Row Number,Calculator ID,Calculator Name,Category,Output Type,Note ID,Note Type,Patient Note,Question,Relevant Entities,Ground Truth Answer,Lower Limit,Upper Limit,Ground Truth Explanation
1,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6477550-1,Extracted,"A 16-year-old female adolescent was referred to our hospital with severe hypertension (systolic pressure 178 mmHg), which was first detected 7 months prior to presentation during a routine annual physical examination. She complained of intermittent headache for about 1 year, and her previous blood pressure, measured 1 month prior to her detection of hypertension, had been normal. She showed mild hypokalemia (3.4 mmol/L) in a routine blood test, and an additional workup considering secondary hypertension was planned. Despite taking amlodipine (0.1 mg/kg twice a day), her blood pressure remained uncontrolled.
Upon admission to our hospital, her systolic and diastolic blood pressures were 155 mmHg (>99th percentile) and 111 mmHg (>99th percentile) respectively. She was 162.8 cm tall (50th–75th percentile) and weighed 55 kg (50th–75th percentile). Physical examination including ophthalmological examination revealed no abnormality other than hypertension, and her family history was negative for hypertension or renal diseases. Laboratory examination revealed normal levels of hemoglobin (14.4 g/dL), serum creatinine (0.57 mg/dL), serum total cholesterol (144 mg/dL), and normal urinalysis. Serum sodium, potassium, chloride, and total carbon dioxide levels were 134 mmol/L, 3.4 mmol/L, 102 mmol/L, and 27 mmol/L, respectively. Plasma renin activity was 9.83 ng/mL/hr (normal, 0.5–3.3 ng/mL/hr), and serum aldosterone level was 77.3 ng/dL (normal, 4–48 ng/dL). Urinary levels of vanillylmandelic acid, epinephrine, norepinephrine, dopamine, metanephrine, and normetanephrine were normal, and plasma levels of epinephrine, norepinephrine, and dopamine were also normal. Chest radiography, electrocardiography, and echocardiography showed normal findings. Renal Doppler ultrasonography revealed an avascular bilobed cyst in the lower pole of the right kidney (). Abdominal computed tomography (CT) angiography showed bilaterally normal renal arteries and an eccentric soft tissue component at the peripheral aspect of the cystic lesion (). The mass remained unenhanced during the arterial phase, and its margin was indistinguishable from the surrounding tissue (). During the delayed phase, its eccentric capsule showed enhancement, and an intact mass could be observed (), consistent with CT findings of JGC tumors.
A right partial nephrectomy was performed, and a clear resection margin was identified. The well-encapsulated mass measured 2.5 cm ×2.2 cm×2.0 cm in size with a partially cystic-appearing cut surface. Microscopic examination revealed sheets of polygonal tumor cells with amphophilic cytoplasm. Immunohistochemical examination showed that the tumor cells stained positive for CD34 and focally positive for CD117 (C-Kit) and smooth muscle actin. ()
Postoperatively, her blood pressure returned to normal (105/63 mmHg) without using any antihypertensive medication. On the 3rd postoperative day, the plasma renin activity (0.52 ng/mL/hr), serum aldosterone (3.9 ng/dL), and serum potassium (3.6 mmol/L) levels returned to normal. Her blood pressure and laboratory findings remained within the reference range over the next 3 years postoperatively until her last follow-up.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [55.0, 'kg'], 'height': [162.8, 'cm'], 'creatinine': [0.57, 'mg/dL'], 'age': [16, 'years']}",141.0403,133.98828,148.09232,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 16 years old. 
The concentration of creatinine is 0.57 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.8 cm, which is 162.8 cm * 1 m / 100 cm = 1.628 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.628 m * 1.628 m) = 20.75171 kg/m^2.The patient's BMI is 20.8, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 54.9174 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 16) * 54.9174 * 0.85) / (0.57 * 72) = 141.0403 mL/min. Hence, the patient's creatinine clearance is 141.0403 mL/min."
2,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-3597915-1,Extracted,"A 56-year-old man was admitted to the renal unit of the tertiary university hospital with symptoms of polyuria with nocturia, and polydipsia with severe thirst for the past 2 months. Initially, the patient visited a local clinic and was diagnosed as type 2 DM with a fasting blood sugar, 150mg/dL. Despite being controlled hyperglycemia with an oral hypoglycemic agent, he continued drinking daily more than 8 L of cold water (about 10 bottles of refrigerated water, 750 ml capacity) and passed large amounts of urine frequently. He had no specific history including head trauma or mental disorder, and denied any pertinent family history. The patient showed no signs of systemic illness such as fever or arthralgia, or neurologic symptoms involving the central nervous system. He has been working as a gardener with 176 cm in height and 68 kg in weight (71 kg before this event). The physical examination was unremarkable with blood pressure of 132/70 mmHg, pulse rate of 80/min, respiratory rate of 16/min, and temperature of 36.8℃. In the laboratory findings, his white blood cell count was 9,700/mm3; hemoglobin, 13.4 g/dL; platelet, 376×103/mm3; sodium, 140 mEq/L; potassium, 3.8 mEq/L; blood urea nitrogen (BUN), 12 mg/dL; creatinine, 1.0 mg/dL and osmolality 295 mOsm/kg water. HbA1c was 7.2% and post-prandial glucose was checked around 180mg/dl with fasting blood sugar of 140 mg/dL. In urine analysis, the urine pH was 6.0; specific gravity 1.006; albumin (-); glucose (-); WBC 0-4/HPF; RBC 0-2/HPF, and osmolality 140mOsm/kg water. Fluid intake and output in 24 hours recorded 9 L in oral water intake from water containers and 11.7 L in urine output. In hormone assays, ACTH was 25.2 pg/mL (reference value, 6.0-76.0 pg/mL), prolactin 8 µg/L (reference value, 0-15 µg/L), cortisol 9.8 µg/dL (referencel value, 5-25 µg/dL), hGH 2.26 ng/mL (reference value, 0.5-17 ng/mL), and TSH 0.99 µU/mL (reference value, 0.5-4.7 µU/mL). Also, angiotensin converting enzyme (ACE) activity was within normal range (reference value, <40 U/L).
On hospital day 5, the patient underwent a water deprivation test according to the method of Miller-Moses test because of persistent polydipsia and polyuria despite blood glucose control. The results are shown in . During dehydration, the patient lost 3kg (4.4% of body weight), and urine osmolality remained hypotonic below 130 mOsm/kg. Basal ADH level was 5.18 pg/dL, and the repeat ADH level following the stimulation by water deprivation was 3.95 pg/dL, which revealed no increment despite the increased serum osmolality up to 300 mOsm/kg from the baseline levels of 285 to 295 mOsm/kg. One puff (5 µg) of desmopressin nasal spray resulted in the increase of urine osmolality to 266 mOsm/kg (>100% increase from the baseline level, 126 mOsm/kg) and in the marked reduction of urine output from 200-410 ml/hr to 44-60 ml/hr. These results were compatible with CDI,, whose causes would be mostly idiopathic because of normal findings in hypothalamus and hypophysis in magnetic resonance imaging (MRI) scan of sella ().
On discharge (hospital day 9), the dose of desmopressin nasal spray (minirin nasal spray®) was adjusted to 1 puff per 12 hrs (10 µg/day), and urine output was markedly reduced to below 2-3 L/day with no more intense thirst. Also, DM was controlled with fasting blood sugar below 115 mg/dL by metformin (novamet GR® 500mg bid) and American Diabetes Association (ADA) recommended diet.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [56, 'years'], 'weight': [68.0, 'kg'], 'height': [176.0, 'cm'], 'creatinine': [1.0, 'mg/dL']}",79.33333,75.36666,83.3,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 56 years old. 
The concentration of creatinine is 1.0 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 176.0 cm, which is 176.0 cm * 1 m / 100 cm = 1.76 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.76 m * 1.76 m) = 21.95248 kg/m^2.The patient's BMI is 22.0, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 68.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 56) * 68.0 * 1) / (1.0 * 72) = 79.33333 mL/min. Hence, the patient's creatinine clearance is 79.33333 mL/min."
3,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-2813128-1,Extracted,"A 34-year-old man was admitted for evaluation of worsening pedal edema. He was apparently healthy until four years back, when he developed edema of both feet and nonpruritic macular skin rash involving both lower limbs. Subsequently, he was detected to have hypertension, proteinuria and mild renal failure (6 months ago). He had no history of arthralgia, Raynaud's phenomenon, paraesthesia or gastrointestinal hemorrhage.
Six weeks prior to admission in our centre, he developed weakness of left upper and lower limbs with slurring of speech and was hospitalized elsewhere. A computerized tomographic scan of head had revealed an infarct in the right middle cerebral artery territory and he was treated with aspirin, statins, and antihypertensives. He made a complete recovery but was detected to have renal failure and was referred to us for further evaluation.
He weighed 74 kg and had a height of 174 cm. He had pallor and bilateral pitting pedal edema. There was no skin rash or lymphadenopathy. Blood pressure was 140/90 mmHg. Examination of cardiovascular system, respiratory system, and abdomen was normal. There were no neurological deficits.
Investigations revealed hemoglobin of 8.79 gm/dL, platelet count of 112000/mm3, total WBC count of 7960/mm3 - with a normal differential count, ESR of 40 mm at end of first hour. Urinalysis showed protein ++++, 6-8 RBCs/HPF; and 24 hour urine protein was 4420 mg. Blood urea was 72 mg/dL and serum creatinine was 3.1 mg/dL with normal serum levels of electrolytes. Liver function tests, PT and aPTT were normal. Serum albumin was 3.6 gm%, serum globulin 3.8 g/dL and serum cholesterol 240 mg/dL. Serum protein electrophoresis was normal. Blood and urine cultures were sterile. HBsAg, antihepatitis C virus (HCV) and HIV antibodies were negative VDRL, cANCA, pANCA, antiphospholipid antibodies, ANA, antids DNA were negative. Serum homocysteine [12 µmol/L] was normal and serum complement levels were reduced (C3:70 mg/dL, C4:18 mg/dL). Serum cryoglobulin assay was positive. On PAGE electrophoresis, the mobility was suggestive of mixed cryoglobulins. HCV RNA was negative in serum [polymerase chain reaction (PCR)]. Qualitative analysis for HCV RNA [by reverse transcriptase-PCR (RT-PCR)] in the cryoprecipitate was negative []. Doppler study of extra cranial carotid and vertebral vessels was normal. Ultra sonogram of abdomen, ECG, and echocardiogram were normal. Bone marrow examination was normal. X-rays of chest, skull spine, and pelvis were normal. Kidney biopsy showed lobular accentuation of glomeruli with mesangial proliferation, mild endocapillary proliferation, and double contour of glomerular basement membrane on light microscopy. Intracapillary eosinophilic PAS positive hyaline deposits were noted []. Interstitium showed mononuclear infiltrates. Immunofluorescence showed mesangial and capillary granular positivity for C3 IgG and IgM.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [34, 'years'], 'weight': [74.0, 'kg'], 'height': [174.0, 'cm'], 'creatinine': [3.1, 'mg/dL']}",33.03435,31.38263,34.68607,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 34 years old. 
The concentration of creatinine is 3.1 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 174.0 cm, which is 174.0 cm * 1 m / 100 cm = 1.74 m. The patient's weight is 74.0 kg. The patient's bmi is therefore 74.0 kg / (1.74 m * 1.74 m) = 24.4418 kg/m^2.The patient's BMI is 24.4, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 69.55913 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 34) * 69.55913 * 1) / (3.1 * 72) = 33.03435 mL/min. Hence, the patient's creatinine clearance is 33.03435 mL/min."
4,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5544981-1,Extracted,"A 67-year-old Japanese woman underwent OWHTO to treat SPONK that had occurred in the left medial femoral condyle (Fig. ). The patient reported the following history of the present illness. Pain in the left knee joint initially occurred at 1 year and 4 months before admission, without any particular trigger. Her former treating physician had provided conservative treatments such as oral administration of anti-inflammatory analgesics, rehabilitation including quadriceps muscle training, and guidance on the use of a cane to relieve weight bearing. However, this treatment was not successful in relieving her symptoms, and she was referred to our department for surgery. The patient had a history of hypertension and hyperlipidemia, and she had been taking oral candesartan and atorvastatin. The patient was a housewife with no noteworthy aspects related to social, family, or environmental history. On physical examination, the patient had a height of 157 cm, a body weight of 62 kg, and a body mass index of 25.2 kg/m2. She reported feeling pain in the medial joint space of the knee during walking, as well as during climbing or descending stairs. At the time of the first admission, her systolic/diastolic blood pressure was 165/97 mmHg. Table provides an overview of the patient’s pain scores in the knee joint, ROM of the knee joint, and knee joint function. Neurological examination revealed no abnormal findings. Similarly, laboratory findings at the time of the first admission did not indicate any abnormality: total protein 7.3 g/dl, albumin 4.6 g/dl, aspartate aminotransferase 22 U/L, alanine aminotransferase 18 U/L, lactate dehydrogenase 213 U/L, alkaline phosphatase 297 U/L, γ-glutamyl transferase 18 U/L, total bilirubin 0.6 mg/dl, Na 142 mEq/L, Cl 104 mEq/L, K 4.5 mEq/L, blood urea nitrogen 21.4 mg/dl, creatinine 0.56 mg/dl, Ca 9.7 mg/dl, inorganic phosphorus 3.7 mg/dl, leukocytes 5100/μl, erythrocytes 5.00 × 106/μl, hemoglobin 14.4 g/dl, hematocrit 43.6%, and platelets 263 × 103/μl.
The HAL-SJ treatment program was divided into five phases []. Phase 1 consisted of preoperative observation from the day of hospital admission until the day of surgery. The patient’s thigh circumference and lower leg length were measured preoperatively to adjust the HAL-SJ to the patient’s physical size, which would ensure appropriate training. We palpated the patient’s quadriceps muscles (vastus medialis, rectus femoris, and vastus lateralis) and attached electrodes to each muscle to detect the bioelectric potentials of the long axis along the belly of each muscle. We instructed the patient to perform knee extension and to contract her quadriceps. On the basis of these data, we instructed the patient to simulate the knee extension training, which would be performed postoperatively. Specifically, the patient sat with her lower leg hanging down naturally, and the height of the chair was adjusted so that the patient’s feet were not in contact with the floor. The patient performed ten knee extensions with HAL-SJ assistance, using the muscle that exhibited the largest bioelectric potential amplitude.
Phase 2 involved surgery (day of surgery). The patient underwent OWHTO (Figs. and ) using TomoFix (DePuy Synthes, Bettlach, Switzerland), artificial bone (OSferion60, β-tricalcium phosphate; Olympus Terumo Biomaterials, Tokyo, Japan), and biplanar osteotomy, as described by Takeuchi et al. []. The preoperative weight-bearing line (WBL) percentage [], calculated on the basis of an anteroposterior weight-bearing radiograph of the affected leg in full knee extension, was 29.6%. The surgery was planned with a target postoperative WBL percentage of 62.5%. The actual enlarged angle and distance of osteotomy were 5.5 degrees and 7 mm, respectively.
Phase 3 consisted of postoperative observation from day 1 to day 7 postoperatively. For postoperative rehabilitation, partial weight bearing was allowed after a non-weight-bearing period of 2 weeks, and full weight bearing began at 4 weeks postoperatively. The patient received rehabilitation training under the guidance of a physical therapist (ROM exercises and muscle-strengthening training) for 20–40 minutes each day, 5 days per week, from the first postoperative day until discharge. For ROM exercises, continuous passive motion training began on the first postoperative day for 1 hour per day and continued every day until discharge. On postoperative day 7, we attached electrodes to the quadriceps muscle to detect the bioelectric potential along the long axis of the rectus femoris muscle belly (Fig. ). Then, the patient was instructed to perform active knee extension exercises that involved contracting her quadriceps, thus simulating training with HAL-SJ (Fig. ).
Phase 4 consisted of HAL-SJ therapy from postoperative day 8 to discharge. The CVC mode of HAL-SJ serves to support the patient’s voluntary motion on the basis of voluntary muscle activity and the assistive torque provided to the knee joint []. In this study, we used the CVC mode, which allowed the operator to adjust the degree of physical support to maintain the patient’s comfort while gradually reducing support as training progressed. In addition to the regular rehabilitation program (Fig. ), the patient performed HAL-JS-assisted knee extension exercises while sitting, which consisted of five sets of ten repetitions per set, twice per week (Fig. ). The training was performed six times before the patient was discharged (postoperative days 8, 10, 15, 17, 22, and 24). The mean training duration, including the time required to put on the HAL-SJ, was 15.5 ± 1.4 minutes (15 minutes, 16 minutes, 17 minutes, 16 minutes, 13 minutes, and 16 minutes during training sessions 1, 2, 3, 4, 5, and 6, respectively). There were no adverse events related to the use of HAL-SJ, and the patient was discharged 30 days after the surgery.
Phase 5 consisted of post-HAL-SJ therapy observation from discharge until 3 months after the end of HAL-SJ therapy, during which the following indicators were assessed: EL, assessed as the difference between the maximum knee joint extension angle during passive exercise and that during active exercise; knee pain rated on the visual analogue scale (VAS); isometric knee extension muscle strength (IKEMS); active ROM before surgery, before and after HAL-SJ training, and at 1 and 3 months after the end of training; and the Japanese Orthopaedic Association (JOA) score [] before surgery, at discharge, and at 1 and 3 months after the end of training. Furthermore, we used lateral radiographs to measure the tibial slope angle (TSA) and Insall-Salvati ratio (ISR) as indicators of patellar tendon shortening before surgery and after implant removal at 1 year after the operation [] (Fig. ). Measurement of knee ROM was performed using goniometry, and the landmarks used in the measurements were the greater trochanter of the femur, proximal head of the fibula, and lateral malleolus. Goniometry was used because it has been reported that goniometric measurements of ROM are more reliable than visual observation, with an accuracy of up to 1.0 degree []. The maximal IKEMS of the operated leg was assessed with the patient in a sitting position, with the hips and knees flexed at 90 degrees. A μTas F-1 handheld dynamometer (Anima Corp., Tokyo, Japan) was fixed to the chair, and two measurements were recorded. Each trial lasted 3–5 seconds, with 30 seconds of rest between trials. The higher score of two valid trials was recorded. All measurements were performed by a single trained physical therapist to eliminate interobserver variability. The EL, VAS, IKEMS, and ROM results are shown in Table . The EL improved from 3 degrees preoperatively to 0 degrees at the end of the sixth HAL-SJ training session, but it returned to 3 degrees at 1 and 3 months after the end of the training. When we compared results obtained before training against those obtained after each of the six training sessions, we observed that three sessions produced improved EL and three sessions produced improved or relatively constant VAS scores immediately after training. However, for the other three sessions, the patient reported increased pain immediately after training, with the greatest increase in pain reported immediately after the first HAL-SJ training session, when the VAS score was 1.7 times higher immediately after training than before training. The EL improved after training sessions 1 and 3, when the patient reported increased knee pain (expressed as the VAS score). However, the EL did not change after training sessions 2 and 4, when the patient reported less knee pain (improved VAS score immediately after training). The patient did not refuse to undergo training because of increased pain. The IKEMS value was the largest preoperatively (17.6 kgf) and decreased to its lowest value (30% of the preoperative strength) before the first HAL-SJ intervention at 8 days after the operation. The IKEMS remained relatively constant throughout HAL-SJ training but recovered to the preoperative value during follow-up (18.7 and 16.6 kgf at 1 and 3 months, respectively, after completion of HAL-SJ training). The active ROM also recovered to the preoperative value by the end of the sixth HAL-SJ training session. Thereafter, the extension ROM did not change, but the flexion ROM was maintained or improved. The JOA score decreased from 60 points preoperatively to 55 points at discharge, but it improved with time, reaching 65 and 85 points at 1 and 3 months, respectively, after the end of HAL-SJ training. Whereas the TSA was maintained at 13.1 degrees before and after the surgery, the ISR decreased from 1.13 preoperatively to 0.97 postoperatively. At 6 months after surgery, the passive ROM was 0–135 degrees, and the JOA score was 90 points. There were no complications throughout the preparation, surgery, or rehabilitation process.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [62.0, 'kg'], 'height': [157.0, 'cm'], 'creatinine': [0.56, 'mg/dL'], 'age': [67, 'years']}",84.0249,79.82366,88.22615,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 67 years old. 
The concentration of creatinine is 0.56 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 157.0 cm, which is 157.0 cm * 1 m / 100 cm = 1.57 m. The patient's weight is 62.0 kg. The patient's bmi is therefore 62.0 kg / (1.57 m * 1.57 m) = 25.15315 kg/m^2.The patient's BMI is 25.2, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 157.0 cm, which is 157.0 cm * 0.393701 in/cm = 61.81106 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.81106 (in inches) - 60) = 49.66544 kg.
Hence, the patient's IBW is 49.66544 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 49.66544 kg + 0.4 * (62.0 kg  - 49.66544 kg) = 54.59926 kg. The patient's adjusted body weight is 54.59926 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 67) * 54.59926 * 0.85) / (0.56 * 72) = 84.0249 mL/min. Hence, the patient's creatinine clearance is 84.0249 mL/min."
5,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-8217860-1,Extracted,"This is a 61-year-old woman who presented with diabetic symptoms and was misclassified as having type 1 diabetes with negative autoimmune-related type 1 diabetes antibodies (Tyrosine Phosphatase antibodies and Glutamic acid Decarboxylase antibodies). She was referred to our center due to uncontrolled diabetes despite the high doses of insulin and the coexistence of severe insulin resistance and decreased body mass index (BMI: 19.4 kg/m2). Age of presentation was 29 years and for the following 30 years she was treated with multiple daily insulin injections with high insulin requirements (5 IU/kg/day) together with metformin 2 g/day for 30 years, but constantly displaying poor glycemic control. Dyslipidemia was observed at the age of 35 years with raised cholesterol levels and severe hypertriglyceridemia despite intense lipid lowering therapy which lately consisted of the combination of fenofibrate 145 mg, rosuvastatin 40 mg/day and omega-3 fatty acids/day together with restricted fat intake. Hypertension was observed at the age of 5 years, and lately treated with the combination of nifedipine 120 mg/day, eplerenone 25 mg/day and hydrochlorothiazide 25 mg/day.
She also had micro- and macrovascular complications of diabetes indicating constantly insufficient glycemic control. She presented peripheral diabetic neuropathy (distal symmetric polyneuropathy) and nephropathy (eGFR: 43 ml/min, albuminuria: 314 mg/24 h). She also suffered from severe cardiovascular disease including peripheral artery disease and hypertrophic cardiomyopathy. Peripheral artery disease presented as intermittent claudication and carotid stenosis, for which she had a right carotid endarterectomy at the age of 52 years old. She was managed with clopidogrel 75 mg/day.
She had menarche at the age of 11, followed by irregular menstruation and then premature menopause at the age of 38. She also reported polycystic ovarian syndrome and never conceived. She underwent hysterectomy due to fibroids at the age of 54. She was diagnosed with osteoporosis at the age of 58 and has since received alendronate 70 mg/week.
It has not been possible to conduct genetic family screening. Her mother and her maternal aunt displayed a lipodystrophy phenotype with fat loss of upper and lower extremities, presented diabetes from the ages of 25 and 28 respectively, and both showed early presentation of cardiovascular disease, presenting as ischemic stroke at the age of 45 years old and myocardial infarction at the same age, respectively. Her mother had reproductive problems and six miscarriages. Two out of four sisters and one brother developed hypertension and dyslipidemia at a young age.
A genetic analysis for lipodystrophy was performed and included the sequence and deletion/duplication analysis of the following genes: ADRA2A, AGPAT2, AKT2, BSCL2, CAV1, CAVIN1, CIDEC, FBN1, KCNJ6, LIPE, LMNA, LMNB2, PCYT1A, PIK3R1, PLIN1, POLD1, PPARG, PSMB8, and ZMPSTE24. The analysis revealed a novel heterozygous mutation in the PPARG gene (c470A>G, p. Glu157Gly, exon3) (The University of Chicago Genetic Services Laboratory). This particular amino acid change has not been described in other patients with PPARG-related disorders, but a different pathogenic sequence change affecting the same amino acid residue (p. Glu157Asp) has been described in a family with PPARG-related lipodystrophy (). In our case the substitution of the negative charged glutamic acid at position 157 by the hydrophobic glycine could possibly lead to the formation of a non-functional protein responsible for the lipodystrophy phenotype. According to missense interpretation by experimental report classifier (MITER) the described mutation is associated with 78.6% probability of causing FPLD3 and 6.5-fold increased risk for type 2 diabetes mellitus.
Examination revealed clinical signs of lipodystrophy of upper and lower limbs and gluteal area. Facial fat and abdominal prominence were also noted. She also had phlebectasia, hirsutism and cervical acanthosis nigricans. The patient mentioned that this phenotype was present from the age of 20 years old. Blood pressure was 175/84 mmHg.She was underweighted with a BMI: 19.40 kg/m2 (weight: 46 kg, height: 154 cm) ().
To assess the degree of regional fat loss in this case, we compared the total and proportional fat content in defined body regions using Dual-energy X-ray absorptiometry (DXA) with a group of healthy, lean postmenopausal women (). The case has a relatively short stature and as a consequence a total lean mass not far from the lower end the 95% confidence interval of the comparators. The total fat mass was drastically lower giving a first indication of a lipodystrophic state. The visceral fat mass was similar to the comparators whilst the proportional fat content in extremities was drastically reduced showing the classic features of peripheral fat loss in partial lipodystrophy ().
At the time of the first evaluation biochemical measurements revealed glycated hemoglobin (HbA1C) of 10%, a total cholesterol of 132 mg/dl of which high density lipoprotein (HDL-C) was 25 mg/dl. There was severe hypertriglyceridemia at 2.919 mg/dl. Further tests confirmed chronic kidney disease (blood urea nitrogen: 49.6 mg/dl, creatinine: 1.3 mg/dl) and albuminuria (314 mg/24 h).
We performed glucagon stimulation test which revealed residual insulin secretion (fasting C-peptide: 2.09 ng/ml, 6 min after 1 mg of glucagon infusion C-peptide: 3.13 ng/ml). Plasma leptin concentration was close to zero (0.43 ng/ml).
Abdominal ultrasound confirmed hepatic steatosis and transient elastography (fibroscan) detected liver stiffness of 18 Kpa. Abdominal Magnetic Resonance Imaging (MRI) was unremarkable apart from hepatomegaly with a liver percentage fat fraction of 9.4%, and an enlarged spleen (). Cardiac MRI revealed left ventricular hypertrophy (maximal wall thickness 17 mm) and myocardial fibrosis in the basal interventricular septum (LGE SCORE 1/48, LGE mass 2%). Two-dimensional echocardiography revealed severe left ventricular hypertrophy, minimal mitral regurgitation, and ejection fraction of 60% ().
After noting her poor glycemic control, her antidiabetic treatment was intensified with empagliflozin 10 mg/daily and liraglutide 1.8 mg/daily, but this resulted only in a slight improvement in glycemic control after 3 months (HbA1c: 9.3%), despite additional strict dietetic management, but without any change in insulin management. We did not observe any change in triglyceride (TG) levels.
Metreleptin was then initiated at 5 mg once daily on top of the current lipid and diabetes management. Glycemic control and hypertriglyceridemia improved within two months of treatment evidenced by decrease of HbA1C from 10 to 8.7% and the reduction of TG from a baseline value of 2.919 to 242 mg/dl. At six months there was further reduction in HbA1C (7.9%) and in TG (198 mg/dl). This improvement was sustained one year after treatment with metreleptin in the same dose (HbA1C: 8%, TG: 185 mg/dl-standard serum determinations are listed in ), (). Insulin doses were reduced from more than 5 to 2.22 IU/kg/day. Blood pressure was also better controlled without any change in anti-hypertensive medication.
At six months of metreleptin treatment a reduced liver fat content was observed (MRI estimated liver percentage fat fraction was reduced from 9.4 to 6.8%). However, liver stiffness assessed by transient elastography remained stable. A repeated DXA scan showed unchanged total fat mass content and cardiac MRI revealed no change (). Reduction in appetite following metreleptin treatment was reported. Hunger scales for the assessment of appetite were not used. Metreleptin treatment was well tolerated with no other adverse effects.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [61, 'years'], 'weight': [46.0, 'kg'], 'height': [154.0, 'cm'], 'creatinine': [1.3, 'mg/dL']}",33.00107,31.35102,34.65112,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 61 years old. 
The concentration of creatinine is 1.3 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 154.0 cm, which is 154.0 cm * 1 m / 100 cm = 1.54 m. The patient's weight is 46.0 kg. The patient's bmi is therefore 46.0 kg / (1.54 m * 1.54 m) = 19.39619 kg/m^2.The patient's BMI is 19.4, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 46.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 61) * 46.0 * 0.85) / (1.3 * 72) = 33.00107 mL/min. Hence, the patient's creatinine clearance is 33.00107 mL/min."
6,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6197009-1,Extracted,"A 51-year-old lady presented to our emergency department because of generalized body ache and marked weakness in both lower extremities for two days duration. She had no history of vomiting, diarrhea, frequent urination, recent use of laxatives or diuretics, current or previous use of lithium, licorice ingestion, or activities leading to profuse sweating. Past medical history was significant for type 2 diabetes mellitus, hypertension, seizure disorder and schizoaffective disorder. She also had a long-term history of alcoholism, consuming two to three pints of vodka every day for about 20 years. Her last drink of alcohol was about 48 hours prior to presentation. On examination, her weight was 79 kg, height 65 inches, body mass index 29.3 kg/m2. Vital signs were stable, temp 98.6°F, heart rate 68 bpm, respiratory rate 18, blood pressure 113/71 mmHg and oxygen saturation 98% on room air. She was alert and oriented, there was no thyromegaly or lymphadenopathy. Cardiac examination revealed a regular sinus rhythm with no murmurs. There were no deformities or edema of the extremities and distal pulses were present. There was no cushingoid facies, buffalo hump or abdominal striae noted. Neurological examination revealed bilateral lower limb weakness of 4/5, with intact sensory system and reflexes. Cranial nerve examination was unremarkable.
Biochemical analysis of the serum showed severe electrolyte disturbances, a potassium level of 2.3 mmol/L (reference 3.6−5.1 mmol/L), magnesium level of 0.9 mg/dL (reference 1.8−3.0 mg/dL), phosphorus level of 2.0 mg/dL (reference 2.4−4.6 mg/dL), corrected calcium level of 7.8 mg/dL (reference 8.9−10.3 mg/dL). Renal function was mildly deranged with Creatinine of 1.35 mg/dL (reference 0.4−1.3 mg/dL) and BUN of 12 mg/dL (reference 8−20mg/dL). The results of hepatic enzymes, AST 113 IU/l (reference 15−41 IU/l), ALT 42 IU/l (reference 17−63 IU/l) was suggestive of alcohol induced hepatic damage. Electrocardiogram (ECG) () showed no arrhythmias, but changes characteristic of hypokalemia with increased amplitude of the U-wave and marked corrected QT segment prolongation (QTc 551 ms). Patient was admitted to intensive care unit for severe hypokalemia management and cardiac monitoring. Aggressive supplementation of electrolytes was initiated (), however despite supplementation with enteral and parenteral potassium as well as magnesium and phosphate, potassium level failed to increase () and subsequently she had a sinus bradycardia followed by asystole. Cardiopulmonary resuscitation was initiated when asystole was noted, return of spontaneous circulation was obtained after 8 minutes of resuscitation. Patient was mechanically ventilated for two days and her own efficient respiration was reestablished, then she was successfully extubated. During the following days, the patient was conscious, alert and oriented to time, place and person. Further laboratory testing revealed thyroid- stimulating hormone level was 1.100 mIU/L (reference 0.45−4.50 mIU/L). Active renin level was 0.653ng/ml/hr (reference 0.167−5.38 ng/ml/hr), aldosterone levels was <0.01 ng/dL (reference 0.00− 30 ng/dL). Creatine kinase (CK) level was 6922 U/L (reference 38–297 IU/L), indicating rhabdomyolysis. The arterial blood gas analysis revealed pH of 7.430, partial pressure of carbon dioxide was 29 mmHg; partial pressure of oxygen was 74 mmHg; HCO3 was 25 mmol/L and base excess of -4.7 mmol/L. Urinalysis showed dilute urine of 1.010 g/mL specific gravity (reference 1.005 to 1.030), Urine pH of 6.5, and no proteinuria. Urine electrolytes were measured on spot urine analysis and twenty-four-hour urine collection, result depicted in . Serial electrocardiogram monitoring showed resolution of ECG changes (). Follow up laboratory tests revealed normalization of electrolytes level (). Post cardiac arrest serial ECGs didn’t reveal any ischemic changes, cardiac enzymes were not elevated and echocardiogram revealed normal left ventricular systolic function, Ejection Fraction of 60–65%. Cardiac arrest was presumed to be secondary to severe hypokalemia and there was no necessity for further cardiac evaluation. She was then discharged from the hospital with recommendations for abstinence from alcohol. Follow up outpatient appointment with primary care physician was provided.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [79.0, 'kg'], 'height': [65.0, 'in'], 'creatinine': [1.35, 'mg/dL'], 'age': [51, 'years']}",51.21163,48.65105,53.77221,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 51 years old. 
The concentration of creatinine is 1.35 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 65.0 in, which is 65.0 in * 0.0254 m / in = 1.651 m. The patient's weight is 79.0 kg. The patient's bmi is therefore 79.0 kg / (1.651 m * 1.651 m) = 28.98231 kg/m^2.The patient's BMI is 29.0, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 65.0 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (65.0 (in inches) - 60) = 57.0 kg.
Hence, the patient's IBW is 57.0 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 57.0 kg + 0.4 * (79.0 kg  - 57.0 kg) = 65.8 kg. The patient's adjusted body weight is 65.8 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 51) * 65.8 * 0.85) / (1.35 * 72) = 51.21163 mL/min. Hence, the patient's creatinine clearance is 51.21163 mL/min."
7,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-2547098-1,Extracted,"A 43-years-old Caucasian male (height 198 cm, weight 115 kg, tobacco smoker – 1 packet of cigarettes/day) was admitted to the intensive care unit (ICU) of a university hospital from a municipal hospital because of multiorgan dysfunction syndrome associated with infection and necrosis of the skin, subcutaneous tissue, and fascia of the left lower leg. The signs and symptoms of the disease – edema and pain affecting the left leg-began 7 days before admission. The patient's medical history was significant for hepatitis C (HCV), treated with ribavarin and interferon, and diabetes mellitus treated with insulin. On the day of admission the HCV-RNA test was negative. A mosquito bite was the probable triggering event.
On admission to the ICU the patient was confused, with a Glasgow Coma Scale (GCS) of 9. He was afebrile, had tachycardia, with a heart rate of 120 beats per minute, hypotension, with a blood pressure of 90/50 mmHg, and relative respiratory insufficiency (oxygen saturation of 88% – 90%). He had moderately-dilated pupils with a delayed light reflex. We noted crepitus over the bilateral lung fields, a tender abdomen with absent bowel sounds, and oliguria. There were numerous hemorrhagic extravasations on the skin. Examination of the left leg revealed diffuse edema of the skin, with marked erythema and necrosis; margins of infection were sharply demarcated, spreading onto the buttock and perineum on the left side (Figure ). Laboratory tests showed a metabolic acidosis, with the following values: base excess -15 mmol/l, lactate level 7.3 mmol/l, PaO2 64 mmHg, platelet count 29,000/mm3, International Normalized Ratio (INR) 2.24, serum creatinine 691.6 μmol/l, bilirubin 62.6 μmol/l, and C-reactive Protein (CRP) 224.6 μg/dl.
The Acute Physiology and Chronic Health Evaluation (APACHE) II score on the day of admission was 31 points and the Sequential Organ Failure Assessment (SOFA) score was 18 points. The patient required fluid resuscitation, endotracheal intubation, mechanical ventilation in BiPAP (bilevel positive airway pressure) mode, continuous intravenous infusion of catecholamines (epinephrine, norepinephrine) and low doses of steroids to restore blood pressure. After obtaining cultures from the affected tissue, blood and bronchoalveolar lavage (BAL) in appropriate media, empirical, broad-spectrum antibiotics were immediately administered (meropenem 3 g/day in a 3-h infusion, vancomycin 3 g/day in continuous infusion, metronidazole 1.5/day in 3 divided doses). Because of progressive organ dysfunction, therapy was started with activated protein C, in doses of 24 μg/kg/h; continuous veno-venous hemofiltration (CVVH) was also started. After several hours, the patient developed atrial fibrillation with a ventricular rate of 140 beats per minute and his blood pressure decreased to 80/50 mmHg. Electrical cardioversion was performed three times, followed by continuous infusion of cordarone (12 mg/kg/day). During this time, intensive fluid resuscitation was administered. During the first day, the patient received 12,800 ml of fluid (colloids and crystalloids). His unstable condition did not allow for early surgical management.
The cultures from the affected areas of skin contained Streptococcus pyogenes and Staphylococcus sciuri. Based on sensitivity results, vancomycin and metronidazole were discontinued, and penicillin G was started at a dose of 60 million units a day (intravenous) in 6 divided doses. Because the patient's poor condition persisted and the microbes were sensitive to clindamycin, it was added at 2.7 g/day in 3 divided doses. In spite of the lack of information about G-pathogens, meropenem was continued. The patient also received 40 g of commercially available gamma-globulin (intravenous), 8 units of packed red blood cells, 6 units of fresh frozen plasma, and 8 units of platelets. After several days his condition improved, with urine output of 100–150 ml/h and resolution of his metabolic acidosis. On the sixth day, the patient's hemodynamic parameters deteriorated again, with tachycardia to 160 beats per minute and a decrease in blood pressure to 85/60 mmHg. CVVH was administered again for detoxification. On the seventh day, the necrotic tissue was surgically excised (Figures , ). We also noted a progressive decline in the white blood cell count to 2,200/mm3, and administered granulocyte colony stimulating factor.
Cultures of the BAL showed 104 colony-forming units/ml of methycillin resistant Staphylococcus aureus (MRSA). (The patient had been a carrier of methycillin susceptible Staphylococcus aureus [MSSA] isolated from his nose vestibule on admission.) Because MRSA also was present in blood cultures and the patient's condition remained poor, linezolid 1.2 g a day in 2 divided doses was initiated based on additional results of susceptibility tests. After 10 days of intensive treatment, the patient was hemodynamically stable, and we discontinued mechanical ventilation. 25 days after admission the patient was discharged to the trauma surgery ward for plastic reconstruction of his wounds.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [43, 'years'], 'weight': [115.0, 'kg'], 'height': [198.0, 'cm'], 'creatinine': [691.6, 'µmol/L']}",17.39476,16.52502,18.2645,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 43 years old. 
The concentration of creatinine is 691.6 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 691.6 µmol. To convert 691.6 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 691.6 µmol creatinine * 1e-06 mol/µmol = 0.00069 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00069 mol creatinine * 113.12 g/mol = 0.07805 g creatinine. To convert 0.07805 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.07805 g creatinine * 1000.0 mg/g = 78.05 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 78.05 mg creatinine/10.0 dL = 7.805 mg creatinine/dL. The concentration value of 691.6 µmol creatinine/L converts to 7.805 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 198.0 cm, which is 198.0 cm * 1 m / 100 cm = 1.98 m. The patient's weight is 115.0 kg. The patient's bmi is therefore 115.0 kg / (1.98 m * 1.98 m) = 29.33374 kg/m^2.The patient's BMI is 29.3, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 198.0 cm, which is 198.0 cm * 0.393701 in/cm = 77.9528 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (77.9528 (in inches) - 60) = 91.29144 kg.
Hence, the patient's IBW is 91.29144 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 91.29144 kg + 0.4 * (115.0 kg  - 91.29144 kg) = 100.77486 kg. The patient's adjusted body weight is 100.77486 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 43) * 100.77486 * 1) / (7.805 * 72) = 17.39476 mL/min. Hence, the patient's creatinine clearance is 17.39476 mL/min."
8,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6408197-1,Extracted,"A 65-year-old female consulted our office for naturopathic primary-care support for a myriad of conditions, which included diabetes with weight gain, chronic fatigue, depression with emotional lability, frequent colds, and recurrent urinary tract infections. The latter was attributed to a medullary sponge kidney as was her history of kidney stones and hypertension. The patient also suffered with long-standing acid reflux and was prone to irritable bowel with diarrhea. She had also suffered with multiple abscesses in the past as well as poor generalized wound healing. A history of fibroadenomas was also noted. The patient recollected, “never being well”, even as a child. She described her diet as a child as “deficient” and consisted mostly of canned beans and bread, which she attributed to her poor socioeconomic status as a child.
Pharmacological management of her diabetic condition included the use of metformin/sitagliptin (1,000 mg/50 mg, taken twice per day) and gliclazide (30 mg), also taken twice per day.
Additional medications included ramipril (5 mg/day), ranitidine (150 mg, twice per day), low-dose aspirin (81 mg/ day), hydrochlorothiazide (25 mg/day), allopurinol (100 mg/ day), citalopram (40 mg/day), and mirabegron (50 mg/day).
Physical examination revealed a 1.69 m (66.5 inch), 88.5 kg (195.0 lb) female. Body mass index was calculated at 31.0 (Obese Class I) (32). Central waist measurement was 112 cm, while her hips measured 118 cm. Blood pressure was 114/64 mmHg, measured at the left brachial artery. Bioimpedance analysis revealed a lean body mass of 49.9 kg (111.0 lbs) and a fat mass of 38.0 kg (84.0 lbs).
Laboratory assessment prior to date of initial consult (June 2017) revealed a HBA1C of 7.8% and a random glucose of 6.5 mmol/L. Total cholesterol (TC) was 4.68 mmol/L, triglycerides (TG) were 2.63 mmol/L, high-density lipoproteins (HDL) was 1.04 mmol/L, low-density lipoproteins (LDL) was 2.44 mmol/L, and TC:HDL was 4.5. Alanine aminotransferase was 55 U/L, while creatinine was 79 μmol/L.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [65, 'years'], 'weight': [88.5, 'kg'], 'height': [1.69, 'm'], 'creatinine': [79.0, 'µmol/L']}",70.16702,66.65867,73.67537,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 65 years old. 
The concentration of creatinine is 79.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 79.0 µmol. To convert 79.0 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 79.0 µmol creatinine * 1e-06 mol/µmol = 8e-05 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 8e-05 mol creatinine * 113.12 g/mol = 0.00905 g creatinine. To convert 0.00905 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00905 g creatinine * 1000.0 mg/g = 9.05 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 9.05 mg creatinine/10.0 dL = 0.905 mg creatinine/dL. The concentration value of 79.0 µmol creatinine/L converts to 0.905 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.69 m. The patient's weight is 88.5 kg. The patient's bmi is therefore 88.5 kg / (1.69 m * 1.69 m) = 30.98631 kg/m^2.The patient's BMI is 31.0, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.69 m, which is 1.69 m * 39.3701 in/m = 66.53547 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.53547 (in inches) - 60) = 60.53158 kg.
Hence, the patient's IBW is 60.53158 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 60.53158 kg + 0.4 * (88.5 kg  - 60.53158 kg) = 71.71895 kg. The patient's adjusted body weight is 71.71895 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 65) * 71.71895 * 0.85) / (0.905 * 72) = 70.16702 mL/min. Hence, the patient's creatinine clearance is 70.16702 mL/min."
9,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4379326-1,Extracted,"The patient is a 78-year-old male patient with renal disease from 9 years ago (March 2005). He has lived in Semnan, Iran. His medical records were reviewed in October 2014. Laboratory findings in the patient at first were as follows: BUN = 22, Cr = 1.3, weight: 60 kg, height: 166 cm, blood pressure 145/95 mmHg. The patient was treated. The BUN and creatinine levels gradually increased and reached to BUN = 43 and Cr = 4 thirty months after the first referral. All laboratory tests were performed in a medical diagnostic laboratory using the calibrated equipment and common methods. The BUN and creatinine levels were measured by auto analyzer TC-6062 manufactured by Tecom Co, China. Blood pressure was measured by the Riester sphygmomanometer (Germany). At that time he had referred for arteriovenous graft and an arteriovenous fistula made by a surgeon. Six months later he had a functional fistula. Patients were treated with the conventional treatment and Eprex. Specific variables in this case were creatinine and GFR. Blood pressure controlled in the range of 110/80 mmHg. The patient's GFR decreased from 20 to 14 cc/min and his last blood pressure was 140/80 mmHg. The mean serum creatinine level was 3, maximum 4.2 and minimum 1.5. At present, the patient is in stage 4 of CKD and under usual medical treatment.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [78, 'years'], 'weight': [60.0, 'kg'], 'height': [166.0, 'cm'], 'creatinine': [1.3, 'mg/dL']}",39.74359,37.75641,41.73077,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 78 years old. 
The concentration of creatinine is 1.3 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.66 m * 1.66 m) = 21.77384 kg/m^2.The patient's BMI is 21.8, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 60.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 78) * 60.0 * 1) / (1.3 * 72) = 39.74359 mL/min. Hence, the patient's creatinine clearance is 39.74359 mL/min."
10,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-7487712-1,Extracted,"A 23-year-old man presented to hospital with a 2-week history of oedema, frothy urine and lower abdominal pain. This is on a background of ulcerative colitis (UC) for which he was on sulfasalazine. He denied any other regular medications, over the counter medications or herbal supplements. His family history included his mother having IgA nephropathy. He was an occasional smoker and rarely consumed alcohol. He denied illicit drug use. On examination, he was mildly tachycardic (105 beats per minute) and normotensive. He was 180 cm tall and weighed 93 kg. He had mild bilateral pitting oedema to his knees. The rest of his examination was unremarkable. Investigations revealed normal renal function with a creatinine of 75 μmol/L, hypoalbuminaemia with a serum albumin of 15 g/l and urinalysis revealing 3+ protein. His urinary albumin to creatinine ratio (uACR) was 944.9 mg/mmol. His total cholesterol was 8.3 mmol/L. GN, vasculitis, infection and myeloma screen (dsDNA, C3 & C4, anti-PLA-2R, hepatitis B & C serology, serum free light chains and serum protein electrophoresis with immunofixation) were negative, with the exception of a positive atypical perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA). Importantly the myeloperoxidase (MPO) and proteinase 3 (PR3) titres were both < 1 IU/ml. ANCA positivity is most likely explained by our patient’s history of UC where ANCA positivity is reported in 60–80% of patients, with a predominant p-ANCA pattern [].
During preparation for renal biopsy our patient was found to have a prolonged activated partial thromboplastin time (aPTT) of 47 s. This corrected on a mixing study. Factor 12 deficiency (29%) was subsequently identified. Haematology opinion was that this conferred no increase in in vivo bleeding risk.
Renal biopsy was undertaken with LM revealing no morphological abnormality (see Fig. ). IF revealed nonspecific trace glomerular deposits of IgM and C3. MCD was the most likely diagnosis. Our patient was consequently commenced on 75 mg oral prednisone daily.
After 1 month our patient achieved complete remission. He was no longer oedematous, his serum albumin was 33 g/l (from 15 g/L) and uACR was 0.7 mg/mmol (from 944.9 mg/mmol). His prednisone was slowly weaned from 75 mg daily to 50 mg daily for a fortnight and then 25 mg daily for a fortnight. Our patient remained in remission with a serum albumin of 39 g/L, total cholesterol of 6 mmol/L and no albuminuria.
The electron microscopy (EM) report from our patient’s renal biopsy returned 2 months later. This revealed patchy foot process effacement, and mesangial expansion with some deposits suggestive of a mesangiopathic process (see Fig. ).
Our patient then suffered a dramatic relapse with the prednisone dose at 20 mg/day. He reported recurrence of frothy urine, 4 kg of weight gain and proteinuria (on urine dipstick given for home monitoring). His prednisone was increased to 25 mg daily but despite this his oedema worsened and proteinuria persisted. Therefore his prednisone dose was further increased to 75 mg daily to induce remission (see Fig. ).
A complete clinical remission was achieved over the next 2 months with serum albumin improving to 38 g/L and total cholesterol to 6.3 mmol/L. At this stage he was commenced on oral cyclosporin 100 mg BD as a steroid sparing agent given the previous failed attempt to wean steroids. Over the next 5 months our patient’s prednisone dosage was weaned more slowly. At a dose of 10 mg prednisone daily he suffered a second relapse with recurrence of oedema in association with albuminuria and hypoalbuminaemia to his previous levels. His prednisone dose was increased back to 50 mg daily and then 75 mg daily to re-induce remission.
Given his multiple relapses, steroid dependence and initial EM report suggestive of a mesangiopathic process, our patient underwent a second renal biopsy. LM was again normal, however IF found significant mesangial deposits of IgM (2–3+) and C3 (2–3+) (see Figs. and ). IgM nephropathy was then consider a possible diagnosis.
This time our patient took longer to achieve remission, requiring 75 mg prednisone daily and an increase in his cyclosporin dose to 125 mg BD. His prednisone dose was again weaned to 25 mg daily. He also self-ceased his cyclosporin. Our patient was adherent to the recommended prednisone dose as he recognised that without it he would relapse, and he felt further relapses would impact his career progression.
After more than 12 months on prednisone 25 mg daily, and a total of 2 years on continuous corticosteroids, our patient agreed to a slow wean of the corticosteroid dose. Our plan was to use anti-human CD20 (Rituximab) if severe nephrosis recurred. He once again relapsed as soon as his prednisone dose reached 20 mg daily. At this stage his prednisone was increased to 50 mg daily, and he received the first of two planned doses of Rituximab 1 g as an outpatient. He suffered no adverse reactions from the rituximab. During this relapse, his serum albumin reached 10 g/L, 24 h urinary protein was 14.76 g/day and his total cholesterol was 11.5 mmol/L (see Fig. ).
Several days after the rituximab infusion, our patient presented to the Emergency Department with a severe headache, nausea and vomiting. His headache had been progressively worsening since the day prior to his rituximab infusion. There were no focal neurological signs on examination. Computed tomography brain (CTB) and computed tomography angiogram (CTA) revealed a right transverse sinus thrombosis and non-occlusive posterior sagittal sinus thrombosis. We found no evidence of any inherited or acquired thrombophilia with extensive testing (anti-thrombin 3, factor V Leiden, lupus anticoagulant, prothrombin gene mutation, protein C & S, JAK 2 mutation analysis and paroxysmal nocturnal haemoglobinuria assay). He was commenced on therapeutic enoxaparin and bridged to warfarin.
He went on to receive a second dose of rituximab 1-month later. Since then he has remained in complete remission (see Fig. ). His prednisone was weaned over the following 6 months, and his prednisone was ceased. A repeat CTB and CTA showed resolution of the transverse sinus and posterior sagittal sinus thromboses and a decision was made to stop anti-coagulation.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [93.0, 'kg'], 'height': [180.0, 'cm'], 'creatinine': [75.0, 'µmol/L'], 'age': [23, 'years']}",168.64572,160.21343,177.07801,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 23 years old. 
The concentration of creatinine is 75.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 75.0 µmol. To convert 75.0 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 75.0 µmol creatinine * 1e-06 mol/µmol = 7e-05 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 7e-05 mol creatinine * 113.12 g/mol = 0.00792 g creatinine. To convert 0.00792 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00792 g creatinine * 1000.0 mg/g = 7.92 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 7.92 mg creatinine/10.0 dL = 0.792 mg creatinine/dL. The concentration value of 75.0 µmol creatinine/L converts to 0.792 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 180.0 cm, which is 180.0 cm * 1 m / 100 cm = 1.8 m. The patient's weight is 93.0 kg. The patient's bmi is therefore 93.0 kg / (1.8 m * 1.8 m) = 28.7037 kg/m^2.The patient's BMI is 28.7, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 180.0 cm, which is 180.0 cm * 0.393701 in/cm = 70.86618 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.86618 (in inches) - 60) = 74.99221 kg.
Hence, the patient's IBW is 74.99221 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 74.99221 kg + 0.4 * (93.0 kg  - 74.99221 kg) = 82.19533 kg. The patient's adjusted body weight is 82.19533 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 23) * 82.19533 * 1) / (0.792 * 72) = 168.64572 mL/min. Hence, the patient's creatinine clearance is 168.64572 mL/min."
11,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5437989-1,Extracted,"An 11-year-old girl was admitted to our hospital with microscopic hematuria and nephrotic-range proteinuria detected by school urinary screening. The patient did not have any characteristic features of Fabry’s disease such as angiokeratoma or neuralgia. On admission, her physical examination was unremarkable (body weight 47.4 kg, body height 157.3 cm), and her blood pressure normal (106/60 mmHg). Laboratory investigations revealed hypoproteinemia (serum total protein 5.6 g/dL, serum albumin 2.9 g/dL, serum IgG 318 mg/dL). All other biochemical investigations were within normal limits: blood urea nitrogen 8 mg/dL, serum creatinine 0.43 mg/dL, IgA 111 mg/dL, C3 140 mg/dL (normal 84 – 151 mg/dL), C4 26 mg/dL (normal 17 – 40 mg/dL). Anti-hepatitis B surface antigen, anti-hepatitis C antibody, and anti-nuclear antibody were negative. Urinalysis findings were 3+ for occult blood and 3+ for the dipstick protein reaction; her 24-hour urine protein excretion was 2.5 g. Light microscopy analysis of the initial renal biopsy specimen revealed diffuse mesangial proliferative glomerulonephritis with fibrocellular crescents in 4 of 13 glomeruli (a). Immunofluorescence revealed granular deposits of IgA (3+) and C3 (1+) in the mesangial areas (b), and electron microscopy revealed paramesangial electron-dense deposits. Based on these findings, a diagnosis of severe IgA nephropathy was made. The patient was treated intravenously with three courses of methylprednisolone (20 mg/kg/day) pulse therapy (MPT), followed by 2 years of alternate-day prednisolone (initially 1 mg/kg and then tapered gradually) combined with an angiotensin receptor blocker (telmisartan 1 mg/kg/day). In addition, a tonsillectomy was performed 3 months after MPT. However, microscopic hematuria and mild proteinuria persisted.
At the age of 13 years, the patient was re-admitted for a second renal biopsy to assess the therapeutic effect. All laboratory investigations were within normal limits: serum total protein 6.3 g/dL, serum albumin 4.0 g/dL, blood urea nitrogen 12 mg/dL, serum creatinine 0.44 mg/dL, IgA 108 mg/dL, C3 96 mg/dL, C4 26 mg/dL. Urinalysis revealed a 2+ value for occult blood and a dipstick protein reaction of 2+; the 24-hour urine protein excretion was 0.5 g. Light microscopy analysis of the second renal biopsy specimen revealed focal segmental mesangial proliferative glomerulonephritis. Immunofluorescence revealed granular deposits of IgA (2+) and C3 (1+) in the mesangial areas, and electron microscopy revealed paramesangial electron-dense deposits. After the second renal biopsy, the patient was additionally treated with three courses of MPT, and her microscopic hematuria disappeared within 6 months.
At the age of 15 years, she was admitted for a third renal biopsy. On admission, her physical examination was unremarkable (body weight 55.9 kg, body height 165 cm), and her blood pressure normal (102/70 mmHg). Laboratory investigations were all within normal limits: serum total protein 6.6 g/dL, serum albumin 4.2 g/dL, blood urea nitrogen 11 mg/dL, serum creatinine 0.48 mg/dL, IgA 135 mg/dL, C3 121 mg/dL, C4 25 mg/dL. Urinalysis was negative for occult blood and the dipstick protein reaction was 2+; her 24-hour urine protein excretion was 0.7 g. Light microscopy analysis of the third renal biopsy specimen revealed minor glomerular abnormalities (a). Immunofluorescence revealed granular deposits of IgA (2+) in the mesangial areas, and electron microscopy revealed paramesangial electron-dense deposits. In addition, numerous myelin-like bodies were first observed in podocytes (b). Low serum α-galactosidase A activity (13.8 Agal U, cut-off value < 20) and increased GL3 excretion in the urine (0.54 mg/mgCr, control 0.1 – 0.4) were also observed. On the basis of these findings, a final diagnosis of concomitant IgA nephropathy (healing stage) and subclinical Fabry’s disease was made.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [15, 'years'], 'weight': [55.9, 'kg'], 'height': [165.0, 'cm'], 'creatinine': [0.48, 'mg/dL']}",171.85692,163.26407,180.44977,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 15 years old. 
The concentration of creatinine is 0.48 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 55.9 kg. The patient's bmi is therefore 55.9 kg / (1.65 m * 1.65 m) = 20.5326 kg/m^2.The patient's BMI is 20.5, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 55.9 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 15) * 55.9 * 0.85) / (0.48 * 72) = 171.85692 mL/min. Hence, the patient's creatinine clearance is 171.85692 mL/min."
12,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5063890-1,Extracted,"A 27-year-old female presented to the Gout Clinic of Peking Union Medical College Hospital with recurrent arthritis and infertility. Fourteen years before presentation, she noticed protrusion of her right ankle but did not undergo evaluation at a hospital. Eight years before presentation, at age 19, she experienced acute pain and swelling of her right ankle. The pain resolved spontaneously but recurred 6 to 7 times/year, involving the bilateral metatarsophalangeal (MTP) joints, bilateral ankles, and right knee. Her serum urate level (SUA) was elevated to 789 μmol/L. A diagnosis of gout was made, and she was prescribed NSAIDs for pain relief and allopurinol and benzbromarone to lower her urate level. However, she discontinued allopurinol and benzbromarone on her own as these medications triggered acute flares. Five years before presentation, she noticed multiple nodules in her MTP joints, ankles, and fingers. The nodules on her feet interfered with normal walking. She also complained of the inability to conceive after 3 years of attempts. Her age at menarche was 14 years, and her cycles were irregular. She was reported to prefer snacks and fatty food during her childhood. Her father had hypertension. Her grandfather had an SUA level greater than 400 μmol/L but without gout. On physical examination, the patient was generally healthy, with a height of 168 cm and a weight of 55 kg. Her blood pressure was 120/80 mmHg. Cardiac and pulmonary examinations were normal. On abdominal palpation, the liver was enlarged with a normal soft texture. A joint examination revealed multiple nodules on the bilateral MTP1 joints, ankles, and fingers.
A serological examination after overnight fasting revealed a SUA level of 548 μmol/L, serum creatinine (Cr) level of 49 μmol/L, fasting glucose level of 3.6 mmol/L, total triglyceride level of 6.22 mmol/L, and total cholesterol level of 6.60 mmol/L. Her resting lactate level was 7.4 mmol/L. Her 24-h urine urate level was 2.262 mmol/24 h, and her fractional excretion of uric acid (FE-UA) was 2.48 %. Her liver enzymes were normal. The estrogen level and basal body temperature curve were normal for her age and menstrual status. Renal ultrasonography revealed normal kidney size with possible calcium deposits in the bilateral renal medulla. Computed tomography (CT) imaging of her abdomen showed hepatomegaly without nodules. The pelvic ultrasonography and salpingography findings were normal. Serum examinations of her parents and her husband were normal.
Whole blood DNA was extracted from all four family members (the patient, both parents, and her husband) after signing an informed consent form. A genetic study was first conducted with a target gene sequencing approach. A search of the OMIM, NIH, and PubMed databases using the key words “FEMALE,” “GOUT,” and “HYPERLACTACIDEMIA” indicated familial juvenile hyperuricaemic nephropathy, glycogen storage disease type I, and glycogen storage disease type II. Next-generation sequencing was used to sequence each of the exons of the UMOD, RENIN, G6PC, SLC37A4, and GAA genes, as well as two SNP loci (rs2231142 and rs72552713) of ABCG2 found in our previous report of a family including a female with gout.
The genetic sequencing results showed that UMOD, RENIN, SLC37A4, GAA and rs72552713 of ABCG2 were all normal in the patient and her family. Sequencing of the G6PC gene revealed composite heterozygous c.190G>T/c.508C>T mutations in the patient, a heterozygous c.190G>T mutation in her father, and a heterozygous c.508C>T mutation in her mother. The genetic analysis of her husband was normal. The c.190G>T mutation was located on exon 1 and encoded a missense mutation of p.V64L, whereas the c.508C>T mutation was located on exon 4 and encoded a nonsense mutation of p.R170X (Fig. ). Sequencing of 50 healthy females and 100 healthy males at the two loci produced normal results. To our knowledge, the c.190G>T mutation has not been reported in previous literature.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [55.0, 'kg'], 'height': [168.0, 'cm'], 'creatinine': [49.0, 'µmol/L'], 'age': [27, 'years']}",129.63167,123.15009,136.11325,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 27 years old. 
The concentration of creatinine is 49.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 49.0 µmol. To convert 49.0 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 49.0 µmol creatinine * 1e-06 mol/µmol = 5e-05 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 5e-05 mol creatinine * 113.12 g/mol = 0.00566 g creatinine. To convert 0.00566 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00566 g creatinine * 1000.0 mg/g = 5.66 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 5.66 mg creatinine/10.0 dL = 0.566 mg creatinine/dL. The concentration value of 49.0 µmol creatinine/L converts to 0.566 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.68 m * 1.68 m) = 19.48696 kg/m^2.The patient's BMI is 19.5, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 55.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 27) * 55.0 * 0.85) / (0.566 * 72) = 129.63167 mL/min. Hence, the patient's creatinine clearance is 129.63167 mL/min."
13,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-7457258-1,Extracted,"A 31-year-old black Congolese female patient, P3G3, who had a pregnancy of 38 weeks and four days, was transferred from a district hospital to a tertiary facility in Kinshasa, Democratic Republic of Congo, for severe preeclampsia with acute on chronic fetal distress. Her past medical history was notable for eclampsia during her first pregnancy in 2011 and preeclampsia in 2013 during her second pregnancy. She had had two cesarean sections for her pregnancies, and she had her antenatal care for her third pregnancy at a referral hospital. She was diagnosed with preeclampsia during her third pregnancy for which she received 250 mg alpha-methyl-dopa twice a day. ​​During the 30th week of gestation, the patient’s systolic blood pressure became labile, oscillating between 140 and 150 mmHg, despite her antihypertension medication. The patient consulted at a district hospital where she underwent a fetal wellbeing ultrasound which did not find anomalies.
The patient was the 7th of 9 children, and her father was hypertensive. She weighed 72 kg for 155 cm, and upon arrival at the authors’ hospital, her blood pressure was 217/152 mmHg. Her heart rate was 101 bpm, her respiratory rate was 24 cpm, and SpO2 was 96% free air. The patient was in pain, she was lucid and coherent, her palpebral conjunctivae were colored, and she had bilateral pitting edema. The fundus height was at 30 cm, the presentation was cephalic, the fetus was bradycardic at 88 bpm, and there were no signs of genital bleeding. The cervix was median, soft, 80% effaced with a 2 cm dilation. Urine deep stick revealed 3+ proteinuria. She had 1.5 mg/dL of creatinine (normal: 0.5–1.5 mg/dL), 22 mg/dL of urea (normal: 10–50 mg/dL), 15,000 white blood cells/ml, 213,000 platelets/ml and 14 g/dL hemoglobin. Based on these findings, we indicated an emergency cesarean section for acute fetal distress, which resulted in the extraction of a dead infant.
Postoperative suites were marked on day two by decompensated anemia (hemoglobin at 7.8 mg/dL) for which the patient was transfused two units of packed red blood cells. On postoperative day three, the patient presented an abdominal effusion, exacerbation of the bilateral pitting edema, blood pressure increase, hematemesis, melena, petechiae, hematuria, and oliguria. Her blood pressure was 215/120 mmHg and she had signs of renal failure (creatinine = 6.9 mg/dL (normal: 0.84–1.21 mg/dL); urea 132.5 mg/dL (normal: 5–20 mg/dL); hyperkalemia at 6.4 mmol/L (normal: 3.5–5 mmol/L); hyponatremia 109 mmol/L (normal: 136–145 mmol/L); hypocalcemia 0.88 mmol/L (normal: 1.12–1.32 mmol/L)), and signs of hepatic failure (AST 135 IU/L, normal: < 33 IU/L; ALT 325 IU/L, normal: < 33 IU/L; prothrombin ratio 100% (normal: 80–110%). PTT was 39 s (normal: 24–35 s), LDH was 1398 IU/L (normal: 120–280 IU/L), and total bilirubin was 0.35 mg/dL (normal: 0-1 mg/dL)). She equally had neutrophilic leukocytosis at 22,180 cells/mm3 and low platelets at 44,000 cells/mm3. Additionally, schistocytes were identified in the peripheral thin smear.
The team excluded TTP and HELLP syndrome as possible causes of the postpartum microangiopathic hemolytic anemia (MAHA). This decision was based on the history, clinical presentation, and laboratory findings. Atypical hemolytic uremic syndrome was retained as the final diagnosis, and in the absence of anti-complement therapy, the patient underwent four sessions of hemodialysis. Hypertension was treated with Nicardipine, 5 mg/hr. IV with a 2.5 mg/hr. increase every 15 min without exceeding 15 mg/hr., and the goal was to lower the systolic blood pressure below 160 mmHg. Hyperkalemia was corrected with insulin and glucose (10 units of insulin dose with 25 g of glucose per each 1 mmol/L of potassium above the normal). A favorable clinical and biologic evolution was observed, and the patient was released for outpatient follow-up on postoperative day 18 (Figs. , and ).
Laboratory tests could not be obtained more frequently due to their financial burden to the patient and her immediate family. The patient had a normal kidney function at postoperative day 160 (urea 24.2 g/dL, creatinine 0.8 mg/dL) and postoperative day 202 (urea 16.9 g/dL, creatinine 0.8 mg/dL). She did not present new episodes of microangiopathic hemolytic anemia.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [31, 'years'], 'weight': [72.0, 'kg'], 'height': [155.0, 'cm'], 'creatinine': [6.9, 'mg/dL']}",10.72574,10.18945,11.26203,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 31 years old. 
The concentration of creatinine is 6.9 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 72.0 kg. The patient's bmi is therefore 72.0 kg / (1.55 m * 1.55 m) = 29.96878 kg/m^2.The patient's BMI is 30.0, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 47.85442 kg + 0.4 * (72.0 kg  - 47.85442 kg) = 57.51265 kg. The patient's adjusted body weight is 57.51265 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 31) * 57.51265 * 0.85) / (6.9 * 72) = 10.72574 mL/min. Hence, the patient's creatinine clearance is 10.72574 mL/min."
14,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4763642-1,Extracted,"A 32-year-old male patient was admitted to the outpatient clinic with complaints of weight gain, dry mouth, and fatigue. In 2002, some eruptions appeared on the skull. Two (2) years later, skin eruptions spread all over his body. At that time, he was diagnosed with psoriasis and prescribed topical clobetasol propionate. He had not been reexamined after that and has been using clobetasol propionate 0.005% routinely for 10 years. He has applied the drug to his arms, legs, and all over the trunk. Over the past year, he put on weight obviously (8 kg). He stopped the treatment 1 month ago, at the time of writing. He has been complaining of dry mouth and fatigue for the last month. On his physical examination, moon face, central adiposity, and purple-red striae on the abdomen under umbilicus were observed. There were scaly patches and erythematous plaques on the skull, interscapular area, sacrum, arms, legs, knees, and elbows []. Other systemic examinations were all normal. Blood pressure was 130/90 mmHg, pulse 75/min, height 1.76 m, weight 77 kg, and body mass index 24.8 kg/m2. On laboratory examination, fasting blood glucose: 152 mg/dL (N: 70-105), creatinine: 1 mg/dL (N: 0.72-1.25), triglyceride: 160 mg/dL (N: 0-200), total cholesterol: 240 mg/dL (N: 0-200), high-density-lipoprotein (HDL)-cholesterol: 44 mg/dL (N: 45-55), low-density-lipoprotein (LDL)-cholesterol: 164 mg/dL (N: 0-130), ALT: 42 u/L (N: 0-55); AST: 27 u/L (N: 0-34); sodium: 140 mmol/L (N: 136-145); potassium: 4.6 mmol/L (N: 3.5-5.1); calcium: 9.9 mg/dL (N: 8.4-10.2); phosphorus: 3.5 mg/dL (N: 2.3-4.7); albumin: 4.6 g/dL (N: 3.2-5.2); intact-parathyroid hormone (iPTH): 38 pg/mL (N: 14-72); 25-OH Vitamin D: 4.9 ng/mL (N: 24-50); white blood cell (WBC) count: 12.76-103 /uL (N: 4.23-9.07); hemoglobin (Hb) count: 14.7 gr/dL (N: 13.7-17.5); platelet: 217-103 /uL (N: 150-400); morning (8 AM) adrenocorticotropic hormone (ACTH): 5.6 pg/mL (N: 0-46); morning (8 AM) serum cortisol: <0.2 μg/dL (5.5 nmol/L) (N: 4.3-22.4). According to these findings, the patient was diagnosed with iatrogenic Cushing's syndrome secondary to topical steroid use. For adrenal insufficiency, 20 mg/day hydrocortisone treatment was commenced, and for vitamin D deficiency, vitamin D replacement. As the patient had high blood glucose levels, dyslipidemia, and large waist circumference (101 cm), he was diagnosed with metabolic syndrome, and a low-calorie diet and exercise were advised. Metformin treatment at a dose of 2000 mg/day was commenced for glucose regulation. The patient consulted at the dermatology department for his psoriasis, and calcipotriol pomade and emollients were prescribed. One (1) month after that, 1 μg tetracosactide i.v. was applied and cortisol levels were measured at 30 min and at 60 min. As both measured levels were below 3 μg/dL, glucocorticoid maintenance treatment was continued.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [77.0, 'kg'], 'height': [1.76, 'm'], 'creatinine': [1.0, 'mg/dL'], 'age': [32, 'years']}",107.05526,101.7025,112.40802,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 32 years old. 
The concentration of creatinine is 1.0 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.76 m. The patient's weight is 77.0 kg. The patient's bmi is therefore 77.0 kg / (1.76 m * 1.76 m) = 24.85795 kg/m^2.The patient's BMI is 24.9, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 71.37017 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 32) * 71.37017 * 1) / (1.0 * 72) = 107.05526 mL/min. Hence, the patient's creatinine clearance is 107.05526 mL/min."
15,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6600489-1,Extracted,"The patient is a 28-year-old Hispanic female with a past medical history of
hypertension, high serum cholesterol, and gastritis who presented to the emergency
room for the evaluation of abdominal pain of 2 days duration. Six months prior, she
had similar pain. An upper gastrointestinal (GI) endoscopy at that time showed
peptic ulcer disease and no other mucosal lesions. The patient had a strong family
history of renal disease and 2 of her siblings required a renal transplant, but she
did not know what kidney pathology they had. Her medications included Lisinopril
oral 10 mg tablet daily and Pantoprazole oral 40 mg daily. On presentation at the
emergency room (ER), her height and weight were 157 cm and 61 kg, respectively, and
her blood pressure was 206/121 mm Hg. On physical examination, the patient had
epigastric tenderness. The rest of her physical examination was unremarkable.
Radiology was ordered to exclude any anatomical abnormality. A computed tomography
scan showed neither atrophy nor enlargement of the kidneys. She then followed up as
an outpatient with a nephrologist shortly after her ER visit. Her laboratory work up
during that visit revealed the following: nephrotic range proteinuria (9.2 g protein
on 24-hour urine collection; reference range, 0-2.5 g/d), hypoalbuminemia (300
µmol/L; reference range, 421-662 µmol/L), hypoproteinemia (50 g/L; reference range,
60-80 g/L), elevated serum creatinine (148.5 µmol/L; reference range, 44-80 μmol/L),
high chloride (110 mmol/L; reference range, 98-106 mmol/L), and low hemoglobin (100
g/L; reference range, 120-160 g/L). The lipid profile showed an increased total
cholesterol level (8.3 mmol/L; reference range, <5.2 mmol/L), elevated
triglycerides (3.7 mmol/L; reference range, <1.70 mmol/L), elevated low-density
lipoprotein fraction (5.9 mmol/L; reference range, <2.6 mmol/L), and decreased
high-density lipoprotein fraction (1.1 mmol/L; reference range, ≥1.55 mmol/L). After
treating her blood pressure, the patient underwent a US-guided renal biopsy.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [61.0, 'kg'], 'height': [157.0, 'cm'], 'creatinine': [148.5, 'µmol/L'], 'age': [28, 'years']}",38.69696,36.76211,40.63181,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 28 years old. 
The concentration of creatinine is 148.5 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 148.5 µmol. To convert 148.5 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 148.5 µmol creatinine * 1e-06 mol/µmol = 0.00015 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00015 mol creatinine * 113.12 g/mol = 0.01697 g creatinine. To convert 0.01697 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01697 g creatinine * 1000.0 mg/g = 16.97 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 16.97 mg creatinine/10.0 dL = 1.697 mg creatinine/dL. The concentration value of 148.5 µmol creatinine/L converts to 1.697 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 157.0 cm, which is 157.0 cm * 1 m / 100 cm = 1.57 m. The patient's weight is 61.0 kg. The patient's bmi is therefore 61.0 kg / (1.57 m * 1.57 m) = 24.74745 kg/m^2.The patient's BMI is 24.7, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 49.66544 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 28) * 49.66544 * 0.85) / (1.697 * 72) = 38.69696 mL/min. Hence, the patient's creatinine clearance is 38.69696 mL/min."
16,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-2693655-1,Extracted,"A 73-yr-old woman with atrial fibrillation presented to the emergency room complaining of chest discomfort, dyspnea, and agitation. The patient had suffered from atrial fibrillation for the last 2 yr. Her medications for the previous 2 yr included diltiazem 90 mg, metoprorol 25 mg, and aspirin 100 mg twice a day. In addition, she had been taking mirtazapine 30 mg, alprazolam 0.25 mg, and zolpidem 10 mg daily for a 6 yr history of dysthymia.
Physical examination showed a blood pressure of 100/83 mmHg, a heart rate of 100 beats/min, and a normal body temperature. Her body weight was 62.3 kg, and she was 158 cm in height. Initial laboratory results were unremarkable with a normal PT of 12.3 sec (INR 1.0). Routine chemical studies indicated normal values for total protein (6.6 g/dL), albumin (3.9 g/dL), aspartate aminotransferase (17 U/L), alanine aminotransferase (10 U/L), alkaline phosphatase (79 U/L), total bilirubin (0.3 mg/dL) blood urea nitrogen (16.4 mg/dL), creatinine (0.6 mg/dL), and electrolytes. Results of hematological studies including complete blood counts were also normal. Mild cardiomegaly was found on the chest radiography. Electrocardiogram showed atrial fibrillation. Echocardiogram revealed mild aortic, mitral, and tricuspid regurgitation and left atrial enlargement (45 mm).
The patient underwent heparinization with an initial bolus administration of 3,600 IU heparin followed by continuous infusion for 6 days. Then the patient was started on 2 or 3 mg of warfarin daily (16.3 mg/week) to prevent thromboembolism, and was discharged after 3 days with a PT of 37.4 sec (INR 2.81). When she revisited the outpatient clinic after 3 days, her PT was found to be 50.0 sec (INR 3.68). After normalization of the patient's PT with warfarin withdrawal for 3 days, 1 or 2 mg/day (10.5 mg/week) of warfarin was prescribed. The PT after 3 days of treatment was 41.6 sec (INR 3.11). The administration of warfarin dose was changed (6.5-10.5 mg/week) continuously, which resulted in a PT of 20.9-43.1 sec (INR 1.64-3.21). She had to discontinue warfarin therapy temporarily 3 times. The difficulty in finding the optimal treatment dose during the induction period of anticoagulation continued for more than 2 month.
The patient continues to receive warfarin therapy at the outpatient clinic monthly and her PT remains within the recommended target therapeutic range (INR 2.0-3.0), even though her warfarin dose has been reduced to 6.5 mg/week.
The patient was genotyped for CYP2C9 after informed consent. DNA was isolated from peripheral blood, and all 9 exons of the CYP2C9 gene were amplified by PCR (-). The PCR products were sequenced using the ABI PRISIM BigDye terminator Cycle sequencing kit and an ABI Prism 3100 Genetic Analyzer (Applied Biosystems, Foster City, CA, U.S.A.). The patient was found to be an intermediate metabolizer with the genotype of CYP2C9*3/*4 ().","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [73, 'years'], 'weight': [62.3, 'kg'], 'height': [158.0, 'cm'], 'creatinine': [0.6, 'mg/dL']}",72.85193,69.20933,76.49453,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 73 years old. 
The concentration of creatinine is 0.6 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 158.0 cm, which is 158.0 cm * 1 m / 100 cm = 1.58 m. The patient's weight is 62.3 kg. The patient's bmi is therefore 62.3 kg / (1.58 m * 1.58 m) = 24.95594 kg/m^2.The patient's BMI is 25.0, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 50.57095 kg + 0.4 * (62.3 kg  - 50.57095 kg) = 55.26257 kg. The patient's adjusted body weight is 55.26257 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 73) * 55.26257 * 0.85) / (0.6 * 72) = 72.85193 mL/min. Hence, the patient's creatinine clearance is 72.85193 mL/min."
17,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-2803985-1,Extracted,"We are presenting a case with acute abdomen, i.e. ileoileal intusussception, caused by Burkitt lymphoma. A sixteen-year-old Caucasian Kosovar boy, presented in the surgical emergency clinic as acute abdomen, with abdominal pain, nausea, vomiting, and problems with defecation and flatulence. The symptoms started three days ago, worsening on admission day.
The patient's height was 178 cm, and his weight was 70 kg. His vital signs were: blood pressure 120/80 mmHg; pulse rate: 76 beats/min; respiratory rate 20/min; body temperature 37.1°C.
During physical examination, a distended, diffusely tender and painful abdomen with lower abdomen rebound was revealed. The patient's skin was pale with sweats.
Plane abdominal radiography showed mechanical obstruction. (Fig. )
The emergency laboratory tests presented as follows: Red blood cells (RBC): 4.61 × 109/L; white blood cells (WBC): 7.3 × 109/L; Hemoglobin (Hgb): 128 g/L; Hematocrit (Htc): 0.42; blood sugar: 5.42 mmol/L; blood urea nitrogen (BUN): 2.6 mmol/L; serum creatinine: 88 μmol/L; BUN/Creat ratio: 8.5; total protein: 72 g/L; albumin: 36 g/l; ALP: 60 IU/L; ALT: 26 IU/L; AST:40 IU/L; direct bilirubin: 5.8 μmol/L; total bilirubin: 20.5 μmol/L; indirect bilirubin: 14.7 μmol/L; Gama GT: 26 IU/L; C-reactive protein: 15.6 mg/L; serum amylase: 30 U/L: electrolytes: Na: 138 mmol/L; K: 3.75 mmol/L; Cl: 102 mmol/L; urinalysis: 2-4 Leucocytes, some bacteria and some uric acid crystals. Blood group: O Rh(D) poz.
Three weeks prior he had been surgically treated as acute abdomen caused by acute appendicitis and Mckelly Diverticulitis. Appendectomy and short resection of the ileum with diverticulum, and end-to-end anastomosis was performed. The immediate post operative period went well. After his discharge, his second hospital admission was two weeks after operation with abdominal pain and constipation problems which released spontaneously after two days.
At his third admission as acute abdomen, urgent laparotomy was performed in general endo tracheal anesthesia on the day after admission. Intra operative findings revealed small bowel dilatation, with intussusceptions of the terminal ileum, 2 cm from ileocecac valve. There were multiple enlarged mesenteric lymph nodes at the meso of the terminal ileum, ascending and the transverse colon, without palpable liver metastases.
We have done des intussusceptions caused by tumor from the wall of the ileum. (Fig. , , )
Adhesions at the anastomosis, and 60 cm above that, were released. The right extended haemicolectomy with end to end ileum-transverse anastomosis was performed. Post operative period went well; blood pressure was 120/80 mmHg, pulse rate beats: 65/min; temp.: 36.7°C. The wound healed per primam. He was treated with frozen fresh plasma (several doses-seven), red blood cells (one dose); antibiotic, analgesics, H2 blockers, vitamins, amino acids, human albumins. He was discharged on the 10th postoperative days, with good bowel movements. He was oriented to the Hematology Department for further treatment, for Burkitt Lymphoma with chemotherapy.
HP opinion: Giemsa staining demonstrated neoplastic lymphocytes infiltration. Immunochemical testing was positive for Burkitt lymphoma (CD10, CD20, CD34, Bcl-2, Ki67, IgM, MIB-1 with a proliferation index of over 90% of neoplastic cells) and c-myc translocation determined by FISH analysis (fusion and split). (Fig. , , , , )","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [16, 'years'], 'weight': [70.0, 'kg'], 'height': [178.0, 'cm'], 'creatinine': [88.0, 'µmol/L']}",118.42392,112.50272,124.34512,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 16 years old. 
The concentration of creatinine is 88.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 88.0 µmol. To convert 88.0 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 88.0 µmol creatinine * 1e-06 mol/µmol = 9e-05 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 9e-05 mol creatinine * 113.12 g/mol = 0.01018 g creatinine. To convert 0.01018 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01018 g creatinine * 1000.0 mg/g = 10.18 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 10.18 mg creatinine/10.0 dL = 1.018 mg creatinine/dL. The concentration value of 88.0 µmol creatinine/L converts to 1.018 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 178.0 cm, which is 178.0 cm * 1 m / 100 cm = 1.78 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.78 m * 1.78 m) = 22.09317 kg/m^2.The patient's BMI is 22.1, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 70.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 16) * 70.0 * 1) / (1.018 * 72) = 118.42392 mL/min. Hence, the patient's creatinine clearance is 118.42392 mL/min."
18,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,usmle-101,Extracted,"A 70-year-old man comes to the emergency room for worsening leg pain and a rash consistent with wet gangrene. He has no history of skin infections but has type 2 diabetes mellitus and has smoked 2 packs of cigarettes daily for 20 years. Three days after admission, he becomes increasingly hypoxic and tachypneic. He is emergently intubated and ventilatory support is initiated. He is 180 cm (5 ft 11 in) tall and weighs 90 kg (198 lb); BMI is 27.8 kg/m2. His pulse is 112/min and his blood pressure is 95/60 mmHg. The ventilator is set at an FIO2 of 100%, tidal volume of 540 mL, respiratory rate of 20/min, and positive end-expiratory pressure (PEEP) of 5 cm H2O. On pulmonary examination, there are diffuse crackles. Cardiac examination shows no abnormalities. Hemoglobin is 11.5 g/dL, serum lactate is 4.0 mmol/L, and serum creatinine is 2.5 mg/dL. An arterial blood gas checked 30 minutes after intubation shows a PaCO2 of 50 mm Hg and a PaO2 of 55 mm Hg. An x-ray of the chest shows new bilateral infiltrates.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [90.0, 'kg'], 'height': [180.0, 'cm'], 'creatinine': [2.5, 'mg/dL'], 'age': [70, 'years']}",31.49818,29.92327,33.07309,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 70 years old. 
The concentration of creatinine is 2.5 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 180.0 cm, which is 180.0 cm * 1 m / 100 cm = 1.8 m. The patient's weight is 90.0 kg. The patient's bmi is therefore 90.0 kg / (1.8 m * 1.8 m) = 27.77778 kg/m^2.The patient's BMI is 27.8, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 180.0 cm, which is 180.0 cm * 0.393701 in/cm = 70.86618 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.86618 (in inches) - 60) = 74.99221 kg.
Hence, the patient's IBW is 74.99221 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 74.99221 kg + 0.4 * (90.0 kg  - 74.99221 kg) = 80.99533 kg. The patient's adjusted body weight is 80.99533 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 70) * 80.99533 * 1) / (2.5 * 72) = 31.49818 mL/min. Hence, the patient's creatinine clearance is 31.49818 mL/min."
19,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4255050-1,Extracted,"A 35-year-old man diagnosed with type 2 diabetes (T2D) eight years ago and treated with intermittent metformin administration visited our clinic. He had a history of a spontaneously healed ureteral stones ten years ago. He was 169.3 cm tall, weighed 51.6 kg, and his body mass index (BMI) was 18 kg/m2. None of his family members had a known history of diabetes. He complained of a warm and painful lesion on his thigh for the last three weeks, but reported no recent history of trauma or injection. Initial physical examination of the painful lesion revealed tenderness and non-pitting edema of the anteromedial right thigh. His blood pressure and body temperature were 120/80 mmHg and 36.4℃, respectively. There was no leukocytosis (white blood cell count: 9,190/µL) and C-reactive protein was normal, but the erythrocyte sedimentation rate was elevated to 62 mm/hr. His glycemic control was very poor, with an HbA1c 14.5% and postprandial glucose of 446 mg/dL. Other biochemistry values were as follows: serum creatinine 0.4 mg/dL, blood urea nitrogen 24 mg/dL, potassium 4.6 mmol/L, sodium 132 mmol/L, calcium 9.1 mg/dL, phosphorus 3.6 mg/dL, alkaline phosphatase 86 U/L, albumin 4.1 g/dL, and creatinine kinase 436 mg/dL. He had proteinuria (trace) and glycosuria (4+) on urinalysis.
Serial blood culture showed no evidence of bacterial infection. As infectious causes were thought to be less likely, we conducted arterial and venous doppler ultrasonography of the extremity to exclude vascular problems such as deep vein thrombosis or peripheral artery disease. There was no evidence of vascular structural abnormality, but an ill-defined hyperechoic lesion and thick fluid collection in the right vastus medialis muscle was found. After four days, the amount of fluid increased, and thus fluid aspiration at the intermuscular fascial plane adjacent to the vastus lateralis was done (). The fluid was clear, watery and serous. Gram stain and culture of the fluid were negative. Magnetic resonance image (MRI) of the right thigh reflected diffuse edema around the vastus medialis with low signal intensity on T1 () and high signal intensity on T2 images (). The three-phase bone scan showed increased blood flow to the right thigh consistent with myonecrosis as shown on the thigh MRI (). The bone scan also revealed increased blood flow at the right medial tibial condyle consistent with an insufficiency fracture, which was subsequently confirmed by X-ray and MRI (). Since these clinical findings and images were highly suggestive of DMI of the right vastus medialis with insufficient fracture of the right tibial condyle, a muscle biopsy was not performed.
Due to the early onset of disease (age 27), no obesity and no family history of T2D, we needed to clearly identify the exact type of his diabetes. Baseline C-peptide level was very low (0.1 ng/mL) and did not sufficiently rise at 6 min after glucagon stimulation test (0.3 ng/mL). Antinuclear antibodies, and anti-IA2 antibody results were not significant, but antibodies to glutamic acid decarboxylase (anti-GAD Ab) were positive (2.0 U/mL). Other immunologic factors were negative. Considering his age, low BMI, positive anti-GAD Ab, and severely decreased C-peptide level, we diagnosed his diabetes as a case of latent autoimmune diabetes in adults (LADA). After we examined microvascular and macrovascular diabetic complications, he was diagnosed with peripheral neuropathy and non-proliferative retinopathy of both eyes as well as microalbuminuria based on spot urine analysis (152 µg/mg Creatinine).
When we evaluated the cause of the insufficiency fracture, we found that his bone mineral density (BMD) was reduced, with T-scores of -3.9 (Z-score -3.3) at L1-L4 and -2.7 (Z-score -2.3) at the femur neck. Due to the young age of the patient, we also evaluated possible etiologies of secondary osteoporosis, including hyperparathyroidism, hyperthyroidism, hypogonadism, and glucocorticoid excess. 25-hydroxy-vitamin D (25-[OH]D) level was also lower than the normal limits (<4 ng/mL, normal range 11.1 to 42.9) and osteocalcin level was slightly decreased (2.4 ng/mL, normal range 2.7 to 11.5). Thyroid function test was normal (free-T4 0.90 ng/dL, normal range 0.77 to 1.94 ng/dL; Thyroid stimulating hormone 2.24 µU/mL, normal range 0.30 to 4.00 µU/mL; T3 120 ng/dL, normal range 80 to 200 ng/dL), and there was no significant finding of thyroid autoantibodies. Parathyroid hormone (PTH) level was 19.6 pg/mL (normal range 13 to 54 pg/mL). C-telopeptide level was within normal limits (0.74 ng/mL, normal range 0.07 to 0.78 ng/mL). Testosterone and follicle stimulating hormone (FSH) levels were also within normal limits (Testosterone 2.19 ng/mL, normal range, 1.8 to 8.96 ng/mL; FSH 4.0 ng/mL, normal range, 2.8 to 9.6 ng/mL), with a slightly low luteinizing hormone level (1.3 ng/mL, normal range, 1.8 to 5.2 ng/mL).
Antibiotics were initially prescribed, but discontinued when bacterial infection was ruled out and DMI was thought to be the most likely clinical diagnosis. Instead, the patient was treated with analgesics such as acetaminophen, application of a long leg splint and bed rest, and multiple daily injections of insulin for strict glucose control. For his osteoporotic fracture, he was administered oral vitamin D and calcium agents. After about two weeks of supportive management, the tenderness and swelling of the right anteromedial thigh gradually reduced and the patient was able to walk without help, and so the splint was removed. 3 months later, when the hyperglycemia was controlled, we have done the oral glucose tolerance test and calculated the insulinogenic index (IGI, delta insulin 30 min-0 min/delta glucose 30 min-0 min). Calculated IGI was 0 (reference range >0.5), which reflects diminished beta-cell function on glucose stimulation. On follow-up ultrasonography after 6 months, the myonecrosis of the right vastus medialis muscle was dramatically resolved and his HbA1c had improved to 5.7%. In addition, his 25-(OH)D level had risen to 58.7 ng/mL after 6 months of treatment. Five months after treatment, the patient complained of frequent injections, so we changed his insulin regimen to a premixed combination insulin injection twice a day. He is currently under follow-up at the outpatient clinic without any evidence of recurrence.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [35, 'years'], 'weight': [51.6, 'kg'], 'height': [169.3, 'cm'], 'creatinine': [0.4, 'mg/dL']}",188.125,178.71875,197.53125,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 35 years old. 
The concentration of creatinine is 0.4 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 169.3 cm, which is 169.3 cm * 1 m / 100 cm = 1.693 m. The patient's weight is 51.6 kg. The patient's bmi is therefore 51.6 kg / (1.693 m * 1.693 m) = 18.00262 kg/m^2.The patient's BMI is 18.0, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 51.6 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation. 
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 35) * 51.6 * 1) / (0.4 * 72) = 188.125 mL/min. Hence, the patient's creatinine clearance is 188.125 mL/min."
20,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,usmle-1585,Extracted,"A 58-year-old patient comes to the physician because of progressive pain and swelling of his left calf for the past 2 days. He has no personal or family history of serious illness. He does not smoke or drink alcohol. His last digital rectal examination and colonoscopy at the age of 50 years were normal. His vital signs are within normal limits. He is 183 cm (6 ft) tall and weighs 80 kg (176 lb); BMI is 24 kg/m2. Physical examination shows redness, warmth, and tenderness of the left calf. The circumference of the left lower leg is 4 cm greater than the right. Dorsiflexion of the left foot elicits pain in the ipsilateral calf. Laboratory studies show:
Hemoglobin 15 g/dL
Leukocyte count 9000/mm3
Platelet count 190,000/mm3
Erythrocyte sedimentation rate 12 mm/h
Serum
Urea nitrogen 18 mg/dL
Creatinine 1.0 mg/dL
Alkaline phosphatase 24 U/L
Aspartate aminotransferase (AST, GOT) 12 U/L
Alanine aminotransferase (ALT, GPT) 10 U/L
Urine
Protein negative
RBC 1/hpf
WBC none
Compression ultrasonography with Doppler shows a non-compressible left popliteal vein with a visible 0.5-cm hyperechoic mass and reduced flow.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [80.0, 'kg'], 'height': [183.0, 'cm'], 'creatinine': [1.0, 'mg/dL'], 'age': [58, 'years']}",88.50162,84.07654,92.9267,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 58 years old. 
The concentration of creatinine is 1.0 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 183.0 cm, which is 183.0 cm * 1 m / 100 cm = 1.83 m. The patient's weight is 80.0 kg. The patient's bmi is therefore 80.0 kg / (1.83 m * 1.83 m) = 23.88844 kg/m^2.The patient's BMI is 23.9, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 77.70874 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 58) * 77.70874 * 1) / (1.0 * 72) = 88.50162 mL/min. Hence, the patient's creatinine clearance is 88.50162 mL/min."
21,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5411536-1,Extracted,"A 43-year old male presented with a history of proteinuria discovered on a routine medical examination in 1985 when he was 22 years old. His medical history was acute pancreatitis at age 17 and hypertension at age 40, and the family history indicated that his nephew had IgA nephropathy. The patient occasionally consumes alcohol, but doesn’t smoke. The patient visited a local doctor and underwent a renal biopsy for suspected active nephritis because of the finding (Table ) of hematuria 3+ protein from pooled urine 0.78 g/day and a plasma creatinine (Cr) level of 1.16 mg/dl [estimated glomerular filtration rate (eGFR) 71 ml/min/1.73 m2]. Pathologic examination revealed IgA nephropathy with partial cellular crescent formation in 1 of the 12 glomeruli, slight mesangial matrix expansion, and mild atrophy of the renal tubule and interstitium. He was followed up without treatment, and the urinary abnormalities resolved spontaneously. He stopped visiting the hospital 3 years after the first visit because of the repeated negative urine analysis and did not visit any other hospital thereafter. He continued to undergo routine medical examinations, which were intermittently positive for microhematuria and proteinuria. His next visit to a medical institution was in 2002 at 38 years of age and revealed urine protein 2+, urine occult blood 1+, plasma Cr 1.13 mg/dl and hypertension. An angiotensin receptor blocker (ARB) was started. After that, he saw a doctor regularly, but hematuria and proteinuria became gradually worse. A relapse of IgA nephropathy was suspected. In March 2009, he was admitted to a hospital for renal biopsy to evaluate the progression of IgA nephropathy.
The patient's general condition at the time of hospitalization was height 163.0 cm, weight 55.0 kg, body mass index 20.7 kg/m2, blood pressure 116/72 mmHg, heart rate 83 beats/min and temperature 36.6 °C. He was lucid with no sign of anemia in the palpebral conjunctiva. No swelling of the throat, abnormal chest auscultation, hard and tender points in the abdominal area or edema of the extremities was observed. Medical examinations (Table ) revealed urine protein 3+ (0.90 g/day), urine occult blood 3+ (RBC 10–19/HPF) and serum Cr 1.63 mg/dl.
Renal biopsy (Fig. ) showed 4 global scleroses, 3 cellular crescent formations and 3 adhesions in 28 glomeruli; moderate expansion of the mesangial matrix; moderate tubular atrophy with mild cell infiltration in the interstitium; and moderate arteriolosclerosis and thickening of interlobular arteries. Immunostaining of IgA confirmed the diagnosis of active chronic-progressive IgA nephropathy.
After admission, the patient was treated with tonsillectomy and steroid pulse therapy. Steroid pulse therapy was given as follows: methylprednisolone was administered continuously at a pulsed dose of 500 mg/day for 3 days, followed by oral prednisolone at a dose of 30 mg continuously for 3 weeks. After completion of the third course, oral prednisolone was initiated at a dose of 30 mg/day every other day after treatment and tapered by 5 mg every 2 months. The after-treatment follow-up was continued for 1 year. The patient underwent tonsillectomy after discharge from the hospital (day 75) and was then followed up at the outpatient clinic. He completed oral prednisolone treatment in approximately a year, but continued taking an ARB during the follow-up period. Clinical remission was achieved 7 months after the initiation of therapy (Table ), and hematuria and proteinuria were no longer observed in this 3-year follow-up period (Fig. ).","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [43, 'years'], 'weight': [55.0, 'kg'], 'height': [163.0, 'cm'], 'creatinine': [1.63, 'mg/dL']}",45.45842,43.1855,47.73134,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 43 years old. 
The concentration of creatinine is 1.63 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.63 m * 1.63 m) = 20.70082 kg/m^2.The patient's BMI is 20.7, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 55.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 43) * 55.0 * 1) / (1.63 * 72) = 45.45842 mL/min. Hence, the patient's creatinine clearance is 45.45842 mL/min."
22,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,usmle-10,Extracted,"A 45-year-old woman comes to the physician because of fatigue and irregular menstrual cycles for the past year. She also complains of recurrent sinus infections. During the past 6 months, she has had increased urinary frequency and swelling of her feet. She has also had difficulty lifting her 3-year-old niece for the past 3 weeks. She was recently diagnosed with depression. She works as a medical assistant. The patient has smoked one half-pack of cigarettes daily for 25 years and drinks four beers on the weekends. Her only medication is escitalopram. She is 160 cm (5 ft 3 in) tall and weighs 79 kg (175 lb); BMI is 31 kg/m2. She appears tired. Her temperature is 37°C (98.6°F), pulse is 80/min, respirations are 18/min, and blood pressure is 140/82 mm Hg. Physical examinations shows neck obesity and an enlarged abdomen. Examination of the skin shows multiple bruises on her arms and legs. There is generalized weakness and atrophy of the proximal muscles. Laboratory studies show:
Serum
Na+ 150 mEq/L
K+ 3.0 mEq/L
Cl- 103 mEq/L
HCO3- 30 mEq/L
Urea nitrogen 19 mg/dL
Creatinine 0.9 mg/dL
Glucose 136 mg/dL
A 1 mg overnight dexamethasone suppression test shows a serum cortisol of 167 nmol/L (N < 50) and a 24-hour urinary cortisol is 425 μg (N < 300 μg). Serum ACTH is 169 pg/mL (N = 7–50). Subsequently, a high-dose dexamethasone suppression test shows a serum cortisol level of 164 nmol/L (N < 50).","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [45, 'years'], 'weight': [79.0, 'kg'], 'height': [160.0, 'cm'], 'creatinine': [0.9, 'mg/dL']}",78.54331,74.61614,82.47048,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 45 years old. 
The concentration of creatinine is 0.9 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 79.0 kg. The patient's bmi is therefore 79.0 kg / (1.6 m * 1.6 m) = 30.85937 kg/m^2.The patient's BMI is 30.9, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 52.38197 kg + 0.4 * (79.0 kg  - 52.38197 kg) = 63.02918 kg. The patient's adjusted body weight is 63.02918 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 45) * 63.02918 * 0.85) / (0.9 * 72) = 78.54331 mL/min. Hence, the patient's creatinine clearance is 78.54331 mL/min."
23,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5175040-1,Extracted,"A 57-year-old-male patient 165 cm tall, and weighing 68 kg in the ASA 1 risk group because of numbness of his left wrist. The biochemical parameters of the patient who was scheduled for operation under regional anesthesia with the diagnosis of carpal tunnel syndrome were as follows; Hb:14.0 mg/dL, Htc:43.0%, Plt:229000/mm3, WBC:6000/mm3, FBG:100 mg/dL, BUN:2817 mg/dL, Creatinine:0.7 mg/dL, AST:20.72 mg/dL, and ALT:12.45 mg/dL. His electrocardiogram (EKC) revealed a HR of 70 bpm with normal sinus rhythm.
Preoperatively the patient was informed about axillary nerve blockade, and his written informed consent was obtained. He didn’t receive any preoperative premedication, and in the operating room, his standard EKG, peripheral O2 saturation (SpO2), and noninvasive blood pressure (NIBP) were monitores. Using a 18 G branule a vein on the back of his left hand was punctured, and 0.09%NaCl infusion at a rate of 200 ml/hr was initiated. Right arm to be operated was positioned at 90° abduction with the torso, and forearm was flexed 90°. After cleansing the surgical field with a sterile antibacterial solution, the site was covered with sterile drape, and a single injection was made with a 22 G x 50 mm needle (Stimuplex® Braun, Melsungen, Germany). Retrograde blood was not observed during negative aspiration.
Using a peripheral nerve stimulator (Stimuplex A; B.Braun Melsungen AG, B.Braun Medical AG CH-6021, Germany) at an intensity of 1.5 mA the nerve was localized. When the intensity of the electrical current was reduced to 0.5 mA, nervous stimuli were observed which made us to think that we were on the innervation site of the nerve to be blocked. Then 40 mL anesthetic solution preprepared by anesthesia technician which we thought to be our routinely used mixture i.e. [20 mL 1% lidocaine (2 ampoules of 2% lidocaine, and 10 mL NaCl 0.09%) and 20 mL 1% prilocaine (10 mL 2% prilocaine, and 10 mL0,09% NaCl)] was injected to the patient with negative suctions after each application of 5 mL. Injection site was compressed for 5 minutes. Nearly 10 minutes later the patient felt numbness on his tongue, irritability, restlessness, agitation, he uttered meaningless words, and moved his arms, and legs senselessly. Decreased peripheral oxygen saturation and presence of peripheral cyanosis led us to make an initial diagnosis of methemoglobinemia, and supportive O2 therapy was initiated via oxygen mask at a rate of 6 lt per minute. We couldn’t measure methemoglobin levels because of lack of necessity facilities. Arterial blood gas measurements were as follows. pH: 7.43 pO2:60.1, and pCO2:44.0. Respiratory distress of the patient increased, and deepened, with a drop in his SpO2 to 76, was intubated under 1 mg/kg propofol, 1 µ/kg fentanyl, and 0.5 mg.kg−1 rocuronium anesthesia to enjure the patency of his airway. For the post-intubation maitenance of anesthesia 50 oxygen –nitrogen, and 1 mac sevoflurane were used. Following induction of anesthesia, hypotension (NIBP: 60/40 mmHg), and bradycardia (HR:40 bpm) developed which required administration of 0.5 mg atropin, and intermittent IV injections of ephedrine (total dose 30 mg). When his health state was stabilized, NIBP values improved, and his HR dropped to 70 bpm with SpO2: 95%, he was amenable for surgery. At the end of the operation which lasted for nearly half an hour, the patient was awakened with injections of 10 µg/kg atropine, and 40 µg/kg neostigmine. Thoughy the patient still continued to articulate meaningless words, and make senseless movements, since he was more cooperative we transferred the patient into the intensive care unit.
When we discerned that in place of 2% lidocaine ampoule which we always requested as a local anesthetic from the pharmacy, 10% lidocaine ampoule was sent, and anesthetic mixture was prepared without checking whether it was 2% lidocaine, we made the diagnosis of local anesthetic intoxication related to wrong formulation of lidocaine rather than methemoglobinemia
During 24-hour monitorization in the intensive care unit his hemodynamic parameters were stable, and his complaints resolved. Then the patient was traansferred to his service with relevant recommendations.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [57, 'years'], 'weight': [68.0, 'kg'], 'height': [165.0, 'cm'], 'creatinine': [0.7, 'mg/dL']}",105.47212,100.19851,110.74573,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 57 years old. 
The concentration of creatinine is 0.7 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.65 m * 1.65 m) = 24.97704 kg/m^2.The patient's BMI is 25.0, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 61.40954 kg + 0.4 * (68.0 kg  - 61.40954 kg) = 64.04572 kg. The patient's adjusted body weight is 64.04572 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 57) * 64.04572 * 1) / (0.7 * 72) = 105.47212 mL/min. Hence, the patient's creatinine clearance is 105.47212 mL/min."
24,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6755925-1,Extracted,"A 51-year-old gentleman, recently diagnosed to have type 2 diabetes mellitus and systemic hypertension, presented to the cardiology outpatient clinic on 28th July 2016 with history of pricking chest pain and shortness of breath for the past 7 years and recurrent attacks of syncope since the previous year. He weighed 49 kg and with a height of 157 cm; body mass index was 19.88 kg/m2. His blood pressure (BP) was 120/80 mmHg and pulse rate was 78/min and regular in rhythm. He was afebrile. Systemic examination was unremarkable.
Laboratory findings revealed hemoglobin of 15.1 g/dL, hematocrit of 47%, white blood cell count of 11,300/mm3 (differential count of neutrophils of 56%, lymphocytes 26%, eosinophils 11%, and monocytes of 7%), and platelet count of 293,000/mm3. Urine on routine examination showed a pH of 6.0, specific gravity of 1015, and was negative for albumin, glucose, red blood cells, and pus cells. Blood glucose fasting was 115 mg/dL and post-prandial was 219 mg/dL with an HbA1C of 7.1%. Blood urea was 27 mg/dL and creatinine was 1.0 mg/dL. Serum electrolytes were as follows: sodium 141 mEq/L, potassium 4.3 mEq/L, chloride 103 mEq/L, and bicarbonate 28 mEq/L. Serum cholesterol was 183 mg/dL, serum triglyceride 121 mg/dL, and serum uric acid 3.9 mg/dl. Two-dimensional (2D) echocardiogram showed normal left ventricular dimensions, no regional wall motion abnormality, and a left ventricular ejection fraction of 69%. Holter monitoring showed occasional supraventricular and ventricular premature complexes. On 2nd August, coronary angiography showed insignificant coronary artery disease with dominant right coronary system and he was discharged with medical advice.
On 3rd August, he attended emergency department with complaints of severe back pain, palpitation, and sweating. His back pain was sudden in onset, gradually progressive, throbbing type, rating 8/10 in pain scale, radiating to the left flank, aggravated by exertion, and partially relieved by rest. He had no other complaints. He was on metformin and calcium channel blocker. He looked anxious, agitated, and restless but was oriented and afebrile. His pulse rate was 112/min, respiratory rate was 28/min, and BP was 210/120 mmHg in the right upper limb and 210/100 mmHg over the left upper limb in supine position. There was no radio-femoral delay. Systemic examination was unremarkable except for a mild tenderness in the lumbar region.
On investigation, electrocardiography, chest X-ray, complete blood counts, liver function tests, 2D echocardiography, urine analysis, and toxicology screen were all within normal limits. Serum amylase and lipase were normal. Blood urea was 58 mg/dL and serum creatinine was 2 mg/dL. Venous blood gas (VBG) analysis showed a pH of 7.21, bicarbonate of 18 mmol/L, base excess of −9.4 mmol/L, and a lactate of 10.81 mmol/L. Serum electrolytes were sodium 138 mmol/L, potassium 3.8 mmol/L, and chloride 108 mmol/L, and anion gap was 12 mmol/L.
The following were considered in the differential diagnosis of this situation: (a) acute mesentric ischemia, (b) aortic dissection (c) hypertensive emergency, and (d) pancreatitis. Contrast-enhanced computed tomography abdomen showed a lesion in the left adrenal gland measuring about 3.5 × 3.2 cm with mild enhancement in the arterial phase, features consistent with pheochromocytoma [: Contrast enhanced CT scan of abdomen showing the mildly enhancing left adrenal mass]. No additional extra-adrenal tumors were seen. There was no evidence of mesenteric ischemia, aortic dissection, or pancreatitis. Upon further questioning his family members, it was known that he was unwell in the previous 6 months with on and off headache, palpitation, and anxiousness, which they attributed to the recently diagnosed diabetes mellitus.
His BP was managed with alpha adreno-receptor blocker and calcium channel blocker. Phenoxybenzamine was added at a dose of 10 mg twice a day and later increased to 20 mg three times daily. Persistent tachycardia and BP were stabilized with addition of beta blocker.
On 5th August 2016, the level of 24-h urine metanephrines was 14,536 mcg (reference range: less than 350 mcg/24 h) and nor-metanephrines was 7,607 mcg (reference range: less than 600 mcg/24 h).
Laparoscopic removal of pheochromocytoma was done under general anesthesia on 12th August 2016. After the surgery, there was a brief episode of hypoglycemia and hypotension, which was managed with 25% dextrose and normal saline, respectively. Azotemia resolved and blood gases were normalized. Pathological examination of the resected mass revealed a well-encapsulated tumor of size 5 cm × 4 cm × 3 cm, without hemorrhage. It showed polygonal and round cells with abundant cytoplasm and increased vasculature. There was no capsular or vascular invasion. Tumor cells were seen in the background of spindle cells with ganglion cells and Schwanian stroma. These features were reported as consistent with a CP–ganglioneuroma of the left adrenal gland []. Immunohistochemistry examination showed positivity for chromogranin, synaptophysin, and S-100 stains and negativity for calretinin in pheochromocytoma cells. Calretinin, chromogranin, synaptophysin, and S-100 stains were positive in the ganglioneuromatous component. Vimentin was positive and cytokeratin was negative. These staining characteristics confirmed the composite nature of the tumor.
At the time of discharge, his blood pressure and blood glucose were normal. Upon review on 28th February 2017, his BP was 130/80 mmHg without antihypertensive medicine. Blood glucose fasting was 90 mg/dL and post-prandial 66 mg/dL, with an HbA1C of 6.1% without any antidiabetic medicine. The levels of 24-h urinary metanephrines and normetanephrines were 62 and 604, mcg, respectively.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [51, 'years'], 'weight': [49.0, 'kg'], 'height': [157.0, 'cm'], 'creatinine': [2.0, 'mg/dL']}",30.28472,28.77048,31.79896,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 51 years old. 
The concentration of creatinine is 2.0 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 157.0 cm, which is 157.0 cm * 1 m / 100 cm = 1.57 m. The patient's weight is 49.0 kg. The patient's bmi is therefore 49.0 kg / (1.57 m * 1.57 m) = 19.8791 kg/m^2.The patient's BMI is 19.9, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 49.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 51) * 49.0 * 1) / (2.0 * 72) = 30.28472 mL/min. Hence, the patient's creatinine clearance is 30.28472 mL/min."
25,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-2981760-1,Extracted,"A 12-year-old boy, average student of class VII, presented with 1 year history of generalized tonic clinic seizures which lasted for 2-3 min. In the initial 2-3 days of his illness, he had 2-3 seizures daily for which he received carbamazepine 200 mg twice daily. Seizure though was controlled, but he started having carpopedal spasms lasting for 1-2 min. His elder brother aged 16 years also had similar illness. Examination revealed that the patient was of average built and nutrition (height 157.5 cm, weight 48kg) and there were no dysmorphic features. The neurological examination was normal except Trousseau’s sign.
The laboratory studies revealed normal hemoglobin and blood counts. His serum calcium was 6 (ionized 4) (normal 8.5-10.8, ionic 4.6-5.3) mg/dl, phosphorus 8 (normal 2.5-4.5) mg/dl, alkaline phosphatase 999 U/l, and magnesium 2.2 mg/dl, blood urea nitrogen 8 mg/dl, and creatinine 0.7 mg/dl. 24-h urinary calcium was 150 (normal 200) mg, phosphorous 0.06 (normal 1) g, and creatinine 1.29 (normal 1-2) g. His calculated TmP/GFR was 2.57 mmol/l (normal 1.15-2.44 mmol/l for 2-15 years age).[] The glomerular filtration rate was 122 ml/min. Serum 25-OH vitamin D was 9.98 (normal 9-47) ng/ml and PTH 335.4 (normal 9-55) pg/ml. His electrocardiogram, electroencephalography, radiograph of hand, feet and pelvis were normal. CT scan revealed bilateral hyperdensity in bilateral caudate, globus pallidus, putamen, and right frontal white matter. Cranial MRI revealed T1 hyperintensity in caudate, globus pallidus, putamen, and dentate nuclei bilaterally. T2 and FLAIR images were normal. He was prescribed calcitrol 0.25 mg twice daily and calcium gluconate 500 mg four times daily without anticonvulsant, on which he was asymptomatic till 1 year follow up.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [12, 'years'], 'weight': [48.0, 'kg'], 'height': [157.5, 'cm'], 'creatinine': [0.7, 'mg/dL']}",121.90476,115.80952,128,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 12 years old. 
The concentration of creatinine is 0.7 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 157.5 cm, which is 157.5 cm * 1 m / 100 cm = 1.575 m. The patient's weight is 48.0 kg. The patient's bmi is therefore 48.0 kg / (1.575 m * 1.575 m) = 19.34996 kg/m^2.The patient's BMI is 19.3, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 48.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 12) * 48.0 * 1) / (0.7 * 72) = 121.90476 mL/min. Hence, the patient's creatinine clearance is 121.90476 mL/min."
26,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6202047-1,Extracted,"A 26-year-old man with progressive chest pain and respiratory distress was transported
as an emergency case to our hospital from the local airport. He had just returned to
Japan from traveling in southeastern Asia for 1 week. He had no relevant past medical
history and was not on medication. He had developed pain in the right lower mandibular
area over the past week. The pain had progressed from the neck to the chest; he
developed a high fever during his journey and could not eat or drink. In the emergency
room, peripheral oxygen saturation was 95% with receiving oxygen at 15 L/min via an
oxygen mask and a reservoir bag. A chest X-ray showed a slightly widened mediastinum
with pleural effusion (). An
ECG revealed widespread ST-elevation (). Physical examination revealed a body mass index of 23.0 kg/m2
(height 168.0 cm; weight 65.0 kg), blood pressure of 121/68 mmHg, average heart rate of
110/min, respiratory rate of 40 breaths/min, body temperature of 37.9°C, and
tenderness and redness in the anterior and bilateral sides of the neck. White blood cell
count was 14,510/µL, neutrophils were 11,320/µL, red blood cell count
was 5.07×106/µL, hemoglobin was 14.7 g/dL, and the platelet
count was 196,000/µL. C-reactive protein level was elevated at 54.52 mg/dL (ref.
0.0–0.14 mg/dL). Blood urea nitrogen and creatinine levels were 45 mg/dL (ref.
8–20 mg/dL) and 1.06 mg/dL (ref. 0.65–1.07 mg/dL), respectively. Lactate
dehydrogenase was elevated to 510 U/L (ref. 124–222 U/L). Creatine kinase and
creatine kinase-MB were 269 (ref. 59–248 U/L) and 11.6 (ref. 0.0–12.0
U/L), respectively. The fasting blood glucose and HbA1c levels were normal. Although
these findings indicated the possibility of acute pericarditis, an ECG did not show any
findings of pericarditis or myocardial dysfunction. Contrast-enhanced CT images revealed
that a large volume of gas had collected in the neck and upper and anterior mediastinum
(). In addition,
an abscess had formed in the retropharyngeal, bilateral sub-mandibular, upper
paratracheal, and mediastinal spaces with pleural effusion and atelectasis in the right
lower basal lobe (). Thus, DNM induced by odontogenic infection with a right mandibular
second or third molar abscess was highly suspected.
A multidisciplinary team, including physicians, otolaryngologists, surgeons, and
intensivists commenced treatment within 2 hours of arrival. He received intravenous 600
mg clindamycin bid and 4.5 g tazobactam/piperacil-lin hydrate qid. A tracheostomy,
bilateral neck drainage, neck fasciotomy, and debridement via a cervical incision were
performed 5 hours after arrival. The blood culture on admission was negative.
Gram-positive cocci were found in sputum and pus, and Streptococcus
pyogenes, Streptococcus constellatus, Fusobacterium
necrophorum, and Peptostreptococcus sp. were found later in
pus culture. Continuous bilateral thoracic drainage began due to the development of a
bilateral pyothorax. Subsequently, the transcervical mediastinal and right mediastinal
areas were drained via thoracotomy. His condition improved steadily, and he was
discharged without any comorbidities on hospital day 63 after admission. Pathological
findings from the excised skeletal muscle and fascia indicated acute inflammation with
necrosis (),
consistent with necrotizing fasciitis, and a large number of Gram-positive cocci were
observed (). Thus, the
radiological diagnosis of DNM was confirmed histologically and bacteriologically.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [65.0, 'kg'], 'height': [168.0, 'cm'], 'creatinine': [1.06, 'mg/dL'], 'age': [26, 'years']}",95.7858,90.99651,100.57509,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 26 years old. 
The concentration of creatinine is 1.06 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 65.0 kg. The patient's bmi is therefore 65.0 kg / (1.68 m * 1.68 m) = 23.03005 kg/m^2.The patient's BMI is 23.0, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 64.12607 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 26) * 64.12607 * 1) / (1.06 * 72) = 95.7858 mL/min. Hence, the patient's creatinine clearance is 95.7858 mL/min."
27,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-8443410-1,Extracted,"A 66-year-old man (body height, 168 cm; body weight, 88.5 kg) experienced dyspnea, a sensation of chest tightness, and back pain for a few days before he was brought to our hospital on an emergency basis. His symptoms became aggravated suddenly as he was about to get off a taxi on his way home from work. He presented with a history of close contact with a coworker with COVID-19 and was waiting for instructions from a public health center.
In the ambulance, the following conditions were documented: Glasgow Coma Scale score, E4V5M6; heart rate, 80/min and irregular; blood pressure, 100/60 mmHg; body temperature, 38.4ºC; oxygen saturation, 98% (O2 delivered with reservoir mask at a rate of 15 L/min). On admission, his white blood cell count was 22,300/µL; hemoglobin, 14.7 g/dL; platelet count, 35 × 104/µL; creatinine level, 2.23 mg/dL; creatine kinase level, 2582 IU/L; creatine kinase myocardial band level, 164 ng/mL; low-density lipoprotein cholesterol level, 97 mg/dL; high-density-lipoprotein cholesterol level, 19 mg/dL; triglyceride level, 173 mg/dL; hemoglobin A1c level, 7.9%; C-reactive protein level, 13.8 mg/dL; troponin T level, 9.640 ng/mL; N-terminal pro-brain natriuretic peptide level, 11753 pg/mL; procalcitonin level, 0.62 ng/mL; d-dimer level, 16.34 µg/mL; and soluble fibrin level, 113.1 µg/mL. An electrocardiogram showed atrial fibrillation; ST-elevation in II, III, aVF, and V2–V6 leads; and ST depression in aVR leads (Figure ). Echocardiography revealed severe hypokinesis extending from the anterior wall to the apex and the inferior wall in left ventricle, with an approximate ejection fraction of 20%. We diagnosed STEMI and decided to perform emergency coronary angiography (CAG). A chest radiograph showed infiltrative shadows in both lungs and tracheal intubation was performed in the emergency outpatient unit (Figure ). Continuous infusion of noradrenaline (0.1 μg/kg/min) was started because his systolic blood pressure dropped below 80 mmHg. After heparin (5,000 U) was administered intravenously, the patient was transferred to the cardiac catheterization room.
CAG was performed by cardiologists, emergency physicians, clinical engineers, nurses, and radiological technologists who donned appropriate personal protective equipment before entering the room. CAG revealed total occlusion of the middle of the right coronary artery (RCA) and left anterior descending artery (LAD; Figure ). After a loading dose of dual antiplatelet therapy (aspirin, 162 mg; clopidogrel, 300 mg), an intra-aortic balloon pump catheter was inserted, and a 7-Fr guiding catheter was inserted into the left coronary artery. We removed white material, which did not at a first glance appear to be a typical thrombus, with an aspiration catheter, but blood flow did not improve. The onset-to-device time and door-to-device time were 116 and 84 minutes, respectively. Subsequent intravascular ultrasonography (IVUS) revealed several structures, which were thought to be thrombi; therefore, we performed plain old balloon angioplasty (Figure ). After the balloon was expanded, blood flow improved slightly in the LAD but not distally. Next, we placed an everolimus-eluting stent (4.0 × 38 mm) in the middle of the LAD, but peripheral blood flow was still not observed. Repeated IVUS revealed severe stenosis caused by plaque with thrombi. An additional balloon was inflated at the distal site, and a cutting balloon was also used. Another everolimus-eluting stent (2.25 × 38 mm) was placed at the distal site, but no blood flow improvements were seen angiographically.
We moved a double-lumen catheter to the distal LAD and performed CAG from the distal LAD, which revealed retrograde blood flow up to the middle of the LAD and collateral circulation from the septal branch to the RCA. Repeated IVUS examination revealed thrombi and plaque at the distal end of the stent and no intrastent blood flow (Figure ). Then, we tried to perform PCI for the total occlusion of RCA, but it was unsuccessful. At this point, 7 hours passed since the patient entered the cardiac catheterization room, and so we finished the procedure. The levels of activated clotting time during PCI were maintained at 280–310 seconds. After PCI, pathological examination proved the aspirated white material was white thrombi. Chest computed tomography performed after PCI showed ground-glass opacities distributed unevenly in both the lungs, as well as left-sided pleural effusion (Figure ). After the patient was transferred to the intensive care unit, he showed pulseless electrical activity, and cardiopulmonary resuscitation (CPR) was initiated. Return of spontaneous circulation was achieved with 1 mg of epinephrine and one cycle of CPR. Veno-arterial extracorporeal membrane oxygenation was considered, but his family decided against it. The blood pressure was maintained through the continuous administration of noradrenaline, dobutamine, and adrenaline. His nasopharyngeal swab was tested with polymerase chain reaction for SARS-CoV-2, and COVID-19-related pneumonia was diagnosed. Remdesivir treatment was initiated at a dose of 200 mg/day on the 5th day of hospitalization and continued at 100 mg/day. Because of the possibility of concomitant bacterial pneumonia, ampicillin sodium/sulbactam sodium (9 g/day) was also administered. However, the patient's oxygenation level worsened, and he died on the 7th day. It was difficult to confirm a main cause of death because we were not permitted to dissect patients due to COVID-19. We assumed that he had died from both cardiogenic shock due to myocardial infarction and septic shock due to covid-19 infection.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [66, 'years'], 'weight': [88.5, 'kg'], 'height': [168.0, 'cm'], 'creatinine': [2.23, 'mg/dL']}",34.04831,32.34589,35.75073,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 66 years old. 
The concentration of creatinine is 2.23 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 88.5 kg. The patient's bmi is therefore 88.5 kg / (1.68 m * 1.68 m) = 31.35629 kg/m^2.The patient's BMI is 31.4, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 64.12607 kg + 0.4 * (88.5 kg  - 64.12607 kg) = 73.87564 kg. The patient's adjusted body weight is 73.87564 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 66) * 73.87564 * 1) / (2.23 * 72) = 34.04831 mL/min. Hence, the patient's creatinine clearance is 34.04831 mL/min."
28,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5695022-1,Extracted,"A 26-year-old man arrived at the emergency department with a seven-day history of hematemesis and melena. He had no previous medical history and did not drink alcohol or used any illicit drug or medication.
Physical examination on admission showed blood pressure of 100/60 mmHg, a temperature of 36°C (96.8°F), a pulse rate of 90/min, and a respiratory rate of 22/min; his height was 1.75 m, weight 98 kg, and BMI 32 kg/m2. He experienced pain with deep palpation in the epigastrium and no organomegaly or lymphadenopathy was identified. The left scrotal sac was enlarged and indurated and there was a mass in the left scrotum that was indistinguishable from the left testis and provoked displacement of structures of the penis and right testis (the right scrotum was empty). No inguinal lymphadenopathy was identified.
Laboratory tests revealed normal liver function. Hemoglobin was 9.13 g/dl, MCV was 87.9 fL, WBC was 11.9 K/uL, neutrophils were 9.81 K/uL, lymphocyte count was 1.59 K/uL, and platelet level was 252 K/uL. Serum glucose level was 106 mg/dl, BUN was 38 mg/dl, creatinine was 0.9 mg/dl, and calcium was 8.9 mg/dl. Serum alpha-fetoprotein (AFP) level was 17,090 ng/mL, lactate dehydrogenase was 1480 U/L (normal range: 91–180 IU/L), and human chorionic gonadotropin level was 287.4 IU/mL.
After resuscitation with crystalloid solutions, he underwent upper endoscopy. The gastroenterologist found abundant active bleeding, for which orotracheal intubation was decided to provide airway protection. The patient was transferred to the intensive care unit. A second upper endoscopy revealed a type 1 isolated gastric varix, treated with cyanoacrylate without complications ().
A scrotal US showed a large heterogeneous image in the left testicle area, with an echogenic and cystic solid component and flow presence with color Doppler assessment.
A contrasted CT scan of the thorax, abdomen, and pelvis showed a liver of normal size and density with multiple retrocrural, retroperitoneal, mesenteric, and left iliac metastatic lymphadenopathy which caused extrinsic compression of the portal vein along with splenic vein partial thrombosis with left-sided portal hypertension and perigastric and perisplenic collateral neovascularization (). A heterogeneous, well defined mass was found in the left testicle, 16.7 × 16.1 × 14.9 cm, with a solid component that was enhanced with the administration of contrast, as well as a cystic component. There was also invasion of the left spermatic cord.
The patient was extubated after surveillance and transferred to the Internal Medicine Department. We started chemotherapy with etoposide 100 mg/m2 and cisplatin 20 mg/m2, and seven days later the patient underwent a left radical orchiectomy by an inguinal approach with left hemiscrotectomy, without complications. Following this intervention, serum alpha-fetoprotein (AFP) level was reduced to 350 ng/mL, and the human chorionic gonadotropin level was 50 IU/mL.
A postoperative biopsy showed a pure testicular teratoma () with glandular formations and the presence of cartilage (a) and respiratory epithelium, with ciliated columnar cells alternating with goblet cells (b).
The patient was discharged after showing clinical improvement to receive ambulatory chemotherapy.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [26, 'years'], 'weight': [98.0, 'kg'], 'height': [1.75, 'm'], 'creatinine': [0.9, 'mg/dL']}",143.34233,136.17521,150.50945,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 26 years old. 
The concentration of creatinine is 0.9 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.75 m. The patient's weight is 98.0 kg. The patient's bmi is therefore 98.0 kg / (1.75 m * 1.75 m) = 32.0 kg/m^2.The patient's BMI is 32.0, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.75 m, which is 1.75 m * 39.3701 in/m = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 70.46466 kg + 0.4 * (98.0 kg  - 70.46466 kg) = 81.4788 kg. The patient's adjusted body weight is 81.4788 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 26) * 81.4788 * 1) / (0.9 * 72) = 143.34233 mL/min. Hence, the patient's creatinine clearance is 143.34233 mL/min."
29,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5588616-1,Extracted,"A 21-year-old Japanese woman was admitted to our hospital because of proteinuria and hematuria. She had been diagnosed at birth with persistent cloaca and congenital esophageal atresia, and underwent enterostomy, cystostomy, and radical esophageal surgery, followed by repair of persistent cloaca and colostomy closure 2 years later. She was followed-up at the pediatric surgery and urology department, and developed with no major problems. Proteinuria and hematuria were detected at routine examination 7 months prior to admission for the first time. No urological problems were detected at a visit to the urology department 3 months before admission. She had mild edema before admission; however its onset had been gradual and it was therefore not clear when the edema had started.
On admission, the patient’s height was 158.6 cm, her weight was 53.0 kg, and her blood pressure was 101/80 mmHg. Physical examination revealed an abdominal midline operation scar and pretibial pitting edema. Urinary examination revealed a protein level of 3+ and 5–9 red blood cells per high-power field. Her urine protein/creatinine ratio was 3.38 g/gCr, blood urea nitrogen was 13.2 mg/dL, serum creatinine was 0.73 mg/dL, and serum albumin was 3.6 g/dL. Serum C3 was 25 mg/dL, C4 was 18.5 mg/dL, and 50% hemolytic unit of complement (CH50) was 13 U/mL. Chromosome G banding revealed a normal karyotype 46XX. Kidney ultrasound showed no kidney deformity. Kidneys size was normal.
A renal biopsy contained 24 glomeruli, all of which showed moderate to severe mesangial hypercellularity and increased homogenous materials in the mesangium. Which were positive with periodic acid-Schiff and were negative with methenamine silver (Fig. ). One glomerulus revealed fibrous crescent formation, and 11 showed segmental double contour of glomerular basement membrane. Immunofluorescence microscopy showed slight staining for fibrinogen, but no staining for IgG, IgA, IgM, kappa light chain and lambda light chain (Fig. ). Electron microscopy showed massive granular deposits in the mesangial area and some subepithelial area (Fig. ). According to these findings, we speculated fibronectin glomerulopathy as a diagnosis. Thus, we performed immunoassays using anti-human fibronectin antibodies. The staining with IST-4, which detects plasma and cell-associated fibronectin, was positive but no staining was observed with IST-9, which stains only cell-associated fibronectin (Fig. ). The mesangial deposits were therefore shown to comprise plasma fibronectin. The patient was finally diagnosed as fibronectin glomerulopathy.
Her family history was investigated further. Although her mother and younger sister had previously been detected to have proteinuria, their urine and blood tests were normal. Her father showed no urinary abnormalities and normal kidney function at his annual health examination. Given that no family history of renal disease could be identified, the current case was determined to be sporadic. The patient and her mother underwent genetic testing of the FN1 gene, which revealed no abnormalities.
Treatment with an angiotensin II receptor antagonist and a sodium-restricted diet were started. However, 10 months after the kidney biopsy, the patient’s proteinuria had increased and her renal function was deteriorated, with a urine protein/creatinine ratio of 9.52 g/gCr, serum creatinine 0.86 mg/dL. Her serum albumin decreased to 2.0 g/dL.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [21, 'years'], 'weight': [53.0, 'kg'], 'height': [158.6, 'cm'], 'creatinine': [0.73, 'mg/dL']}",98.3677,93.44931,103.28608,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 21 years old. 
The concentration of creatinine is 0.73 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 158.6 cm, which is 158.6 cm * 1 m / 100 cm = 1.586 m. The patient's weight is 53.0 kg. The patient's bmi is therefore 53.0 kg / (1.586 m * 1.586 m) = 21.07024 kg/m^2.The patient's BMI is 21.1, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 51.11425 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 21) * 51.11425 * 0.85) / (0.73 * 72) = 98.3677 mL/min. Hence, the patient's creatinine clearance is 98.3677 mL/min."
30,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-3306738-1,Extracted,"A 41-year-old male was referred to our Nephrology Unit because of worsening of kidney function and proteinuria. He was born at term of a normal pregnancy from apparently healthy, nonconsanguineous parents. The patient's early development was normal and he had no evident clinical problem until 18 years of age, when he developed seizures triggered by light and recurrent headaches. He was prescribed Valproic Acid and started a discontinuous follow-up in Neurology. In 1991 (age 22) EEG revealed well-represented alpha background activity, with a complex wave-peak after 7-10 flashes/sec, an expression of an epileptogenic photosensitive centroencephalic focus. In 1992, in the presence of signs of myopathy (asthenia, increase of serum lactate, myalgia), a muscle biopsy showed non-specific changes (occasional small red sub-sarcolemmal deposits, showing oxidative enzymatic activity). In 1992 the patient's sister (3 years younger) developed generalized seizures and myopathy. Genetic counseling suggested the presence of a mitochondrial disease.
Detection of the 3243A > G mutation of mitochondrial DNA confirmed the diagnosis of MELAS syndrome in the patient, his sister, his mother and one of the mother's sisters.
In the subsequent decade, he started and discontinued different types of anticonvulsant therapy (including Lamotrigine and Phenobarbital), and developed recurrent seizures, with imaging evidence of an ischemic lesion in the left hemisphere, progressive bilateral sensorineural hearing loss and sensitive distal polyneuropathy with increasing muscle weakness. On various occasions, lactic acidosis was found (lactic acid 10-13.5 mmol/L; normal <2 mmol/L).
In July 2009 (age 39) he was diagnosed with diabetes mellitus (weight loss, polyuria and polydipsia); at diagnosis, glycated hemoglobin was 19.6% and glycemia <500 mg/dL. Insulin treatment was started. Soon after diagnosis, he developed a sepsis due to Klebsiella pneumoniae. A CT scan, performed on the suspicion of a pyelonephritis focus, showed a solid hypervascularized mass, highly suggestive of neoplasia, in the right kidney. During hospitalization, serum creatinine was 0.9 mg/dL; 24-hour proteinuria was absent at repeated urinalysis; glomerular filtration rate (eGFR) was 62 mL/min (Cockcroft and Gault formula). He was normotensive (usual blood pressure 120/80 mmHg) and remained so during follow-up.
In November 2009 the patient underwent right nephrectomy. At surgery, a second small superficial tumor was detected. The histological examination identified a renal oncocytoma (2 cm); a smaller lesion (0.5 cm) had an appearance highly suggestive of chromophobe carcinoma. However, the lesion could also represent a tumoral focus of tubular oncocytosis and a precursor of another oncocytoma (Figures and ). The cytogenetic analysis was not performed, in this case; however, the two lesions are highly correlated, and a further definition was considered as of minor clinical relevance.
At hospital discharge, serum creatinine was 1.17 mg/dL with mild proteinuria (30 mg/dL). In the same year the patient's sister developed breast cancer and was identified as a carrier of the BRCA-2 mutation. However, the other family members, including our patient, preferred not to perform genetic testing for the BRCA mutation.
In January 2011 the patient was referred to our center. Glycemic control was good (glycated hemoglobin 6.5% on Repaglinide). Blood pressure was normal, without therapy. Cognitive impairment and psychomotor agitation, choreiform movements and intentional tremor, nystagmus and lower limb muscle weakness, hypotrophy and severe muscle wasting were present (height 155 cm, weight 36 Kg, BMI: 15). His speech was slow, slurred but coherent, and he appeared severely depressed. His last biochemical tests were: serum creatinine 2.1 mg/dL (eGFR 23 mL/min), proteinuria 3.6 g/24 hours, low-normal total proteins (6.2 g/dL) and normal serum albumin (3.7 g/dL). EKG was normal; no sign of cardiomyopathy was detected. Further tests showed: low IgG levels (499 mg/dL), normal IgA and IgM (213 and 115 mg/dL respectively); high PTH (445 pg/mL); moderate acidosis (pH 7.227; HCO3 22.8; SBE -3.7; normal lactates: 1.2 mmol/L); antinuclear antibodies and ANCA were negative.
Renal ultrasounds showed moderate medullary hyperechogeneity, consistent with tubulo-interstitial or vascular damage.
The rapid progression of kidney disease, with the development of nephrotic proteinuria, led us to review the samples of kidney tissue at a distance from the cancer lesions.
Of note, the changes were recorded before the onset of proteinuria and in the absence of hypertension, both at nephrectomy and over the follow-up.
Morphological examination revealed a widespread interstitial fibrosis and marked vascular changes characterized by intimal fibrosis of arcuate and interlobular arteries with a wedge-shaped area of interstitial fibrosis and tubular atrophy extending to the renal capsule suggestive of ischemic damage (Figure ). Hyaline arteriolosclerosis (Figures and ) and signs of chronic inflammation were also seen. These severe vascular lesions were the basis of the different glomerular alterations including ischemic and obsolescent glomeruli. The obsolescent glomeruli amounted to approximately 50% of the more than 100 glomeruli sampled. Some rare glomeruli (about 5-10%) showed focal segmental glomerulosclerosis, which in this context can be interpreted as consequent to the vascular alterations.
As the patient subsequently developed nephrotic syndrome, these lesions suggest that silent ischemic changes may result in the development of focal segmental glomerulosclerosis secondary to nephron loss, at least in some cases of MELAS-related nephropathy.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [41, 'years'], 'weight': [36.0, 'kg'], 'height': [155.0, 'cm'], 'creatinine': [2.1, 'mg/dL']}",23.57143,22.39286,24.75,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 41 years old. 
The concentration of creatinine is 2.1 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 36.0 kg. The patient's bmi is therefore 36.0 kg / (1.55 m * 1.55 m) = 14.98439 kg/m^2.The patient's BMI is 15.0, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 36.0 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation. 
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 41) * 36.0 * 1) / (2.1 * 72) = 23.57143 mL/min. Hence, the patient's creatinine clearance is 23.57143 mL/min."
31,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-8019405-1,Extracted,"A 67-year-old man in good health reported numbness and weakness of his lower legs in June 2010. He presented to the clinic due to the spread of the symptoms to his upper limbs. Magnetic resonance imaging revealed multiple lacuna infarctions. Laboratory analysis revealed anemia (hemoglobin [Hb], 9.8 g/dL) and renal dysfunction (creatine, 2.7 mg/dL). He was admitted to a nearby hospital for further examination and was diagnosed with hypertension and multiple mononeuropathy. In addition, laboratory findings revealed increased levels of C-reactive protein (CRP, 16.82 mg/dL). After 8 days in the hospital, severe right-flank pain suddenly occurred, and anemia worsened (Hb, 6.8 g/dL). Abdominal computed tomography (CT) without enhancement revealed a right perirenal hematoma. He was then transferred to our hospital for investigation and treatment.
On admission, his height was 156.0 cm, and his weight was 54.5 kg (approximately 2-kg loss over months). His blood pressure was 192/114 mm Hg; pulse, 98 bpm; and body temperature, 37.1 ℃. On physical examination, palpebral conjunctiva was pallid, and he had severe right-flank pain with muscular defense. No skin rush was evident in the extremities, although hypesthesia was detected by neurologic examination. Laboratory findings on admission are presented in Table . The results of the urine tests were as follows: protein levels, 2.4 g/g⋅Cr; occult blood 3+ by dipstick test; red blood cells ≧ 100/high-power field; and sediment contained granular cast 2+ . The results of serum examinations were as follows: white blood count, 13,610/µL (with 74.0% neutrophils and 16.0% eosinophils); hemoglobin, 6.2 g/dL; platelet count, 32.1 × 104/µL; alkaline phosphatase, 1,867 IU/L; γ-glutamyl transpeptidase (γ-GTP), 360 IU/L; blood urea nitrogen, 39 mg/dL; Cr, 1.3 mg/dL; erythrocyte sedimentation rate, 156 mm; C-reactive protein, 11.5 mg/dL; immunoglobulin (Ig) G, 2533 mg/dL; IgA, 306 mg/dL; IgM, 106 mg/dL; C3, 83 mg/dL; C4, 15 mg/dL; and CH50, 48 U/mL. ANA, PR3-ANCA, MPO-ANCA, anti-GBM antibody, and HBs-antigenemia were not detected. Contrast-enhanced CT revealed bilateral pleural effusion, right small renal infarction, and right perirenal hematoma. CT angiography revealed multiple small aneurysmal dilatations in the intrarenal branches of the bilateral renal arteries and the intrasplenic branches of the splenic artery (Fig. a–c). Emergency selective coil embolization was conducted to the right renal artery aneurysm, which was responsible for the bleeding (Fig. ). To obtain a definitive diagnosis, we performed a left sural nerve biopsy (Fig. ). We confirmed a small arterial occlusion with inflammatory cell infiltration in the sural nerve tissue, although a histological examination did not reveal fibrinoid necrosis or granuloma. Collectively, and based on his clinical and radiographic findings, we diagnosed polyarteritis nodosa.
On the fifth hospital day, we started oral prednisolone therapy at 40 mg/day. On the 8th and 15th hospital days, intravenous methylprednisolone pulse (500 mg/day) therapy was started for 3 consecutive days. Although these therapies suppressed the disease activity, including inflammatory response, urine protein, and pleural effusion, the patient failed to achieve remission. Intravenous pulse cyclophosphamide therapy was, therefore, given on the 30th day. Clinical symptoms such as numbness and weakness of limbs gradually diminished, and laboratory findings dramatically improved. Moreover, contrast-enhanced CT revealed the disappearance of pleural effusion and the decreased size of perirenal hematoma concomitant with aneurysms. The patient was then transferred to another hospital for rehabilitation training (Fig. ).","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [54.5, 'kg'], 'height': [156.0, 'cm'], 'creatinine': [2.7, 'mg/dL'], 'age': [67, 'years']}",19.99987,18.99988,20.99986,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 67 years old. 
The concentration of creatinine is 2.7 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 156.0 cm, which is 156.0 cm * 1 m / 100 cm = 1.56 m. The patient's weight is 54.5 kg. The patient's bmi is therefore 54.5 kg / (1.56 m * 1.56 m) = 22.39481 kg/m^2.The patient's BMI is 22.4, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 53.25993 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 67) * 53.25993 * 1) / (2.7 * 72) = 19.99987 mL/min. Hence, the patient's creatinine clearance is 19.99987 mL/min."
32,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-2923787-1,Extracted,"A 43-yr-old female visited a nearby hospital because of abnormal shadows including multiple nodules and reticular shadows on chest radiography found at an annual medical checkup in 2005. A bronchoscopic examination was performed. They were unable to obtain a biopsy specimen from one of the nodules in S10 of the left lung because the patient had a strong bleeding tendency. She was referred to this hospital for further examination on June 30, 2005.
On admission, her height was 157.5 cm and weight, 50.3 kg. Her consciousness was clear. The conjunctivas were anemic and not jaundiced. Her heart sounds were normal. Fine crackles were audible in the right lower lung field. The abdomen was not distended. Her inguinal lymph nodes were palpable and no other superficial lymph nodes were palpable. She was experiencing slight polyarthralgia, however, radiography films showed no joint anomalies.
The laboratory data were: erythrocyte sedimentation rate, 119 mm/1 hr; white cell count, 8,900/µL; hemoglobin, 8.4 g/dL; platelet count, 39.4×104/µL; serum aspartate aminotransferase, 22 IU/L; alanine aminotransferase, 22; total protein, 9.7 g/dL; albumin 2.6; creatinine, 0.48; PT, 13.1 sec (INR 1.45); aPTT, 39.6 (control, 10.4); fibrinogen, 750 mg/dL; KL-6, 277 U/mL (reference range <500); C-reactive protein, 11.7 mg/dL (<0.3); serum immunoglobulin (Ig)G, 4,570 (870-1740); IgA, 491(110-400), IgM, 706 (35-220), CH50, 52.3 U/mL (30-50), soluble IL-2 receptor, 1,400; serum IL-6, 6.8 pg/mL (<4); rheumatoid factor (RF), 1,330 IU/mL (<20). Autoantibodies, including antinuclear antibody, anti-ds-DNA, anti-Sm, anti-RNP, cytoplasmic antineutrophil cytoplasmic antibody (ANCA), and myeloperoxidase-ANCA were all negative. M-protein was not noted in serum immunoelectrophoresis. Bone marrow aspiration showed hyperplasia with no abnormal morphology on smear specimens.
Chest radiographys showed multiple nodules and reticular shadows mainly in the lower lung field. Chest CT scan disclosed a slight enlargement of the mediastinal lymph nodes, centrilobular nodules, thin-walled cysts, the thickening of the bronchovascular bundles, and ground-grass opacities, all of these findings were compatible with those of lymphocytic interstitial pneumonia (LIP; ) (, ). 67Gallium citrate scintigraphy did not reveal any evident accumulation.
A lung surgeon and a thoracic physician declined to perform a lung biopsy because of her bleeding tendency (bleeding time: 6 min 30 sec) and poor general condition. A biopsy of an inguinal lymph node was obtained for making a definite diagnosis (). She was diagnosed with MCD and undifferentiated arthritis based on the characteristic pathology of the specimen of the inguinal lymph node, CT findings of the bilateral lung lesions and laboratory data.
She was initially administered intravenous corticosteroid (methylprednisolone, 500 mg/day, 3 consecutive days) followed by oral corticosteroid (methylprednisolone, 16 mg/day), and, 375 mg/m2 rituximab every week for 4 weeks. The polyarthralgia instantly disappeared; however, none of the other clinical and laboratory parameters were fully resolved. Therefore the therapeutic regimen was changed to tocilizumab (8 mg/kg, every 2 weeks), oral corticosteroid (methylprednisolone, 16 mg/day) on October 25, 2005. The patient requested that the interval between tocilizumab to be increased to more than every two weeks. The dose of corticosteroid in combination with tocilizumab should be kept as low as possible to avoid various side effects, such as osteoporosis, hyperglycemia, and hypertension. It is indicated for the treatment of rheumatoid arthritis in Japan. The addition of tacrolimus to the regimen was considered to fulfill such requirements. Both the possible merits and demerits of the drug were explained to the patient and her oral consent was obtained. Tacrolimus (3 mg/day) was introduced on November 10, 2005. Laboratory findings, including anemia, hypergammaglobulinemia, and an increase in acute phase proteins responded to this regimen (). The enlargement of mediastinal lymph nodes and abnormal shadows were also partially alleviated (). The intervals of the tocilizumab-administration sessions were extended from every 2 weeks to every 3 weeks from January 2006. Oral corticosteroid was gradually tapered from 16 mg/day finally to 4 mg/day. The dose of tacrolimus has been unchanged. The disease activity has been totally suppressed for 36 months by this maintenance regimen.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [43, 'years'], 'weight': [50.3, 'kg'], 'height': [157.5, 'cm'], 'creatinine': [0.48, 'mg/dL']}",119.56727,113.58891,125.54563,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 43 years old. 
The concentration of creatinine is 0.48 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 157.5 cm, which is 157.5 cm * 1 m / 100 cm = 1.575 m. The patient's weight is 50.3 kg. The patient's bmi is therefore 50.3 kg / (1.575 m * 1.575 m) = 20.27715 kg/m^2.The patient's BMI is 20.3, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 50.11819 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 43) * 50.11819 * 0.85) / (0.48 * 72) = 119.56727 mL/min. Hence, the patient's creatinine clearance is 119.56727 mL/min."
33,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-8005225-1,Extracted,"This case involves an unmarried 25-year-old phenotypic Japanese female, 154.1 cm in height and 48.5 kg in weight, and without a notable medical, family, or psychosocial history. She did not consume alcohol, tobacco, or any drugs. The patient was examined at the age of 18 at a gynecology clinic for primary amenorrhea where, given the patient’s active involvement in competitive track and field, she was diagnosed with athletic amenorrhea without further tests being conducted. Afterwards, the patient underwent no treatment and did not experience menstruation. Moreover, the patient had not engaged in sexual intercourse up to this point.
Upon examination by a local physician with the main complaint of abdominal distention, the patient was referred to our hospital with a suspected ovarian tumor, as a giant 17 cm tumor was found in the pelvis. The inspection of the external genitalia revealed clitoral hypertrophy and narrowing of the vaginal opening (Fig. ). Pelvic magnetic resonance imaging (MRI) revealed a tumorous lesion in the pelvis measuring 218 × 115 × 178 mm, containing a mixture of cystic and solid components. The uterus could not be found. The cystic components contained blood, and the solid portion had a contrast effect (Fig. ). Examination by 18F-fluorodeoxyglucose (FDG)-positron emission tomography/computed tomography revealed FDG accumulation in the tumor and in enlarged abdominal para-aortic lymph nodes. Blood tests revealed the following levels: white blood cells (WBC): 10.7/μL × 103; hemoglobin: 10.1 g/dL; platelets: 412/μL × 104; C-reactive protein (CRP): 18.1 mg/dL; total protein: 7.7 g/dL; albumin: 3.8 g/dL; urea nitrogen: 8 mg/dL; creatinine: 0.53 mg/dL; total bilirubin: 0.6 mg/dL; aspartate aminotransferase (AST): 30 IU/L; alanine aminotransferase (ALT): 8 IU/L; follicle-stimulating hormone (FSH): 52.4 mU/mL; luteinizing hormone (LH): 34.4 mU/mL; estradiol (E2): < 10 pg/mL; progesterone (P4): 0.66 ng/mL; and testosterone: 0.25 ng/mL. Serum alpha-fetoprotein (2.4 ng/mL) was within the normal range, but serum beta-human chorionic gonadotropin (5.86 ng/mL), lactate dehydrogenase (4574 µg/L), and CA125 (165 µg/mL) were elevated. Urinalysis was normal. As DSD was suspected because of the appearance of the pelvic tumor, chromosome testing was performed. The karyotype was found to exhibit 45,X/46,XY mosaicism, and the patient was diagnosed with MGD. Since the pelvic tumor was considered to be a gonadal tumor, a resulting complication of MGD, an exploratory laparotomy was performed in order to arrive at a definitive pathologic diagnosis of the tumor.
A physical examination revealed a patient who looked unwell, with blood pressure of 119/77 mmHg, heart rate of 117 beats per minute, and body temperature of 38.7 °C. Neurological examination was unremarkable and did not offer any substantial information. Surgical findings revealed marked adhesions between the tumor and the surrounding organs, making excision difficult. Therefore, only a biopsy of the tumor was performed (Fig. a, b). The final pathological diagnosis was “seminoma” (Fig. ). Consequently, the patient was diagnosed with clinical stage IIB testicular cancer (seminoma) with MGD.
Postoperative systemic chemotherapy was started promptly, consisting of bleomycin, etoposide, and cisplatin (BEP). At the time of the fourth course of BEP, tumor markers had normalized (Fig. ). Marked tumor reduction was confirmed with imaging, and subsequently the patient underwent interval debulking surgery. Surgery involved bilateral gonadectomy and resection of disseminated peritoneal lesions (Figs. a, b, ). Pathological examination of the excised specimens was consistent with necrosis of the seminoma due to the effect of chemotherapy. No viable tumor remains were found. No further chemotherapy was administered, and the initial course of treatment was completed. We notified the patient regarding MGD, and she decided her future sex as female. Therefore, we proposed some surgical options for clitoromegaly or vaginal stenosis. However, she did not wish to pursue those at that time.
Currently, 4 years and 11 months after the initial treatment, there has been no recurrence of the tumor. In addition, the patient has been on postoperative hormone replacement therapy in the form of an estradiol/norethindrone acetate patch and psychotherapy continuously.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [25, 'years'], 'weight': [48.5, 'kg'], 'height': [154.1, 'cm'], 'creatinine': [0.53, 'mg/dL']}",120.49542,114.47065,126.52019,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 25 years old. 
The concentration of creatinine is 0.53 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 154.1 cm, which is 154.1 cm * 1 m / 100 cm = 1.541 m. The patient's weight is 48.5 kg. The patient's bmi is therefore 48.5 kg / (1.541 m * 1.541 m) = 20.4238 kg/m^2.The patient's BMI is 20.4, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 47.03944 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 25) * 47.03944 * 0.85) / (0.53 * 72) = 120.49542 mL/min. Hence, the patient's creatinine clearance is 120.49542 mL/min."
34,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6877966-1,Extracted,"A 19-year-old male with sickle cell anemia, being treated with folic acid, presented to the emergency department of Samtah General Hospital, Jizan, Saudi Arabia, with fever, nausea, headache, and yellowish discoloration of sclera. Patient was living in Jizan, an endemic area of malaria, which raised suspicion of malaria infection. Patient looked unwell, conscious, and alert. His vital signs were normal except the temperature which was high (38.5 degree C). Chest examination was normal and the cardiovascular system showed normal first and second heart sounds with no added sound. Fundus examination was normal. Other systemic reviews were unremarkable. Patient was admitted in the medical ward, and baseline laboratory investigations revealed the following remarkable laboratory values: white blood cells 12 × 109/L (normal range: 4.5 to 11.0 × 109/L); hemoglobin 7.3 g/dL (normal range: 13.8 to 17.2 g/dL); mean corpuscular volume 72 fL/red cell (normal range: 80–96 fL/red cell); platelet count 62 × 103/μL (normal range: 150–400 × 103/μL); reticulocyte 2.6% (normal range: 0.5% to 2.5%); aspartate transaminase 89 U/L (normal range: 10 to 40 U/L); alanine transaminase 78 U/L (normal range: 7 to 56 U/L); total bilirubin 600 μmol/L (normal range: 1.71 to 20.5 μmol/L); direct bilirubin 200 μmol/L (normal range: less than 5.1 μmol/L); and sodium 149 mmol/L (normal range: 136–145 mmol/L), whereas the following laboratory values were found to be in normal ranges: alkaline phosphatase 120 IU/L (normal range: 44 to 147 IU/L); random blood glucose 7.2 mmol/L (normal range: 4.4–8.9 mmol/L); potassium 4.9 mmol/L (normal range: 3.6–5.2 mmol/L); magnesium 0.9 mmol/L (normal range: 0.6–1.1 mmol/L); calcium 2.3 mmol/L (normal range: 2.2–2.7 mmol/L); phosphate 1.4 mmol/L (normal range: 1.12–1.45 mmol/L); creatinine 78 mmol/L (normal range: 60–110 mmol/L); and urea 3.7 mmol/L (normal range: 2.5–7.1 mmol/L).
ECG initially showed normal sinus rhythm, and chest X-ray was normal. The patient had no previous history of cardiac arrhythmias, and his baseline ECG was normal (). Peripheral blood smear revealed P. falciparum (ring form) with parasitemia index 10%. His body weight was 74 kg and height 166 cm.
Patient was diagnosed with severe P. falciparum malaria based on clinical presentation and laboratory investigations and started on intravenous artesunate 170 mg (2.4 mg/kg) bolus slowly over 2 minutes at 0 hour, 12 hours, and 24 hours, and every 24 hours thereafter for 5 days. The powder for injection was reconstituted with 5% sodium bicarbonate and diluted in an equal volume of normal saline. He was started on paracetamol 500 mg tablet orally as needed every 6 hours. Patient was clinically improving and temperature subsided. After 4 hours of the third dose of artesunate, the patient became sick, faint, and suddenly arrested. Resuscitation was done for 32 minutes, ECG was done and showed wide complex ventricular tachycardia, and QTc (Bazett) was 516 msec (). Electrolytes were in the normal limits: sodium 136 mmol/L; potassium 4.3 mmol/L; magnesium 0.8 mmol/L; and calcium 2.1 mmol/L. Tachycardia was managed by administration of amiodarone (150 mg i.v. for 10 minutes). The patient revived and kept in ICU for further observation. There was no worsening of hemolytic anemia during and after the treatment with artesunate. The treatment plan was not changed; the next dose of artesunate was after 24 hours of the third dose (last dose given before event happened). The patient clinically improved, fever subsided, and the temperature decreased with paracetamol to 37.4°C, and he was walking and conversing normally. The treatment was completed by oral artesunate 100 mg + sulfadoxine 500 mg/pyrimethamine 25 mg tablets (3-day course).","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [19, 'years'], 'weight': [74.0, 'kg'], 'height': [166.0, 'cm'], 'creatinine': [78.0, 'mmol/L']}",0.12759,0.12121,0.13397,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 19 years old. 
The concentration of creatinine is 78.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from mmol to mg. The mass of creatinine is 78.0 mmol. To convert 78.0 mmol of creatinine to mol, multiply by the conversion factor 0.001, giving us 78.0 mmol creatinine * 0.001 mol/mmol = 0.078 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.078 mol creatinine * 113.12 g/mol = 8.82336 g creatinine. To convert 8.82336 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 8.82336 g creatinine * 1000.0 mg/g = 8823.36 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 8823.36 mg creatinine/10.0 dL = 882.336 mg creatinine/dL. The concentration value of 78.0 mmol creatinine/L converts to 882.336 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 74.0 kg. The patient's bmi is therefore 74.0 kg / (1.66 m * 1.66 m) = 26.85441 kg/m^2.The patient's BMI is 26.9, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 166.0 cm, which is 166.0 cm * 0.393701 in/cm = 65.35437 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.35437 (in inches) - 60) = 62.31505 kg.
Hence, the patient's IBW is 62.31505 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 62.31505 kg + 0.4 * (74.0 kg  - 62.31505 kg) = 66.98903 kg. The patient's adjusted body weight is 66.98903 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 19) * 66.98903 * 1) / (882.336 * 72) = 0.12759 mL/min. Hence, the patient's creatinine clearance is 0.12759 mL/min."
35,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5385225-1,Extracted,"A 24-year-old man with a protein-losing gastroenteropathy due to an intestinal lymphangiectasia was treated with glucocorticoids (prednisolone, 7.5 mg/day) and developed low-grade fevers 7 months before admission. He did not have any remarkable life histories. Five months before admission, the man complained of headaches, fatigue, and a hearing abnormality. Then, he experienced nausea, diarrhea, and drowsiness for 6 days and subsequently sought evaluation at our hospital. The physical examination at the time of admission revealed that he was slow to respond (Japan Coma Scale 1-1). The following measurements were obtained: height, 161.2 cm; weight, 51.0 kg; BMI, 19.6 kg/m2; blood pressure, 119/78 mmHg; heart rate, 62 bpm; and body temperature, 37.4°C. The remainder of the examination findings were normal, without any signs of meningitis.
The initial laboratory data showed a white blood cell count of 11700/μL, with 87.0% neutrophils (86% segmented and 1% band neutrophils), 2.0% lymphocytes, 10%monocytes, 0% eosinophils, 1% metamyelocytes, hemoglobin = 15.7 g/dL, and a platelet count of 157,000/μL. The serum C-reactive protein level was slightly elevated (0.80 mg/dL). Although the serum sodium level was slightly decreased (130 mEq/L), the potassium (4.6 mEq/L), chloride (97 mEq/L), creatinine (0.59 mg/dL), fasting glucose (85 mEq/L), and HbA1c (5.1%) concentrations were normal.
An abdominal computed tomography (CT) showed bilateral adrenal enlargement (right, 10.0 × 20.0 mm; left, 29.0 × 29.0 mm). A retrospective analysis of the CT images revealed that the enlargement in the left adrenal gland developed 5 months before admission (), which coincided with the onset of fevers and headaches. Subsequently, the bilateral adrenal enlargement progressed (). The differential diagnosis of adrenal enlargement includes metastatic carcinoma, bilateral adrenal hyperplasia, tuberculosis, and fungal infections. A whole-body examination failed to find a primary malignant lesion. The QuantiFERON-TB test and HIV antibody titer were negative.Although there were no signs of meningeal irritation, a diagnostic lumbar puncture was performed. The cerebrospinal fluid revealed an increased white blood cell count (240/μL), a normal protein level, a decreased glucose level (0.10 g/l), and a positive cryptococcal antigen titer. The pathologic specimen showed the presence of yeast-like organisms, such as Cryptococcus spp. on Alcian blue staining, which was subsequently determined to be Cryptococcus neoformans.
Although the level of serum adrenocorticotropic hormone (ACTH) was elevated (131.3 pg/mL; normal range, 7.2–63.3 pg/mL) at the time of the diagnosis of cryptococcosis (), cortisol release in response to ACTH (Cortrosyn), which was evaluated 1 day after prednisolone cessation, was increased (). Oral prednisolone (7.5 mg/day) was then resumed as treatment for the protein-losing gastroenteropathy. The other endocrinological data of adrenal gland ruled out the possibility of pheochromocytoma and aldosterone-secreting tumors in this patient ().
Amphotericin B (250 mg/day) was initiated, followed by the addition of fluconazole (400 mg/day). The symptoms improved gradually after beginning antifungal treatment. Fluconazole alone was continued after discharge. After the initiation of antifungal treatment, the elevated ACTH levels were decreased and varied during the treatment (), suggesting a stressed condition with infection at the diagnosis and unstable absorption of prednisolone due to the protein-losing gastroenteropathy. Mild hyponatremia probably due to relative adrenal insufficiency was improved to the normal range (138 mEq/L) one month after the initiation of the antifungal treatment.
An abdominal CT, which was routinely obtained during follow-up, showed that the size of the adrenal glands decreased following antifungal therapy and became normal without any abnormal findings, including calcifications, 6 months after starting treatment ().","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [24, 'years'], 'weight': [51.0, 'kg'], 'height': [161.2, 'cm'], 'creatinine': [0.59, 'mg/dL']}",139.26554,132.30226,146.22882,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 24 years old. 
The concentration of creatinine is 0.59 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 161.2 cm, which is 161.2 cm * 1 m / 100 cm = 1.612 m. The patient's weight is 51.0 kg. The patient's bmi is therefore 51.0 kg / (1.612 m * 1.612 m) = 19.62638 kg/m^2.The patient's BMI is 19.6, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 51.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 24) * 51.0 * 1) / (0.59 * 72) = 139.26554 mL/min. Hence, the patient's creatinine clearance is 139.26554 mL/min."
36,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6196924-1,Extracted,"A 24-year-old man arrived at the emergency department with a four-month history of pain and swelling of the left testicle. A week ago, he developed progressive edema in the lower limbs, which was followed 48 hours before admission by dysesthesia and paraparesis as well as urinary incontinence. He had no previous medical history and did not consume alcohol or use any illicit drug or medication.
Physical examination on admission showed a blood pressure of 100/60 mmHg, a temperature of 36°C, a pulse rate of 90/min, and a respiratory rate of 22/min; his height was 1.75 m, weight 98 kg, and BMI 32 kg/m2. He referred bilateral paresthesia of the lower limbs and pain on mobilization of the lumbar spine. The left scrotal sac was enlarged and indurated, and there was a mass in the left scrotum that was indistinguishable from the right testis and provoked displacement of the penis and right testis. No inguinal lymphadenopathy was identified. When examining both lower extremities, we found edema without fovea. Neurological examination revealed hypoesthesia, areflexia, and decreased muscle strength.
Laboratory tests revealed normal liver function. Hemoglobin was 9.13 g/dL, MCV was 87.9 fL, WBC was 11.9 K/μL, neutrophil count was 9.81 K/μL, lymphocyte count was 1.59 K/μL, and the platelet level was 252 K/μL. Serum glucose was 148 mg/dL, BUN was 38 mg/dL, creatinine was 1.3 mg/dL, and calcium was 8.9 mg/dL. Serum alpha-fetoprotein (AFP) was 11.28 ng/mL, lactate dehydrogenase was 1687 U/L (normal range 91–180 IU/L), and human chorionic gonadotropin level was 10.05 IU/mL.
A scrotal ultrasound showed a hypoechoic oval-shaped infiltrative lesion in the left testicle of 6.1 × 3.2 × 2.7 cm, associated with a large left hydrocele, with an estimated volume of 450 mL. Microcalcifications were seen in both testis.
A contrasted CT scan of the thorax, abdomen, and pelvis showed bilateral supraclavicular adenopathies and multiple round pulmonary nodules with well-defined edges of bilateral and diffuse distribution. In the liver, there were two hyperdense lesions: one larger lesion of 4.8 × 2 cm located in hepatic segment IV and a second lesion of 1.9 cm in segment VIII, with partially defined borders and enhancement to contrast administration. There was also a large retroperitoneal ganglionar conglomerate of 10 × 6 cm, which infiltrated the spinal cord.
An MRI of the dorsal and lumbar spine showed a large and heterogeneous retroperitoneal conglomerate which invaded the left psoas muscle and infiltrated the spinal cord through the intervertebral foramina of T11 with displacement of the L1 vertebral body (). Metastatic infiltration of the vertebral bodies L3–L5 was also seen ().
A diagnosis of clinical stage IIIC testicular cancer was established with a poor prognosis due to nonpulmonary visceral metastases. After initial treatment with high-dose intravenous corticosteroids, the case was evaluated by a multidisciplinary oncological team. Three fractions of external beam radiotherapy were given. He then underwent a left radical orchiectomy by an inguinal approach with a left hemiscrotectomy, without complications. A postoperative biopsy showed a pure embryonal carcinoma with invasion of the spermatic cord and necrosis of more than 50% of its surface. After finishing 10 fractions of radiotherapy for a total of 30 Gy, and improving his renal function with intravenous crystalloids, the patient received his first cycle of chemotherapy (CT). We planned a CT regimen based on bleomycin, etoposide, and cisplatin (BEP), repeated every 21 days for a total of four cycles.
After the eighth day of CT, the patient presented sudden dyspnea at rest that progressed to hypoxemic respiratory failure. Due to this condition, we decided to perform orotracheal intubation and the patient was then transferred to the intensive care unit. An angio-CT revealed the presence of bilateral pulmonary thromboembolism. Despite the treatment received, the patient died three days later.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [24, 'years'], 'weight': [98.0, 'kg'], 'height': [1.75, 'm'], 'creatinine': [1.3, 'mg/dL']}",100.978,95.9291,106.0269,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 24 years old. 
The concentration of creatinine is 1.3 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.75 m. The patient's weight is 98.0 kg. The patient's bmi is therefore 98.0 kg / (1.75 m * 1.75 m) = 32.0 kg/m^2.The patient's BMI is 32.0, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.75 m, which is 1.75 m * 39.3701 in/m = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 70.46466 kg + 0.4 * (98.0 kg  - 70.46466 kg) = 81.4788 kg. The patient's adjusted body weight is 81.4788 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 24) * 81.4788 * 1) / (1.3 * 72) = 100.978 mL/min. Hence, the patient's creatinine clearance is 100.978 mL/min."
37,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-8022680-1,Extracted,"A 185-cm, 75-kg, 46-year-old man with an American Society of Anesthesiologists physical status 3 and a 15 pack-year history of smoking as well as postoperative nausea and vomiting, cannabis use, and gastroesophageal reflux presented for median sternotomy with open resection of a left-sided, biopsy-proven 13.1 × 9.4 × 4.5-cm type B-1 thymoma with distal tracheal deviation (Figures , ). The patient had initially presented with unrelated symptoms that led to a chest X-ray. This incidentally revealed the mediastinal mass, which was subsequently further evaluated. The patient had no family history of muscular dystrophies or electrolyte abnormalities. Although the original frozen section was read as lymphoma, final cytology confirmed thymic origin.
On the morning of the surgery, the patient denied dyspnea, orthopnea, double vision, difficulties chewing, speaking, or swallowing, or peripheral muscle weakness. Airway examination revealed a Mallampati IV classification with appropriate mouth opening and prognathism without restriction of neck movement. No stridor was appreciated in the sitting or supine position.
After discussion with the procedural team about vessels at risk for surgical sacrifice, a 20-G left radial arterial catheter was placed preoperatively using local anesthesia. Preoperative arterial blood gas (ABG) and other laboratory studies showed no significant abnormalities, preserved renal function with normal estimated glomerular filtration rate, a serum creatinine of 1.0 mg/dL, a serum blood urea nitrogen of 14 mg/dL, and a serum potassium of 4.5 mmol/L.
Anxiolysis was achieved using midazolam, and the patient was induced with intravenous ketamine combined with sevoflurane via a nasal continuous positive airway pressure device (SuperNO2VATM; Vyaire Medical, Mettawa, IL, USA), ensuring preservation of spontaneous ventilation. A 20-mg bolus of intravenous propofol was administered to facilitate placement of a size 4 igelⓇ supraglottic airway (Intersurgical Ltd., Wokingham, Berkshire, UK). Bronchoscopy was performed through the supraglottic airway to obtain visualization of the left main bronchus and secondary carina. Propofol was incrementally titrated until spontaneous ventilation was temporarily halted and capacity to provide adequate positive pressure ventilation was ensured. Reassuring bronchoscopy findings and ventilation allowed titration of rocuronium and uneventful placement of a left-sided 37-French, double-lumen endotracheal tube via direct laryngoscopy. Appropriate positioning was confirmed under bronchoscopic visualization.
The surgical resection was technically challenging given local tumor invasion into the left lung parenchyma as well as bilateral mediastinal parietal pleura. The resection required significant tumor manipulation, and the left phrenic nerve could not be spared by the cardiothoracic surgeons (Figure ). To help improve surgical conditions, intermittent alternating left and right lung isolation was required. The patient tolerated this well without significant desaturation. Hypercarbia levels were maintained within acceptable ranges anticipated for one-lung ventilation, especially compared to thoracoscopically assisted cases with carbon dioxide insufflation.
After considerable tumor manipulation requiring intermittent breath holds, an intraoperative ABG was obtained to assess oxygenation and ventilation status, revealing a potassium of 6.5 mmol/L. To confirm this value, another ABG drawn by a different physician showed a potassium of 6.2 mmol/L. In an effort to remove further confounding factors, a different anesthesia technician ran a third confirmatory ABG that returned a potassium of 6.1 mmol/L, a pH of 7.27, partial pressure of carbon dioxide of 56 mmHg, hemoglobin of 12.6 g/dL, bicarbonate of 24.7 mmol/L, a base deficit of 2.4 mmol/L, a sodium of 133 mmol/L, a chloride of 107 mmol/L, ionized calcium of 1.09 mmol/L, and a glucose of 133 mg/dL (Table ). T-waves were not peaked, and there were no other notable abnormalities on electrocardiogram.
The patient was given 50 mEq of sodium bicarbonate and 6 g of calcium gluconate over 45 min. A five-unit bolus of insulin was administered intravenously with 12.5 g of dextrose, and an insulin infusion was started at 2 units/hour and titrated up to 5 units/hour. Given frequent one-lung ventilation and intermittent respiratory cessation, β-agonist therapy and hyperventilation were deferred. Diuretic therapy was avoided given implementation of other therapies, adequate urine production, and a lack of electrocardiographic changes or other symptoms. The patient’s potassium level improved to 5.2 mmol/L by the end of the procedure without evidence of hypoglycemia, and he produced 800 mL of urine. The patient’s temperature was 36.4°C at the beginning, 36.1°C during, and 37.1°C at the end of the surgery. After successful conclusion of the procedure, the patient’s respiratory mechanics were evaluated using negative inspiratory force and rapid shallow breathing index, and he was extubated uneventfully and transferred to the intensive care unit. The patient did not experience any further hyperkalemia during his hospital stay and was discharged on postoperative day 3. At follow-up, the patient expressed appreciation for the care he received.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [46, 'years'], 'weight': [75.0, 'kg'], 'height': [185.0, 'cm'], 'creatinine': [1.0, 'mg/dL']}",97.91667,93.02084,102.8125,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 46 years old. 
The concentration of creatinine is 1.0 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 185.0 cm, which is 185.0 cm * 1 m / 100 cm = 1.85 m. The patient's weight is 75.0 kg. The patient's bmi is therefore 75.0 kg / (1.85 m * 1.85 m) = 21.91381 kg/m^2.The patient's BMI is 21.9, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 75.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 46) * 75.0 * 1) / (1.0 * 72) = 97.91667 mL/min. Hence, the patient's creatinine clearance is 97.91667 mL/min."
38,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-2769420-1,Extracted,"We present the case of a 19-year-old Hispanic female previously healthy, whose relevant medical history only included smoking 4 cigarettes a day for one year. The patient was admitted to our hospital for left periorbital pain, ipsilateral ocular motor nerve palsies and diplopia. Four days prior to admission, the patient started with first episode in her life of severe left periorbital pain; 48 hours later, she also presented limited left eye movements, ipsilateral palpebral ptosis and horizontal diplopia. Pain did not cede after the administration of NSAID, which was the reason why the patient decided to resort to the ER for examination.
At the hospital, she was submitted to a thorough physical examination by a multidisciplinary team integrated by three ophthalmologists, a neurologist and three specialists in internal medicine. The results of the physical and neuro-ophthalmologic examination were weight 89 kg, height: 1.57 mt, BMI 36 kg/m2, 20/20 vision, normal eye fondues bilaterally, left palpebral ptosis, exotropia of the primary look of the left eye, paresis of the third, fourth and sixth left cranial nerves, and hypoesthesia over the first and second division of the left trigeminal nerve. The right eye and the rest of the physical examination did not show further abnormalities ().
Since the beginning, we considered Tolosa-Hunt syndrome as a possibility, but started the clinical approach as a painful ophthalmoplegia. Her initial laboratory tests showed white blood cell count, 8.500/ml; red blood cell count, 4.86×106/μl; haemoglobin, 15.1 g/dl; platelets, 293×103; glucose, 98 mg/dl, blood urea nitrogen, 8 mg/dl; creatinine, 0.6 mg/dl; ELISA for HIV, negative; D-Dimer, 271 ng/ml (<500 ng/ml). Thyroid function tests showed TSH, 1.00 μUI/ml (0.34-5.60); Total T3, 0.96 ng/ml (0.87-1.78); free T 3, 2.64 pg/ml (2.50 y 3.90); free T4, 0.76 ng7 dl (0,54-1.64); Total T4, 10.72 μg/dl (6.09-12.23). The cerebral spinal fluid reported 2 mononuclear cell/uL; glucose, 51 mg/dl; proteins, 15 mg/dl; ADA and PCR in CFS for tuberculosis and cultures were negative. ANA´s, were positive in a homogenous pattern 1:40; anti-dsDNA, 15.1 U/ml (0-9.6); c-ANCA, positive 1:40 and x-ANCA, 1:20. CT scan of brain and paranasal sinus, MRI and MRA of the brain were normal.
Since the studies showed no abnormalities and we excluded neoplasic, infectious, vascular, thyroid and metabolic causes of painful ophthalmoplegia, we decided to start treatment for Tolosa-Hunt Syndrome with metilprednisolne 1 gr IV daily for 3 days, and noticed significant response of the left periorbital pain, palpebral ptosis and the ipsilateral ocular motor nerve palsies in the next 72 hours. At day 4, we changed treatment to prednisone at 1 mg/kg daily. One week later, we initiated steroid tapering every week, and at week 6 the patient was asymptomatic and her neuro-ophthalmologic examination was completely normal. Today the patient is still on prednisone 10 mg/day ().","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [89.0, 'kg'], 'height': [1.57, 'm'], 'creatinine': [0.6, 'mg/dL'], 'age': [19, 'years']}",155.70171,147.91662,163.4868,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 19 years old. 
The concentration of creatinine is 0.6 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.57 m. The patient's weight is 89.0 kg. The patient's bmi is therefore 89.0 kg / (1.57 m * 1.57 m) = 36.10694 kg/m^2.The patient's BMI is 36.1, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.57 m, which is 1.57 m * 39.3701 in/m = 61.81106 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.81106 (in inches) - 60) = 49.66544 kg.
Hence, the patient's IBW is 49.66544 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 49.66544 kg + 0.4 * (89.0 kg  - 49.66544 kg) = 65.39926 kg. The patient's adjusted body weight is 65.39926 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 19) * 65.39926 * 0.85) / (0.6 * 72) = 155.70171 mL/min. Hence, the patient's creatinine clearance is 155.70171 mL/min."
39,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6820813-1,Extracted,"A 32-year-old Japanese woman was admitted to our hospital for evaluation of microscopic hematuria with a positive family history. Urinary occult blood had been detected during a health checkup at the age of 29 years, while 11–30 erythrocytes per high-power field (HPF) were seen in the urinary sediment at the age of 31 years. Her grandfather had required hemodialysis, but his renal disease was unknown.
On admission, the patient was 153.0 cm tall and weighed 44 kg, with a blood pressure of 108/75 mmHg, heart rate of 82/min, and temperature of 37.4 °C. There was no peripheral edema and no purpura, neuropathy, or arthritis.
Laboratory tests revealed that the white blood cell count was 5500/μL, hemoglobin (Hb) was 15.0 g/dL, and the platelet count was 29.9 × 104/μL. In addition, serum albumin was 4.8 g/dL, blood urea nitrogen was 14 mg/dL, creatinine was 0.79 mg/dL, eGFR was 68.6 mL/min/1.73m2, aspartate aminotransferase (AST) was 19 IU/L, and alanine aminotransferase (ALT) was 21 IU/L, and γ-glutamyl transpeptidase was 18 IU/L. C-reactive protein was 0.0 mg/dL, while IgG was 961 mg/dL and IgA was 149 mg/dL (normal 110–410). Complement components C3 and C4 were 78 and 10 mg/dL, and CH50 was 37 U/mL (normal 30–50). Immunological tests including anti-double-stranded DNA antibody and antinuclear antibody suggesting autoimmune diseases were all negative. The activated partial thromboplastin time (APTT) was 29.5 s (normal 27–40) and the prothrombin time (PT) was 106.5% (normal > 75). Urinary protein excretion was 0.02 g/day, and the sediment contained 11–30 erythrocytes per HPF and detected dysmorphic red blood cells. Computed tomography (CT) of the chest and abdomen showed that her kidneys were normal in size with no morphological abnormalities. Definite nut cracker phenomenon in CT was not detected before renal biopsy.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [44.0, 'kg'], 'height': [153.0, 'cm'], 'creatinine': [0.79, 'mg/dL'], 'age': [32, 'years']}",71.01266,67.46203,74.56329,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 32 years old. 
The concentration of creatinine is 0.79 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 153.0 cm, which is 153.0 cm * 1 m / 100 cm = 1.53 m. The patient's weight is 44.0 kg. The patient's bmi is therefore 44.0 kg / (1.53 m * 1.53 m) = 18.79619 kg/m^2.The patient's BMI is 18.8, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 44.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 32) * 44.0 * 0.85) / (0.79 * 72) = 71.01266 mL/min. Hence, the patient's creatinine clearance is 71.01266 mL/min."
40,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5434261-1,Extracted,"A 66-year-old man was transferred to our hospital because of confusion, severe general fatigue, and dyspnea of 1-week duration. The patient had chronic kidney disease related to diabetic nephropathy. Although we strongly recommended initiation of chronic HD, the patient refused the treatment.
The patient had a 15-year history of type 2 diabetes mellitus with triopathy. Other medical history included hypertension of unknown duration that was being treated with amlodipine besylate, losartan, and carvedilol. There was no prior history of seizures, neurological symptoms, loss of vision or other underlying illnesses, or use of any other drugs. Upon arrival at our outpatient department, the patient had severe dyspnea.
On admission (day 0), the patient had mild confusion and anasarca. His height was 168 cm; body weight, 74 kg; blood pressure, 124/43 mmHg; and body temperature, 35.7°C. Urinalysis showed 1+ proteinuria and 2+ occult blood, − glucose, and − ketone and urinary sediment revealed 1–4 erythrocytes, 1–4 leukocytes, 1–4 squamous cells, and 0-1 transitional cells per HPF, but no casts. Blood tests showed low hemoglobin (4.6 g/dL), white blood cell count of 5240/µL (82.3% neutrophils, 12.8% lymphocytes, 1.1% eosinophils, 3.6% monocytes, and 0.2% basophils), and thrombocytopenia (platelet count 84 × 103/µL). Blood chemistry showed blood urea nitrogen (BUN) of 222 mg/dL; serum creatinine, 25.4 mg/dL; total protein, 5.7 g/dL; albumin, 3.3 g/dL; lactate dehydrogenase, 403 IU/L; aspartate aminotransferase, 46 IU/L; alanine aminotransferase, 44 IU/L; serum sodium, 139 mmol/L; and serum potassium, 6.1 mmol/L, glucose 97 mg/dL. Serological tests showed C-reactive protein of 0.2 mg/dL. Coagulation parameters were normal. Chest X-ray showed congestion of the lung fields. The patient had pulmonary edema and uremic symptoms (vomiting and consciousness disorder). We performed brain MRI and electroencephalogram (EEG) to evaluate cerebral function.
T2-weighted fluid attenuated inversion recovery (FLAIR) MRI showed several old, small brain infarcts (Figures and ). Diffusion-weighted MR imaging (DWI) did not show increased apparent diffusion coefficient (ADC), which would be suggestive of vasogenic edema. EEG showed frequent slow waves, consistent with metabolic encephalopathy ().
The patient was placed on short-duration HD (2 hours) with smaller surface area (cellulose triacetate; membrane area: 0.7 m2) and low blood flow (100 mL/min) to avoid DDS (). His consciousness gradually improved and he did not develop symptoms of DDS.
On day 15, we repeated MRI and EEG. T2-weighted FLAIR MRI showed increased signal intensities bilaterally in the cortical and subcortical areas of the occipital lobe (Figures and ). DWI demonstrated no hyperintense signal alterations in these regions. He had no cerebral infarcts, but the ADC was elevated in bilateral occipital lesions (Figures and ). Thus, although the patient did not have clinical symptoms of DDS, we diagnosed that he had asymptomatic brain edema. EEG on day 15 had been compared with the findings on admission; namely, the slow waves on EEG had decreased, consistent with improving uremic encephalopathy. The patient underwent vascular access surgery for HD and continued maintenance HD. On day 29, a third MRI was performed and showed return to findings on admission ().
The patient was discharged on regular intermittent HD without any neurological deficits. No further neurological disturbances were noted during 1-year follow-up.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [66, 'years'], 'weight': [74.0, 'kg'], 'height': [168.0, 'cm'], 'creatinine': [25.4, 'mg/dL']}",2.75459,2.61686,2.89232,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 66 years old. 
The concentration of creatinine is 25.4 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 74.0 kg. The patient's bmi is therefore 74.0 kg / (1.68 m * 1.68 m) = 26.21882 kg/m^2.The patient's BMI is 26.2, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 64.12607 kg + 0.4 * (74.0 kg  - 64.12607 kg) = 68.07564 kg. The patient's adjusted body weight is 68.07564 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 66) * 68.07564 * 1) / (25.4 * 72) = 2.75459 mL/min. Hence, the patient's creatinine clearance is 2.75459 mL/min."
41,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4307179-1,Extracted,"A 70-year-old Caucasian man (weight: 75kg; height: 165cm) with T2DM, hypertension and prostatic hypertrophy was referred to our unit for CRC treatment. His usual medications included metformin (3000mg/day), irbesartan/hydrochlorothiazide 150mg/12.5mg/day and tamsulosin (0.4mg/day).
Ten weeks after receiving pre-operative chemoradiotherapy, the patient underwent a low anterior rectal resection with a diverting ileostomy. Metformin treatment was suspended 3 days before the operation.
The patient’s post-operative course was uneventful. His renal function was normal; his blood glucose was between 150mg/dl and 200mg/dl after a meal; and his stoma output was approximately 600ml/day.
Metformin therapy was resumed 5 days after surgery, when the patient returned to a normal diet. He was discharged to home in good condition on the ninth post-operative day.
Two weeks later, he returned to our department because of nausea, vomiting and diffuse abdominal pain. In the preceding days, he had noticed an increased stoma output that required him to empty the stoma bag four or five times per day. He also referred to being anuric for the preceding 24 hours.
During his examination, the patient appeared dehydrated and had tachypnea and a reduced level of consciousness. His blood pressure was 90/60mmHg, and his pulse rate was 90/min. His laboratory tests showed acute kidney injury (AKI) (creatinine, 8.94mg/dl; blood urea nitrogen, 324mg/dl) with severe lactic acidosis (pH, 6.99; partial pressure of carbon dioxide, 12mmHg; base excess, -26.9 mM).
Aggressive hydration with crystalloids and intravenous bicarbonate infusion was initiated. The patient’s internal jugular vein was cannulated, and he was promptly transferred to the hemodialysis unit. Hemodialysis was performed for 6 hours and repeated 12 hours later for 3 hours using bicarbonate-buffered dialysate. His chemical profile and clinical condition then improved dramatically. His acidosis resolved over the course of 24 hours; his spontaneous diuresis resumed after 48 hours; and his renal function recovered. The patient was discharged 8 days after admission with a serum creatinine level of 2.5mg/dl and a blood urea nitrogen concentration of 50mg/dl. His ileostomy was closed about 1 month later, and he did not experience any further similar episodes. At a follow-up examination almost 1 year later, he was well and disease-free.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [75.0, 'kg'], 'height': [165.0, 'cm'], 'creatinine': [8.94, 'mg/dL'], 'age': [70, 'years']}",7.26945,6.90598,7.63292,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 70 years old. 
The concentration of creatinine is 8.94 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 75.0 kg. The patient's bmi is therefore 75.0 kg / (1.65 m * 1.65 m) = 27.54821 kg/m^2.The patient's BMI is 27.5, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 61.40954 kg + 0.4 * (75.0 kg  - 61.40954 kg) = 66.84572 kg. The patient's adjusted body weight is 66.84572 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 70) * 66.84572 * 1) / (8.94 * 72) = 7.26945 mL/min. Hence, the patient's creatinine clearance is 7.26945 mL/min."
42,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-7249747-1,Extracted,"We present a case of severe AKI with rhabdomyolysis in a 49-year-old, experienced, competitive male trail runner (weight 66 kg, height 183 cm, body mass index 19.7 kg/m2, running 5-6 times/ week, training load 70-100 km/week) who presented six days after a 110-km trail race to the accident and emergency department. He participated in one of Europe’s toughest ultra-trail race, the Grossglockner Ultra-Trail, a 110-km trail race with 6.500 m positive climb and an average elevation higher than 2,000 m for at least half of the course, including technically difficult terrain and trails. He finished the race in a time of approximately 18 hours (overall winning time of 14:40:14 hr:c). Prior to the event, he was free of injury, otherwise fit and healthy, non-smoker, with no other past medical history of note. Blood tests approximately six months before the event showed a normal renal function (creatinine 1 mg/dL, glomerular filtration rate [GFR] >90 mL/min/1.73 m2). Immediately prior to the event, he ingested 500 mg of naproxen and 20 mg of esomeprazole. Throughout the race, he consumed little oral fluids (approximately 4 litres of fluids in total, during approximately 18 hours of running). There was no urination throughout the race. Immediately after crossing the finish line, he started to re-hydrate and increased his fluid intake ad libitum and shortly thereafter had one episode of chocolate brown urination. He felt fine, with some post-race fatigue and subsequently returned home. The following day he noticed some mild generalised swelling with oliguria, despite regular food and fluid intake. After two days, urination returned to normal, but the generalised oedema increased over the following days with a combined weight gain of approximately 10 kg. Subsequently, he felt generally tired and fatigued, and at this stage he presented to the local accident and emergency department six days post-event. Biochemically the diagnosis of severe AKI with rhabdomyolysis was made. Conservative measures with intravenous and oral fluid therapy were instigated, and renal replacement therapy was contemplated. However, his kidney function gradually improved, as well as elevated potassium levels, with conservative measures; therefore renal replacement therapy was not required. Further investigations included abdominal radiographs (due to abdominal extension), ultrasounds of both kidneys, urine analysis (dip stick and microscopic) and serial laboratory blood tests, as well as cardiac assessment, including ECG. Radiological imaging and cardiological assessment were unremarkable, as well as blood gas analysis, without signs of metabolic acidosis. The patient remained hospitalised for two weeks, and on discharge his renal function and clinical symptoms had improved considerably. Subsequent regular blood test demonstrated a gradual return of his creatinine levels after approximately six months. Estimated laboratory GFR remained reduced, with no evidence of microproteinuria (albumin-to-creatinine ratio) (Table ). At this point, he was allowed to return to gradual aerobic activity under close supervision of his sports physician.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [66.0, 'kg'], 'height': [183.0, 'cm'], 'creatinine': [1.0, 'mg/dL'], 'age': [49, 'years']}",83.41667,79.24584,87.5875,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 49 years old. 
The concentration of creatinine is 1.0 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 183.0 cm, which is 183.0 cm * 1 m / 100 cm = 1.83 m. The patient's weight is 66.0 kg. The patient's bmi is therefore 66.0 kg / (1.83 m * 1.83 m) = 19.70796 kg/m^2.The patient's BMI is 19.7, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 66.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 49) * 66.0 * 1) / (1.0 * 72) = 83.41667 mL/min. Hence, the patient's creatinine clearance is 83.41667 mL/min."
43,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4532033-1,Extracted,"A 44-year-old woman was admitted to our hospital for the evaluation of Cushing’s syndrome. She was diagnosed as hypertension at a local clinic in 1986 but recieved no antihypertensive medication. She developed headache, nausea and vomiting in Feb, 1990 and was admitted to the department of neurosurgery with diagnosis of Rt. cerebellar hemorrhage. After discharge, she has been followed for treatment of hypertension. During the follow-up period, she was found to have the Cushingoid features and transferred to the Department of Internal Medicine for the evaluation of Cushing’s syndrome.
The family and other past medical history were not contributory.
On admission, blood pressure was 150/110 mmHg, pulse rate 78/min, body temperature 36.5°C, respiration rate 18/min and height was 164cm and body weight was 77kg.
On physical examination, she was shown to have central obesity. Her face was round and plethoric. She had pink conjunctivae and white sclerae.
On auscultation of the chest, breathing sounds were normal and the heart sound was regular without murmur. On examination of the abdomen, she was found to have striae. Further examination revealed no abnormal finding.
Laboratory studies included hemoglobin 12.7g/dl, WBC 6700/mm3 with 75% neutrophils and 23% lymphocytes, platelet 261,000/mm3, total protein 7.2g/dl, albumin 4.2g/dl, total bilirubin 0.7mg/dl, direct bilirubin 0.3mg/dl, ALT 17unit, AST 19 unit, alkaline phosphatase 65U/L, BUN 20mg/dl and creatinine 1.1mg/dl. The concentrations of Na, K, CI and Ca were normal. FBS was 116mg/dl and HbA1c was 3.1%. Urinalysis was normal.
The results of low and high dose dexamethasone suppression test were shown in .
Chest PA and skull series revealed no abnormal findings.
By her history and physical examination, we suspect she had Cushing’s syndrome and then measured 24hr urine free cortisol and performed low dose dexamethasone suppression test. After this study, high dose dexamethasone suppression test was done to differentiate the etiology of Cushing’s syndrome. The levels of plasma cortisol were not suppressed and plasma ACTH level was very low. Abdominal CT scanning was done under the impression of adrenocortical tumor but revealed no abnormal mass in the adreanal gland first. Therefore we performed pituitary fossa MRI to rule out Cushing’s disease associated with micronodular adrenal hyperplasia. MRI reveals atrophic pituitary gland with empty sella. At that time, we didn’t decide the treatment modality for this patient because of poor general condition.
Instead, follow-up study was recommended. Follow-up abdominal CT scan, 3 years after the first study, revealed 2cm-sized hypodense mass in the upper pole of lt, adrenal gland (). So, explorative laparotomy was done under the impression of lt, adrenal adenoma. At operation field, no abnormal adrenal mass was found but the surgeon performed lt, adrenalectomy. The cut surface of surgical specimen showed multiple black pigmented nodules with pale atrophic cortex ().
On the microscopic finding, pigmented micronodular dysplasia with cortical atrophy was found (, ).
After operation, her blood pressure was normalized, and follow-up hormonal levels were also improved.
We concluded that her Cushing’s syndrome resulted from primary pigmented nodular adrenocortical disease and we plan the contralateral adrenalectomy.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [44, 'years'], 'weight': [77.0, 'kg'], 'height': [164.0, 'cm'], 'creatinine': [1.1, 'mg/dL']}",66.354,63.0363,69.6717,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 44 years old. 
The concentration of creatinine is 1.1 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 164.0 cm, which is 164.0 cm * 1 m / 100 cm = 1.64 m. The patient's weight is 77.0 kg. The patient's bmi is therefore 77.0 kg / (1.64 m * 1.64 m) = 28.62879 kg/m^2.The patient's BMI is 28.6, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 164.0 cm, which is 164.0 cm * 0.393701 in/cm = 64.56696 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.56696 (in inches) - 60) = 56.00401 kg.
Hence, the patient's IBW is 56.00401 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 56.00401 kg + 0.4 * (77.0 kg  - 56.00401 kg) = 64.40241 kg. The patient's adjusted body weight is 64.40241 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 44) * 64.40241 * 0.85) / (1.1 * 72) = 66.354 mL/min. Hence, the patient's creatinine clearance is 66.354 mL/min."
44,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-7838889-1,Extracted,"Male patient, 26 years old, kitchen assistant, originated from Taxco, Guerrero and living there until he emigrated to Texas, United States, in 2016, where he was diagnosed with B lymphoblastic leukemia in January 2017. He received four cycles of unspecified chemotherapy with apparent remission of the disease and came back to Mexico (Cuernavaca, Morelos). He was admitted to the National Institute of Cancer in Mexico City in November 2017, where he was diagnosed with early relapse. From November 2017 to January 2018, he received chemotherapy for relapse with BFM like protocol (L-Asparaginase, Vincristine, Daunorubicin, and Prednisone). He did not receive any antifungal prophylaxis. On day +23 he was presented with febrile neutropenia, with no etiologic agent identified. An empirical treatment of five days of Meropenem was administered, with resulting in fever remission. He was discharged 6 days after his admission, asymptomatic but with persistent neutropenia.
Two days later, he had come back with an acute abdomen, although afebrile. Vital constants at admission were: BP: 107/78 mmHg, HR: 90 bpm, RR: 20 rpm, T °: 36.5 °C, weight: 55 Kg, height: 1.62 m, BMI: 21 Kg/m2. His blood tests showed leukocytes of 0.32 × 103/μL, absolute neutrophils 0.0032 x103/μL, hemoglobin 5.7 g/dL, platelets 35 × 103/μL, creatinine 0.66 mg/dL, ALT 174 IU/L, AST 82 IU/L, ALP 1004 IU/L, GGT 572 IU/L, total bilirubin 8 mg/dL, conjugated bilirubin 6.4 mg/dL, unconjugated bilirubin 1.62 mg/dL, LDH 287 IU/L, albumin 1.7 mg/dL, C reactive protein 8.4 mg/dL. The patient underwent exploratory laparotomy which revealed sigmoid perforation. Sigmoidectomy and colostomy were performed. The initial pathology report was diverticulum perforation. Forty-eight hours later, he presented moderate diffuse abdominal pain, and temperature > 38 °C. The blood cultures were negative. Administration of Meropenem, caspofungin and Filgastrim was empirically initiated. Contrast abdominal tomography (CT) showed diffuse liver lesions consistent with liver abscesses ().
A liver biopsy of the lesions was performed under ultrasound guidance; the aerobic, anaerobic and Sabouraud dextrose agar cultures were negative. The pathology showed granulomatous hepatitis with extensive necrosis; Grocott’s stain evidenced hyaline hyphae. The histopathology of the sigmoid surgical specimen was reviewed again and then reported as transmural ischemic necrosis, acute and chronic peritonitis, and positive Grocott’s stain with the same hyphae described in the liver ().
Hyalohyphomycosis was concluded. The serum galactomannan was negative. Pulmonary involvement was not seen by tomography. The antifungal treatment was changed from caspofungin to intravenous Voriconazole on day 23. The patient had gradual clinical improvement the neutropenia was remitted and was discharged with a treatment of oral voriconazole 200 mg bid. He was, at that time, in complete remission of leukemia.
Three weeks later he was readmitted for abdominal pain in the right hypochondrium with fever without neutropenia; he reported bad adherence to oral antifungal treatment for economic reasons. The new abdominal CT showed the persistence of liver abscesses. Exploratory laparotomy plus drainage were performed finding abscesses in segments II, IV and VI. The anaerobic culture grew Bacteroides fragilis; he completed 14 days of Metronidazole. The fungal culture was negative. The pathology report was extensive granulomatous hepatitis with necrosis and negative Grocott’s stain. The patient received 2 weeks of intravenous Voriconazole plus 6 weeks of the same oral antifungal. At the end of treatment, the abdominal CT showed only one residual lesion of 16 mm. A timeline of the case is shown in .
He did not present further complications of the infectious process. However, six months later, while undergoing hematopoietic stem-cell transplant evaluations, he presented a relapse of leukemia and he decided to stop the antineoplastic treatment. He died seven months later.
A paraffin block of the first liver biopsy was requested, and DNA extraction was performed. Genomic DNA was extracted from the paraffin-embedded tissue sample using a DNeasy blood and tissue kit (Qiagen, Ventura, CA, USA) according to the manufacturer’s instructions before preliminary removal of paraffin by extraction with xylene protocol. The molecular identification was performed by 18S-ITS1-5.8S-ITS2-25S rRNA gene amplification using a set of primers previously reported to identify fungi species (5′-TCCGTAGGTGAACCTTGCGG-3′) and ITS4 (5′-TCCTCCGCTTATTGATATGC-3′). A PCR product of 500 bp was amplified, purified and sequenced in both directions; nucleotide sequence was determined with Taq FS Dye Terminator Cycle Sequencing Fluorescence-Based Sequencing and analyzed on an Applied Biosystems 3730 DNA sequencing system (Foster City, CA, USA). The sequence was edited with Vector NTI program and homology search was performed in the GenBank database (nucleotide blast), finding a 100% identity with Fusarium graminearum complex strain HUT59 []. (). The sequences used are shown in .","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [26, 'years'], 'weight': [55.0, 'kg'], 'height': [1.62, 'm'], 'creatinine': [0.66, 'mg/dL']}",131.94444,125.34722,138.54166,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 26 years old. 
The concentration of creatinine is 0.66 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.62 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.62 m * 1.62 m) = 20.95717 kg/m^2.The patient's BMI is 21.0, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 55.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 26) * 55.0 * 1) / (0.66 * 72) = 131.94444 mL/min. Hence, the patient's creatinine clearance is 131.94444 mL/min."
45,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4052557-1,Extracted,"A 52-year-old female patient was referred to our clinic because of the recent discovery of hypercalcemia in a routine oncological control. Her oncologist, assuming that the diagnosis was most likely to be tumor-induced hypercalcemia, referred her to an endocrinologist, who undertook further tests to reveal the etiology of hypercalcemia. The physical examination revealed her to be eupneic, blood pressure of 120/80 mmHg with 84 beats per second. The patient had a history of left breast carcinoma. Our patient had undergone a left mastectomy one year previously (estrogen-receptor positive, progesterone-receptor positive, Her2 negative) and received letrozole without any complications until hospitalization. She remained well and achieved a complete response without an increase of carcinoembryonic antigen (CEA, (normal value <5 ng/mL)) or carbohydrate antigen 15-3 (CA 15-3, normal value: 0.5–29 IU/mL) since ten months.
Currently she is 1.62 m tall, weighting 62 kg, with a body mass index (BMI) of 23 kg/m2 and using letrozole only for the indication prescribed. She had started a course of letrozole ten months earlier. Her family history was unremarkable. As her hypercalcemia was mild and did not elicit any symptoms, she did not require immediate measures to correct this.
Investigations to determine the cause of the hypercalcemia were performed. Initial laboratory evaluation showed hypercalcemia at 11 mg/dL, iPTH as 15 pg/mL normal albumin 4.3 g/dL, and phosphorus level 3.5 mg/dL (Normal: 2.5–4.8) and creatinine 0.57 mg/dL. 24 h urinary calcium excretion was found to be 247 mg/day (normal: 100–300 mg/day). Further blood tests demonstrated that alkaline phosphatase level was 64 U/L (35–104) and 25-hydroxy vitamin D level was 22 ng/mL (normal: 20–30) within normal limits. A dual energy X-ray absorptiometry (DEXA) scan was performed, which revealed mild osteopenia at the left femoral neck (T score: −1.6). No previous bone mineral density (BMD) measurement had been taken prior to this.
On other days, our patient's serum calcium and iPTH level returned to within normal range without any medications. When we analyzed the sequence of laboratory tests, there were episodes of calcium and iPTH levels with fluctuating on repeat analyses over a period of ten months between 9.5–11 mg/dL (, normal: 8.5–10.2 mg/dL) and 11–17 pg/mL (, normal: 12–65), respectively.
A workup investigation to exclude other causes of hypercalcemia was done. She underwent an extensive evaluation including careful history, family history, physical examination, and lab work to exclude possible other causes of hypercalcemia. Parathyroid hormone related peptide was 0.28 pmol/L (normal: 0–1.3) and bone scan was normal, thus making malignancy-related hypercalcemia unlikely. Computed tomography of thorax, neck and abdomen, and PET-BT did not reveal any malignancy.
Although serum phosphorus was normal and iPTH was not increased, in order to rule out hyperparathyroidism, evaluation of the parathyroid glands was performed using ultrasound and MIBI scan, which were normal. Clinically, patients with FHH (familial hypocalciuric hypercalcemia) have relative hypocalciuria and inappropriately normal or elevated iPTH in the face of persistent mild hypercalcemia, none of which our patient had.
In addition to malignancy-related hypercalcemia, the differential diagnosis of hypercalcemia includes calcium supplements hypervitaminosis D, milk-alkali syndrome, granulomatous diseases, medications, inflammatory and rheumatic diseases, and other endocrine disorders.
25-hydroxy vitamin D level was not elevated ruling out hypervitaminosis D. Tuberculin test, computed tomography of thorax, and bone survey were normal, thus ruling out a granulomatous process (tuberculosis or sarcoidosis). Erythrocyte sedimentation rate and ANA level were normal, ruling out inflammatory and rheumatic diseases. Thyroid-stimulating hormone and free thyroid hormones should be checked to help rule out hyperthyroidism. Free T4, Free T3, and TSH were normal, ruling out hyperthyroidism, and there were no signs or symptoms suggestive of Cushing disease, adrenal insufficiency, acromegaly, or pheochromocytoma. Normal prolactin level and IGF-I in the age- and gender-matched normal range excluded the diagnosis of prolactinoma and acromegaly in our patient, respectively. Basal cortisol level was 19 μg/dL, and therefore we could rule out adrenal insufficiency. An overnight dexamethasone suppression test (DST) was done. After a 1-mg dose DST, the plasma cortisol level was 0.8 μg/dL. Hence, we could rule out Cushing syndrome. A 24-hour total urinary metanephrines and fractionated catecholamines were within normal range. She had no evidence of leukemia and lymphoma and a normal complete blood count. Serum electrophoresis was negative for monoclonal proteins. She indicated no symptoms of peptic ulcer, and there was neither exogenous vitamin D intake nor family history of endocrinopathy. She had no history of taking vitamin A, calcium supplements, and thiazide medication and no recent history of immobilization. Assessment of bone metabolism using markers of bone turnover could yield useful information and guide management decisions in our case. Urinary hydroxyproline level was significantly increased (35 mg/24 h/m2; normal: 22–55 years—8.5–23.5 mg/24 h/m2).
Because of sufficient vitamin D level, oral bisphosphonate was administered and letrozole was restarted at one-half dose (1.25 mg). She was discharged and we closely follow up patient's serum calcium, CEA, CA 15-3, and for distant metastasis.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [62.0, 'kg'], 'height': [1.62, 'm'], 'creatinine': [0.57, 'mg/dL'], 'age': [52, 'years']}",98.7728,93.83416,103.71144,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 52 years old. 
The concentration of creatinine is 0.57 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.62 m. The patient's weight is 62.0 kg. The patient's bmi is therefore 62.0 kg / (1.62 m * 1.62 m) = 23.62445 kg/m^2.The patient's BMI is 23.6, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 54.19299 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 52) * 54.19299 * 0.85) / (0.57 * 72) = 98.7728 mL/min. Hence, the patient's creatinine clearance is 98.7728 mL/min."
46,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5968287-2,Extracted,"In July 2016, a 16-year-old Japanese female was admitted to our hospital with abdominal distention. CT revealed 4 huge cysts in the left kidney, while the right kidney was normal. The total volume of the 4 cysts was 9,215 mL, and all cysts were Bosniak category I (Fig. ). Although nephrectomy had been recommended at the previous hospital where she was first assessed, both the patient and her parents preferred to avoid surgery and wanted to explore further therapeutic options.
On admission, she was 155.1 cm tall and weighed 56.5 kg, with a blood pressure of 124/87 mm Hg and body temperature of 36.5°C. Abdominal distention was noted. Laboratory findings were as follows (Table ): white blood cell count, 4,200/μL; red blood cell count, 3.94 × 106/μL; hemoglobin, 12.2 g/dL; platelet count, 284 × 103/μL; total protein, 7.1 g/dL; albumin, 4.5 g/dL; blood urea nitrogen, 5.3 mg/dL; Cre, 0.63 mg/dL; and CRP, 0 mg/dL. Genetic testing was performed (including PKD1 and PKD2) according to the previous method [], but no abnormalities were detected.
Because intracystic bleeding had occurred in case 1 after catheter drainage, prophylactic TAE was performed in this patient to avoid bleeding. A total of 8 platinum microcoils were used to block the branches of the left renal artery encircling the cyst walls (Fig. ). Subsequently, a total volume of 9,400 mL of cyst fluid was removed. Then, sclerotherapy was performed by daily infusion of minocycline hydrochloride for 7 days and the catheters were removed. Cytology for the cystic fluid was negative for malignancy. Serum Cre increased to 0.93 mg/dL immediately after TAE, but then improved to 0.63 mg/dL within 1 week. After 1 year, the total cyst volume was decreased to 633 mL (Fig. ).","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [56.5, 'kg'], 'height': [155.1, 'cm'], 'creatinine': [0.63, 'mg/dL'], 'age': [16, 'years']}",111.40652,105.83619,116.97685,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 16 years old. 
The concentration of creatinine is 0.63 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.1 cm, which is 155.1 cm * 1 m / 100 cm = 1.551 m. The patient's weight is 56.5 kg. The patient's bmi is therefore 56.5 kg / (1.551 m * 1.551 m) = 23.48685 kg/m^2.The patient's BMI is 23.5, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 47.94497 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 16) * 47.94497 * 0.85) / (0.63 * 72) = 111.40652 mL/min. Hence, the patient's creatinine clearance is 111.40652 mL/min."
47,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5729455-2,Extracted,"A 47-year-old Japanese man was admitted to our hospital for evaluation of renal disease in May 2013. Edema of the lower limbs was initially noted in August 2012. He consulted a local clinic in February 2013 with generalized edema and weight gain to 113 kg. Proteinuria was detected (5.2 g daily). His anasarca was treated with furosemide (100 mg daily) and restriction of salt and fluid intake (to 6 g of salt and 700 mL of water daily), achieving weight reduction to 90.0 kg. He had a history of drinking one-third of a bottle of whisky daily for 34 years starting from 13 years old. On admission, he was 174 cm tall and weighed 90.0 kg, with a blood pressure of 144/88 mmHg and bilateral lower limb edema. Laboratory findings are shown in Table . Total protein was 6.0 g/dL, albumin was 2.7 g/dL, urea nitrogen was 23 mg/dL, and Cre was 1.66 mg/dL. In addition, 24-h urinary protein excretion was 1.17 g and the urine sediment contained more than 100 erythrocytes per high-power field.
Computed tomography showed gastric varices with anastomoses to the left renal vein, as well as cirrhosis and splenomegaly.
This patient was also diagnosed as having alcoholic cirrhosis due to his 34-year history of alcohol abuse and negative tests for HBV and HCV infection. As with case 1, renal biopsy was performed to evaluate his renal disease.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [47, 'years'], 'weight': [90.0, 'kg'], 'height': [174.0, 'cm'], 'creatinine': [1.66, 'mg/dL']}",60.48694,57.46259,63.51129,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 47 years old. 
The concentration of creatinine is 1.66 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 174.0 cm, which is 174.0 cm * 1 m / 100 cm = 1.74 m. The patient's weight is 90.0 kg. The patient's bmi is therefore 90.0 kg / (1.74 m * 1.74 m) = 29.72652 kg/m^2.The patient's BMI is 29.7, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 174.0 cm, which is 174.0 cm * 0.393701 in/cm = 68.50397 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.50397 (in inches) - 60) = 69.55913 kg.
Hence, the patient's IBW is 69.55913 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 69.55913 kg + 0.4 * (90.0 kg  - 69.55913 kg) = 77.73548 kg. The patient's adjusted body weight is 77.73548 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 47) * 77.73548 * 1) / (1.66 * 72) = 60.48694 mL/min. Hence, the patient's creatinine clearance is 60.48694 mL/min."
48,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6182792-1,Extracted,"A 78-year-old (height 163.3 cm, weight 61.3 kg) Japanese man was admitted to our intensive care unit (ICU) after esophagectomy with gastric reconstruction for esophageal cancer. His body temperature was 36.9 °C and heart rate was 96 beats/minute. His blood pressure was 148/68 mmHg on ICU admission. Physical and neurological examinations were not significant. His past medical history included appendectomy (8 years of age) and lumber canal stenosis (70 years of age). He did not smoke cigarettes but drank Japanese alcohol (360 ml/day). Regarding family history, his elder brother died of esophageal cancer.
On ICU day 5, he developed new onset fever up to 38.0 °C, increase in sputum, and hypoxemia with 90% arterial oxygen saturation by pulse oximetry (SpO2) with mask oxygen at 10 L/minute with bilateral pulmonary coarse crackles. Therefore, he was intubated. A chest X-ray revealed diffuse bilateral pulmonary infiltrates predominantly in his right lung with pleural effusion (Fig. ). Laboratory findings revealed white blood cell count 5.7 × 109/L, red blood cell count 2.25 × 1012/L, hemoglobin 7.3 g/dL, hematocrit 21.4%, platelet 145 × 109/L, aspartate aminotransferase 54 U/L, alanine aminotransferase 55 U/L, total bilirubin 4.11 mg/dL, albumin 2.2 g/dL, urea nitrogen 38 mg/dL, creatinine 0.83 mg/dL, C-reactive protein 18.7 mg/dL, and urinary creatinine 95 mg/dL after intubation. Because sputum culture revealed Streptococcus pneumoniae on ICU day 7, the antibiotic was changed from cefmetazole to meropenem.
He underwent a long period of mechanical ventilation, ultimately undergoing tracheostomy on ICU day 38. Although his oxygenation was good with partial pressure of arterial oxygen/fraction of inspired oxygen (PaO2/FIO2) > 300 mmHg, restrictive pulmonary dysfunction developed: tidal volume 230–240 mL, static compliance 14–15 mL/cmH2O with 10 cmH2O pressure support ventilation, respiratory rate 34 beats/minute, and partial pressure of arterial carbon dioxide (PaCO2) 46 mmHg. We tried to wean him from mechanical ventilation with support by HFT setting the flow at 40 L/minute with FIO2 of 0.25 because the maximum inspiratory flow of the ventilator was 40 L/minute during 10 cmH2O pressure support ventilation. By setting the flow at the same rate as the ventilator, we hoped to reduce his inspiratory effort. HFT was used in the daytime, and a ventilator with 5 cmH2O pressure support with 5 cmH2O positive end-expiratory pressure (PEEP) was used at night for the first 8 days. In the next 8 days, HFT was used around the clock. Table presents the respiratory parameters during HFT. Under respiratory support with HFT, his condition was stable, and his physiotherapy rehabilitation continued uneventfully. The HFT optimally delivered humidified gas, which improved the thinning of his bronchial secretions. He was discharged from the ICU to the general ward on ICU day 127. His physiotherapy rehabilitation continued for 2 months, and he was transferred to a rehabilitation hospital on day 201 of hospitalization.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [61.3, 'kg'], 'height': [163.3, 'cm'], 'creatinine': [0.83, 'mg/dL'], 'age': [78, 'years']}",62.11428,59.00857,65.21999,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 78 years old. 
The concentration of creatinine is 0.83 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.3 cm, which is 163.3 cm * 1 m / 100 cm = 1.633 m. The patient's weight is 61.3 kg. The patient's bmi is therefore 61.3 kg / (1.633 m * 1.633 m) = 22.98731 kg/m^2.The patient's BMI is 23.0, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 59.87015 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 78) * 59.87015 * 1) / (0.83 * 72) = 62.11428 mL/min. Hence, the patient's creatinine clearance is 62.11428 mL/min."
49,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-3572805-1,Extracted,"The patient is a female whose age is 25 and undergoing medical treatment of Crohn's disease that is an inflammatory bowel disease after diagnosis of cryptogenic multifocal ulcerous enteritis and the nutrition team received the request to attempt high protein meal to improve hypoalbuminemia along protein-losing enteropathy.
The patient suffered from anemia continuously since when she was 4 years old, but could not find the specific reason for that, however, while implementing capsule endoscope to find the reason, the capsule was stuck at the upper part of ileum then the patient took small bowel resection. At that time, weight was normal by 49.4 kg (100% of IBW), but it decreased down to 37.0 kg (75% of IBW) by 25% for a year as weight loss continued, then reached the status of severe underweight at 33.3 kg (68% of IBW) at the time of hospitalization in 2010. She also suffered from ascites and subcutaneous edema with hypoalbuminemia (1.3 g/dL), however, abdominal discomfort and edema of face occurred from 2007 and diuretic was used to control ascites from 2009. She took the injection of albumin intermittently as the outpatient to improve hypoalbuminemia, but there was no effect.
The patient was in severe underweight that was included in 68% of IBW with 153 cm height and 33.3 kg body weight and in excessive malnutrition of protein-energy that marasmus was mixed at total protein by 2.7 g/dL and albumin by 1.3 g/dL from biochemical examination. Other blood test indices were 89 mg/dL for cholesterol, 7.5 for BUN, 0.28 Cr, 6.9 mg/dL for Ca, 33/19 IU/L for AST/ALT, 8.1 g/dL for hemoglobin, and 1.7 for CRP.
The foods for the patient were extremely restricted due to abdominal discomfort and the varieties were limited. In case of eating out, the symptoms of abdominal pain and diarrhea appeared and had meals at home most of the time. According to survey results of her dietary history, the patient consumed spinach and broccoli only after complete boiling and avoided the intake of other vegetables because she thought abdominal discomfort got worse if she had high-fiber foods. The patient appealed that abdominal discomfort occurred even when she consumed a bottle of vegetable juice little by little for a whole day. In case of ingesting fruits, she limited the quantity because she had burning feeling in her stomach because of sourness of the fruits. The patient also did not like the sweet taste of fruits, and there was nearly no intake of fruits. The patient had the meals mainly with rice and some fishes she could eat and intake of most nutrients such as calorie, carbohydrate, fat, protein, vitamin and minerals was very insufficient below 30-40% of required amount.
The foods the patient had were too limited considering her preference and abdominal discomfort. However, the motive and participation of the patient were willing to be induced to increase the intake by setting the goal of nutrition management so that she could minimize the supply of intravenous alimentation and increase oral feeding as much as possible considering that she was in the condition that could use gastrointestinal tract as an young female who were supposed to do social activities actively. First, low reside diet with low contents of dietary fiber was provided and supplementary snack was provided two or three times a day for the purpose of reducing discomfort and increase intake, although the amount was only slightly increased due to abdominal discomfort. Standard formula such as Ensure and Greenbia which have low contents of fiber as the nutritional supplementing beverage was recommended and tried, but the patient appealed the abdominal pain after ingesting them. And component nutrition solution (Monowell) that was produced for purpose of providing the nutrients to the patient of colitis was tried, but it could not be continued because she appealed abdominal discomfort. Despite the efforts of increasing oral feeding in various types, the intake was 800-900 kcal, 34 g protein (24-27 kcal/kg, 1 g/kg) a day falling into 40-50% of required intake, and it was insufficient to satisfy with the required intake though it increased comparing with the time of entering the hospital.
Because it was difficult to increase oral feeding, supplementation of calories and protein were required to increase the weight and improve hypoproteinemia. After discussion with the medical team, the use of protein supplement was suggested. The references of Umar & DiBaise [] and Braamskamp et al. [] that recommended 2.0-3.0 g protein/kg/day were referred for positive balance of protein in protein-losing enteropathy and the goal of nutrient supply was set to 40-50 kcal/kg and 2.5 g protein/kg considering the condition of excessive underweight. Nutrition intervention was implemented continuously to increase oral feeding by providing gruel or soup as the snack and insufficient protein from oral feeding was supplemented with protein supplement (Promax, >90% protein) ().
It was guided to take protein supplement with the meal by providing it twice a day for breakfast and dinner after discussion with the patient and instructed her to consume protein supplement with gruel, water and yogurt in the way that the patient could eat. Twenty g was provided a day when providing protein supplement at first, but actual intake stopped at degree of 1/2 and it was increased up to target goal 55 g slowly for about 2 weeks starting from intake of protein 10 g a day considering adaptability of the patient, and the adaptability was good for the period of increase without abdominal discomfort. Blood testing including BUN, Cr, and electrolytes was monitored monitored continuously to check load on kidney along intake of high protein meal (2.5 g protein/kg). The patient discharged from the hospital about 4 weeks after hospitalization, however, there was weight loss by 1.0 kg from 33.3 kg to 32.3 kg while ascites were controlled and stabilized after treatment and serum albumin was improved from 1.3 to 2.5. She discharged from the hospital in the condition without discomfort after increasing protein powder up to target amount.
After discharge, she visited the hospital regulary as the outpatient for about 10 months and was managed (total 8 times by every 2 weeks and one-two months after discharge). She kept 55 g (morning 30, lunch 5, dinner 20) of protein supplements for about 5 months and 35 g for about 2 months and 25 g along the improvement of the patient. Body weight increased gradually from 32.3 kg (65% of IBW) to 44.0 kg (89% of IBW) by about 36% for the period of continuous management () and serum albumin concentration was kept above 2.8 in average without the injection of albumin (). And, the performance status that the patient felt was improved from 4 points of 'very tired' to 2 points of 'a little tired' out of 5-points scale measurement and input of diuretic stopped owing to the improvement of edema and ascites from the time of 4th month after discharging from the hospital. During this period, the results of blood test such as BUN, Cr and electrolytes were within the normal range.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [25, 'years'], 'weight': [33.3, 'kg'], 'height': [153.0, 'cm'], 'creatinine': [0.28, 'mg/dL']}",161.46205,153.38895,169.53515,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 25 years old. 
The concentration of creatinine is 0.28 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 153.0 cm, which is 153.0 cm * 1 m / 100 cm = 1.53 m. The patient's weight is 33.3 kg. The patient's bmi is therefore 33.3 kg / (1.53 m * 1.53 m) = 14.2253 kg/m^2.The patient's BMI is 14.2, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 33.3 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation. 
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 25) * 33.3 * 0.85) / (0.28 * 72) = 161.46205 mL/min. Hence, the patient's creatinine clearance is 161.46205 mL/min."
50,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6878684-1,Extracted,"A 37-year-old man presented with the chief complaint of loin pain. He had no abnormalities in growth and development and had a healthy constitution; however, he once had an approximately 1-week episode of convalescence for loin pain after exercising in junior high/high school. Hypouricemia was noted on every biochemical examination in health check with a UA level of < 1 mg/dL. However, until now, his renal function and urine findings had been normal, and there was no history of examination at a medical institution. Bilateral loin pain developed during walking. The patient expected an improvement in the pain from walking; hence, he engaged in intensive exercise, including swimming for 1 h, fast walking / jogging for 2 km, and active muscle training for approximately 2 h. However, the pain worsened and persisted. He was then examined at the Department of Urology at our hospital. Renal calculi were ruled out via computed tomography (CT), but with a creatinine (Cr) level of 3.7 mg/dL, acute kidney injury with hyperbilirubinemia was diagnosed. The patient was then examined at the Department of Nephrology at our hospital. The following day, renal function further worsened with a Cr level of 4.1 mg/dL, and the patient was hospitalized on an emergency basis for detailed testing and treatment.
He had no notable medical history and no constitutional jaundice. The patient’s older sister was reported to have hypouricemia, but the UA level was unknown. He also had no history of allergy and was a non-smoker and an occasional drinker. His physical characteristics were as follows: height, 166 cm; weight, 66.8 kg; body mass index, 24.2 kg/m2; blood pressure, 135/53 mmHg; heart rate, 53 beats/min; body temperature, 37.0 °C; lucid; no anemia of the palpebral conjunctiva; no jaundice of the bulbar conjunctiva; no oral cavity findings; no swelling of the cervical lymph nodes; bilateral costovertebral angel tenderness; no pedal edema; no arthralgia; no cutaneous findings; and no neurological findings.
The blood and urine test results of the patient are shown in Table . The blood test results revealed renal function damage, hyperbilirubinemia in indirect bilirubin dominance, slight increase in C-reactive protein level, elevated fibrinogen levels, slight increases in creatine kinase (CK) and myoglobin levels, and hypouricemia. However, no data could be found suggestive of a collagen disease or vascular disease, and there were no findings indicative of hemolysis without anemia and elevated LDH.
The urine test results did not reveal any abnormal urinary findings. There were no urinary microscopic evidence, tubular epithelial cells, granular cast, epithelial cell cast, uric acid crystals, microscopic hematuria, and eosinophiluria. However, there were aciduria and mild elevation in myoglobin, whereas tubular injury markers were almost normal. Prerenal failure was suggested by a fractional excretion of sodium (FENA) level of 0.61, and fractional excretion of UA (FEUA) was markedly elevated at a level of 50.5%. CT examination revealed bilateral renal swelling, but there were no hepatobiliary structural abnormalities and no other abnormal findings. Contrast-enhanced CT was not performed because of the renal dysfunction. Instead, renal magnetic resonance imaging (MRI) was performed, and the T2-weighted image showed a cuneiform low-signal area suggestive of heterogeneous ischemia (Fig. a, b).
For the differential diagnosis, medical history was gathered, and laboratory investigations were conducted. There had been no issues during growth and development; the patient had never experienced any liver injury, and bilirubin levels had been within the normal range at every yearly health check. There was no past history of fatty liver, viral hepatitis, or congenital liver disease. Furthermore, hepatitis B virus surface antigen, hepatitis B virus core antibody, and hepatitis C virus antibody are all negative. No chronic liver injury, neurological injury, or urinary abnormalities were detected. Based on these findings, Fanconi syndrome and Wilson’s disease were excluded. No inappropriate secretion of antidiuretic hormone, malignant tumors, diabetes, or diarrhea was detected. The patient did not receive NSAIDs, antihyperuricemics, herbal supplements, nephrotoxic drugs, or contrast agents. There were no hypotension, infection, or sepsis. Urinary microscopic evidence showed a lack of tubular injury, and tubular injury markers were almost normal; these findings were negative for ATN. Low FENA suggested prerenal acute failure. However, the patient blood pressure was normotensive, and the oral mucous membrane and skin turgor were normal. There was no body weight loss compared to his usual weight, and dehydration was absent. Moreover, the state of the patient fulfilled the diagnostic criteria for ALPE []. Based on the findings of renal failure and loin pain after exercise, minor elevation in CK and myoglobin, hypouricemia, and increase in FEUA as well as the MRI findings of bilateral renal swelling and cuneiform low-signal areas, we made a diagnosis of RHUC and ALPE. At that time, the cause of hyperbilirubinemia was unknown.
The patient’s progress was favorable, and he was kept under observation while undergoing bed rest, fluid replacement, and nutrition therapy. On day 4, the Cr level had improved to 3.4 mg/dL, and the patient was discharged on day 5. One month later, his renal function had recovered, with a Cr level of 0.98 mg/dL, and bilirubin levels also normalized to 0.9 mg/dL. However, the UA level was 0.8 mg/dL, indicating severe RHUC. This progress is shown in Table . Considering the patient’s familial history of RHUC, we performed genetic testing using next-generation sequencing at the Tokyo Medical and Dental University. We performed comprehensive genetic analysis, including that for SLC22A12 encoding URAT1 and SLC2A9 encoding GLUT9, which are genes causing RHUC, and SLC34A1, EHHADH, HNF4A, and SLC2A2, which are genes causing Fanconi syndrome; however, the results could not identify the responsible mutation. Based on the patient’s family history, we considered the possibility of a new genetic mutation causing RHUC and considered exome sequencing (full genetic analysis). However, the patient’s family did not provide consent for genetic testing, and thus we were not able to identify the gene in question. To prevent ALPE, we advised the patient to avoid intense exercise; since then, ALPE has not recurred.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [37, 'years'], 'weight': [66.8, 'kg'], 'height': [166.0, 'cm'], 'creatinine': [4.1, 'mg/dL']}",21.74272,20.65558,22.82986,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 37 years old. 
The concentration of creatinine is 4.1 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 66.8 kg. The patient's bmi is therefore 66.8 kg / (1.66 m * 1.66 m) = 24.24154 kg/m^2.The patient's BMI is 24.2, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 62.31505 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 37) * 62.31505 * 1) / (4.1 * 72) = 21.74272 mL/min. Hence, the patient's creatinine clearance is 21.74272 mL/min."
51,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4339863-1,Extracted,"Mr. AD was a 25-year-old student who was an active footballer until ten days prior to presentation to Cardia Heart Clinic (CHC), Kano, Nigeria, when he started having dyspnoea on exertion, which progressed to dyspnoea at rest, associated with orthopnoea, paroxysmal nocturnal dyspnoea, easy fatigability, abdominal and leg oedema, upper right abdominal discomfort, easy satiety, and subsequently cough with frothy sputum. He denied having urinary symptoms, fever, or other symptoms. Prior to his self-referral to CHF, he had visited another clinic where a chest X-ray, complete blood count, and renal function assessment were carried out.
Physical examination revealed a young man in mild respiratory distress. There were no skeletal anomalies or digital clubbing, and he was 1.76 meters tall with body weight of 68 Kg. His axillary body temperature was 37.1°C, oxygen saturation on room air was 91%, and he had bilateral pitting pedal oedema extending to the shins. He had regular heart rate of 104 beats/minute, blood pressure of 100/80 mmHg, raised jugular venous pressure (approximately 8 cm), displaced apex, third heart sound with loud component of second heart sound, and grade IV mitral regurgitation and grade III tricuspid regurgitation murmurs. There were bilateral basal crepitations, soft and tender hepatomegaly of 12 cm below the right costal margin, and mild ascites. Other aspects of physical examination were not remarkable.
Chest X-ray revealed cardiomegaly, pulmonary venous congestion, and minimal left pleural effusion. Electrocardiogram showed sinus tachycardia with bifascicular block (complete right bundle branch block plus left posterior hemiblock). Echocardiogram (see Figures and ) revealed absent interatrial septum (common atrium) with deformed mitral and tricuspid valves (MV and TV, resp.), which were severely regurgitant. The right ventricle was dilated with a basal diameter of 50 mm, but left ventricular (LV) end diastolic diameter was normal (39 mm), and LV was hypercontractile (LV ejection fraction (LVEF) = 90%). His mean pulmonary artery systolic pressure was approximately 36.8 mmHg, consistent with moderate pulmonary hypertension. The pulmonary veins and superior vena were normally positioned. The pericardium was mildly thickened with moderate pericardial effusion (average echo free space = 15.5 mm). Fibrin strands were not seen within the effusion. The complete blood count showed total white blood cell count of 11.6 × 109/L, neutrophils = 8.3 × 109/L, lymphocytes = 2.6 × 109/L, haemoglobin = 16.3 g/dL, haematocrit = 54.9%, and platelets = 522 × 109/L. Serum creatinine was 92 μmol/L, and other renal function parameters were all normal.
The overall diagnosis was ADHF with preserved LVEF and progressive secondary pulmonary hypertension, caused by CA, associated with moderate pericardial effusion and indirect evidence suggestive of acute bacterial infection.
After the initial cardiac evaluation at CHC which is an out-patient facility, the patient was immediately referred to the emergency unit of a tertiary level hospital in the city for admission and further treatment. The patient gave a written informed consent for his case to be reported. Unfortunately, the patient died about 20 hours after admission at the tertiary level hospital, but details of the in-patient management are not available to us, and postmortem examination was not carried out.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [68.0, 'kg'], 'height': [1.76, 'm'], 'creatinine': [92.0, 'µmol/L'], 'age': [25, 'years']}",106.69068,101.35615,112.02521,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 25 years old. 
The concentration of creatinine is 92.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 92.0 µmol. To convert 92.0 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 92.0 µmol creatinine * 1e-06 mol/µmol = 9e-05 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 9e-05 mol creatinine * 113.12 g/mol = 0.01018 g creatinine. To convert 0.01018 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01018 g creatinine * 1000.0 mg/g = 10.18 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 10.18 mg creatinine/10.0 dL = 1.018 mg creatinine/dL. The concentration value of 92.0 µmol creatinine/L converts to 1.018 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.76 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.76 m * 1.76 m) = 21.95248 kg/m^2.The patient's BMI is 22.0, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 68.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 25) * 68.0 * 1) / (1.018 * 72) = 106.69068 mL/min. Hence, the patient's creatinine clearance is 106.69068 mL/min."
52,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4172392-1,Extracted,"A 44 year old Caucasian female (weight: 65 kg height: 170 cm) with a history of bipolar disorder and Wolf-Parkinson-Withe syndrome was transferred from a local hospital to our intensive care unit due to somnolence with a GCS (Glasgow Coma Scale) of 9 and polyuria after acute lithium intoxication. The patient was treated with a lithium medication for years. She took 4 tablets of perazindimalonat, 29 tablets of lithium (0.022 g Lithium per pill) and 10 tablets of zolpidemtartrat in suicidal attempt. On admission to our emergency room the patient’s history could not be obtained due to somnolence. Patient’s heart rate was 60 bpm, blood pressure was 120/80 mmHg, respiratory rate 14 per minute, cardiac and pulmonary auscultation were unremarkable as was the remainder of the physical exam. The patient was polyuric (4 l urine in 24 hours). Laboratory work-up showed a serum creatinine of 57 μmol/l, a serum sodium of 140 mmol/l and a serum potassium of 4.0 mmol/l. Liver function test, blood gas analysis and whole blood count were normal. Lithium serum level on admission was 3.9 mmol/l. Subsequently it rose to a concentration of 4.2 mmol/l two hours after admission. Due to the combination of the rising lithium serum level and the neurological symptoms the patient was transferred to the ICU for monitoring and the critical care nephrology department was consulted.
For fast reduction of lithium levels an intermittent hemodialysis using the GENIUS dialysis batch system (FMC, Germany) with a 90 liters dialysate tank volume and a 1.3 m2 F60S polysulfone high-flux dialyzer (FMC, Germany) was started. Blood and dialysate flow rate was started at 350 ml/min. As the patient woke up and became more vigilant but also agitated after one dialysis treatment, the flow rate had to be reduced to 200 ml/min to avoid frequent system alarms and the need to restrain the patient. Ultrafiltration rate was adjusted at minimum rate of 50 ml/h. Anticoagulation was provided by unfractionated heparin medication with an initial bolus of 1000 IE and a continuous dose of 500 IE per hour. Lithium serum levels were measured right before the start of the treatment, as well as within an interval of 15 minutes, 30 minutes, 1 hour, 2 hours and 3.5 hours after treatment initiation. One of the peculiarities of the GENIUS dialysis system is that fresh and spent dialysate are separated by virtue of temperature differences and difference in uremic solute concentration []. To prevent an early contamination of the fresh with the spent dialysate as seen in GENIUS therapy in patients without renal failure [], dialysis therapy was stopped after 4 hours of treatment. Plasma dialyzer clearance rates were measured 30 minutes and 3 hours after dialysis initiation using established dialyzer clearance equations reported previously []. Lithium dialyzer clearance was calculated according to the following equation: Kplasma = QB × (1 – Hct/100) × ((Cart – Cven)/Cart). Pre dialyzer concentrations (Cart) and post dialyzer concentration (Cven) were drawn at a time of minimal ultrafiltration (50 ml/h).
After the marked clinical improvement already occruing after the first hour of intermittent hemodialysis a subsequent extended dialysis with dialysate and blood flow of 140 ml/min was initiated right after the completion of the first dialysis session using a second GENIUS machine. As there was no gap between treatments a rebound could not be assessed.During the first dialysis lithium serum level was lowered by 71.5%. Plasma dialyzer clearance rate was 177.4 ml/min after 30 minutes of dialysis at a blood flow of 350 ml/min and 129.6 ml/min after 3 hours of dialysis at a blood flow of 260 ml/min. We mixed the total spent dialysate of the first dialysis tank by air insufflation and collected a sample for laboratory measurement. Lithium dialysate level was 0.4 mmol/l in the dialysate tank of 90 liters volume. Accordingly we found a total amount of 250 mg of lithium in the total spent dialysate. 5.5 hours after the initiation of the second dialysis therapy serum lithium level was 0.79 mmol/l (Figure ). No neurological symptoms were detectable after the patient woke up fully. Blood pressure rose to 175/85 mmHg prompting treatment with urapidil. Crystalloids were administered to compensate for polyuria. The morning after admission, the patient had fully recovered. Intensive monitoring was no longer required and the patient was retransferred to the psychiatric hospital. Blood pressure rose meanwhile up to 175/85 mmHg and urapidil therapy was initiated. Crystalloid solutes were administered to provide adequate fluid supply during polyuria. The morning after admission, the patient had fully recovered. Monitoring was no longer required and the patient was retransferred to the psychiatric hospital.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [44, 'years'], 'weight': [65.0, 'kg'], 'height': [170.0, 'cm'], 'creatinine': [57.0, 'µmol/L']}",102.54595,97.41865,107.67325,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 44 years old. 
The concentration of creatinine is 57.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 57.0 µmol. To convert 57.0 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 57.0 µmol creatinine * 1e-06 mol/µmol = 6e-05 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 6e-05 mol creatinine * 113.12 g/mol = 0.00679 g creatinine. To convert 0.00679 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00679 g creatinine * 1000.0 mg/g = 6.79 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 6.79 mg creatinine/10.0 dL = 0.679 mg creatinine/dL. The concentration value of 57.0 µmol creatinine/L converts to 0.679 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 65.0 kg. The patient's bmi is therefore 65.0 kg / (1.7 m * 1.7 m) = 22.49135 kg/m^2.The patient's BMI is 22.5, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 61.43709 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 44) * 61.43709 * 0.85) / (0.679 * 72) = 102.54595 mL/min. Hence, the patient's creatinine clearance is 102.54595 mL/min."
53,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-3746150-1,Extracted,"A 61-year-old female visited the emergency room complaining of sudden abdominal pain and nausea after overeating. She visited a local clinic where she underwent abdominal CT and was prescribed an analgesic, but the pain did not subside, so she visited our hospital. Her medical and social histories were noncontributory. At admission, her blood pressure was 120/80 mm Hg, pulse rate 68 per minute, respiratory rate 18 per minute, body temperature 36.9℃, height 157 cm, weight 50 kg, and BMI 20.3. She denied a history of weight loss. The physical examination revealed an acutely ill-looking appearance with epigastric tenderness. The complete blood count showed leukocytes 10,600/µL, hemoglobin 13.3 g/dL, and platelet count 208,000/µL. The blood chemistry showed total bilirubin 0.5 mg/dL, aspartate aminotransferase 18 U/L, alanine aminotransferase 13 U/L, amylase 106 U/L, blood urea nitrogen 23 mg/dL, creatinine 0.67 mg/dL, and C-reactive protein 0.26 mg/dL.
The initial abdominal X-ray revealed a large amount of food distending the stomach and mild gas accumulation in the small and large bowel (). An abdominal CT taken at the local clinic showed a hugely distended stomach and duodenum (). The aortomesenteric distance on CT was 7.4 mm which was decreased than normal mean aortomesenteric distance of 10 to 28 mm in healthy people. Conventional barium studies, which still play an important role for diagnosis of SMA syndrome, could not be performed because of severe gastroptosis and distended stomach. Then we performed esophagogastroduodenoscopy (EGD) and EUS to rule out intestinal intraluminal obstruction and gastric or duodenal ulcer disease that might be secondary to reflux or that might constitute a primary pathology mimicking SMA syndrome. EGD revealed a huge amount of food in the stomach (). Since that EUS could give us more information about surrounding organs which can directly compress the duodenum, we performed linear EUS (EG3870-UTK; Pentax, Tokyo, Japan). This did not show any abnormality of the gallbladder, common bile duct or pancreas. However, it showed the SMA running almost parallel to the abdominal aorta, with an aortomesenteric angle of 10° (normal range, 38° to 65°), confirming the diagnosis of SMA syndrome (, Supplementary Video 1 [available online at ]). The patient was managed conservatively with bowel rest and intravenous fluids. The abdominal pain and nausea were relieved and the patient started a soft diet on day 5 of admission and was discharged on day 7 of admission without any symptoms.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [61, 'years'], 'weight': [50.0, 'kg'], 'height': [157.0, 'cm'], 'creatinine': [0.67, 'mg/dL']}",69.13421,65.6775,72.59092,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 61 years old. 
The concentration of creatinine is 0.67 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 157.0 cm, which is 157.0 cm * 1 m / 100 cm = 1.57 m. The patient's weight is 50.0 kg. The patient's bmi is therefore 50.0 kg / (1.57 m * 1.57 m) = 20.2848 kg/m^2.The patient's BMI is 20.3, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 49.66544 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 61) * 49.66544 * 0.85) / (0.67 * 72) = 69.13421 mL/min. Hence, the patient's creatinine clearance is 69.13421 mL/min."
54,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5712145-1,Extracted,"The patient was a 55-year-old man in whom leukocytosis and systemic enlarged lymph nodes had been pointed out on positron emission tomography-computed tomography (PET-CT), which had been performed in an annual health check four years previously. The urinalysis findings at that time were normal without hematuria or proteinuria. He was referred to a hematologist in a regional hospital. Peripheral blood flow cytometry revealed that the percentages of lymphocytes that were positive for cluster of differentiation (CD)5, CD19, CD20, and CD23 to be 97.5%, 91.7%, 80.7%, and 84.3%, respectively. He was diagnosed with CLL Rai stage II. At the time, his serum creatinine level was 0.69 mg/dl and he was not taking any medications, including traditional Chinese medicines. He was followed up without treatment, and his serum creatinine level remained normal for three and a half years. However, his serum creatinine level gradually increased from 1.11 to 2.66 mg/dL in the 6 months before he presented to our hospital. He was referred to our hospital to undergo an evaluation for progressive renal dysfunction.
On admission, his height was 167 cm, and his body weight was 70 kg. His body temperature was 36.8 °C, and his heart rate was 60 beats per minute. His blood pressure was 108/69 mmHg. A physical examination revealed the palpable enlargement of the cervical and inguinal lymph nodes, liver, and spleen. The laboratory data on admission are summarized in Table . The patient’s urinary protein level was 0.23 g per day without any occult blood. The levels of urinary N-acetyl-β-D-glucosaminidase and β2 microglobulin were high. Leukocytosis was observed (91.8% lymphocytes). The blood urea nitrogen and serum creatinine levels were 40 mg/dL and 3.89 mg/dL, respectively. The patient was negative for myeloperoxidase antineutrophil cytoplasmic antibody, proteinase3-antineutrophil cytoplasmic antibody, M-protein, and Bence Jones protein. The patient was also showed negative results for the interferon gamma release assay (IGRA). The patient’s angiotensin-converting enzyme (ACE) level was normal. No bilateral hilar adenopathy or infiltration was detected on a chest radiograph. No uveitis was detected in an ophthalmic examination. Abdominal echography showed that the right and left kidneys were 10.7 × 4.8 cm and 10.6 × 5.3 cm in size, respectively.
A renal biopsy obtained 53 glomeruli, 30 of which showed global sclerosis and 11 of which were collapsed without glomerular lesions. Immunofluorescence staining of immunoglobulin G (IgG), IgA, IgM, C3, C1q, and fibrinogen was negative. Tubulointerstitial injury with the interstitial infiltration of lymphocytes was observed in 90% of the total area, and there were some non-caseating epithelioid cell granulomas with Langhans giant cells (Fig. ). Ziehl-Neelsen staining for acid-fast bacilli was negative (Fig. ). Immunohistochemistry was performed with the T-cell marker CD3 and B-cell markers CD5, CD20, and CD23 (Fig. ). The interstitial area was strongly positive for CD5 and CD20, positive for CD3 and weakly positive for CD23. The area inside or in the vicinity of the epithelioid cell granulomas was positive for CD3 and CD5 and negative for CD20 and CD23.
We determined that progressive renal dysfunction had occurred due to the diffuse infiltration of CLL cells in the interstitial area of the kidneys, and the patient was treated with two cycles of cyclophosphamide. The treatment was unable to attenuate the progression of the renal dysfunction, and the patient ultimately required maintenance hemodialysis due to end-stage renal failure.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [55, 'years'], 'weight': [70.0, 'kg'], 'height': [167.0, 'cm'], 'creatinine': [3.89, 'mg/dL']}",20.00946,19.00899,21.00993,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 55 years old. 
The concentration of creatinine is 3.89 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 167.0 cm, which is 167.0 cm * 1 m / 100 cm = 1.67 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.67 m * 1.67 m) = 25.0995 kg/m^2.The patient's BMI is 25.1, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 167.0 cm, which is 167.0 cm * 0.393701 in/cm = 65.74807 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.74807 (in inches) - 60) = 63.22056 kg.
Hence, the patient's IBW is 63.22056 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 63.22056 kg + 0.4 * (70.0 kg  - 63.22056 kg) = 65.93234 kg. The patient's adjusted body weight is 65.93234 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 55) * 65.93234 * 1) / (3.89 * 72) = 20.00946 mL/min. Hence, the patient's creatinine clearance is 20.00946 mL/min."
55,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4421390-1,Extracted,"A 47-year-old man was admitted to our hospital for evaluation of proteinuria in June 2004. He had a history of blood transfusion in 1977, due to unexpected bleeding after tooth extraction. In 1996, he was diagnosed with haemophilia A and chronic hepatitis associated with HCV infection. In November 2002, he complained of swelling and pain of the lower limbs. After the diagnosis of neuropathy caused by cryoglobulinaemia, prednisolone (20 mg/day) was administered, and improvement was observed. Prednisolone was stopped after 6 months. In June 2004, the patient noticed oedema and purpura on both lower extremities, and was admitted.
He was 164 cm in height and weighed 62.6 kg. The blood pressure was 170/90 mmHg. Urinalysis revealed proteinuria (2.6 g/day) and microscopic haematuria. The serum protein, albumin and creatinine levels were 6.9 g/dL, 3.1 g/dL and 1.30 mg/dL, respectively. Serologic workup included positive cryoglobulin and rheumatoid factor (430 IU/mL). Liver function tests were normal. The test for HCV antibody was positive, and serum HCV RNA was detected at a high level (392 KIU/mL) by a PCR assay. The HCV genotype was group 1. The plasma factor VIII activity was 6%. A renal biopsy was not considered because of the risk of bleeding. Based on the presumption of proteinuria caused by HCV-associated nephritis with cryoglobulinaemia, treatment was commenced with anti-viral agents, consisting of injections of interferon-α of 6 million units six times/week combined with oral administration of ribavirin 400 mg/day. After discharge, serum HCV RNA disappeared, and proteinuria was reduced to 0.8 g/day. However, there were sustained episodes of leukocytopaenia (800/μL) and anaemia (haemoglobin as low as 8.8 g/dL), and side effects of interferon-α and ribavirin, and treatment was ceased 2 months later. Serum HCV RNA levels rose, again, to 307 KIU/mL, proteinuria increased to 7.7 g/day and serum albumin was decreased to 2.6 g/dL.
In order to treat the patient, based on a definite diagnosis, the patient was advised to receive a renal biopsy, despite possible bleeding risk due to haemophilia A. This was because presumption of a diagnosis without a renal biopsy, as in the first admission, could not allow us an expensive and risky treatment with a combination of pegylated interferon and ribavirin in conjunction with lenograstim and epoetin α injection. The patient was re-admitted for a renal biopsy in January 2005. Before undergoing this, an increase of serum factor VIII by intravenous administration of recombinant factor VIII (octocog alfa, Kogenate® FS; Bayer Health Care Pharmaceuticals, Berkley, CA, USA) was noted, as shown in Table . Based on these findings, a biopsy was performed in the morning, 30 min after a bolus injection of 4000 units of recombinant factor VIII, and with two passes of an automatic 16-gauge core biopsy needle (ACECUT for Nephro-Biopsy, CREATE MEDIC CO., LTD, Yokohama, Japan). The plasma factor VIII activity 30 min after the administration was 91%. In the evening of the day of biopsy, and the following morning and evening, three bolus administrations of 3000 units of factor VIII were added. After the renal biopsy, ultrasonography of the kidney did not detect haematoma, and the blood count did not show a decrease in haemoglobin.
Light microscopic examination of the renal biopsy specimen revealed MPGN (Figure ). Immunofluorescent microscopy revealed positive staining of C3, Ig M and Ig G (Figure ). Electron microscopy revealed subendothelial deposits. Based on this definite diagnosis obtained from the renal biopsy, we determined to perform antiviral therapy with agents to overcome side effects, even though the therapy may be expensive. Anti-viral treatment was initiated, consisting of injection of pegylated interferon 80 μg/week and oral administration of ribavirin 400 mg/day, combined with lenograstim and epoetin α injections to avoid leukocytopaenia and anaemia, respectively. The patient was then discharged. Serum HCV RNA disappeared and proteinuria was reduced to 2.6 g/day. However, there was sustained leukocytopaenia and anaemia despite the lenograstim and epoetin α injections, and so anti-viral treatment was stopped, 3 months later. After two more months, serum HCV RNA levels rose to 309 KIU/mL, and proteinuria was increased to 6.0 g/day. The patient was admitted to our hospital for the third time in June 2005. According to the next therapy of cryoglobulinaemic MPGN associated with HCV infection [], daily oral prednisolone (40 mg/day) was started. Prednisolone was tapered, and cyclosporine A (150 mg/day) was added. One month after the treatment, proteinuria decreased to 0.2 g/day, and serum albumin increased to 3.4 g/dL.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [47, 'years'], 'weight': [62.6, 'kg'], 'height': [164.0, 'cm'], 'creatinine': [1.3, 'mg/dL']}",60.11616,57.11035,63.12197,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 47 years old. 
The concentration of creatinine is 1.3 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 164.0 cm, which is 164.0 cm * 1 m / 100 cm = 1.64 m. The patient's weight is 62.6 kg. The patient's bmi is therefore 62.6 kg / (1.64 m * 1.64 m) = 23.27484 kg/m^2.The patient's BMI is 23.3, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 60.50401 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 47) * 60.50401 * 1) / (1.3 * 72) = 60.11616 mL/min. Hence, the patient's creatinine clearance is 60.11616 mL/min."
56,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-3772920-1,Extracted,"Nineteen year-old-man, known case of Type 2 Diabetes mellitus for 4 y on 1 g metformin twice daily since diagnosis of his diabetes. He was in his usual state of health till he presented to the emergency department reporting nausea, vomiting and epigastric pain for 3 d.
On physical examination, his height was 170 cm and body weight 99 kg; body mass index (BMI) 34.3 kg/m2, looked mildly dehydrated. Vitals signs were stable. Systemic examination was unremarkable, apart from mild epigastric tenderness.
Laboratory investigations showed HbA1c 7.7%, Creatinine 58 µmol/L, Amylase 462 units/l (normal range < 100), Lipase 1378 units/l (0–60), white blood cells 16.8/mm3 (4–11) 80% of which was neutrophils, CRP 258 mg/l (0–5), Mg 0.76 mmol/l (0.7–1.05), Ca 2.17 mmol/l (2.2–2.6), AST 18 units/l (< 39), ALT 34 units/l (< 41), TG 0.95 mmol/l (< 2.3), Lactate 1.4 mmol/l (0.5–1.6). Abdominal Ultrasound and ERCP were done for the patient, results showed no gallstones and clear biliary tract, respectively. CT confirmed the diagnosis of acute pancreatitis, with no identifiable cause.
The patient was admitted to ICU for close monitoring and further investigation. Normalization of Amylase and Lipase was reached after Metformin cessation, and Supportive treatment in the form of IV insulin and IV fluids. Other potential causes of pancreatitis were excluded. Patient was discharged home in stable condition after 2 weeks.
Few days later, after re-exposure to Metformin, he presented with recurrence of his previous symptoms, and elevation of Amylase and Lipase was documented.
As a result, Metformin was suspended with improvement of his symptoms and biochemical profile.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [99.0, 'kg'], 'height': [170.0, 'cm'], 'creatinine': [58.0, 'µmol/L'], 'age': [19, 'years']}",195.93013,186.13362,205.72664,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 19 years old. 
The concentration of creatinine is 58.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 58.0 µmol. To convert 58.0 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 58.0 µmol creatinine * 1e-06 mol/µmol = 6e-05 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 6e-05 mol creatinine * 113.12 g/mol = 0.00679 g creatinine. To convert 0.00679 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00679 g creatinine * 1000.0 mg/g = 6.79 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 6.79 mg creatinine/10.0 dL = 0.679 mg creatinine/dL. The concentration value of 58.0 µmol creatinine/L converts to 0.679 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 99.0 kg. The patient's bmi is therefore 99.0 kg / (1.7 m * 1.7 m) = 34.25606 kg/m^2.The patient's BMI is 34.3, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 65.93709 kg + 0.4 * (99.0 kg  - 65.93709 kg) = 79.16225 kg. The patient's adjusted body weight is 79.16225 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 19) * 79.16225 * 1) / (0.679 * 72) = 195.93013 mL/min. Hence, the patient's creatinine clearance is 195.93013 mL/min."
57,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-8102657-1,Extracted,"The patient was an 84-year-old man with a height of 176 cm and a body weight of 80 kg who was scheduled for minimally invasive posterior spine fusion (T9–L3) for the treatment of a lumbar compression fracture. He had a history of hypertension, atrial fibrillation, and chronic kidney disease and was taking amlodipine and apixaban (5 mg twice daily). Preoperative serum examination indicated moderate loss of kidney function, which was confirmed by a serum creatinine level of 1.05 mg/dL and an estimated glomerular filtration rate of 52 mL/min/1.73 m2. Preoperative coagulation tests indicated prolonged values for both APTT and PT-international normalized ratio (40.1 s and 1.7, respectively). Although temporary interruption of apixaban is commonly recommended for the perioperative period (usually 48–72 h before surgical procedures, such as spine surgery, with high bleeding risk) [], the patient continued apixaban until the night before surgery, according to the instruction of his cardiologist.
We considered it necessary to evaluate the residual anti-Xa effect of apixaban for the estimation of perioperative bleeding and potential need for transfusion; therefore, we implemented the use of ClotPro in combination with the conventional blood tests performed at our hospital’s central laboratory. ClotPro uses RVV as the reagent to activate coagulation. Because RVV specifically cleaves factor X to Xa, clotting time (CT) is prolonged by anti-Xa drugs, such as apixaban, in a dose-dependent manner [, ]. We examined blood cell count, PT, APTT, and plasma fibrinogen level at four time points: after anesthesia induction, at the end of surgery, on postoperative day (POD) 1, and on POD 6. We simultaneously performed the ClotPro assay, an ecarin chromogenic assay (ECA), to detect the effect of direct thrombin inhibitors such as dabigatran [], and a fibrinogen concentration assay. Blood samples for outsourced chromogenic anti-Xa assay were collected at the same time points.
Anesthesia was induced with propofol and rocuronium, and was maintained with desflurane and continuous infusion of remifentanil. The results of coagulation tests after anesthesia induction indicated delayed thrombin production (Table ) (Fig. ). All members of the surgical team recognized the residual effects of apixaban, and we prepared fresh frozen plasma for excessive bleeding. Fortunately, the volume of bleeding was 440 mL, and we did not perform a transfusion. Considering the balance of the risk of postoperative bleeding and the result of the RVV test on the morning of POD 1, which was in the normal range, we resumed apixaban at a decreased dose of 2.5 mg twice daily on POD 1. The CT for the RVV test on POD 6 was prolonged to 93 s, which was shorter than the preoperative value (167 s) (Table ). Although the patient had minor subconjunctival hemorrhaging after the resumption of apixaban, he was discharged without major bleeding or thrombotic complications.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [80.0, 'kg'], 'height': [176.0, 'cm'], 'creatinine': [1.05, 'mg/dL'], 'age': [84, 'years']}",55.42378,52.65259,58.19497,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 84 years old. 
The concentration of creatinine is 1.05 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 176.0 cm, which is 176.0 cm * 1 m / 100 cm = 1.76 m. The patient's weight is 80.0 kg. The patient's bmi is therefore 80.0 kg / (1.76 m * 1.76 m) = 25.82645 kg/m^2.The patient's BMI is 25.8, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 176.0 cm, which is 176.0 cm * 0.393701 in/cm = 69.29138 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.29138 (in inches) - 60) = 71.37017 kg.
Hence, the patient's IBW is 71.37017 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 71.37017 kg + 0.4 * (80.0 kg  - 71.37017 kg) = 74.8221 kg. The patient's adjusted body weight is 74.8221 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 84) * 74.8221 * 1) / (1.05 * 72) = 55.42378 mL/min. Hence, the patient's creatinine clearance is 55.42378 mL/min."
58,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5318337-1,Extracted,"A 50-year-old Japanese male was referred to our hospital due to albuminuria and hyperuricemia. At 40 years of age, the patient had been diagnosed with hyperuricemia (8.4 mg/dL) in another clinic but did not receive follow-up treatment at that time. Then, at 50 years of age, he visited the same clinic and was again diagnosed with hyperuricemia (9.0 mg/dl) and high UAE (390 mg/g.cr), leading to admission to our hospital for a detailed examination of CKD. He had no history of smoking or major diseases, excluding hyperuricemia, and no family history of renal diseases. Clinical examination and laboratory tests at admission showed the following characteristics: height 170 cm, weight 68 kg, blood pressure 130/82 mmHg, heart rate 70 beats/min, serum UA 9.2 mg/dL, UAE 388.6 mg/g.cr, urinary L-FABP 28.8 µg/g.cr (normal range <8.4 µg/g.cr), serum creatinine 1.32 mg/dL, estimated glomerular filtration ratio 46.6 mL/min/1.73 m2, no hematuria, normal proteinemia (serum total protein 7.0 g/dL, serum albumin 4.2 g/dL), normoglycemia (fasting blood sugar 96 mg/dL, HbA1c 5.6%), and normal lipid profile (low-density lipoprotein cholesterol 126 mg/dL, triglycerides 96 mg/dL, high-density lipoprotein cholesterol 66 mg/dL). Plasma serology was negative for antinuclear antibody, antiglomerular basement membrane antibody, myeloperoxidase antineutrophil cytoplasmic antibody (ANCA), proteinase 3-ANCA, hepatitis C antibody, and hepatic B antigen. Serum complement and immunoglobulin levels were within normal limits, and the FMD value was 5.4% (normal range >6.0%).
A renal biopsy was performed on day 3 after admission. Renal histopathology showed renal arteriolar hyalinosis and arteriolar wall thickening, tubular atrophy, and interstitial fibrosis, but only minor changes in the glomeruli (Fig. ). These findings were compatible with renal arteriolopathy related to hyperuricemia []. In addition, immunohistochemistry for deposition of immunoglobulin G (IgG), IgM, IgA, C3, and C1q were all negative. The patient was therefore diagnosed with hyperuricemic arteriolopathy. Because of its potential renal protective effect described earlier, topiroxostat treatment (160 mg/day) was initiated on day 7. The serial changes in laboratory data pre- and post-topiroxostat treatment are shown in Table . The patient’s serum UA level decreased from 9.2 to 7.4 mg/dL after 3 months and 6.4 mg/dL after 6 months, while UAE decreased from 388.6 to 288.2 mg/g.cr after 3 months and 88.4 mg/g.cr after 6 months. The urinary L-FABP level also decreased from 28.8 to 24.2 µg/g.cr after 3 months and 19.8 µg/g.cr after 6 months. In addition, FMD increased slightly from 5.4 to 5.6% after 3 months and 5.8% after 6 months. Other parameters, including blood pressure, renal function, and lipid profile, showed only minor changes during the 6-month treatment period. No adverse drug reaction was observed.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [68.0, 'kg'], 'height': [170.0, 'cm'], 'creatinine': [1.32, 'mg/dL'], 'age': [50, 'years']}",62.44043,59.31841,65.56245,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 50 years old. 
The concentration of creatinine is 1.32 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.7 m * 1.7 m) = 23.52941 kg/m^2.The patient's BMI is 23.5, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 65.93709 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 50) * 65.93709 * 1) / (1.32 * 72) = 62.44043 mL/min. Hence, the patient's creatinine clearance is 62.44043 mL/min."
59,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5735468-1,Extracted,"A 28-year-old woman, gravida 2 para 0 who complained of headache and persistent epigastric or right upper quadrant pain for 1 h with dizziness, blurred vision, nausea, and vomiting, was admitted to our hospital at 35 weeks and 2 days’ gestation. The patient's body weight was 67 kg and height was 161 cm. She was healthy before the pregnancy and did not undergo any regular prenatal examinations. The baby was conceived naturally. Written consent of publishing of this paper was obtained from the patient when she was discharged.
The patient was drowsy and had an anemic appearance. Physical examination revealed axillary temperature of 37.1°C, high blood pressure (BP) (190/110 mmHg) with a heart rate of 102 beat/min, and respiratory rate of 22 breath/min. Chest auscultation revealed clear breath sounds without rales. Tenderness over the right upper quadrant was noted. Bilateral lower extremity pitting edema was observed.
Laboratory tests were as follows: urine protein, 2+; urine occult blood, 3+; red blood cells, 2.68 × 1012/L; hemoglobin, 91 g/L; white blood cells, 9 × 109/L; platelets, 92 × 109/L; aspartate aminotransferase, 331.4 U/L; alanine aminotransferase, 116.1 U/L; albumin, 26.3 g/L; total bilirubin, 35.4 μmol/L; indirect bilirubin, 21.4 μmol/L; plasma urea nitrogen, 8.9 mmol/L; and creatinine, 134.1 μmol/L. HELLP syndrome was diagnosed based on the above laboratory test findings.
Computerized tomography performed showed multiple cerebral infarctions in the bilateral temporal and basal ganglia regions and a thin layer of hemorrhagic lesion in the left temporoparietal cortex. Ultrasound revealed changes in the liver parenchyma and a small amount of abdominal effusion. Fetal heart monitor showed that fetal heart rate was 106 beat/min and irregular. The decision was made to perform an emergency cesarean section to terminate pregnancy as soon as possible.
The patient was treated immediately with intravenous magnesium sulfate and 5–10 μg/min nitroglycerin, sublingual 10 mg nifedipine, and intramuscular 100 mg phenobarbital sodium. Coagulation function showed prothrombin time, 12.3 s; activated partial thromboplastin time, 43.2 s; and fibrinogen, 2.6 g/L. The patient did not drink or eat for 12 h.
The patient was positioned supine with left side tilt in the operating room. American Society of Anesthesiologists grade was evaluated as III–E. A preanesthetic evaluation showed a Class II Mallampati airway with mild oral mucosa swelling. Standard monitoring (electrocardiography, pulse oximetry, and noninvasive BP) was attached to the patient. Respiratory frequency was 20 breath/min, and pulse oxygen saturation was 98%. BP was 175/102 mmHg with a heart rate of 96 beats/min.
Ringer's lactate solution was administered at a rate of 200 ml/h. After the surgical area was disinfected and sterile drapes were placed, 100 μg remifentanil and 60 mg propofol were injected slowly. When the patient lost consciousness, the operation began. Then, an injection of 100 mg succinylcholine was given for intubation. Nitroglycerin 2 μg/kg was administered for blood control. Anesthesia was maintained with infusions of propofol at a rate of 300–400 mg/h and remifentanil at a rate of 0.6 mg/h. Fentanyl and cisatracurium were administered intermittently as needed after the umbilical cord was clamped. In 3 min after the beginning of surgery, a female neonate was delivered, and then resuscitation was initiated by the neonatal team. The neonate was immediately intubated with Apgar scores of 1 and 5 at 1 and 5 min, respectively. The patient received 20 IU oxytocin by the intravenous route followed by intramuscular 250 μg carboprost tromethamine. During surgery, the patient was hemodynamically stable. Before delivery of the baby, we managed to control BP at the range of 140–160/80–100 mmHg.
Since the patient's admission, no urine output was observed; hence, after proper intravenous infusion and blood transfusion, 20 mg furosemide was administered by the intravenous route and 40 mg was repeated 20 min later. After a while, a small amount of urine flew out. Dexamethasone of 10 mg and 125 ml of 20% mannitol was given. According to the result of blood gas analysis, 150 ml of 5% sodium bicarbonate was infused.
During surgery, multiple spontaneous hemorrhagic lesions in the peritoneum were found. Blood samples were drawn and sent for laboratory tests. Blood routine showed that her platelet count, red blood cell count, and hemoglobin were reduced to 68 × 109/L, 2.00 × 1012/L, and 61 g/L, respectively. Coagulation function indicated fibrinogen, 1.8 g/L; prothrombin time, 17.4 s; activated and partial thromboplastin time, 53.2 s. On the base of the result, the diagnosis of HELLP syndrome was confirmed, and then 50 mg heparin was intravenously administered.
The operation lasted for 75 min. One unit of packed red blood cells and 1 unit of fresh frozen plasma were transfused. A total of 300 ml lactated Ringer's solution was given during the entire period in the operative room. Urine output was 40 ml.
After the surgery, the patient was transferred to the Intensive Care Unit and extubated 2 h later. A total of 1 unit of platelets and 1 unit of fresh frozen plasma was transfused in the Intensive Care Unit, according to platelet count (4.1 × 109/L), coagulation profile, and evidence of active bleeding. Subsequently, the patient's coagulation profile was normalized and platelet count increased to 146 × 109/L on the 1st postoperative day. Urine output increased gradually, and then plasma urea nitrogen and creatinine were within the normal ranges on the 3rd day after the operation. The edema gradually vanished 4 days after operation and the patient was discharged 6 days later uneventfully.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [28, 'years'], 'weight': [67.0, 'kg'], 'height': [161.0, 'cm'], 'creatinine': [134.1, 'µmol/L']}",52.82821,50.1868,55.46962,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 28 years old. 
The concentration of creatinine is 134.1 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 134.1 µmol. To convert 134.1 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 134.1 µmol creatinine * 1e-06 mol/µmol = 0.00013 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00013 mol creatinine * 113.12 g/mol = 0.01471 g creatinine. To convert 0.01471 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01471 g creatinine * 1000.0 mg/g = 14.71 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 14.71 mg creatinine/10.0 dL = 1.471 mg creatinine/dL. The concentration value of 134.1 µmol creatinine/L converts to 1.471 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 161.0 cm, which is 161.0 cm * 1 m / 100 cm = 1.61 m. The patient's weight is 67.0 kg. The patient's bmi is therefore 67.0 kg / (1.61 m * 1.61 m) = 25.84777 kg/m^2.The patient's BMI is 25.8, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 161.0 cm, which is 161.0 cm * 0.393701 in/cm = 63.38586 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.38586 (in inches) - 60) = 53.28748 kg.
Hence, the patient's IBW is 53.28748 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 53.28748 kg + 0.4 * (67.0 kg  - 53.28748 kg) = 58.77249 kg. The patient's adjusted body weight is 58.77249 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 28) * 58.77249 * 0.85) / (1.471 * 72) = 52.82821 mL/min. Hence, the patient's creatinine clearance is 52.82821 mL/min."
60,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6225725-1,Extracted,"We present the case of a 61-year-old woman with a history of total hysterectomy owing to a uterine fibroid at the age of 35 years. Nine days before admission to our hospital, she developed an itchy rash covering the whole body. Seven days before admission to our hospital, she visited a dermatologist who prescribed oral and topical medicines; however, there was no improvement. Three days before admission to our hospital, she visited a physician for general malaise and loss of appetite. Liver function disorder was detected by blood tests (AST (aspartate aminotransferase), 165 U/L; ALT (alanine transaminase), 291 U/L; ALP (alkaline phosphatase), 840 U/L; γ-GTP (γ-glutamyl transpeptidase), 373 U/L) and thickening of the gallbladder wall was seen on abdominal echo imaging. She was referred to our department of gastroenterological medicine. However, on the day of her visit to our hospital, she experienced a dull headache and blurred vision on attempting to get out of bed. The itching increased and she was brought to our emergency outpatient department. On admission, her clinical parameters were as follows: height, 162 cm; weight, 46.5 kg; JCS (Japan Coma Scale), 0; temperature, 36.6 °C; blood pressure, 126/82 mmHg; pulse, 77 bpm; and peripheral capillary oxygen saturation (SpO2), 96% (room air). Conjunctival congestion and jaundice were present, and breathing sounds were normal. Several erythemas (millimeter size), itching sensations on the face, body, and upper and lower extremities, partially fused wheals, and small papules were also observed (Fig. , ). There was no dryness of the mouth, pedal edema, decreased body weight, purpura, superficial lymph nodes, or nocturnal sweating. Laboratory results are shown in the Table . The results (creatinine (Cr) 3.08 mg/dL) indicated rapid decline in renal function compared to the tests conducted 3 days prior to admission (Cr 0.74 mg/dL). In addition, liver function tests were also abnormal. The patient was referred to the nephrology department and admitted to our hospital for examination and treatment.
Abdominal computed tomography (CT) showed slight enlargement of both kidneys (right, 12 × 7 cm; left, 11 × 6 cm) (Fig. ). Hepatitis virus antigen/antibody tests were negative on admission and there was no history of drinking; however, hepatobiliary enzymes were elevated. In addition, abdominal CT showed splenohepatomegaly (Fig. ). For the systemic rash, the patient was referred to the dermatology department on the day of admission, and a skin biopsy was performed. The rash was suspected to be an adverse effect of a drug; therefore, use of the previously prescribed drug was discontinued. The patient was also referred to the ophthalmology department for her blurred vision. Cataracts and uveitis were observed, along with increased intraocular pressure (IOP) (left IOP, 14 mmHg; right IOP, 13 mmHg). Abdominal CT did not reveal obstruction of the urinary tract, thus ruling out postrenal failure. Assuming the possibility of a prerenal failure, we administered extracellular fluid to maintain the hemodynamics. However, there was no improvement in renal function. We then suspected rapidly progressive renal failure with renal parenchyma involvement, or interstitial failure. Among the causes of rapidly progressive renal failure, we suspected nephrotoxic medications or glomerulonephritis due to membrane-type lupus nephritis or renal lymphoma. During hospitalization, her IOP further increased (left IOP, 35 mmHg; right IOP, 37 mmHg), for which various eye drops (steroids, prostaglandin-related drugs, beta-blocking drugs, adrenergic alpha 2 receptor agonists, carbonic anhydrase inhibitors, rho kinase inhibitors) were administered. However, there was no improvement. We administered oral steroids (prednisolone 30 mg/day) to prevent blindness and protect the kidneys. An improvement in the eye symptoms was detected. On day 3 of hospitalization, we performed a renal biopsy to determine the cause of rapidly progressive renal failure. In addition, after renal biopsy, we administered pulse steroid therapy (methylprednisolone 500 mg/day for 3 days) to protect the kidneys and further improve the eye symptoms (Fig. ). The response to pulse steroid therapy was good and renal function gradually improved (day 3 of hospitalization, Cr 3.22 mg/dL; day 5, Cr 2.06 mg/dL; day 8, Cr 1.13 mg/dL) (Fig. ). One complete course of pulse steroid therapy was administered and the dose of prednisolone was decreased to 20 mg/day from day 18. Elevated hepatobiliary enzymes gradually improved with steroids (Fig. ). The systemic rash and itching sensation began to dissipate, although pigmentation was still visible. Her vision improved and IOP decreased, thus blindness was prevented. On day 22, a diagnosis of tubulointerstitial nephritis due to tubulointerstitial infiltration of PTCL-NOS was made, based on the results of renal biopsy (hematoxylin-eosin staining showed the presence of atypical lymphocytes; immunostaining showed that CD2, CD3, and CD4 were positive and CD5, CD7, CD8, and CD20 were negative) (Fig. , , , ) and a Ki-67 score of approximately 80%. We also diagnosed subcutaneous tissue infiltration of PTCL-NOS, based on the results of skin biopsy (hematoxylin-eosin staining showed the presence of atypical lymphocytes; immunostaining showed that CD2, CD3, and CD4 were positive and CD5, CD7, CD8, and CD20 were negative) (Fig. , , , ) and a Ki-67 score of approximately 80%. We performed flow cytometric analysis of the kidney and skin tissue, which showed similar results. We performed Southern blot analysis on kidney and skin tissue, but we could not obtain the result because of small amount of DNA. A presumptive diagnosis of PTCL-NOS to the liver and spleen and existence of Uveitis masquerade syndrome [] due to PTCL-NOS was made based on the clinical course. Since lymph node lesions were not seen on imaging, we assumed that the lesions were limited to extralymphatic organs. In addition, we performed a spinal fluid test and found an atypical lymphocyte count of 5%. These atypical lymphocytes showed the same findings on flow cytometric analysis as those in the kidney and skin. The patient was referred to the hematology department and initial CHOP therapy was administered on day 23 of hospitalization.
For 8 months after admission, seven courses of CHOP therapy (Vincristine 1.4 mg/m2, Doxorubicin 50 mg/m2, Cyclophosphamide 750 mg/m2, Prednisolone 100 mg/day day1-day5) were administered and positron emission tomography/CT was performed. No enhanced uptake of FDG (fluorodeoxyglucose) was seen in any principal organs or lymph nodes, indicating complete remission. There was no significant change in the size of the liver; however, a decrease in the size of the spleen and both kidneys was seen.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [46.5, 'kg'], 'height': [162.0, 'cm'], 'creatinine': [3.08, 'mg/dL'], 'age': [61, 'years']}",14.08042,13.3764,14.78444,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 61 years old. 
The concentration of creatinine is 3.08 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.0 cm, which is 162.0 cm * 1 m / 100 cm = 1.62 m. The patient's weight is 46.5 kg. The patient's bmi is therefore 46.5 kg / (1.62 m * 1.62 m) = 17.71834 kg/m^2.The patient's BMI is 17.7, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 46.5 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation. 
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 61) * 46.5 * 0.85) / (3.08 * 72) = 14.08042 mL/min. Hence, the patient's creatinine clearance is 14.08042 mL/min."
61,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4251529-1,Extracted,"A 47-year-old Hispanic male presented with lower back pain, and lethargy. The symptoms started approximately 1 week before presentation. The patient denied having any upper respiratory symptoms, rash, or joint pain. The patient also denied having any gross hematuria, foamy urine, or any other urinary symptoms. The patient’s history included GPA, diagnosed by a renal biopsy 2 years ago, diabetes mellitus, hypertension, hyperlipidemia, and diverticulosis requiring colostomy.
His medication at the time included simvastatin, lisinopril, azathioprine, and insulin. His azathioprine was reduced from 200 mg/day to 100 mg/day 6 months before presentation. He had recently lost his job and insurance, and denied smoking, alcohol use, or any substance abuse. On physical examination, he was afebrile. His blood pressure was 99/51 mmHg, pulse was 74 beats/minute, and respiration rate 18 breaths/minute, height was 165 cm, and weight was 97 kg. He was in no apparent distress. The patient’s lungs were clear, heart sounds were regular without any murmur, rub, or gallop, the abdomen was soft, and no edema or skin rash was present.
Laboratory data revealed the patient’s blood urea nitrogen (BUN) to be 73 mg/dL and serum creatinine (Scr) 5.2 mg/dL with otherwise normal electrolytes, hemoglobin 12.7 mg/dL, platelets 257,000/mm3, albumin 3.5 mg/dL, and normal liver enzymes. Two years prior to current presentation his Scr level was 1.5 mg/dl. Urinalysis showed large protein, large blood, many dysmorphic red blood cells and red blood cell casts. The urine protein to creatinine ratio was 2.03 mg/mg. Renal sonogram revealed kidney sizes of 11.3 cm and 10.6 cm on right and left kidneys, respectively, without any evidence of obstruction and an unremarkable bladder with no significant postvoid residual volume.
The patient was started on high dose pulse methylprednisolone intravenously (1 g/day for 3 days), and his azathioprine dose was increased to 200 mg/day. His serology showed normal complement titers, negative hepatitis profile, and mildly elevated rheumatoid factor at 24 IU/ml (normal <14). ANCA serology showed proteinase-3 (PR3) antibody (anti-PR3, cytoplasmic c-ANCA) reactive at low levels −4.1 (<1.0 reported as negative) and negative myeloperoxidase (MPO) antibody (anti-MPO, perinuclear p-ANCA). Anti-GBM titers were negative.
Based on clinical presentation and the patient’s past medical history, it was presumed that the most likely cause of worsening renal function was a relapse of GPA. However, very low levels of anti-PR3 antibodies, and the questionable duration of the progression of the patient’s renal disease prompted the nephrology team to proceed with a repeat kidney biopsy.
The kidney biopsy showed focal segmental necrotizing and crescentic glomerulonephritis, with weak linear staining of IgG, which was not seen on previous biopsy. Out of 19 glomeruli examined, nine showed complete or near complete global sclerosis. Crescents were seen in eleven of 19 glomeruli. The other biopsy findings included moderate tubular atrophy, moderate interstitial fibrosis with inflammation, and moderate arteriosclerosis ( and ). The pathologist reported findings suggestive of moderate disease activity and moderate chronicity. Although the biopsy indicated some evidence of chronic disease, there was still significant active disease that should be treated. Provided that the disease process responded to the treatment, there was a possibility of at least partial recovery of renal function.
The biopsy findings presented a treatment dilemma. The patient had a history of GPA and initially presented with PICGN and crescentic glomerulonephritis with negative IF findings 2 years previously (). At that time, he was treated with pulse methylprednisolone followed by 6 months of oral prednisone and cyclophosphamide, which successfully induced remission. His renal function had improved; Scr decreased from 3.1 mg/dL to 1.5 mg/dL and proteinuria decreased from 2.3 g/day to <500 mg/day. He was then switched to maintenance immunosuppression with azathioprine. At the time of his initial presentation, his anti-PR3 level was >100 U/ml. After initial induction therapy, anti-PR3 level was reduced below assay limits and remained negative during follow up.
This patient was treated with pulse dose of intravenous methyl prednisolone 1 g/day for 3 days followed by maintenance oral prednisone at 1 mg/kg/day. He was also treated with monthly intravenous cyclophosphamide (15 mg/kg). Three months later, the patient had partially responded with proteinuria decreasing to 800 mg/day and Cr stabilizing to 2.8 mg/dL.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [47, 'years'], 'weight': [97.0, 'kg'], 'height': [165.0, 'cm'], 'creatinine': [5.2, 'mg/dL']}",18.7902,17.85069,19.72971,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 47 years old. 
The concentration of creatinine is 5.2 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 97.0 kg. The patient's bmi is therefore 97.0 kg / (1.65 m * 1.65 m) = 35.62902 kg/m^2.The patient's BMI is 35.6, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 61.40954 kg + 0.4 * (97.0 kg  - 61.40954 kg) = 75.64572 kg. The patient's adjusted body weight is 75.64572 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 47) * 75.64572 * 1) / (5.2 * 72) = 18.7902 mL/min. Hence, the patient's creatinine clearance is 18.7902 mL/min."
62,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5411553-3,Extracted,"A 51-year-old man was admitted to our hospital for renal biopsy. Proteinuria had been detected when the patient was approximately 30 years of age, and he had experienced tonsillitis several times. The patient had been diagnosed with PV with an abnormality of the JAK2 gene 3 years earlier. Renal biopsy was planned because his proteinuria had become more apparent over the past 2 years.
The patient’s height, weight, and blood pressure were 165 cm, 66 kg, and 120/73 mmHg, respectively. His consciousness level was alert, and he appeared healthy. No remarkable abnormalities were found in the heart, lungs, or abdomen, and pitting edema was not observed.
The laboratory data were as follows: hemoglobin, 15.3 g/dl; hematocrit, 48.1 %; platelets, 326,000/μl; white blood cells, 8,400/μl; C-reactive protein, <0.2 mg/dl; blood urea nitrogen, 22.2 mg/dl; serum creatinine, 1.4 mg/dl; total cholesterol, 194 mg/dl; total protein, 7.1 g/dl; albumin, 4.1 g/dl; globulin, 3.0 g/dl; lactate dehydrogenase, 169 IU/l; aspartate aminotransferase, 17 IU/l; alanine aminotransferase, 23 IU/l; total bilirubin, 0.5 mg/dl; γ-glutamyl transpeptidase, 21 IU/l; alkaline phosphatase, 276 IU/l; Na, 139 mmol/l; K, 4.7 mmol/l; and Cl, 106 mmol/l. Urinalysis showed 4+ proteinuria (1.2 g/day) and no evidence of hematuria.
Renal biopsy was performed (Fig. ) and 22 glomeruli could be evaluated, 5 of which showed global sclerosis. Histological findings included mesangial proliferative glomerulonephritis with crescents and focal segmental necrosis. Arteriosclerotic changes were also observed. Immunofluorescence staining was positive and revealed strong immunoreactivity for IgA and C3. Electron microscopy showed electron-dense deposits in the mesangium. He was diagnosed with IgA nephropathy. Tonsillectomy plus steroid pulse therapy and an angiotensin II receptor blocker were selected as treatments for the patient. His proteinuria and hematuria disappeared after 6 months.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [66.0, 'kg'], 'height': [165.0, 'cm'], 'creatinine': [1.4, 'mg/dL'], 'age': [51, 'years']}",54.22072,51.50968,56.93176,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 51 years old. 
The concentration of creatinine is 1.4 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 66.0 kg. The patient's bmi is therefore 66.0 kg / (1.65 m * 1.65 m) = 24.24242 kg/m^2.The patient's BMI is 24.2, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 61.40954 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 51) * 61.40954 * 1) / (1.4 * 72) = 54.22072 mL/min. Hence, the patient's creatinine clearance is 54.22072 mL/min."
63,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,usmle-3434,Extracted,"A 48-year-old woman comes to the physician for the evaluation of 24-hour blood pressure monitoring results. Over the last 3 months, she has had intermittent nausea, decreased appetite, and increasing weakness and fatigue during the day. She has been treated twice for kidney stones within the past year. Her current medications include lisinopril, amlodipine, and furosemide. She is 178 cm (5 ft 10 in) tall and weighs 97 kg (214 lb); BMI is 31 kg/m2. Her blood pressure is 152/98 mm Hg. Physical examination shows no abnormalities. Serum studies show:
Na+ 141 mEq/L
Cl− 101 mEq/L
K+ 4.5 mEq/L
HCO3− 24 mEq/L
Calcium 12.9 mg/dL
Creatinine 1.0 mg/dL
Twenty-four-hour blood pressure monitoring indicates elevated nocturnal blood pressure.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [48, 'years'], 'weight': [97.0, 'kg'], 'height': [178.0, 'cm'], 'creatinine': [1.0, 'mg/dL']}",86.89835,82.55343,91.24327,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 48 years old. 
The concentration of creatinine is 1.0 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 178.0 cm, which is 178.0 cm * 1 m / 100 cm = 1.78 m. The patient's weight is 97.0 kg. The patient's bmi is therefore 97.0 kg / (1.78 m * 1.78 m) = 30.61482 kg/m^2.The patient's BMI is 30.6, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (70.07878 (in inches) - 60) = 68.68119 kg.
Hence, the patient's IBW is 68.68119 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 68.68119 kg + 0.4 * (97.0 kg  - 68.68119 kg) = 80.00871 kg. The patient's adjusted body weight is 80.00871 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 48) * 80.00871 * 0.85) / (1.0 * 72) = 86.89835 mL/min. Hence, the patient's creatinine clearance is 86.89835 mL/min."
64,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-7746474-1,Extracted,"A 13-year-old, previously fit and well, male presented with pain and swelling to his right lower leg. A bone cyst was identified on imaging including plain radiographs and MRI scans (Figures and ). He underwent curettage on three occasions, including one with a bone graft, with recurrence on each occasion. An ABC was confirmed on biopsy on tissue obtained during curettage. En bloc resection of the proximal tibia was not thought to be viable due to the extent of disease and involvement of major neurovascular structures. Vascular embolization was not possible because no feeding vessels were identified on angiogram. Throughout this period, he had ongoing severe leg pain, was unable to weight-bear or attend school, and was at significant risk of pathological fracture.
Denosumab therapy was subsequently commenced following discussion of a bone tumour treatment multidisciplinary team. The weight at the start of treatment was 36 kg, with a height of 161 cm. The patient received four doses of subcutaneous denosumab (70 mg/m2) on a weekly basis for four weeks with significant improvement in pain, allowing him to return to school shortly after, although he was still immobile. There was a subtle initial radiological response with a slight reduction in size of the lesion. There was asymptomatic mild hypocalcaemia (corrected calcium 2.03 mmol/L; normal range 2.25–2.74 mmol/L) in the early stages of treatment which was treated with oral calcium supplementation (calcium carbonate 1.25 g daily). He remained on this supplementation throughout treatment. The patient went on to receive six further doses of denosumab at four-week intervals at the same dose.
On review following six months of treatment, there was ongoing radiological improvement, with bony consolidation (). The patient remained pain free, and he began partial weight-bearing over the subsequent few months. However, there was also evidence of some calcification of the lower limb growth plates, possibly as a result of denosumab therapy. Therefore, the dose interval was increased initially to two months, and then at 12 months of treatment, to three months.
After 18 months of treatment, the patient was walking without protection and fully weight-bearing without pain. The ABC was stable radiologically, and the dosing interval was further increased to four months.
On review after 27 months of treatment (following the 17th dose; cumulative dose 1554 mg), the patient remained pain free and was able to play gentle sport. Given the good response, the plan was for two further doses of denosumab every six months before stopping therapy.
On presentation for the first six-month dose, the patient was found to have a blood pressure of 170/100 mmHg. He reported he had felt generally unwell for several weeks with malaise, anorexia, polyuria, and headaches. His weight was 47 kg which was significantly lower than his last clinic review four months earlier when it was 50.7 kg, demonstrating a weight loss of 3.7 kg. Height was static in this four-month period at 172 cm. Initial blood tests demonstrated hypercalcaemia (corrected calcium 4.04 mmol/L). There were normal levels of phosphate (1.35 mmol/L; normal range 0.74–1.55 mmol/L) and alkaline phosphatase (201µ/L; normal range 55–236µ/L). 25-Hydroxyvitamin D2 was <5 nmol/L, and 25-hydroxyvitamin D3 was 84 nmol/L (normal range >50 nmol/L). In addition, there was an acute kidney injury (AKI) with a creatinine of 293 µmol/L (normal range 46–102 µmol/L) and a urea of 13.4 mmol/L (normal range 2.5–6.7 mmol/L). His parathyroid hormone level on presentation was suppressed at 1.0 pmol/L (normal range 1.1–6.9 pmol/L). Urine calcium/creatinine ratio was high at 3.62 mm/mm Cr (normal range 0–0.6 mm/mm Cr), however was not performed until 11 days after presentation and initial management. Lab values on this presentation and in subsequent management are summarised in .
Initial management was with intravenous (IV) fluids, IV furosemide (60 mg six hourly), and cessation of the supplemental calcium. There was no initial biochemical improvement, with corrected calcium peaking at 4.18 mmol/L and creatinine at 314 µmol/L. 200 units of calcitonin, initially subcutaneously, and then intravenously, was introduced once a day with limited improvement in calcium level and renal function, despite increasing to twice daily dosing over a nine-day period. Therefore, two doses of IV pamidronate (0.25 mg/kg and then 0.5 mg/kg, 24 hours apart) were given. Bisphosphonate therapy led to the normalisation of calcium levels (corrected calcium 2.74 mmol/L) within three days, with subsequent improvement to normal range of the high creatinine (97 µmol/L) a further three days later. Amlodipine (2.5 mg daily), which had been commenced to control the hypertension, could also be stopped at this stage with no adverse effect on the now normal blood pressure. He was discharged the following day.
Calcium levels were monitored closely following discharge with a further episode of rebound hypercalcaemia (corrected calcium 3.44 mmol/L), with an associated AKI (creatinine 115 µmol/L), 13 days after initial pamidronate treatment (). A further dose of IV pamidronate (0.5 mg/kg) was given, again with a positive response (corrected calcium 2.50 mmol/L four days later). A further episode occurred two weeks later (corrected calcium, 3.15 mmol/L), this time successfully treated with IV zoledronic acid (0.05 mg/kg).
A bone density scan (DEXA scan) was performed approximately two months following the third episode of hypercalcaemia and was within normal range, with a Z-score of 0.5 for the lumbar spine and 1.0 for the whole body (normal range >−2.0). Recurrence of hypercalcaemia has not subsequently occurred, and the patient remains mobile and pain free 16 months since the last denosumab dose and nine months since the third and last episode of hypercalcaemia. Now at 18 years old, his fatigue and appetite, without the need for a low calcium diet, have improved and he is gaining weight (now 53.8 kg).","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [53.8, 'kg'], 'height': [172.0, 'cm'], 'creatinine': [97.0, 'µmol/L'], 'age': [18, 'years']}",80.60222,76.57211,84.63233,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 18 years old. 
The concentration of creatinine is 97.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 97.0 µmol. To convert 97.0 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 97.0 µmol creatinine * 1e-06 mol/µmol = 0.0001 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.0001 mol creatinine * 113.12 g/mol = 0.01131 g creatinine. To convert 0.01131 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01131 g creatinine * 1000.0 mg/g = 11.31 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 11.31 mg creatinine/10.0 dL = 1.131 mg creatinine/dL. The concentration value of 97.0 µmol creatinine/L converts to 1.131 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 172.0 cm, which is 172.0 cm * 1 m / 100 cm = 1.72 m. The patient's weight is 53.8 kg. The patient's bmi is therefore 53.8 kg / (1.72 m * 1.72 m) = 18.18551 kg/m^2.The patient's BMI is 18.2, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 53.8 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation. 
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 18) * 53.8 * 1) / (1.131 * 72) = 80.60222 mL/min. Hence, the patient's creatinine clearance is 80.60222 mL/min."
65,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5984920-1,Extracted,"A 45-year-old Caucasian woman presented with abdominal pain, nausea, and vomiting for 17 h. At 22 h prior to admission, she went out to dinner and drank one glass of wine. A few hours after the meal, she developed epigastric and left upper quadrant abdominal pain that was moderate, persistent, cramping, and aching; the pain radiated to her left middle back and arm without exacerbating or alleviating factors. The pain was associated with nausea, vomiting, and she could not tolerate any oral intake. She felt thirsty and had polyuria and positional lightheadedness. She reported no fever, chills, chest pain, cough, sputum production, dysuria, hematuria, diarrhea, hematochezia, and melena.
On further questioning, the patient shared that she had a history of gestational glucose intolerance 6 years ago, and has had occasional impaired fasting glucose of 81–107 mg/dL for the past 6 years. She began following an American Diabetes Association (ADA) diet 2 years ago and lost 25 lb. Additionally, she had a past medical history of supraventricular tachycardia, irritable bowel syndrome, social alcohol use, cholecystectomy, and thyroid papillary adenocarcinoma status post partial thyroidectomy complicated by postsurgical hypothyroidism. Home medications included metoprolol tartrate, levothyroxine, and meloxicam. The patient reported no family history of diabetes.
Temperature 97.7 °F, pulse 130 bpm, respiratory rate 28 bpm, BP 134/71 mmHg, weight 87 kg, height 1.68 m, BMI 31 kg/m2, SpO2 99% on room air.
The patient was in moderate distress. There was no acanthosis nigricans. Cardiovascular system revealed tachycardia. A pulmonary exam revealed tachypnea, accessory muscle usage with moderate respiratory distress. Abdominal exam revealed central obesity, normoactive bowel sounds, left upper quadrant and epigastric tenderness to palpation, no rigidity or guarding. No costovertebral angle tenderness.
CBC: WBC 25.9 × 109/L, hemoglobin 14.7 g/dL, hematocrit 45.8%, platelet 386 × 109/L, MCV 100.2 µm3. BMP: sodium 135 mmol/L, potassium 7.4 mmol/L, chloride 89 mmol/L, bicarbonate 5 mmol/L, BUN 37 mg/dL, creatinine 1.27 mg/dL, glucose 931 mg/dL, eGFR 46 mL/min.
Liver chemistry: Total bilirubin 0.2 mg/dL, AST 23 U/L, ALT 54 U/L, ALP 138 U/L, total protein 7.5 g/dL, albumin 4.5 g/dL. Calcium 8.7 mg/dL, phosphate 1.4 mg/dL, magnesium 2.1 mg/dL. VBG: pH 6.92. Repeated ABG 2 h later: pH 7.21, pCO2 16 mmHg, pO2 129 mmHg, HCO3− 6.4 mmol/L, SaO2 98% on 2 L/min oxygen by nasal cannula. Beta-hydroxybutyrate 28 mmol/L, lactic acid 4.0 mmol/L. Urinalysis showed urine ketones 80 mg/dL, leukocyte esterase negative, urine culture no growth. HbA1c 6.4%. Lipid profile: triglycerides 89 mg/dL, total cholesterol 144 mg/dL, LDL 91 mg/dL, HDL 35 mg/dL. TSH 3.12 mIU/mL, free T4 1.26 ng/dL. Troponin I < 0.01 ng/mL.
Ultrasonography of the abdomen revealed mild hepatic steatosis, incidental mild to moderate right-sided hydronephrosis, status post cholecystectomy. ECG on admission: sinus rhythm, HR 126 bpm, peaked T waves at lead V2–V6 consistent with hyperkalemia, no ischemic changes.
All procedures performed in this study were in compliance with the ethical standards of the institutional and/or national research committee and with the 1964 Declaration of Helsinki and its later amendments or comparable ethical standards. Informed consent was obtained from the individual participant for being included in the study.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [87.0, 'kg'], 'height': [1.68, 'm'], 'creatinine': [1.27, 'mg/dL'], 'age': [45, 'years']}",62.32484,59.2086,65.44108,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 45 years old. 
The concentration of creatinine is 1.27 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.68 m. The patient's weight is 87.0 kg. The patient's bmi is therefore 87.0 kg / (1.68 m * 1.68 m) = 30.82483 kg/m^2.The patient's BMI is 30.8, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.68 m, which is 1.68 m * 39.3701 in/m = 66.14177 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.14177 (in inches) - 60) = 59.62607 kg.
Hence, the patient's IBW is 59.62607 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 59.62607 kg + 0.4 * (87.0 kg  - 59.62607 kg) = 70.57564 kg. The patient's adjusted body weight is 70.57564 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 45) * 70.57564 * 0.85) / (1.27 * 72) = 62.32484 mL/min. Hence, the patient's creatinine clearance is 62.32484 mL/min."
66,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-8494847-3,Extracted,"Male, 52 years old, with a 17-year history of DM, was admitted for evaluation of acute renal dysfunction (from 0.8 mg/dL to 1.1 mg/dL of serum creatinine, 79.7 mL/min/1.73 m2 to 68.4 mL/min/1.73 m2 of eGFR) for 56 day intervals). Treatment with dapagliflozin 5 mg daily was started from 5 months before this admission. The patient’s height was 164.5 cm and weight increased from 80 to 82 kg following dapagliflozin treatment. Urinary protein was 0.08 g/day, and negative for ketones. The patient’s blood pressure was 122/74 mmHg; HbA1c, 7.4%; blood sugar level, 108 mg/dL; and plasma renin activity was 36.8 ng/ml/hr (normal 0.3–2.9). Renal biopsy was performed to evaluate renal dysfunction.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [52, 'years'], 'weight': [82.0, 'kg'], 'height': [164.5, 'cm'], 'creatinine': [1.1, 'mg/dL']}",77.08229,73.22818,80.9364,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 52 years old. 
The concentration of creatinine is 1.1 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 164.5 cm, which is 164.5 cm * 1 m / 100 cm = 1.645 m. The patient's weight is 82.0 kg. The patient's bmi is therefore 82.0 kg / (1.645 m * 1.645 m) = 30.30275 kg/m^2.The patient's BMI is 30.3, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 164.5 cm, which is 164.5 cm * 0.393701 in/cm = 64.76381 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.76381 (in inches) - 60) = 60.95676 kg.
Hence, the patient's IBW is 60.95676 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 60.95676 kg + 0.4 * (82.0 kg  - 60.95676 kg) = 69.37406 kg. The patient's adjusted body weight is 69.37406 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 52) * 69.37406 * 1) / (1.1 * 72) = 77.08229 mL/min. Hence, the patient's creatinine clearance is 77.08229 mL/min."
67,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6682344-1,Extracted,"A 50-year-old female presented to our hospital with generalized abdominal pain. The pain had been intermittent and was occurring spontaneously, every two to three weeks, for the last year. Her current episode spanned over 15 days and had gradually been increasing in intensity. The pain radiated to the back and was associated with three episodes of non-projectile, non-bilious vomiting. The pain had no association with meals. The review of systems revealed undocumented weight loss and reduced appetite. She had a history of Grade 3 ductal carcinoma of the left breast, treated with mastectomy and chemoradiotherapy 10 years previously. She had also undergone a laparoscopic cholecystectomy 15 years ago. Family history was not significant for any illness. At the time of presentation, she was being treated for Helicobacter pylori gastritis with triple therapy. There was no history of smoking, drug, or alcohol use.
At the time of presentation to the emergency room (ER), the patient was in severe pain. The patient was of short stature and lean, and was visibly distressed. At the time of presentation to the ER, she was hypotensive with a systolic blood pressure (SBP) ranging from 64 to 81 mm Hg and a diastolic blood pressure (DBP) of 30-40 mm Hg and tachycardic (Pulse = 131-150 bpm). She was afebrile. General physical examination revealed pallor and dehydration of conjunctival and oral mucosae. On abdominal examination, there was generalized tenderness but no guarding. Gut sounds were audible. The remaining physical examination was unremarkable. Resuscitation with intravenous fluids was initiated. A central venous catheter was placed to monitor fluid status and for the administration of norepinephrine. Tramadol was given to manage the pain and heparin sodium subcutaneously for deep venous thrombosis (DVT) prophylaxis.
Laboratory investigations revealed anemia (hemoglobin 8.9 gm/dl) and renal dysfunction (creatinine 2.2 mg/dl). Arterial blood gas suggested metabolic acidosis with respiratory compensation. The calculated serum osmolarity was 288 mOsm/kg and anion gap (corrected for albumin) was 26 (Table ).
Following volume resuscitation, she underwent a contrast-enhanced CT scan that showed significantly distorted bowel anatomy with abnormally dilated enhancing proximal and mid-jejunal loops. The presence of a midgut volvulus, affirmed by the presence of the whirlpool sign was noted (Figure ). No congenital malrotation could be identified. The superior mesenteric artery was significantly attenuated representing occlusion, and there was non-enhancement of distal jejunal and ileal loops. These findings suggested mesenteric ischemia. There was no evidence of pneumatosis intestinalis or pneumoperitoneum. The liver was unremarkable.
Following successful resuscitation, an emergency laparotomy was performed. No underlying anatomic abnormality that could direct us towards the cause of the volvulus could be identified. Therefore, a presumptive diagnosis of primary midgut volvulus was made. Approximately 250 cm of gangrenous distal jejunum, ileum and cecum were resected (Figure ). Seventy-five centimeters of duodenojejunum remained but had questionable viability in some areas. The abdomen was irrigated with three liters of fluid. The two stapled ends were left in place without an anastomosis. The fascia was not closed and the skin was approximated using towel clips.
The patient was shifted to the intensive care unit (ICU) and extubated. During the next 48 hours, she remained hemodynamically stable off vasopressors. She was afebrile, required minimal supplemental oxygen, and produced adequate urine. Anticoagulation was maintained via heparin sodium infusion.
She underwent a re-look laparotomy 48 hours later. Approximately 100 cc of thin murky fluid was found in the peritoneal cavity. The residual small bowel was viable with pulsatile mesenteric vessels throughout the remaining mesentery. There were no areas of necrosis identified. A side to side functional end to end stapled anastomosis was created between the mid jejunum and ascending colon. The fascia was closed and the skin left open.
She was again shifted to the ICU, and extubated a day later. Total parenteral nutrition (TPN) was initiated. The surgical wound was open and daily dressings were done. She was transferred to a special care unit (SCU) on day 5 of admission where she remained for a day before being shifted to the ward (day 6). She maintained adequate urine output and had multiple bowel movements every day from the sixth day of admission.
A complete nutritional assessment for this patient was done. She weighed 40 kg with a height of 155 cm, BMI of 18 kg/m2, and an ideal body weight of 48 kg. To meet her nutritional requirements, it was determined that she needed 1400-1800 kcal/day (35-45 kcal/kg/day). This was further split into 80 gm of protein, 175 gm of carbohydrates and 42 gm of fat. She was kept nil per oral (NPO) till the 2nd post-operative day, following the re-look procedure. During this time, she was kept on a TPN formula consisting of 10 gm of nitrogen, 200 gm of dextrose and 20 gm of fat, with a caloric value of 1130 kcal. Her TPN formula was subsequently adjusted to include 12 gm of nitrogen, 20 gm of fat, 260 gm of dextrose, 10 ml of multivitamin and 5 ml zinc sulfate, amounting to 1384 kcal. She was started on a soft diet on the 3rd post-operative day along with the new TPN formula. She was then progressed to a regular diet along with TPN. On the 6th post-operative day, TPN was discontinued and oral intake was supplemented with full-strength Ensure, at 200 ml twice a day. She was discharged on the 9th post-operative day on a regular diet, along with Ensure.
On her first visit to the outpatient clinic four days post-discharge, her weight was 35 kg and she was documented to have had multiple bowel movements (an average of four per day) at home. On subsequent monthly visits that continued for the next eight months, her weight remained fairly stable, going up to 36 kg; and she was found to be tolerating her diet well. She had no active complaints during these visits and her physical examination revealed adequate granulation tissue developing at the wound site.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [40.0, 'kg'], 'height': [155.0, 'cm'], 'creatinine': [2.2, 'mg/dL'], 'age': [50, 'years']}",19.31818,18.35227,20.28409,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 50 years old. 
The concentration of creatinine is 2.2 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 40.0 kg. The patient's bmi is therefore 40.0 kg / (1.55 m * 1.55 m) = 16.64932 kg/m^2.The patient's BMI is 16.6, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 40.0 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation. 
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 50) * 40.0 * 0.85) / (2.2 * 72) = 19.31818 mL/min. Hence, the patient's creatinine clearance is 19.31818 mL/min."
68,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4204687-1,Extracted,"A 31-year-old man with CD was admitted to the hospital because of severe abdominal pain and diarrhea. He had been diagnosed with CD 10 years previously, but he was lost to follow-up, during which he experienced repeated exacerbations and remissions. The patient had taken mesalazine 3,000 mg/day and azathioprine 50 mg/day and had started infliximab one year prior to admission. With infliximab, the patient experienced immediate relief of diarrhea and abdominal pain, but obstructive symptoms had gradually worsened. He complained of abdominal pain, increased borborygmus, decreased oral intake, and a decrease in body weight. Abdominal CT scan and small bowel series revealed an ileocolic fistula, multiple ulcers, and severe stricture of the small bowel (). Vital signs (blood pressure, 120/80 mmHg; pulse rate, 80 beats/min; respiratory rate, 20 beats/min; body temperature, 36.9℃) were normal. He has a height of 171 cm, a weight of 53 kg, and a BMI of 18.1 kg/m2. The patient had a chronically ill appearance with pale conjunctiva, mild tenderness in the lower abdomen, and accentuated bowel sounds. Liver and spleen were not palpable. Pitting edema could be seen on both lower limbs. Laboratory testing revealed anemia with a hemoglobin level of 8.7 g/dL, leukocyte count of 3,970/mm3, and platelet count of 265,000/mm3. Serum chemistry tests were consistent with severe malnutrition: AST/ALT 53/29 IU/L, BUN/creatinine 15/0.64 mg/dL, total protein/albumin 4.3/2.2 g/dL, and total cholesterol 88 mg/dL. ESR and CRP level were 35 mm/h and 2.1 mg/dL, respectively. Both anti-Saccharomyces cerevisiae-antibodies IgA and IgG were negative, and the patient's CDAI was about 261 points. He had been experiencing approximately 25 liquid stools per week, severe abdominal pain, and a very poor sense of well-being. To improve the patient's condition, wide resection of involved bowel and colostomy would be needed; however, because of a psychological reaction to personal disfigurement and the need to relearn bowel habits, he strongly refused colostomy. Therefore, we decided to perform a small and large bowel segmental resection and primary repair.
Gross findings during surgery included an abscess connected to the terminal ileum, bladder adhesion, a jejuno-sigmoid fistula, and huge inflammatory masses. An ileocecectomy, jejunal resection, and sigmoid colon resection were performed, followed by primary repair of the jejunum, rectum, and sigmoid colon (). Fortunately, 220 cm of the small bowel remained after surgery. However, one week postoperatively, the patient developed a high fever and abdominal pain. Abdominal CT scan revealed a fistula connected to an intraperitoneal abscess (). The patient was started on intravenous antibiotics, and the abscess was drained percutaneously. A total of four percutaneous drainages were performed. The drainage fluid was dark yellow and highly viscous but gradually cleared after continuous use of antibiotics. However, despite no further evidence of infection (white blood cell count 4,270/mm3 and CRP 0.3 mg/dL), approximately 30-50 cc of fluid issued from every drain daily, even one month after the operation.
The patient was started on 5 mg/kg of infliximab to treat the postoperative fistula and prevent a recurrence. After infliximab therapy was initiated, drainage decreased dramatically to less than 10 cc a day. In follow-up abdominal CT scans, the abscess in the abdominal cavity and the postoperative fistula disappeared (). The percutaneous drainages were consecutively removed, the patient began receiving oral nutrition, and the intravenous antibiotics were stopped. The patient quit smoking, and infliximab was injected to prevent disease recurrence. Three months after surgery, the patient looked healthy and reported passing stools once or twice a day. His body weight increased by 8 kg, BMI increased to 20.9 kg/m2, and his CDAI decreased to 60. In follow-up laboratory exams, the patient's hemoglobin level was 12.7 g/dL, total protein and albumin were 6.9/3.9 g/dL, and total cholesterol was 130 mg/dL.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [31, 'years'], 'weight': [53.0, 'kg'], 'height': [171.0, 'cm'], 'creatinine': [0.64, 'mg/dL']}",125.36892,119.10047,131.63737,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 31 years old. 
The concentration of creatinine is 0.64 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 171.0 cm, which is 171.0 cm * 1 m / 100 cm = 1.71 m. The patient's weight is 53.0 kg. The patient's bmi is therefore 53.0 kg / (1.71 m * 1.71 m) = 18.12524 kg/m^2.The patient's BMI is 18.1, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 53.0 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation. 
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 31) * 53.0 * 1) / (0.64 * 72) = 125.36892 mL/min. Hence, the patient's creatinine clearance is 125.36892 mL/min."
69,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-3048475-1,Extracted,"A 22-year-old South Indian man with a previous history of Fontan surgery at the age of 13 for double outlet right ventricle with severe pulmonary stenosis and straddling tricuspid valve presented with a spiking high-grade fever of 25-day duration. He had no history of cough, ear discharge, respiratory infection, dysuria, diarrhea, gastrointestinal distress or vomiting.
His past history included surgery for a brain abscess at the age of 13, Fontan surgery at the age of 13, ocular surgery for retinal detachment at the age of 16, and multiple small skin abscesses chiefly on his left foot, which recurred after treatment and led to an excision of an abscess on his foot. At the age of 20, he was diagnosed with protein-losing enteropathy.
The last echocardiography performed before his hospitalization showed a right to left flow in the Fontan circuit, signifying a flow of de-oxygenated blood from the intended pulmonic to the systemic circulation.
On physical examination, he was found to be febrile with a temperature of 39°C on admission, a pulse rate of 88 per minute, a respiratory rate of 26 per minute, blood pressure of 98/60 mmHg, and oxygen saturation of 89 percent in room air. A head to toe examination identified clubbing of his nails, a median sternotomy scar, mild abdominal distension and pedal edema. His teeth and oral cavity were found to be normal. He was 174 cm tall and weighed 51 kg.
His laboratory data on admission showed the following: white blood cells (WBCs) 14,000/mm3, neutrophils 84.5 percent, lymphocytes 8.3 percent, eosinophils 0.2 percent, erythrocyte sedimentation rate 45 mm/hour, hemoglobin 10.1 g/dL, urea 19 mg/dL, serum creatinine 0.6 mg/dL, sodium 122 mmol/L, potassium 3.7 mmol/L, total protein 3.7 g/dL, serum albumin 1.3 g/dL and serum globulin 2.4 g/dL. He tested negative for hepatitis B surface antigen, hepatitis C virus and human immunodeficiency virus. A further work-up for immune deficiency could not be performed for logistical reasons. A urine analysis showed 20-25 red blood cells and 10-12 WBCs per high-power field.
A 2 D echocardiography revealed no vegetations. An ultrasound scan revealed a mass in his left kidney measuring 7.2 × 4 cm. A computed tomography (CT) scan showed a hypodense area in the lower pole of his left kidney measuring 5.28 × 6.22 cm, consistent with a renal abscess, which was percutaneously aspirated and grew highly sensitive Staphylococcus aureus. Special staining for acid-fast bacilli was negative. Figure shows the CT images. His blood cultures were repeatedly negative. One of the urine cultures grew Escherichia coli and Enterococcus species. The E. coli was sensitive to amikacin, cefoperazone and/or sulbactam, gentamicin, imipenem, meropenem, natamycin, nitrofurantoin, and piperacillin and/or tazobactam. The Enterococcus species was sensitive to amoxicillin and clavulanic acid, gentamicin, imipenem, linezolid, meropenem and nitrofurantoin.
On the basis of the sensitivity of the S. aureus isolated from the abscess, he was treated with intravenous gentamicin, 80 mg at eight-hourly intervals, and with intravenous teicoplanin, 400 mg once per day.
He continued experiencing spikes of high-grade fever, and a repeat ultrasound after 12 days of appropriate therapy showed only minimal resolution of the lesion. Surgery was anticipated. A technetium-99 m renogram was performed to see the split function of the kidney with the abscess and to determine whether or not a partial nephrectomy could be performed. The renogram revealed a total glomerular filtration rate of 94 mL/min, with the left kidney contributing 36 mL/min and the right kidney 58 mL/min, and no evidence of obstruction. Figure shows the results of the technetium-99 m renogram.
In view of the persistence of the abscess, he underwent a surgical exploration of the renal bed. An attempt was made to carry out a partial nephrectomy of the affected region. However, this failed and so a left nephrectomy was performed. Figure shows the nephrectomy specimen. Figures and show the histopathological picture.
Post-operatively, his fever subsided and the antibiotic coverage was continued for one week with teicoplanin and gentamicin. At the time of his discharge, his serum creatinine level was 1.1 mg/dL.
A histopathological examination of the diseased kidney revealed infiltrates of lymphocytes, plasma cells and histiocytes. The replacement of renal parenchymal tissue by sheets of foamy histiocytes admixed with neutrophils was observed and this was consistent with xanthogranulomatous pyelonephritis. A special stain for acid-fast bacilli was negative. Clinical, radiological and histopathological examinations failed to provide any evidence of an obstructive lesion in his urinary tract or of renal calculi.
Two weeks after his discharge from hospital, he complained of fever. A CT scan of his abdomen was performed and a residual renal bed abscess was found. A pigtail catheter was inserted and daily aspiration and antibiotic instillation were performed. A week later he was discharged again, with oral antibiotics.
About seven months after the surgery, he remained in a perfect state of health without reports of further infection. This also signified the absence of inherent immune deficiency.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [22, 'years'], 'weight': [51.0, 'kg'], 'height': [174.0, 'cm'], 'creatinine': [0.6, 'mg/dL']}",139.30556,132.34028,146.27084,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 22 years old. 
The concentration of creatinine is 0.6 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 174.0 cm, which is 174.0 cm * 1 m / 100 cm = 1.74 m. The patient's weight is 51.0 kg. The patient's bmi is therefore 51.0 kg / (1.74 m * 1.74 m) = 16.84503 kg/m^2.The patient's BMI is 16.8, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 51.0 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation. 
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 22) * 51.0 * 1) / (0.6 * 72) = 139.30556 mL/min. Hence, the patient's creatinine clearance is 139.30556 mL/min."
70,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6751414-1,Extracted,"A 77-year-old man presented with a complaint of a lump on the upper abdominal wall for several weeks. His performance status (PS) was Grade 2 (Height, 168 cm; Weight, 58 kg; BMI, 20 kg/m2). He had a history of appendicitis that was operated upon. On physical examination, the tumor was located on the upper left side of the abdominal wall measuring around 5 cm with poor mobility and partial ulceration but without pain (Fig. ). At a nearby hospital, he had previously undergone physical examination and computed tomography (CT) for his symptoms. Advanced gastric cancer with invasion to the skin of the abdominal wall was suspected and, for more specific investigation and therapy, he was referred to our department. We obtained informed consent from all participants, and all procedures therapy were performed in accordance with the Declaration of Helsinki.
His blood investigation revealed the following: hemoglobin 8.7 g/dL, white blood cell count 6,060 /μL, platelets 321,000 /μL, prothrombin time-international nomarized ratio (PT-INR) 1.05, sodium 140 mmol/L, potassium 4.2 mmol/L, chlorine 105 mmol/L, creatinine 0.91 mg/dL, aspartate aminotransferase (AST) 13 U/L, alanine aminotransferase (ALT) 10 U/L, alkaline phosphatase 249 U/L, γ-guanosine triphosphate cyclohydrolase (γ-GTP) 14 U/L, LD 156 U/L, total bilirubin 0.8 mg/dL, C-reactive protein 0.41 mg/dL, carcinoembryonic antigen-S (CEA-S) 1.6 ng/mL, alpha-fetoprotein 1.83 ng/mL and carbohydorate antigen 19–9 (CA 19–9) <2 U/mL. There was moderate anemia but there was no organ failure and or elevation of tumor marker.
On Upper gastrointestinal endoscopy, a Type 3 tumor that measured around 40 mm was observed occupying from the angle of the stomach to the anterior wall of the antrum of the stomach (Fig. ).
On biopsy, the histological type was revealed as tubular adenocarcinoma (tub1) and immunostaining for HER2 was negative.
Thoracoabdominal enhanced CT revealed invasion of the tumor from the anterior wall of the stomach to the lateral region of the liver and infiltration from the abdominal wall to the skin. There was no evidence of metastasis or ascites (Fig. ).
On the basis of these findings, we diagnosed advanced gastric cancer (L-Less, Gre, type 3, 40 mm, tub1), cT4b (SI; liver, skin) N0M0 c Stage IIIA. Initially we anticipated chemotherapy considering that the patient's PS was Grade 2 and the defect of abdominal wall was too large for surgery. In addition, the patient did not want to undergo surgery. S-1+Cisplatin (SP) therapy was performed as first-line therapy every 3 weeks [].
Obvious shrinkage of the tumor invasion to the skin was observed, and we determined that PR was obtained at the end-point of 4th course of SP therapy. However, because of malaise (Grade 2), we had to set a 1-month interval. During the interval, the invasion to the skin gradually increased again; hence, another two courses of SP regimen were added with decreased dose. After six courses of SP therapy had been completed, PR was obtained again by the re-shrinkage of the skin tumor on physical examination and upper gastrointestinal endoscopy and CT (Fig. , ). At this point, the patient was not amenable to surgery or chemotherapy; hence, we adopted a “wait-and-see” approach. During this period, the skin tumor underwent re-growth gradually for which RAM/PTX therapy (3-week administration at 1-week intervals) was introduced as the second line chemotherapy, 2 months after the previous one []. Over the course of therapy, anemia (Grade 3) and neutropenia (Grade 2) were observed and we were compelled to skip one administration each of PTX in course 2 and 3but RAM dosage was completely administrated through all five courses (Fig. ). Throughout the second line of therapy, the skin tumor kept decreasing visually and enhanced abdominal CT revealed the shrinkage of the primary tumor and the invasion to the lateral area of the liver and skin. Similar findings were observed on gastrointestinal endoscopy; and hence, we determined that PR was obtained again (Fig. ). Since his general condition was observed have improved, we planned to perform surgery with the aim of reaching a chemotherapy-free status.
We performed open total gastrectomy with D2 lymph nodes dissection (Roux-en-Y reconstruction) with combined partial resection of the skin, abdominal wall, and liver. There were no findings of the peritoneal dissemination, metastasis to the liver, or ascites (Fig. ). The components separation method was performed for abdominal wall closure with the defect of the skin by exposure of the anterior sheath of abdominal rectal muscles and resection of partial aponeurosis of the right external abdominal oblique muscle.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [77, 'years'], 'weight': [58.0, 'kg'], 'height': [168.0, 'cm'], 'creatinine': [0.91, 'mg/dL']}",55.76923,52.98077,58.55769,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 77 years old. 
The concentration of creatinine is 0.91 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 58.0 kg. The patient's bmi is therefore 58.0 kg / (1.68 m * 1.68 m) = 20.54989 kg/m^2.The patient's BMI is 20.5, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 58.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 77) * 58.0 * 1) / (0.91 * 72) = 55.76923 mL/min. Hence, the patient's creatinine clearance is 55.76923 mL/min."
71,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,usmle-819,Extracted,"A 48-year-old woman comes to the emergency department because of increasingly severe right upper abdominal pain, fever, and nonbloody vomiting for 5 hours. The pain is dull and intermittent and radiates to her right shoulder. During the past 3 months, she had recurring abdominal discomfort after meals. She underwent an appendectomy at the age of 13 years. The patient has hypertension, type 2 diabetes mellitus, and chronic back pain. She takes bisoprolol, metformin, and ibuprofen daily. She is 171 cm (5 ft 6 in) tall and weighs 99 kg (218 lb); BMI is 35 kg/m2. She appears uncomfortable and is clutching her abdomen. Her temperature is 38.5°C (101.3°F), pulse is 108/min, and blood pressure is 150/82 mm Hg. Abdominal examination shows right upper quadrant abdominal tenderness and guarding. Upon deep palpation of the right upper quadrant, the patient pauses during inspiration. Laboratory studies show:
Hemoglobin 13.1 g/dL
Leukocyte count 10,900/mm3
Platelet count 236,000/mm3
Mean corpuscular volume 89/μm3
Serum
Urea nitrogen 28 mg/dL
Glucose 89 mg/dL
Creatinine 0.7 mg/dL
Bilirubin
Total 1.6 mg/dL
Direct 1.1 mg/dL
Alkaline phosphatase 79 U/L
Alanine aminotransferase (ALT, GPT) 28 U/L
Aspartate aminotransferase (AST, GOT) 32 U/L
An x-ray of the abdomen shows no abnormalities.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [48, 'years'], 'weight': [99.0, 'kg'], 'height': [171.0, 'cm'], 'creatinine': [0.7, 'mg/dL']}",119.48085,113.50681,125.45489,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 48 years old. 
The concentration of creatinine is 0.7 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 171.0 cm, which is 171.0 cm * 1 m / 100 cm = 1.71 m. The patient's weight is 99.0 kg. The patient's bmi is therefore 99.0 kg / (1.71 m * 1.71 m) = 33.85657 kg/m^2.The patient's BMI is 33.9, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 171.0 cm, which is 171.0 cm * 0.393701 in/cm = 67.32287 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (67.32287 (in inches) - 60) = 62.3426 kg.
Hence, the patient's IBW is 62.3426 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 62.3426 kg + 0.4 * (99.0 kg  - 62.3426 kg) = 77.00556 kg. The patient's adjusted body weight is 77.00556 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 48) * 77.00556 * 0.85) / (0.7 * 72) = 119.48085 mL/min. Hence, the patient's creatinine clearance is 119.48085 mL/min."
72,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6381477-1,Extracted,"A 43-year-old man (55 kg, 165 cm) was admitted to our hospital to undergo aortic valve replacement for treatment of infective endocarditis and aortic regurgitation. His initial laboratory data were as follows: hemoglobin level, 8.2 g/dL; hematocrit, 25.8%; platelet count, 180,000/μL, blood urea nitrogen level, 35.0 mg/dL; creatinine level, 5.18 mg/dL; troponin I level, 1.42 ng/mL; prothrombin time/international normalized ratio, 1.45; activated prothrombin time, 44.9 seconds; and C-reactive protein level, 8.6 mg/dL.
The patient’s vital signs in the operating room were stable. Local anesthesia was administered using 2% lidocaine, and a 20-G arterial catheter was inserted into the right radial artery. General anesthesia was then induced. We used etomidate at 0.2 mg/kg for sedation, sufentanil at 0.02 μg/kg/min for analgesia, and rocuronium at 0.6 mg/kg for neuromuscular blockade. The patient had no history of cervical surgery and had not recently undergone insertion of a catheter into the IJV.
After intubation, the patient was positioned to facilitate insertion of the AVA catheter () into the right IJV. In an effort to expand the right IJV, the head was lowered approximately 5 degrees and the face was pointed toward the left. The skin was aseptically prepared, the IJV was punctured with a needle tip under static ultrasound guidance with marking of anatomical landmarks, blood was aspirated, and a guidewire was inserted. The guidewire was inserted until it reached approximately 25 cm from the end of the syringe and was advanced no further to avoid arrhythmia. The presence of the guidewire within the IJV was confirmed by ultrasonography (). After a slight incision was made using a scalpel, the AVA catheter combined with a vessel dilator was advanced along the guidewire. No resistance was felt during entry of the dilator along the guidewire into the IJV. When the dilator was considered to have passed the IJV, the sheath was pushed forward; however, the dilator and guidewire were unable to be pulled backward. We assumed that the guidewire tip had become stuck to the vessel wall; therefore, we gently moved the dilator and guidewire back and forth in an attempt to loosen them. Despite these efforts, the dilator and guidewire were not removed simultaneously; instead, the guidewire was removed first, followed by the dilator. Upon pulling the guidewire out, we found that its end was bent and curved ().
We considered that the catheter was in the appropriate position despite the fact that the guidewire tip was twisted upon removal. We attempted to irrigate the vessel lumen with saline to remove air and prevent blood clot formation, but the blood was not regurgitated. We assumed that the sheath was malpositioned and thus repeated the ultrasound examination, which revealed that the AVA catheter sheath was folded inside the right IJV ().
We gently withdrew the AVA catheter to avoid additional injury. The AVA catheter was pulled out with no resistance, and the IJV was manually compressed for 5 minutes. We observed traces of small pleats in the end of the AVA catheter sheath, and we considered that they had been caused by folding and stretching of the end of the sheath upon removal. After removing the AVA catheter, we attempted to gain access to the left IJV. Left IJV catheterization using a new AVA catheter and subsequent performance of the operation were uneventful. At 6 and 12 hours postoperatively, we observed no tenderness, swelling, or color change at the right IJV catheterization site, and no further examination was performed thereafter.
Ethical permission was obtained from the Chonnam National University Hospital Institutional Review Board (CNUH-EXP-2017-283). Written informed consent was obtained from the patient.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [43, 'years'], 'weight': [55.0, 'kg'], 'height': [165.0, 'cm'], 'creatinine': [5.18, 'mg/dL']}",14.30448,13.58926,15.0197,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 43 years old. 
The concentration of creatinine is 5.18 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.65 m * 1.65 m) = 20.20202 kg/m^2.The patient's BMI is 20.2, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 55.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 43) * 55.0 * 1) / (5.18 * 72) = 14.30448 mL/min. Hence, the patient's creatinine clearance is 14.30448 mL/min."
73,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4400448-1,Extracted,"A 17-year-old girl presented herself in our emergency department in the morning after suicidal ingestion of 250–300, 325 mg acetylsalicylic acid (Aspirin®). She announced that she had ingested the tablets on the previous evening. She developed vomiting and tinnitus prior to admission. She was 167 cm tall and weighed 52 kg. Her blood pressure was 132/74 mmHg, heart rate 110/min and the respiratory rate 26/min. She was alert, her pupillary response slightly delayed, she had mild epigastric tenderness and the bowel sounds were diminished. Her blood values were as following: pH 7.51, pO2 121 mmHg (16.1 kPa), pCO2 18 mmHg (2.38 kPa), HCO3
− 14 mmol/L, lactate 0.8 mmol/L, sodium 142 mmol/L, potassium 3.2 mmol/L, chloride 123 mmol/L, ionized calcium 0.98 mmol/L, creatinine 72 μmol/L (0.81 mg/dL). The serum salicylate concentration was 6.4 mmol/L (88 mg/dL).
We administered 100 mL sodium bicarbonate 8.4%, 40 mmol potassium, 2 mg tropisetron and 80 mg esomeprazole intravenously. Furthermore, a central venous catheter was introduced into the internal jugular vein and haemodialysis was begun. Haemodialysis was continued until the salicylate levels decreased sufficiently. The clinical course was uneventful and we transferred her to our psychiatric department.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [17, 'years'], 'weight': [52.0, 'kg'], 'height': [167.0, 'cm'], 'creatinine': [0.81, 'mg/dL']}",93.22016,88.55915,97.88117,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 17 years old. 
The concentration of creatinine is 0.81 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 167.0 cm, which is 167.0 cm * 1 m / 100 cm = 1.67 m. The patient's weight is 52.0 kg. The patient's bmi is therefore 52.0 kg / (1.67 m * 1.67 m) = 18.64534 kg/m^2.The patient's BMI is 18.6, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 52.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 17) * 52.0 * 0.85) / (0.81 * 72) = 93.22016 mL/min. Hence, the patient's creatinine clearance is 93.22016 mL/min."
74,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-2811977-1,Extracted,"The patient was a 40-year-old unmarried male who was symptomatic since last 7 years for progressive ataxia. He also complained of clumsiness in fine activities including writing. There was a history of slurring of speech for the past 2 years. In addition, he had also noted a paucity of facial, axillary and pubic hair and impotence including absence of early morning erections. Many indigenous medications were consumed for the same. Past history was significant for bouts of diarrhea since his early twenties.
Clinical examination revealed a well nourished, moderately built adult with a BMI of 21 kg/sq.m. His arm span was 182 cm with a height of 170 cm. Hypoandrogenism was seen with reduced facial, axillary and pubic hair []. Gynecomastia was present. General physical examination was normal. Higher mental functions were normal with an MMSE of 30/30. Speech revealed scanning dysarthria. Cranial nerve examination revealed bilateral gaze evoked nystagmus with fast phase in direction of gaze. Saccades and pursuit were normal. Fundus examination was unremarkable. No pyramidal or sensory findings were noted. Romberg's test was negative. Ankle reflexes were bilaterally hypoactive. Bilaterally symmetric dysmetria, dyssynergia, incoordination, and truncal ataxia were noted. Stance was broad based with gait ataxia. In summary, this man had a progressive pan-cerebellar syndrome with evidence of hypogonadism. In view of the history of recurrent diarrhea, a possibility of gluten ataxia was considered.
Hb = 11.3 gm% with a normocytic normochromic picture. Total leukocyte counts = 8,700/ cu.mm; platelets adequate. Fasting blood sugar level = 84 mg/dl; 2 hour post lunch sugar = 106 mg/dl. Blood urea nitrogen = 13 mg/dl; serum creatinine = 0.6 mg/dl; sodium = 142 mEq/L; potassium = 4.1 mEq/L Serum calcium = 8.9 mg/dl; phosphorus = 4.2 mg/dl. Total proteins = 7.5 g/dl; serum albumin level = 3.9 g/dl. AST levels = 22 IU; ALT levels= 23 IU; Alkaline phosphatase = 110 IU. Total cholesterol = 119 mg%; serum triglyceride= 206 mg%. HIV ELISA and other viral markers were negative. Stool routine and microscopy revealed minimal fat globules; no occult blood or parasites. Serum vitamin B12 levels = 795.7pg/ml; vitamin E levels = 7.60 mg/L (6–19 mg/L). Serum FSH levels = 1.11 mIU/ml (1.4–18.1 mIU/ml); LH levels = 0.30 mIU/ml (1.5–9.3 mIU/ml). Serum testosterone levels = 0.33 ng/ml (2.7–10.7 ng/ml) T3=125 ng/dl; T4= 9.5 μg/dl; TSH=4.46 μU/ml. Testicular volume – Right = 9 cc and Left = 10.5 cc (normal = 13–19 cc). Nerve conduction studies revealed bilaterally attenuated H reflexes with normal Sensory Nerve Action Potentials (SNAPs) and Compound motor action potentials (CMAPs). Magnetic Resonance Imaging (MRI) of the brain revealed gross cerebellar atrophy []. On gastroscopy there was mild gastric atrophy with mild duodenitis in the D1 segment. Histopathology of biopsy specimens from both areas revealed features which were consistent with celiac sprue (short flattened villi, intra-epithelial lymphocytic infiltrates, increased villous-crypt ratio) [].
Serum IgA Anti-Gliadin Antibodies (AGA) = 31.2 U/ml (n = ≤11 U/ml) Serum IgG Anti-gliadin Antibodies= 17.4 U/ml (n = 11–17 U/ml). Serum IgA Anti-tissue Transglutaminase (TTG) = 168.90 U/ml (0–20 U/ml) Serum IgA Anti-endomysial Antibodies (EMA) = 243.40 U/ml (0–20 U/ml)
On the basis of the above findings, patient was diagnosed to have gluten ataxia and enteropathy with additional hypogonadotropic hypogonadism. He has been initiated on a gluten-free diet and is under evaluation for hormonal replacement therapy.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [70.0, 'kg'], 'height': [170.0, 'cm'], 'creatinine': [0.6, 'mg/dL'], 'age': [40, 'years']}",152.63215,145.00054,160.26376,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 40 years old. 
The concentration of creatinine is 0.6 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.7 m * 1.7 m) = 24.22145 kg/m^2.The patient's BMI is 24.2, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 65.93709 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 40) * 65.93709 * 1) / (0.6 * 72) = 152.63215 mL/min. Hence, the patient's creatinine clearance is 152.63215 mL/min."
75,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6264997-1,Extracted,"A 53-year-old woman was admitted to the local hospital after 1 d of convulsions leading to loss of consciousness. After the attack (approximately 20 min), the patient eventually became conscious. Six months prior, she reported having paroxysmal palpitation attacks (5-20 min each), which spontaneously subsided, and had suffered occasional headaches, without sweating or chest pain. Consequently, medical attention was never sought.
Computed tomography (CT) of the head showed no abnormalities; but this historically normotensive patient produced a blood pressure (BP) reading of 230/100 mmHg. Nicardipine hydrochloride (3 μg/kg per min; Astellas Pharma Tech Co, Ltd, Tokyo, Japan) was administered for BP control, which was achieved approximately 8 h later (160/90 mmHg), and the convulsions disappeared. However, treatment was withdrawn without rebound effect following a sudden drop in BP (nadir: 53/35 mmHg). She was then transferred to our facility.
At the time of admission, the patient was somnolent but could be aroused and appeared dispirited, evoking a Glasgow coma score of 9 (E, 2; M, 4; V, 3). She presented with watery diarrhea > 10 times/d (total volume, 800-1200 mL/24 h). At a height of 162 cm and a body weight of 82 kg, her baseline vital signs were as follows: BP, 68/44 mmHg; heart rate, 92 bpm; respiratory rate, 18 bpm; and temperature, 36.8 °C. There was flushing of the face and neck (Figure ) and sensitivity to percussion in the region of the left kidney. Thyromegaly, rales (neither lung by auscultation), cardiac murmurs, abdominal tenderness, and palpable lumps were not observed.
Laboratory tests showed that hematocrit and hemoglobin were within standard reference ranges and did not deviate significantly in several repeat attempts. Other results were as follows: glucose, 17.2 mmol/L (3.9-6.1); creatinine, 289.9 μmol/L (45-84); troponin I (TnI), 0.14 ng/mL (0.010-0.023); creatine kinase (CK), 230 ng/L (45-145); and CK-MB, 15 ng/L (2.0-7.2). A battery of biochemical tests, including liver function studies, blood gas analysis, blood coagulation indices, and electrolyte (K, Na, Cl, Ca, P, and Mg) levels, returned essentially normal results. The electrocardiogram showed T-wave inversion and slight ST-segment depression (0.1-0.2 mv) in leads V1-V6, II, III, and AVF. Coronary arteriography confirmed no coronary artery obstruction. By ultrasonic cardiography (UCG), the following parameters were determined: interventricular septal thickness, 10-12 mm; width of posterior left ventricular wall, 10 mm; left ventricular end-diastolic (156 mL) and end-systolic (69 mL) volumes; stroke volume, 87 mL; and ejection fraction, 56%. CT studies of the patient’s head and chest were not abnormal, but on the enhanced abdominal CT, a solitary mass of the left adrenal gland was identified, with signs of bleeding (Figure ). In addition, blood and urinary CAT concentrations and urinary vanillylmandelic acid were significantly elevated (Table ).
Treatment included copious intravenous fluid replacement (0.9% NaCl, 4000 mL/24 h), with potassium supplementation (KCl, 3-6 g/24 h), and an intravenous dopamine drip (12 μg/kg per min; Shanghai Fenge Pharmaceutical Co, Ltd, Shanghai, China) was initiated. The patient’s BP increased slightly in response, with systolic pressures still fluctuating from 80-100 mmHg. There was no mental improvement or resolution of facial and neck flushing, and despite complete solid/liquid fasting, the diarrhea persisted. Besides, we administered the patient with continuous intravenous insulin to keep the blood glucose around 10 mmol/L. We rechecked CK, CK-MB, TnI, and electrocardiogram every 6 h. The patient’s myocardial enzymes and TnI levels gradually returned to normal, and the ischemic manifestations on electrocardiogram were also significantly improved. This symptomology was not typical of pheochromocytoma. Given the array of hormones implicated in neuroendocrine tumors, significant elevation of plasma VIP (Table ) was subsequently verified through additional diagnostics, whereas other substances [plasma pancreatic polypeptide, adrenocorticotropic hormone, somatostatin (SST), thyroid hormones, parathyroid hormone, calcitonin, adrenomedullin, and urine 5-hydroxy indoleacetic acid] remained normal.
To control diarrhea and facial flushing, the patient received intramuscular injections of octreotide (0.1 mg/8 h; Novartis International AG, Basel, Switzerland) on day 3 after admission, followed by a surprisingly rapid rise in BP. After 24 h, the dopamine drip was discontinued, and her BP had reached 123/75 mmHg. The patient’s mental state also cleared significantly, and she was more alert; the facial and neck flushing was relieved; and diarrhea was less frequent. On day 5 after admission, she was completely conscious, her facial and neck skin had returned to normal, and the diarrhea had stopped. At this point, she developed paroxysmal hypertension (peak BP: 190/100 mmHg), for which oral terazosin hydrochloride (2 mg/d; Abbott Laboratories, Chicago, IL, United States) was given.
After 20 d, left laparoscopic adrenalectomy was performed. The mass of the left upper kidney and an encapsulated, posteriorly placed hematoma (due to rupture) were located. When dissecting this mass, the patient’s BP again climbed to 240/130 mmHg. No other abdominal tumors were discovered, and the right adrenal gland was morphologically normal. The resected mass measured 7 cm × 4.5 cm. On cut section, it was soft and yellow-brown, demonstrating two subcapsular clefts of 2-4 cm (Figure ). In histological sections, the tumor cells were nested or arranged in trabecular pattern, with variably sized, pleomorphic nuclei. Their cytoplasm was abundant, showing basophilic or amphophilic stippling. A compressed rim of normal adrenal cortex was retained at the tumor’s edge, and there was no obvious intervening septum (Figure ).
Immunohistochemical staining properties were as follows: Syn (+), CgA (+), S-100 (+), CK (-), and KI67 (< 5% +) (Figure -G). On this basis, the histopathological diagnosis was adrenal pheochromocytoma. We then pursued immunohistochemical staining for VIP and SST receptor 2 (SSTR2), confirming 60%-70% cytoplasmic VIP positivity of pheochromocytoma cells. No positively stained ganglioneuroma component was evident (Figure ). Nearly all tumor cell membranes demonstrated SSTR2 positivity (Figure ).
After surgery, the patient discontinued octreotide and terazosin hydrochloride and recovered uneventfully from surgery. Her BP and heart rate returned to normal levels, as did various hormonal concentrations; and symptoms such as headache, palpitation, chest pain, facial flushing, and diarrhea were no longer problematic. During a 6-mo follow-up period, she seemed in good health and was symptom-free.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [53, 'years'], 'weight': [82.0, 'kg'], 'height': [162.0, 'cm'], 'creatinine': [289.9, 'µmol/L']}",20.45267,19.43004,21.4753,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 53 years old. 
The concentration of creatinine is 289.9 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 289.9 µmol. To convert 289.9 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 289.9 µmol creatinine * 1e-06 mol/µmol = 0.00029 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00029 mol creatinine * 113.12 g/mol = 0.0328 g creatinine. To convert 0.0328 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.0328 g creatinine * 1000.0 mg/g = 32.8 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 32.8 mg creatinine/10.0 dL = 3.28 mg creatinine/dL. The concentration value of 289.9 µmol creatinine/L converts to 3.28 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.0 cm, which is 162.0 cm * 1 m / 100 cm = 1.62 m. The patient's weight is 82.0 kg. The patient's bmi is therefore 82.0 kg / (1.62 m * 1.62 m) = 31.24524 kg/m^2.The patient's BMI is 31.2, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.77956 (in inches) - 60) = 54.19299 kg.
Hence, the patient's IBW is 54.19299 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 54.19299 kg + 0.4 * (82.0 kg  - 54.19299 kg) = 65.31579 kg. The patient's adjusted body weight is 65.31579 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 53) * 65.31579 * 0.85) / (3.28 * 72) = 20.45267 mL/min. Hence, the patient's creatinine clearance is 20.45267 mL/min."
76,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6787412-1,Extracted,"A 75-year-old man was admitted to our hospital for further evaluation of subacute renal failure. He had no past history associated with bronchial asthma or drug administration and no other medical problems, history of smoking, habitual drinking, or family history of renal disease. Upon admission, his body weight was 51.0 kg, height was 171.0 cm (body mass index 17.4), temperature was 36.8°C, and blood pressure was 125/74 mm Hg. The lymph nodes were not palpable, and there were no signs of leg edema. The peripheral white blood cell count was 4,600/mm3, with 3,450 neutrophils/mm3 and 92 eosinophils/mm3; the hematocrit was 27.1′; the red blood cell count was 2,710,000/mm3, hemoglobin was 8.9 g/dL, and the platelet count was 156,000/mm3. Laboratory serological findings were as follows: total protein 7.5 g/dL, albumin 4.4 g/dL, creatinine 3.3 mg/dL, urea nitrogen 46.9 mg/dL, and C-reactive protein 0.6 mg/dL. The serum IgG and IgG4 levels were 1,614.0 and 235.0 mg/dL, respectively. Serum protein electrophoresis showed no signs of gammopathy. Slight hypocomplementemia in C4 (C3 83 mg/dL, C4 21.7 mg/dL, CH50 49 U/mL) was also observed. Antinuclear and antineutrophil cytoplasmic antibodies, antiglomerular basement membrane antibody, SS-A and SS-B antibodies, as well as cryoglobulin were all negative. Serum angiotensin-converting enzyme, soluble interleukin-2 receptor, and tumor marker levels were within normal limits. Urinalysis showed proteinuria of 0.9 g/day without hematuria and increasing levels of NAG (22.8 IU/L) and α1-MG (85 mg/L). Whole-body CT and magnetic resonance imaging showed no pleural effusion, ascites, lymph node swelling, or enlargement of organs, except for diffuse enlargement of the kidneys (Fig. ). The longest diameter of the kidneys was > 12 cm. A whole-body gallium scan showed no abnormal accumulation.
Percutaneous renal needle biopsy showed diffuse infiltration of abundant lymphocytes and IgG4-positive plasma cells and storiform fibrosis, which is specific to IgG4-RKD, in the interstitium on light microscopy. There were no signs of injury of the glomeruli or basement membrane. No crescent forms were observed in glomeruli. Slight linear deposition of C3 was observed in the tubules on immunofluorescence microscopy, and no electron-dense deposits were observed (Fig. ). Immunohistochemically, IgG4-positive plasma cells were markedly observed in the interstitium (> 10 IgG4-positive plasma cells/high-power field), and the ratio of IgG4-positive plasma cells to IgG-positive plasma cells was > 90′ (Fig. ).
The diagnosis of IgG4-RKD was reached based upon the above-described findings, and the patient was started on prednisolone at a dose of 0.6 mg/kg/day (30 mg/day). Serum IgG4 and creatinine levels and urinary α1-MG level improved temporarily; however, renal insufficiency continued to advance as the prednisolone was tapered. It became necessary to decrease the dose of the steroid after the onset of severe steroid psychosis. He lost his appetite and became malnourished, and we abandoned the additional therapy because of the risk of infection. The renal function did not improve and maintenance dialysis was initiated. Serum creatinine as well as urinary NAG and α1-MG levels became exacerbated as the prednisolone was tapered. However, the serum IgG4 level continued to decline. Moreover, the diffuse enlargement of kidneys, which was detected by CT, did not improve from the initiation of steroid therapy to the initiation of hemodialysis.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [75, 'years'], 'weight': [51.0, 'kg'], 'height': [171.0, 'cm'], 'creatinine': [3.3, 'mg/dL']}",13.95202,13.25442,14.64962,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 75 years old. 
The concentration of creatinine is 3.3 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 171.0 cm, which is 171.0 cm * 1 m / 100 cm = 1.71 m. The patient's weight is 51.0 kg. The patient's bmi is therefore 51.0 kg / (1.71 m * 1.71 m) = 17.44126 kg/m^2.The patient's BMI is 17.4, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 51.0 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation. 
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 75) * 51.0 * 1) / (3.3 * 72) = 13.95202 mL/min. Hence, the patient's creatinine clearance is 13.95202 mL/min."
77,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4376932-1,Extracted,"Our patient was a 54-year-old male who presented with anuria, fever, and lower-leg edema. On June 3, 2012, the patient visited the urology department of a local community hospital with macroscopic hematuria and dysuria. He was diagnosed with acute prostatitis and began treatment with levofloxacin hydrate, loxoprofen sodium hydrate, and cernitin pollen extract. However, his condition did not improve, and he subsequently developed lower extremity numbness, bilateral flank pain, and diarrhea, followed by anuria. On June 11, he visited another hospital in his community and was eventually transferred to our hospital on June 13 for inpatient treatment of possible acute kidney injury.
Physical examination on admission revealed the following: height 175 cm; body weight 80 kg; systolic and diastolic blood pressure values 179 and 102 mm Hg, respectively; pulse 98 beats/min (regular), and body temperature 37.9°C. The patient had a normal mental status despite persistent headache. His palpebral conjunctivae indicated signs of anemia. Radiographic images showed no abnormal findings. Both lower limbs were edematous. The results of clinical laboratory tests obtained on admission are summarized in table . Urinalysis showed high protein levels (3 g/l), blood (+++), pyuria, and a fractional sodium excretion rate of 20.3%. Hematological analyses of peripheral blood yielded a white blood cell count of 9.61 × 109 cells/l (neutrophils 85.0%, lymphocytes 8.5%), a red blood cell count of 3.44 × 1012 cells/l, a hemoglobin level of 100 g/l, the presence of fragmented red blood cells, and a platelet count of 90 × 109 cells/l. C-reactive protein levels were as high as 160,900 μg/l. The fibrinogen degradation product level was 1.168 g/l, the prothrombin time was 45.6 s, and the fibrinogen level was 4.1 g/l. These measurements resulted in a disseminated intravascular coagulation score of 6 points. Serum biochemistry tests yielded a blood urea nitrogen level of 58.1 mmol/l and a creatinine level of 2,044 μmol/l, suggesting significant renal impairment. The lactate dehydrogenase level was 765 IU/l, and the haptoglobin level was below 1.2 μmol/l. The patient had hypoproteinemia, as evidenced by a total serum protein level of 58 g/l and an albumin level of 24 g/l. Serum samples were negative for anti-nuclear antibodies as well as myeloperoxidase- and proteinase 3-specific antineutrophil cytoplasmic autoantibodies, although anti-GBM antibody levels were high at 230 ELISA units. Stool examination was negative for occult blood, intestinal pathogens, and verotoxins. Plain chest radiographs revealed no alveolar hemorrhage or other abnormal signs. On interview, the patient reported a history of cervical disc herniation diagnosed at the age of 52 years. He had no noteworthy family history and was not taking any medications on a regular basis at the time of admission to our hospital.
Changes in platelet counts, lactate dehydrogenase levels, and mean blood pressure over time during the 119-day hospital stay are schematically represented in figure , along with major therapeutic interventions. Computed tomography (CT) imaging conducted on admission indicated renal atrophy and ascites, but no collapse of the inferior vena cava. These findings negated the possibility of prerenal and postrenal failure and suggested an acute aggravation of chronic kidney disease rather than a typical acute kidney injury. Since the patient had not undergone regular medical checkups, it was not clear whether proteinuria had existed in the past. During the early hospitalization period, we administered γ-globulin, diuretics, and hemodialysis, under the assumption that the patient had either sepsis- or drug-induced acute kidney injury. Peripheral blood smears revealed the presence of fragmented red blood cells (hospital day 2), suggesting hemolytic uremic syndrome (HUS) resulting from food poisoning caused by Escherichia coli O-157:H7 or other pathogenic strains. However, the patient had no diarrhea and was negative for intestinal pathogens and verotoxins. Epistaxis developed on hospital day 4, platelet counts and hemoglobin levels decreased to 29 × 109 cells/l and 55 g/l, respectively, and the lactate dehydrogenase level rose to 1,253 IU/l. The patient's anemia was unresponsive to erythropoiesis-stimulating therapy, and frequent blood transfusions were required (i.e., a total of 16 units of irradiated red cell concentrates). His fever remained in the range of 38-39°C despite treatment with γ-globulin. The patient was diagnosed with TMA [thrombotic thrombocytopenic purpura (TTP) or HUS] based on the following findings: thrombocytopenia, hemolytic anemia evidenced by anemic signs and elevated lactate dehydrogenase levels, signs of renal impairment, fever, bleeding episodes (i.e., epistaxis), neuropsychiatric manifestations (i.e., headache), direct and indirect Coombs test results, and haptoglobin levels below 1.2 μmol/l.
Assays conducted several days later indicated an ADAMTS13 activity of 31.6% (reference range 70-120%), and ADAMTS13 inhibitors were negative. Serum factor H measured by the ELISA method was 0.473 g/l (the standard value of factor H ranges from 0.3 to 0.6 g/l). These findings led us to administer plasma exchange therapy with a total of 30 units of fresh frozen plasma, starting on hospital day 8. On hospital day 15, steroid pulse therapy (3 methylprednisolone doses of 1,000 mg/day) was initiated to lower the elevated anti-GBM antibody level. Following the completion of this 3-day course, the patient was given oral prednisolone at a starting dose of 50 mg/day, which was gradually tapered and discontinued. After this, platelet counts rose to 197 × 109 cells/l, and kidney biopsy was conducted on hospital day 22 (fig. ). Seventeen glomeruli examined by optic microscopy all showed destructive patterns with characteristic architecture ranging from atypical proliferative changes to global sclerosis. Renal arterioles, both afferent and efferent, showed extensive endothelial cell edema and swelling, indicative of glomeruloid changes. Renal tubules showed focal atrophy with massive lymphocyte infiltration. Congo red staining of the biopsy specimen was negative. Electron microscopy showed that the loss of glomerular structure observed under optic microscopy was the result of an extensive and dense extracellular deposition of fibrillar components, which were larger in diameter than amyloid fibers and aggregated to form large bundles. Immunofluorescence analysis for immunoglobulin G and third component (C3) deposits was not carried out because of glomerular collapse. Available findings supported the diagnosis of FGN involving severe glomerular destruction. On hospital day 29, a second course of steroid pulse therapy was started due to significantly decreased platelet counts.
On hospital day 46, the mean blood pressure values started to increase gradually. Although the target body weight was lowered and arotinolol hydrochloride and methyldopa hydrate were added to nifedipine and candesartan cilexetil, these measures did not achieve successful blood pressure control.
On hospital day 56, the patient had a mild seizure. T2-weighted fluid-attenuated inversion recovery (FLAIR) magnetic resonance scans of the bilateral cerebellum, occipital lobe, and parietal lobe showed multiple high-intensity areas, suggesting a diagnosis of reversible posterior leukoencephalopathy syndrome (fig. ). Despite antihypertensive therapy with imidapril hydrochloride, carvedilol, nifedipine, and nitroglycerin infusion, hypertension persisted, and the patient's headache continued. On hospital day 61, generalized convulsions recurred, and head CT images showed multiple hemorrhagic lesions in the right temporal, right parietal, and right frontal lobes (fig. ). Doses of intravenous hemostatic medications were increased, while antihypertensive agents were administered nasogastrically. Blood pressure levels gradually decreased with the increase in platelet counts, starting around hospital day 65. On hospital day 72, the patient started rehabilitation exercises. The patient recovered enough to walk with a cane (fig. ). He was transferred to a rehabilitation hospital on hospital day 119.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [54, 'years'], 'weight': [80.0, 'kg'], 'height': [175.0, 'cm'], 'creatinine': [2044.0, 'µmol/L']}",3.84477,3.65253,4.03701,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 54 years old. 
The concentration of creatinine is 2044.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 2044.0 µmol. To convert 2044.0 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 2044.0 µmol creatinine * 1e-06 mol/µmol = 0.00204 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00204 mol creatinine * 113.12 g/mol = 0.23076 g creatinine. To convert 0.23076 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.23076 g creatinine * 1000.0 mg/g = 230.76 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 230.76 mg creatinine/10.0 dL = 23.076 mg creatinine/dL. The concentration value of 2044.0 µmol creatinine/L converts to 23.076 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 175.0 cm, which is 175.0 cm * 1 m / 100 cm = 1.75 m. The patient's weight is 80.0 kg. The patient's bmi is therefore 80.0 kg / (1.75 m * 1.75 m) = 26.12245 kg/m^2.The patient's BMI is 26.1, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 70.46466 kg + 0.4 * (80.0 kg  - 70.46466 kg) = 74.2788 kg. The patient's adjusted body weight is 74.2788 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 54) * 74.2788 * 1) / (23.076 * 72) = 3.84477 mL/min. Hence, the patient's creatinine clearance is 3.84477 mL/min."
78,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-2827053-1,Extracted,"A 36-year-old, previously healthy Hispanic female with no significant past medical history and no prior history of hypertension presented to the emergency room with sharp retrosternal chest pain radiating to the back. She was 165 centimeter tall and weighed 70 kilogram. She was a housewife and mother of two living children. She smoked one pack of cigarettes a day for more than ten years. For 3 months prior to presentation, she had been taking 18-20 tablets of caffeine-based weight loss pills daily, which was higher than the recommended daily dose. Each tablet contains 60-100 mg of caffeine and she was taking 1080 mg to 2000 mg of caffeine daily. She denied the use of other medications, stimulants, herbal, alcohol and illicit drugs. She said that she had lost approximately 20-25 kilograms in last 3 months. No family history of hypertension, diabetes or coronary artery disease. She denied palpitation, chest pain, insomnia, headache, abdominal pain or increase in urination.
On presentation, her blood pressure was found to be 220/110 mm Hg in right arm and 230/118 mm Hg in left arm. Her initial work-up included an electrocardiogram which showed T-wave inversion in leads III, aVF and V6. A complete blood count showed hemoglobin 12.9 g/dl (normal: 12.0-16.0 g/dl), white blood cell count 15.1 k/ul (normal: 4.0-11.0 k/ul) and platelet count 231 k/ul (normal: 150-450 k/ul). Serum basic metabolic panel showed sodium 132 mmol/L (normal: 135-145 mmol/L), potassium 3.3 mmol/L (normal: 3.5-5.3 mmol/L), chloride 103 mmol/L (normal: 95/105 mmol/L), bicarbonate 23 mmol/L (normal: 22-31 mmol/L), creatinine 1.3 mg/dl (normal: 0.6-1.3 mg/dl), calcium 8.3 mg/dl (normal: 8.6-10.3 mg/dl), and anion gap 6 mmol/L (normal: 7-17 mmol/L). Liver function test showed normal aspartate transaminase (15 U/L; normal: 0-55 U/L), alanine transaminase (23 U/L; normal: <45 U/L), alkaline phosphatase (55 U/L; normal: 34-104 U/L) and albumin (3.5 g/dl,normal:3.0-5.1 g/dl). Urinalysis showed only elevated specific gravity of 1.031(normal: 1.005-1.03). There were no crystals, protein and glucose in the urinalysis. Troponin I level was less than 0.030 ng/ml (normal: 0.0-0.049 ng/ml). Urine and serum toxicology screens were negative for cocaine, amphetamine, marijuana, benzodiazepines, barbiturates and phencyclidine. A chest X-ray did not show any infiltrate, consolidation, effusion or mediastinal widening. A computed tomography aortogram showed aortic dissection involving the posterior aspect of the arch extending into the common iliac arteries and right proximal external iliac artery. The dissection extended into the left subclavian and axillary arteries. There was narrowing of the origin of the right renal artery due to dissection (Stanford type B dissection) (Figure ,Figure , & Figure .)
She was started on intravenous esmolol and nitroprusside for blood pressure control and was admitted to the medical intensive care unit. During hospitalization, her blood pressure remained well controlled with amlodipine. All other investigations for a secondary cause of hypertension were negative.Patient was discharged home and upon follow-up 2 week later, her blood pressure remained well controlled with low dose amlodipine.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [70.0, 'kg'], 'height': [165.0, 'cm'], 'creatinine': [1.3, 'mg/dL'], 'age': [36, 'years']}",58.69318,55.75852,61.62784,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 36 years old. 
The concentration of creatinine is 1.3 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.65 m * 1.65 m) = 25.71166 kg/m^2.The patient's BMI is 25.7, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 56.90954 kg + 0.4 * (70.0 kg  - 56.90954 kg) = 62.14572 kg. The patient's adjusted body weight is 62.14572 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 36) * 62.14572 * 0.85) / (1.3 * 72) = 58.69318 mL/min. Hence, the patient's creatinine clearance is 58.69318 mL/min."
79,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6545029-1,Extracted,"A 28-year-old Togolese woman was admitted to the Gynecology Department of Kara University Hospital with a 1-week history of bleeding and pelvic pain. She reported her age at first menstrual period as 14 years old and her age at first sexual intercourse as 15 years old. She did not smoke, drink alcohol, or take contraceptive pills. She did not report any history of sexually transmitted infections. The patient had no medical, obstetric, social, environmental, or special family history. She had never received an intervention, and she had a good psychosocial state.
Clinical examination revealed an axillary temperature of 38 °C, body weight of 54 kg, and height of 1.68 m. The patient’s blood pressure was 100/60 mmHg, and her pulse was good. Her general condition was good. Upon inspection, her conjunctivas were moderately hyperemic, and her abdomen palpated normally but was painful on palpation of the pelvic region. There was palpable lymphadenopathy in the region of the inguinal lymph nodes. Her gynecological speculum examination showed a macroscopically healthy uterine cervix. The result of examination of her external genitalia was normal. Her neurological examination and other investigations were unremarkable. The result of biological explorations, namely hemoglobin, was normal (13.5 g/dl). Her renal biology was normal (urea 0.22 g/L, creatinine 9 mg/L, blood glucose 0.9 g/L). The result of her hepatic evaluation was also normal (transaminases 19 IU/L, phosphatases 104 IU/L, γ-glutamyltransferase 21 IU/L). The result of her human immunodeficiency virus serology test was negative.
Abdominal ultrasound showed regular thickening of the endometrium, measuring 19 mm thick, and no substantial masses (Fig. ). Her ovaries were normal in size. Biopsy with curettage of the endometrium was performed.
Anatomopathological examination with hematoxylin and eosin (H&E) staining showed neoplastic cells of an epidermoid nature with bridges of unions arranged in lobules, often centered, with dyskeratotic maturation. Cellular atypia of epidermoid cells, particularly anisokaryosis, and mitotic figures were noted (Fig. ). Immunohistochemistry (IHC) investigations showed positivity for anti-epithelial membrane antigen markers and anti-pancytokeratin 1 (KL1+) markers of tumor cells (Figs. and ). The cells were negative for chromogranin A, actin, S100, estrogen receptor (ER), and progesterone receptor (PR). Positive staining for Ki-67 (antigen of cell multiplication) was observed in 50% of the tumor cells. In situ hybridization demonstrated HPV genotype 16/18. A diagnosis of PSCC of the endometrium associated with HPV genotype 16/18 was made.
Total hysterectomy with bilateral adnexectomy and bilateral inguinal dissection were performed. The inguinal dissection revealed a total of five ganglia (three lymph nodes on the right and two lymph nodes on the left). The cervix, fallopian tubes, and ovaries were macroscopically normal. Histologically, the tumor consisted of well-differentiated epidermoid cells with union bridges and dyskeratotic maturation invading the middle third of the myometrium. The diagnosis of a well-differentiated, invasive SCC of the endometrium was confirmed. There was no differentiation of adenocarcinoma, and no squamous metaplasia or dysplasia was observed. No tumor cells were seen in the cervix, the fallopian tubes, the ovaries, the omentum, or the lymph nodes.
The histoprognostic grade was classified as FIGO (International Federation of Gynecology and Obstetrics) stage IB, corresponding to pT1N0M0. The patient received three cycles of docetaxel (75 mg/m2, day 1, pump in) combined with carboplatin (200 mg/m2, day 1, drop in) chemotherapy.
After 3 and 6 months of follow-up, the patient was well, without recurrence.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [28, 'years'], 'weight': [54.0, 'kg'], 'height': [1.68, 'm'], 'creatinine': [9.0, 'mg/L']}",79.33333,75.36666,83.3,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 28 years old. 
The concentration of creatinine is 9.0 mg/L. We need to convert the concentration to mg/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 9.0 mg creatinine/10.0 dL = 0.9 mg creatinine/dL. The concentration value of 9.0 mg creatinine/L converts to 0.9 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.68 m. The patient's weight is 54.0 kg. The patient's bmi is therefore 54.0 kg / (1.68 m * 1.68 m) = 19.13265 kg/m^2.The patient's BMI is 19.1, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 54.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 28) * 54.0 * 0.85) / (0.9 * 72) = 79.33333 mL/min. Hence, the patient's creatinine clearance is 79.33333 mL/min."
80,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5879769-1,Extracted,"A 51-year-old male taxi driver was admitted to Fukuoka City hospital with high fever (40 °C) and a shaking chill despite his use of over-the-counter antipyretics. He was transferred to the emergency department about 14 h after the symptoms onset. His medical history included bronchial asthma, pneumonia, and a surgical procedure for the resection of bilateral orbital tumors at 40 years of age. The patient had neither a history of contact with sick persons nor of any travel abroad. His body height was 160 cm and his body weight was 52 kg.
At the time of admission, his vital signs were as follows: blood pressure, 108/74 mmHg; heart rate, 90 beats/min; respiratory rate, 40 breaths/min; body temperature, 40.1 °C; and Glasgow Coma Scale, E4V4M6 (total 14/15). Upon physical examination, a swelling of the bilateral eyelids (Fig. ) and petechiae were detected on the conjunctiva. Some dental caries, purpura and petechiae were noted on the limbs (Fig. ), and 1–2 cm sized swollen lymph nodes noted at submandibular and inguinal areas were remarkable. Neck stiffness was not detected. Laboratory data on admission revealed high inflammation (white blood cell 13,500 μL, and c-reactive protein 12.29 mg/dL), normocytic anemia (Hemoglobin 8.7 g/dL), high protein and low albumin levels (total protein 12.3 g/dL and albumin 2 g/dL), renal failure (serum creatinine 4.52 mg/dL), hyperkalemia (6.12 mEq/L), proteinuria and hematuria (Table ). Computed tomography showed enlargement of the liver and bilateral kidneys (Fig. ) in addition to swelling of the cervical, supraclavicular, axillary, mediastinal, and celiac lymphadenopathy.
Severe infectious disease was suspected, and we started ceftriaxone 1 g intravenously every 12 h after drawing a blood culture. However, purpura spread rapidly and the progression of drowsiness and fever was sustained on the 2nd hospital day. We performed a lumbar puncture and the turbid spinal fluid analysis revealed meningeal inflammation (white blood cell count, 2370 /fields; protein, 293 mg/dL; and glucose, 16 mg/dL), which was compatible with bacterial meningitis (Fig. ). Gram-staining of the spinal fluid showed gram-negative diplococci. The blood culture also became positive for gram-negative diplococci. We strongly suspected that the septic status of the patient’s meningitis and bacteremia was due to N. meningitidis. We increased the dose of ceftriaxone to 2 g intravenously every 12 h. The patient’s general status and consciousness then improved and his fever subsided. On the 5th hospital day, the patient’s fever (38 °C) re-appeared with hypotension, hyponatremia and eosinophilia, which led to a suspicion of relative adrenal insufficiency due to meningococcemia. We started a daily intravenous administration of 300 mg hydrocortisone on the 7th hospital day, and tapered the regimen to a daily oral administration of hydrocortisone on the 11th hospital day. Ceftriaxone was stopped on the 12th hospital day. No recurrence of infection was observed and he was discharged on the 25th hospital day. The clinical course is summarized in Fig. .
We investigated the patient’s co-morbidities and performed microbiological analysis of the strain. His past surgical history (bilateral orbital tumors), his symptoms (swelling lachrymal glands and lymph nodes), the elevated levels of IgG4 (3200 mg/dL) and immunoglobulin E (304 IU/ml), and hypocomplementemia (C3 37 mg/dL, C4 7 mg/dL, and CH50 < 12.0 U/ml) were the characteristics of Mikulicz’s disease included in IgG4-related disease. Furthermore, a biopsy of the patient’s lymph nodes confirmed the presence of IgG4-related disease (IgG4/IgG index 100%). We prescribed oral prednisolone 30 mg a day on the 19th hospital day. In addition, the strain of N. meningitidis was identified as non-typable. The sequence type (ST) was identified as ST-11448, which belongs to ST-23 (ST-23 complex), the most common ST in Japan []. Moreover, we also analyzed the N. meningitidis strain according to PorA and FetA typing, which has a higher resolution power than that of ST, and identified that the PorA VR1, PorA VR2 and FetA were 5, 2–82, and F4–1, respectively. These results suggested that this N. meningitidis strain was a non-capsulated derivative of the domestic ST-23 strain. (See ).","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [52.0, 'kg'], 'height': [160.0, 'cm'], 'creatinine': [4.52, 'mg/dL'], 'age': [51, 'years']}",14.22075,13.50971,14.93179,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 51 years old. 
The concentration of creatinine is 4.52 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 52.0 kg. The patient's bmi is therefore 52.0 kg / (1.6 m * 1.6 m) = 20.3125 kg/m^2.The patient's BMI is 20.3, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 52.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 51) * 52.0 * 1) / (4.52 * 72) = 14.22075 mL/min. Hence, the patient's creatinine clearance is 14.22075 mL/min."
81,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-2783101-1,Extracted,"A 44-year-old caucasian man underwent his second kidney transplantation. His induction regimen included thymoglobulin, methilprednisolone and rituximab. Because of increased risk of humoral rejection he underwent 5 plasmapheresis sessions before transplant. He was 1.6 m tall, and weighted 70 kg.
The maintenance immunosuppressive regimen included methilprednisolone, tacrolimus and micophenolate. Delayed graft function occurred and a renal biopsy done in the first week after transplant showed signs of probable humoral rejection. Gammaglobulin and plasmapheresis were started with mild improvement of renal function.
His medical history includes chronic renal failure secondary to focal and segmental glomerulonephritis, first renal transplantation 23 years before the present admission and on dialysis for the last 10 years, hepatitis C and left eye blindness of unknown etiology. He had no relevant family history and did not smoke or drink alcohol.
During first two months his post-transplant course was complicated by surgical wound infection, urinary fistula, nosocomial pneumonia due to Haemophilus influenzae, and abdominal wall abscess due to Acinetobacter baumanii.
One month after transplant the patient developed severe left sided headaches and blurred vision. He was hypertensive (150/90 mmHg with a usual blood pressure between 90-60 and 70-50) and a right temporal visual field deficit was detected. Computed Tomography (CT) showed a left occipital cortico-subcortical hypodense area. (Figure )
Serum creatinine was 3,79 mg/dl, tacrolimus level was 6.8 (normal 5-20), platelets were 137.000/ml. Other laboratory test results are shown in table .
A Neurology consultant suggested ischemic stroke as the cause, aspirin was started and permissive hypertension was allowed.
Twelve hours later he had an episode of left-sided motor focal seizures followed by left hemiparesis and was admitted to the intensive care unit. He was alert and oriented. Blood pressure was 165/71, temperature 36.3°C, heart rate 88, pulse oximetry 100% on room air, respiratory rate 18. The neurological exam showed left arm and left leg weakness and bilateral amaurosis. A new CT scan showed bilateral occipital hypodensities and hemorrhagic foci. (Figure ) Diphenilhydantoin was started. Brain Magnetic Resonance Image (MRI) showed bilateral occipital hyperintese lesions in Fluid Attenuated Inversion Recovery (FLAIR) and T2, a small area of cortical left occipital lobe restricted diffusion on Diffusion Weighted Image (DWI) and GRE sequence compatible with hemorrhage. (Figure , , , ) MRI venous and arterial angiography showed no abnormalities. (Figure ,)
With a diagnosis of Reversible Posterior Leukoencephalopathy Syndrome (RPLS) blood pressure was controlled with intravenous labetalol (2 doses of 10 mg). Neurologic findings including cortical blindness returned to normal within 48 hs.
A follow-up CT 17 days later showed decreasing hypodensity in left occipital and parietal lobes with improvement of the hemorrhagic foci and almost complete resolution of the right occipital lesions. (Figure )","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [70.0, 'kg'], 'height': [1.6, 'm'], 'creatinine': [3.79, 'mg/dL'], 'age': [44, 'years']}",21.85723,20.76437,22.95009,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 44 years old. 
The concentration of creatinine is 3.79 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.6 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.6 m * 1.6 m) = 27.34375 kg/m^2.The patient's BMI is 27.3, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.6 m, which is 1.6 m * 39.3701 in/m = 62.99216 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.99216 (in inches) - 60) = 56.88197 kg.
Hence, the patient's IBW is 56.88197 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 56.88197 kg + 0.4 * (70.0 kg  - 56.88197 kg) = 62.12918 kg. The patient's adjusted body weight is 62.12918 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 44) * 62.12918 * 1) / (3.79 * 72) = 21.85723 mL/min. Hence, the patient's creatinine clearance is 21.85723 mL/min."
82,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-3728599-1,Extracted,"The recipient was a 63-year-old Japanese male who had been suffering from hepatitis C cirrhosis since the age of 37 years. He had undergone endoscopic variceal ligation for esophageal varices at the age of 58 years. His liver function had gradually become decompensated and he had developed hepatic encephalopathy 5 months before admission. He had had cryptogenic chronic nephritis from the age of 19 years and started hemodialysis at the age of 60 years. He had no other complications such as diabetes, hypertension or hemodialysis-related complications. His height was 159 cm and his weight was 53 kg before hemodialysis and 51 kg after hemodialysis. His Child-Pugh score was 10 (grade C) with a total bilirubin level of 0.9 mg/dl, an albumin level of 3.4 g/dl and a prothrombin time of 68% (international ratio 1.25). He was seropositive for hepatitis C virus (HCV) antibodies but seronegative for HCV RNA. The levels of blood urea nitrogen and creatinine were 61 and 9.01 mg/dl, respectively. His model for end-stage liver disease score was 22. A computed tomography scan revealed the presence of liver cirrhosis, splenomegaly and developed collateral vessels such as splenorenal shunt, recanalized paraumbilical vein and gastric varices. No definite hepatocellular carcinomas were detected (fig. ). The bilateral kidneys were very atrophic, which was consistent with irreversible renal failure (fig. ). In summary, he had decompensated hepatitis C cirrhosis without serum HCV RNA. He had non-diabetic renal failure after 3 years on hemodialysis. He showed good general function except for the liver and kidney failure. Therefore, the patient was expected to have a good prognosis after LDLT.
The donor was his healthy 58-year-old wife with identical blood type to the recipient. The right lobe graft was procured using a typical method described elsewhere [, , , , ]. The actual graft weight was 546 g, which accounted for 50.4% of the recipient's standard liver volume.
In the recipient, intraoperative continuous hemodiafiltration (CHDF) without water removal was started immediately via the right femoral vein after laparotomy. The CHDF provided a stable acid-base and electrolyte balance. A total hepatectomy and implantation were performed under stable hemodynamics using an extracorporeal veno-venous bypass. The V5, right inferior hepatic vein and right hepatic vein of the right lobe graft were reconstructed to have a co-orifice using the left internal jugular vein and explanted portal vein grafts of the recipient at the backtable according to our usual method [, ]. Operative time was 14 h 22 min. The anhepatic, cold ischemic and warm ischemic times were 140, 169 and 65 min, respectively. The blood loss was 2,000 g, for which 10 units of red cell concentrate, 10 units of fresh-frozen plasma and 30 units of platelet concentrate were transfused.
The postoperative courses of the recipient and the donor were uneventful. CHDF was continued until postoperative day 4, at which point CHDF was converted to hemodialysis. The amount of water removal was appropriately adjusted according to blood pressure, central venous pressure and body weight. The drained ascites was below 500 ml/day and all abdominal drains were removed by postoperative day 6 except for the biliary stents (table ). Other than the renal replacement therapy and dose modulation of renal excretory drugs such as acyclovir, the perioperative management of the recipient was typical, as previously described [, , , , ]. Immunosuppression was induced with intravenous methylprednisolone and then switched to oral prednisolone, cyclosporin A and mycophenolate mofetil. He left the intensive care unit on postoperative day 5 and was discharged on postoperative day 36 with good hepatic function.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [51.0, 'kg'], 'height': [159.0, 'cm'], 'creatinine': [9.01, 'mg/dL'], 'age': [63, 'years']}",6.05346,5.75079,6.35613,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 63 years old. 
The concentration of creatinine is 9.01 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 159.0 cm, which is 159.0 cm * 1 m / 100 cm = 1.59 m. The patient's weight is 51.0 kg. The patient's bmi is therefore 51.0 kg / (1.59 m * 1.59 m) = 20.17325 kg/m^2.The patient's BMI is 20.2, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 51.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 63) * 51.0 * 1) / (9.01 * 72) = 6.05346 mL/min. Hence, the patient's creatinine clearance is 6.05346 mL/min."
83,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4400491-1,Extracted,"A 70-year-old man who had a low-grade fever was treated with antibiotics and a nonsteroidal anti-inflammatory drug. About 1 week after a fall, general malaise and peripheral edema appeared. He was admitted to our renal department and his condition was diagnosed as rapidly progressive glomerulonephritis. He had no family history of kidney disease. Physical examination findings included the following: height 160 cm; weight 45 kg; body temperature 37.2°C; blood pressure 137/72 mmHg; edema present in both of the lower legs. The rest of the physical examination was unremarkable. A further clinical workup indicated kidney failure with MPO-ANCA-positive vasculitis, supported by the following laboratory data: serum creatinine 2.19 mg/dL (200 µmol/L), eGFR 23.7 (mL/min/1.73 m2); eGFR (mL/min/1.73 m2) = 194 × serum creatinine−1.094 × age−0.287) [] urea nitrogen 48.0 mg/dL (19 mmol/L), C-reactive protein 7.39 mg/dL, MPO-ANCA 276 EU (reference <20 EU), negative serologic tests for PR-3-ANCA and anti-glomerular basement membrane antibodies, and urinalysis showed protein (+) and blood (3+). Microscopic examination of urine showed numerous erythrocytes and casts. A percutaneous kidney biopsy was performed 1 day after the admission. In light microscopy, 15 glomeruli were included. The renal specimen shows a fibrinoid necrosis with cellular crescent and apoptosis-like appearance of neutrophils (A). Then, the serial sections were immunostained for citrullinated histone using anti-citrullinated histone H3 peptide antibodies [], for MPO using an antiserum against MPO and for PAD4 using anti-PAD4 antibodies in a coupled reaction with peroxidase-conjugated goat anti-rabbit IgG antibodies (B–D). Strong positivities for citrullinated histone, MPO and PAD4 were distributed throughout the foci. The three antibodies were recognized to be distributed in cytoplasmic and extracellular sites, as well as the nuclei of the cells of the foci. More exactly, double immunofluorescence staining of the section revealed the codistribution of significant signals of MPO and citrullinated histone in the fibrinoid necrosis of the cellular crescent in the lesion (). The three other glomeruli with fibrocellular crescents showed no immunostaining for citrullinated histione, MPO and PAD4 (). In the 11 glomeruli showing only minor abnormalities, almost no signals were found throughout the sections. The other view field of the sections exhibited a typical fibrinoid necrosis of the interlobular artery (A). Some immunostains for citrullinated histone, MPO and PAD4 were distributed in the extracellular and cytoplasmic sites, as well as in the nuclei, of the cells throughout the lesion (B–D). More directly, double immunofluorescence staining of the section indicated the codistribution of MPO and PAD4 in the fibrinoid necrosis of the interlobular artery (). MPO-AAV was recognized as belonging to the focal class, according to the histopathologic classification []. No immunoglobulin or complement deposition was found. Immunostaining of renal biopsy sections from a patient with anti-glomerular basement membrane glomerulonephritis revealed no signals of PAD4, citrullinated histone and MPO in the cellular crescent of glomerulus in the lesion (). The occurrence of NET components is likely to be specific for a type of renal disease.
First, the patient received steroid pulse therapy consisting of a series of three intravenous infusions of 1 g methylprednisolone plus 40 mg/day oral prednisolone for 30 days, and then (for induction therapy) 50 mg/day oral cyclophosphamide. After 60 days, the patient successfully entered into complete remission, as evidenced by the following laboratory findings: serum creatinine 0.62 mg/dL (60 µmol/L); eGFR 80.5 (mL/min/1.73 m2); C-reactive protein 0.2 mg/dL, MPO-ANCA 20 EU (reference < 20 EU) and urine protein (−) and blood (−). He has remained in remission for 3 years without intermittent relapse.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [70, 'years'], 'weight': [45.0, 'kg'], 'height': [160.0, 'cm'], 'creatinine': [2.19, 'mg/dL']}",19.97717,18.97831,20.97603,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 70 years old. 
The concentration of creatinine is 2.19 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 45.0 kg. The patient's bmi is therefore 45.0 kg / (1.6 m * 1.6 m) = 17.57812 kg/m^2.The patient's BMI is 17.6, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 45.0 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation. 
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 70) * 45.0 * 1) / (2.19 * 72) = 19.97717 mL/min. Hence, the patient's creatinine clearance is 19.97717 mL/min."
84,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-2481241-1,Extracted,"A 52-year-old white male with O2-dependent COPD, hypertension, GERD, idiopathic gastroparesis, and chronic low back pain was noted to have persistent hypokalemia in the 2.7–3.3 meq/L range over more than 2 years. He complained also of chronic generalized weakness and fatigue. He denied nausea or vomiting, but did have occasional loose stools. The hypokalemia persisted despite discontinuation of diuretic treatment for hypertension and fludrocortisone that had been prescribed briefly for orthostatic hypotension. There was no improvement with aggressive oral potassium supplementation in amounts up to 120 meq per day. The patient's serum potassium level normalized on three occasions when he was hospitalized and given supplemental potassium (COPD exacerbations in 7/06 and 1/07, pseudoseizures in 7/07), but the hypokalemia promptly recurred after discharge from the hospital (Figure ). His medications were paroxetine, trazodone, pregabalin, sustained-release morphine, loratadine, isosorbide mononitrate, lisinopril, metoprolol, simvastatin, omeprazole, metoclopramide, potassium chloride, calcium/vitamin D tablets, alendronate, and mometasone, tiotropium, and albuterol inhalers. He smoked one-half pack of cigarettes per day and did not drink alcohol.
On physical examination, he was a chronically ill-appearing man wearing a nasal cannula. Height was 69 inches, weight 205 pounds. There were no cushingoid facies, buffalo hump, or abdominal striae. Vital signs were temperature 98.6 degrees, pulse 95, respiratory rate 14, blood pressure 128/73. There was no thyromegaly or lymphadenopathy. Lungs showed decreased breath sounds and mild expiratory wheezes bilaterally. Heart sounds were regular with no murmurs, rubs, or gallops. The abdomen was soft and non-tender, with no masses or organomegaly. Extremities showed no edema, clubbing or cyanosis. The neurologic examination revealed mild generalized muscular weakness (4+/5) and normal deep tendon reflexes.
Laboratory results include serum sodium 137 mg/dL, potassium 3.0 mg/dL, chloride 95 mmol/L, CO2 30.0 mmol/L, blood urea nitrogen 5 mg/dL, creatinine 0.8 mg/dL, calcium 9.3 mg/dL, phosphorus 4.1 mg/dL, albumin 3.6 g/dL, ferritin 126 ng/mL, hemoglobin 12.7 g/dL, white blood cell count 10.6 K/cmm, and platelet count 160 K/cmm. Serum aldosterone was 4.8 ng/dL (normal 4–31 ng/dL) and the plasma renin activity was 0.33 ng/mL/hr (normal 1.31–3.96 ng/mL/hr upright, 0.15–2.33 ng/mL/hr supine). Spot urine potassium was 8.6 mEq/L, urine sodium was < 10 mEq/L, and urine chloride was 16 mmol/L.
In the absence of a clear explanation for this patient's chronic hypokalemia, he was asked to give the details of his diet. He admitted to drinking 4 liters of Pepsi-Cola per day for the past several years. It was his habit to sip cola slowly but almost continuously, throughout the day. When hospitalized, he had stopped drinking cola and his potassium levels had temporarily normalized. In early May 2008, he decreased his cola intake to 2 liters per day, with a resultant increase in the serum potassium from 3.0 to 3.5 mg/dL (Figure ).","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [205.0, 'lbs'], 'height': [69.0, 'in'], 'creatinine': [0.8, 'mg/dL'], 'age': [52, 'years']}",121.63332,115.55165,127.71499,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 52 years old. 
The concentration of creatinine is 0.8 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 69.0 in, which is 69.0 in * 0.0254 m / in = 1.7526 m. The patient's weight is 205.0 lbs so this converts to 205.0 lbs * 0.453592 kg/lbs = 92.98636 kg. The patient's bmi is therefore 92.98636 kg / (1.7526 m * 1.7526 m) = 30.27287 kg/m^2.The patient's BMI is 30.3, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 69.0 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.0 (in inches) - 60) = 70.7 kg.
Hence, the patient's IBW is 70.7 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 70.7 kg + 0.4 * (92.98636 kg  - 70.7 kg) = 79.61454 kg. The patient's adjusted body weight is 79.61454 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 52) * 79.61454 * 1) / (0.8 * 72) = 121.63332 mL/min. Hence, the patient's creatinine clearance is 121.63332 mL/min."
85,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-3658343-1,Extracted,"A 50-year-old man, weighing 80 kg, who was 1.58 m tall (body mass index = 32 kg/m2) was admitted to the emergency room with a traumatic amputation of the right upper limb up to about 5 cm distal to the elbow joint and a contused lacerated wound (CLW) extending circumferentially around the left distal forearm. Both the wounds were badly contaminated and the amputated limb was bleeding. He was on Tab. Amlodipine 5 mg once daily for hypertension and, Glipizide 5 mg once daily and Metformin 500 mg twice daily for type-2 diabetes mellitus since 2 years. He was also a known case of HOCM and had undergone alcohol ablation of the interventricular septum one year ago.
He was conscious and oriented. His pulse rate was 120/m and the blood pressure (BP) in his left lower limb was 210/120 mmHg (mean arterial pressure (MAP) = 150 mmHg). A systolic murmur was heard over the left parasternal area. The respiratory system examination was normal. The mouth opening was one-and-a-half fingers breadth, he had Mallampati airway class-3 and the upper two incisors were loose and broken. Neck extension was restricted and the thyromental distance was three fingers breadth.
His haemoglobin was 11 g/dl, blood sugar was 173 mg/dl, blood urea was 26 mg/dl, serum creatinine was 1.3 mg/dl and serum electrolytes were normal. An electrocardiogram revealed a left bundle branch block with left ventricular hypertrophy []. Echocardiography showed a thickened interventricular septum, systolic anterior motion of the anterior mitral leaflet, left ventricular outflow tract gradient of 60 mmHg, left ventricular ejection fraction of 45%, good right ventricular function and no mitral regurgitation. A chest X-ray showed cardiomegaly with no signs of congestive cardiac failure. The cervical spine X-ray revealed spondylotic changes at C5-C7.
An intravenous access was secured on the left foot. The right dorsalis pedis artery was cannulated and continuous BP monitoring was initiated. Intravenous fentanyl 150 μg and labetalol 10 mg, followed by an infusion of 2 mg/min, were administered. After 20 min, his heart rate decreased to 106/min and BP to 196/114 mmHg (MAP 140 mmHg). He was scheduled for emergency hemostasis and debridement of the amputated limb and contused lacerated wound. The patient was nil-by-mouth for 2 h.
In the operation theater, after applying the standard monitors, the right subclavian vein was cannulated and central venous pressure (CVP) monitoring was initiated. The initial CVP was 4 mmHg. The BP had decreased to 180/110 mmHg (MAP = 133 mmHg) and pulse rate to 90-100/min. It was decided to achieve the hemostasis and debride the amputated limb first, and follow it up with debridement of the CLW.
Right brachial plexus block was performed via a supraclavicular approach using a 23 G needle. After eliciting paraesthesia, a mixture of 6 ml 2% lignocaine and 18 ml 0.5% bupivacaine was injected slowly with frequent aspirations. He was sedated with intravenous midazolam 2 mg following initiation of the block. The debridement and revision amputation were completed in 120 min. Following this, left axillary block was performed with a mixture of 8 ml 2% lignocaine and 30 ml 0.25% bupivacaine using a multiple injections technique. Both the blocks worked adequately. Intraoperatively, the pulse rate and MAP were maintained at 80-90/min and 110-120 mmHg, respectively. The total blood loss was 500-550 ml. The blood sugar was monitored hourly, and it was maintained between 100 and 200 mg/dl with insulin infusion. The surgeries were uneventful and the patient was shifted to the intensive care unit. Analgesia lasted for 6 h post-operatively, which was managed further with fentanyl infusion.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [50, 'years'], 'weight': [80.0, 'kg'], 'height': [1.58, 'm'], 'creatinine': [1.3, 'mg/dL']}",62.54093,59.41388,65.66798,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 50 years old. 
The concentration of creatinine is 1.3 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.58 m. The patient's weight is 80.0 kg. The patient's bmi is therefore 80.0 kg / (1.58 m * 1.58 m) = 32.04615 kg/m^2.The patient's BMI is 32.0, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.58 m, which is 1.58 m * 39.3701 in/m = 62.20476 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.20476 (in inches) - 60) = 55.07095 kg.
Hence, the patient's IBW is 55.07095 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 55.07095 kg + 0.4 * (80.0 kg  - 55.07095 kg) = 65.04257 kg. The patient's adjusted body weight is 65.04257 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 50) * 65.04257 * 1) / (1.3 * 72) = 62.54093 mL/min. Hence, the patient's creatinine clearance is 62.54093 mL/min."
86,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4805222-1,Extracted,"A 16-year-old male presented to our outpatient clinic with complaints of bilateral pain and swelling along his Achilles tendon in the past four weeks. He stated that the pain was usually worse during and after walking. He was a high school student and was not involved in any sport activity. A closer questioning revealed a transient hematuria which had occurred two weeks ago. Medical history was unremarkable otherwise. Family history was also negative for known diseases including cancers.
Physical examination revealed normal findings except for tenderness and swelling in the area where the patient complained of pain. The height of the patient was 172 cm (50th percentile) and his weight was 63 kg (50th percentile). Pubertal stage conformed to Tanner 4 according to Tanner staging. Blood pressure was 110/70 mmHg.
Total blood count was normal. Blood chemistry showed a serum calcium level of 14.4 mg/dL (N: 8.4-10.6 mg/dL), phosphate: 2.4 mg/dL (N: 2.3-4.7 mg/dL), alkaline phosphatase: 245 U/L (N: 40-360 mg/dL), magnesium: 0.8 mmol/L (N: 0.5-1.1 mg/dL), creatinine: 0.8 mg/dL, total protein: 7.7 g/dL, albumin: 4.1 g/dL, alanine aminotransferase: 15 U/L, and aspartate aminotransferase: 19 U/L. Serum glucose and prolactin levels were within normal limits. Urinary calcium/creatinine ratio was 0.2. Parathormone (PTH) level was 512 pg/mL (N: 5-65 pg/mL). Anteroposterior and lateral radiograms of both ankles were normal. A superficial ultrasonography performed using GE logic5P Doppler Sonography device and linear probe (7-12 MHz) revealed calcific nodules and increased Doppler signals surrounding the nodules, which were localized in both Achilles tendons on the longitudinal Doppler sections (). Renal ultrasonography was normal. Intravenous saline infusion (3000 mL/day), furosemide (1 mg/kg every six hours) and prednisolone (60 mg/day) were started. Neck ultrasonography revealed a 12x10 mm hypoechoic lesion near the left thyroid lobe, suggesting a parathyroid adenoma. The dual-phase 15 mCi Technetium-99m (99mTc) sestamibi scanning revealed increased activity in the left thyroid lobe, indicating parathyroid adenoma. On the second day of admission, it was observed that the hypercalcemia did not respond to medical treatment and the patient was admitted to pediatric intensive care unit due to severe hypercalcemia (calcium: 18 mg/dL). Serum calcium levels decreased to 13 mg/dL after intravenous calcitonin (0.8 IU/kg/d) was added to the treatment.
A minimally invasive parathyroidectomy was planned. On the day of surgery, serum PTH level was 1222 pg/mL. PTH level was measured intraoperatively 10 minutes after the left superior gland was excised and detected to be decreased more than 50% of the initial PTH level. The left inferior gland was apparently normal. Left superior parathyroid gland was excised guided by gamma probe.
On post-operative day 3, the laboratory data were: calcium: 9.9 mg/dL, phosphate: 3.9 mg/dL, alkaline phosphatase: 176 U/L, and PTH: 12.5 pg/mL. After parathyroidectomy, the swelling also resolved and the patient had some relief from his pain. On the follow-up visit two months after the surgery, the tenderness over the Achilles tendon and the flow pattern on Doppler examination had both disappeared.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [16, 'years'], 'weight': [63.0, 'kg'], 'height': [172.0, 'cm'], 'creatinine': [0.8, 'mg/dL']}",135.625,128.84375,142.40625,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 16 years old. 
The concentration of creatinine is 0.8 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 172.0 cm, which is 172.0 cm * 1 m / 100 cm = 1.72 m. The patient's weight is 63.0 kg. The patient's bmi is therefore 63.0 kg / (1.72 m * 1.72 m) = 21.29529 kg/m^2.The patient's BMI is 21.3, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 63.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 16) * 63.0 * 1) / (0.8 * 72) = 135.625 mL/min. Hence, the patient's creatinine clearance is 135.625 mL/min."
87,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5815706-1,Extracted,"A 69-year-old patient (G6 P6) (height, 155 cm; weight, 66 kg) reported vaginal prolapse for several years and incontinence, abdominal pain and hematuria. Comorbidities: type 2 diabetes for 20 years, circulatory failure, paroxysmal atrial fibrillation, anaemia, urinary tract infection, hypertension, chronic biliary gastritis, cervical osteoarthritis.
Physical examination on admission revealed anterior vaginal and uterine walls prolapse, with 8 cm in diameter large ulcerated lesion (Fig. ) located on the anterior vaginal wall. Diagnostic biopsy of the lesion revealed squamous cell carcinoma (Fig. ).
Additional tests: hemoglobin 11.0 g/dL (12.0–16.0); hematocrit 33.9% (37.0–47.0); erythrocytes 4.34 × 106/uL (4.00–5.00); MCV 78.1 fL (80–94); MCH 25.3 pg (27.0–31.0); MCHC 32.4 g/dL 931.0–37.0); RDW-SD 48.3 fL (36.4–46.3); RDW-CV 17.7% (11.7–14.4); Blood Plate 296 × 103/Ul (140–400); plate distribution width (PDW) 11.6 fL (9.80–16.20); MPV 9.8 fL (9.40–12.50); platelet large cell ratio (P-LCR) 24.1% (19.10–46.60); WBC 8.12 × 103/ul (4.0–10.0); Macro R 6.7%; Micro R 7.9%; total protein 7.1 g/dL (range 6.3–8.2); chlorides 112.0 mmol/L (98.0–107.0); activated partial thromboplastin time (APTT) 29.0 s (25.9–36.6); prothrombin time 9.2 s (7.6–11.4); Prothrombin index 103.7% (80.0–120.0); INR 1.0 (0.9–1.3); D-dimer 2 208.8 ng/mL (<500.0); fibrinogen 503.9 mg/dL (180.0–400.0); glomerular filtration rate (GFR) 27 mL/min/1.73 m2 (>60.0); glucose 115 mg/dL (70–99); creatinine 1.85 mg/dL (0.52–1.04); urea 66 mg/dL (15–43); potassium 4.9 mmol/L (3.5–5.1); sodium 144.0 mmol/L (137.0–145.0); TSH 0.50 uIU/mL (0.27–4.20).
Sagittal pelvic CT showed protruded vagina, infiltrated bladder wall, uterus, and rectum. In frontal CT scan of abdomen, enlarged pelvic iliac nodes, hydronephrosis of the left kidney with left hydroureter, in the right kidney nephrostomic catheter were observed (Fig. ).
Cystoscopy-mucosal lesions were found in the bladder (Fig. ). The diagnostic biopsies were collected from the urethra and the bladder (Fig. ).
Symptomatic treatment included: InsulinueGensulin R t.i.d. (2–6 units)sc, Amlodypinum 2 × 10 mg, 0.9%NaCl 2 × 500 ml iv., Clexan (Enoxaparinumnatricum) 2 × 0.6 sc, Ramiprilum 5 mg 1 × 1, Captoprilum 25 mg 1 × 1.
The patient was disqualified from surgery due to the severity of the disease, lymph node metastases, and coexisting comorbidities. Only palliative nephrostomy was performed.
The patient signed informed consents. In our case the patient accepted regular and proved diagnosis and therapy in Clinical Department of Urology, so the ethical approval was not necessary.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [69, 'years'], 'weight': [66.0, 'kg'], 'height': [155.0, 'cm'], 'creatinine': [1.85, 'mg/dL']}",24.97033,23.72181,26.21885,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 69 years old. 
The concentration of creatinine is 1.85 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 66.0 kg. The patient's bmi is therefore 66.0 kg / (1.55 m * 1.55 m) = 27.47138 kg/m^2.The patient's BMI is 27.5, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 47.85442 kg + 0.4 * (66.0 kg  - 47.85442 kg) = 55.11265 kg. The patient's adjusted body weight is 55.11265 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 69) * 55.11265 * 0.85) / (1.85 * 72) = 24.97033 mL/min. Hence, the patient's creatinine clearance is 24.97033 mL/min."
88,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5624279-1,Extracted,"A 44-year-old Japanese woman was admitted to our hospital for evaluation of abdominal distension. She was 164 cm tall and weighed 74 kg, with a blood pressure of 143/93 mm Hg. Laboratory tests revealed that her serum creatinine (Cre) value was 0.91 mg/dL, the estimated glomerular filtration rate (eGFR) was 53.7 mL/min/1.73 m2, and her albumin level was 3.6 g/dL. In addition, the total bilirubin level was 0.7 mg/dL, aspartate aminotransferase was 23 IU/L (normal range: 13–33), alanine aminotransferase was 15 IU/L (normal range: 8–42), lactate dehydrogenase was 173 IU/L (normal range: 103–190), alkaline phosphatase was 268 IU/L (normal range: 117–350), γ-glutamyl transpeptidase was 74 IU/L (normal range: 9–109), and C-reactive protein was 0.8 mg/dL. Urinary protein excretion was 0.1 g/day, and the urine sediment contained 1–4 erythrocytes per high-power field. Magnetic resonance imaging and computed tomography showed bilateral enlarged polycystic kidneys and a massive polycystic liver (Fig. ). ADPKD was diagnosed, since her mother had this disease. Liver volume was calculated to be 10,173 mL, indicating advanced PLD, while the total kidney volume was calculated as 2,614 mL by a previously reported method [].
First, 3 large cysts were treated by aspiration and sclerotherapy using minocycline hydrochloride according to a reported method []. Her abdominal fullness improved immediately after 1,750 mL of cyst fluid was removed, but the improvement was only temporary. Liver volume increased to 9,750 mL again after 6 months, along with the exacerbation of abdominal symptoms. Tolvaptan therapy was started at a dose of 60 mg daily to treat renal involvement (Cre of 0.89 mg/dL and eGFR of 54.6 mL/min/1.73 m2). After 1 month of tolvaptan therapy, abdominal fullness showed improvement and liver volume decreased to 9,219 mL, while it decreased further to 8,963 mL after 12 months of treatment and to 8,345 mL after 17 months. Total kidney volume was 2,714 mL at the start of tolvaptan therapy, while it was 2,640 mL after 1 month and 2,832 mL after 17 months. There was no significant change in kidney volume during the 17-month treatment period, and renal function was also unchanged (Cre of 0.92 mg/dL and eGFR of 52.3 mL/min/1.73 m2).","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [44, 'years'], 'weight': [74.0, 'kg'], 'height': [164.0, 'cm'], 'creatinine': [0.91, 'mg/dL']}",78.71362,74.77794,82.6493,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 44 years old. 
The concentration of creatinine is 0.91 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 164.0 cm, which is 164.0 cm * 1 m / 100 cm = 1.64 m. The patient's weight is 74.0 kg. The patient's bmi is therefore 74.0 kg / (1.64 m * 1.64 m) = 27.51338 kg/m^2.The patient's BMI is 27.5, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 164.0 cm, which is 164.0 cm * 0.393701 in/cm = 64.56696 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.56696 (in inches) - 60) = 56.00401 kg.
Hence, the patient's IBW is 56.00401 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 56.00401 kg + 0.4 * (74.0 kg  - 56.00401 kg) = 63.20241 kg. The patient's adjusted body weight is 63.20241 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 44) * 63.20241 * 0.85) / (0.91 * 72) = 78.71362 mL/min. Hence, the patient's creatinine clearance is 78.71362 mL/min."
89,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-3350132-1,Extracted,"A 69-year-old man was admitted to a hospital in the South of Brazil, with weight loss, weakness, and difficulty to swallow. In the last 4 months, he had anorexia, asthenia, and difficulty to swallow any food. When he tried to eat, he felt nausea and sometimes vomited. He had lost 7 kg. He denied fever or other symptoms. He was an active smoker that had smoked 100 pack-years. He did not abuse alcohol or other drugs. He had arterial hypertension, type 2 diabetes mellitus with HbA1c: 6.5% one month earlier and mild chronic obstructive pulmonary disease. He had presented three no disabling ischemic strokes. He was taking hydrochlorothiazide 25 mg, simvastatin 20 mg, and acetylsalicylic acid 100 mg, once a day; and captopril 50 mg TID. His father died of sudden death at 83 years old, and his mother died of stroke at 80 years old. His brother died of esophageal cancer with 55 years old. He lived with his wife. His physical examination revealed an alert, oriented man, with blood pressure: 120/70 mmHg; heart rate: 72 bpm; respiratory rate: 20 rpm; axillary temperature: 36°C; pulse oximetry: 95%; weight: 33.5 kg; height: 1.53 m; BMI: 14.3 kg/m2. There were several lymph nodes the cervical region, the larger one with 1.5 cm, and digital clubbing. Other aspects of his physical examination were normal. Two months before admission, chest radiography showed signs of chronic obstructive pulmonary disease, micronodules and linear opacities in the upper lobes, and a small consolidation in the lower left lobe. The initial laboratory evaluation revealed hemoglobin = 8.6 g/dL (normal range: 13–14.2 g/dL); VCM = 88.9 fL (80–100 fL); leukocytes = 7220/μL (4000–10000/μL); neutrophils = 2758/μL (1800–7500/μL); eosinophils = 606/μL (40–500/μL); basophils = 87/μL (<100/μL); monocytes = 477/μL (120–1000/μL); lymphocytes = 3292/μL (1000–4000/μL); platelets: 409000/μL (150–400 × 103/μL); serum sodium: 134 mEq/L (135–145 mEq/L); potassium: 5.2 mEq/L (3.5–5.1 mEq/L); creatinine: 0.64 mg/dL (0.5–1.2 mg/dL); ureic nitrogen: 21 mg/dL (5–20 mg/dL); calcium: 7.8 mg/dL (8.5–10.4 mg/dL); albumin: 3.0 g/dL (3.5–5.0 g/dL); ALT: 17 U/L (<31U/L); glucose: 94/mg/dL (70–99 mg/dL). An upper gastrointestinal endoscopy was normal, and a nasojejunal tube was inserted. The patient remained with the same symptoms, receiving food and liquids through a nasojejunal tube. In the sixth day after admission, after being submitted to chest and abdomen computerized tomography, he developed fever (39.5°C), confusion, blood pressure 160/110 mmHg, heart rate: 120 bpm, pulse oximetry: 95%. He received intravenous dipyrone. A few moments later, his blood pressure dropped to 80/40 mmHg, and intravenous saline solution was infused. A blood sample to measure serum ACTH and cortisol was drawn. In the next two days, he had no fever, and two samples of blood culture were negative. In the following days, the patient developed severe hyponatremia (sodium = 122 mEq/L and 119 mEq/L), and postural hypotension was identified (supine resting = 122/60 mmHg and standing = 100/60 mmHg). The results of computed tomography of chest and abdomen are shown in Figures and . Serum cortisol and ACTH were, respectively, 1.03 μg/dL (4.3–22.4 μg/dL) and 626 pg/mL (12–46 pg/mL), and serum TSH was 8.06 μU/mL (0.35–5.5 μU/mL). The patient received intravenous hydrocortisone, and hydrochlorothiazide was discontinued. Electrolyte abnormalities, anorexia, and difficulty to swallow are resolved. A biopsy of the left adrenal gland showed signet-ring cell adenocarcinoma with areas of necrosis. In the immunohistochemical study, the cells were positive for CK7, TTF-1, and CEA, and negative for CK20, vimentin, CA19.9, CD10, prostatic specific antigen, and thyroglobulin. Therefore, the diagnosis of adenocarcinoma of pulmonary origin was made. Bone and brain metastases were not evident in bone scintigraphy and brain computerized tomography. A few days later, the patient was switched to 5 mg oral prednisone and 0.1 mg of fludrocortisone and was discharged to his home. One month after initiating glucocorticoids, he came to the outpatient oncology division. He was eating normally, his weight increased to 40.1 kg, but he refused the palliative chemotherapy offered.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [69, 'years'], 'weight': [33.5, 'kg'], 'height': [1.53, 'm'], 'creatinine': [0.64, 'mg/dL']}",51.61675,49.03591,54.19759,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 69 years old. 
The concentration of creatinine is 0.64 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.53 m. The patient's weight is 33.5 kg. The patient's bmi is therefore 33.5 kg / (1.53 m * 1.53 m) = 14.31074 kg/m^2.The patient's BMI is 14.3, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 33.5 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation. 
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 69) * 33.5 * 1) / (0.64 * 72) = 51.61675 mL/min. Hence, the patient's creatinine clearance is 51.61675 mL/min."
90,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6230595-1,Extracted,"A 45-year-old male with no past medical history was transferred to our tertiary care facility after presenting to a community hospital with a one-week history of generalized abdominal pain, jaundice, dark urine, and lower extremity edema. His initial evaluation revealed severe hyperbilirubinemia and elevated transaminases, prompting his transfer. He denied any alcohol consumption for the previous twenty years or intravenous drug use. He had no medical history, was taking no medications prior to presentation, except a multivitamin. He denied taking any herbal supplements and his family history was unremarkable. He was married and employed as an auto mechanic.
On examination, he was notably jaundiced and cachectic in appearance with a height of 1.7 m, weight of 82.5 kg, and body mass index (BMI) of 28.3 kg/m2. He was afebrile with a pulse of 95 beats per minute, respiratory rate of 16 breaths per minute, and pulse oxygen saturation of 95% while on room air. He had marked scleral icterus; proptosis was noted. On thyroid examination, he had a large symmetrical, non-tender goiter with audible bruit. Heartbeat was irregularly irregular. His abdomen was mildly tender diffusely without ascites or organomegaly. Mild bilateral lower extremity edema was present. Skin was warm to the touch. A fine tremor was noted; asterixis of hands was intermittently present.
Initial laboratory evaluation revealed a hemoglobin of 12.1 g/dL (13.5-16.5), platelet count of 115 k/µL (150-400), and white blood cell count of 11.8 k/µL (4.5-11). His international normalized ratio (INR) was 2.4. His serum sodium was 128 mmol/L (137-147), potassium of 4.3 mmol/L (3.5-5.1) with creatinine of 1.77 mg/dL (0.4-1.24), blood urea nitrogen (BUN) of 57 mg/dL (7-25) and serum glucose 159 mg/dL (70-100). Notably, his total bilirubin was 19.8 mg/dL (0.3-1.2), direct bilirubin 13.8 mg/dL (<0.4), alkaline phosphatase 332 U/L (25-110), aspartate aminotransferase (AST) 86 U/L (7-40), and alanine aminotransferase (ALT) 50 U/L (7-56). His gamma-glutamyltransferase was 20 U/L (9-64). Total iron was 32 mcg/dL (50-185), percent iron saturation 11% (28%-42%), total iron binding capacity (TIBC) was 283 mcg/dL (270-380), and ferritin 121 ng/mL (30-300). The patient also had negative serology for hepatitis A, B, and C.
A workup for thyroid dysfunction demonstrated a thyroid-stimulating hormone (TSH) of 0.026 mcg/mL (0.35-5.00) with a free T4 of 4.3 ng/dL (0.6-1.6), free T3 4.6 pg/mL (2.1-3.9), and total T3 125 ng/dL (87-180). TSH receptor antibody was>40 IU/L (0.00 −1.75) and thyroid peroxidase (TPO) antibody was >1000 IU/mL (<5.61). An ultrasound of the patient's thyroid was notable for a mildly enlarged heterogeneous and hypervascular thyroid without nodularity. Based on these findings along with his presenting symptoms and signs, the patient was diagnosed with Graves’ disease.
In light of worsening cholestatic jaundice (Figure ), a thorough hepatology evaluation was undertaken for potential autoimmune, infectious, and primary hepatobiliary causes of cholestasis. The laboratory testing were all negative. Cardiac evaluation was notable for an ejection fraction of 55%-60% with right ventricular dilation and moderate mitral regurgitation. Moderate left atrial and severe right atrial enlargement was found with elevated central venous pressure as well as pulmonary artery pressure. Abdominal ultrasound demonstrated increase echogenicity of the liver and revealed trace abdominal and pelvic ascites. Further workup for cholestatic jaundice included a computed tomography scan of the abdomen and pelvis, which was notable for fatty liver, cardiomegaly, and diffuse irregular appearance of bones with prominent trabecula. Endoscopic retrograde cholangiopancreatography (ERCP) showed normal caliber common bile duct and common hepatic duct with normal intrahepatic ducts, without filling defects, strictures, or stenosis. Endoscopic ultrasound (EUS) was notable for normal pancreatic parenchyma as well as normal pancreatic and common bile ducts. The patient subsequently underwent transjugular liver biopsy with unremarkable hepatic vein pressures and a corrected sinusoidal pressure gradient of 5-6 mm Hg (normal). Pathology showed cholestasis and mild ductal proliferation with focal pericholangitis but no hepatic steatosis, fibrosis, hepatocellular injury, or necrosis. Periodic acid-Schiff (PAS) diastase digestion showed normal glycogen content without unusual intrahepatic inclusions; hepatic iron stores were normal.
Prior to transfer to our facility, he was initially stabilized with intravenous diltiazem drip 5 mg per hour titrated for rate control of his atrial fibrillation with rapid ventricular response, in combination with hydrocortisone 50 mg every eight hours and propylthiouracil (PTU) 150 mg every six hours for management of thyrotoxicosis. Due to concern for fulminant liver failure, urgent transfer was pursued to our facility. Upon arrival, the patient's thyrotoxicosis and resultant atrial fibrillation and diastolic heart failure were managed aggressively given his calculated Burch-Wartofsky score of 45. PTU was stopped in light of FDA black box warning, and methimazole was initiated at a dose of 20 mg every 8 hours; corticosteroids were continued for management of thyroid storm until normalization of total T3. The patient experienced gradual improvement in his free T4 (Figure ). His atrial fibrillation was managed with oral digoxin 125 µg after digitalizing doses and metoprolol 100 mg oral twice daily.
While the index of concern for acute liver failure prompted a swift and extensive investigation, it was entirely negative for primary hepatobiliary causes of his cholestasis including ERCP, EUS, and transjugular liver biopsy. Based on negative rheumatologic, autoimmune, and infectious causes workup, it was concluded that his cholestatic jaundice was related to Graves’ disease related thyrotoxicosis. This clinical hunch was further solidified with his clinical and metabolic improvement (Table ). Total bilirubin was 13.9 mg/dL on admission to the outside facility, peaking 17 days later at 39.1 mg/dL and improving to 14.0 mg/dL two weeks following discharge. An important point that needs to be made was his high bone-specific alkaline phosphatase, which was markedly elevated at 103 mcg/L (0-20), demonstrating a high bone turnover state related to his hyperthyroidism. The patient was discharged two weeks after his hospitalization with plans for definitive outpatient management of Graves’ disease.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [82.5, 'kg'], 'height': [1.7, 'm'], 'creatinine': [1.77, 'mg/dL'], 'age': [45, 'years']}",54.09144,51.38687,56.79601,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 45 years old. 
The concentration of creatinine is 1.77 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.7 m. The patient's weight is 82.5 kg. The patient's bmi is therefore 82.5 kg / (1.7 m * 1.7 m) = 28.54671 kg/m^2.The patient's BMI is 28.5, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.7 m, which is 1.7 m * 39.3701 in/m = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 65.93709 kg + 0.4 * (82.5 kg  - 65.93709 kg) = 72.56225 kg. The patient's adjusted body weight is 72.56225 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 45) * 72.56225 * 1) / (1.77 * 72) = 54.09144 mL/min. Hence, the patient's creatinine clearance is 54.09144 mL/min."
91,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4421407-1,Extracted,"A male patient, born in 1990, first presented with a kidney stone when he was 10 years old, but the stone had passed spontaneously, and no further testing was done at that time. At the age of 20, he presented with a second episode of renal colic. Proteinuria and microscopic haematuria were also noticed, for which he was referred to a nephrologist.
On examination, he was a lean young man with normal height and stature. Height was 175 cm, and weight was 59 kg. Systemic examination was unremarkable. Blood pressure was 107/74 mmHg.
Laboratory examination showed an elevated serum creatinine of 130 μmol/L (1.44 mg/dL) (eGFR 62 mL/min/1.73 m2). Serum alkaline phosphatase level was 122 U/L with elevated bone fraction of alkaline phosphatase. Other blood tests were normal. Twenty-four-hour urine collection showed proteinuria of 2.981 g/day consisting mainly of low-molecular-weight proteins. Calciuria was 8.3 mmol/day (334 mg/day) or 5.7 mg/kg/day (normal < 4). Urine sediment analysis was normal ().
Ultrasonography, CT scan and MRI revealed normal kidney size and contour but bilateral multiple cysts. The cysts were mainly localized in the cortex, and they had a benign simple appearance. Furthermore, bilateral nephrolithiasis and intraparenchymal calcification consistent with nephrocalcinosis were seen ( and ).
Renal biopsy had been performed in another centre and had shown normal light microscopy, normal electron microscopy, and negative immunofluorescence.
After the acute renal colic, transurethral stone extraction was performed. Stone analysis showed a stone consisting of calcium phosphate and calcium oxalate.
Family history was negative for renal disease or renal colic. The patient had no siblings. The parents underwent a renal ultrasound examination: both had normal morphology of their kidneys without cysts, but one asymptomatic nephrolithiasis was found in the father.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [30, 'years'], 'weight': [59.0, 'kg'], 'height': [175.0, 'cm'], 'creatinine': [1.44, 'mg/dL']}",62.59645,59.46663,65.72627,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 30 years old. 
The concentration of creatinine is 1.44 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 175.0 cm, which is 175.0 cm * 1 m / 100 cm = 1.75 m. The patient's weight is 59.0 kg. The patient's bmi is therefore 59.0 kg / (1.75 m * 1.75 m) = 19.26531 kg/m^2.The patient's BMI is 19.3, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 59.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 30) * 59.0 * 1) / (1.44 * 72) = 62.59645 mL/min. Hence, the patient's creatinine clearance is 62.59645 mL/min."
92,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-7728984-2,Extracted,"Case 2 A 67-year-old male (height, 173.6 cm; weight, 65.5 kg) was admitted for treatment of two hepatic nodules (16 mm at S2/4 and 12 mm at S2) suggestive of hepatocellular carcinoma in the left lobe of liver due to alcoholic hepatitis (T2, N0, M0, Stage II). Preoperative laboratory examination showed the following: PLTS, 109,000/µL; PT-ACT, 74%; PT-INR, 1.14; Fib, 203 mg/dL; D-dimer, 0.9 µg/mL; ALB, 3.8 mg/dL; T-Bil, 1.29 mg/dL; Cre, 0.9 mg/dL; eGFR, 65.1 mL/min/1.73 m2; CRP, 0.11 mg/dL; indocyanine green retention rate at 15 min (ICGR15), 45.7%; and a Child–Pugh A score of 6 points. Consequently, laparoscopic microwave coagulation therapy was planned for this patient. Since PVT and congestion of portal blood flow were observed in the left and 4th segment branch of the portal vein after microwave coagulation therapy by endoscopic ultrasonography during surgery, administration of antithrombin III concentrate with enoxaparin was administered for 5 days after surgery. Enhanced CT on POD 5 revealed a thrombosis in the segment 4th branch of the portal vein (Fig. ), and the patient was administered with 60 mg edoxaban as a result. Consciousness disorder occurred on POD 15, and CT examination revealed cerebellar hemorrhage with ventricular perforation (Fig. ). Blood examination at this time revealed the following: PLTS, 181,000/µL; PT-ACT, 52%; PT-INR, 1.39; Fib, 224 mg/dL; D-dimer, 5.6 µg/mL; ALB, 3.7 mg/dL; T-Bil, 1.23 mg/dL; Cre, 1.23 mg/dL; eGFR, 88.5 mL/min/1.73 m2. Although cerebellar hemorrhage was successfully treated by craniotomy hematoma evacuation with ventricular drainage, the consciousness disorder persisted. The patient was transferred to another medical facility for rehabilitation 49 days after brain surgery.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [67, 'years'], 'weight': [65.5, 'kg'], 'height': [173.6, 'cm'], 'creatinine': [0.9, 'mg/dL']}",73.78858,70.09915,77.47801,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 67 years old. 
The concentration of creatinine is 0.9 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 173.6 cm, which is 173.6 cm * 1 m / 100 cm = 1.736 m. The patient's weight is 65.5 kg. The patient's bmi is therefore 65.5 kg / (1.736 m * 1.736 m) = 21.73411 kg/m^2.The patient's BMI is 21.7, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 65.5 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 67) * 65.5 * 1) / (0.9 * 72) = 73.78858 mL/min. Hence, the patient's creatinine clearance is 73.78858 mL/min."
93,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5424333-1,Extracted,"A 69 year-old post-menopausal woman presented to her primary care physician with several months of increasing terminal hair growth on her face, torso, and arms, requiring shaving. There was also recession of the hairline, but no clitoromegaly. An initial endocrine evaluation demonstrated a markedly elevated serum total testosterone of 160 ng/dL (normal 5-32 ng/dL). ACTH level was normal, and the DHEA-S level was below assay detection. Initial transvaginal pelvic ultrasound demonstrated two simple cysts measuring 11 × 12 × 8 mm and 11 mm, and a 6 × 6 × 7 mm hypoechoic structure in the right adnexa; the left ovary was not visualized. A follow-up transvaginal pelvic ultrasound demonstrated a normal right ovary measuring 17 × 5 mm and a 13 × 9 mm left paratubal cyst; the left ovary was again not seen. An MRI of the pelvis did not demonstrate any adnexal masses, and an adrenal MRI was unremarkable as well.
Her past obstetrical history was notable for six pregnancies, one vaginal delivery, one tubal ectopic pregnancy, and four 2nd trimester spontaneous abortions. Her past medical history included Crohn’s disease status-post total colectomy and ileostomy. Her condition was complicated further by fistula formation through an appendectomy scar, stoma relocation, hernia repair, and development of a secondary large parastomal hernia. These operations resulted in scarring of the inside of her entire abdomen and replacement of her left lower quadrant by the large parastomal hernia. She also had chronic renal insufficiency with the serum creatinine elevated to 1.3-1.6 mg/dL. Other less significant factors in her medical history were renal stones status-post surgical removal, polymyalgia rheumatica, restless leg syndrome, asthma, arthritis, and osteoporosis, and depression.
On physical examination, the patient’s height was 63 in and weight was 157 lb (body mass index, 27.9 kg/m2). Her blood pressure was 122/81 mmHg. Skin examination confirmed the presence of extensive hirsutism of the face, neck and chin, and significant frontotemporal balding.
Her medications at initial evaluation included an albuterol inhaler, fluticasone, benzonatate, lactobacillus, calcium carbonate, cholecalciferol, cyanocobalamin, fenofibrate, omeprazole, zolpidem, citalopram, gabapentin, hydrocodone, pramipexole, furosemide, and zoledronic acid, none of which are known to have androgenic side effects.
Her family history was non-contributory.
Given the low levels of DHEA-S and normal adrenal imaging, an adrenal source for the testosterone was thought to be unlikely, and an ovarian source was suspected. The patient was referred to a gynecologic oncologist for possible surgical exploration and oophorectomy; however, she was deemed to be a poor operative candidate due to her multiple prior abdominal surgeries and massive lower left quadrant parastomal hernia. The patient was then referred to the reproductive endocrinology clinic for possible medical management.
Physical examination confirmed a cheerful, elderly white female with an evident shaven beard, and hairline recession. Laboratory testing demonstrated: testosterone 100.6 ng/dL (normal 2.9-40.8 ng/dL), FSH 112.1 mIU/mL (normal 25.8-134.8 mIU/mL), LH 62.4 mIU/mL (normal 7.7-58.5 mIU/mL), and estradiol 9 pg/mL (normal 0-47 pg/mL). Her hemoglobin A1c at this time was 5.9% (normal <6.0%). Lipid levels several months prior to presentation were: cholesterol 142 mg/dL (normal <200 mg/dL), HDL 51 mg/dL (normal >40 mg/dL), triglycerides 101 mg/dL (normal <150 mg/dL), and a calculated LDL 71 mg/dL (normal <129 mg/dL). A recommendation was given to start a GnRH agonist (leuprolide) to determine whether her testosterone production was gonadotropin-responsive. However, the patient did not start the GnRH agonist at that time for two reasons. First, the testosterone level had decreased somewhat on its own, though it was still quite elevated (160 ng/dL to 100 ng/dL). Second, the patient’s health insurance, Medicare, would not cover the off-label use of the medication, and the patient could not afford an out-of-pocket cost of ~ $1000/month for the intramuscular depot injection of leuprolide.
Over the next two years, the patient had a progression of her symptoms, including continued scalp hair loss requiring a wig, increased body and facial hair requiring daily shaving, increased body odor and libido, and a deepening of the voice. Several high-resolution transvaginal ultrasounds over these two years continued to demonstrate a grossly normal right ovary (1.7 cm × 0.5 cm) The left ovary was visualized on the most recent ultrasound, and was also grossly normal (1.7 cm × 0.5 cm). Total testosterone levels remained elevated up to 151 ng/dL (normal 8-60 ng/dL). Because the patient continued to be a high risk surgical candidate with no clear surgical target, the patient was referred back to the reproductive endocrinology clinic to reconsider medical management.
At the time of that appointment, her testosterone had increased to 187.4 ng/dL (normal 2.9-40.8 ng/dL) and free testosterone was 1.3 pg/mL (normal 0.14-1.72 pg/mL). The patient was started on 20 U (1 mg) of daily subcutaneous injection of leuprolide (~$300/month), which her husband helped her administer at home. Two weeks later, testosterone levels had normalized to 23.9 ng/dL, confirming gonadotropin-responsive testosterone secretion, most likely of ovarian etiology.
Unfortunately, two months after starting leuprolide, the patient reported significant “hot flashes”, difficulty sleeping, and feeling anxious and depressed. On laboratory evaluation, the total and free testosterone levels were suppressed to below assay range <2.5 ng/dL (normal 2.9-40.8 ng/dL) and <0.43 pg/mL (normal 0.14-1.72 pg/mL), respectively. The patient was advised to use half of an estradiol/norethindrone acetate patch twice weekly to relieve symptoms. However, her depressive symptoms and fatigue persisted even in the presence of add-back therapy, and given the high cost of the medication not covered by Medicare, the patient decided against pursuing further attempts at increasing progestin add-back therapy and discontinued the leuprolide one month later (three months after starting injections). At follow-up 2 weeks after discontinuing leuprolide, the patient’s testosterone had increased slightly to 6.5 ng/dL (normal 2.9-40.8 ng/dL).
Her lipid levels at this time were as follows: cholesterol 149 mg/dL (normal 100-199 mg/dL), HDL 39 mg/dL (normal 40-80 mg/dL), triglycerides 280 mg/dL (normal 35-150 mg/dL), and a calculated LDL 54 mg/dL (normal 50-129 mg/dL). The patient’s hemoglobin A1c level was 6.4% (normal <6.0%); with the aim of lowering her glucose levels and potentially ameliorating the hirsutism, she was subsequently started on metformin. At the last check-in, six months after discontinuing leuprolide therapy, her testosterone level increased to 85.24 ng/dL (normal 14-76 ng/dL), and she reported still having to shave her chin, but not as frequently as in the past. She reported being generally in good spirits, although low on energy secondary to having been recently hospitalized for medical complications unrelated to the elevated testosterone.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [69, 'years'], 'weight': [157.0, 'lbs'], 'height': [63.0, 'in'], 'creatinine': [1.6, 'mg/dL']}",31.39331,29.82364,32.96298,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 69 years old. 
The concentration of creatinine is 1.6 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 63.0 in, which is 63.0 in * 0.0254 m / in = 1.6002 m. The patient's weight is 157.0 lbs so this converts to 157.0 lbs * 0.453592 kg/lbs = 71.21394 kg. The patient's bmi is therefore 71.21394 kg / (1.6002 m * 1.6002 m) = 27.81099 kg/m^2.The patient's BMI is 27.8, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 63.0 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.0 (in inches) - 60) = 52.4 kg.
Hence, the patient's IBW is 52.4 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 52.4 kg + 0.4 * (71.21394 kg  - 52.4 kg) = 59.92558 kg. The patient's adjusted body weight is 59.92558 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 69) * 59.92558 * 0.85) / (1.6 * 72) = 31.39331 mL/min. Hence, the patient's creatinine clearance is 31.39331 mL/min."
94,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-3172664-1,Extracted,"On July 30, 2010, a 25-yr-old man was admitted to our hospital because of bilateral loin pain and nausea just after severe physical activity, and that was 2nd episode since 1 month before. He had played football and jogging on a regular base since he was 20 yr old, but there was no problem. He had completed military service in Korea without any medical problem. Five days prior to his visit, he had run thousands of meters for an employment test of a local security company. Just after the test, he got vomiting and loin pain. He endured the symptoms for a few days, but oliguria developed the day before he was admitted. He had experienced same symptoms after same physical activity test, 1 month ago. On admission, he had oliguria. Height and weight were 171 cm and 81 kg. Blood pressure was 143/85 mmHg and body temperature was 36.3℃. Physical examination did not reveal any abnormalities except bilateral costovertebral angle tenderness. Laboratory tests showed the following: hemoglobin 12.6 g/dL, hematocrit 35.9%, leukocyte count 6,160/µL with normal differentiation, platelet 209,000/µL, total protein 6.7 g/dL, serum sodium 139 mEq/L, potassium 4.4 mEq/L, chloride 107 mEq/L, BUN/Cr 29.0/4.31 mg/dL, CK/LDH 87/259 U/L, CRP 1.24 mg/dL, uric acid 2.0 mg/dL, spot urine sodium 45 mEq/L, urine myoglobin(-), 24-hr urine sodium 179 mM/day, potassium 3 mM/day, chloride 231 mM/day, uric acid 517 mg/day, Cr 1.68 g/day, fractional excretion of sodium 4.6%, and fractional excretion of uric acid 66%. The kidney sonographic image showed left kidney/right kidney 12.3/12.9 cm and no abnormal echo texture. After 9 days of admission, marked hypouricemia became apparent with the improvement of renal function: BUN was 18.4 mg/dL, serum creatinine 1.66 mg/dL, and serum uric acid 1.4 mg/dL. Gene analysis was done under the diagnosis of exercise-induced ARF associated with idiopathic renal hypouricemia. Peripheral blood sample for gene analysis was obtained from the patient. DNA sequence analysis of the exon 1, 3, and 4 (hot spot for mutations) of the URAT1 gene was undertaken. Gene analysis revealed a homozygous nonsense mutation (c.G774A, p.Trp258Stop) in the exon 4 of the URAT1 gene (). After 11 days of admission, he was discharged with the improvement of renal function (BUN 17.1 mg/dL, serum creatinine 1.14 mg/dL).","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [25, 'years'], 'weight': [81.0, 'kg'], 'height': [171.0, 'cm'], 'creatinine': [1.14, 'mg/dL']}",101.58552,96.50624,106.6648,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 25 years old. 
The concentration of creatinine is 1.14 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 171.0 cm, which is 171.0 cm * 1 m / 100 cm = 1.71 m. The patient's weight is 81.0 kg. The patient's bmi is therefore 81.0 kg / (1.71 m * 1.71 m) = 27.70083 kg/m^2.The patient's BMI is 27.7, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 171.0 cm, which is 171.0 cm * 0.393701 in/cm = 67.32287 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.32287 (in inches) - 60) = 66.8426 kg.
Hence, the patient's IBW is 66.8426 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 66.8426 kg + 0.4 * (81.0 kg  - 66.8426 kg) = 72.50556 kg. The patient's adjusted body weight is 72.50556 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 25) * 72.50556 * 1) / (1.14 * 72) = 101.58552 mL/min. Hence, the patient's creatinine clearance is 101.58552 mL/min."
95,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6107824-1,Extracted,"A 72-year-old woman experienced a light fall while taking a walk around her house on March 28, 2015. She visited the outpatient department of Konyang University Hospital after 3 days of injury with a complaint of mild pain in her left forearm although she was able to move the forearm. The patient weighed 66 kg and height was 159 cm. She had no prodromal symptom in the left forearm and had no restrictions in daily activities and walking. Furthermore, comorbidities such as hypertension, diabetes mellitus, thyroid disease, or gynecologic cancer, were absent. She was neither a smoker nor a drinker of alcohol. She had a past history of fracture of the left distal radius and ulnar styloid and was treated with closed reduction and percutaneous pinning in 2008. Since 2008, after the fracture of the left wrist, she had been continuously taking oral alendronate (a dosage of alendronic acid 70 mg/wk) of bisphosphonates for osteoporosis.
There were no signs of skin abrasion, ecchymosis, and swelling in the left forearm, but tenderness on the proximal border of the ulna was noted. She complained of discomfort during rotation of the injured forearm although range of motion of the left elbow and wrist was not limited. We confirmed a complete shaft fracture without comminution and minimal displacement in the proximal one-third of the ulna on radiographs of the left forearm (). This fracture showed a combined configuration of a transverse fracture line and an oblique fracture line. Radiographs of the contralateral forearm and both femurs did not show any findings of fracture. Also, the whole body bone scan showed no hot uptake except for hot-uptake in the left proximal forearm consistent with fracture (). Bone mineral density measured by dual-energy X-ray absorptiometry was 0.776 mg/cm2 (T score, −2.4), 0.858 g/cm2 (T score, −0.3) and 0.912 g/cm2 (T score, 0.1) at the lumbar spine, right hip, and left hip, respectively. The results of laboratory tests at the time of presentation were as follows: serum creatinine, 0.57 mg/dL (normal, 0.51 to 1.17 mg/dL); blood urea nitrogen, 9.8 mg/dL (normal, 8 to 20 mg/dL); alkaline phosphatase, 60 IU/L (normal, 40 to 120 IU/L); osteocalcin, 18.34 ng/mL (postmenopausal, 13 to 48 ng/mL); C-telopeptide, 0.593 ng/mL (postmenopausal, < 1.00 ng/mL); procollagen III peptide, 0.81 U/mL (normal, 0.3 to 0.8 U/mL); and urine N-telopeptide, 50.68 nM BCE/mM (normal, 5.0 to 65.0 nM BCE/mM).
The fracture was fixed using a 3.5-mm dynamic compression plate without bone graft (). We applied a cast immobilization to the patient for 4 weeks postoperatively and allowed light daily activities later. Union of the fracture was achieved at 6 months after surgery (). Bisphosphonate therapy was stopped immediately after surgery and restarted after the union of fracture.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [66.0, 'kg'], 'height': [159.0, 'cm'], 'creatinine': [0.57, 'mg/dL'], 'age': [72, 'years']}",80.68041,76.64639,84.71443,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 72 years old. 
The concentration of creatinine is 0.57 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 159.0 cm, which is 159.0 cm * 1 m / 100 cm = 1.59 m. The patient's weight is 66.0 kg. The patient's bmi is therefore 66.0 kg / (1.59 m * 1.59 m) = 26.10656 kg/m^2.The patient's BMI is 26.1, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 159.0 cm, which is 159.0 cm * 0.393701 in/cm = 62.59846 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.59846 (in inches) - 60) = 51.47646 kg.
Hence, the patient's IBW is 51.47646 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 51.47646 kg + 0.4 * (66.0 kg  - 51.47646 kg) = 57.28588 kg. The patient's adjusted body weight is 57.28588 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 72) * 57.28588 * 0.85) / (0.57 * 72) = 80.68041 mL/min. Hence, the patient's creatinine clearance is 80.68041 mL/min."
96,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5385993-1,Extracted,"A 14-year-old girl was admitted to our emergency department with a four-day history
of generalized myalgia, muscular weakness and dark urine. On the day of admission,
she noted much-reduced diuresis and had difficulty walking. During the previous
days, the patient had been participating in a dance festival in hot conditions.
There was no past history of muscle cramps or hospital admissions due to
rhabdomyolysis. She was the only child of non-consanguineous parents.
At presentation, she was dehydrated. Her blood pressure was 120/60 (90th
percentile). Her muscle strengths in the proximal and distal muscles of the upper
and lower extremities were 4/5. Deep tendon reflexes were normal, and there was no
neurologic deficit. The remainder of her physical examination was normal. Her weight
was 57kg, and her height was 165cm.
The laboratory evaluation revealed ARF with a blood urea nitrogen of 263mg/dL (range
19.3 - 44.9mg/dL), a blood creatinine of 9.59mg/dL (range 0.60 - 1.30mg/dL) and a
glomerular filtration rate calculated according to the original Schwartz formula of
11.6mL/min/1.73m2. The blood gases showed metabolic acidosis (pH
7.30; HCO3 17.7mmol/L; base excess - 7.9; lactate 1.4mmol/L). Blood
biochemistries were as follows: sodium 129mmol/L (range 136 - 145mmol/L), potassium
6.12 (range 3.4 - 5.1mmol/L), ionized calcium 1.03mmol/L (range 1.13 - 1.32mmol/L),
phosphorus 9.3mg/dL (3.1 - 5.5mg/dL), magnesium 1.8mg/dL (range 1.6 - 2.3mg/dL),
myoglobin 28173mg/dL (range 9 - 82mg/dL), creatine kinase > 400,000UI/L (range 28
- 142UI/L), aspartate aminotransferase 3266UI/L (range 0 - 26), alanine
aminotransferase 1310UI/L (range 19 - 44UI/L).
Because of massive rhabdomyolysis, the patient was admitted to our pediatric
intensive care unit and was given intravenous fluid combined with diuretic therapy
to reverse ARF, glucose and insulin therapy to correct hyperkalemia and calcium
gluconate to prevent cardiac arrhythmias secondary to ion changes. During the first
hours of admission, she presented anuria that was unresponsive to medical therapy.
After eight hours of receiving supportive therapy, she was started on continuous
veno-venous hemodiafiltration (Gambro Prismaflex® System, Lisbon;
Portugal).
A hemodialysis catheter (12F; triple lumen) was inserted in the right femoral vein.
Hemodiafltration was performed using the hemofilter ST 60, and heparin was the
anticoagulant chosen. The following initial settings were used: blood-pump
150mL/min, dialysate (Prismasol 4®) 1000mL/hr, pre-filter
replacement solution (Prismasol 4®) 500mL/hr, post-filter
replacement solution (Prismasol 4®) 500mL/hr and fluid removal
50mL/hr. During the first two days of therapy, the main problem with
hemodiafiltration was easy coagulability of the hemofilter due to high levels of
myoglobin in circulation. To overcome this problem, higher pre-dilution flow rates
were used (maximum 1500mL/h). After 48 hours, she had asymptomatic hypophosphatemia
of 2.7mg/dL that was corrected after adding phosphorous to the replacement
solutions. On day 5, intermittent hemodialysis was started, and three sessions on
alternate days were performed. A calcium antagonist was prescribed on day six due to
worsening hypertension.
Signs and symptoms were controlled with medical treatment and renal replacement
therapy. Creatinine kinase and myoglobin returned to normal values in two weeks. Her
diuresis started to recover after the second day of therapy. At discharge, her renal
function was recovering, and she had a glomerular filtration rate of
88.9mL/min/1.73m2.
Regarding the investigation of the underlying insult, an acylcarnitine analysis by
tandem mass spectrometry of the patient's dried blood spot revealed a deficiency of
very long-chain acyl-CoA dehydrogenase (VLCAD). A genetic study revealed the
following mutations in compound heterozygosity of the VLCAD gene: p.P65Tfs*7 (c.
187_192insA) and p.R336H (c.1097G > A).
Frequent meals with carbohydrate-rich intake before exercise and restriction of
long-chain fatty acids intake along with medium-chain fatty acid supplementation
were recommended to prevent further attacks.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [14, 'years'], 'weight': [57.0, 'kg'], 'height': [165.0, 'cm'], 'creatinine': [9.59, 'mg/dL']}",8.82721,8.38585,9.26857,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 14 years old. 
The concentration of creatinine is 9.59 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 57.0 kg. The patient's bmi is therefore 57.0 kg / (1.65 m * 1.65 m) = 20.93664 kg/m^2.The patient's BMI is 20.9, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 56.90954 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 14) * 56.90954 * 0.85) / (9.59 * 72) = 8.82721 mL/min. Hence, the patient's creatinine clearance is 8.82721 mL/min."
97,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6031942-1,Extracted,"We report the case of a 67-year-old male with kidney dysfunction. His past medical history included thyroidectomy due to hyperthyroidism at the age of 30 years. In 2006, the patient was admitted to our hospital for cerebral infarction, diabetes, hypertension, hyperuricemia, and dyslipidemia. Since that time, the patient had been prescribed the following medicines: levothyroxine sodium hydrate, 25 μg/day; amlodipine basilate OD, 5 mg/day; valsartan, 160 mg/day; feburostat, 10 mg/day; and atorvastatin calcium hydrate, 5 mg/day. Rapid types of insulin, such as the 16-unit Novo RapidN and the 10-unit Novolin RN had been used. The levels of uric acid are 4.90 mg/dL, and blood pressure was 140/70 mm Hg. The levels of FT3, FT4, TSH, and total cholesterol and triglyceride were within normal limits. An ophthalmologist diagnosed him with diabetic proliferative retinopathy and performed photocoagulation therapy. In November 2015, a serum urea nitrogen level of 56.0 mg/dL, a serum creatinine (s-Cr) level of 3.9 mg/dL and an estimated glomerular filtration rate (eGFR) of 13.4 mL/min indicated renal dysfunction at another division.
Due to a recent increase in frothy urine, the patient was transferred to our nephrology division for a further treatment. At the time of the first visit to our division, body height was 160 cm and weight was 68 kg (BMI: 26.6). He showed slight obesity (obesity criteria in Japan: a BMI of more than 25.0). Laboratory data from the time of his first visit to our division in March 2016 showed a fasting plasma glucose level of 121 mg/dL and a HbA1c (national and glycohemoglobin standardization program: NGSP) of 6.9%. Thus, we moved him to a DPP-4 inhibitor, i.e., saxagliptin hydrate of 5 mg/day. High-density urine and a strongly positive proteinuria quantified at 2.62 g/gCr were found. Urine ketone bodies were negative, and there was a negative urine occult blood reaction, which resulted in a clinical diagnosis of diabetic nephropathy. The frothy (with small bubbles) urine meant that there was a high dose of protein in the urine. A serum urea nitrogen level of 60.7 mg/dL, a s-Cr level of 4.9 mg/dL, and an eGFR of 10.2 mL/min showed a progressive renal dysfunction. Antiglutamic acid decarboxylase antibodies in sera were negative (normal value: < 1.5 U/mL).
In the Japanese Society of Nephrology (JSN) classification, the causal disease, eGFR, and albuminuria (proteinuria) levels have to be determined. eGFR is divided into 5 stages, from GFR 1 to 5, and albuminuria (proteinuria) is divided into 3 stages, from A1 to 3, as shown in Figure . According to this classification, he was diagnosed as follows; chronic kidney disease (CKD); cause diabetes (type 2); GFR G5, (eGFR range: < 15 min/mL); and albuminuria, A3 (albuminuria range: > 300 mg/gCr). A definite diagnosis of diabetic nephropathy could not be made without renal biopsy. Kidney function, i.e., eGFR, was not improved by previous medications. We added on a minimal dosage of AST-120 (Kremezin®) of 2 g/day because of his severe constipation. After 3 months of AST-120 therapy, eGFR increased to 18.1 mL/min/1.73m2 (with a s-Cr of 2.90–2.72 mg/dL). Although he used some laxative products (senna 1 g/day and sennnoside 12 mg/day), he could not continue to take AST-120 and then completely stopped the drug 8 months after starting. Kidney function then abruptly declined (eGFR of 7.3 mL/min/1.73 m2; s-Cr of 6.7 mg/dL) and progressed to end-stage kidney disease (ESKD), as shown in Figure . In June 2017, he was introduced to hemodialysis (HD).","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [68.0, 'kg'], 'height': [160.0, 'cm'], 'creatinine': [4.9, 'mg/dL'], 'age': [67, 'years']}",12.68999,12.05549,13.32449,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 67 years old. 
The concentration of creatinine is 4.9 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.6 m * 1.6 m) = 26.5625 kg/m^2.The patient's BMI is 26.6, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.99216 (in inches) - 60) = 56.88197 kg.
Hence, the patient's IBW is 56.88197 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 56.88197 kg + 0.4 * (68.0 kg  - 56.88197 kg) = 61.32918 kg. The patient's adjusted body weight is 61.32918 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 67) * 61.32918 * 1) / (4.9 * 72) = 12.68999 mL/min. Hence, the patient's creatinine clearance is 12.68999 mL/min."
98,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-2966711-1,Extracted,"A 70-year-old woman (height: 156 cm, body weight: 48 kg) with lower abdominal pain was admitted and associated symptoms were fever, nausea, vomiting and diaphoresis which started from the day previous to her admission. On abdominal computed tomography (CT), right ovarian cyst in size of 2.5 cm was found, and an acute appendicitis was diagnosed by an abdominal ultrasonography. An elective operation was scheduled under the collaboration of gynecology and general surgery.
In the patient's past medical history, she had taken digoxin, dilatrend, nitrate, telmisartan, and thiazide for 5 years because of hypertension, congestive heart failure, AF, and right coronary artery 90% stenosis on coronary angiography. An electrocardiogram before operation showed AF with ventricular response 90-100 times/min, left ventricular hypertrophy. Cardiomegaly and pleural effusion were found on chest X-ray. On transthoracic echocardiography (TTE), ejection fraction was 55% and left atrial enlargement, right atrial enlargement and eccentric hypertrophy with decreased mobility of the inferior wall of the left ventricle were shown. A moderate aortic valve insufficiency, aortic valve sclerosis, mild aortic stenosis, and severe posterior mitral valve leaflet calcification were also found and the width of mitral valve measured by pressure half-time was 1.92 cm2. A chronic cerebral infarction in the right posterior cerebral artery was found on brain CT with symptoms of dysarthria. Signs of dehydration on physical examinations with prerenal azotemia of FeNa 0.1% and serum creatinine of 1.7 mg/dl on blood test led us to start an fluid therapy. The serum creatinine was decreased to 1.3 mg/dl after the fluid therapy.
Glycopyrrolate 0.2 mg IM was premedicated at 30 minutes pre-operation. The patient's blood pressure (BP) was 130/50 mmHg, ventricular response 90-100 times/min, and arterial oxygen saturation 97% when she arrived at the operation room. A right radial artery was cannulated with great caution before the induction of anesthesia. The induction of anesthesia was initiated with injecting 2 ml of 2% lidocaine to reduce injection pain and propofol (Diprivan® AstraZeneca, UK) and remifentanil (Ultiva® GlaxoSmithKline, UK) were injected using a target-controlled infuser (Orchestra® Fresenius Vial, France). After confirming the patient's being unconscious, rocuronium 40 mg was injected and then endotracheal intubation was performed with close monitoring of arterial blood pressure. Ventilation with 100% O2 was given while central venous catheterization was placed in right jugular vein. After the induction of anesthesia, the patient's vital sign showed no hemodynamic disorder with systolic BP 130-150 mmHg, diastolic BP 40-60 mmHg, ventricular response approximately 100-110 times/min, and central venous pressure (CVP) 8-9 mmHg. The effect site concentration was injected as 2.5-3.0 µg/ml of propofol and and 2.0 ng/ml of remifentanil.
After the lower abdomen laparotomy at obstetrics and gynecology for the right ovary cystectomy, a small bowel infarction from jejunum to ileum was detected. The authors suspected a mesenteric arterial embolism based on the patient's previous medical history. A transesophageal echocardiology (SonoSite MicroMaxx, Bothell, USA) probe was immediately inserted and a spontaneous echo contrast (SEC or ""smoke"") in the left atrium (LA) and a 13 × 18 mm size thrombus in the LAA was detected (). The findings in TEE made a mesenteric arterial embolism highly suspicious for the cause of the small bowel infarction. A segmental resection and intestinal anastomosis were performed by the department of general surgery. No hemodynamic instability was observed through whole procedure of operation and the patient was transferred to the intensive care unit with endotracheal tube inserted. After confirming her awareness and the absence of any neurologic disorder, extubation was performed in intensive care unit. To minimize the risk of hemorrhage of the anastomosis site, anticoagulation was performed with caution under the collaboration of general surgery and cardiology. It was started with low molecular weight heparin 3 days after the operation and oral warfarin was added 5 days after the operation. After 4 weeks, cardioversion was successfully performed to turn into normal sinus rhythm.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [70, 'years'], 'weight': [48.0, 'kg'], 'height': [156.0, 'cm'], 'creatinine': [1.3, 'mg/dL']}",30.51282,28.98718,32.03846,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 70 years old. 
The concentration of creatinine is 1.3 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 156.0 cm, which is 156.0 cm * 1 m / 100 cm = 1.56 m. The patient's weight is 48.0 kg. The patient's bmi is therefore 48.0 kg / (1.56 m * 1.56 m) = 19.72387 kg/m^2.The patient's BMI is 19.7, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 48.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 70) * 48.0 * 0.85) / (1.3 * 72) = 30.51282 mL/min. Hence, the patient's creatinine clearance is 30.51282 mL/min."
99,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6194623-1,Extracted,"A 79-year-old woman initially presented with diabetes in 2008. Her HbA1c level was 8.8%, and treatment with an oral hypoglycemic agent was initiated. At that time, the patient also reported swelling on the anterior surface of her neck in the area of the thyroid gland; therefore, she sought consultation at an ambulatory otolaryngology clinic. She was diagnosed with papillary thyroid carcinoma with metastasis to the right cervical lymph nodes. In 2011, a pulmonary tumor was detected; it was resected via thoracoscopy and a diagnosis of metastatic thyroid cancer was confirmed. In December 2012, her serum creatinine level was 0.57 mg/dL, with no evidence of proteinuria. In 2013, the patient underwent resection of the right lobe of the thyroid gland, including bilateral dissection of the paratracheal lymph nodes and the right parotid lymph node.
In January 2016, the patient experienced exacerbation of her unresectable thyroid cancer; therefore, oral administration of 10 mg lenvatinib was initiated.
The findings of the pretreatment laboratory assessment were as follows: normal blood pressure (118–132/64–77 mmHg); creatinine (Cr), 0 .72 mg/dL; and albumin (Alb), 3.8 g/dL, respectively, and her estimated glomerular filtration rate (eGFR) was 58 mL/min/1.73 m2. In addition, the urine sample test showed negative results for red blood cells (1–4/HPF), and the urine qualitative analysis showed negative results for protein. However, after initiation of treatment (Fig. ), the patient developed hypertension that required treatment with candesartan (8 mg/day). By February 2016, her Cr level had increased to 0.82 mg/dL, and her eGFR and Alb levels had decreased to 51 mL/min/1.73 m2 and 3.5 g/dL, respectively. She also developed hypertension (blood pressure, 140–170/60–70 mmHg). Based on these findings, we added a daily dose of amlodipine (5 mg/day) to her treatment; thereafter, the dose was increased to 10 mg/day. By March 2016, her Cr level continued to increase to 0.84 mg/dL, and her eGFR and Alb level continued to decrease (49 mL/min/1.73 m2 and 3.0 g/dL, respectively). Her blood pressure increased to 150/60 mmHg, and the candesartan dose was increased to 12 mg/day. However, she developed lower limb edema. In April 2016, she was diagnosed with acute kidney injury and nephrotic syndrome. Development of generalized edema and weight gain were noted, her Cr level increased to 1.17 mg/dL, and her eGFR decreased to 34 mL/min/1.73 m2. Measurements of other relevant parameters were as follows: total protein (TP), 5.1 mg/dL; Alb, 2.5 mg/dL; total creatinine (TC), 329 mg/dL; low-density lipoprotein (LDL), 204 mg/dL; and urinary protein, 11.78 g/gCr. The patient was referred to our institution for further evaluation and treatment.
On admission, the patient’s medications included lenvatinib (10 mg), glimepiride (0.5 mg), pioglitazone (915 mg), alogliptin (925 mg), candesartan (12 mg), and amlodipine (10 mg). On physical examination, her height was 155 cm, weight was 55 kg (usual weight, 44 kg), body mass index was 21.4 kg/m2, blood pressure was 142/60 mmHg, heart rate was 72 beats/min, temperature was 36.2 °C, and respiratory rate was 20 breaths/min. A surgical scar from her thyroidectomy was visible on the anterior aspect of her neck. In addition, bilateral edema of her lower limbs was evident. Significant medical history included a uterine myoma, appendicitis, and a fundal hemorrhage due to diabetic retinopathy at the ages of 50, 51, and 77 years, respectively. Her family history was negative, and she had no known allergies. The patient was a non-smoker and only consumed alcohol socially. Her urine and blood laboratory data are summarized in Table . Large quantities of urine protein and urine occult bleeding, anemia, renal function disorder, hypoalbuminemia, and hypercholesterolemia were observed. Urinary Bence-Jones proteins, increased ferritin, hypergammopathy, low-complement blood symptoms, and ANCA and ds-DNA antibodies were not observed, however.
Multiple pulmonary metastases were observable on computed tomography (CT) imaging. Although there was no evidence of malformation of the kidneys, generalized edema and thoraco-abdominal fluid were observed.
Considering the development of elevated blood pressure and nephrotic syndrome after administration of lenvatinib, drug-induced nephrotic syndrome was suspected as the primary clinical diagnosis. Therefore, lenvatinib treatment was discontinued.
The patient’s diabetes was controlled well with the use of oral hypoglycemic agents (HbA1c of 5.7%). However, her blood pressure remained high at 140–145/50–60 mmHg despite treatment with oral antihypertensive agents. Because of her history of diabetic retinal hemorrhage, papillary thyroid carcinoma with relatively new onset of distant metastasis, hematuria, low selectivity index (0.247), information based on the negative findings of hypocomplementemia, absence of MPO-ANCA, PR3-ANCA, ds-DNA antibodies, we thought that minimal change nephrotic syndrome (MCNS), membranoproliferative glomerulonephritis (MPGN), and rapidly progressive glomerulonephritis (RPGN) would not be correct diagnoses.
Because it is necessary to differentiate FSGS from diabetes nephrosis syndrome and secondary membranous nephropathy due to a malignant tumor, and because most TKIs are type I or type II and lenvatinib has novel binding ability (type V), we performed a renal biopsy.
Renal biopsy using light microscopy (Fig. ) revealed that 7 of 16 glomeruli had complete hyalinization, and that glomeruli with incomplete hyalinization showed partial glomerular collapse (arrow in Fig. ); FSGS was confirmed because the glomeruli showed lobular and segmental expansion. Vacuolar degeneration of the podocytes (see arrow in Fig. ) and enlarged endothelial cells with a thickened loop were evident, suggesting endothelial injury (arrow head in Fig. ). Thrombotic microangiopathy was absent. The mesangial matrix slightly increased, but the mesangial cells did not increase (Fig. ). Periodic acid methenamine silver (PAM) staining showed mesangial interposition-like changes and a duplicated basal membrane (arrow head in Fig. ). The endarterium was slightly thickened and the arterioles showed partial hyaline consolidation.
Immunofluorescence (Fig. ) of the IgG showed nonspecific staining, no linear pattern, and negative results. Only IgA, IgM, C3, and C4 were granular and slightly positive in the mesangial areas, and there was no staining of the loop wall. C1q was negative.
Vacuolar degeneration of podocytes (arrow in Fig. ) was observed on electron microscopy (Fig. ). The loops were thickened and a duplicated basal membrane was observed. Mesangial interposition-like changes were found (arrow in Fig. ), and endothelial cells invaded the basal membrane (arrow head in Fig. ).
Electron-dense deposits suggesting immune complexes were not observed. Foot process effacement was almost 60–70%. It suggested that this is a case of podocytopathy and not a secondary effect of hypertensive/hyperfiltration injury.
The mesangial matrix slightly increased, but there was no nodular glomerulosclerosis such as a Kimmelstiel-Wilson lesion or IgG immunofluorescence staining with a linear pattern along the basement membrane, thereby suggesting that the diagnosis was not advanced stage disease that could lead to diabetes nephrosis syndrome. The glomeruli showed lobular expansion, but mesangial cells were not increased and an electron-dense deposit was not observed; therefore, the diagnosis was not MPGN.
With regard to morphologic variants of FSGS based on the Columbia classification, the collapsing variant of FSGS is diagnosed because of the presence of collapsed glomeruli.
Treatment included the discontinuation of lenvatinib, dietary modifications, and the use of palliative diuretics. The patient’s weight decreased over the course of the subsequent 2 weeks (loss of 8.7 kg from admission weight) but showed improvement in the edema of her lower limbs. Glycemic control was achieved. Because nephrotic syndrome was improved after discontinuation of lenvatinib therapy, and because diabetic changes in the kidneys including increased thickness of the mesangial matrix were mild, we confirmed a diagnosis of secondary FSGS caused by lenvatinib.
The patient was discharged on day 11 after admission. Although her renal function status did not improve from that on admission (Cr, 1.16 mg/dL; eGFR, 35 mL/min/1.73 m2) to that at discharge (Cr, 1.17 mg/dL; eGFR, 34 mL/min/1.73 m2), her proteinuria did improve from 11.8 g/day on admission to 5.4 g/day at discharge. She was followed-up on an outpatient basis, and her proteinuria continued to gradually decrease over time. In July 2017, her Cr level was 1.04 mg/dL and eGFR was 39 mL/min/1.73 m2, with complete remission of urinary protein (qualitative urinary protein, 116 mg/gCr) and no evidence of hematuria. A period of 15 months was required to achieve complete remission after discontinuation of lenvatinib treatment. Chronic kidney disease (CKD; stage G3bA1) was diagnosed. Regular follow-up examinations are performed at our outpatient clinic.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [79, 'years'], 'weight': [55.0, 'kg'], 'height': [155.0, 'cm'], 'creatinine': [1.17, 'mg/dL']}",29.45455,27.98182,30.92728,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 79 years old. 
The concentration of creatinine is 1.17 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.55 m * 1.55 m) = 22.89282 kg/m^2.The patient's BMI is 22.9, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 47.85442 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 79) * 47.85442 * 0.85) / (1.17 * 72) = 29.45455 mL/min. Hence, the patient's creatinine clearance is 29.45455 mL/min."
100,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-7234858-1,Extracted,"On April 6, 2018, a 49-year-old Korean man with end stage renal disease (ESRD) was transferred to our hospital for kidney transplantation. He visited emergency room at local hospital due to nausea and vomiting one month ago. Laboratory findings revealed renal failure (blood urea nitrogen 137 mg/dL, serum creatinine 20.5 mg/dL) and anemia (hemoglobin 9.1 g/dL) and metabolic acidosis on arterial blood gas analysis (pH 7.3, bicarbonate 16.4 mEq/L). Routine urinalysis revealed no proteinuria or hematuria. Complement levels were normal range and autoantibodies (Antinuclear antibody and antineutrophil cytoplasmic antibody) were negative. Chest PA showed no cardiomegaly or pulmonary edema, and Kidney-Ureter-Bladder radiography (KUB) was non-specific. Kidney ultrasonography revealed diffusely increased echogenicity and kidney size was smaller than normal (8.2 × 5.0 cm). The abdominal computed tomography showed no evidence of stone in both kidneys ().
Due to uremic symptoms, emergency hemodialysis was started and the kidney biopsy was performed to identify the cause of ESRD. The kidney biopsy showed foci of tubular damage with deposition of translucent crystals of different shapes which are predominantly intraluminal, and confirmed these crystals as calcium oxalate crystals using polarized light (). Final report of pathology was chronic tubulointerstitial nephritis with oxalate crystal deposits and a change of ESRD.
He was an office worker. He received regular national health examination including renal function and urinalysis, and both results were normal until two years before admission. His height and body weight were 167 cm and 70 kg. Body mass index was 25 kg/m2. Review of medical history revealed no history of kidney stone, diabetes, hypertension and operation. He had no medical family history. From the drug history, he had taken Chaga mushroom powder for 5 years due to atopic dermatitis. Initially, he had taken 3 g daily for 4 years following company's recommendation and 9 g of powder for another year because his symptom did not improve.
Based on pathologic finding (oxalate nephropathy) and drug history (long-term exposure to Chaga mushroom), we suspected the association between Chaga mushroom and oxalate nephropathy in our case. Thus, we requested oxalate content of remained Chaga mushroom to researcher/clinical pharmacology division of Catholic Medical center clinical research coordinating center of Korea. Measurement of oxalate was performed by high performance liquid chromatography (HPLC), and analysis revealed extremely high content of oxalate in Chaga mushroom powder (0.14 g of oxalate per 1 g of Chaga mushroom powder).
We finally diagnosed this case as Chaga mushroom-induced oxalate nephropathy with kidney biopsy findings, drug history and high content of oxalate. Clinical course of our case was unfavorable. Renal function has not recovered and he is on maintenance hemodialysis for 18 months.
This study was approved by the Institutional Review Board (IRB) of the Catholic University of Korea (IRB No. 2019-3713-0001) and an informed consent was received from the patient and a caregiver. The images are published under agreement of the patient.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [49, 'years'], 'weight': [70.0, 'kg'], 'height': [167.0, 'cm'], 'creatinine': [20.5, 'mg/dL']}",4.06493,3.86168,4.26818,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 49 years old. 
The concentration of creatinine is 20.5 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 167.0 cm, which is 167.0 cm * 1 m / 100 cm = 1.67 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.67 m * 1.67 m) = 25.0995 kg/m^2.The patient's BMI is 25.1, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 167.0 cm, which is 167.0 cm * 0.393701 in/cm = 65.74807 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.74807 (in inches) - 60) = 63.22056 kg.
Hence, the patient's IBW is 63.22056 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 63.22056 kg + 0.4 * (70.0 kg  - 63.22056 kg) = 65.93234 kg. The patient's adjusted body weight is 65.93234 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 49) * 65.93234 * 1) / (20.5 * 72) = 4.06493 mL/min. Hence, the patient's creatinine clearance is 4.06493 mL/min."
101,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5297160-1,Extracted,"A 61-year-old woman was admitted because of sudden onset of confusion and slurred speech. In preparation for an elective outpatient colonoscopy she had commenced bowel preparation four hours earlier with sodium picosulfate/magnesium citrate (PICOLAX ®). As instructed, she had ingested two liters of water and two liters of tea, albeit within two hours. Shortly thereafter, she felt nauseous, dizzy and vomited repeatedly. Her husband found her confused with unintelligible speech and unsteady gait and called the ambulance.
On physical examination, the patient appeared agitated and her speech was incomprehensible. She weighed 56 kg and her height was 168 cm (BMI 19.9 kg/m2). Vital signs were as follows: Afebrile, blood pressure 132/66 mmHg, pulse 82 beats/min. The patient was clinically euvolemic and could follow verbal commands. No lateralizing signs were found on neurological examination but generalized tremor was present. Acute CT scanning of the brain did not reveal any abnormalities.
Her medical records showed a history of hypothyroidism for which she took levothyroxine. She was a non-smoker and did not drink alcohol. Family history was unremarkable and there was no history of diuretic use or anorexia, as corroborated by her husband.
In the emergency department, biochemistry results were as follows: Serum sodium 122 mmol/l, potassium 3.1 mmol/l, chloride 87 mmol/l, BUN 14.8 mg/dl, creatinine 1.1 mg/dl, uric acid 4.1 mg/dl, glucose 108 mg/dl. Serum osmolality was 251 mOsm/kg. In view of the patient’s symptoms and the clear time of onset, acute hyponatremia was deemed likely and treatment with hypertonic saline (3%) at a rate of 50 ml/h was commenced. Urine osmolality was not done on admission but was 232 mOsm/kg with a urinary sodium of 39 mmol/l when tested two hours later. Thyroid-stimulating hormone was suppressed under replacement therapy. The sodium level increased to 128 mmol/l within the ensuing four hours. In parallel, the patient’s symptoms abated. Twelve hours after admission, she had voided 2600 ml of urine and her mentation and electrolytes had normalized.
On further questioning, it transpired that the patient had had very limited food intake prior to the scheduled procedure. On the day before admission (two days before the endoscopy appointment), her diet consisted of carrot-ginger soup with white bread for lunch and rusk with tea for dinner. The next day, a breakfast consisting of two slices of plain toast and a cup of coffee, followed by a broth at lunchtime, was all she had to eat. No additional salt had been added to her meals. Furthermore, the patient had been taking a nonsteroidal anti-inflammatory drug (NSAID) for the last five days because of shoulder pain (Diclofenac 50 mg bid). A diagnosis of hyponatremic encephalopathy due to acute water intoxication facilitated by poor dietary solute intake was made. On follow-up appointment 1 week later, the patient was well and electrolytes were normal. Adrenal function was tested and found to be intact.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [61, 'years'], 'weight': [56.0, 'kg'], 'height': [168.0, 'cm'], 'creatinine': [1.1, 'mg/dL']}",47.4798,45.10581,49.85379,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 61 years old. 
The concentration of creatinine is 1.1 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 56.0 kg. The patient's bmi is therefore 56.0 kg / (1.68 m * 1.68 m) = 19.84127 kg/m^2.The patient's BMI is 19.8, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 56.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 61) * 56.0 * 0.85) / (1.1 * 72) = 47.4798 mL/min. Hence, the patient's creatinine clearance is 47.4798 mL/min."
102,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-7588675-1,Extracted,"The patient was an 18-year-old man who had been complaining of exertional cough and dyspnea for 4 months. He had no medical and familial history. He graduated from junior high school but did not go to high school or work. He presented to our hospital after visiting a general practitioner for epigastric discomfort and nausea. At that time, urinalysis revealed massive proteinuria. On the next day, he was referred and admitted to our hospital for a thorough examination. He had no history of hypertension, human immunodeficiency virus (HIV) infection, drug abuse, ureteral reflux, premature birth, or any other diseases.
On admission, physical examination revealed a body temperature of 36.7°C, a body weight of 62 kg, and a height of 168 cm. Blood pressure was 157/85 mm Hg. There were evident leg edema, bilateral inguinal lymphadenopathy, and no skin lesions. The laboratory findings revealed decreased serum total protein (5.9 g/dL) and albumin (2.6 g/dL); normal serum creatinine (SCr, 0.9 mg/dL) and eGFR (95 mL/min/1.73 m2); elevated LDL cholesterol (224 mg/dL); and slightly elevated serum calcium (10.6 mg/dL). BNP level was remarkably elevated (1,850 pg/mL). Urinalysis revealed a subnephrotic level of urinary protein (3.0 g/day), microhematuria (5–9/HPF), no leukocyturia, and no bacteria. The soluble interleukin 2 receptor level was elevated (2,905 U/mL); serum angiotensin-converting enzyme (ACE) level was normal (14.2 U/L); renin activity was remarkably elevated (39 ng/mL/h); plasma aldosterone level was within normal limits (184 pg/mL). The urinary N-acetyl-glucosaminidase level was remarkably elevated (85.6 IU/L). Hepatitis B virus surface antigen, hepatitis C virus antibody, and HIV antigen and antibody were all negative. Immunoglobulins, complements, rheumatoid factor, antinuclear antibody, and antineutrophil cytoplasmic antibodies were all negative. Tuberculin test was negative.
The chest X-ray showed enhanced pulmonary congestion and no detectable hilar lymphadenopathy. In contrast, chest computed tomography (CT) revealed hilar lymphadenopathy without fibrosis in any lung field. Furthermore, abdominal CT revealed bilateral normal-sized kidneys and bilateral inguinal lymphadenopathy. Gallium-67 scintigraphy revealed uptakes in the pulmonary hilum, mediastinum, bilateral submaxillary glands, bilateral parotid glands, and bilateral inguinal regions. Echocardiography detected severe cardiac dysfunction (ejection fraction 25%), diffuse akinesis of the ventricular wall, and atrial septal defect, but it did not detect thinning of the interventricular septum base. However, electrocardiogram-gated cardiac CT revealed thinning of the interventricular septum base, and this finding was supported by a cine magnetic resonance imaging. Cardiac dysfunction and thinning of the ventricular septum base were supportive findings of cardiac sarcoidosis.
On the first admission, the patient received treatment for heart failure and hypertension, including temocapril hydrochloride, calcium channel antagonist, carvedilol, spironolactone, and carperitide. Thereafter, the urinary protein level decreased to <1 g/day, and the heart failure and hypertension improved. On the 30th hospital day, the patient was discharged. The inguinal biopsy that was performed as outpatient procedure detected granulomas; therefore, the diagnosis was sarcoidosis. On the 69th day, the SCr level gradually increased to 2.00 mg/dL (eGFR 39.4 mL/min/1.73 m2) and the urinary protein-to-creatinine ratio increased to 3.2 g/gCr. At this time, the serum albumin and LDL cholesterol levels were 3.7 g/dL and 134 mg/dL, respectively. Therefore, he was readmitted for renal investigation.
Subsequent renal biopsy revealed the presence of 32 glomeruli, 8 of which showed global sclerosis. Mesangial proliferation, crescent formation, or epithelial change was not observed. In 4 glomeruli, segmental sclerotic lesions were found near the vascular pole and were classified as the perihilar variant of FSGS [] (Fig. ). The diameter of the Bowman's space of the FSGS lesions was maintained at approximately 200–230 μm. Conversely, several ischemic glomerular changes were found, including atrophic Bowman's capsule, glomerular tuft shrinking, and global sclerosis (Fig. ). Tubulointerstitial fibrosis and inflammatory cell infiltration accounted for 70% of the renal parenchyma. Mononuclear cell infiltration, giant cells, and noncaseous granulomas in the tubulointerstitium were noted. The majority of the granulomas involved small arteries and/or arterioles, many of which had intimal wall thickness, reduplicated internal elastic lamina, and narrow lumen (Fig. ). Many of the epithelioid cells of these granulomas were arranged concentrically around the artery/arteriole and formed a multilayer structure.
Immunostaining by an enzyme-labeled antibody method revealed focal and segmental deposits of IgM (1+) in the glomerular lesions. In the tubulointerstitium, no significant deposits of IgG, IgA, IgM, C1q, and C3 were found. Immunohistochemistry revealed CD68-positive macrophage accumulation in the tubulointerstitial granulomas but not in the glomeruli. Electron microscopy did not detect any glomeruli. Based on these findings, the pathological diagnosis was tubulointerstitial granulomatous angiocentric vasculitis with FSGS.
He received oral prednisolone 30 mg/day after the renal biopsy revealed renal sarcoidosis. At 27 days after the initiation of steroid therapy, the SCr level decreased to 1.60 mg/dL (eGFR 50.2 mL/min/1.73 m2), with a simultaneous decrease in the urinary protein-to-creatinine ratio to <0.5 g/gCr. Thereafter, oral prednisolone was tapered to 25 mg/day, and the patient was discharged on the 38th day of the second hospital stay (the 108th day).
After discharge, his blood pressure stabilized. Later in the clinical course, nifedipine could be reduced, and temocapril was discontinued. Echocardiography showed recovery of cardiac function (ejection fraction 55.4%). Oral prednisolone was gradually tapered to 2 mg/day after 8 years of steroid initiation, and the SCr level decreased to 1.22 mg/dL (eGFR 60.6 mL/min/1.73 m2) after 8.8 years of the initial presentation. The urinary protein-to-creatinine ratio was maintained at <0.3 g/gCr. No other immunosuppressants were used. No relapse in the clinical course has occurred at the time of writing this manuscript.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [62.0, 'kg'], 'height': [168.0, 'cm'], 'creatinine': [0.9, 'mg/dL'], 'age': [18, 'years']}",116.7284,110.89198,122.56482,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 18 years old. 
The concentration of creatinine is 0.9 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 62.0 kg. The patient's bmi is therefore 62.0 kg / (1.68 m * 1.68 m) = 21.96712 kg/m^2.The patient's BMI is 22.0, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 62.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 18) * 62.0 * 1) / (0.9 * 72) = 116.7284 mL/min. Hence, the patient's creatinine clearance is 116.7284 mL/min."
103,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6311974-1,Extracted,"A 38-year-old man presented to an emergency department with progressive weakness and decreased urine output after having vomited up to 20 times per day over a period of 7 days. The patient was referred to our intensive care unit. Before medical consultation, he was healthy, and no other symptoms were reported. Diarrhea, fever, chills, or abdominal pain was absent.
Clinical examination revealed a patient of normal weight (height: 180 cm, weight: 70 kg). Blood pressure and heart rate were elevated (150/80 mmHg, 105/min); the respiratory rate was normal (13/min), but oxygen saturation was low (89%). During blood pressure measurement, a positive Trousseau sign was noted. The mucous membranes were dry, and the physical examination was otherwise unremarkable.
Arterial blood gas analysis revealed a metabolic alkalosis with partial respiratory compensation (pH: 7.71 [7.35–7.45], base excess: 40.5 mmol/l [-2-3 mmol/l], pCO2: 56.1 mmHg [32–45 mmHg], pO2: 43.5 mmHg [83–108 mmHg], bicarbonate: 72.2 mmol/l [21–26 mmol/l], lactate: 2.8 mmol/l [0.5–1.6 mmol/l], chloride: 52 mmol/l [98–106 mmol/l], sodium: 130 mmol/l [136–146 mmol/l], potassium: 2.4 mmol/l [3.5–5.1 mmol/l], ionized calcium: 0.77 mmol/l [1.15–1.29 mmol/l] and glucose: 165 mg/dl [70–105 mg/dl]).
Ultrasound revealed a distended and full stomach; the inferior vena cava was collapsing on inspiration. Otherwise, the ultrasound was unremarkable. The electrocardiography [] showed a prolonged QT interval (QTc 547 ms).
Laboratory tests were consistent with acute kidney injury (creatinine: 5.2 mg/dl, urea: 176 mg/dl); liver function tests, coagulation tests, albumin, lipase, procalcitonin, total calcium, hemoglobin, and thyroid-stimulating hormone were normal. Leukocytes were minimally elevated (11500/μl).
We suspected a prerenal acute kidney injury and a hypochloremic metabolic alkalosis due to gastric losses of HCl and fluids. Initial management consisted of oxygen therapy to correct hypoxemia and intravenous fluid therapy with normal saline and potassium chloride. Initially, a balanced crystalloid solution was infused, and later normal saline with KCl (40 mmol/l) was used because of the higher chloride content. Metoclopramide was administered to promote gastric emptying. To prevent further gastric losses of HCl, a proton-pump inhibitor was given. The patient was put on nihil per os for 24 h.
After 24 h, a total of 4.5 l of crystalloid fluid was infused. There was no further vomiting. A repeated bedside ultrasound revealed an empty stomach. The pH was corrected to 7.49, bicarbonate was reduced to 48.6 mmol/l, base excess was 23.4, chloride was 69 mmol/l, and potassium was still low at 2.8 mmol/l. There was hypoventilation with a pCO2 of 68.4 mmHg. We noted onset of diuresis. After 72 h of fluid therapy, the acid-base and electrolyte status was normal. Creatinine had decreased to 3.5 mg/dl. Small meals were tolerated.
Since there was no evidence of an infectious etiology for the excessive vomiting and the ultrasound had shown a distended stomach, an upper gastrointestinal endoscopy was performed []. A significant stenosis of the duodenum was diagnosed. Although there was no ulcer visible, an occult ulcer was deemed to be possible. A portal hypertensive gastropathy was diagnosed while esophageal varices were absent. Helicobacter pylori testing was positive, so an eradication therapy was initiated. A repeated endoscopy confirmed the stenosis, but again, no ulcer was seen. Since a focused abdominal ultrasound did not reveal the reason for the stenosis, a magnetic resonance imaging scan was performed to rule out malignancy such as pancreatic or gallbladder cancer or a thrombosis of the mesenteric vein. There was no evidence of malignancy or cirrhosis. An endosonography was done without evidence of malignancy or mesenteric vein thrombosis. At that point, the stenosis had partly resolved, and endoscopic passage was possible. We concluded that the temporary duodenal stenosis was caused most likely by portal hypertension of unknown etiology, and our differential diagnosis included idiopathic noncirrhotic portal hypertension after exclusion of cirrhosis and portal vein obstruction.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [38, 'years'], 'weight': [70.0, 'kg'], 'height': [180.0, 'cm'], 'creatinine': [5.2, 'mg/dL']}",19.07051,18.11698,20.02404,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 38 years old. 
The concentration of creatinine is 5.2 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 180.0 cm, which is 180.0 cm * 1 m / 100 cm = 1.8 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.8 m * 1.8 m) = 21.60494 kg/m^2.The patient's BMI is 21.6, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 70.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 38) * 70.0 * 1) / (5.2 * 72) = 19.07051 mL/min. Hence, the patient's creatinine clearance is 19.07051 mL/min."
104,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5830324-1,Extracted,"A 67-year-old Japanese man was diagnosed with stage IV non-small-cell lung cancer with malignant pleural effusion in June 2015. His kidney function was normal at that time (creatinine 0.78 mg/dl, estimated glomerular filtration rate 76.2 ml/min/1.73 m2). His medical history included atrial fibrillation and gastroesophageal reflux disease. He had no known history of food or drug allergy. He did not drink but had smoked 40 cigarettes per day since at the age of 20 years. His family history was unremarkable. Despite receiving first-line chemotherapy (bevacizumab combined with pemetrexed plus cisplatin followed by maintenance pemetrexed infusion), the lung cancer progressed. Thus, nivolumab was initiated at a dose of 3 mg/kg every 2 weeks in April 2016. His baseline serum creatinine level before nivolumab therapy was 1.2 mg/dl, and red or white blood cells were not noted in urinalysis. Owing to general fatigue and appetite loss, 10 mg oral prednisolone daily was initiated in July 2016. Four months later, when the oral prednisolone treatment was tapered to 5 mg daily, sterile pyuria was noted and the creatinine level increased to 1.64 mg/dl. Since his creatinine level continued to increase, nivolumab was discontinued (a total of 19 cycles had been performed), and the patient was referred to the nephrology department in January 2017.
His medications at the time of referral included aspirin 100 mg, warfarin 1.0 mg, prednisolone 2.5 mg, and lansoprazole 15 mg per day. He also used indacaterol/glycopyrronium inhaler once-daily. He had been receiving lansoprazole for more than 4 years without significant adverse effects, including kidney injury. He denied using non-steroidal anti-inflammatory drugs or other nephrotoxic agents. His weight was 49.9 kg, height was 168 cm, body temperature was 36.7 °C, pulse rate was 84/min with an irregular rhythm, and blood pressure was 102/60 mmHg. Breath sounds were reduced in the left lower lung field. His heart sounds were normal without audible murmurs. The liver, spleen, and kidneys were not palpable. Tenderness in the costovertebral angle was unclear. Skin rash, joint pain, or swelling was absent, and the oral mucosa was intact. No neurological abnormalities were noted. Laboratory investigations showed blood urea nitrogen value of 23.2 mg/dl, creatinine level of 2.39 mg/dl, and urinary beta-2 microglobulin level of 21,398 μg/l. Urine microscopy revealed numerous white blood cells (100–999 cells/high-power field) along with white blood cell casts. Blood and urine cultures were negative. Other laboratory findings are summarized in Table . Computed tomography (CT) revealed no possible focus of infection. A kidney biopsy was performed to clarify the cause of the acute kidney injury (AKI). The biopsied specimen contained 17 glomeruli. Two of the glomeruli were globally sclerosed but the remaining 15 showed no apparent mesangial proliferation, hypercellularity, or crescent formation. The infiltration of lymphocytes and plasma cells was conspicuous in the interstitial space and it was accompanied by mild edema and fibrosis. Tubulitis was frequently observed with mild to moderate tubular atrophy in the cortical area, but granuloma formation was not noted. Immunohistochemistry demonstrated no significant immune deposits in the glomeruli or tubules. Inflammatory cells were predominantly composed of CD4-positive cells (Fig. ). A diagnosis of ATIN was made. As anti-PD-1 therapy could disrupt the immune tolerance to medications that had been safely used for a long time by enhancing T-lymphocyte activation, we reassessed the patient’s current medications. PPIs have been recently recognized as important offending drugs in the development of drug-induced ATIN, so lansoprazole was discontinued. His creatinine level showed rapid improvement in 3 days (decreasing from 2.74 to 1.82 mg/dl), and the sterile pyuria disappeared. The patient then received steroid therapy (500 mg intravenous methylprednisolone for 3 days followed by 1 mg/kg/day oral prednisolone), and his creatinine levels eventually stabilized around 1.7 mg/dl. DLST for lansoprazole was positive. The detailed methodology for the DLST has been described in a prior publication []. The patient’s clinical course is shown in Fig. . Since the size of the lung cancer and serum carcinoembryonic antigen level remained unchanged, the patient was followed up carefully without re-initiating nivolumab. Urinary beta-2 microglobulin level remained within normal range.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [67, 'years'], 'weight': [49.9, 'kg'], 'height': [168.0, 'cm'], 'creatinine': [2.39, 'mg/dL']}",21.16864,20.11021,22.22707,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 67 years old. 
The concentration of creatinine is 2.39 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 49.9 kg. The patient's bmi is therefore 49.9 kg / (1.68 m * 1.68 m) = 17.67999 kg/m^2.The patient's BMI is 17.7, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 49.9 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation. 
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 67) * 49.9 * 1) / (2.39 * 72) = 21.16864 mL/min. Hence, the patient's creatinine clearance is 21.16864 mL/min."
105,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-2556317-1,Extracted,"A 55 year old post menopausal Caucasian female presented with vitiligo on her face, arms and legs. Her past medical history included only mild asthma requiring only intermittent bronchodilators without glucocorticoids. There was no other significant personal or family medical history. Clinical examination showed a well woman, weight of 69.1 kg, height 1.67 metre (body mass index ~25). Her blood pressure was 120/75 lying and 120/70 sitting with a regular pulse of 78 beats per minute. There were 3 vitiligo patches each measuring approximately 3 × 5 cm on her forehead, anterior abdomen and left cubital fossa. No goitre or liver enlargement was detected. Biochemical investigations are as follow: sodium 130 mmol/L (reference range (RR), 136–146), potassium 5.4 mmol/L (RR, 3.5–5.5), chloride 99 mmol/L (RR, 98–108), bicarbonate 21 mmol/L (RR, 24–30), urea 9.1 mmol/L (3.0–7.0), creatinine 90 umol/L (RR, 40–90), bilirubin 18 μmol/L (6–10), alanine aminotransferase 105 IU/L (RR, < 50), aspartate aminotransferase 56 IU/L (RR, < 45), alkaline phosphatase 136 IU/L (RR, < 110), γ-glutamyl transferase 40 IU/L (< 60), albumin 33 g/L (RR, 35–45), plasma aldosterone 172 pmol/L (RR, 80–1040), plasma renin activity > 35.7 ng/mL/hr (RR, 1.2–2.8). In essence, they showed mild hyperkalaemic metabolic acidosis and hepatocellular dysfunction. Because the latter persisted, chronic hepatitis C was confirmed with positive serology of genotype 1. The liver biopsy showed changes consistent with chronic persistent hepatitis, the inflammatory and fibrotic changes were both graded 1 according to the scoring method []. Together with additional biochemical and immunological studies, other causes of persistent abnormal liver function tests were excluded. In view of her vitiligo, hepatitis C and biochemical disturbance, the Adrenocorticotropin (ACTH) stimulation test (AST), also known as the Cosyntropin or Short Synacthen test, was performed which revealed the presence of subclinical adrenal insufficiency (AI), additional file . Further investigations for the causes of AI revealed positive adrenal cell antibody (ACA) serology. Computerised tomographic scan showed small adrenal glands bilaterally with normal anatomy and appearance.
The patient underwent routine combination treatment of Interferon-α2β (IFN) and Ribavirin (RBV) for 48 weeks for her genotype 1 HCV infection. The patient's subclinical adrenal disease was also followed closely using salivary as well as serum cortisol levels to assess the hypothalamo-pituitary-adrenal axis (HPA) every 12 weeks, starting at baseline, during treatment, 6 and 12 month follow-ups. The results suggested a progressive decline of her adrenal function during the treatment phase. Glucocorticoid replacement therapy was seriously considered but with apprehension due to possible exacerbation of the hepatitis. The risks were discussed in detail with the patient and her family and it was decided to continue with anti-viral therapy but without glucocorticoid supplement. The patient and her husband were counselled comprehensively regarding the emergency management of Addisonian crisis, provided with a carrying note and required to wear an alert bracelet. Other immediate family members were also involved in her management plan, with her consent. Her management plan was also forwarded to the local hospital Emergency Department and Hepatitis C Service. Fortunately, there was no crisis other than the common side effects of the treatment regimen. Her pattern of steroid profile and ACA returned to its pre-existing state and remained unchanged at 6 and 12 month follow-up after the cessation of therapy. The patient has remained well since but her subclinical AI persists.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [55, 'years'], 'weight': [69.1, 'kg'], 'height': [1.67, 'm'], 'creatinine': [90.0, 'µmol/L']}",57.88256,54.98843,60.77669,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 55 years old. 
The concentration of creatinine is 90.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 90.0 µmol. To convert 90.0 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 90.0 µmol creatinine * 1e-06 mol/µmol = 9e-05 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 9e-05 mol creatinine * 113.12 g/mol = 0.01018 g creatinine. To convert 0.01018 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01018 g creatinine * 1000.0 mg/g = 10.18 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 10.18 mg creatinine/10.0 dL = 1.018 mg creatinine/dL. The concentration value of 90.0 µmol creatinine/L converts to 1.018 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.67 m. The patient's weight is 69.1 kg. The patient's bmi is therefore 69.1 kg / (1.67 m * 1.67 m) = 24.77679 kg/m^2.The patient's BMI is 24.8, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 58.72056 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 55) * 58.72056 * 0.85) / (1.018 * 72) = 57.88256 mL/min. Hence, the patient's creatinine clearance is 57.88256 mL/min."
106,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-7495872-1,Extracted,"A 38-year-old female living donor (height 162.3 cm; weight 53.5 kg; body mass index 20.3 kg/m2) was scheduled for elective laparoscopic right hepatectomy for LT. She was clinically acceptable for donation surgery according to multidisciplinary assessments based on living liver donation guidelines [, ]. She had no history of diabetes mellitus, hypertension, cerebro- and cardiovascular diseases, hepatitis or pneumothorax, and there were nonspecific physical findings. The CXR and chest CT image findings were nonspecific, and there was no evidence of fatty liver or focal hepatic lesions in abdominal CT images. Sinus rhythm was recorded on an electrocardiogram. A central venous catheter (Arrow 7 Fr catheter; Teleflex, Wayne, PA, USA) was implemented to administer intravenous fluids and medications without complications in the right internal jugular vein under sonographic guidance, and the patency of catheterization was confirmed by CXR. Her laboratory findings were as follows: hemoglobin, 12.0 g/dL; white blood cell count, 6.94 × 109/L (neutrophils, 57.2%); platelet count, 271,000/μL; creatinine, 0.64 mg/dL; albumin, 4.2 g/dL; aspartate and alanine aminotransferase, 19 U/L and 11 U/L, respectively; total bilirubin, 0.39 mg/dL; and prothrombin time, 111.6% (INR: 0.94).
Balanced anesthesia was induced with 100 mg propofol (Fresenius Kabi, Bad Homburg, Germany) and 50 mg rocuronium (Merck Sharp & Dohme Corp., Kenilworth, NJ, USA), and was maintained with desflurane (Baxter, Deerfield, IL, USA) in oxygen/medical air (FiO2 50%) with volume-controlled mechanical ventilation (tidal volume: 400 mL; respiration rate: 12/min; inspiration and expiration ratio: 1:2). A neuromuscular block was maintained with rocuronium. Her vital signs (i.e., systolic [SBP] and diastolic [DBP] blood pressure; heart rate [HR]; and body temperature) and hypnotic depth (bispectral index monitor; Medtronic, Minneapolis, MN, USA) were continuously monitored and managed, as appropriate (Table ).
A laparoscopic hepatectomy was performed using the five-trocar technique and the trocars were placed uneventfully. Abdominal CO2 insufflation was performed with a pressure of 10–12 mmHg. The patient was placed in a 30° head-up position to assist with surgical exposure. The harmonic scalpel (Ethicon Inc., Cincinnati, OH, USA), with transaction and hemostasis of the liver around tissues, was meticulously applied for liver mobilization.
Saturation of peripheral oxygen (SpO2) decreased to 90%, and airway peak pressure reached 35 cmH2O 30 min after beginning the laparoscopic surgery. Chest auscultation revealed normal breath sounds over the left chest but reduced breath sounds on the right. Because we assumed that this could be due to kinking or migration of the endotracheal tube or due to obstructive secretions in the endotracheal tube, we carefully checked the tube and smoothly toileted inside the tube using a fiberoptic bronchoscope. Chest auscultation and movement seemed to recover during inspiration and expiration. However, airway peak pressure abruptly reached 38 cmH2O again and tidal volume simultaneously decreased to 180 mL. Her hemodynamic parameters began to change as SpO2 was 88%, end-tidal CO2 increased to 48 mmHg, SBP/DBP decreased to 82/41, and HR reached 110 beats/min. As a result, a sonographic examination of the lungs (Affiniti 70C ultrasound system; Philips, Amsterdam, the Netherlands) was performed to rule out pneumothorax, but we verified the lung points as a sonographic marker for occult pneumothorax in both anterior apical zones (Fig. ). A pneumothorax was suspected, and the surgeon was asked to temporarily pause the surgery and cease gas insufflation. Lung ultrasound using a sterile drape was meticulously performed in the anterior apical zone (i.e., the mid-clavicular line at the second to third intercostal space) and lateral zone (i.e., the lateral-clavicular line at lateral and slightly superior to the nipple) with the patient in the supine position, and the stratosphere sign was identified as a critical marker for pneumothorax (Fig. ). Portable CXR verified a right-dominant large pneumothorax with a small degree of left lung collapse; thus, a chest tube was inserted on the right side without complications (Fig. ). After passive decompression using a chest tube, her hemodynamic parameters fully recovered, and the surgery continued laparoscopically with the chest tube inserted and close monitoring of the left-side lung field using lung ultrasound and respiratory monitoring. The surgeon explored both the diaphragm and surrounding structures to detect any defects or injuries, but there were no specific abnormal findings (Fig. ). The surgery was completed uneventfully, and after manual deflation of the abdomen, an alveolar recruitment maneuver (i.e., manual inflation of 30 cmH2O for 30 s) was performed several times. We confirmed the return of both equal breath sounds, and the donor was extubated and transported to the postanesthesia care unit.
The postoperative recovery course was uneventful, and follow-up CXR and CT images revealed complete resolution of the two-sided pneumothorax (Fig. ). She was discharged on postoperative day 5 without any complications.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [53.5, 'kg'], 'height': [162.3, 'cm'], 'creatinine': [0.64, 'mg/dL'], 'age': [38, 'years']}",100.66081,95.62777,105.69385,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 38 years old. 
The concentration of creatinine is 0.64 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.3 cm, which is 162.3 cm * 1 m / 100 cm = 1.623 m. The patient's weight is 53.5 kg. The patient's bmi is therefore 53.5 kg / (1.623 m * 1.623 m) = 20.31032 kg/m^2.The patient's BMI is 20.3, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 53.5 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 38) * 53.5 * 0.85) / (0.64 * 72) = 100.66081 mL/min. Hence, the patient's creatinine clearance is 100.66081 mL/min."
107,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-7171609-1,Extracted,"A 23-year-old man who was previously fit army personnel presented to our emergency department (ED) with a history of intermittent postprandial vomiting and leg cramps for one month which had worsened two days before his presentation where he vomited for ten times a day. He also had no loin pain or haematuria. Clinically, he was alert, not pale, neither jaundice nor cachexic, and without any abnormality on physical examination. On arrival, his blood pressure (BP) was 130/73 mmHg, pulse rate of 92 beats per minute, and oxygen saturation of 98% under room air.
The initial blood investigations in ED showed severe metabolic alkalosis with hypokalaemia, hypocalcaemia, and renal impairment. Blood urea was 9.1 mmol/L, serum creatinine of 218.3 μmol/L (eGFR 35.5 ml/min/1.73 m2), potassium of 1.6 mmol/L, and sodium of 126 mmol/L. Venous blood gas showed metabolic alkalosis with pH of 7.56, bicarbonate of 62 mmol/L, pCO2 of 73.3, mm Hg, pO2 of 29.1, and SO2 of 52.2%. Corrected serum calcium was 2.04 mmol/L while serum phosphate was 1.0 mmol/L. Full blood count showed haemoglobin of 12.2 g/L, total white blood cell count of 10.2 × 109/L, and platelet of 302 × 109/L. Meanwhile, C-reactive protein was 0.28 mg/dL. There were no baseline investigations for comparison and also no arterial blood gas results.
Shortly after reviewing him, he developed generalised tonic seizure followed by cardiac arrest with pulseless electrical activity. The blood pressure was not recordable; hence, cardiopulmonary resuscitation was carried out for a total of 70 minutes, with 14 direct current shocks delivered for ventricular tachycardia and fibrillation before he regained full and sustained recirculation. He was intubated and required inotropic support for persistent hypotension despite adequate volume resuscitation. He had 300 ml of urine following urinary bladder catheterisation after the resuscitation, which was most likely reflective of residual urine prior to the collapsed, but later he became anuric and was initiated on renal replacement therapy.
Placement of nasogastric tube (NG) postintubation drained almost 2 L gastric content, and even after emptying, he was unable to tolerate feeding via the tube. He required multiple corrections for hypokalaemia and hypocalcaemia with intravenous potassium chloride and calcium gluconate infusion, respectively. CT thorax, abdomen, and pelvis was done and showed distended elongated stomach with air contrast level (). There was no enhancing lesion or compression at the pylorus and antrum of the stomach. However, the D3 segment of the duodenum was significantly smaller in calibre at the precaval and preaortic region with lack of mesenteric fat. There was a reduced aortomesenteric angle measuring 21 degrees (normal: 25–60 degree) with reduced distance measuring 8 mm (normal: 10–28 mm). The contrast was seen opacifying the duodenum, jejunum and ileal loops.
He required intermittent haemodialysis and extubated after four days and could give more detailed histories which help to exclude the possibility of congenital related disorders or drug abuse which were not present. He was well before but gave a history of progressive weight loss with intermittent vomiting, which goes back to almost a year. Although it was not initially alarming, for the past two months, he lost 2 kilograms, despite normal appetite and no associated diarrhoea or vomiting. His body mass index on admission was 17.8 kg/m2 only with a weight of 48 kg and height of 1.64 m.
He had a full neurological recovery but remained intolerance to NG feeding. Gastroscopy examination showed Forrest 3 ulcer at D1, pinhole D1-D2 junction, which was dilated during the scope, and the nasojejunal (NJ) tube was inserted to facilitate oral feeding. He was given parenteral nutritional support throughout the hospital stay together with oral erythromycin ethylsuccinate as a prokinetic agent until he tolerates the tube feeding very well. He was then successfully discharged without the feeding tube after one month of admission. His renal function was also gradually recovered (). He was taken off dialysis support after three months. With proper dietary advice, he gained five kilograms in a span of four months.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [23, 'years'], 'weight': [48.0, 'kg'], 'height': [1.64, 'm'], 'creatinine': [218.3, 'µmol/L']}",31.33789,29.771,32.90478,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 23 years old. 
The concentration of creatinine is 218.3 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 218.3 µmol. To convert 218.3 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 218.3 µmol creatinine * 1e-06 mol/µmol = 0.00022 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00022 mol creatinine * 113.12 g/mol = 0.02489 g creatinine. To convert 0.02489 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.02489 g creatinine * 1000.0 mg/g = 24.89 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 24.89 mg creatinine/10.0 dL = 2.489 mg creatinine/dL. The concentration value of 218.3 µmol creatinine/L converts to 2.489 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.64 m. The patient's weight is 48.0 kg. The patient's bmi is therefore 48.0 kg / (1.64 m * 1.64 m) = 17.84652 kg/m^2.The patient's BMI is 17.8, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 48.0 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation. 
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 23) * 48.0 * 1) / (2.489 * 72) = 31.33789 mL/min. Hence, the patient's creatinine clearance is 31.33789 mL/min."
108,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-7382311-1,Extracted,"In March 2017, a 56-year-old Japanese woman was diagnosed by a dermatologist in the outpatient clinic of the neighboring hospital with palmoplantar pustulosis (PPP) including skin ulcers and erosion on both feet and fingers. Following this diagnosis, the patient began to suffer left leg pain, with the pain increasing. Prednisolone was administrated at the dose of 20 mg daily, but the pain continued. This resulted in the patient being admitted to the authors' hospital for the examination of the left femur pain in January 2018.
On admission, the patient was 156.2 cm tall and weighed 55.4 kg, with a blood pressure of 124/65 mmHg. Laboratory tests were conducted including serum creatinine (1.19 mg/dL), and C-reactive protein (0.2 mg/dL). Rheumatoid factor (RF) was negative at 1 U/mL (normal: <10 U/mL), cyclic citrullinated peptide (CCP) antibodies were negative at <0.5 U/mL (normal <4.5 U/mL), and all autoantibodies were negative, including antinuclear antibody (ANA). Serum complement component 3 (C3) was 106 mg/dL (normal: >86 mg/dL), complement component 4 (C4) was 18 mg/dL (normal: >17 mg/dL), and total complement (CH50) was 44 U/mL (normal: >30 U/mL). The serum level of immunoglobulin G (IgG) was 1705 mg/dL (normal: 870 to 1700 mg/dL), immunoglobulin A (IgA) was 265.9 mg/dL (normal: 110 to 410), and immunoglobulin M (IgM) was 61.2 mg/dL (normal: 33 to 190). Alkaline phosphatase (ALP) was 258 IU/L (normal: 117 to 350), bone ALP was 60.3 μg/L (normal: 3.8 to 22.6), tartrate-resistant acid phosphatase (TRAP)-5B was 848 mU/dL (normal: 250 to 760), and intact parathyroid hormone was 117 pg/mL (normal: 25 to 117) ().
Plain radiography and computed tomography showed thickening of the bone on the outer portion of left femur, which bone scintigraphy with 99mTc–methylene diphosphonate showed intense radioactive uptake (a).
A diagnosis of SAPHO syndrome was given due to characteristic skin manifestations (including palmoplantar pustulosis) and bone manifestations (including hyperostosis). Bone biopsy was performed to investigate the pathogenesis of this disease after tetracycline double labeling with the schedule of 02-7-02-25.
Bone biopsy was performed as follows. A 5 cm vertical skin incision was made just above the lesion. Incision of the vastus lateralis and periosteum revealed incorrect bone cortex. The part was perforated to 1.5 cm × 0.8 cm. Upon reaching the defect in the bone cortex, there were a hematoma and a tissue looked like normal bone inside, from which a specimen was taken. No abscess or infected granulation tissue were detected.
Bone histomorphometrical analysis and immunohistological analysis was performed according to previously described methods (). The normal value of bone histomorphometrical analysis is referred according to the report of . We must note the followings: It is not the value of the femoral diaphysis, but the value of iliac bone. In addition to it has not been age-adjusted.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [56, 'years'], 'weight': [55.4, 'kg'], 'height': [156.2, 'cm'], 'creatinine': [1.19, 'mg/dL']}",40.78419,38.74498,42.8234,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 56 years old. 
The concentration of creatinine is 1.19 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 156.2 cm, which is 156.2 cm * 1 m / 100 cm = 1.562 m. The patient's weight is 55.4 kg. The patient's bmi is therefore 55.4 kg / (1.562 m * 1.562 m) = 22.70637 kg/m^2.The patient's BMI is 22.7, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 48.94103 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 56) * 48.94103 * 0.85) / (1.19 * 72) = 40.78419 mL/min. Hence, the patient's creatinine clearance is 40.78419 mL/min."
109,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5216608-1,Extracted,"A 71-year-old Japanese woman, non-smoker, with a history of cholelithiasis, hypertension, and dyslipidaemia, was referred to our hospital for evaluation of nephrotic syndrome. The patient had been diagnosed with hypertrophic cardiomyopathy 6 months previously.
On physical examination, the patient was 155.0 cm tall. She weighed 46.0 kg and showed a systolic ejection murmur from the left sternal border to the apex and pitting leg oedema. The remainder of the examination was unremarkable. On blood analysis, hypoalbuminemia (1.7 g/dL), proteinuria (4.5 g/gCr), and serum IgG M-protein were detected. Serum free light chain (SFLC) assay showed an increase in free lambda chain with a decreased kappa/lambda ratio (kappa SFLC: 7.8 mg/L, normal 3.3–19.4 mg/L; lambda SFLC: 70.5 mg/L, normal 5.7–26.3 mg/L; kappa/lambda ratio: 0.11, normal 0.3–1.3). On the other hand, SAA (5.6 μg/mL) and immunoglobulin were within normal limits. Creatinine (0.8 mg/dL), brain natriuretic peptide (325.8 pg/mL), and carcinoembryonic antigen (6.4 ng/mL) were elevated. Chest radiography showed a nodule, 2.1 cm in diameter, in the right upper lung field. Computed tomography revealed a nodule with marginal irregularity and bronchodilatation in the right upper lobe, hilar mediastinal lymph node enlargement, slight bilateral pleural effusion, pericardial effusion, and ascites (Fig. ).
Pathological examination of transbronchial biopsy samples of the lung nodule yielded a diagnosis of adenocarcinoma (Fig. ). In addition, interstitial deposition of amorphous material that stained positively for Congo red with apple-green birefringence in the polarized view, and an amyloid P component was found in the tissues surrounding the tumour and in the subcarinal lymph node (Fig. : lung; g, k: subcarinal lymph node). Enlargement of the subcarinal lymph node was not due to cancer metastasis. In addition, biopsy samples of gastric and duodenal mucosa, bone marrow, and cardiac muscle stained positively for Congo red with apple-green birefringence in the polarized view, and amyloid P component (Fig. : duodenal mucosa; i, m: bone marrow). Only the subcarinal lymph node and the cardiac muscle stained positively for anti-lambda light chain antibodies. Furthermore, positive staining for RAGE was detected only in the lung tumour cells (Fig. ). The bone marrow demonstrated a normal population of plasma cells with slight atypia.
Finally, the case was diagnosed as lung adenocarcinoma, Stage IA (cT1bN0M0), and primary systemic AL amyloidosis with nephrotic syndrome and cardiomyopathy.
Because the patient displayed rapidly worsening edema and cardiac amyloidosis with elevated brain natriuretic peptide, she was given a poor prognosis rather than that expected with early-stage lung adenocarcinoma and was treated with dexamethasone (20 mg/day) and diuretics. The oedema, mainly due to the nephrotic syndrome with severe proteinuria, pleural effusion, and brain natriuretic peptide levels were not responsive to treatment. The patient died after 3 months despite dexamethasone and bortezomib treatment in another hospital.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [71, 'years'], 'weight': [46.0, 'kg'], 'height': [155.0, 'cm'], 'creatinine': [0.8, 'mg/dL']}",46.83854,44.49661,49.18047,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 71 years old. 
The concentration of creatinine is 0.8 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 46.0 kg. The patient's bmi is therefore 46.0 kg / (1.55 m * 1.55 m) = 19.14672 kg/m^2.The patient's BMI is 19.1, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 46.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 71) * 46.0 * 0.85) / (0.8 * 72) = 46.83854 mL/min. Hence, the patient's creatinine clearance is 46.83854 mL/min."
110,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-7544376-1,Extracted,"A 58-year-old obese woman presented to the emergency department of our hospital with recurrent episodes of constrictive chest pain during exercise within the last 2 weeks (de novo AP). She described similar symptomatology a few years ago, but she did not have any medical evaluation at that time. The patient denied shortness of breath during daily activities, dizziness, or syncope. Her past medical history revealed type 2 diabetes mellitus, arterial hypertension, and dyslipidemia, with an estimated 10-year risk of fatal cardiovascular disease of 3% according to SCORE risk chart. She was on chronic ambulatory medication with bisoprolol 5 mg quaque die (QD), perindopril 5 mg QD, atorvastatin 20 mg QD, and metformin 1000 mg bis in die with good medication adherence. There was no family history of cardiac diseases.
Focused clinical examination on admission revealed class I obesity (height = 156 cm, weight = 80 kg, body mass index = 33 kg/m2); blood pressure was 120/65 mm Hg, heart rate was 56 bpm, heart and lung sounds were normal with no audible cardiac murmurs, respiratory rate was 17 breaths/min and peripheral oxygen saturation was 98% in ambiental air.
Laboratory workup revealed impaired fasting glucose (112 mg/dL = 6.2 mmol/L), high values for total cholesterol (210 mg/dL = 5.43 mmol/L), LDL-cholesterol (157 mg/dL = 4 mmol/L) and tryglicerides (157 mg/dL = 1.76 mmol/L), high NTproBNP (1120 pg/mL) and normal myocardial necrosis markers, including serial determination of myoglobin (33–28 ng/mL, cut-off value 60 ng/mL), high-sensitive cardiac troponin I (23-8-13 ng/L, cut-off value 54 ng/L), and creatinkinase (CK/CK-MB = 61/21– 84/15–52/17 UI/L, cut-off value 280/22 U/l). Routine liver and kidney function blood tests were within normal range (serum creatinine: 0.85 mg/dL = 75 μmol/L, blood urea nitrogen: 15.85 mg/dL = 5.66 mmol/L, AST = 32 U/L, ALT = 47 U/L).
The resting ECG on admission during pain-free interval showed biphasic T-waves with terminal negative component (+/−) in leads V2 to V6, DIII, aVF and minimal ST depression in leads DI and aVL (Fig. ).
Transthoracic echocardiography revealed interventricular septum and anterior wall hypokinesia with preserved global left ventricular ejection fraction (55%) and mild mitral regurgitation.
We established the diagnosis of low-risk non-ST-segment elevation acute coronary syndrome with a Global Registry of Acute Coronary Events risk score of 92 points.
The patient was admitted to the cardiac intensive care unit and monitored with continuous telemetry. Following her presentation, the patient was immediately started on aspirin 300 mg loading dose followed by 75 mg QD orally, clopidogrel 600 mg loading dose followed by 75 mg QD orally, atorvastatin 80 mg QD orally, and a bolus of 5000 IU of unfractioned heparin. Keeping in mind that our patient presented ECG findings compatible with type A Wellens pattern, which is highly specific (89%) for critical LAD stenosis, the patient underwent cardiac catheterization the same day. Coronary angiography showed subocclusive dynamic obstruction of the LAD due to MB (Figs. and ). The ECG taken the next day showed diffuse T waves flattening (Fig. ).
The patient was managed conservatively. Her hospital course was uneventful and she was discharged on pharmacological therapy (clopidogrel, bisoprolol, amlodipine, atorvastatin, and metformin) with well-controlled symptoms on follow-up.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [58, 'years'], 'weight': [80.0, 'kg'], 'height': [156.0, 'cm'], 'creatinine': [0.85, 'mg/dL']}",69.76373,66.27554,73.25192,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 58 years old. 
The concentration of creatinine is 0.85 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 156.0 cm, which is 156.0 cm * 1 m / 100 cm = 1.56 m. The patient's weight is 80.0 kg. The patient's bmi is therefore 80.0 kg / (1.56 m * 1.56 m) = 32.87311 kg/m^2.The patient's BMI is 32.9, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 156.0 cm, which is 156.0 cm * 0.393701 in/cm = 61.41736 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.41736 (in inches) - 60) = 48.75993 kg.
Hence, the patient's IBW is 48.75993 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 48.75993 kg + 0.4 * (80.0 kg  - 48.75993 kg) = 61.25596 kg. The patient's adjusted body weight is 61.25596 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 58) * 61.25596 * 0.85) / (0.85 * 72) = 69.76373 mL/min. Hence, the patient's creatinine clearance is 69.76373 mL/min."
111,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5729381-1,Extracted,"An 18-year-old man with nausea, general malaise, and back pain was admitted to our hospital. Past medical history was only relevant for facial bone fracture, and he was not taking any regular medications. Ten days before admission, he had developed a cough, and his temperature was 36.7°C. He visited a nearby clinic, where he was diagnosed with a common cold, and was prescribed 300 mg of cefcapene pivoxil hydrochloride, 75 mg of diprophylline, 75 mg of methoxyphenamine hydrochloride, 15 mg of noscapine, 6 mg of chlorpheniramine maleate, and 1 mg of dequalinium chloride per day for 3 days. Five days before admission, he again visited the clinic due to coughing and was prescribed 500 mg of levofloxacin, 75 mg of diprophylline, 75 mg of methoxyphenamine hydrochloride, 15 mg of noscapine, and 6 mg of chlorpheniramine maleate. Three days before admission, he performed some extremely demanding training (five 500-m sprints) and developed epigastric pain with vomiting that evening. He visited the clinic for a third time, where acute gastroenteritis was diagnosed. Fluid was intravenously administered for 2 days, after which he went back home.
On the day of admission, the clinic doctor found that his creatinine and blood urea nitrogen (BUN) levels were extremely high, and he was referred to our hospital.
His height was 178 cm, and his body weight was 80 kg. His blood pressure was 140/92 mmHg, pulse was 52 beats/min, and body temperature was 37.2°C. He did not have abnormal skin turgor, dry mucous membranes, or edema. Serum creatine kinase levels were normal, and serum creatinine and BUN levels were elevated at 7.51 mg/dL (reference range: 0.40-1.20 mg/dL) and 55.2 mg/dL (reference range: 8.0-20.0 mg/dL), respectively. His uric acid (UA) levels were also elevated, at 18.3 mg/dL (reference range: 2.0-6.0 mg/dL). Serum myoglobin level was 75 ng/mL (reference range: <60 ng/mL). Urinalysis revealed 2+ protein by dipstick, whereas the urinary protein to creatinine ratio was 0.81. The urine occult blood reaction was negative, and urinary myoglobin was undetectable.
Kidney ultrasound showed no abnormalities in their size and shape. However, on the pulse Doppler ultrasound, the resistance indexes of the interlobar arteries were over 0.8 on both kidneys, suggesting low perfusion at the level of the interlobar arteries of kidneys (Figure A).
Based on the typical symptoms, such as bilateral back pain, and findings from the pulse Doppler ultrasound, we made the diagnosis of ALPE.
Along with oral intake, intravenous potassium-free fluid (Solita-T No.1®, AY PHARMACEUTICALS CO., LTD, Tokyo, Japan) was administered by 500 mL/day over the next 4 days. He had an adequate urinary output exceeding 1000 mL/day, and his nausea and loin pain remitted.
When serum creatinine level decreased to 1.5 mg/dL, 40 mL of iodine contrast dye was administered, and 24 hours later, we performed noncontrast CT. This delayed CT scan showed patchy, wedge-shaped, high-density areas on both kidneys, due to a delay in excretion of contrast (Figure B).
The patient's symptoms fully resolved and he was discharged 12 days after admission. The time course of his biochemical measurements is shown in Figure .","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [18, 'years'], 'weight': [80.0, 'kg'], 'height': [178.0, 'cm'], 'creatinine': [7.51, 'mg/dL']}",17.12691,16.27056,17.98326,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 18 years old. 
The concentration of creatinine is 7.51 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 178.0 cm, which is 178.0 cm * 1 m / 100 cm = 1.78 m. The patient's weight is 80.0 kg. The patient's bmi is therefore 80.0 kg / (1.78 m * 1.78 m) = 25.24934 kg/m^2.The patient's BMI is 25.2, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 73.18119 kg + 0.4 * (80.0 kg  - 73.18119 kg) = 75.90871 kg. The patient's adjusted body weight is 75.90871 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 18) * 75.90871 * 1) / (7.51 * 72) = 17.12691 mL/min. Hence, the patient's creatinine clearance is 17.12691 mL/min."
112,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4804144-1,Extracted,"Mild proteinuria had been incidentally detected in a 22-year-old woman during a regular health check-up 2 years prior to presentation. She visited a local clinic for a follow-up check. She took medication to treat hyperlipidemia for 1 year and did not take any other drugs including diuretics or laxatives. She was admitted to our hospital for evaluation of persistent mild proteinuria.
The prenatal course was unremarkable. On physical examination, her height was 153 cm, her body weight was 49 kg and her blood pressure was 100/60 mm Hg. No edema was found, and normal muscle strength and reflexes were noted. The rest of the physical examination was unremarkable. The laboratory examination revealed blood urea nitrogen of 10.9 mg/dL, creatinine of 0.68 mg/dL, sodium of 137 mmol/L, potassium of 2.59 mmol/L, chloride of 94.7 mmol/L, magnesium of 2.05 mEq/L, and bicarbonate of 31.2 mEq/L. Serum levels of IgG, IgA, IgM, C3, and C4 were normal. Anti-nuclear antibody was negative. Urinalysis showed a specific gravity of 1.007, trace protein, pH 8.0, and no red blood cells. The spot urine protein/creatinine ratio was 0.95 g/g creatinine. Abdominal sonography revealed normal-sized kidneys, without nephrocalcinosis or stones. Plasma renin activity was elevated at 27.98 ng/mL/hr (normal range, 0.50 to 1.90 ng/mL/hr in a supine position), but serum aldosterone was 13.2 pg/mL within normal limits (normal range, 1 to 16 pg/mL in a supine position). The urine prostaglandin E2 level was elevated at 2,815 ng/day (normal range, 400 to 620 ng/day). These findings suggested BS or pseudo-BS/GS caused by vomiting or diuretics.
Light microscopy of renal biopsy demonstrated 14 glomeruli, two of which were globally sclerotic. Most glomeruli appeared moderately increased in size and cellularity due to prominence of the mesangium and JGA. Five glomeruli showed marked enlargement with hyperplasia () and hypergranulosis of the JGA (). The mesangium was diffusely expanded due to mild to moderate increase in cells and matrix (). There was moderate tubular atrophy and interstitial fibrosis with infiltration of lymphocytes. The interlobular arteries and arterioles displayed mild to moderate intimal fibrous thickening and medial sclerosis. Immunofluorescence revealed weak positive (1+) staining for IgG, IgA, and fibrinogen and trace (+/–) of staining for C3 and lambda in the mesangium (). Electron microscopy revealed mild increase in the mesangial cells and matrix with rare small mesangial electron-dense deposits and hyperplastic juxtaglomerular cells with increased electron dense renin and progranules ().
Genetic analysis revealed a homozygous deletion of exon 1–14 and heterozygous deletion of exon 15–19 in the CLCNKB gene (). Her father had heterozygous deletion of exon 1–14 (), and her mother had heterozygous deletion of all examined exons of the CLCNKB gene (). However, her parents displayed no renal symptoms or abnormal renal function.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [22, 'years'], 'weight': [49.0, 'kg'], 'height': [153.0, 'cm'], 'creatinine': [0.68, 'mg/dL']}",94.32496,89.60871,99.04121,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 22 years old. 
The concentration of creatinine is 0.68 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 153.0 cm, which is 153.0 cm * 1 m / 100 cm = 1.53 m. The patient's weight is 49.0 kg. The patient's bmi is therefore 49.0 kg / (1.53 m * 1.53 m) = 20.93212 kg/m^2.The patient's BMI is 20.9, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 46.04337 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 22) * 46.04337 * 0.85) / (0.68 * 72) = 94.32496 mL/min. Hence, the patient's creatinine clearance is 94.32496 mL/min."
113,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-7154233-1,Extracted,"A 15-year-old male complained of strong fatigue after intense exercise since childhood. He had no remarkable medical history apart from allergic rhinitis. After entering high school, he often felt unwell, especially in the morning, and frequently missed classes. He was diagnosed as having orthostatic dysregulation and prescribed amezinium metilsulfate 10 mg/day, but his symptoms persisted. Eight days after the start of treatment he was switched to etilefrine 5 mg/day. However, his fatigue progressively worsened. He was found vomiting and unresponsive after collapsing in the bathroom on the eighth night following the prescription change and taken to the hospital by his family. In the emergency room he exhibited mild consciousness disturbance (Glasgow Coma Scale: E4V4M6) and complained of right lower abdominal pain. Laboratory tests (blood and urine), whole-body computed tomography, and head magnetic resonance imaging did not indicate any abnormalities (serum creatinine level 1.0 mg/dL, uric acid level 7.2 mg/dL). His conscious state and abdominal pain were improved on the next day, but his blood pressure gradually increased from 100/60 to 180/80 mm Hg and his serum creatinine level rose from 1.0 to 5.5 mg/dL during 5 days of admission. He was then transferred to our institution for the treatment of AKI and severe hypertension.
At the time of admission to our hospital the patient was fully conscious and alert. His body temperature was 37.2°C, blood pressure was 161/98 mm Hg, heart rate was 83 beats/min, and respiratory rate was 17 breaths/min. His height was 174 cm and his body weight was 54 kg. Physical examination detected no signs of dehydration, rash, or other abnormalities of the neck, chest, abdomen, or extremities. He had been taking loratadine 10 mg/day for his allergic rhinitis for several months. Both loratadine and etilefrine had been discontinued upon admission to the previous hospital. There was no family history of kidney dysfunction, and he reported no episodes of intense exercise other than daily commuting by bicycle to school. No alcohol consumption, smoking, or illegal drug use were reported. His laboratory data at the time of transfer to our hospital are summarized in Table . Urinalysis showed mild proteinuria (0.66 g/gCr) and elevation of the tubulointerstitial injury marker β2 microglobulin (1,498 μg/L). Hematuria was not observed. His serum level of uric acid was low at 3.2 mg/dL and his fractional excretion of uric acid was high at 49.7%. Laboratory markers of rhabdomyolysis, diabetes mellitus, infection, and collagen diseases such as creatine phosphokinase, hemoglobin A1c, C-reactive protein, and autoimmune antibodies were all within normal range. An electrocardiogram disclosed left anterior hemiblock and nonspecific intraventricular conduction delay that had been detected when he was an elementary school student. A chest X-ray revealed no abnormalities. Ultrasound echography showed bilateral mild kidney swelling with increased renal cortical echogenicity (Fig. ). No stenotic lesions were detected in the aorta or renal arteries, although the resistance index of the intrarenal arteries was slightly high (left 0.69, right 0.69), indicating a circulatory disturbance in the renal microvessels. Hydronephrosis and renal calcification were absent. An ultrasound-guided kidney biopsy performed 3 days after arrival at our hospital showed mild interstitial edema, vascular endothelial cell swelling in the renal interlobular arterioles, and no obvious signs of acute tubular necrosis (ATN) (Fig. ). Treatment with continuous intravenous infusion of extracellular fluids and nicardipine gradually improved his kidney function and hypertension. His serum uric acid level decreased to 1.0 mg/dL (Fig. ), and his fractional excretion of uric acid was at 55.9% at 10 days after admission. He was ultimately diagnosed as having AKI with RHUC and discharged 12 days after transfer to our hospital. Hypouricemia was found in his parents and a sister, indicating a hereditary condition. However, genetic screening did not detect any known causative RHUC mutations on URAT1/SLC22A12 or GLUT9/SLC2A9","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [54.0, 'kg'], 'height': [174.0, 'cm'], 'creatinine': [5.5, 'mg/dL'], 'age': [15, 'years']}",17.04545,16.19318,17.89772,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 15 years old. 
The concentration of creatinine is 5.5 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 174.0 cm, which is 174.0 cm * 1 m / 100 cm = 1.74 m. The patient's weight is 54.0 kg. The patient's bmi is therefore 54.0 kg / (1.74 m * 1.74 m) = 17.83591 kg/m^2.The patient's BMI is 17.8, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 54.0 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation. 
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 15) * 54.0 * 1) / (5.5 * 72) = 17.04545 mL/min. Hence, the patient's creatinine clearance is 17.04545 mL/min."
114,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5057249-1,Extracted,"A 48-year-old male (178 cm, 60 kg, body mass index 18.9 kg/m2) was scheduled for urethral scrotal fistula repair. He had been diagnosed with anxiety disorder, imprisoned for illegal drug use, and diagnosed some 15 years previously with hepatitis C. Ten years before visiting our hospital, he experienced a mental status change, was hyperammonemic, but with normal liver function, and was diagnosed with citrullinemia type II based on biochemical assay results. He had never experienced ascites or esophageal varix, but had experienced recurrent uncompensated hyperammonemia, for which he was taking arginine and sodium benzoate. Prior to transfer to our hospital, he had been living in a sanatorium in a bed ridden state with slurred speech and motor weakness. Subsequent brain computed tomography demonstrated progressive diffuse brain atropy.
The patient was admitted to our urology department for urethral fistula repair and cystolitholapaxy. Preoperative electrocardiographic and chest x-ray findings were normal, and pre- and post-operative serum ammonia levels were illustrated in Fig. (normal value 12-66 μg/dL). Serum ammonia level fluctuations were controlled by daily lactulose enema and intravenous arginine and sodium benzoate. The medical team involved prescribed a 1000 kcal/day diet with a PFC ratio of 14 %:27 %:59 %. Preoperatively, his blood pressure was 100/50 mm Hg, heart rate 88 beats/min, and body temperature 39.3 °C, and he had a scrotal abscess. His preoperative laboratory data were as follows: hematocrit 31.3 %, platelet count 161 × 103/ml, blood urea nitrogen (BUN) 10.4 mg/dl, creatinine (Cr) 0.5 mg/dl, prothrombin time (PT) 14.5 sec (INR 1.34), activated partial thromboplastin time (aPTT) 38.5 sec, serum albumin 2.4 g/dl, aspartate aminotransferase 88 IU/L, alanine aminotransferase 43 IU/L, total bilirubin 0.5 mg/dl, direct bilirubin 0.32 mg/dl, and serum gamma-glutamyl transferase 349 IU/L, the latter of which was moderately elevated (normal 0-72U/L).
Surgery was performed 5 days after admission. He was not administered premedication and in the operating theatre his vital signs were monitored by pulse-oximetry, ECG, and a non-invasive blood pressure device. Spinal anesthesia was performed using 12 mg of 0.5 % hyperbaric bupivacaine using a 25-gauge Quinke needle to block the T6 thoracic level. Dexmedetomidine was administered for sedation during surgery. Plasma solution (600 ml; sodium chloride 5.26 g, sodium gluconate 5.02 g, sodium acetate hydrate 3.68 g, potassium chloride 0.37 g, and magnesium chloride 0.3 g per liter; Plasma solution A inj., CJ Health Care, Korea) was infused during the 120 min operation, which involved open cystolitholapaxy, fistula repair, and removal of the abscess pocket, and estimated blood loss was 100 ml. No adverse event occurred during surgery. The surgical team planned a second-look operation after fever control had been achieved and confirmed the absence of bacterial growth in the surgical wound. No neurologic events of significance occurred before the second operation despite poorly controlled serum ammonia levels.
Twenty days after the first operation, while still hospitalized, the patient underwent a second operation under spinal anesthesia (T8 with 12 mg of 0.5 % hyperbaric bupivacaine) for wound repair and cystoscopic examination; 0.9 % normal saline was used as distension medium during the cystoscopic examination. During the 60 min operation, 400 ml of plasma solution was infused. The patient did not experience any change in consciousness level, despite fluctuating serum ammonia levels, during his 43-day hospital stay.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [60.0, 'kg'], 'height': [178.0, 'cm'], 'creatinine': [0.5, 'mg/dL'], 'age': [48, 'years']}",153.33333,145.66666,161,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 48 years old. 
The concentration of creatinine is 0.5 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 178.0 cm, which is 178.0 cm * 1 m / 100 cm = 1.78 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.78 m * 1.78 m) = 18.937 kg/m^2.The patient's BMI is 18.9, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 60.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 48) * 60.0 * 1) / (0.5 * 72) = 153.33333 mL/min. Hence, the patient's creatinine clearance is 153.33333 mL/min."
115,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4870939-1,Extracted,"Case 1 (the proband), a 27-year-old man, was admitted because of a 7-year history of proteinuria. He had been born at full term and his growth and development had been normal. There was no family history of renal disease. Physical findings were as follows: height 174.0 cm, weight 71.5 kg, body mass index 23.6, and blood pressure 120/80 mm Hg. He did not suffer from deafness. The rest of the physical examination was unremarkable. Urine dipstick analysis was negative for occult blood and 2+ for protein. Urinary protein was 1.6–3.0 g/day. The urinary sediment contained <1 erythrocyte and 3–5 leukocytes per high-power field. Hematocrit was 43.0%, hemoglobin concentration 15.2 g/dl, platelet count 277,000/μl, and leukocyte count 6,200/μl. The serum urea nitrogen level was 15.4 mg/dl, creatinine 1.0 mg/dl, uric acid 7.9 mg/dl, cholesterol 222 mg/dl, total protein 7.2 g/dl, and albumin, 4.9 g/dl. IgG level was 1,070 mg/dl, IgA 139 mg/dl, and IgM 84 mg/dl. Total complement level was 35 IU/l, C3 72 mg/dl, C4 29.5 mg/dl, and C1Q 12.8 mg/dl. Antinuclear antibody was negative. The remaining autoimmune serological findings were within the normal range, and serum viral hepatitis markers were negative. Abdominal computed tomography and ultrasound showed slightly small kidneys with bilateral cysts. Funduscopic examination by portable ophthalmoscope was normal. On the eighth hospital day, a right renal biopsy was performed. Under light microscopy, ten glomeruli and a localized area of tubular atrophy were found (fig. ). One glomerulus was obsolescent and in another there was segmental sclerosis with hyaline deposits near the vascular pole (fig. ). Other glomeruli were slightly enlarged and had essentially minor changes, but in several segments a questionable increased mesangium was observed (fig. ). By immunofluorescence, no significant deposits of immunoglobulins or complement components were found, except for weak granular mesangial and paramesangial IgM deposits. From the clinical and histological findings, idiopathic FSGS was considered as a tentative diagnosis. Initially he was treated with platelet aggregation inhibitor and low-protein diets in our outpatient clinic, but the treatment was interrupted 3 months after admission. At the age of 31 years, he visited our hospital again to be checked for proteinuria. His urinary protein was 51 mg/dl and 0.8 g/day, his serum urea nitrogen level was 17.3 mg/dl, and creatinine was 1.1 mg/dl. To clarify the indication of prednisolone, a second renal biopsy was performed. Under light microscopy, only five glomeruli were found, but significant histological changes were not observed expect for focal tubular atrophy with mild interstitial cell infiltration. The patient was treated with 40 mg/day of prednisolone with gradual tapering for 18 months in our outpatient clinic, but the proteinuria was steroid-resistant and remained at about 1.0–1.5 g/day. His renal function gradually worsened. At the age of 52 years, his urinary protein was 64 mg/dl and his serum creatinine level 1.73 mg/dl.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [27, 'years'], 'weight': [71.5, 'kg'], 'height': [174.0, 'cm'], 'creatinine': [1.0, 'mg/dL']}",109.16919,103.71073,114.62765,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 27 years old. 
The concentration of creatinine is 1.0 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 174.0 cm, which is 174.0 cm * 1 m / 100 cm = 1.74 m. The patient's weight is 71.5 kg. The patient's bmi is therefore 71.5 kg / (1.74 m * 1.74 m) = 23.61607 kg/m^2.The patient's BMI is 23.6, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 69.55913 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 27) * 69.55913 * 1) / (1.0 * 72) = 109.16919 mL/min. Hence, the patient's creatinine clearance is 109.16919 mL/min."
116,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4844913-1,Extracted,"Our patient was a 76-year-old white female with a past medical history of chronic kidney disease (CKD), baseline creatinine 1.85 mg/dL (estimated glomerular filtration rate 27 ml/min/1.73 m2; creatinine range 1.5-2.5 mg/dL six months prior to admission), hypertension, gout and psoriatic arthritis, who was admitted to the hospital for evaluation of elevated creatinine (4.83 mg/dL). She had no previous history of major surgeries. She did have a remote history of therapeutic use of arsenic for psoriasis approximately four decades earlier. She also had past history of heavy nonsteroidal anti-inflammatory drugs use up till three years earlier, when she had an episode of AKI. Her family history was unremarkable. She had only a remote history of smoking. Six weeks earlier, she has been started on orlistat 120 mg three times a day for weight loss. The rest of her medications included vitamin-C supplementation (500 mg/day) calcium carbonate, sevelamer hydrochloride and sodium bicarbonate supplementation for CKD, pantoprazole and monthly infliximab infusions for psoriatic arthritis. Physical exam was non-contributory, with a weight of 71 kg, height 1.55 m and blood pressure of 144/61 mm Hg. Her body mass index calculated at 29.5 kg/m2. Urinalysis with microscopy was unremarkable, except for 5 WBCs/high power fields with no crystals or cast formation. Extensive serologic work-up (antinuclear antibody, anti-neutrophil cytoplasmic antibodies, hepatitis-B and C studies, serum protein electrophoresis with measurements of serum free light chains) remained unremarkable. Uric acid was only mildly elevated at 7.2 mg/dL. Parathyroid hormone level returned within normal limits. During the diagnostic work-up, however, renal ultrasound noted multiple non-obstructing stones. Despite appropriate medical therapy, including volume expansion and correction of serum bicarbonate, creatinine rose to 5.40 mg/dL. Due to the ongoing diagnostic uncertainty a percutaneous kidney biopsy was performed, revealing calcium oxalate crystals within tubular lumens with associated interstitial inflammation with associated features of acute tubular necrosis (-). A subsequent, 24-hour urine collection confirmed increased oxalate excretion (69.5 mg/24 hour; normal for the laboratory: 9.7 - 40.5 mg/24 hour specimen). Heavy metal screen (arsenic, cadmium, lead, mercury) from blood and 24-hour urine collection was unremarkable. Renal replacement therapy with intermittent hemodialysis was initiated for 5 consecutive sessions in eight days, which she tolerated well. Initial serum oxalate was 45 mm/l (normal <27, reporting limit > 10; ARUP Laboratories, Salt Lake City, UT/National Medical Services, Willow Grove, PA); subsequent values returned undetectable after renal dialysis begun. Repeated 24-hour urine collection before discharge documented ongoing excessive oxalate excretion (75 mg/24 hour) (.).
During follow-up, despite good medical compliance, she failed her per os calcium-carbonate therapy to achieve effective gastrointestinal oxalate chelation. Thereafter, being aware of the potential interaction between proton pump inhibitor (PPI) and reduced bioavailability of CaCO3 (,), she was changed to calcium citrate 1040 mg three times daily with meals for the purposes of gastrointestinal oxalate binding agent and to decrease urinary oxalate excretion (). Twenty-two months after her initial hospital presentation she continues to do well and serum creatinine gradually decreased to the 2.01–2.32 mg/dL range (estimated glomerular filtration rate 20-24 ml/min/1.73 m2) (). Urine oxalate excretion came under acceptable control with per os calcium-citrate dosed at 2080 mg, to be taken three times a day with meals ( ).","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [71.0, 'kg'], 'height': [1.55, 'm'], 'creatinine': [4.83, 'mg/dL'], 'age': [76, 'years']}",8.93412,8.48741,9.38083,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 76 years old. 
The concentration of creatinine is 4.83 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.55 m. The patient's weight is 71.0 kg. The patient's bmi is therefore 71.0 kg / (1.55 m * 1.55 m) = 29.55255 kg/m^2.The patient's BMI is 29.6, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.55 m, which is 1.55 m * 39.3701 in/m = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 47.85442 kg + 0.4 * (71.0 kg  - 47.85442 kg) = 57.11265 kg. The patient's adjusted body weight is 57.11265 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 76) * 57.11265 * 0.85) / (4.83 * 72) = 8.93412 mL/min. Hence, the patient's creatinine clearance is 8.93412 mL/min."
117,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-3475914-1,Extracted,"A 15-year-old boy was referred for genetic testing due to hypergonadotrophic hypogonadism. He was the third child born to a non-consanguineous couple (mother 34 years, father 45 years).The antenatal period was complicated by gestational hypertension. The baby was delivered by a lower segment caesarean section at 38 weeks. He weighed 2.650 kg at birth. There were no postnatal complications.
His gross motor milestones were age appropriate. The parents had noticed speech delay and hyperactivity at the age of about 2 years. He has been regularly followed up by a child psychiatrist for attention deficit hyperactive disorder and he was on methylphenidate. Except for one episode of febrile convulsions, there was no history of a seizure disorder. He has had intermittent episodes of bronchial asthma and several episodes of food allergies. He has learning disabilities and poor social interactions. He has had recurrent dental caries. A history of peripheral vascular disease and deep vein thrombosis, reported to be associated with the condition, was not elicited.
Examination showed a tall boy with a height of 180 cm and an arm span of 190 cm. He weighed 70 kg. His body mass index was 21.6 kg/m2. There were no facial dysmorphic features. Psychometric assessment found him to have an IQ between 80 and 90 (Test of Nonverbal Intelligence, Third Edition) with a reduction in span of attention. He had reduced facial and body hair, acne, gynaecomastia, small bilateral descended testis (3–4 ml), small penis, and intention tremors. Pubic hair Tanner stage was II.
Investigations showed hypergonadrotropic hypogonadism, testosterone 0.95 ng/ml (range 0.18–1.5 ng/ml), FSH of 54.8 mIU (range 0.7–11.1 mIU/ml), and LH of 22.3 mIU/ ml (range 0.8–7.6 mIU/ml). Thyroid functions were normal [TSH 1.63 μIU/ml (range 0.4–4.0μIU/ml), free T4 0.881 ng/dl (range 0.78–2.19 ng/dl)]. Ultrasound scan of abdomen showed a small right kidney located in the pelvis. DMSA (dimercaptosuccinic acid) scan confirmed the small right kidney located in the pelvis with reduced function (27%) and a small cortical defect in the superior pole. The left kidney was normal with adequate function (73%). Blood urea (26.7 mg/dl) and serum creatinine (0.9 mg/dl) were within the normal range. Fasting plasma glucose level was 109 mg/dl (70–100 mg/dl). No congenital cardiac defects were seen in the echocardiogram.
The karyotype performed on peripheral lymphocytes showed the presence of the 48,XXYY chromosome compliment in all the cells analyzed []. He was commenced on depot testosterone therapy.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [15, 'years'], 'weight': [70.0, 'kg'], 'height': [180.0, 'cm'], 'creatinine': [0.9, 'mg/dL']}",135.03086,128.27932,141.7824,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 15 years old. 
The concentration of creatinine is 0.9 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 180.0 cm, which is 180.0 cm * 1 m / 100 cm = 1.8 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.8 m * 1.8 m) = 21.60494 kg/m^2.The patient's BMI is 21.6, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 70.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 15) * 70.0 * 1) / (0.9 * 72) = 135.03086 mL/min. Hence, the patient's creatinine clearance is 135.03086 mL/min."
118,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,usmle-1978,Extracted,"A 68-year-old woman comes to the physician because of increasing heartburn for the last few months. During this period, she has taken ranitidine several times a day without relief and has lost 10 kg (22 lbs). She has retrosternal pressure and burning with every meal. She has had heartburn for several years and took ranitidine as needed. She has hypertension. She has smoked one pack of cigarettes daily for the last 40 years and drinks one glass of wine occasionally. Other current medications include amlodipine and hydrochlorothiazide. She appears pale. Her height is 163 cm (5 ft 4 in), her weight is 75 kg (165 lbs), BMI is 27.5 kg/m2. Her temperature is 37.2°C (98.96°F), pulse is 78/min, and blood pressure is 135/80 mm Hg. Cardiovascular examination shows no abnormalities. Abdominal examination shows mild tenderness to palpation in the epigastric region. Bowel sounds are normal. The remainder of the examination shows no abnormalities. Laboratory studies show:
Hemoglobin 10.2 g/dL
Mean corpuscular volume 78 μm
Mean corpuscular hemoglobin 23 pg/cell
Leukocyte count 9,500/mm3
Platelet count 330,000/mm3
Serum
Na+ 137 mEq/L
K+ 3.8 mEq/L
Cl- 100 mEq/L
HCO3- 25 mEq/L
Creatinine 1.2 mg/dL
Lactate dehydrogenase 260 U/L
Alanine aminotransferase 18 U/L
Aspartate aminotransferase 15 U/L
Lipase (N < 280 U/L) 40 U/L
Troponin I (N < 0.1 ng/mL) 0.029 ng/mL
An ECG shows normal sinus rhythm without ST-T changes.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'weight': [75.0, 'kg'], 'height': [163.0, 'cm'], 'creatinine': [1.2, 'mg/dL'], 'age': [68, 'years']}",44.66686,42.43352,46.9002,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 68 years old. 
The concentration of creatinine is 1.2 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 75.0 kg. The patient's bmi is therefore 75.0 kg / (1.63 m * 1.63 m) = 28.22839 kg/m^2.The patient's BMI is 28.2, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 163.0 cm, which is 163.0 cm * 0.393701 in/cm = 64.17326 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.17326 (in inches) - 60) = 55.0985 kg.
Hence, the patient's IBW is 55.0985 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 55.0985 kg + 0.4 * (75.0 kg  - 55.0985 kg) = 63.0591 kg. The patient's adjusted body weight is 63.0591 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 68) * 63.0591 * 0.85) / (1.2 * 72) = 44.66686 mL/min. Hence, the patient's creatinine clearance is 44.66686 mL/min."
119,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4886904-1,Extracted,"A 40-year-old Japanese man was admitted to our hospital to undergo a laparoscopic cholecystectomy. An unknown hypokalemia [potassium (K) 2.7 mmol/L] was found and he was referred to our department presurgery. He had been hospitalized in another hospital for periodic paralysis due to unknown severe hypokalemia (K 1.7 mmol/L) 4 months prior. He and his father, who had died of a stroke, had been diagnosed with nephrocalcinosis in their 20s. None of his three siblings had any medical history. His physical and laboratory findings were as follows: height, 182 cm; weight, 81.5 kg; blood pressure, 120/78 mmHg. No abnormalities were observed in a physical examination. His audibility test was normal. In a blood examination, his serum creatinine level was elevated at 1.44 mg/dL (127.3 μmol/L). His serum K level was low, at 2.7 mmol/L, while his sodium (Na), chlorine (Cl), calcium (Ca), phosphorus (P) and magnesium (Mg) levels were all normal, at 144 mmol/L, 108 mmol/L, 8.7 mg/dL, 2.7 mg/dL and 2.6 mg/dL, respectively. The venous bicarbonate () level was at the lower limit of the normal range, at 22.8 mmol/L. His blood anion gap was normal at 13.2. His complete blood counts were all normal. The levels of immunoglobulins and complements were all within normal limits, and he tested negative for antinuclear, anti-SS-A and anti-SS-B antibodies. The plasma renin activity (normal: 0.1–2) and plasma aldosterone concentration (normal: 35.7–240) were 0.7 ng/mL/h and 141.1 pg/mL, respectively. The spot urinary pH was 7.5 and the fractional excretion of K was inappropriately normal, at 10.3%, even in a hypokalemic state. The urinary Ca/creatinine ratio (mol) was 0.70. The urinary anion gap was positive at 30.9 (=Na 67 mmol/L + K 13.9 mmol/L – Cl [minus sign] 50 mmol/L). Abdominal CT revealed medullary nephrocalcinosis in both kidneys. A bone mineral density test showed normal levels. We suspected dRTA and started a prescription of potassium aspartate and sodium/potassium citrate during the perioperative period. The level of serum K was corrected to within the normal range at 3.6 mmol/L. Black-pigmented stones in the patient's gallbladder were detected after a successful laparoscopic cholecystectomy.
After suspension of the prescription for 7 days, the hypokalemia became advanced (K 3.0 mmol/L), while metabolic acidosis was not evident ( 29.3 mmol/L). We performed ammonium chloride (NH4Cl), furosemide–fludrocortisone and HCO3− loading tests (Figures – ). The NH4Cl loading test demonstrated that the patient had dysfunction in both urinary acidification and net acid excretion under the acid loading condition (Figure A–C). In the furosemide–fludrocortisone loading test, the potential to secrete H+ into the lumina at distal nephrons with an enhanced negative charge was extremely weak (Figure A). In this test, instead of H+, the patient's K secretion increased sharply compared with a healthy control (Figure B). In the bicarbonate loading test, the patient's basal H+ secretion dysfunction was also demonstrated (Figure A); conversely, the tubular maximal reabsorption rate of () was elevated compared with the control (Figure B).
We performed comprehensive genetic testing for known causal genes of RTA in the patient using next-generation sequencing (NGS) technology based on the capturing method (Agilent Technologies). The genes SLC4A1 (encoding AE1), ATP6V1B1, ATP6V0A1, ATP6V0A4 (encoding the B1, a1 and a4 subunits of V-ATPase, respectively), SLC4A4 (encoding NBCe1-A), SLC34A1 (encoding NaPi-2a) and CA2 were all examined simultaneously. The detected mutations were narrowed down to those that might be disease-causing mutations according to the following two filters: one for novel variants that have not been reported previously or for variants with minor allele frequencies (MAFs) of up to 1% in the four single nucleotide polymorphism (SNP) databases [Human Genetic Variation Database (Japanese) [], 1000 Genomes [], ESP6500 [], Exome Aggregation Consortium []] and a second one for variants except for synonymous mutations if the variants are in the coding region. Consequently, only one mutation, which is a novel heterozygous mutation in ATP6V0A4 (exon 15, c.C1631T, p.S544L) was detected. As shown in Figure , the detected variants were validated with conventional Sanger sequencing and the result was consistent with that of the NGS diagnosis. Moreover, to confirm whether a large structural variant such as a large deletion or insertion exists as the second mutation, we performed the copy number variation (CNV) analysis for all the targeted genes by using CONTRA (). Briefly, this is CNV detection software using NGS data, and it calls copy number gains and losses for each target region by comparing the normalized sequencing depth from control samples. We used the sequence data from seven individuals as controls and did not find any large deletions or insertions in the patient. The results of CNV detection extracting the ATP6V0A4 region are shown in . There were no regions where relative sequencing depth was significantly changed compared with the controls, indicating that this patient did not have large deletions in ATP6V0A4, thus he was believed to be a heterozygous carrier of the ATP6V0A4 mutation. In addition, it was confirmed at the same time that other tested genes (SLC4A1, SLC4A4, ATPV1B1, ATPV0A1, etc.) did not have any CNVs.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [40, 'years'], 'weight': [81.5, 'kg'], 'height': [182.0, 'cm'], 'creatinine': [1.44, 'mg/dL']}",74.07719,70.37333,77.78105,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 40 years old. 
The concentration of creatinine is 1.44 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 182.0 cm, which is 182.0 cm * 1 m / 100 cm = 1.82 m. The patient's weight is 81.5 kg. The patient's bmi is therefore 81.5 kg / (1.82 m * 1.82 m) = 24.60452 kg/m^2.The patient's BMI is 24.6, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 76.80323 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 40) * 76.80323 * 1) / (1.44 * 72) = 74.07719 mL/min. Hence, the patient's creatinine clearance is 74.07719 mL/min."
120,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,usmle-9010,Extracted,"A 55-year-old man presents to the physician with tiredness, lethargy, bone pain, and colicky right abdominal pain for 1 month. He has no comorbidities. He does not have any significant past medical history. His height is 176 cm (5 ft 7 in), weight is 88 kg (194 lb), and his BMI is 28.47 kg/m2. The physical examination is normal, except for mild right lumbar region tenderness. Laboratory studies show:
Hemoglobin 13.5 g/dL
Serum TSH 2.2 mU/L
Serum calcium 12.3 mg/dL
Serum phosphorus 1.1 mg/dL
Serum sodium 136 mEq/L
Serum potassium 3.5 mEq/L
Serum creatinine 1.1 mg/dL
Urine calcium Elevated
An ultrasound of the abdomen reveals a single stone in the right ureter without hydroureteronephrosis. Clinically, no evidence of malignancy was observed. An X-ray of the long bones reveals diffuse osteopenia with subperiosteal bone resorption. The serum parathyroid hormone level is tested and it is grossly elevated.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [88.0, 'kg'], 'height': [176.0, 'cm'], 'creatinine': [1.1, 'mg/dL'], 'age': [55, 'years']}",83.73584,79.54905,87.92263,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 55 years old. 
The concentration of creatinine is 1.1 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 176.0 cm, which is 176.0 cm * 1 m / 100 cm = 1.76 m. The patient's weight is 88.0 kg. The patient's bmi is therefore 88.0 kg / (1.76 m * 1.76 m) = 28.40909 kg/m^2.The patient's BMI is 28.4, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 176.0 cm, which is 176.0 cm * 0.393701 in/cm = 69.29138 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.29138 (in inches) - 60) = 71.37017 kg.
Hence, the patient's IBW is 71.37017 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 71.37017 kg + 0.4 * (88.0 kg  - 71.37017 kg) = 78.0221 kg. The patient's adjusted body weight is 78.0221 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 55) * 78.0221 * 1) / (1.1 * 72) = 83.73584 mL/min. Hence, the patient's creatinine clearance is 83.73584 mL/min."
121,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4421631-1,Extracted,"A 70-year-old woman with a history of hypertension and osteoporosis presented with progressive renal insufficiency, abnormal fatigue for several months and increasing shortness of breath during exercise. Five months previously, an invasive ductal breast carcinoma (pT2, pTis, pN0, cM0 and R0) had been diagnosed, and the patient underwent breast-conserving tumour resection, followed by adjuvant radiotherapy and treatment with a non-steroidal aromatase inhibitor. On admission, the patient appeared to be in a good general condition (weight 53 kg, height 168 cm and BMI 19 kg/m2) and seemed only slightly affected. Vital signs were normal (blood pressure 130/60 mmHg and heart rate 80 bpm), and physical examination was unremarkable. The patient’s medication included letrozole, calcium and vitamin D3. Previous administration of alendronate had been stopped before admission. Laboratory testing showed impaired renal function with a creatinine of 297 μmol/L and an estimated glomerular filtration rate (GFR) of 14 mL/min/1.73 m2. Serum calcium level was significantly elevated (3.6 mmol/L) in the presence of slightly lowered serum albumin (31 g/dL). A blood count showed normocytic anaemia (haemoglobin 11,5 g/dL), leucocytopaenia (2840/μL) and a normal platelet count; a differential blood count revealed significant lymphocytopaenia (227/μL). Further biochemical tests demonstrated hyperphosphataemia (2.4 mmol/L) but normal values for parathyroid hormone and C-reactive protein. Urinalysis showed signs of prevailing tubulointerstitial nephritis with minor leucocyturia, predominant tubular proteinuria and mild haematuria.
A diagnostic work-up was performed to establish the cause of hypercalcaemia and bicytopaenia and to identify the underlying renal disease. A skeletal scintigraphy ruled out bone metastatic disease, and abdominal ultrasound did not show any isolated metastases or a tumour mass. Renal ultrasound demonstrated kidneys of normal size with hyperechoic parenchyma and hypoechoic pyramids as well as signs of nephrocalcinosis. Computed tomography of the chest revealed two new very small nodular lesions in both upper lobes; however, there was no notion of enlarged intrathoracic lymph nodes. Spirometric testing was within the normal range (FEV1 85%, VCin 99%, FEV1/VCin 90% and pO2 84 mHg). Subsequent bronchoscopy showed a macroscopically normal bronchial system, and bronchoalveolar lavage did not reveal suspicious cells or any infectious pathogen but a lymphocytic cell profile with an elevated T4/T8 ratio of 5.5. A renal biopsy was performed: histopathology displayed a few moderate epithelioid cell granulomas with interstitial nephritis, slight nephrocalcinosis and moderate focal tubular atrophy, suggesting sarcoid nephropathy (A and B). Bone marrow biopsy demonstrated impaired haematopoiesis with slight siderosis, moderate plasmocytosis and surprisingly also an epithelioid cell granuloma (C), consistent—although non-specific—with manifestation of sarcoidosis. Immunophenotyping of the bone marrow revealed CD138/CD19-positive plasma cells, but no light chains or any other B- or T-cell clonal disease. Revision of a lymph node biopsy, previously performed for staging of the breast cancer, also revealed an epithelioid cell granuloma (D). Further laboratory testing was negative for immunological antibodies, including antinuclear antibodies and c- and p-ANCAs, but showed elevated serum levels for angiotensin-converting enzyme (137 U/L, normal < 52). Echocardiography demonstrated moderate left ventricular hypertrophy with normal systolic function and slight diastolic dysfunction.
Altogether, a diagnosis of sarcoidosis with renal, pulmonary, bone marrow and lymph node involvement was made, while cardiac manifestation was suspected. Treatment with prednisolone resulted in significantly improved renal function within several days, normalized calcium and phosphate values, and led to a haemoglobin and leucocyte count within the normal range. Follow-up studies 3 months later showed an almost normal serum creatinine level of 108 μmol/L with an estimated GFR of 46 mL/min/1.73 m2, a normalized ACE level and regressive pulmonary lesions.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [70, 'years'], 'weight': [53.0, 'kg'], 'height': [168.0, 'cm'], 'creatinine': [297.0, 'µmol/L']}",12.90472,12.25948,13.54996,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 70 years old. 
The concentration of creatinine is 297.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 297.0 µmol. To convert 297.0 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 297.0 µmol creatinine * 1e-06 mol/µmol = 0.0003 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.0003 mol creatinine * 113.12 g/mol = 0.03394 g creatinine. To convert 0.03394 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.03394 g creatinine * 1000.0 mg/g = 33.94 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 33.94 mg creatinine/10.0 dL = 3.394 mg creatinine/dL. The concentration value of 297.0 µmol creatinine/L converts to 3.394 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 53.0 kg. The patient's bmi is therefore 53.0 kg / (1.68 m * 1.68 m) = 18.77834 kg/m^2.The patient's BMI is 18.8, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 53.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 70) * 53.0 * 0.85) / (3.394 * 72) = 12.90472 mL/min. Hence, the patient's creatinine clearance is 12.90472 mL/min."
122,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6392561-1,Extracted,"A 51-year-old woman visited our outpatient clinic because of latent tuberculosis infection detected by a screening examination performed by a healthcare worker. She had no relevant prior medical history. Laboratory findings were normal with a serum creatinine (Cr) level of 0.76 mg/dL (normal 0.6–1.5 mg/dL) and blood urea nitrogen (BUN) level of 12.8 mg/dL (normal 8–23 mg/dL). Antituberculosis treatment was started with isoniazid at 300 mg/d and rifampicin at 600 mg/d. During the 25-day antituberculosis therapy regimen, she complained of nausea, vomiting, general weakness, and edema. Serum Cr and BUN levels were 1.0 and 18 mg/dL, respectively. Rifampicin and isoniazid were discontinued. However, her symptoms progressed for 4 days and urinalysis revealed 4+ proteinuria (normal negative). She was admitted to the hospital for more detailed examinations.
On admission, her blood pressure was 110/80 mm Hg, body temperature was 36.5°C, height was 158 cm, and body weight was 68.6 kg. She had gained 8.6 kg in body weight over the preceding 1 month. The results of physical examination were unremarkable except for pitting edema on both lower extremities. Laboratory findings were as follows: white blood cell count 7490/mm3 (normal 4000–10,000/mm3) with 63.1% neutrophils and 1.4% eosinophils, hemoglobin 13.6 g/dL (normal 12–16 g/dL), platelet count in peripheral complete blood 295,000/mm3 (normal 140,000–440,000/mm3), BUN 45 mg/dL, serum Cr 1.72 mg/dL, total protein 3.67 g/dL (normal 6.5–8.2 g/dL), albumin 1.73 g/dL (normal 3.5–5.0 g/dL), total bilirubin 0.67 mg/dL (normal 0.1–1.2 mg/dL), aspartate transaminase 116 IU/L (normal 10–35 IU/L), alanine transaminase 94 IU/L (normal 0–40 IU/L), total cholesterol 453 mg/dL (normal 120–200 mg/dL), sodium (Na) 133 mEq/L (normal 135–145 mEq/L), potassium 5 mEq/L (normal 3.5–5.5 mEq/L), and chloride 103 mEq/L (normal 98–110 mEq/L). Urinalysis showed specific gravity >1.050 (normal 1.005–1.03), osmolality 687 mOsm/kg (normal 300–900 mOsm/kg), urine Na <10 mEq/L, and urinary Cr 267.34. The calculated fractional sodium excretion was 0.02%. The creatinine urine to plasma ratio was 155. Urinary sediment did not show either red blood cells or granular casts. A 24-h urine sample contained 12.2 g of protein. Serum and urine electrophoresis results showed no M-spike and nonselective proteinuria. The patient was negative for hepatitis B, hepatitis C, HIV, and syphilis serological markers. Rheumatoid factor, antinuclear antibody, antineutrophil cytoplasmic antibody, and antiglomerular basement membrane antibody tests were all negative. In addition, results for complement 3 (144.3 mg/dL, normal 90–180 mg/dL), complement 4 (32.4 mg/dL, normal 10–40 mg/dL), immunoglobulin G (551 mg/dL, normal 700–1600 mg/dL), immunoglobulin A (267 mg/dL, normal 70–400 mg/dL), and immunoglobulin M (111 mg/dL, normal 40–230 mg/dL) were negative. Chest X-ray revealed a small amount of bilateral pleural effusion (Fig. A). The patient was treated with torsemide at a dose of 50 mg/d for edema.
Renal biopsy was performed at 1 week after discontinuation of medication. However, she developed dyspnea and pulmonary edema on the day of the procedure (Fig. B). As we suspected nephrotic syndrome with acute nonoliguric renal failure, we performed dialysis and oral administration of prednisolone at 60 mg/d. Acute renal failure was confirmed with temporary loss of renal function that required dialysis, and with peaked serum Cr (2.68 mg/dL) that more than 3-fold increase in baseline Cr (0.76 mg/dL). Renal biopsy revealed nonsclerotic glomeruli with normocellularity and a mild focal tubular injury pattern on light microscopy (Fig. A and B). No deposition of immunoglobulins or complement components was observed in the glomeruli. Electron microscopy showed diffuse loss of the podocyte foot processes of glomerular epithelial cells, but the glomerular basement membrane showed normal thickness and architecture, consistent with MCD (Fig. A and B).
The diagnosis was confirmed to be MCD. Heavy proteinuria developed after using antituberculosis agents. We speculated that this was a case of antituberculosis medication-induced nephrotic syndrome and toxic hepatitis. Following discontinuation of rifampicin and isoniazid with the aid of prednisolone therapy, the patient's nausea, vomiting, and pulmonary edema improved after 1 week of steroid therapy, and dialysis was stopped. Her body weight recovered from 68.6 to 60.7 kg at 3 weeks after discontinuation of rifampicin and isoniazid, and she was then discharged. Proteinuria became negative and renal function tests showed normal results at 4 weeks (serum Cr, 0.86 mg/dL; BUN, 24.7 mg/dL). Furthermore, her albumin and cholesterol levels were 3.15 g/dL and 276 mg/dL, respectively, at 4 weeks after stopping the drugs. Prednisolone was then tapered and withdrawn 3 months after initiation. Recurrence of proteinuria was not observed during a 3-month follow-up. The patient's clinical course is summarized in Fig. .
Informed consents were obtained from the patient for the publication of clinical details and accompanying images. As this study is a clinical case report, no ethical committee approval was required for its conduction, which is in compliance with the institutional and national policies concerning research approvals.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [51, 'years'], 'weight': [68.6, 'kg'], 'height': [158.0, 'cm'], 'creatinine': [0.76, 'mg/dL']}",79.88398,75.88978,83.87818,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 51 years old. 
The concentration of creatinine is 0.76 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 158.0 cm, which is 158.0 cm * 1 m / 100 cm = 1.58 m. The patient's weight is 68.6 kg. The patient's bmi is therefore 68.6 kg / (1.58 m * 1.58 m) = 27.47957 kg/m^2.The patient's BMI is 27.5, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 50.57095 kg + 0.4 * (68.6 kg  - 50.57095 kg) = 57.78257 kg. The patient's adjusted body weight is 57.78257 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 51) * 57.78257 * 0.85) / (0.76 * 72) = 79.88398 mL/min. Hence, the patient's creatinine clearance is 79.88398 mL/min."
123,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4919844-1,Extracted,"A 41-year-old African woman weighing 72 kg and 169 cm tall, with American Society of Anesthesiologists physical status class I, was referred to our hospital because of tumefaction of the neck. Her clinical examination revealed an isolated parotid mass without associated lymphadenopathy. She had no pain or peripheral facial nerve palsy. The magnetic resonance imaging results were in favor of a pleomorphic adenoma (Figs. and ), and the patient was scheduled for a parotidectomy with general anesthesia.
The results of the patient’s cardiovascular examination were normal, with a noninvasive blood pressure of 131/71 mmHg and a heart rate of 79 beats/minute. Her respiratory examination revealed no dyspnea or snoring. Her oxygen saturation was 98 % on room air. An examination of her upper airway demonstrated good opening of the mouth and good mobility of the cervical spine (Mallampati class I). Her laboratory test results were a urea plasma concentration of 0.18 g/L, a creatinine level of 6 mg/L, blood glucose level of 0.99 mg/dl, hemoglobin concentration of 15.1 g/dl, platelet count of 213,000/mm3, prothrombin time of 12.9 seconds, and international normalized ratio of 1.2. Her chest x-ray and electrocardiogram (ECG) were unremarkable.
After written informed consent was obtained from the patient, it was decided to use general anesthesia during the procedure. Upon the patient’s arrival in the operating theater, intravenous access was established and standard anesthesia monitoring (three-lead ECG, peripheral oxygen saturation, noninvasive blood pressure) was instituted.
Neuromuscular monitoring was performed using acceleromyography. Following calibration, the ulnar nerve was supramaximally stimulated with a square pulse of 0.2-ms duration delivered as train-of-four (TOF) pulses at intervals of 15 seconds. The resulting contractions of the adductor pollicis muscles were quantified by using an acceleromyographic monitor (Infinity® Trident® NMT SmartPod®; Dräger, Lübeck, Germany). The TOF ratio and time interval from injection of the reversal agent to TOF ratio 0.9 were recorded.
Before induction of anesthesia, midazolam 2 mg was administered intravenously as premedication. After 5 minutes of adequate preoxygenation, anesthesia was initiated with fentanyl (2.5 μg/kg) and propofol (3 mg/kg) without significant hemodynamic changes. To facilitate tracheal intubation, rocuronium (0.5 mg/kg) was administered after effective mask ventilation. Once there was no twitching in response to TOF stimulation (1 minute, 45 seconds), the patient’s airway was successfully secured after the first attempt with a 7.0-mm endotracheal tube. The endotracheal tube was connected to a closed “low-flow” anesthetic breathing circuit. Ventilation was controlled to maintain normocapnia with a tidal volume of 8 ml/kg, a respiratory rate of 12 breaths/minute, and peak inspiratory pressure of 20 cmH2O. Anesthesia was maintained with isoflurane (1 %) in a mixture of oxygen and nitrous oxide (50 %:50 %). The end-tidal concentrations of anesthetic and carbon dioxide were measured continuously using a multiple gas monitor. The depth of anesthesia was monitored by bispectral index (BIS), and body temperature was maintained using heating blankets. The patient was placed in supine position and with slight Trendelenburg tilting of the table and the patient’s head turned to the left side. A bolus dose of fentanyl was administered before starting the skin incision to maintain a BIS score between 40 and 60. After the surgical incision was made (15 minutes after induction), there was no response on the basis of TOF ratio. Neuromuscular block was reversed with sugammadex (4 mg/kg). The TOF reached 0.9 after 5 minutes. No hemodynamic or respiratory changes were noted. We stopped the neuromuscular transmission (NMT) monitoring after obtaining a TOF ratio above 0.9 in three consecutive measurements.
The inspired isoflurane concentration was gradually increased to 1.8 % to prevent movement during critical phases of the surgical procedure after reversing neuromuscular blockade. The parotid gland was carefully dissected under magnification with facial nerve monitoring. The facial nerve was identified using the NIM 2.4 nerve integrity monitoring system (MEDTRONIC-XOMED, Jacksonville, FL, USA), and after 1 h surgical conditions were good for the removal of the tumor.
The patient was extubated when fully awake after a smooth emergence from anesthesia. Her oxygen saturation was 99 % with 2 L/minute of supplemental oxygen. Her postoperative course was uneventful, and no evidence of facial nerve paralysis was noted in the postinterventional surveillance room. The patient was discharged to home after 5 days of hospitalization.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [41, 'years'], 'weight': [72.0, 'kg'], 'height': [169.0, 'cm'], 'creatinine': [6.0, 'mg/L']}",126.84629,120.50398,133.1886,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 41 years old. 
The concentration of creatinine is 6.0 mg/L. We need to convert the concentration to mg/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 6.0 mg creatinine/10.0 dL = 0.6 mg creatinine/dL. The concentration value of 6.0 mg creatinine/L converts to 0.6 mg creatinine/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 169.0 cm, which is 169.0 cm * 1 m / 100 cm = 1.69 m. The patient's weight is 72.0 kg. The patient's bmi is therefore 72.0 kg / (1.69 m * 1.69 m) = 25.2092 kg/m^2.The patient's BMI is 25.2, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 169.0 cm, which is 169.0 cm * 0.393701 in/cm = 66.53547 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.53547 (in inches) - 60) = 60.53158 kg.
Hence, the patient's IBW is 60.53158 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 60.53158 kg + 0.4 * (72.0 kg  - 60.53158 kg) = 65.11895 kg. The patient's adjusted body weight is 65.11895 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 41) * 65.11895 * 0.85) / (0.6 * 72) = 126.84629 mL/min. Hence, the patient's creatinine clearance is 126.84629 mL/min."
124,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-8223295-1,Extracted,"The patient was a 71-year-old Japanese woman who was diagnosed with chronic kidney disease due to ADPKD 3 years previously. She received surgical clipping for an unruptured aneurysm of the right middle cerebral artery 4 years earlier. She did not drink alcohol and was a non-smoker. She was taking amlodipine for hypertension, topiroxostat for hyperuricemia, and ferric citrate hydrate for hyperphosphatemia. Continuous erythropoietin receptor activator was administered subcutaneously for renal anemia once a month. She was followed up in an outpatient clinic and suddenly developed right abdominal pain one month previously. As abdominal computed tomography (CT) showed a ruptured liver cyst in the right lobe, which had not been observed seven months previously (Fig. a, b), she was admitted to our hospital. While her white blood cell count was within the normal range at 5900/µL, C-reactive protein was a little high at 0.4 mg/dL. She was treated with bed rest and intravenous cefmetazole administration (1 g/day) on suspicion of cyst infection. Oral acetaminophen 500 mg was occasionally used when needed, and her symptoms improved with conservative management and she was discharged from the hospital after one week. Although she was asymptomatic for a while, she noticed bilateral leg edema, abdominal distension, and general malaise at one month after hospital discharge. Since abdominal CT showed massive ascites (Fig. c), she was admitted to our hospital again.
On admission, her height was 166 cm, and her body weight was 62 kg. A physical examination revealed the following: body temperature, 37.2 °C; blood pressure, 114/73 mmHg; pulse, 94 beats/min; and oxygen rate, 97% on room air. Abdominal distention was observed without tenderness, and pitting edema was observed in the bilateral legs. The laboratory data are shown in Table . Her serum creatinine, alkaline phosphatase, γ-glutamyl transpeptidase, total bilirubin, and CA19-9 were 5.2 mg/dL, 1992 U/L, 355 U/L, 3.1 mg/dL, and 5006 U/mL, respectively.
Abdominal paracentesis revealed amber transparent ascites (Fig. d) and the bilirubin and CA19-9 concentrations were high at 13.3 mg/dL and 244,700 U/mL, respectively. Ascites culturing and cytology were negative. She was diagnosed with biliary peritonitis due to a ruptured liver cyst. Hemodialysis was initiated due to the exacerbation of chronic kidney disease. As conservative treatment did not improve her symptom, drainage of the ascites was initiated from day 11. The outflow of the ascites was 1000 mL per day and there was no tendency to decrease. Drip infusion cholangiography (DIC)-CT revealed that the ruptured cyst in the right posterior segment S6 of the liver was enhanced with contrast medium (Fig. e). Three-dimensional views of DIC-CT showed communication between the ruptured cyst and an intrahepatic bile duct (Fig. f, g). Because of her markedly high CA19-9 levels in serum and ascites, upper endoscopy and repeated ascites cytology were required to rule out cancer. On day 24, oral cefditoren pivoxil (100 mg/day) was initiated because her C-reactive protein was still high at 7.4 mg/dL. On day 31, she was transferred to a university hospital, and the ascites culture on the same day was found to be positive for Enterococcus faecalis. Abdominal surgery was performed. The surface of the liver became yellowish due to bile leakage and a ruptured necrotic cyst was observed on the right liver lobe (Fig. h). After removing the necrotic roof, the orifice that was the source of the bile leakage was identified and sutured (Fig. i). As gallbladder stones had been pointed out, cholecystectomy was performed at the same time. Cholangiography showed no stones in the common bile duct. Intravenous flomoxef sodium (0.5 g/day) was initiated for 3 consecutive days, followed by intravenous sulbactam/ampicillin (1.5 g/day) for 12 days. Abdominal CT one month after the operation showed no recurrence of ascites and she was discharged on day 49. Hemodialysis treatment was discontinued immediately after discharge because her urine volume had increased and her creatinine level had decreased to 3.8 mg/dL. There has been no recurrence of ascites since then.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [71, 'years'], 'weight': [62.0, 'kg'], 'height': [166.0, 'cm'], 'creatinine': [5.2, 'mg/dL']}",9.05676,8.60392,9.5096,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 71 years old. 
The concentration of creatinine is 5.2 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 62.0 kg. The patient's bmi is therefore 62.0 kg / (1.66 m * 1.66 m) = 22.49964 kg/m^2.The patient's BMI is 22.5, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 57.81505 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 71) * 57.81505 * 0.85) / (5.2 * 72) = 9.05676 mL/min. Hence, the patient's creatinine clearance is 9.05676 mL/min."
125,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4028530-1,Extracted,"A 50-year-old woman was referred to our hospital because of persistent hypercalcemia after surgical removal of a parathyroid carcinoma. The patient had undergone an endoscopic parathyroidectomy using a bilateral axillo-breast approach for a right lower parathyroid adenoma 2 years earlier at a local hospital. The tumor was reported as having no histological features suggestive of malignancy. The serum calcium level was returned to normal after surgery. However, approximately 2 years after surgery, the patient's serum calcium level was found to be elevated again, and an enlargement of the left lower parathyroid gland was detected. The patient underwent conventional parathyroidectomy to remove a left lower parathyroid tumor, with a subsequent histological diagnosis consistent with parathyroid carcinoma. Despite the removal of the left lower parathyroid tumor, her serum calcium levels remained high for 2 months, prompting the referral.
Upon presentation, the patient complained of mild fatigue, anorexia, and constipation. Her family history was unremarkable for cancers or endocrine neoplasias. Physical examination revealed no significant abnormality except her previous surgical neck scar. The patient's weight was 46.1 kg, her height 154 cm, and her body mass index 19.4 kg/m2. On laboratory examination, her serum calcium level was 15.0 mg/dL (ionized calcium, 1.95 mmol/L) and serum phosphorus level 3.6 mg/dL. Serum alkaline phosphatase was elevated at 481 IU/L. Her serum parathyroid hormone (PTH) level was elevated markedly (540.2 pg/mL). Blood urea nitrogen on admission was 26.1 mg/dL with a serum creatinine of 1.7 mg/dL. Urine analysis showed low specific gravity, leukocyturia (24/HPF), and mild erythrocyturia (4 to 5/HPF).
A 99mTc-sestamibi scan was performed and demonstrated focal abnormal uptake in the upper mediastinal area in the 2-hour delayed image (). A subsequent 18F-fluorodeoxyglucose (FDG) positron-emission tomography (PET)/computed tomography (CT) imaging study revealed a mass in the soft tissue at the anterior border of the sternum, with focally increased FDG uptake (maxSUV, 2.6) that correlated with the initial 99mTc-sestamibi scan (). The patient displayed reduced bone mineral density at the lumbar spine (L1-4, 0.889 g/cm2; T-score, -1.9 SD) and at the proximal femur neck (0.695 g/cm2; T-score, -1.7 SD). There were no definite radiographic findings or signs of trabecular bone resorption in the skull or other bones, apart from mild subperiosteal bone resorption in the third metacarpal bone. A whole-body bone scan with 99mTc MDP showed diffuse, subtle uptake in the skull and long bones. An abdominal CT scan showed bilateral medullary nephrocalcinosis. Preoperatively, we marked the outline of the mass on the skin, based on the imaging and manual palpation ().
Based on the preoperative findings, the patient underwent an anterior chest wall mass resection. A frozen section revealed pathological parathyroid tissue, and a wide local resection of the tumor with surrounding structures was performed. A final pathological examination revealed a 2.3-cm parathyroid carcinoma with fibrous bands, numerous mitoses, nuclear pleomorphisms, and foci of capsular invasion (). An intraoperative PTH test showed an 82% decline from the pre-excision level (540.1 pg/mL) to the postexcision level (97.5 pg/mL). The postoperative serum PTH and calcium levels dropped significantly to 57.6 pg/mL and 9.3 mg/dL, respectively. Both levels remained stable and within the normal ranges with temporary oral calcium supplementation. Her hospital course was otherwise uncomplicated, and she was subsequently discharged.
During the patient's outpatient follow-up period, the serum PTH and calcium levels remained near the upper limits of normal. However, approximately 1 year later, her serum PTH level was elevated to 84.1 pg/mL, and a new mass was palpated in the upper portion of her left breast upon physical examination. A 99mTc-sestamibi scan and 18F-FDG PET/CT imaging were performed, revealing an abnormal lesion in the upper area of her left breast (). Subsequently, tumor resection was performed, and the pathological report demonstrated parathyroid carcinoma metastasis. Her postoperative serum PTH and calcium levels dropped significantly to 38.9 pg/mL and 9.5 mg/dL, respectively. We are currently watching her cautiously, conducting serial blood examinations and, more specifically, serum PTH and calcium measurements.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [50, 'years'], 'weight': [46.1, 'kg'], 'height': [154.0, 'cm'], 'creatinine': [1.7, 'mg/dL']}",28.8125,27.37187,30.25313,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 50 years old. 
The concentration of creatinine is 1.7 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 154.0 cm, which is 154.0 cm * 1 m / 100 cm = 1.54 m. The patient's weight is 46.1 kg. The patient's bmi is therefore 46.1 kg / (1.54 m * 1.54 m) = 19.43835 kg/m^2.The patient's BMI is 19.4, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 46.1 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 50) * 46.1 * 0.85) / (1.7 * 72) = 28.8125 mL/min. Hence, the patient's creatinine clearance is 28.8125 mL/min."
126,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5290507-1,Extracted,"A 31-year-old man visited our hospital for evaluation of dyspnea and malaise. He had been ill for 1 week prior to admission. His dyspnea gradually started to worsen 2 days prior to admission. One day before admission, he could not get out of the bathtub because of severe dyspnea. The following day, he was found in the bathtub by his family after about 10 h had passed and was transported to our hospital.
The patient had been diagnosed with mild dilated cardiomyopathy without coronary artery stenosis and valvular insufficiency 2 years previously, and diuretics were prescribed by the clinic. However, he stopped taking the diuretics and returning for regular checkups. On arrival to our hospital, his height was 163 cm, weight was 115.4 kg, and vital signs were as follows: blood pressure, 82/53 mmHg; regular heart rate, 125 beats/min; oxygen saturation, 100% (oxygen mask, 6.0 L/min); respiratory rate, 42 breaths/min, and body temperature, 38.7°C. Physical examination revealed peeling skin on his buttocks and pressure marks associated with the long bath time extending from the back over the buttocks. Wheezing and moist rales were heard in the lungs.
Laboratory examination showed the presence of inflammation (white blood cell count, 13,100 cells/μL; C-reactive protein, 16.7 mg/dL; procalcitonin, 41.95 ng/mL), renal impairment (blood urea nitrogen, 53.0 mg/dL; creatinine, 1.55 mg/dL), thrombocytopenia (platelet count, 3.9 × 104/μL), heart failure (N-terminal pro-brain natriuretic peptide, 49,804 pg/mL), and coagulation system abnormalities (D-dimers, 20.6 μg/mL; P-fibrin degradation products, 44.5 μg/mL).
Transthoracic echocardiography (TTE) at admission showed diffuse hypokinesis of wall motion and an ejection fraction of 56% without vegetation. An enlarged heart shadow and a patchy shadow were observed in the right middle lung field on a chest X-ray. Whole-body computed tomography (CT) showed nodules in the right middle lobe of the right lung, suspicious for septic emboli, along with splenomegaly.
Two sets of blood cultures were obtained. Under a preliminary diagnosis of disseminated intravascular coagulation and systemic inflammatory response associated with infection, intravenous administration of meropenem was initiated at 1 g every 8 h. The next day, both sets of blood cultures exhibited growth of Gram-positive streptococci (BD BACTEC blood culture system, Becton, Dickinson and Company, Sparks, Maryland, USA). The antimicrobial treatment was then switched from meropenem to combination therapy comprising ampicillin at 2 g every 8 h and clindamycin at 600 mg every 8 h for toxic shock. The Gram-positive culture was identified as SDSE (VITEK 2 system; BioMerieux Japan, Tokyo, Japan) on the third day. TTE on the third day revealed a reduction in the ejection fraction to 46%, emergence of severe mitral valve regurgitation, and a 5-mm vegetation on the anterior leaflet mitral valve (Fig. ). Using the modified Duke criteria, we diagnosed IE (one major criterion and three minor criteria) caused by SDSE. The ampicillin and clindamycin were continued.
A whole-body CT scan on hospital day 12 revealed a hemorrhagic infarction of the right frontal lobe (Fig. A), abscesses on the right frontal and occipital lobes, and an aneurysm of the mesenteric artery (Fig. B). A rapidly progressive new aneurysm emerged (as shown by comparison of the CT examinations on days 1 and 12) during the clinical course of SDSE bacteremia, and radiological examination was compatible with an infected aneurysm. Therefore, we diagnosed infectious aneurysms caused by SDSE. On day 18, gentamicin was added at 60 mg every 24 h with dose adjustment according to the patient's renal function. Because of the possibility of brain hemorrhage and concern about worsening infection due to embolization, we decided not to perform surgical and radiological intervention. On hospital day 41, the patient complained of sudden abdominal pain, and an abdominal CT scan revealed that the infected aneurysm of the splenic artery had ruptured and caused massive bleeding (Fig. A); there was a significant increase in the size of the aneurysm in the upper mesenteric artery (Fig. B), and new aneurysms were present in the right colic artery. Transcatheter arterial embolization (TAE) for the aneurysms of the splenic and upper mesenteric arteries was performed (Fig. ). A follow-up abdominal CT performed on day 68 demonstrated organized aneurysms of the right colic artery without intestinal ischemia or any additional bleeding.
The antimicrobial agents were adjusted according to the patient's renal function, and the ampicillin was increased to 12 g per day. The intravenous clindamycin and gentamicin were continued for 10 weeks, and the ampicillin was continued for 11 weeks. Several blood cultures were performed throughout the treatment period, but none were positive. A follow-up TTE on hospital day 70 demonstrated organization of the vegetation. The patient was discharged in good clinical condition after 3 months of treatment.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [115.4, 'kg'], 'height': [163.0, 'cm'], 'creatinine': [1.55, 'mg/dL'], 'age': [31, 'years']}",80.01059,76.01006,84.01112,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 31 years old. 
The concentration of creatinine is 1.55 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 115.4 kg. The patient's bmi is therefore 115.4 kg / (1.63 m * 1.63 m) = 43.43408 kg/m^2.The patient's BMI is 43.4, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 163.0 cm, which is 163.0 cm * 0.393701 in/cm = 64.17326 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.17326 (in inches) - 60) = 59.5985 kg.
Hence, the patient's IBW is 59.5985 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 59.5985 kg + 0.4 * (115.4 kg  - 59.5985 kg) = 81.9191 kg. The patient's adjusted body weight is 81.9191 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 31) * 81.9191 * 1) / (1.55 * 72) = 80.01059 mL/min. Hence, the patient's creatinine clearance is 80.01059 mL/min."
127,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4370314-1,Extracted,"A 65-year-old Japanese man was diagnosed with HIV infection in October 2005. There were no comorbidities, including hypertension, diabetes mellitus and dyslipidemia. cART, comprising lamivudine, abacavir and atazanavir/ritonavir (300 mg of atazanavir boosted by 100 mg of ritonavir), was started to treat his low CD4+ T-cell count (205 cells/μL) and high HIV-RNA (230 000 copies/mL) in June 2006. Soon after the initiation of cART, both proteinuria and hematuria emerged (1+ and 1+ on dipstick test, respectively) and his renal function started to decline slowly, yet there were no crystalline precipitates in the urine. Serum creatinine (Cr) increased from 0.6 to 1.0 mg/dL in June 2009, and to 1.4 mg/dL in February 2012, with persistent proteinuria (1+) and occult hematuria (2+) on a dipstick test. As serum Cr increased to 1.7 mg/dL, he was admitted to the Department of Nephrology in April 2012. The cART regimen remained unchanged, since the control of HIV infection was good at the time.
On admission, his blood pressure was 102/78 mmHg and pulse rate 98 beats per minute. His height was 154 cm and his weight was 35.4 kg (body mass index, 14.9 kg/m2). There were no particular abnormalities on physical examination. The blood data were as follows: white blood cell count 6400/μL; red blood cell count 387 × 104/μL; hemoglobin 12.5 g/dL; platelet count 27.0 × 104/μL; serum urea nitrogen 21 mg/dL; serum Cr 1.7 mg/dL; serum sodium 139 mEq/L; serum potassium 4.5 mEq/L; serum chloride 103 mEq/L and serum C-reactive protein 0.49 mg/dL. Urine dipstick test showed pH 6.0, proteinuria (1+), and occult blood (3+). The urinary concentrations of biomarkers for tubular damage, which was corrected for urinary Cr concentrations, were as follows: N-acetyl-β-d-glucosaminidase (NAG), 12.0 IU/gCr (normal level of NAG concentration, 0.0–7.0 IU/L) and β2M, 391 μg/gCr (normal level of β2M concentration, 27–265 μg/L), respectively. The daily amount of urinary protein was 250 mg. Urinary sediments included 50–99 red blood cells/high power field (HPF), 20–29 white blood cells/HPF and small amounts of crystalline precipitation (no detail for its shape). Infrared spectroscopic analysis was implemented to test whether the urinary crystalline precipitation included atazanavir crystals. In brief, the patient's urine was stored for 24 h, and some of the urine was centrifuged for 2 min at 2000 rpm. The supernatant was used for infrared spectroscopic analysis, and the spectrum of the infrared absorbance was compared with that of the standard for atazanavir analysis (Santa Cruz Biotechnology, Inc., Dallas, TX, USA). This analysis strongly indicated that the urinary crystalline precipitation of the patient included atazanavir crystals (Figure ). The first renal biopsy was performed in May 2012. The kidney tissue contained eight glomeruli, one of which (12.5%) was globally sclerotic. The remaining glomeruli showed no convincing histological changes indicating renal failure. In contrast, interstitial nephritis, accompanied by diffuse inflammatory infiltrates consisting of lymphocytes and plasma cells, was noted (Figure A). Moreover, needle-shaped crystalline precipitation, likely in the epithelia of the tubule, surrounded by multinuclear giant cells, was very characteristic (Figure B). Immunohistochemistry was negative. Electron microscopy showed no electron-dense deposits in the glomeruli; however, crystalline precipitation was confirmed within the tubular epithelial cells (Figure C). In June 2012, atazanavir was replaced by raltegravir, but renal function did not improve. From November 2012, 6 months after the first renal biopsy, oral prednisolone was started at the initial dose of 0.75 mg/kg daily for 4 weeks, and was slowly decreased in the subsequent 5 months. However, serum Cr remained constant at 1.5 mg/dL. In August 2013 (1 year and 3 months after the first renal biopsy), a second renal biopsy contained 28 glomeruli, 5 of which (17.9%) were globally sclerotic. The remaining 23 glomeruli had unremarkable changes. Needle-shaped crystals surrounded by lymphocytes and multinuclear giant cells in the tubulointerstitial compartment were completely removed. Sclerotic findings of glomeruli and intrarenal arterioles including interlobular arteries were more prominent than those observed in the first renal biopsy. Additionally, tubular atrophy and interstitial-fibrosis developed further, although the severe interstitial inflammation was almost cured (Figure D). Immunohistochemistry and electron microscopy showed no characteristic findings.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'weight': [35.4, 'kg'], 'height': [154.0, 'cm'], 'creatinine': [1.7, 'mg/dL'], 'age': [65, 'years']}",21.69118,20.60662,22.77574,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 65 years old. 
The concentration of creatinine is 1.7 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 154.0 cm, which is 154.0 cm * 1 m / 100 cm = 1.54 m. The patient's weight is 35.4 kg. The patient's bmi is therefore 35.4 kg / (1.54 m * 1.54 m) = 14.92663 kg/m^2.The patient's BMI is 14.9, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 35.4 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation. 
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 65) * 35.4 * 1) / (1.7 * 72) = 21.69118 mL/min. Hence, the patient's creatinine clearance is 21.69118 mL/min."
128,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-8556051-1,Extracted,"A 46-year-old Korean woman presented with a 1-month history of progressive generalized edema since November, 2020. She had a history of malignant melanoma on the left posterior side of the thigh that was treated with wide local excision on May 29, 2019. Because of metastasis to the left sentinel and inguinal lymph nodes, she received pembrolizumab 200 mg every 21 days for 1 year, from July 10, 2019 to July 3, 2020. During pemblizumab treatment, she was started on levothyroxine for hypothyroidism, presumably an immune-related AE of pembrolizumab. Four months after the cessation of pembrolizumab, she developed generalized edema, most notable in the periorbital area and both hands and legs, which gradually worsened. She denied taking any new medication or personal and family history of kidney disease. Her baseline observations on admission were as follows: height, 165 cm; weight, 70 kg; blood pressure, 140/80 mm Hg; heart rate, 74 bpm and regular; and temperature, 36.4°C. Clinical examination revealed grade 3 pitting edema in both lower legs. Four months before the onset of the edema, her blood pressure was 120/70 mm Hg, body weight was 65 kg, and body mass index was 23.88 kg/m2. Laboratory findings were as follows: white blood cell count 10,940/μL (reference range 3800–11,000/μL); hemoglobin 12.5 g/dL (reference range 11.2–15.0 g/dL); platelet count 208 × 103/μL (reference range 140–420 × 103/μL); total protein 5.71 g/dL (reference range 6.0–8.0 g/dL); albumin 2.84 g/dL (reference range 3.3–5.2 g/dL); blood urea nitrogen 5.4 mg/dL (reference range 6–26 mg/dL); creatinine 0.66 mg/dL (reference range 0.4–1.2 mg/dL); estimated glomerular filtration rate 105.9 mL/min per 1.73 m2; total cholesterol 238 mg/dL (reference range 0–200 mg/dL); urine red blood cells 6 to 10 cells/high power field (reference range 0–2 cells/high power field); and urine protein to creatinine ratio 3277 mg/g (reference range 0–150 mg/g). Urine dipstick for protein was negative before pembrolizumab treatment. Human immunodeficiency virus antigen and antibody results were negative. A contrast-enhanced computed tomography scan of the abdomen showed normal sized kidneys (right kidney: 9.6 cm; left kidney: 10.7 cm) and no evidence of vaso-occlusive processes in the renal arteries.
She underwent kidney biopsy for suspected glomerulonephritis. Light microscopic findings of biopsy specimens showed that up to 36 glomeruli, 2 glomeruli exhibited segmental sclerosis with atrophied tubules and fibrosis in the interstitium (Fig. A, B). Electron microscopy revealed wide effacement of the epithelial cell foot processes (Fig. C). Immunofluorescence microscopy showed no immune complexes or autoantibody deposition.
After ruling out other causes of secondary FSGS, she was diagnosed with FSGS caused by pembrolizumab. The patient was started on irbesartan and furosemide to treat high blood pressure, proteinuria, and edema. She did not resume treatment with pembrolizumab and immunosuppressive therapy was not applied. After 2 months, the features of nephrotic syndrome resolved and the urine protein-to-creatinine ratio decreased to 203 mg/g.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [46, 'years'], 'weight': [70.0, 'kg'], 'height': [165.0, 'cm'], 'creatinine': [0.66, 'mg/dL']}",104.49165,99.26707,109.71623,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 46 years old. 
The concentration of creatinine is 0.66 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.65 m * 1.65 m) = 25.71166 kg/m^2.The patient's BMI is 25.7, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 56.90954 kg + 0.4 * (70.0 kg  - 56.90954 kg) = 62.14572 kg. The patient's adjusted body weight is 62.14572 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 46) * 62.14572 * 0.85) / (0.66 * 72) = 104.49165 mL/min. Hence, the patient's creatinine clearance is 104.49165 mL/min."
129,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-6389502-1,Extracted,"The patient was a 34-year-old Japanese man, whose family history included a father with hypertension, and a mother that suffered a subarachnoid hemorrhage, but which did not include either a consanguineous marriage or any incidence of renal cysts. At the age of 31, the patient presented with mild albuminuria, and a serum creatinine (Cr) level of 2.98 mg/dL. At the age of 34, the patient was admitted to hospital with a creatinine level of 8.2 mg/dL.
Upon admission, the patient's height, weight, and blood pressure were 179 cm, 58 kg, and 126/80 mm Hg, respectively. The patient exhibited anemia (Hb 8.2 g/dL), azotemia (Cr 8.38 mg/dL), hyperphosphatemia, metabolic acidosis, and secondary hyperparathyroidism; thus, he was diagnosed with ESRD. An abdominal ultrasonography revealed that, although the size of both kidneys appeared to be normal, the patient's renal parenchyma showed increased brightness. We performed a percutaneous renal biopsy; histologically, six of 16 glomeruli displayed global sclerosis, along with mild cellular infiltration, conspicuous interstitial fibrosis, renal tubular atrophy, and cystoid irregular dilation (Figure ), suggesting an NPHP diagnosis. We performed targeted sequencing using a next-generation sequencer, with the approval by the research ethics committee of Tokyo Medical and Dental University in accordance with the Declaration of Helsinki and the patient's written informed consent. A homozygous full gene deletion of NPHP1 (NM_000272.3:g110879716-110962709) was resultantly identified, as well as heterozygous substitutions in PKD1 (NM_0001009944.2:c.6395T>G(p.Phe2132Cys)) (Figure ), BBS1 (NM_024649.4:c.908T>C(p.Val303Ala)), and INPP5E (NM_019892.4:c.1652C>T(p.Thr551Met)).","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [34, 'years'], 'weight': [58.0, 'kg'], 'height': [179.0, 'cm'], 'creatinine': [8.2, 'mg/dL']}",10.41328,9.89262,10.93394,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 34 years old. 
The concentration of creatinine is 8.2 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 179.0 cm, which is 179.0 cm * 1 m / 100 cm = 1.79 m. The patient's weight is 58.0 kg. The patient's bmi is therefore 58.0 kg / (1.79 m * 1.79 m) = 18.10181 kg/m^2.The patient's BMI is 18.1, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 58.0 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation. 
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 34) * 58.0 * 1) / (8.2 * 72) = 10.41328 mL/min. Hence, the patient's creatinine clearance is 10.41328 mL/min."
130,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-5859759-1,Extracted,"A 57-year-old gravida 6, para 3, Asian Taiwanese woman presented to our hospital for scheduled surgery due to endometrial cancer. At admission, her body temperature was 36.8 °C, pulse rate 78 beats/minute, respiratory rate 20/minute, and blood pressure 136/98 mmHg. Her family and environmental history were unremarkable. She did not receive surgery before nor take any medication for systemic disease, such as diabetes mellitus or hypertension. She was a housekeeper. She did not smoke tobacco or consume alcohol. On physical examination, she had normal breathing sound, without wheezing or crackle, and a regular heartbeat without murmur. Her abdomen was soft with normoactive bowel sound on auscultation. Her extremities were freely moveable without edema. She exhibited severe morbid obesity (body weight, 128.4 kg; height, 155.7 cm; BMI, 52.9 kg/m2). Her daily activities were independent most of the time, except for some episodes of exertional dyspnea. Computed tomography (CT) revealed a ventral hernia with a large fascial defect (Fig. ). There were no clinical symptoms, such as abdominal pain or tenderness. She underwent total abdominal hysterectomy, bilateral salpingo-oophorectomy, and ventral herniorrhaphy with Goretex mesh (GORE DUALMESH®).
Her early postoperative course was smooth. She consumed water on postoperative day (POD) 3, a clear-liquid diet on POD5, and a semi-liquid diet on POD7. She began bedside ambulation, and half of her stitches were removed on POD10. However, progressive dyspnea was noted after bedside ambulation. Intra-abdominal free air with elevation of right-side hemidiaphragm was noted by chest X-ray (Fig. ) on POD14. There was no abdominal tenderness or rebounding pain, but there was moderate abdominal distension. She was kept under close observation and began nil by mouth (NPO) for possible visceral perforation.
Two days later (POD16), severe dyspnea and extensive abdominal distention were noted. Her respiratory rate was elevated to 26/minute with accessory muscle use. Arterial blood gas analysis (under simple O2 mask, 10 L/minute) showed: pH, 7.42; partial pressure of carbon dioxide in arterial blood (PaCO2), 44.8 (mmHg); partial pressure of oxygen in arterial blood (PaO2), 86.2 (mmHg); bicarbonate (HCO3-), 28.5 (mmol/L); blood oxygen saturation (SpO2), 96.7%; and blood pressure, 102/75 mmHg. Laboratory tests revealed leukocytosis with a white blood cell (WBC) count of 12,900/uL, hemoglobin (Hb) 12.6 g/dL, and platelet count 310,000/uL. Her C-reactive protein (CRP) was elevated at 165.7 mg/dL. Serum creatinine was 0.99 mg/dL, while serum sodium was 131 mmol/L, and potassium was 3.9 mmol/l. A physical examination showed severe abdominal distension without rebound pain. A pelvic examination demonstrated good healing of the vaginal cuff without leakage. CT showed a large amount of intra-peritoneal free air with little ascites (Fig. ). Because clinical visceral perforation was less likely, under the impression of pneumoperitoneum, in this emergent situation, an 8-Fr. pigtail catheter was inserted under CT guidance for decompression. A massive amount of gas was drained. Subsequently, her dyspnea and abdominal distention dramatically subsided. She re-started oral intake on POD20, and the abdominal pigtail catheter was removed on POD24 after no more free air was revealed by chest X-ray. No further abdominal distention was noted, and she was discharged on POD28. The clinical course of the endometrial cancer and repaired hernia were well at the 1-year follow-up.","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [57, 'years'], 'weight': [128.4, 'kg'], 'height': [155.7, 'cm'], 'creatinine': [0.99, 'mg/dL']}",79.62903,75.64758,83.61048,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 57 years old. 
The concentration of creatinine is 0.99 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.7 cm, which is 155.7 cm * 1 m / 100 cm = 1.557 m. The patient's weight is 128.4 kg. The patient's bmi is therefore 128.4 kg / (1.557 m * 1.557 m) = 52.96486 kg/m^2.The patient's BMI is 53.0, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.7 cm, which is 155.7 cm * 0.393701 in/cm = 61.29925 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.29925 (in inches) - 60) = 48.48828 kg.
Hence, the patient's IBW is 48.48828 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 48.48828 kg + 0.4 * (128.4 kg  - 48.48828 kg) = 80.45297 kg. The patient's adjusted body weight is 80.45297 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 57) * 80.45297 * 0.85) / (0.99 * 72) = 79.62903 mL/min. Hence, the patient's creatinine clearance is 79.62903 mL/min."
131,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-7391090-1,Extracted,"A 75-year-old Japanese male with end-stage renal disease due to antineutrophil cytoplasmic antigen (ANCA)-associated vasculitis had been receiving continuous ambulatory peritoneal dialysis (CAPD) for 9 years. He also had an implanted defibrillator (cardio-resynchronized therapy with defibrillator) to treat chronic heart failure resulting from a myocardial infarction. He had a poor appetite and general malaise without abdominal pain or fever. These symptoms gradually worsened, and he was hospitalized. At the time of admission, his blood pressure was 94/52 mmHg, his height was 165 cm, and his weight was 53 kg. At auscultation, no gallop rhythm was heard, and his extremities were not edematous. The laboratory parameters at the time of admission were as follows: white blood cells, 8080/μL; hemoglobin, 13.5 g/dL; platelets, 121 × 103/μL; total protein, 5.2 g/dL; albumin, 1.8 g/dL; lactate dehydrogenase, 309 U/L; glutamate oxaloacetate transaminase, 25 U/L; glutamate pyruvate transaminase, 19 U/L; blood urea nitrogen, 28 mg/dL; creatinine, 4.97 mg/dL; sodium, 125 mmol/L; potassium, 2.7 mmol/L; chlorine, 91 mmol/L; calcium, 6.8 mg/dL; phosphorus, 4.1 mg/dL; C-reactive protein, 0.092 mg/dL; procalcitonin, 0.21 ng/mL; BNP, 319 pg/mL; intact parathyroid hormone, 149 pg/mL; and β2-microglobulin, 23.4 μg/mL. Chest X-ray revealed bilateral free air in the abdomen (). Subsequent computed tomography of the abdomen revealed marked PP (Figures and ).
Peritonitis due to perforation of the digestive tract was suspected, but the possibility of perforation was considered very low because of the absence of abdominal pain, fever, and turbidity of dialysis drainage. Insufficient priming (air removal) at the time of peritoneal dialysis bag replacement was suspected, and the patient was instructed on how to perform sufficient priming. As a result, the free air in his abdominal cavity gradually disappeared ().","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [75, 'years'], 'weight': [53.0, 'kg'], 'height': [165.0, 'cm'], 'creatinine': [4.97, 'mg/dL']}",9.62721,9.14585,10.10857,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 75 years old. 
The concentration of creatinine is 4.97 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 53.0 kg. The patient's bmi is therefore 53.0 kg / (1.65 m * 1.65 m) = 19.4674 kg/m^2.The patient's BMI is 19.5, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 53.0 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 75) * 53.0 * 1) / (4.97 * 72) = 9.62721 mL/min. Hence, the patient's creatinine clearance is 9.62721 mL/min."
132,2,Creatinine Clearance (Cockcroft-Gault Equation),lab test,decimal,pmc-4400518-1,Extracted,"A 60-year-old man was referred to Japanese Red Cross Koga Hospital with the main complaint of proteinuria and hypertension in September 2008. At another clinic, proteinuria had been identified in 2003, and hypertension and hyperlipidemia had been diagnosed in 2007. A medication regimen of amlodipine (2.5 mg/day) and pitavastatin (2 mg/day) began in January 2008. The patient had no history of diabetes or other glomerular diseases. Physical findings at the first visit to our hospital were the following: height 157.6 cm, body weight 68.0 kg, body mass index (BMI) 27.4, blood pressure (BP) 148/91 mmHg, pulse rate 73 beats/min, body temperature 36.4°C and the tonsils were not enlarged. Blood examination showed blood urea nitrogen 3.89 mmol/L (10.9 mg/dL), serum creatinine 88.4 μmol/L (1.00 mg/dL), uric acid 39.2 μmol/L (6.6 mg/dL), serum albumin 43 g/L (4.3 g/dL), total cholesterol 4.87 mmol/L (188 mg/dL), immunoglobulin (Ig) G 13.49 g/L (1349 mg/dL), IgA 4.35 g/L (435 mg/dL) and IgM 0.83 g/L (83 mg/dL). Autoimmune serological findings and tumor markers such as CEA and CA19-9 were within normal ranges. Urine examination revealed proteinuria (protein and creatinine ratio) 0.67 g/g Cr and urinary red blood cells at 3 per high power field. Urinary protein was determined by Protein Assay Rapid Kit (Wako; Pure Chemical Industries Ltd, Tokyo, Japan). Renal biopsy was not performed because the patient refused it. We added candesartan (2 mg/day), an angiotensin II receptor antagonist, to decrease BP and proteinuria []. As a result, the BP decreased while in our hospital to within the normal range (120–130/80–85), but proteinuria increased gradually. In September 2010, he complained of repetitive apnea during sleep which his wife had noticed and pointed out to him. Therefore, we decided to screen for sleep apnea by first performing pulse oximetry (PULSOX-Me300; Teijin Pharma Ltd, Tokyo, Japan) and Epworth Sleepiness Scale (ESS), a questionnaire about daytime sleepiness []. In these tests, 3% oxygen desaturation index by pulse oximetry was 56.88 (normal range < 5) and ESS score was 10 (normal range ≤ 10). As these results indicated severe sleep apnea, polysomnography (PSG) was performed for a detailed examination (Sleep Watcher E; Teijin Pharma, Ltd and Compumedics Ltd, Victoria, Australia). We then diagnosed severe OSA based on the following data: total apnea–hypopnea index (AHI) 78.3 events per h, obstructive AHI 77.6 events per h, average oxygen saturation (SaO2) 94.0%, minimum SaO2 65.0% and cumulative time percentage of total sleep time when SaO2 was <90% (SaO2 <90%) 20.7% ( and ).
After obtaining informed consent, CPAP treatment using a nasal mask (AutoSet C; Teijin Pharma Ltd and ResMed, Sydney, Australia) was initiated. The setting of the device was auto-titration mode (pressure 4.0–20.0 cm H2O), and we instructed the patient to use it overnight. This device could store compliance and efficacy data, which were downloaded using software at follow-up visits every month. At 3 months after CPAP initiation, CPAP usage days and daily hours were 96.4% and 5.3 h, respectively (). Then, PSG was performed to evaluate the effect of CPAP on OSA. The data exhibited clear improvement of OSA: total AHI, 6.1 events per h; average SaO2, 96.0%; minimum SaO2, 93.0% and SaO2 <90%, 0% (). Importantly, total elimination of saturated oxygen levels <90% indicated the disappearance of severe hypoxia during sleep. Along with the reduction of apnea and hypopnea events, proteinuria also clearly decreased ( and ), although no other medication was changed. In addition, home BP in the morning, which was measured within 1 h after waking as described previously [, ], decreased mildly ( and ). Then, we stopped amlodipine at 5 months after CPAP initiation (). Heart rate (HR) and pulse rate rise index-6, the number of pulse rate increases ≥6 per h determined by pulse oximetry, decreased clearly after CPAP treatment (). On the other hand, an apparent change of BMI was not found during the period (). At 6 months after CPAP initiation, the low level of proteinuria (≤0.3 g/g Cr) had continued (). In addition, average proteinuria for 6 months after CPAP was markedly lower (0.3 g/g Cr) than before CPAP treatment (1.2 g/g Cr).","What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [60, 'years'], 'weight': [68.0, 'kg'], 'height': [157.6, 'cm'], 'creatinine': [1.0, 'mg/dL']}",66.69471,63.35997,70.02945,"The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 60 years old. 
The concentration of creatinine is 1.0 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 157.6 cm, which is 157.6 cm * 1 m / 100 cm = 1.576 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.576 m * 1.576 m) = 27.37767 kg/m^2.The patient's BMI is 27.4, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 157.6 cm, which is 157.6 cm * 0.393701 in/cm = 62.04728 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.04728 (in inches) - 60) = 54.70874 kg.
Hence, the patient's IBW is 54.70874 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 54.70874 kg + 0.4 * (68.0 kg  - 54.70874 kg) = 60.02524 kg. The patient's adjusted body weight is 60.02524 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 60) * 60.02524 * 1) / (1.0 * 72) = 66.69471 mL/min. Hence, the patient's creatinine clearance is 66.69471 mL/min."
133,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3914169-1,Extracted,"A 63-year-old female on maintenance hemodialysis was admitted to our hospital for an initial generalized tonic seizure suffered at home. Just after admission, a second generalized tonic seizure was observed. During the seizure, conjugate eye deviation toward the upper left was noted. On admission, her pulse rate was 92 beats/min, blood pressure 134/92 mm Hg, and body temperature 36.5°C. Neither abnormal heart sounds nor rales were noted on auscultation. Brain computed tomography (CT) and magnetic resonance imaging (MRI) showed no mass lesion, hemorrhage, or infarction (Figures and ). Electroencephalography showed repetition of intermittent high-amplitude irregular slow waves in the right frontal lobe (). Based on these findings, the patient was diagnosed with generalized partial seizures. After administration of phenytoin sodium, the seizures resolved, and neurological findings normalized. According to her medical record, she had no history of diabetes mellitus or coronary artery disease, nor any family history of coronary artery disease. She had been stable on maintenance hemodialysis for 32 years, and the appropriate dry weight was maintained. Kt/V (urea) was 1.48. Her administration had included fentanyl patch, etizolam, rabeprazole sodium, celecoxib, lactomin, camostat mesilate, tocopherol nicotinate, acetaminophen, and mecobalamin. On admission, electrocardiogram (ECG) was normal.
On the second hospital day, ECG showed inverted T waves and QT prolongation in all leads without chest pain, dyspnea, or any other cardiac symptoms. Neurological findings were normal. Blood test findings were as follows: creatinine, 6.46 mg/dL; blood urea nitrogen, 55 mg/dL; sodium, 141 mEq/L; potassium, 5.3 mEq/L; calcium, 8.9 g/dL; phosphorus, 7.0 mg/dL; hemoglobin, 12.3 g/dL; aspartate aminotransferase, 19 IU/L; alanine aminotransferase, 8 IU/L; creatine kinase, 312 IU/L; and cardiac troponin t-test, negative (Troponin T kit; TROP T sensitive, Roche Diagnostics, Mannheim, Germany: cutoff value is 0.1 ng/mL). Thoracoabdominal computed tomography (CT) did not show any abnormal findings. Echocardiography demonstrated left apical akinesis. On the third hospital day, the patient underwent cardiac catheterization. While coronary angiography showed normal coronary arteries, left ventriculography showed extensive severe hypokinesis in the anteroseptal and apical segments with hyperkinesis in the basal segments (). Based on these findings, the patient was diagnosed with takotsubo cardiomyopathy.
We followed with serial ECG monitoring for several weeks. Her clinical course of takotsubo cardiomyopathy was uneventful and seizure had not been seen. After two months, left ventricular apical wall motion abnormalities on echocardiography had reversed, and the inverted T waves and QT prolongation on ECG had also resolved ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [63, 'years'], 'creatinine': [6.46, 'mg/dL']}",6.74752,6.41014,7.0849,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 63 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 6.46 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (6.46/0.7)**-1.2 * 0.9938**63 * 1.012 = 6.74752.
Hence, the GFR value is 6.74752 ml/min/1.73 m²."
134,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3696308-1,Extracted,"A 66-year-old male, known diabetic for last 1 year was hospitalized with pain in right upper quadrant of abdomen for 20 days and breathlessness at rest for 5 days. No written reports of blood sugar levels were available with patient at the time of admission. On verbal enquiry, he reported that blood sugars were always below 140 mg%. His blood sugars were well-controlled on medical nutrition therapy (diet with low glycemic index). He had never taken any anti-diabetic drugs. During this admission, blood investigations revealed fasting blood sugar of 142 g/dl, white blood cell count of 12700/c.mm, platelets of 48000 lacs/c.mm. Renal profile showed blood urea nitrogen of 33.4 mg/dl, creatinine of 1.7 mg/dl, sodium of 129 meq/l, and potassium of 3.9 meq/l. Liver function tests revealed total bilirubin level of 6.6 mg/dl, direct bilirubin level of 5.8 mg/dl, alanine amino-transferase level of 75 u/l, aspartate amino-transferase level of 103 u/l, alkaline phosphatase level of 202 u/l, total protein level of 5.8 g/dl and albumin level of 2.9 g/dl. Hepatitis B surface Antigen (HBsAg) and anti Hepatitis C virus (HCV) were negative. Chest X-ray revealed right mid zone pneumonia and ultrasound abdomen was normal. Urine routine revealed 10-12 pus cells/high power field and later urine culture grew Escherichia coli. He was empirically started on i.v. moxifloxacin (400 mg) at admission and was managed symptomatically. Twenty four hours later i.v. cefepime/tazobactum combination was also added based on urine culture sensitivity report. After 16 h of hospitalization patient developed tremors, sweating and was found to have blood glucose level of 58 mg/dl. He was administered 10% dextrose intravenously, which relieved his symptoms. The patient had repeated episodes of hypoglycemia for subsequent 3 days (blood glucose levels 77, 44, 54 mg/dl) despite regular administration of intravenous 10% dextrose. Moxifloxacin was discontinued after 3 days, after it was suspected to cause the hypoglycemia. After stopping moxifloxacin, his blood sugar levels increased after 24 h and he developed hyperglycemia (blood sugars-273, 324, 298 mg/dl) and required insulin treatment. The patient was discharged on recovery after 10 days of hospitalization. At 1 month follow-up, his liver function tests and kidney function tests were normal. He continued to require insulin for glycemic control even 1 month after his discharge. His last blood sugars level was 115 mg% with insulin.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [66, 'years'], 'creatinine': [1.7, 'mg/dL'], 'sex': 'Male'}",43.91108,41.71553,46.10663,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 66 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.9)**-1.2 * 0.9938**66 * 1.0 = 43.91108.
Hence, the GFR value is 43.91108 ml/min/1.73 m²."
135,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8267016-1,Extracted,"The patient was a 45-year-old male with a past medical history of intermittent asthma, hypertension, and type 2 diabetes mellitus who presented to the emergency department (ED) via ambulance status post fall in the context of phencyclidine (PCP) intoxication. Initially in the ED the patient was urinating on the floor, attempting to fight staff members, and uncooperative with examination. Intravenous haloperidol 5 mg and midazolam 4 mg were administered for agitation, after which the patient was able to tolerate medical evaluation and management. Additional history was limited at this time given the patient’s intoxicated state. The patient was unable to participate in a formal review of systems given his altered mental status (AMS). Initial vital signs were blood pressure 146/83 mm Hg, pulse 104 beats per minute, temperature 98.4 °F, respiratory rate 18 breath per minute, and oxygen saturation 98%. Physical examination was grossly normal aside from a 3 cm stellate forehead laceration. Apart from a leukocytosis of 15 K/mm3, complete blood count, and comprehensive metabolic panel were within normal limits. Pertinent normal laboratory test results included a sodium of 140 mmol/L, blood urea nitrogen of 15, and a creatinine of 0.87 mg/dL. Urine drug screen was positive for benzodiazepines and PCP. Urinalysis was positive for only bacteria and nitrites along with 6 to 9 epithelial cells per high-power field suggesting possible contamination. Urine cultures were not obtained. Computerized tomography (CT) imaging demonstrated left zygomaticomaxillary complex fractures without acute intracranial pathology. CT imaging of the patient’s cervical spine did not demonstrate any acute pathology. While in the ED, the patient’s forehead laceration was sutured. The patient was admitted to an inpatient medicine unit for further management of his AMS and facial fracture.
On admission, the patient was somnolent, oriented only to self, and unable to engage with the admission assessment. An extensive AMS workup was completed, which included ammonia, vitamin B12 and folate levels, thyroid-stimulating hormone, blood cultures, C-reactive protein, repeat comprehensive metabolic panel/complete blood count, syphilis screen, and repeat head CT. Aside from a mildly elevated C-reactive protein of 2.6 mg/dL and leukocytosis of 14.2 K/mm3 the remainder of the patient’s laboratory test results was within normal limits. Specific laboratory tests of interest pertinent to a delirium workup returned within normal limits as follows: ammonia 15 µmol/L, thyroid-stimulating hormone 0.4, vitamin B12 576 pg/mL, and folate 22.9 ng/mL. The differential diagnosis for the patient’s AMS remained wide, so he was placed on the Clinical Institute Withdrawal Assessment for Alcohol protocol and started on intravenous thiamine as a history of alcohol use could not be ruled out. The patient was also given a 3-day course of intravenous ceftriaxone considering equivocal urinalysis findings. Plastic surgery was consulted and recommended nonemergent elective repair of the facial fractures, but treatment was deferred as the patient remained altered and could not consent to the procedure.
Per family collateral, the patient worked part-time as a mechanic, lived alone, performed all activities of daily living independently, and did not have any history of neurologic or psychiatric disease. Family was unable to provide any additional information regarding the patient’s substance use. The patient did not receive any additional lorazepam per Clinical Institute Withdrawal Assessment for Alcohol protocol or for vital sign abnormalities consistent with alcohol withdrawal. Aside from his tachycardia on initial presentation in the ED, the patient did not demonstrate tachycardia after admission to the inpatient medicine unit. On the third hospital day, the patient’s AMS persisted, and neurology was consulted and evaluated the patient for additional causes of encephalopathy.
On the consulting neurologist’s initial examination, the patient remained lethargic, oriented only to self, unable to follow complex commands, and hypophonic with increased speech latency. No focal cranial nerve deficit was appreciated; however, the patient exhibited hypertonicity with significant oppositional paratonias in all 4 extremities along with bilaterally upgoing plantar reflexes. Magnetic resonance imaging (MRI) and electroencephalography (EEG) were ordered per neurology recommendations. EEG did not demonstrate epileptiform activity or generalized slowing. However, MRI revealed a restricted diffusion/focal hyperintensity within the splenium of the corpus callosum on diffusion-weighted imaging (DWI) and fluid-attenuated inversion recovery (FLAIR) images, respectively. MRI findings on FLAIR, DWI, and ADC (apparent diffusion coefficient) are highlighted in . In consideration of the patient’s recent exposure to neuroleptics, persistent encephalopathy, and significant oppositional paratonias, the possibility of an atypical variant of NMS contributing to the patient’s delirium was likely. Despite the likelihood of atypical NMS, in considering the wide differential diagnosis of callosal lesions the probability of the MRI lesion representing a new infarct remained. Therefore, the patient was placed on standing aspirin 325 mg along with atorvastatin 40 mg daily. CT angiography of the head and neck was completed and was unremarkable. The patient was also started on standing benztropine 1 mg twice daily for atypical NMS. Of note, lorazepam was not used as there was concern for additional central nervous system depression in an already somnolent and delirious patient.
By the seventh hospital day, the patient became more alert, had improved orientation, was able to complete 2 step commands with prompting, and had reduced cogwheeling on examination. Additionally, the patient’s leukocytosis had down-trended to 13.2 K/mm3. The scheduled benztropine was also discontinued. The patient did not require any physical restraints or tranquilizers for agitation after admission. The patient’s MRI was repeated 11 days after initial imaging, which redemonstrated the corpus callosum splenium hyperintensity on FLAIR imaging and without restricted diffusion on DWI. The patient was instructed to repeat imaging as an outpatient to confirm the diagnosis of subacute callosal infarct versus transient splenial lesion of another etiology. The patient was recommended to be discharged to a rehabilitation facility to further manage his physical deconditioning and was subsequently lost to follow-up.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [45, 'years'], 'creatinine': [0.87, 'mg/dL'], 'sex': 'Male'}",100.51429,95.48858,105.54,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 45 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.87 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.87/0.7)**-0.302 * 0.9938**45 * 1.0 = 100.51429.
Hence, the GFR value is 100.51429 ml/min/1.73 m²."
136,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3968600-1,Extracted,"An 8-year-old male child presented with a history of facial puffiness and edema of one year duration. He was diagnosed to have nephrotic syndrome and was treated by a local physician with steroids. He did not improve, however, and was referred to this hospital for further management.
There was no family history of kidney disease. He is the first child of non-consanguineous marriage. There was no history of drug ingestion including exposure to mycotoxins or other herbal medicines. No history of recurrent respiratory symptoms. On examination, patient had stunted growth with moon facies, secondary to steroids and had clinical features of rickets.
His investigations revealed hemoglobin of 10 g/dl, blood urea 33 mg/dl and serum creatinine 0.7 mg/dl. His liver functions revealed hypoalbuminemia of 2.6 g/dl. His liver enzymes were within normal limits. He was human immunodeficiency virus non-reactive and hepatitis B surface antigen and hepatitis C virus and 24 h urine protein was 3565 mg/dl. Complete urine examination showed 2+ albumin, 4-6 red blood cells and granular casts. Ultrasound revealed normal sized kidneys with normal echotexture.
He was started on cyclophosphamide. However, there was no response even after 6 months. Hence a kidney biopsy was done. Biopsy showed 23 glomeruli, four of whom showed segmental sclerosis []. Basement membrane and cellularity were normal in the uninvolved glomeruli. Tubular epithelial cells revealed changes diffusely. The lining cells in many cells revealed enlarged nuclei with lobulated appearance. These cells are larger than the normal tubular epithelial cells []. There was chromatin clumping giving a hyperchromatic appearance. Mitoses were sparse. There is atrophy of the tubules with thickening of tubular basement membrane. There is interstitial fibrosis and interstitial mild lymphomononuclear infiltration [].
Immunohistochemical stains for BK virus and cytomegalovirus were negative. Ki-67 index was low. Immunofluorescence did not reveal any significant immune deposits.
He is under regular follow-up and his last creatinine has increased to 1.2 mg/dl.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [8, 'years'], 'creatinine': [1.2, 'mg/dL'], 'sex': 'Male'}",95.66516,90.8819,100.44842,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 8 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.2 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.2/0.9)**-1.2 * 0.9938**8 * 1.0 = 95.66516.
Hence, the GFR value is 95.66516 ml/min/1.73 m²."
137,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5518485-2,Extracted,"A 58-year-old Thai female patient with hypertension, hyperlipidemia, and type 2 diabetes mellitus was infected with HIV 1.5 years ago. She had been taking antiretroviral drugs including tenofovir, emtricitabine, and boosted darunavir thereafter and achieved virological control after 6 months of therapy. Her CD4-positive T-lymphocyte count was 532/mm3 (40%). Her other medications were amlodipine 5 mg/day, enalapril 10 mg/day, fenofibrate 300 mg/day, and metformin 500 mg/day. She gradually developed anorexia, nausea, and fatigue over two weeks' duration. She also noticed a decrease in her daily urine volume and new-onset nocturia together with swelling in both of her legs particularly in the evening. She reported no fever, rash, or joint pain. She denied taking over-the-counter medication or nonsteroidal anti-inflammatory drugs. On examination, she was alert and had normal vital signs except for mild hypertension (body temperature 37.0°C, pulse rate 70/min, respiratory rate 16/min, and blood pressure 140/70 mmHg). She also had mildly pale conjunctivae and pitting edema in both of her legs. Laboratory tests showed severe azotemia (BUN 21.4 mmol/L, Cr 1,370 µmol/L) compared to baselines labs 1 month earlier (Cr 124 µmol/L). She also had hyponatremia, hypokalemia, metabolic acidosis, and elevated muscle enzyme (sodium 127 mEq/L, potassium 5.5 mEq/L, chloride 94 mEq/L, bicarbonate 10 mEq/L, and creatine phosphokinase 1,904 U/L; normal value 22–165 U/L). Urinalysis revealed isosthenuria, albuminuria, leukocyturia, and microhematuria without dysmorphic RBC (specific gravity 1.010, proteinuria 2+, glucose negative, WBC 3–5/hpf, and RBC 20–30/hpf). Renal ultrasonography demonstrated normal size but mildly increased parenchymal echogenicity of both kidneys without hydroureter or hydronephrosis. AKI was diagnosed. Differential diagnoses of AKI included tenofovir-induced ATN, HIV-associated nephropathy/immune complex glomerulonephritis, and rhabdomyolysis.
RRT was initiated soon after admission due to uremia and volume overload. After successful insertion of flexible double-cuff PD catheter, automated PD (Homechoice cycler; Baxter) using total dialysate (Dianeal; Baxter) volume of 10 L was started (fill volume of 2 L, five cycles, therapy time 12 hours) on the first day of admission resulting in adequate control of fluid, electrolytes, and acid-base balance. The doses of PD by total weekly Kt/V and total weekly CCr were 3.63 and 91.94 L/week, respectively. Renal biopsy was later performed revealing evidence of acute granulomatous interstitial nephritis (AIN) and ATN without evidence of glomerular or vascular injury. Antiretroviral drugs-induced ATN/AIN was diagnosed. The attending physician then switched antiretroviral regimen to stavudine/lamivudine/boosted darunavir regimen. During fourth week of admission, her urine volume had increased to 0.8–1.0 L per day but the measured renal CCr was still low (6.62 mL/min/1.73 m2). She was discharged from the hospital anyway and was prescribed to continue automated PD during night time at home (night intermittent PD; NIPD) at a similar dose (fill volume of 2 L, five cycles, therapy time 12 hours). Eventually, PD was successfully discontinued 9 months after the onset of AKI in August 2014. At that time, her serum Cr was 159 µmol/L, and measured renal CCr was stable at 17.3 mL/min/1.73 m2 with daily urine volume of 2,480 mL. Afterwards, she remained in chronic kidney disease (CKD) stage 4 with stable renal function for another whole year.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [58, 'years'], 'creatinine': [1370.0, 'µmol/L']}",2.43574,2.31395,2.55753,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 58 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1370.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 1370.0 µmol. To convert 1370.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 1370.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00137 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00137 mol Serum Creatinine * 113.12 g/mol = 0.15497 g Serum Creatinine. To convert 0.15497 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.15497 g Serum Creatinine * 1000.0 mg/g = 154.97 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 154.97 mg Serum Creatinine/10.0 dL = 15.497 mg Serum Creatinine/dL. The concentration value of 1370.0 µmol Serum Creatinine/L converts to 15.497 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (15.497/0.7)**-1.2 * 0.9938**58 * 1.012 = 2.43574.
Hence, the GFR value is 2.43574 ml/min/1.73 m²."
138,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7006151-1,Extracted,"A 55-year-old previously healthy man from the western province of Sri Lanka was admitted to Colombo South Teaching Hospital (CSTH) 18 h after an HNV bite. He was initially managed in a peripheral hospital and later transferred as he was anuric for 8 h. He also had vomiting and loose stools. Fang marks were seen on the fifth left toe with pain, minimal swelling and two blisters on the dorsum of the foot. The killed snake was identified by the medical officer as an HNV. He was conscious and rational with a pulse rate of 100 bpm, blood pressure 150/100 mmHg and oxygen saturation of 98%. There was no bleeding tendency or neurological manifestations. Bedside whole blood clotting time was less than 20 min on admission to the peripheral hospital and at 18 h when seen at the CSTH. Polyvalent antivenom was not given as it is ineffective in neutralizing HNV toxicity and carry a high risk of side effects.
Initial investigations revealed, haemoglobin 13.2 g/dl, white cells 13.2 × 109/L, platelets 68 × 109/L, serum sodium 143 mmol/L, serum potassium 4.2 mmol/L and serum creatinine 3.2 mg/dl. On the 2nd day, haematological investigations revealed, haemoglobin 10.5 g/dl, white blood cells 14.1 × 109/L and platelets 58 × 109/L, whole blood clotting time > 20 min, PT/INR 1.7 (reference range: < 1.1) and APTT 48 s (30–40s). Total bilirubin 62.14 μmol/L (5–21) with direct bilirubin 10.08 μmol/L (< 3.4), serum alanine aminotransferase (ALT) 171 U/L (10–40), serum aspartate aminotransferase (AST) 808 U/L (10–35), Creatine kinase (CK) 750 U/L (15–105), serum lactate dehydrogenase (LDH) 2370 U/L (230–460) and serum creatinine was 409 μmol/L (70–120). Blood picture revealed fragmented red cells and thrombocytopenia suggestive of microangiopathic haemolytic anaemia (MAHA). In view of thrombotic microangiopathy (TMA), he was transfused with fresh frozen plasma with the improvement of INR and APTT. The patient was commenced on haemodialysis due to acute kidney injury (AKI).
On the 3rd day, he became tachypneic with de-saturation and blood gases revealed PH 7.21, PCO2 45 mmHg, PO2 31 mmHg HCO3 12.4 mEq/L. He was intubated and started on mechanical ventilation. Bleeding through the endotracheal tube was noted but there was no bleeding from elsewhere. Chest x-ray revealed bilateral alveolar shadowing suggestive of pulmonary haemorrhages (Fig. ). At this time his platelet count was 56 × 109/L, INR 1.1, APTT 40 s, thrombo-elastometry showed only a deficiency of platelets. Due to the life-threatening nature of the situation, he was commenced on intravenous methylprednisolone 1 g pulse therapy daily along with FFP and platelet transfusions. There was a rapid improvement of hypoxia with the resolution of chest x-ray changes during the next 48 h. We discontinued steroid therapy after 3 days as there was no further bleeding and chest x-ray changes were resolving (Fig. ).
Because of, persistent TMA as evidenced by a further drop in haemoglobin (8 mg/dl) and platelets (28 × 109/L) plasmapheresis was commenced and continued for 6 cycles. Despite the effective treatment of TMA, the patient went on to develop dry gangrene of toes on both feet (Fig. ). Renal function did not improve and required long term maintenance haemodialysis. He underwent renal transplantation 11 months after the incident due to end-stage renal disease.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [55, 'years'], 'creatinine': [3.2, 'mg/dL'], 'sex': 'Male'}",22.01121,20.91065,23.11177,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 55 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.2 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.2/0.9)**-1.2 * 0.9938**55 * 1.0 = 22.01121.
Hence, the GFR value is 22.01121 ml/min/1.73 m²."
139,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4379634-1,Extracted,"A 16-year-old boy presented with history of vomiting and headache of 15 days duration. On evaluation, he was found to have blood pressure of 160/80 mmHg. He had a history of consumption of anabolic steroids (dexona + dianabol [methandrostenolone] combination) for general body development for a duration of 3 months.
Laboratory studies revealed a serum creatinine of 2.27 mg/dl, urine protein to creatinine ratio of 6, proteinuria of 4.7 g in 24 h. Urine microscopy showed 10-12 white blood cells and 5-40 red blood cells per high power field. His liver function tests (LFT) were normal. There was no jaundice or evidence of cholestasis. Tests for antibodies to HIV, hepatitis B and C viruses were negative. There was no biochemical evidence of a TMA. Ultrasound examination of both kidneys revealed Grade II renal parenchymal changes.
The renal biopsy showed global glomerulosclerosis in four of the 15 glomeruli, with the remaining showing mesangial and endocapillary cell proliferation with paramesangial capillary wall thickening. The extra glomerular compartment showed interstitial fibrosis amounting to 20%, aggregates of mononuclear inflammatory cells, tubular atrophy, microcystic dilatation of tubules with hyaline casts and necrotic cells in nonatrophic tubular lumina [].
The immunofluorescence (IF) done on two glomeruli revealed arborizing mesangial deposits of IgA (3+), IgG (2+ to 3+) and C3 (2+ to 3+) with extension into the paramesangial capillary walls. There was no staining for IgM, C1q or C4. Electron microscopic examination of seven glomeruli showed abundant paramesangial electron-dense deposits, focally extending subendothelially into peripheral capillary loops. Segmental thinning and splitting of glomerular basement membranes (GBMs) were present, suggestive of primary IgAN. One glomerulus showed segmental [Figures and ] and another showed global collapse with corrugated GBMs and pseudocrescent formation [Figures –], features consistent with CG. Foot process effacement was extensive. Endothelial tubuloreticular inclusions were absent, in keeping with the patient's negative serology for HIV and other viral infections. There was no evidence of TMA.
The final diagnosis was CG associated with IgAN. The patient was treated with oral prednisolone and mycophenolate mofetil with therapeutic drug level monitoring and strongly recommended to abstain from further use of body-building drugs. On follow-up after 6 months, the patient has achieved partial remission with proteinuria decreasing to 1.6 g/24 h. But serum creatinine remained high at 2.96 mg/dl. The patient is continuing therapy and is on regular follow-up.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [16, 'years'], 'creatinine': [2.27, 'mg/dL']}",42.35768,40.2398,44.47556,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 16 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.27 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.27/0.9)**-1.2 * 0.9938**16 * 1.0 = 42.35768.
Hence, the GFR value is 42.35768 ml/min/1.73 m²."
140,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6423434-1,Extracted,"Between August 2017 and September 2017 in Tehran, a 59-year-old man was brought in the Emergency Department with fever, disorientation, and agitation which had developed over the previous two days. He had also suffered from a three-month period of nausea and abdominal pain along with a progressive weight loss of 17 kg. He had used opium every day for 20 years. His current medication included omeprazole 20 mg daily and ondansetron 4 mg bid.
On physical examination, the patient was agitated and disoriented. He had an axillary temperature of 37.4 °C, blood pressure of 110/70 mmHg, pulse of 100 per minute, and a respiratory rate of 18 per minute. He looked pale. Neurologically, he was awake but disoriented. No other abnormalities were found.
Laboratory tests showed an elevated urea (50 mg/dl), creatinine (1.7 mg/dl), sodium (153 mmol/L), and leukocytosis of 13000 per mm3 with a shift to left (75% neutrophil, 20% lymphocyte, and 5% mixed cells), a low hemoglobin of 10.3 mg/dl with a mild hypochromic microcytic smear; evaluation for hemolysis was negative. Other metabolic evaluations including glucose were normal. Serum drug screening revealed a positive level for opiates. The brain computerized tomography (CT) scan, electroencephalography (EEG), and his cerebrospinal fluid (CSF) analysis were normal. As we could not rule out herpetic encephalitis with these data, he was commenced on intravenous acyclovir 750 mg every 12 hours and subcutaneously methadone 5 mg every 12 hours to control opioid withdrawal syndrome as well as providing electrolyte correction. After two days, his consciousness had not changed. Repeated evaluation of CNS, including brain Magnetic resonance imaging (MRI) and CSF analysis, showed normal results.
To further the evaluation of his abdominal pain, the abdominal ultrasound and CT scan were requested which revealed a coarse echo of the liver and a diameter of the portal vein of 13 mm. The upper and lower endoscopy showed gastritis and internal hemorrhoid. The Magnetic resonance cholangiopancreatography (MRCP) was normal. On the third day of admission, he had experienced a tonic-clonic seizure. EEG showed evidence of encephalopathy, but his brain CT scan remained normal. On the fourth day of admission, his gastric secretion changed to coffee-ground appearance. Finally, he had a cardio-pulmonary arrest and passed away. After his death, we received a negative result of his CSF herpes virus (HSV) polymerase chain reaction (PCR), and his serum lead level showed 98 µg/dl.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [59, 'years'], 'creatinine': [1.7, 'mg/dL'], 'sex': 'Male'}",45.86498,43.57173,48.15823,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 59 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.9)**-1.2 * 0.9938**59 * 1.0 = 45.86498.
Hence, the GFR value is 45.86498 ml/min/1.73 m²."
141,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7263708-1,Extracted,"A 68-year-old non-smoking Caucasian man initially transferred from a different hospital for evaluation of a brain lesion found on imaging. The patient has a medical history pertinent to BPH, and his family history was relevant for a father with colon cancer.
Six months earlier, his primary care physician (PCP) evaluated him for worsening urinary symptoms and subsequently referred him to a urologist. Upon further evaluation, his prostate-specific antigen (PSA) level was normal at 3 ng/mL, and his digital rectal examination was normal, for which a cystoscopy with prostate GreenLight™ (Boston Scientific, Marlborough, MA) enucleation was performed for BPH diagnosis. Five months later and one month before this admission, he discerned progressive worsening of double vision. His PCP examined and referred him to an ophthalmologist, who diagnosed him with third cranial (oculomotor) and sixth cranial (abducens) nerve palsy, which was subsequently confirmed by a neurologist.
Subsequently, the patient was admitted to the other hospital, and upon admission, he was found to have an acute kidney injury (AKI) and hyperkalemia. Laboratory studies showed white blood cells of 27 x 10^3/µL, hemoglobin of 11.5 g/dL, and platelet count of 201 K/µL. His chemistry was pertinent for sodium of 134 mmol/L, potassium of 6.5 mmol/L, chloride of 103 mmol/L, bicarbonate level of 10 mmol/L, a glucose of 159 mg/dL, creatinine of 13 mg/dL, uric acid of 19.6 µmol/L, chromogranin A of 656 µg/L, and PSA of 22.67 ng/mL. He received hemodialysis and underwent bilateral percutaneous nephrostomy, after which his AKI resolved. An abdominal CT scan showed findings consistent with diffuse metastatic disease to the lungs, liver, and peritoneum, and brain MRI showed brain lesions. Therefore, he was, subsequently, transferred to our hospital for further care.
Upon evaluation in our hospital, imaging showed findings consistent with earlier recognized lesions at the other hospital (Figures -). The patient was, therefore, seen by a multidisciplinary team of a neurosurgeon, an ophthalmologist, a medical oncologist, and a radiation oncologist. Biopsies of a perirectal mass showed a high-grade neuroendocrine tumor. The oncologist who saw him diagnosed him with metastatic SCC of the lung; therefore, he was started on one cycle of carboplatin/etoposide chemotherapy during his hospitalization, which he tolerated well and was discharged home.
A senior oncologist saw the patient, reviewed all his radiographic images, and questioned the initial diagnosis of lung SCC based on the patient’s clinical presentation of urinary obstruction, hydronephrosis, and AKI. Hence, the original tumor location speculated to be consistent with a high-grade neuroendocrine tumor/SCC originating from the urinary tract. The senior oncologist, therefore, advised cystoscopy for prostate biopsy, which was declined by consulting urologist because the “prostate exam was normal.” Consequently, the senior oncologist sent the patient to a second urologist who performed cystoscopy and informed the patient that everything was normal. The senior oncologist had a thorough discussion to explain the necessity of a meticulous endoscopic urethral examination and prostate biopsy. Subsequently, the patient took the senior oncologist’s advice, went back to the urologist, and underwent a repeat diagnostic cystoscopy. This time, biopsies of the urethra were taken and confirmed a high-grade large cell neuroendocrine carcinoma. 
 
The tissue specimen from this case was compared to the patient’s previous perirectal mass biopsy and was found to have similar features. Immunohistochemical (IHC) stains were negative for CK7, CK20, PSA, and prostate-specific acid phosphatase. Scattered individual cells were positive for nuclear NKX 3.1 and cytoplasmic CK5. Moreover, there was diffuse variable positivity for nuclear p63 with greater than 80% of nuclei were positive for p53 and diffuse strong positivity for CD56, thyroid transcription factor 1 (TTF-1), and synaptophysin (Figure ).
Based on the clinical history of disease distribution, the pathologist considered the neoplasm to be likely of either prostate or urinary bladder origin. Subsequently, the senior oncologist reviewed the urethral biopsy, remained suspecting the primary site of cancer to be originating from the prostate. Therefore, he advised for prostate biopsy. Finally, the patient underwent transrectal ultrasound-guided prostate biopsy, which confirmed that all 12 cores were positive for prostate SCC (Figure ). The pathology findings confirmed the senior oncologist’s initial surmise that the metastatic cancer origin was from the genitourinary tract, likely involving prostate extending into the urethra.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [68, 'years'], 'creatinine': [13.0, 'mg/dL'], 'sex': 'Male'}",3.77554,3.58676,3.96432,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 68 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 13.0 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (13.0/0.9)**-1.2 * 0.9938**68 * 1.0 = 3.77554.
Hence, the GFR value is 3.77554 ml/min/1.73 m²."
142,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8573490-1,Extracted,"A 63-year-old male with history of alcoholic cirrhosis, without any significant valve disorder, and without history of drug abuse (MELD score of 13 as of a month ago) presented to the hospital with abdominal pain for the past 3 weeks. He had no prior history of ascites and never underwent a paracentesis. He had multiple admissions in the past for alcohol withdrawal with the most recent hospitalization 3 weeks ago. On examination, he was cachectic, icteric, and had a holosystolic murmur which was heard best at the apex with radiation to the axilla. His abdomen was diffusely tender and distended. There were erythematous, purpuric macules, and papules scattered diffusely on hands, legs, and feet bilaterally ().
Admission labs were white blood cell count of 16.8 k/uL, hemoglobin of 10 g/dl, platelets of 292 k/uL, prothrombin time 27.8 s, sodium of 125 mEq/L, potassium of 4.8 mmol/L, urea of 54 mg/dL, creatinine 3.3 mg/dL, bilirubin 9.1 mg/dL, alanine transaminase (ALT) of 24 U/L, aspartate transaminase (AST) of 76 U/L, alkaline phosphatase of 93 U/L, lactic acid dehydrogenase (LDH) 829 U/L, total protein of 7.4 g/dL, albumin of 2.6 g/dL, and INR of 2.3. One month ago, labs were essentially normal, except for a bilirubin of 4.4 mg/dL, and hemoglobin of 10.5 g/dL. His current MELD score was 38 points. Paracentesis was performed on the ascitic fluid which showed a cell count of 2000 cells/mm3 with neutrophilic predominance with polymorphonuclear cell count PMN of 700 cells/mm3. The admission lab values are mentioned in .
Patient was empirically started on Piperacillin and Tazobactam. Patient blood culture revealed gram-positive cocci in clusters and 750 mg of Vancomycin was added 2 days later (given high suspicion of healthcare-associated infection which is defined as infections that develop in less than 48 h after admission or previous exposure to healthcare setting in the preceding 90–180 days).
 Final culture was positive for MSSA. Paracentesis fluid culture revealed MSSA as well. Echocardiogram showed vegetation on the mitral valve 17 mm × 4 mm (). Antibiotics were changed to cefazolin. The patient was not a candidate for surgery in spite of embolic events due to a high Mayo surgical risk of 40% mortality within 7 days. His kidney function continued to deteriorate. Urine studies showed UNa of 79 mEq/L, U creatinine of 50.2 mg/dL, and FENa of 4.1%. Patient had a daily electrocardiography (EKG) which did not show an AV block. No persistent fever or bacteremia was noted. He had hepatorenal syndrome (HRS) for which he was initially started on octreotide, midodrine, albumin without response, and eventually needed hemodialysis. He was discharged to rehab with long-term intravenous antibiotics for a total of 6 weeks. Patient’s repeat echocardiogram showed improvement in valve function with clearance of vegetation (). Even with the clearance of infection, patient’s clinical course continued to deteriorate with multiple admissions for refractory symptomatic ascites, hepatic hydrothorax, recurrent pleural effusion, acute liver failure and encephalopathy. He was not a candidate for transplantation due to active alcohol abuse within last 6 months. He underwent placement of palliative peritoneal drainage catheter and transferred to tertiary care for transjugular intrahepatic portosystemic shunt (TIPS). The improved survival seen in patients with HRS from TIPS made us refer him for the same.
 Other factor affecting success from TIPS is pre-TIPS bilirubin which was 2.6 mg/dL in his case.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [63, 'years'], 'creatinine': [3.3, 'mg/dL']}",20.18362,19.17444,21.1928,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 63 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.3/0.9)**-1.2 * 0.9938**63 * 1.0 = 20.18362.
Hence, the GFR value is 20.18362 ml/min/1.73 m²."
143,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-250,Extracted,"A 71-year old man is brought to the emergency department because of progressively worsening shortness of breath and fatigue for 3 days. During the last month, he has also noticed dark colored urine. He had an upper respiratory infection 6 weeks ago. He underwent a cholecystectomy at the age of 30 years. He has hypertension, hyperlipidemia, and type 2 diabetes mellitus. He immigrated to the US from Italy 50 years ago. Current medications include simvastatin, lisinopril, and metformin. He appears pale. His temperature is 37.1°C (98.8°F), pulse is 96/min, respirations are 21/min, and blood pressure is 150/80 mm Hg. Auscultation of the heart shows a grade 4/6 systolic murmur over the right second intercostal space that radiates to the carotids. Laboratory studies show:
Leukocyte count 9,000/mm3
Hemoglobin 8.3 g/dL
Hematocrit 24%
Platelet count 180,000/mm3
LDH 212 U/L
Haptoglobin 15 mg/dL (N=41–165)
Serum
Na+ 138 mEq/L
K+ 4.5 mEq/L
CL- 102 mEq/L
HCO3- 24 mEq/L
Urea nitrogen 20 mg/dL
Creatinine 1.2 mg/dL
Total bilirubin 1.8 mg/dL
Stool testing for occult blood is negative. Direct Coombs test is negative. Echocardiography shows an aortic jet velocity of 4.2 m/s and a mean pressure gradient of 46 mm Hg.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [71, 'years'], 'creatinine': [1.2, 'mg/dL'], 'sex': 'Male'}",64.65324,61.42058,67.8859,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 71 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.2 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.2/0.9)**-1.2 * 0.9938**71 * 1.0 = 64.65324.
Hence, the GFR value is 64.65324 ml/min/1.73 m²."
144,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2769482-1,Extracted,"A 73-year-old Caucasian male presented to the Emergency Department (ED) in June 2008 with a history of collapse without loss of consciousness while mobilizing to the toilet in the early hours of the morning. This occurred on the background of a 6 day history of general unwellness. He was conscious and orientated on arrival but was slightly drowsy. Other than clinical features of dehydration and mild central abdominal adiposity with a waist: hip ratio of 1.04, there were no other significant clinical signs. His random plasma glucose (RPG) on arrival was 59.1 mmol/L. His height was 1.76 meters (m) and weight was 90 kilograms (kg) making the body mass index (BMI) 29.0 kg/m2. The patient was previously fit and well without any known co-morbidities. He was on no regular medication. There was no family history of diabetes or other significant conditions. He was a non-smoker and consumed no alcohol. He works as a farm equipment evaluator. There was no history of specific weight loss over the preceding months. His general practitioner (GP) had performed a fasting plasma glucose test on him in February 2008 which showed a value of 6.4 mmol/L. This was repeated within 2 weeks and the repeated value was 6.1 mmol/L. Glycosylated haemoglobin (HbA1c) was also done and was 6.3%. Subsequent 75 gram (g) oral glucose tolerance test (OGTT) produced a value of 15.3 mmol/L, 14.1 mmol/L and 7.6 mmol/L 30 minutes, 1-hour and 2-hours post glucose load respectively. He was managed with dietary modification and exercise.
His sodium (Na) was 150 mmol/L, potassium (K) 4.6 mmol/L, urea 26.1 mmol/L and creatinine (Cr) 237 micromol/L. Calculated osmolality was 394.4 mOsm/kg. Arterial blood gas sampling (ABG) showed a pH of 7.36, pCO2 4.9 kPa, pO2 11.0 kPa, bicarbonate 20 mmol/L and BE -1 mmol/L. Lactate was mildly elevated at 1.4 mmol/L. β-hydroxybutyrate (β-OHB) was slightly elevated at 3.67 mmol/L. Repeat HBA1c was 8.1%. Besides a small amount of ketones and glycosuria, urine testing revealed nil else of concern. Full septic screen was done; white cell count (WCC) and differential showed mildly raised WCC at 12.5 × 109 and neutrophils at 10.9 × 109 with the rest of differential count being normal, CRP was 4, urine microscopy, culture and sensitivity was normal and chest radiograph was normal. Thyroid function was normal. Lipid profile was also normal.
The patient was diagnosed with T2DM based on his presentation, age and absence of anti-Glutamic Acid Decarboxylase 65 (Anti-GAD 65), Insulinoma Antigen-2 (IA-2) and Islet Cell (ICA) antibodies. His acute presentation was consistent with hyperglycaemic hyperosmolar state (HHS) and acute renal failure secondary to dehydration. He was treated with intravenous insulin and intensively rehydrated with close attention to electrolyte balance. He improved considerably and renal function normalized. He was started on Metformin 500 mg twice daily (BID) increasing to 1 g BD and Penmix 30 subcutaneous insulin at a dose of 12 units BD increasing to 30 units BD. 5 days after the acute event, a 1 mg intravenous (IV) glucagon stimulation test was done at 9.00 am with blood samples for glucose and C-peptide taken at baseline, 5, 10 and 15 minutes.
Patient had been fasted for 15 hours overnight and medications were withheld until after the test. The glucose values were 6.3 mmol/L, 15.1 mmol/L, 16.3 mmol/L and 16.6 mmol/L at baseline, 5, 10 and 15 minutes respectively. Corresponding C-peptide values were 0.21 nmol/L, 0.42 nmol/L, 0.47 nmol/L and 0.51 nmol/L respectively. He was finally discharged after 7 days of hospital care with clinic follow up in 2 months. His average capillary blood glucose (CBG) was 6.7 mmol/L and range 6.5-7.7 mmol/L on discharge.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [73, 'years'], 'creatinine': [237.0, 'µmol/L'], 'sex': 'Male'}",23.97077,22.77223,25.16931,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 73 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 237.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 237.0 µmol. To convert 237.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 237.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00024 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00024 mol Serum Creatinine * 113.12 g/mol = 0.02715 g Serum Creatinine. To convert 0.02715 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.02715 g Serum Creatinine * 1000.0 mg/g = 27.15 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 27.15 mg Serum Creatinine/10.0 dL = 2.715 mg Serum Creatinine/dL. The concentration value of 237.0 µmol Serum Creatinine/L converts to 2.715 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.715/0.9)**-1.2 * 0.9938**73 * 1.0 = 23.97077.
Hence, the GFR value is 23.97077 ml/min/1.73 m²."
145,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6089461-1,Extracted,"A male farmer patient of 53 years old, previously healthy, from the interior of Minas Gerais, Brazil, was admitted to the emergency room with a 6-day history of fever, myalgia, headache, and low back pain that progressively worsened over this period. On admission, he presented jaundice, fever (38 °C), heart rate of 98 bpm and blood pressure 120 x 70 mmHg. On an initial laboratory workup drew attention the total bilirubin of 13.6 mg/dL (reference range [RR], 0.2-1.4 mg/dL) with direct bilirubin of 6.11 mg/dL (RR; 0.0-0.3) and indirect bilirubin of 7.55 mg/dL, RR; 0.2-1.2 mg/dL), aspartate transaminase [AST] of 10,740 UI/L (RR; 15-37 UI/L) and alanine transaminase [ALT] of 3,120 UI/L (RR; 30-65 UI/L); renal failure (serum creatinine level of 3.21 mg/dL, [RR; 0.7-1.2 mg/dL] and urea of 77 mg/dL, [RR; 0.2-1.4 mg/dL]) and thrombocytopenia (platelet count 33,000/mm3, [RR; 13-400x103/mm3]). On the day 7 after admission, a positive molecular test for yellow fever was available. The patient was referred to the intensive care unit (ICU) of an Infectious Disease Referral Hospital because of the worsening clinical status characterized by mental confusion, which progressed to hepatic encephalopathy, ascites, respiratory failure, and bleeding at the puncture sites. An antimicrobial regimen was empirically started with piperacillin/tazobactam, and transfusion of fresh frozen plasma (800 mL), lactulose and glycerin enema were administered. The abdominal ultrasound revealed the presence of moderate ascites and signs of nephropathy, but the absence of bile ducts’ dilation and signs of chronic fibrosing liver disease. As the clinical course demanded, the patient was started on hemodialysis. Although no microorganism was isolated on cultures, the antibiotics were also empirically changed for meropenem, vancomycin, and polymyxin B due to the suspicion of peritonitis, ascending leukocytosis and severe hypotension requiring vasoactive drugs administration. Despite a normal echocardiography, on the D9 after the ICU admission, the patient unexpectedly presented a Mobitz II second degree AV followed by a total atrioventricular block, cardiogenic shock, and death.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [53, 'years'], 'creatinine': [3.21, 'mg/dL']}",22.20342,21.09325,23.31359,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 53 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.21 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.21/0.9)**-1.2 * 0.9938**53 * 1.0 = 22.20342.
Hence, the GFR value is 22.20342 ml/min/1.73 m²."
146,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-6106,Extracted,"A 30-year-old man with history of intravenous drug use and methamphetamine-associated chronic thromboembolic pulmonary hypertension (CTEPH) is brought to the emergency department by his girlfriend for worsening abdominal pain and fevers. The patient said the pain was initially around his umbilicus, but he is now experiencing intense tenderness near his groin. He was initially prescribed rivaroxaban, but due to insurance issues, he was switched to warfarin for management of CTEPH two weeks ago. His temperature is 102°F (38.9°C), blood pressure is 95/60 mmHg, pulse is 95/min, respirations are 22/min. He states that his blood pressure usually runs low. His physical exam is notable for an unremarkable cardiac exam, bibasilar crackles, and RLQ tenderness with rebound tenderness when the LLQ is palpated. Laboratory results are shown below:

Hemoglobin: 11 g/dL
Hematocrit: 35 %
Leukocyte count: 16,000/mm^3 with normal differential
Platelet count: 190,000/mm^3

Serum:
Na+: 137 mEq/L
Cl-: 100 mEq/L
K+: 3.7 mEq/L
HCO3-: 23 mEq/L
BUN: 40 mg/dL
Glucose: 110 mg/dL
Creatinine: 0.8 mg/dL
Ca2+: 9.1 mg/dL
AST: 34 U/L
ALT: 45 U/L

International normalized ratio (INR): 6.2
Prothrombin time (PT): 40 seconds
Partial thromboplastin time: 70 seconds

Blood type: O
Rhesus: Positive
Antibody screen: Negative

A clinical diagnosis is made and supported by the surgical consult team in lieu of imaging. The next operating room for an add-on procedure will not be available for another 5 hours. Appropriate medical therapy is initiated.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [30, 'years'], 'creatinine': [0.8, 'mg/dL'], 'sex': 'Male'}",113.17345,107.51478,118.83212,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 30 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.8 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.8/0.7)**-0.302 * 0.9938**30 * 1.0 = 113.17345.
Hence, the GFR value is 113.17345 ml/min/1.73 m²."
147,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-1307,Extracted,"A 36-year-old man is brought to the emergency department by his neighbor because of altered mental status. He was found 6 hours ago stumbling through his neighbor's bushes and yelling obscenities. The neighbor helped him home but found him again 1 hour ago slumped over on his driveway in a puddle of vomit. He is oriented to self but not to place or time. His temperature is 36.9°C (98.5°F), pulse is 82/min, respirations are 28/min, and blood pressure is 122/80 mm Hg. Cardiopulmonary exam shows no abnormalities. He is unable to cooperate for a neurological examination. Muscle spasms are seen in his arms and jaw. Serum laboratory studies show:
Na+ 140 mEq/L
K+ 5.5 mEq/L
Cl- 101 mEq/L
HCO3- 9 mEq/L
Urea nitrogen 28 mg/dL
Creatinine 2.3 mg/dL
Glucose 75 mg/dL
Calcium 7.2 mg/dL
Osmolality 320 mOsm/kg
Calculated serum osmolality is 294 mOsm/kg. Arterial blood gas shows a pH of 7.25 and lactate level of 3.2 mmol/L (N=< 1 mmol/L). Examination of the urine shows oxalate crystals and no ketones.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [36, 'years'], 'creatinine': [2.3, 'mg/dL'], 'sex': 'Male'}",36.8188,34.97786,38.65974,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 36 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.3/0.9)**-1.2 * 0.9938**36 * 1.0 = 36.8188.
Hence, the GFR value is 36.8188 ml/min/1.73 m²."
148,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6796602-1,Extracted,"An 80-year-old female with no past surgical history was brought into the Emergency Department (ED) of a public teaching hospital with concern for altered mental status. She had a past medical history of atrial fibrillation (for which she was taking apixaban), two prior cerebrovascular accidents, hypertension, insulin-dependent diabetes mellitus, and Stage 3 chronic kidney disease with a baseline serum creatinine of 1.3–1.5 mg/dL.
Upon evaluation, the patient had a Glasgow Coma Score of 8 (E(2)V(2)M(4)) and was unable to provide any history. Initial vitals showed a temperature of 97.8 °F, heart rate of 73 beats/min, blood pressure of 118/65, respiratory rate of 18 breaths/min, and oxygen saturation of 97% on room air. On examination, her abdomen was distended and diffusely tender to palpation. Laboratory results showed an elevated serum creatinine of 5.0 mg/dL consistent with acute kidney injury (AKI). Serum electrolytes, white blood cell count, serum lactate, and coagulation tests were within normal limits. The patient underwent a CT scan of the abdomen and pelvis without contrast, which showed a large dilated loop of proximal jejunum with evidence of mesenteric twist concerning for a closed loop SBO ().
Given the patient’s age and medical comorbidities, her estimated American College of Surgeons National Surgical Quality Improvement Program intraoperative mortality risk was 19%, and the risk of serious complications was 35% []. However, due to the acute decline in mental status, AKI, and concerning abdominal exam, emergent surgical intervention was recommended to the next of kin. After obtaining consent, we proceeded with an exploratory laparotomy.
After intravenous fluid resuscitation and perioperative antibiotics, the patient underwent general anesthesia and intubation. Upon entering the abdomen, we noted several decompressed loops of small bowel, as well as a dilated loop of jejunum densely adherent to the mesentery of the SMA and transverse colon. We also noted twisting of the mesentery and numerous adhesions of the small bowel to the mesentery, retroperitoneum, and surrounding structures. During our lysis of adhesions, we noted a large mesenteric defect through which a loop of jejunum had become trapped, causing the closed loop SBO. Moreover, the cecum was visualized in the right upper quadrant instead of its usual anatomical location in the right lower quadrant of the abdomen (A). It became apparent that the adhesions were in fact Ladd bands (A), and that our patient had an intestinal malrotation. After completely lysing the Ladd bands, we then proceeded with a Ladd procedure for malrotation. We first detorsed the mesentery through counterclockwise rotation. The segment of jejunum involved in the internal hernia appeared viable, so no bowel resection was performed. We then mobilized and rotated the cecum and the ascending and transverse colon towards the left, also performing an appendectomy. After straightening out and relocating the duodenum to the right hemiabdomen, the final position of abdominal contents was consistent with that seen after a completed Ladd procedure (B).
The patient’s postoperative course was accompanied by resolution of AKI but complicated by delirium and prolonged ileus. Initial high-volume bilious output from her nasogastric tube prompted a CT scan that showed no evidence of SBO, and confirmed the new position of the cecum on the left (). The patient was discharged following clinical improvement and ability to tolerate a diet. She was seen in clinic two weeks later and reported feeling well, with no obstructive symptoms.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [80, 'years'], 'creatinine': [5.0, 'mg/dL'], 'sex': 'Female'}",8.25547,7.8427,8.66824,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 80 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 5.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (5.0/0.7)**-1.2 * 0.9938**80 * 1.012 = 8.25547.
Hence, the GFR value is 8.25547 ml/min/1.73 m²."
149,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4295059-1,Extracted,"A 60-year-old female suffering from frontal lobe epilepsy was presented to our hospital with a mental obtundation.
We have treated the patient for a period of 5 years and have registered an electroencephalogram (EEG) with ictal fast activity in the right frontocentral area. A brain MRI showed a T2 high, T1 low signal intensity of a single lesion without enhancement in the right anterior basal frontal lobe white matter (). She used to have partial seizures with a secondary generalization, and she has been on 1,200 mg/day VPA for the last 4 years. Generalized tonic-clonic seizures (GTCSz) were well controlled, but partial seizures of left head version following left arm clonus occurred one to two times per several months. We added LEV to VPA and increased the daily dosage of LEV to 1,000 mg/day. Her partial motor seizures ceased and her EEG showed normal findings ().
Eight months later, mental obtundation developed insidiously. The neurologic findings showed no ataxia or nystagmus, and routine hematological and biochemical laboratories presented a normal complete blood count (WBC 6,600/mm3, Hb 13.4 g/dL, platelet 168,000/mm), electrolyte (Na 138 mmol/L, K 4.1 mmol/L), renal (BUN 11.1 mg/dL, Creatinine 0.72 mg/dL), and thyroid function test (free T4 1.230 ng/dL, TSH 0.779 uIU/mL). Her creatinine clearance was of 75.6 mL/min. However, her liver function test showed a mild impairment (aspartate aminotransferase 46 IU/L, alanine aminotransferase 44 IU/L, γ-glutamyl transferase 656 IU/L), and the serum ammonia level was high (154 umol/L, normal: 12 to 47 umol/L). An abdomen computed tomography (CT) with a contrast enhancement showed no remarkable finding, except for a 0.6 cm-sized liver cyst. The blood concentrations of VPA was of 82.4 ug/mL (therapeutic range: 50–100 ug/mL). The EEG presented an intermittent generalized delta slowing (). We suspected the possibility of side effects associated with LEV because she tolerated medication with VPA for 4 years and stopped LEV. Her mental function was gradually restored, with a decrease in the blood ammonia level (56 umol/L), and the generalized slowing disappeared in a follow-up EEG (). We added carbamazepine to treat for partial seizures, and the patient was asymptomatic until the last visit in July 2014.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [60, 'years'], 'creatinine': [0.72, 'mg/dL'], 'sex': 'Female'}",95.65927,90.87631,100.44223,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 60 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.72 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.72/0.7)**-1.2 * 0.9938**60 * 1.012 = 95.65927.
Hence, the GFR value is 95.65927 ml/min/1.73 m²."
150,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4700638-5,Extracted,"Case 5: A 71-year-old woman had longstanding sicca symptoms and chronic hypokalaemia. She presented to hospital with diarrhea with severe hypokalaemia (2.1 mmol/L) and paralysis. The diarrhea was due to a colonic villous adenoma, for which she underwent a hemicolectomy. She was referred to our service for her hypokalaemia which persisted after her surgery. She reported sicca symptoms, arthralgia and systemic upset with associated positive pSS serology. dRTA was confirmed by urinary acidification testing. She underwent renal biopsy which demonstrated TIN with heavy staining for C9 along tubular basement membranes (negative staining for immunoglobulin). Potassium and bicarbonate supplements were commenced along with prednisolone 20 mg/day and hydroxychloroquine 200 mg/day. She was intolerant of both of these (dyspepsia and rash respectively) and developed worsening renal function off immunosuppression (serum creatinine rose from 97 to 159 μmol/L). MMF (1 g/day) was introduced with resolution of her renal impairment and improvement in her extra-renal symptoms.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [71, 'years'], 'creatinine': [159.0, 'µmol/L']}",29.55294,28.07529,31.03059,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 71 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 159.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 159.0 µmol. To convert 159.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 159.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00016 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00016 mol Serum Creatinine * 113.12 g/mol = 0.0181 g Serum Creatinine. To convert 0.0181 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.0181 g Serum Creatinine * 1000.0 mg/g = 18.1 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 18.1 mg Serum Creatinine/10.0 dL = 1.81 mg Serum Creatinine/dL. The concentration value of 159.0 µmol Serum Creatinine/L converts to 1.81 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.81/0.7)**-1.2 * 0.9938**71 * 1.012 = 29.55294.
Hence, the GFR value is 29.55294 ml/min/1.73 m²."
151,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6381853-1,Extracted,"A 42-year-old Saudi male from Jizan, with a comorbidity of hypertension and type 2 diabetes mellitus diagnosed 6 years prior (well controlled by oral antidiabetic agents: metformin 1000 mg twice daily and gliclazide 30 mg once daily), presented with impaired renal function and hematuria. After basic laboratory investigations, kidney biopsy was performed. Histological examination with light microscope revealed a global sclerosed glomeruli, minimal interstitial fibrosis and tubular atrophy []. A diagnosis of glomerulonephritis of unknown etiology was made and treatment with mycophenolate (1 g PO twice daily) and prednisone (20 mg PO once daily) was initiated.
After 3 months, the patient presented with a 3-week history of fever, abdominal pain and fatigue. The fever was subjective, intermittent, associated with chills and rigors, especially at night, and not relieved by paracetamol. The abdominal pain was intermittent, diffuse and colicky in nature and was associated with nausea and vomiting without blood (2–3 times/day). During these 3 weeks, the patient's appetite decreased, owing to which he lost 7 kg in weight. In addition, the patient reported a history of animal contact (goat and sheep), ingestion of raw goat milk and swimming in the valley water. There was no history of rash, cough, hemoptysis, jaundice, diarrhea, constipation, dysuria, change in urine color, arthralgia, visual disturbances, oral ulcers, genital rash, discharge or contact with tuberculosis patients.
On physical examination, the patient was found to be obese, sweating, not jaundiced or cyanosed. He was conscious, alert and oriented to time, place and person. His vital signs were as follows: body temperature, 38.6°C; pulse rate, 98 beats/min; respiratory rate, 24 breaths/min; blood pressure, 125/85 mmHg; and oxygen saturation, 100% on room air. He was pale, with normal jugular venous pressure and no oral ulcers or thrush. Abdominal examination revealed mild epigastric tenderness and a palpable liver 4 cm below the costal margin with a 15-cm liver span. The rest of the examinations were within normal limits.
Laboratory investigations on admission revealed a white blood cell (WBC) count of 2.65/mcL (neutrophils, 72.1%; lymphocytes, 23.2%; monocytes, 4%; and eosinophils, 0.7%). Results of other hematological examinations were as follows: hemoglobin level, 8.8 g/L; erythrocyte sedimentation rate, 88 mm/h; platelet count, 87,000/mcL; and reticulocyte count, 1.28%. Level of ferritin was 1000 ng/mL, with a transferrin saturation of 11.22 mg/dL. Estimation of electrolytes showed sodium 138 mEq/L, potassium 3.2 mEq/L and bicarbonate 25 mmol/L. Liver function tests showed that total protein was 6.1 g/dL, albumin 3.2 g/dL, total bilirubin 1.2 mg/dL, alanine transaminase 71 IU/L, aspartate transaminase 42 IU/L, alkaline phosphatase 179 IU/L and gamma-glutamyl transferase 447 IU/L. International normalized ratio was 0.8. Renal function tests showed that blood urea nitrogen was 12 mg/dL and creatinine 2.15 mg/dL. Level of lactate dehydrogenase was 732 U/L and C-reactive protein 53 mg/L. Urine analysis showed 2–5 WBCs/high-power field and 10–25 red blood cells/high-power field with no nitrites. Sickling test and direct/indirect Coombs test were negative, and the stool test result was normal.
Chest X-ray and electrocardiogram were normal. Abdominal ultrasound showed an enlarged liver (16.2-cm liver span) and a mildly enlarged spleen (14 cm in length). Kidneys were normal in size, with a mild increase in the echogenicity of renal parenchyma, but no hydronephrosis or ascites.
The serological tests for viral hepatitis, human immunodeficiency virus, Epstein–Barr virus, cytomegalovirus, Toxoplasma and Brucella were negative. Rheumatoid factor, antinuclear antibody, antineutrophil cytoplasmic antibody, antiglomerular basement membrane antibody, anti-Sjögren's syndrome A and B antibodies and cryoglobulin were negative. Malaria smear and blood cultures were also negative.
The patient's condition continued to deteriorate and he developed continuous fever of up to 40.5°C. Repeated tests after 5 days revealed the following: WBC, 1.4/mcL; hemoglobin, 6.7 g/dL; platelet, 55,000/mcL; creatinine, 3.3 mg/dL; C-reactive protein, 151 mg/L; total bilirubin, 2.9 mg/dL; alkaline phosphatase, 460 IU/L; alanine aminotransferase, 80 IU/L; aspartate aminotransferase, 138 IU/L; gamma-glutamyl transferase, 651 IU/L; albumin, 2.5 g/dL; and lactate dehydrogenase, 1400 U/L.
Bone marrow aspirate showed mild hypocellular marrow with no evidence of dysplasia or malignancy. Bone marrow culture for Brucella was negative. Further, Leishman-Donovan bodies were not detected by light microscope. Polymerase-chain reaction test for the diagnosis of tuberculosis, serological tests for dengue fever and Q fever as well as β-D-Glucan and galactomannan antigen tests were all negative. Liver biopsy showed granulomatous hepatitis with extramedullary hematopoiesis. After 1 week of admission, the patient was treated empirically with broad-spectrum antibiotic (meropenem intravenously, 1 g every 8 h for 6 days); however, there was no improvement.
Additional serological testing using enzyme-linked immunosorbent assay (ELISA) releveled the presence of anti-Leishmania antibodies. Based on this, the patient was started on liposomal amphotericin B course as a treatment for VL (4 mg/kg intravenous on Days 1–5, 10, 17, 24, 31 and 38), despite the lack of a definitive diagnosis. After 1 week, the patient improved clinically, the fever subsided, the laboratory parameters began to improve and at the end of liposomal amphotericin B course, all tests returned to normal.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [42, 'years'], 'creatinine': [3.3, 'mg/dL'], 'sex': 'Male'}",22.9996,21.84962,24.14958,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 42 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.3/0.9)**-1.2 * 0.9938**42 * 1.0 = 22.9996.
Hence, the GFR value is 22.9996 ml/min/1.73 m²."
152,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3958989-1,Extracted,"A 52-year-old African American female was brought to the emergency department for generalized abdominal discomfort, altered mental status, diarrhea, fevers and chills for 4-5 days. Her past medical history was significant for alcohol abuse and alcohol-related liver cirrhosis. In the emergency department, vital signs were as follows: Blood pressure of 74/42 mmHg, heart rate of 112 beats/min, respiratory rate of 20 breaths/min and temperature of 98.6 F. Remarkable findings on physical examination included jaundice as well as abdominal distention and tenderness to palpation, especially in the right upper quadrant. There was no rash or ulcers. As per family, she did not have recent travels or exposure to sick people. They denied having domestic animals at home or any contact to the patient with pets. She was placed on mechanical ventilation and admitted to the medical intensive care unit. Admission diagnosis was systemic inflammatory response syndrome with sepsis and septic shock with multi-organic dysfunction syndrome, presumptively secondary to community-acquired pneumonia, possible biliary tract infection (ascending cholangitis), probable spontaneous bacterial peritonitis (SBP) and alcoholic hepatitis. Aggressive intravenous fluids resuscitation with crystalloids along with vasopressors was initiated. Blood, urine, respiratory cultures and Legionella urine antigen were obtained. Empiric intravenous antimicrobial therapy, composed by piperacillin/tazobactam (2.25 g every 8 h) and azithromycin (500 mg every 24 h), was initiated.
Laboratory results on admission were: A complete blood cell count of 21,000/mm3(90% neutrophils), a platelet count of 51,000/mm3, a sodium level of 127 mEq/L, a potassium level of 5.3 mEq/L, a bicarbonate level of 15 mEq/L and a creatinine level of 6.3 mg/dl. Aspartate aminotransferase and alanine aminotransferase levels were 121 and 65 IU/L, respectively. Alkaline phosphatase level was 290 IU/L, gamma-glutamyl transpeptidase level was 290 U/L and lactate dehydrogenase level was 482 U/L. Total bilirubin level was 14.5 mg/dl, with a direct bilirubin level of 10.1 mg/dl. Lactic acid level was 6.4 mg/dl. Prothrombine time was 25.2 s, with an INR of 2.29. Serum alcohol level was within the normal limits. Arterial blood gases showed a pH of 7.15, a pCO2 of 23, and a pO2 of 132 while the patient was receiving mechanical ventilation with FIO2 of 60%. Chest X-ray showed left lung infiltrate with pleural effusion.
After 24 h of admission, patient remained in critical condition and requiring maximum doses of vasopressors, despite of what it seems to be the appropriate empiric antimicrobial therapy. Blood cultures drawn of admission grew P. multocida. Blood culture system Bact-Alert 3D® was used for the recovery of the organism. No polymerase chain reaction analysis was performed. Isolate was tested sensitive to piperacillin/tazobactam and azithromycin. No minimal inhibitory concentrations for these antimicrobials were reported. In spite of all medical efforts, general medical condition deteriorated and patient expired on day 3 of admission.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [52, 'years'], 'creatinine': [6.3, 'mg/dL'], 'sex': 'Female'}",7.44604,7.07374,7.81834,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 52 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 6.3 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (6.3/0.7)**-1.2 * 0.9938**52 * 1.012 = 7.44604.
Hence, the GFR value is 7.44604 ml/min/1.73 m²."
153,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4421666-1,Extracted,"A 71-year-old man with a past history of carcinoma of the prostate was admitted in August 2011, feeling unwell and with new-onset weakness of the quadriceps muscles for the past 2 days. He had initially received a diagnosis of adenocarcinoma of the prostate in May 2011 and he had been treated with cyproterone acetate 300 mg since June 2011. He had also been on aspirin 75 mg and simvastatin 40 mg unchanged for the past 2 years.
On admission, here, he appeared unwell but normotensive and afebrile. He had weakness of his lower limbs (power 2/5) with normal reflexes. Serum creatinine was 338 μmol/L and liver function tests were also markedly abnormal [alanine transaminase 887 U/L (normal < 41 U/L), γ-glutamyltransferase 111 U/L (normal < 41 U/L)]. Previous serum creatinine results and liver function were all normal. Urine dipstick was positive for blood but urine microscopy was negative. Ultrasound showed normal sized kidneys and normal liver parenchyma. The creatine kinase was 78820 U/L. A complete virology and immunology screen, including Jo-1 antibodies, was negative.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [71, 'years'], 'creatinine': [338.0, 'µmol/L'], 'sex': 'Male'}",15.98073,15.18169,16.77977,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 71 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 338.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 338.0 µmol. To convert 338.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 338.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00034 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00034 mol Serum Creatinine * 113.12 g/mol = 0.03846 g Serum Creatinine. To convert 0.03846 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.03846 g Serum Creatinine * 1000.0 mg/g = 38.46 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 38.46 mg Serum Creatinine/10.0 dL = 3.846 mg Serum Creatinine/dL. The concentration value of 338.0 µmol Serum Creatinine/L converts to 3.846 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.846/0.9)**-1.2 * 0.9938**71 * 1.0 = 15.98073.
Hence, the GFR value is 15.98073 ml/min/1.73 m²."
154,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4084408-1,Extracted,"A 64-year-old woman was admitted to the hospital after experiencing acute visual deficits. Her symptoms resolved within 24 hours and were consistent with a transient ischemic attack (TIA). The patient's past medical history was significant for paroxysmal atrial fibrillation, migraines, and hypertension. Prior medical records indicated that she was taking 325 mg of aspirin once a day for paroxysmal atrial fibrillation. The patient did not take any additional medications. Her family and social history were unremarkable. On physical exam, her blood pressure was 170/116 mmHg and heart rate was 88 bpm with a respiratory rate of 20 and oxygen saturation of 98%. The patient had an irregularly irregular heart rate and rhythm with a soft midpeaking systolic murmur best appreciated at the right upper sternal border. No carotid bruits were appreciated. An electrocardiogram showed atrial fibrillation with a ventricular rate of 88 bpm and no significant ST or T wave changes. Remarkable lab values included a prothrombin time of 11.4 s, 0.5 mg/dL creatinine, 71 mg/dL HDL, 105 mg/dL LDL, and 103 mg/dL triglycerides. CT angiography of the head and neck was unremarkable except for mild carotid bulb calcifications. Brain MRI revealed old ischemic changes in the periventricular and subcortical white matter consistent with possible old strokes. A transthoracic echocardiogram (TTE) noted a round echodense mass measuring 20 × 23 mm attached to the mitral valve annulus, along the atrioventricular groove and adjacent to the posterior mitral leaflet (). The mass was described as having a smooth border, possibly tumor versus thrombus. There was mild mitral valve thickening with mild mitral regurgitation, but no stenosis or LV outflow tract obstruction. There was aortic valve sclerosis without stenosis. The left ventricle had a normal size with a preserved ejection fraction (69% LVEF biplane) and no wall motion abnormalities. Given the abnormal valvular findings, a transesophageal echocardiogram (TEE) was recommended. It revealed a well-circumscribed echogenic and nonmobile mass attached to the posterior mitral valve annulus measuring 19 × 23 mm (). The subvalvular mitral apparatus was intact and the left atrial appendage did not show a thrombus. Based on the size, shape, and location of the mass, the differential diagnosis included myxoma versus caseous mitral annular calcification. A nongated contrast-enhanced chest CT scan showed a 17 × 18 mm round hyperdense mass along the inferior mitral valve annulus (). The mass was described as having a heterogenous calcification pattern with a hypoattenuated necrotic center of 100 Hounsfield units. These findings were consistent with caseous mitral annular calcification. In light of the newly identified ischemic changes on her brain MRI and most recent CVA episode, there was concern for possible embolization from the CMAC complex. The patient was evaluated by cardiothoracic surgery and was deemed an operable candidate, but the patient declined surgery. Given these findings and a calculated CHADS2 score of 3, the patient was started on rivaroxaban, a factor Xa inhibitor for stroke management. She was followed closely with a repeat TTE 6 months later revealing no changes in the size or appearance of the mass.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [64, 'years'], 'creatinine': [0.5, 'mg/dL'], 'sex': 'Female'}",104.66976,99.43627,109.90325,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 64 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.5 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.5/0.7)**-0.241 * 0.9938**64 * 1.012 = 104.66976.
Hence, the GFR value is 104.66976 ml/min/1.73 m²."
155,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6208011-1,Extracted,"In January 2018, an 85-year-old Japanese woman was referred to our hospital with vascular purpura on her lower limbs, chest, and abdomen. She was a housewife and reported no recent travel history. There was no history of urticarial or other allergic symptoms, and she had no familial history. She had no history of smoking tobacco and alcoholism. She had a previous history of hypertension treated with amlodipine besylate for 20 years and no other medication (she was not administered new drugs). She described no trigger factors for purpura. Her vital signs were as follows: temperature, 37.2 °C; pulse, 86 beats per minute; blood pressure, 120/78 mmHg; and respiratory rate, 18 breaths per minute.
A physical examination revealed significant pitting edema in both lower legs, and the confluence of palpable purpura that formed several patches of different sizes in her lower limbs, chest, and abdomen (Fig. ). There were no remarkable features in her heart, lungs, or abdominal examinations. A neurological examination revealed no abnormalities. She was afebrile and there were no signs of an infectious focus in examinations of each system. Laboratory tests showed a white blood cell count (WBC) of 23.3 × 109/L, eosinophil cell count of 13.5 × 109/L, red blood cell count (RBC) of 299 × 1010/L, hemoglobin (Hb) concentration of 9.2 g/dL, and platelet count of 152 × 109/L (Table ). The serum total protein level was 8.2 g/dL (normal range, 6.9–8.2 g/dL), the lactate dehydrogenase (LDH) level was 280 IU/L (normal range, 106–211 IU/L), the aspartate transaminase level was 50 U/L (normal range, 5–40 U/L), the alanine transaminase level was 40 U/L (normal range, 5–35 U/L), the alkaline phosphatase level was 1564 U/L (normal range, 104–338 U/L), and the C-reactive protein level was 6.6 mg/dL (normal range, below 0.3 mg/dL). The serum creatinine level was 2.1 mg/dL (normal range, 0.40–0.80 mg/dL) and nephrotic-range proteinuria was noted. Hypocomplementemia with elevated C1q levels was observed. Serum antinuclear antibodies, perinuclear anti-neutrophil cytoplasmic antibodies, and cytoplasmic anti-neutrophil cytoplasmic antibodies were all negative. Cryoglobulins and the hepatitis B and C panels were negative. The serum β2-microglobulin level was 13.5 μg/dl (normal range, < 2.0 μg/dl), and immunoglobulin G (IgG), immunoglobulin E (IgE), and κ-light chain concentrations were 43.8 g/L (normal range, 8.7–17 g/L), 2455 IU/mL (normal range, 10–340 IU/mL), and 515 mg/dL (normal range, 3.3–19.4 mg/dL), respectively. Serum protein electrophoresis disclosed a monoclonal spike in the γ-globulin region and urine electrophoresis also revealed a monoclonal spike. Serum immunofixation electrophoresis confirmed the presence of an IgG-κ chain monoclonal M component. A bone marrow (BM) examination showed that plasma cells and eosinophils were 16.2% and 28.6%, respectively (Fig. ). A karyotype analysis showed 46,XX (20/20 cells). Interphase fluorescence chromosomal in situ hybridization (FISH) of BM cells revealed no gene abnormalities in 1q21, RB1, P53, D13S319, or IgH. A skeletal survey X-ray found no osteolytic lesions. A biopsy sample of accessory salivary glands showed no amyloidosis. A skin biopsy sample revealed LV showing angiocentric, neutrophilic segmental inflammation with endothelial cell swelling and fibrinoid necrosis on blood vessel walls (Fig. ). A cellular infiltrate around the vessels showed leukocytoclasia of neutrophil nuclei. IgG or IgA deposits around the vessel walls were not clear. Although hypocomplementemia was noted, no manifestations suggesting autoimmune diseases and cryoglobulinemia were observed. Allergic purpura was less likely because of the absence of abdominal pain and arthralgia. Drug-induced purpura was also not suspected because no causative drug was being taken.
The serum level of IFN-γ, which was secreted by Th1, was lower than 0.1 IU/ml (normal range, lower than 0.1 IU/mL) (Table ). Serum levels of IL-4, IL-5, and IL-6 secreted by Th2 were 50.3 pg/mL (IL-4 normal range, lower than 6 pg/mL), 56.1 pg/mL (IL-5 normal range, lower than 3.9 pg/mL), and 76.2 pg/mL (IL-6 normal range, lower than 4 pg/mL), respectively. IL-3, granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-10, and TGF-β levels were lower than 31 pg/mL (IL-3 normal range, lower than 31 pg/mL), lower than 8 pg/mL (GM-CSF normal range, lower than 8 pg/mL), 45 pg/mL (IL-10 normal range, lower than 5 pg/mL), and 8.74 ng/mL (TGF-β normal range, 1.56–0.24 ng/mL), respectively.
Our patient was diagnosed as having MM IgG-κ chain type, stage IIIA according to the Durie-Salmon system and stage II according to the International Staging System. Following a definite diagnosis, she received a VRD regimen: bortezomib, 1.0 mg/m2, days 1, 4, 8, and 11; lenalidomide, 15 mg/day, days 1–21, and dexamethasone 20 mg/day, days 1, 2, 4, 5, 8, 9, 11, and 12. After one course of the treatment, the cutaneous manifestation rapidly improved (Fig. ). Laboratory tests showed a WBC count of 5.4 × 109/L, eosinophil cell count of 0.2 × 109/L, RBC count of 305 × 1010/L, Hb concentration of 10.6 g/dL, and platelet count of 286 × 109/L (Table ). The serum total protein level was 7.6 g/dL, the LDH level was 204 U/L, the aspartate transaminase level was 15 U/L, the alanine transaminase level was 12 U/L, the alkaline phosphatase level was 332 U/L, and the C-reactive protein level was 0.13 mg/dL. The serum creatinine level was 0.82 mg/dL and serum levels of complement bodies were normalized. Serum concentrations of IgG, IgE, and the κ-light chain decreased (13.2 g/L, 218 IU/mL, and 24.2 mg/dL, respectively). The serum level of IFN-γ was elevated (6.5 IU/mL). Serum levels of IL-4, IL-5, IL-6, IL-10, and TGF-β decreased (< 6 pg/mL, < 3.9 pg/mL, 3.4 pg/mL, < 5 pg/mL, and 0.48 ng/mL, respectively). In the fluorescence-activated cell sorting (FACS) analysis of peripheral blood mononuclear cells, the ratio of Th1/Th2 increased. A BM examination showed decrease of plasma cells (3%). She achieved and maintained a very good partial response (VGPR) following VRD regimen for nine cycles without recurrence of LV and eosinophilia.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [85, 'years'], 'creatinine': [2.1, 'mg/dL'], 'sex': 'Female'}",22.66406,21.53086,23.79726,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 85 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.1 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.1/0.7)**-1.2 * 0.9938**85 * 1.012 = 22.66406.
Hence, the GFR value is 22.66406 ml/min/1.73 m²."
156,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4886917-1,Extracted,"A 75-year-old Caucasian male with essential hypertension and recurrent metastatic melanoma presented with systemic morbilliform rash and AKI. The patient was initially diagnosed with invasive cutaneous melanoma of the left nasolabial fold [American Joint Committee of Cancer (AJCC) Stage IIc; T4b, N0, M0. BRAF V600/NRAS-wild-type] and underwent local excision with clear margins. Seven months later, he presented with significant weight loss and a palpable mass in his left submandibular area. PET-CT revealed an FDG-avid left submandibular lymph node and a liver lesion without any brain metastasis [AJCC Stage IV, M1c; Eastern Cooperative Oncology Group (ECOG) performance status 0]. Biopsy confirmed recurrence of malignant melanoma and combination therapy of nivolumab (1 mg/kg) and ipilimumab (3 mg/kg) was initiated. Routine blood test after his second cycle of treatment revealed a creatinine of 3.96 mg/dL, compared with a baseline of 0.91 mg/dL 3 weeks prior, indicating AKI (Table ). Urinalysis revealed 2+ protein (albumin/creatinine ratio 42.4 mg/gCre), RBC 8/hpf and WBC 9/hpf. Urine sediments showed granular casts and WBC casts (FigureA and B). There was no history suggestive of dehydration or exposure to nephrotoxic agents such as antibiotics, contrast or analgesics. His only medications were nivolumab and ipilimumab. He was allergic to sulfa and ciprofloxacin.
On physical examination, vitals revealed a temperature of 36.4°C, a pulse of 93/min, a blood pressure at 178/80 mmHg, a respiratory rate of 20/min and body weight of 73.1 kg (an increase of 5 kg from his pre-treatment weight). A non-tender submandibular mass was palpable. His lungs were clear to auscultation and 1+ bilateral lower extremity edema were noted. A morbilliform eruption rash was noted on his chest, abdomen and back (FigureC). There was no change in the oral mucosa. A renal ultrasound showed no evidence of hydronephrosis, although the kidneys were slightly enlarged bilaterally (right 12.4 cm and left 13.0 cm). The decision was then made to pursue a kidney biopsy to further define the etiology of the patient's severe AKI.
The kidney biopsy contained 34 glomeruli, of which 4 were globally sclerosed. The remaining glomeruli showed wrinkled glomerular capillary loops and narrowing of Bowman's space, suggestive of hypoperfusion. Cellularity and architecture was normal and no active inflammation of the tuft, necrotizing lesions or cellular crescents was noted (not shown). There was diffuse extensive interstitial inflammation associated with moderate interstitial edema (FigureA). The infiltrates were primarily composed of lymphocytes and plasma cells with admixed eosinophils and neutrophils. Granuloma or granulomatous lesions were not noted. There were frequent tubulitis and various degenerative changes, with focal flattening of the epithelium and occasional mitoses. Several tubules contained necrotic cellular debris, granular casts and periodic acid–Schiff-positive hyaline casts.
Immunofluorescence staining revealed no significant immune deposits in the glomeruli. Tubular basement membranes showed focal fine granular deposition of C3 (1+). The interstitium revealed intense fibrin deposits (not shown). Immunohistochemistry showed extensive T-cell-dominant infiltrates (FigureB and C), of which ∼10–20% were strongly positive for cytotoxic enzymes including granzyme B (FigureD) and perforin (FigureE). Foxp3+ regulatory T cells were also present in the interstitium (FigureF).
The patient was treated with a steroid pulse [solumedrol 500 mg intravenous (IV) × 3 days] followed by a taper (prednisone 60 mg daily). Although his creatinine initially improved to 2.41 mg/dL over the course of a week, it had increased to 4.64 mg/dL when he was readmitted the following week with symptoms of a fever and a rash (Table and Figure). There was no laboratory evidence of hypophysitis or hepatitis at the time (Table ). Skin biopsy revealed interface dermatitis involving adnexal structures with superficial perivascular lymphohistiocytic infiltrates. Peripheral immune characterization revealed highly proliferative circulating CD4+ and CD8+ T cells (measured by the percentage of Ki67+ cells, FigureA–C) in combination with an expansion of effector memory T cells (TEM, CD45RA-negative CCR7-negative, FigureD and E). Furthermore, serum cytokine analysis revealed a strikingly high level of pro-inflammatory cytokines (IL-1Ra, CXCL10 and TNF-α) (FigureF–H) and soluble IL-2 receptor (32 400 pg/mL; reference range <1033 pg/mL). Due to these findings, the patient's steroid dose was increased (solumedrol 140 mg IV twice a day) and mycophenolate mofetil (MMF; 1000 mg twice a day) was added to intensify treatment. Creatinine peaked at 7.31 mg/dL and then improved to 3.37 mg/dL over 10 days (Figure). The patient's rash dramatically improved and eventually resolved. Two weeks later, the patient was again admitted with a fever of 38.4°C and 3 days of bloody diarrhea. While his creatinine had remained stable, he was found to be pancytopenic (WBC 1.25 × 103/µL with 92% neutrophils, hemoglobin 9.2 g/dL, platelets 37 × 103/µL). The patient subsequently developed septic shock and deceased in spite of aggressive treatment with broad-spectrum antibiotics and vasopressor support. Blood culture turned out to be positive for pan-sensitive Pseudomonas aeruginosa. Autopsy demonstrated hemorrhagic colitis with no histological evidence of viable tumor in his liver.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [75, 'years'], 'creatinine': [3.96, 'mg/dL']}",15.05115,14.29859,15.80371,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 75 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.96 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.96/0.9)**-1.2 * 0.9938**75 * 1.0 = 15.05115.
Hence, the GFR value is 15.05115 ml/min/1.73 m²."
157,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,trec-ct-2022-22,Extracted,"A 15-year-old boy with mild intellectual disability is brought to the office by his parents for a routine physical examination.  The boy is going to a school for students with learning disabilities.  The patient was adopted, and his immunizations are up to date.  Review of the patient's medical records is notable for cytogenetic studies that showed a small gap near the tip of the long arm of the X chromosome, which is consistent with fragile X syndrome, an X-linked disorder. The defect is an unstable expansion of trinucleotide repeats (CGG) in the fragile X mental retardation 1 (FMR1) gene, located on the long arm of the X chromosome. He is not using any medications and vital signs are within normal levels. His blood chemistry analysis as bellow:
Blood Chemistry Value      Normal Range     Patient Value
Glucose                    90-120 mg/dl     95 mg/dl
BUN (Blood Urea Nitrogen)  7-24 mg/dl       10 mg/dl
Creatinine                 0.7-1.4 mg/dl    0.8 mg/dl
Calcium                    8.5-10.5 mg/dl   9 mg/dl
Sodium                     134-143 mEq/L    135 mEq/L
Potassium                  3.5-4.5 mEq/L    3.7 mEq/L
Chloride                   95-108 mEq/L     98 mEq/L
CO2                        20-30 mEq/L      25 mEq/L
Blood pH                   7.38-7.42        7. 39","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [15, 'years'], 'creatinine': [0.8, 'mg/dL'], 'sex': 'Male'}",124.23949,118.02752,130.45146,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 15 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.8 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.8/0.7)**-0.302 * 0.9938**15 * 1.0 = 124.23949.
Hence, the GFR value is 124.23949 ml/min/1.73 m²."
158,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8083874-1,Extracted,"A 73-year-old Japanese woman was brought to an emergency room due to difficulty in urinating. At the age of 70, she was diagnosed with complete eversion of uterine prolapse and type 2 diabetes mellitus (T2DM), but she hesitated to get any medical treatment. Her vital signs were as follows: temperature, 36.8°C; blood pressure, 96/50 mmHg; heart rate, 30 beats/min; oxygen saturation, 84 % (room air). shows laboratory data in an emergency room. Diabetes-associated data were as follows: plasma glucose, 241 mg/dl; hemoglobin A1c (HbA1c), 9.3%. Liver and renal function was markedly elevated as follows: asparate aminotransferase (AST), 567 U/L; alanine transaminase (ALT), 196 U/L; alkaline phosphatase (ALP) 214 U/L; γ-glutamyl transpeptidase (γ-GTP), 33 U/L; lactate dehydrogenase (LDH), 1670 U/L; creatinine (CRE), 3.27 mg/dl; blood urea nitrogen (BUN), 37 mg/dl. In addition, her inflammation markers were markedly elevated probably due to the development of DIC: white blood cell, 36,260 /μL (neutrophil, 93.0%); C-reactive protein, 15.54 mg/dl; procalcitonin, 278.70 Ng/mL; platelets, 9.2 × 104/μL; prothrombin percentage activity, 65.8%; fibrinogen, 288 mg/dl; D-dimer, 69.60 μg/mL; antithrombin III activity, 62.5%. As shown in , her abdominal and pelvic computed tomography (CT) on admission revealed renal calculus, hydronephrosis, lower shift of bladder, urinary tract and severe uterine prolapse. In addition, as shown in , she suffered from emphysematous cystitis and pyelonephritis both of which contained some gas inside the organ. Same pathogenic bacteria (Escherichia coli) were detected in blood and urine. Since we thought that uterus prolapse was possibly involved in the aggravation of the conditions in this subject, we performed prolapsed uterus reduction and ureteral stenting. In addition, we also started antibiotics therapy for emphysematous cystitis and pyelonephritis (3 g/day of meropenem) and treated DIC. In abdominal and pelvic CT taken 10 days after admission, hydronephrosis was improved, although renal calculus was observed. In addition, pelvic CT revealed that lower shift of bladder (red arrow) and severe uterine prolapse (white arrow) were improved (). Finally, we successfully treated emphysematous cystitis and pyelonephritis, and she was transferred from intensive care unit to general ward at day 10. After then, we stopped meropenum and started 3.0 g/day of cefazolin, and after several days later we changed cefazolin to 300 g/day of cefdinir (). Her renal function and inflammatory markers were gradually normalized and she was finally discharged about 1 month after admission.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [73, 'years'], 'creatinine': [3.27, 'mg/dL'], 'sex': 'Female'}",14.35343,13.63576,15.0711,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 73 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 3.27 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (3.27/0.7)**-1.2 * 0.9938**73 * 1.012 = 14.35343.
Hence, the GFR value is 14.35343 ml/min/1.73 m²."
159,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7809723-1,Extracted,"A 72-year-old Bahraini female known to have type 2 diabetes mellitus, resistant systemic hypertension, hyperlipidaemia, and peripheral artery disease (PAD) with a history of stenting distal abdominal aorta (12 mm × 40 mm S.M.A.R.T control self-expanding stent) and right common iliac artery (7 mm × 17 mm Express LD) in 2014 was referred to our cardiac centre for evaluation of repeated episodes of FPE.
On arrival, she was in mild dyspnoea and oliguric. Her blood pressure was 182/105 mmHg, and her heart rate was 109 b.p.m. Physical examination has revealed bilateral basal crackle with no audible cardiac murmur and periumbilical, high-pitched bruits. Her electrocardiogram showed QRS voltage criteria for left ventricular hypertrophy, which was confirmed with a transthoracic echocardiogram that revealed concentric left ventricular hypertrophy with Grade II diastolic dysfunction and normal left ventricular size and systolic function with no regional wall motion abnormality. Baseline Creatinine was 225 µmol/L (reference range 44–88 µmol/L) and hence we performed the coronary angiogram with minimal contrast (18 cc only) to rule out underlying coronary artery disease in view of multiple risk factors and troponinaemia, which showed coronary calcifications but no flow-limiting disease in the epicardial coronaries. Since the patient had resistant systemic hypertension with abdominal bruits, non-selective renal angiography was conducted and showed bilateral heavily calcified high-grade ostioproximal RAS. While we were sorting out a strategy for ad hoc intervention for the tight renal arteries she desaturated, her blood pressure raised to 240/130 mmHg, her heart rate increased to 130 b.p.m., and her respiration rate was 26/min with diffuse bilateral fine crackles. Considering acute florid pulmonary oedema and being anuric despite large dose of diuretics, we aborted the procedure and timely inserted the right internal jugular dialysis line and transferred her to the cardiac care unit for urgent haemodialysis.
The next day, after full stabilization, we brought her back to the Cath lab for renal angioplasty. We decided for the left transradial approach for two reasons: the left radial artery has a shorter distance to the renal arteries than the right radial artery and the angles of the renal arteries off the aorta favour a radial approach than a retrograde femoral access.
Under local anaesthesia, the left radial artery access was achieved with a 7-Fr sheath. We managed to navigate a 90 cm sheath across an unexpected left subclavian stenosis with balloon dilatation (Figure and B) and slide it subsequently across a tortuous descending aorta using NaviCross microcatheter and Terumo Glidewire Advantage, which was exchanged to Hi-Torque supracore guidewire thereafter to land the sheath into the abdominal aorta.
A 7-Fr multipurpose guide catheter engaged the right renal artery, and a selective renal angiogram confirmed the presence of critical calcified stenosis at the proximal part of the right renal artery (Figure ).
The lesion crossed with Hi-Torque BMW 0.014 × 300 cm guidewire. Intravascular ultrasound pullback showed a very high superficial and deep calcium burden in the proximal segment of the right renal artery with a 5.2 cm reference vessel diameter (Figure ). Considering severe calcifications, we decided to proceed with shockwave lithotripsy using a 4.0 mm × 12 mm, 138 cm shockwave C2 IVL balloon with a total of 80 pulses. Fair expansion of the 4.0 mm IVL balloon at 6 atmospheres was achieved (Figure and D). Now, without further balloon dilation, a 5.0 mm × 18 mm Resolute Onyx stent was deployed at 14 atmospheres with a good final angiographic result (Figure ).
The same procedure was applied for the left renal artery after confirmation of tight osteoproximal lesion with selective injection (Figure ). This time, the IVUS study showed a larger vessel diameter of 7.1 cm with severe semi-circumferential calcium arc (Figure ) that we overcame successfully with 6.0 mm × 60 mm, 110 cm shockwave M5 IVL balloon (10 rounds each of 30 pulses) at 6 atm (Figure and D). Once the lithotripsy treatment is completed, a 7.0 mm × 17 mm Express SD Renal stent was deployed at 10 bar. Final angiography demonstrated an excellent position of the stent and confirmed patency of the left renal artery (Figure ). The patient tolerated the procedure well and was transferred to the cardiology ward for further monitoring. A few hours later, we noticed a dramatic improvement of blood pressure measurements and urine output. She required one more haemodialysis session to enhance renal recovery and minimize the risk of contrast induced-nephropathy and was successfully discharged to home 48 h post-procedure.
In the 2-week of follow-up, she was asymptomatic, serum creatinine almost normalized (96 µmol/L, reference range 44–88 µmol/L) with adequate blood pressure control. Three months after discharge, renal function recovered completely and return to normal (Creatinine 81 µmol/L, reference range 44–88 µmol/L) with good blood pressure control on amlodipine 10 mg o.d. only.
In our institution, there are no standards for routine duplex or imaging follow-up after renal angioplasty unless mandated clinically.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [72, 'years'], 'creatinine': [81.0, 'µmol/L'], 'sex': 'Female'}",67.47388,64.10019,70.84757,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 72 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 81.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 81.0 µmol. To convert 81.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 81.0 µmol Serum Creatinine * 1e-06 mol/µmol = 8e-05 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 8e-05 mol Serum Creatinine * 113.12 g/mol = 0.00905 g Serum Creatinine. To convert 0.00905 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00905 g Serum Creatinine * 1000.0 mg/g = 9.05 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 9.05 mg Serum Creatinine/10.0 dL = 0.905 mg Serum Creatinine/dL. The concentration value of 81.0 µmol Serum Creatinine/L converts to 0.905 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.905/0.7)**-1.2 * 0.9938**72 * 1.012 = 67.47388.
Hence, the GFR value is 67.47388 ml/min/1.73 m²."
160,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4885209-1,Extracted,"A 34-year-old male presented with multiple asymptomatic pigmented raised lesions over the trunk, bilateral upper and lower limbs for last two months. He had history of fever and weight loss (>10% total body weight) for the past six months. History of swelling of bilateral lower limbs, scrotum, and penis was present since one month. He gave history of unprotected sexual exposures with multiple female partners. On examination, the patient had pallor, generalized lymphadenopathy, bilateral pitting pedal edema, and hepatosplenomegaly. Cutaneous examination revealed multiple discrete to grouped violaceous macules, papules, nodules and plaques measuring 0.2 cm × 0.2 cm to 0.5 cm × 3 cm over the trunk, bilateral upper and lower limbs []. Cutaneous lesions over the lower abdomen and left thigh were coalescing to give a “cobblestone appearance” []. Oral cavity showed two well-defined violaceous patches over the hard palate []. On investigation, he had low hemoglobin (6.9 g/dl), deranged renal function parameters (urea - 69 mg/dl and creatinine - 1.9 mg/dl) and massive bilateral pleural effusion on chest X-ray. Serology for HIV-1 was positive by enzyme-linked immunosorbent assay and negative for HIV-2, and his CD4 count was 573/mm3. Histopathology of skin biopsy specimen revealed proliferation of endothelial cells with formation of slit-like vascular spaces in the upper and middle dermis. Spindle-shaped endothelial cells were arranged in solid cords and fascicles admixed with variable lymphoplasmacytic infiltrate, hemorrhage, and lymphatic-like dilated spaces [Figures and ]. Promontory sign, characterized by protruding of new vessels into the lumen of existing large vessel, was also demonstrated []. On immunocytochemistry, endothelial cells were positive for CD31 [] and CD34. A final diagnosis of AIDS-associated disseminated KS was made but unfortunately the patient died before starting HAART because of recurrent massive pleural effusion.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [34, 'years'], 'creatinine': [1.9, 'mg/dL'], 'sex': 'Male'}",46.88574,44.54145,49.23003,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 34 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.9 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.9/0.9)**-1.2 * 0.9938**34 * 1.0 = 46.88574.
Hence, the GFR value is 46.88574 ml/min/1.73 m²."
161,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5437989-1,Extracted,"An 11-year-old girl was admitted to our hospital with microscopic hematuria and nephrotic-range proteinuria detected by school urinary screening. The patient did not have any characteristic features of Fabry’s disease such as angiokeratoma or neuralgia. On admission, her physical examination was unremarkable (body weight 47.4 kg, body height 157.3 cm), and her blood pressure normal (106/60 mmHg). Laboratory investigations revealed hypoproteinemia (serum total protein 5.6 g/dL, serum albumin 2.9 g/dL, serum IgG 318 mg/dL). All other biochemical investigations were within normal limits: blood urea nitrogen 8 mg/dL, serum creatinine 0.43 mg/dL, IgA 111 mg/dL, C3 140 mg/dL (normal 84 – 151 mg/dL), C4 26 mg/dL (normal 17 – 40 mg/dL). Anti-hepatitis B surface antigen, anti-hepatitis C antibody, and anti-nuclear antibody were negative. Urinalysis findings were 3+ for occult blood and 3+ for the dipstick protein reaction; her 24-hour urine protein excretion was 2.5 g. Light microscopy analysis of the initial renal biopsy specimen revealed diffuse mesangial proliferative glomerulonephritis with fibrocellular crescents in 4 of 13 glomeruli (a). Immunofluorescence revealed granular deposits of IgA (3+) and C3 (1+) in the mesangial areas (b), and electron microscopy revealed paramesangial electron-dense deposits. Based on these findings, a diagnosis of severe IgA nephropathy was made. The patient was treated intravenously with three courses of methylprednisolone (20 mg/kg/day) pulse therapy (MPT), followed by 2 years of alternate-day prednisolone (initially 1 mg/kg and then tapered gradually) combined with an angiotensin receptor blocker (telmisartan 1 mg/kg/day). In addition, a tonsillectomy was performed 3 months after MPT. However, microscopic hematuria and mild proteinuria persisted.
At the age of 13 years, the patient was re-admitted for a second renal biopsy to assess the therapeutic effect. All laboratory investigations were within normal limits: serum total protein 6.3 g/dL, serum albumin 4.0 g/dL, blood urea nitrogen 12 mg/dL, serum creatinine 0.44 mg/dL, IgA 108 mg/dL, C3 96 mg/dL, C4 26 mg/dL. Urinalysis revealed a 2+ value for occult blood and a dipstick protein reaction of 2+; the 24-hour urine protein excretion was 0.5 g. Light microscopy analysis of the second renal biopsy specimen revealed focal segmental mesangial proliferative glomerulonephritis. Immunofluorescence revealed granular deposits of IgA (2+) and C3 (1+) in the mesangial areas, and electron microscopy revealed paramesangial electron-dense deposits. After the second renal biopsy, the patient was additionally treated with three courses of MPT, and her microscopic hematuria disappeared within 6 months.
At the age of 15 years, she was admitted for a third renal biopsy. On admission, her physical examination was unremarkable (body weight 55.9 kg, body height 165 cm), and her blood pressure normal (102/70 mmHg). Laboratory investigations were all within normal limits: serum total protein 6.6 g/dL, serum albumin 4.2 g/dL, blood urea nitrogen 11 mg/dL, serum creatinine 0.48 mg/dL, IgA 135 mg/dL, C3 121 mg/dL, C4 25 mg/dL. Urinalysis was negative for occult blood and the dipstick protein reaction was 2+; her 24-hour urine protein excretion was 0.7 g. Light microscopy analysis of the third renal biopsy specimen revealed minor glomerular abnormalities (a). Immunofluorescence revealed granular deposits of IgA (2+) in the mesangial areas, and electron microscopy revealed paramesangial electron-dense deposits. In addition, numerous myelin-like bodies were first observed in podocytes (b). Low serum α-galactosidase A activity (13.8 Agal U, cut-off value < 20) and increased GL3 excretion in the urine (0.54 mg/mgCr, control 0.1 – 0.4) were also observed. On the basis of these findings, a final diagnosis of concomitant IgA nephropathy (healing stage) and subclinical Fabry’s disease was made.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [15, 'years'], 'creatinine': [0.48, 'mg/dL'], 'sex': 'Female'}",143.36503,136.19678,150.53328,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 15 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.48 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.48/0.7)**-0.241 * 0.9938**15 * 1.012 = 143.36503.
Hence, the GFR value is 143.36503 ml/min/1.73 m²."
162,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7387068-1,Extracted,"A 45-year-old man, known to have diabetes mellitus type 2 and FHTG (diagnosed based on genetic testing) from past six years, not compliant with his treatment (atorvastatin 10 mg bedtime and metformin 500 mg twice daily), presented to a tertiary hospital with a one-day history of abdominal pain and three episodes of vomiting. The patient had experienced similar symptoms six years ago. He denied eating food from a restaurant, although he reported that his diet is high in carbohydrates and fat. On clinical examination, abdominal tenderness was elicited, and no eruptive xanthomas were present. His blood test result on the day of admission was not reported as it was highly lipemic. Pertinent laboratory tests showed: lipase 242 IU/L (reference: 13-60), amylase 41 IU/L (reference: 28-100), albumin 33 g/L (reference: 35-52), and creatinine 40 micromol/L (reference: 62-106). Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were not recorded as the sample was lipemic. Total cholesterol was 592.8 mg/dl (reference: 150.8-201); high-density lipoprotein (HDL), 15.8 mg/dl (reference: 42.5-61.8); and triglycerides, 3587.2 mg/dl (reference: 44.2-150.5). Low-density lipoprotein (LDL) was not recorded. HbA1c was 9.7% (reference: 4.6-6.2). His venous blood gas showed a pH of 7.42 (reference: 7.35-7.45) and HCO3 of 25 mmol/L (reference: 22-26). He had a CT scan without contrast on the day of admission, which was suggestive of AP.
The patient was diagnosed with HTG-AP. On day 1, the patient was kept nil per mouth and started on a continuous infusion of normal saline at 135 ml/hr for 24 hours. On day 2, he was reviewed by the endocrinologist and recommended starting IV insulin infusion 4 units/hr and dextrose normal saline IV fluids until the TG level falls below 443 mg/dl. Besides, atorvastatin (40 mg once daily (OD)), fenofibrate (145 mg OD), omega-3 (1 g OD), and aspirin (100 mg OD) were given. On day 3, his abdominal pain resolved, and the CT scan with contrast revealed acute pancreatitis (Figure ). On day 6, his lipase level reduced to normal (40 IU/L), and TG level came down to 673.1 mg/dl; he was discharged.
On discharge, the patient was kept on insulin glargine 40 units bedtime, insulin NovoRapid® four units three times daily with 1 g metformin twice daily. All oral medications (atorvastatin, fenofibrate, omega-3 fatty acids, and aspirin) were continued. Four days after discharge, the patient was seen in the clinic by the endocrinologist. His lipase levels were normal (21 IU/L), and TG was at 549.1 mg/dl.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [45, 'years'], 'creatinine': [40.0, 'µmol/L'], 'sex': 'Male'}",122.49287,116.36823,128.61751,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 45 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 40.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 40.0 µmol. To convert 40.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 40.0 µmol Serum Creatinine * 1e-06 mol/µmol = 4e-05 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 4e-05 mol Serum Creatinine * 113.12 g/mol = 0.00452 g Serum Creatinine. To convert 0.00452 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00452 g Serum Creatinine * 1000.0 mg/g = 4.52 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 4.52 mg Serum Creatinine/10.0 dL = 0.452 mg Serum Creatinine/dL. The concentration value of 40.0 µmol Serum Creatinine/L converts to 0.452 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.452/0.7)**-0.302 * 0.9938**45 * 1.0 = 122.49287.
Hence, the GFR value is 122.49287 ml/min/1.73 m²."
163,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4967670-1,Extracted,"A 31-year-old Caucasian woman was diagnosed with lupus in 2011. She initially presented with arthritis, serositis (pleuritis), autoimmune hemolytic anemia, idiopathic thrombocytopenia (ITP), positive antinuclear antibody (ANA), Smith and RNP antibodies, and low complement levels. She also has a history of autoimmune hepatitis and diabetes mellitus type 1. She was initially treated with intravenous immunoglobulin (IVIG), rituximab, and splenectomy. Her disease was relatively stable on hydroxychloroquine 200 mg BID and mycophenolate mofetil (MMF) 500 mg twice a day. In June 2013, she presented with complaints of dyspnea, lower extremity swelling, fevers, anorexia, and jaundice.
Initial workup revealed worsening of chronic anemia with hemoglobin of 5.2 g/dL (her baseline, 8–10 g/dL, and normal, 11.2–15.7 g/dL), hyperbilirubinemia with total bilirubin of 9.2 mg/dL (normal, 0.2–1.2 mg/dL), direct bilirubin of 6.4 mg/dL (normal, 0.0–0.3 mg/dL), alkaline phosphatase of 250 μ/L (normal, 35–104 μ/L), normal ALT and AST, and a right-sided pleural effusion on chest X-ray. She was treated for a flare of autoimmune hemolytic anemia with IVIG, blood transfusions, intravenous pulse doses of methylprednisolone, empiric treatment with broad spectrum antibiotics for pleural effusion, and continuation of the home dose of hydroxychloroquine 200 mg daily and MMF 500 mg twice a day. Antibiotics were stopped after pleural fluid and blood cultures were found to be negative. Liver biopsy showed iron overload in hepatocytes and no significant inflammation or fibrosis.
Her creatinine increased from a baseline of 0.8 to 1.8 mg/dL and peaked at 2.81 mg/dL (normal, 0.5–1.10 mg/dL) on the fifth day of hospitalization. Urinalysis showed large protein and blood, and urine microscopy showed many red blood cells (RBCs) with few dysmorphic RBCs and many granular casts, fatty casts, and white blood cell casts but no RBC casts. Urine random protein/creatinine ratio was elevated at 2.49 (normal < 0.15).
Renal biopsy () showed glomeruli with cellular and fibrocellular crescents, focal segmental necrosis, and mild interstitial and tubular injury. IF showed only trace C3, IgM, and fibrinogen deposits. Electron microscopy (EM) showed endothelial and podocyte injury with glomerular basement membrane (GBM) remodeling; no electron dense immune deposits were seen. The findings were consistent with pauci-immune crescentic glomerulonephritis with focal acute activity and mild chronic changes.
Additional laboratory testing revealed a positive ANA with a titer of 1 : 640 (homogenous pattern), elevated anti-Smith antibody of >8.0 (normal, 0.0–0.9 AI), RNP antibody of 7.2 (normal, 0.0–0.9 AI), p-ANCA at >1 : 640 (normal, <1 : 20), anti-myeloperoxidase (MPO) antibodies at 86.0 U/mL (normal, 0.0–9.0 U/mL), anticardiolipin IgM at 27 U/mL (normal, 0–12 U/mL), and positive lupus anticoagulant. She had a low C3 level of 56 mg/dL (normal, 90–180 mg/dL) and normal C4 level. Anti-double stranded DNA antibodies (dsDNA), c-ANCA, anti-proteinase 3 (PR-3) antibodies, and beta-2 glycoprotein antibodies were negative.
Based on biopsy results, MMF was switched to cyclophosphamide 175 milligrams daily orally. Creatinine returned to normal and her anemia improved. She was tapered off of cyclophosphamide and switched to azathioprine for maintenance therapy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [31, 'years'], 'creatinine': [2.81, 'mg/dL'], 'sex': 'Female'}",22.3567,21.23887,23.47453,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 31 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.81 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.81/0.7)**-1.2 * 0.9938**31 * 1.012 = 22.3567.
Hence, the GFR value is 22.3567 ml/min/1.73 m²."
164,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6559684-1,Extracted,"A 40-year-old Hispanic man with a past medical history of human immunodeficiency virus (HIV) was brought to the emergency department complaining of right upper extremity (RUE) weakness and numbness for four days with associated bitemporal headache and generalized fatigue. The patient reported first time use of intranasal cocaine and heroin, after which he lost consciousness and woke up approximately four hours later with new onset RUE and headache. His cluster of differentiation 4 (CD-4) count was reported above 500 cells/mm3 and viral load (VL) was undetectable. The patient did not have any known CNS complications in the past.
On physical examination, his blood pressure was 151/97 mm Hg and pulse was 82 and regular. He was alert and cooperative. His cranial nerves were intact. His motor exam, however, was abnormal in the RUE with 3/5 arm strength and wrist drop; the strength and tone of the other extremities were normal throughout. Deep tendon reflexes were normal bilaterally, but his gait could not be evaluated. His sensory function decreased to pin sensation at the RUE and normal sensation was noted in the rest of the extremities and face. Laboratory testing was normal except for an elevated creatinine of 6.9 mg/dl, creatine phosphokinase (CPK) of 7855 IU/l, alanine transaminase (ALT) of 139 IU/l, and aspartate transaminase (AST) of 109 IU/l. Urine toxicology was positive for metabolites of cocaine and heroin. Magnetic resonance imaging (MRI) of the brain was done and it revealed two areas of increased T2/FLAIR signal within the medial aspect of both basal ganglia, measuring 16 mm in the right and 12 mm on the left involving each globus pallidus and the genu of the internal capsule, as can be seen in Figures -. His chest radiography was normal, computerized tomography (CT) of the brain, as can be seen in Figure , and cervical spine were normal. His electrocardiogram was normal.
In the subsequent days, his kidney function and rhabdomyolysis improved. The patient remained fully awake, alert and oriented, but the weakness of his RUE persisted. The patient decided to leave against medical advice despite full explanation of the risk of leaving.
The patient was contacted over the phone and he informed us that he followed up with his primary care physician and reported improvement of the weakness. He received physical therapy and was independent in all activities of daily living and functional mobility. His only limitation was a moderate decrease in fine motor coordination of the RUE.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [40, 'years'], 'creatinine': [6.9, 'mg/dL']}",9.60993,9.12943,10.09043,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 40 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 6.9 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (6.9/0.9)**-1.2 * 0.9938**40 * 1.0 = 9.60993.
Hence, the GFR value is 9.60993 ml/min/1.73 m²."
165,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6776198-1,Extracted,"A 56-year old man with multiple comorbidities (severe obesity, moderate chronic renal failure, chronic obstructive pulmonary disease, smoking, cirrhosis, atrial fibrillation, coronary artery disease) presented to the out-patient clinic complaining intermittent claudication (Rutherford category 3) at right lower limb since 2 weeks. He received mitral valve replacement with coronary artery bypass graft three months before for acute endocarditis (Streptococcus gallolyticus), followed by brain septic embolization.
Physical examination revealed absence of right lower limb pulses with mild hypothermia and abdominal pain at deep palpation of the right lower quadrant without pulsating masses. Duplex ultrasound (DUS) found a perfused abdominal mass with 69mm in diameter in the right lower quadrant with steno-occlusion of right iliac axis. An emergency computer tomography angiography (CTA) revealed a right common iliac artery pseudoaneurysm (62x64 mm) with occlusion of external iliac artery, patency of hypogastric and recanalization of the right common femoral artery.
At admission, the patient had no fever and no leukocytosis (white blood cells=6,76x10^3), with anemia (Hb=9.1 g/dl), mild chronic renal failure (creatinine: 2.1 mg/dl) and high C reactive protein (CRP=97.2 mg/l). No blood culture or positron emission tomography were performed for absence of signs of concurrent systemic infection. No systemic antibiotics was undertaken for the same reason.
The following day, the patient underwent a digital subtraction angiography (DSA) () through left brachial access (6F-sheath introducer, 90cm in length).
The embolization of the hypogastric artery with coils (Balt SPI™ and Cook Mreye™) and of the common iliac artery with Plug (16 mm-Amplatzer Vascular Plug II™) was performed.
The post-procedural DSA revealed the complete exclusion of the hypogastric artery, and the pseudoaneurysm (). The reperfusion of ipsilateral common femoral artery was maintained by collateral circulation.
During the post-operatory period, no hypotension or ischemia of the right lower limb occurred. A CTA confirmed the exclusion of the pseudoaneurysm. Similar findings were highlighted at CTA performed in the third post-procedural day. At discharge (6th post-procedural day), the patient had no fever, no leukocytosis (WBC=5,66x10^3) with stable anemia (Hb=9.1 g/dl) and renal function (creatinine=1.6 mg/dl). The abdominal pain disappeared, the right leg was normothermic and in hemodynamic compensation without rest pain, acute ischemia or neurological deficit.
After one month, a CTA referred the exclusion of the pseudoaneurysm with a gradual reduction in the size. After 10 months, other CTA showed the complete resolution of the pseudoaneurysm () and the revascularization of the right common femoral artery by collateral circulation.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [56, 'years'], 'creatinine': [2.1, 'mg/dL']}",36.26267,34.44954,38.0758,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 56 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.1/0.9)**-1.2 * 0.9938**56 * 1.0 = 36.26267.
Hence, the GFR value is 36.26267 ml/min/1.73 m²."
166,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8712212-1,Extracted,"A 35-year-old male presented with chief complaints of severe back pain and dehydration. Hours earlier, his family found him floating in a hot tub outside his parent’s suburban home, exposed to the midday summer heat of central Texas. His past medical history was pertinent for bipolar type schizoaffective disorder and substance use disorder (methamphetamines, marijuana, and cocaine). In the past, he had been admitted for his schizoaffective disorder and recently had been released from a correctional facility where he had been incarcerated for drug-related offenses. Collateral history from the patient’s family revealed the patient was recently released from a correctional facility and missed an appointment to receive a long-acting injectable antipsychotic (risperidone), but he was otherwise unmedicated and had no psychiatry follow-up. He was brought to the emergency department under a police order of emergency detention (POED) with chief complaints of extreme back pain and the sense that his house was “full of snakes.” The patient requested the medical team to perform a “full-body transplant” to alleviate his back pain and so he would be able to move on to “a new life.” The patient disclosed that he had been in the hot tub for several hours because it would, “protect [him] from the mind-controlling electric machine which creates these snakes that attack [him].” The patient denied any recent recreational or illicit substance use. The remainder of the history was deferred due to the patient’s psychosis. Initially, the patient was infused with two liters of Ringer's lactate solution in the emergency room and given a sitter to prevent him from leaving the patient care room.
Physical examination
On general inspection, the patient had a first-degree burn covering his bilateral upper torso, arms, and calves. He smelled of salt and appeared very dehydrated with dry mucus membranes of the mouth. Capillary refill was delayed to roughly four seconds and his forehead was covered in a fine coat of salt. Vital signs were pertinent for sinus tachycardia to the 120s and systolic blood pressure in the 110s/60s (mmHg). However, the patient was hemodynamically stable and did not require intensive stabilization or surgical intervention.
Laboratory results
A complete blood count (CBC), complete metabolic panel (CMP), urinalysis, toxicology screen, and HIV test were obtained. The patient’s urine sample was a dark brown color, like that of a dark tea, which led the team to order a creatine kinase (CK) level. The patient’s CK serum level was elevated at approximately 90,000 mg/dL (22 to 198 mg/dL). The patient’s urinary toxicology screen was positive for both benzodiazepines and methamphetamines. The CMP revealed a creatinine of approximately 5 mg/dL, significantly elevated blood urea nitrogen (BUN), and mild transaminitis, while other laboratory values were within normal limits (Table ). While awaiting laboratory findings, the primary care team ordered an abdominal ultrasound (US), which demonstrated no acute changes or morphologic alterations to the kidney parenchyma, ureters, or other urinary structures. Furthermore, the abdominal US did not demonstrate findings on the liver, gall bladder, or other gastrointestinal structures. These laboratory values and the imaging study led the primary medicine team to consult the nephrology team for potential hemodialysis for acute renal failure (ARF) secondary to rhabdomyolysis.
Consultant team’s recommendations for management
Based on the patient’s clinical condition, the nephrology team recommended aggressive IV fluid resuscitation at 200 mL/hr to facilitate the renal clearance of myoglobin. The nephrology team acknowledged that if the patient’s creatinine kinase levels continued to increase, they may need to begin hemodialysis. However, they were hopeful that conservative management would permit physiological recovery. As the patient faced a life-threatening condition and clearly lacked the capacity to refuse treatment, the psychiatry team acknowledged that they would likely need to file for an order of protective custody (OPC) to ensure that he would not be able to leave in his altered state, they also stated that they would start 1 mg of oral risperidone given once daily to treat his psychosis and baseline schizoaffective disorder and adjust the medications as needed from there.
Psychiatric complications
Shortly after starting treatment for the ARF, the patient complained that he had no issues with his kidneys and that he wanted a transfer to another location to obtain a new body, exclaiming that “if you don’t even have a muscle regeneration machine, how can you call this a hospital?”. He stated that he did not want the IV catheter placed, the fluids given, or an X-ray taken as he “doesn’t want his plasma taken out.” After his mother arrived, the patient successfully removed his IV catheter and attempted to leave against medical advice (AMA), which he was unable to do secondary to his POED. The patient became increasingly agitated and required 5 mg of haloperidol, 2 mg of lorazepam, and 50 mg of diphenhydramine by intramuscular injection. Despite this, he continued to be agitated and aggressive, which necessitated another intramuscular injection of 5 mg of haloperidol and 2 mg of lorazepam. Reestablishing IV access proved to be very difficult leading to a six-hour delay in resuming fluid infusion.
Over the following days, the patient was amenable to taking oral risperidone. However, he also called the police a total of four times stating that he was being held against his will and that the hospital was working to harm him. These accusations necessitated the medical team to collaborate with the police. With the support of the head of security, the team summoned a police officer from another floor to “answer the call” from the patient. The officer kindly explained that they had received his call, but that he had a legal order to remain in the hospital, and that it was important to listen to the doctors and take his medications. The patient agreed to take an oral dose of risperidone and expressed his willingness to restart the IV fluids. This helped resolve some of the patient’s guardedness, allowing for continued IV restoration of fluid status without the patient removing his catheter. Over the next several days, the patient’s urine output normalized, and laboratory tests returned reassuring serum creatinine levels. The primary care team transitioned the patient from IV fluid replacement to aggressive oral fluid replacement and the IV catheter was removed, which surprisingly alleviated nearly all of the patient’s paranoid ideations and distrust toward the medical team. After a total of 11 days of hospitalization, during which pharmacy, physical therapy, occupational therapy, and case management all worked to ensure his proper physical and social care, the nephrology team and internal medicine team cleared him for discharge to inpatient psychiatry for treatment of his schizoaffective disorder. He was discharged on a 0.1 mg clonidine extended-release patch to be replaced weekly, 1 mg of risperidone taken orally twice daily, and 800 mg of sevelamer to be taken three times a day with meals. He and his parents were given education regarding his adherence to his medications, major signs and symptoms associated with medication use, and finally his rehabilitation plan for after the psychiatric hospitalization was discussed with the patient and his case manager.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [35, 'years'], 'creatinine': [5.0, 'mg/dL'], 'sex': 'Male'}",14.59083,13.86129,15.32037,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 35 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 5.0 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (5.0/0.9)**-1.2 * 0.9938**35 * 1.0 = 14.59083.
Hence, the GFR value is 14.59083 ml/min/1.73 m²."
167,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-9449,Extracted,"A 70-year-old man presents to the Emergency Department after 3 days of shortness of breath, orthopnea, and lower limb edema. His personal history is significant for a myocardial infarction 6 years ago that required revascularization and hypertension. His medication consists of simvastatin and lisinopril.  In the ED, he has a blood pressure of 100/80 mm Hg, a pulse of 88/min, a respiratory rate of 28/min, and a temperature of 36.5°C (97.7°F). On physical examination, he has jugular vein distention, displaced point of maximal impulse (PMI), an S4-gallop, a holosystolic murmur, and 2+ pitting edema up to the mid calf.  He is started on furosemide, carvedilol, and oxygen therapy. After 6-hours of continued therapy, his blood pressure remains low, and his serum creatinine is found to be 1.9 mg/dL.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [70, 'years'], 'creatinine': [1.9, 'mg/dL'], 'sex': 'Male'}",37.48042,35.6064,39.35444,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 70 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.9 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.9/0.9)**-1.2 * 0.9938**70 * 1.0 = 37.48042.
Hence, the GFR value is 37.48042 ml/min/1.73 m²."
168,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7768448-1,Extracted,"A 72-year-old man was referred to our hospital from a suburban nephrology center because of prolonged fever and persistent enterococcal bacteremia. The patient was suffering from chronic renal failure, undergoing regular hemodialysis sessions three times per week through a permanent right internal jugular venous catheter. He was a chronic smoker with chronic obstructive pulmonary disease, and had been operated on for lung decortication because of amiantosis 18 years prior to admission (since then he was under methylprednisolone therapy). Furthermore, he had high blood pressure and single vessel coronary artery disease for which he was treated with successful angioplasty the previous year, and was compliant to antihypertension and anticoagulant therapy.
The patient had sought medical consultation 35 days before in the nephrology center where he was having hemodialysis, because he had high fever (up to 39 °C). Blood cultures were drawn and were processed in the nephrology center’s laboratory, resulting in the isolation of Enterococcus spp. from two culture vials with a susceptibility profile that included vancomycin: sensitive (MIC: 4 μg/mL), ampicillin: sensitive, daptomycin: sensitive, dalfopristin/quinopristin: resistant, gentamicin synergy: sensitive, ciprofloxacin: sensitive, and linezolid: sensitive. The patient received daptomycin and ciprofloxacin for 21 days. After the completion of antibiotic therapy he presented again with fever at the nephrology center, new blood cultures were drawn, and he started again receiving daptomycin. Two days later, during hemodialysis, he suffered from chills, and after completion of the session developed fever. In the next hemodialysis session, the same symptoms occurred (chills and fever), and gentamicin was added to his therapy. The nephrology clinic’s laboratory in the meantime isolated again Enterococcus spp. from the blood culture. He was treated with antibiotic lock therapy of the central venous catheter with gentamicin, and was referred to University General Hospital Attikon for further evaluation and treatment.
On the day of admission to our hospital, the following laboratory results were obtained: hemoglobin 10.4 g/dL, leukocytes 13,590/μL (Neutrophils 87%), platelets 295,000/μL, creatinine 3.8 mg/dL, C-reactive protein 61 mg/L, and procalcitonine 2.7 ng/mL. The physical examination was normal except for a holosystolic mitral valve murmur upon cardiac auscultation. Initially he continued the therapeutic regimen he had started at the nephrology center (antibiotics only on the haemodialysis days of Tuesday, Thursday and Saturday). On Tuesday and Thursday, he was receiving daptomycin 300 mg IV, and on Saturday the dose was 450 mg. On all haemodialysis days he was receiving gentamicin 240 mg IV before the haemodialysis session and gentamicin 80 mg IV after each session. On the first day at the hospital six blood cultures were drawn and two more on the following day, and all were incubated with the standard BACTEC system (Becton Dickinson, Sparks, NV, USA). On the second day of his hospital stay, five of the blood cultures were positive with Gram-positive coccus forming chains. On the third day, two more cultures were positive with the same coccus. The central venous catheter was removed on the third day of stay. The isolate from all seven blood culture bottles was identified as E. casseliflavus. The colonies in standard Columbia agar exhibited distinct yellow pigment, the coccus was positive for motility [], and the biochemical profile examined by Phoenix (Becton Dickinson, Sparks, NY, USA) and Vitek 2 (BioMerieux, Marcy-l’Etoile, France) matched E. casseliflavus. The antibiotic susceptibility phenotype included vancomycin: sensitive (MIC: 4 μg/mL), ampicillin: sensitive (MIC: 1 μg/mL), daptomycin: sensitive (MIC: 2 μg/mL), dalfopristin/quinopristin: resistant (MIC: 8 μg/mL), gentamicin synergy: sensitive (MIC: 16 μg/mL), ciprofloxacin: sensitive (MIC: 1 μg/mL), and linezolid: sensitive (MIC: 4 μg/mL). The MICs were determined by Vitek 2, Phoenix and E-tests while following the EUCAST breakpoints for all antibiotics (with the sole exception of the daptomycin MIC which was compared to the CLSI breakpoint). Furthermore, a multiplex PCR detecting vanA, vanB, vanC, vanD, vanE and VanG genes was performed and was positive for vanC, further corroborating the biochemical diagnosis []. The central venous catheter was cultured but there was no growth of any pathogen. The urine cultures were also negative.
The transesophageal echocardiogram was negative for vegetations and the fundoscopy was negative for Roth spots in the retina. A colonoscopy revealed numerous diverticula mainly in the sigmoid colon. CT scans of the head, thorax and abdomen were performed revealing a thrombus in the anterior vena cava near the distal end of the central venous catheter, and a pulmonary embolus at the lower lobe of the right lung involving the respective lobar artery and segmental branches.
After the fourth day in our hospital the patient’s antibiotic therapy was changed to a combination of ampicillin 2gr IV every 8 h and ceftriaxone 2gr IV every 12 h, which he received for a total of 6 weeks. He also received anticoagulant therapy for the pulmonary embolus. He was released from the hospital after a total stay of seven weeks, afebrile, with negative blood cultures.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [72, 'years'], 'creatinine': [3.8, 'mg/dL'], 'sex': 'Male'}",16.11263,15.307,16.91826,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 72 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.8 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.8/0.9)**-1.2 * 0.9938**72 * 1.0 = 16.11263.
Hence, the GFR value is 16.11263 ml/min/1.73 m²."
169,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5521117-1,Extracted,"A 54-year-old Sri Lankan woman who had recently been diagnosed with rheumatoid arthritis presented to our hospital with worsening bilatateral leg swelling and facial puffiness of 1 month’s duration, accompanied by oliguria. She had no frothy urine or hematuria. She did not have exertional breathlessness or orthopnea, and she had no history suggestive of a cardiac or hepatic cause of edema. She was not diabetic or hypertensive. Her rheumatoid arthritis had been diagnosed 8 months earlier, when she presented with bilateral symmetrical polyarthritis involving the small joints of her hands with significant morning stiffness of 2 hours’ duration. Her rheumatoid factor was positive at a high titer. She was commenced on methotrexate 10 mg weekly and infrequent nonsteroidal anti-inflammatory drugs, with good symptom control achieved.
Her physical examination revealed that she had bilateral pitting leg edema and periorbital edema. She was not pale or icteric. No malar rash, vasculitic rash, or distal gangrene was seen. She had evidence of mild synovitis of the small joints of the hands bilaterally with no deformities. No generalized lymphadenopathy or hepatosplenomegaly was noted. Her pulse rate was 90 beats per minute; her blood pressure was 170/100 mmHg; and her jugular venous pressure was elevated to 7 cm with an undisplaced cardiac apex and normal heart sounds. A fundus examination did not reveal papilledema. Her lungs were clear with equal breath sounds bilaterally. The results of the rest of the examination were normal. Her laboratory investigation results are provided in Table .
A diagnosis of crescentic glomerular nephritis was made. The patient was started on atorvastatin, enalapril, and diuretics. Intravenous methylprednisolone 1 g was given for 3 consecutive days, followed by 1 mg/kg oral prednisolone. She was started on intravenous cyclophosphamide 500 mg every 2 weeks for a total of six doses. She gradually had increasing urine output and was symptomatically better, with improving renal function. Her serum creatinine level was 110 μmol/L at her last clinic visit after 3 months of treatment.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [54, 'years'], 'creatinine': [110.0, 'µmol/L'], 'sex': 'Female'}",51.51665,48.94082,54.09248,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 54 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 110.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 110.0 µmol. To convert 110.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 110.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00011 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00011 mol Serum Creatinine * 113.12 g/mol = 0.01244 g Serum Creatinine. To convert 0.01244 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01244 g Serum Creatinine * 1000.0 mg/g = 12.44 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 12.44 mg Serum Creatinine/10.0 dL = 1.244 mg Serum Creatinine/dL. The concentration value of 110.0 µmol Serum Creatinine/L converts to 1.244 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.244/0.7)**-1.2 * 0.9938**54 * 1.012 = 51.51665.
Hence, the GFR value is 51.51665 ml/min/1.73 m²."
170,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4939672-1,Extracted,"An 82-year-old male patient with a diagnosis of metastatic gastric cancer presented to the emergency department after an episode of confusion and fall. Until 2 weeks prior to this event, the patient was functionally independent with a performance status of ECOG 1, but recently displayed increasing confusion, unsteady balance, numerous falls, and sometimes difficulty with speech. There was no significant tobacco, alcohol, or recreational drug use history. His past medical history was significant for peripheral neuropathy affecting his feet, hypertension, and hypothyroidism. He was diagnosed with gastric cancer 11 months prior by stomach wall biopsy demonstrating poorly differentiated adenocarcinoma with signet ring cells. Staging CT scans showed metastases to the omentum, retroperitoneum, diaphragmatic lymph nodes, and malignant ascites. He initially began standard chemotherapy with carboplatin and paclitaxel, with a partial response which lasted for several months. Six months later, he was switched to capecitabine due to disease progression, which was poorly tolerated and discontinued after 1 cycle. Subsequently he received ramucirumab single-agent therapy at the dose of 8 mg/kg given intravenously. He received four doses, each spaced 2 weeks apart, with the last dose 2 weeks prior to presentation.
His physical exam was significant for orientation to person only and ataxia on the finger-nose-finger test. Initial laboratory results were within normal limits except for creatinine 1.6 mg/dl, BUN 30 mg/dl, and TSH 14.24 mIU/l with normal T4 1.2 ng/dl. Cardiac telemetry did not show any evidence of arrhythmia. CT of the head did not show any acute changes to explain the patient's symptoms. Carotid Doppler ultrasound was negative for significant stenosis. Transthoracic and transesophageal echocardiogram was negative for thrombus or severe atrial dilation; it did note a patent foramen ovale with a very small amount of right-to-left shunting. MRI with gadolinium of the brain revealed multifocal mildly increased diffusion signals with a corresponding increased T2 and FLAIR signal, likely subacute, involving the bilateral cerebellar hemispheres, bilateral occipital lobes, and bilateral parietal cortex (fig. ), confirming multifocal ischemic stroke, while in the hospital the patient underwent physical and occupational therapy and did achieve improvement in his symptoms. However, due to his poor prognosis and overall decline in functional status it was decided by the patient and his family to be discharged home with hospice.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [82, 'years'], 'creatinine': [1.6, 'mg/dL'], 'sex': 'Male'}",42.75164,40.61406,44.88922,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 82 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.6 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.6/0.9)**-1.2 * 0.9938**82 * 1.0 = 42.75164.
Hence, the GFR value is 42.75164 ml/min/1.73 m²."
171,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6246990-1,Extracted,"We present the case of a 39 years old female patient, hospitalized in the Dermatology clinic of Emergency County Hospital in september 2014, for ulcerative lesions on the left hallux and the second and third left toes, associated with pain and difficulties in walking. Moreover, the patient presented inflammatory pain of the radio-carpal joint, asthenia, dyspneea and myalgia, especially in upper limbs. The patient was diagnosed in 2007 with overlap syndrome-systemic lupus erythematosus, antiphospholipid syndrome, systemic sclerosis-diffuse form and dermatomyositis, based on laboratory findings-presence of antinuclear antibodies-ANA, anti-dsDNA antibodies, anti-Scl70 and anti-U1-RNP antibodies, increased levels of creatine kinase-CK, positive biopsy for systemic sclerosis and dermatomyositis. The histopathological exam, for skin biopsy, revealed atrophic epidermis with hyperpigmentation of the basal layer, with straight lines of the basal membrane and papilloma areas; underlying dense collagen sclerosis, with hyaline areas, partial atrophy of skin and dermal appendages, and for muscle biopsy: degeneration of skeletal muscle fibers and interstitial inflammatory infiltrate.
From the personal history, we note multiple spontaneous abortion in the first 3-4 weeks of pregnancy. The pathologic history reveals chronic kidney disease, an ischemic stroke in 2011 (objectivized by computed tomography and magnetic resonance), hypertension, coronary cardiac disease and cardiac insufficiency treated and monitored periodically by the cardiologist.
On admission, the clinical exam revealed a patient with a facies with lack of frontal folds, pinched nose, retraction of the lips, with limited oral aperture, Cushing conformation, telangiectasia on the cheeks and livedo reticularis, with poikilodermic aspect (), pale chest with sharply demarcated and erythematous papulo-squamous lesions (Fig.1), left hallux ulceration, of 1.5/1 cm, with a haematic scall, ulcerations of 0.5cm on the second and third toe, dry eyes, diffuse alopecia, muscular hypotonia and hypokinesia, muscle atrophy of the shoulder and pelvic girdle. We found inflammatory signs in radio-carpal, metacarpophalangeal (MCP) joints and proximal interphalangeal (PIP) joints. The pulmonary and cardiac clinical exam showed no pathological findings. The muscular testing, using MMT-8 scale, that included evaluation of axial, bilateral proximal and distal muscles for upper and lower limbs, showed a score of 91, of 150 maximum.
The biological analyses show mild normochromic, normocytic anemia, inflammatory syndrome (ESR 38/60mm and CRP 6mg/dl), creatinine of 1.92mg/dl, urea 69mg/dl, normal aminotransferases, CK 250U/l; urinalysis: presence of albumin, a few leucocytes and red blood cells; proteinuria/24 hours-650mg/24h. The immunological tests show a low complement: C4 8.3mg/dl and C3 80mg/dl; anti-dsDNA antibodies 425UI/ml.
The chest X-ray shows interstitial pulmonary fibrosis, mostly in medium and inferior areas. The cardiac ultrasonography, performed with 5 days before the admission in our department, showed a mild systolic and diastolic dysfunction, pulmonary hypertension and small pericardial effusion.
In order to assess the peripheric microcirculation, we performed nailfold capillaroscopy, that showed avascular areas (), dilated capillaries, frequent haemorrhages (; ), bushy capillaries, multiple capillaries with increased tortuosity () and giant capillaries (), findings specific to a late scleroderma pattern.
The treatment included intravenous administration of synthetic analogue of prostacyclin PGI2-Iloprost for 3 days and local measures, like antiseptic solutions and epithelization agents.
The patient also continued the chronic treatment prescribed by the rheumatologist: corticotherapy-Methylprednisolone 32mg/day, immunosuppressive drugs-Azathioprine 100mg/day, peripheric vasodilators-Pentoxiretard 800mg/day, and cardiologist-antihypertensive drugs-Atacand 32mg/day, Norvasc 5mg/day, platelets antiaggregant-Aspenter 75mg/say and antithrombotic-Vessel due F 2 capsules/day.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [39, 'years'], 'creatinine': [1.92, 'mg/dL'], 'sex': 'Female'}",33.59586,31.91607,35.27565,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 39 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.92 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.92/0.7)**-1.2 * 0.9938**39 * 1.012 = 33.59586.
Hence, the GFR value is 33.59586 ml/min/1.73 m²."
172,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2779295-1,Extracted,"A 7-yr-old boy presented with left knee joint pain, abdominal pain, and purpuric rash on the lower extremities. He was managed with oral prednisolone and supportive care under the impression of HSP at the private clinic for three days. However above symptoms did not improve. Additionally abdominal distension, diarrhea, hematochezia, and melena were developed, so he was transferred to our hospital. On admission, laboratory investigations revealed hemoglobin 12.5 g/dL, white blood cell count 19,200/µL, platelet count 388,000/µL, C-reactive protein 0.69 mg/dL, blood urea nitrogen 11.3 mg/dL, and serum creatinine 0.7 mg/dL. Serum electrolyte, liver enzymes, blood coagulation tests, antinuclear antibody, rheumatoid factor, antistreptolysin O, and urinalysis were normal. Abdominal radiography showed air-fluid levels and abdominal ultrasonography was normal. The patient was treated with intravenous hydration and 1 mg/kg per day methylprednisone. At follow up, the clinical findings such as arthralgia, abdominal pain, bloody stool, and purpuric rash improved gradually over four days. On the 5th hospital day he became pyrexial and developed right iliac fossa pain and tenderness with guarding. White blood cell count was 21,900/µL and C-reactive protein was 8.58 mg/dL. Ultrasonography showed distended appendix surrounded by hyperechoic inflamed fat. On abdominal exploration there was an appendiceal perforation in the appendiceal tip, and pus was present in the periappendiceal area. Microscopically the appendix showed hemorrhagic ulceration of mucosa, gangrenous necrosis throughout wall, and the mucosa showed abundant infiltration of inflammatory cells and eosinophilic fibrinoid materials. Some of the small blood vessels in the submucosa showed fibrinoid necrosis with neutrophilic infiltrations (). Following the operation the colicky abdominal pain, fever, and leukocytosis were resolved, but two days after operation he developed scalp edema, scrotal swelling, and purpuric rash on buttock. Two weeks after operation he was discharged without any clinical symptoms, however microscopic hematuria (5-9 RBC/HPF) has persisted subsequent two months. Six months after operation his recovery was complete.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [7, 'years'], 'creatinine': [0.7, 'mg/dL'], 'sex': 'Male'}",135.95065,129.15312,142.74818,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 7 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.7 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.7/0.7)**-0.302 * 0.9938**7 * 1.0 = 135.95065.
Hence, the GFR value is 135.95065 ml/min/1.73 m²."
173,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4150947-1,Extracted,"A 54-year-old female patient, with a history of stage IVB squamous cell carcinoma of cervix, was treated by concurrent chemoradiotherapy 6 years ago. Subsequently, 6 months later, bilateral hydroureteronephrosis was found by the follow-up computerized tomography (CT), which showed the stricture segment included the middle third and lower third of both ureters. The level of serum creatinine increased from 1.0 to 2.7 mg/dL. She underwent bilateral insertion of double-J catheter to facilitate the upper urinary tract drainage. Unfortunately, the follow-up CT showed persistent bilateral hydronephrosis (left side worse than right side). Additionally, the renal function deteriorated and a gradual change of serum creatinine from 2.4 to 6.5 mg/dL was found. She underwent right insertion of a parallel second double-J catheter and left percutaneous nephrostomy (Figure ). The level of serum creatinine decreased to 2.6 mg/dL. It was possible due to the complication of retroperitoneal fibrosis and bilateral ureteral strictures following previous radiation therapy. Afterward, she had periodic change of the right side double-J stents and left percutaneous nephrostomy.
She presented with deterioration of creatinine level from 2.6 to 4.0 mg/dL and repeated catheter-related infection in recent 1 year and transferred to our hospital. Consideration of the stricture length of bilateral ureters, we planned the surgical treatment of segmental resection of bilateral ureteral stricture accompanied with bilateral Boari flap and ureteroneocystostomy.
We made a lower midline transperitoneal incision. After exposing bilateral ureters and bladder, we found a contracted bladder, generalized fibrotic change in the pelvis and bilateral long-segment ureteral strictures including middle third and lower third of ureters. We isolated the both ureters by sharp and blunt dissection and found the both dilated ureters above the junction of middle third and upper third of ureters. It was not available for the procedure of bilateral Boari flap because that the bladder was contracted and the length of bilaterally healthy ureters was not long enough, even though the bilateral upper ureters and bilateral kidneys had been mobilized.
We transected the bilateral ureters at the middle third of ureters, and placed a 3–0 synthetic absorbable stay suture in the proximal cut end of the bilateral ureters and ligated the distal stump of the bilateral ureters. After mobilizing the bladder, a psoas hitch onto the left psoas tendon was done with three interrupted sutures. We designed a Boari flap with the width 2.5 cm at the tip and 5 cm wide at the base. The right ureter was brought to the left side through the retrocolon channel. The bilateral ureters were reconstructed into a common channel, then directly anastomosed the common channel of both ureters to the edge of the Boari flap (Figure ). Prior to closure, we inserted two double-J catheters into both ureters. We placed two closed-suction drains at the site of perivesical region and Cul-de-sac, and closed the surgical wound.
After operation, she recovered uneventfully and was discharged on postoperative day 7. We removed the two double-J catheters on the fourteenth postoperative day. 18 months latter, a follow-up sonography showed mild hydronephrosis on right kidney and the level of serum creatinine was 2.4 mg/dL (Figure ).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [54, 'years'], 'creatinine': [2.4, 'mg/dL']}",23.41416,22.24345,24.58487,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 54 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.4 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.4/0.7)**-1.2 * 0.9938**54 * 1.012 = 23.41416.
Hence, the GFR value is 23.41416 ml/min/1.73 m²."
174,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3806345-3,Extracted,"A 44-year-old male who had been on hemodialysis for 2 years underwent a living-relative transplant with his brother as the donor. His baseline renal disease was unknown. Induction therapy consisted of thymoglobulin and maintenance immunosuppression corticosteroids, tacrolimus at 0.15 mg/kg to achieve a trough level of 6–10 ng/dL, and MPA at 1440 mg/day; prophylaxis against infection consisted of ganciclovir and trimethoprim/sulfamethoxazole. At the time of discharge on POD 4, his creatinine was 125.53 μmol/L (1.42 mg/dL). On POD 8, a biopsy performed because of a creatinine increase showed Banff Ia cellular rejection, which was treated successfully with three pulses of methylprednisolone. On POD 13, a control biopsy showed mesangiolysis and double contours (). C4d staining was negative, there was no sign of glomerulitis or capillaritis, and detection of anti-HLA antibodies by Luminex was negative. Associated causes were ruled out, and it was suspected that the TMA was drug-related. At the time of the TMA diagnosis, no DSA was detected, and laboratory test values were as follows: creatinine 178.57 μmol/L (2.02 mg/dL), platelet count 218000/mm3, tacrolimus trough level 6.9 ng/dL hemoglobin 88 g/L, LDH 230 IU/L, total bilirubin 8.20 μmol/L, and haptoglobin 1.06 g/L, and no schistocytes were found. Tacrolimus treatment was suspended, and belatacept was initiated at 10 mg/kg on days 1, 5, 14, 28, 60, and 90; maintenance treatment was 5 mg/kg once a month for 1 year. The creatinine level decreased. On POD 31, a control biopsy showed Banff IIa cellular rejection that was treated with ATG. Administration of belatacept continued as planned. On POD 40, a biopsy showed no sign of rejection or TMA; his creatinine level was 122.88 μmol/L (1.39 mg/dL).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [44, 'years'], 'creatinine': [1.39, 'mg/dL']}",64.10874,60.9033,67.31418,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 44 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.39 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.39/0.9)**-1.2 * 0.9938**44 * 1.0 = 64.10874.
Hence, the GFR value is 64.10874 ml/min/1.73 m²."
175,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5401727-1,Extracted,"A 39-year-old male was admitted for work-up of occult infection due to recurrent fevers, nausea, nonbilious emesis, and occipital headache for three weeks. Prior history was notable for traumatic brain injury in 1995 complicated by subarachnoid hemorrhage with subsequent placement of a ventriculoperitoneal (VP) shunt.
At presentation, the patient was tachycardic (HR: 130 per minute) and febrile (103 F) with urticarial plaques involving trunk, arms, and legs. Initial laboratory studies were notable for serum creatinine of 2.0 mg/dL, hemoglobin of 9.7 g/dL, C3 of 45 mg/dL (normal: 98–162), C4 of 9 mg/dL (normal: 16–43), and rheumatoid factor > 100 international units/mL (normal: <15). Urine microscopy did not reveal dysmorphic red cells or cellular casts. Cerebrospinal fluid showed elevated protein, decreased glucose, and gram stain with moderate leukocytosis but no organisms. Brain computed tomography indicated stable findings of his prior surgeries. The patient was given intravenous vancomycin. During the admission, a 24-hour urine collection revealed 1.4 grams of protein. Blood and cerebrospinal cultures remained negative for growth. However, serum creatinine only improved to 1.6 mg/dL (baseline: 0.98–1.1 mg/dL), so a renal biopsy was performed. Following the biopsy, the patient's renal insufficiency began improving, and this recovery was thought to be secondary to successful treatment of the infection. Vancomycin was discontinued at this time in light of negative blood cultures and the consultant neurosurgeon did not feel shunt removal was necessary at that time.
With regard to the renal biopsy, the glomeruli showed mesangial hypercellularity and segmental endocapillary proliferation with a single glomerular crescent containing hyaline droplets. Another glomerulus showed a sclerotic segment. There was no evidence of tubular cell vacuoles. The glomerular basement membranes were not thickened. Immunofluorescence was done with fluorochrome conjugated antibodies against human IgG, IgA, IgM, C3, C1q, fibrin, kappa light chain, and lambda light chain, using appropriate controls. A total of four glomeruli were identified. The glomeruli showed focal segmental 2+ IgM and 3+ C3 mesangial staining in three of the glomeruli. The glomeruli were negative for the other stains. The tubular basement membranes were negative for all of the aforementioned stains.
Electron microscopy showed that the foot processes of the podocytes were subtotally effaced. Rare, small, subendothelial osmiophilic electron-dense deposits were identified. Subepithelial deposits were not present. Spikes or duplicated basement membranes were not identified. Segmentally, there were increased numbers of endothelial and mononuclear cells. The mesangial matrix was mildly expanded and there was slightly increased mesangial cellularity with a few osmiophilic electron-dense deposits identified in the mesangium. These electron-dense deposits were not identified in the tubular basement membranes (see Figures –). The final biopsy report's diagnosis was acute interstitial nephritis with tubular epithelial necrosis and segmental endocapillary proliferation with increased mesangial hypercellularity.
Two months after the renal biopsy, the patient was readmitted for recurrent symptoms similar to his initial presentation. Vital signs and exam were unremarkable. Laboratory data on readmission were notable for serum creatinine of 1.7 mg/dL, hemoglobin of 8.8 g/dL, C3 of 63 mg/dL, C4 of 15 mg/dL, and rheumatoid factor > 100 international units/mL. Cranial imaging did not show acute findings. On subsequent hospital day, the patient had repeat cerebrospinal fluid studies which showed the presence of Gram-positive organisms. He was restarted on antibiotics and the VP shunt was removed emergently. Cerebrospinal fluid culture resulted in the growth of Propionibacterium acnes and shunt hardware culture grew coagulase-negative Staphylococcus. As per infectious disease consultant's recommendations, the patient was treated with two weeks of intravenous vancomycin and ampicillin. Repeat blood cultures were negative and no further antimicrobial treatment was required.
At 1-month follow-up in the clinic, the patient had persistent skin lesions; he was otherwise asymptomatic with no headaches, dizziness, nausea, vomiting, fevers, or chills. Microscopic hematuria had completely resolved, C3 had increased to near normal levels, and serum creatinine had improved but not to baseline. Mild proteinuria persisted. Rheumatoid factor was normal. Serum creatinine was 1.2 and hemoglobin was 11.2 g/dL.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [39, 'years'], 'creatinine': [1.2, 'mg/dL']}",78.89011,74.9456,82.83462,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 39 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.2 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.2/0.9)**-1.2 * 0.9938**39 * 1.0 = 78.89011.
Hence, the GFR value is 78.89011 ml/min/1.73 m²."
176,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7505622-1,Extracted,"A 79-year-old African American male with a past medical history of hypertension presented with a static slurred speech that manifested with sudden onset two days prior to his hospital visit in late January of 2020. Following the slurred speech the next day he had chills, however, did not record his body temperature at home. He initially considered his symptoms as a minor flu, however, later decided to seek medical care due to nonresolving speech impairment. On presentation, he was febrile with an oral temperature of 100oF. His blood pressure was 124/74 mmHg. He endorsed compliance of his antihypertensive medication. He did not give a history of tobacco abuse, shortness of breath, cough, or intermittent palpitation. Physical examination showed an irregular pulse at the rate of 96 beats/min, respiratory rate at 18 breaths/min, and fine crackles in bilateral lower lungs on auscultation. His blood oxygen saturation level was 95%. Neurological examination was unremarkable except mild dysarthria. From his dysarthria assessment it was inferred that he had a low pitched phonation, impaired prosody for the sentence “ I am hungry”, lack of hypo- or hyper-nasality, decreased rate of repetitions (repeated the word “buttercup” only four times in five seconds), impaired articulation of the word “PresbyEpiscopal” and letters “P, B, F”, but with normal articulation of the words “la-la-la”. The initial National Institute of Health Stroke Scale (NIHSS) was one.
The real-time reverse transcription polymerase chain reaction (RT-PCR) analysis of SARS-CoV-2 infection tested positive from the nasopharyngeal swab. Pertinent initial laboratory findings showed a white blood cell count of 9.3 (4.5-11 K/μL), lymphocyte count of 0.6 (1.2-3.4 K/μL), and giant platelet morphology with normal count. He had mild elevated creatinine 2.4 (0.7-1.5 mg/dL) and procalcitonin levels 0.19 (0.02-0.10 ng/mL). His interleukin-6 92 (0-6.3 pg/mL), ferritin 505 (15-150 ng/L), and D-dimer 1201 (0-230 ng/mL) levels were abnormal. His cardiac troponin levels were normal, but the transaminase levels were elevated. The electrocardiogram showed an AF with a rapid ventricular response (Figure ).
The CHA2DS2-VASc score was four (calculated from his risk factors: age, hypertension, and stroke). A pulmonary CT scan showed bilateral peripheral ground glass opacities without pulmonary embolism (Figure ), and a brain MRI showed a punctate left frontal lobe infarction (Figure ).
A magnetic resonance angiogram of the head and neck showed no significant stenosis and transthoracic echocardiogram showed normal systolic function, moderate left atrial enlargement without thrombus or atrial septal defect (Figure ).
The patient was treated with IV unfractionized heparin infusion at the rate of 15 units/kg/hour and metoprolol tartrate 25 mg two times a day. The COVID-19-associated pneumonia was treated with oral azithromycin and hydroxychloroquine and was closely monitored in the ICU setting. Still, after a week, the patient got an increased respiratory distress as a consequence of a cytokine storm and required mechanical ventilation. The laboratory findings during this time showed highly abnormal interleukin-6 330 (0-6.3 pg/mL) level. The patient was treated with IV steroids and tocilizumab, but his condition further deteriorated, complicated by a multi-system organ failure, including septic shock, acute respiratory distress syndrome, acute myocardial injury (NT-proBNP 936 pg/mL), acute kidney injury, and dyselectrolemia. Despite aggressive supportive measures that included hemodialysis, the patient died two and half weeks after his admission.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [79, 'years'], 'creatinine': [2.4, 'mg/dL'], 'sex': 'Male'}",26.77603,25.43723,28.11483,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 79 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.4 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.4/0.9)**-1.2 * 0.9938**79 * 1.0 = 26.77603.
Hence, the GFR value is 26.77603 ml/min/1.73 m²."
177,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4157190-1,Extracted,"A three and half year old male child was referred to our department for DMSA scintigraphy for evaluation of renal scarring. Renal function tests (RFTs) were within normal limits (Blood Urea Nitrogen: 12 mg/dl, Serum Creatinine: 0.4 mg/dl). Voiding cystourethrogram (VCUG) and renal ultrasonography (USG KUB) were also normal except for mild left hydronephrosis. 60 MBq of Tc-99m DMSA was administered IV after adequate hydration and the scintigraphy was performed 3 hours later. The anterior and posterior images showed no definite delineation of renal cortical outline with high background tracer activity and hence pinhole images could not be acquired []. The child had no recent history of UTI to suggest any recent acute renal insult. A detailed enquiry then revealed that the child is a suspected case of Lowe's syndrome and had bilateral cataracts operated in his first year of age, history of global developmental delay and abnormal behavioral pattern. Biochemical analysis revealed hyperchloremic normal anion gap metabolic acidosis (NAGMA) and alkaline urine with associated hyperphosphaturia, hypercalciuria, nonselective aminoaciduria, and glycosuria indicative of Fanconi type of proximal renal tubular acidosis. Suspecting the proximal tubular disorder as the cause of the discrepancy, an EC renal dynamic study was performed. Sequential dynamic images were acquired in posterior view after intravenous administration of 65 MBq of Tc-99m EC. Dynamic imaging showed adequate perfusion and renal cortical tracer uptake of both kidneys along with adequate background tracer clearance indicating adequate renal function []. This case depicts the key role of proximal renal tubule membrane integrity in the uptake of DMSA.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [5, 'years'], 'creatinine': [0.4, 'mg/dL'], 'sex': 'Male'}",162.99745,154.84758,171.14732,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 5 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.4 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.4/0.7)**-0.302 * 0.9938**5 * 1.0 = 162.99745.
Hence, the GFR value is 162.99745 ml/min/1.73 m²."
178,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2576186-1,Extracted,"A 61-year-old Caucasian male was brought to the ER with an initial diagnosis of acute ST-elevation myocardial infraction by the emergency medical services (EMS). On further questioning, the patient denied history of chest pain, but complained of sudden onset generalized weakness and numbness. The patient had developed weakness of his legs and difficulty in passing urine one hour before arriving in the ER. Patient denied recent infections, headaches, nausea, vomiting, trauma or a similar neurological episode before. The patient had end stage renal failure due to poorly controlled diabetes and hypertensive heart disease for many years. He had been on routine hemodialysis thrice a week with each dialyzing session lasting for four hours for the past three years. The last dialysis was done the day prior to presentation. His medications included metoprolol 100 mg twice a day, simvastatin 40 mg daily, aspirin 81 mg daily and 70/30 insulin 30 units subcutaneously twice a day.
On examination, the patient's had a temperature of 98.2°F, respiratory rate of 20 per minute, heart rate of 90 beats per minute and a blood pressure of 150/90 mmHg. Examination of the cardiovascular system showed normal heart sounds with no murmurs. The respiratory system and gastrointestinal systems were normal. Central nervous system examination revealed an alert, awake and oriented patient with normal cranial nerve function. He had symmetrical and equal weakness of the lower limbs more than in the upper limbs. The muscle tone and the reflexes were also weaker in the lower limbs compared to the upper limbs. There was no sensory deficit. In the ER, blood tests including chemistry and complete blood count were sent. A bed side EKG and a chest X-ray were performed.
Based on the initial two EKG strips done by the EMS and the subsequent two EKGs done in the ER (Figure: , , , ) and the clinical back ground of end stage renal failure the diagnosis of hyperkalaemic flaccid paralysis was made. The patient was given 10 ml of 10% calcium gluconate intravenously followed by 10 units of regular insulin, and 50 ml of 50% dextrose. The patient also received 30 ml of sodium polystyrene sulfonate (Kayexalate) orally that was repeated every hour till the patient developed a diarrhea.
Subsequently the patient's blood results showed potassium of 6.2 mEq/L, blood urea nitrogen (BUN) of 152 mg/dl and creatinine level of 8.50 mg/dl. Patient was rushed for emergency dialysis. After three hours of dialysis, the patient recovered completely from his weakness and was able to walk. His post dialysis potassium level was 4.0 mEq/L, BUN was 47 mg/dl and creatinine was 3.57 mg/dl. The EKG had reversed back to sinus rhythm, heart rate of 88 per minute, normal T waves and ST segment (Figure ).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [61, 'years'], 'creatinine': [8.5, 'mg/dL'], 'sex': 'Male'}",6.56622,6.23791,6.89453,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 61 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 8.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (8.5/0.9)**-1.2 * 0.9938**61 * 1.0 = 6.56622.
Hence, the GFR value is 6.56622 ml/min/1.73 m²."
179,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8099007-1,Extracted,"A 70-year-old male with a history of atherosclerosis, coronary artery disease, congestive heart failure, atrial fibrillation on anticoagulation, femoral artery aneurysm repair, and cholecystectomy 20 years ago, presented to the emergency department with one week of abdominal pain, nausea, and vomiting. On presentation, he was noted to be hemodynamically stable, jaundiced, and epigastric abdominal tenderness. Laboratory studies revealed a hemoglobin of 10.6 g/dL, creatinine of 3.51 mg/dL (patient baseline of 1.0 mg/dL), total bilirubin 9.5 mg/dL, alkaline phosphatase 953 units/L, aspartate aminotransferase (AST) 66 units/L, alanine aminotransferase (ALT) 58 units/L, and lipase 1529 units/L (upper limit of normal is 60 units/L).
A CT abdomen and pelvis was performed without IV contrast due to acute kidney injury (Figure ). This revealed a large heterogeneous and hyperattenuating structure at the level of the head of the pancreas close to the superior mesenteric artery (SMA) with associated mass effect on the duodenum and obstruction of the common bile duct. Marked dilatation of the intra and extra-hepatic biliary tree was also noted. These findings were not seen on CT abdomen with contrast four months prior.
Based on this presentation and findings, the patient was admitted to the hospital. Given that the large heterogeneous structure seen on the non-contrast CT was close to the SMA and the head of the pancreas, the differential diagnosis included ruptured SMA aneurysm, SMA pseudoaneurysm, hemorrhagic pancreatic mass, and pancreatic cancer. The modality and urgency of treatment of each of these diagnoses vary greatly. Despite the patient’s acute kidney injury, a CT angiography of the abdomen was performed (Figures , ) as a large SMA aneurysm or pseudoaneurysm would potentially necessitate urgent interventions by either vascular surgery or interventional radiology.
The CT angiography of the abdomen revealed fusiform aneurysmal degeneration of the proximal abdominal aorta. There was an overall beaded appearance, irregular narrowing, and mural thickening involving multiple visceral media and large size arteries, including the celiac artery, splenic artery, superior mesenteric artery, gastroduodenal artery, and right renal artery. A replaced right hepatic artery arising off the SMA extended into the previously described large heterogeneous mass, which appeared to be a hematoma 9.1 x 6.8 x 8.4 cm in size, centered posterior to the head of the pancreas. There were multiple areas of contained active bleeding and pseudoaneurysm formation within this hematoma marginating from branches of the replaced right hepatic artery (Figures , ). Given these concerning findings, vascular surgery and interventional radiology were urgently consulted, but the degree of involvement of multiple vessels precluded any interventions. The patient was discharged with home hospice and passed away two weeks later.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [70, 'years'], 'creatinine': [3.51, 'mg/dL']}",17.94487,17.04763,18.84211,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 70 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.51 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.51/0.9)**-1.2 * 0.9938**70 * 1.0 = 17.94487.
Hence, the GFR value is 17.94487 ml/min/1.73 m²."
180,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8651372-1,Extracted,"The patient is a 64-year-old male with a medical history of hypertension, chronic kidney disease, atrial fibrillation, heart failure with reduced ejection fraction (nonischemic cardiomyopathy) with left ventricular ejection fraction of 35%, and ventricular tachycardia with ICD in place on amiodarone and mexiletine, who presented after experiencing a shock by his ICD twice on the day of admission. The patient complained of palpitations on the day of admission and denied having chest pain, shortness of breath, cough, or loss of consciousness. On physical exam, his blood pressure was 109/71 mmHg, heart rate was 100 beats per minute, respiratory rate was 18 breaths per minute, oxygen saturation was 96% on room air, and temperature was 97.8 F. He was alert and oriented, had clear breathing sounds, bilateral, no heart murmurs, and no leg swelling. EKG showed ventricular paced rhythm with underlying atrial fibrillation. Significant laboratory showed an increase in his creatinine to 1.7 mg/dl from a baseline of 1.2 mg/dl and a TSH of 16 uIU/mL and normal free thyroid hormone levels. The ICD interrogation showed multiple sustained monomorphic ventricular tachycardia episodes. During his hospital stay, his workup revealed positive UDS for amphetamine on 2 separate occasions (urine toxicology screen), but the patient adamantly denied using amphetamine or any other illicit drugs. He ultimately underwent confirmatory drug testing for amphetamine (quantitative urine amphetamines), which was negative. Ultimately, the patient underwent successful VT ablation and was discharged home.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [64, 'years'], 'creatinine': [1.7, 'mg/dL']}",44.46069,42.23766,46.68372,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 64 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.9)**-1.2 * 0.9938**64 * 1.0 = 44.46069.
Hence, the GFR value is 44.46069 ml/min/1.73 m²."
181,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4559782-1,Extracted,"A 49-year-old cachectic female patient with a body weight of 30 kg who was hospitalized for prerenal acute renal failure due to poor oral intake developed tonic clonic seizures that lasted for two minutes and showed signs of confusion afterwards. On laboratory analysis, she had an increased blood urea nitrogen level of 30.5 mg/dL and a creatinine level of 1.09 mg/dL. Serum electrolyte levels, hepatic function tests, and bleeding parameters were within normal limits. Her complete blood count was normal except for anemia (hemoglobin: 11.3 g/dL). She did not have any signs of infection and had negative blood and urine cultures. She was slightly hypertensive with a maximum systolic blood pressure of 140 mm Hg and a diastolic blood pressure of 90 mm Hg. She did not have any known history of a neurological disease but had undergone bilateral lung transplantation due to idiopathic pulmonary fibrosis 6 months ago and was on immunosuppressive treatment with tacrolimus. Plasma tacrolimus concentration was 8 ng/mL and it was within normal limits. She underwent magnetic resonance imaging (MRI) examination of the brain. On MRI, there were extensive hyperintense lesions predominantly in the subcortical and deep white matter of the left frontotemporoparietal lobe including the splenium of the corpus callosum and basal ganglia on fluid attenuation inversion recovery (FLAIR) images (). The lesions were iso to hyperintense on diffusion-weighted images (DWI) () and hyperintense on apparent diffusion coefficient (ADC) maps without any signs of restricted diffusion (). On contrast-enhanced three-dimensional T1-weighted images, lesions showed patchy enhancement (). Time-of-flight MR angiogram revealed high-grade occlusion of the left MCA (), but she did not undergo any further imaging with computed tomography (CT) or conventional angiography. The imaging findings were interpreted as a subacute infarction in the left MCA territory and the patient was given aspirin therapy. The patient did not experience any other seizures and her mental confusion disappeared the next day. She underwent follow-up CT imaging 5 days later and it showed a newly developed small intraparenchymal hematoma in the left temporal lobe which was interpreted as hemorrhagic transformation. Right frontal subdural widening and a small subarachnoid hemorrhage along the right side of the anterior interhemispheric fissure were also noted (). Aspirin was stopped immediately. The patient had a short-term follow-up with CT in the first two weeks and did not have a follow-up MRI examination until two years later. MRI examination performed two years later revealed complete disappearence of the lesions along with persisting left MCA occlusion and an old hemorrhagic focus in the left temporal lobe (). This reversibility of ischemic lesions was quite unexpected and led to re-evaluation of the first MRI examination of the patient. ADC hyperintensity which is representative of vasogenic edema, contrast enhancement, involvement of the splenium of the corpus callosum which is supplied by posterior circulation rather than the MCA, initially neglected presence of subtle hyperintensity in the contralateral external capsule (), and parenchymal hemorrhage led to the retrospective diagnosis of atypical unilateral presentation of PRES in the appropriate clinical setting.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [49, 'years'], 'creatinine': [1.09, 'mg/dL'], 'sex': 'Female'}",62.27666,59.16283,65.39049,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 49 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.09 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.09/0.7)**-1.2 * 0.9938**49 * 1.012 = 62.27666.
Hence, the GFR value is 62.27666 ml/min/1.73 m²."
182,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7461861-1,Extracted,"The 90-year-old Chinese gentleman presented to our hospital with progressively worsening left knee joint and left ankle pain for 1 week, accompanied by mild lower abdominal pain and constipation for 2 days. Medical history included 10 years of gout with irregular treatment, hypertension, chronic kidney failure (CKD) stage 3, and permanent pacemaker implantation due to atrial fibrillation. Apart from eating oysters 1 week before admission, he had not eaten anything different from the usual.
On admission, his vital signs were normal. Physical examination revealed swollen left knee and left ankle with tenderness and a soft abdomen with tenderness of right lower quadrant without rebound tenderness. Murphy's sign was negative. Laboratory tests showed that white blood cell (WBC) count, percentage of neutrophils, and C-reactive protein (CRP) were mildly elevated, and mild transaminitis was also identified (). Stool routine was normal. After intestinal obstruction was excluded by abdominal radiology, he was treated with an intramuscular injection of 7 mg compound betamethasone once for gout attack and 30 mL oral lactulose for constipation.
In the subsequent 2 days, he appeared with persistent diarrhea and ongoing lower abdominal pain with fever of up to 39.4°C. Repeat investigations recognized markedly elevated WBC count, CRP, and procalcitonin, and creatine increased significantly with a peak value of 414 μmol/L (). The stool routine revealed yellow watery stool with 1 to 3 WBCs per high-power field, and Clostridium difficile test was negative. Blood and stool cultures were pending; thus, intravenous ceftriaxone sodium 2 g daily was started empirically. Shortly afterward, blood and stool cultures revealed Salmonella group D with resistance to ampicillin and sensitivity to chloramphenicol, trimethoprim/sulfamethoxazole, ceftriaxone, and azithromycin. Meanwhile, although with enough fluid intake, his blood pressure sharply dropped to 88/52 mm Hg. Considering septic shock, treatment was upgraded to intravenous meropenem 1 g every 12 h (half dosage concerning renal insufficiency).
One day later, his temperature returned to normal, and diarrhea improved, whereas abdominal pain was not resolved. Physical examination revealed abdominal tenderness without definite location and no rebound tenderness, and Murphy's sign was positive. Bedside ultrasound (US) suggested enlarged gallbladder, sludge formation, and no gallstones were identified. The abdominal computed tomography (CT) scan revealed acute cholecystitis and appendicitis (). Then he was transferred to gastrointestinal surgery and underwent laparoscopic cholecystectomy, appendicectomy and enterolysis. Postoperative pathology revealed acute gangrenous cholecystitis () and chronic appendicitis with focal acute inflammation changes (). Bile culture was positive for Salmonella group D. He recovered after surgery and was discharged after 5 days of intravenous ceftriaxone and metronidazole.
Pathological sections of gallbladder and appendix tissues were sent for NGS analysis (see for details). The results identified 9,591 Salmonella enterica reads in gallbladder tissue, covering 6.33% of the nucleotide sequences, and 51 S. enterica reads in appendix tissue, covering 0.04% of the nucleotide sequences. Epstein-Barr virus (EBV, HHV-4) reads of 50 and 43 were also detected in the gallbladder and appendix tissues, respectively (). EBV-encoded RNA (EBER) by in situ hybridization for appendix tissue was negative.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [90, 'years'], 'creatinine': [414.0, 'µmol/L'], 'sex': 'Male'}",11.34206,10.77496,11.90916,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 90 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 414.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 414.0 µmol. To convert 414.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 414.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00041 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00041 mol Serum Creatinine * 113.12 g/mol = 0.04638 g Serum Creatinine. To convert 0.04638 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.04638 g Serum Creatinine * 1000.0 mg/g = 46.38 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 46.38 mg Serum Creatinine/10.0 dL = 4.638 mg Serum Creatinine/dL. The concentration value of 414.0 µmol Serum Creatinine/L converts to 4.638 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (4.638/0.9)**-1.2 * 0.9938**90 * 1.0 = 11.34206.
Hence, the GFR value is 11.34206 ml/min/1.73 m²."
183,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4094861-1,Extracted,"A 17-year-old 6-week-pregnant female was admitted for nausea and vomiting for a suspected morning sickness. At admission patient was found to have a mild fever of 99 F, hemoglobin of 6.5 mg/dL, and serum creatinine at 6.47 mg/dL. Baseline creatinine six months earlier was 0.6 mg/dL. A thrombotic thrombocytopenic purpura was suspected despite normal platelets and hence she was admitted to the hospital for further workup. Vital signs at admission were temperature of 99 F, heart rate of 90–100 beats per minute, respiratory rate of 14 cycles per minute, and blood pressure of 120–130/80 s. Physical exam was consistent with a normal female who was moderately built without any evidence of fluid overload like raised jugular venous distension and facial or leg edema. Heart and lung exam were within normal limits. Patient's neurological exam was intact. Laboratory findings were as follows: hemoglobin 6.51 mg/dL, white blood cell count 10.3 k/mm3, platelets 384 k/mm3, sodium 136 mEq/L, potassium 4.4 mEq/L, chloride 107 mEq/L, bicarbonate 21 mEq/L, blood urea nitrogen 26 mg/dL, and creatinine 6.47 mg/dL. Iron studies showed iron deficiency anemia with iron of 25 mcg/dL, total iron binding capacity of 185 mcg/dL, iron saturation of 14%, and transferrin of 132 mg/dL. Urine analysis at admission showed urine pH of 6.5, specific gravity of 1.009, urine protein of 2+, and urine blood of 3+ with too numerous RBCs to count; urine glucose, ketones, bilirubin, and leukocyte esterase were all negative. Other tests that were ordered were antiglomerular basement membrane antibodies which were high at 156 units. Complement C3 and C4 levels were high at 195 and 57, respectively. Antineutrophil antibody, antineutrophil cytoplasmic antibody, antiproteinase 3, anti-Smith, and ds DNA were negative. Other miscellaneous lab tests like HIV antibody, hepatitis A IgM antibody, hepatitis B surface antigen, hepatitis B core IgM antibody, hepatitis C antibody, and antistreptolysin O Ab were all negative.
On the second day of hospitalization the patient underwent a kidney biopsy for a suspected anti-GBM disease. The preliminary biopsy results based on the hematoxylin and eosin stains showed acute necrotizing and crescentic glomerulonephritis. Final pathology results showed acute crescentic glomerulonephritis with no globally obsolescent glomeruli, moderate interstitial inflammation, and mild fibrosis. The final images of the pathology slides are shown in Figures and .
Patient was given 2 units of PRBC after admission with a posttransfusion Hb at 8.9 mg/dL. Peripheral smear did not show any schistocytes and hence the diagnosis of TTP was ruled out. All the labs and pathology suggested acute anti-GBM disease. On hospital day 3 plasmapheresis and high dose methylprednisolone at 1 gm/day were begun. See for creatinine trend. Creatinine peaked to 7.48 on day 5 and the patient was slowly becoming oliguric, showing sign of fluid overload with pedal edema and lung crackles on physical exam and hence was initiated on intermittent hemodialysis on day 5 of hospitalization. Patient received a total of 3 doses of methylprednisolone at 1 gm/day and then was started on prednisone at 60 mg/day from day 4.
To prevent further renal injury the option of adding cyclophosphamide was discussed but was not done due to possible fetal adverse outcomes. On day 17 of hospitalization the patient had a spontaneous abortion. After abortion cyclophosphamide was not started due to patient's request and hence she was managed with plasmapheresis and high dose prednisone. The plasmapheresis sessions were started on day 3 and continued daily until discharge (day 25). Traditional plasmapheresis with albumin replacement and sometimes 70% albumin with 30% normal saline replacement that lasted for 3 hours every day was the technique used. She was never started on cyclophosphamide and slowly became hemodialysis independent in about 2 months from discharge. At about 6 months from discharge the patient lost to follow up. It was deemed that the acute anti-GBM flare-up was pregnancy related.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [17, 'years'], 'creatinine': [6.47, 'mg/dL']}",8.9657,8.51741,9.41399,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 17 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 6.47 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (6.47/0.7)**-1.2 * 0.9938**17 * 1.012 = 8.9657.
Hence, the GFR value is 8.9657 ml/min/1.73 m²."
184,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5872390-1,Extracted,"We present the case of a 41-year-old man who had been diagnosed with type 1 DM in junior high school. He was 168 cm tall and weighed 90.0 kg (body mass index, 31.9 kg/m2). His baseline serum creatinine (sCr) level was 79.6 μmol/L and his urinary protein level was 0.3 g/gCr. His blood pressure was well controlled with an aldosterone receptor blocker. DM control was poor (haemoglobin A1c 9.0–10.0%) under intensive conventional insulin therapy. His diabetic retinopathy was simple type. Pregabalin, duloxetine and mexiletine were also used for diabetic neuropathy. His family history was not significant except cerebral infarction in his grandmother. He initially visited a primary care unit because of general fatigue and high fever and was given oral levofloxacin. However, he later called an urgent care unit because of swelling and pain in his genitals. He was diagnosed with Fournier gangrene and admitted to our hospital (Fig. , clinical course). Table showed urinary, blood and culture examination on admission. Inflammatory markers were elevated (white blood cell count 25,700/μL with left shift and C reactive protein 28.8 mg/L). Renal function was slightly abnormal (Blood urine nitrogen 22.0 mg/dL, sCr 91.1 μmol/L) and proteinuria was detected. Blood culture was negative. Escherichia coli and Enterococcus faecalis were detected from wound culture. Free air was noted in his genital area via computed tomography (CT) scan (Fig. ). He underwent debridement and received tazobactam/piperacillin (PIPC/TAZ) 4.5 g every 8 h and intravenous VCM 1.5 g every 12 h. Because his trough VCM level was still low (9.24 μg/mL, 15–20 μg/mL is for complicated infections []) and sCr stable (83.1 μmol/L) on day 3, intravenous VCM increased to 1.5 g every 8 h. Thereafter, he developed pitting pedal edema, weight gain (10 kg), reduced urine volume (100 mL/day), increased sCr (416.4 μmol/L) and trough VCM level (80.48 μg/mL) on day 6, which suggested VCM-induced AKI. Urinary examination results, which included N-acetyl-beta-D-glucosaminidase of 32.0 U/L, α1-microgloblin of 25.7 mg/L, and β2-microgloblin of 1800 μg/L, were also consistent with AKI. CT scan showed no signs of hydronephrosis or renal atrophy (Fig. ). Gallium scintigraphy showed significant accumulation in both kidneys (Fig. ).
VCM and PIPC/TAZ were switched to ampicillin/sulbactam (ABPC/SBT), and frequent haemodialysis was performed on days 6–17, a total of seven times over 12 days (seven 4-h sessions with a blood flow rate of 120–150 mL/min and dialysate flow rate of 500 mL/min). Ethylene vinyl alcohol membrane was used on days 6 and 7, whereas polysulfone membrane was used on days 9, 11, 12, 14, and 17. His urine volume began to increase as his plasma VCM levels gradually decreased. A renal biopsy was performed on day 18 to rule out other renal disorders and evaluate for diabetic nephropathy. ABPC/SBT was switched to ciprofloxacin on day 13 because of a rash that developed mainly on his abdomen and back, and clindamycin was added on days 16–22. He was discharged on day 49 without haemodialysis and antibiotics (sCr, 145.0 μmol/L). Eight months later, his sCr was decreased to 109.6 μmol/L.
The specimen included 16 glomeruli with cortex (no medulla). Subcapsular and medullary ray fibrosis was found in 10% of the specimen on Masson staining (Fig. ). Glomeruli showed no sclerotic or inflammatory changes, but mild mesangial expansion without significant depositions of immunoglobulin or complement in immunofluorescence was found. Nodular lesions were not detected (Fig. ). Focal but severe AIN (Fig. ) and tubular epithelium injury with nuclear denudation or tubular dilatation (ATN) (Fig. ) were detected. Interstitial monocyte infiltration and tubulitis were mainly distributed in the medullary ray lesions (Fig. ). There were no obvious eosinophilic infiltrations or granular lesions in the specimen. Mild intimal fibrosis was found in some of the small interlobular arteries, and mild hyalinosis was also noted in an arteriole. In summary, the kidney biopsy showed that ATN and focal AIN with mild diabetic nephropathy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [41, 'years'], 'creatinine': [79.6, 'µmol/L'], 'sex': 'Male'}",109.30996,103.84446,114.77546,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 41 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 79.6 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 79.6 µmol. To convert 79.6 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 79.6 µmol Serum Creatinine * 1e-06 mol/µmol = 8e-05 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 8e-05 mol Serum Creatinine * 113.12 g/mol = 0.00905 g Serum Creatinine. To convert 0.00905 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00905 g Serum Creatinine * 1000.0 mg/g = 9.05 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 9.05 mg Serum Creatinine/10.0 dL = 0.905 mg Serum Creatinine/dL. The concentration value of 79.6 µmol Serum Creatinine/L converts to 0.905 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (0.905/0.9)**-1.2 * 0.9938**41 * 1.0 = 109.30996.
Hence, the GFR value is 109.30996 ml/min/1.73 m²."
185,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7686952-1,Extracted,"A 50-year-old male having a history of multiple myeloma (IgG kappa), on weekly elotuzumab infusion for last five weeks (last infusion four days before admission) along with lenalidomide and dexamethasone presented to emergency with four-day symptoms of shortness of breath, fatigue and malaise. He also reported dry cough. He denied having fever, chills, night sweats, chest pain, abdominal pain, nausea, vomiting, diarrhoea, urinary changes and lower extremity swelling. The patient was diagnosed with pulmonary embolism a month back. Compliance of the patient with therapeutic dose enoxaparin was documented. On initial evaluation, the patient was hypoxic requiring 2-3-litres oxygen, later increased to 15 litres high flow nasal cannula, and eventually stabilized on bilevel positive airway pressure (BiPAP). On physical examination, he had a temperature of 101.3 F, and faint crackles (heard bilaterally at bases) on chest examination. Cardiovascular, gastrointestinal, and neurological examinations were normal.
Laboratory tests revealed thrombocytopenia (platelets (PLT) 16 x 109/L) and anaemia (Hb 7.8 g/dl) consistent with initial baseline values, acute kidney injury (creatinine 1.28 mg/dl), mild pro-BNP elevation (394 pg/ml) with insignificant electrocardiogram abnormality. Viral respiratory pathogens polymerase chain reaction (PCR), COVID-19 PCR, legionella, and streptococcal urine antigens were negative. CT Chest with pulmonary embolism protocol demonstrated the decreased size of previously seen filling defect within right lower lobe segmental artery but new bilateral diffuse ground-glass opacities (Figure ). Elotuzumab induced pneumonitis, sepsis, pulmonary edema, and multifocal pneumonia were taken as a differential diagnosis. The patient was admitted, blood and urine cultures were sent and started on vancomycin along with meropenem. Normal systolic function (ejection fraction 50%), normal wall motion with no right to left shunt were observed on echocardiogram with bubble study. Continued administration of antibiotics with an observation period of one to two days was suggested by the haematologist along with administration of corticosteroids for possible elotuzumab induced pneumonitis if the patient did not improve under the antibiotics.
The patient continued to have shortness of breath requiring 10-15-litres oxygen on high flow nasal cannula and intermittent BIPAP over the next 24 hours. He was started on methylprednisolone (125 mg) every six hours after consultation with the haematologist. This brought down the oxygen requirement to 6 litres/min the next day, but the malaise persisted. Antibiotics were stopped since the urine and blood cultures were negative. Significant improvement was observed on the fourth day of intravenous methylprednisolone as the patient ambulated comfortably. He was not requiring any oxygen, was ambulating without difficulty. The patient was discharged with a prescription of prednisone (40 mg) daily with prolonged taper: 40 mg daily for the first two weeks, 10 mg weekly for next three weeks. Marked improvement of the bilateral opacities was observed after three weeks on chest x-ray (Figure ). After an additional three weeks, CT chest was ordered, but patient decided to discontinue chemotherapy due to adverse effects, low functional status and opted for hospice care.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [50, 'years'], 'creatinine': [1.28, 'mg/dL']}",68.18314,64.77398,71.5923,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 50 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.28 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.28/0.9)**-1.2 * 0.9938**50 * 1.0 = 68.18314.
Hence, the GFR value is 68.18314 ml/min/1.73 m²."
186,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7302721-1,Extracted,"A 77-year-old gentleman with a past medical history significant for hypertension, hyperlipidemia, chronic kidney disease and recent cerebrovascular accident presented to the emergency department with two weeks of intention tremors increasing in intensity to the extent that he was unable to walk. He also reported limited oral intake secondary to nausea over approximately the same period. Medication reconciliation was notable for omeprazole and furosemide. Vital signs in the emergency department were within normal limits, and physical exam was notable only for significant generalized tetany that worsened with intention. The patient’s electrocardiogram (EKG) revealed normal sinus rhythm with multiple premature atrial contractions (Figure ).
Initial laboratory results showed a creatinine of 1.18 mg/dL (which is at the patient’s baseline), sodium of 143 mmol/L, potassium of 3.3 mmol/L, phosphate of 2.5 mg/dL, calcium of 7.4 mg/dL and an undetectable magnesium level of <0.6 mg/dL. Additionally, parathyroid hormone was elevated to 79 pg/mL (reference range = 15-65 pg/mL).
In the emergency department, he was given 20 milliequivalents oral potassium replacement and one gram of intravenous magnesium sulfate with immediate improvement of his tetany. Omeprazole and furosemide were discontinued on admission, and causes of hypomagnesemia were evaluated. Both random urine and 24-hour urine magnesium testing did not reveal evidence of renal magnesium wasting. Furthermore, in the setting of recent occipital and cerebellar infarcts, magnetic resonance imaging of the patient’s brain was performed, which showed only encephalomalacia of the left occipital region from his prior ischemic stroke without evidence of an acute infarct as possible etiology (Figure ).
The patient required aggressive electrolyte replacement of magnesium, calcium, phosphate and potassium throughout his hospital course. He was asymptomatic at the time of discharge on hospital day 5 and was prescribed oral magnesium, calcium and vitamin D replacement. Discharge laboratory results were notable for stable creatinine, sodium of 139 mmol/L, potassium of 4.3 mmol/L, phosphate of 2.4 mg/dL, calcium of 8.4 mg/dL and a magnesium level of 1.8 mg/dL. Repeat magnesium level one week after discharge remained stable at 2.2 mg/dL. The patient remained on magnesium supplemental for a period of eight months after discharge before this was discontinued by his primary care physician. His measured serum magnesium level three months after discontinuation was within normal limits at 2.1 mg/dL.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [77, 'years'], 'creatinine': [1.18, 'mg/dL'], 'sex': 'Male'}",63.55407,60.37637,66.73177,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 77 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.18 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.18/0.9)**-1.2 * 0.9938**77 * 1.0 = 63.55407.
Hence, the GFR value is 63.55407 ml/min/1.73 m²."
187,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5139696-1,Extracted,"A 55-year-old white male presented to emergency room with pain in the abdomen, hematemesis, and melena. The abdominal pain was ongoing for 2 months, in the left upper quadrant, at times worsened with eating, and had abruptly increased in severity on the morning of admission associated with a few bouts of hemetemesis and melena. He denied any chest pain or shortness of breath.
His past medical history was significant for hypertension, hyperlipidemia, diabetes mellitus and coronary artery disease. He was on metformin, aspirin, simvastatin and metoprolol. He denied any other NSAID use. He had a thirty pack year history of smoking, drank alcohol occasionally and denied any illicit drug use.
On examination his temperature was 97degrees, heart rate was 102/ minute, sinus tachycardia, blood pressure was 135/85 mmHg, respiratory rate 13/ minute, oxygen saturation was 100% on two liters of oxygen. He was pale and uncomfortable. His abdomen was soft, tender in the left upper quadrant with bowel positive sounds. Rectal examination was grossly heme-positive. The rest of the physical examination was within normal limits.
Laboratory results showed white cell count of 11.4 K/mcL, hemoglobin 8.1 gm/dl, hematocrit 25 %, platelet count 372 K/mcL, normal renal panel, blood urea nitrogen 14 mg/dl, creatinine 1.1 mg/dl, glucose 231 mg/dl and lactic acid level was 7 mmol/L. Prothrombin time was 11.9 seconds, International Normalized Ratio was 1.1 and Partial thromboplastin time was 27.6 seconds. Computed tomography (CT) scan of abdomen at that time showed a small 2.5 x 2.6 cm infrarenal aortic aneurysm and 2.1 cm right common iliac artery aortic aneurysm.
He became hemodynamically unstable later with blood pressure of 79/ 39mm Hg, heart rate of 140/ minute. Emergent CT scan with contrast showed active contrast extravasation into the stomach from the splenic artery, raising the possibility of penetrating gastric ulcer involving these vessels (). Following that, he underwent emergent splenic arteriogram which confirmed an area of active contrast extravasation from the mid portion of the splenic artery beyond the dorsal pancreatic artery (). The splenic artery was embolized with 6 mm x 14 cm fibered micro coils both proximal and distal to the site of extravasation. Follow-up splenic and celiac arteriogram showed flow in the splenic artery to the level of the dorsal pancreatic but not distal. He did well over the next day but the left sided abdominal pain returned. Repeat contrast enhanced CT scan showed continued extravasation of blood into the stomach and he was taken to operating room. The stomach had a very large ulcer which was penetrating into the pancreas. The top of this ulcer was only 2 cm away from the esophagus, and therefore to perform resection of the ulcer, a total gastrectomy had to be performed. Splenectomy was also performed since the spleen was found to be infarcted.
Histopathology of the spleen revealed evidence of hemorrhagic infarction without evidence of vasculitis or vascular dysplasia identified. The gastric ulcer was 5.4 x 3.7 cm, with granulation tissue, gastric mucosa with fresh hemorrhage and reactive changes. No Helicobacter pylori organisms were identified. No malignancy was identified.
The patient recuperated and was later on discharged home.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [55, 'years'], 'creatinine': [1.1, 'mg/dL'], 'sex': 'Male'}",79.27801,75.31411,83.24191,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 55 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.1/0.9)**-1.2 * 0.9938**55 * 1.0 = 79.27801.
Hence, the GFR value is 79.27801 ml/min/1.73 m²."
188,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2769309-1,Extracted,"An 80-year-old man (ethnic origin: German, nationality: German) with the medical history of Parkinson’s disease consulted his neurologist because of paresthesia in his lower extremities. The patient had 40 pack-years smoking history but had quit 26 years earlier. His medical history showed mitral valve insufficiency grade 2, hypertension and hypercholestererolemia. The social history, family history and review of systems were otherwise unremarkable. The physical examination revealed a generally light reduced state of health, normal vital signs, no fever, with bilaterally clear lung fields and no lymphadenopathy. His routine lab values, including complete blood count and chemistries showed elevated creatinine (1.87 mg/dl) and urea (93 mg/dl) as well as normochromic normocyteric anaemia. After readjustment of medical therapy, chest X-ray was done to exclude a paraneoplastic cause of the above-mentioned symptom. Chest X-ray revealed a solid contrast-enhancing mass in the right upper lobe (RUL). Based on these finding CT-scan was ordered and demonstrated a 1.4 × 3.1 cm pulmonary mass in the lateral segment of the RUL associated with 2.2 cm node in precarinal and 2.4 cm node paraaortal position (). A flexible bronchoscopy and transbronchial biopsy of a parabronchial lymph node were performed. The endoscopic findings revealed no endobronchial lesion. Microbiological cultures of the gained bronchial secretion showed no evidence of the growth of germs, fungi or mycobacteria and the pathology report was negative for malignancy. CT-guided needle biopsy showed also no evidence of malignant tumour. PET-CT scan was performed to assess mediastinal nodal disease, and showed high fluorodeoxyglucose (FDG) uptake in the RUL lesion with maximum standardized uptake value (SUVmax) of 6.9 (). Further uptake was detected in precarinal (SUVmax: 6.4), infracarinal (SUVmax: 6.4) and paraaortal (SUVmax: 4.0) lymph nodes as well in a lymph node at the left main bronchus () corresponding to N3 disease. The TNM classification after PET staging was NSCLC T2 N3 M0 (UICC IIIB). It was decided to proceed to thoracotomy in order to obtain histological confirmation. A right lateral thoracotomy was performed and wedge resection of the RUL. The pathologist’s intraoperative examination resulted in NSCLC (squamous cell carcinoma, T2) in the RUL. Additionally stage adapted lymph node dissection was performed. Surprisingly microscopic examination of the resected RUL tissue revealed except the squamous cell carcinoma signs of granulomatous inflammation. Numerous epitheloid cell granulomas were also found in all resected lymph nodes, which were free of malignancy. In summary, histological diagnosis was pulmonary sarcoidosis in addition to NSCLC. Resected margins and pleural surface were free of malignancy. The following TNM classification arose from the pathological examination: pT2, pN0, M0, G2, R0. Postoperative progress was satisfactory and the patient was discharged 7 days after surgery. Due to the reduced general state of health, no secondary lobectomy or adjuvant chemotherapy was indicated.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [80, 'years'], 'creatinine': [1.87, 'mg/dL'], 'sex': 'Male'}",35.89953,34.10455,37.69451,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 80 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.87 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.87/0.9)**-1.2 * 0.9938**80 * 1.0 = 35.89953.
Hence, the GFR value is 35.89953 ml/min/1.73 m²."
189,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4038523-1,Extracted,"A 73-year-old man without any significant past medical history presented with 10 days of cough and dyspnea, accompanied by loss of appetite. Dyspnea worsened gradually, with the patient becoming unable to walk to the bathroom, so he was brought to the hospital by ambulance. He denied any significant past medical history or family history, and was not on any medication. He even denied any previous attendances for health care. He had smoked one pack of cigarettes per day for 53 years. He also drank one can of beer and two 180 mL bottles of Japanese sake daily. He lived with his wife, and his son lived nearby.
Upon arrival, he appeared sick and looked to be in pain. Blood pressure was 113/50 mmHg, pulse rate was 135 per minute, respiratory rate was 27 per minute, temperature was 37.8°C, and oxygen saturation level was 93% on room air. Examination of his head, eyes, ears, nose, and throat was unremarkable. His neck was supple. Cardiac auscultation revealed tachycardia but no murmur. A coarse crackle was heard in the right lower lung. The rest of his physical examination was unremarkable.
Blood tests showed elevated white cells (33,200 per μL), lactate dehydrogenase 1,340 IU/L, and creatinine 2.5 mg/dL. Arterial blood gas (on oxygen of unknown amount) showed a pH of 7.347, pCO2 31.1 mmHg, pO2 53.3 mmHg, HCO3− 16.6 mEq/L, an anion gap of 17 mEq/L, and a delta anion gap of 5 mEq/L. Chest radiography showed infiltration in the lower lobes bilaterally, particularly on the right ().
Based on his history, physical examination, and laboratory findings, a diagnosis of severe pneumonia was made, with a score of 3 on the CURB-65 (British Thoracic Society Community Acquired Pneumonia Severity Calculations and Guidelines) and a score of V on the Pneumonia Severity Index. He was admitted to the intensive care unit, but did not require mechanical ventilation. Sputum staining showed many Gram-positive diplococci, suggesting that S. pneumoniae was the organism causing his pneumonia (Geckler’s category 5 with unknown Millar-Jones classification, ). Retrospectively, Gram-negative cocci were also seen but were not detected on initial microscopic examination. Ceftriaxone 2 g once daily and azithromycin 500 mg once daily were administered, both intravenously.
On the following day, his respiratory function deteriorated. He was intubated and placed on mechanical ventilation that afternoon. Because Gram staining of aspirates from the lower respiratory tract revealed decreased organisms and his cardiac function remained good, acute respiratory distress syndrome or another complication such as congestive heart failure was suspected rather than worsening of pneumonia. However, because of the patient’s deteriorating condition, his antibiotics were changed to meropenem 1 g twice a day and levofloxacin 750 mg once a day both intravenously. On the third day after admission, his respiratory function remained unchanged. The inspired oxygen fraction was set at 1.0. Intravenous methylprednisolone 80 mg was added. He also developed atrial fibrillation and hypotension, which led to addition of diltiazem and noradrenaline. On the fourth day after admission, his respiratory function and blood pressure improved. His inspired oxygen fraction decreased to 0.65 and his vasopressor was discontinued. On the fifth day after admission, the sputum culture result on admission was reported, which revealed meropenem-resistant S. pneumoniae and Moraxella catarrhalis (). The M. catarrhalis was beta-lactamase-producing but detailed susceptibility testing was not done. Two sets of blood cultures were negative. Based on the susceptibility pattern of S. pneumoniae, meropenem was discontinued and only intravenous levofloxacin was continued.
Analysis for resistant genes revealed gPRSP (pbp1a + pbp2x + pbp2b gene variants) and the capsular antigen was 19F; this is included in both the 7-valent and 23-valent pneumococcal vaccines. Because it seemed unusual for a patient to have acquired such a resistant organism without a history of access to health care, a more detailed history was taken from the patient. Apparently his two grandchildren (aged 3 years and 2 months) visited his house 3 days prior to the onset of his symptoms, and the 3-year-old grandchild had cold symptoms at that time. Throat cultures from both of them revealed S. pneumoniae with the same susceptibility pattern, the same genes for development of resistance, and the same capsular antigen. It was postulated that transmission of S. pneumoniae to the patient occurred via one of his grandchildren. Neither the patient nor his grandchildren had received any type of pneumococcal vaccination.
On day 9 after admission, the patient developed diarrhea. A stool Clostridium difficile toxin assay was positive, and levofloxacin was discontinued. He was treated with oral metronidazole. His pneumonia resolved promptly, but his hospitalization was complicated by status epilepticus, presumably due to metabolic encephalopathy, gastrointestinal bleeding, pleural effusion, and cardiac arrest on changing his endotracheal tube. The patient was discharged from the intensive care unit one month after admission, and transferred to another hospital 2 months later.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [73, 'years'], 'creatinine': [2.5, 'mg/dL'], 'sex': 'Male'}",26.46536,25.14209,27.78863,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 73 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.5/0.9)**-1.2 * 0.9938**73 * 1.0 = 26.46536.
Hence, the GFR value is 26.46536 ml/min/1.73 m²."
190,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7427037-1,Extracted,"A 46-year-old Caucasian male from Arkansas with a past medical history of multiple sclerosis, plaque psoriasis presented with generalized weakness of 1 week duration. He also had associated fever and chills for the past day. He did admit to multiple tick bites (2 days ago) from recent travel in Arkansas prior to the symptoms starting. He does not know the duration of tick attachment and did not notice any engorged ticks on removal. On examination, he had a fever of 100.5 °F and a heart rate of 70 beats per minute that was irregularly irregular. Significant laboratory values include a white blood cell count of 4200/µL with 77% neutrophils, platelets of 83 000/µL. Sodium was 131 mEq/L. His BUN (blood urea nitrogen) was 12 mg/dL and creatinine was 1.4 mg/dL. Liver enzymes were within normal limits. Electrocardiogram (EKG) obtained showed variable block atrial flutter with heart rate <100 beats per minute (prior EKG showed normal sinus rhythm; ). The patient was treated empirically with doxycycline, intravenous fluids, and metoprolol tartrate. E chaffeensis immunoglobulin M (IgM) Ab was positive with titers >1:40 consistent with tick-borne illness due to E Chaffeensis. The patient’s symptoms improved over the next couple of days and eventually discharged. Repeat EKG 1 month later showed normal sinus rhythm ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [46, 'years'], 'creatinine': [1.4, 'mg/dL'], 'sex': 'Male'}",62.77394,59.63524,65.91264,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 46 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.4 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.4/0.9)**-1.2 * 0.9938**46 * 1.0 = 62.77394.
Hence, the GFR value is 62.77394 ml/min/1.73 m²."
191,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5484569-1,Extracted,"A 63-year-old male with end-stage kidney disease due to diabetic nephropathy had been undergoing continuous ambulatory peritoneal dialysis for 3 years when he sought medical advice regarding the appearance of grouped red crusts on the left and right sides of his abdomen. The problem initially started as the development of painful erythematous vesicles on the left flank corresponding to the T11 dermatome approximately 15 days prior to presentation and on the right side of his abdomen 5 days previously. The patient reported a history of prodromal pain on the left side of the abdominal region approximately 3 weeks prior to the onset of this disease. A few days later, grouped vesicular eruptions developed, lasting approximately 1 week. Thereafter, the lesions became encrusted; some of them healed with residual scarring and pigmentation, but new painful vesicular lesions appeared on the right side of his abdomen at almost the same level as that observed on the left side (T11 dermatome) (). A physical examination revealed the patient to be afebrile, alert, and oriented, and no abnormalities other than the cutaneous manifestation were found. Laboratory evaluations revealed hemoglobin 11.7 g/dL, hematocrit 35.4%, white blood cell count 10,800/μL (neutrophils 71.1%, lymphocytes 14.1%, monocytes 6.3%, eosinophils 6.5%, basophils 2.0%), platelet counts 33,0000/μL, blood urea nitrogen 40 mg/dL, serum creatinine 17.68 mg/dL, fasting blood sugar 151 mg/dL, and hemoglobin A1c 8.4%, while the chest X-ray findings and liver function were normal. The characteristic cutaneous manifestation encouraged us to ascribe the disease to HZ duplex bilateralis, and he was given a single dose of 250 mg oral valaciclovir. Overall, the patient’s clinical course was favorable, and the pain subsided without any complications. Finally, elevated serum titers of both anti-VZV immunoglobulin (Ig)M (IgM index 2.9, cut-off index 0.8) and IgG (3,400 IU/mL) were confirmed.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [63, 'years'], 'creatinine': [17.68, 'mg/dL']}",2.69301,2.55836,2.82766,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 63 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 17.68 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (17.68/0.9)**-1.2 * 0.9938**63 * 1.0 = 2.69301.
Hence, the GFR value is 2.69301 ml/min/1.73 m²."
192,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6607589-1,Extracted,"A 26-year-old Sinhalese woman was transferred from a local hospital with a history of reduced urine output, shortness of breath, reduced level of consciousness, abdominal pain, vomiting, and mild degree fever of 2 days’ duration. Her bilateral lower limbs were edematous but she was not pale or icteric. Her pulse rate was 112 beats per minute and blood pressure was 140/70 mmHg. An abdominal examination did not reveal organomegaly. Bilateral lower zone crepitations were noted on lung auscultation. Her respiratory rate was 20 cycles per minute and oxygen saturation was 97% on air. She had right-sided lower motor type facial nerve palsy. Glasgow Coma Scale was 13/15. The rest of the neurological examination including other cranial nerves and ophthalmoscope examination was unremarkable.
Our initial working diagnosis was leptospirosis with acute kidney injury and treatment was initiated accordingly (intravenously administered antibiotic and hemodialysis via femoral vascular catheter), but we could not explain the cranial nerve involvement. The following day she came out with the history of a suicide attempt in which she had self-ingested brake oil (amount not clear) after a conflict with her husband.
On admission her renal functions were deranged with serum creatinine of 352 μmol/ L, blood urea of 14.1 mmol/l, Na+ 140 mmol/l, and K 5.2 mmol/l. Arterial blood gas showed pH 7.08, partial pressure of oxygen (PO2) 94, partial pressure of carbon dioxide (PCO2) 28, bicarbonate (HCO3) 13.8, and base excess − 18 mEq per liter. Her serum osmolality was 339 mosmols with an osmolar gap of 20 mOsm/kg and anion gap was 32 mEq/l. Although relevant, her urine was not examined for calcium oxalate crystals. Full blood count showed hemoglobin of 12.7 g/dl, platelet of 185 × 106/L, and white cell count of 15.2 × 106/L. Her C-reactive protein was 22 mg/dl. Her random blood sugar was 92 mg/dl. Her blood and urine cultures were negative. Her pro-calcitonin levels were within normal range. A chest X-ray did not reveal any abnormality such as consolidation or pleural effusion. A non-contrast computed tomography (CT) scan of her brain was normal. Leptospira antibody tested after 10 days of disease was negative. She was started on initial consecutive daily dialysis followed by every other day dialysis which yielded a considerable improvement in renal functions. After 10 days of hospital stay she was discharged with residual facial nerve palsy. Over the course of 3 months’ clinic follow-up she had complete renal and neurological improvement.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [26, 'years'], 'creatinine': [352.0, 'µmol/L']}",15.28473,14.52049,16.04897,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 26 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 352.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 352.0 µmol. To convert 352.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 352.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00035 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00035 mol Serum Creatinine * 113.12 g/mol = 0.03959 g Serum Creatinine. To convert 0.03959 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.03959 g Serum Creatinine * 1000.0 mg/g = 39.59 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 39.59 mg Serum Creatinine/10.0 dL = 3.959 mg Serum Creatinine/dL. The concentration value of 352.0 µmol Serum Creatinine/L converts to 3.959 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (3.959/0.7)**-1.2 * 0.9938**26 * 1.012 = 15.28473.
Hence, the GFR value is 15.28473 ml/min/1.73 m²."
193,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8334176-1,Extracted,"A 26-year-old man with a history of acute lymphoblastic leukemia (ALL) in childhood and end-stage kidney failure due to IgA nephropathy received a deceased donor kidney transplant at the age of 21, mismatched for 3 HLA antigens (one mismatch in HLA-A, HLA-B, and HLA-DR). Two years after kidney transplantation (KTx), an indication biopsy for an increase in serum creatinine (sCr) levels showed a mixed T-cell rejection (Banff 4/IB) and acute AMR with positive donor-specific antibodies (DSA; anti-HLA DQB1 and DQA1) while receiving triple maintenance immunosuppressive regimen (tacrolimus/mycophenolate mofetil/steroid). The rejection was treated with high-dose steroids, antithymocyte globulin, plasmapheresis, intravenous immunoglobulins (IVIg), and rituximab. After 3 years of stable kidney function with sCr in the range between 150 and 180 μmol/L, we observed a progressive deterioration of kidney function with a sCr value of 240 μmol/L and a 24-h proteinuria of 3.4 g/day before entering the study protocol. The kidney biopsy revealed chronic active AMR ().
Due to the history of childhood ALL, which was treated with a combination chemotherapy (vincristine, doxorubicine, methotrexate, cyclophosphamide, cytarabine), we first performed a bone marrow aspiration, which showed non-specific reactive changes. The treatment protocols were approved by National Ethic Committee (approval no. 0120-215/2018/4). The written informed consent was obtained from the patient. After completion of the standard of care therapy (including corticosteroids, membrane plasmapheresis, and IVIg), the patient received MSCs therapy according to the study protocol, consisting of 3 x 106 cells/kg, applied at 1-week intervals. Details of the MSCs cultures and criteria for bench release are described in the Supplementary documentation ().
After the first dose of MSCs the patient reported short term nausea. One week later after the second dose of MSCs nausea, blepharitis and diarrhea developed, with their remission after 24 h. This was associated with a slight deterioration in kidney function, which we attributed to prerenal causes (). When the patient was referred for the third dose of MSCs (2 weeks after the first dose), the symptoms had completely disappeared. The evening after the third dose of MSCs was administered, the patient was admitted to the emergency department due to abdominal cramps, vomiting, and diarrhea. A further deterioration of the kidney function was observed (sCr of 390 μmol/L), accompanied by newly developed ascites and abdominal lymphadenopathy.
Although indicators of inflammation remained normal throughout the course of treatment, the initial clinical presentation was suspicious for infection. Therefore, the manufacturing process of MSCs was reevaluated and contamination by infectious agents during cultivation or before release was ruled out. An expanded diagnostic investigation () ruled out common and opportunistic infections, including Herpes viruses 6, 7, and 8, CMV, HIV, and EBV viremia, bacteremia, gastrointestinal infections, and the possibility of intestinal bacterial overgrowth syndrome. Endoscopic biopsies of the colon and duodenum showed mucosal edema without inflammatory cell infiltration or apoptotic bodies. Given the normal concentrations of complement components and absence of fetal bovine albumin in the cell medium (platelet lysate was used instead), a serum disease-like syndrome did not seem likely. A capillary leak variant syndrome, associated with sudden capillary hyperpermeability, resulting edemas and hypoalbuminemia, was considered. Therefore, antihistamines and methylprednisolone were administered at a dosage of 1.5 mg per kg body weight. After administration of high-dose steroids, the symptoms disappeared, and the dose was reduced during the next 10 days. At this point, sCr stabilized in the range of 300 μmol/l.
Two weeks later (i.e., 5 weeks after the last dose of MSCs), there was a recurrence of abdominal symptoms (nausea, diarrhea, ascites), this time followed by resistant hypertension, a further deterioration of kidney function (sCr of 380 μmol/l), an increase in proteinuria (7.3 g per day), and signs of hemolysis and pancytopenia. Tacrolimus trough levels were very low (<2 ng/ml), despite an increase of the dosage and assured adherence to therapy. The abdominal CT scan showed ascites, thickening of the intestinal wall (especially the jejunum), lymphadenopathy and an enlarged spleen. Transcriptomic analysis by the molecular microscope diagnostic system (MMDx) () of the subsequent kidney biopsy showed persistence of AMR, although the molecular classifiers of inflammation and AMR were lower compared to the biopsy before application of MSCs (inflammation score of 1.06 vs. 3.19, and AMR score of 0.63 vs. 0.94, respectively; ). In addition, the MFI levels of DSA decreased and we had no reason to assume a further deterioration of AMR.
Cytokine assessment after MSCs treatment (at the time of onset of symptoms) showed increased levels of IL-2R and IL-8, while other cytokines, including TNF-α and IL-6, were within near normal ranges and not consistent with a cytokine storm (, for details see ). Comparative analysis of T and B lymphocyte subsets before and after MSC therapy showed a transient decrease in all lymphocyte subsets with an increase in the ratio of activated T lymphocytes that occurred concomitantly with worsening of symptoms and the appearance of pancytopenia (). Bone marrow examination was consistent with trilineage dysplasia and a secondary myelodysplastic syndrome attributable to potentiated immunosuppressive therapy. It is more likely, however, that the changes in the bone marrow were of reactive origin. Morphologically, there was no evidence of parvovirus B19 infection of the bone marrow.
The kidney allograft failed 2 months after MSCs transplantation and hemodialysis was initiated. After administration of granulocyte colony stimulating factor (G-CSF) and reintroduction of methylprednisolone at a dose of 1 mg/kg, leukopenia improved minimally, and gastrointestinal symptoms worsened after each application of GCS-F. Therefore, the steroids and GCS-F were discontinued. The patient's general condition gradually deteriorated with progressive malaise, vomiting/diarrhea, generalized edema, and laboratory signs of hypoalbuminemia and agranulocytosis. The clinic's expert council made the empirical decision to end a life-threatening situation by removing the failed kidney transplant. After the transplant nephrectomy, the cell counts recovered almost instantly (). At this time, parvovirus B19 viremia was also detected. After treatment with high-dose IVIg, the parvovirus B19 infection resolved. Retrospectively, parvovirus B19 was detected by PCR in both the preimplantation kidney biopsy (6 years before MSC therapy) and in the kidney graft after MSC therapy. The patient is currently on chronic hemodialysis, remains aviremic and no further MSCs associated adverse events were observed during the 24-month follow-up period. Patohistologic analysis of the explanted kidney was consistent with advanced AMR, glomerular and vascular thrombotic microangiopathy (TMA), and extensive tubular injury ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [26, 'years'], 'creatinine': [240.0, 'µmol/L'], 'sex': 'Male'}",32.10919,30.50373,33.71465,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 26 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 240.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 240.0 µmol. To convert 240.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 240.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00024 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00024 mol Serum Creatinine * 113.12 g/mol = 0.02715 g Serum Creatinine. To convert 0.02715 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.02715 g Serum Creatinine * 1000.0 mg/g = 27.15 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 27.15 mg Serum Creatinine/10.0 dL = 2.715 mg Serum Creatinine/dL. The concentration value of 240.0 µmol Serum Creatinine/L converts to 2.715 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.715/0.9)**-1.2 * 0.9938**26 * 1.0 = 32.10919.
Hence, the GFR value is 32.10919 ml/min/1.73 m²."
194,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3420417-1,Extracted,"Mr. B is a 59-year-old African American male with a long history of bipolar disorder, maintained on fluphenazine decanoate, and lithium carbonate for over 30 years without any incidence of toxicity. His past medical history is significant for hypertension, Type II diabetes, and morbid obesity. He presented with a 1-week history of increasing confusion and lethargy, slurred speech, urinary incontinence, worsening tremor, and gait difficulties. He was found lying on the floor beside his bed on the day of presentation. The family was unaware of how long the patient had been lying there but found him awake and alert, unable to lift himself off the floor. About 2 weeks before presentation, his antihypertensive regimen was modified with a doubling of the dose of Valsartan to 320 mg/day, in addition to his regular lisinopril 20 mg/day. His other medications were lithium carbonate 450 mg twice daily and fluphenazine decanoate 37.5 mg every 3 weeks (last administered 3 weeks before admission). His last recorded lithium level was 0.7 just prior to the above medication changes. Other relevant baseline laboratory results a few weeks before onset of symptoms included Na-134 mEq/L, K-4.1, BUN, 23, and Cr. 2.4 mg/dL.
Collateral history from his outpatient psychiatrists revealed that patient had been stable on the above regimen of lithium and fluphenazine decanoate with no medication changes made within the past 6 months.
On examination in the ER, the patient was in moderate distress, dehydrated asking for water to drink. His vital signs were fluctuating with temperature ranging from 99.3 to 100.1, heart rate from 75 to 102, and BP from 123/69 to 223/112 all over a period of 6 hours. Cardiovascular and respiratory exams were unremarkable. Neurological exam revealed slurred speech, hand tremors, and rigidity in the extremities with decreased motor strength in the upper extremities and lower extremities. Patient was oriented to place and person but not to time.
Admission labs showed a leukocytosis of WBC-22.6, neutrophil count of 87.9%; sodium was 142 mEq/L; potassium was 3.5 mEq/L, bicarbonate 20.1 mmol/L; BUN 35 mg/dL; creatinine 4.1 mg/dL; blood glucose 145, troponin I 5.64; CPK 6008; CK (MB) isoenzyme 36.7 and a lithium level of 1.20 mEq/L. Blood, urine and sputum cultures yielded no growth. CT/MRI brain showed old frontoparietal infarct, and EEG was reported as within normal limits for drowsiness and briefly aroused state with no epileptiform discharges. CSF from spinal tap was unremarkable.
Patient was commenced on IV fluid hydration and broad-spectrum antibiotics. Lithium was discontinued and fluphenazine decanoate was not administered. Repeated blood cultures yielded no growth, and thus antibiotics were discontinued. Patient showed gradual improvement in his mental status, he had no problems with articulation, and he was fully orientated within a week of admission. His lithium levels had decreased to 0.89 on day 5 and 0.55 on day 7, and his renal function was back to baseline. Patient's vital signs stabilized, and there was minimal rigidity at the time of discharge.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [59, 'years'], 'creatinine': [4.1, 'mg/dL'], 'sex': 'Male'}",15.94701,15.14966,16.74436,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 59 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 4.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (4.1/0.9)**-1.2 * 0.9938**59 * 1.0 = 15.94701.
Hence, the GFR value is 15.94701 ml/min/1.73 m²."
195,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6046178-1,Extracted,"A 55-year-old Caucasian male was admitted to our hospital with a history of biventricular systolic heart failure due to ischemic cardiomyopathy and chronic stage IV kidney disease due to diabetic nephropathy; one month earlier, he had been approved for combined heart-kidney transplant. He recently had increased fatigue and dyspnea, weight gain of 8 kg, and serum creatinine that increased from 2.3 mg/dL to 3.7 mg/dL despite outpatient inotropic and diuretic therapy. Other comorbidities included antiphospholipid syndrome under warfarin management, multiple myocardial infarctions, with 2 coronary artery bypass grafting procedures, placement of biventricular automated implantable cardioverter-defibrillator, and placement of left ventricular assist device (HeartWare) 5 months earlier.
On hospital day (HD) 14, after optimization of hemodynamics with diuretics and inotropic support, the patient was listed for heart-kidney transplant and transferred to the intensive care unit. On HD 24, the patient was taken to the operating room for combined heart-kidney transplant; however, only orthotopic heart transplantation (OHT) was possible. During the OHT, acute right ventricular graft dysfunction developed, resulting in cardiogenic shock, requiring placement of VA-ECMO support through central cannulation and withholding of the single-kidney transplantation. VA-ECMO was utilized to allow the newly transplanted heart to rest and recover and to optimize hemodynamics and volume status in order for the patient to eventually receive the single-kidney transplantation. Simultaneously, he received support with vasopressin 0.04 U/min, dobutamine 10 mcg/kg/min, epinephrine 0.01 mcg/kg/min, and full-dose anticoagulation with heparin 9.5 U/kg/hour. Tables and show the initial and subsequent laboratory results and ECMO parameters.
On post-OHT day 1, after the patient had improved volume and cardiovascular status, adequate urine output (1,660 mL/24 hours), and stable laboratory testing parameters, the heparin infusion was reduced to 5.5 U/kg/hour (i.e., low dose) and the patient underwent deceased-donor renal transplantation (DDRT). During the DDRT procedure, the patient received 1 unit of packed red blood cells and had no complications. After DDRT, the patient required epinephrine at 0.03 mcg/kg/min, dobutamine at 10 mcg/kg/min, and heparin at 5.5 U/kg/hour.
During the first 48 hours after DDRT, the patient's urine output was adequate (1,900 mL in 24 hours) and his serum creatinine concentration decreased to 2.0 mg/dL. On post-DDRT day 2 (post-OHT day 3), after repeated transesophageal echocardiography showed improved right ventricular function and optimal volume status, the patient underwent ECMO decannulation, chest washout, and sternal closure without complication. His renal function continued to improve, and his anticoagulation was discontinued. The only inotropic support needed was dobutamine at 7.5 mcg/kg/min. On post-DDRT day 5 (post-OHT day 6), the patient was successfully weaned from mechanical ventilation and on post-DDRT day 18 (post-OHT day 19) was transferred to the posttransplant care unit for further care.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [55, 'years'], 'creatinine': [2.0, 'mg/dL'], 'sex': 'Male'}",38.68904,36.75459,40.62349,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 55 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.0 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.0/0.9)**-1.2 * 0.9938**55 * 1.0 = 38.68904.
Hence, the GFR value is 38.68904 ml/min/1.73 m²."
196,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2878709-1,Extracted,"A 57-year-old male presented with complaints of low grade fever for 10 days; dry cough, progressive breathlessness and right-sided chest pain of seven days duration. There was no history of wheezing or hemoptysis. There was no past history of any cardiac illness, pulmonary tuberculosis, COPD, blood transfusion or previous hospitalization. The patient gave history of diabetes mellitus diagnosed 10 years back and presently well-controlled on oral hypoglycemic agents. He was also a known hypertensive for seven years, well-controlled with drugs.
On physical examination, the patient was conscious and alert with a pulse rate of 110 beats per minute, blood pressure of 140/70 mmHg, and a respiratory rate of 36 breaths per minute. The accessory respiratory muscles were active. The patient was febrile with temperature 100.8°F. There was no pallor, clubbing, lymphadenopathy, icterus, cyanosis, or pedal edema. Examination of the chest revealed reduced movements on right side, and stony dull note in right infrascapular, infra-mammary and axillary regions with decreased breath sounds. Rest of the physical examination was unremarkable.
Investigations showed hemoglobin-10.9 gm%, total leukocyte count-11,400/cu mm, differential leukocyte count-P78 L06 M5 E11, erythrocyte sedimentation rate -38 mm, random blood sugar-505 mg%, blood urea-89 mg%, serum creatinine-2.3 mg%, serum proteins-5.4 gm%, albumin-2.8 gm%, alanine aminotransferase-128 IU/l, aspartate aminotransferase-142 IU/l. Urine routine examination showed albumin in traces and sugar-4+ and ketones were absent. Electrocardiograph showed sinus tachycardia. Arterial blood gases were suggestive of uncompensated metabolic acidosis (pH: 7.297, partial pressure of carbon dioxide: 23 mmHg, partial pressure of oxygen: 119 mmHg, bicarbonate: 10.9 mEq/L) which might have been due to severe sepsis. His chest radiograph [] showed right pleural effusion. A diagnostic thoracocentesis was performed and thin pus was aspirated. Pleural fluid cell count was 4200 (P-73%, L-18%, M-09%), glucose: 134 mg%, protein: 5.2 gm%, and lactate dehydrogenase: 1621 IU/l. Acid fast bacilli (AFB) smear and Gram's stain were negative, and pyogenic culture was sterile.
Early initiation of a combination of empirical intravenous antibiotics, amoxycillin-clavulanic acid and cefepime, was started. Inter-costal chest tube drainage was done and about 1500 ml thin pus drained. Even after four days of treatment there was no clinical improvement as fever persisted and patient remained tachypnoeic, toxic, febrile and breathless. Inter-costal drainage of about 150-200 ml of thin pus was noted daily. Chest ultrasonography (USG) was suggestive of right multi-loculated empyema. Contrast enhanced computed tomography (CT) scan of chest showed right sided empyema with multiple loculations but no pleural thickening. There was no mediastinal lymphadenopathy or lung parenchymal involvement. Mantoux test was negative. Medical thoracoscopy was performed and another 750 ml of thin pus aspirated. A large number of fibrinous adhesions with multiple loculations were seen. Diaphragm and pleural surfaces were lined with fibrinous exudates. Pleural fluid and pleural biopsy specimens were sent for pyogenic, fungal and AFB culture. Pleural fluid smears[] showed septate fungal hyphae. Intravenous voriconazole was started with a loading dose of 400 mg twice on first day followed by 200 mg twice daily. He was taken up for surgical intervention due to persistent toxemia and multiloculated empyema. Thoracotomy revealed tough fibrinous adhesions with multiloculated fluid collection with pleural thickening. The right lower lobe showed multiple superficial cavitatory lesions measuring one-two cms. Complete parietal pleurectomy was done along with surgical resection of part of the right lower lobe. Pleural fluid, pleural and lung tissue cultures grew Aspergillus fumigatus, whereas the bacterial cultures and AFB smears were negative in all the samples. The hematoxyllin and eosin staining of pleural biopsy sample was positive for aspergillar hyphae []. The postoperative period was uneventful and he was continued with voriconazole. His general condition improved rapidly. The toxemic state, fever and breathlessness subsided. His kidney function tests settled to normal. The patient was discharged after 14 days on oral Voriconazole which was continued for three months. He was followed up to eight months and showed good clinical and radiological recovery.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [57, 'years'], 'creatinine': [2.3, 'mg/dL']}",32.31086,30.69532,33.9264,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 57 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.3/0.9)**-1.2 * 0.9938**57 * 1.0 = 32.31086.
Hence, the GFR value is 32.31086 ml/min/1.73 m²."
197,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3741981-1,Extracted,"A 57-year-old gentleman was referred with high grade intermittent fever with chills since 3 months. He was a longstanding type 2 diabetic, on oral hypoglycemic agents with a fairly good sugar control. He did not have any constitutional symptoms like weight loss or anorexia. He was normotensive and had no specific urinary symptoms. Other than the fever for which he consumed paracetamol, he was fairly asymptomatic. There were no clinical clues to the etiology for the fever on systemic examination.
The complete blood count of the patient showed an Hemoglobin 11 g/dL, total leukocyte count 10,100 (polymorphs 85, lymphocytes 13% and eosinophils 2%) and a normal platelet count of 2.73 lacs. Liver function tests were essentially normal with a bilirubin of 0.7 mg/dL, alanine aminotransferase/ALT of 36 and 31 IU/L, serum albumin 3.84 g/dL, and serum globulin 2.46 g/dL. Renal function tests showed BUN 55 mg/dL, serum creatinine 1.5 mg/dL, and normal serum electrolytes. The urine analysis was essentially bland with no albumin, 1-2 pus cells, and no red cells.
Test results during these 3 months revealed an erythrocyte sedimentation rate of 90 mm at the end of 1 h and two high C-reactive protein levels of 35.8, 24, and 18.5 mg/L (Normal up to 6 mg/L). Complete blood count, urine examination, chest radiology, and 2D Echo performed to investigate the cause of the fever were all normal. Blood and urine cultures were also negative. Serum Ferritin and complement levels were normal. anti-nuclear antibodies and anti-neutrophil cytoplasmic antibody were negative. angiotensin converting enzyme levels were normal. Tumor marker profile was negative. Enzyme immunoassays for tuberculosis and brucellosis were negative. He was treated empirically with antibiotics during this period with no permanent relief.
The abdominal ultrasound was also essentially normal. A whole body computed tomography (CT) scan revealed multiple lymph nodes measuring 1.5-4 cm in the mediastinum and retrocarinal region reported to be of inflammatory/infective etiology. Fine needle aspiration of the lymph node was reported as non-specific lymphadenitis. The contrast CT abdomen revealed heterogeneous enhancement of both kidneys with hypodensities at the lower pole [].
Given the clinical presentation and the clinical possibilities of vasculitis and lymphoma, and the kidney findings on CT, a renal biopsy was performed. The conspicuous feature was presence of expansile interstitial fibrosis with a plasma cell rich interstitial infiltrate that were accompanied by a few lymphocytes and occasional eosinophil []. Some areas of the biopsy showed storiform fibrosis. There were neither neutrophils nor granulomas. The fibro inflammatory process was seen to extend into the peri-nephric tissue and had resulted in significant tubular loss. The remaining tubules showed thickening of their basement membranes. The glomeruli revealed diffuse capillary wall thickening but there were no changes of diffuse or nodular diabetic glomerulopathy. The arteries revealed mild medial thickening. The pathologic features raised the suspicion for IgG4 related tubulointerstitial nephritis. Immunofluorescence was negative for IgG, IgA, IgM, C3 and C4. IgG4 immunohistochemistry was performed which showed numerous IgG4 expressing plasma cells amounting to at least 15 per high power field (HPF) []. The pathologic diagnosis was IgG4 related tubulointerstitial nephritis. Corresponding serum IgG4 level was 5.9 g/L (N-0.01-1.3 g/L). The diagnosis of IgG4 mediated nephropathy was made on the basis of the clinical history, CT scan findings, histopathology, immunohistochemistry, and serology. He was initiated on a dose of 40 mg prednisolone (0.5 mg/kg/day) and his fever defervesced within 24 h. The steroids were continued and tapered over the next 5 months. His serum creatinine touched a baseline of 1.2 mg/dL at the end of 2 months therapy with steroids. Although an attempt was being made to taper down the steroids further, his fever recurred at a steroid dose of 5 mg/day. He was therefore initiated on Mycophenolate Mofetil (MMF) with a dose of 1 g b.i.d to which his fever responded again. Steroids were stopped by the end of the 5th month and MMF was continued. The serum IgG4 levels progressively declined from a peak of 5.9 g/L to 2.04 followed by 1.55 g/L by the end of the 4th month. The patient continued to be on a dose of 2 g of MMF per day. The CT scan repeated after 6 months showed a significant regression in the mediastinal and retrocarinal lymphadenopathy and resolution of the original hypodense foci in the kidneys.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [57, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Male'}",53.96503,51.26678,56.66328,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 57 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.5/0.9)**-1.2 * 0.9938**57 * 1.0 = 53.96503.
Hence, the GFR value is 53.96503 ml/min/1.73 m²."
198,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4783560-1,Extracted,"A 58-year-old male presented to his primary care physician with central abdominal pain and distension. His past medical history was significant for hypertension, hyperlipidemia, and end-stage renal disease secondary to hypertensive kidney disease requiring hemodialysis. This was performed via arteriovenous fistula starting 8 years prior to being seen. He denied any history of peritoneal dialysis and his only abdominal surgery was a right inguinal hernia repair approximately 4 years before. Unfortunately, the operative report was unavailable to us and he was unsure if mesh was used. CT of the abdomen and pelvis with oral and intravenous contrast showed a 17.2 × 14.6 × 17.3 cm large pelvic cystic tumor with separate loculated areas in the right upper abdomen adjacent to the gastric antrum. A smaller fluid collection in the right midabdomen between the mesocolon of the proximal transverse colon/hepatic flexure and small intestine, ascites, and thickened omentum were also seen (Figures 
–). Hounsfield units for the cystic regions were 24. There was also a loculated right pleural effusion. The appendix could not be visualized (). The prior right inguinal hernia repair with possible mesh could be seen adjacent to the pseudocyst (). He presented to the surgical oncology clinic for further workup. At the time, he only complained of abdominal pain and distension without any other associated symptoms. His baseline creatinine was 5.3 mg/dL (normal 0.6–1.3 mg/dL). His white blood cell count was 4.4 k/uL (normal 4–10.8 K/uL), albumin was 3.6 g/dL (normal 3.8–5.0), and carcinoembryonic antigen (CEA) was 3.6 (normal < 3.5). The patient was a nonsmoker and denied weight loss.
He underwent a bronchoscopy that showed extrinsic compression from the loculated effusion. Washings showed atypical cells but no malignancy was identified. His information was reviewed and discussed in our gastroenterology multidisciplinary conference and a decision was made to proceed with surgical exploration and resection of the large intra-abdominal tumor. Given the possibility for mucinous tumor, surgical debulking as well as potential intraperitoneal chemotherapy was also discussed.
During surgery, the tumor was found to be adherent to the omentum and anterior abdominal wall and was unable to be separated requiring resection of a portion of peritoneum. This was suspected to be close to the region of the hernia repair, although it was difficult to discern if scar tissue or tumor caused the inability to separate the tumor from the peritoneum. No mesh was encountered in this space. The mass was also adherent to the right colon but was able to be separated with careful dissection. It was not attached to the appendix, but this was removed given the original concern for mucinous ascites. The tumor appeared encapsulated with a tan-yellow capsule and multiple thick adhesions were encountered (). Multiple nonencapsulated pockets of ascites were also found throughout the abdomen consistent with findings on the CT. The pocket in the right midabdomen was removed intactly and also appeared as a tan-yellow cystic structure. His surgery included an exploratory laparotomy, excision of the intra-abdominal tumor with appendectomy, greater and lesser omentectomy, excision of the falciform ligament, and peritoneal stripping at the area of attachment to the abdominal wall.
Final pathology revealed an intact large cystic mass measuring 19 × 15 × 9 cm (). Grossly, the lesion was tan-yellow and smooth and had a dull external surface with thin fibrous adhesions. Upon opening the cyst, a large amount of hemorrhagic fluid was seen. The inner wall was covered by a friable slightly necrotic and hemorrhagic appearing exudate. Microscopic examination showed the cystic wall was composed of fibrous tissue with mild chronic inflammation and hemosiderin deposits (). The luminal surface was lined by granulation tissue and fibrin. Recent hemorrhagic material was also noted attached to the luminal surface. The fibrous wall measured up to 0.8 cm thick. Microscopic evaluation revealed organizing hemorrhage with surrounding dense fibrous cyst wall and stromal reactive changes. There was no evidence of neoplasm within the cyst wall, nor was any concerning neoplasm found within the appendix or omentum (). Pathology at our institution as well as at the Mayo Clinic confirmed the final diagnosis to be a giant pseudocyst. The appendix, omentum, smaller cystic structure, and falciform were all without malignancy. The smaller cyst showed fibroadipose tissue with chronic inflammation and hemorrhage.
The patient recovered well postoperatively without complication and was discharged home on postoperative day 6. Most recent imaging performed approximately 3 months later showed no intraperitoneal recurrence, but he required a right thoracentesis for a recurrent pleural effusion. CEA was not rechecked given that no carcinoma was found.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [58, 'years'], 'creatinine': [5.3, 'mg/dL'], 'sex': 'Male'}",11.79207,11.20247,12.38167,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 58 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 5.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (5.3/0.9)**-1.2 * 0.9938**58 * 1.0 = 11.79207.
Hence, the GFR value is 11.79207 ml/min/1.73 m²."
199,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8111648-1,Extracted,"A 30-year-old male with a history of live related renal transplant (LRRT) 3 years back, who was doing well on triple immunosuppression, presented with low grade fever and throat pain for 5 days with 2 days of myalgias. There was no history of cough, haemoptysis, breathlessness, chest discomfort, vomiting, dysuria, or abdominal pain. Pulse rate was 104 per minute, and BP was 130/80. Systemic examination was unremarkable except for a subcentrimetric submandibular lymph nodes. Temperature was 100.2 Fahrenheit. Laboratory evaluation revealed total leucocyte count 6600/microliter with lymphopenia (12%) with a normal haemoglobin; cultures were sterile and the result of liver function test was normal. Urine examination result was normal. The serum creatinine was 0.8mg/dL, with normal x-ray chest and ultrasound abdomen and graft. Cytomegalovirus (CMV) and BK viral markers were negative. C-reactive protein was elevated (12mg/l). RT PCR for SARS-CoV2 turned out to be positive. The patient was put on azithromycin, oseltamivir and continued on the same dose of tacrolimus 1mg BD, and prednisolone dose increased from 5mg to 20mg OD, while the dose of mycophenolate mofetil halved from 1000 mg to 500mg daily in 2 divided doses. The patient became afebrile on day 3 of hospitalization. Lymphopenia improved completely by day 9 of hospital stay. Repeat RT PCR was negative on day 17. Renal functions remained stable throughout the hospital stay and the patient was discharged on the same immunosuppression as was commenced in hospital; and after a total of 4 weeks, his immunosuppression was back to preinfection dose and the patient was doing well.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [30, 'years'], 'creatinine': [0.8, 'mg/dL'], 'sex': 'Male'}",113.17345,107.51478,118.83212,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 30 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.8 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.8/0.7)**-0.302 * 0.9938**30 * 1.0 = 113.17345.
Hence, the GFR value is 113.17345 ml/min/1.73 m²."
200,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3684486-1,Extracted,"Previously healthy 6-week-old boy, born to a GIII PIII, birth weight 2900g, was admitted to the district hospital with fever, vomiting and oliguria persisting for several hours. Family history was of no significance. On admission, infant's general condition was poor. A distended abdomen, tense and tender on palpation, was noted. Urethral catheterization was difficult. Laboratory investigations revealed: WBC 3.7 K/u, Hb 8.4 g/dl, urea 70 mg/dl, CRP 132.3 mg/l, procalcitonine >200 ng/ml, and uncompensated metabolic acidosis. Urine microscopy revealed pyuria and few fresh red cells. Ultrasound examination showed a left kidney measuring 70 mm in length with a dilated pelvi-calyceal system and an enlarged hydronephrotic right kidney measuring 90 mm in length. Treatment was started with cefotaxime, vancomycin, dopamine and furosemide. The infant's general condition improved, but CRP continued to rise (281.5 mg/l). Serum urea, creatinine and procalcitonine were 98.0 mg/dl, 1.0 mg/dl and 180.74 ng/ml, respectively. Blood and urine cultures were negative. A diagnosis of bilateral hydronephrosis was made.
On the 2nd day of hospitalization the infant was transferred to our Department. A distended abdomen with a right sided large palpable mass was found. Laboratory tests showed CRP 309.4 mg/l, urea 116 mg/dl, creatinine 1.81 mg/dl, Hb 10.5 g/dl and compensated metabolic acidosis. Urine output in less than 24-hours measured about 280 ml. Cefotaxime and vancomycin were discontinued and meropenem commenced. Abdominal ultrasound demonstrated left kidney 7×2.8 cm, with mild pelvic dilatation, and right kidney 11×6.6 cm with a dilated and deformed collecting system. The upper and middle calyces seemed mostly dilated with a total volume of about 216 ml, pelvic volume 3 ml. Right kidney parenchyma was compressed. The bladder was empty. Hydronephrosis was considered, but a suspicion of kidney compression by an extraneous cystic structure was also raised. Due to worsening of the infant's condition and equivocal ultrasound images, he was qualified for an urgent laparotomy.
During surgery a huge cyst was found in the peritoneal cavity, encircling almost the whole right kidney and connected to the renal capsule by its capsule. The cyst contained about 500 ml of watery bright fluid which was resected revealing that its wall was a fragment of the anterior wall of the renal capsule. Drains were set up to postoperative sites. Additionally, the bladder was noted to have a thick and hard wall.
In the following 24-hours renal function improved (urea 47 mg/dl, creatinine 0.95 mg/dl), CRP decreased to 65 mg/dl. Urine output was 2-5 ml/h. Bright yellow draining fluid, about 20 ml/h, was noted to have similar biochemical properties to urine: urea 496 mg/dl, urea nitrogen 231.8 mg/dl, creatinine 9 mg/dl. Follow up abdominal ultrasound reported a slightly wider right pelvi-calyceal system, with a small fluid collection near the upper pole (). Voiding cystourethrography showed trabeculated bladder wall. Cystoscopy revealed urethral structures which could correspond to disrupted posterior urethral valves. Valve ablation was performed. Histopathologically the wall of the resected cyst turned out to be the right kidney capsule and was reported as Pseudocystis in inflammatione chronica. Retrospectively spontaneous kidney rupture due to posterior urethral valves was diagnosed.
After 21 days of treatment, inflammatory markers and renal function normalized. Renoscintigraphy performed 6 weeks post surgery revealed cumulative renogram curves of both kidneys, the right kidney (operated) contributing 81.5% of renal function and the left kidney 18.5%. At 20 months follow up review both renal function parameters and blood pressure values were normal. Ultrasound examinations revealed persisting mild dilatation of both pelvi-calyceal systems. History regarding urinary tract infection was negative.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [6, 'weeks'], 'creatinine': [0.95, 'mg/dL'], 'sex': 'Male'}",133.07946,126.42549,139.73343,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 6 weeks old. This means the patient is 0 years old.
The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.95 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (0.95/0.9)**-1.2 * 0.9938**0 * 1.0 = 133.07946.
Hence, the GFR value is 133.07946 ml/min/1.73 m²."
201,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4411889-1,Extracted,"In January 2006, a 33-year-old woman was diagnosed with SLE, based on malar rash, positive ANA (1 : 640, mixed pattern), high titer of anti-dsDNA (140 IU/mL, normal <10), and autoimmune hemolytic anemia. Since then, she received immunosuppressive medications including prednisolone, azathiopurine, and hydroxychloroquine. In January 2007, splenectomy was performed on account of refractory hemolytic anemia and thrombocytopenia. In June 2007, severe nephritic syndrome with urine daily protein loss (DPL) 8 g developed. She received renal biopsy, and the biopsy revealed membranous glomerulonephritis. Monthly pulses of cyclophosphamide combined with pulse corticosteroids therapy was initiated thereafter; however, the response was poor. Persistent proteinuria (urine DPL: 5 to 10 g) was still found. In November 2007, she presented with intermittent abdominal pain in the emergency room. Physical examination revealed decreased bowel sound, positive shifting dullness, rebounding tenderness in the right lower quadrant, left costovertebral-angle tenderness, and peripheral bilateral leg edema. Laboratory data revealed the following results: WBC, 4,700/mm3 (normal 4,500–11,000); hemoglobin, 13.3 g/dL (normal 12–16); platelets, 179,000/mm3 (normal 150,000–400,000); BUN, 23 mg/dL (normal 7–20); creatinine, 0.4 mg/dL (normal 0.5–1); alanine aminotransferase, 28 U/L (normal <31); aspartate transaminase, 18 U/L (normal <31); albumin, 1.7 g/dL (normal 3.4–4.8); d-dimer, 3,516 ng/mL (normal <500); fibrinogen, 933 mg/dL (normal 200–400). The urine DPL was 10.3 g. Immunological studies were as follows: positive LA; aCL-IgG, 55 U/mL (normal <15); aCL-IgM, 19.6 U/mL (normal <15); anti-dsDNA, 394 IU/mL; C3, 48.8 mg/dL (normal 90–180); C4, 16.8 mg/dL (normal 10–40), and the serological test for syphilis was negative. Antithrombin III was 59% (normal 70–120). Multidetector-row computed tomography (MDCT) demonstrated a wedge-shaped infarction involving the right kidney (), as well as segmental thrombus in the inferior vena cava (IVC) and main portal vein (). Initially, the patient was managed with anticoagulants (low-molecular-weight heparin) and intravenous methylprednisolone 250 mg daily for three days. However, right lower quadrant abdominal pain with acute renal failure (serum creatinine: 2.5 mg/dL) progressed. Elevation of anti-dsDNA (412 IU/mL) and reduction of C3 and C4 (40 and 9 mg/dL) were also found from following laboratory data. Acute SLE flare with acute renal failure and multiple thrombus events was impressed. Due to poor response for anticoagulant and methylprednisolone therapy, plasma exchange was carried out 5 times by using fresh frozen plasma as the replacement fluid, followed by corticosteroids pulse therapy (1,000 mg intravenous methylprednisolone for 3 days). After therapy, she recovered and was discharged on the 14th hospital day with normal d-dimer and a targeted international normalized ratio (INR) of 2.5. The patient's renal functions were within normal range. Decreased serum levels of anti-dsDNA, and increased C3 and C4 was also found. The patient had no recurrent symptoms of thrombus or emboli in the following three months. Until now, she visited outpatient department regularly and received medication including prednisolone, hydroxychloroquine, and azathiopurine.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [33, 'years'], 'creatinine': [2.5, 'mg/dL']}",25.40535,24.13508,26.67562,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 33 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.5 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.5/0.7)**-1.2 * 0.9938**33 * 1.012 = 25.40535.
Hence, the GFR value is 25.40535 ml/min/1.73 m²."
202,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5514834-1,Extracted,"A 28-year-old male (weight 70.6 kg) presented with edema, gross painless hematuria, and uremic symptoms since 2 weeks. He was nondiabetic, normotensive, and nonalcoholic. Habit of smoking 2–3 cigarettes/day was there since 2 years. On examination, there was bilateral pitting edema, pallor, and normal blood pressure (130/80 mmHg). Urinalysis showed 3+ protein, plenty of red blood cells (RBCs), and RBC casts. Complete blood count revealed hemoglobin, 10.3 g/dl; total leukocyte count, 14,830 cells/mm3; and platelets, 2.3 lakhs cells/mm3. Serum creatinine was 16.5 mg/dl. Serum electrolytes and complements were normal. Total serum calcium was 7.1 mg/dl. Viral markers (hepatitis C virus, hepatitis B surface antigen, human immunodeficiency virus) and antinuclear antibody, antineutrophil cytoplasmic antibody were also negative. Ultrasonogram revealed 12.9 cm kidney size bilaterally with increased echoes. Renal biopsy was performed in view of RPGN.
Renal histology showed four glomeruli, all of which possessed circumferential active cellular crescents and fibrinoid material deposition []. Capillary tufts were nonproliferative but had disruption of capillary basement membranes and Bowman's capsule. Severe acute tubular injury was noticed. There was no giant cell reaction. Immunofluorescence panel (Dako: IgG, IgA, IgM, C3, C1q, kappa, and lambda) showed strong linear uninterrupted staining with IgG (4+ on a scale of 0–4) and kappa (4+ on a scale of 0–4) along glomerular capillary walls (GCW) in all seven glomeruli [Figure –]. Rest of the panel was negatively stained. Further subclass of IgG performed showed positive staining with IgG1 (3+ on a scale of 0–4) along GCW and negative for IgG2, IgG3, and IgG4 [Figure –]. All seven glomeruli in immunofluorescence core possessed circumferential crescents. Ultrastructure of kidney retrieved from paraffin block did not show any powdery or electron-dense deposits in glomeruli and tubular basement membranes.
A diagnosis of anti-GBM crescentic glomerulonephritis with monoclonality (IgG1-kappa light chain restriction) was made. Further detailed post-biopsy serum investigations are shown in .
The patient was treated with intravenous (IV) methyl prednisolone 500 mg, 1 dose of cyclophosphamide 500 mg, and subsequently switched to oral steroids 1 mg/kg/day. Eight sessions of plasmapheresis were performed in addition to regular hemodialysis. Targeted therapy including bortezomib-based regimen was discussed with patient attendants, but they were hesitant due to financial constraints and the patient was lost to follow-up.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [28, 'years'], 'creatinine': [16.5, 'mg/dL'], 'sex': 'Male'}",3.63723,3.45537,3.81909,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 28 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 16.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (16.5/0.9)**-1.2 * 0.9938**28 * 1.0 = 3.63723.
Hence, the GFR value is 3.63723 ml/min/1.73 m²."
203,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5956757-1,Extracted,"A 39-year-old man with CF and CF-related diabetes came to our Unit due to symptoms of pulmonary exacerbation. At the same time, he started to present gross hematuria, back pain and headache. At admission, laboratory analysis showed increase in serum creatinine of 1.5 mg/dl together with hematuria and mild proteinuria (1 g/24 h). Intravenous antibiotics for pulmonary exacerbation (piperacillin/tazobacatam and colimycin) were started and a renal biopsy performed to investigate the cause of hematuria and renal failure. Biopsy was consistent with IgAN (see Fig. ), with morphological features of mesangial and endocapillary hypercellularity (Oxford classification M1, E1, S0, T0) [] As the patient presented dyspepsia, he was offered upper gastrointestinal endoscopy with duodenal biopsies (one from duodenal bulb and three from descending duodenum). Duodenal mucosa was reported as normal on hematoxylin/eosin stain. While compatible HLA alleles for celiac disease (DQ2) were identified, both serum anti-endomysium (EMA) and anti-tissue transglutaminase antibodies (anti-tTG) were negative. It has been demonstrated that coeliac IgA targets intestinal TG2 early in disease development even when serum celiac autoantibodies are not present. Extraintestinal deposits of coeliac IgA further indicate that humoral immunity may have a pathogenetic role []. Therefore, double immunofluorescence on duodenal mucosa was performed to detect mucosal deposits of anti-tissue transglutaminase type 2 using the technique described by Karponay-Szabo et al., with some modification []. Briefly, 5 μm sections from the duodenal specimen included in optimal cutting temperature (OCT) compound were obtained and stored at − 80° in liquid nitrogen. Sections were fixed in acetone and incubated with Normal Rabbit Serum (Calbiochem Germany) for 20 min to block nonspecific sites. Sections were then incubated with anti-tissue transglutaminase type 2 (anti-tTG-2) from mouse (CUB7402 from Neomarker, Fremont CA) for one hour, and then with secondary antibodies conjugated with fluorochromes to detect total IgA (in green using Polyclonal Rabbit anti-Human IgA/FICT from Dako, Denmark) and anti-tTG-2 (in red using Polyconal Rabbit anti-Mouse RPE F (ab’) 2 from Dako, Denmark) for 30 min. The overlap of green and red (yellow) indicates the deposits of anti-tTG2. Analysis was performed on confocal microscopy. The same technique was performed on 5 μm renal sections. In both cases, an overlap of green and red in yellow was seen, thus demonstrating deposits of tTG-2 (Fig. , and ). In particular, in renal biopsies, deposits of tTG-2 that topographically replicated mesangial deposits of IgA (Fig. ) were detected.
Given the morphological features of IgAN, and the presence of proteinuria, steroid therapy was started according to a standardized six month’s protocol []. After one month, proteinuria decreased to 100 mg/24 h and hematuria resolved. Steroids were stopped after six months of treatment. The patient continued on a gluten containing diet.
Considering that intestinal deposits of anti-tissue transglutaminase IgA are predictive of forthcoming enteropathy [] after one year arepeat upper endoscopy was performed even though anti-tTG were still negative. At this time, a Marsh 2 type duodenal pathology was detected (Fig. , ). A gluten free diet was started (for a complete timeline history see Additional file : Table S1).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [39, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Male'}",60.3574,57.33953,63.37527,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 39 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.5/0.9)**-1.2 * 0.9938**39 * 1.0 = 60.3574.
Hence, the GFR value is 60.3574 ml/min/1.73 m²."
204,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4508971-1,Extracted,"A 38-year-old Turkish male was admitted to our outpatient clinic for hypercalcemia. Before entering our clinic, hypercalcemia has been detected in another medical center. History revealed, that he took ace inhibitor in combination with thiazide diuretic for hypertension. Due to the complications, like hypopotassemia this medicine was replaced with calcium channel blockers. In his family history, none of his first degree relatives had hypertension. His father died at 47 years of age due to biliary tract cancer. His three children were diagnosed with West Syndrome. One of them died at the age of 13 months, while the other 9 months of age. His third child is 2 years old and living with the respiratory support equipment. He also has a 13-year-old healthy son. There is no other significant clinical data in his medical history.
On his physical examination: blood pressure—150/90 mmHg, pulse −74 per minute, rhythmic. His general clinical appearance was good. The other systemic and laboratory findings were the following: complete blood count and thyroid function tests were normal: serum Ca level: 10.9 mg/dl (8.8–10.2), inorganic P: 2.4 mg/dl (2.7–4.5), Mg: 2.3(1.6–2.6), albumine: 3.9 g/dl, parathormone (PTH): 200 pg/ml (12–88), Na: 138 mmol/l, K+: 2.8 mmol/l, glucose: 85 mg/dl, creatinine: 0.84 mg/dl, alanine transaminase: 24 U/l, white blood cells 8 ML, hemoglobin 14 g/dl, platelet 219 C-reactive protein 0.4 mg/dl (0–0.8), alkaline phosphatase 61 U/l (38–126), 25-OH vitamin D3 22 ng/ml (14–66). Calcium level in 24-h urine: 251 mg/day, inorganic P: 88 mg/day, and K+ value in spot urine: 66 mmol/l. Aldosterone level was measured after normalization of his serum potassium level (result: 26.9 ng/dl). Plasma renin activity was <0.15 ng/ml/h. The patient was detected for multiple endocrine neoplasia syndromes. Levels of catecholamine and its metabolites in 24-h urine were normal. In the low dose (1 mg) dexamethasone suppression test, serum cortisol level was suppressed to the normal range. Serum prolactin, thyroid-stimulating hormone, adrenocorticotropic hormone, growth hormone, insulin-like growth factor 1 and calcitonin were normal.
Thyroid ultrasound revealed a 24 × 14 × 12.5 mm hypoechoic nodular lesion at the upper posterior part of the right thyroid lobe, within the thyroid capsule (intrathyroidal parathyroid adenoma?). MIBI (Technetium (99mTc) sestamibi) scintigraphy of parathyroid glands was consistent with the ultrasound finding. Abdominal magnetic resonance imaging revealed 1.6 cm adrenal gland mass consistent with adenoma, cystic lesions in both kidneys with the largest (3 cm in length) in the right kidney and also on this side 11 mm lesion which may be consistent with angiomyolipoma. Pituitary magnetic resonance imaging was normal.
The patient was operated for parathyroid adenoma. At the 3rd day after the operation, serum Ca level was found to be 9.5 mg/dl, inorganic P—3.6 mg/dl and parathyroid hormone—62 pg/ml. Pathological examination of the surgery material revealed parathyroid adenoma. The patient post operatively was followed during the 2 months with spironolactone therapy for his hypertension. This medication was stopped soon after, due to its side effects like erectile dysfunction. Post-surgery, which was conducted for the lesion (1.6 cm) identified on the left adrenal gland revealed adrenal aldosterone producing adenoma. Follow up the adrenal surgery, his blood pressure came to normal ranges and hypokalemia were improved. Blood potassium and calcium levels were within normal ranges. Genetic screening revealed negative mutation of MENIN gene.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [38, 'years'], 'creatinine': [0.84, 'mg/dL'], 'sex': 'Male'}",106.10536,100.80009,111.41063,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 38 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.84 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.84/0.7)**-0.302 * 0.9938**38 * 1.0 = 106.10536.
Hence, the GFR value is 106.10536 ml/min/1.73 m²."
205,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4849970-1,Extracted,"A 49-year-old white male presented to the emergency department with a chief complaint of
spontaneous weight loss (20 kg in 1 year) and arthralgia. He reported development of
erythematous lesions on the earlobes and anterior surface of the thighs 3 weeks before
presentation. Medical history was positive for arterial hypertension that was diagnosed
2 years before but not treated, and alcohol and cocaine dependence. The patient was
receiving psychiatric care for depression. Current medications included 1 mg/day
risperidone, 40 mg/day fluoxetine, and 500 mg/day sodium valproate, the latter for
seizures during alcohol and cocaine withdrawal. He denied any prior kidney conditions,
and his baseline serum creatinine measured 1 year before was 0.8 mg/dL. Physical
examination revealed erythematous, slightly hypochromic skin lesions on the anterior and
posterior surfaces of the thighs and flanks bilaterally, as well as edema and purpuric
areas with foci of central necrosis. The auricula was edematous and purpuric, with focal
necrosis, as shown in .
Laboratory tests on admission were as follows: urinalysis with 51 leukocytes/μL, 960
erythrocytes/μL, spot urine protein-to-creatinine ratio 1.20, serum creatinine 4.56
mg/dL, hemoglobin 7.3 g/dL, platelets 290,000/μL, WBC 3,800/μL, and serum albumin 4.1
g/dL. Complement levels were within normal limits (C3, 89 mg/dL; C4, 14 mg/dL).
Anti-nuclear and anti-dsDNA antibodies, lupus anticoagulant, rheumatoid factor,
cryoglobulins, and HBV, HCV, and HIV serologies were negative. ANCA testing was positive
(titers >1:320), with anti-myeloperoxidase (anti-MPO) antibody 109 IU/mL (positive if
>5 IU/mL) and anti-proteinase 3 (anti-PR3) antibody 35 IU/mL (positive if >10
IU/mL). Renal ultrasonography findings were normal.
Skin biopsy revealed a neutrophilic vasculitis in small vessels with eosinophils,
leukocytoclasia, and fibrinoid necrosis (). Skin immunofluorescence showed focal and granular deposits of C3 in venules.
There were a total of twenty-five glomeruli in kidney biopsy, with cellular crescents
and intra-glomerular necrosis in eight. There were no globally sclerosed glomeruli.
Podocyte hypertrophy, focal mesangiolysis, a diffuse and chronic inflammatory infiltrate
in the tubulointerstitium, and interstitial fibrosis and tubular atrophy in 10% of total
cortical area were also observed ().
Immunofluorescence findings revealed no deposits of IgG, IgM, IgA, C1q, C3, fibrinogen,
kappa and lambda, which was consistent with a pauci-immune crescentic
glomerulonephritis. The findings of retiform purpura, crescentic glomerulonephritis, and
positive anti-MPO and anti-PR3 antibodies were compatible with exposure to
levamisole-contaminated cocaine. Pulse corticosteroid therapy was instituted with
intravenous methylprednisolone, 500 mg/day for 3 days. During his hospital stay, the
patient exhibited a recurrence of elevated creatinine and onset of new cutaneous
lesions. A second methylprednisolone pulse therapy was performed (1 g/day for 3 days)
and cyclophosphamide 1000 mg iv was administered, which were followed
by an improvement of cutaneous lesions and renal function. The patient was discharged on
60 mg/day prednisone, with a plan to receive monthly iv
cyclophosphamide pulse therapy depending on clinical response. Guidance was provided on
the importance of continued psychiatric care and abstinence from cocaine.
One week after discharge, the patient returned asymptomatic but reporting a relapse of
cocaine use. A sample of cocaine powder used by the patient was sent to the Rio Grande
do Sul State Poison Control Center for testing to confirm presence of cocaine and
levamisole. Serial urine samples were collected for an immunochromatographic drug screen
test (Abon¯, Biopharm, China), and confirmatory testing was performed by gas
chromatography-mass spectrometry (GC/MS) in an Agilent¯ 7890A/5975C system
(USA). Urine toxicology screen was positive for cocaine and levamisole, and the
percentage of each compound measured in the first cocaine powder sample was 62.8% of
cocaine, 32.2% of levamisole, and 5% of an unidentified substance.
As there had been no significant improvement in renal function, the decision was made to
continue immunosuppressive therapy and intensify psychiatric follow-up. One month after
hospital discharge, the patient reported abstinence from cocaine, which was confirmed by
negative urine samples for cocaine or levamisole, and exhibited progressive improvement
of renal function (). On January 2016, in
the last follow-up visit, his blood pressure was 130/80 mmHg, he had a weight gain of 8
kg, and laboratory tests showed serum creatinine of 1.97 mg/dL, urinalysis with 14
leukocytes/μL, 12 erythrocytes/μL, and urine protein-to-creatinine ratio of 0.34, as
presented in . ANCA titers had decreased
to 1:160.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [49, 'years'], 'creatinine': [1.97, 'mg/dL'], 'sex': 'Male'}",40.89503,38.85028,42.93978,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 49 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.97 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.97/0.9)**-1.2 * 0.9938**49 * 1.0 = 40.89503.
Hence, the GFR value is 40.89503 ml/min/1.73 m²."
206,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-1966,Extracted,"A 24-year-old woman with 45,X syndrome comes to the physician because of diarrhea for 4 months. She also reports bloating, nausea, and abdominal discomfort that persists after defecation. For the past 6 months, she has felt tired and has been unable to do her normal chores. She went on a backpacking trip across Southeast Asia around 7 months ago. She is 144 cm (4 ft 9 in) tall and weighs 40 kg (88 lb); BMI is 19 kg/m2. Her blood pressure is 110/60 mm Hg in the upper extremities and 80/40 mm Hg in the lower extremities. Examination shows pale conjunctivae and angular stomatitis. Abdominal examination is normal. Laboratory studies show:
Hemoglobin 9.1 mg/dL
Leukocyte count 5100/mm3
Platelet count 200,000/mm3
Mean corpuscular volume 67 μmm3
Serum
Na+ 136 mEq/L
K+ 3.7 mEq/L
Cl- 105 mEq/L
Glucose 89 mg/dL
Creatinine 1.4 mg/dL
Ferritin 10 ng/mL
IgA tissue transglutaminase antibody positive
Based on the laboratory studies, a biopsy for confirmation of the diagnosis is suggested, but the patient is unwilling to undergo the procedure.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [24, 'years'], 'creatinine': [1.4, 'mg/dL'], 'sex': 'Female'}",53.87765,51.18377,56.57153,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 24 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.4 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.4/0.7)**-1.2 * 0.9938**24 * 1.012 = 53.87765.
Hence, the GFR value is 53.87765 ml/min/1.73 m²."
207,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7875644-1,Extracted,"A 50-year-old female patient who had been diagnosed with HIV 6 months previously under highly active antiretroviral therapy (HAART) was admitted for abdominal pain and mass syndrome of the left flank evolving for a month with a weight loss of 12 kg, in whom the clinical examination found a conscious patient, normotensive, with tenderness in the left flank, absence of clinical Cushing syndrome, or hyperandrogenism; the rest of the clinical examination is unremarkable.
The thoracic abdominopelvic scan () objectified a voluminous retroperitoneal tumor process centered on the left adrenal compartment badly limited irregular, containing zones of necrosis, measuring135 × 110 × 129 mm 10 HU of density, which infiltrates the great gastric curvature, the body and the tail of the pancreas without a dividing line, and the splenic vein which is laminated. Outside comes at intimate contact with a spleen includes the upper pole of the left kidney. Posteriorly, it arrives at the contact of the vertebral bodies D10, 11, and 12 and invades the left diaphragmatic pillar, the psoas muscle, and the square of the left lumbar region. Thus, it encompasses the celiac trunk and the renal artery over their entire circumference and the abdominal aorta over a circumference > 180° comes into contact with the superior mesenteric artery, and the common hepatic artery without a sign of invasion comes into contact with the inferior vena cava with a border of separation in places, associated with perilesional lymphadenopathy the largest 19 mm, left inferior lobar parenchymal nodule of 7 mm, and left supraclavicular lymphadenopathy the largest 13 mm.
Biological exploration revealed a negative endogenous hypersecretion of cortisol, negative urinary methoxylated metabolites, and no hypersecretion of androgens.
Creatinine was 5.56 mg/L, urea 0.27 g/L, natremia 139 mEq/L, kalmia 3.6 mEq/L, calcemia 100 mg/L, hemoglobin 12.3 g/dL, white blood cells 3110/mm3, and platelets 198,000/mm3, and the liver function test was unremarkable.
The patient was placed on level 2 analgesic treatment. A percutaneous biopsy of the mass was taken, showing a proliferation of atypical plasma cells. No intact tissue of the adrenal gland was found. Immunohistochemistry study revealed a negative expression of CD3 and CD20 excluding a plasmablastic lymphoma and a positive expression of CD138 and lambda light chains confirming the diagnosis of adrenal plasmacytoma ().
Further serum investigation by immunoelectrophoresis of Bence-Jones proteins was made showing a high level of lambda light chains at 45.8 mg/L (normal level between 4 and 25.1 mg/L) with the normal level of kappa light chains at 6.2 mg/L (normal level between 5.2 and 22.17 mg/L). X-rays of the skeleton did not show lesions. A sternal suction biopsy did not show any plasmacytic infiltration. The diagnosis of a solitary adrenal plasmacytoma was established.
The patient was transferred to the oncology for chemotherapy and radiotherapy. But unfortunately, she died after 3 months of following up.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [50, 'years'], 'creatinine': [5.56, 'mg/L'], 'sex': 'Female'}",111.30741,105.74204,116.87278,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 50 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 5.56 mg/L. We need to convert the concentration to mg/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 5.56 mg Serum Creatinine/10.0 dL = 0.556 mg Serum Creatinine/dL. The concentration value of 5.56 mg Serum Creatinine/L converts to 0.556 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.556/0.7)**-0.241 * 0.9938**50 * 1.012 = 111.30741.
Hence, the GFR value is 111.30741 ml/min/1.73 m²."
208,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5875003-1,Extracted,"Our case involved a 32 year-old woman affected by CF diagnosed at 6 months old, with renal diseases and hypertension in her family medical history. She also suffered from reactive arthritis since 19 years old in steroid and hydroxychloroquine therapy and had been diagnosed with CF-related diabetes at the age of 21.
After a fever episode (treated with ciprofloxacin) in October 2015 the patient’s laboratory tests showed Haemoglobin 8.2 mg/dl, serum creatinine 2 mg/dl, creatinine clearance 62 ml/min, hypocomplementemia C3. Her urinalysis pointed out hematuria (10–20 RBC/field of view) with 60% of dysmorphic erythrocytes, without proteinuria. The first clinical suspicion was a post-infectious glomerulonephritis. After that, a close follow up was conducted until December 2015. The persistent laboratory results over 8 weeks required kidney biopsy to be performed to exclude other causes of nephritic syndrome.
Light microscopy pointed out 5 sclerotic glomeruli out of 23. Main pattern was diffuse endocapillary proliferation, segmental in only a few glomeruli, with neutrophil (and less frequently lympho-monocyte) infiltration. Mesangium was characterized by deposits as well as hypercellularity and increased mesangial matrix. Interstitium showed mild edema and inflammatory cells, as well as between Tubular Basement Membrane and the above cells. A few arteries presented a fibrous intimal thickening. Arteriolar hyalinosis manifested too (Fig. and ).
Immunofluorescence assay proved strong C3 staining (3+) in granular deposits in mesangium and glomerular basement membrane (GBM). Staining was less evident in tubuli (2+). IgA staining was focal in mesangium and in only a few arteriolar walls (2+). The presence of IgG only into tubular cells was explained as the result of re-absorption (Fig. ).
The deposits were well characterized by electron microscopy. They were localized to a greater extent in mesangium, but the assay demonstrated their presence also in subendothelial and subepithelial spaces. Their confluent electrondense appearance, instead of the intensely osmiophilic ribbon-shaped deposits pathognomonic for DDD, allowed to conclude for a C3 glomerulonephritis (Fig. and ).
Complement system dysregulation was tested and resulted in a strong terminal pathway activation proved by high levels of sC5b-9 complex, amounting to 1588 ng/ml (normal value < 400 ng/ml).
Both genetics and C3NeF were investigated to determine the etiology of this altered control of alternative pathway. Next generation sequencing (NGS) showed polymorphism in CFH (p.V62I in SCR1) and THBD (p.A473V) already known as pathogenic for C3GN, as well as a mutation in C3 (p.R102G) associated only with age-related macular degeneration (AMD) so far.4
Our patient is now treated with Angiotensin-converting-enzyme inhibitors (ACEI) added to her current Cystic Fybrosis and Reactive Arthritis therapies to preserve her kidney function.
After two years of disease her renal function is stable with serum creatinine 1.7 mg/dl, creatinine clearance 50 ml/min, 24 h proteinuria 270 mg, hypocomplementemia for C3 (14 mg/dl) and haemoglobin 9.4 mg/dl.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [32, 'years'], 'creatinine': [1.7, 'mg/dL'], 'sex': 'Female'}",40.60837,38.57795,42.63879,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 32 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.7)**-1.2 * 0.9938**32 * 1.012 = 40.60837.
Hence, the GFR value is 40.60837 ml/min/1.73 m²."
209,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7990347-1,Extracted,"A 55-year-old male with ESRD due to hypertensive nephrosclerosis on PD, diabetes mellitus type two, chronic anemia, and hypertension presented to the hospital with emotional lability for three days. Several days prior to the patient’s presentation, he was prescribed valacyclovir, for orolabial herpes. The patient’s wife noticed that her husband was more confused at home, with frequent emotional outbursts and frequent emotional liability. On presentation to the emergency room, he was confused about why he was crying and denied feelings of depression or suicidal ideation. Other than recent diarrhea, he denied any other symptoms. Of note, the patient did not have any history of physiatric illness, alcohol, or drug use.
On physical exam, his vitals revealed a temperature of 36.7 °C, blood pressure of 158/97 mmHg, heart rate of 86 beats/min, and saturating at 96% on room air. He had no focal neurological deficits, or other concerning exam findings, though would cry intermittently during interviews. His labs showed sodium of 140 mmol/L, potassium 3.2 mmol/L, chloride 100 mmol/L, carbon dioxide 23 mmol/L, glucose 70 mg/dL, blood urea nitrogen (BUN) of 35 mg/dL, creatinine of 17.70 mg/dL, calcium of 6.4 mg/dL, magnesium of 1.4 mg/dL, and phosphorus of 9.8 mg/dL. White blood cell count of 8.6 10e9/L, red blood cell count of 3.93 10e12/L, hemoglobin of 11.6 g/dL, hematocrit of 34.4%. The patient also had an anion gap of 17. Blood and urine cultures were negative. The urine drug screen was also negative. The folic acid level was 10 ng/mL, B12 level was 650 pg/mL. Computerized tomography (CT) of the head showed no acute intracranial abnormality (Figure ). There was no concern for infection or issues with PD. Nephrology was consulted to manage PD; however, after reviewing the history, it was discerned that he will need more frequent PD exchanges after recently being prescribed valacyclovir. After one day of increased PD exchanges, the patient’s emotional state improved significantly.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [55, 'years'], 'creatinine': [17.7, 'mg/dL'], 'sex': 'Male'}",2.82655,2.68522,2.96788,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 55 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 17.7 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (17.7/0.9)**-1.2 * 0.9938**55 * 1.0 = 2.82655.
Hence, the GFR value is 2.82655 ml/min/1.73 m²."
210,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4364005-1,Extracted,"A 43-year-old Caucasian male was referred to Internal Medicine with complaints of left cervical mass, anorexia, and 10 kg of unintentional weight loss in 2 months. He denied any other subjective complaints, including difficulty in swallowing, breathing, or urinary symptoms. On examination, a nontender, firm mass with approximately 3 cm in diameter was present in the left cervical region, fixed to the underlying tissues. There were also nodes palpable in the left axillar and bilateral inguinal region. Subsequent computed tomography (CT) scan of the neck, thorax, and abdomen showed multiple adenopathies involving retroperitoneum, inguinal, iliac, left axillar and left cervical regions, signs of pronounced bone metastasis, and bilateral hydronephrosis (Figures and ). A biopsy of the neck lymphadenopathy was performed and interpreted as probable adenocarcinoma, strongly positive for prostate specific antigen in immunohistochemical study. Full blood count, biochemical investigation, and prostate specific antigen (PSA) were abnormal: creatinine 3.9 mg/dL (reference range (RR) 0.7–1.4 mg/dL), blood urea nitrogen (BUN) 93 mg/dL (RR: <50 mg/dL), PSA 583 ng/mL, alkaline phosphate 1592 U/L (RR: 40–130 U/L), and LDH 1086 U/L (RR: 135–225 U/L). Following consultation by urology, a digital rectal exam revealed a firm, fixed, and enlarged prostate, highly suspicious of prostate cancer. The patient denied family history of malignant neoplasms, including prostate cancer, and was never subjected to prostate exam or PSA test. He was then submitted to urgent bilateral ureteral stenting due to obstructive acute renal failure secondary to invasion of the ureteral meatus by prostate carcinoma. Transrectal ultrasonography guided prostate biopsy revealed bilateral adenocarcinoma with a Gleason score 3 + 5 = 8. The Tc-99m whole body scan confirmed the previous tomography suspicion of axial, sternum, and cranium bone metastasis (). The patient initiated complete androgen blockage and zoledronic acid. Three months later his cervical lymph node enlargement had regressed and serum PSA had decreased to 3.48 ng/mL. Unfortunately 5 months after initiation of hormonal treatment the patient presented with complaints of left red eye, exophthalmos, and sudden decrease in visual acuity (). Head CT showed an intracranial mass originating in the sphenoid bone and compressing the left eye ball. PSA had increased to 80.82 ng/mL and testosterone remained within castration level (<50 ng/dL). Chemotherapy with docetaxel associated with prednisolone was initiated after failure of standard hormonal manipulations and the patient presented clinical improvement with reduction of exophthalmos and pain complaints. After 5 cycles of docetaxel the PSA level increased to 370 ng/mL. The docetaxel, prednisolone, and zoledronic acid therapy was then substituted for denosumab and cabazitaxel, with good clinical and analytical response (current PSA level of 37 ng/mL).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [43, 'years'], 'creatinine': [3.9, 'mg/dL'], 'sex': 'Male'}",18.70503,17.76978,19.64028,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 43 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.9 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.9/0.9)**-1.2 * 0.9938**43 * 1.0 = 18.70503.
Hence, the GFR value is 18.70503 ml/min/1.73 m²."
211,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6629601-1,Extracted,"A 63-year-old man was admitted to the nephrology department for further evaluation of renal impairment and hypocalcemia. The patient was clinically diagnosed with TSC at another tertiary hospital approximately 40 years ago and had a history of hypertension and diabetes. He had not undergone thyroid or parathyroid gland surgery. Several episodes of seizures occurred when he was young. These were managed with anticonvulsants, which were maintained until several years ago. He had also been taking unidentified herbal medicine due to fatigue for a month. He had no cognitive or behavioral problems. He had large bilateral renal AMLs and underwent transcatheter arterial embolizations due to left and right side hemorrhages 24 years and 2 weeks ago, respectively. His two sons were also diagnosed with TSC based on genetic test results.
On admission, the patient complained of general weakness and muscle tremor without other neurologic symptoms, such as tetany or seizure. Physical examination revealed trace peripheral edema and facial angiofibroma only. His blood pressure was 113/67mmHg, with a pulse rate of 87/min, a respiratory rate of 18/min, and body temperature of 36.9℃. His initial laboratory findings were as follows: white blood cells, 12,760/mm3; hemoglobin, 7.9 g/dL; platelets, 365 K/mm3; blood urea nitrogen, 54 mg/dL; serum creatinine, 5.26mg/dL; alkaline phosphatase, 98 IU/L; magnesium, 2.1mg/dL; total calcium, 3.7 mg/dL (corrected calcium, 4.5mg/dL); ionized calcium, 0.591mmol/L; phosphrous, 5.0mg/dL; and albumin, 3.0 mg/dL. An electrocardiogram showed QT prolongation (QT 440 ms, QTc 508ms). Computed tomography (CT) demonstrated enlarged and distorted kidneys due to numerous AMLs and a large number of tiny nodules in both lungs, consistent with renal and pulmonary manifestations of TSC(). His baseline kidney function was not determined due to the lack of previous medical records; however, severely destructed renal parenchyma detected in CT suggested progression to advanced chronic kidney disease (CKD). Bone mineral density was within normal range (the lowest value was −0.6 for the total femur). To determine the cause of the hypocalcemia, hormonal status related to calcium homeostasis was examined, including parathyroid hormone (PTH) 44 pg/mL, 25-(OH) vitamin D3 9 ng/mL, and 1,25-(OH) 2 vitamin D3 2.8 pg/mL (reference range, 19.6-54.3 pg/mL). Urinary calcium concentration was very low(<0.8mg/dL), and the urinary calcium/creatinine ratio was <0.013mg/mg Cr. The fractional excretion of calcium(FECa) was 0.015.
The patient was initially treated with oral calcitriol 0.25 mg/day, calcium acetate 4.26 g/day, and cholecalciferol 400 IU/day, and intravenous calcium gluconate 2 g/day was administered on the first 2 days (). After 5 days of intensive calcium replacement, the total calcium concentration increased from 3.7 to 6.1mg/dL and ionized calcium from 0.591 to 0.749mmol/L, and his tremor improved. At the outpatient clinic 1 month after discharge, the total and ionized calcium levels were measured as 7.9mg/dL and 0.945mmol/L, respectively, with continuous administration of calcitriol 0.25mg/day and calcium citrate 750mg/cholecalciferol 400 IU/day.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [5.26, 'mg/dL'], 'sex': 'Male'}",11.53541,10.95864,12.11218,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 63 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 5.26 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (5.26/0.9)**-1.2 * 0.9938**63 * 1.0 = 11.53541.
Hence, the GFR value is 11.53541 ml/min/1.73 m²."
212,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6751855-1,Extracted,"An 82-year-old woman with type 2 diabetes mellitus and chronic renal failure was admitted to the hospital with a 7-day history of fever, delirium, and dyspnea. She had undergone an aortic valve replacement (Perceval sutureless bioprosthesis) 18 months prior due to aortic stenosis. The immediate post cardiac surgery period was complicated by paroxysmal atrial fibrillation, transudative left-sided pleural effusion, and oligoanuric renal failure. She did not present any infectious complications and the median sternotomy incision closed normally. Between 1 and 14 months after aortic surgery, she was admitted to the hospital five times because of severe clinical heart failure of unclear cause and some episode of paroxysmal atrial fibrillation. No fever or other signs of infection were detected at all this time, and did not receive any antibiotic treatment. A transesophageal echocardiogram performed 3 months after surgery showed an aortic prosthesis without alterations. On physical examination, her temperature was 39 °C, she was confused and tachypneic. A 3/6 systolic ejection murmur in the aortic position and basal crackles were identified. She presented grade II uninfected pressure ulcers on heels and sacrococcygeal region. Laboratory tests showed a normal blood cell count, a serum creatinine of 2.14 mg/dL, and an increased C-reactive protein (13 mg/dL) and hyperglycemia (628 mg/dL). A chest X-ray showed bilateral pleural effusion and interstitial pulmonary edema. Two sets of aerobic and anaerobic blood culture bottles were drawn at admission, and empiric ceftriaxone (2 g daily) and levofloxacin adjusted to renal function (250 mg daily, intravenous) were started. After 26 to 80 h of incubation into the BACTEC FX system (Becton, Dickinson and Company), all four blood culture bottles were positive. Gram stain showed coryneform gram-positive bacilli with occasional branching forms. After incubation on CNA agar and chocolate agar, colonies were less than 2 mm in size, glistening and yellow. The colonies penetrated into the agar upon further incubation. On the 5th day of admission, blood cultures were again obtained, and the same organism grew in 1 of the 4 bottles. The isolates were initially identified by matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS, Bruker Daltonics) as C. cellulans. Thereafter, the identification was confirmed by API Coryne strip (bioMérieux; code number 7572767), which was an “excellent identification” for C. cellulans with a reliability of 99.9%, and by sequencing the 16S rRNA (using the BLAST Sequence Analysis Tool of GenBank database), showing a 100% similarity with C. cellulans and 99.8% with C. funkei. Antimicrobial susceptibility tests were performed using a microdilution microtiter panel MICroSTREP plus 6 (MicroScan Walk Away, Beckman Coulter). Following EUCAST breakpoints criteria for Corynebacterium, the isolate was susceptible or presumably susceptible (for antibiotics without EUCAST breakpoints, but with low MIC) to amoxicillin-clavulanate (MIC = 2 mg/L), daptomycin (MIC = 0.5 mg/L), levofloxacin (MIC = 2 mg/L), linezolid (MIC≤1 mg/L), tetracycline (MIC≤1 mg/L), trimethoprim-sulfamethoxazole (MIC = 0.006 mg/L) and vancomycin (MIC = 0.5 mg/L), and resistant or presumably resistant to amikacin (MIC = 32 mg/L), cefotaxime (MIC> 2 mg/L), ciprofloxacin (MIC> 2 mg/L), clindamycin (MIC> 2 mg/L), erythromycin (MIC = 1 mg/L), gentamycin (MIC = 4 mg/L), imipenem (MIC = 4 mg/L), meropenem (MIC = 8 mg/L) and rifampin (MIC = 1 mg/L). The MICs of amoxicillin-clavulanate, cefotaxime, meropenem, trimethoprim-sulfamethoxazole and vancomycin were also determined by Etest® (bioMérieux) using Mueller-Hinton agar plus 5% blood, and similar results were found.
On the 7th day, a transthoracic echocardiogram did not show alterations. Therapy was switched to amoxicillin-clavulanate (1 g three times daily, intravenous), and new blood cultures obtained 24 h later were negative. A transesophageal echocardiogram performed on the 9th day of stay revealed an echogenic and mobile vegetation of 6 × 9 mm on the prosthetic aortic valve attached to the commissure between the right coronary cusp and the non-coronary cusp. Prosthetic valve function was otherwise normal. On the 11th day, amoxicillin-clavulanate was switched to vancomycin adjusted to renal function (750 mg daily) plus linezolid (600 mg twice daily, intravenous). Surgical replacement was considered inappropriate in this patient due to comorbidity, advanced age, limited mobility and family rejection. In the following days, she developed severe anemia, acute confusional state and refractory heart failure. End-of-life decision-making was implemented, prioritizing symptom control, and antibiotic therapy was switched back to amoxicillin-clavulanate on day 22nd of admission. On the 28th day, she was discharged to another hospital for palliative care, dying 7 days later because of sepsis and severe heart failure. A postmortem examination was not performed.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [82, 'years'], 'creatinine': [2.14, 'mg/dL'], 'sex': 'Female'}",22.57394,21.44524,23.70264,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 82 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.14 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.14/0.7)**-1.2 * 0.9938**82 * 1.012 = 22.57394.
Hence, the GFR value is 22.57394 ml/min/1.73 m²."
213,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3195138-1,Extracted,"A 61-year-old man with continuous high-grade intermittent fever associated with chills and rigor (8 days), hiccup (8 days), nausea (1–2 days), and breathlessness (1 day) reported to the outpatient department (OPD) of Neelachal Hospital Pvt Ltd, Bhubaneswar. The patient was administered with arteether 150 mg i.v. OPD in another private clinic prior to admission. The patient was a known case of hypertension with cerebrovascular accident (CVA) and right-sided hemiparesis since 13 years and was on atenolol 75 mg, amlodipine 7.5 mg, amiloride 40 mg, and aspirin 50 mg once daily.
At the time of admission, the patient was confused with temperature 104°F, pulse 110/min, blood pressure 130/80 mmHg, respiration rate 40/min, SPO2 96%, pallor, and normal blood sugar and ultrasonography (USG) of whole abdomen. An increase in serum urea (76 mg/dl), serum creatinine (3.2 mg/dl), serum glutamic oxaloacetic transaminase (40 IU/L), serum glutamic pyruvic transaminase (49 IU/L), and total leukocytic count/TLC (10600) was observed. tests for Plasmodium vivax, Plasmodium falciparum, Hepatitis C Virus (HCV), and Australian antigen were found to be negative.
The patient was diagnosed as a case of sepsis with ARF and was administered with antibiotics such as ceftriaxone and tazobactam for 4 days. However, arteether 150 mg i.v. once daily was continued as the patient belonged to a malaria prone area. There was no relief in any of the symptoms and the serum urea and creatinine levels increased progressively daily. The urine output however remained normal. Hence, on the 5th day the two antibiotics were replaced by teicoplanin and meropenem. Hemodialysis was started from the 6th day. On the 7th day, the symptoms start abated, but the serum urea (116 mg/dl) and creatinine (4.3 mg/dl) levels and the TLC (11900/cumm) were raised. On the 10th day, there was an increase in serum urea (168 mg/dl) and creatinine (4.34 mg/dl) levels and TLC (21600/cumm). Hence, the two antibiotics and arteether were stopped and administration of three diuretics (Furosemide 40 mg twice daily, torsemide 20 mg twice daily, and metolazone 5 mg once daily) and one antibiotic (Cefotaxime 1 g twice daily) were started in addition to hemodialysis once in every 3–4 days. The nephrologists administered three diuretics together with the objective that increased urination would decrease serum urea and creatinine. On the 12th day however, the TLC (31000), serum urea (219 mg/dl), and creatinine (4.64 mg/dl) increased further. The day after hemodialysis, urea and creatinine levels decreased but again increased requiring another dialysis within 3–4 days. Hence, tigecycline 50 mg twice daily on the 17th day and caspofungin 50 mg once daily on the 24th day were added. On the 29th day, the TLC decreased and another antibiotic (doripenem 250 mg twice daily) was added. On the 35th day, all the antibiotics were stopped as the TLC became almost normal (11000/cumm). However, the serum urea (400 mg/dl) and creatinine (3.6 mg/dl) remained high. The patient was diagnosed as a case of CRF and dialysis at regular intervals was recommended.
After consultation with a nephrologist from another organization, on the 41st day, two diuretics (torsemide 20 mg twice daily and metolazone 5 mg once daily) were stopped. The next day (42nd day) urea and creatinine levels decreased to 208 mg/dl and 2.2 mg/dl, respectively. On the 43rd day, furosemide was stopped. The serum urea and creatinine levels started decreasing and by 60th day, they were normal (TLC 7700/cumm, urea 27 mg/dl, and creatinine 1.1 mg/dl). Dialysis was not required further after stopping the administration of diuretics.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [61, 'years'], 'creatinine': [1.1, 'mg/dL'], 'sex': 'Male'}",76.3742,72.55549,80.19291,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 61 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.1/0.9)**-1.2 * 0.9938**61 * 1.0 = 76.3742.
Hence, the GFR value is 76.3742 ml/min/1.73 m²."
214,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5518485-1,Extracted,"A 49-year-old Dutch male patient came to King Chulalongkorn Memorial Hospital (KCMH) with a complaint of low-grade fever and profuse sweating at night for 1 week. Three weeks earlier, he was diagnosed HIV infection when antiretroviral medications comprising of tenofovir, emtricitabine, and efavirenz were prescribed. He denied taking any over-the-counter drugs. The physical examination was unremarkable except for a body temperature of 38°C. He also had normotension (blood pressure 125/75 mmHg) without orthostatic hypotension or other signs of volume depletion. The chest X-ray showed miliary pulmonary nodules compatible with miliary tuberculosis which was later confirmed by positive polymerase-chain-reaction for Mycobacterium tuberculosis in his sputum. Disseminated tuberculosis was promptly diagnosed, and antituberculosis treatment (isoniazid, rifampicin, pyrazinamide, and ethambutol) was planned. However, he also had severe azotemia at admission (BUN 53.6 mmol/L, Cr 1,230 µmol/L) in contrast to his baseline values from one month earlier (Cr 115 µmol/L). At that time, there were no evidences of uremic symptoms or volume overload, and he still voided 500 mL of urine per day. Urinalysis revealed isosthenuria with bland urinary sediments (specific gravity 1.010, pH 5.0, albuminuria trace, glycose negative, WBC 0-1/hpf, and RBC 0-1/hpf). Renal ultrasonography demonstrated normal size and contour of both kidneys. Urine biomarker for renal tubular injury, neutrophil gelatinase-associated lipocalin (NGAL), was markedly elevated (7,891 ng/mL). Acute kidney injury was diagnosed and likely caused by nephrotoxic acute tubular necrosis (ATN) even though a renal biopsy had not been done. In the absence of other offending drugs or conditions, tenofovir was suspected to be a causal drug for ATN resulting in an adjustment of the antiretroviral regimen (abacavir, lamivudine, and raltegravir).
In the absence of uremic symptom or volume overload, PD was, nevertheless, initiated due to high level of nitrogen catabolites. The flexible double-cuffed PD catheter was inserted on day 4 of admission, and automated PD (Homechoice cycler®; Baxter) using a total dialysate (Dianeal®; Baxter) volume of 10 L (initial fill volume of 700 mL, 14 cycles, 20 hours) was promptly started on the same day of the catheter insertion. PD dose was gradually increased to achieve the total dialysate volume of 20 L per day in the next few days. The delivered dose of PD by total weekly Kt/V and total weekly creatinine clearance (CCr) were 3.23 and 97.84 L/week, respectively. After a week of automated PD, nitrogen catabolites decreased gradually (BUN 27.8 mmol/L, Cr 840 µmol/L). At one month, his urine volume had increased to 1 L per day, but measured renal CCr was still at 4 mL/min/1.73 m2 which reflected inadequate recovery of renal function. He was discharged on day 31 of admission with continuation of automated PD at a total dialysate volume of 10 L per day. At follow-up visit, the patient showed gradually improvement in renal function and the dose of PD was tapered accordingly. Eventually, PD could be discontinued at 4 months after the onset of AKI. The patient attained stable serum Cr of 124 µmol/L and measured CCr of 29 mL/min/1.73 m2 afterwards.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [49, 'years'], 'creatinine': [124.0, 'µmol/L'], 'sex': 'Male'}",63.96379,60.7656,67.16198,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 49 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 124.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 124.0 µmol. To convert 124.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 124.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00012 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00012 mol Serum Creatinine * 113.12 g/mol = 0.01357 g Serum Creatinine. To convert 0.01357 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01357 g Serum Creatinine * 1000.0 mg/g = 13.57 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 13.57 mg Serum Creatinine/10.0 dL = 1.357 mg Serum Creatinine/dL. The concentration value of 124.0 µmol Serum Creatinine/L converts to 1.357 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.357/0.9)**-1.2 * 0.9938**49 * 1.0 = 63.96379.
Hence, the GFR value is 63.96379 ml/min/1.73 m²."
215,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7682974-1,Extracted,"A 30-year-old woman and known case of liver transplantation due to decompensated cirrhosis secondary to autoimmune hepatitis from 5 years ago was admitted to the emergency room of Taleghani Hospital, a teaching referral hospital in Tehran, Iran, with fever, chills, watery (non bloody) diarrhea, nausea, vomiting, abdominal pain, and loss of appetite. She had experienced an episode of rejection 2 years after her liver transplant manifested by an elevation in liver enzymes up to 3 times the upper limit of normal and a total bilirubin increase. Fortunately, abnormal liver function tests completely responded to the typical pulse regimen of methylprednisolone. After that, she underwent an inevitable splenectomy because of severe pancytopenia, multiple tortuous venous collaterals and multiple hypodense parenchymal infarcts in the spleen attributed to huge splenomegaly and hypersplenism. At the time of admission, physical examination revealed her vital signs to be body temperature: 39oC, heart rate: 110 beats per minute, respiratory rate: 21 times per minute, and blood pressure: 120/75 mmHg. Her cardiac and chest examination were unremarkable. Her chest spiral CT scan showed no specific abnormality ().
The patient’s abdomen was soft, but a generalized abdominal tenderness was remarkable in her physical examination. Her liver function profile showed aspartate aminotransferase (AST): 18 IU/l, alanine aminotransferase (ALT): 15 IU/l, alkaline phosphatase (ALP): 254 IU/l, total bilirubin: 0.4 mg/dl, direct bilirubin: 0.2 mg/dl, albumin: 3.8 gr/dl. Her coagulopathy parameters were PT=13 seconds, INR=1, and PTT=32 seconds. Stool exam was non inflammatory without WBC or RBC and no evidence of parasitic infection. Urine, blood, and stool cultures were all negative. Complete blood counts (CBC) were as follows: white blood cells (WBC)=10100 cells per cubic millimeter, hemoglobin (Hb)=10.1 gr/dl, mean corpuscular volume (MCV)=79.6 fl, platelet (Plt)=310000 per microliter. C-reactive protein (CRP) was 18 mg/l and erythrocyte sedimentation rate (ESR) was measured 22 mm/hr. Kidney function tests were BUN=23 mg/dl, and creatinine=2.1 mg/dl at the time of admission and 1.4 mg/dl at the time of discharge, natrium=139 meq/l and Kalium=4.2 meq/l. Trough level of tacrolimus was 8.7 ng/ml, which is within accepted range. CMV PCR and toxin A&B stool assays for clostridium difficile were negative. The patient previously took cellcept 1500 mg per day in divided doses, prograf (tacrolimus) 4 mg per day in divided doses, prednisolone 10 mg per day, aspirin 80 mg daily, levothyroxine 200 microgram daily, calcium-vitamin D supplement, folic acid 1 mg per day, and ferrous sulfate 60 mg daily. Initially, the patient was asked to discontinue cellcept because of an increased risk of developing severe sepsis in such circumstances. Hydration and empiric antibiotic therapy were started. Nephrology consult was requested because of a rise in serum BUN and creatinine level probably due to prerenal azotemia. Ultrasonography revealed a decrease in kidney size and an increase in corticomedullary differentiation, indicating an episode of acute kidney injury in addition to a preexisting chronic kidney disease. Moreover, ultrasonography findings revealed a normal orthotopic liver in size and contour. Normal intra and extra biliary ducts were detected. Color Doppler ultrasound demonstrated normal flow, size and patency of orthotopic vessels including portal vein, superior mesenteric vein, inferior venacava, and splenic vein before and at anastomosis sites.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [30, 'years'], 'creatinine': [2.1, 'mg/dL']}",31.90753,30.31215,33.50291,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 30 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.1 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.1/0.7)**-1.2 * 0.9938**30 * 1.012 = 31.90753.
Hence, the GFR value is 31.90753 ml/min/1.73 m²."
216,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3914222-1,Extracted,"A 57-year-old Caucasian female with a history of hypertension came to the emergency department (ED) for evaluation of worsening nonproductive cough and exertional dyspnea for 2 weeks. She had gone to her primary care physician for the above-mentioned symptoms and was given cephalexin. Despite completing the course of antibiotic, her symptoms progressed. She developed a diffuse body rash 2 days after starting cephalexin and complained of diffuse joint pain and malaise for 2 weeks. She denied having abdominal pain, fever, or hemoptysis and was not using any other nephrotoxic drugs including over the counter medications. Laboratory studies performed by the primary care physician 2 weeks prior, to presentation, including renal function tests, were unremarkable.
Vital signs in the ED were BP: 132/86, P: 118, R/R: 20, and afebrile. Oxygen saturation was 94% on 2 L/min nasal cannula and lung auscultation was normal. She had a diffuse maculopapular rash on the anterior chest wall, trunk area, and all extremities. Laboratory results showed sodium 127 mmol/L (132–150 mmol/L), potassium 3.8 mmol/L (3.5–5.5 mmol/L), bicarbonate 22.7 mmol/L (23–31 mmol/L), BUN 38 mg/dL (5–23 mg/dL), creatinine 4.39 mg/dL (0.44–1.03 mg/dL), chloride 93 mmol/dL (91–110 mmol/dL), calcium 8.3 mg/dL (8.7–10.2 mg/dL), and anion gap 9.3 (3–11). Urine analysis at admission showed specific gravity 1.006 (1.010–1.025), blood 3+, ph 5 (4.5–8.5), protein 1+, RBC ≥ 100, WBC 0–5, negative nitrites, negative leukocyte esterase, and no casts. WBC count at admission was 8400 with no shift, and hemoglobin and hematocrit were 8.8 and 25.8, respectively. Chest X-ray showed no acute pulmonary pathology. At the time of admission, the differential diagnoses were (1) drug-induced interstitial nephritis, (2) postinfectious glomerulonephritis, (3) acute tubular necrosis, and (4) pulmonary-renal syndrome including Goodpasture's syndrome, microscopic polyangiitis, or Wegener's granulomatosis.
Cephalexin was stopped and she was started on IV hydration but responded poorly and remained oliguric. Additional laboratory studies revealed negative urine eosinophils, normal C3 and C4 levels, and negative ANA, rheumatoid factor, and ASO titers. ANCA at admission was positive at ≥1 : 20 with a perinuclear pattern, confirmed as MPO (myelo-peroxidase) ANCA on ELISA. Anti-GBM IgG antibody was positive with titer 234 au/mL (0–19 au/mL). Repeated chest X-ray on day 4 and day 5 revealed development of bilateral alveolar infiltrates. She underwent bronchoscopy which showed evidence of alveolar hemorrhage, and lung biopsy which disclosed acute fibrinous and interstitial pneumonia with interstitial neutrophils but no granulomas. Renal biopsy also was performed.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [57, 'years'], 'creatinine': [4.39, 'mg/dL'], 'sex': 'Female'}",11.13452,10.57779,11.69125,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 57 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 4.39 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (4.39/0.7)**-1.2 * 0.9938**57 * 1.012 = 11.13452.
Hence, the GFR value is 11.13452 ml/min/1.73 m²."
217,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6890328-1,Extracted,"A 41-year-old man was transferred to the intensive care unit of a local hospital (Quzhou, China) because of severe rhabdomyolysis with AKI and acute respiratory distress syndrome (ARDS), on October 28, 2018. Twenty years ago, he had dark-colored urine after exercise. Approximately 15 years ago, he had the same symptom after severe cold with high fever; he was diagnosed with rhabdomyolysis, from which he recovered after general treatment. In the present condition, the patient reported of high fever, general malaise, myalgia, dyspnea, and dark-colored urine, and then progressed to anuria. An annual physical examination of the patient revealed no abnormal renal function. He never smoked and was an occasional drinker. He belonged to the ethnic Han community and had no prior family history of this disease. Physical examination on admission revealed oliguria, suppurated tonsils, poor hemoglobin saturation, alert consciousness, normal neurological signs and reflexes, arterial blood pressure of 165/95 mm Hg, and heart rate of 112 bpm. The initial laboratory investigations showed positive test results for inflammation (circulating leukocytes, 32.3 × 109/L; C-reactive protein, 58.5 mg/L), high serum myogenic enzyme levels (aspartate aminotransferase, alanine aminotransferase, lactic dehydrogenase, and creatine kinase were 2 420, 623, 1 531, and 136 365 IU/L, respectively), and evidence of AKI at 48 h (proteinuria, 3+; urine occult blood test, 3+; blood urea nitrogen, 4.59–23.78 mmol/L; serum creatinine, 88.3–510 μmol/L). The serological test results for cytomegalovirus, Epstein–Barr virus, anti-glomerular basement membrane antibody, antinuclear autoantibodies, and other autoantibodies were negative. He was diagnosed with rhabdomyolysis with AKI and ARDS. The patient recovered successfully from ARDS with intubation and ventilator support, as well as continuous renal replacement therapy (CRRT); he was then removed from hemodialysis on day 48 of illness. Although he had normal 24-hour urine volumes, his renal function recovered gradually with abnormal serum creatinine during the 3-month follow-up period (Fig. ).
Repetitive rhabdomyolysis following fever or exercise prompted us to investigate genetic and metabolic disorders. The blood carnitine level was detected by high performance liquid chromatography-tandem mass spectrometry and whole exome sequencing after obtaining a signed consent form.
Adiacyl carnitine [C6DC] and 3-hydroxyoctadecyl carnitine [C18:1OH] were twice the normal upper limit (see Table, Supplemental Content, which illustrates the increased level of blood carnitine). The level of other carnitines was marginally higher than the normal upper limit. The abnormal carnitine levels showed carnitine metabolism dysfunction. There were 2 novel heterozygous and relatively rare mutation sites of CPT II (c.482G>A and c.1493G>T) (Fig. ).
The missense mutation c.482G>A leads to an amino acid change of p.Arg161Gln. Its frequency is <1%‰ in the Genome Aggregation Database (gnomAD) and 0.2‰ in the general East Asian population. This variant has not been included in the 1000-genome project (genomic data for 2504 individuals from 5 populations), Exome Aggregation Consortium (ExAC) Exome Sequencing Project v. 6500 (ESP6500), Taiwan 500, CG69 (69 individuals with complete genomes), and local databases. The variant c.482G>A has not been reported. Neither the Human Gene Mutation Database (HGMD) nor ClinVar database (public archive of relationships among sequence variation and human phenotype) includes the mutation. The functional prediction showed the variant to be pathogenic. The predicted REVEL (Rare Exome Variant Ensemble Learner) and ClinPred (Prediction Tool to Identify Disease-Relevant Nonsynonymous Single-Nucleotide Variants) were 0.746 and 0.786, respectively.
The mutation c.1493G>T leads to an amino acid change of p.Arg498Leu. Its frequency in the general population is <1‰ in the ExAC and gnomAD databases and 0 in East Asian population. The variant is not included in the 1000 genome, ESP6500, Taiwan 500, cg69, and local databases. The variant c.1493G>T has not been reported. Neither the HGMD nor ClinVar database includes the mutation. The functional prediction showed it to be pathogenic; the predicted REVEL and ClinPred were 0.978 and 0.999, respectively.
The mutation c.1493G>T was verified using maternal peripheral blood. However, as paternal peripheral blood was not collected, the variation source of c.482G>A could not be determined. Furthermore, a genetic test related to the clinical phenotype was conducted; we did not identify any more gene mutations in the patient. Through bioinformatics analysis, data filtering, and comprehensive analysis, no pathogenic variation was found in the 59 genes recommended by the American College of Medical Genetics and Genomics Guidelines.
At 4 weeks after recovery, his urine output was almost normal. The blood creatinine kinase activity returned to the normal range without any muscle pain symptom. However, the patient refused renal biopsy. Even after >140 days of follow up, his renal function was abnormal, and was diagnosed as chronic kidney disease stage 3a with persistent microalbuminuria. He was then administered valsartan tablets at a dosage of 80 mg per day and L-carnitine supplements as the main course of treatment.
The research was approved by the ethics committee of Zhejiang Provincial People's Hospital. Patient has provided informed consent for publication of the case.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [41, 'years'], 'creatinine': [510.0, 'µmol/L'], 'sex': 'Male'}",11.83906,11.24711,12.43101,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 41 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 510.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 510.0 µmol. To convert 510.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 510.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00051 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00051 mol Serum Creatinine * 113.12 g/mol = 0.05769 g Serum Creatinine. To convert 0.05769 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.05769 g Serum Creatinine * 1000.0 mg/g = 57.69 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 57.69 mg Serum Creatinine/10.0 dL = 5.769 mg Serum Creatinine/dL. The concentration value of 510.0 µmol Serum Creatinine/L converts to 5.769 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (5.769/0.9)**-1.2 * 0.9938**41 * 1.0 = 11.83906.
Hence, the GFR value is 11.83906 ml/min/1.73 m²."
218,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-453,Extracted,"Two hours after admission to the hospital for dialysis, a 63-year-old woman has severe pain in her lower back. The pain is 8 out of 10 in intensity and radiates down the legs. She underwent a laparoscopic cholecystectomy 4 years ago. She has hypertension, chronic kidney disease, type 2 diabetes mellitus, and major depressive disorder. She lives with her daughter and reports frequent fights with her at home. Her current medications include sertraline, insulin, enalapril, sodium bicarbonate, and sevelamer. She appears uncomfortable. Her temperature is 37.3°C (99.1°F), pulse is 102/min, respirations are 15/min, and blood pressure is 132/94 mm Hg. There is severe tenderness on palpation over the L2 vertebra; range of motion is limited. Neurologic examination shows no focal findings. Laboratory studies show:
Hemoglobin 10.1 g/dL
Leukocyte count 8,700/mm3
Platelet count 130,000/mm3
Serum
Na+ 136 mEq/L
Cl- 101 mEq/L
K+ 5.1 mEq/L
Calcium 8.2 mg/dL
Urea nitrogen 33 mg/dL
Glucose 190 mg/dL
Creatinine 3.8 mg/dL
An x-ray of the spine shows a wedge compression fracture of the L2 vertebra.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [3.8, 'mg/dL'], 'sex': 'Female'}",12.75507,12.11732,13.39282,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 63 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 3.8 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (3.8/0.7)**-1.2 * 0.9938**63 * 1.012 = 12.75507.
Hence, the GFR value is 12.75507 ml/min/1.73 m²."
219,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7357330-1,Extracted,"A 72-year-old African-American male with a history of hypertension, diabetes mellitus, and stage IV pancreatic adenocarcinoma status post gastric-biliary bypass and chemoradiation therapy presented with a one-day history of coffee-ground emesis. On admission, he was afebrile and hemodynamically stable. Physical examination was remarkable for severe muscle wasting, cachexia, and abdominal distention with decreased bowel sounds. Laboratory examination revealed bicarbonate 19 mEq/L, chloride 98 mEq/L, lactate 3.8 mmol/L, sodium 138 mEq/L, random blood glucose 212 mg/dL, blood urea nitrogen (BUN) 23 mg/dL, creatinine (Cr) 1.9 mg/dL, albumin 2.1 g/dL, white blood cell (WBC) 9.4 K/uL, hemoglobin 9.8 g/dL, and international normalized ratio (INR) 1.2. CT abdomen with oral contrast revealed gastric distention with a transition point at the level of duodenal bulb/pyloric region and large volume ascites.
He was initially suspected to have gastric outlet obstruction due to the imaging findings. Esophagogastroduodenoscopy (EGD) showed diffuse exudative esophagitis involving most of the esophagus with clear demarcation line between the necrotic esophagus and gastric mucosa (Figure ).
Biopsies were taken for pathology. Gastroenterostomy anastomosis from his prior surgery was noted in the distal stomach, which showed no luminal stenosis. A large infiltrating mass, consistent with the known pancreatic cancer, was noted in the distal second part of the duodenum, obstructing the duodenal lumen (Figure ).
The patient was kept nil per os and was started on intravenous pantoprazole. Pathology report of esophageal biopsy showed fibrin-inflammatory debris. Special stain for Gomori methenamine silver (GMS) was positive for scattered budding yeasts, and rare fungal pseudohyphae or hyphae. The patient was prescribed a course of oral fluconazole to treat Candida esophagitis; however, he was lost to follow-up.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [72, 'years'], 'creatinine': [1.9, 'mg/dL'], 'sex': 'Male'}",37.01711,35.16625,38.86797,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 72 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.9 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.9/0.9)**-1.2 * 0.9938**72 * 1.0 = 37.01711.
Hence, the GFR value is 37.01711 ml/min/1.73 m²."
220,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-6209,Extracted,"A 27-year-old woman presents to the emergency department with weakness of her legs which has progressed to an inability for her to stand. The patient works as a school teacher in Alaska and regularly goes hiking and camping. She recently returned from a camping trip where she hiked through tall brush and drank from mountain streams. The patient was also involved in a motor vehicle accident 2 days ago but did not seek treatment. The patient has a medical history that is unremarkable and is currently taking multivitamins and other than a recent bout of diarrhea is generally healthy. Her temperature is 99.5°F (37.5°C), blood pressure is 120/68 mmHg, pulse is 120/min, respirations are 17/min, and oxygen saturation is 98% on room air. Physical exam is notable for a very anxious woman with 1/5 strength of the patient’s lower extremities and 2/5 strength of her trunk muscles with diminished sensation. Laboratory studies are ordered as seen below.

Hemoglobin: 15 g/dL
Hematocrit: 43%
Leukocyte count: 6,500/mm^3 with normal differential
Platelet count: 194,000/mm^3

Serum:
Na+: 138 mEq/L
Cl-: 102 mEq/L
K+: 4.4 mEq/L
HCO3-: 24 mEq/L
BUN: 20 mg/dL
Glucose: 120 mg/dL
Creatinine: 1.0 mg/dL
Ca2+: 10.2 mg/dL
pH: 7.44
PaCO2: 10 mmHg
PaO2: 90 mmHg
AST: 12 U/L
ALT: 10 U/L

The patient complains about difficulty breathing. Repeat laboratory values are notable for the findings below.

pH: 7.35
PaCO2: 30 mmHg
PaO2: 80 mmHg

The patient is intubated and sent to the MICU.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [27, 'years'], 'creatinine': [1.0, 'mg/dL'], 'sex': 'Female'}",79.18799,75.22859,83.14739,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 27 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.0/0.7)**-1.2 * 0.9938**27 * 1.012 = 79.18799.
Hence, the GFR value is 79.18799 ml/min/1.73 m²."
221,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6375024-1,Extracted,"A 35-year-old diabetic male with chronic kidney disease (CKD) stage 5 due to biopsy-proven immunoglobulin A nephropathy and on hemodialysis thrice weekly since 14 months presented with acute onset pain of calf muscle in right lower limb, immediately after dialysis session. It was presumed to be muscle fiber tear secondary to intense muscle cramps and he was treated with analgesics. Pain worsened over the week, with patient experiencing severe pain while walking. Ultrasound examination revealed intense muscle edema. No area of liquefaction suggestive of abscess was seen. He had poor glycemic control, with glycosylated hemoglobin being 8.6%. He had hemoglobin of 9.7 g/dl; total leucocyte count (TLC) of 8790 cells/mm3, with polymorphonuclear neutrophils constituting 70%. Serum creatinine was 11.5 mg/dl, serum creatine phosphokinase (CPK) was 365 units/liter (normal reference range 24–175 units/liter), and calcium, phosphorus, and albumin were within normal limits. Magnetic resonance imaging (MRI) of the involved limb showed hyperintense signal in the upper gastrocnemius muscle on T2-weighted images []. He was treated with analgesics and antiplatelet agents, clopidogrel 75 mg with aspirin 150 mg/day. Three days later patient had relief of symptoms and he was able to walk without a limp for the first time since the pain started. The muscles became supple and gradually over the next 2 weeks, the pain disappeared. There was no recurrence over the ensuing period of nearly 26 months.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [35, 'years'], 'creatinine': [11.5, 'mg/dL'], 'sex': 'Male'}",5.3704,5.10188,5.63892,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 35 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 11.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (11.5/0.9)**-1.2 * 0.9938**35 * 1.0 = 5.3704.
Hence, the GFR value is 5.3704 ml/min/1.73 m²."
222,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7791697-1,Extracted,"In November 2019, a 37-year-old man with no underlying disease presented with pain, a rash, and swelling in the right thigh. Two days prior, he was stung by a sea anemone while scuba diving in Cebu, Philippines. He was administered a tetanus injection at a hospital in Philippines. We made the diagnosis based on the characteristic shape of the wounds, which were caused by a sea anemone tentacle, and the patient’s statement.
On admission, generalized swelling and redness were observed on the right leg. A 20 × 15 cm wound and a purpuric, reticulated patch were observed on the right thigh (Fig. a). His blood pressure was 100/60 mmHg, and his body temperature was 36.6 ℃. His white blood cell count was 17,900 cells/mm3, hemoglobin level was 13.9 g/dL, platelet count was 303,000/mm3, blood urea nitrogen (BUN) level was 51 mg/dL, creatinine level was 5.12 mg/dL, aspartate aminotransferase level was 370 IU/L, alanine aminotransferase level was 209 IU/L, and serum creatine phosphokinase level was 401 IU/L (1-171 IU/L). Urine blood was + 2 positive, and RBC count was 0–1/HPF. Rhabdomyolysis was suspected, and subsequently, fluid therapy was initiated.
On day three, his platelet count rapidly decreased (36,000 cells/mm3); and renal dysfunction (BUN and creatinine concentrations were 85 and 9.86 mg/dL, respectively) gradually worsened. Oliguria was confirmed along with worsening pulmonary edema. Therefore, we initiated conventional hemodialysis.
On day four, his body temperature was 38.4 ℃ and C-reactive protein (CRP) concentration was 5.097 mg/dL. We suspected sepsis due to cellulitis and initiated broad-spectrum antibiotics. His white blood cell count was 10,760 cells/mm3, and leukocytosis was better than that at the time of the emergency visit. Fever was observed only once (38.4 ℃), and subsequently, his body temperature was normal. His blood pressure was also stable. Blood culture test results were negative; therefore, cellulitis was confirmed without diagnosis of sepsis. We also excluded disseminated intravascular coagulation since the results in our case fulfilled only two of the four Korean Society of Thrombosis and Hemostasis disseminated intravascular coagulation (DIC) criteria. DIC can be diagnosed when three or more of the following diagnostic criteria are satisfied: (1) Positive fibrin degradation products or D-dimer, (2) Platelet count < 100,000 cells/mm3, (3) Fibrinogen concentration < 150 mg/dL, and (4) prothrombin time (PT) ≥ 3 sec or activated partial thromboplastin time (aPTT) ≥ 5 sec []. In our case, the D-dimer and fibrinogen concentrations were 5.48 µg/mL (0-0.5 µg/mL) and 542 mg/dL, respectively, and PT and aPTT were 12 sec (0.4–13.3 sec) and 29.6 sec (23.2–39.4 sec), respectively.
The hemoglobin levels decreased to 7.4 g/dL with progressive thrombocytopenia and renal dysfunction. His blood lactate dehydrogenase (LDH) level was 3,354 IU/L (150–550 IU/L), and his haptoglobin levels decreased to 10 mg/dL (50–320 mg/dL). Schistocytes were observed on the peripheral blood (PB) smear, and the patient complained of a mild headache. We suspected thrombotic microangiopathy syndrome based on microangiopathic hemolytic anemia, thrombocytopenia, and renal dysfunction. Thrombotic thrombocytopenic purpura (TTP) could not be ruled out until ADAMTS-13 results were available. Therefore, we performed a plasma exchange until ADAMTS-13 results were obtained. Complement sampling was performed prior to plasma exchange. The concentrations of serum complement 3 and complement 4 were 109.9 mg/dL (90–180 mg/dL) and 35.6 mg/dL (10–40 mg/dL), respectively, antinuclear antibody was negative, concentrations of antineutrophil cytoplasmic antibody was 0.21 U/mL (≤ 0.9 U/mL), anti-glomerular basement membrane antibody was 0.8 U/mL (< 20.0 U/mL), and ADAMTS-13 was 46.9%. Since TTP was excluded based on normal ADAMTS-13 level, we discontinued plasma exchange. After discontinuation of plasma exchange, the platelet count began to increase. The genetic test results associated with atypical HUS were normal. Genetic testing was performed at the Department of Laboratory Medicine, Samsung Seoul Hospital. A total of 18 genes (C3, C4BPA, C4BPB, CD46, CFB, complement factor H (CFH), CFHR1, CFHR2, CFHR3, CFHR4, CFHR5, CFI, DGKE, LMNA, THBD, MMACHC, PLG, ADAMTS-13) were tested. No clinically significant variants were detected in any of the 18 genes, including the CFH gene that accounts for about 22% of atypical HUS. Based on the above results, the patient was diagnosed with HUS caused by a sea anemone toxin. We continued conventional treatment that included hemodialysis, blood transfusion, and antibiotic administration. The wound turned necrotic, and it was debrided and dressed with betadine-soaked dressings (Fig. b).
On day 10, the hemoglobin level and platelet count normalized. In addition, the urine volume gradually increased, and hemodialysis was discontinued. The serum creatinine level was 7.2 mg/dL, LDH level decreased, and haptoglobin level normalized.
On day 21, the CRP level was 0.874 mg/dL. Therefore, we discontinued antibiotic administration. The wound was healing (Fig. c), and there was no pain or swelling on the right thigh. Even after discontinuing hemodialysis, the serum creatinine level continued to decrease and serum hemoglobin level remained stable (Fig. ). Additionally, the serum haptoglobin level, LDH level, platelet count, and schistocyte count on the PB smear were stable (Figs. and ). We continued wound dressing, blood tests and kept him under close observation. Finally, he was discharged on day 28. Six months after discharge, his serum creatinine level, hemoglobin level, and platelet count were normal.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [37, 'years'], 'creatinine': [5.12, 'mg/dL'], 'sex': 'Male'}",14.00613,13.30582,14.70644,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 37 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 5.12 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (5.12/0.9)**-1.2 * 0.9938**37 * 1.0 = 14.00613.
Hence, the GFR value is 14.00613 ml/min/1.73 m²."
223,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8013637-1,Extracted,"A 76-year-old man with comorbidities including hypertension, dyslipidemia, chronic renal disease (serum creatinine: 1.6 mg/dL), ischemic coronary disease, and Behçet’s disease underwent percutaneous coronary artery intervention through the right femoral artery with a 6 Fr sheath, and the Angio-Seal device was used for the closure of the access site. Three days after discharge, the patient experienced intermittent claudication, and he was re-admitted to our hospital. The ankle-brachial pressure index (ABI) had worsened starting from before, to immediately after, and 3 days after the intervention (1.03, 0.88, and 0.63, respectively). Procedure-related arterial stenosis was suspected, and he was referred to the Department of Vascular Surgery.
An initial survey with DUS revealed a heterogeneous echogenic mass in the proximal superficial femoral artery (SFA) that caused hemodynamically significant stenosis, which was indicated by high blood flow of more than 4 m/s ( and ()). The “anchor” of the Angio-Seal, which should be tagged to the intra-arterial lumen, cannot usually be observed as such a mass. Therefore, we assumed that the collagen sponge connected to the suture was misplaced into the arterial lumen. Contrast-induced computed tomography (CT) revealed that the access site was in the SFA and was adjacent to arterial wall calcification (). Surgical re-intervention was required for the stenosis with clinical ischemic symptoms, high blood flow on DUS, and low ABI. We considered endovascular intervention, including stenting or stent-grafting, to be contraindicated in this case because the punctured site was located in the inguinal region, a so-called “non-stenting zone.”
An incision in the femoral artery revealed the intra-arterial lumen with an artifact mass, granulation, and small blood clots (). After atherectomy and patchplasty, the ABI improved to the normal range (1.06).
The pathological findings revealed that the resected specimen included a sponge-like artifact and granulation accompanied by inflammatory cells. The postoperative course was uneventful, and the patient was discharged on postoperative day 3.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [76, 'years'], 'creatinine': [1.6, 'mg/dL'], 'sex': 'Male'}",44.37709,42.15824,46.59594,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 76 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.6 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.6/0.9)**-1.2 * 0.9938**76 * 1.0 = 44.37709.
Hence, the GFR value is 44.37709 ml/min/1.73 m²."
224,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6235430-1,Extracted,"A 48-year-old male farmer, born in Jaguaribe and living in Pereiro, in the State of Ceara, Northeast Brazil, had hematuria, enlarged abdomen and skin pallor. After 5 months, he evolved with disorientation and dyspnea on exertion and was taken to the hospital. Physical examination showed skin and mucous membrane pallor, hepatosplenomegaly and lower-limb edema.
The patient had a history of cigarettes and alcohol consumption. The first laboratory tests showed creatinine 4.3 mg/dL, urea 246 mg/dL (), hypergammaglobulinemia in plasma protein electrophoresis, in urinalysis 369 red cells per high-power field and proteinuria (1+/4+). Due to evident signs of AKI, classified as KDIGO 3, hemodialysis was started. On the same day, rK39 antigen test was positiveand a bone marrow aspirate evidenced amastigote-like forms of Leishmania donovani, confirming VL diagnosis. Leishmania antigen dosage was not performed. Serologies for hepatitis virus B, C and HIV were negative. Complement test levels were C3-55 mg/dL and C4- 15 mg/dL. VDRL, p-ANCA, c-ANCA, FAN and anti-ds-DNA tests showed negative results. Renal biopsy showed rapidly progressive, post-infectious glomerulonephritis with mesangial hypercellularity and endocapillary proliferation (). Immunofluorescence was positive for IgM, C3 and C1q. The Polymerase Chain Reaction (PCR) assay for Leishmania on the renal biopsy was not performed. Treatment consisted of liposomal amphotericin B 200 mg a day for 7 days and 1 g of methylprednisolone a day for three days. Renal function improved and dialysis was discontinued (). The transthoracic echocardiography showed ejection fraction (EF) of 51%, significant tricuspid regurgitation and moderate mitral regurgitation, mild pericardial effusion in the left ventricle (LV) and significant pericardial effusion in the left atrium, with eccentric LV hypertrophy. The patient was discharged with the following prescriptions: enalapril, amlodipine and prednisone 60 mg/day. Five months later, the man sought medical care at the emergency room due to symptoms of cardiac decompensation, wheezing, irregular heart rhythm with a fourth heart sound. The electrocardiography showed atrial fibrillation and the transthoracic echocardiography showed EF of 25%, moderate mitral regurgitation, atrial fibrillation (AF) and dilated cardiomyopathy showing systolic function worsening. He also had positive IgG antibodies for Chagas disease by two methods (ELISA – titer > 1.8 and IFA – titer > 1:160), but there was no need for dialysis during this second hospitalization and the heart condition was defined as a complication of chronic Chagas disease. After compensating for his medical condition, the patient was discharged, is currently receiving outpatient care, and is no longer taking prednisone (the patient has already weaned it). He is currently receiving enalapril, 5 mg a day, carvedilol 12.5 mg twice a day, digoxin 0.25 mg a day, spironolactone 25 mg, furosemide 40 mg/day and warfarin 7.5 mg/day.
Clinical and laboratory findings, after the patient was discharged from the hospital, confirmed the patient's renal function improvement throughout the months ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [48, 'years'], 'creatinine': [4.3, 'mg/dL']}",16.12757,15.32119,16.93395,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 48 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 4.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (4.3/0.9)**-1.2 * 0.9938**48 * 1.0 = 16.12757.
Hence, the GFR value is 16.12757 ml/min/1.73 m²."
225,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3914125-1,Extracted,"A 50-year-old woman with a past medical history of hypertension treated with lisinopril and chronic obstructive pulmonary disease was seen by her primary care physician five months prior to admission presenting with lower abdominal pain. Her review of systems was negative at the time except for decreased bowel movements. After being diagnosed with constipation the patient presented again one month later with lower abdominal pain localized to the left lower quadrant and low grade fevers. The patient was sent home with ciprofloxacin and metronidazole for 14 days for suspicion of diverticulitis.
Though the symptoms abated somewhat the patient again presented with pain suggestive of cholecystitis. She underwent an abdominal computed tomography scan () which incidentally identified a confluent soft tissue mass tracking along the retroperitoneum encasing the surrounding vessels. Seemingly not related to her current symptoms the patient was asked to follow up with another radiological scan in a few months. A hepatobiliary iminodiacetic acid scan confirmed cholecystitis and a cholecystectomy was performed.
One month later though her initial pain had resolved after the surgery she complained of a constant low grade pain described as progressively worsening, nonradiating, and epigastric accompanied by nausea, vomiting, fatigue, and anorexia for 5 days. She reported recent decrease in urine output and 20 pound weight loss over the last 4 months. The patient denied fevers, chills, dysuria, diarrhea, constipation, or blood in stool or urine.
Physical Exam with blood pressure 162/91 mmHg, pulse 79 bpm, temperature 98°F (36.7°C), respiratory rate 18, and SpO2 99% on room air. She was alert, well appearing, and in no distress, oriented ×3. Abdomen was nondistented, bowel sounds were normal, slight epigastric tenderness without hepatosplenomegaly, rebound, or guarding. Rest of her exam including neck, chest, cardiac, back, and extremities exam was within normal limit.
Her pertinent labs included Sodium 146 mEq/L, Potassium 5.1 mEq/L, Creatinine 8.18 mg/dL (baseline 0.8 mg/dL), white blood cell count 10.4 K/uL, hemoglobin 13.1 g/dL, hematocrit 40.5%, and platelets 383 K/uL ().
In the emergency department, she was able to spontaneously urinate but amount was subjectively decreased. The mild bilateral hydronephrosis on renal ultrasound suggested obstructive pathology. A urologic consultation was requested for suspicion of postobstructive uropathy. The next morning she underwent a retrograde pyelogram demonstrating bilateral hydronephrosis, extrinsic compression, and medial deviation of the ureters, particularly on the right (). Ureteral stents were placed with relief of her obstructive uropathy.
Her renal function and electrolytes were followed for the risk of electrolyte abnormalities due to postobstructive diuresis. Over the course of days her renal function returned to baseline and she was discharged with a plan for surgical ureterolysis and open biopsy one month later. Surgical pathology confirmed tissue consistent with inflammation and ruled out any evidence of malignancy thus making the final diagnosis idiopathic retroperitoneal fibrosis (). The patient remained asymptomatic for 1 year and then lost followup.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [50, 'years'], 'creatinine': [8.18, 'mg/dL'], 'sex': 'Female'}",5.51102,5.23547,5.78657,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 50 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 8.18 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (8.18/0.7)**-1.2 * 0.9938**50 * 1.012 = 5.51102.
Hence, the GFR value is 5.51102 ml/min/1.73 m²."
226,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4421529-1,Extracted,"Our patient was a 56-year-old white male, who was referred to the Nephrology Clinic for a 1-week history of worsening dyspnoea on exertion, hypertension, pedal oedema and a recent increase in his serum creatinine level. Six months prior to presentation, he was diagnosed with coronary artery disease (CAD) for which he required coronary artery stent placement. His home medications included aspirin, clopidogrel, hydrochlorothiazide, atorvastatin, enalapril and metoprolol.
On examination, the patient was obese and had bilateral pitting oedema up to the knees. His blood pressure was 196/100 mmHg (baseline was 130/86 mmHg), and pulse 66 beats/min. He had no rash, purpura or leg ulcers. Laboratory analysis revealed worsening of the serum creatinine level to 1.9 mg/dL (167.96 µmol/L; laboratory range: 0.7–1.4 mg/dL) from a baseline of 1.3 mg/dL (114.92 µmol/L). He had an associated nephrotic range proteinuria (urine protein/creatinine ratio 11 918 mg/g creatinine), microscopic haematuria, and markedly elevated rheumatoid factor of 123 IU/mL (123 IU/mL; laboratory range: <20 IU/mL). In addition, there was a decreased level of complement C4 7 mg/dL, (0.07 g/L; laboratory range: 16–47 mg/dL) with a normal level of complement C3 98 mg/dL, (0.98 g/L; laboratory range: 90–180 mg/dL). Serologic analysis revealed a negative anti-nuclear antibody (ANA), anti-glomerular basement membrane antibody, anti-neutrophilic cytoplasmic antibody and hepatitis B surface antigen (HBsAg). The levels of immunoglobulin G (IgG), immunoglobulin A (IgA) and immunoglobulin M (IgM) were normal. The hepatitis C RNA was 58 100 IU/mL (58 100 IU/mL; laboratory range <5 IU/mL). In view of acute renal failure in the presence of markedly elevated RF, nephrotic syndrome and active HCV serology, a presumptive diagnosis of cryoglobulinaemic glomerulonephritis was made.
The patient refused antiviral therapy. He was thus treated symptomatically. An angiotensin receptor blocker (ARB) and a calcium channel blocker (CCB) were added to achieve blood pressure control. In addition, he continued to receive aspirin (325 mg) and clopidogrel (75 mg) as part of the management for his CAD. Even though the blood pressure improved to 130/86 mmHg after the addition of ARB and CCB, his nephrotic syndrome and renal failure worsened over the next 5 months (). The patient ultimately agreed to a renal biopsy 6 months after the initial presentation. This showed features of MPGN type 1, but with no overt evidence of intracapillary globular accumulations of eosinophilic material (‘protein thrombi’) and no ultrastructural features of cryoglobulin ().
The patient continued to refuse anti-HCV therapy, and his creatinine increased to 2.8 mg/dL (247.52 µmol/L; laboratory range: 0.7–1.4 mg/dL) in the eighth month after presentation. Subsequently, and without any change in his therapy or medication regimen, an unexpected gradual partial resolution of his nephrotic syndrome was seen, which was also associated with an improvement of his serum creatinine and a normalization of his C4 level. There was no decrease in the viral load or the level of rheumatoid factor. The HCV RNA was 58 100 IU/mL (58 100 IU/mL) on presentation and 44 524 IU/mL (44 524 IU/mL) in the 12th month. The pertinent laboratory values over the 12-month period are summarized in .","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [56, 'years'], 'creatinine': [2.8, 'mg/dL'], 'sex': 'Male'}",25.67635,24.39253,26.96017,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 56 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.8 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.8/0.9)**-1.2 * 0.9938**56 * 1.0 = 25.67635.
Hence, the GFR value is 25.67635 ml/min/1.73 m²."
227,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5579934-1,Extracted,"A 31-year-old man, originally from Morocco, was admitted to Leiden University Medical Center (LUMC, The Netherlands) complaining of leg edema in February 2000. The patient had a history of recurrent episodes of inflammation, fever and serositis. The patient was diagnosed with nephrotic syndrome due to amyloidosis secondary to FMF. His family had 7 siblings with consanguineous parents. At that time, no genetic mutations were found. After another episode of FMF in 2009, the patient presented with renal failure and nephrotic syndrome that did not respond to conservative therapy (angiotensin-converting-enzyme inhibitors, diuretics, nonsteroidal anti-inflammatory drugs, cyclosporine and colchicine). He was suspected not to be compliant with treatment. A bilateral nephrectomy was performed to halt the progressive catabolism due to unrestrained renal protein loss. The patient, a Dutch resident, required chronic dialysis. At this time, there was no evidence of clinical cardiac involvement by amyloidosis. In 2011, he received a left kidney transplant from his elder brother, a resident of Spain, who had no medical history of note (the preoperative evaluation of his clinical status and renal function were unremarkable). The kidney donation and transplantation were performed in the Netherlands. The recipient received a standard immunosuppression protocol (cyclosporine, mycophenolic acid and prednisolone). After transplantation, the recipient’s postoperative course was unsatisfactory, with a 10% decrease in serum creatinine levels on 3 consecutive days during the first postoperative week. His renal function subsequently improved, although slowly, and he developed massive proteinuria (18 g/day) and elevated serum amyloid A levels and was diagnosed with nephrotic syndrome. A graft transplant biopsy showed extensive amyloid deposition. The patient underwent treatment with colchicine (0.5 mg/12 h, adjusted for renal function), anakinra (100 mg/day), prednisolone (10 mg/day), mycophenolic acid (540 mg/12 h) and cyclosporine (150 mg/12 h). After 6 months, the patient presented a serum creatinine level of 2.10 mg/dL (185.6 μmol/L) and proteinuria of 0.25 g/day. After 20 months, the graft was functioning well, with a serum creatinine level of 2.40 mg/dL (212.1 μmol/L), undetectable serum amyloid A levels and proteinuria of 0.20 g/day. After 62 months and at the time of this report, his serum creatinine was 2.05 mg/dL (182 μmol/L), Modification of Diet in Renal Disease (MDRD) value of 35 mL/min/1.73 m2 and proteinuria of 0.44 g/day.
An apparently healthy 45-year-old man, originally from Morocco and a resident of Spain for 12 years, was considered a living kidney donor for his younger brother. His medical history and examination was compatible for a living related kidney donation procedure. A thorough physical examination showed no abnormalities, and the laboratory work-up included urine analysis, urine culture, blood test and liver function, the results of which were all within normal ranges. Other studies revealed a serum creatinine level of 1 mg/dL (88.4 μmol/L), creatinine clearance of 113 mL/min/1.73 m2, a 24-h urine protein level of 100 mg and a C-reactive protein (CRP) level of 6 mg/dL (normal range < 5 mg/dL). A computed tomography (CT) angiography of his abdomen showed both kidneys had a perfect configuration with a single renal artery and vein, a normal excretory system and normal appearance of the bladder. After the kidney donation in 2011, the patient presented nausea, vomiting and diarrhea and developed an erysipelas-like erythema of the lower legs. On the fifth postoperative day, he presented a serum creatinine level of 2.08 mg/dL (184 μmol/L). With the diagnosis of prerenal renal failure, the patient was started on IV fluids, which resulted in partially improved renal function. He was released from hospital on the seventh day after the kidney transplantation and was readmitted 3 days later for dyspnea and chest pain. At that time, his serum creatinine level had increased to 2.20 mg/dL (197 μmol/L). Nineteen days after the transplantation, the patient presented a serum creatinine level of 4.80 mg/dL (424.3 μmol/L), proteinuria of 25 g/day and a serum amyloid A level of 85 mg/L. A renal biopsy showed 8 glomeruli, one of which was globally sclerosed and all were pathological. There was extensive expansion of the mesangium, with periodic acid-Schiff (PAS)-positive eosinophilic material, which also caused occlusion of the glomerular capillaries. The eosinophilic material also invaded the blood vessels and was stained with Congo Red. The interstitium presented fibrosis and a diffuse lymphocytic infiltrate. There was also a component of acute tubular necrosis with regeneration. The patient underwent treatment with colchicine (0.5-1 mg/12 h, adjusted for renal function) and anakinra (100 mg/day). After 4 weeks, the patient presented a serum creatinine level of 3.80 mg/dL (339 μmol/L), proteinuria of 16 g/day and an undetectable serum amyloid A level. Treatment with candesartan (2 mg/day) was then started. Fourteen weeks after the kidney donation, the patient had a serum creatinine level of 1.93 mg/dL (171 μmol/L) and proteinuria of 7.5 g/day. He remained on regular colchicine (0.5 mg/12 h), anakinra (100 mg/48 h), candesartan (4 mg/day) and enalapril (5 mg/day) for 4 months. After 20 months, the patient was in good clinical condition. The serum creatinine level had stabilized at 1.50 mg/dL (132.6 μmol/L), creatinine clearance was 61 mL/min/1.73 m2 (MDRD of 53.3 mL/min/1.73 m2), and proteinuria was 2.6 g/day. An echocardiogram revealed an ejection fraction of 60%. Although the possibility of anakinra withdrawal was considered, we decided on indefinite therapy with anakinra and colchicine due to the satisfactory response. After 62 months and at the time of this report, the patient was taking colchicine (0.5 mg/12 h), anakinra (100 mg/48 h) and atorvastatin (40 mg/day). His serum creatinine level was 1.40 mg/dL (123.7 μmol/L), his creatinine clearance was 67.4 mL/min/1.73 m2 (MDRD of 55.7 mL/min/1.73 m2) and his proteinuria was 1.1 g/day.
An initial genetic study on the recipient was conducted in 2000 with negative results. A second genetic analysis was performed in 2011 after the living transplantation on both brothers. Briefly, genomic DNA was prepared from 200 μL of whole blood, using a commercial kit. Hot spot testing for exons 2 (c.278 to c.910) and exon 10 (c.1900 to c.2346) of the FMF gene (MEFV), as well as exons 3, 4-5, 6-7 including introns 2,4 and exons 6 9, 11, by direct PCR and automated sequencing revealed homozygosity in the MEFV gene (c.2082G > A; p.M694I; National Amyloidosis Centre, University College London Medical School, London, UK). The reason p.M694I was not found in 2000 is not known, given that this founder mutation had been already described in 1998 [, ]. This missense mutation has a founder effect in the African Mediterranean population (Lebanon 12.6%; Tunisia; 13%, Syria 4.8%; Egypt 20.6%), and dates back more than 8500 years (Lebanon) (Mediterranean Founder Mutation Database). This change has been established as a pathogenic variant (Clin Var: RCV000220431.2) in a recessive condition.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [31, 'years'], 'creatinine': [2.05, 'mg/dL'], 'sex': 'Male'}",43.60572,41.42543,45.78601,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 31 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.05 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.05/0.9)**-1.2 * 0.9938**31 * 1.0 = 43.60572.
Hence, the GFR value is 43.60572 ml/min/1.73 m²."
228,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3692155-1,Extracted,"A 54-year-old Indian male with diabetes mellitus and hypertension presented with right loin pain, fever, and tiredness since 1 week. He had undergone meatotomy and circumcision 3 years ago. A year later, there was recurrence of poor urinary stream.
On examination, he was febrile, blood pressure was 140/70 mmHg, chest was clear and there were no murmurs over heart on auscultation. Abdomen was soft on palpation and there was significant tenderness over the right loin. Urethral meatus was pin hole and there were changes of lichen sclerosis in the skin over glans.
Investigations showed 1+ proteinuria, 18-20 white blood cells, and 10-15 red blood cells on urine analysis; hemoglobin, 13 g/dL; total leukocyte count, 17.1 × 103/mm3; differential count polymorphs, 89%; lymphocytes, 9%; eosinophils, 1% and monocytes, 1%; platelet count, 108 × 103/mm3; serum creatinine, 3.5 mg/dL; metabolic acidosis; and serum albumin, 2.2 g/dL. Electrocardiography revealed sinus tachycardia, leftward QRS axis, and poor R wave progression over chest leads. There was right turbid hydro-ureteronephrosis on ultrasonogram abdomen. Transthoracic echocardiogram (TTE) revealed regional wall motion abnormalities, normal valves, and mild left ventricle (LV) systolic dysfunction (ejection fraction 45%).
He was started on cefoperazone-sulbactam and amikacin (with dose adjusted for renal function pending cultures). Insulin infusion was required for control of severe hyperglycemia. Planning ureteric stenting, he underwent cystoscopy on day 0; there was penile urethral stricture and visual internal urethrotomy was performed followed by right ureteric stenting. There was purulent hydronephrotic drip following the stent insertion.
Blood and urine grew E. coli. Levofloxacin was substituted for amikacin based on anti-biogram 5 days after admission to minimize the risk of nephrotoxicity. He was continued on two antibiotics as he was still sick and febrile with persisting leukocytosis (22.0 × 103/mm3; 22.0 × 109/L). Evaluation for focal renal and prostatic abscesses with abdominal and transrectal ultrasound was negative. There was some improvement in renal function following these measures and serum creatinine was 2.4 mg/dL on day 6.
He developed a new grade 3 systolic murmur over the apex of the heart along with clinical and radiological signs of congestive cardiac failure on day 6; repeat TTE revealed flail mitral valve, severe mitral regurgitation, a small echogenic mass on the tip of anterior mitral leaflet suggestive of vegetations on the mitral valve, and dilated left atrium and left ventricle []. Amikacin was restarted with dose modified for renal function and levofloxacin was stopped. Cardiac failure was managed with intravenous frusemide. He had an episode of transient weakness of right upper limb that lasted for less than 12 h on day 7, suggesting a possible embolic transient ischemic attack (TIA) in middle cerebral artery territory. With worsening cardiac failure and respiratory distress, he was intubated and started on dobutamine infusion and ventilator support the same day. There was progressive decline in renal function from day 6. Serum creatinine was 3.2 mg/dL (282.8 μmol/L) on day 9. Repeat cultures were sterile.
In view of persistent fever, IE and congestive cardiac failure, valve replacement was carried out on day 9. Mitral valve had vegetations over the anterior leaflet; chordae were necrotic and there were abscesses over the papillary muscles []. Mitral valve excision and replacement with 27 mm St. Jude Medical Biocor™ was carried out along with two vessel coronary artery bypass grafting as there was 100% occlusion of left anterior descending artery and long segment stenosis of proximal left coronary artery on angiogram. Transesophageal echocardiography (TEE) at the end of the procedure showed no residual mitral incompetence.
His overall clinical status gradually and steadily improved; he could be successfully weaned off ventilator. Smear from the resected valve showed numerous pus cells on gram-stain and scanty growth of E. coli on culture. Repeat cultures on day 16 were sterile. He was continued on cefoperazone sulbactam for 6 weeks and alternate day amikacin for 4 weeks (with periodic monitoring of serum creatinine). Acitrom was added for anticoagulation. Serum creatinine declined to 1.9 mg/dL on day 19 and 1.7 mg/dL on day 50. Cultures continued to be sterile more than 2 weeks after discontinuation of all antibiotics. At last visit (22 months since first presentation), he was clinically comfortable and serum creatinine was 1.6 mg/dL; there was no further episode of urinary infection and there was no valve regurgitation.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [54, 'years'], 'creatinine': [1.6, 'mg/dL'], 'sex': 'Male'}",50.88397,48.33977,53.42817,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 54 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.6 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.6/0.9)**-1.2 * 0.9938**54 * 1.0 = 50.88397.
Hence, the GFR value is 50.88397 ml/min/1.73 m²."
229,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4165057-1,Extracted,"A 42-year-old man, who had live related donor renal transplantation 18 years ago, and was taking azathioprine 100 mg and prednisolone 10 mg once daily as immunosuppesive agents, developed new onset diabetes mellitus 6 months after transplantation and was on insulin since then. He has a stable graft function without any rejection episode. Three and half years ago he developed a small ulcer on the skin over right knee joint which was operated, after which he had remained asymptomatic for 3 years. He then developed papulo-nodular lesions and erythematous plaques with multiple discharging sinuses at that site which had developed after a minor trauma. These lesions gradually evolved to multiple discharging sinuses []. Prior to his visit to us he consulted surgeon to remove the ulcers. The surgeon operated thrice but after each surgery the sinuses and ulcer increased in number and size. On examination, there were scattered erythematous papules and nodules with necrotic ulcerations and multiple discharging sinuses. There was no lymphadenopathy. Histopathology revealed a granulomatous suppurative infiltrate extending to the entire dermis and numerous ectatic blood vessels. Many hyaline hyphae and unicellular fungal elements were seen in the infiltrate and within the vascular spaces. Gomori Methenamine staining showed hyphae of more than 1μm in diameter and reproductive structures represented by microconidia and chlamydospore like structures, suggesting a presumptive diagnosis of non-Aspergillus hyalo-hypho-mycosis. Sabouraud-Dextrose agar culture without cycloheximide grew whitish grey cottony colonies suggestive of Fusarium species. Successive subcultures performed on potato dextrose agar, then put on lactophenol cotton blue mount which showed sickle-shaped multiseptatedmacroconidia; and one-to two-celled microconidia formed from unbranched phialides, conidiophores and chlamydospores typical of Fusarium [Figures and ]. Laboratory investigations revealed impaired renal function, with raised serum creatinine levels (2.8 mg/dl) and blood urea levels (87 mg/dl). Three consecutive blood cultures were negative. X-ray of the chest and gastrointestinal tract, as well as an abdominal ultrasound, showed no abnormalities. Itraconazole was started at 100 mg twice daily, which led to after 6 weeks.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [42, 'years'], 'creatinine': [2.8, 'mg/dL'], 'sex': 'Male'}",28.01221,26.6116,29.41282,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 42 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.8 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.8/0.9)**-1.2 * 0.9938**42 * 1.0 = 28.01221.
Hence, the GFR value is 28.01221 ml/min/1.73 m²."
230,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3132331-1,Extracted,"A 39 year-old Caucasian man was transferred from an outlying facility for management of a psoas abscess diagnosed on computerized tomography (CT) scan of abdomen and pelvis. He complained of low back pain for 2 weeks. He denied any fever, trauma, tingling, numbness, bladder, or bowel disturbances. Past medical history was unremarkable except for an abscess on his right forearm and right scrotal area following a tick bite which was draining a couple of days before he started having back pain. Physical exam revealed tachycardia, tachypnea and minimal costovertebral angle tenderness bilaterally. Rest of the physical exam including neurological exam was within normal limits. Laboratory data revealed white blood cell count 33.8 thousand/mm3 (neutrophils count 31,900/mm3 and bands 24%), hemoglobin 11.9 gm/dl, sodium 124 mmol/l, potassium 4.5 mmol/l, blood urea nitrogen 24 mg/dl, creatinine 1.1 mg/dl, total protein 7.3 gm/dl, albumin 1.5 gm/dl. Urinalysis was significant for small amount of blood, red blood cells (8/hpf), white blood cells (10/hpf) and occasional white blood cell casts. Urine color, specific gravity and PH were within normal limits.
A CT scan of the abdomen without contrast done at an outlying facility revealed possible psoas abscess and left renal abscess []. Magnetic resonance imaging (MRI) of the lumbar spine confirmed the findings including multiple abscesses in the psoas muscles bilaterally and spondylitis involving L1–L4. CT guided biopsy of the left paravertebral mass as well as blood culture grew MRSA. Patient was started on vancomycin and levofloxacin with a plan to continue these antibiotics for at least 4–6 weeks.
During the hospital course, his condition started improving clinically; however his renal function started deteriorating and he developed acute renal failure. His blood urea nitrogen and creatinine increased from a baseline of 12 mg/dl and 1.1 mg/dl, respectively, to 24 and 2.4 mg/dl within 20 days of hospitalization and these values continued to increase. Within the next 2 weeks his blood urea nitrogen and creatinine were increased to 43 and 7.4 mg/dl, respectively. After 2 weeks of antibiotic treatment urine output decreased significantly. He was started on hemodialysis as he developed volume overload. Vancomycin and levofloxacin were stopped and the patient was started on linezolid, which also was stopped after six days as the patient developed an apparent allergic skin reaction. He was then started on daptomycin. The time course of serum creatinine is shown in .
During this time period patient was evaluated for the cause of acute renal failure. His urine analysis at this point revealed red blood cells 56/hpf, a few dysmorphic red blood cells, WBCs <1/hpf, no eosinophils, proteinuria with urine protein to creatinine ratio 2.94, fractional excretion of sodium 7.67, and fractional excretion of urea 124.5; urine microscopic exam revealed few muddy brown casts. The urine color was brown and specific gravity was normal. His renal function did not return to baseline after a few days of hemodialysis. Considering the possibility of acute glomerulonephritis, the patient underwent CT guided biopsy of the right kidney, which revealed IgA dominant PIGN with extensive acute tubular injury and acute interstitial nephritis. Light microscopy showed glomeruli with mild to moderate increase in the mesangial matrix and cellularity, with cellular crescents in 2 of the 3 glomeruli sampled, and fibrinoid necrosis in one of these. In addition, rare hump shaped deposits were visualized overlying the glomerular basement membrane in the capillary notch area []. Correspondingly, immunofluorescence (IF) microscopy showed 2+ mesangial and segmental capillary loop staining for IgA and C3 while IgG was negative []. Electron microscopy showed scattered mesangial deposits and rare subepithelial hump type deposits []. These findings were characteristic of IgA dominant postinfectious glomerulonephritis. The biopsy also showed acute tubular injury and a hypersensitivity drug induced acute interstitial nephritis, with widespread tubultitis and interstitial nephritis in areas away from the crescents.
The patient received pulse doses of steroids followed by oral steroids. He was discharged with arrangements to receive intravenous antibiotics and hemodialysis. His creatinine at the onset of the steroid therapy was 5.5 mg/dl, which improved after 2 weeks of treatment, at which point he was removed off hemodialysis. On follow up at three months and at one year, his creatinine was 1.7 and 1.3 mg/dl, respectively.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [39, 'years'], 'creatinine': [1.1, 'mg/dL']}",87.57272,83.19408,91.95136,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 39 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.1/0.9)**-1.2 * 0.9938**39 * 1.0 = 87.57272.
Hence, the GFR value is 87.57272 ml/min/1.73 m²."
231,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4421477-1,Extracted,"A 37-year-old male presented to renal clinic for routine follow-up for PKD. His initial diagnosis of PKD was made after an evaluation of an episode of painless gross haematuria at age 27. Physical examination at that time was normal except for the blood pressure that was 148/86 mmHg. His past medical history is unremarkable, specifically for no history of flank pain, renal colic or symptomatic kidney stones. He takes no medications. He has no family history of renal disease, kidney stones or PKD. Computed tomography scanning at initial presentation revealed marked renal volume enlargement, greater than 50 cystic lesions in each kidney bilaterally all consistent with simple cysts (Figure ). Additionally, hepatic cysts and colonic diverticuli were noted. Finally, several renal parenchymal calcifications were noted, thought to be consistent with retained bilateral nephrolithiasis. Serum creatinine at that time was 1.3 mg/dL. Urinalysis at initial presentation was notable for specific gravity of 1.005, pH 7.5, trace blood and no proteinuria. He was diagnosed with PKD in accordance with Ravine's criteria [].
He has done well over time with only an occasional episode of painless gross haematuria, always associated with physical sports activity. His hypertension has worsened prompting treatment with an angiotensin receptor blocker, irbesartan 75 mg orally per day.
On recent routine follow-up evaluation, the patient was asymptomatic with normal physical examination. Blood pressure was 132/76 mmHg. Urinalysis revealed a specific gravity of 1.005, pH 7.5, no protein, trace blood and numerous hexagonal-shaped crystals (Figure ). The patient was further evaluated with a 24-h urine collection that revealed 1645 mg/day cystine, creatinine 2100 mg and volume 3010 mL. Since the patient was asymptomatic, no specific pharmacologic treatment was given. He was counseled about the increased risks of nephrolithiasis, and hydration strategies were discussed. The patient remains in good health and has yet to develop a symptomatic kidney stone over a 3-year follow-up period.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [37, 'years'], 'creatinine': [1.3, 'mg/dL']}",72.56213,68.93402,76.19024,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 37 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.3/0.9)**-1.2 * 0.9938**37 * 1.0 = 72.56213.
Hence, the GFR value is 72.56213 ml/min/1.73 m²."
232,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6531112-1,Extracted,"A 77-year-old, Asian male patient (weight: 60 kg, height: 165 cm) with end-stage renal disease (ESRD) undergoing periodic hemodialysis, was hospitalized due to acute exacerbation of chronic obstructive pulmonary disease. He had no known history of psychosis prior to admission to the hospital. His social history was positive for alcohol consumption (25 mL a day for 10 years) and smoking (40 cigarettes a day for 30 years).
On admission, the patient was conscious and oriented to person, time, and place. Complete neurological examination including mental state was normal. The patient was in shortness of breath with the following vital signs: temperature 36.2 °C, blood pressure 156/91 mmHg, pulse 98 beats/min, and respiratory rate 20 per minute. He reported progressively worsening cough productive of yellow purulent sputum. Bilateral moist crackles were heard in both lungs on auscultation but with no wheezing. Markers of systemic inflammation were elevated (white blood cell count [WBC] 10.25 × 103/μL, C-reactive protein [CRP] 57.50 mg/L, procalcitonin [PCT] 0.49 ng/mL). Laboratory analysis revealed increased baseline serum creatinine (10.63 mg/dL, estimated creatinine clearance 4.94 mL/min). His liver function was moderately impaired and classified into Child-Pugh class B. Chest computed tomography (CT) scan showed diffuse inflammation and interstitial change and a small amount of pleural effusion in bilateral lungs.
Intravenous moxifloxacin was initiated 400 mg daily as empiric treatment for pulmonary infection on hospital day 1. A sputum sample was collected for microbiological culture before initiation of antibiotics and the result came back negative. On day 12, the patient was feeling tired and weak with hyperthemia (38.1 °C), hypertension (184/91 mm Hg), and worsened shortness of breath (26 beats/min). Plasma indicators for infection were elevated (WBC 11.50 × 109/L, neutrophils 97.1%, PCT 22.10 ng/mL). On the 13th day, moxifloxacin was switched to meropenem 500 mg intravenous every 8 hours. On 16th day, sputum culture revealed multidrug-resistant (MDR) A baumannii (resistant to carbapenem but sensitive to tetracycline). Then intraveous tigecycline was added to the regimen at a loading dose of 100 mg followed by 50 mg every 12 hours.
Fourteen hours after tigecycline initiation, the patient became confused, disoriented to location, and the time. He had difficulty understanding instructions and was clearly disturbed in attention during the conversation. He was agitated, fearing that people around him were trying to harm him. Then he became verbally aggressive toward his family members and medical staff. His mental disorder worsened in the next 2 to 3 hours then he began having hallucinations, seeing a huge ball in the ceiling and asking the nurse to take it down so he could eat it. He asked other people to gather together and said he had important things to announce. His Confusion Assessment Method, which is a valid tool for the detection of delirium, was negative prior to the initiation of tigecycline, but became positive after it was started. His clinical manifestations also met the key features listed by the Diagnostic and Statistical Manual of Mental Disorders fifth edition (DSM-V) criteria from the American Psychiatric Association that characterizes delirium.[
No focal neurological disease was noted after neurological examination. A computerized tomographic scan of the head was then performed, and no abnormalities were identified. Oxygen supplementation (4 L/min via nasal cannulae) was initiated after the arterial blood gas analysis showed hypoxemia (pH 7.41; PaCO2 25 mmHg; PaO2 68 mmHg; Na+ 132 mEq/L; K+ 5.5 mEq/L). The patient did not have any prior history of mental illness. Drug-induced delirium was suspected and tigecycline was speculated to be the most likely offending agent after medication review (Table ). Since his delirium was treated with little success with olanzapine, tigecycline therapy was discontinued the next morning after the patient stayed awake the whole night. During the following day after discontinuation of tigecyline, the patient's mental state improved and delirium cleared slowly. He restored the ability of focus and orientation. Perceptual disturbances disappeared, and no visual illusions or vague delusions of harm were noted again.
Meanwhile, markers of systemic inflammation were elevated (WBC 43.91 × 109/L, neutrophils 98.2%, PCT 34.04 ng/mL, CRP 89.09 mg/L). On Day 19, antibiotic therapy was switched to meropenem (i.v., 500 mg q8 h) combined with minocycline (p.o., 400 mg q12 h), and amikacin (i.v., 200 mg qd). The regimen continued for 5 days but the patient did not respond well, showing even higher systemic inflammation markers and exacerbated dyspnea. Antibiotic therapy was switched to meropenem 500 mg every 8 hours, and he started again on tigecycline 50 mg every 12 hours on 24th day with no loading dose.
In the morning of Day 25, the patient showed reduced psychomotor activity, decreased speech, but no obvious hallucinations. He had no idea of the time of day, nor where he was, although the day before he was fully orientated. The patient experienced a hypoactive state of delirium. CT examination of the chest showed increased inflammatory pulmonary lesions in bilateral lungs. Blood gas analysis revealed hypoxemia without carbon dioxide retention, and the electrolytes were found to be within range. Also, no significant changes in blood profile like levels of liver enzymes or serum creatinine was observed compared with the last test taken before the delirium appeared again. Tigecycline was discontinued and delirium resolved in the afternoon. Antibiotic treatment was then switched to levofloxacin (i.v., 600 mg qd) and minocycline (p.o., 100 mg q12 h). But the patient did not respond well to the present antibiotic therapy and his dyspnea exacerbated. He was transferred to the intensive care unit 6 days later as mechanical ventilation was required. Unfortunately, the patient died of recurrent attacks of left heart failure probably caused by uncontrolled serious infections on 33th day.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [77, 'years'], 'creatinine': [10.63, 'mg/dL'], 'sex': 'Male'}",4.54529,4.31803,4.77255,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 77 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 10.63 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (10.63/0.9)**-1.2 * 0.9938**77 * 1.0 = 4.54529.
Hence, the GFR value is 4.54529 ml/min/1.73 m²."
233,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5735466-1,Extracted,"A 26-year-old female patient weighing 35 kg, presented with strangulated umbilical hernia. Her previous medical records revealed she was a known case of DCMP and chronic kidney disease since 2 years. She was presently on treatment with tablet digoxin 0.25 mg, tablet furosemide 40 mg, and tablet carvedilol 12.5 mg once a day. She gave a history of repeated hospital admissions in the past 2 years with features suggestive of congestive heart failure (CHF) and was on regular twice weekly maintenance hemodialysis, last being 2 days before the surgery.
On preanesthetic evaluation, her heart rate was 96 beats/min, regular; blood pressure was 106/72 mmHg; respiratory rate was 16 breaths/min. On auscultation grade, three ejection systolic murmurs were audible. There were no rhonchi or crepitations. Air entry was equal bilaterally. There was no hepatomegaly, ascitis, or pedal edema. The skin overlying the hernia appeared necrosed.
The preoperative 12 lead electrocardiogram (ECG) revealed normal sinus rhythm. Echocardiography demonstrated global hypokinesia, poor systolic function with LVEF of 28%, all 4 chambers dilated, severe mitral regurgitation, tricuspid regurgitation, pulmonary regurgitation, and moderate pulmonary artery hypertension. Chest radiograph revealed cardiomegaly with normal lung fields. Her investigations showed Hb 7.9 g/dl, total leukocyte count TLC 12.9 × 1000/μl, platelet count 219 × 1000/mm3, urea 28.9 mg/dl, creatinine 3.6 mg/dl, sodium 138 mEq/L, potassium 4.5 mEq/L, international normalized ratio of 1.05.
A high-risk written and informed consent was obtained in view of cardiac and renal disease. After shifting to the operating room, an 18-gauge intravenous (IV) cannula was secured. Under strict aseptic precautions, an 18-gauge epidural catheter was inserted into the epidural space at T10-11 interspace using loss of resistance to air technique. A 22-gauge right radial arterial cannula was secured since the left hand had an arteriovenous fistula. Under local anesthesia, a 7 Fr, 15 cm triple lumen central venous catheter was inserted into a right internal jugular vein under ultrasound guidance for intensive hemodynamic monitoring.
The following parameters were monitored: Two lead ECG (II and V5), invasive blood pressure, central venous pressure (CVP), oxygen saturation by pulse oximetry, end-tidal carbon dioxide, body temperature, and urine output. FloTrac® continuous cardiac monitoring was done to monitor cardiac output, cardiac index and stroke volume variability (SVV).
Anesthesia was induced with injection etomidate 0.2 mg/kg, injection fentany l 3 μg/kg. Injection cisatracurium 0.15 mg/kg IV was given to facilitate intubation with size 7.0 mm endotracheal tube. Anesthesia was maintained with 50% air in oxygen, desflurane 4%–6%, and intermittent boluses of 1 mg cisatracurium. An epidural infusion of 0.05% ropivacaine with 2 μg/ml fentanyl was started at 5 ml/h. The CVP was maintained between 8 and 10 cmH2O, cardiac output of 6.8 L/min, cardiac index of 5.5 L/min/m2, and systemic vascular resistance (SVR) of 835 dyne/s/cm5. Arterial blood gas revealed a pH of 7.381, pO2193 mmHg, pCO232.1 mmHg, base excess - 5.8 mmol/L, HCO3− 18.6 mmol/L.
We started injection noradrenaline infusion at 0.08 μg/kg/min and injection dobutamine infusion at 5 μg/kg/min which were tapered slowly towards the end of surgery. Surgeons found only ascitic fluid as the sac contents which was then aspirated. There was no bowel or omentum. The neck of the hernia was found to be very narrow, and defect was closed without a mesh. The procedure lasted for 90 min. Blood loss was about 100 ml. Intraoperatively, a total of 400 ml of normal saline was given. Paracetamol 500 mg IV was given as a means to achieve multimodal analgesia. At the end of surgery, after the return of respiratory efforts, the residual neuromuscular blockade was reversed with injection glycopyrrolate 0.01 mg/kg and injection neostigmine 0.05 mg/kg and extubated. The patient had stable hemodynamics throughout the procedure []. The patient was shifted to surgical recovery room, and all the intraoperative monitoring was continued postoperatively. A continuous epidural infusion of 0.05% ropivacaine with 1 μg/ml fentanyl was continued postoperatively.
All her preoperative medications were continued as per the recommended scheduled dosing and timing. The patient was shifted from the recovery room after 4 h. She underwent dialysis on the postoperative day 1 and was then discharged on postoperative day 4.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [26, 'years'], 'creatinine': [3.6, 'mg/dL'], 'sex': 'Female'}",17.13158,16.275,17.98816,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 26 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 3.6 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (3.6/0.7)**-1.2 * 0.9938**26 * 1.012 = 17.13158.
Hence, the GFR value is 17.13158 ml/min/1.73 m²."
234,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-1994,Extracted,"A 73-year-old man comes to the physician because of progressive fatigue and shortness of breath on exertion for 3 weeks. He has swelling of his legs. He has not had nausea or vomiting. His symptoms began shortly after he returned from a trip to Cambodia. He occasionally takes ibuprofen for chronic back pain. He has a history of arterial hypertension and osteoarthritis of both knees. He had an episode of pneumonia 4 months ago. His current medications include lisinopril and hydrochlorothiazide. He has no history of drinking or smoking. His temperature is 37°C (98.6°F), pulse is 101/min, and blood pressure is 135/76 mm Hg. Examination shows pitting edema of the upper and lower extremities. Laboratory studies show:
Hemoglobin 14.1 g/dL
Leukocyte count 6,800/mm3
Platelet count 216,000/mm3
Serum
Urea nitrogen 26 mg/dL
Creatinine 2.9 mg/dL
Albumin 1.6 g/L
Urine
Blood negative
Protein 4+
Glucose negative
Renal biopsy with Congo red stain shows apple-green birefringence under polarized light.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [73, 'years'], 'creatinine': [2.9, 'mg/dL'], 'sex': 'Male'}",22.14768,21.0403,23.25506,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 73 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.9 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.9/0.9)**-1.2 * 0.9938**73 * 1.0 = 22.14768.
Hence, the GFR value is 22.14768 ml/min/1.73 m²."
235,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6013953-1,Extracted,"A 79-year-old Japanese woman with a weight of 72 kg who has been maintained on anti-hypertensive drugs, including hydralazine, for more than 10 years, was advised on acute onset of proteinuria and microscopic hematuria by her family doctor. At this time, her serum creatinine (Cr) level was within normal range (0.8 mg/dl). One month later, however, the Cr level was elevated to 1.6 mg/dl. Therefore, she was referred to our hospital for admission.
On admission, vital signs revealed body temperature of 36.9 °C, blood pressure of 150/70 mmHg, and pulse rate of 80 per minute. The white blood cell count was 8700/μl with 2.0% eosinophils, red blood cell count was 307 × 104/μl, and platelet count was 26.6 × 104/μl. The following values indicated renal dysfunction; blood urea nitrogen: 25.0 mg/dl, Cr: 1.9 mg/dl, urinary protein: 2.5 g/day, and the presence of microscopic hematuria. Dysmorphic red blood cells were noted in the urine sample microscopically. In the serum, MPO-ANCA was 107 IU/ml (normal limit, 3.5 IU/ml), whereas C-reactive protein (CRP) was 0.2 mg/dl. PR3-ANCA and other ANCAs, including anti-elastase and anti-lactoferrin antibodies, were negative. The titer of anti-nuclear antibody (ANA) was less than 1:40. Anti-DNA antibody was negative. Complement values were as follows: C3 162.2 mg/dl (normal range, 71–135 mg/dl) and C4 37.7 mg/dl (normal range, 11–34 mg/dl). Renal biopsy revealed pauci-immune necrotizing crescentic glomerulonephritis (Fig. ).
Hydralazine-induced MPO-AAV was considered regardless of absence of skin involvement, elastase- and lactoferrin-ANCAs, anti-nuclear and anti-DNA antibodies, and hypocomplementemia, which are usually observed in the disease []. By discontinuation of the causative drug, the serum Cr level decreased gradually. At 10 months later, the serum Cr and MPO-ANCA levels recovered to 1.1 mg/dl and 13 IU/ml, respectively. Proteinuria and microscopic hematuria also disappeared. Since the clinical course was consistent with hydralazine-induced MPO-AAV and the serum CRP level was not high throughout the clinical course, no additional medication was administered.
After another 6 months of observation, the serum Cr and MPO-ANCA levels were re-elevated (Cr, 2.0 mg/dl; MPO-ANCA, 195 IU/ml) and proteinuria and microscopic hematuria were re-appeared. The titer of ANA was 1:40. Other ANCAs, including PR3-ANCA, and anti-DNA antibody were negative even at this time. Complement values were as follows: C3 149.4 mg/dl and C4 38.5 mg/dl. Renal biopsy was performed again and revealed cellular crescents in some glomeruli (Fig. ). These findings suggested the relapse of MPO-AAV. Since she had fever (38.3 °C), and the serum CRP level was elevated to 10.0 mg/dl at this time, administration of 30 mg prednisone (0.5 mg/kg body weight) was initiated. The illness improved rapidly, and remission was achieved 5 months after the beginning of treatment. The patient has remained in remission thereafter (Table ).
This study was approved by the Ethical Committee of Osaka General Medical Center (Permission No. 29-C0313) and the Ethical Committee of Faculty of Health Sciences, Hokkaido University (Permission No. 15–90). After acquisition of written informed consent from the patient, serum samples were obtained at the disease onset (Serum A; MPO-ANCA, 107 IU/ml), at relapse (Serum B; MPO-ANCA, 195 IU/ml), at 3 months after treatment (Serum C; MPO-ANCA, 4.5 IU/ml), and at remission (Serum D; MPO-ANCA, 2.4 IU/ml).
To assess the involvement of NETs in the pathophysiology of this patient, we determined the NET degradation activity in the serum samples at first. In brief, peripheral blood neutrophils from a healthy volunteer were seeded in slide chambers (1 × 106/ml), incubated for 15 min at 37 °C, and then made to react with 100 nM phorbol myristate acetate (PMA; Sigma-Aldrich, St. Louis, MO) for 3 h at 37 °C. We have confirmed that this stimulation induces NETs conspicuously []. After washing with PBS, the cells were incubated in 10% Serum A, B, C, or D for 6 h at 37 °C. For positive control, 10% serum of a healthy volunteer (49 years old, male) was employed. This sample exhibited the average value for NET degradation in our previous study []. To stop the serum nuclease activity, 2 mM EDTA was added, and then the remaining cells on the slides were fixed with 4% paraformaldehyde (PFA) followed by mounting with the solution containing DAPI. Photomicrographs (magnification, × 200) were taken randomly under a fluorescent microscope (6 fields/well of chamber slides), and then the residual NET area was determined using Image J software. NET degradation rate (%) was calculated as follows; {(residual NET area, incubated with PBS) – (residual NET area, incubated with serum) / (residual NET area, incubated with PBS)} × 100. As a result, the NET degradation activity was entirely low in Sera A, B, C, and D compared with the healthy control (Fig. ). Correspondingly, the DNase I activity as determined using ELISA kit (Orgentec GmbH, Mainz, Germany) was low in Sera A (21.7%), B (28.3%), C (22.8%), and D (33.5%) compared with the healthy controls {mean ± standard deviation (SD), 52.6 ± 12.1%}.
Next, we determined the NET induction activity of IgG, which was isolated from the serum samples, using immunoadsorbent columns (Protein G HP SpinTrap, GE Healthcare, Tokyo, Japan). Contamination of endotoxin in the IgG samples was ruled out using the Limulus test kit (Wako Pure Chemical, Osaka, Japan). Peripheral blood neutrophils from a healthy volunteer were seeded in slide chambers (1 × 106/ml), pre-treated with 5 ng/ml TNF-α for 15 min at 37 °C to express MPOs on the cell surface, and then made to react with 250 μg/ml of the IgG samples. Serum IgG samples from a 65-year-old woman patient with MPO-AAV (MPO-ANCA, 93.2 IU/ml) and the healthy volunteer were employed as positive and negative controls, respectively. These samples exhibited the average values for NET induction in our previous study []. After incubation for 3 h at 37 °C, the supernatants were removed and the remaining cells on the slides were fixed with 4% PFA. Finally, the remaining cells were mounted with the DAPI-containing solution. Photomicrographs (magnification, × 200) were taken randomly under a fluorescent microscope (6 fields/well of chamber slides), and then the rates of NET-forming neutrophils were determined using ImageJ software. As a result, the NET induction activity was high in Sera A, B, and C, whereas that in Serum D was equivalent to the healthy control (Fig. ).
Lastly, we conducted immunofluorescent (IF) tests to determine the presence of ANETA in the serum samples. Briefly, peripheral blood neutrophils from a healthy volunteer were seeded in slide chambers (1 × 106/ml), incubated for 15 min at 37 °C, and then made to react with 20 nM PMA for 2 h at 37 °C. After washing with PBS, the cells were fixed with 4% PFA, and then made to react with 250 μg/ml of the IgG samples for 1 h at 37 °C. After washing with PBS, the cells were next allowed to react with 1:5000 dilution of FITC-conjugated anti-human IgG antibodies for 1 h at 37 °C followed by mounting with the solution containing DAPI. As shown in Fig. , ANCA was detected in Sera A and B but not in Sera C or D; thus, these findings were consistent with the ELISA titers of MPO-ANCA. On the other hand, ANETA was detected in Sera B and C but not in Serum A or D.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [79, 'years'], 'creatinine': [2.0, 'mg/dL'], 'sex': 'Female'}",24.94428,23.69707,26.19149,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 79 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.0/0.7)**-1.2 * 0.9938**79 * 1.012 = 24.94428.
Hence, the GFR value is 24.94428 ml/min/1.73 m²."
236,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-10845,Extracted,"A 55-year-old African American male presents to his primary care physician with complaints of persistent back pain and fatigue over 12 months. Physical examination reveals a blood pressure of 190/150 mm Hg, and laboratory tests reveal hyperlipidemia and a serum creatinine level of 3.0 mg/dL. 4.5 g of protein are excreted in the urine over 24 hours. Renal biopsy shows eosinophilic, acellular material in the glomerular tuft and capillary walls that display apple green-colored birefringence in polarized light upon Congo red tissue staining.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [55, 'years'], 'creatinine': [3.0, 'mg/dL'], 'sex': 'Male'}",23.78365,22.59447,24.97283,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 55 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.0 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.0/0.9)**-1.2 * 0.9938**55 * 1.0 = 23.78365.
Hence, the GFR value is 23.78365 ml/min/1.73 m²."
237,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5954322-1,Extracted,"A 10-year-old spayed female American Shorthair cat was referred to the Matthew J Ryan
Veterinary Hospital of the University of Pennsylvania (MJR-VHUP) for renal
transplantation. The cat had a 1 year history of polyuria and polydipsia, and was
diagnosed with polycystic kidney disease (PKD) by the referring veterinarian. During
physical examination, both kidneys were markedly enlarged based on palpation. No
other masses or organomegaly were appreciated, and peripheral lymph nodes were
palpably within normal limits.
Initial hematologic analysis revealed a normocytic, normochromic, non-regenerative
anemia (hematocrit 17.5%; reference interval [RI] 31.70–48.00%) and a lymphopenia
(lymphocytes 0.414 ×103/μl; RI 0.800–6.100 ×103/μl). Serum
biochemical analysis revealed moderate azotemia (blood urea nitrogen [BUN] 68 mg/dl
[RI 15–32 mg/dl]; creatinine 2.7 mg/dl [RI 1.0–2.0 mg/dl]), hyperphosphatemia
(phosphorus 6.8 mg/dl; RI 3.0–6.6 mg/dl) and mild hypomagnesemia (magnesium 1.8
mg/dl; RI 1.9–2.6 mg/dl). Urinalysis revealed borderline hyposthenuria (urine
specific gravity 1.008), mild glucosuria (1+) and mild proteinuria (trace). No
abnormalities were found when examining the urine sediment. A urine protein to
creatinine ratio (1.32; RI 0–0.5) confirmed proteinuria. A concurrent urine culture
was negative for any pathogens. Serum total thyroxine (1.49 μg/dl; RI 1.00–4.00
μg/dl) was within normal limits.
Thoracic radiographs were obtained to screen for concurrent disease and revealed no
abnormalities. On abdominal ultrasound, multiple variably sized bilateral renal
cysts and hepatic cysts were noted, consistent with PKD. Pyelectasia was observed,
likely secondary to renal insufficiency. Cysts were as large as 19.2 mm in diameter
in the left kidney and 23.5 mm in the right kidney.
The cat was systemically healthy aside from IRIS stage 3 chronic kidney disease (CKD)
secondary to PKD and was considered an appropriate candidate for renal
transplantation. The cat was administered darbepoetin (1 μg/kg SC) 8 days prior to
surgery, blood typed and cross-matched to identify a compatible donor cat. An
additional dose of darbepoetin (1 μg/kg SC) was administered 1 day prior to the
procedure. Immunosuppression was initiated 4 days prior to surgery with ciclosporin
(3 mg/kg PO q12h). Prednisolone (0.5 mg/kg PO q24h) was administered beginning on
the day of the procedure in conjunction with ciclosporin for further
immunosuppression.
During surgery, the abdomen was routinely entered and explored. The right kidney was
severely enlarged and polycystic with neovascularization to the aorta and caudal
vena cava. An anomalous bifurcation of the caudal vena cava was observed at the
level of the adrenal glands. The right kidney was firmly adhered to the surrounding
tissues, and although both kidneys were polycystic, the right appeared more severely
affected than the left. Because of how grossly diseased and enlarged the right
native kidney appeared, an intraoperative fine-needle aspirate was performed.
Cytology revealed proteinaceous fluid, a moderate number of macrophages, rare
neutrophils and few small lymphocytes, suggestive of chronic inflammation associated
with a cystic or seromatous mass. No neoplastic cells were observed. A right
nephrectomy was performed prior to transplantation and the entire native kidney was
submitted for biopsy. Owing to the firm adhesions to the body wall and surrounding
tissues, extensive dissection was necessary to remove the right native kidney. The
donor kidney, provided by a cat in the MJR-VHUP renal transplant colony, was
harvested and transplanted as previously described following removal of the right
native kidney (). Although the allograft kidney
was observed to be of normal color and firm consistency following transplantation,
suggesting adequate perfusion, no urine production was identified.
Postoperatively, the cat was maintained on a fentanyl continuous rate infusion (CRI;
2–3.5 μg/kg/h). The morning after the procedure, the cat appeared bright, was
ambulatory and readily ate and drank small amounts. However, throughout the day the
cat’s appetite began to decline. Owing to the decreased appetite, the ciclosporin
dosage was decreased accordingly (2.5 mg/kg PO q12h), and ondansetron (0.2 mg/kg IV
q8h) and pantoprazole (1 mg/kg IV q24h) were administered. Serum biochemical
analysis revealed azotemia (BUN 70 mg/dl [RI 15–32 mg/dl], creatinine 2.4 mg/dl [RI
1.0–2.0 mg/dl]), hypo calcemia (calcium 7.3 mg/dl; RI 9.1–11.2 mg/dl) and
hyperphosphatemia (phosphorus 8.2 mg/dl; RI 3.0–6.6 mg/dl). A focal ultrasound of
the allograft kidney revealed venous and arterial Doppler signal throughout the
entire allograft and the allograft renal vein and arteries, indicating adequate
blood flow. No evidence of obstruction was observed. Despite a prior intraoperative
transfusion of packed red blood cells, the cat remained anemic (hematocrit 22%; RI
31.70–48.00%) so another unit of packed red blood cells was administered.
Two days following the procedure, the cat developed watery, mucoid diarrhea, which
appeared to be causing irritation of the perineum. Foci of erythema and erosions
were also appreciated in the inguinal and medial thigh regions. Metronidazole (10
mg/kg IV q12h) was administered in addition to the cat’s other medications. Fentanyl
CRI was discontinued and buprenorphine (0.01–0.015 mg/kg IV q8h) was administered
for further analgesia.
Anorexia continued and a nasoesophageal feeding tube was placed 4 days
postoperatively. The cat’s clinical condition continued to progressively decline
with development of marked obtundation and signs of sepsis. Hypotension (systolic
blood pressure 64 mmHg) and severe hypoglycemia (blood glucose 30 mg/dl; RI
67.0–168.0 mg/dl) occurred. Hypoglycemia was initially treated with a dextrose bolus
(0.5 g/kg IV) and a 5% dextrose CRI (1 ml/kg/h). Ceftazidime (40 mg/kg IV q6h) and
clindamycin (10 mg/kg IV q12h) were also administered. Hypotension was treated with
a norepinephrine (0.5 μg/kg/min) CRI, a vasopressin (0.5 mIU/kg/min) CRI and a whole
blood transfusion (40 ml total). Hematologic analysis revealed a marked neutrophilia
(neutrophils 31.06 ×103/μl; RI 2.30–11.60 ×103/μl) with a
concurrent left shift (band neutrophils 6.21 ×103/μl; RI 0.00–0.10
×103/μl).
Five days following surgery, the cat began to show neurologic signs consisting of
anisocoria, delayed-to-absent palpebral reflexes and menace response bilaterally and
intractable seizures. At this time, biopsy results of the right native kidney
removed at surgery were received and histopathology showed an infiltrative
epithelial neoplasm composed of tubules of polygonal-to-cuboidal cells separated by
a desmoplastic stroma. The neoplastic cells exhibited marked anisocytosis and
anisokaryosis with prominent nucleoli, occasional binucleation and frequent mitotic
figures. These histologic features were consistent with a renal cell carcinoma (RCC)
(,). Owing to the cat’s
declining clinical condition and the diagnosis of RCC, humane euthanasia was elected
6 days postoperatively.
Post-mortem histologic evaluation of the erosive skin lesions in the inguinal and
perineal regions demonstrated severe regional epidermal and dermal necrosis with a
suppurative dermatitis and panniculitis. Blood vessels in these sections often
contained fibrin thrombi, exhibited fibrinoid vascular necrosis and occasionally
necrotizing vasculitis (). Although definitive evidence of bacteremia was not identified, the
clinical signs and postmortem lesions were highly suggestive of an acute
inflammatory response. Given the histologic lesions in the skin, ischemic dermal
necrosis secondary to thromboembolic (TE) disease with subsequent bacterial invasion
was suspected. Similar lesions were identified in the digital and metatarsal pads of
the left pelvic limb during necropsy (). Primary necrotizing dermatitis due
to diarrhea and urine scalding seemed much less likely based on the vascular changes
noted on histology but could not be definitively ruled out. Further supporting TE
disease, multifocal acute intravascular fibrin thrombi were distributed throughout
multiple other tissues, including the allograft kidney, heart, right adrenal gland
and one of the anomalous branches of the caudal vena cava (). The allograft kidney had multiple
fibrin thrombi within the vessels of the renal cortex and corticomedullary junction
and foci of segmental acute tubular necrosis with tubular casts (,). No evidence of inflammation suggesting
rejection was found within the allograft or at the vascular anastomoses. No lesions
were found in histologic sections of the brain; however, focal vascular lesions or
peracute ischemic events without appreciable histomorphologic changes could not be
excluded as possible causes of the cat’s neurologic signs. Metabolic derangements
could have also contributed. Cysts found in the left native kidney, liver and
pancreas were consistent with PKD.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [10, 'years'], 'creatinine': [2.7, 'mg/dL'], 'sex': 'Female'}",26.72637,25.39005,28.06269,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 10 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.7 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.7/0.7)**-1.2 * 0.9938**10 * 1.012 = 26.72637.
Hence, the GFR value is 26.72637 ml/min/1.73 m²."
238,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5295655-1,Extracted,"A 30-year-old non-smoker male, carpenter by occupation was detected to have end-stage renal disease due to chronic glomerulonephritis in 2006. He remained on intermittent hemodialysis till he received a renal allograft from his 50 years old mother in August 2008. He was not given induction therapy. He received triple immunosuppression that included oral prednisolone, mycophenolate mofetil and tacrolimus in therapeutic doses. Due to financial constraints, mycophenolate mofetil was replaced with oral azathioprine 100 mg a day after 3 months of renal transplantation. He maintained normal graft function. Four years after transplant, he presented with hoarseness of voice of 2 months duration. This was insidious in onset, progressively increasing and was not associated with neck pain, voice fatigue and cough. There was no relief with voice rest. There was no history of fever, hemoptysis and weight loss.
His general physical and systemic examination was essentially unremarkable. There was no tenderness or bruit over the graft kidney. The local examination of the nose, throat and ear did not show any gross abnormality. Flexible fiberoptic laryngoscopy showed an exophytic growth on the vocal process of the left arytenoid, extending anteriorly till the anterior commissure. The growth was excised under general anaesthesia and the base fulgurated. The tissue was sent for histopathological and microbiological examination, to evaluate for neoplastic and fungal pathology.
On investigations, the complete blood count (CBC) showed mild anemia with hemoglobin of 12.5 gm/dl and normal total and differential leukocyte and platelet counts. Urine examination showed absence of proteinuria and hematuria. The blood biochemistry revealed blood urea and serum creatinine of 40 mg/dl and 1.5 mg/dl respectively. His serology tests for hepatitis B surface antigen and antibodies to hepatitis C virus, Human immunodeficiency virus and cytomegalovirus were negative. Chest x-ray was normal. Biopsy from laryngeal mass lesion exhibited a polypoidal appearance lined by stratified squamous epithelium underneath which sheets of histiocytes containing numerous spores of cryptococcus of variable sizes were seen (). The PAS stain highlighted the fungus spores (). While, clinically there were no signs and symptoms of meningitis, the cerebrospinal fluid (CSF) examination was done that was negative for cryptococcal meningitis. Patient was treated with oral fluconazole 400 mg per day for 6 months and recovered completely. Since fluconazole has interaction with calcineurin inhibitors, the dose of tacrolimus was decreased to 1 mg twice a day maintaining the blood levels in the therapeutic range.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [30, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Male'}",63.83217,60.64056,67.02378,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 30 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.5/0.9)**-1.2 * 0.9938**30 * 1.0 = 63.83217.
Hence, the GFR value is 63.83217 ml/min/1.73 m²."
239,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7427638-1,Extracted,"A 46-year-old male was admitted to a hospital in the Metropolitan Area of Belo Horizonte, Minas Gerais, Brazil, with leg edema progressing since six months prior to hospitalization, associated with foamy urine and weight gain of 10 Kg. The patient had a history of systemic hypertension, hyperuricemia, dyslipidemia, and recurring use of non-steroid anti-inflammatory drugs. Physical examination revealed he had edema on both legs (2+/4+). His blood pressure was normal (BP 120x60 mmHg) and he breathed normally in ambient air. The patient was on amoxicillin/clavulanic acid for community-acquired pneumonia. His renal function was preserved (serum creatinine: 0.86 mg/dL) and he did not have fluid and electrolyte disorders or anemia (Hb: 12.1 mg/dL). Urine tests showed urinary protein (3+/3+) and hematuria with erythrocyte dysmorphism (30%), 4.0 g of urinary protein over 24 hours, hypoalbuminemia (albumin: 1.5 mg/dL), and hypercholesterolemia (total cholesterol: 217 mg/dL). Serology tests for HIV, hepatitis B and C, VDRL, ANA, RF, and ANCA were negative. C4 level: 35.5 mg/dL; C3 level: 126.3 mg/dL. His transthoracic echocardiogram showed an ejection fraction of 65% without ventricular dysfunction, while venous ultrasound examination of the legs did not reveal signs of deep venous thrombosis. The patient was suspected for glomerular disease, and a kidney biopsy was thus ordered. Examination of biopsy specimens on a light microscope showed glomeruli with a slightly expanded mesangial matrix and increased mesangial hypercellularity, a diffusely thickened GBM with small spikes (), and preserved tubulointerstitial and vascular spaces. Immunohistochemistry analysis with fluorescein revealed a speckled pattern along the basement membrane stained positive for IgG, C3, Kappa and Lambda. Mesangial expression of IgA, C3, Kappa and Lambda was also found ( to ). Peroxidase immunohistochemistry showed a strong granular pattern along the basement membrane stained positive for IgG1, IgG4, THSD7A, and PLA2R ( to ). Examination with an electron microscope helped to identify electron-dense subepithelial and mesangial immune deposits with diffuse podocyte foot process alterations, including flattening and effacement ( and ). These alterations are consistent with stage II membranous nephropathy associated with IgA nephropathy stained positive for PLA2R and THSD7A. The patient underwent examination with upper gastrointestinal endoscopy, colonoscopy, and chest/abdomen computed tomography scans, and was tested for serum CEA and CA 19-9, but relevant alterations were not found. The patient is stable and has had steady decreases in urine protein levels (3.5 grams/24 hours after two months). He is currently on dual RAAS blockade, hemodynamically stable, and free of renal function alterations.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [46, 'years'], 'creatinine': [0.86, 'mg/dL']}",100.24046,95.22844,105.25248,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 46 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.86 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.86/0.7)**-0.302 * 0.9938**46 * 1.0 = 100.24046.
Hence, the GFR value is 100.24046 ml/min/1.73 m²."
240,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4440474-2,Extracted,"A 60-year-old Caucasian female received her annual influenza vaccination in November 2009, and 53 days later, in January 2010, she was hospitalized for evaluation of acute renal graft failure.
In September 2008, she received a living-related donor renal transplant (HLA-A, B, DR mismatch 1-2-1) and afterwards had stable kidney function with a plasma creatinine level of 90 µmol/L and without detectable albuminuria (20 October 2009). Her native renal disease was unknown. Her hypertension was treated with a calcium channel blocker, and she had a pacemaker due to sinus node dysfunction. She received immunosuppressive treatment with prednisolone 5 mg once daily, mycophenolate mofetil 500 mg twice daily and tacrolimus 3 mg once daily.
At admission, she complained of nausea and swelling of the face and lower limbs, which started after the vaccination. Plasma creatinine was elevated to 250 µmol/L. Urine dip stick showed no red blood cells, but 24-h urine collection revealed microalbuminuria of 100 mg (23 January 2010). Medical investigation included polyomavirus, ANCA (MPO and PR3), anti-GBM, ANA, anti-DNA, C3, C4, Ig-screening and CMV antigenemia—all of which were within normal limits.
Ultrasound of the graft did not reveal urinary obstruction, and there were no signs of infection. Renal biopsy showed acute cellular rejection (type IA according to the Banff classification) with severe interstitial oedema, interstitial inflammation (i2) and focal moderate tubulitis (t2). There were no signs of humoral rejection, and C4d staining was negative. Flow cytometric crossmatch was negative.
Treatment with methylprednisolone 500 mg daily was initiated. Despite 4 days of treatment, plasma creatinine was still 422 µmol/L. Chronic dialysis was initiated in November 2010.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [60, 'years'], 'creatinine': [422.0, 'µmol/L'], 'sex': 'Female'}",9.93995,9.44295,10.43695,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 60 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 422.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 422.0 µmol. To convert 422.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 422.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00042 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00042 mol Serum Creatinine * 113.12 g/mol = 0.04751 g Serum Creatinine. To convert 0.04751 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.04751 g Serum Creatinine * 1000.0 mg/g = 47.51 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 47.51 mg Serum Creatinine/10.0 dL = 4.751 mg Serum Creatinine/dL. The concentration value of 422.0 µmol Serum Creatinine/L converts to 4.751 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (4.751/0.7)**-1.2 * 0.9938**60 * 1.012 = 9.93995.
Hence, the GFR value is 9.93995 ml/min/1.73 m²."
241,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5819634-1,Extracted,"An 81-year-old female presented to the emergency department (ED) complaining of progressive shortness of breath over the preceding few weeks. Other symptoms include weight loss of 30 lb over 5 months, pain in both knees and hips, as well as swelling and numbness in her right-hand fingers. Patient had been following regularly at the cardiology clinic. She had extensive past medical history significant for chronic kidney disease (CKD) stage III, hypertension, coronary artery disease and history of remote myocardial infarction complicated by right ventricular (RV) aneurysm with mural thrombus treated with warfarin therapy, and sick sinus syndrome managed with a pacemaker. She also had remote colon cancer treated with partial colectomy.
On arrival to the ED, she was afebrile, had tachypnea and tachycardia with stable blood pressure. Physical exam revealed fine crackles along the bases and absent pedal edema. She had wide spread hyper pigmented macules and papules over the back and extremities. Initial laboratory workup showed creatinine 2.84 mg/dL, hemoglobin (Hb) 8.2 g/dL, brain natriuretic peptide (BNP) 317 pg/mL and normal troponin level. Electrocardiogram (EKG) showed ST changes along the inferior leads with low voltage QRS (). Transthoracic echocardiography (TTE) revealed a large circumferential pericardial effusion with tamponade physiology (). Previously seen RV mural thrombus was not identified. Pericardiocentesis was performed with 700 mL of frankly bloody pericardial fluid drained, and a pigtail catheter was left in place for passive dependent drainage (). Pericardial fluid analysis showed a hemorrhagic exudate without evidence of infection or malignancy based on normal microbiology studies and cytology results.
Further tests showed an erythrocyte sedimentation rate (ESR) 109 mm/h, C-reactive protein (CRP) 10.5 mg/L and normal thyroid function test. She had positive serology for ribonucleoprotein antibodies at 1.9 consistent with a diagnosis of MCTD. Further serology tests were negative for anti-dsDNA, ribosomal P protein, anticentromere Ab, Sjogren’s syndrome A and B, Jo1 Ab and Scl-70 Ab.
Computed tomography (CT) scan of the chest, abdomen, and pelvis showed no evidence of malignancy, and tumor markers including CA19-9, CA125 and CEA were negative. Follow-up echocardiogram during admission showed rapidly re-accumulating pericardial effusion. Accordingly, she had a sub-xiphoid pericardial window placed and pericardial tissue biopsy revealed acute and chronic fibrinous pericarditis (). Patient responded to empiric therapy with intravenous prednisone. Prior to discharge, echocardiography showed left ventricular ejection fraction (LVEF) of 30-35% with only a trivial pericardial effusion. Given the high risk for recurrence of a pericardial effusion and lack of a mural thrombus, warfarin was held.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [81, 'years'], 'creatinine': [2.84, 'mg/dL'], 'sex': 'Female'}",16.1742,15.36549,16.98291,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 81 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.84 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.84/0.7)**-1.2 * 0.9938**81 * 1.012 = 16.1742.
Hence, the GFR value is 16.1742 ml/min/1.73 m²."
242,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8559581-1,Extracted,"An 18-year-old male with a history of recurrent pharyngitis presented with a sore throat, fever, and progressive shortness of breath for 10 days. The patient had been previously evaluated at an outpatient urgent care clinic where both monospot and streptococcal RADT had been negative. He had been given a prescription for prednisolone for presumed bronchitis, which he had taken for two days prior to admission. He denied any history of sick contacts, travel, use of intravenous drugs, or recent dental intervention.
Upon admission to our hospital, the patient was febrile, tachycardic, hypotensive, and in respiratory distress. Physical exam revealed generalized neck pain aggravated by movement, right-sided swollen neck, and lymphadenopathy. The cardiac examination did not reveal any murmurs but pulmonary auscultation revealed bilateral coarse crackles. Abdominal, musculoskeletal, and neurological examinations were unremarkable.
Laboratory findings revealed the following results: white blood cell count: 24 k/µL (4.40-11.30 k/µL) with bandemia; platelet count: 26 k/µL (145-445 k/µL); and serum creatinine: 2.65 mg/dL (0.50-0.90 mg/dL). The liver function test was within the normal range.
The patient’s condition deteriorated and he was emergently intubated. He developed acute respiratory distress syndrome (ARDS) and required prone positioning to allow for improved oxygenation. Chest radiograph (Figure ) and subsequent CT scan (Figure ) revealed multifocal pulmonary consolidation and nodules. A transesophageal echocardiogram was negative for valvular vegetations. Blood cultures revealed F. necrophorum, group F Streptococcus, and Gemella sp. Venous duplex ultrasound of the neck revealed a thrombus in the right IJV. The patient was subsequently diagnosed with LS. Intravenous ampicillin-sulbactam was initiated and a single dose of gentamicin was given. The patient subsequently defervesced, with extubation on day 18 of hospitalization, and was discharged on day 29 with an additional two-week course of amoxicillin-clavulanic acid. He did not receive anticoagulants. No further studies were performed for clot progression and/or resolution as the patient was lost to follow-up.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [18, 'years'], 'creatinine': [2.65, 'mg/dL'], 'sex': 'Male'}",34.74291,33.00576,36.48006,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 18 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.65 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.65/0.9)**-1.2 * 0.9938**18 * 1.0 = 34.74291.
Hence, the GFR value is 34.74291 ml/min/1.73 m²."
243,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5348141-1,Extracted,"A 37-year-old Asian lady presented to the emergency department with sudden onset of back pain and fainting. She was an epileptic, had mental retardation, and a history of progressive low abdominal fullness since a year. Physical examination revealed facial angiofibromatosis, a tender palpable mass in the lower abdomen and ecchymosis over the flank. Relevant routine blood laboratory investigations were (values [reference range]): white blood count 9.8 × 109 /L (4–11), hemoglobin 6.1 g/dL (12–15), creatinine 1.59 mg/dL (0.8–1.3). A contrast-enhanced abdominal CT revealed multiple bilateral renal angiomyolipoma (AML), with confined retroperitoneal hemorrhage around the left kidney. An extensive pelvic tumor, 153.12 × 100.03 mm in the transverse plane, was also seen almost filling the pelvic cavity, resulting in compression of the urinary bladder, uterus, rectum, and small bowel. Genetic studies revealed TSC-2 gene mutation. A diagnosis of tuberous sclerosis (TSC) associated with bilateral AML and pelvic LAM was made and supportive care was instituted. Everolimus 10 mg/day was prescribed after informed consent. She made an uneventful recovery without surgery. Follow-up CT scans showed marked regression of the bilateral AML and pelvic LAM (Fig. ). We used the Response Evaluation Criteria in Solid Tumors, RECIST, Version 1.1, to measure tumor response in an objective manner, in both patients. The largest pelvic tumor diameter was measured serially and the RECIST calculator showed that the pelvic mass (target lesion) shrunk to 105.72 mm within 4 months (–30.72%) and to 74.64 mm at 12 months (–50.98%). There was also notable regression of the renal AML (nontarget lesions) bilaterally. This amounted to a partial response. Adverse effects of the drug were explained in detail, and sought at follow-up sessions, but none were found except mild stomatitis (Table ). No dose adjustment was necessary. Her epileptic seizures were also well controlled by the drug.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [37, 'years'], 'creatinine': [1.59, 'mg/dL'], 'sex': 'Female'}",42.65527,40.52251,44.78803,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 37 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.59 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.59/0.7)**-1.2 * 0.9938**37 * 1.012 = 42.65527.
Hence, the GFR value is 42.65527 ml/min/1.73 m²."
244,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8361506-1,Extracted,"The patient is a 53-year-old African American female with a past medical history of
hypertension and diabetes mellitus type 2 who presented to the emergency department
with altered mental status. Her family reported that she had been feeling unwell for
3 days. Her symptoms subsequently progressed to altered mentation and dyspnea. In
the emergency department, initial vital signs include a temperature of 36.6 °C,
heart rate of 112 beats per minute, blood pressure of 140/72 mm Hg, respiratory rate
of 28 breaths per minute, and oxygen saturation of 96% on room air. On physical
examination, the patient was confused and agitated. She was tachypneic and
tachycardic on heart and lung examination. Laboratory tests () revealed leukocytosis with a
white blood cell count of 19.9 × 109/L, absolute neutrophils of 89.3%,
and a platelet count of 507 × 109/L. The basic metabolic panel revealed a
sodium level of 131 mmol/L, potassium of 6.2 mmol/L, chloride of 104 mmol/L, total
CO2 of 6, glucose level >38.8 mmol/L, BUN (blood urea nitrogen) of
25 mmol/L, creatinine of 362.5 µmol/L, high anion gap of 28, and acetone was large.
Arterial blood gas revealed a high anion gap metabolic acidosis with compensatory
respiratory alkalosis. Computed tomography (CT) of the head without contrast was
unremarkable. The patient was started on intravenous fluids and insulin infusion and
was transferred to the intensive care unit to manage DKA and acute kidney
injury.
In the intensive care unit, the patient’s DKA resolved, and altered mentation
improved significantly over 3 days; however, her renal function progressively
worsened. Her BUN and serum creatinine continued to trend up, and she became
oliguric. Given these changes, an Udall catheter was placed for hemodialysis. Of
note, the patient had a creatinine level of 88 µmol/L and BUN of 3.6 mmol/L on her
outpatient blood work 2 months before this presentation.
In the days following treatment, the patient became febrile, with a
Tmax of 39.1 °C and tachycardic, but she remained
hemodynamically stable. A septic workup was performed, and empiric broad-spectrum
antibiotics were started along with antipyretics. Blood cultures grew K
pneumoniae. Ultimately, a CT scan of the abdomen and pelvis with oral
contrast showed several hypoattenuating hepatic lesions and heterogeneous splenic
hyperattenuation concerning for splenic infarcts. Magnetic resonance imaging of the
abdomen and pelvis to further characterize these lesions revealed about 8 lesions in
the left hepatic lobe, with the largest lesion measuring 3.9 × 3.2 × 3.7 cm in size,
within segment 3 of the left hepatic lobe concerning for hepatic abscess. There were
also numerous ill-defined peripherally located lesions within the spleen concerning
for abscesses. Piperacillin/tazobactam was de-escalated to ceftriaxone along with
metronidazole. Percutaneous drainage of the left hepatic lobe abscess through
Interventional Radiology guidance yielded 30 mL of pus that grew K
pneumoniae as well (see and ).
The patient’s overall condition improved, and repeat blood cultures were negative.
Her renal function stabilized, and dialysis was discontinued. A repeat CT scan of
the abdomen and pelvis revealed worsening of several ill-defined hypoattenuating
splenic lesions with adjacent perisplenic fluid, which required percutaneous
drainage of the splenic abscesses.
Likewise, her hospital course was complicated by acute right femoral, popliteal, and
peroneal vein deep vein thrombosis, for which she was started on high-range heparin
infusion, which was discontinued after 2 days due to a steep decline in hemoglobin
level. An inferior vena cava filter was subsequently inserted. A colonoscopy
revealed a 15-mm polyp in the cecum and nonbleeding hemorrhoids. Her hemoglobin
level subsequently stabilized following blood transfusions. She continued to improve
clinically on the current antibiotic regimen. Ultimately, she was discharged to
complete a 6-week course of antibiotics through a peripherally inserted central
catheter line to follow-up outpatient with nephrology, infectious disease, and
primary care physician.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [53, 'years'], 'creatinine': [362.5, 'µmol/L']}",12.49291,11.86826,13.11756,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 53 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 362.5 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 362.5 µmol. To convert 362.5 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 362.5 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00036 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00036 mol Serum Creatinine * 113.12 g/mol = 0.04072 g Serum Creatinine. To convert 0.04072 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.04072 g Serum Creatinine * 1000.0 mg/g = 40.72 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 40.72 mg Serum Creatinine/10.0 dL = 4.072 mg Serum Creatinine/dL. The concentration value of 362.5 µmol Serum Creatinine/L converts to 4.072 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (4.072/0.7)**-1.2 * 0.9938**53 * 1.012 = 12.49291.
Hence, the GFR value is 12.49291 ml/min/1.73 m²."
245,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7338606-3,Extracted,"The patient is a 25-year-old woman who presented at age 16 with lower extremity edema when she was approximately six months pregnant. Kidney biopsy at that time revealed DDD with 45% active crescents and marked acute tubulointerstitial injury (). On immunofluorescence, approximately half the glomeruli had capillary wall and/or mesangial staining for C3 (4+) in a segmental confluent granular to pseudolinear pattern. On electron microscopy, capillary walls were irregular and segmentally had thickened with osmiophilic deposits which segmentally transformed and replaced the lamina densa. There were scattered aggregates of electron dense deposits in a subepithelial and intramembranous distribution, and a pathological diagnosis of DDD was made. At that time the serum creatinine was 0.99 mg/dl, with normal C3 89.5 [76–165 normal range] and C4 80.1 (16–48 normal range). The patient declined treatment at that time because of concern about taking medications during her pregnancy.
Six days after a full-term delivery, she presented to a different hospital with abdominal pain, dysuria, and worsening edema. Labs were significant for creatinine 4.1 mg/dL, albumin 1.6 g/dL, and urine protein-to-creatinine ratio of 9.3 g/g. In addition, there was isolated depression of C3 at 54.1 [76–165 normal range] with normal C4 37.5 [16–48 normal range]. A repeat kidney biopsy again showed DDD with extensive crescent formation. The tubulointerstitium showed interstitial inflammation with focal intratubular neutrophils and cellular debris suggestive of acute pyelonephritis, as well as evolving parenchymal scarring (). On electron microscopy, few and large, “hump-like” subepithelial deposits were noted. She was treated with intravenous antibiotics, one dose of intravenous methylprednisolone 500 mg, and five sessions of plasma exchange. She also started hemodialysis at that time.
Genetic testing was performed as part of a transplant evaluation. A C3 glomerulonephritis (C3GN)/DDD genetic susceptibility panel, including C3, CFB, CFH, CFHR1, CFHR2, CFHR1, CFI, MCP (CD46) identified no known mutations. In addition, C3Nef, Factors B, H, and I, Factor H autoantibody, and soluble C5b-9 levels were within normal limits (reference range <1).
The patient was activated on the kidney transplant list. After 9 years on dialysis, the patient underwent a deceased donor kidney transplant (donor in 30 s, terminal creatinine 1 mg/dl). She received basiliximab for induction immunosuppression and tacrolimus, mycophenolate mofetil, and prednisone for maintenance immunosuppression. Her post-transplant course was significant for expected delayed graft function given cold ischemia time of 19 h requiring hemodialysis for two sessions post-transplant. She was monitored closely with no evidence of proteinuria or intermittent microscopic hematuria. She is now over 1-year post-transplant with a creatinine of 0.9 mg/dl and no evidence of proteinuria or hematuria to indicate recurrent disease.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [25, 'years'], 'creatinine': [0.9, 'mg/dL']}",90.98511,86.43585,95.53437,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 25 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.9 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.9/0.7)**-1.2 * 0.9938**25 * 1.012 = 90.98511.
Hence, the GFR value is 90.98511 ml/min/1.73 m²."
246,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8225443-1,Extracted,"A 77-year-old Caucasian male with a past medical history of insulin-dependent diabetes mellitus, dyslipidemia, hypertension, and chronic kidney disease stage IIIa presented to the emergency department due to bilateral lower extremity pain. The patient was diagnosed and treated for lower extremity cellulitis. Due to pain of his lower extremities with ambulation, the patient requested an indwelling urinary catheter. Therefore, urinary catheter placement was performed on the patient's request. Prior to discharge to the skilled nursing facility, discontinuation of the indwelling urinary catheter was recommended multiple times to the patient, but he refused the catheter's removal. He was discharged to the skilled nursing facility after having completed his antibiotic course. He was to continue furosemide, gabapentin, and also nystatin cream for prophylactic prevention of fungal infection on his feet bilaterally.
Nearly three weeks after discharge to the skilled nursing facility, the patient was brought to the emergency department by emergency medical services due to signs of a possible stroke observed at the facility. He was demonstrating dysarthria, right-sided facial droop, and right-sided weakness. These symptoms were first noted about 2.5 hours prior to arrival. Computed tomography head showed no acute abnormality. The patient was not a candidate for alteplase due to an elevated INR.
Initial emergency department vitals showed a temperature of 38.3. After blood cultures were drawn, a single dose of one gram of ceftriaxone was given to the patient. Later that day, the patient's antibiotics were broadened to vancomycin and cefepime. On his physical exam, the patient's speech remained dysarthric, and he also exhibited a right-sided facial droop with right-sided weakness. The indwelling urinary catheter from his previous admission was still in place. His labs were remarkable for a creatinine level of 3.50, a blood urea nitrogen of 105, a potassium level of 5.2, and a serum bicarbonate of 17. His white blood cell count was within normal limits. Computed tomography angiography of the head and neck vessels was performed in the emergency department even with his acute on chronic kidney injury with a creatinine of 3.50. The computed tomography scans revealed a 50% to 70% stenosis of the left carotid artery and a less than 50% stenosis of the right carotid artery at the bifurcation. The patient underwent magnetic resonance imaging of the brain the following day, which revealed no signs of an acute stroke.
Upon returning to his hospital room after his magnetic resonance imaging scan, the patient was observed to be unresponsive with no palpable pulses. Cardiopulmonary resuscitation was started. Once return of spontaneous circulation was achieved, the follow-up electrocardiogram did not reveal any ST-segment or T-wave changes concerning for ischemia or infarction. Transthoracic echocardiogram with a bubble study revealed an ejection fraction estimated at 50% to 55% without any wall motion abnormalities and a negative bubble study. Alarmingly, the echocardiogram reported “a possible vegetation attached to the tricuspid valve with a separate possible vegetation attached to the Eustachian valve.” It also reported mild-to-moderate tricuspid regurgitation.
At this time, the patient's blood cultures returned positive for fungal growth. Urine cultures were drawn following the blood culture results, and those cultures also demonstrated fungal growth. The patient's blood and urine cultures were finalized as Candida lusitaniae, and the patient continued on micafungin 150 mg daily. As this organism is highly uncommon, multiple blood cultures were drawn. However, on 3 different days, the blood cultures resulted positive for C. lusitaniae.
As the days progressed, the patient displayed findings consistent with an anoxic brain injury. Therefore, the decision was made with the family to withdraw care, and the patient expired soon after.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [77, 'years'], 'creatinine': [3.5, 'mg/dL'], 'sex': 'Male'}",17.23932,16.37735,18.10129,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 77 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.5/0.9)**-1.2 * 0.9938**77 * 1.0 = 17.23932.
Hence, the GFR value is 17.23932 ml/min/1.73 m²."
247,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7993970-1,Extracted,"A 68-year-old male with a solitary kidney, had a history of multiple abdominal surgeries due to adenocarcinoma of sigmoid colon, including left hemi-colectomy and right nephrectomy with adjuvant chemo-radiation therapy. On follow-up, a recurrent tumor was diagnosed at the bowel anastomotic site, including a mass invasion into the distal left ureter. Following the resection of the tumor and the involved segment of the left ureter, a temporary colostomy was created, and ureteroneocystotomy using combined Boari flap and Psoas hitch techniques were applied to reestablish urinary continuity.
Three years later, laboratory examinations revealed a serum creatinine of 3.4mg/dL (baseline 1.4mg/dL). Physical examination was unremarkable and renal ultrasound (US) demonstrated severe left hydronephrosis. Further antegrade imaging through a percutaneous nephrostomy which was inserted to by-pass the obstruction, confirmed the presence of a 2cm long ureteral stricture above the previous flap formation (). Serum creatinine decrease to 1.6mg/dL following insertion of percutaneous nephrostomy. Absence of tumor recurrence was confirmed with PET-CT and cystoscopy.
A re-do Boari flap was performed, using an open approach: the healthy ureter was transected above the stenotic segment at the level of the previous flap. The ureter was re-implanted to a newly formed Boari flap, which was harvested again from the bladder wall (). The postoperative period was uneventful, the urethral catheter and the double J stents were removed 2 and 6 weeks, respectively. Postoperative follow-up imaging showed no urine leak after the surgery before the removal of the urethral catheter (). A 10-year follow-up showed no hydronephrosis and no aggravation of the kidney function.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [68, 'years'], 'creatinine': [3.4, 'mg/dL']}",18.87714,17.93328,19.821,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 68 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.4 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.4/0.9)**-1.2 * 0.9938**68 * 1.0 = 18.87714.
Hence, the GFR value is 18.87714 ml/min/1.73 m²."
248,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7502416-1,Extracted,"The patient was a 68-year-old male nursing home resident, with a past medical history of diabetes mellitus, hypertension, and stage IV chronic kidney disease. He denied any history of tobacco, alcohol, or substance use. After an outbreak of COVID-19 at his residence, a routine polymerase chain reaction (PCR) test was done, which confirmed COVID-19 infection two days prior to presenting to the emergency department (ED). The patient complained of loss of appetite and nausea for one week while denying any respiratory symptoms. In the ED, he was afebrile and saturating 97% on room air. On examination, he appeared dehydrated and lethargic, while his lung sounds were clear and his abdomen was soft and non-tender. Laboratory workup on admission revealed white blood cell (WBC) 8900 ug/L without lymphopenia, sodium 136 mmol/L, blood urea nitrogen (BUN) 77 mg/dl, creatinine 6.6 mg/dl, glucose 46 mg/dl, procalcitonin 6.04 ng/ml, C-reactive protein (CRP) 158 mg/L, aspartate aminotransferase (AST) 27 U/L, alanine aminotransferase (ALT) 20 U/L, alkaline phosphatase (ALP) 123 U/L and total bilirubin of 0.5 mg/dl. The chest radiograph showed a faint patchy opacity in the left perihilar region (Figure ). He was admitted for acute on chronic kidney injury and hypoglycemia due to poor oral intake. He was also empirically covered with antibiotics for possible superimposed bacterial pneumonia.
Over the next few days, the patient's kidney function improved with hydration. He had persistent nausea, vomiting, and anorexia, but no abdominal pain. A non-contrast abdominal computed tomography (CT) scan revealed peripancreatic fat stranding, greatest around the tail, with mild duodenal wall thickening and adjacent fat stranding, likely from pancreatitis. The gallbladder appeared normal, without wall thickening or surrounding inflammatory changes, and the common bile duct was not dilated (Figure ). Amylase and lipase levels were elevated at 1030 U/L and 2035 U/L, respectively, but the triglyceride and calcium levels were normal. The patient was kept on bowel rest, and given continuous intravenous fluids and antiemetics. Throughout the admission, he did not have any respiratory signs or symptoms, nor did he require oxygen supplementation. Repeat chest radiograph did not show any focal consolidations. The patient's appetite eventually improved, and his diet was advanced. He was discharged seven days later back to his nursing home with a follow-up appointment.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [68, 'years'], 'creatinine': [6.6, 'mg/dL'], 'sex': 'Male'}",8.51644,8.09062,8.94226,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 68 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 6.6 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (6.6/0.9)**-1.2 * 0.9938**68 * 1.0 = 8.51644.
Hence, the GFR value is 8.51644 ml/min/1.73 m²."
249,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-942,Extracted,"A 46-year-old woman comes to the physician for a routine health examination. She was last seen by a physician 3 years ago. She has been healthy aside from occasional mild flank pain. Her only medication is a multivitamin. Her blood pressure is 154/90 mm Hg. Physical examination shows no abnormalities. Serum studies show:
Sodium 141 mEq/L
Potassium 3.7 mEq/L
Calcium 11.3 mg/dL
Phosphorus 2.3 mg/dL
Urea nitrogen 15 mg/dL
Creatinine 0.9 mg/dL
Albumin 3.6 g/dL
Subsequent serum studies show a repeat calcium of 11.2 mg/dL, parathyroid hormone concentration of 890 pg/mL, and 25-hydroxyvitamin D of 48 ng/mL (N = 25–80). Her 24-hour urine calcium excretion is elevated. An abdominal ultrasound shows several small calculi in bilateral kidneys. Further testing shows normal bone mineral density.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [46, 'years'], 'creatinine': [0.9, 'mg/dL'], 'sex': 'Female'}",79.84526,75.853,83.83752,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 46 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.9 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.9/0.7)**-1.2 * 0.9938**46 * 1.012 = 79.84526.
Hence, the GFR value is 79.84526 ml/min/1.73 m²."
250,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7286590-2,Extracted,"The second case is a 16-year-old male with a history of high-grade reflux nephropathy, solitary left kidney, and neurogenic bladder on intermittent Foley catheterization every three hours. The patient had stage 4 CKD with an elevated serum creatinine of 6.1 mg/dL (baseline 3.0 mg/dL) in December 2016, which warranted the placement of a left nephrostomy tube. The nephrostomy tube was removed in March 2017. He presented to the ED with nausea and vomiting four days after left nephrostomy tube removal. There was no trauma or contact with contaminated water. He was afebrile and denied flank pain. The nephrostomy site did not appear to be infected. Creatinine was 5.0 mg/dL and blood urea nitrogen (BUN) was 55 mg/dL. The mother was concerned for pyelonephritis, but ultrasound at the time did not show any significant changes in the left kidney. A midstream urine culture grew 70,000 cfu/mL L. adecarboxylata. Susceptibility panel showed that it was sensitive to ampicillin, ampicillin/sulbactam, cefazolin, gentamicin, nitrofurantoin, and tobramycin. The patient was discharged home with oral cephalexin. A week later, the patient presented back at the ED with left flank pain and intermittent vomiting, but no fever. He was not compliant with the antibiotic regimen due to complex social situation. He was hospitalized and started on IV ceftriaxone. Creatinine improved at 4.3 mg/dL, BUN remained elevated at 53 mg/dL, and albumin was decreased at 3.5 g/dL. Urinalysis was significant for 2+ proteinuria, but absence of white blood cells, leukocyte esterase, nitrite, and bacteria. Ultrasound (Figure ) showed a hypodense mass in the left mid-kidney concerning for a possible abscess or a callous reaction to prior nephrostomy. Urine culture was negative for organisms, and the patient no longer experienced any left flank pain after 24 hours. He was afebrile and denied nausea and vomiting. The patient was discharged home on cefdinir. There was no symptomatic recurrence, and renal ultrasound at follow-up was stable.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [16, 'years'], 'creatinine': [4.3, 'mg/dL'], 'sex': 'Male'}",19.67891,18.69496,20.66286,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 16 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 4.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (4.3/0.9)**-1.2 * 0.9938**16 * 1.0 = 19.67891.
Hence, the GFR value is 19.67891 ml/min/1.73 m²."
251,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6842836-1,Extracted,"A 16-year-old male patient with Wilson's disease who was followed-up at pediatric gastroenterology for 5 years admitted to the pediatric emergency department for myoclonic contractions on the whole body. From the review of the patient's history, it was detected that the patient was using D-penicillamine as a chelating agent. D-penicillamine was discontinued, and trientine treatment was initiated due to neurological problems and tremor on the hands while the patient was using D-penicillamine until 1 month before. In the first physical examination in the pediatric emergency department, pulse was 98/min, respiratory count was 24/min, and TA was 130/85 mm Hg. The eyeballs were sunken, the skin reduced turgor, and deep tendon reflexes were normoactive. Values in the complete blood count were as follows: hemoglobin: 14 g/dL, platelet count: 250.000/µL, leukocyte count: 24.400/µL. In the urine analysis, density was 1035, and protein 3+ and abundant erythrocytes were determined in microscopy. The biochemical tests revealed the followings: BUN 60 mg/dL, creatinine 2.34 mg/dL, uric acid 9.5 mg/dL, sodium 139 mmol/L, potassium 5.2 mmol/L, phosphorus 8 mg/dL, AST 5053 U/L, ALT 6398 U/L, LDH 1400 U/L, and creatinine clearance 13.5 mL/min. Complements (C3, C4) and IgA values were within the normal range, and viral serology was negative. Prothrombin time was 15.1 seconds, aPTT was 29 seconds, fibrinogen was 281 mg/dL, and the direct Coombs test was negative. Blood gas values were as follows: pH 7.32, pCO 29, HCO 14.9, and BE –10.1. Creatine kinase (CK) level was 15197 U/L, and myoglobin in the blood and urine was above 3900 ng/mL. The echocardiographic evaluation was found to be normal; dimensions of the kidneys were normal on the urinary system ultrasonography, and an increase in parenchyma echogenicity (consistent with grade II parenchymal disease) was noted. Rhabdomyolysis and acute renal failure were considered, so the patient was not hydrated. He was admitted to the pediatric intensive care unit with the diagnosis of acute renal failure due to rhabdomyolysis. Rhabdomyolysis was associated with trientine, and trientine treatment was stopped. The CK value of the patient increased up to 546.326 at the 36th hour of hospitalization and then followed a falling trend (). Continued renal replacement therapy was started, and hemodiafiltration was performed with a 12 Fr hemodialysis catheter placed in the internal jugular vein for 3 days. Then, the patient was taken to the routine hemodialysis program for 3 days a week. The patient began to urinate on the 24th day of intensive care unit admission. Creatinine levels gradually decreased and normalized on day 28. Written informed consent was obtained from the family.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [16, 'years'], 'creatinine': [2.34, 'mg/dL']}",40.84174,38.79965,42.88383,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 16 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.34 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.34/0.9)**-1.2 * 0.9938**16 * 1.0 = 40.84174.
Hence, the GFR value is 40.84174 ml/min/1.73 m²."
252,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7441249-1,Extracted,"A 46-year-old man with HCV infection and dysuria for 1 wk was referred to our department for HCV therapy assessment in September 2018. Genotyping revealed HCV 3b. Initial viral load was 5.8 lgIU/mL. Liver stiffness was 8.0 kPa by liver transient elastography (Fibroscan®).
At 8 wk later, the patient started taking oral tamsulosin hydrochloride (0.2 mg/d) because of dysuria. Forty-eight hours later, the patient complained of progressive bilateral lower extremity edema and facial edema, which did not change with posture. No redness or swelling was present, and there was no skin ulceration in the lower limbs. The patient did not complain of lower limb pain, and there was no limited range of motion of the lower limbs. High-resolution Doppler ultrasound of the arteries and veins of the lower limbs showed no flow alterations.
The patient had a history of intravenous drug abuse and received methadone maintenance therapy. He also took tamsulosin hydrochloride intermittently for benign prostatic hypertrophy (BPH) during the past 3 years.
Physical examination at admission revealed no remarkable findings.
The laboratory findings (Table ) showed alanine aminotransferase at 118 IU/L (reference range < 50 IU/L), aspartate aminotransferase at 66 IU/L (reference range < 40 IU/L), gamma glutamyl transferase at 127 IU/L (reference range < 60 IU/L) and creatinine at 53.26 μmol/L (reference range 57-111 μmol/L). Echocardiogram showed normal ejection fraction and diastolic function.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [46, 'years'], 'creatinine': [53.26, 'µmol/L'], 'sex': 'Male'}",113.73943,108.05246,119.4264,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 46 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 53.26 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 53.26 µmol. To convert 53.26 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 53.26 µmol Serum Creatinine * 1e-06 mol/µmol = 5e-05 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 5e-05 mol Serum Creatinine * 113.12 g/mol = 0.00566 g Serum Creatinine. To convert 0.00566 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00566 g Serum Creatinine * 1000.0 mg/g = 5.66 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 5.66 mg Serum Creatinine/10.0 dL = 0.566 mg Serum Creatinine/dL. The concentration value of 53.26 µmol Serum Creatinine/L converts to 0.566 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.566/0.7)**-0.302 * 0.9938**46 * 1.0 = 113.73943.
Hence, the GFR value is 113.73943 ml/min/1.73 m²."
253,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5842533-2,Extracted,"We report the case of a 35-year-old female patient. SLE was diagnosed in 2013. The first disease manifestation was nephrotic syndrome. The patient underwent renal biopsy with evidences of ISN/RPS class IV-G (A) LN. She was initially treated in another hospital with a low-dose IV CYC regimen (6 fortnightly pulses at a fixed dose of 500 mg) according to EURO-LUPUS protocol followed by azathioprine 50 mg/twid []. After 3, 6 and 12 months, no renal response was achieved. The patient has been followed in our Lupus Clinic since the end of 2014. She manifested constitutional symptoms (low degree fever and fatigue), mucocutaneus symptoms (malar rash and oral aphthous ulceration), low complement fragment C3 0.34. mg/dL (reference range 0.9–1.8) and C4 0.03 mg/dL (reference range 0.1–0.4) and anti-dsDNA positivity (100 UI/ml). Her 24-h proteinuria was 4400 mg, creatinine was 1.1 and the urine analysis showed 20 erythrocytes per high power field and 10 leucocytes per high power field. The disease activity according BILAG was: constitutional C, musculoskeletal D, mucocutaneous B, renal A. The patient was considered refractory to the therapy. IV methylprednisolone at a dosage of 1000 mg/day for 3 days was started, followed by prednisone 50 mg/day (about 1 mg/Kg). The patient was treated with MMF at a dose of 500 mg/twid, gradually increased to 1000 mg/twid. After a month, the patient presented with epigastralgia and persistent aqueous diarrhoea. The MMF dosage was reduced to the maximum tolerated dose of 1000 mg/day. At the end of the second month of therapy, no renal response was achieved. We decided to introduce combination therapy of IV Belimumab 10 mg/Kg with a low dose of MMF (1000 mg/day) and prednisone 1 mg/Kg/day. After 3 months of combination therapy, complete renal response was achieved and prednisone therapy was tapered to 10 mg/day. At the end of the induction cycle, we noticed a strong improvement of fatigue (FACIT-Fatigue from 20 to 48). After 2 years of starting therapy with Belimumab, a complete renal response was maintained with SELENA-SLEDAI below 6 (Fig. ).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [35, 'years'], 'creatinine': [1.1, 'mg/dL'], 'sex': 'Female'}",67.20166,63.84158,70.56174,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 35 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.1 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.1/0.7)**-1.2 * 0.9938**35 * 1.012 = 67.20166.
Hence, the GFR value is 67.20166 ml/min/1.73 m²."
254,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8565703-1,Extracted,"We present the case of an 84-year-old left-handed, white female, nonsmoker, nonalcoholic, who presented to the emergency department (ED) on 09/23/19 in the early evening shortly after experiencing dysarthria and transient left-hand tremor (around 18:30) concerning for an acute stroke. She was not a candidate for Alteplase (tPA) due to recent stroke and current use of apixaban.
She has a history of hypertension, non-insulin dependent diabetes mellitus, atrial fibrillation diagnosed in 2017 (paroxysmal AF with spontaneous reversal at the time of diagnosis and which was initially treated with 2.5 mg of apixaban twice daily) with 1 prior cardiovascular accident (CVA) in the left frontotemporal infarction seen on MRI on 08/09/2019, no tPA was administered.
Earlier that evening prior to arriving to the ED, the patient was eating dinner and abruptly noticed that she had tonic jerky movements of her left hand which she could not control. The episode lasted a few minutes. Subsequently, she noticed right facial droop, slurred speech and expressive aphasia. She denied diplopia or difficulty swallowing. She denied weakness in her extremities. She endorses previous history of abrupt onset expressive aphasia which lasted 3-4 days or so during the CVA on 08/09/2019 (positive on MRI as stated above). She was on apixaban 2.5 mg twice a day (BID) by mouth (p.o.) at the time which was increased to 5.0 mg BID p.o. upon discharge. Physical examination was grossly unremarkable other than noted left corner of the mouth facial droop and slurred speech per the admitting physician. NIHSS stroke scale was 2.
In the ED, an electrocardiogram (EKG) revealed sinus rhythm with heart rate of 89 beats per minutes, right bundle branch block, T wave inversions in inferior leads and poor R-wave progression as read by the cardiologist. The report of the brain computed tomography (CT) without contrast obtained at 19:33 showed no acute intracranial hemorrhage, midline shift or mass effect but revealed age indeterminate infarct in the left frontal lobe per the reading radiologist. CT angiography performed at 19:51 reported no focal flow-limiting stenosis, occlusion or aneurysm involving the anterior and posterior circulation of the brain nor any hemodynamically significant stenosis or occlusion involving the major arterial vessels of the neck. Brain MRI ( and ) performed at 22:05 revealed subacute infarct in the left frontal lobe at the gray-white matter junction. There was an acute infarct involving the right frontotemporal cortex just above the right sylvian fissure and chronic ischemic changes and cortical atrophy. An echocardiogram performed on 09/23/2019 at 21:54 reported an ejection fraction estimated at 60-65% with grade I diastolic dysfunction and no gross regional wall motion abnormalities. There was aortic valve calcification without hemodynamically significant stenosis.
Laboratory findings were grossly unremarkable: white blood cell (WBC)=7.1 10*3/ uL, hemoglobin (Hb)=13.0 g/dL, hematocrit (Hct)=38.3%, platelets (PLT)=250 10*3/ uL, prothrombin time (PT)=13.1 seconds (secs), activated partial thromboplastin time (aPTT)=30.6 secs, INR=1.0. Myocardial enzymes (troponins I) were unremarkable (<0.015, <0.015, <0.015). Electrolytes were grossly unremarkable. Blood urea nitrogen (BUN)=22 mg/dL, Creatinine=1.260 mg/dL. Glucose=228 mg/dL. Hepatocytolysis enzymes were grossly unremarkable (AST 35, ALT 83, Alkaline phosphatase 103). She was administered 324 mg of aspirin orally and admitted for further evaluation.
Regarding clinical and pharmacological history at the time of this current presentation, for anticoagulation due to her history of AF, she was on apixaban 5 mg p.o. daily (qd). For rate control, she was reportedly on oral diltiazem 120 mg daily and for rhythm control, oral sotalol 80 mg BID. In addition, the patient was on rosuvastatin 20 mg daily qd p.o for cardiovascular event prevention and metoprolol succinate 25 mg qd p.o. for hypertension. Canaglifozin 300 mg p.o. daily and sitagliptin 100 mg p.o. daily for diabetes. Levothyroxine 88 mcg p.o. daily for hypothyroidism. For the past month prior to this ED visit, she had been complaining of headaches localized over the forehead, more so on the left side, off and on. She has history of chronic headaches in the past and was diagnosed to have temporal arteritis. She was followed by a rheumatologist and treated with oral methotrexate 2.5 mg daily and 12.5 mg once a week on Thursdays as well as oral prednisone 2-3 mg a day. She suffers from major depressive disorder and was on oral paroxetine 20 mg once daily.
Upon admission, most of the aforementioned medications were withheld except for apixaban, metoprolol and paroxetine. Permissive hypertension was allowed for the first 24 hours. The patient’s BP remained in systolic BP between 125-170 and diastolic between 55-77 during that timeframe. The patient was noted to have paroxysmal atrial fibrillation and was in sinus rhythm at the time of the encounter with the cardiologist around 21:59 on the day of admission. Metoprolol was discontinued by day 1 (09/24/2019) by the cardiologist after noticing heart rate sustaining in the 60s beats per minutes. Sotalol was resumed on day 1 and administered throughout her hospital stay. Lipid profile on 09/24/2019 revealed triglycerides of 81 mg/dL, cholesterol of 185 mg/dL, low density lipoprotein (LDL) of 94 mg/dL, high density lipoprotein (HDL) of 75 mg/dL. LDL goal was less than 70 mg/dL hence atorvastatin at a higher dose of 80 mg p.o. qd was started on day 1 and maintained throughout her hospital course. Levetiracetem was initiated at 1000 mg IV q12 hours upon admission due to possible right focal motor seizure involving her involuntary left hand clonic type activity. It was subsequently reduced to 500 mg IV q 12 hours on day 4 and discontinued upon discharge due to no further seizure like activities. 2 mg of oral prednisone once daily was resumed on day 1 to continue management for her history of temporal arteritis as well as her daily levothyroxine and 81 mg of p.o. aspirin. Apixaban was discontinued on day 1 and she was bridged the same day to warfarin with heparin drip (discontinued on 10/02/2019). She was administered 5 mg p.o. daily of warfarin which was continued throughout the hospitalization with occasional administration of a 2.5 mg dose instead (on 10/01, 10/02 and 10/04) An INR goal of 2.0-2.5 was targeted and it remained between 1.0 to a peak of 2.3 on the day of discharge.
Repeat CT scan of the brain (on 09/27/19 and 10/02/19) were negative for hemorrhagic conversion or any other acute intracranial changes. She remained neurologically stable from the time of admission to the day of discharge on 10/06/2019. She was able to ambulate without assistance despite mild weakness in the left leg proximally and she remained in sinus rhythm on tele-monitoring throughout her hospital stay. Her dysarthria was very minimal prior to discharge with no significant changes in her facial weakness. She was recommended to continue to do facial exercises as well as physical and occupational therapy upon discharge. Apixaban, diltiazem, metoprolol, paroxetine and rosuvastatin were discontinued during this admission and rosuvastatin 40 mg p.o daily, warfarin 4 mg p.o daily, amlodipine 2.5 mg p.o daily, aspirin 81 mg p.o daily and vitamin B12 1000 mg p.o daily were added to her list of ambulatory meds. Medications for temporal arteritis, diabetes, hypothyroidism were renewed and for atrial fibrillation only sotalol was renewed.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [84, 'years'], 'creatinine': [1.26, 'mg/dL']}",42.09759,39.99271,44.20247,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 84 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.26 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.26/0.7)**-1.2 * 0.9938**84 * 1.012 = 42.09759.
Hence, the GFR value is 42.09759 ml/min/1.73 m²."
255,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7243648-1,Extracted,"A 93-year-old Caucasian female presented to the Emergency Department of our hospital with worsening pain in the right upper abdomen, loss of appetite and vomiting.
The patient’s symptoms started a few days before presentation with recurrent progressive episodes of pain in the right upper abdomen, vomiting and loss of appetite.
The patient had a history of myocardial infarction, asymptomatic cholelithiasis, and renal dysfunction.
The patient did not have a fever. Physical examination showed tenderness in the right upper abdomen.
Blood analysis revealed an increased C-reactive protein of 228 mg/L (normal range < 10 mg/L) with mild leukocytosis of 10.2 × 109/L. Pre-existing renal dysfunction had worsened with an increase in creatinine level to 214 μmol/L (normal range between 45-80 μmol/L) due to dehydration. Alanine transaminase, aspartate transaminase and bilirubin were normal. Alkaline phosphatase and gamma-glutamyl transpeptidase were increased to 286 U/L and 644 U/L, respectively. Urine analyses and electrocardiogram showed no abnormalities.
Abdominal ultrasound showed a gallstone in the gallbladder and widened intrahepatic bile ducts, and the distal part of the common bile duct could not be visualized. Gastroscopy (Figure ) revealed fluid retention caused by a massive obstructive stone in the bulbus. Abdominal CT scanning demonstrated a fistula between the gallbladder and the bulbus and a large impacted stone in the bulbus (Figure ).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [93, 'years'], 'creatinine': [214.0, 'µmol/L'], 'sex': 'Female'}",18.59418,17.66447,19.52389,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 93 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 214.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 214.0 µmol. To convert 214.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 214.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00021 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00021 mol Serum Creatinine * 113.12 g/mol = 0.02376 g Serum Creatinine. To convert 0.02376 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.02376 g Serum Creatinine * 1000.0 mg/g = 23.76 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 23.76 mg Serum Creatinine/10.0 dL = 2.376 mg Serum Creatinine/dL. The concentration value of 214.0 µmol Serum Creatinine/L converts to 2.376 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.376/0.7)**-1.2 * 0.9938**93 * 1.012 = 18.59418.
Hence, the GFR value is 18.59418 ml/min/1.73 m²."
256,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5703689-1,Extracted,"During our regular interdisciplinary endometriosis discussion rounds, we were presented with a 39-year-old patient who suffered from chronic pain, which she rated as 7 to 8 on the visual analog scale (VAS) of 0 to 10 (0 correlating with no pain and 10 severe unbearable pain). Her previous medical history included a laparoscopic endometriosis clearance, with resection of the visible foci, performed in 2001. These included foci in both fossa ovarica, pouch of Douglas, plica vesicouterina, and left pelvic wall, which were removed by means of bipolar coagulation. Endometriotic foci in the vicinity of the left ureter, however, were only treated superficially. Postoperatively, open surgery, which would allow for exposure of the ureter, was suggested, yet firmly refused by the patient. Instead, to relieve the left hydronephrosis (observed as grade I–II), double J stents were placed and administration of gonadotropin-releasing hormone (GnRH) analogues was initiated. Medical therapy was continued for 6 months, after which therapy was extended with the combined oral anticontraceptive pill.
Noteworthy comorbidities are Hashimoto's thyroiditis and arterial hypertonia. In 2005, given the existing urological problems and a suspected nephrolithiasis, an extracorporeal shockwave lithotripsy (ESWL) was performed in the left kidney after a new ureteral stent was placed. According to the patient, however, no kidney stones or stone fragments were removed during that treatment. After the placement of the double J stents, a renal scintigraphy showed that the flow rate of left kidney was 40%; after furosemide administration, the renal flow rate was adequate. Nevertheless, as before, the organ was still dilated. The patient denied further surgical interventions, although the kidney and ureter functions were continuously monitored and did not reveal any significant regression.
However, increased complaints in 2014 demanded a visit to our clinic. We suspected an advanced endometriosis coinciding with rectovaginal nodule and ureteral and periureteral infiltration resulting in the formation of hydroureter as well as hydronephrosis grade II as shown by computed tomography (CT,
). Scintigraphy of the left kidney showed a flow rate of merely 36% (
). Furthermore, her blood creatinine level was elevated to 1.05 µg/dL.
We chose to perform a laparoscopic procedure to remove all visible and palpable endometrioma inside and outside the pelvis as well as ureterolysis and intraoperative resection of the rectovaginal nodule. On top, supracervical hysterectomy, because of suspected adenomyosis, was performed. Simultaneously, we placed a 6-Fr double J stent in the left ureter to relieve the left kidney. The latter procedure was strenuous and could only be done after the corresponding endometriomas were laparoscopically removed. There were no postoperative complications, and the patient experienced a dramatic improvement of all symptoms, including a significant decrease in pain (VAS 2). After 6 months, the double J stent was removed. Initially, the patient remained free of symptoms and no deterioration of hydronephrosis was observed.
Nevertheless, 1 year later, a kidney scintigraphy showed a further deterioration of the kidney flow rate to 27% (ÓReilly grade II) and an increasing obstruction.
Despite furosemide treatment, hardly any flow was observed in the left kidney. As such, the prevesical ureter was not only restenosed, but also further reduced in its function because of limited peristalsis. To address this, we suggested a laparoscopic ureteral reimplantation surgery (
). At this point, it is important to mention that we had suspected the ureter infiltration to have been present for several years already. Yet, for over more than a decade, the patient firmly refused any form of surgical intervention, even though multiple clinicians and centers recommended surgery and warned her about potential risks and consequences of not doing so. Resection of the affected ureter, when infiltration was suspected and obstructive uropathy or even hydronephrosis occurred, should have been performed immediately.
The procedure was performed as follows. After cystoscopy and placement of yet another 6-Fr double J stent, the endometriomas in the pelvis were removed during laparoscopic exploration. The juxtavesical ureter was fixed in endometriosis tissue. Only at the level of the vessel intersection, we found sufficiently large inconspicuous anatomic conditions of the ureter, which could serve for reimplantation. Thus, to reach the bladder, a distance of at least 10 cm had to be bypassed. In such cases, the psoas hitch procedure is indicated.
We chose to perform this technique laparoscopically as opposed to the usual open surgical approach. For this purpose, the entire bladder was mobilized toward the lateral right wall, to be pulled toward the likewise exposed psoas muscle (“Hitch” preparation). Next, the hitch suture fixation was applied on the left bladder wall, so it could be attached to the psoas muscle at the end of the operation. This was an important step, as this part of the bladder was hard to reach after completion of anastomosis. While sparing the double J stent, the already mobilized ureter was severed shortly below the vessel intersection, and the stent was carefully pulled from the bladder. After closure of the distal ureter with a Roeder knot, the bladder was opened below the fixation sutures with endoscopic assistance, keeping the perforation small. As such, we gained access to the ureter lumen, and by use of forceps, the double J stent-equipped ureter could be pulled from the abdominal cavity into the bladder. The ureterocystostomy was performed according to Dreikorn et al;
the ureter was merely fixed extravesically and then latched onto the bladder without tunneling. The anastomosis was done with a total of eight 3–0 sutures. First, two anterior sutures were made to compose the entire bladder and fix the ureter in such a manner that it could be integrated into the bladder wall. Then, each suture was repeated laterally, medially, and posteriorly. After testing the integrity of the sutures with cystoscopy, the psoas bladder hitch fixation suture was fixed and attached to the psoas. Because of applying the psoas hitch procedure, the anastomosis was free of tension. Next, the placement of an extraperitoneal Robinson drainage and the closure of the peritoneum were performed so that the anastomosis and the drainage were lying extraperitoneally.
No postoperative complications occurred. After cystography (
) and contrast CT of the urinary tract, the patient could be discharged after 8 days of hospitalization and transferred to outpatient care without any discomforting symptoms.
The patient continued to be monitored during follow-up. Her creatinine levels returned within the normal range. Examinations of the renal flow showed no aberrations; yet, the hydronephrosis persisted as a “morphologically fixed” aberration due to 15 years of dilatation, and the function of the left kidney remained reduced at 31%. The hormone therapy was no longer continued.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [39, 'years'], 'creatinine': [1.05, 'µg/dL'], 'sex': 'Female'}",540.37042,513.3519,567.38894,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 39 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.05 µg/dL. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µg to mg. The mass of Serum Creatinine is 1.05 µg. To convert 1.05 µg of Serum Creatinine to mg, multiply by the conversion factor 0.001, giving us 1.05 µg Serum Creatinine * 0.001 mg/µg = 0.00105 mg Serum Creatinine. The volume units is dL so no volume conversion is needed. Hence, the concentration value of 1.05 µg Serum Creatinine/dL converts to 0.00105 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.00105/0.7)**-0.241 * 0.9938**39 * 1.012 = 540.37042.
Hence, the GFR value is 540.37042 ml/min/1.73 m²."
257,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2878422-1,Extracted,"A 20-year-old woman presented with vesicovaginal (VVF) and rectovaginal fistula (RVF) due to obstructed labor. She underwent a temporary transverse colostomy followed by two failed attempts of VVF repair. One year later, the RVF was repaired successfully by the vaginal route and a simultaneous continent cutaneous urinary diversion procedure (right colon pouch with Mitrofanoff continence mechanism) was performed. She was then lost to follow-up and could not come even for colostomy closure due to poor socioeconomic condition. She presented after 10 years when she noticed a gritty sensation while passing catheter for pouch emptying. On evaluation, she had normal renal functions, with serum creatinine of 1.0 mg%, while an intravenous urogram revealed a large pouch full of stones []. In view of the large stone bulk, she was subjected to open surgical removal of stones with simultaneous colostomy closure. Stone analysis revealed that the stones were composed of calcium, magnesium and ammonium phosphate.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [20, 'years'], 'creatinine': [1.0, 'mg/dL'], 'sex': 'Female'}",82.71159,78.57601,86.84717,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 20 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.0/0.7)**-1.2 * 0.9938**20 * 1.012 = 82.71159.
Hence, the GFR value is 82.71159 ml/min/1.73 m²."
258,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4105386-1,Extracted,"A 55 year-old woman was admitted to Inha University Hospital with abdominal pain, distension, and oliguria. She had undergone radical hysterectomy for uterine cervical cancer and received post-operative concurrent chemoradiation therapy 13 years previously. After a 5-year follow-up period, there was no evidence of the disease state and the patient was asymptomatic, and thus, regular follow-up was discontinued. At the time of admission, she had a 20 pack-year smoking history and consumed 1-2 bottles of alcohol per day, 3-4 times per week. Four days before admission, she visited another hospital with nausea, vomiting, abdominal pain, and abdominal distension of 7 days duration that started after drinking. Physician recommended admission because of the presence of features of acute kidney injury (blood urea nitrogen (BUN): 78mg/dL, creatinine: 4.9mg/dL), but she refused. Four days after discharge, she was admitted at the emergency department of our hospital due to aggravation of her symptoms. She had an acute ill-looking appearance, and her blood pressure, heart rate, respiration rate, and body temperature were 153/112mmHg, 109 pulses per minute, 20 per minute, and 36.6℃, respectively. She complained of general weakness, anorexia, weight loss (6 kg per 1 month), abdominal pain and distension, oliguria, and generalized edema. Physical examination revealed a dry tongue and skin. Chest auscultation showed a regular heart beat without murmur and clear breath sounds without crackle. She had moderate abdominal distension with hypoactive bowel sounds, and mild direct and rebound tenderness of the whole abdomen without organomegaly or a palpable mass. She had edematous lower legs but there was no definite pre-tibial pitting edema. Laboratory findings were as follows: BUN 162.9 mg/dL (reference range, 7.8-26), creatinine 7.74 mg/dL (0.3-1.2), pH 7.24, HCO3- 11.6mmol/L, pCO2 28 mmHg, sodium 119mEq/L, potassium 6.1mEq/L, serum osmolality 313mOsm/Kg. Complete blood cell count results showed mild leukocytosis (13,600/mm3 with 90% neutrophils), elevated hemoglobin (16.5 g/dL), and a normal platelet count. Liver function and coagulation battery tests were normal. Computed tomography (CT) without contrast media showed bilateral hydroureteronephrosis and a large amount of ascites but no evidence of liver cirrhosis (). During hospitalization, her urine output was less than 500mL per day and her renal function, including hyperkalemia and metabolic acidosis, were not improved by conservative management. Hemodialysis was performed for 2 days after admission, but oliguria was not improved. Paracentesis showed no evidence of malignancy or infection. Cell count and chemistry of ascites were as follows: RBC 2/mm3, WBC 42/mm3, polymorphonuclear leukocyte count 11%, glucose 152mg/dL, protein <1.0 g/dL, LDH 25U/L, BUN and creatinine level were not evaluated. On the third hospital day, bilateral percutaneous nephrostomy catheters were inserted, a large amount of urine was drained, her creatinine level decreased dramatically (2 and 4 days after catheter insertions creatinine levels were 1.45 and 0.73mg/dL, respectively), and ascites decreased simultaneously without additional paracentesis. Contrast enhanced CT showed improved hydronephrosis and ascites without evidence of malignancy or an obstructing stone. To determine the cause of the obstruction and to resolve the obstruction by D-J stent insertion, retrograde pyelography was performed. During the procedure, a severe urethral stricture was found, and after urethral dilation, contrast leakage revealed a bladder wall defect open to the peritoneal cavity at the posterior bladder wall (). Multiple bladder wall thinning and severe inflammation were visualized during cystoscopy but no mass or ureteral stricture. The patient was transferred to our urology department and open abdominal surgery was performed to repair the ruptured bladder wall. After surgery, she was well and her renal function remained normal.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [55, 'years'], 'creatinine': [4.9, 'mg/dL']}",9.88088,9.38684,10.37492,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 55 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 4.9 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (4.9/0.7)**-1.2 * 0.9938**55 * 1.012 = 9.88088.
Hence, the GFR value is 9.88088 ml/min/1.73 m²."
259,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3263066-1,Extracted,"A 27-year-old man with end-stage kidney disease from chronic glomerulonephritis received a renal allograft from his mother in 2005 using prednisolone, cyclosporine and azathioprine, without induction therapy. During the immediate post transplant period, he received three intravenous pulses of methylprednisolone 1 g each daily for acute cellular rejection. He did not develop major infections till the current episode. His weight was 58 kg. He had stable graft function, with serum creatinine at 1.6 mg/dl and was on prednisolone 10 mg/d, azathioprine 100 mg/d and cyclosporine 175 mg/d, with the trough (C0) and 2-hour (C2) cyclosporine levels being 368 and 1280 ng/ml, respectively, at 6 months after transplantation.
Three years after transplantation, he presented to us with 4 months history of fever, weight loss of 16 kg in 4 months, episodic small volume diarrhea and diffuse abdominal pain with occasional hematochezia. He did not have pulmonary or other gastrointestinal symptoms. He discontinued cyclosporine 4 months prior to visiting our center. At presentation, he was on prednisolone (10 mg/d) and azathioprine (100 mg/d). On examination, his weight was 38 kg, and pulse rate, blood pressure, respiratory rate were normal. He was pale but did not have icterus or peripheral lymphadenopathy or allograft tenderness. He had a diffuse, ill-defined, firm, tender mass (9 × 7 cm) in the right hypochondrium. There was no hepatosplenomegaly or ascites.
Laboratory investigations revealed anemia (hemoglobin of 6.7 g/dl), a total leukocyte count of 4200/mm3, a normal platelet count and serum albumin of 2.2 g/dl. He had renal allograft dysfunction (serum creatinine of 3.1 mg/dl) with normal electrolyte profile and liver enzymes. His chest radiograph revealed an ill-defined minimal haziness in the right upper and midzones with minimal pleural effusion. Ultrasonogram of abdomen showed an intussusception mass measuring 7.1 × 5.0 × 10.1 cm in the right hypochondrium with a few enlarged mesenteric nodes and fat within and adjacent to it []. The renal allograft appeared normal. Computed tomogram (CT) scan of abdomen with rectal contrast revealed an ileocolic intussusception up to the hepatic flexure with multiple enlarged mesenteric nodes and mesenteric fat pulled into it []. The ascending colon was thick. The para-aortic, mesenteric and para-iliac nodes were enlarged and showed central necrosis.
The patient underwent an emergency exploratory laparotomy with resection of the ileocolic intussusception, the adjacent ascending colon and terminal ileum []. Histopathological examination of the ileocolic intussusception revealed fragments of a lymph node with extensive caseation necrosis and many acid-fast bacilli (AFB). The proximal polypoidal lesion of the intussusceptum and the mucosal ulcerations of the intussuscepient colonic segment revealed dense inflammatory infiltrates of lymphocytes and plasma cells, along with microabscesses in the submucosa and lamina propria, transmural granulomas with epitheloid histiocytes, lymphocytes; Langhans type multinucleated giant cells and central foci of caseation [Figure and ]. Long, curved and beaded AFB, morphologically typical of Mycobacterium tuberculosis (MTB), were detected in all the above-mentioned lesions [].
On the first postoperative day, the patient received hydrocortisone 100 mg thrice daily, but azathioprine was discontinued due to leukopenia (WBC count 1900/mm3). He received granulocyte colony stimulating factor for leukopenia. On the second postoperative day, he was weaned off mechanical ventilation. On the fourth postoperative day, he received ATT with isoniazid 300 mg/d, rifampicin 450 mg/d, pyrazinamide 750 mg/d and ethambutol 400 mg/d. On the fifth postoperative day, 36 hours after starting ATT, he developed tachycardia, tachypnea, hypotension, oliguria and worsening of pulmonary oxygenation [partial pressure to inspired fraction of oxygen ratio (P–F ratio)]. The chest radiograph revealed worsening of the preexisting haziness. However, there was no bacteremia or evidence of invasive fungal infection.The total leukocyte count had remained about 4500 cells/mm3 during this period. His condition subsequently worsened, and he received broad-spectrum antibiotics (piperacillin with tazobactam) while routine cultures remained sterile. A tracheal aspirate showed numerous AFB morphologically typical of MTB, though there was no growth in culture. In addition, tracheal aspirate grew mixture of non-fermenting gram negative bacilli and Candida glabrata, which were probably contaminants. He continued to develop worsening features of a systemic inflammatory response syndrome, lung infiltrates, and disseminated intravascular coagulation. Steroids were continued, antibiotics were changed empirically to meropenem with teicoplanin and liposomal amphotericin B. The patient died on the 11th postoperative day. The next of kin declined post-mortem examination.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [27, 'years'], 'creatinine': [3.1, 'mg/dL']}",27.21561,25.85483,28.57639,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 27 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.1/0.9)**-1.2 * 0.9938**27 * 1.0 = 27.21561.
Hence, the GFR value is 27.21561 ml/min/1.73 m²."
260,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8206272-1,Extracted,"A 21-year-old swiss-indonesian man was referred to our nephrology clinic in June 2019. He had end-stage renal disease with a creatine value of 907 μmol/l (). Previously, at the age of 14 years, an asymptomatic, increased blood pressure of 158/102 mmHg was discovered during a school-based examination, and he was investigated at the children's hospital of Lucerne, Switzerland. His medical history revealed swollen eyelids in the morning for the last 3 years. Clinical examination was regular except for bilateral ankle edema. Further workup identified a nephrotic syndrome with a protein to creatine ratio of 586 mg/mmol, a serum albumin concentration of 27 g/L, total cholesterol of 9.5 mmol/l (), and microhematuria with 30% dysmorphic erythrocytes. Screening for hepatitis B and C was negative, and autoantibodies (antinuclear antibodies, anti dsDNA antibodies, antineutrophil cytoplasmic antibodies, and antiglomerular basement membrane antibodies) were negative. Echocardiography showed mild left ventricular hypertrophy. The renal biopsy established the diagnosis of LPG. It showed glomerular capillary dilatations with lipoprotein thrombi with lamella formation (). No fibrin thrombi, fragmented erythrocytes or fibrinoid necrosis suggestive of aHUS was seen. Chronic changes in the form of secondary focal segmental scleroses and mild interstitial fibrosis with tubular atrophy were already present. By immunohistochemistry, mild to moderate unspecific depositions of IgM and C5b-9 within the glomeruli were detected. IgA, IgG, and C3c were negative within the glomeruli. Transmission electron microscopy showed the characteristic concentrically layered and vacuolated lipoprotein thrombi (). Analysis of APOE revealed E3/E3 genotype. Sequencing of the APOE gene detected a heterozygous 9-bp deletion in exon 4 (NM_000041.3: c.480_488del (p.Leu162_Lys164del, traditional nomencalture: 142_144del)), resulting in a 3-amino acid deletion in a region involved in receptor binding of the apo E molecule and previously associated with LPG (, ). In the literature, this mutation is often named APOE Tokyo/Maebashi (). A grandfather of the patient in Indonesia received a kidney transplant at the age of about 60 years. Otherwise, the family history brought to light no renal disease in either of the patient's parents. The patient has no siblings. Therapy was started with an ACE-inhibitor (enalapril 10 mg/d) and a lipid-lowering agent (atorvastatin 20 mg/d). As the patient emigrated to Indonesia soon after the diagnosis, medical follow-up was lost.
In June 2019, after his return to Switzerland, he complained about fatigue, epigastric pain, and a dizzy sensation. Blood pressure was 171/106 mmHg. No edema was noticed. In contrast to the findings 7 years earlier, the lipid profile was normal. The laboratory results showed progressive thrombocytopenia and coombs-negative hemolytic anemia with fragmentocytes (), and the diagnosis of thrombotic microangiopathy (TMA) was made. At this time, C3 levels were reduced. ADAMTS13 activity was 100% (). We started dialysis in July 2019, shortly after his first emergency consultation in our clinic. Due to a paracentral scotoma (left > right) fundoscopic exam was performed, which showed hypertensive retinopathy. A magnetic resonance imaging (MRI) of the brain was normal. A detailed, further analysis of the complement system revealed a functional complement defect () and the presence of a homozygous aHUS risk allele for CFHR1, CFHR1*B (). Factor H antibodies were negative. Currently, the patient is listed for renal transplantation. We plan to treat the patient with the C5 inhibitor eculizumab during the first 3–6 months after transplantation. Close monitoring of the complement activity, i.e., CH50 test and C3 levels, will be required. Also, protocol biopsies will help us to detected aHUS and LPG recurrence at an early stage. Depending on posttransplant lipid levels and the results of protocol biopsies, we plan to treat the patient with fibrates as their use can induce clinical remission in some patients with LPG ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [21, 'years'], 'creatinine': [907.0, 'µmol/L']}",6.69202,6.35742,7.02662,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 21 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 907.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 907.0 µmol. To convert 907.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 907.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00091 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00091 mol Serum Creatinine * 113.12 g/mol = 0.10294 g Serum Creatinine. To convert 0.10294 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.10294 g Serum Creatinine * 1000.0 mg/g = 102.94 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 102.94 mg Serum Creatinine/10.0 dL = 10.294 mg Serum Creatinine/dL. The concentration value of 907.0 µmol Serum Creatinine/L converts to 10.294 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (10.294/0.9)**-1.2 * 0.9938**21 * 1.0 = 6.69202.
Hence, the GFR value is 6.69202 ml/min/1.73 m²."
261,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7490107-1,Extracted,"A 74-year-old gentleman, known to have hypertension and diabetes mellitus, presented to our emergency department with a 4-day history of intermittent subjective fever of no specific periodicity and rigors associated with generalized headache, altered mentation, body malaise, nausea, and vomiting. He reported no history of loss of consciousness, abdominal pain, or change in stool habits/urine color. The patient denied history of recent trauma or falls, and the rest of the systemic review was unremarkable. The patient resided in a malaria-endemic region and reported to have previous uncomplicated malarial infections that were successfully treated with oral anti-malarials.
On clinical examination, he was an elderly gentleman febrile (38.7 °C), tachypneic, and disoriented with good nutritional status. He was not jaundiced or cyanosed. Initial vitals were pulse rate of 103 beats/min in sinus rhythm, respiratory rate of 23 breaths/min, with slightly borderline low blood pressure of 96/60 mmHg and saturating at 98% on room air. On systemic examination he had normal vesicular breath sounds and a normal abdominal examination. While awaiting initial work up, in view of the findings the patient received intravenous (IV) resuscitation and analgesia.
The complete blood count (CBC) revealed a white blood cell count (WBC) of 8.2 × 103/μL, hemoglobin (Hb) of 11.5 g/dL, and thrombocytopenia of 46,000/mm3. The renal profile revealed elevated creatinine 117 μmol/L and BUN 10.5 mmol/L with slightly low sodium of 131 mmol/L. The rest of serum electrolytes, liver, and coagulation profile were normal. Chest X-ray was normal. Peripheral blood smear for malaria demonstrated P. falciparum with high parasitemia with more than 1000 trophozoites/200 WBC, HPF (high power field). He was subsequently admitted to the intensive care unit (ICU) as a case of severe malaria evident by high parasitemia and altered mentation.
He was then commenced on an intravenous artesunate-based regimen as per the national malaria treatment protocol with other supportive measures. With marked improvement in both clinical status and lab parameters, he was subsequently shifted to the general ward after 3 days of ICU stay. While in the ward (day 5 post admission), he acutely developed features of acute abdomen characterized by progressive, dull, constant generalized abdominal pain more so on the left upper quadrant associated with nausea and several episodes of non-bilious vomiting. The rest of the review was unremarkable.
On review, he was lying still in bed, anxious, afebrile, diaphoretic, tachycardic, tachypneic, and hypotensive but saturating well on room air. He had a slightly distended abdomen which was tender on superficial palpation with inaudible bowel sounds on auscultation. In view of the above, urgent CBC, grouping/crossmatch, formal abdominal ultrasound, and contrast-enhanced CT scan of the abdomen were performed. CBC revealed a low Hb of 7.1 g/dL (compared to 8.9 mg/dl the day prior). Ultrasound showed hypoechoic nodular cystic area ( and ) and CT scan revealed hyperdense intrasplenic hematoma surrounded by hypodense subcapsular hematoma. Post-contrast CT images demonstrated splenic laceration on the superolateral aspect in addition to the hematoma as well as intraperitoneal free fluid. These findings were in line with grade 3 splenic injury ( and ).
The findings of spontaneous splenic rupture were attributed to the consequence of severe malaria due to P. falciparum infection as there was no evidence of other documented etiologies such as trauma or other infectious causes. Blood products were mobilized, adequate resuscitation was done, and after thorough discussion with the patient and family the patient was taken to the operating theatre for explorative laparotomy and splenectomy.
Intra-operatively 2.5 L of frank blood without purulence was evacuated. The spleen was enlarged and very firm with a long laceration on the upper pole extending laterally involving the fine covering capsule and not much of the splenic parenchyma. Splenectomy was done. He had an uneventful postoperative period and 7 days later he was discharged home fully recovered with scheduled clinic visits for post-splenectomy care.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [74, 'years'], 'creatinine': [117.0, 'µmol/L']}",54.75313,52.01547,57.49079,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 74 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 117.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 117.0 µmol. To convert 117.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 117.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00012 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00012 mol Serum Creatinine * 113.12 g/mol = 0.01357 g Serum Creatinine. To convert 0.01357 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01357 g Serum Creatinine * 1000.0 mg/g = 13.57 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 13.57 mg Serum Creatinine/10.0 dL = 1.357 mg Serum Creatinine/dL. The concentration value of 117.0 µmol Serum Creatinine/L converts to 1.357 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.357/0.9)**-1.2 * 0.9938**74 * 1.0 = 54.75313.
Hence, the GFR value is 54.75313 ml/min/1.73 m²."
262,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5885127-3,Extracted,"A 12-year-old girl weighing 17 kg presented with lumbosacral meningomyelocele. She had no sensory deficit over the anterior abdominal wall. Her medical history included scoliosis, hydrocephalus, and spina bifida. She was scheduled for laparoscopic insertion of a peritoneal dialysis catheter. Her physical examination did not reveal any significant findings. Hemoglobin, hematocrit, platelet count, coagulation profile, liver enzymes, bilirubin levels, blood glucose level, serum sodium and potassium levels were within normal limits in preoperative investigations. Blood urea level was 80 mg/dl and serum creatinine level was 2.4 mg/dl. There were no abnormal findings on the preoperative chest x-ray (). Preoperative investigations revealed elevated urea and creatinine levels.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [12, 'years'], 'creatinine': [2.4, 'mg/dL'], 'sex': 'Female'}",30.40331,28.88314,31.92348,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 12 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.4 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.4/0.7)**-1.2 * 0.9938**12 * 1.012 = 30.40331.
Hence, the GFR value is 30.40331 ml/min/1.73 m²."
263,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6874932-1,Extracted,"A 61-year-old woman presented with symptoms of intractable nausea and vomiting for 10 days. Her past medical history included permanent hypothyroidism and hypoparathyroidism from subtotal thyroidectomy due to a huge multinodular goiter 2 years earlier. Her thyroid condition was well controlled with levothyroxine 600 μg per week. She was also prescribed with 2,400 mg of elemental calcium and 1 μg of alfacalcidol per day. On the last follow-up, 2 months prior to this visit, she was in good health with normal calcium and thyroid function levels. A thorough medical history review discovered that she had been taking different preparations of over-the-counter alfacalcidol, 0.25 μg to 1 μg/tablet for 6 weeks. She also increased the daily calcium supplement up to 4,800 mg of elemental calcium per day to control her tingling sensation. On physical examination, the patient was drowsy and moderately dehydrated. Her vital signs and neurological examination were unremarkable. Laboratory investigations showed profound hypercalcemia, mild hypophosphatemia and azotemia: serum calcium 17.08 mg/dL (8.5–10.5), phosphate 2.1 mg/dL (2.5–4.5), albumin 3.5 mg/dL and creatinine 2.0 mg/dL. Her venous pH was 7.46 and electrolytes showed mild hypokalemia and metabolic alkalosis: sodium 135 mEq/L potassium 3.4 mEq/L, chloride 95 mEq/L, and bicarbonate 29 mEq/L. Low levels of intact PTH 6.07 pg/mL (15–65), 25-OH vitamin D 19 ng/mL (>20) with a normal level of 1,25(OH)2 vitamin D 25.4 pg/mL (19.9–79.3) and normal levels of PTHrP were shown. Her thyroid function test was normal: FT4 1.35 ng/dL (0.80–1.80) and TSH 2.52 μIU/mL (0.35–4.10). The electrocardiography (ECG) showed sinus rhythm with normal QTc interval (410 ms). Her amylase and lipase levels were not elevated. The presumptive diagnosis of CAS was proposed from her triad of hypercalcemia, metabolic alkalosis, and renal insufficiency. She responded well to intravenous hydration with isotonic normal saline (4 L/d), subcutaneous calcitonin (200 IU q 8 h) and discontinuation of calcium and vitamin D supplements. Her clinical symptoms and serum calcium level returned to normal within 2 days of treatment. The patient was discharged on the 4th day of hospitalization and was prescribed with 2,000 mg of calcium carbonate and 0.5 μg of alfacalcidol daily. During the follow-up after 6 months, she did not have experienced episode of hypercalcemia and her renal function returned to baseline level.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [61, 'years'], 'creatinine': [2.0, 'mg/dL'], 'sex': 'Female'}",27.89903,26.50408,29.29398,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 61 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.0/0.7)**-1.2 * 0.9938**61 * 1.012 = 27.89903.
Hence, the GFR value is 27.89903 ml/min/1.73 m²."
264,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4421525-3,Extracted,"A 50-year-old African American man with type 1 diabetes mellitus and ESRD underwent simultaneous kidney and pancreas transplantation. His operative course and immediate post-operative course were uncomplicated. His immunosuppression consisted of mycophenolate mofetil, tacrolimus and a prednisone taper over 6 months. Preoperative SCr was 9.05 mg/dL [690.2 mmol/L] with a nadir of 0.99 mg/dL [75.5 mmol/L].
Six weeks after transplantation he was noted to have an asymptomatic rise in his SCr to 2.5 mg/dL [190.7 mmol/L]. He had no uveitis, rash, fever, arthralgia, purpura or pulmonary symptoms such as shortness of breath, cough or haemoptysis. Physical examination was normal.
All possible culprit drugs, including lisinopril, metoclopramide and ferrous sulphate, were discontinued. A serologic work-up was initiated, including serum antinuclear antibodies, double-stranded DNA antibodies, ANCA and anti-glomerular basement membrane antibodies (anti-GBM). Because of concerns for acute rejection, he was empirically placed on corticosteroids and transplant kidney biopsy was performed. The biopsy revealed several interstitial non-caseating granulomas, some of which were in a periglomerular distribution, with disruption of the Bowman's capsules (E). Crescents, viral inclusions or vasculitis were not identified. AFB and GMS stains and C4d immunostain were negative.
A repeat biopsy was performed 2 weeks later, which showed similar glomerular and tubulointerstitial histology. In addition, several cross sections of arcuate and interlobular calibre arteries had mild to moderate intimal arteritis (F), worrisome for acute vascular rejection (Banff grade IIa). Overall, the aetiology was unclear and the differential diagnosis included infection, drug reaction, necrotizing granulomatous vasculitis and acute vascular rejection.
The aetiology of granulomatous interstitial nephritis in this patient was unclear. Despite stopping all possible offending agents and empiric treatment with corticosteroids, the SCr continued to rise, up to 5.05 mg/dL [385.1 mmol/L] 2 weeks after the first transplant kidney biopsy.
Both the initial and follow-up biopsies showed evidence of vasculitis and periglomerular granulomatous inflammation. The biopsy results plus uncertainty regarding the exact nature of his primary disease raised the possibility of recurrent glomerulonephritis. However, serologic work-up for pauci-immune glomerulonephritis and GBM antibody-mediated disease was negative. Although his pancreas allograft continued to function well, his kidney function progressively worsened, and he was reinitiated on haemodialysis soon thereafter.
The recipient of the mate kidney had prolonged delayed graft function, subsequently dying within 3 months of transplantation. Patients receiving other mate organs (including liver, lung and intestine) have been reported as doing well without impaired organ function.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [50, 'years'], 'creatinine': [5.05, 'mg/dL'], 'sex': 'Male'}",13.13347,12.4768,13.79014,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 50 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 5.05 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (5.05/0.9)**-1.2 * 0.9938**50 * 1.0 = 13.13347.
Hence, the GFR value is 13.13347 ml/min/1.73 m²."
265,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6579338-1,Extracted,"A 76-year-old Caucasian male with a history of chronic kidney disease (CKD) stage 3, type 2 diabetes complicated by neuropathy and retinopathy (HbA1c 8.6%), atrial fibrillation on dabigatran, hypertension (HTN), coronary artery disease status post (s/p) three-vessel coronary artery bypass grafting (CABG), heart failure with preserved ejection fraction (HFpEF), peripheral artery disease (PAD) with prior right below knee amputation (BKA) and recent left lower extremity transmetatarsal amputation, and Lisfranc amputation presented due to worsening left foot wound dehiscence. The patient was seen by podiatry prior to initial presentation, where left foot osteomyelitis was suspected given the worsening discharge, odor, and erythema. In consultation with vascular surgery, the left foot was deemed unsalvageable and amputation was recommended.
Initial vitals were significant for temperature 100.3 degrees Fahrenheit (normal range 97.7-99.5 degrees Fahrenheit), pulse 79 (normal range 60-100), blood pressure 138/70 (normal 120/80), respiratory rate 20 (normal range 12-20), with 94% oxygen saturation on room air (normal range 95-100%). On admission, labs were significant for a normal white blood cell (WBC) count of 8.6 K/cmm (normal range 3.6-11.0) with evidence of acute kidney injury (AKI) superimposed on chronic kidney disease (CKD) Stage 3 with a creatinine of 1.7 mg/dL (patient's baseline of 1.1 mg/dL, normal range 0.7-1.5 mg/dL). Radiographic studies of the affected foot revealed air pockets distal to the second and third cuneiforms, felt to represent the extension of deep wounds, raising concerns for chronic osteomyelitis. The patient was started on vancomycin, aztreonam, and metronidazole, given a prior history of piperacillin/tazobactam allergy, and was admitted to medicine for further management. During hospitalization, the patient’s kidney function continued to worsen (Cr: 1.7 mg/dL -> 2.7 -> 3.7 -> 4.4 -> 4.7 -> 5.7 mg/dL) with poor urine output (100-150 cubic centimeters (cc) daily or 0.05-0.07 mL/kg/hr, normal range 800-2000 mL or 1-2 mL/kg/hr). Blood cultures showed 48 hours no growth to date (NGTD) while wound cultures were positive for Staphylococcus aureus with gram-negative rods. Given worsening AKI and positive wound cultures, infectious disease and nephrology were consulted. With concern for medication-induced AKI, the decision was made to switch the patient to monotherapy with intravenous (IV) ertapenem 500 mg daily. However, the patient’s renal function continued to deteriorate, a temporary hemodialysis catheter was placed, and he was initiated on hemodialysis. The differential for the etiology for this patient’s AKI was extensive and included vancomycin-induced nephrotoxicity, obstructive causes (ruled out with no hydronephrosis seen on renal ultrasound and normal bladder scan), vascular causes (no renal artery stenosis or arteriolosclerotic occlusive disease observed on renal artery Doppler ultrasound), autoimmune causes (anti-nuclear antibody (ANA) negative), and vasculitides (antineutrophil cytoplasmic antibody (ANCA) studies negative). The patient required aggressive fluid removal with hemodialysis and ultrafiltration as he remained volume overload and continued to require supplemental oxygen.
Following a five-day clopidogrel washout, a renal biopsy was performed to further workup the etiology of this patient’s anuric AKI. Light microscopy of the kidney biopsy demonstrated diffuse endocapillary proliferative, exudative glomerulonephritis, and increase in mesangial cell counts, consistent with infection-related glomerulonephritis (Figure ). In addition, moderate to severe nodular glomerulosclerosis with prominent hyalinization was present in glomerular capillary loops, consistent with chronic kidney disease secondary to diabetic nephropathy (Figure ). Direct immunofluorescence staining for complement C3 revealed positive glomerular wall and coarsely granular mesangial staining (Figure ). Per the biopsy report, other sites revealed tubular atrophy and interstitial fibrosis (moderate) and arterio/arteriolosclerosis (severe) (not shown). In short, the patient’s renal biopsy results were consistent with acute infection-related glomerulonephritis in the setting of CKD, likely secondary to HTN and diabetes.
Left ankle disarticulation (left guillotine below knee amputation (BKA)) was performed by vascular surgery to treat the patient’s left foot osteomyelitis 28 days after initial admission, after which he completed IV ertapenem for 72 hours at the recommendation of the infectious disease team. Despite an initial reported improvement in urine output to 200 cc daily (0.010 mL/kg/hr, normal range 1-2 mL/kg/hr) following the procedure, the patient remained hemodialysis-dependent on outpatient follow-up, reporting <100 cc urine output per day (0.05 mL/kg/hr, normal range 1-2 mL/kg/hr) per interview in the two weeks following surgery.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [76, 'years'], 'creatinine': [1.7, 'mg/dL'], 'sex': 'Male'}",41.26331,39.20014,43.32648,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 76 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.9)**-1.2 * 0.9938**76 * 1.0 = 41.26331.
Hence, the GFR value is 41.26331 ml/min/1.73 m²."
266,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5121444-1,Extracted,"A 70-year-old woman was presented with loin pain of 2 months and unable to stand and walk for 2 weeks, with no comorbidities. In her physical examination, there were blood pressure of 130/80 mmHg, body temperature of 37.3°C, a pulse of 86 bpm, and grade 3 motor weakness of lower limbs. Biochemical profile of the patient was identified as glucose 98 mg/dL, blood urea nitrogen 198 mg/dL, serum creatinine 3,5 mg/dL, uric acid 17,4 mg/dL total protein 9,8 gr/dL, serum albumin 4,0 gr/dL, calcium 6,5 mg/dL, phosphate 8,7 mg/dL, potassium 5,1 mmol/L, LDH 856 IU/L, white cell count 11 000 mm3/uL, Hb 5,7 gr/dL, Htc 17%, and platelet count 28 000/mm3. Arterial blood gas analysis was evaluated as metabolic acidosis (pH 7,22, HCO3 13 mEq/L, PCO2 27 mmHg, and PO2 96 mmHg). A radiography of the thoracal spine showed a compression fracture of the T12 vertebra. In serum protein electrophoresis, M-band was documented. Serum immunoglobulin Ig G was 5,6 g/dL. Serum and urine protein immunofixation revealed kappa light chain. Bone marrow aspiration smear showed abnormal plasma cells. Bone marrow biopsy showed plasma cells accounting for 90% of all cells; normal erythroid and myeloid cells were markedly suppressed. Immunohistochemistry examinations revealed kappa positive.
Our patient fulfilled clinical (acute renal injury) and laboratory criteria (hyperuricemia, hyperphosphatemia, and hypocalcemia) of TLS according to the Cairo and Bishop criteria []. The diagnosis of MM and spontaneous TLS were established. Medical treatment was initiated upon of TLS. The patient was treated with hydration, allopurinol, calcium gluconate, and sodium bicarbonate. After one week of initiating treatment, laboratory data showed glucose 117 mg/dL, blood urea nitrogen 48 mg/dL, serum creatinine 0,9 mg/dL, uric acid 3,2 mg/dL, serum albumin 3,5 gr/dL, calcium 7,8 mg/dL, phosphate 2,7 mg/dL, potassium 4,9 mmol/L, LDH 724 IU/L, white cell count 5300 mm3/uL, Hb 10,4 gr/dL, Htc 30,3%, and platelet count 40 000/mm3. Arterial blood gas analysis was normal.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [70, 'years'], 'creatinine': [3.5, 'mg/dL']}",13.47828,12.80437,14.15219,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 70 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 3.5 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (3.5/0.7)**-1.2 * 0.9938**70 * 1.012 = 13.47828.
Hence, the GFR value is 13.47828 ml/min/1.73 m²."
267,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2967566-1,Extracted,"A 68-year-old Japanese male with systemic AL amyloidosis was admitted with fatigue, exertional dyspnea, and bilateral lower-extremity edema. He had been diagnosed with systemic AL amyloidosis in 1999, on the basis of the results of histopathological examination of the biopsied tissues of his kidney and bone marrow. After diagnosis, he was successfully managed with 21 courses of intermittent MP chemotherapy for seven years. Two months before admission, he developed exertional dyspnea. One month before admission, his dyspnea had become worse, and his chest radiograph showed bilateral pleural effusion, with the effusion on the right side being more severe. Thoracocentesis was performed with removal of one litre of yellow serous fluid from the right hemithorax. Pleural fluid analysis revealed that his nucleated cell count was 2600/mm3 (24% neutrophils, 71% lymphocytes); total protein concentration, 0.4 g/dl (a pleural fluid to serum ratio, 0:11); lactate dehydrogenase level, 26 IU/l (two-thirds normal upper limit for serum, 154 IU/l and a pleural fluid to serum ratio, 0:12); total cholesterol content, 11 mg/dl; and glucose level, 118 mg/dl. These findings were consistent with transudative pleural effusion. The pleural fluid cytology was negative for malignancy. The pleural fluid was cultured for bacteria (aerobic and anaerobic), fungi, and mycobacteria, and the results were negative.
Since the pleural effusion was refractory to aggressive administration of diuretics, thoracentesis with removal of one litre of serous fluid was repeated once every week. Although his symptoms were alleviated, the patient's pleural effusion gradually increased and the pleural fluid returned to the pre-drainage level after one week. The composition of the pleural fluid remained the same at all instances of drainage.
He was admitted to our hospital for treatment of refractory pleural effusion. On admission, he appeared to be comfortable while resting. He was 158.7 cm tall and weighed 65.2 kg. His body temperature was 36.5°C; blood pressure was 124 over 69 mm Hg; and his pulse rate, regular at 84 beats per minute. Diminished breath sounds in the right lower lung, slight inspiratory coarse crackles in the left basal lung, and lower extremity edema were observed. The results of the other clinical examinations were normal. Laboratory tests revealed that his blood urea nitrogen (31 mg/dl) and serum-creatinine (1.3 mg/dl) levels were elevated; creatinine clearance rate was low (39 ml/min/1.73 m2); 24-hour urine protein was 3.5 g per day; and total protein content (4.6 g/dl) and serum-albumin levels (1.6 g/dl) were low. These findings were indicative of renal insufficiency and nephritic syndrome. However, his renal function and his serum-albumin levels remained the same as those observed one year before. The serum protein electrophoresis was negative for a monoclonal spike. Bence-Jones proteins were not detected in the urine. All his immunoglobulin levels were normal. His hemoglobin level was 12.4 g/dl, platelet count 12 × 104/mm3, and white blood cell count, 5900/mm3, with a normal differential count. His levels of troponin T (below 0.01 mg/dl) and the C-reactive protein (0.2 mg/dl) were also normal. No other abnormalities were detected in any other laboratory tests. Our patient's echocardiogram showed symmetrical thickening of the left ventricular (LV) wall with slightly high echoic lesions (interventricular septum wall thickness, 14 mm; posterior LV wall thickness, 15 mm at systolic phase) and almost normal cardiac function (fractional shortening, 40%; LV ejection fraction, 0.71). These results were suggestive of infiltrative cardiomyopathy, and not acute heart failure caused by cardiac compensation.
At admission, his chest radiograph image showed a moderate effusion on the right side and slight effusion in the left. The computed tomography imaging of his chest revealed moderate pleural effusion in the right lung and atelectasis of the right lower robe (Figure ).
Thoracentesis was performed with removal of one litre of serous fluid from the right hemithorax on the second hospital day. The level and composition of the effusion were the same as those seen before. VAD chemotherapy was administered on the third day. He did not develop serious bone marrow suppression or complications. A week after the administration of VAD chemotherapy, his chest radiograph revealed significant improvement. Moreover, he did not have dyspnea or general fatigue. However, the edema in his lower extremities showed no improvement, and no obvious change was seen in cardiac indices; pleural effusion did not recur until he was discharged from the hospital (Figure ). The results of the clinical test did not change (creatinine clearance rate, 35 ml/minute/1.73 m2; daily proteinuria, 3.4 g; serum-albumin, 1.6 g/dl). He was discharged from our hospital on his 31st hospital day.
Since then, he has continued receiving intermittent MP chemotherapy. Pleural effusion did not recur for six months after he became ambulatory. However, he had a recurrence of right pleural effusion and was managed with VAD chemotherapy. Although his right pleural effusion did not increase while treating with VAD chemotherapy, the recurrence occurred immediately after VAD chemotherapy had finished. Hence, in 2006, he underwent chemical pleurodesis for recurrent right pleural effusion. After pleurodesis, his pleural effusion has not increased after he received intermittent MP chemotherapy in 2010.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [68, 'years'], 'creatinine': [1.3, 'mg/dL'], 'sex': 'Male'}",59.83824,56.84633,62.83015,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 68 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.3/0.9)**-1.2 * 0.9938**68 * 1.0 = 59.83824.
Hence, the GFR value is 59.83824 ml/min/1.73 m²."
268,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4839245-1,Extracted,"A 41-year-old male, known to have hypertension on amlodipine, has presented to our hospital with bilateral recurrent colicky flank pain several weeks. The patient had a history of the spontaneous passage of several stones during the past years. There was no history of previous UTIs or family history of urinary stones. Physical examination was unremarkable. Urine analysis showed microscopic hematuria and urine culture showed no growth. Creatinine was 130 mmol/dl, and other blood works were within normal range. Plain X-ray of the urinary tract [] has showed two radiopaque shadows overlying the course of abdominal part of the ureter (white arrows) in each side. Bilateral multiple renal stones (black arrows) were also seen. Excretory urography [Figure and ] has demonstrated bilateral complete duplication of the ureters, with mild to moderate hydronephrosis in the right side, and moderate to severe hydronephrosis in the left side (black stars). Each of the four ureteral limbs was harboring a single stone at the abdominal segment (white arrows). The ureteral stones ranged from 7 to 23 mm in length and 5–11 mm in width.
Cystoscopy was performed under general anesthesia and revealed four ureteric orifices, with two ureteric orifices on each side at their normal anatomic position. Through one of the left ureteric orifices, retrograde pyelography demonstrated the ureteral limb with the obstructing stone, and a 0.038-inch Terumo guidewire was manipulated to pass above the stone. A small caliber 7 Fr semi-rigid ureteroscope was easily steered up to the stone, and holmium laser lithotripsy was done. The ureteroscope was withdrawn, keeping the guidewire in place. The same technique was repeated in the ipsilateral second ureteral limb, followed by the two contralateral ureteral limbs, keeping a guidewire in each limb. The four ureters were successfully rendered stone free in a single session. Four double-J stents, one in each ureter, were inserted after removal of all ureteric stones.
The patient passed the uneventful postoperative course. After that, the patient has received few extracorporeal shock wave lithotripsy (ESWL) sessions for the bilateral renal stones. The double-J stents were removed under local anesthesia after clearance of all stones.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [41, 'years'], 'creatinine': [130.0, 'mmol/dL']}",0.00097,0.00092,0.00102,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 41 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 130.0 mmol/dL. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from mmol to mg. The mass of Serum Creatinine is 130.0 mmol. To convert 130.0 mmol of Serum Creatinine to mol, multiply by the conversion factor 0.001, giving us 130.0 mmol Serum Creatinine * 0.001 mol/mmol = 0.13 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.13 mol Serum Creatinine * 113.12 g/mol = 14.7056 g Serum Creatinine. To convert 14.7056 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 14.7056 g Serum Creatinine * 1000.0 mg/g = 14705.6 mg Serum Creatinine. The volume units is dL so no volume conversion is needed. Hence, the concentration value of 130.0 mmol Serum Creatinine/dL converts to 14705.6 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (14705.6/0.9)**-1.2 * 0.9938**41 * 1.0 = 0.00097.
Hence, the GFR value is 0.00097 ml/min/1.73 m²."
269,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8142808-1,Extracted,"The following case is of an elderly male who presented with metabolic encephalopathy and failure to thrive that was found to have persistently positive NP RT-PCR for SARS-CoV-2 over several weeks despite a lack of symptoms typically attributed to SARS-CoV-2 infection [].
A 90-year-old male with hypertension (HTN), well-controlled type 2 diabetes mellitus (DM2), hyperlipidemia (HLD), coronary artery disease, mild Alzheimer's dementia, and chronic kidney disease (CKD) stage 3 presented to the emergency department (ED) with generalized weakness and recurrent falls for the past few days. He was diagnosed with a possible urinary tract infection owing to an otherwise negative workup including a computed tomography (CT) head and chest radiograph (CXR). He did not initially undergo a NP RT-PCR for SARS-CoV-2 on admission due to restrictions on testing at that time. He was discharged from the ED with oral antibiotics to his assisted living facility (ALF). Four days later, he returned to the ED with encephalopathy, progressive generalized weakness, and inadequate oral intake requiring admission to the inpatient medical ward. To note: the day after admission, the patient's ALF reported an infection at their facility; however, our patient did not undergo a NP RT-PCR at that time as he had no indication for testing consistent with the Centers for Disease Control and Prevention (CDC) testing algorithm [] (note: testing criteria have since been updated). Pertinent findings on presentation included a dry oropharynx, right lower lobe crackles, ecchymosis on lower extremities, and a significant encephalopathy. Initial workup revealed a serum creatinine of 2.46 (baseline 1.8), a procalcitonin of 0.16, and a normal CXR. He was diagnosed with failure to thrive, metabolic encephalopathy, and acute kidney injury (AKI) on CKD stage 3. He was initially treated with isotonic saline for volume repletion and general supportive care. On hospital day (HD) four, the patient's metabolic encephalopathy persisted despite rehydration and resolution of his AKI warranting further investigation. Aside from a CRP of 57.4, his lab work, blood cultures, repeat procalcitonin (0.19), magnetic resonance imaging (MRI) of the brain, repeated CXR, and electroencephalogram (EEG) were unrevealing. Although the patient did not meet CDC testing criteria at that time, he underwent NP-PCR for SARS-CoV-2 on HD nine. On HD 10, NP-PCR for SARS-CoV-2 was positive and the patient was placed on modified droplet precaution while exposed staff members were instructed to self-quarantine for 14 days. A lumbar puncture (LP) was performed given the concern for encephalopathy related to COVID-19. PCR on CSF was negative for SARS-CoV-2. His encephalopathy improved by HD 20 without additional therapies; unfortunately, his discharge was delayed secondary to persistently positive SARS-CoV-2 PCR tests (). On HD 30, CRP was retested and found to be improved at 8.4. He was discharged on HD 33 after two consecutive negative RT-PCR results. During his hospital course, he remained afebrile without pulmonary symptoms, imaging findings, supplemental oxygen requirements, or other signs of infection. All blood, urine, and LP cultures remained negative, and his metabolic encephalopathy was attributed to an atypical COVID-19 infection. Modified droplet precautions were removed once he had two consecutive negative NP RT-PCR tests, and he was discharged to his ALF without further follow-up or subsequent hospitalizations [].","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [90, 'years'], 'creatinine': [2.46, 'mg/dL']}",24.27541,23.06164,25.48918,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 90 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.46 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.46/0.9)**-1.2 * 0.9938**90 * 1.0 = 24.27541.
Hence, the GFR value is 24.27541 ml/min/1.73 m²."
270,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7733431-1,Extracted,"A 56-year-old Caucasian female with a history of mechanical mitral valve replacement presented to the emergency room with acute kidney injury. The patient also reported the presence of low-grade fever, fatigue, weight loss of 24 pounds, and decreased appetite for 3 months. During the period of subacute symptoms, the patient presented to the health-care system several times. The patient denied the presence of any night sweats, chills, skin rash, viral symptoms, or hemoptysis. Past medical history was positive for diabetes mellitus type 2, hypertension, and atrial fibrillation, whereas the patient had surgical history of mitral valve replacement due to severe mitral valve regurgitation, coronary artery bypass grafting, carotid endarterectomy, aortic valve repair, and placement of a surgical mesh after urinary bladder surgery. Medications at the time of admission included warfarin, amiodarone, and metoprolol. The patient was vitally stable; however, physical examination revealed a 4/6 diastolic murmur on the apical area along with significant tenderness on the left upper chest wall which radiated toward the back. The patient. had no Janeway lesions and had no exposure to tame animals.
Blood workup showed pancytopenia and elevated creatinine of 5.9 mg/L, potassium of 6.1 mEq/L, C-reactive protein of 61 mg/dL, and International Normalized Ratio (INR) of 4.78. Urine analysis showed hematuria with mild proteinuria and mixed cellular cast. Light microscopic study of urine, liver function tests, serology for viral hepatitis, antinuclear antibody, antineutrophil cytoplasmic antibodies, and cryoglobulin were within the normal range. Bacterial isolates were recovered from four of four blood cultures within 14–28 h of collection using the standard automated instrumentation (BacT-Alert System, FA Plus and FN Plus bottles, BioMeriuex, Durham, NC, USA). Following subculture to sheep blood agar, isolated colonies of Gram-positive cocci were evaluated in duplicate from each of the four cultures using MALDI-TOF mass spectrometry (Vitek MS, BioMeriuex), with all giving uniformly high probability scores (99.9%) for the identity of E. durans.[] Antimicrobial susceptibility testing was performed on a representative isolate from each bacteremia episode using an automated phenotypic method (Vitek 2, GP75, BioMeriuex) or standard disc diffusion and gradient diffusion (E-test, BioMeriuex) []. Transesophageal echocardiogram (TEE) showed vegetation of 0.8 cm × 0.3 cm on the medial aspect of the annulus of the mechanical mitral valve []. An abdominal computed tomography (CT) scan showed splenomegaly with splenic infarction. After the initial assessment, the patient was admitted to the medicine ward, and multidisciplinary teams, including nephrology, infectious disease, radiology, and cardiac surgery, were consulted.
At admission, the patient was placed on intravenous fluids as conservative management for kidney injury and empiric antibiotic therapy consisting of daptomycin, cefepime, and metronidazole was initiated, whereas warfarin was halted due to supra-therapeutic INR levels. Daptomycin was eventually switched to combination ampicillin and ciprofloxacin when blood cultures revealed E. durans sensitive to ampicillin, ciprofloxacin, daptomycin, gentamicin, and vancomycin. Gentamicin was avoided due to kidney injury. Blood cultures after 72 h of antibiotics therapy were sterile. The patient improved significantly, and on the 10th day of hospitalization, the patient was discharged home with the recommendation to complete a 6-week course of intravenous antibiotics. Meanwhile, warfarin was resumed as INR stabilized at 2.33 mg/dL. In the 5th week of therapy, the patient developed peripheral eosinophilia; therefore, ampicillin was switched to daptomycin.
Three months after the completion of antibiotic therapy, the patient presented to the emergency department with hemiplegia, left-sided facial palsy, and aphasia. Laboratory studies showed creatinine of 7.27 mg/dL, blood urea nitrogen of 79, and INR of 7.2. CT scan of the brain showed right frontal intraparenchymal hemorrhage with subarachnoid extension and a 3-mm leftward midline shift. Repeated CT scan showed a progression of hemorrhage; therefore, the patient underwent right decompressive craniotomy. Four sets of blood cultures were drawn and through above-mentioned modality, they were positive for E. durans []. Transesophageal echocardiography was negative for any vegetation []. Combination antibiotic therapy was initiated, and follow-up blood culture after 48 h was sterile. The patient remained intubated and underwent continuous renal replacement therapy. Despite the definitive management, the patient developed multiple organ failure. A discussion with the family was arranged where they decided to move patient to the inpatient hospice for comfort measures where she eventually died on the 26th day of admission.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [56, 'years'], 'creatinine': [7.27, 'mg/dL'], 'sex': 'Female'}",6.1163,5.81048,6.42211,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 56 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 7.27 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (7.27/0.7)**-1.2 * 0.9938**56 * 1.012 = 6.1163.
Hence, the GFR value is 6.1163 ml/min/1.73 m²."
271,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4432425-1,Extracted,"A 31-year-old Caucasian man was admitted to a hospital with severe renal failure. He presented with a 1 week history of sudden onset of severe lower back and loin pain accompanied by swelling of both lower limbs and reduced urine output. He had no past medical or family history, and was an ex-smoker. Apart from his work as a taxi driver, there was no history of immobility, long airline journeys or major physical exertion. He took no regular medication. His blood pressure was 149/70 mmHg, pulse 100/min. Abdomen was distended without a palpable mass. Bladder was empty after catheterization and he remained anuric. Biochemically, he had severe renal failure (creatinine 1167 μmol/L = 13.2 mg/dL). His white cell count was 12 800 × 106/mL, C-reactive protein 283 mg/L, erythrocyte sedimentation rate 55 mm and serum albumin 41 g/L. His clotting profile was normal, d-dimer was 15 570 ng/mL (normal below 250) and creatinine kinase was 51 IU/mL.
A central venous dialysis catheter was inserted into the right femoral vein. The operator reported difficulty in cannulating the vein but on haemodialysis high venous pressure and poor blood flow were noted. This catheter was removed and further haemodialysis was carried out via a right internal jugular venous catheter.
The next day, computed tomography (CT scan-venous phase contrast) of thorax, abdomen and pelvis revealed complete venous thrombotic occlusion extending from both common femoral veins to the supra-renal inferior vena cava (IVC), and both the renal veins were occluded with oedematous kidneys (). No malignancy was seen.
The interventional radiologists started thrombolytic therapy: initially, venous access was gained in the left femoral vein and digital subtraction venography demonstrated near-occlusive thrombus extending from the femoral vein to the supra-renal IVC as seen on CT. At this point, a 20 cm Cragg-McNamara thrombolysis catheter (EV3) was placed along the length of the IVC and a recombinant tissue plasminogen activator (rTPA) was administered as a bolus of 5 mg, followed by a continuous infusion of 1 mg/h for 12 h. A simultaneous infusion of unfractionated heparin at a rate of 500 IU/h was given through the femoral vascular access sheath for 48 h. Repeat venography at 12 and 48 h showed some minor improvements but still significant residual thrombus. Then, renal venography and thrombolysis were attempted via a right internal jugular vein approach after placement of a vascular access sheath. Imaging from here identified supra-renal IVC stenosis, which was angioplastied with a 12 mm diameter balloon. Venography showed heavy thrombus burden within the left renal vein and thrombus at the origin of the right renal vein. A new Cragg-McNamara (EV3) thrombolysis catheter was positioned in the left renal vein thrombus and further rTPA bolus (four pulse spray of 1 mg) followed by continuous infusion (1 mg/h) was given. Right renal vein patency was gained by suction thrombectomy of the thrombus at its origin and balloon angioplasty of the same region to disperse residual thrombus. Venography 48 h later showed complete patency of both renal veins; the supra-renal IVC stenosis was apparent and a 22 mm × 80 mm Sinus XL stent was deployed across this successfully. Venography then demonstrated patency of the IVC and both renal veins.
Urine output resumed on the third day of starting thrombolysis, oedema gradually settled and the creatinine level continued to improve (). The antiphospholipid screen was negative [protein C 130 U/dL (66–122), protein S 112 U/dL (74–146), antithrombin III 134 U/dL (75–140), activated protein C ratio 2.99 [>2.1], factor V Leiden absent, lupus anticoagulant negative, anti-β2-glycoprotein I antibodies 2 U/mL (0–20), cardiolipin antibodies IgG <12 U/mL (0–12) and IgM <10 U/mL (0–10)]. The patient was anticoagulated with warfarin. Magnetic resonance venography () at 3 months confirmed patency of all veins and the stented IVC segment. Eight months after initial presentation, the creatinine level was still normal at 76 μmol/L.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [31, 'years'], 'creatinine': [13.2, 'mg/dL'], 'sex': 'Male'}",4.66616,4.43285,4.89947,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 31 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 13.2 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (13.2/0.9)**-1.2 * 0.9938**31 * 1.0 = 4.66616.
Hence, the GFR value is 4.66616 ml/min/1.73 m²."
272,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4955219-1,Extracted,"A 47-year-old male reported a seven day history of influenza-like symptoms, including general malaise, chills, dry cough, chest-pain, shortness of breath, and temperatures of up to 39.5 °C, which did not respond to paracetamol or ibuprofen. The patient worked as a veterinary researcher in a laboratory where experimental intranasal infections with C. abortus were developed in sheep. The patient carried out these infections using a suspension of C. abortus sprayed into both nostrils with a multi-dose spray pump, as described previously []. Ten days after the sheep infections, the patient showed the first symptoms.
The initial medical examination identified crackling sounds during lung auscultation. A chest x-ray showed areas of consolidation of the lower lobe of the left lung, indicating a pan-lobar pneumonia (Fig. ). Blood and biochemical tests revealed a non-significant increase in mean corpuscular hemoglobin (MCH), as well as a slight increase in urea and creatinine levels: 50.3 and 1.3 mg/dl respectively. By contrast, the C-reactive protein level was very high, 8.9 mg/dl, normal values being <0.5 mg/dl. These high values suggested a bacterial infection rather than a viral infection, in which case the values would be lower [].
Serological analyses with several ELISA tests (all of them from Vircell Microbiologist, Granada, Spain) using specific IgG and IgM monoclonal antibodies (MoAb) were negative against Mycoplasma pneumoniae, Legionella pneumophila (serogroup 1-7), Rickettsia conorii and Chlamydia pneumoniae.
Due to the suspicion of C. abortus infection, serum and sputum samples from the patient were sent to a laboratory at the Animal Health Department of the Murcia University (Spain) for further analysis.
A C. abortus-specific serological test, performed using an ELISA kit (ID Screen Chlamydophila abortus indirect multi-species, IDvet), revealed high IgM and IgG optical densities (OD) in the serum samples (Table ). The serum samples were tested with a peroxidase-conjugated anti-human IgG or IgM (Sigma), and the OD were determined (DigiScan with DigiWin Software, ASYS Hitech). In addition, two serum samples from asymptomatic work colleagues were analyzed with the same ELISA kit. As might be expected, both colleagues showed antibody production against C. abortus, but with a lower OD than the patient, especially for IgM production (Table ). It was therefore assumed that antibody production on the part of the patient was due to a clinical episode and not to a progressive sensitization to C. abortus.
C. abortus was isolated from the sputum using a McCoy cell monolayer, as described previously []. Positive cell cultures were identified by an immunofluorescence assay using the C. abortus-specific anti-MOMP FA2H10 MoAb []. The MoAb was produced using BALB/c mice and purified by immunoafinity, and was chosen because it is specific for an oligomer of the outer membrane protein of C. abortus (named as C. psittaci, serotype 1).
C. abortus DNA was detected in the sputum sample and also in the cell culture isolates by PCR analysis. Total DNA was extracted with a commercial kit (DNeasy tissue kit, Qiagen) and was used as a template for a C. abortus-specific PCR, using primers pmp-F (5′-CTC ACC ATT GTC TCA GGT GGA-3′) and pmp-R821 (5′-ACC GTA ATG GGT AGG AGG GGT-3′) for the target gen pmp 90/91 [], which allow the sensitive amplification of 821-bp length DNA fragments. In order to confirm the specific presence of C. abortus in the sputum sample as well as in the cell isolates, the amplicons were sequenced (ABI Prism 3130). The PCR products showed 100 % identity to the C. abortus AB7 strain sequence obtained using MEGA5 software and BLAST® program. This C. abortus strain was the same strain as that used in the experimental infections in ewes carried out by the patient [].
Once diagnosed, the patient was treated with antibiotics (levofloxacin, initial intravenous dose of 500 and 500 mg orally every 24 h for 10 days; and clarithromycin 500 mg every 12 h for 10 days), mucolytic carbocysteine lysine (2.7 g orally every 24 h), glucocorticoids (beclomethasone dipropionate inhaler 100 μg every 12 h) and non-steroidal anti-inflammatory drugs (paracetamol 1 g orally in case of fever or pain). This treatment resulted in successful recovery of the patient in 2 weeks without sequels.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [47, 'years'], 'creatinine': [1.3, 'mg/dL'], 'sex': 'Male'}",68.18675,64.77741,71.59609,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 47 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.3/0.9)**-1.2 * 0.9938**47 * 1.0 = 68.18675.
Hence, the GFR value is 68.18675 ml/min/1.73 m²."
273,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5998720-1,Extracted,"A 32-year-old male was admitted for renal failure. Five years ago, diabetes mellitus (DM) had been diagnosed on the evaluation of unintentional weight loss. Six months before present admission, pulmonary tuberculosis (PTB) was diagnosed. Investigations at that time including kidney and liver function tests, complete blood count, and urine analysis were normal; X-ray chest revealed bilateral reticulonodular infiltrates and small thin-walled cavities; sputum smear for acid-fast bacilli was negative; computed tomography (CT) scan of thorax revealed bilateral multiple centrilobular nodules with adjacent ground glass opacities, fibro-bronchiectatic changes in upper lobes and multiple necrotic mediastinal lymph nodes. Since there was past history of PTB with drug default, antitubercular treatment (ATT) was started as per category II of DOTS (thrice a week combined regime of streptomycin for 2 months, pyrazinamide for 3 months, and isoniazid, rifampicin, and ethambutol for 8 months). Three months ago, progressive increase in serum creatinine was noted, and he was investigated at another hospital. Serum creatinine was 7.1 mg/dl, complete blood count, liver function tests, and urine analysis were normal; 24 h urine protein was 100 mg; tests for HIV, hepatitis B and C virus infection were negative, and ultrasonography of kidney showed normal-sized kidneys. Kidney biopsy was performed; light microscopy had revealed only one glomerulus with normal morphology, mild interstitial edema with lymphocytic and neutrophilic infiltrates and few tubules with changes of acute injury and oxalate crystal deposition. Dose-modified rifampicin-free ATT had been continued, however, renal function had declined further. One month before the present admission, hemodialysis was initiated due to uremic symptoms. summarizes the trend of renal function. In the present admission, investigations were as follows: Hb 9.5 g/dl, WBCs 7800/cmm, platelets 2.4 lac/cmm, serum. creatinine 11.4 mg/dl, total bilirubin 0.6 mg/dl, SGOT 18 IU/L, SGPT 38 IU/L, serum calcium 8.8 mg/dl, serum phosphorus 5.8 mg/dl; Urine analysis-trace protein, 1–2 red blood cells, and 3–4 pus cells/hpf, no crystalluria; 24 h urine protein-94 mg. Fundoscopy revealed changes of mild non-proliferative diabetic retinopathy. Serum complement level was normal, antinuclear antibody and anti-neutrophil cytoplasmic antibody tests were negative. Kidney biopsy was repeated; it revealed 14 viable glomeruli with mild mesangial expansion without evidence of hypercellularity, nodular glomerulosclerosis, or glomerular basement membrane (GBM) alterations []. Tubules showed extensive inspissation of refractile calcium oxalate (CaOx) crystals in tubular epithelial cells and lumina with acute tubular injury []. The crystals showed strong birefringence under polarized light. Mild interstitial edema was observed with lymphocytic infiltrates; tubular atrophy and interstitial fibrosis in 25% of the cortex. Eosinophilic infiltrates or acute tubular necrosis was not seen. Immunofluorescence was negative. Electron microscopy showed mild thickening of GBM (mean thickness 475.3 nm). Electron-dense deposits were absent. Diagnosis of oxalate nephropathy with mild diabetic nephropathy (Class IIa) was made. Urine Oxalate:Creatinine ratio was 41 mg/g (normal <32) indicating hyperoxaluria. He had no clinical features of primary hyperoxaluria. He had no history of renal calculi, recurrent abdominal pain, diarrhea, abdominal surgery, recurrent respiratory tract infections or infertility, consumption of herbal or nonprescription medicines, or alcohol consumption. Due to the presence of DM and significant weight loss, chronic pancreatitis (CP) was suspected.[] Further investigations revealed: Serum amylase 96 IU/L (normal 25–140), lipase (325 IU/L, normal 40–190), CT abdomen revealed diffuse calcification of head [], body and tail of pancreas. Magnetic resonance cholangiopancreatography confirmed severe atrophy of pancreas with multiple calcific foci in the parenchyma and pancreatic duct []. Fecal elastase-1 level was low (90 μg/g of stool, normal >200). These features were diagnostic of chronic calcific pancreatitis[] and hyperoxaluria. He was treated with pancreatic enzyme supplementation, calcium carbonate, sodium bicarbonate, pyridoxine, and increased fluid intake for oxalate nephropathy. ATT was continued without rifampicin. However, the patient remained dialysis dependent at 6-month follow-up.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [32, 'years'], 'creatinine': [11.4, 'mg/dL']}",5.52919,5.25273,5.80565,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 32 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 11.4 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (11.4/0.9)**-1.2 * 0.9938**32 * 1.0 = 5.52919.
Hence, the GFR value is 5.52919 ml/min/1.73 m²."
274,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8547566-1,Extracted,"A 27-year-old woman presented to the Emergency Department complaining of asthenia, adynamia and weight loss associated with lower urinary tract symptoms and subfebrile temperature. Ten years before, she had undergone a pediatric en-bloc kidney transplant because of end-stage kidney disease secondary to perinatal asphyxia syndrome. Asphyxia can lead to multi-organ dysfunction and a redistribution of cardiac output to maintain cerebral, cardiac and adrenal perfusion while potentially compromising renal, gastrointestinal and skin perfusion as circulatory response.
One allograft was located in the right iliac fossa (upside-down implantation with ureteric anastomosis following Lich-Gregoir technique, violet in Fig. ) and the other in the right flank (end-to-side uretero-ureteral anastomosis with native right kidney, blue and orange in Fig. ). The en-bloc graft was made to rest on the right psoas muscle, and the graft vena cava was anastomosed terminolaterally to the recipient external iliac vein using 6–0 polypropylene suture. The graft aorta was also anastomosed terminolaterally to the right external iliac artery using 7–0 polypropylene suture.
Our patient presented other comorbidities as well such as hypertension, asymptomatic, bilateral cataracts, intellectual disability, sensorineural hearing loss and Wolff–Parkinson–White syndrome (WPW pattern or preexcitation consisting of a short PR interval and prolonged QRS with an initial slurring upstroke—“delta” wave—in the presence of sinus rhythm) with episodic palpitations and lightheadedness. Anthropometric features are : height 125 cm, weight 25 kg, BMI = 14.2. She reported 10 kg weight loss in the last 5 months due to depression symptoms associated with COVID-19 (coronavirus disease) quarantine. Her daily medication was: prednisone 4 mg, amlodipine 5 mg, atenolol 25 mg, enalapril 2.5 mg, mycophenolic acid 250 mg/250 mg and tacrolimus 2 mg/2 mg.
The main abnormalities in the laboratory data were white blood cells count 15,654/mm3, serum creatinine level 1 mg/dl (baseline: 0.6 mg/dl), lactate 3.6 mmol/l and pH 7.39.
Non-contrast computed tomography (NCCT) scan showed staghorn calculi in the kidney allograft implanted in the right iliac fossa composed of at least 3 stones of 12.5 mm, 13.7 mm and 10 mm located in superior, medium and inferior calyx, respectively (530 Hounsfield Units) (Fig. ). Moreover, both the right flank transplanted kidney and the right native kidney had severe pelvicalyceal dilation because of two ureteral stones of 6.7 mm and 5.9 mm impacted in the uretero-ureteral anastomosis (450 to 510 HU). Finally, a 7.2-mm stone was reported in the lower calyx of her right native kidney (457 HU).
Initial management consisted in hospital admission and empiric treatment with ceftriaxone. After 24 h of empiric ceftriaxone and following our COVID19 protocol, an attempt to perform primary URS of the ureteral stones was carried out. Nevertheless, once the guidewire (Sensor™ PTFE-Nitinol Guidewire with Hydrophilic Tip, Boston Scientific®) passed through the ureteral stones, purulent material came out from the ureteral meatus. Due to this finding, we decided to take an upper urinary tract urine sample for culture, place a double pig-tail stent and a bladder catheter, and stop the procedure. She stayed 9 days in-hospital for management of postobstructive polyuria and was discharged with oral antimicrobial agents (ciprofloxacin and fluconazole) and without the bladder catheter.
Definitive operative treatment of urolithiasis was performed three weeks thereafter. The traditional lithotomy position, in this unprecedented patient, allowed both antegrade and retrograde access. After removing ureteral stent, semirigid ureteroscopy (8Fr, Richard Wolf, Germany®) and Holmium-YAG laser lithotripsy of the ureteral stones (120 W, Lumenis®) were carried out. Retrograde intrarenal surgery (RIRS) (Flex X2, Karl Storz®) was required to treat the stone located in the inferior calyx of the native kidney. Fragmentation of the stones was executed using these laser settings: 0.8 J and 10 Hz. Fragments were removed using a nitinol stone-retrieval frontal basket (NGage, Cook Medical®).
At the meantime, upper pole puncture of the right iliac fossa allograft was performed under ultrasound (US) guidance by a second endourologist. Endovision puncture was not attempted in order to protect the reusable flexible ureteroscope from an extreme proximal ureteral kinking loop (Fig. B).
Tract dilation was accomplished using one-shot dilator to establish a 21-Fr working channel over the guidewire. Mini-PNL (MIP Storz 12 Fr Nephroscope ®) was performed with Holmium-YAG laser dusting of the stones (settings: 0.5 J and 50 Hz). Stone fragments and dust were flushed out through the sheath by vortex effect. After most of the stone fragments had been removed, antegrade flexible nephroscopy (Flexible Fiber-Cystoscope 15Fr, Richard Wolf, Germany®) was conducted to search for residual stones in locations that were inaccessible with the rigid nephroscope (Fig. C). A 14-Fr 100% silicon nephrostomy tube and a bladder catheter were left in place. Operating time was 120 min. Estimated blood loss was approximately 50 cc.
Postoperative NCCT scan, performed 12 h postoperatively, showed neither residual fragments nor suggestive signs of immediate postoperative complications (Fig. ). Both the nephrostomy and the bladder catheter were removed the following day. The patient remained in hospital for 3 days because of tacrolimus blood levels fluctuation. Neither early nor late onset postoperative complications occurred.
After 10 months from discharge, the patient remains stone-free. She is now under magnesium supplement and nitrofurantoin 100 mg daily prophylaxis since crystallographic analysis showed ammonium magnesium phosphate as the main component of the stones. Every six months ultrasound will be performed as follow-up.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [27, 'years'], 'creatinine': [1.0, 'mg/dL'], 'sex': 'Female'}",79.18799,75.22859,83.14739,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 27 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.0/0.7)**-1.2 * 0.9938**27 * 1.012 = 79.18799.
Hence, the GFR value is 79.18799 ml/min/1.73 m²."
275,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3847001-1,Extracted,"A 72-year-old female was admitted with generalized edema. Her general medical condition had been stable for 2 weeks before presenting to the district clinic with a fever and myalgia. She had no history of renal disease. She denied taking any drug except acetaminophen for fever relief. The patient had a persistent fever and subsequently developed generalized edema. On physical examination, the patient was confused, acutely ill-looking, and showed grade 3 pitting edema of both lower extremities. An ecchymotic 3-cm plaque with a 1-cm black eschar was observed over the right lower abdomen (). At the time of admission, she had a blood pressure of 85/55 mmHg, a respiratory rate of 30 per minute, and a body temperature of 39.4℃. Laboratory studies revealed anemia (a hemoglobin level of 10.6 g/dL and a hematocrit of 33.0%) and leukocytosis (a white blood cell count of 17,420/mm3, neutrophils 78.4%, lymphocytes 12.3%, and monocytes 7.7%). Other relevant parameters included a total protein of 6.2 g/dL, a serum albumin of 2.5 g/dL, a blood urea nitrogen of 22.2 mg/dL, a serum creatinine of 1.57 mg/dL, and a total cholesterol of 250 mg/dL. Urinalysis revealed a 4+ proteinuria without significant casts and hematuria. The 24-hour urinary protein excretion was 5.4 g with a random urine protein to creatinine ratio of 9.14.
The anti-Tsutsugamushi antibody test was strongly positive (1:2,560), but was otherwise unremarkable (negative antinuclear antibody, negative anti-dsDNA antibody, negative antistreptolysin O, serum C3 82.6 mg/dL, and serum C4 20.7 mg/dL). Tsutsugamushi disease was diagnosed based on the clinical and laboratory findings. Renal ultrasound revealed normal-sized kidneys with increased echogenicity. Percutaneous renal biopsy was performed under ultrasonographic guidance to identify the cause of the nephrotic syndrome. Light microscopy of the renal biopsy specimen demonstrated diffusely and globally thickened glomerular basement membranes with subepithelial spikes and double contours (). Tubulointerstitial changes were unremarkable. Immunofluorescent staining revealed fine granular deposition of immunoglobulin G along the peripheral capillary wall (). Transmission electron microscopy showed that the glomerular basement membrane was diffusely thick with relatively evenly-spaced intramembranous electron dense deposits. The glomerular epithelial foot processes were diffusely effaced (). Based on these pathologic findings, the patient was diagnosed with membranous glomerulonephritis (MGN).
The patient was treated with doxycycline (200 mg/day). After 5 days of treatment with antibiotics, her clinical symptoms and signs, including fever, weakness, and hypotension, greatly improved. After 4 weeks of treatment, her urinary protein:creatinine ratio was 0.9, serum albumin levels rose to 3.7 g/dL, and the edema resolved. The patient was discharged 5 weeks after admission.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [72, 'years'], 'creatinine': [1.57, 'mg/dL']}",34.83649,33.09467,36.57831,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 72 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.57 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.57/0.7)**-1.2 * 0.9938**72 * 1.012 = 34.83649.
Hence, the GFR value is 34.83649 ml/min/1.73 m²."
276,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7813934-1,Extracted,"An 81-year-old female with a past medical history significant for coronary artery disease, active left femoral vein deep vein thrombosis on warfarin, hypothyroidism, atrial fibrillation, and type 2 diabetes presented to the emergency department from a skilled nursing facility for evaluation of abdominal pain. The patient had been experiencing four days of abdominal pain, nausea, vomiting, and diarrhea. She noted her vomitus had a feculent odor. No blood was noted in the patient's emesis or bowel movements. The patient reported that ""food goes right through me"".
On physical examination, the patient was ill-appearing with a heart rate of 150/min in rapid atrial fibrillation, respiratory rate of 22/min, blood pressure of 100/60 mmHg, and oral temperature of 37.5°C. Abdominal exam was consistent with peritonitis with guarding in all four quadrants of the abdomen, which was most significant in the right lower quadrant. Of note, there was no palpable crepitus or overlying skin changes. Resuscitation was initiated with two liters of normal saline IV fluids.
Labs demonstrated leukocytosis to 19,600/μL, hemoglobin of 9.0 g/dL, and a platelet count of 370,000/μL. Her international normalized ratio (INR) was 2.6. A metabolic panel was significant for creatinine 1.56, a significant increase from baseline. Her lactic acid was elevated at 4.0. An abdominal CT scan with intravenous contrast was obtained that showed a 9.0 x 4.8 cm fluid collection and gas anterior to the bladder (Figures -). The gas appeared to track upward into the anterior abdominal wall with extensive subcutaneous gas present (Figure ). Also noted were thickening of the cecum and appendix and bilateral hydronephrosis and hydroureter (Figure ).
General surgery service was consulted for emergent laparotomy after anticoagulation reversal. She was given four units of fresh frozen plasma and vitamin K 10 mg IV for warfarin reversal, and ceftriaxone 1 g IV, and metronidazole 500 mg IV.
Exploratory laparotomy revealed unusual findings. Upon entrance into the abdominal wall, there was clear separation of the peritoneum from the overlying necrotic transversalis fascia extending down into the pelvis. A dense fibrotic ring covering the base of the cecum was discovered, and the appendix had perforated. There was a large collection of dishwater-like, foul-smelling fluid that extended deep into the space of Retzius (i.e. retropubic space). This collection was consistent with periappendiceal abscess. Its cultures grew out Escherichia coli, Pseudomonas aeruginosa, and Proteus mirabilis. The dome of the bladder was noted to be necrotic and ruptured, and in direct contact with the abscess. In summary, the general surgeon performed an appendectomy, drainage of the periappendiceal abscess, repair of the bladder perforation, resection of necrotic tissue of the abdominal wall, and abdominal washout prior to closure of the abdomen. Urology service was consulted intraoperatively for assistance in the management of bladder perforation via telephone.
Postoperatively, the patient remained intubated in critical condition, requiring low-dose norepinephrine infusion. Antibiotics were tailored to the cultures, with a regimen of clindamycin, cefepime, and metronidazole. On post-operative day 13, the patient’s urine output decreased significantly, and a repeat CT scan was performed, demonstrating free fluid in the abdomen likely representing urine, as well as persistent subcutaneous gas in the abdominal wall. The patient was taken back to the operating room, and it was found that she had progressive necrosis of the bladder wall with a perforation at the site of the initial repair and gross spillage of urine. There was also evidence of ongoing necrotizing fasciitis of the peritoneum and anterior abdominal wall, contributing to the continued septic shock. She underwent abdominal wall debridement, washout, and repeat repair of the bladder perforation. On post-operative day 19, the patient’s septic shock did not improve and care was withdrawn, and the patient died shortly thereafter.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [81, 'years'], 'creatinine': [1.56, 'mg/dL'], 'sex': 'Female'}",33.19368,31.534,34.85336,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 81 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.56 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.56/0.7)**-1.2 * 0.9938**81 * 1.012 = 33.19368.
Hence, the GFR value is 33.19368 ml/min/1.73 m²."
277,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5689439-1,Extracted,"An 87-year-old woman had been in good health until one and a half years before when coughing, bilateral ear fullness, and hearing impairment appeared. She consulted a pulmonary medicine office. Idiopathic pulmonary fibrosis (IPF) was diagnosed from the chest computed tomography (CT) findings. She was followed without treatment. Two months later, she consulted an otolaryngologist and was diagnosed with bilateral otitis media. She was treated with medications and received bilateral myringotomies, but the otitis media remained refractory. Four weeks earlier, nocturnal cough and anorexia had appeared. She consulted a community hospital. Blood tests disclosed a leukocyte count of 11 300/μL, hemoglobin 8.3 g/dL, and creatinine 0.56 mg/dL. Chest CT scan showed no change of IPF. Garenoxacin at a dose of 200 mg per day was prescribedfor 7 days without improvement. Five days before, low-grade fever appeared. She was referred to our division. Past myringotomies were observed in both tympanic membranes. Late inspiratory fine crackles were heard at the base of the lungs. AAV was strongly suspected from the history, especially intractable otitis media. Laboratory values were as follows: leukocyte count 11 800/μL; hemoglobin 8.8 g/dL; platelet count 373 000/μL; aspartate aminotransferase (AST) 18 IU/L; alanine aminotransferase (ALT) 12 IU/L; creatinine 0.52 mg/dL; CRP 6.2 mg/dL; and erythrocyte sedimentation ratio (ESR) 85 mm/h. Urinalysis disclosed trace hematuria and no proteinuria. Myeloperoxidase (MPO)-ANCA was positive at 43.5 U/mL. Proteinase 3 (PR3)-ANCA was negative. She was admitted to the division of rheumatology for examination. On admission, livedo reticularis was observed in both legs. Skin biopsy of the lesion showed leukocytoclastic vasculitis without fibrinoid necrosis in small arteries and veins located in the dermis and subcutaneous tissue (Figure ). She was diagnosed with MPA. Oral prednisolone at a dose of 20 mg per day was administered, and all symptoms including otitis media improved markedly.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [87, 'years'], 'creatinine': [0.52, 'mg/dL']}",89.8655,85.37223,94.35877,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 87 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.52 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.52/0.7)**-0.241 * 0.9938**87 * 1.012 = 89.8655.
Hence, the GFR value is 89.8655 ml/min/1.73 m²."
278,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6458895-1,Extracted,"A 57-year-old male from Thailand with long-standing psoriatic arthritis presented with diffuse scaling of his skin. He was being treated for psoriatic arthritis with adalimumab, leflunomide, and topical clobetasol, but had stopped taking all medications two weeks prior to presentation. At baseline, the patient was a gardener and able to complete all his activities of daily living. However, during the disease course, he noticed diffuse skin scaling and had diarrhea, leading to fatigue. His only joint complaint was chronic left ankle pain, and he denied oral ulcers. Physical exam revealed diffuse yellow scaling covering his entire body with underlying erythema and tenderness without mucosal involvement (Figures and ). Empiric antibiotics were started until blood cultures ruled out infection. Labs were notable for a creatinine of 3.3 mg/dL, with no prior history of renal disease, calcium 7.8 mg/dL, phosphate 5.9 mg/dL, bicarbonate 13.0 mmol/L, urine pH 5.0, and uric acid of 12.7 mg/dL (). The patient was admitted to the intensive care unit given >80% of body surface area involvement and acute renal failure. He received 4 L of normal saline for initial resuscitation. On day 2, the patient was determined to be euvolemic based on clinical exam with moist mucous membranes. Despite aggressive fluid administration, renal function did not improve, and creatinine continued to rise and peaked at 4.61 mg/dL, with phosphate of 7.0 mg/dL and 48 hours of anuria. Renal ultrasound showed 5 mm nonobstructing renal calculi in the left kidney and small echogenic kidneys consistent with chronic kidney disease (). Subsequent urine microscopy showed diffuse polymorphic uric acid crystals, consistent with uric acid crystal-induced nephropathy (). He was managed with rasburicase, urinary alkalinization, and fluids. The underlying erythrodermic psoriasis was treated with restarting leflunomide, topical isotretinoin, and clobetasol. His renal function improved dramatically; urine output, uric acid, and electrolytes normalized. He was discharged on topical clobetasol and leflunomide and new addition of secukinumab with little to no skin involvement.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [57, 'years'], 'creatinine': [3.3, 'mg/dL']}",20.95102,19.90347,21.99857,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 57 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.3/0.9)**-1.2 * 0.9938**57 * 1.0 = 20.95102.
Hence, the GFR value is 20.95102 ml/min/1.73 m²."
279,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5946557-1,Extracted,"The patient is a 78-year-old Caucasian male, former smoker (40 pack-year history of tobacco use), with medical history of chronic obstructive pulmonary disease (COPD) and prostate cancer status postradical prostatectomy and subsequent radiation therapy complicated by radiation colitis who presented to the emergency department with recent onset shortness of breath and altered mental status per family members. The patient reported that he had been experiencing a productive cough and subjective fevers for the past 2 days. The night before presentation, the patient’s wife noted that he was confused and was unable to get into bed. On these mentioned findings, the patient was rushed to the emergency department. On further questioning, the patient disclosed a recent hospitalization 2 months prior for a COPD exacerbation and suspected bowel obstruction.
On presentation, the patient was hypotensive with a blood pressure of 92/61, tachycardic with heart rate of 130, tachypneic with respiratory rate of 25, and hypoxic with oxygen saturation of 71%. The patient was afebrile with a temperature of 99.9°F (37.7°C). At this time, the patient was alert and oriented. On physical examination, breath sounds were diminished in all lung fields bilaterally along with scattered crackles throughout. While in the emergency department, the patient was started on noninvasive positive pressure ventilation with BiPAP. On initial laboratory studies, the patient had a leukocytosis (white blood cell 30.6 with 12% bands), lactic acidosis (lactic acid of 3.6 mmol/l), and acute kidney injury with creatinine of 1.5 mg/dl (baseline 0.8 mg/dl). Chest X-ray showed a left upper and lower lobe opacity concerning for pneumonia []. The patients calculated pneumonia severity index was 131, which correlates with a suggested Class V management strategy. Considering this classification and its associated mortality of 27%–31.1%, our patient was admitted to the intensive care unit for acute on chronic hypoxic hypercapnic respiratory failure secondary to left-sided pneumonia. Soon after admission, the patient’s condition deteriorated requiring intubation with mechanical ventilation. The patient was started on broad-spectrum antibiotics with vancomycin, piperacillin-tazobactam, and azithromycin for what was thought to be healthcare-associated pneumonia (HCAP).
On the 2nd day of hospitalization, initial blood cultures returned positive for P. multocida, confirmed by blood chocolate agar [] and gram stain []. At this point, additional history obtained from the patient’s family revealed ownership over five cats and a deep involvement in their care and grooming. A thorough physical examination was performed; however, no scratch or bite marks were identified on the patient nor were any signs of skin infection or abscess found. Following the identification of P. multocida, the patient’s antibiotic regimen was switched to ampicillin-sulbactam. Several days after initiating targeted antibiotic therapy, the patients clinical status improved, leading to successful extubation and discharge on the 18th day of hospitalization. The patient was sent to an extended care facility with amoxicillin-clavulanic acid, with instructions to complete a total of 14 days of antibiotic therapy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [78, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Male'}",47.35777,44.98988,49.72566,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 78 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.5/0.9)**-1.2 * 0.9938**78 * 1.0 = 47.35777.
Hence, the GFR value is 47.35777 ml/min/1.73 m²."
280,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8040450-1,Extracted,"A 17-year-old obese female with a nonsignificant past medical history presented to the emergency room (ER) because of fever, cough, and shortness of breath. Onset 7 days before admission with ungraded fever and cough, was aggravated by dyspnea, which prompted her to call the emergency medical services (EMS). The EMS reported that the patient’s oxygen saturation was in the low 80s, so she was placed on a non-rebreather mask (NRM) and transferred to the hospital. Upon arrival in the ER, the patient looked lethargic, in severe respiratory distress, and could only speak two to three words per sentence. On arrival, vitals were as follows: blood pressure (BP) 98/69, pulse 140, respiratory rate 30, saturation 98% on NRM, and temperature of 38.4 °C. On physical examination, there were fine crepitations in both lung fields. Real-time polymerase chain reaction (PCR) for COVID-19 was performed, which came back positive. Chest X-ray showed patchy bilateral opacities (). Other laboratory studies revealed white blood cell (WBC): 13.7 × 103/µL, hemoglobin (Hb): 12.5g/dL, erythrocyte sedimentation rate (ESR): 95 mm/h, D-dimer: 0.72 µg/mL, C-reactive protein (CRP): 17.1 mg/dL, ferritin: 251.2 ng/mL, blood urea nitrogen (BUN): 6mg/dL and creatinine: 0.5mg/dL. The patient was admitted to the pediatric intensive care unit (ICU); the NRM was switched to high-flow nasal cannula (HFNC) (45 L per minute (LPM) at 50% FiO2) and was started on hydroxychloroquine, azithromycin, vitamin C, and zinc, which were standard of care at the time. Remdesivir was requested from the Department of Health but was not readily available due to limited supply. On day 2 of admission, her condition worsened, with a respiratory rate in the 40 s, severe respiratory distress with the use of accessory muscles. She was then placed on a non-invasive positive pressure ventilation machine on continuous positive airway pressure (CPAP) mode to improve the oxygenation. The chest X-ray also showed worsening in her lung infiltrates (). At this point, she had a very low threshold for intubation due to her worsening clinical state. This prompted the medical team to discuss other options available to manage the patient, and it was finally decided to start on immunomodulators for compassionate use. So the patient was started on baricitinib 4 mg oral dose, given daily for 5 days.
On day 3, there was a marked improvement in the patient’s clinical status, no longer in respiratory distress, with a respiratory rate 18 - 22; she looked comfortable, not using any accessory muscles. Vitals showed BP 116/55 mm Hg, heart rate (HR) 97, temperature of 37.1 °C. Oxygen delivery mode was deescalated from CPAP back to HFNC 50 LPM and 50% FiO2, which was further deescalated to Venturi mask, and then nasal cannula. Repeat chest X-ray showed a marked improvement in the opacities.
By day 6 of admission, the patient was comfortable with ambient air, saturating 98%. The patchy opacities on the chest X-ray was resolving significantly; and the inflammatory markers are improved (). She was discharged home on day 8 and scheduled for follow-up in the pediatric clinic.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [17, 'years'], 'creatinine': [0.5, 'mg/dL'], 'sex': 'Female'}",140.20664,133.19631,147.21697,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 17 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.5 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.5/0.7)**-0.241 * 0.9938**17 * 1.012 = 140.20664.
Hence, the GFR value is 140.20664 ml/min/1.73 m²."
281,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4783551-1,Extracted,"A 60-year-old man presented with few days of jaundice, generalized fatigue, and dark urine. On admission, he had a bilirubin level of 836 μmol/L (normal < 24), direct bilirubin of >580 μmol/L (normal < 5), ALP of 235 U/L (normal 40–130), GGT of 340 U/L (normal < 60), AST of 236 U/L (normal < 45), ALT of 75 U/L (normal < 45), albumin of 21 g/L (normal 38–52), and serum creatinine of 135 μmol/L (normal 60–105). His creatinine 6 months earlier had been 80 μmol/L.
He had been taking flucloxacillin 500 mg daily intermittently for 3 months to treat skin folliculitis. He stopped the antibiotics 6 weeks prior to his presentation. There was no history of substance or alcohol abuse. He was on no other regular medications.
On Examination. He was afebrile and had BMI of 30, BP of 125/80, and heart rate of 70/min. His JVP was +2 cm above the sternal angle, with mild peripheral oedema, clear chest on auscultation, and nontender liver extending 3 cm below the costal margin.
The screen for viral and metabolic causes of hepatitis was unremarkable. An abdominal CT with contrast showed hepatomegaly with diffuse fatty changes but no biliary dilatation. The serum bilirubin continued to rise reaching a peak of 881 μmol/L on day 8. A liver biopsy was performed and showed panacinar steatosis, moderate steatohepatitis (NAFLD score 5/8), portal fibrosis, and cholestasis. An ERCP was normal. The diagnosis was flucloxacillin-induced hepatitis.
The patient's serum creatinine continued to rise and peaked at 581 μmol/L on day 16 despite adequate hydration and avoidance of nephrotoxins. In addition, the patient had persistent severe hypokalemia with serum potassium levels consistently <3 mmol/L despite the potassium replacement. Arterial blood gas was not suggestive of renal tubular acidosis with serum bicarbonate level of 26 mmol/L and pH of 7.46.
On day 3, his urine sodium was 33 mmol/L, urine potassium 42 mmol/L, and urine osmolality 420 mmol/kg. The transtubular potassium gradient was >10 and the serum potassium at the time of specimen collection was 2.7 mmol/L indicating renal cause for his hypokalemia. The urinary protein/creatinine ratio was slightly raised at 39 mg/mmol (normal < 23) and otherwise bland urine sediment. The urine output averaged 1.5 L per day from the day of admission.
A renal USS showed normal sized kidneys at 128 mm and 125 mm with no obstruction, normal echotexture, and perfusion; a renal biopsy was performed.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [60, 'years'], 'creatinine': [135.0, 'µmol/L'], 'sex': 'Male'}",49.61496,47.13421,52.09571,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 60 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 135.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 135.0 µmol. To convert 135.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 135.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00014 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00014 mol Serum Creatinine * 113.12 g/mol = 0.01584 g Serum Creatinine. To convert 0.01584 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01584 g Serum Creatinine * 1000.0 mg/g = 15.84 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 15.84 mg Serum Creatinine/10.0 dL = 1.584 mg Serum Creatinine/dL. The concentration value of 135.0 µmol Serum Creatinine/L converts to 1.584 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.584/0.9)**-1.2 * 0.9938**60 * 1.0 = 49.61496.
Hence, the GFR value is 49.61496 ml/min/1.73 m²."
282,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4333874-1,Extracted,"A 54-year-old non-diabetic and non-hypertensive Asian man presented to us with the complaint of recurrent episodes of bilateral pedal pitting swelling along with abdominal distension and periorbital oedema for the preceding 25 years approximately. The swelling subsides when he visits a local physician and receives a short course of diuretics. There was no associated history of dyspnoea, jaundice, upper gastrointestinal (GI) bleed or recurrent episodes of diarrhoea.
A physical examination revealed bilateral pedal oedema, periorbital puffiness, ascites (grade 2), bilateral pleural effusion and mild pallor. He was investigated thoroughly to delineate the cause of anasarca. His blood reports were as follows: haemoglobin 10gm%, serum albumin 1.5gm/dL and serum globulin 3.0gm/dL. Renal function tests revealed urea 30mg% and creatinine 0.9mg/dL. Electrolytes, bilirubin and liver enzymes were within normal limits. His coagulation profile is as follows: prothrombin time 12 seconds (control 12 seconds) and activated partial thromboplastin time 36 seconds (control 35 seconds). Fasting lipid profile showed hypertriglyceridaemia and hypercholesterolaemia. Urine routine examination was 3+ for albumin; his 24-hour urine for albumin was 660mg, with urine output of 800mL in 24 hours. His previous medical records showed higher magnitude of proteinuria and on a few occasions it was approximately 1500mg in 24 hours. An abdominal diagnostic paracentesis was done which strikingly showed milky white colour (Figure ). Routine analysis of ascitic fluid revealed: cell count 154/mm3 (lymphocyte predominant); serum–ascitic albumin gradient 1.2; and adenosine deaminase 6u/L and TG 213mg%. Ascitic fluid culture for bacteria including Mycobacterium tuberculosis was negative. A lymphangiogram was done to find the presence of any obstruction in his lymphatic system, which turned out to be normal (Figure ). A contrast-enhanced computed tomography scan of his abdomen revealed no neoplasm but did reveal the existence of splenic lymphangiectasia (Figure ). An upper GI endoscopy was performed to rule out any feature of portal hypertension; it revealed duodenal lymphangiectasia. His echocardiography was within normal limits, ruling out cardiac cause of ascites.
In view of demonstrated urinary protein loss and presence of dyslipidaemia, a renal biopsy was performed. The renal biopsy (Figure ) showed the presence of focal segmental glomerulosclerosisa (FSGS); not otherwise specified. A total of 18 glomeruli were examined of which two showed segmental sclerosis with adhesion to Bowman’s capsule. Glomeruli were stained for immunoglobulin (Ig G, IgM, IgA, C3, C1q, kappa and lambda light chains. All were negative.
Thus the issue of anasarca was addressed and the patient was put on oral steroids. He responded very well and the steroids could be gradually tapered off without recurrence of symptoms. However, the issue of widespread lymphangiectasia remained unresolved even after thorough search and imaging analysis.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [54, 'years'], 'creatinine': [0.9, 'mg/dL']}",94.07458,89.37085,98.77831,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 54 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.9 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.9/0.7)**-0.302 * 0.9938**54 * 1.0 = 94.07458.
Hence, the GFR value is 94.07458 ml/min/1.73 m²."
283,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6077600-1,Extracted,"A 59-year-old male was scheduled for elective open retropubic prostatectomy for a benign enlarged prostate weighing approximately 65 grams. The patient's weight was 89 kg, ASA physical status II, diagnosed with essential hypertension two years ago, and controlled with ACE-I, Ramipril 10 mg once daily. No other morbidities were associated and no other medications were taken by the patient. The preoperative assessment did not reveal any other abnormality related to anaesthesia with normal vital signs, omitting Ramipril for 48 hours before the operation and normal baseline laboratory results including renal profile (creatinine 87 micromole/L, urea 7.9 mmol/L, Na 140 mmol/L, and K 4.1 mmol/L).
Following discussion with the patient and the surgical team, the anaesthetic plan was general anesthesia (GA) with postoperative patient-controlled analgesia (PCA) with morphine. Relatively uneventful induction of GA by propofol (2mg/kg), fentanyl (100 micrograms), and rocuronium (0.6 mg/kg) with endotracheal intubation, radial arterial cannulation for IBP monitoring, and two wide-bore peripheral cannulas (18G) were inserted. Induction was accompanied by hypotension (BP dropped from 112/68 to 73/46) and bradycardia (HR dropped from 78/min. to 38/min.) that required two successive doses of ephedrine each 6 mg were followed by restoration of BP and HR. Baseline arterial blood gas (ABG) after positioning was normal (). At 2 hours after the start of surgery, the estimated blood was about 350 ml and the urinary output (UOP) was 120 ml (over 2 hours) with mean arterial pressure (MAP) being maintained above 70 mmHg without further vasopressors required other than the initial 12 mg of ephedrine required immediately after induction. An arterial blood gas (2 hours after start of surgery) was initially performed for monitoring haemoglobin level showed hyperkalaemia (6.1 mmol/L) with acidosis (pH 7.33 and PCo2 6.2 kPa). The initial explanation was respiratory acidosis, and ventilation parameters were increased. Twenty-five minutes later ABG showed a decrease of PCo2 to normal with normal anion gap acidosis and increasing potassium to 6.5 mmol/L. Hyperkalaemia was treated with glucose-insulin (10 units of insulin added to 1 litre of glucose 10%) and mild hyperventilation and furosemide (20 mg bolus) with a change of the maintenance fluid from compound lactate solution to normal saline with the same rate (225ml/h). Forty minutes later, these measures had reduced potassium from 6.5 mmol/L to 4.1 mmol/L.
Despite normalization of potassium level (k 4.1 mmol/L) following the measures mentioned above, the acidosis persisted with maintained normal bicarbonate level and normal PCo2 (). From the time of normalized potassium, the acidosis required three hours to normalize which was two hours after recovery from GA. The presence of acidosis did not affect emergence from anaesthesia or recovery of the patient.
Postoperative follow-up of the renal function tests and electrolytes () revealed normalization over a period of two days postoperatively with the patient restored intake of ACE-I on day one postoperatively with no effect on potassium level.
At the end of surgery, the estimated blood loss was about 635 ml, UOP was 700 ml (over an operative time of 4 hours), and the infused fluids included 450 ml of Hartman's solution (over the first 2 hours), 950 ml of 0.9% normal saline, and 500 ml of Gelofusine 4% (over the second 2 hours) in addition to 1 litre of glucose 10% with insulin. No blood transfusion was required and no MAP <70 mmHg was recorded.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [59, 'years'], 'creatinine': [87.0, 'µmol/L'], 'sex': 'Male'}",84.86382,80.62063,89.10701,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 59 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 87.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 87.0 µmol. To convert 87.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 87.0 µmol Serum Creatinine * 1e-06 mol/µmol = 9e-05 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 9e-05 mol Serum Creatinine * 113.12 g/mol = 0.01018 g Serum Creatinine. To convert 0.01018 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01018 g Serum Creatinine * 1000.0 mg/g = 10.18 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 10.18 mg Serum Creatinine/10.0 dL = 1.018 mg Serum Creatinine/dL. The concentration value of 87.0 µmol Serum Creatinine/L converts to 1.018 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.018/0.9)**-1.2 * 0.9938**59 * 1.0 = 84.86382.
Hence, the GFR value is 84.86382 ml/min/1.73 m²."
284,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4531180-1,Extracted,"An 81-year-old male with a history of chronic renal insufficiency, three myocardial infarctions, four coronary stents, and end-stage heart failure presented to an outside hospital in June 2013 for destination LVAD placement (HeartMate II, Thoratec). Prior to LVAD placement, he did not have hematuria. However, as an inpatient, he developed gross hematuria and ultimately underwent transurethral resection of bladder tumor. Pathology revealed muscle-invasive high-grade urothelial carcinoma (UC) with squamous differentiation. Metastatic workup included a CT chest, abdomen, and pelvis as well as a bone scan, which were both unremarkable.
After discharge, the patient's bladder cancer management was referred to our tertiary center, which is also an advanced heart failure referral center with considerable LVAD experience. By July 2013, he had recovered well from his LVAD placement with improved energy and exercise tolerance along with decreased dyspnea. Following a discussion of the risks and benefits, the decision was made for surgical resection with ileal conduit diversion. Neoadjuvant chemotherapy was considered but not pursued given the risks of thromboembolism and infection, preexisting renal insufficiency, and patient preference.
The patient was evaluated by anesthesia and cardiology preoperatively and cleared for surgery. He had previously been on aspirin 81 mg, but this was held for one week in preparation for surgery. The patient was bridged from warfarin to therapeutic enoxaparin (1 mg/kg twice daily) for 5 days with the last dose being 24 hours prior to surgery. In August 2013, the patient was preadmitted before surgery. Per protocol, he was given antimicrobial prophylaxis, alvimopan, and heparin 5000 u subcutaneous on the morning of surgery. Preoperative hemoglobin was 11.9 g/dL, and INR was 1.3.
After intubation, bilateral transversus abdominis blocks were performed for adjunctive pain control. Radical cystoprostatectomy, bilateral pelvic lymphadenectomy, and ileal conduit diversion were performed without complication. Intraoperatively, 3.6 L crystalloid, 250 mL 5% albumin, and 1 unit pRBC were administered. The patient had 265 mL of urine output and 600 mL of blood loss. A Jackson-Pratt drain and ureteral stents were left in place, and the patient was extubated. Total room time was 270 minutes, and time from incision to close was 133 minutes.
After surgery, the patient was admitted to the cardiothoracic intensive care unit (CICU) and given subcutaneous heparin every 8 hours. Postoperative investigations noted initially stable cardiopulmonary status (chest X-ray shown in ). Complete blood counts were drawn every 8–12 hours, and INR was checked daily. On postoperative day (POD) 1, he was transferred out of the CICU on aspirin 81 mg daily but no further anticoagulation given an INR of 2.1. By POD3, the patient's hemoglobin had decreased from 9.7 g/dL immediately after surgery to 7.5 g/dL. He was given 1 u pRBC and furosemide, but the patient became hypoxic. He was transferred back to the CICU and a bumetanide drip was initiated. He received another unit of blood once stabilized, and his hemoglobin increased to 10.7 g/dL.
The patient's diet was advanced on POD7 after passing flatus. From POD9 to POD11, there was a slow downtrend in hemoglobin. On POD11, a CT demonstrated free fluid of mixed heterogeneity in the paracolic gutters and pelvis, consistent with organizing hematoma (). Over the next 72 hours, 4 units of pRBC and 4 units of FFP were given for anemia and an INR of 3.8. Afterwards, the patient required no further transfusions, suggesting a self-resolving bleed. He also underwent left thoracentesis for a pleural effusion with 1.8 L of straw-colored transudate removed. Despite maintained hemodynamics, the remainder of his hospitalization was prolonged due to pain (located near the surgical incision) and anticoagulation monitoring. The acute pain service was consulted on POD15 and assisted with inpatient pain management and the transition to a home analgesia regimen. Warfarin was initiated on POD13 at an INR of 1.5. On POD20, he was discharged with an INR of 2.0 and hemoglobin of 9.8 g/dL, stable over 6 days. Final pathology revealed T2aN0 high-grade UC with squamous differentiation, 26 negative nodes, and negative margins.
The patient's last follow-up was 18 months after cystectomy. Surveillance imaging showed no signs of recurrence. The patient continues to do well from a urologic and cardiac standpoint, including stable renal function (creatinine 1.4 mg/dL), satisfactory ostomy care, and appropriate activity tolerance.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [81, 'years'], 'creatinine': [1.4, 'mg/dL'], 'sex': 'Male'}",50.4945,47.96977,53.01923,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 81 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.4 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.4/0.9)**-1.2 * 0.9938**81 * 1.0 = 50.4945.
Hence, the GFR value is 50.4945 ml/min/1.73 m²."
285,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7114002-1,Extracted,"A 37-year-old male presented to us with complaints of vague abdominal pain, headache, episodic palpitation, dizziness and blurring of vision for the last 6 months. There was no history of pedal edema, shortness of breath or decreased urine output. He was a known hypertensive for past 2 years. There was no other significant illness in past. He was opium addict for last 10 years. He denied any history of alcohol or other drug abuse. Family history was not remarkable. He was on calcium channel blockers, diuretics and Angiotensin receptors blockers (ARBs) for hypertension with good compliance. His blood pressure was uncontrolled in past few months with repeated visits to the hospital with episodes of hypertensive urgency. On physical examination, he was afebrile, with a pulse rate of 94/min, blood pressure of 190/110 mm hg (No significant difference in all limbs). Systemic examination was unremarkable except grade 2 hypertensive retinopathy. Laboratory analysis revealed normal hematological indices. Further investigations showed serum creatinine of 1.14 mg/dl, blood urea nitrogen of 15 mg/dl, and random blood glucose of 96 mg/dl. Urinalysis was also unremarkable. Serum sodium and potassium were 138 mmol/l and 4.9 mmol/l respectively. 24-hour urinary metanephrine levels were within normal limits (131 μg, normal 25-312 μg). 2D echocardiography did not show any abnormality. Computed tomography of abdomen with urogram revealed an enlarged right kidney (12.6 × 5.2 cm) and right moderate hydronephrosis [ and ]. There was no abnormal dilatation of ureter, no calculus noted in kidney or ureter. The left kidney was normal, no mass is seen in bilateral adrenal glands. We tried to explore the cause of hypertension due to the persistent resistant hypertension. After ruling out the common renal parenchymal, vascular and endocrine causes of hypertension, unilateral hydronephrosis was considered the possible reason for secondary hypertension.
The patient was advised renal 99mTc-DTPA (diethylene-triamine-pentaacetate) scan after urology consultation to assess renal function and drainage pattern, which showed hydronephrotic right kidney with obstructed drainage at the level of PUJ (pelvic ureteric junction). Due to resistant hypertension and differential function less than 40%, The laparoscopic guided pyeloplasty was performed. His blood pressure returned to normal after 3 weeks of procedure, with reduction in the dose and number of antihypertensive (on amlodipine 5 mg twice/day). The patient was doing well at 3 months of follow-up with antihypertensive drugs were tapered gradually. 6 months later the patient now continues to remain symptoms free without any antihypertensive.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [37, 'years'], 'creatinine': [1.14, 'mg/dL'], 'sex': 'Male'}",84.94861,80.70118,89.19604,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 37 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.14 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.14/0.9)**-1.2 * 0.9938**37 * 1.0 = 84.94861.
Hence, the GFR value is 84.94861 ml/min/1.73 m²."
286,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7860652-1,Extracted,"A 44-year-old woman who was current smoker (25 packs/year), with hypertension and peripheral arterial disease diagnosed 2 and 1 years ago, respectively, presented with asthenia, nausea, and vomiting during the previous 2 weeks. The physical examination was unremarkable, except by blood pressure of 140/70 mmHg, body mass index of 22.1 kg/m, and pallor. Relevant laboratory findings were hemoglobin of 7 gr/dL, creatinine of 4 mg/dL, albumin 3.5 gr/dL, sodium 128 mEq/L, potassium 4.5 mEq/L, hypercholesterolemia (244 mg/dL, reference value >200 mg/dL), and proteinuria of 7.4 grams in 24 hours. Anti-nuclear antibodies, anti-glomerular basement membrane antibodies, anti-neutrophil cytoplasmic antibodies, human immunodeficiency virus, hepatitis B and C virus tested negative. Renal ultrasound showed normal sized kidneys without obstruction. Percutaneous renal biopsy () was performed demonstrating 27 glomeruli, of which 23 were globally sclerosed, with global nodular mesangial matrix expansion, which stained blue with the Masson trichrome, and was Congo Red negative by light microscopy (LM). By Immunofluorescence (IF), there was no immune deposit, except by the linear staining accentuation of glomerular basement membrane (GBM) and tubular basement membranes (TBM) for Immunoglobulin G and albumin. By electron microscopy (EM), glomerular basement membranes thickness was increased, with laminated and healed areas. There was >50% of interstitial fibrosis and proportional tubular atrophy. Arterioles showed moderate hyalinosis and interlobular arteries mild media thickening. Analyzing the data of the medical history, physical examination, and laboratory and histological findings, ING was diagnosed.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [44, 'years'], 'creatinine': [4.0, 'mg/dL'], 'sex': 'Female'}",13.49802,12.82312,14.17292,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 44 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 4.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (4.0/0.7)**-1.2 * 0.9938**44 * 1.012 = 13.49802.
Hence, the GFR value is 13.49802 ml/min/1.73 m²."
287,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4504063-3,Extracted,"A 43-year-old man presented with a 1-month history of left foot swelling with no other associated complaints or significant medical history. The swelling was mildly tender in the left fifth metatarsal bone with no reddish color or throbbing sensation. Radiography revealed multiple mild but expansive lytic bone lesions in the bilateral distal tibia and left fifth metatarsal bone (Fig. –). Biopsy of the left fifth metatarsal bone and left distal tibia lesions revealed numerous osteoclast-like giant plurinuclear cells without necrosis, mitoses, or histological signs of malignancy; these findings were compatible with a giant cell tumor of the bone. The patient underwent excision of the left fifth metatarsal bone and curettage of the lesion in the left distal tibia. Three weeks after surgery, the first medical and laboratory follow-up examinations revealed a serum calcium level of 2.91 mmol/L (reference range, 2.08–2.80 mmol/L), ALP level of 1154 U/L (reference range, 45–132 U/L), and PTH level of 1084.45 pg/ml (reference range, 15–88 pg/ml). A review of the patient’s medical records revealed hypercalcemia, which had been underestimated at the first examination. The patient had no family history of parathyroid disease. The creatinine level was 51 μmol/L (reference range, 45–133 μmol/L).
PHPT was suspected. Enhancement CT of the neck revealed a round mass measuring 2.7 × 1.4 cm behind and below the left thyroid lobe and a round lesion measuring 1.5 × 1.0 cm located in the left thyroid lobe (Fig. ). Parathyroidectomy was performed. Histological examination confirmed the diagnosis of adenoma of the left parathyroid gland and papillary thyroid carcinoma of the left thyroid lobe. Biochemical data observed before and after parathyroidectomy are shown in Table . After a review of bone slices, the final diagnosis was a brown tumor probably due to long-standing underestimated PHPT.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [43, 'years'], 'creatinine': [51.0, 'µmol/L'], 'sex': 'Male'}",115.88149,110.08742,121.67556,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 43 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 51.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 51.0 µmol. To convert 51.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 51.0 µmol Serum Creatinine * 1e-06 mol/µmol = 5e-05 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 5e-05 mol Serum Creatinine * 113.12 g/mol = 0.00566 g Serum Creatinine. To convert 0.00566 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00566 g Serum Creatinine * 1000.0 mg/g = 5.66 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 5.66 mg Serum Creatinine/10.0 dL = 0.566 mg Serum Creatinine/dL. The concentration value of 51.0 µmol Serum Creatinine/L converts to 0.566 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.566/0.7)**-0.302 * 0.9938**43 * 1.0 = 115.88149.
Hence, the GFR value is 115.88149 ml/min/1.73 m²."
288,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6719630-1,Extracted,"A 78-year-old male with a history of hypertension and hypothyroidism presented to an outside hospital with edema, anorexia, and abdominal pain. Computed tomography (CT) imaging demonstrated focal hypoperfusion of the medial right kidney with bilateral perinephric stranding and suspected phlegmon/abscess formation, which was interpreted as being consistent with bilateral pyelonephritis. Additional imaging findings included pleural effusions, colonic wall thickening adjacent to the suspected perinephric abscess, thought to be a reactive process, and a small pelvic fluid collection. Antibiotics were initiated to treat the working diagnosis of pyelonephritis, and the patient was transferred to our tertiary care facility for surgical consideration in the setting of worsening respiratory function.
On arrival, the patient endorsed worsening edema and pain. Bloodwork was sent to the laboratory for testing, and notable values included the following: white blood cell count 20.1 K/mm3 (reference range [RR]; 4.8-10.8 K/mm3), hemoglobin 7.4 g/dL (RR; 14-18 g/dL), platelet count 37 K/mm3 (RR; 140-440 K/mm3), lactic acid 15 mmol/L (RR; 0.4-2.3 mmol/L), urea nitrogen 67 mg/dL (RR; 7-20 mg/dL), and creatinine 2.5 mg/dL (RR; 0.7-1.3 mg/dL). He was found to be nonreactive for HIV-1 and HIV-2 antibodies. These lab values, which were indicative of acute kidney injury, further supported the clinical impression of pyelonephritis. The renal status continued to worsen both clinically and based on laboratory values, and the patient ultimately became anuric and required continuous renal replacement therapy (CRRT). Concurrently, increasing difficulty of breathing necessitated intubation and mechanical ventilation. Surgical intervention was declined due to the patient’s poor condition and unclear benefit, and the clinical teams continued to administer broad-spectrum antibiotics and supportive care. Over the next several days, his condition deteriorated with refractory shock thought to be secondary to sepsis, nonfunctioning kidneys, and frequent ectopic arrhythmias requiring cardioversion. Care was withdrawn due to severe multisystem organ failure, and the patient was pronounced dead six days after initial presentation to the outside hospital. An autopsy was requested by clinicians and approved by the patient’s next-of-kin due to his rapid decline and several unexplained clinical features at death, such as frequent ectopic beats and severe, refractory shock. An autopsy limited to the chest and abdomen was performed two days following death.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [78, 'years'], 'creatinine': [2.5, 'mg/dL'], 'sex': 'Male'}",25.65504,24.37229,26.93779,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 78 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.5/0.9)**-1.2 * 0.9938**78 * 1.0 = 25.65504.
Hence, the GFR value is 25.65504 ml/min/1.73 m²."
289,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5549489-1,Extracted,"A 42-year-old man receiving APD therapy for approximately one year was admitted to the hospital with diffuse abdominal pain and cloudy dialysate for two days. His medical history included diabetes mellitus (DM) type 2, hypertension, and coronary heart disease but no episodes of peritonitis. He was smoking for twenty years. Physical examination was normal without hypotension, fever, and diffuse abdominal tenderness, and no finding of infection was observed at the catheter exit site or tunnel. His laboratory tests were as follows: hemoglobin: 10.4 g/dL; white blood cell count (WBC): 6390/mm3 (with 76% neutrophils); BUN: 47 mg/dL; creatinine: 5,55 mg/dL; albumin: 3.8 gr/dL; erythrocyte sedimentation rate: 102 mm/h; C-reactive protein (CRP): 22 mg/dL; and peritoneal fluid WBC: 10.380 cells/mm3 (with 90% neutrophils). Gram stain was negative and standard dialysate culture technique was performed. Ceftazidime 1 × 1 g intraperitoneal and piperacillin/tazobactam 3 × 2,25 g intravenous empiric treatment had been started because of the patient's septic condition. On the third day of the treatment, peritoneal fluid and blood cultures identified A. lwoffii that was sensitive to many antibiotics. Clinical and laboratory improvement (peritoneal fluid WBC 300/mm3 and CRP 13 mg/dL) were prominently observed on the third day of treatment; therefore antibiotic treatment was exactly continued and the control dialysate culture was sterile. He was given antibiotic treatment for 15 days to cure the peritonitis and discharged without any problems.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [42, 'years'], 'creatinine': [5.55, 'mg/dL'], 'sex': 'Male'}",12.32496,11.70871,12.94121,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 42 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 5.55 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (5.55/0.9)**-1.2 * 0.9938**42 * 1.0 = 12.32496.
Hence, the GFR value is 12.32496 ml/min/1.73 m²."
290,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-5194,Extracted,"A 25-year-old man is brought to the emergency department by his fiancée for altered mental status. She states that they got in a fight that morning. She later got a text from him at work that said he was going to kill himself. She rushed back home and found him unconscious on the living room floor surrounded by his prescription pill bottles. The patient is sedated but conscious and states that he thinks he swallowed “a bunch of pills” about 2 hours ago. He also complains of nausea. The patient’s medical history is significant for bipolar disorder and chronic back pain from a motor vehicle accident. He takes lithium and oxycodone. The patient’s temperature is 99°F (37.2°C), blood pressure is 130/78 mmHg, pulse is 102/min, and respirations are 17/min with an oxygen saturation of 97% on room air. On physical exam, the patient is drowsy, and his speech is slurred, but he is fully oriented. He has horizontal nystagmus, is diffusely hyperreflexic, and has a mild tremor. His initial electrocardiogram shows sinus tachycardia. Labs are obtained, as shown below:

Serum:
Na: 143 mEq/L
K+: 4.3 mEq/L
Cl-: 104 mEq/L
HCO3-: 24 mEq/L
BUN: 18 mg/dL
Creatinine: 1.5 mg/dL
Glucose: 75 mg/dL
Lithium level: 6.8 mEq/L (normal 0.6 mEq/L – 1.2 mEq/L)

An intravenous bolus of 1 liter normal saline is given.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [25, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Male'}",65.84831,62.55589,69.14073,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 25 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.5/0.9)**-1.2 * 0.9938**25 * 1.0 = 65.84831.
Hence, the GFR value is 65.84831 ml/min/1.73 m²."
291,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2933483-2,Extracted,"A 73-year-old 61-kg male hypertensive and diabetic with peripheral vascular disease (PVD) patient was posted for emergency lower limb below knee amputation for gangrene of foot. Patient was a known alcoholic and smoker (30 pack years), had symptoms of syncopal attacks, dyspnoea and easy fatigability. Patient was on tab. atenolol 25 mg OD, tab. aspirin 75 mg OD, tab. clopidogrel 75 mg OD, tab. pentoxyfilline 400 mg TID for the past 4 months. Investigation showed serum creatinine levels of 1.5 mg/dl, blood sugar 212 mg/dl, Bleeding Time and Clotting Time 4 and 6.5 minutes, respectively. Electrocardiogram showed hypertrophied left ventricle and T inversions. Echocardiogram [] revealed severe aortic stenosis with a mean gradient of 112 mm Hg with left ventricular hypertrophy.
Nerve blocks were performed with similar approaches as in case 1. Femoral nerve block was performed with mixture of 10 ml of 0.5% bupivacaine, 4 ml of isotonic saline 0.9% and 6 ml of 2% lignocaine (total volume 20 ml). Sciatic block was performed with 25 ml of 0.5% bupivacaine. Adequate block was achieved in 30 minutes. Surgery was completed uneventfully. Complete sensory and motor recovery was seen after 9 hours. An ultrasound-guided evaluation was carried out in the postoperative period (at 2nd and 10th hours) to rule out haematoma at the sites of injections.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [73, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Male'}",48.85357,46.41089,51.29625,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 73 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.5/0.9)**-1.2 * 0.9938**73 * 1.0 = 48.85357.
Hence, the GFR value is 48.85357 ml/min/1.73 m²."
292,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5137935-1,Extracted,"A 47-year-old Hispanic male presented to our emergency department with severe neck pain. He has had intermittent episodes of neck pain with radiation down his spine and lower extremities for the past year. It was described as a sharp and sometimes cramping, 8–10/10 in intensity, intermittent and was triggered by activity like lifting heavy objects. Two weeks prior to admission he was evaluated at a local clinic for the same complaints, treated with ibuprofen and referred to our rheumatology clinic where a workup was in progress.
His pain became more intense prompting him to seek medical attention and was admitted to our hospital for evaluation. He noted that he had been more fatigued lately with generalized malaise. He had difficulty climbing stairs and moving from a sitting to a standing position but was able to eat with a fork/spoon and comb his hair without any difficulty. He reported that his fingers turned blue on exposure to cold weather. He occasionally had joint pains with swelling and redness of multiple joints, associated with morning stiffness lasting at least 30 min. He also reported noticing frothy urine for the past year.
His past medical history was significant for hypothyroidism and hypertension. His medications consisted of lisinopril, aspirin and levothyroxine. He had no allergies. He denied any family history of thyroid, autoimmune or rheumatological diseases. He was a landscaper by profession. He denied smoking cigarettes, alcohol use or illicit drug use.
On examination, he was a young Hispanic male in some distress from the neck pain. He had unremarkable vital signs with a BMI of 25. His physical examination was normal. X-rays of his chest and spine were normal. His blood work revealed anemia with hemoglobin of 11 g/dl, marked hypoalbuminemia of 1.7 g/dl and a total protein of 3.6 mg/dl. He had a blood urea nitrogen of 33 mg/dl and serum creatinine of 1.0 mg/dl. His triglycerides were elevated at 265 mg/dl, cholesterol of 209 mg/dl and a calculated LDL of 132 mg/dl. His previous blood work done a few days ago at our rheumatology clinic showed an elevated erythrocyte sedimentation rate of 53 mm/h, TSH 10.6 and free T4 1.27 ng/ml. A urinalysis showed 1+ blood with 9 RBC, hyaline and granular casts but no RBC casts, protein of greater than 600 mg/dl with a urine protein-creatinine ratio of 4 grams/gram of creatinine. HIV, hepatitis B and C serologies were negative. Antinuclear antibody was positive with a titer of 1:640 and a peripheral pattern.
A nephrologist and a rheumatologist were consulted. Given normal renal function, microscopic hematuria and massive proteinuria, membranous nephropathy secondary to SLE was suspected. Further workup revealed a low C3 of 76 mg/dl, a normal C4 of 36 mg/dl and the anti-dsDNA titer was positive at 29 IU/ml. Renal biopsy was done and it revealed immune-complex-mediated diffuse segmental proliferative and membranous nephritis with features of focal cellular and fibrocellular crescents (8–10%). The segmental active glomerular lesions were in approximately 79–83% of sampled glomeruli, which were characterized by segmental endocapillary hypercellularity, hyaline ‘pseudothrombi’ (intraluminal immune aggregates), duplication of glomerular basement membrane (GBM) and, cellular and fibrocellular crescent. There was no significant tubulointerstitial chronic injury. The biopsy was diagnostic for lupus nephritis class IV-S (A/C) and V by ISN/RPS 2004 classification (). He was started on prednisone, hydroxychloroquine and mycophenolate mofetil. Four months after initiating therapy he started to show improvement in his proteinuria. He continues to have a normal renal function ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [47, 'years'], 'creatinine': [1.0, 'mg/dL'], 'sex': 'Male'}",93.41831,88.74739,98.08923,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 47 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.0 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.0/0.9)**-1.2 * 0.9938**47 * 1.0 = 93.41831.
Hence, the GFR value is 93.41831 ml/min/1.73 m²."
293,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6323659-1,Extracted,"On 16 December 2011, a 40-year-old white woman was hospitalized with dyspnea and a small-volume hemoptysis that had started 2 weeks before. She reported asthenia, but no weight loss, cigarette smoking (20 pack-years) that was not stopped afterwards, no exposure to toxic chemicals. Her medical history included pre-eclampsia during her two pregnancies, but no previous pulmonary disease or family history of renal/cardiac/pulmonary diseases. No other relevant finding was recorded.
Clinical examination upon admission highlighted apyrexia, hypertension (184/105 mmHg), pulse rate of 96 beats/minute, and skin pallor. A chest X-ray showed bilateral infiltrates, and the thoracic CT scan indicated diffuse and bilateral ground-glass opacification. The laboratory work-up showed normocytic normochromic anemia (hemoglobin level of 7 g/dL), but normal platelet and leucocyte counts. The creatinine level of 614 μmol/L (50 μmol/L in June 2011) indicated acute renal failure. Due to respiratory failure and renal impairment, the patients received three daily boluses of methylprednisolone (500 mg) followed by 1 mg/kg/day of prednisone.
A bronchoscopy performed on day 4 after hospitalization revealed the presence of hematic traces with a Golde score of 197 (bacterial cultures were negative). Serologic tests for auto-antibodies (antinuclear antibodies, ANCA, and anti-GBM antibodies) were negative, and the hemolytic complement fractions within the normal values (C3 = 1.22 g/L and C4 = 0.28 g/L). The ELISA test for anti-GBM antibodies using purified collagen IV alpha3 chain was negative. The renal biopsy showed fibrinoid necrosis in 10 glomeruli (among the 29 assessed; 34.5%), glomerulosclerosis in 30% of glomeruli, and cellular glomerular crescents in 28%. Immunofluorescence analysis revealed linear deposition of IgG, compatible with GS.
The patient underwent daily PLasmatic EXchanges (PLEX) for 11 days and started oral immunosuppressive therapy (100 mg of cyclophosphamide per day) on day 13 of the prednisone treatment. Due to severe renal failure and anuria, hemodialysis (3 times per week) was started on December 20, 2011. Hemoptysis stopped rapidly, but diuresis was not improved. At day 37 of hospitalization, due to neutropenia (<1G/L), the cyclophosphamide treatment was reduced to 75 mg per day, and then discontinued after 3 months. The patient remained on dialysis. As the serologic tests were all negative in 2011, the anti-GBM antibodies could not be monitored, but the patient did not show any other GS symptom in the following years.
In 2014, when the patient was still taking 5 mg of prednisone per day, a new episode of hemoptysis occurred confirmed by bronchoscopy. This was associated with acute pneumonia of the left lung lower lobe, with favorable outcome after treatment with prednisone (50 mg per day for 1 week) and fluoroquinolone-based antibiotic therapy.
In March 2015, the patient received a living donor (her mother) kidney transplant. In the years from the GS episode to the kidney transplant, all serologic tests for auto-antibodies were negative. Conversely, panel-reactive antibodies against class I and class II antigens were detected, but not against the donor’s human leukocyte antigen (HLA) (identical HLA profiles for donor and patient). Anti-Epstein Barr virus and cytomegalovirus IgGs were detected in serum samples from donor and recipient. The patient was induced with anti-thymocyte globulin (rabbit) and received standard immunosuppressive therapy with mycophenolate mofetil (MMF), tacrolimus (residual serum tacrolimus between 6 and 8 ng/mL), and prednisone. After the graft, the creatinine level was stabilized between 110 and 130 μmol/L. She developed new onset diabetes after transplantation that was treated with metformin and repaglinide.
In November 2016, microscopic hematuria without any proteinuria or renal dysfunction (creatinine level = 104 μmol/L) was detected. In February 2017, the patient was hospitalized because of hemoptysis and anuric acute renal failure (creatinine level = 1696 μmol/L). Like in 2011, blood pressure was increased (220/113 mmHg). The laboratory work-up showed normocytic normochromic anemia (hemoglobin level of 10.4 g/dL), platelet count of 100G/L, and normal leucocyte levels. At this time, the patient was taking tacrolimus (5 mg per day; residual tacrolimus level = 4.2 ng/mL), MMF (500 mg twice per day), and prednisone (5 mg per day). The serologic tests for auto-antibodies (antinuclear antibodies, ANCA, and anti-GBM antibodies) were negative, and the hemolytic complement factors within normal levels (CH50 = 79 U/mL, C3 = 1.28 g/L and C4 = 0.35 g/L). Renal biopsy of the transplanted kidney (25 glomeruli) confirmed the GS relapse with glomerulosclerosis in 36% of the analyzed glomeruli, cellular glomerular crescents in 56%, and linear IgG deposition on the GBM (Fig. ).
The patient underwent daily PLEX for 14 days, and received prednisone (500 mg/day for the first 3 days followed by 1 mg/kg/day). At the end of the 14th PLEX, a bronchoscopy indicated active hemoptysis with the presence of 99.5% sideroblasts and a Golde score of 200. Due to the absence of effect, PLEX was stopped and intravenous infusion of cyclophosphamide (500 mg/m2 every 21 days) was introduced combined with prednisone (5 mg per day) and tacrolimus (2 mg twice per day).
After five infusions of cyclophosphamide the patient has now recovered and the anemia is under control with EPO supplementation. Conversely, the grafted kidney does not work, and the patient needs hemodialysis 3 times per week. Tacrolimus has been stopped.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [40, 'years'], 'creatinine': [1696.0, 'µmol/L'], 'sex': 'Female'}",2.10267,1.99754,2.2078,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 40 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1696.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 1696.0 µmol. To convert 1696.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 1696.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.0017 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.0017 mol Serum Creatinine * 113.12 g/mol = 0.1923 g Serum Creatinine. To convert 0.1923 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.1923 g Serum Creatinine * 1000.0 mg/g = 192.3 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 192.3 mg Serum Creatinine/10.0 dL = 19.23 mg Serum Creatinine/dL. The concentration value of 1696.0 µmol Serum Creatinine/L converts to 19.23 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (19.23/0.7)**-1.2 * 0.9938**40 * 1.012 = 2.10267.
Hence, the GFR value is 2.10267 ml/min/1.73 m²."
294,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4924496-3,Extracted,"A 30-year-old female, historically normotensive, nondiabetic presented to us with 2 years history of pedal edema and periorbital swelling. On evaluation in 2011, her urine examination revealed Alb - 3+, pus cells - 18–20. Twenty-four hours urinary protein had been 1.8 g/day. Kidney function tests revealed creatinine of 1.3 mg/dl. The right kidney was 8.8 × 2.9 in size and left kidney was 7.8 cm × 3.3 cm in size with normal hepatobillary and pelvic system. Her anti-nuclear antibody titer (an ANA was 5.84 IU/ml, positive >1.2 IU/ml). The patient had been reluctant for renal biopsy. She had been treated with oral steroids and angiotensin receptor blocking agents. She presented to our department on November 2013. A full evaluation was sought. Her urine examination revealed Alb 2+, RBC 1–2, pus cells 4–5. Twenty-four hours urinary protein estimation was 1.38 g/day. Serum creatinine was 1.85 mg/dl. ANA, anti-dsDNA had been negative. Patient was subjected to renal biopsy. The examination of the renal tissue revealed up to seven glomeruli, one was globally sclerosed. Rest of the glomeruli displayed variably enlarged capillary tufts with patchy, segmental, and mild mesangial matrix expansion. Extracapillary cells (chiefly podocytes) were enlarged and displayed a foamy/finely vacuolated cytoplasm. No mesangial or endocapillary proliferation was noted and the peripheral glomerular capillary loops did not show significant thickening. There was no evidence of tuft necrosis/crescent formation or segmental sclerosis in the sampled glomeruli [].
Foci of tubular atrophy and interstitial fibrosis were seen involving approximately 15–20% of the sampled cortical parenchyma. The atrophic tubules contained inspissated hyaline casts. An associated, mild to moderate chronic interstitial inflammatory infiltrate was seen. The nonatrophic tubules showed patchy loss of brush borders with epithelial attenuation. The arteries sampled showed medial thickening and mild fibrointimal hyperplasia with elastic reduplication.
On differential immunofluorescence (DIF), sections included up to nine glomeruli exhibiting the following immunostaining features-IgA negative, IgG - 3+, IgM - Trace, C3 - negative, C1q - 3+/4+, kappa light chains - 1+/2+, lambda light chains - 2+. The entire staining pattern above was predominantly mesangial. The glomeruli exhibited nonproliferative morphology with variably enlarged capillary tufts exhibiting patchy, segmental, mild mesangial matrix expansion, and prominent enlarged extracapillary cells (chiefly podocytes) which display a foamy/finely vacuolated cytoplasm.
Further special stains were performed on this biopsy. Periodic acid–schiff (PAS) stained, frozen-sections of saline preserved tissue revealed intracytoplasmic PAS-positive granules within the podocytes/parietal epithelial cells. On examination of unstained frozen-sections under polarized light, these granules showed a Maltese cross pattern. With these DIF findings of non specific mesangial entrapment of complement and immunoglobulin, a possibility of renal involvement in a metabolic disorder viz., FD was suggested.
The pedigree analysis revealed that the patient had three brothers and one sister. Clinical examination showed angiokeratoma and corneal haziness in father and one of the brothers. Enzyme levels in all members had been sent.
The clinical characteristics of the studied population is shown in .","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [30, 'years'], 'creatinine': [1.85, 'mg/dL'], 'sex': 'Female'}",37.14926,35.2918,39.00672,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 30 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.85 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.85/0.7)**-1.2 * 0.9938**30 * 1.012 = 37.14926.
Hence, the GFR value is 37.14926 ml/min/1.73 m²."
295,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7872500-1,Extracted,"A 61-year-old previously healthy female was transferred from an outside hospital for a second opinion for a liver transplant. She first noticed fatigue, weakness, and abdominal swelling three months prior to her admission at the outside hospital. CT of the abdomen with contrast showed cirrhosis and multiple masses with arterial enhancement in her liver. She underwent a liver biopsy. Pathology was reported as a low-grade vascular tumor. She presented to a larger academic center where she underwent an exploratory laparotomy with open liver biopsy to further investigate the liver lesions. There was no visual evidence of omental spread. The pathology was reviewed by multiple tertiary centers specializing in hepatic malignancies and was reported as a low-grade vascular lesion, which was likely small vessel neoplasm. After denial for LT secondary to an unknown low-grade vascular tumor, she presented to our medical center. MRI of the liver showed multiple enhancing liver masses (Figure ). Oncology was consulted and she was diagnosed with benign liver vascular tumors with an overall favorable prognosis.
She was listed for liver transplant with a model for end-stage liver disease-sodium (MELD-Na) score of 25. The patient had normal renal function prior to her admission with a creatinine level of 0.79 mg/dL, which increased to 3.3 mg/dL after her admission which was thought to be secondary to hepatorenal syndrome (HRS) type I. Her creatinine level did not improve despite medical management and hemodialysis (HD) was initiated prior to transfer to the University Medical Center. She continued on HD for approximately 10 weeks prior to her LT and was listed for combined liver and kidney transplant.
She underwent an orthotopic liver transplant 10 weeks after presenting to the UNMC. Microscopic evaluation of the tumor cells showed positive immunohistochemical staining for the ETS-related gene and was negative for human herpesvirus-8. A Ki-67 labeling index of the solid areas was approximately 30%. Overall, the amount of necrosis and the elevated mitotic rate was sufficient to classify the tumor as a Federation Nationale des Centres de Lutte le Cancer grade 3 of three angiosarcomas (Figure ).
She was scheduled for a living donor kidney transplant three days after her liver transplant, but it was postponed due to increased urine output on postoperative day four. Her creatinine level was 2.22 mg/dL and blood urea nitrogen was 73 mg/dL at the time of discharge.
She was undergoing routine image testing every three months after transplantation. Unfortunately, she was found to have a recurrence in the form of innumerable liver and bone lesions at 16 months post-transplantation. Despite starting her on chemotherapy with taxol, the patient passed away 31 months post-LT.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [61, 'years'], 'creatinine': [2.22, 'mg/dL'], 'sex': 'Female'}",24.61509,23.38434,25.84584,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 61 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.22 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.22/0.7)**-1.2 * 0.9938**61 * 1.012 = 24.61509.
Hence, the GFR value is 24.61509 ml/min/1.73 m²."
296,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5996786-1,Extracted,"A 63-year-old man was admitted to the hospital with generalized weakness, fever and weight loss for 6 months. Blood tests showed a creatinine level of 5.29mg/dl, an urea of 169mg/dl, a C-reactive protein of 297.7mg/L and urinalysis with leukocyturia.
Plain abdominal radiograph demonstrated right renal staghorn calculi (). Computed tomography (CT) images showed obstructive stone, dilated calyces and renal parenchymal atrophy with exuberant fibrofatty proliferation ( and ). Final diagnosis was xanthogranulomatous pyelonephritis with extensive lipomatosis.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [63, 'years'], 'creatinine': [5.29, 'mg/dL']}",11.45695,10.8841,12.0298,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 63 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 5.29 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (5.29/0.9)**-1.2 * 0.9938**63 * 1.0 = 11.45695.
Hence, the GFR value is 11.45695 ml/min/1.73 m²."
297,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5822868-1,Extracted,"A 70-year-old male presented with urgency, urinary incontinence, and nocturia for five days. The patient was known to have benign prostatic hyperplasia (on Tamsulosin) and had a long- standing history of anaemia. No palpable abdominal mass was detected during the physical examination. His laboratory evaluation revealed anaemia (haemoglobin: 8.5 mg/dl, MCV: 80 fl, MCH 24.8 pg, MCHC 30.9 gm/dl, WBC 14 × 103/microliter, creatinine 90 micromole/dl, and platelet 156 ng/ml).
Ultrasound of the renal system showed a right renal mass. An abdominal computed tomography (CT) revealed an ill-defined infiltrative 4 cm renal mass in the mid to lower pole region of the right kidney, involving the renal parenchyma, renal hilum, and the renal pelvis (). Similar findings were also noted on a magnetic resonance imaging (MRI) which also revealed a tumour thrombus extending along the entire course of the right renal vein and projecting into the right side of the lumen of the inferior vena cava ().
A right laparoscopic radical nephroureterectomy with thrombectomy of the inferior vena cava was performed. The right kidney was enlarged, solid, and adherent to perirenal adipose tissue. The middle and lower part of right ureter were dilated. The thrombus was gently milked from the inferior vena cava and removed separately.
Gross examination of the nephrectomy specimen showed a 5.5 × 4.5 × 4.5 cm greyish tan friable mass arising in the renal pelvis, projecting into the proximal ureter, and extensively infiltrating the adjacent renal parenchyma ().
Histological examination revealed a high grade urothelial carcinoma with sarcomatoid differentiation. The tumour was arising in the renal pelvis with infiltration of the renal parenchyma and extension into renal sinus and the renal vein. Carcinoma in situ involving the adjacent urothelium was noted ().
The sarcomatoid elements were composed of spindle shaped cells with marked nuclear pleomorphism and high mitotic activity (Figures and ).
Extensive areas of tumour necrosis were also seen. The resection margin of the ureter was free of tumour. The tumour thrombus from the inferior vena cava was composed of high grade urothelial carcinoma along with the sarcomatoid component ().
On immunohistochemistry the carcinoma component was positive for CK7, CK20, p63, p53, and GATA-3, while the sarcomatous component stained strongly and diffusely positive for vimentin. Both components did not show any staining for desmin or smooth muscle actin ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [70, 'years'], 'sex': 'Male', 'creatinine': [90.0, 'µmol/L']}",79.25223,75.28962,83.21484,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 70 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 90.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 90.0 µmol. To convert 90.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 90.0 µmol Serum Creatinine * 1e-06 mol/µmol = 9e-05 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 9e-05 mol Serum Creatinine * 113.12 g/mol = 0.01018 g Serum Creatinine. To convert 0.01018 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01018 g Serum Creatinine * 1000.0 mg/g = 10.18 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 10.18 mg Serum Creatinine/10.0 dL = 1.018 mg Serum Creatinine/dL. The concentration value of 90.0 µmol Serum Creatinine/L converts to 1.018 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.018/0.9)**-1.2 * 0.9938**70 * 1.0 = 79.25223.
Hence, the GFR value is 79.25223 ml/min/1.73 m²."
298,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3109786-1,Extracted,"A seven-year old girl presented to emergency room with 5 months history of intermittent fever, joint pain, severe anemia, and distended abdomen. She was treated outside by alternative medicine (‘naturopathy’) based on severe diet restrictions consisting of few pieces of bread and vegetables for several months. She was also misdiagnosed, hence treated wrongly as a case of congestive heart failure. Bilateral renal enlargement was mistaken for congested hepatosplenomegaly. No proper evaluation for abdominal distention was made at this time.
At admission to our hospital, physical examination revealed an emaciated child with severe anemia and bilateral palpable kidneys. Clinically they were symmetrical, non-cystic, and non-tender. Routine laboratory evaluation showed a blood urea nitrogen level of 16 mg/dl, serum creatinine 0.9 mg/dl, and uric acid was 7.8 mg/dl. Creatinine clearance was 52 ml per minute. Her hemoglobin was 3.2 g/dl, total leukocyte count 7900/mm3, and platelet count 2.53 × 104/mm3. Peripheral smear showed moderate anisocytosis with macrocytes, polychromatic cells, normocytes, and few microcytic normochromic cells suggesting hemolytic anemia. Reticulocyte count was 4.5 percent. Serum calcium was 10.2 mg/dl, phosphorous 3.1 mg/dl, and uric acid 9.8 mg/dl. Liver function tests were normal. The erythrocyte sedimentation rate was 38 mm/h and C-reactive protein was 1.4 mg/dl. Tuberculin skin test and serological assays for EB virus and virus were negative. Serum compliment and quantitative estimation of immuno-globulins were non-contributory. Urinalysis revealed trace protein but no active sediments. Repeated urine cytology revealed no malignant cells. Ultrasound of abdomen revealed marked bilateral renal enlargement with homogenous cortical echogenicity. The kidneys measured 17.9 × 6.8 × 7.1 and 16.6 × 6.8 × 7.1 cm. There was mild hepatomegaly without evidence of any focal lesion. Intrahepatic vascular and biliary radicles were normal. A plain computed tomography (CT) scan of abdomen confirmed bilateral diffused renal enlargement with decreased attenuation suggestive of diffuse infiltrative disease. There was mild hepatomegaly but no evidence of hydronephrosis or intra-abdominal lymphadenopathy []. Chest X-ray showed normal lung parenchyma and a normal size heart without any mediastinal lymphadenopathy, which was confirmed by CT scan.
Percutaneous renal biopsy showed extensive infiltration of interstitium by monomorphic neoplastic cells, some of which were round with round nuclei and scanty cytoplasm. Tumor cells were arranged in a tubular pattern at places. Tumor infiltration was found confined to interstitium without involving glomeruli or tubule [Figure and ]. CD45 showed surface positivity in all cells []. Bone marrow biopsy was unremarkable, as were the head and chest CT scans. In view of angulation of all nucleoli, mucosa-associated lymphoid tissue (maltoma), a form of PRL was entertained.
She was put on combination chemotherapy consisting cyclophosphamide, intravenous vincristine 2 mg/M2and shifted to a medical oncology unit where she was started on combination chemotherapy with CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisolone). She developed serious leucopenia (total leukocyte count of 900/cmm) on sixth postchemotherapy day, needing temporary suspension of therapy and institution of broad spectrum antibiotics.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [7, 'years'], 'creatinine': [0.9, 'mg/dL'], 'sex': 'Female'}",101.76266,96.67453,106.85079,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 7 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.9 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.9/0.7)**-1.2 * 0.9938**7 * 1.012 = 101.76266.
Hence, the GFR value is 101.76266 ml/min/1.73 m²."
299,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4635960-2,Extracted,"A 53-year-old male with severe pneumonia was transferred from another hospital. He had a four-day history of flu with cough and fever (39.4°C), having recently complained of dyspnea and progressive edema of the lower extremities. Physical examination revealed hypotension (blood pressure, 80/50 mmHg) and tachycardia (140 bpm). Auscultation of the thorax showed decreased breath sounds in the right lung and crackles in the left lung base. At admission, a chest X-ray revealed right pleural effusion and a CT scan showed right pleural effusion with collapse of the right lower and middle lobes associated with extensive effusion. Laboratory tests at admission revealed a white blood cell count of 30.2 × 109 cells/L (92% neutrophils and 3.6% lymphocytes), a platelet count of 956 × 109/L, a serum C-reactive protein level of 15.84 mg/dL, a serum creatinine concentration of 1.32 mg/dL, a serum sodium level of 135 mEq/L, and a serum potassium level of 5.6 mEq/L.
A chest X-ray performed on the second day of hospitalization showed progression of the disease process: an opacity involving nearly all of the right lung and further enlargement of cardiopericardial silhouette ( A). Echocardiography showed severe pericardial effusion affecting the entire cardiac silhouette. Pericardiocentesis yielded 640 mL of exudative fluid, the culture of which was negative. Pericardial and thoracic drainage was performed; purulent fluid was obtained in a sterile manner from the chest drain. Examination of the pleural fluid showed a pH of 6.95, a glucose level of 5 mg/dL, proteins at 47.4 g/L, and an LDH content of 5,347 U/L. A second chest X-ray showed consolidation in the right lung, minimal pleural fluid, and a normal cardiac silhouette ( B). A urinary pneumococcal antigen test was negative. Pleural fluid culture was positive for S. pneumoniae that was susceptible to erythromycin, levofloxacin, and penicillin. The isolate was S. pneumoniae serotype 1.
The patient received empirical antibiotic treatment with the piperacillin-tazobactam combination (4.5 g/8 h) and levofloxacin (500 mg twice a day for 5 days). The latter was continued because the pneumococcus was susceptible to it. The patient was discharged on the twelfth day, after withdrawal of the pericardial and pleural drains.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [53, 'years'], 'creatinine': [1.32, 'mg/dL'], 'sex': 'Male'}",64.49666,61.27183,67.72149,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 53 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.32 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.32/0.9)**-1.2 * 0.9938**53 * 1.0 = 64.49666.
Hence, the GFR value is 64.49666 ml/min/1.73 m²."
300,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6964961-2,Extracted,"A 63-year-old African American female with a history of chronic venous stasis ulcers, an unknown history of renal disease presented to the ED with complaints of epigastric pain, nausea, and vomiting for 10 days. On presentation, vitals were within normal limits and physical examination was unremarkable except for chronic ulcers on bilateral lower extremities. Her initial lab results were significant for a potassium of 2.0 mMol/L, bicarbonate of 17 mMol/L, AG of 16 mMol/L, blood urea nitrogen (BUN) of 85 mg/dL, and creatinine of 3.9 mg/dL. The rest of the labs are outlined in Table . Electrocardiogram (EKG) showed normal sinus rhythm (Figure ). The patient was given 120 mEq of KCL, started on IVF, and admitted for the management of hypokalemia, renal impairment, and abdominal pain workup. On further questioning, she reported taking ibuprofen 800 mg on an average of 10-12 tablets/day for the past 10 months to help with the pain from chronic venous stasis ulcers. She denied taking any other medications, having diarrhea, and episodes of hypokalemia in the past.
Potassium on day two of admission remained low at 2.3 mMol/L and even after 180 mEq of KCL was repleted, it continued to be low at 2.7 mMol/L on day four. Meanwhile, the urine potassium/creatinine ratio was obtained on day four, and it was 20.6 mEq/gm, indicating urine loss of potassium. The patient remained normotensive, and the serum aldosterone was 2 ng/dL, ruling out hyperaldosteronism. The urine anion gap was found to be positive 12.7 and urine pH was 6 pointing toward the distal renal tubular acidosis (dRTA).
After ruling out the other possible etiologies, a diagnosis of ibuprofen-induced hypokalemia and distal RTA was reached. She was aggressively treated with fluid and electrolyte replacement, as shown in Figure , along with the cessation of ibuprofen. The patient was discharged on day 11 after persistent normal potassium levels were observed and serum creatinine improved to 2.2 mMol/L with a plan to follow up as an outpatient. During hospitalization, she received a total of 640 mEq of KCL replacement and her potassium was 3.8 mMol/L on the day of discharge.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [3.9, 'mg/dL'], 'sex': 'Female'}",12.36362,11.74544,12.9818,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 63 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 3.9 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (3.9/0.7)**-1.2 * 0.9938**63 * 1.012 = 12.36362.
Hence, the GFR value is 12.36362 ml/min/1.73 m²."
301,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7149248-1,Extracted,"A 46-year-old Japanese man without a remarkable medical history visited our hospital with chief complaints of fever, fatigue, generalized edema, and abdominal distention. His fever started two weeks prior to admission. Abdominal distention and edema gradually worsened, and he gained 7 kg of weight within two weeks, despite low food intake owing to loss of appetite. He denied previous episodes of infectious diseases. At initial presentation, he appeared exhausted. His vital signs were as follows: body temperature, 37.8 °C; blood pressure, 160/93 mmHg; heart rate, 109 beats/min; respiratory rate, 22 breathes/min; and oxygen saturation, 90% with room air. On physical examination, generalized pitting edema was observed. His heart sounds were normal, but his lung sounds were weak at the lung base on both sides. Jaundice was not observed, but a distended abdomen and hepatomegaly were observed. Blood test results on the day of admission revealed an elevated white blood cell (WBC) count (14,600/μL), mild anemia (hemoglobin level, 11.1 g/dL), thrombocytopenia (platelet count, 11.1 × 104/μL), renal impairment (blood urea nitrogen level, 60.7 mg/dL and serum creatinine level, 2.94 mg/dL), an elevated C-reactive protein (CRP) level (14.25 mg/dL), an elevated ALP level (768 U/L), polyclonal hypergammaglobulinemia (immunoglobulin G [IgG], 2461 mg/dL), and an elevated IgG4 level (235 mg/dL). Immunological screening test results for autoantibodies were negative, except for positive antinuclear antibody (× 40) and anti-SS-A antibody. Polymerase chain reaction for HHV-8 DNA in a serum sample was negative (Table ). Computed tomography (CT) performed on the day of admission revealed massive pleural effusions and ascites, generalized mild lymphadenopathy (< 1.5 cm in diameter), and hepatosplenomegaly (Fig. ). Echocardiography performed on day 2 revealed normal wall motions without any sign of valvular disease, but a collapsed inferior vena cava was observed (maximum diameter < 5 mm). 18F–fluorodeoxyglucose positron emission tomography (FDG-PET) revealed no apparent FDG uptake, except for slight uptake in the para-aortic lymph nodes (Fig. ). Considering the positive anti-SS-A antibody finding, lip biopsy was performed on day 6, but the pathological findings did not meet the criteria for Sjögren syndrome (SjS). On ophthalmological examination, keratoconjunctivitis was not observed; however, bilateral optic edema was remarkable (Fig. ). Serum IL-6 and plasma VEGF levels were assessed in a blood sample obtained on day 9, and both were elevated (25.2 pg/mL and 224 pg/mL, respectively). Abdominal paracentesis was performed on the same day, and the levels of IL-6 and vascular endothelial growth factor (VEGF) in ascites were remarkably high (3310 pg/mL and 335 pg/mL, respectively). Bone marrow examination was performed on day 9. Bone marrow aspiration was dry tap, and bone marrow biopsy revealed a mild increase in megakaryocytes and mild reticulin myelofibrosis on silver impregnation staining (Fig. ). Biopsy of a cervical lymph node was performed on day 10, and the pathological findings were compatible with a mixed-type MCD histology (Fig. ). We suspected TAFRO syndrome and methylprednisolone (mPSL) pulse therapy (500 mg/day for three consecutive days) was initiated on day 10 after lymph node biopsy, followed by intravenous PSL (40 mg/day) and oral CsA administration. The disease severity of TAFRO syndrome one day prior to treatment initiation was very severe (grade 5) []. After the initiation of immunosuppressive treatment, the patient became afebrile and the CRP level returned to the normal range within two weeks. However, the patient’s platelet count and serum creatinine level as well as his overall condition did not improve, even after the initiation of immunosuppressive treatment (Fig. ). A central venous catheter was inserted and total parenteral nutrition was started as he could not eat owing to loss of appetite and refusal of tubal feeding. Diuretics, including furosemide, potassium canrenoate, trichlormethiazide, and tolvaptan were administered during hospitalization; however, the amount of ascites did not decrease (Fig. ). Urinalysis performed on day 25 revealed mild proteinuria (0.34 g/day) with a fractional excretion of sodium of 5.1% and a fractional excretion of urea nitrogen (FEUN) of 20.7%. Because urinalysis was performed under diuretics use, considering FEUN level and intravascular hypovolemia on echography, intravenous fluid replacement was performed to correct the pre-renal factor responsible for renal impairment. However, the patient’s volume depletion and blood pressure did not respond well to intravenous fluid replacement. Abdominal paracentesis was again performed on day 40, and it revealed persistently high levels of IL-6 and VEGF (4320 pg/mL and 421 pg/mL, respectively). Although urine volume was initially preserved with diuretic administration, the patient became oliguric from day 47 and anuric from day 49. He was hemodynamically unstable on day 50 (body temperature, 37.5 °C; blood pressure, 84/52 mmHg; heart rate, 109 beats/min; respiratory rate, 24 breaths/min; oxygen saturation, 95% with room air). As the patient was undergoing immunosuppressive therapy and his CRP levels increased by 10.08 mg/dL on the same day, systemic examination was performed to rule out the possibility of infectious disease. Analysis of ascites was performed on the same day, revealing purulent ascites, and Escherichia coli was isolated. E. coli was also isolated from blood cultures. CT of the chest showed a mass in the right lung (Fig. ) in addition to scattered appearance of high intensity regions in the myocardium, which were newly observed (Fig. ). Blood tests performed on day 50 revealed elevated β-d-glucan levels (23.0 pg/mL) and positive cytomegalovirus (CMV) antigenemia (41 cells/5 × 104 WBCs on the C7-HRP test). Aspergillus, Candida mannan, and Cryptococcus neoformans antigens were negative. We suspected bacterial peritonitis and fungal pneumonia. Intravenous meropenem, vancomycin, and caspofungin were initiated on the same day. Continuous renal replacement therapy (CRRT) using a polymethyl-methacrylate membrane was also initiated on the same day because anuria did not improve and the patient was hemodynamically unstable. Conditions of CRRT were as follows: mode, continuous hemodiafiltration; dialysis membrane, CH-1.8 W (Toray Medical Co., Ltd., Tokyo Japan); and anticoagulant, nafamostat mesilate. The blood, dialysate, substitute, and filtration flow rates were 100 mL/min, 400 mL/h, 400 mL/h, and 800 mL/h, respectively.
However, approximately 10 h after CRRT initiation, cardiac arrest (ventricular fibrillation followed by pulseless electrical activity) suddenly occurred. Return of spontaneous circulation (ROSC) was achieved by cardiopulmonary resuscitation with epinephrine injections. STEMI was suspected from electrocardiography findings obtained immediately after ROSC (Fig. ). Echocardiography performed immediately after ROSC revealed a generalized hypokinesis and akinesia of the anterior wall, septum, and apex without any apparent calcification of the cardiac wall. Blood tests performed after ROSC revealed a slightly elevated serum creatine kinase-MB level (80 U/L, normal range: < 25 U/L) and a remarkably elevated troponin I level (1.2904 ng/mL, normal range: < 0.0262 ng/mL), indicating the acute phase of MI. Emergent coronary angiography (CAG) was performed on the same day. On CAG, complete occlusion of the left anterior descending coronary artery was observed, and reperfusion was achieved through percutaneous old balloon angioplasty (Fig. ). An intra-aortic balloon pump was inserted to increase coronary blood flow and improve cardiogenic shock. However, even after successful coronary intervention, the patient was still hemodynamically unstable. Despite intensive care, the patient died on day 52.
Autopsy was performed after obtaining consent from the patient’s relatives. The histological findings of autopsy are shown in Fig. . In this case, multiple infections, including bacterial peritonitis (small abscesses were observed in the abdominal space, and gram-positive cocci and gram-negative rods were identified), systemic CMV infection (including the lungs, pancreas, and adrenal glands), and Trichosporon asahii infection in the lungs (T. asahii was isolated from sputum culture) were observed. Intravascular invasion of fungal hyphae was noted in the lungs. On histological evaluation of the heart, coagulation necrosis and neutrophil infiltration were observed, findings that were compatible with MI that occurred a few days before the autopsy. Considering that intravascular invasion of fungal hyphae was observed, embolization caused by fungal hyphae was a possible cause of MI in this case. Necrotic changes were observed in most internal organs. We considered multiple organ failure due to multiple severe infections and circulatory failure due to MI as the main causes of death in this patient. Although there was no stenotic lesion and vascular calcification was not apparent in the left anterior descending coronary artery, myocardial calcification was noted. Calcification in the skeletal muscle cells of the diaphragm and iliopsoas muscle without vascular calcification was also noted. The pathological findings of the kidney were compatible with thrombotic microangiopathy (TMA) and endothelial injury was noted, although fibrin thrombi were not observed in arterioles. IgA, IgG, and IgM were negative on immunofluorescence. Tubulointerstitial changes could not be evaluated because most of the tissue was necrotic due to changes after death and circulatory failure prior to death. In the bone marrow reevaluation, the number of megakaryocytes did not increase, and reticulin myelofibrosis was not remarkably changed. In the lymph node reevaluation, infiltration of plasma cells was decreased, and immunosuppressive therapy appeared partially effective, although the amount of ascites and IL-6 levels in ascites did not decrease in the present case. Fibrotic changes in the fat tissue of the anterior mediastinum were noted.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [46, 'years'], 'creatinine': [2.94, 'mg/dL']}",25.77011,24.4816,27.05862,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 46 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.94 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.94/0.9)**-1.2 * 0.9938**46 * 1.0 = 25.77011.
Hence, the GFR value is 25.77011 ml/min/1.73 m²."
302,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5487311-3,Extracted,"A 38-year-old Indonesian woman living in United States for ten years with ESRD due to IgA nephropathy on hemodialysis for 10 years received a DDKT in 2015 (6 antigen mismatch, PRA 0%). She received induction with alemtuzumab and solumedrol and was maintained on tacrolimus, mycophenolate mofetil, and prednisone. There were no surgical complications or episodes of acute rejection in the post-transplant period. Allograft function was excellent with serum Cr of 1.0 mg/dL. Pre-transplant work up was notable for positive TST with normal CXR. She was started on INH immediately after transplant and received nine months of therapy for LTBI. One month after completing INH therapy, she was admitted with persistent fevers, night sweats and acute kidney injury, serum Cr of 2 mg/dL. Fever work up showed adenovirus in the blood and urine. There was increased flurodeoxyglucose uptake in the kidney allograft on positron emission tomography scan. Biopsy of the kidney transplant showed necrotizing granulomatous interstitial nephritis. Differential diagnosis of the granulomatous interstitial nephritis included renal transplant TB and adenovirus infection. Renal pathology changes were not consistent with adenovirus infection. AFB smear and cultures were negative in the urine and renal biopsy specimens. Due to persistent fevers, worsening renal function and clinical suspicion for TB, she was started on RIPE and Moxifloxacin. Moxifloxacin was added as a fifth agent due to concern for INH resistance given she was treated with INH monotherapy for LTBI. Fevers, night sweats and AKI resolved on treatment without addition of cidofovir, which supported the diagnosis of renal transplant TB. Her IS was modified with discontinuation of MMF. She is currently maintained on tacrolimus and prednisone. She completed 6 mo of ATT and is cured of TB. Renal allograft function is stable with Cr of 1.3 mg/dL.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [38, 'years'], 'creatinine': [1.3, 'mg/dL']}",53.97793,51.27903,56.67683,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 38 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.3 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.3/0.7)**-1.2 * 0.9938**38 * 1.012 = 53.97793.
Hence, the GFR value is 53.97793 ml/min/1.73 m²."
303,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7869636-1,Extracted,"A 33-year-old married woman with two previous uneventful pregnancies was admitted from the emergency department of our hospital with bilateral lower limb edema for 7 days, breathlessness at rest, and oliguria since 4 days. She had no complaints of hematuria, hemoptysis, malar rash, arthralgia, oral ulcers, photosensitivity, or hair loss. Her serum creatinine done 3 years earlier was 1.15 mg/dl. Prior to admission at our hospital, she was detected to have a serum creatinine of 17 mg/dl and had received two sessions of hemodialysis and 500 mg of intravenous methylprednisolone. At the time of admission, she was afebrile and had tachycardia. Her blood pressure of 140/90 mmHg and oxygen saturation was 94% on room air. Physical examination revealed jugular venous distension and bilateral lower limb edema. Examinations of oral cavity and respiratory system were within normal limits; there were no visible rashes. Investigations showed hemoglobin of 7.2 g/dl, platelet count of 240,000/μl with no schistocytes. Urine examination showed 3+ proteinuria, 8–10 red cells, and 50–55 leucocytes. Serum lactate dehydrogenase was 585 IU/L; serum levels of complement C3 were marginally low (88 mg/dl, Normal = 90–180 mg/dl) while C4 levels were normal (22 mg/dl, Normal = 10–40 mg/dl). Ultrasonogram showed bilateral swollen kidneys with preserved corticomedullary differentiation and normal parenchymal echogenicity. She was dialyzed on two consecutive days for pulmonary edema. Renal biopsy showed arteriolar TMA in acute phase with acute tubular injury. Immunofluorescence staining for IgG, IgM, IgA, C3, C1q, κ and λ was negative.
Serum anti-factor H antibody level was 495 AU/L (Normal range: 0–100 AU/L) and plasma ADAMTS-13 activity was normal (60%). Plasma exchange (PEX) with 4.2 L of volume for volume replacement with fresh frozen plasma was started for TMA, secondary to dysregulation of complement alternative pathway. She received five daily PEX till platelets and LDH normalized, followed by nine PEX on alternate days, along with hemodialysis as required. Urine output gradually increased and after one month the patient became dialysis-independent. She was discharged with a serum creatinine of 3.3 mg/dl. Follow-up 45 days after the diagnosis showed serum creatinine of 2.4 mg/dl.
Multiplex ligation-dependent probe amplification (MLPA) for copy number variation (CNV) of genes involved in alternate complement pathway was carried out [SALSA MLPA P236-A3 probemix, MRC Holland] on DNA extracted from the peripheral blood. The MLPA results, when compared to a sample from a known healthy control run in parallel, showed an ~1.5X increase in relative signal intensity for one probe targeting the terminal region of the CFH gene (exon 23) and a ~50% reduction in signal for one probe targeting exon 6 of the CFHR1 gene []. These findings suggest a duplication and deletion in these regions, respectively, which in turn, indicate a gene conversion event between the CFH and CFHR1 genes. Clinical exome sequencing using the Illumina Trusight One platform did not detect any clinically relevant sequence variant in any of the complement pathway related genes (CFH, CFI, CD46/MCP, C3)or ADAMTS13. A functional assay for factor H as previously described by Sanchez Coral et al.[] was performed. It showed a 33% lysis of sheep erythrocytes as compared to 5% with control plasma from healthy blood donors. The healthy donor plasma also inhibited the lysis inducedin vitro by the patient's plasma in a dose-dependent manner [].","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [33, 'years'], 'creatinine': [17.0, 'mg/dL']}",2.54633,2.41901,2.67365,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 33 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 17.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (17.0/0.7)**-1.2 * 0.9938**33 * 1.012 = 2.54633.
Hence, the GFR value is 2.54633 ml/min/1.73 m²."
304,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8170122-1,Extracted,"An 81-year-old Caucasian man with a history of hypertension, type 2 diabetes mellitus, cardiovascular disease, hyperlipidemia, and benign prostate hypertrophy presented with a fall at home without witnessed syncope or seizures. His medications consisted of clopidogrel, enalapril, finasteride, gabapentin, glimepiride, sitagliptin, metformin, and tamsulosin.
At presentation at the Mount Sinai Medical Center, Brooklyn, New York, in September 2020, the patient complained of weakness, fatigue, and frequent urinations. His body temperature was 39.0 °C, and blood pressure was 150/95 mm Hg, with a pulse rate of 98 beats/minute and oxygen saturation rate of 98%. He was alert and oriented, with unremarkable lung and cardiovascular examination. Laboratory findings showed leukocytes, 6.6 × 103/µL; hemoglobin, 12.2 g/dL; thrombocytes, 89 × 103/µL; glucose, 235 mg/dL; sodium, 134 mEq/L; potassium 4.6 mEq/L; bicarbonate, 16 mEq/L; calcium, 8.5 mEq/L; serum creatinine (Scr) 1.1 mg/dL; blood urea nitrogen (BUN), 29 mg/dL; creatine phosphokinase (CPK), 9,128 IU/L; prothrombin time, 13.4 s; partial thromboplastin time, 25.3 s. Urinalysis and urinary microscopy demonstrated glucose, erythrocytes, and trace protein and no casts. A chest X-ray showed clear lungs. COVID-19 infection was diagnosed based on a reverse transcriptase-polymerase chain reaction test that detected acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in a throat swab sample. Initial treatment was supportive, with nasal cannula oxygen, doxycycline, and thrombosis prophylaxis with apixaban.
On day 5 after admission, the condition of the patient worsened. He became more tachypneic, with oxygen saturation decreased to 87% on nasal cannula. There were no episodes of hemodynamic instability. He developed non-oliguric deterioration of kidney function, with Scr and BUN increased to a maximum level of 5.8 mg/dL and 124 mg/dL, respectively. Arterial blood gas on non-rebreather mask showed pH 7.25, Pa O2 78 mmHg, Pa CO2 31 mmHg, and HCO3 13 meq/L. Chest X-ray showed diffuse patchy bilateral infiltrates. The patient was transferred to the Intensive Care Unit (ICU), started BiPAP therapy, intravenous steroids, and was given convalescent plasma. Over the next 48 hours, his respiratory status started improving, with Scr decreasing to 1.2 mg/dL, and CPK to 280 IU/L (). He was changed to high-flow oxygen therapy (HFOT) () and given 5 days of remdesivir treatment.
In the following period, the patient showed gradual respiratory improvement and diuresis. At 20 days after admission, he was discharged from the ICU, and after 43 days, when his throat swab test for coronavirus became negative, he was discharged home. At the time of discharge, Scr level was 0.9 mg/dL.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [81, 'years'], 'creatinine': [0.9, 'mg/dL'], 'sex': 'Male'}",79.53259,75.55596,83.50922,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 81 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.9 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.9/0.7)**-0.302 * 0.9938**81 * 1.0 = 79.53259.
Hence, the GFR value is 79.53259 ml/min/1.73 m²."
305,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8606724-1,Extracted,"A 61-year-old male with a past medical history of diabetes mellitus, dyslipidemia, and hypertension presented to the emergency department (ED) with pain and swelling of the left scrotum for 48 h. The pain was constant, throbbing, and exacerbated by movement. It was localized to the posterior left hemi-scrotum with radiation to the right hemi-scrotum. The patient reported a 3-day history of subjective fever, chills, dysuria, urgency, frequency, and urinary retention. He denied any trauma to the scrotum and had no history of sexually transmitted infections.
On initial evaluation, his temperature was 98.7 F, blood pressure 156/60 mm Hg, heart rate 69 beats per minute, respiratory rate 18 breaths per minute, 98% oxygen saturation on room air. On physical examination, he was in no acute distress. Cardiac, respiratory, and abdominal examinations were unremarkable. Urogenital exam revealed swelling and erythema of the left hemi-scrotum and significant tenderness to palpation and swelling of the left epididymis. The penis was swollen and erythematous (). There was no crepitus, bullae, blisters, or skin discoloration. Prehn sign was negative. Cremasteric reflex was absent bilaterally. Blue dot sign was negative.
Initial serum labs showed a white blood cell (WBC) count of 29,600/μL with 91.2% neutrophils, hemoglobin 9.7 g/dL, glucose 244 mg/dL, blood urea nitrogen 39 mg/dL, creatinine 1.9 mg/dL, c-reactive protein (CRP) 27.2 mg/dL, and creatinine kinase 345 U/L. Urinalysis was cloudy, negative for leukocyte esterase and nitrites, with 4+ protein, 2+ glucose, 1.0 EU/dL urobilinogen, 3+ blood, negative for ketones, few red blood cells, and rare WBCs. HIV and RPR were negative. Blood and urine cultures were negative. Ultrasound of the scrotum and testicles revealed that the left epididymis was extremely complex and hyper vascular, possibly secondary to epididymitis. Testicular duplex showed a normal testicular duplex scan. FG severity index 7.
He was started on levofloxacin for suspected epididymitis. Urology was consulted and saw him 22 h after admission; he had developed a 3 cm necrotic lesion with fluctuance on the posterior aspect of the left hemi-scrotum. He was emergently taken for incision and drainage. The entire dartos fascia and the lower half of the scrotum were removed with a wide swathe of the perineal area, as shown in . Quarter inch Penrose drains were placed bilaterally extending from the bilateral inguinal area to the dependent area of the wound in the perineum. IV antibiotics were changed to piperacillin-tazobactam and linezolid. Two days later, general surgery performed a diverting colostomy at the level of the sigmoid colon. This was completed to allow for adequate healing of the affected area. Urology then performed another debridement as the remaining scrotal skin edges were necrotic. A vacuum dressing, set at 125 mm Hg, was utilized for 12 days to decrease pressure over the wound, to gently extract fluids from the wound, to help pull the edges of the wound together, and to improve overall healing.
Surgical tissue cultures were negative and gram stain showed rare gram-negative rods and rare gram-positive cocci. He was eventually switched to oral antibiotics (linezolid, levofloxacin, and metronidazole) and transferred to a subacute medical facility where he could undergo hyperbaric oxygen therapy. The patient has healed well with no complications and is scheduled for a colostomy reversal this month.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [61, 'years'], 'creatinine': [1.9, 'mg/dL']}",39.63817,37.65626,41.62008,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 61 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.9 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.9/0.9)**-1.2 * 0.9938**61 * 1.0 = 39.63817.
Hence, the GFR value is 39.63817 ml/min/1.73 m²."
306,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3978405-1,Extracted,"A 57-year-old Japanese man was admitted to our hospital with pleural effusion, massive ascites, and leg edema in March 2010. Physical examination revealed hyperpigmentation, hemangiomas, and gynecomastia. The patient had no neurological symptoms; however, the deep tendon reflexes were absent. Chest radiography revealed cardiomegaly and bilateral pleural effusion. Computed tomography of the abdomen revealed hepatosplenomegaly and massive ascites (). Blood examination showed moderate renal dysfunction (serum creatinine 1.81 mg/dL, blood urea nitrogen 44 mg/dL). The diagnosis of POEMS syndrome was made based on the following findings: peripheral neuropathy (mild decrease of the median nerve conduction velocity), organomegaly (hepatosplenomegaly), endocrinopathy (gynecomastia), serum monoclonal protein elevation (IgA lambda 1295 mg/dL), skin changes (hyperpigmentation and hemangioma), plasma VEGF elevation (700 pg/mL; normal <117 pg/mL), and evidence of extravascular volume overload (edema, pleural effusion, and massive ascites). While there were 5.4% plasma cells in bone marrow aspirate and biopsy, neoplastic plasma cells were not observed. The ratio of serum-free kappa and lambda light chain was within normal range. The diagnostic process of this patient was described in the previous report []. The patient had the renal involvement of POEMS syndrome and the renal biopsy was helpful for making a precise diagnosis [].
Initially the patient refused medication for POEMS syndrome. However, the ascites increased gradually in size, necessitating regular drainage from July 2010, with the average drainage volume per session being 6000 mL. From December 2010, drainage was necessitated three times a month (average drainage volume: 18 liters/month).
The patient gave consent for undergoing treatment. We started treatment with lenalidomide (10 mg/day for 21 days of a 28-day cycle) and once-weekly dexamethasone (10 mg). While the ascites and plasma VEGF concentration reduced dramatically (VEGF: 64 pg/mL), the treatment could not be continued due to deterioration of the renal function. After discontinuation of the lenalidomide (once-weekly dexamethasone was continued to be administrated), the patient's renal function recovered to its pretreatment level; however, the ascites began to increase again in size. We then restarted the treatment with a lower dose of lenalidomide (5 mg every other day for 11 days of a 28-day cycle) and dexamethasone (10 mg/week). The ascites gradually began to reduce in size in response to this treatment. While the plasma level of VEGF increased transiently (244 pg/mL at 6 months after the retreatment), it decreased finally to be within normal range (73 pg/mL and 26 pg/mL at 12 and 18 months after the retreatment, resp.). By the end of the seventh course of retreatment, the ascites had completely disappeared (). The patient did not want to undergo high-dose chemotherapy with autologous stem cell transplantation as a consolidative therapy. At the time of writing, the patient remains on maintenance therapy with very-low-dose lenalidomide and dexamethasone and is free of ascites. The median nerve conduction velocity has increased slightly (about 10%) and the renal function improved (serum creatinine: 0.93 mg/dL, blood urea nitrogen: 13 mg/dL). Although the level of serum IgA is tending to decline, the pace of reduction is considerably slow (1002 mg/dL and 981 mg/dL at 12 and 18 months after the retreatment, resp.).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [57, 'years'], 'creatinine': [1.81, 'mg/dL']}",43.07325,40.91959,45.22691,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 57 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.81 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.81/0.9)**-1.2 * 0.9938**57 * 1.0 = 43.07325.
Hence, the GFR value is 43.07325 ml/min/1.73 m²."
307,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8637396-1,Extracted,"A 34-year-old Hispanic female was admitted with the chief complaint of a painful nonhealing abdominal wound for 2 weeks duration. The patient initially developed few scabs in the infra umbilical area which led to frequent itching and irritation. She used plain cotton gauze with vaseline ointment to treat them by herself. The scabs later turned into ulcers. Her past medical history was significant for ESRD, and she has been on continuous ambulatory peritoneal dialysis (CAPD) for 5 years, gastroesophageal reflux disease, obesity, anemia of chronic kidney disease (CKD), secondary hyperparathyroidism of renal origin, and coccidioidomycosis infection. Her chronic renal disease was from amphotericin B drug toxicity secondary to previous disseminated coccidioidomycosis treatment. The patient had a history of uncontrolled hyperparathyroidism with an intact parathyroid hormone level as high as 2400 picograms/milliliter (pg/mL) and an elevated phosphorus level of 10 mg/dL as an outpatient. These were values 6 months before the current hospitalization. This was difficult to control mainly because of financial constraints in getting the medications and nonadherence to prescribed phosphate binders. Home medications include sevelamer carbonate 3200 milligrams (mg) 3 times a day with meals. The patient lived at her parent’s home and has stopped working because of multiple medical issues. The patient denied any history of smoking, alcohol, or illicit drug use. Her peritoneal dialysis prescription was 4 daytime exchanges of 2-L peritoneal dialysate fluid, each bag composed of 2.5% dextrose and each exchange for 4 hours daily. Her weekly Kt/V was 2.1, with no residual kidney function.
Vital signs on presentation were, temperature of 98.6 Fahrenheit (F), pulse rate of 84 beats per minute (bpm), respiratory rate of 18 breaths per minute, blood pressure 117/59 mm Hg, and oxygen saturation of 99% on room air. Physical examination showed a morbidly obese female in mild distress due to abdominal pain. Abdominal examination revealed multiple tender indurated ulcers with surrounding erythema and black eschar in the lower abdomen section ( and ) along with skin ulceration with exposed subcutaneous tissue and granulation in lateral walls ( and ). The rest of the physical examination was non-significant.
Laboratory data revealed elevated white blood count (WBC) 21,000/mm3, hemoglobin 8.5 g/dL, platelets 526,000/mm3, sodium 131 mmol/L, potassium 3.4 mmol/L, blood urea nitrogen 59 mg/dL, creatinine 13.26 mg/dL, albumin 3.3 g/dL, calcium 8.6 mg/dL, phosphorus 8.3 mg/dL, parathyroid hormone 712 pg./mL, C reactive protein 129.8 mg/L, CAPD fluid was not positive for an infection, and blood cultures were negative for any infection. Computerized tomography (CT) abdomen and pelvis with and without contrast revealed anterior abdominal wall subcutaneous calcification. Parathyroid imaging by 29.2 mCi Technetium 99m Sestamibi scan revealed no abnormal radiotracer accumulation to suggest parathyroid adenoma.
To the patient was initially treated with empiric antibiotics until the infection was ruled out and was also started on sodium thiosulphate 25 g in sterile water intravenous infusion over 30 minutes, 3 times a week for 3 months. Due to unavailability of dermatologist and skilled surgeons, skin biopsy was not possible. The peritoneal dialysis regimen was intensified with the patient switching to continuous cycler peritoneal dialysis and doing 6 exchanges throughout the night with 2.5-L peritoneal dialysate fluid, each bag composed of 2.5 % dextrose and each exchange for 2.5 hours. The patient underwent 4-gland parathyroidectomy with implantation of half of the right superior parathyroid gland on the right forearm. The patient also received aggressive wound care daily. The calciphylaxis lesions healed completely in 3 months with intense peritoneal dialysis, sodium thiosulfate infusion for 3 months, and parathyroidectomy. The dialysis modality was never changed to hemodialysis during the management of calciphylaxis lesions.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [34, 'years'], 'creatinine': [13.26, 'mg/dL'], 'sex': 'Female'}",3.40957,3.23909,3.58005,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 34 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 13.26 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (13.26/0.7)**-1.2 * 0.9938**34 * 1.012 = 3.40957.
Hence, the GFR value is 3.40957 ml/min/1.73 m²."
308,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8460550-1,Extracted,"A 79-year-old Japanese man presented with an abnormal shadow on chest radiography during an annual check-up. His family history was unremarkable. The patient had been treated for diabetes, and he was a current smoker (smoking index of 3680). The chest radiograph showed an ill-defined nodule of ~25 mm in diameter in the left lower lung field. Chest computed tomography revealed an ill-defined nodule of ~25 mm in diameter in the left S9a area without lymph node involvement (Figure ).
Blood examinations showed a slightly elevated carcinoembryonic antigen (5.9 ng/ml) but normal ranges of cytokeratin fragment and progastrin-releasing peptide. The blood glucose level was high (164 mg/dl), with 9.1% HbA1c. Other than renal dysfunction with a creatinine level of 1.10 mg/dl and blood urea nitrogen level of 28.3 mg/dl, the haemogram and renal and hepatic functions were within normal ranges. Squamous cell carcinoma was detected via transbronchial lung biopsy. At the time of bronchoscopy, a nodule of ~1 mm in diameter with a smooth surface was observed at the orifice of the left B8a (Figure ). Pathological diagnosis of the tumour revealed typical carcinoid. The bronchial tumour cannot be detected on the chest CT image (Figure ).
After controlling hyperglycaemia, left lower lobectomy with mediastinal lymph node dissection was performed based on the diagnosis of cT1cN0M0 stage IA. Pathology revealed a 23 × 23 × 23 mm (same invasive dimension) tumour, which was a keratinizing squamous cell carcinoma (Figure ) without lymph node metastases or pleural involvement. The surgical stage was IA3 with pT1cN0M0. Moreover, a tumour (0.8 mm in diameter) was located at the orifice of the left B8 and was limited in the bronchial mucosa without invasion of the bronchial cartilage (Figure ). A ribbon-like arrangement with positivity for chromogranin A and synaptophysin was observed. The Ki67 labelling index was <1%. Necrosis or mitosis was not observed. Finally, typical bronchial carcinoid was diagnosed (Figure ). The squamous cell carcinoma did not include any carcinoid component at all. The patient was alive without recurrence 2 years after the surgery.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [79, 'years'], 'creatinine': [1.1, 'mg/dL'], 'sex': 'Male'}",68.28551,64.87123,71.69979,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 79 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.1/0.9)**-1.2 * 0.9938**79 * 1.0 = 68.28551.
Hence, the GFR value is 68.28551 ml/min/1.73 m²."
309,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5192594-1,Extracted,"A 73-year-old man who had been suffering from left flank pain for 20 days was referred to our outpatient clinic for evaluation and treatment. No significant past medical or surgical history was elicited. No palpable abdominal mass was detected during the physical examination. His laboratory evaluation revealed mild renal function impairment (white blood cell count [WBC] 9.41 × 109/L, hemoglobin [Hb] 144 g/L, percentage of neutrophil cell 78.4%, platelet count [PLT] 234 × 109/L, lactate dehydrogenase [LDH] 528 U/L, blood urea nitrogen [BUN] 6.70 mmol/L, creatinine [Cr] 124.3 μmol/L, C-reactive protein [CRP] 28.0 mg/L, and erythrocyte sedimentation rate [ESR] 37). Urinalysis showed microscopic hematuria and proteinuria.
A plain abdominal X-ray revealed a suspected left renal mass. A three-phase computed tomography (CT) urography revealed left hydronephrosis and multiple space-occupying lesions in the left renal pelvis and left medium and lower ureter. The left renal parenchyma was totally invaded and multiple enlargements of lymph nodes were seen in the aortocaval area. Thus, a TCC was highly suspected. Furthermore, an abdominal CT angiography showed a tumor thrombus in the left renal vein. No obvious metastasis was observed on chest CT except for some tiny nodules.
As the preoperational diagnosis was TCC from the left renal pelvis with the left renal vein thrombus, left laparoscopic radical nephroureterectomy with thrombectomy and regional lymphadenectomy were performed. No neoplasm was observed in intraoperative cystoscopy examination. The left kidney was enlarged, solid, and adherent to perirenal fat. The left medium and lower ureter was dilated, solid, and adherent to iliac vessels. The thrombus was gently milked back into the left kidney and removed along with the kidney.
Gross examination of the specimen showed necrosis in the left renal calyx and wall of the left medium and lower ureter. Postoperative histopathological examination revealed high-grade TCC (16 × 9 × 10 cm) (according to the 2004 WHO classification), which infiltrated parenchyma and perirenal fat diffusely and extended into the renal vein. Postoperative histopathology also showed multiple para-aortic lymphatic metastases, of which the biggest one was 6 cm (pT4N3M0). No microscopic lymphovascular invasion was observed. The margin of the ureter was negative.
No significant event was observed during the perioperative period. The patient underwent chemotherapy in another center, but the regimen was not recorded. The patient died 2 months after the operation.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [73, 'years'], 'creatinine': [124.3, 'µmol/L'], 'sex': 'Male'}",55.09472,52.33998,57.84946,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 73 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 124.3 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 124.3 µmol. To convert 124.3 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 124.3 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00012 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00012 mol Serum Creatinine * 113.12 g/mol = 0.01357 g Serum Creatinine. To convert 0.01357 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01357 g Serum Creatinine * 1000.0 mg/g = 13.57 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 13.57 mg Serum Creatinine/10.0 dL = 1.357 mg Serum Creatinine/dL. The concentration value of 124.3 µmol Serum Creatinine/L converts to 1.357 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.357/0.9)**-1.2 * 0.9938**73 * 1.0 = 55.09472.
Hence, the GFR value is 55.09472 ml/min/1.73 m²."
310,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3809353-2,Extracted,"A 72-years-old male patient (ASA 3; BMI 23.1 kg/mq body surface area) underwent general anesthesia for thoracic aorta aneurysmectomy. Preoperative blood test did not show any significant alteration but Kaliemia 5.1 mmol/L and serum creatinine 1.29 mg/dL; electrocardiogram showed a sinus rhythm (68 bpm); echocardiogram reported a good global kinesis (ejection fraction 60%; left ventricle end-diastolic volume 78 ml). Eight years before, he experienced a myocardial infarction treated with percutaneous angioplasty and stenting. Aneurism maximum diameter was 6.7 cm.
Nitrate was not administered even during clamping phase; conversely, hemodynamics needed to be supported by Dopamine administration (8–10 mcg/kg/min).
Surgical approach consisted of thoraco-phreno-laparotomic incision, and before left emithorax opening, OLV started and TV lowered at 6 mL/kg.
After 100 minutes from the beginning, surgeon clamped aorta 5 cm below the isthmus. The clamping phase lasted 105 minutes.
Before aortic clamping patient received N-acetyl-cysteine 2 g i.v. bolus, Methyl-Prednisolone 2 g i.v. bolus, and Mannitol 18% 100 ml, aiming to protect kidney and as free-radicals scavenging.
Global intraoperative fluid administration was 8500 mL including 4 units of red blood cells and 4 units of fresh frozen plasma; bleeding resulted in about 2000 mL and 625 mL was readministered by a red cells storage device. Subarachnoid fluid withdrawal was 100 mL.
Postoperatively, he was admitted to ICU, awakened, and successfully extubated on the day after. Patient did not experience any neurological postoperative complication and was dismissed to ward after 2 days and left hospital 15 days after the operation.
In both of the two cases, aortic aneurysm involved the supradiaphragmatic tract of the vessel.
General anesthesia was induced with Fentanyl 1 mcg/kg i.v. + Propofol 2 mg/kg i.v. after preanesthesia administration of Morphine 5 mg + Atropine 0.5 mg i.m. Orotracheal intubation (double-lumen tube n.39) was performed after myorelaxation with cis-Atracurium 10 mg i.v. bolus and further administration of 0.15 mg/kg every 30 minutes. Anesthesia continued with administration of a gas mixture of air and oxygen (FiO2 0.5-0.6, according to blood gas-analysis (BGA) results) and Sevoflurane 1-2%. Mechanical ventilation setting was tidal volume (TV) 5–8 mL/kg according to one-lung ventilation (OLV) or bilateral lung ventilation (BLV) phase; respiratory rate was 12 apm and it was modified to assure normal pCO2; positive end-expiratory pressure (PEEP) was 5–7 cmH2O.
Intraoperative monitoring included electrocardiogram (D2 and V5) and ST line analysis, heart rate (HR), not-invasive blood pressure (NIBP) and invasive blood pressure (IBP) after right radial artery line insertion connected with FloTrac/Vigileo sensor (Edwards Lifesciences, Irvine, USA) for Cardiac Output (CO; Cardiac Index, CI) monitoring, peripheral oxygen saturation (SpO2), central venous pressure (CVP), end-tidal carbon dioxide (EtCO2), and diuresis. A subarachnoid catheter was inserted (Lumbar Drainage Catheter 46 cm, Codman and Shurtleff, Inc., Raynham, MA, USA) at lumbar level L3-L4 and connected to standard multichannel patient monitoring system to measure intrathecal pressure (P
Lq) and withdraw CSF to lower it when necessary. Transesophageal echocardiogram (TEE) was used to value cardiac performance, particularly during the clamping period. BGA was tested after surgical incision, after OLV starting, every 15 minutes during aortic clamping, after unclamping, and after BLV restoring ().
Postoperative analgesia started before the end of operation with i.v. infusion of a saline solution containing Morphine 30 mg/50 ml (2.1 mL/h). After the operation, the patient was sedated with Propofol 100 mg/h and admitted to ICU as planned to continue postoperative care and monitoring.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [72, 'years'], 'creatinine': [1.29, 'mg/dL'], 'sex': 'Male'}",58.91137,55.9658,61.85694,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 72 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.29 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.29/0.9)**-1.2 * 0.9938**72 * 1.0 = 58.91137.
Hence, the GFR value is 58.91137 ml/min/1.73 m²."
311,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5884240-3,Extracted,"An asymptomatic 45-year-old female was detected to be heterozygous during family screening (AFD affected father). Echocardiographic examination showed thickened mitral papillary muscle, LV wall thickness 11/12 mm, and mild degree of diastolic dysfunction. Testing for AF disease was performed: alpha-galactosidase level was normal (0.2 nmol/spot/21 h; normal range >0.12 nmol/spot/21 h) and a heterozygous mutation was detected (c.[902G>T]). Thereafter, heart MRI was performed; there was no late gadolinium enhancement or signs of myocardial fibrosis, examination considered as completely normal. Furthermore, brain MRI was normal. Renal biopsy showed typical zebra bodies located in podocytes and partly in epithelial tubular cells. Laboratory analysis showed normal renal function: creatinine level 76 µmol/L, endogenous creatinine clearance 81 mL/min/1.73 m2, albuminuria 5.1 mg/L, and proteinuria 78 mg/24 h (Figures and ).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [45, 'years'], 'creatinine': [76.0, 'µmol/L'], 'sex': 'Female'}",79.81102,75.82047,83.80157,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 45 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 76.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 76.0 µmol. To convert 76.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 76.0 µmol Serum Creatinine * 1e-06 mol/µmol = 8e-05 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 8e-05 mol Serum Creatinine * 113.12 g/mol = 0.00905 g Serum Creatinine. To convert 0.00905 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00905 g Serum Creatinine * 1000.0 mg/g = 9.05 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 9.05 mg Serum Creatinine/10.0 dL = 0.905 mg Serum Creatinine/dL. The concentration value of 76.0 µmol Serum Creatinine/L converts to 0.905 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.905/0.7)**-1.2 * 0.9938**45 * 1.012 = 79.81102.
Hence, the GFR value is 79.81102 ml/min/1.73 m²."
312,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7437116-1,Extracted,"A 43-year-old male, known to be deaf, mute, and blind, presented to the ED accompanied by his daughter. She said that he had multiple episodes of diarrhea and vomiting for two days.
He was morbidly obese and diabetic, taking insulin. He had a history of coronary artery disease and had two coronary stents.
Taking more history asking about the presence of blood in the stool revealed that his daughter did not enter with him to the bathroom. As the patient was blind, deaf, and mute, diarrhea history also came under doubt at this point. What we could understand was that he had abdominal pain somewhere, vomited a few times, and entered the bathroom several times a day for two days.
He was vitally stable. Blood pressure was 130/76 mmHg, pulse was 92 beats per minute, respiratory rate was 16 breaths per minute, and the temperature was 37.3°C.
On examination, the patient was lying on the bed flat, looking well, morbidly obese. He was conscious, moving all limbs, had no rash, no neck rigidity. His chest was clear bilaterally, with no added sounds. His abdomen was lax with no localized tenderness, and hernia orifices were unremarkable. He was pointing to his epigastrium and right flank when asked for pain location. His extremities did not show redness, hotness, edema, or signs of deep vein thrombosis.
Investigations
Blood tests showed mild leukocytosis (WBCs 12000), mild anemia (Hb 11 g/dL), normal platelet count, mild elevation in kidney function (creatinine 120 mmol/L), slight elevation in liver function (alanine transaminase 70, aspartate transaminase 84), average bilirubin level, and mild elevation in amylase. Electrocardiogram (ECG) showed normal sinus rhythm and no signs of new ischemia. A chest X-ray showed no pneumonic patches or air under the diaphragm. The bedside ultrasound did not add so much as the patient was morbidly obese.
More blood tests, urine tests, and an official ultrasound (USG) for the abdomen were ordered. The lipase was normal. Troponin was negative.
The USG showed normal liver echotexture. The gall bladder wall thickness was average. The gall bladder showed no stones inside, and there were no signs of cholecystitis. The aorta was normal in caliber with no dilatation all over its course till the bifurcation. The left kidney had an average size with no hydronephrosis or stones. The right kidney showed moderate to severe hydronephrosis.
The urine analysis showed blood and mild leucocytes. So, the suspicion of renal colic became close in the picture of right moderate hydronephrosis, mild acute renal function derangement, and the blood in the urine.
CT of the kidney and the urinary bladder (CT KUB) was ordered, which revealed a big stone 1.2 cm in the mid of the right ureter with right moderate to severe hydronephrosis and perinephric fat strandings (Figures -).
Differential diagnosis
Many differential diagnoses were considered for a case of upper abdominal pain. The patient could have gastritis, gastroenteritis, acute pancreatitis, acute cholecystitis, renal colic, pneumonia, and acute myocardial infarction.
The lab investigations, in this case, helped rule out other differential diagnoses and reach a final diagnosis.
Ultrasound and blood tests ruled out gastritis and gastroenteritis. Lipase and amylase were normal, so the diagnosis of acute pancreatitis was out of consideration. There was a mild increase in liver enzymes, but no jaundice and no abnormality were seen in the liver and the gall bladder during USG, so the diagnosis of acute cholecystitis was also ruled out.
Chest X-ray was normal, so there was no question of pneumonia. Troponin and ECG also came out to be normal.
The USG showed hydronephrosis in the right kidney along with blood and WBCs in urinalysis. These findings prompted the suspicion of urinary tract stone, which was confirmed on CT KUB as it is the gold standard for the diagnosis of renal stones.
Treatment, outcome, and follow-up
The patient’s pain was controlled by simple analgesia. He was admitted to the urology department, where he underwent a ureteroscopy to remove the obstructing stone, and a Double-J (DJ stent) was inserted. The patient improved and was discharged home after two days without complications. He did not develop pain or hematuria. He followed with the urology department for three months.
Emotional challenges while dealing with this patient
The patient was in pain when he presented, but he could not communicate in any way because he was blind, mute, and deaf. His family communicated with him by touch. They used to hold his hands, draw some shapes, and point to some parts of his body. He was able to reply to his daughter’s touch with similar actions, and she delivered the translated message to the clinical team.
It was an emotionally overwhelming experience in multiple ways. Firstly, seeing how hard it was for the person to describe his problem and specifically pain at that time due to many disabilities was distressful. Secondly, we were not able to get the proper information from the patient, so it was hard to make differential diagnoses. There was a feeling of helplessness because we were not able to do something based on clinical findings. Even his daughter thought it was gastroenteritis because he went to the bathroom multiple times in the last two days. Later we figured out that it was because of dysuria and increased frequency of urination rather than diarrhea. Moreover, the patient was vomiting because of pain and not gastroenteritis.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [43, 'years'], 'creatinine': [120.0, 'mmol/L']}",0.01667,0.01584,0.0175,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 43 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 120.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from mmol to mg. The mass of Serum Creatinine is 120.0 mmol. To convert 120.0 mmol of Serum Creatinine to mol, multiply by the conversion factor 0.001, giving us 120.0 mmol Serum Creatinine * 0.001 mol/mmol = 0.12 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.12 mol Serum Creatinine * 113.12 g/mol = 13.5744 g Serum Creatinine. To convert 13.5744 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 13.5744 g Serum Creatinine * 1000.0 mg/g = 13574.4 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 13574.4 mg Serum Creatinine/10.0 dL = 1357.44 mg Serum Creatinine/dL. The concentration value of 120.0 mmol Serum Creatinine/L converts to 1357.44 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1357.44/0.9)**-1.2 * 0.9938**43 * 1.0 = 0.01667.
Hence, the GFR value is 0.01667 ml/min/1.73 m²."
313,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3109787-1,Extracted,"A 67-year-old man was admitted with fever, cough, sore throat, breathlessness, muscle and joint pains of 1-week duration. He was a case of CKD stage 4 with hypertension (treated with amlodipine 5 mg twice a day) and diabetes mellitus of 1-year duration (on regular insulin, 5 IU three times a day).
On examination, he was obese (body mass index - 31 kg/m2) with blood pressure of 112/57 mmHg, temperature 39°C, respiratory rate of 36 breaths per minute, heart rate of 116 beats per minute, and oxygen saturation of 72% on room air which improved on high flow oxygen mask to 94%. The chest radiograph (posthemodialysis) revealed bilateral upper and middle zone pulmonary infiltrates.
Laboratory investigations revealed hemoglobin, 9.6 gm/L; total white cell count, 15.6 × 103/μl (differential count: 86% neutrophils, 6% lymphocytes, 6% monocytes, and 2% eosinophils); platelet count, 1.2 × 105/μl; serum creatinine (SCr), 7.8 mg/dl; alanine aminotransferase, 84 units/l (normal range: 0 – 40 units/l); aspartate aminotransferase, 176 units/l (normal range: 5 – 34 units/l); serum bilirubin, 3.5 mg/dl; serum albumin, 2.5 gm/dl; creatine phosphokinase, 900 U/l (normal range: 15 – 105 U/l); lactate dehydrogenase, 302 IU/l (normal range: 100 – 190 IU/l); lactate, 5.2 mmol/l (normal range: 0.4-2.0 mmol/l); and fasting/postprandial blood sugar of 130/180 mg/dl. Multiple blood, urine, and sputum cultures were sterile. On routine checkup 1 month prior to admission, his creatinine was 3 mg/dl. He was treated with antibiotics (Imipenem-cilastatin and clindamycin) and urgent HD during which 2 l of fluid was removed. An additional 2 l fluid was removed during a second HD. However his respiratory status did not improve, clinical condition deteriorated with rising body temperature, worsening hypoxia and dyspnea. He was transferred to the intensive care unit, intubated, and mechanically ventilated on day 2 of admission. Arterial partial pressure of oxygen/fraction of inspired oxygen was 125 mmHg. Acute Physiology and Chronic Health Evaluation (APACHE) II, Sequential Organ Failure Assessment (SOFA) scores, Multiple Organ Dysfunction Score, and Murray scores were 33, 12, 13, and 2.75, respectively. H1N1 virus was identified by reverse transcription polymerase chain reaction from his nasal and throat swabs. Oral oseltamivir, 75 mg on alternate days and amantadine 100 mg BID were initiated and continued for 10 days. He had history of exposure to H1N1 in community, and had not been vaccinated with seasonal influenza/pneumococcal vaccine within the last year. He received alternate day HD, and ionotropes were administered for 2 days. Repeat sputum culture on day 6 did not identify pathogenic organisms. On clinical improvement, he was extubated on day 6 and discharged on day 12. On follow-up three weeks later, his SCr was 3.3 mg/dl (CKD stage 4) and urine output was 1.2 l/day. He did not require dialysis after discharge. No adverse effects of oseltamivir were noted.
Protective measures like extensive use of surgical masks and N 95 respirators in addition to goggles, gowns, and gloves, strict application of universal precautions as well as liberal use of gel-alcohol hand sanitizer, limitation and control of entries; prompt isolation of suspected cases were implemented in order to limit the spread of the infection in dialysis units. All close contacts including health care workers received oseltamivir (75 mg for 10 days) and did not develop any influenza like illness.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [67, 'years'], 'creatinine': [7.8, 'mg/dL'], 'sex': 'Male'}",7.01291,6.66226,7.36356,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 67 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 7.8 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (7.8/0.9)**-1.2 * 0.9938**67 * 1.0 = 7.01291.
Hence, the GFR value is 7.01291 ml/min/1.73 m²."
314,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5516357-1,Extracted,"A 70-year-old Asian man with ESRD due to nephrosclerosis complained of chest discomfort during exercise and was referred to our hospital. He had been receiving hemodialysis for 20 years, and had a past medical history of hypertension, hyperuricemia, and reflux esophagitis. He had no history of thromboembolism or endocarditis. He smokes one pack of cigarettes per day, and drinks socially.
He had no significant social and environmental history. His medication list included amlodipine, allopurinol, ferric citrate hydrate, and lansoprazole. He had no family history of cardiovascular diseases.
He was afebrile, with a blood pressure of 114/50 mmHg and a regular pulse rate of 61 beats per minute. His oxygen saturation was 96% on ambient air. There was no evidence of lung rales, cardiac murmur, and abdominal tenderness. His neurological examinations were unremarkable. Blood investigations showed: hemoglobin 14.0 mg/dl, white blood cells 4700/mm3, and platelets 134,000/mm3. His liver and renal function tests revealed total bilirubin 0.4 mg/dl, aspartate aminotransferase 24 IU/l, alanine aminotransferase 34 IU/l, blood urea nitrogen 54.2 mg/dl, and serum creatinine 11.1 mg/dL. His C-reactive protein was 0.16 mg/dl. His serum electrolyte tests were within normal limits, including calcium and inorganic phosphorus. In addition, his brain natriuretic peptide was raised at 605.1 pg/dl. His blood cultures were negative.
A chest X-ray showed mild cardiomegaly without pulmonary congestion (Fig. ). An electrocardiogram suggested left ventricular hypertrophy with nonspecific ST-T wave changes (Fig. ). A transthoracic echocardiogram revealed MAC and a highly mobile mass (8 × 6 mm) attached to the ventricular side of the posterior mitral valve leaflet (Fig. ). The echogenicity of the mass was similar to MAC. The mitral valve was mildly thickened with mild mitral stenosis. Left ventricular systolic function was normal. Cardiac computed tomography demonstrated a calcified cardiac mass in the mitral annulus with heavy MAC (Fig. ). As the mass was highly mobile, suggesting a high risk of embolization, he underwent surgical resection of the mass. Intraoperative findings demonstrated a severely calcified mitral annulus and attachment of the calcific mass to the P2 segment of the mitral valve. Surgical resection was performed successfully.
Macroscopic findings of the resected mass showed a yellowish colored and partially calcified mass (7 mm in diameter; Fig. ). A histopathological examination revealed multiple nodular amorphous calcifications and fibrous connective tissue. There were no identifiable myxoma or malignancy cells (Fig. ). Consequently, the diagnosis of CAT was confirmed. He recovered uneventfully and was discharged without any complications.
No evidence of tumor recurrence was detected after the surgery, and he is doing well after 6 months of follow-up.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [70, 'years'], 'creatinine': [11.1, 'mg/dL'], 'sex': 'Male'}",4.50735,4.28198,4.73272,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 70 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 11.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (11.1/0.9)**-1.2 * 0.9938**70 * 1.0 = 4.50735.
Hence, the GFR value is 4.50735 ml/min/1.73 m²."
315,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5733951-1,Extracted,"A right-handed 81-year-old man with a history of ischemic stroke, hypertension, hyperlipidemia, hypothyroidism, and chronic kidney disease presented to the Emergency Department with dizziness, nausea, dysarthria, and change in mental status. Further history revealed that he had two prior ischemic strokes, in 2003 and 2007, with residual right-sided weakness. Subsequently, he had been on aspirin/dipyridamole for stroke prevention.
On initial examination, the patient was afebrile with a blood pressure of 162/81, heart rate of 77 beats per minute, and oxygen saturation of 98% on room air. He was alert and oriented to person but disoriented to location and time. On neurological examination, he was found to have poor memory, fair concentration, mild dysarthria and nonfluent aphasia, poor knowledge, and limited judgement. Pupils were equally round and reactive to light with intact extraocular movements. Facial sensation was intact bilaterally. No facial weakness was appreciated and tongue was midline on protrusion. Motor examination was nonfocal without a pronator drift. Sensory examination was intact to light touch, proprioception, and pinprick. Reflexes were symmetrical and coordination was normal.
Laboratory studies revealed a white blood cell count of 12,600/μL, platelet count of 155,000/μL, sodium level of 141 mEq/L, potassium level of 4.3 mEq/L, glucose level of 123 mg/dL, and serum creatinine level of 1.50 mg/dL. An electrocardiogram showed a normal sinus rhythm and a 2D echocardiogram did not reveal any valvular or wall motion abnormalities. Telemetry monitoring in the hospital did not reveal any atrial fibrillation.
An outpatient computed tomography (CT) scan showed no acute findings. CT angiogram (CTA) of the head revealed a remote infarct in the left parietal lobe and diminished flow within the distal left middle cerebral artery branches. The CTA further showed a PTA supplying the mid and distal basilar artery () and severe atherosclerosis and stenosis of the proximal ICA ().
Magnetic resonance imaging (MRI) of the brain showed several areas of restricted diffusion in the posterior left temporal and frontal lobes, right occipital lobe, and bilateral cerebellar hemispheres consistent with subacute infarcts.
Two days after admission, the patient was noted to be nonverbal and somnolent. Motor examination revealed right-sided hemiplegia. A repeat MRI of the brain showed new areas of restricted diffusion in the left frontoparietal region, and also in the brain stem, bilateral superior cerebellar, and occipital regions. Findings were most consistent with emboli originating from the severely atherosclerotic left ICA, reaching the posterior fossa via the PTA (). After reviewing the images with a neuroradiologist, it was determined that the new acute infarcts found in the occipital lobes, superior cerebellum, and thalamus were within the PTA territory.
The patient was transferred to the neuroscience intensive care unit for monitoring with a systolic blood pressure goal of 180 to 200. A carotid duplex showed 80% to 99% stenosis of the proximal left ICA. Subsequently, the patient underwent a left carotid endarterectomy with bovine patch angioplasty one week after admission with no complications. His neurological examination improved slowly and the patient was eventually discharged to a skilled nursing facility for rehabilitation with no recurrence of ischemic stroke.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [81, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Male'}",46.48237,44.15825,48.80649,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 81 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.5/0.9)**-1.2 * 0.9938**81 * 1.0 = 46.48237.
Hence, the GFR value is 46.48237 ml/min/1.73 m²."
316,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4602609-1,Extracted,"A 55-year-old white male was referred to our outpatient clinic because of a computed tomography (CT) finding of a large abdominal mass and left inguinal adenopathy. No significant medical history was reported. At our evaluation, he reported a remittent and dull pain on his left flank, which had prompted a further diagnostic evaluation by his general practitioner. Laboratory values were notable for mild anemia (Hb = 13.1 g/dL; normal range, 14–16 g/dL), moderate lymphopenia (620/mm3, normal range, 1000–3500/mm3), and raised serum creatinine levels (1.7 mg/dL). Serum LDH levels were normal (348 U/L, normal range, 100–450 U/L), as serum electrophoresis and liver function. The CT scans of the chest, abdomen, and pelvis showed multiple scattered nodular lesions in the lungs (the greater of which measured 1.6 cm); marked left hydronephrosis was present, caused by a diffuse thickening of the pelvic connective tissue, compressing the left ureter and surrounding the bladder, the prostate, and ileopsoas muscles. Multiple left inguinal adenopathies were evident, the larger of which measured 2.6 cm. A biopsy of the most accessible inguinal lymph node had been performed, but no evidence of malignant lymphoma was found at histological examination. Given the strong clinical suspicion for a neoplastic disease, a new biopsy of the largest inguinal adenopathy was performed, which exhibited fat necrosis and chronic granulomatous inflammation with giant cells. At the positron emission tomography (PET) scan, both the pelvic masses and the pulmonary nodules showed remarkable metabolic avidity to 18-FDG (Fig. ). A diagnostic bone marrow biopsy was proposed, but the patient refused the procedure. After these tests and before a new clinical evaluation, the patient developed acute abdominal pain with fever and was hospitalized in a nearby local clinic. An urgent laparotomy was performed. Intraoperative examination did not confirm the finding of an intraabdominal mass seen at the CT scan; a large pelvic abscess was instead found, with evidence of colonic perforation, bladder-colonic fistula, and completely necrotic bladder. Large adenopathies were also absent. Surgical intervention included partial colonic, total bladder, and omental resection with terminal colostomy to the left side, suturing of the remaining bladder, and fashioning of a bilateral nephrostomy. All the surgical specimens were submitted for pathological examination.
Grossly, the intestinal wall appeared thickened and hardened with a 3-cm large perforation. The cut surface was whitish with areas of frank necrosis and the overlying mucosa featured erosions and ulcerations. The bladder wall appeared extensively necrotic.
On histology, the intestinal submucosa and muscularis propria layer displayed a mild small lymphocytic infiltrate within an edematous and necrotic stroma, with scattered atypical mononuclear larger cells, sometimes provided with a conspicuous nucleolus and a relatively abundant cytoplasm. In the intestine, the large cells were B lymphocytes (CD20+/CD79a+/CD3−) with strong IRF4 expression and active cycling (Ki67 80%). No clear-cut expression of germinal center markers (BCL6 and CD10), CD30, BCL2, and κ or λ light chains could be observed, although no positive internal controls were present for BCL6. The immunohistochemical staining for cytomegalovirus and in situ hybridization (ISH) for EBER proved negative. The accompanying population of small lymphocytes was mainly composed of CD3+ cells with both helper (CD4+) and cytotoxic (CD8+) phenotype, and rare CD20+ B cells (Fig. ). T lymphocytes did not display evident cytological abnormalities; regular representation of other T-cell markers (CD2, CD5, CD7; Fig. ) was observed; molecular studies for clonal rearrangement of TCR-gamma gene proved negative (Supplementary Fig. 1S, ). Molecular studies for clonal rearrangement of IgH gene did not provide any reliable result, likely because of the abundant coagulative necrosis and tissue autolytic degeneration. The specimen from the bladder showed extensively necrotic tissue with scattered lymphoid infiltration and no evidence of large atypical cells.
The histological and immunohistochemical features of the lymphoid infiltrate prompted the differential diagnosis between a primary aggressive B-cell lymphoproliferative disorder and an abnormal inflammatory hyper-reaction with secondary perforation and involvement of the colonic and bladder wall, in the light of the referred absence of a properly defined mass at surgical examination and presence of a large abscess instead.
After the intervention, the patient entered a septic state confirmed by repeated findings of Gram-negative bacteria from blood and abdominal drainage cultures. Notwithstanding extensive antibacterial treatment, the septic state persisted. The finding of increasing pulmonary nodules at the chest CT scan prompted the execution of a transbronchial biopsy of a 3-cm nodular lesion in the left lung, which resulted nondiagnostic. Also, pleural fluid obtained from thoracentesis proved sterile, and cytological examination of the sediment did not find cells. Given the strong suspicion for B-cell lymphoma, the resistance to multiple antibacterial treatments, and the evidence for growing abdominal and pulmonary lesions, the possibility of a treatment with Rituximab was discussed. However, owing to the poor clinical conditions, the patient was deemed unfit even for this treatment.
Approximately 2 months after the hospitalization, the patient developed a massive intra-abdominal hemorrhage. He underwent immediate surgical intervention, but attempt to stop the bleeding was unsuccessful. The patient died during the intervention. A large mass in the left iliac fossa was found and sent for pathological examination (Figs. and ).
On histology, the sample was diffusely necrotic and edematous, with a dispersed loose mixed lymphocytic and granulocytic inflammatory infiltrate within which large cells, cytologically more atypical than those previously observed in the intestine, were seen, either scattered singly or focally surrounding small blood vessels as perivascular cuffs. These cells expressed CD20, IRF4, and BCL6, with negativity for CD3, CD10, and BCL2. The strong diffuse positivity for the c-Myc protein (>90%) and the extremely high Ki67-index confirmed the aggressive nature of the neoplastic process. Again, ISH for EBER proved negative and the clonal rearrangement of IgH genes was not assessable.
A diagnosis of an extranodal EBV-negative high-grade large B-cell lymphoma with massive necrosis and angiocentric pattern of growth was addressed, although the unique histological features did not allow to classify this tumor within any of the recognized WHO entities.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [55, 'years'], 'creatinine': [1.7, 'mg/dL'], 'sex': 'Male'}",47.02028,44.66927,49.37129,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 55 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.9)**-1.2 * 0.9938**55 * 1.0 = 47.02028.
Hence, the GFR value is 47.02028 ml/min/1.73 m²."
317,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4389168-1,Extracted,"A 32-year-old woman presented with twin pregnancy after in vitro fertilisation at a gestational age of 24 weeks + 3 days because of imminent preterm labour. She had stage-4 chronic kidney disease due to lupus nephritis that had been diagnosed 15 years earlier. Before pregnancy, the woman was treated with prednisolone and hydroxychloroquine. Her blood pressure was controlled with labetalol and methyldopa. Before pregnancy, her urinary protein level was 0.4 g/L (normal value < 0.1 g/L). At admission, her blood pressure was 110/80 mmHg and heart rate 88 beats per min and regular. Plasma creatinine was 258 µmol/L (normal values < 80 µmol/L) and blood urea nitrogen was elevated to 20 mmol/L (normal values < 7.8 mmol/L). Haemoglobin was reduced to 6.3 mmol/L (normal values, 7.0–10.0 mmol/L), whereas alanine aminotransferase (7 U/L), lactate dehydrogenase (169 U/L) and platelet counts (191 × 109/L) were in the normal range. Clinical examination showed uterus contractions and shortening of the cervix indicating threatening preterm labour. Continuous infusions of the tocolytic substance, atosiban, and an oxytocin receptor antagonist were administered to halt premature labour. However, contractions reinstated when atosiban was paused. Ultrasound examinations were performed using a Voluson ultrasound machine (General Electric Healthcare, Amersham, UK) with the woman in a semi-recumbent position. Amniotic fluid volume was measured according to the standardized techniques using the single deepest pocket measurement giving the vertical dimension of the largest pocket of amniotic fluid measured at a right angle to the uterine contour [, ]. The single deepest pocket measurement is interpreted as normal amniotic fluid volume (2.1–8.0 cm) and polyhydramnios (>8.0 cm). Ultrasound showed diamniotic and dichoriotic twins with estimated weights of 609 and 693 g, respectively. Repeated ultrasound evaluations confirmed intrauterine growth restriction in twin 1 by 24.7 % and twin 2 by 14.3%, respectively, and polyhydramnios as the cause of imminent preterm labour (A). Because of the well-known association between polyhydramnios and elevated uraemic toxins, intrauterine growth restriction and threatening preterm labour of premature children, haemodialysis treatments were started to reduce uraemic toxins, including blood urea nitrogen (B). Dialysis was administered 6 days per week for 3 h each using a biocompatible haemodialysis membrane. After initiation of haemodialysis treatment, ultrasound evaluation showed a significant decrease in amniotic fluids and reduction in the clinical complaints. At a gestational age of 28 weeks + 4 days, pre-eclampsia developed showing an elevated maternal blood pressure, elevated liver enzymes as well as an elevated pulsatility index in the arteria umbilicalis. Thus, we were forced to deliver by Caesarean section. Birth weights of the twins were 941 and 1164 g, respectively (C). Six weeks after delivery and cessation of haemodialysis, the mother's plasma blood urea nitrogen was 18 mmol/L, and plasma creatinine was 264 µmol/L. When the twins were seen last at the age of 12 months, the psychomotor development was uneventful.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [32, 'years'], 'creatinine': [258.0, 'µmol/L']}",21.03586,19.98407,22.08765,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 32 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 258.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 258.0 µmol. To convert 258.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 258.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00026 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00026 mol Serum Creatinine * 113.12 g/mol = 0.02941 g Serum Creatinine. To convert 0.02941 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.02941 g Serum Creatinine * 1000.0 mg/g = 29.41 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 29.41 mg Serum Creatinine/10.0 dL = 2.941 mg Serum Creatinine/dL. The concentration value of 258.0 µmol Serum Creatinine/L converts to 2.941 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.941/0.7)**-1.2 * 0.9938**32 * 1.012 = 21.03586.
Hence, the GFR value is 21.03586 ml/min/1.73 m²."
318,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4208581-1,Extracted,"SM, a 55-year-old female, in established renal failure secondary to adult polycystic kidney disease, received a living unrelated renal transplant through an exchange donor program. The kidney was implanted in the left iliac fossa. Her past medical history included a mechanical aortic valve replacement, cerebrovascular accident, and ascending thoracic aortic aneurysm treated by aortic root replacement and was maintained on long-term warfarin. One week prior to her transplantation, her warfarin was replaced with enoxaparin 60 mg daily.
The donor renal vein was thin walled and cut short requiring the recipient's long saphenous vein to be harvested and used as a cuff to lengthen it. The kidney had three arteries: a small upper polar artery which was ligated, a middle artery that was anastomosed end to side to the external iliac artery, and a medium sized lower polar artery that was anastomosed end to end to the inferior epigastric artery.
Postoperatively, she was put on a heparin infusion at a rate of 15 units/kg/hour with a targeted activated plasma thromboplastin time (APTT) ratio of 1.5–2.0. Immunosuppression comprised induction with basiliximab and maintenance on tacrolimus, mycophenolate mofetil, and prednisolone.
A routine ultrasound scan performed on the first postoperative day showed global perfusion of the kidney, but a deep fluid collection of about 5 cm diameter was seen at the lower pole. Given an APTT ratio of 3.5, the heparin dose was reduced to 11 units/kg/hour. On the second postoperative day, she developed frank haematuria and her haemoglobin (Hb) level dropped from a preoperative level of 10.8 g/dL to 8 g/dL. A CT scan was performed which confirmed a large retroperitoneal haematoma (15 cm in diameter) with layered density but no evidence of active bleeding (). At reexploration of the transplant, the haematoma was evacuated and the kidney was noted to be well perfused without any obvious active bleeding point. Heparin (7.5 units/kg/hour) was restarted on the next day (postoperative day three) maintaining the APTT ratio within the target range until postoperative day five when this was switched to enoxaparin 80 mg daily. The dose of enoxaparin was increased to 120 mg on day 7 as the transplant function improved.
SM experienced several complications following transplantation including CMV viraemia, pulmonary oedema, late urine leak managed conservatively, and recurrent urinary sepsis treated with antibiotics. On postoperative day 27, she developed pedal oedema, pain in the right hip, and thigh especially on moving as well as a 3 cm swelling in the right groin. In addition, there was a significant amount of bruising in the right flank extending into the thigh and upper calf associated with paraesthesia, significant discomfort, and weakness in the right leg. She also became hypotensive (81/53 mmHg) and required resuscitation with three units of packed cells and protamine 50 mg as her Hb dropped to 4.8 g/dL and anti-Factor Xa level was 0.97. Enoxaparin was stopped. An abdominal and pelvic CT scan showed bilateral psoas haematomata (). A repeat CT scan performed on the 31st postoperative day found no change in the haematomata apart from an extension to other retroperitoneal sites.
By the 36th postoperative day, she was restarted on warfarin and a CT scan showed a mature haematoma (with gas locules) around the transplant kidney as well as the bilateral psoas haematomata. Linezolid was added to the antibiotic regimen and later switched to Teicoplanin based on a urine culture which grew enterococcus. Antibiotics were continued for four weeks in one form or another. Her mobility was severely impaired when she developed the psoas haematomata, effectively confining her to her bed in the initial period. Regular physiotherapy was carried out throughout and she made steady progress. On postoperative day 78, she was discharged to a local community hospital where her rehabilitation continued for a further 16 days. She then continued her convalescence at home. By eight months after her transplantation, she had returned to her pretransplant levels of fitness. At her last clinic visit (18 months after transplantation), she stated that she had returned to full fitness with regular outdoor activities and her transplant function was excellent with a creatinine of 97 μmol/L (MDRD 54 mL/min).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [55, 'years'], 'creatinine': [97.0, 'µmol/L'], 'sex': 'Female'}",57.39525,54.52549,60.26501,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 55 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 97.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 97.0 µmol. To convert 97.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 97.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.0001 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.0001 mol Serum Creatinine * 113.12 g/mol = 0.01131 g Serum Creatinine. To convert 0.01131 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01131 g Serum Creatinine * 1000.0 mg/g = 11.31 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 11.31 mg Serum Creatinine/10.0 dL = 1.131 mg Serum Creatinine/dL. The concentration value of 97.0 µmol Serum Creatinine/L converts to 1.131 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.131/0.7)**-1.2 * 0.9938**55 * 1.012 = 57.39525.
Hence, the GFR value is 57.39525 ml/min/1.73 m²."
319,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-379,Extracted,"A 66-year-old white man comes to the physician because of a 10-day history of fatigue and lower leg swelling. Over the past 6 months, he has had a 3.6-kg (8-lb) weight loss. He has chronic bronchitis and uses an albuterol inhaler as needed. He has smoked one pack of cigarettes daily for 44 years and drinks one alcoholic beverage daily. His temperature is 37°C (98.6°F), pulse is 88/min, and blood pressure is 120/75 mm Hg. He appears thin. Examination shows 2+ pretibial edema bilaterally. Cardiopulmonary examination shows no abnormalities. Laboratory studies show:
Hemoglobin 11.2 g/dL
Leukocyte count 8500/mm3
Platelet count 130,000/mm3
Serum
Urea nitrogen 23 mg/dL
Glucose 77 mg/dL
Creatinine 1.6 mg/dL
Albumin 1.8 mg/dL
Total cholesterol 475 mg/dL
Urine
Blood negative
Glucose negative
Protein 4+
WBC 0–1/hpf
Fatty casts numerous
An x-ray of the chest shows a right upper lobe density. A CT scan of the chest shows a 2.5 x 3.5 x 2-cm right upper lobe mass.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [66, 'years'], 'creatinine': [1.6, 'mg/dL'], 'sex': 'Male'}",47.22466,44.86343,49.58589,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 66 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.6 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.6/0.9)**-1.2 * 0.9938**66 * 1.0 = 47.22466.
Hence, the GFR value is 47.22466 ml/min/1.73 m²."
320,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7393746-1,Extracted,"A 52-year-old woman presented with intermittent left lower quadrant pain that had started in 2017. She was diagnosed with systemic lupus erythematosus 19 years ago and had been taking oral corticosteroids since then. Her past medical history also showed steroid-induced diabetes mellitus, hypertension, and hypothyroidism, which was treated with levothyroxine. Menopause occurred when she was in her thirties.
On her first visit to the emergency department in another tertiary hospital in May 2018, she underwent abdominal pelvic computerized tomography (APCT), which showed a multiloculated lesion on the left adnexa, with left ovary involvement and hydrosalpinx or pyosalpinx. Under the impression of a TOA, she was admitted and received conservative care including intravenous (IV) antibiotics for 15 days. However, the pain in her left lower quadrant persisted. She visited the emergency department for the second time in July 2018. APCT was performed again, which revealed a slightly increased multiloculated, rim-enhancing lesion compared with the previous APCT findings. Again, the impression was TOA; however, APCT showed a newly developed wall enhancement of the left ureter due to either secondary change or combined ureteritis. Because of persistent pain, she agreed to undergo surgery. On August 3, 2018, the patient underwent laparoscope-guided bilateral salpingo-oophorectomy. The pathology report showed chronic active inflammation with foam cell collection in her left ovary and both salpinges.
Because the surgery did not alleviate her pain, she underwent both APCT and magnetic resonance imaging in April 2019, which revealed a 7-cm irregular mass in her left adnexa and an infiltrative lesion in her uterus, suggestive of endometrial cancer. Imaging results also showed left ureter invasion by the left adnexal tumor. As prophylactic management, a left ureter stent was inserted. Furthermore, she underwent dilatation and curettage for diagnosis. Pathological examination showed chronic active inflammation with foam cell collection, consistent with the finding in the previous laparoscopic surgery.
The patient visited the emergency department of our hospital on May 20, 2019. She had sepsis and a body temperature of >39°C; blood culture revealed the presence of extended-spectrum beta-lactamase–producing Escherichia coli. The cervix culture taken at the emergency department also showed the presence of the same organism. Her initial blood urea nitrogen level was 45.6 mg/dL, and her creatinine level was 2.75 mg/dL, which implied septic postrenal acute kidney injury. For septic shock evaluation, she underwent APCT without contrast, which revealed newly developed mild hydronephrosis of the left kidney. The left adnexal mass remained the same as that seen in April 2019 (). We started initial shock management in the emergency department and conservative care including an IV antibiotic (meropenem) for bacteremia and left percutaneous nephrostomy (PCN) for left hydronephrosis and acute kidney injury.
After her recovery from septic shock, the patient underwent debulking surgery on June 4, 2019. During the surgery, severe adhesion in the pelvis involving the peritoneum, rectum, uterus, and left ureter was noted. Multiple hard and catheter-shaped foreign body–like materials were observed in the left parametrium and left pararectal space and near the left internal iliac artery. Caseous necrotic materials had spread deep into the left pelvic and paravaginal space. Total hysterectomy and debulking operation of the left pelvic mass, including left pelvic lymph nodes, were performed.
The final pathology showed foamy histiocyte aggregation and acute and chronic inflammation with numerous Michaelis-Gutmann bodies, consistent with malakoplakia (). According to the recommended treatment for malakoplakia, we continued IV administration of tazoperan after the surgery. After the culture from peritoneal fluid cytology showed ceftazidime-sensitive E. coli, we changed the antibiotic to ceftazidime 1 g twice a day.
However, her creatinine level increased gradually to 4.48 mg/dL after the surgery. A retrograde pyelogram showed patent left ureter and dye spillage from the right ureter. Right PCN was performed. A computerized tomography scan performed on postoperative day 9 showed recurrence of a 9-cm mass in her left pelvis. Hence, we again administered tazoperan. On postoperative day 21, the patient was referred to a general hospital for further conservative care with IV antibiotics.
On July 24, approximately 1.5 months after surgery, she underwent left PCN removal and right PCN clamping. On August 2, the patient returned to the emergency department with complaints of fever and right flank pain that had started on the previous day. She presented with right costovertebral angle tenderness and pyuria and was admitted to the urology department with a diagnosis of right acute pyelonephritis. On August 9, the anterograde pyelogram showed leakage at the right ureter, which was similar to the previous retrograde pyelogram finding. Right PCN exchange was performed. After conservative care with IV antibiotics, the patient was discharged on August 12. On September 10, direct ureteroneocystostomy was attempted; however, only right PCN exchange was performed because the ureter was short.
The patient has been closely followed up through outpatient visits to both urology and obstetrics and gynecology departments.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [52, 'years'], 'creatinine': [4.48, 'mg/dL'], 'sex': 'Female'}",11.20987,10.64938,11.77036,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 52 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 4.48 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (4.48/0.7)**-1.2 * 0.9938**52 * 1.012 = 11.20987.
Hence, the GFR value is 11.20987 ml/min/1.73 m²."
321,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4342062-1,Extracted,"A 36-year-old Puerto Rican woman was hospitalized to our institution in March 2010 because of nephrotic syndrome and hemolytic anemia. Seven years before admission, she was diagnosed with SLE manifested by constitutional symptoms, malar rash, photosensitivity, oral ulcers, alopecia, Raynaud's phenomenon, arthritis, myalgias, lymphadenopathy, lymphopenia, anemia, positive antinuclear antibodies (ANA), elevated anti-dsDNA antibodies, and hypocomplementemia (C3 and C4). Early during the course of disease, she developed autoimmune pancreatitis, serositis, and membranous glomerulonephritis. Initially, she was treated with corticosteroids (including intravenous [IV] methylprednisolone therapy), hydroxychloroquine, IV pulse cyclophosphamide, and azathioprine. However, she had either partial clinical response or adverse events to these drugs for which she was started on mycophenolate mofetil in 2007. She achieved good clinical response with this therapy.
One month before admission, mycophenolate mofetil was discontinued due to severe diarrhea resulting in a severe SLE exacerbation. Upon admission she had oral ulcers, an erythematous maculopapular rash on her face, neck, and upper extremities, and anasarca. Initial laboratories showed a white blood cell (WBC) count of 6.6 × 109/L, neutrophil count of 6.3 × 109/L, lymphocyte count of 1.3 × 109/L, platelet count of 100 × 109/L, and hemoglobin of 8.7 g/dL. The peripheral blood smear revealed slight hypochromasia, anisocytosis, and poikilocytosis and the presence of reticulocytes. No schistocytes were seen. The reticulocyte count was elevated at 2.6% and the haptoglobin was decreased at 5.8 mg/dL. She had a serum creatinine of 1.53 mg/dL that rapidly worsened to 2.29 mg/dL after 48 hours. Serum albumin was decreased at 1.8 g/dL. The urinalysis showed >50 red blood cells (RBC)/high power field (hpf), 0–4 leukocytes/hpf, 3+ protein, and 0–2 granular casts/hpf. The urine protein-to-creatinine ratio was 2.1 which worsened to 8.6 eleven days later. The Westergren sedimentation rate was elevated at 48 mm/hr. Complement C3 and C4 were decreased at 14.6 mg/dL (90–180 mg/dL) and 2.0 mg/dL (10–40 mg/dL), respectively. Anti-dsDNA antibodies were not elevated.
The patient was treated with methylprednisolone 250 mg IV every six hours for 3 days, followed by methylprednisolone 1-2 mg/kg/day. Mycophenolate mofetil was restarted. During her hospital course she developed several complications including seizures, oliguria requiring transient hemodialysis, hypertensive crisis, and ascites. Rituximab 675 mg (375 mg/m2) IV weekly was started. Fifteen days after the first rituximab dose (7 days after the second infusion), the WBC count decreased to 2.8 × 109/L, neutrophil count to 2.0 × 109/L, and lymphocyte count to 0.6 × 109/L (). The next day, platelets decreased to 52 × 109/L. Cell counts continued to decrease with a nadir of 0.8 × 109/L for leukocytes, 0.3 × 109/L for neutrophils, and 28 × 109/L for platelets, 19 days after the first rituximab dose. Conversely, hemoglobin levels increased during this time. Thirty-nine days after the first rituximab dose (12 days after the fourth and final infusion), WBC and platelet counts returned to normal limits.
She responded favorably to rituximab therapy. Renal function improved and proteinuria significantly decreased. Upon discharge she had a WBC count of 4.6 × 109/L, neutrophil count of 3.3 × 109/L, platelet count of 122 × 109/L, hemoglobin of 11.4 g/dL, and serum creatinine of 0.9 mg/dL. She was discharged on prednisone 60 mg daily, hydroxychloroquine 200 mg twice daily, and mycophenolate mofetil 500 mg twice daily. Prednisone dose was gradually decreased until discontinued. After 4 years of follow-up the patient remained in clinical remission with normal WBC and platelet counts and renal function.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [36, 'years'], 'creatinine': [0.9, 'mg/dL']}",84.96875,80.72031,89.21719,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 36 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.9 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.9/0.7)**-1.2 * 0.9938**36 * 1.012 = 84.96875.
Hence, the GFR value is 84.96875 ml/min/1.73 m²."
322,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6701887-1,Extracted,"A 40-year-old female with no significant past medical history who was seen by her primary care physician for fatigue and workup revealed low hemoglobin, so she was asked to go to the emergency department (ED) for further evaluation. The patient has been complaining of fatigue, nausea, diarrhea, dysuria, and urinary frequency for more than seven days prior to presentation. On physical examination, the patient was pale, had mild abdominal tenderness, and left flank fullness was felt. Labs were repeated in the ED and were remarkable for a hemoglobin of 6.5 g/dL (down from 10 g/dL three months prior), white blood cell (WBC) count of 18 x 109/L, creatinine of 1.87 mg/dL (baseline is 1 mg/dL) with blood urea nitrogen (BUN) of 24 mg/dL. Urinalysis was remarkable for numerous WBC, positive bacteria, and nitrite. The patient received one unit of packed red blood cells and was started on ceftriaxone for urinary tract infection (UTI). No source of active bleeding was identified.
Gastroenterology team was consulted for the anemia, and they performed esophagogastroduodenoscopy (EGD) which was normal. Subsequently, they performed a colonoscopy which detected a fistula opening with surrounding nodularity close to the splenic flexure of the colon with a small amount of pus noted coming out of it (Figure ).
Shortly after, the patient spiked a fever of 102.7F. C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were both elevated. Based on the colonoscopy findings and the new fever, a computed tomography (CT) scan of the abdomen and pelvis with contrast was performed and it revealed chronic left kidney pyelonephritis with multiple contiguous abscesses in the inferior left kidney with a staghorn calculus concerning for XGP; it also showed the fistula between the left kidney and the splenic flexure of the colon (Figures -). The patient underwent exploratory laparotomy, takedown and repair of renocolic fistula, partial omentectomy, and left nephrectomy by urology and general surgery teams. The patient had an uncomplicated postoperative course and was discharged home on postoperative day six with stable hemoglobin of 8 g/dL.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [40, 'years'], 'creatinine': [1.87, 'mg/dL']}",34.46167,32.73859,36.18475,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 40 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.87 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.87/0.7)**-1.2 * 0.9938**40 * 1.012 = 34.46167.
Hence, the GFR value is 34.46167 ml/min/1.73 m²."
323,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8009464-1,Extracted,"A 77-year-old male with uncontrolled diabetes mellitus type II presented to our hospital with sudden onset hematuria and altered mental status. He was in his usual state of health, until about a week before the hospital presentation when he began to have generalized body fatigue. Symptoms developed into supra-pubic discomfort associated with frequency, urgency, dysuria, and gross hematuria involving the passage of clots. A day before the hospital visit, he was alert, oriented, and able to converse normally, but on the day of admission, he had been delirious and agitated for few hours. A review of systems was negative for weight changes, history of malignancy, urolithiasis, exposure to industrial chemicals, history of gastrointestinal tract disease, radiation therapy, and trauma.
Past medical histories were significant for coronary artery disease, diabetes mellitus type II, hypertension, benign prostatic hyperplasia, and gastroesophageal reflux disease. He had had coronary artery bypass surgery, a total metatarsal amputation due to chronic recurrent osteomyelitis, and angioplasty with stent placement in the lower extremity. There was no known drug allergy and home medications were atorvastatin, clopidogrel, metoprolol succinate, glargine, liraglutide, losartan, tamsulosin, famotidine. He resided in a house, had a 35 pack-year cigarette smoking, drank alcohol occasionally, and denied recreational drug use. Family history was significant for diabetes mellitus II, ischemic stroke, and transient ischemic attack.
On examination, the patient’s temperature was 100.6°C, his heart rate was 90 beats per minute, blood pressure 143/94 mm Hg, respiratory rate 18 beats per minute, and oxygen saturation 99% on room air. He appeared obese, confused, and agitated. He was alert to self, but not to time, place, or situation. The patient’s pupils were round and reactive to light. He was anicteric and dry mucosal, with a supple neck. The patient’s lungs exhibited decreased bilateral breath sounds due to body habitus. His heart had a regular rate and rhythms, as well as normal S1 and S2 sounds, with no gallops, rubs, or murmur. The abdomen displayed normative bowel sounds, was soft, and non-distended. There was no guarding, but there was tenderness at the suprapubic and costovertebral regions. Anal-rectal sphincter tone was normal and there was no mass in the rectum. The patient’s prostate was diffusely enlarged with normal palpation and the genitourinary examination showed gross hematuria, with clots. Testes were bilaterally descended with minimal atrophy. The patient’s extremities showed no ankle pitting edema. The results of the remaining examinations conducted were unremarkable.
Laboratory findings were significant for elevated lactate (2.7 mg/dl) (0.5-1.9), leukocytosis (28,100/uL), hemoglobin (Hgb) (11.1 gm/dl), hematocrit (HCT) (33.7%), and platelets (223 K/uL). The comprehensive metabolic panel was unremarkable, except for serum creatinine (1.6 mg/dl) (0.7-1.3), glucose (270 mg/dl) (74-106), and HbA1c (7.7%). Urinalysis revealed macroalbuminuria (>300 mg/dl), glucosuria (>1000 mg/dl), and ketonuria, leukocyte esterase, and leukocyturia (25-50 white blood cells per field, and too-numerous-to-count red blood cells per field). Prothrombin time (PT), partial thromboplastin time (PTT), international normalized ratio (INR), and ammonia levels were all normal. Electrocardiograph and chest X-ray results were both unremarkable. Computed tomography (CT) of the head was negative for acute pathology. CT of the abdomen and pelvis revealed dense material within the bladder, and air within the bladder wall, bilateral hydronephrosis, and hydroureter (Figures -).
The patient was fitted with a urinary (Foley) catheter. Blood and urine cultures were obtained, and broad-spectrum antibiotics of intravenous piperacillin-tazobactam and vancomycin were started. Throughout the hospital course, specialists in infectious disease and urology were consulted. Concerns for pyelonephritis, nephrolithiasis, urolithiasis, malignancy, gastrointestinal tract, and central nervous etiology were all low after extensive investigation. The patient’s symptoms were caused by urinary outlet obstruction in the setting of enlarged benign prostatic hyperplasia. After two days, the blood culture was negative, but the urine culture grew Escherichia coli (10,000-50,000 CFU/ml), sensitive to ceftriaxone. The antibiotic was de-escalated to ceftriaxone. The patient’s mental and clinical status improved on day 6. He was discharged with outpatient intravenous ceftriaxone (2 gm every 24 hours for 14 days), a urinary (Foley) catheter, and outpatient follow-up. At his three-week visit, the patient’s urinalysis and culture were normal. Pelvic sonography revealed normal bladder wall thickening and no intraluminal gas.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [77, 'years'], 'creatinine': [1.6, 'mg/dL'], 'sex': 'Male'}",44.10195,41.89685,46.30705,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 77 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.6 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.6/0.9)**-1.2 * 0.9938**77 * 1.0 = 44.10195.
Hence, the GFR value is 44.10195 ml/min/1.73 m²."
324,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5440791-1,Extracted,"A 2-year, 11-month-old Hispanic female presented to her primary care physician's office with swelling of the hands and face following one week of fever, sore throat, and malaise. A screening urine analysis (U/A) revealed 3+ protein and blood with numerous red blood cells per high power field. Further work-up also demonstrated anemia (Hb of 8.5 g/dl) and several electrolyte imbalances with azotemia (BUN 116 mg/dl and Cr 7.3 g/dl) prompting immediate transfer to our Children's Hospital for further evaluation and management.
On admission, examination revealed a pale child with bilateral mild pedal edema and blood pressure of 125/71 mm Hg. She was afebrile, mildly tachycardic, and saturating at 100% in room air and parents denied any h/o joint pain/swelling or skin rash. Her urine output was noted to be darker and less frequent over the past few days.
Past medical history was significant for an admission about 7 months back with respiratory distress and presumed pneumonia. Labs at that time were significant for severe anemia (Hb 6.9 g/dl) and iron deficiency. Initial chest X-ray showed bilateral diffuse peribronchial cuffing and nodular opacities with concerns for severe bronchiolitis/bronchopneumonia (). Patient was started on empiric antibiotic coverage but respiratory distress worsened to the point of requiring ventilator support. A work-up at that time showed elevated erythrocyte sedimentation rate (113 mm/hr) and negative serology for antinuclear antibody. A respiratory viral pathogen array came back positive for rhino virus. Patient's clinical condition continued to deteriorate and patient was placed on extracorporeal membrane oxygenation (ECMO). During this time patient was also started on high dose methylprednisolone with presumptive exaggerated inflammatory response to her viral pneumonia in a bid to reduce inflammation. Patient had a dramatic response to steroids and was off ECMO in 2 days and off ventilator support within a week time. A U/A done during this past hospital stay showed 1+ blood and no protein and a chemistry panel showed normal renal function with a serum creatinine of 0.41 mg/dl.
Work-up during this current admission confirmed anemia (Hb 7.8 g/dl) with a slightly elevated white blood cell count (10,400/mm3) and platelet count (234,000/mm3). Serum chemistry panel was abnormal for hyperkalemia (6 mmol/L), metabolic acidosis (Hco3 of 8 mmol/L), hypocalcemia (5.6 mg/dl), hyperphosphatemia (8.9 mg/dl), and renal failure (BUN 120 mg/dl and Cr 7.01 mg/dl). Further work-up involved evaluation as to identify the cause of glomerulonephritis and showed normal complement levels, normal coagulation profile, negative serology for viral etiology, lupus, and ANCA titers. Parathyroid hormone levels were elevated indicating a state of chronic kidney damage. ESR was elevated at 24 mm/hr but lesser than the prior admission value of 113 mm/hr and a CRP was not checked during the current admission. Urine protein to creatinine ratio was in the nephrotic range and antiglomerular basement membrane (GBM) titers were sent. Urine output recorded was between 1.5 and 2 ml/kg/hr during the initial few days but progressively got oliguric (0.3 to 0.5 ml/kg/hr) from the first week onwards. Renal ultrasound showed normal sized kidneys (right and left kidney around 7.2 cm) with increased cortical echogenicity bilaterally. A comparison of lab values during prior hospital stay and current admission is provided in .
Patient underwent emergent hemodialysis to correct electrolyte imbalances. We proceeded with a renal biopsy to ascertain a tissue diagnosis for the glomerulonephritis. 12 glomeruli were available for light microscopic examination. 9/12 glomeruli showed global sclerosis (). Remaining glomeruli showed cellular to fibrocellular crescents (). The interstitium is involved by a dense inflammatory infiltrate composed of lymphocytes, plasma cells, and scattered eosinophils. No definite granulomas were identified. Immunofluorescence showed intense linear glomerular capillary staining with IgG, Kappa, and lambda chains (). The renal biopsy findings were consistent with anti-GBM mediated crescentic glomerulonephritis.
Patient was started on high dose methylprednisolone and plasmapheresis once the biopsy results were consistent with anti-GBM disease. Anti-GBM titers (IgG antibody) also came back elevated at 1.1 units (Normal < 1) confirming the diagnosis. The subtle elevation in anti-GBM titers could be secondary to the possibility of a serological remission though chronic damage to the kidneys has already happened as documented by the amount of fibrosis on renal biopsy. Unfortunately anti-GBM titers were not checked during the initial pneumonia like presentation 7 months back which likely represented the initial acute episode. With every other day plasmapheresis, anti-GBM titers started trending down but renal function did not recover. With the extent of global sclerosis noted in renal biopsy and with the very high PTH levels, chances for renal recovery remained slim. Rituximab was used as an alternate immunosuppressive agent instead of cyclophosphamide taking into consideration the amount of chronic damage noted on renal biopsy in an attempt to reduce infectious risk. Patient received a total of 5 sessions of plasmapheresis with no improvement in renal function and was transitioned to peritoneal dialysis. During the inpatient stay she suffered a hypertensive crisis with seizures and the control of blood pressure required multiple antihypertensive agents. Anti-GBM titers were periodically monitored by lab work on a monthly basis and remained negative on maintenance immunosuppression with mycophenolate and low dose prednisone. Patient received a diseased donor kidney transplant, 2 months back, and is currently doing well with normal renal function.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [2, 'years', 11, 'months'], 'creatinine': [7.01, 'mg/dL'], 'sex': 'Female'}",8.9397,8.49272,9.38668,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 2 years, and 11 months old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 7.01 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (7.01/0.7)**-1.2 * 0.9938**2 * 1.012 = 8.9397.
Hence, the GFR value is 8.9397 ml/min/1.73 m²."
325,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8373194-1,Extracted,"A 93-year-old female presented to the ED with complaints of two episodes of black, tarry stool over the previous 24 hours that turned lime-green in color when it contacted the water in the toilet bowl. She expressed personal concern for GI hemorrhage, as she had a similar episode of melena one year prior and was subsequently found to have a gastric ulcer thought to be secondary to non-steroidal anti-inflammatory drug (NSAID) use. The ulcer was treated with endoscopic ablation and the patient had been symptom free since that time. Further past medical history included hypertension and stage III chronic kidney disease. Her only home medications included a daily multivitamin and an omega-3 polyunsaturated fatty acid supplement.
A detailed history obtained in the ED revealed that she had eaten a fast-food hamburger and frozen beverage the evening prior to the onset of her perceived melanotic stool. Further questioning revealed that the hamburger bun and beverage were both dyed black in color as a promotional event by the fast-food restaurant in celebration of Halloween. She denied ongoing NSAID use that had seemingly contributed to her previously mild upper GI bleed (UGIB).
The patient was hemodynamically stable with a blood pressure of 132/79 millimeters of mercury, a heart rate of 74 beats per minute, a respiratory rate of 16 breaths per minute, and an oxygen saturation of 96% on room air. She denied abdominal discomfort. Serology testing showed a chronic and otherwise stable hemoglobin of 11.0 grams per deciliter (g/dL) (reference range 11.5–15.5 g/dL), a blood urea nitrogen (BUN) of 17 milligrams per deciliter (mg/dL) (8–28 mg/dL), a creatinine of 1.8 mg/dL (0.5–1.5 mg/dL), and a BUN to creatinine ratio of 9.4.
Digital rectal exam done in the ED revealed a bright, lime-green stool without obvious evidence of melena or hematochezia. A guaiac FOBT (gFOBT) was performed. Despite the grossly bright, lime-green appearance of the specimen, this turned dark green to black in color with a blue hue when developer was introduced. Appearance of occult blood in stool specimens is considered when a blue coloration is appreciated on the indicator card. However, given the duration of the patient’s symptoms, the absence of acute anemia, the lack of observed melena on digital rectal exam, and the history of recent ingestion of artificially dyed food, a false positive gFOBT was considered.
A shared decision-making discussion on inpatient observation vs close outpatient follow-up was done with the gastroenterologist, the emergency physician, and the patient. Given the absence of melena on digital rectal exam, a stable hemoglobin level near her baseline, and patient preference, she was felt to be reasonable for close outpatient follow-up. Further, she had a calculated Glasgow-Blatchford Bleeding Score of 1, which would suggest a predicted survivability without intervention at a sensitivity of 98.6%. Following a four-hour observation period, she remained asymptomatic and without observed melena. The patient was discharged home with close outpatient follow-up the next day.
A repeat hemoglobin level obtained 12 hours after ED discharge was unchanged at 11.2 g/dL. A one-year follow-up of the patient’s medical record from her primary physician showed no return visits to the ED, and no diagnostic or therapeutic colonoscopy had been performed. Her hemoglobin levels remained stable within her baseline range of 11.0 to 12.3 g/dL in the one-year period since ED discharge.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [93, 'years'], 'creatinine': [1.8, 'mg/dL'], 'sex': 'Female'}",25.94572,24.64843,27.24301,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 93 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.8 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.8/0.7)**-1.2 * 0.9938**93 * 1.012 = 25.94572.
Hence, the GFR value is 25.94572 ml/min/1.73 m²."
326,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5570079-1,Extracted,"A 67-year-old Caucasian gentleman presented to his primary care physician with a chief complaint of hematochezia. A mass 1–2 cm above the anal verge was noted on digital rectal examination. Further historical evaluation detailed a history of progressive constipation, thin bowel movements, and an unintentional 15-pound weight loss over a 2-month period. At 50 years of age, he underwent a screening colonoscopy that was without mass or polyp. He had not undergone repeat colorectal screening since. His past medical history included seasonal allergies, hypercholesterolemia, and prostate cancer treated 17 years prior. There was no family history of known colorectal malignancy.
He was referred to a gastroenterologist who performed a diagnostic colonoscopy. A friable, exophytic mass was encountered 1 cm proximal to the anal verge. The pathology specimen stained positively with synaptophysin, chromogranin and TTF-1, which is consistent with small cell neuroendocrine carcinoma (Fig. ).
He was subsequently referred to a colon and rectal surgeon. Prior to this appointment, he was admitted to a small community hospital with abdominal discomfort and leukocytosis. Records from this facility demonstrated admission serum sodium of 122 mEq/L for which he was given two liters of intravascular normal saline. Laboratory evaluation was not repeated before his transfer to our hospital.
He was transferred to our institution the following day. At that time, he had a temperature of 36.5°C, pulse of 107 beats per minute, blood pressure of 135/62 mm/Hg, respiratory rate of 15 breaths/min, and an oxygen saturation of 94% on room air. His physical examination was remarkable for a palpable lower abdominal mass, a palpable rectal mass, and absence of peripheral edema. Serum laboratory evaluation returned the following results: hemoglobin level of 10.5 mg/dL, white blood cell count of 18 000, creatinine of 1.8 mg/dL, serum sodium of 118 mEq/L, glucose of 133 and serum osmolarity of 260 mOsm/kg. A CT scan of the abdomen and pelvis exhibited a 9.4 × 8.5 × 15.9 cm3 mass involving the posterior bladder, distal sigmoid, and proximal rectum. Urine electrolyte evaluation returned the following values: sodium of 73 mEq/L, potassium of 22.8 mEq/L and osmolarity of 432 mOsm/kg. The patient’s hyponatremia promptly resolved with fluid restriction and administration of tolvaptan, a competitive vasopressin receptor antagonist.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [67, 'years'], 'creatinine': [1.8, 'mg/dL'], 'sex': 'Male'}",40.74599,38.70869,42.78329,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 67 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.8 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.8/0.9)**-1.2 * 0.9938**67 * 1.0 = 40.74599.
Hence, the GFR value is 40.74599 ml/min/1.73 m²."
327,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4204721-1,Extracted,"A 74-year-old man with a history of cerebral infarction was admitted with watery diarrhea that had lasted for 1 month. PEG had been performed 9 months prior to this admission. The patient's condition had been stable for 8 months after PEG. Vital signs and laboratory results upon admission were as follows: blood pressure, 80/40 mmHg; body temperature, 36.8℃; white blood cell count, 18,300/µL; hemoglobin level, 13.2 g/dL; BUN level, 10.3 mg/dL; creatinine level, 0.9 mg/dL; urine white blood cell count, high. His septic condition improved after adequate hydration and the administration of broad-spectrum antibiotics. However, the postprandial watery diarrhea persisted. On the 12th day of hospitalization, an upper endoscopy revealed a gastrocolic fistula and the internal bumper of the PEG tube was not seen (). The feeding tube was withdrawn after the upper endoscopy. On the same day, a colonoscopy also revealed a gastrocolic fistula in the transverse colon (). Several metal clips were applied to seal the gastrocolic fistula opening (). Abdominal CT performed before upper endoscopy showed that the bumper of the feeding tube had migrated into the colonic lumen () and revealed a fistula tract between the stomach and colon (). In a radiologic study using gastrografin administered through the nasogastric tube 1 week later, there was no leakage of dye (). The patient was discharged with a nasogastric tube for feeding after the external opening of the gastrocolocutaneous fistula was closed. The patient has been alive in a nursing home for 3 months after discharge from the hospital.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [74, 'years'], 'creatinine': [0.9, 'mg/dL'], 'sex': 'Male'}",83.07152,78.91794,87.2251,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 74 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.9 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.9/0.7)**-0.302 * 0.9938**74 * 1.0 = 83.07152.
Hence, the GFR value is 83.07152 ml/min/1.73 m²."
328,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4421228-1,Extracted,"A 71-year-old woman presented at the outpatient clinic for the first time in 1973 with diffuse bone pain mainly in both wrists, shoulders and the spine. Clinical examination showed limb deformities (genu varum of the left leg, genu valgum of the right leg) and short stature (142 cm). At that time, she had already experienced multiple spontaneous fractures of the right and left femur. There was no family history of bone disorders (mother and father as well as seven brothers and sisters were healthy).
Laboratory tests at that moment showed: sodium 141 mmol/L (normal range 133–145), potassium 3.9 mmol/L (3.5–5.1), chloride 104 mmol/L (95–108), bicarbonate 23 mmol/L (23–29), calcium 9.8 mg/dL (8.4–10.2), phosphate 1.7 mg/dL (2.4–4.5), serum creatinine 0.72 mg/dL and alkaline phosphatase 120 U/L (53–141). Hyperparathyroidism was excluded. Urine analysis showed a daily phosphate excretion of 597 mg (300–1300), a daily calcium excretion of 39 mg (100–250) and a daily creatinine excretion of 852 mg (660–2200), corresponding to a fractional renal excretion of phosphate of 67%. At that time, the diagnosis of a congenital disorder with hypophosphataemia due to renal phosphate wasting, resulting in osteomalacia was considered. Treatment with oral phosphate and vitamin D replacement was initiated, resulting in a normalization of her serum calcium and phosphate. The following years, a few episodes of symptomatic hypo- and hypercalcaemia (with nausea and vomiting) could not be prevented. Figure shows the evolution over the years of the serum calcium and phosphate levels. Figure shows the evolution of the daily urinary excretion of calcium and phosphate.
In 1988, she developed hyperparathyroidism with a serum PTH (parathyroid hormone) level of 305 pg/mL (PTH-COOH-terminal assay, normal range 10–80). Ultrasonography showed a left retrothyroidal, hypoechogenic nodule with a diameter of 10 mm, which was proven to be a parathyroid adenoma at subsequent surgery. Her postoperative serum PTH level was 91.9 pg/mL (PTH-intact assay, normal range 10–65). In 1994, the serum intact PTH level rose to 714 pg/mL, and an asymptomatic hypercalcaemia of 11.4 mg/dL was noted. Ultrasonography showed a large node (diameter 18 mm) in the dorsal, inferior side of the right thyroid lobe and a smaller node (diameter 6 mm) in the dorsal, inferior side of the left thyroid lobe. A total parathyroidectomy was performed, with subcutaneous reimplantation of one small parathyroid gland piece, superficial to the left musculus sternocleidomastoideus. Pathological examination of all resected parathyroid tissue showed diffuse multinodular hyperplasia. Postoperatively, the serum PTH level dropped to 5 pg/mL. In the year 2000, the PTH serum level rose again to 337 pg/mL, while an asymptomatic hypercalcaemic episode (serum calcium level 12.5 mg/dL) was noted, leading to surgical removal of the remaining parathyroid tissue.
In the 90s, she developed chronic kidney disease stage IV (serum creatinine level between 1.5 and 2.5 mg/dL, corresponding to a creatinine clearance of 20–30 ml/min) (Figure ), associated with a minimal proteinuria (0.3 g/24 h). Repeated renal ultrasonography during follow-up showed bilateral small kidneys (7–8 cm in length), with a thin hyperechoic cortex. In June 2007, a CT scan of the abdomen showed bilateral diffuse, small medullary calcifications in both kidneys (Figure ). Moreover, an 8-cm tumoural mass was noted in the inferior pole of the left kidney. In July 2007, a retroperitoneoscopic radical left nephrectomy was performed. Postoperatively, chronic intermittent haemodialysis had to be initiated. Pathological examination of the left kidney showed a renal clear cell carcinoma, without invasion of the surrounding tissues, compatible with a Fuhrman histological grade 3 lesion and an anatomic pT2N0M0 tumour (2002 TNM staging system). Pathological examination of the surrounding kidney tissue showed important interstitial fibrosis and tubular atrophy. There was an interstitial lymphocytic infiltrate. Moreover, several interstitial calcifications were present (Figure ). Since the resection of the renal clear cell carcinoma was curative, no adjuvant therapy was given. Up until now, 8 months postoperatively, no tumour recurrence has occurred.
The patient has one daughter, one grandson and one granddaughter. None of them have bone abnormalities.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [71, 'years'], 'creatinine': [0.72, 'mg/dL'], 'sex': 'Female'}",89.33383,84.86714,93.80052,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 71 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.72 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.72/0.7)**-1.2 * 0.9938**71 * 1.012 = 89.33383.
Hence, the GFR value is 89.33383 ml/min/1.73 m²."
329,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5607972-1,Extracted,"A 21-year-old man from a remote area in Western Australia was initially referred by the general practitioner (GP) to the renal service in 2001 with peripheral oedema and a family history of “nephritis” in his deceased grandfather. Serum creatinine was 150 μmol/L and urinary protein 1.5 g/24 h.
Renal biopsy at the time revealed focal segmental glomerulosclerosis (FSGS) with three out of six glomeruli revealing segmental sclerosis. The patient received corticosteroids with no improvement in proteinuria, therefore corticosteroids were tapered and ceased after three months.
Ten years later, the patient was in stage 4 chronic kidney disease and had relocated to the Metropolitan area. Arteriovenous fistula was created in anticipation for future need for dialysis. Two months after relocating, the patient developed status epilepticus and required admission to the intensive care unit (ICU). Magnetic resonance imaging (MRI) of the brain revealed multifocal, bi-hemispherical white matter lesions. (). Brain biopsy was performed which revealed minor and essentially nonspecific findings with no morphological changes diagnostic of an active vasculitis. In view of multiple cerebral infarcts and the well-recognized fact that a considerable proportion of cerebral biopsies performed in such cases could be non-diagnostic, the patient was treated for primary central nervous system (CNS) vasculitis. He received six doses of monthly IV cyclophosphamide followed by azathioprine for 12 months along with tapering dose of steroids. He had developed cortical blindness and required prolonged neurologic rehabilitation. He required ongoing hemodialysis, started during the above admission.
Twelve years after initial presentation, at 33 years of age, the patient was undergoing regular, uneventful maintenance hemodialysis and was assessed for suitability for renal transplant. He was found to have severe left ventricular hypertrophy on electrocardiogram (ECG) during renal transplant work up, despite having normal blood pressure and not being on any antihypertensive medications. Dobutamine stress test revealed severe dynamic left ventricular outflow obstruction and the possibility of familial hypertrophic cardiomyopathy was suggested. Coronary angiography was essentially normal.
A detailed assessment of the family history at this stage revealed that patient’s maternal grandfather had died in his thirties of renal failure presumably secondary to “chronic nephritis.” Patient’s mother was a single child of this person and had four children including one elder son aged 56 years who was apparently normal, and two younger daughters. The other family members had no symptoms to raise concerns. The patient is unmarried and has no children. With multi-system involvement (kidneys, CNS and heart) and positive family history, FD was suspected.
Blood sample was then sent to the national reference laboratory after explaining the suspected diagnosis of FD and its implications. Low leucocyte AGAL levels (0.2 n mol/min/mg protein [normal 0.7-3.3]) confirmed the diagnosis.
Molecular analysis of GLA gene revealed that the patient was hemizygous for p.N34T mutation resulting in the replacement of an asparagine residue with threonine residue, a mutation that has not been reported previously.
The initial renal biopsy was retrieved and reviewed by EM at this point and revealed the characteristic laminated electron-dense lipid deposits in endothelial cells and macrophages giving rise to zebra stripe and myelin body appearances ().
The patient was started on Fabrazyme (Alfa galactosidase beta; 1 mg/kg fortnightly) infusions to be continued for life. One year follow up revealed no further seizures (on anti-epileptic therapy), transient ischemic attack (TIA) or stroke, while continuing on maintenance haemodialysis.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [21, 'years'], 'creatinine': [150.0, 'µmol/L'], 'sex': 'Male'}",58.21568,55.3049,61.12646,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 21 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 150.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 150.0 µmol. To convert 150.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 150.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00015 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00015 mol Serum Creatinine * 113.12 g/mol = 0.01697 g Serum Creatinine. To convert 0.01697 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01697 g Serum Creatinine * 1000.0 mg/g = 16.97 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 16.97 mg Serum Creatinine/10.0 dL = 1.697 mg Serum Creatinine/dL. The concentration value of 150.0 µmol Serum Creatinine/L converts to 1.697 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.697/0.9)**-1.2 * 0.9938**21 * 1.0 = 58.21568.
Hence, the GFR value is 58.21568 ml/min/1.73 m²."
330,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7880830-1,Extracted,"A 69-year-old female with a past medical history of hypertension, hyperlipidemia, type 2 diabetes mellitus, morbid obesity, and chronic kidney disease stage 3A with baseline creatinine of 1.3-1.9 was complaining of shortness of breath for two days and was found unresponsive at home by her husband. Emergency medical services were called. En-route to the emergency room, she was found pulseless and initial rhythm showed ventricular fibrillation. The patient received CPR for 45 minutes, direct current cardioversion counter shocks of 360 J each, total of 1080 J were implemented and multiple boluses of epinephrine, amiodarone, lidocaine, and magnesium were given to restore effective cardiac rhythm. After the third attempt of defibrillation she converted to sinus rhythm. She was then transferred to the ICU. Her initial arterial blood gas was suggestive of respiratory acidosis with pH of 7.14, Pco2 of 84, and Po2 of 98. She was intubated with pressure support mechanical ventilation with the following settings: FiO2 of 100 %, respiratory rate of 32, tidal volume of 400 mL, and positive end expiratory pressure of 5. Her vital signs after the event were as follows; blood pressure of 110/80 mmHg, pulse was 110/min, and oxygen saturation was at 95% with the ventilation setting. Electrocardiogram after the event showed sinus tachycardia. Chest roentgenogram was suggestive of mild pulmonary edema. Her troponin level was 0.18 ng/mL (normal range <0.04 ng/mL) followed by 0.44 ng/mL and 0.43 ng/mL. On examination the patient was minimally following command. Her breath sound was coarse bilaterally with no other remarkable physical examination findings. Her initial laboratory work up showed potassium of 4 mmol/L (normal reference 3.7-5.1 mmol/L), blood urea nitrogen of 35 mg/dL (normal reference 6-24 mg/dL), and creatinine of 1.70 mg/dL (normal reference 0.50-1.10 mg/dL). Echocardiography of the heart showed ejection fraction of 50%-55% and motion wall abnormality of basal, mid anterior, and inferior wall suggestive of underlying MI, which was a new finding as compared to the old report. Cardiac catheterization could not be performed due to her critical condition. On second day of her hospitalization, she started became anuric (urine output <100ml/24 h) and her creatinine started rising up causing acute kidney injury (AKI). Her further laboratory works up during the hospital course are listed in the table (Table ). Her urinalysis showed no red blood cells, pyuria or bacteria, but did show some granular casts. A renal ultrasound was negative for obstruction, and her fractional sodium was found to be 4.5%. The patient’s CK level peaked at 6380 U/L (normal range 26-192 U/L), myoglobin was >20,000 ng/mL (normal range 9-83 ng/mL), and myocardial bound (CK-MB) isoenzyme of CK was 4.5 ng/mL (normal range 0-3.6 ng/mL). The patient’s renal function did not improve with fluid loading as a part of resuscitation post CPR initially considering it to be prerenal cause or with stress dose furosemide (1 mg/kg) after the diagnosis of intrinsic AKI was made. However, her plasma creatinine rose to 5.71 mg/dL. She was started on hemodialysis. However, her kidneys continued to show minimal renal recovery and the patient was transferred to a long-term care facility. Elective left heart catheterization was done after a month later as per cardiology recommendation. She was found to have total occlusion in the right coronary artery (RCA) and received percutaneous coronary intervention to RCA. However, her renal recovery has been minimal and the patient still receiving hemodialysis three times a week.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [69, 'years'], 'creatinine': [5.71, 'mg/dL']}",7.53796,7.16106,7.91486,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 69 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 5.71 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (5.71/0.7)**-1.2 * 0.9938**69 * 1.012 = 7.53796.
Hence, the GFR value is 7.53796 ml/min/1.73 m²."
331,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7011916-1,Extracted,"A 67-year-old man with past medical history of coronary artery disease (CAD) status post coronary artery bypass graft (CABG), history of alcoholism, and history of chronic kidney disease stage 3 presented with chest pain for 1 week. Chest pain was intermittent, left sided, 8/10 in severity, non-radiating, dull in nature, exacerbated by exertion and mildly relieved by rest. Remaining review of system was negative. He stopped taking all his cardiac medications for 1 year. Vitals were as follows: blood pressure 130/76 mm Hg, pulse 142/beat per minute respiratory rate 18/min. Pulse oximetry was 97% on 2 L nasal cannula. Cardiac examination was significant for tachycardia with irregularly irregular pulse but no murmur, rub or gallops. Lungs were clear to auscultation. Other system examinations were unremarkable. Laboratory data showed sodium 137 (136 - 145 mmol/dL), potassium 5.1 (3.5 - 5.2 mmol/dL), chloride 105 (96 - 110 mmol/dL), bicarbonate 22 (24 - 31 mmol/dL), blood urea nitrogen (BUN) 37 (5 - 25 mg/dL), creatinine 1.85 (0.44 - 1.0 mg/dL), glucose 130 (70 - 99 mg/dL), aspartate transaminase (AST) 176 (10 - 42 IU/L), alanine transaminase (ALT) 208 (10 - 60 IU/L), international normalized ratio (INR) 1.39, and thyroid stimulating hormone (TSH) 6.87 (0.3 - 4.5 IU/mL). Serum troponin was 0.01 (reference value < 0.04 ng/mL). Electrocardiogram (EKG) showed 2:1 atrial flutter. Initially patient was given cardizem and β-blocker boluses but heart rate did not improve. He was loaded with amiodarone 150 mg intravenous push (IVP) over 10 min and continued on amiodarone drip 1 mg/min over 6 h. Heparin drip was started for anticoagulation. On the following day morning labs showed significantly elevated liver enzymes and worsening renal function from his base line on the day of admission. AST was 4,250 (10 - 42 IU/L), ALT 2,422 (10 - 60 IU/L), and INR 2.28. Creatinine was 3.2 mg/dL (0.44 - 1.0 mg/dL), and BUN 44 mg/d reference value (5 - 25 mg/dL). At that moment patient was hemodynamically stable with blood pressure (BP) of 105/55 mm Hg, HR 70 beats per min and pulse ox of 95% on room air. Six hours later, patient became confused and unable to protect his airways. A rapid response was called, and the patient was intubated for airway protection and transferred to intensive care unit (ICU). Amiodarone was immediately stopped. Right upper quadrant ultrasound, a computed tomography (CT) of the chest, abdomen and pelvis without contrast were normal. Blood cultures, toxicology screen including acetaminophen level, hepatitis panel, antinuclear antibodies (ANAs), anti-smooth muscle antibody (ASMA), antimitochondrial antibody (AMA) were all negative. Alpha-1 antitrypsine (A1AT) was 126 (90 - 200 mg/dL), and ceruloplasmin 18 (17 - 54 mg/dL). Hereditary hemochromatosis mutation with C282Y heterozygote and H63D was negative. Patient was immediately started on N-acetylcysteine drip for 72 h. Patient’s liver enzymes continued to rise and peaked at 21,000 (10 - 42 IU/L) for AST and 9,020 (10 - 60 IU/L) for ALT (, ). Total bilirubin increased to 3.9 (, ). INR was 3.8 (day 3 of admission) (). Patient was deemed not a candidate for liver transplant due to history of alcoholism and acute-on-chronic kidney injury. As patient’s kidney function continued to worsen, he was started on hemodialysis (on the fifth day). His platelets count began to drop on day 3. Heparin-induced thrombocytopenia was suspected and heparin was stopped. Heparin-induced platelet antibodies with reflex to serotonin were positive. Patient was started on argatroban but serotonin release assay came back negative. Patient was successfully extubated to nasal cannula on day 8. LFTs improved and came down AST 79, ALT 192, and albumin of 2.5. INR was falsely high when patient was receiving argatroban () but improved after argatroban was stopped. Kidney function eventually improved, and he did not need more hemodialysis.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [67, 'years'], 'creatinine': [3.2, 'mg/dL'], 'sex': 'Male'}",20.42828,19.40687,21.44969,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 67 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.2 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.2/0.9)**-1.2 * 0.9938**67 * 1.0 = 20.42828.
Hence, the GFR value is 20.42828 ml/min/1.73 m²."
332,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6206852-1,Extracted,"We present the case of a 77-year-old ambulatory man with hypertension, sarcoidosis, complete atrioventricular block status post-pacemaker implantation, chronic kidney disease due to FSGS, and right facial nerve paralysis, who presented with sporadic gait and right face numbness. He was diagnosed with sarcoidosis by biopsy of a tumor in front of the right tibia 14 years before presentation. Since the tumor and abdominal lymphadenopathy were the only manifestation of sarcoidosis and no other signs of organ involvement were present, he received no immunosuppressive treatment. The abdominal lymphadenopathy had been stable over time. Nine years before presentation, he was referred to our nephrology clinic to determine the cause of chronic kidney disease. His serum creatinine level was 1.2 mg/dL and he had proteinuria of 0.4 g per day. Hematuria was not present. Renal biopsy revealed six globally sclerotic glomeruli among all 34 glomeruli (18%) and some residual glomeruli with segmental sclerosing lesions, but no involvement of sarcoidosis. He was diagnosed with primary FSGS. Since the proteinuria was mild, he did not receive immunosuppressive treatment.
One year after that, the patient experienced palpitations and was diagnosed with complete atrioventricular block. Coronary angiography showed no significant stenosis of the coronary arteries, and he underwent pacemaker implantation. Whether sarcoidosis contributed to the complete atrioventricular block was unclear. The abdominal lymphadenopathy and the dyskinesia of the ventricular septum were stable and did not progress over time.
The patient was stable for eight years, until when he started to suffer from sporadic gait and right face numbness that occurred and resolved within a day every few weeks. Three months later, the symptoms recurred along with sudden dysarthria and left limbs weakness. Physical findings were notable for pronator drift on the left side. Perfusion computed tomography (CT) with iodinated contrast and CT angiography revealed no ischemic lesions or occlusion of major cerebral arteries. The symptoms disappeared three hours after the onset. A transient ischemic attack (TIA) was suspected, and he was admitted to the stroke unit. Ultrasonography revealed no stenosis of the internal carotid arteries, and transesophageal echocardiogram showed no abnormalities of the atrial septum. His pacemaker detected paroxysmal atrial fibrillation, which was presumed to be the etiology of the TIA. Thus, edoxaban 30 mg per day was started and he was discharged after one week of hospitalization.
One month after his discharge, his left leg started to swell and his gait worsened. Urinary protein excretion was 0.6 g per day, serum creatinine was at the baseline level of 1.6 mg/dL, and serum albumin level was 3.8 g/dL. Although no coagulopathy was found, ultrasonography revealed left femoral vein thrombosis that was 41 mm long. Edoxaban was stopped, and heparin was administered intravenously for two weeks. Low mobility due to his gait was presumed to be the cause of development of deep vein thrombosis (DVT). The patient was switched to warfarin and was discharged, but the left leg edema persisted. Three months later, he developed complications of urinary retention and constipation.
Four months after discharge, the patient presented to the emergency department with sudden left leg pain and inability to walk. The entire left lower limb was slightly pale and had slow pitting edema. The left dorsal artery was not palpable, and the left femoral artery was barely palpable. Contrast CT revealed occlusion of the left femoral and superficial femoral arteries together with the known DVT in the left femoral vein (Fig. , ). Emergency thrombectomy for acute arterial occlusion was performed and the leg perfusion resumed. The emboli (maximum of 23 mm in diameter) were sent for pathological examination. The patient was admitted to the hospital and started on heparin infusion in place of oral warfarin. The history of recent TIA implied hypercoagulable state, but again no coagulopathy was found. While malignancy screening was being planned, the pathology of the arterial emboli revealed an unusual and surprising finding: the surface of the thrombi was filled with large atypical lymphoid cells (Fig. ) and was covering the necrotic interior of the thrombi. Immunohistochemical analysis showed that the tumor cells on the surface and the necrotic interior of the thrombi were positive for CD20 and CD79a but negative for CD3 (Fig. , ), which is characteristic of B cells. Leukocytosis was absent (white blood cell, 4,000/μL; segmented neutrophil, 55%; lymphocyte, 34%; monocyte, 9%; eosinophil, 2%). Serum soluble interleukin-2 receptor level was 1,548 U/mL (normal, 122–496 U/mL); lactate dehydrogenase (LDH) level, 808 U/L (normal, 120–245 U/L); LDH-2 fraction, 39% (normal, 28–35%), and LDH-3 fraction, 32% (normal, 21–27%). These findings were consistent with large B-cell lymphoma with intravascular proliferation, but the etiology of the aortic thrombi was unclear.
The hematology consultation team considered that the patient needed further biopsy to determine the etiology. Bone marrow biopsy showed normocellular marrow with normal maturation, but with infiltration of CD79a-positive large atypical lymphoid cells within the small vessels (Fig. , ). Although no lymphadenopathy was detected on palpation, CT scan showed swollen bilateral axillary and inguinal lymph nodes, which were up to 30 mm in diameter. While surgical biopsy of the right axillary lymph node and random skin biopsy were planned for diagnosis, the patient developed a complication of sepsis presumably due to pyelonephritis on hospital day nine. Piperacillin/tazobactam and vancomycin were started. Because partial thromboplastin time was prolonged, biopsies were withheld. Although white blood cell and neutrophil counts were improving, the patient died due to sudden respiratory and cardiac arrest on hospital day twelve. The patient had a do-not-resuscitate order. His family agreed to an autopsy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [77, 'years'], 'creatinine': [1.6, 'mg/dL'], 'sex': 'Male'}",44.10195,41.89685,46.30705,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 77 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.6 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.6/0.9)**-1.2 * 0.9938**77 * 1.0 = 44.10195.
Hence, the GFR value is 44.10195 ml/min/1.73 m²."
333,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7397629-1,Extracted,"A 62-year-old man with ESRD secondary to diabetes presented to Toronto General Hospital with shortness of breath on exertion for 3 years. His co-morbidities include type 2 diabetes, coronary artery disease, gout, hypertension, hyperlipidemia, hypothyroidism, asthma, and obstructive sleep apnea treated by continuous positive airway pressure (CPAP). His mobility was limited by dyspnea (especially with stairs). Given his poor functionality, he was unable to complete any formal exercise program. He denied any chest pain, orthopnea, and paroxysmal nocturnal dyspnea.
He was diagnosed with asthma 10 years ago with pulmonary function testing (PFTs). His pulmonary obstruction was not substantiated by a methacholine challenge. At that time, he presented with shortness of breath on exertion, chest tightness, and occasional cough. He had a remote history of smoking and occasional alcohol use. He was regularly seen in our chronic kidney disease program 3 years prior to the initiation of renal replacement therapy. At that time, PFTs showed a decrease in lung volumes and airflow obstruction with normal diffusive capacity. Based on symptom severity, his inhaler regime included salbutamol (100 mcg) 2 puffs twice daily, ipratropium (17 mcg) 2 puffs twice daily, salmeterol – fluticasone (50/500) 2 puffs twice daily, montelukast 10 mg once daily, ciclesonide (160 mcg) 2 puffs once daily and tiotropium (1.25 mcg) 2 puffs once daily (Table ).
At the time of hemodialysis initiation, his vital signs were stable, body weight was 99 kg, and there was pronounced bilateral edema. His cardiac examination revealed normal heart sounds with no audible murmurs. There were no abnormal pulmonary findings.
His initial laboratory testing were consistent with ESRD (urea 40 mmol/L, creatinine 775 μmol/L, hemoglobin 107 g/L, ferritin 280 ng/mL, potassium 4.4 mmol/L, bicarbonate 22 mmol/L, calcium 2.27 mmol/L, phosphate 1.93 mmol/L, albumin 36 g/L, intact parathyroid hormone (PTH) 28 pmol/L and an urine protein creatinine ratio 704 mg/mmol).
He was initiated on conventional hemodialysis (4 h per session, 3 times a week) in February 2018 due to volume overload. He adhered to his dialysis treatment schedule, and his weight gradually decreased by 7 kg in 3 months. His respiratory symptoms improved, and he was able to exercise using a stationary bicycle without exertional dyspnea. However, he remained dependent on bronchodilators (Table ). PFTs were repeated in April 2018 (see Table ). Of note, there was no evidence of airflow limitation. Additional diagnostic tests included a normal electrocardiogram and chest X-ray (Fig. ). Transthoracic echocardiogram showed an ejection fraction of 55%. Ventricular and atrial assessments showed normal geometry and function bilaterally. CT scan of thorax demonstrated no evidence of interstitial thickening, air trapping, pulmonary edema, or bronchiectasis.
During 8 weeks of home hemodialysis training, his weight decreased by another 5 kg. The patient’s symptom gradually improved, he denied dyspnea on exertion, or asthmatic attack. His asthmatic medication was tapered as shown in Table . He was converted to nocturnal home hemodialysis in June 2018. His hemodialysis prescription was 8 h per session, 4 times a week via left radio-cephalic AV fistula with bicarbonate base dialysate. The remaining dialysis treatment parameters were noted below: Revaclear®; Polyethersulfone membrane, surface area of 1.8 m2, urea mass transfer area coefficient (KoA) 1439 mL/min, ultrafiltration coefficient (UFC) 54 ml/hr./mmHg, Blood flow rate (Qb) 350 ml/min and dialysate flow rate (Qd) 500 ml/min.
Within 3 months of home hemodialysis, our patient reported further improvement of dyspnea. He indicated that his activities were no longer limited by his respiratory symptoms, and he was able to climb 2 flights of stairs.
His asthma medications were subsequently tapered completely as shown in Table .
Routine hemodialysis laboratory data were collected after 3 months of home hemodialysis initiation. His results reflected his intensive hemodialysis prescription (urea 18 mmol/L, creatinine 554 mmol/L, hemoglobin 123 g/L, bicarbonate 23 mmol/L, albumin 41 g/L, calcium 2.29 mmol/L, phosphate 1.35 mmol/L and PTH 37.9 pmol/L.) His urea reduction ratio was 85% with a single-Pool Kt/V of 2.53. Moreover, the patient had a diagnostic methacholine test, and excluded any pulmonary obstruction. His pulmonary function is shown in Table .","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [62, 'years'], 'creatinine': [775.0, 'µmol/L']}",6.33717,6.02031,6.65403,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 62 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 775.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 775.0 µmol. To convert 775.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 775.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00077 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00077 mol Serum Creatinine * 113.12 g/mol = 0.0871 g Serum Creatinine. To convert 0.0871 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.0871 g Serum Creatinine * 1000.0 mg/g = 87.1 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 87.1 mg Serum Creatinine/10.0 dL = 8.71 mg Serum Creatinine/dL. The concentration value of 775.0 µmol Serum Creatinine/L converts to 8.71 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (8.71/0.9)**-1.2 * 0.9938**62 * 1.0 = 6.33717.
Hence, the GFR value is 6.33717 ml/min/1.73 m²."
334,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6787834-1,Extracted,"A 53-year-old man was referred to our hospital for evaluation and management of hypertension and hypokalemia. He was diagnosed with hypertension at the age of 40 years, and his blood pressure was poorly controlled with a calcium channel blocker (nifedipine at 40 mg/d). He also had a past medical history of vasospastic angina and was a nonsmoker and social drinker. In addition, he had no family history of cardiovascular diseases. On admission, the patient was 168 cm tall and weighed 59 kg. He was afebrile, with a blood pressure of 161/96 mm Hg and a regular pulse of 61 beats per minute. There was no evidence of lung rales, cardiac murmurs, or an abdominal bruit. His neurological examination was unremarkable. Laboratory tests revealed that his serum creatinine level was 1.1 mg/dL, urea nitrogen level was 19 mg/dL, and serum sodium level was 140 mEq/L. He also exhibited hypokalemia with a serum potassium concentration of 2.9 mEq/L; however, he had no subjective symptoms, including muscle weakness. Plasma renin activity (PRA), plasma aldosterone concentration (PAC), and aldosterone-to-renin ratio (ARR) were <0.1 ng/mL/h, 292 pg/mL, and >2920, respectively. Other adrenal hormone levels were within normal limits. A chest radiograph and transthoracic echocardiogram showed no significant findings. An electrocardiogram suggested nonspecific ST-T wave changes with premature atrial contractions.
Primary hyperaldosteronism was suspected, and therefore, a captopril challenge test and a saline infusion test were performed. All these investigations revealed positive test results (Table ), which confirmed a diagnosis of PA. A low-dose dexamethasone suppression test to exclude the diagnosis of subclinical Cushing's syndrome was negative. An abdominal computed tomography (CT) scan was performed, which showed a left adrenal mass (13 mm) (Figure ). In adrenocorticotropic hormone (ACTH)-stimulated AVS, although aldosterone hypersecretion was observed in the left adrenal gland, the lateralization of the disease was not determined due to incomplete cannulation of the right adrenal vein (Table ). The criteria of successful cannulation were based on the current Expert Consensus Statement.
131I-adosterol scintigraphy under dexamethasone suppression showed an equivalently increased uptake in both adrenal glands (Figure ). Because we could not exclude the bilateral PA, including aldosterone-producing adenoma (APA) with microadenoma in the right adrenal gland, we performed the medical therapy with mineralocorticoid receptor antagonists (MRA). Although we administrated multiple antihypertensive agents including an MRA (eplerenone at 100 mg/d), an angiotensin II receptor blocker (azilsartan at 40 mg/d), a dual action beta blocker/alpha-1 blocker (carvedilol at 20 mg/d), a calcium channel blocker with an increased dose (nifedipine at 80 mg/d), an alpha-1 blocker (doxazosin at 2 mg/d), and an alpha-2 agonist (guanabenz at 4 mg/d), a home reading of the patient's blood pressure was above 140/90 mm Hg. Moreover, he needed a large quantity of potassium chloride to compensate for his hypokalemia.
Despite intensive medical therapy, he underwent percutaneous coronary intervention due to stable angina. Following this, we performed AVS again, but the right adrenal vein was not successfully cannulated (Table ). We discussed further the indication for surgery and decided to remove the left adrenal gland. After laparoscopic left adrenalectomy, his blood pressure and serum potassium remained normal after the withdrawal of eplerenone, doxazosin, guanabenz, and potassium chloride and a dose reduction of azilsartan (at 20 mg/d), carvedilol (at 10 mg/d), and nifedipine (at 10 mg/d). The PRA and PAC were 0.8 ng/mL/h and 57.1 pg/mL, 3 months after the adrenalectomy, respectively. Macroscopic findings of the resected specimen showed a yellowish colored nodule (13 mm in diameter) in the adrenal gland. We confirmed a diagnosis of an adrenocortical adenoma based on a histopathologic examination (Figure ); we also confirmed that the tumor cells were rich in the cytoplasm and were eosinophilic without malignant cells.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [53, 'years'], 'creatinine': [1.1, 'mg/dL'], 'sex': 'Male'}",80.27027,76.25676,84.28378,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 53 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.1/0.9)**-1.2 * 0.9938**53 * 1.0 = 80.27027.
Hence, the GFR value is 80.27027 ml/min/1.73 m²."
335,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7772176-1,Extracted,"A 76 year-old-man with DM controlled on metformin was admitted for a decline in his overall well-being. His friends reported he had become fatigued, forgetful, less involved, missed medications, and had lost some weight. He reported passing foul-smelling dark urine but denied dysuria, frequency, fevers, chills, or rigors. He denied abdominal pain, nausea, vomiting, or a history of recent urinary bladder instrumentation.
On admission, his oral temperature was 98°F, blood pressure was 166/94 mmHg, pulse was 66 beats per minute and the respiratory rate was 18 breaths per minute. His physical examination was unremarkable, and he was alert and oriented to person, place and year. Complete blood count was normal, but serum creatinine was 1.7 mg/dl. Other electrolytes, including sodium, were normal. His glycosylated hemoglobin was 5.6%. Computed tomography (CT) of the brain showed moderate to severe small vessel ischemic changes but no acute abnormality. Rapid plasma reagin (RPR) was negative, and vitamin B12 and thyroid-stimulating hormone levels were normal. Urinalysis revealed pyuria and urine culture grew > 100,000 CFU/mL Escherichia coli and Klebsiella pneumoniae. Blood cultures obtained on admission were negative. CT images of the chest, abdomen, and pelvis performed to rule out malignancy showed diffuse bladder wall thickening with air seen circumferentially within the bladder wall (Figures -).
Based on his clinical presentation, microbiologic and radiologic findings, he was diagnosed with emphysematous cystitis, a rare complication of lower urinary tract infection. He was initially treated with empiric intravenous piperacillin/tazobactam then discharged to a nursing facility on ertapenem (Escherichia coli strain was an extended spectrum beta-lactamase producer). A urinary catheter was inserted for effective bladder drainage, and he completed a total of 14 days of antibiotic therapy. After completion of antibiotic therapy, a repeat CT of the abdomen and pelvis showed complete resolution of the bladder wall emphysematous changes.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [76, 'years'], 'creatinine': [1.7, 'mg/dL'], 'sex': 'Male'}",41.26331,39.20014,43.32648,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 76 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.9)**-1.2 * 0.9938**76 * 1.0 = 41.26331.
Hence, the GFR value is 41.26331 ml/min/1.73 m²."
336,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4421736-1,Extracted,"A 68-year-old woman presented with 1-week of weakness, dyspnea and several episodes of hemoptysis. Her medical history included hypertension, aortic stenosis [aortic valve area of 1.09 cm, mean gradient 19.74 mmHg on two-dimensional echocardiography (2DE)] and chronic obstructive pulmonary disease related to a 60-year smoking history. One month prior to presentation, she had experienced stiffness in her shoulders and was started on a corticosteroid, sulfasalazine and methotrexate for presumed rheumatoid arthritis. She had no recent history of a gastrointestinal illness.
At presentation, she was normotensive (121/76 mmHg). Her hemoglobin was 13.3 g/dL (133 g/L), platelets 241 × 109/L and serum creatinine 1.7 mg/dL (150 μmol/L). Blood cultures were negative, and chest X-ray showed non-specific bilateral interstitial markings. She was admitted with a presumptive diagnosis of congestive heart failure and pneumonia. Her sulfasalazine and methotrexate were held.
Transthoracic 2DE revealed normal left ventricular function and unchanged aortic stenosis. Her right ventricular systolic pressure was estimated to be 57 mmHg. Urinalysis showed trace protein and moderate blood. Abdominal ultrasound revealed normal-sized kidneys without evidence of obstruction.
By her 12th day of admission, her hemoglobin was 9.9 g/dL (99 g/L), platelets 63 × 109/L, serum creatinine 5.9 mg/dL (523 μmol/L) and blood urea nitrogen 120 mg/dL (43 mmol/L). Her LDH was 442 U/L, haptoglobin 1.1 mg/dL (0.11 g/L) and reticulocyte count 143 × 109/L. An autoimmune workup was positive for anti-nuclear antibody (ANA) in anti-centromere pattern (1:320). Her C4 was normal at 0.18 g/L, and C3 was mildly decreased at 0.87 g/L. Antineutrophil cytoplasmic antibodies, rheumatoid factor and antiextractable nuclear antigen antibodies were negative. Red blood cell fragmentation was noted on her blood film, prompting a renal biopsy that was consistent with a TMA (). She was transferred to a tertiary care hospital for PLEX.
Her ADAMTS-13 activity (drawn prior to the first cycle of PLEX) was estimated by qualitative collagen binding assay and was normal []. She was started on an angiotensin receptor blocker that was eventually changed to an angiotensin-converting enzyme-inhibitor following discontinuation of PLEX. She required ongoing hemodialysis and platelet transfusions. Bone marrow biopsy was normal. She received nine daily 1–1.5 plasma volume exchanges with cryosupernatant plasma, without a response in platelet count [platelets were 49 × 109/L and hemoglobin 8.4 g/dL (84 g/L) on Day 9]. PLEX was discontinued due to lack of response.
A thoracic computed tomography scan demonstrated a 4.4 cm by 3.1 cm mediastinal mass which was not seen on chest X-ray as well as enlarged mediastinal lymph nodes (largest 1.5 cm) and pleural effusions (). A biopsy was not pursued because of her deteriorating status. She died on her 31st day of admission following sudden onset of confusion and hepatitis.
Autopsy findings included an acute organized lung injury, extensive steatohepatitis and renal cortical infarctions. A high-grade malignancy was found in her mediastinum involving multiple lymph nodes. Tumor cells showed marked variability in size and shape, with nuclei having a characteristic ‘salt and pepper’ pattern by hematoxylin and eosin staining (). Immunostaining on the largest node was positive for CD56, synaptophysin, chromogranin (), low-molecular weight cytokeratin and pan-keratin but was negative for TTF-1, S100 and CD45. Transmission electron microscopy revealed intracytoplasmic membrane-bound neuroendocrine granules within tumor cells (). Overall, these findings were consistent with neuroendocrine carcinoma and did not support a diagnosis of melanoma, lymphoma or bronchogenic carcinoma. No definitive primary lesion was identified.
A post-mortem quantitative enzyme immunoassay for ADAMTS-13 activity using frozen serum demonstrated actually revealed mild deficiency prior to PLEX at 0.45 U/mL [].","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [68, 'years'], 'creatinine': [1.7, 'mg/dL'], 'sex': 'Female'}",32.4623,30.83918,34.08541,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 68 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.7)**-1.2 * 0.9938**68 * 1.012 = 32.4623.
Hence, the GFR value is 32.4623 ml/min/1.73 m²."
337,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-1387,Extracted,"A 38-year-old woman comes to the physician because of persistent diarrhea and fatigue for 1 month. She has had up to 12 watery stools per day. Sometimes she awakens at night because she has to defecate. She has abdominal bloating and cramps. She has had a 2-kg weight loss in the past month. She returned from a trip to Costa Rica 7 weeks ago. She has a history of bronchial asthma and bulimia nervosa. She works as a nurse. She does not smoke and drinks 1–2 beers on the weekend. Current medications include fish oil, a multivitamin, and a salbutamol inhaler. Her temperature is 36.8°C (98.2°F), pulse is 65/min, and blood pressure is 100/75 mm Hg. Examination shows dry mucous membranes. Abdominal and rectal examinations are unremarkable. Laboratory studies show:
Hematocrit 46%
Leukocyte Count 6,500/mm3
Platelet Count 220,000/mm3
Serum
Na+ 136 mEq/L
K+ 3.2 mEq/L
Cl- 102 mEq/L
HCO3- 33 mEq/L
Mg2+ 3.3 mEq/L
Urea nitrogen 14 mg/dL
Creatinine 0.8 mg/dL
Abdominal ultrasound shows no abnormalities. Colonoscopy shows dark colored mucosa with interspersed white spots. Biopsies of colonic mucosa are obtained and sent for pathological evaluation.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [38, 'years'], 'creatinine': [0.8, 'mg/dL'], 'sex': 'Female'}",96.65854,91.82561,101.49147,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 38 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.8 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.8/0.7)**-1.2 * 0.9938**38 * 1.012 = 96.65854.
Hence, the GFR value is 96.65854 ml/min/1.73 m²."
338,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4145832-1,Extracted,"A 52-year-old Caucasian woman presented to a healthcare center with high fever, sore throat, itchy rash, generalized muscle pain, and nausea, which had continued for 15 days. The patient’s husband and son had similar complaints over the same period. She was administered Penicillin G, antihistaminic and antipyretic drugs. Because her condition did not improve, she was referred to a dermatology clinic with the suspicion of urticarial vasculitis. She received antihistaminic and depot steroid treatment there and a consultation with the infectious diseases department was requested. Her body temperature was 39°C (centigrade), her pulse rate was 96 beats/minute, and respiratory rate was 22 breaths/minute at first examination. She had a generalized maculopapular rash spread over her entire body, even the palms of her hands and the soles of her feet. Our patient had bilateral cervical and axillary painful and mobile lymphadenopathies.
Her laboratory test results were as follows; serum urea: 151mg/dL (normal range: 10 to 50mg/dL), serum creatinine: 2.6mg/dL (normal range: 0.6 to 1.1mg/dL), lactate dehydrogenase (LDH): 608U/L (normal range: 207 to 414U/L), total protein: 5.8g/dL (normal range: 6.4 to 8.3g/dL), albumin: 2.7g/dL (normal range: 3.8 to 5.1g/dL), white blood cell (WBC) count: 22,300/μL (normal range: 4300 to 10,300/μL), red blood cell (RBC) count: 4.02×106/μL (normal range: 4.38 to 5.75×106/μL), hemoglobin: 12.4g/dL (normal range: 13.6 to 17.2g/dL), erythrocyte sedimentation rate (ESR): 45mm/h, C-reactive protein (CRP): 52mg/L (normal range: 0 to 5.0mg/L).
Abdominal ultrasonography (USG) revealed that hepatomegaly was present. All other intra-abdominal structures were normal. Her cervical USG revealed a large number of reactive lymphadenopathies at submandibular, submental, posterior cervical, upper and lower jugular regions bilaterally and at the right and left submandibular regions. Some of them were conglomerated. There were also several reactive lymphadenopathies at both her axillary regions, which were observed on the axillary ultrasonography. A thoracic computed tomography (CT) scan was performed because our patient’s chest radiography revealed several uncertain nodular lesions. The thoracic CT scan presented widespread areas of air trapping. Bilateral multiple lymphadenopathies were present in the aortic pulmonary, prevascular, precarinal, paratracheal, subcarinal and left supraclavicular regions.
Levofloxacin treatment was initiated empirically at the dermatology clinic. On the fifth day, this treatment was discontinued and our patient was transferred to the infectious diseases clinic because there was no improvement in her signs and symptoms.
Measles, Rubella, Epstein-Barr virus (EBV), Cytomegalovirus (CMV), Toxoplasma immunglobulin (Ig) M tests were reported to be negative. The tests for Ricketsiosis, Coxiellosis, Brucellosis and Tularemia were reported to be negative. The autoimmune markers were studied to exclude a rheumatologic disease and found to be negative.
On the twelfth day of admission, our patient’s WBC count increased to 35,000μL and her hemoglobin decreased to 10.6g/dL (normal range: 13.6 to 17.2g/dL). Therefore, our patient was referred to the hematologists. A total of 45% polymorphonuclear leukocytes (PMN) (50% band form), 40% lymphomonositer cells (50% atypical lymphocytes), and 11% eosinophils were identified in her peripheral blood smear. Dysplasia was also present in neutrophils. A bone marrow biopsy and tests were performed, yielding no positive results.Desquamation spread over her entire body (Figure ), an evident erythematous rash on her palms and soles, dyspnea, chest pain and hypertension developed in the following days. Kawasaki syndrome was suspected. Our patient consulted with a chest diseases specialist and a cardiologist. An electrocardiogram and echocardiogram were performed and no cardiologic cause was found for her symptoms. Bronchodilator and antihypertensive agents were added to the treatment.
After insistent efforts of repeated medical history taking, we learned that the patient’s son had brought mercury home from school in a bottle and had spilled it on the hot stove. All of the family members (mother, father and son) were exposed to this environment of dense mercury fumes for a long period of time. Because mercury fumes are colorless and odorless, they were unable to detect it. Approximately 10 hours after this event, our patient’s husband developed dyspnea, hypertension, tachycardia, high fever and sore throat. He was admitted to the healthcare institution with these complaints. A physical examination of the patient revealed no pathological findings other than hypertension (tension arterielle (TA): 160/100mmHg) and erythema in the legs. His laboratory test results showed leucocytosis (WBC count: 13,200/μL (normal range: 4300 to 10300/μL)). Other laboratory findings were considered normal. His complaints improved with the supportive treatment administrated at the respiratory diseases clinic of the hospital. He was discharged after eight days of hospitalization, but a personality disorder developed in the following days.
The 14-year-old son suffered from high fever, sore throat, skin rash, diarrhea, and dyspnea. He was admitted to the pediatric hospital with these complaints. A physical examination revealed the following: fever: 39°C, TA: 110/50mmHg, respiratory rate: 20 breaths/minute, pulse: 104 beats/minute. A generalized maculopapular rash was spread over the patient’s entire body, and he was identified with hyperemia in the conjunctivas and cervical and bilateral axillary lymphadenopathy. Rhoncuses were determined in the lungs by oscultation. No abnormal laboratory findings, other than leucocytosis (WBC count: 11,100/μL (normal range: 4300 to 10,300/μL)) were identified. The patient was initially given empirical doxycycline and bronchodilator therapy based on the family history. A thoracic CT scan was performed. Consolidation areas containing air bronchograms were detected in the paracardiac region in the right lung middle zone. Ceftriaxone and clarithromycin were included in his treatment. The tests performed revealed no findings of infection. Material was submitted to the reference laboratory for blood and urine mercury level tests upon persistent fever on day 10 of hospitalization.
The son’s serum and urine mercury levels were analyzed using the inductively coupled plasma - mass spectrometer (ICP-MS) method in the reference laboratory. His serum mercury level was 130μg/L (normal range: 0.6 to 59μg/L), and his urine mercury level was 31μg/L (normal range: 0.1 to 20μg/L). He received chelating therapy after high levels of mercury were identified in his blood. Therefore, our patient’s serum and urine mercury levels were analyzed using the ICP-MS method in the reference laboratory. Her serum mercury level was 207μg/L (normal range: 0.6 to 59μg/L), and her urine mercury level was 524μg/L (normal range: 0.1 to 20μg/L).
The diagnosis of mercury intoxication was also corroborated by the consulted toxicologist. The toxicologist recommended the administration of penicillamine instead of dimercaprol as our patient recovered from the acute period. A dosage of 300mg of penicillamine every six hours was administered for seven days. Her clinical and laboratory test results were significantly improved by the treatment. No side effects of penicillamine were seen and our patient was discharged.
Her husband’s serum mercury level was 197μg/L (normal range 0.6 to 59μg/L), and his urine mercury level was 412μg/L (normal range 0.1 to 20μg/L). Therefore, he received the same treatment as his wife.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [52, 'years'], 'creatinine': [2.6, 'mg/dL'], 'sex': 'Female'}",21.53605,20.45925,22.61285,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 52 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.6 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.6/0.7)**-1.2 * 0.9938**52 * 1.012 = 21.53605.
Hence, the GFR value is 21.53605 ml/min/1.73 m²."
339,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8418825-1,Extracted,"A 63-year-old woman with a past medical history of diabetes, hypertension, and hypothyroidism presented for evaluation of repeat episodes of an itchy rash on her body after exposure to the sun, as well as recurrent erythema on her abdomen that appeared each time she cooked at a stove. Both of her skin conditions had been present for at least three years. She provided a photograph of periumbilical erythematous hives on her abdomen that repeatedly developed when she would cook at the countertop stove (Figure ). Her current medications included levothyroxine, losartan, and metoprolol.
In addition, she would develop hives not only in sun-exposed but also in sun-covered areas after being outside. To demonstrate the lesions, prior to a follow-up visit she stood outside in the parking lot for 15 minutes with her pants and sandals on. Extremely pruritic, erythematous urticarial lesions developed on both covered and exposed areas of her legs and arms (Figure , ). Skin biopsies from both an affected area on her left anterior thigh and a normal-appearing site on her left lateral thigh were performed (Figure ).
Microscopic examination of the lesional skin biopsy showed widening of the spaces between the collagen bundles, consistent with edema. In addition, occasional eosinophils were present not only in the dermal blood vessels but also in the dermis (Figure ). In contrast, the biopsy from the normal-appearing skin did not show any pathologic alteration; there was neither increased space between the collagen bundles nor eosinophils in the dermis (Figure ).
Laboratory studies were performed. These included a complete blood count, comprehensive metabolic panel, serum protein electrophoresis, thyroid-stimulating hormone, thyroxine, triiodothyronine as well as tests for complement components, DNA antibodies, HIV antibodies, rheumatoid factor, ribonucleic protein antibody, scleroderma-70 antibodies, Sjogren syndrome A antibody, Sjogren syndrome B antibody, Smith antibody, and thyroid antibodies (peroxidase). All of the studies were either negative or normal except for a blood urea nitrogen/creatinine ratio of 23 (normal, six to 22), creatinine level of 1.05 mg/dL (normal, 0.50-0.99 mg/dL), and thyroid peroxidase antibodies of 157 IU/mL (normal, less than nine IU/mL).
Correlation of the clinical history, pathologic changes, and laboratory studies established not only a diagnosis of solar urticaria but also heat urticaria. Her initial management included histamine 1 (H1) and histamine 2 (H2) antihistamines, specifically fexofenadine 180 milligrams and famotidine 20 milligrams in the morning, and hydroxyzine 10 milligrams and famotidine 20 milligrams in the evenings. She tolerated this therapeutic regimen without any adverse effects.
A follow-up visit showed that all symptoms and lesions resolved and did not recur even with occasional exposure to sunlight when she took the medications as prescribed. However, any variance of treatment resulted in recurrence of her urticaria, specifically when going outside. She continues to be managed on her current therapy without any additional flares of urticaria.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [1.05, 'mg/dL'], 'sex': 'Female'}",59.70296,56.71781,62.68811,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 63 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.05 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.05/0.7)**-1.2 * 0.9938**63 * 1.012 = 59.70296.
Hence, the GFR value is 59.70296 ml/min/1.73 m²."
340,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6020510-1,Extracted,"A 25-year-old female with no prior medical history presented to the emergency department due to high fever (up to 39°C) since 3 days. She complained of left flank pain and gross hematuria. On physical examination, left costovertebral angle tenderness was noted. The urinalysis confirmed the hematuria (2055 red blood cells per high-power field). The urinary dipstick was negative for leukocyte esterase and for nitrites, but significantly positive for albuminuria (2+). On microscopic examination of the urine, pyuria was minimal (6 white blood cells per high-power field) and no bacteriuria was noted. She denied having taken antibiotics before presentation. Urine and blood cultures were obtained. The laboratory tests revealed a significantly elevated C-reactive protein (CRP = 28 mg/dl), a high erythrocyte sedimentation rate (107 mm/h), and an elevated creatinine (1.21 mg/dl) with normal blood urea nitrogen (16 mg/dl).
She was admitted to the internal medicine ward with a preliminary diagnosis of acute pyelonephritis, and she was started on intravenous ceftriaxone. A contrast-enhanced computed tomography the next day revealed a hypoenhancing region in the upper pole of the left kidney, suggestive of pyelonephritis (). However, considering the significant hematuria in the absence of pyuria and bacteriuria, and the persistently elevated creatinine (1.55 mg/dl on day 3), a nephrologist was consulted. Microscopic evaluation of the urinary sediment revealed dysmorphic red blood cells suggesting glomerular disease (2 red blood cell casts and 60–80 red blood cells per high-power field with >10% of G1 cells and >80% dysmorphic erythrocytes). The spot urine protein to creatinine ratio obtained on the 5th day of hospital stay was also elevated (929 mg/g). Furthermore, both urine and blood cultures came back negative, and no fever was recorded during the hospital stay. Ceftriaxone was discontinued after 7 days of treatment.
A biopsy of the left kidney was performed at the 6th day of hospital stay and confirmed a diagnosis of IgA nephropathy (immunofluorescence was strongly positive for mesangial IgA deposition, complement component C3, and lambda light chains and moderately positive for IgM). The patient denied any recent respiratory tract infection symptoms. Other lab tests sent during her hospital stay were normal (lactate dehydrogenase, anti-neutrophil cytoplasmic antibodies, antinuclear antibodies, anticardiolipin IgG and IgM, anti-beta-2 glycoprotein I IgG and IgM, protein electrophoresis, serum complement C3c and C4 level, rheumatoid factor, and transesophageal echocardiography). She was started on lisinopril 5 mg daily. Furthermore, considering the significant proteinuria, the elevated creatinine and the negative prognostic features of the biopsy, (M1E1S1T0C1 according to the Oxford classification []) she was started on glucocorticoids (three-day pulse of methylprednisolone 1g in months 1, 3, and 5 in addition to oral prednisolone 0.5 mg/kg every other day for 6 months) []. At follow-up at 2 months, both creatine (0.86 mg/dl) and the spot urine protein to creatinine (114 mg/g) were normal. CRP at follow-up was 0.4 mg/dl.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [25, 'years'], 'creatinine': [0.86, 'mg/dL'], 'sex': 'Female'}",96.08668,91.28235,100.89101,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 25 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.86 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.86/0.7)**-1.2 * 0.9938**25 * 1.012 = 96.08668.
Hence, the GFR value is 96.08668 ml/min/1.73 m²."
341,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7916314-1,Extracted,"An 83-year-old man had a two-year history of proteinuria (2+) that had become worse in the year before admission. He complained of progressive proximal lower limb muscle weakness for 10 months before admission. He was admitted to our hospital because of upper and lower limb, neck flexor and extensor, and flexor and extensor digitorum muscle weakness, and pitting edema of the legs. He had a medical history of atrial fibrillation and hypertension. He had smoked five cigarettes per day for the decade before he turned 30.
On admission, predominantly proximal symmetrical muscle weakness and leg pitting edema were observed. His manual muscle testing (MMT) scores were: neck flexion = 4; neck extension = 4; deltoids = 3; biceps brachii = 3; triceps brachii = 3; flexor and extensor muscles of the hand = 4; flexor and extensor digitorum muscle = 3; iliopsoas = 2; gluteus maximus = 2; quadriceps = 2; hamstring = 2; flexor and extensor muscles of the foot = 5. His blood pressure was 120/80 mmHg. Laboratory tests on admission showed serum creatinine and albumin levels of 0.7 mg/dL and 2.9 g/dL, respectively, and his urinary protein creatinine ratio was 7.3 g/gCr, suggesting nephrotic syndrome. Serum creatine kinase (820 U/L), aldolase (13.7 IU/L), and urinary myoglobin levels were initially elevated, but after admission they normalized and myoglobinuria disappeared. All autoantibodies (i.e., antinuclear antibodies [ANA], anti-double stranded DNA [anti-dsDNA] antibodies, anti-Ro/SS-A antibodies, anti-La/SS-B antibodies, anti-aminoacyl tRNA synthetase [anti-ARS] antibodies, anti-cyclic citrullinated peptide [anti-CCP] antibodies, anti-mitochondrial M2 [AMA2] antibodies, acetylcholine receptor [AChR] antibodies, and anti-muscle-specific kinase [anti-MuSK] antibodies) were negative. Although serum immunoglobulin (Ig) G was decreased (705 mg/dL), IgA (159 mg/dL) and IgM (37 mg/dL) were within normal range. Bence Jones protein (BJP)-lambda was observed in both the blood and urine, the serum free light chain lambda was 533 mg/L, the serum kappa/lambda ratio was 0.046, and the M protein level was 0.575 g/dL. The plasma cell count in the bone marrow was 0.7%, indicating MGUS. Magnetic resonance imaging (MRI) scan showed proximal lower limb muscle atrophy and edema, including the quadriceps femoris, obturator, and gluteus maximus muscles (Fig. ). Needle electromyogram was performed in the first dorsal interosseous, deltoid, and iliopsoas muscles. Although it showed fibrillation potential and positive sharp waves, it also showed complex repetitive discharge, low amplitude, and early recruitment, suggestive of myogenic changes. Nerve conduction study of the median, ulnar, tibial, and sural nerves was normal (Table ). Therefore, the patient was diagnosed with myopathy as the cause of the predominantly proximal symmetrical muscle weakness.
A muscle biopsy of the right vastus lateralis muscle was performed on the 25th day of admission. Light microscopy showed a small cluster of atrophic angulated fibers in addition to mild fiber size variation on hematoxylin and eosin (HE)–stained sections. On nicotinamide adenine dinucleotide-tetrazolium reductase (NADH-TR), some fibers minimally lacked oxidative activity (Fig. a). On modified Gomori trichrome, one atrophic fiber was filled with fine cytoplasmic inclusions (Fig. b). Although we thought they were reminiscent of nemaline bodies, we could not confirm the nature of this structure as a sample for electron microscopic study was not available. Congo red positivity in the sarcolemma membrane and vascular walls was observed (Fig. c, d, e). Immunofluorescence staining of frozen muscle tissue showed that lambda and kappa light chains were negative (Fig. ). Considering the clinical course and histopathological findings, the patient was diagnosed with amyloid myopathy.
A percutaneous renal biopsy was performed on the 35th day of admission to determine the cause of nephrotic syndrome. Light microscopy showed an accumulation of eosinophilic, amorphous deposits in the mesangial region and part of the capillary walls in HE-stained sections (Fig. a), periodic acid–Schiff–stained sections (Fig. b), and periodic acid–methenamine-silver–stained sections (Fig. c), which were determined to be amyloid proteins as they were stained positive by direct fast scarlet staining (Fig. d). Amyloid proteins were also observed in the blood vessel walls. As these amyloid proteins were positive for p-component staining and negative for amyloid A staining, β2-microglobulin, and pre-albumin, we diagnosed the patient with AL amyloidosis. Approximately 40% interstitial fibrosis and tubular atrophy was observed. Immunofluorescence staining of frozen tissue showed that lambda light chains were positive in the mesangial region (Fig. a). Staining with IgG, IgA, IgM, complement component 3 (C3)c, C1q, and kappa light chains were negative (Fig. b). Electron microscopy showed amyloid fibrils in the mesangial region (Fig. ). Thus, the patient was diagnosed with AL amyloidosis caused by BJP-lambda.
Each examination was subsequently performed for systemic amyloidosis. Although echocardiography showed mild left ventricular diastolic dysfunction without characteristic findings for cardiac amyloidosis such as a classical granular sparkling appearance, we did not exclude cardiac amyloidosis because 1) both serum NT-pro brain natriuretic peptide (BNP) (369.7 pg/mL) and troponin T levels (0.166 ng/mL) were elevated and 2) the patient had a history of atrial fibrillation. Amyloid protein was negative in the colon biopsy. Finally, the patient was diagnosed with AL amyloidosis involving the kidneys, muscles, and possibly the heart.
The patient was treated with MD (melphalan, 8 mg and dexamethasone, 20 mg daily for 4 days) therapy for AL amyloidosis. Although his cardiac function and respiratory function did not decline, the muscle weakness grew worse, and the nephrotic syndrome, renal insufficiency, and serum free light chain level did not improve. Twenty-one months after therapy commenced, the serum creatinine level had increased to 1.2 mg/dL, and his MMT scores were: neck flexion = 3; neck extension = 3; deltoids = 2–3; biceps brachii = 2–3; triceps brachii = 2–3; flexor and extensor muscles of the hand = 2–3; flexor and extensor digitorum muscle = 2–3; iliopsoas = 1–2; gluteus maximus = 1–2; quadriceps = 1–2; hamstring = 1–2; flexor and extensor muscles of the foot = 2–3.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [83, 'years'], 'creatinine': [1.2, 'mg/dL']}",60.00373,57.00354,63.00392,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 83 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.2 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.2/0.9)**-1.2 * 0.9938**83 * 1.0 = 60.00373.
Hence, the GFR value is 60.00373 ml/min/1.73 m²."
342,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8104137-1,Extracted,"A 55-year-old woman was consulted to evaluate renal dysfunction from the department of head and neck surgery. Two months ago, oral cavity cancer, histologically squamous cell carcinoma, was diagnosed. A 2.4 × 1.6 × 2.0 cm sized enhanced mass around the right retromolar trigon in neck computed tomography (Fig. A). The mass extended to the right buccal space and invaded part of the pterygoid muscle. Focal segmental glomerulosclerosis positron emission tomography/computed tomography showed FDG-avid mass lesion around the right retromolar trigon (Fig. B). When diagnosing oral cavity cancer, the renal function was normal, except for 1+ proteinuria on urinalysis. Surgeons decided to be treated with 1 cycle of neoadjuvant chemotherapy (docetaxel and cisplatin) and wide tumor excision.
One month after neoadjuvant chemotherapy and surgery, generalized edema with heavy proteinuria and severe renal dysfunction developed. On physical examination, a coarse breathing sound with rhonchi was heard in both lower lung fields, and 2+ pretibial pitting edema on both lower extremities was noted. Laboratory findings revealed a white blood cell count of 7090/mm3, hemoglobin level of 9.9 g/dL, platelet count of 287,000/mm3, blood urea nitrogen level of 58 mg/dL, serum creatinine level of 3.67 mg/dL, and serum albumin level of 2.7 g/dL. Urinalysis revealed 4+ proteinuria with hematuria. The urine protein/creatinine ratio was 17578.51 mg/g. Viral markers for hepatitis B, C, and human immunodeficiency virus were negative. Anti-nuclear antibody, anti-neutrophil cytoplasmic antibody, and C3/C4 levels were within normal limits. We performed the ultrasound-guided renal biopsy. The findings showed segmental or global collapse of glomerular capillaries with marked hyperplasia and swelling of overlying epithelial cells, suggesting a collapsing variant of FSGS (Fig. ). There is patchy mononuclear inflammatory cell infiltration in the interstitium and mild interstitial fibrosis with tubular loss and atrophy. Electron microscopic findings showed diffuse effacement of the foot process of the external capillary surface, segmental wrinkling of the glomerular basement membrane, and no immune deposits in the mesangium.
Initially, we prescribed oral prednisolone at a dose of 1 mg/kg/day. Despite immunosuppressive treatment, renal function has deteriorated. We performed hemodialysis after internal jugular vein catheterization. After 23 sessions of hemodialysis and high-dose oral glucocorticoid treatment, renal function slowly recovered to a serum creatinine level of 1.6 mg/dL and started to taper the glucocorticoid. Eight months after initial treatment, we discontinued oral prednisolone and checked urinalysis and renal function regularly. After 2 and half years of follow-up, the patient was in a cancer-free state and maintained normal renal function (Fig. ).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [55, 'years'], 'creatinine': [1.6, 'mg/dL']}",37.85185,35.95926,39.74444,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 55 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.6 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.6/0.7)**-1.2 * 0.9938**55 * 1.012 = 37.85185.
Hence, the GFR value is 37.85185 ml/min/1.73 m²."
343,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4190298-1,Extracted,"The patient was a 62 year-old Caucasian man with a long-standing history of essential hypertension and a 4-year history of MM (IgG kappa subtype). The latter was diagnosed after suffering a T7 compression fracture. At that time, his kidney function was normal (serum creatinine: 0.9 mg/dL (79.56 μmol/L)) and his blood pressure was fairly well controlled on four agents (carvedilol extended-release 80 mg daily, diltiazem 60 mg three times daily, valsartan 320 mg daily and hydralazine 25 mg three times daily). As initial therapy for MM, he received melphalan for conditioning, four cycles of lenalidomide and dexamethasone, followed by autologous HSCT. Three months later, his kidney function remained within normal limits. He subsequently developed a few episodes of volume depletion associated with transient increases in serum creatinine level, after which his serum creatinine stabilized at a level of 1.4 mg/dL (123.76 μmol/L). Ten months after HSCT, he was started on bortezomib, cyclophosphamide and dexamethasone (VCD) due to progression of MM. He received five cycles of VCD. His blood pressure remained fairly well controlled with no changes to his anti-hypertensive regimen. Fifteen months after the first HSCT and 1 month after completing VCD, he underwent a second autologous HSCT for relapse. This time, the hospital course was complicated with septic shock and a severe bout of AKI, with serum creatinine peaking at 7.4 mg/dL (654.16 μmol/L). After requiring four weeks of acute hemodialysis, he partially regained kidney function, ultimately being discharged from the hospital with a new baseline serum creatinine of 2.1 mg/dL (185.64 μmol/L). At the time of discharge, his antihypertensive regimen was modified to avoid blockade of the renin-angiotensin system in the setting of AKI. Accordingly, he was switched to hydralazine 50 mg three times daily, diltiazem extended-release 360 mg daily, metoprolol 200 mg twice daily and a clonidine patch 0.3 mg/24 h.
Seventeen months after the second HSCT, a follow-up bone marrow biopsy specimen revealed persistent plasma cell infiltration. As a result, he was initiated on carfilzomib (20 mg/m2; followed by 27 mg/m2, four weeks apart), thalidomide 100 mg daily and dexamethasone 20 mg per week. Six weeks after the initiation of chemotherapy, the patient developed abrupt worsening of lower extremity edema and his hypertension became more difficult to control. After being stable with four agents (hydralazine, diltiazem, metoprolol and clonidine) averaging a blood pressure of 142/74 mmHg during previous office visits, he presented with a blood pressure of 206/100 mmHg (Figure ). His physical examination also revealed pallor, but otherwise no additional abnormalities. Laboratory data showed: hemoglobin 8.2 g/dL (5.09 μmol/L), platelet count 53 K/cumm, serum creatinine 2.1 mg/dL (185.64 μmol/L), lactate dehydrogenase 183 IU/L, haptoglobin 23 mg/dL (0.23 g/L), total bilirubin 0.6 mg/dL (10.26 μmol/L), C3 112.3 mg/dL (1.123 g/L) (normal range: 88–201 mg/dL), C4 54.4 mg/dL (0.544 g/L) (normal range: 16–47 mg/dL), albumin 2.8 g/dL (28 g/L), serum kappa free light chain 82.4 mg/dL (normal range: 0.33-1.94), serum lambda free light chain 0.69 mg/dL (normal range: 0.57-2.63), serum free kappa/lambda ratio 119.42 (normal range: 0.26-1.65). Urinalysis showed 300 mg/dL protein on dipstick but no hematuria or pyuria. Urine protein electrophoresis showed elevated kappa light chain in the gamma zone at 11.9 mg/dL (232 mg per 24 hours) and a 24-hour urine collection revealed 2.6 grams of protein (53.3% albumin). Previous testing had shown presence of low-grade proteinuria (less than 0.5 grams per day) (Table ). In addition to his antihypertensives, he was also taking acyclovir, citalopram, esomeprazole, zolpidem, tramadol and aspirin. He required the addition of eplerenone 25 mg daily, nifedipine extended-release 90 mg daily and benazepril 30 mg daily, for a total of 7 antihypertensives. Despite the 7-drug combination, he remained hypertensive averaging 190/95 mmHg.
A renal sonogram revealed a right kidney of 10.8 and a left kidney of 10.6 cm of longitudinal diameter with moderately increased cortical echogenicity. Following acute reduction of blood pressure with intravenous labetalol, an ultrasound-guided percutaneous kidney biopsy was performed to evaluate the newly developed overt proteinuria. Histological examination of the biopsy specimen on light microscopy disclosed 8 out of 17 globally sclerotic glomeruli, some mesangiolysis (Figure a), moderate interstitial fibrosis and tubular atrophy, and severe arteriolar hyalinosis. There was no evidence of myeloma cast nephropathy. No thrombi were identified in the glomerular capillaries or arterioles. Congo red stain was negative. Immunofluorescence showed 4 out of 14 glomeruli with global sclerosis and one small artery that stained intensely for fibrin (Figure b), C1q, IgM and C3. The corresponding H&E-stained cryosection showed a thrombus in that artery. The specimen was negative for linear deposition of IgG or kappa along the glomerular and tubular basement membranes. Electron microscopy of one glomerulus showed diffuse foot process effacement, endothelial cell swelling and some loops with flocculent material between the endothelial cell and the glomerular basement membrane (Figure c). There was no immune complex deposition or finely granular electron dense deposits along the glomerular or tubular basement membranes. In summary, the findings were consistent with TMA, glomerular podocytopathy, hypertensive-related injury and chronic scarring.
After the results of the kidney biopsy were reviewed and discussed, carfilzomib was discontinued. Eight weeks later, proteinuria slightly improved to 1 gram on a 24 hour urine collection. His serum creatinine remained stable at 1.7 mg/dL (150.28 μmol/L) at that time. His arterial blood pressure improved significantly averaging 135/75 mmHg on 5 agents. Due to progression of MM and a joint decision of not pursuing further treatment, the patient died four months later.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [62, 'years'], 'creatinine': [2.1, 'mg/dL'], 'sex': 'Male'}",34.93444,33.18772,36.68116,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 62 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.1/0.9)**-1.2 * 0.9938**62 * 1.0 = 34.93444.
Hence, the GFR value is 34.93444 ml/min/1.73 m²."
344,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3502826-1,Extracted,"A 21-year-old female patient with a history of bladder exstrophy (BE) was referred to our department for dysuria-hematuria syndrome and recurrent febrile urinary tract infections (UTIs).
Her surgical history started on the fourth day of life. During the first procedure, she underwent bladder closure without osteotomy in a staged reconstructive approach. At 6 years for low bladder capacity, a gastrocystoplasty was performed to correct low bladder capacity. At the age of 10, she underwent a bilateral ureteral reimplantation (UR) according to Cohen for hydronephrosis secondary to vesicoureteral reflux (VUR) due to high bladder pressure. The last procedure was performed at 19 years with the removal of umbilical endometriosis.
On physical examination (), she presented with lower midline and Pfannenstiel scars due to previous procedures, pubis diastasis, bifid clitoris, stenotic and anteriorly displaced vagina, and short perineum with the anus directly behind the urogenital diaphragm. No alterations on blood tests, with normal renal function (creatinine 0.7 mg/dL). Urine culture showed >100.000 CFU of E. coli sensitive to ceftriaxone. Antibiotic was prescribed for 7 days. To treat the dysuria-hematuria syndrome, a proton pomp inhibitor (PPI) therapy was started.
A severe bilateral hydronephrosis, greater on the left, associated to a compression of renal parenchyma, was apparent at ultrasonography (US) and was confirmed at the CT scan (), with an AP pelvic diameter of 33 mm on the right and 43 mm on the left. Right and left ureters presented diameters of 23 and 40 mm, respectively. A high postvoid residual volume was evident.
The patient refused self-intermittent clean catheterisation. She allowed us to perform cystourethroscopy under general anaesthesia; this showed a long and twisting urethra with a bladder full of mucus without alterations of urothelial and gastric mucosa. Cross trigonal ureteral meatus were stenotic bilaterally, and retrograde stenting was not possible. During the same procedure, a retrograde cystourethrogram was executed without evidence of VUR. One month later, she elected to undergo open surgery.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [21, 'years'], 'creatinine': [0.7, 'mg/dL'], 'sex': 'Female'}",126.10947,119.804,132.41494,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 21 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.7 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.7/0.7)**-0.241 * 0.9938**21 * 1.012 = 126.10947.
Hence, the GFR value is 126.10947 ml/min/1.73 m²."
345,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4637796-1,Extracted,"A 79-year-old female presented with gradual deterioration of mental status for 1 month. For 2 months prior to admission, she had had intermittent right upper abdominal pain, vomiting, constipation, anorexia and significant weight loss. Her medical conditions were hypertension and dyslipidemia, and she was receiving treatment with amlodipine and simvastatin. She was a passive smoker and did not drink alcohol. There was no history of malignancy in her family.
The patient was admitted to another hospital for investigation. Kidney, ureter and bladder (KUB) X-ray visualized a large right staghorn stone (fig. ), and a retrograde pyelogram showed right staghorn renal calculi with partial obstruction and left middle ureter stricture (fig. ). A diuretic renal scan was interpreted as a nonfunctioning right kidney and fair renal function of the left kidney. Serum blood urea nitrogen and creatinine were 52 mg/dl (reference range 7–18) and 6.8 mg/dl (reference range 0.67–1.17), respectively. She was rehydrated with normal saline and then referred to our hospital for relief of left ureteric obstruction.
On examination, the patient appeared lethargic and dehydrated. Her blood pressure was 160/87 mm Hg and her pulse rate was 93 beats/min. She had no fever and mild pallor. Two lymph nodes, 0.7 and 1 cm in diameter, were palpated in the left supraclavicular area. She had nonpitting edema on both legs that was more pronounced on the right leg with the presence of Homan's sign. Deep vein thrombosis was suspected.
Urinary examination showed a pH of 5, white blood cells of 1–2/high-power field and red blood cells of 0–1 cells/high-power field. Furthermore, blood chemistries revealed serum total calcium of 14.8 mg/dl (reference range 8.5–10.1), serum phosphorus of 3 mg/dl (reference range 2.5–4.9) and serum creatinine of 2 mg/dl (reference range 0.67–1.17). Her corrected calcium adjusted with albumin was 15.93 mg/dl. Serum intact parathyroid hormone (PTH) was investigated and found to be 11.5 pg/ml (reference range 15–65). In the settings of old age, weight loss and deep vein thrombosis, humoral hypercalcemia of malignancy was mostly suspected. Unfortunately, we could not confirm the diagnosis with PTH-related protein (PTH-rP) due to test unavailability in our country.
Renal ultrasound visualized large right staghorn calculi and moderate left hydronephrosis with proximal hydroureter (fig. ). Doppler ultrasound showed acute extensive deep vein thrombosis of both legs along the external iliac vein, the common femoral vein, the proximal deep femoral vein to the popliteal vein. Thrombosis completely occluded the right leg and partially the left leg. There was minimal right pleural effusion on chest X-ray, with no abnormal pulmonary nodules. In searching for the primary site of malignancy, a left supraclavicular lymph node biopsy was performed. Histopathology was compatible with metastatic squamous cell carcinoma. Computed tomography of the chest and abdomen showed an infiltrative tumor with extensive involvement of the right kidney, the right pelvocalyceal system, the right adrenal gland, the right lobe of the liver and the adjacent right hemidiaphragm and psoas muscle (fig. ). There were inferior vena cava invasion and multiple metastases in both hepatic lobes and intra-abdominal lymph nodes. The final diagnosis was advanced-stage squamous cell carcinoma of the right renal pelvis.
To rescue left kidney function, a left retrograde pyelogram with double J stent was performed. The treatment of hypercalcemia was first intravenous saline rehydration. After restoration of volume status, serum creatinine levels decreased from 2.0 to 1.7 mg/dl. Then the patient was prescribed 60 mg of pamidronate, an intravenous bisphosphonate. Four days later, serum calcium level subsided to 10.16 mg/dl. It was decided that long-term therapy would be the best supportive care. The patient was discharged to a primary care hospital and passed away 1 month later.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [79, 'years'], 'creatinine': [1.7, 'mg/dL'], 'sex': 'Female'}",30.31574,28.79995,31.83153,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 79 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.7)**-1.2 * 0.9938**79 * 1.012 = 30.31574.
Hence, the GFR value is 30.31574 ml/min/1.73 m²."
346,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2913916-1,Extracted,"A 21 year old male patient was referred to our institution following unsuccessful surgery for presumed hydatid disease of the right lobe of the liver. The initial operation was performed in a district hospital; an open approach was performed and an attempt to drain/resect the lesion failed. The operation was aborted and a percutaneous drain was inserted at the site of surgery. The patient was in hospital for 2 weeks with no improvement. The family decided to transfer him to our institution which is a tertiary care center specialized in hepatobiliary surgery.
On admission, the patient was in respiratory distress with severe abdominal pain, distension and lower limb edema. The alpha-fetoprotein (AFP) at the time of diagnosis was 3.6 U/mL (range 1-9), carcinoembryonic Ag (CEA) 2.2 ng/mL (range 0-4) and human chorionic gonadotropin (Beta- HCG) 3.6 mlU/mL (< = 4). The laboratory tests included INR median 1.4 (range 0.9-1.1), serum bilirubin (Total) 1.4 mg/dL (range 0-1.2), serum aspartate aminotransferase (AST) 113 IU/L (range 0-50), gamma-glutamyl transferase 95 IU/L (range 0-50), creatinine 0.6 mg/dL (range 0.5-1.2), platelet count 680 × 109/L (range 150-400) and haemoglobin 11 g/dl (range 13-18). ELISA test was negative for hydatid disease Serology was negative for hepatitis B, C and HIV.
A computed tomography (CT) scan of the abdomen revealed a large, well defined lesion with intracystic septations occupying the right hepatic lobe measuring 22 × 19 × 23.6 cm containing the percutaneous drain (Figure ). Significant abdominal ascites was noted.
A technically challenging extended right hepatectomy was performed. Histopathology revealed an unusual neoplasm composed of irregular spindle cells showing moderate pleomorphism and brisk mitotic activity (Figure ). Immunohistochemical studies showed positive staining for vimentin and a positive cytokeratin AE1/3. Diagnosis was made of a stage III undifferentiated embryonic sarcoma (UES). The patient was discharged home day 16 post-resection. Adjuvant chemotherapy was recommended and the patient elected to be treated in his native country. Three weeks post-discharge he re-presented to our institution with a fungating abdominal wall mass at the site of previous percutaneous drain insertion. CT scan revealed a new lesion in segment II and an intra-abdominal lesion extending through the drain site 5 cm outside the skin (Figure ). The skin lesion was resected and histopathological examination revealed metastatic UES. He elected to go back to his country of origin where he received adjuvant chemotherapy which was ifosfamide plus etoposide alternating with actinomycin-D, vincristine every 3 weeks for 6 months. He is currently 5 months post-resection and a recent CT scan showed no evidence of disease recurrence.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [21, 'years'], 'creatinine': [0.6, 'mg/dL']}",130.55248,124.02486,137.0801,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 21 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.6 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.6/0.7)**-0.302 * 0.9938**21 * 1.0 = 130.55248.
Hence, the GFR value is 130.55248 ml/min/1.73 m²."
347,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3999574-1,Extracted,"A 64-year-old gentleman with a history of autoimmune autonomic dysfunction and gastroparesis on a background of type 2 insulin-dependent diabetes mellitus presented to our hospital with abdominal pain and diarrhea. He did not have any history of coronary artery disease or other cardiovascular comorbidities. The patient was initially started on MMF 1,000 mg twice daily 2 years prior for autoimmune autonomic dysfunction. This was subsequently raised to 1,500 mg twice daily 4 months preceding the patient's presentation. The diarrhea had started 2 months prior to presentation, with up to eight episodes of non-bloody diarrhea per day. Abdominal pain was of recent onset with a 4-day history of lower abdominal stabbing pain most severe in the left lower quadrant and reported as constant and progressive in nature. He also had decreased appetite, weight loss, sensation of bloating and intermittent nausea. He did not have any history of coronary artery disease or other cardiovascular comorbidities. The patient had undergone esophagogastroduodenoscopy within the past year, which had been unremarkable. A colonoscopy 5 years prior had shown diverticulosis, but otherwise been normal.
On examination, his vital signs were normal, and he had diffuse abdominal tenderness with increased intensity in the left lower quadrant area. Initial investigations revealed an elevated white blood cell count of 17.9 × 109 cells/l (normal 3.5–10.5 × 109 cells/l) with normal hemoglobin and platelet count. An elevated creatinine of 1.8 mg/dl (normal 0.6–1.2 mg/dl) was also noted. Abdominal X-ray showed no obstruction. Stool examination for microbiology including Clostridium difficile was negative. Initial management included hydration with intravenous fluids, empiric antibiotics and analgesia. Further work-up with CT of the abdomen and pelvis with contrast revealed segmental wall thickening and pericolic inflammation at the splenic flexure and proximal descending colon without evidence of diverticulitis. Flexible sigmoidoscopy revealed a segmental erythematous mucosa and multiple ulcers in the sigmoid colon, descending colon, splenic flexure and proximal transverse colon, suggesting a mucosal injury pattern consistent with ischemic colitis (fig. ). However, biopsies showed dilated damaged crypts, eosinophilic epithelial changes and crypt abscesses with apoptotic bodies, a pattern of injury highly suggestive of MMF-related colitis (fig. ). There was no evidence of cytomegalovirus infection.
MMF therapy was subsequently discontinued and the patient was discharged following improvement of symptoms with follow-up in an outpatient clinic 5 weeks later. During this visit, his abdominal pain and diarrhea had improved rapidly and significantly. He is scheduled for a repeat colonoscopy in 4 months’ time to assess the extent of mucosa recovery.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [64, 'years'], 'creatinine': [1.8, 'mg/dL'], 'sex': 'Male'}",41.51336,39.43769,43.58903,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 64 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.8 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.8/0.9)**-1.2 * 0.9938**64 * 1.0 = 41.51336.
Hence, the GFR value is 41.51336 ml/min/1.73 m²."
348,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-9445,Extracted,"An 83-year-old woman with fever, malaise, and cough for the past 24 hours is brought to the emergency department. She lives in an assisted living facility, and several of her neighbors have had similar symptoms. She has a past medical history of hypertension treated with lisinopril. Her temperature is 38.9°C (102.2°F), pulse is 105/min, respirations are 22/min, and blood pressure is 112/62 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 88%. Her leukocyte count is 10,500/mm3, and serum creatinine is 0.9 mg/dL. An X-ray of the chest shows bilateral reticulonodular opacities in the lower lobes. Serum procalcitonin level is 0.06 µg/L (N < 0.06 µg/L).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [83, 'years'], 'creatinine': [0.9, 'mg/dL'], 'sex': 'Female'}",63.43251,60.26088,66.60414,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 83 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.9 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.9/0.7)**-1.2 * 0.9938**83 * 1.012 = 63.43251.
Hence, the GFR value is 63.43251 ml/min/1.73 m²."
349,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7427458-1,Extracted,"A 79-year-old male with a past medical history of CMML diagnosed 4 years prior, anemia related to CMML and CKD receiving erythropoiesis-stimulating agent, hypertension, and chronic kidney disease stage 3 (baseline creatinine 1.8 mg/dL) presented with one day of decreased urination and an unintentional 20 pound weight loss and fatigue over the preceding three months.
The patient’s blood pressure was 141/84 mmHg, pulse 104 beats per minute, respiratory rate 16 respirations per minute, SpO2 96%, and temperature of 36.6°C. The physical exam did not reveal any abdominal tenderness to palpation but did reveal splenomegaly. There was no palpable cervical, supraclavicular, axillary, or inguinal lymphadenopathy.
Laboratory evaluation was significant for profound leukocytosis, 88.5 × 103 cells per mm3, with 24.0% monocytes compared to his baseline WBC 4.5–7 × 103 cells per mm3 over the preceding 4 years. Additional laboratory abnormalities were significant for uric acid 19.8 mg/dL and creatinine 2.94 mg/dL as well as potassium 4 mmol/L, phosphorus 4 mg/dL, calcium 9.2 mg/dL, and albumin 3.2 g/dL. Urinalysis was significant for protein 200 mg/dL, 20/LPF granular casts, and 7/LPF hyaline casts. A renal ultrasound measured the left kidney as 10.2 cm long, with at least two cysts the largest at 3.5 cm, and without hydronephrosis. The right kidney measured as 10.5 cm long, with one cyst at 2 cm, and also without hydronephrosis. The CT of the chest, abdomen, and pelvis identified splenomegaly with a splenic diameter of 14.6 cm. No renal calculi were appreciated. Also visualized were several borderline subcentimeter retroperitoneal and pelvic lymph nodes.
Peripheral blood smear was performed and revealed a myeloid predominance with left shift and a small blast population (0.6%) as well as monocytic phenotypic aberrance (see ). Subsequently, a bone marrow biopsy was performed which identified 20–25% of CD 34+ blasts and morphologic features consistent with AML with monocytic differentiation (see and ). Flow cytometry showed prominent monocytes which demonstrated loss of expression of HLA-DR and CD14 as well as coexpression of CD56. Next generation sequencing (NGS) revealed a pathogenic mutation in the NPM1 gene.
With presenting hyperuricemia and acute on chronic kidney injury, he received one dose of rasburicase 3 mg IV given concern for early TLS with concomitant initiation of daily allopurinol. He commenced cytoreduction with hydroxyurea 1000 mg twice daily and after 48 hours, his white blood cell count and uric acid down-trended to 48.5 × 103 cells per mm3 and 5.5 mg/dL respectively. Creatinine also trended down to 1.98 mg/dL.
Due to the patient’s performance status and age, hematology offered reduced-intensity therapy consisting of azacitidine with or without venetoclax or best supportive care rather than intensive induction chemotherapy. Ultimately, the patient elected for home hospice services and passed away 10 days later.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [79, 'years'], 'creatinine': [2.94, 'mg/dL'], 'sex': 'Male'}",20.98858,19.93915,22.03801,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 79 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.94 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.94/0.9)**-1.2 * 0.9938**79 * 1.0 = 20.98858.
Hence, the GFR value is 20.98858 ml/min/1.73 m²."
350,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5959307-1,Extracted,"A 90-year-old male with a history of diabetes mellitus, hypertension, hyperlipidemia, chronic kidney disease stage 2, and stroke was admitted for hypertensive emergency with a blood pressure of 200/105 mmHg, altered sensorium, and acute kidney injury. His physical examination showed bilateral crackles, a distended abdomen, decreased bowel sounds, and right upper quadrant tenderness. Blood workup showed a white cell count of 10.5 K/cmm3, a hemoglobin level of 13 g/dl, a platelet count of 185,000/cmm3, a creatinine level of 1.12 mg/dl, a potassium level of 2.7 mEq/L, a magnesium level of 1.8 mEq/L, and a thyroid stimulating hormone (TSH) level of 1.75 U/mL. On imaging, the chest radiograph demonstrated marked elevation of the right diaphragm and interposition of the hepatic flexure of the colon between the diaphragm and the liver, along with marked gaseous distension of the colon in the upper abdomen (Figure ). His blood pressure was initially managed with intravenous nicardipine drip that was later transitioned to oral calcium channel blockers, beta blockers, and thiazide diuretics. For his abdominal symptoms, he was treated conservatively with supportive management: kept NPO (nil per os/ nothing through the mouth), intravenous fluids, and electrolyte replacement. All anticholinergic medications and calcium channel blockers were discontinued. The patient did not show any symptomatic improvement with 48 hours of conservative management, at which point an abdominal computed tomography (CT) was obtained with oral contrast, which was consistent with pseudo-obstruction. After reviewing the images, a decision was made to continue close monitoring with no immediate need for surgical decompression (Figures , ). On day 5 of admission, the patient improved clinically with resolution of the abdominal pain, constipation, and bloating. He tolerated oral intake and was discharged home a day later with a follow-up outpatient visit, which he failed to show-up for.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [90, 'years'], 'creatinine': [1.12, 'mg/dL'], 'sex': 'Male'}",62.4061,59.2858,65.52641,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 90 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.12 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.12/0.9)**-1.2 * 0.9938**90 * 1.0 = 62.4061.
Hence, the GFR value is 62.4061 ml/min/1.73 m²."
351,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4421204-1,Extracted,"The patient is a 69-year-old male who presented to the emergency room complaining of severe fatigue and weakness. He had a history of IgG λ MM diagnosed ∼2.5 years ago after presenting with back pain and was found to have vertebral metastases. A bone marrow exam revealed marked interstitial monoclonal λ plasma cell infiltrate. The patient was initially treated with radiation to his spine, followed by a course of thalidomide and dexamethasone. He developed steroid-induced myopathy and his chemotherapy was changed to bortezomib. He also developed fatigue and vomiting on this medication and was noted to have rising free serum λ chains. His regimen was changed to doxorubicin, carmustine, cyclophosphamide and melphalan. He received two cycles but had progression of disease with rising λ chains and prolonged thrombocytopenia. Subsequently, he failed the stem cell collection and was deemed poor candidate for high-dose stem cell transplantation. He was started on oral cyclophosphamide and prednisone and was able to tolerate this therapy well with stable light chain disease for ∼1 year. He was given a brief chemotherapy holiday but was started on lenalidomide 15 mg daily once his serum λ chains began to rise. At the time lenalidomide was initiated the patient's serum creatinine was stable at 1.7 mg/dl (0.6–1.3 mg/dl), free serum λ chains 28.5 mg/dl (0.57–2.63 mg/dl). Of note, the patient was also receiving monthly zoledronic acid for treatment of bone disease for 26 months. Three weeks after lenalidomide was started the patient presented to the hospital with fatigue, weakness, orthostatic symptoms, thirst and polyuria. His upright and supine blood pressures were 83/45 and 110/79, respectively. The laboratory data revealed acute renal failure, hypernatremia, hypokalemia, hypophosphatemia, hypouricemia and metabolic acidosis with serum pH of 7.29 and anion gap of 7 (Table ). The serum λ light chains were 5.76 mg/dl. Urinalysis showed pH of 7.0 and glucosuria with normal serum glucose level. Twenty-four hour urine collection revealed 1.8 g of protein. Urine osmolality was 128 mOsml/kg. The patient's urine output was noted to be 6.1 l in the first 24 h after admission. Fractional excretion of sodium was 4.33% and fractional excretion of phosphate was 65.5%. Twenty-four hour potassium excretion was calculated to be 70 mEq. He underwent hydration with aggressive electrolyte and bicarbonate supplementation. His electrolyte abnormalities improved and urine output decreased over the next several days. He was discharged home 12 days after admission but required oral potassium, phosphorus and bicarbonate supplementation. At two-month follow-up, he was able to discontinue oral supplementation as the electrolyte abnormalities resolved. His renal function improved and the glucosuria also resolved (Table ). However, his serum λ light chains started to rise (Table ).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [69, 'years'], 'creatinine': [1.7, 'mg/dL'], 'sex': 'Male'}",43.09939,40.94442,45.25436,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 69 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.9)**-1.2 * 0.9938**69 * 1.0 = 43.09939.
Hence, the GFR value is 43.09939 ml/min/1.73 m²."
352,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-2797,Extracted,"Ten days after being discharged from the hospital, a 42-year-old man comes to the emergency department because of reduced urine output for 3 days. Physical examination is normal. Serum creatinine concentration is 2.9 mg/dL. Urinalysis shows brownish granular casts and 2+ proteinuria. Renal biopsy shows patchy necrosis of the proximal convoluted tubule with sloughing of tubular cells into the lumen and preservation of tubular basement membranes.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [42, 'years'], 'creatinine': [2.9, 'mg/dL'], 'sex': 'Male'}",26.85712,25.51426,28.19998,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 42 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.9 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.9/0.9)**-1.2 * 0.9938**42 * 1.0 = 26.85712.
Hence, the GFR value is 26.85712 ml/min/1.73 m²."
353,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8114252-1,Extracted,"A 52-year-old Black woman was noted to have a prolonged aPTT before her elective kidney biopsy. The patient had been recently diagnosed with Sjögren’s syndrome and started on steroids. She then developed acute kidney injury associated with a positive antinuclear antibody (ANA) concerning for systemic lupus erythematosus (SLE) complicated by lupus nephritis. She had a history of bulimia with a recent weight gain of 11 kg during the past 2 months. The patient’s preprocedure tests revealed a prolonged aPTT of 106.4 seconds (reference interval = 25-32 seconds), with a repeat value of 83 seconds, as well as rapid progression of renal dysfunction with an elevation of creatinine from 1.1 to 1.8 mg/dL in the past 2 months. Given abnormal coagulation laboratories, she was instead admitted for an expedited workup in the setting of rapidly progressive renal dysfunction with a new disorder of coagulation. The patient had normal PT of 10.3 seconds (reference interval = 9.4-12.5 seconds), platelet count of 248 000/µL (reference interval = 200-450 000/μL), and fibrinogen level of 212 mg/dL (reference interval = 150-400 mg/dL). Thrombin time was slightly increased (18.7 seconds; reference interval = 12-14 seconds). von Willebrand factor (vWF) antigen test was elevated to 374 IU/dL (reference interval = 50-200 IU/dL). Other laboratory results were notable for stable normocytic anemia (hemoglobin 10.8 g/dL), with iron studies consistent with anemia of chronic diseases (ferritin 729 mg/L, transferrin 197 mg/dL, total iron-binding capacity 256 µg/dL). A mixing study was ordered. The patient presented with high-grade proteinuria, anasarca, hypoalbuminemia, and urine sediment notable for fat droplets and lipid-laden casts, all consistent with acute nephrotic syndrome. Thus, a decision was made to pursue renal biopsy to further understand kidney disease and guide treatment.
Her current medication list included hydroxychloroquine, torsemide, prednisone, lisinopril, potassium chloride, and sumatriptan. The patient did not have any medical or family history of abnormal hemorrhagic or thromboembolic events. She had an uncomplicated Cesarean section in the past without any bleeding complications. She reported a prolonged aPTT of around 200 seconds in her sister, found incidentally through routine laboratory tests before shoulder surgery, without further hematology follow-up. The patient’s physical examination did not show any evidence of ecchymoses, purpura, or petechiae.
The patient underwent the planned kidney biopsy after receiving 3 units of fresh frozen plasma (FFP) in light of the prolonged aPTT, which corrected the aPTT to 27 seconds. Kidney biopsy pathology showed class V membranous disease as well as evidence of proliferative disease with crescents. Possible causes of isolated prolongation of aPTT were considered, including heparin administration, inherited intrinsic pathway factor deficiencies, including XII, XI, IX, and VIII, factor inhibitors, and von Willebrand disease. The patient’s laboratory studies before biopsy indicated normal PT as well as a normal activity of factors VIII, IX, XI, XII, vWF, and HMWK. The lupus anticoagulant (LA) screen was positive, but the confirmatory test was negative. Anti-cardiolipin antibodies and β-2-glycoprotein 1 (immunoglobulins G and M) levels were normal. The plasma PK assay revealed low activity at 15% consistent with mild PK deficiency (reference interval = normal >50%, mild deficiency = 5% to 49%, severe deficiency ≤5%). The plasma PK was measured indirectly by quantifying the amidolytic activity of kallikrein by using a synthetic chromogenic substrate. Antigenic assays for evaluation of structure or quantity of PK were not available.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [52, 'years'], 'creatinine': [1.8, 'mg/dL'], 'sex': 'Female'}",33.48167,31.80759,35.15575,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 52 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.8 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.8/0.7)**-1.2 * 0.9938**52 * 1.012 = 33.48167.
Hence, the GFR value is 33.48167 ml/min/1.73 m²."
354,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4421621-1,Extracted,"A 36-year-old male, with no symptoms and no past medical history, exhibited hypertension (166/113 mmHg) during a medical check-up. His primary doctor started him, in a phased manner, on amlodipine 5 mg/day, candesartan 2 mg/day and carvedilol 2.5 mg/day. He was subsequently referred to our centre. The physical findings on admission were almost normal (blood pressure 138/93 mmHg); however, his serum creatinine level was 2.65 mg/dL. Urinalysis showed proteinuria (1 +) but no haematuria. On ultrasonography, both kidneys were atrophic and showed a diffuse increase of echogenicity. The number (1.29/mm2) and diameter (200 μm) of the glomeruli were diagnostic of oligomeganephronia. Continuing with the safe treatment, he has maintained his serum creatinine level at 2.5–3.0 mg/dL for 3.5 years.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [36, 'years'], 'creatinine': [2.65, 'mg/dL'], 'sex': 'Male'}",31.06333,29.51016,32.6165,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 36 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.65 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.65/0.9)**-1.2 * 0.9938**36 * 1.0 = 31.06333.
Hence, the GFR value is 31.06333 ml/min/1.73 m²."
355,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4544255-1,Extracted,"A 19-year-old man complained of recurrent fever and lower back pain for a month. He had
a history of scalded mouth syndrome with no regular antibiotic or antifungal drug
treatment six months prior to hospitalization. He had neither history of taking
immunosuppressors, nor of any disease indicative of immunodeficiency. He had, however,
received the Bacillus Calmette-Guérin (BCG) vaccine during childhood. On admission, his
vital signs included an oral temperature of 39 ºC, heart rate of 92 beats per minute,
respiratory rate of 20 breaths per minute and blood pressure of 130/80 mmHg. Physical
examination revealed a 9×8cm mass in the right of the patient's neck, but no lesions
were found on the oral mucosa. The remainder of the systemic examination was
unremarkable.
Laboratory results included a leukocyte count of 14800×103/mm3,
serum glucose level of 143 mg/dL, blood urea nitrogen of 40 mg/dL and creatinine level
of 1.7 mg/dL. Inflammatory markers were elevated with an erythrocyte sedimentation rate
(ESR) of 120 mm/h and C-reactive protein (CRP) level of 11.1 mg/L. Both a tuberculin
skin test and human immunodeficiency virus (HIV) antibody exam were negative.
Comprehensive immunological studies, including serum immunoglobulins and complement
levels, tests for cell-mediated immunity (NK, CD3, CD4, CD8, CD4/CD8 and CD19) and
autoantibody tests, were normal. 1, 3-β-D-glucan assay levels and the galactomannan test
were normal. Blood cultures were also negative. Whole-body positron emission
tomography/computed tomography (PET/CT) revealed multiple abscesses in the right of the
patient's neck, liver and right psoas major area respectively (); and there was a raised uptake of [18F] FDG in
vertebral bodies of T11, T12 and L1. Consequently, percutaneous abscess drainage was
conducted on the upper body using B-mode ultrasonography and drained brown fluids (30
mL, 280 mL and 130 mL, respectively, ) were
sent to the microbiology lab. Also, drainage tubes were inserted into abscesses in the
liver and psoas major, but were removed after no drainage took place. Results of the
Chromagar Candida Medium (Chromagar, France) cultures were positive for Candida
albicans (), but no acid-fast
bacilli were detected. The germ tube test was positive and the documented diagnosis
using API 20C Aux systems (BioMeriux, France) was Candida albicans,
which was sensitive to amphotericin B, fluconazole, itraconazole, voriconazole,
caspofungin and 5-fluorocytosine. Based on antifungal guidelines and susceptibility
tests, he was treated with intravenous 35 mg amphotericin B daily (0.5 mg/kg per day).
The patient responded to antifungal therapy and his fever abated after ten days of
treatment. Abscess detection using B-mode ultrasonography revealed that the extent of
infection in the upper body had greatly decreased at the end of three-week antifungal
therapy.
However, there was no improvement in the patient's lower back pain. Spinal magnetic
resonance imaging (MRI) showed altered signal intensity in T11, T12, L1 and unique
osteolytic lesions in upper vertebral bodies (). Subsequently, computed tomography (CT) guided percutaneous vertebral
biopsy specimens from the T12 vertebrae revealed caseous material and the acid fast
bacilli were identified (, ). Also, the aspirate culture showed growth of the
M. tuberculosis. Chest CT, urine and sputum examinations were
normal. Taking histological and microbiological findings into consideration, the patient
was treated with antitubercular therapy (rifampicin, isoniazid, pyrazinamide,
ethambutol) for 12 months. In addition, he was treated with a total dose of 1500 mg of
amphotericin B, while oral fluconazole and 5-flucytosine were subsequently prescribed
for six months. By his 2-year follow up, there were complete resolutions of the lesions
in the upper vertebral bodies and no evidence of new abscesses.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [19, 'years'], 'creatinine': [1.7, 'mg/dL'], 'sex': 'Male'}",58.81952,55.87854,61.7605,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 19 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.9)**-1.2 * 0.9938**19 * 1.0 = 58.81952.
Hence, the GFR value is 58.81952 ml/min/1.73 m²."
356,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4525392-1,Extracted,"A 32-year-old female presented to the emergency room with a chief complaint of marked edema of 5 days' duration. Past medical history included: Bipolar disorder, panic disorder, hypothyroidism, and hidradenitis suppurativa. Her daily home medications included lithium carbonate 900 mg, synthroid 75 μg, cymbalata 60 mg, nortryptiline 30 mg, cipralex 30 mg, gabapentin 600-900 mg, and ibuprofen 200 mg. The patient had been on a stable dose of lithium for approximately 5 years experiencing no side effects. She presented to the hospital with a 5-day history of severe fatigue, migraine-like headaches, lethargy, and significant anasarca. Associated with these symptoms were upper extremity tremors as well as polyuria and polydipsia. She denied chest pain, shortness of breath, constitutional symptoms, and any urinary symptoms. Social history included 10-pack year history of tobacco.
On admission, the patient's vital signs were: Blood pressure 115/61, heart rate 61 beats/min, respiratory rate 20 breaths/min, and oxygen saturation 96% on room air. The patient was afebrile. There was generalized + 2 edema of lower extremities, upper extremities, and periorbital regions. Minimal bibasilar crackles were appreciated. The remainder of the cardiovascular and abdominal examination was unremarkable.
Blood work showed a plasma creatinine level of 119 μmol/L (baseline 69 μmol/L) and a blood urea of 10.4 mmol/L. Urine dipstick showed a specific gravity of 1.016, pH 7.5, and 4 + protein; and was negative for glucose, ketones, and nitrites. Microscopy revealed oval fat bodies and free fat droplets. The urine albumin to creatinine ratio was 973.4 mg/mmol and 24-h urine protein was 15.69 g. On admission, serum lithium level was 2.66 mmol/L (therapeutic 0.50-1.50 mmol/L). Serum sodium was 130 mmol/L, potassium 4.5 mmol/L, chloride 105 mmol/L, and bicarbonate 27 mmol/L. A complete blood count demonstrated hemoglobin 106 g/L, white blood cell count 9.46 × 109 /L, and platelet count 234 × 109 /L. Serum albumin was low at 20 g/L; but all liver enzymes, total bilirubin, and coagulation studies were within normal limits. Thyroid-stimulating hormone was 18.90 mU/L and free T4 8.2 pmol/L. Serology for hepatitis B and C, anti-double stranded deoxyribonucleic acid, antineutrophilic cytoplasmic antibodies, ribonucleoprotein, Sjogren's syndrome, scleroderma, inflammatory myositis, and Smith antibody were all negative. Antinuclear antibody was slightly positive on admission. Chest radiographs revealed nonspecific bibasilar infiltrates. Abdominal ultrasound demonstrated normal kidneys with no renal calculi or hydronephrosis.
Lithium treatment was discontinued immediately and the patient was treated conservatively with fluids. Initially the patient refused renal biopsy. Once stabilized, she was discharged from the hospital and lithium remained discontinued. At 2 months follow-up, the patient experienced worsening anasarca, significant acute kidney injury (AKI; serum creatinine 209 μmol/L), and persistent proteinuria. She was readmitted to the hospital and subsequently underwent a renal biopsy, when at the time her creatinine peaked at 348 μmol/l. On light microscopy, there was no global sclerosis, crescent formation, or necrotic lesions capillary wall thickness was normal. There was evidence of moderate focal interstitial fibrosis []. Immunofluorescence did not demonstrate any immune deposits. Electron microscopy revealed widespread fusion of podocyte foot processes affecting more than 75% of the surface of glomerular capillary loops []. No electron dense deposits were evident. A diagnosis of MCD secondary to lithium use was established and the patient was started on high dose corticosteroids, initially intravenously, but changed to oral prednisone 80 mg daily on discharge. Over the next 2 months of follow-up, the patient's creatinine, proteinuria, and edema all decreased significantly and she was tapered to oral prednisone 40 mg. At her 4 months follow-up, her albumin/creatinine ratio had decreased to 220 mg/mmol and she remained on oral prednisone 40 mg daily. Her edema as well as AKI had resolved. The progression of renal and glomerular failure is illustrated in .","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [32, 'years'], 'creatinine': [119.0, 'µmol/L']}",53.21799,50.55709,55.87889,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 32 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 119.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 119.0 µmol. To convert 119.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 119.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00012 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00012 mol Serum Creatinine * 113.12 g/mol = 0.01357 g Serum Creatinine. To convert 0.01357 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01357 g Serum Creatinine * 1000.0 mg/g = 13.57 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 13.57 mg Serum Creatinine/10.0 dL = 1.357 mg Serum Creatinine/dL. The concentration value of 119.0 µmol Serum Creatinine/L converts to 1.357 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.357/0.7)**-1.2 * 0.9938**32 * 1.012 = 53.21799.
Hence, the GFR value is 53.21799 ml/min/1.73 m²."
357,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8439411-1,Extracted,"A 76-year-old man with chronic obstructive pulmonary disease and type II diabetes mellitus presented to the emergency department with fever, dyspnea on exertion, and lethargy. At presentation, his temperature was 102.4°F, heart rate 59 beats per minute, blood pressure 105/44 mmHg, and oxygen saturation was 98% on a 6 L nasal cannula. Examination revealed bounding carotid pulses, a grade 2/6 early blowing diastolic murmur at the left lower sternal border, and diminished lung sounds at the bases. Laboratory profile showed leukocytosis of 19.65 k/µL, acute-on-chronic kidney injury with blood urea nitrogen of 72 mg/dL and creatinine of 2.92 mg/dL, lactic acid 3.1 mmol/L, pro-B-type natriuretic peptide 15,342 pg/mL, high-sensitivity troponin 136 ng/L, aspartate aminotransferase 129 U/L, and alanine aminotransferase of 115 U/L. Serial electrocardiogram showed complete heart block with alternating bundle branch morphology and junctional escape (Figure ), requiring a transvenous pacemaker.
A transthoracic echocardiogram showed normal biventricular function, moderate aortic insufficiency with no evidence of aortic abscess, and hypokinetic mid-distal anteroseptal segments. Cardiac pacing was set to 100 beats per minute to limit diastolic time and reduce aortic insufficiency. Despite aggressive therapy with broad-spectrum antibiotics including vancomycin and cefepime for less than two days, he decompensated and required emergent intubation and was placed on epinephrine and vasopressin. Blood cultures grew Aerococcus urinae. He developed methicillin-sensitive Staphylococcus aureus ventilator-associated pneumonia. Antibiotics were de-escalated and he was treated with a 14-day course of ampicillin-sulbactam.
A transesophageal echocardiogram revealed a 1.7 cm × 2.7 cm paravalvular aortic root abscess occupying the noncoronary sinus and left ventricular outflow tract with severe aortic regurgitation (Figure ).
Computed tomography (CT) of the chest, abdomen, and pelvis was performed to identify a potential infectious source. Due to wall motion abnormalities and concern for coronary embolization, the study was performed with gating, and ventricular pacing was decreased to 50 beats per minute to optimize coronary artery visualization (Figures , ).
CT confirmed the abscess with accompanying subaortic pseudoaneurysm along the aorto-mitral curtain, pyelitis, and cystitis. No acute coronary artery pathology was identified. The patient underwent emergent aortic valve replacement, debridement of subaortic pseudoaneurysm, and bovine pericardial patch repair of the aorta (Figure ). After the pneumonia was treated, he was treated with penicillin G for six weeks from the time of the aortic valve surgery. His postoperative hemodynamics improved, and a leadless pacemaker was planned when blood cultures cleared.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [76, 'years'], 'creatinine': [2.92, 'mg/dL'], 'sex': 'Male'}",21.55973,20.48174,22.63772,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 76 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.92 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.92/0.9)**-1.2 * 0.9938**76 * 1.0 = 21.55973.
Hence, the GFR value is 21.55973 ml/min/1.73 m²."
358,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4460636-1,Extracted,"A 77-year-old Korean man presented to our hospital with an axillary mass. The presence of amyloid in the subsequent excisional biopsy prompted a bone marrow biopsy, related laboratory tests, and pertinent imaging studies, including computed tomography (CT). Ultimately, a diagnosis of primary amyloidosis was rendered.
Despite the patient’s advanced age, melphalan/dexamethasone combination therapy was elected. After three cycles of this regimen, detectable masses grew smaller and his serum kappa/lambda ratio normalized, so treatment continued. However, serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) rose precipitously after six cycles of therapy.
Our patient denied use of other medications (including herbal or dietary supplements), smoking, or consumption of alcohol, and there was no history of blood transfusion. On physical examination, he was alert, with normal blood pressure, pulse, and respiratory rate. No direct or rebound tenderness of the abdomen was evident.
Laboratory tests yielded the following values: white blood cell count, 2,720/mm3 (40.1% neutrophils, 43.5% lymphocytes, 1.4% eosinophils); hematocrit, 10.6g/dL; platelet count, 111,000/mm3; prothrombin time, 11.8 seconds; AST level, 454.1IU/L; ALT level, 496.3IU/L; total bilirubin, 1.34mg/dL; direct bilirubin, 1.04mg/dL; albumin, 3.11g/d; alkaline phosphatase (ALP), 142U/L; gamma-glutamyl transferase (rGTP), 126U/L; blood urea nitrogen (BUN), 17.2mg/dL; and creatinine (Cr), 1.28mg/dL.
Prior to initiating chemotherapy, our patient had been screened twice for hepatitis, testing negative for hepatitis B surface antigen (HBsAg, 0.41S/Co) and positive for antibodies to HBsAg (HBsAb, 55.0mIU/mL). No further serologic testing was pursued at this juncture, but after receiving chemotherapy, HBsAg seroconversion (5,592S/Co) and loss of HBsAb (0.62mIU/mL) were documented. Repeat testing generated the same results, so screening was expanded to include hepatitis B envelope antigen (HBeAg, negative (0.27S/Co)), antibodies to HBeAg (HBeAb, positive (0.02S/Co)), and antibodies to hepatitis B core antigen (immunoglobulin M (IgM) HBcAb, negative (0.27S/Co); immunoglobulin M (IgG) HBcAb, positive (2.2S/Co)). A massive HBV DNA burden (67,322,328 copies/mL) was also determined by real-time polymerase chain reaction (PCR).
Given a lack of HBV vaccination by history, the patient’s baseline HBsAb positivity was attributed to innate (naturally acquired) immunity. Hence, this acute bout of hepatitis was considered HBV reactivation. Entecavir antiviral treatment was then administered, gradually restoring normal liver function within three weeks. Five months later, AST and ALT levels were 40IU/L and 12IU/L, respectively. At this point, he also tested negative for HBsAg and positive for HBsAb, with PCR-determined HBV DNA level at 3,600 copies/mL (Figure , Table ). Continued chemotherapy for primary amyloidosis was declined, and he died unexpectedly seven months later.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [77, 'years'], 'creatinine': [1.28, 'mg/dL'], 'sex': 'Male'}",57.64343,54.76126,60.5256,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 77 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.28 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.28/0.9)**-1.2 * 0.9938**77 * 1.0 = 57.64343.
Hence, the GFR value is 57.64343 ml/min/1.73 m²."
359,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6572507-1,Extracted,"The patient is a 62-year-old woman who was brought to the emergency department (ED) with 2 episodes of sudden onset substernal chest pain, each episode lasting for 30 min. Her chest pain had resolved at the time of arrival. Prior to that, she had felt nauseous which was usual for her after her chemotherapy. Chest pain was followed by right-sided, sharp diffuse abdominal pain which lasted for 10 min and resolved spontaneously. She had received her last chemotherapy infusion 2 days prior to the episode. She denied any fever, chills, cough or shortness of breath. She was diagnosed of NSCLC with bone metastases (epidermal growth factor receptor negative and PD-L1-80%) a year ago for which she underwent radiation therapy of left hip and right upper ribs, completed palliative chemotherapy with 6 cycles of pemetrexed 500 mg/m2/dose, carboplatin 550 mg, and pembrolizumab 200 mg followed by same doses of pemetrexed and pembrolizumab maintenance every 3 weeks with last dose 2 days prior to presentation. The patient had been on pembrolizumab for 6 months prior to the decline in renal function. Other past medical history included stage IA right breast cancer (estrogen receptor+ (90%), progesterone receptor+ (3–5%), and human epidermal growth factor receptor 2-negative invasive ductal carcinoma) for which she underwent a bilateral mastectomy, 6 cycles of cyclophosphamide, methotrexate, and fluorouracil, and tamoxifen for 5 years 20 years ago, hypothyroidism, and hyperlipidemia. Her home medications included levothyroxine 75 µg daily, folic acid 1 mg daily, pantoprazole 40 mg daily, rosuvastatin 5 mg nightly, dexamethasone 8 mg two doses before and after chemotherapy, olanzapine 10 mg nightly, lorazepam 0.5 mg as needed, ondansetron 8 mg as needed, prochlorperazine 10 mg as needed, and promethazine 25 mg as needed. She had smoked a pack a day for 15 years before quitting 27 years ago.
On examination, vitals were stable with a temperature of 36.7 °C (98.1 °F), blood pressure 139/82 mm Hg, pulse 79 beats per minute, respiratory rate 18 breaths per minute, and she was maintaining saturation on room air. Chest, cardiac, and abdominal examinations were unremarkable. Her hemoglobin was 9.1 g/dL (reference range: 12.0–16.0 g/dL), platelet count was 556,000/µL (reference range: 13,000–400,000/µL), and white count was 10,700/µL (reference range: 4800–10,800/µL) with neutrophil count of 9800/µL (reference range: 2000–8000/µL), monocyte count of 400 (reference range: 100–1300/µL), and immature granulocyte count of 260/µL (reference range: 0–30/µL). Serial troponins and electrocardiograms were non-suggestive of an acute coronary syndrome. Her creatinine was 1.69 mg/dL (reference range: 0.6–1.3 mg/dL). It was 1.72 two days prior above her baseline of 0.6–0.9. Although d-dimer was 1.02 (reference range: <0.53 µg/mL), computed tomography (CT) pulmonary embolism protocol was not done as ultrasound lower extremity vein bilateral was negative and there was low clinical suspicion for pulmonary embolism. CT without contrast of chest/abdomen/pelvis showed decreasing right upper lobe mass and surrounding consolidation. She had bilateral enlarging metastatic lung nodules. Hepatic metastases were not identified but contrast was not used. Bone metastases were unchanged. Her kidneys and urinary tract on CT and urinalysis were unremarkable. Her acute kidney injury (AKI) was thought to be related to poor oral intake and vomiting related volume depletion. The patient was discharged home and was recommended hydration and repeat labs in a few days. Her creatinine on the day of discharge was 1.83 mg/dL.
Two days post discharge, the patient called her oncologist and told that she had started feeling sick on the same day after she was discharged. She complained of fever with maximum recorded temperature was 102.7 °F along with chills and rigors. She had multiple episodes of vomiting and poor intake. She was directly admitted to the hospital. At presentation, her vitals were stable with a temperature of 37.0 °C (98.6 °F), blood pressure 140/71 mm Hg, pulse 84 beats per minute, and respiratory rate 20 breaths per minute. Chest, cardiac, and abdominal examinations were unremarkable. Her mucous membranes were moist. Her hemoglobin was 8.2 g/dL (reference range: 12.0–16.0 g/dL), platelet count was 257,000/µL (reference range: 13,000–400,000/µL), white count was 2600/µL (reference range: 4800–10,800/µL) with neutrophil count of 1500/µL (reference range: 2000–8000/µL), monocyte count of 0/µL (reference range: 100–1300/µL), and immature granulocyte count of 50/µL (reference range: 0–30/µL). Her low cell counts were thought to be related to her chemotherapy. No eosinophilia was noted in complete blood count during hospitalization or prior to presentation. Her urinalysis was negative for infection but showed 30 mg /dL (1+) proteinuria. Her blood and urine cultures showed no growth. Her creatinine was elevated at 3.70 mg/dL and this was again thought to be related to volume depletion. The patient was started on intravenous fluids. Her renal ultrasound was unremarkable. With suspicion for pembrolizumab as a potential cause for acute kidney injury, future infusions were held. The patient was given a dose of IV methylprednisone 80 mg (1 mg/kg) and planned to be started on prednisone 80 mg daily next day. She was planned for a renal biopsy to rule out medication-related injury. Her creatinine progressively improved during her 5-day-stay and was 2.10 on discharge. We think this was with discontinuation of pembrolizumab. Her renal biopsy showed evidence of acute tubular injury, focal interstitial inflammation (lymphocytes, plasma cells, few eosinophils, few neutrophils) with focal mild tubulitis, 14% globally sclerotic glomeruli, mild arterial thickening, and mild interstitial fibrosis (). This was thought to be secondary to pembrolizumab which was permanently discontinued. She was started on docetaxel 125 mg every 3 weeks. She has received 3 cycles so far. With non-improvement in kidney function, prednisone dose was increased to 1 mg/kg/day (70 mg) for a course of 3 months. Sulfamethoxazole-trimethoprim and pantoprazole were started for prophylaxis. Her creatinine even after 5 months is still elevated. Her new creatinine baseline is around 1.8–2.0. Pertinent case details are summarized in .","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [62, 'years'], 'creatinine': [1.83, 'mg/dL'], 'sex': 'Female'}",30.84485,29.30261,32.38709,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 62 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.83 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.83/0.7)**-1.2 * 0.9938**62 * 1.012 = 30.84485.
Hence, the GFR value is 30.84485 ml/min/1.73 m²."
360,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3221906-1,Extracted,"A 49-year-old previously healthy male was admitted to the hospital with fever and pain in the left calf. Two months before admission, the patient had fever, chills and myalgias, especially in the leg. He visited a local clinic and had taken medication for a total of three weeks. However the fever, which was remittent, did not completely resolve. A few weeks before admission, he had painful and erythematous lesions in both thighs, which gradually disappeared. One week before admission, he developed pain in the left calf and a headache. He denied overseas travel, sick exposures, or history of trauma.
Upon physical examination, the patient's blood pressure was 90/60 mm Hg, pulse was 80 beats per minute, an temperature was 38℃. He had periodontitis and dental caries. The first and second heart sounds were normal and no heart murmurs were heard. No lymphadenopathy or hepatosplenomegaly was noted. The patient's left calf was slightly erythematous, swollen and tender. His lower extremities were otherwise normal, and the remainder of the examination was unremarkable.
Laboratory values upon admission were as follows: white blood cell count, 11,700 /mm3 with 70.3% neutrophils; hemoglobin, 13.7 g/dL; platelet count, 254,000/mm3; blood urea nitrogen, 8.1 mg/dL; serum creatinine, 1.0 mg/dL; glucose, 136 mg/dL; alanine aminotransferase, 16 U/L; aspartate aminotransferase, 29 U/L; C-reactive protein, 7.91 mg/dL. Urinalysis showed no abnormalities. Chest X-ray and electrocardiography were unremarkable.
On the third hospital day, magnetic resonance imaging (MRI) of his left calf revealed inflammation in the medial belly of the gastrocnemius muscle without abscess (). Empiric antimicrobial therapy for myositis was started with ceftriaxone and clindamycin intravenously. Considering the unusual location of inflammation and his history of no previous trauma, metastatic infection from an unrecognized primary site was also considered. On the sixth day of admission, a small, palpable, tender erythematous lesion was observed on the left thumb, suggestive of an Osler's node. Transthoracic echocardiography and transesophageal echocardiography were then performed, which revealed normal sized cardiac chambers and normal systolic function of the left ventricle. All cardiac valves were clean and only trivial mitral regurgitation was noted. An elongated, villous, 5.6×1.8 cm mass arising from the posterior wall of the left atrium () was found. The initial blood cultures drawn at the time of admission yielded Streptococcus bovis resistant to gentamicin. A diagnosis of infected left atrial myxoma was made and antimicrobial therapy was continued. On the seventh hospital day the patient complained of continuing headache and noncontrast brain magnetic resonance imaging incidentally showed an infarction of the left cerebellar hemisphere that was attributed to embolization from the infected myxoma. On the tenth hospital day an abdominal CT scan was conducted to check for additional foci of infection, which revealed multiple splenic infarcts. After twelve days of antibiotics, the patient's fever had resolved and after 19 days of antibiotics the patient underwent excision of the mass.
In the operating room, the mass was found to have a base of about 9 mm () and was attached to the posterior wall of the left atrium. Unexpectedly, multiple tiny and nodular vegetations of less than 1 mm in size were found on the endocardium of the left atrium and P2 and P3 portion of the posterior mitral leaflet () and posterior mitral annulus. Since they were too firmly attached to be removed without mitral valve injury, the mass was resected and mitral valve replacement was conducted using a Saint-Jude 29 mm prosthetic valve.
The pathology of the excised mass showed a partially myxoid and papillomatous surface and microscopically ischemic necrosis and focal abscesses (). Focal microabscesses and multinodular vegetations with sizes of less than 1 mm were present on the mitral valve, which was consistent with subchronic endocarditis.
The patient rapidly recovered without postoperative complications and was discharged 12 days after the operation. Three sets of blood cultures drawn during the perioperative period yielded no growth of any organisms.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [49, 'years'], 'creatinine': [1.0, 'mg/dL']}",92.26351,87.65033,96.87669,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 49 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.0 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.0/0.9)**-1.2 * 0.9938**49 * 1.0 = 92.26351.
Hence, the GFR value is 92.26351 ml/min/1.73 m²."
361,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-1608,Extracted,"Nine days after being treated for a perforated gastric ulcer and sepsis, a 78-year-old woman develops decreased urinary output and malaise. She required emergency laparotomy and was subsequently treated in the intensive care unit for sepsis. Blood cultures grew Pseudomonas aeruginosa. The patient was treated with ceftazidime and gentamicin. She has type 2 diabetes mellitus, arterial hypertension, and osteoarthritis of the hips. Prior to admission, her medications were insulin, ramipril, and ibuprofen. Her temperature is 37.3°C (99.1°F), pulse is 80/min, and blood pressure is 115/75 mm Hg. Examination shows a healing surgical incision in the upper abdomen. Laboratory studies show:
Hemoglobin count 14 g/dL
Leukocyte count 16,400 mm3
Segmented neutrophils 60%
Eosinophils 2%
Lymphocytes 30%
Monocytes 6%
Platelet count 260,000 mm3
Serum
Na+ 137 mEq/L
Cl- 102 mEq/L
K+ 5.1 mEq/L
Urea nitrogen 25 mg/dL
Creatinine 4.2 mg/dL
Fractional excretion of sodium is 2.1%.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [78, 'years'], 'creatinine': [4.2, 'mg/dL'], 'sex': 'Female'}",10.30407,9.78887,10.81927,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 78 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 4.2 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (4.2/0.7)**-1.2 * 0.9938**78 * 1.012 = 10.30407.
Hence, the GFR value is 10.30407 ml/min/1.73 m²."
362,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5750783-1,Extracted,"A 53-year-old male presented with 1 month history of abdominal pain, anorexia, and nausea. His medical history was positive for coronary artery disease and coronary artery bypass graft (CABG) surgery was performed on him, about 45 days prior to admission. He was relatively well when he developed abdominal pain accompanied by anorexia and nausea. The patient had sought medical attention for his abdominal discomfort, and bilateral large solid adrenal masses were detected in his abdominal ultrasonography. He also mentioned an unintentional weight loss and generalized darkening of the skin during this period.
He was admitted to the under study hospital with the impression of adrenal failure. Serum sample for basal cortisol and adrenocorticotropic hormone (ACTH) was taken in the basal state, and then, after giving 250 μg of synthetic ACTH, serum cortisol was measured again. He responded to administration of high doses of intravenous hydrocortisone with remission of symptoms. On admission, clinical examination revealed low blood pressure (90/60 mmHg), body temperature 37°C, the pulse rate 88 beat/minute, and respiratory rate of 18 breath/ minute. He looked well and was in no acute distress. There was generalized increased pigmentation of the skin. No Cushingoid appearance was detected and there was no palpable lymph node. Physical examination of lungs and heart were unremarkable and his abdomen was flat without palpable mass or hepatosplenomegaly. Laboratory investigations revealed normal liver function test, hemoglobin 11.1 g/dL, white blood cell 8.5 × 103, with normal differential count and platelet 200 × 103. Blood chemistries showed Na 125 mEq/L, K 5.2 mEq/L, blood urea nitrogen (BUN) 35 mg/dL, creatinine (Cr) 1.8 mg/dL, normal blood sugar, lactate dehydrogenase (LDH) 1277 U/L, erythrocyte sedimentation rate (ESR) 110 mm/hour, and normal lipase and amylase levels. The ultrasound of the abdomen revealed bilateral large solid adrenal masses without lymphadenopathy or organomegaly.
A contrast-enhanced computerized tomography (CT) scan of the abdomen with adrenal protocol demonstrated bilateral large heterogeneously enhancing adrenal lesions, 8.5 × 6.5 cm in the Rt. and 7.5 × 5.7 cm in the left adrenal, without calcification ().
The masses were non-homogeneous and their precontrast Hounsfield score was 65 in the left and 73 in the right side. Also, there was no significant washout of the contrast agent and no other pathology was detected. Since adrenal metastasis from an unknown malignant disease was suspected, CT scan of the chest and pelvis was performed and no primary tumor was found. His upper endoscopy and colonoscopy also revealed no abnormal finding. Further biochemical evaluation showed normal alpha-fetoprotein (AFP), prostate-specific antigen (PSA), cancer antigen (CA) 19-9, U/mL, β-hCG, and CEA, and low dehydroepiandrosterone sulphate (DHEAS) levels and 24-hour urine metanephrines were 4.1 μg/day (0 - 350 μg/day).
Clinical suspicion of primary adrenal insufficiency was confirmed by an elevated baseline plasma ACTH of 99 pg/mL, a low plasma cortisol of 0.7 μg/dL (normal value of 12 - 25 μg/dL) and insufficient peak cortisol response of 1.9 μg/dL to ACTH stimulation (normal value of > 18 μg/dL). Bone marrow examination revealed no abnormality.
The patient was treated with high doses of intravenous hydrocortisone and rehydrated with sodium chloride infusion resulting in complete remission of symptoms and normalization of biochemistry. Subsequently, a CT-guided biopsy of the mass lesion was performed and microscopic examination of the material revealed diffuse large B-cell lymphoma.
Immunohistochemistry was positive for CD43, CD79, leukocyte common antigen (LCA), and Pax.5, but did not stain for CD3, CK, CK20, and cytokeratin (AE1/AE3). The proliferative fraction detected by Ki-67 was high and the diagnosis of B-cell lymphoma was confirmed ().
Chemotherapy was started on him. At the end of the third cycle, there was a transient clinical improvement despite no change in size of the tumors. But, the patient worsened thereafter and died 5 months after starting the chemotherapy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [53, 'years'], 'creatinine': [1.8, 'mg/dL']}",44.45278,42.23014,46.67542,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 53 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.8 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.8/0.9)**-1.2 * 0.9938**53 * 1.0 = 44.45278.
Hence, the GFR value is 44.45278 ml/min/1.73 m²."
363,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6477550-1,Extracted,"A 16-year-old female adolescent was referred to our hospital with severe hypertension (systolic pressure 178 mmHg), which was first detected 7 months prior to presentation during a routine annual physical examination. She complained of intermittent headache for about 1 year, and her previous blood pressure, measured 1 month prior to her detection of hypertension, had been normal. She showed mild hypokalemia (3.4 mmol/L) in a routine blood test, and an additional workup considering secondary hypertension was planned. Despite taking amlodipine (0.1 mg/kg twice a day), her blood pressure remained uncontrolled.
Upon admission to our hospital, her systolic and diastolic blood pressures were 155 mmHg (>99th percentile) and 111 mmHg (>99th percentile) respectively. She was 162.8 cm tall (50th–75th percentile) and weighed 55 kg (50th–75th percentile). Physical examination including ophthalmological examination revealed no abnormality other than hypertension, and her family history was negative for hypertension or renal diseases. Laboratory examination revealed normal levels of hemoglobin (14.4 g/dL), serum creatinine (0.57 mg/dL), serum total cholesterol (144 mg/dL), and normal urinalysis. Serum sodium, potassium, chloride, and total carbon dioxide levels were 134 mmol/L, 3.4 mmol/L, 102 mmol/L, and 27 mmol/L, respectively. Plasma renin activity was 9.83 ng/mL/hr (normal, 0.5–3.3 ng/mL/hr), and serum aldosterone level was 77.3 ng/dL (normal, 4–48 ng/dL). Urinary levels of vanillylmandelic acid, epinephrine, norepinephrine, dopamine, metanephrine, and normetanephrine were normal, and plasma levels of epinephrine, norepinephrine, and dopamine were also normal. Chest radiography, electrocardiography, and echocardiography showed normal findings. Renal Doppler ultrasonography revealed an avascular bilobed cyst in the lower pole of the right kidney (). Abdominal computed tomography (CT) angiography showed bilaterally normal renal arteries and an eccentric soft tissue component at the peripheral aspect of the cystic lesion (). The mass remained unenhanced during the arterial phase, and its margin was indistinguishable from the surrounding tissue (). During the delayed phase, its eccentric capsule showed enhancement, and an intact mass could be observed (), consistent with CT findings of JGC tumors.
A right partial nephrectomy was performed, and a clear resection margin was identified. The well-encapsulated mass measured 2.5 cm ×2.2 cm×2.0 cm in size with a partially cystic-appearing cut surface. Microscopic examination revealed sheets of polygonal tumor cells with amphophilic cytoplasm. Immunohistochemical examination showed that the tumor cells stained positive for CD34 and focally positive for CD117 (C-Kit) and smooth muscle actin. ()
Postoperatively, her blood pressure returned to normal (105/63 mmHg) without using any antihypertensive medication. On the 3rd postoperative day, the plasma renin activity (0.52 ng/mL/hr), serum aldosterone (3.9 ng/dL), and serum potassium (3.6 mmol/L) levels returned to normal. Her blood pressure and laboratory findings remained within the reference range over the next 3 years postoperatively until her last follow-up.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [16, 'years'], 'creatinine': [0.57, 'mg/dL'], 'sex': 'Female'}",136.69591,129.86111,143.53071,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 16 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.57 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.57/0.7)**-0.241 * 0.9938**16 * 1.012 = 136.69591.
Hence, the GFR value is 136.69591 ml/min/1.73 m²."
364,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5438001-1,Extracted,"A 78-year-old Caucasian woman presented with a 3-week history of cough, intermittent hemoptysis and epistaxis, weight loss, pleuritic chest pain, malaise, and arthralgia, but no joint pain or swelling. The primary physician had made a diagnosis of multifocal pneumonia based on symptoms and chest radiographic findings, and the patient was placed on a 2-week course of antibiotics (amoxicillin and azithromycin). At that time, the SCr was 0.9 mg/dL. The patient returned to the emergency department 2 weeks later with worsening cough, chest pain radiating to the shoulders, reduction in urine output, worsening malaise, arthralgia, anorexia, nausea, and vomiting.
Examination revealed an elderly woman, not in obvious respiratory distress, pale, not cyanosed, with no pitting pedal edema. There was no skin rash or mucosal ulceration. The sinuses were not tender. Pulse was 99 beats/min and regular, blood pressure was 114/64 mmHg. The precordium was normoactive, and the 1st and 2nd heart sounds were heard. The patient was tachypneic, with a RR 23 cycles/min. Oxygen saturation was 98% at room air and coarse breath sounds were heard in all the lung fields.
A basic metabolic panel revealed: sodium 128 mmol/L, potassium 3.8 mmol/L, bicarbonate 11 mmol/L (23 – 31 mmol/L), BUN 82 mg/dL (9.8 – 20 mg/dL), SCr 8.3 mg/dL (0.6 – 1.1 mg/dL), chloride 99 mmol/L, calcium 9.1 mg/dL (8.5 – 10.5 mg/dL), and anion gap 20 (5 – 15). SCr was 0.8 mg/dL and 1.2 mg/dL 2 and 1 weeks previously, respectively. During admission SCr increased to 9.4 mg/dL within 24 hours.
Urine dipstick was positive for blood and protein. Fractional excretion of sodium (FE Na) and FE urea were 7.5% and 63.6%, respectively. Urinary protein Cr ratio was 2.7.
Urine microscopy showed numerous eumorphic red blood cells (RBC), some dysmorphic RBC, a few white blood cells (WBC) and few granular casts. WBC count at admission was 10,000/cm3, and hemoglobin concentration was 7.7 g/dL.
Renal ultrasound revealed normal sized kidneys with increased echogenicity and no hydronephrosis. Chest radiograph showed persistence of a mass-like opacity in the right upper lobe similar to that seen on chest X-ray on the outpatient visit. Computerized tomography (CT) revealed multifocal spiculated nodules and masses within both lungs; the largest measuring ~ 3.3 × 4.8 cm in the right upper lobe, thought to represent an obstructing mass with resultant adjacent atelectasis. Further workup revealed normal C3 and C4 levels, negative ANA, ASO titers, and rheumatoid factor. C-ANCA was positive directed against PR3; titer > 8 Antibody Index (AI) (< 1.0 AI). P-ANCA was negative. Her anti-GBM IgG antibody was also positive > 8 AI (< 1.0AI), and C-reactive protein was elevated 24.5 mg/dL (< 0.5 mg/dL). Serology for hepatitis B, hepatitis C, and HIV were all negative. Serum and urinary protein electrophoresis were unremarkable. Renal and CT-guided lung biopsies were performed.
Light microscopy revealed 4 corticomedullary cores with 28 glomeruli, 5 of which were obsolescent. 16 glomeruli demonstrated cellular crescents with marked fibrinoid necrosis (). Obliteration of Bowman’s capsules and periglomerular giant cells were noted in a few glomeruli (). A marked acute and chronic interstitial infiltrate was present. Numerous red cell casts were noted. Mild tubular atrophy was accompanied by mild interstitial fibrosis. Arteries were sclerotic with no inflammation. A Congo red stain was negative.
Immunofluorescence was performed on 5 glomeruli, all of which had cellular crescents. Bright capillary loop staining was seen with antisera specific for IgG (2+; scale trace through 3+), C3 (1+), and κ and λ light chains (both 2+) (). Fibrinogen stained the crescents. No tubular basement membrane staining was seen.
Ultrastructural examination of single glomerulus demonstrated diffuse fibrinoid necrosis and marked endocapillary hypercellularity with numerous breaks in the capillary loop basement membrane. There were no immune complex-type electron dense deposits or tubuloreticular inclusions. Proximal convoluted tubular and peritubular capillary profiles were unremarkable. The CT-guided lung biopsy revealed multiple cores with necrotizing granulomatous inflammation and focal vasculitis with associated multinucleated giant cells (, ). A single fragment showed hemorrhage with focal organization. An assessment of anti-GBM antibody nephritis with 57% active crescents and ANCA-positive vasculitis presenting predominantly with extra-renal manifestations (granulomatosis with polyangiitis) was made.
Dialysis was initiated. The patient was immediately commenced on high-dose IV methylprednisolone 500 mg daily for 3 days, followed by high-dose oral prednisolone 60 mg. The patient also received 4 doses of IV rituximab 375 mg/m2 weekly as part of induction therapy (as per the RAVE trial), and 6 sessions of alternate day therapeutic plasma exchange (TPE) []. The anti-GBM antibodies disappeared and the PR3 ANCA dropped to 1.8 AI in 10 weeks. The patient is still dialysis-dependent 3 months later, but has had full resolution of respiratory and other systemic symptoms.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [78, 'years'], 'creatinine': [9.4, 'mg/dL'], 'sex': 'Female'}",3.91881,3.72287,4.11475,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 78 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 9.4 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (9.4/0.7)**-1.2 * 0.9938**78 * 1.012 = 3.91881.
Hence, the GFR value is 3.91881 ml/min/1.73 m²."
365,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5625662-1,Extracted,"A 74-year-old female visited our emergency room, complaining of fever and mental deterioration. Her initial vital signs were as follows: pulse rate 111/min, blood pressure 100/60 mmHg, and body temperature, 38.9 °C. On physical examination, no abnormal findings were detected except for left costovertebral angle tenderness. On initial laboratory tests, she had thrombocytopenia (platelet counts, 62 K/mm3). There were no findings of leukocytosis or prothrombin time prolongation. Serum levels of blood urea nitrogen and creatinine were 38.6 mg/dL and 0.6 mg/dL, respectively. The results of liver function tests were within normal limits. The level of C-reactive protein was elevated to 19.24 mg/dL. E. coli grew in urine and blood cultures. She was finally diagnosed with acute pyelonephritis and treated with intravenous administrations of ceftriaxone 2 g once daily for 4 days, and then ciprofloxacin 400 mg twice daily for 10 days. She recovered after systemic antibiotics treatment.
At presentation, diffuse and slate gray-bluish pigmented patches were noticed on her face and nails. Neurologic examination showed that the patient’s motor powers of the upper and lower extremities were grade IV and III, respectively. Five years before presentation, the patient had ingested soluble silver-NPs for a year for the purpose of health promotion. She used a colloidal silver generator, which produces 5 ppm of colloidal silver water in a single cycle by electrolysis using silver electrodes. She gave a detailed account to have ingested 0.8-1.2 l of colloidal silver solution daily for approximately 12 months.
Her facial discoloration was first noticed 2 years before presentation. She first experienced muscle weakness of both upper and lower extremities 1 year before presentation. As her muscle weakness gradually worsened, she visited a different hospital seeking a diagnosis 2 months prior to visiting our hospital. She was diagnosed to have inflammatory myopathy after pathological tests of samples obtained from her left thigh muscle at the other hospital, and received steroid therapy. Despite taking oral prednisolone 1 mg per kg body weight per day, she did not show any clinical improvement.
Upon admission to our hospital, serology testing for connective tissue disease-associated autoantibodies including dermatomyositis was performed and there were no abnormal findings for anti-Jo1, anti-Ro/La, or the fluorescent antinuclear antibody, anti-ds DNA, anti-CCP Ab, anti-U1RNP, anti-Sm, or anti-neutrophil cytoplasmic antibody. We performed chest and abdomen computed tomography (CT) to exclude cancer-associated myopathy and did not find any other tumorous lesions. We also performed endoscopic gastro-duodenoscopy and colonoscopy, but observed no discoloration on the gastrointestinal mucosa and no silver particles in biopsy specimens.
Ocular argyrosis was not found in the cornea or conjunctiva. The histopathologic results of skin biopsies from pigmented areas of forehead and nose revealed brown-black granules in the basement membrane of sweat gland epithelium that measured less than 1.0 um in diameter, which are diagnostic findings of argyria (Fig. ). We reviewed outside pathology slides obtained from the left thigh muscles and found markedly degenerated myofibers with disorganization of myofibrils without inflammatory reactions, consistent with unspecified myopathy, rather than inflammatory myopathy (Fig. ). We performed electromyography and nerve conduction studies for muscle weakness, which revealed diffuse, mild motor dominant polyneuropathy of both upper and lower extremities. A heavy metal analysis of hair samples including arsenic, mercury, cadmium, and bismuth showed all levels within acceptable ranges and copper levels below normal. We diagnosed the patient with generalized argyria with myopathy and polyneuropathy. She was transferred to a rehabilitation institution after slowly tapering off of steroids on the 22nd day of hospital admission.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [74, 'years'], 'creatinine': [0.6, 'mg/dL'], 'sex': 'Female'}",94.13009,89.42359,98.83659,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 74 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.6 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.6/0.7)**-0.241 * 0.9938**74 * 1.012 = 94.13009.
Hence, the GFR value is 94.13009 ml/min/1.73 m²."
366,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4421438-2,Extracted,"The patient was a 34-year-old Caucasian man, without toxic habits, with chronic renal failure stage V due to membranous glomerulonephritis but he had no other remarkable medical history. He was studied for receiving a preemptive kidney transplantation but there were no contraindications.
Study of a possible living donor (the patient’s 71-year-old mother) was performed. No contraindications for donation were found but she carried an MGUS with two monoclonal proteins, IgG kappa and IgA lambda. A bone marrow examination showed 8% plasma cells. The M-protein concentration in the serum was 10 g/L and serum free light chains lambda and kappa were 14.4 and 16 mg/L, respectively, with a normal ratio.
Kidney transplantation was carried out in May 2007 with no complications and renal function progressively improved. The patient was discharged 1 week after the procedure. Currently, 36 months after the transplantation, the patient has a serum creatinine level of 1.8 mg/dL (159 μmol/L) and a 24-h urinary protein excretion of 200 mg.
Induction immunosuppressive treatment consisted of basiliximab, mycophenolate mofetil, prednisone and tacrolimus. Three months after transplantation, tacrolimus was switched to sirolimus for the same reasons as in Case 1. The patient is currently receiving sirolimus and mycophenolate mofetil.
The patient has developed no immunological or infectious complications and serum protein electrophoresis and serum immunofixation revealed no monoclonal proteins.
No complications have occurred in the donor and there is no evidence of MGUS progression. Renal function is normal.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [34, 'years'], 'creatinine': [1.8, 'mg/dL']}",50.02857,47.52714,52.53,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 34 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.8 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.8/0.9)**-1.2 * 0.9938**34 * 1.0 = 50.02857.
Hence, the GFR value is 50.02857 ml/min/1.73 m²."
367,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7674717-1,Extracted,"A 46 years old woman patient admitted for worsening pancytopenia for 1 mo.
The patient had her regular hemodialysis scheduled at the nephrology department and we were consulted by the nephrology department for pancytopenia. Bone marrow biopsy and reverse transcriptase-polymerase chain reaction (RT-PCR) tests were performed. Bone marrow examination showed hypercellular marrow with 54% promyelocytes. Cytogenetics revealed FISH for t (15:17) in 10 of 20 cells, while RT-PCR revealed the PML/RARα fusion gene. She received induction chemotherapy with all-trans retinoic acid (ATRA) and idarubicin. After induction chemotherapy, follow-up bone marrow biopsy was performed; however, morphologic remission for promyelocyte was observed, and molecular remission was not achieved. Therefore, the first consolidation chemotherapy with idarubicin was provided with sustained ATRA administration, and molecular remission was confirmed a month later. Unfortunately, after the second consolidation chemotherapy, she was lost to follow-up. She maintained only her regular hemodialysis schedule at the nephrology department where pancytopenia was reconfirmed.
The patient has been on regular hemodialysis for 15 years due to chronic glomerulonephritis.
She has been gotten only erythropoietin treatment for mild anemia.
No signs of bleeding such as mucosal bleeding or petechia, commonly observed in APL patients, were noted. Her vital signs were stable.
The complete blood count results was normal in parentheses, as shown below: White blood cells (WBCs): 1080 × 103/μL (4.0–10.0 103/μL); hemoglobin: 8.9 g/dL (12-16 g/dL); platelets: 69 × 103/μL (150-400 103/μL); absolute neutrophil count (ANC): 420 × 103/μL (1.5-7.5 103/μL). Blood biochemistry results were as follows: Total bilirubin: 0.55 mg/dL (0.2-1.1 mg/dL); aspartate aminotransferase: 23 U/L (5-40 U/L); alanine aminotransferase: 17 U/L (5-40 U/L); albumi: 4.54 g/dL (3.5-5.2 g/dL); blood urea nitrogen: 86.6 mg/dL (8-20 mg/dL); creatinine: 11.6 mg/dL (0.5-1.3 mg/dL); C-reactive protein (CRP): 0.13 mg/dL (0-0.5 mg/dL). The results of the coagulation profile were as follows: Prothrombin time (PT): 11.3 s (9.4-12.5 s); activated partial thromboplastin time: 31.9 s (28.0-44.0 s); fibrinogen: 189 mg/dL (200-400 mg/dL); D-dimer: 9537 (0-255 ng/mL).
Bone marrow examination and RT-PCR tests were performed for the evaluation of pancytopenia. Bone marrow aspiration demonstrated relapsed APL with promyelocytes comprising 40% of differential leukocyte counts, as well as the t (15:17) (q22; q12) translocation and RML/RARα fusion transcript.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [46, 'years'], 'creatinine': [11.6, 'mg/dL'], 'sex': 'Female'}",3.71527,3.52951,3.90103,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 46 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 11.6 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (11.6/0.7)**-1.2 * 0.9938**46 * 1.012 = 3.71527.
Hence, the GFR value is 3.71527 ml/min/1.73 m²."
368,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6547289-1,Extracted,"A 63-year old female patient was admitted to the hospital for fatigue, jaundice, and large-volume ascites.
PNH was diagnosed 2 years earlier when she was admitted for anemia, but she was lost to follow-up. Six weeks before current admission, portal vein thrombosis was diagnosed and enoxaparin 60 IU twice daily was initiated.
The abdomen was distended, and the liver was enlarged 4 cm below the right costal margin. The spleen was mildly enlarged.
Blood analysis revealed hemoglobin of 10.8 g/dL, white blood cell count 5.4 × 109/L, platelets 171 × 109/L, reticulocytes 6.5%, international normalized ratio 1.0, total bilirubin 4 mg/dL, direct bilirubin 2.6 mg/dL, aspartate transaminase 28 IU/L, alanine transaminase 12 IU/L, alkaline phosphatase 456 IU/L, glutamyl transpeptidase 248 IU/L, total protein 6.6 g/dL, albumin 3.3 g/dL, lactate dehydrogenase (LDH) 650 U/L, serum haptoglobin < 7 mg/dL, creatinine 1.7 mg/dL, urea 81 mg/dL. Ascitic fluid had a serum-ascites albumin gradient of 1.7 g/dL (ascitic fluid total protein 3 g/dL, albumin 1.6 g/dL). Hepatitis B and C and human immunodeficiency virus serology was negative. Direct globulin test was negative.
In Doppler ultrasonography of splenoportal axis, recanalization of the portal vein and large abdominal portosystemic anastomoses were evident. Hepatic veins were patent. Magnetic resonance imaging showed hepatomegaly and confirmed the above findings. No esophageal or gastric varices were demonstrated in endoscopy. Ascites was refractory to diuretics and multiple large volume paracenteses were required. Due to the absence of a clear etiology of portal hypertension, a liver biopsy was performed.
Changes of portal venopathy with portal fibrosis and sclerosis and features of nodular regenerative hyperplasia were demonstrated. A spectrum of portal vein lesions was seen in interlobular portal tracts included in the biopsy, ranging from portal venule herniation in the periportal parenchyma, to slit-like stenosed portal venules and sclerosed portal tracts without a visible portal venule. In addition, parenchymal ischemic changes indicative of decreased venous outflow, mild focal sinusoidal and perivenular fibrosis, mild cholestasis, and mild secondary siderosis were noted. There was no bridging fibrosis or cirrhosis (Figure ). The overall changes supported the diagnosis of INCPH.
The flow cytometry at this point revealed that 16.5% of her red blood cells were PNH, 4.1% were partially deficient for CD59, and 12.4% lacked CD59 completely; 63% of her granulocytes and 60% of monocytes were PNH.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [1.7, 'mg/dL'], 'sex': 'Female'}",33.48762,31.81324,35.162,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 63 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.7)**-1.2 * 0.9938**63 * 1.012 = 33.48762.
Hence, the GFR value is 33.48762 ml/min/1.73 m²."
369,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6201034-1,Extracted,"A 43-year-old Asian male was transferred to our hospital after undergoing a drainage procedure for a gluteal abscess at another hospital. He was known to have poorly controlled diabetes, and hyperlipidemia on treatment; he was also a heavy smoker for more than 20 years. The complaints started 3 weeks prior to presentation with fever and gluteal abscess which was drained surgically (). The fever persisted despite receiving a combination of gentamycin and penicillin. Two days later, the patient’s condition deteriorated with the onset of shortness of breath and orthopnea. Two sets of blood culture performed on 6 August 2017 grew CoNS, which was considered a contaminant. Further evaluation via transthoracic echocardiography revealed the presence of large vegetation on the aortic valve with severe regurgitation and moderate size vegetation on mitral and tricuspid valve with moderate regurgitation plus aortic root abscess. He was subsequently transferred to our hospital for cardiac surgery.
On arrival, his condition had worsened as evidenced by fever with a temperature of 38.9°C, tachycardia (142 beats/minute), hypotension (96/54 mm Hg), and blood oxygen saturation level of 91%. Laboratory tests revealed a white blood cell count of 14,000/mm3 with 81% neutrophils while kidney profile showed acute renal failure with urea 19.5 mmol/L and creatinine 533 µmol/L. His C-reactive protein level was 200 mg/L.
He was admitted to the intensive care unit and parenteral vancomycin was initiated based on the knowledge of a previous culture of CoNS from the referring hospital. The condition of the patient deteriorated further the next day with refractory heart failure and pulmonary edema due to the extensive valvular lesions and insufficiency with worse blood gas values and desaturation (SpO2, 84%). He was intubated and continuous renal replacement therapy was initiated with a good response as demonstrated by the normalization of his blood pressure and blood gases.
The microbiologist in our hospital issued the result of the positive blood culture of CoNS, which was identified as S. lugdunensis by using MicroScan Walkaway 96 Plus commercial system. The decision to add cefazolin was based on the antibiogram which showed the isolate to be sensitive to almost all antibiotics tested including oxacillin. A transesophageal echocardiogram confirmed the presence of a large vegetation on the aortic valve with regurgitation and moderate vegetations on the mitral and tricuspid valves with regurgitation and aortic root abscess (Figures ). The general condition worsened with refractory heart failure and pulmonary edema due to the extensive valvular lesions and insufficiency.
An emergency open heart surgery was then performed to replace all valves and drain the aortic root abscess. His postoperative clinical course was uneventful with vancomycin and cefazolin as a combination of antibiotics administered over a period of 6 weeks. He was subsequently discharged in a stable condition ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [43, 'years'], 'creatinine': [533.0, 'µmol/L'], 'sex': 'Male'}",11.16578,10.60749,11.72407,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 43 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 533.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 533.0 µmol. To convert 533.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 533.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00053 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00053 mol Serum Creatinine * 113.12 g/mol = 0.05995 g Serum Creatinine. To convert 0.05995 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.05995 g Serum Creatinine * 1000.0 mg/g = 59.95 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 59.95 mg Serum Creatinine/10.0 dL = 5.995 mg Serum Creatinine/dL. The concentration value of 533.0 µmol Serum Creatinine/L converts to 5.995 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (5.995/0.9)**-1.2 * 0.9938**43 * 1.0 = 11.16578.
Hence, the GFR value is 11.16578 ml/min/1.73 m²."
370,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7294369-1,Extracted,"A 48-year-old gentleman with no known comorbidities presented with epigastric discomfort, early satiety, and unintentional weight loss of 18 kg in 1 year. He had a significant family history of gastric cancer in his older brother, ovarian and breast cancer in his mother, and breast cancer in his maternal grandmother. Computed tomography scan () revealed circumferential thickening of distal gastric body as well as thoracic, abdominal, and retroperitoneal lymphadenopathy. Esophagogastroduodenoscopy (EGD) revealed an exophytic mass. Biopsy was positive for adenocarcinoma with signet ring features (). Positron emission tomography scan showed avidity in the supraclavicular and thoracic lymph nodes. He was diagnosed with stage IV gastric adenocarcinoma and started on FOLFOX chemotherapy.
Four days after receiving the first cycle of FOLFOX, the patient was brought to the hospital by his family for confusion and altered mentation. Vitals signs on presentation were within normal limits, with temperature of 36.3 °C, heart rate of 89 beats per minute, blood pressure of 129/98 mm Hg, and a pulse oximetry of l00% on room air. On physical examination, he was drowsy and disoriented to person, place, and time. Neurologic examination, limited by altered mentation, revealed spontaneous movement of all 4 extremities. Patellar and ankle reflexes were 2+, and biceps and supinator reflexes were 3+ bilaterally. Cardiopulmonary and abdominal examinations were benign.
Computed tomography scan of head was negative for intracranial bleeding. Laboratory findings () were remarkable for elevated serum creatinine of 4.1 mg/dL, elevated phosphorus of 6.9 mg/dL, and elevated uric acid of 14.8 mg/dL. Calcium and potassium levels were within normal limits. He was admitted to the intensive care unit for uremic encephalopathy in the setting of TLS. Electroencephalography showed moderate generalized slowing, reflective of diffuse nonspecific cerebral dysfunction, without epileptiform activity.
He was managed with aggressive hydration and one dose of rasburicase. Over the next 2 days, his mentation and neurologic examination improved, with the patient successfully demonstrating orientation to person, place, and time. His electrolyte abnormalities improved (), with serum creatinine of 1.3 mg/dL, uric acid of 1.7 mg/dL, and phosphorus of 2.2 mg/dL. He was transferred to the general medicine floor and was discharged in stable condition.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [48, 'years'], 'creatinine': [1.3, 'mg/dL'], 'sex': 'Male'}",67.76399,64.37579,71.15219,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 48 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.3/0.9)**-1.2 * 0.9938**48 * 1.0 = 67.76399.
Hence, the GFR value is 67.76399 ml/min/1.73 m²."
371,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6791640-1,Extracted,"A 71-year-old white man presented with hypertension and ileocolonic stricturing CD since 1974. He had undergone 3 surgeries including ileocecectomy and 2 small bowel resections in 1975, 1986, and 2007. Current medications include 6-mercaptopurine, amlodipine, metoprolol, vitamin D, calcium, and a multivitamin. He was previously treated with sulfasalazine and oral mesalamine. He sparingly required oral steroids throughout his life. In October 2018, he presented for a 5-month history of worsening watery diarrhea and unintentional weight loss. Stool studies, including Clostridium difficile, were negative. Colonoscopy to the neoterminal ileum revealed a Rutgeerts score of i3. He was started on oral budesonide as a bridge to biologic therapy.
After starting 9 mg of budesonide, the patient immediately began to experience weakness and muscle aches. Three weeks later, these symptoms progressed and he was unable to walk or lift his arms above his head. He presented to the hospital, and laboratory tests revealed magnesium 0.8 mg/dL, potassium 1.7 mmol/L, creatinine 1.52 mg/dL, creatine phosphokinase 15,913 IU/L, calcium 7.1 mg/dL, albumin 3.7 g/dL, aspartate aminotransferase 253 U/L, alanine aminotransferase 125 U/L, and lactate dehydrogenase 734 IU/L. Urinalysis showed 3+ blood and 0–3 red blood cells. Laboratory values 2 months before were unremarkable, despite having chronic diarrhea for several months (Table ). He was diagnosed with rhabdomyolysis. Intravenous fluids and electrolyte replacement were initiated. The patient felt that the onset of symptoms correlated with the initiation of budesonide, so the medication was held. Over the course of the week, his symptoms improved drastically and ultimately resolved, correlating with creatine phosphokinase and potassium improvement. He followed up 3 weeks later, asymptomatic and with normal laboratory values (Table ).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [71, 'years'], 'creatinine': [1.52, 'mg/dL'], 'sex': 'Male'}",48.68504,46.25079,51.11929,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 71 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.52 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.52/0.9)**-1.2 * 0.9938**71 * 1.0 = 48.68504.
Hence, the GFR value is 48.68504 ml/min/1.73 m²."
372,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6398059-1,Extracted,"A 54-year-old male with IgA nephropathy had a kidney transplant, with chronic graft dysfunction (basal creatinine 2.7 mg/dL) due to biopsy-proven chronic thrombotic microangiopathy, attributed to tacrolimus. He had no previous history of diabetes, toxic habits, or liver disease, and he was HIV negative. Twelve months after transplantation, he was on treatment with everolimus (trough levels 6-8ng/mL) and prednisone 10 mg/24h.
The patient consulted in the emergency department due to an erythematous cutaneous lesion that had appeared 48 hours prior to the consultation, slightly painful. He did not report fever, trauma, or intense exercise. He had preserved general state and vital signs: BP 155/90, HR 85/min, basal SpO2 98%, and temperature of 37°C. Physical examination revealed a diffuse erythematous lesion on his left torso, indurated, and poorly delimited (). Blood analysis showed C-reactive protein 19 mg/dL, creatine-kinase 88 U/L, creatinine 3.5 mg/dL, hemoglobin 104 g/L, leucocytes 4.62·109/L [neutrophils 4.2·109/L, lymphocytes 0.3·109/L], platelets 224·109/L, and prothrombin time 100%. A CT-scan was performed immediately, which showed thickening of left pectoral muscles and trabeculation of adjacent adipose tissue, without collections or gas (). Given the suspicion of an infectious process, empirical treatment was started with ceftazidime and linezolid, and the patient was hospitalized. No microorganisms were isolated in blood cultures. Staphylococcus aureus methicillin-sensitive (MSSA) was isolated in nasal swab. One week later, despite antibiotic treatment, the lesion presented progressive fluctuating consolidation. An MRI was performed then, revealing a pectoral septated collection (59x52x42mm) () and confirming the diagnosis of pyomyositis. No signs of endocarditis as primary process were detected in the echocardiogram. MSSA was isolated in purulent fluid obtained by endoscopic ultrasound fine-needle aspiration. The lesion was surgically debrided and treatment was changed according to the sensitivity of the antibiogram to clindamycin and levofloxacin, for a duration of 4 weeks, achieving complete resolution of the process.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [54, 'years'], 'creatinine': [3.5, 'mg/dL']}",19.89039,18.89587,20.88491,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 54 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.5/0.9)**-1.2 * 0.9938**54 * 1.0 = 19.89039.
Hence, the GFR value is 19.89039 ml/min/1.73 m²."
373,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4323913-1,Extracted,"A 40-year-old male presented with facial puffiness and edema of lower extremities of 7 months duration. He had no history of bony pain, oral ulcers, arthralgia, skin rashes or any features suggestive of connective tissue disorder. On examination patient had pitting edema of lower limbs with no pallor, icterus or skin rashes. Blood pressure was 110/70 mm Hg. Systemic examination was normal. Urine microscopic examination revealed 4 + proteinuria with no active sediments. Twenty-four hours urine protein was 6.9 g. Renal function tests revealed blood urea nitrogen of 25 and serum creatinine of 2.06 mg/dl respectively. Patient had hemoglobin of 138 g/L, total leucocyte count of 11 × 109/L with normal differential counts and platelet count of 3.4 lakhs/micro litre. Serum total protein and albumin were 5.5 and 2.5 g/dl respectively. Liver function tests were normal. Patient's serum tested negative for hepatitis B surface antigen, antibodies for hepatitis C virus and human immunodeficiency virus-I/II. Antinuclear factor, rheumatoid factor, cryoglobulin and antineutrophil cytoplasmic antibodies were negative and serum complement levels were normal (C3 = 110 mg/dl and C4 = 20 mg/dl). Serum total cholesterol and triglyceride were 352 and 328 mg/dl. Ultrasonography revealed normal sized kidneys. With clinical diagnosis of nephrotic syndrome, ultrasound guided percutaneous kidney biopsy was performed.
Light microscopic examination showed eight glomeruli, all showed diffuse thickening of glomerular capillary walls with lifting up of podocytes. Jones silver stain revealed spikes []. No endocapillary or mesangial proliferative, tubulointerstitial and vascular alterations were noted. Immunofluorescence showed granular polyclonal IgG, kappa light chain and deposition of monoclonal IgG3 and C3 along glomerular capillary loops with intensity being 3 + on a scale of 0-3+ []. IgA, IgM, lambda light chain and complement (C1q) were negative. No deposition along tubular basement membranes was observed. Therefore, a diagnosis of MGN with monoclonal IgG3-kappa deposition was made on renal biopsy.
Urine and serum immunoelectrophoresis showed no monoclonal proteins. Serum kappa and lambda light chain concentrations were 1088 and 208 mg/dl respectively with κ/λ ratio of 5.2 (normal - 0.26-1.52). Skeletal survey did not reveal any abnormalities. Bone marrow examination revealed 3% plasma cells. With a diagnosis of monoclonal gammopathy with MGN, patient was started on treatment with 6 monthly cycles of velcade-thalidomide-dexamethasone (VTD) regimen (bortezomib - 1.3 mg/m2 on 1st, 4th, 7th and 11th days, thalidomide - 200 mg/day and dexamethasone - 30 mg/kg on 1st-4th and 7th-11th days of month). After 6 monthly cycles of VTD therapy, patient had reduction in proteinuria to 3.1 g/day with serum creatinine and albumin of 0.9 mg/dl and 3.1 g/dl respectively. Repeat serum free light assay revealed kappa and lambda light chain of 29 and 14 mg/dl respectively (κ/λ ratio: 2.01).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [40, 'years'], 'creatinine': [2.06, 'mg/dL'], 'sex': 'Male'}",40.99193,38.94233,43.04153,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 40 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.06 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.06/0.9)**-1.2 * 0.9938**40 * 1.0 = 40.99193.
Hence, the GFR value is 40.99193 ml/min/1.73 m²."
374,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7793217-2,Extracted,"A 70-year-old man with ischaemic cardiomyopathy was referred to our institution for catheter ablation of ventricular tachycardia (VT) storm. Eight years prior to his presentation, he had undergone coronary artery bypass grafting, endoventricular circular patch plasty, mitral valve plasty, tricuspid annuloplasty, and CRT-D implantation with an LV lead also surgically implanted for NYHA Class IV HF, reduced LVEF of 24%, and QRS width of 154 ms. He has also suffered from chronic obstructive pulmonary disease and chronic kidney disease (serum creatinine level, 1.99 mg/dL). Physical examination revealed a pansystolic murmur (IV/VI) over the apex and no lower-limb oedema. His BNP level was elevated to 500 pg/mL. Echocardiography revealed an LVEF of 20% and pulmonary hypertension [tricuspid regurgitation pressure gradient (TRPG) of 43 mmHg].
One day after admission, catheter ablation was performed under CARTO guidance (Biosense Webster Inc., Diamond Bar, CA, USA). CARTO mapping revealed a low-voltage area in the anterior and septal walls (). After elimination of all abnormal potentials within the low-voltage area, no VT could be induced.
However, the patient developed progressively worsening dyspnoea and hypotension even under optimized medical therapies including oral intake of carvedilol of 10 mg, spironolactone of 50 mg, furosemide of 40 mg, tolvaptan of 15 mg, and amiodarone of 200 mg and intravenous infusion of dobutamine at 5 μg/min/kg. Despite an improved LVEF of 35%, TRPG elevation to 90 mmHg was observed on echocardiography and respirator support was required. We were aware of the development of CAVB and a change in the QRS morphology during junctional escape rhythm that suggested injury to the left posterior fascicle (). We thought his haemodynamic deterioration was induced by RV and LV dyssynchrony due to CAVB caused by catheter ablation because the VT episodes were completely eliminated. We therefore decided to add a pacing lead (Model 3830, Medtronic, Inc.) at the HB region (). Although we initially placed the lead at the site where a HB potential was recorded, the pacing threshold at that site was too high to obtain stable permanent pacing. Alternatively, the lead was implanted at a more distal (ventricular) site where a possible right bundle branch potential was recorded (). During HBP, the QRS duration was not significantly shortened (186 ms, ), so we applied BiVHB+LV pacing. Fortunately, because a DF-1 lead was originally used as a defibrillator lead, we could connect the HBP lead to the RV pacing port. The pin of the original RV pacing lead was covered with a silicon cap and abandoned. Following the application of BiVHB+LV pacing, the QRS narrowed from 167 to 127 ms with an optimized AV delay (atrial-HB delay: 140 ms) and VV delay (HB-LV delay: 40 ms) (). Over the week following the upgrade to BiVHB+LV, his haemodynamics improved dramatically. Although RV-SD and LV-SD had worsened from 52 to 82 ms and 75 to 189 ms after ablation, respectively, BiVHB+LV reversed the RV-SD to 53 ms and LV-SD to 82 ms (). Unfortunately, he died from a non-cardiac cause, acute non-occlusive mesenteric infarction, 4 months after the upgrade although he had remained free from HF until that time.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [70, 'years'], 'creatinine': [1.99, 'mg/dL'], 'sex': 'Male'}",35.45562,33.68284,37.2284,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 70 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.99 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.99/0.9)**-1.2 * 0.9938**70 * 1.0 = 35.45562.
Hence, the GFR value is 35.45562 ml/min/1.73 m²."
375,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4150159-1,Extracted,"A 53-year-old black male with ESRD undergoing renal transplant evaluation was referred for a screening nuclear stress test. His medical history was otherwise notable for human immunodeficiency virus with a normal CD4 count and undetectable viral load on antiretroviral therapy. He was asymptomatic on arrival to the laboratory. Notable laboratory evaluation included the following (reference ranges shown parenthetically): Hemoglobin, 10.6 g/dL (13.5-17.5 g/dL); and creatinine 6.8 mg/dL (0.8-1.3 g/dL). Physical examination revealed an obese male with blood pressure (BP) of 158/100; pulse 75 beats/min, and saturation of 96% on room air.
He underwent pharmacologic nuclear stress testing per protocol. After 1.5 min of low-intensity ambulation he received IV regadenoson followed by technetium-99 injection. He reported transient shortness of breath and lightheadedness. There were no ischemic changes on the electrocardiogram. When he returned for stress imaging 45 min later he reported severe fatigue, nausea, and headache. An IV was restarted and 125 mg of IV aminophylline was administered. Symptoms quickly resolved, and stress images were acquired without issue. Perfusion imaging revealed no evidence of myocardial infarction or ischemia.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [53, 'years'], 'creatinine': [6.8, 'mg/dL'], 'sex': 'Male'}",9.02018,8.56917,9.47119,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 53 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 6.8 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (6.8/0.9)**-1.2 * 0.9938**53 * 1.0 = 9.02018.
Hence, the GFR value is 9.02018 ml/min/1.73 m²."
376,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4049046-1,Extracted,"This was a case report of a 77-year-old African American male patient with a past medical history of hypertension, cerebrovascular accident, bladder cancer, chronic renal insufficiency, right nephrectomy and multiple hospitalizations for sepsis presented to the hospital with a change in mental status, worsening renal failure and leukocytosis. He complained of watery non-bloody diarrhea. His stool test for C. difficile toxin was positive. The laboratory findings on admission revealed white blood count of 35.7 K/uL, hemoglobin of 16.0 mg/dL, platelets of 258 K/uL, Albumin of 2.2 mg/dL and creatinine of 2.5 mg/dL.
The patient was initially treated with oral vancomycin. On day 4 of antibiotic treatment, the diarrhea persisted. IV metronidazole was added to the therapeutic regimen. On day 15, in light of poor response to dual therapy, a sigmoidoscopy was performed showing severe pseudomembranous colitis. The patient developed severe sepsis with worsening leukocytosis, hypoalbuminemia and renal failure. A second sigmoidoscopy was performed on day 21 showing worsening of the pseudomembranous colitis with no improvement. After 25 days of dual oral vancomycin and IV metronidazole antibiotic therapy, a single dose of IVIG 400 mg/kg was administered over 12 h. The number of bowel movements per day immediately started to decrease with subsequent resolution in the patient's diarrhea, fever and leukocytosis. There was no recurrence following the IVIG therapy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [77, 'years'], 'creatinine': [2.5, 'mg/dL'], 'sex': 'Male'}",25.8151,24.52435,27.10586,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 77 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.5/0.9)**-1.2 * 0.9938**77 * 1.0 = 25.8151.
Hence, the GFR value is 25.8151 ml/min/1.73 m²."
377,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-7604,Extracted,"A 7-year-old boy is rushed to the emergency room after developing severe abdominal pain with nausea and vomiting for a day at a summer camp. He also has a bad cough and generalized muscle weakness. He was doing fine until these symptoms started on day 3 of his camp. Past medical history obtained from his parents on the phone was significant for recurrent nephrotic syndrome controlled by prolonged corticosteroid therapy. His blood pressure is 110/75 mm Hg, axillary temperature is 38.9°C (102.0°F) and random blood sugar is 49 mg/dL. On examination, he appears somnolent. His heart has a regular rate and rhythm and his lungs have rhonchi and focal wheezing, bilaterally. Results of other lab investigations are:
Sodium 131 mEq/L
Potassium 5.1 mEq/L
Chloride 94 mEq/L
Bicarbonate 16 mEq/L
Urea 44 mg/dL
Creatinine 1.4 mg/dL
A respiratory culture is positive for type A influenza.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [7, 'years'], 'creatinine': [1.4, 'mg/dL'], 'sex': 'Male'}",80.00528,76.00502,84.00554,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 7 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.4 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.4/0.9)**-1.2 * 0.9938**7 * 1.0 = 80.00528.
Hence, the GFR value is 80.00528 ml/min/1.73 m²."
378,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3669580-1,Extracted,"A 69 year old male patient was a known case of hypertension and receiving tablet atenolol 25 mg once a day since 3 years. He was diagnosed with spindle cell carcinoma on left thigh and was operated for it. Before surgery, he was given tablet furesemide 40 mg once a day and his anti-hypertensive drug was continued. On discharge after surgery, he was asked to continue his antihypertensive therapy with tablet atenolol 25 mg once a day and was also prescribed tablet ranitidine 150 mg twice a day, a combination of diclofenac 50 mg with serratiopeptidase 10 mg thrice a day and another combination of ampicillin 250 mg and cloxacillin 250 mg thrice a day for a total duration of 7 days.
After 7 days, he visited outpatient department with complaints of swelling over legs and decreased frequency of micturition. On examination, the patient was alert and his pulse and blood pressure were within normal limits. He had no pallor, icterus, lymphadenopathy or clubbing but he had pedal edema. His respiratory, cardiovascular and central nervous systems were within normal limits.
On investigation, it was found that his plasma creatinine and urea were raised to 9.4 mg/dl and 99 mg/dl respectively. Among the electrolytes, plasma potassium and sodium were 4.9 mEq/L and 133 mEq/L, respectively. These values of these tests when done 4 days prior to surgery were creatinine 1 mg/dl, urea of 17 mg/dl, potassium 4.6 mEq/L and sodium 141 mEq/L. Urine proteins were within normal range with total protein 6.8 g/dl (normal 6.0-8.3 g/dl) urine albumin 3.47 g/dl (normal 3.2-5.0 g/dl) and urine globulin 3.34 g/dl (normal 3.2-5.0 g/dl). Urinary sodium was decreased 14.1 mEq/L (normal 25-50 mEq/L) and so the osmality to 34.2 mEq/L (normal values 100-260 mEq/L).
Following the deranged report, his diclofenac was stopped and his investigations were repeated the following day, on day 5, day 10 and after 1 month. His plasma creatinine and urea levels didn’t show significant change on the following day but on day 5 the values started to drop towards normality with plasma creatinine 3.2 mg/dl, potassium 3.6 mEq/L and sodium 137 mEq/L. His pedal edema was also subsiding showing clinical improvement.
On subsequent visit, on day 10, his creatinine level further came down to 1.5 mg/dl, urea to 21 mg/dl, potassium 3.2 mEq/L and sodium 140 mEq/L. After one month, all the values returned within the normal range with creatinine 1.5 mg/dl and urea 16 mg/dl.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [69, 'years'], 'creatinine': [1.5, 'mg/dL']}",50.08415,47.57994,52.58836,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 69 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.5/0.9)**-1.2 * 0.9938**69 * 1.0 = 50.08415.
Hence, the GFR value is 50.08415 ml/min/1.73 m²."
379,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2967010-1,Extracted,"A 36-yr-old female patient was admitted for severe anemia in July 2002. She had been diagnosed with chronic kidney disease caused by immunoglobulin A (IgA) nephropathy. In October 2000, she began to receive rEPO therapy with Epokine (CJ Corp, Seoul, Korea), an EPO-α product, at a dose of 4,000 IU/week on subcutaneous (SC) route for anemia. Her hemoglobin (Hb) level was maintained at 10-12 g/dL before hemodialysis. In January 2002, she was started on hemodialysis, and her Hb level was maintained at 8-10 g/dL under EPO-α treatment at a dose of 3,000-6,000 IU/week. Eleven months after the start of hemodialysis, her Hb level dropped to 5.3 g/dL, although she was treated with rEPO-α at a dose of 12,000 IU/week. Even with the cumulative ESA dose of 224,000 IU over 26 months, her anemia did not improve. Therefore, she was transfused with two units of packed red blood cells every three weeks to maintain her Hb level despite the ESA treatment (12,000-15,000 IU/week). Meanwhile, she received three types of rEPO-α products (Epokine, Espogen [LG Life Sciences, Seoul, Korea], and Eporon [Dong-A Pharmaceutical Co., Ltd., Seoul, Korea]) and one rEPO-β (Recormon [Roche, Basel, Switzerland]) product transiently, but her anemia did not improve at all.
Initial laboratory test values on admission were as follows: leukocyte count, 4,610 cells/µL; Hb, 5.4 g/dL; platelet count, 113,000 cells/µL; reticulocytes, 0.27%; total iron binding capacity, 220 µg/dL (39.38 µM/L); ferritin, 1,760 µg/L; iron, 201 µg/dL (35.98 µM/L); parathyroid hormone, 23 ng/L; blood urea nitrogen, 83 mg/dL (29.63 mM/L); creatinine, 12.3 mg/dL (1,087.32 µM/L); C-reactive protein, 0.75 mg/dL. Serologic tests for hepatitis viruses, cytomegalovirus, Epstein-Barr virus, human immunodeficiency virus, and parvovirus B19 were all negative. Thoracic computed tomographic scans or abdominal sonography showed no evidence of an abnormal mass such as thymoma or lymphoma. Bone marrow examination showed reduced cellularity (0-20%) and severe erythroid hypoplasia, whereas thrombopoiesis was in the low normal range and granulopoiesis was normal, findings consistent with PRCA ().
In June 2003, anti-EPO antibodies were screened by competition enzyme-linked immunoassay (ELISA). The result of ELISA showed 1.9 times higher antibody titer in patients serum compared with in control serum, and ESA treatment was discontinued. The PRCA did not respond to oxymetholone treatment from June 2003 to July 2003. Although we considered immunesuppressive therapies, she refused to receive the treatments. In September 2003, the antibody was also identified by radioimmunoprecipitation assay, their binding capacity was 5.6 IU/mL. In the neutralizing capacity test, her serum showed complete inhibition of colony formation by normal marrow cells when stimulated by 0.5 IU of rEPO-α in an in vitro bioassay.
After then, she remained transfusion-dependent, Espogen was restarted from January 2004, but there was no response. After she was switched to Recormon on SC route, the transfusion requirement decreased and her anemia showed slight improvement. However, her Hb level decreased to 5.3 g/dL again in April 2005. Despite the increased dose of Recormon up to 15,000 IU/week, her Hb level did not recover. In June 2005, the patient was started on another type of ESA therapy, 40 µg/week of Aranesp (darbepoetin-α, Amgen Inc., San Francisco, CA, USA) subcutaneously, but her anemia did not seem to improve. Although darbepoetin-α was replaced with Recormon, there was a big decline in her Hb level again in April 2006. Later, darbepoetin-α (50 mcg/week) was reintroduced, following which her Hb level started to recover slowly and she did not require transfusions from August 2006. Her Hb level increased up to 12.1 g/dL under 20 µg/week of darbepoetin-α treatment in December 2006.
In July 2007, anti-EPO antibodies were still detectable by radioimmunoprecipitation testing, but the concentration was too low for titration. Similarly, biosensor immunoassay (Biacore 3000; GE Healthcare Life-science Corp., UK) detected antibodies against both EPO-α and darbepoetin-α, but their titers were below the quantifiable levels of 80 ng/mL and 100 ng/mL, respectively. The neutralizing capacity was not detected in an in vitro bioassay. Until now, the patient is on subcutaneous darbepoetin-α treatment and the Hb level is maintained at around 9-11 g/dL ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [36, 'years'], 'creatinine': [12.3, 'mg/dL'], 'sex': 'Female'}",3.68523,3.50097,3.86949,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 36 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 12.3 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (12.3/0.7)**-1.2 * 0.9938**36 * 1.012 = 3.68523.
Hence, the GFR value is 3.68523 ml/min/1.73 m²."
380,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8314078-1,Extracted,"A 50-year-old female patient presented to our university hospital with fever and nonproductive cough. Her medical history included chronic hypertension (treated with bisoprolol) and chronic renal impairment, which was managed conservatively without hemodialysis. The patient tested positive for COVID-19 through reverse transcriptase polymerase chain reaction (RT-PCR) detection assay for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Laboratory tests showed hyperkalemia (potassium level was 6 mmol/L), metabolic acidosis, high serum urea (200 mg/dL), and serum creatinine level of 11 mg/dL. The patient underwent emergent hemodialysis, and on day two of hospitalization, she was transferred to our isolation hospital dedicated to patients with COVID-19 infection. On admission, a computed tomography (CT) scan of the chest was performed and showed bilateral ground-glass appearance, mild right-sided pleural effusion, and enlarged cardiac silhouette (most probably pericardial effusion, ).
Upon admission to the isolation ICU, a physical examination of the patient revealed blood pressure of 150/90 mmHg, heart rate of 100 beats per minute, respiratory rate of 22 breaths per minute, and oxygen saturation (SpO2) of 88%. The patient was placed in the prone position with venturi oxygen mask delivering an FiO2 of 50%, resulting in a subsequent increase of the SpO2 to 92%. Arterial blood gases (ABG) analysis showed PaO2 to FiO2 ratio (P/F ratio) of 100. The laboratory results at that time showed ferritin 1200 ng/mL (normal 13 - 150), troponin 149 ng/L (normal 2 - 100), D-dimer 3.4 mg/mL (normal up to 0.5), CRP 159 mg/L (normal < 6), and total CK 300 U/L (normal 0 - 190) with normal value of CK-MB. We started methylprednisolone 2 mg/kg. On the following day, the patient was intubated and placed on mechanical ventilation secondary to progressively worsening respiratory distress. Norepinephrine infusion was started to stabilize blood pressure. The ECG showed sinus tachycardia and diffuse low QRS voltage. The patient suddenly developed pulmonary edema, and oxygen saturation decreased rapidly to the point of hypoxemic cardiac arrest. Immediately, 1 mg epinephrine was injected intravenously, FiO2 was placed at 100%, and chest compressions were started simultaneously. The patient responded with return of spontaneous circulation after 4 minutes of cardio-pulmonary resuscitation (CPR). The patient remained hypotensive (systolic blood pressure less than 90 mmHg) that required the addition of an inotropic infusion (epinephrine).
There were no cardiologists in the isolation hospital; thus, the ICU physician performed bedside transthoracic echocardiography (TTE, ), which revealed a large circumferential pericardial effusion around the entire heart with signs of early right ventricular diastolic collapse, a dilated but collapsing inferior vena cava, and lack of regional wall motion abnormalities. Using telemedicine technology, the intensivist sent the TTE video accompanied by the patient’s medical records to a cardiologist. The cardiologist confirmed the diagnosis and recommended urgent pericardiocentesis. The intensivist performed echo-guided pericardiocentesis using a central venous catheter, removing ~ 600 mL of clear serous fluid using the subcostal approach. A significant rise in blood pressure was noted along with improvement of the hemodynamic parameters. A sample from the pericardial fluid aspirate was sent to the laboratory for further analysis, and follow-up monitoring by TTE showed no pericardial effusion (). The patient had a hemodialysis session with ultrafiltration of 1.5 liters. After dialysis, the hemodynamics continued to improve, and vasopressor drugs were decreased. Oxygen saturation increased, and FiO2 requirement subsequently decreased. The results of pericardial fluid aspirate supported serous contents, but the laboratory did not examine it for the presence of SARS-COV-2.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [50, 'years'], 'creatinine': [11.0, 'mg/dL'], 'sex': 'Female'}",3.86247,3.66935,4.05559,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 50 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 11.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (11.0/0.7)**-1.2 * 0.9938**50 * 1.012 = 3.86247.
Hence, the GFR value is 3.86247 ml/min/1.73 m²."
381,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3593173-1,Extracted,"A 67-year-old female presented with chronic edema of the lower abdomen, perineum, and bilateral lower extremities. Renal function was abnormal (BUN/creatinine 22/1.52). Echocardiography showed normal function of both ventricles, however the right-sided pulmonary veins were not identified. The systolic pulmonary arterial pressure was 34 mmHg. Computerized tomography (CT) angiography showed total interruption of the IVC below the hepatic veins and confirmed the abnormal return of the right-side pulmonary veins into the subdiaphragmatic IVC below an IVC obstruction (). There were IVC collaterals to the azygos vein draining into the superior vena cava and hepatic veins draining directly into the right atrium (). At the time of surgery, a posterior lateral thoracotomy incision was made, and the chest was opened through the ninth intercostal space. The eighth and ninth ribs were divided posteriorly. Division of the diaphragm was extended medially to the hiatus of the IVC. The right side of the retrohepatic IVC was exposed by retroperitoneal dissection (). The patient underwent retrohepatic cavoatrial bypass from right atrium to the suprarenal IVC with a PTFE 16-mm ringed graft (Gore-Tex, W. L. Gore & Associates, Inc., Flagstaff, AZ, USA; ). The preoperative CVP and IVC pressure were 8 and 13 mmHg and the postoperative IVC pressure was 8 mmHg. The patient recovered without any complications. Her symptoms were resolved. The graft has remained patent on images obtained two years following the surgery. The patient has taken warfarin and aspirin to maximize the graft patency.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [67, 'years'], 'creatinine': [1.52, 'mg/dL'], 'sex': 'Female'}",37.35998,35.49198,39.22798,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 67 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.52 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.52/0.7)**-1.2 * 0.9938**67 * 1.012 = 37.35998.
Hence, the GFR value is 37.35998 ml/min/1.73 m²."
382,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4236634-1,Extracted,"A 52-year-old man was admitted with complaints of skin rash and burning sensation. He had noticed erythematous, variable-sized macules and patches on the dorsum of his feet and ankles (Figure ), as well as swelling and redness on both metacarpophalangeal joints. He had ingested a raw extract of D. quinqueloba as a traditional remedy (Figure ). The following day, he experienced symptoms of nausea, vomiting, and diarrhea. He had a history of hyperthyroidism and was treated with 5 mg of methimazole once daily. He denied the use of any other medication or supplements except for D. quinqueloba. On admission, the patient was afebrile, with normal blood pressure and pulse rate. Laboratory studies revealed the following values: white blood cell count, 9,900/mm3; absolute eosinophil count, 900/mm3; hemoglobin, 15.3 g/dL; platelet count, 193,000/mm3; aspartate aminotransferase, 27 U/L; alanine aminotransferase, 11 U/L; and total bilirubin, 0.65 mg/dL. Serological tests showed that the levels of anti-neutrophil cytoplasmic antibody, antinuclear antibody, complements, and double-stranded DNA were within the normal range. The urine output was 4.0 L/day. The serum creatinine level was 2.7 mg/dL, and blood urea nitrogen was 33.0 mg/dL. The level of immunoglobulin (Ig) E was markedly increased at 1320.0 IU/mL (institution laboratory reference of <100 IU/mL). Urinalysis showed a sodium concentration of 50 meq/L, fractional excretion of sodium of 3.77%, protein 1+, and blood 3+. The 24-hour urinary protein excretion was 930 mg/day. The kidney ultrasonography revealed slightly large and hyper-echogenic but morphologically normal kidneys, no scarring, good cortical preservation, and no evidence of hydronephrosis. On day 3, biopsies of the skin (Figure ) and kidney (Figure ) were performed. The kidney specimen contained 26 glomeruli, with no evidence of global or segmental sclerotic lesions. The glomerular basement membranes appeared normal, and there was no glomerular proliferation, inflammation, or other abnormality. Most of the changes involved the renal tubules and interstitium. Moreover, the interstitium was diffusely expanded by edema, with infiltrates composed of eosinophils, lymphocytes, and neutrophils. A limited number of red blood cell (RBC) casts were observed in the renal tubules and RBC extravasation was observed in the interstitium. Immunofluorescence staining was negative for IgA, IgM IgG, C3, C4, as well as kappa and lambda chains. Electron microscopy revealed no evidence of foot process effacement or electron-dense deposits. The pathologic findings of the kidney biopsy were compatible with those of AIN. The renal function progressively improved, and the patient was discharged with a serum creatinine of 1.1 mg/dL.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [52, 'years'], 'creatinine': [2.7, 'mg/dL']}",27.49732,26.12245,28.87219,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 52 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.7 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.7/0.9)**-1.2 * 0.9938**52 * 1.0 = 27.49732.
Hence, the GFR value is 27.49732 ml/min/1.73 m²."
383,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-5351,Extracted,"A 30-year-old man presents to his primary care physician complaining of headaches. He states that over the past month he has been trying to study for an accounting exam, but he finds it increasingly more difficult to focus due to his headaches. He also complains of lower extremity muscle cramping. He has no significant past medical history and takes ibuprofen and acetaminophen as needed. The patient’s temperature is 98°F (36.7°C), blood pressure is 168/108 mmHg, and pulse is 75/min. Labs are obtained, as shown below:

Serum:
pH (VBG): 7.50
Na: 146 mEq/L
K+: 3.2 mEq/L
Cl-: 104 mEq/L
HCO3-: 32 mEq/L
Urea nitrogen: 20 mg/dL
Creatinine: 1.1 mg/dL
Glucose: 85 mg/dL

An ultrasound reveals a hypoechoic lesion within the right adrenal gland. A 2 cm right-sided homogeneous adrenal mass is confirmed with computed tomography.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [30, 'years'], 'creatinine': [1.1, 'mg/dL'], 'sex': 'Male'}",92.61427,87.98356,97.24498,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 30 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.1/0.9)**-1.2 * 0.9938**30 * 1.0 = 92.61427.
Hence, the GFR value is 92.61427 ml/min/1.73 m²."
384,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5352960-1,Extracted,"A 69-year-old man was admitted to hospital with abdominal discomfort, tenderness, and dyspeptic complaints in August 2010. Abdominal ultrasonography revealed paraaortic lymphadenopathy and the patient was referred to the hematology department. He had no history of hypertension, diabetes mellitus, smoking, or alcohol use. The physical examination showed no sign of peripheral lymphadenopathy or hepatosplenomegaly. Laboratory results showed hypochromic microcytic anemia with a hemoglobin level of 11.9 g/dL, mean corpuscular volume (MCV) of 78 fl, erythrocyte sedimentation rate of 66 mm/h, and C-reactive protein level of 64 mg/L (normal range: 0-6 mg/L). The reticulocyte count was normal. There was no iron, folic acid, or vitamin B12 deficiency according to the laboratory results. All biochemical parameters were within normal range. Serologic tests for hepatitis, human immunodeficiency virus, Brucella, cytomegalovirus, Epstein-Barr virus, and HHV-8 were all negative. Serum immunoelectrophoresis demonstrated polyclonal hyperglobulinemia. Bone marrow aspiration and biopsy revealed normocellular findings. A computed tomography scan demonstrated a paraaortic lymphadenopathy (6 cm in diameter). Total lymph node excision was performed and the result of the pathologic specimen was reported as Castleman’s disease of the plasma cell type (Figure ). After operation, the patient was followed until July 2013, and he was in remission state according to laboratory and imaging studies. Follow-up laboratory results in 2011 showed that the erythrocyte sedimentation rate was 55 mm/h and the C-reactive protein was 25 mg/L. Follow-up laboratory results in 2012 showed that the erythrocyte sedimentation rate was 35 mm/h and the C-reactive protein level was 9.6 mg/L. During the patient’s last hematology visit in 2013, a physical examination revealed normal findings. Laboratory parameters showed that his hemoglobin level was 13.7 g/dL, the erythrocyte sedimentation rate was 33 mm/h, and the C-reactive protein level was 9.6 mg/L. All biochemical parameters were within normal range. Serum immunoelectrophoresis and protein electrophoresis were normal. Radiologically, there were millimetric lymph nodes in the paraaortic area. The patient stopped routine follow-up hematology visits after July 2013 and was not seen for three years due to the lack of complaints. In June 2016, the patient was admitted to the hematology department with complaints of nausea, vomiting, abdominal pain, and edema in the distal extremities. A physical examination revealed pale skin and conjunctiva without hepatosplenomegaly. Laboratory examinations revealed normochromic normocytic anemia (Hct, 25.7%; Hb, 9.6 g/dL; MCV, 87 fl) and elevated erythrocyte sedimentation rate (80 mm/h) and C-reactive protein (76 mg/L). The results of the laboratory findings were as follows: Glucose 95 mg/dL, BUN 75 mg/dL, creatinine 6.2 mg/dL, Na 139 mmol/L, K 5.0 mmol/L, Ca 8.2 mmol/L, phosphorus 5.2 mmol/L, uric acid 6.6 mg/dL, total cholesterol 223 mg/dL, LDL 126 mg/dL, GGT 15 U/L, ALP 97 U/L, AST 10 U/L, ALT 6 U/L, total protein 5.9 g/dL, albumin 2.4 g/dL, LDH 213 U/L, CPK 20 U/L, and serum iPTH level 151 pg/mL (15-65). The urine stick test revealed a positive result for protein (+++), but there were no erythrocyte or leukocyte casts in the microscopic evaluation of the urine sediment. The 24-h urine protein level was 10 g. ANA, anti-ds DNA, anti-GBM and ANCA profiles were all negative. The patient did not have any chronic inflammatory conditions such as tuberculosis, malaria, rheumatoid arthritis, or familial Mediterranean fever. The patient was referred to the nephrology department. An abdomen ultrasonography noted normal sized kidneys and a normal parenchymal thickness with increased grade 2 renal cortical echogenicity. All other findings were normal. A kidney biopsy was performed, which suggested AA-type amyloidosis (Figure ). Metabolic acidosis and uremic symptoms had occurred, oliguria developed, and creatinine clearance was decreased to 10 mL/dk. The patient was admitted for veno-venous hemodialysis intervention via a double-lumen dialysis catheter in the jugular vein. Hematologic assessment demonstrated that CD was in remission according to imaging studies. A PET-CT scan only reported multiple millimetric lymph nodes without FDG uptake in the paraaortic area. Hemodialysis intervention was continued three times a week due to progressive deterioration of kidney functions. The patient was discharged from hospital two weeks later with a hemodialysis catheter and followed weekly. Two months later, he was considered to have end stage renal disease and underwent routine hemodialysis intervention via a created arteriovenous fistula.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [69, 'years'], 'creatinine': [6.2, 'mg/dL'], 'sex': 'Male'}",9.12304,8.66689,9.57919,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 69 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 6.2 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (6.2/0.9)**-1.2 * 0.9938**69 * 1.0 = 9.12304.
Hence, the GFR value is 9.12304 ml/min/1.73 m²."
385,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6158991-1,Extracted,"A 74-year-old man, retired civil servant, presented through surgery outpatient clinic with 1-year history of bilateral scrotal and lower-limb swelling. The scrotal swelling was gradual in onset, painless, and progressively worsened with involvement and partial engulfment/burying of his penis. The bilateral lower-limb swelling was painless and not associated with breathlessness or orthopnea. There was no lower urinary tract symptom. There was no history of trauma, pelvic/groin surgery, and irradiation.
For the above complaints, he went to traditionalist who gave oral concoction and scrotal injection and made cuts/incisions on the scrotum and lower extremities all to no avail. He then decided to present to our center.
On examination, he was an elderly man with no obvious distress, anicteric, afebrile, and pale, with bilateral symmetrical pitting leg edema and scarification marks all over the lower extremities.
His pulse rate was 88 beats/min, respiratory rate was 18 cycles/min, blood pressure was 100/80 mmHg, and temperature was 37°C. The chest was clinically clear.
Abdominal and rectal examination was unremarkable with prostate barely enlarged with benign features.
External genitalia showed edematous scrotum and penis. Scrotum measured 15 cm ×15 cm, was nontender and thickened with hyperkeratotic penoscrotal skin with the testes barely palpable.
An impression of genital lymphedema secondary to chronic cellulitis from multiple local incisions and herbal application was made. He was admitted into the male surgical ward, investigated, and resuscitated.
Requested laboratory and radiological investigations with results include full blood count (FBC): hematocrit:24%, white blood cell: 6.6 × 103/ml, neutrophil: 36%, lymphocyte: 59%, monocyte: 04%, and eosinophil: 01%; platelet: 268 × 103/ml; erythrocyte sedimentation rate: 120 mm/h; serum PSA (total: 158.4 ng/ml; % free: 19.4); urinalysis: normal; skin snip and blood film for microfilaria were negative; retroviral screening was negative; S/E/U/Cr: Na: 141, K: 4.5, Cl: 100, HCO3: 21, urea: 5.9, and creatinine: 200. Abdominopelvic USS showed enlarged irregular prostate with nodular changes and lobulated margins highly suggestive of cancer of prostate, bilateral hydronephrosis, and multiple bilateral superficial inguinal lymphadenopathy.
Three units of blood were transfused to optimize the patient with posttransfusion hemogram of 10.6 g/dl. He was commenced on oral antibiotics, haematinics and diuretics. His limbs were also elevated on a pillow.
He had transrectal prostate biopsy and inguinal lymph node biopsy, with histopathology revealing adenocarcinoma of prostate Gleason score 8 [see for tissue photomicrograph].
We counseled him on the options of medical or surgical androgen deprivation therapy (ADT).
He opted for medical ADT, and we commenced monthly subcutaneous Goserelin 3.6 mg. He was discharged to be seen monthly on follow-up and Goserelin injection. For financial reasons, he was irregular with his injections but received a total of four doses in 7 months. His leg and scrotal swelling disappeared, and we lost him to follow-up.
Seven months later (14 months from the first presentation), he presented again with recurrence of scrotal swelling but no leg swelling. We offered the option of orchidectomy which he consented to and had. After a visit 2 weeks later, we lost him yet again to follow-up.
He only presented 24 months later (38 months from the first presentation) with recurrence of penoscrotal swelling and a new onset of nodular cutaneous growths on the lower abdomen on both lumbar regions around the area of subcutaneous Goserelin injection. These nodules were painless and progressively involved the entire lower abdomen below the umbilicus [Figures and ].
An impression of Kaposi's sarcoma to rule out metastatic skin nodules was made. Skin biopsy showed the lesion to be metastatic adenocarcinoma of prostate [see Figures and for photomicrograph]. PSA done then was 122 ng/ml, and he was commenced on tablet stilbesterol, vasoprin and hematinics. He died about 18 months from the onset of the skin metastasis and 56 months from first presentation and diagnosis of prostate cancer.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [74, 'years'], 'creatinine': [200.0, 'µmol/L'], 'sex': 'Male'}",29.65608,28.17328,31.13888,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 74 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 200.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 200.0 µmol. To convert 200.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 200.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.0002 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.0002 mol Serum Creatinine * 113.12 g/mol = 0.02262 g Serum Creatinine. To convert 0.02262 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.02262 g Serum Creatinine * 1000.0 mg/g = 22.62 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 22.62 mg Serum Creatinine/10.0 dL = 2.262 mg Serum Creatinine/dL. The concentration value of 200.0 µmol Serum Creatinine/L converts to 2.262 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.262/0.9)**-1.2 * 0.9938**74 * 1.0 = 29.65608.
Hence, the GFR value is 29.65608 ml/min/1.73 m²."
386,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-4766,Extracted,"A 37-year-old woman with a history of a kidney transplant presents with a cough, fever, and fatigue. Her symptoms started 1 week ago and have been steadily worsening. She has a history of IV drug use and worked in the past as a commercial sex work in her 20's. She recently traveled to Malasia 1 month ago. Her temperature is 101°F (38.3°C), blood pressure is 114/64 mmHg, pulse is 110/min, respirations are 19/min, and oxygen saturation is 93% on room air. Her physical exam is notable for bilateral coarse breath sounds. Laboratory values are ordered as seen below.

Serum:
Na+: 140 mEq/L
Cl-: 102 mEq/L
K+: 4.7 mEq/L
HCO3-: 22 mEq/L
BUN: 30 mg/dL
Glucose: 96 mg/dL
Creatinine: 1.5 mg/dL (baseline 1.4 mg/dL)
Ca2+: 9.1 mg/dL

A chest radiograph is obtained as seen in Figure A and a CT scan of the chest is obtained as seen in Figure B.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [37, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Female'}",45.74459,43.45736,48.03182,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 37 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.5 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.5/0.7)**-1.2 * 0.9938**37 * 1.012 = 45.74459.
Hence, the GFR value is 45.74459 ml/min/1.73 m²."
387,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7947333-1,Extracted,"A 16-year-old female with a five-day history of headache, fever, persistent vomiting, and complete loss of vision in both eyes was referred to the Ophthalmology unit from the children's emergency room of Abia State University Teaching Hospital. One month prior to presentation, she noticed a gradual, painless reduction in vision which was ignored.
The eye examination findings were as follows:
Visual acuity was no light perception in both eyes. A left divergent squint was noted with defective inward movement of the left eye. Also noted was a right nasal subconjunctival haemorrhage. Both corneas were clear. Both pupils were markedly dilated and not reactive to light (). On fundoscopy/slit lamp examination, there was a white pupil, marked disc, and retina oedema. () Soft and hard exudates were seen, left hazy media, and a macular scar was noted. The intraocular pressure (IOP) were 37mmHg and 28mmHg in the right and left eyes, respectively.
A diagnosis of ocular hypertension, and bilateral ERD was made, secondary to CRF and hypertensive complications. Senior Loken syndrome was the differential diagnosis.
A B-mode ocular ultrasound was requested.
She was placed on gutt 0.005% latanoprost/0.5% timolol, a drop in each eye, nocte; gutt 0.1% brimonidine, a drop in each eye, twice daily; gutt 0.1% diclofenac, vitreolent (0.3% potassium iodide and 0.3% sodium iodide) and 0.1% flurometholone, a drop in each eye, q.i.d.
The latanoprost/timolol and brimonidine are ocular antihypertensives used for the reduction of the IOP. Diclofenac was used for pain and inflammation. Fluorometholone is a low dose steroid used for its anti-inflammatory properties.
She was reviewed by the physicians and the following parameters were noted:
On presentation, her metabolic status showed the level of urea: 40.7 m/l (2.4–8.3), creatinine: 11.92mg/dl (0.6–1.1), potassium: 6.7 (3.4–5.2), chlorine: 91 (96–107), sodium: 133 (138–149), bicarbonate: 14 (24–30). Random blood sugar 245mg/dl; the urine specific gravity was 1.020, PH was 6.0, protein +++. Blood+++.
The systemic blood pressure (BP) was 220/140mmHg (>99 percentile for age). Systemic hypertension was managed with amlodipine 10mg daily, lisinopril 10mg daily, and intravenous furosemide 20mg daily. The hemoglobin level was 7g/dl on admission and she was transfused with 6 units of whole blood all through her stay in the hospital. A dialysis regimen of 3 times weekly was also recommended.
The B-mode ocular ultrasound scan showed normal sized and shaped globes. ( and ) The anterior chambers and the lenses were normal. There were thick echogenic membranes which are V-shaped, attached to the optic disc and ora serrata in the vitreous body on both sides. There were scattered ill-defined collections of slightly echogenic particles as well as a freely mobile membrane in the left vitreous body. The optic nerve shadows were normal. There was limited medial movement of the left eye. The movements of other extraocular muscles were within normal limits. An impression of bilateral retinal detachment with left-sided vitreous hemorrhage was made.
A renal ultrasound scan showed bilateral small kidneys measuring 8.61cm × 3.4cm and 8.31 × 4.28cm on the right and left sides respectively (). (Normal kidney sizes for her age are 10.74±1.35cm and 11.0 ±1.15cm on the right and left side, respectively.) There was a grade 3 increase in renal parenchymal echoes with the loss of corticomedullary echo differentiation. There were no renal cysts, calculi, or calyceal dilatation. Also noted was pelvic ascites. A diagnosis of bilateral chronic renal parenchymal disease with pelvic ascites was made.
She was discharged on request one month after admission and was placed on a weekly follow-up at the pediatric outpatient clinic.
In the third month of follow up, the ophthalmic review showed improvement of left eye visual acuity to hand movement. There was a reduction in the IOP to 35mmHg and 23mmHg in the right and left eyes, respectively. This recording was after her fourth hemodialysis. At this time, the systemic BP was 160/100mmHg.
The patient was inconsistent with hemodialysis due to financial constraints. She had only six hemodialysis treatments over seven months, prior to her demise.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [16, 'years'], 'creatinine': [11.92, 'mg/dL'], 'sex': 'Female'}",4.3335,4.11682,4.55018,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 16 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 11.92 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (11.92/0.7)**-1.2 * 0.9938**16 * 1.012 = 4.3335.
Hence, the GFR value is 4.3335 ml/min/1.73 m²."
388,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4010026-1,Extracted,"A 74-year-old man, a retired railroad conductor, with a history of hypertension, hyperlipidemia, and noninsulin-dependent diabetes mellitus presented to our Emergency Department with a several-day history of increasing shortness of breath associated with a new-onset chest pain. ECG performed in the Emergency Department showed a right bundle branch block, left ventricular hypertrophy, and left atrial enlargement. Troponin I was elevated at 77.28 ng/mL. (Beckman-Coulter's Access AccuTnl Assay; reference range 0.00–0.04) The remainder of the cardiac enzymes were essentially normal: myoglobin (50 ng/mL), CK-MB (5.2 ng/mL), and creatine kinase (74 IU/L). D-Dimer was normal at 0.33 mcg/mL. BUN was 13 mg/dL and creatinine was normal at 0.65 mg/dL (reference range 0.64–1.27). Standard Acute Coronary Syndrome protocol was initiated, and the patient was admitted to the hospital. Transthoracic echocardiography showed left ventricular hypertrophy, mild diastolic dysfunction, and a normal ejection fraction with no evidence of wall motion abnormality. Troponin levels remained elevated throughout the entire hospitalization, in continued disproportion to the other cardiac enzymes, (Myoglobin, CK-MB, and CK) which remained either normal or very mildly elevated throughout.
His hospital course was complicated by bibasilar pneumonia and atelectasis requiring multiple bronchoscopies, intubation with ventilatory support, and ultimately a tracheostomy; bilateral lower extremity deep venous thromboses, for which he underwent successful inferior vena cava filter placement; a progressive thrombocytopenia which proved to be Heparin-Induced Thrombocytopenia-antibody positive; and finally, a life-threatening bleeding duodenal ulcer.
A complete blood count trend analysis revealed a significant two-week down-trending of the patient's hemoglobin and hematocrit values; retrospectively a result of the slowly bleeding ulcer. Troponin levels was obtained serially throughout. is a graph showing all the patient's troponin I levels recorded at our hospital, with a juxtaposed graphing of his hemoglobin levels.
As the duodenal ulcer proved to be incendiary, and refractory to temporizing measures, the patient ultimately developed hemorrhagic shock and was taken emergently to the operating room where he underwent an exploratory laparotomy with pyloroplasty and successful suture ligation of the ulcer.
In addition to extensive resuscitation with normal saline, the patient had required a total of 18 units of PRBC. 12 of these units were given within 24 hrs. Intraoperatively, the patient received 5 units of PRBC, 10 units of FFP, and 5 units of platelets.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [74, 'years'], 'creatinine': [0.65, 'mg/dL']}",91.65023,87.06772,96.23274,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 74 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.65 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.65/0.7)**-0.302 * 0.9938**74 * 1.0 = 91.65023.
Hence, the GFR value is 91.65023 ml/min/1.73 m²."
389,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5487311-1,Extracted,"A 63-year-old Vietnamese male with end stage renal disease due to IgA nephropathy received an expanded criteria deceased donor kidney transplant (DDKT) in 2012 (5 antigen mismatch, 5% panel reactive antibody, PRA). He received induction with alemtuzumab and solumedrol and was maintained on tacrolimus and mycophenolate mofetil. There were no surgical complications or episodes of acute rejection in the post-transplant period. Allograft function stabilized with a serum creatinine (Cr) of 1.8 mg/dL. His past medical history was notable for incarceration in Vietnam, prior hepatitis B exposure with protective anti-Hepatitis B surface antibody, positive tuberculin skin test (TST) and a non-calcified nodule on chest X-ray (CXR). He had been in the United States for twenty years prior to his transplant. He did not receive isoniazid (INH) prophylaxis before undergoing kidney transplant. At one-year post-transplant, he was admitted with fever, palpitations and 3 cm non-tender submental lymph node. Labs were notable for acute kidney injury (AKI) with Cr of 3 mg/dL and urinary retention that resolved with urinary catheter placement and treatment for an enlarged prostate. CXR revealed bilateral pleural effusions and a large pericardial effusion. Fine needle aspiration of the lymph node and pericardial fluid grew Mycobacterium tuberculosis (MTB). He received anti-tubercular therapy (ATT) with 2 mo of Rifampin, INH, Pyrazinamide and Ethambutol (RIPE) and 4.5 mo of INH and Rifampin (IR). His treatment course was complicated by transaminitis with reactivation of hepatitis B leading to end stage liver disease. He was treated with tenofovir with resolution of transaminitis. Patient completed 6.5 mo of ATT and has been cured of TB. His kidney transplant failed three years later due to BK nephropathy, and he was initiated on hemodialysis.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [63, 'years'], 'creatinine': [3.0, 'mg/dL']}",22.62926,21.4978,23.76072,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 63 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.0 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.0/0.9)**-1.2 * 0.9938**63 * 1.0 = 22.62926.
Hence, the GFR value is 22.62926 ml/min/1.73 m²."
390,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-1297610-1,Extracted,"A 38-year-old male underwent a hiking tour on a hot, humid day in late July 2003. At the end of this exhausting trip he complained of dizziness, finally falling into an 'apathic' state. On the arrival of the emergency physician, the patient suffered from a generalized epileptic seizure. Subsequently, the comatose patient (Glasgow Coma Scale 6 (E 1, V 1, M 4)) developed respiratory insufficiency and cardiovascular failure (blood pressure 60/20 mmHg, heart rate 166/min). He was immediately intubated (using fentanyl (0.3 mg), etomidate (40 mg) and midazolam (20 mg)) and transported to our neurological intensive care unit (NICU).
On admission, the patient was deeply sedated and under analgesia, but still suffering from hypotension requiring immediate use of catecholamines (norepinephrine). The patient had normal weight (body mass index = 24) and no significant previous medical history. The initial cerebral computed tomography (CT) scan in combination with CT angiography did not reveal any pathologies and, to exclude an infectious origin for the central nervous system dysfunction, a lumbar puncture was carried out yielding normal cerebrospinal fluid. An initial extensive laboratory work up revealed impaired liver function (glutamic-oxaloacetic transaminase 312U/l (normal range: 10 to 50 U/l), glutamic-pyruvic transaminase 244 U/l (normal range: 10 to 50 U/l), gamma-glutamylcyclotransferase 94 U/l (normal range: 10 to 66 U/l) and a prothrombin time of 60% (normal range: 70 to 130%). Serum creatinine levels as well as blood urea nitrogen (BUN) were elevated (creatinine 2.6 mg/100 ml (normal range: 0.8 to 1.3 mg/100 ml) and BUN 30 mg/100 ml (normal range: 5 to 25 mg/100 ml)) indicating the beginning of renal failure. This situation was further complicated by rhabdomyolysis with elevation of myoglobin and creatine kinase (CK) (myoglobin peak level 33.124 μg/l (day 2), normal range: 0 to 116 μg/l) and CK peak level 102.4 U/l (day 4), normal range: 38 to 174 U/l.
At the time of admission, core body temperature measured by urinary bladder probe (Foley catheter; Kendall Curity, Mansfield, MA, USA), was 40.8°C. During the first 20 h of treatment, conventional temperature control methods including high-dose non-steroidal anti-inflammatory drugs (NSAIDs) (acetylsalicylic acid 1000 mg and paracetamol 2000 mg) and opioids (pethidine 100 mg), as well as external cooling devices such as cooling blankets (Blanketrol II®, Cincinnati Sub-Zero, Cincinnati, OH, USA) and Bair Hugger® (Arizant Healthcare Inc, Eden Prairie, MN, USA), which were applied for 8 h, did not lead to any significant decrease in core body temperature (Figure ). Because of subsequent deterioration of the patient's condition and insufficient conventional temperature control, an aggressive treatment approach with a novel intravascular cooling system (CoolGard 3000® and Cool Line™, Alsius, Irvine, CA, USA) was begun. The heat-exchange catheter (Cool Line™) was placed into the left superior vena cava and cooled saline was infused through a closed loop system into two heat-exchange balloons located near the distal end of the catheter. The temperature of the saline solution was adjusted automatically by the CoolGard 3000®, which is an external temperature control unit, according to feedback to the external pump/refrigerant device from a microthermister attached to a Foley bladder catheter. Target temperature was set at 37°C for the first 25 h of intravascular treatment and subsequently at 37.5°C. Target temperature was reached within 7 h at a maximum cooling rate of 0.6°C/h and 'cooling' was prolonged at this level.
Multiple organ dysfunction and secondary rhabdomyolysis led to increased levels of myoglobin and CK (myoglobin peak level 33.124 μg/l (day 2), CK peak level 102.4 U/l (day 4)). To prevent imminent renal failure, forced diuresis was initiated and continued for 40 h using high-dose furosemide and fluids, resulting in an urinary excretion rate of more than 400 ml/h, leading to a fluid turnover of up to 24,000 ml/24 h. With this aggressive measure, we suceeded in avoiding the use of extracorporal hemofiltration and the renal parameters returned to normal values within 3 days.
Core body temperature was maintained at about 37°C and subsequently maintained at 37.5°C (± 0.2°C) with the use of the intravascular catheter over the next 5 days (Figure ). Several attempts to stop the active cooling within this period (Figure ) led to an immediate steep increase of core body temperature, which forced us to prolong this very efficacious endovascular treatment. Finally, after 111.5 h, CoolGard® treatment was stopped, since most of the laboratory parameters had stabilized; the patient did not suffer from hyperthermia thereafter.
To confirm the diagnosis of severe heat stroke and to measure the systemic inflammatory response [], we analyzed levels of plasma cytokines and serum chemokines 60 h after admission. The results are shown in Table : soluble interleukin (IL) receptor (sIL-2R) 1500 pg/ml, IL-4 3 pg/ml, IL-6 204 pg/ml, IL-8 40 pg/ml and tumor necrosis factor alpha (TNF alpha) 38 pg/ml (IL-4, IL-6, IL-8, TNF alpha analyzed by immunoenzymometric assay, Biosource, Nivelles, Belgium; IL-2R analyzed by immunoenzymometric assay, Immunotec, Marseille, France). On days 5 and 7 after admission, the values of IL-6 had decreased to 96 pg/ml (day 5) and 34 pg/ml (day 7), respectively.
Initially diagnosed aspiration pneumonia as well as sinusitis maxillaris diagnosed on the initial cerebral CT scan, were treated with tazobactam/piperacilline and clindamycin. On day 3, somatosensoric potentials did not show any pathologic results. The patient was extubated on day 8 and transferred to a regular neurological ward on day 12 with neither signs of any focal neurological nor overt cognitive deficits. At the time of discharge from the NICU, laboratory parameters had returned to normal values.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [38, 'years'], 'creatinine': [2.6, 'mg/dL']}",31.38868,29.81925,32.95811,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 38 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.6 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.6/0.9)**-1.2 * 0.9938**38 * 1.0 = 31.38868.
Hence, the GFR value is 31.38868 ml/min/1.73 m²."
391,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-2041,Extracted,"A 59-year-old man comes to the emergency department because of worsening nausea and reduced urine output for the past 3 days. One week ago he had a 4-day episode of abdominal pain, vomiting, and watery, nonbloody diarrhea that began a day after he returned from a trip to Mexico. He has not been able to eat or drink much since then, but the symptoms resolved 3 days ago. He has a history of tension headaches, for which he takes ibuprofen about 10 times a month. He also has gastroesophageal reflux disease and benign prostatic hyperplasia. His daily medications include pantoprazole and alfuzosin. He appears pale. His temperature is 36.9°C (98.4°F), pulse is 120/min, and blood pressure is 90/60 mm Hg. Examination shows dry mucous membranes. The abdomen is soft without guarding or rebound. Laboratory studies show:
Hemoglobin 14.8 g/dL
Platelet count 250,000/mm3
Serum
Na+ 147 mEq/L
Cl- 102 mEq/L
K+ 4.7 mEq/L
HCO3- 20 mEq/L
Urea nitrogen 109 mg/dL
Glucose 80 mg/dL
Creatinine 3.1 mg/dL
Urinalysis shows no abnormalities.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [59, 'years'], 'creatinine': [3.1, 'mg/dL'], 'sex': 'Male'}",22.30416,21.18895,23.41937,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 59 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.1/0.9)**-1.2 * 0.9938**59 * 1.0 = 22.30416.
Hence, the GFR value is 22.30416 ml/min/1.73 m²."
392,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5941725-1,Extracted,"The patient is a 63-year-old male with a history of ESRD of unclear etiology, who underwent an uncomplicated cadaveric renal transplant with a creatinine nadir of 1.3 mg/dl. Approximately 6 months postop his creatinine level demonstrated an increase (1.78 mg/dl) and he developed new proteinuria in the setting of medical noncompliance. He underwent workup for allograft dysfunction, which included a normal renal transplant ultrasound; negative testing for DSA, BK virus, and CMV; review of blood tacrolimus levels; and maintenance of blood pressure control.
He underwent a standard ultrasound-guided renal transplant biopsy under sedation with the interventional radiology team, with two cores obtained from the lower pole of the transplant kidney. No complications were observed during the procedural imaging. He was not on any anticoagulants nor antiplatelet medications at the time of the procedure. Per standard practice, the patient was monitored for four hours after the procedure, had no pain and no significant bleeding on his dressing, and had normal vital signs. He was voiding normal yellow urine prior to discharge that afternoon.
The following day, his biopsy results confirmed acute T-cell-mediated rejection (Banff Grade IIB). He was contacted and admitted to the hospital for planned thymoglobulin infusion that evening. On arrival, his vitals were normal with a BP of 133/88 mmHg; however, over the course of the evening, his blood pressure rose to a max of 170/102 mmHg and he developed nausea. His admission labs returned with a notable creatinine rise from 1.31 to 4.46 mg/dl. His hemoglobin was stable at 12.1 g/dl with normal platelets and coagulation profile. He denied pain or any issues with urinating, including hematuria or low urine volume, since his biopsy. His exam was benign—no back, flank, or abdominal tenderness.
The precipitous uptick in his creatinine level combined with his hypertension and mild nausea raised concerns for complication from his recent renal biopsy. A renal transplant ultrasound was obtained, which demonstrated a subcapsular hematoma () in addition to decreased color Doppler flow at the inferior pole of the transplant kidney. These findings prompted urgent operative intervention. The patient underwent an exploratory laparotomy which revealed subcapsular hematoma spanning the entire allograft with circumferential compression. This was treated surgically with generous capsulotomy, releasing approximately 500 cc of clotted blood. Meticulous inspection of the allograft failed to identify a primary bleeding source, but hemostasis was achieved with a combination of electrocautery and topical hemostatics (Surgicel Original Hemostat, Surgicel Fibrillar Hemostat). The allograft appeared pink and well perfused at the conclusion of the procedure. An intraoperative ultrasound () confirmed interval improvement in color flow at the superior pole and periphery of the kidney as compared to the preoperative exam. A Jackson-Pratt drain was placed prior to closing the abdomen.
A repeat transplant kidney ultrasound was performed on postoperative day 1, again documenting improved vascular flow in the transplant kidney with normal resistive indices (0.6–0.7) and patent venous drainage; no perinephric fluid nor hydronephrosis was identified. The patient recovered well and showed immediate improvement in his creatinine (); he was discharged on postoperative day 3 after removal of his drain and completion of three total doses of IV thymoglobulin for his rejection. At the time of discharge, his vitals were stable with blood pressure ranges of 112–127/70–88 mmHg. His creatinine was 1.79 mg/dl and his CBC was normal. His wounds healed well, his blood pressure returned to baseline, and his creatinine level at clinic follow-up on June 21, 2017, was 1.30 mg/dl.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [1.3, 'mg/dL'], 'sex': 'Male'}",61.72823,58.64182,64.81464,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 63 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.3/0.9)**-1.2 * 0.9938**63 * 1.0 = 61.72823.
Hence, the GFR value is 61.72823 ml/min/1.73 m²."
393,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5637642-1,Extracted,"A 33-year-old otherwise healthy male presented to emergency room after referral from an urgent care unit after his chest X-ray showed multifocal pneumonia. His symptoms started with high grade-fever and rigors for the last 9 days. He later developed sore throat, difficulty swallowing, productive cough and progressive dyspnea. He denied any sick contacts, romantic relationships, recent travel, tuberculosis exposure, recent dental procedure or exposure to animals.
On presentation, his vitals included a temperature of 104°F, pulse-140/min, blood pressure −104/53 mmHg, respiratory rate-33/min and oxygen saturation-89% on ambient air.
On physical examination, he appeared toxic and scleral icterus was noticed. The oropharynx examination showed right tonsillar swelling with erythema but without exudates. A firm immobile non-tender right submandibular swelling was present. No tongue swelling, dental caries/abscesses were identified. Axillary and cervical lymph nodes were not appreciated. No skin rash, joint swelling, needle or track marks were noticed. Chest examination showed bilateral rhonchi. Central nervous, cardiovascular and gastrointestinal systems were unremarkable.
Initial laboratory evaluation showed elevated white blood count (WBC) 21k/µl (neutrophils 81%, lymphocytes 4%, bands 13%), hemoglobin 16.1 mg/dl, platelet count of 41 k/µl, blood urea nitrogen 46 mg/dl, creatinine 2.12 mg/dl (baseline normal), total bilirubin 5 mg/dl (direct bilirubin 2.4 mg/dl) and alkaline phosphatase 261 U/L. Arterial blood gas revealed marked hypoxia requiring high flow nasal cannula.
Chest X-ray showed bilateral airspace opacities and patchy ground glass opacities consistent with multifocal pneumonia ().
He was resuscitated aggressively with intravenous fluids for septic shock from possibly pulmonary source and started empirically on vancomycin, cefepime, and levofloxacin. Bedside ultrasound of submandibular swelling revealed a clot in right internal jugular vein followed by an urgent CT scan of neck which revealed 3.3 × 2.7 × 3.1 cm fluid collection representing an abscess in the right palatine tonsil with a phlegmon and non-occlusive thrombus in the right internal jugular vein consistent with the diagnosis of Lemierre’s syndrome (, )).
CT chest showed several hypodense foci of the lower lobes worrisome for phlegmon or early abscess formation and cavitary lesions in the right upper lobe (). Infectious disease and ENT were consulted and antibiotics were broadened to include clindamycin due to possible lung abscesses and cefepime was changed to meropenem due to its increased efficacy against anaerobes. A repeat ultrasound of neck veins didn’t show extension of the clot so anticoagulation was held.
The patient’s respiratory status deteriorated and he had to be intubated for worsening hypoxia. Bed side incision and drainage of the peritonsillar abscess was done by ENT which grew group-C streptococci. Antibiotics were narrowed to ampicillin-sulbactam after blood cultures came back positive for gram negative rods which were later identified as Fusobacterium species. His hospitalization course was complicated by acute respiratory distress syndrome(ARDS) requiring bi-level ventilation, intermittent pressor support and chest tube placement for persistent pleural effusions. Later, his kidney function deteriorated requiring hemodialysis for fluid overload. Antibiotics were changed to levofloxacin and metronidazole on day 10 of hospitalization as the decline in renal function was attributed to either interstitial nephritis from penicillin or septic acute tubular necrosis from the overwhelming infection. He continued to have recurrent fevers which led to repeat CT chest on day 15 of admission showing worsening of interstitial opacities and increase in the number of pulmonary cavities. Repeat cultures of blood, urine, and sputum were done which were negative including stool studies, bronchoalveolar lavage, and pleural fluid analysis. Same antibiotics were continued and gradually his fever resolved. His respiratory status continued to improve with improvement of hypoxia. The patient was extubated on day 21 of hospitalization. He never underwent tracheostomy and percutaneous endoscopic gastrostomy (PEG). He was also found to have right upper extremity deep venous thrombosis diagnosed by ultrasound after he was noticed to have swelling of right upper extremity. He was started on heparin initially and later bridged to warfarin. His kidney function improved and dialysis wasn’t required anymore. Levofloxacin was discontinued after a month and metronidazole was continued for a total of 6 weeks of antibiotics. He did well post discharge and warfarin was discontinued after three months.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [33, 'years'], 'creatinine': [2.12, 'mg/dL'], 'sex': 'Male'}",41.36596,39.29766,43.43426,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 33 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.12 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.12/0.9)**-1.2 * 0.9938**33 * 1.0 = 41.36596.
Hence, the GFR value is 41.36596 ml/min/1.73 m²."
394,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8169095-1,Extracted,"A 61-year-old man was referred to the emergency department of our hospital by his assistant physician due to asthenia, nausea, and anorexia during the previous month coupled with rapidly deteriorating renal function. The past medical history included dyslipidemia, controlled arterial hypertension, partial thyroidectomy, and stable untreated psoriatic arthritis with no other known associated connective tissue or autoimmune conditions. The patient was also accompanied by a cardiologist due to a history of syncope but no chronic cardiomyopathy, arrhythmia, or coronary disease was found in the aetiologic investigation. The patient denied any knowledge of diabetes, stroke, or any infectious diseases. His family history was negative for thrombotic disorders as well as autoimmune conditions and otherwise unremarkable. He was on ivabradine 5 mg/day, telmisartan 80 mg + amlodipine 5 mg/day, and rosuvastatin 10 mg/day. No pharmacological allergies were known.
The patient did not present fever, weight loss, or arthralgia and no skin changes were apparent. Haematuria, dysuria, and foamy urine were not reported and the patient did not exhibit respiratory symptoms or hemoptysis. Eye redness/pain and headache were not mentioned and the patient denied mucous dryness or ulceration. No gastrointestinal symptoms were pointed out. No new drugs or toxic/herbs, namely herbal remedies or teas, were identified. The patient had no contact with domestic or farm/wild animals and had not traveled abroad recently.
On physical examination at admission, blood pressure was 174/86 mmHg, heart rate was 78 bpm with a rhythmic pulse, respiratory rate was 18/min, and the temperature was 36.5ºC. The air oxygen saturation was 94%. The pallor of the skin and mucous membranes was apparent. No anomalies were found in cardiopulmonary auscultation and the abdominal examination was unremarkable. No peripheral edema was found and capillary perfusion time was normal (<2 sec). The patient presented bilateral ankle swelling with no external inflammatory signs or pain, that he described as chronic and unaltered. Neurological examination at admission was normal.
Investigation
The most relevant performed laboratory studies and normal reference values are detailed in Table . A complete hemogram revealed mild anemia with normal white blood cells (WBC) and platelet counts; no schistocytes were found on peripheral blood smear ruling out, thrombotic microangiopathy coagulation tests were within normal range. Lactate dehydrogenase, total bilirubin, and haptoglobin were also normal, making hemolysis unlikely. C-reactive protein was only mildly elevated (23.1 mg/L). Creatine kinase and myoglobin levels were normal. Serum protein electrophoresis profile was typical and immunoglobin levels and light chain proteins in the serum were within normal range.
Urea and serum creatinine were markedly elevated at admission (206 mg/dL and 8.01 mg/dL, respectively), but the electrolyte panel showed only slight hyperkalemia (5.6 mEq/L) and hyperphosphatemia (4.9 mg/dL) with no other deviations. Uric acid was also elevated. Mild elevation of parathyroid hormone (PTH) with low 25-OH-vitamin D and normal calcium suggested a subacute process. Complementary testing found no abnormalities in lipidic profile, cytocholestasis markers, thyroid function, serum iron, transferrin and ferritin, and vitamin B12 and folic acid levels.
The urinalysis showed marked erythrocyturia with slight proteinuria and leukocyturia that coupled with hypertension suggested a nephritic process but no pathological casts were found in urinalysis.
Regarding immunology markers, ANCA-MPO titer was 72 U/mL (normal value <20) and anti-GBM titer was 216.0 U/mL (normal value <7), both demonstrating a frank elevation. Serum tests for anti-streptolysin O, anti-nuclear antibodies, anti-cyclic citrullinated peptides, rheumatoid factor, anti-double-stranded DNA, anti-extractable nuclear antigens (ENA), and anti-cardiolipin antibody titers were negative and there was no complement consumption. Anti-treponemal tests, human immunodeficiency virus, hepatitis B virus, and hepatitis C virus serologies were also negative.
Given the positivity of ANCA-MPO and anti-GBM autoantibodies, renal biopsy was performed, confirming the diagnosis (Figure ). The biopsy material allowed the observation of a total of 21 glomeruli with 47.6% of crescentic glomeruli (eight cellular crescents and two fibrocellular crescents). There were five sclerotic glomeruli and the remaining presented mesangial proliferation. There was also a moderate degree of tubular atrophy associated with interstitial scarring and inflammation and signs of haematuria as well. Immunofluorescence for immunoglobulin G (IgG) revealed linear deposits along the glomerular basement membrane and weaker staining in the tubular basement membranes, compatible with this entity. The lung CT showed no abnormalities.
Treatment
The patient was readily started on a high dose of methylprednisolone (1 g/day for three days) followed by a maintenance dose of 1 mg/kg of prednisolone. He was started on intravenous cyclophosphamide during the hospital stay and administered a cumulative dose of 5 g. Daily plasmapheresis with albumin reposition was initiated and continued for a total of 10 consecutive days and in alternate days for five more days. Renal function support with hemodialysis was needed shortly after diagnosis. Pneumocystis jirovecii prophylaxis with trimethoprim/sulfamethoxazole three times a week was also provided, as the patient was on high dose corticosteroids and immunosuppressant therapy.
Outcome and follow-up
The patient evolved with significant improvement of his systemic symptoms and despite maintaining adequate diuresis, renal function recovery was not obtained which motivated a regular hemodialysis program initiation. In what concerns antibody titers, steep descent in anti-GBM titers was noted at discharge (anti-GBM 7.9 U/mL) and ANCA-MPO titers normalized and both were persistently within normal levels during a follow-up of two years.
The patient was advised to seek medical attention immediately if abnormal symptoms presented to evaluate vasculitic relapse. Medical follow-up appointments were scheduled to assure an adequate multidisciplinary approach. Prednisolone was tapered and eventually stopped five months following hospital admission and there was no need for reinstitution.
Despite clinical and analytical stability, since the patient is hemodialysis-dependent (two sessions per week, three hours per session), a referral for a renal transplant was considered and is ongoing [].","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [61, 'years'], 'creatinine': [8.01, 'mg/dL'], 'sex': 'Male'}",7.05113,6.69857,7.40369,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 61 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 8.01 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (8.01/0.9)**-1.2 * 0.9938**61 * 1.0 = 7.05113.
Hence, the GFR value is 7.05113 ml/min/1.73 m²."
395,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7661643-2,Extracted,"A 46 years old Chinese Singaporean woman complained of two episodes of central chest pain at rest, 3 hours apart, with increasing intensity. At ED triage her blood pressure was 138/78 mm Hg, heart rate of 89 beats per minute and oxygen saturation of 98% on room air. Her initial electrocardiogram looked normal, but her troponin I level was raised to 1465 ng/L. Her laboratory investigations revealed a normal hemoglobin of 14.1 g/dL, and creatinine of 41 μmol/L. She was diagnosed with a non ST-segment MI and was loaded with aspirin and ticagrelor. Coronary angiography revealed two tandem high-grade stenotic lesions in the mid and distal LAD artery (Figure ). IVUS showed mild fibrotic plaques with significant intramural hematoma causing intraluminal narrowing (Figure ). Balloon angioplasty was performed with a 2.0 mm balloon, as there was on-going angina, this was followed by implantation of a 2.25 × 33 mm drug-eluting stent across the lesions to prevent re-occlusion, with good result on IVUS. Her left ventricular function was preserved on echocardiogram. Her cardiovascular risk factors included newly diagnosed hyperlipidemia (low-density lipoprotein 3.36 mmol/L) and hypertension (140/80 mm Hg). Her BMI was 22.1 kg/m2. She was discharged the following day with aspirin, ticagrelor, atorvastatin, bisoprolol, and lisinopril.
After 2 days, she was readmitted for recurrent chest pain that coincided with onset of her menstrual cycle. The initial concern was whether she had progression or recurrence of SCAD but her electrocardiogram was normal and the troponin I level was not higher than before. Her full body computed tomography angiogram did not reveal extracoronary arteriopathy. She was discharged the following day with spontaneous resolution of her chest pain. On follow-up, she continued to experience recurrent chest pain episodes, and had to be reviewed frequently outpatient in the women's heart health clinic. Her electrocardiogram and troponin I level remained normal during each chest pain episode. She was treated with beta-blocker and nitrate therapy. Eventually, her symptoms abated with completion of the cardiac rehabilitation program, which gave her confidence in performing her usual physical activities and exercise. She also received coaching from the occupational therapist on healthy lifestyle habits and stress management strategies. She completed 6 months of dual antiplatelet therapy, and was maintained on lifelong single antiplatelet agent. She remained on beta-blockade, angiotensin converting enzyme-inhibitor, and low dose statins.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [46, 'years'], 'creatinine': [41.0, 'µmol/L']}",119.9507,113.95316,125.94823,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 46 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 41.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 41.0 µmol. To convert 41.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 41.0 µmol Serum Creatinine * 1e-06 mol/µmol = 4e-05 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 4e-05 mol Serum Creatinine * 113.12 g/mol = 0.00452 g Serum Creatinine. To convert 0.00452 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00452 g Serum Creatinine * 1000.0 mg/g = 4.52 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 4.52 mg Serum Creatinine/10.0 dL = 0.452 mg Serum Creatinine/dL. The concentration value of 41.0 µmol Serum Creatinine/L converts to 0.452 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.452/0.7)**-0.241 * 0.9938**46 * 1.012 = 119.9507.
Hence, the GFR value is 119.9507 ml/min/1.73 m²."
396,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6875423-1,Extracted,"An 86-year-old woman (2 gravida, 2 para), who was presented with an increased pelvic mass, was referred to our facility. She had undergone surgery to repair an umbilical hernia one year previously, and a large abdominal mass with broad calcification, measuring 16 × 13 × 13.1 cm (longitudinal × transverse × anteroposterior), was identified by plain computed tomography (CT) before the hernia repair surgery. The mass was consistent with a uterus containing calcified uterine fibroids (). The patient felt the increased pelvic mass and experienced gastric discomfort related to the stomach being compressed by the mass, resulting in complete appetite loss for the previous week. She was also presented with continuous uterine bleeding and urinary discomfort. The latest CT examination showed that the myomatous uterus significantly increased in size, measuring 27 × 16.5 × 17 cm (), and the calcified lesion was largely displaced (Figures and ).
On admission, her height was 150 cm and body weight was 60 kg. Her body temperature was 35.8°C, pulse rate was 81/min, and blood pressure was 88/40 mmHg. Although she was lucid, her Eastern Cooperative Oncology Group (ECOG) performance status was level 3, accompanied by disabling fatigue []. Her abdomen was distended by an irregular hard mass equivalent to 28 weeks' gestation. There was mild tenderness without rebound tenderness on the mass. On pelvic examination, the portio was normal and no vaginal bleeding was observed. Transabdominal ultrasound showed a large pelvic mass with peripheral calcification suggestive of uterine fibroids. Both ovaries were undetectable and minimal ascites was observed. Both kidneys were normal, with no dilatation of the renal pelvis and ureter. Plain CT images revealed that the uterine cervix was elongated and moved upward compared with its position one year before ().
Blood tests showed an elevated white blood cell count (32,500/μL), low hemoglobin levels (9.9 g/dL), elevated C-reactive protein (16.4 mg/dL), and high serum creatinine (2.45 mg/dL). We initially suspected a malignant tumor arising from the uterus or ovary, such as uterine leiomyosarcoma, carcinosarcoma, or ovarian cancer, based on the patient's advanced age, abnormal uterine bleeding, rapidly growing abdominal mass, and ascites. Therefore, we performed cervical cytology, endometrial cytology, and a puncture of the pouch of Douglas to assess the cytology of the ascites. The results of all cytological examinations were negative for malignancy. Transvaginal ultrasonography revealed that the endometrium was thin; therefore, we did not perform an endometrial biopsy. On the second hospital day, the patient's vital signs were stable, but her ECOG performance status fell to level 4. She was completely confined to the bed and could not carry out any self-care tasks; this change in status was accompanied by delirium. Paralytic ileus developed and her bowel was decompressed with a gastric tube. A small amount of uterine bleeding was observed, and her urine volume gradually decreased. Her hemoglobin level decreased (8.5 g/dL), and her white blood cell count (37,800/μL) and serum creatinine levels (3.5 mg/dL) were elevated. On the third hospital day, she remained in a state of delirium. Hemorrhagic fluid was collected from the pouch of Douglas by a needle aspiration. The preoperative diagnosis was degeneration and infection of the large myomatous uterus; however, the relationship between the diagnosis and the deleterious change in her general condition remained unknown. During emergency surgery, the uterus was found to be rotated 360 degrees clockwise at the level of the isthmus (). The rotated uterus had suffered total infarction. A small amount of hemorrhagic fluid was present in the peritoneal cavity. A part of the small intestine was compressed by the uterus. We performed a total abdominal hysterectomy and bilateral salpingo-oophorectomy. The weight of the uterus was 3.8 kg. The postoperative course was uneventful, and the patient was discharged on the seventh postoperative day. Histopathology showed fibroids and extensive uterine and adnexal hemorrhagic infarcts consistent with uterine torsion.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [86, 'years'], 'creatinine': [3.5, 'mg/dL'], 'sex': 'Female'}",12.20164,11.59156,12.81172,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 86 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 3.5 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (3.5/0.7)**-1.2 * 0.9938**86 * 1.012 = 12.20164.
Hence, the GFR value is 12.20164 ml/min/1.73 m²."
397,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5977029-1,Extracted,"An 86-year-old woman with known history of coronary artery disease and sick sinus syndrome was admitted to the hospital with dyspnea, orthopnea, and exertional dizziness. Physical exam revealed bibasilar crackles, a grade 5 crescendo-decrescendo murmur, elevated JVP, and lower extremity edema. Laboratory findings were pertinent for creatinine of 1.73, BUN of 45, and NT-pro-BNP of 10k. The rest of her physical exam and laboratory was normal. Electrocardiogram showed normal sinus rhythm with known left bundle branch block. 2D echocardiogram demonstrated severe aortic stenosis with mean aortic valve pressure gradient of 68.6 mmHg and peak velocity of 5.15 m/s with preserved systolic function. She received intravenous diuretics with some clinical improvement. She was seen and evaluated by cardiothoracic surgeon for evaluation of aortic valve replacement but deemed high risk for surgical aortic valve replacement with an estimated surgical mortality by Society of Thoracic Surgeons score of 8.1%. Cardiac computed tomography angiography was done as part of transcatheter aortic valve replacement evaluation and showed severely calcified aortic leaflets with short and low left coronary system with coronary ostial height of 8.4 mm (). Special attention was paid to the left coronary leaflet calcification and the short and low coronary ostium. Coronary angiography revealed 50% LAD stent restenosis, diffuse distal LCX disease, and 90% proximal RCA stenosis. A drug-eluting stent was implanted to the right coronary artery. The decision then was made to proceed with TAVI utilizing coronary protection technique during the procedure. TAVR was then undertaken from the right femoral artery through a 14F Edwards arterial sheath. Two 300 mm long Prowater wires were advanced to the LAD and LCX arteries. With rapid ventricular pacing over a long Amplatz extra stiff wire, balloon aortic valvuloplasty using an Edward 4 × 23 mm balloon with simultaneous root aortography to see how the left main flow was performed (). There was flow compromise in the left main system to TIMI-2 flow; the wires were deformed and the large piece of calcium in the left cusp moved right over the left main coronary artery (). We therefore made decision to place two 3.5 × 12 mm Robel bare-metal stents in the LAD and LCX. An Edward 23 mm SAPIEN 3 valve with rapid ventricular pacing was then deployed followed by deploying the two stents in a kissing fashion, and an excellent result was obtained (). Position of the valve and function was confirmed by aortography and transesophageal echocardiography (TEE). The left main coronary flow was excellent. The patient tolerated the procedure well and recovered uneventfully and was discharged 2 days after the procedure without complications. At 30-day follow-up, she has notable improvement of her symptoms and physical activity with NYHA class I from class IV symptoms.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [86, 'years'], 'creatinine': [1.73, 'mg/dL']}",28.42134,27.00027,29.84241,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 86 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.73 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.73/0.7)**-1.2 * 0.9938**86 * 1.012 = 28.42134.
Hence, the GFR value is 28.42134 ml/min/1.73 m²."
398,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4384670-1,Extracted,"A 73-year-old woman with a history of hypertension and type 2 diabetes was admitted to the emergency department after 2 days of general weakness, anorexia, vomiting and diarrhea. She was hypotensive, and her mentality was deeply drowsy. She was intubated, ventilated and administered massive fluid resuscitation immediately. Her pharmacologic regimen included metformin 2,000 mg, glimepiride 8 mg, telmisartan/hydrochlorothiazide 80/12.5 mg, amlodipine 10 mg, nifedipine 30 mg, alprazolam 0.5 mg, pantoprazole 20 mg, trimetazidine dihydrochloride 40 mg, and bisoprolol 10 mg. Her physical examination revealed no abnormalities other than severe dehydration. Laboratory results showed leukocytosis (19,660/mm3, 81.4%) with left shift and anemia and levels of hemoglobin of 6.8 g/dL, blood glucose of 419 mg/dL, sodium of 130 mEq/L, potassium of 8 mEq/L, and chloride of 96 mEq/L. Acute renal failure was noted, with a blood urea nitrogen level of 70.6 mg/dL and serum creatinine level of 5.8 mg/dL, and the creatinine clearance was calculated as 7 mL/min/1.73 m2 using the Modification of Diet in Renal Disease (MDRD) formula. The last creatinine level measured before admission was 1.6 mg/dL. Analysis of arterial blood gases indicated a high anion gap (31.5 mEq/L), metabolic acidosis (pH 6.9), and bicarbonate 2.5 mEq/L. Liver function tests were within normal ranges. The serum lactate level was elevated at 9.2 mmol/L. Despite forced diuresis after massive rehydration, urine output was absent and acidosis was aggravated. Continuous venovenous hemodialysis was started using bicarbonate buffered solution. Twenty-four hours of renal replacement therapy led to progressive improvement of metabolic acidosis with pH values of 7.16, 7.36, and 7.41 and bicarbonate values of 6, 12, and 24 mEq/L on each subsequent day. The urinary output also increased progressively. Two days later, the patient returned to a normal mental state with stable vital signs without inotropics or ventilator support. Renal function was improved as indicated by a serum creatinine level of 1.63 mg/dL. After 15 days, the patient was discharged.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [73, 'years'], 'creatinine': [5.8, 'mg/dL']}",7.21605,6.85525,7.57685,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 73 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 5.8 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (5.8/0.7)**-1.2 * 0.9938**73 * 1.012 = 7.21605.
Hence, the GFR value is 7.21605 ml/min/1.73 m²."
399,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4010012-1,Extracted,"An 82-year-old woman, independent as regards activities of daily life, was admitted into the emergency department due to accidental fall at home with consecutive immobilization for a period of approximately 12 hours. Her medical history includes hypertension, dyslipidemia, non-insulin-dependent diabetes, and mild chronic renal insufficiency (baseline creatinine 1.4 mg/dL).
The accidental fall caused right femur periprosthetic supracondylar fracture, which is pending surgery. Blood sample analysis at admission was the following: creatinine 8.74 mg/dL, urea 210 mg/dL with anuria compatible with kidney injury according to RIFLE criteria [], and the patient was transferred to the intensive care unit (ICU).
At the time of admission to the ICU, blood sample analysis showed the following: creatinine 8.76 mg/dL, urea 202 mg/dL, and potassium 6.4 mEq/L, and arterial blood gas analysis showed metabolic acidosis: pH 7.02, −24.6 base excess, serum bicarbonate 4.3 mEq/L, partial pressure of oxigen 79 mmHg and partial pressure of carbon dioxide 16.9 mmHg of creatine phosphokinase (CK) 9475 U/L, with oliguria. Continuous venovenous hemofiltration (CVVHF) with (Edwards Aquarius, Irvine-based Edwards Lifesciences Corp. Lone Peak Parkway, Draper, UT 84020, USA Irvine, CA, USA) 1,2 polysulphone m2 membrane was started with the sequent parameters: 180 mL/min blood flow, predilution flow of 1000 mL, postdilution of 1000 mL, removal of 100 mL/hour, prefilter pressure of 180 mmHg and effluent pressure of 70 mmHg, with prefilter/effluent relationship 30/70. Due to the fact that the patient was breathing with difficulty and was progressively showing clinical and analytical deterioration, a chest radiograph was performed, which showed bilateral infiltrates compatible with distress syndrome with right-lower lobe consolidation added. Endotracheal intubation and mechanical ventilation was conducted the second day at ICU. Blood culture, bronchoalveolar lavage, culture of the fracture site, and sputum cultures were conducted. The last one showed Staphylococcus aureus and Neisseria meningitides colonization and the right femur periprosthetic sample showed Pseudomonas aeruginosa, so meropenem 1 g every 12 hours was administered. The patient was hemodynamically unstable, and thus she was invasively monitored, requiring inotropic support with norepinephrine presenting septic shock with acute circulatory failure with persistent arterial hypotension despite adequate fluid resuscitation. Radiological and clinical improvement allowed extubation, and due to creatinine level improvement (1.03 mg/dL), urea (59 mg/dL) and CK (137 U/L) it was decided to withdraw CVVHF. The patient had a favorable outcome with spontaneous dieresis and was eupneic without respiratory support, hemodynamically stable, and afebrile.
Within a week of their stay in our critical care unit, scheduled surgery was performed for her right femur periprosthetic supracondylar fracture, with spinal anesthesia without incidents. After surgery she moved back to our critical care unit, where she remained eupneic and hemodynamically stable with spontaneous diuresis and good renal function (creatinine 0.92 mg/dL), so after 12 hours in RU, she was discharged to ward.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [82, 'years'], 'creatinine': [0.92, 'mg/dL'], 'sex': 'Female'}",62.1668,59.05846,65.27514,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 82 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.92 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.92/0.7)**-1.2 * 0.9938**82 * 1.012 = 62.1668.
Hence, the GFR value is 62.1668 ml/min/1.73 m²."
400,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7591977-1,Extracted,"A 66-year-old female with a history of rheumatoid arthritis on prednisone 5 mg daily, T2DM, CKD, AI secondary to chronic steroid use, and recent hospitalization for methicillin-resistant Staphylococcus aureus (MRSA) osteomyelitis still on antibiotics, now admitted for cholangitis treatment, suddenly presents unexplained hyperkalemia. At the time of admission, the patient was started on piperacillin-tazobactam for cholangitis and on TMP-SFX for a history of MRSA osteomyelitis. She also received stress-dose steroids for 48 hours with immediate clinical improvement. The patient's hospitalization was prolonged (more than 30 days) and complicated by acute kidney injury, hyperkalemia, and nonanion gap metabolic acidosis (NAGMA) outlined as follows. The patient also had a history of hypertension treated with lisinopril 5 mg daily, which was initially discontinued and restarted during the hospitalization (day 30) at the increased dose of 10 mg daily given severe hypertension. On day 33, the patient's creatinine rose to 1.5 mg/dL from a baseline of 1.2 mg/dL, and her previously normal potassium (K) increased to 5.5 mmol/L (). This was thought to be related to lisinopril, which was discontinued. Off lisinopril, her kidney function recovered, but unexpectedly, hyperkalemia worsened to 6.3 mmol/L, and she presented a new-onset NAGMA with serum bicarbonate 17.5 mmol/L. The abnormally elevated K was then attributed to TMP-SMX-induced hyperkalemia, so TMP-SFX was switched to doxycycline, and the patient was given patiromer. Despite these interventions, both hyperkalemia and NAGMA persisted (K, 6.3 mmol/L and bicarbonate, 19.6 mmol/L on day 35). At that point, urine electrolytes and venous blood gas were obtained, demonstrating a positive urine anion gap and venous pH of 7.31. The urinalysis was normal with pH of 7, no evidence of infection, and absence of proteinuria, glycosuria, and microhematuria. Plasma renin activity was 0.95, and aldosterone levels were undetectable; however, the treatment with ACE-I could affect the interpretation of this test. The picture was now consistent with type IV RTA, so the patient was started on oral sodium bicarbonate 1300 mg three times a day with the resolution of NAGMA. Despite the discontinuation of possible culprit medications, the patient was still hyperkalemic. Finally, considering her cAI with a likely component of hypoaldosteronism worsened by lisinopril, fludrocortisone 0.1 mg was added daily with immediate normalization of K (from 5.2 mmol/L to 4.4 mmol/L). This happened the fourth day after stopping lisinopril (). The patient had to continue the daily therapy with both sodium bicarbonate and fludrocortisone to maintain normal K levels and acid-base status and did not experience any electrolyte imbalance or worsening hypertension, while on the mineralocorticoid replacement therapy, as a demonstration that, she was indeed aldosterone-deficient. Of note, cortisol and adrenocorticotropic hormone levels were not measured during this admission as the patient's diagnosis of adrenal insufficiency was well established, and she was on treatment.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [66, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Female'}",38.19535,36.28558,40.10512,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 66 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.5 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.5/0.7)**-1.2 * 0.9938**66 * 1.012 = 38.19535.
Hence, the GFR value is 38.19535 ml/min/1.73 m²."
401,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3544066-1,Extracted,"A 60-year-old lady, a known case of type 2 diabetes mellitus for 15 years and hypertension for 3 years, presented to the clinic with fever, chills, and bilateral loin pain of 4 days duration. No other co-morbidities like chronic kidney disease or coronary artery disease were known in her in the past and she was apparently in normal state of health prior to the presenting illness.
She developed high-grade fever with chills and rigors. Fever was accompanied by dysuria and bilateral loin pain which was constant and aching in nature. Two days following the onset of fever and loin pain, she developed hematuria and subsequently her urine output started declining and she was anuric at the time of admission to the hospital. She also experienced severe generalized muscle ache. There was no arthralgia, skin rash or hemoptysis. Her medications included glipizide and multivitamin.
At the time of admission, she was conscious, irritable, febrile, and tachypneic. Her conjunctivae appeared suffused. There was no icterus, purpura, or lymphadenopathy. Muscle tenderness in limbs was noted. Her pulse was 104/min, BP–110/70 mm Hg, respiratory rate 23/min, temperature 101°F, oxygen saturation 95% at room air. Rales were appreciated in the basal regions of the chest. Examination of abdomen revealed no organomegaly, but both renal angles were tender on palpation.
Investigations revealed hemoglobin of 10.8 g/dL; leukocyte count of 28400 cells/μL; differential count revealed polymorphs 91%, lymphocytes 8%; platelet count 60000/μL. The blood film revealed normocytic normochromic RBCs, neutrophilic leucocytosis with toxic granulations. No hemoparasites were detectable. Urine analysis revealed 1+ protein, 40-50 WBCs/high power field, 20-25 RBCs/high power field, bile salts and pigments - negative, ketone-negative. Blood sugar on admission was 208 mg/dL; blood urea nitrogen 74 mg/ dL; serum creatinine 5.4 mg/dL; serum sodium 138 mmol/L; potassium 4.8 mmol/L; bicarbonate 7.0 mmol/L; chloride 104 mmol/L; plasma anion gap +27 mmol/L, pO290 mm Hg., pCO226 mm Hg. Serum total bilirubin measured 2.1 mg/dl; SGOT – 44 U/L; SGPT – 34 U/L; alkaline phosphatase – 242 U/L; serum total protein 6.5 g/L; and serum albumin measured 2.4 g/ dL. Urine culture revealed significant growth of E. Coli., (>105 colony forming units/ ml) sensitive to ciprofloxacin, amikacin, and ceftriaxone. However, blood culture grew no organism. Ultrasonogram of the abdomen revealed bilaterally enlarged kidneys with hydroureteronephrosis. No radioopaque lesion could be made out in the ultrasonogram or X-ray KUB region. An MR urogram performed to further evaluate the obstruction [] revealed bilateral renal papillary necrosis (RPN) with bilateral midureteric obstruction.
Thrombocytopenia and severe myalgia prompted a search for leptospirosis, a common cause of AKI in this part of the country. The organism could not be isolated from the urine or blood. However, the MAT (Microscopic Agglutination Test) done in the second week of the illness detected Leptospira icterohemorrhagica; serovar hardjo. Serologic investigations for dengue were negative.
She was subjected to a USG-guided renal biopsy which revealed acute tubular necrosis, interstitial inflammation, and mild mesangial proliferation [Figure –].
The patient was treated with hemodialysis and her antibiotics included benzyl penicillin and ceftriaxone. Gradually, the fever settled, her general condition stabilized, and renal function started to improve. By the 20th day of the illness, serum creatinine was 1.7 mg/ dL and platelet count was 190,000/μL and patient was discharged. Follow-up at 3 months revealed a serum creatinine of 1.4 mg/dL.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [60, 'years'], 'creatinine': [5.4, 'mg/dL'], 'sex': 'Female'}",8.5242,8.09799,8.95041,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 60 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 5.4 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (5.4/0.7)**-1.2 * 0.9938**60 * 1.012 = 8.5242.
Hence, the GFR value is 8.5242 ml/min/1.73 m²."
402,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-6622,Extracted,A 36-year-old woman presents with increased tiredness and lethargy for the past 4 weeks. Investigations show her hemoglobin level to be 8.6 gm/dL and serum creatinine of 4.6 mg/dL. The serum is negative for antinuclear antibodies (ANA) and positive for C3 nephritic factor. Urinalysis shows a 3+ proteinuria. The renal biopsy demonstrates hypercellular glomerulus with electron dense deposits along the glomerular basement membrane.,"Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [36, 'years'], 'creatinine': [4.6, 'mg/dL'], 'sex': 'Female'}",11.99612,11.39631,12.59593,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 36 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 4.6 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (4.6/0.7)**-1.2 * 0.9938**36 * 1.012 = 11.99612.
Hence, the GFR value is 11.99612 ml/min/1.73 m²."
403,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4964694-3,Extracted,"A 12-year-old girl presented with 2 months history of low grade intermittent fever and arthralgia. She was pale, normotensive with no significant lymphadenopathy or hepatosplenomegaly. Investigations showed blood urea nitrogen (BUN) 12 mg/dl, creatinine 1.3 mg/dl, total white blood cell count (TLC) 6600/mm3, hemoglobin, 10 g/dl and platelets, 2.6 lakhs/mm3. Peripheral smear showed microcytic hypochromic anemia. There was no proteinuria, serum corrected calcium was 9 mg/dl, lactate dehydrogenase 135 U/L, and uric acid 6 mg/dl. Viral serology for hepatitis B, hepatitis C, and HIV 1 and 2 were negative. Chest radiograph was normal. Ultrasound showed bilateral diffusely enlarged echogenic kidneys with right kidney 11.8 cm and left kidney 12 cm. Computed tomography (CT) showed bilateral enlarged kidneys with a solitary para-aortic node measuring 1.4 cm. CT chest was normal. Percutaneous kidney biopsy was performed. Histopathology showed renal parenchyma with diffuse infiltration of intermediate sized cells that obliterate majority of the renal architecture. Only rare tubules and morphologically normal glomeruli were observed. The cells displayed large nuclei with scant cytoplasm. Immunofluorescence (IF) staining was negative for IgG, IgM, IgA, C3, C1q, kappa, and lambda light chains. Immunohistochemistry (IHC) were positive for CD20, PAX5 (strongly and diffuse), CD10 and terminal deoxynucleotidyl transferase (TdT) and negative for CD3 and CD34 []. Bone marrow examination of this patient did not reveal any atypical cells. These findings are diagnostic of precursor B-LBL stage IV. She was started on chemotherapy but developed septicemia and succumbed to the overwhelming infection.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [12, 'years'], 'creatinine': [1.3, 'mg/dL'], 'sex': 'Female'}",63.45157,60.27899,66.62415,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 12 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.3 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.3/0.7)**-1.2 * 0.9938**12 * 1.012 = 63.45157.
Hence, the GFR value is 63.45157 ml/min/1.73 m²."
404,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3283759-1,Extracted,"A 74-year-old woman was admitted to the hospital for diarrhea and epigastric pain. She had a history of hypertension, diabetes mellitus, chronic kidney disease, dilated cardiomyopathy, and permanent AF for 5 years (). Echocardiography performed 3 months before admission revealed severe global left ventricular hypokinesia (ejection fraction=19% by Simpson's method) and an enlarged left atrium (left atrial volume index=40 mL/m2). Her medications included digoxin (0.125 mg daily), warfarin (2 mg daily), ramipril (10 mg daily), furosemide (40 mg daily), spinolactone (25 mg daily), and carvedilol (25 mg daily).
On examination, her heart rate was 41 bpm, and blood pressure was 110/70 mm Hg. Heart sounds were regular, and there were no murmurs or thrills. An electrocardiogram (ECG) revealed junctional rhythm at a rate of 35 bpm and a QRS duration of 136 msec (). Admission laboratory results showed severe hyperkalemia (serum potassium 8.3 mEq/L), high blood urea nitrogen (62.4 mg/dL), creatinine of 4.0 mg/dL, glucose of 248 mg/dL, and low sodium (131 mM) and hemoglobin (7.2 g/dL) levels. Arterial blood gas analysis on room air showed a pH of 7.400, pCO2 of 41.6 mm Hg, pO2 of 102.8 mm Hg, and HCO3- of 26.0 mmol/L.
The patient was immediately treated with intravenous calcium chloride, followed by intravenous glucose/insulin and a sodium bicarbonate infusion. On hospital day 2, the serum potassium level was 5.3 mEq/L and the ECG showed sinus bradycardia at a rate of 53 bpm with an 80 ms QRS duration (). On hospital day 3, the ECG revealed a normal sinus rhythm at a rate of 67 bpm, and the serum potassium level was within normal limits (4.3 mEq/L). The patient was discharged 6 days after admission, and the ECG at discharge showed normal sinus rhythm at a rate of 65 bpm with occasional premature ventricular complexes. At the 10 day and 1 month follow-ups, the ECG at an outpatient clinic had returned to AF and serum potassium levels were within the normal range.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [74, 'years'], 'creatinine': [4.0, 'mg/dL']}",11.20057,10.64054,11.7606,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 74 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 4.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (4.0/0.7)**-1.2 * 0.9938**74 * 1.012 = 11.20057.
Hence, the GFR value is 11.20057 ml/min/1.73 m²."
405,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2693867-1,Extracted,"A three-year old, previously healthy boy was brought to us because of intermittent fever for seven days and foamy urine for five days. On admission, his body temperature was 39.5℃ and blood pressure was 100/60 mmHg. The throat was mildly injected without exudate or ulceration. A few thumb tip-sized cervical lymph nodes were detected bilaterally, which were non-tender and movable. Both liver and spleen were palpable with three finger-breaths. The edge of the liver was sharp, and the surface was smooth without tenderness. The urogenital examination was normal. One of his maternal cousins had proteinuria since age of three and was diagnosed as having Dent's disease by genetic testing. His maternal grandfather also had a history of proteinuria since childhood, and developed chronic renal failure several years before.
Initial laboratory investigations revealed: hemoglobin 10.4 g/dL, platelet 191,000/µL, and WBC 24,710/µL (neutrophils 21%, lymphocytes 44%, atypical lymphocytes 28%, and monocytes 7%). The blood biochemistry results were as follows; blood urea nitrogen 11 mg/dL, creatinine 0.4 mg/dL, total protein 7.4 g/dL, albumin 4.2 g/dL, and aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase were 98, 153, and 565 IU/L, respectively. EBV VCA IgM Ab was positive, and other viral markers including hepatitis B virus, hepatitis C virus, hepatitis A virus and cytomegalovirus were all negative. Urinalysis revealed two positive albuminuria with some hyaline and granular casts, but hematuria was not detected. Urinary protein excretion was 2,780 mg/day, and urinary calcium excretion was 2.7 mg/kg/day. Urinary β2-microglobulin was 163 µg/mL. The urinary protein electrophoresis revealed: albumin 34.9% and total globulin 65.1%. The SDS-PAGE of urine protein showed a mixed glomerular and tubular pattern of proteinuria. Serum C3 and C4 were 213.8 and 71.5 mg/dL, respectively. Serum IgG, IgA, and IgM were 1,590, 153, and 230 mg/dL, respectively. ASO titer, anti-double strands-DNA, and rheumatoid factor were negative. Renal ultrasonography revealed no abnormal findings.
Initially, EBV infection was easily diagnosed on the basis of typical clinical features and the positive serologic test. In addition, severe low-molecular weight proteinuria supported the possibility of underlying Dent's disease. However, nephrotic range proteinuria with a considerable proportion of albuminuria could not be explained by EBV infection and/or underlying Dent's disease. Thus, kidney biopsy was carried out to rule out a superimposing glomerular disease.
Total nineteen glomeruli were identified by light microscopic examination of the biopsied renal tissue. The glomeruli, tubules, interstitium, and blood vessels looked almost normal. However, electron microscopic examination disclosed a small amount of mesangial deposits with focal moderate effacement of epithelial foot processes. Immunofluorescence microscopic examination revealed mesangial C1q (++) and IgG (+) deposits with a granular pattern (). In situ hybridization of EBV was negative (data not shown).
The mutational analysis of the CLCN5 gene revealed a C-to-T point mutation that replaces the 637th codon of arginine to a stop codon. This nonsense mutation was the same one detected in his maternal cousin previously (the patient 1 in reference 5).
Leukocytosis and abnormal liver function were normalized within seven days with conservative management, and atypical lymphocytosis disappeared completely within three weeks. However, proteinuria persisted, and enalapril (2 mg/kg/day) was started by the twentieth day of hospitalization, which decreased the urine protein/creatinine ratio by approximately 50% a after six months.
Follow-up of EBV serologic markers after a month revealed positive VCA-IgM, VCA-IgG, and EA(DR)-IgG antibodies. About five months later, negative conversion of VCA-IgM Ab and positive conversion of EBNA-IgG Ab were noted.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [3, 'years'], 'creatinine': [0.4, 'mg/dL'], 'sex': 'Male'}",165.03757,156.78569,173.28945,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 3 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.4 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.4/0.7)**-0.302 * 0.9938**3 * 1.0 = 165.03757.
Hence, the GFR value is 165.03757 ml/min/1.73 m²."
406,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-12301,Extracted,"A 46-year-old man presents to your primary care office for follow-up. He has hypertension, which has been well-controlled with furosemide. He is a former smoker with a 5 pack-year history and drinks 2 alcoholic drinks twice per week. You saw him 3 months ago for chronic knee pain. At that time, radiographic imaging showed moderate arthritis of the right knee. As a result, the patient started taking an over-the-counter pain reliever with substantial relief. At today's appointment, you note that his blood pressure is elevated. Examination of his feet shows 1+ pitting edema in his bilateral lower extremities (Figure A). You order lab-work, which is notable for: Na 140 mEq/L; K 4.7 mEq/L; Cr 1.2 mg/dL; AST 20 U/L; ALT 20 U/L; Albumin 5.0 g/dL. An echocardiogram shows an ejection fraction of 60%.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [46, 'years'], 'creatinine': [1.2, 'mg/dL'], 'sex': 'Male'}",75.52931,71.75284,79.30578,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 46 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.2 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.2/0.9)**-1.2 * 0.9938**46 * 1.0 = 75.52931.
Hence, the GFR value is 75.52931 ml/min/1.73 m²."
407,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8510665-1,Extracted,"An 83-year-old man with a past medical history significant for coronary artery disease, hyperlipidemia, hypertension, and chronic kidney disease presented to the emergency department with a 6-week history of worsening bilateral lower extremity swelling and 1 week of increased shortness of breath. He also endorsed dyspnea on exertion and a weight gain of 8 pounds in the past 2 weeks. Of note the patient did not have a prior history of congestive heart failure (CHF) and previous echocardiograms revealed normal heart function.
Approximately 3 weeks prior to presentation, the patient underwent preoperative testing at a different facility in preparation for primary hip arthroplasty. Nuclear stress test at the time showed multivessel coronary artery disease, left ventricular ejection fraction of 40% and abnormal myocardial perfusion. Echocardiogram revealed the presence of severe left ventricular hypertrophy with an abnormal strain pattern and an inferobasilar aneurysm. The patient was then scheduled at that facility for a coronary angiogram but was deferred due to elevated creatinine. His anti-hypertensives losartan and chlorthalidone were discontinued at discharge due to the elevated creatinine. The patient was directed to follow up with his cardiologist whom he scheduled an appointment in 4 weeks’ time.
In the time between the preoperative testing and presentation to our hospital, the patient reported initially feeling well. He endorsed a healthy lifestyle with the ability to exercise and walk miles without any difficulty. He was employed as a physical education teacher. As the lower extremity swelling worsened, he started to develop shortness of breath limiting his activity level which prompted his visit to the emergency room.
On arrival to our hospital, the patient’s vital signs were all within normal limits and his blood pressure was well controlled despite the recent discontinuation of some of his anti-hypertensives (). Physical examination exhibited leg edema, crackles on auscultation and flat neck veins. Laboratory results showed an elevated brain-type natriuretic peptide (BNP) (1,761 ng/L), troponin (0.31 ng/mL), blood urea nitrogen (BUN) (55 mg/dL) and creatinine (3.46 mg/dL) (). According to medical records, his baseline creatinine ranged 1.4 - 1.8 mg/dL. Urine analysis revealed hematuria and proteinuria suggesting nephrotic syndrome (). Electrocardiogram (EKG) displayed low-voltage normal sinus rhythm. Repeat echocardiogram at our hospital confirmed the severe left ventricular hypertrophy with reduced ejection fraction of 46-50% but also revealed a strain pattern suggestive of cardiac amyloidosis.
The patient underwent laboratory investigation for amyloidosis due to the echocardiogram findings. Total urine protein was elevated (1.19 g/L) and positive for monoclonal free lambda light chains (Bence-Jones protein). Serum protein electrophoresis (SPEP) showed markedly decreased total protein, hypoalbuminemia, hypogammaglobulinemia and increased alpha-2-globulin. It also revealed a monoclonal protein peak migrating in the beta-globulin region making up 0.21 g/dL of the total 0.67 g/dL, a second monoclonal protein peak migrating in the gamma globulin region making up 0.10 g/dL of the total 0.22 g/dL with markedly increased free lambda light chains and markedly decreased kappa/lambda ratio.
Diagnostic testing for amyloidosis was initiated with a fat pad biopsy that upon Congo red staining was indeterminate for amyloid deposition. Bone marrow biopsy of the left iliac crest showed extensive interstitial infiltrate of atypical plasma cells (80-90%) in the form of diffuse sheets that is consistent with multiple myeloma. An X-ray skeletal survey was negative for any osteolytic lesions. The patient was scheduled for positron emission tomography (PET) on a later date at an outpatient center.
The patient was initially started on a daily dose of 40 mg intravenous dexamethasone. Once the multiple myeloma diagnosis was confirmed with bone marrow biopsy, the patient received two rounds of “CyBorD” chemotherapy treatment: cyclophosphamide, bortezomib and dexamethasone. CHF medications and diuretics were administered to manage volume overload secondary to cardiac amyloidosis. As treatment progressed, serial labs indicated increased uric acid production (12.3 mg/dL) that was treated with one-time rasburicase and managed thereafter with allopurinol. He also received “Granix” (tbo-filgrastim) to reduce the duration of severe neutropenia while undergoing chemotherapy. After 9 days of initial hospitalization, the patient was scheduled for a third chemotherapy session and discharged to home.
Seven days later, the patient presented again to our facility with continued symptoms of worsening dyspnea and generalized edema. Additionally, he tested positive for a urinary tract infection and was started on antibiotics. Blood work revealed acute on chronic kidney disease with significantly worse creatinine of 5.40 mg/dL compared to previous admission. He was promptly started on hemodialysis. Next morning, the patient became hypoxic and hypotensive requiring transfer to the intensive care unit where vasopressors, inotropes and bilevel positive airway pressure (BiPAP) were initiated. Shortly thereafter, the patient went into cardiac arrest and resuscitation efforts were unsuccessful.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [83, 'years'], 'creatinine': [3.46, 'mg/dL'], 'sex': 'Male'}",16.83854,15.99661,17.68047,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 83 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.46 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.46/0.9)**-1.2 * 0.9938**83 * 1.0 = 16.83854.
Hence, the GFR value is 16.83854 ml/min/1.73 m²."
408,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8340372-1,Extracted,"A 58-year-old Caucasian female presented to her local emergency department with fever and diarrhea. The patient developed nonbloody, large-volume diarrhea after eating take-out 11 days ago, with four to five bowel movements per day. During this time, she also experienced fevers, chills, nausea, vomiting, general malaise, and weakness. In addition, she observed leaking and drainage around her G-tube site with associated erythema and intense abdominal pain. The patient denied sick contacts or recent travel.
Her past medical history includes obesity, orthostatic hypotension, hyperlipidemia, chronic kidney disease, nephrolithiasis, gastrojejunal ulcer, Kawasaki’s disease, subdural hemorrhage, epilepsy, chronic pain syndrome, and anxiety. The patient’s past surgical history includes burr-hole craniotomy, lithotripsy, cholecystectomy, Roux-en-Y gastric bypass complicated by chronic refractory marginal ulceration and small bowel obstruction requiring two resections, ventral hernia repair, and gastrostomy tube insertion.
The patient was pregnant six times and had six miscarriages (G6P0060). She lives with her husband and adopted son with good social support. She is currently unemployed. The patient denies ever smoking and does not drink alcohol. Familial history consists of diabetes, heart disease, and nephrolithiasis in the patient’s mother. Her father had glaucoma, nephrolithiasis, and prostate cancer.
Medications before admission included pantoprazole 40 mg twice a day, sucralfate 1 g twice a day, ondansetron 4 mg twice a day as needed for nausea, midodrine 10 mg three times a day, fludrocortisone 0.1 mg twice a day, atorvastatin 40 mg daily, levetiracetam 1500 twice a day, methadone 10 mg every 8 hours, and lorazepam 0.5 mg daily as needed for anxiety. She was also on daily vitamin A, D3, and B-complex supplements and a monthly cyanocobalamin 1000 μg intramuscular injection, in addition to a nutritional supplement Isosource 1.5 Cal that is administered through the G-tube once every night.
Due to her complex past surgical history, the patient was sent from her local emergency department to our hospital. At presentation, the patient was febrile to 101 ℉. Blood pressure was 110/72 mmHg, and heart rate was 84 beats per minute. Further examination revealed diffuse abdominal tenderness with erythema and purulent drainage around the G-tube site on the left upper quadrant. The general examination showed a thin patient who is alert and oriented. Mucous membranes were moist. Lungs were clear to auscultation as she was breathing comfortably on room air. Heart sounds were regular without murmurs. Extremities were warm with intact pulses bilaterally and no edema. However, she had moderate muscle loss for her age. Skin was intact except for the previously mentioned erythema around the G-tube. Neurological examination revealed normal speech with comprehension, intact cranial nerves II–VII, XI, and XII, and 5/5 motor strength in all four extremities. Sensation was intact to light touch and pinprick throughout. Romberg test was negative. Gait was slowed owing to weakness but showed normal balance.
Serum chemistry showed sodium of 136 mmol/L, potassium of 2.9 mmol/L, chloride of 111 mmol/L, bicarbonate of 20 mmol/L, magnesium 1.2 mg/dL, calcium 6.1 mg/dL, and serum creatinine 1.0 mg/dL. Liver function tests showed low albumin of 2.5 g/dL, total bilirubin of 0.3 mg/dL, alkaline phosphatase of 86 U/L, alanine aminotransferase (ALT) of 13 U/L and aspartate aminotransferase (AST) of 21 U/L. Complete blood count showed a white blood cell count of 3.97 × 109 /L, hemoglobin of 12.6 g/dL, hematocrit of 39.6%, and platelet count of 239 × 109 /L. Urinalysis showed normal appearance and color, specific gravity of 1.020, without detecting red blood cells (RBC), white blood cells (WBC), ketones, glucose, leukocytes esterase, or nitrites. A stool sample was sent for Clostridium difficile and a molecular enteric panel but was pending at that time. Two out of two blood cultures that were collected at her local emergency department were positive for Gram-negative rods. An abdominal radiograph confirmed G-tube location overlying the stomach and a computed tomography (CT) abdomen/pelvis with contrast showed nonspecific skin thickening and subcutaneous fat stranding along the G-tube insertion site (Fig. ). Due to a prior history of penicillin and sulfa anaphylactic reactions, the patient was empirically treated with intravenous ciprofloxacin 400 mg every 8 hours for bacteremia, and oral clindamycin 450 mg every 8 hours for the cellulitis surrounding her G-tube site, in addition to intravenous fluid resuscitation with normal saline at 75 mL/hour and electrolyte repletion with oral potassium chloride 20 mEq for four total doses, and intravenous magnesium sulfate 4 g once.
A fluoroscopy G-tube study revealed no contrast leak or evidence of obstruction. On day 1 of hospitalization, the molecular enteric stool panel was positive for the Salmonella species. On day 4, two out of two blood cultures grew Salmonella enteritidis with susceptibilities to ampicillin, ceftriaxone, and trimethoprim/sulfamethoxazole. The patient was then transitioned from intravenous ciprofloxacin to a 14-day course of intravenous ceftriaxone 2 g every 24 hours. We resumed tube feeds through the G-tube on day 5 after a successful clamping trial. On day 6, the patient was somnolent and difficult to arouse, with poor skin turgor and dry mucous membranes. Vital signs remained within normal limits; T max of 98.6 ℉, blood pressure of 98/65 mmHg, and heart rate of 95 beats per minute. Laboratory results were significant for a serum creatinine level of 5.25 mg/dL and non-anion gap metabolic acidosis with sodium of 131 mmol/L, chloride of 105 mmol/L, and serum bicarbonate of 18 mmol/L. These clinical and laboratory findings of dehydration suggested the development of prerenal acute kidney injury (AKI) in the setting of prolonged GI volume loss. The patient was resuscitated with half normal saline containing 75 mEq sodium bicarbonate additive at 125 mL/hour. On day 8, the patient’s mental status improved but her G-tube began to leak, prompting clamping of the G-tube. The patient was encouraged to increase oral intake. Intravenous fluids were discontinued on day 9, as she was able to tolerate oral foods and liquids well. No further leakage was seen around her G-tube site. On day 13, the patient was discharged home with a peripherally inserted central line to finish a 14-day course of intravenous ceftriaxone (2 g every 24 hours).
Following completion of a 14-day course of intravenous ceftriaxone, the patient made a full recovery with resolution of her diarrhea and abdominal pain. Tube feeds were resumed without further issues. At a 4-month follow-up visit with her bariatric surgeon, the patient reports that she is doing well and happy with her progress. Electrolytes and serum creatinine were all within normal limits. The patient was readmitted 6 months following her initial hospitalization for abdominal pain and hematemesis due to a large marginal ulcer. She improved with conservative measures including bowel rest (nothing per os) and maintenance intravenous fluids, and was discharged 2 days later. At the time of discharge, her hemoglobin remained stable at 11.2 g/dL, and she was able to tolerate an oral diet. She continues to follow up with her bariatric surgeon in clinic with no recurrence of fever or diarrhea.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [58, 'years'], 'creatinine': [1.0, 'mg/dL']}",65.30224,62.03713,68.56735,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 58 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.0/0.7)**-1.2 * 0.9938**58 * 1.012 = 65.30224.
Hence, the GFR value is 65.30224 ml/min/1.73 m²."
409,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8312766-1,Extracted,"The patient is a 42-year-old male with no prior medical history who presented with two weeks of productive cough with yellowish sputum associated with shortness of breath, fatigue, weight loss (about 10 pounds in four weeks), loss of appetite and subjective fever. The patient denied chills, nausea, vomiting, night sweats, recent travel and sick contacts. In addition, the patient noted for the last 4-6 months a swelling of lymph nodes predominantly in the submandibular area. In addition, one month before presentation, he developed a vesicular rash on the left subcostal area spreading to his back. The rash was initially blisters and later became crusted lesions. The patient denied tobacco use although used cannabis regularly and admitted to occasional alcohol use. The patient had 50 female sexual partners with inconsistent barrier protection and denied having a primary care provider for several years.
Vital signs at admission were remarkable for temperature of 103.3F, pulse of 132 per minute, respiratory rate of 20. On examination the patient was in mild distress, with diminished breath sounds on right hemithorax, non-tender firm bilateral anterior and posterior cervical lymphadenopathy bilaterally in the supraclavicular and inguinal area. On skin, the patient presented with left-sided crusted lesions along the T5 dermatome region. Laboratory results showed white blood count of 6.9 x 109/L (normal range: 4.5 to 11 x 109/L), serum creatinine of 1.6 mg/dl (normal range: 0.5 to 1.1 mg/dl), whole blood lactic acid of 2.9 mmol/L (normal range: 0.5 to 2.2 mmol/L) and COVID-19 test PCR was negative. Chest X-ray showed a possible pleural-based mass and residual effusion with mass effect on the right lung. The chest CT with contrast showed extensive mediastinal and axillary adenopathy, a large loculated right pleural effusion, patchy bilateral pulmonary infiltrates and a small pericardial effusion. Neck CT showed extensive bilateral lymphadenopathy up to 3 cm, including a necrotic left submandibular node. Adenopathy extended inferiorly through the supraclavicular region and into the chest. The CT of the abdomen and pelvis showed extensive lymphadenopathy. Findings were concerning for lymphoma with differential diagnosis of metastatic disease vs. infectious process (Figure ).
The patient underwent chest tube placement on the right hemithorax, and 2.4 liters of pleural fluid was drained on the first day. Results of pleural fluid analysis yielded to be exudative in nature, with a high count on lymphocytes, which was suspicious for malignancy or tuberculosis. The patient was placed on airborne isolation precautions.
HIV testing was positive for HIV-1 with CD4 count found on 111 cells/mm3 (normal range: 500 to 1,200 cells/mm3), viral load was found on 91,548 copies/ml and the QuantiFERON-TB Gold test was positive.
Urine culture was negative. Four sets of blood cultures were obtained with no growth, three sputum acid-fast bacilli (AFB) smear were negative and culture showed no growth. Pleural fluid culture grew AFB. The left inguinal lymph node was excised and the final biopsy results showed caseating granulomatous inflammation, granulomas were composed of epithelioid histiocytes and occasional multinucleated giant cells, focal caseous necrosis was noted. Additionally, flow cytometry showed no evidence of B-cell or T-cell non-Hodgkin lymphoma. Pulmonary and Infectious Disease (ID) consults recommended to start RIPE (rifampin, isoniazid, pyrazinamide and ethambutol) TB treatment along with bactrim, for pneumocystis pneumonia prophylaxis (PCP).
Infectious Disease recommended to start Highly Active Antiretroviral Therapy (HAART) approximately eight weeks after initiation of TB therapy to avoid immune reconstitution inflammatory syndrome (IRIS).
Ophthalmology was consulted for baseline examination due to treatment with ethambutol. They recommended monitoring kidney function as renal disease could increase risk of ethambutol and isoniazid induced optic neuropathy. Baseline color vision was documented with no current metamorphopsia or scotoma, optic nerve appeared sharp and pink. Follow-up with Ophthalmology was arranged in six months.
The patient continued to have persistent fever. Pleural fluid AFB resulted positive for rare mycobacterium tuberculosis complex by DNA probe. Vancomycin and Azactam were started for broader coverage on top of RIPE therapy with PCP prophylaxis. Since the patient continued to have persistent fever, chest CT was repeated and showed pleural fluid thickening with persistent fluid collection concerning for possible empyema. Repeat procalcitonin downtrended to 0.10 ug/ml (normal range: <0.5 ug/dl) without leukocytosis and subsequently we stopped treatment with Vancomycin and Azactam. The Department of Health (DOH) was informed about the patient's case and recommended to pleural decortication, as such the patient was transferred to a more specialized facility with a TB unit.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [42, 'years'], 'creatinine': [1.6, 'mg/dL'], 'sex': 'Male'}",54.82682,52.08548,57.56816,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 42 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.6 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.6/0.9)**-1.2 * 0.9938**42 * 1.0 = 54.82682.
Hence, the GFR value is 54.82682 ml/min/1.73 m²."
410,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4315802-1,Extracted,"A 59 year old male patient was diagnosed with seronegative RA and received treatment with methotrexate (MTX) and prednisolone. Four years after the diagnosis of RA, he presented with a productive cough, haematuria, proteinuria (6.84 g/24 hours) and decline in renal function (serum creatinine (SCr) rising from 119 to 270 mmol/L). He had an acute phase response (CRP 33 mg/L, ESR 134 mm/h) and was PR3-ANCA positive (67 U/ml, normal range 0–3). The RhF and anti-CCP remained negative. A CT scan of the chest showed multiple air filled cavitating structures and CT scan of his sinuses revealed extensive bony defects in the antronasal regions and thickening of the maxillary and frontal sinuses. A kidney biopsy demonstrated focal necrotising vasculitis lesions. As a result a diagnosis of Granulomatosis with polyangiitis(GPA) was made and he was treated with pulsed methylprednisolone, oral prednisolone and intravenous cyclophosphamide. His renal function improved (SCr 115, proteinuria 0.58 g/24 hours) and his pulmonary lesions regressed.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [59, 'years'], 'creatinine': [270.0, 'mmol/L'], 'sex': 'Male'}",0.0057,0.00541,0.00599,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 59 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 270.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from mmol to mg. The mass of Serum Creatinine is 270.0 mmol. To convert 270.0 mmol of Serum Creatinine to mol, multiply by the conversion factor 0.001, giving us 270.0 mmol Serum Creatinine * 0.001 mol/mmol = 0.27 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.27 mol Serum Creatinine * 113.12 g/mol = 30.5424 g Serum Creatinine. To convert 30.5424 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 30.5424 g Serum Creatinine * 1000.0 mg/g = 30542.4 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 30542.4 mg Serum Creatinine/10.0 dL = 3054.24 mg Serum Creatinine/dL. The concentration value of 270.0 mmol Serum Creatinine/L converts to 3054.24 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3054.24/0.9)**-1.2 * 0.9938**59 * 1.0 = 0.0057.
Hence, the GFR value is 0.0057 ml/min/1.73 m²."
411,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4377761-1,Extracted,"A 77-year-old male, with stable chronic kidney disease stage 3, type 2 diabetes and peripheral vasculopathy, was admitted to our hospital for treatment of a badly healing diabetic ulcer on the right hallux. Empirical therapy with intravenous flucloxacillin was started. A wound swab subsequently showed growth of methicillin sensitive Staphylococcus aureus. His maintenance therapy, consisting of metformin, low dose aspirin and candesartan, was continued. Delayed healing prompted a vascular work-up, followed by percutaneous transluminal angioplasty of the right external iliac artery. Despite these interventions, the ulcer deteriorated and 2 weeks later the right hallux had to be amputated. During the ensuing 2 weeks, the surgical wound healed reasonably well, but the patient's general condition degraded with progressive nausea and anorexia. Physical examination revealed discrete abdominal tenderness and diminished bowel sounds. Biochemistry showed no major inflammation, but serum creatinine had risen from a baseline value of 1.3–2.0 mg/dL, which led to the cessation of metformin and candesartan. His glycaemia remained well controlled. During the next 24 h, he became hypotensive (70/30 mmHg) and started to hyperventilate vigorously. He was started on intravenous (IV) fluids and was transferred to the intensive care unit (ICU). Results of blood samples taken upon admission to the ICU, and additional blood and urine tests, obtained 12 h later, are summarized in Table . An abdominal computed tomography-angioscan was performed with iso-osmolar contrast after intravenous administration of isotonic NaHCO3 and allowed to rule out intestinal ischaemia. His blood pressure ameliorated slightly and diuresis remained well preserved.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [77, 'years'], 'creatinine': [2.0, 'mg/dL'], 'sex': 'Male'}",33.74161,32.05453,35.42869,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 77 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.0 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.0/0.9)**-1.2 * 0.9938**77 * 1.0 = 33.74161.
Hence, the GFR value is 33.74161 ml/min/1.73 m²."
412,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2931142-1,Extracted,"A 35-year-old woman was admitted to our hospital with complaints of anorexia, nausea, episodic vomiting and loss of appetite for the last seven days and decreased urine output for two days, complete urine shut down since one day. She denied any history of fever, pain abdomen, dysuria, hemeturia and pedal edema. She did not have diabetes or hypertension.
Physical examination revealed a middle age woman in no acute distress. Blood pressure was 110/70 mm of Hg. The pulse was 82 beats/min and regular. She had mild pallor. Rest of the systemic examination was unremarkable. Initial laboratory work up revealed: hemoglobin 9.6gm/dl, packed cell volume- 28.3%, total leukocyte count-12900/mm3. Routine urine examination showed specific gravity of urine 1.005, pH>6, urinary albumin- 1, WBC- 12-15/high power field and RBC’s – negative. Renal profile was done and values were: blood urea nitrogen 45mg/dl, creatinine 12.03 mg/dl, uric acid 9.30 mg/dl, calcium 7.83 mg/dl, phosphorus 4.96 mg/dl, serum total proteins 6.0 g/dl, albumin 3.0 g/dl, globulin; 3.0 g/dl, spot urine for protein creatinine ratio 6.0. Patient was negative for HIV 1and 2, hepatitis B surface antigen, HCV antibodies. Complement factor C3 and C4 were within normal limits. Patient was worked up for vasculitis and connective tissue disorder with ANA, Anti dsDNA, c-ANCA, p-ANCA and anti glomerular basement membrane antibodies and all the parameters were negative. Ultrasonography of the abdomen revealed bilateral bulky kidneys with mild increase in cortical reflectivity and cortico medullary differentiation was normal.
In view of worsening azotemia she was initiated on hemodialysis. Kidney biopsy was performed in view of acute onset of unexplained renal failure, after four sessions of hemodialysis. The histopathological finding showed that the glomeruli were normocellular, there was mild increase in mesangial matrix, tubules showed multiple fractured casts and crystals within the casts. There was polymorpho nuclear and histiocytic reaction around the crystals with denudation of tubular epithelium. A few casts showed giant cell reaction around them. There was focal interstitial infiltrate of lymphocytes and plasma cells []. Immuno histochemical staining was done to demonstrate the presence of light chains and which showed the positive lambda and negative kappa chains []. Electron microscopy showed sclerosed and totally obliterated glomerulus. The tubules contained casts of condensed osmophilic material and large vacuoles in the surrounding epithelial cells.
Based on the history, clinical features and laboratory investigations, patient was diagnosed as cast nephropathy suggestive of plasma cell myeloma. This was further confirmed with the help of serum protein electrophoresis which showed M band in gamma region. Urine Bence-Jones protein was absent and serum immune fixation (qualitative) was positive for monoclonal gammopathy in lambda region, which was quantitated and values were as follows: free kappa light chain 37.20 (normal 3.3-19.4) mg/l, free lambda light chain 8220.00 (5.71-26.3) mg/l, free kappa/lambda ratio; below 0.01 (0.26-1.65). Increased plasma cells (22%) were seen in bone marrow aspiration and bone marrow biopsy was consistent with plasma cell myeloma.
She was treated with five cycles of plasma exchange therapy along with regular hemodialysis. Her plasma exchange prescription included two liters of exchange/cycle (35 ml/kg) with blood flow of 100 ml/min, simultaneously replaced albumin and fresh frozen plasma in 50:50 mixtures using heparin as anticoagulant. Along with plasmapheresis she was started on bortezomib (2 mg IV bolus on 1, 4, 8, 11th day) and dexamethasone 40 mg/day for first three days under the guidance of a haematologist in each cycle. At the end of the first cycle, her urine output improved significantly and she went off hemodialysis. Her renal function also improved and her serum creatinine levels stabilized at 3 mg/dl without requiring haemodialysis. Her tumor burden also came down in a significant manner. At the end of first cycle of chemotherapy her serum free lambda light chain levels dropped from 8220 mg/l to 136 mg/l. Her serum-free kappa/lambda ratio came back to normal (0.30). She was treated with two more cycles of chemotherapy with 10 days of rest in between each cycle. Similarly, her serum-free light chain, serum creatinine and protein electrophoresis was performed at the end of each cycle. At the end of the 3rd cycle her renal function returned to normal (serum creatinine 1.0 mg/dl). Her tumor burden also returned to normalcy (serum free lambda light chain-25 mg/l) without having M band in protein electrophoresis and now she is under complete remission.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [35, 'years'], 'creatinine': [12.03, 'mg/dL'], 'sex': 'Female'}",3.80831,3.61789,3.99873,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 35 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 12.03 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (12.03/0.7)**-1.2 * 0.9938**35 * 1.012 = 3.80831.
Hence, the GFR value is 3.80831 ml/min/1.73 m²."
413,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4421525-2,Extracted,"A 57-year-old Caucasian man with ESRD due to haemolytic uraemic syndrome with thrombotic thrombocytopenic purpura underwent living-unrelated kidney transplantation. He received induction immunosuppression with rATG and was maintained on tacrolimus, mycophenolate mofetil and prednisone. His operative course was uncomplicated, and he had excellent allograft function with an SCr nadir of 1.1 mg/dL [83.9 mmol/L].
His allograft function remained stable until ~1 month after transplantation, at which time his SCr rose to 2.4 mg/dL [183.0 mmol/L]. On physical examination, he was afebrile, normotensive and his allograft site was non-tender to palpation. Imaging studies of his allograft showed moderate hydronephrosis and he underwent double-J stent and nephrostomy tube placement. His SCr peaked at 5.9 mg/dL [449.9 mmol/L]. Despite structural decompression, SCr remained high, and transplant kidney biopsy revealed granulomatous interstitial inflammation with minimal necrosis (C). An AFB stain was negative, but GMS stain revealed yeast forms morphologically suggestive of Histoplasma species (D).
Based on his initial clinical presentation and preliminary biopsy results, this patient was thought to have eosinophilic granulomatous interstitial nephritis due to trimethoprim–sulfamethoxazole. Soon afterwards, however, histochemical staining revealed budding yeast forms, and serum and urine studies for histoplasmosis antigen and antibody were positive. His immunosuppression was decreased and he was placed on itraconazole. Studies for blastomycosis, cryptococcus and coccidiomycosis were negative.
SCr improved to 1.4 mg/dL [106.8 mmol/L] and the nephrostomy tube was removed. Imaging studies showed evidence of a urethral stricture, for which he is scheduled to undergo repair.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [57, 'years'], 'creatinine': [1.4, 'mg/dL'], 'sex': 'Male'}",58.62303,55.69188,61.55418,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 57 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.4 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.4/0.9)**-1.2 * 0.9938**57 * 1.0 = 58.62303.
Hence, the GFR value is 58.62303 ml/min/1.73 m²."
414,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6453850-1,Extracted,"A 53-year-old man with no history of specific disease presented with abdominal pain. He visited another hospital and underwent laboratory tests and abdominal computed tomography. He was diagnosed with chronic hepatitis B and liver cirrhosis (LC) associated with hepatocellular carcinoma (HCC) and was referred to our hospital for further work-up and suitable treatment.
At the time of admission, the patient’s blood pressure and pulse rate were 140/90 mm Hg and 90 beats per minute, respectively. Further, his breathing rate and body temperature were 22 breaths per minute and 36.4°C, respectively. Abdominal distension and shifting dullness were observed, whereas no palpable mass, tenderness, or rebound tenderness was detected in the abdomen. The results of complete blood cell count were as follows: white blood cell count, 5,630/mm3; hemoglobin, 9.7 g/dL; hematocrit, 28.5%; and blood platelet count, 73,000/mm3. Moreover, the results of serum biochemical test were as follows: total protein, 6.0 g/dL; albumin, 1.8 g/dL; total bilirubin, 1.53 mg/dL; aspartate aminotransferase, 95 IU/L; alanine aminotransferase, 15 IU/L; alkaline phosphatase, 697 IU/L; gamma-glutamyltranspeptidase, 166 IU/L; blood urea nitrogen, 19.4 mg/dL; and creatinine, 1.0 mg/dL. Prothrombin time and activated partial thromboplastin time were within normal limits.
Abdominal ultrasonography, dynamic magnetic resonance imaging, and esophagogastroduodenoscopy (EGD) were performed, and ultimately, the patient was diagnosed with LC, HCC infiltrating both the liver lobes with portal vein thrombosis, grade 2 esophageal varices with red color sign, and type 2 gastroesophageal varices (GOV2). On day 4 of hospitalization, he underwent prophylactic endoscopic variceal ligation (EVL) and transarterial chemoembolization in accordance with the Barcelona Clinic Liver Cancer guidelines for HCC. Despite appropriate management, the patient’s liver function gradually deteriorated, and esophageal variceal bleeding (EVB) and hepatic encephalopathy recurred during admission.
On day 12 of hospitalization, he presented with hematemesis (400 mL of blood) resulting from EVB and was immediately transferred to the intensive care unit. EGD and therapeutic EVL, along with aggressive blood volume resuscitation and intravenous administration of terlipressin, were performed to control EVB but failed because of unstable vital signs and massive bleeding. SB tube insertion (All Silicone Sengstaken–Blakemore Tube®; Create Medic Co., Yokohama, Japan) was performed as subsequent treatment, and medical therapy including administration of terlipressin was continued. On day 13 of hospitalization, grade 2 hepatic encephalopathy developed, and the SB tube was abruptly cut off because of the patient’s irritability.
Emergency EGD showed esophageal and gastric balloon transection from the SB tube, which remained fully inflated and impacted. We attempted to deflate the balloon using various methods based on previous reports. Endoscopic injection needle (WS-2416PN2504; Omnimed Ltd., England, UK) and endoscopic cutter (FS-5L-1; Olympus, Tokyo, Japan) were initially used, but the balloon, having thick elastic walls, was not easily punctured. We subsequently used endoscopic hot biopsy forceps (FD-1U-1; Olympus) and employed argon plasma coagulation, which proved unsuccessful as the balloon, which was made of silicone, had excellent electrical insulating and heat-resistant properties. On the presumption that a sharper and more rigid instrument could cut the balloon, we finally chose and used endoscopic scissors (FS-3L-1; Olympus) to perforate the balloon (), and the deflated balloon was gently removed using an endoscopic snare (SD-210U-10; Olympus) without any complication ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [53, 'years'], 'creatinine': [1.0, 'mg/dL']}",89.99657,85.49674,94.4964,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 53 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.0 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.0/0.9)**-1.2 * 0.9938**53 * 1.0 = 89.99657.
Hence, the GFR value is 89.99657 ml/min/1.73 m²."
415,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7424659-1,Extracted,"A 65 year-old white female patient had been previously evaluated an outside facility for recent development of edema and CKD. She had a history of hypertension diagnosed at age 58 on treatment with angiotensin II receptor blocker. At time of her initial evaluation (at an outside facility) her serum creatinine was 1.1–1.2 mg/dL and urine analysis demonstrated proteinuria +++. She underwent a kidney biopsy that showed a FSGS lesion and presence of focal myelin figures within podocytes (zebra bodies). GLA sequencing for FD was negative. She had no history of prior exposure to silica, amiodarone or hydroxychloroquine, which can be associated with lesions resembling zebra bodies on EM. Her mother was diagnosed with FSGS at age 69 years, then developed end-stage renal disease, 2 years later, and was on dialysis until her 80s when she died. The patient’s father had died due to liver cancer. She has two healthy brothers, ages 56 and 63, and two healthy sons who are 39 and 40 years old.
Due to the inconsistency between the EM findings and the genetic analysis, and to obtain further clarification regarding the diagnosis, the patient was referred to Mayo Clinic 4 years after the first evaluation. She had no history of acroparesthesias, angiokeratomas, transient ischemic attacks, hypohidrosis, parapelvic cysts or any other FD-related signs or symptoms []. One son had negative biochemical testing and the other had negative genetic testing for FD. Physical examination was unremarkable including no evidence of corneal abnormalities in ophthalmological evaluation. Laboratory evaluation is presented on Table . Cardiac and brain magnetic resonance imaging were unrevealing. To further evaluate the cause of her renal disease, she underwent a repeat kidney biopsy. On light microscopy (LM) there were 30% globally sclerotic glomeruli and one glomerulus showed segmental sclerosis with podocyte capping. Few glomeruli showed duplication of the glomerular basement membranes. There was mild tubular atrophy and interstitial fibrosis (Fig. a) involving 25% of the cortex sampled accompanied by mild chronic interstitial inflammation. Some podocytes with bubbly cytoplasm were seen on LM (Fig. b). No glomeruli were seen in the immunofluorescence. There was 3+ focal tubular casts staining for IgA, kappa, and lambda with 2+ IgM. The medullary tissue was negative for IgG, C1q, C3, albumin, and fibrinogen. On EM, several podocytes contained myeline figures resembling zebra bodies (Fig. c and d) with podocytes displaying mild to moderate foot process effacement involving approximately 30% of the total peripheral capillary surface area. No myelin figures were seen within endothelial cells, mesangial cells, peritubular capillaries, or tubular cells. No beaded collagen fibrils were seen within the glomerular basement membranes. GLA deletion/duplication testing for FD gene was repeated and was negative. Due to the inconclusive biochemical and genetic testing, she was referred to the Department of Clinical Genomics for further evaluation. To further evaluate the cause of her renal biopsy findings, RNA sequencing of kidney tissue was performed through a research program in the Center for Individualized Medicine []. No variants, aberrant expression, aberrant splicing changes, or allelic imbalance was detected within GLA by RNA analysis. Moreover, there was no sign of skewed X chromosome expression. To search for other possible genetic explanation for her symptoms, whole exome sequencing was performed on the kidney tissue and revealed a pathogenic variant in LMX1B (NM_002316.3:c.737G > A, p.Arg246Gln), which is associated with NPLRD in multiple families. The variant was Sanger confirmed to be germline on DNA extracted from the patient’s blood. Her renal disease progressed and 2 years after presentation to the Mayo Clinic the patient received a kidney transplant from a deceased donor.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [65, 'years'], 'creatinine': [1.2, 'mg/dL'], 'sex': 'Female'}",50.23467,47.72294,52.7464,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 65 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.2 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.2/0.7)**-1.2 * 0.9938**65 * 1.012 = 50.23467.
Hence, the GFR value is 50.23467 ml/min/1.73 m²."
416,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-264,Extracted,"A 5-year-old African-American boy is brought to the physician because of fatigue and night sweats for the past month. During this time, he has also lost 3 kg (6.6 lbs). Before the onset of symptoms, he had been healthy except for a febrile seizure as an infant. His brother had chickenpox 2 months ago. He is at the 75th percentile for height and 50th percentile for weight. He appears markedly fatigued. His temperature is 38°C (100.4°F), pulse is 95/min, respirations are 19/min, and blood pressure is 100/60 mm Hg. Lung and cardiac examination is normal. There are enlarged, nontender lymph nodes bilaterally in the neck. The abdomen is soft and nontender. A complete blood count shows:
Leukocyte count 8,000/mm3
Hemoglobin 9.1 g/dL
Hematocrit 26.9%
Platelet count 34,000/mm3
Serum
Na+ 135 mEq/L
K+ 4.5 mEq/L
Cl- 101 mEq/L
HCO3- 27 mEq/L
Urea nitrogen 9 g/dL
Creatinine 0.7 g/dL
Ca2+ 8.8 mg/dL
PCR testing demonstrates a 9:22 chromosomal translocation.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [5, 'years'], 'creatinine': [0.7, 'mg/dL'], 'sex': 'Male'}",137.65225,130.76964,144.53486,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 5 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.7 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.7/0.7)**-0.302 * 0.9938**5 * 1.0 = 137.65225.
Hence, the GFR value is 137.65225 ml/min/1.73 m²."
417,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5966893-1,Extracted,"A 52-years-old man showing worsening of interstitial pneumonitis and presenting with microscopic hematuria and proteinuria was referred to our department. His interstitial pneumonitis was diagnosed 11 years ago, and since then, he had shown persistent serological positivity for MPO-ANCA. MPA was therefore suspected, and he was carefully followed-up without any medications.
After the referral, his proteinuria progressed to nephrotic syndrome. Physical examination showed bilateral fine crackles and pitting edema in the feet. His urinary protein excretion was 15.9 g/g urinary creatinine. Urinary microscopic examination showed massive erythrocytes. The results of blood examination were as follows: white blood cell count, 12.4 × 103/μL; hemoglobin, 13.5 g/dL; platelet count, 529 × 103/μL; serum creatinine, 1.99 mg/dL; urea nitrogen, 17 mg/dL; total protein/albumin (TP/Alb), 6.4/2.5 g/dL; total cholesterol, 245 mg/dL; immunoglobulin G (IgG), 1103 mg/dL; and IgA/M, 416/89 mg/dL. The C-reactive protein level was 1.2 mg/dL, and hypocomplementemia was absent. The ANCA titer for MPO was 19.4 U/mL, and the proteinase 3 (PR3) titer was within the normal range. Viral antibodies for HBV, HCV, and human immunodeficiency virus (HIV) were negative. His chest X-ray suggested exacerbation of interstitial pneumonitis. Computed tomography scans did not show any evidence of malignant tumors.
We diagnosed the patient with MPA clinically, and renal biopsy was performed. Light microscopy observations showed crescents in 13 of 28 glomeruli (Fig. ) as well as global glomerulosclerosis in 4 of 28 glomeruli. The biopsy also showed diffuse and global spike formation of the glomerular capillary walls (Fig. ). Immunofluorescence staining showed granular 2+ deposition of IgG (Fig. ) and complement C3 and ± deposition of IgM and complement C1q on the glomerular capillary walls. Electron microscopy showed subepithelial electron-dense deposits, spike formation of the glomerular basement membrane throughout the deposits, and effacement of the podocyte foot processes (Fig. ).
All of the IgG subclasses were positive on the glomerular capillary walls. Immunoperoxidase staining showed that the glomerular capillary walls were positive for MPO (Fig. ). In addition, although serum anti-PLA2R antibody level without any medications, measured by enzyme-linked immunosorbant assay at the day of renal biopsy, was negative, glomerular PLA2R was clearly detected (Fig. ). PLA2R staining was completely negative in the negative control (without the primary antibody, data not shown). According to these findings, the patient was diagnosed with ANCA-associated glomerulonephritis (mixed class) [] with MN-lesions.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [52, 'years'], 'creatinine': [1.99, 'mg/dL'], 'sex': 'Male'}",39.65549,37.67272,41.63826,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 52 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.99 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.99/0.9)**-1.2 * 0.9938**52 * 1.0 = 39.65549.
Hence, the GFR value is 39.65549 ml/min/1.73 m²."
418,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4387343-1,Extracted,"A 57-year-old white female with a past medical history significant for ESRD on HD admitted with right buttock abscess with overlying cellulitis. One-week prior, she presented to a local emergency room with right buttock boil. No intervention was undertaken and she was sent home on oral trimethoprim/sulfamethoxazole (TMP/SMX). She did not fill her prescription nor sought further care till this admission. In the emergency room, she complained of fever, chills and throbbing pain at the abscess site. She had no other skin lesions or complaints. The patient’s past medial history is significant for hypertension, which led to her ESRD. She has been on HD for 16 years. She did not have recent hospitalization within the past 6 months nor she had history of methicillin - resistant S. aureus colonization or infection.
On examination, she was awake and oriented but in obvious pain. She had an oral temperature of 38.6°C. Her heart rate was 112 beats/min and her blood pressure was 118/62 mmHg. Her heart, lung and abdominal examination were unremarkable. She had a right-sided femoral arterio-venous graft with a strong thrill and no overlying redness. This arterio-venous graft was placed 2 years ago, after she ran out of upper body HD access sites. Her right buttock showed a warm, tender, fluctuant area with surrounding redness. There were no other skin lesions. She was admitted with sepsis secondary to a complicated right buttock skin infection. She was started empirically on ceftaroline (600 mg intravenously once then 200 mg every 12 h) for her complicated skin infection and the surgical service consulted.
Blood testing showed a white blood cell count of 36.9×109/L, hemoglobin of 11.1 g/dL and creatinine of 4.8 mg/dL. Electrolytes and liver function tests were within normal limits. Non-contrast computed tomography scans of the pelvis showed right buttock cellulitis with few gas bubbles in the soft tissues ().
The patient underwent incision and drainage of the right buttock abscess. Her blood cultures were negative but purulent secretions from the right buttock grew S. lugdunensis. Transthoracic echocardiography was negative for valvular vegetations. The bacterium was methicillin-resistant but was susceptible to vancomycin, ciprofloxacin, clindamycin, erythromycin, TMP/SMX, tetracycline, rifampin and linezolid. Bacterial identification was performed by Microscan WalkAway plus system (Siemens, Berlin-Munich, Germany). Her condition improved markedly with the subsequent initiation of negative pressure wound therapy (). On the 11th hospital day, she was discharged home to finish 2 more weeks of oral doxycycline (100 mg every 12 h). The patient was followed in the outpatient clinic and showed complete healing of her infection.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [57, 'years'], 'creatinine': [4.8, 'mg/dL']}",10.00321,9.50305,10.50337,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 57 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 4.8 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (4.8/0.7)**-1.2 * 0.9938**57 * 1.012 = 10.00321.
Hence, the GFR value is 10.00321 ml/min/1.73 m²."
419,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8059041-1,Extracted,"An 85-year-old man with a history of BP presented with right forearm swelling and erythema for 3 days. The patient had a history of atrial fibrillation, chronic obstructive pulmonary disease, and diabetes mellitus. He was diagnosed with BP about 7 years ago when he presented with a similar rash. The diagnosis of BP was made based on a punch biopsy showing subepidermal bullae containing a dense inflammatory infiltrate with prominent eosinophils. Direct immunofluorescence revealed a strong linear staining pattern of the basement membrane zone with immunoglobulin G and C3. Since then, he has been having similar although less severe recurrent episodes about once every 1 to 2 years involving lower and upper extremities with complete remission in between, every time treated successfully with short courses of intramuscular, oral, and topical steroids. He also required methotrexate maintenance therapy for the initial episode. Medications included insulin, metoprolol, gabapentin, simvastatin, warfarin, lisinopril, tamsulosin, and furosemide. Examination revealed swelling, erythema, and warmth of the right upper extremity from the mid upper arm all the way to the hand ( and ) along with a few deep tense bullae formation of 2 to 3 cm (). Laboratory investigations revealed the following: leukocytes 9.3 × 10 9/L, hemoglobin 13.7 g/dL, creatinine 1.83 mg/dL, platelets 248 × 10 9/L, procalcitonin <0.05 ng/mL, lactic acid 2.3 mmol/L, and negative blood cultures. The patient was initially started on broad-spectrum antibiotics due to suspicion of infectious etiology. However, due to the absence of fever and elevated inflammatory markers, the antibiotics were discontinued, and oral prednisone 40 mg daily was initiated with tremendous and rapid response. His eruption had cleared with no new bullae at the 1-week outpatient follow-up with his dermatologist. The prednisone was tapered accordingly.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [85, 'years'], 'creatinine': [1.83, 'mg/dL'], 'sex': 'Male'}",35.71514,33.92938,37.5009,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 85 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.83 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.83/0.9)**-1.2 * 0.9938**85 * 1.0 = 35.71514.
Hence, the GFR value is 35.71514 ml/min/1.73 m²."
420,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4940809-1,Extracted,"A 74-year-old man with an unremarkable medical history was referred to the Roubaix Hospital emergency department on November 13th 2012. The reasons for his consultation were headaches, vomiting, walking trouble, and dysarthria of sudden onset a few hours ago. His vital signs were blood pressure: 156/57 mmHg, heart rate: 103/min, and body temperature: 95°F (35°C). The first examination of the patient revealed cerebellar signs such as ataxia, apraxia, and dysarthria. The initial level of consciousness was normal (Glasgow Coma Score (CGS) 15). The head CT scan was normal, without ischemic or hemorrhagic stroke. Because of meningeal signs, a lumbar puncture was performed and found only 2 cells per mm3. The neurological investigations were completed by a brain magnetic resonance imaging (MRI), confirming the absence of ischemic or hemorrhagic stroke. A brainstem stroke was also discarded, and the basilar artery was permeable.
Few hours later, the patient deteriorated and presented coma (GCS 7), requiring intubation and mechanical ventilation. He was then transferred to our intensive care unit. The first lab results revealed a nonspecific inflammatory syndrome (white blood cells: 25,000/μL, C-RP: 96 mg/L) and renal failure (creatinine: 266 μmol/L, urea: 13.8 mmol/L). All standard toxic substances were negative (alcohol, barbiturates, benzodiazepines, tricyclic antidepressants, and carbon monoxide). The chest X-ray revealed an alveolar infiltrate of the right lung. The renal ultrasound was normal.
Initial management included mechanical ventilation, sedation, volemic expansion, broad spectrum antibiotics to treat a possible meningitis, and intravenous acyclovir to treat a possible herpetic encephalitis.
Early evolution was marked by the persistence of shock requiring vasopressive support (norepinephrine). A few hours later, the patient presented an acute coronary syndrome, complicated by severe arrhythmias, namely ventricular fibrillation, responsible for a cardiogenic shock with a left ventricular ejection fraction (LVEF) at 30%.
Because of multiorgan failure, including cerebral, renal, pulmonary, and cardiac dysfunctions, several diagnoses were suspected. Normal levels of complement system’s proteins and plasma protein electrophoresis were not in favor of an autoimmune disease. c-ANCA antibodies, anti-glomerular basement membrane antibodies, antinuclear, and lupus anticoagulant antibodies were negative, allowing to rule out Wegener’s granulomatosis, Goodpasture’s syndrome, and lupus erythematosus. Finally, a thrombotic microangiopathy was also suspected, but ADAMST 13 activity was normal. In addition, there was no hemolytic anemia, neither thrombopenia. It should be noted that viral serologies such as HIV and B and C hepatitis were also negative.
After discussion with the radiologist and the neurologist, it appeared that the first MRI might have been realized too early. A second one was then performed on November 16th (day 4). It showed several abnormalities as follows: hyperintense lesions of thalami (Figure a), dentate nuclei (Figure b), posterior white matter in the brainstem pons, and periaqueductal gray matter of the midbrain (Figure c) on fluid-attenuation inversion recovery (FLAIR) and diffusion weighted-sequences.
At day 7, the son of the patient brought us the answer: an old empty extinguisher (Figure ). The patient used it in the morning of his consultation to unclog his sink and he inhaled the content of the extinguisher, which contained methyl bromide. A blood sample was sent to specialized toxicology laboratory in Paris. The methyl bromide blood level was over 120 mg/L (normal level <0.05 mg/L). Assuming a 12-day half-life for methyl bromide [], his serum bromide was probably much higher at his admission (7 days before the blood sample). Four weeks later, methyl bromide was still positive in the patient’s blood (Figure ).
Several authors have studied methyl bromide’s neurotoxicity and reported similar brain MRI results. Bilateral strikingly symmetrical high signal intensity on T2-weighted and FLAIR sequences have been reported in the bilateral dentate nuclei of the cerebellum, periventricular area of the fourth ventricle, dorsal medulla (inferior olivary nuclei, restiform bodies, vestibular nuclei), dorsal pons, periaqueductal gray matter, superior and inferior colliculi, posterior putamen, subthalamic nuclei, and corpus callosum. These lesions were hypointense on T1-weighted images and devoid of mass effect. Post-gadolinium studies demonstrated no enhancement [-]. These lesions were thought to be related to local injury due to ischemia resulting from vasospasm, to increased axonal and interstitial water content, and also to a direct effect of the methyl bromide on Purkinje cells’ nucleic acid [,].
As regards to the cardiovascular system, the patient presented an acute coronary syndrome at day 2, responsible for a cardiogenic shock. The diagnosis was made based on the combination of an elevated troponin up to 54 μg/L and changes in the 12-lead electrocardiogram. There was indeed a de novo ST elevation and a Pardee wave in the inferolateral territory, with mirror images in the anterior territory. The transthoracic echocardiography revealed kinetics abnormalities in the corresponding territories and a decreased left ventricle ejection fraction at 30%. The patient also presented ventricular fibrillation, reversed after three external electric shocks. Given the fact that the patient was highly unstable, presented acute renal failure, and in the hypothesis of a septic shock, we decided not to perform an angiocoronarography immediately. The cardiogenic shock was controlled after 4 days of cardiotropic treatment by dobutamine, and the electrocardiogram was back to anterior state within 48 h, under cover of a treatment by double platelet anti-aggregation. One month later, the LVEF increased at 50%.
The angiocoronarography performed around day 40 found normal coronary arteries. The assumption of a myocardial infarction induced by the methyl bromide himself was then not confirmed. The major etiological hypothesis for this cardiac and/or coronary distress is a side effect of the severe initial shock with low cardiac output. Indeed, initial cardiac ultrasound showed localized kinetics abnormality, well correlated with electrocardiogram, which did not suggest a stress cardiomyopathy such as Takotsubo (no contrast between apex and basis of the left ventricle). A direct cardiotoxicity of the methyl bromide is quite unlikely because no similar case has been described in the literature.
As regards to renal failure, the urinary balance showed a proteinuria at 2.15 g/day. The renal ultrasound showed no obstruction of the urinary tract, two kidneys of normal size, and a good corticomedullary differentiation.
The renal function got worse to reach a real anuria with creatininemia at 575 μmol/L and ureamia at 38,2 mmol/L. Extrarenal epuration was required for 11 days. We used a continuous venovenous hemofiltration instead of intermittent dialysis because of hemodynamic unstability. A normal renal function was finally reached in 16 days, with a creatininemia at 90 μmol/L, and a normal urinary output. This renal failure seems to be of renal type. On the first blood sample from the emergency ward, creatinine level is already more increased than the urea is. The natriuresis was never locked. Moreover, the early volemic expansion and hemodynamic stabilization had no effect on renal function and diuresis. This renal failure can easily be explained by the methyl bromide himself [].
As regards to respiratory failure, ventilator-associated pneumonia was suspected at day 4. The patient presented hyperthermia at 101.3°F (38.5°C), an important inflammatory syndrome with C-RP at 195 mg/L and a right alveolar infiltrate on the chest X-ray. Two days later, in spite of a broad-spectrum antimicrobial treatment (Tazocilline), it progressed to acute respiratory distress syndrome (ARDS) with a PaO2/FiO2 ratio at 80 and bilateral diffuse alveolar syndrome on the chest X-ray. There was no argument in favor of a cardiogenic pulmonary oedema, in spite of the concomitant ventricular dysfunction, because the left ventricular filling pressures were low. The patient required specific ARDS ventilation and curarization. Finally, ARDS quickly resolved, and the patient did not require prone positioning. The pulmonary evolution was also marked by the occurrence at day 8 of a pneumothorax under mechanical ventilation, which had to be been drained by a chest tube.
All the respiratory events were obviously not the result of direct injury of the intoxication but were induced by the neurological injury, requiring intubation and mechanical ventilation.
Delayed weaning from the ventilator was partly related to ventilator-associated pneumonia. In addition, the patient presented a polyneuropathy with tetraparesia. ICU-acquired weakness or “critical illness polyneuropathy” was confirmed by an electromyogram showing a peripherical neurogenic disturbance. It was certainly favored by 56 days of mechanical ventilation and the severity of the multiple organ failure []. However, this kind of peripheral neuropathy has also been frequently described in cases of methyl bromide poisoning [-]. On top of this, the methyl bromide intoxication resulted in central neurological effects, such as delayed awakening, and alertness disorders. Moreover, the patient experienced swallowing disorders, probably due to the methyl bromide intoxication itself [,]. A percutaneous tracheotomy was performed because of weaning difficulties.
Finally, the patient was decanulated after 56 days of mechanical ventilation. A brain MRI, performed 6 months later, showed that most of the lesions had improved. It remained only sequels on the left internal capsule and specifically the thalamus and the dentate nucleus. According to the literature, brain MRI lesions due to methyl bromide toxicity are frequently reversible [,,]. He has been transferred to a rehabilitation department specialized in rehabilitation of neurological patients. To date, he is back home. After hours of physical and speech therapy, he still faces sequels such as dysarthria and ataxia and needs a Zimmer to walk by himself.
As far as pathophysiology is concerned, several mechanisms seem to be the cause of the methyl bromide toxicity. Most of the authors have described a cellular toxic effect. Indeed, following a methylation reaction, the methyl bromide conjugates itself with glutathione to make methylglutathione, which is highly toxic for the respiratory chain [-]. A second cause often described is the modulation of the inhibitory neurotransmitter γ-aminobutyric acid receptor within the cerebellar and vestibular systems [,,]. A third hypothesis attributes toxicity to methyl bromide metabolites such as methanethiol and formaldehyde [,]. Another suggested mechanism is that methyl bromide rapidly inhibits creatine kinase activity in all regions of the brain and in other target organs. Creatine kinase is an enzyme catalyzing the conversion of adenosine triphosphate and creatine to adenosine diphosphate and phosphocreatine [,].","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [74, 'years'], 'creatinine': [266.0, 'µmol/L'], 'sex': 'Male'}",20.68531,19.65104,21.71958,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 74 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 266.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 266.0 µmol. To convert 266.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 266.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00027 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00027 mol Serum Creatinine * 113.12 g/mol = 0.03054 g Serum Creatinine. To convert 0.03054 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.03054 g Serum Creatinine * 1000.0 mg/g = 30.54 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 30.54 mg Serum Creatinine/10.0 dL = 3.054 mg Serum Creatinine/dL. The concentration value of 266.0 µmol Serum Creatinine/L converts to 3.054 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.054/0.9)**-1.2 * 0.9938**74 * 1.0 = 20.68531.
Hence, the GFR value is 20.68531 ml/min/1.73 m²."
421,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-5483,Extracted,"A 69-year-old man presents to the emergency department with shortness of breath that has been worsening over the past month. The patient states that he has had worsening shortness of breath that has progressed to shortness of breath with simple activities and minor exertion. When he was unable to climb the stairs to his house today, he decided to come to the emergency department. The patient has a past medical history of poorly managed diabetes mellitus, hypertension, end stage renal disease, and obesity. His current medications include insulin, metformin, lisinopril, hydrochlorothiazide, and ibuprofen. The patient is notably non-compliant with his medications. An EKG and chest radiograph are normal. The patient had dialysis two days ago and attends most of his appointments. Laboratory values are ordered and are seen below:

Serum:
Na+: 135 mEq/L
K+: 4.5 mEq/L
Cl-: 100 mEq/L
HCO3-: 19 mEq/L
Urea nitrogen: 29 mg/dL
Glucose: 75 mg/dL
Creatinine: 2.5 mg/dL
Ca2+: 9.2 mg/dL
Mg2+: 1.7 mEq/L
AST: 11 U/L
ALT: 11 U/L

Leukocyte count and differential:
Leukocyte count: 4,500/mm^3
Platelet count: 150,000/mm^3
Neutrophil: 54%
Lymphocyte: 25%
Monocyte: 3%
Eosinophil: 1%
Basophil: 1%

Hemoglobin: 8.2 g/dL
Hematocrit: 22%
Mean corpuscular volume: 82 µm^3

The patient appears comfortable at rest but demonstrates notable shortness of breath when exerting himself. His temperature is 99.5°F (37.5°C), pulse is 89/min, blood pressure is 144/85 mmHg, respirations are 10/min, and oxygen saturation is 97% on room air. Pulmonary and cardiac exam are within normal limits.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [69, 'years'], 'creatinine': [2.5, 'mg/dL']}",27.132,25.7754,28.4886,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 69 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.5/0.9)**-1.2 * 0.9938**69 * 1.0 = 27.132.
Hence, the GFR value is 27.132 ml/min/1.73 m²."
422,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4393463-1,Extracted,"A 62-year-old man with type 2 diabetes mellitus and hypertension presented with generalized weakness. The patient had undergone partial penectomy 5 months earlier for a mass, which was diagnosed histologically as squamous cell carcinoma, moderately to well differentiated, condylomatous subtype. The neoplasm involved the entire glans and distal part of the urethra, with up to 1.5 cm depth of invasion (Stage T3). No lymph node dissection was performed at the time of surgery. Physical examination showed the trace edema of lower extremities but was otherwise unremarkable. Laboratory data on admission were significant for hypercalcemia with a serum calcium of 13.4 mg/dL (3.35 mmol/L) and increased serum creatinine at 2.3 mg/dL (203.3 μmol/L). Urinalysis showed pH 5, 2+ proteinuria and granular casts (2–4/low-power field). A computed tomographic scan revealed lymphadenopathy in mediastinum, inguinal regions and external iliac lymph nodes. Bone scintigraphy showed increased uptake in the skull, ribs, shoulders, vertebral bones and left sacroiliac joint, consistent with metastasis. The hypercalcemia was treated with intravenous fluid and bisphosphonate, with significant improvement. However, the patient's serum creatinine rapidly increased to 8.1 mg/dL (716 μmol/L) in 2 weeks. Nephrology was consulted and a kidney biopsy was performed.
Microscopic examination showed acute interstitial nephritis characterized by diffuse interstitial edema and infiltration by mononuclear and polymorphonuclear leukocytes including neutrophils. The interstitial inflammatory changes were associated with widespread acute tubular injury. The glomeruli showed features of diabetic nephropathy including nodular mesangial sclerosis. One of the glomeruli was partially obliterated by a proliferative epithelial lesion with crescent-like features involving the capillary tuft and adjacent urinary space (A and B). Epithelial cells comprising this lesion were cytologically atypical and showed feature suggestive of squamous differentiation including the eosinophilic cytoplasm, distinct cell borders and occasional intercellular bridges. Many of these cells had large irregular nuclei, and prominent eosinophilic nucleoli (A and B). Occasional mitotic figures and apoptotic bodies were also identified (A). The glomerular capillary involved with this lesion was markedly distended and completely filled by atypical epithelial cells. A few of these cells were also identified in the adjacent proximal tubules. A review of the partial penectomy specimen, previously diagnosed as squamous cell carcinoma, showed a strong similarity between the cancer cells of the primary neoplasm and the atypical epithelial cells found in the kidney biopsy (data not shown). Taken together with the squamous features of the intraglomerular epithelial cells, this finding was most suggestive of glomerular involvement by metastatic squamous cell carcinoma of the penile origin.
Immunohistochemical studies were performed to confirm the squamous differentiation and neoplastic nature of the intraglomerular proliferative epithelial lesion. The atypical intraglomerular epithelial cells were positive for cytokeratin (CK) 5 (EP1601Y, Cell Marque; C) and p63 (BC4A4, Cell Marque; D), markers of squamous cell carcinoma [, ], and negative for WT1 (6F-H2, Dako, podocyte marker), CK8 (35bH11, Cell Marque, parietal epithelial cell marker) and CD31 (JC/70A, Dako, endothelial marker) (data not shown). Atypical cells with similar cytologic and immunoreactive features were identified within the urinary space of an additional glomerulus (data not shown).
Based on the histologic and immunohistochemical findings, the lesion was diagnosed as intraglomerular metastatic squamous cell carcinoma of penile origin. The patient's clinical condition deteriorated despite supportive care, including dialysis, to the extent that systemic chemotherapy could not be administered. The patient was kept on palliative care until his demise 3 weeks after the kidney biopsy. No autopsy was performed.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [62, 'years'], 'creatinine': [2.3, 'mg/dL'], 'sex': 'Male'}",31.32157,29.75549,32.88765,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 62 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.3/0.9)**-1.2 * 0.9938**62 * 1.0 = 31.32157.
Hence, the GFR value is 31.32157 ml/min/1.73 m²."
423,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5803725-1,Extracted,"An 89-year-old man presented to our emergency room with a 2-day history of upper abdominal pain, nausea, and vomiting that had been present for 2 days. He had a history of type 2 DM, hypertension, and dementia and was bedridden. His vital signs were stable. On physical examination, his abdomen was tender to palpation over the epigastrium without rebound tenderness or guarding. Laboratory values were as follows: sodium 143 mmol/L, potassium 3.2 mmol/L, total bilirubin 0.5 mg/dL, creatinine 0.99 mg/dL, urea nitrogen 22.7 mg/dL, C-reactive protein 4.08 mg/dL, hemoglobin A1c 6.2%, hemoglobin 9.9 g/dL, leukocyte count 12,200 mm3, platelet count 215,000 mm3, and lactate 0.9 mmol/L. Abdominal X-ray and a computed tomography scan of the abdomen revealed a dilated stomach with significant fluid collection, GOO, and GP due to a 42 × 40 mm mass composed of fat and air densities (Fig. ). Emergency esophagogastroduodenoscopy (EGDS) revealed two gastric bezoars, one of which was incarcerated in the pyloric region. We used various endoscopic devices to successfully break and remove the bezoars. EGDS procedures were performed with a conventional single-accessory channel endoscope (GIF-Q260J; Olympus Medical Systems, Tokyo, Japan). First, we performed fragmentation with endoscopic forceps and a water jet. However, this was insufficient to extract the obstruction. Therefore, we used an endoscopic snare to cut the bezoars into several pieces and removed them with an endoscopic net (Fig. ). Follow-up endoscopy confirmed that the gastric bezoars had been completely removed (Fig. ).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [89, 'years'], 'creatinine': [0.99, 'mg/dL'], 'sex': 'Male'}",72.81611,69.1753,76.45692,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 89 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.99 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (0.99/0.9)**-1.2 * 0.9938**89 * 1.0 = 72.81611.
Hence, the GFR value is 72.81611 ml/min/1.73 m²."
424,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4348984-1,Extracted,"A 75-year-old male presented to the emergency room complaining of left-sided ischemic chest pain for 5 hours. The pain increased during the hour prior to presentation and was associated with shortness of breath. There were no other symptoms.
He has hypertension, diabetes, dyslipidemia and chronic renal impairment.
Physical examination was unremarkable apart from a few bilateral basal rales. ECG in the emergency room showed ST elevation more than 1 mm in leads III and AVF and 3 mm ST depression in leads V2 - V6 and leads I and AVL. There was no evidence of right ventricular infarction. CXR showed normal mediastinum and right lower zone infiltrate []. Echocardiography showed ejection fraction (EF) 45% and severe hypokinesia of inferior wall and inferobasal segment. Serum troponin was initially normal but peaked to 181 ng/ml.
White blood cell (WBC) was 36,200 cells/mcL (mainly neutrophils); hemoglobin was 12.3 g/dL; platelet count 402000/mmo; sodium was 131 mmol/L; and potassium was 5.0 mmol/L. Random blood sugar was 9.7 mmol/L; creatinine was 141 mmol/L; and urea 9.6 mmol/L; ALT was normal; low density lipoprotein 2.35 mmol/L; triglycerides 1.06 mmol/L; and high density lipoprotein 1.42 mmol/L.
Streptokinase (1.5 million units) was started immediately according to standard protocol. He was commenced on aspirin 81 mg daily, clopidogrel 75 mg daily, simvastatin 40 mg nocturnal, carvedilol 6.25 mg BD, amlodipine 5 mg daily, and fosinopril 20 mg daily.
After streptokinase, chest pain and shortness of breath resolved for the first 72 hours and there was significant improvement of the ECG (>50% resolution of ST elevation). However after 72 hours, he started to complain of dry cough and shortness of breath at rest, inspite of oxygen. He was given furosemide but without response.
Hemoglobin dropped to 8.9 g/dL with no external bleeding, WBC decreased to 24000 g/L. ABG showed hypoxia (PO2= 7.8 kpa; CO23.9 kpa; pH 7.32; O289%; HCO315.3 mmol/L).
CXR showed increased bilateral basal reticular infiltrate and new right lower lobe opacity not seen on admission []. Repeated echocardiography was comparable to the previous examination.
He was started on empirical antibiotic treatment, two units of packed red blood cells were given and HRCT was ordered to rule out interstitial lung disease or infection.
A few hours later, SaO2 started to drop again and urine output decreased to 20 mL/h, despite intravenous (IV) furosemide. Creatinine jumped to 438 mmol/L and ALT increased to 1383 IU/L. Urgent consultations from different specialties were requested. The patient underwent elective mechanical ventilation and urgent bronchoscopy.
Bronchoscopy showed blood coming from the bronchial tree, mainly from left lower lobe with pale mucosa and no evidence of infection []. Bronchoalveolar lavage was performed and specimens were taken for hemosiderin-laden macrophages, cultures, and cytology.
On the above basis, the respirology team confirmed the diagnosis of pulmonary hemorrhage. Aspirin, clopidogrel, and enoxaparin were stopped.
Tranexamic acid 500 mg IV every 8 hours was started.
On the 4th hospital day, the patient reinfarcted as evidenced by elevation of troponin and CK MB, with new ST depression more than 2 mm in leads V2 - V4. Echocardiography showed further drop in EF to 30% with extension of infarction but no mechanical complications. Tranexamic acid was stopped.
On the 5th hospital day, the patient developed atrial fibrillation that required both synchronized cardioversion of 200 joules and amiodarone infusion. All cultures were negative.
The patient went into cardiogenic shock and multiorgan failure on the 6th hospital day and passed away.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [75, 'years'], 'creatinine': [141.0, 'µmol/L']}",45.19575,42.93596,47.45554,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 75 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 141.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 141.0 µmol. To convert 141.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 141.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00014 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00014 mol Serum Creatinine * 113.12 g/mol = 0.01584 g Serum Creatinine. To convert 0.01584 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01584 g Serum Creatinine * 1000.0 mg/g = 15.84 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 15.84 mg Serum Creatinine/10.0 dL = 1.584 mg Serum Creatinine/dL. The concentration value of 141.0 µmol Serum Creatinine/L converts to 1.584 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.584/0.9)**-1.2 * 0.9938**75 * 1.0 = 45.19575.
Hence, the GFR value is 45.19575 ml/min/1.73 m²."
425,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-1186,Extracted,"A 55-year-old woman comes to the physician because of a 6-month history of worsening fatigue. During this time, she has noted a decrease in her exercise capacity and she becomes short of breath when walking briskly. She has had occasional streaks of blood in her stools during periods of constipation. She was diagnosed with type 1 diabetes mellitus at the age of 24 years and has a history of hypertension and hypercholesterolemia. She does not smoke or drink alcohol. Her current medications include insulin, lisinopril, aspirin, and atorvastatin. Her diet mostly consists of white meat and vegetables. Her pulse is 92/min and blood pressure is 145/92 mm Hg. Examination shows conjunctival pallor. Cardiac auscultation shows a grade 2/6 midsystolic ejection murmur best heard along the right upper sternal border. Sensation to pinprick is decreased bilaterally over the dorsum of her feet. The remainder of the examination shows no abnormalities. Laboratory studies show:
Hemoglobin 9.2 g/dL
WBC count 7,200/mm3
Erythrocyte count 3.06 million/mm3
Mean corpuscular volume 84 μm3
Platelets 250,000/mm3
Reticulocyte count 0.6 %
Erythrocyte sedimentation rate 15 mm/h
Serum
Na+ 142 mEq/L
K+ 4.8 mEq/L
Ca2+ 8.1 mEq/L
Ferritin 145 ng/mL
Urea nitrogen 48 mg/dL
Creatinine 3.1 mg/dL
A fecal occult blood test is pending.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [55, 'years'], 'creatinine': [3.1, 'mg/dL'], 'sex': 'Female'}",17.11579,16.26,17.97158,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 55 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 3.1 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (3.1/0.7)**-1.2 * 0.9938**55 * 1.012 = 17.11579.
Hence, the GFR value is 17.11579 ml/min/1.73 m²."
426,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4228718-1,Extracted,"A 49-year-old female with metastatic urothelial carcinoma of the bladder was transferred to our tertiary care institution from another hospital with hypoxia, tachycardia, and chest pain. Three days previously, she received her first cycle of palliative chemotherapy consisting of cisplatin (75 mg/m2) and infusional 5-fluorouracil (1000 mg/m2/day × 4 days). Her body surface area was 1.84 m2 and her body mass index was 26.9 kg/m2. She had no previous history of cardiac disease, diabetes, dyslipidemia, or smoking. Prior to transfer, the patient was assessed in the emergency department for nausea, vomiting, and hypovolemia. An initial working diagnosis of undifferentiated shock was made, for which she received four litres of intravenous crystalloid with minimal urine output.
Upon transfer, the patient was in respiratory distress, with an oxygen saturation of 93 percent measured by pulse oximetry, on 100 percent oxygen via nonrebreather facemask. She subsequently became cyanotic and hypotensive, requiring endotracheal intubation and mechanical ventilation. Blood pressure decreased to 96/52 mm Hg with clinical evidence of hypoperfusion and multiorgan system dysfunction, requiring vasopressor and inotropic support. A venous blood gas revealed a pH of 7.10, a pCO2 of 61 mm Hg, and an HCO3 of 19 mmol/L. Serum lactate and creatinine were elevated at 5.7 mmol/L and 361 μmol/L, respectively. Serum troponin I was also elevated, with a peak value of 2.91 μg/L 24 hours after transfer. Chest radiographs revealed bilateral areas of patchy consolidation with pleural effusions. A computed tomography pulmonary angiogram ruled out an embolism but confirmed bilateral airspace consolidation in all 5 lobes. Bronchoscopy and lavage were performed, which ruled out evidence of obstruction or infection. An electrocardiogram demonstrated ST segment elevation in the precordial leads and in the limb leads, with no reciprocal ST segment depression ().
A transthoracic echocardiogram (while on inotropic support) revealed moderate biventricular dysfunction with a left ventricular ejection fraction of 44%. A provisional diagnosis of cardiogenic shock was established, and the patient was transferred to the intensive care unit for supportive care.
While in the intensive care unit, intravenous milrinone, phenylephrine, norepinephrine, and vasopressin were required to maintain adequate blood pressure and cardiac output. Blood, urine, and sputum cultures were obtained, and empiric antibiotics were administered. The patient's renal function continued to deteriorate, and continuous renal replacement therapy was subsequently initiated. Over the course of several days, the patient's cardiac output and hypoxemic respiratory failure improved, vasopressors and inotropes were discontinued, and she was extubated and transitioned to intermittent hemodialysis. Her renal function slowly recovered, and hemodialysis was eventually discontinued. The initial ST segment changes resolved, with no evidence of Q waves on serial ECGs (Figures and ).
A follow-up transthoracic echocardiogram five days after admission revealed improvement in left ventricular function, with a left ventricular ejection fraction off inotropes of 59%. Throughout the patient's hospital course, blood, urine, and sputum cultures remained negative.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [49, 'years'], 'creatinine': [361.0, 'µmol/L']}",12.8076,12.16722,13.44798,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 49 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 361.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 361.0 µmol. To convert 361.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 361.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00036 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00036 mol Serum Creatinine * 113.12 g/mol = 0.04072 g Serum Creatinine. To convert 0.04072 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.04072 g Serum Creatinine * 1000.0 mg/g = 40.72 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 40.72 mg Serum Creatinine/10.0 dL = 4.072 mg Serum Creatinine/dL. The concentration value of 361.0 µmol Serum Creatinine/L converts to 4.072 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (4.072/0.7)**-1.2 * 0.9938**49 * 1.012 = 12.8076.
Hence, the GFR value is 12.8076 ml/min/1.73 m²."
427,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4432414-1,Extracted,"A 44-year-old Bangladeshi man was admitted to hospital with a history of cough, hemoptysis and dyspnea of 1-day duration. He had previously been healthy until he developed coryza symptoms about 1 week prior to presentation. There was no history of chronic cough, weight loss, night sweats or recent travel outside the USA. The patient had smoked half a pack of cigarettes per day for 15 years but denied a history of exposure to any environmental or industrial exposure to any agents with known pulmonary toxicity. He denied passage of cola-colored urine or gross hematuria. His medications were bismuth subsalicylate for gastroesophageal reflux disease and daily multivitamins.
On examination, his vital signs showed a blood pressure of 143/81 mmHg, pulse of 90 beats/min, temperature of 37°C and respiratory rate of 20. Cardiac examination was normal, but diffuse pulmonary rales were heard in both lung fields on chest auscultation. The rest of his physical examination was normal. The hematocrit was 44% and hemoglobin was 12 g/dL. The white cell count was 4.5 k/mm3, platelet of 196 k/mm3 and a prothrombin time with a normalized international ratio of 0.96. His blood urea nitrogen was 19 mg/dL (6.78 mmol/L) and serum creatinine was 0.96 mg/dL (84.48 mmol/L). Urinalysis was significant for 3+ blood, and >50 rbc/hpf with dysmorphic red cells and 2+ protein. Serologies for antineutrophil cytoplasmic antibodies (ANCA), antinuclear antibodies (ANA), rheumatoid factor, antiglomerular basement membrane antibody (anti-GBM), hepatitis B and C and viruses influenza A and B, adenovirus, enteroviruses, herpes simples I and II, cytomegalovirus, Coxiella burnetti, Mycoplasma pneumonia were all negative. A tuberculin skin test was negative. Sputum cultures for bacterial, fungal and mycobacteria were negative.
A CT scan of the chest with contrast () showed diffuse alveolar bilateral patchy infiltrates, with some emphysematous changes. The lung infiltrates had a ground glass appearance. The patient was admitted to the intensive care unit for closer monitoring, and started on empiric antibiotic therapy for possible pneumonia to exclude Goodpasture's syndrome in view of hemoptysis and hematuria. Further laboratory tests including ANA, anti-GBM IgG, complements, viral hepatitis screen, ESR, CRP, VWF, ANCA, sputum AFB ×3 and coagulation panel, were all within normal limits. An upper gastrointestinal endoscopy to investigate hemocult-positive stool did not reveal any active evidence of gastro-intestinal bleeding.
He continued to have massive (>500 mL/day) hemoptysis and hematuria with subsequent decline in the hematocrit necessitating transfusion of a total of 3 units of packed red cells. He underwent bronchoscopy and bronchoalveolar lavage which showed the presence of hemosiderin-laden macrophages and bloody exudate. To establish the cause of the pulmonary–renal presentation of this patient, a kidney biopsy was done.
Renal biopsy () showed mesangial proliferative glomerulonephritis with IgA deposition. The patient was started on intravenous cyclophosphamide 1 g and prednisone 60 mg daily. Over a 4-day period, his hemoptysis gradually resolved, and hemoglobin and hematocrit stabilized at 10.9 gm/dL and 32.1%, respectively. The patient was then started on intravenous cyclophosphamide infusion 1 gm monthly with daily oral prednisone tapered by 10 mg every month. He completed six cycles of monthly cyclophosphamide. Prednisone was tapered off over an additional 2-month interval. There has been no recurrence of hemoptysis and the patient has since stopped smoking ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [44, 'years'], 'creatinine': [0.96, 'mg/dL'], 'sex': 'Male'}",99.95616,94.95835,104.95397,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 44 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.96 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (0.96/0.9)**-1.2 * 0.9938**44 * 1.0 = 99.95616.
Hence, the GFR value is 99.95616 ml/min/1.73 m²."
428,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4556817-1,Extracted,"A 43-year-old African American male presented to the Division of Oral Oncology at the University of Mississippi Cancer Institute with the chief complaint of swelling in his right mandible that had been present for approximately one year (). Oral exam revealed a 5.0 × 7.0 cm bulbous mass arising from the mandible and obliterating the right side of the oral cavity. The mass was ulcerated due to occluding with the opposing dentition. The patient denied pain but reported difficulty in eating. A computed tomography (CT) scan (Figures and ) showed an expansile osseous lesion, involving the entire height of the mandible and extending from the right first premolar all the way posteriorly to involve the ramus and coronoid process. This lesion caused severe bony destruction of the mandible, eroding through both buccal and lingual cortices and filling the right half of the oral cavity.
The patient's past medical history was significant for end stage renal disease (ESRD). He was on hemodialysis and was followed by a nephrologist. He had secondary HPT which was not well controlled, with a PTH level of 1,818 pg/mL at the time of presentation (normal range (NR) 11 to 77 pg/mL). This was thought to be likely due to noncompliance with his medications and due to refractory disease. The remainder of his labs was as follows: Ca 8.4 (NR 9–10.5 mg/dL), P 5.3 (NR 3.0–4.5 mg/dL), blood urea nitroge 28 (NR 8–20 mg/dL), and creatinine 7.17 (NR 0.7–1.3 mg/dL).
Based on the past medical history, this lesion was highly suspicious for BTHPT. However, given the rarity of brown tumors and the clinical appearance and size of this lesion, other osseous and odontogenic tumors could not be excluded. An incisional biopsy was performed and histologic examination confirmed the diagnosis of BTHPT.
Microscopically, the lesion was composed of a highly cellular proliferation of bland spindle-shaped fibroblastic cells with numerous multinucleated giant cells () and spicules of woven bone. The osteoclastic giant cells were scattered throughout the cellular stroma and surrounded small spicules of bone (). Small blood vessels, extravasated red blood cells, and focal deposits of hemosiderin were seen throughout the lesion, especially toward the periphery. The native bone showed evidence of intense bone resorption secondary to osteoclast hyperactivity and marrow fibrosis, consistent with secondary hyperparathyroidism (). The histologic appearance of the lesion was akin to central giant cell reparative granuloma.
A discussion was held with the patient and treating nephrologist. Given the extent of the tumor and the uncontrolled underlying disease, it was decided that surgical intervention was the best option. Segmental resection with minimal margins was performed because marginal resection or enucleation procedures were deemed not feasible due to the limited amount of bone. This was done via a transcervical lip splitting approach due to limited access from the extensive size of the tumor (Figures 
– and supplemental video in Supplementary Material available online at ). A microvascular free tissue transfer was not performed at that time because the treating nephrologist did not feel the patient could tolerate a lengthy surgery. Virtual surgical planning was utilized to help plan the mandibular resection as well as the reconstruction bar placement (). Postoperatively, the patient's hospital course was uneventful. He was followed up by the inpatient nephrology team and continued to receive dialysis while he remained in the hospital.
The patient was followed up for several weeks after surgery, and initial healing was within normal limits. Unfortunately, the patient was noncompliant with long term follow-up despite very extensive efforts to get him rescheduled. This noncompliance may have potentially contributed to the initial presentation of the tumor.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [43, 'years'], 'creatinine': [7.17, 'mg/dL']}",9.00768,8.5573,9.45806,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 43 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 7.17 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (7.17/0.9)**-1.2 * 0.9938**43 * 1.0 = 9.00768.
Hence, the GFR value is 9.00768 ml/min/1.73 m²."
429,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3141156-1,Extracted,"An 18-year-old female presented with gradually progressive intraoral swelling over the left palate since childhood. Apart from the swelling, she did not have any other complaint like pain or difficulty in swallowing. This was possibly the reason why she presented late. On local examination, the swelling was measuring 8 × 3 cm in size, hard in consistency, and nontender with irregular surface and margins.
The patient was assessed preoperatively as Ameican Society of Anaesthesiologists (ASA) grade I. Preoperative investigations were as follows: Haemoglobin 13.2 g%, blood urea 14 mg/dl, serum creatinine 0.7 mg/dl and blood sugar level (BSL) 70 mg%. X-ray paranasal sinuses was within normal limits.
She was posted for surgery under general anaesthesia. She was pre-medicated with injection Glycopyrrolate 0.2 mg intramuscular 45 minutes prior to surgery. All the preoperative vital parameters were normal. An intravenous line was secured with a 20-gauge cannula. She was pre-oxygenated with 100% O2. Injection Ondansetron 4 mg, injection Ranitidine 50 mg, injection Midazolam and injection Fentanyl were administered as preinduction drugs. General anaesthesia was induced with Sodium Thiopentone and intubated under the effect of Scoline. Nasal intubation was done with 32 FG flexometallic ETT. After inflation of cuff, throat packing and fixing of ETT, anaesthesia was maintained on O2 + N2O and Isoflurane with Vecuronium as long-acting muscle relaxant. The patient was kept on intermittent positive pressure ventilation. All vital parameters were maintained in normal range during surgery. Injection Voveran was given intramuscularly to maintain analgesia.
During surgery, while cutting the portion of palate involved by the mass lesion with a Giglisaw, it was observed that the reservoir bag of Bain's circuit collapsed fully. Both the surgeon and the anaesthetist realised at the same time that this was due to complete transection of the flexometallic tube with the Giglisaw. There was difficulty in removing both the proximal and distal ends of the transected tube because of intact nylon rings. Hence, tracheostomy was performed by the surgeon within 90 seconds. We continued 100% O2 through the same circuit. The oxygen saturation had dropped to 82% during tracheostomy. Portex 8 mm ID cuffed tracheostomy tube was used and the cuff was inflated with 6 ml of air. Intermittent positive pressure ventilation was continued with 100% oxygen. The patient stabilised within 3 minutes with oxygen saturation of 99%. Once the airway was established, cuff of the transected ETT was punctured and remnants of the flexometallic ETT were removed []. The surgery was continued and completed uneventfully in the next 30 minutes. All vital parameters remained normal during the procedure. The patient was reversed with injection Neostigmine and atropine intravenously and monitored for 30 minutes.
Postoperatively, the patient was conscious, responding to pain and obeying verbal commands with a pulse rate of 108/min and a BP of 126/80 mm of Hg. SaO2 was 98% on air. She was shifted to ICU for observation and tracheostomy care.
On the 2nd postoperative day, she was transfused with one pint of blood as there was haematemesis on the same day that she was shifted to the ward.
On the 4th postoperative day, tracheostomy tube was removed. Further recovery was uneventful.
On the 9th postoperative day, the patient was discharged.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [18, 'years'], 'creatinine': [0.7, 'mg/dL']}",128.48449,122.06027,134.90871,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 18 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.7 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.7/0.7)**-0.241 * 0.9938**18 * 1.012 = 128.48449.
Hence, the GFR value is 128.48449 ml/min/1.73 m²."
430,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8612778-1,Extracted,"We present the case of a 40-year-old male who six months prior underwent an orthotopic liver transplant secondary to primary sclerosing cholangitis on chronic immunosuppressive therapy. He presented to the emergency room with complaints of sudden onset fever ongoing for three days associated with nausea, vomiting, and diarrhea (about five to six watery bowel movements per day). He also endorsed fatigue. He denied chest pain, shortness of breath, headache, confusion, or vision changes. His immunosuppressive medications consisted of prednisone, mycophenolate mofetil, tacrolimus, and valganciclovir. He previously had cytomegalovirus (CMV) viremia, for which he was treated with valganciclovir. Serial CMV PCR was negative, and the valganciclovir dose was decreased to a maintenance dose.
At the time of initial presentation, he was febrile with a maximum temperature of 38.9°C, blood pressure 93/55 mmHg, pulse 101 beats/min, and oxygen saturation 98% on room air. He was alert, oriented, cooperative, and in no apparent distress. The physical exam was unremarkable, with no rashes or lesions noted.
Initial labs revealed sodium of 130 mEq/L, potassium 5.6 mEq/L, chloride 105 mEq/L, creatinine 1.60 mg/dL, albumin 4.6 g/dL, total bilirubin 1.2 mg/dL, AST 44 U/L, ALT 51 U/L, WBC 1.70 thou/mcL with absolute neutrophil count of 0.6 thou/mcL, platelets 40 thou/mcL, and hemoglobin 8.7 g/dL. CMV PCR was negative. Blood cultures were sent and were subsequently negative. A chest X-ray did not reveal any acute abnormalities. Abdominal ultrasound showed findings consistent with medical renal disease only. Gastrointestinal PCR panel was negative for enterotoxigenic E. coli, Giardia, Norovirus, Salmonella, Shiga-like Toxin producing E. coli, Plesiomonas shigelloides, Vibrio, Yersinia enterocolitica, enteroaggregative E. coli, Cyclospora cayetanensis, Entamoeba histolytica, Adenovirus F 40/41, Astrovirus, Sapovirus, Enteropathogenic E. coli, and Shigella/Enteroinvasive E. coli. Clostridium difficile and SARS-CoV-2 PCR were negative. Serum Cryptococcus neoformans and histoplasmosis antigens were negative. Acute hepatitis A, B, and C panel was negative. Rocky Mountain spotted fever IgM titer and Rickettsia typhi IgM and IgG antibodies were negative. Urinalysis was unremarkable.
He was started on empiric vancomycin, meropenem, and micafungin (doses adjusted for renal function) without any clinical improvement in 48 hours. His immunosuppressive medication doses were reduced appropriately. His fever persisted, and renal function, as well as liver functions, declined rapidly (), prompting an infectious disease consult. On further questioning, the patient revealed he worked as a resource manager in a state park and is exposed regularly to ticks; he did not recall any obvious tick bites and had never had to pluck out a tick from his skin. He denied eating unpasteurized goods and did not consume uncooked meat or fish. He had not been swimming in public pools.
Given this history, intravenous doxycycline for presumptive ehrlichiosis was initiated on hospital day 3 while awaiting studies. Subsequently, E. chaffeensis PCR returned positive. He required a short ICU stay for vasopressor support due to septic shock. Given his severe acute kidney injury and creatinine clearance decline to <15 mL/min, hemodialysis was initiated on hospital day 4. His immunosuppressive medication regimen was initially held on admission and later changed to prednisone and tacrolimus, while mycophenolate was discontinued.
After initiation of doxycycline, clinical improvement was noted both in symptoms and laboratory indices (). He completed a 10-day course of doxycycline and was taken off hemodialysis on hospital day 10. The patient was discharged home in a stable condition and, since his discharge, has continued to do well.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [40, 'years'], 'creatinine': [1.6, 'mg/dL']}",55.51305,52.7374,58.2887,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 40 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.6 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.6/0.9)**-1.2 * 0.9938**40 * 1.0 = 55.51305.
Hence, the GFR value is 55.51305 ml/min/1.73 m²."
431,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4993914-1,Extracted,"A 68-year-old female was referred to our service for evaluation of erythema and swelling of the right elbow. She was admitted to the hospital 12 days before because of an infected left foot ulcer that required debridement and intravenous antibiotic therapy. Six weeks prior to admission she was seen by a pain management specialist for swelling of the right elbow and she was diagnosed with olecranon bursitis. She was treated with bursa aspiration and corticosteroid injection. Cultures were reportedly negative. One to two weeks after the procedure, she had worsening of swelling, as well as pain and erythema of the olecranon bursa. She did not report fever, weight loss, fatigue, or weakness.
Her past medical history was remarkable for RA diagnosed at 30 years of age, arterial hypertension, peripheral vascular disease, and asthma. Her surgical history included amputations of the first and second toes of the left foot and two tendon repairs (left hand and left shoulder). She received multiple therapies for RA including auranofin, methotrexate, leflunomide, and etanercept. Her last treatment was golimumab, which she used for 4 years. She did not have further follow-up with her rheumatologist and stopped this treatment about 2 years before onset of olecranon bursitis.
On initial evaluation, she had normal vital signs. Scleromalacia was noted bilaterally. Examination of the upper extremities showed ulnar deviation of the metacarpophalangeal joints and swan neck deformities bilaterally. The left wrist had marked limitation of flexion and extension. The right olecranon bursa was tender and swollen, and the overlying skin was erythematous (). Range of motion of the right elbow was not limited. She had multiple subcutaneous nodules in the right leg and a stage IV ulcer on the medial aspect of the left foot. Generalized muscle atrophy was observed. The rest of the examination was unremarkable.
Laboratory tests showed a white blood cell count of 6.8 × 103/μL, lymphocytic count of 1.2 × 103/μL, hemoglobin of 9.6 g/dL, and platelet count of 344 × 103/μL. Serum creatinine was 0.5 mg/dL and blood urea nitrogen was 17 mg/dL. Wound cultures were negative. Chest X-ray showed mild prominence of the pulmonary markings in the right infrahilar region.
The olecranon bursa was aspirated and 9 mL of hemorrhagic fluid was obtained. No crystals were observed under polarized microscopy. Fluid analysis showed a white blood cell count of 3.1 × 103/μL (41% neutrophils, 30% lymphocytes, and 29% monocytes). Bacterial cultures were negative. Fungal culture was positive for Candida parapsilosis; this was sensitive to anidulafungin, micafungin, caspofungin, 5-flucytosine, voriconazole, itraconazole, and fluconazole. The VITEK 2 system (bioMérieux, Inc., Hazelwood, Missouri, USA) was used for fungus identification. The Sensititre YeastOne system (Trek Diagnostic Systems, Cleveland, Ohio, USA) was utilized to determine antifungal susceptibility.
She was treated with caspofungin 50 mg intravenously daily for 13 days. Four aspiration procedures were required (every 3–5 days) due to fluid reaccumulation. All samples were cultured but only the first two were positive for Candida parapsilosis. After intravenous therapy, fluconazole 200 mg orally daily was prescribed for one week. She responded well to this therapy but had recurrent swelling of the bursa. Bursectomy was recommended but she did not wish to proceed with the intervention or receive further treatment. After 3 months of follow-up, she continued to have fluid in the olecranon bursa and had some discomfort in the area.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [68, 'years'], 'creatinine': [0.5, 'mg/dL'], 'sex': 'Female'}",102.09799,96.99309,107.20289,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 68 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.5 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.5/0.7)**-0.241 * 0.9938**68 * 1.012 = 102.09799.
Hence, the GFR value is 102.09799 ml/min/1.73 m²."
432,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7792301-1,Extracted,"A 70-year-old Thai man with a 5-year history of primary myelofibrosis, hypertension, pulmonary hypertension due to left-sided heart disease, asthma, and osteoporosis presented with an erythematous swollen left leg for 7 days (Fig. ). He also complained of fever, dyspnea on exertion, and orthopnea for 6 days. He had multiple ulcers on his right foot for 10 days, and was treated with ceftriaxone for 3 days prior to hospitalization. He received ruxolitinib for treatment of primary myelofibrosis for 4 years. His other medications included warfarin, omeprazole, furosemide, diltiazem, spironolactone, bisoprolol, and seretide evohaler for his pulmonary and heart diseases.
Ruxolitinib was initiated in November 2015 after the patient developed pancytopenia following hydroxyurea and allopurinol treatment. Total duration of ruxolitinib therapy was 48 months, and the most recent dose was 20 mg/day. He denied smoking and alcohol drinking. He reported no exposure to herbal drug use or animals, and he had no known tuberculosis contact.
Physical examination revealed a low-grade fever [temperature (T) 38.3 °C], blood pressure (BP) 117/64 mmHg, pulse 72/min, respiratory rate 24/min, oxygen saturation 85% at room air, and 98% with oxygen cannula 3 l per minute (LPM). He was alert, had mild pallor, and was tachypneic. Cardiovascular examination showed jugular vein distension with apical and parasternal heaving, loud P2, and irregular pulse. Fine crepitations were detected at both lower lung fields. Abdominal examination revealed mild splenomegaly. Ill-defined erythematous swelling of the left leg with mild tenderness, and multiple ulcers at his right foot with minimal pus discharge were noted. Neurological examination and other systems were unremarkable.
Complete blood count (CBC) revealed a white blood cell count (WBC) of 21,130 cells/μL (81% neutrophil, 9% band form, 5% metamyelocyte, and 2% promyelocyte), hemoglobin (Hb) level of 7.2 g/dL, platelet (PLT) count of 536,000 cells/μL, blood urea nitrogen (BUN) of 23.9 mg/dL, and serum creatinine (SCr) of 1.21 mg/dL. Liver function tests showed direct bilirubin (DBIL) of 0.66 mg/dL, total bilirubin (TBIL) of 0.45 mg/ dL, aspartate transaminase (AST) of 16 U/L, alanine transaminase (ALT) of 10 U/L, alkaline phosphatase (ALP) of 84 U/L, albumin (ALB) of 2.8 g/dL, and total protein of 5.4 g/dL. The urinalysis was unremarkable. Chest radiograph (CXR) showed bilateral interstitial infiltration with blunt costophrenic angles and increased cardiothoracic ratio. One of his 2 blood cultures grew round budding yeasts on the fourth day after blood collection, which were identified as C. neoformans (Fig. ). Serum cryptococcal antigen was positive at a titer of 1:2. Lumbar puncture was attempted; however, no cerebrospinal fluid was collected.
On the admission date, the patient was empirically treated with intravenous ceftazidime and azithromycin. Following the blood culture result, intravenous amphotericin B deoxycholate 50 mg/day (0.87 mg/kg/day) and oral fluconazole 800 mg/day were added. The patient was improved. Subsequently, the patient developed acute kidney injury (AKI) and the antifungal agent was changed to liposomal amphotericin B 180 mg (3 mg/kg/day). The patient received induction therapy with 28 days of intravenous amphotericin B plus fluconazole 800 mg/day, followed by oral fluconazole at the dose of 400 mg/day thereafter. However, ruxolitinib was still continued.
After 1 month of hospitalization and antifungal treatment, the patient developed new onset of fever and worsening of the lesion on his left leg. Intravenous vancomycin was initiated for empirical treatment of suspected nosocomial skin and soft tissue infection. Skin biopsy at the left leg lesion was performed. The tissue pathology showed suppurative granuloma involving dermis and subcutis that suggested mycobacterial skin and soft tissue infection, and Ziehl-Neelsen staining demonstrated numerous acid-fast bacilli (Fig. ). Tissue mycobacterial culture revealed positive organisms from acid-fast stain, and isolate identification by INNO-LiPA assay technique from liquid medium was compatible with M. haemophilum. The mycobacterium colony grew on chocolate plate agar after 42 days of incubation, but failed to grow on solid (Lowenstein-Jensen) medium.
The patient was treated with levofloxacin 750 mg/day, rifampicin 300 mg/day, and ethambutol 800 mg/day; however, the patient was not improved after 7 days of antimicrobial treatment. He then developed septic shock and expired on the 48th day of hospitalization.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [70, 'years'], 'creatinine': [1.21, 'mg/dL'], 'sex': 'Male'}",64.41194,61.19134,67.63254,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 70 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.21 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.21/0.9)**-1.2 * 0.9938**70 * 1.0 = 64.41194.
Hence, the GFR value is 64.41194 ml/min/1.73 m²."
433,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8111443-1,Extracted,"A 58-year-old male with clinical history of autosomal dominant polycystic kidney disease who previously underwent left total nephrectomy (in 2003) and renal transplantation (in 2003, 18 years prior to presentation) presents to the emergency department with acute onset right abdominal pain that gradually worsened over the span of 5 days. On arrival, the patient was afebrile and vital signs were stable. Physical examination revealed tenderness to deep palpation in the right lower quadrant and right flank.
Initial laboratory workup was as follow: White Blood Cell Count 16.1 × 109/L, Hemoglobin 16.9 g/dL, Hematocrit 49.7%, Platelet 454 109/L, Red Blood Cell Count 6.22 million/mm3, International Normalized Ratio (INR) 1.2, serum sodium 134 mEq/L, serum potassium 3.7 mEq/L, serum chloride 104 mEq/L, serum creatinine 1.04 mg/dL, blood urea nitrogen 15 mg/dL, and serum Lactate 0.9 mmol/L. Urine analysis was clean, reported as negative for glucose, bilirubin, ketones, blood, leukocytes, and protein, occasional bacteria, pH of 6.0 and specific gravity of 1.008. Urine Culture was reported no growth for 5 days.
CT abdomen and pelvis with intravenous contrast was performed. A wide-neck right lower quadrant incisional hernia was noted, with stranding and inflammation within the hernial sac ( and ). A distended tubular structure with mucosal enhancement was identified in the hernial sac, which was arising from the cecum. Based on imaging findings differential diagnoses included appendicitis, incarcerated hernia, or colonic diverticulitis. No intraperitoneal free air or pneumatosis was present. On comparison with prior CT abdomen and pelvis (6 months prior to presentation), a normal vermiform appendix was noted protruding into the incisional hernial sac (), making appendicitis as the leading differential for patients’ presentation.
Of note, other specific differential diagnosis to be considered in patients with renal transplantation include: perioperative acute tubular necrosis, renal allograft compartment syndrome, renal allograft torsion, acute or chronic renal transplant rejection, renal artery stenosis, renal vein thrombosis, arteriovenous fistula, perinephric fluid collection from infection or hematoma, renal artery pseudoaneurysm, urinary obstruction, graft pyelonephritis, opportunistic or community-acquired infection and donor-related malignancy .
Subsequently, exploratory laparotomy was performed which revealed a perforated appendicitis within the incisional hernial sac, confirming the diagnosis. Pathology reported as acute transmural appendicitis with perforation and ischemic changes. Viable proximal and distal mucosal margins and uninvolved by inflammatory process. Following surgery, the patient made an uneventful recovery.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [58, 'years'], 'creatinine': [1.04, 'mg/dL']}",83.23019,79.06868,87.3917,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 58 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.04 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.04/0.9)**-1.2 * 0.9938**58 * 1.0 = 83.23019.
Hence, the GFR value is 83.23019 ml/min/1.73 m²."
434,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-2298,Extracted,"A 58-year-old female comes to the physician because of generalized fatigue and malaise for 3 months. Four months ago, she was treated for a urinary tract infection with trimethoprim-sulfamethoxazole. She has hypertension, asthma, chronic lower back pain, and chronic headaches. Current medications include hydrochlorothiazide, an albuterol inhaler, naproxen, and an aspirin-caffeine combination. Examination shows conjunctival pallor. Laboratory studies show:
Hemoglobin 8.9 g/dL
Serum
Urea nitrogen 46 mg/dL
Creatinine 2.4 mg/dL
Calcium 9.8 mg/dL
Urine
Protein 1+
Blood 1+
RBCs none
WBCs 9-10/hpf
Urine cultures are negative. Ultrasound shows shrunken kidneys with irregular contours and papillary calcifications.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [58, 'years'], 'creatinine': [2.4, 'mg/dL'], 'sex': 'Female'}",22.83887,21.69693,23.98081,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 58 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.4 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.4/0.7)**-1.2 * 0.9938**58 * 1.012 = 22.83887.
Hence, the GFR value is 22.83887 ml/min/1.73 m²."
435,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-3434,Extracted,"A 48-year-old woman comes to the physician for the evaluation of 24-hour blood pressure monitoring results. Over the last 3 months, she has had intermittent nausea, decreased appetite, and increasing weakness and fatigue during the day. She has been treated twice for kidney stones within the past year. Her current medications include lisinopril, amlodipine, and furosemide. She is 178 cm (5 ft 10 in) tall and weighs 97 kg (214 lb); BMI is 31 kg/m2. Her blood pressure is 152/98 mm Hg. Physical examination shows no abnormalities. Serum studies show:
Na+ 141 mEq/L
Cl− 101 mEq/L
K+ 4.5 mEq/L
HCO3− 24 mEq/L
Calcium 12.9 mg/dL
Creatinine 1.0 mg/dL
Twenty-four-hour blood pressure monitoring indicates elevated nocturnal blood pressure.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [48, 'years'], 'creatinine': [1.0, 'mg/dL'], 'sex': 'Female'}",69.49253,66.0179,72.96716,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 48 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.0/0.7)**-1.2 * 0.9938**48 * 1.012 = 69.49253.
Hence, the GFR value is 69.49253 ml/min/1.73 m²."
436,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3594647-1,Extracted,"The first patient was a 60-year-old man presenting with an asymptomatic, 6.0 cm expanding infrarenal AAA (). He underwent a renal transplantation 21 years prior to his current presentation due to renal failure secondary to diabetes and hypertension. The renal artery of the transplanted kidney arose from the right internal iliac artery. His renal function was marginal due to chronic rejection with creatinine and blood urea nitrogen (BUN) values of around 4.0 mg/dL and 50 mg/dL, respectively. His AAA was repaired with a Zenith (Cook Medical Inc., Bloomington, IN, USA) bifurcated stent graft. A 30 mm × 117 mm Zenith main body device was placed through the left common femoral artery with ""preclose technique"" using 7F Proglide (Abbott Vascular, Redwood City, CA, USA). An 18 mm × 71 mm limb extender was used as the ipsilateral extension. A 24 mm × 71 mm was used as contralateral extension. A type Ib endoleak arising from the right iliac artery was noted on the completion angiogram (). Another 24 mm × 54 mm limb extender was placed to overcome this type Ib endoleak. There was no endoleak with final angiogram (). There was no change in renal perfusion after EVAR according to the completion angiogram. A total of 30 mL of Visipaque (iodixanol) was used for this patient. The total fluoroscopic time was 90 minutes. The patient's renal function was slightly decreased after EVAR (creatinine and BUN of 4.1-4.4 mg/dL and 53-58 mg/dL, respectively). The hemodialysis was not needed after EVAR. The aggravation of chronic rejection led to hemodialysis 4 months after EVAR. Over the following 12 months, no types of endoleak were detected as evaluated by serial colorized duplex scan.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [60, 'years'], 'creatinine': [4.0, 'mg/dL'], 'sex': 'Male'}",16.32476,15.50852,17.141,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 60 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 4.0 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (4.0/0.9)**-1.2 * 0.9938**60 * 1.0 = 16.32476.
Hence, the GFR value is 16.32476 ml/min/1.73 m²."
437,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-8996,Extracted,"A 49-year-old woman presents to the family medicine clinic with concerns about her weight. She has been constantly gaining weight for a decade now as she has not been able to control her diet. She has tried exercising but says that she is too lazy for this method of weight loss to work. Her temperature is 37° C (98.6° F), respirations are 15/min, pulse is 67/min, and blood pressure is 122/88 mm Hg. Her BMI is 30. Her labs from her past visit show:
Fasting blood glucose: 149 mg/dL
Glycated hemoglobin (HbA1c): 9.1%
Triglycerides: 175 mg/dL
LDL-Cholesterol: 102 mg/dL
HDL-Cholesterol: 35 mg/dL
Total Cholesterol: 180 mg/dL
Serum creatinine: 1.0 mg/dL
BUN: 12 mg/dL
Serum:  
  Albumin: 4.2 gm/dL
  Alkaline phosphatase: 150 U/L
  Alanine aminotransferase:      76 U/L
  Aspartate aminotransferase: 88 U/L
After discussing the long term issues that will arise if her health does not improve, she agrees to modify her lifestyle and diet.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [49, 'years'], 'creatinine': [1.0, 'mg/dL'], 'sex': 'Female'}",69.06168,65.6086,72.51476,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 49 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.0/0.7)**-1.2 * 0.9938**49 * 1.012 = 69.06168.
Hence, the GFR value is 69.06168 ml/min/1.73 m²."
438,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5642814-1,Extracted,"A 71-year-old Chinese woman presented to the emergency department (ED) with a generalized body rash of one-day duration. The rash started one day after the patient reinitiated allopurinol treatment for the spontaneous onset of bilateral ankle pain associated with redness and swelling. The patient reported two days of intermittent fever ranging from 100.4 °F to 101.4 °F. She denied the history of recent travel, tick bite, pain in other joints, and myalgias. Past medical history included hypertension, dyslipidemia, diabetes mellitus, and recently diagnosed gout. She was recently diagnosed with gout and allopurinol therapy was initially started four weeks prior to her current presentation.
The patient revealed that she was hospitalized with a similar rash, high-grade fever, and upper abdominal pain two weeks previously. The patient took allopurinol for one week and stopped it after her ankle pain resolved. Physical examination revealed right upper quadrant tenderness, and palpation elicited Murphy's sign (associated with acute cholecystitis). Skin examination revealed a petechial, non-blanching rash on all extremities. A poorly defined, diffuse, and nonscaling erythematous maculopapular rash covered the trunk. The vital signs were—heart rate: 135 beats/min, respiratory rate: 25/min, and temperature: 102.9 °F. In the ED, she developed hypotension of 90/60 mmHg.
A computed tomography (CT) scan of the abdomen demonstrated nonspecific pericholecystic fluid and periportal edema. Abdominal ultrasonography revealed a thickened gallbladder wall measuring 7 mm and the presence of pericholecystic fluid. There were no visible stones. No intra or extrahepatic bile duct dilatation was noted. The proximal common bile duct (CBD) measured 3.5 mm. The initial laboratory evaluation revealed white cell count (WBC): 2.3 x 103/µL (4-11 x 103/µL), platelet count: 158 x 103/µL (150-450 x 103/µL), lactate: 3.9 mEq/L (0.5-1.3 mEq/L), blood urea nitrogen (BUN): 12 mg/dL (10-26 mg/dl), creatinine: 1.4 mg/dL (0.6-1.3 mg/dL), total bilirubin: 2.2 mg/dL (0.2-1 mg/dl), direct bilirubin: 0.7 mg/dL (0 to 0.3 mg/dL), aspartate aminotransferase (AST): 71 IU/L (7-40 IU/L), alanine aminotransferase (ALT): 56 IU/L (0-40 IU/L), alkaline phosphatase (ALP): 100 IU/L (70-230 IU/L) , and serum lipase: 45 IU/L (0-140 IU/L). Therein, the patient was diagnosed with acute AC.
Intravenous (IV) vancomycin (1500 mg), cefepime (2 gm), and methylprednisolone (60 mg) were administered in addition to aggressive fluid resuscitation. Percutaneous cholecystostomy and drain placement were accomplished without complications. Blood and urine cultures were persistently negative. Resolution of the rash occurred on Day 3 of hospitalization and, subsequently, the corticosteroid therapy was discontinued. On the fourth hospital day, laboratory data included WBC: 12.9 x 103/uL, platelets: 52 x 103/uL, total bilirubin: 2.4 mg/dL, direct bilirubin: 1.5 mg/dL, lactate: 1.3 mEq/L, and creatinine: 0.8 mg/dL. On the fourth, fifth, and sixth hospital days, eosinophil percentages were 17%, 14.2%, and 9.5%, respectively. The European Registry of Severe Cutaneous Adverse Reactions (RegiSCAR) score was four, suggesting the possibility of the drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome. Antimicrobial therapy was changed to IV ceftriaxone and IV metronidazole on the fourth day. The patient showed significant improvement in the rash and started tolerating oral feeding. She was discharged from the hospital on Day 8. At the time of discharge, the etiology of acute AC had not been determined with certainty. Allopurinol was not discontinued at the time of discharge.
Five days after hospital discharge, the patient developed left-sided ankle pain and again took one dose of 300 mg allopurinol. Within 24 hours, a diffuse erythematous rash all over her body recurred, and she returned to the emergency department. Examination revealed temperature: 103.7 °F, heart rate: 117 beats/minute, respiratory rate: 20/minute, and blood pressure: 161/61 mmHg. A morbilliform rash was present over the pubic symphysis. A petechial rash was noted on both legs (Figure ) as well as on the upper extremities (Figure ).
The oral mucosa was uninvolved. The left ankle was warm and tender to touch and a mild effusion was present. Laboratory data included WBC: 9.4 x 103 /uL (4-11x103/μL), eosinophil: 31% (1%-3%), neutrophils: 72.5% (57-67%), C-reactive protein: (CRP) 9.100 mg/dL (1-3 mg/dL), erythrocyte sedimentation rate (ESR): 90 mm/hr (0-20mm/hr), lipase: 170 U/L (0-140 U/L), B-type natriuretic peptide (BNP): 177 pg/mL (0-100pg/mL), and uric acid: 5.9 mg/dL (2.1-6.3 mg/dl). Radiographic imaging of the chest, abdomen, and pelvis did not reveal any abnormalities. The diagnosis of ""possible"" DRESS syndrome due to allopurinol hypersensitivity was made on a RegiSCAR score of three. Intravenous methylprednisolone (40 mg) was administered twice daily for six to seven days. Significant resolution of the rash occurred during treatment. The upper left arm was almost cleared of the rash (Figure ). Residual post-inflammatory changes were noted on both legs (Figure ). Corticosteroid therapy was discontinued. The patient was educated about her allergy to allopurinol and about not taking this medication in the future.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [71, 'years'], 'creatinine': [1.4, 'mg/dL'], 'sex': 'Female'}",40.22178,38.21069,42.23287,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 71 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.4 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.4/0.7)**-1.2 * 0.9938**71 * 1.012 = 40.22178.
Hence, the GFR value is 40.22178 ml/min/1.73 m²."
439,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4294446-1,Extracted,"A 56-year-old previously healthy Caucasian female presented with edema, hypertension, and rapidly progressive renal failure. Three months prior to presentation, the patient's serum creatinine was 1.9 mg/dl. At the time of admission, her creatinine was 8 mg/dl. Urinalysis showed protein (2+), red blood cells (2+), and her 24-hour urine protein was 11.6 grams. In addition to having a normocytic normochromic anemia, her serum IgG was 372 mg/dl (694–1,618), free kappa light chain (LC) was 339.0 mg/dl (0.33–1.94), free lambda LC was 5.91 mg/dl (0.57–2.63), and the kappa/lambda ratio was 57.36 (0.26–1.65). Serum IgA, IgM, C3, and C4 were normal. Urine immunofixation showed kappa 275 mg/dl (0.14–2.42), lambda 5.93 mg/dl (0.02–0.67), and 24-hour urine kappa light chain excretion of 4.3 grams. ANA, antineutrophil cytoplasmic antibody, anti-GBM, cryoglobulin, hepatitis B surface antigen and HIV were all negative. Notably, her hepatitis C virus (HCV) antibody was positive, but HCV was undetectable by PCR. Renal ultrasound showed normal sized kidneys with moderately increased bilateral renal echogenicity. A bone survey showed no lytic lesions. Bone marrow biopsy revealed an abnormal kappa positive plasma cell population (CD138-positive) representing 5% or less of the cellularity (fig. ). Flow cytometry confirmed an abnormal CD56+ plasma cell population with an elevated kappa/lambda ratio of 6.2, suggestive of a plasma cell neoplasm.
On the kidney biopsy, 37 glomeruli were present, 7 of which were obsolescent. Ten glomeruli had cellular to fibrocellular crescents (fig. ), with focal fibrinoid necrosis (fig. ). Most glomeruli exhibited global proliferation, with mesangial and endocapillary hypercellularity as well as lobular accentuation. Double contour formation of the glomerular basement membrane was frequently seen (fig. ). Congo red staining for amyloid was negative.
Direct immunofluorescence staining showed 4+ smudgy to coarse granular mesangial, segmental linear glomerular capillary wall (fig. ), as well as diffuse linear tubular basement membrane, and arterial wall staining for IgG (fig. ). IgG subclass staining demonstrated 2–3+ deposition in these locations only for IgG2 (fig. ), with faint staining of mesangial nodules for IgG4. Both IgG1 and IgG3 staining were negative. Staining for light chains was negative for lambda, with trace to 1+ for kappa in expanded mesangial regions and scant staining of basement membranes (fig. ). Staining for C3 was 3+ in the glomerular mesangium, segmental glomerular capillary walls, and focal artery and arteriole walls. Tubular casts stained 2–3+ for IgA, kappa, and lambda.
Electron microscopy revealed significant effacement of podocyte foot processes. The mesangial regions were moderately expanded by matrix and contained finely granular electron dense material (fig. ) with vague fibrils in a few segments (fig. ). A band of finely granular electron dense material was present along some glomerular basement membranes and in rare tubular basement membranes (fig. ).
The pathological findings in this case were consistent with IgG2 heavy chain monoclonal immunoglobulin deposition disease. In two previous studies [, ], the following criteria were used for the diagnosis of HCDD: staining for a single class of Ig (γ, α, µ) on glomerular and/or tubular basement membranes, negative or minimal staining for light chain (κ or λ), and typical finely granular basement membrane-dominant electron dense deposits. Although Aucouturier et al. [] suggested the hallmark of HCDD is CH1 deletion of γ-heavy chains, staining for CH1 is not necessarily required for a diagnosis []. The present case meets the criteria for γ2-HCDD, making it the fifth case reported in the literature to our knowledge. Light microscopy demonstrated a general pattern consistent with MPGN; however, the presence of crescents and fibrin are unusual for many conditions that result in an MPGN pattern. The differential diagnosis was broad, encompassing diseases that produce an MPGN pattern and/or crescentic disease, including: MPGN type 1, C3 glomerulopathy, proliferative glomerulonephritis with monoclonal immunoglobulin deposits, fibrillary glomerulopathy, and autoimmune diseases. Given the proliferative pattern, antineutrophil cytoplasmic antibody-associated small vessel vasculitis and anti-GBM glomerulonephritis were less likely. Immunofluorescence demonstrated an immune complex-associated process related to the deposition of IgG2 molecules that did not appear to be associated with significant light chain deposits. The Congo red staining was negative. While some areas of expanded mesangium contained vague fibrillar structures, they were not typical of amyloid, were slightly thinner than expected for fibrillary glomerulopathy, and lacked classic features for cryoglobulin. The lack of significant associated kappa light chain deposits in the present case was surprising, given the large quantity in serum and urine.
The patient's renal function did not improve despite pulsed steroids, followed by prednisone and oral cyclophosphamide, and therefore, hemodialysis was started. Three months into treatment, her serum kappa/lambda ratio decreased dramatically to 2.2; however, the patient remains dialysis-dependent. Recently, her treatment regimen has been changed to weekly bortezomib, cyclophosphamide and dexamethasone.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [56, 'years'], 'creatinine': [8.0, 'mg/dL']}",5.45283,5.18019,5.72547,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 56 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 8.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (8.0/0.7)**-1.2 * 0.9938**56 * 1.012 = 5.45283.
Hence, the GFR value is 5.45283 ml/min/1.73 m²."
440,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7509571-1,Extracted,"A 56-year-old man presented to the emergency department with bleeding (>700 cc) around his colostomy site persisting for two days. The patient denied any pain with the bleeding, fever, chills, sweats, weakness, abdominal pain, nausea, vomiting, or diarrhea. The patient denied any history of smoking, alcohol, or any other substance abuse. The patient's surgical history included a remote colectomy with permanent colostomy for stage IV colon cancer and a subsequent colostomy revision and hernia repair (8 and 6 years, respectively, before this episode), after experiencing a massive bleed from a parastomal varices. The patient has a medical history of hypertension, hyperlipidemia, diabetes, hypothyroidism, colon cancer, obstructive sleep apnea, and obesity.
The patient's current medications upon presentation in the emergency department included pioglitazone, ipratropium bromide, insulin glargine, montelukast, levocetirizine, atorvastatin, azelastine, bisoprolol, levothyroxine, lisinopril, metformin, triamcinolone, and aspirin. The patient's blood pressure was 128/84 mmHg. The patient's white blood cell count was 3,970 cells/µL, platelet count was 119,000/µL, and red blood cell count was low at 4.080 million cells/uL. His hemoglobin and hematocrit levels were 13.7 g/dL and 39.2%, respectively. His sodium was below normal, and he was hypochloremic (135 mmol/L and 95 mmol/L, respectively), glucose was elevated at 313 mg/dL, and creatine was normal at 0.8 mg/dL. His liver function was normal, aside from slightly elevated alanine transaminase of 64 international units/L.
Given the recurrent bleeding over several days, surgery was consulted to evaluate the bleeding. No further bleeding was elicited, and the patient was discharged. However, the patient returned to the emergency department the next day reporting 50 cc of dark red blood while emptying his colostomy bag. Vascular surgery and gastroenterology were consulted. A right upper quadrant ultrasound demonstrated a gallstone, no pericholecystic fluid or wall thickening, and common bile duct diameter of 6 mm without intrahepatic biliary ductal dilatation. The liver measured 20 cm in length with the portal vein slightly dilated at 1.1 cm. Furthermore, the portal vein showed hepatopedal blood flow with a velocity of 14.6 cm/s. The liver echotexture was also hyperechogenic suggesting mild hepatic steatosis. Visualization of the pancreas was normal.
The colonoscopy performed through the stoma was without abnormality. EGD showed a normal esophagus without any esophageal varices and a normal duodenum; however, mild portal hypertensive gastropathy was found diffusely in the entire stomach. A CT scan of the abdomen showed the main portal vein to be slightly dilated measuring 14 mm. The superior mesenteric vein was also dilated measuring 15 mm. Mesenteric veins extending into the parastomal hernia were also dilated. As shown in , the CT scan demonstrated a parastomal hernia with accompanying dilated parastomal varices. Given the lack of further bleeding, the patient was released and given instructions on how to reduce the risk of further bleeding from the parastomal varices. The patient subsequently had another episode of massive bleeding (>700 cc) occurring two years after the incident described herein, which resolved sponstaneously after the patient aggressively debrided the vascular erosion and applied manual compression. No rebleeding has occurred in the year since the last incident.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [56, 'years'], 'creatinine': [0.8, 'mg/dL'], 'sex': 'Male'}",96.27607,91.46227,101.08987,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 56 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.8 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.8/0.7)**-0.302 * 0.9938**56 * 1.0 = 96.27607.
Hence, the GFR value is 96.27607 ml/min/1.73 m²."
441,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5325746-1,Extracted,"A 51-year-old female presented to the emergency department after several episodes of hematemesis and severe epigastric pain. She had a past medical history of pulmonary sarcoidosis, ADPKD requiring bilateral nephrectomy and left kidney transplant, and is currently on immunosuppressive therapy. On admission, her vitals were stable. Her hemoglobin was 9.8 g/dl. Her total bilirubin was 0.2 mg/dl, alkaline phosphates 74 U/L, aspartate aminotransferase 24 U/L, alanine aminotransferase 20 U/L, blood urea nitrogen 49 mg/dl, and creatinine 1.07 mg/dl. Electrolytes were normal. She underwent emergent esophagogastroduodenoscopy (EGD), which showed grade 3 esophageal varices and four of them were banded. Octreotide and pantoprazole drip were administered. A computed tomography (CT) scan of the abdomen showed ascites with polycystic liver, nodular contour, and several sites of calcifications (most likely calcified granulomas) (Figure ). An abdominal ultrasound showed a heterogeneous liver with mild contour and patent portal circulation. A previous magnetic resonance imaging (MRI) of the pelvis, which was done two years ago, showed similar small cysts in the parenchyma; however, the calcifications and nodularity of the liver were new. Diagnostic paracentesis revealed serum to ascitic albumin gradient (SAAG) of 1.9 consistent with portal hypertension. The patient was started on non-selective beta blocker for stabilization of varices. Ceftriaxone was given for prophylaxis for spontaneous bacterial peritonitis. The patient’s bleeding was controlled, and the hemoglobin level was stable during the hospital stay. She refused further workup including liver biopsy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [51, 'years'], 'creatinine': [1.07, 'mg/dL']}",62.88898,59.74453,66.03343,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 51 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.07 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.07/0.7)**-1.2 * 0.9938**51 * 1.012 = 62.88898.
Hence, the GFR value is 62.88898 ml/min/1.73 m²."
442,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3118316-1,Extracted,"The patient is a 77 year old male with a history of prostate cancer for which he was treated with brachytherapy (radiation seeds) 10 years ago. Patient had also a transurethral resection of prostate due to urinary obstruction complicated by multiple tract infections one year prior to his current presentation. At present, patient was admitted for decreased urinary output. Laboratory work up revealed a creatinin level of 10 mg/dl, with metabolic acidosis, thought to be secondary to acute kidney injury. Computer tomography imaging studies showed bilateral hydronephrosis grade 2, with obstruction of the ureters at the uretero-vesicle junction for which percutaneous nephrostomy tubes were placed. A cystourethrogram was also performed and revealed colo-urethral fistula in the region of the prostatic urethra, extending to the rectum. The bladder lumen was irregular and small, corresponding to thickened bladder wall seen on CT. Patient was taken to surgery for cystprostatectomy, ileal conduit and repair of the recto- urethral fistula.
The cystprostatectomy specimen was composed of a portion of prostate (4.2 × 2.7 × 2.5 cm), urinary bladder (7.5 × 5 cm) and the surrounding fat. The entire prostatic gland was replaced by a white firm irregular tumor mass. The bladder mucosa was very congested, diffusely irregular but no mucosal growths or luminal masses were present. The thickness of the bladder wall ranged from 0.5 to 1.0 cm.
Microscopic sections from the prostate showed an infiltrating tumor mass forming nests and cords (Figure ). No benign prostatic glands were identified. Cytologically, the cells were large, cohesive, with abundant glassy eosinophilic cytoplasm and well defined cell borders. Keratinization was noted (Figure ). The tumor showed focal necrosis (Figure ). Areas with less differentiated cells with high grade nuclei infiltrating singly into the stroma were identified (Figure ). The morphological appearance was compatible with poorly differentiated squamous cell carcinoma. No other differentiation (adenocarcinoma or urothelial carcinoma) was seen. The tumor replaced the entire prostate, extending into seminal vesicles, periprostatic and perivesicle soft tissue (Figure ). Lymphovascular (Figure ) and perineural (Figure ) invasion were present. There were also areas of necrosis with calcifications consistent with therapy effect (Figure ). Sections from the urinary bladder wall revealed inflamed and mainly denuded transitional mucosa with underlying granulation tissue. Where present, the urothelium was hyperplastic with focal frond-like proliferation. Although, cytologically, the urothelial cells were slightly enlarged, the nuclear to cytoplasmic ratio was maintained and the nuclear polarity was preserved (Figure ). This degree of atypia was less than that of the tumor cells and was considered to represent reactive changes, secondary to the inflammatory process. No areas of high grade urothelial carcinoma were identified. The lamina propria and detrusor muscle of the bladder were infiltrated by the squamous cell carcinoma (Figure ) that also extended, focally, into the urothelial mucosa (Figure ). Immunohistochemistry studies, using a battery of prostate specific antibodies, showed viable neoplastic cells staining positive for racemace/AMACR (Figure ) and negative for Prostate specific antigen (PSA), Prostate specific membrane antigen (PSMA), Prostate specific acid phosphatase (PSAP) and P501S (553-amino acid protein that is localized to the Golgi complex and expressed in both benign and neoplastic prostate tissues). Interestingly, AMACR also stained the endothelial cells in the vessels adjacent to the tumor (Figure ).
A final diagnosis of squamous cell carcinoma involving the prostate and urinary bladder was rendered. The question that arose was whether the squamous carcinoma developed through divergent differentiation from prostatic adenocarcinoma following treatment, represented squamous differentiation of an urothelial carcinoma, or it was the second primary prostatic malignancy in this patient.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [77, 'years'], 'creatinine': [10.0, 'mg/dL'], 'sex': 'Male'}",4.89105,4.6465,5.1356,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 77 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 10.0 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (10.0/0.9)**-1.2 * 0.9938**77 * 1.0 = 4.89105.
Hence, the GFR value is 4.89105 ml/min/1.73 m²."
443,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3852275-1,Extracted,"A 58-year-old female, from Chhattisgarh, Central India, presented with a persistent discharging sinus from the right gluteal region for two years. She had previously received an intramuscular injection in the right gluteal region at another centre for fever and back pain. Subsequently she developed multiple abscesses over the right gluteal region that required incision and drainage on two occasions. She had been treated presumptively for tuberculosis with a 6-month course of antituberculous drugs (two months of Isoniazid, Rifampicin, Pyrazinamide, and Ethambutol followed by four months of Isoniazid and Rifampicin) with no apparent clinical improvement.
On examination, there was a subcutaneous, nontender, indurated swelling in the right gluteal region with a single sinus opening with serous and nonfoul smelling pus discharge. Systemic examination was normal. Her laboratory values were hemoglobin 11.6 g%, white cell count 7000/mm3, platelets—2,50,000/mm3, fasting blood sugar 90 mg%, postprandial blood sugar 130 mg%, serum Creatinine 1.0 mg%, chest X-ray normal, and erythrocyte sedimentation rate of 15 mm at one hour.
A provisional diagnosis of a soft tissue infection due to atypical mycobacteria was made. The sinus tract was excised and a portion of the specimen was sent for histopathological as well as mycological examinations. Haematoxylin and eosin stained sections revealed inflammatory granulation tissue and foreign body granulomas with necrosis in the sinus tract. Two days postoperatively a blackish discoloration of the edge of the surgical wound was noted and was debrided. A calcofluor white preparation of the debrided tissue revealed broad, irregular, and aseptate hyphae. Culture on Sabouraud's dextrose agar showed a creamy white, waxy, and glabrous colony with many radial folds. On performing lactophenol cotton blue wet mount of the fungus, aseptate hyphae, and numerous globose, smooth walled zygospores with characteristic conjugation beaks were observed (). The fungus was identified as Basidiobolus ranarum. There was an excellent response to oral potassium iodide in our patient with complete resolution in six months ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [58, 'years'], 'creatinine': [1.0, 'mg/dL']}",65.30224,62.03713,68.56735,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 58 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.0/0.7)**-1.2 * 0.9938**58 * 1.012 = 65.30224.
Hence, the GFR value is 65.30224 ml/min/1.73 m²."
444,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7481148-2,Extracted,"A 43-year-old man was diagnosed with familial ADPKD at the age of 34. His kidneys were bigger than normal and contained numerous cysts; he had no liver cysts and normal laboratory tests with slightly high Cr (1.1 mg/dL). Disease symptoms were controlled for 5 years with enalapril, amlodipine, and allopurinol. In December 2018, infinite bleeding renal cysts were detected, and Cr was 1.55 mg/dL. Due to the ADPKD rapid progression, tolvaptan was initiated on 4 May 2019 at the regular dose, 45-0-15. After 17 doses of treatment, blood tests revealed a 5–6 fold increase of CK (from 154 to 854 UI/mL) and a moderate increase in LDH (364 UI/L). Cr did not increase during this time, and the patient did not have symptoms. Tolvaptan was stopped, while other treatments continued, and CK and LDH (307UI/L) gradually recovered after 6 weeks.
Both patients suffered a dramatic CK elevation after receiving tolvaptan and neither showed symptoms. They had no history of CK elevation and reported not having taken any other drug, phytotherapy, or special diet and not having performed extreme exercise that could justify CK elevation []. The LDH increase was minor; however, it is usually high in ADPKD due to cyst breakage. In the absence of any other justification for CK elevation and since CK decreased after tolvaptan discontinuation, it is probable that tolvaptan caused CK elevation in both cases [] (Fig. ).
These are the first cases of tolvaptan-induced CK elevation reported. It is well-known that tolvaptan causes hepatotoxicity in ADPKD patients [] but not in other patients []. Since CK elevation is caused by muscle damage [], we hypothesize that tolvaptan might damage ADPKD patients’ myocytes and hepatocytes by the same mechanism, probably related with intracellular cAMP reduction. Since CK elevation might be underestimated in ADPKD patients receiving tolvaptan, we suggest that CK should be monitored in these patients.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [43, 'years'], 'creatinine': [1.55, 'mg/dL'], 'sex': 'Male'}",56.60281,53.77267,59.43295,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 43 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.55 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.55/0.9)**-1.2 * 0.9938**43 * 1.0 = 56.60281.
Hence, the GFR value is 56.60281 ml/min/1.73 m²."
445,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4976193-1,Extracted,"A 56-year-old woman was referred to a High Specialized Medical Unit with a diagnosis of persistent primary hyperparathyroidism and multiple pathologic fractures.
The patient had no familial history of bone disease or any other chronic-degenerative disease. She had no diabetes, hypertension, or other pathological antecedents. There was no tobacco or alcohol consumption. She presented 3 years earlier with nephrolithiasis and hip fracture due to a fall from her own height that conditioned prostration and limitation of daily living activities. In her local hospital, she fulfilled biochemical criteria for PHPT. No localization studies were performed. She underwent parathyroidectomy with resection of left superior parathyroid and biopsy of left inferior parathyroid; final histopathology reported hyperplasia (the slides of the first histology could not be revised). The surgery was made in another state with surgeons and pathologists inexperienced in parathyroid surgery. The patient persisted with hypercalcemia and elevated levels of PTH during the first 6 months of clinical follow-up; thus, she was sent to our Medical Unit for additional evaluation.
During the first visit to our center, the patient was found with generalized bone pain. On the physical examination, she had normal vital signs including blood pressure 100/80 mmHg, heart rate 86 per minute, and body mass index (BMI) 19 kg/m2; she was bedridden and with multiple bone deformities and contractures due to pathologic fractures in thoracic and pelvic extremities.
Laboratory tests reported elevated levels of calcium (14 mg/dL; reference range: 8.4–10.2 mg/dL), low serum phosphorus (2.3 mg/dL; reference range: 2.7–4.5 mg/dL), normal levels of magnesium (2.2 mg/dL; reference range: 1.6–2.6 mg/dL), azotemia with elevated creatinine (2.4 mg/dL; reference range: 0.4–1.2 mg/dL) and urea (59 mg/dL; reference range: 10–50 mg/dL), elevation levels of Intact PTH (iPTH) (1648 pg/mL; reference range: 10–65 pg/mL), severe vitamin D deficiency (<5 ng/mL; sufficiency 30 ng/mL and deficiency < 10 mg/dL), and elevated levels in alkaline phosphatase (1580 UI/L, reference range: 40–129 UI/L) (). Gonadotropins, thyroid function test, cortisol, and IGF-1 levels were normal for the age of the patient. We corroborated biochemical persistence of PHPT.
Radiographically, chest and pelvis X-ray showed severe widespread cortical bone loss, cysts, brown tumors, and multiple pathological fractures because of severe cystic fibrous osteitis (Figures and ). No localization studies for parathyroid pathologies could not be performed due to the duration of the studies and the pain induced by the position required to perform them.
We initiated treatment with aggressive intravenous hydration with 0.9% sodium chloride solutions, loop diuretics, and intravenous calcitonin 48 hours before surgery. An experienced head and neck surgeon performed the second surgical bilateral neck exploration with radioguided minimally invasive parathyroidectomy using hand-held gamma probe, evidencing an ectopic adenoma approximately 4 cm in larger diameter ().
Postoperatively, the patient presented symptomatic hypocalcemia, with a nadir of 6.8 mg/dL and biochemical evidence of hungry bone syndrome, requiring treatment with intravenous calcium up to 2 mg/kg/min, intravenous magnesium, and oral calcitriol replacement. Despite intensive multidisciplinary approach, the patient had a torpid clinical evolution and died a month later from respiratory complications due to nosocomial pneumonia.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [56, 'years'], 'creatinine': [2.4, 'mg/dL'], 'sex': 'Female'}",23.12473,21.96849,24.28097,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 56 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.4 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.4/0.7)**-1.2 * 0.9938**56 * 1.012 = 23.12473.
Hence, the GFR value is 23.12473 ml/min/1.73 m²."
446,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5477882-2,Extracted,"A 53-year-old man was admitted to our hospital for evaluation of anaemia and generalized lymphadenopathy. He had been diagnosed with diabetes mellitus 5 years ago, which was well managed with glibenclamide. On admission, the serum creatinine level was 1.47 mg/dL, blood urea nitrogen was 19 mg/dL, haemoglobin was 9.5 g/dL, total serum protein was 12.9 g/dL, serum albumin was 1.7 g/dL and CRP was 13.7 mg/dL. Urine analysis showed microhaematuria and proteinuria of 2.6 g/24 h. Serum protein electrophoresis results showed a polyclonal gammopathy with an increased level of IgG of 8680 mg/dL. Serum IL-6 was markedly elevated to 62.2 pg/mL. Collagen vascular disease workup was negative. There was no evidence of diabetic retinopathy or neuropathy. Histological findings of the right inguinal enlarged lymph nodes were compatible with the plasma cell type of CD.
The renal biopsy showed 10 glomeruli, 3 of which exhibited global sclerosis. The remaining glomeruli showed diffuse mesangial stalk thickening and hyalinosis of both afferent and efferent arterioles. There was patchy infiltration of plasma cells and lymphocytes in the interstitium (Figure E). The immunofluorescence study showed no significant staining of glomeruli. Electron-dense deposits were absent. The biopsy findings were compatible with interstitial nephritis associated with plasma cell infiltration, superimposed on pre-existing early diabetic glomerulosclerosis.
He was treated with 8 mg/kg tocilizumab intravenously every 2 weeks without concomitant immunosuppression. Within 3 months of treatment, his anaemia, hypoalbuminaemia, inflammation and polyclonal gammopathy were all improved. Furthermore, serum creatinine and proteinuria decreased to 1.12 mg/dL and 0.4 g/24 h, respectively (Figure ). He has been free of symptoms with stabilized renal function for 1 year while maintained on tocilizumab treatment.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [53, 'years'], 'creatinine': [1.47, 'mg/dL'], 'sex': 'Male'}",56.682,53.8479,59.5161,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 53 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.47 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.47/0.9)**-1.2 * 0.9938**53 * 1.0 = 56.682.
Hence, the GFR value is 56.682 ml/min/1.73 m²."
447,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4168289-2,Extracted,"A 38-year-old African man, with no cardiovascular or renal disease and a medical history with repeated emission of rust urine after intense drumming on a bongo-djembè, was admitted to the emergency department with nausea, flank pain and rust urine emission.
Two days before, the patient had played in a prolonged hand-drumming session (the same musical event previously described) maintaining poor hydration with a karkade-based infusion imported from Senegal.
At presentation, the blood chemistries were notable for creatinine 1043 μmol/L, urea 65 mmol/L with no abnormalities in the dipstick urine specimen, haemoglobin 8.5 mmol/L, platelet count 157 000/mm3, leucocytes 4920/ mm3, uric acid 0.59 mmol/L, calcium 2.1 mmol/L, phosphorus 2 mmol/l and cholesterolaemia 5.43 mmol/L.
Further investigations revealed 24-h proteinuria of 0.3 g and hepatitis serology positive for HBV infection with no anti-HBs antibodies.
Serology for rhabdomyolysis, vasculitis and connectivitis, complementaemia and immunoglobulin dosing were all in the normal range.
Blood samples were negative for the presence of substances derived from drug consumption, and biochemical analysis in the karkade beverage did not reveal any nephrotoxic contaminants/herbs. Renal ultrasound and chest X-ray were unremarkable.
The patient first underwent renal replacement therapy with haemodialysis in an emergency setting and was subsequently rehydrated.
As a result, a polyuria phase lasting 2–3 days preceded a rapid renal function improvement, and control chemistries performed 1 month later confirmed the complete normalization of serum creatinine (88 μmol/L).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [38, 'years'], 'creatinine': [1043.0, 'µmol/L'], 'sex': 'Male'}",5.1295,4.87303,5.38598,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 38 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1043.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 1043.0 µmol. To convert 1043.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 1043.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00104 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00104 mol Serum Creatinine * 113.12 g/mol = 0.11764 g Serum Creatinine. To convert 0.11764 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.11764 g Serum Creatinine * 1000.0 mg/g = 117.64 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 117.64 mg Serum Creatinine/10.0 dL = 11.764 mg Serum Creatinine/dL. The concentration value of 1043.0 µmol Serum Creatinine/L converts to 11.764 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (11.764/0.9)**-1.2 * 0.9938**38 * 1.0 = 5.1295.
Hence, the GFR value is 5.1295 ml/min/1.73 m²."
448,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4317725-1,Extracted,"A 50-year-old Caucasian male with a history of alcohol and injection-drug abuse, chronic HCV infection, coronary heart disease, and idiopathic renal function impairment (creatinine clearance < 60 mL/min) for preceding four months attended in the emergency department with uremic symptomatology. He was dysphonic (O2 saturation, 85%) and hypertensive (blood pressure, 185/90 mmHg) and had prominent hepatosplenomegaly with mild peripheral edema; he had no palpable lymph nodes, skin rash, or other manifestations of systemic diseases. Laboratory analyses results were as follows: metabolic acidosis (pH, 7.123; and HCO3-, 8.6 mmol/L); mild hyperkalemia (K+, 5.7 mmol/L); hyperphosphatemia (PO43-, 10 mg/dL); hypoalbuminemia (albumin, 2.8g/L); anemia (hematocrit, 21.2%; and hemoglobin, 6.8 g/dL); thrombocytopenia (platelet, 72 × 10³/μL); lactate dehydrogenase,185 U/L; and severe renal failure (serum creatinine, 9.9 mg/dL; and urea, 199 mg/dL) with signs of glomerular involvement (urine red blood cells, 40 to 60/HPF; and 24-hour urine proteins, 3.06 g).
The clinical and laboratory findings on admission necessitated the immediate start of hemodialysis. Subsequent ultrasound studies revealed hepatosplenomegaly, two kidneys of normal size (right kidney, 11.7 cm; and left kidney, 11.5 cm), and parenchymal thickness (right kidney, 10 mm; and left kidney, 9.9 mm). There was no clinical or radiological sign of lymph nodes involvement. Further laboratory testing by immunological assay (ANA, anti-dsDNA, ASMA, AMA, C-ANCA, P-ANCA, and C3 complement levels) had negative results except for serum proteins electrophoresis, which showed a monoclonal gammopathy of IgM. At the same time, urine immunofixation revealed the presence of albumin, IgM, and kappa light chains, type I cryoglobulinemia, and low C4 complement levels. Considering the history of the patient and after excluding and treating all other causes of renal function deterioration, our diagnostic approach pointed towards an HCV-related renal offence in the context of cryoglobulinemia. However, the rapid decline of renal function and the absence of mixed cryoglobulinemia suggested performing the renal biopsy. While the histopathological examination of the specimen was consistent with the initial suspicion, indicating MPGN (), the immunofluorescence study revealed two unusual findings: dominant monoclonal IgMκ deposits in glomerular basement membrane and infiltration of the interstitium by abundant strongly IgM-positive lymphoid cells (). The presence of CD20 cell marker was distinctive while CD5 was absent. According to these findings, a bone marrow biopsy was performed. The histopathological examination revealed plasmacytic differentiation of small B cells and the immunophenotyping results were positive for CD20 and negative for CD5. These findings were consistent with SMZL. The patient became hemodialysis dependent and received no treatment for the lymphoproliferative disease and was monitored regularly for possible transformation to a high-differentiated lymphoma.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [50, 'years'], 'creatinine': [9.9, 'mg/dL']}",5.85554,5.56276,6.14832,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 50 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 9.9 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (9.9/0.9)**-1.2 * 0.9938**50 * 1.0 = 5.85554.
Hence, the GFR value is 5.85554 ml/min/1.73 m²."
449,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8288603-3,Extracted,"A 51-year-old Caucasian male with hypertrophic cardiomyopathy and recurrent ventricular tachycardia with LVAD placement two years prior presentation for bridge to transplantation presented with complaints of low grade fevers with concern for recurrent infection involving the LVAD line exit site (see Figure ). More than three weeks prior, he had debridement of the site and cultures grew Staphylococcus pseudintermedius and Staphylococcus epidermidis. He underwent debridement, line repositioning and flap closure. On presentation, he was afebrile and hemodynamically stable. On exam, serosanguinous drainage was noted on the LVAD site dressing overlying the abdomen. His white blood cell count was 15.72 x 103/μL, hemoglobin 13.2 g/dL, and creatinine 1.7 mg/dL. A CT scan of the abdomen and pelvis denoted an ill-defined high-density fluid measuring 4.4 x 5.7 cm with subtle adjacent fat stranding in the right upper and mid aspect of the abdomen, which crossed adjacent to the driveline. Thus, additional cultures were obtained with further debridement.
AFB cultures from the LVAD exit site were notable for Mycobacterium abscessus subs. massiliense, and he was started empirically on imipenem and tigecycline intravenously, and oral azithromycin. The patient was discharged, but was subsequently readmitted due to gastrointestinal intolerance to tigecycline. As such, this was replaced by omadacycline, which he later was unable to tolerate as well. Over the next five months, the patient’s clinical status deteriorated and he had numerous readmissions. A decision was made for him to be on lifelong therapy with oral clofazamine and azithromycin (see Table ). However, his last admission to the hospital was for confusion and electrolyte disturbances for which he required urgent dialysis. His poor inpatient clinical course led to comfort care measures being instituted as per request, and he subsequently expired.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [51, 'years'], 'creatinine': [1.7, 'mg/dL'], 'sex': 'Male'}",48.20469,45.79446,50.61492,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 51 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.9)**-1.2 * 0.9938**51 * 1.0 = 48.20469.
Hence, the GFR value is 48.20469 ml/min/1.73 m²."
450,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5971374-1,Extracted,"We present a 48-year-old woman with significant past medical history of uncontrolled diabetes type 2, former intravenous drug user, human immunodeficiency virus, noncompliant with antiretroviral therapy, untreated hepatitis C virus, and epilepsy who presented with a severe sore throat. She reported these symptoms for the last 3 days, which were gradual in onset, mild in intensity, accompanied by nausea and difficulty swallowing, and that progressed within hours into difficulty breathing. She denied any fevers or chills, cough, runny nose or earaches, any palpitations, anxiety, heat intolerance, or weight loss.
On physical examination, she was noted to be afebrile, tachycardia into 120s, dyspneic, and hypotensive. She had a tender anterior neck swelling without palpable lymph nodes. No exudates were noted in the oropharynx. She had bilateral wheezing without stridor. The rest of the systemic examination was unremarkable.
Laboratory tests revealed leukocytosis with bands; platelets were reduced to 30 000/mL. Chemistry revealed sodium of 135 mmol/L, potassium of 2.9 mmol/L, blood urea nitrogen of 32 mg/dL, and creatinine of 2.67 mg/dL. The thyroid function test revealed thyroid-stimulating hormone to be within the normal range at 3.740 µIU/mL with elevated free thyroxine (T4) and free tri-iodothyronine (T3) at 2.33 µg/dL and 5.16 ng/dL, respectively. Antithyroperoxidase antibodies and thyroglobulin antibodies were negative. Her CD4 count was 7 cells/mm3, with 873 000 viral copies/mL.
Urine analysis revealed significant pyuria and bacteriuria. Due to the acute kidney injury, a noncontrast CT scan of the neck was done, which showed fat stranding in the anterior cervical region and around the thyroid gland with marked narrowing of the subglottic airway. An ultrasound of the thyroid gland failed to reveal any obvious fluid collections to suggest an abscess or features of AST-like increased vascularity. Based on these findings, we considered subacute thyroiditis as the probable differential.
She was admitted to the intensive care unit and placed on broad-spectrum antibiotics, piperacillin-tazobactam with vancomycin. Highly active antiretroviral therapy along with bactrim and azithromycin prophylaxis, acyclovir, and fluconazole for opportunistic infections were started.
Her blood cultures came back positive with MRSA; hence, only vancomycin was continued. A transthoracic echocardiography and carotid Doppler ultrasound were inconclusive. Urine cultures also grew MRSA. By day 4 of hospitalization, the patient had worsening neck pain and stridor. She was taken for a stat contrast CT-neck, which revealed multiple abscesses in the thyroid as well as in the retropharyngeal space (). She was taken to the operating room for transoral and transcervical drainage of the thyroid abscesses. She was intubated postprocedure for possible airway edema and observed in the intensive care unit. The cultures from the abscesses also grew MRSA. In the setting of persistent bacteremia and suspicion for endocarditis, a transesophageal echocardiography was done with no evidence of vegetations. She was successfully extubated and her repeat thyroid hormone studies postdrainage were in euthyroid ranges. However, by day 7, she again developed worsening neck pain, fevers, and lactic acidosis. Repeat CT scan of the neck showed re-accumulation of abscesses. She was taken to the operating room again for surgical exploration and drainage. She improved postprocedure. She was given a total 14 days intravenous vancomycin. She was successfully discharged from the hospital.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [48, 'years'], 'creatinine': [2.67, 'mg/dL'], 'sex': 'Female'}",21.38576,20.31647,22.45505,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 48 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.67 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.67/0.7)**-1.2 * 0.9938**48 * 1.012 = 21.38576.
Hence, the GFR value is 21.38576 ml/min/1.73 m²."
451,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3544062-1,Extracted,"A 50-year-old man presented with the complaint of swelling of feet and facial puffiness of 1 month duration accompanied by oliguria. There was no hematuria or turbid urine. There was no history of exertional breathlessness or orthopnea. His appetite was fairly well preserved and his bowel movements were regular. He was not a diabetic or hypertensive and had no significant illness in the past.
On examination, he had pallor, pitting pedal edema, and facial puffiness. His blood pressure was 120/80 mmHg. Respiratory system examination revealed bilateral basal crepitations. Abdominal examination showed the presence of ascites without any evidence of organomegaly. Laboratory examination showed hemoglobin of 10 mg/ dL, total leukocyte count of 14.4 × 109/L with 76% of polymorphs in differential count. Biochemical parameters were as follows: random blood sugar 127 mg/dL, serum creatinine 1.4 mg/dL, blood urea 34 mg/dL, and serum albumin 0.9 g/dL. Serum electrolytes and liver function tests were normal. Erythrocyte sedimentation rate was 140 mm/h. Urine analysis showed 3+ protein, 2–3 pus cells/hpf, and inactive sediments. Urine protein creatinine ratio was 4.6 g/g. Chest X-ray showed bilateral pleural effusion. Abdominal sonogram showed moderate ascites with bilateral pleural effusion and bilateral normal-sized kidneys.
Serum protein electrophoresis showed normal pattern lacking “M-spike.” Renal biopsy was carried out to ascertain the nature of glomerular pathology. Light microscopy showed 24 glomeruli, all of which showed pale, eosinophilic, acellular, weakly periodic acid-Schiff (PAS)-positive material in the mesangium and basement membrane, focally forming nodules []. Congophilia and apple-green birefringence were documented. There was no interstitial fibrosis or tubular atrophy. Minimal amount of amyloid material was seen in the wall of interlobular arteries. Immunofluorescence showed ten viable glomeruli that were negative for IgG, IgA, IgM, C3c, C1q, and fibrin. Immunohistochemical studies were positive for amyloid A protein in the deposits []. There was no light chain restriction. Bone marrow examination and skeletal profile ruled out plasma cell dyscrasia. Serum rheumatoid arthritis (RA) factor was negative. A diagnosis of renal amyloid A (AA) amyloidosis causing secondary nephrotic syndrome was reached and the patient was put on enalapril, atorvastatin, and diuretics. He was also initiated on colchicine 1.2 mg/day.
He returned for follow-up after 1 month with complaints of anorexia, nausea, and oliguria. He had discontinued treatment 3 weeks before. On evaluation, he had anasarca and had blood pressure of 130/80 mmHg. Clinically, the patient had persisting bilateral pleural effusion and ascites. Laboratory tests were as follows: hemoglobin 6.5 g/dL, blood urea 157 mg/dL, serum albumin 1.8 g/ dL, and serum creatinine 6.5 mg/dL. Urine analysis showed 3+ protein and 10–12 RBCs/hpf. RBC casts and granular casts were seen. Doppler study ruled out renal vein thrombosis. Antineutrophil cytoplasmic antibody (by immunoblot assay) was negative and serum C3 was 93.8 mg/dL (normal, 90–180 mg/dL). Considering the rapid deterioration of renal function and sudden drop in hemoglobin, renal biopsy was repeated. Fourteen viable glomeruli were seen on light microscopy, of which 30% of them showed active cellular crescents occupying circumferentially in addition to amyloid deposits []. There was no fibrinoid necrosis of the tufts. Vessel wall had minimal amyloid deposits and no area of necrotizing vasculitis was seen. Immunofluorescence showed eight viable glomeruli that were negative for IgG, IgA, IgM, C3c, C1q, and fibrin. There was no light chain restriction with kappa and lambda light chains.
The patient was treated with large doses of diuretics. Injectable methylprednisolone (1g) was given on three consecutive days. Inj. cyclophosphamide 500 mg was given. The patient gradually had increasing urine output and was symptomatically better at discharge, with serum creatinine improving to 3.5 mg/dL. Unfortunately, he was lost to follow-up.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [50, 'years'], 'creatinine': [1.4, 'mg/dL'], 'sex': 'Male'}",61.23156,58.16998,64.29314,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 50 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.4 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.4/0.9)**-1.2 * 0.9938**50 * 1.0 = 61.23156.
Hence, the GFR value is 61.23156 ml/min/1.73 m²."
452,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8010803-1,Extracted,"A 70-year-old man presented at a regional general hospital because of a protracted cough and hemoptysis manifesting for the last 2 months. He had a 98-pack-year history of cigarette smoking but had quit smoking at 67 years of age. At the presentation, he was found to have 3+ proteinuria and microscopic hematuria with an increased serum creatinine (sCr) level of 3.3 mg/dL despite having no apparent history of renal disease. Ten days later, he showed an increase in the titer of anti-myeloperoxidase-ANCA (MPO-ANCA) to 33.2 U/ml, but no increase in anti-proteinase 3-ANCA or anti-glomerular basement membrane antibodies was revealed, so he was referred and admitted to our hospital for a further workup. Other medical histories included hypertension and emphysema, for which he had received sporadic medical care, while the renal parameters had not been monitored on a regular basis. No exposure to a specific environment or activity was noted.
At the time of the admission (clinical day 1), the patient had a temperature of 36.9°C, a pulse of 98 beats/minute, and a blood pressure of 155/88 mmHg. There were no rashes or petechiae. Renal sonography of both kidneys revealed the preservation of the size with slightly elevated renal cortex echogenicity, while a chest radiograph showed a round circumscribed solitary lesion at the right pulmonary hilar region, and subsequent chest computed tomography (CT) revealed a solid mass in the right upper lobe anterior segment with distinct lymphadenopathy (). The laboratory data on admission are summarized in . A 24-hour urine specimen contained 2.4 g of protein, and his Cr clearance was 24.0 mL/minute.
A renal biopsy performed on clinical day 1 () revealed 3 cores of renal parenchyma with 10 glomeruli, 3 of which were globally sclerotic. Although no evidence of vasculitis was confirmed in the blood vessels, the glomeruli showed cellular crescents with focal segmental necrotizing lesions. Marked interstitial infiltration of inflammatory cells was also noticed. An immunofluorescence analysis revealed no significant staining for C1q or fibrinogen or immunoglobulins, while electron microscopy failed to demonstrate the presence of deposits in the biopsy specimens. Thus, a diagnosis of MPO-ANCA-associated crescentic glomerulonephritis accompanied by a presumed right pulmonary neoplasm was made.
Thereafter, fluctuation in the patient’s sCr level, ranging from 2.77 mg/dL to 3.00 mg/dL was noted until clinical day 11, when the patient showed a sCr level of 2.74 mg/dL and started to receive oral prednisolone (PSL) at 30 mg/day, while a transbronchial lung biopsy performed on clinical day 14 led to a clinical diagnosis of stage IIIC (T4N3M0) squamous cell lung carcinoma in accordance with the American Joint Committee on cancer-tumor-node-metastasis classification (8th edition). The patient was subjected to chemotherapy consisting of paclitaxel and carboplatin on clinical day 52. Although no favorable responses were noted for the pulmonary disease, the MPO-ANCA titer became negative approximately 4 months after the renal biopsy while he was still being treated with oral PSL (10 mg/day). His sCr levels finally settled around 1.94 mg/dL, so he was never on renal replacement therapy. However, the patient ultimately died of respiratory failure 13 months after the initial presentation.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [70, 'years'], 'creatinine': [3.3, 'mg/dL'], 'sex': 'Male'}",19.32378,18.35759,20.28997,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 70 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.3/0.9)**-1.2 * 0.9938**70 * 1.0 = 19.32378.
Hence, the GFR value is 19.32378 ml/min/1.73 m²."
453,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5747944-1,Extracted,"A 67-year-old woman who had been previously treated for RA at a medical clinic presented with abdominal pain and chronic diarrhea, and was referred to our Internal Department. Her vital signs were normal, but pedal edema was present. The remainder of the physical examination findings were unremarkable.
Laboratory values were as follows: serum creatinine, 0.47 mg/dL; urea nitrogen, 10 mg/dL; serum total protein/albumin, 5.2/2.0 g/dL; immunoglobulin (Ig) G, 1002 mg/dL; IgA/M, 111/69 mg/dL. C-reactive protein (CRP), 4.9 mg/dL; rheumatoid factor, 38 IU/mL (reference range, < 15 IU/mL); anti-cyclic citrullinated peptide antibody, 124 U/mL (reference range, < 4 U/mL); matrix metalloproteinase-3, 248.4 ng/mL (reference range, 17.3 ~ 59.7 ng/mL); SAA, 193.2 μg/mL (reference range, < 8 μg/mL). Antinuclear antibody was undetectable, and urinary protein excretion was 0.5 g per gram urinary creatinine.
A computed tomography scan showed a right renal tumor suggestive of renal cell carcinoma. Right nephrectomy (May, 20XX) was performed and confirmed the diagnosis of clear cell carcinoma. The non-cancerous part of the renal tissue contained 365 glomeruli; 57 glomeruli were globally sclerotic. In addition, deposition of amorphous eosinophilic material was observed at vascular poles and mesangial regions (Fig. ). These deposits were Congo red- and AA-positive (Fig. and ). Tubular atrophy and interstitial fibrosis were moderate. Immunofluorescence staining showed no deposition of complements or Igs, including light chains. Electron microscopy revealed randomly disposed, rigid, nonbranching fibrils compatible with amyloid deposition (Fig. ) and effacement of podocyte foot processes.
Colonoscopy revealed amyloid deposition in addition to inflammation of the colon (February, 20XX, Fig. ). Biopsy of the duodenum also revealed amyloid deposition. The patient was therefore diagnosed with renal cell carcinoma and AA amyloidosis.
We initiated treatment with for RA, but her proteinuria gradually increased to the nephrotic range (Fig. ). was replaced with TCZ, and her proteinuria began to improve considerably and eventually resolved (February, 20XX + 1). Her gastrointestinal symptoms were also alleviated. In addition, the levels of SAA decreased to the reference range. However, repeat colon biopsy (July, 20XX + 1), performed after her gastrointestinal symptoms resolved (November, 20XX), showed persistence of amyloid deposition, although it had decreased compared to that observed on the initial biopsy (Fig. ).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [67, 'years'], 'creatinine': [0.47, 'mg/dL'], 'sex': 'Female'}",104.27841,99.06449,109.49233,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 67 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.47 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.47/0.7)**-0.241 * 0.9938**67 * 1.012 = 104.27841.
Hence, the GFR value is 104.27841 ml/min/1.73 m²."
454,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6448469-1,Extracted,"A 54-year-old woman presented to the cardiovascular (CV) outpatient clinic with dyspnea on exertion aggravated for 1–2 months. In addition, low systolic blood pressure (up to 60 mmHg) in both upper arms was one of the referred reasons. She was followed up for RA for 24 years and had regular medical treatment at a nearby rheumatology clinic.
On physical examination, she was alert and looked well despite the low blood pressure on her upper arms. However, the blood pressure in both lower extremities was appropriate (up to 160 mmHg). Mild pitting edema on both legs and puffy face were also noted. With regard to the upper extremities, a rheumatoid nodule was found on the right wrist and both hands were deformed and deviated to the ulnar side, compatible with RA.
Serum biochemical profile was unremarkable, while renal dysfunction (creatinine level, 2.5 mg/dL) with proteinuria was observed. The serological markers of RA were characterized with the following values: anticyclic citrullinated peptides, 150.6 U/mL; RA factor, 73.8 IU/mL; and antinuclear antibody, 1:40 (homogeneous type). Erythrocyte sedimentation rate, 32 mm/h; C-reactive protein level, 0.2 mg/dL.
She was controlled with broad-spectrum medications, including methotrexate, methylprednisolone, hydroxychloroquine, sulfasalazine, and nonsteroid anti-inflammatory drugs (NSAIDs).
Electrocardiography revealed normal sinus rhythm with a left ventricular (LV) hypertrophic pattern. Echocardiographic study revealed global hypokinesia with reduced ejection fraction (35%) and LV concentric hypertrophy with apical aneurysm, in which multiple, small thrombi were embedded []. Mitral inflow showed a restrictive pattern (E/A ratio, 3.6; isovolumic relaxation time, 50 ms; deceleration time, 130 ms; E/e’ ratio, 21.0).
Coronary computed tomography angiography revealed 70%–80% stenosis of the proximal left anterior descending artery and 70% stenosis of the diagonal branch and luminal narrowing of the descending abdominal aorta []. Cardiac magnetic resonance (MR) imaging revealed diffuse, circular, and patched late gadolinium enhancements in the hypertrophied myocardium [Figure –]. It is interesting that the best inversion time (TI) for myocardial nulling was greatly shortened (120 ms) on the TI-scout sequence. These findings were also consistent with cardiac amyloidosis (CA). The serum levels of free kappa and lambda light chains measured to rule out AL-type CA were within their normal ranges. MR angiography revealed total occlusion of both the subclavian and carotid arteries in the proximal portion, with multiple collateral flow to the upper neck and head side [].
According to CV imaging, the final diagnosis was RA associated with Takayasu's arteritis (TA), reactive CA, and ischemic heart disease with coronary artery stenosis. Anticoagulation cleared the apical thrombus from the LV cavity, and medications for ischemic treatment were maintained. However, she refused surgery for revascularization of the carotid, subclavian, and coronary arteries and opted for medical treatment with regular follow-up.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [54, 'years'], 'creatinine': [2.5, 'mg/dL']}",22.29483,21.18009,23.40957,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 54 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.5 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.5/0.7)**-1.2 * 0.9938**54 * 1.012 = 22.29483.
Hence, the GFR value is 22.29483 ml/min/1.73 m²."
455,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7457498-1,Extracted,"The patient was a 77-year-old man who was admitted to our institution due to a gastric GIST detected at a local hospital. The patient first visited the Department of Internal Medicine for an examination. He had no specific complaints other than slight indigestion. The gastric GIST was located on the lesser curvature of the upper body of the stomach. The tumor diameter was approximately 5 cm according to the findings of esophagogastroduodenoscopy (EGD) performed at the local hospital. He had hypertension, which was well controlled with antihypertensive drugs. He had no significant surgical or family history.
On physical examination, the patient’s vital signs, including blood pressure, heart rate, body temperature, respiratory rate, and oxygen saturation at room air, were normal. No specific findings were observed on abdominal examination. Another EGD was performed that showed the known lesion (a gastric GIST) on the lesser curvature of the upper body and a new flat-elevated lesion on the lesser curvature of the lower body, leading to a suspicion of EGC (Fig. ). Computed tomography findings confirmed the presence of a GIST in the stomach (Fig. a) and revealed two new lesions. One lesion was suspected to be a 4-cm submucosal tumor on the anterior wall of the upper body of the stomach (Fig. b). The other lesion was a wall thickening of the descending colon that demonstrated the possibility of malignancy (Fig. c). Upon colonoscopy, a 3-cm ulceroinfiltrative mass was observed from 25 to 28 cm above the anal verge (Fig. ). Positron emission tomography showed no distant metastasis, including in the liver and both lung fields. Biopsy results revealed two gastric GISTs with spindle cell neoplasm and synchronous gastric and colon cancers that were well-differentiated adenocarcinomas. We decided to perform cooperative laparoscopic surgery. The patient’s hemogram showed a white blood cell count of 11,210/μl and hemoglobin levels of 14.5 g/dl. Blood chemistry findings were as follows: albumin, 4.6 g/dl; creatinine, 0.91 mg/dl; blood urea nitrogen, 10.8 mg/dl; and total bilirubin, 1.12 mg/dl. Serum tumor marker levels were also within normal limits: carcinoembryonic antigen, 2.8 ng/ml, and carbohydrate antigen 19-9, 19.0 U/ml.
Laparoscopic surgery was performed according to the standard laparoscopic procedure, and the first 12-mm port was inserted through the umbilicus. For gastrectomy, two operator ports were made on the right upper side of the patient’s abdomen (upper port = 5 mm and lower port = 12 mm). Additional ports were inserted into the right lower (12 mm) and left lower (12 mm) abdominal areas for colectomy. Laparoscopic near-total gastrectomy with D1+ lymph node dissection and left hemicolectomy were performed sequentially without significant events. The stomach and colon were removed through the umbilicus by extending the incision of the umbilical port. In the stomach specimen, we found a 1-cm incidental lesion of a submucosal tumor located on the greater curvature of the high body (Fig. ). After the surgery, the patient proceeded with sips of water on the second day and began a soft diet on the fourth day. He was discharged 7 days after the surgery without immediate complications.
Histopathological examination of the EGC revealed a well-differentiated adenocarcinoma with negative resection margins that were staged IA (T1aN0M0) according to the American Joint Committee on Cancer (AJCC) Cancer Staging, 8th edition []. Three gastric GISTs (5.5 cm, 4 cm, and 1 cm) posed an intermediate risk as suggested by the modified National Institutes of Health classification system (mitotic index, ≤ 5/50 high-power fields) []. Immunohistochemical findings were as follows: c-KIT (+), CD34 (+), DOG-1 (+), S-100 (−), desmin (−), and a low proliferative activity indicated by Ki-67 (Fig. ). The descending colon lesion was identified as a well-differentiated adenocarcinoma with negative resection margins and was staged IIA (T3N0M0), with low risk, according to the AJCC Cancer Staging 8th edition []. No mutations were detected in the K-ras, N-ras, and B-raf genes. In the molecular testing of the colon cancer specimen, tumor cells were confirmed to be diffusely and strongly positive for the epidermal growth factor receptor. Furthermore, the microsatellite instability test showed the status to be stable (microsatellite stable). On the follow-up appointment, the patient was stable without any symptoms and did not require any adjuvant systemic chemotherapy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [77, 'years'], 'creatinine': [0.91, 'mg/dL'], 'sex': 'Male'}",86.80647,82.46615,91.14679,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 77 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.91 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (0.91/0.9)**-1.2 * 0.9938**77 * 1.0 = 86.80647.
Hence, the GFR value is 86.80647 ml/min/1.73 m²."
456,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6396525-1,Extracted,"An 81-year-old Asian man presented to our department complaining of fever since the preceding day. The patient had been under treatment for the previous 3 years for chronic heart failure and chronic renal failure. He did not have a history of malignancy, diabetes mellitus, cytotoxic therapy, or corticosteroid use, and no foreign bodies had been implanted. The patient’s family history was unremarkable. Physical examination revealed a heart rate of 101 beats/min, blood pressure of 87/48 mmHg, respiratory rate of 20 breaths/min, temperature of 37.0 °C, and oxygen saturation of 87% on room air. He had no caries or periodontitis. Results of respiratory, cardiac, and abdominal examinations were unremarkable. Limb examination demonstrated mild edema of both legs. Abdominal computed tomography (CT) showed a low-density mass in the right iliopsoas muscle indicative of an iliopsoas abscess (Fig. ). The patient’s white blood cell count, C-reactive protein (CRP), and procalcitonin levels were 19,400/μl, 13.35 mg/dl, and 3.950 ng/ml, respectively. Serum blood urea nitrogen and creatinine were elevated at 77.2 mg/dl and 3.69 mg/dl, respectively. A CT-guided percutaneous drainage of the psoas abscess was performed, and an indwelling catheter was placed. Gram staining of the drained fluid revealed many neutrophils and Gram-positive streptococci. On the basis of these findings, a presumptive diagnosis of iliopsoas abscess caused by Streptococcus species was made, and treatment with ampicillin/sulbactam (ABPC/SBT) 1.5 g, administered intravenously every 8 h, was initiated. Results of organism cultures of the abscess and blood were positive, and P. micra was identified by using the API ZYM system (Sysmex-bioMérieux Co. Ltd., Tokyo, Japan), with the organism exhibiting susceptibility to penicillin G, ampicillin, clindamycin, and meropenem. By day 7, the patient’s white blood cell count normalized. By day 20, his CRP level was decreased to 0.35 mg/dl. Therefore, the pigtail catheter was removed. The patient died of peritonitis due to colon diverticulum perforation after 5 weeks of treatment. An autopsy revealed no right iliopsoas abscess at the time of death.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [81, 'years'], 'creatinine': [3.69, 'mg/dL'], 'sex': 'Male'}",15.78215,14.99304,16.57126,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 81 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.69 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.69/0.9)**-1.2 * 0.9938**81 * 1.0 = 15.78215.
Hence, the GFR value is 15.78215 ml/min/1.73 m²."
457,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5965212-1,Extracted,"An 86-year-old female presented to the emergency department (ED) after sustaining a head injury following a mechanical ground-level fall. Upon interviewing the family, it was determined that the patient was taking dabigatran. She had a left-sided blepharohematoma, left sided facial edema, blood on her lips, and a non-displaced fracture of the right mandible. Her medical history was significant for atrial fibrillation for which she was taking dabigatran 75mg twice daily with unknown timing of her last dose. Further history included hypertension, coronary artery disease, and a previous cerebral vascular accident. Pulse and blood pressure on admission were 118 beats per minute and 178/105 mm Hg respectively. She was alert and oriented to person, place, time, and situation, without focal neurological deficits. Her National Institutes of Health Stroke Scale was zero and her Glasgow Coma Scale was 15.
The computed tomography (CT) showed signs of trace subarachnoid hemorrhage in the Sylvian fissures bilaterally and chronic bilateral subdural hygromas ( and ). Laboratory findings showed an activated partial thromboplastin time (aPTT) of 30.8 seconds (s) (normal range 24.5–35.7 s), a mildly elevated prothrombin time (PT) of 12.7 s (normal 10.1–12.6 s) and a serum creatinine 1.17 mg/dL. The neurosurgery service, as well as the clinical pharmacy specialist for the ED, were consulted to initiate treatment with 5g of idarucizumab immediately to prevent further hemorrhage. Serial CT showed stabilization of the bleeding without further progression. Six days after admission the patient was transferred to a rehabilitation unit without incident.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [86, 'years'], 'creatinine': [1.17, 'mg/dL'], 'sex': 'Female'}",45.44403,43.17183,47.71623,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 86 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.17 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.17/0.7)**-1.2 * 0.9938**86 * 1.012 = 45.44403.
Hence, the GFR value is 45.44403 ml/min/1.73 m²."
458,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4553271-2,Extracted,"An 80-year-old man was hospitalized because of heart failure with cardiorenal dilemma. His past medical history included coronary bypass surgery, ischemic cardiomyopathy, chronic kidney disease, chronic obstructive pulmonary disease, prostate cancer treated with total androgen deprivation, and type 2 diabetes, treated with diet only. His medication included pantoprazole, enoxaparin, aspirin, bumetanide, carvedilol, atorvastatin, bicalutamide, darbepoetin alfa, macrogol laxatives, and fluticasone, salmeterol, and tiotropium inhalation therapy. He had been admitted with pulmonary edema, for which continuous venovenous hemofiltration (CVVH) was started. Afterwards, he was transferred to the nephrology ward for continuation of chronic intermittent hemodialysis. He had a residual diuresis of 600 mL per 24 hours. An indwelling urinary catheter had been placed on the first day of hospitalization to monitor urinary output.
On the 13th day of hospitalization, the urine inside the urine bag suddenly turned purple (see ). The patient had a burning sensation in the lower abdomen. Vital parameters were unremarkable. Physical examination showed bilateral basal crepitations on auscultation, systolic cardiac murmur, mild peripheral edema, and indwelling urinary catheter with remarkable purple color of the collecting bag, while the urine in the tubing before the bag had a normal color. Laboratory assessment showed anemia (hemoglobin 8.9 g/dL) with mild macrocytosis, normal leukocyte count and differentiation, and platelets of 115 × 109/L. Creatinine before dialysis was 3.11 mg/dL and blood urea nitrogen was 48 mg/dL. Liver function tests were normal. CRP was 23 mg/L (reference value < 5 mg/L). Urine analysis showed pyuria and trace hematuria; urinary pH was 8.5. Culture was positive for Escherichia coli. The indwelling catheter was removed. The patient was treated with amoxicillin for 7 days. He was discharged in good health, with continuation of thrice-weekly hemodialysis. Shortly thereafter, the patient developed urinary obstruction for which a permanent suprapubic catheter was placed. The purple urine color never recurred.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [80, 'years'], 'creatinine': [3.11, 'mg/dL'], 'sex': 'Male'}",19.49783,18.52294,20.47272,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 80 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.11 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.11/0.9)**-1.2 * 0.9938**80 * 1.0 = 19.49783.
Hence, the GFR value is 19.49783 ml/min/1.73 m²."
459,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6376492-1,Extracted,"A previously healthy 11-month-old girl presented with failure to thrive and dyspnoea secondary to cardiac dysfunction. She was found to be hypertensive. Blood pressure measurements demonstrated a persistent systolic pressure over 180 mm Hg. She was initiated on antihypertensive and diuretic medication. There was no family history of significance and no stigmata of autoimmune disease or neurofibromatosis. There was no syndromic phenotype. Biochemistry revealed marginally renal function (creatinine 25 mmol/L), but urinalysis was normal. Vasculitic screen was negative. Echocardiogram revealed left ventricular dysfunction and hypertrophy. Renal Doppler ultrasound demonstrated a reduced blood flow through a comparatively smaller right kidney (1 SD below mean) with abnormal spectral trace in the right renal artery. Divided renal function was estimated at 30% on the right and 70% on the left. No dysplastic changes were seen. Dimercaptosuccinic acid (DMSA) demonstrated a small right kidney and a divided renal function of 6% on the right and 94% on the left.
At this time, the patient was referred to our tertiary centre for a review at a multidisciplinary team (MDT) meeting to consider angioplasty versus nephrectomy as a treatment. The tests had not at this point identified any pathology in the left kidney (which DMSA had demonstrated to contribute to 94% of renal function), renal function was only slightly deranged, and bilateral RAS was thought to be usual. The decision was made to perform a right nephrectomy in the belief that the poorly functioning right kidney, and associated reduced renal perfusion, was driving a compensatory hypertensive response via the renin-angiotensin system. This was confirmed on biochemical assay of renin and aldosterone levels. At this point, she was taking 5 different classes of antihypertensive medication and the DMSA had shown only 6% function from the right kidney.
The nephrectomy was performed and the resected right kidney demonstrated no histological abnormality such as fibromuscular dysplasia (FMD). There was compensatory hypertrophy of the left kidney on follow-up ultrasound (>2 SDs above the mean), but the hypertension persisted and the marginally impaired renal function did not improve (thought due, in part, to the Angiotensin converting enzyme (ACE) inhibitor). Spectral analysis demonstrated abnormal waveforms suggestive of RAS of the solitary left kidney. Following further MDT meeting discussion, it was decided to attempt angioplasty of the left renal artery.
Percutaneous transluminal angioplasty was performed via a 4Fr vascular sheath in the right common femoral artery. Angiogram demonstrated no aortic coarctation but a tight ostial stenosis of the left renal artery () suggestive of possible unifocal FMD. The stenosis was crossed and angioplastied with both 2 and 3 mm conventional balloons (Sterling, Boston Scientific, Massachusetts, United States), but there was failure to relieve the stenosis () despite high inflation pressures. As the use of a cutting balloon and its inherent risk had not been discussed or consented for the decision was made to stop and the use of a cutting balloon discussed in the paediatric urology meeting. A second attempt was scheduled for 3 months later. The MDT decision was to have a renal transplant surgeon available during PTA so that, should a complication, such as dissection, arise with loss of the solitary kidney, then the kidney could be auto transplanted and re-anastomosed in the pelvis. Using a 6Fr sheath, an over-the-wire 3 mm × 15 mm cutting balloon (Boston Scientific) was used over a 0.014 wire () to relieve the stenosis. The stenosis was post dilated with 3.5 mm × 20 mm balloon with excellent angiographic results and release of the stenosis (). There were no immediate complications.
During the month following cutting balloon angioplasty, there was an improvement in blood pressure and antihypertensive medications were slowly weaned off. Three months following treatment, she had stopped 2 antihypertensives and 1 was reduced, leaving her taking 2 antihypertensives. The parents reported increased wet nappies, thought perhaps due to increased renal perfusion. Echocardiogram revealed improved left ventricular function. In addition, the biochemical profile demonstrated an improvement in renal function with a reduction in creatinine. At 1 year of follow-up, she had stopped all antihypertensives and remained with stable good blood pressure and normalised end-organ function.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [11, 'months'], 'creatinine': [25.0, 'mmol/L']}",0.10711,0.10175,0.11247,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 11 months old. This means the patient is 0 years old.
The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 25.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from mmol to mg. The mass of Serum Creatinine is 25.0 mmol. To convert 25.0 mmol of Serum Creatinine to mol, multiply by the conversion factor 0.001, giving us 25.0 mmol Serum Creatinine * 0.001 mol/mmol = 0.025 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.025 mol Serum Creatinine * 113.12 g/mol = 2.828 g Serum Creatinine. To convert 2.828 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 2.828 g Serum Creatinine * 1000.0 mg/g = 2828.0 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 2828.0 mg Serum Creatinine/10.0 dL = 282.8 mg Serum Creatinine/dL. The concentration value of 25.0 mmol Serum Creatinine/L converts to 282.8 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (282.8/0.7)**-1.2 * 0.9938**0 * 1.012 = 0.10711.
Hence, the GFR value is 0.10711 ml/min/1.73 m²."
460,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4310434-1,Extracted,"A 42-year-old African-American man, who underwent kidney transplantation for end-stage renal disease due to hypertension, presented to the emergency department with lightheadedness, palpitations and a reported home blood pressure of >220/110 mmHg. Six weeks prior, he had received a kidney from a 30-year-old deceased donor who died from a gunshot wound. The donor renal anatomy was notable for three renal arteries: two main renal arteries on a common aortic patch and a third superior pole renal artery on a separate aortic patch. The superior pole artery supplied ∼20% of the graft. It had been transected during procurement, but was repaired in an end-to-end fashion with running continuous sutures. During transplantation, two separate aortic cuff anastomoses were made to the external iliac artery. Reperfusion of the kidney was normal and the kidney functioned immediately. The immunosuppression regimen included basiliximab induction and maintenance tacrolimus, mycophenolate mofetil and corticosteroids. The postoperative course was uncomplicated except for new onset of atrial fibrillation, which was resolved with cardioversion. The blood pressure after kidney transplantation ranged between 125/70 and 175/105 mmHg on metoprolol tartrate 100 mg and nifedipine 90 mg twice daily. After addressing medication compliance, antihypertensive medications were adjusted. On the day of the presentation to the emergency department, the patient's antihypertensive medications included clonidine 0.2 mg three times a day, labetalol 200 mg and nifedipine 90 mg twice daily. He appeared diaphoretic, with a blood pressure of 235/122 mmHg and a heart rate of 87 bpm. Physical examination revealed bilateral lung rales without peripheral edema or abdominal pain.
Laboratory tests were significant for a serum creatinine, which had increased from a post-transplant baseline of 1.4 to 2.2 mg/dL over 4 days. The tacrolimus trough level was slightly elevated at 18.3 ng/mL (target 8–15 ng/mL), which suggested against allograft rejection. Urine and blood cultures were negative. Chest X-ray showed evidence of pulmonary edema. Electrocardiogram revealed no evidence of cardiac ischemia or arrhythmia. The patient was admitted to the intensive care unit and administered a nicardipine drip, but his blood pressure remained elevated. Given the presence of refractory hypertension and flash pulmonary edema, TRAS was suspected. Duplex sonography was performed and revealed a hilar pseudoaneurysm adjacent to one of the main donor renal arteries measuring 3.1 × 3.2 × 3.1 cm, with a peak systolic velocity of 457 cm/s in the transplant renal artery. Angiography demonstrated a bi-lobed pseudoaneurysm arising from the distal anastomosis and extrinsically compressing the main transplant artery and limiting flow (Figure ).
The following day, the patient was taken to the operating room for pseudoaneurysm repair. Due to extensive abdominal adhesions from prior surgeries, repair of the pseudoaneurysm was aborted, and the pseudoaneurysm was controlled by placement of a covered endoluminal stent to the external iliac artery. This led to surgical embolization of the allograft. The blood pressure improved significantly postoperatively. Finally, the allograft was removed. On the pathologic examination of the explanted kidney, there was extensive coagulative necrosis, reactive acute inflammation and vascular thrombi, which was compatible with infarction. In the residual viable kidney parenchyma, there were vascular changes suggestive of malignant hypertension. There was no evidence of rejection. In summary, this is a case of hypertensive crisis and flash pulmonary edema in a kidney transplant recipient, as a result of transplant renal artery narrowing due to compression of a pseudoaneurysm.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [42, 'years'], 'creatinine': [2.2, 'mg/dL'], 'sex': 'Male'}",37.41363,35.54295,39.28431,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 42 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.2 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.2/0.9)**-1.2 * 0.9938**42 * 1.0 = 37.41363.
Hence, the GFR value is 37.41363 ml/min/1.73 m²."
461,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5469569-3,Extracted,"A 28-year-old woman with a family history of IgAN presented in January 2014 at the emergency care unit with macrohematuria, fever and an unspecific skin rash on her buttocks in conjunction with a viral upper respiratory tract infection. BP was 139/74 mmHg. She had previously experienced macrohematuria without rashes during viral infections. At this first visit, her creatinine was 217 µmol/L, CRP 36 mg/L, p-alb 29 g/L and U-dipstick 3+ for hematuria and proteinuria. U-sediment contained 4–10 Erys and 2–5 granular casts/hpf. Two weeks later, BP was 107/62 mmHg, creatinine had spontaneously decreased to 109 µmol/L, but the urine ACR was 160 mg/mmol. At the time of renal biopsy, 1 month after the first visit, creatinine had again increased to 233 µmol/L, p-alb was 26 g/L and U-sediment again contained granular casts. Histopathologic examination revealed a diagnosis of IgAN with cellular crescents in 5 of 17 glomeruli (31%) with an Oxford classification of M1E0S1T1. Treatment was started with MEP pulses, followed by PSL. RTX was given on days 10 and 24 after diagnosis. (For doses, see Table and Figure.) A month later, the creatinine level was 78 µmol/L and albuminuria was 1.9 g/day. PSL was tapered over 12 months, prolonged due to persistent proteinuria (urine ACR 77–102 mg/mmol). After 13 months the patient became pregnant and angiotensin-converting enzyme inhibitor (ACEi) had to be stopped, but proteinuria continued to decrease and the urine ACR was 8.8 mg/mmol in October 2015 when she was 30 weeks into her pregnancy. The patient was lost to follow-up due to her move to another town.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [28, 'years'], 'creatinine': [233.0, 'µmol/L'], 'sex': 'Female'}",24.97983,23.73084,26.22882,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 28 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 233.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 233.0 µmol. To convert 233.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 233.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00023 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00023 mol Serum Creatinine * 113.12 g/mol = 0.02602 g Serum Creatinine. To convert 0.02602 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.02602 g Serum Creatinine * 1000.0 mg/g = 26.02 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 26.02 mg Serum Creatinine/10.0 dL = 2.602 mg Serum Creatinine/dL. The concentration value of 233.0 µmol Serum Creatinine/L converts to 2.602 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.602/0.7)**-1.2 * 0.9938**28 * 1.012 = 24.97983.
Hence, the GFR value is 24.97983 ml/min/1.73 m²."
462,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5641498-1,Extracted,"A 60-year-old woman presented to the emergency department with left hip pain after falling down. The simple X-ray revealed transverse subtrochanteric fracture of the left femur with displacement of the distal part. The patient had been on a monthly risedronate for osteoporosis. Otherwise, she had been well until this event. She was admitted and underwent open reduction and internal fixation on the following day. The computed tomography demonstrated another incomplete subtrochanteric fracture line on the medial side of the right femur. In addition, low bone mineral density (T-score, -2.7) and multiple rib fractures were noted on dual-energy X-ray absorptiometry and bone scan, respectively.
Oddly, the urine dipstick test revealed a strong positivity for glucose at the serum glucose level of 126mg/dL. The blood chemistry and arterial blood gas analysis showed hypokalemia, hyperchloremic metabolic acidosis, hypophosphatemia, hypouricemia, and elevated alkaline phosphatase (ALP) level with a modestly decreased kidney function (). The urine anion gap, fractional excretion or daily excretion of several electrolytes, and transtubular potassium gradient are shown in : positive urine anion gap in the setting of normal anion gap metabolic acidosis, normoglycemic glucosuria, enhanced potassium secretion leading to hypokalemia, and renal wasting of phosphate. These findings were consistent with Fanconi syndrome with renal tubular acidosis (RTA). Moreover, her serum sodium level increased up to 151mmol/L on the sixth day of admission, although 0.9% normal saline or hypotonic fluid was administered. The urine osmolality was inappropriately low(190mOsm/kg), despite adequate plasma antidiuretic hormone secretion to increased serum osmolality (304 mOsm/kg); such a finding reflected a urine concentration defect. Potassium citrate powder was administered daily with intravenous potassium phosphate replacement.
A renal biopsy was performed to determine the cause of chronic kidney disease and associated renal tubule dysfunction. The light microscopy showed a mild degree of interstitial nephritis and focal acute tubular injury with normal glomerulus (). However, the immunofluorescence and electron microscopy did not reveal any abnormal finding.
Further investigations revealed a speckled pattern of antinuclear antibodies (ANA) (1:160) with positivity for both anti-SS-A and anti-SS-B antibodies. She had a history of gritty sensation in the eyes and decreased tear flow on the Schirmer's test. Based on the clinical history and laboratory findings, interstitial nephritis associated with Fanconi syndrome, RTA, and nephrogenic diabetes insipidus secondary to Sjögren's syndrome were diagnosed. It was likely that RTA and hypophosphatemia were responsible for the multiple fractures, suggesting osteomalacia overlapping with osteoporosis.
When the total carbon dioxide (CO2) level increased to 24.7mmol/L via the administration of potassium citrate, the fractional excretion of bicarbonate and urine-to-blood CO2 tension gradient (U-B pCO2) were calculated as <15% and <20mmHg, respectively, indicating distal RTA. Furthermore, her urine pH level persistently ranged from 6.5 to 8.0, which supported this type of RTA (). Thereafter, she has been on prednisolone and hydroxychloroquine with potassium citrate powder and maintained normal serum potassium, phosphate, and total CO2 level. The ALP level also decreased to the normal range. However, the serum creatinine level increased to 2.0 mg/dL after 17 months ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [60, 'years'], 'creatinine': [2.0, 'mg/dL']}",28.07308,26.66943,29.47673,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 60 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.0/0.7)**-1.2 * 0.9938**60 * 1.012 = 28.07308.
Hence, the GFR value is 28.07308 ml/min/1.73 m²."
463,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8238594-1,Extracted,"A 34 year-old Thai man from Prajin Buri, a province in rural East Thailand, presented with a 4-month history of low-grade fever and multiple discrete painful umbilicated erythematous papules on his face, as well as a 40 kg weight loss from his previous normal weight of 110 kg and height of 170 cm. Two weeks prior to admission (PTA), he developed odynophagia, painful nodular ulcers on his tongue, and hoarseness of his voice. One week PTA, he had dyspnea on exertion. His medical history was unremarkable, and he denied using any pills, herbs, or intravenous drugs. His occupation was that of a car mechanic. He mentioned that he had not traveled to other locations in the previous three months. Physical examination revealed blood pressure of 90/50 mmHg, regular heart rate of 110/min, respiratory rate of 24/min, and body temperature of 38.3°C, mildly pale conjunctivae, multiple papules with central necrosis on his face painful nodular ulcers on his tongue and palate, diffuse fine crackles in both lungs, jugular vein engorgement, a positive left ventricular heave and a grade III/VI diastolic rumbling murmur at mitral valve area, hepatosplenomegaly, and mild pedal edema. The complete blood count (CBC) analysis showed a Hb of 11.1 g/dL, white blood cell of 5,350 × 103/μL, and platelets of 140,000/μL. Blood chemistries showed urea nitrogen of 56 mg/dL, creatinine of 1.98 mg/dL, total bilirubin of 4.9 mg/dL, direct bilirubin of 3.09 mg/dL, aspartate aminotransferase of 42 U/L, alanine aminotransferase of 25 U/L, alkaline phosphatase of 147 U/L, albumin of 3.1 g/dL, corrected calcium of 13.4 mg/dL, phosphorus of 3.1 mg/dL, intact parathyroid hormone of <1.2 (normal: 15–65) pmol/L, and 1,25-OH2 vitamin D of 152 (normal: 19.9–79.3) pg/mL. Anti-HIV serology testing showed negative results. Cardiomegaly with pulmonary congestion was seen on chest radiography. Transthoracic echocardiography indicated a left ventricular ejection fraction of 54%, moderate aortic regurgitation, severe rheumatic mitral stenosis, and multiple oscillating masses on the anterior mitral valve leaflet ranging from 1.5 cm to 2.4 cm in diameter (, yellow arrows). Skin scraping of the facial lesion exhibited both extracellular and intracellular yeast-like organisms with buddings, 2–4 μm in size, on Wright's stain, most likely Histoplasma. As a result, disseminated histoplasmosis and endocarditis were diagnosed, and 3 mg/kg/day intravenous liposomal amphotericin B was administered immediately. The patient had a profound cardiogenic shock and atrial fibrillation one day after being admitted to the hospital, and echocardiography indicated a mechanical obstruction of the mitral valve orifice caused by the vegetation. Three large vegetations on the anterior mitral valve leaflet were identified during emergency open-heart surgery (), and a mechanical prosthetic mitral valve was placed. Histopathology examination of the vegetation showed many yeast-like organisms. However, the patient's condition deteriorated, and he died four days after the operation from intractable multiorgan failure. The sputum and vegetation cultures grew H. capsulatum (Figures and ) after 1 week of incubation.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [34, 'years'], 'creatinine': [1.98, 'mg/dL']}",44.62178,42.39069,46.85287,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 34 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.98 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.98/0.9)**-1.2 * 0.9938**34 * 1.0 = 44.62178.
Hence, the GFR value is 44.62178 ml/min/1.73 m²."
464,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8406562-1,Extracted,"The patient was a 49-year-old man with chronic renal insufficiency. He underwent right renal transplantation in the Chinese People's Armed Police Force General Hospital in November 2016. Following transplantation, the patient underwent immunosuppression therapy, which included tacrolimus, prednisone, and myfortic, resulting in the return of normal renal function in the patient.
Two years later, the level of sCr in the patient gradually increased from normal to 274 mmol/L during routine laboratory testing. Enhanced MRI demonstrated multiple, variably sized quasi-circular lesions with slightly short signal intensity on T1WI, slightly long signal intensity on T2WI, and high signal intensity on DWI. The larger size lesion was about 4.66 cm by 3.10 cm (Fig. ). PET-CT revealed a soft tissue mass in the pelvis of the transplanted kidney (with an elevated SUV of 2.6), and multiple metastatic hypermetabolic soft tissue density nodules can be observed in the parenchyma of the transplanted kidney (with a maximum SUV of 2.9). No metastatic hypermetabolic lesions were observed in any other parts of the body.
A puncture biopsy of the transplanted kidney was performed, and the results indicated large neoplastic cells. The immunohistochemistry examination revealed the following: CD34 (few +), CD68 (KP1) (few +), CD163 (-), lysozyme (few +), MPO (+), Ki-67 (>70% +), CD3 (few +), CD20 (-), TdT (few +), CD15 (-), CD117 (+), FISH: EBER(-). Bone marrow biopsy showed no evidence of leukemic infiltration (Fig. ), with normal chromosomes (46, XY). Examinations of fusion genes for both acute lymphoblastic leukemia and myeloid leukemia were negative. NGS examinations of the transplanted kidney was performed on 34 commonly mutated genes in AML (listed in ) and showed mutations of KRAS (NM_004985:exon2:c.G35A:p.G12Drs121913529), DNMT3A (NM_022552:exon15:c.1675delT:p.C559fs) , and no gene mutations in the bone marrow. Eventually, the patient was diagnosed with de novo MS in the transplanted kidney. Detailed information on the donor was not available, but the other transplant recipient did not have any problems in the transplanted kidney.
The patient underwent systemic chemotherapy in our hospital in October 2019, and received DA regimen chemotherapy (daunorubicin 100 mg on days 1-3 and cytarabine 170 mg on days 1-7). The patient responded well to the treatment, and the size of the mass in the transplanted kidney decreased and the level of sCr decreased to 192 mmol/L. The patient underwent a second cycle of DA regimen chemotherapy 30 days later. The size of the biggest lesion decreased to 2.5cm by 1.8cm, but the level of sCr remained at around 180 mmol/L. Therefore, we changed the chemotherapy regimen to cytarabine 2.5 g every 12h on days 1, 3, and 5, and etoposide 100 mg on days 1-3 for 3 cycles. However, 3 days after the 5th cycle of the revised chemotherapy regimen, the patient presented with progressive generalized motor weakness and slurred speech, without headache and vomiting, and the patient couldn’t stand and walk without assistance. A routine blood test showed WBC 4×109/L, NEUT 3.84×109/L, HGB 94.3 g/L, and PLT 44×109/L. The patient’s liver function, serum ions, and other metabolic panels were within normal limits, except that the level of sCr was 157 mmol/L. Head CT and MRI did not show any new abnormal acute findings, and it was presumed that the neurologic symptoms experienced by the patient were a result of cytarabine neurotoxicity. Thereafter the patient was treated with prednisone 40 mg twice a day for 3 days, which led to a significant improvement in his symptoms. After recovering from the neurologic symptoms, the patient refused to continue chemotherapy and allogeneic hematopoietic stem cell transplantation. The patient was followed up on April 20, 2021 and he could speak fluently, but sometimes walked with an unsteady step. The size of the biggest lesion in the transplanted kidney decreased to 1.7 cm and the level of sCr was maintained at around 200mol/L.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [49, 'years'], 'creatinine': [200.0, 'mmol/L']}",0.0087,0.00826,0.00913,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 49 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 200.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from mmol to mg. The mass of Serum Creatinine is 200.0 mmol. To convert 200.0 mmol of Serum Creatinine to mol, multiply by the conversion factor 0.001, giving us 200.0 mmol Serum Creatinine * 0.001 mol/mmol = 0.2 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.2 mol Serum Creatinine * 113.12 g/mol = 22.624 g Serum Creatinine. To convert 22.624 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 22.624 g Serum Creatinine * 1000.0 mg/g = 22624.0 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 22624.0 mg Serum Creatinine/10.0 dL = 2262.4 mg Serum Creatinine/dL. The concentration value of 200.0 mmol Serum Creatinine/L converts to 2262.4 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2262.4/0.9)**-1.2 * 0.9938**49 * 1.0 = 0.0087.
Hence, the GFR value is 0.0087 ml/min/1.73 m²."
465,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5381035-1,Extracted,"The patient was an 81-year-old Caucasian woman with a history of persistent right-sided flank pain with no associated symptoms including dysuria, hematuria, frequency, or urinary retention. She had no history of prior abdominal surgery, trauma, or congenital defects. Given the unclear etiology, we obtained cross-sectional imaging which demonstrated a right-sided Bochdalek diaphragmatic hernia incarcerating her proximal ureteral segment (Fig. ). Initially, she was managed conservatively with surveillance monitoring since her pain was tolerable and her renal function was preserved. Although her kidney function remained unchanged, follow-up imaging at the next visit surprisingly demonstrated an interval increase in hydroureteronephrosis (Fig. ). Additionally, the entrapped ureteral portion had progressed with now obvious hydronephrosis of the renal pelvis. A Tc-99m MAG-3 nuclear medicine renal scan with furosemide confirmed our suspicion – she had moderate obstruction of the right kidney. This study also demonstrated an asymmetric split function with 64% left and 36% right in the setting of a stable baseline creatinine (0.7mg/dL).
In attempt to reduce the entrapped ureter and unobstruct the right kidney, a double-pigtail ureteral stent was endoscopically placed. We were able to reduce the herniation with the use of a super stiff wire and a standard soft stent was placed in the usual retrograde fashion. During her stent exchanges, it became apparent that the herniated ureteral segment was enlarging as the curl of the double-J stent retracted into the distal ureter requiring ureteroscopy to visualize and engage. Longer stents were used to ensure that the distal curl remained in the bladder lumen despite recurrent herniation. Stiffer stents were also used however these maneuvers eventually were no longer able to straighten and reduce the ureter, leaving it entrapped in the thoracic cavity. After several stent exchanges were completed, the patient became symptomatic with ureteral stent discomfort including flank pain, urinary frequency and urgency. Due to concern that her diaphragmatic defect was enlarging, we discussed definitive surgical options with her; nephrectomy versus resection and anastomoses of her right ureter with diaphragmatic hernia repair. She ultimately opted to preserve her right kidney and proceed with open-resection reduction and repair.
We approached her open surgical repair through a standard supra-11 incision carried down through her flank muscles where we entered the retroperitoneal space. First, we freed her affected kidney from the surrounding tissue and then identified the incarcerated ureteral segment using our previously placed stent. The redundant ureter was mobilized out of the diaphragmatic defect and returned to the retroperitoneal abdominal cavity. We closed her diaphragmatic defect using interrupted 0 silk sutures, and then excised the redundant proximal ureteral segment where we spatulated and reapproximated the proximal and distal ends. Last, we replaced the patient’s ureteral stent and completed the anastomosis over a 7-French x 26 cm double-J ureteral stent. Due to the dissection of the renal hilum and perinephric tissue, the kidney appeared to have more mobility. To help maintain proper drainage and reduce tension on the anastomosis, we performed a nephropexy, securing the posterior aspect of the kidney to the flank muscles with a 0 silk. From there, we performed the standard two-layered incision closure.
The patient had an uncomplicated post-operative course and was discharged home after regaining bowel function and returning to her baseline physical activity on post-operative day three. There were no complications during surgery or recovery. Two months later, we removed her ureteral stent and obtained follow-up imaging which demonstrated repair of the diaphragmatic defect without hernia recurrence (Fig. ). We also repeated the Tc-99m MAG-3 nuclear medicine renal scan, which now demonstrated normal clearance of the previously obstructed right kidney. Post operative creatinine was 0.7 mg/dL with no obstruction detected. Split cortical function was 54% left and 46% right; an improvement the patient’s preoperative findings.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [81, 'years'], 'creatinine': [0.7, 'mg/dL'], 'sex': 'Female'}",86.83349,82.49182,91.17516,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 81 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.7 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.7/0.7)**-0.241 * 0.9938**81 * 1.012 = 86.83349.
Hence, the GFR value is 86.83349 ml/min/1.73 m²."
466,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4323911-1,Extracted,"A 60-year-old male with type 2 diabetes mellitus of 5 years’ duration, on oral hypoglycemic drugs with good control of blood sugars and documented coronary artery disease with a baseline serum creatinine of 1.2 mg/dl, presented with intermittent fever, weight loss and anorexia of 2-month duration. There was no alteration in bowel habits, ecchymosis, purpura, chronic cough, long-standing headache and pain abdomen. On examination, he was hemodynamically stable, pallor was present and there was no edema or lymphadenopathy. Per-abdomen, cardiovascular and respiratory system examinations were unremarkable. On evaluation, he had hemoglobin of 8 g/dl and peripheral smear showed normocytic and normocytic picture. Total leukocyte and platelet counts were 6900/μl and 2.5 × 105/μl, respectively. Alanine transaminase, aspartate transaminase, serum albumin, total bilirubin and alkaline phosphatase were 28 U/L, 16 U/L, 4 g/dl, 0.4 mg/dl and 97 U/L, respectively. Renal functions were deranged with serum creatinine and blood urea nitrogen of 8.5 mg/dl and 235 mg/dl, respectively. However, his urine output was adequate. Serum uric acid was high (13 mg/dl) and lactate dehydrogenase was elevated (1400 IU/dl). Serum protein electrophoresis didn’t reveal monoclonal proteins. Urine analysis showed 1+ albumin and no red blood corpuscles or white blood cells. Twenty-four hour urinary protein was 500 mg/dl. Ultrasound of kidney ureter bladder showed right kidney of 12.3 cm and left kidney of 12.4 cm with echogenic contents suggestive of calculi. Both kidneys were globular in outline with raised cortical echotexture. Antinuclear antibody (by immunofluorescence), anti-neutrophilic cytoplasmic antibodies (by immunofluorescence and ELISA) were negative. Complement factor 3 and 4 were 108 mg/dl and 44 mg/dl, respectively. Hepatitis B surface antigen, human immunodeficiency virus-I/II and anti-hepatitis C viral serology were negative. With a provisional diagnosis of rapidly progressive renal failure (RPRF), kidney biopsy was done.
Histopathological examination revealed [] diffuse interstitial infiltration with lymphomatous cells with morphology suggestive of high-grade non-Hodgkin's lymphoma (NHL) and immunohistochemistry showed [] CD20 positivity of the lymphomatous cells, suggestive of diffuse large B-cell, non-Hodgkin's lymphoma (DLBCL). To further characterize the disease, positron emission tomography-computed tomography (PET-CT) was done, which demonstrated avid flurodeoxy glucose (FDG) uptake in enlarged left and right kidneys with standardized uptake value (SUV) max of 18.5 and 9.5, respectively. A note was made of 9 mm calculus in left kidney lower calyx. Avid FDG uptake was also seen in multiple hypodense areas in both lobes of liver (SUV max 13.8), largest being 7.9 cm × 5.5 cm in the left lobe [] and intense patchy uptake in the bone marrow of multiple bones in axial and appendicular skeleton. Bone marrow examination did not reveal any infiltration with lymphomatous cells. Patient was diagnosed as extranodal NHL, in the form of PRL with RPRF and secondary hepatic involvement. His disease was staged as IV BE according to Ann Arbor staging system and his international prognostic index score was 5/5. Chemotherapy was initiated with rituximab, cyclophosphamide, hydroxydaunorubicin, vincristine and prednisolone (R-CHOP) regimen. Twenty days post-chemotherapy, patient's well-being improved; he became afebrile and his serum creatinine came down to 1.2 mg/dl from 8.5 mg/dl.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [60, 'years'], 'creatinine': [1.2, 'mg/dL'], 'sex': 'Male'}",69.23113,65.76957,72.69269,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 60 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.2 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.2/0.9)**-1.2 * 0.9938**60 * 1.0 = 69.23113.
Hence, the GFR value is 69.23113 ml/min/1.73 m²."
467,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-9608,Extracted,"A 54-year-old man presents to the emergency department with a severe diffuse abdominal pain, nausea, and vomiting. The patient states that the pain acute onset approximately 3 hours ago and has not improved. He denies any fever or chills. His last bowel movement was yesterday morning which was normal. The patient has a history of hypertension and infectious endocarditis 7 years ago. Current medications are hydrochlorothiazide and lisinopril. Patient denies any history of gastrointestinal disease although notes he frequently has abdominal discomfort after meals. Vital signs are as follows: blood pressure 150/90 mm Hg, heart rate 87/min, respiratory rate 22/min, and temperature of 37.4℃ (99.3℉). On physical examination, the patient is agitated and appears to be in significant pain. Lungs are clear to auscultation. The cardiac exam is significant for a 2/6 pansystolic grade murmur best heard at the apex and the presence of a pulse deficit. The abdomen is soft and nondistended, but there is tenderness to palpation in the periumbilical region. No rebound or guarding. Bowel sounds are present.
Laboratory tests show the following results:
RBC count 4.4 x 106/mm3
Hemoglobin 12.9 g/dL
Hematocrit 35%
Leukocyte count 12,400/mm3
Platelet count 312,000/mm3
Serum:  
Na+ 140 mEq/L
Cl- 103 mEq/L
K+ 4.4 mEq/L
HCO3 20 mEq/L
Base deficit -4
BUN 11 mg/dL
Glucose 97 mg/dL
Creatinine 1.1 mg/dL
Ca2+ 10.7 mg/dL
Lactate 7.6 mmol/L
Amylase 240 U/L
Stool guaiac negative
EKG is significant for findings consistent with atrial fibrillation and left ventricular hypertrophy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [54, 'years'], 'creatinine': [1.1, 'mg/dL'], 'sex': 'Male'}",79.7726,75.78397,83.76123,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 54 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.1/0.9)**-1.2 * 0.9938**54 * 1.0 = 79.7726.
Hence, the GFR value is 79.7726 ml/min/1.73 m²."
468,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5920258-1,Extracted,"A 44-year old female presented to our centre in late 2015 with bilateral lower limb pain and weakness following trivial trauma. She was known to have Type 1 renal tubular acidosis on regular follow-up with the nephrology unit since the age of 35. Prior to the admission, the patient was ambulating mostly independently with an occasional walking aid due to left hip pain. Unfortunately, a trivial fall landing in the sitting position following a vasovagal episode had rendered the patient immobile. On arrival at the emergency unit, she was conscious and alert. Though her vital signs were found to be normal, she appeared lethargic, albeit able to converse and give a full history. Clinically, systemic examination was unremarkable except for tenderness over both hip regions. Her main initial investigations suggested metabolic acidosis with a blood pH of 7.220 and bicarbonate of 14.4mmol/L. Total white blood count was elevated at 17 x 103 mmol/L. Renal profile revealed mild dehydration with a blood urea of 4.7 mmol/L and blood creatinine at 127 mmol/L, which was later corrected during her admission. Her potassium level was normal at 3.9mmol/L. She had hypocalcemia at 1.60mmo/l and hypophosphatemia at 0.59mmol/l. Albumin levels were normal at 35g/dl, but alkaline phosphatase (ALP) was mildly elevated.
All investigations pointed towards poor control of her renal tubular acidosis leading to a systemic metabolic state with hypocalcemia and hypophosphatemia. The raised ALP was likely due to increased osteoblastic activity, a result of the osteomalacia. Further history taking revealed that the patient had not been compliant with the Shohl’s solution (mixture of citric acid and sodium citrate) which was prescribed by the nephrologist, claiming it to be distasteful. Further history revealed a previous fracture neck of left femur in 2010 which had been managed with internal fixation. Poor compliance to her RTA treatment was established after a thorough review. Despite suffering from a chronic renal disorder, the patient had no evidence of renal failure as the glomerular function was normal with no uremia. Therefore, we decided to distance the patient’s case from that of those with chronic renal failure with renal osteodystrophy.
Plain radiographs () revealed left intertrochanteric fracture with previous screw fixation for fracture of neck of left femur intact, with a contralateral right neck of femur fracture. While awaiting surgery, she was co-managed by a multi-speciality team which included the orthopaedic, nephrology and medical unit. Bilateral lower limb skin traction was applied till the day of surgery.
The bilateral proximal femoral fractures were treated surgically. A right total hip arthroplasty and left proximal femur nail (Synthes A2) fixation were performed in one setting. We performed a right total hip arthroplasty as the fracture involved an intracapsular component. As for the left sided extracapsular intertroncteric fracture, an intramedullary internal fixation was deemed best in view of the healed previous neck of femur fracture. The decision also was influenced by the need to provide primary stability in either limb to allow early rehabilitation, thus the decision for right total hip arthroplasty. The patient had an uneventful surgery and recovery and was discharged well with regular follow ups in the clinic to monitor progress with plain radiographs (). Awareness of the patient's current condition as well as emphasis over the importance of compliance were ensured to obtain good control of her RTA. At just over a year, patient had became independently ambulatory.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [44, 'years'], 'creatinine': [127.0, 'mmol/L'], 'sex': 'Female'}",0.01159,0.01101,0.01217,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 44 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 127.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from mmol to mg. The mass of Serum Creatinine is 127.0 mmol. To convert 127.0 mmol of Serum Creatinine to mol, multiply by the conversion factor 0.001, giving us 127.0 mmol Serum Creatinine * 0.001 mol/mmol = 0.127 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.127 mol Serum Creatinine * 113.12 g/mol = 14.36624 g Serum Creatinine. To convert 14.36624 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 14.36624 g Serum Creatinine * 1000.0 mg/g = 14366.24 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 14366.24 mg Serum Creatinine/10.0 dL = 1436.624 mg Serum Creatinine/dL. The concentration value of 127.0 mmol Serum Creatinine/L converts to 1436.624 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1436.624/0.7)**-1.2 * 0.9938**44 * 1.012 = 0.01159.
Hence, the GFR value is 0.01159 ml/min/1.73 m²."
469,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4550805-1,Extracted,"A 27-year-old Latina woman received a living related transplant from her mother for end stage renal disease (ESRD) secondary to advanced lupus nephritis and presented with nephrotic range proteinuria 6 months after transplantation.
The patient was diagnosed with systemic lupus erythematosus (SLE) at age of 17. During the course of the disease she fulfilled the American College of Rheumatology (ACR) criteria including malar rash, arthritis, pericarditis, class IV/V lupus nephritis, leucopenia, lymphopenia, and positive antinuclear (ANA) and anti-double-stranded DNA (anti-dsDNA) antibodies. The patient's lupus nephritis was treated with glucocorticoids, multiple doses of cyclophosphamide, mycophenolate mofetil, and rituximab. Despite aggressive treatment, she progressed to ESRD and required renal transplantation. She received a kidney from her mother, which was donor/recipient CMV +/−. The patient has been negative for anti-Ro, anti-La, anti-Sm, anti-RNP, β2 glycoprotein I, and lupus anticoagulant. The anticardiolipin antibody (ACLA), although reported as positive at one occasion which prompted the use of aspirin for prophylaxis, has been consistently negative ever since. She also has a history of hypertension and hypothyroidism due to Hashimoto's thyroiditis.
The surgery and hospital course after transplantation were uneventful and the patient was discharged with excellent urine output and creatinine level of 1.0 mg/dL. Six months later she developed nephrotic range proteinuria at 4.6 mg/mg () and her creatinine levels progressively rose to 2.5 mg/dL. However, she lacked edema, hypoalbuminemia, and hypercholesterolemia. Her medications at the time included tacrolimus, 4 mg in the morning and 3 mg in the evening, mycophenolate mofetil 500 mg bid, prednisone 5 mg/d, hydroxychloroquine 200 mg bid, enalapril 10 mg/d, aspirin 81 mg/d, trimethoprim-sulfamethoxazole 400–80 mg/d, valganciclovir HCl 450 mg/d, levothyroxine 0.15 mg/d, and omeprazole 20 mg/d. A kidney biopsy was performed that showed minimal glomerular change by light microscopy and diffuse podocyte foot process effacement by electron microscopy, consistent with MCD (Figures and ). There was no evidence of acute cellular, antibody-mediated, or vascular rejection or immune-complex-mediated glomerulonephritis. In particular, immunofluorescence exam did not reveal significant glomerular staining for IgG, IgA, and C3. There was granular glomerular staining in mesangial regions and capillary loops for 1+ IgM while the tubulointerstitial compartment was negative for immunoglobulins or complement components. Arteries and arterioles stained 1+ for C3 but peritubular capillaries were negative for C3d and C4d. The serum C3 and C4 levels were within the normal range and anti-dsDNA antibody was 1+. Consequently, she received pulse methylprednisolone followed by oral prednisone to treat presumed MCD. She did not respond to treatment, while two additional subsequent renal biopsies were also consistent with MCD. In the following 12 months the patient developed several episodes of acute renal failure characterized by increasing proteinuria and creatinine levels that were attributed to dehydration. Her serum albumin levels decreased down to 2.7 g/dL secondary to ongoing protein loss in urine. However, this effect was transient and coincided with one of the peaks of her proteinuria (7.5 g). Otherwise, her albumin during this course usually ranged between 3 and 4 g/dL. Multiple ultrasounds of the kidney were performed. Initially they were normal showing patent renal artery and vein with good perfusion of the transplant on color and power Doppler. However, subsequently the studies exhibited mild hydronephrosis of the transplant kidney and turbulence in the right external iliac vein proximal to the attachment of the transplanted renal vein that was suggestive of narrowing. Eventually, because of worsening proteinuria and creatinine (9.7 mg/mg and 3.4 mg/dL, resp.), magnetic resonance imaging (MRI) of the pelvis without contrast was done for further investigation and revealed diminished signal intensity in the right iliac artery. A subsequent angiogram revealed a normal right iliac artery and renal transplant arterial anastomosis but outlined stenosis of the right external iliac vein adjacent to the transplant anastomosis with a pressure gradient of 7 mmHg between the common iliac vein and the external iliac vein. Balloon angioplasty of the right external iliac vein partially corrected the stenosis with a postangioplasty gradient of 2-3 mmHg. A few weeks later recurrent renal dysfunction necessitated a second venogram that showed restenosis and culminated in angioplasty and stent placement with pressure gradient improving from 10 mmHg to 0. After the stent deployment and dilation to 12–14 mm in diameter, a thrombus was identified within the stent which was aspirated. There was no thrombus seen prior to stenting which leads to the assumption that this was a procedure-related complication. Subsequently, the patient received one month of renally dosed enoxaparin as prophylaxis to decrease the possibility of in-stent thrombosis. Following the procedure, the proteinuria and creatinine levels steadily declined and reached her baseline of 300 mg/day and 1.5 mg/dL, respectively, at one-year follow-up ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [27, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Female'}",48.67991,46.24591,51.11391,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 27 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.5 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.5/0.7)**-1.2 * 0.9938**27 * 1.012 = 48.67991.
Hence, the GFR value is 48.67991 ml/min/1.73 m²."
470,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4279845-1,Extracted,"A 59-year-old female visited an emergency room of Gachon University Gil Medical Center due to dyspnea that had lasted for five days. The initial blood pressure in her right arm was 220/100 mmHg, and her respiration rate was 40 breaths per minute. Chest radiography revealed cardiomegaly, a prominent aortic notch, and pulmonary edema, which explained her tachypnea and arterial hypoxemia (). The laboratory data was as follows: creatine kinase-MB, 1.20 ng/mL; troponin I, 0.08 ng/mL; brain natriuretic peptide, 5,850 pg/mL; creatinine, 1.3 mg/dL; C-reactive protein, 12.30 mg/L; and an erythrocyte sedimentation rate of 1.1 mm/hr. An electrocardiogram showed sinus tachycardia with a Q wave on V1, ST segment elevation from V1 to V3, and T wave inversion on anterior precordial and inferior limb leads. Echocardiography showed akinesia of the anterior wall anteroseptum, and inferoseptum from the low middle left ventricle to the apex with thinning and a preserved ejection fraction of 50% with left ventricular hypertrophy. The medical history taken from the patient’s family revealed that she had been diagnosed with hypertension, Takayasu’s arteritis, and cerebral infarction at another hospital fifteen years ago. In addition, an aortic bypass graft procedure carried out to treat thoracic aortic stenosis 15 years ago. When the patient presented to an emergency room of Gachon University Gil Medical Center she had left hemiparesis as the sequel of her previous stroke.
Computed tomography revealed severe stenosis in the descending thoracic aorta and diffuse circumferential wall calcifications (). Wall thickening was also observed in the distal portion of the aortic arch and in the left common carotid artery. Between the proximal descending thoracic aorta and supraceliac abdominal aorta, there was a bypass graft, which had a 3-cm pseudoaneurysm at the proximal anastomosis and severe luminal stenosis at its proximal segment.
Endovascular repair was performed to treat the pseudoaneurysm and graft stenosis simultaneously. Under general anesthesia, the descending aorta was accessed via a right common femoral artery puncture. After the narrowed proximal portion of the graft was dilated with a 12×4 cm balloon catheter (Ultrathin; Boston Scientific, Natick, MA, USA), a tapered stent graft (proximal diameter 32 mm, distal diameter 24 mm, length 10 cm; Seal, S&G Biotech Co., Seongnam, Korea) was implanted from the proximal descending aorta into the bypass graft. The bare stent portion of the stent graft was deployed proximally to the left subclavian artery. To relieve the stenosis at the middle portion of the graft, a bare metal stent 28 mm in diameter and 8 cm in length (Hercules; S&G Biotech Co.) was implanted. The absence of a pressure gradient between the stent graft and the distal native aorta was confirmed before the catheter and sheath were removed.
The patient was extubated three days after the endovascular stent graft procedure. Postoperative computed tomography showed good stent graft patency in the descending thoracic aorta and that the pseudoaneurysm was thrombosed ().
The patient was discharged uneventfully with no pressure difference between the right arm and the legs. She showed no complications for three years after the stent graft procedure, and a follow-up computed tomography scan showed that the graft was patent and that the size of the pseudoaneurysm remained unchanged.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [59, 'years'], 'creatinine': [1.3, 'mg/dL'], 'sex': 'Female'}",47.36909,45.00064,49.73754,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 59 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.3 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.3/0.7)**-1.2 * 0.9938**59 * 1.012 = 47.36909.
Hence, the GFR value is 47.36909 ml/min/1.73 m²."
471,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5907197-1,Extracted,"A 52-year-old Chinese female farmer was referred to our hospital in August 2014 because of bilateral leg swelling since approximately 2 weeks. She had a history of malar rash and intermittent generalized arthralgia since 3 months. She also had a history of right thyroid papillary carcinoma, for which subtotal thyroidectomy was performed in 2009. Postoperatively, she was administered L-Thyroxine therapy and was followed up annually. The dosage of L-Thyroxine at admission was 50 μg daily. She was a non-smoker and had developed menopause at the age of 50 years. The family history was unremarkable. Physical examination showed a blood pressure of 130/80 mmHg, malar rash, clear breath sounds, normal heart sounds, and grade 3 lower-extremity pitting edema. There was no redness or swelling over joints. Her serum creatinine level was 1.37 mg/dL (121 μmol/L); serum albumin level was 2.3 g/dL (23 g/L); white blood cell (WBC) count was 2700/μL; lymphocyte count was 600/μL. Urinary protein excretion was 5.3 g/d. Serological tests for antinuclear antibody (ANA; 1:320, speckled pattern), anti-Smith (Sm) antibody, and anti-SS-A antibody were positive. Antineutrophil cytoplasmic antibody (ANCA), hepatitis B surface antigen, and hepatitis C antibody were negative. She had low serum complement levels (C3, C4). Anti-streptolysin O titer, and rheumatoid factor were within normal range. Urine microscopy showed 20–30 red blood cells and 3–8 WBCs per high-power field. Electrocardiogram, chest radiograph and kidney ultrasound were unremarkable.
Based on clinical and laboratory findings, a diagnosis of SLE, lupus nephritis (LN) and nephritic syndrome was established. One week later, a percutaneous renal biopsy was performed. Light microscopy showed that there were 38 glomeruli, with a mild increase in mesangial cellularity and mesangial matrix. There were no signs of endocapillary proliferation. Glomerular basement membranes were thickened and spikes were noticed on Jones silver staining (Fig. a, b). On immunoflurescence examination, the mesangium and glomerular capillary wall were found positive for IgG (3+), IgA (1+), IgM (2+), C3 (2+), C1q (2+), and FRA (1+). Electron microscopy showed irregular thickening of the glomerular basement membranes, mesangial hypercellularity, proliferation of the mesangial matrix, and electron-dense subepithelial, intramembranous, subendothelial and mesangial deposits. These findings were consistent with Class V + IV(G)-A lupus nephritis.
After the diagnosis, we instituted treatment with intravenous methylprednisolone 500 mg/d for 3 days, followed by 1 mg/kg oral prednisolone daily. In addition, she received omeprazole (20 mg, twice a day), rocaltrol (0.25 μg, once a day), and caltrate D (300 mg, twice a day) for symptomatic treatment. Ten days after treatment, the WBC counts were restored to normal levels. Subsequently, intermittent intravenous cyclophosphamide treatment was added. After four-week treatment, the edema was largely resolved; her serum albumin level was 2.4 g/dL (24 g/L) and her urinary protein excretion was 4.0 g/d. She was discharged from the hospital and followed up monthly. Eight months later, her urinary protein excretion was 1.2 g/d, serum creatinine level was 1.1 mg/dL (97 μmol/L), and serum albumin level was 3.0 g/dL (30 g/L). There was no recurrence of rashes or arthralgia. Her condition continued to improve for about 15 months (until November 2015), at which time, the dosage of prednisolone was 12.5 mg daily and that of total cyclophosphamide was 8 g. Then she experienced exacerbation of symptoms with exertional dyspnea and frequent cough and sputum. She was hospitalized again. Sputum culture showed streptococcus pneumoniae and thoracic computed tomography revealed numerous well-defined cysts (Fig. ). Meanwhile, she developed recurrence of lupus nephritis. We instituted prednisolone 1 mg/kg daily combined with mycophenolate mofetil 0.75 g twice a day after the control of infection. A diagnosis of pulmonary LAM was made based on lung biopsy performed at another hospital (Fig. ). Patient only agreed to receive symptomatic treatment, i.e., oxygen supplementation, ipratropium and acetylcysteine. The patient refused to receive sirolimus and estrogen. In the following years, lupus nephritis was stable (partial remission); her serum creatinine level was 1.45 mg/dL (128 μmol/L), serum albumin concentration was 2.9 g/dL (29 g/L), and urine protein to creatine ratio was 2.3. The dosage of oral prednisone was 20 mg daily and mycophenolate mofetil was 0.5 g twice a day. However, she experienced progressive dyspnea. CT re-examination confirmed progressive multiple thin-walled pulmonary cysts and bullae in both lungs, along with interstitial pulmonary fibrosis (Fig. ). She died in December 2016 due to severe respiratory failure and cor pulmonale.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [52, 'years'], 'creatinine': [1.45, 'mg/dL'], 'sex': 'Female'}",43.40028,41.23027,45.57029,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 52 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.45 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.45/0.7)**-1.2 * 0.9938**52 * 1.012 = 43.40028.
Hence, the GFR value is 43.40028 ml/min/1.73 m²."
472,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8517457-1,Extracted,"An 81-year-old male presented to our emergency department (ED) with painless post-prandial epigastric discomfort for five days. He had a 12-year history of RCC, chronic obstructive pulmonary disease, hypertension, and chronic renal failure. The patient was receiving chemotherapy for RCC. A month ago, he has taken 40 mg of methylprednisolone for chronic obstructive pulmonary disease exacerbation for 3 days, and he was on 5 mg of axitinib (Inlyta; Pfizer, New York, NY, USA) daily for the past year. His vital signs were within the normal range. Apart from elevated blood urea nitrogen (55.5 mg/dL, 9.0–23.0 mg/L) and creatinine (1.7 mg/dL, 0.7–1.3 mg/dL) levels, his blood tests (complete blood count with differential count, liver function tests, coagulation tests, electrolytes, and lactate level, etc.) were within normal ranges. Plain abdominal radiography and abdominal computed tomography (CT) without contrast revealed diffuse PI, predominantly in the jejunum, with a large amount of intra-abdominal free air (). Following a suspicion of bowel perforation, an exploratory laparotomy was performed. However, during the operation, we only found PI, which occupied 20 cm of the bowel wall 1 m away from the ileocecal valve without ischemic changes or bowel perforation (). On postoperative day (POD) 4, the patient started eating soft foods and did not develop any complications. On POD 8, plain abdominal radiography was performed, which showed the absence of any free air. However, the patient developed diarrhea after resuming foods. On POD 17, abdominal CT was repeated, which showed the absence of PI or pneumoperitoneum. The patient was discharged on POD 34 without any complications.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [81, 'years'], 'creatinine': [1.7, 'mg/dL'], 'sex': 'Male'}",39.99991,37.99991,41.99991,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 81 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.9)**-1.2 * 0.9938**81 * 1.0 = 39.99991.
Hence, the GFR value is 39.99991 ml/min/1.73 m²."
473,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7402428-1,Extracted,"A 63-year old female was referred to our hospital with progressively increasing shortness of breath for 15 days. She was being treated as a community-acquired pneumonia patient at some other hospital. Her course of illness at that hospital was complicated with the development of right-sided hydropneumothorax, for which she had underwent right-sided tube thoracostomy. Her condition did not improve, and she was referred to our hospital. On presentation her blood pressure was 110/60 mmHg, pulse was 110/min, and oxygen saturation was 95% on 10 L of oxygen. She had severe subcutaneous emphysema on face and chest. There was a chest tube placed on the right side. On chest auscultation bilateral crackles were audible. Rest of the examination was unremarkable. She was a known case of hypertension and poorly controlled diabetes mellitus, her glycated hemoglobin (HbA1c) on admission was 8.7%. She was on metformin and Humulin N. During hospitalization her blood sugar remained elevated for which Insulin Glargin 24 units was added with increased dose of Humulin N. There was no prior history of diabetic neuropathy, retinopathy, or nephropathy.
On presentation her complete blood count showed hemoglobin of 12.7 g/dL and white cell count of 14.8 x 103/L with 84.4% neutrophils. Blood urea nitrogen was 15 mg/dL, creatinine was 1.0 mg/dL, and random blood sugar was 294 mg/dL. Chest radiograph revealed significant subcutaneous emphysema with right-sided pneumothorax, pneumomediastinum along with pneumopericardium (Figure ). High resolution computed tomography (HRCT) scan confirmed pneumothorax with pneumomediastinum, pneumopericardium, right-sided necrotizing consolidation, and mal-positioning of chest tube (Figure ).
The patient was started on piperacillin/tazobactam, vancomycin, and a new chest tube was inserted on the right side. Due to no improvement in her condition, surgical intervention was planned. The patient refused surgical intervention and was discharged home on IV antibiotics with chest tube on suction. She again presented 10 days later with fever and purulent discharge from the chest tube. Pus was sent to laboratory for Gram stain and culture. Antibiotics were changed to colistin and meropenem. Pleural fluid analysis showed total leukocyte count of 99020/cu mm with 90% polymorphs and glucose of 7 mg/dL. Gram stain of pleural pus revealed numerous pus cells and fungal hyphae on smear and culture grew Trichosporon spp. and Fusarium spp. Fusarium spp. was identified based on phenotypic gross and microscopic morphology, while Trichosporon spp. was identified to genus level based on colony morphology, urease production, and microscopic morphology on corn meal agar. Susceptibility testing for both organisms was not performed. No bacterial growth was obtained on sputum, blood, and pleural culture. As tuberculosis is endemic in Pakistan, she was also evaluated for TB and mycobacterial culture was negative.
Amphotericin B deoxycholate was started and antibiotics were stopped after the third day of admission. Empyema was drained through chest tube and the chest tube was kept in place for eight weeks. She became afebrile after initiation of antifungal but developed acute kidney injury, electrolyte imbalance, and vomiting. Amphotericin B was replaced with voriconazole 200 mg twice daily which was continued for eight weeks. She tolerated the treatment very well and her condition improved gradually, and the chest tube was successfully removed after eight weeks. Follow up chest radiograph showed significant improvement (Figure ).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [1.0, 'mg/dL'], 'sex': 'Female'}",63.30282,60.13768,66.46796,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 63 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.0/0.7)**-1.2 * 0.9938**63 * 1.012 = 63.30282.
Hence, the GFR value is 63.30282 ml/min/1.73 m²."
474,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2917397-1,Extracted,"A 77 year old Caucasian female presented to emergency room on 09/06/2009 with left sided chest pain of three days duration. Her pain was sharp, 8/10 in intensity, nonexertional, radiated to interscapular region, and initially relieved by over the counter medications. She denied any fever, cough, nausea, vomiting, diaphoresis, shortness of breath and, palpitation. Other review of systems was unremarkable.
Past medical history included hypertension, dyslipidemia, obstructive sleep apnea, atrial fibrillation and coronary artery disease. She had bare metal stent placement in left anterior descending artery in 06/09, angioplasty for in stent restenosis in 08/09 and a pacemaker implantation for sick sinus syndrome on 09/01/2009. Her medications included lisinopril, atenolol, simvastatin, aspirin, clopidogrel, warfarin, and dofetilide.
On physical examination she was morbidly obese, was in moderate distress. Her vital signs included temperature of 98.7°F, pulse rate 63/minute, regular in rate and rhythm, blood pressure (BP) 141/62 mmHg, respiratory rate (RR) 18/min SpO2 97%, jugular venous pressure (JVP) was not elevated and there was no pulsus paradoxsus. Auscultation of heart and lungs was unremarkable. Examination of other systems was normal.
Admission electrocardiogram (EKG) revealed new T wave inversions in the lead II, III, AVF and QS complexes and T wave Inversions in V1-V6 as seen in the previous EKG (Fig. ). Admission chest X-ray showed normal cardiac silhouette with presence of pacemaker leads, normal lung fields and mediastinum.
Her initial set of cardiac enzymes, complete blood count (CBC), basic metabolic panel (BMP) and urine analysis were normal. She was admitted with diagnosis of unstable angina. Treatment with heparin, eptifibatide and nitroglycerine was begun. Her repeat EKG on 09/07/09 showed ST depressions in the inferior leads, repeat cardiac enzymes were normal, however her chest pain continued to persist. 2D Echocardiogram (ECHO) on 09/07/09 revealed ejection fraction (EF) of 65%, without any pericardial effusion. Chest pain continued to persist, became hypotensive and oliguric, blood pressure medications were with held. Repeat CBC and BMP revealed elevated WBC 15,800/μl and hemoglobin of 9.4 gm/dl. Serum creatinine changed from 1.13 to 3.01 and blood urea nitrogen increased from 29 to 53. Urine analysis revealed 15-20 white blood cells per high power field (HPF), positive leukocyte esterase and nitrite, 5-10 red blood cells per HPF.
In view of leucocytosis, increased renal parameters and pyuria septic shock secondary to urinary tract infection was considered and transferred to Intensive care unit (ICU). After fluid resuscitation, broad spectrum antibiotics were intiated. On 09/09/09 in ICU the patient was in distress and continued to have chest pain. Vital signs were significant for pulse rate 90/min, regular, BP 70 mmHg, RR of 22/min, SpO2 95%. Auscultation of heart and lungs was unremarkable. Central venous pressure was 15 cm of water. Intravenous vasopressor therapy was intiated. As her chest pain continued to persist, a non-contrast computerized tomography (CT) of the chest was done which revealed hemorrhagic pericardial effusion (Figs. and ) with lead perforation of the right atrium which was subsequently confirmed by 2D ECHO (Fig. )
She underwent pericardial window for drainage and evaluation of lead perforation. During surgery the screw in right atrium had gone through the right atrial wall and caused the perforation. Surgeons over sew the atrial wall and drained 200 cc of pericardial fluid. Her post operative recovery was uneventful and discharged home on the fifth day.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [77, 'years'], 'creatinine': [3.01, 'mg/dL']}",15.46426,14.69105,16.23747,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 77 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 3.01 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (3.01/0.7)**-1.2 * 0.9938**77 * 1.012 = 15.46426.
Hence, the GFR value is 15.46426 ml/min/1.73 m²."
475,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5882333-3,Extracted,"A 76-year-old man was referred to our hospital that was diagnosed with HCV GT1b infection and nephrotic syndrome 11 years ago. He did not have surgery, blood transfusions, tattoos, or abuse of drugs at that time. He did not drink alcohol and had no family history of HCV infection. He had a medical history of drug-induced liver injury of benzbromarone [–] and received a transfusion for renal anemia 9 years ago.
He received dialysis shunt surgery on the left forearm in 2015. He was an interferon-treatment naïve patient. He was treated with HCV NS5A inhibitor ombitasvir (25 mg)/HCV NS3/4A inhibitor paritaprevir (150 mg)/ritonavir (100 mg) daily in 2016 []. However, this treatment was discontinued on day 12 because of renal dysfunction (serum creatinine 8.23 mg/dL) with hyperpotassemia (serum potassium 5.6 mEq/L). HCV RNA disappeared at week 4 but relapsed on week 8 after stopping the treatment. Renal dialysis was performed three times weekly one month later after stopping the treatment (Figure ).
The laboratory data at the start of retreatment are shown in Table . He had no sign of cirrhosis. HCV NS5A-L31 and -Y93 sequencing using a real-time PCR system and a cycling probe assay [] revealed he had no HCV NS5A RASs. He began retreatment with grazoprevir (100 mg daily) and elbasvir (50 mg daily) at 13 months after the initial DAA treatment. He also took ursodeoxycholic acid (600 mg daily), rabeprazole sodium (10 mg daily), carvedilol (10 mg daily), losartan potassium (2.5 mg daily)/hydrochlorothiazide (12.5 mg daily) and febuxostat (10 g daily). He received full doses of both grazoprevir and elbasvir for 12 weeks, and no adverse events were observed. RVR and SVR12 were achieved (Figure ).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [76, 'years'], 'creatinine': [8.23, 'mg/dL']}",6.2176,5.90672,6.52848,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 76 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 8.23 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (8.23/0.9)**-1.2 * 0.9938**76 * 1.0 = 6.2176.
Hence, the GFR value is 6.2176 ml/min/1.73 m²."
476,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5478768-1,Extracted,"A 45-year-old woman with hypothyroidism and hypertension and a history of chronic kidney disease had presented with chronic diarrhea and weight loss of 10 kg for the past 8 months. She had anemia, and her hemoglobin level was 10.3 g/dL; total leukocyte count was 7,600×103/dL; and platelet count was 2.34×103/dL. She also exhibited impaired renal function with BUN and creatinine levels of 67 mg/dL and 2.1 mg/dL, respectively. She had hypoalbuminemia with an albumin level of 2.7 g/dL. The results of the liver function test were normal, and her total bilirubin level was 0.9 mg/dL; direct bilirubin level was 0.2 mg/dL; aspartate transaminase level was 26 IU/L; alanine transaminase level was 20 IU/L; and ALP level was 117 IU/L. Electrocardiograph showed left ventricular hypertrophy, and the chest radiograph showed no abnormalities. To determine the cause of diarrhea, we performed the routine stool examination and culture, which were noncontributory. Further, the results of serological examination for celiac disease (IgA anti-tissue transglutaminase antibody) were negative. Her upper gastrointestinal endoscopy revealed typical scalloping and grooving with nodularity (). Multiple samples were taken from the second part of the duodenum and biopsy was performed, which showed subtotal atrophy of the duodenal villous pattern (). The patient had been prescribed telmisartan 40 mg daily for hypertension for the past 1 year. After discontinuation of telmisartan and switching to amlodipine, diarrhea subsided, renal function improved, and significant weight gain was observed. Follow-up endoscopy showed normal duodenal folds 4 months after discontinuation of telmisartan.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [45, 'years'], 'creatinine': [2.1, 'mg/dL']}",29.06551,27.61223,30.51879,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 45 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.1 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.1/0.7)**-1.2 * 0.9938**45 * 1.012 = 29.06551.
Hence, the GFR value is 29.06551 ml/min/1.73 m²."
477,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3305563-1,Extracted,"A 69-years old male known for post alcoholic liver cirrhosis was admitted at the Division of Internal Medicine through the Emergency Room because of abdominal pain and distension, diarrhea and oliguria. Physical examination revealed abdominal distension because of severe ascites. Murphy and Blumberg signs were not evocable. Laboratory data showed: white blood cells 5.3 10^9/L; haemoglobin 12.6 g/dL; platelets 98 10^9/L; AST/ALT 66/90 U/L; PT ratio 1.10; aPTT ratio 0.92; total bilirubin 0.75 mg/dL; Albumin 41.8 g/L; α-Fetoprotein 249.6 ng/mL; Creatinine 1.06 mg/dL. Child-Pugh class was A7 (the patient took 2 points for ascites). An abdominal ultrasonography revealed severe ascites, multiple lesions in the left liver and absence of blood flow in the left portal vein branch. A paracentesis was then placed with drainage of 3 liters of clear ascites. The day following admission hematemesis and melena occurred due to bleeding from oesophageal varices: the patient underwent upper gastrointestinal endoscopy which revealed III grade blue varices, with red signs and with blood clots in the gastric fundus. Endoscopic band ligation of oesophageal varices was performed with success. Abdominal dynamic computed tomography (CT) revealed low density confluent lesions in all phases in the left lobe of the liver (Figure ), an hyper-enhanced portal vein during the arterial phase (Figure ) and a tumor thrombus in the left portal vein causing a filling defect (Figure ), ascites and splenomegaly. The patient was diagnosed with HCC with severe intratumoral APS, which caused portal hypertension that lead to oesophagogastric varices and hypersplenism. Since the main cause of the portal hypertension was the APS, transcatheter arterial embolization (TAE) was performed twice. The preliminary angiography confirmed the presence of APS (Figure ) and during the first TAE, branches coming from left hepatic artery were embolized (Figure ). When a control CT scan was performed, it revealed a persistent contrast enhancement of the APS (Figure ) that was refurnished from an arterial vessel coming from the left gastric artery (Figure ). A second angiography and subsequent embolization managed to stop APS refilling. Therefore, after two days a left hepatectomy was performed. Pathological examination revealed a trabecular HCC with satellitosis, vascular invasion and necrosis (pT3a, G3), a tumor thrombus in the left branch of the portal vein, and active cirrhosis in liver parenchyma. The postoperative course was complicated by mild signs of liver failure with ascites (about 700 mL die) which resolved after treatment with diuretics and iv administration of albumin (Grade II according to Dindo-Clavien classification of complications following surgery) []. The patient was discharged in postoperative day (POD) 16. The patient is alive and disease free at 8 months after left hepatectomy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [69, 'years'], 'creatinine': [1.06, 'mg/dL'], 'sex': 'Male'}",75.97012,72.17161,79.76863,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 69 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.06 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.06/0.9)**-1.2 * 0.9938**69 * 1.0 = 75.97012.
Hence, the GFR value is 75.97012 ml/min/1.73 m²."
478,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6669421-1,Extracted,"We report here a forty nine years old male who is a known case of hypertension, diabetes and end-stage renal disease secondary to membranous glomerulonephritis, and who remained in regular hemodialysis for two years before getting a cadaveric transplant. He had an induction with anti thymocyte globulin and was maintained on triple immunosuppressive regimen and his best creatinine post transplant was 1.4 m/dL. After 2 months, he came with productive cough, high grade fever and mild leukocytosis (WBC count of 11.3 x 103). On examination he was stable, conscious and oriented.
On chest examination, bronchial breathing was heard and the chest radiograph showed solid consolidations in the right upper lung lobe (). Subsequently performed, a high resolution CT chest depicted a mass-like consolidation in right upper lobe () measuring 7cm x 10 cm with air bronchogram. Bronchoscopy was performed and biopsies were taken, which revealed filamentous gram-stain positive bacteria. The sample was negative for Ziehl-Neelsen staining for acid fast bacillus. Polymerase chain reaction (PCR) for tuberculosis (TB) and subsequent culture for TB was negative. On routine TTE, the patient had a mobile mass (0.3 cm x 0.85 cm) attached to the posterior leaflet of mitral valve (). This was an incidental finding as pre-transplant TTE was normal. A PCR for Nocardia came out to be positive.
Based on the above mentioned studies, the patient was started on IV TMP-SMX (Trimethoprim- sulfamethoxazole) and Imipenem and this combination was continued for four weeks. Our patient received initial induction therapy with IV TMP-SMX (Trimethoprim- sulfamethoxazole) and Imipenem and this combination was continued for four weeks. The patient showed swift recovery, with frequent radiological imagings showing gradual improvement of lung consolidation. Intracardic mass disappeared after two weeks of treatment. Following the response to antibiotic therapy, the patient was kept on maintenance dose of oral TMP-SMX 960 mg once a day for six months.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [49, 'years'], 'creatinine': [1.4, 'mg/dL'], 'sex': 'Male'}",61.61357,58.53289,64.69425,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 49 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.4 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.4/0.9)**-1.2 * 0.9938**49 * 1.0 = 61.61357.
Hence, the GFR value is 61.61357 ml/min/1.73 m²."
479,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6639570-1,Extracted,"A 78-year-old woman underwent medical follow-up after surgery for bladder cancer, and a mass in the upper part of the pelvis was revealed by abdominal CT. She only had a history of hyperlipemia and had no history or family history of neurofibrosis and malignant diseases. She had no digestive symptoms, and her appetite had been normal. She had a soft abdomen and no pain, but the physical examination was positive for a 3-cm induration in the midline below the umbilicus. Laboratory findings included hemoglobin 11.8 g/dL, white blood cell count 6.2 × 103/μL, C-reactive protein 0.1 mg/dL, platelet count 252 × 103/μL, creatinine 0.67 mg/dL, alanine transaminase 21 U/L, and aspartate transaminase 23 U/L. They showed no abnormalities, and tumor markers (CEA: 0.1 ng/mL, CA19-9: 23 U/mL) were within normal limits. Enhanced abdominal CT demonstrated a 25 × 30 × 35 mm mass in the upper part of the pelvis, and the tumor was suspected to originate from the small intestine (Fig. ). No enlarged lymph nodes or distant metastases were demonstrated. Colonoscopy showed only polyps. Therefore, with the diagnosis of a submucosal tumor of the small intestine, possibly gastrointestinal stromal tumor (GIST), she underwent laparotomy, at which partial intestinal resection was performed with a mechanical side-to-side anastomosis with a 1-cm margin from the tumor. Intraoperatively, the tumor was palpated in the wall of the small intestine.
Pathologically, a hard submucosal tumor of 4.5 × 3.4 × 2.4 cm was detected macroscopically (Fig. ). Histologically, relatively uniform spindle-shaped cells were formed, in a palisading pattern, from the lamina propria to the subserous lamina of the small intestine. Immunohistochemical examination demonstrated that the tumor cells were positive for S100, and negative for αSMA, desmin, CD34, and c-Kit (Fig. ). The MIB1 index was low, and no findings indicating malignancy were observed. Hence, the tumor was diagnosed as schwannoma, and the patient was discharged 10 days after operation. However, 12 days after discharge, she died of asphyxia.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [78, 'years'], 'creatinine': [0.67, 'mg/dL'], 'sex': 'Female'}",89.40769,84.93731,93.87807,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 78 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.67 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.67/0.7)**-0.241 * 0.9938**78 * 1.012 = 89.40769.
Hence, the GFR value is 89.40769 ml/min/1.73 m²."
480,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-3088,Extracted,"A 22-year-old man comes to the physician because of a 2-week history of cough and decreased urination. The cough was initially nonproductive, but in the last few days he has coughed up small amounts of blood-tinged sputum with clots. He has not had any fevers, chills, or weight loss. He has smoked one pack of cigarettes daily for 5 years. Pulse is 115/min and blood pressure is 125/66 mm Hg. Physical examination shows dried blood around the lips. Serum studies show a creatinine of 2.9 mg/dL. Results of a serum antineutrophil cytoplasm antibody test are negative.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [22, 'years'], 'creatinine': [2.9, 'mg/dL'], 'sex': 'Male'}",30.41442,28.8937,31.93514,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 22 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.9 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.9/0.9)**-1.2 * 0.9938**22 * 1.0 = 30.41442.
Hence, the GFR value is 30.41442 ml/min/1.73 m²."
481,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5937041-1,Extracted,"A 14-year-old Kazakh girl who had ongoing difficulties in starting the stream of urine and intermittent interruption of the urinary stream while voiding, and bedwetting since her early years (persistent since she was 2 years old), which was stressful for both the parents and child.
Since that time, the girl has been treated by pediatricians using traditional methods (fluid and diet restriction, lifting and waking, dry bed training, bladder training and retention control, anticholinergic medication) without any success.
Her past medical history included regular medical checkups because of agenesis of her right kidney and pelvic ectopy of the single left kidney, a cyst of the bladder, and bedwetting. She had never had hematuria. Surgical interventions had not taken place. She is the second child of five in her family. The other family members do not have health problems.
On physical examination she was well. Her blood pressure was 100/60 mmHg. Her pulse was 82 beats/min. A urine analysis was normal. Her renal function was normal with a creatinine of 90 μmol/L. Examination of other systems revealed an agenesis of her vagina.
On radiologic examination: on sonography her right kidney was not visualized; her left kidney was located in the pelvic region, and was 51.8 × 62.8 cm in size. Her urinary bladder volume was 156 cm3, and on the right side of the wall a cystic mass 23 × 20 mm in size was visualized (ureterocele?). A contrast media computed tomography (CT) scan revealed agenesis of her right kidney, pelvic ectopy of her left kidney; on the right side of the urinary bladder there was a cystic mass 24 × 17 mm in size (papilloma, ureterocele, mixed tumor); and agenesis of her uterus and vagina (Mayer-Rokitansky-Küster-Hauser syndrome) was also detected (Fig. ).
On intravenous urography, her right kidney was not visualized, there was normal functioning of the left kidney located in the pelvic region, and excretory (descending) cystography shows a shadow of reduced density on the right side of the urinary bladder wall 23 × 20 mm in size (cystic mass, ureterocele) (Fig. ).
On the right extremity of the interureteric ridge, in the projection of the missing right ureteric orifice, a round-shaped cystic mass, 24 × 20 mm in size was seen, covered by a normal mucous membrane, located close to the bladder neck and protruding into the internal urethral meatus.
Based on the clinical presentation, sonographic, radiologic and endoscopic findings we concluded that some cystic masses (mixed tumor, dermoid cyst) of the bladder cause bladder irritation with symptoms of lower urinary tract obstruction and bedwetting. However, we considered the possibility of a relationship of this mass with the right kidney agenesis, because of its location in the same area of the missing right ureteric orifice, so we decided to perform transvesical surgery rather than transurethral surgery.
Transvesical access found a round-shaped mass, 24 × 20 mm in size, located on the right extremity of the interureteric ridge, covered by normal mucous membrane of the bladder. This mass was located close to the bladder neck and was protruding into the internal urethral meatus (Fig. ). We discovered that it was attached to the bladder wall. Excision of the bladder mass was performed. During surgery, multiple cystic masses containing dark-brown liquid were excised. The integrity of the urinary bladder wall was restored. The urinary bladder was drained by a size 16 Foley urethral catheter.
After removing the urethral catheter (at 48 h), our patient was free from her symptoms of bedwetting, difficulty in starting the stream of urine, and intermittent interruption of the urinary stream while voiding.
In order to study the tissue with a light microscope, the specimen was fixed in formalin (10%), cut into sections of 5 μm and stained with hematoxylin and eosin. At histology (Figs. , , , , , , and ), malformation of renal structures typical of rudimentary multicystic dysplastic kidney was observed: a tubular structure lined with cubic epithelium, dilated distal tubules and collecting ducts with their transformation into stretched cysts; disorganized structures of renal calyces and pelvis that transformed into the cysts; atrophy of renal tubules; thickening of the basement membrane, resembling wall of cysts; malformed glomeruli and tubules are lacking proper organization, interstitial and periglomerular fibrosis, and nonspecific cellular infiltration.
At 3 year, 8.5 month follow-up of the patient, she had no recurrence of bedwetting, difficulty in starting the stream of urine or intermittent interruption of the urinary stream while voiding. She was followed up with clinical and radiological examinations. Retrograde cystogram (February 1, 2018) showed normal urinary bladder, no cystic mass was seen (Fig. ).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [14, 'years'], 'creatinine': [90.0, 'µmol/L'], 'sex': 'Female'}",84.03788,79.83599,88.23977,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 14 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 90.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 90.0 µmol. To convert 90.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 90.0 µmol Serum Creatinine * 1e-06 mol/µmol = 9e-05 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 9e-05 mol Serum Creatinine * 113.12 g/mol = 0.01018 g Serum Creatinine. To convert 0.01018 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01018 g Serum Creatinine * 1000.0 mg/g = 10.18 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 10.18 mg Serum Creatinine/10.0 dL = 1.018 mg Serum Creatinine/dL. The concentration value of 90.0 µmol Serum Creatinine/L converts to 1.018 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.018/0.7)**-1.2 * 0.9938**14 * 1.012 = 84.03788.
Hence, the GFR value is 84.03788 ml/min/1.73 m²."
482,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4309029-1,Extracted,"A 58-year-old female with medical history significant for liver cirrhosis secondary to hepatitis C infection, chronic obstructive pulmonary disease, diabetes mellitus, and hypertension presented to the hospital for increasing abdominal distension, weakness, and confusion. She was first diagnosed with chronic nonhepatitis B hepatitis in 1983, later revised to hepatitis C cirrhosis in 1992, and underwent pegylated interferon plus ribavirin treatment for three months in 2002; however, she ceased treatment due to adverse effects leading to noncompliance. Since 2011, the patient has been undergoing evaluation for liver transplantation on outpatient basis and no prior hospitalizations were reported due to complications from liver disease.
At presentation, patient's encephalopathic and physical examination was remarkable for abdominal distension with tenderness. Laboratory findings demonstrated serum sodium of 118 mMol/L, potassium of 6.4 mMol/L, chloride of 114 mMol/L, blood urea nitrogen of 57 mg/dL, and creatinine of 4.8 mg/dL (baseline: 0.8 mg/dL). The patient was found to be oliguric, urine microscopy demonstrated “muddy brown casts” consistent with acute tubular necrosis, and after extensive workup this was determined as secondary to hepatorenal physiology. Patient's renal status continued to deteriorate to eventual anuria, hyperkalemia refractory to medical management, and encephalopathy, for which a vascular catheter was fitted into the right internal jugular vein under ultrasound guidance without difficulty and care, and the patient was transferred to the intensive care unit for continuous venous-venous hemofiltration (CVVH) therapy. The patient received a 5-day total of CVVH and, on hospital day 7, with creatinine clearance of 15.32 mL/min, the patient shuttled to catheterization lab, where 15 mL of Isovue-300 contrast was used for safe placement of a right-sided tunneled venous catheter for scheduled triweekly hemodialysis sessions. Contrast enhanced X-ray fluoroscopy demonstrated persistent left superior vena cava (). Upon careful review of current and past imaging studies, a contrast enhanced computed tomography (CT) of the thorax, abdomen, and pelvis and a magnetic resonance imaging (MRI) of abdomen which were conducted as part of outpatient workup for liver transplantation corroborated the existence of both PLSVC and HSK ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [58, 'years'], 'creatinine': [4.8, 'mg/dL'], 'sex': 'Female'}",9.94119,9.44413,10.43825,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 58 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 4.8 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (4.8/0.7)**-1.2 * 0.9938**58 * 1.012 = 9.94119.
Hence, the GFR value is 9.94119 ml/min/1.73 m²."
483,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8462866-1,Extracted,"An 83-year-old Caucasian female with a past medical history of hypothyroidism, hypertension, asthma, and osteoporosis presented to the emergency department complaining of bilateral lower extremity swelling for the past four months. She denied chest pain, shortness of breath, orthopnea, palpitations, fatigue, night sweats, and unintentional weight loss. She also denied dysphagia, tongue swelling, changes in bowel habits, headache, numbness, tingling in the extremities, changes in vision, skin changes, or easy bruising. She had no known history of diabetes, heart failure, or renal disease. On physical examination, vitals revealed temperature 96.8° Fahrenheit, blood pressure 125/77 mmHg, heart rate 71 beats per minute, respiratory rate 12 breaths per minute, and oxygen saturation 98% on room air. The remainder of the exam demonstrated 3+ leg edema bilaterally up to the knees. She was awake, alert, and oriented to person, place, and time. Cardiac exam revealed a regular rhythm with no murmurs while the lungs were clear to auscultation bilaterally and the abdomen was benign. In addition to a lack of neurological deficits, she had no macroglossia, lymphadenopathy, or jugular venous distension. Evaluation of the skin revealed no thinning, thickening, rashes, or ecchymosis. Initial laboratory studies revealed BUN 18.1 mg/dL, creatinine 0.84 mg/dL, total protein 4.8 g/dL, albumin 2.3 g/dL, TSH 3.92 uIU/mL, free T4 6.6 μg/dL, and NT-proBNP 401 pg/mL. AST, ALT, and a complete blood count did not show any abnormal values. An electrocardiogram revealed a normal sinus rhythm without low voltage complexes or dysrhythmia and normal chest X-ray. A subsequent echocardiogram found normal left and right ventricular function with no valvular abnormalities. Urine studies found a total urine protein of 257.8 mg/dl, with a 24-hour urine study revealing 12,374 mg of protein. Subsequent urine and serum protein electrophoresis noted high free lambda light chains of 26.84 mg/dL and 47.7 mg/dL, respectively, and a low Kappa/Lambda urine ratio of 0.77 (). A renal biopsy was performed and demonstrated renal amyloidosis of the AL type with monoclonal IgG lambda involving the glomeruli and arteriolar vessels (). Further work-up including serum immunofixation and flow cytometry were not consistent with multiple myeloma (). A 24-hour urine collection was negative for Bence Jones protein. Bone marrow biopsy did not reveal evidence of amyloidosis or plasma cell dyscrasia and was negative for Congo red stain. A fluorodeoxyglucose PET/CT scan showed non-specific findings for multiple myeloma. A diagnosis of renal-limited amyloidosis was made and the patient initiated treatment with bortezomib, melphalan, and steroids. Shared decision making was employed to refer the patient to a well-known amyloid program for further management; however, the patient declined the referral.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [83, 'years'], 'creatinine': [0.84, 'mg/dL']}",68.9077,65.46232,72.35309,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 83 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.84 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.84/0.7)**-1.2 * 0.9938**83 * 1.012 = 68.9077.
Hence, the GFR value is 68.9077 ml/min/1.73 m²."
484,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7885150-1,Extracted,"A 63-year-old woman with the history of hypertension presented to the emergency department during COVID-19 pandemic with significant shortness of breath on minimal exertion and fatigue for 3 weeks. Patient was hypoxic to 74% and tachypneic to 30 breaths/min and required endotracheal intubation. Physical exam was unremarkable. Shortly, thereafter, she became persistently hypotensive requiring vasopressor support. Electrocardiogram revealed sinus rhythm with rate of 70 bpm, tall R wave in V2 and symmetric T wave inversions in precordial leads (). Chest radiograph post intubation showed bilateral patchy infiltrates. Initial severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) PCR test was negative while the second PCR for SARS-CoV-2 done 24 h later returned positive.
Initial troponin T was 0.07 ng/ml with maximum at 0.22 ng/ml (reference range < 0.01 ng/ml) and NT-proBNP was 12 945 pg/ml. Elevated white blood cell count (21.1 × 103/μl), creatinine (1.45 mg/dl), C-reactive protein (25.9 mg/dl) and ferritin (546 ng/ml) and D- Dimer 4.34 (ref range ≤ 0.63 mg/l) was noted. Serial ECGs remained stable.
Patient remained persistently hypoxic with PaO2/FiO2 ratio of 85 which along with CXR findings is suggestive of severe acute respiratory distress syndrome (ARDS). Central venous oxygen saturation of 62% suggested the possibility of mixed shock.
Computed tomography angiogram of chest was deferred due to hemodynamic instability and refractory hypoxemia. Systemic anticoagulation with heparin and broad-spectrum antibiotics was initiated. Due to institutional COVID-19 policy for transthoracic echocardiography to minimize personnel exposure, focused cardiac ultrasound (FoCUS) was performed, which revealed mildly increased right ventricular cavity size with flattened septum in systole and diastole along with bowing of interatrial septum toward the left supporting ECG findings of right ventricular strain (, ). Due to suspected massive pulmonary embolism (PE) alteplase 50 mg was given intravenously over 120 min. This resulted in significant improvement of hemodynamics, perfusion indices and oxygenation within next 12 h to the extent that hypotension resolved despite being on high PEEP protocol for ARDS.
After 24 h, patient was noted to be unresponsive despite being off sedation. Urgent computed tomography (CT) of head revealed multifocal infarcts of both cerebral and cerebellar hemispheres with associated mass effects concerning for acute ischemic infarcts. Follow-up CT in 12 h revealed hemorrhagic transformation and anticoagulation with heparin was held. Due to concern for cardioembolic phenomenon, FoCUS with agitated saline was done that showed early right to left shunt consistent with patent foramen ovale (PFO) (, ). Doppler ultrasound of legs did not reveal deep venous thrombosis (DVT). No evidence of atrial fibrillation was noted on prolonged cardiac monitoring. Antiphospholipid antibody syndrome workup was negative.
Patient remained intubated for 20 days due to poor mental status but was eventually successfully liberated from mechanical ventilation. She was discharged on apixaban 5 mg BID for PE. After 5 months of continuous physical, neurological and nutritional improvement, TEE was done which confirmed the PFO ( and ). She was referred for PFO closure.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [1.45, 'mg/dL'], 'sex': 'Female'}",40.53045,38.50393,42.55697,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 63 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.45 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.45/0.7)**-1.2 * 0.9938**63 * 1.012 = 40.53045.
Hence, the GFR value is 40.53045 ml/min/1.73 m²."
485,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4678057-1,Extracted,"A 46-year-old woman with a medical history of SCD and end stage renal disease (ESRD) underwent renal transplantation two years before this biopsy. She was found to have elevated serum creatinine up to 1.4 mg/dL from baseline of 0.9 mg/dL, and her renal graft was biopsied to rule out rejection.
The hematoxylin and eosin (HE) sections revealed three biopsy cores with 10 glomeruli. None of the glomeruli was either segmentally or globally sclerosed. There was no glomerulitis or double contours of glomerular basement membranes noted. Except for focal tubular atrophy, the majority of renal tubules were back-to-back without significant interstitial fibrosis (). The proximal tubules were mildly dilated with focal disruption of the brush borders. There was no significant inflammatory infiltration in the renal parenchyma, tubulitis, or vasculitis. BK virus staining was negative with a good positive control. C4d staining by immunofluorescent method was negative in peritubular capillaries. There was no specific glomerular staining for IgA, IgG, IgM, C1q, C3, kappa, or lambda light chain. An immunohistochemical stain for kidney injury molecule-1 (KIM-1) was positive along the luminal surface of some proximal tubules (), consistent with acute tubular injury. Approximately 20% of proximal tubules stained 1+ to 2+ positive for iron (), implying that the ATI was associated with iron/heme deposition from hemolyzed sickled RBCs into the renal tubules. Two glomeruli were present on Methylene Blue Azure II stained sections. Ultrastructurally, there was good preservation of foot processes. Focal thickening of glomerular basement membranes was noted. Some irregular shaped RBCs were identified in the glomerular capillary loops, consistent with sickled RBCs (). No immune complex deposits were present in the mesangial areas, subendothelial or subepithelial spaces. In summary, the mild ATI was most likely associated with iron nephrotoxicity secondary to recurrent SCN.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [46, 'years'], 'creatinine': [1.4, 'mg/dL'], 'sex': 'Female'}",46.98795,44.63855,49.33735,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 46 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.4 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.4/0.7)**-1.2 * 0.9938**46 * 1.012 = 46.98795.
Hence, the GFR value is 46.98795 ml/min/1.73 m²."
486,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3840817-1,Extracted,"A 60-year-old male was referred to our department in April 2011 by his nephrologist due to an increase in his serum creatinine to 140.8 µmol/L (1.6 mg/dL), haematuria of 290 erythrocytes/µL and spot urine protein–creatinine ratio (UPCR) of 1.9 g/g. He had also developed hypertension during the previous months. His medical history was uneventful, and physical examination did not show any pathologies. He subsequently underwent renal biopsy showing pauci-immune extracapillary-proliferative glomerulonephritis (4 of 14 crescents) with mild tubular atrophy and interstitial fibrosis (20%), as well as lymphohistiocytic infiltration (A). Polymorphonuclear leukocytes were present in the glomerulus and in the interstitium. Immunofluorescence revealed minimal mesangial deposits of C3 and complement complex C5b-9 as well as IgM. Immunofluorescence for IgA, IgG and fibrinogen was negative. No amyloid deposits or myeloma casts were identified. Serum C3 and C4 complement levels were normal. Serum ANCAs and cryoglobulines showed negative results. No anti-glomerular basement membrane antibodies were present. The patient received four monthly cycles of cyclophosphamide i.v. along with steroids. Informed consent was obtained from the patient prior to submission of this manuscript. During therapy, serum creatinine stabilized to 132.0 µmol/L (1.5 mg/dL), proteinuria (UPCR) decreased to 0.5 g/g and haematuria improved to 32 erythrocytes/µL, respectively. Maintenance treatment with azathioprine was started and the patient returned to the care of his nephrologist.
After 10 months, the patient was referred to our service again with newly diagnosed macrohaematuria, increased UCPR of 5 g/g and elevated serum creatinine of 169.8 µmol/L (1.93 mg/dL). A thorough investigation revealed an increased serum β2-microglobulin of 3.5 mg/L and a pathological serum IgG kappa/lambda free light-chain ratio of 5.2 (normal value: 0.26–1.65) due to elevated serum IgG kappa light chains of 74.0 mg/L (normal range: 3.3–19.4 mg/L). A bone marrow biopsy showed an increase of monoclonal kappa-positive plasma cells to 10%. Re-evaluating the initial renal biopsy, no evidence of light-chain deposition disease, fibrillary glomerulonephritis or amyloidosis was present.
A new renal biopsy was performed, again showing pauci-immune extracapillary-proliferating glomerulonephritis (4 of 10 crescents) with mild interstitial fibrosis. In this biopsy, there was also no evidence of classical myeloma-associated kidney disease. Due to the relapse of rapidly progressive glomerulonephritis after cyclophosphamide therapy and leucopenia during azathioprine treatment, we decided to administer two doses of 1 g of rituximab i.v. within 4 weeks and maintained the patient on a reduced dose of azathioprine in combination with cyclosporine A [, ]. Unfortunately, the patient showed rapid deterioration of his renal function within the following 8 weeks to a serum creatinine level of 303.6 µmol/L (3.45 mg/dL), an increase of proteinuria to 9 g/g and an increase of haematuria. The serum kappa/lambda free light-chain ratio also increased to 9.1. Because of the underlying plasma cell dyscrasia and rapidly worsening kidney function, we decided to start the patient on the proteasome inhibitor bortezomib (1.3 mg/m2 body surface i.v. on Days 1, 8, 15, 22) in combination with dexamethasone based on the treatment recommendations for multiple myeloma. After the first cycle of bortezomib/dexamethasone, serum creatinine decreased to 140.8 µmol/L (1.6 mg/dL), and urinalysis showed reduced proteinuria of 2 g/g. A control biopsy was performed revealing residual sclerosed crescents, completely sclerosed glomeruli, mild interstitial fibrosis and tubular atrophy (B). No signs of active extracapillary proliferations were detected. After the second cycle of bortezomib/dexamethasone, the patient showed clinical remission with serum creatinine levels of 103.8 µmol/L (1.18 mg/dL), minimal proteinuria of 0.48 g/g, no haematuria and well-controlled hypertension. Maintenance therapy of monthly bortezomib was initiated, and the patient showed stable serum creatinine values as well as stable proteinuria with 8 months of follow-up.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [60, 'years'], 'creatinine': [1.18, 'mg/dL'], 'sex': 'Male'}",70.64159,67.10951,74.17367,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 60 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.18 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.18/0.9)**-1.2 * 0.9938**60 * 1.0 = 70.64159.
Hence, the GFR value is 70.64159 ml/min/1.73 m²."
487,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-3900,Extracted,"A 47-year-old man comes to the physician for a routine health maintenance examination. He states that he has felt fatigued and dizzy on several occasions over the past week. He has back pain for which he takes ibuprofen. Digital rectal examination shows no abnormalities. Laboratory studies show a hemoglobin concentration of 15 g/dL, a serum urea nitrogen concentration of 22 mg/dL, a serum creatinine concentration of 1.4 mg/dL, and a serum calcium concentration of 8.4 mg/dL. His prostate-specific antigen (PSA) level is 0.3 ng/mL (N < 4.5). An intravenous infusion of para-aminohippurate (PAH) is administered and its clearance is calculated. The patient's effective renal plasma flow is estimated to be 660 mL/min (N = 500–1350). The filtration fraction is calculated to be 9% (N = 17–23).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [47, 'years'], 'creatinine': [1.4, 'mg/dL'], 'sex': 'Male'}",62.38474,59.2655,65.50398,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 47 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.4 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.4/0.9)**-1.2 * 0.9938**47 * 1.0 = 62.38474.
Hence, the GFR value is 62.38474 ml/min/1.73 m²."
488,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-798,Extracted,"Two days after undergoing emergent laparotomy with splenectomy for a grade IV splenic laceration sustained in a motor vehicle collision, a 54-year-old man develops decreased urinary output. His urine output is < 350 mL/day despite aggressive fluid resuscitation. During the emergent laparotomy, he required three units of packed RBCs. He has type 2 diabetes mellitus and is on an insulin sliding scale. His vital signs are within normal limits. Physical examination shows a healing surgical incision in the upper abdomen and multiple large ecchymoses of the superior right and left abdominal wall. His hematocrit is 28%, platelet count is 400,000/mm3, serum creatinine is 3.9 mg/dL, and serum urea nitrogen concentration is 29 mg/dL. Urinalysis shows brown granular casts.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [54, 'years'], 'creatinine': [3.9, 'mg/dL']}",17.46817,16.59476,18.34158,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 54 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.9 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.9/0.9)**-1.2 * 0.9938**54 * 1.0 = 17.46817.
Hence, the GFR value is 17.46817 ml/min/1.73 m²."
489,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7255085-1,Extracted,"A 70-year-old Caucasian female patient suffering from left knee primary osteoarthritis underwent fully cemented TKA under regional anesthesia. Past medical history included arterial hypertension, long-standing, well-controlled, insulin-dependent diabetes, glaucoma, and mild obesity. The procedure was uneventful, a standard postoperative protocol was followed with partial weight-bearing, and she was discharged home 48 hours postoperatively. The patient had a low-grade fever during the first two postoperative days. Analgesics, non-steroidal anti-inflammatory drugs (NSAIDs), and anticoagulation were prescribed, as well as physiotherapy. The day after discharge, she felt unwell with muscle aching body fatigue and developed a temperature of 38°C. The clinical examination by a physician at home was focused on the surgical wound and the local hematoma absorption, and she was treated with oral antibiotics (cefuroxime 500 mg twice a day) NSAIDs, paracetamol, hydration, and observation. Attention was not turned to chest symptoms that were mild at the time with occasional coughing and intermittent chest pain. Despite antibiotic treatment, the patient had persistent periodic high fever up to 38.5°C, myalgia, fatigue, and malaise along with mild coughing. On the sixth postoperative day, a second physician consultation by the telephone this time switched the antibiotic therapy to moxifloxacin 400 mg twice a day. The high temperature did not subside, the antibiotics made no difference to the symptoms, the wound remained red and mildly inflamed, coughing became intense, but the patient did not have difficulty in breathing.
On the tenth postoperative day, the patient turned up in our emergency department exhausted with high temperature up to 38.5°C, seeking orthopedic assistance for a knee infection. She was unable to ambulate, suffering from whole-body myalgia, generic malaise, and persistent cough but no dyspnea. On knee clinical examination, the wound was mildly inflamed with no effusion; thus, there was no suspicion of infection and aspiration deemed not necessary. The patient had an unrestricted passive knee range of motion 0-100 degrees, and the knee radiographs demonstrated stable, well-aligned implants with no signs of effusion (Figures -).
Upon admission, blood tests revealed a white blood count of 7.400/mm3 (range:3.900-11.100/mm3) with a differential of 83% polymorphonuclears and 14% lymphocytes, reduced hemoglobin of 9.5 g/dl (range=11.8-14.8 g/dL) and hematocrit of 28.7% (range: 37-46%), normal platelet of 279 x 103/mm3 (range 150-400 x 103/mm3), and elevated serum creatinine 1.38 mg/dl (range: 0.57-1.11 mg/dl), creatine phosphokinase 299U/L (range: 29-168U/L), and lactate dehydrogenase 513U/L (range: 125-220U/L). The blood coagulation test and urinalysis were normal. The C-reactive protein test was not performed on admission.
An infectious disease internist and pulmonologist were called upon to help diagnose and assist in managing the suspected infection. Chest radiograph revealed pneumonia of both lungs with ground-glass typical bilateral, multifocal, peripheral opacities due to an infectious organism (Figure ). Consequently, coronavirus-19 disease (COVID-19) was suspected. The patient was admitted to a specially dedicated ward for suspected COVID-19 patients where pneumonia from SARS-CoV-2 was diagnosed. The patient was transferred to a COVID reference hospital and treated according to the COVID-19 protocol; she marginally escaped intubation though she went through significant respiratory distress for several days and is now slowly recovering.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [70, 'years'], 'creatinine': [1.38, 'mg/dL'], 'sex': 'Female'}",41.1776,39.11872,43.23648,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 70 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.38 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.38/0.7)**-1.2 * 0.9938**70 * 1.012 = 41.1776.
Hence, the GFR value is 41.1776 ml/min/1.73 m²."
490,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6037334-1,Extracted,"A 43-year-old Caucasian male with a medical history significant for intravenous (IV) drug use presented to the emergency department with restlessness, agitation, and profuse sweating. He reported no pain in the chest, neck, back, or abdomen. He denied a history of diabetes mellitus, hypertension, coronary artery disease, or connective tissue disease and was not taking any medication. He reported smoking one pack per day for the last 20 years. On presentation, he had a blood pressure of 120/32 mmHg; pulse of 90 beats per min; temperature of 100.1 F, and respiratory rate of 24 breaths/min. His oxygen saturation was 95% on two-liter of oxygen. He was fully oriented but found to be agitated and restless. A cardiovascular examination revealed grade 3/6 decrescendo diastolic murmur heard best on the left parasternal border on expiration. There were clear breath sounds bilaterally with no audible wheezes or crackles. The abdominal and neurological exams were benign.
His electrocardiogram showed nonspecific T wave changes in V1-V2 with sinus rhythm. His chest X-ray was unremarkable as well. The laboratory reports were normal except for creatinine of 2.5 mg/dl. Based on the history of IV drug abuse and auscultation consistent with a murmur and low-grade fever, the presumptive diagnosis of infective endocarditis was made. Blood cultures were drawn and empiric broad-spectrum antibiotics were started. A transthoracic echocardiogram (TTE) was ordered to look for possible valvular pathology/vegetation. TTE showed aortic root dilatation and aortic insufficiency along with the possibility of dissection in the ascending aorta. A computed tomography (CT) angiogram was ordered emergently that revealed aortic dissection involving the ascending aorta, arch (Figures -) with an aneurysm measuring up to 5.5 cm, extending into the descending aorta (Figures -). Emergent aortic root replacement along with ascending aorta and hemi-arch replacement were performed. The postoperative course was uneventful and he was discharged in a stable condition.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [43, 'years'], 'creatinine': [2.5, 'mg/dL'], 'sex': 'Male'}",31.89393,30.29923,33.48863,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 43 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.5/0.9)**-1.2 * 0.9938**43 * 1.0 = 31.89393.
Hence, the GFR value is 31.89393 ml/min/1.73 m²."
491,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3811690-1,Extracted,"A 53-year-old female presented to our hospital complaining of a 6-month history of backache. Judging from the blood testing results, she had hypercalcemia, and alkaline phosphatase (ALP) was increased to 1,253 U/L (normal range, 35 to 130); the patient was sent to the endocrinology department. Her past history was significant for a surgical procedure for fibrocystoma of her right humerus 20 years ago, and she had donated one of her kidneys to a relative 7 years previously. She had taken atorvastatin 10 mg, amlodipine 5 mg, and omega-3 fatty acid 1,000 mg daily for the past 3 years to treat high blood pressure and dyslipidemia. The patient had been misdiagnosed with a thyroid nodule and hypothyroidism at another hospital 4 years previously and had immediately been prescribed levothyroxine 50 µg/day. At that time, the thyroid ultrasonography revealed two nodules that were 0.3 and 0.5 cm in diameter on her right lobe and another nodule that was 2.3×1.3 cm in size that was projected backwards. She had fine needle aspiration cytology for the nodule on the left lobe, and this had revealed a benign nodule. She had been followed up every 6 months by neck ultrasonography. Two years later, when the nodule on the left lobe of the thyroid had increased in size to 2.9×1.7 cm, they carried out radiofrequency ablation. However, the thyroid nodule remained the same size even after the radiofrequency ablation, so they monitored its size every 6 months for 2 more years (). During that time, the patient began experiencing backache and visited the orthopedics department of our hospital where she was suspected of having metabolic bone disease due to the high serum ALP value.
The patient presented with generalized weakness and fatigue without other hypercalcemic symptoms. The peripheral blood examination was as follows: leukocyte count, 7,020/mm3; hemoglobin, 9.3 g/dL; platelet count, 249,000/mm3; prothrombin time (PT), 14.4 seconds (normal range, 11.9 to 14.3); activated partial thromboplastin time (aPTT), 31.3 seconds (normal range, 29.1 to 43.5); serum iron, 65 µg/dL (normal range, 40 to 160); total iron binding capacity (TIBC), 258 µg/dL (normal range, 230 to 430); transferrin saturation, 25%; and ferritin, 158.6 ng/mL (normal range, 13 to 150). Serum chemistry values were also obtained: blood urea nitrogen, 26.9 mg/dL; creatinine, 1.98 mg/dL; glucose, 110 mg/dL; ALP, 1,011 U/L; aspartate aminotransferase, 23 U/L; and alanine aminotransferase, 11 U/L. Serum calcium was 14.6 mg/dL, phosphate was 3.5 mg/dL, and ionized calcium was 7.2 mg/dL. Serum protein and serum albumin were 6.9 and 3.7 g/dL, respectively. The results of the serum electrolyte test revealed that sodium was 135.7 mmol/L, potassium was 4.3 mmol/L, chloride was 104.0 mmol/L, and serum osmotic pressure was 286 mOsm/kg. According to the serum lipid examination, the total cholesterol was 146 mg/dL, triglyceride was 95 mg/dL, high density lipoprotein was 33 mg/dL, and low density lipoprotein was 79 mg/dL. A thyroid function test found T3 was 108.9 ng/dL (normal range, 80 to 200), thyroid stimulating hormone was 0.40 mIU/L (normal range, 0.27 to 4.2), and free T4 was 0.74 ng/dL (normal range, 0.93 to 1.70). Under dual energy X-ray absorptiometry-based bone density examination, the T-score of the lumbar region was -1.4, while the T-scores of the neck were -1.2 on the left and -1.8 on the right. Except for the fifth lumbar vertebra, which had spondylolisthesis, nothing remarkable was found on magnetic resonance imaging.
According to further blood tests, 25-hydroxyvitamin D3 was 9.6 ng/mL (normal range, 4.8 to 52.8), and 1,25-dihydroxyvitamin D3 was 10.5 pg/mL (normal range, 19.6 to 54.3), while the intact parathyroid hormone (iPTH) was 1,911 pg/mL (normal range, 15 to 65). When we performed bone scanning with 99mTc, the amount of cortical bone radioactive isotope uptake increased very high (). Because we suspected hyperparathyroidism, we carried out a 99mTc sestamibi scan and suspected the lesion that had been previously diagnosed as a left thyroid nodule was likely a parathyroid adenoma (). Using thyroid Doppler ultrasonography, we discovered a hypervascular adenoma that was 5-cm-sized solid mass with similar echo of surrounding thyroid tissue in the center, and slightly low echo in outer part in the inferior site of left thyroid gland (), while on the right thyroid parenchyma we discovered two thyroid nodules, 0.3 and 0.5 cm each in diameter, that the patient had had 4 years before. We performed neck computed tomography and found there was no neck lymph node metastastasis and local invasion of other organs ().
The patient received both hydration and diuretic treatments until she underwent a surgical operation to control the hypercalcemia; she also had pamidronate 90 mg intravenous injections twice a week. On the 11th day after hydration and diuretic treatment, her condition had improved; serum calcium was reduced to 11.6 mg/dL, and creatinine improved to 1.11 mg/dL. On the 12th day, the patient had left parathyroid excision and was diagnosed with a parathyroid adenoma (). Following the surgical procedure, iPTH normalized to 42.5 pg/mL, but calcium and vitamin D were prescribed for 9 months to cure the hypocalcemia that had developed due to hungry bone syndrome. It has been a year since the surgical operation, and her calcium, phosphate, ALP, and iPTH all remain at normal levels.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [53, 'years'], 'creatinine': [1.98, 'mg/dL'], 'sex': 'Female'}",29.67802,28.19412,31.16192,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 53 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.98 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.98/0.7)**-1.2 * 0.9938**53 * 1.012 = 29.67802.
Hence, the GFR value is 29.67802 ml/min/1.73 m²."
492,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7870202-1,Extracted,"An 82-year-old male experiencing bilateral edema at the lower extremities after a fall was referred for evaluation. Upon examination, rapid renal deterioration was noted as serum creatinine rose from 2.32 to 3.12 mg/dL over the course of 3 weeks, after which he was subsequently referred to our hospital and admitted with suspected rapidly progressive glomerulonephritis. Medical history included hypertension and hyperuricemia during a previous hospitalization. The patient consumed high levels of alcohol; daily intake of 300 to 500 ml Japanese sake. Additionally, he had been taking amlodipine 5 mg/day and febuxostat 10 mg/day.
Upon admission, physical examination and laboratory findings determined the following profiles: height at 155 cm, weight 63.4 kg, and BMI 26.2 kg/m2. Blood pressure was slightly elevated at 151/67 mmHg and serum creatinine levels had increased to 5.18 mg/dL. A complete blood count indicated: white blood cell was 5400 / ml (neutrophil 60%), hemoglobin was 11.2 g/dL and platelet count was 8,6000/ml. Chemical analysis showed total protein at 5.1 mg/dl, albumin at 1.9 g/dl, LDL-cholesterol at 143 mg/dL, and triglyceride at 123 mg/dL. Urinalysis revealed 3+ proteinuria and 3+ hematuria. In urine sediment, red blood cell count was greater than 100 per high-power field. The spot urine protein level was 4.5 g/g creatinine. Serological examination revealed a high level of IgA at 557 mg/dL. Other immunoglobulins measured were normal; IgG 1234 mg/dL and IgM 55 mg/dL. Testing for anti-nuclear antibody (ANA) was positive at 1:40 with a speckled pattern. However, anti-double-stranded DNA antibody gave negative results. In addition, myeloperoxidase-antineutrophil cytoplasmic antibodies (ANCA) and proteinase 3-ANCA were not detected. At time of hospitalization complement levels were unaffected: C3 66 mg/dL (normal range 65 to 135) and C4 25 mg/dL. After 6 days, C3 slightly decreased to 64 mg/dL in spite of the acute inflammatory phase, however, then increased again and remained within normal range.
A kidney biopsy was performed and the specimen was shown to contain 17 glomeruli, with 7 global sclerosis. Light microscopy showed various characteristics, such as subendothelial deposits including wire loop lesions, endocapillary proliferation, and cellular crescents in the glomeruli (Fig. A-C). immunofluorescence (IF) revealed strong positive staining for IgA and C3 along the glomerular capillary. In contrast, IgG, IgM, C1q, and C4d were weakly stained, in particular C1q (Fig. D-I). Non-structured massive electron dense deposits were observed in the subendothelial and mesangial area using electron microscopy (Fig. J, K)
Treatment was initiated with intravenous methylprednisolone 500 mg/d as a steroid pulse therapy for 3 days, followed by oral prednisolone 25 mg/d as it was considered rapidly progressive glomerulonephritis. As strong positive staining of IgA and C3 was observed compared to IgG and C1q, we suspected IRGN and therefore included further testing of NAPlr and plasmin activity to determine infection. Whilst presence of infection was not clear from the tests performed on blood culture, head non-contrast computed tomography (CT), contrast CT from chest to abdomen and lumbar magnetic resonance imaging; positive NAPlr and plasmin activity was detected in the glomeruli (Fig. A, B). Immunosuppressive therapy was halted because of a poor response to this treatment by the patient, and hemodialysis was initiated. His Renal function did not recover and hemodialysis was continued. Two months after dialysis initiation, he was transferred to another hospital for maintenance hemodialysis treatment.
Further investigation confirmed that IgA and Gd-IgA1 staining merged in IF (Fig. C, D, E). In addition, high levels of serum Gd-IgA1 (9.3 μg/mL) were detected by ELISA. As this result is high compared to that seen in other kidney diseases,[ the final diagnosis of IgA-dominant IRGN was concluded.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [82, 'years'], 'creatinine': [5.18, 'mg/dL']}",10.44001,9.91801,10.96201,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 82 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 5.18 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (5.18/0.9)**-1.2 * 0.9938**82 * 1.0 = 10.44001.
Hence, the GFR value is 10.44001 ml/min/1.73 m²."
493,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6683587-1,Extracted,"An 84-year-old female patient was admitted to the hospital with weakness, lethargy and infectious secretions of the umbilicus. She was treated for elevated urea and creatinine levels and infectious secretions from the umbilicus emerging a week before. A long piece of gauze had been left in the patient’s abdomen 21 years before after she had undergone hysterectomy, and no interventions had been performed to remove it. Moreover, her family did not have any detailed information about this problem.
Clinical examinations and accurate umbilicus explorations showed a 0.5-mm fibrin and smelly umbilical secretions. The fibrin was found to be a gauze thread attached to a long piece of gauze that could not be easily removed from the umbilicus despite the effort made to remove it from the umbilicus ().
The results of laboratory tests upon the patient admission were as follows: White blood cells (WBC)=11210/mm3, hemoglobin=12.5 gr/dl, potassium (K)=3.5 meq/l, urea=67 mg/dl and creatinine=1.5 mg/dl.
The patient was therefore identified as a candidate for laparotomy. Direct abdominal explorations showed a long piece of gauze attached to a band and a metal ring with a 3-cm diameter and a large abscess containing 200 ml of infectious secretions ().
Severe adhesions of the intestines to each other and to the long gauze were observed. The abdomen and pelvis were frozen and the long gauze was skillfully removed and the abscess was drained. The 10×10 cm cavity created in the site of the gauze was irrigated. An approximately 1-cm fistula or laceration was also observed in the ileum due to the foreign body. The site of the fistula was therefore repaired. The patient was transferred to the Intensive Care Unit (ICU) after the surgery.
Five days later, the fistula repair failed. The patient was treated with Total Parenteral Nutrition (TPN) for two months and her clinical and para-clinical symptoms were carefully monitored. The fistula was not, however, repaired and considerable gastrointestinal secretions were continuously drained from the fistula.
The patient was again identified as a candidate for surgery after suppressing the inflammation and infection of the fistula. Adhesions were released, and the resection and anastomosis of the intestines were performed.
One week later, the secondary restoration of the abdominal wall was performed and the abdomen was sutured. The patient was discharged from the hospital in good health conditions ten days after the final surgery.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [84, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Female'}",34.15013,32.44262,35.85764,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 84 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.5 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.5/0.7)**-1.2 * 0.9938**84 * 1.012 = 34.15013.
Hence, the GFR value is 34.15013 ml/min/1.73 m²."
494,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8294950-1,Extracted,"A 52-year-old Hispanic male with newly diagnosed diabetes mellitus, hypertension, and ischemic cardiomyopathy presented with a one-month history of nonradiating right thigh erythema, pain, and swelling. He worked as a warehouse clerk; however, due to the severe, debilitating pain to his right thigh, the patient was on disability. He required maximal assistance in ambulation and, at times, even a wheelchair. He denied a history of fever, physical trauma, or intravenous drug use. The patient reported several emergency department and urgent care visits prior to our evaluation with no significant improvement on oral antibiotics for presumed cellulitis. Vital signs on presentation included blood pressure 108/69 mm Hg, heart rate 77 beats per minute, temperature 37.5°C, respiratory rate 18, and 96% on room air. On physical examination, a hard, tender, erythematous 7 × 4 inch right anterior thigh mass with accompanying right upper thigh edema was noted (as shown in ). Distal pulses were 2+ on palpation. Right lower extremity had 3+ pitting edema, while the left lower extremity had 2+ pitting edema. Severe tenderness was also noted in the right groin region with associated painful groin lymphadenopathy.
White blood cell count was 10.7 × 10^3 cells/mcl; other laboratory tests did show signs of systemic inflammation including elevated erythrocyte sedimentation rate 49 mm and elevated C-reactive protein 7.98 mg/dL. Aldose value was 3.8 units/L. The patient had an elevated creatinine 1.31 mg/dL, blood urea nitrogen 25 mg/dL, urine albumin/creatinine ratio 1,342.8 mcg/mg Cr, and creatinine kinase 844 unit/L, hemoglobin A1c (HbA1c) was 10.3%, and blood cultures were negative. Laboratory values to diagnose polymyositis and dermatomyositis were negative. A venous Doppler ultrasound of the right leg was negative for deep vein thrombosis. Magnetic resonance imaging (MRI) without contrast of the femur demonstrated bilateral inflammatory changes with disproportionate enlargement and diffuse heterogeneity of the right vastus medialis muscle with patchy areas of intramuscular hemorrhage, extensive subcutaneous edema, interfascial free fluid, and severe myositis (as shown in ).
Due to lack of improvement of symptoms on antibiotics and poorly controlled diabetes, the diagnosis of diabetic muscle infarction was considered. The treatment consisted of analgesia, low-dose aspirin, bed rest, and close outpatient follow-up. Upon discharge from the hospital, the patient was referred to a tertiary center for muscle biopsy; however, this was delayed due to the coronavirus disease 2019 (COVID-19) pandemic. Three months after being discharged from the hospital, the patient endorsed a significant size reduction of right thigh mass, complete resolution of pain, and endorsed being able to ambulate without assistance. With time, rest, and excellent adherence to low-dose aspirin, he no longer required a biopsy due to complete resolution of symptoms.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [52, 'years'], 'creatinine': [1.31, 'mg/dL'], 'sex': 'Male'}",65.49398,62.21928,68.76868,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 52 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.31 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.31/0.9)**-1.2 * 0.9938**52 * 1.0 = 65.49398.
Hence, the GFR value is 65.49398 ml/min/1.73 m²."
495,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4206014-1,Extracted,"A 56-year-old man, Afghan origin, with a history of significant weight reduction in a period of three months (about 20 kg), was admitted to the hospital. In the past medical history, one year before hospitalization, he had the history of low back pain and underwent disk hernia operation in India. Six months after disc hernioraphy, low back pain continued and the patient came back to India for further evaluation. On the second visit and evaluation, the patient’s laboratory tests revealed normal complete blood count (CBC), normal liver and renal function tests. Erythrocyte sedimentation rate (ESR) was 15 mm/1st hr. Also the serum calcium, phosphorus, parathyroid hormone (PTH), serum protein, electrophoresis and upper gastrointestinal endoscopy were normal. At this time, the patient was prescribed six Vitamin D ampoules (300,000 IU), however, the drugstore gave him 60 Vitamin D ampoules. After returning to the country of origin (Afghanistan), he injected 40 Vitamin D ampoules (one vitamin D ampoule each week). During this period of time, the patient had 30 Kg weight loss and then returned to Iran and was admitted in our hospital. Besides weight loss, he also had the complaint of pruritus, nausea and vomiting. Primary evaluation revealed a serum creatinine of 4 mg/dl, serum calcium of 12 mg/dl, serum phosphorus of 3 mg/dl, serum intact PTH of 2.7 ng/ml (normal: 10-65 ng/ml), and vitamin D level of >400 nmol/l (normal: 47.7-144 nmol/l). Also the patient had serum hemoglobin of 9.8 g/dl, hematocrit of 30% and ESR of 55 mm/1st hr. For further evaluation, a bone marrow aspiration and biopsy were performed, which were normal. Moreover, the results of serum protein electrophoresis, urine and serum immunoglobulin electrophoresis were normal. The serum angiotensin converting enzyme (ACE) and PSA level was normal. PSA as well as skull, chest and pelvic X-rays were normal. To find further information on the renal damage a renal biopsy was also performed. On light microscopy, the glomeruli had normal morphology and architecture (). There was no vasculopathy. The main pathology was found in the tubulointerstitial compartment. The interstitial area harbored significant inflammatory cell infiltration, predominantly mononuclear cells, associated with mild tubular atrophy and interstitial fibrosis. Both tubular dilatation and calcified necrotic debris in the tubular lumina were evident. Tubular cell degeneration was also seen (). On immunofluorescence study, there was no deposition of IgA, IgG, IgM, C3, C1q or fibrin. The diagnosis was tubulointerstitial nephritis, mostly chronic and compatible with the clinical diagnosis of vitamin D intoxication due to dispensing error. The patient was treated for hypercalcemia. Prednisolone, 1 mg/kg was started and gradually tapered. Serum creatinine and calcium level gradually decreased. However, serum vitamin D level continued to be high, even after one year. The patient returned to his country with serum creatinine of 1.5 mg/dl and calcium of 10 mg/dl. A low dose prednisolone (7.5 mg/day) was continued. We were updated on his laboratory results regularly. After two years, the last serum creatinine test showed a value of 1.2 mg/dl.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [56, 'years'], 'creatinine': [1.2, 'mg/dL'], 'sex': 'Male'}",70.97501,67.42626,74.52376,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 56 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.2 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.2/0.9)**-1.2 * 0.9938**56 * 1.0 = 70.97501.
Hence, the GFR value is 70.97501 ml/min/1.73 m²."
496,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8026824-1,Extracted,"A 67-year-old Caucasian male patient presented to the Emergency Department with fever, pain, swelling and bruising of his left thigh. He denied trauma to the leg.
A month before presentation, he was admitted for evaluation of painless jaundice. At the time of admission, his laboratory results showed acute kidney failure (serum creatinine 446 µmol/L, urea 10.7 mmol/L), normocytic anaemia (haemoglobin 90 g/L, mean corpuscular volume 86 fL), elevated liver enzymes [aspartate aminotransferase (AST) 2.6 µkat/L, alanine aminotransferase (ALT) 3.6 µkat/L, gamma-glutamyl transferase (GGT) 12.1 µkat/L, alkaline phosphatase (AP) 12.1 µkat/L] and elevated bilirubin levels (186/145 µmol/L), indicating cholestasis. Malignant stenosis of the distal common bile duct was discovered upon abdominal computed tomography (CT) scan with no evidence of distant metastases (Figure ). He underwent endoscopic retrograde cholangiopancreatography with stent placement in order to overcome the stenosis (Figure ). Kidney function tests (serum creatinine 369 µmol/L), liver enzymes (AST 1.9 µkat/L, ALT 3.67 µkat/L, GGT 3.87 µkat/L, AP 9.86 µkat/L) and bilirubin levels (149/124 µmol/L) improved, however, levels of haemoglobin remained low (86 g/L). His case was discussed at a multidisciplinary cancer team meeting and surgical treatment was proposed.
His background medical history was remarkable for arterial hypertension, hypercholesterolemia and stage 3 chronic kidney disease.
Upon admission the patient was alert, oriented and cooperative. He was febrile with body temperature of 38.1 °C, blood pressure of 135/72 mmHg, heart rate of 71/min and oxygen saturation of 100%. Physical examination revealed swelling and large suffusion on his left thigh.
Laboratory results showed severe normocytic anaemia (haemoglobin 65 g/L, mean corpuscular volume 93.0 fL), elevated liver enzymes (AST 1.08 µkat/L, ALT 1.68 µkat/L, GGT 10.86 µkat/L, AP 10.72 µkat/L) and bilirubin levels (52/33 µmol/L) and moderately raised inflammatory parameters (C-reactive protein 63 mg/L, white blood cell 9.4 × 109/L, procalcitonin 0.31 ng/mL). Coagulation tests showed normal prothrombin time/international normalized ratio (1.03). Laboratory values upon admission are summarized in Table .
Deep vein thrombosis was excluded with a venous point-of-care ultrasound. Ultrasound of the soft tissues of the left thigh revealed a large hematoma (13 cm × 5 cm × 3 cm) in one of the muscles of the anterior/extensor compartment. Later on, when no significant improvement in haemoglobin level (73 g/L) was observed despite treatment with multiple erythrocyte transfusions, a CT angiography of the abdomen and lower limbs was performed. Here, hematoperitoneum with a large haematoma in the left iliacus muscle (5 cm × 9 cm × 29 cm) and left femoral rectus muscle (7 cm × 5 cm × 30 cm; previously described) was discovered, both with multiple active bleeding sites (Figure ).
After presentation, the patient received three units of packed red blood cells and was admitted for further treatment and evaluation. Antibiotic treatment due to cholangitis, confirmed upon abdominal ultrasound, was initiated and another endoscopic retrograde cholangiopancreatography was performed to replace the poorly functioning choledochal stent. A haematologist was consulted and ordered additional coagulation tests that revealed elevated activated partial thromboplastin time (aPTT; 92 s), normal prothrombin time (1.00) and international normalized ratio (1.00), solely reduced FVIII activity (1%) and appearance of anti-FVIII antibodies, with titre of 30 Bethesda units (BU)/mL (Table ). Von Willebrand factor (vWF) antigen, vWF activity and vWF ristocetin cofactor activity were normal.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [67, 'years'], 'creatinine': [446.0, 'µmol/L'], 'sex': 'Male'}",11.70444,11.11922,12.28966,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 67 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 446.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 446.0 µmol. To convert 446.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 446.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00045 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00045 mol Serum Creatinine * 113.12 g/mol = 0.0509 g Serum Creatinine. To convert 0.0509 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.0509 g Serum Creatinine * 1000.0 mg/g = 50.9 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 50.9 mg Serum Creatinine/10.0 dL = 5.09 mg Serum Creatinine/dL. The concentration value of 446.0 µmol Serum Creatinine/L converts to 5.09 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (5.09/0.9)**-1.2 * 0.9938**67 * 1.0 = 11.70444.
Hence, the GFR value is 11.70444 ml/min/1.73 m²."
497,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6125993-1,Extracted,"We report a 77-year-old Caucasian female who had presented to nephrology clinic with a history of multiple sclerosis in remission who was noted to have progressive weakness for 2 months prior to presentation. Suspicion for a multiple sclerosis flare was low since her electrolytes were grossly abnormal with a serum calcium of 13.7 mg/dL and a serum creatinine of 2 mg/dL on June 23, 2017, increased from baseline of 8 – 9 mg/dL (calcium) and 0.9 – 1.1 mg/dL (creatinine). Ionized calcium was measured at 1.54 mmol/L (reference range 1.09 – 1.29 mmol/L), confirming the hypercalcemia noted on chemistry. Patient had initially been taking cholecalciferol 2,000 units PO daily for osteoporosis prophylaxis which were stopped, but this failed to improve the serum calcium. Parathyroid hormone (PTH) was appropriately suppressed at low normal 18 – 21 pg/mL (reference range 11 – 51 pg/mL), PTH-related peptide was in range at 17 pg/mL (reference range 14 – 27 pg/mL) which was not consistent with hypercalcemia of malignancy. The patient had normal sodium and alkaline phosphatase values. Urinalysis showed only 1+ proteinuria and was otherwise normal, and the kidney ultrasound demonstrated normal kidney structure. 25-hydroxy vitamin D level was 28 – 37 ng/mL (reference range: 20 – 50 ng/mL), but 1,25-dihydroxy vitamin D levels remained elevated despite stopping any supplements and remained elevated for nearly 2 months. 1,25-dihydroxy vitamin D peak level was 158 pg/mL (reference range: 19.9 – 79.3 pg/mL) and remained elevated between 100 and 113 pg/mL despite stopping vitamin D supplements. Urine protein electrophoresis and serum electrophoresis were negative or an M-spike, immunofixation was only positive in serum with IgG-κ monoclonal being found. κ- and λ-light chains were only slightly skewed towards IgG-κ > IgG-λ with a ratio of 2.32, ruling out monoclonal gammopathy as the etiology for the hypercalcemia.
The patient’s hypercalcemia continued to cause acute kidney injury, her calcium reached 12.6 mg/dL, she was hospitalized where she was given IV fluids, furosemide, and pamidronate. A high resolution CT scan did not show any lymphadenopathy or pulmonary pathology (), and angiotensin-converting enzyme levels were elevated at 100 U/L and 102 U/L for 2 draws. After the aforementioned treatment, her serum calcium decreased to 10.5 mg/dL.
When her serum calcium increased to 11.8 mg/dL, she was given denosumab 120 mg formulation in the interim leading to the return of serum calcium to 10.5 mg/dL. Since infectious causes of granulomatous diseases, such as tuberculosis and fungal infections, were in the differential diagnosis corticosteroids were not given empirically. While the high level of angiotensin-converting enzyme suggested possible sarcoidosis, we considered the low specificity of the test to demand more definitive tissue diagnosis could be obtained. Thus, corticosteroids were deferred until definite diagnosis, and denosumab was prescribed in the interim to control hypercalcemia.
See for graphs of serum calcium, PTH, 25-hydroxy vitamin D, 1,25-dihydroxy vitamin D, angiotensin-converting enzyme level, and serum creatinine levels. Mycobacterial serologies, coccidiomycosis, and other fungal serologies were negative as well.
It was during this time that granulomatous disease, specifically sarcoidosis was suspected. She underwent PET scan with findings of upper lobe predominant peri-bronchial wall thickening, diffuse lymphadenopathy and flourodeoxyglucose (FDG) uptake throughout pulmonary parenchyma. This was suggestive of a granulomatous process such as sarcoidosis. No other focus of FDG uptake in a pattern that suggests malignancy was found, and no splenic involvement was seen. See for PET scan image and findings.
When the patient’s creatinine increased to 2.58 mg/dL with a serum calcium of 11 mg/dL, the patient was admitted for definitive diagnostic procedures. Bone marrow biopsy and a transbronchial lymph node biopsy were obtained. The patient’s serum calcium and serum creatinine normalized with hydration and subcutaneous calcitonin injection. Biopsy results showed diffuse non-necrotizing/non-caseating granulomata in lung and bone marrow confirming diagnosis of systemic sarcoidosis. Cultures from lung biopsy were negative for mycobacteria, fungal elements, or bacteria. The sarcoidosis staging was rated at stage 0 according to lung imaging, but with a high enough burden of disease to cause significant hypercalcemia. Please see for details of biopsy findings and bone marrow biopsy results. The patient started 20 mg of prednisone after diagnosis with improvement of hypercalcemia down to serum calcium of 10.2 mg/dL. She is receiving 3 times weekly hydration with IV normal saline to help prevent dehydration which helped decrease serum creatinine to 1.58 mg/dL. The patient was not on TNFi (tumor necrosis factor) to suggest secondary sarcoidosis. Her multiple sclerosis was stable as well. She was started on plaquenil for maintenance treatment of the diagnosed sarcoidosis.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [77, 'years'], 'creatinine': [2.58, 'mg/dL']}",18.60653,17.6762,19.53686,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 77 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.58 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.58/0.7)**-1.2 * 0.9938**77 * 1.012 = 18.60653.
Hence, the GFR value is 18.60653 ml/min/1.73 m²."
498,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6541993-1,Extracted,"A 28-year-old male patient was admitted to endocrinology outpatient clinic with complaints of impaired balance, hearing loss, and numbness in the hands for a long time. There were type 1 diabetes mellitus, hypopituitarism, and short-term myoclonic jerks after head trauma in his medical history. The drugs he used were insulin aspart, insulin glargine, and carbamazepine. In the family history there was a consanguineous marriage between the parents. His family did not have any history of HDR syndrome. Vital signs upon admission found a blood pressure of 100/70 mmHg, heart rate of 84 beats/min, and body temperature of 36.6°C. He was not mentally retarded. In the neurological examination, the patient was awake, oriented, and cooperative with exam; cranial nerves, motor strength, sensory testing, and proprioception were all intact; only ataxic gait was present. Hair in the face and axillary and inguinal regions was decreased, bilateral testes were small, and gynecomastia was present. All other examinations were normal.
In laboratory examination, the following are found: leukocyte: 8.6 103/ml (4-10), hemoglobin: 10.8 gr/dl (12.1-17.2), MCV: 99.7 fL (82.2-99), platelet: 119 103/ml (150-400), glucose: 386 mg/dL (70-100), urea: 80 mg/dL (16.6-48.5), creatinine: 1.9 mg/dL (0.70-1.2), sodium: 161 mmol/L (136-145), potassium: 4.48 mmol/L (3.5-5.1), calcium: 5.68 mg/dL (8.4-10.2), phosphorus: 5.7 mg/dL (2.5-4.5), albumin: 4.02 g/dL (3.5-5.2), HbA1c: 7.6% (4-6), TSH: 1.42 mU/L (0.27-4.2), free T4: 0.546 ng/dL (0.93-1.7), free T3: 1.53 ng/L (2-4.4), iPTH: 19.90 ng/dL (12-88), FSH: 1.3 U/L (1.7 -12), LH: 7.67 IU/L (1.24-8.62), total testosterone: 8.88 ng/dL (249-836), cortisol: 10.15 mcg/dL (6.02-18.4), prolactin: 8.19 mcg/L (4.4- 15.2), B12: 273.2 ng/L (197-771), folic acid: 1.9 mcg/dL (3.89-20), urine analysis Ph: 5.5, density: 1014, microalbumin in spot urine: 0.34 mg/dl (0-2), microprotein in spot urine: 36.3 mg/dl (0-15), creatinine in spot urine: 227.61 (39-259) mg/dl, serum osmolarity: 394 mOsm/KgH2O (285-295), and urine osmolarity: 590 mOsm/KgH2O (50-1200). On abdominal ultrasonography, the size of left kidney was preserved, long axis of right kidney was 8.5 cm, and there was a minimal reduction in cortex thickness and a grade 1 increase in right kidney parenchyma echogenicity. As a result of laboratory and imaging findings, in addition to the diagnosis of type 1 diabetes mellitus and hypopituitarism, chronic kidney disease, primary hypoparathyroidism, and megaloblastic anemia due to folic acid deficiency were detected.
The audiogram showed a moderate mix type sensorineural hearing loss in the left ear and mild sensorineural hearing loss at increased frequencies in the right ear []. There were no pathological findings on eye examination. Bilateral symmetrical calcifications were detected in the basal ganglia, vermis, and cerebellum in brain CT []. There were no pathological findings in the pituitary MRI.
HDR syndrome was considered because of the diagnosis of primary hypoparathyroidism, hearing loss, and nondiabetic chronic kidney disease in addition to type 1 diabetes mellitus, hypopituitarism, and epilepsy. The patient's electrolyte and hormone replacement therapies were held. The symptoms and signs improved and the patient was taken to regular follow-up program.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [28, 'years'], 'creatinine': [1.9, 'mg/dL'], 'sex': 'Male'}",48.66837,46.23495,51.10179,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 28 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.9 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.9/0.9)**-1.2 * 0.9938**28 * 1.0 = 48.66837.
Hence, the GFR value is 48.66837 ml/min/1.73 m²."
499,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8462187-1,Extracted,"A 64-year-old Chinese man was admitted to our hospital with edema that had persisted over 4 mo.
The patient reported edema of the face and lower limbs, particularly in the afternoon, and he had not received any special treatment for this symptom.
No other relevant history of past illness was reported.
No other relevant family history was reported.
On examination, the patient presented with multiple nodules and lumps with a smooth surface that could be seen throughout the body (Figure ). Enlargement of the cervical, axillary, and inguinal lymph nodes was clearly observed.
Laboratory examinations revealed severe proteinuria (3.77 g/24 h; normal range, 0–0.15 g/24 h), hypoalbuminemia (1.8 g/dL), hyperlipidemia (cholesterol 15.7 mmoL, triglyceride 3.34 mmol/L), and increased serum creatinine levels (152 μmoL; normal range, 44–133 μmoL). These clinical parameters suggested that the patient’s symptoms were a result of nephrotic syndrome.
A kidney biopsy was performed and the analysis of nine glomeruli revealed one glomerulus indicative of glomerulosclerosis and one indicative of segmental glomerulosclerosis with peripheral podocytosis, vacuolation, and granular degeneration in the renal tubular epithelial cells (Figure and ). These pathological findings were indicative of FSGS, not otherwise specified (NOS). Immunohistochemistry of the kidney revealed that the glomerular capillary loop, peritubular capillary, and arterioles were positive for CD34 (Figure ), and the proximal tubule cells were positive for CD117 (Figure ) but negative for DOG1. Fat degeneration and necrosis were observed in the lymph node, and no tumor metastasis was revealed (Figure ). Hematoxylin and eosin staining of the skin showed spindle cell tumor-like hyperplasia, which was slightly heteromorphic with focal necrosis and rarely mitotic (Figure ). Immunohistochemistry staining revealed that the tumor cells were positive for CD34, Bcl-2, CD99, Ki67, and vimentin but negative for smooth muscle actin (SMA) and S-100. Representative immunohistochemical staining for CD34 is shown in Figure . The diagnosis was a desmoid tumor (DT) based on the above immunohistochemistry results.
Then, gastroscopy was performed and the results revealed a 0.6 cm mucosal mass that was hard to the touch, and poor mobility could be seen in the greater curvature of the stomach (Figure ). Several 0.4-2 cm masses were observed in the anterior wall of the middle and upper of the gastric fundus with fractured surfaces and fresh blood (Figure ). Moreover, pathological examination revealed the destruction of the gastric solid membrane structure and spindle cell tumor-like hyperplasia with mild dysplasia (Figure ), and epithelioid cells were occasionally seen with 6-8 mitotic figures/50 high power fields (Figure ). CD117 (Figure ), CD34 (Figure ), and SMA were positive by immunohistochemistry, and DOG1 was probably positive, and S-100 and CK were negative. These findings supported the diagnosis of GIST. Additional immunohistochemistry revealed that the skin was positive for CD117 (Figure ) and DOG1 (Figure ), the two most sensitive and specific markers for the diagnosis of GIST[]. In addition, a heterozygous missense mutation was found in the NPHP4 gene of the patient (NPHP4: NM_015102: exon17: c.2198G>A: p.G733D), which explained the occurrence of GIST and FSGS and indicated that this was not a random association[].","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [64, 'years'], 'creatinine': [152.0, 'µmol/L'], 'sex': 'Male'}",44.55502,42.32727,46.78277,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 64 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 152.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 152.0 µmol. To convert 152.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 152.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00015 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00015 mol Serum Creatinine * 113.12 g/mol = 0.01697 g Serum Creatinine. To convert 0.01697 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01697 g Serum Creatinine * 1000.0 mg/g = 16.97 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 16.97 mg Serum Creatinine/10.0 dL = 1.697 mg Serum Creatinine/dL. The concentration value of 152.0 µmol Serum Creatinine/L converts to 1.697 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.697/0.9)**-1.2 * 0.9938**64 * 1.0 = 44.55502.
Hence, the GFR value is 44.55502 ml/min/1.73 m²."
500,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5165133-1,Extracted,"A 78-year-old Japanese woman was found to have anaemia and reticular shadows on her chest X-ray during a health examination, for which she came to our hospital. She did not have any symptoms, including fever, cough, and purulent sputum, at that time. Her dietary habits were normal and she had not experienced any weight loss. Her haemogram and serum biochemistry revealed the following: haemoglobin: 7.8 (11.3–15.2) g/dL, MCV: 78.5 (79–100) fL, MCHC: 29.5 (30.7–36.6)%, serum iron: 62 (43–172) μg/dL, ferritin: 67.2 (4.6–204.0) ng/dL, unsaturated iron-binding capacity: 188 (137–327) μg/dL, vitamin B12: 470 (180–914) pg/mL, folic acid: 3.8 (3.1–9.7) ng/mL, blood urea nitrogen: 20.9 (8–22) mg/dL, creatinine: 1.13 (0.4–0.7) mg/dL, sodium: 145 (138–146) mEq/L, potassium: 3.5 (3.6–4.9) mEq/L, and chlorides: 109 (99–109) mEq/L. Her faecal occult blood test was negative. We diagnosed the cause of anaemia as defective iron utilization, and we followed up her laboratory data and chest X-ray findings to clarify the cause of defective iron utilization.
Three months later, she was admitted to the hospital with renal failure, chest radiograph abnormality, and severe anaemia. She had a past medical history of hypertension but had never smoked and had no history of tuberculosis (TB). She had not been exposed to any fine particles. She did not have fever or any respiratory symptoms, such as breathlessness, cough, haemoptysis, dyspnoea, and chest pain.
Physical examination showed a body temperature of 36.3°C and no crackles were audible on auscultation. Her chest X-ray showed persistence of the reticular shadows in the right middle and lower lung fields. In addition, a calcified lesion was observed in the left middle part (). Chest computed tomography (CT) showed a ground glass shadow and consolidation in the right upper and lower lobes with left sided pleural thickening and calcification (Figures –). Her laboratory findings at this time were haemoglobin 6.9 g/dL, white blood cell count 6,600 (3,500–9,000)/μL, blood urea nitrogen 61.5 mg/dL, creatinine 2.56 mg/dL, C-reactive protein (CRP) 0.0 (<0.3) mg/dL, erythrocyte sedimentation rate (ESR) 90 (2–15) mm/h, myeloperoxidase (MPO)-ANCA 54 (<10) EU, proteinase 3 (PR3)-ANCA <10 (<10) EU, and anti-glomerular basement membrane (GBM) antibody <10 (<10) EU. More than 100 counts per high power field of red blood cell (RBC) casts were found on urinalysis.
Renal biopsy was performed and pathological evaluation of the specimen revealed cellular crescent formations and lobulation in more than half the glomeruli (). Evaluation of bronchoalveolar lavage fluid (BALF) revealed increased RBC counts, and cytology indicated that 90% of the detected macrophages were haemosiderin-laden. These findings indicated the presence of alveolar haemorrhage and, hence, she was diagnosed as MPA. She did not consent to undergo surgical lung biopsy at this time. We initially planned to treat her with corticosteroids and intravenous cyclophosphamide (IVCY), and, therefore, we first started treatment with corticosteroid therapy (prednisolone 50 mg/day) (). After prednisolone therapy at this dose for 14 days, we started tapering it by 10 mg every 2 weeks, and once the dose of 20 mg was reached we tapered it by 5 mg every 4 weeks. This resulted in improvement in the renal failure, anaemia and lung abnormalities and, hence, IVCY was not required. Once the corticosteroid dose was reduced to 5 mg, it was combined with azathioprine. Currently, the patient is on maintenance therapy with corticosteroids (prednisolone 3 mg/day) and azathioprine (5 mg/day) without relapse of lung and renal lesions. She has been carefully followed up for development of TB by examination of chest X-rays once a month and sputum culture every three months, but with no TB prophylaxis.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [78, 'years'], 'creatinine': [2.56, 'mg/dL'], 'sex': 'Female'}",18.66465,17.73142,19.59788,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 78 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.56 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.56/0.7)**-1.2 * 0.9938**78 * 1.012 = 18.66465.
Hence, the GFR value is 18.66465 ml/min/1.73 m²."
501,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4287030-1,Extracted,"A 70-year-old male came to the hospital with fracture of the left femur. X-ray of the left femur showed a lytic lesion in the subtrochanteric region. Laboratory investigations revealed hemoglobin level of 10.2 g/dL, white blood cell count of 8200/µL, blood urea of 21 mg/dL, creatinine of 1.1 mg/dL, serum Ca2+ of 9.1 mg/dL, total protein of 7.8 g/dL, and albumin of 3.01 g/dL (A:G=0.63). Open reduction and internal fixation were done using a dynamic hip fixator, but there was no healing of the fracture even after 5 months. A biopsy from the fracture site showed sheets of CD138-positive plasma cells with kappa light chain restriction. Bone marrow was normocellular with normal hemopoietic cells and plasma cells constituted 2% of the nucleated differential count. Serum β2-microglobulin was 6.3 ng/L and M spike was 0.74 g/dL. Immunofixation electrophoresis revealed the M spike in the β-globulin region to be of IgA kappa. Bence Jones proteins were absent in the urine. No other lytic or soft tissue lesions were detected in a whole-body MRI scan. Hence, a diagnosis of SBP was made. The patient received radiotherapy (26 cycles) to the left femur over a period of 1 month with a total dose of 5000 cGy. Four months after completion of radiotherapy, a repeat serum protein electrophoresis showed an M spike measuring 2.31 g/dL in the β-globulin region, β2-microglobulin of 5.965 mg/L, total protein of 8.6 g/dL, albumin of 3.2 g/dL, and an A:G ratio of 0.59. The patient complained of diffuse abdominal pain, swelling, and constipation. Abdominal ultrasound revealed a heterogeneous, hypervascular mass of 9.4x6.2 cm in the left suprarenal area, displacing the pancreas anteriorly, and large peripancreatic lymph nodes. Non-contrast CT imaging showed a mass (6.6x4.5 cm) near the pylorus with multiple peripancreatic lymph nodes and a left suprarenal retroperitoneal mass. Colonoscopic examination was normal. Tru-Cut biopsy from the retroperitoneal mass revealed extramedullary plasmacytoma (). Blood analysis showed a hemoglobin level of 10.8 g/dL, serum calcium of 8.1 mg/dL, and creatinine of 1.09 mg/dL. Urine analysis did not reveal any Bence Jones proteins. Bone marrow aspirate showed 2% plasma cells. Bone marrow biopsy showed no increase or clusters of plasma cells. A whole-body PET-CT scan showed multiple metabolically active mass lesions in the retroperitoneum and peripancreatic lymph nodes. The uptake in the lungs, liver, spleen, remainder of the lymph node group regions, and skeletal system was within normal limits. A diagnosis of PCM was made. The patient was treated with chemotherapy with subcutaneous injection of bortezomib and dexamethasone. There was a decrease in the size of the mass after chemotherapy, but the patient’s condition deteriorated and he died 2 months after initiation of chemotherapy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [70, 'years'], 'creatinine': [1.09, 'mg/dL'], 'sex': 'Male'}",73.01247,69.36185,76.66309,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 70 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.09 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.09/0.9)**-1.2 * 0.9938**70 * 1.0 = 73.01247.
Hence, the GFR value is 73.01247 ml/min/1.73 m²."
502,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5045256-1,Extracted,"A 54-year-old man presented to the emergency department with recurrent abdominal pain and a palpable abdominal mass. He had suffered from an intermittent epigastric pain for 3 months. There was no abnormality in gastroscopy and colonoscopy. In abdominal computed tomography (CT) (), there was a calcified 4-cm-sized aneurysm in the SMA, a calcified 12-mm-sized dilatation of the splenic artery, and a nonfunctional right kidney with hydronephrosis. His medical history was not remarkable. He was not a smoker and had no other atherosclerotic risk factors. The family history was negative for connective tissue diseases, aneurysms and sudden deaths. On physical examination, the abdomen was scaphoid, and a 4-cm-sized pulsatile mass was palpated. There was no tenderness over the mass or in the abdomen. Blood pressure was 120/80 mmHg; body temperature was 36.5°C. There was a complete atrioventricular (AV) block on electrocardiogram. Laboratory tests revealed a white cell count of 6,230/mL, platelet count of 171,000/mL, aspartate aminotransferase 32 U/L, alanine aminotransferase 19 U/L, serum creatinine 1.77 mg/dL, p-amylase 75 U/L and lipase 114 IU/L. Genetic tests for connective tissue diseases and immunologic tests for rheumatic evaluation were not performed. However, there was no evidence of other diseases. He had an emergency operation for the visceral artery aneurysms.
In operative findings, a 4-cm-sized SMA aneurysm was identified at the SMA after the proximal jejunal branch. The splenic artery aneurysm was not resected because it was relatively small and heavily calcified. After distal and proximal control of the SMA, the aneurysm was opened. The aneurysmal wall was very thick and heavily calcified. After the aneurysm sac was opened, the posterior jejunal branch was controlled. The aneurysm was partially resected. An aneurysmal portion of the SMA was replaced with a great saphenous vein graft. There was no ischemic bowel. On CT angiography at 14 months postoperatively (), there was a small aneurysmal dilatation in the distal SMA. A chylous ascites was drained for 10 weeks. However, he finally recovered without any problems. Since then, his postoperative course was uneventful. An echocardiogram was checked, and left ventricular hypertrophy, complete AV block was confirmed. Five months later, he underwent another operation for an exacerbating hydronephrosis. He recovered without any sequelae.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [54, 'years'], 'creatinine': [1.77, 'mg/dL']}",45.07721,42.82335,47.33107,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 54 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.77 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.77/0.9)**-1.2 * 0.9938**54 * 1.0 = 45.07721.
Hence, the GFR value is 45.07721 ml/min/1.73 m²."
503,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3505635-1,Extracted,"A 68-year-old female was referred to the department of internal medicine for a hypercalcemic crisis. Originally, she was admitted to a psychiatric ward for confusion. Laboratory findings revealed hypercalcemia 4.62 mmol/L and confirmed PHPT with an iPTH level of 2479 pg/mL. The clinical signs of PHPT were dominated by those typical for the hypercalcemic syndrome—significant mental changes, dehydration, and impaired renal function (creatinine 147 μmol/L; normal range: 44–104 μmol/L). In her history, no standard manifestations of PHPT were found (). The neck was negative to palpation.
A US scan showed a solid, mostly hypoechoic mass in the lower pole of the right thyroid lobe, with roughened echo structure, increased vascularization, undulate margins, a size of 2.8 × 2.3 × 1.8 cm, and 6 mL in volume (). In the context of the PHPT diagnosis, the mass was considered to be an intrathyroidal parathyroid gland. Given its nonhomogeneous structure it was classified as suspicious. Ultrasound-guided fine-needle aspiration biopsy (US-FNAB) was performed. Cytologic smears showed cell clusters with apparent anisonucleosis, atypical nuclei, and only locally present small differentiated cells with clear cytoplasm. The finding was highly suggestive of PCa. Aspirate from the mass showed iPTH above 2500 pg/mL.
Combining subtraction scintigraphy (99mTc-MIBI and 99mTcO4
−) with two-phase technetium-99m sestamibi (99mTc-MIBI) revealed only low accumulation of the radiopharmaceutical at the caudal pole of the right thyroid lobe which was considered nonspecific (probably caused by degenerative and neoplastic changes in the parathyroid).
The thyroid was removed completely, including the tumor. Histologically, the finding was described as a clear cell PCa with fibrosis and hyalinization.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [68, 'years'], 'creatinine': [147.0, 'µmol/L'], 'sex': 'Female'}",32.53118,30.90462,34.15774,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 68 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 147.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 147.0 µmol. To convert 147.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 147.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00015 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00015 mol Serum Creatinine * 113.12 g/mol = 0.01697 g Serum Creatinine. To convert 0.01697 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01697 g Serum Creatinine * 1000.0 mg/g = 16.97 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 16.97 mg Serum Creatinine/10.0 dL = 1.697 mg Serum Creatinine/dL. The concentration value of 147.0 µmol Serum Creatinine/L converts to 1.697 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.697/0.7)**-1.2 * 0.9938**68 * 1.012 = 32.53118.
Hence, the GFR value is 32.53118 ml/min/1.73 m²."
504,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4421519-1,Extracted,"A 71-year-old Japanese man developed advanced chronic renal failure due to nephrosclerosis and underwent surgery to insert and embed a Tenckhoff peritoneal dialysis (PD) catheter on 27 December 2007. His medications were candesartan cilexetil, diltiazem hydrochloride, furosemide, spironolactone, bayaspirin, alfacalcidol and calcium carbonate. At the beginning of December 2007, he experienced a pruritic maculopapular rash affecting his arms and anterior chest with eosinophilia (eosinophils 16.6%, 1700/mm3). After administration of the antihistamine agent for 2weeks, his symptoms subsided. He had no other history of allergic disease, including bronchial asthma or food sensitivity, other than this episode.
On 31 January 2008, CAPD treatment was initiated immediately after confirming that serum blood urea nitrogen was 26.8 mmol/L (75 mg/dL), and creatinine was 954.7 μmol/L (10.8 mg/dL). Two days after commencing CAPD, a cloudy effluent was noted. He had no clinical symptoms, and physical examination was unremarkable. Investigation revealed an elevated number of leucocytes in the peritoneal fluid (310/μL) with 29% eosinophils, 11% neutrophils, and 60% lymphocytes and monocytes. Repeated culture of dialysis fluid failed to reveal any organisms. Blood culture and PCR for Mycobacterium tuberculosis, Mycobacterium
avium and Mycobacterium
intracellulare were negative. We diagnosed eosinophilic peritonitis, and intraperitoneal administration of antibiotics was discontinued.
Mild eosinophilic peritonitis with peripheral blood eosinophilia continued for 18 months. During this period, white cell count in peritoneal effluent was 200–1060/μL, and eosinophils were 20–30%. In addition, C-reactive protein was 0.04–2.01 mg/dL (0.36 ± 0.47, mean ± SD). Repeated examination of the stool revealed no parasite ova. Anti-nuclear antibody, anti-proteinase 3 and anti-myeloperoxidase antibodies, and monoclonal protein were negative. Immunoglobulin E (IgE) levels did not increase during the course, and IgE radioimmunosorbent tests for food, animals and house dust were all negative.
Peritoneal equilibration test with Dianeal-N PD-4 (Baxter, Tokyo, Japan) was performed twice at 6 and 12 months after initiation of PD. The ratio of creatinine concentration in dialysate and plasma (D/P Cr) values was 0.82 and 0.81, which indicates high peritoneal transporter status. Candesartan, diltiazem, furosemide and spironolactone were switched to losartan potassium, cilnidipine, eplerenone and torasemide, and antihistamine medication was restarted. However, the extent of cloudiness in peritoneal effluent did not change. He refused to take corticosteroids.
After PD treatment for 18 months, early gastric cancer was found, and laparoscopic partial gastrectomy was performed. We then evaluated the parietal peritoneum biopsied during gastrectomy. CAPD was resumed; however, eosinophilic peritonitis continued, and D/P Cr levels (0.82) did not change 5 months after operation.
Pathologically, mesothelial cells were seen as a monolayer covering the surface of the peritoneum. Numerous eosinophils were observed in the blood vessels, and some were present in the interstitium (). On immunohistochemistry, we detected increased chymase- and tryptase-positive mast cell infiltration, as compared with previously reported control tissue []. However, macrophage infiltration and CD-31- and pathologische anatomie Leiden-endothelium (PAL-E)-positive blood vessels were not elevated in comparison with previous control data [] () (Supplementary Data). No evidence of parasites, granulomas or vasculitis was identified.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [71, 'years'], 'creatinine': [954.7, 'µmol/L'], 'sex': 'Male'}",4.65706,4.42421,4.88991,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 71 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 954.7 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 954.7 µmol. To convert 954.7 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 954.7 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00095 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00095 mol Serum Creatinine * 113.12 g/mol = 0.10746 g Serum Creatinine. To convert 0.10746 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.10746 g Serum Creatinine * 1000.0 mg/g = 107.46 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 107.46 mg Serum Creatinine/10.0 dL = 10.746 mg Serum Creatinine/dL. The concentration value of 954.7 µmol Serum Creatinine/L converts to 10.746 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (10.746/0.9)**-1.2 * 0.9938**71 * 1.0 = 4.65706.
Hence, the GFR value is 4.65706 ml/min/1.73 m²."
505,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3635627-1,Extracted,"A 62-year-old diabetic woman on chronic hemodialysis for 7 months was admitted to our hospital because of general weakness and constipation for 1 week. She was bed-ridden for 1 month because of a fracture of L3-L4 spine due to a pedestrian traffic accident. Her vital signs were within normal ranges, and she had no fever. Physical examination revealed soft but distended abdomen and hypoactive bowel sounds. Plain abdominal radiographs showed large bowel distension with stool impaction (). Laboratory data showed hemoglobin of 8.6 g/dL, hematocrit 25.8%, random glucose 258 mg/dL, blood urea nitrogen 24.8 mg/dL, serum creatinine 4.1 mg/dL, sodium 129 mEq/L, potassium 4.5 mEq/L, calcium 8.0 mg/dL, phosphorus 1.7 mg/dL, and C-reactive protein 48.1 mg/L. The serum magnesium level was 3.0 mg/dL, and was 2.2 mg/dL 1 week ago (normal range, 1.8-2.6 mg/dL). She had taken magnesium-containing laxative (magnesium hydroxide 1500 mg per day) for a month, which was prescribed by another clinic. Therefore, magnesium hydroxide was discontinued and other laxatives were given.
On the 3rd hospital day, the patient became lethargic and showed somnolence. Physical examination showed generally hypoactive deep tendon reflex, abdominal distension with no bowel sounds, and severe tenderness on the lower abdomen. Her vital signs were; blood pressure: 90/60 mm Hg, pulse rate: 90 beats/minute, and body temperature: 37.0℃. Electrocardiogram revealed normal sinus rhythm. The serum magnesium level was rapidly increased to 6.0 mg/dL. Plain abdominal radiographs showed more distended large bowel loops compared with those on admission. Computed tomography (CT) showed diffuse and marked dilatation of large bowel loops with fecal impaction, compatible with megacolon. The clinical course and the serum magnesium level are shown in . Calcium gluconate was infused for a temporary antagonizing effect of hypermagnesemia. Nasogastric tube and rectal tube were inserted for gastrointestinal decompression. Hemodialysis was performed daily for hypermagnesemia correction. After three consecutive hemodialyses, the serum magnesium decreased to 3.3 mg/dL and vital signs became normal. The patient started to have bowel movements, and abdominal distension subsided slightly with defecation. On the 11th hospital day, she complained of severe abdominal pain again. Diffuse abdominal tenderness and rebound tenderness were noticed. She was hypotensive (blood pressure 90/50 mm Hg) with a rapid pulse of 100/minute and febrile (37.5℃). The serum magnesium level was 3.1 mg/dL. Follow-up abdominal CT showed large air fluid levels in the upper pelvic cavity, representing gastrointestinal perforation (). Emergent Hartmann's operation was performed. Operative finding was necrosis of the transverse colon and rectum, and histologic findings were gangrenous colitis with microperforation and serosal abscess of the colon and rectum. After the operation, her abdominal pain was resolved and vital signs became normal.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [62, 'years'], 'creatinine': [4.1, 'mg/dL']}",11.71611,11.1303,12.30192,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 62 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 4.1 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (4.1/0.7)**-1.2 * 0.9938**62 * 1.012 = 11.71611.
Hence, the GFR value is 11.71611 ml/min/1.73 m²."
506,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4465706-1,Extracted,"A 76-year-old female with type 2 diabetes mellitus (hemoglobin A1c 6.3 on metformin therapy), overweight (BMI 28), and history of benzodiazepine and opiate use was found at home confused and lethargic, surrounded by water bottles containing pink fluid. A red-and-white pill with a #5 inscribed (likely acetaminophen/oxycodone) was next to her, along with dark brown emesis stains. She was taking high doses of acetaminophen (sometimes exceeding 8 Extra Strength tabs daily) for back and leg pain for the past year. She used to take hydrocodone/acetaminophen but was no longer being prescribed this medication. She had been depressed and was previously on sertraline but had self-discontinued the drug for unknown reasons. Although she was never formally diagnosed with dementia, her daughter mentioned she had difficulty taking care of herself and was not eating, drinking, and taking medications appropriately for several weeks at least. She became progressively somnolent and was admitted to the ICU.
On admission, venous blood gas revealed serum pH 6.84, serum bicarbonate 5.8 mmol/L, and anion gap 22.2 mmol/L (Na = 138 mmol/L, Cl = 110 mmol/L), consistent with an anion gap metabolic acidosis. Other laboratory values included BUN 52.6 mg/dL, creatinine = 2.1 mg/dL, elevated beta-hydroxybutyrate (4.2 mmol/L), normal lactate 1.5 mmol/L, and random blood sugar 213 mg/dL. See for additional laboratory values. Serum osmolality was elevated at 324 mOsm/kg. As her calculated osmolality was 306.6 mOsm/kg (Na = 138 mmol/L, BUN = 52.6 mg/dL, and glucose = 213 mg/dL), there was an osmolal gap of 17.4 mOsm/kg. Her potassium was 7.5 mmol/L, but an EKG showed no peaked T waves (). However, she was given intravenous bicarbonate, insulin, glucose, calcium, and nebulized albuterol to treat the hyperkalemia. Given the elevated anion and osmolal gap and suspicion for ethylene glycol or methanol ingestion, 2 doses of fomepizole (670 mg IV Q12H) and 2 hemodialysis sessions were initiated while drug levels of these alcohols were still pending.
Serum and urine drug screens returned negative for ethylene glycol, methanol, ethanol, isopropanol, acetaminophen, and salicylates, but there were elevated levels of acetone (11 mg/dL) in the urine. Serum acetone was however not detectable. Her daughter later reported seeing a bottle of nail polish remover in her mother's house, though a direct ingestion history was not available. Due to the elevated beta-hydroxybutyrate and acetone levels, starvation ketosis was also entertained, and the patient was given thiamine along with intravenous glucose followed by enteral nutrition with close monitoring for refeeding syndrome. After a 5-day stay in the ICU, her mental status improved with supportive care. She was unable to clearly recount what occurred prior to her hospital admission, however. Creatinine returned to baseline of 0.8 mg/dL. She was transferred to the general floor and discharged to a nursing facility.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [76, 'years'], 'creatinine': [2.1, 'mg/dL'], 'sex': 'Female'}",23.96883,22.77039,25.16727,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 76 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.1 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.1/0.7)**-1.2 * 0.9938**76 * 1.012 = 23.96883.
Hence, the GFR value is 23.96883 ml/min/1.73 m²."
507,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5670091-1,Extracted,"A 66-year-old Caucasian male inpatient was transferred from the neurological ward to the emergency department (critical care unit) of the same hospital because of decreased consciousness. His medical history included poorly controlled type 2 diabetes mellitus, atrial fibrillation and cardiovascular disease.
The patient had been admitted to the department of cardiology 17 days earlier because of a myocardial infarction. He underwent successful percutaneous coronary intervention and felt well during the first days of hospitalisation. The patient developed focal pontine stroke [National Institutes of Health Stroke Scale (NIHSS) 7] 12 days later and was subsequently transferred to the neurology ward for further care. The patient experienced moderate dysarthria, some degree of hemiparesis and limb ataxia but was otherwise alert and responsive. However, reduced general condition with moderately severe disability kept the patient bedridden and necessitated intensified nursing care, including assistance with drinking and personal care, including bodily functions (modified Rankin scale 4). The patient was transferred to the emergency department 5 days later because of progressive loss of consciousness. Figure highlights the medically relevant events that occurred during hospitalisation.
On admission to the emergency department, the patient was stuporous (Glasgow coma scale 10; eye response 3, motor response 4, verbal response 3), had elevated body temperature (38.5 °C) and low blood pressure (95/50 mmHg) and appeared to be dehydrated. Laboratory findings included severe hypertonic hypernatraemia (164 mmol/l), hyperglycaemia (322 mg/dl), excessive glucosuria (3935 mg/dl) and impaired kidney function (creatinine 2.1 mg/dl). Chest X-ray (posterioranterior) showed patchy consolidations in upper lung fields. Table gives a summary of laboratory test results, the patient’s medical history and a list of his medications.
Diagnostic work-up primarily focused on the differential diagnosis of hypernatraemia as it was the predominant laboratory finding and considered the cause of impaired consciousness.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [66, 'years'], 'creatinine': [2.1, 'mg/dL'], 'sex': 'Male'}",34.07609,32.37229,35.77989,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 66 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.1/0.9)**-1.2 * 0.9938**66 * 1.0 = 34.07609.
Hence, the GFR value is 34.07609 ml/min/1.73 m²."
508,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5549307-1,Extracted,"A 14-year-old Han Chinese woman with a history of neurogenic bladder for more than 10 years was admitted to our Department because of coma for 12 h. The patient complained for diplopia without fever or diarrhea 4 days before her coma with no incentive. She had no limb weakness and was treated with Vitamin B1and mecobalamine. Her previous medical history included neurogenic bladder caused by spina bifida occulta for 12 years and hydronephrosis diagnosed 1 year before. Sometimes she had urine retention, but she received no treatment for the neurogenic bladder except for urethral catheterization occasionally. She had no seizures and no fever. On admission, physical examination revealed that she was unconscious. The pupils did not react to light and presented different sizes in each eye (left pupil diameter, 2.5 mm; right pupil diameter, 4 mm). On stimulation, she could move her 4 limbs spontaneously. There were exaggerated deep tendon reflexes over both legs and the right Barbinski sign was positive. However, her vital signs were stable: Blood Pressure (BP) was 120/81 mmHg; pulse rate, 76 beats/min; body temperature, 36.5 °C; breath, 12 times/min. Non-contrast brain computed tomography (CT) after the onset of her coma revealed diffuse brain stem hypodensity. Brain MRI acquired 4 h after the coma onset in the county hospital showed high signal at the dorsal part of the pontine base and the mid brain on fluid-attenuated inversion-recovery (FLAIR) imaging and T2-weighted imaging. However, diffusion-weighted images presented normal signal (Fig. ). The non- contrast abdominal CT preformed on the next day of admission showed chronic obstructive uropathy with a distended bladder, severe hydronephrosis and dual renal atrophy.
Blood analysis immediately after admission revealed renal failure [Urea nitrogen: 23.87 mmol/L, Creatinine: 566.8 μmol/L], and anemia [RBC: 2.5 × 1012/L, HGB: 79 g/L]. Arterial blood gas analysis revealed metabolic acidosis [pH 7.09 (7.35–7.45)]. Liver function was normal.
The patient was diagnosed with UE due to chronic renal failure and metabolic acidosis. She was immediately treated with 200 ml of bicarbonate at 5% conducted by quick intravenous injection, followed by 100 ml intravenous injection of bicarbonate at 5% once a day and 1.0 g of bicarbonate administered orally three times per day for 3 days. Simultaneously, she underwent urethral catheterization to relieve the urine retention. She was revived without diplopia 3 days after admission and the reviewed blood analysis after urethral catheterization showed that her renal function was returning to a normal level (Urea nitrogen: 13.10 mmol/L, Creatinine: 294 μmol/L); hence, dialysis was not necessary. She was treated with hypodermically administered erythropoietin 3000u twice a day, and ferrous sulfate 0.3 g orally thrice a day for the anemia. She was discharged 14 days after the admission without diplopia and any mental disturbance. She was still with the ureteral catheter because of the hydronephrosis. Two weeks after the discharge, the catheter was removed when abdomen ultrasonic showed decreased hydronephrosis. Follow-up MRI performed 2 months after the discharge revealed complete resolution of the brainstem UE (Fig. ). Reviewed blood analysis after 2 months of discharge showed that her renal failure still persisted (Urea nitrogen: 13.10 mmol/L, Creatinine: 190.3 μmol/L). However, she had no neurological disturbance or urinary retention. She underwent the comprehensive bladder-retraining program to avoid urinary retention and her renal function was regularly assessed once a month.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [14, 'years'], 'creatinine': [566.8, 'µmol/L'], 'sex': 'Female'}",9.17196,8.71336,9.63056,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 14 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 566.8 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 566.8 µmol. To convert 566.8 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 566.8 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00057 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00057 mol Serum Creatinine * 113.12 g/mol = 0.06448 g Serum Creatinine. To convert 0.06448 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.06448 g Serum Creatinine * 1000.0 mg/g = 64.48 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 64.48 mg Serum Creatinine/10.0 dL = 6.448 mg Serum Creatinine/dL. The concentration value of 566.8 µmol Serum Creatinine/L converts to 6.448 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (6.448/0.7)**-1.2 * 0.9938**14 * 1.012 = 9.17196.
Hence, the GFR value is 9.17196 ml/min/1.73 m²."
509,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8453423-1,Extracted,"A 61-year-old male patient with advanced heart failure under LVAD support presented to the emergency department with worsening dyspnoea, NYHA Class IV, and massive lower extremity and scrotal oedema. A continuous-flow LVAD had been implanted 7 years ago due to dilated cardiomyopathy with heart failure refractory to medical therapy. During LVAD support, the patient developed morbid obesity (body mass index 41 kg/m2) and chronic driveline infection. At presentation, arterial pulse was absent with normal capillary refill time. The core temperature was normal. The neurologic exam was unremarkable. Electrocardiogram demonstrated VF (). Interrogation of the implanted cardioverter defibrillator revealed VF while anti-tachycardic therapy had been previously deactivated due to RV lead malfunction. Left ventricular assist device interrogation showed no acute deviations of pump flow and power readings from the patient’s baseline (pump flow 6.0 L/min, power 5.0 W). Laboratory testing showed elevated serum creatinine (2.3 mg/dL, reference, 0.9–1.3 mg/dL) and N-terminal prohormone of brain natriuretic peptide (39 330 pg/mL, reference, <125 pg/mL). Serum lactate level in venous blood was 3.5 mmol/L (reference, 0.5–1.6 mmol/L). Trans-oesophageal echocardiography was then performed that depicted global akinesia of all cardiac chambers with profound dilation of the right ventricle and faint movements of the tricuspid valve leaflets, a situation resembling Fontan circulation ( and Videos 1 and 2). We initiated intravenous furosemide to relieve congestion and performed external defibrillation after excluding intracardiac thrombosis with trans-oesophageal echocardiography. After multiple unsuccessful attempts to restore normal rhythm with external defibrillation, oral amiodarone was initiated followed again by multiple unsuccessful defibrillations. Due to morbid obesity despite multiple dietary consultations and the patient’s wish not to proceed to bariatric surgery due to the high procedural risk, listing for heart transplantation was not possible. It was a shared decision to refrain from performing catheter ablation in the setting of severe comorbidities including morbid obesity, severe renal failure, chronic driveline infection, and incessant VF. The patient eventually developed end-stage renal failure and died due to complications of sepsis.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [61, 'years'], 'creatinine': [2.3, 'mg/dL']}",31.51697,29.94112,33.09282,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 61 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.3/0.9)**-1.2 * 0.9938**61 * 1.0 = 31.51697.
Hence, the GFR value is 31.51697 ml/min/1.73 m²."
510,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2900043-1,Extracted,"Eight year old girl, weighing 14kg presented with diminished vision for six months. Cataract was diagnosed in both the eyes. She was full term normally delivered child, detected to have esophageal atresia & imperforate anus after few hours of birth. She also had absent radius. A single kidney was accidentally detected on sonography.
At 30 hours of life she had undergone feeding gastrostomy, colostomy & esophageal pouch was created. At the age of 1½ years, she had undergone anal pull through surgery & colostomy closure was done. At the age of 2 years, esophageal atresia was corrected by formation of tube of colon anastomosing with stomach; subsequently esophageal pouch was closed. At the age of 6 years she presented with anuria & diagnosed to have renal hypertension and chronic renal failure due to single kidney. She was on hemodialysis initially once a week now twice a week. Prior to the day of surgery, she had undergone hemodialysis. She was on oral amlodepin 5mg BD & Losartan 50mg ½ HS since 2 years. She had deafness since 8 months, using hearing aids and now presented with diminution of vision of both the eyes, diagnosed as bilateral cataract.
On clinical examination, (Fig. –), she was malnourished, weighing 14 Kg & height of 100cm. She was deaf, non-cooperative and unable to stand due to weakness. Her left arm was short due to Radial aplasia. Right arm & forearm had AV fistula. Her pulse rate was 120/min regular; blood pressure 160/100mmHg measured on left upper arm and body temperature was normal. She was pale, no icterus or cyanosis was observed. Her spine was normal. In cardiovascular system, S1\S2 was normal with soft systolic murmer. On respiratory system examination, airentry was equal on both the sides; there were no foreign sounds. Mallampati classification could not be elicited, as child was un-cooperative.
The blood investigations reported haemoglobin 6.9gm%, blood group B+, haematocrit 19%, random blood sugar 75mg, bleeding time 2 min 5 sec, prothrombin time 13 sec & I.N.R. 1:1. Before dialysis, blood urea was elevated to 70mg/dl, serum creatinine 5.3mg/dl & serum potassium 5.6mmol/L. After dialysis, blood urea was reduced to 15mg/dl, serum creatinine 1.8mg/dl & serum potassium 3.7mmol/L. Her ECG showed sinus tachycardia and in chest X-ray, there was cardiomegaly. On 2-D echo, mild concentric LVH, diastolic dysfunction, ejection fraction 60% was reported.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [8, 'years'], 'creatinine': [1.8, 'mg/dL'], 'sex': 'Female'}",44.02014,41.81913,46.22115,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 8 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.8 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.8/0.7)**-1.2 * 0.9938**8 * 1.012 = 44.02014.
Hence, the GFR value is 44.02014 ml/min/1.73 m²."
511,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8201711-1,Extracted,"A 69-year-old man was admitted to our hospital on Jan 25, 2020 with a complaint of fever and abdominal pain for 1 days’ duration. The patient was diagnosed with hypertension and cerebral infarction 10 years ago, and also with a medical history of renal anemia and cholecystectomy. In 2014, the patient was diagnosed with IgA nephropathy by a renal biopsy and was treated with diet. In 2018, the patient progressed to chronic kidney disease stage 5 and underwent peritoneal dialysis for 2 years until this admission.
At the emergency department on Jan 25, 2020, his physical examination showed a body temperature of 38.6 °C, a blood pressure of 206/95 mmHg, a pulse rate of 85 beats/min, and a respiratory rate of 18 breaths/min. He complained tenderness and rebound pain in his abdomen, with pitting lower extremity edema. Redness or discharge was not found near the peritoneal catheter. Laboratory tests revealed a white blood cell count (WBC) of 13.9 × 109/L with 80.7% neutrophils, a hemoglobin (Hb) level of 74 g/L, a C-reactive protein (CRP) level of 96.7 mg/L, a procalcitonin (PCT) level of 3 ng/ml, a B-type natriuretic peptide (BNP) level of 939 pg/mL, an urea level of 25.27 mmol/L and a creatinine level of 924.2 μmol/L. Routine testing of the PD effluent revealed a yellow and muddy appearance with positive results in the Rivalta test, WBC count of 13,363 × 106/L (neutrophils: 98%). Peritoneal dialysis-associated peritonitis was diagnosed initially. The PD effluent was collected for bacterial culture.
Being admitted to the Nephrology ward later in the same day, another PD effluent was collected for bacterial culture before starting an empirical antibiotic therapy. Then, the patient was empirically treated with ceftizoxime intravenously (2 g bid iv) and intraperitoneal injection of teicoplanin (0.2 g qd ip) for 7 days. On Feb 1, a gram-positive bacterium was found from PD effluent culture. Therefore, teicoplanin (0.2 g qd iv) and imipenem (0.5 g qd ip) were administered based on the antimicrobial susceptibility testing for the next 4 days. Due to the low blood concentration of teicoplanin and intraperitoneal catheter removed on Feb 5, the treatment was adjusted to teicoplanin (0.4 g qd iv) and imipenem (0.5 g q12h iv). With the continuous treatment with teicoplanin and imipenem for 15 days, the infection symptom was improved with a normal body temperature of 36.6 °C, a PCT level of 0.7 ng/ml and a CRP level of 76.8 mg/L. Routine testing of the peritoneal fluid were within normal ranges. Peritoneal dialysis effluent culture and intraperitoneal catheter culture also showed negative result.
Thereafter, arteriovenous fistula angioplasty was performed for hemodialysis on Feb 15 and the patient developed fever (38 °C) and disturbance of consciousness on the first day after surgery. No cerebral hemorrhage and cerebral infarction were found by cranial Computed Tomography (CT). Considered the toxicity, imipenem was switched to biapenem. However, the patient’s symptoms and signs did not improve, and the laboratory test indicators gradually increased. On Feb 17, elevated PCT (0.801 ng/mL) and CRP (76.8 mg/L) was observed. Blood culture showed a negative result, and amikacin was given instead of biapenem for the treatment. On Feb 20, the patient still had a fever (37.8 °C) and thick sputum. Laboratory examination revealed a PCT of 1.34 ng/mL, a CRP of 58.5 mg/L, a ESR of more than 140 mm/h, a Hb of 45 g/L. The fecal occult blood test was positive and the blood culture was negative. High resolution CT of the thorax showed inflammatory manifestations including pulmonary cord, flocculent shadow and exudate. Unfortunately, the patient died on Feb 25 due to septic shock and multi-organ failure.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [69, 'years'], 'creatinine': [924.2, 'µmol/L'], 'sex': 'Male'}",4.90026,4.65525,5.14527,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 69 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 924.2 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 924.2 µmol. To convert 924.2 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 924.2 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00092 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00092 mol Serum Creatinine * 113.12 g/mol = 0.10407 g Serum Creatinine. To convert 0.10407 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.10407 g Serum Creatinine * 1000.0 mg/g = 104.07 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 104.07 mg Serum Creatinine/10.0 dL = 10.407 mg Serum Creatinine/dL. The concentration value of 924.2 µmol Serum Creatinine/L converts to 10.407 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (10.407/0.9)**-1.2 * 0.9938**69 * 1.0 = 4.90026.
Hence, the GFR value is 4.90026 ml/min/1.73 m²."
512,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5552637-1,Extracted,"A 79-year-old male was referred due to significant coronary artery stenosis noted by coronary computed tomographic angiography (CTA). Coronary CTA showed 3-vessel coronary artery and LM disease involving bifurcation with long and heavily calcified lesions of high syntax score of 33. Laboratory investigation revealed normal renal function (serum creatinine 0.85 mg/dL). Transthoracic echocardiography revealed absence of regional wall motion abnormality and pharmacologic techneitum-99m myocardial single photon emission computed tomography revealed reversible defect in the inferior wall. To minimize the risk of CIN, intravenous normal saline infusion and usage of iso-osmolar iodine contrast was done. Initial coronary angiography revealed total occlusion of distal right coronary artery (RCA) and LM disease involving bifurcation (). RCA lesion was successfully revascularized with 2.5×13 mm sized Orsiro (Biotronik, Berlin, Germany) stent implantation with total 100cc of contrast volume ().
Staged PCI for treatment of LM bifurcation lesion was done via femoral access one week later. Initial left coronary angiography was done with 6 cc injection of contrast dye (). Prior to PCI, initial angiogram which had already been performed one week ago with same angle of projection was uploaded to the monitor for PCI guidance. After advancing a guide wire into both left anterior descending (LAD) and left circumflex artery (LCX) without use of contrast dye, pre-stent IVUS was performed to determine optimal proximal and distal stent landing zones, stent diameter and length (). Recording of position of IVUS transducer on fluoroscopic image was useful to determine the distal landing zone of stent (, arrow). Based on the angiographic and IVUS findings, two stent technique in a culotte fashion was performed with fluoroscopic guidance, but without the use of contrast dye. Both branches were pre-dilated with 3.5×15 mm non-complaint balloon. Then, a 3.5×23 mm XIENCE Alpine (Abbott Vascular, Santa Clara, CA, USA) stent was deployed at 11 atm in LM to LCX (). The stent was re-crossed and the un-stented branch was dilated with 2.0×12 mm and 3.5×23 mm non-complaint balloons. The 3.5×38 mm XIENCE Alpine stent was positioned towards the LM to LAD at 14 atm (). The first stent was re-crossed and final kissing balloon inflation was performed with two 3.5×15 mm non-compliant balloons (). Post-stent IVUS confirmed optimal stent deployment without acute complications; minimal lumen area was 8.5 mm2 in proximal LAD and 7.4 mm2 in ostial LCX (). After confirmation of stent optimization with post-stent IVUS examination, final second angiography with 6 cc contrast injection revealed successful results (). During the two stent technique in a culotte fashion for LM bifurcation lesions, successful results were achieved with minimal amount of contrast dye and only two angiographic imaging under the IVUS guidance. This patient was clinically stable for 2 days without CIN (Serum creatinine 0.74 mg/dL). This patient was discharged 2 days after PCI and has been uneventful.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [79, 'years'], 'creatinine': [0.74, 'mg/dL'], 'sex': 'Male'}",85.43196,81.16036,89.70356,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 79 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.74 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.74/0.7)**-0.302 * 0.9938**79 * 1.0 = 85.43196.
Hence, the GFR value is 85.43196 ml/min/1.73 m²."
513,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3109784-1,Extracted,"A 20-year-old woman presented with pain and swelling of both knees from last 10 days that started while coming downstairs and progressively increased. She was unable to stand without support. There was no significant medical history. On examination, she was afebrile, asthenic, and pale; pulse was 80 beats/min, blood pressure was 130/80 mmHg. Both knees were swollen and tender, and revealed defects above low-lying patellae. There was no active extension possible against gravity; patellar reflex could not be elicited on either side. Laboratory investigations revealed hemoglobin of 7.5 g/dL. Urinalysis showed albuminuria (1+), urinary sediment had 3–4 red cells/high power field; there were no casts, pus cells, or sugar; 24-h urinary protein excretion was 1.5 g/d. Blood chemistry results were as follows: blood urea of 130 mg/dL, serum creatinine 6 mg/dL with estimated creatinine clearance of 19.3 mL/min; serum calcium was 9 mg/dL, phosphate was 5 mg/dL, parathyroid hormone (PTH) level was 600 pg/mL; blood pH was 7.2, bicarbonate level was 16 mEq/L, potassium was 3 mEq/L; sodium and liver function tests were normal. Serological tests did not suggest any evidence of hepatitis (B, C) or HIV infection; antinuclear antibodies and antidouble stranded antibodies were absent.
X-ray of knees showed slightly low-lying patella with diminished bulk of quadriceps tendon just above the patella in either knee [Figures and ]; soft tissue calcification was seen in the suprapatellar region of the right knee []. T2-weighted MRIs in sagittal plane revealed discontinuity between distal quadriceps tendon and upper pole of patella in both knee joints with the intervening space filled with hyperintense signal intensity, in definite contrast to hypointense signal intensity of tendon [Figures and ]; small joint effusion was seen in the suprapatellar region on either side [Figures and ]. Bones, menisci, and cruciate ligaments were normal. A diagnosis of bilateral spontaneous quadriceps tendon rupture with stage IV CKD with hyperparathyroidism and metabolic acidosis was made.
Patient was treated with intravenous fluids, sodium bicarbonate, and potassium chloride judiciously, and monitored carefully for the correction of acidosis and hypokalemia. Immediate cause of hypokalemia could not be ascertained; however, the potassium levels remained normal after initial correction. Ultrasound showed bilateral small and echogenic kidneys with loss of corticomedullary differentiation. Renal biopsy revealed advanced glomerulosclerosis. After stabilization, surgical repair of the quadriceps tendons was performed by fixing the tendon to the patella through nonabsorbable sutures. Knees were splinted in extension followed by gradual weight bearing after 4 weeks and complete weight bearing at 7–8 weeks. She gradually gained the power and movements in her knees and could stand independently after 4 months. Peritoneal dialysis was continued and her PTH level came down with continued vitamin D therapy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [20, 'years'], 'creatinine': [6.0, 'mg/dL']}",9.63352,9.15184,10.1152,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 20 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 6.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (6.0/0.7)**-1.2 * 0.9938**20 * 1.012 = 9.63352.
Hence, the GFR value is 9.63352 ml/min/1.73 m²."
514,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4808535-1,Extracted,"A 65-year-old male visited a community hospital complaining of urinary retardation, dysuria, and gross hematuria. The patient had history of hypertension, hyperuricemia, and hyperlipidemia. He had no family history of prostate cancer, and his prostate-specific antigen (PSA) value was 1.6 ng/mL (normal range: 0–4 ng/mL). A physical examination revealed low-grade fever. Administration of 4 mg of alpha blocker did not relieve his symptoms.
Laboratory evaluations were as follows: hemoglobin (Hb), 9.6 g/mL, hematocrit (Ht), 28.9%, leukocytes, 8200 cells/mL, glucose, 175 mg/dL, creatinine, 0.65 mg/dL, and C-reactive protein (CRP), 17.96 mg/dL. Urinalysis noted 30–40 WBCs/hpf and 5–9 RBCs/hpf. Urine cytology is Class IIIa.
Abdomen and pelvic computed tomography (CT) scan and magnetic resonance imaging (MRI) showed a lobular lesion with irregular edge and fluid collection in the left lobe of prostate ().
Chest CT scan in the presence of a dye showed bilateral, bizarre pulmonary nodules with cavitation and an enhancing mass of about 6.5 cm at its largest diameter ().
This patient was admitted to a hospital for intensive examination.
Thus, a transurethral resection of the prostate (TURP) as part of tissue sampling and a bronchoscopic examination were performed. Histologic examination of the prostate revealed accumulation and cellular infiltration of neutrophils and lymphocytes as well as histiocytosis and necrotizing tissues. These findings were consistent with those of GPA (). Histologic examination of lung lesions also showed accumulation and cellular infiltration of neutrophils and lymphocytes as well as histiocytosis with fibrinoid necrosis ().
Cerebral MRI showed that T2WI high-iso signal occupied the area from right lateral maxillary to ethmoid sinus involving a fluid collection.
An immunologic investigation showed positive c-ANCA with high anti-PR3 activity (296 U/mL).
We diagnosed GPA as the systemic disease considering these results, and the patient was treated in the department of respiratory medicine.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [65, 'years'], 'creatinine': [0.65, 'mg/dL'], 'sex': 'Male'}",96.92652,92.08019,101.77285,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 65 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.65 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.65/0.7)**-0.302 * 0.9938**65 * 1.0 = 96.92652.
Hence, the GFR value is 96.92652 ml/min/1.73 m²."
515,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5968655-1,Extracted,"A 74-year-old female who had been diagnosed with hypertension 15 years prior to presentation, hypothyroidism 8 years before presentation, and aortic stenosis 2 years before presentation, presented with the first episode depression of insidious onset for the past 9 months, precipitated by a life stressor. Exploration of history revealed that initially she developed sadness of mood, anhedonia, tiredness, bleak and pessimistic views of future, disturbed sleep, and poor appetite. Over the next 2–3 months, the symptoms progressed further, and she additionally developed suicidal ideations, poor attention and concentration, low self-esteem, and delusion of poverty. She had received adequate trials of tablet escitalopram (10–20 mg/day for 3 months) and sertraline (up to 150 mg/day) along with quetiapine (50–100 mg) for 6 weeks without much improvement in psychopathology. While receiving the combination of sertraline and quetiapine, she developed side effects in the form of bradykinesia, rigidity, and tremors.
When evaluated for the first time at the inpatient setting at our center, she was found to have sadness of mood, marked psychomotor retardation, delusion of poverty, suicidal ideations, marked sleep disturbances, and poor oral intake. A diagnosis of severe depression with psychotic symptoms was considered.
She was receiving tablet torsemide 20 mg/d and tablet amlodipine 5 mg/d for hypertension, and tablet thyroxine 50 μg/day for the hypothyroidism. On investigation, she was found to have features suggestive of raised serum urea (55 mg/dl) and creatinine levels (1.6 mg/dl), which were considered to be suggestive of prerenal acute renal failure most likely due to reduced oral intake. All other investigations in the form of hemogram, serum electrolytes, liver function tests, and X-ray chest were found to be within normal limits. Initially, she was treated with tablet mirtazapine up to 22.5 mg/day for 3 weeks, but there was no improvement. However, during this period, her renal status improved over 1 week with oral rehydration and renal diet. Following this, ECT was considered. On further investigation, her echocardiography revealed severe aortic stenosis (aortic value area 0.8 cm2 [normal values - 2.5–4.5 cm2]) with the normal left ventricular function. The aortic stenosis velocity was 4.3 m/s and left ventricular ejection fraction was 60%–65%. Her electrocardiogram revealed T wave inversion in leads I, II, aVL, V4–V6. History was again reviewed and patient had no history suggestive of dyspnea, angina, syncope, and congestive heart failure.
She was cleared for ECT under high-risk consent and it was decided to administer ECT in a setting where all the equipments for cardiopulmonary resuscitation were available in case of any cardiac emergency. ECT was administered without the use of anticholinergics and injection esmolol was given before ECT. She was properly oxygenated during the ECT procedure. Throughout the procedure and 2 h after the procedure, her electrocardiogram, blood pressure, heart rate, and oxygen saturation were closely monitored. She received nine effective bilateral modified ECTs, all of which were uneventful and by the end of ECT course, and she achieved clinical remission and was discharged on tablet mirtazapine 30 mg/day. She has been maintaining well thereafter for the past 2 years.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [74, 'years'], 'creatinine': [1.6, 'mg/dL'], 'sex': 'Female'}",33.63318,31.95152,35.31484,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 74 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.6 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.6/0.7)**-1.2 * 0.9938**74 * 1.012 = 33.63318.
Hence, the GFR value is 33.63318 ml/min/1.73 m²."
516,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5005662-1,Extracted,"A 54-year-old woman presented to the emergency department after 2 days of lower limb weakness and bilateral ankle pain. She had a known history of type 2 diabetes mellitus, diabetes mellitus nephropathy with chronic kidney disease, and chronic gouty arthritis. She was orally administered 0.6 mg colchicine once or twice daily for 8 months. She reported no recent traumatic event, alcohol ingestion, or substance abuse.
Four days before visiting our emergency department, the patient was discharged from our nephrology ward after undergoing treatment for a urinary tract infection. During her hospitalization, she was administered intravenous cefazolin for 7 days. Her current maintenance medications including oral colchicine (0.9 mg, once daily) were also prescribed. She still experienced dysuria, urgency, and lower abdominal fullness. Repeated urinalysis revealed the presence of yeast. She was diagnosed with fungal cystitis and administered a 7-day course of oral fluconazole (100 mg) once daily. On day 5 of the course, she was discharged and asked to continue treatment with oral colchicine (0.6 mg, twice daily) and fluconazole to complete the 7-day course.
The initial physical examination revealed an arterial blood pressure of 133/69 mmHg, a pulse rate of 89 beats/min, a respiratory rate of 19 breaths/min, and body temperature of 36.6 °C. She had bilateral tenderness in her ankles with general weakness. Neurological examination revealed marked symmetrical weakness (Medical Research Council grade 4/5). Her sensation and coordination were intact. She had no rash or lymphadenopathy. Her chest plain film showed no active lung lesion and borderline heart size. Cardiac echography revealed preserved left ventricle systolic function without cardiac chamber dilatation. Initial laboratory investigations revealed hyperkalemia (6.2 mmol/L vs. normal: 3.4–4.7 mmol/L), and elevated blood urea nitrogen (181 mg/dL vs. normal: 7–20 mg/dL), serum creatinine (11.16 mg/dL vs. normal: 0.5–1.2 mg/dL), and creatine kinase (CK, 803 U/L vs. normal: 24–120 U/L) levels. Her liver function tests showed elevated alanine aminotransferase (ALT, 112 U/L vs. normal: 0–40 U/L) levels. She had a decreased white blood cell count (2830 cells/mL vs. normal: 4000–9900 cells/mL) and hemoglobin levels (9.7 g/dL vs. normal: 12–16 g/dL). Anemia, indicated by the reduced hemoglobin level, is a common complication of chronic kidney disease. Cholesterol levels, amylase, direct and indirect bilirubin, C-reactive protein, rheumatoid factor, and thyroid hormones were all within their normal ranges.
Motor nerve conduction studies revealed prolonged distal latency, slow nerve conduction velocity, delayed F-wave latency on four limbs, and low compound muscle action potential amplitude in the bilateral peroneal and tibial nerves. Hoffmann’s reflex study showed no response in both lower limbs. Sensory nerve conduction studies revealed slow nerve conduction velocities in bilateral median nerves across the wrist, and relatively low sensory nerve action potential amplitude in four limbs. Needle electromyography demonstrated severely active denervation in both the lower limbs.
She was diagnosed with neuromyopathy based on clinical presentation and laboratory studies. On admission, her anti-inflammatory drugs were changed to corticosteroids for gouty arthritis, and colchicine was withdrawn. Ten days after the cessation of colchicine, her laboratory values returned to the normal range (potassium 4.1 mmol/L; ALT 41 U/L; white blood cell count 5540 cells/mL), with the exception of the hemoglobin level (9.6 g/dL). Her weakness disappeared gradually.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [54, 'years'], 'creatinine': [11.16, 'mg/dL'], 'sex': 'Female'}",3.70284,3.5177,3.88798,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 54 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 11.16 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (11.16/0.7)**-1.2 * 0.9938**54 * 1.012 = 3.70284.
Hence, the GFR value is 3.70284 ml/min/1.73 m²."
517,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7142028-1,Extracted,"A 72-year-old female was referred to our hospital with unresolved dyspnea. She had a history of hypertension, diabetes, asthma, and cerebral infarction. Two weeks before admission, dyspnea and cough developed. She was admitted to the local hospital for 10 days and was on antibiotics, including a third generation cephalosporin (ceftriaxone) and carbapenem (meropenem), resulting from suspected pneumonia.
At admission, she had resting dyspnea. Her body temperature was 37.1°C, heart rate 108 beats/min, blood pressure 140/80 mmHg, respiratory rate 24 breaths/min, and oxygen saturation 84% while receiving oxygen via a nasal cannula at a rate of 5 L/min. Physical examination was notable for crackles without wheezing in the lungs and pitting edema in both lower legs. Arterial blood gas analysis showed pH 7.33, PCO2 52 mmHg, PO2 56 mmHg, HCO3- 20.6 mM/L, and O2 saturation 84.6%. Laboratory tests revealed the following values: white blood cell count 8,840/µL, hemoglobin 11.2 g/µL, platelet count 393 K/µL, total bilirubin 0.17 mg/dL, aspartate aminotransferase 20 IU/L, alanine aminotransferase 14 IU/L, alkaline phosphatase 97 IU/L (range, 30–120 IU/L), gamma glutamyl transferase 46 IU/L (range, 5–39 IU/L), blood urea nitrogen 29.9 mg/dL, creatinine 0.69 mg/dL, C-reactive protein 27.57 mg/L (range, 0–5 mg/L), activated partial thrombin time 25.8 sec (range, 23–35 sec), and international normalized ratio 1.15. The level of brain natriuretic peptide and D-dimer were 1,921 pg/mL (range, 0–150 pg/mL) and 5.8 μg/mL (range, 0–0.5 μg/mL), respectively; other laboratory results were unremarkable. Electrocardiogram showed sinus tachycardia at a rate of 110 beats/min, T wave inversion in V1-4, poor R-wave progression, and rightward axis deviation, known as ‘right ventricle (RV) strain.’
Transthoracic echocardiography (TTE) () showed RV dilatation with reduced systolic function, moderate tricuspid valve regurgitation (proximal isovelocity surface area radius, 5.1 mm; jet area, 7.5 cm2), left ventricle septal flattening during the systolic phase, inferior vena cava plethora, and moderate PH (pulmonary artery systolic pressure [PASP], 65.7 mmHg; mean pulmonary arterial pressure, 44 mmHg) without obvious atrial or ventricular septal defect. Left ventricular systolic function was preserved with an ejection fraction of 71%. Contrast–enhanced chest computed tomography (CT) with pulmonary arteriography was performed. CT showed the presence of multiple small consolidative lesions in both lung fields without evidence of pulmonary thromboembolism. A pulmonary function test showed moderate obstructive lung defect with good response to bronchodilator (forced expiratory volume in 1 sec [FEV1]/forced vital capacity [FVC] 78%, pre-FEV1 0.79 L, 43%→post-FEV1 0.99 L, 58%). A 15% decrease in the diffusing capacity of the lung for carbon monoxide was noted.
Given these findings, right-sided heart failure originating from untreated asthma and acute decompensation caused by community-acquired pneumonia was suggested as the initial diagnosis. However, despite antibiotics and proper diuretic-based heart failure therapy, her dyspnea gradually worsened. On the 12th hospital day (HD), oxygen was supplied using a high flow nasal cannula (FiO2, 0.4; flow, 40 L/min), and oxygen saturation was maintained within the range of 90%–95%.
On the 14th HD, contrast-enhanced whole-body CT and ventilation/perfusion lung scans were performed to determine the cause of clinical deterioration. Chest CT showed numerous centrilobular nodules with “tree-in-bud” sign and pleural-enhancing nodules (). Abdominopelvic CT showed a 3-cm less enhancing mass with ill-defined margins located at the pancreatic head and neck region, in addition to upstream pancreatic duct dilatation (). A ventilation lung scan showed no significant decreased activity while a perfusion lung scan revealed multifocal peripherally distributed small perfusion defects in the bilateral lung fields (). Moreover, serum carbohydrate antigen 19-9 level was elevated 77.9 U/mL (range, 0–35 U/mL); therefore, an endoscopic ultrasonographic-guided biopsy was needed for histopathological confirmation of pancreatic cancer. However, it was impossible to obtain the biopsy due to the unbearable severe dyspnea and opposition of the patient’s family. 18F-2-fluoro-2-deoxy-D-glucose-positron emission tomography integrated with computed tomography (FDG-PET/CT) was performed for diagnosis and staging of pancreatic cancer after discussion with the Pancreatobiliary Department (). This test showed an intensive hypermetabolic mass at the pancreatic head and neck portion with multiple common hepatic, portocaval, aortocaval, hepatoduodenal, para-aortic, left common iliac, mediastinum, right lower paratracheal, and right interlobar lymph node metastases in addition to numerous tiny bilateral lung and both pleural metastases.
According to these clinical and radiologic findings, PTTM secondary to advanced pancreatic cancer was suggested as the final diagnosis. The clinical stage was TxN2M1, stage IV according to the 8th edition of the American Joint Committee on Cancer staging system []. Since the disease continuously progressed to multi-organ failure, including respiratory failure and acute kidney injury, only supportive care could be provided, and the patient died on the 27th day after diagnosis.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [72, 'years'], 'creatinine': [0.69, 'mg/dL'], 'sex': 'Female'}",92.15148,87.54391,96.75905,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 72 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.69 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.69/0.7)**-0.241 * 0.9938**72 * 1.012 = 92.15148.
Hence, the GFR value is 92.15148 ml/min/1.73 m²."
518,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5852897-1,Extracted,"A 73-year-old male with alcoholic cirrhosis complicated by prior spontaneous bacterial peritonitis on ciprofloxacin prophylaxis presented to the emergency department with fever, abdominal pain, and nausea. On admission he had normal vital signs. His abdomen was distended and diffusely tender with a positive fluid wave. Laboratory results revealed a leukocytosis to 18,200 cells/mL, stable liver function tests, and a creatinine of 1.8 mg/dL. His Model for End-Stage Liver Disease (MELD) score was 18 on initial presentation. Paracentesis revealed hazy peritoneal fluid with 2,590 white blood cells of which 2,434 were neutrophils. He was started on vancomycin and ertapenem for sepsis secondary to spontaneous bacterial peritonitis but progressively worsened clinically. On day 4 of hospitalization, the patient became tachycardic and hypotensive with a leukocytosis of 29,900 cells/mL. Repeat paracentesis revealed 2,670 neutrophils. A CT scan of the abdomen did not show evidence of focal infection or gastrointestinal perforation. Peritoneal fluid cultures revealed Lactobacillus paracasei as the sole pathogen isolated from both aerobic and anaerobic plates. The isolate was resistant to carbapenems and sensitive to clindamycin and penicillin. The patient was switched to clindamycin and high-dose intravenous penicillin (2 million units every 4 hours) for Lactobacillus coverage. Despite a rapid improvement in his peripheral leukocytosis and hemodynamic measures, the patient's creatinine continued to rise rapidly. He ultimately developed type 2 hepatorenal syndrome with anuric renal failure. He was transitioned to comfort care and died of multiorgan failure.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [73, 'years'], 'creatinine': [1.8, 'mg/dL'], 'sex': 'Male'}",39.25354,37.29086,41.21622,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 73 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.8 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.8/0.9)**-1.2 * 0.9938**73 * 1.0 = 39.25354.
Hence, the GFR value is 39.25354 ml/min/1.73 m²."
519,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8583227-1,Extracted,"A sixty-one-year-old man with a significant two-year past medical history of bilateral lower extremity weakness and a left parasellar meningioma presented with anorexia, intermittent dysphagia, and early satiety with intermittent nausea, vomiting, and diarrhea from which he had been suffering for the past three months. During this time, he experienced a 20-pound unintentional weight loss. He was not taking any medications known to cause peripheral neuropathy; additionally, he reported a 20 pack/year smoking history and denied alcohol or illicit substance use.
Prior to admission, in January 2016, he had undergone extensive workup for similar symptoms of abdominal pain, nausea, vomiting, and dysphagia. The resulting workup included a CT of the chest, abdomen, and pelvis that demonstrated a fatty infiltrative change in the liver and a kidney, ureter, and bladder X-ray that showed a nonobstructive abdominal gas pattern with no dilated bowel loops or masses identified. An esophagogastroduodenoscopy done in March 2016 demonstrated dysphagia likely secondary to underlying neurologic issues, along with a small hiatal hernia, and an MRI that June revealed an unchanged left middle cranial fossa mass consistent with meningioma.
Upon presentation in July 2016, our patient reported bilateral lower extremity pain present over the past six months, which had been attributed to distal axonal motor neuropathy by electromyogram and nerve conduction studies by his outpatient neurologist. He characterized his pain as alternating between throbbing or shooting up his legs, and that he had been started on pregabalin six months prior with some amelioration of his symptoms. Oxcarbazepine had been recently added to his medication, with some results. He also reported weakness in both his feet since receiving radiation therapy for meningioma two years prior, requiring the use of a walker to ambulate.
In the emergency department, his creatinine was elevated to 1.31 mg/dL from a baseline of 0.9 mg/dL, and troponins were elevated threefold with a normal EKG. His physical exam was significant for splenomegaly and small-volume perihepatic ascites contributing to abdominal distension. He was admitted for acute kidney injury.
A CT of his abdomen and pelvis was obtained, revealing small-volume peri-hepatic ascites, splenomegaly (Figure ), and incidentally-noted expansile lesions of the left ischium, acetabulum, and ilium (Figure ).
Due to these findings and noted bilateral lower extremity neuropathic weakness, we obtained further testing to corroborate our suspicions of a plasma cell disorder. Laboratory data were significant for monoclonal gammopathy (bi-clonal IgG lambda on serum protein electrophoresis), as well as marked endocrinopathy: adrenal insufficiency with a low AM cortisol of 3.6 ug/dL; hypothyroidism with a TSH of 3.76 uIU/mL and low free thyroxine (T4) of 0.45 ng/dL; and hypogonadism with low free testosterone of 0.3 pg/mL. His VEGF levels were elevated to 377 pg/mL. Bone marrow core biopsy confirmed our suspicions of a plasma cell dyscrasia; the core biopsy was 50% cellular, with plasma cells comprising 7% of the smear cellularity, and of which approximately half were noted to be immunophenotypically abnormal.
Given his polyneuropathy, organomegaly, endocrinopathy, IgG lambda, skin changes (leukonychia and rubor in his extremities), and extravascular fluid overload, he was diagnosed with POEMS syndrome. He was initiated on lenalidomide and dexamethasone following diagnosis, and eventually received an autologous stem cell bone marrow transplant.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [61, 'years'], 'creatinine': [1.31, 'mg/dL'], 'sex': 'Male'}",61.92875,58.83231,65.02519,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 61 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.31 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.31/0.9)**-1.2 * 0.9938**61 * 1.0 = 61.92875.
Hence, the GFR value is 61.92875 ml/min/1.73 m²."
520,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-4901,Extracted,"A 32-year-old man with a history of chronic alcoholism presents to the emergency department with vomiting and diarrhea for 1 week. He states he feels weak and has had poor oral intake during this time. The patient is a current smoker and has presented many times to the emergency department for alcohol intoxication. His temperature is 97.5°F (36.4°C), blood pressure is 102/62 mmHg, pulse is 135/min, respirations are 25/min, and oxygen saturation is 99% on room air. On physical exam, he is found to have orthostatic hypotension and dry mucus membranes. Laboratory studies are ordered as seen below.

Serum:
Na+: 139 mEq/L
Cl-: 101 mEq/L
K+: 3.9 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 9.8 mg/dL

The patient is given normal saline, oral potassium, dextrose, thiamine, and folic acid. The following day, the patient seems confused and complains of diffuse weakness and muscle/bone pain. An ECG and head CT are performed and are unremarkable.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [32, 'years'], 'creatinine': [1.1, 'mg/dL'], 'sex': 'Male'}",91.46941,86.89594,96.04288,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 32 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.1/0.9)**-1.2 * 0.9938**32 * 1.0 = 91.46941.
Hence, the GFR value is 91.46941 ml/min/1.73 m²."
521,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3652045-1,Extracted,"In July 2012, a 91-year-old Italian male patient was admitted to the Internal Medicine Unit of the Perugia General Hospital complaining from fatigue, anorexia, weight loss of 10 Kg in few weeks, and arthralgia. The patient's medical history revealed that he was suffering from myelodysplastic syndrome, complicated by autoimmune hemolytic anemia since March 2012, treated with periodic blood transfusions, alpha recombinant human erythropoietin 40,000 IU/week subcutaneously, and since the last month, with prednisone 25 mg/day, cutting down the dosage by half every week. The patient completed corticosteroid therapy few days before admission. He suffered also from previous ischemic stroke, moderate renal insufficiency, psychosis, and chronic obstructive pulmonary disease.
On admission the examination showed low-grade fever (37.2°C), fatigue, nonproductive cough, bilateral basal crackles, and wheezes at chest auscultation. His blood pressure was 118/78 mmHg, the heart rate was 82 beats per minute, the respiratory rate was 20 breaths per minute, and oxygen saturation measured by pulse oximetry was 95%. The patient's body weight was 76 kg. No other significant abnormalities were found. Two sets of blood cultures were drawn from different peripheral sites at the same time.
Main laboratory tests performed on admission showed hemoglobin 10.2 g/dL, leukocytes 11.3 × 103/μL (neutrophils 77%, lymphocytes 16%, and monocytes 6.3%), platelets 202 × 103/μL, sedimentation rate 42 mm/h, creatinine 1.95 mg/dL, albumin 2.7 g/dL, and gamma globulin 29.5% with two monoclonal bands in gamma region. Other blood-chemistry tests did not show significant pathological values. The chest X-ray performed on admission disclosed multiple nodular acinar opacities throughout both lungs with diffuse interstitial thickening. The Mantoux skin test showed negative result. A sputum sample was collected, and Gram stain showed more than 25 neutrophils per low-power field and normal upper respiratory tract bacterial population, but no potential pathogens present. Culture was negative for common bacterial pathogens. A presumptive diagnosis of community-acquired pneumonia in immunocompromised patient was made, and antimicrobial therapy with ceftriaxone 2 g intravenously/die was started. In spite of that, the patient's conditions slightly worsened over the next couple of days, with decreased level of consciousness and low-grade fever (≤37.5°C) episodes every day. On the fourth day, the aerobic bottle of the first blood culture set flagged positive. Gram staining of positive bottle revealed branching Gram-positive rods () that were also weakly acid-fast on modified Kinyoun stain (). On the basis of these findings, Nocardia spp. bacteremia was suspected and ceftriaxone was replaced with trimethoprim/sulfamethoxazole 160/800 mg intravenously three times daily, plus linezolid 600 mg intravenously twice daily. Positive blood culture was subcultured, and after 2 days of incubation very small colonies appeared on Columbia blood agar and were identified by MALDI-TOF MS (Bruker Daltonics, Bremen, Germany) as Nocardia farcinica, with a score of 1.879 (). On the fifth day after subculturing, N. farcinica identification was confirmed by conventional biochemical tests. The isolate was susceptible to trimethoprim/sulfamethoxazole, linezolid, ciprofloxacin, and amikacin but resistant to ceftriaxone, clarithromycin, and imipenem. Ciprofloxacin 200 mg intravenously twice daily was added. Sputum, collected again soon after presumptive diagnosis of nocardiosis, was cultured for Nocardia spp., but resulted negative after 10 days of incubation.
On day 10 the patient's level of consciousness deteriorated to a state of light coma, difficult to awaken, with worsening shortness of breath. Oxygen saturation measured by pulse oximetry showed values of 89%; therefore oxygen therapy was started via nasal cannula at 2 liters per minute (FiO2 28%). A computerized tomography (CT) scan of the brain was performed, and it showed multiple enhancing focal lesions in the frontal regions (), midbrain, and in the cerebellum, and a chest CT scan showed multiple nodular lesions and bilateral pleural effusion (). Unfortunately, the patient was suffering from psychosis, and although in a coma, he was uncooperative when awakened; therefore a thoracentesis could not be performed. For the same reason, the patient refused noninvasive mechanical ventilation, and oxygen therapy was continued via nasal cannula and then via Venturi mask with further increases. The patient died on day 18 of hospitalization.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [91, 'years'], 'creatinine': [1.95, 'mg/dL'], 'sex': 'Male'}",31.88204,30.28794,33.47614,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 91 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.95 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.95/0.9)**-1.2 * 0.9938**91 * 1.0 = 31.88204.
Hence, the GFR value is 31.88204 ml/min/1.73 m²."
522,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4260427-1,Extracted,"A 34-year-old man was admitted to our hospital with a 4-month history of diffuse abdominal pain and body weight loss, progressing in 3 months to muscle weakness, abdominal distension, nausea, vomiting, and stiff painful swelling of his neck. His previous history included a fluctuating tumoral mass in the left maxillary region for the last six years, causing mild dysphagia and limiting movement of the temporomandibular joint. The pathological examination was consistent with a chronic inflammatory process. Later on he presented right palpebral ptosis with protrusion of the eyeball and chronic dry cough, with transbronchial biopsy examination revealing chronic pneumonitis and irregular septal fibrosis.
On examination he was afebrile, with blood pressure 120/80 mmHg, with pale mucous membranes, anterior neck swelling and stiffness with local hyperemia, without palpable lymph nodes, reduced pulmonary expansion, diffuse abdominal pain, and rigidity on palpation. The remainder of the physical examination was unremarkable.
On admission laboratory tests revealed the following: hemoglobin 9.0 g/dL, white blood cell count 21,390/mm3, platelet count 808,000/mm3, total bilirubin 2.89 mg/dL (direct bilirubin 2.26 mg/dL), calcium 8.2 mg/dL, creatinine 0.4 mg/dL, aspartate transaminase 25.7 mg/dL, alanine transaminase 16.6 mg/dL, and alkaline phosphatase 417 mg/dL. Search for antinuclear antibodies (ANA), anti-SSA/Ro, and ANCA showed negative results. Serum protein electrophoresis and immunofixation showed polyclonal hypergammaglobulinemia. Serum IgG4 was 264 mg/dL (reference value ≤140 mg/dL). Ultrasonography of the neck showed soft tissues swelling. Abdominal ultrasonography was normal.
The patient developed daily fever, asthenia, diarrhea, profuse coughing, and intense dyspnea. Chest radiography revealed bilateral parenchymal infiltration, multiple pulmonary nodules, and consolidation in the lower right hemithorax. As the patient's clinical condition was not improving, despite the use of broad spectrum antibiotics (piperacillin/tazobactam, meropenem) and mechanical ventilation, pulse therapy with methylprednisolone 1 g was started and used for three days, with considerable clinical and radiological improvement. After this, prednisone 50 mg/day was initiated and he was discharged in good general condition. After two-year follow-up, he has been well on lower dose (5 mg/day) of prednisone. In the last few months, after abrupt voluntary discontinuation of his medication, there was a mild relapse of the disease which remitted with the reintroduction of 20 mg/day of prednisone. The patient remains asymptomatic with low doses of steroids, maintaining complete resolution of respiratory, eye, and neck symptoms which were assumed to be manifestations of the same disease.
A reanalysis (with immunohistochemical staining) of the histological sample from previous maxillary biopsy revealed chronic inflammatory infiltrate rich in plasma cells with areas of fibrosis and erosion. Immunohistochemistry showed mixed population of B and T lymphocytes and an increased amount of positive IgG4 cells (up to 55 IgG4-positive plasma cell per high power field; IgG4/IgG ratio of 45%) ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [34, 'years'], 'creatinine': [0.4, 'mg/dL']}",136.09795,129.29305,142.90285,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 34 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.4 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.4/0.7)**-0.302 * 0.9938**34 * 1.0 = 136.09795.
Hence, the GFR value is 136.09795 ml/min/1.73 m²."
523,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2769279-1,Extracted,"A 38-year-old, Turkish, Caucasian female patient presented with complain of intermittant cramping abdominal pain, nausea and vomiting which aggravated in the last 2 weeks. She had a history of cholecystectomy, performed 8 years ago. On physical examination, signs of anemia, jaundice and severe weight loss were inspected. The abdomen was distended and tender to palpation in the epigastrium and right upper quadrants with guarding, accompanied by reduced bowel sound. Laboratory examination revealed anemia (Hemoglobin: 8.1 g/dl), leukocytosis (13800/mm3), increase of erythrocyte sedimentation rate in first hour (105 mm/h), bilirubinemia (total bilirubin: 3 mg/dl and direct bilirubin: 1.82 mg/dl), increase of alchaline phosphatase (321 U/dl) and blood amilase (304 U/dl), prerenal azotemia (BUN: 50 mg/dl and creatinin: 1.24 mg/dl) and hypoalbuminemia (2.9 g/l). The levels of tumor markers were within the normal limits except CA-125, which was increased to 111 IU/dl. The abdominal ultrasound and computed tomography scan revealed a complex cystic retroperitoneal mass, 30 cm in diameter, extending from the subhepatic space down into the pelvis and was thought to be arised from the head of the pancreas. Dilatation of the intrahepatic and extrahepatic bile ducts and the Wirsung’s duct were accompanied by parenchymal calcifications and atrophy of the pancreas. The mass involved the porta hepatis and vascular structures, compressed the celiac trunk and superior mesenteric artery. The collecting system of the right kidney was dilated ( and ).
After one week of supportive treatment and transfusion of 2 units of blood, the patient underwent surgery. The exploration of the abdomen revealed a cystic mass, extending from the liver to the pelvis retroperitoneally, which elevated the cecum, ascending colon and partially transverse colon. The mass was perforated during the dissection and an abundant bile drainage was observed. The frozen section of the biopsy, taken from the capsule of this cystic mass showed no evidence of malignancy. Thereafter, the mass was thought to be a huge retroperitoneal biloma. The porta hepatis, the common bile duct and the duodenum were explored. In the retropancreatic portion of the common bile duct, a perforation site with a dimension of 3 × 3 cm was inspected and a Foley catheter was placed through this hole for a peroperative cholangiography which revealed dilatation of intrahepatic bile ducts was and normal level of biliary tract drainage into the duodenum. Thereafter, the retroperitoneum was cleansed with saline and drained and biloma was excised. The perforation site was repaired with 3/0 silk sutures with omentoplasty. T-tube placement was performed on the proximal choledochus and a peroperative cholangiography was repeated, which demonstrated a stricture in the common bile duct but free passage of contrast media into the duodenum ().
No complication was observed during early follow-up. On the postoperative 10th day, the T-tube was withdrawn following a cholangiography which revealed a sufficient passage of contrast medium into the duodenum and no leakage out of the biliary tract. There was no abdominal pathology, except findings of chronic pancreatitis and dilatation of the common bile duct, at ultrasonography imaging performed 3 months after the operation.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [38, 'years'], 'creatinine': [1.24, 'mg/dL'], 'sex': 'Female'}",57.1271,54.27074,59.98345,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 38 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.24 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.24/0.7)**-1.2 * 0.9938**38 * 1.012 = 57.1271.
Hence, the GFR value is 57.1271 ml/min/1.73 m²."
524,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2769432-1,Extracted,"A 79-year-old Caucasian Italian female was admitted to our hospital for dyspnea and referred lower left limb pain. Her past medical history included systemic hypertension for ten years, type 2 Diabetes Mellitus and chronic obstructive pulmonary disease.
At the admission she was markedly dyspneic, pale and had a pulse rate of 120 beats per minute. The blood pressure was 125/95 mmHg. At pulmonary auscultation there was evidence of broncospasm without signs of congestion.
The lower left leg was warm but pulseless. The oxygen saturation was reduced at about 82-85% in room air. Examination of arterial blood gases revealed hypocapnic hypoxia (pO2 46 mmHg, pCO2 21 mmHg, pH 7.52) and the electrocardiogram showed right axis deviation and inverted T waves in the anterior leads (V1-V3).
The laboratory examinations showed significant leukocytosis (21300/mm3), increased blood glucose and serum creatinine levels (Cr. 2.4 mg/dL), with D-dimer levels moderately high (715 ng/ml).
Echocardiography imaging revealed right ventricular dilatation and elevated transtricuspid systolic gradient with indirect signs of high pulmonary hypertension. The whole-body CT showed a massive thrombus in the main right and left pulmonary artery, extended to lobar branches (). Moreover, the abdomen CT demonstrated the almost entirely occlusion of the superior mesenteric artery () and of the right renal artery, by a floating clot in the lumen, (), resulting in renal hypoperfusion and further worsening of its function (Cr. 3.9 mg/dL). An embolic occlusion of the left external iliac artery was also evident. The Echo Doppler of her lower legs didn’t reveal signs of deep vein thrombosis, showing instead the whole thrombotic occlusion of poplytea artery. There was no evidence of ischemic lesions at the CT scan of brain.
Transesophageal echocardiography (TEE) excluded the presence of intracardiac thrombi but it revealed a significant interatrial septum’s aneurysm with long tunnel-type patent foramen ovale (PFO). The presence of other anatomic anomalies, frequently associated with patent foramen ovale [], such as Chiari’s Network or a prominent Eustachian Valve were also excluded. A saline contrast echocardiography confirmed the presence of PFO and demonstrated a right-to-left shunt during Valsalva maneuver ().
Because of the hemodynamic stability, the patient’s age and the absence of contraindications to thrombolisis, the woman was treated with i.v. tPA (10 mg bolus followed by 90 mg infusion over 2h) and i.v. heparin with progressive improvement of clinical conditions and dyspnea.
During the following days the kidney function gradually improves with a reduction of hematic creatinine from 3.9 to 1.3 mg/dL. A repeat CT one week later showed a partial resolution of pulmonary embolism and the reduction of renal, mesenteric and iliac thrombosis, while the left poplytea artery’s occlusion persisted.
Her anticoagulation work up showed no evidence of factor V Leiden or prothrombin gene mutation, antiphospholipid antibody screening was negative and level of homocysteine was normal. Levels of protein C, S and antithrombin III were unreliable in the context of an acute thromboembolic event or during antithrombotic therapy. Other predisposing factors for venous thromboembolism as metastatic solid tumors or lymphoproliferative disorders were excluded.
The patient was discharged 8 days after admission and no recurrent embolic episode was observed. She has to keep on assuming life-long oral anticoagulant therapy. PFO closure was not performed because our patient required a life-long anticoagulation therapy; the presence of a long tunnel-type PFO may give rise to technical problems in realizing device implantation and finally there are no clear guidelines based on randomized trials for therapy if patent foramen ovale is present.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [79, 'years'], 'creatinine': [3.9, 'mg/dL']}",11.19256,10.63293,11.75219,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 79 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 3.9 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (3.9/0.7)**-1.2 * 0.9938**79 * 1.012 = 11.19256.
Hence, the GFR value is 11.19256 ml/min/1.73 m²."
525,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4089319-1,Extracted,"A 30-year-old man from suburbs of the city with renal failure was admitted for renal transplantation (RTx) from his 36-year-old HLA-identical (6/6) brother in January 2012. He was subjected to open right nephrectomy due to persistent pyuria in March 2012. Histopathology revealed chronic tubulointerstitial nephritis leading to end-stage renal disease. He was cleared for transplantation in June 2012. Before placing the renal allograft in the right iliac fossa, an enlarged lymph node was found and sent for histopathology. This was followed by an uneventful transplantation. Histopathology of the lymph node revealed necrotic lymphatic filled with coiled adult worms of Wuchereria bancrofti (microfilaria) () with double uteri in female worms. Subsequently after diethylcarbamazine citrate (DEC) challenge test, his peripheral blood also showed microfilarial worms (), however he never had tissue/peripheral blood eosinophilia. He was therefore treated with a single dose of 400 mg albendazole followed by DEC, 6 mg/kg body weight for 14 days. Eight months post-transplantation he was maintaining stable graft function with serum creatinine of 1 mg/dL on maintenance immunosuppression of 0.06 mg/kg/day of tacrolimus, 360 mg of mycofenolate sodium twice a day, and 10 mg/day prednisone. On screening, none of his family members had evidence of filariasis.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [30, 'years'], 'creatinine': [1.0, 'mg/dL'], 'sex': 'Male'}",103.83628,98.64447,109.02809,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 30 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.0 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.0/0.9)**-1.2 * 0.9938**30 * 1.0 = 103.83628.
Hence, the GFR value is 103.83628 ml/min/1.73 m²."
526,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6375021-1,Extracted,"A 63-year-old man, known diabetic for 7 years with blood sugars controlled with oral hypoglycemics presented in October 2015 at a local hospital with mild dull aching upper abdominal pain and no constitutional symptoms. Investigations revealed anemia with hemoglobin of 7 g/dl and serum creatinine of 5.5 mg/dl with normal sized kidneys on ultrasonography. He underwent upper gastrointestinal endoscopy, which was normal. Within 1 week, serum creatinine increased to 10 mg/dl. He did not seek medical advice following this and started taking alternate medications. He remained asymptomatic for the next 6 months after which he developed uremic symptoms. Investigations revealed hemoglobin of 5 g/dl and serum creatinine 15 mg/dl. Tests for hepatitis B, C, and HIV viruses were negative. He was started on maintenance hemodialysis and received packed red blood cell transfusion (3 units) during initial dialysis. He underwent RT at another center with the wife as donor in May 2016.
He was induced with anti-thymocyte globulin and maintenance therapy compromised of tacrolimus, mycophenolate mofetil, and prednisolone. He had delayed graft function, which was attributed to intraoperative hypotension. Graft biopsy done on postoperative day 2 showed acute tubular necrosis. He remained oliguric even after 2 weeks and came to our institute for a second opinion. His general and systemic examination was unremarkable except for mild pallor. His blood workup showed anemia (hemoglobin 8.2 g/dl). Tacrolimus Co level was 7 ng/ml. Urine examination was unremarkable. Ultrasound and Doppler of the graft kidney were normal. We advised for a repeat graft biopsy, which showed evidence of MCN [] with lambda (λ) light chain restriction [] and proximal tubulopathy []. Serum protein electrophoresis did not show any myeloma band while immunofixation electrophoresis showed a discrete band in lambda region. Serum-free light chain assay showed λ predominance, with free λ chain of 8350 mg/L, while free kappa (k) was 39 mg/L (k/λ ratio of 0.005). Bone marrow examination revealed 10% plasma cells. Skeletal survey showed lytic lesion in humerus. Serum calcium was normal.
With a final diagnosis of MM with MCN and light chain proximal tubulopathy (LCPT), he was started on plasmapheresis and chemotherapy with bortezomib and high-dose prednisolone. However, the patient had sudden cardiac death during dialysis 1 week after starting chemotherapy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [15.0, 'mg/dL'], 'sex': 'Male'}",3.28025,3.11624,3.44426,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 63 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 15.0 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (15.0/0.9)**-1.2 * 0.9938**63 * 1.0 = 3.28025.
Hence, the GFR value is 3.28025 ml/min/1.73 m²."
527,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7329524-1,Extracted,"A 78-year-old male with past medical history significant for CKD stage 3 known to have a left sided inguinal hernia presented to the Emergency department with two weeks of intermittent suprapubic tenderness, dysuria, frequency, urgency, frothy urine as well as nausea and vomiting. Workup on admission revealed an elevated creatinine of 2.8 mg/dl from a baseline of 1.5 mg/dl, with leukocytosis of 7000. Urine analysis was performed that revealed large leukocyte esterase, urine WBC greater 180, and white blood cell clumps. The patient was diagnosed with acute kidney injury as well as a urinary tract infection. Computed tomography of the abdomen and pelvis revealed duplicated left sided pelvis and ureters with the left inguinal hernia containing the ureters with cystic ureteral dilation within the herniation sac as well as moderate left hydroureteronephrosis (Figs. and ). The patient was managed with volume repletion and antibiotics for his urinary tract infection. There was some improvement in kidney function although not to his previous baseline. He was discharged with an outpatient urology follow up and was subsequently readmitted for an elective paraperitoneal inguinal hernia repair with a Kumpe catheter placement up to the left kidney externalizing through the urethral meatus.
When it comes to the inguinal hernia repair, a large portion of the herniated extraperitoneal fat was freed from its incarcerated position in the scrotum and then dissected back to the internal ring. A typical mesh repair was not done in order to avoid placing the mesh in direct contact with the ureter causing erosions as well as ureteral structuring further down the line. Thus, the internal ring was primarily closed first to maintain the ureter in a reduced position deep to the ring then a Lichtenstein repair was done using a polypropelene patch that was sutured to the tissues overlying the pubic tubercle medially to the shelving edge of the inguinal ligament inferiorly and to the conjoined tendon superiorly, laterally the arms of the patch were passed around the spermatic cord at the internal ring and sutured together and to the tissue lateral to the internal ring.
Following the surgery, he had recovery of kidney function to the previous baseline serum creatinine of 1.5 mg/dl. (Table ) (Fig. ).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [78, 'years'], 'creatinine': [1.5, 'mg/dL']}",47.35777,44.98988,49.72566,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 78 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.5/0.9)**-1.2 * 0.9938**78 * 1.0 = 47.35777.
Hence, the GFR value is 47.35777 ml/min/1.73 m²."
528,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5398301-1,Extracted,"A 76-year-old man was admitted in June 2014 due to progressive deterioration of renal function, loss of appetite, and asthenia. Nine months prior to his admission (September 2013), he was diagnosed with effort angina and infrarenal abdominal aortic aneurysm. At the beginning of October 2013, he was found to have unprovoked PE for which he had received oral warfarin, delivering a prothrombin time-international normalized ratio (PT-INR) of 1.7 to 2.1 (reference range: 0.9-1.2) with a favorable clinical course. He had no history of renal disease, and steady serum creatinine (sCr) levels ranging between 0.96 and 1.12 mg/dL (reference range: 0.63-1.03 mg/dL) were noted until mid-December 2013. His sCr level was 1.89 mg/dL in mid-March 2014 and increased to 7.33 mg/dL in early June 2014. Therefore, he was referred and admitted to our hospital for further examination. His medical history included a diagnosis of acute myocardial infarction at 58 years of age. He had been a smoker for more than 40 years but denied the use of any drugs.
At the time of admission, the patient was alert and had a temperature of 36.4°C, a heart rate of 89 beats/min, and a blood pressure of 176/94 mm Hg. His physical examination revealed livedo reticularis on the soles of his toes and a blue-purple discoloration of all toes bilaterally (), whereas his feet were warm to the touch and the peripheral pulse remained intact. Laboratory examinations revealed the following: blood urea nitrogen (BUN), 64 mg/dL (reference range: 8-20 mg/dL); sCr, 7.23 mg/dL; white blood cell count, 9800/µL (reference range: 3900-9800/µL); eosinophils, 1092/µL (reference range: 0-400/µL); platelet count, 166 × 103/µL (reference range: 130-369 × 103/µL); erythrocyte sedimentation rate (ESR), 59 mm/h (reference range: 0-10 mm/h); serum albumin, 3.5 g/dL (reference range: 6.9-8.4 g/dL); triglycerides, 203 mg/dL (reference range: 40-185 mg/dL); low-density lipoprotein (LDL) cholesterol, 129 mg/dL (reference range: <139 mg/dL), fibrinogen, 410 mg/dL (reference range: 129-271 mg/dL); fibrin/fibrinogen degradation products, 13.5 µg/mL (reference range: 0-5 µg/mL); D-dimer, 5900 µg/L (reference range: 0-1500 µg/L); PT-INR, 1.76; C3, 104 mg/dL (reference range: 86-160 mg/dL); C4, 45 mg/dL (reference range: 17-45 mg/dL); and C-reactive protein, 0.49 mg/dL (reference range: 0-0.14 mg/dL). Tests for anti-neutrophil cytoplasmic antibodies, anti-glomerular basement membrane antibodies, hepatitis B virus surface antigen (HBsAg), anti-HBsAg antibodies, and antibodies to the hepatitis C virus were all negative. His urine was trace positive for protein, 2+ for occult blood, and contained 0.09 g of protein in a 24-hour specimen, whereas his creatinine clearance was 3.9 mL/min. The urinary excretion of β2-microglobulin and N-acetyl-beta-d-glucosaminidase was 22 856 µg/L (reference range: <200 µg/L) and 5.4 U/g·Cr (reference range: 0.9-2.4 U/g·Cr), respectively. A computed tomographic scan revealed a calcified thoracic aorta without a dimensional disorder and an infrarenal aortic aneurysm with a maximum diameter of approximately 4.4 cm. Diagnostic noncontrast-enhanced T2-weighted half-fourier-acquired single-shot turbo spin ecocho (HASTE) magnetic resonance imaging subsequently revealed hypointense areas and bright signals, which were suggestive of an atheromatous plaque consisting of lipids and fibrous tissues, respectively, in the abdominal aorta (). Oral warfarin was discontinued on admission, and the patient was subjected to empirical treatment with pravastatin at a dose of 10 mg/day combined with limaprost alfadex at a dose of 30 µg/day. A 5-mm-deep punch biopsy was performed on clinical day 7 within the territory of livedo reticularis on the lateral aspect of the left first toe. Typical biconvex needle-shaped empty spaces, suggestive of cholesterol clefts, were observed within the lumen of the arteriole in the subcutis (). A diagnosis of CES was made based on pathological and imaging findings as well as clinical manifestations.
Due to the elevated D-dimer level of 10 600 µg/L confirmed on clinical day 8, the decision was made to resume anticoagulation therapy despite our failure to detect deep venous thrombotic lesions using ultrasonography. The patient was treated with intravenous heparin and then switched to warfarin 2.5 mg/day on clinical day 30. Oral prednisolone (PSL) at a dose of 20 mg/day was also initiated on clinical day 22, resulting in the amelioration of eosinophilia and cutaneous manifestations within a few days and the subsequent stabilization of sCr levels at approximately 4.3 mg/dL. His elevated blood pressure was also controlled at approximately 120-130/70-80 mm Hg with irbesartan (100 mg/day) and amlodipine besilate (5 mg/day). However, sCr levels started to increase when PSL was tapered to 5 mg/day. The patient developed general fatigue, appetite loss, decline in urine output, and progressive swelling in both legs without any calf pain at the end of September 2014, with an elevated sCr level of 8.07 mg/dL, and was readmitted for further examinations. Similar to his initial admission, a laboratory analysis at this point revealed mild hypoalbuminemia (3.6 g/dL), whereas echocardiography and chest radiograph findings did not support the concurrent presence of heart failure. The relationship between deteriorated cutaneous manifestations and recurrent eosinophilia of 1365/µL resulted in the diagnosis of relapsed CES. The patient received hemodialysis (HD). After the resumption of an increased dose of PSL (15 mg/day) and the addition of a transient session of LDL apheresis (LDL-A) to the therapeutic regimen, his cutaneous manifestations improved and eosinophilia disappeared; however, severely deteriorated renal function did not recover, and he was finally started on a periodic HD program with favorable volume control ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [76, 'years'], 'creatinine': [7.23, 'mg/dL']}",7.26335,6.90018,7.62652,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 76 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 7.23 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (7.23/0.9)**-1.2 * 0.9938**76 * 1.0 = 7.26335.
Hence, the GFR value is 7.26335 ml/min/1.73 m²."
529,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4949650-1,Extracted,"The patient, a 65-year-old woman of Indian origin, presented with poor mobility and recurrent falls. She underwent investigation and was found to have hypercalcemia (serum adjusted-calcium concentration = 2.77 mmol/L, normal range = 2.20–2.60 mmol/L) in association with normal serum concentrations of phosphate (0.85 mmol/L; normal range = 0.70–1.40 mmol/L), creatinine (45 µmol/L; normal range = 40–130 µmol/L), PTH (5.9 pmol/L; normal range = 1.0–7.0 pmol/L), and serum 25-hydroxyvitamin D (52 nmol/L; normal >50 nmol/L). Urinary calcium-to-creatinine clearance ratio was low at 0.01 (normal >0.02). These findings are consistent with a diagnosis of FHH, although there appeared to be an absence of a family history of hypercalcemia, based on the patient not having knowledge of any relatives who suffered from symptomatic hypercalcemia and the relatives not being available for medical assessment. DNA sequence analyses of the CASR and AP2S1 genes had not identified any abnormalities. Informed consent was obtained for the study using protocols approved by the Multi-Centre Research Ethics Committee (UK) (MREC/02/2/93).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [45.0, 'µmol/L'], 'age': [65, 'years']}",106.58194,101.25284,111.91104,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 65 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 45.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 45.0 µmol. To convert 45.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 45.0 µmol Serum Creatinine * 1e-06 mol/µmol = 4e-05 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 4e-05 mol Serum Creatinine * 113.12 g/mol = 0.00452 g Serum Creatinine. To convert 0.00452 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00452 g Serum Creatinine * 1000.0 mg/g = 4.52 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 4.52 mg Serum Creatinine/10.0 dL = 0.452 mg Serum Creatinine/dL. The concentration value of 45.0 µmol Serum Creatinine/L converts to 0.452 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.452/0.7)**-0.241 * 0.9938**65 * 1.012 = 106.58194.
Hence, the GFR value is 106.58194 ml/min/1.73 m²."
530,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8627579-1,Extracted,"A 60-year-old Polish male with a history of alcoholism, liver cirrhosis, and hepatocellular carcinoma presented with respiratory distress, purpuric rash on both lower extremities, and acute kidney injury (AKI) via referral from his primary medical doctor. He was on Nivolumab for hepatocellular cancer and had received a total of 16 doses. Nivolumab was, however, skipped a month prior to presentation on account of rising blood urea nitrogen (BUN) and creatinine as well as the onset of the purpuric rash. On physical examination, he was tachypneic but able to sustain a conversation, he had papular, purpuric rash prominent on both lower extremities. Labs showed elevated BUN/creatinine at 52/3.6, baseline creatinine of 1.4, hyperkalemia of 5.1, and metabolic acidosis with bicarbonate of 11, and blood gas PH of 7.12. Urinalysis was positive for proteinuria and microscopic hematuria. Labs were negative for c-ANCA, p-ANCA, atypical ANCA, and complement levels were within normal limits. He was admitted for AKI superimposed on chronic kidney disease based on elevated BUN/creatinine and worsening renal function. Serologic tests were negative including ANCA panel and complement levels were within normal limits. A skin biopsy was done which showed leukocytoclastic vasculitis as well as a kidney biopsy which showed focally crescentic IgA nephropathy (Figures -). He was started on methylprednisolone 1 g daily for three days and subsequently maintained at 1 mg/kg of prednisone. The purpuric rash resolved in response to steroid treatment, but his renal function continued to get worse requiring intermittent hemodialysis. His hospital course was complicated by septic shock, he was on the maximum dose of norepinephrine on the day of his death, 18 days after admission.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [3.6, 'mg/dL'], 'age': [60, 'years']}",18.5249,17.59865,19.45115,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 60 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.6 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.6/0.9)**-1.2 * 0.9938**60 * 1.0 = 18.5249.
Hence, the GFR value is 18.5249 ml/min/1.73 m²."
531,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7195636-1,Extracted,"An 81-year-old Colombian male presented to the hospital with a 4-day history of productive cough and 2-week history of fevers and chills. His past medical history was significant for hypertension, hyperlipidemia, diabetes mellitus, and chronic heart failure with preserved ejection fraction. In the Emergency Department (ED), he was febrile to 38.7°C and bradycardic at 55 beats/min. Initial physical exam demonstrated an obese, diaphoretic male with poor dentition. He was mildly tachypneic with decreased breath sounds and an audible grade III/VI systolic ejection murmur in the right second intercostal space. There was significant pitting edema in his extremities, with chronic venous stasis changes, and his right lower extremity was warm and erythematous. Laboratory studies revealed a leukocytosis of 25,000 cells/μl (4.8–10.8 cells/μl) with 87% neutrophils, 7% monocytes, 2% lymphocytes, and 4% band forms, and serum chemistries were remarkable for hyperkalemia with a potassium level of 6.5 mmol/L (3.5–5.5 mmol/L) and elevated creatinine of 1.67 mg/dL (0.7–1.3 mg/dL). An electrocardiogram revealed a third-degree heart block with a wide complex escape rhythm (). He was admitted to the Cardiac Intensive Care Unit, and electrophysiology (EP) service was consulted for external transvenous pacer placement. An infectious disease consultation was obtained to evaluate optimal timing for placement of a permanent pacemaker as the initial blood cultures were reported to contain Gram-positive cocci in chains, later identified as Streptococcus pseudoporcinus by the clinical microbiology laboratory using the Vitek 2™ system and the VT2 GP ID™ card. Transthoracic echocardiogram demonstrated a preserved ejection fraction with moderate aortic regurgitation (AR) but without evidence of valvular vegetations. The infectious disease consultant considered the source of his bacteremia to be due to right lower extremity cellulitis. The patient received 2 g of intravenous ceftriaxone daily. Repeat blood cultures obtained on hospital day 3 remained negative after five days so permanent pacemaker placement was scheduled. Upon transfer to the EP lab, the patient experienced respiratory failure requiring mechanical ventilation. The chest radiograph demonstrated dense airspace disease of bilateral lung fields. He continued to be febrile despite appropriate parenteral therapy. A repeat fever workup was unrevealing other than the urinalysis demonstrating proteinuria and increased RBCs. His creatinine remained elevated throughout his stay. Fevers were postulated to be due to beta-lactam agent use; therefore, the antibiotic regimen was changed to intravenous vancomycin. Cardiothoracic surgery was consulted for the moderate AR seen on an initial echocardiogram, and they recommended a transesophageal echocardiogram (TEE). During the procedure, the patient suffered a pulseless electrical activity (PEA) cardiac arrest with return of spontaneous circulation after five minutes of cardiopulmonary resuscitation. Repeat chest radiograph demonstrated pulmonary edema. The TEE revealed a mobile echodensity seen on the ventricular aspect of the right coronary cusp of the aortic valve with severe AR and a mobile echodensity on the atrial aspect of the mitral valve with moderate mitral regurgitation (Figures and ). In spite of full critical care support, he again suffered PEA arrest and eventually the family decided to withdraw care and he died on hospital day 23.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.67, 'mg/dL'], 'age': [81, 'years']}",40.86373,38.82054,42.90692,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 81 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.67 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.67/0.9)**-1.2 * 0.9938**81 * 1.0 = 40.86373.
Hence, the GFR value is 40.86373 ml/min/1.73 m²."
532,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7250032-1,Extracted,"A 68-year-old female patient was admitted to our hospital with complaints of fatigue, muscle pain, and a decreased urine output for the previous 2 weeks. She had a history of diabetes mellitus after acute pancreatitis for nearly 11 years, accompanied by peripheral vascular disease and peripheral neuropathy. Moreover, she had suffered from dyslipidemia for about 2 years. Her regular medications included insulin (totaling 16 units daily) and mecobalamin (3 tablets daily). 250 mg micronized fenofibrate daily was initiated to control hypertriglyceridemia 5 months ago. She had no history of liver, muscle, or kidney disease, and had not caught a cold recently. She also denied hypertension, coronary heart disease, or thyroid disease. Diffuse tenderness of muscles and pretibial oedema were detected on physical examination. No obvious abnormality was found in chest X-ray, abdominal ultrasonography, and cardiac ultrasonography. The electrocardiogram showed sinus rhythm without alteration of ST segment. On the basis of the above data, there was no evidence of acute myocardial infarction.
The results of the laboratory examination on admission were as follows: creatine kinase (CK): 8385 IU/L (normal: 24–174 IU/L), aspartate aminotransferase: 716 IU/L (normal: 0–40 IU/L), alanine aminotransferase: 68 IU/L (normal: 0–40 IU/L), lactate dehydrogenase: 1244 IU/L (normal: 103–227 U/L), serum creatinine: 97.63 μmol/L (normal: 41–81 μmol/L), blood urea nitrogen: 14.79 mmol/L (normal: 1.7–8.3 mmol/L), myoglobin: 1075 ng/mL (normal: 25–72 ng/mL), troponin T: 37.28 ng/L (normal: 0–14 ng/L). Antinuclear antibody, anti-JO-1 antibody, anti-double-stranded DNA antibody, anti-centromere antibody, anti-mitochondrial antibody M2, and rheumatoid factor were all negative. Thyroid stimulating hormone (TSH), total thyroxin 3 (TT3), and total thyroxin 4 (TT4) were normal. No significant abnormality was found in other laboratory tests. Therefore, a diagnosis of rhabdomyolysis and secondary ARF due to fenofibrate monotherapy was made.
Because of the serious side effect, fenofibrate was discontinued. Fluid infusion, urine alkalization with sodium bicarbonate, diuretic with torasemide, and hepatoprotection were performed subsequently. The patient's complaints were ameliorated and urine output increased gradually during the hospitalization. On the fifth day of treatment, serum urea nitrogen and creatinine returned to normal range. Although the patient's CK concentration decreased to 2184.8 U/L, which did not return to baseline level, she was discharged 6 days after hospitalization and monitored as an outpatient. Two weeks after discharge, the patient's symptoms disappeared, and serum CK, creatinine, and myoglobin were completely normal (Table ).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [97.63, 'µmol/L'], 'age': [68, 'years']}",52.93743,50.29056,55.5843,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 68 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 97.63 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 97.63 µmol. To convert 97.63 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 97.63 µmol Serum Creatinine * 1e-06 mol/µmol = 0.0001 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.0001 mol Serum Creatinine * 113.12 g/mol = 0.01131 g Serum Creatinine. To convert 0.01131 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01131 g Serum Creatinine * 1000.0 mg/g = 11.31 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 11.31 mg Serum Creatinine/10.0 dL = 1.131 mg Serum Creatinine/dL. The concentration value of 97.63 µmol Serum Creatinine/L converts to 1.131 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.131/0.7)**-1.2 * 0.9938**68 * 1.012 = 52.93743.
Hence, the GFR value is 52.93743 ml/min/1.73 m²."
533,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8189304-1,Extracted,"A 67-year-old man was referred to our facility for extensive left lower extremity (LLE) venous ulcers. He reported an increase in the size and number of LLE venous ulcers, which initially developed 6 months prior. He failed previous wound and compressive management with plastic surgery as well as multiple oral and intravenous antibiotic regimens. He was Clinical-Etiology-Anatomical-Pathophysiology (CEAP) Class 6 upon referral. Initial vitals were normal. Physical exam revealed significant bilateral leg oedema, with purple discolouration and increased skin pigmentation on both sides, most pronounced in the calf area. Findings were worse on the left side with 4+ LLE oedema and multiple large ulcers with diameter up to 7 cm involving the anterior, posterior, and medial aspects of the left calf with associated warmth to touch and tenderness. The right lower extremity (LE) was asymptomatic and without venous ulcers. Peripheral pulses in the bilateral LE were 2+. The remainder of the physical exam was normal. He denied chest pain, dyspnoea, claudication, trauma, palpitations, syncope and any history of pulmonary embolism, pulmonary artery hypertension, chronic heart failure, and smoking.
The patient has a history of hypertension, sleep apnoea on continuous positive airway pressure therapy (CPAP), hyperlipidaemia, obesity, chronic atrial fibrillation on apixaban 5 mg BID, chronic venous insufficiency (CEAP Class 6), and bilateral chronic femoral DVT.
Initial labs were unremarkable (Hgb 14.2 g/dL, WBC 7.9 × 109 per L, Plt 329 × 10−3 per μL, Na 142 mEq/L, K 4.5 mEq/L, Glu 94 mg/dL, Cr 0.95 mg/dL, INR 1.2, CRP 2.5 mg/L). Lower extremity venous ultrasound (US) revealed evidence of chronic DVTs involving the bilateral proximal, mid and distal femoral (FV), popliteal (PV), and left peroneal veins (PerV). He had evidence of reflux within the common FVs and the PVs. Lower extremity arterial US showed no significant peripheral artery disease with normal toe-brachial indices.
With non-healing LLE venous ulcers related to severe venous hypertension exacerbated by chronic DVT involving the LFVs and LPVs, we suspected PTS with superimposed left leg venous stenosis/compression. We considered Left femoral vein (LFV) and left popliteal vein (LPV) mechanical thrombectomy as an option during catheterization, keeping in mind that this intervention in this context is technically difficult with mixed odds of success given his chronic thrombus burden. He was taken to the catheterization lab where US-guided LPV access was undertaken.
Selective LFV venogram revealed extensive organized thrombus within the LFV below the left common FV (LCFV) confluence with the saphenous and profunda veins. There was complete occlusion of the proximal and mid-LFV () (Video 1). Furthermore, the proximal and mid-LFV demonstrated chronic thrombus and PTS changes. Thereafter, intravascular ultrasound (IVUS) Visions PV.035 Digital IVUS Catheter (Philips, Amsterdam, the Netherlands) of the left iliolumbar vein (ILV) confirmed its patency without evidence of compression, stenosis, or DVT. It demonstrated significant scarring and a ‘rubbery’ appearance of the venous walls throughout the LFV. Using IVUS imaging, the superior and mid-distal portions of the LFV appeared most impacted with chronic thrombus (). Subsequently, he underwent high pressure venoplasty of the LCFV and entire LFV with 10 × 40 mm Dorado balloon (Bard, Tempe, AZ, USA). The mid-LFV had an area of very high-grade stenosis that would not yield. AngioSculpt balloon 6 × 40 mm (AngioScore, Brandin Court Fremont, CA, USA) was used similarly without success. The high-grade LFV occlusion demonstrated a persistent ‘dog-bone/waist’ appearance (). We then decided to perform intravascular shockwave lithotripsy (IVSL) empirically. Shockwave balloon 7 × 60 mm (Shockwave Medical, Fremont, CA, USA) was therefore positioned at the level of the mid-LFV and 180 pulses at 2, 4, and 6 atmospheres were delivered to prime the lesion for further intervention. Subsequently, TurboHawk LX extended tip device (Medtronic, Minneapolis, MN, USA) was empirically used for multiple passes of ad hoc ‘venous atherectomy’ along the affected segment, resulting in retrieval of a significant amount of red, rubbery organized material suggestive of chronic DVT. Venoplasty with 7 × 20 mm cutting balloon (Boston Scientific, Marlborough, MA, US) finally yielded the mid-LFV culprit lesion successfully ().
Post-intervention venogram revealed improved flow, but with high-grade stenosis at the level of the LCFV and superior portion of the LFV. Therefore, further venoplasty was performed using 10 × 40 mm Dorado balloon.
Subsequent IVUS demonstrated patent LCFV and LFV with significantly improved luminal diameter and gain. However, we visualized both residual organized and fragmented thrombus. Mechanical thrombectomy with FlowTriever device (Inari Medical, Irvine, CA, USA) then yielded the thrombus fragment. Intravascular ultrasound-guided venoplasty using Cook Advance 12 × 40 mm balloon (Cook Medical LLC, Bloomington, IN, USA) was performed on the affected superior portion of the LFV at the level of the initially occlusive cap and within the mid-LFV at the level of the aforementioned high-grade occlusive stenosis. Final post-intervention IVUS and venogram demonstrated patent LFV with improved lumen and recovered anterograde LFV flow throughout, and towards the LCFV (, Video 2). He tolerated the procedure well without complications and received aspirin and IV heparin with activated clotting time maintained at therapeutic levels.
The patient was seen in an office visit at 2, 8, and 12 weeks post-intervention. Symptoms had improved with resolution of LE oedema to +1 and resolution of venous ulcers. He continued wound care, chronic anticoagulation, and compressive therapy. Repeat US at every follow-up showed no re-occlusion of the LFV.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [0.95, 'mg/dL'], 'age': [67, 'years']}",87.72907,83.34262,92.11552,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 67 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.95 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (0.95/0.9)**-1.2 * 0.9938**67 * 1.0 = 87.72907.
Hence, the GFR value is 87.72907 ml/min/1.73 m²."
534,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8288603-1,Extracted,"An 80-year-old Caucasian male with chronic kidney disease and dilated cardiomyopathy with LVAD as destination therapy presented to the emergency room with nausea and chills. His LVAD had been placed eight years prior to presentation and his clinical course was complicated by chronic driveline infections predominantly due to Serratia and Staphylococcus epidermidis, and the use of chronic antimicrobial prophylaxis with cefdinir.
On admission, he was afebrile and hemodynamically stable. On exam, his driveline dressing was soaked with yellow fluid which was also emanating from his left lower quadrant suggesting the presence of a sinus tract (see Figure ). His white blood cell count was 10.04 x 103/μL, hemoglobin 10.5 g/dL, and creatinine 0.8 mg/dL. Blood cultures were unremarkable. A computed tomography (CT) scan of his abdomen and pelvis did not demonstrate any collections involving his LVAD. While in hospital, our team was made aware of positive acid-fast bacilli (AFB) cultures from his driveline done a month ago at an outside facility. Therefore, the patient was taken to the operating room for irrigation and debridement (I&D), and flap closure of his LVAD site. He was deemed a high-risk surgical candidate for device removal. Accordingly, he was empirically treated with imipenem and tigecycline intravenously, and oral azithromycin. The AFB cultures and Mycobacterium PCR collected intraoperatively yielded positive results for Mycobacterium abscessus subs. massiliense (see Table ).
Due to gastrointestinal-related intolerance, the patient preferred to remain off antibiotics intermittently during his inpatient stay. Eventually, tigecycline was switched to amikacin. However, after a few days his gastrointestinal complaints recurred. His most recent regimen was amikacin, cefoxitin, and azithromycin. Ultimately, the patient opted for home with hospice, antibiotics were discontinued, and he expired.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [0.8, 'mg/dL'], 'age': [80, 'years']}",82.92666,78.78033,87.07299,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 80 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.8 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.8/0.7)**-0.302 * 0.9938**80 * 1.0 = 82.92666.
Hence, the GFR value is 82.92666 ml/min/1.73 m²."
535,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3969001-1,Extracted,"A 26-year-old woman with previous operation of bladder exstrophy presented supra pubic pain, bloody vaginal discharge and dysuria since about one year ago was treated only medically. She was a case of bladder exstrophy and underwent bladder reconstruction when she was 5 years old. She had been operated 21 years ago in another country and we couldn’t provide her detailed past surgical history. She was on hemodialysis since 12 years ago because of ESRD (end stage renal disease). Her urine volume had gradually decreased in the past 12 years and she was extremely oliguric since about 2 years ago. She also had urinary incontinency but since she was extremely oliguric her incontinency was not prominent. Her physical examination showed a low midline incision of her previous surgery and an anteriorly displaced vagina with bifid clitoris. The patient was a candidate for renal transplant, and her preoperative evaluation abdominal radiograph had been taken. Her radiography showed large stones in the bladder that one of them was around the metallic wire used for fixation of the symphysis pubis in her previous surgery (). Her ultrasonograghy showed multiple bladder stones with no report of vaginal stone. So she was admitted and prepared for surgery. Her pre-operative lab data showed: BUN 35 mg/dL, creatinine 5.2 mg/dL, K 5.3 mEq/L, Na 140 mEq/L, blood WBC 8700 (62%PMN, 21%MN and 15.7% other) and U/C: E. coli greater than 105 CFU/mL.
In preoperative cystoscopy the bladder was full of multiple stones and not suitable for cystolitholapaxy. So we opened the abdominal wall with a short low midline incision and after opening the bladder removed the bladder stones (). After that we also palpated another stone which was located behind the bladder in her vaginal cavity. The stone was around the metallic wire and because of its connections appeared unremovable. We cut the wire and then removed the large stone located there (). A great amount of pus exited from the vaginal cavity after removing the stone, so we irrigated there with normal saline until no evidence of pus was observed (). She didn’t have vaginal fistula. After stone removal and irrigation, the vaginal cavity collapsed and we simply repaired the introitus with simple absorbable sutures. Then we put a Foley catheter in the bladder and reconstruct the bladder and abdominal layers anatomically. She was treated with intravenous antibiotics after surgery. After 20 days her urine culture was sterile. The patient was good in her post-operative period and then was referred to kidney transplant team.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [5.2, 'mg/dL'], 'age': [26, 'years']}",11.01936,10.46839,11.57033,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 26 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 5.2 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (5.2/0.7)**-1.2 * 0.9938**26 * 1.012 = 11.01936.
Hence, the GFR value is 11.01936 ml/min/1.73 m²."
536,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6642778-1,Extracted,"We present the case of an 84-year-old male with past medical history of hypertension, benign prostatic hyperplasia, former alcohol and cocaine abuse, chronic kidney disease stage 3A, severe malnutrition, and frequent falls who presented from a nursing home for elective left heart catheterization. The patient had an NSTEMI two months earlier but had refused catheterization at the time with new left ventricular systolic dysfunction and an ejection fraction of 45%.
During the catheterization, the patient developed hypertensive emergency with flash pulmonary edema and the procedure had to be aborted. He was admitted to the Cardiac Critical Care Unit for hypertensive emergency and was started on antihypertensive drips. Urine drug screen was negative. He was weaned off the drips after 36 hours. After which he developed labile blood pressures, fluctuating in minutes, and ranging from 68/31 mmHg to 323/115 mmHg with his heart rate ranging from 90 bpm to 140 bpm. These blood pressure readings were measured in four extremities with a manual manometer and confirmed with an arterial line. During the rapid shifts in blood pressure the patient would develop blank staring episodes and nonresponsiveness that would last approximately 30 seconds to 1 minute. An immediate head CT showed no acute ischemic changes, hemorrhagic stroke, or cerebral edema. Electroencephalogram showed generalized slowing consistent with moderate metabolic encephalopathy. In addition, the patient developed acute kidney injury with maximum creatinine of 2.6 mg/dl from a baseline of 1.3 mg/dl.
Workup of the labile blood pressure, including an abdominal CT scan without contrast because of the patient's kidney injury revealed a large 9.4 x 8.7 x 8.1 cm round, slightly lobulated left suprarenal mass with mixed cystic and solid components and no calcifications with Hounsfield units ranging from 15 to 45. Free serum metanephrines (MN) were 104 nmol/L (reference range 0.0-0.49 nmol/L) and normetanephrines (NMN) were 24 nmol/L (reference range 0.0-0.89 nmol/L), with a ratio of MN to NMN of 4:1, which were drawn at the peak of a hypertensive cycle. Because of the labile blood pressures, the patient was on no antihypertensive medications, including alpha or beta blockers or calcium channel antagonists, at the time when then the serum and urine metanephrines were drawn. His UDS was negative for cocaine and the patient was not on tricyclic antidepressant or other drugs that can cause false positive elevations of plasma and urinary catecholamines or metanephrines []. The findings confirmed the diagnosis of pheochromocytoma.
The patient was started on prazosin and, however, developed worsening hypotension again, even while receiving aggressive fluid resuscitation. After the patient was euvolemic, the prazosin was able to be titrated up to goal with stabilization of his blood pressure. Due to his advanced age, severe malnutrition, no family support, worsening mental status, and comorbidities he was deemed not an appropriate surgical candidate. Patient was discharged under hospice care.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [2.6, 'mg/dL'], 'age': [84, 'years']}",23.57907,22.40012,24.75802,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 84 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.6 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.6/0.9)**-1.2 * 0.9938**84 * 1.0 = 23.57907.
Hence, the GFR value is 23.57907 ml/min/1.73 m²."
537,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4315802-3,Extracted,"A 33 year old woman was diagnosed with seronegative RA. She was intolerant of methotrexate, sulphasalazine and azathioprine, and was treated with etanercept with improvement in her symptoms. Thirty four years later, she developed a vasculitic rash on her legs, and was noted to have acute kidney injury (SCr 211 μmol/L), haematuria and proteinuria (1.55 g/24 hours). She was ANCA negative, but a renal biopsy demonstrated pauci-immune focal necrotizing glomerulonephritis with moderate chronic damage. She was diagnosed with MPA and treated with pulsed methylprednisolone, oral prednisolone and pulsed intravenous cyclophosphamide, following which she had an improvement of renal function (SCr 129 μmol/L) and proteinuria (0.3 g/24 hours).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [129.0, 'µmol/L'], 'age': [67, 'years']}",38.8583,36.91539,40.80121,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 67 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 129.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 129.0 µmol. To convert 129.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 129.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00013 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00013 mol Serum Creatinine * 113.12 g/mol = 0.01471 g Serum Creatinine. To convert 0.01471 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01471 g Serum Creatinine * 1000.0 mg/g = 14.71 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 14.71 mg Serum Creatinine/10.0 dL = 1.471 mg Serum Creatinine/dL. The concentration value of 129.0 µmol Serum Creatinine/L converts to 1.471 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.471/0.7)**-1.2 * 0.9938**67 * 1.012 = 38.8583.
Hence, the GFR value is 38.8583 ml/min/1.73 m²."
538,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-4444,Extracted,"A 62-year-old homeless man presents to the emergency department with severe chest pain. The patient states he has felt unwell for the past several days and endorses lower back pain, chest pain, pain with swallowing, a cough, and a subjective fever. Several weeks ago, the patient had dental pain which he has been treating by drinking alcohol. His temperature is 104°F (40.0°C), blood pressure is 114/64 mmHg, pulse is 120/min, respirations are 22/min, and oxygen saturation is 92% on room air. Exam is notable for submandibular erythema and a coarse, rasping sound when auscultating the heart sounds. A CT of the chest is performed as seen in Figure A and an ECG is performed as seen in Figure B. Laboratory values are notable for a troponin of 1.0 ng/mL (normal < 0.4 ng/mL) and a creatinine of 2.5 mg/dL.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [2.5, 'mg/dL'], 'age': [62, 'years']}",28.33928,26.92232,29.75624,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 62 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.5/0.9)**-1.2 * 0.9938**62 * 1.0 = 28.33928.
Hence, the GFR value is 28.33928 ml/min/1.73 m²."
539,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2783061-1,Extracted,"A 21-year-old Caucasian man with histologically proven (renal biopsy) Goodpasture's disease since spring 2006 was admitted to our hospital after two generalized tonic-clonic seizures with preceding neuropsychological symptoms of decreased alertness and slowed executive functions. The patient was found to be somnolent, with elevated blood pressure of 180/90 mmHg and a second generalized seizure. Aspiration during the seizure required intubation and mechanical ventilation until the third day after admission.
Regarding his past medical history, the patient was first treated for a rapid progressive glomerulonephritis (RPGN) in another hospital when Goodpasture's disease was diagnosed histologically through renal biopsy (linear deposition of immunoglobulins along the basement membrane) and detection of anti-GBM antibodies in the plasma. A cyclophosphamide pulse therapy was administered, but renal disease progressed and hemodialysis became necessary and the cyclophosphamide therapy was terminated. One month later, renal replacement therapy was switched to continuous ambulatory peritoneal dialysis. Four months later, the patient was readmitted because of a pulmonary complication with anemia due to tracheal suffusions and microbleeds in combination with a gastrointestinal reflux disease. Cyclophosphamide therapy was reintroduced with monthly administration of 1 g as a bolus, initially. Immunosuppressive treatment yielded good elimination of anti-GBM antibodies. However, a consequent immunosuppressive therapy of at least 6 months duration had never been maintained. In summary, the patient received three therapy cycles before admission to our hospital with the central nervous system symptoms, but neither cyclophosphamide nor steroids had been given on a regular basis.
Routine laboratory tests showed an elevation of creatinine (1107 μmol/l, normal value: 72-127 μmol/l) and serum urea (16.4 mmol/l, normal value: 3.0-9.2 mmol/l), while blood cell count, electrolytes, blood gas analysis and liver enzymes were normal. A chest X-ray was consistent with pneumonia after aspiration. Cranial computed tomography was normal. Cerebral magnetic resonance imaging (MRI) revealed multiple T2- and fluid-attenuated inversion recovery (FLAIR)-hyperintense lesions subcortically, predominantly located in the posterior dorsal and lateral white matter as well as in the cerebellar white matter, consistent with cerebral edema (Figures and ). The lesions did not enhance contrast media nor did they match a pattern of ischemic infarctions. The time-of-flight angiography did not detect vasculitic stenosis.
After extubation, the patient presented a mild psycho-syndrome with cognitive slowing and deficits in mnestic function. Apart from a positive Babinski sign on the left, his neurological state was normal. Due to the initial presentation with pneumonia, high-dose steroid therapy was not administered. Since anti-GBM antibodies were elevated (200 U/mL, normal value: <10 U/mL), plasmapheresis was started, alternating with continuous veno-venous hemofiltration. During this therapy, the psycho-syndrome resolved and the MR-morphological alterations almost diminished in parallel (Figure ). Anti-GBM antibodies scaled down to 21 U/mL after five cycles of plasmapheresis initiated at day 6 (substitution of 4 litre albumin at each session) and one pulse of 1 g cyclophosphamide at day 13 (Figure ). Antinuclear antibodies were negative at all times. The patient was dismissed in a neurologically and neuropsychologically healthy condition under continued oral cyclophosphamide therapy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [21, 'years'], 'creatinine': [1107.0, 'µmol/L']}",5.27274,5.0091,5.53638,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 21 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1107.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 1107.0 µmol. To convert 1107.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 1107.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00111 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00111 mol Serum Creatinine * 113.12 g/mol = 0.12556 g Serum Creatinine. To convert 0.12556 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.12556 g Serum Creatinine * 1000.0 mg/g = 125.56 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 125.56 mg Serum Creatinine/10.0 dL = 12.556 mg Serum Creatinine/dL. The concentration value of 1107.0 µmol Serum Creatinine/L converts to 12.556 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (12.556/0.9)**-1.2 * 0.9938**21 * 1.0 = 5.27274.
Hence, the GFR value is 5.27274 ml/min/1.73 m²."
540,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7102483-1,Extracted,"We report a 2-year 11-month-old male on chronic hemodialysis secondary to polycystic kidney disease (PCKD) who underwent bilateral nephrectomy. He had a compound heterozygous phosphomannomutase 2 promoter and missense mutation, accounting for PCKD and congenital hyperinsulinism. His left kidney was removed in February 2017 due to respiratory insufficiency from mass effect. Seven months later, with significantly reduced kidney function, he underwent a left nephrectomy due to respiratory compromise and hypertension. Following his second nephrectomy, he began intermittent hemodialysis five days a week; decreased to four days a week after 6 months.
Prior to his second nephrectomy, he was being treated for hypertension with an angiotensin-converting enzyme inhibitor, beta-blocker, and furosemide. After the second nephrectomy, his intradialytic systolic blood pressure used to be around 68 mmHg. For this reason, he was started on 2.5 mg midodrine during hemodialysis for systolic blood pressure below 90 mmHg. His ultrafiltration was minimized to avoid further hypotensive episodes during hemodialysis. Despite that, his systolic blood pressure stayed around 60 mmHg. Other medications included diazoxide, omeprazole, levothyroxine, and darbepoetin. He was G-tube fed without salt restriction. His blood work five days prior to presentation demonstrated normocytic, mild anemia (hemoglobin 95 g/L) with a reticulocyte count of 20 × 109/L. His electrolytes were grossly normal (sodium 136 mmol/L, potassium 3.8 mmol/L, chloride 91 mmol/L, and calcium 2.77 mmol/L) and his albumin was low at 30 g/L. Creatinine was elevated at 421 μmol/L. His echocardiogram showed normal biventricular function.
In June 2018, 9 months after initiating hemodialysis, he presented to the emergency department with an unsteady gait and difficulty focusing and following objects starting approximately two hours after completion of hemodialysis that day. Parents noted a pupil size change from small to large bilaterally, documented at 8 mm. On his initial neurological examination, his pupils were dilated but responsive, and he had poor visual acuity and an unsteady gait. He was otherwise alert, oriented, and comfortable. Vitally, his blood pressure was 59/33 mmHg, heart rate was 92 bpm, and he was afebrile. Laboratory findings on admission demonstrated a normocytic, mild anemia with a hemoglobin level of 101 g/L and an MCV of 92.7 fL. His sodium was found to be low at 127 mmol/L, with a potassium level of 4.4 mmol/L, and a chloride level of 98 mmol/L. Repeat blood work displayed a sodium level of 134 mmol/L, and thus, no hypertonic saline was administered. Creatinine was elevated at 166 μmol/L. Tox screen was negative, and AST, ALT, and INR were all normal. He had no history of trauma, toxin ingestion, sick contact exposure, or seizure activity.
Head CT displayed nonspecific findings of bifrontal subcortical white matter hypodensities. MRI displayed multiple foci of increased fluid-attenuated inversion recovery signal, mainly on bilateral subcortical white matter of the frontal lobes and corona radiata. Optic nerve size and signal intensity were normal (). Ophthalmology noted decreased visual acuity to hand motion and optic disk pallor, and diagnosed optic nerve atrophy. He was treated with a five-day course of intravenous pulse methylprednisolone (15 mg/kg, 225 mg daily). Enteral midodrine was administered three times a day, and fluids were titrated for a blood pressure goal above 70/40 mmHg.
He was discharged after steroid treatment with a diagnosis of bilateral AION. Ophthalmology follow-up two months after his acute presentation revealed his vision to be 20/800 in the left eye and 20/30 in the right eye (). He continued midodrine until his related living donor kidney transplant. He is currently stable and normotensive six months posttransplant. His vision at 10 months following his initial presentation is 20/40 in the right eye and no light perception in the left.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [421.0, 'µmol/L'], 'age': [2, 'years', 11, 'months']}",19.04738,18.09501,19.99975,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 2 years, and 11 months old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 421.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 421.0 µmol. To convert 421.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 421.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00042 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00042 mol Serum Creatinine * 113.12 g/mol = 0.04751 g Serum Creatinine. To convert 0.04751 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.04751 g Serum Creatinine * 1000.0 mg/g = 47.51 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 47.51 mg Serum Creatinine/10.0 dL = 4.751 mg Serum Creatinine/dL. The concentration value of 421.0 µmol Serum Creatinine/L converts to 4.751 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (4.751/0.9)**-1.2 * 0.9938**2 * 1.0 = 19.04738.
Hence, the GFR value is 19.04738 ml/min/1.73 m²."
541,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7594425-1,Extracted,"An 85-year-old woman presented with a bulky tumor in the collecting system of a congenital solitary left kidney. Her past medical history includes significant chronic obstructive pulmonary disease with a 2 pack-day smoking history more than 50 years. She has a history of recurrent low-grade non-muscle invasive bladder cancer (NMIBC) for the last 7 years for which she received intravesical BCG treatments. Her last recurrence in the bladder was 3 months prior showing non-invasive low-grade urothelial carcinoma.
Laboratory tests revealed normal renal function including serum creatinine of 0.69 mg/dl. A computerized tomography (CT) scan with a urographic phase demonstrated lobulated urothelial thickening of the left renal pelvis without hydronephrosis (Fig. ). CT imaging of the chest did not identify metastatic disease.
The patient underwent flexible ureteroscopy and nephroscopy with ureteral washing and biopsy. A sessile tumor greater than 2 cm was visualized in the renal pelvis towards the upper pole infundibulum. Two adequate specimens were obtained in order to determine the disease grade and were consistent with low grade urothelial carcinoma.
After a detailed discussion with the patient about the risks, benefits, and possible complications of KSS, the patient elected to undergo percutaneous treatment with laser ablation of the UTUC in her solitary kidney. Prior to the procedure, a lower pole percutaneous nephrostomy tube was successfully placed under sedation by Interventional Radiology.
The patient was positioned in prone split leg position. We cystoscopically confirmed that there was no tumor recurrence in the bladder. A guidewire was passed through the nephrostomy tube, ureteroscopically grasped with a nitinol basket and was taken out to achieve through-and-through access. After placing a 12.7 French ureteral access sheath under fluoroscopy, we visualized the renal pelvis again using the ureteroscope and dilated the percutaneous tract with a balloon dilatator under direct vision and placed a 28 French Amplatz sheath, which allowed the introduction of a 24 French continuous-flow cystoscope (Richard Wolf, CITY) with normal saline for irrigation. Importantly, the ureteral access sheath was left to optimize drainage, provide low pressure in the renal pelvis, and limit any tumor seeding in the bladder.
After systematic exploration of the collecting system, the boundaries of the large sessile tumor were visualized, and the renal pelvis mass was vaporized with the 532 nm laser in a systematic manner with continuous irrigation of normal saline through the cystoscope. GreenLight XPS LBO 180W laser console (Boston Scientific, Malborough, MA) was used with an extended application (EA) 600 micron side-fire fiber (Boston Scientific, Malborough, MA). The mass was vaporized using a setting of 40 watts; to coagulate any bleeders, the power was set at 20 watts. Care was taken to stay in near-contact with the mass during vaporization, using visible bubbles as feedback of efficient vaporization and hemostasis of the tumor bed without charring tissue. The hemostasis was achieved effectively in a very short duration at low power. Total energy used during the procedure was 39,515 J. After satisfactory tumor ablation, an 8-French nephroureteral catheter was inserted under fluoroscopic and cystoscopic guidance to maintain adequate urinary drainage.
The patient was discharged home on postoperative day 2 with the nephroureterostomy catheter open to drainage. The catheter was subsequently clamped and removed two weeks later without complications. Follow up included cystoscopy and CT urogram at 3 months. CT urogram demonstrated focal thickening in the upper pole urothelium without obvious recurrence. Ureteroscopy was performed at 6 months which demonstrated minimal residual or recurrent disease (5 mm in upper pole calyx) that was successfully ablated (thulium laser). Excellent treatment response was observed throughout the remaining collecting system. At the same time two small papillary low-grade bladder tumors were resected, followed by intravesical gemcitabine. The patient is now at 8 months of follow up and remains well, with plans for ongoing cross sectional imaging, cystoscopic and ureteroscopic follow up. Throughout the treatment, we did not observe any deleterious consequences to renal function. In the accompanying video (Additional file ), we present our technique for KTP Green-light laser vaporization of UTUC via a percutaneous approach.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [0.69, 'mg/dL'], 'age': [85, 'years']}",84.99418,80.74447,89.24389,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 85 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.69 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.69/0.7)**-0.241 * 0.9938**85 * 1.012 = 84.99418.
Hence, the GFR value is 84.99418 ml/min/1.73 m²."
542,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6509785-1,Extracted,"We describe a case of a 36-year-old black African woman with two previous live births by cesarean section and two previous miscarriages who was referred in her fifth pregnancy after 6 weeks of amenorrhea. Her serum quantitative β-human chorionic gonadotropin (bHCG) was 16,124 mIU/ml. However, an intrauterine or extrauterine pregnancy could not be located on a transabdominal ultrasound scan.
A copper intrauterine contraceptive device had been removed 2 months prior to her last menstrual period. She reported using one cycle of clomiphene 50 mg with the hope of achieving a twin pregnancy.
She had delivered twice by cesarean section for failure to progress. Her last two pregnancies had been first-trimester miscarriages; one was managed expectantly, and the other was surgically evacuated, though the actual procedure was unknown to the patient. She did not have any chronic medical illness and was not receiving any medication prior to this presentation. She stayed in a city suburb that was well serviced. She was a school principal in her second marriage with no children in the current relationship. She did not smoke or drink alcohol.
On examination, she had a normal blood pressure of 113/70 mmHg and a pulse rate of 98 beats/min. Her body temperature was 37.5 °C. On examination, her cardiorespiratory and neurological systems were normal. Her abdomen was soft and not tender. The result of her pelvic examination was normal. TVUS showed a gestational sac of 13 mm with irregular margins and a visible yolk sac located on the anterior isthmic portion of the uterus, raising suspicion of a cesarean section scar ectopic pregnancy. She declined a Doppler ultrasound evaluation scheduled for the next day. She was scheduled to have serial bHCG evaluations every 48 h.
A repeat serum quantitative bHCG done 48 h after the initial test revealed a level of 21,521 mIU/ml, a 33% rise. She defaulted follow-up until 1 week later, when she presented with pelvic pain of increasing intensity for 5 days. An urgent transvaginal scan was performed. A fetal pole with active cardiac activity (crown-rump length 0.9 cm) in a gestational sac was located in the anterior low myometrium. The sac traversed the full width of the anterior myometrium, with the posterior margin of the sac abutting the anterior margin of endometrium and the anterior margin of the sac extending to a subserosal location in a fairly exophytic fashion. There was evidence of trophoblastic circulation on Doppler examination. There was no endometrial fluid or free pelvic fluid (Fig. ).
She was immediately admitted for a diagnostic laparoscopy/hysteroscopy and possible excision of the scar pregnancy if confirmed. A preoperative complete blood count showed hemoglobin 13.4 g/dl, white blood cells 7.2 × 103/μl, and platelet count 243 × 103/μl. The patient’s kidney function was normal with sodium 135 mmol/L, potassium 4.9 mmol/L, urea 3.5 mmol/L, and creatinine 65 μmol/L. The patient’s liver function test results were also normal. She had a negative result in a blood test for human immunodeficiency virus. Urinalysis did not show abnormalities. The patient’s random blood sugar was 5.6 mmol at admission. At laparoscopy, the bladder was adherent high on the anterior uterine wall, and the ectopic pregnancy was not visualized (Fig. ). At hysteroscopy, there were extensive adhesions within the lower endometrial cavity, which obscured visibility. There was no active intracavitary bleeding ruling out a threatened or inevitable miscarriage. We could not visualize any obvious bulge in the cervical canal suggestive of a cervical ectopic pregnancy. Because of the uncertainty of the location of the pregnancy due to adhesions, excision was postponed. Postoperatively, the patient became unstable with low blood pressure, systolic pressure range of 82 to 95 mmHg and diastolic pressure range of 40 to 55 mmHg, and a pulse rate range of 64 to 73 beats/min, but without active vaginal bleeding or use of medications inducing persistent hypotension. Anesthesia had been induced with etomidate 16 mg and suxamethonium 100 mg, and maintenance was initiated with isoflurane 0.8–1.5%. Intra- and perioperative analgesia was induced with fentanyl 200 mg intravenously (IV), indomethacin 100 mg rectally, and paracetamol 1 g IV. Antibiotic prophylaxis was with ceftriaxone 1 g IV and metronidazole 500 mg IV. This prompted us to order an urgent MRI scan to map the location of the pregnancy in the immediate postoperative period. MRI confirmed the TVUS findings of a cesarean section ectopic scar extending to the serosa (Fig. ).
An emergency laparotomy was then performed on the same day. The abdomen was entered through a Pfannenstiel incision along the old skin scar. A transverse incision was made in the upper uterine segment just above the adherent bladder. The products of conception were removed with forceps, and the gap in the anterior myometrium at the old scar was seen and felt. There was massive bleeding from the implantation site. Twenty milliliters of vasopressin (20 U diluted in 100 ml) in normal saline was administered into the bleeding myometrium edges. The edges were apposed in layers with VICRYL suture (Ethicon, Somerville, NJ, USA) to repair the defect. Estimated blood loss was 2000 ml. The patient was transfused with 1 U of packed cells intraoperatively. She was continued on the same intravenous antibiotics and analgesia that had been commenced after the laparoscopy. Her hemoglobin count on day 1 postoperatively was 8 g/dl, and she declined any further transfusion. Oral iron and folic acid supplementation was commenced.
The patient’s postoperative recovery was uneventful, and she was discharged on day 4 after surgery. Histology confirmed the presence of decidua and chorionic villi. The patient wanted a child because she was in a new relationship, but she was no longer sure of her future fertility plans after the ectopic pregnancy. A levonorgestrel implant was inserted 2 weeks postoperatively. The patient last attended physical review at 6 weeks, and she was well with no problems related to the surgery at a telephone review at 3 months postoperatively.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [36, 'years'], 'creatinine': [65.0, 'µmol/L']}",115.72324,109.93708,121.5094,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 36 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 65.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 65.0 µmol. To convert 65.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 65.0 µmol Serum Creatinine * 1e-06 mol/µmol = 6e-05 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 6e-05 mol Serum Creatinine * 113.12 g/mol = 0.00679 g Serum Creatinine. To convert 0.00679 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00679 g Serum Creatinine * 1000.0 mg/g = 6.79 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 6.79 mg Serum Creatinine/10.0 dL = 0.679 mg Serum Creatinine/dL. The concentration value of 65.0 µmol Serum Creatinine/L converts to 0.679 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.679/0.7)**-0.241 * 0.9938**36 * 1.012 = 115.72324.
Hence, the GFR value is 115.72324 ml/min/1.73 m²."
543,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4904563-1,Extracted,"A 67-year-old male, originally from Southeastern Europe, was admitted to hospital in 2011 after a 12 × 6 × 8 cm perirenal abdominal aortic aneurysm (AAA) was found on ultrasound during workup for acute lower back and abdominal pain. The patient had a previous AAA open repair 5 years earlier with no complications. He also had chronic renal disease secondary to hypertension (baseline serum creatinine 140–180 μmol/L), past history of heavy smoking (quit 5 years earlier, total pack years unknown), and chronic mechanical low back pain managed medically for the last four years. He had immigrated to Canada from Southeastern Europe in 2009 and was living in Southern Alberta. He had previously worked as a mechanical technician. He denied any recent or past exposures to farm animals or unpasteurized dairy products. The patient denied fatigue, weight loss, night sweats, fevers, or chills. Vital signs were normal and the patient was afebrile. Physical exam demonstrated poor distal pulses and a palpable aorta with the remainder of the exam being normal. Laboratory workup revealed a longstanding normocytic anemia (Hgb 125 g/L) and elevated creatinine (174 μmol/L). Liver enzymes and function were within normal limits. C-reactive protein was elevated at 156.8 mg/L.
Computed tomography (CT) angiogram demonstrated an 11.8 × 14.3 cm perirenal saccular abdominal pseudoaneurysm arising from the posterior aspect of the proximal anastomosis of his abdominal aortic graft repair (). The sac extended posteriorly with extensive destruction of L1, L2, and L3 vertebral bodies (). Follow-up magnetic resonance imaging revealed L2-L3 disk space destruction that caused a moderate degree of spinal stenosis and severe left neural foraminal compromise at the L2-L3 level. It was noted that a smaller (11.4 × 7.3 cm) aortic mass with L1–L3 destruction was observed on noncontrast CT 1 year prior to his presentation, though no interventions were taken at that time. Based on the CT and MRI findings, it was felt that the pseudoaneurysm was most likely a complication from the patient's previous AAA repair (anastomotic pseudoaneurysm). Infection was not suspected.
The patient underwent an open, redo repair of his abdominal aortic aneurysm and bilateral renal artery reconstruction. The operation revealed a contained AAA rupture with large amounts of purulence and massive erosion of the patient's adjacent lumbar spine with exposure to anterior elements but no visible dura. Pathology demonstrated normal appearing atherosclerotic plaque with no signs of infection or granulomas.
One day after operation the patient developed respiratory distress as a result of renal failure from prerenal acute tubular necrosis. He was transferred to the intensive care unit for mechanical ventilation. During his stay he had recurrent fevers (Tmax 39.2) despite prolonged (approximately 1 month) treatment of piperacillin/tazobactam and vancomycin for presumed mycotic aneurysm. Aerobic and anaerobic bacterial and fungal cultures of blood and infected vascular tissue were negative, including cultures specific for Mycoplasma, Brucella, and Mycobacteria. Screening for human immunodeficiency virus, hepatitis B, hepatitis C, and syphilis was negative. After 1 month, Q fever serology results returned positive with phase I IgG serological titer of 1 : 2048 and phase II 1 : 1024, consistent with a diagnosis of chronic Q fever. Coxiella burnetii IgM was negative. PCR on the vascular tissue, completed postmortem, was positive for C. burnetii.
The patient was treated for chronic Q fever with doxycycline 100 mg twice daily and hydroxychloroquine 200 mg daily, with plan for reassessment once fully recuperated. Response to treatment was verified by repeat Q fever serology 20 months later revealing decreased titers of 1 : 512 (phase I) and 1 : 256 (phase II).
Though the patient had multiple complications during his 3-month hospital stay, the patient was successfully discharged to another centre for ongoing rehabilitation and shortly thereafter returned home with his family. He died 18 months later (22 months since admission) from hypoxia and multiorgan failure secondary to an acute pulmonary embolism (PE) confirmed on CT angiography. The PE was not thought to be related to Q fever since the patient had previously improved from his hospital stay and had decreasing phase I and II serological titers.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [174.0, 'µmol/L'], 'age': [67, 'years']}",37.63888,35.75694,39.52082,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 67 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 174.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 174.0 µmol. To convert 174.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 174.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00017 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00017 mol Serum Creatinine * 113.12 g/mol = 0.01923 g Serum Creatinine. To convert 0.01923 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01923 g Serum Creatinine * 1000.0 mg/g = 19.23 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 19.23 mg Serum Creatinine/10.0 dL = 1.923 mg Serum Creatinine/dL. The concentration value of 174.0 µmol Serum Creatinine/L converts to 1.923 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.923/0.9)**-1.2 * 0.9938**67 * 1.0 = 37.63888.
Hence, the GFR value is 37.63888 ml/min/1.73 m²."
544,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6510563-1,Extracted,"A 70-year-old Indian male with a history of a Gleason 7 (3+4) prostate cancer who underwent aborted prostatectomy a week prior, presented with weakness, abdominal distention, decreased urine output, increased lower extremity edema, and constipation for five days. On exam, his vital signs were normal. His abdomen was soft but distended, and bilateral lower extremities showed pitting edema to the level of the knees. Initial laboratory studies were notable for sodium of 117 mmol/L, potassium of 6.3 mmol/L, creatinine of 9.92 mg/dL, and white blood cell count of 21 x 108/L. Computed tomography (CT) of the abdomen and pelvis was remarkable for diffuse urinary bladder wall thickening extending to the level of the seminal vesicles, bilateral hydronephrosis, diffuse peritoneal carcinomatosis with moderate ascites, and small low-density lesions in the right lower lobe of the liver too small to characterize (Figure ). The patient subsequently underwent emergent hemodialysis followed by interventional radiology guided nephrostomy tube placement. Nuclear medicine (NM) bone scan did not show definitive evidence of osseous metastases.
Given the rarity of peritoneal involvement of prostate cancer, the pursuit of confirmatory testing was necessary to evaluate for other primary cancers. In addition, the patient’s origin from a tuberculosis endemic region raised concern for possible peritoneal tuberculosis. Ascitic fluid cytology studies confirmed the presence of malignant cells. Immunohistochemistry staining positive for prostate-specific antigen (PSA) and Ber-EP4 (a monoclonal antibody used to distinguish between adenocarcinoma and reactive mesothelium) was compatible with primary prostate adenocarcinoma (Figures -) []. However, the hematoxylin and eosin (H&E) staining also showed focal signet-ring cell features concerning for possible gastrointestinal carcinoma primary (Figure ). Ascitic fluid cultures for acid-fast bacilli, Mycobacterium tuberculosis polymerase chain reaction (PCR) and Quantiferon assays, were negative. The patient declined further tissue analysis via cystoscopy.
The patient was treated with androgen deprivation therapy (ADT), which included leuprolide and bicalutamide. Extensive discussions were held with regard to the addition of docetaxel to ADT according to the chemo-hormonal therapy vs. androgen ablation randomized trial for extensive disease in prostate cancer (CHAARTED) [], but the patient declined as he felt too weak. The patient’s total serum PSA decreased from 38.2 ng/ml to 4.7 ng/ml over four months. Repeat staging CT scan of the abdomen and pelvis that was done five months after the initiation of therapy showed an overall improvement in the peritoneal carcinomatosis. However, there was an increase in the size of some nodules in the omentum as well as a new soft tissue mass extending into the seminal vesicle consistent with progressive disease (Figure ). NM bone scan was negative for osseous metastases and patient’s serum PSA was 192.
The patient was deemed castrate-resistant with plans to start on abiraterone and prednisone therapy. Before the patient could start therapy, he developed hematuria, requiring admission to the hospital for bladder outlet obstruction from compressive effects of the mass. Repeat CT scans showed increased tumor burden including the progression of the peritoneal carcinomatosis. Although the patient was out of the window of benefit per the CHAARTED trial, he was started on docetaxel given his high volume disease while continuing his Lupron. After cycle six of docetaxel, his total serum PSA down-trended to 3.38 ng/ml with repeat CT imaging showing the response in almost all target lesions, except for an increase in the size of a nodule at the vesicoureteral junction. Given the concern for progression, the patient was subsequently started on abiraterone and prednisone. After six months of therapy, the patient had progression with worsening peritoneal carcinomatosis and a noted increase in his PSA to 4.66 ng/ml. After discussion with the patient regarding his goals for treatment, it was decided to start therapy with cabazitaxel. After one cycle of therapy, the patient had improvement of his symptoms with a decrease in his PSA. Upon completion of his fourth cycle, however, the patient developed sepsis, requiring admission to the hospital. Given his worsened functional status, the patient was deemed an unsuitable candidate for further chemotherapy and was later transitioned to home hospice.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [9.92, 'mg/dL'], 'age': [70, 'years']}",5.15816,4.90025,5.41607,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 70 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 9.92 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (9.92/0.9)**-1.2 * 0.9938**70 * 1.0 = 5.15816.
Hence, the GFR value is 5.15816 ml/min/1.73 m²."
545,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3577482-1,Extracted,"Our case was a 30-year-old Moroccan man without significant past medical history. The patient consulted us for left back pain associated with urinary symptoms of urinary frequency, and macroscopic hematuria for the past six months. The physical examination revealed an exhausted patient. The patient presented with anorexia and significant weight loss: his weight had fallen by 10kg in six months. The urogenital examination found a left epididymitis and normal prostate size with slight loss of elastic consistence; his prostate was firmer than usual for a young patient and without nodules.
Laboratory investigations were performed and showed appropriate kidney function with a creatinine of 66.2μmol/L, an inflammatory syndrome with an erythrocyte sedimentation rate of 120mm/hour and a C-reactive protein of 200mg/L, whereas the remaining laboratory investigations were unremarkable. The patient then underwent a renal and pelvic ultrasound which showed left hydronephrosis and hydroureter. This examination was completed by a computed tomography (CT) urography that revealed a left ureterohydronephrosis in the left lumbar ureter secondary to focal wall thickening (Figure ). Thus, it was thought that we revealed a ureteral tumor. However, considering the irritative voiding symptoms, epididymal symptoms, and slight indurations of the prostate, we suggested a Koch’s bacillus assessment of the patient’s urine of which the results proved strongly positive.
The treatment consisted of establishing a ureteric double-J stent to drain the left kidney, followed by antituberculous antibiotics.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [66.2, 'µmol/L'], 'age': [30, 'years']}",113.51747,107.8416,119.19334,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 30 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 66.2 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 66.2 µmol. To convert 66.2 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 66.2 µmol Serum Creatinine * 1e-06 mol/µmol = 7e-05 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 7e-05 mol Serum Creatinine * 113.12 g/mol = 0.00792 g Serum Creatinine. To convert 0.00792 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00792 g Serum Creatinine * 1000.0 mg/g = 7.92 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 7.92 mg Serum Creatinine/10.0 dL = 0.792 mg Serum Creatinine/dL. The concentration value of 66.2 µmol Serum Creatinine/L converts to 0.792 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.792/0.7)**-0.302 * 0.9938**30 * 1.0 = 113.51747.
Hence, the GFR value is 113.51747 ml/min/1.73 m²."
546,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2808612-1,Extracted,"A 65-yr-old male patient was admitted to Chonnam National University Hospital because of fever and chills with drowsy mental status after hemodialysis. His symptoms and signs were acute onset. Fifteen years earlier, he was found to have diabetes and well controlled by insulin and oral hypoglycemics, and to have hypertension. Five years earlier, he had developed chronic renal failure due to diabetic complication. Three years earlier, he was operated native brachiocephalic arteriovenous fistula formation on his left arm and has been taken maintenance hemodialysis with 3 sessions in each week. Other past medical history including tuberculosis, hepatitis or abdominal surgery had not been known. He was non-smoker, and non-alcoholics. There was no history of trauma. His blood pressure was 130/80 mmHg and his body temperature was 38.1℃ on admission. On physical examination, there was diffuse tenderness on the abdomen, especially on the left hypochondrium. There was ecchymosis around the left brachiocephalic arteriovenous fistula area with tenderness and swelling. Auscultation of his chest revealed diastolic cardiac murmurs on apex.
On chest radiography and electrocardiogram, there was cardiomegaly. Biochemical analysis revealed that hemoglobin level was 8.2 g/dL, white blood cell count 11,500/µL, platelet count 84,000/µL, blood urea nitrogen level 25.0 mg/dL, and serum creatinine level 4.6 mg/dL, sodium 140 mEq/L, potassium 4.7 mEq/L, chloride 97 mEq/L, aspartate aminotransferase 28 IU/L, alkaline phosphatase 81 IU/L, serum albumin 3.4 g/dL, C-reactive protein 25.97 mg/dL, erythrocyte sedimentation rate 31 mm/hr, fibrinogen degradation product <5 µg/mL, D-dimer 0.4 mg/L (reference value 0-0.3), aPTT 37.3 sec, PT 13.1 sec/INR 1.08, and fibrinogen 716 mg/dL.
Abdominal sonography revealed two hypoechoic space occupying lesions and one cystic lesion in the spleen (). To differentiate splenic abscess or infarction, abdominal computed tomography (CT) was performed. Abdominal CT revealed multiple septated cystic lesions in the spleen, the largest 4.3 cm, and 2 cm low attenuated lesion in the left buttock area, compatible with multiple splenic abscesses and an abscess in the left buttock area (). We performed 2D-echocardiography, and found mobile hyperechoic mass on posterior mitral valve leflet tip with calcified valve. His brain CT was normal. We obtained blood samples at two different sites for bacteriologic culture and then started empirical antibiotics with ceftriaxone and aminoglycoside. He had continuous fever and left hypochondrial pain. Blood culture revealed methicillin sensitive Staphylococcus aureus (MSSA). We changed the antibiotics with cefazoline based on the drug sensitivity test. Inflammatory signs and hypoechoic lesions in the spleen did not respond to antibiotic therapy. On the 4th hospital day, emergency splenectomy was performed for the splenic abscess based on blood culture and abdominal CT. We aspirated blood from the evacuated spleen for bacteriologic culture and sent the evacuated spleen to pathologist for histologic diagnosis (). MSSA was cultured from the evacuated splenic blood, too. The pathologic findings showed splenic abscesses and infarction (). Antibiotic therapy was continued and he became afebrile. CBC findings and other chemical laboratory findings were returned to normal.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [4.6, 'mg/dL'], 'age': [65, 'years']}",13.38149,12.71242,14.05056,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 65 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 4.6 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (4.6/0.9)**-1.2 * 0.9938**65 * 1.0 = 13.38149.
Hence, the GFR value is 13.38149 ml/min/1.73 m²."
547,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5358041-1,Extracted,"During the last influenza season a 6-month-old boy born to Turkish, unrelated healthy parents, was admitted after 5 days of febrile bronchitis and without any history of recent diarrhea, with pallor, edema of the eyelids and reduced urine output. Hemolytic anemia (hemoglobin 5.7 g/dL (10.1–13.1 g/dL)), thrombocytopenia (58/nL (150–500/nL)), and renal failure with raised serum creatinine (1.42 mg/dL (0.2–0.5 mg/dL)) lead to the diagnosis of HUS. A blood smear showed schistocytes, the urine analysis proteinuria and an ultrasound enlarged hyperechogenic kidneys. ADAMTS13 activity was normal, while complement activation could be confirmed by mildly reduced serum C3 (69 mg/dL (90–180 mg/dL)) and increased plasma terminal complement complex sC5b-9 (450 ng/ml (<320 ng/ml)). We could not detect any pathogenic enterobacteria (enterohemorrhagic E. coli, Yersina-, Shigella-, Campylobacter species) by culture and no Shiga toxin by PCR in multiple stool samples. A nasopharyngeal swab showed presence of Influenza B DNA by multiplex-PCR and genotyping identified the subtype Yamagata.
Subsequently, genomic analysis of the patient’s CFH, CFI, C3 and MCP genes by Sanger-sequencing identified a pathogenic heterozygous mutation in the MCP gene (c.104G > A (p.Cys35Tyr)) confirming the diagnosis of aHUS []. In addition, quantitative MLPA-analysis showed a suspicious signal of a non-allelic homologous recombination (NAHR) in the regulators of complement activation gene cluster (RCA) on chromosome 1 []. Meanwhile, we had started the patient on the antiviral drug Oseltamivir, antihypertensive medication and symptomatic treatment. After initial spontaneous recovery the patient developed clinical signs of relapse. Eculizumab treatment was started immediately after vaccination against meningococcal diseases. This resulted in a complete and sustained remission ever since (Fig. ). Previously not immunized, the patient will now be vaccinated against influenza with quadrivalent vaccines for maximum protection before each start of the upcoming seasons.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.42, 'mg/dL'], 'age': [6, 'months']}",82.15488,78.04714,86.26262,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 6 months old. This means the patient is 0 years old.
The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.42 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.42/0.9)**-1.2 * 0.9938**0 * 1.0 = 82.15488.
Hence, the GFR value is 82.15488 ml/min/1.73 m²."
548,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6031599-1,Extracted,"A 67-year-old male patient presented with a three-day history of diarrhea. He had received 14 months of dasatinib therapy (100 mg/day) for the treatment of CML, and He had chronic kidney disease. Physical examination revealed no fever and mild abdominal pain without any tenderness. At hospitalization, he had white blood cell (WBC) count of 19,430/mm3 (lymphocyte, 71%), hemoglobin (Hb) level of 8.0 g/dl, platelet count of 239,000/mm3, and a blood urea nitrogen/creatinine ratio of 85.2/3.08 mg/dl. On the 2nd day, his WBC count declined sharply to 8,720/mm3 (lymphocyte 20%), and he developed hematochezia without thrombocytopenia on 3rd day of admission. At this point, his blood and stool cultures tested negative. Dasatinib-induced hemorrhagic colitis was suspected, and a total colonoscopy revealed edematous and friable mucosa, along with a loss of vascularity from the cecum to rectum (). His symptoms did not improve upon the discontinuation of dasatinib and with conservative care. After 4 days of admission, biopsy tissue showed positive CMV-specific IHC staining, and a blood CMV real time quantitative polymerase chain reaction (RQ-PCR) also tested positive (760 copies/ml). His symptoms subsided following 19 days of ganciclovir (5 mg/kg IV q12hr) administration. Dasatinib was re-started subsequently, and the CMV colitis did not relapse (15 months).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [3.08, 'mg/dL'], 'age': [67, 'years']}",21.38706,20.31771,22.45641,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 67 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.08 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.08/0.9)**-1.2 * 0.9938**67 * 1.0 = 21.38706.
Hence, the GFR value is 21.38706 ml/min/1.73 m²."
549,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8655043-1,Extracted,"A 46-year-old African male with a past medical history of essential HTN presented to the emergency department with a five days history of cough, shortness of breath, diarrhea, muscle cramping, fatigue, poor oral intake and decreased urinary output. The patient was tested positive for COVID-19 one day prior to admission. On further examination, the patient was febrile, hemodynamically stable with a blood pressure of 125/57 mmHg with a mean arterial pressure of 77 mmHg, heart rate of 83 bpm, respiratory rate of 24 per minute, and oxygen saturation was 93%. The patient was adequately oxygenated on a 2 L nasal cannula. Initial lab report revealed 133 meq/L of Na, chloride 88 meq/L, potassium 6.3 meq/L, calcium 8 meq/L, creatinine 23 mg/dL, BUN 195 mg/dL, creatinine kinase 1,200 U/L, lactate dehydrogenase (LDH) 212 U/L, C-reactive protein 126.6, and elevated D-dimer 4,433 (Table ). Arterial blood gas showed bicarbonate 6 meq/L, CO2 6 mmol/L, anion gap 41 mmol/L, PH 7.17. His liver function panel was normal. Urinary analysis showed protein >600 mg/dL, blood 1+, creatinine 404.6 mg/dL, and urine protein electrophoresis was 1,735 mg.
EKG findings were non-significant for hyperkalemia, Chest x-ray was negative for the acute process of viral infection (Figure ). Since the patient was dehydrated he was started on 2 L of normal saline followed by 1 g of calcium gluconate. Repeat potassium was 7.7 meq/L. Therefore, the patient was admitted to the COVID ICU followed by a nephrology consultation. Since remdisivir is not a good drug of choice in renal dysfunction, 6 mg of decadron was started and sodium bicarbonate drip was started at 150 mL/hr. Additional investigation including color Doppler ultrasound of lower extremities was done due to high D-dimer and was negative for deep vein thrombosis. Ultrasound of kidney and urinary bladder was also negative for hydronephrosis. Despite the lack of improvement in supportive treatment, the patient was scheduled for hemodialysis. Subsequently his renal function and electrolytes status improved. Creatinine decreased to 3.1 mg/dL, creatinine kinase 895 IU/L, and the anion gap trended to 15. On discharge, potassium was 4.4 meq/L, creatinine was 2.9 mg/dL and he was sent home on room air with four more days of decadron and pulmonary rehabilitation exercise was done to enhance the recovery from COVID-19 pneumonia.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [2.9, 'mg/dL'], 'age': [46, 'years']}",26.19723,24.88737,27.50709,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 46 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.9 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.9/0.9)**-1.2 * 0.9938**46 * 1.0 = 26.19723.
Hence, the GFR value is 26.19723 ml/min/1.73 m²."
550,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7278321-1,Extracted,"On May 3, 2019, a 34-year-old man was admitted to our hospital due to agitation, auditory
hallucinations, and abdominal pain for 2 days. Four years prior to admission, the patient
had been diagnosed with chronic renal failure and hypertension. Since then, he had undergone
stable continuous ambulatory peritoneal dialysis using 2.5% peritoneal dialysis fluid four
times per day. The ultrafiltration volume was about 1,000 mL. The patient had a fever 3 days
before admission with a peak temperature of 37.8°C, accompanied by dizziness and discomfort
in his neck. He took ibuprofen and his temperature returned to normal, but there was no
significant improvement in dizziness. A local physician initiated an infusion treatment
(clindamycin 0.6 g + normal saline 250 mL, dexamethasone 5 mg, vitamin C 200 mg + normal
saline 250 mL), which slightly improved the patient’s dizziness. One day later, the patient
reported discomfort in his upper abdomen accompanied by restlessness, auditory
hallucinations, and emotional agitation. He continued to receive peritoneal dialysis. The
patient visited our hospital accompanied by his family; he was diagnosed with chronic renal
failure, hypertension, chronic left cardiac dysfunction, and a symptomatic mental disorder.
Signed informed consent was obtained from the patient, and this study was approved by the
ethics review committee of the Lianyungang No. 1 People’s Hospital.
The patient had a history of hypertension lasting more than 6 years, with a maximum blood
pressure of 200/100 mmHg. He was treated with nifedipine controlled-release tablets, 20 mg
twice a day, and metoprolol tartrate tablets, 47.5 mg once a day orally. The patient had
also suffered from chronic left ventricular dysfunction for several years. Echocardiogram
showed cardiac enlargement, a decrease in ventricular activity and cardiac function,
valvular regurgitation of the second and tricuspid valve, and severe pulmonary hypertension
(pulmonary artery systolic pressure 97 mmHg; left ventricular ejection fraction 28%). He had
no history of medication allergies.
Physical examination showed that the patient had a temperature of 36.4°C, blood pressure of
99/65 mmHg, and heart rate of 55 beats per minute. The patient was restless, agitated, and
kept complaining about upper abdomen discomfort. He could not respond to questions when
asked about his medical history. A few abnormal breath sounds (moist rales) were revealed
when listening to the chest with a stethoscope (auscultation). The patient’s peritoneal
dialysis catheter was stable and fixed in place. No edema in the lower limbs was noted.
Laboratory examination revealed the following results: leukocyte count of
12.98 × 109/L, neutrophil ratio of 84.8%, lymphocyte percentage of 7.2%,
hemoglobin level of 137 g/L, platelet count of 344 × 109/L, blood creatinine
level of 1,687.8 µmol/L, blood urea nitrogen level of 33.64 mmol/L, potassium level of
3.23 mmol/L, chlorine level of 89.7 mmol/L, calcium level of 1.85 mmol/L, phosphorus level
of 3.87 mmol/L, and sodium level of 137.4 mmol/L. There was no obvious abnormality observed
on head and chest computed tomography (CT). Electroencephalogram on day 2 of hospitalization
showed moderately abnormal brain topography and basic rhythm (). Blood ammonia and blood glucose were
normal.
At admission, the clindamycin treatment was discontinued, and peritoneal dialysis was
strengthened. The patient was treated with low-calcium peritoneal dialysis solution
(lactate-G2.5%) 2,000 mL intraperitoneal injection, five times a day; reducing glutathione
1,200 mL intravenous injection, once a day; calcium gluconate 1 g + 5% glucose intravenous
injection 20 mL, once a day; 250 mL of sodium bicarbonate intravenous injection, once a day;
alprostadil 10 µg + saline 100 mL intravenous injection, once a day; and other support
treatments. No antibiotics were administered during the hospitalization. On the night of 3
May, the patient’s anxiety and excitement increased. He began throwing and damaging his
personal belongings. The doctor on duty administered diazepam 5 mg static push, olanzapine
2.5 mg orally, and haloperidol 5 mg intramuscular injection assisted sedation. On 4 May, the
patient’s abdominal pain eased and irritability gradually diminished. The patient was able
to remember information and control his emotions. On 8 May, he was discharged from the
hospital without any neurological deficits.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1687.8, 'µmol/L'], 'age': [34, 'years']}",2.93658,2.78975,3.08341,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 34 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1687.8 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 1687.8 µmol. To convert 1687.8 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 1687.8 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00169 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00169 mol Serum Creatinine * 113.12 g/mol = 0.19117 g Serum Creatinine. To convert 0.19117 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.19117 g Serum Creatinine * 1000.0 mg/g = 191.17 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 191.17 mg Serum Creatinine/10.0 dL = 19.117 mg Serum Creatinine/dL. The concentration value of 1687.8 µmol Serum Creatinine/L converts to 19.117 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (19.117/0.9)**-1.2 * 0.9938**34 * 1.0 = 2.93658.
Hence, the GFR value is 2.93658 ml/min/1.73 m²."
551,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4109115-1,Extracted,"In December 2012, a 39-year-old Chinese woman complaining of anuria with lower abdominal pain visited our hospital. She had not received unremarkable medical treatments before except for the right lateral allogeneic renal transplantation in 2009 at another hospital (hereafter referred to as Hospital A) owing to uremia. Initially, she had a good postoperative recovery via routinely taking the antirejection immunosuppressants cyclosporin A and prednisone. Simultaneously, she took calcitriol to manage commonly encountered HPT and osteoporosis after renal transplantation []. However, she had undergone anuria with lower abdominal pain 6 months ago, which was diagnosed as acute unilateral ureteral obstruction. Subsequently, the patient had been receiving retrograde internal 6F ureteral double J stenting provided by Bard-InLay and discharged from Hospital A. Unfortunately, she had been harassed by the identical symptoms 2 months later. Although Bard-InLay stent was the most commonly used auxiliary implement in urological interventions for its tapered tip and lubricious coating to facilitate smooth insertion and effective negotiation around obstructions, clinicians in Hospital A had substituted domestic ureteral stent brand of YZB/Jiangsu-0038-2004 for Bard-InLay, in view of different adaptabilities to the stents caused by racial diversity and personality. Surprisingly, only 3 weeks later, it is necessary for the patient to receive the third double J stent placement to solve the extremely same problem of anuria and abdominal symptoms. Even so, this last try in Hospital A was still invalid after one month.
After viewing the medical history, we began to make a physical examination for her. She had unremarkable physical signs except for a suffering moon face and slight abdominal bulge and pain. Routine blood investigation file revealed red blood cells, white blood cells, and platelet counts of 4.11 × 1012/L, 10.38 × 109/L, and 322 × 109/L, respectively. Besides, the following data were obtained: total protein, 54.8 g/L; albumin, 29.0 g/L; glucose, 4.69 mmol/L; urea nitrogen, 2.84 mmol/L; creatinine, 61 μmol/L; potassium, 3.30 mmol/L; sodium, 135.5 mmol/L; chlorinum, 103.1 mmol/L; magnesium, 0.63 mmol/L; phosphonium, 1.00 mmol/L; intact PTH, 32.1 pg/mL; 24-hour urine calcium, 4.42 mmol/L; and calcium, 2.19 mmol/L. For the imaging diagnosis, type-B ultrasound revealed moderate hydronephrosis of the transplanted kidney in the right lateral of pelvic cavity. Kidney-ureter-bladder (KUB) radiography clearly showed the stent modified by cutting a length of 9 cm from one end of the classical 25 cm full-length double J ureteral stent to improve its clinical acceptability (as the donor kidney is usually placed in a lower position in the pelvic cavity) (, red arrows, and ). After careful and detailed examinations, we conducted the operation to substitute a new Bard-InLay internal 6F double J stent for the originally blocked one. Subsequently, infrared spectrum analysis elucidated that the calculi in the completely blocked stent consisted of whewellite, weddellite, and carbonated apatite (Figures and , red arrows and dashed lines). The patient's urine volume reached 4300 mL the next whole day after operation. Besides, her kidney function tests and multiple urine cytologies were absolutely normal. After discontinuing calcitriol, the patient was found to be calculi-free and the 9-month follow-up showed a good recovery without stent obstruction or anuria with lower abdominal pain, which she had been confronting several times before receiving the appropriate management in our hospital.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [61.0, 'µmol/L'], 'age': [39, 'years']}",113.58411,107.9049,119.26332,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 39 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 61.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 61.0 µmol. To convert 61.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 61.0 µmol Serum Creatinine * 1e-06 mol/µmol = 6e-05 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 6e-05 mol Serum Creatinine * 113.12 g/mol = 0.00679 g Serum Creatinine. To convert 0.00679 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00679 g Serum Creatinine * 1000.0 mg/g = 6.79 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 6.79 mg Serum Creatinine/10.0 dL = 0.679 mg Serum Creatinine/dL. The concentration value of 61.0 µmol Serum Creatinine/L converts to 0.679 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.679/0.7)**-0.241 * 0.9938**39 * 1.012 = 113.58411.
Hence, the GFR value is 113.58411 ml/min/1.73 m²."
552,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6374990-1,Extracted,"A 39-year-old female presented with complaints of generalized abdominal distension, weight loss, swelling of legs, and muscle weakness extant for several weeks. Her past medical history was significant for a well-controlled HIV infection of 6 years on highly active anti-retroviral therapy, hypertension, ESRD secondary to HIV-associated nephropathy, and secondary hyperparathyroidism. She was a non-smoker and had no history of alcohol or drug abuse. Her initial renal biopsy revealed collapsing focal glomerular sclerosis, microcystic dilation of renal tubules, lymphocytic interstitial infiltrates, and interstitial fibrosis. She received chronic cycler-assisted peritoneal dialysis (PD) for 5 years and was well controlled clinically regarding uremic and volume status with no abnormalities regarding color, viscosity, or volume of exchanges. Subsequently, she was transitioned to intermittent hemodialysis (HD) due to personal preferences. A few weeks after the transition to intermittent HD, ascites of unclear etiology developed, ultimately requiring repeated large-volume paracentesis with ~ 5 – 7 L ascitic fluid removals every other week.
There were no associated symptoms of coughing, palpitations, or shortness of breath. She was chronically anuric. Vital signs showed blood pressure of 160/80 mmHg, heart rate 74 beats/min (regular), respiratory rate 16/min and temperature 36.9 °C. Oxygen saturation was 98% on ambient room air. Her physical examination was remarkable for moderate ascites and edema of the lower extremities. Otherwise neurological, respiratory, and cardiovascular examinations were normal without organomegaly and without clinical stigmata or symptoms of chronic liver disease or heart failure.
Laboratory investigations showed normocytic, normochromic anemia with a hemoglobin of 10 g/dL and uncorrected serum calcium of 8.6 mg/dL. Other labs were as follows: CD4 T-cell count: 600/mm3, HIV viral load: 986 copies/mL (reference: < 40 copies/mL), serum creatinine: 10.3 mg/dL, aspartate aminotransferase: 13 U/L (normal range: 5 – 34 U/L), alanine aminotransferase: 17 U/L (5 – 45 U/L), bilirubin: 0.4 mg/dL, prothrombin time INR: 1.01, serum albumin: 2.3 mg/dL, serum amylase: 105 IU/L (27 – 130 U/L), serum lipase: 40 IU/L (8 – 78 U/L). Her tumor antigens (Ag) were within reference range for cancer antigen (CA) 15-3 and CA19-9. CA 125 levels were repeatedly elevated (197 – 416 U/mL (normal: < 34.9 U/mL)), but no further follow-up was obtained. Analysis of the ascites fluid showed an albumin level of 1.5 g/dL and protein of 3.5 g/dL. The serum-to-ascites albumin gradient was < 1.1 excluding portal hypertension as a cause of ascites. The culture of peritoneal fluid was negative for acid-fast bacilli. There were no fungi seen by calcofluor white stain. Histoplasma Ag and Aspergillus Ag were negative. The pancreas was reported normal on computed tomography. Her β-2 microglobulin was elevated to 47.30 mg/L (normal: 0.80 – 2.3). Serum protein electrophoresis showed hypoalbuminemia and decreased total protein, with minimal monoclonal M-component only (IgG-κ 0.30 g/dL in the γ zone). Immunofixation electrophoresis showed polyclonal immunoglobulins (Ig) with polyclonal light chains. κ and λ light chains were increased to 66.86 mg/dL (normal: 0.33 – 1.94) and 18.55 mg/dL (normal: 0.57 – 2.63), respectively, yielding a ratio of 3.6 (normal: 0.26 – 1.65) (). Ascitic fluid analysis showed a marked increase in plasma cells with an abnormal κ : λ ratio, i.e., > 5 : 1.
Liver biopsy was essentially normal, hence an omental biopsy was performed which on immunohistochemistry showed similar findings as the ascitic fluid with predominant κ and faint λ staining (). Multiple myeloma work-ups with skeletal surveys revealed no focal osseous lesions, apart from the osseous changes of hyperparathyroidism. Accordingly, the diagnosis of omental EMP with malignant ascites was established. Omental resection and radiation were offered to the patient, but she refused further intervention. Two years of follow-up, she remained stable without any further complication, apart from requiring regular paracenteses.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [10.3, 'mg/dL'], 'age': [39, 'years']}",4.47551,4.25173,4.69929,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 39 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 10.3 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (10.3/0.7)**-1.2 * 0.9938**39 * 1.012 = 4.47551.
Hence, the GFR value is 4.47551 ml/min/1.73 m²."
553,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3521645-2,Extracted,"The patient is a man who is currently 24 years old. No abnormality had been noted in the perinatal period, nor was there any contributory or past medical history. His parents were unrelated; however, they were divorced soon after his birth. No inherited kidney disease or other congenital anomalies of the kidney were found in his maternal family members. The patient was brought to our department because of edema that developed after influenza at 3 years of age. Proteinuria, hypoproteinemia, and mild renal dysfunction were present, and the patient was admitted. On physical examination, facial edema was present, but ascites was absent. Mild mental retardation was noted, but motor function was normal. Semiqualitative urinary protein was 4+ (5.4 g/day). Serum total protein was 4.2 g/dl, and albumin was 2.1 g/dl, indicative of NS. BUN was 33 mg/dl and creatinine was 1.4 mg/dl, showing mild renal hypofunction. Urinary β2-MG was 1,020 μg/day, representing a mild increase; however, the urine concentrating ability remained normal at this time. Steroid therapy (2 mg/kg/day) was initiated, but urinary protein levels did not decrease. Kidney biopsy was performed, obtaining 23 glomeruli; changes were minimal. In the uriniferous tubular interstitium, tubular epithelial cell detachment, focal thickening and atrophy of the tubular basement membrane, and mild interstitial fibrosis were observed (Fig. a). Immunofluorescence showed no deposition of any immunoglobulin type or of complement. Localization of nephrin and CD2AP was normal. The patient was diagnosed with steroid-resistant NS. CyA treatment was initiated, obtaining a type I incomplete remission. A second kidney biopsy was performed at 5 years of age because of increased proteinuria. Glomerular enlargement had progressed, and segmental sclerotic lesions were noted in some glomeruli. Based on the later findings, FSGS was diagnosed (Fig. b, arrow). In a third specimen at 8 years of age, tubular atrophy, tubular interstitial fibrosis, and glomerular segmental sclerotic lesions had progressed (Fig. c, d). The median glomerular diameter was 73.5 μm in the specimen obtained at 5 years (25 glomeruli evaluated), slightly larger than in age-matched children (55–60 μm); the number of glomeruli per unit area was 5.8/mm2, within the normal range. However, in the next specimen, the number of glomeruli had decreased (4.7/mm2) and glomerular diameter increased. Since we were not able to obtain consent for gene analysis from his mother, the mode of inheritance remains unclear.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [24, 'years'], 'creatinine': [1.4, 'mg/dL']}",71.97829,68.37938,75.5772,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 24 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.4 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.4/0.9)**-1.2 * 0.9938**24 * 1.0 = 71.97829.
Hence, the GFR value is 71.97829 ml/min/1.73 m²."
554,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8187818-1,Extracted,"A 67-year-old male underwent a live, related renal artery transplant due to Stage IV Chronic Kidney Disease secondary to biopsy proven IgA nephropathy. Patient has a past medical history of Type II Diabetes Mellitus, HTN, OSA, bladder cancer s/p TURP, systolic heart failure with implanted defibrillator, dyslipidemia, and obesity with BMI of 38.0 kg/m2. He is a retired maintenance worker and never smoker with no alcohol use. The kidney of his biological brother was transplanted into the right iliac fossa with end to side anastomosis of graft renal vessels to the external iliac vessels. The surgical course was uneventful. Surgery was performed by a board certified transplant surgeon with over 10 years of experience at a regional community practice. Pre-operative creatinine was 3.3 mg/dl. Post-operative creatinine was 3.1 mg/dl and increased to 3.3 mg/dl on post-operative day one. Urine output was satisfactory at 220 ml/h. Immediate post-operative ultrasound showed no evidence of perinephric fluid collection and low-normal renal artery peak systolic velocity measures of 41 cm/s at the hilum, 46 cm/s at the mid-portion, and 57 cm/s at the anastomosis with resistive indices of 0.6 at the upper, middle, and lower pole. On post-operative day one, repeat ultrasound revealed decreasing renal artery peak systolic velocities at the hilum (32 cm/s) and mid-portion (33 cm/s), but increased peak systolic velocity at the anastomosis (129 cm/s) with resistive indices of 0.73 at the upper, 0.63 at the middle, and. 0.60 at the lower pole. Follow-up renal nuclear medicine scan showed delayed perfusion to the renal transplant. Renal CO2 angiogram demonstrated evidence of kinking of the transplant's renal artery (). Renal angiogram with judicious contrast supported this finding as well (). Attempted balloon angioplasty revealed a lesion that did not behave like a true stenosis in that very little resistance was encountered during inflation with no stricture noted in the balloon (). Renal angiogram showed continued kinking after deflation of the balloon (). This evaluation and attempted angioplasty was performed by a board certified interventional radiologist with more than 15 years of experience at a regional community practice. Due to unsuccessful angioplasty and evidence of mechanical kinking on renal angiogram, the patient underwent surgical evaluation, and a renal artery kink was identified 1.5 cm distal to the anastomosis. The graft was repositioned with upper pole placed in the posterior pelvis and lower pole positioned towards the incision to avoid kinking of the vasculature. The operative course was uneventful. Post-operative ultrasound revealed increasing peak renal artery systolic velocities at the hilum (268 cm/s, high-resistance wave form), mid-portion (128 cm/s), and anastomosis (173 cm/s, high-resistance wave form) with resistive indices of 0.51 at the upper, 0.58 at the middle, and 0.60 at the lower pole. Serum creatinine decreased to 2.8 mg/dl on post-operative day one and 2.1 mg/dl on post-operative day two. Urine output remained strong at 2.5l in 24 h post-op indicating successful repositioning. The patient developed a seroma and borderline evidence of rejection on renal biopsy in the continued post-operative course. At two months follow up the patient is stable with a creatinine of 1.3 mg/dl.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.3, 'mg/dL'], 'age': [67, 'years']}",60.21155,57.20097,63.22213,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 67 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.3 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.3/0.9)**-1.2 * 0.9938**67 * 1.0 = 60.21155.
Hence, the GFR value is 60.21155 ml/min/1.73 m²."
555,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3350214-1,Extracted,"A 42-year-old male patient was admitted with an 18-month history of progressive abdominal distension and mild dullaching diffuse abdominal pain. He used to have vague abdominal discomfort and did not have specific characteristic pain. Patient did not have any history of fever, jaundice, or vomiting. Also there was no history of weight loss, and he had maintained a good appetite. Hematemesis and melena were also absent. There were no specific urinary or bowel complains.
Clinical examination showed a huge and symmetric distension. No abdominal mass was palpable. The swelling was dull on percussion, but there was no shifting dullness. Examination of other systems was unremarkable.
The serum analysis and complete blood count was performed, and blood urea was 1,65 g/L, creatinine was 78 mg/L, hemoglobin was 11 g/dL, and hematocrit was 51.4%. Blood sugar, serum amylase, liver function tests, and serum calcium, phosphate, and electrolytes were within normal limits. Urine examination did not reveal any abnormality, and urine culture was sterile.
Diagnostic aspiration from abdominal swelling revealed urine. Ultrasonography revealed a large hypoechoic mass lesion occupying nearly the whole abdomen with multiple septate internal echoes. kidneys were not visualized separately. The liver was displaced upwards. A CT scan of the abdomen, without intravenous contrast, was done to further delineate the site of obstruction. It revealed a giant bilateral hydronephrosis and a huge bladder which occupied the intraperitoneal and pelvic cavities (Figures and ). No abdominal mass or calculi were seen. Following this, a total of about 20 L of urines fluid was drained by urethral catheterization over a period of 3 days. There was minimal improvement in the renal function, urea was 1,30 g/L, creatinine was 60 mg/L.
Ultrasonography control showed significant regression of the dilatation, but the large bilateral kidney hydronephrosis was still present.
The cystoscopy confirmed the huge bladder and showed a bladder neck obstruction (), and then a trans-urethral neck incision was performed. Hyporeactive bladder was found in urodynamic analysis, and a cystofix suprapubic bladder catheter was introduced percutaneously. The postoperative period was uneventful. Follow-up US examinations demonstrated nearly complete disappearance of the hydronephrosis; laboratory findings and urine culture were normal.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [78.0, 'mg/dL'], 'age': [42, 'years']}",0.51692,0.49107,0.54277,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 42 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 78.0 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (78.0/0.9)**-1.2 * 0.9938**42 * 1.0 = 0.51692.
Hence, the GFR value is 0.51692 ml/min/1.73 m²."
556,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4397714-1,Extracted,"A 75-year-old female presented to a local clinic with a history of fever, nausea, vomiting, and anorexia lasting for 2 days. Medical history was significant only for arterial hypertension, obesity (body mass index 29), and urinary incontinence. She was treated by oral antihypertensive therapy and solifenacin for her overactive bladder.
Physical examination revealed fever with body temperature of 101.3°F (38.5°C), tachypnea with respiratory rate of 25 breaths/min, normal hemodynamic parameters with blood pressure 125/57 mmHg, and pulse 80 beats/minute. The laboratory investigations yielded an inflammatory process and moderate renal impairment. The white blood cell count was 37.6 × 109/L with neutrophils 85%. Hemoglobin was 100.2 g/L. The platelet count was normal 263 × 109/L, and fibrinogen was 32.89 μmol/L. C-reactive protein was 591 mg/L; the serum gammaglutamyltransferases level was increased up to 276 U/L. The alkaline phosphatases level was 168 U/L. The bilirubin was 9.7 μmol/L. The urea nitrogen and creatinine serum levels were, respectively, 18 mmol/L and 282 μmol/L. The other laboratory tests for blood chemistry panel and liver function were normal. Few minutes after her admission, the patient's blood pressure dropped dramatically with anuria and hypoxemia, so she received oxygen therapy (10 L/min with a reservoir mask) and intravenous fluid therapy with 1,500 mL of crystalloid (Ringer lactate) and 500 mL of colloid (6% hydroxyethyl starch 130/0.4).Urgent abdominal computed tomography (CT) scan permitted the diagnosis of EPN showing a pyonephrosis of the right kidney and presence of pneumaturia in the collecting system and in a cyst located in the lower pole of the right kidney (Figure ). The pelvi-caliceal cavities of the right kidney appeared slightly dilated. After blood cultures, intravenous antibiotic therapy was initiated with amoxicillin/clavulanic acid 1 g and ofloxacin 200 mg. Despite antibiotic therapy and supportive measures, the patient's clinical condition rapidly deteriorated towards a septic shock with multiple organ dysfunction syndrome. The patient required mechanical ventilator support and intravenous vasopressor (norepinephrine). She was promptly transferred to our hospital to undergo urgent ureteral stenting.
On admission to the operating room, protective ventilation settings (controlled mandatory ventilation, tidal volume of 7 mL/kg of predicted body weight, respiratory rate 20 breaths/min, FiO2 1.0) resulted in a PaO2/FiO2 ratio at 122. Hemodynamic parameters with continuous intravenous norepinephrine 0.4 gamma/kg/min showed pulse 90 beats/min and mean arterial pressure 69 mmHg, and the patient was still anuric. A right retrograde cystoscopic pyelogram revealed a moderate pelvi-caliceal dilatation and also allowed a right ureteral open-ended stenting with drainage of a pyuria.
The patient was subsequently admitted to our ICU. Antibiotics were switched to intravenous ceftriaxone (2 g/day) plus ofloxacin (200 mg twice a day) and metronidazole (500 mg every 8 h). Septic shock improved in the following 2 days. Her renal function recovered without need of renal replacement therapy and with equal diuresis of both kidneys. Despite improvement of the patient's condition, we observed a reascension of WBC at day 3 (50 × 109/L). Gynecological examination with hysteroscopy excluded genital infection. CT scan showed a persistent posterior abscess of the right kidney with inflammatory infiltration of the perirenal space. After discussion with urologists and radiologists, a percutaneous CT scan-guided drainage was performed by a radiologist who placed a stent in the abscess and collected a hemic and purulent fluid. The patient's condition rapidly improved, so she was extubated on day 8. On day 11, the CT scan-guided drainage was complicated by a fistula, with the urinary tract successfully treated by a double J stenting of the right ureter.
Microscopic examination of urine collected by cystoscopy from the right pelvi-caliceal cavity showed presence of pyuria, Gram stain detected gram-positive bacilli, and culture was positive with A. meyeri 105 CFU/mL with the use of Vitek 2 ANC card (bioMérieux, Marcy l'Etoile, France). Antibiotherapy was finally switched to amoxicillin 2 g × 3 per day according to the antibiogram for a duration of 3 months against A. meyeri. As advised by our infectious disease specialists, ofloxacin (200 mg twice a day) was maintained for 21 days covering a hypothetic non-diagnosed coinfection with gram-negative bacilli. Metronidazole was stopped at day 5 after identification of A. meyeri. At day 10, the patient was finally discharged from the ICU to the department of urology in stable condition. She recovered a normal renal function and was transferred back to her home at day 24. She underwent an abdominal CT scan 2 months later (Figure ) showing regression of the right pyonephrosis with normal parenchyma, no dilatation, and persistence of a right renal cyst of reduced diameter. Four months later, ureteroscopic examination revealed no abnormality and double J stenting was retrieved.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [282.0, 'µmol/L'], 'age': [75, 'years']}",14.73103,13.99448,15.46758,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 75 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 282.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 282.0 µmol. To convert 282.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 282.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00028 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00028 mol Serum Creatinine * 113.12 g/mol = 0.03167 g Serum Creatinine. To convert 0.03167 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.03167 g Serum Creatinine * 1000.0 mg/g = 31.67 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 31.67 mg Serum Creatinine/10.0 dL = 3.167 mg Serum Creatinine/dL. The concentration value of 282.0 µmol Serum Creatinine/L converts to 3.167 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (3.167/0.7)**-1.2 * 0.9938**75 * 1.012 = 14.73103.
Hence, the GFR value is 14.73103 ml/min/1.73 m²."
557,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7243385-1,Extracted,"The patient is a 44-year-old African American male, with a history of diabetes and hypertension, who presented to the emergency department on December 30, 2018, with complaints of joint pain, leg swelling, mild abdominal pain, and a rash. His symptoms began 5 days before admission with lower extremity arthralgia and swelling. The pain progressed and a diffuse rash appeared over his back, legs, and abdomen. Physical examination was notable for palpable purpuric lesions distributed extensively across the lower extremities, abdomen, and back (). Laboratory studies were significant for acute kidney injury (AKI) with a serum creatinine of 1.4 mg/dL, hematuria and proteinuria >1 g/day. His baseline creatinine was 1 mg/dL 3 months ago.
Nephrology was consulted, and a clinical diagnosis of IgAV was made based on his symptoms, palpable purpura, and renal failure. The patient was admitted and started on intravenous hydration and an nonsteroidal anti-inflammatory drug (NSAID) for pain. On hospital day 2, his creatinine sharply increased to 2.4 mg/dL. Urinalysis revealed active sediment with hematuria and proteinuria. Acute glomerulonephritis from IgAV was suspected. The NSAID was stopped and changed to acetaminophen-hydrocodone. Glucocorticoid therapy was started with pulse dose intravenous methylprednisolone daily for 3 days followed by oral prednisone. Kidney biopsy was performed. Light microscopy demonstrated diffuse proliferative changes with endocapillary hypercellularity, infiltration of polymorphonuclear neutrophils within capillary loops, and segmental fibrinoid necrosis (, ). There were no cellular crescents, interstitial inflammation, fibrosis, or tubular atrophy. On immunofluorescence, there was granular staining of the glomeruli with IgA, C3, and Lambda light chains consistent with diffuse proliferative and exudative glomerulonephritis with IgA dominant immune complex deposits ().
Treatment with high-dose prednisone was continued. His serum creatinine decreased to 1.3 mg/dL. However, the purpuric rash became more widespread involving his mouth and throat, and the lesions on his legs grew larger. He continued to complain of abdominal pain. On hospital day 8, 6 days after starting glucocorticoid therapy, the abdominal pain worsened and was even more intense on hospital day 9. A computed tomography (CT) scan of the abdomen was performed and showed extensive pneumatosis of the gut wall consistent with bowel ischemia ().
He underwent urgent surgery that night. On laparotomy, he was found to have a perforation in the duodenum along with ischemic necrosis of 6 feet of the jejunum and the entire ascending colon. The necrosed jejunum and ascending colon were resected and a vacuum-assisted closure of the wound was placed. After the surgery, the patient was critically ill in the intensive care unit with hypotension requiring high-dose vasopressors including vasopressin and norepinephrine. His urine output dropped significantly, creatinine increased to 4.5 mg/dL, and his serum potassium increased to 6.0 mg/dL. He was losing fluid from his abdominal wound. Continuous renal replacement therapy (CRRT) was started in the intensive care unit with a permcath. He underwent a repeat exploratory laparotomy that revealed contamination but no evidence of ischemia or leak. The colon looked viable. On hospital day 12, the patient had another exploratory laparotomy and a small bowel anastomosis with ileostomy. The surgical wound had delayed closure despite wound care and vacuum-assisted closure of the wound. The wound was large and widely open involving the entire thickness of the muscles of the anterior abdominal wall ().
His condition was further complicated by gastrointestinal bleeding requiring embolization of the bleeding vessel by interventional radiology. He developed bilateral deep vein thromboses and underwent placement of an inferior vena cava filter. He had a prolonged course on mechanical ventilation and was switched from CRRT to every other day hemodialysis. Over the next few weeks, his condition slowly improved and his urine output gradually increased.
He was extubated on hospital day 22 and was eventually discharged after a 6-week hospital stay complicated by multiple surgeries, infections, delayed wound healing, and cytopenia. During the admission, he received multiple units of blood products including 19 packed red blood cell transfusions, 2 platelet transfusions, 3 fresh frozen plasma transfusions, and 1 cryoprecipitate. His kidney function slowly improved, and he was taken off dialysis. On discharge, his serum creatinine was 1.42 mg/dL, and his blood urea nitrogen was 28 mg/dL. An appointment was made for him to follow-up with nephrology.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.42, 'mg/dL'], 'age': [44, 'years']}",62.4869,59.36255,65.61124,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 44 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.42 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.42/0.9)**-1.2 * 0.9938**44 * 1.0 = 62.4869.
Hence, the GFR value is 62.4869 ml/min/1.73 m²."
558,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5411553-3,Extracted,"A 51-year-old man was admitted to our hospital for renal biopsy. Proteinuria had been detected when the patient was approximately 30 years of age, and he had experienced tonsillitis several times. The patient had been diagnosed with PV with an abnormality of the JAK2 gene 3 years earlier. Renal biopsy was planned because his proteinuria had become more apparent over the past 2 years.
The patient’s height, weight, and blood pressure were 165 cm, 66 kg, and 120/73 mmHg, respectively. His consciousness level was alert, and he appeared healthy. No remarkable abnormalities were found in the heart, lungs, or abdomen, and pitting edema was not observed.
The laboratory data were as follows: hemoglobin, 15.3 g/dl; hematocrit, 48.1 %; platelets, 326,000/μl; white blood cells, 8,400/μl; C-reactive protein, <0.2 mg/dl; blood urea nitrogen, 22.2 mg/dl; serum creatinine, 1.4 mg/dl; total cholesterol, 194 mg/dl; total protein, 7.1 g/dl; albumin, 4.1 g/dl; globulin, 3.0 g/dl; lactate dehydrogenase, 169 IU/l; aspartate aminotransferase, 17 IU/l; alanine aminotransferase, 23 IU/l; total bilirubin, 0.5 mg/dl; γ-glutamyl transpeptidase, 21 IU/l; alkaline phosphatase, 276 IU/l; Na, 139 mmol/l; K, 4.7 mmol/l; and Cl, 106 mmol/l. Urinalysis showed 4+ proteinuria (1.2 g/day) and no evidence of hematuria.
Renal biopsy was performed (Fig. ) and 22 glomeruli could be evaluated, 5 of which showed global sclerosis. Histological findings included mesangial proliferative glomerulonephritis with crescents and focal segmental necrosis. Arteriosclerotic changes were also observed. Immunofluorescence staining was positive and revealed strong immunoreactivity for IgA and C3. Electron microscopy showed electron-dense deposits in the mesangium. He was diagnosed with IgA nephropathy. Tonsillectomy plus steroid pulse therapy and an angiotensin II receptor blocker were selected as treatments for the patient. His proteinuria and hematuria disappeared after 6 months.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.4, 'mg/dL'], 'age': [51, 'years']}",60.85193,57.80933,63.89453,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 51 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.4 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.4/0.9)**-1.2 * 0.9938**51 * 1.0 = 60.85193.
Hence, the GFR value is 60.85193 ml/min/1.73 m²."
559,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6454690-1,Extracted,"An 89-year-old Japanese woman was admitted to our hospital because of general fatigue, nausea, muscle weakness of the lower limbs, and ophthalmoplegia that had appeared 2 months earlier and gradually worsened. She noticed diplopia at 1 year before this hospitalization. None of her family members had a history of renal or autoimmune disease. There was no past history of allergic diseases such as bronchial asthma. The patient had never smoked. She had been diagnosed with hypertension and treated with an angiotensin-receptor antagonist (losartan, 50 mg daily).
The physical examination identified a slight fever, anemic conjunctiva, eyelid ptosis, and muscle weakness of the lower limbs; her blood pressure was 135/67 mmHg. The laboratory examination revealed elevated serum levels of creatinine (1.91 mg/dL, 170 μmol/L) and C-reactive protein (8.12 mg/dL). A hemogram showed anemia (hemoglobin concentration, 9.2 g/dL), but her white blood cell count was in the normal range (5400 /μL). On urinalysis, occult blood and protein and cellular (granular and red blood cell) casts were detected. Her urinary protein excretion was 2.13 g/g creatinine. The serological examination revealed an elevated level of serum IgG (3494 mg/dL), but serum complement levels were within normal limits: the serum C3 level was 95.1 mg/dL, the serum C4 level was 21.7 mg/dL, and the serum CH50 level was 44.7 U/mL. Positivity for MPO-ANCA (176 U/mL) and PR3-ANCA (125 U/mL) was observed, but rheumatoid factor, antinuclear antibody, anti-glomerular basement membrane antibody, cryoglobulin, and monoclonal immunoglobulin were not detected.
We also assayed for various types of ANCA in the patient’s serum. A sample was collected in a separator tube before the patient’s initial treatment and was separated at 1000 g for 15 min. The diluted serum sample was measured by an enzyme-linked immunosorbent assay (ELISA) using a Wieslab® ANCA panel kit (EuroDiagnostica, Malmo, Sweden), in duplicate. The ELISA plate was read on a microplate reader (Sunrise Remote®: Tecan Japan, Kanagawa, Japan) set at 405 nm wavelength. The patient showed positivity for azurocidin-ANCA (optical density [OD] ratio: 4.05, normal: < 3.0), but not bactericidal/permeability increasing protein (BPI)-ANCA (OD ratio: 1.61, normal: < 3.0), cathepsin G-ANCA (OD ratio: 1.20, normal: < 3.0), elastase-ANCA (OD ratio: 0.99, normal: < 3.0), lactoferrin-ANCA (OD ratio: 2.77, normal: < 3.0) or lysozyme-ANCA (OD ratio: 1.47, normal: < 3.0) [see Additional file ].
The patient’s symptoms and inflammatory findings did not improve with antibiotic treatment (ceftriaxone, 2 g daily for 6 days), and her serum creatinine level deteriorated to 2.42 mg/dL (Fig. ). On abdominal ultrasound examination, her kidney size was relative small (right, 78 mm × 40 mm; left, 87 mm × 46 mm). We diagnosed rapidly progressive glomerulonephritis.
Light microscopic findings of a renal biopsy sample showed cellular crescents in 50% of 14 obtained glomeruli, and a fibrocellular crescent was revealed in one of those glomeruli. Mononuclear inflammatory cell infiltration to the interstitium was widely observed. Vasculitis was not observed, but intimal thickening of the interlobular arterial walls was seen (Fig. ). On immunofluorescence findings, immunoglobulins and complement components were not detected. We therefore diagnosed microscopic polyangiitis with cellular-type renal involvement.
Chest X-rays showed a wide mediastinum, and chest computed tomography (CT) and magnetic resonance imaging (MRI) revealed a 40-mm-sized lobulated tumor in the anterior mediastinum (Fig. ). On additional serological examination, anti-acetylcholine-receptor antibody was present (0.9 nmol/L), but anti-muscle specific kinase (MuSK) antibody was not detected. We thus additionally diagnosed myasthenia gravis with thymoma.
After the renal biopsy, the patient was treated with 500 mg/day of methylprednisolone for three consecutive days, followed by 30 mg/day (0.8 mg/kg) of oral prednisolone. Rituximab 500 mg (375 mg/m2) was intravenously administered, but it was discontinued after only one administration because of an adverse effect (atrial fibrillation). Three months after the remission induction therapy, the patient’s MPO-ANCA was decreased to 25.3 U/mL, PR3-ANCA was decreased to 15.2 U/mL, and elevated serum IgG level was normalized to 1297 mg/dL. Her symptoms had improved; at 2 months after the initiation of treatment, anti-acetylcholine-receptor antibody became negative and the size of her thymoma had decreased to approx. 20 mm (Fig. ). However, hemodialysis was initiated at 1 month after this treatment because the patient’s renal function was deteriorated. Her renal function did not unfortunately recovered, and she was moved to another hospital 3 months after the therapy because she needed rehabilitation for her muscle weakness due to disuse syndrome.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [1.91, 'mg/dL'], 'age': [89, 'years']}",24.77176,23.53317,26.01035,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 89 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.91 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.91/0.7)**-1.2 * 0.9938**89 * 1.012 = 24.77176.
Hence, the GFR value is 24.77176 ml/min/1.73 m²."
560,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7826221-1,Extracted,"A 60-year-old female with history of hypertension, type 2 diabetes, and history of deep vein thrombosis on chronic anticoagulation with warfarin, who was transferred from outside hospital (OSH), was presented for evaluation of cholecystoduodenal fistula.
Her initial presentation includes a 2-day history of right upper quadrant abdominal pain associated with nausea, dark bilious emesis, and the absence of flatus/bowel movements in the last 24 hours. Abdominal/pelvic computed tomography (CT) with contrast from OSH revealed cholecystoenteric fistula from the fundus of the gallbladder to the 2nd portion of the duodenum with 3.5 cm gallstone within the duodenum, and with 2.5 cm gallstone within common bile duct (CBD) with extensive pneumobilia (). Initial labs on presentation were unremarkable (total bilirubin -0.6 mg/dL, WBC −10.7 × 103/μL and Creatinine -0.8 mg/dL) except elevated alkaline phosphatase -336 units/L and INR -6.8. Upon her arrival, she underwent magnetic resonance cholangiopancreatography with double Eovist contrast and delays (MRCP) to help further delineate biliary anatomy, which revealed similar findings from the CT with the change of duodenal stone migrating to proximal jejunum and a better visualization of the fistula ().
After appropriate resuscitation and gastric decompression, the patient underwent exploratory laparotomy, partial cholecystectomy, take-down of cholecystoenteric fistula, duodenal repair, jejunostomy with extraction of stone and primary closure, choledochotomy with common bile duct exploration and extraction of a large stone and closure using interrupted absorbable sutures, and intraoperative cholangiogram. Intraoperatively, the gallbladder was first opened, and an intraop cholangiogram was performed which delineated the CBD anatomy (). Next, we identified one of the impacting gallstones at the proximal jejunum just distal to the ligament of Treitz (). We performed enterotomy for stone extraction and closed the incision in the Heineke-Mikulicz fashion. Based on patient's presentation and risk factors, we decided to proceed with cholecystectomy and fistula take-down. A partial cholecystectomy was performed with anterior wall take-down due to severe inflammation and altered anatomy and concerns that otherwise will injure the CBD. When addressing the CBD impacting stone, we first attempted a transcystic approach to extract the stone but failed due to the size of the stone. Therefore, we performed a transverse choledochotomy, through which stone was extracted in pieces using the Randall stone forceps and was closed via interrupted absorbable sutures (). A decision was made to not perform external drainage of the CBD with a T-tube, because the duct was large to 2.5 cm in diameter, and there was good drainage on completion cholangiogram (). Lastly, fistula on the duodenum side was closed in 2 layers utilizing the Heineke-Mikulicz method (). A JP drain was placed in the gallbladder bed near the duodenal fistula site before closure.
Pathology report confirmed the stones from the proximal jejunum and the CBD are 3.8 x 3.6 x 2.9 cm and 2.5 x 2.2 x 2.0 cm, respectively. Tissue from duodenal fistula showed mucosal erosion and acute inflammation with fibrosis on pathology report.
During her postoperative course, CT A/P with oral contrast was obtained on postop day (POD) 3 which revealed no obvious leak. Based on the unremarkable CT scan and benign clinical picture, we decided to start her on a clear liquid diet on POD 5. Immediately following diet change, JP drain acutely changed its content from serosanguinous fluid to dark bilious fluid. We suspected a leak from duodenal repair due to the extremely high amylase level detected in drain fluid. Because the patient at the time was clinically stable, no signs of peritonitis and sepsis, a repeated CT A/P with oral contrast on POD6 showed no extravasation of contrast from the duodenum, for which we proceeded with conservative medical management. Octreotide was started and the patient was maintained on nothing per OS along with starting total parenteral nutrition. On day 9 a nasojejunal tube distal to the duodenal suture line was inserted via esophagogastroduodenoscopy (EGD), during which we further evaluated for duodenal leak using contrast injection. EGD revealed inflammation in the second portion of duodenal wall opposite the major papilla without a good visualization of perforation or leak. The patient was started on enteral feeding with no issues.
HIDA scan was also performed and did not reveal a biliary leak. With consistent low JP drain output and negative scans, she was given a clear liquid diet trial again on POD13, and she tolerated diet well. The patient was discharged on POD15, tolerating regular diet, and having minimal JP drain output. JP drain was pulled out during a follow-up visit.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [60, 'years'], 'creatinine': [0.8, 'mg/dL']}",84.29815,80.08324,88.51306,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 60 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.8 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.8/0.7)**-1.2 * 0.9938**60 * 1.012 = 84.29815.
Hence, the GFR value is 84.29815 ml/min/1.73 m²."
561,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4448518-1,Extracted,"A 103-year-old (body mass index [BMI]=27.2) African-American female from an assisted living home presented for left hip pinning of a femoral neck fracture following a fall from a wheelchair. Preoperative evaluation revealed an elderly women moaning in distress from severe excruciating left hip pain. After she was diagnosed with a left femoral neck fracture, she was scheduled for a hip pinning procedure under subarachnoid anesthesia. Past medical history was significant for hypertension, congestive heart failure, atrial fibrillation, osteoporosis, renal insufficiency, right lower extremity lymphedema with cellulitis, and peripheral vascular disease. She had a history of right tibial fracture and was taking furosemide, morphine, and enoxaparin. She had no history of known allergy.
Preoperative laboratory reports were significant for blood urea nitrogen (BUN) 35, creatinine (Cr) 1.75, hemoglobin (Hgb) 9.4, platelets 113, and international normalized ratio (INR) 1.1. Preoperative vital signs were blood pressure (BP) 120/70, heart rate (HR) 87. Blood gas analysis revealed a pH 7.39, CO240, PO285. In the operating room (OR) at 16:45, the patient was placed into the right lateral decubitus position. Approximately 500 ml of normal saline solution was given as preload prior to the spinal blockade. At 17:00 nasal cannula O2was administrerd, while maintaining good spontaneous ventilation and with 2 mg of midazolam injected intravenously. Following local skin infiltration, a 25G 5-inch Pencan brand spinal needle was used to access the subarachnoid space, with free flow of clear cerebrospinal fluid (CSF). Multiple attempts by an experienced, pain fellowship trained anesthesiologist were necessary to obtain CSF due to severe scoliosis and multiple bony osteophytes. Hyperbaric bupivacaine, 1.5 ml of 0.75% (11.25 mg), with 15 mcg of fentanyl was injected into the subarachnoidal space. Adequate analgesia was not reached for approximately 45 min, at which time she developed a dense sensory level of anesthesia to the T12 level. Once this level was obtained, the remainder of the procedure was uneventful. Postoperativly, the patient was comfortable, and she returned to full alert status after one and half hours. At the end of the surgery, she had BP 126/78, HR 91, RR 18, Temperature 37.0°C, SaO2100%. Laboratory results showed PT 10.8, INR 1.1, albumin 3.3, Na 138. She received 1.5 L of crystalloids and estimated blood loss was 100 ml, urine output 200 ml. She also received 1 unit of blood and 250 mL of red blood cells (RBC).","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [1.75, 'mg/dL'], 'age': [103, 'years']}",25.21953,23.95855,26.48051,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 103 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.75 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.75/0.7)**-1.2 * 0.9938**103 * 1.012 = 25.21953.
Hence, the GFR value is 25.21953 ml/min/1.73 m²."
562,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5715608-2,Extracted,"A 61-year-old woman diagnosed with kappa light-chain multiple myeloma in September 2009 was initially treated with lenalidomide, bortezomib, and dexamethasone. Upon disease progression in 2010, she received cyclophosphamide, bortezomib, and dexamethasone. In 2011, with worsening in her disease status, the patient underwent high-dose melphalan followed by autologous hematopoietic stem cell infusion. Post-transplant, the patient received radiotherapy with 20-Gy over 10 fractions to the lytic lesions in both hips and femur. She remained in remission until 2014, but with disease relapse, she was retreated with bortezomib and dexamethasone. Unfortunately, her disease status worsened, and she was initiated on newly approved carfilzomib and dexamethasone. She was able to attain a partial response. On day five, cycle nine of this treatment, the patient presented to the hospital with chest discomfort and shortness of air that was progressively worsening over 5 days. On presentation, she had elevated blood pressure, Cr of 5.45 mg/dL (from 1.45 mg/dL), Hb of 7.6 g/dL (from 10.3 g/dL), and Plt count of 37 × 109/L (from 174 × 109/L) along with LDH of 867 IU/L and haptoglobin of <10 mg/dL. PBS was consistent with increased schistocytes. She was emergently started on PLEX; however, her renal function continued to rapidly decline requiring hemodialysis (HD). The patient's underlying multiple myeloma disease status and laboratory work-up including free kappa light chain, serum-free lambda light chain, and kappa-to-lambda ratio remained unchanged. Upon receiving results of ADAMTS13 activity of 100%, the patient initiated eculizumab therapy. Within 2 weeks of initiating 900 mg IV (weekly) eculizumab, her labs normalized (Fig. ), and her clinical status significantly improved. She was weaned off HD around 6 weeks (Fig. ) in the outpatient setting. Patient was maintained on 1200 mg IV eculizumab every 2 weeks from 5th week after initial 900 mg IV every week dosing for 4 weeks in outpatient settings.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [5.45, 'mg/dL'], 'age': [61, 'years']}",8.37817,7.95926,8.79708,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 61 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 5.45 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (5.45/0.7)**-1.2 * 0.9938**61 * 1.012 = 8.37817.
Hence, the GFR value is 8.37817 ml/min/1.73 m²."
563,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6663283-1,Extracted,"A 59-year-old male with a past medical history of diabetes, hypertension, stroke, and congestive heart failure presented to the emergency department for epigastric pain, chest pain, and hyperglycemia. Initial vital signs were blood pressure 195/86, heart rate 104, respiratory rate 19, oxygen saturation 96% on room air, and temperature 37.1°C. Laboratory values were significant for acute kidney injury (AKI) with new elevated creatinine (2.2), troponin-T elevation (0.57), creatine kinase (CK) total (3,124), and CK-muscle/brain (CKMB; 11.1). The patient was promptly started on insulin for hyperglycemia. An electrocardiogram was performed, showing regular rhythm with Q waves and ST elevation in V1 and V2 (Figure ) without significant ST depressions, which was similar to an old electrocardiogram (Figure ). As noted earlier, the patient had elevated troponins so interventional cardiology was promptly consulted through our transfer center. The interventional cardiology team reviewed all the electrocardiograms, and recommendations included non-emergent catheterization, to repeat the electrocardiogram in two hours, and to administer aspirin, intravenous (IV) heparin, IV nitroglycerin, and pain control.
The patient was observed in the emergency department for serial exams. Subsequently, the noninterventional cardiologist was consulted and he agreed with interventional cardiology’s assessment and plan for the case. A repeat two-hour electrocardiogram was similar to the initial electrocardiogram (Figure ). During his course in the emergency department, the patient’s chest pain was resolving, but he started complaining of gradual onset abdominal and back pain that was refractory to all pain medications. He then started complaining of bilateral lower extremity paresis and anesthesia. On reevaluation, he had no palpable dorsalis pedis or posterior tibial pulse and no detectable pulse by Doppler or ultrasound. The compartments were soft and the distal extremities warm.
CT scans were performed, which showed a filling defect in the distal infrarenal aorta that was confirmed to be a distal infrarenal aortic saddle thrombus extending into the bilateral common iliac arteries (Figure ). Additionally, an intraventricular thrombus was identified that was thought to be the cause of the aortic thrombus (Figure ). Neurology was consulted at the time of intracardiac thrombus diagnosis and agreed to not give thrombolytics because the patient stated that he had a prior history of nonsurgical hemorrhagic cerebrovascular accident (CVA). However, they did agree with anticoagulation and to obtain an MRI/magnetic resonance angiography (MRA) brain/neck at admission to assess the showering of thrombi to the brain. The patient was transferred emergently to the operating room for vascular surgery to perform emergent thrombectomies and bilateral lower extremity four-compartment fasciotomies.
The patient had multiple tests during his hospital course, showing that the damage caused by the 1.7 cm cardiac intramural thrombus involvement had been diffuse. His MRI brain showed multiple subacute infarcts, indicating that the intramural cardiac thrombus had been present for weeks before he came to the emergency department. He also had right inferior pole renal infarcts that were age-indeterminate. On repeat testing, the size of the cardiac thrombus was shown to decrease after anticoagulation during hospital admission.
The patient’s hospital course included anticoagulation and hemodialysis due to rhabdomyolysis, causing acute tubular necrosis. He also had eventual stent placement during admission for subcritical CAD. The patient was in the intensive care unit for three weeks for frequent postoperative neurologic checks, respiratory support, and dialysis support; he was then discharged to inpatient rehabilitation six weeks after that. He now requires a wheelchair for mobility due to paraplegia and a urinary catheter for incontinence but does not require dialysis.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [2.2, 'mg/dL'], 'age': [59, 'years']}",33.65989,31.9769,35.34288,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 59 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.2 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.2/0.9)**-1.2 * 0.9938**59 * 1.0 = 33.65989.
Hence, the GFR value is 33.65989 ml/min/1.73 m²."
564,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6006632-1,Extracted,"The patient is currently a 93-year-old female who was first referred to us at age 64 because of edema involving both legs to the thighs and above, and 12 g of proteinuria in 24 h. Her renal function was within normal limits. The creatinine clearance was 80 mL/min, her BUN was 14 mg/dL, and her serum creatinine was 0.9 mg/dL. Her serum albumin was 1.1 mg/dL. Her total serum cholesterol was greater than 300 mg/dL. Repeat 24-h proteinuria was 13 g. A renal biopsy was classic for membranous nephropathy by light, immuno-, and electron microscopy criteria. No malignancies were discovered, and tests for systemic lupus and other collagen diseases were negative. She was seronegative for human immunodeficiency virus and hepatitis B and C. She had never received gold salts, nor did she take nonsteroidal anti-inflammatory drugs. Thus, she had idiopathic membranous nephropathy by clinical criteria.
A conservative trial of furosemide and an angiotensin enzyme inhibitor was attempted with no reduction in her proteinuria. She became orthostatic when the dose of furosemide was increased in an attempt to relieve her symptoms of leg stiffness and difficulty with ambulation. She remained weak and relatively immobilized.
After 4 months of the above treatment, she was treated with the steroid and chlorambucil protocol described by Ponticelli et al. [, ]. There was no response for 2 months, but her serum albumin began to rise to 2 mg/dL by month 3. Her 24-h albumin excretion continued to be 10 mg/24 h. By month 4, her albuminuria was no longer present. Her 24-h protein excretion had fallen to less than 100 mg. She completed the full 6-month course and remained in complete remission for 5 years. There was no proteinuria, and all blood chemistries remained within normal limits.
Five years after her complete remission, the nephrotic syndrome recurred with edema, proteinuria, hyperlipidemia, etc. The therapy was repeated for the 6-month course of alternating prednisone and chlorambucil exactly as administered previously, but there was no response. Two months later, a course of intravenous immunoglobulin [] was attempted with a 2-month induction period and 4 months of infusions every 3 weeks with no effect on her proteinuria. This protocol was terminated at the patient's request because she had lost patience.
She was then treated with 20 mg of prednisone on alternate days plus cyclosporine 4 mg/kg daily []. Within 3 months, she was in complete remission. Her dose of prednisone was tapered to 0 by 6 months, and her dose of cyclosporine was reduced to 25 mg daily.
She remained in remission for another 7 years, but her nephrotic syndrome again recurred. The prednisone/cyclosporine regimen was repeated for 6 months with no response. She was then treated with alternate-day prednisone as before plus mycophenolate 500 mg twice daily []. Once again, she had a complete remission after 3 months.
The steroids were tapered to 0 after 6 months, and the mycophenolate was continued at 125 mg twice daily. She remained in complete remission until 7 years later when she developed cytomegalovirus colitis that remitted upon discontinuation of the mycophenolate and treatment with ganciclovir. She remains in complete remission 10 years later on no treatment.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [0.9, 'mg/dL'], 'age': [93, 'years']}",59.60762,56.62724,62.588,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 93 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.9 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.9/0.7)**-1.2 * 0.9938**93 * 1.012 = 59.60762.
Hence, the GFR value is 59.60762 ml/min/1.73 m²."
565,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6701889-1,Extracted,"The patient was a 79-year-old female who presented to the emergency department with an eight-hour history of abdominal pain associated with nausea and vomiting. She also complained of obstipation for the past day as well as right hip pain. Her past medical and surgical history includes right upper lobectomy for adenocarcinoma of the lung in 2008, left nephrectomy for renal cell carcinoma, prior pulmonary embolism, hypertrophic cardiomyopathy and Stage IV chronic kidney disease. Her vital signs on admission showed tachycardia and hypotension. On examination, decreased bowel sounds and mild distended was observed. A computer tomography (CT) scan of the abdomen and pelvis was performed and showed small bowel obstruction with air-fluid levels as well as a right-sided obturator hernia with a loop of small bowel which appeared incarcerated inside (Figures , ). Initial laboratory studies showed mild leukocytosis with a WBC of 10.7, hemoglobin of 15 and hematocrit of 44.3. Creatinine was at a baseline level of 1.8. The patient had a nasogastric (NG) tube placed in the ER with an output of 500 cc of bilious output and was resuscitated with crystalloid and brought to the operating room.
The patient was deemed unstable to undergo a laparoscopic approach and she underwent an infraumbilical midline laparotomy through which the right-sided obturator hernia was gently reduced. The bowel was inspected and was deemed to be healthy and viable. The obturator hernia was then repaired using a polypropylene mesh plug. She had an uneventful recovery. The nasogastric tube was removed on POD 2 and the patient was started on clear liquids diet. She regained full bowel function on post-operative day 3. The patient subsequently had her diet advanced to a regular diet which she tolerated until discharge.
The patient returned to the emergency room six months later with the sudden onset of left hip pain associated with lower abdominal pain while walking. Soon thereafter, the patient began belching but did not develop nausea or vomiting. She underwent a CT scan of the abdomen and pelvis in the ED that demonstrated a left-sided obturator hernia as well as small bowel obstruction (Figures , ). The patient was otherwise hemodynamically stable, and her laboratory studies were within normal limits. The patient was taken for an urgent midline laparotomy through her prior incision and the left obturator hernia was reduced. Intraoperatively, the bowel appeared viable and did not require any resection. The obturator hernia was repaired in a similar manner as the initial surgery with a polypropylene mesh plug. She was extubated the morning after her surgery. Recovery proceeded in a timely fashion as in her previous hospitalization. Her NG tube was removed on post-operative day 2 and she was started on a clear liquid diet. Her diet was advanced, and she remained asymptomatic until discharge.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [1.8, 'mg/dL'], 'age': [79, 'years']}",28.30609,26.89079,29.72139,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 79 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.8 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.8/0.7)**-1.2 * 0.9938**79 * 1.012 = 28.30609.
Hence, the GFR value is 28.30609 ml/min/1.73 m²."
566,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-8397,Extracted,"After hospitalization for urgent chemotherapy to treat Burkitt’s lymphoma, a 7-year-old boy develops paresthesias of the fingers, toes, and face. Blood pressure is 100/65 mm Hg, respirations are 28/min, pulse is 100/min, and temperature is 36.2°C (97.2°F). Inflating a blood pressure cuff on the boy’s arm produces carpal spasm. He has excreted 20 mL urine in the past 6 hours. Laboratory studies show the following:
Hemoglobin 15 g/dL
Leukocyte count 6,000/mm3 with a normal differential serum
K+ 6.5 mEq/L
Ca+ 6.6 mg/dL
Phosphorus 5.4 mg/dL
HCO3− 15 mEq/L
Uric acid 12 mg/dL
Urea nitrogen 54 mg/dL
Creatinine 3.4 mg/dL
Arterial blood gas analysis on room air:
pH 7.30
PCO2 30 mm Hg
O2 saturation 95%
Febuxostat is initiated.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [7, 'years'], 'creatinine': [3.4, 'mg/dL']}",27.58656,26.20723,28.96589,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 7 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.4 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.4/0.9)**-1.2 * 0.9938**7 * 1.0 = 27.58656.
Hence, the GFR value is 27.58656 ml/min/1.73 m²."
567,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-657,Extracted,"A 56-year-old man comes to the physician for a follow-up examination. Two weeks ago, he was treated for an acute gout attack of the metatarsophalangeal joints of his right big toe. His symptoms improved with naproxen. He has had three other similar episodes of joint pain in his toes and ankles during the last year that improved with over-the-counter analgesics. He does not currently take any medications. He used to drink 3–5 beers daily but has recently cut down. He is a chef at a steakhouse. His temperature is 37.0°C (98.6°F), pulse is 76/min, and blood pressure is 147/83 mm Hg. Examination of his right big toe shows minimal tenderness; there is no warmth or apparent deformity. The remainder of the examination shows no abnormalities. His serum creatinine concentration is 0.9 mg/dL.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [0.9, 'mg/dL'], 'age': [56, 'years']}",92.91167,88.26609,97.55725,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 56 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 0.9 mg/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.9/0.7)**-0.302 * 0.9938**56 * 1.0 = 92.91167.
Hence, the GFR value is 92.91167 ml/min/1.73 m²."
568,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-3504,Extracted,"A 69-year-old white man comes to the physician because of a 15-day history of fatigue and lower leg swelling. Over the past 8 months, he has had a 3.8-kg (8.3-lb) weight loss. He has smoked one pack of cigarettes daily for 48 years. Vital signs are within normal limits. He appears thin. Examination shows 2+ pretibial edema bilaterally. An x-ray of the chest shows a right upper lobe density. Laboratory studies show:
Hemoglobin 11.3 g/dL
Leukocyte count 8600/mm3
Platelet count 140,000/mm3
Serum
Urea nitrogen 25 mg/dL
Glucose 79 mg/dL
Creatinine 1.7 mg/dL
Albumin 1.6 mg/dL
Total cholesterol 479 mg/dL
Urine
Blood negative
Glucose negative
Protein 4+
WBC 0–1/hpf
Fatty casts numerous
Light microscopic examination of a kidney biopsy reveals thickening of glomerular capillary loops and the basal membrane.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.7, 'mg/dL'], 'age': [69, 'years']}",43.09939,40.94442,45.25436,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 69 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.9)**-1.2 * 0.9938**69 * 1.0 = 43.09939.
Hence, the GFR value is 43.09939 ml/min/1.73 m²."
569,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7789149-2,Extracted,"A 58-year-old Chinese man presented with a one-and-a-half-year history of proteinuria. His initial SCr was normal and was treated with tacrolimus and glucocorticoid. However, the patient experienced acute kidney injury with SCr increasing to 1.98 mg/dl afterwards and Tacrolimus was suspended. Then, he switched to oral cyclophosphamide (total 8 g), but reached no remission of proteinuria. To further evaluate the cause of proteinuria, he was admitted to our division in August 2017.
His past medical history and family history was of no significance. On admission, the physical examination revealed a blood pressure of 120/70 mmHg, temperature of 36.5 °C, heart rate of 70/min, and respiratory rate of 18/min. No organomegaly was noticed. Other signs were normal.
After admission, his urinalysis revealed proteinuria 2+ without hematuria. Urine protein excretion was 4.67 ~ 11.117 g/d. His serum albumin 46.9 g/L, SCr level was 1.67 mg/dl, calcium 2.48 mmol/L, uric acid was 510 μmol/L (90–360 μmol/L), serum lactate dehydrogenase level 145 IU/L and cTnI 0.001 ng/ml. Complete blood count showed WBC 4.1 × 109/L, hemoglobin 133 g/L and platelet count 136 × 109/L. Liver enzymes were normal. His serum IgG was 4.33 g/L, IgA was 0.19 g/L, and IgM was 0.13 g/L. Plasma C3 level was 0.873 g/L, and C4 level was 0.411 g/L. Monoclonal IgDλ spike was identified in the serum and urine by immunofixation electrophoresis. Free κ light chain was 8.95 (3.30–19.40) mg/L and free λ light chain was 3775 (5.71–26.30) mg/L. Ultrasonic examination showed enlarged kidneys with increased echogenicity. Electrocardiogram was normal. Echocardiography showed left ventricular ejection fraction was 81.9% and there was mild mitral valve regurgitation and aortic valve regurgitation. Bone marrow aspiration smear revealed 20% of plasma cells. CD38 and CD138 positive cells accounted for 16.6% of bone marrow cells with λ light chain restricted expression as determined by bone marrow flow cytometry. HBsAg, anti-HCV, anti-HIV, TP-Ab, anti-nuclear antibodies, anti-neutrophil cytoplasmic antibodies, anti-glomerular basement membrane antibody and PLA2R antibodies were all negative.
To further identify the kidney pathological type, the patient underwent renal biopsy on August 3rd, 2017. Immunofluorescence staining on frozen tissue revealed λ++ linear depositing along the glomerular capillary wall and tubular basement membrane, and κ was negative (Fig. a). There are also some intratubular casts showing strong staining for λ++. No significant deposits for IgG, IgA, IgM, C3 and C1q in the glomeruli. Light microscopic examination showed 37 glomeruli and one was globally sclerosed. The glomeruli revealed mild segmental mesangial proliferation (Fig. b) and some glomeruli showed ischemic change. Tubular epithelial cells exhibited granular degeneration and focal tubular atrophy. Periodic acid-Schiff (PAS) pale protein casts were noticed in the tubular lumens with fibrillary changes (Fig. c), and the protein casts were Congo-red positive (Fig. d) showing apple-green birefringence with polarized microscopy. On electron microscopy, the glomeruli basement membrane showed ischemic change without any deposits (Fig. e). But there were fine granular deposits along the tubular basement membrane (Fig. f).
The final diagnosis of this patient was multiple myeloma (IgDλ) with light chain deposition disease along the tubular basement membrane and MCN with diffuse amyloid casts. The patient was treated with 6 cycles of bortezomib and dexamethasone followed by 3 cycles of lenalidomide, dexamethasone and bortezomib therapy. He achieved very good partial remission (VGPR). Fifteen months after the renal biopsy, his bone marrow plasma cells decreased to 4%. He was on maintaining therapy with IRD (ixazomib, lenalidomide, and dexamethasone) until now. Twenty-seven months after renal biopsy, his SCr was 1.5 mg/dl, and there was no sign of systemic amyloidosis.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.5, 'mg/dL'], 'age': [58, 'years']}",53.63045,50.94893,56.31197,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 58 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.5 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.5/0.9)**-1.2 * 0.9938**58 * 1.0 = 53.63045.
Hence, the GFR value is 53.63045 ml/min/1.73 m²."
570,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,trec-ct-2021-38,Extracted,"The patient is a 35-year-old woman with myasthenia gravis, class IIa. She complains of diplopia and fatigue and weakness that affects mainly her upper limbs. She had a positive anti-AChR antibody test, and her single fiber electromyography (SFEMG) was positive. She takes pyridostigmine 60 mg three times a day. But she still has some symptoms that interfere with her job. She is a research coordinator and has 3 children. Her 70-year-old father has hypertension.  She does not smoke or use illicit drugs. She drinks alcohol occasionally at social events. Her physical exam and lab studies were not remarkable for any other abnormalities.
BP: 110/75
Hgb: 11 g/dl
WBC: 8000 /mm3
Plt: 300000 /ml
Creatinine: 0.5 mg/dl
BUN: 10 mg/dl
Beta hcg: negative for pregnancy","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [0.5, 'mg/dL'], 'age': [35, 'years']}",125.35754,119.08966,131.62542,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 35 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.5 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.5/0.7)**-0.241 * 0.9938**35 * 1.012 = 125.35754.
Hence, the GFR value is 125.35754 ml/min/1.73 m²."
571,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8182221-1,Extracted,"A 58-year-old male with a past medical history of prostate cancer presented to our facility
with worsening confusion, weakness, and oliguria. Prostate biopsy 5 months prior to
admission showed Gleason 4+3 T2aN0M0 prostate adenocarcinoma, for which he was treated with
combined brachytherapy and external beam radiation. He developed left lower extremity and
weakness after treatment. MRI of lumbar spine showed degenerative changes but no
attributable etiology for his weakness was evident. Around the same time, he also started
developing short-term memory loss.
On presentation to our facility, complete blood count was unremarkable, and creatinine was
5.97 mg/dL. Baseline creatinine was 0.85 mg/dL 6 months prior to admission. Urinalysis
revealed specific gravity 1.017, large occult blood, white blood cells (WBC) 15 to 25 cells,
trace ketones, and no evidence of infection. Due to oliguric acute kidney injury with
altered mental status suggestive of uremia, dialysis was initiated. Workup for the confusion
including noncontrast MRI brain showed extensive white matter changes. Cerebrospinal fluid
(CSF) analysis showed glucose 29 mg/dL, protein 120 mg/dL, WBC 68 cells/mm3 with
77% lymphocytes, and red blood cells 119 cells/mm3. Computed tomography (CT) scan
of chest, abdomen, and pelvis showed pleural effusion and mildly enlarged subcarinal lymph
node. Infectious workup was also negative. Urine microalbumin to creatinine ratio was 851
(0-28) and urine protein to creatinine ratio was 1.81 (normal less than 0.20). Serum protein
electrophoresis (SPEP) was positive for M spike. Immunofixation electrophoresis showed IgM
kappa monoclonal protein and second IgM monoclonal protein with probable kappa light chain.
IgM kappa monoclonal protein #1 concentration was 0.2 g/dL and IgM monoclonal protein #2
concentration was less than 0.1 g/dL. Urine protein electrophoresis showed M spike and urine
immunofixation electrophoresis showed Bence Jones protein, kappa type. Free kappa light
chain was 924 mg/dL (3.3-19.4 mg/dL), free lambda light chain was 24 mg/dL (5.7-26.3 mg/dL),
with a kappa/lambda ratio of 38.2 (0.26-1.65). A kidney biopsy was ultimately performed,
which showed extensive glomerular and arteriolar IgM kappa hyaline thrombi and glomerular
features of thrombotic microangiopathy. A few kappa light chain restricted casts were seen
suspicious for light chain nephropathy. Findings were deemed secondary to IgM kappa
monoclonal protein. A subsequent bone marrow biopsy was consistent with lymphoplasmacytic
lymphoma. Lymphoid aggregates were composed of CD20 positive B cells with admixed CD138
positive plasma cells with kappa predominance (-). Karyotype showed normal cytogenetics and molecular studies detected a MYD88
L265P mutation. CXCR4 mutation was not detected. HIV and hepatitis B tests were negative. He
was treated with methylprednisolone 500 mg for 3 days followed by a prednisone taper. He
also underwent 2 sessions of plasmapheresis as viscosity was not available at that time and
patients had concerning symptoms of hyperviscosity. Later on, his serum viscosity turned out
to be normal (1.5 centipoises). Dialysis was discontinued prior to discharge from hospital
as his kidney function recovered with good urine output (creatinine 2.81 mg/dL).
Subsequently, a month later, his creatinine in the follow-up hematology clinic visit was
1.35 mg/dL. He had a follow-up with nephrology and no more dialysis was needed. He was then
initiated on treatment with rituximab, cyclophosphamide, and dexamethasone (RCD). IgM level
at the time of treatment initiation was 1402 mg/dL. It increased to 1650 mg/dL after 1 month
and 1877 mg/dL after 2 months. He was readmitted 3 months after initiation of chemotherapy
with a 30-minute episode of right-sided facial weakness, slurred speech, and right upper
extremity weakness. CT head showed severe white matter changes with scattered areas of
enhancement with surrounding vasogenic edema. CT angiography was unremarkable. CSF studies
showed opening pressure of 17, glucose 70 mg/dL, protein 72 mg/dL, WBC 4
cells/mm3, and red blood cells 4 cells/mm3. No definitive etiology
was again attributable to these findings. A month later, he was readmitted with seizures.
His hospital course was complicated by atrial fibrillation with rapid ventricular rate and
aspiration pneumonia. He was started on eliquis. MRI brain showed persistent extensive
periventricular leukomalacia. He was placed on dexamethasone. He continued to have issues
with memory loss and weakness. He benefited with RCD treatment with continued stabilization
of his renal function but his M protein was overall unchanged. After 5 cycles of RCD, his
IgM was 1108 mg/dL. His SPEP showed an IgM monoclonal spike of 0.8 with kappa light chain
specificity. Another lumbar puncture was pursued after holding his steroids for 2 weeks and
the CSF analysis indicated elevated protein, decreased glucose, and elevated WBC with
lymphocytic predominance. His lumbar puncture was abnormal but not definitive for diagnosis
of CNS involvement by lymphoma. Brain biopsy was discussed but patient deferred the
procedure. A repeat MRI was done that showed progression of white matter enhancement (). Due to the persistent
imaging findings, suspicion of CNS involvement by lymphoma was high. As he had been treated
with multiple courses of steroids, the diagnostic yield of CSF for definitive diagnosis was
likely low. He was started on ibrutinib 420 mg daily. Eliquis was held in consultation with
cardiology. After initiation of therapy, the patient noted dramatic improvement in memory
and weakness. Repeat MRI brain after 2 months of ibrutinib showed complete resolution of
intracranial enhancement (). His IgM protein as well as his M spike have largely remained stable since. The
patient is currently tolerating ibrutinib well with no complications.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [5.97, 'mg/dL'], 'age': [58, 'years']}",10.22237,9.71125,10.73349,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 58 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 5.97 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (5.97/0.9)**-1.2 * 0.9938**58 * 1.0 = 10.22237.
Hence, the GFR value is 10.22237 ml/min/1.73 m²."
572,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5439064-1,Extracted,"Our patient was a 40-year-old African American male with a past medical history of diabetes mellitus, hypertension, and hyperlipidemia who was in his normal state of health prior to hospital admission. According to the patient's family, he recently traveled from Las Vegas and upon returning abruptly developed fevers, chills, and worsening dyspnea two days prior to presentation. Per history, he had no prior cardiac or pulmonary disorders. He had excellent performance status including vigorous daily physical activity prior to his hospitalization and was compliant with his oral medications. Family denied any recent sick contacts or prior hospitalizations. The patient smoked for 20 years with cessation 6 months prior to presentation. He drank alcohol socially and did not use illicit drugs. Initial vital signs revealed a temperature of 39.5° Celsius, heart rate of 130 beats per minute, blood pressure of 156/101 millimeters of mercury (mmHg), respiratory rate of 30 breaths per minute, and oxygen saturation 92% on room air. On physical exam, the patient had evidence of accessory muscle use with crackles at the lung bases bilaterally. He was tachycardic but no murmur or gallop was noted. His extremities were cool to touch without edema bilaterally.
His labs were remarkable for an elevated lactic acid 3.4 millimoles/liter, elevated troponin 1.01 nanograms/milliliter, creatinine 1.84 milligrams/deciliter, a white blood cell count of 16.2 k/microliter, and a beta-natriuretic peptide level of 443 picograms/milliliter. Cardiac troponins and beta-natriuretic peptide remained persistently elevated on repeat lab work. Other nonspecific markers of inflammation were elevated including erythrocyte sedimentation rate 90 millimeters/hour, C-reactive protein 2.2 milligrams/deciliter, and ferritin 931 nanograms/deciliter. Electrocardiogram demonstrated tachycardia and T-wave inversions in leads V4, V5, and V6. Chest X-ray showed bilateral interstitial infiltrates which prompted initiation of broad-spectrum antibiotics. Noninvasive positive pressure ventilation was initially attempted without success. The patient subsequently required mechanical ventilation secondary to worsening hypoxemic respiratory failure as evidenced by a low partial pressure of oxygen on arterial blood gas monitoring (). Ventilator mechanics yielded a plateau pressure of 27 mmHg with an applied positive end-expiratory pressure of 15 centimeters of water. Bronchoalveolar lavage (BAL) was positive for respiratory syncytial virus, subtype A.
Given his progressive hypotension and impending cardiogenic shock, the patient underwent emergent cardiac catheterization yielding nonobstructive coronary disease. A pulmonary artery catheter was placed with a mean pulmonary artery pressure of 38 mm/Hg and wedge pressure documented at 28 mm/Hg. The patient's pulmonary hypertension was thought to be secondary to elevated left heart pressures given the elevated wedge pressure. He required maximum vasopressor support with norepinephrine, vasopressin, dopamine, and milrinone. An intra-aortic balloon pump was inserted for refractory shock. Viral myocarditis was considered the leading diagnosis at this point given his clinical presentation and worsening cardiopulmonary status.
Due to his progressive cardiopulmonary failure, the patient required venoarterial extracorporeal membrane oxygenation (VA-ECMO). An intraoperative transesophageal echocardiogram was performed which showed normal size and function of the right ventricle and severely depressed left ventricular systolic function. These findings were consistent with a transthoracic echocardiogram, which showed an estimated ejection fraction of 10–15% (). Given his instability, the patient underwent central cannulation for VA-ECMO with left ventricular vent for left heart decompression.
On postoperative day one, the patient showed marked improvement in his hemodynamics with minimal vasopressor support needed. The intra-aortic balloon pump was removed and the patient was liberated from mechanical ventilation on postoperative day two. Follow-up chest X-ray showed improvement in the interstitial edema pattern previously noted on prior imaging (). Given his excellent lung compliance and rapid resolution of pulmonary pathology, cardiogenic pulmonary edema from decompensated left sided heart failure was favored over acute respiratory distress syndrome.
Transthoracic echocardiogram performed seven days after admission demonstrated continued reduction in systolic function with an ejection fraction of 20–25% (). As the patient improved clinically, explantation from ECMO occurred 20 days postoperatively. Follow-up echocardiogram showed improvement in his ejection fraction to 35–40% (). Repeat cardiac biomarkers trended downward and were within normal limits at this time indicating myocardial recovery. The patient was subsequently discharged and was doing well on outpatient follow-up and was compliant with his heart failure medication regimen. Due to the rapid resolution of his pulmonary pathology, it was believed that the duration of VA-ECMO served as a bridge to recovery from cytokine-induced myocardial inflammation secondary to RSV as exemplified by serial imaging.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.84, 'mg/dL'], 'age': [40, 'years']}",46.94158,44.5945,49.28866,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 40 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.84 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.84/0.9)**-1.2 * 0.9938**40 * 1.0 = 46.94158.
Hence, the GFR value is 46.94158 ml/min/1.73 m²."
573,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5297489-1,Extracted,"A 56-year-old man had received a living related kidney transplant for an end stage renal disease of unknown etiology in 1997. The patient was on triple immunosuppression with steroids, azathioprine, and cyclosporine and had stable graft function. He was followed-up regularly in the renal transplant clinic and the immediate post-transplant period was uneventful. In 2001, the serum creatinine was gradually increased to 3 mg/dl. He underwent an allograft biopsy, which revealed an interstitial nephritis/tubular atrophy grade II. The cyclosporine dosage was reduced (150 mg/day given twice daily) to minimize the chronic nephrotoxicity and MMF (2 g/day in two divided doses) was substituted for azathioprine to control chronic allograft nephropathy. At that time, the patient was afebrile and had a normal physical examination. After conversion, serum creatinine level fell to 2.5 mg/dl. However, he presented with complaints of severe abdominal pain, vomiting, loss of appetite and fever requiring hospital admission twelve days later. MMF was withdrawn but cyclosporine and prednisolone were continued.
On admission, physical examination revealed a moderately dehydrated patient with temperature of 37.8°C, blood pressure of 105/55 mm Hg, heart rate of 110 beats/min, and respiratory rate of 22 breaths/min. Abdominal examination showed a moderately distended abdomen with epigastric tenderness, but no mass or rigidity. Laboratory tests demonstrated a serum amylase level of 1550 U/L (normal range, 30 U/L to 110 U/L), and a serum lipase concentration of 364 U/L (normal range, 5.6 U/L to 51.3 U/L). There was a mild rise in serum creatinine value (2.8 mg/dl). A complete blood count showed a white blood cell count of 11.4×109/L with 65% neutrophils, a hematocrit level of 32.6%. Liver transaminases, total bilirubin, alkaline phosphatase, glucose, lipid profile and electrolytes tests were within the normal ranges. Evaluation for infectious etiology revealed a negative work-up for cytomegalovirus (CMV) antigen. Blood testing for CMV and Epstein–Barr virus (EBV), by PCR was also negative. The electrocardiogram showed normal QRS complexes. Computed tomography of the abdomen demonstrated an enlarged and heterogeneous of his pancreas with poorly delineated borders, consistent with acute pancreatitis. His gallbladder, biliary duct system and spleen were normal. Acute pancreatitis was diagnosed on the basis of laboratory data and imaging findings during hospital admission. He had no history of pancreatitis or other its risk factors. The patient was resuscitated with intravenous fluid and cyclosporine was withdrawn. However, he developed hypotension and respiratory failure requiring transfer to the intensive care unit for ventilatory and inotropic support. Unfortunately, his symptoms worsened, and despite an intensive care, his clinical state deteriorated and he died one week later and autopsy findings demonstrated acute necrotizing pancreatitis. There were no evidence of gallstones or cancer.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [2.8, 'mg/dL'], 'age': [56, 'years']}",25.67635,24.39253,26.96017,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 56 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.8 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.8/0.9)**-1.2 * 0.9938**56 * 1.0 = 25.67635.
Hence, the GFR value is 25.67635 ml/min/1.73 m²."
574,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6691829-1,Extracted,"A 70-year-old man was admitted to the hospital because he had been suffering from edema of the lower extremities for 1 month. He had a 5-year history of renal dysfunction, bile duct stenosis, and an inflammatory pancreatic mass. Additionally, 5 years prior to the presentation, he had a baseline serum creatinine level of 200 μmol/L. At that time, the patient had undergone choledochal stent implantation. Three years ago, the stent had been removed, and he had begun to take oral prednisone 30 mg/day. The bile duct stenosis and pancreatic mass had been successfully eliminated, so the prednisone treatment had been discontinued 3 months prior to presentation. In the past month, he had experienced rapid progression of renal function. His medical history also included hypertension and diabetes. With the exception of bilateral lower limb edema, the findings from the physical examination conducted at the time of presentation were unremarkable.
Laboratory tests showed that his white blood cell count was 5.06 × 109/L; hemoglobin, 87 g/L; platelet count, 126 × 109/L; CRP, 30.23 mg/L; erythrocyte sedimentation rate, 80 mm/H; serum nitrogen, 32.79 mmol/L; serum creatinine, 555.8 μmol/L; and serum albumin, 32.7 g/L. He had normal liver function with normal amylase and lipase levels. Urine analysis showed that the protein level was 2+; red blood cell count, 80/μL; urine gravity, 1.010; urinary albumin/creatinine ratio, 330; 24-h urine protein, 0.98–1.22 g; and urine neutrophil gelatinase-associated lipocalin (NGAL), 236 ng/mL.
Immunological tests showed that the concentrations of serum C3 (complement 3) and serum C4 (complement 4) were lower than normal at 0.355 and <0.066 g/L respectively. Further, the patient had polyclonal hypergammaglobulinemia, as the total serum immunoglobulin G (IgG) level had increased to 31.7 g/L. However, the serum IgA and IgM concentrations were normal. The patient was negative for anti-self-antibodies, including antinuclear antibody, anti-double-stranded antibody, anti-Sjogren’s syndrome A antibody, anti-Sjogren’s syndrome B antibody, anti-proteinase 3, and anti-myeloperoxidase anti-neutrophil cytoplasmic antibody. Analysis of the IgG subtypes showed that the serum IgG1 level and the serum IgG4 level were obviously elevated at 23.7 g/L (4.90–11.40) and 10.90 g/L (0.08–1.40), respectively. The mCRP autoantibodies level was also elevated at 64.25%.
Kidney ultrasound examination showed that both kidneys were of normal size (10.6 × 5.2 cm and 10.6 × 5.6 cm), with uniform echo frequency and clear corticomedullary boundaries; moreover, there were no mass lesions. Chest computed tomography showed that there were multiple nodules in the both lungs. The abdominal radiography findings were unremarkable.
The renal biopsy specimen exhibited severe tubulointerstitial changes, but the glomerulus shows no specific finding (). In particular, storiform fibrosis () and inflammatory cells infiltration including plasma cells () were marked in the interstitium. Immunofluorescence staining revealed that IgM, IgA, and C3 were present at low levels in the granular mesangial area. Electron microscopy demonstrated that there were no electron-dense deposits in the glomeruli. Immunohistochemical staining showed that most plasma cells in the interstitium were positive for CD138, and there were seven IgG4-positive plasma cells and thirteen IgG-positive plasma cells in the same area of serial sections). So, the percentage of IgG4-positive plasma cells among the total IgG-positive plasma cells was 53%.
We prescribed 25 mg/day oral prednisone and 0.6 g of cyclophosphamide (CTX) every month by intravenous infusion. The patient had been followed up for 6 months at the time of writing this paper. In the most recent follow-up examination, the serum creatinine level had decreased to 194 μmol/L, the serum C3 and serum C4 levels had increased to 0.668 and 0.209 g/L, respectively, and were close to normal, the serum IgG1 level was normal at 10.2 g/L, and the IgG4 level had considerably decreased to 3.72 g/L. Therefore, the dose of prednisone was decreased to 12.5 mg/day, and the cumulative dose of CTX was 3.6 g until to the time of writing this paper. Changes in renal function, as indicated by the serum creatinine level, during the follow-up are depicted in .","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [555.8, 'µmol/L'], 'age': [70, 'years']}",8.83513,8.39337,9.27689,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 70 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 555.8 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 555.8 µmol. To convert 555.8 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 555.8 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00056 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00056 mol Serum Creatinine * 113.12 g/mol = 0.06335 g Serum Creatinine. To convert 0.06335 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.06335 g Serum Creatinine * 1000.0 mg/g = 63.35 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 63.35 mg Serum Creatinine/10.0 dL = 6.335 mg Serum Creatinine/dL. The concentration value of 555.8 µmol Serum Creatinine/L converts to 6.335 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (6.335/0.9)**-1.2 * 0.9938**70 * 1.0 = 8.83513.
Hence, the GFR value is 8.83513 ml/min/1.73 m²."
575,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4522993-1,Extracted,"This is a 35-year-old man with a history of ESRD who was receiving conventional hemodialysis for the last 5 years. He was submitted to chest radiography as part of routine annual cardiac screening. As associated comorbidity he had hypertension which has been treated with atenolol, atensin and amlodipine. His blood pressure was within the target limits, although much higher in lower limbs, generating a high ankle brachial index (ABI) of 1.3. He also had secondary hyperparathyroidism. The last routine blood test showed calcium 9.0 mg/dL, phosphate 5.7 mg/dL, potassium 4.7 mEq/L, creatinine 7.4 mg/dL, alkaline phosphatase 175 U/L, and parathyroid hormone 1,745 pg/mL. The chest radiography revealed a tunneled venous catheter, and incidentally found demarcated images on cardiac area (). The necklace shape extends from the cardiac apex to the base. A small circular shape is also displayed, superimposed on the first one. The lesions seen in this image correspond to a calcified right coronary and aortic valve. Parathyroidectomy (PTX) was indicated, but unfortunately, this patient had sudden cardiac death few months after this radiography had been taken. FGF-23, accessed afterward, was 1,327 pg/mL.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [7.4, 'mg/dL'], 'age': [35, 'years']}",9.1152,8.65944,9.57096,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 35 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 7.4 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (7.4/0.9)**-1.2 * 0.9938**35 * 1.0 = 9.1152.
Hence, the GFR value is 9.1152 ml/min/1.73 m²."
576,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7813086-1,Extracted,"A 32-year-old woman who had a history of recurrent stone formation and previous several urological procedures presented to our facility with pelvic pain mainly on the right side and severe dysuria of a few days duration. Reviewing her records revealed a poor dietary control, high protein intake, and high urinary uric acid for long periods. Her body mass index was 41. Five weeks prior to this presentation, she had presented to another healthcare facility with bilateral, mainly left, flank pain associated with fever of two days duration. Imaging at that time showed bilateral small upper ureteric stones with bilateral hydronephrosis and her serum creatinine was 1.65 mg/dl (normal range: 0.7-1.20). So, she underwent an emergency bilateral JJ stent insertion after which her creatinine returned to normal.
At our facility, a plain x-ray of the abdomen showed a fragmented left stent at the level of L4 (Figure A). The tip of the straight end of the lower fragment was protruding out of the external urethral meatus (Figure B). So, this piece was removed in the emergency room. Urinalysis showed pyuria, and there was no bacterial growth. Subsequently, she underwent bilateral ureteroscopy. On the left side, the stent was removed and the ureteric stone was fragmented. Right rigid ureteroscopy showed no ureteric stones, and removal of the upper fragment of the stent using forceps has failed, and this piece was unintentionally pushed back to the renal pelvis. This was removed using flexible ureterorenoscopy and a basket.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [1.65, 'mg/dL'], 'age': [32, 'years']}",42.08948,39.98501,44.19395,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 32 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.65 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.65/0.7)**-1.2 * 0.9938**32 * 1.012 = 42.08948.
Hence, the GFR value is 42.08948 ml/min/1.73 m²."
577,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3464797-1,Extracted,"We report the case of a 61-year-old Tunisian woman presented to the emergency unit with a 4-hour history of abdominal pain, diffused at both flanks without hematuria. Her medical history was significant for diabetes, hypertension and atrial fibrillation, besides her surgical history indicates left pneumectomy for pulmonary tuberculosis. Her medications consisted of aspirin, metformin, furosemide, and metoprolol. Physical examination showed vital signs as follows: body temperature of 37.2°C, blood pressure of 150/85 mmHg, heart rate of 133 beats per minute, respiratory rate of 20 breaths per minute; the abdomen was soft with slight tenderness in the renal angles. The remainder of the examination was normal.
An electrocardiogram showed atrial fibrillation. A biological analysis showed high serum creatinine levels (205μmol/L); her aminotransferases were twice normal the normal levels and her lactate dehydrogenase (LDH) level had increased to (8,636IU/L) with high leukocytosis at 15,000 cells/mm3. A urine analysis showed no hematuria or infection. A serum analysis done one month previously showed that her creatinine level was normal (93μmol/L). Nephrolithiasis and mesenteric ischemia were strongly suspected to be the causes for this acute pain.
Ultrasounds of the abdomen were performed and showed peri-renal fluid collection with heterogeneous parenchyma (Figure ). Contrast-enhanced helical computed tomography (CT) images showed: a thrombus in the left auricle, an increase in kidney’s size besides to perirenal edema and multiple parenchymal perfusion defects of both kidneys that are related to segmental distal arterial lesions which suggest arterial thromboembolic disease. Aorta and renal arteries were permeable with no atherosclerotic plaque; the renal vein and inferior vena cava were both less permeable. Figure .
Subsequent transesophageal echocardiography confirmed the presence of a thrombus in the left atrium without valvular vegetations Figure .
We concluded that it was a bilateral renal infarction of embolic origin caused by migration of an embolus from the left atrium. In addition to analgesic, continuous IV infusion of heparin was administered at the curative dose of 18 units/kg/hour and the outcome was favorable: the abdominal pain disappeared besides to a decrease of serum creatinine to (115 μmol/ l) after 3 days. One month later, the creatinine levels declined to 95 μmol/ l so we also concluded that acute renal failure was due to the infarction.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [205.0, 'µmol/L'], 'age': [61, 'years']}",24.06766,22.86428,25.27104,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 61 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 205.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 205.0 µmol. To convert 205.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 205.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.0002 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.0002 mol Serum Creatinine * 113.12 g/mol = 0.02262 g Serum Creatinine. To convert 0.02262 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.02262 g Serum Creatinine * 1000.0 mg/g = 22.62 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 22.62 mg Serum Creatinine/10.0 dL = 2.262 mg Serum Creatinine/dL. The concentration value of 205.0 µmol Serum Creatinine/L converts to 2.262 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.262/0.7)**-1.2 * 0.9938**61 * 1.012 = 24.06766.
Hence, the GFR value is 24.06766 ml/min/1.73 m²."
578,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4129213-1,Extracted,"A 51-yr-old Korean male visited the emergency room with complaints of high fever, chills, and abdominal pain in August 2013. He described the pain as increasing progressively in intensity, worsening after meals, and accompanied by nausea. He also suffered from diarrhea twice. He was diagnosed with Graves' disease 2 weeks ago, and was being treated with MMI (20 mg per day). His other medications included bisoprolol and 100 mg aspirin for atrial fibrillation. He did not have any history of drug or food allergies. He denied the use of tobacco, alcohol, and any dietary supplements. His family history was unremarkable, and did not include thyroid disease or gastrointestinal disorders.
Upon admission, his vital signs were as follows: blood pressure of 100/70 mmHg, heart rate of 121 beats per minute, a respiratory rate of 21 times per minute, and a body temperature of 39.0℃. He had a slightly enlarged thyroid gland, but there was no pharyngeal injection. Physical examination revealed tenderness in the epigastric and upper abdomen without rebound tenderness, guarding, or rigidity.
The results of blood tests were as follows: white blood cell count of 5,460/µL, hemoglobin of 16.3 g/dL, and platelet count of 103,000/µL. Biochemical parameters were glucose of 222 mg/dL, triglycerides of 113 mg/dL, blood urea nitrogen of 30.3 mg/dL, creatinine of 1.45 mg/dL, sodium of 133.8 mM/L, potassium of 3.9 mM/L, chloride of 97.3 mM/L, aspartate transaminase of 34 IU/L, alanine transaminase of 46 IU/L, alkaline phosphatase of 46 U/L, total bilirubin of 2.60 mg/dL, C-reactive protein (CRP) of 46.7 mg/L, amylase of 86 IU/L (normal range: 29-110), and lipase of 86 IU/L (normal range: 14-60).
A thyroid function test at the first visit revealed TSH of 0.01 mIU/L (normal range: 0.27-4.20), free T4 of 3.89 ng/dL (normal range: 0.93-1.70), total T3 of 199.8 ng/dL (normal range: 80-200), anti-TPO antibody of 17.84 (normal range: 0-34), and TSH-receptor antibody of 8.8 IU/L (normal range: 0.00-1.75). In Tc-99m thyroid scan, the uptake ratio was 4.8%. There was no elevation of serum antibodies for respiratory viruses including adenovirus, influenza, parainfluenza, and rhinovirus. He also tested negative for serum antibodies against tsutsugamushi, leptospira, and hantavirus.
The following day, MMI therapy was restarted after holding 42 hr because his fever had subsided and there was no evidence of agranulocytosis. However, 5 hr after he took the second dose of MMI (10 mg), abdominal pain and fever (39.2℃) developed again. At that time, laboratory studies showed a white blood cell count of 5,580/µL (72.7% neutrophils and 1.9% eosinophils), total bilirubin of 1.84 mg/dL, and CRP of 26.0 mg/L. His serum amylase and lipase levels increased to 265 IU/L and 682 IU/L, respectively. Electrophoresis revealed that his pancreatic amylase isoenzyme levels were elevated. An abdominal CT revealed a swollen pancreas with peripancreatic inflammatory fat stranding, suggestive of acute pancreatitis (). An abdominal ultrasound was then performed, which showed no evidence of cholelithiasis or biliary duct dilatation ().
After the withdrawal of MMI, his fever and abdominal pain improved, and pancreatic enzyme levels began to decrease and finally normalized (). We measured IgG and IgG4 to exclude autoimmune pancreatitis. The serum levels of IgG and IgG subclass-4 were in the normal range (901.5 mg/dL, normal range: 700-1,600; and 349 mg/L, normal range: 30-2,010, respectively). The serologic typing of HLA alleles revealed DRB1*0803 and DQB1*0601. After discharge, PTU (50 mg t.i.d) was prescribed for treatment of Graves' disease and his hyperthyroidism was gradually controlled without any side-effects.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.45, 'mg/dL'], 'age': [51, 'years']}",58.34268,55.42555,61.25981,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 51 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.45 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.45/0.9)**-1.2 * 0.9938**51 * 1.0 = 58.34268.
Hence, the GFR value is 58.34268 ml/min/1.73 m²."
579,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3780919-1,Extracted,"A 78-year-old female patient who had loss of appetite, lethargy, disorientation, and speech disturbance for several days came to our hospital in emergency room due to mental deterioration. About a month before the hospital visit, the patient had femur neck fracture caused by hitting on a table and then received hip arthroplasty under spinal anesthesia. At the time of the visit, blood pressure, body temperature, pulse rate, and respiratory rate were 120/70 mmHg, 36.5℃, 70 times/minute, and 20 times/minute, respectively, and the patient responded to pains but couldn't communicate. Brain magnetic resonance imaging (MRI) was carried out in order to check the occurrence of cerebrovascular event but acute lesion was not observed. Laboratory test showed the result of leukocyte count 6,530/µL, hemoglobin 11.3 g/dL, platelet count 197,000/µL, blood urea nitrogen 36.9 mg/dL (8-23), serum creatinine 3.67 mg/dL (0.6-1.2), fractional excretion of sodium (FENa) 5.9%, serum albumin 3.3 g/dL (3.2-4.5), sodium 143.4 mEq/L (136-142), potassium 3.3 mEq/L (3.8-5.0), corrected calcium concentration 3.96 mg/dL (9-11), phosphorus 2.5 mg/dL (2.3-4.7), parathyroid hormone (PTH) 486.6 pg/mL (12-88), ionized calcium 1.8 mg/dL (4-4.8), and magnesium 1.4 mg/dL (1.3-2.1). The corrected calcium concentration was calculated utilizing equation of 'total calcium concentration in serum (mg/dL) + (0.8 × (4.0 - serum albumin concentration [g/dL])'. On electrocardiography, corrected QT interval (519 msec) was prolonged, but Trousseau's phenomenon or Chvostek's sign was not exhibited. In the past medical history, no special diseases such as hypertension and diabetes were present and the patient was a non-smoker and a non-drinker. When the patient had femur neck fracture about a month ago, bone mineral density (BMD) was measured utilizing dual-energy X-ray absorptiometry (DXA; Hologic QDR-4500W; Hologic, Inc., Bedford, MA, USA). In result, osteoporosis was considered with T-scores of -3.9 and -3.4 in lumbar spine (L1-4) and hip, respectively (). Therefore, 5 mg of zoledronate (Aclasta®) was injected intravenously for 15 minutes on the day after the surgery and then calcium supplements were continuously being given until visiting the emergency room. In the blood test at the time of injecting zoledronate intravenously, serum creatinine concentration was 2.83 mg/dL and corrected calcium concentration was 8.4 mg/dL.
The patient was diagnosed intravenous zoledronate-induced hypocalcemia and then 20 mL of calcium gluconate (diluted in 100 mL of normal saline) and 1 µg/day of vitamin D (calcitriol, Bonky®) were started to inject intravenously. From the day after the intravenous injection of calcium, the patient showed gradual improvement in consciousness as well as lethargy and fatigue. However, in spite of continuous supplying of oral calcium carbonate, 3 g/day, and oral vitamin D, 0.5 µg/day, serum calcium concentration was not improved as much with 4.68 mg/dL of corrected calcium concentration in 2 weeks after the hospital visit. In the follow up examination performed in out-patient clinic after discharging from the hospital, serum creatinine concentration was 3.14 mg/dL and calcium concentration was 7.2 mg/dL (4 weeks after the symptom occurrence) and 9.3 mg/dL (4 months after the symptom occurrence) ().","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [3.14, 'mg/dL'], 'age': [78, 'years']}",14.60805,13.87765,15.33845,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 78 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 3.14 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (3.14/0.7)**-1.2 * 0.9938**78 * 1.012 = 14.60805.
Hence, the GFR value is 14.60805 ml/min/1.73 m²."
580,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4942527-1,Extracted,"A 72-year-old man visited the Emergency Department with hematochezia. He had mild abdominal pain with a bloating sensation. He denied being nauseous or vomitous and experiencing hematemesis. He had been taking aspirin to treat angina for 10 years. He had a past history of melena due to a duodenal ulcer 2 years earlier. At admission, the patient's vital signs were within normal ranges. Physical examination did not reveal abdominal tenderness. Laboratory investigations revealed the following: white blood cell count, 8,910/mm3 (44.0% neutrophils); hemoglobin, 12.6 g/dL; hematocrit, 38.0%; platelet count, 125 × 103/mm3; prothrombin time, 13.2 seconds (international normalized ratio, 1.08); creatinine, 1.34 mg/dL; serum Na, 139 meq/L; and serum K, 4.8 meq/L.
Esophagogastroduodenoscopy showed gastric and duodenal ulcers, but no evidence of acute bleeding. Colonoscopy showed dark blood fill without definitive evidence of bleeding foci in the entire colon or rectum and revealed that active bleeding originated from the orifice of the appendix (). Otherwise, few diverticula without bleeding were present in the proximal part of the ascending colon and the cecum. No blood clots were found in the proximal part of the ileocecal valve. On the double-phase abdominopelvic computer tomography scan, we noted mild wall thickening in the appendix.
A laparoscopic appendectomy and cecum wedge resection were performed. The appendix appeared grossly to be mildly edematous and hyperemic on the serosal surface and had a maximum diameter of 8 mm and a length of 48 mm. A small ulcer-like lesion was found on the mucosa of the middle part of the appendix (). Microscopically, the submucosa of the appendix was widened with aggregates of dilated vessels, most of which were veins. The submucosal veins pierced the circular and the longitudinal muscle layers of the appendix (). The patient had no hematochezia or melena after surgery. The patient was discharged uneventfully eight days after surgery.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.34, 'mg/dL'], 'age': [72, 'years']}",56.28349,53.46932,59.09766,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 72 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.34 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.34/0.9)**-1.2 * 0.9938**72 * 1.0 = 56.28349.
Hence, the GFR value is 56.28349 ml/min/1.73 m²."
581,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4267133-1,Extracted,"A 75-year-old Japanese man was admitted to our hospital in June 2010 for consciousness disturbance. After admission, cerebral infarctions and a left atrium (LA) mass were identified on computed tomography (CT). He had previously been diagnosed with RCC and had undergone hand-assisted laparoscopic nephrectomy in October 2006 (pT2N0M0). Subsequently, multiple lung metastases and mediastinal lymph node metastases were detected on chest CT in April 2008. His Karnofsky performance status score was 100, and Memorial Sloan-Kettering Cancer Center risk classification was “favorable”. The patient was therefore treated with three doses per week of subcutaneous interferon-alpha at 5 million units. However, owing to progression of lung metastases and the appearance of a pubic bone metastasis, treatment was changed to sorafenib at 800 mg/day in August 2009. In January 2010, radiotherapy (total: 39 Gy in 13 fractions) was added owing to progression and pain of the pubic bone metastasis. At that time, sorafenib was changed to everolimus at 10 mg/day. In July 2010, a solid mass was found in the LA on routine CT of the lungs.
At the time of admission, vital signs were stable, with blood pressure at 132/84 mmHg and heart rate at 64 beats/min. Laboratory tests results indicated anemia (hemoglobin, 9.3 g/dL) and renal failure (creatinine, 2.0 mg/dL), and electrocardiography revealed sinus rhythm.
Transthoracic echocardiography showed a 42 × 24 mm mass in the LA that moved without extension into the outflow tract (Figure ). The right atrium and interatrial septum appeared normal. CT of the chest and abdomen revealed multiple metastatic tumors of the lungs, lymph nodes and pubic bone, but no IVC involvement, and the LA mass was unclear (Figures and ).
The appearance of the LA mass was consistent with myxoma, but the history of RCC raised the possibility of an intracardiac metastatic mass. Finally, the LA mass was surgically resected to prevent sudden death from acute heart failure or embolism resulting from tumor separation. Although the tumor had grown into the right superior pulmonary vein as the site of lymph node metastasis, the mass was completely resected.
Pathological assessment of the LA tumor revealed clear cell RCC that was diagnosed as a metastasis from the original RCC. After surgery, the patient did not experienced symptom of heart disease, such as dyspnea, chest pain, or syncope. However, multiple brain metastases were found subsequently, and the patient died from progressive disease 4 months postoperatively.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [2.0, 'mg/dL'], 'age': [75, 'years']}",34.16393,32.45573,35.87213,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 75 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.0 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.0/0.9)**-1.2 * 0.9938**75 * 1.0 = 34.16393.
Hence, the GFR value is 34.16393 ml/min/1.73 m²."
582,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8023184-1,Extracted,"We described a 56-year-old male patient that was referred to our intensive care unit (ICU) for TMA/HUS and acute respiratory failure. Two years before admission, he had upper-right lung lobectomy to treat a localized non-seminoma germ cell tumour. In the 2 months preceding the admission to the ICU, he received a chemotherapy regimen combining cisplatin, bleomycin and etoposide for relapse of the malignancy. On admission, serum creatinine was 620 μmol/L (77 μmol/L at baseline), urinary protein to creatinine ratio was 2.2 g/g and microscopic haematuria was identified. Haemolytic anaemia with schistocytes and thrombocytopenia was identified. Blood pressure was 180/100 mmHg. Search for Shiga toxin in stool, circular dichroism (CD) 46 deficiency or anti-factor H or anti-ADAMTS13 antibodies was negative. Complement componentsC3, C4 and CH50 were normal. Chest computed tomography scan showed interstitial lung disease suggestive of bleomycin-related lung fibrosis. Diagnosis of bleomycin-induced HUS was retained.
Daily plasma exchanges were started at Day 1 and dialysis at Day 2. Acute respiratory distress syndrome required mechanical ventilation at Day 1. Because TMA was still active, salvage therapy by eculizumab was started at Day 5 after anti-pneumococcal and anti-meningococcal vaccination (900 mg weekly, intravenously). Ceftriaxone was used as anti-bacterial prophylaxis. As shown in , eculizumab administration was followed by rapid correction of haemolysis, normalization of haptoglobin levels and an increase in platelets to 100 000/mL. No relapse of the TMA occurred. However, no renal recovery was observed and lung fibrosis progressed despite protective ventilation and secondary introduction of steroids and tocilizumab. Worsening of the lung compliance ultimately led to fatal respiratory failure at Day 25.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [620.0, 'µmol/L'], 'age': [56, 'years']}",8.53175,8.10516,8.95834,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 56 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 620.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 620.0 µmol. To convert 620.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 620.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00062 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00062 mol Serum Creatinine * 113.12 g/mol = 0.07013 g Serum Creatinine. To convert 0.07013 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.07013 g Serum Creatinine * 1000.0 mg/g = 70.13 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 70.13 mg Serum Creatinine/10.0 dL = 7.013 mg Serum Creatinine/dL. The concentration value of 620.0 µmol Serum Creatinine/L converts to 7.013 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (7.013/0.9)**-1.2 * 0.9938**56 * 1.0 = 8.53175.
Hence, the GFR value is 8.53175 ml/min/1.73 m²."
583,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4873190-1,Extracted,"A 47-year-old man was hospitalized at the Care for Business Medical Center and Hospital in Lusaka, Zambia, with initial complaints of frequent episodes of headache, fever, dizziness, body malaise, and erythematous skin rashes. Rapid diagnostic tests for malaria (Immuno Chromatographic Test and blood slide), typhoid (IgG/IgM), and tick fever (Weil Felix) were all negative. The history of the patient revealed that he owned a wildlife safari lodge in KNP, about 16 kilometres from the Itumbi Safari Camp.
The patient had just returned from the Park following heightened tourist peak visits around the festive holidays. Together with colleagues, he had been involved in a two-day pursuit of an injured wild animal that was wounded by poachers and needed clinical intervention. This pursuit led the team to be exposed to the deep forest and far-flung areas within KNP. The patient reported being bitten multiple times by tsetse flies and other biting arthropods.
Following centrifugation of the patient’s blood, microscopic examination of Giemsa-stained thin buffy coat smears revealed the presence of several trypanosomes (), which, given the patient’s travel history, were thought to be T. b. rhodesiense. As shown in , loop-mediated isothermal amplification (LAMP) results confirmed the trypanosomes positive for the T. b. rhodesiense-specific human serum resistance-associated (SRA) gene. Blood test results were as follows: Alanine aminotransferase 114.3 U/L, bilirubin 82.7 μmol/L, creatinine 42.1 μmol/L, urea 2.78 mmol/L, leukocytes 4.8 × 109 cells/L, and platelets 18 × 109/L.
Although the patient had a packed cell volume (PCV) value of 42% (reference 42% to 54%), he was critically ill. He was progressively getting weaker, having episodes of unconsciousness, and eventually became comatose. He was placed on assisted breathing ventilator as he could not breathe on his own. The presence of T. b. rhodesiense, which was only in the patient’s blood and not in the cerebrospinal fluid (CSF), coupled with ≤5 white blood cells (WBCs)/mm3 in the CSF, signified early-stage HAT, which was treated with Suramin [] along with supportive therapy. A Suramin dose of 1 gram (g) dissolved in 5 centimetre cubed (cm3) of sterile water was administered slowly and intravenously on days 1, 3, 5, 14, and 21. The patient showed a tremendous improvement on the second day by returning to normal consciousness and was thus removed from the ventilator. He appeared brighter and more alert and was responsive to treatment. Before and after each treatment, a sample of blood was collected. Thin buffy coat slides were regularly examined by microscopy to track the course of the disease. His blood was cleared of all parasites after the fifth day of treatment and all clinical signs receded. The patient was hospitalized for observation until all treatment was completed. Other people that were in his company during his stay in the area were screened using microscopy and LAMP and were all negative.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [42.1, 'µmol/L'], 'age': [47, 'years']}",120.97867,114.92974,127.0276,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 47 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 42.1 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 42.1 µmol. To convert 42.1 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 42.1 µmol Serum Creatinine * 1e-06 mol/µmol = 4e-05 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 4e-05 mol Serum Creatinine * 113.12 g/mol = 0.00452 g Serum Creatinine. To convert 0.00452 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00452 g Serum Creatinine * 1000.0 mg/g = 4.52 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 4.52 mg Serum Creatinine/10.0 dL = 0.452 mg Serum Creatinine/dL. The concentration value of 42.1 µmol Serum Creatinine/L converts to 0.452 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is less than or equal to 0.9 mg/dL, A = 0.7 and B = -0.302.
Plugging in these values, we get 142 * (0.452/0.7)**-0.302 * 0.9938**47 * 1.0 = 120.97867.
Hence, the GFR value is 120.97867 ml/min/1.73 m²."
584,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8221701-1,Extracted,"Our patient is a 67-year-old Spanish-speaking male with history of hypertension, hyperlipidemia, and chronic bilateral osteoarthritis of the knees, who was admitted to our hospital for anasarca and shortness of breath. Over the 3 months prior to initial presentation, he noticed worsening bilateral lower extremity pitting edema, abdominal swelling, and orthopnea. He also endorsed having nausea, vomiting, and diarrhea. Furthermore, he reported making less urine than before, accompanied by urine frothiness.
On initial examination, his blood pressure was 168/67 mm Hg. He had notable anasarca and a brain natriuretic peptide in the 2000s. There was 4+ pitting edema of his lower extremities up to the thighs. His lungs were clear and there was no respiratory distress. Initial urinalysis showed elevated urine protein of >500 mg/dL with 5 to 10 white blood cells/high power field (WBC/HPF) and 20 to 30 granular casts/HPF. His baseline serum creatinine (SCr) in 2018 was 0.5 to 0.6 mg/dL, but his SCr on initial admission was 2.1 mg/dL. Albumin was 2.0 g/dL, and urine protein:creatinine ratio (UPCR) was 6132 mg/g. Extensive proteinuria workup was done, revealing of 7 g protein/24 h, 3600 mg/24-h albuminuria. The proteinuria was mostly albuminuria nearly 60% with 40% of proteinuria being non-albumin proteinuria.
Further workup, including HIV, hepatitis B, hepatitis C, antinuclear antibody, rapid plasma reagin, anti-Rho, double-stranded DNA, and complements C3 and C4, was all negative or within normal limits. Serum and urine protein electrophoresis showed no monoclonal spikes. Renal ultrasound demonstrated normal cortical echogenicity and contour for both kidneys, with right measuring 13.2 cm and left measuring 13.0 cm.
A percutaneous sonographic guided renal biopsy was done and was composed of renal cortex and contained at least 33 non-sclerotic glomeruli. The glomerular capillary loops were mildly thickened and exhibited segmental subtle spikes and pinholes. Podocytes appeared reactive. There was no mesangial or endocapillary hypercellularity. There were no large endocapillary deposits, necrotizing lesions, segments of sclerosis, or crescents. There was patchy acute tubular injury associated with mild patchy interstitial inflammation associated with foci of tubulitis and scattered eosinophils. There was mild interstitial fibrosis/tubular atrophy (~15%). Immunofluorescence studies demonstrated segmental granular glomerular capillary wall staining with immunoglobulin G (IgG, trace), immunoglobulin M (IgM, trace), C1q (trace-1+), kappa (trace), and lambda (trace) light chains. There was no extra-glomerular staining. The M-type phospholipase A2 receptor (PLA2R) stain was negative. Electron microscopic analysis demonstrated diffuse podocyte foot process effacement with frequent microvillous transformation and condensation of actin cytoskeletal filaments. Glomerular basement membranes were variable thickening with segmental subepithelial and intramembranous electron lucencies and subepithelial remodeling (spike/pinholes) and showed rare small granular subepithelial and intramembranous deposits. Minimal mesangial electron densities were present. No deposits displayed any significant fibrillary or microtubular substructure. There were no tubuloreticular inclusions or immune complex-type deposits present in any other location (see ).
Diagnosis of MN (stage IV of IV) and mild AIN was rendered. Because the degree of podocyte foot process effacement was felt to be more extensive than would be expected given the somewhat segmental and low-grade MN, the possibility of a superimposed podocytopathy (MCD) was raised. The time course of the worsening proteinuria was also felt to be incompatible with the relatively chronic stage of the MN. The constellation of biopsy findings raised the suspicion for an underlying allergic/drug-induced etiology.
In light of this biopsy-proven diagnosis of MN, PLA2R [Anti Phospholipase A2 Receptor Antbiody] serology, anti-THSD7A [Anti Thrombospondin Type 1 Domain Contaning 7A Antibody], and anti-NELL [Anti Neural Epidermal Growth Factor-Like 1 Protein Antibody] were sent, and anti-PLA2R and anti-THSD7A came back negative.
 Anti-NELL was sent, but after discussion with the Mayo Clinic laboratory, it could not be performed due to a lack of current approval as a commercially approved assay. The patient had no signs of systemic lupus erythematosus, no indications of malignancy (on recent computed tomography (CT) imaging studies and colonoscopy), and no evidence of chronic infections or sarcoidosis to suggest any other etiologies for a secondary MN. Lyme IgG and IgM were sent to investigate Lyme nephritis and were not detected, as Lyme disease has been reported to cause a diverse spectrum of glomerular disease.
Given the concern for a potential drug-induced MN, lack of serologic evidence for a primary form, and its low-grade chronic nature, immunosuppressants such as cyclophosphamide or rituximab were not pursued. The patient was further diuresed with metolazone 5 mg and furosemide 80 mg IV (intravenous) twice a day with improvements to his urine output and edema. Prednisone 10 mg daily was also started for his worsening SCr, which peaked at 5.6 mg/dL about 1 month after initial presentation. When the patient came to our clinic a month later, his symptoms had drastically improved. The patient lost around 24 pounds of water weight with noticeable improvements to his edema. Upon further investigation at that time, the patient finally recalled that he had been frequently taking ibuprofen 9 months prior to symptom manifestation. He was taking 400 mg of ibuprofen three to four times a day; he had no heavy metal exposure, industrial exposure, or new vaccines in the time prior to development of anasarca. He had been using over-the-counter ibuprofen at lower doses (once a day) nearly daily for his chronic knee pain for 10 months prior to his intensification of therapy years before stopping due to inefficacy and advice of nephrologists regarding NSAID nephrotoxicity.
The findings suggesting NSAID-induced injury were tempered by finding of elevated urine copper levels. A 24-h urine panel for heavy metals showed undetectable levels of arsenic, zinc, cadmium, mercury, and lead. Copper levels were elevated at 27.1 µg/dL (upper limit of normal value 3.2 µg/dL) with a caveat that this is known to occur in high-grade proteinuria and with cirrhosis which the patient had. The patient also underwent workup for cirrhosis, including exclusion of Wilson’s disease; the patient ceruloplasmin level was within normal limits at 27 mg/dL. Eye examination did not reveal Kayser Fleischer rings as well. The liver findings were attributed by hepatology to non-alcoholic fatty liver disease (NAFLD). Unfortunately, given the patient’s financial status and insurance status, hair sampling for heavy metal toxicity was not financially viable or practical in this particular situation.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [2.1, 'mg/dL'], 'age': [67, 'years']}",33.86481,32.17157,35.55805,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 67 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.1/0.9)**-1.2 * 0.9938**67 * 1.0 = 33.86481.
Hence, the GFR value is 33.86481 ml/min/1.73 m²."
585,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2740182-1,Extracted,"A 78-year-old African American female was admitted with multiple painful ulcers on the lower extremities and possible septicemia. Her medical history included coronary artery disease, peripheral vascular disease, end-stage renal disease on hemodialysis for 7 months, insulin-dependent diabetes, hypertension, hypothyroidism, chronic obstructive pulmonary disease and asthma. Her surgical history included thyroidectomy and left upper extremity graft in October 2005 which failed to maturate and patient did not follow up. Patient was admitted in March 2006 for symptoms of worsening of lower extremity swelling and paroxysmal nocturnal dyspnea when her laboratory results showed BUN-141 mg/dl and creatinine-8.1 mg/dl. Patient underwent fistulogram which showed multiple high-grade stenosis. She had internal jugular catheter placed at the time and was started on daily hemodialysis. When she was discharged 6 days later, her BUN was 33 mg/dl and creatinine was 5.4 mg/dl. She was advised to follow with the dialysis center three times weekly, however patient remained noncompliant with intermittent dialysis. Since the September 2006 hospitalization as described on the case she was dialyzed regularly on Tuesday, Thursday & Saturday. She also had right lower extremity angiogram with an attempted right superficial femoral arterectomy and angioplasty which failed because of severely calcified vessels and multiple wound debridements in the past 3-4 months. Drug therapy included aspirin 81 mg daily, pentoxifylline 400 mg 3 times daily, lisinopril 40 mg daily, amlodipine 10 mg and minoxidil 2.5 mg daily, insulin 70/30 22 units every morning and 12 units every evening, atorvastatin 40 mg daily, albuterol and atrovent inhalers as needed, levothyroxine 150 mcg daily, PhosLo 2 caps 3 times daily, cinacalcet 30 mg daily, colace 100 mg twice daily, hydrocodone 500 mg as needed. Patient denied any exposure to tobacco, ethanol, and intravenous drug abuse. She had 2 children and lived with her son and daughter-in-law who are the primary caretakers. Family history included chronic kidney disease, hypertension, coronary artery disease and diabetes.
Six months prior to presentation, she was found to have significant hyperparathyroidism (serum intact parathormone of 1133 pg/ml [normal, 10-65]) and hypercalcemia of 11.1 mg/dl [normal, 8.5-10.5]. Meanwhile, she developed 7 × 4 cm ulcer on the posterior aspect of right calf after a burn which remained non-healing for more than 2 weeks. She complained of severe local pain and continued developing multiple ulcerations on both lower extremities. Wound care and pain management was attempted as outpatient. Admission followed due to worsening of ulcerations and poor pain control. On admission, physical examination revealed obese (Ht-154 cm, Wt-84 kgs, BMI-35) African American female in distress due to pain with marked abdominal adiposity, absent pedal pulses and extensive lesions on the hips, buttocks, and proximal thighs with surrounding erythema, induration and dark eschar ( & ). No other pertinent physical findings were present. Laboratory studies showed serum calcium of 8.6 mg/dl (normal, 8.5-10.5), serum phosphorous of 3.7 mg/dl (normal, 2.5-5.0), calcium-phosphorous product - 31.8, parathormone of 155 pg/ml (normal, 10-65), urea of 35 mg/dl (normal, 7-20) and creatinine of 4.3 mg/dl (normal, 0.8-1.3), alkaline phosphatase-145 IU (normal, 70-230 IU), and serum albumin-1.9 g/dl (normal, 3.5-5.5 g/dl).
X-ray of lower extremities revealed extensive arterial calcifications within the femoral, popliteal artery and smaller branches. Nuclear medicine scan of parathyroid showed adenoma of the right lobe. With significant multiple co morbidities of diabetes, peripheral vascular disease and end stage renal disease, we considered the possibilities of ischemic ulcers and superimposed infection. The patient underwent several investigations, including a lower extremity angiogram with an attempted right superficial femoral arterectomy and angioplasty which failed because of severely calcified vessels and multiple wound debridements in the past 3-4 months. Hypercoagulable state with cryoglobulinemia was also ruled out, with the results of protein C, protein S and antithrombin-3 being in the normal range.
A biopsy of the lower extremity ulcer demonstrated circumferential vascular mural calcification affecting small and medium sized blood vessels with degeneration of elastic fibers and absence of inflammation (). During her hospitalization, despite attempts to control deterioration (wound care, pain control, hemodialysis and parenteral antibiotics), leg wounds and general condition worsened over the next 3-4 weeks. She exhibited periodic disorientation. Upon multiple discussions with the family on different treatment options and overall poor prognosis, the patient’s family opted for comfort care under Hospice. Patient expired two days later.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [4.3, 'mg/dL'], 'age': [78, 'years']}",10.01719,9.51633,10.51805,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 78 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 4.3 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (4.3/0.7)**-1.2 * 0.9938**78 * 1.012 = 10.01719.
Hence, the GFR value is 10.01719 ml/min/1.73 m²."
586,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4495505-1,Extracted,"A 63-year-old male presented with intermittent gross hematuria and anemia. He had undergone a Y-graft surgery for an abdominal aortic aneurysm 3 years earlier. A computed tomography (CT), 1 year after Y-graft surgery revealed that the right ureter had crossed the distal anastomosis of the vascular graft. Two years after the surgery, the ureter was observed to be extrinsically compressed by fibrosis at the site of its crossing over the Y-graft and a ureteral stent was placed at another hospital, 7 months before presentation to us. Cystoscopy revealed hematuria from the right ureteric orifice, suggesting the possibility of AUF. The patient was transferred to our hospital after transfusion of four units of red cell concentrates. Laboratory data showed anemia with a hemoglobin concentration of 9.7 g/dL (normal, 13.5–17.0 g/dL), a hematocrit level of 28.9% (normal, 40–50%), an elevated serum creatinine level of 1.41 mg/dL (normal, 0.4–0.8 mg/dL) and a slightly elevated C-reactive protein concentration of 0.40 mg/dL (normal, 0.00–0.30 mg/dL). He was hemodynamically stable and a urine bacterial culture was negative. At the time of consultation at our hospital, contrast-enhanced CT of the abdomen revealed a possible fistula between the right common iliac artery and the ureter, although no flow of contrast medium to the ureter was detected []. The CT showed that the process originated at the level of the distal anastomosis of a vascular Y-graft [Figure and ]. Right hydronephrosis with intraureteral blood clots were present. The patient was diagnosed with AUF associated with the Y-graft. An elective endovascular surgery was performed by vascular surgeons following embolization of the right internal iliac artery to prevent endoleak caused by backflow from the right internal iliac artery. Arteriography at the operation detected no leak from the artery to the ureter []. A stent covered by expanded polytetrafluoroethylene (Fluency Plus, Bard Inc., Covington, GA, USA; diameter 10 mm; length, 80 mm) was placed via the right femoral artery. The right ureteral stent was removed after the treatment. Extrinsic obstruction caused by inflammatory fibrotic change was considered to be so dense that it was impossible to treat the ureteral stricture. Neither antiplatelet nor anticoagulation drugs were prescribed. Two weeks after treatment, contrast-enhanced CT showed disappearance of the fistula and improvement of right hydronephrosis. Six months after the endovascular surgery, severe right hydronephrosis was observed with an elevated serum creatinine level of 1.42 mg/dL. Retroperitoneoscopic nephrectomy was performed because we were concerned about recurrence of the fistula. No bleeding from the right residual ureter has been observed.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.42, 'mg/dL'], 'age': [63, 'years']}",55.52261,52.74648,58.29874,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 63 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.42 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.42/0.9)**-1.2 * 0.9938**63 * 1.0 = 55.52261.
Hence, the GFR value is 55.52261 ml/min/1.73 m²."
587,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3509375-1,Extracted,"An 82-year-old male was admitted by one-month history of swelling and small pustules that progressed to ulcers with purulent drainage in his right hallux. Medical history includes recurrent gout attacks since 8 years ago, hypertension, diabetes mellitus, hypothyroidism, and chronic kidney failure in medical management, aortic valve replacement, and myocardial revascularization. He lived in Buga, Colombia, and worked in agriculture but had lived in Chiclayo, Peru, for six years; both are endemic areas of P. brasiliensis [, ].
At exam, the hallux was edematous with limited range of motion and mild pain, erythema, and two ulcers of 2 cm on the lateral and medial aspect of the foot. The patient was afebrile, and findings on general medical and pulmonary tests were unremarkable. A plain radiograph of the foot revealed a lytic lesion with cortical disruption in the proximal phalanx of the right hallux associated with soft tissue swelling (). The chest radiograph was normal. Laboratory studies showed a PCR of 4.47 mg/dL (0–0.5 mg/dL), BUN 42 mg/dL (8–23 mg/dL), serum creatinine of 1.7 mg/dL, TSH level of 6.4 mIU/L, albumin 2.6 g/dL, white blood cell count of 8 × 103/uL with a normal differential, hemoglobin of 11.2 g/dL, hematocrit of 35%, and platelets of 390.000 K/uL. HIV test was negative. Blood and urine cultures were reported as negative. An amputation of the hallux was done. The microbiology laboratory received the sample of drainage right hallux for bacteriological study, to which Gram stain was initially performed and fungal structures were observed like a large, round, fairly thick-walled cells with single and multiple buddings. Direct examination, with KOH 10%, observed unique spherical yeast budding and also observed crystal needle-shaped structures, which observed polarized light filters with characteristic of monosodium urate crystal. At 35°–37°C on liquid medium, was obtained multiple budding “pilot wheel” morphology of P. brasiliensis. Histopathological study and bone cultures for aerobic, anaerobic, and fungal growth were done. The pathology report was consistent with osteomyelitis. Histologic examination revealed multiplebudding cells consistent with P. brasiliensis () and confirmed by isolation of the fungus in cultures and serological complementary diagnosis with agar gel immunodiffusion.
A diagnosis of a secondary infection by P. brasiliensis in a chronic gouty arthritis (right hallux) was made, and therapy with itraconazole was initiated without evidence of adverse effect. The patient's clinical course was satisfactory.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.7, 'mg/dL'], 'age': [82, 'years']}",39.75191,37.76431,41.73951,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 82 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.9)**-1.2 * 0.9938**82 * 1.0 = 39.75191.
Hence, the GFR value is 39.75191 ml/min/1.73 m²."
588,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7954254-1,Extracted,"A 59-year-old woman with ischaemic cardiomyopathy presented for OHT. She has a past medical history of Stage D heart failure (EF 20%) on home milrinone therapy, coronary artery disease with PCI to right coronary artery, hypertension, insulin-dependent diabetes mellitus, and Stage 3 chronic kidney disease. She was admitted from home for prospective heart transplantation. She was in her usual state of health without worsening shortness of breath, orthopnoea, or paroxysmal nocturnal dyspnoea. The induction of anaesthesia, sternotomy, and commencement of cardiopulmonary bypass (CPB) were without complications. She underwent cardiectomy and implantation of donor heart in the usual fashion. She had an unremarkable intraoperative course.
Post-operatively, she was on stable doses of inotropes/vasopressors in the form of epinephrine at 0.1 mcg/kg/min, milrinone at 0.25 mcg/kg/min, and vasopressin at 1.2 units/h. Swan-Ganz catheter monitoring revealed low cardiac indices and low filling pressures. On physical examination, she was intubated and sedated, cardiac examination revealed normal S1/S2 with no additional sounds, murmurs, rubs, or gallops. It was difficult to assess JVP due to the presence of Swan-Ganz catheter. Laboratory evaluation revealed an acute kidney injury with a creatinine of 1.6 mg/dL, elevated lactic acid up to 14 mmol/L, with decrease in bicarbonate down to 14. AST was elevated to 397 and ALT up to 262. Four hours later, she remained tachycardic and hypotensive requiring escalating doses of norepinephrine, epinephrine, and vasopressin. She was resuscitated with 5 L of crystalloid and albumin without improvement in hypotension. She notably developed progressive abdominal distention corresponding with fluid resuscitation.
Transoesophageal echocardiography (TOE) showed a small hyperdynamic left ventricle with diastolic internal diameter of 2.57 cm. Transgastric right ventricular (RV) view showed a small underfilled RV (). At the IVC-RA junction, there was an area of flow acceleration with a near-constant flow with velocity 2 m/s (). Intrahepatic IVC was 3 cm in diameter while SVC diameter was 1.4 cm. The suspicion of IVC obstruction was confirmed after volume resuscitation; the IVC-RA flow acceleration increased and became more phasic with respiration with peak velocity of 2 m/s, with gradient across the IVC and RA of approximately 16 mmHg ().
A central venous catheter was inserted into the left femoral vein and transduced to measure the pressure in the IVC which was found to be 26 mmHg. The transduced gradient across the SVC and IVC was ∼18 mmHg; consistent with the measured TOE gradient of 16 mmHg.
She was emergently taken back to the operating room. Following the initiation of CPB and right atriotomy, it was immediately evident that an obstruction existed at the IVC anastomosis with a thickened Eustachian valve and the existing sutures. The Eustachian valve was completely excised. The IVC orifice and anastomosis were confirmed as widely patent and the anterior wall of the anastomosis was closed. Transoesophageal echocardiography following Eustachian valve resection showed resolution of IVC-RA pressure gradient ().
Post-operatively, her haemodynamics showed hypervolaemia reflected by a CVP >15 mmHg. Aggressive diuresis with furosemide was initiated. Hours later, she was weaned off inotropic and vasopressor support. Her cardiac index improved to >2.0 with a mixed venous oxygen saturation (SvO2) of 72.7%. She subsequently had an uncomplicated post-operative course and overall recovery. During her follow-up visit, she had excellent graft function with no signs or symptoms of heart failure and was leading an excellent quality of life.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [1.6, 'mg/dL'], 'age': [59, 'years']}",36.92182,35.07573,38.76791,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 59 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.6 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.6/0.7)**-1.2 * 0.9938**59 * 1.012 = 36.92182.
Hence, the GFR value is 36.92182 ml/min/1.73 m²."
589,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4107385-1,Extracted,"A 27-year-old African American female was referred for nephrotic syndrome in 2012. In 2005, during her first pregnancy, she had developed proteinuria and preeclampsia. The proteinuria subsided after she had given birth; however, it recurred during a second pregnancy in 2006 and increased to the nephrotic range. The second pregnancy was otherwise uneventful, and after delivery, the degree of proteinuria trended down to a nadir of 120 mg/g creatinine by 2009. She subsequently presented to our hospital in 2012 when the proteinuria again increased, reaching 4,600 mg/24 h (or 2,900 mg/g creatinine).
The patient had no past medical history of diabetes, hypertension, or other systemic illnesses. She was not taking any medications, had no known allergies and denied ever smoking or having used illicit drugs. Of note, both her father and maternal grandmother had type 2 DM and her father had had a stroke at age 50.
On examination, her blood pressure was 100/60 mm Hg and her BMI was 33. There was no edema, acanthosis nigricans, or hirsuitism. Fundoscopy did not reveal any diabetic retinopathy. Laboratory values included 0.7 mg/dl serum creatinine, 167 mg/dl total cholesterol, 42 mg/dl HDL cholesterol, and 77 mg/dl triglycerides. Urinalysis showed 3+ proteinuria with no hematuria. Tests for HIV, RPR, HBV, HCV, ANA, C3, and C4 were all negative or normal. Fasting glucose was 80 mg/dl and HbA1C was 5.8%. Renal ultrasound revealed kidneys 12 cm in size.
A renal biopsy was obtained in October 2012. Of the 7 glomeruli present, none were globally or partially sclerotic. Glomerulomegaly was not present. Using an eyepiece micrometer, the mean glomerular diameter was 175 ± 12 μm, a value within the reported normal range. One glomerulus evidenced segmental hyalinosis. Otherwise, the glomeruli were unremarkable by light microscopy (fig. ). Evidence of chronicity such as interstitial fibrosis and tubular atrophy was absent. Immunofluorescence microscopy revealed mild (1–2+) pseudolinear staining of the glomerular basement membrane (GBM) for IgG. No other immunoglobulin classes or complement components were detectable. Electron microscopy showed that the lamina densa of the GBMs were diffusely thickened, averaging 700–900 nm (fig. ). The podocytes were not vacuolated and, importantly, their foot processes were not effaced (fig. ). The endothelial cells were swollen with loss of fenestrations. Hyaline deposits were also noted in the glomerular capillary wall (fig. ), a finding corresponding to the light microscopic changes mentioned above.
Our patient was serially evaluated for impaired glucose metabolism. Fasting blood glucoses ranged from 80 to 111 mg/dl (with only two values ≥100 mg/dl). HbA1C ranged from 5.6 to 5.9%. Fluorescein angiography was negative for diabetic retinopathy. An oral glucose tolerance test (OGTT) was normal with a 2-hour glucose level of 109 mg/dl. The homeostasis model assessment of IR (HOMA-IR) was elevated at 2.93 and 3.74, a result that indicates IR (normal value: 1) in the face of adequate insulin secretion to maintain normoglycemia and a normal OGTT.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [27, 'years'], 'creatinine': [0.7, 'mg/dL']}",121.49031,115.41579,127.56483,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 27 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.7 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.7/0.7)**-0.241 * 0.9938**27 * 1.012 = 121.49031.
Hence, the GFR value is 121.49031 ml/min/1.73 m²."
590,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5827907-2,Extracted,"A 32-year-old female with a past medical history of dyspepsia presented to the outpatient gastroenterology clinic with complaints of bloating and abdominal gas despite proton pump inhibitor (PPI) therapy. The patient also reported experiencing early satiety, no significant reflux, and occasional vomiting. She denied any associated fever, nausea, chills, or weight loss. The patient also denied smoking, but reported occasional binge drinking. Abdominal examination was soft, non-tender, and non-distended. Laboratory findings showed white blood cell count was 3,700/mm3 (normal range: 4,800 - 10,800/mm3), hemoglobin 12.1 g/dL (12.0 - 16.0 g/dL), hematocrit 37% (37-47%), and platelet count 188,000/mm3 (130,000 - 400,000/mm3). Blood urea nitrogen and creatinine were normal at 7 mg/dL (8 - 27 mg/dL) and 0.7 mg/dL (0.8 - 2.0 mg/dL), respectively. Vital signs were stable and within normal limits.
Upper endoscopy showed mild erythematous mucosa of the stomach. Biopsy specimens revealed mild gastritis without evidence of Helicobacter pylori. A gastric diverticulum was found in the antrum, which appeared to have normal appearing mucosa. Upon further entry, there appeared to be two smaller diverticula within the larger diverticulum (). In this case, a UGS was performed to characterize the morphology of the diverticulum which returned normal.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [0.7, 'mg/dL'], 'age': [32, 'years']}",117.77053,111.882,123.65906,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 32 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.7 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.7/0.7)**-0.241 * 0.9938**32 * 1.012 = 117.77053.
Hence, the GFR value is 117.77053 ml/min/1.73 m²."
591,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7771102-1,Extracted,"A 72-year-old Caucasian female with past medical history significant for remote history of supracervical hysterectomy for uterine fibroids presented to the emergency room with complaints of diplopia, left eye pain, and gradually worsening left-sided headache of one week duration. She had also been experiencing mild intermittent vaginal bleeding for several months. Ophthalmologic exam revealed left lateral rectus muscle restriction and was otherwise unremarkable. She didn’t have history of abnormal pap smear; however, her last pap smear had been over thirty years ago. Pelvic examination revealed a large necrotic mass occupying the vaginal vault approximately 7 cm in size with parametrial involvement appreciated on bimanual exam. Remainder of physical examination was unremarkable. Past medical history was only significant for a 45-pack year history of smoking and history of iron deficiency anemia related to GI arteriovenous malformation.
Biopsy of the cervical mass revealed an infiltrating poorly differentiated squamous cell carcinoma. MRI of the pelvis revealed a large mass in the expected area of the cervix measuring 6.7 × 3.6 × 7.3 cm in size with extension through the left lateral parametrium into the mesorectal fat, as well as a 2 cm long segment of abutment to the posterior bladder wall, partial encasement of the urethra, and invasion into the anterior rectal wall (A–C). MRI of the orbit was performed, which revealed an enhancing mass measuring 1.2 × 1.1 × 1.4 cm in the lateral aspect of the left orbit displacing the left lateral rectus muscle superiorly and medially resulting in lateral rectus palsy (D and E). A transvaginal ultrasound revealed a 6.9 cm solid mass replacing the expected location of the cervix and/or vaginal cuff. A contrast enhanced computerized tomography (CT) scan revealed a 5.2 × 8.1 cm mass in the region of the cervix extending into the vagina. Laboratory work-up was significant for anemia, with hemoglobin of 10.1 and hematocrit of 30.6. A basic metabolic panel was unremarkable with a normal creatinine of 0.67.
To further evaluate for metastasis, a whole-body positron emission tomography (PET) scan revealed intense uptake in the cervix with a maximum standard uptake value (SUV) of 20.3 as well as uptake of two adjacent pelvic lymph nodes in the left pelvis lateral to the cervix with SUV of 5.0. There was also asymmetrical FDG uptake in the left posterior orbit and no evidence of uptake in other distant organs such as liver, lung, or distant lymph nodes.
Orbital biopsy was performed and revealed poorly differentiated carcinoma, consistent with nonkeratinizing squamous cell carcinoma. Immunohistochemical stains performed were positive for CK5/6 and P16 (A and B) and negative for P40 supporting HPV associated malignancy in this patient with a cervical primary neoplasm. Given that the biopsy confirmed metastasis to the left orbit, she was ultimately diagnosed with Stage IVB squamous cell carcinoma of the cervix.
She completed palliative 3D conformal radiation to the left retroorbital mass and pelvis with 30 Gy over 10 fractions for both locations. Concurrent radiosensitizer chemotherapy wasn’t administered. She tolerated radiation well with mild vulvar and perineal skin toxicity, which subsequently healed without complications. Following completion of radiation, chemotherapy was initiated with carboplatin AUC 6, paclitaxel 175 mg/m2, and bevacizumab 15 mg/kg every 3 weeks. Carboplatin was selected opposed to cisplatin (unlike GOG 240) due to favorable toxicity profile.
She completed a total of six planned cycles of chemotherapy. Subsequently surveillance was planned and repeat imaging with contrast enhanced CT scan after completing six cycles of chemotherapy showed a positive response (A and B). She tolerated chemotherapy without significant side effects, and her double vision had resolved since radiation treatment to the left orbit. About 4 months after completing chemotherapy, she was found to have diffuse brain metastases detected on MRI. She received whole brain radiation therapy with 30 Gy over 10 fractions. Shortly after that she developed right cerebellar intracranial hemorrhage from hemorrhagic metastasis, obstructive hydrocephalus and bilateral cerebellar tonsillar herniation leading to brain stem compression and death.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [0.67, 'mg/dL'], 'age': [72, 'years']}",92.80704,88.16669,97.44739,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 72 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.67 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.67/0.7)**-0.241 * 0.9938**72 * 1.012 = 92.80704.
Hence, the GFR value is 92.80704 ml/min/1.73 m²."
592,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4546076-1,Extracted,"A 60-year-old woman with lupus nephritis and ischemic cardiomyopathy developed emesis, abdominal discomfort, diarrhea and acute renal allograft dysfunction 6 months after combined heart-kidney transplantation. The most recent kidney transplant was her third and was performed through a midline abdominal incision. The right common iliac artery and vein were used for inflow and outflow, respectively. Maintenance immunosuppression included tacrolimus, mycophenolate mofetil, and prednisone. Fluconazole was recently re-initiated for prophylaxis against fungal infections.
Physical examination was remarkable for blood pressure 98/64 mmHg, pulse 111 bpm, minimal skin tenting, mild diffuse abdominal tenderness including over the renal allograft, and coarse resting upper extremity tremors. Laboratory testing revealed macrocytic anemia (hemoglobin 10.1 g/dL; normal: 12–15.5) and metabolic acidemia (bicarbonate 18 mmol/L; normal: 22–29). Serum creatinine was elevated at 4.2 mg/dL (normal: 0.8–1.3; baseline: 1.0). Urinalysis was notable for mild proteinuria, hematuria, pyuria, and renal epithelial cells. Serum BK virus levels by PCR were elevated (73,300 copies/mL). A 12-h tacrolimus trough level was supratherapeutic at 27.8 ng/mL (goal: 5–8 ng/mL).
Renal allograft ultrasound showed hydronephrosis and a CT scan of the abdomen and pelvis (Fig. ) demonstrated significant dilatation of the cecum and proximal allograft ureter (arrow). She underwent surgical exploration. The distal small bowel and proximal colonic mesentery had herniated posterior to the intraperitoneal allograft ureter (Fig. ), resulting in cecal volvulus and allograft ureteral obstruction. A right hemicolectomy was performed. Postoperatively, she experienced no significant complications. Tacrolimus and fluconazole were temporarily discontinued. Within a few weeks, her renal allograft function improved (serum creatinine 0.9 mg/dL) and BK virus levels were reduced in the setting of reduced immunosuppressive drug target levels.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [4.2, 'mg/dL'], 'age': [60, 'years']}",11.52463,10.9484,12.10086,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 60 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 4.2 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (4.2/0.7)**-1.2 * 0.9938**60 * 1.012 = 11.52463.
Hence, the GFR value is 11.52463 ml/min/1.73 m²."
593,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5637966-1,Extracted,"A 50-year-old Filipino woman with a past medical history of MCTD, diagnosed 7 years prior, presented to the emergency department with complaints of shortness of breath, chest pain with a “bubble” like sensation, and diaphoresis with minimal exertion. She also had positive Raynaud’s phenomenon. Ten days prior she went to the emergency department for self-limited shortness of breath at which time her creatinine (CRE) was 0.8 mg/dL. Two months prior she was started on hydroxychloroquine 400 mg/day and prednisone 60 mg/day for a MCTD flare that manifested as muscle weakness. Her other home medications were amlodipine 5 mg/day, aspirin 81 mg/day, topical nitroglycerin to fingers 6 times/day as needed, alendronate 70 mg/week, and calcium carbonate/vitamin D3 daily. She has never smoked, never used illicit drugs, and denies consumption of alcoholic beverages.
The patient’s vital signs were unremarkable with a blood pressure reading of 116/80 mm Hg. Physical examination was remarkable for mild distress, a systolic murmur, crackles to mid lung fields, and a blanchable maculopapular rash on the chest.
Complete blood count reveled a leukocyte count of 9.1/mm3 and a platelet count of 205 000/mm3. Hemoglobin was 8.3 g/dL. Biochemical investigations were remarkable for elevated serum urea (53 mg/dL) and CRE (4.3 mg/dL). Liver enzyme tests revealed a total bilirubin of 1.5 mg/dL, an alanine transaminase level of 70 IU/L, and an alkaline phosphatase level of 124 IU/L. Serum lactate dehydrogenase was 343 U/L, and serum haptoglobin was 38 mg/dL (ref 30-200 mg/dL). Urine analysis revealed ++protein, ++white blood cells, 10 to 20 RBC/hpf (red blood cells per high-power filed), and granular casts. Urine microscopy was not done due to suspected diagnosis being MCTD flare. Her spot urine protein to creatinine ratio was 0.8 g/day. Her autoimmune workup was positive for speckled antinuclear antibody (1 in 2560), anti-RNP-topoisomerase I and -Smith antibodies. Complements C3 and C4 were decreased (39 and 7 mg/dL, respectively). Anti–double stranded DNA, -Scl 70, -JO1, -SS-A, -SS-B, and -centromere antibodies were negative. Cytoplasmic-staining (C)-ANCA and perinuclear-staining (P)-ANCA were both negative.
Abdominal ultrasound revealed gallbladder wall thickening. Computed tomography of the chest without contrast showed fibrotic inflammatory changes in the posterior basal segments, bronchial thickening with infiltrates suggestive of bronchopneumonia, an enlarged pulmonary artery, and moderate sized pleural effusions (right greater than left). Echocardiography showed an ejection fraction of 55%, a pulmonary artery pressure of 26 mm Hg, and a moderate sized pericardial effusion.
The patient was diagnosed with a MCTD flare, renal failure, and pneumonia. Hydroxychloroquine was discontinued. She was started on nifedipine, for worsening Raynaud’s phenomenon, methylprednisone 500 mg intravenous daily, vancomycin, and pipercillin/tazobactram. Her CRE continued to deteriorate (5.2 mg/dL), and her blood pressure continued to rise to 150/90 mm Hg. She was sent for a kidney biopsy. On day 4 methylprednisone was discontinued (for concern of precipitating SRC) and captopril (titrated to maximum dose within 72 hours) was started. On day 6 the patient developed oliguria and signs of hypervolemia. Hemodialysis was initiated every other day for a total of 6 sessions. The renal biopsy showed 9 available glomeruli with rare intraglomerular thrombi, moderately thickened vessels without onion skinning proliferation, or mucoid changes in their walls. No hypercellularity, necrosis, or crescent formation was seen. None of the glomeruli were globally sclerotic. One glomerulus had a thrombus within an afferent arteriole at the hilum (). Multiple red cell casts within tubular lumina were noted with mild interstitial fibrosis. The tubules were dilated with flattening of the tubular epithelial cells, suggestive of marked acute tubular injury. Immunofluorescence microscopy revealed no deposition of IgG, IgA, IgM, C3, and C1q. There was no evidence of SRC or other forms of hemolytic-uremic syndrome (HUS)-type thrombotic microangiopathy. The findings of intraglomeruli thrombi were most compatible with thrombotic thrombocytopenia (TTP).
On day 8 the patient became acutely altered. Her complete blood count reveled a platelet count of 80/mm3 and hemoglobin level of 5.8 g/dL. Laboratory data revealed an elevated lactic acid dehydrogenase level of 466 U/L and a decreased haptoglobin level of <10 mg/dL. Complements C3 and C4 were both still decreased (42 and 6 mg/dL, respectively), and serum cardiolipin IgG was positive. A peripheral smear revealed fragmented red blood cells and anisocytosis. She was transfused multiple units of packed red blood cells without improvement. Due to the worsening MAHA along with the aforementioned presentation she was started on plasma exchange (using thawed plasma at 1.0 volume exchanges) for presumed thrombotic thrombocytopenia. On day 9 laboratory values for ADAMT-13 and atypical HUS (aHUS) were drawn and sent out. Methylprednisone 500 mg intravenous daily and mycophenolate at 1000 mg twice daily (chosen over cyclophosphamide due to lack of crescents, pauci-immune glomerulonephritis, and necrotizing inflammation on renal biopsy) were added to further control the MCTD flare. Treatment with eculizumab was considered but the patient refused. Daily pulse dose steroids at 500 mg was restarted with plasma exchange and continued (total of 6 exchanges received) until day 11. There was minimal response of a rise in platelets to plasma exchange with a count of 79/mm3 after her last treatment. Her last hemodialysis received was on day 13 at which time her CRE was 4.8 mg/dL. Over the month of hospitalization her serum CRE and urine output continued to improve and she was discharged with a CRE of 1.7 mg/dL and platelet count of 273/mm3. Her discharge medications were mycophenolate 500 mg twice daily, nifedipine extended release 60 mg/day, and lisinopril 20 mg/day. She was seen in clinic 6 weeks later, and her serum CRE had returned to 0.8 mg/dL. ADAMTS-13 activity later resulted as 67%, but was drawn after first plasma exchange session. The complement serologies for aHUS were sent to an outside speciality lab for processing, but the blood work was not resulted to improper collection.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [50, 'years'], 'creatinine': [0.8, 'mg/dL']}",89.70737,85.222,94.19274,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 50 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.8 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.8/0.7)**-1.2 * 0.9938**50 * 1.012 = 89.70737.
Hence, the GFR value is 89.70737 ml/min/1.73 m²."
594,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4421570-1,Extracted,"A 39-year-old female presented with an 8-day history of fever, myalgia, back pain, nausea and vomiting, visual impairment, anuria and weight gain of 9 kg within 1 week. Neither cough nor dyspnea was reported. She had no previous medical history and no regular medication. She is a florist by profession and exposed to moss collected in the forest. She does regular mountain biking tours.
On admission, she was severly ill. Jugular vein congestion was present; auscultation and percussion of the lungs were pathologic. The abdomen was tender and painful on palpation and suspicious for ascites. All other findings were unremarkable. Abnormal laboratory findings on admission were white blood count (WBC) 13/nL, platelets 84 /nL, lactate dehydrogenase (LDH) 285 U/L, creatinine 5.4 mg/dL, urea 69 mg/dL, uric acid 6.5 mg/dL and C-reactive protein (CRP) 68 mg/L (normal < 5) as well as proteinuria and hematuria. All other values were unremarkable.
Kidney ultrasound revealed bilateral kidney enlargement with hyperechogenic parenchyma. A chest X-ray and abdominal computed tomography (CT) (non-enhanced due to renal impairment) were performed with the findings presented in .","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [5.4, 'mg/dL'], 'age': [39, 'years']}",9.71348,9.22781,10.19915,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 39 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 5.4 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (5.4/0.7)**-1.2 * 0.9938**39 * 1.012 = 9.71348.
Hence, the GFR value is 9.71348 ml/min/1.73 m²."
595,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7798777-1,Extracted,"A 75-year-old female presented to the emergency department with dyspnoea. She had been treated for recurrent lower respiratory tract infections by the general practitioner (GP) with oral antibiotics (12 cases in the past 14 months). Her relevant medical history included chronic kidney disease stage 3 (baseline creatinine 80–110 µmol/L), polymyalgia rheumatica requiring long-term steroids, asthma and chronic back pain. The pneumonia diagnosis was confirmed by a chest radiograph and CT showing multifocal nodular consolidation in the right lower lobe with cavitations and blood cultures were taken that grew Staphylococcus aureus.
Her medical history otherwise included depression, hypercholesterolaemia, gastro-oesophageal reflux disease, spondylosis, glaucoma, hypertension, lacunar stroke, transient ischaemic attack, vitamin B12 deficiency and vascular dementia.
Her long-term treatment included hydromorphone, paracetamol, topiramate, paracetamol–codeine–doxylamine, doxylamine, colecalciferol, aspirin, duloxetine, pantoprazole, prednisolone, docusate, macrogol, hydroxocobalamin, salbutamol and denosumab.
On presentation, she was initially afebrile, heart rate of 95 bpm, respiratory rate of 25 breaths per minute and oxygen saturation of 96%. On examination, there were crackles on the right base, dual heart sounds with no murmurs and no peripheral stigmata of infective endocarditis. She was subsequently treated for pneumonia and urinary tract infection with intravenous piperacillin–tazobactam. The working diagnosis was S. aureus bacteraemia secondary to a pulmonary source.
The patient was transferred to the closest tertiary hospital as the eventual need for further investigations, including a trans-oesophageal echo, was anticipated in the context of S. aureus bacteraemia. The treatment of her bacteraemia was eventually changed to intravenous flucloxacillin (2 g four times daily) once sensitivities were confirmed. Flucloxacillin was planned to continue for a further 5 weeks via peripherally inserted central catheter (PICC) on an 8 g/24 hours infuser that was monitored via hospital in the home (HITH).
Four weeks into the HITH treatment, the patient developed nausea and was investigated with blood results that showed worsening renal function associated with HAGMA. She was subsequently referred back to the regional hospital. Her heart rate was 105 bpm, respiratory rate of 20 breaths per minute and O2 sat 98% on room air. At that point, HAGMA was attributed to an acute kidney injury (AKI). Following adequate fluid resuscitation, HAGMA and AKI persisted. She was investigated for the AKI with a renal ultrasound which was negative and there were no eosinophils found in the urine. Interstitial nephritis secondary to flucloxacillin use was considered as another reason for her AKI but was deemed unlikely. The treatment plan was to commence sodium bicarbonate 840 mg once daily following consultation with the renal team. Ultimately, further investigations for the AKI were completed at the tertiary hospital. The HAGMA was suspected to be caused by the concurrent use of flucloxacillin and paracetamol. As a result of this, flucloxacillin was changed to cefazolin and the patient transferred again to a tertiary facility pending further investigations as well as suspected pulmonary embolism following reports of chest pain.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [110.0, 'µmol/L'], 'age': [75, 'years']}",45.20916,42.9487,47.46962,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 75 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 110.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 110.0 µmol. To convert 110.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 110.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00011 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00011 mol Serum Creatinine * 113.12 g/mol = 0.01244 g Serum Creatinine. To convert 0.01244 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01244 g Serum Creatinine * 1000.0 mg/g = 12.44 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 12.44 mg Serum Creatinine/10.0 dL = 1.244 mg Serum Creatinine/dL. The concentration value of 110.0 µmol Serum Creatinine/L converts to 1.244 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.244/0.7)**-1.2 * 0.9938**75 * 1.012 = 45.20916.
Hence, the GFR value is 45.20916 ml/min/1.73 m²."
596,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6964363-1,Extracted,"The patient was an 82-year-old white male with a history of ischemic cardiomyopathy status postcardiac stenting, history of heart failure with reduced ejection fraction (HFrEF with ejection fraction (EF): 20–25%) with implantable cardiac defibrillator (ICD), chronic atrial fibrillation on dabigatran, obstructive sleep apnea (OSA), chronic kidney disease (CKD) stage III, carpal tunnel syndrome, and gout who presented with fatigue, acute hematuria, and urinary retention. He was a nonsmoker, did not endorse regular alcohol use, and denied any illicit drug use. His family history was noncontributory. His vitals at presentation were temperature 36.3°C, heart rate 80 beats per minute, blood pressure 100/70 mm Hg, and oxygen Saturation 93% on room air. Home medications included bumetanide 1 mg daily, metolazone 1.25 mg twice a week, carvedilol 12.5 mg daily, and dabigatran 75 mg twice a day. Complete blood count (CBC) was unremarkable, and basic metabolic panel (BMP) showed creatinine of 2.2 mg/dl (near baseline). NT-pro-BNP was elevated at 18,500 pg/ml (baseline 2000s). Troponin was elevated at 0.36 ng/ml.
Urology was consulted, and patient underwent cystoscopic evaluation for hematuria. Clot evacuation and fulguration of diffuse bladder lesions were performed. Bladder biopsy was also obtained, and subepithelial amyloid deposits were identified based on Congo-red stain.
In the following days, the patient developed intermittent episodes of atrial fibrillation with rapid ventricular rate, hypotension, liver dysfunction, and acute kidney injury secondary to acute tubular necrosis. Aspartate aminotransferase (AST) peaked at 3000 (U/L) and alanine aminotransaminase (ALT) at 2000 (U/L). Remaining liver function tests showed alkaline phosphatase 50 (U/L), bilirubin 3-4 mg/dl, hyperammonemia (72 mcmol/L) and elevated international normalized ration (INR) around 4. Computed tomography imaging of chest, abdomen, and pelvis was negative for any acute process but showed cardiomegaly that was seen in the plain chest radiography as well. Workup for any acute infectious or inflammatory processes (viral markers, acetaminophen levels, and autoimmune markers) for evaluation of acute liver dysfunction did not reveal any alternate diagnosis, thereby suggesting acute decompensation from shock liver.
Echocardiogram demonstrated worsening of ejection fraction (EF) to 10–15% with concentric left ventricle hypertrophy, impaired left ventricular diastolic dysfunction, thickened interventricular septum more than 12 mm, normal biventricular dimensions, biatrial dilation with no significant valvular abnormalities (findings compatible with cardiac amyloidosis) (). Magnetic Resonance Imaging (MRI) was not performed due to underlying CKD. His condition continued to deteriorate, and he was transferred to the cardiac care unit for acute decompensated heart failure. He was started on milrinone infusion with transient improvement in his cardiac function and end organ perfusion.
He was evaluated for cardiac resynchronization therapy upgrade but deemed unstable from medical standpoint to undergo the procedure.
Hematology team was consulted and performed biochemical workup for amyloidosis. Serum protein electrophoresis (SPEP) did not show an M-spike. Serum-free light analysis (kappa/lambda ratio 2.9) and urine immunofixation studies were not significant ruling out evidence for plasma cell dyscrasias. Meanwhile, the mass spectrometry analysis of the bladder biopsy specimen confirmed wild-type transthyretin (ATTRwt) consistent with senile systemic amyloidosis. Immunohistochemical analysis was not performed as mass spectrometry has been demonstrated to be a well-validated technique to diagnose and classify amyloidosis [, ]. Genetic testing can help clarify if the disease was hereditary or not but was not performed in this case and remains a limitation.
Multiple specialties including internal medicine, hematology, cardiology, and critical care were involved in the patient care, but despite aggressive management, patient's condition gradually deteriorated. Due to the poor prognosis in the setting of multiple comorbidities and decompensated heart failure, the patients' family decided to stop further treatment and focus on patients comfort only which was facilitated by the palliative care team. The patient passed away shortly thereafter from cardiac arrest, and the diagnosis was acute on chronic cardiac failure from senile systemic amyloidosis.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [2.2, 'mg/dL'], 'age': [82, 'years']}",29.17357,27.71489,30.63225,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 82 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.2 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.2/0.9)**-1.2 * 0.9938**82 * 1.0 = 29.17357.
Hence, the GFR value is 29.17357 ml/min/1.73 m²."
597,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5573093-1,Extracted,"A 36-year-old woman with X linked AS (COL4A5, very rare heterozygous nonsense mutation-c.1117C>T, p.Arg373stop in exon 19), chronic kidney disease, hypertension, and obesity presented to the emergency room with the acute onset of substernal chest and neck pain. Chest pain was associated with exertion. Her pain radiated to both arms and was associated with numbness. She did not have a past history of oral contraceptive pill use and was not pregnant at this time. She was previously prescribed lisinopril for hypertension; however her blood pressure was poorly controlled due to noncompliance in taking her medication over the past month. Her blood pressure was 150/100 mmHg six weeks prior to the admission.
The patient was diagnosed with AS at 23 years of age when she was being considered as a kidney donor for her brother. The diagnosis of AS was confirmed by genetic test and renal biopsy. She was asymptomatic at that time and had no renal, ocular, or auditory manifestations of AS. Later, she developed chronic kidney disease and hypertension. She denied a history of tobacco use/abuse. There was a family history of AS in her brother with AS who underwent two renal transplantations.
On physical exam she had a temperature of 36.3°C, a blood pressure of 152/100 mmHg, a heart rate of 60 beats per minute, and a respiratory rate of 10 breaths per minute. Repeat blood pressure in the ER was 138/88 mmHg. ECG showed transient 1 mm ST-segment elevation in the inferior leads (II, III, and aVF). The serum troponin I was 28 ng/ml (normal range 0–0.01 ng/ml). Serum creatinine was 2.19 mg/dL.
Heparin and aspirin were promptly administered. A decision was made to perform emergent coronary angiography, which showed a localized dissection (red arrow in ) of the mid left circumflex coronary artery. This dissection resulted in a luminal compression of the coronary artery leading to 40% narrowing of its lumen. Percutaneous balloon angioplasty and drug eluting stent placement (blue arrow in ) were successfully performed. Echocardiography revealed a normal ejection fraction with mild inferolateral wall hypokinesis. She improved clinically with resolution of the chest pain. Following the procedure, she received aspirin, prasugrel, metoprolol tartrate, amlodipine, and atorvastatin. During the hospitalization, her blood pressure was in the range of 118–141/64–89 mmHg.
Six months after procedure she presented to a clinic with a complaint of dyspnea on exertion and atypical chest pain. An exercise stress test with echocardiography did not demonstrate ischemia.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [2.19, 'mg/dL'], 'age': [36, 'years']}",29.22922,27.76776,30.69068,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 36 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.19 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.19/0.7)**-1.2 * 0.9938**36 * 1.012 = 29.22922.
Hence, the GFR value is 29.22922 ml/min/1.73 m²."
598,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6429644-1,Extracted,"Our patient is a 73-year-old Chinese woman with history of hepatitis B, hypertension, insulin-dependent diabetes mellitus, chronic kidney disease (stage III), and hepatocellular carcinoma (HCC), who initially presented to the hospital for elective trans-arterial embolization of the HCC. She successfully underwent bland embolization of the right hepatic lobe for the HCC, but was admitted for monitoring due to concern for post-embolization syndrome with right upper quadrant pain, low grade fever, and elevation of transaminases and bilirubin. Over the next 48 h, she developed encephalopathy and oliguria with an upward trending creatinine to 4.36 mg/dL from a baseline value of 2.0 mg/dL, along with azotemia of 80 mg/dL. She was subsequently transferred to the medical intensive care unit (ICU) to receive urgent hemodialysis (HD) for contrast-induced acute tubular necrosis. The patient tolerated her initial dialysis session well; no fluid was removed. She underwent a repeat HD session on the second day. Approximately 20 min after starting HD, the patient became dyspneic and complained of back pain. She was noted to have tachycardia and hypotension with heart rate in the 140 beats/min range and blood pressure of 90/50 mm Hg, respectively. Her respiratory rate was 30 breaths/min and her oxygen saturation in the low 80s.
On physical examination, the patient was found to have audible inspiratory stridor and was given two doses of racemic epinephrine via nebulizer along with 10 mg dexamethasone intravenous injection. HD was stopped and her symptoms improved. The following day, another session of HD was attempted. She again developed dyspnea, tachycardia, and hypotension. Dialysis was stopped and the decision was made to change the HD filter from an EO sterilized filter to a polyethersulfone dialyzer which is steam sterilized. HD was re-initiated with the new filter. Patient symptoms improved and she tolerated the remainder and subsequent sessions of HD without any further complication. Sepsis was considered; this was, however, ruled out with chest imaging that did not reveal infiltrates suggestive of infection and negative blood and urine cultures. The post-embolization syndrome resolved during the ICU stay.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [4.36, 'mg/dL'], 'age': [73, 'years']}",10.16317,9.65501,10.67133,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 73 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 4.36 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (4.36/0.7)**-1.2 * 0.9938**73 * 1.012 = 10.16317.
Hence, the GFR value is 10.16317 ml/min/1.73 m²."
599,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5120452-1,Extracted,"A 72 year old African male from Wum, in the far North west region of Cameroon, presented with a 3 year history of lower urinary tract symptoms (LUTS) both obstructive and irritative in nature; and an International Prostate Symptom Score (IPSS) of 22 with a moderate degree of bother, which culminated in an episode of acute urinary retention for which he sought a consult at our health services. The patient like most in his neighbourhood used water from a nearby stream for his baths and claims he had never received any preventive chemotherapy against schistosomiasis.
On examination, the patient was anxious with a tender, renitent hypogastic swelling which increased the zeal to urinate on palpation. A diagnosis of bladder outlet obstruction due to a benign prostate hypertrophy was advocated. Blood samples were collected and a transurethral catheter was placed which relieved the symptoms; with collection of 800 ml of clear urine.
Results of investigations showed: a normal full blood count; prostate specific antigen value of 4.21 ng/dl; normal size and structure of the prostate on ultrasound; serum urea = 321 mg/dl, serum creatinine = 3.2 mg/dl, serum K+ = 6 mEq/l and a microscopic haematuria on urinalysis. A follow up renal ultrasound showed a decrease in the size of the kidneys.
On day 2, the patient started having macroscopic hematuria with blockage of urinary catheter. A suprapubic puncture was done with extraction of several live worms which were confirmed to be S. haematobium in the laboratory (Fig. ). The patient was then placed on praziquantel 40 mg/kg and hemodialysis.
Day 6 of hospitalization was marked by the onset of pyuria and fever and the patient was placed on broad spectrum antibiotics and a urine culture requested. We finally lost the patient on day 9 of admission due to sepsis from a urinary tract infection.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [3.2, 'mg/dL'], 'age': [72, 'years']}",19.80281,18.81267,20.79295,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 72 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 3.2 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (3.2/0.9)**-1.2 * 0.9938**72 * 1.0 = 19.80281.
Hence, the GFR value is 19.80281 ml/min/1.73 m²."
600,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-10636,Extracted,"A 68-year-old female presents to her primary care physician with a 7-month history of fatigue and low back pain. Her pain is not improved by over the counter analgesics. Laboratory analysis is notable for a calcium level of 11.5 mg/dL, creatinine level of 2.0 mg/dL, and blood urea nitrogen level of 30 mg/dL. Large eosinophilic casts are seen on renal biopsy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [2.0, 'mg/dL'], 'age': [68, 'years']}",26.7105,25.37497,28.04603,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 68 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 2.0 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (2.0/0.7)**-1.2 * 0.9938**68 * 1.012 = 26.7105.
Hence, the GFR value is 26.7105 ml/min/1.73 m²."
601,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6165619-1,Extracted,"An 18-year-old male with no past medical history presented as an outside hospital transfer for acute respiratory failure. Approximately 2 months before, he began to have a cough associated with intermittent hemoptysis. He was evaluated at an urgent care clinic and received antibiotics without resolution of his symptoms. At that time, his renal function and urinalysis were within the normal limits. He denied history of joint pain or subjective joint swelling. Dyspnea progressed, and he was taken to his local hospital. On transfer, patient was intubated and on mechanical ventilation.
On physical examination, he was intubated and sedated. Lungs were with coarse breath sound bilaterally. There was bilateral swelling of his knees.
Laboratory studies showed hemoglobin of 8.4 g/dL, WBC count of 5.6/L with a lymphopenia, platelet count of 126/L, creatinine of 1.6 mg/dL, INR of 1, and PTT of 26.6 seconds. Urinalysis was with 41 red blood cells, and protein to creatinine ratio was 0.94. Anti-nuclear antibody (ANA) was greater than 12, anti-dsDNA was 507 IU/mL, C3 was 63 mg/dL, C4 was 8 mg/dL, and anti-cardiolipin IgM was 15.8 mpl.
His anti-smith,anti-MPO,anti-PR3,anti-cardiolipin IgG, anti-beta 2 glycoproteins IgG/IgM, anti-GBM, lupus anticoagulant, and cryoglobulins were negative.
Blood and sputum cultures were negative. Chest X-ray showed bibasilar airspace disease (Figure ). Bronchoalveolar lavage showed progressively hemorrhagic aliquots (Figure ).
He was treated with pulse dose methylprednisolone for three days, one dose of intravenous cyclophosphamide, and five days of plasmapheresis. Shortly after, he was extubated and weaned to room air. His hemoptysis resolved with stabilization of his hemoglobin. He was discharged in the stable condition.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.6, 'mg/dL'], 'age': [18, 'years']}",63.65276,60.47012,66.8354,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 18 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.6 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.6/0.9)**-1.2 * 0.9938**18 * 1.0 = 63.65276.
Hence, the GFR value is 63.65276 ml/min/1.73 m²."
602,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-7716301-1,Extracted,"An 85-year-old female presented to emergency room with vomiting and abdominal pain.
An elderly female patient presented with symptoms of intermittent abdominal pain around epigastric and umbilical area. The pain was dull aching 5/10 intensity that had been present for 1 mo and gradually worsened over the last 2 wk. The abdominal pain was non-radiating, exacerbated by food intake and had no associated relieving factors. Vomiting intermittently for the last 2 wk and increased in intensity over the past 48 h; it was non-blood stained and non-foul smelling. The patient had a history of loss of appetite and weight loss of about 15 Lbs. over the 1-mo duration. Her last bowel movement was 2 d prior to admission, with a normal consistency but black tarry in color. Review of systems unremarkable.
Past medical history included hypertension, cerebrovascular accident, diabetes, and chronic kidney disease stage 3. Family history did not reveal anything of significance to her present illness.
Family history did not reveal anything of significance to her present illness.
Heart rate of 110 beats per minute, blood pressure of systolic 80’s, temperature 36.4 °C, respiratory rate of 18. The patient abdomen was mildly distended, with tenderness in the mid epigastric region, no organomegaly, and normal bowel sounds.
Blood tests revealed elevated troponin of 86, electrocardiogram showed ST segment depressions likely demand ischemia from the acute illness. Basic metabolic panel showed creatinine of 3.1 (baseline was 1.4), potassium of 3.2, alkaline phosphatase of 177, Alanine transaminase of 53, aspartate transaminase of 53, and lactic acid of 2.3. On complete blood count, her white cell count of 20.78 neutrophilic leukocytosis, and hemoglobin of 9.8.
An abdominal computed tomography (CT) scan showed a 4.5 cm × 4.7 cm partially calcified mass at the gastric pylorus causing gastric outlet obstruction (Figure ).
Endoscopy showed an ulcerated fistulous opening and a large 5 cm impacted gallstone in the duodenal bulb (Figure ). Endoscopic nets and baskets were used in an attempt to remove the stone, but this approach was unsuccessful.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [3.1, 'mg/dL'], 'age': [85, 'years']}",14.20257,13.49244,14.9127,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 85 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 3.1 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (3.1/0.7)**-1.2 * 0.9938**85 * 1.012 = 14.20257.
Hence, the GFR value is 14.20257 ml/min/1.73 m²."
603,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6188736-1,Extracted,"The patient was a 60-year-old man who was diagnosed with alcoholic liver cirrhosis and type 2 diabetes when he was 50 years old. His drinking history was 540–720 mL Japanese sake per day for 35 years, and his smoking history was 30 cigarettes per day for 30 years. His ascites increased in 2008 when he was 57 years old, and he repeatedly exhibited symptoms of hepatic encephalopathy. Due to the liver cirrhosis symptoms, the patient was treated with several medications including furosemide, spironolactone, lactulose, and total amino acid preparation. To prevent the complications of liver cirrhosis, coil embolization to a portal venous shunt was performed twice. The patient was admitted to our hospital in June 2012 because of slowly progressive renal impairment and nephrotic syndrome.
Upon admission, the patient's height and weight were 166 cm and 64 kg, respectively. His body temperature was 36.7°C and his blood pressure was 150/60 mmHg. His consciousness was clear. His abdomen was slightly expanded but exhibited no tenderness. The liver and spleen were not palpable. No rash or purpura was noted on the skin. Diabetic and/or hypertensive changes were not observed in the ocular fundus.
The laboratory findings on admission were hemoglobin level of 9.4 g/dL (normal range 13.5–17.6 g/dL), platelet count of 11x104/μL (normal range, 13.1–36.2x104/μL), prothrombin time measurement of 68% (normal range, 70–130%), total bilirubin level of 0.9 mg/dL (normal range, 0.3–1.2 mg/dL), NH3 level of 85 mg/dL (normal range, 30–80 mg/dL), blood urea nitrogen level of 41 mg/dL (normal range, 8–20 mg/dL), serum creatinine concentration of 1.77 mg/dL (normal range, 0.5–1.1 mg/dL), serum total protein level of 5.7 g/dL (normal range, 6.7–8.3 g/dL), serum albumin level of 2.1 g/dL (normal range, 3.5–5.2 g/dL), total cholesterol of 188 mg/dL (normal range, 120–219 mg/dL), and HbA1c of 5.8% (normal range, 4.3–5.8%). The serum levels of IgG were 1558 mg/dL (normal range, 870–1700 mg/dL), of IgA were 481 mg/dL (normal range, 110–410 mg/dL), of IgA1 were 398 mg/dL (normal range, 50–314 mg/dL), of IgA2 were 83 mg/dL (normal range, 10–156 mg/dL), and of IgM were 219 mg/dL (normal range, 35–220 mg/dL). The serum levels of free κ and λ light chains were 149.0 mg/L (normal range, 3.3–19.4 mg/L) and 106.0 mg/L (normal range, 5.7–26.3 mg/L). The serum free light chain ratio was within normal range. The serum level of complement factor C3 was 79 mg/dL (normal range, 65–135 mg/dL), of C4 was 17 mg/dL (normal range, 13–35 mg/dL), and of CH50 was 41.1 U/mL (normal range, 30–50 U/mL). All of the other serology findings including anti-nuclear antibody, hepatitis B virus surface antigen, hepatitis C virus antibody, anti-neutrophil cytoplasmic antibody, and anti-glomerular basement membrane antibody were negative. There was no M-spike on serum and urine protein electrophoresis. A serum test for a cryoglobulin precipitation was negative.
The urinary sediments showed many red blood cells in high power fields together with granular casts and dysmorphic red blood cells. The urinary protein excretion was 4.7 g/day. The 24-hour creatinine clearance was 45 mL/min. Computed tomography revealed liver deformity with moderate accumulation of ascites. The kidneys were normal in size and there were no signs of urinary tract obstruction.
The renal biopsy specimens contained a total 28 glomeruli, 12 of which were globally sclerotic. The degree of interstitial fibrosis/tubular atrophy was 50–60% of the total biopsy specimen identified. Moderate fibrous intimal hyperplasia was observed in the arcuate artery. Diffuse segmental double-contours of the glomerular basement membrane and mesangial cell hypercellularity were identified in nonsclerotic glomeruli, exhibiting a membranoproliferative glomerulonephritis-like pattern (). Some glomeruli showed moderate-to-severe endocapillary hypercellularity, accompanied by fibrocellular crescents (). Fluorescent immunostaining showed granular staining of IgA and C3, but not of IgG, IgM, or C1q, on glomerular capillaries and some mesangial areas (Figures –). Among the IgA subtypes, staining of IgA1 (GenWay Biotech, San Diego, CA, USA) was observed, but staining of IgA2 (GenWay Biotech) was not identified (Figures and ). With light chain immunostaining, only κ (SouthernBiotech, Birmingham, AL, USA) was identified and no λ staining (SouthernBiotech) was seen (Figures and ). On electron microscopy, the glomerular capillary walls showed double contours. Electron-dense deposits were found in the paramesangium and around the subendothelial space of the glomeruli (). No organized structure deposits were identified (). Based on these findings, this case was histologically diagnosed as diffuse membranoproliferative glomerulonephritis with monoclonal IgA1-κ deposits.
Because this case was accompanied by moderately advanced decompensated liver cirrhosis, there was a concern that the patient may have serious side effects due to aggressive treatment such as the administration of corticosteroids. Thus, supportive treatment based on medications such as RAS inhibitors/diuretics, in addition to dietary therapy including salt restriction/branched-chain amino acid administration, was selected. Although these treatments led to a modest decrease in the urinary protein excretion, the patient's renal dysfunction slowly progressed and finally resulted in end-stage renal failure and initiation of dialysis therapy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.77, 'mg/dL'], 'age': [60, 'years']}",43.42612,41.25481,45.59743,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 60 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.77 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.77/0.9)**-1.2 * 0.9938**60 * 1.0 = 43.42612.
Hence, the GFR value is 43.42612 ml/min/1.73 m²."
604,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,usmle-7828,Extracted,"A 46-year-old man presents to a clinic with a complaint of intermittent flank pain bilaterally for 5 days. The pain is colicky in nature and radiates to the groin. The patient took an old prescription (hyoscyamine) and got some relief. He has nausea, but had not vomited until now. Although he has a history of renal stones, he denies any blood in the urine or stool and gives no history of fevers, changes in bowel habits, or abdominal distension. He does not have joint pain. On examination of the abdomen, the is no organomegaly and the bowel sounds are normal.
The blood test report reveals the following:
Serum calcium 8.9 mg/dL
Serum uric acid 8.9 mg/dL
Serum creatinine 1.1 mg /dL
The urinalysis shows the following:
pH 6.0
Pus cells none
RBCs 1–2/HPF
Epithelial cells 1/HPF
Protein negative
Ketones negative
Crystals oxalate (plenty)
An abdominal ultrasound shows echogenic medullary pyramids with multiple dense echogenic foci in both kidneys, that cast posterior acoustic shadows.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.1, 'mg/dL'], 'age': [46, 'years']}",83.84203,79.64993,88.03413,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 46 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 1.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.1/0.9)**-1.2 * 0.9938**46 * 1.0 = 83.84203.
Hence, the GFR value is 83.84203 ml/min/1.73 m²."
605,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3816164-1,Extracted,"A 63-year-old Korean woman with a past medical history of hypertension and a 25-year history of SLE presented with a 3-week history of shortness of breath. She had been treated with hydroxychloroquine 400 mg/day and varying doses of prednisone between 5 and 15 mg/day for the SLE. Additionally, the hypertension was under control with carvedilol 25 mg/day. On examination, her blood pressure was 110/70 mmHg, pulse rate was 112 beats/min, respiratory rate was 24 breaths/min, and body temperature was 36.5℃. Jugular venous distention was noted on inspection. On cardiac auscultation, her rhythm was noted to be tachycardic but regular, weak summation gallops were heard at the cardiac apex, and no pericardial friction rubs were appreciated. Blood tests showed a white blood cell count of 4000/mm3 (normal, 4300-9400/mm3), hemoglobin of 11.5 g/dL (normal, 12-14.3 g/dL) and platelet count of 67000/mm3 (normal, 169-365/mm3). The C-reactive protein level was found to be 0.29 mg/L (normal, 0-0.75 mg/L). A blood chemistry panel revealed a blood urea nitrogen level of 25.0 mg/dL (normal, 7-20 mg/dL), creatinine of 1.3 mg/dL (normal, 0.5-1.5 mg/dL), total protein of 6.7 g/dL (normal, 6.0-8.3 gm/dL), and albumin of 3.2 g/dL (normal, 3.5-4.5 mg/dL). Analysis of the urinary sediment revealed 1-4 white blood cells/high power field (hpf), many red blood cells/hpf, and trace levels of proteinuria. Cardiac enzymelabs were drawn and found to be elevated: CK-MB of 8.7 U/L (normal, 0.6-6.3 U/L), troponin-I of 0.35 ng/mL (normal, 0.0-0.2 ng/mL), and pro-brain natriuretic peptide of 8110 pg/mL (normal, 0-125 pg/mL). Chest X-ray revealed an enlarged cardiac silhouette and an electrocardiogram revealed ST elevation in leads V1-6 (). Immunofluorescence tests were negative for double-stranded DNA antibodies and anti-extractable nuclear antigen antibodies (anti-Ro and anti-La). Complement levels were found to be low (C3 0.39 g/L, normal 0.8-1.7 g/L; C4 0.04 g/L, normal 0.12-0.36 g/L). Viral markers for cytomegalovirus, Coxsackie virus B type 2, herpes simplex virus, and Epstein-Barr virus were all negative. Echocardiography demonstrated moderate left ventricular systolic dysfunction [left ventricular ejection fraction (LVEF) was 42%] with apical akinesia but no evidence of pericardial effusion (). Echocardiography performed 2 years earlier showed mild concentric left ventricular hypertrophy with a LVEF of 70%. A coronary angiography showed normal coronary arteries.
We suspected takotsubo cardiomyopathy. However there was no trigger event as physical and emotional stress. The patient was treated with angiotensin converting enzyme inhibitor, furosemide, and intravenous nitrates. The dose of glucocorticoids was between 0.5 to 1 mg/kg for the control of SLE activity. Her dyspnea gradually improved, however, a three-week follow-up echocardiography test revealed persistent apical ballooning and a newly developed apical thrombus (size, 1.10 × 2.12 cm) () with no significant improvement in LVEF. Heparin was then administered followed by oral anticoagulation therapy with warfarin. There were no embolic events during the patient's hospital stay. On the 35th day of hospital admission, follow-up echocardiography showed slightly improved wall motion of the left ventricular apex with a partially resolved thrombus and a LVEF of 50%. Although cardiac enzymes remained elevated (CK-MB 12.80 U/L and troponin-I 0.64 ng/mL), the patient was discharged on oral anticoagulation therapy.
Three months later, she was readmitted to the hospital due to a severe herpes zoster outbreak on her left shoulder. Cardiac enzymes were again found to be elevated (CK-MB 8.8 U/L and troponin-I 0.98 ng/mL). Electrocardiography revealed persistent ST segment elevation () and echocardiography revealed mild apical hypokinesia with a LVEF 50%, but no apical thrombus (). During her hospital stay she developed a mild fever and candidemia which was treated with an intravenous antifungal agent. Unfortunately, she developed septic shock and expired on day 54 of hospital re-admission.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [1.3, 'mg/dL'], 'age': [63, 'years']}",46.20522,43.89496,48.51548,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 63 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.3 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.3/0.7)**-1.2 * 0.9938**63 * 1.012 = 46.20522.
Hence, the GFR value is 46.20522 ml/min/1.73 m²."
606,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3512245-1,Extracted,"A 60-year-old female presented with a two-week history of occasional vague abdominal pain that, over a period of four days, had become more severe and localized to the right upper quadrant of the abdomen. This was associated with vomiting, which relieved pain. There was history of dyspepsia for the past 4 years. On examination, the patient was mildly dehydrated without any icterus. The abdomen was distended and tender without evidence of hernia. Bowel sounds were present. Ryle's tube aspirate was bilious and around 1 litre/24 hours. Plain radiographs of abdomen and chest were normal. Potassium and sodium levels were decreased (3.2 and 124 milli equivalent/litre). Amylase was slightly raised to the level of 125.5 IU/L. Urea and creatinine levels were 84 and 1.7 milligram/dL. Her haemoglobin level was 11.2 g/dL. The white cell counted 10 × 109/L. Liver function tests were normal.
Ultrasound examination (done on Xario XG, model number SSA 580, Toshiba color Doppler ultrasound scanner) revealed dilated stomach and duodenum till its 3rd part. No calculus was detected in gallbladder or duodenum. Liver and kidneys were normal. There was no ascites. Contrast enhanced computed tomography (CT) scan was performed on a multidetector CT scanner (Model-GE Light speed VCT XTe, whole body 64 Slice CT system, GE Healthcare, Milwaukee, USA). The scan parameters were as follows: 5 mm collimation, 2.5 mm interslice interval, 0.6 seconds rotation time, 15 mm table speed per rotation at 120 KV and automatic mA. Images were acquired in portal venous phase after injecting 90 mL of nonionic iodinated contrast material intravenously at 2.5 mL/s with a pressure injector followed by 20 mL of normal saline flush at the same rate. The multidetector computed tomography (MDCT) scan revealed a cholecysto-duodenal fistula with second part of duodenum. There was a large gallstone measuring 3.2 cm in the proximal 3rd part of the duodenum. Pneumobilia was also seen. Stomach and duodenum were dilated (Figures and ).
On laparotomy, multiple adhesions were found between stomach, gallbladder, duodenum, and omentum with inferior surface of liver. Fundus of gallbladder was adherent to 2nd part of duodenum, suggestive of a fistulous tract. The fistulous tract was excised, and the 2nd part of duodenum was opened simultaneously (). Duodenotomy was extended, and a black impacted stone was retrieved from the same site measuring 4 × 2.5 cm (Figures and ). Primary closure of oedematous duodenum was done. Covering gastrojejunostomy and cholecystectomy was also performed simultaneously. Postoperative period was uneventful, and the patient was discharged on 10th postoperative day.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [1.7, 'mg/dL'], 'age': [60, 'years']}",34.1183,32.41238,35.82422,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 60 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 1.7 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.7/0.7)**-1.2 * 0.9938**60 * 1.012 = 34.1183.
Hence, the GFR value is 34.1183 ml/min/1.73 m²."
607,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5887274-2,Extracted,"A 58-year-old man was referred with a 4-week history of fatigue, dyspnoea and a dry cough. Routine blood tests revealed an increased creatinine of 250 µmol/L from 97 µmol/L. He had been on adalimumab 40 mg monthly for 5 years for rheumatoid arthritis (RA).
On physical examination he had bibasal coarse crepitations, with a BP of 140/86 mmHg and a bland urine dipstick. His creatinine increased to 555 µmol/L with a urea of 38 mmol/L, resulting in clinical uraemia. A pyraexia (38.2°C) developed, with rapidly worsening respiratory symptoms. CT of the thorax showed diffuse ground glass change and bilateral mediastinal lymphadenopathy. He was commenced on intermittent haemodialysis. Antimicrobial treatment was initiated with intravenous amoxicillin/clavulanic acid, oral clarithromycin, clindamycin and primaquine.
Blood tests showed a peak corrected calcium of 3.05 mmol/L. Serum ACE levels were elevated at 100 UECA. A vasculitic screen, connective tissue screen, complement levels, serum protein electrophoresis and immunoglobulin levels were normal. Blood cultures, hepatitis, HIV screen, Chlamydia, Brucella, Mycoplasma and leptospirosis serology were negative. Extensive testing to exclude TB as the unifying diagnosis was negative. Bronchoscopy and bronchoalveolar lavage samples were negative for Pneumocystis pneumonia, cytomegalovirus, TB and cryptococcal antigen. There was no relevant travel or occupational exposure to indicate further testing for histoplasmosis. Antimicrobial therapy was discontinued.
Renal biopsy showed granulomatous nephritis without evidence of necrosis. An endobronchial ultrasound and fine-needle aspiration cytology demonstrated granulomatous lymphadenitis.
Adalimumab was withdrawn and empiric prednisolone 60 mg daily was commenced. He remained dialysis dependent for 3 months. Four months after discontinuing adalimumab, dialysis was successfully stopped and steroid therapy was tapered slowly. His kidney function stabilized to a creatinine of 160 μmol/L with resolution of his respiratory symptoms clinically and radiographically. He is currently on methotrexate with good control of his RA.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [160.0, 'µmol/L'], 'age': [58, 'years']}",42.8062,40.66589,44.94651,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 58 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 160.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 160.0 µmol. To convert 160.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 160.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00016 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00016 mol Serum Creatinine * 113.12 g/mol = 0.0181 g Serum Creatinine. To convert 0.0181 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.0181 g Serum Creatinine * 1000.0 mg/g = 18.1 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 18.1 mg Serum Creatinine/10.0 dL = 1.81 mg Serum Creatinine/dL. The concentration value of 160.0 µmol Serum Creatinine/L converts to 1.81 mg Serum Creatinine/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (1.81/0.9)**-1.2 * 0.9938**58 * 1.0 = 42.8062.
Hence, the GFR value is 42.8062 ml/min/1.73 m²."
608,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4850250-1,Extracted,"A previously healthy, 38-year-old lady with a history of chronic alcohol use (0.5–1.0 gallon of vodka per day) presented with a three-week history of progressive weakness and generalized fatigue. She complained of paresthesias and weakness in her feet, which progressed proximally and involved her hands. She presented to the hospital after falling and injuring her feet due to inability to walk. She had previously seen her primary care physician and was started on folate supplements. She also complained of diarrhea but denied any anorexia, dysgeusia, cramps, or spasms. On physical examination, the patient was noted to be afebrile, and her blood pressure was 148/78 mmHg. Cardiopulmonary and abdominal exam were normal. Neurological exam showed intact cranial nerves, 4/5 strength bilaterally in upper and lower extremities, diminished triceps, and patellar and Achilles tendon reflexes. There was decreased sensation to temperature, pinprick, vibration, and proprioception that followed a stocking/glove distribution up to the knees and elbows, bilaterally. Neither Chvostek's nor Trousseau's signs were present. Laboratory analysis revealed the following: potassium: 2.9 mEq/L (3.5–5.0), total calcium: 7.3 mg/dL (8.6–10.6), albumin: 3.4 g/dL (3.0–4.8), magnesium: 0.8 mg/dL (1.7–2.4), phosphorus: 5.0 mg/dL (2.5–5.0), intact parathyroid hormone (iPTH): 31.8 pg/mL (12–88), 25 (OH) vitamin D3: 9 ng/mL (25–80), creatinine: 0.66 mg/dL (0.5–1.04), bicarbonate: 25 mmol/L (23–31), AST: 162 U/L (13–40), ALT: 61 U/L (9–51), lipase: 471 U/L (0–220), folate: 5.6 ng/mL (3–20), vitamin B12: 442 pg/mL (240–930), tissue transglutaminase IgA: 3 units (0–19), and hemoglobin: 11.8 g/dL (11.6–15.0). In addition, the patient was noted to have elevated homocysteine levels and normal levels of B12 and folate. Urine studies were significant for urine potassium: 27.7 mmol/L, urine calcium: 20 mg/dL, urine magnesium: 23 mg/dL, and urine creatinine: 103.6 mg/dL. The fractional excretion of magnesium was calculated to be 26%, indicating renal magnesium wasting. The significant electrolyte abnormalities as well as possible folate and B12 deficiency seemed to account for her generalized weakness. Her history of heavy alcohol consumption was thought to have caused her laboratory abnormalities and symptoms. The patient was treated initially with two grams of magnesium intravenously for one day and then switched over to oral magnesium oxide replacement (800 mg three times a day) for seven days. She was also given vitamin B12 and folate replacements. Given the vitamin D deficiency on the labs, which could contribute to the hypocalcemia, the patient was discharged on high dose of vitamin D supplementation.
The normal iPTH levels in the setting of hypocalcemia seemed inappropriate. Once the hypomagnesemia was corrected, the iPTH levels were rechecked and an appropriate rise was noted. Soon after, the hypocalcemia resolved as well. The preceding treatment allowed for an appropriate rise in her PTH levels, which then allowed for the correction of the hypokalemia and hypocalcemia that had been refractory to oral replacements (). The patient's overall condition and weakness improved after two weeks of treatment.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [0.66, 'mg/dL'], 'age': [38, 'years']}",115.07715,109.32329,120.83101,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 38 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.66 mg/dL. Because the patient's gender is female and the creatinine concentration is less than or equal to 0.7 mg/dL, A = 0.7 and B = -0.241.
Plugging in these values, we get 142 * (0.66/0.7)**-0.241 * 0.9938**38 * 1.012 = 115.07715.
Hence, the GFR value is 115.07715 ml/min/1.73 m²."
609,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4389158-1,Extracted,"A 47-year-old woman was referred to our renal outpatient clinic with rapidly progressive renal failure. In the past, she only reported a spontaneous miscarriage at 39 years of age. Five months before the referral, she developed a rash on her arms, trunk and legs and a few spots on the face. The rash was erythematous, made of round patches with slight elevation. The initial diagnosis by dermatologists was one of urticarial rash. She was treated with antihistamines achieving a slight improvement.
Two months later, she began to have speech difficulties, weakness and pain in her legs along with diminished knee reflexes. The laboratory values showed C-reactive protein (CRP) 43 mg/L, erythrocyte sedimentation rate (ESR) 40 mmL/h ANCA positive with PR3 < 1.23 U/mL and MPO Abs 46.21 U/mL, serum creatinine 75 µmol/L. An electromyogram suggested widespread myopathy (). Urinary dipstick was positive for protein (++), blood (++) and nitrites (+). At this point, DM was suspected and she was treated with prednisolone 40 mg and azathioprine 50 mg daily. Chest and abdominal computed tomography (CT) did not reveal any malignancy.
One month later, her laboratory results showed that she had rapidly progressive renal failure. As a result, she was admitted to the Renal Department for further investigations including kidney biopsy. The laboratory results were haemoglobin 91 g/L, white cell count (WBC) 12.1 × 109/L, platelets 389 × 109/L, ESR 112 mm/h, CRP 237 mg/L, creatinine 365 µmol/L, urea 18 mmol/L, potassium 5.1 mmol/L, creatinine kinase 22 µ/L and urine albumin:creatinine ratio (UACR) 19.8 mg/mmol. The repeat ANCA screen was positive with a peri-nuclear pattern, MPO-ANCA 37.61 U/mL and PR3-ANCA negative. C3 and C4 levels were 73 mg/dL (normal range 65–135) and 24 (normal range 13–35), respectively. The urinalysis showed red cells 5–10 × 106 cells/mL with occasional dysmorphic erythrocytes. The urine culture, chest X-ray, anti-glomerular basement membrane (GBM) antibodies, anti-nuclear antibody (ANA), extractable nuclear antibody (ENA), anti-smooth muscle antibody (anti-SMA), myeloma screen, hepatitis B and C serology and human immunodeficiency virus (HIV) serology were all negative. On examination, the rash was slightly improved but persisted on the arms and trunk. The weakness and speech difficulties disappeared but she complained of arthralgia in the small joints. There was no evidence of pulmonary involvement.
The kidney biopsy yielded 19 glomeruli, 4 of which were globally sclerosed, while the remainder showed focal segmental necrotizing glomerulonephritis with a wide variability in severity (some were almost normal whereas others showed extensive necrosis with crescent formation). and the residual segments of the non-necrotic glomeruli tufts showed non-specific mesangial thickening and Bowman's capsule was also focally thickened. The surrounding renal cortex showed focal acute-on-chronic inflammatory changes. Small- and medium-sized vessels showed no evidence of vasculitis. Immunofluorescence showed focal segmental deposition of IgG along with capsular C3 deposition.
Based on these findings, a diagnosis of ANCA-associated focal and segmental necrotizing glomerulonephritis with crescent formation was made and cyclophosphamide 100 mg and prednisolone 60 mg per day were started. Three months later, measurement of thiopurine methyltransferase (TPMT) showed a low-activity, cyclophosphamide treatment was switched to mycophenolate mofetil 500 mg twice daily. Since then we have observed a progressive recovery in her renal function, which remains stable after 6 months with a creatinine of 134 µmol/L and UACR 10 mg/mmol (). The prednisolone dose was tapered slowly to 5 mg/day.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [134.0, 'µmol/L'], 'age': [47, 'years']}",44.00519,41.80493,46.20545,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 47 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 134.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Serum Creatinine from µmol to mg. The mass of Serum Creatinine is 134.0 µmol. To convert 134.0 µmol of Serum Creatinine to mol, multiply by the conversion factor 1e-06, giving us 134.0 µmol Serum Creatinine * 1e-06 mol/µmol = 0.00013 mol Serum Creatinine. To convert from mol Serum Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00013 mol Serum Creatinine * 113.12 g/mol = 0.01471 g Serum Creatinine. To convert 0.01471 g of Serum Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01471 g Serum Creatinine * 1000.0 mg/g = 14.71 mg Serum Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 14.71 mg Serum Creatinine/10.0 dL = 1.471 mg Serum Creatinine/dL. The concentration value of 134.0 µmol Serum Creatinine/L converts to 1.471 mg Serum Creatinine/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (1.471/0.7)**-1.2 * 0.9938**47 * 1.012 = 44.00519.
Hence, the GFR value is 44.00519 ml/min/1.73 m²."
610,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-6695237-1,Extracted,"A 54-year-old female, with a past medical history significant for a recent diagnosis of diffuse cutaneous systemic sclerosis, hypertension, and chronic kidney disease stage three, and a history of adrenal insufficiency presented to the emergency room due to generalized weakness. The patient reported that her weakness started in the lower extremities and had been progressively worsening with difficulty both standing up and sitting. She was unable to walk for the past week. She also reported unintentional weight loss of 70 pounds for the past nine months, inadequate oral intake, decreased urine output, accompanied by dry eyes and mouth, with erythematous non-pruritic and non-painful rash in the inner thighs and buttocks.
On admission, vital signs were only significant for a blood pressure of 160/80 mmHg. The physical examination was remarkable for loss of wrinkles, maculopapular rash, bilateral lower extremity with pitting edema up to the ankles, and skin breakdown in the inner thighs and sacral area. Neurological examination was normal except for decreased motor strength 3/5 in the upper extremities and 2/5 in the lower extremities. Laboratory work-up was significant for a hemoglobin level of 10.8 g/dl (normal 12-15.5 g/dl), potassium 5.8 mmol/L (normal 3.4-5.1 mmol/L), magnesium 1.5 mg/dl (normal 1.7-2.4 mg/dl), bicarbonate 14 mmol/L (normal 21-32 mmol/L), worsening creatinine 6.83 mg/dl (normal 0.51-0.95 mg/dl) (baseline creatinine 1.8-2.1 mg/dl, six months ago), and blood urea nitrogen (BUN) 107 mg/dl (normal 6-20 mg/dl). An electrocardiogram (EKG) showed a normal sinus rhythm with no other changes and her chest X-ray showed no abnormalities (Figure ). The initial treatment consisted of treatment for hyperkalemia with regular insulin 10 units, dextrose, and polystyrene sulfonate. The patient was admitted for further workup of kidney dysfunction and weakness. The rheumatology team recommended immunologic workup, kidney biopsy, and intravenous fluid resuscitation.
During the second day of hospital admission, the patient started to complain of sudden onset chest pain and shortness of breath. Her vital signs were significant for blood pressure 170/90 mmHg, 115 beats per minute, and tachypnea with an oxygen saturation of 89%. The patient was placed on 4 liters of oxygen via a nasal cannula. Her physical examination was remarkable for non-reproducible substernal chest pain, right lower lobe crackles, diffused wheezing throughout, and marked pitting edema in bilateral lower extremities up to the knee. Intravenous fluids were stopped, and a trial of albuterol inhaler was given, with no improvement. As part of the initial workup, the laboratory was remarkable for elevated troponin 0.07 ng/ml (normal <0.05 ng/ml), d-dimer 2.5 mg/l (normal <0.57 mg/l) and procalcitonin 19.9 ng/ml (normal<0.10 ng/ml). A new electrocardiogram (EKG) showed sinus tachycardia with no ischemic changes, and chest X-ray showed current ground-glass densities with interstitial opacities bilaterally (Figure ). The patient was transferred to the medical intensive care unit (MICU) for further care.
At arrival to the MICU, she was progressively getting worse and using accessory respiratory muscles. Her arterial blood gas (ABG) showed pH 7.20 unit (normal 7.35-7.45 unit), CO2 22 mmHg (normal 32-45 mmHg) and O2 54 mmHg (normal 83-108 mmHg) on 6 L through a nasal cannula. The patient was transitioned to bilevel positive airway pressure (BiPAP), but no improvement was achieved. Later, ABG with worsening acidosis and CO2 retention (PH 7.15 and CO2 45), a potassium level of 6.2 mmol/L (normal 3.4-5.1 mmol/L), BUN 150 mg/dl (normal 6-20 mg/dl), and creatinine 7.9 mg/dl (normal 0.51-0.95 mg/dl). The decision was made to proceed with intubation for ventilatory support; she was started on empiric antibiotics (ceftriaxone and azithromycin), intravenous heparin for suspected pulmonary embolism, and emergent dialysis for worsening uremia. Repeated chest X-ray after intubation showed worsening bilateral diffuse interstitial opacities concerning for different etiologies, including pleural effusion, pneumonia, or pulmonary hemorrhage (Figure ). Later during the day, a small amount of blood through the endotracheal tube (ETT) was noted, thereby intravenous heparin was held.
At this point, owing to the findings of worsening kidney function, fluid overload, and persistent hypertension with systolic blood pressure >200/100 mmHg, the primary diagnosis was SRC. Management includes starting the patient on angiotensin-converting enzyme (ACE) inhibitor. Further extensive investigations only showed lower levels of decreased hemoglobin 7.7 g/dl (normal 12-15.5 g/dl), low complement C3 40mg/dl (normal 79-152mg/dl), and high lactate dehydrogenase (LDH) levels of 625 U/L (normal 82-240 U/L). The peripheral smear showed mildly hypochromic anemia and rare polychromatophilic cells. Imaging included transthoracic echocardiogram that revealed concentric hypertrophy, ejection fraction 50%-55%, and grade one diastolic dysfunction. Bilateral lower extremities ultrasound gave no evidence of deep venous thrombosis. Computed tomography of the chest showed bibasilar atelectatic changes, no gross evidence of interstitial lung disease, and cardiomegaly (Figure ).
During the fourth day of hospitalization, the patient's condition worsened, with persistent moderate to large amounts of blood through the ETT with a significant drop in the hemoglobin to 5.7 g/dl (normal 12-15.5 g/dl) from which she received a unit of packed red blood cells. Bronchoscopy was later done, revealing moderate thick bloody secretions in the tracheobronchial tree consistent with pulmonary hemorrhage. Intravenous steroids were held to avoid the worsening of SRC. The kidney biopsy reported an acute thrombotic microangiopathy type pattern with severe vascular involvement, most consistent with scleroderma renal crisis associated with tubular necrosis (Figure ).
Ultimately, the patient was transferred to a tertiary scleroderma center, in which she significantly improved after supportive treatment and infusion with cyclophosphamide. The patient was successfully extubated and was transitioned to acute inpatient rehabilitation.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [7.9, 'mg/dL'], 'age': [54, 'years']}",5.60505,5.3248,5.8853,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 54 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 7.9 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (7.9/0.7)**-1.2 * 0.9938**54 * 1.012 = 5.60505.
Hence, the GFR value is 5.60505 ml/min/1.73 m²."
611,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-2627261-1,Extracted,"A 68-year-old man presented with a 3-week history of abdominal discomfort, nausea and skin eruption on his entire body. There was no past medial history of hepatolithiasis, recurrent peptic ulcer, abdominal operation, allergic disease, generalized skin eruption or food sensitivity. The laboratory investigations revealed a white blood cell count of 12.86 × 103/µl. There was peripheral eosinophilia ranging from 7% to 52% (normal: 0-7.2%). The total IgE was 593 IU/ml (normal: 0-170 IU/ml). Stool examination and an enzyme-linked immunosorbent assay (ELISA) test to detect parasite infestation showed negative results. The blood urea nitrogen (BUN) was 40 mg/dl (normal: 10-26 mg/dl) and the serum creatine was 2.1 mg/dl (normal: 0.6-1.3 mg/dl). An ultrasound scan for evaluation of acute renal failure yielded negative results except for pneumobilia. Because of the absence of prior sphincterotomy, a surgical bypass procedure or recent endoscopic retrograde cholangiopancreatography (ERCP), we inferred the existence of enterobiliary fistula. The acute renal failure was slightly improved and we then performed multidetector computed tomography (MDCT) for further evaluation. MDCT revealed diffuse submucosal thickening from the antrum of the stomach to the duodenal bulb and a bezoar at the first portion of duodenum. But enterobiliary fistula was not clearly detected (). Gastrointestinal endoscopy showed large ulcers with a geographic pattern from the antrum of the stomach to the duodenal bulb (). The duodenum revealed severe stricture involving the second portion and a soft bezoar at the first portion of the duodenum. MRCP demonstrated that there was pneumobilia in the gall bladder and common bile duct (CBD). In addition, cholecystoduodenal fistula and a suspected choledocoduodenal fistula were observed (). The results of the UGI were similar to those of the MRCP, and the other findings were mucosal fold thickening and nodularity involving the antrum and severe stricture involving the second portion of the duodenum (). Biopsy samples were obtained at the ulcer bed, and they showed marked eosinophilic infiltration (). We adopted the criteria shown in for evaluating the tissue eosinophilia; severe eosinophilia (over 70 eosinophils/× 400 field) was demonstrated in the lamina propria of the gastric mucosa. The diagnosis was enterobiliary fistula complicating eosinophilic gastroenteritis. After steroid therapy, there was interval improvement of both the ulcer and duodenal luminal narrowing on the follow up endoscopy.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [2.1, 'mg/dL'], 'age': [68, 'years']}",33.65485,31.97211,35.33759,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 68 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.1 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.1/0.9)**-1.2 * 0.9938**68 * 1.0 = 33.65485.
Hence, the GFR value is 33.65485 ml/min/1.73 m²."
612,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-5965203-1,Extracted,"A 69-year-old man with a past medical history of untreated hypertension, chronic back pain, and heavy smoking was brought in by ambulance to a community emergency department (ED) for severe bilateral leg pain and paraplegia. He had been unable to ambulate and remained lying on the floor for the prior three days. The patient also admitted to chronic low back pain that had worsened over the preceding week and not improved with his usual pain medications of naproxen and aspirin. He had no other complaints and denied any fevers or chills.
The patient’s initial vital signs were as follows: temperature 36.6 degrees Celsius, blood pressure 157/84 mmHg, heart rate 95 beats/min, respiratory rate 38 breaths/min, oxygen saturation 94% on room air. On physical examination, the patient appeared cachectic and chronically ill. His cardiac exam revealed a regular heart rate and rhythm without murmur. He had no palpable femoral, popliteal, or dorsalis pedis pulses bilaterally. A Doppler ultrasound performed at bedside further demonstrated a lack of pulses bilaterally from the femoral to the dorsalis pedis arteries. Abdominal examination showed a scaphoid, soft, non-tender abdomen without a pulsatile mass. There was no midline spinal tenderness or step-offs on musculoskeletal examination. Neurological evaluation demonstrated complete sensory loss from T10 and ending on the S1dermatome bilaterally. He had 5/5 motor strength in both upper extremities and 0/5 strength in hip flexion and extension as well as ankle dorsiflexion and plantar flexion bilaterally. The dermatological examination of the lower extremities revealed pale, cold, and mottled-appearing skin from the hips to the ankles bilaterally.
Initial laboratory data for the patient revealed white blood cells (WBC) 26.9 x109/L with neutrophil count 88.8%, hemoglobin 14.3 g/L, hematocrit 44.4%, and platelets 288 x 109/L complete metabolic panel showed the following: sodium (Na) 127 mmol/L, potassium (K) 7.3 mmol/L, chloride (Cl) 99 mmol/L, carbon dioxide (CO2) 18 mmol/L, blood urea nitrogen (BUN) 82 mg/dL, creatinine (Cr) 4.4 mg/dL, glucose 123 mg/dL, alanine transaminase 288 units/L, aspartate transaminase 1,372 units/L, albumin 3.4g/dL, alkaline phosphatase 86 units/L, direct bilirubin 1.0 mg/dL, indirect bilirubin 0.2 mg/dL, and total bilirubin 1.2 mg/dL. Prothrombin time, international normalized ratio, and partial thromboplastin time were 11.0, 1.0, and 26.9 seconds, respectively. Lactic acid was 3.36 mmol/L and creatinine kinase was 111,693 units/L. Troponin was also elevated at 3.850 ng/mL, and the electrocardiogram showed diffuse and deep T-wave inversions in the inferior, anterior, and lateral leads.
Point-of-care ultrasound of the abdominal aorta revealed a linear hyperechoic shadow in the aorta. Chest radiograph displayed a mildly tortuous ectatic aorta and evidence of chronic obstructive pulmonary disease (COPD). CT of the chest demonstrates a Stanford Type B aortic dissection (). The dissection starts from the subclavian and extends well into the infrarenal region of the abdominal aorta with significant mural thrombosis. On three-dimensional reconstructed images of the CTA abdominal aorta and bilateral lower extremities with runoff, significant stenosis is visible in both renal arteries, especially in the left (). The right lower extremity demonstrates near-complete occlusion of the right common iliac artery and both internal and external iliac arteries. The popliteal artery and arteries below the right knee are occluded. No blood flow to the right lower extremity is noted. The left lower extremity also demonstrates severe narrowing with moderate thrombosis in the iliac arteries with complete occlusion of the left external iliac artery. The left popliteal artery is likewise occluded, and no blood flow to the left lower extremity is visible. In addition to the above findings, intramuscular gas is seen in the thighs bilaterally, raising suspicion for myonecrosis ().
In the ED, the patient was aggressively resuscitated with an initial two-liter bolus of normal saline. A central venous catheter was inserted in the left internal jugular vein and the patient was started on an intravenous (IV) esmolol drip. He also received IV heparin, calcium chloride, sodium bicarbonate, insulin, glucose, and morphine during his ED stay. Shortly thereafter, the patient was taken for emergent dialysis in the intensive care unit (ICU) to further correct his electrolyte abnormalities, renal failure, and rhabdomyolysis prior to operative treatment. The laboratory abnormalities were partially corrected to a WBC of 17.5 with neutrophil count of 79.7%, K of 6.6, BUN of 87 and Cr at 3.6. The patient subsequently underwent open bilateral iliofemoral aortic popliteal thrombectomy, stent placement in the abdominal aorta and bilateral iliac arteries and bilateral femoral endarterectomy and patch angioplasty. While in the operating room, the patient became hypotensive and bradycardic and eventually suffered cardiopulmonary arrest. Despite a brief return of spontaneous circulation after resuscitative efforts, the patient died shortly thereafter in the ICU.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [4.4, 'mg/dL'], 'age': [69, 'years']}",13.76787,13.07948,14.45626,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 69 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 4.4 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (4.4/0.9)**-1.2 * 0.9938**69 * 1.0 = 13.76787.
Hence, the GFR value is 13.76787 ml/min/1.73 m²."
613,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-8617802-1,Extracted,"A 65 year old woman, who had undergone a radical hysterectomy and postoperative radiotherapy (total dose, 50 Gy) for uterine endometrial cancer 21 years prior, was admitted to our hospital with acute abdominal pain. The patient had symptoms of peritoneal irritation with rebound tenderness and was suspected to have generalized peritonitis with inflammatory findings (white blood cell (WBC), 11,000/µL; neutrophils, 85.2%; C-reactive protein (CRP), 3.50 mg/dL; platelet, 30.7 × 10⁴/µL; procalcitonin, 17.35 ng/mL) and renal failure (blood urea nitrogen (BUN), 52.3 mg/dL; creatinine (Cre), 3.73 mg/dL). Plain computed tomography (CT) showed only massive ascites, but showed no findings of gastrointestinal perforation, such as free air. Ascites collected by puncture were neither purulent nor bloody. Conservative treatment was performed because of stable vital signs and the patient’s will. Considering bacterial peritonitis, the antibiotics tazobactam/piperacillin (7.75 g/day) were administered. On day 3 after admission, the abdominal symptoms and inflammatory findings improved (WBC, 4800/µL; Neutrophils, 59.6%; CRP, 0.71 mg/dL). On day 4 after admission, renal failure improved (BUN, 9.1 mg/dL; Cre, 0.53 mg/dL), and contrast-enhanced CT was performed, showing no remarkable findings for the cause of generalized peritonitis (). In addition, no abnormalities were found on esophagogastroduodenoscopy or total colonoscopy. Recurrence of uterine endometrial cancer was suspected; however, tumor markers did not elevate (carcinoembryonic antigen (CEA), 0.9 ng/dL; carbohydrate antigen 19-9 (CA19-9), 6.6 u/mL), and a CT showed no disseminated nodules. The tumor markers and adenosine deaminase (ADA) in the ascites also did not elevate (CEA, 0.5 ng/dL; CA19-9, 3.2 U-mL; ADA, 2.1 u/L). The cytology of ascites was class II and was dominated by WBC (especially neutrophils), reflecting generalized peritonitis. Although the cause of the generalized peritonitis could not be identified, conservative treatment, including intravenous fluid treatment without eating, in addition to antibiotics, led to the disappearance of ascites and the patient’s discharge on day 15.
Five months after the first admission (second-time admission), the patient was readmitted for the same symptoms. The cause was still unclear; however, the patient recovered with conservative treatment. Eleven months after the first admission (third-time admission), the patient was readmitted for the same episode of acute abdominal pain.
To investigate the cause of generalized peritonitis, a trial laparotomy was suggested; however, the patient refused the procedure. Fourteen months after the first admission, the patient was readmitted for the fourth time with generalized peritonitis. A plain CT, on the day of the fourth admission, showed massive ascites and partial wall thinning in the dome of the bladder (). A urine culture revealed a urinary tract infection (Klebsiella oxytoca detected) along with urinalysis (WBC in urine, 2+). Since the patient complained of dysuria, a cystoscopy was performed just after the inflammatory findings improved. The cystoscopy showed no tumor or fistula but showed granular edematous mucosa in the same part of wall thinning on CT at the fourth admission (). Based on these findings, SBR was diagnosed as the cause of recurrent generalized peritonitis. We suggested surgery of suturing and omentoplasty to the wall thinning in the dome of the bladder; however, the patient declined it because of the invasiveness. Instead of the surgery, the patient received a long-term bladder catheter placement, leading to no recurrence of generalized peritonitis for 2 years.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [3.73, 'mg/dL'], 'age': [65, 'years']}",12.88162,12.23754,13.5257,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 65 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 3.73 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (3.73/0.7)**-1.2 * 0.9938**65 * 1.012 = 12.88162.
Hence, the GFR value is 12.88162 ml/min/1.73 m²."
614,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-4732999-1,Extracted,"The patient is a 42-year-old asymptomatic woman with no past medical history referred to us on account of a hyperechoic right kidney mass and IVC thrombus found on routine abdominal ultrasound. Physical examination was unremarkable, and laboratory values were within normal limits, with hemoglobin of 13.2 g/dL and creatinine of 0.85 mg/dL. Computed tomographic (CT) scan of the abdomen confirmed a 3-cm right upper pole renal mass with central fat attenuation and a 5-cm level II IVC thrombus (extension into the right renal vein and IVC below the level of the hepatic veins; A and B). Shortly after imaging diagnosis, she presented with a 1-week history of pleuritic chest pain and shortness of breath in the recumbent position. Urgent chest CT angiogram showed a pulmonary tumor embolus (−65 HU) in the right anterior segmental branch of the pulmonary artery, with a corresponding infarct in the medial segment of the right lower lung lobe. The CT also revealed multiple bilateral lung cysts, suggesting a diagnosis of LAM.
She underwent a right radical nephrectomy and IVC thrombectomy through a modified Chevron incision. With full mobilization of the right kidney, control of the IVC proximal and distal to the thrombus, and the contralateral renal vein, a free-floating thrombus was easily delivered intact through an anterior ellipsoid cavotomy. Subsequent to IVC repair, a right radical nephrectomy was performed without perioperative complications. The patient fared well postoperatively and was discharged home on postoperative day 4.
Gross specimen examination revealed a 2.5 × 2.2 × 2.0 cm fatty tumor located in the upper pole of the right kidney, extending into the renal sinus. There was a 6.8 × 0.9 cm tumor thrombus protruding through the renal vein, without involvement of the vein wall (A). Microscopic examination revealed a tumor composed of adipose tissue predominantly, scattered thick-walled blood vessels, and minor smooth muscle cells surrounding abnormal vessels (B). Immunophenotypic expression includes positive staining for melanocytic markers (HMB-45) and smooth muscle markers (SMA, smooth muscle actin). S-100 immunostain showed positive cytoplasmic staining.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [0.85, 'mg/dL'], 'age': [42, 'years']}",87.66808,83.28468,92.05148,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 42 years old. The patient's gender is Female, and so the patient's gender coefficient is 1.012.
The concentration of Serum Creatinine is 0.85 mg/dL. Because the patient's gender is female and the creatinine concentration is greater than or equal to 0.7 mg/dL, A = 0.7 and B = -1.2.
Plugging in these values, we get 142 * (0.85/0.7)**-1.2 * 0.9938**42 * 1.012 = 87.66808.
Hence, the GFR value is 87.66808 ml/min/1.73 m²."
615,3,CKD-EPI Equations for Glomerular Filtration Rate,lab test,decimal,pmc-3639672-1,Extracted,"A 45 year-old Hispanic male presented to the emergency department (ED) with complaints of weakness and myalgias for the preceding month with worsening on the days prior to admission. Physical exam was grossly unremarkable and vital signs were stable. He was found to be anemic with hemoglobin of 7.8 g/dL. In addition he had a platelet count of 73,000/mL. Other pertinent laboratory findings included a blood urea nitrogen (BUN) of 41 mg/dL, creatinine of 2.6 mg/dL, calcium 12.3 mg/dL and ionized calcium level was 1.59. Total protein was 7.6 g/dL and albumin was 4.1 g/dL. The patient's chest radiograph showed increased vascular markings and reticulonodular opacifications (see ). Computed tomography (CT) scans of chest also revealed diffuse ground-glass nodular opacities, with numerous poorly defined nodules measuring 3–10 mm in diameter both (see ). A skeletal survey revealed punched-out defects consistent with multiple myeloma (MM). The patient underwent a Technetium (Tc) 99 bone scan, which revealed diffuse activity in the lung with significant lighting up of the pulmonary parenchyma, consistent with metastatic pulmonary calcification (see ).
A subsequent serum protein electrophoresis revealed elevation of the free lambda light chain to 14,400 mg/L (normal range 5.71–26.3 mg/L). A bone marrow biopsy revealed massive plasmacytosis. The patient underwent standard therapy for his anemia and hypercalcemia and was seen by the oncology and nephrology services. Once discharged the patient was eventually lost in followup due to medical noncompliance. Our last search indicated that the patient has expired due to hypoxia and noncompliance with the hemodialysis sessions.","Using the 2021 CKD-EPI Creatinine equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [45, 'years'], 'creatinine': [2.6, 'mg/dL']}",30.05149,28.54892,31.55406,"The formula for computing GFR is 142 x (Scr/A)**B x 0.9938**age x (gender_coeffcient), where the ** indicates an exponent operation, Scr is the concentration of serum creatinine in mg/dL and gender_coefficient is 1.012 if the patient is female, else the coeffient is 1. The coefficients A and B are dependent on the patient's gender and the patient's creatinine concentration.
The patient is 45 years old. The patient's gender is Male, and so the patient's gender coefficient is 1.0.
The concentration of Serum Creatinine is 2.6 mg/dL. Because the patient's gender is male and the creatinine concentration is greater than or equal to 0.9 mg/dL, A = 0.9 and B = -1.2.
Plugging in these values, we get 142 * (2.6/0.9)**-1.2 * 0.9938**45 * 1.0 = 30.05149.
Hence, the GFR value is 30.05149 ml/min/1.73 m²."
616,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6132167-1,Extracted,"A 78-year-old man visited our emergency room with unconsciousness. According to his family, he was poisoned with pesticide (glyphosate) for self-injury purpose. Two years ago, he had a history of cerebral infarction, and he was taking aspirin and medication for hypertension. During gastric lavage in the local clinic emergency room, his heart rate and respiration decreased. Then, he was transferred to the intensive care unit after intubation.
Intensive care such as continuous renal replacement therapy and mechanical ventilation was performed in the intensive care unit, and colistin and minocycline were administered for pneumonia. Pulmonary thromboembolism was confirmed by chest computed tomography (CT), and anticoagulant therapy was performed. Acute acalculous cholecystitis occurred simultaneously, and a percutaneous transhepatic GB drainage tube was inserted.
After 2 months of intensive treatment, the patient's condition improved, and cholecystectomy was planned. He underwent laparoscopic cholecystectomy, and there were no remarkable details of the surgery.
On the first day postoperatively, the drainage changed to bile. The patient's vital signs were as follows: blood pressure, 160/105 mm Hg; pulse rate, 143 beats/min; respiratory rate, 37 breaths/min; and body temperature, 39°C. There was tenderness and rebound tenderness in the whole abdomen, and CT showed pneumoperitoneum and diffuse fluid collection in the right perihepatic space (Figure ). We diagnosed him as having bile peritonitis, and reoperation was decided.
On relaparoscopic examination, there was a large amount of bile juice around the GB bed and perihepatic space, and suction and irrigation were performed. The cystic duct stump was confirmed, but there was no leakage. In the GB bed, a leak was observed in a small duct-like structure, which was regarded as an aberrant duct, and the operation was terminated after primary repair (Figure ).
Until 6 days postoperatively, hemoserous fluid was drained from the drainage tube. However, from postoperative day 7, the fluid changed to bile, and a percutaneous drainage (PCD) catheter was inserted into the GB bed area after performing CT.
On postoperative day 9, endoscopic retrograde cholangiopancreatography (ERCP) was performed, and a leak was detected in the branch of the right posterior hepatic duct, which was regarded as an aberrant subvesical bile duct (Figure ). Endoscopic sphincterotomy (EST) and insertion of an endoscopic retrograde biliary drainage (ERBD) stent (7 French, 5 cm) were performed (Figure ).
One month after ERBD stent insertion, ERCP was performed again to confirm that there was no leak, and then, the ERBD stent was removed (Figure ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': True, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'age': [78, 'years'], 'Stroke': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 78 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
617,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5932498-1,Extracted,"A 74-year-old male with a past medical history of coronary artery disease, congestive cardiac failure, permanent atrial fibrillation status-post nodal ablation, and placement of a biventricular pacemaker presented to the hospital with complaints of generalized fatigue. The patient denied other constitutional symptoms including chest pain, dyspnea, abdominal pain, diarrhea, or dysuria. Vitals were as follows: afebrile, blood pressure 116/80, pulse 72, respiratory rate 21, and saturating well on 3 litres/minute nasal cannula. Physical examination showed pitting edema in bilateral lower extremities till knees, decreased bibasilar breath sounds, and jugular venous distension. There was no rash, painful nodes or splinter hemorrhages. Holosystolic murmur was heard at the apex, JVD ∼18 cm H2O. Laboratory investigations showed normal WBC count, neutrophilia with 17 bands, 26 lymphocytes, and 8 monocytes. CRP was elevated at 4.3. The patient also had a troponin level of 0.22; however, this was found to be chronically elevated. Chest X-ray showed cardiomegaly, but no pulmonary vascular congestion, consolidation, nor effusions. Urinalysis did not show any evidence of infection. Overnight, the patient developed fever with a maximum temperature of 39.2°C.
Blood cultures turned positive for Gram-positive rods at which time the patient was started on vancomycin. Echocardiogram was performed due to concerns of endocarditis and showed left ventricular ejection fraction 20–25%, severe diffuse hypokinesis, moderate mitral and tricuspid regurgitation, and a 1 mm mobile strand in the left atrium attached to pacer lead concerning vegetation. Final blood cultures revealed Listeria monocytogenes, and two sets of subsequent cultures grew listeria. TEE was not performed as it would not have changed management. The patient was not a surgical candidate for pacemaker removal due to comorbidities and advanced heart failure. Antibiotic therapy with vancomycin was continued. Ampicillin was not used due to high sodium content in the infusion in setting of decreased systolic function. The patient received 6 weeks of IV vancomycin followed by oral suppression with amoxicillin. There was appropriate clinical response to the abovementioned treatment with resolution of fever and subjective improvement.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Hypertension history': True, 'Vascular disease history': True, 'age': [74, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 74 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
618,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-12610,Extracted,"A 76-year-old man is brought to the emergency department by his daughter because he has been feeling lightheaded and almost passed out during dinner. Furthermore, over the past few days he has been experiencing heart palpitations. His medical history is significant for well-controlled hypertension and diabetes. Given this presentation, an electrocardiogram is performed showing an irregularly irregular tachyarrhythmia with narrow QRS complexes. The patient is prescribed a drug that decreases the slope of phase 0 of the ventricular action potential but does not change the overall duration of the action potential.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': False, 'age': [76, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
619,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7485475-1,Extracted,"A 73-year-old man was referred to the Emergency Department of our University Hospital because of fever, dry cough, and worsening dyspnea after contacts with two sons recently diagnosed with COVID-19. No gastrointestinal (GI) symptoms were present. History revealed multimorbidity characterized by type 2 diabetes mellitus, hypertension, atrial fibrillation, multivessel coronary artery disease (requiring repeated percutaneous angioplasty with stenting two years before), and a recent diagnosis of primary cutaneous large B-cell lymphoma (PCLBCL) leg type, localized at the right leg without extra-nodal involvement, which was treated with local radiotherapy two months before.
The presenting clinical and imaging picture suggested a severe acute respiratory syndrome (SARS). The patient was severely hypoxemic (paO2/FiO2 less than 100), chest X-ray, and computerized tomography (CT) () revealed bilateral interstitial pneumonia. SARS-CoV-2 infection was diagnosed through polymerase chain reaction on a nasopharyngeal swab, and the patient was admitted to a dedicated COVID-19 area. High flows of oxygen and continuous positive airways pressure (CPAP) were started, and the patient was stimulated to pronation. Electrocardiogram confirmed atrial fibrillation with a normal QTc interval. Initial blood analysis showed C-reactive protein 263 mg/L, leukocytosis (16,610/mm3) with neutrophilia (15,940/mm3) and marked lymphocytopenia (260/mm3), ferritin 487 mcg/L, D-dimer 719 mcg/L, fibrinogen 8.91 g/L, LDH 287 U/L, lactate 2.9 mmol/L. Hemoglobin, platelets, creatinine, and liver enzymes were in the normal range. Lymphocyte subpopulations analysis revealed a marked reduction of CD4+ T-cells (100/mm3). Revision of previous records excluded any prior immunodeficiency. Empirical treatment was started with hydroxychloroquine 200 mg BID (after a loading dose of 400 mg BID for the first 24 hours), lopinavir/ritonavir 100/25 mg BID, methyl-prednisolone 80 mg OD (1 mg/kg) with subsequent tapering, and enoxaparin at therapeutic doses. Overall, the duration of the antiviral and methyl-prednisolone treatments was ten days. After an initial critical phase, the respiratory failure slowly improved so that the patient could be gradually weaned from CPAP from day 14 after admission.
However, on day 18, the patient developed epigastric pain, melena, hypotension, tachycardia, and a substantial drop of hemoglobin levels (from 14.5 to 10.6 g/dL). After hemodynamic stabilization with intravenous fluids and transfusion with two units of red blood cells, an upper endoscopy was performed, which showed multiple large and confluent ulcers in the first and second portions of the duodenum (), suggesting a Cytomegalovirus (CMV) duodenitis. The diagnosis was confirmed by the positivity of circulating CMV-DNA (6,080 IU/mL titer) and by duodenal histopathological findings (). CMV serologic test showed positive IgG (154 U/mL; positive ≥ 14 U/mL) and borderline IgM at diagnosis. Helicobacter pylori and Epstein-Barr encoded RNA were not found on the histologic specimens.
Enoxaparin was immediately stopped, and ganciclovir (5 mg/kg BID) was started. The patient also underwent a CT-scan of the abdomen, which showed pancreatitis with a non-homogeneous pattern of the pancreatic head and peripancreatic fluid collection (). Pancreatic amylases and lipases were only slightly increased (59 and 63 U/L, respectively). The clinical evolution was favorable, as abdominal pain disappeared, and pancreatic enzymes returned within the normal range in few days, allowing early enteral refeeding. The CMV-DNA titer dropped to 1,320 IU/mL after 12 days of treatment with ganciclovir. On day 43 from admission, the patient was successfully discharged by the COVID Unit.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [73, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Vascular disease history': True, 'Diabetes history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 73 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
620,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8059103-1,Extracted,"We report the case of a 51-year-old Moroccan woman admitted to the cardiovascular intensive care unit after mitral valve replacement surgery. Her medical history was significant for organic mitral disease (mild mitral stenosis and severe regurgitation) with preserved left ventricular function, enlarged left atrium, atrial flutter, irritable bowel, and depression. She had been taking acenocoumarol (4 mg) for the last two years to prevent thromboembolic events. The surgical procedure consisted of valvular replacement surgery with a mechanical prosthesis. No thrombus was detected in the left atrium during the perioperative period. During the weaning of the cardiopulmonary bypass (73 min), the patient exhibited supraventricular tachycardia, which was reduced using amiodarone.
During the postoperative period, the hemodynamics were stable without any inotropic or vasopressor agents, and the cardiac rhythm was regular. In the postoperative stage, the patient received fluids, an intravenous curative dose of unfractionated heparin (UFH), and antalgics. The blood test results are presented in Table . Three days later, the patient reported generalized abdominal pain that spread to the flanks with hematuria, constipation, and vomiting. Physical examination showed the following vital signs: body temperature, 37.2°C; blood pressure, 110/78 mmHg; heart rate, 77 beats per minute; respiratory rate, 22 breaths per minute; and swollen abdomen with a slight stiffness in the renal angles. The rest of the examination results were normal.
Pyelonephritis or mesenteric ischemia was strongly suspected as the cause of her acute pain. The workup revealed high serum creatinine levels, high lactate dehydrogenase (LDH) levels, high leukocytosis, and high C-reactive protein (CRP) levels. Urine analysis showed macroscopic hematuria and aseptic leukocytosis. An abdominal CT scan without contrast showed fecal impaction and infiltration of perirenal fat. Duplex Doppler ultrasound showed aspects of bilateral multifocal cortical renal infarctions (Figure ), which suggested arterial thromboembolic disease.
The aorta and renal arteries were permeable with no atherosclerotic plaques. Both the renal vein and inferior vena cava were permeable. Transthoracic and transesophageal echocardiography showed neither intracardiac nor valvular prosthesis thrombus or endocarditis vegetation. The estimated left ventricular ejection fraction was 38% with elevated left ventricular filling pressure. The systolic pulmonary arterial pressure was approximately 46 mmHg.
We concluded that it was a bilateral renal infarction of probable embolic origin, despite curative heparin. A progressive increase was observed in serum creatinine levels up to 70 mg/L after four days. The urine output up to now was preserved. One month later, the creatinine level increased to 95 mg/L, and the patient was diagnosed with chronic kidney disease.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': True, 'Hypertension history': True, 'Vascular disease history': False, 'age': [51, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 51 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
621,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4583844-1,Extracted,"A 70-year-old male patient presented himself to the emergency department due to having had productive cough for one week. He has a past history of type 2 diabetes mellitus, stage III chronic kidney disease, hypertension, old pulmonary tuberculosis, and poliomyelitis. He also received a mechanical valve replacement for severe tricuspid regurgitation and has been taking warfarin for 10 years. He was admitted with the diagnosis of community-acquired pneumonia, and received amoxicillin/clavulanic acid.
On the second day after admission, the patient developed massive upper gastrointestinal bleeding with a remarkable decrease of hemoglobin from 11.1 g/dL to 7.6 g/dL. He had a profound coagulopathy with prothrombin time (PT) of 43.4 s, international normalized ratio (INR) of 4.07, and activated partial thromboplastin time (aPTT) of 63.2 s. The platelet count was 252,000/μL. Warfarin was discontinued. He received blood component therapy and Vitamin K1 to correct anemia and coagulopathy. He also received intravenous esomeprazole. The panendoscopic examination showed an ulcer on the duodenal bulb with an active oozing vessel on the ulcer crater (Fig. -). Hemostasis was performed with epinephrine injection and hemoclipping (Fig. -).
The patient had abdominal pain, gastrointestinal bleeding and hypotension one day after the endoscopic procedure. Hemoglobin was further dropped to 5.8 g/dL, and coagulopathy was worsened with PT of 60.4 s, INR of 5.69, and aPTT of 60.1 s despite of aggressive component therapy. Total serum bilirubin level was rapidly elevated from 1.68 mg/dL to 6.00 mg/dL. Acute pancreatitis was also suspected with a lipase level of 3743 IU/L. Computed tomography of the abdomen showed a 14.4 cm × 7 cm intramural hematoma at the second portion of duodenum (Fig. -). The stomach was distended which indicated gastric outlet obstruction. He also had air retention in the portal vein and wall of esophagus, stomach and bulb (Fig. - to ).
The patient developed respiratory failure and shock, and he received support with mechanical ventilation. His bleeding tendency was corrected by vitamin K1 and blood component therapy. Hemodynamic instability was promptly resolved within two days. Abdominal ultrasonography taken six days later showed the finding of complete resolution of the duodenal hematoma, and was confirmed with endoscopy two weeks later (Fig. ). But, his renal function was progressively worsened, and the patient and his family declined hemodialysis therapy. The patient died of renal failure on the 40th day after admission.
Depending on the involved site of gastrointestinal tract, clinical presentation of PI is usually nonspecific, varying from chest pain, diarrhea, constipation, abdominal pain, abdominal distension, nausea, vomiting, to gastrointestinal bleeding, or even no symptom [, , ].
Gastric pneumatosis has been described in various circumstances, including patients who have hemorrhagic radiation gastritis after Argon plasma coagulation [], gastric ulcer [], corrosive injury of stomach, status post endoscopy, gastric outlet obstruction, duodenal obstruction, nasogastric tube placement [], hepatectomy with vascular reconstruction, obstructive pulmonary disease with bleb rupture [], and high-dose dexamethasone therapy []. It can be divided into two categories: first, gastric emphysema, implying benign condition and usually being managed by conservative treatment; and second, emphysematous gastritis, suggesting emergent condition, and surgical intervention being critical for life-saving. Mclaughlin et al. have proposed to use the term gangrenous PI/nongangrenous PI instead of emphysematous gastritis/gastric emphysema, to avoid misleading [].
IDH is also a rare condition that mostly occurs after a blunt abdominal trauma because that the duodenum has rich submucosal vascular supply and is fixed in retroperitoneum []. IDH has also been reported as clinical finding associated with anticoagulant therapy, blood dyscrasia, pancreatic disease, collagen vascular disease [], and diagnostic/therapeutic endoscopy [] such as endoscopic retrograde cholangiopancreatography with sphincterotomy and biliary stone retrieval []. It tends to occur in patients with liver cirrhosis, coagulopathy and hemodialysis especially []. IDH is usually confined from the first portion to the second portion of the duodenum due to the barrier of pylorus and ligament of Treitz. Typical symptoms of IDH include epigastric pain, vomiting, and hematochezia. Acute pancreatitis is the most frequent comorbidity in those patients []. Thandassery et al. reported a rare case in a patient who developed intramural duodenal hematoma after endoscopic retrograde cholangiopancreatogram (ERCP) with sphincterotomy and biliary stone extraction with subsequent of acute pancreatitis, biliary and gastric outlet obstruction after ERCP []. Our patient also had the triad of above symptoms. We also observed rapid decline of hemoglobin level in our patient and this observation has been described in other case reports [, ]. We suggest that the patients should be suspected to have IHD if they have the tetrad of acute pancreatitis, biliary obstruction, gastric outlet obstruction and rapid decline of hemoglobin after an endoscopic examination.
In uncomplicated cases, IDH usually resolves spontaneously with conservative treatment in 1–3 weeks []. Sadio et al. have reported a case in a patient with intramural gastric hematoma after endoscopic injection therapy, and have found that patient’s hematoma disappear six days later []. In our patient, the IDH was spontaneously resolved under abdominal sonography six days after the endoscopy.
To our best knowledge, less than 10 cases of patients with esophageal pneumatosis have been reported [, ], and no esophagogastroduodenal pneumatosis has been reported. The mechanism of PI has been experimentally proved that dissection of the gas from intraluminal to the intramural compartment is due to increased intra-abdominal pressure combined with mucosal defect []. We hypothesize that the findings of our patient are derived from the similar mechanism. The air was inflated from the defect of the needle injection site after endoscopic hemostasis for duodenal ulcer hemorrhage, and warfarin-associated coagulopathy precipitated the formation of IDH, which further dissected the duodenal wall, leading to inflated air entering into the duodenal, gastric and esophageal wall. The inflated air finally entered the portal vein through the portal circulation system.
Traditionally, once the pneumoporta is recognized along with PI, surgical intervention is preferred due to the concern of having ischemic bowel. But, PI is a radiological finding with wide spectrum of clinical severity and outcome. Surgical or conservative treatment should be considered according to the underlying etiology []. In this patient, esophagogastroduodenal pneumatosis and intramural duodenal hematoma were resolved spontaneously six days later. Therefore, we suggest that conservative treatment and close clinical assessment should be considered as an initial management for patients who complicate with IDH and PI after an endoscopic procedure. But, surgery is needed for those patients if the diseases progress or complications persist.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': False, 'age': [70, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 70 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
622,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8086050-1,Extracted,"We present a case of a 79-year-old independent female who was referred to our breast unit with a left breast lump. Her past medical history included bilateral implant-based breast augmentation in 1970, hypertension, myocardial infarction in 1979 and 1982, coronary stents, atrioventricular (AV) node ablation, and atrial fibrillation (AF). There was no relevant family history, and the general examination was unremarkable. Breast examination revealed bilateral hard 50 mm masses in each breast's centre, denoting grade IV capsular contracture (as per Baker scale []) and likely failed breast implants, with no other palpable suspicious lumps or axillary or supraclavicular lymphadenopathy.
Bilateral mammogram and ultrasound scan showed an impalpable, right breast, 10 mm, suspicious mass, which was cored and clipped under ultrasound scan guidance. They also showed bilateral failed collapsed breast implants (Figures -).
After discussing her care in our multidisciplinary meeting, we preceded with right breast radiofrequency identification (RFID) tag-guided wide local excision (Figure ), patent blue and radioactive directed sentinel lymph node biopsy (SLNB) and bilateral explantation surrounded by a rim of normal breast tissue (Figure ).
The patient had smooth postoperative recovery and was discharged the following day, seen in the clinic the following week with good aesthetic results and no postoperative complications were noted.
Final histology revealed a fully excised, right breast, 17 mm, invasive ductal carcinoma, grade II, with intermediate-grade solid and comedo ductal carcinoma in situ, estrogen receptors (ER) 8, progesterone receptors (PR) 8 and human epidermal growth factor receptor 2 (HER2) negative, and SLNB 0/2. The bilateral collapsed implants showed an extensively calcified capsule lined by a band of dense hyaline fibrous tissue showing patchy dystrophic calcification, with mild chronic inflammation, occasional foreign body giant cells, and fat necrosis noted but no evidence of Breast Implant-Associated Anaplastic Large Cell Lymphoma (BIA-ALCL). Based on the final histology, the patient was offered right breast radiotherapy, followed by endocrine treatment.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [79, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 79 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
623,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3588394-1,Extracted,"An 81-year-old right-handed male presented with acute onset of sound volume loss, inability to swallow and speak, inability to move tongue, and difficulties in chewing the foods. The past medical history was remarkable for diabetes mellitus, hypertension, coronary artery disease, and benign prostate hypertrophy. His first cerebral vascular event presenting with right-sided arm and leg weakness was observed about 4 years ago and his weakness was recovered completely. However, he has not used suggested antiplatelet treatment up to now. The family history was unremarkable.
In neurological assessment, he was aphonic, but his verbal and reading perception was normal. He was able to answer the questions with signs and writing. The pupillary, corneal reflexes, and extraocular movements were intact. The left nasolabial sulcus disappeared. He was not able to open the mouth, protrude the tongue, show the teeth, whistle, chew, and swallow. The tongue was on the midline and immobile. No tongue atrophy, fibrillation, and deviation were observed. The taste sensation was intact. Palatal, laryngeal, blink, and gag reflexes, spontaneous smiling, and yawning were protected. The upper and lower limbs muscles strengths were 5/5. Deep tendon reflex was normoactive. Babinski response was absent. Extrapyramidal, coordination, and sensory examinations were normal. No vocal cord paralysis was detected on the laryngoscopic examination. The laboratory investigation including liver and kidney function, complete cell count, urinalysis, and erythrocyte sedimentation rate was normal. A transthoracic echocardiogram showed biatrial dilatation, mild calcification of mitral and aortic valves, and mild aortic and mitral valves insufficiency. A doppler ultrasonography of carotid and vertebral arteries was unremarkable. The magnetic resonance imaging (MRI) of brain indicated right frontal opercular acute infarct with 3.3 × 2.6 cm on dimensions () and bilateral chronic inferior frontal gyrus infarct (). He was treated with 300 mg acetylsalicylic acid daily and was placed nasogastric tube for feeding due to lack of swallowing function. At the end of the 3rd week, he had nonsense sounds and was able to open the mouth. However, there was no improvement in speech, chewing, and swallowing functions.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': True, 'age': [81, 'years'], 'Stroke': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 81 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 6 + 1 = 7.
The patient's CHA2DS2-VASc Score is 7."
624,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3658340-1,Extracted,"A 35-year-old woman with the following characteristics was posted for emergency caesarean delivery in view of intra-uterine growth retardation and foetal tachycardia: Second gravida at 35 weeks of gestation with TA, AR and hypertension for 5 years, on treatment with tablet methyldopa 500 mg, amlodipine 5 mg and extended release metoprolol 50 mg, each, twice daily.
Her pulse rate was 114/min and BP was 183/78 mmHg in right arm supine position. Volume of upper limb pulses appeared to be bilaterally equal on palpation. However, right radial pulse was collapsing in nature along with radio-femoral delay. Grade four early diastolic murmur, loudest in aortic area, with palpable thrill-radiating to left sternal border was present. Examination of other systems and investigations were unremarkable. Two dimensional (2D) echocardiogram revealed narrowing of thoracic and abdominal aorta to 9 mm with a high blood flow velocity of 2.0 m/s. Ascending aorta and aortic arch were dilated along with moderate AR. Left ventricular ejection fraction was 58% with normal biventricular systolic function and normal pulmonary artery pressure. Doppler performed 5 years back showed high resistant flows in common, internal and external carotid arteries bilaterally, with possible proximal stenosis of right subclavian artery (SCA).
Baseline vitals in the operating room were as follows: Heart rate of 115/min, non-invasive blood pressure (NIBP) of 188/78 mmHg in right upper limb and SPO2 of 97% [].
Anaesthetic plan was lumbar epidural anaesthesia with invasive radial arterial BP monitoring prior to placing the epidural. Since the doppler report showed possible stenosis of right SCA, left radial arterial line was secured and the invasive BP (IBP) was 112/55 mmHg. Lower limb arterial monitoring was not considered due to narrowing of thoraco-abdominal aorta. Epidural catheter was secured in L1-L2 intervertebral space, and the position was confirmed with test dose of 3 ml of 2% preservative free lignocaine. Patient was positioned supine with a wedge under the right buttock. To achieve a sensory block up to T6 level, 10 ml of 0.5% ropivacaine was given in 5-ml increments every 10 minutes. There was a drop in IBP to 80/40 mmHg along with a drop of NIBP to 122/60 mmHg after the epidural over 10 minutes. We treated the drop in IBP with 6 mg ephedrine boluses to avoid any cerebral or utero-placental hypoperfusion. There was ill-sustained increase in IBP and NIBP after each bolus (3 boluses provided). BP increased up to 122/64 mmHg, while the NIBP increased up to 198/94 mmHg after the third bolus of ephedrine. Patient complained of headache after each bolus of ephedrine. Possibility of over treating IBP leading to headache was considered after ruling out possibilities of monitoring error. On-table doppler ultrasound of upper limb arteries was performed specifically looking at the luminal diameter and amplitude of pulsations. Both were reduced in the left radial and axillary artery when compared to the right radial and axillary artery. Right radial pulsation was collapsing in nature, which is expected in AR. Thereafter, we considered treating using the NIBP values of the right upper limb. Meanwhile, the baby delivered was shifted to neonatal intensive care unit in view of prematurity. Rest of the intra-operative period was uneventful. Postoperatively, the patient was monitored in a high dependency unit. Post-operative aortogram revealed normal right SCA and diffuse disease of the left distal SCA, which confirmed our intra-operative findings.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Diabetes history': False, 'Vascular disease history': True, 'age': [35, 'years'], 'Stroke': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 35 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
625,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3024586-1,Extracted,"A 78-year-old Caucasian woman with no known past medical history presented to the emergency department with complaints of bilateral lower extremity edema and erythema with a clear serous discharge. The patient first noticed some small blisters on her left lower extremity which subsequently opened with some clear serous drainage. She also experienced progressively worsening swelling first of the left lower extremity and then her right lower extremity which prompted her to come into the hospital. Except for a cough, the patient had no other symptoms.
Preliminary evaluation at the emergency department indicated the patient had cardiomegaly and bilateral pleural effusions with a BNP of 1260. She also had atrial fibrillation with rapid ventricular response. The patient was not complaining of any chest pain, fevers, chills, nausea, vomiting or diarrhea. Her chest x-ray showed evidence of cardiac enlargement with interstitial densities and bilateral air-space processes possibly associated with asymmetric pulmonary edema. Large bilateral pleural effusions were noted, with the left greater than the right side. Incidentally, some evidence indicating a compression fracture of indeterminate age involving the upper lumbar/lower dorsal spine was observed.
The patient had no known medical history. In fact, she had not been seen by a physician for the last 15 years. Besides taking aspirin occasionally, she was not on any medications. She did not use alcohol, tobacco or illicit drugs. Physical examination did not reveal any specific concerns other than bilateral lower extremity edema.
CT angiogram of the chest showed large bilateral pleural effusions with bilateral lower lobe enhancing volume loss and worse on the left. Cardiomegaly was noted and there was no evidence for a pulmonary embolus. In addition, there was no evidence of deep venous thrombosis in the venous Doppler studies of her lower extremities bilaterally.
Echocardiogram indicated the left ventricle with some mild hypertrophy. Systolic function was normal with an ejection fraction estimated at about 60%. The right ventricle was mildly enlarged and mildly hypokinetic. The left atrium showed marked enlargement and the right atrium was moderately enlarged as well. The aortic valve was mildly sclerotic and trileaflet. The pulmonic valve was unremarkable. The mitral valve showed flail motion of the posterior leaflet and there was a small mobile echo seen in the left atrium which strongly indicated endocarditis as the cause for pulmonary edema. Doppler examination showed severe mitral regurgitation that tracked underneath the anterior leaflet along the interatrial septum. There was mild aortic insufficiency. The inferior vena cava was dilated indicating elevated right atrial pressure and the pulmonary systolic pressure was estimated at about 50 mmHg.
Gram positive cocci in diploids, tetrads, and clusters were isolated from three sets of blood cultures. The organism was catalase positive and produced a negative coagulase reaction by SlidexTM (BioMérieux, NC). The Vitek 2 GP card (BioMérieux, MO) identified the bacterium as Staphylococcus warneri. It produced acid from trehalose and lacked phosphatase enzyme, two key characteristics that differentiate this species from S. epidermidis - one of the most recognized CoNS [].
The patient was initially treated with Unasyn, 3 grams IV every 6 hours for presumed bilateral lower extremity cellulitis. After the diagnosis of bacterial endocarditis was made and supported by the echo-cardiographic results, the patient was started on nafcillin with gentamicin following consultation with the infectious diseases specialist. In addition, congestive heart failure was treated initially with lasix IV and subsequently with lasix orally. Atrial fibrillation was rate controlled with diltiazem. Gentamicin was later discontinued due to acute renal failure, and the patient was discharged with a PICC line for treatment with 2 grams Nafcillin intravenously every 4 hours for a total of 6 weeks. Repeat blood cultures were negative for 48 hours prior to discharge.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': False, 'Diabetes history': False, 'Vascular disease history': False, 'age': [78, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 78 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
626,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4027656-1,Extracted,"A 75-year-old right-handed woman was admitted because of the abrupt development of mental confusion, left hemiparesis, and dysarthria. She was previously healthy. One day before admission, she developed weakness in her left arm and disorientation, followed 20 hours later by inappropriate speech, agitation, and dysarthria. She had a history of hypertension and diabetes, but no history of psychiatric illness. She had no family history of affective illness.
On admission, she showed partially impaired orientation to time, but had well-preserved orientation to place and person. The neurological examination revealed left homonymous hemianopsia, but no obvious motor or sensory deficits. She appeared agitated, and was talkative with an elated, euphoric mood. She also had a reduced need for sleep and pressured speech. She tended to touch the examiner while speaking. She showed no deficits in the line bisection and cancellation tasks, but was unable to copy an interlocked pentagon. She was also unable to draw a clock. Three days later, she developed motor weakness (grade 4) and hypesthesia in her left arm and face. Dysarthria developed along with persistence of her restlessness and manic features. The motor deficits and dysarthria were improved the next day, but the sensory deficit was unchanged.
Routine serologic testing and electrocardiography were all normal. Initial brain magnetic resonance imaging (MRI) with diffusion-weighted images (DWI) was performed on admission, which revealed an acute infarction in the right parietal lobe with subtle involvement of the posterior temporal area (). Magnetic resonance angiography (MRA) revealed an obstruction of portion M1 of the right middle cerebral artery (). Repeat MRI on the fourth hospital day after the motor deficits developed revealed that the infarction had increased in size (). Brain 2-deoxy-2-[18F]fluoro-D-glucose positron emission tomography (18F-FDG PET) performed 13 days after admission showed reduced FDG uptake in the right hemisphere, which was most severe in the right parietal lobe and left cerebellum ().
When she was discharged 2 weeks after admission, her neurological deficits had improved. Her restlessness and manic symptoms had also partially alleviated without treatment. After 13 months, her neurological deficits and manic symptoms had resolved completely, except for the left-sided visual field defect. Repeated brain 18F-FDG PET showed that the previous reduction in FDG uptake in the right hemisphere had improved ().",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': False, 'age': [75, 'years'], 'Congestive Heart Failure': False, 'Stroke': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 75 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 6. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 6 + 1 = 7.
The patient's CHA2DS2-VASc Score is 7."
627,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8184267-1,Extracted,"An 85-year-old man with a medical history significant for ASH, hypertension,
hyperlipidaemia, and severe aortic stenosis presented to our centre for worsening dyspnoea
with the New York Heart Association (NYHA) Class III symptoms with no reported angina nor
syncope. On physical examination, his blood pressure was 130/80 mmHg, heart rate was 76
b.p.m. Cardiac auscultation was remarkable for an aortic systolic murmur best heard at the
second intercostal space with a significant decrease in S2. The transthoracic echocardiogram
(TTE) showed ASH with a diastolic septal diameter of 17 mm, a fixed LVOT gradient of
11 mmHg, moderately calcified aortic valve associated with severe stenosis (mean gradient of
42 mmHg, the maximal velocity of 4.05 m/s, the continuity equation was not applicable to
calculate aortic valve area due to accelerated jet in the LVOT), an ejection fraction (EF)
of 60%, and normal systolic pulmonary artery pressure. Cardiac catheterization revealed
normal coronary angiogram. He had a low risk for open-heart surgery (Logistic Euro score
7.96%, STS score 2.9%) with a frail physical state for which the Heart team decided to refer
him for TAVI. Computed tomography and angiography showed ASH with a moderately calcified
aortic valve, mild LVOT calcifications (), and an accessible femoral route.
The TAVI procedure was performed with a 26 mm Sapien 3 bioprosthetic valve (Edwards
Lifesciences, Irvine, CA, USA). The initial result was acceptable, with no PVL nor coronary
obstruction. We noticed an upward movement of the valve during implantation (). There was no pre- nor post-dilations required. No
electrical or access site complications were encountered. The patient was transferred to the
cardiac ward.
Later that day, the patient developed chest discomfort associated with atrial fibrillation
with a rapid ventricular response at 130 b.p.m. and non-specific ST-T changes. A TTE showed
normal EF, a mean aortic gradient of 8 mmHg, a fistula jet reaching from the LVOT to the RA,
no right ventricular dilation, no right atrial dilation, and no pericardial effusion.
Transoesophageal echocardiogram showed mild PVL, and an LVOT pseudo-aneurysm, that is
associated with an LVOT to the RA fistula. The fistula's jet was lining the tricuspid valve
plane with a maximal gradient of 123 mmHg (). A post-procedure computed
tomography (CT) scan showed that the bioprosthesis was well placed with no significant PVL,
no coronary artery obstruction. At the level of the LVOT, there exists a small
pseudo-aneurysm of 5 mm, immediately upstream of the valve prosthesis. It is extended by a
fistulous track towards the RA of an ∼2 mm diameter, where the jet flushes parallel to and
outlining the tricuspid valve plane ().
The patient remained asymptomatic during the course of the hospitalization and was
discharged home on Day 7 post-TAVI. The follow-up TTE was done 1 month later showed a
persistence of the fistula with an increase in size (from 2 to 2.95 mm) and an increased
colour jet and gradient (maximal gradient 166 mmHg) ( and ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [85, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 85 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
628,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7489164-1,Extracted,"A 77-year-old female patient with a five-month history of stroke, right-sided weakness and left knee contracture presented to our Physical Medicine and Rehabilitation Department. Following the onset of stroke, the patient was initially treated in an intensive care unit (ICU) before being transferred to the neurology ward. Following discharge from the ward, a monoarthritis of the left knee developed. According to the patient’s relatives, the patient’s knee was evaluated by an orthopedics and traumatology team; however, no details of the evaluation/investigations/ treatment applied are known. To date, the patient had not partaken in a home exercise program or received physical therapy. The patient’s past medical history included hypertension, atrial fibrillation, heart failure and a right total knee replacement five years previously due to osteoarthritis. Prior to development of the stroke, the patient was independent of activities of daily living.
Physical examination revealed a Glasgow Coma Score of 12 with motor and sensory aphasia. There was a flaccid paralysis of the right side. No spasticity was detected. The patient was incontinent of urine and feces. Examination of the musculoskeletal system revealed bilateral painful and limited ROM of the hips and left knee contracture. There was no effusion of the joints. The patient’s Functional Independence Measure[] score was 23.
The patient’s initial routine blood tests were normal. The erythrocyte sedimentation rate was 69 mm/hour and the C-reactive protein was 11.4 mg/L. An anteroposterior X-ray of the
pelvis revealed extensive bilateral periarticular HO (Figure 1). A two-way bilateral X-ray of the knees revealed a total knee replacement on the right side and extensive osteoarthritis of the left knee (Figure 2). Pharmacological treatment with indomethacin was commenced. The Orthopedics and Traumatology Department was consulted for further management of the bilateral hip HO and left knee contracture. Initially, arthroscopic debridement of the left knee was recommended; however, the patient’s relatives did not consent to the procedure. Due to the patient’s limited cooperation, immobility, poor right-sided motor recovery, bilateral limited hip movement and left knee contracture, it was decided that she would gain little benefit from an active inpatient rehabilitation program. The patient was discharged with appropriate analgesia and a home exercise plan with a view to follow-up in the outpatient clinic in a month’s time.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Vascular disease history': False, 'age': [77, 'years'], 'Congestive Heart Failure': True, 'Stroke': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 5 + 2 = 7.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 7. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
629,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2769479-1,Extracted,"A 77-year-old Dutch Caucasian woman presented with a 2-day history of slight headache and progressive walking problems. No recent head trauma had occurred. Past medical history was extended including diabetes, ischemic stroke, hypertension and heart failure. She had been using among others an oral anticoagulant agent because of atrial fibrillation and mitral valve replacement. Neurological examination was unremarkable except for a disturbed heel to shin coordination test and an inability to walk without support. Results of laboratory studies revealed no significant abnormalities and an International Normalized Ratio of 2.6. Computed tomography of the brain showed a 5 mm thick linear hyperdense lesion extending along the right side of the interhemispheric fissure (). Because of the stable neurological condition the patient was admitted for observation and treated conservatively. The anticoagulant agent was stopped and gradual improvement was noticed in a few days. Five days after admission she was able to walk without assistance and she was discharged from the hospital. Two weeks later the patient was in excellent condition. Computed tomography of the brain revealed no signs of a rebleed and showed a hypodense lesion representing the known interhemispheric subdural hematoma of older age ().",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Diabetes history': True, 'age': [77, 'years'], 'Congestive Heart Failure': True, 'Stroke': True}",8,8,8,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 5 + 2 = 7.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 7. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 7 + 1 = 8.
The patient's CHA2DS2-VASc Score is 8."
630,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8275952-1,Extracted,"We report on a case of a 73-year-old man who presented to our emergency department due to progressive shortness of breath (). He was an ex-smoker (30 pack-years of cigarette smoking), with a medical history of dyslipidemia, arterial hypertension, atrial fibrillation, PAD, and left main coronary artery disease (CAD), which led to CABG surgery four months previously. His medical therapy included warfarin, antihypertensive drugs, statin, and a proton-pump inhibitor. Since surgery, he felt a gradual reduction in functional capacity with significant worsening of dyspnea in the last three days. On physical examination, the patient was mildly dyspnoic at rest and had low blood pressure (BP) readings of 105/74 mm Hg on the right arm and 97/69 mm Hg on the left arm. Heart sounds were quiet and irregular. Lung sound was clear bilaterally, with the exception of fine crackles in the right base. Jugular venous pressure was mildly elevated, and there was no evidence of peripheral edema. The rest of physical examination was unremarkable. Electrocardiogram (ECG) showed atrial fibrillation with a rate of 90 beats per minute (bpm), incomplete left bundle branch block, and diffuse T wave inversion in precordial leads. Laboratory tests demonstrated markedly elevated NT-proBNP levels of 3564 ng/L (reference levels <0.73 mg/L), mild increase in serial high sensitive troponin essays (hsTnT) of 31 ng/L and 51 ng/L (reference levels <14 ng/L), and normocytic anemia of 115 g/L (reference levels 138-175 g/L). The chest x-ray displayed an enlargement of the cardiac silhouette with mild pleural effusion and cranial redistribution of pulmonary vasculature, suggesting heart failure. Given the patient`s symptoms, CT pulmonary angiography was also requested to rule out pulmonary embolism. The test did not show signs of pulmonary embolus but showed a large circulatory pericardial effusion (). The patient was admitted to the coronary care unit. The bedside echo showed global hypocontractility of the left ventricle (ejection fraction of 40%) with a confirmed large circulatory pericardial effusion and increased respiratory variations in mitral and tricuspid inflow. Pericardiocentesis was performed with the drainage of 1500 mL of sanguineous effusion over a couple of days. The control laboratory tests showed an hsTnT increase (1865 ng/L) without the progression of clinical symptoms and without echographic or ECG changes. Coronary angiography showed significant stenosis of the left subclavian artery just proximal to the functional LIMA graft to the left anterior descending artery, which indicated the presence of CSSS. While the sudden hsTnT increase could have been explained by pericardiocentesis and consequential hemodynamic changes, myocardial strain, or mild myocardial trauma, it is likely that CSSS had significantly aggravated myocardial perfusion in specific hemodynamic circumstances following pericardiocentesis. Although subclavian bruit was absent, DUS of upper extremities showed reduced blood flow in the left arm, while CTA confirmed the previous angiographic finding and the anomalous origin of the left vertebral artery from the aorta (). As a result, percutaneous transluminal angioplasty was performed. A stent was implanted in the stenotic subclavian artery, followed by optimal blood flow across the treated vessel (). The procedure's success was later also confirmed with control DUS. Control echocardiographic study revealed the absence of pericardial effusion and improvement in cardiac systolic function, which correlated with the patient` s clinical recovery. The patient was discharged from the hospital in a stable condition.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [73, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Vascular disease history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 73 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
631,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8647273-1,Extracted,"We report the case of a 32-year-old Chinese patient who had a history of two pregnancy-related thromboembolic events. These events were cerebral vein-venous sinus thrombosis at 5 gestational weeks (GW) when she was 27 years old and left lower thrombosis following a miscarriage in her second pregnancy in the first trimester at 29 years old. At that point, she was then treated with warfarin.
After routine assessments were performed in the patient at 32 years old, no inherited or acquired risk factors for thrombosis or related family history were discovered, except for AT activity. Her AT activity was only 37% (normal range: 75%–125%) (Berichrom Antithrombin III; Siemens, Erlangen, Germany) while the AT antigen (BN ProSpec system AT-III; Siemens) was 93% (normal range: 80%–120%). The D-dimer concentration was 0.2 µg/mL D-dimer units (normal range: 0–0.5 µg/mL D-dimer units), platelet aggregation in response to arachidonic acid was 82% (normal range: 60%–80%), the prothrombin time was 13.5 s (normal range: 10.3–16.6 s), and the activated partial thromboplastin time was 32 s (normal range: 25.1–36.5 s). Her fibrinogen concentration was 1.13 µg/mL (normal range: 0–5 µg/mL), protein C activity was 98.8% (normal range: 70%–140%), protein S activity was 93.8% (normal range: 63.5%–149%), and homocysteine concentration was 9.8 µmol/L (normal range: 3–17 µmol/L). Antiphospholipid antibodies, including lupus anticoagulant, anticardiolipin, and beta-2 glycoprotein I-dependent anticardiolipin antibodies, were negative.
The SERPINC1 gene in this patient was then analyzed by the gold standard Sanger fluorescent sequencing method in which all exons, exon-intron boundaries, and the promoter region were examined (ABI PRISM 3130; Applied Biosystems, Foster City, CA, USA). Molecular analysis showed a heterozygous mutation, which led to a tyrosine to cysteine change at amino acid position 95, compatible with a type II HBS defect (). On the basis of the findings of a low AT activity level, normal AT antigen level, and genetic result, we made the diagnosis of type II hereditary AT deficiency. Unfortunately, her parents were not available for laboratory assessment for AT activity and genetic testing.
When the patient was 31 years old, she consulted her doctor because she wanted to become pregnant again. At the start of her pregnancy, thromboprophylaxis with self-injection of LMWH at 4100 units every 12 hours with FFP 1 unit weekly was prescribed to replace warfarin because of its adverse effects on the fetus. She had arachidonic acid and D-dimer concentrations measured fortnightly, while her AT activity and anti-Xa measurements were checked monthly throughout pregnancy (). Her serum AT activity level remained at 30% to 40%, but no thrombosis occurred during pregnancy. Her plasma D-dimer concentrations ranged from 0.2 to 1.5 µg/mL D-dimer units, which were within the expected range for pregnant women. Nevertheless, peak anti-Xa activity levels ranged from 0 to 0.29 IU/mL in the second trimester. This activity was not consistent with the required dose ranging from 0.5 to 1 U/mL 2 to 4 hours following the injection. This finding indicated the phenomenon of HR.
After 14 GW, she used LMWH as a bridge to warfarin, then she continued warfarin therapy before delivery. The international normalized ratio was monitored weekly to achieve a level between 2.0 and 3.0. She resumed LMWH and FFP from 37 GW. A cesarean section was scheduled at 37+4 GW. The patient delivered a healthy, 3165-g girl with Apgar scores of 10 at both 1 and 5 minutes. There were no adverse effects of the anticoagulation therapies. The patient and her newborn were discharged without morbidity 7 days later. She continued the same doses of LMWH with FFP, which was replaced with oral anticoagulant therapy from 6 weeks after delivery. The patient and her infant were healthy with no sequelae or adverse events at a follow-up visit 6 weeks after delivery.
The reporting of this study conforms to the CARE guidelines.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [32, 'years'], 'Hypertension history': False, 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 32 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
632,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7891801-2,Extracted,"A 65-year-old male with past medical history of diabetes mellitus, deep venous thrombosis on apixaban, myocardial infarction, hypertension, atrial fibrillation, hypoalbuminemia, emphysema, and morbid obesity presented to the emergency department from a nursing home. The patient complained of abdominal pain, nausea, vomiting, and diarrhea for 24 hours. The patient mentioned an inability to tolerate solid food for approximately one year. The physical examination showed no acute distress, no respiratory distress, atrial fibrillation with rapid ventricular response, and the abdomen was obese and non-tender, without rebound or guarding. An NG tube was placed. His vital signs revealed a temperature of 36.5 °C, blood pressure 143/119 mmHg , pulse 163 beats/minute, respiratory rate 19 breaths/minute, and oxygen saturation 99%. Laboratory evaluation showed WBC count of 26 k/μL with 90% neutrophils, albumin 1.4 mmol/L, BNP 2,300 pg/mL, international normalized ratio 1.4, BUN 22 mg/dL, and creatinine 1.1 mg/dL. A CT scan of the abdomen and pelvis with intravenous contrast showed severe distention of the stomach and duodenum with extensive gas in the wall of the dependent portion of the stomach and extension of gas into the adjacent gastric veins, portal vein, and portal vein branches within the liver [Figure ].
The branches of the celiac artery and SMA were patent. The patient was resuscitated with crystalloids, given broad-spectrum antibiotics, NG tube for gastric decompression, diltiazem infusion for atrial fibrillation, and admitted to the ICU. The patient declined any surgical intervention.
On the second day in the hospital, the patient showed improvement with his abdominal pain, now a 4/10 down from 10/10 on admission. The patient remained on a diltiazem drip for his atrial fibrillation with rapid ventricular response. His abdomen was soft and non-tender; however, his NG tube output was approximately 1 L of bilious fluid. On the third day, the NG tube output was 900 mL of bilious fluid overnight and he had no bowel movement since admission. The WBC reduced to 12,000/μL and he had a benign abdominal examination. CT scan was done with enteral and intravenous contrast to assess for bowel obstruction. It showed that the stomach was now decompressed and there was decreased air within the wall of the stomach and the previously seen air within the left gastric vein and the gastroepiploic veins had resolved [Figure ].
The small intestines, appendix, and colon appeared normal. The patient’s diet was progressed as he tolerated and he was discharged back to the skilled nursing facility on the tenth day.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': True, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': True, 'age': [65, 'years']}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
633,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6419387-1,Extracted,"An 82-year-old female with secondary post-herpetic uveitic glaucoma of the right eye presented at the Department of Ophthalmology for an elective trans-scleral laser cyclophotocoagulation. She had a history of chronic heart failure, arterial hypertension, hyperlipidemia, depression and Hodgkin’s lymphoma in remission. Her regular medications included acetylsalicylic acid, bisoprolol, isosorbide mononitrate, telmisartan, atorvastatin and escitaloprame. The patient denied having any allergies. On preoperative assessment she weighed 62 kg, her height was 162 cm and her blood pressure (BP) was 166/83 mmHg with 70/min heart rate (HR). Physical examination was unremarkable.
The patient’s orbit was anatomically normal. She was given a retrobulbar block to the right eye with 2 mL of 0.5% levobupivacaine and 2 mL of 2% lidocaine. No mydriatic agent was used. She did not move her eye during the procedure. Aspiration for blood was negative. Upon injection, no resistance was felt. 2-3 minutes after the injection, she started yawning and feeling progressively drowsy; anaesthesiology team was immediately called. 5-8 minutes after the injection she became unresponsive to verbal and tactile stimuli; her Glasgow Coma Scale (GCS) score was 3. On arrival of the team she had developed bradycardia with hypotension, her HR was 40/min, BP 50/30 mmHg and blood oxygen saturation (SpO2) 85%. 10 mg of ephedrine was promptly administered intravenously (i.v.) with no significant effect, continued by 3 i.v. doses of 0.1 mg adrenaline 2 minutes later. Concurrently the patient developed respiratory arrest, her SpO2 had fallen to 54%, BP was 163/100 mmHg with HR 93/min. A bolus of 200 mL intravenous lipid emulsion (ILE) was given. Anaesthesia was induced with 50 mg of propofol, the patient was intubated and mechanically ventilated, and her vitals had stabilized (SpO2 98%, BP 113/60 mmHg, HR 92/min). She was additionally sedated with 5 mg of midazolam. Because of persistent hypotension (RR 92/58), 500 mL of hydroxyethyl starch (HES 130/0.4) in isotonic sodium chloride solution was also administered.
Surgery was cancelled and the patient was relocated to the ICU. She was additionally sedated with midazolam and propofol, then gradually shifted through supportive ventilation techniques to spontaneous ventilation and extubated 6 hours after admission. There was no need for vasoactive support, oxygen or fluid replacement therapy. Blood test results were within normal range. Her BP was 140/60 mmHg, HR 71/min, SpO2 95%, without additional oxygen. Her GCS score was 15. The next day she was discharged to the Department of Ophthalmology, where the intended procedure was performed under general anaesthesia. The patient was discharged home 6 days later, she was stable and had not suffered any consequences from the adverse reaction.
Informed consent has been obtained from the patient to use the data presented in this case report.
The research has been complied with all the relevant national regulations, institutional policies and in accordance the tenets of the Helsinki Declaration.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'age': [82, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 82 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 5.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
634,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6368202-1,Extracted,"This case report presents an 80-year-old female with past medical history of Marfan syndrome with extensive cardiovascular manifestations including coarctation of the aorta, mechanical aortic valve and mitral valve replacement, heart failure with reduced ejection fraction (25–30%), and atrial fibrillation. The patient was admitted to the emergency general surgical service for complaints of acute onset colicky periumbilical abdominal pain, progressive abdominal distension, nausea and vomiting for 2 days. Emesis was described as non-bloody and non-bilious. Other pertinent history included one bowel movement 12 h prior to admission, which was non-bloody and inability to pass flatus for more than 24 h. No previous episode of abdominal pain of similar nature were elicitated. Physical examination was significant for mild abdominal distension and generalized tenderness to palpation in all quadrants without signs of peritonitis. Patient was afebrile and hemodynamically stable. Significant laboratory findings were INR of 2.20 (on warfarin for valve replacement), hyponatremia of 125, acute kidney injury with creatinine of 1.56. computed tomography (CT) of the abdomen/pelvis was significant for high-grade small bowel obstruction with a swirling of the superior mesenteric artery (SMA) and superior mesenteric vein (SMV) suggesting rotation of intestinal mesentery (Fig. ) []. The SMV was located to the right of SMA, a reliable finding against intestinal malrotation [] (Fig. ). Further, there was no radiologic evidence of malrotation like transposition of SMA and SMV, the horizontal part of the duodenum not reaching medioventral line, and malposition of ileocecal junction []. The INR was not reversed with FFP and Vitamin K due to concern for stroke. Emergent exploratory laparotomy within 6 h of admission was performed which was significant for midgut volvulus with the small bowel rotating around the base of mesentery a complete 360°. There were no signs of ischemia, and hence manual untwisting of the bowel was performed [, ]. The cecum was noted to be on the right lower quadrant and ligament of Treitz was on the left upper quadrant. The small bowel mesentery was noted to appear long with narrow base and floppy likely contributing to hypermobility of the small bowel. The patients postoperative course was uneventful, and she was discharged to skilled nursing facility for further rehabilitation.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Hypertension history': True, 'Vascular disease history': True, 'age': [80, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 80 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
635,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3120651-1,Extracted,"A 70-year-old right-handed female was brought to the emergency room 35 min after the sudden onset of a stroke. She arrived at the hospital at 11.35 a.m. with dysarthria, right homonymous hemianopsia, dense right hemiplegia, and partial gaze palsy.
Neurological deficit on presentation was assessed using the National Institutes of Health Stroke Scale (NIHSS) with a score of 24. She had a past medical history of hypertension, hyperlipidemia, atrial fibrillation, and hereditary hemorrhagic telangiectasia.
On general medical evaluation she was alert but disorientated. Her blood pressure was 170/80, serum glucose value 89 mg/dl, and cholesterol 213 mg/dl.
At 12:00 she underwent an emergent brain CT scan, which revealed no hemorrhage and only a mild front left hypodensity in the insular area. The Alberta Stroke Program Early CT Score was 8. CT angiogram showed an occlusion of the left M1 trunk, and CT perfusion (CTP) revealed a mismatch among the CBF (cerebral blood flow), MTT (mean transit time), and CBV (cerebral blood volume) maps (Figure ).
All stroke patients arriving at our hospital undergo an emergent brain CT scan, CT angiogram (CTA), and CT perfusion (CTP), according to a protocol agreed upon by neurologists and intensivists.
On the basis of the presence of penumbra, the decision was taken to transfer the patient to an angiographic ward.
Because the angiographic suite was busy with other procedures, an angiography was performed 6 h after the onset of symptoms without any change in her clinical condition. It confirmed an occlusion of the main M1 trunk with excellent collateral circulation from the leptomeningeal anterior cerebral artery and retrograde opacification of the distal M1 segment.
An angiogram was obtained by pulling back the microcatheter to show the extent of the thrombus.
According to exclusion criteria of the SITS-MOST Study Protocol [], Rendu Osler syndrome represents an absolute contraindication for rt PA infusion.
We opted for a mechanical thrombectomy performed more than 6 h after the onset of the stroke with a Hyperform 4 mm × 7 mm balloon angioplasty (EV3) positioned inside the thrombus. Recanalization was achieved with rapid inflations (duration of the inflation, maximum 10 s) at different levels of the M1 trunk.
At the end of the procedure, the artery was recanalized. Thrombolysis in Cerebral Infarction Perfusion Categories (TICI) was grade 3 (Figure ).
Follow-up CTP after 24 h and 7 days revealed persistence of the mismatch (Figure ).
NIHSS score at 24 h was 8, and the Rankin scale at 3 months documented a slight disability (Modified Rankin Score 2).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Diabetes history': False, 'Vascular disease history': False, 'age': [70, 'years'], 'Congestive Heart Failure': True, 'Stroke': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 70 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 6. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
636,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7772857-1,Extracted,"A 67-year-old man presented with a mass on the intergluteal cleft and lymphadenopathy in both inguinal regions. There was no history of pain, fever, malaise, nausea, vomiting, constipation, bloody diarrhea, or abdominal distension. Past medical history included Systemic arterial hypertension in treatment. He first noticed it 1 year before and it had progressively increased in size to 2.5 × 2.5 cm. The mass was soft, non-tender, and freely mobile in the subcutaneous tissue with normal-appearing overlying skin. Examination revealed bilateral inguinal lymphadenopathy (right of 1 cm and a ganglionic conglomerates of 4.5 × 7 cm in left inguinal region). Mohs surgery was performed, and a tumor and ganglion biopsy was taken, histopathological examination revealed high-grade malignancy of primary cutaneous appendages of skin with basaloid differentiation of squamous cells, glandular and alveolar tubule, in some areas myxoid degeneration, microcalcifications, lymphatic and vascular permeation; the tumor was less than 1 mm from the edges of the section and from the surgical bed and ganglion right inguinal lymphatic with metastasis of malignant neoplasm mixed with high skin grade (Fig. and ).
An abdominal computed tomography (CT) with intravenous contrast was performed in which a solid tumor lesion in intergluteal cleft of 2.3 cm, as well as a giant adenopathy in left inguinal region (4.5 cm conglomerate) was reported. Contrast chest CT reported bilateral pulmonary nodules (right 6.4 mm and left basal 1.1 cm) and bilateral axillary and cervical adenopathies. The diagnosis was EPC with areas of epidermoid, basal cell and sebaceous differentiation. No perineural lymphatic invasion, lymph node with carcinoma metastasis (Fig. and ). He started chemotherapy based on etoposide, vincristine, carboplatin.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [67, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 67 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
637,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4144368-1,Extracted,"The case we present here is about a 69-year-old male patient who presented to our hospital with substernal chest pain associated with shortness of breath of 10 days duration and one episode of loss of consciousness one day back. The patient denied chest trauma, fever, or chills. He was a past smoker and taking medicines for systemic hypertension, type-2 diabetes mellitus, and long-standing atrial fibrillation. He was on aspirin, atorvastatin, atenolol, amlodipine, and metformin. In the emergency room, his systolic blood pressure was found to be of 170/90 mmHg with heart rate of 45 beats/min. Family history was unremarkable for any cardiovascular illness. Patient was conscious with no focal neurological deficit. Physical examination was within normal limits except for a soft systolic murmur at the apex. Complete blood count and serum biochemistry were within normal limits. Electrocardiography showed atrial fibrillation with slow ventricular response and ST segment depression of 3 mm in leads V2 and V6 with T-wave inversion. Laboratory studies did not show any elevation in cardiac enzymes. A computed tomography scan of the head showed normal findings. He was taken to the cardiac catheterization laboratory for the placement of a temporary pacemaker and coronary angiography (CAG).
Temporary pacemaker was inserted via right femoral vein and kept in the right ventricle. CAG was performed via right femoral artery approach. Selective cannulation of the left coronary artery revealed a normal left main coronary artery bifurcating into the left anterior descending (LAD) and the left circumflex artery (LCX). There were non-obstructive lesions in the mid-LAD as well as at the first diagonal branch. LCX had minor atherosclerotic plaques. RCA was hooked with Judkins right catheter 3.5 × 6 French (Cordis). Selective cannulation of the RCA revealed a dissection within the proximal segment of an uplifted tortuous (Shepherd’s Crook morphology) RCA with the normal flow down the distal vessel ( and ).
The dissection was treated by direct stenting (3.5 mm × 24 mm, Partner Sirolimus Eluting Stent, Lepu Medical), after which the dissection disappeared (). Three days later, his heart rate was in a range of 60-70 beats/min and temporary pacemaker was removed. His subsequent stay in the hospital was uneventful and discharged free of symptoms on the 5th day. At 6 month follow-up, patient remained chest pain free.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': True, 'age': [69, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 69 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
638,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4620391-1,Extracted,"We report the case of a 58-year-old male that presented to our Emergency Department with complaints of acute interscapular back pain and bilateral lower extremities weakness.
Patient's medical history was significant for diabetes mellitus type II, hypertension, dyslipidemia, and atrial fibrillation. His surgical history consisted of umbilical hernia repair and left hip arthroplasty. Patient had no allergies and had stopped smoking many years ago. He was diagnosed with atrial fibrillation 30 days prior to admission, for which he was started on rivaroxaban 20 mg once daily. The rest of his medications included atorvastatin, fish oil, sitagliptin, quinapril, and triamterene-hydrochlorothiazide.
On the day of admission, the patient admitted waking up at 3:00 am with sudden onset, sharp, interscapular back pain. He denied any similar pain in the past. The patient first presented to another institution, where he started having bilateral lower extremities numbness, which progressed rapidly to bilateral weakness. At this point, he was still able to walk but with difficulty. He was then transferred to our institution, where his weakness became more pronounced. Patient denied any other neurologic symptoms. There was no history of trauma. Prior to this, he had a left hip arthroplasty three weeks earlier, which was performed under spinal (lumbar) anesthesia, without complications. Rivaroxaban was stopped three days before the surgery. Postoperatively he did not receive nonsteroidal anti-inflammatory drugs and was restarted on the OAC few days later. Moreover, he reported driving for almost 7 hours from Elmira (New York) to Staten Island (New York) one day prior to presentation.
Initial physical examination revealed an alert and oriented patient in no acute distress, with a Glasgow Coma Scale score of 15. His blood pressure was 148/98 mmHg; heart rate was 82 beats/min and irregular; body temperature was 98.7°F; respiratory rate was 18 breaths/min. Cardiopulmonary and abdominal exams were within normal limits. Tenderness was elicited over the upper thoracic spine. There were no neurological deficits in the cranial nerves or upper limbs. The motor strength in both lower limbs was of Medical Research Council grade 0/5. A sensory level was evident at the level of T2 with positive bilateral Babinski reflexes.
Initial laboratory assays included a hemoglobin concentration of 11 g/dL, a platelet count of 176 × 109/L, an activated partial thromboplastin time (aPTT) of 36.6 seconds, a prothrombin time (PT) of 18.4 seconds, and an international normalized ratio (INR) of 1.6. Kidney function and liver enzymes were normal. Electrocardiogram and chest radiograph were unremarkable. A noncontrast computerized tomography (CT) of the brain was negative for bleed, and a CT of the chest was also negative for dissection.
The clinical presentation combined with findings on the neurological exam pointed towards a spinal pathology. Moreover, a spinal bleed was strongly suspected given the history of recent spinal anesthesia in addition to the rivaroxaban use. An emergent cervical and thoracic magnetic resonance imaging (MRI) demonstrated an acute 6.3 × 0.6 × 1.6 cm intradural hematoma from C7 to T2, with spinal cord edema (). Neurosurgical intervention was not deemed an option at this point given that the increased risk of rivaroxaban-induced bleeding outweighed the benefits. Therefore, a conservative management was adopted, including close neurological monitoring in the intensive care unit along with high dose intravenous dexamethasone (100 mg once followed by 10 mg every 6 hrs). Patient was also offered prothrombin complex concentrate (PCC), but he declined to proceed with this therapeutic option given its potential side effects, such as prothrombotic state, as well as its uncertain efficacy in similar spinal bleed. He was started instead on aminocaproic acid.
The following day, patient's neurological exam had improved. Sensory level was down to T4-T5, and motor strength was 4/5 in the right lower extremity while it remained 1/5 on the left lower extremity. Given the increased risk of bleeding, especially taking into account the minor improvement in the patient's condition, surgical intervention was delayed for three days, to allow complete elimination of rivaroxaban. On hospital day 4, patient underwent a successful and uneventful anterior C7 corpectomy with resection of a large intradural hematoma. Postoperatively, his neurological exam continued to improve slowly, and he was discharged for intensive rehabilitation 5 days after the surgery. A repeat MRI done 6 weeks later showed almost complete resolution of the spinal hemorrhage ().",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': False, 'age': [58, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 58 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 1 + 1 = 2.
The patient's CHA2DS2-VASc Score is 2."
639,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2639604-1,Extracted,"A 71-year-old Caucasian man with a past medical history significant for type-2 diabetes, coronary artery disease, atrial fibrillation, chronic pericardial effusion and hypothyroidism presented with 5 weeks of increasing fatigue and 1 day of dizziness.
Physical examination revealed that the patient was afebrile, had a blood pressure of 140/90 mmHg, an irregularly irregular heart rate of 102 beats per minute and a respiratory rate of 16 breaths per minute. There was no pulsus parodoxus. Examination of the head and neck showed pale conjunctiva, no palpable lymphadenopathy, jugular venous distension or bruits. Auscultation of the chest revealed scattered rhonchi. The patient was mildly tachycardic with no S3 or S4 heart sounds, murmurs or rubs appreciated. There was no hepatosplenomegaly, clubbing, cyanosis or edema and stools were guaiac negative.
An electrocardiogram (EKG) on admission demonstrated atrial fibrillation with a rapid ventricular response with low voltage QRS complexes; electrical alternans were not present. The chest radiograph showed a very minimal pleural effusion with no cardiomegaly, infiltrates or masses.
Laboratory analysis revealed a white blood-cell count of 12,900/L, with a normal differential, and a hemoglobin and hematocrit of 7.2 g/dl and 23.4%, respectively. The platelet count was 387 thousand/L. The red cell indices were microcytic and iron studies revealed an iron deficiency anemia. Liver function tests were normal. The lactate dehydrogenase (LDH) was 167 U/L (within normal limits). The thyroid-stimulating hormone (TSH) was 16.49 mcIU/ml and the free T3 was 57 mcg/ml.
The patient was admitted for anemia and worked up for a gastrointestinal bleed. Three units packed red blood cells were transfused. Upper endoscopy revealed a mass just below the gastroesophageal junction and three nonbleeding gastric ulcers. To further evaluate the gastric mass, an endoscopic ultrasound (EUS) was performed demonstrating a 30 × 17 mm polypoid mass visualized in the gastric cardia limited to the mucosa/submucosa. The biopsy revealed gastric adenocarcinoma, staged as T1N0M0 by EUS, and was Helicobacter pylori-negative.
A two-dimensional echocardiogram was preformed to evaluate an 8-month old pericardial effusion. It demonstrated a 2.0 × 2.7 cm mass associated with the right atrium (RA). To better define the mass and its anatomic relationship within the RA, several imaging procedures were performed: 1) transesophageal echocardiogram (TEE) showing a 5.7 cm2 shaped echodensity within the wall of the RA and a second, 16 cm2 echodensity, that extended across the atrioventricular groove (Figure ); 2) a contrast computed tomography (CT) of the chest, abdomen and pelvis negative for metastasis, but significant for a large pericardial effusion without pericardial thickening and a 2.6 × 2.1 cm filling defect in the right atrial appendage (Figure ); and 3) a cardiac MRI demonstrating a homogenous enhancing mass along the lateral wall of the right atrium. A positron emission tomography (PET) scan demonstrated a hypermetabolic region in the heart corresponding to the mass observed on CT.
At this point, our differential diagnosis included a primary gastric adenocarcinoma with metastasis to the heart as well as two separate primary neoplastic processes (one involving the heart and one involving the stomach).
To determine the etiology of the cardiac mass, a biopsy was accomplished via a pericardial window through an anterolateral thoracotomy. At thoracotomy, the parietal pericardium appeared normal. Visual inspection revealed several nodular areas over the body of the right atrium, superior vena cava (SVC) and inferior vena cava (IVC). There was no evidence of a thickened, constrictive layer surrounding the heart. Two hundred milliliters of straw-colored fluid was recovered from the pericardial cavity. The fluid was negative for malignant cells and consisted of a few benign and reactive mesothelial cells mixed with inflammatory cells and proteinaceous debris. Viral, bacterial and mycobacterial cultures of the pericardial fluid were negative. Biopsy revealed a normal parietal pericardium and myocardium. However, the visceral pericardium showed a lymphoplasmocytic infiltrate diagnostic of epicarditis (Figure ). After thoracotomy, the patient had a partial gastrectomy to remove the adenocarcinoma. The postoperative course was complicated by infection, requiring a 3-month stay in the intensive care unit. During this time, there was no evidence suggestive of constrictive physiology. Since the patient continued to remain asymptomatic from the epicarditis, no further imaging studies or procedures were performed to follow the ""mass."" The patient eventually succumbed to infection.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': True, 'age': [71, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 71 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
640,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6530056-1,Extracted,"A 68-year-old woman visited our emergency department (ED) because of a sudden attack of severe back pain. The pain developed so suddenly that the ED physician provided a tentative diagnosis of aortic dissection. Chest and abdominal computed tomography (CT) with contrast enhancement revealed no findings related to the pain and both aortic dissection and any aortic involvement were excluded. The ED physician prescribed non-steroidal anti-inflammatory drugs. The next day, the patient presented to the outpatient department and was admitted for further examination. She had medical histories of asthma and atrial fibrillation, was not receiving any medication, was a current smoker, and was not an alcohol consumer. She owned a corgi dog that lived in her house and she had been bitten and scratched by the dog daily.
Upon admission, her body temperature was 37.5 °C, with blood pressure 127/48 mmHg, heart rate 84 beats per minute and oxygen saturation 95% in ambient air with no accelerated respiration. She looked very ill suffering from the severe back pain. A physical examination did not note spinal knocking pain, neurological abnormality, or any other specific findings. A laboratory test revealed a white blood cell count of 13,360 cells/mm3 (normal value: 3900–9800 cells/mm3), platelet count of 17.0 × 104/μL, serum creatinine level of 0.66 mg/dL, and C-reactive protein level of 18.5 mg/dL (normal value: 0–0.5 mg/dL). Re-performed enhanced CT and plane magnetic resonance imaging (MRI) of the spine was not diagnostic.
On the second hospital day, Gram-negative bacilli were detected in her blood cultures. We started intravenous meropenem 1 g every 8 h, based on a provisional diagnosis of spinal epidural abscess or vertebral osteomyelitis/discitis. P. multocida was identified, and drug susceptibility was confirmed by the Vitek2 system with GN and AST-N228 card, bioMérieux (Table ) []. Then, the antimicrobial treatment was switched to intravenous ampicillin 2 g every 6 h.
On the eighth hospital day, MRI was re-performed with gadolinium-contrast to confirm the diagnosis. T2-weighted imaging and T1-weighted imaging with gadolinium enhancement revealed an epidural abscess at the Th5–6 level (Fig. ). We decided to withhold a surgery and continued the conservative treatment because of absence of a neurological deficit. On the twenty-fourth hospital day, the abscess had disappeared on the plane MRI. The antimicrobial treatment was switched to oral levofloxacin 500 mg every 24 h before hospital discharge. In total, 12-week antibiotic treatment was completed. She visits our hospital with another medical condition which is unrelated to this episode, and no recurrence occurred in 5 years after the treatment was completed.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'age': [68, 'years'], 'Diabetes history': False, 'Vascular disease history': False, 'Congestive Heart Failure': False, 'Stroke': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 68 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
641,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4616515-1,Extracted,"This is the case of a 73-year-old woman affected by hepatitis B virus (HBV)-related cirrhosis. The HBV infection was diagnosed in 1981, when she underwent gastrectomy for complicated gastric ulcer. In February 1998, she underwent treatment with 3 million units of Interferon alpha 3 times per week per 24 weeks, without obtaining a biochemical and virological response. She was admitted to our Liver Unit in 1999. She appeared to be in satisfactory general clinical condition and reported being affected by osteoporosis (for which she was treated with calcium and cholecalciferol). She had no history of heart, lung, kidney, metabolic, or thyroid diseases. A needle liver biopsy was performed and histological cirrhosis was diagnosed. At that time the HBV-DNA quantification showed 330,000 copies/ml (COBAS AmpliPrep System, Roche Diagnostics, Monza, Italy) and therapy with 100 mg/die of lamivudine was therefore started. The treatment was promptly and persistently efficacious. Subsequently, the patient regularly attended the outpatient clinic of our liver unit. In February 2010, as a consequence of a slight increase of HBV-DNA levels (up to 300 IU/ml), tenofovir dipivoxil 245 mg/die therapy was introduced, replacing lamivudine.
On November 3, 2011 the alpha-fetoprotein level rose to 217.5 ng/ml and an HCC nodule measuring 14 mm in diameter located in the right lobe was diagnosed by contrast iodine-enhanced computed tomography (CECT). Iodopride at a concentration of 370 mg/ml was the contrast medium used and it was administered intravenously at a dosage of 1.2 ml per kilogram of body weight. In December 2011, the patient underwent percutaneous radiofrequency ablation of the lesion and was subsequently followed up with periodic CECT examinations, according to AASLD practice guidelines; a total of 3 CECTs were performed without the occurrence of any side effect. In occasion of the CECT control on February 5, 2013, the patient appeared to be in good general clinical condition, the blood pressure was 130/80 mm Hg, the electrocardiogram (ECG) was normal, the heart rate was 68 beats per minutes (bpm), the blood tests were normal, HBV-DNA was undetectable. However, 4 hours after the CECT scan with iodine contrast medium administration the patient complained of palpitations, dizziness, and epigastric pain. The blood pressure was 100/60 mm Hg, radial pulse was frequent and irregular, and ECG revealed the presence of high frequency AF (120 bpm). The cardiac enzymes, evaluated every 6 hours from the onset of AF for 24 hours, were persistently within normal ranges. She was treated intravenously with amiodarone 5 mg/kg for the first hour and subsequently at the dosage of 50 mg/hour for maintenance and with subcutaneous 6000 IU/die of enoxaparin. Twenty-four hours after onset of symptoms, there was a reversion to sinus rhythm and on February 6 the patient was discharged from the hospital (Figures and ). During hospitalization, an echocardiographic examination was performed which showed the presence of mitral annulus calcification with mitral insufficiency of moderate degree and mild enlargement of the left atrium.
Four months later the patient was scheduled for a further CECT scan control. At admission on June 10, she exhibited laboratory tests—including thyroid hormone values—within normal limits, she had no symptoms, her liver disease was compensated, the blood pressure was 110/60 mm Hg, the ECG revealed a sinus rhythm with heart rate of 68 bpm. One hour after the intravenous iodide contrast medium administration, she complained about an intense chest pain without any irradiation. The blood pressure was 100/70 mm Hg, her heart rate was irregular with 150 bpm and ECG analysis identified AF. The cardiac enzyme levels were within normal ranges. Therapy with aiodarone was promptly started but this time it had no clinical effect. Therefore the patient underwent electrical cardioversion, which succeeded in reverting to sinus rhythm (Figures and ). During hospitalization a neck ultrasonography examination was performed that showed an increased volume of the thyroid, many small hypo-echoic nodules (diameter <0.5 cm) and swollen cervical lymph nodes. Thyroid tests revealed a profile of subclinical hyperthyroidism [TSH 0.146 μIU/ml (normal range 0.3–4.2); FT3 0.9 ng/ml (normal range 0.87–1.78); FT4 9.12 μg/dl (normal range 6.09–12.23)]. On June 13, 2013 treatment with flecainide 100 mg/die was started; the patient showed no signs of AF and she was discharged from the hospital. Thereafter the patient underwent surveillance of HCC by both ultrasound and magnetic resonance examinations without showing recurrence of hepatic neoplasm so far. She did not experience any new episodes of AF (indeed, she is under flecanide treatment until today), hormone thyroid values remained within normal ranges and no further treatment for thyroid dysfunction was necessary.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Hypertension history': False, 'Diabetes history': False, 'Vascular disease history': False, 'age': [73, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 73 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
642,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2859592-2,Extracted,"A 58-year-old right-handed woman with a history of diabetes mellitus (DM), hypertension, IHD, and chronic kidney disease, on maintenance dialysis presented to the ICU from the dialysis unit when the doctors found her developing sudden onset of right-sided weakness after the completion of the dialysis. She was immediately assessed by a neurologist in the ICU, where she was found to have right-sided hemiplegia with right upper motor neuron facial palsy with dysarthria. Her pulse and blood pressure were stable. She was shifted for the CT brain scan immediately which revealed a hyperdense left middle cerebral artery (MCA) with old bilateral basal ganglia lacunar infarcts. She was diagnosed to have acute left MCA stroke with unknown mechanism and received IV tPA 80 minutes after the stroke.
Following the infusion of IV tPA, the power of left arm and leg improved.Approximately two hours after the completion of tPA,she developed sudden onset of chest pain with cardiovascular collapse. Her blood pressure was 60 mm Hg systolic with pulse rate of 30/min. Immediately, she was started on inotropes. ECG revealed ST segment elevation in anterior leads. Intravenous atropine was started. A temporary pacemaker was inserted. Her troponin-T was sent which was elevated to 7.63. Echocardiogram revealed an ejection fraction of 15% with hypokinetic anterior and lateral wall. There was no cardiac thrombus.
Her baseline ECG was reassessed which showed QS pattern in II, III, aVF indicating an old inferior wall myocardial infarction. Neurological examination revealed that she was unresponsive to verbal commands. Pupils were dilated bilaterally (3 mm) in size and reactive. She had a withdrawal response in her left arm and leg. The mechanism of myocardial injury was postulated to be thrombolytic mediated distal embolization of the proximal thrombus in the coronary arteries. Again the patient succumbed before the arrangement for coronary angiography could be made.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': True, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': True, 'age': [58, 'years'], 'Stroke': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 58 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
643,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8526917-1,Extracted,"We describe the case of an 18-year-old woman with chest pain radiating to the left arm at rest. Her past medical history was unremarkable, apart from Graves’ disease on treatment with methimazole at a dosage of 5 mg/die. She came to our attention in 2020, when she was admitted to the emergency department (ED) for the onset of sharp chest pain radiated to the left arm and to the trapezius ridge. Pain was less severe when in a seated position and more severe when in a supine position, when breathing deeply or during coughing. No episodes of fever, diarrhoea, respiratory symptoms, or myalgia were reported in the previous days. In the ED, the pain was persistent; laboratory findings showed no significant abnormalities. In particular, cardiac markers, D-dimer, complete blood count, C-reactive protein, and procalcitonin were normal. The ECG () showed tachycardia at 128 b.p.m. and diffuse, concave (‘saddle-shaped’) and non-specific ST-segment elevations in all leads except aVR and V1, and PR-segment depression except aVR. Analgesic drugs were administered and the patient was then hospitalized in the Cardiology Department for further diagnostic and therapeutic assessment. On physical examination, blood pressure was 141/63 mmHg and body temperature 36.5°C. On cardiac auscultation, S1 and S2 heart sounds were normal and no pathological murmur was reported; no friction rub was heard. Absence of jugular vein distension and no pulsus paradoxus was reported. Laboratory tests were repeated and showed no significant abnormalities: serum Beta 2 microglobulin, electrolytes, lactate dehydrogenase, and transaminases (ALT, AST) were normal and renal function was not impaired, thus ruling out uraemic pericarditis. Thyroid-stimulating hormone (TSH) was suppressed (<0.0008 mIU/L, local lab normal reference range: 0.4–4 mIU/L) and serum-free thyroxine 4 was increased (61.24 pg/mL, reference range: 8–19 pg/mL); cardiac markers and acute-phase proteins were still negative. Antithyroid therapy was optimized, increasing methimazole dosage to 10 mg TID, and oral propanolol 10 mg TID was introduced. Laboratory tests for autoimmune diseases were performed and the antinuclear antibody panel, lupus anti-coagulant, and anti-neutrophil cytoplasm antibodies were negative. Additionally, anti-mitochondrial (AMA, M2), anti-extractable nuclear antigens, anti-actin smooth muscle antibodies, and anti-Scl-70 (topoisomerase I) antibodies were negative, excluding systemic autoimmune and auto-inflammatory causes of pericardial diseases such as systemic lupus erythematosus, scleroderma and vasculitis. Tests for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (nasopharyngeal swab), Epstein–Barr virus, human immunodeficiency virus, hepatitis C virus, Enterovirus, Parvovirus B19, and Adenovirus were also negative, so that the main viral infectious causes of pericarditis were excluded. Transthoracic echocardiography showed normal left ventricular ejection fraction (EF = 65%), absence of valvular diseases, no pericardial effusion, and normal right ventricular dimensions and function. Thoracic non-ECG-gated CT angiography was then performed () and acute aortic and pulmonary diseases were ruled out. The CT showed the presence of a pericardial effusion with slightly increased density (with radiological characteristic not consistent with blood nature) having a maximum thickness of 15 mm in the upper mediastinum. To characterize this effusion, gadolinium cardiac magnetic resonance imaging (MRI) was performed and the effusion turned out to be an extrapericardial mass of 73 × 51 mm () located in the upper mediastinum. A minimal pericardial effusion was found near the anterior mid-basal wall of the left ventricle where the mass had contact with the pericardium. The pericardium, however, showed no signs of infiltration by the mass and no late gadolinium enhancement was described. In view of this and in the absence of surrounding lymphadenopathies, the haematology specialist indicated biopsy of the mass, which was then performed through video-assisted thoracoscopic surgery. Histological analysis showed true thymic hyperplasia and, from an anatomopathological point of view, prevalence of thymic cortex with various Hassall’s bodies in the absence of lymphoid infiltration was described. After the improvement of the symptoms, the patient was discharged and ambulatory follow-up was planned. At the 1-month follow-up visit on 4 November 2020, the patient was asymptomatic, TSH levels were normal (3 mIU/L), anti-TSH receptor antibodies (TRAb) were 10 IU/L (vs. 35.50 IU/L on admission; reference range <0.55 IU/L), and a 12-month cardiac MRI was planned.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [18, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 18 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
644,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4637487-1,Extracted,"A 70-year-old Caucasian man with a previously diagnosed, IgG-kappa multiple myeloma presented with a 3-month history of worsening dyspnea, dysphagia, and weight loss. The diagnosis of multiple myeloma was established one year prior to presentation with a serum kappa free light chain (K-FLC) level of 685 mg/dL and a lambda FLC level of 0.13 mg/dL (kappa/lambda (K/L) ratio of 5269). The patient had no lytic bone lesions or liver or heart involvement and had a normocellular bone marrow with 70% plasma cells. He was never noted to have macroglossia or albuminuria. His past medical history was otherwise notable for hypertension, type II diabetes mellitus, atrial fibrillation, and chronic kidney disease with Bence Jones proteinuria (K-FLC proteinuria of 691 mg/dL). Upon initial evaluation, the patient was hypoxic to 78% in room air. He appeared tachypneic, with an increased work of breathing and accessory muscle use. Auscultation revealed overall reduced breath sounds, bibasilar crackles, and an irregular cardiac rhythm with a holosystolic grade III/VI murmur loudest at the cardiac apex.
The patient's arterial blood gas revealed a pH of 7.31, a pCO2 of 60, and a pO2 of 60 mmHg. His labs otherwise revealed an bicarbonate of 33 mmol/L, a creatinine of 2.55 mg/dL (increased from a baseline of 1.2 mg/dL), a hemoglobin of 10.3 g/dL, and a white blood cell count of 7.4 × 103 per μL. The patient also had a B-type natriuretic peptide level of 572 pg/mL and serial cardiac troponin I levels of 0.22, 0.22, and 0.21 ng/mL drawn 6 to 8 hours apart. His K-FLC level was 1379 mg/dL with L-FLC of 0.65 mg/dL (K/L-FLC ratio of 2121).
A chest radiograph showed mild pulmonary vascular congestion with small bilateral pleural effusions. His echocardiogram was notable for elevated pulmonary artery systolic pressure of 64 mmHg, biatrial dilatation with normal sized ventricles, and a preserved ejection fraction. A ventilation-perfusion scan was negative for acute or chronic pulmonary embolus.
Subsequently, the patient was admitted to the cardiac stepdown unit for inotropic diuresis and noninvasive positive pressure ventilation (NIPPV). After diuresis, a right heart catheterization (RHC) revealed PA pressure of 34/9/18 mmHg (systolic/diastolic/mean) and a pulmonary capillary wedge pressure of 10 mmHg.
Despite effective diuresis, the patient went into a worsening hypercapnic respiratory failure with almost continuous dependence on NIPPV. His pulmonary function tests revealed restrictive physiology with FEV1 of 61%, FVC of 58%, and FEV/FVC of 104%. A subsequent nerve conduction study was suggestive of bilateral phrenic axonal neuropathy.
With his worsening dysphagia and respiratory muscle weakness, the course was further complicated by aspiration pneumonitis. A barium swallow esophagram showed narrowing of the gastroesophageal junction and tertiary contractions in the esophagus. An upper endoscopy was unrevealing and biopsy samples were negative for amyloidosis, confirmed by lack of Congo red staining (not shown). A fat pad biopsy was also negative for amyloid.
Due to deteriorating cardiopulmonary and renal status, the patient was transferred to our cardiac intensive care unit. A repeat RHC was performed and a right ventricular biopsy was diagnostic of cardiac amyloidosis. The patient subsequently received 3 doses of bortezomib and dexamethasone but passed away soon after from the multiorgan system failure, approximately 5 weeks after admission.
Autopsy revealed IgG-kappa amyloid deposits in the left and right ventricles (), the diaphragm (), and the gastroesophageal junction (). There was no demyelination, amyloid deposition, or other abnormalities of the phrenic nerves (), nor was there amyloid infiltration of the lung parenchyma.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [70, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Vascular disease history': False, 'Diabetes history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 70 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
645,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6359131-1,Extracted,"The patient was a 59-year-old male who presented to our emergency department with a complaint of a 5-h duration of lower abdominal pain. He had a previous history of atrial fibrillation and had taken warfarin, digoxin, and bisoprolol. A physical examination revealed tenderness to palpation of the right lower abdomen without signs of peritoneal irritation. Laboratory data showed slight leukocytosis (WBC 8700/mm3) with slightly elevated C-reactive protein (CRP 0.43 mg/dL).
A computed tomography (CT) image revealed a dilated cecum surrounded by free air, while the appendix was intact (). The preoperative diagnosis was perforation of the cecum. We planned to perform an urgent laparoscopic surgery.
During the laparoscopy, the cecum was found to be dilated and discoloured ().
About 10 h after symptoms onset, we performed a laparoscopic-assisted ileocecal resection. After the resection of the damaged intestine, extracorporeal end to end anastomosis was performed. The specimen revealed localized ischemic change on the anti-mesenteric side of the cecum (). Microscopically, the transluminal ischemic change was confirmed.
The lesion was diagnosed as isolated cecal necrosis. On day three postoperative, the patient developed a small intestinal perforation caused by sticking on the drainage tube, and he underwent ileostomy. After that, the patient progressed uneventfully, and the patient underwent closure of the ileostomy on the 51st postoperative day.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False, 'age': [59, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 59 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
646,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8263222-1,Extracted,"A 59-year-old female patient presented with a personal history of non-insulin-treated diabetes mellitus, dyslipidemia, and hypertension, usually medicated with metformin, perindopril, and simvastatin.
The patient attended to emergency service (ES) due to epigastric pain and feeling of fullness, for which was submitted to dioctyl sulfosuccinate enema and later discharged. Due to the persistence of the complaints and, now, with progressive tiredness, the patient frequented the ES two days later, where she underwent an abdominal ultrasound, which revealed pericardial effusion.
Objectively, on admission, the patient was conscious, oriented, collaborative, eupneic at rest and hemodynamically stable with rhythmic heart tones, no murmurs, decreased vesicular murmur in the right pulmonary base, free and defenceless abdomen, and lower limbs without oedema.
The patient displayed on electrocardiogram a sinus rhythm, 90 bpm heart rate, low amplitude QRS complexes, and nonspecific alterations in ventricular repolarization; chest X-ray was performed with increased cardiothoracic index and bilateral pleural effusion, especially at the base of the right hemithorax; echocardiogram was with large pericardial effusion “swinging heart” and partial collapse of the right heart chambers. The patient is admitted to the cardiac intensive care unit, in the context of cardiac tamponade.
During hospitalization, the patient underwent: pericardiocentesis, with a total drainage of 1250 cc, whose fluid, according to the pathological anatomy, evidenced neoplastic cells. She also underwent a thoracic-abdominal-pelvic computed tomography which revealed bilateral pleural effusion, with adjacent parenchymal atelectasis, slight pericardial effusion (), and zones on the left side, with clear pericardial thickening suggestive of pericardial metastasis, after intravenous contrast. Several nodules in all lung lobes were indicative of metastases. The patient also underwent fine-needle aspiration biopsy of a cervical nodule, which has shown to be a melanoma metastasis. Later on, it was found out that the patient had malignant melanoma with inguinal ganglion metastasis in 1995 and completed chemotherapy, cutaneous excision, and lymphadenectomy in 1996.
During hospitalization, the patient had several periods of paroxysmal atrial fibrillation, despite chemical cardioversion with amiodarone. The patient was discharged with oral anticoagulation and digoxin, as an effective heart rate management agent.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': True, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': False, 'age': [59, 'years'], 'Congestive Heart Failure': True, 'Stroke': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 59 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
647,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4506443-1,Extracted,"A 68-year-old Caucasian woman, with active tabagism (40 pack-years), obstructive sleep apnoea syndrome under continuous positive airway pressure (CPAP) via nasal mask, and hypothyroidism secondary to a partial thyroidectomy in 1979, was investigated by her practitioner for fatigue in 2010. The current treatment at that time was aspirin 100mg per day, levothyroxine 100μg per day, and lorazepam 1mg per day. Her family history was negative for any hematologic malignancy.
A hemoglobin (Hb) level of 177g/L and hematocrit (HCT) level of 55% was found, with slight leukocytosis at 12.3G/L, but there was no other abnormality found on her blood smear, especially no left deviation or myelemia. Therefore it was initially interpreted as secondary erythrocytosis.
In 2012 a rise in her Hb level was noted and she was seen at our institution for further investigation. Her test results indicated a Hb level of 180g/L, a HCT level of 55%, a leukocytes count of 16G/L with normal differentiation, a thrombocytes count of 294G/L, and a reticulocytes count of 67G/L. Her arterial blood gas levels were: partial pressure of oxygen in the arterial blood (PaO2) of 8.8kPa, partial pressure of carbon dioxide in the arterial blood (PaCO2) of 4.7KPa, carboxyhemoglobin at 8.6%, a pH of 7.42, and a base excess of -1.2mmol/L with oxygen saturation at 95%. Her lactate dehydrogenase value was 527U/L (normal value: <450U/L), with her liver test results showing normal function. Her erythropoietin and ferritin values were low at 2.3U/L (normal value: 8 to 22U/L) and 16μg/L (normal value: 30 to 300μg/L), respectively. In this context, polycythemia vera was suspected, but could not be confirmed by molecular biology analysis as she was negative for the JAK2 V617F mutation. Interestingly, her vitamin B12 level was very high at 1,703pg/mL (normal value: 185 to 1,060pg/mL).
Her blood marrow biopsy revealed a slight hypercellularity with discrete hyperplasia and slight atypia of megakaryopoiesis, normal erythropoiesis with discrete signs of dyserythropoiesis without hyperplasia, and normal myelopoiesis. These abnormalities were aspecific and not suggestive for a MPN. Based on hyperleukocytosis and a high vitamin B12 level, we searched for the BCR-ABL1 fusion gene, which was surprisingly positive. Her bone marrow conventional cytogenetic analysis revealed a female karyotype with the presence of the Philadelphia chromosome (t (9; 22) (q34; q11.2)) in 85% of metaphases.
An interphase fluorescence in situ hybridization (FISH) analysis confirmed the BCR-ABL1 rearrangement in 88.5% of interphases analyzed. In light of these results we diagnosed a BCR-ABL1-positive CML, in chronic phase, with a low risk Sokal score (0.62). Given the presence of the Philadelphia chromosome (t (9; 22) (q34; q11.2)), we did not search for exon 12 mutations.
We started a therapy of imatinib mesylate (daily dose of 400mg) on 13 April 2012, and she showed relatively good tolerance. Under treatment, she obtained a complete hematological response at three months, including rapid disappearance of her erythrocytosis (see Figure ), normalization of absolute neutrophil count (see Figure ) with complete cytogenetic response and major molecular responses being observed at six months (see Figure ). These responses were considered optimal according to European LeukemiaNet criteria 2010 and 2013 [].",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False, 'age': [68, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 68 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
648,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7192128-1,Extracted,"A 59-year-old male with hypertension, chronic kidney disease, and paroxysmal atrial fibrillation (AF) was referred for catheter ablation due to an increasing frequency of symptomatic AF episodes over the past year despite antiarrhythmic drug (ADD) therapy. After discussion of the risks and benefits of catheter ablation and different modalities for pulmonary vein (PV) isolation (PVI), the patient opted to undergo visually guided laser balloon (LB) ablation. A baseline transthoracic echocardiogram revealed normal left ventricular ejection fraction (55%) and left atrial (LA) volume index (32.1 mL/min).
After informed consent was obtained, the patient was brought to the electrophysiology (EP) laboratory and placed under general anesthesia for the procedure. Percutaneous femoral venous access was obtained using ultrasound guidance and modified Seldinger technique. An 8-French (Fr) intracardiac echocardiography (ICE) catheter (AcuNav™; Biosense Webster, Diamond Bar, CA, USA) was advanced into the right atrium (RA) and a three-dimensional (3D) electroanatomic shell was created of the RA, LA, superior vena cava (SVC), and coronary sinus (CS) ostium and integrated into the CARTO® 3 mapping system (CARTOSOUND®; Biosense Webster, Diamond Bar, CA, USA). A five-spline multielectrode mapping catheter (Pentaray®; Biosense Webster, Diamond Bar, CA, USA) was advanced to the inferior vena cava (IVC)–RA junction and a 3D fast anatomic map of the RA cavity, ostium, proximal body of the CS, and SVC was created. A detailed map of the course of the right phrenic nerve (PN) was also developed during high-output pacing from the mapping catheter’s distal poles beginning at the right innominate artery–SVC junction and sweeping down to the SVC-RA junction (. Next a 7-Fr decapolar catheter (Biosense Webster, Diamond Bar, CA, USA) was positioned in the CS using electroanatomic mapping (EAM) guidance and previously acquired anatomy as visual landmarks.
The multispline mapping catheter was then exchanged for a long 0.032-in J-wire, which was positioned in the SVC under ICE visualization (ie, high in the RA with a posterior tilt) without the use of fluoroscopy (. A 63-cm-long SL1 sheath (Abbott Laboratories, Chicago, IL, USA) was advanced over the long 0.032-in J-wire into the SVC under ICE visualization. The 0.032-in J-wire was then exchanged for a BRK-1 transseptal needle (Abbott Laboratories, Chicago, IL, USA), and brief fluoroscopy was used to confirm that the tip of the transseptal needle did not extend beyond the tip of the SL1 dilator. The proximal end of the BRK-1 needle apparatus was connected to alligator cables (Abbott Laboratories, Chicago, IL, USA) and a pin box to facilitate live tracking of the needle tip on the CARTO® 3 mapping system (CARTOSOUND®; Biosense Webster, Diamond Bar, CA, USA). Under EAM guidance, the transseptal assembly was pulled down from the SVC onto the fossa ovalis (. The presence of interatrial septal tenting was visually confirmed on ICE imaging in the plane of the PVs. Successful puncture of the interatrial septum with the BRK-1 needle was confirmed on ICE by the presence of bubbles within the LA, and the SL1 was advanced into the LA. The BRK-1/dilator assembly was exchanged for the multispline mapping catheter, and a 3D map of the LA and PVs was created.
The multispline mapping catheter was removed, and an Amplatz super stiff guidewire (Boston Scientific, Natick, MA, USA) was advanced through the SL1 sheath and placed into the left superior PV (LSPV) under ICE imaging (. While maintaining constant ICE visualization of this wire in the LSPV, the SL1 sheath was exchanged for a 12-Fr steerable sheath-dilator assembly (CardioFocus, Marlborough, MA, USA). The LB catheter (HeartLight Excalibur™; CardioFocus, Marlborough, MA, USA) was advanced through the 12-Fr sheath and into the LA cavity. Under ICE visualization, the soft, atraumatic tip of the LB catheter was directly advanced into an upper branch of the LSPV without tactile resistance (. The catheter’s balloon was then manually inflated under endoscopic and ICE visualization (. The ideal antral position of the equatorial surface of the LB was confirmed on ICE by the presence of the balloon’s proximal end within the LA cavity and by endoscopic landmark visualization (. If the position of the catheter’s distal end interferes with obtaining coaxial alignment of the balloon with the PV ostium, the LB can be pulled back into the LA cavity while still inflated ( and the PV can be reengaged by gently pushing forward with the LB while viewing on ICE until the tip is advanced into a different side branch.
Following delivery of a circumferential lesion set around the LSPV antrum, the LB was deflated and withdrawn from the LSPV. Under ICE visualization, the sheath was deflected until the catheter tip was pointing directly toward the ostium of the left inferior PV (LIPV) (. The LB catheter was advanced into the LIPV and inflated until antral balloon contact was confirmed with endoscopic and ICE visualization (. A similar circumferential laser lesion set was created to isolate the LIPV (.
To cannulate the right inferior PV (RIPV) under ICE visualization, we utilized a “hockey-stick” maneuver. First, the LB catheter was withdrawn until just the atraumatic tip was exposed beyond the 12-Fr sheath. While still facing the left PVs, we maximally deflected the sheath and withdrew the assembly toward the interatrial septum while maintaining a curve on the sheath. To avoid damage to the LA posterior wall during this maneuver, brief fluoroscopy was used to reconfirm that the LB catheter’s soft tip remained beyond the sheath prior to RIPV cannulation. Using ICE, the 12-Fr sheath was rotated clockwise until the sheath–catheter assembly was visualized in the same plane as the RIPV (. Following cannulation of the RIPV and inflation of the LB using the aforementioned steps, the decapolar catheter was removed from the CS and aligned with previously tagged sites of PN capture. While pacing at a suprathreshold output, an antral circumferential RIPV lesion set was created while simultaneously limiting the likelihood of PN injury by monitoring the compound motor action potential amplitude and manually assessing diaphragmatic movement.
For cannulation of the right superior PV (RSPV), the ICE catheter was advanced superiorly with slight posterior deflection until the vein was visualized. After withdrawing the LB catheter from the RIPV, deflection on the 12-Fr sheath was released and the sheath–catheter assembly was slowly clocked until the LB catheter was seen in the same plane as the RSPV on ICE (. The LB catheter was then advanced into the RSPV and circumferential ablation was performed while monitoring for PN injury as described above.
After LB ablation of all four PVs was visually completed, the LB catheter was exchanged for a multielectrode mapping catheter and a postablation high-density voltage map was created of the LA and PVs, confirming entrance block (. Pacing from the multielectrode catheter positioned at the ostium of each PV was used to demonstrate exit block. The LB catheter–sheath assembly was then removed from the LA. After checking the final activated clotting time, protamine was administered intravenously and all remaining sheaths and catheters were removed. Hemostasis was obtained with manual pressure.
There were no complications during the procedure. The final ICE images of the pericardial space revealed no evidence of pericardial effusion. The patient resumed his direct oral anticoagulation regimen the same evening and was discharged from the hospital the following day. His AAD was discontinued three months after ablation and he experienced no recurrence of AF during eight months of follow-up.
Overall, the total procedure time was 146 minutes and the LA dwell time was 59 minutes. The fluoroscopy setting was 7.5 frames per second. The fluoroscopy time required to obtain transseptal access was 0.3 minutes. The total fluoroscopy time in the LA to accomplish PVI and confirm bidirectional block of all four PVs was 0.2 minutes. Thus, the total procedural fluoroscopy time was 0.5 minutes.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Diabetes history': False, 'Vascular disease history': False, 'age': [59, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 59 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
649,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3214513-1,Extracted,"A 55-year-old woman with no past medical problems was referred to our ED from a local hospital with acute pulmonary edema. She was seen in that hospital twice previously with episodes of acute pulmonary edema that was treated with intravenous diuretics. She had an appointment with cardiologist after a month. Clinical examination revealed normal vital signs, normal JVP, bibasilar rales and a very faint mid-diastolic murmur heard at the apex of the heart without an opening snap. Her ECG was normal. Chest X-ray showed no cardiomegaly but there was pulmonary congestion. In view of recurrent pulmonary edema in the absence of obvious causes for pulmonary edema and a long waiting for cardiologist consultation, a bedside transthoracic echocardiographic examination of the heart was performed using the ATL HDI 5000 machine to rule out any gross abnormalities in the heart. Bedside transthoracic echocardiographic examination showed a large rounded mass protruding from the left atrium into the left ventricle [Figures and ]. This mass was relatively fixed at mitral valve causing diastolic obstruction of mitral inflow and ‘functional’ mitral stenosis leading to recurrent pulmonary edema. The mass seemed to be attached to lower part of interatrial septum and the echocardiographic appearance of the mass was pathognomic of atrial myxoma. The patient underwent urgent surgery to remove the mass. At surgery interatrial septum was intact with an 8×4 cm mass seen attached from low interatrial septum with a small pedicle and occupying whole of mitral annulus. The mass was excised from the atrial septum which was secured by a patch closure. It weighed 64 gm and the histology of the specimen showed abundant hyaline and myxoid stroma containing small groups of tumor cells, compatible with the diagnosis of atrial myxoma.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [55, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 55 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
650,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7275196-1,Extracted,"A 77-year-old Caucasian woman initially presented with pancytopenia, referred from the primary care physician to the hematology/oncology clinic for further evaluation in April 2019. Her past medical history was notable for paroxysmal atrial fibrillation, hyperlipidemia, and recurrent allergic sinusitis. She was on metoprolol, apixaban, and ezetimibe. On presentation, she was afebrile with a blood pressure of 126/80 mm Hg, a heart rate of 72 beats/min (regular), and a respiratory rate of 16 breaths/min. A comprehensive physical examination was unremarkable.
The laboratory data revealed pancytopenia with a platelet count of 116 × 1,000/mm3, a white blood cell count of 1.7 × 1,000/mm3 with 25% neutrophils, and a hemoglobin level of 9.5 g/dL with a mean corpuscular volume of 80.9 fL/cell and a red blood cell distribution width of 22.9. Flow cytometry was unremarkable. All other laboratory investigations, including a liver function test, creatinine, thyroid function tests, and a hepatitis panel, were also within normal limits. Her iron studies and hemoglobin electrophoresis results were also normal.
She was initially suspected of having α-thalassemia, but a bone marrow biopsy in May 2019 demonstrated findings consistent with AML positive for IDH2 mutation with 16% marrow blasts/promonocytes without circulating blasts. Due to the diagnosis of AML with IDH2 mutation, she was advised against bone marrow transplantation given her age. She was started on a regimen of 5-azacitidine and enasidenib. Prophylactic antiviral, antifungal, and antibiotic medications were also initiated.
After 2 weeks, she was scheduled for the second cycle of chemotherapy. However, it was held off as she reported having subjective fevers associated with headache, frontal sinus pressure, and loss of appetite. Computed tomography of the sinuses showed evidence of inflammatory disease. She was treated with amoxicillin/clavulanic acid (Augmentin) for a presumed diagnosis of bacterial sinusitis. A few days later, her second dose of chemotherapy was administered. During a follow-up visit, her laboratory data revealed hyperbilirubinemia of 3.8 mg/dL, which raised a concern for differentiation syndrome. Therefore, she was started on dexamethasone 8 mg twice a day.
On her next follow-up visit, she complained of dyspnea. Her physical examination was notable for diminished breath sounds at the lung bases and bilateral pitting edema. The chest radiograph confirmed bilateral pleural effusions. A 2D echocardiogram showed a preserved left ventricular ejection fraction. She was treated with oral furosemide along with steroids and pantoprazole. Apixaban was held due to pancytopenia. During this time, she was hospitalized for dehydration in the setting of furosemide use and reduced oral intake. An EKG showed rapid atrial fibrillation. Her laboratory data showed a worsening hyperbilirubinemia up to 5.5 mg/dL, and new-onset hyperthyroidism with TSH less than 0.02 ng/dL and elevated free T4 of 2.1 ng/dL. An I-123 thyroid scan showed slightly increased uptake in the upper portion of the right thyroid lobe with no suppression in the remainder of the gland, consistent with thyroiditis. Rate control of atrial fibrillation was achieved with uptitration of β-blocker; methimazole was avoided due to concerns for bone marrow suppression.
Due to persistent hyperbilirubinemia despite being on steroids, the dosage of enasidenib was reduced to half. After the dose reduction, repeat total bilirubin started trending down to 4.4 mg/dL. A few weeks later, during a follow-up visit, she was feeling better and was switched to a steroid taper. Her free T4 levels also trended down to 1.5 ng/dL. Subsequently, she started her third cycle of chemotherapy with a reduced dose of enasidenib (50 mg). During a follow-up visit, her dyspnea and fatigue were noted to have improved and her thyroid panel and bilirubin levels had normalized.
She was able to complete cycles 4/5 and 5/5 of azacytidine with enasidenib uneventfully. Her antifungal and antibiotics were discontinued due to normalization of her absolute neutrophil count.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [77, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
651,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5985765-1,Extracted,"A 73-year-old woman was admitted to our hospital because of deterioration of memory and abnormal behavior for more than 1 year. According to her medical records, this patient had suffered from major depressive disorder for more than 40 years and initiated antidepressive therapy 10 years before this admission. She had taken mirtazapine and olanzapine for 1 year, and her mood improved and stabilized. She gradually stopped these medications under the surveillance of her doctor. Four years before admission, the patient suffered from acute cerebral infarction, which was possibly caused by atrial fibrillation. Her emotional level went down after this cerebrovascular accident. She became depressed and nervous, had difficulty in falling asleep, and would complain that somebody wanted to hurt her and her family members. She felt hopeless about her life and lay in bed every day. During that period, she hardly spoke and refused to eat. She was brought to our hospital, and cranial magnetic resonance imaging (MRI, 1.5T) revealed multiple encephalomalacia in the right cerebellar hemisphere, left occipital lobe, and left pons, along with ischemic changes in the bilateral periventricular regions and bilateral centrum semiovale (). She was then sent to our department for further treatment. On admission, she was diagnosed with depressive syndrome caused by cerebral infarction and atrial fibrillation. Quetiapine (300 mg per night) combined with venlafaxine (225 mg per day) were prescribed. Her condition gradually stabilized in the following 2 months. This patient continued to take these medications, and 2 years before this admission, the dose of venlafaxine was reduced to 150 mg per day, and quetiapine 200 mg per night.
On this admission, the patient was well-orientated, but euphoric, childish, loss of self-insight, and abnormal behavior, such as garbage sorting and picking flowers, was observed. No hallucination or delusion was reported. Laboratory examinations, including routine blood test, biochemical profiles, tumor markers, infectious diseases, and thyroid function, were all within the normal reference ranges. Cranial MRI scanning was performed again, and the findings were similar to the previous examination (). No acute cerebrovasuclar events were reported.
The patient scored 18/30 on the Mini-Mental State Examination, and she had graduated from a senior high school. According to the Diagnostic and Statistical Manual of Mental Disorders (fifth edition), she was diagnosed with vascular neurocognitive disorder, with behavioral disturbance. Accordingly, venlafaxine was discontinued and the dose of quetiapine was increased to 400 mg per night. Meanwhile, donepezil 5 mg per night was also added for improving her cognitive function. However, she became emotionally unstable and fragile in the next 2 days, often crying and making noises by herself. The patient repetitively complained that she was abandoned by her children, and she would sometimes cry and sometimes smile for no reason. Escalating the dose of quetiapine to 600 mg per night also showed no significant improvement.
Due to the poor treatment outcome, donepezil was discontinued and memantine at a dose of 10 mg per night was initiated. Her symptoms visibly ameliorated in 2 days. However, after taking memantine for 1 week, the patient became more and more excited and talkative. She could not stop talking and repetitively sought doctors for chatting. She laughed all the time, and even began to practice Tai chi in the ward. In view of her overexcitement, memantine was stopped and lithium carbonate 300 mg twice a day was prescribed. After ensuing the serum concentration of lithium was within the normal reference range, the dose of lithium carbonate was increased to 300 mg 3 times a day. Her emotions finally stabilized after taking lithium carbonate for 5 days.
The Institute Ethical Committee of the First Affiliated Hospital, Zhejiang University School of Medicine, approved this case study. Written informed consent for publication of this case and any accompanying image was obtained from our patient and her guardian.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': True, 'Transient Ischemic Attacks History': True, 'Vascular disease history': False, 'age': [73, 'years'], 'Congestive Heart Failure': False, 'Stroke': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 73 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
652,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5987242-1,Extracted,"A 69-year-old Caucasian woman presents with confusion, headache, generalized weakness, ataxia, and increased agitation on the second day following a CT myelogram during which she received L2-L3 interspace lumbar puncture with fluoroscopic guided injection of 15 cc Omnipaque (Iohexol) 300, a nonionic water-soluble contrast material, in the prone position using a 20-gauge spinal needle. There were no complications during the procedure and after an adequate observation period the patient was discharged in a stable condition.
Her past medical history includes chronic back pain with spinal stenosis, diabetes, coronary artery disease, hyperlipidemia, colitis, gout, atrial fibrillation, and sick sinus syndrome. Her surgical history includes pacemaker placement, hysterectomy, and tonsillectomy. She has no known allergies. Her medication includes aspirin, allopurinol, amlodipine, colchicine, furosemide, gabapentin, metformin, pravastatin, metoprolol, pregabalin, and spironolactone.
On physical examination, the patient's vitals were stable. She was noted to be restless, agitated, and disoriented to place and had hyperactive deep tendon reflexes. She had no focal neurological deficits. Except for a mild elevation in WBC of 13.0, her laboratory values including CBC, CMP, urine analysis, and toxicity screen were all within normal limits.
A head CT revealed new supratentorial bilateral vasogenic edema with loss of all sulci and with poor differentiation of white and gray matter (). There was no evidence of any compression of the quadrigeminal plate cistern or fourth ventricle on imaging. These findings were not visualized on previous imaging. Patient was admitted to the neurology intensive care unit (ICU) and was treated with mannitol, corticosteroids, and seizure prophylaxis. She was discharged in a stable condition after a 5-day admission with resolution of both clinical symptoms and radiographic findings of cerebral edema on head CT ().",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': True, 'age': [69, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 69 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
653,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8519794-1,Extracted,"A 72-year-old female patient presented to the emergency department (ED) after a primary care physician referral for tachycardia, who saw her with complaints of epigastric discomfort, vomiting, and loss of appetite for the past 2 days. An electrocardiogram (ECG) at the clinic revealed a narrow complex tachycardia of 169 beats/min. She was admitted for ischemic stroke 6 months earlier and was on aspirin. During that admission, PSVT developed but was successfully treated with intravenous (IV) adenosine. She was reviewed by the cardiologist, and 2D echocardiography was performed, which did not reveal any underlying structural heart abnormalities. In addition, an electrophysiological study confirmed the underlying etiology of PSVT as AVNRT.
On arrival, she was alert with a temperature of 37.3°C; heart rate of 170 beats/min; respiratory rate of 25 cycles/min; blood pressure of 112/81 mm/Hg; and oxygen saturation of 97% on room air. Her physical examination was normal. The ECG revealed a narrow complex tachycardia suggestive of AVNRT due to the presence of retrograde conduction of P waves in leads I and aVR (). Previous ECG documented in electronic health records did not show any signs of pre-excitation for AVRT from an accessory pathway or prolonged QTc syndrome. She was observed on continuous cardiac rhythm monitoring throughout her ED stay.
Vagal maneuver (Valsalva) was attempted without success. A carotid sinus massage was not performed as the patient had a stroke history. IV adenosine at 6 mg was given for pharmacological conversion. Shortly after IV adenosine administration, the patient became unresponsive and developed a generalized tonic-clonic (GTC) seizure. Pulse was absent, and the cardiac monitor revealed ventricular fibrillation (VF). Cardiopulmonary resuscitation was immediately started together with the preparation for defibrillation. However, just before defibrillation, the seizure spontaneously aborted and she had a palpable pulse with a return of spontaneous circulation (ROSC). The whole episode of seizure and VF lasted for approximately 8–10 s. The cardiac monitor revealed a normal sinus rhythm conversion and the patient spontaneously regained consciousness. Repeat vital signs were stable with a heart rate of 72 beats/min; blood pressure of 102/62 mm/Hg, and oxygen saturation of 99% on room air.
A rhythm strip () review recorded during the IV adenosine administration revealed an initial suppression of the AV conduction lasting for approximately 6 s interspersed, with non-conducted P waves and ventricular escape beats (), in which the last escape beat triggered the onset of VF (), which lasted for approximately 8 s. The VF duration corresponded to the GTC seizure duration, indicating a convulsive syncope secondary to VF resulting in seizure. The patient does not have any history of epilepsy. This was followed by spontaneous VF termination and continued AV conduction suppression with a period of aberrantly conducted supraventricular impulses () before sinus rhythm reversion (). A repeat ECG post adenosine administration did not reveal any pre-excitation features ().
Blood investigations were done in the ED upon patient arrival before adenosine administration. These included a complete blood count with hematocrit level, serum electrolytes, and thyroid function test, which all revealed normal results. Coupled with her normal physical examination without signs of dehydration and ECG that was not suggestive of sinus tachycardia, the possibility of dehydration as a contributory factor to the tachycardia was ruled out. The patient was admitted to the High Dependency Unit (HDU) under cardiology. During admission, her serial cardiac enzymes were normal. Her symptoms of epigastric discomfort and vomiting were attributed to gastritis. She had another episode of SVT in the HDU, which was successfully converted with IV diltiazem. Myocardial perfusion imaging was negative for ischemia, and the transthoracic echocardiography revealed a normal ejection fraction without regional wall motion abnormalities. An electrophysiological study was not performed during this admission due to her advanced age and other co-morbidities. She was discharged stable after a few days and was started on long-term oral diltiazem.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': True, 'Vascular disease history': False, 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Stroke': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
654,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4857320-1,Extracted,"A 63-year-old woman was admitted to our department because of pain and limitation in motion in the left hip for 2 years after primary total hip arthroplasty with hybrid prosthesis for avascular necrosis of the femoral head 15 years ago. The patient underwent mitral commissurotomy because of mitral stenosis 30 years ago, when she complicated with atrial fibrillation, since then she had been taking aspirin 100 mg once daily. The patient presented absolute arrhythmia and uneven first heart sound on auscultation. Electrocardiogram demonstrated atrial fibrillation. X-ray film of the pelvis and the left femur revealed osteolysis around the femoral stem and subsidence of femoral component.
The patient was diagnosed as aseptic loosening of the femoral component after total hip arthroplasty and underwent revision total hip arthroplasty with cementless acetabular component and cementless modular stem and allograft for bone defects in both sides. Aspirin was discontinued 7 days before surgery. The procedure was performed uneventfully. The patient began to take rivaroxaban 10 mg 12 h after surgery, which was planned once daily for 35 days. The patient was told to start functional exercises of the left lower extremity as soon as tolerated and began to ambulate with crutches with the left lower extremity free of weight bearing on the 15th day postoperatively.
The patient felt sudden numbness, tingling in the right lower extremity, and inability to move it after having a nap on the 17th postoperative day. Physical examination: pulse 80/min and blood pressure (BP) 120/70 mmHg mentally conscious, with pupils round, symmetrical, and sensitive to light. There was loss of sensation, paresis, and decreased skin temperature for the right lower extremity, with pedis artery impalpable on the right side and normal pedis artery on the left side.
The color Doppler showed that there was insufficient blood flow with low vascular tension in the right lower extremity, which suggested stenosis or incomplete obstruction proximal to the popliteal artery. Computed tomography (CT) angiography showed that there was complete occlusion of the right common iliac artery and the beginning of internal and external iliac arteries, with no collateral circulation from the contralateral side (), which caused narrowing of arteries of the right lower extremity.
The patient underwent an emergency digital subtraction angiography (DSA; ) and catheter-directed thrombolysis combined with balloon angioplasty. The procedure was performed by a contralateral retrograde approach under regional anesthesia. Initially, catheter-directed thrombolysis was performed with urokinase 300,000 units for half an hour. Subsequent angiography showed antegrade flow with large residual thrombi. Then, a balloon was used to get patent recanalization (), followed by urokinase 500,000 units pumped into the right common iliac artery for 24 h. Post-procedure angiography demonstrated smooth blood flow without filling defects in the previously occluded arteries (). The feeling of tingling in the right lower extremity disappeared soon after balloon angioplasty. The right pedis artery got palpable and skin temperature gradually returned to normal. Sensation gradually recovered with disappearing of numbness in the right lower extremity. No presentation of ischemia-reperfusion injury, such as swelling of the right lower extremity, increased creatinine, or hyperkalemia, was detected.
After the procedure, the patient received subcutaneous low-molecular-weight heparin calcium 4100 units twice daily for 2–3 days, warfarin 2.5 mg once daily for half a year, and aspirin 100 mg once daily for life time. The international normalized ratio (INR) was maintained within 2–3. The procedure went uneventfully without any complications, and the patient was fine at the 2-year follow-up. Informed consent was obtained from the patient for publication of this case report. The institutional review board of The Third Hospital of Changsha does not require ethics approval for reporting individual cases.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [63, 'years'], 'Congestive Heart Failure': True, 'Stroke': True, 'Transient Ischemic Attacks History': True, 'Thromboembolism history': True, 'Vascular disease history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 63 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
655,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4369576-1,Extracted,"A 54-year-old man presented to our Accident and Emergency (A&E) department complaining of pain in his right knee. The patient has slipped off the bottom two steps of the staircase, without suffering any direct impact to his knee. He was still able to mobilize for 10 yards afterwards, before hearing a ‘pop’ and immediately experienced pain to his right knee.
There was no previous injury to patient's right knee. His past medical history included atrial fibrillation and squamous cell penile carcinoma of the glans penis, requiring partial penectomy and urethral reconstruction, and subsequent radical right inguinal lymph node (ILN) dissection 16 years ago (limited to borders of the femoral triangle) for lymphatic metastases, with clear dissections margins. Patient has never received any radiotherapy or chemotherapy treatment. He has been free from disease recurrence since, and continued to have annual surveillance follow-up. Following ILN dissection, patient developed right lower limb lymphoedema, with episodes of intermittent swelling of his right thigh, which became more frequent over the last 3 years. Patient was on warfarin, paracetamol and codeine. There was no family history of musculoskeletal, autoimmune disease, diabetes or other systemic disease.
Physical examination showed knee swelling, a high riding patella with a palpable gap below the patella. The patient was unable to weight bear and could not perform active knee extension on his right knee. There was no obvious laceration or injury to the knee. Neurovascular examination was normal. Apart from ectopic ossification of the patellar tendon, plain radiograph showed no evidence of acute fracture or joint effusion (Fig. ). Because of the unusual mechanism of injury and the initial ultrasound performed in A&E which suggested a rupture of the quadriceps and patella tendon, magnetic resonance imaging (MRI) was performed and demonstrated complete rupture of the patellar tendon from the inferior pole of patella, an almost complete shearing of quadriceps tendon off the patella and chronic tendinosis in the mid-portion of patellar tendon (Fig. ).
Surgery was performed on the knee. A midline longitudinal incision was made, revealing a complete rupture of the patellar tendon from the inferior pole of the patella, torn medial and lateral retinacular fibres, and near complete shearing of 90% of the quadriceps tendon (Fig. ). The patellar tendon was anchored trans-osseously with 5 TiCron™ (Covidien) sutures, and further strengthened with 2/0 vicryl sutures using the Kessler technique. Both the quadriceps tendon and retinaculum were primarily repaired using 2/0 vicryl sutures. Postoperatively, the knee was immobilized in a long leg back slab for 2 weeks, followed by cylinder cast for 4 weeks. Patient was gradually worked towards full weight bearing afterwards. At 8 weeks post-surgery, patient was able to fully extend his knee, and perform straight leg raise against gravity. His range of flexion improved with physiotherapy from 30° to 100° at 3 months following surgery.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [54, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 54 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
656,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6295750-1,Extracted,"A 71-year-old Hispanic male was referred for a 2-month history of dysphagia and left oropharyngeal fullness in early 2014. His past medical history was significant for hypertension, dyslipidemia, atrial fibrillation, and WT of the left parotid gland in 2008 ( and ()) for which he received a left superficial parotidectomy and developed Frey syndrome (). He was currently smoking with a history of 27.5 pack years. Physical examination was significant for left oropharyngeal soft palate fullness without ulceration.
Magnetic resonance imaging (MRI) studies of the head and neck showed a small, submucosal ovoid shaped nodule, 8 mm in diameter, with a peripheral ring of enhancement of the left oropharyngeal airway () (). A more careful review of pre-parotidectomy imaging revealed the presence of the oropharyngeal lesion at that time (). Surgical excision was recommended for diagnostic and curative purposes. The patient underwent excision of the mass with a 3 mm margin. Surgical pathology of this specimen was reported as WT ( and ()) (). There were no complications in the postoperative period and no evidence of recurrence.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [71, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 71 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
657,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7733742-1,Extracted,"A 76-year-old man visited the hospital complaining of dry cough and right-sided neck pain. He had a past medical history of type 2 diabetes, angina pectoris, atrial fibrillation, hypertension, hyperlipidemia, and hepatitis B and a 20 pack-year history of smoking. A computed tomography (CT) scan showed a mass with a thick-walled cavity in the right upper lobe of the lung (). A transbronchial lung biopsy revealed proliferation of spindle cells which were immunohistochemically positive for cytokeratin and vimentin.
Although the limited size of the biopsy specimen made a thorough analysis difficult, we confirmed spindle cells by hematoxylin and eosin (H&E) staining (), which aided in diagnosing the patient with spindle cell carcinoma of the lung. While gene mutation test results for epidermal growth factor receptor mutations and anaplastic lymphoma kinase rearrangement were negative, programmed death ligand-1 (PD-L1) expression was observed in more than 90% of the tumor cells of the lung biopsy tissue () by immunohistochemistry (IHC) using the PD-L1 IHC 22C3 pharmDx antibody (clone 22C3; Dako North America Inc.). A positron emission tomography (PET)-CT scan showed fluorodeoxyglucose uptake in the mediastinal and hilar lymph nodes, right adrenal gland, and right trapezius muscle, which was consistent with his symptom (). Based on all these findings, the patient was diagnosed with advanced lung cancer, spindle cell carcinoma, cT4N2M1c, stage IVB.
From April 2017, the patient began receiving 200 mg pembrolizumab intravenously every 3 weeks. The lung and metastatic tumors dramatically decreased in size after 9 weeks, and tumor regression was maintained after 21 weeks, as indicated by the reduced fluorodeoxyglucose uptake observed in the PET-CT scan (). The tumor continued to reduce in size, and the patient’s complaint of neck pain was resolved.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': True, 'age': [76, 'years'], 'Congestive Heart Failure': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
658,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2873323-3,Extracted,"Patient A3 is the elder sister of patient A1. She is an 86 year-old woman with a clinical history of hypertension, type 2 diabetes mellitus, sensorineural hearing impairment, osteoarthritis, hypercholesterolemia and coronary heart disease. She had a mild left motor hemiparesis at the age of 74 years due to a lacunar brain infarct. Memory impairment appeared and mild dementia was diagnosed by a general practitioner, with CERAD and an MMSE score of 22. There were no focal neurological signs except for an absence of tendon reflexes. Brain CT revealed lacunar changes in the right hemisphere but no atrophic findings.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': True, 'age': [86, 'years'], 'Congestive Heart Failure': False, 'Stroke': True}",8,8,8,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 86 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 7 + 1 = 8.
The patient's CHA2DS2-VASc Score is 8."
659,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3542926-1,Extracted,"A 64-year-old male presented to the emergency department as a “stroke alert” with new left-sided facial droop and aphasia one hour prior to arrival. The patient had a past medical history of hypertension, coronary artery disease, and ischemic cardiomyopathy with heart failure. Emergency Medical Services (EMS) stated that on their arrival to the scene, the patient had aphasia, left-sided facial droop and was somnolent. EMS reported that the patient had a Glascow Coma Score of 14, and the patient was easy to arouse to verbal stimuli. Pertinent positives in the review of systems included neck stiffness, nausea, vomiting, speech change, headache, and loss of balance. The patient's vital signs on arrival included blood pressure of 179/102 mm Hg, pulse rate of 79 beats per minute, temperature 36.9 degrees Celsius (oral), respiratory rate of 20 breaths per minute, and a pulse oximeter reading of 97%. Pertinent physical exam findings included an expressive aphasia, left-sided facial droop, nonfatiguable horizontal and vertical nystagmus bilaterally, full range-of-motion of the neck, no pronator drift bilaterally with normal strength in the upper and lower extremities bilaterally, past-pointing of the left upper extremity on finger-to-nose examination, and two plus pitting edema of the lower extremities bilaterally.
The patient underwent a CT with angiography of the head and neck per the department's stroke protocol (see Figures , , and ) which revealed a 25 mm basilar aneurysm with partial thrombosis and no evidence of rupture with a secondary saccular aneurysm of the left posterior cerebral artery. The neurosurgery and neurology services were both consulted with no direct intervention recommended. The patient was started on anticoagulation with heparin due to thrombus within the aneurysm and MRI performed (). A radial arterial line was placed and the patient was kept normotensive prior to being admitted to the neurology intensive care unit without further decompensation prior to transport.
On hospital day three, the patient became difficult to arouse and his heparin infusion was discontinued. An emergent noncontrast CT of the head () revealed diffuse blood products in the subarachnoid spaces and early ventricular dilation. The patient was reevaluated after returning from CT and found to have fixed, midposition pupils, absent corneal reflexes, and no response to painful stimuli. The patient was made Do Not Resuscitate (DNR) due to his terminal condition and he subsequently expired.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Vascular disease history': True, 'age': [64, 'years'], 'Congestive Heart Failure': True, 'Stroke': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 64 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
660,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4280491-1,Extracted,"An 80-year-old female was admitted for a routine total hip replacement. She was previously receiving warfarin for paroxysmal atrial fibrillation and this had been discontinued prior to surgery. A cementless total hip replacement was performed through a direct anterior approach using a Trinity Cluster Shell, a ceramic liner, and a lateralized Metafix femoral stem with ceramic head (Corin, UK). On the evening following uneventful surgery, she was comfortable and had normal neurovascular status. She commenced mobilization and was making good progress the following day. Due to long-standing atrial fibrillation, warfarin was restarted the day after surgery for prophylaxis. Three days after surgery her haemoglobin was 6.8 g/dL and she was transfused 4 units of blood. Overnight she developed severe pain requiring opiate analgesia and she subsequently required another transfusion of 4 units two days later. At this stage, the patient had developed a foot drop and was unable to stand. An MRI scan () demonstrated a large posterior haematoma deep to the iliotibial band and tensor fascia lata. Examination demonstrated numbness below the knee and she was unable to dorsiflex or plantarflex her foot, consistent with a sciatic nerve palsy.
A posterior approach was used to evacuate the posterior haematoma and explore the sciatic nerve. The nerve was in continuity with no evidence of trauma other than compression from overlying haematoma. Gluteus medius was contractile. Haematoma was also evacuated from the anterior wound, and an arthrotomy was performed with lavage of the hip joint. No active bleeding was identified.
Sensation subsequently improved in the lower leg, but she continued to have a foot drop.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False, 'age': [80, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 80 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
661,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4943297-1,Extracted,"A 72-year-old male patient with recurrent subcutaneous abdominal wall abscesses was referred to our dermatological inpatient unit at the University Hospital in Zurich, Switzerland. The abdominal skin problems had begun one and a half years before, after subcutaneous insulin injections in the underbelly region had been initiated. Within few days, the patient noticed a development of a small red indurated but indolent nodule in the right umbilical region. The patient's medical history included insulin-dependent diabetes mellitus type 2, atrial fibrillation with oral anticoagulation and a previous percutaneous coronary intervention due to a myocardial infarction. Five months later, local subcutaneous abscesses developed in the central abdominal wall region. The patient was referred to a nearby hospital for surgical wound debridement and received postoperative antibiotic treatment with oral amoxicillin and clavulanic acid. In the following months, there were several recurrences of abdominal wall abscesses turning into ulcers followed by repeated subsequent surgical debridements, excisions of abdominal wall fistulas, negative pressure wound therapies, as well as antibiotic therapies (amoxicillin and clavulanic acid).
As the abscesses with ulcer formation did not improve in the long term, the suspicion of pyoderma gangrenosum arose and the patient was referred to our clinic for further dermatological investigations. At hospital admission, the patient was in a good clinical condition, without fever or infection signs. Clinical examination revealed three 2- to 5-cm-large oval ulcers with granulation tissue on the lower right central abdominal area, with slightly erythematous but not undermined boarders (fig. ). Laboratory findings did not indicate a systemic infection with CRP 7 mg/l (range <5 mg/l), leukocytes 9 G/l (range 3.0–9.6 G/l). The differential diagnosis encompassed ulcers of either infectious, vasculitic or exogenous origin, open abdominal wall fistulas with ulcer formation as well as pyoderma gangrenosum.
Bacterial swabs from the ulcers showed only the presence of the commensal skin flora. Pathergy phenomenon could not be detected clinically. The patient had no personality changes that would imply an obsessive-compulsive disorder resulting in self-mutilation. Serological vasculitis screen with antinuclear antibodies, ANCA, rheumatoid factor, complement C3/4 fraction, and hepatitis B and C serology was negative. Imaging studies of the abdomen with contrast-enhanced computed tomography (CT) and magnetic resonance imaging (MRI) illustrated an abdominal subcutaneous fluid collection but no abdominal fistulas. A deep skin biopsy of the ulcers was performed and tissue culture started (for bacteria, fungi and mycobacteria). Histology revealed mixed inflammatory cellular infiltrates of neutrophils and histiocytes with granuloma and abscess formation in the dermis. No pathogen could be verified in different stainings (PAS, Grocott, Ziehl-Neelsen) (fig. ). After 6 days of cultivation, skin biopsy tissue culture showed rapid growth of non-tuberculous mycobacteria (NTM), which were identified by 16S rRNA gene sequencing as Mycobacterium wolinskyi. The patient underwent surgical excision and primary closure of all abdominal ulcers with material being sent for further tissue culturing. The subsequent mycobacterial culture also yielded rapidly growing M. wolinskyi. Based on the antibiotic susceptibility test results (table ), the patient was treated with intravenous amikacin (500 mg per day) for 1 month in combination with oral moxifloxacin (400 mg per day) and minocycline (100 mg twice a day) therapy for a total of 6 months. The patient responded well to this combination therapy with complete resolution of the clinical symptoms and no recurrence of infection at a 6-month follow-up (fig. ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Diabetes history': True, 'Vascular disease history': True, 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
662,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8049151-1,Extracted,"A 66-year-old woman with type 2 diabetes mellitus, atrial fibrillation on warfarin, as well as a recent diagnosis of Graves disease (positive thyroid-stimulating immunoglobulins and radioactive iodine uptake of 99%) was transferred to our facility with a diagnosis of drug-induced liver injury with resultant acute liver failure. She had initially presented with several weeks of malaise after being started on methimazole for her Graves disease, and she had taken this medication for only 4 days. Initial laboratory findings included markedly elevated liver transaminases, and her international normalized ratio (INR) was also high (Figures and ). Although she was being assessed and stabilized in the emergency department, she developed rapid deterioration of her mental status with lethargy, weakness, and progressed to frank confusion and somnolence. This led to urgent endotracheal intubation to ensure airway protection. To evaluate her confusion, an magnetic resonance imaging of the brain was obtained which did not show any acute intracranial pathology but noted findings suggesting chronic small vessel ischemic disease and mild diffuse cerebral atrophy. Based on the findings of coagulopathy and progressive encephalopathy in the setting of acute liver injury, she was diagnosed as having acute liver failure, N-acetylcysteine was started, and she was transferred to our transplant center for evaluation for liver transplantation.
Her medications were reviewed thoroughly, and the possibility of liver injury secondary to methimazole was entertained, as this was a new medication, so it was initially discontinued. On evaluation, she was afebrile but in atrial fibrillation with a heart rate of 118. She was initially hypotensive at 86/49 mm Hg. She was believed to have a Burch-Wartofsky Point Scale of 55, thus highly suggestive of severe thyrotoxicosis/thyroid storm. A comprehensive etiological workup was undertaken which yielded a negative antinuclear antibody and anti-smooth muscle antibody; negative viral serology for hepatitis A, B, and C, human immunodeficiency virus, and herpes simplex virus. She had a normal creatine kinase, and her serum acetaminophen and salicylate levels were below detectable range. She underwent a urine toxicology screen that was negative for alcohol and other drugs. A complete abdominal ultrasound with Dopplers was notable for a grossly normal liver with mild steatosis but no structural or vascular abnormalities. A portable chest radiograph noted mild pulmonary edema and cardiomegaly. A transthoracic echocardiogram was obtained as well, and this was significant for a left ventricular ejection fraction of 36%, with an enlarged right ventricle, moderately reduced right ventricular function, and a dilated inferior vena cava. Her thyroid function tests revealed undetectable thyroid-stimulating hormone and elevated free thyroxine hormones (free T4 and T3) (Figure ). A diagnosis of thyrotoxicosis was made with resultant congestive cardiac failure and subsequent congestive hepatopathy. She was started on high-dose intravenous methylprednisolone and restarted on her methimazole. She improved clinically and had laboratory normalization of her INR and liver tests. She was ultimately discharged, clinically stable, to follow-up in the outpatient endocrinology clinic.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Diabetes history': True, 'Vascular disease history': False, 'age': [66, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 66 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
663,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7137410-2,Extracted,"A 61-year-old Chinese woman presented with a history of upper right abdominal cramping with vomiting and fever for 10 h. The patient developed the above symptoms after eating greasy food 10 h ago; she vomited her stomach contents and bile repeatedly, but did not experience hematemesis. Fever occurred after the abdominal pain, and the highest body temperature was 38.8 °C. She did not present with chills, jaundice, constipation or diarrhea. Apart from these observations, the patient had a history of intermittent bloating after meals for at least 20 years, and she denied the symptoms of steatorrhea. The patient has had type 2 diabetes for 12 years, and metformin and glimepiride were used to control the DM; her fasting blood sugar level fluctuates from approximately 7–10 mmol/L. She also has congenital scoliosis. Her family medical history was unremarkable.
The patient’s body temperature was 38.9 °C, and her BMI was 32 kg/m2. The physical examination revealed mild abdominal muscle tension, tenderness in the right upper quadrant, and positive Murphy’s sign. The hematological examinations showed a high white blood cell count (14.4*10^9 /L) and an elevated neutrophil percentage (87.7%). The blood biochemistry tests showed high blood sugar (12.1 mmol/L), low K+ (2.9 mmol/L) and low total cholesterol levels (6.2 mmol/L). The abdominal CT including coronal reconstruction and sagittal reconstruction image showed multiple stones in the gallbladder, and the gallbladder wall was rough and had mild edema (Fig. a). The body and tail of the patient’s pancreas were absent; in the area where the tail of the pancreas should be, we only observed blood vessels of the spleen (Fig. b-i). Since the patient had no evidence of bile duct stones, MRCP was not performed in the emergency department.
So the preoperative diagnosis is acute cholecystitis, cholelithiasis, agenesis of the dorsal pancreas, and pancreatic exocrine insufficiency were not excluded. We gave the patient gastric decompression. Cefminox were used to control the infection, and magnesium sulfate was used as a cholagogue. In addition, to relieve her symptoms, we used anisodamine, metoclopramide and famotidine. Rehydration therapy and potassium supplementation were conducted simultaneously. After the patient recovered from the acute stage, she underwent laparoscopic cholecystectomy; 1.8 g pancreatin enteric-coated capsules were given per day continuously to relieve the symptoms of pancreatic exocrine function.
The patient’s symptoms completely improved after the drug regimen in the acute stage, and she had no abdominal pain after the LC surgery. After 3 weeks of pancreatic enzyme replacement therapy, she said that her symptoms of bloating after meals significantly improved.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [61, 'years'], 'Congestive Heart Failure': False, 'Diabetes history': True, 'Vascular disease history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 61 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 1 + 1 = 2.
The patient's CHA2DS2-VASc Score is 2."
664,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5564149-1,Extracted,"A 74-year-old male patient was admitted to the Department of Advanced General Dentistry at Yonsei University College of Dentistry on 2014, for a chief complaint of loosening of the restoration that was covering his teeth (). The patient had experienced a stroke in 2000 and was taking warfarin, 2.5 mg PO bid, due to atrial fibrillation. In addition, the patient was taking medications for hypertension (candesartan, atorvastatin, spironolactone, and carvedilol). At the time of admission, his INR value was 4.76. Clinical examination and radiological findings indicated the presence of residual root in the maxillary right second molar while existing restoration of the maxillary left canine, first premolar, and second premolar had fallen out. The Department of Cardiology at our hospital was consulted to determine whether the patient was operable and whether warfarin could be discontinued or changed. The response to the consultation was that the patient could receive dental treatments, and, in case of a high risk of bleeding, heparinization on an inpatient basis or use of low molecular weight heparins (LMWH) on an outpatient basis would be possible. Accordingly, extraction of the maxillary right residual root and prosthetic treatment following crown lengthening on the maxillary left canine, first premolar, and second premolar was planned. The treatment plan for the maxillary and mandibular missing posterior teeth (maxillary left first and second molars and mandibular right second molar) was to be reestablished after treating the area of chief complaint.
Warfarin was discontinued from three days prior to the treatment, and from two days prior to treatment, LMWH (Enoxaparin, Clexane, Sanofi-Aventis, France), 60 mg bid. was injected subcutaneously. On the day of treatment, LMWH injection was discontinued and full-mouth supragingival scaling and extraction of the maxillary right residual root were performed. Crown lengthening was performed by ostectomy of the alveolar bone after flap elevation on the area around the maxillary left canine and first and second premolars. In addition, dental pulp extirpation was performed on the maxillary left canine and second premolar. After suturing the area with 4–0 vicryl suture, hemostasis was confirmed by gauze biting for 1 hr. Starting from the evening of the day of treatment, subcutaneous injection of LMWH and warfarin administration was initiated. LMWH was continued for two more days. On the following day, hemostatic status was confirmed while dressing the area and the stitches were removed after one week. Subsequently, endodontic and prosthetic treatments were completed without discontinuing warfarin.
About one year after treatment completion, implant placement was planned on the left maxillary first and second molars (). Since medication was switched from warfarin to 20 mg of rivaroxaban (Xarelto, Bayer HealthCare AG, Germany) two months earlier, consultation was requested on whether surgery was feasible and whether the medication should be discontinued, to which the response was to discontinue rivaroxaban from the morning of the day before the procedure and to restart as soon as possible afterwards. The day of surgery, his systolic and diastolic blood pressures were 133 and 80 mmHg, respectively. After local anesthesia on the left maxillary first and second molars using 2 ampoules of 2% lidocaine containing 1:100,000 epinephrine, two implants (diameter 5.0 mm and length 8.0 mm) were placed with full thickness flap elevation () and a healing abutment (diameter 5.5 mm) was screwed onto the implants (). After suturing with 4–0 vicryl suture, pressure was applied with gauze to stop the bleeding and the patient was discharged on the same day after confirming that the bleeding had stopped.
On the day after the procedure, since there were no signs of infection or bleeding, the patient was instructed to restart rivaroxaban. On post-operative day (POD) 6, the patient visited the dental emergency room at our hospital around 4 AM for a chief complaint of spontaneous bleeding at the surgical site. Oozing bleeding in the area was observed, and pressure was applied with a gauze to stop the bleeding for about one hour, after which the patient was discharged after confirming that the bleeding had stopped (). On the same day, the patient visited our department again at about 5 PM for re-bleeding at the surgical site that had started about an hour earlier. However, the bleeding could not be stopped, despite applying pressure with gauze; therefore, oxidized regenerated cellulose (ORC) was applied to the bleeding area. After about an hour, the bleeding had stopped, but because of the possibility of continued bleeding, the decision was made to discontinue rivaroxaban for one day. On the next day (POD 7), the patient was admitted to the dental emergency room again at about 1 AM for bleeding in the same area. Slightly pulsating oozing bleeding was observed in the same area and the existing ORC was removed and new ORC was applied while simultaneously applying pressure with gauze to stop the bleeding. On POD 8, since no further bleeding was observed, the patient was instructed to restart rivaroxaban. One week thereafter (POD 14), the stitches were removed.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'age': [74, 'years'], 'Stroke': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 74 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
665,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-2908,Extracted,"A 76-year-old woman comes to the physician for a routine examination. She has a history of hypertension well controlled with diet and exercise. She has no history of smoking or illicit drug use. She walks one mile daily. Her pulse is 68/min, respirations are 16/min, and blood pressure is 119/76 mm Hg. Physical examination shows no abnormalities.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [76, 'years'], 'Hypertension history': True, 'Diabetes history': False, 'Transient Ischemic Attacks History': False, 'Stroke': False, 'Thromboembolism history': False, 'Vascular disease history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
666,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7869292-1,Extracted,"A 69-year-old female patient presented to the emergency department with a severe headache and painful swelling in the right temporoparietal area. She also had a painless lump on her sternum. The lesion in the scalp had been growing during the past 4 months, and the lesion on the sternum had been present for the past 2 months. She denied any head or thorax trauma history. Her medical history was unremarkable except for warfarin therapy due to atrial fibrillation and hypertension. Her neurological examination was intact, and the infection markers were negative. The patient was referred to the neurosurgery outpatient clinic. Magnetic resonance imaging (MRI) revealed a lesion in the right temporoparietal area which caused local bone erosion. Together with the bone erosion, dural and scalp involvement were seen [].
Thorax and abdominal computed tomography was planned for a probable primary lesion, but there was not a suggestive focus except bone erosion on sternum just beneath the painless lump. Surgery was performed for diagnostic purposes for the skull pathology. The pathologic bone part was removed following the scalp incision. The dural area was also removed because the dura was also affected, and then, duraplasty was performed. The removed lesion was sent for histopathological examination. Since the diagnosis was not definite during the surgery, cranioplasty was planned after the confirmation of the diagnosis and treatment strategy. The pathology showed widespread strong positivity with CD20, bcl-2, bcl-6, and CD10, moderate positivity on the ground with CD5 and CD3 observed with a small number of T-lymphocytes. It was negative for CD56, thyroid transcription factor-1 and pancytokeratin were negative, and Ki-67 proliferation index was around 80% []. The specimen was diagnosed with high-grade diffuse large B-cell lymphoma []. The cerebrospinal fluid sample was not taken from the patient. Since the patient had no previous history of lymphoma, the patient was not considered bone marrow involvement before the histopathologic results. The patient was referred to a center with the oncology department. To the best of our knowledge, the patient is still under the treatment of the referenced oncology clinic. . The patient consent form was obtained.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Hypertension history': True, 'Vascular disease history': False, 'age': [69, 'years'], 'Stroke': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 69 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
667,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6243370-1,Extracted,"A 75-year-old female with well-controlled hypertension presented with a 2-week history of palpitations. On examination, her pulse was regular at 76 bpm, blood pressure was 150/70 mmHg and auscultation revealed a continuous murmur heard over the precordium. She had no signs of heart failure. Resting electrocardiogram (ECG) was within normal limits, and the chest X-ray showed prominent pulmonary arteries on the left side, but normal heart size and clear lung fields. Transthoracic echocardiogram revealed normal left ventricular systolic function with normal ejection fraction at 65%. There was impaired relaxation with Grade 1 diastolic dysfunction. The right ventricular structure and function were normal and there were no significant valvular lesions, with only trivial mitral and tricuspid regurgitation. 24-h Holter monitoring demonstrated a normal heart rate profile, with frequent isolated ventricular and supraventricular ectopic beats, and one episode of broad complex tachycardia of 4 beats. She had blunted heart rate response to exercise and the maximum heart rate was 102 bpm despite completing Stage 3 of the normal Bruce protocol. At peak exercise, the blood pressure dropped from 150/94 mmHg to 90/68 mmHg, and this was associated with presyncope.
Coronary angiography showed a large communication between the left anterior descending (LAD) artery and the main pulmonary artery. In addition, there was another smaller communication that appeared to run from the right coronary artery (RCA) to the pulmonary artery. She was subsequently referred for CT coronary angiography (CTCA), which was performed using a 64-slice multidetector CT scanner using prospective ECG-gated acquisition. This confirmed the presence of a large complex fistula, between the main pulmonary conus and both the LAD and proximal RCA, with cavernous malformation of the fistula segment to the LAD (–). There were two branches of the fistula, the larger branch communicating to the LAD and a further smaller branch to the RCA. The scan also showed minimal plaque burden in the RCA. The patient was reluctant to consider surgical correction of the fistulae, and as she was largely asymptomatic, medical management was pursued. 13 years following the initial diagnosis, she remains asymptomatic with normal left and right ventricular echocardiographic parameters on follow-up.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Diabetes history': False, 'Vascular disease history': False, 'age': [75, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 75 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
668,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8383607-1,Extracted,"We present the case of a diabetic 48-year-old man with non-ischemic dilated cardiomyopathy, associated with heart failure with severely reduced ejection fraction, complete heart block (CHB), and permanent atrial fibrillation. The patient had a past cardioembolic stroke with left hemiparesis and had a record of recurrent urinary tract infections (UTIs) associated with suprapubic cystostomy due to urethral stenosis. A CRT-D generator (Quadra Assura MP St Jude Medical) was implanted the year before due to CHB with a single lead pacing cardioverter-defibrillator implanted (ICD), due to QRS < 120 ms and high probability of widening in the near future.
One month earlier he was admitted in the emergency department (ED) for fever and low back pain, being discharged with a UTI diagnosis and ciprofloxacin.
Again, he was admitted in the ED with fever, severe low back pain, anorexia, and weight loss. On physical examination, fever (39.1 °C), painful palpation of the lumbar spinal apophysis, and absent cardiac audible murmur, or cutaneous embolic phenomena were remarked. Electrocardiography showed atrial fibrillation with complete left bundle branch block with QRS > 150 ms, and TTE was unremarkable for the presence of vegetations. Prior blood cultures (BC) identified C. striatum, with sensitivity to tetracycline and vancomycin, and resistance to gentamicin, clindamycin, ciprofloxacin, and penicillin G; so did a new pair of BC with the same sensitivity profile. Vancomycin therapy was initiated. BC collected on the second day of antibiotic was sterile. Ten days after admission TEE showed vegetation at the auricular face of the tricuspid valve, in the posterior leaflet, +/- 6 mm, heterogeneous contours, with two mobile projections with +/- 6 mm, with no apparent device lead involvement ().
Lumbar computed tomography (CT) scan showed irregularities in the L1 - L2 vertebral platforms, which were absent in the previous examination, 1 month earlier. Due to the incompatibility of the CRT-D device, it was not possible to perform magnetic resonance imaging (MRI). However, a lumbar spondylodiscitis diagnosis was presumed.
TEE was repeated (day 29) in the fourth week of vancomycin therapy, similar to the previous one namely regarding the presence of vegetation. Surgical removal of the CRT-D device was proposed, but the patient was considered as having a very high overall surgical risk. So he was managed with medical treatment alone. He was discharged after completing 49 days of vancomycin, with clinical resolution and serial negative blood cultures.
Again, 42 days after hospital discharge, the patient was readmitted, in cardiogenic shock, with respiratory failure, acute kidney injury, and ischemic hepatitis requiring dobutamine. As soon as dysfunctions improved he was transferred to our nursery. Again, BC showed the presence of C. striatum, with the same sensitivity profile and presumptively sensitive to daptomycin (minimum inhibitory concentration (MIC) = 0.023 µg/mL). Neither TTE at admission nor TEE performed 5 days after, showed cardiac vegetation. Vancomycin was started (day 3), requiring several adjustments due to frequent toxic levels. The patient developed acute kidney injury (day 12) suspecting renal toxicity due to vancomycin; and therapy was changed to daptomycin10 mg/kg. A systolic murmur not present at admission was noticed (day12), and TTE was repeated with evidence of vegetations adhering to the device lead in its auricular path near the tricuspid valve (). Daptomycin therapy was continued without new febrile events or elevated inflammatory markers, and with sterile serial BC. On the 81st day of daptomycin (inpatient day 93), the patient underwent surgical intervention with the removal of CRT-D and implantation of a cardiac resynchronization therapy pacemaker (CRT-P) (Quadra Allure MPP St Jude Medical), with epicardial electrodes and the device placed in an abdominal loca. ICD was not implanted due to the absence of therapies in the past, in addition to frailty and life expectancy < 1 year. Electrode tips were sterile. He completed 15 days of daptomycin after the intervention. No evidence of recurrence of infection was found in follow-up consultation 6 months after discharge.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [48, 'years'], 'Congestive Heart Failure': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': False, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 48 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
669,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6575106-1,Extracted,"A 58-year-old male with a history of well-controlled hypertension, chronic smoking, and recently diagnosed biopsy-confirmed small cell lung cancer (SCLC) of the left upper lobe presented to the hospital with a left field cut, right gaze palsy, and left hand weakness (). He had previously been admitted to an outside hospital after developing sudden-onset tonic-clonic seizures and expressive aphasia. A magnetic resonance imaging (MRI) scan of the brain at that time revealed scattered subcentimeter ischemic infarcts in the right and left frontal lobes, right parietal lobe, and the left cerebellar hemisphere. He was transferred to our institution for further management.
Upon admission, the patient was admitted to the neurosciences intensive care unit for further monitoring. He was placed on continuous electroencephalographic monitoring. Computed tomography (CT) of the brain showed new mild hypodensities in the right subcortical frontal lobe with stable hypodensities in the periventricular white matter, left subcortical frontal and left occipital lobes (). A transthoracic echocardiogram (TTE) revealed a moderately dilated left atrium with a 40 × 39 mm spherical echogenic, heterogeneous mass originating from a left pulmonary vein (, ). Given that the patient had no significant cardiovascular history, it was concluded that the embolic infarcts were likely secondary to tumor shower from the left atrial metastasis from his primary SCLC. The patient was scheduled to undergo cardiac MRI imaging to further characterize the left atrial lesion and extent of invasion, but given the risk of intubation and sedation, this was deferred. A CT-angiogram and chest X-ray of the chest was conducted which demonstrated encasement of the left main pulmonary artery with direct extension of the left pulmonary vein and left atrium (, ).
In the setting of metastatic left atrial invasion with metastatic thromboembolic spread to the brain, the patient was started on anticoagulation with a heparin drip in the hospital and later transitioned to enoxaparin. His neurologic status improved and he was transferred to the oncology service for initiation of chemotherapy. After initiation, he developed atrial fibrillation with rapid ventricular response that was subsequently controlled with metoprolol. He was discharged in stable condition from the hospital and has been following up with his oncologist and cardio-oncologist for continued management of SCLC.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': True, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Diabetes history': False, 'Vascular disease history': True, 'age': [58, 'years'], 'Stroke': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 58 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
670,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6439371-1,Extracted,"An 87-year-old woman was transferred to our centre for revision of a pacing lead 2 months after implantation of a dual chamber pacemaker. After finding failure of capture on the passive fixation ventricular lead, chest radiography had been performed and showed the lead to be outside the cardiac silhouette, apparently in the left pleural space. The patient had no significant comorbidities and her recorded observations were stable, including height of 156 cm, weight of 64 kg, and a body mass index of 26.3 kg/m2.
We extracted and replaced the lead under general anaesthesia with cardiac surgical cover. Due to the anticipated risk of bleeding into the pericardial or pleural cavities, we performed a peri-procedural TOE and used invasive haemodynamic monitoring. The TOE probe was a standard model (Philips X7-2t) and there were no reports of difficulty or undue resistance with probe insertion. The TOE was performed for a total duration of 15 min. This enabled a review of the cardiac structure and function at the start of the procedure, and the TOE probe was left in situ for the rest of the case. The TOE was used again at the end of the procedure to rule out any pericardial effusion or other structural changes. This patient did not have a history of heart failure and TOE confirmed good left ventricular systolic function. The right ventricle was of normal size and systolic function. A new active fixation right ventricular lead (CapSureFix 5076, Medtronic) was placed in a mid-septal position using left cephalic venous access. This new lead achieved satisfactory sensing and pacing threshold parameters.
The perforating lead, a passive fixation model (CapSure Novus, Medtronic) was removed with the aid of a Liberator® Beacon® Tip Locking Stylet (Cook Medical). With gentle traction only, the lead was freed and removed entirely. There was no immediate haemodynamic disturbance and at procedure conclusion, there was no evidence of pericardial or significant pleural collections on repeat TOE. The offending lead, including the tip, was inspected and no overt abnormality was evident.
Upon recovery from general anaesthesia, the patient complained of severe chest pain and became hypotensive, requiring intravenous fluids. Emergency chest radiography showed a pneumomediastinum and pleural effusion (Figure ); a transthoracic echocardiogram showed no pericardial effusion and only a small pleural effusion. The initial clinical impression was that this was pulmonary injury from the original offending pacing lead that perforated into the pleural cavity. A computed tomography thorax was performed and reported as confirming the chest radiograph findings only (Figure ).
The patient remained systemically unwell with low grade pyrexia, despite broad spectrum antibiotic therapy (intravenous ertapenem was advised by microbiologists as empirical cover; all blood cultures were negative). Her blood pressure was 102/80 mmHg, and she had episodes of tachycardia, in atrial fibrillation at 150 b.p.m. Without supplemental oxygen, her saturations dropped to 90%. Inflammatory markers were markedly raised with a climbing C-reactive protein (CRP) of 433.3 and white cell count of 16. Albumin was low at 16. In our laboratory, the normal reference range for CRP is 0-10 mg/L, for WCC it is 4-119/L and for albumin, the normal range is 35-50 g/L. Kidney function and urine output remained stable and she was cognitively intact. Alongside her deteriorating clinical condition, the pleural effusion also increased in size, raising the possibility of an empyema, so a video-assisted thoracoscopic surgical procedure was performed to drain it. This unexpectedly revealed food material in the chest cavity. A gastrografin study (Figure ) confirmed the presence of oesophageal perforation, with continued communication to the pleural space. The patient was transferred urgently for a surgical review and possible surgery.
Correspondence from the district general hospital confirmed that the patient was managed conservatively. At 1-year post-event, the patient is well but has not regained her premorbid health status.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False, 'age': [87, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 87 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
671,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7431306-1,Extracted,"A 53-year-old male with a history of atrial fibrillation and an aortic aneurysm presented to our ED by Emergency Medical Services (EMS) with acute onset of right-sided weakness. Per EMS report, he was found to have right-sided weakness, aphasia, and left gaze preference approximately one hour prior to arrival. Initial vital signs upon arrival included an irregular heart rate (HR) of 99 beats per minute (bpm), blood pressure (BP) of 155/78 mmHg, a respiratory rate (RR) of 21 breaths per minute, a temperature of 97.4⁰F, and an oxygen saturation of 100%. A National Institutes of Health Stroke Scale (NIHSS) of 16 was calculated during initial evaluation with points given for inability to perform simultaneous tasks, aphasia, right upper extremity weakness, right lower extremity weakness, and gaze deviation. A stroke alert was called, and the neurology service was consulted. The patient’s electrocardiogram (ECG) showed atrial fibrillation with a rate of 83 without other significant features (Figure ).
Chest x-ray showed a widened mediastinum with enlarged aortic contour (Figure ). CT noncontrast of the head and CT angiography (CTA) of the head and neck showed findings consistent with an early middle cerebral artery (MCA) infarct with an embolus to the M1 segment of the left MCA with extension to the proximal M2 segments, in addition to dissection of the left internal carotid artery extending into the left subclavian artery (Figure ).
Given concern for an AD based on the chest X-ray and left internal carotid artery dissection, CTA of the aorta was obtained. CTA showed an ascending thoracic aneurysm with Stanford type A dissection from the aortic valve to the level of the renal arteries with extension to the left internal carotid artery (Figures , ).
The patient was started on esmolol and nicardipine intravenous drips to optimize heart rate and BP with a goal heart rate of 60 bpm and goal systolic BP of 120 mmHg. The case was discussed with the neurology and cardiothoracic surgery services. Given the finding of an LVO stroke, the interventional neurology service was also consulted. The consulting physicians did not think the patient was an optimal candidate for either immediate endovascular therapy or surgical aortic repair. In conjunction with cardiothoracic surgery, the decision was made to transfer the patient to a center with an aortic specialist for operative repair. The patient was maintained on the esmolol and nicardipine infusions and in stable condition until the time of transfer. While in the ED, the patient’s neurologic exam was unchanged with persistence of his right hemiplegia, aphasia, and left gaze preference. He was ultimately transferred to a center for potential definitive care of his AD and was lost to follow-up.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Transient Ischemic Attacks History': True, 'Vascular disease history': True, 'age': [53, 'years'], 'Congestive Heart Failure': False, 'Stroke': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 53 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 0 + 2 = 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
672,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5336689-1,Extracted,"Mrs. M.R, a 65-year-old South Indian woman, visiting family in Australia, was admitted in January 2015 for the management of new congestive cardiac failure (CCF).
She had been recently discharged from a different hospital with symptoms consistent with community-acquired pneumonia and managed with intravenous ceftriaxone and azithromycin followed by amoxicillin/clavulanate and roxithromycin. Investigations at this time included a chest X-ray demonstrating right lung lower zone consolidation, and blood and sputum cultures were negative for routine pathogens; sputum acid-fast bacilli (AFB) smears were negative. She subsequently developed worsening bilateral peripheral limb oedema, increasing exertional dyspnoea and paroxysmal nocturnal dyspnoea, and was admitted to our hospital for further management. Clinical examination was consistent with congestive cardiac failure with evidence of atrial fibrillation. Additionally the patient was found to have cervical and parotid lymphadenopathy measuring approximately 1–2 cm in size.
Her past medical history included ischaemic heart disease, atrial fibrillation, hypertension, osteoarthritis, asthma, herpes zoster (6 months prior to admission), laparotomy in 1968 for an unclear indication, and total hysterectomy in 1991. Further history revealed a 6-month history of 5 kg weight loss with no anorexia, and she denied fevers and night sweats. There was no other travel history besides to Australia. She had been married since the age of 19 and denied other sexual partners. There was no history of tattoos or injecting drug use. She had no animal contact or gardening activities.
Initial laboratory investigations revealed pancytopenia with a normocytic anaemia: haemoglobin 80 g/L (115–165 g/L), mean cell volume 84 fL (80–96 fL), white cell count 3.0 × 109/L (4–11 × 109/L), with normal neutrophils 2.5 × 109/L (2–7.5 × 109/L) and lymphopenia 0.2 × 109/L (1–4 × 109/L), and platelets 55 × 109/L (150–400 × 109/L). Her chest X-ray was consistent with fluid overload with bilateral pleural effusions and there was evidence of right lung lower zone consolidation.
Given the pancytopenia, lymphadenopathy and weight loss, Mrs. M.R proceeded to have computerised tomography (CT) of the neck, chest, abdomen and pelvis. This revealed widespread mediastinal, hilar and peritoneal lymphadenopathy as well as multiple peripherally enhancing cystic lesions within the right parotid gland, raising the possibility of tuberculous adenitis. A positron emission tomography scan demonstrated metabolically active retroperitoneal, mesenteric and inguinal lymph nodes. Transthoracic echocardiography revealed normal left ventricular size and function, impaired right ventricular systolic function as well as diastolic dysfunction, and severe pulmonary hypertension (pulmonary artery systolic pressure 57 mmHg + right atrial pressure). CT pulmonary angiogram did not reveal evidence of pulmonary embolus, and screening tests for connective tissue disorders as a cause for secondary pulmonary hypertension were unremarkable. In view of her country of origin and respiratory symptoms, sputum AFB smears were repeated and were negative. Quantiferon-Gold testing was indeterminate.
Given her unexplained lymphadenopathy and weight loss, Mrs. M.R went on to have human immunodeficiency virus testing. The HIV-1/2 enzyme immunosorbent assay (EIA) (Roche) at our hospital was unexpectedly strongly positive on two occasions and the sample was sent to the Victorian Infectious Diseases Reference Laboratory for confirmation. The HIV-1/2 EIA using different platforms (Genscreen and Liaison XL) was also positive but the HIV-1 p24 antigen was negative. The HIV-1 western blot was negative. This prompted testing for HIV-2, performed at the National Reference Laboratory, using an in-house HIV-2 western blot (Fig. ) and the BioRad Multispot EIA assay, which is able to differentiate between HIV-1 and HIV-2 antibodies. Both tests confirmed HIV-2 infection. HIV-2 viral load (VL) was performed using a research-based assay and was detected at 3260 copies/mL. Resistance testing demonstrated susceptibility to all protease inhibitors and nucleoside reverse transcriptase inhibitors; resistance to non-nucleoside reverse transcriptase inhibitors was consistent with HIV-2. Her CD4 T cell count was 118 cells/µL (17%) (650–2000 cells/µL; 35–59%). Further questioning revealed the patient received a blood transfusion in 1991 during her hysterectomy in India; no other risk factors for HIV infection were determined, and her husband tested negative for HIV-1 and HIV-2.
Given this new diagnosis of HIV-2 infection, a number of potential differential diagnoses were considered for Mrs. M.R’s pancytopenia, widespread lymphadenopathy, weight loss and ongoing respiratory issues. Multiple lymph node aspirates and core biopsies, bone marrow aspirate and trephine, and bronchoscopy were performed and did not reveal a microbiological or haematological diagnosis; investigations for mycobacterial, fungal and opportunistic infections were negative on all specimens.
She was commenced on anti-retroviral therapy with fixed-dose combination emtricitabine 200 mg + tenofovir 300 mg daily and ritonavir (200 mg)-boosted lopinavir 800 mg daily, a regimen widely available in India. She was also commenced on trimethoprim-sulfamethoxazole for Pneumocystis jiroveci prophylaxis. Within 2 months her VL was undetectable and her CD4 cell count was improving, after an initial decline. Her pancytopenia improved and her lymphadenopathy regressed over the next 2 months and these were subsequently attributed to HIV-2 infection.
Mrs. M.R continued on anti-retroviral treatment and remained well until she returned to India.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Hypertension history': True, 'Vascular disease history': True, 'age': [65, 'years'], 'Congestive Heart Failure': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
673,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5241449-1,Extracted,"A 78-year-old Caucasian female was referred to hematology after her primary physician noted a persistent elevation in her serum ferritin level. Her primary concern was a profound sense of fatigue and recent erratic control of her thyroid medication despite years of stability. She had developed atrial fibrillation within the year prior to detection of the elevated ferritin. In the remote past, she had breast cancer treated with lumpectomy, radiation therapy, and adjuvant chemotherapy. She was actively being treated for hyperlipidemia, gastroesophageal reflux with Barrett's esophagus, and vitamin B12 deficiency. There was no family history of unexplained liver disease.
She was a healthy appearing woman who looked younger than her stated age. Her sclera were not icteric. The liver and spleen were not palpable. She had no stigmata of chronic liver disease. Her cardiac rhythm was regular with a normal rate.
Laboratory data revealed hemoglobin of 12.5 g/dL (12.0–16.0) with normal WBC and platelets. Liver transaminases and alkaline phosphatase levels were normal. PT was 10.7 sec (9.1–12.0), and INR was 0.97 (0.90–1.10). Serum ferritin was 1,379 ng/mL (10–162 ng/mL). Serum iron was 77 μg/dL (25–156), TIBC was 226 μg/dL (250–450), and transferrin saturation was 34% (20–50). She did not carry any of the mutations C282Y, H63D, or S65C.
MRI of the abdomen demonstrated iron deposition in the liver and spleen compatible with secondary hemochromatosis. Liver biopsy documented increased iron uptake in the hepatocytes and Kupffer cells (). There was focal periportal fibrosis but no cirrhosis. The dry weight iron content in a biopsy of liver tissue was 6,153 μg/g (270–1,600 μg/g).
The iron supplements were discontinued. She was prescribed one 300–350 mL phlebotomy of whole blood per week. After approximately 4 phlebotomies, her hemoglobin fell to 9.7 while her ferritin remained elevated. Erythropoietin injections were added in an attempt to minimize delays and interruptions in the phlebotomy schedule, and with some difficulty, she tolerated 17 phlebotomies over a span of 5 months. Her hemoglobin the week following her 17th phlebotomy was 8 g/dL despite the erythropoietin stimulants. Her ferritin at that point was 65 ng/mL. She had one more phlebotomy about six months later when her ferritin rose again to more than 100 ng/mL. After that, because of the symptoms induced by the procedure and based on the rationale that she had no apparent mutation causing excessive absorption, we have accepted the normal range for our lab as our goal. To date, the iron saturation has remained less than 30% and her ferritin has remained stable between 70 and 100 ng/mL.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [78, 'years'], 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 78 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
674,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8716163-1,Extracted,"A 66-year-old Caucasian male presented to the ER reporting blood in the urine with increased fatigue for the past three days. He explained that the urine was slightly red and progressively worsened to gross bloody hematuria. The patient had been on aspirin and ticagrelor (DAPT therapy) for eight months prior to hospitalization immediately following cardiac stenting for acute coronary syndrome. The patient was also taking rivaroxaban (15 mg) and amiodarone (200 mg) for paroxysmal atrial fibrillation. The rivaroxaban was stopped five months prior to the current hospital admission due to epistaxis. The patient reported that he had started calisthenic exercises for the past two months prior to presentation. He had been sore occasionally following these exercises. On review of symptoms, the patient denied dysuria, abdominal pain, flank pain, fever, trauma, or injury. His past medical history was significant for myocardial infarction, paroxysmal atrial fibrillation, hypertension, and hypercholesterolemia. His medication regimen included amiodarone 200 mg once a day, Rosuvastatin 20 mg every evening, ticagrelor 90 mg every 12 hours, aspirin 81 mg once a day, metoprolol tartrate 50 mg every 12 hours, pantoprazole 40 mg every morning before breakfast, and alprazolam 1 mg as needed for anxiety.
The only medication that was new to his regimen was the alprazolam, prescribed for anxiety two months prior to presentation. The patient had been adherent to his medication regimen for the past eight months. He denied any alcohol, tobacco, or recreational drug use. Vitals on admission were blood pressure 164/74 mmHg, pulse 71 beats per minute, respiratory rate of 20 respirations per minute, temperature 97.9 degrees Fahrenheit and pulse oximetry of 98% on room air. His initial labs were significant for low RBC count and platelets at 127,000/mm3. Differential analysis showed slight anisocytosis, macrocytes, ovalocytes, and abnormal RBC morphology. Complete metabolic panel showed an increased creatinine of 1.70 mg/dL (with a glomerular filtration rate [GFR] of 41 ml/min), alkaline phosphatase of 232 u/L, aspartate aminotransferase (AST) of 1,290 U/L, and alanine aminotransferase (ALT) of 766 U/L. The creatine kinase measured two days after admission was 33,030 U/L. The patient’s hepatitis panel, coagulation panel, thyroid panel, and acetaminophen level were all within normal limits. Urinalysis showed proteinuria with 100 mg/dl, a few squamous epithelial cells, large amounts of blood with few RBCs, and 3-5 WBCs, without leukocytosis. A CT scan of the abdomen and pelvis without contrast showed no nephrolithiasis or appendicitis (Figure ). The ultrasound of the right upper quadrant showed no pathological findings of the kidney or the liver.
On admission, amiodarone and rosuvastatin were stopped due to the patient’s transaminitis. IV hydration therapy was started on admission due to the AKI. Later on in the patient’s course of treatment, after rhabdomyolysis was diagnosed, anti-Jo antibodies and antinuclear antibodies were measured and found to be negative. On the day the patient was discharged, five days after the initial encounter, the patient’s condition had progressively improved, which was evidenced by the patient’s level of serum creatine improving to 1.28 mg/dL (with a GFR of 56 ml/min), alkaline phosphatase of 215 U/L, AST of 614 U/L, ALT of 650 U/L and a creatine kinase of 10,297. The patient's admission and discharge day's laboratory values are listed in Table .",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [66, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Vascular disease history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 66 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
675,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8501465-1,Extracted,"An 85-year-old male with a medical history of hypertension, hyperlipidemia, benign prostatic hyperplasia, stage III chronic kidney disease, and vasovagal syncope was brought to the emergency department (ED) and complained of left upper extremity shaking and an abrupt, non-localized headache that started a day prior to admission associated with tinnitus, vision changes, generalized weakness, nausea, vomiting, and new left upper extremity weakness. There was no report of loss of consciousness, incontinence, or tongue biting. Family history was remarkable for coronary artery disease in his father. He smoked two packs of cigarettes per day for about 32 years. His daily home medications were aspirin 81 milligrams (mg), atorvastatin 40 mg, lisinopril - hydrochlorothiazide 20 - 25 mg, atenolol 25 mg, and finasteride 5 mg. On arrival, his Glasgow Coma Scale (GCS) score was 15 (E 4, V 5, and M 6), and his NIH Stroke Scale/Score (NIHSS) was 2 (1 each for limb ataxia and dysarthria). Initial vitals were a blood pressure of 174/83 mmHg, heart rate of 151 beats per minute, respiratory rate of 18 breaths per minute, temperature of 98.4℉, and oxygen saturation (SpO2) of 98% on room air. On physical examination, he was alert and oriented to name, place, and time. Cranial nerves II to XII were intact. Strength was 5/5 in the upper and lower extremities. Sensations were intact, with no dysmetria noted. The cardiopulmonary examination was only remarkable for an irregular heartbeat. Other examination findings were noncontributory. The laboratory results on admission are presented in Table .
Electrocardiogram confirmed new-onset atrial fibrillation with a rate of 132 beats per minute with no ST or T-wave changes. A non-contrast computed tomography (CT) scan of the head was negative for cerebral hemorrhage and showed no signs of large vessel territory infarct. He was not a candidate for tissue plasminogen activator (tPA) due to the delayed onset of symptoms. He was started on diltiazem and anticoagulated with low-intensity heparin drips for new-onset atrial fibrillation. CT angiogram (CTA) of the head and neck revealed 50% to 60% stenosis at the right proximal internal carotid artery, 30% stenosis at the left proximal internal carotid artery, and mild stenosis at the origin of the right/left vertebral artery. Echocardiogram was remarkable for an ejection fraction of 55%-60% with mild mitral regurgitation.
On the second day of hospitalization, the patient developed hypoxia, new-onset stridor, persistent coughing spells, shortness of breath, dysmetria on the finger to nose testing (left more than right), and altered mental status. On assessment, there was expressive aphasia, left upper extremity weakness (3/5), and disorientation noted. He received racemic epinephrine, 125 mg solumedrol, and helical oxygen 4L due to concern for an allergic reaction. A repeat CT scan of the head revealed an acute infarct in the left inferior to medial cerebellar hemisphere with mild associated hemorrhagic conversion. Associated mass effects, including compression of the fourth ventricle and mild left cerebellar tonsillar herniation, was also noted (Figure ). Protamine sulfate was administered and heparin/aspirin was discontinued. Neurosurgery was consulted and a decision was made with the patient and family to not pursue any surgical interventions due to the risks. Bedside laryngoscopy done by an otolaryngologist revealed partial limitation of bilateral vocal cord abduction on inspiration, possibly due to cerebellar hemorrhage and mass effect on cranial nerve X. The patient was transferred to the neurointensive care unit (ICU) and his cerebral edema was treated with 3% hypertonic saline. The patient never required intubation and an MRI was not completed due to patient refusal.
The patient improved over one week and was discharged to a rehabilitation center. Twenty-three days later, a repeat CT scan of the head showed an evolution of the left cerebellar infarct with patchy low attenuation of cerebellar hemorrhage that appeared slightly smaller when compared to prior imaging (Figure ). On an outpatient follow-up visit three weeks later, his stridor had significantly improved.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Vascular disease history': True, 'age': [85, 'years'], 'Stroke': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 85 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
676,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5839003-1,Extracted,"A 64 year old male presented with sudden onset quadriparesis. He had acute onset pain in both lower limbs which was followed by lower limb weakness. Meantime he had also noticed weakness of both upper limbs. There was no history of preceding back or neck pain. He was also unable to pass urine and faeces. There had not been any history of trauma. He has been ambulant and apparently healthy prior to this illness. He gave a history of smoking of sixteen pack years. There was no past or family history of cardiovascular diseases. There was no history of high risk sexual behaviour.
The patient was averagely built with no features of Marfan syndrome. On examination both the lower limbs had reduced tone and the power was of Medical Research Council {MRC} grade 0/5. Both knee and ankle jerks were absent with equivocal plantar response. The pain and temperature sensory examination revealed a sensory level at T1. However the vibration and proprioception were both spared. The examination of upper limbs revealed weak elbow extension MRC power grade being 4/5. Intrinsic hand muscles power was also reduced to grade 3/5 bilaterally. However biceps and brachioradialis power was 5/5. The biceps and brachioradialis reflexes were normal. The triceps reflex was diminished on right side and absent on the left. Thus a lesion at spinal cord level lower cervical/ upper thoracic C7/T1 was clinically suspected especially of the anterior cord region sparing the dorsal columns. There were no areas of spinal tenderness.
The abdominal examination revealed a palpable distended bladder with relaxed anal sphincter tone. Cardiac and respiratory system examination was essentially normal. The mental status and cognition were unaffected. The patient was immediately catheterized and basic investigations carried out.
Magnetic Resonant Imaging (MRI) panspine showed increased T2 signal intensity in the anterior aspect of cervico-dorsal spinal cord extending from C5 to T10 level. High signal areas revealed the characteristic ‘owl eye’ appearance on axial imaging (Figs. and ). The involved areas showed diffusion restriction on Diffusion Weighted Imaging (DWI). Cervical, thoracic and lumbosacral vertebral bodies and discs were of normal alignment with mild degenerative changes without significant thecal indentation or paravertebral abnormalities. Compressive myelopathy was also excluded. The lower thoracic aorta showed aneurysmal dilatation with a mural thrombus.
The chest Xray revealed a widened mediastinum. A CT aortogram done thereafter confirmed an aneurysmal dilalatation of the root, ascending, arch and proximal descending thoracic aorta. The abdominal aorta was normal. The diameters of the ascending aorta and arch were 5.6 cm, 5.8 cm respectively (Fig. ). It can be categorized as Extent 1 according to the Crawford classification of thoracoabdominal aortic aneurysms. There were marked intimal irregularities and calcified atherosclerotic plaques with a small mural thrombus.
The complete blood count, C reactive protein, renal and liver functions were within normal ranges. The ESR was 32 mm/ first hour and Venereal Disease Research Laboratory (VDRL) test was non reactive. HIV 1 and 2 antibodies were negative. Blood and urine cultures were all sterile. The LDL cholesterol was 86 mg/dL and HbA1c was 5.4%. Antinuclear antibody and Antineutrophilic cytoplasmic antibodies were negative. Two Dimentional Echocardiography revealed a mild left ventricular hypertrophy with an ejection fraction of 60% and dilated aortic root of 4 cm in size.
The patient was assessed by both vascular surgical and cardiothoracic teams. However the patient was declining surgical interventions. He was then commenced on rehabilitation and transferred to a dedicated rehabilitation centre.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Hypertension history': False, 'Diabetes history': False, 'Vascular disease history': True, 'age': [64, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 64 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 0 + 1 = 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
677,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2628898-1,Extracted,"An 85-year old lady presented as an emergency with sudden onset of severe left sided abdominal pain and vomiting for two days. This was associated with constipation for 3 days. She had a past medical history of atrial fibrillation, angina, and pulmonary embolism for which she was anticoagulated with warfarin. There was no history of trauma.
On examination she was haemodynamically stable. Her abdomen was generally tender, maximal tenderness being in the left hypochondrium and left lumbar region, associated with some guarding and rigidity. Bowel sounds were present and the rectal examination was unremarkable.
The blood tests revealed normal haemoglobin, marginally raised white cell count (12.5) and C- reactive protein (25.3), and a grossly deranged International Normalised Ratio (INR) of 8.9. Her renal and liver functions function tests were within normal limits. An erect Chest X-ray and supine abdominal films were both unremarkable. Computed Tomography (CT) Scan showed a long abnormal loop of thick walled jejunum with a small amount of free fluid in the intraperitoneal cavity (Figure and ).
A diagnosis of spontaneous intramural haematoma of the jejunum was made. She was treated conservatively with nil by mouth, intravenous fluids, and nasogastric suction. Fresh frozen plasma and vitamin K were given to normalise her clotting parameters. Her symptoms subsided gradually over the next couple of days and she was gradually started on fluid and diet. The clotting parameters normalized and she was discharged home on normal diet six days later.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': True, 'Vascular disease history': True, 'age': [85, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 85 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
678,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5644815-1,Extracted,"A 77-year-old male with past medical history of hypertension, mechanical aortic valve replacement (AVR), rectal carcinoma status post partial colectomy and colostomy was admitted with paroxysmal atrial fibrillation and volume overload. His heart was 110-120 and BP was 130/85 on initial presentation. The patient was started on diltiazem drip in the emergency department which was continued along with his home dose of warfarin. He also received 80 mg of IV Lasix given his volume overload status as evident on physical examination as the patient had positive jugulovenous distension and +1 bilateral pitting edema on lower extremities. An initial chest x-ray obtained demonstrated pulmonary vascular congestion, bilateral effusion and mild interstitial edema.
The patient underwent regadenoson stress test as part of ischemia workup which was negative. A transthoracic echocardiogram (TTE) was obtained that was significant for mildly dilated left atrium, moderate to severely impaired left ventricular systolic function with an ejection fraction estimated at 30% and normal diastolic function. No wall motion abnormality was detected on TTE. The patient was diuresed further with IV Lasix 40 mg and lisinopril and spironolactone were initiated. He underwent DC cardioversion (DCCV) as diltiazem did not convert him to sinus rhythm in 24 hours. His rhythm changed to normal sinus rhythm (NSR) post DCCV. Amiodarone was started after cardioversion for maintenance of NSR and warfarin dose was adjusted.
Following the night after DCCV, the patient underwent cardiac arrest and CPR was initiated. CPR continued for 60 minutes with the patient being in torsades de pointes (ventricular fibrillation) for the first 50 minutes after which the rhythm changed to pulseless electrical activity. Return of spontaneous circulation (ROSC) was achieved after 60 minutes. The patient was immediately intubated and shifted to cardiac intensive care unit. Blood pressure was initially maintained with four pressors (epinephrine, norepinephrine, dopamine, vasopressin) with a target mean arterial pressure (MAP) of greater than 65. Continuous renal replacement therapy (CRRT) was begun for acute renal failure with anuria complicated with severe anion gap metabolic acidosis. The patient also developed lactic acidosis, leukocytosis and shock liver as evident with elevated liver function tests (LFT) and International Normalized Ratio (INR). He was also started on piperacillin/tazobactam for suspected infection and pan-cultures were obtained. Pain was controlled with fentanyl drip.
Over the course of next few days, the patient's blood pressure improved and he was weaned off all vasopressors. He became more awake and alert and responded to commands. Tracheostomy was performed for prolonged mechanical ventilation. The patient had worsening point of care (POC) blood glucose and elevated ketones in the blood and urine. He was started on insulin drip which resulted in better control of his POC glucose. Antibiotics were switched to meropenem and linezolid for worsening leukocytosis and micafungin was added for fungal coverage. Abdominal computed tomography (CT) was obtained which demonstrated acute pancreatitis (Figure ). Lipase was sent that came back normal. A CT-angiography (CTA) obtained prior to cardiac arrest as part of the workup for abdominal aortic aneurysm was unremarkable for any signs of pancreatic abnormalities (Figure ). Cultures obtained from the central line, peripheral, urine and sputum did not yield any organism. Lactic acidosis resolved, white blood cell (WBC) trended down and abdominal pain improved. Linezolid and micafungin were discontinued based on infectious disease recommendation as infectious etiology was less likely, however, meropenem was continued for empiric coverage for total 14 days. Insulin drip was switched to NPH insulin with correction factor while the patient was on tube feeding. The patient was successfully weaned off of ventilator and physical therapy and occupational therapy were initiated for rehabilitation.
Unfortunately, the patient developed worsening abdominal pain and elevated bilirubin in the following days. A CT scan and ultrasound of abdomen and pelvis were consistent with the development of cholecystitis without any evidence of gallstones. The patient underwent endoscopic ultrasound (EUS) with endoscopic retrograde cholangiopancreatography (ERCP) which revealed 2-3 cm stricture in the common bile duct. Pancreatic duct and common bile duct were stented and good bile flow was demonstrated. Despite this, the patient continued to endorse abdominal pain and enteral feeding was paused. Total parenteral nutrition (TPN) was initiated to provide bowel rest. The patient developed septic shock with elevated lactate and BP was barely managed with four pressors. Family was counseled and the patient passed away shortly after he was transitioned to comfort care.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Hypertension history': True, 'Vascular disease history': False, 'age': [77, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
679,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7105085-1,Extracted,"A 68-year-old male presented for total thyroidectomy due to amiodarone-induced thyrotoxicosis. Past medical history included ischemic cardiomyopathy (left ventricular ejection fraction 37%) supported by a Heartmate 3 LVAD (Abbott Laboratories, Lake Bluff, Illinois) biventricular implantable cardioverter-defibrillator (BiV-ICD) placement, atrial fibrillation on chronic amiodarone, hypertension, and obesity. The patient had presented to the hospital a month prior, in cardiogenic shock, with a further decrease of his ejection fraction to 21%. He required an intra-aortic balloon pump and subsequent placement of a Heartmate 3 LVAD. The hospital course was further complicated by a tenuous volume status requiring alternating diuretic dosing with pressor/albumin support. More importantly, the patient was diagnosed with amiodarone-induced thyrotoxicosis. Despite maximal medical treatment (methimazole, high dose prednisone, and cholestyramine), thyroid-stimulating hormone (TSH) levels remained <0.005 (0.27-4.2 µUI/ml). Total thyroidectomy was recommended by a multidisciplinary care team (endocrinologist, endocrine surgeon, and cardiologist).
Preoperative transthoracic echocardiography showed LVAD present with mildly decreased right ventricular function. The electrocardiogram demonstrated sinus rhythm with premature ventricular complexes and a left bundle branch block.
Due to concerns about the patient’s cardiac status, it was decided to perform the surgery under MAC/superficial cervical block, with general anesthesia as a back-up option. The patient was brought to the operating room and his LVAD was connected to the operating room power source. An arterial line was placed for constant blood pressure measurements in addition to standard American Society of Anesthesiologists (ASA) monitoring. Per discussion with the surgical team, a bipolar cautery was used for the procedure so as not to interfere with the ICD function. The patient was given 2 mg of midazolam and an alfentanil infusion was started at 1.2 mcg/kg/min. He was additionally given 500 mcg bolus of alfentanil prior to the cervical block performed by the surgical team. Intravenous (IV) fluid was infused at 50 ml/hour and there was no vasopressor or blood transfusion requirement during the case. The patient tolerated the procedure extremely well from a hemodynamic standpoint (Figure ) as well as the pain, comfort, and awareness standpoint. No conversion to general anesthesia or advanced airway was necessary for the case.
After completion of the surgery, he recovered in the intensive care unit in stable condition. There were no reported complications at postoperative follow-up.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Hypertension history': True, 'Diabetes history': False, 'Vascular disease history': True, 'age': [68, 'years'], 'Congestive Heart Failure': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 68 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
680,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7505381-2,Extracted,"A 74-year-old man, weighing 54 kg (body mass index: 21), was diagnosed with an epiretinal membrane and scheduled for left total vitrectomy. His medical history was significant for hypertension and non-insulin-dependent diabetes. There was no history of PCI or coronary angiography. The patient's physical status score was II according to the American Society of Anesthesiologists. During the preoperative evaluation, the patient described his functional capacity as good and denied experiencing any symptoms of HF. Physical examination did not reveal any signs of congestive HF. The preoperative ECG showed non-specific T wave abnormalities and atrial fibrillation (Fig. ). TTE revealed ischemic heart disease with normal LV size and function (EF: 65%), grade 2 diastolic dysfunction with left atrial enlargement, regional wall motion abnormalities (inferior wall hypokinesia and antero-lateral wall hypokinesia), and no significant valvular pathology. Preoperative TTE revealed, LVEF = 65%, E/A = 2.64, and E/e′ = 16.43 (Fig. ). The patient was taking spironolactone 25 mg and furosemide 40 mg for treatment of cardiac disease. The preoperative cardiology consultation estimated the surgical risk of the patient to be low (<1%) considering his blood pressure was stable and functional capacity was good.
The procedure was performed under general anesthesia and endotracheal intubation with routine monitoring as in Case 1. Anesthesia was induced using propofol, and intubation was performed following rocuronium-induced muscular relaxation. Anesthesia was maintained using sevoflurane (1.5–2.0 vol%) and an air–oxygen mixture (FiO2 0.5). Muscle relaxation was maintained using intermittent doses of intravenous rocuronium titrated to keep the train of 4 to less than 2 twitches.
The perioperative blood pressure was stable and the surgery lasted for approximately 80 minutes. The patient experienced mild bleeding and fluid replacement was performed with 200 mL of normal saline. Postoperatively, all anesthetic agents were discontinued and the residual neuromuscular block was reversed using 15 mg pyridostigmine and 0.4 mg glycopyrrolate. The patient was responsive to verbal commands, and was extubated immediately after adequate spontaneous ventilation was ensured. He was then transferred to the PACU. On arrival, the SpO2 was evaluated and found to be 99%; 30 minutes after arrival, it gradually decreased to 93%. Therefore, the patient was reintubated. Suctioning of the trachea revealed pink frothy sputum. Postoperative chest radiograph was obtained immediately (Fig. ) and the ECG was evaluated (Fig. ). The patient was transferred to the SICU without extubation for further management. In the SICU, 20 mg furosemide was injected intravenously, and infusion of 10 μg/kg/min dobutamine was continued. The patient received an additional dose of furosemide and his respiratory status improved over the next 12 hours. On postoperative day 1, his vital signs were stable and there were no signs of respiratory disturbance. On postoperative day 2, he was transferred to the general ward in an overall stable condition and then discharged on postoperative day 3 without any complications. No abnormalities were observed during the follow-up period of 4 weeks.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': False, 'age': [74, 'years'], 'Congestive Heart Failure': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 74 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
681,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4960328-1,Extracted,"A 50-year-old female with a past medical history of SLE diagnosed 20 years ago, ESRD on hemodialysis and atrial fibrillation on anticoagulation, presented to the emergency department after a syncopal episode. The patient was sitting on the side of her bed when she suddenly lost consciousness falling to the floor striking the right side of her face. She sustained significant facial trauma; however there were no signs of intracranial hemorrhage on CT scan of the brain. She described palpitations with chest pressure prior to the event. Initial electrocardiogram (ECG) reported by emergency medical services did not reveal any acute arrhythmias, such as TdP. Due to the complaints of chest pressure she was evaluated for cardiac ischemia utilizing cardiac biomarkers, CKMB and Troponin I. A total of three sets were completed every eight hours apart; all studies were reported within normal limits ruling out cardiac ischemia. Troponin I values were less than 0.045 ng/mL and CKMB values were all less than 0.5 ng/mL. ECG on presentation revealed 1st-degree AV block with corrected QT (QTc) interval of 689 ms (). Patient's ECG from two years prior showed a baseline prolonged QTc interval of 500 (). She was evaluated for reversible causes of QT interval prolongation including electrolyte derangements, medications, and SLE flare. Her electrolytes were within normal limits including potassium (3.9 mmol/L), magnesium (2.3 mg/dL), phosphorous (4.2 mg/dL), and calcium (9.0 mg/dL). C3 levels were low, with normal C4 and ESR, and anti-dsDNA was negative making SLE flare unlikely. Patient continued to have dialysis on her normally scheduled days.
After evaluation by electrophysiology there was concern for presumed TdP due to her clinical presentation and grossly abnormal QTc interval. She was placed on mexiletine 150 mg BID and was initially recommended to have defibrillator implantation to protect against sudden cardiac death from cardiac arrhythmias. Evaluation of the patient's medications revealed that she was taking HCQ for the past two years for treatment of refractory SLE. HCQ was discontinued and the patient's QT interval slowly decreased to a QTc interval of 500 over the next 7 days (). She was monitored on the telemetry unit for one week and did not have any further arrhythmic events. After further discussion with the patient's Cardiologist and Rheumatologist she had been noted to have a prolonged QTc interval of approximately 500 ms while on therapy with HCQ. She was trialed off the medication for two months without resolution of the QT interval abnormality, possibly due to undiagnosed underlying SLE cardiomyopathy. The patient's ejection fraction on echocardiography one year prior was estimated at 65% with Doppler parameters consistent with abnormal relaxation suggesting heart failure with preserved ejection fraction. Implantable defibrillator placement was discussed with the patient prior to admission due to the prolonged baseline QTc interval. However, she was reluctant to proceed as she did not want indwelling devices due to concern for possible Permacath placement in the future for dialysis if her arteriovenous fistula malfunctioned.
The risks and benefits of continuing HCQ were discussed with the patient, and she decided she wanted to continue the medication due to well controlled SLE flares. She had noted adverse reactions to steroid therapy and limited treatment options for SLE due to her underlying renal failure. We discussed the risks of recurrent syncopal episodes if she was to continue HCQ therapy, and the high risk for intracranial bleed while on anticoagulation if she was to have another syncopal episode. Final recommendations were made to proceed with defibrillator placement if she was to continue with HCQ to protect against life threatening arrhythmias. She had a subcutaneous defibrillator placement and was to be restarted on HCQ as an outpatient with dose reduction and close monitoring of QTc interval.
At three-month follow-up the patient remained off HCQ as after discussion with her Rheumatologist the risks related to syncope and possible intracranial bleed while on anticoagulation treatment greatly outweighed the benefits of HCQ therapy. She continues to be closely monitored for SLE flares, and treatment decisions are to be strategized as clinical issues arise. Subcutaneous implantable defibrillator interrogation showed no recorded events at three months. Her ECG continues to show a prolonged QTc interval of 508 ms. Due to the prolonged QTc interval she is still at high risk of ventricular arrhythmias despite discontinuation of HCQ. Therefore, the subcutaneous implantable defibrillator is providing secondary prevention of sudden cardiac death due to prolonged QT interval.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Diabetes history': False, 'Vascular disease history': True, 'age': [50, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 50 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
682,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-11396,Extracted,"A 56-year-old man was brought to the emergency department by his wife when he passed out for 5 seconds after dinner at home. He says that he recalls feeling lightheaded moments prior to passing out and also had some palpitations. Otherwise, he has been feeling fatigued recently and has had some shortness of breath. His previous medical history is significant for diabetes that is well controlled on metformin. An EKG is obtained showing fast sawtooth waves at 200/min. He is administered a medication but soon develops ringing in his ears, headache, flushed skin, and a spinning sensation.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Diabetes history': True, 'Vascular disease history': False, 'age': [56, 'years'], 'Stroke': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 56 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 0 + 1 = 1.
The patient's CHA2DS2-VASc Score is 1."
683,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8130342-1,Extracted,"A 72-year-old man presented with three months’ history of progressive dysphagia for solid and liquid foods. He also had frequent instances of regurgitation of food without any symptoms of chest pain or heartburn, while his body weight remained constant. His Eckard score was 5 points which consist of dysphagia each meal and daily regurgitation. He had underlying hypertension and dyslipidemia and was taking losartan 50 mg/day and simvastatin 20 mg/day. He denied any history of smoking, alcohol drinking, or family history of cancer. Physical examination and basic laboratory tests were within normal limits.
Upper GI endoscopy demonstrated circular folds like a winding staircase in the lower esophagus, which is classically known as a corkscrew esophagus (Fig. a), and a normal esophagogastric junction (Fig. b). A barium esophagogram showed constriction and curling of the esophageal lumen resembling a corkscrew (Fig. ). He underwent HRM which showed 6 of 10 swallows with a DCI > 8000 mmhg-s-cm (the median with interquartile range of DCI was 16,597 [8736–30,397] mmhg-s-cm), a distal latency (DL) was normal at 6.5 s (the median with interquartile range of DL was 5.4 [3.3–5.7] s), and integrated relaxation pressure (IRP) was borderline high at 15.5 mmHg (Fig. ). During the procedure, we observed quite good lower esophageal sphincter relaxation during wet swallowing.
Based on this HRM study, we made a diagnosis of an esophago-gastric junction (EGJ) outflow obstruction with hypercontractile (JH) esophagus. The patient was treated with a calcium blocker and proton pump inhibitor for one month after which his symptoms markedly reduced. After the treatment, the Eckard scores declined from 5 to 1, consisting of occasional dysphagia.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Diabetes history': False, 'Vascular disease history': False, 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
684,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7213680-1,Extracted,"A 64-year-old male patient was referred to the emergency department of our hospital, with a four-day history of spontaneous abdominal pain radiating on the posterior aspect of the left thigh. He reported no trauma history, but during the past few hours, pain had severely deteriorated. In regards to his past medical history, the patient was on treatment for hypertension and atrial fibrillation. In particular, he was on an angiotensin II receptor blocker and on warfarin as an oral anticoagulant.
The patient was afebrile, and his vital signs were within normal values (blood pressure 115/78 mmHg, heart rate 82 beats/min, SpO2 99%). Physical examination revealed diffuse abdominal pain, radiating on the posterior aspect of the left thigh. Peripheral vascular examination was within normal values on both lower limbs, with palpable pulses and capillary refill time of less than two seconds. Neurological condition, on the other hand, was impaired on the left lower limb, and objective deficiencies were obvious. Examination revealed reduced strength of the left lower limb. The patient was unable to straight leg raise, to flex the hip or the knee, and had developed hypoesthesia on the anterior aspect of the thigh. The patella reflex was absent on the affected side.
Laboratory data revealed prolonged prothrombin time with an international normalized ratio (INR) level of 4.5, and a haematocrit and haemoglobin decrease of 33.1% and 10.7 g/l, respectively. The rest of the full laboratory analysis was within normal values. Imaging studies included abdominal ultrasound scan (US), lumbar spine, and pelvis CT scans. Lumbar spine pathology was excluded, and a large retroperitoneal haematoma was unveiled within and around the left iliopsoas muscle (35 cm x 9 cm x 6 cm) (Figure ).
The patient was admitted to the hospital, and warfarin anticoagulation regimen was intermitted. Prolonged INR was reversed within 48 hours with the aid of vitamin K administration. A new CT scan was performed on day 3 post-admission. No change in the size of the haematoma was revealed (Figure ). At that point, there was a consultation with the radiology department whether the haematoma could be percutaneously drained; however, the CT scan revealed a clotted formation that would not allow for successful drainage.
The patient was managed conservatively. Physical therapy had been initiated by day 1 post-admission. The patient was discharged after six days of hospitalization and after pain management had been established. Nerve conduction studies were performed three weeks later and revealed left femoral nerve palsy. A new CT scan was performed two months post-discharge and unveiled absorption and a significantly reduced size of the haematoma (Figure ). The patient demonstrated gradual improvement and recovered after eight months of physiotherapy and rehabilitation. This included almost complete motor and complete sensory function restoration of the left femoral nerve.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [64, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 64 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
685,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2614940-1,Extracted,"A 77 year old lady presented with a two week history of shortness of breath and acute onset palpitations and chest pain. She had also developed an acute confusional state for two days prior to her admission. She had been admitted five months ago with an episode of chest infection which was successfully treated with antibiotics. In the previous four years she had suffered from an episode of transient ischaemic attack (TIA).
Previous investigations had shown a normal computer tomography (CT) scan of the head, active rheumatoid arthritis and osteoarthritis. On this occasion she was afebrile, normotensive and had an irregularly irregular pulse rate of 150 bpm. Further cardiovascular, respiratory and abdominal examination was unremarkable and a detailed neurological examination did not reveal any significant abnormality.
An electrocardiogram showed fast atrial fibrillation (AF) for which she was treated with digoxin, warfarin & beta blocker for further optimisation. An in-patient trans-thoracic echocardiogram (TTE) demonstrated a mobile mass in the left atrium (figure ). Subsequent trans-oesophageal echocardiography (TOE) revealed a mobile large left atrial mass (2.7 cm × 3.5 cm) attached to the fossa ovalis region in the inter-atrial septum, prolapsing into the left ventricle through the mitral valve in diastole (figure &).
The patient declined surgical treatment in view of the risks involved, & died a few weeks later whilst on conservative therapy.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': True, 'Hypertension history': False, 'Vascular disease history': False, 'age': [77, 'years']}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
686,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5052862-1,Extracted,"A 52-year-old male patient, who had been experiencing left fronto-temporal headache with left ocular pain for 1 day, was admitted to the ED. The day before admission, the man had experienced headache and ocular pain for 3 hours, and then recovered spontaneously. On the day of admission, the symptoms had recurred abruptly and persisted. The headache was dull, and ocular pain was more severe in the lean-forward position. He also complained of blur red vision and lacrimation in the left eye in the supine position. The headache had occurred spontaneously without any history of trauma. He has no past medical history without hypertension.
The patient’s vital signs at the time of admission into the ED were as follows: blood pressure, 170/105 mmHg; heart rate, 68 beats/min; respiratory rate, 18 breaths/min; body temperature 36.1°C. His mental status was clear. Ophthalmologic examination revealed normal visual field, extra-ocular movement and light reflex. Laboratory findings were unremarkable. To rule out brain lesion, we performed computed tomography (CT) of the brain. No parenchymal lesion or bony deformity was seen in the brain ().
Consult to neurologist and ophthalmologist was done due to rule out cluster headache and glaucoma. Neurologist ordered brain magnetic resonance angiography (MRA) of the brain to rule out cavernous carotid fistula. The results were normal (). Neurologist requested ophthalmologist consult.
The initial ophthalmologic examination revealed normal findings, including normal visual acuity (visus oculi dextri, 1.0 diopter [D], visus oculi sinistri [VOS], 1.0 D), and normal intraocular pressure (normal range, 12 to 22 mmHg). But the patient kept complaining of pain and painkillers were ineffective. We reviewed the CT scan of the brain, and observed lens subluxation in the left eye (). So we consulted to ophthalmologist again. It revealed protrusion of the vitreous body into the anterior chamber, posterior subcapsular opacity, phacodonesis, and lens subluxation toward the nasal area of the left eye, and the ophthalmologist decided him to out-patient department follow up for the possibility of operation.
Spontaneous zonulysis of the left eye was diagnosed. The symptoms were attributed to a temporary pupillary block and angle closure glaucoma attack. So we recommended him to visit outpatient department and explained the possibility of laser iridectomy in case of aggravation of disease.
After 3 days, he visited the ophthalmologic out-patient department, and initial examination showed fluctuation of vision scale (initial exam VOS 0.1 D; after 1hour exam VOS 0.9 D) in left eye. The intraocular pressure was normal but slit lamp examination revealed further prolapse of the vitreous body into the anterior chamber.
There was more progressive inferior dislocation of left lens due to zonulysis in dilated funduscopic examination otherwise normal finding in right eye (). The patient was discharged and an operation was scheduled for 2 days later.
After 2 days, the left eye had been rendered aphakic because of complete dislocation of the lens. Left pars plana vitrectomy (PPV) and intra ocular lens (IOL) fixation were recommended by the ophthalmologist. However, the patient wanted to undergo the operation in his hometown and hence, was discharged.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': False, 'Diabetes history': False, 'Vascular disease history': False, 'age': [52, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 52 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
687,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6968510-1,Extracted,"A 67-year old right-hand-dominant male was referred to our plastic surgery department with a 3 year history of a swelling on his right middle fingertip with no prior history of trauma to the digit. The mass had been slowly enlarging over the preceding 3–4 months, was becoming increasingly tender and occasionally bled due to a superficial abrasion on the surface. The patient had a past medical history of Grave’s disease, atrial fibrillation and a perforated gastric ulcer.
Examination revealed a 2 × 1.5cm mass over the distal pulp and hyponychium of the right middle finger. The swelling was mildly tender and there was an area of superficial ulceration centrally (). The digit was neurovascularly intact with normal range of motion and no evidence of local erythema, inflammation or discolouration. The working differential diagnosis following initial consultation included glomus tumour, ganglion cyst and haemangioma, thus the patient was booked for surgery without prior imaging.
One month following referral, the patient underwent excision biopsy of the lesion which was not found to be communicating with bone, nerve or tendon and the intra-operative impression was that of a ganglion cyst (). The initial histopathology examination reported a circumscribed multinodular predominantly solid tumour () ulcerating the overlying epidermis. There were focal papillary projections with tubular/ductal structures () where ducts were lined by a double layer of epithelium consisting of inner cuboidal cells and an outer myoepithelial layer (). There was also evidence of lymphovascular invasion (), focally high mitotic activity () and the tumour was shown to abut the margins. Immunohistochemistry was performed () confirming a myoepithelial cell population expressing smooth muscle actin, calponin, D2-40 () and p63 (). The tumour was classified as digital papillary adenocarcinoma. The histopathology sections were sent to an external institution for expert opinion and the diagnosis affirmed with recommendation of complete excision and close follow-up. This recommendation was echoed when the case was discussed at the local multi-disciplinary meeting.
The patient underwent partial amputation of the digit () and computed tomography (CT) scan of thorax, abdomen and pelvis, which showed no evidence of distant disease. The histology report on the wider excision specimen confirmed no invasion of underlying bone and margins free of tumour (residual tumour in wider specimen 0.5 mm). This patient is currently 1 year disease-free and will be followed closely in the outpatient department with clinical examination, yearly chest X-ray and additional imaging as needed for at least a ten year period.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': False, 'Diabetes history': False, 'Vascular disease history': False, 'age': [67, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 67 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
688,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-10003,Extracted,"A 58-year-old woman presents to the emergency department with difficulty breathing and a sensation that her heart was racing for the past 3 days. She adds that she has lost weight over the last 7 weeks, despite a good appetite, and is anxious most of the time with difficulty sleeping at night. She has smoked 10 cigarettes per day for the past 15 years. Her blood pressure is 100/55 mmHg, temperature is 36.5°C (97.7°F), and pulse is irregular with a rate of 140–150/min. On physical examination she is thin, frail, and appears anxious. Her palms are sweaty and there are fine tremors on extension of both hands. She has a palpable smooth thyroid mass. Examination of the eyes reveals bilateral exophthalmos. An electrocardiogram is obtained and shown in the picture.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Hypertension history': False, 'Diabetes history': False, 'Vascular disease history': False, 'age': [58, 'years'], 'Congestive Heart Failure': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 58 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
689,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3325618-1,Extracted,"A 49-year old man was referred to us with painless sudden visual loss in his right eye. Eight days prior to his visit, he received chiropractic manipulation on his neck in a prone position for approximately 10 minutes to improve neck and shoulder stiffness. Immediately after rising, he was unable to see with his right eye. When he first visited our clinic, the best corrected visual acuity in the right eye was hand motion, while the left eye was at 20 / 20. Anterior segment examination was unremarkable, and the right eye had a relative afferent pupillary defect. There was cherry-red spot in the macula in his right eye (), and the arterio-venous transit time in the fluorescein angiogram was delayed (). A cervical color Doppler showed stenosis of the right internal carotid artery () with diffuse atherosclerotic plaques in the right common carotid artery (). The right anterior communication artery was not visible by magnetic resonance angiogram ().
The patient had been taken hospitalization twice previously because of cerebral infarction. He has suffered from dysarthria, which is sequela of cerebral infarction. He has taken medicine for hypertension and diabetes mellitus for 5 years.
In our case of central retinal artery occlusion, the usual emergency efforts to restore retinal circulation such as ocular digital massage and anterior chamber paracentesis were not performed because eight days had already passed. We prescribed ginko biloba extract (Tanamin; Yuyu Pharmacy, Seoul, Korea), 3 tablets per day. Three years after the patient's first visit, the best corrected visual acuity of his right eye was 20 / 200.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': True, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': True, 'age': [49, 'years'], 'Stroke': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 49 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
690,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7451151-1,Extracted,"A previously healthy 20-year-old female patient presented at the emergency department with 4 days history of concurrent severe right-sided pleuritic chest pain and moderate ipsilateral clavicular pain, shortness of breath on exertion, as well as combined right upper limb weakness and bilateral fingertip numbness. No other symptoms were reported. She accounted no recent travel or family history, including neurofibromatosis.
On admission, the ECG and troponins were found to be within normal limits. However, the ensuing chest X-ray (CXR) showed a large oval mass-like density in the posterior segment of the right upper lobe [].
The complementary CT scan of the chest with contrast showed a low density 7.2 × 10.5 × 8.3 cm mass in the posterior segment of the right upper lobe with no nodular enhancement, potentially originating at the right T5-T6 neural foramen. A 16 mm thick right pleural effusion was also described []. Although nonspecific, the findings suggested the presence of a peripheral nerve sheath tumor such as neurofibroma or schwannoma.
The ensuing MRI with gadolinium demonstrated a large (at least 7.2 × 9.2 × 8.5 cm) T1 isointense and a mild T2 hyperintense (heterogenic) mass relative to the muscle and within the right upper/mid posterior hemithorax. A focal contrast-enhancing protrusion of the right posterior medial aspect of the mass extending into the right T5-6 neural foramen suggested that the mass emanated from the neural foramen []. Of note, the bronchoalveolar lavage cultures were found negative for pulmonary pathogens, including acid-fast bacilli, chlamydia, Mycobacterium marinum, Mycobacterium avium, Nocardia, Legionella, yeast, fungus, or viruses.
In view of the patient’s age, concurrent symptomatology, Karnofsky Performance Scale (KPS) of 70 (mainly due to presenting symptoms), size of the lesion, and topoanatomical constraints, we decided to remove the tumor using a right- sided posterolateral thoracotomy followed by a perilesional dissection; the mass was successfully freed from the corresponding posterior rib and transverse process. We then proceeded to follow the pedicle into the right T5-T6 foramen, ultimately achieving “en bloc” tumor resection including the proximal nerve root. No spinal fluid leak or persistent bleeding was noted; the surgical site was closed accordingly and without complications.
The microscopic examination of the collected samples demonstrated a well-circumscribed encapsulated tumor composed of interlacing fascicles of bland spindled cells with alternating areas of hyper- and hypocellularity, thick hyalinized vessels, and occasional areas of nuclear palisading (Verocay bodies). Areas of lipidized/xanthoma cells were also noted. Non-neoplastic nerve structures were found adjacent to the neoplasm. No significant atypia or mitotic activity was seen. Finally, the immunohistochemical staining proved positive for S-100 protein, SOX-10 while negative for p63, PAX-8, neurofilament, and desmin. The findings confirmed the diagnosis of schwannoma [].[]
The patient was transferred to the intensive care unit postoperatively; her evolution at the hospital proved uncomplicated with follow-up serial CXRs remaining unremarkable []. The patient was discharged 7 days following surgery. A CT scan of the chest 1 month postsurgery showed normal findings [ and ]. In view of her good prognosis, adjuvant chemotherapy or radiotherapy was deemed not necessary at this stage. The patient has remained asymptomatic since her discharge from hospital; her KPS is of 100 currently (6 months postsurgery). As expected, she remains on follow-up. Due to the low risk of recurrence after schwannoma resection, repeated CT scan will be scheduled after 12 months postsurgery.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': False, 'Diabetes history': False, 'Vascular disease history': False, 'age': [20, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 20 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
691,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3789314-1,Extracted,"A 58-year old Caucasian male with a history of recurrent paroxysmal AF came to the Emergency Department (ED) with the complaint of epistaxis. He had a history of end stage renal disease (ESRD) on hemodialysis. His cardiologist had started him on dabigatran etexilate 150 mg twice a day about 4 months ago. He was previously on warfarin, but side effects including multiple episodes of minor epistaxis and gastrointestinal bleeds requiring transfusions warranted the switch to dabigatran etexilate. His CHADS2 score was 5, supporting the need for anticoagulation to prevent future stroke events []. Since being started on dabigatran etexilate, he has been tolerating it except for minor epistaxis. On the day of ED presentation, the patient awoke to find himself in a pool of blood. His vital signs were unremarkable on arrival to the hospital. Because of persistent epistaxis, an inflatable balloon epistaxis device was placed in the right nostril in the ED, with good hemostasis. He was admitted to the hospital for monitoring and further work-up.
Abnormal labs at the time of admission included a prothrombin time (PT) of 63 seconds, INR of 8.8, activated partial thromboplastin time (aPTT) of 105.7 seconds, and elevated BUN and creatinine of 73 mg/dL and 4.12 mg/dL, respectively. His hemoglobin and hematocrit were frequently checked, and they remained stable around 12 mg/dL and 37 mg/dL, respectively, not requiring any pRBC transfusions. The patient had not missed any dialysis session prior to admission. The supratherapeutic INR was thought to be secondary to dabigatran etexilate, and the medication was held. Other possible causes of supratherapeutic INR were excluded, including Vitamin K deficiency and severe liver disease, as laboratory values showed normal liver function test (LFT), albumin, and Vitamin K levels. He was given fresh frozen plasma (FFP), and ENT was consulted for additional packing. As dabigatran etexilate was a new anticoagulation agent at the time, the hospital did not have a reversal protocol for dabigatran etexilate toxicity in place and thus FFP was used. He remained stable clinically and the INR and aPTT trended downward after holding the dabigatran and continuing his scheduled dialysis session the following day. INR was 1.7 at the time of discharge and his aPTT had normalized. After a 5-day hospital stay, he was discharged. He went home without anticoagulants as his recurrent bleeds were thought to be a substantial morbidity risk outweighing the benefit of stroke prevention.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False, 'age': [58, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 58 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
692,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7906080-1,Extracted,"A 50-year-old man presented to the ED in late May 2020 with sudden onset excruciating pain on the posterior aspect of the right lower leg for two hours. The patient described a history of runny nose, sore throat, and noticed some palpitations over the previous five days. The patient had no reported past medical or surgical history. The patient was a nonsmoker, not an alcoholic with no history of illicit drug abuse. Family history was nonsignificant for a hereditable condition or vascular abnormalities. Initial vital signs were significant for a temperature of 98.8°F, a blood pressure of 129/76 mmHg, a heart rate of 78 beats/min, a respiratory rate of 18 cycles/min, and a body mass index of 31 kg/m2. On pulse oximetry, the patient was maintaining oxygen saturation on room air at 96%.
On physical examination, the right posterior tibial artery and right dorsalis pedis artery were not palpable. Femoral and popliteal arteries were palpable bilaterally. The rest of the systemic examination is otherwise unremarkable. The 12 lead electrocardiogram (ECG) showed an irregular heart rate of 70 beats/min and was identified as new-onset atrial fibrillation (AF) (Figure ). The cardiac enzymes were within the normal limit. Afterward, the patient had a real-time reverse transcriptase-polymerase chain reaction (RT-PCR) test of a nasopharyngeal swab specimen for SARS-CoV-2, and the result returned positive. Initial laboratory values showed a D-dimer level of 0.583 mcg/mL (Normal < 0.4 mcg/mL). Other laboratory results, including troponin T, thyroid-stimulating hormone value (TSH), complete blood count (CBC), comprehensive metabolic panel (CMP), and glycated hemoglobin (HbA1c) were unremarkable. A complete hypercoagulable workup, including measurements of factor V Leiden, protein C, protein S, and antithrombin III was unremarkable.
Droplet and contact precautions ensued in addition to contact and eye protection. Symptomatic treatment with antipyretic paracetamol was initiated. Computed tomography angiography (CTA) of the lower extremity showed partial right popliteal artery block (Figure ). Vascular surgery was involved, and the patient underwent catheter-directed therapy, including endovascular clot extraction to the right popliteal artery. The patient also initiated a therapeutic dose of enoxaparin of 1 mg/kg twice daily and oral warfarin with an international normalized ratio (INR) target between 2 and 3. The symptoms gradually improved and there was a notable improvement in his right posterior tibial and dorsal pedal pulses. He spent three days in the surgical intensive care unit (SICU) for observation.
The patient received the SARS-CoV-2 treatment protocol of the hospital at that time. Azithromycin, oseltamivir, paracetamol, vitamin C, zinc sulfate, and hydroxychloroquine were given in addition to bisoprolol and omeprazole. A transthoracic echocardiogram (TTE) showed a normal size of the left ventricle and normal global systolic left ventricular function (ejection fraction of 55%) with no regional wall motion abnormality. The pressure and size of the right and left atrium were normal with no valvular abnormalities.
In SICU, on the third day while the patient was under observation, he developed a dull abdominal pain mainly on the left side that required IV morphine. His abdomen was soft, nondistended, with no guarding or rebound tenderness and no organomegaly noticed on palpation. The CTA of the abdomen and pelvis with IV contrast revealed left kidney lower pole infarction (Figure ) and high-grade narrowing of the anterior splenic artery thrombosis with multiple splenic infarctions involving the anterior and inferior aspects (Figure ). The decision was to put the patient under observation for any concurrent complications and to be treated accordingly.
Over the course of the next week, the abdominal pain resolved, and the patient was transferred to the SARS-CoV-2 facility for quarantine. Five days later, he developed a symptom of blurry vision and headache, the patient denied having any similar symptoms before or had any eye discomfort. Focused neurological examination detected left homonymous hemianopia. Otherwise, it was unremarkable. Afterward, the ophthalmology team evaluated the patient and ordered magnetic resonance angiography (MRA) of the head. The latter showed the right occipital lobe subacute infarcts (Figure ). The stroke team decided to continue anticoagulation with an INR target of 2-3, with a consultation to physical and occupational therapy.
Four days later, a second RT-PCR nasopharyngeal swab was taken, which came back negative. The D-dimer level during the hospital stay continued to elevate, the last upon discharge was 4.74 mcg/mL. He was discharged home with an instruction to maintain direct-acting oral anticoagulant (DOAC), atorvastatin, aspirin, and bisoprolol with a close outpatient follow-up plan to an AF clinic for possible electrical cardioversion and a referral to a neuro-ophthalmologist clinic for rehabilitation therapy. On follow up, a transesophageal echocardiogram with saline study has been done which was normal with no cardiac shunts, intracardiac mural thrombus, and cardiac tumors. The patient was evaluated in the follow-up clinic with no vascular complaints or deterioration in his symptoms.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': True, 'Hypertension history': False, 'Diabetes history': False, 'Vascular disease history': True, 'age': [50, 'years'], 'Congestive Heart Failure': False, 'Stroke': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 50 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 0 + 2 = 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
693,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6849010-1,Extracted,"A 50-year-old female was referred for open heart surgery under the diagnosis of mitral stenosis and aortic regurgitation combined with atrial fibrillation. She had a history of percutaneous mitral valvuloplasty for mitral stenosis 11 years earlier. Her dyspnea worsened over the last 3 years and she was in New York Heart Association (NYHA) functional class III at presentation. She was in good physical shape, weighing 66 kg, and had no neuromuscular abnormalities on physical examination. She had no underlying disease either. She underwent mitral and aortic valve replacement in addition to maze procedure for the atrial fibrillation without events. The ischemic time was 208 minutes and the total bypass time was 246 minutes, respectively. Immediately after surgery in the ICU, higher doses of inotropics and vasopressors were necessary to maintain her blood pressure (BP) (systolic BP around 80 mmHg with dopamine 10 mcg/kg/min, dobutamine 10 mcg/kg/min, norepinephrine 0.5 mcg/kg/min and vasopressin 4 unit/h). Her cardiac index measured by a Swan-Ganz catheter ranged from 2.2 L/min/m2 to 2.4 L/min/m2. Hypoxia was noted as well (PaO2 75 mmHg with FiO2 1.0 and PEEP 5 cmH2O). PaO2 rose to 93.7 mmHg with increasing positive end expiratory pressure (PEEP) to 7 cmH2O. We did not apply higher PEEP because of hemodynamic instability. Vasopressin and norepinephrine were tapered off gradually. On postoperative day 1, she showed complete mental recovery. She opened eyes spontaneously, meeting gaze and obeyed command. Yet, her marginal hemodynamics and arterial blood gas profile (systolic BP 80−90 mmHg with dopamine 10 mcg/kg/min and dobutamine 10 mcg/kg/min, PaO2 around 70 mmHg with FiO2 1.0 and PEEP 4 cmH2O) required further ventilatory support. Fentanyl and vecuronium were given intermittently in a bolus of 50−100 mcg and 2−4 mg respectively until she was switched to the simultaneous intermittent mandatory ventilation (SIMV) mode on the second postoperative day. However, her respiratory status, which seemed to have improved slightly (PaO2 76.9 mmHg with FiO2 0.7 and PEEP 7 mmHg), gradually deteriorated again as reflected by increasing pulmonary infiltrate and worsening PaO2. Superimposed recurrent atrial fibrillation and high fever (38℃−39℃) worsened her condition. On postoperative day 4, her respiratory rate rose up to 40/min and she was put back on the controlled mandatory ventilation mode again. Continuous infusion of fentanyl and vecuronium was initiated at the rate of 100 mcg/hr and 4 mg/hr respectively and she was paralyzed over the next 6 days. The intermittent interruption of the infusion was attempted in order to access mental status and neurologic deficit. Neuromuscular monitoring was not considered. Bispectral index monitoring was not considered either because fentanyl was administered in low dosage. Daily spontaneous awakening trial and breathing trial were largely postponed until the improvement of pulmonary infiltrate and blood gas profile was evident. Meanwhile, antibiotics were changed from vancomycin to meropenem plus amikacin empirically although no microorganism was documented from blood cultures. Hydrocortisone sodium succinate (solu-cortef 150 mg a day) was administered intravenously for 3 days to overcome acute pulmonary dysfunction. Total serum bilirubin level had increased, peaking 15.4 mg/dl on postoperative day 7, only to decline gradually thereafter. Serum aminotransferase did not elevate beyond 175 IU/L. Blood urea nitrogen and serum creatinine were in the acceptable ranges.
Her pulmonary infiltrate had significantly improved on postoperative day 9 and she managed to be put on SIMV mode on postoperative day 10. Thereafter, recovery was slow yet straightforward and she was barely extubated on postoperative day 14. After the extubation, though her blood gas profile was in an acceptable range, her respiratory pattern was shallow and labored. Sonographic assessment of the chest wall and diaphragm movement was not considered as the respiratory muscle incoordination was evident by physical assessment alone. She complained that she could not move at all. Limply waggling of her finger tips and toe tips was at her best. Her mental recovery was full and her senses were intact. No lateralizing sign was seen. She had no history of neuromuscular disorder. A neurological examination demonstrated symmetrical muscle weakness in both upper and lower extremities (Medical Research Council grade II) and decreased deep tendon reflexes. Normal results were observed on the mini-mental state examination, as well as on cranial nerve and sensory tests. No Babinski sign or ankle clonus was observed. Initally, we thought that it was due to the delayed effect of longstanding muscle relaxant administration. However, weakness of the extremities lasted longer than expected and she remained in bed for the next couple of weeks. She had to be intermittently catheterized because of voiding difficulty. Brain computerized tomography revealed no remarkable findings. Postoperative echocardiography on postoperative day 25 revealed well-functioning prosthetic valves and normal ventricular function.
Neurologic consultation suggested CINM as a cause and thus recommended electromyography (EMG) and nerve conduction velocity (NCV) study as well as acetylcholine receptor antibody test to rule out myasthenia gravis. Bedside physical therapy by professionals was encouraged following the initial studies.
Although the blood level of acetylcholine receptor antibody, creatine phosphokinase, and aldolase were in normal range, the result of EMG and NCV showed a pattern of diffuse axonal motor dominant polyneuropathy (). On EMG, fibrillation potentials and positive sharp waves, that reflects active denervation or myopathy, observed on plenty muscles with reduced recruitment pattern (). These electrophysiologic findings were consistent with of CINM.
She was transferred to the rehabilitation center and her condition and motor weakness gradually improved with time. On postoperative day 52, follow up NCV study revealed that compound motor action potentials markedly improved to a normal range and EMG study was normal (). She eventually recovered and discharged on postoperative day 64, still in a state of mild weakness of her extremities, but leading a daily life without support.
Now she has been followed for 2 year, and is completely free of neurologic symptoms, and living a normal life.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [50, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False, 'Stroke': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 50 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
694,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5791500-1,Extracted,"A 68-year-old male was admitted for transseptal transcatheter mitral valve replacement for mitral stenosis and regurgitation. His comorbidities included paroxysmal atrial fibrillation (AF), coronary artery disease, congestive heart failure, and ischemic cerebral vascular accident. At the time of surgery, the patient was in SR with distinct “P“ waves on the electrocardiogram (EKG). During intraoperative transesophageal echocardiography (TEE) examination, the LA contractility was demonstrated with distinct mitral inflow E and A waves, and atrial systolic reversal waves of pulmonary venous inflow []. Simultaneous interrogation of the LAA with pulse wave Doppler (PWD) demonstrated characteristic dyssynchronous contraction and relaxation waves suggesting a non-SR [ and ]. There was no spontaneous echo contrast (SEC) or thrombus in the LAA and ejection velocity was >20 cm/s []. The patient underwent a successful transseptal mitral valve replacement procedure with a 26 mm Sapien 3 valve (Edwards Lifesciences Corporation, Irvine, California, USA). The postoperative course was uneventful and patient remained in SR and was discharged after 1 day of oral aspirin and clopidogrel therapy. He was noncompliant with medications and suffered a massive embolic stroke a week after discharge and died a week after the procedure.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [68, 'years'], 'Congestive Heart Failure': True, 'Stroke': True, 'Thromboembolism history': True, 'Vascular disease history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 68 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
695,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7014744-1,Extracted,"A 62-year-old man was admitted to the neurology department complaining of an inability to see in the right eye for 2 days along with acute headache. He had a history of atrial fibrillation in rheumatic heart disease and suffered an ischaemic stroke in the left frontotemporal parietal lobe 4 years ago. The right limb of the patient was left with sequelae of mild paralysis, and he gradually developed mild vascular dementia; however, he could communicate with family members normally in daily life. He suffered symptomatic epilepsy due to ischaemic stroke 2 years ago, and effective antiepileptic drugs (500 mg levetiracetam bid and 500 mg valproic acid bid) were prescribed. At the first medical evaluation, the arterial pressure was 170/100 mmHg, and arterial blood lactic acid was 3.3 mmol/L. Liver function, renal function, electrolytes, erythrocyte sedimentation rate, procalcitonin, cerebrospinal fluid examination, syphilis antibody and HIV testing were normal. Neurological examination revealed a cognitive decline wherein the patient could not accurately answer questions or simply reply with short sentences or words. Ophthalmological examination found that when the patient’s eyes were unshielded, he needed to walk with help to distinguish orientations. Neither eye of the patient could read a visual chart clearly, but he could grasp a pen when shaken in front of both eyes, suggesting macular avoidance or partial visual field avoidance. The patient suffered sudden visual impairment, acute headache and progressive dementia, which suggested that the lesion may be located in the cerebral cortex. An MRI was then performed, which showed marked diffuse cortical hyperintensities in the left temporoparietal and occipital lobes on T2 and diffusion-weighted images. The apparent diffusion coefficient map demonstrated decreased signal intensity in the area of interest compared with the control region. Thus, the lesion was identified, while the differential diagnosis was relatively difficult. The patient had rheumatic heart disease and atrial fibrillation, which were risk factors for arterial cerebral infarction. However, CT angiography did not find corresponding vascular occlusion, and the lesion was not consistent with the vascular distribution. Thus, arterial cerebral infarction was excluded. The patient did not have drug or poison contact. Liver function, kidney function and plasma glucose were normal. Metabolism or toxic encephalopathy was less possible. Reversible posterior leukoencephalopathy syndrome (RPLS) was another possible diagnosis, as it could present with similar symptoms and the elevated blood pressure obtained at admission. However, the lesion was located on one side of the cortex, and the focus was a cytotoxic brain oedema. RPLS was less likely because its focus is often vasogenic oedema and symmetric. The lesion was located in the cortex of the left temporoparietal occipital lobes, and the lactate level was increased at admission. MELAS could not be completely ruled out. However, the patient did not have exercise intolerance in the past and had a rather older age. We found that the lactic acid level was normal. These clinical data did not suggest a diagnosis of MELAS. One day after hospitalization, the patient suffered limb twitches of the right lower limb lasting for approximately 1 min., and his wife told us that the patient was more taciturn than he had been in the past week, which she ignored at the beginning. Consequently, continuous EEG monitoring was performed, which found continuous sharp wave discharges, especially in the regions of the left temporal, parietal and occipital lobes. The patient had a history of epilepsy, acute headache, and visual and cognitive impairment. MRI found cytotoxic brain oedema in the left temporoparietal and occipital lobes, and EEG found sharp waves discharges mainly in the regions of the left central, parietal and occipital lobes. Taken together, these findings were most consistent with NCSE. Continuous intravenous administration of diazepam and oral addition of the antiepileptic drug topiramate (50 mg bid) were prescribed. After that, the patient recovered quickly, and follow-up EEG monitoring was normal. A follow-up MRI was performed 11 days later, which showed that the abnormal signal of the left parietooccipital occipital lobes was markedly attenuated (Fig. ). We concluded that the abnormal and reversible imaging on the MRI was TPMA.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [62, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': True, 'Thromboembolism history': True, 'Vascular disease history': True, 'Diabetes history': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 62 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
696,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8018225-1,Extracted,"A 54-year-old female Caucasian patient with past medical history of paroxysmal atrial fibrillation, heart failure with preserved ejection fraction, Hodgkin’s lymphoma in remission, rheumatoid arthritis, and splenectomy was admitted to our hospital with one week of malaise, fever dry cough and shortness of breath. She also noted abdominal bloating and bilateral leg swelling. She denied chest pain. There was no history of trauma or recent surgery. At the time, she was on digoxin, diltiazem, and furosemide. Her vaccines were up to date. She had no history of cigarrete smoking, alcohol drinking comsuption or recreational drug use. She reported severe allergic reaction to penicillin. Physical examination on admission showed a frail middle-aged woman in no acute distress. Blood pressure 128/90 mmHg, pulse 130 irregular beats/min, respiratory rate 20 breaths/min, axillary temperature 97.6˚ Fahrenheit and oxygen saturation of 96% on room air. Body mass index was 16 kg/m2. Cardiovascular exam was remarkable for normal S1 and S2 and irregular rhythm. No murmurs or gallops were appreciated. Jugular venous distension was noticed. Pulmonary auscultation was remarkable for decreased breath sounds at the lung bases. The abdomen was mildly distended and there was hepatomegaly on palpation. Bilateral pitting edema 2+ was observed in the lower extremities. White blood count was 9500 cells/ul, hemoglobin 13,6 g/dl, blood urea nitrogen 22 mg/dl, creatinine 0,64 mg/dl, B-type natriuretic peptide 144 pg/ml, troponins negative and electrolytes within normal range.
Electrocardiogram (EKG) revealed atrial fibrillation with rapid ventricular response and generalized low voltage QRS (Figure ). Chest X-ray showed bilateral moderate-sized pleural effusions with evident blunting of both costophrenic angles. Cardiomegaly was noted. CT of the chest showed moderate pericardial effusion, moderate right pleural effusion and small left pleural effusion, without evidence of pulmonary embolism. CT of the abdomen was significant for hepatic edema and mild ascites. Doppler ultrasound of the lower extremities showed no signs of deep venous thrombosis. Transthoracic echocardiogram (TTE) showed normal left ventricular function and large circumferential pericardial effusion (Figure ).
Patient underwent pericardial window and right chest tube placement. Pleural and pericardial fluid were sent for analysis. The results are summarized in the Table .
After seven days of incubation, both pleural and pericardial fluid grew C. acnes. Pericardial tissue histology showed pericarditis with fibrinous exudate and organization. Due to penicillin allergy, the patient was treated initially with ceftriaxone and transitioned to oral linezolid at discharge. After two weeks of linezolid, she developed vision loss. Due to concerns about drug-induced optic neuritis, linezolid was switched to doxycycline for more two weeks. Her symptoms eventually resolved. New echocardiogram two weeks later showed reduction of pericardial and pleural effusion.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': False, 'Diabetes history': False, 'Vascular disease history': False, 'age': [54, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 54 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
697,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7188380-1,Extracted,"A 77-year-old man with past medical history significant for atrial fibrillation, insomnia and post-traumatic stress disorder (PTSD) who has been in his usual state of health presented initially with complaints of shortness of breath on exertion, cough, generalized weakness, fatigue and decreased appetite for almost 2 to 3 weeks. He was initially treated for suspected community-acquired pneumonia with antibiotics. He had a complete blood count (CBC) done that showed white blood cell (WBC) count of 21,000, platelet count of 27,000 and hemoglobin of 12 g/dL. At baseline, he had normal hemoglobin, WBC count and platelet count. Given the abnormal blood test results and lack of any symptomatic improvement, a computed tomography (CT) scan of the chest, abdomen and pelvis was done which showed diffuse lymphadenopathy in the mediastinum (), axilla (), retroperitoneal lymphadenopathy () and bilateral pleural effusions ().
Given the findings of elevated WBC count, thrombocytopenia and diffuse lymphadenopathy, hematology/oncology was consulted. Subsequently, he had a bone marrow biopsy done which showed hypercellular marrow with non-necrotizing granulomatous inflammation (). In view of the diffuse lymphadenopathy and non-necrotizing granulomatous inflammation in bone marrow, a diagnosis of sarcoidosis was considered initially and he was treated with steroids, which did not show any improvement.
Due to the non-diagnostic bone marrow biopsy and lack of response to steroids, he later underwent a biopsy of the left anterior cervical lymph node. Pathology showed findings consistent with AITL. The sections showed lymph node tissue with architectural effacement by a polymorphous infiltrate predominantly composed of small lymphoid cells with irregular nuclei, inconspicuous nucleoli, coarse chromatin and pale cytoplasm. Scattered larger cells with irregular nuclei, variably prominent nucleoli and moderate pale cytoplasm are also present (). There is an associated arborizing proliferation of vessels (), follicular dendritic cells () and macrophages consistent with AITL. Acid fast bacteria (AFB) and Gomori methenamine silver (GMS) special stains were performed and were negative for mycobacterial and fungal organisms, respectively. In-situ hybridization study for Epstein-Barr virus (EBV)-encoded RNA (EBER) was negative. Proliferation index by Ki-67 was elevated at 30-40%.
Subsequently, the patient was started on chemotherapy with cyclophosphamide, adriamycin, vincristine, prednisone (CHOP) regimen. He received one cycle of the CHOP regimen after which unfortunately he had bowel perforation, and the cause of his bowel perforation was unclear. Later, the patient and family did not want to have any aggressive intervention and chose to keep him comfortable and he subsequently passed away.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Diabetes history': False, 'Vascular disease history': False, 'age': [77, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
698,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6107326-1,Extracted,"We report the case of a 64-year-old male whose medical history included hypertension, type II diabetes mellitus, and ischemic dilated cardiomyopathy with a history of heavy smoking (2 package/day for 30 years). The patient had undergone a coronary artery bypass grafting 10 years ago.
While being on routine outpatient follow-up due to suddenly worsening heart failure, with signs of systemic edema resulting in dyspnea, extreme fatigue and hypotension, the patient was categorized to have Interagency Registry for Mechanically Assisted
Circulatory Support (INTERMACS) II effort capacity. Further need for serious inotropic support placed the patient in the 'bridge to transplant', status Ib category. Consequently, the patient was implanted with a centrifugal type flow LVAD (Heartmate III, St. Jude Medical, Abbott) and was started on anticoagulation therapy with enoxaparin sodium 6000 IU subcutaneously twice daily (Figure ).
At post-operative day 20, he presented with melena accompanied with haemoglobin (Hb) levels falling from 11 to 6.4 g/dL, which prompted an upper gastrointestinal endoscopy revealing gastric cancer located at the cardia starting 1.5 cm distal to the Z-line, protruding into the gastric lumen at the posterior wall. Due to the patient's high-risk cardiovascular condition, enoxaparin was maintained at the therapeutic level twice daily at 6000 IU.
Biopsy indicated a signet-ring cell adenocarcinoma which with subsequent positron emission tomography-computed tomography (PET-CT) demonstrated no distant organ metastasis (Figure ).
After necessary preoperative assessment by anaesthesiologists and cardiologists, and under full therapeutic anticoagulation protocol (enoxaparin sodium 6000 IU twice daily), it was decided to proceed with a proximal gastric resection due to potentially life-threatening upper gastrointestinal haemorrhage. Since the LVAD was implanted at the left upper quadrant, an upper midline incision was found feasible, and proximal gastrectomy with extended D1 dissection was then performed. We performed resection of the proximal stomach using linear staplers, with a consecutive application of end-to-end circular 28 mm stapler for end-to-side esophagogastrostomy performed on the anterior surface of the stomach. Choice of this particular technique was justified due to the significantly shorter duration (20 minutes for resection-dissection-anastomosis) of the procedure in the light of having a shorter suture row on fundus and one anastomosis to deal with instead of three separate suture rows/anastomoses for Roux-en-Y reconstruction after total gastrectomy.
The pathology report indicated a poorly differentiated pT3N2(10/15)M0 signet-ring cell adenocarcinoma with negative resection margins. Originating from esophagogastric junction tumor was revealed to have perineural and lymphovascular invasion.
The early postoperative period was without major complications. The intravenous fluid administration was restricted in order to limit systemic edema. Since no postoperative bleeding occurred, there was no need to adjust the anticoagulation regimen. The patient experienced minor superficial surgical site infection and was discharged home on postoperative day 11 on a normal diet with necessary adjustments. No major complications were seen. Since then the patient has been followed-up for nine months till date, perfectly tolerating a normal diet.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': True, 'age': [64, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 64 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
699,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7295563-1,Extracted,"The patient described in this report was a woman, aged 35 years, married with two children, and had a history of relapsing episodes of paroxysmal AF, for which flecainide controlled-release was prescribed (January 2017) at the dose of 100 mg once daily. Subsequently, due to the reappearance of AF runs during the 24-h Holter recording, associated with annoying palpitations, the patient was offered the radiofrequency ablation, which she refused. The controlled-release flecainide was therefore cancelled and replaced by the addition of bisoprolol 2.5 mg once daily plus amiodarone 200 mg daily. The echocardiogram () was characterized by a severely depressed (23%) left ventricular ejection fraction (LVEF) due to uniform dilatation of the left ventricle and moderate secondary mitral insufficiency. Thus, considering the echocardiographic picture compatible with the diagnosis of idiopathic dilated cardiomyopathy, the therapy was supplemented by ramipril at the dose of 5 mg once a day, plus a mineralocorticoid receptor antagonist, i.e., canrenone 25 mg daily, plus furosemide 25 mg daily. In addition, due to the incumbent risk of cardioembolic events related to recurrent paroxysmal AF episodes, the patient was given rivaroxaban at the dose of 15 mg once daily. In January 2018, despite the patient’s close adherence to therapy, she started complaining about dyspnea related to minimal physical activity (New York Heart Association (NYHA) class III). The deterioration of the hemodynamic and clinical picture was related to the worsening of the functional mitral insufficiency and the occurrence of intermittent left bundle branch block. For the worsening mitral regurgitation the patient was offered a MitraClip procedure that she refused (February 2018). The echocardiogram revealed a severe dilation of the left ventricle with end-diastolic volume of 107 mL and end-systolic volume of 82 mL, and severely reduced LVEF (32%) with left atrial volume index (LAVI) of 38 mL/m2. During the follow-up, in July 2018, her ventricular function was still severely reduced (LVEF 32%) and LAVI was about 38 mL/m2, despite the cardioprotective therapy. Therefore, ramipril was suspended, and after 48 h sacubitril/valsartan therapy was initiated, at the dosage of 24/26 mg twice daily in add-on to therapy with furosemide 25 mg quaque altera die (qod), carvedilol 12.5 mg twice daily, canrenoate 25 mg once daily, and rivaroxaban 20 mg once daily. In February 2019, sacubitril/valsartan was up titrated to 49/51 mg/bis in die (bid). In May 2019, sacubitril/valsartan was up titrated to 97/103 mg/bid, but patient had symptomatic hypotension, so the dosing was reduced to 49/51 mg/bid. At the subsequent follow-up visit, sinus rhythm was restored and LVEF progressively recovered, with a marked reduction of chamber dimensions and cardiac volumes. In May 2019, LVEF was 35%, and LAVI was reduced to 30 mL/m2. At present, the patient is in good conditions and furosemide dosing has been curtailed to the 25 mg qod ().
The patient whose clinical description constitutes the subject of the present article, gave informed consent to participate in the study, and provided informed consent for publication.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': True, 'Vascular disease history': False, 'age': [35, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 35 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
700,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7676778-1,Extracted,"A 63-year-old female presented to the emergency department with a two-day history of cough, neck swelling, dysphagia, and dysphonia. She was taking warfarin for atrial fibrillation. Vital signs were normal, and she was not in respiratory distress. Further examination revealed hoarseness and multiple ecchymoses over the anterior aspect of her neck (), as well as a sublingual haematoma ().
Immediate anesthesiology and otorhinolaryngology consultations were requested. Non-contrast computed tomography and endoscopic examination revealed a hematoma extending from the retropharyngeal space of the suprahyoid neck, down into the infrahyoid neck to the level of the thyroid cartilage, causing significant mass effect on the airway and right vocal cord ().
The patient’s international normalised ratio (INR) was supratherapeutic, measuring greater than 10. She was managed conservatively, with 10 mg of vitamin K, 3000 units of prothrombin complex concentrate (PCC), as well as 10 milligrams of dexamethasone, and observed in the intensive care unit (ICU). She was transferred to the surgical observation unit the following day, and discharged home six days later.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'age': [63, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 63 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
701,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6978820-1,Extracted,"A 63-year-old male on peritoneal dialysis presented to the home dialysis clinic with
a chief complaint of cloudy effluent. The patient was started on empiric
intraperitoneal vancomycin and gentamicin for suspected peritonitis as the patient
was allergic to penicillin. The patient developed severe itching, rash, and dry
heaves after 10 minutes of intraperitoneal antibiotics dwell and was drained. The
patient was sent to the emergency room for further management. The patient also had
bilateral lower extremity cellulitis for 2 weeks, which was not getting better with
oral cefalexin as an outpatient. He also admitted that he was not able to ambulate
for a week and was having excruciating pain in the lower extremities on ambulating
only short distances. The patient was admitted to the hospital for management of
peritonitis and cellulitis. He was started on intravenous daptomycin and
aztreonam.
The past medical history was significant for atrial fibrillation, type 2 diabetes,
coronary artery disease, coronary artery bypass grafting, end-stage renal disease on
peritoneal dialysis, mechanical mitral, and aortic valve repair on anticoagulation,
implantable cardioverter-defibrillator. Outpatient medications include alprazolam 2
mg twice a day, bupropion 150 mg twice a day, calcitriol 0.25 µg daily, carvedilol
25 mg twice a day, furosemide 80 mg daily, losartan 100 mg daily, simvastatin 80 mg
daily, and warfarin 3 mg daily. The patient was an ex-smoker and denied any intake
of alcohol or drugs. Physical examination showed implantable
cardioverter-defibrillator placement, has a mechanical click at the left lower
sternal border, soft systolic ejection murmur, peritoneal dialysis catheter in place
with no exit site infection, and bilateral lower extremity ulcerations, which had an
eschar with surrounding erythema and were exquisitely tender on palpation.
The peritoneal fluid analysis sent from the dialysis clinic revealed 206 nucleated
cells, 5% segmented neutrophils, 90% lymphocytes, and 5% eosinophils. The
antibiotics were continued for 2 days in the hospital and were stopped as there was
no growth in the peritoneal dialysis fluid, and repeated cell counts remained
insignificant. The infectious disease specialist actively followed the patient since
the day of admission to the hospital. During the hospitalization, the patient was
evaluated by the vascular surgeon for nonhealing lower extremity ulcers. The patient
was started on sodium thiosulfate for suspected calciphylaxis. The patient underwent
lower extremity angiogram with right anterior tibial artery angioplasty for
excruciating right lower extremity pain, which was cold and appeared necrotic. The
patient developed retroperitoneal hematoma post angioplasty, secondary to
supratherapeutic international normalized ratio, and the patient was managed
conservatively by stopping warfarin for 3 days and administering fresh frozen
plasma. The pain became unbearable for the patient despite angioplasty, and the
patient underwent right above knee amputation. The patient subsequently developed
left lower extremity pain and blisters during the hospital stay, and the patient
underwent angiogram with angioplasty and recanalization of the totally occluded left
anterior tibial artery. The vascular interventions and retroperitoneal hematoma
prolonged the hospital stay. The patient continued to receive renal replacement
therapy through peritoneal dialysis.
One month into the hospital admission, the peritoneal fluid was analyzed for
suspicion of peritonitis, as the effluent was cloudy. Peritoneal fluid cell count
revealed 3520 nucleated cells, 41 red blood cells, 91% neutrophils, 1% lymphocyte,
8% eosinophils, and gram stain revealed more than 100 white blood cells/low-power
field; no organisms were seen. The patient was started on empiric intraperitoneal
amikacin and ceftriaxone. The effluent culture from aerobic bottle grew N
farcinica, identified by MALDI-TOF (matrix-assisted desorption
ionization time-of-flight) technique. Oral linezolid was added to the antibiotic
regimen after the organism was identified. The susceptibilities are mentioned in
. The general
surgery team removed the peritoneal dialysis catheter. Computed tomography of the
head, chest, abdomen, and pelvis was done for suspected disseminated nocardiosis,
which revealed discrete noncalcified mass measuring 3.3 cm in the left apex. Mixed
density masses identified in the right lower abdominal quadrants of 4.1 cm and 5.9
cm that could represent infectious or prior resolving retroperitoneal hematoma. The
patient’s family opted against any aggressive interventions, including the biopsy of
the lung mass, and it was decided to treat with oral linezolid for 6 months. The
patient passed away, unfortunately, despite treatment as the clinical condition
deteriorated.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Diabetes history': True, 'Vascular disease history': True, 'age': [63, 'years'], 'Congestive Heart Failure': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 63 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
702,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7847568-1,Extracted,"A 66-year-old Japanese male patient had received regorafenib (160 mg/day) as an anticancer treatment for metastatic colorectal carcinoma. His medical history included hypertension, diabetes mellitus, dyslipidemia, chronic heart failure, deep vein thrombosis (DVT), and permanent pacemaker implantation due to complete atrioventricular block. His DVT had been managed with low-dose apixaban (5 mg/day; body weight: 75 kg, creatinine: 1.0 mg/dL) to avoid bleeding complications.
Two months ago, he had suffered from non-ST-elevation myocardial infarction with the high-lateral (HL) branch as the culprit lesion, accompanied by chest discomfort; the HL branch occlusion was treated with balloon dilation only to avoid the need of a long-term triple antithrombotic therapy. At the same time, coronary angiography (CAG) revealed severe stenosis in the proximal left anterior descending (LAD) artery. A fractional flow reserve value of 0.72 confirmed a physiologically significant lesion. After PCI for the HL branch, regorafenib was withdrawn temporarily, and a triple antithrombotic therapy (aspirin: 100 mg/day, prasugrel: 3.75 mg/day, and apixaban: 5 mg/day) was successfully continued for two months without bleeding complications. Subsequently, the patient underwent PCI for severe stenosis in the LAD lesion two months after PCI for HL, as he demonstrated good tolerance to the triple antithrombotic therapy. Other medications administered included bisoprolol (1.25 mg/day), enalapril (2.5 mg/day), furosemide (20 mg/day), esomeprazole (20 mg/day), amlodipine (5 mg/day), sitagliptin (50 mg/day), mitiglinide (30 mg/day), and insulin degludec (9 units). In addition, routine blood testing revealed an elevated level of B-type natriuretic peptide (BNP), normal kidney function, high value of HbA1c, and mild anemia (BNP: 191.6 pg/mL, creatinine: 0.68 mg/dL, estimated glomerular filtration rate: 89.3 mL/minute/1.73 m2, HbA1c: 8.4%, hemoglobin: 9.9 g/dL, and platelet count: 318 × 103/µL). He was classified as having a high thrombotic and bleeding risk at this time, according to the CREDO-Kyoto thrombotic and bleeding risk scores. A sirolimus-eluting stent, which is a drug-eluting stent (DES) (Ultimaster Tansei 3.5/38 mm; Terumo Corporation, Tokyo, Japan), was implanted in the LAD lesion without malapposition or significant under-expansion, as confirmed by intravascular ultrasound imaging (IVUS) analysis (Fig. ). After PCI for the LAD, regorafenib was resumed because it exhibited a clinical effect on the patient's cancer. Nevertheless, the patient was admitted to our hospital for congestive heart failure with dyspnea one month later (BNP: 1,512.5 pg/mL). Echocardiography demonstrated new severe hypokinesis of the anteroseptal wall and apex. Despite continued triple antithrombotic therapy, CAG revealed focal and eccentric contrastive defects in the previous LAD stent, and OFDI confirmed ST (Fig. a–e). A 3.5/20 mm perfusion balloon (Ryusei, Kaneka Medical, Tokyo, Japan) was inflated for 3 min using an embolic protection device (Fig. f). CAG and OFDI confirmed optimal initial gain in the ST site and thrombolysis in myocardial infarction flow grade 3, with no complications including distal emboli (Fig. g–k). Antithrombotic therapy was further enhanced temporarily to prevent the recurrence of ST; it included aspirin (100 mg/day), ticagrelor (120 mg/day), and apixaban (10 mg/day). The administration of regorafenib was discontinued after PCI for ST in the LAD, and aspirin and ticagrelor were discontinued 1 and 2 months later, respectively. No further thromboembolic events (including definite/probable ST) were observed, and heart failure was managed well. However, he died due to the progression of metastatic colorectal carcinoma about 3 months after ST onset.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': True, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': True, 'age': [66, 'years'], 'Congestive Heart Failure': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 66 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 6 + 1 = 7.
The patient's CHA2DS2-VASc Score is 7."
703,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6966909-1,Extracted,"An 83-year-old male with a history of myocardial infarction was scheduled to undergo OPCAB. His medical history included chronic kidney disease, paroxysmal atrial fibrillation, type ΙΙ diabetes mellitus (DM), and dyslipidemia. He took low-dose oral aspirin (100 mg/day) until the day of the surgery because of his history of myocardial infarction.
The left internal thoracic artery was initially anastomosed to the left anterior descending artery (LAD) using gauze pads under the left ventricle and application of a tissue stabilizer (Octopus™, Medtronic Inc., Minneapolis, MN). After completion of LAD anastomosis, two DPSs were placed in the posterior pericardium between the inferior vena cava and the left lower pulmonary vein (LLPV), exposing the lateral to inferior walls. The saphenous vein graft was sequentially anastomosed to the obtuse marginal and the posterior descending arteries with the application of tissue stabilizer. Flowmetry showed both grafts provided excellent flow to the arterial territories. At the end of the OPCAB, his hemodynamic parameters were stable, and surgical bleeding was well controlled. In addition, TEE showed good cardiac contraction and no hematoma in either the pericardial or the intrathoracic spaces.
The patient was extubated 21 h after the surgery in the intensive care unit. About an hour after extubation, he lost consciousness and exhibited ventricular tachycardia. He was soon resuscitated with cardioversion and amiodarone infusion. A diagnosis of cardiac tamponade was made based on transthoracic echocardiogram findings although bleeding from mediastinal and pericardial drainage tubes was < 10 mL/h for 12 h, and he was taken to the operation theater for emergency re-exploration. Intraoperative TEE revealed a small amount of pericardial effusion; however, there is a huge hematoma in the left thoracic cavity, including an area just adjacent to the LLPV (Fig. ). Surgical inspection supported that the location of the hematoma was consistent with TEE findings. His hemodynamics stabilized after removal of the hematoma. The location of hematoma implied bleeding from the LLPV due to DPSs, leading to a huge hematoma. His postoperative course was uneventful.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Diabetes history': True, 'Vascular disease history': True, 'age': [83, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 83 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
704,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8180152-1,Extracted,"The patient is a 72-year-old man capable of independently performing activities of daily living. Regarding his medical history, he developed gastric ulceration at 18 years of age and underwent partial gastric resection. He was treated with rivaroxaban 10 mg / day for atrial fibrillation. Also, he regularly inhales formoterol fumarate for managing bronchial asthma. He used to smoke 20 cigarettes/day and drink more than three cups of sake between 20 and 65 years of age. He reported no positive history of food or drug allergy.
Approximately 40 days before admission to our department, the patient developed pain in the lower left abdominal region. Eight days later, he visited a hospital where he underwent non-contrast computed tomography (CT) of the abdomen that showed multiple colonic stenosis. Colon cancer was suspected, and the patient was admitted to the facility immediately. The patient also had fever (38 °C) on admission and, therefore, underwent thoracoabdominal contrast-enhanced CT that showed pulmonary thromboembolism (Fig. ). Therefore, the dose of rivaroxaban was increased from 10 mg/day to 30 mg/day on Day 14 (days numbered from day of admission at the first facility).
Then, he underwent fasting treatment and received maintenance intravenous fluids. On Day 14 of hospitalization, he underwent colonoscopy that showed stenosis in the hepatic flexure of the transverse colon and a circumferential ulcer of the sigmoid colon. On administration of a contrast, a 55-mm stenosis was found in the transverse and descending colon (Fig. ). Pathological examination of the stenosed colon tissue revealed intranuclear inclusion bodies and a positive immunostaining for anti-CMV antibodies and CMV antigens (CMV DNA viral load was not performed). Consequently, the patient was administered 5 mg/kg ganciclovir (GCV) every 12 h since Day 27. Although the patient’s abdominal pain was relieved by the treatment, the fever was not alleviated.
Although the coagulation profile of the patient was normal on the day of admission (Day 1), an abnormal coagulation profile was seen on Day 25; the international normalized ratio of prothrombin time (PT-INR) was elevated (8.35) and the activated partial thromboplastin time (APTT) was prolonged (170.8 s). As a result, rivaroxaban was discontinued. Up till then, the patient had received a total of 18 units of fresh-frozen plasma (FFP) and 180 mg of vitamin K. However, the coagulation profile had not improved. Although the platelet count was 113 × 109 cells/L on admission, the count began decreasing since Day 25 till it reached 73 × 109 cells/Lon Day 31. Therefore, to further explore the cause of the coagulation abnormality and continue the treatment of CMV colitis, the patient was transferred to our hospital on Day 32.
On admission to our facility, the patient’s clinical findings were as follows: Height, 163 cm; weight, 51 kg; body temperature, 36.8 °C; pulse rate, 108 beats/min; blood pressure, 118/92 mmHg; respiratory rate, 12 breaths/min; and oxygen saturation, 90% on ambient air. Breathing sounds were heard with coarse cracks on the dorsal surface of the lungs bilaterally. The heartbeat was irregular, but no heart murmur was heard. The abdomen was flat and soft, and there was no spontaneous pain; however, there was tenderness on palpation in the right hypochondrium and iliac regions. No peritoneal irritation was observed. Bilateral to the chest, approximately 20 scattered erythematous papules (~ 1 cm in length) were found; no superficial lymph nodes were palpable. Purpuric spots and pain were present on the right fifth finger, whereas only purpuric spots were seen on the left second and third fingers (Fig. ). A peripherally inserted central catheter that was placed in the left upper arm at the previous facility was present.
Table shows the patient’s laboratory data upon his admission to our hospital (Day 35 from the day of admission at the first facility).
These were as follows: White blood cell count, 14.54 × 109 cells/L; C-reactive protein, 1847.62 nmol/L; platelet count, 60 × 109 cells/L; and normocytic anemia. There was no significant abnormality in the peripheral blood; however, biliary enzymes were elevated (alkaline phosphatase: 20.02 μkat/L; γ- glutamyltransferase: 1.62 μkat/L). The coagulation disorder was apparent (PT-INR, 4.37; APTT, 154.1 s) but the D-dimer level was virtually unchanged (2.1 mg/L) and the level of fibrin degradation products was normal (3.6 mg/mL). Levels of thrombin-antithrombin complex (2.6 ng/mL) and plasmin-α2 plasmin inhibitor complex (< 0.2 ng/mL) were also normal. However, soluble interleukin-2 receptor (sIL-2R) was elevated (8540 U/mL), factor II activity was marginally reduced (49.1%), factor X activity was reduced to 59.7%, factor V activity was < 1.0%, and ADAMTS13 activity had decreased to 18%. Abdominal CT showed splenomegaly with a maximum splenic length of 9.6 cm and enlargement of axillary, left superior fossa, and paraortic lymph nodes. On Day 1, the patient had a maximum splenic length of 7.6 cm, indicating that the splenomegaly had increased since then.
Figure shows the clinical course after admission at the first facility. The administration of 5 mg/kg GCV every 12 h was continued. The purpura on the right hand observed at the time of admission to our facility widened. A total of 16 units of FFP were transfused to the patient at our hospital for 3 days (from Day 35, Day 4 from the admission to our hospital) but the coagulation profile did not improve. Since this patient had CMV enteritis, we considered vasculitis or malignant lymphoma as the cause based on the purpura on the fingertips, truncal rash, increasing splenomegaly, high alkaline phosphatase (ALP) level, high sIL-2R level, low platelet count, and PT-INR and APTT prolongation. A biopsy of the skin rash on the right lateral surface of the abdomen and of a left axillary lymph node was performed on Day 34 and Day 36 (Day 3 and 5 from the admission to our hospital), respectively. However, there were no indications of vasculitis or malignant lymphoma.
On Day 35 (Day 4 from the admission to our hospital), the patient developed bacteremia caused by Staphylococcus aureus and Fusobacterium species. He was treated with meropenem (MEPM) 2 g/day and vancomycin (VCM; trough ≥15 μg/mL). On Day 37 (Day 6 from the admission to our hospital), his abdominal pain worsened, and he went into shock. Non-contrast CT of the abdomen showed extensive free air in the abdominal cavity, which led to the diagnosis of gastrointestinal perforation that warranted an emergency surgery. During the operation, scattered necrotic changes were observed in the small intestine. A 1-cm perforation was found 10 cm to the right from the top of the transverse colon; the colon was resected from the ileum to the perforated area (Fig. ). An additional excision was performed on the left side of the transverse colon because of stool drainage from that region. Subsequently, ileal colostomy was performed, and a stoma was placed in the right lower abdomen. The surgical specimen of the ileum showed a perforation in the transverse colon, necrosis due to ischemic changes associated with circulatory failure, and numerous thrombi, including microthrombi, in the small- and medium-sized arteriovenous ducts (Fig. ). There was no evidence of lymphoma, vasculitis, or ulcerative colitis on pathological examination. We performed cardiac ultrasound scan multiple times, but no valve destruction was seen. In addition, a second blood culture was negative. Abnormal coagulation and multiple thrombosis were present before the onset of staphylococcal bloodstream infection. Furthermore, the pathology of the intestine showed no invasion by S. aureus. Therefore, we thought that Staphylococcal bloodstream infection had little to do with abnormal coagulation and multiple thrombosis. Because of the drug sensitivities of S. aureus and Fusobacterium species and the presence of intestinal perforation, VCM was discontinued, and only MEPM (1 g, 12 hourly) was administered from Day 39 (Day 8 from the admission to our hospital) onward. The thrombocytopenia and coagulation abnormalities observed preoperatively improved slightly and normalized postoperatively. In addition, the activities of factor II, factor X, factor V, and ADAMTS13 normalized. There was no evidence of vasculitis, lymphoma, or any other thrombotic disease; therefore, the final diagnosis was multiple microthrombi caused by CMV enteritis that mimicked thrombotic microangiopathy-like conditions. GCV administration was continued until Day 57 (Day 26 from the admission to our hospital).
On Day 88 (Day 57 from the admission to our hospital), the patient was transferred to the previous hospital for rehabilitation. One year has passed since he was discharged from the hospital; no recurrence has been observed since.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': False, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
705,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-10982,Extracted,"A 55-year-old male presents to the emergency department with dyspnea and palpitations. He does not smoke cigarettes or consume alcohol, and past medical history is insignificant. Blood pressure is 115/75 mmHG and heart rate is 125/min. Heart rhythm is irregularly irregular. After initial treatment with IV digoxin the patient's heart rate drops to 85/min and remains irregular.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': False, 'Diabetes history': False, 'Vascular disease history': False, 'age': [55, 'years'], 'Congestive Heart Failure': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 55 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
706,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-520,Extracted,"A 66-year old man comes to the physician because of fatigue for 6 months. He says that he wakes up every morning feeling tired. Most days of the week he feels sleepy during the day and often takes an afternoon nap for an hour. His wife says he snores in the middle of the night. He has a history of heart failure and atrial fibrillation. His medications include aspirin, atorvastatin, lisinopril, metoprolol, and warfarin. He drinks 1–2 glasses of wine daily with dinner; he does not smoke. He is 175 cm (5 ft 9 in) tall and weighs 96 kg (212 lb); BMI is 31.3 kg/m2. His blood pressure is 142/88 mm Hg, pulse is 98/min, and respirations are 22/min. Examination of the oral cavity shows a low-lying palate. Cardiac examination shows an irregularly irregular rhythm and no murmurs. The remainder of the examination shows no abnormalities.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [66, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 66 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
707,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7675879-1,Extracted,"A 78-year-old Caucasian male with non-ischemic dilated cardiomyopathy, who had
received a cardiac resynchronization therapy device (a CRT-D) 2 years earlier at our
center, was brought to our clinic in an emergency situation for an electric storm
(ES) with repeated shock delivery. ES is the sequela of a state of cardiac
electrical instability leading to multiple episodes of ventricular arrhythmia in a
short period of time and is commonly defined as the occurrence of at least three
sustained episodes of appropriate ventricular tachycardia, ventricular fibrillation
or ICD shock during a 24-h period.
During the 2 years after biventricular implantation of an implantable
cardioverter-defibrillator (ICD), the patient referred moderate improvement in
general conditions, corresponding to an increase in the ejection fraction from 28%
to 34% with functional improvement from III to II New York Heart Association (NYHA) class. Medical therapy included bisoprolol 5 mg, ramipril 10 mg, furosemide 75 mg,
and aldactone 25 mg. During periodic checks of the device, no significant
ventricular arrhythmias had emerged that required anti-tachycardia therapy with
shock delivery or anti-tachycardia pacing (ATP), or that fell within the window of
monitoring, except for rare ventricular triplets. About 10 days before the current
hospitalization, the patient experienced fever, which after 2 days was associated
with anosmia and ageusia, in the absence of cough, dyspnea, or other symptoms. SpO2
by percutaneous pulse oximetry was constantly around 95%, which was similar to
levels prior to the febrile episode. On the advice of his general practitioner, home
therapy with HCQ was initiated (400 mg BID on day 1, followed by 200 mg BID for a
total period of 6 days), 5 days before admission.
Upon arrival at the emergency department, blood pressure was 130/70 mmHg, heart rate
80 bpm, temperature was 36.8 °C, and oxygen saturation was 96% while breathing
ambient air. The patient had cold sweats and was clearly agitated. Blood glucose was
within normal limits. Arterial gases, lactate and electrolytes were within normal
ranges. Blood tests revealed high levels of hs-troponin T, creatine kinase-MB, and
NT-proBNP (), and
a slight increase in creatinine (1.3 mg/dL, corresponding to creatinine clearance of
46.37 mL/ min by Cockcroft-Gault formula). Tisdale score, which at the last visit 2
months earlier was 5 (low risk) was 11 (high risk). Chest X-ray did not detect any
notable pulmonary changes and confirmed regular placement of the leads. A 12-lead
electrocardiogram (ECG) revealed a sequential biventricular pacemaker rhythm (). Interrogation of
the device revealed, during the last 6 hours, the presence of numerous episodes of
sustained and non-sustained ventricular tachycardia (VT), which in three occasions
reverted with ATP and on eight occasions with shock delivery of 41 Joules (). In addition, the
device showed functionality parameters within normal limits and superimposable on
previous control visits with 98% of correct biventricular stimulation.
The patient was admitted to the intensive care unit, sedated with propofol,
intubated, and administered intravenous metoprolol and magnesium sulfate.
Nasopharyngeal swab was positive for SARS-CoV-2 by reverse transcription polymerase
chain reaction (RT-PCR), and did not have a very high viral load of 27
cycle-threshold, while the search for common cardiotropic infectious agents was
negative. Echocardiographic examination revealed deterioration of cardiac
contractility, in the absence of specific contractile deficits, with an ejection
fraction that had decreased to levels seen prior to implantation of the
biventricular ICD. Urgent coronary angiography showed no evidence of obstructive
coronary artery disease. Upon arrival at the emergency department, while checking
the biventricular ICD, an ECG was also done in the absence of pacing, with the
observation of spontaneous electrical activity, highlighting a QTc of 483 ms; at
electrocardiogram (ECG) performed 2 months earlier, the QTc was 446 ms (). The only change in
therapy was the introduction of HCQ, and after consultation with an infectious
disease specialist the drug was discontinued (it had been administered for a total
of 6 days). This was followed by progressive improvement in the QTc and parallel
regression of ventricular arrhythmias. On the second day, therapy with propofol was
stopped, and on the fourth day therapy with oral beta-blockers was restarted.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [78, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 78 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
708,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4636106-1,Extracted,"A 48-year-old man was brought to the emergency care unit with a 2-week history of malaise and headache followed by abnormal behavior over the last week, when he presented a depressed mood and an alteration in his mental status with disorientation, uncooperativeness, and self-aggressiveness. Indeed, the patient attempted suicide by trying to hang himself. There was no history of any previous similar episodes, psychiatric diseases, fever, other signs of infection, head trauma, or abuse of illegal substances.
The patient was previously diagnosed with hypertension and diabetes mellitus, and was taking enalapril, metformin and glicazide. There were no reports of tobacco or alcohol consumption, nor any familial history of psychiatric diseases.
On the initial examination, the patient was ruddy, afebrile, and hydrated. His heart rate was 87 beats per minute; arterial pressure was 140/110 mmHg, respiratory rate was 14 breaths per minute; and capillary glycemia was 237 mg/dL.
The cardiovascular, pulmonary, abdominal, and skin examination was normal. The mental status on admission showed a Glasgow Coma Scale (GCS) of 10, and he was uncooperative, inattentive, and disorientated. His pupils were normal and no motor deficit was detected.
The initial laboratory work-up and the brain computerized tomography were normal. A cerebrospinal fluid (CSF) examination (lumbar puncture) was performed and the results are presented in . The diagnosis of encephalitis due to the herpes simplex virus (HSV) was suspected and intravenous acyclovir was promptly prescribed, as recommended by Studahl et al.. Polymerase chain reaction for HSV was not requested due to its unavailability. The electroencephalogram was normal.
After 7 days of anti-viral therapy (acyclovir, 10 mg/kg, tree times daily), no clinical improvement was observed, and indeed a new CSF examination resulted in worsened cytological and biochemical parameters (). Therefore, serum fluorescent treponemal antibody and the Venereal Disease Research Laboratory (VDRL) were requested that resulted positive. The VDRL title was 1/128. The VDRL in the CSF also resulted in the same title (1/128). shows the electrophorectic profile of the CSF proteins. Intravenous crystalline G penicillin at a dosage of 24 million units per day in six divided doses over 14 days was prescribed and acyclovir was discontinued on the eighth day. The magnetic resonance imaging (MRI) of the brain revealed oval spots of hyperintensity on T2-weighted and fluid attenuated inversion recovery (FLAIR) sequences involving subcortical white matter of the superior frontal gyri.
Marked clinical improvement was observed after 30 hours of antibiotic therapy. The patient achieved a GCS of 15 and started managing his basic daily living activities. However, he started complaining of visual and auditory hallucinations with persecutory content that were controlled after the administration of risperidone.
At the end of the penicillin therapy, the patient’s wife reported his normal behavior. He was discharged to continue medical monitoring in the outpatient clinic.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': False, 'age': [48, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 48 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 1 + 1 = 2.
The patient's CHA2DS2-VASc Score is 2."
709,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3555400-1,Extracted,"Mr. E. K. P was a 77-year-old Chinese gentleman who presented to our institution with 3 days history of fever associated with chills and rigors. There were no other constitutional symptoms. Prior to the current admission, he was treated for a liver abscess which had resolved. The patient's past medical history included tablet-controlled Type 1 diabetes mellitus, a previous cholecystectomy, and a previous repair of a perforated peptic ulcer.
On examination, he was found to be afebrile with stable vital signs. There were bilateral basal lung crepitations on auscultation. The rest of the systemic examination was unremarkable. Blood investigation showed elevated glucose level of 18.2 mmol/l. Full blood count revealed leukocytosis with total count of 23.7 × 109/l and mild thrombocytopenia with a platelet count of 139 × 109/l. Liver function test showed mild elevation of alkaline phosphatase and γ-glutaryl transaminase.
A supine chest radiograph was performed on admission which was also unremarkable. Ultrasound of the hepatobiliary system was performed on admission to exclude recurrent liver abscesses, which also turned out to be negative.
The patient was admitted for blood glucose control and antibiotic treatment. Repeat physical examination in the ward revealed bronchial breathing in the right lower zone with crepitations and signs of a right pleural effusion which was confirmed on a right decubitus chest radiograph. He was then treated for community-acquired pneumonia and was started on intravenous Imipenem (Tienem®). Patient responded clinically well initially to the treatment.
However, despite treatment, C-reactive protein and erythrocyte sedimentation rate (ESR) levels remained elevated at 17.1 mg/dl and 75 mm/h, respectively. A leukocyte labeled scintigraphy was then performed to exclude other foci of infection, which turned out to be negative except for an intense tracer uptake in the left distal thigh. A fused single-photon emitter computed tomography and computed tomography (SPECT-CT) was performed, and a diagnosis of a left popliteal vein aneurysm was made. No evidence of thrombosis was noted.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Diabetes history': True, 'Vascular disease history': False, 'age': [77, 'years'], 'Stroke': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
710,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8237380-1,Extracted,"A 57-year-old woman with a past medical history of atrial fibrillation, hypertension, cervical spine injury with C5-C6 fusion, congestive heart failure, and mitral valve endocarditis status post mechanical mitral valve replacement seven years ago presented with sudden onset of left-sided weakness and an inability to stand. These symptoms were associated with a two-week history of fever, chills, myalgia, and anorexia. She denied headache, nausea, vomiting, chest pain, or shortness of breath. On examination, the patient’s temperature was 37 °C (98.6 °F), pulse rate was 73 beats per minute, respiratory rate was 19 breaths per minute, and blood pressure was 166/63 mmHg. She was saturating at 98% on ambient room air. The cardiovascular exam revealed a grade 2/6 systolic murmur and grade 3 pedal edema. The oral exam showed absent dentition, and the musculoskeletal exam revealed bilateral palmar Dupuytren’s contractures and multiple scratch wounds on the lower extremities with no evidence of cellulitis or lymphangitis. The central nervous system exam revealed left-sided hemiparesis. The rest of the physical examination was unremarkable. Her social history was significant for a 25 pack-year history of smoking (she had quit 15 years ago), occasional alcohol use, and no illicit drug use. She admitted to sustaining scratch injuries while playing with her two dogs; further questioning revealed that the dogs had subsequently licked the wounds.
Laboratory testing showed a normal white blood cell count of 5.2 x 109/L (normal range: 4.0-10.0 x 109/L), low hemoglobin of 10.4 gm/dL (normal range: 12.0-16.0 gm/dL), and hematocrit of 31.5% (normal range: 35-45%). The basic metabolic panel was within normal limits. Chest radiography revealed bibasilar subsegmental atelectasis with a minimal left pleural effusion. CT of the head revealed a large right frontal hematoma with midline shift (Figure ), and CT angiogram indicated active extravasation of contrast.
The patient underwent emergent craniotomy with hematoma evacuation. A mycotic aneurysm with cerebritis was found intraoperatively, and the aneurysm was clipped. An external ventricular device (EVD) was placed. She remained intubated and was started on broad-spectrum antimicrobial therapy, including intravenous (IV) vancomycin and cefepime. Blood cultures yielded growth of Pasteurella spp., which were susceptible to all antibiotics tested. Minimum inhibitory concentrations (MIC) were as shown in Table .
Subsequently, her therapeutic regimen was switched to penicillin G 24 million units IV by continuous infusion every 24 hours. Because of the presence of a mycotic aneurysm and the fact that the patient also had a prosthetic mechanical mitral valve, CT imaging of the chest and abdomen was carried out, which showed wedge-shaped hypodense areas in the spleen (Figure ).
Transesophageal echocardiogram (TEE) revealed 1-cm mobile vegetation on the mechanical mitral valve. Repeat blood cultures 48 hours after the initiation of antibiotics were negative for bacterial and fungal growth. A week postoperatively, the EVD was removed, and a repeat CT angiogram of the brain showed no evidence of residual aneurysm or arteriovenous malformation. A repeat TEE two weeks later revealed that the prosthetic mitral valve vegetation was increasing in size (1.2 cm) compared to the vegetation seen on the previous TEE. Hence, the patient underwent redo sternotomy, removal of the in-situ mechanical mitral prosthetic valve, and implantation of a mitral bioprosthetic valve. The mechanical mitral prosthetic valve that was surgically removed was negative for bacterial and fungal growth. Although the patient`s postoperative course was complicated by atrial fibrillation, her condition gradually improved, and she was discharged to a rehabilitation center to complete a six-week course of IV penicillin G 24 million units administered via continuous infusion every 24 hours, counting from the day of valve replacement. The patient was found to be doing well at her four-week follow-up appointment.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [57, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': True, 'Vascular disease history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 57 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
711,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6022317-1,Extracted,"An 82-year-old Caucasian male was admitted to our hospital in December 2016 with dyspnea, hemoptysis, and impaired general condition. He also presented with pseudoparalysis of his left shoulder due to severe pain. The medical record included ischemic heart disease (coronary artery bypass grafting in 1994), atrial fibrillation, low malignant prostate cancer, gout, and diabetes mellitus type II. Six months prior to admission, the patient had all teeth in his upper mouth removed prior to being fitted with dentures. This dental procedure was complicated with severe inflammation, and the patient was treated several times with oral antibiotics.
On admission, the patient was septic with fever and in a condition with pulmonary congestion and bilateral oedema in his lower limbs. Vital parameters included a blood pressure of 148/62 mmHg, a heart rate of 84 beats/min, oxygen saturation of 81% without oxygen supplementation, respiratory frequency at 26 per minute, and a rectal temperature of 38.8°C. Arterial blood gasses showed a normal pH (7.44), low partial pressure of carbon dioxide (3.5 kPa) and oxygen (7.2 kPa) in arterial blood, and low oxygen saturation (89%). On physical examination, the patient's left shoulder was tender and warm and had an anterior nonerythematous swelling. Cardiac auscultation did not reveal any murmur, and the neurologic examination was normal. The electrocardiogram revealed normofrequent atrial fibrillation and right bundle branch block.
The initial blood samples showed leucocytosis (14.7 × 109/L) with dominance of neutrophilic granulocytes, haemoglobin level of 7.1 mmol/L, and C-reactive protein (CRP) of 216 mg/L.
Chest X-ray showed no infiltrates but was consistent with pulmonary stasis. An X-ray of the left shoulder showed no signs of inflammation.
Blood cultures (three bottles with 10 ml each) and two samples of synovial fluids from the left shoulder were sent to the laboratory. Next day, growth of Gram-positive cocci was seen in one of the three blood culture bottles and in both synovial fluids. Matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) was performed on all three isolates using Microflex™ LT MALDI-TOF-System (Bruker, Karlsruhe, Germany; two databases: 1829023 Maldi Biotyper Compass Library and 8254705 Security ref. Library 1.0 for MALDI Biotyper 2.0), and they were diagnosed as S. equi subspecies zooepidemicus with a score between 2.37 and 2.63. Whole-genome sequencing of the blood culture isolate was performed by 251-bp paired-end sequencing (MiSeq; Illumina) and confirmed the species and subspecies type diagnosed by MALDI-TOF MS. The isolate carried a novel sequence type (ST379), and a phylogenetic analysis using FastTree v2.1.5 of the concatenated MLST alleles () found it to cluster in a branch containing ST60, ST135 and ST162. An analysis using the iTOL implementation at revealed that seven related isolates with those ST types were reported in the database from various hosts (cow (n=1), dog (n=1), and horse (n=5)). The sequence data has been uploaded to ENA with the following Study and Read accession IDs: PRJEB24181 and ERR2233447, respectively. Antibiotic susceptibility testing using the Epsilometer test (E-test) (bioMérieux, Marcy-l'Etoile, France) showed that the isolate was susceptible to penicillin (0.016 microgram/ml), ampicillin (0.032 microgram/ml), amoxicillin (0.047 microgram/ml), cefuroxime (0.016 microgram/ml), erythromycin (0.094 microgram/ml), clindamycin (0.38 microgram/ml), vancomycin (0.5 microgram/ml), imipenem (0.012 microgram/ml), and rifampicin (0.012 microgram/ml). The isolate was intermediate susceptible to gentamicin (12 microgram/ml).
Antibiotic treatment the first two days was intravenous cefuroxime 1.5 gram administered three times daily, which was changed to intravenous high-dose benzylpenicillin, initially a dose of 2 million international units (IU) four times a day. The monotherapy with benzylpenicillin was supplemented with intravenous gentamicin in intervals (five days in total). On day three, transthoracic and transesophageal echocardiography (TTE and TEE, resp.) demonstrated a vegetation on the aortic valve () with a minimal aortic insufficiency. There were no signs of paravalvular abscesses and no stenosis of the affected valve. Ejection fraction was normal. The patient was diagnosed with aortic valve endocarditis without indication for acute operation. According to the national Danish guidelines for infective endocarditis, the benzylpenicillin dosage was increased to 5 million IU four times a day.
On day three, CRP levels were increasing as well as the pain and oedema in his left arm. On day five, arthroscopic revision of the left shoulder was performed and three biopsies were taken, but none of these cultures showed further growth of the pathogen. The rotator cuff was almost completely degenerated, and the humeral head was devoid of its hyaline cartilage. Ten days later technetium-99m bone scintigraphy showed intense activity in the left shoulder, suspicious of osteitis (). The bone scintigraphy revealed no other focus of infection. On day 17, control transesophageal echocardiography was performed. At this time, the examination showed no suspicious signs of endocarditis, and the vegetation that was previously seen on the aortic valve could not be visualised.
The patient was sent to a dentist, which did not reveal any oral focus. The patient's clinical condition improved gradually, and he was discharged from our hospital after five weeks (36 days) with oral antibiotics (oral amoxicillin 1 g × 3 pr. day and oral rifampicin 600 mg × 2 pr. day) for further two months. In total, he received antibiotics for almost three months (87 days). During the admission, the patient lost approximately 17 kilograms in weight, primarily fluid associated with his septic condition as well as fluid from some of degree cardiac decompensation and lung stasis.
The patient was followed up in the Out-Patient Clinics for Infectious Diseases and Cardiology, which included blood samples and control transthoracic echocardiography. None of the subsequent examinations indicated signs of recurrence. The patient regained normal function in his left shoulder.
The patient reported that he had daily contact with animals including horses, though he did not recall any illness in the four horses he had taken care of the past year. He denied consuming unpasteurized milk products.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [82, 'years'], 'Hypertension history': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 82 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
712,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8422536-1,Extracted,"Here, we reported a 41-year-old female with a medical history of obesity and diabetes type 2, who underwent surgical resection of a frontal parasagittal with no intraoperative surgical and anesthetic complications and developed complete blindness on awakening as a complication. Postoperative ophthalmological examination revealed bilateral mydriasis and non-reactive to light in both eyes, although bilateral mydriasis can occur after general anesthesia.[] Fluorescein angiography showed adequate choroidal filling in both eyes with delayed arterial phase and all subsequent phases; as well as, in late phases an absence of bilateral optic nerve staining occurred, confirming a bilateral CRAO []. The photopic and scotopic electroretinogram showed a prolonged latency and decreased extent of the a and b waves. Postoperative digital subtraction angiography was performed showing adequate blood flow through both OAs and a significant decrease in bilateral choroidal blush []. The echocardiography performed did not reveal vegetations or other valvular alterations. Carotid Doppler showed mild non-obstructive diffuse atheromatosis and type I atheroma plaques in both common carotids, both with biphasic flow, without stenosis and with preserved flow velocities. Whole-body vessels CTA scans were not contributory. Different hematological tests were normal. Brain MRI showed no suggestive lesions of stroke in the DWI sequence and intra-orbital segment hyperintensity in T2-weighted sequences, suggesting for bilateral optic nerve infarction []. Patient started an early treatment with hyperbaric chamber sessions, continuing with this at discharge, even if patient reported only a very slight improvement in the visual deficit, referring only shadows in her peripheral visual field.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Diabetes history': True, 'Vascular disease history': True, 'age': [41, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 41 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
713,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5965434-1,Extracted,"A 71-year-old man presented to an outside emergency department (ED) with chief concerns of abdominal pain and anorexia that had been present for four weeks. Findings of an extensive work-up were subsequently unrevealing, including normal results of colonoscopy, esophagogastroduodenoscopy, colon biopsy, mesenteric Doppler studies, and computed tomography (CT) of the abdomen and pelvis. Video capsule endoscopy demonstrated a questionable adynamic ileus. Treatment with dicyclomine hydrochloride, polyethylene glycol 3350, tramadol, and simethicone had failed to relieve symptoms. The patient’s family decided to sign him out of the outside hospital from the inpatient service and drive him directly to our ED for evaluation in the middle of the night.
On initial presentation to our ED, the patient complained of left-sided abdominal pain described as aching and one episode of hematuria. Past medical history included osteoarthritis, hypertension, chronic obstructive pulmonary disease, coronary artery disease, nonischemic cardiomyopathy, chronic atrial fibrillation, embolic stroke, and mediastinal thymoma with sternotomy and subsequent pleural effusion and empyema. Initial findings were as follows: temperature 36.6°C oral, blood pressure 142/95 mm Hg, pulse 106 beats per minute, oxygen saturation 98% while breathing room air, and respiratory rate of 16 breaths per minute. Physical examination findings and results of laboratory analysis were reassuring except for an international normalized ratio of 5.5 and evidence of hemoconcentration. The patient was given intravenous (IV) fluids and 1,000 mg of acetaminophen and was then dismissed. Results of urine culture were positive for growth of more than 100,000 colony-forming units of Salmonella species 72 hours later.
Per protocol, the positive urine culture results were flagged and presented to the physician working clinically. On the basis of the patient’s prior presentation and the rarity of Salmonella in the urine, the patient was asked to return immediately for reevaluation. On return to the ED, the patient’s wife expressed sincere confusion and disappointment as she tried to explain how her husband, a hardworking man, was told to “walk it off” and that his irritable bowel syndrome was “just something he had to learn to live with.” The patient appeared pale and acutely ill with closed eyes and persistent moaning. Findings at presentation were temperature 37.2°C oral, blood pressure 102/55 mm Hg, pulse 93 beats per minute, oxygen saturation 95% while breathing room air, and respiratory rate of 22 breaths per minute. Pain was rated as 10 on a scale of 0 to 10. Positive physical examination findings included flat neck veins, dry mucous membranes, healed scars on the chest, and left lower quadrant abdominal pain without tenderness or peritoneal signs, inguinal tenderness, or adenopathy. Sepsis work-up and blood cultures were ordered, as was CT because of concern for possible disseminated infection. The patient was given 1 gram of ceftriaxone, IV fluids, and hydromorphone.
CT showed a contained pseudoaneurysm in the descending thoracic aorta (4.7×4.0×5.7 cm) about 2 cm in diameter from the native aortic wall to the outer edge of the outpouching; it had a bilobed appearance and a total craniocaudal measurement of 2.6 cm for both outpouchings ( and ). The inferior-most origin of the pseudoaneurysm was noted about 3 cm above the origin of the celiac artery. Surrounding hematoma was seen on the descending thoracic aorta with inflammation and “old” hematoma settling down into the diaphragm.
The patient was admitted to a vascular surgery service, and IV ceftriaxone therapy was continued before surgical resection and replacement of a segment of the descending thoracic aorta with a cryopreserved aortic interposition graft. After a two-week hospital stay, the patient was dismissed receiving outpatient IV antibiotic infusion therapy.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': True, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Vascular disease history': True, 'age': [71, 'years'], 'Congestive Heart Failure': True, 'Stroke': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 71 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
714,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5588490-1,Extracted,"A 68-year-old male with hypertension presented with episodes of recurrent syncope with ECG showing complete heart block []. In addition, the patient has a history of angina and doubtful history of a previous myocardial infarction.
The patient was stabilized by putting in temporary pacemaker lead through the left femoral vein as the right femoral venous puncture could not be done despite multiple attempts. Echocardiography showed low left ventricular (LV) systolic ejection functions and tricuspid regurgitation. The patient was further planned for coronary angiography for accessing the status of coronaries which revealed severe multivessel coronary artery disease [Figures and ].
Immediately after completing the coronary imaging, the patient developed intermittent capture loss of temporary pacemaker, manipulation of the temporary lead proved to be difficult, and the patient developed asystole [] and was unresponsive despite multiple attempts of lead manipulation. Cardiopulmonary resuscitation was started, and atropine and adrenaline infusion started, but no rhythm could be established. As a desperate last-ditch effort, a second 6F temporary lead was advanced through femoral artery sheath into LV apex and pacing commenced at higher threshold [].
Within a few moments, hemodynamics improved and the patient became responsive. The right pacemaker lead was then successfully negotiated in the right ventricular (RV) apex, and parameters checked followed by taking out of LV lead. The patient was shifted to the intensive care unit in a stable condition and underwent permanent pacemaker implantation subsequently.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Vascular disease history': True, 'age': [68, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 68 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
715,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2917397-1,Extracted,"A 77 year old Caucasian female presented to emergency room on 09/06/2009 with left sided chest pain of three days duration. Her pain was sharp, 8/10 in intensity, nonexertional, radiated to interscapular region, and initially relieved by over the counter medications. She denied any fever, cough, nausea, vomiting, diaphoresis, shortness of breath and, palpitation. Other review of systems was unremarkable.
Past medical history included hypertension, dyslipidemia, obstructive sleep apnea, atrial fibrillation and coronary artery disease. She had bare metal stent placement in left anterior descending artery in 06/09, angioplasty for in stent restenosis in 08/09 and a pacemaker implantation for sick sinus syndrome on 09/01/2009. Her medications included lisinopril, atenolol, simvastatin, aspirin, clopidogrel, warfarin, and dofetilide.
On physical examination she was morbidly obese, was in moderate distress. Her vital signs included temperature of 98.7°F, pulse rate 63/minute, regular in rate and rhythm, blood pressure (BP) 141/62 mmHg, respiratory rate (RR) 18/min SpO2 97%, jugular venous pressure (JVP) was not elevated and there was no pulsus paradoxsus. Auscultation of heart and lungs was unremarkable. Examination of other systems was normal.
Admission electrocardiogram (EKG) revealed new T wave inversions in the lead II, III, AVF and QS complexes and T wave Inversions in V1-V6 as seen in the previous EKG (Fig. ). Admission chest X-ray showed normal cardiac silhouette with presence of pacemaker leads, normal lung fields and mediastinum.
Her initial set of cardiac enzymes, complete blood count (CBC), basic metabolic panel (BMP) and urine analysis were normal. She was admitted with diagnosis of unstable angina. Treatment with heparin, eptifibatide and nitroglycerine was begun. Her repeat EKG on 09/07/09 showed ST depressions in the inferior leads, repeat cardiac enzymes were normal, however her chest pain continued to persist. 2D Echocardiogram (ECHO) on 09/07/09 revealed ejection fraction (EF) of 65%, without any pericardial effusion. Chest pain continued to persist, became hypotensive and oliguric, blood pressure medications were with held. Repeat CBC and BMP revealed elevated WBC 15,800/μl and hemoglobin of 9.4 gm/dl. Serum creatinine changed from 1.13 to 3.01 and blood urea nitrogen increased from 29 to 53. Urine analysis revealed 15-20 white blood cells per high power field (HPF), positive leukocyte esterase and nitrite, 5-10 red blood cells per HPF.
In view of leucocytosis, increased renal parameters and pyuria septic shock secondary to urinary tract infection was considered and transferred to Intensive care unit (ICU). After fluid resuscitation, broad spectrum antibiotics were intiated. On 09/09/09 in ICU the patient was in distress and continued to have chest pain. Vital signs were significant for pulse rate 90/min, regular, BP 70 mmHg, RR of 22/min, SpO2 95%. Auscultation of heart and lungs was unremarkable. Central venous pressure was 15 cm of water. Intravenous vasopressor therapy was intiated. As her chest pain continued to persist, a non-contrast computerized tomography (CT) of the chest was done which revealed hemorrhagic pericardial effusion (Figs. and ) with lead perforation of the right atrium which was subsequently confirmed by 2D ECHO (Fig. )
She underwent pericardial window for drainage and evaluation of lead perforation. During surgery the screw in right atrium had gone through the right atrial wall and caused the perforation. Surgeons over sew the atrial wall and drained 200 cc of pericardial fluid. Her post operative recovery was uneventful and discharged home on the fifth day.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Diabetes history': False, 'Vascular disease history': True, 'age': [77, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
716,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4421490-1,Extracted,"A 73-year-old female patient with hypertensive nephrosclerosis was started on haemodialysis via a tunnelled line in July 2008. Her other comorbid conditions included atrial fibrillation and right heart failure with severe pulmonary hypertension (pulmonary artery pressure 83 mmHg) due to pulmonary emboli. Her medication included ramipril 5 mg once daily (OD), bisoprolol 3.75 mg OD (evenings) and sildenafil 25 mg three times daily. Following implantation of her tunnelled line, she underwent three uneventful haemodialysis sessions. The fourth haemodialysis session was started with the patient in good mood and with a blood pressure of 123/71 mmHg. After 8 min of dialysis the patient became unresponsive without peripheral pulse. Dialysis was stopped, and resuscitation was just being initiated when the patient regained consciousness after administration of 1L of fluid. There had been no kinking of any of the tubing. The chest was clear and there was no cardiac murmur; the abdomen was soft. The patient was afebrile. Dialysis was stopped. An electrocardiogram showed no new changes and troponin T was normal. A bedside ultrasound excluded pleural and pericardial effusion and showed no free intra-abdominal fluid. The inferior vena cava was dilated, in keeping with known right-sided heart failure. Dialysis was discontinued and the patient received oxygen. During that day she made an uneventful recovery. Her C-reactive protein was normal and serum haemoglobin was unchanged. Serum potassium was not elevated. We continued to search for something that was different on the day she had her fourth haemodialysis session and came up with the timing: the uneventful sessions had started at 17.00 p.m., 10.45 a.m. and 15.00 p.m., respectively. The fourth haemodialysis session had been started at 9.00 a.m. We hypothesized that her medication was at fault and ascertained that it had been the only session in close vicinity to sildenafil ingestion (given at 8.00 a.m., lunchtime and 18.00 p.m.). We then tried to schedule all dialysis sessions 3 h after the last sildenafil dose. No further episodes occurred. However, several sessions later the patient was inadvertently called for dialysis again at around 9.00 a.m. and sustained an episode similar to the first although less severe. Sildenafil was stopped entirely, the patient was discharged and no further episodes occurred.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': True, 'Hypertension history': True, 'Vascular disease history': True, 'age': [73, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 73 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
717,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5385507-1,Extracted,"A 79-year-old male presented to the emergency department with acute left elbow pain. His past medical history was significant for diabetes mellitus, osteoarthritis, transient ischemic attack and paroxysmal atrial fibrillation, for which he was prescribed warfarin. He woke on the morning of his presentation with pain and swelling in the elbow, which worsened over 6 hours before he arrived in the emergency department. He had no history of trauma and was non-ambulatory due to chronic pain from arthritis; he required assistance with all transfers from bed to a chair. There was no fever, rash, or other acute arthralgia. He reported that his most recent international normalized ratio (INR) measured 3 days ago was in the therapeutic range.
On physical examination, his temperature was 36.6°C, pulse 77 beats per minute, respiratory rate 16 per minute, and blood pressure of 157/87 mmHg. His left elbow was swollen and warm posterolaterally. There was no erythema or ecchymosis. He had no bony tenderness along the joint, upper arm, or forearm. Range of motion of the elbow was markedly limited secondary to pain.
The treating physician performed point-of-care ultrasound to evaluate the swelling and suspected effusion. Using a high-frequency 10-5 MHz transducer (Sonosite, Bothell, WA, USA), both lateral longitudinal and posterior transverse images of the joint were obtained. The ultrasound images demonstrated a complex, compressible effusion with mixed hyperechoic and hypoechoic content, consistent with a hemarthrosis (, ) [-]. No layering fluid was appreciated to suggest lipohemarthrosis from an intra-articular fracture. Radiographs of the elbow were subsequently obtained, which re-demonstrated an effusion without evidence of fracture (). Laboratory studies were subsequently available, and notable for an INR of 7.9 and hemoglobin 12.8 g/dL.
Given the clinical history, absence of trauma or fever, and markedly supratherapeutic INR, a diagnosis of a spontaneous hemarthrosis was made. Although the elbow is an unusual location for a spontaneous hemarthrosis, the point-of-care ultrasound findings consistent with acute bleeding supported the diagnosis and decision to avoid arthrocentesis to further investigate the cause of the effusion. In the absence of bony tenderness or a history of trauma, the ultrasound findings of bleeding without cortical disruption helped obviate the need for computed tomography or magnetic resonance imaging to evaluate for occult fracture.
The patient was managed conservatively, with a focus on symptom control. He was given oral and intravenous analgesia. The affected extremity was placed in a splint and sling for comfort, with a compression bandage applied to the elbow to facilitate hemostasis. Given the degree of pain associated with the hemarthrosis, his coagulopathy was reversed with oral vitamin K to accelerate INR normalization. He was discharged with instructions to follow up with his physician in 2 days. In serial follow-up visits, he reported progressive decrease in pain and swelling and ultimately symptom resolution. He and his primary care physician ultimately elected to discontinue anticoagulation.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Diabetes history': True, 'age': [79, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 79 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
718,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4400477-1,Extracted,"A 67-year-old man was referred for a rising creatinine level from 88 to 906 µmol/L (1.0–10.3 mg/dL) over a 4-month period. He had a history of upper and lower back pain of 4 months duration and was treated by pregabaline, oxycodone and naproxen. He had a weight loss of 13 kg and complained of nycturia, gross haematuria, fatigue, nausea and occasional vomiting. Physical examination revealed normal vital signs and temperature. The patient appeared euvolemic, presented asterixis without focal neurological deficit, poor dental hygiene with multiple cavities and severe parodontis, an apical holosystolic murmur radiating to the axillary region and an enlarged spleen.
On admission, his serum creatinine level was 906 µmol/L (10.3 mg/dL) and urea nitrogen 33 mmol/L (92 mg/dL). His urine sediment showed 0.3–0.8 g/L proteins with more than 100 erythrocytes/high power field. C-ANCA using an immunofluorescence technique was positive at a titre of 1/80. Anti-PR3 were positive at 85 U/mL (<20 U/mL) and anti-myeloperoxidase were negative using enzyme-linked immunosorbent assay (QUANTA Lite® PR3 and QUANTA Lite® MPO, Inova Diagnostics®, San Diego). C3 was low (0.66 g/l [N:0.90–1.80]) and C4 was normal, but these results were available only 8 days after admission. Table presents the initial laboratory data.
Haemodialysis was required on the second day of admission. Transthoracic echocardiography showed severe mitral regurgitation with a 9 × 27 mm pannus and a 4-mm vegetation attached to the anterior mitral leaflet, with multiple microperforations. The transoesophageal echocardiography confirmed severe mitral regurgitation with an 11 × 13 mm vegetation on the anterior leaflet, and moderate aortic and tricuspid regurgitation. A kidney biopsy revealed focal necrotizing glomerulonephritis without significant endocapillary or mesangial proliferation (). The glomeruli showed cellular crescents (4/21) and/or fibrinoid necrosis (3/21) with mildly increased mesangial matrix. The tubulointerstitial compartment revealed mild tubular atrophy and moderate-to-severe interstitial oedema. Severe acute tubular injury was also present. Vessels showed nothing but focally severe arteriosclerosis. Immunofluorescence microscopy revealed primarily mesangial immune complex deposits with focal capillary loop involvement in a full-house pattern with strongly positive C3, IgM and C1q, moderately positive IgG and mildly positive IgA (). Electron microscopy showed subendothelial () and mesangial electron dense deposits with focal mesangial interposition. No tubuloreticular inclusions were found. In the context of a probable endocarditis, ceftriaxone and gentamicin were started, and methylprednisolone 500 mg IV ID was given for 3 days followed by daily prednisone (50 mg) for 2 weeks in an attempt to treat the necrotizing glomerulonephritis.
On Day 3, several blood cultures grew slow-growing streptococcus-like gram-positive bacteria that yielded Gemella haemolysans by conventional biochemical identification methods. The bacterial strain was sent to the reference laboratory for identification by sequencing of the 16S ribosomal RNA gene using a previously described method [] and was identified as G. sanguinis. A positron emission tomography–computed tomography (CT) scan revealed signs of spondylodisciitis at C6-7 and L3-4 levels. A CT-scan showed splenomegaly (14.8 cm cephalocaudal length) with an infarct of 4.2 × 2.4 cm. No pulmonary abnormalities were noted on the CT-scan. Vancomycin and gentamicin were given from Days 4–6, and subsequently vancomycin was replaced by penicillin G upon receipt of in vitro susceptibility analysis. The patient underwent mitral and aortic valve replacement on Day 17. Valve cultures were negative, but histological examination showed devitalized gram-positive cocci. The patient received penicillin and gentamicin until Day 69.
One month after admission, dialysis was stopped, and by the third month, the creatinine level decreased to 62 µmol/L (0.7 mg/dL), c-ANCA level decreased to 1/40, anti-PR3 and blood cultures were negative. presents the case history.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [67, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 67 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
719,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8712209-1,Extracted,"We present the case of an 80-year-old female patient known to have ischemic heart disease, heart failure with reduced ejection fraction, and atrial fibrillation. Almost 20 years before her current presentation, the patient had a history of ascending cholangitis post endoscopic retrograde cholangiopancreatography, complicated by an iatrogenic esophageal perforation requiring surgical repair and cholecystectomy. In 2015, the patient had another abdominal perforation secondary to an ischemic bowel due to arterial emboli.
The patient presented with a one-week history of abdominal pain, dysuria, and fever. Her vitals showed a blood pressure of 86/55 mmHg and a heart rate of 127 beats per minute, which recovered after 500 mL of normal saline. Her urine dipstick revealed 100 leukoestrase and positive nitrites. Basic blood investigations were normal, and cultures were sent. She was started on Ceftriaxone 1 g once a day to treat her urinary tract infection. The cultures came back negative apart from blood cultures which grew V. cholera within a day of incubation (Table shows the antibiotics' sensitivity).
The patient was clinically improving but to identify the bacteremia source, a stool culture was sent, and abdominal computed tomography (CT) was arranged. The stool culture was negative, and the CT showed a common bile duct dilatation with a heterogeneous enhancement of the liver, representing cholangitis, but no obstruction was observed (Figure ).
Since the patient was improving and her CT findings were related to her previous surgeries, no intervention was done.
She completed a seven-day course of Ceftriaxone, and repeated blood culture did not grow any organism. She was discharged home, but a few days later, she returned with severe sepsis without a clear focus. Cultures were sent, and the results showed Clostridium perfringens bacteremia. She was started on an intravenous metronidazole loading dose of 750 mg, and then she was kept on 375 mg every 6 hours as a maintenance dose. The patient's condition worsened as her level of consciousness and blood pressure dropped, requiring norepinephrine infusion and intubation. Her intensive care unit stay was complicated with ventilator-associated pneumonia. After two days, the patient's condition deteriorated, and she passed away.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': True, 'Hypertension history': True, 'Vascular disease history': True, 'age': [80, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",8,8,8,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 80 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 5 + 2 = 7.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 7 + 1 = 8. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 8.
The patient's CHA2DS2-VASc Score is 8."
720,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2772243-1,Extracted,"A 74-year-old Caucasian female was admitted to the hospital for rapid atrial fibrillation and lower limb cellulitis. While being treated with anti-arrhythmic agents and antibiotics, she developed non projectile bilious vomiting and watery diarrhoea. Her surgical history included an appendicectomy 17 years ago and a hysterectomy followed by radiotherapy for endometrial carcinoma seven years ago. Her regular medications were digoxin, warfarin, clopidogrel, and metoprolol.
On clinical examination, she appeared in no acute distress. Her heart rate was 134 per minute in atrial fibrillation, her blood pressure was 124/56 mmHg, her respiratory rate was 25/min, and her temperature was normal. The abdomen was distended with increased bowel sounds and mild tenderness in the right iliac fossa. There was no rebound tenderness, rigidity, or guarding and no discrete mass was palpable. The rest of the systemic examination was unremarkable. Blood investigations revealed deranged renal function with a blood urea of 5.2 mmol/L (2.5-6.1) and creatinine of 186 micromoles/L (50-110). Liver function tests were normal with bilirubin 7 micromoles/L (<21), ALT 26U/L (<33), AST 36U/L (<45), GGT 28U/L (<30), and ALP 116 U/L (30–115). Her white cell count was 27.2×109/L (3.9-11.1) and hemoglobin was 14.1 gm/dL with normal coagulation parameters.
She underwent an oral-contrast enhanced CT scan of the abdomen (intravenous contrast was not administered due to renal impairment), which showed a markedly distended stomach with dilated small bowel loops [], but free gas or fluid collection were not noted. The presence of gas in the distended bowel wall could not be ruled out. There were multiple streaks of gas in a branching pattern seen throughout the liver parenchyma []. Her history was revisited but there was no previous hepatobiliary disease or endoscopic retrograde cholangiopancreatography.
In view of the possibility of intestinal obstruction with a low probability of bowel necrosis, the patient underwent an exploratory laparotomy. The operative findings were small bowel obstruction due to fibrotic adhesions with no visible evidence of intestinal ischaemia or necrosis. The abdomen was closed after resection of the adhesions. Her bowel function returned to normal in 3 days and she was discharged from the hospital after 2 weeks.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [74, 'years'], 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 74 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
721,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4016326-2,Extracted,"A 56-year-old woman was referred to our outpatient clinic because of progressive exertional dyspnoea. She had undergone closure of a ventricular septum defect when she was 3 years old. At the age of 49, she developed paroxysmal atrial fibrillation. Because she was highly symptomatic and the atrial fibrillation turned out to be resistant to medical therapy, she underwent His bundle ablation and VVI-pacemaker implantation. There were bilateral superior caval veins but no connection between the left subclavian vein and the right superior caval vein, so the pacemaker was implanted on the right side. She had remained asymptomatic for 5 years. She was now referred to our outpatient clinic because of deterioration of her exercise capacity and progressive dyspnoea on exertion.
At physical examination, her saturation was 92 % at rest, which dropped to 72 % after mild exercise. Transthoracic echocardiography revealed a moderately dilated right ventricle with a normal systolic function and severe tricuspid valve insufficiency due to tricuspid annular dilation in combination with retraction of the septal leaflet caused by the pacemaker lead. The systolic PAP was estimated at 30 mmHg using the tricuspid insufficiency signal. Colour Doppler showed a flow signal from the left to the right atrium suggesting an atrial septum defect (ASD) (Fig. ). After infusion of agitated saline contrast, a right-to-left shunt at atrial level was seen, suggesting a patent foramen ovale or an ASD with right-to-left shunting. Transoesophageal echocardiography confirmed an 8 mm defect in the posterior part of the interatrial septum with bidirectional flow matching the diagnosis of ASD type UCS. Cardiac CT showed a PLVCS draining into a dilated coronary sinus, which was partially unroofed causing communication with the left atrium (Fig. ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'age': [56, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 56 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
722,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6364951-1,Extracted,"An 84-year-old woman, known to have atrial fibrillation and hypertension, presented with impaired memory and altered mental status. On physical examination, no lymphadenopathy or organomegaly was detected. A neurological examination revealed mild dysmetria in the left upper extremity. Her white cell count was 25,100 × 1012/l, with 61% lymphocytes. Magnetic resonance imaging (MRI) of the brain revealed a homogeneously enhancing cerebellar mass causing mass effect on the tectum and obstruction at the level of the aqueduct associated with the hydrocephalus (Figures -).
The patient underwent a bilateral posterior fossa craniotomy and tumor resection, followed by the insertion of an external ventricular drain. Intraoperatively, the mass was thought to be intra-parenchymal. After surgery, she recovered well, with no new neurological deficits. Histopathology revealed an infiltrating and highly mitotic neoplasm composed of malignant lymphoid cells (Figures -). In situ hybridization (ISH) for Epstein–Barr virus (EBV) was negative. Fluorescence in situ hybridization (FISH) demonstrated no gene rearrangements in B-cell lymphoma 2 (BCL2), (BCL6), and MYC. Polymerase chain reaction (PCR) amplification and capillary gel electrophoresis per the BIOMED-2 protocol were performed on paraffin-embedded tissue, revealing a peak in the immunoglobulin heavy chain (IGH) consistent with a clonal process. The findings were diagnostic of an EBV negative, diffuse large B cell lymphoma (DLBCL).
A bone marrow core biopsy was performed due to low white blood cell (WBC) count, which revealed the involvement of a low-grade lymphoid process (Figures -). Flow cytometric immunophenotyping revealed a Lambda-monotypic, CD5 negative B cell population expressing CD19, CD23, CD22 (dim), and partial CD20 while lacking CD10 and FMC7. Aside from the lack of CD5 expression, the morphologic and immunophenotypic findings were consistent with chronic lymphocytic leukemia/small cell lymphoma. A diagnosis of small B cell lymphoma was rendered, with an offered differential diagnosis including CLL, marginal zone lymphoma, mantle cell lymphoma (CD5 negative), follicular lymphoma (CD10 negative), and lymphoplasmacytic lymphoma. Although the lack of CD5 expression makes mantle cell lymphoma a more reasonable differential, multiple studies have reported cases of CD5 negative CLL [-], with an incidence ranging from 7% to 20% among all CLL cases []. Hence no further investigations to rule out mantle cell lymphoma were required.
As mentioned above, molecular studies performed on the paraffin-embedded tissue from the brain biopsy revealed an immunoglobulin heavy chain (IGH) rearrangement consistent with a clonal process. We endeavored to perform a similar analysis on a sample from the patient's bone marrow biopsy, as the presence of an identical gene rearrangement would have provided support for a relationship between the two neoplasms. However, per standard protocols, the bone marrow core biopsy was acid decalcified for next day processing, compromising the integrity of the DNA necessary for the PCR. Therefore, performing an IGH rearrangement studies on the bone marrow biopsy was not a viable option, and a definitive genetic link between the two neoplastic processes could not be established.
The positron emission tomography/computed tomography (PET/CT) scan showed no other areas of hypermetabolic involvement. Given her advanced age, she might not have tolerated the toxic effect of methotrexate. Therefore, she received one cycle of temozolomide and whole-brain radiation therapy (WBRT). A follow-up CT scan at six months showed no residual tumor. Approximately 10 months following her initial diagnosis, she had a recurrence in the posterior fossa, which was confirmed by MRI. She passed away within one month of recurrence.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Vascular disease history': False, 'age': [84, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 84 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
723,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4099427-1,Extracted,"A 76 year old woman with primary hypertension was referred to our hospital for catheter ablation of persistent AF. She was suffering from exertional dyspnoe since two years ago which became more sever since the last 3 months. Persistent AF was initially diagnosed due to ischemic stroke on December 2011. Due to high risk of bleeding with anticoagulation, an Amplatzer LAA occluder (puck and disc type, AGA Medical Corp., Minneapolis, MN) was implanted in another hospital. Transesophageal echocardiography (TEE) was performed to exclude LAA thrombus before ablation procedure which confirmed that the LAA occluder was in the LAA. An angio CT of pulmonary veins was performed which showed three and two pulmonary veins in the right and left side, respectively. Compressed LIPV was suspected with an oval shape appearance in short axis (8 mm in CT angio), the other veins were in normal sizes ().
During the ablation study, stable sinus rhythm was at the beginning of the procedure. Two 8.5 F SL1 sheaths (St. Jude Medical, Inc., MN, USA) were advanced to the left atrium (LA) by a modified Brockenbrough Technique. After transseptal catheterization, intravenous heparin was administered to maintain an activated clotting time of 250 to 300 seconds. Additionally, continuous infusions of heparinized saline were connected to the transseptal sheaths (flow rate of 10 ml/h) to avoid thrombus formation or air embolism. Electroanatomical mapping was performed with a 3.5-mm-tip catheter (ThermoCool, Biosense-Webster, Diamond Bar, CA, USA) during SR by using CARTO 3 system (Biosense-Webstar, CA, USA). Mapping at the ridge between the left inferior pulmonary vein (LIPV) and LAA in anterior part showed significant decrease in impedance (about 70-80 Ohm), which suggested the catheter contact to the metal device ().
Selective PV angiography showed that the right sided and left superior pulmonary veins (LSPV) had normal sizes but the LIPV was compressed with the atrial part of the occluder (the diameter of the vein in distal part just before the ostium was around 50 percent smaller than that of its proximal part ().
There was no pressure gradient by pulling back from the distal to the LA with a multipurpose catheter 7F (St Jude Medical, USA). Circumferential radiofrequency (RF) lesions were delivered at the area with normal impedance that resulted in the complete PV isolation. Therefore, RF ablation was not necessary to deliver at the area with low impedance. The patient discharged home after 24 hours holter monitoring (stable SR) with Dabigatran for 3 months. Dyspnoe was slightly better.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [76, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': True, 'Vascular disease history': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 6. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
724,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4633557-1,Extracted,"A 77-year-old Hispanic woman was admitted to our hospital with the vague complaints of “not feeling well.” The patient was diagnosed with ET and positive JAK 2 mutation seven years ago with a platelet count stable at 750 × 109/UL. She has been treated with aspirin only. There was no documented history of bleeding, thrombosis, or other symptoms. Her other medical comorbid included benign essential hypertension, heartburn, osteoarthritis, and depressive disorder. Over an eighteen-day period the patient has had two consecutive six-day duration hospitalizations, for chest pain and fall, respectively. She was lastly discharged five days prior to this new admission. In those 2 previous admissions she received subcutaneous heparin for deep venous thrombosis (DVT) prophylaxis. At the time of the current admission her vitals were unremarkable, and so was the rest of the physical examination.
The first set of blood works revealed the following: hemoglobin 14.9 g/dL (reference range 12–15.5 g/dL); white blood cell count 31.6 × 103/UL (reference range 4.8–10.8/UL) with 92.6% neutrophils; platelet count 285 × 109/UL (reference range 150–400/UL); BUN 71 (reference range 6–20 mg/dL); creatinine 3.6 mg/dL (reference range 0.5–1.5 mg/dL); ALT 8624 mg/dL (reference range 5–40 mg/dL); AST 13824 mg/dL (reference range 9–36 mg/dL); troponin T 0.952 ng/mL (reference <0.100 ng/mL); total creatinine kinase 193 Unit/L (reference range 20–200 Unit/L); creatinine kinase MB 4.77 ng/mL (reference range <0.500 ng/mL).
During this admission, serum cardiac markers were elevated, and electrocardiographic changes were nonspecific. Intravenous heparin was started for (non-ST-elevation myocardial infarction) NSTEMI. Further record review showed that the platelet count decreased by more than 50% (platelet count 285 × 109/UL on CBC at the time of the current admission compared to the platelet count of 750 × 109/UL at the time of the previous discharge 5 days ago). Furthermore, the platelet count reached a nadir of 216 × 109/UL. UFH was discontinued, but direct thrombin inhibitor was not started because suspicion for HIT was deemed to be low. An echocardiogram showed atrial fibrillation, low normal left ventricular ejection fraction (EF). Dabigatran was started for atrial fibrillation. On the second day of admission the kidney function improved on IV hydration, and the patient underwent cardiac catheterization. The study showed patent coronary arteries. In the late evening of day two, the patient became acutely confused and agitated. Computer tomography scan (CT) and magnetic resonance imaging (MRI) of the brain showed multiple tiny infarcts in the right cerebellum, right occipital and left frontal lobes. An ultrasound of the lower extremities showed acute right popliteal vein thrombosis. An inferior vena cava (IVC) filter was placed. On day five of hospitalization heparin platelet factor 4 (HPF4) antibody test came back negative. Positive test does not necessarily indicate the presence of thrombosis or thrombocytopenia, since only a minority of PFH4/heparin antibodies activate the platelets. Further confirmatory test (Serotonin Release Assay) C14-SRA was sent on day six of hospitalization which came back positive. Whilst awaiting for the gold standard test of C14-SRA, patient was continued on Dabigatran for new onset atrial fibrillation which, after the confirmed diagnosis of HIT, was discontinued and Lepirudin started. On twelfth day, the patient complained of discomfort at the right groin. Examination revealed ecchymosis with a pulsatile nontender mass at the right groin. Duplex of the right groin showed pseudoaneurysm of the right common femoral artery; Lepirudin was discontinued. On thirteenth day, the patient underwent successful obliteration of the pseudoaneurysm by in situ thrombin injection. The patient was observed in the hospital for two more days. Subsequently no bleeding or thrombotic event occurred. After discontinuing heparin, platelet count progressively increased to reach 815 × 109/UL at the time of discharge, . The patient was discharged only on aspirin because she did not opt to continue on anticoagulation owing to bleeding risk.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': True, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Vascular disease history': True, 'age': [77, 'years'], 'Congestive Heart Failure': False, 'Stroke': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
725,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6650453-1,Extracted,"A 48-year-old female patient presented to the emergency department (ED) after CPR due to VF that occurred after a seizure. Four years prior, she presented to other hospital ED and discharged after observation for a condition where her arms were raised and her limbs were stretched continually for approximately 1 min while sleeping after an episode of alcohol intake. She did not undergo any particular tests and neither was she administered any drugs, under the assumption that these symptoms were temporary and had been caused by alcohol intake. Three years prior, a similar episode occurred during sleep, for which some medical tests were conducted such as electrocardiogram (ECG), brain MRI, and electroencephalogram (EEG), but no conclusive results were reported. Drugs were also prescribed but not taken by the patient. One and a half year prior, the patient experienced another relapse again during sleep at dawn. According to the statement given by her husband who witnessed the episode at the time, for approximately 1 min while sleeping, the patient groaned with her mouth shut tightly, her arms raised, limbs stretched, and did not respond when called. Subsequently, her body collapsed, she stopped breathing for approximately 30–40 s, and then she breathed in a concentrated manner. Urination and post-ictal confusion were also noted. The patient had no family history of epilepsy or no medical history of febrile convulsion in the past, and only reported of the inability to sleep well and waking up frequently due to a burning sensation in the foot. In the previous hospital, the patient underwent video-EEG and polysomnography in an epilepsy monitoring unit (EMU) for two days to investigate the cause under the putative diagnosis of restless legs syndrome and nocturnal bilateral tonic seizure – frontal lobe epilepsy. Based on EEG findings, there was no inter-ictal epileptiform discharge and an intermittent slow wave was observed in the right frontotemporal area, but it was equivocal, and therefore, no clear abnormality was reported. Subsequently, administration of pramipexole and pregabalin was started to control the rare nocturnal seizures and symptoms of the restless legs syndrome under the putative diagnosis of restless legs syndrome and unknown etiologic epilepsy – bilateral tonic seizure.
On the day before current admission, her epileptic seizure relapsed during sleep but she recovered consciousness immediately; thus, she did not come to the hospital. In the evening of the admission day, while conversing with her children, she suddenly had a general tonic-clonic type seizure for 2–3 mins and emergency medical services (EMS) were informed as she did not recover consciousness immediately after the seizure like in previous episodes and her breathing was almost negligible. Following the instructions of the EMS center, her family started CPR. After the paramedics arrived, spontaneous circulation was restored after CPR and 2 times of defibrillation as VF was indicated by the AED findings (). At the time of ED arrival, the patient was stupor and her vital signs and oxygen saturation were normal with a blood pressure of 121/82 mmHg, pulse rate of 80 beats per minute, respiratory rate of 16 breathes per minute, and body temperature of 36.2°C. ECG performed immediately after arrival showed a sinus rhythm with a heart rate of 78 beats per minute and QTc duration of 401 ms (). The initial arterial blood gas analysis (ABGA) showed a pH of 7.35, PCO2 21 mmHg, PO2 134 mmHg, HCO3 11.6 mEq/L, and a lactate level of 6.1 mg/dL. Approximately 10 min after arrival, she regained consciousness but Todd’s paralysis in the right limbs and global aphasia were shown. The repeat ABGA showed that all values had recovered to normal levels. All other blood test results were normal, including electrolyte and myocardial enzyme levels. Levetiracetam was administered intravenously in the ED. Brain diffusion MRI showed no abnormality. Thereafter, the patient was admitted to the cardiology intensive care unit (ICU) and received a full cardiologic work-up. After admission to the ICU, her consciousness was maintained in an alert state, the paralysis in the right limbs and aphasia resolved completely, and the EEG showed normal results. Transthoracic echocardiography performed on the day after admission showed that the left ventricle ejection fraction (LVEF) was reduced to 44%, and left ventricle global hypokinesia and moderate systolic dysfunction were observed. After that, consecutively performed coronary angiography (CAG), spasm provocation test, cardiac MRI, and 24-hr Holter monitoring showed normal results. For the purpose of preventing sudden cardiac death (SCD), the insertion of an implantable cardiac defibrillator (ICD) was recommended. The patient was discharged without any complications 6 days after the procedure. Currently, levetiracetam administration is being maintained by the neurology department and her condition is being periodically followed by the cardiology department under the diagnosis of aborted SCD due to VF and heart failure with mid-range ejection fraction.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [48, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 48 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
726,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7343312-1,Extracted,"A 71-year-old man presented to the ED with a two-day history of bilateral lower extremity pain. He initially experienced left lower extremity pain and cold sensation which progressed to the right lower extremity. Pertinent past medical history included type 2 diabetes mellitus, hypertension, coronary artery disease with percutaneous coronary intervention (PCI) to the right coronary artery (RCA) 18 years prior, peripheral arterial disease (PAD) with bilateral superficial femoral artery stenting two years prior and atrial fibrillation with recent ablation.
Physical exam revealed cold lower limbs and there was bilateral absence of dorsalis pedis and posterior tibial pulses. He had decreased sensation to light touch with preserved strength. The remainder of the physical exam including heart and lung auscultation was unremarkable. Arterial Doppler studies showed occluded stent grafts in the superficial femoral arteries and popliteal arteries bilaterally. A subsequent CT angiogram of his lower extremities confirmed these findings, revealing minimal flow within the dorsal right calf arteries, with no flow being identified within the left calf arteries (Figure ).
His initial laboratory results were remarkable for hemoglobin 12.4 g/dL, mean corpuscular volume 104.3, white blood cell (WBC) count 4.6 k/uL, and platelet count 46 k/uL. He was incidentally noted to have 30% peripheral blasts with features consistent with APL on peripheral smear review for thrombocytopenia which prompted a hematology consultation (Figure ). Coagulation panel showed prothrombin time 17.9, international normalized ratio (INR) 1.5, D-dimer >20 ug/mL, and fibrinogen 86 mg/dL. He subsequently underwent bone marrow biopsy which revealed a t(15:17) promyelocytic leukemia/retinoic acid receptor alpha (PML-RARA) positive and 66% confirming diagnosis of APL (Figure ).
After a multidisciplinary discussion with vascular surgery and hematology, the patient was deemed to be very high risk for any surgical intervention and was continued on heparin drip. The following day, the patient reported numbness and weakness in his right lower extremity which resolved spontaneously, and the patient opted for continued observation and chemotherapy. Given the possibility of emergent intervention and concern for poor wound healing, the patient was started only on single agent all-trans retinoic acid (ATRA) alone instead of full-regimen chemotherapy.
His hospital course was complicated by atrial fibrillation with rapid ventricular response and subsequently developed ST elevation myocardial infarction (STEMI) needing emergency balloon angioplasty, subsequently sustained a cardiopulmonary arrest (Figure ). Despite a brief return of spontaneous circulation, the patient deteriorated rapidly and expired.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': True, 'age': [71, 'years'], 'Stroke': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 71 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
727,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7186085-1,Extracted,"We present an 85-year-old male with a past medical history of obesity, type two diabetes, atrial fibrillation, diastolic heart failure, chronic kidney disease (CKD) stage three, and coronary artery disease. The patient had a history of non-ST elevation myocardial infarction (NSTEMI) four weeks before the current admission, requiring a drug-eluting stent (DES) to the left anterior descending (LAD) artery. He also had a history of significant gastrointestinal bleed in the past month, for which apixaban was stopped. The patient was admitted to our hospital with worsening shortness of breath and found to have bilateral pleural effusions, right greater than left. He was afebrile and did not have any symptoms of pneumonia. The patient was started on IV furosemide and had an initial diagnostic, small-bore, ultrasound-guided tap from the right pleural effusion that was uneventful and yielded straw-colored 1000 mL of fluid. The pleural fluid analysis was mildly exudative based on Light’s lactate dehydrogenase (LDH) criteria, but cytology was negative as well as Gram stain, bacterial, and fungal cultures. Autoimmune screening, including anti-nuclear antibody (ANA) and extractable nuclear antigen (ENA), was negative. In anticipation of a potential repeat pleural tap, the patient's aspirin was stopped. One week later, the patient was getting more short of breath, and chest X-ray revealed recurrent bilateral effusions worse on the right side. Echocardiogram showed features of diastolic dysfunction, with a left ventricular ejection fraction of 55% and no significant valvular disease. Arterial blood gas (ABG) was suggestive of hypercapnic respiratory failure; thus, he was started on non-invasive ventilation (NIV) and shifted to the ICU. He underwent a second, uneventful pleural tap on the right side, that yielded 1500 mL of straw-colored fluid. Analysis again showed an exudate with negative bacterial, fungal cultures, and cytology. CT scan of the chest showed basal atelectasis with significant pleural effusions, no lung masses, or lymph nodes enlargement (Figure ). The patient was transferred to the step-down unit, completed a 10-day course of antibiotics for possible community-acquired pneumonia, although sputum and blood cultures remained negative. One week later, the patient again clinically deteriorated and was admitted to ICU with hypercapnic respiratory failure and worsening pleural effusions. He initially required continuous bilevel positive airway pressure (BiPAP) ventilation until he stabilized. He had a third, right-sided thoracocentesis under ultrasound-guidance from a posterior approach, atraumatic, and yielded 1500 mL of clear thin yellow fluid. The patient had a follow-up chest X-ray 20 min later that showed improvement in the previously seen right-sided pleural effusion and no pneumothorax. However, two hours later, the patient was suddenly getting sweaty, tachypneic, lethargic while on BiPAP. His blood pressure (BP) was reading 60/40 mmHg, heart rate was dropping to 40 bpm, and he was less responsive. There was minimal air entry on auscultating the right chest with dullness to percussion, and no signs of any pain or tenderness. ABG showed hypoxia and a stable PCO2 level. Immediate chest X-ray showed a new 3.5 cm hemothorax on the right side (Figure ).
He was given 1 L of IV fluids, norepinephrine for BP support, and an urgent right-sided IC surgical drain was inserted, which immediately drained 1.7 L of blood.
The patient had a central line insertion, and three units of packed red blood cells (PRBC) transfused. Repeat hemoglobin after the second transfused unit was still below baseline at 6 g/L (from 8 g/L). He clinically started to improve after the hemothorax drainage, was more responsive, and pressor requirement was decreased. Overnight he received two units of platelets, and clopidogrel was stopped. The next day, the IC surgical drain still had around 800 mL output of serosanguinous fluid, but he was clinically back to his baseline as before this event. CT scan of the chest with IV contrast did not show any active bleeding into the pleural space but showed complex right-sided effusion. The IR team performed IC arteries angiogram to diagnose the site of the injured vessel. That was done within 24 h of the event and was negative. The cardiothoracic surgery team was consulted for possible video-assisted thoracoscopic surgery (VATS) procedure in the right pleural space. The patient continued to improve, and after a few days we removed the surgical drain, and transferred him out to the step-down unit with cardiothoracic surgical team following up on his care.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': True, 'age': [85, 'years'], 'Congestive Heart Failure': True, 'Stroke': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 85 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
728,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5987319-3,Extracted,"An 87-year-old woman was referred to our hospital for treatment of AF with palpitation and dyspnea (). She related a history of treatment for hypertension and cerebral infarction but no history of heart failure and/or arrhythmia. Upon arrival, her BP was 102/54 mmHg and HR was 151 bpm. Her heart rhythm often spontaneously alternated between AF and sinus rhythm (). Echocardiography demonstrated preserved cardiac contractility with an EF of 64%, indicating heart failure with preserved EF. She was administered verapamil (5 mg) injection; however, there was no decrease in HR or frequency of rhythm alternation. Next, bisoprolol transdermal patch (4 mg) was applied to her chest. Her HR trends were significantly decreased after 6 hours on the bisoprolol transdermal patch and the frequency and duration of AF decreased until 24 hours after administration (). Moreover, her symptoms were improved.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'age': [87, 'years'], 'Congestive Heart Failure': False, 'Stroke': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 87 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 6. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
729,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-7626,Extracted,"A 76-year-old man presents after an acute onset seizure. He lives in a retirement home and denies any previous history of seizures. Past medical history is significant for a hemorrhagic stroke 4 years ago, and type 2 diabetes, managed with metformin. His vital signs include: blood pressure 80/50 mm Hg, pulse 80/min, and respiratory rate 19/min. On physical examination, the patient is lethargic. Mucous membranes are dry. A noncontrast CT of the head is performed and is unremarkable.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [76, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
730,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3819262-1,Extracted,"A 35-year-old Caucasian male patient who worked as an environmental engineer had a medical history of recurrent episodes of acute pharyngitis, essential hypertension, hypercholesterolemia, and occasional abdominal pain and bloating. He had no recent travel history. His family history included immunoglobulin (Ig) A deficiency in his 18-month-old son and a several-year history of nonspecific colitis in his father. Regular medications were nifedipine CR (30 mg/day) and rosuvastatin (5 mg/day).
The patient initially presented to his family physician with a symmetrical polyarthralgia involving his knees and hands, odynophagia, temporal headache, retro-ocular pain, and an intermittent fever (maximum of 38°C). He was initially managed with an antibiotic (azithromycin) and anti-inflammatory agents without resolution of symptoms. One week later, he developed oral mucosal lesions and a vesicular rash on his palms and soles (Figures and ). In April 2011, 3 weeks after the initial presentation, he was admitted to the emergency room at the Curry Cabral Hospital (Lisbon) with compressive retrosternal pain, without dyspnea or a productive cough. The odynophagia was persistent, with worsening of the headache and arthralgia.
The emergency staff noted nonexudative oropharyngitis and tender cervical lymphadenopathy with normal cardiorespiratory examination findings and absence of a pericardial friction rub. He had abdominal tenderness in the right lower quadrant without guarding. There were no vesicles on the palms of his hands or soles of his feet, but the skin had a scalded appearance. There was slight ST-segment depression on the inferior leads (II, III, and aVF) of the electrocardiogram (ECG) and mildly increased levels of troponin I and creatine kinase-MB fraction. The diagnosis of myopericarditis was considered. He started ibuprofen at 400 mg three times a day and was admitted for further workup.
As an inpatient, his condition slowly improved. His fever resolved and he was discharged with only slight fatigue during strenuous exercise. The skin vesicles disappeared and progressed to scaliness (Figure ).
Laboratory examination showed positive serology for coxsackie A9 (IgM with a titer of 1:160) 1 week after the disappearance of the vesicular rash. It is assumed that a titer of >1:80 is predictive of a diagnosis of the infection in question. In addition, he was positive for IgA anti-transglutaminase 25 (<20 U/mL) and IgA anti-gliadin 77 (<25 U/mL) antibodies, with higher titers during follow-up after discharge (59 and 60 U/mL, respectively). He had normal immunoglobulin levels and was negative for antinuclear antibody (ANA), anti-DNA antibody (dsDNA), and p- and c-anti-neutrophil cytoplasmic antibody (ANCA). Serology for viral hepatitis and human immunodeficiency virus were negative. Endoscopy revealed a normal appearance of the gastric and duodenal mucosae, and biopsy showed slight mucosal architecture disruption.
An echocardiogram showed a normal left ventricle, slightly hypertrophic interventricular septum, normal systolic function (ejection fraction of 60%), and left atrium in the upper limit of the normal range. The ECG findings and cardiac biomarker levels returned to normal after 5 days.
To ameliorate the abdominal pain and bloating, a gluten-free diet was introduced, and this proved to be helpful with normalization of the anti-transglutaminase and anti-gliadin antibodies 6 months later.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [35, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 35 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
731,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8254656-1,Extracted,"A 76-year-old female with a medical history of atrial fibrillation, congestive heart failure (CHF) on pacemaker, hypertension, and asthma presented to the emergency department with the chief complaint of right upper quadrant abdominal pain of seven days duration. The patient described the pain as gradual in onset, which progressively worsened over two days duration. The pain was dull in quality, radiated to her right shoulder, worsened with meals, taking a deep breath, and moving. She described the severity of pain as 8/10; it was associated with nausea and vomiting of ingested matter for the past three days. She denied any alleviating factors. Furthermore, the patient complained of dry cough and gradual worsening of shortness of breath which started seven days ago. Shortness of breath was both at rest and while walking. The patient also had intermittent low-grade fever with a T-max of 100.8°F in the past three days. Otherwise, she denied chest pain, leg swelling, hemoptysis, yellowish discoloration of the eye, change in stool color, diarrhea, or constipation.
Upon initial evaluation and physical exam, the patient was fully awake and oriented to person, place, and time. Initial vitals were as follows: respiratory rate of 23 breaths/min, oxygen saturation of 86% on room air which later improved to 94% with 2 L of oxygen via nasal cannula, blood pressure of 127/87 mmHg, pulse rate of 89 bpm, and temperature of 98.6°F. Head, eyes, ears, nose, and throat (HEENT) exam revealed pink conjunctiva and nonicteric sclera, dry tongue, and buccal mucosa. On respiratory system exam, she had mild tachypnea with a respiratory rate of 23 breaths/min and bilateral coarse crackles with rhonchi. Heart sounds were irregularly irregular, S1 and S2 well heard no murmur or gallop. Jugular venous pressure (JVP) was flat, and no distended neck veins. The abdomen was slightly distended abdomen which moved with respiration. The patient had marked right upper quadrant tenderness on both superficial and deep palpation with significant guarding and rigidity, and murphy’s sign was positive. She had no costovertebral angle tenderness or suprapubic tenderness. Extremity exam revealed mild pretibial and pedal trace edema. Laboratory tests revealed a white blood cell (WBC) count of 5,800 k/uL, hemoglobin of 13.2 g/dL, platelet of 170,000 k/uL, blood urea nitrogen (BUN) of 17 mg/dL, creatinine of 0.7 mg/dL, brain natriuretic peptide (BNP) of 398 pg/mL,aspartate transaminase (AST) of 21 u/L, alanine transaminase (ALT) of 14 u/L, alkaline phosphatase 62 u/L, and total bilirubin of 1.4 mg/dL. Inflammatory markers were elevated with C-reactive protein (CRP) of 68 mg/dL, lactate dehydrogenase (LDH) of 278 u/L, and D-dimer of 0.77 mg/L FEU (fibrinogen equivalent units)​​​​​​. ​Procalcitonin was within normal limits (0.20 ug/L). Blood cultures showed no growth in two bottles. COVID-19 nasal swab test was positive. Chest X-ray showed bilateral interstitial infiltrates typical of viral interstitial pneumonia (Figure ). Ultrasound of the gallbladder showed gallbladder wall thickness with mild pericholecystic fluid collection and no gallstone suggestive of acalculous acute cholecystitis (Figures , ). The most recent echocardiogram showed a left ventricular ejection fraction (LVEF) of 50%.
The patient was admitted to the COVID-19 unit with the diagnosis of acute hypoxic respiratory failure due to COVID-19 pneumonia and acute acalculous cholecystitis. She was treated with dexamethasone, remdesivir, and vitamin supplements. The patient also received supportive care with oxygenation via nasal cannula. Anticoagulation with Eliquis from her home medication was continued for the atrial fibrillation and deep vein thrombosis (DVT) prophylaxis. Empiric antibiotic coverage was initiated for acalculous cholecystitis with Zosyn after evaluation by the general surgeon. The patient was kept on nothing by mouth, and cholecystectomy was postponed as the patient clinically improved with empiric antibiotic coverage. The patient completed a 5-day course of remdesivir as an inpatient and eventually weaned off oxygen. Abdominal pain was significantly resolved, and oral feeding was resumed on the third day of her admission. Eventually, she was discharged home with oral Augmentin and the remaining dose of dexamethasone as well as vitamin supplements. She was given a follow-up appointment with general surgery as an outpatient for elective cholecystectomy after six weeks.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [76, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Vascular disease history': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
732,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7056952-1,Extracted,"A 52-year-old woman with rheumatic heart disease and atrial fibrillation was scheduled to undergo a mitral valve replacement and Maze operation for severe mitral stenosis. She had a history of decompressive craniectomy due to cerebral swelling and right middle cerebral artery infarction 1 year prior, and sequela included persistent weakness of her left side. Preoperative transthoracic echocardiography revealed normal left ventricular systolic function (ejection fraction, 63%) and no regional wall motion abnormalities. Anesthesia induction and maintenance were performed as usual, and routine cardiac anesthesia monitoring was conducted. The mitral valve replacement was a 27-mm St. Jude Medical valve prosthesis (St. Jude Medical, Saint Paul, MN, USA), and the Maze operation proceeded well under cardiopulmonary bypass (CPB). Myocardial protection was performed via an infusion of cold cardioplegia via the aortic root cannula. Intraoperative transesophageal echocardiography showed no paravalvular leakage. Immediately after an aortic cross clamp, the cardiac activity was converted to normal sinus rhythm but returned to atrial fibrillation after a few minutes. Left ventricular systolic function remained normal. The patient was weaned from the CPB. After the operation, the patient was transferred to the ICU. The patient’s vital signs were controlled through administration of dobutamine and norepinephrine, and tachycardia was controlled through amiodarone. The patient’s blood pressure was maintained at 110/60 mmHg, and her oxygen saturation was greater than 97%. Extubation was performed the day after the operation. However, at 2 days postoperatively, the patient complained of dyspnea and chest discomfort, and electrocardiogram (ECG) revealed a premature ventricular complex. Transthoracic echocardiography revealed decreased left ventricular ejection fraction to 26% and akinesia of the middle and apical wall of the left ventricle (). Takotsubo cardiomyopathy was suspected, but coronary artery disease could not be completely ruled out. On the 4th postoperative day, the patient developed pulmonary edema and hypoxemia. The patient’s systolic blood pressure was 80 mmHg, and heart rate was 150 beats/min. The ECG showed atrial fibrillation with a rapid ventricular response. The doses of norepinephrine, dobutamine, and epinephrine were continuously increased. Transthoracic echocardiography showed a continuously worsening ejection fraction. The patient was intubated, and we decided to perform ECMO insertion because coronary angiography and management were not possible at the time due to the patient’s condition. The results of laboratory tests were as follows: creatine kinase-MB, 1.5 μg/L; troponin I, 1.73 ng/ml; and brain natriuretic peptide (BNP), 4,073 pg/ml. The ECG showed atrial fibrillation with ST and T wave abnormality. The QT interval was 266 ms. Vasopressor support with norepinephrine was continued. Coronary angiography was performed under ECMO, and the results were normal. Thus, Takotsubo cardiomyopathy was confirmed, and conservative treatment and supportive care were maintained. At 11 days postoperatively, the ECG showed QT prolongation (582 ms). At 21 days postoperatively, transthoracic echocardiography revealed that the left ventricular ejection fraction had recovered to 38%, and the ECMO was subsequently removed. Extubation was performed at 30 days postoperatively, and the patient was transferred to the general ward at 33 days postoperatively. At 35 days postoperatively, the patient’s left ventricular ejection fraction had recovered to 58%. The changes in BNP and serum troponin I levels are shown in .
The patient was discharged on the 60th postoperative day after receiving rehabilitation for left-sided weakness. One year after the operation at a follow-up visit, the patient was without any complications and medicated with digitalis, diuretics, and warfarin.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [52, 'years'], 'Congestive Heart Failure': True, 'Stroke': True, 'Transient Ischemic Attacks History': True, 'Thromboembolism history': True, 'Vascular disease history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 52 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
733,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8426069-1,Extracted,"An 83-year-old female presented to the operating room to undergo an elective suprapubic catheter placement for chronic urinary retention secondary to a hypotonic bladder. Past medical history included hypertension, aortic stenosis, atrial fibrillation, transient ischemic attack, peripheral vascular disease, five vaginal deliveries, and longstanding pelvic floor dysfunction. The patient weighed 53 kilograms. Preoperative cystoscopy revealed a grossly trabeculated bladder consistent with long-standing urinary retention. A trial of clean intermittent catheterization was found undesirable by the patient, and a urethral catheter was placed. After discussion regarding long-term options, the patient decided to proceed with SPC.
In the operating room, cefazolin 1 g was administered intravenously on induction of procedural sedation. The bladder was distended with approximately 500 mL of normal saline instilled through a urethral catheter and adequately palpated. A spinal needle was used to infiltrate the tract with 0.5% Marcaine without epinephrine. The spinal needle was then advanced into the bladder, and urine was aspirated. A trocar was passed, and an 18 French Foley catheter was advanced into the bladder. Hematuria was noted, and continuous bladder irrigation (CBI) was started through the urethral catheter. The patient was transferred to the post anesthesia care unit (PACU) in stable condition. Within one hour of surgery, nausea, vomiting, rigors, pyrexia (temperature 39°C), and significant hypertension (229/165 mmHg) became apparent. On examination, the patient was alert and the abdomen was moderately distended and firm. Intravenous labetalol was administered, and a stat computed-tomography (CT) scan of the abdomen and pelvis was ordered to rule out bowel injury. Marked hypotension (82/50 mmHg) was then noted, and blood cultures as well as intravenous crystalloid resuscitation were ordered. The CT scan showed no evidence of bowel puncture and confirmed appropriate placement of the suprapubic catheter tip within the bladder.
The patient was then transferred to the intensive care unit (ICU) for management of postoperative septicemia. Fluid resuscitation and empirical antibiotics were administered until blood cultures and sensitivities were available. Vasopressors were required overnight and discontinued on postoperative day one, as was the CBI and the urethral catheter. The suprapubic catheter was well positioned and draining clear, yellow urine. White blood cell counts peaked at 30.6 × 109/L. Blood cultures were positive for Enterococcus faecalis and Proteus mirabilis, for which the patient completed a seven-day course of piperacillin-tazobactam. P. mirabilis was sensitive to ampicillin, cefazolin, ciprofloxacin, gentamicin, and trimethoprim/sulfa, while E. faecalis showed sensitivity to ampicillin, gentamicin synergy, streptomycin synergy, and vancomycin.
The admission was further complicated by increased left ventricular afterload in the context of aortic stenosis, leading to poor coronary perfusion (postoperative troponin I peaking at 1917 ng/L) during the hypertensive episode in PACU. Coronary angiography was performed, and severe disease in the first obtuse marginal artery was treated with a drug-eluting stent. The patient was discharged in stable condition on postoperative day ten.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': True, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Diabetes history': False, 'Vascular disease history': True, 'age': [83, 'years'], 'Stroke': False}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 83 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
734,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6457404-1,Extracted,"A 62-year-old female with a history of ESRD and on hemodialysis was referred to our electrophysiology department due to paroxysmal AF. Anticoagulation therapy with warfarin was started because her CHADS2-VASc score was 4 (hypertension, diabetes, congestive heart failure, and female gender), as well as amiodarone therapy for rhythm control. Transthoracic echocardiography demonstrated enlarged left atrium (LA) with a reduced left ventricular ejection fraction (25%). The coronary angiogram demonstrated no significant stenosis at the epicardial coronary artery. Transesophageal echocardiography (TEE) revealed a thrombus in the LAA ( & ). We targeted an INR of 2.0–2.5 with a monthly check up; however, labile INR was documented with time in a therapeutic range (TTR) of 45.8%. With maintaining warfarin and amiodarone, the patient experienced syncope. Tachycardia–bradycardia syndrome was documented, and therefore, a catheter ablation was planned. However, after approximately 2 years of warfarin anticoagulation therapy, TEE detected remaining thrombus (). Therefore, warfarin was switched to a direct factor Xa inhibitor, apixaban at 5mg bid. Patient’s PT and INR values were 19.4 and 1.78, respectively, at the time of replacement. Apixaban was initially prescribed at 2.5 mg bid as opposed to 5 mg bid recommended by the package labeling for fear of bleeding complications, and it was increased to 5 mg bid a month later. After 4 months of apixaban treatment, TEE revealed complete resolution of the LAA thrombus ( & ). Finally, catheter ablation was performed without complications, and the patient has since been in the sinus rhythm under continued anticoagulant treatment with apixaban. No thromboembolic or bleeding event occurred during the 26 months of the follow-up after the catheter ablation.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': False, 'age': [62, 'years'], 'Congestive Heart Failure': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 62 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
735,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3684099-1,Extracted,"A 76-year-old Caucasian man came to our observation because of lumbar pain and epigastric discomfort. He was taking ibuprofen orally 400 mg bid as an analgesic treatment for 1 month. About his clinical history, 1 year before the admission, he had suffered from acute coronary syndrome during an episode of atrial tachyfibrillation treated with percutaneous transluminal coronary angioplasty and stenting, and subsequently a biologic prosthetic mitral valve had been implanted due to severe mitral insufficiency. He was on regular treatment with warfarin, atorvastatin, and bisoprolol tablets. At the admission to our ward we stopped ibuprofen. He demonstrated a state of mild confusion and irritability. Laboratory tests showed sodium 116 mmol/L and chloride 84 mmol/L; hepatic and renal tests, as well as the other routine blood tests, were normal, with uric acid 2.5 mg/dL and urea 37 mg/dL. Duration of hyponatremia was unknown. The patient appeared clinically normovolemic (blood pressure 126/76 mmHg without orthostatic hypotension, heart rate 86 bpm) and showed no signs of heart or renal failure. We performed thyroid function tests and measurement of urinary cortisol excretion that resulted normal. After the evidence of low plasma osmolality (252 mOsm/L), high Uosm (561 mOsm/L), and high urinary sodium (160 mmol/L), a diagnosis of SIADH was formulated. To determine the etiopathogenesis of the syndrome, we performed brain MR, total body CT scan, radionuclide bone scan, serologic tests for Chlamydia, Legionella, and Mycoplasma: all tests resulted normal.
We started infusion of a slightly hypertonic saline solution (1.2% at a rate of 60 mL per h) for 3 days without significant sodium changes; since the patient was taking warfarin and therefore we could not prepare immediately a central iv line to allow the infusion of a more hypertonic solution (3% saline), we decided to treat the patient with tolvaptan, an oral AVP V2 receptor antagonist, initially at the dosage of 7.5 mg daily, checking plasmatic sodium level every 6 hours, and after 5 days at the dosage of 15 mg daily. The patient was encouraged to drink water if he felt thirsty. The changes of sodium level associated with the treatment are presented in . After 8 days of treatment the patient showed progressive increase of sodium levels up to normal values and fully recovered clinically. In the following weeks tolvaptan was prescribed at progressively titrated dosage to full suspension (at day 40); afterwards the sodium levels remained normal without any type of treatment.
Our diagnostic conclusion was drug-induced SIADH, due to the use of ibuprofen, with a complete recovery of normal sodium levels induced by the treatment with a V2 receptor antagonist.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [76, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
736,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6803739-1,Extracted,"A 51-year-old lady presented with cough and shortness of breath. The symptoms started in the morning after waking up from sleeping. The cough was productive of pink-colored sputum and she was using accessory muscles to breathe. The family members noticed that she was also drowsy, confused, and not responding to them for about 30 min. Afterwards, she was fully aware of the surroundings; however, she could not recall what happened. They measured her blood glucose and it was 8.5 mmol/L. The past medical history was significant for a resected right temporal meningioma 3 years back and type 2 diabetes mellitus with well controlled HbA1c. Home medications are phenytoin 200 mg twice daily, lamotrigine 200 mg three times daily, escitalopram 10 mg once daily, and metformin/sitagliptin 1000/50 mg twice daily. The patient is known to experience seizures despite those anti-epileptic medications.
On examination, she was afebrile (37.3°C), hypotensive (89/47 mmHg), and hypoxic (82% oxygen saturation on room air). Respiratory exam showed bilateral crackles up to the mid zones bilaterally. Neurological examination did not reveal any abnormality. The initial laboratory tests ordered upon admission are shown in .
Arterial Blood Gases (ABG) on Room Air. pH 7.41 (7.35–7.45), PaO2 48.8 mmHg (83–108), PaCO2 35 mmHg (35–45), HCO3 22.5 mmol/L (21–28), PaO2/FiO2 ratio: 232 (normal ratio is approximately 500).
ABG on Room Air after 2 Days. pH 7.43 (7.35–7.45), PaO2 90 mmHg (83–108), PaCO2 36 mmHg (35–45), HCO3 24.5 mmol/L (21–28), PaO2/FiO2 ratio: 429 (normal ratio is approximately 500).
CXR on Admission. Multiple confluent and patchy air space opacities noticed diffusely involving both lung fields ().
CXR after 2 Days. Bilateral lung opacities appear significantly resolved as compared to the previous chest radiograph ().
ECG. Sinus tachycardia with premature ventricular complexes ().
Trans-Thoracic Echocardiography. Good global contractility and no resting regional wall motion abnormality. Normal Left ventricle systolic function. Ejection fraction 58%–60%.
The patient received 1.5 L of intravenous normal saline boluses, she was connected to noninvasive ventilator—Continuous positive airway pressure (CPAP) machine with empirical IV. antibiotic to cover aspiration pneumonia and admitted to MICU for observation. There, she stayed for 2 days and showed marked improvement clinically and in the requirements of oxygen. Repeated CXR showed dramatic resolution of bilateral lung opacities without giving furosemide (). Compliance to anti-convulsant medications was emphasized, and she was maintaining oxygen saturation above 95% on room air upon discharge.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': False, 'Diabetes history': True, 'Vascular disease history': False, 'age': [51, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 51 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 1 + 1 = 2.
The patient's CHA2DS2-VASc Score is 2."
737,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5155631-1,Extracted,"A 90-year-old Caucasian female presented to the eye casualty with a 2-day history of headaches, nausea, and a painful, red left eye with reduced vision.
Past ocular history included stable primary open angle glaucoma, right-eye cataract surgery and bilateral age-related macular degeneration (AMD). The left eye was known to have a disciform scar, amblyopia, and hand movements vision. Her medical history included atrial fibrillation, chronic congestive heart failure, hypertension, hypercholesterolaemia, chronic kidney disease stage 3, and a previous cerebral vascular accident. She was on oral warfarin, furosemide, ramipril, and simvastatin.
At presentation, the corrected Snellen visual acuity was 6/15 in the right and hand movements in the left eye. The right eye was pseudophakic and had moderate dry AMD. The IOP in the left eye was 55 mm Hg, the ocular surface was deeply inflamed, the cornea oedematous, and the pupil fixed and mid-dilated.
Nevertheless, the anterior chamber (AC) was moderately deep on van Herick's test (grade 3), showing a red hue secondary to haemolysed red blood cells (Fig ). The angles and fundus could not be appropriately assessed due to the oedematous cornea and dense cataract.
The international normalised ratio (INR) was 7.7, while all other haematological and biochemical tests were within normal limits. Ultrasound biomicroscopy (UBM) of the left anterior segment showed normal AC depth and open angles but the ocular ultrasound of the posterior segment revealed a diffuse suprachoroidal and vitreous haemorrhage (Fig ). The patient was admitted and required intravenous acetazolamide, topical ocular hypotensive medications, dexamethasone 0.1%, cyclopentolate 1%, and oral glycerol to achieve a IOP of less than 21 mm Hg. Warfarin was omitted and the patient was given 5 mg of oral vitamin K which reduced the INR to 1.9. Warfarin was then re-started and the INR kept within the low therapeutic range.
Despite good IOP and INR control, van Herick's grade progressed from 3 to 0 between the third and the sixth day of her hospital stay. Angle closure was confirmed on repeated ocular UBM (Fig ). Considering the pathophysiology of the angle closure and the visual prognosis, YAG laser peripheral iridotomy was not performed.
A vitreo-retinal opinion was sought, but drainage of the haemorrhage was not considered appropriate due to the risk of recurrent haemorrhage and poor prognosis.
Two months following the acute event, the left eye was comfortable, the corneal oedema had largely resolved, the AC was quiet and returned to its normal depth. Gonioscopy showed open angles and a reddish-brown pigment on the trabecular meshwork. The IOP was well-controlled without any ocular hypotensive agents. Despite the poor visual outcome, the patient was pleased that the left eye returned to be comfortable.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Thromboembolism history': True, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Vascular disease history': True, 'age': [90, 'years'], 'Congestive Heart Failure': True, 'Stroke': True}",8,8,8,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 90 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 5 + 2 = 7.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 7 + 1 = 8. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 8.
The patient's CHA2DS2-VASc Score is 8."
738,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4344978-1,Extracted,"A fifty five year old gentleman with no past history of diabetes mellitus or hypertension, presented a history of a Cerebrovascular event three years ago followed by complaints of rotatory vertigo for three years. Episodes lasted 5-10 minutes but there was no hearing loss, tinnitus or hyperacusis associated with the vertigo. This episodic vertigo had been more frequent in the recent past. It was not associated with any headache or preceding aura. His Cerebrovascular event was diagnosed as left-sided lateral medullary syndrome with left hemi paresis, left Horner syndrome and left upper motor neuron facial palsy. MRI suggested multiple lacunar infarcts in the left medullar region. Over time the patient had shown slow but progressive improvement in all neurological deficits.
At the time of presentation he had residual intermittent nasal regurgitation, dysphagia to solid food, and change in voice. He also had tingling sensation, paresthesia, and decreased touch sensation of the left half of his face and the right side of his body. He had no history of seizures.
Neurological examination revealed decreased sensation on the left half of the face and the right side of the body. Cranial nerve examination revealed that the Vagus nerve (right vocal cord palsy) and the trigeminal nerve (decreased touch sensation with paresthesia over the left half of the face) were affected; furthermore, gag reflex was sluggish. Cerebellar signs were positive on the left side with ipsilateral tilt on Romberg’s test. He had a wide-based gait with difficulty in turning. There was no significant spontaneous nystagmus. Gaze nystagmus was present on the left. Dix–Hallpike revealed non fatigueable left-beating horizontal nystagmus with no latency in sitting as well as supine positions.
He had saccadic intrusions of the smooth pursuit evident in Electronystagmography (). Optokinetic test was normal. Caloric tests revealed bilateral hyperactive response () pure tone audiometry and impedance audiogram was within normal limits.
Subjective visual vertical (SVV) and subjective visual horizontal (SVH) were tested using a pre-programmed computed equipment (MUS_VS-V1.3.2.RevB-Synapsis company). The subject was seated in a darkened room (to avoid any visual cues). Head and neck was stabilized in an erect neutral position using a headband fixed to the patient’s high back chair. The stimulus was projected on a large screen monitor mounted at a distance of 2 metres, in front of the patient.
The patient was fitted with a contour mask with binocular vision fitted with a set of 3 obturators so as to further reduce the chance of any visual cues. The stimulus was a projected vertical illuminated ‘line’ on the screen provided by the software from the SVV and SVH equipment. It was presented at a preset angle (between 5 degrees and 30 degrees) in a random fashion. He was required to adjust the ‘line’ to absolutely vertical and horizontal as perceived by him, using a joy stick (remote controlled potentiometer). For the dynamic assessment, the background was made to rotate clockwise or anti-clockwise. It was repeated six times, each for static and dynamic settings and values were recorded. The above procedure was in accordance with standard recommendations (,).
Static SVV was 1.45 degree and static SVH was 1.81 degree, which was within normal values. The dynamic SVV and SVH were found to be 5.48 degrees and 3.08 degrees which were noticeably abnormal ().
Imaging three years after a Cerebrovascular event revealed an old left PICA (posterior inferior cerebellar artery) infarction and MRA suggested absence of flow in the left vertebral artery. He was advised a short course of vestibular suppressants and prolonged vestibular rehabilitation exercise. He was significantly relieved of his symptoms after four months.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': True, 'Transient Ischemic Attacks History': True, 'Hypertension history': False, 'Diabetes history': False, 'Vascular disease history': False, 'age': [55, 'years'], 'Stroke': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 55 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 0 + 2 = 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
739,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6993326-1,Extracted,"A 50-year-old otherwise healthy male patient was emergently referred by his primary care physician with recurrent unprovoked syncope which led to multiple hospital visits.
The patient was on beta blocker therapy for supraventricular and ventricular extrasystole, as well as arterial hypertension. There were no other prior medical conditions.
At the time of admission to our hospital, the patient had experienced four episodes of transient loss of consciousness; the last episode lasted 30 s and took place in the office of the primary care physician. The first episode took place after mowing the lawn and caused a minor head trauma leading to his admission to the hospital. A head CT after this incident was deemed normal (Fig. ); the physical and neurologic exams, as well as repeat EEGs revealed no pathologies.
There were no syncope provoking factors. Since there had been a recent death in the family causing the patient increased psychosocial stress, psychogenic pseudosyncope was also considered. After each episode of transient loss of consciousness, the patient was fully alert and oriented. The patient reported no family history of sudden cardiac death or other cardiovascular diseases.
In 24-h Holter monitoring ordered by the primary care physician, a 6 s sinoatrial arrest had been documented. Later, in our clinic, asystole of 12 s was documented (Fig. ). During the episodes, there were no clinical signs of generalized seizure (no involuntary movements, tongue bite, incontinence, postictal confusion).
After ruling out Lyme disease, relevant coronary artery disease, a structural heart disease, and pulmonary embolism, a dual chamber magnetic resonance (MR) conditional pacemaker was implanted.
On the first postoperative day, the patient suffered another transient loss of consciousness. During this episode we observed sinus rhythm transitioning to atrial pacing by the device without a pause on telemetric monitoring. This event prompted a neurological consultation. Again, the clinical neurological exams showed no pathological findings; however during EEG, a hyperventilation provocation test triggered a focal seizure (Fig. ). Therapy with antiepileptic medication was initiated; at this time the patient’s medication list consisted of an angiotensin-converting-enzyme (ACE) inhibitor because of arterial hypertension, and both acetylsalicylic acid and a statin due to coronary artery sclerosis. He was transferred to a neurology clinic.
Subsequent neurological exams in the neurology clinic, including EEG testing for photosensitive epilepsy triggering and a hyperventilation test, as well as duplex sonography of extra- and intracranial arteries showed normal results and the patient was discharged without changes to his medications.
Six months later, the patient presented with focal seizures, aphasia, and recollection difficulties. Stage IV glioblastoma was diagnosed by CT and MRI and treated surgically (Fig. ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Diabetes history': False, 'Vascular disease history': False, 'age': [50, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 50 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
740,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-1738,Extracted,"Two days after an uncomplicated laparoscopic abdominal hernia repair, a 46-year-old man is evaluated for palpitations. He has a history of hypertension, type 2 diabetes mellitus, and a ventricular septal defect that closed spontaneously as a child. His father has coronary artery disease. Prior to admission, his only medications were hydrochlorothiazide and metformin. He currently also takes hydromorphone/acetaminophen for mild postoperative pain. He is 180 cm (5 ft 11 in) tall and weighs 100 kg (220 lb); BMI is 30.7 kg/m2. His temperature is 37.0°C (99°F), blood pressure is 139/85 mmHg, pulse is 75/min and irregular, and respirations are 14/min. Cardiopulmonary examination shows a normal S1 and S2 without murmurs and clear lung fields. The abdominal incisions are clean, dry, and intact. There is mild tenderness to palpation over the lower quadrants. An electrocardiogram is obtained and shown below.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': False, 'age': [46, 'years'], 'Congestive Heart Failure': False, 'Stroke': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 46 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 1 + 1 = 2.
The patient's CHA2DS2-VASc Score is 2."
741,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5803689-2,Extracted,"An 88-year-old retired man with arterial hypertension, chronic alcohol use, and polyneuropathy presented with left hand weakness and wrist drop upon waking up. Upon examination, he showed left-sided flaccid weakness of the hand digits, impaired wrist extension (Fig. ), decreased brachioradialis reflex, and absent Hoffmann's, Tromner's, and Babinski signs, with sensory loss on the posterior surface of the hand but preserved sensory function on the lateral and medial borders. Electromyography performed 72 h after the ictus showed that the extensor carpi radialis longus (radial nerve), the abductor pollicis brevis (median nerve), and the first dorsal interosseous (ulnar nerve) functions were intact.
Brain MRI revealed restricted diffusion in the right pre- and post-central gyrus (Fig. ). The spinal cord MRI results were normal. A carotid artery duplex scan showed less than 50% stenosis. The echocardiogram demonstrated left ventricular hypokinesia and an increased left atrial diameter (46 mm). A carotid artery duplex scan showed stenosis of less than 50%. The laboratory tests, an electrocardiogram, and a 24-hour Holter monitoring were normal. The patient was managed in the stroke unit with conservative treatment. The probable aetiology of the patient's symptoms was determined to be a cardioembolic stroke.
The sensorimotor loss resolved completely within 1 month of rehabilitation therapy, and no evidence of recurrent or new events was reported during the 6-month follow-up.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Diabetes history': False, 'Vascular disease history': False, 'age': [88, 'years'], 'Congestive Heart Failure': False, 'Stroke': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 88 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
742,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6009768-1,Extracted,"A 72-year-old woman was admitted to our hospital with a chief complaint of palpitations due to drug-refractory AF to undergo RFCA. She underwent a total right lung excision due to bronchiectasia at an age of 23 years old. Her physical examination and laboratory analysis yielded no abnormalities. Her 12 lead electrocardiogram exhibited normal sinus rhythm, but a counter clockwise rotation (Figure A). Her echocardiograms yielded no evidence of clinically overt structural and/or organic heart disease including right ventricular dysfunction and dilation, and pulmonary hypertension, and a normal ejection fraction of 70% and left atrial (LA) dimension of 30 mm. Her chest X-ray (Figure B) and computed tomography (CT) (Figure C) revealed a severely right-sided dislocation of the heart. The CT also revealed that the area of the atrial septum was small and parallel in the 40° left anterior oblique (LAO) view and perpendicular to the 50° right anterior oblique (RAO) view (Figure C). Thus, before the transseptal puncture, right atriography was performed in those views (Figure A,B). A temperature probe (SensiTherm™, St. Jude Medical, St. Paul, MN, USA) for monitoring the esophageal temperature and a guidewire were inserted and placed between the level of the left superior and inferior pulmonary veins (PVs) and in the ascending aorta, respectively. Then, a double transseptal puncture was carefully performed under guidance of an intracardiac echogram (Ultra ICE catheter; EP Technologies, Boston Scientific Corporation, San Jose, CA, USA) (Figure C). After an open irrigated 3.5-mm-tip ablation catheter (FlexAbility™, St. Jude Medical, St. Paul, MN, USA) and circular mapping catheter (Optima™, St. Jude Medical, St. Paul, MN, USA) were positioned in the LA, the LA was reconstructed by a 3D mapping system (EnSite NavX/Velocity™ Cardiac Mapping System, St. Jude Medical, St. Paul, MN, USA). The left atriography (Figure D) and EnSite voltage map (Figure E,F) revealed that the right PVs had a blind edge, but had PV potentials. The left PVs’ stenosis or occlusion might be fatal complication in this present case. Thus, to prevent those complications, a circumferential PVAI was performed and the radiofrequency energy did not deliver in the PV, especially left PVs, under electroanatomic guidance with the 3D mapping system (Figure H,I) until the achievement of bidirectional conduction block between the LA and PVs under the administration of isoproterenol (Figure G). Because the run of the phrenic nerve was unknown, the procedure was performed while confirming the diaphragmatic movement by fluoroscopy. Because firing from the superior vena cava (SVC) was induced under an intravenous administration of isoproterenol, an SVC isolation was additionally performed. Then, program stimulation could no longer induce any arrhythmias including AF. She has remained well without any symptoms or medications for 1 year after the RFCA.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
743,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6988214-1,Extracted,"A 78-year-old Japanese man presented with declining renal function, proteinuria, and hematuria. He had started to experience gross hematuria 7 months before admission. Examination by the Urology Department revealed no evidence of urinary tract neoplasia. He was therefore transferred to the Nephrology Department.
His medical history included hepatitis B virus and hepatitis C virus carrier status with an undetectable viral titer, gastric carcinoma (post-surgery), cerebral infarction, hypertension, paroxysmal atrial fibrillation, and non-tuberculous mycobacterial infection. The patient had no history of cutaneous rashes or ulcers. He was under medication with apixaban, amlodipine, losartan and febuxostat. However, to perform a kidney biopsy, apixaban was discontinued at his first visit to the Nephrology Department.
Laboratory investigations at the time of kidney biopsy are shown in Table . A serum creatinine concentration of 3.51 mg/dL corresponded to an estimated glomerular filtration rate (eGFR) of 14 mL/min/1.73m2 (revised equations for estimated GFR from serum creatinine in Japan []). The patient had anemia with a hemoglobin concentration of 7.9 g/dL. White blood cells, platelet counts and liver function were within normal ranges. C-reactive protein was 0.33 mg/dL. Serologic testing for antineutrophil cytoplasmic antibodies, antinuclear antibodies, and cryoglobulins were all negative, and C3, C4 and CH50 titers were within the reference ranges. Urinalysis showed protein (4+) and blood (3+), and 24-h urinary protein was 4.5 g. Serum and urine electrophoresis and immunofixation showed the presence of an IgG-κ band (serum IgG 1.177 mg/dL, κ/λ ratio 2.8). However, no proliferation of monoclonal plasma cells was detected in a bone marrow aspirate (only 3.2% plasma cells). Accordingly, a diagnosis of IgG-κ type monoclonal gammopathy of unknown significance was made. Additionally, computed tomography scanning revealed no evidence of malignancy.
Fifteen glomeruli were identified in a renal biopsy, three of which showed global sclerosis under light microscopy. The remaining glomeruli showed lobular accentuation of the glomerular capillary tufts with diffuse mesangial expansion. Endocapillary proliferation with neutrophilic infiltration was noted. Peripheral capillary walls were thickened and had double contours. Subendothelial deposits negative for periodic acid methenamine silver staining and positive for periodic acid Schiff (PAS) staining were observed. Cellular crescents were also present in six glomeruli. There was moderate interstitial fibrosis and tubular atrophy (50%) (Fig. a–c). There were no remarkable changes in vessels.
Immunofluorescence studies showed that C3c was dominantly positive between the capillary walls and mesangial area. Capillary walls were also positive for IgM and regions of the mesangial area were weakly positive for fibrinogen. IgG, IgA, C1q, kappa and lambda light chains were all negative (Fig. d–f).
Ultrastructural examination revealed the presence of unique subendothelial deposits characterized by randomly arranged large fibrils with large central bores and double layer structures (Fig. a, b). The mean diameter of the fibrils was 185 nm (range, 150–220 nm). These deposits resembled those described in two patients diagnosed with cryofibrinogen-associated glomerulonephritis []. In addition, diffuse foot process effacement and a mild increase in mesangial matrix were present. Electron dense deposits characteristic of C3 nephropathy and hump-like subepithelial deposits were not observed.
Cryofibrinogen was detected in this patient’s serum (Fig. ). Using prewarmed equipment, the patient’s blood was collected into both anticoagulant-free tubes and tubes containing EDTA. Both serum and plasma were prepared by centrifuging at 2000×g for 30 min at 37 °C. Serum and plasma were chilled to 4 °C for 48 h and analyzed for precipitation. Precipitate was found only in plasma, not in serum. When the precipitate was warmed to 37 °C, it redissolved. Ultrastructural examination of the cryoprecipitate revealed similar structures to the glomerular subendothelial deposits (Fig. c).
Furthermore, LC-MS/MS on laser microdissected glomeruli from paraffin sections was performed as previously described [], and revealed increased levels of fibrinogen α, β, and γ chains, fibronectin, filamin-A, and C3 (Fig. ). These substances have been detected in patients previously reported as having cryofibrinogen-associated glomerulonephritis [, ]. IgG1, IgA1, and kappa light chain were also detected at levels comparable to those in a control. There were small amounts of proteins associated with amyloidosis such as amyloid P component and apolipoprotein A. We measured the peptide concentrations of the samples by fluorometric peptide assay (Thermo Scientific, San Jose, CA, USA) prior to LC-MS/MS analysis.
A diagnosis of cryofibrinogen-associated glomerulonephritis was made on the basis of the characteristic electron microscopic findings in the glomeruli and cryoprecipitate and results of LC-MS/MS.
After diagnosis, the patient refused to receive any additional treatment, and his renal function rapidly decreased (Fig. ). He underwent hemodialysis 4 months after diagnosis. One month after the initiation of hemodialysis, he suddenly died, but an autopsy was not performed. Clinical data were extracted by electronic health record under the consent of the patient and patient’s family.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': False, 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Vascular disease history': True, 'age': [78, 'years'], 'Congestive Heart Failure': True, 'Stroke': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 78 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
744,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3914183-1,Extracted,"A 74-year-old black man with history of end-stage renal disease maintained on hemodialysis for five years, coronary artery disease, peripheral vascular disease, atrial fibrillation on anticoagulation with warfarin, pacemaker placement for symptomatic bradycardia 10 years ago, diabetes mellitus, hypertension, and colon cancer was referred to an outpatient vascular access center for thrombosed right forearm loop graft, which has been in use for three years. Thrombolysis was performed using 4 mg of alteplase and 8000 units of heparin, followed by mechanical thromboaspiration. An eighty percent stenosis at the genu of the graft was found which was dilated with a balloon catheter. No central venous stenosis was seen.
Follow-up imaging of the entire access circuit after the thrombolysis demonstrated patency of the access. The patient's vital signs were stable throughout the procedure and afterwards, and his INR prior to thrombolysis was 2.0. After completion of the procedure, the patient was noted to be lethargic and aphasic with right-sided hemiparesis.
The patient was then transferred to the emergency room of our hospital. At time of admission, his blood pressure was 150/80 mmHg, heart rate was 60 beats/minute and regular. The neurological examination was significant for dysarthria, right ptosis, occasional vertical nystagmus, dense right upper motor neuron facial paresis, left tongue deviation, and right hemiplegia. His lungs were clear and he had a grade 2/6 systolic murmur at the left sternal border. The right forearm graft had a good bruit. His electrocardiogram showed ventricular pacing. Noncontrast head computed tomography (CT) revealed a hypodensity within the left posterior parietal lobe (). A CT angiography of the brain and neck showed a small distal basilar filling defect near the left superior cerebellar artery and terminal bifurcation. The patient was not a candidate for intravenous tissue plasminogen activator due to therapeutic INR and he was past the 3-hour window.
A transthoracic echocardiogram with bubble study was performed due to strong suspicion of an embolic event, which showed right-to-left shunting, normal sized left atrium, and no evidence of intracardiac thrombus. It also revealed an elevated right ventricular systolic pressure and severe tricuspid regurgitation (an echocardiogram from 2010 showed similar findings of elevated right sided pressure and tricuspid regurgitation). A CT of the chest with pulmonary embolism (PE) protocol was not performed due to low clinical suspicion for pulmonary embolism because the patient had normal oxygen saturation on room air, no respiratory symptoms, and there were no electrocardiographic changes suggestive of pulmonary embolism.
The patient was continued on anticoagulation with warfarin. He underwent physical rehabilitation and subsequently regained some functional ability in his right upper extremity. He was discharged to a subacute rehabilitation facility, but was readmitted one month later for sepsis and died during that admission.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'Thromboembolism history': True, 'Hypertension history': True, 'Diabetes history': True, 'Vascular disease history': True, 'age': [74, 'years'], 'Stroke': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 74 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
745,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7991460-1,Extracted,"A 66-year-old female with ESRD secondary to hypertensive nephrosclerosis presented to our hospital complaining of bilateral lower extremity pain. Her past medical history included coronary artery disease, diastolic congestive heart failure, cerebrovascular disease, and chronic atrial fibrillation on warfarin for 3 years. She had progressed to ESRD and had been started on thrice-weekly HD 5 months prior to presentation. Physical examination was notable for several tender erythematous subcutaneous nodules with necrosis on her thighs and calves bilaterally (Fig. ).
The monthly biochemical data and dialysis clearance profiles are shown in Table . Her outpatient dialysis clearance was inadequate and her bone mineral parameters were uncontrolled prior to presentation. Other pertinent laboratory findings on presentation included a C-reactive protein level of 25.90 mg/L (normal, <10 mg/L) and homocysteine >50 µmol/L (normal, 5–15 µmol/L). Notably, she was taking calcium acetate as a phosphate binder and receiving intravenous paricalcitol, a 1,25-vitamin D analog, with each outpatient dialysis treatment.
She underwent an extensive investigation during the index admission for presumed CUA. A magnetic resonance imaging scan, without use of intravenous gadolinium, demonstrated areas of abnormal signal intensity within the thigh muscles highly suggestive of soft-tissue calcification. Echocardiography showed severe mitral valve calcification with restriction of both leaflets, as well as severe sclerosis of the aortic valve; both had advanced compared with echocardiography performed 6 months prior to admission. A non-iodinated contrast computerized tomography scan of the chest revealed extensive atherosclerotic calcification of the coronary arteries, mitral valve, aorta, bronchial walls, and small arteries supplying the breasts, axillae, and chest wall.
A punch skin biopsy was performed − instead of a wedge biopsy, to avoid complications such as infection, bleeding, and pain − on the periphery of the subcutaneous lesion on her left thigh corresponding to the increased signal intensity on the MRI. This yielded a mural calcification of a single deep dermal blood vessel without microvascular thrombosis, necrosis, or extravascular calcium and phosphate deposits (Fig. ).
Serial bone scintigraphy demonstrated metastatic pulmonary CUA. Five months prior to admission, a bone scintigraphy was obtained to evaluate the cause of her rib pain (Fig. ); it showed no activity in the lungs or soft tissues. The bone scintigraphy at the time of CUA diagnosis, however, demonstrated extensive increased activity throughout the lungs and lower extremities (Fig. ).
The clinical diagnosis of CUA was made based on the physical characteristics of the lesions, risk factors, and bone scintigraphy, despite having no histological evidence of microvessel thrombosis or necrosis on the punch skin biopsy. We excluded other differential diagnoses of CUA, such as warfarin necrosis, cholesterol embolization, atherosclerosis, ischemic ulcers, and early stages of nephrogenic systemic fibrosis.
After CUA was diagnosed, lanthanum carbonate (Fosrenol®) 500 mg 2 tablets with meals, in lieu of calcium-containing oral phosphate binders, was initiated to control her bone mineral parameters. Warfarin was discontinued, due to its ability to inactivate vitamin K-dependent carboxylation of matrix Gla protein (MGP). There were no alternative anticoagulants offered, since the patient was deemed at high risk for bleeding after the skin biopsy. HD was optimized to improve her dialysis clearance.
Despite adequate dialysis clearance and optimal control of bone mineral parameters, a repeat bone scintigraphy performed 1 month after the diagnosis showed no changes in metastatic CUA (Fig. ). Because of the lack of clinical improvement, we initiated treatment with STS after each HD session, beginning at a dose of 5 g intravenously with titration to 10 g. The patient did not experience gastrointestinal side effects or develop metabolic acidosis from STS. Clinically, we observed slight improvement of the localized CUA on the patient's thighs, but the metastatic pulmonary CUA on the last bone scintigraphy obtained 2 months after the diagnosis remained unchanged (Fig. ).
Severe pain from CUA and depression marked her hospital course. Poor nutrition, as evident by her low serum albumin and phosphorus, failed to heal her CUA lesions. She requested cessation of all treatment 2 months after the diagnosis, and she expired shortly thereafter. There was no autopsy performed.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'Transient Ischemic Attacks History': True, 'Hypertension history': True, 'Diabetes history': False, 'Vascular disease history': True, 'age': [66, 'years'], 'Congestive Heart Failure': True, 'Stroke': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 66 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
746,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4626627-2,Extracted,"A 53-year-old man was admitted to hospital, complaining weakness of all four limbs with dysphonia for 3 months, which deteriorated to quadriparesis in 7 days. A neurological examination revealed dysarthria with right-sided hemiplegia (Grade 0) and moderate left-sided hemiparesis (Grade 3). The patient had a history of drinking, hypertension diabetes and nonsmoking. He had three recurrent posterior circulation strokes during the past 3 months. The private MRI showed extensive brainstem and cerebellar infarct. CT angiography showed severe stenosis in left vertebral artery (V2/3 junction to V3 segment) and moderate stenosis in middle BA (Fig. A). CT perfusion showed a very poor perfusion in the posterior circulation regions (Fig. B). Before admission, the patient was given oral prescription of aspirin 80 mg daily and atorvastatin 40 mg daily for 3 months. After admission, he was given aspirin 80 mg daily, clopidogrel 75 mg daily together with atorvastatin 40 mg daily and totally 29 daily 1-h ECP treatment sessions. The right-sided limb power increased gradually over time during ECP. After completion of 29 sessions of ECP treatment, the right-sided upper limb power increased to 4 grade and lower limb power increased to 3 grade. However, the DSA still showed a high-grade stenosis of about 70% in left V3 segment and 60% stenosis in middle BA (Fig. A). A wingspan stenting was successfully inserted into the severe stenosed segment of left V3 (Fig. B). After stenting, CT perfusion showed significant improvement of cerebral perfusion over the posterior circulation regions (Fig. C). At a 30-day follow-up, his condition was stable with wheelchair walking. At a 12-month follow-up, the patient was independent (mRS ≤ 2), although he rejected to perform DSA.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [53, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Vascular disease history': True, 'Diabetes history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 53 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
747,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4190867-1,Extracted,"History of present illness: a female patient aged 75 years old, suffering from unstable walking and inaccurate hand holding for 8 months. Eight months before admission, the patient experienced unstable walking without obvious inducement and sometimes fell down, similar to being drunk. During the last 6 months before admission, she exhibited inaccurate hand holding. During the last three months before admission, she experienced limb numbness. During the last half month before admission, she felt dizziness, without nausea, vomiting, head distention, disturbance of consciousness, urinary and fecal incontinence, and tinnitus or deafness. She was diagnosed as having an aging brain using cranial CT in the outpatient clinic of Fengxian Central Hospital. She was hospitalized for further treatment. Since onset, the patient had normal appetite, normal sleep, and normal urine and stool, and did not display signs of influenza or fever.
History of past illness: hypertension, maximum 160/90 mmHg (1 mmHg = 0.133 kPa); taking Zhenjujiangya tablets.
Family history: four sisters; two had similar diseases and died from cardiovascular disease.
On admission observations were as follows: body temperature, 36.7°C; heart rate, 69 beats/minute; blood pressure, 135/85 mmHg; respiration, 20 times/minute; showing normal heart and lung function; normal abdomen examination.
Nervous system examination revealed: clear mind, equivocal language, dialogue relevant to the subject, normal orientation and possessiveness, mask-like face, two pupils of the same size with a diameter of 0.3 cm, light reflex, horizontal nystagmus, normal visual acuity, without hemianopia; symmetrical nasolabial fold, normal lifting of the soft palate, positive pharyngeal reflex; limb muscle force of grade IV, gear wheel-like increase of limb muscle tension, radial periosteal hyperreflexia, patellar tendon hyperreflexia, with physical reflex, bilateral positive Babinski sign; inaccurate nose touch, inaccurate heel-knee-tibia test, sensory disturbance of limb extremities; positive Romberg's sign; tuning fork hypopallesthesia of both limbs.
Auxiliary examination showed normal blood examination, electrolyte, cardiac troponin I, myoglobin and creatine kinase-MB isoenzyme, clotting mechanism, hepatic function, renal function, blood glucose, glycosylated hemoglobin, myocardial enzyme, blood lipid, homocysteine, stool, thyroid function and tumor index. Transcranial Doppler sonography revealed an increased blood flow resistance index. Brainstem auditory evoked potential was normal. Nerve conduction velocity: the motor conduction velocity of the right median nerve was slightly low. The sensory conduction velocities of the median and ulnar nerves were normal. The amplitude of the motor conduction velocity of the right common peroneal nerve was low. The wave form of the sensory conduction velocity of the left superficial peroneal nerve was dispersing. The frequency of the F wave of the median nerve was low. The latency of the F wave of the ulnar nerve was normal. Hoffmann's reflex of the bilateral tibial nerve was within the normal range.
Using 1.5 T permanent magnet magnetic resonance equipment (Phillips, Amsterdam, the Netherlands), the parameters of the spin-echo sequence were as follows: axial, sagittal T1 weighting (repetition time = 500 ms, echo time = 30 ms) and axial T2 weighting (repetition time = 5 000 ms, echo time = 102 ms), 5–8 mm gap, matrix 256 × 256. The plane through the midbrain aqueduct and the fourth ventricle at the cerebellomedullary cistern was designated the measurement plane. On the workstation, the following parameters were measured using computer function keys[]: (A) the distance between the midpoint of the anterior border of the cerebral peduncle and the midpoint of the midbrain aqueduct; (B) shortest distance between the midpoint of the anterior border of the pons and the floor of the fourth ventricle; (C) the distance between the midpoint of the anterior and posterior borders of the medulla oblongata; (D) shortest distance between the floor and top of the fourth ventricle; (E) shortest anteroposterior diameter of the pontine cistern; (F) anteroposterior diameter of the medullar cistern (shortest distance between the midpoint of the anterior border of the medulla oblongata and the clivus). Accuracy of the above-described indices was 0.1 mm. Each parameter was measured twice, and an average value was obtained ().
MRI displayed cerebellar and brainstem atrophy ().
A total of 3 mL of ulnar vein blood was separately obtained from the MJD patient and her son, treated with ethylenediamine tetraacetic acid anticoagulant, and stored at 4°C in the Molecule Room of Huashan Hospital. Total DNA was extracted, and the SCA3/MJD gene was amplified by PCR. Primer sequences were in accordance with reference 11 as follows: upstream: SCA3-F, 5º-CCAgTgACTACTTTg ATTCg-3º; downstream: SCA3-R, 5º-TggCCTTTCACA TggATgTg-3º. Primers were synthesized by Sangon Biotech Co., Ltd. (Shanghai, China). Total reaction volume was 25 μL: DNA extract 2 μL, 20 mM forward and reverse primers each 0.5 μL, 5 U/L TaqDNA polymerase 0.2 μL, 25 mM dNTP 10 μL, 10 × buffer solution (MgCl2 15 mM) 4 μL, R110 and R6G fluorescein-labeled dUTP 0.25 μL. These reagents were purchased from Perkin-Elmer, Fremont, CA, USA. Double distilled water was used as required. Using a PCR thermocycler (9600 DNA thermal cycler, Perkin-Elmer, USA), cycling conditions were 3 minutes at 95°C, 40 seconds at 94°C, 50 seconds at 56°C, 40 seconds at 72°C for 30 cycles, followed by 7 minutes at 72°C. An Abiprism™ 310 genetic analyzer was utilized for capillary electrophoresis and fragment length analysis using the following parameters: electrophoretic medium, POP-4 gel; electrophoresis condition, 15 kV for 24 minutes; capillary, 47 cm (length) × 50 μm (inner diameter). Using the capillary tube method for Stp-PCR, the reaction was run on a low melting point agarose gel, followed by column purification. PCR products were concentrated using a cryogenic vacuum apparatus. Results revealed an abnormal number of CAG repeats and mutation of the SCA3/MJD gene. Agarose gel electrophoresis showed an abnormal amplified band ().
By Stp-PCR sequencing, the CAG repeat number was found to be 77 in the mutated allele, which exceeded the normal range ()",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [75, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Diabetes history': False, 'Transient Ischemic Attacks History': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 75 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 6. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
748,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5816879-1,Extracted,"We present the case of a 90-year-old female with symptomatic severe AS. She described an episode of presyncope and progressive dyspnea on exertion (NYHA Class III). Medical history included hypertension, hypercholesterolemia, paroxysmal atrial fibrillation, stroke, peripheral vascular disease (PVD), and an ascending aortic aneurysm. She lived independently with Katz index of 6/6. Transthoracic echocardiogram (TTE) confirmed severe AS (mean gradient 40 mmHg; aortic valve area 0.8 cm2), concomitant moderate aortic regurgitation, and preserved left ventricular function (ejection fraction 55%).
Given the patient's severe symptoms, advanced age, and associated comorbid illnesses, the patient was considered for TAVI. Multislice computed tomography (MSCT) showed a heavily calcified, tortuous iliofemoral vasculature (minimal lumen diameter (MLD) right: 5.7 mm; left: 5.8 mm), small subclavian arteries (MLD: 4.5 mm), and a bovine aortic arch (). MSCT identified an infrarenal abdominal aortic aneurysm (AAA) (maximum diameter: 46 mm). The diameter of the ascending aortic aneurysm was 60 mm. The trileaflet aortic valve was heavily calcified (annular dimensions: mean diameter 26.4 mm; area 542 mm2; perimeter 84.4 mm) ().
The institutional Heart Team considered her to be at excessive risk for surgical aortic valve replacement (SAVR): EuroSCORE II 17.10%; Society of Thoracic Surgeons predicted risk of mortality 7.9%. A conservative management strategy was initially considered; however the patient and her family pressed for TAVI due to debilitating symptoms. Given the ascending aorta and aortic branch anatomy, a transfemoral TAVI with a surgical femoral arterial cut-down was considered to be the most appropriate vascular access route for implantation of a self-expanding transcatheter heart valve (THV). The periprocedural plan did not include transition to cardiopulmonary bypass as the patient had been declined traditional cardiac surgery by the institutional Heart Team.
Under general anesthesia, the left common femoral artery was exposed, and an 18 Fr Cook (Cook Inc., Bloomington, IN, USA) vascular access sheath was inserted just cranial to a heavily calcified arterial segment. Sheath advancement to the descending aorta was challenging, though ultimately successful (Video ). Heparin was administered to maintain an activated clotting time of >300 seconds. The stenotic aortic valve was crossed with some difficulty, and a stiff guide wire was placed in the left ventricle. Preimplant balloon aortic valvuloplasty was performed with an 18 mm NuMED balloon (NuMED Inc., Hopkinton, NY, USA) under rapid ventricular pacing. A 31 mm Medtronic CoreValve (Medtronic, Minneapolis, MN, USA) was deployed at an appropriate depth (3–6 mm), and transesophageal echocardiography and aortography suggested excellent valve function with mild paravalvular aortic regurgitation (Videos and ).
Closure of the femoral arteriotomy was performed with a 6.0 Prolene. Control femoral angiography, however, showed occlusion of the common femoral artery just caudal to the puncture site (; Video ), and an area of extensive calcific plaque was observed on the screening MSCT (). In light of the extensive calcific disease, it was deemed that percutaneous recanalization of the artery would be impossible, and a common femoral endarterectomy was performed (). The patient subsequently required further surgical exploration for ongoing bleeding and needed transfusion with 10 units of packed red blood cells. She recovered quickly and was ambulating independently on discharge to respite care (postoperative day 8).
The patient underwent routine follow-up, including outpatient review and surveillance echocardiography. Follow-up TTE at 6 months showed normal valve function, mean gradient of 6 mmHg, and mild paravalvular leak. Repeat MSCT showed a well-positioned valve, with the outflow floating in the ascending aortic aneurysm, without evidence of in situ thrombus, and no expansion of the ascending or descending aortic aneurysms (). The patient remains asymptomatic at 12-month follow-up and will continue to undergo surveillance echocardiography annually.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [90, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Thromboembolism history': True, 'Vascular disease history': True, 'Diabetes history': False}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 90 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
749,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8323361-1,Extracted,"A 75-year-old man with a 7-year history of epithelioid mesothelioma and a right sided IPC presented to the pleural clinic with a history of 2–3 weeks of a malodourous, purulent fluid drainage via the IPC. The patient was Eastern Cooperative Oncology Group performance status 0 and was under the ambulatory pleural service but managed his pleural collections independently in the community. The IPC had been inserted 3½ years ago for a right-sided loculated hydropneumothorax that had developed after a radical extended pleurectomy, decortication and diaphragmatic patch surgery for mesothelioma. The rationale for the IPC was recurrent effusions and associated infections requiring repeat chest drains in the area of the postoperative hydropneumothorax.
The patient was asymptomatic and apyrexial. The pleural fluid cultured Klebsiella oxytoca and Enterococcus faecalis. He was treated with the oral fluoroquinolone, ciprofloxacin and given advice and guidance on infection prevention strategies when handling the IPC and pleural drainage apparatus. A couple of weeks later it was decided to replace the IPC as an elective procedure due to the long duration of the IPC, a persistent low-grade purulent discharge, concerns about bacterial colonisation and history of a similar infection episode a year ago.
On the day of the procedure, the patient reported that the IPC had partially migrated out of the pleural cavity and the tunnelled subcutaneous tract due to loss of integrity of the IPC cuff and thus came out easily without any intervention. The IPC tip was sent for culture.
On clinical examination, blood pressure was 133/77 mm Hg, pulse rate was 77 beats per minute, respiratory rate was 18 breaths/min and the body temperature was 36.6°C with oxygen saturation 98% on room air. Lung auscultation revealed inspiratory crackles at the right lower lung zone. The laboratory test revealed white cell count (WCC) count 11.3×109/L, haemoglobin 108 g/L, platelets 430 x10ˆ9/L and C reactive protein 71 mg/L. Bedside thoracic ultrasound scan was consistent with a hydropneumothorax.
The same day the patient underwent an uneventful IPC insertion under local anaesthesia and mild sedation with 1 mg of intravenous midazolam. Satisfactory IPC placement was confirmed on a post procedure chest radiograph ().
One and half hours postprocedure, the patient had a witnessed sudden drop in conscious level with associated seizure like activity. The patient was immediately assessed by the cardiac arrest team where blood pressure, heart rate and oxygen saturations were maintained within the reference range throughout. Glasgow Coma Scale (GCS) was 4 (eyes opening 1, verbal response 1 and motor response 2). General examination did not demonstrate any peripheral stigmata of systemic air embolism and no retinal air bubbles were seen in funduscopic examination. An acute stroke was suspected and an urgent CT head was performed. Repeat blood tests revealed WCC 9.4×109/L, haemoglobin 107 g/L, platelet 408x10ˆ9/L, blood urea 4.0 mmol/L, serum creatinine 73 umol/L, estimated glomerular filtration rate >90, C reactive protein 70 mg/L, alanine transaminase 9 iu/L. ECG was in sinus rhythm and no ischaemic changes were noted. CT head revealed multiple serpiginous pockets of air along the cerebral fissure, with features that were highly suggestive of an embolism and multiple wedge-shaped areas of infarction involving the cerebral hemispheres (). CT chest revealed satisfactory positioning of the IPC with no aetiology for the acute deterioration (). The patient was admitted to the intensive care unit for high flow oxygen therapy and head down ventilation.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [75, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': False, 'Stroke': True, 'Transient Ischemic Attacks History': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 75 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
750,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6787157-1,Extracted,"An 87-year-old Japanese man with a history of chronic atrial fibrillation, hypertension, and aortic regurgitation status post aortic valve replacement was hospitalized for recurrent episodes of dizziness during his daily activities and exercises. His usual daily medication included warfarin (3.5 mg/day), azosemide (30 mg/day), spironolactone (25 mg/day). His 12-lead electrocardiogram showed bradycardia and atrial fibrillation. Twenty-four-hour Holter electrocardiogram revealed the total of 87 138 heart beats per day and pauses longer than 3.7 seconds in the daytime, which were considered to be the underlying cause of the recurrent episodes of dizziness (Figure ). The presence of chronic atrial fibrillation with symptomatic ventricular pause that was suggestive of transient arterioventricular block made this patient a candidate for the placement of a leadless pacemaker. The right femoral vein was punctured with the anatomical landmark method, in which the physicians firstly identify the location of arterial pulsation below an inguinal ligament and then puncture the 1 cm medial side of the site since the femoral vein usually accompanies with the medial side of femoral artery. A guide wire and a 27 French steerable sheath were inserted under fluoroscopy. The leadless pacemaker (Micra Transcatheter pacing system, Medtronic, VVI setting; 60 bpm) was then deployed successfully. Amplitude and pacing threshold were in the normal range. No major bleeding was observed/reported from the puncture site during the procedure.
After removal of the large caliber sheath, subcutaneous Z-stich was performed to achieve hemostasis. Soon after the removal of the sheath, arterial bleeding was observed from the puncture site despite manual compression after the venous sheath removal. Although bleeding from the puncture site was stopped after three hours of compression, shunt sounds on suggesting the presence of an arteriovenous fistula (AVF) were observed. Sonographic assessment was subsequently performed, and the presence of an AVF was diagnosed (Figure ).
Contrast computed tomography (CT) scan was performed to determine the cause/etiology of the fistula. CT scan revealed that the right DFA was branching off the medial side of the femoral artery 3 cm below the inguinal ligament, passing above the femoral vein (Figure ). Simultaneous presence of contrast in both artery and vein revealed an AVF. Since the patient had no apparent symptoms other than mild pain and hematoma at the puncture site, it was decided not to perform an urgent fistula closure operation. Blood testing showed an increase in serum BNP (180 pg/mL to 813 pg/mL) due to the AVF. However, during the follow-up period of six months, the patient did not complain of any symptom, such as dizziness, puncture site pain, and dyspnea related to AVF.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [87, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 87 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
751,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6369389-1,Extracted,"A 67-year-old women presented to the hospital with worsening dyspnea and cough for 4 d.
Her symptoms worsened after mild activities and relieved after rest without taking any medication.
She had a long-term history of AF.
On admission, she was fully conscious, with a blood pressure of 110/70 mmHg, an irregular heart rate of 105 bpm on auscultation and oxygen saturation of 92% on room air. She had mild edema in the lower limbs. Her weight was 58 kg and the remainder of her physical examination was normal.
Laboratory tests revealed normal platelets, hemoglobin, electrolytes, liver function markers, renal function markers (serum creatinine and estimated glomerular filtration rate), cardiac troponin-T, and routine coagulation measurements (prothrombin time [PT], international normalized ratio, and activated partial thromboplastin time [aPTT]). However, her N-terminal pro-brain natriuretic peptide was 5364.00 pg/mL (reference, < 450.00 pg/mL), D-dimer level was 5.65 μg/mL (reference, 0.001–0.50 g/mL), and PaO2 was 60.5 mmHg (reference, 80-100 mmHg). Her electrocardiogram suggested AF, and her transthoracic echocardiogram revealed a left atrial diameter of 51 mm and an ejection fraction of 48%.
Lower limb venous compression ultrasonography showed a deep vein thromboembolism (DVT) involving bilateral intermuscular veins. Furthermore, computed tomography pulmonary angiography confirmed the presence of an embolus in both upper lobes of the pulmonary artery (Figure ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Hypertension history': False, 'Thromboembolism history': True, 'age': [67, 'years'], 'Stroke': True, 'Transient Ischemic Attacks History': False, 'sex': 'Female'}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 67 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
752,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-1570479-1,Extracted,"A 24-year-old female presented a thumb-sized subcutaneous tumor mass in the right side of the pubic region for two years. Because she felt that the tumor size and the pain were gradually increasing, she consulted us for medical care. She had never been pregnant or experienced dysmenorrhea.
Manipulation in the right groin region showed that the mass was located just above the right edge of the pubic tubercle and was a 2 × 3 cm subcutaneous tumor with a slightly rough surface, unclear borderline, and mild tenderness. While no adhesion to the skin and only slight adhesion to the subcutaneous fat tissue were observed, the tumor was firmly attached to the floor without mobility. No remarkable skin region was observed. The laboratory data showed no signs of inflammation with WBC 6400/μl and CRP 0.1 and only slight anemia with Hb 11.8 g/dl. Image analysis of a pelvic CT revealed an irregular subcutaneous mass just above the right edge of the pubic tubercle with the same X-ray absorbance density as that of the muscle. The radiographic diagnosis was that of an inflammatory tumor. Consequently, as the preoperative diagnosis, we considered an inflammatory reaction of a lymph node or a dermoid cyst.
During the operation, we easily approached the mass through an incision on the medial side of the right groin region. The mass could be manually released from its adhesion to the subcutaneous fat tissue, but was firmly attached to the uterine round ligament with a poorly demarcated borderline. Therefore, we removed the tumor with a part of the uterine round ligament attached. Neither an inguinal hernia nor a sac was observed. From the macroscopic view, fat tissue was attached to the surface of the tumor. The cross section presented a whitish-yellow color with an irregular round shape; the indistinct boundary adhered to the surrounding fat tissue. Small spots containing brownish mucus were observed. The H&E staining of the removed tissue showed several small hollow glands scattered inside the tumor with a stromal structure. The hollow glands were lined with columnar epithelial layers and surrounded by proliferated stromal cells (Fig. ). Immunohistochemical analyses revealed that antibodies against CA125 (Fig. ), estrogen receptor (Fig. ), progesterone receptor (Fig. ), CD10 (Fig. ), and COX-2 (Fig. ) stained positively, but no staining of the CA19-9 antibody was observed. Although five antibodies that we chose had positive staining in the endometrial tissue, there were several differences in the degree of stainability among them. The CA125 antibody stained weakly, mainly in the inner and outer surfaces of the cytoplasm in the glandular endothelial cells, without staining the nuclei of the endothelial and stromal cells. The estrogen receptor, progesterone receptor, and COX-2 antibodies stained both in the stromal and endothelial cells. However, estrogen and progesterone receptor antibodies stained positively only in the nucleus and not the cytoplasm. The estrogen receptor antibody stained more positively in the endothelial cells than in the stromal cells, while the progesterone receptor antibody stained strongly and more positively in the stromal cells than in that of the endothelial cells. COX-2 had stained stronger in the cytoplasm and the nuclei of the endothelial cells than in that of the stromal cells. CD10 stained strongly positive in only the cytoplasm of the stromal cells. These findings indicated that the tumor that had adhered to the uterine round ligament had originated from the endometrial tissue.
After the operation, we consulted an obstetrician and a gynecologist. Neither uterine adenomyosis nor pelvic endometriosis was detected using manipulation, ultrasound examination, and MRI scan. The serum CA125 level was 19.9 U/ml, which is within the normal range. No recurrence of the tumor was observed one year after the operation.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [24, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 24 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
753,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7873810-2,Extracted,"An 81-year-old male presented to the emergency department after being found collapsed. He was delirious, pyrexial, and dyspnoeic. Five years prior to this, he had undergone bioprosthetic AVR and CABG, for critical aortic stenosis and significant coronary artery disease.
His medical history also included: moderate left ventricular systolic dysfunction (LVSD), psoriasis, and iron deficiency anaemia.
Medications included: furosemide 40 mg BD, lansoprazole 30 mg OD, atorvastatin 80 mg OD, saubitril/valsartan 49/51 mg BD, bisoprolol 1.25 mg OD, epleronone 25 mg OD, ferrous Sulphate 200 mg BD, and aspirin 75 mg OD.
At presentation, the blood pressure was 78/60 mmHg, heart rate 120 b.p.m., respiratory rate 38 b.p.m., oxygen saturations 77% on air, and he had a temperature of 37.8°C. On physical examination, he appeared breathless at rest, had bi-basal fine crepitations, a soft systolic murmur, and bilateral pitting oedema. Initial laboratory investigations revealed a haemoglobin of 113 g/L, white cell count of 11.14 × 109/L (neutrophil count 9.81 × 109/L), C-reactive protein 150 mg/L, creatinine 506 μmol/L (eGFR 9 mL/min; baseline creatinine 100–160 μmol/L), and creatinine kinase 74 U/L. Twelve-lead electrocardiogram (ECG) showed 1st degree heart block and old left bundle branch block.
The admission differential diagnosis was broad; however, the presence of sepsis in the context of cardiac valve surgery and new 1st degree heart block made infective endocarditis and possible aortic root abscess the primary concern.
Urgent echocardiography showed severe LVSD, although no clear evidence of endocarditis or valvular vegetations. The overall impression was that of decompensated heart failure with reduced ejection fraction, secondary to sepsis of unknown source. The patient was urgently transferred to the intensive care unit (ICU) for inotropic support and haemofiltration.
Three peripheral blood cultures returned positive for Klebsiella pneumoniae, a Gram-negative bacterium. Treatment with intravenous Piperacillin with Tazobactam was initiated. A CT abdomen and pelvis did not reveal a specific source for the Gram-negative bacteraemia.
After initially stabilizing in ICU for several days, the patient deteriorated again with worsening dyspnoea and evidence of decompensated heart failure. Serial laboratory investigations revealed rising inflammatory markers. A repeat CT scan of the thorax, abdomen, and pelvis showed new occlusion of the superior mesenteric artery and right lower lobe pneumonia. Repeat transthoracic echocardiogram was organized due to the identification of a new petechial rash, a new harsh systolic murmur, and lengthening PR interval on ECG. This demonstrated a complex aortic root lesion, with aortic valve dehiscence and RA septal wall vegetations (Figure ). On colour flow mapping, there was communication between the LV and RA—the Gerbode defect (Figure ).
Transoesophageal echocardiogram and CT of the aortic root were arranged, however, the patient deteriorated rapidly before these were completed. Following discussion with the patient and his family, the decision was made for symptom control and palliative management. He died peacefully shortly after.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [81, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 81 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
754,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5618982-1,Extracted,"An 83-year-old right-handed woman presented at the emergency room reporting a
90-minute history of sluggish speech and left side weakness. Her past medical
history was marked by hypertension and hypercholesterolemia. The initial neurologic
examination showed left side facio-brachio-crural paresis, left hypoesthesia,
dysarthria and left side extinction on double tactile and visual stimulation.
Approximately 20 minutes later, she developed massive neglect of her left side,
being able only to describe the pictures localized on the right side of the “cookie
theft picture”. She preferred right side gaze spontaneously, but there was neither
sustained conjugate eye deviation nor gaze palsy. Extrinsic ocular movements were
full on smooth pursuits and hemianopsia was not present. The National Institute of
Health Stroke Score (NIHSS) was 7.
Computed tomography (CT) of the brain was normal on initial evaluation, but a
conjugated rightward shift of the eyes, or “eyes sign”, was present. (). Intravenous rt-PA was administered 180
minutes after the onset of symptoms. The patient made an almost full recovery,
remaining only with a mild flattening of the naso-labial fold and asymmetry on
smiling (NIHSS of 1). At follow up 24 hours later, brain magnetic resonance imaging
(MRI) confirmed an infarct in the right insular subcortical region (subinsular
territory) (). Despite recovering from
hemispatial neglect, the patient remained unaware of her recent stroke and slight
neurological deficits (anosognosia). Initially she denied any neurologic problem.
After receiving an explanation concerning the illness, she accepted the fact she had
suffered a stroke, although this appeared to have had little impact on her behavior.
The patient remained free of hemispatial neglect at the follow up visit.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [83, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Diabetes history': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 83 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 6. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
755,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5353419-1,Extracted,"A 68-year-old woman with a history of rheumatic mitral stenosis and atrial fibrillation presented with dyspnea NYHA class III, palpitations, and ankle edema for 3 months. She had worsened during the past 6 days. She had been diagnosed with rheumatic mitral stenosis 30 years back, on irregular follow-up and not compliant with injectable penicillin. Physical examination revealed a blood pressure of 100/80 mm Hg and an irregular heart rate of 136 beats/min. Auscultation revealed a loud S1 at the apex, a diastolic rumble at the apex, and a holosystolic murmur at the lower left sternal border. Chest radiography revealed a marked cardiomegaly with a cardiothoracic ratio of 95% suggesting massively dilated right atrium (RA) and left atrium (LA).
Two-dimensional echocardiogram [Figures and ] revealed a giant LA measuring 15.2 cm × 10.1 cm, an area of 170 cm2, and a volume of 1326 mL. RA was 13.1 cm × 7.05 cm, with a volume of 760 ml. The mitral valve was thickened with a planimetered mitral valve area of 1.2 cm2. The mean LA-left ventricular diastolic gradient was 4.5 mm Hg. The left ventricular size was small with an ejection fraction of 60%. The right ventricle was small with right ventricular dysfunction which was evident from a reduced tricuspid annular plane systolic excursion of 10 mm and a right ventricular ejection fraction of 35%. Tricuspid valve was thickened with noncoaptating leaflets and severe tricuspid regurgitation as evident from vena contracta width of 0.8 cm and hepatic vein systolic flow reversal [Video –].
The patient was stabilized with intravenous furosemide, amiodarone, oral digoxin, warfarin, and spironolactone. The patient did not consent to surgery and hence was discharged home after medical stabilization.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [68, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 68 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
756,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7263103-1,Extracted,"A 78-year-old male, originally from China, with a past medical history of hypertension, diabetes, paroxysmal atrial fibrillation, and a stroke with residual left-sided deficit and waxing and waning mental status was brought to the hospital for weakness, urinary incontinence, confusion, and poor oral intake. On the day of his presentation, the patient was noted to appear weak on the left side more so than at baseline. The patient was brought to the emergency department as a stroke code; computed tomography (CT) scan of the head ruled out acute stroke. Vital signs were significant for a heart rate of 94 beats per minute and respiratory rate of 31 breaths per minute. The patient was admitted to the hospital for sepsis and workup for possible toxic, metabolic, or infectious insults leading to recrudescence.
The patient was started on empiric antibiotics, which were narrowed when blood cultures revealed gram-negative bacteremia speciating to Klebsiella pneumoniae, ampicillin-resistant, but sensitive to ceftriaxone. A CT scan of the abdomen and pelvis demonstrated the presence of a large cystic region with air-fluid level in the left lobe of the liver ( and ). Under the suspicion that this lesion was the source of the patient’s bacteremia, the patient underwent percutaneous drainage of the lesion by Interventional Radiology, which produced 80 cc of purulent fluid, also growing ampicillin-resistant, ceftriaxone-sensitive Klebsiella pneumoniae. While a stool ova and parasite examination on the patient was negative, further workup revealed that the patient was positive for Entamoeba histolytica antibody in the serum, detected via enzyme-linked immunosorbent assay and indicative of either current or prior infection. The patient had lived in the United States for several years, had no recent travel history and, to the knowledge of his family, had never been diagnosed or treated for E histolytica infection in the past; as such, he was started on metronidazole and paromomycin for extraluminal amoebic infection after completing the course of ceftriaxone to treat what appeared to have been a superimposed bacterial infection of a previously subclinical amoebic liver abscess (ALA).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [78, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': True, 'Thromboembolism history': True, 'Vascular disease history': False, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 78 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
757,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8449517-1,Extracted,"An 86-year-old male presented to our emergency department (ED) with complaints of shortness of breath (SOB) and dyspnea on minimal exertion. The patient had a past medical history significant for chronic obstructive pulmonary disease (COPD), congestive heart failure with preserved ejection fraction, and atrial fibrillation on anticoagulation with warfarin, hypertension, dyslipidemia, a cerebrovascular accident without any residual deficits, seizures, benign prostatic hyperplasia (BPH), and a recently diagnosed left lower extremity DVT. The patient presented via EMS to our emergency department from home as a “CPAP alert.” The patient was placed on CPAP en route to the hospital because, at home, he had a SpO2 of 77% on room air and was notably short of breath. The patient’s respiratory status rapidly improved with CPAP and upon arrival to the ED, he was placed on supplemental oxygen via nasal cannula at 4 liters per minute and was saturating well with SpO2 of 98%. Upon further history, the patient endorsed dyspnea, in addition to left leg pain and swelling for the past month. He did not seek earlier medical care secondary to other issues at home. He also reported intermittent abdominal pain associated with eating as well as watery diarrhea for the past month. He denied fever, chest pain, nausea, vomiting, syncope, or any other complaints on review of systems.
In the ED, the patient was found to have a left lower extremity DVT, bilateral pulmonary embolism diagnosed by CTPA, as well as a left atrial appendage thrombus (Figures -).
Labs were significant for a supratherapeutic INR of 7.5 and an elevated activated partial thromboplastin time (aPTT) of 54.7 seconds. Also, N-terminal proBNP levels were elevated at 2831 pg/ml, troponin-I was not elevated. Twelve-lead ECG showed atrial fibrillation with a normal rate. A cardiologist was consulted, who recommended initiation of subcutaneous enoxaparin despite a supratherapeutic INR and vitamin K reversal with oral phytonadione. The plan included transitioning the patient to a direct oral anticoagulant (DOAC), such as apixaban, prior to discharge. Hematology was consulted to weigh in on the evaluation of this hypercoagulable state despite being appropriately anticoagulated with warfarin. The patient was admitted to the cardiovascular ICU in stable but guarded condition.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [86, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': True, 'Diabetes history': False}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 86 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
758,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2533017-1,Extracted,"An 88-year-old man presented with a 6-month history of dysphagia for solid foods and significant weight loss. He denied any symptoms of odynophagia. He denied any hoarseness of the voice, neck pain or breathlessness. There was no change in bowel habit or blood in the stools. His calorific intake was solely dependent on protein supplement drinks. His previous medical history was of type 2 diabetes, hypercholesterolaemia, hypertension, atrial fibrillation and glaucoma.
On examination he was cachetic and pale. His weight was 54 kg. The rest of his physical examination was unremarkable. His full blood count showed a normocytic anaemia (10.3 g/dl) with a normal ferritin level. Liver function was normal apart from an albumin of 28 g/l. Erythrocyte sedimentation rate and thyroid stimulating hormone were normal. An endoscopy was performed to exclude an intrinsic cause for the patient's symptoms. This showed chronic atrophic gastritis but no cause for the dysphagia. Video fluoroscopy was performed which showed a bony prominence impeding swallow at the level of C3. A lateral cervical spine radiograph showed anterior osteophyte formation, most marked at the C3/C4 vertebrae and consistent with DISH (Figure ).
He was commenced on nasogastric feeding, as there was evidence of aspiration on video fluoroscopy. He was referred to the spinal surgeons but they did not feel surgery was appropriate due to the patient's frail condition and comorbidities. A percutaneous endoscopic gastrostomy tube was placed 3 weeks later. The patient died 6 weeks after admission, from complications secondary to an unrelated septic arthritis of the shoulder.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': False, 'age': [88, 'years'], 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False, 'sex': 'Male'}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 88 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
759,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5643875-1,Extracted,"A 78-year-old man presented to the emergency department of Sina Hospital, Tehran, Iran, with complaints of pain and coldness of the left lower extremity, which had suddenly occurred at 11 a.m. On arrival at our emergency department at 2 p.m., he was conscious. Bradycardia (heart rate = 45/min) and high blood pressure (165/80 mmHg) were detected. The respiratory rate and temperature were normal. On examination, the left lower extremity was cold. The left femoral artery pulse was detected, but the pulses of the left popliteal, dorsalis pedis, and posterior tibialis arteries were absent. Impaired sensory examination was noted. The muscle force of the left lower limb was 4/5. At baseline, laboratory tests revealed hemoglobin of 13.4 mg/dL, platelet of 294,000 cells/µL, white blood cell of 8,100 cells/µL, urea of 24 mg/dL, and serum creatinine of 1.06 mg/dL. Arterial blood gas showed no significant abnormal findings. Electrocardiography revealed sinus bradycardia. On color Doppler sonography of the left limb, the common femoral artery had high resistance and stenotic blood inflow as far as 2 centimeters above the bifurcation of the common femoral artery. No blood inflow was detected in the superficial and deep femoral, popliteal artery, and anterior and posterior tibialis arteries. A mildly hyperechoic thrombosis was seen in the superficial and deep femoral arteries. The findings were suggestive of acute arterial obstruction.
While the patient was under observation in the emergency department, he had a sudden onset of loss of consciousness and left hemiplegia. On examination, the pupils were normal in size and reactive to light. Aphasia and facial asymmetry were noted. The upper and lower left limbs were plegic. After neurology and cardiovascular consultation, echocardiography and brain computed tomography (CT) scan were done. Echocardiography revealed a large mobile mass in the left atrium protruding into the left ventricle (). Brain CT scan was negative for neurological findings; therefore, brain magnetic resonance imaging (MRI) without contrast was requested. On MRI, an abnormal bright signal in the periventricular white matter in both cerebral hemispheres in favor of microvascular ischemic changes was reported. In addition, acute infarction was detected in the right insula, external capsule, putamen, and caudate nucleuses (). After primary treatment, angiography was performed; it demonstrated a normal inflow in the right and left iliac arteries and the aorta. A cutoff was shown in the proximal portion of the common femoral artery, and runoff was reported in the deep femoral artery and the proximal portion of the superficial arteries. Subsequently, the patient underwent emergent surgery.
After local anesthesia, an incision was made over the left inguinal area. Thrombectomy was performed with a Fogarty catheter (3, 4 French). A fatty-like mass from the bifurcation of the common femoral artery and a thrombotic mass from the proximal portion of the superficial and deep femoral arteries were removed. The pulsatile inflow and palpable pulses of the left femoral, popliteal, dorsalis pedis, and posterior tibialis arteries were restored after surgery. The specimen was sent to the pathology center of Sina Hospital. The histological findings of the embolus were suggestive of a cardiac myxoma (). The patient was referred to the cardiac surgery department for further evaluation and treatment. After open-heart surgery, the patient was hospitalized for 10 days in the intensive care unit. Gradually, the patient’s consciousness and lower limb blood flow improved. He was discharged from the hospital with full awareness and improved lower extremity muscle function 2 weeks after surgery.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [78, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Thromboembolism history': True, 'Vascular disease history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 78 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
760,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6681501-1,Extracted,"The patient was a 69-year-old Hispanic man with no family history of cardiovascular or hematological diseases. He was a heavy smoker with a history of 15 pack-years. He was retired and not an alcoholic. He had a history of arterial hypertension, revascularized ischemic heart disease, and aortic valve replacement 10 years earlier, in addition to five coronary stents, chronic peripheral arterial disease of the lower limbs, and an aneurysm of the infrarenal aorta and left primitive iliac artery (Fig. a, b). He underwent endovascular surgery with an Endurant II stent (Medtronic, Minneapolis, MN, USA) and a successful right hypogastric artery embolization (Fig. a–d). There were no complications in the postoperative period; he received ambulatory anticoagulant therapy with low-molecular-weight heparin and subsequent change to warfarin, but with little adherence to the initial treatment. In addition, he received atorvastatin 40 mg daily, acetaminophen 1 g every 8 hours, clonidine 150 mg every 8 hours, losartan 50 mg every 12 hours, nimodipine 60 mg every 4 hours, phenytoin 300 mg/night, and bisacodyl 10 mg daily. He did not receive any antibiotics before the surgery; after the surgery, he received norfloxacin 400 mg every 12 hours for 7 days to treat a urinary tract infection.
Two months after surgery, he was admitted to the emergency room with blood pressure of 97/52 mmHg, heart rate 79 beats/minute, respiratory rate 20 breaths/minute, and temperature of 36 °C. He presented with sudden pain in his lower left limb with signs of ischemia (absence of popliteal and pedis pulses, paleness and coldness of the extremity, motor and sensitivity loss), a partially normal neurological examination regarding orientation, with compromise of superficial and deep sensitivity of the lower limbs. He had laboratory test results of white blood cell count of 15,2 x10^3/uL, neutrophils 82%, lymphocytes 17%, hemoglobin 15.2 g/dL, hematocrit 44.5%, platelets 154 x10^3/uL, blood urea nitrogen 14.3 mg/dL, creatinine 0.87 mg/dL, and initial international normalized ratio (INR) in subtherapeutic range (INR 1.05–1.95). He was diagnosed with an exacerbation of his chronic peripheral arterial disease with an arterial duplex of his lower limbs, showing moderate atheromatous process of lower limb arteries, with acute left femoral popliteal artery occlusion from its origin extending to the anterior and posterior tibial arteries and pedis artery. The patient was initiated on intravenous unfractionated heparin (UFH) and dual antiplatelet therapy achieving anticoagulation goals with subsequent gradual improvement of limb ischemia. After 48 hours of observation, he had a sudden pain in his lumbar region associated with absence of sphincter control and loss of strength of his lower limbs with a Medical Research Council scale score of 0/5 (complete paralysis). Contrast-enhanced magnetic resonance imaging (MRI) was performed, which revealed extensive dorsal myelopathy from T3–T4 to T11–T12 (Fig. a–d) of compressive and/or ischemic nature, and extensive spinal cord infarction was determined. Twenty-four hours later, despite the established antihypertensive treatment, he presented with a hypertensive emergency with acute target organ damage. Anti-ischemic management was initiated, and it was decided to stop heparin due to possible excessive anticoagulation. During the evolution of this presentation, he had headaches; hence, cerebral computed tomographic angiography was performed, which showed supra- and infratentorial intraparenchymal hemorrhage and thalamic hematoma. An intensive care unit stay as well as rehabilitation for the subsequent management of his symptoms and stabilization of comorbidities was required.
After commonly agreeing with the family, he was discharged for home healthcare planning. When discharged, the patient’s pure motor deficit in his lower extremities persisted, along with absence of sphincter control and presence of mild cognitive impairment, specifically in memory. Seven months after outpatient treatment, with progressive worsening of complications of his disease with depression, recurrent infections, and skin ulcers, the patient died.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [69, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': True, 'Stroke': False, 'Diabetes history': False, 'Transient Ischemic Attacks History': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 69 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
761,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-7836,Extracted,"A 73-year-old woman arrives at the emergency department due to intense central chest pain for 30 minutes this morning. She says the pain was cramping in nature and radiated down her left arm. She has a history of atrial fibrillation and type 2 diabetes mellitus. Her pulse is 98/min, respiratory rate is 19/min, temperature is 36.8°C (98.2°F), and blood pressure is 160/91 mm Hg. Cardiovascular examination shows no abnormalities. ECG is shown below.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [73, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 73 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
762,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8559208-1,Extracted,"The patient of interest is a 59-year-old man with history of ascending aortic aneurysm, atrial fibrillation, congestive heart failure with a reduced ejection fraction, bilateral lower extremity venous stasis ulcers, stage 3 chronic kidney disease, and multinodular goiter. The patient was brought to the emergency department by ambulance following a ground-level fall while ambulating in his home. At the time of the fall, the patient stated he felt his heart racing, but denied dyspnea, chest pain, or loss of consciousness. The patient noted the deterioration of his health in the prior month during which time he stated that he was unable to properly care for his bilateral lower extremity wounds. The patient frequently attempted to clean his wounds with water and a washcloth during his daily bandage changes.
On presentation to the emergency department, he was found to be in septic shock with blood pressure of 84/53 mm Hg, heart rate of 124 beats per minute, and lactate of 3 mg/dL. His physical examination was remarkable for 3 lower extremity ulcers below the knee. On the right extremity, the patient had 2 medial ulcers measuring 8 × 5 cm (depth to the muscle tissue) and 6 × 3 cm. On the left extremity, he had 1 medial ulcer measuring 8 × 5 cm (depth to the muscle tissue). All 3 ulcers had necrotic skin and subcutaneous tissue manifested with maggots.
Initial laboratory values were also significant for C-reactive protein (CRP) of 6.97 mg/L, creatinine of 3.54 mg/dL, elevated troponin of 0.06 ng/mL (which subsequently increased to 9.8 ng/mL), and elevated white blood cell (WBC) count of 14.8 × 103 cells per mL with 83.6% neutrophils. Electrocardiogram (ECG) showed atrial fibrillation with rapid ventricular rate. Chest X-ray showed an enlarged heart with a tortuous aorta. X-ray imaging of the tibia and fibula was negative for osteomyelitis but showed bilateral areas of subcutaneous gas formation suspicious of a gas-forming organism.
The patient was admitted to the intensive care unit (ICU) for treatment of septic shock and non-ST elevation myocardial infarction. Sepsis bundle was initiated with careful fluid resuscitation due to his heart failure and vasopressor support with norepinephrine. On admission, 2 sets of blood cultures from separate sites and a urine culture were obtained prior to the initiation of antibiotic treatment. He was then started on broad-spectrum antibiotics for focused coverage of skin and soft tissue infection with vancomycin and piperacillin/tazobactam. Acute coronary syndrome protocol was initiated given the patient’s elevated troponins along with amiodarone for treatment for chronic atrial fibrillation refractory to digoxin. The patient was subsequently taken to the operating room for debridement of bilateral lower extremity necrotic skin and soft tissue. Thorough debridement demonstrated that muscle tissue was not involved.
On the first set of blood cultures, both the aerobic and anaerobic bottles grew gram negative rods and gram positive cocci resembling Staphylococcus species which were ultimately identified as S fonticola and methicillin-sensitive Staphylococcus aureus (MSSA). Of the second set of blood cultures, only the aerobic bottle grew gram negative rods resembling enterics which were ultimately identified as S fonticola. S fonticola was resistant only to amoxicillin/clavulanate (). Urine culture was unremarkable. On completion of blood culture susceptibility results, on the fourth day of hospitalization, vancomycin was discontinued and piperacillin/tazobactam was de-escalated to ceftriaxone.
Cardiac echocardiogram demonstrated dilation of all cardiac chambers with mild concentric left ventricular hypertrophy. Left ventricular systolic function was severely depressed with an estimated ejection fraction of 15% to 20%. Diastolic function was unable to be assessed due to atrial fibrillation. The patient was also noted to have abnormal septal motion secondary to bundle branch block with abnormal regional wall motion due to underlying coronary acute disease and myocardial infarction. The right ventricle was noted to be moderately dilated with mild to moderate reduced right ventricular systolic function with systolic pressure of 45 mm Hg and moderate tricuspid regurgitation.
On improvement and transfer from ICU to regular unit, transesophageal echocardiogram (TEE) was performed which demonstrated severe left ventricular systolic dysfunction with an ejection fraction of 15% to 20% and severe low-flow low-gradient aortic valve stenosis. In addition, TEE demonstrated a mitral valve vegetation measuring less than 1 cm attached to the posterior annulus (). A mobile echo density measuring 0.8 × 1.6 cm consistent with a thrombus was also seen in the left atrium. The source of infection leading to the infective endocarditis was determined to be the patient’s chronic bilateral lower extremity skin infection. The patient also underwent cardiac catheterization which revealed severe 2 vessel coronary artery disease.
In consultation with infectious diseases, ceftriaxone was changed to cefepime in the milieu of infective endocarditis, due to increased incidence of inducible amp-C beta-lactamase production among Serratia species with use of ceftriaxone.
 For effective treatment of infective endocarditis, the duration of cefepime treatment was determined to be 6 weeks due to low suspicions of coinfection with MSSA.
The patient was discharged to a skilled nursing facility to complete intravenous antibiotic therapy and obtain appropriate wound care. The patient had an uneventful recovery after completing 6 weeks of antibiotic therapy. Further outpatient management included a multidisciplinary approach with cardiology, nephrology, and infectious disease in addition to primary care.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [59, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 59 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
763,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4000642-5,Extracted,"A 65-year-old male with a past medical history of end stage renal disease status after kidney transplant, atrial fibrillation, and hypertension presented to the emergency room with complaints of abdominal pain for one week. He was known to have a failed kidney transplant at the time of admission as per his outpatient visit records. The suspicion for an infection or infarction of the kidney graft was high based on the patient being on immunosuppressant medications and having atrial fibrillation, respectively. His laboratory data are presented in . No urine was available for analysis as the patient was a hemodialysis patient. Blood cultures were negative. A CT of the abdomen and pelvis showed an edematous transplanted kidney with air in the intraparenchymal region and the urinary bladder (). The patient also had a small bowel obstruction. Early goal directed therapy with fluids and antibiotics was started. He was started on empiric IV Unasyn (). The concern for a more fulminant EPN was high and the patient was taken to the operating room for an emergent transplant nephrectomy and hemicolectomy with small bowel resection. Postoperatively the patient developed acute respiratory failure secondary to Acinetobacter pneumonia and had to be admitted to the intensive care unit (ICU) service. He was started on IV Imipenem to which he responded with resolution of his pneumonia. He developed an ileus and required a course of total parenteral nutrition. In the ICU the patient developed Clostridium difficile colitis. He was successfully treated for Clostridium difficile colitis with oral Vancomycin. He made complete clinical recovery and was transferred to the medical floor where his clinical course was eventful for resolution of cough, dyspnea, fever, diarrhea, and abdominal pain. He was discharged on a course of IV Imipenem and IV Unasyn to complete a total of 14 days.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [65, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
764,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-9242,Extracted,"A 77-year-old man presents to the emergency department complaining of feeling like “his heart was racing” for the last 8 days. He denies any chest pain, dizziness, or fainting but complains of fatigue, difficulty breathing with exertion, and swelling of his legs bilaterally for the last 2 weeks. He has had hypertension for the last 25 years. He has a long history of heavy alcohol consumption but denies smoking. His blood pressure is 145/70 mm Hg and the pulse is irregular at the rate of 110/min. On examination of his lower limbs, mild pitting edema is noted of his ankles bilaterally. On cardiac auscultation, heart sounds are irregular. Bibasilar crackles are heard with auscultation of the lungs. An ECG is ordered and the result is shown in the image. Transesophageal echocardiography shows a reduced ejection fraction of 32% and dilatation of all chambers of the heart without any obvious intracardiac thrombus.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [77, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
765,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6624151-1,Extracted,"A 55-year-old man with a history of type II diabetes mellitus, hypertension, obstructive sleep apnea, and depression developed pleuritic chest pain and shortness of breath, and had a syncopal episode during a car trip from Texas to Cleveland. In the emergency room (ER), his blood pressure was 120/83 mmHg, pulse 119/min, respiratory rate 22/min, temperature 36.6oC, and oxygen (O2) saturation was 93% on room air. Physical exam was notable for an obese male in no acute distress with tachycardia, regular rhythm, clear lungs, shallow breaths without accessory muscle usage, and mild epigastric tenderness. His electrocardiogram (ECG) demonstrated sinus tachycardia at 117 bpm with a deep S wave in lead I, a small Q wave and inverted T wave in lead III (Figure ).
Initial laboratory testing was significant for serum sodium 132 mmol/L, creatinine 1.6 mg/dL, ProBNP 3188pg/mL, and initial troponin 0.12, peaking at 0.2 on hospital day two. Computed tomography (CT) chest showed bilateral submassive pulmonary emboli in multiple branches of the right and left upper and lower lobe pulmonary arteries, with no indication of a saddle embolus or main pulmonary artery thrombus (Figures -).
The patient was started on an intravenous (IV) heparin drip and thrombolytics were deferred due to perceived hemodynamic stability and timing of presentation. While in the ER, he became more tachycardic with heart rate 130-140 bpm, and developed jugular venous distention and acute hypoxemia requiring 3 liters (L) nasal cannula to maintain normal O2 saturation. He was admitted to the medical intensive care unit (MICU) due to possible signs of acute decompensation.
In the MICU, ultrasound revealed a right popliteal deep vein thrombosis (DVT); an inferior vena cava filter was considered, but the patient was considered hemodynamically stable and placement of a filter was deferred. Over the second and third hospital days, he remained tachycardic at 105-130/min with blood pressures in the 110/80 mmHg range and stable O2 saturations on 3L per nasal cannula. Transthoracic echocardiogram revealed right ventricular strain and a mobile structure in the right atrium, possibly consistent with thrombus. On hospital day four, he remained hemodynamically stable but experienced mild pleuritic chest pain and shortness of breath. On hospital day five, the patient was switched from IV heparin to enoxaparin 120 mg twice daily with a two-hour overlap; he was noted to have a transient O2 desaturation but remained normotensive. In the early hours of day six, he became diaphoretic and developed sustained tachycardia at 140/min with a blood pressure of 100/70 mmHg. He then developed chest pain and worsening dyspnea and lethargy, and was found to be in atrial flutter with 2:1 block. In the early afternoon, while speaking with the medical team and later while working with physical therapy, the patient complained of worsening shortness of breath, and was noted to be diaphoretic and persistently tachycardic at 120/min. Shortly thereafter, he lost consciousness and was found to be in cardiac arrest. He was treated per advanced cardiac life support (ACLS) protocol with temporary restoration of circulation, but became asystolic and was pronounced dead after 30 minutes.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [55, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': True, 'Vascular disease history': False, 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 55 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
766,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6367120-1,Extracted,"A 47-year-old Caucasian male with a past medical history of uncontrolled diabetes mellitus, hypertension, gastroesophageal reflux disease, and anxiety presented to the emergency department with a chief complaint of right foot swelling. The patient reported that the swelling started two weeks prior to the presentation but denied any associated pain. The patient denied injury or trauma to the foot. An X-ray of the right foot revealed old fracture deformities but no evidence of an acute osseous lesion. A lower extremity Doppler ultrasound was performed and ruled out the presence of deep vein thrombosis (DVT). The patient also endorsed dysuria, dribbling, and urinary retention over the previous day but adamantly refused placement of a catheter. When the patient was told that he would be discharged from the emergency department, he began complaining of chest tightness, shortness of breath, and nausea, all of which he denied on a review of symptoms during the initial evaluation. He stated that the chest discomfort had been present all day, was non-radiating, and rated at a 4/10 in severity. Electrocardiography (EKG) and cardiac enzymes were within normal limits. The patient was admitted for further evaluation.
During the hospitalization, the patient developed multiple additional complaints that after appropriate workup, ultimately did not lead to a specific diagnosis. The patient worked with physical therapy and occupational therapy, which established that the patient was difficult to assess, as his functional mobility issues were inconsistent. He was noted to have deficits in balance, endurance, and safety awareness, which affected the patient’s ability to perform the activities of daily living. Of note, one of the physical therapists documented that the patient was witnessed alone in his room, walking without difficulty while texting on his phone.
On hospital day four, the patient was displeased when told that he was being discharged, as he desired further workup for his complaints. While preparing to leave, he had an unwitnessed fall in his room. The patient stated that he hit his head and was in pain but was unable to localize the pain. There was no evidence of acute trauma on physical exam. Regardless, the fall prompted a computed tomography (CT) scan of the brain without contrast to rule out any acute intracranial trauma. Incidentally, the CT scan revealed bilateral symmetric calcifications of the basal ganglia, putamen, caudate, thalami, dentate nuclei of the cerebellum, and cerebral white matter, consistent with Fahr's disease (Figure ). Laboratory values, such as parathyroid hormone (PTH), thyroid stimulating hormone (TSH), T3, and T4, were all within the normal reference limits. Serum calcium was mildly decreased, ranging from 8.1 - 8.4 mg/dL during the admission. After being informed of the CT scan findings, the patient revealed that his deceased mother suffered from a rare diagnosis. Further investigation, with the patient's permission, revealed a prior CT scan with similar calcifications in the basal ganglia and cerebellum, consistent with Fahr's disease.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [47, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 47 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 1 + 1 = 2.
The patient's CHA2DS2-VASc Score is 2."
767,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2396650-1,Extracted,"A 63-year-old man presented to the Accident and Emergency department with a history of mild frontal headache and progressive right-sided weakness. He was on bendrofluazide and atenolol for hypertension which was controlled.
On examination, he was fully conscious and haemodynamically stable with a pulse of 65 beats per minute and blood pressure of 105/72. Systemic examination was normal. Power was 3/5 in the right arm and leg with the right plantar reflex upgoing. There was progression of neurological signs 24 hours after admission, until the power was 0/5 in the affected limbs with mild slurring of speech 72 hours later. There was no evidence of fluctuating neurological signs. His higher mental functions were intact throughout his hospital admission. The electrocardiogram confirmed sinus rhythm at 60 beats per minute. The chest X-ray was unremarkable.
He was admitted and underwent an urgent computed tomography (CT) scan of the brain. The initial CT (Figure ) was performed 6 hours after the collapse. The hospital had access to a magnetic resonance imaging (MRI) scanner once a week and the next available slot was 6 days later. During the weekend following admission he was transferred to the stroke unit and reviewed twice daily. His neurological deficits deteriorated stepwise with 2/5 power in his right arm and leg at 36 hours progressing to 0/5 with mild slurring of speech around 72 hours post admission on Monday. There were no features suggestive of raised intracranial pressure. He had no altered sensorium. His case was discussed with the radiologist and the medical physician on call during the weekend. It was felt there was no need for an urgent repeat scan and all agreed the progression was likely to be due to the stroke. The radiologist reviewed the initial scan over the weekend and had no concerns about the calcified area, which was judged less likely to be a bleed, although this could not be ruled out. The decision was to perform a scan on Monday morning to confirm that the deterioration was due to the stroke and the suspected calcified area was not a bleed.
A repeat CT brain scan was performed after the weekend on the third day after admission (Figure ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [63, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 63 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
768,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7772839-1,Extracted,"An 87-year-old woman was transferred to the emergency department with mild consciousness cloudiness and swallowing disturbance. She had a history of myocardial infarction 7 years before and had been taking aspirin, isosorbide and lipid-lowering drugs. She had mild, untreated diabetes mellitus. On examination, her consciousness level was 4-4-6 on the Glasgow Coma Scale. Her blood pressure was 128/94 mm Hg and her heart rate was 103/min without arrhythmia. She showed severe dysphagia and hoarseness, but palatal movement and gag reflex were normal and there was no tongue deviation. Except for mild gait ataxia, which was suspected to be of cerebellar origin, no motor or sensory impairment was observed. Bilateral limb tendon reflexes tended to be decreased, but other neurological signs were negative. Blood tests, including a complete blood count, electrolytes, and renal and liver functions were all normal. Fasting glucose level was 170 mg/dL. Chest X-ray and electrocardiogram were noncontributory. Head CT showed a high-density area at the right dorsolateral medulla (Fig. ). However, CT angiography performed at the same time did not reveal the cause of the hemorrhagic lesion; there was no aneurysm, cavernous malformation or tumor (Fig. ).
After hospitalization, aspirin intake was discontinued, and anti-hypertensive drugs were initiated. Her consciousness level returned to normal within a few days. Due to the swallowing disturbance, nutrition was provided via a feeding tube. Rehabilitation training stabilized her walking and reduced the symptoms of ataxia. She could speak clearly by the 10th hospital day and she was able to take food orally on the 30th hospital day.
The patient underwent 1.5-T MRI scans of the brain on the 8th and 40th hospital days. The 40th day scan still showed a low signal intensity lesion on the right dorsolateral medulla in the T2* sequence image (Fig. ). MRA conducted at the same time again did not reveal any vascular anomaly or tumor. Diffusion tensor tractography, performed on the same day (40th hospital day) as the second MRI using our previously reported technique [], showed a decreased volume of the right cortico-mesencephalic tract (Fig. ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [87, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 87 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
769,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7852472-1,Extracted,"A 64-year-old female presented to the emergency department after an episode of syncope and sudden onset right hemiplegia. One week prior, she had experienced a syncopal episode that resulted in a minor car accident without serious injury. On further history, the patient reported having experienced several pre-syncopal events, discoordination and episodic loss of fine motor skills in the previous 2 weeks. There was no associated history of fevers or weight loss and there were no significant risk factors for bacterial endocarditis such as intravenous drug use, implantable cardiac devices, rheumatic fever or dental decay.
The patient had a history of achondroplasia/metaphyseal dysplasia and a family history of multiple sclerosis. There was no history of hypertension, dyslipidaemia, diabetes mellitus or prior vascular disease.
On examination, tone was increased in the right upper and lower limbs and muscular power in the right limbs was reduced to movement against gravity. There was reduced sensation to pinprick and fine touch on the right side of the body. Knee and elbow reflexes were brisker on the right than the left and the right plantar reflex was upgoing.
The cardiovascular, respiratory and gastrointestinal examinations were normal except for very prominent splinter haemorrhages ().
Initial investigations were as follows: haemoglobin 137 g/L, WCC 9.3 × 109, neutrophils 8.0 × 109, platelet count 147 × 109, D-dimer 18.5 (NR < 0.5), troponin 1621 ng/L (NR < 11), PT 12.3 secs (NR 10.0–14.0), APTT 29 secs (NR 26–36), creatinine 48 umol/L and eGFR > 90.
The patient was admitted for further investigation. MRI brain demonstrated multiple sites of ischaemic change in both the anterior and posterior circulation (). A cardiac embolic source was considered and TTE demonstrated a small hypoechoic focus 6 mm ×3 mm on the aortic annulus reported as representing either thrombus or atheroma. Further serological testing ruled out autoimmune and inflammatory conditions. A CT aortogram + coronary angiogram to exclude dissection or coronary artery disease given the rise in troponin noted an incidental pelvic mass () thought to be arising from the adnexa. A confirmatory pelvic ultrasound reported a lesion arising from the right ovary with complex and vascular structure. CA 125 was >1500 (normal ref < 100). The patient was transferred to a tertiary centre with specialist onco-gynaecological and general surgical services for biopsy, which confirmed stage III high-grade serous ovarian cancer.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [64, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Vascular disease history': False, 'Stroke': True, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 64 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
770,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4852782-1,Extracted,"A 75-year-old gentleman presented to the accident and emergency department (A&E) following an episode of fall at home and was found by his wife on a bathroom floor. Initial neurological examination revealed global aphasia with right-sided hemiparesis. He was noted to be incontinent of urine.
His medical history included atrial fibrillation, hypertension, benign prostatic hypertrophy and chronic obstructive pulmonary disease. His medications included warfarin, tamsulosin, seretide, felodipine and candesartan. He has no physical disability, independent prior to hospital admission. On presentation, he was hemodynamically stable with a GCS of 11/15 (E4/V1/M6). Initial blood parameters including inflammatory markers were within normal limits. Each episode of seizures lasted less than a minute. They were all self-terminating. He was commenced on phenytoin infusion. CT brain revealed an old lacunar infarct in the left basal ganglia. He was transferred to the stroke ward for further observation and treatment. It was noted he had been developing further seizure clusters despite IV phenytoin. Each seizure episode lasted between 3 and 5 min. Nursing documentation revealed at least 20 stereotypical movements within the first 24 h.
On the second day of his admission, his CRP had risen and he was commenced treatment for aspiration pneumonia. MRI brain was unremarkable with no evidence of temporal or meningeal enhancement (). Lumbar puncture was delayed in view of his abnormal INR. His random blood sugar measurement was recorded at 30 mmol/L with HbA1c measurement of 14.8%. He was commenced on IV insulin with subsequent reduction of seizure frequency. He was seizure free within 24 h and discharged uneventfully with oral metformin. He was reportedly still seizure free on annual review without any anti-epileptic medication.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [75, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': False, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 75 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
771,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5118523-1,Extracted,"A 44-year-old male with a history notable for a bicuspid aortic valve that was repaired 19 years ago via a Ross procedure (pulmonary autograft replacement of the aortic valve and cadaveric allograft replacement of the pulmonary valve) was admitted for evaluation of 2-3 months of persistent daily fevers up to 39.4°C, headaches, night sweats, and marked fatigue of unknown origin. Review of systems was remarkable for a week of mild painless hematochezia. He was using aspirin frequently for control of his fevers. His family and social history were unremarkable beyond owning a pet dog. He reported a dental cleaning approximately 5 months prior to presentation. At the time of presentation, he had undergone extensive infectious and rheumatologic evaluations for persistent but undifferentiated fevers. Blood cultures obtained three months prior to admission, and again one week prior to admission at a separate facility in Bactec Plus aerobic and anaerobic FAN bottles, processed in a Bactec 9120 system (Becton Dickinson), were negative after 5 days of incubation.
On physical examination the patient was febrile to 38.8°C. He was diaphoretic but otherwise well appearing. He had no evidence of dental or periodontal disease and no visible oropharyngeal abnormalities. Cardiovascular examination was notable for an old III/VI holosystolic murmur greatest at the left lower sternal border, radiating to the back, and an old II/VI diastolic murmur best appreciated over the RUSB. The pulmonary exam was unremarkable. Abdominal exam was notable for slight tenderness to palpation in the RLQ. On rectal exam, no perianal lesions were noted and there were no masses in the rectal vault; he had brown, guaiac positive stools but no melena. No other findings of endocarditis were appreciated.
Laboratory evaluation revealed a hematocrit that was decreased to 30.7% from a preillness baseline of 48%, an erythrocyte sedimentation rate (ESR) of 44 mm/hr, C-reactive protein (CRP) of 55 mg/L, and creatinine of 1.01 mg/dL. His white blood cell count was 6,000 per mcL. A urinalysis with sediment was notable for 1+ blood, and 2 red blood cells per high-powered field on microscopy. Transthoracic and transesophageal echocardiography revealed mild, diffuse thickening of the mitral valve with trace mitral regurgitation and focal thickening of the pulmonic valve homograft, which were highly suggestive of a valvular vegetation. There was stable, severe dilation of the aortic root. These findings were confirmed with cardiac magnetic resonance imaging.
Blood cultures were sent on the day of admission and processed with the BacT/ALERT system (bioMerieux) and on day 2 grew thin, tapered Gram-variable rods from an anaerobic FAN bottle. Subcultures grew only on Brucella agar plates incubated within an anaerobic chamber, and Gram stain of the culture revealed thin Gram-negative rods with tapered ends. This isolate was negative for oxidase and spot indole testing. The patient was started on vancomycin, ceftriaxone, and metronidazole for empiric coverage. Multiple blood cultures continued to be positive for Gram-negative rods from anaerobic FAN bottles, and Gram-variable rods were also subsequently isolated from both aerobic and anaerobic FAN bottles over the following 2 days during which the patient was taking antibiotics. Despite the positive blood cultures, the patient defervesced and felt better following the administration of antibiotics. Blood cultures drawn on day 3 of antibiotic treatment were negative and remained negative after 5 days. At discharge, the isolate was still not identified.
Additional work-up with gas-liquid chromatography revealed a large peak for lactic acid and a small peak for acetic acid. The appearance on Gram stain, aerotolerance noted on further passage, and lactic acid production were most consistent with Leptotrichia species. A RapID ANAII test, which uses conventional and chromogenic substrates for species identification, did not reveal any satisfactory matches. Isolates were sent for 16S rRNA sequencing as a definitive diagnosis was unattainable via conventional phenotypic methods. Following 16S rRNA sequencing, a search of the Isentio RipSeq 16S database yielded a match with a 99.9% identity for L. goodfellowii and 7.3% difference separating it from another related species.
The patient was discharged on piperacillin/tazobactam and metronidazole as these antibiotics had demonstrated clinical effectiveness in a previous case report []. Antibiotic susceptibility testing of the isolates via Etest showed sensitivity to ceftriaxone (MIC 0.016 μg/mL), clindamycin (MIC 0.016 μg/mL), metronidazole (MIC 0.25 μg/mL), and penicillin (MIC 0.125 μg/mL). Following the availability of susceptibility data, the patient was switched to ceftriaxone and metronidazole and in total completed a 6-week course of antibiotics. He was then started on chronic suppressive therapy with penicillin V potassium, which was complicated by elevated liver transaminases and discontinued. He was then started on cefpodoxime, which he has tolerated well. Cardiac surgery was under consideration but ultimately deferred as he has been otherwise asymptomatic and with stable cardiac imaging since his hospitalization.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [44, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 44 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 0 + 1 = 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
772,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6738249-1,Extracted,"A 70-year-old woman presented to the emergency room with symptoms of total aphasia and right unilateral spatial neglect. She had a history of bronchial asthma, dyslipidemia, and type 2 diabetes. Dyslipidemia and type 2 diabetes were noted from the age of 62. The onset of symptoms was 46 min prior to presentation to the emergency room. Her neurological findings confirmed mixed aphasia (she could not obey simple commands), neglect of the right half of her body, and left conjugated deviation. No obvious paralysis or sensory disturbances were noted. Deep tendon reflex was normal, and no pathological reflex was observed. Her NIH Stroke Scale (NIHSS) was 7. Her baseline MRI revealed no obvious high signal in DWI (Fig. ). Fluid-attenuated inversion recovery (FLAIR) confirmed FLAIR vessel hyperintensities in the left middle cerebral artery (MCA) (Fig. ). Magnetic resonance angiography (MRA) showed partial obstruction in the distal part of the left MCA (Fig. ), which may have been an artifact. To make a definitive diagnosis, perfusion-weighted imaging (PWI) was additionally performed to assess the tissue at risk. Our automated software showed 12 mL of Tmax >6 s of hypoperfusion in the left MCA region, which matched the lesion side. Because the ischemic core calculated by an apparent diffusion coefficient (ADC) <620/10−3 mm2/s was not present, this case was diagnosed as DWI-negative DWI-PWI-mismatched AIS (Fig. ). Carotid vascular ultrasound showed no stenosis in the bilateral common carotid artery or internal carotid artery. We diagnosed her as AIS, and intravenous rt-PA therapy was administered 22 min after entering the MRI suite. She responded well to the reperfusion therapy, and her NIHSS was 0 after leaving the MRI suite. No further deterioration of neurological signs was observed during her admission. A FLAIR scan on the 9th day showed an ischemic change in the same lesion as the perfusion abnormality. This area was also identical to the obstructed left MCA seen on MRA. Transthoracic echocardiography did not reveal any apparent cardiac dysfunction or intracardiac thrombus. Nonvalvular atrial fibrillation was observed on day 2 of admission, and we diagnosed her stroke subtype as a cardiogenic cerebral embolism. Direct oral anticoagulant (dabigatran 300 mg/day) was prescribed at the time she was discharged to her home.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'age': [70, 'years'], 'Stroke': True, 'Diabetes history': True, 'Transient Ischemic Attacks History': True, 'sex': 'Female'}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 70 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
773,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5851773-1,Extracted,"A 65-year-old Chinese male, who worked as an aid man before retirement, had a 9-month history of temporary but progressive substernal burning sensation with acid bilges of shoulders and arms, and profuse sweating at night. Each episode lasted for 1 h and recovered spontaneously, without any triggers. Previously, he was diagnosed with reflux esophagitis for which he was prescribed some acid-inhibitory medicines which was, however, not effective. He suffered the above-mentioned symptoms again 1 night with higher severity than before with palpitation and weakness. His blood pressure (130/110 mm Hg) and heart rate (55 beats/min) were measured, was accordingly prescribed 3 grain of traditional Chinese pills, fosinopril 5 mg, and metoprolol 25 mg and was taken to the emergency room. His personal history revealed a 25 pack-year smoking history, a 40-year drinking history, and a snoring habit at night. However, his medical, family, and psychosocial histories were normal. Interestingly, his ECG showed coved ST-segment elevation of approximately 0.3 to 0.8 mV in precordial leads V1–V3 and 0.5 to 0.7 mV in standard limb leads II, III, aVF, and “mirror change” in leads I, aVL (Fig. A and B). Unfortunately, the echocardiogram was not taken immediately due to occasional reason. No arrhythmia was recorded. Laboratory tests showed no abnormalities. He was treated with intravenous nitroglycerin injection and exhibited dim consciousness with sweating, pallor, and cold limbs after that. In about 5 min after the treatment, the patient gained consciousness. The ECG, at this stage, was unremarkable (Fig. A and B). Coronary angiography demonstrated moderate stenosis of the left anterior descending branch (Fig. A and D). An echocardiogram taken after that was normal. VSA was diagnosed. He also underwent sleep monitoring with a result of moderate obstructive sleep apnea. The patient was treated with diltiazem, aspirin, isosorbide mononitrate, and rosuvastatin and counseled extensively on quitting cigarettes and alcohol. We followed up the patient at half a year after his being discharged. He was compliant of taking the prescribed pills on schedule and there was no reoccurrence of the symptoms. Written informed consent for publication was obtained from the patient.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [65, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
774,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5698791-1,Extracted,"A 58-year-old Caucasian male with a history of metastatic melanoma presented with severe weakness. The patient was initially diagnosed with cutaneous melanoma of the back in May 2008 (American Joint Committee of Cancer (AJCC) Stage 1b; T2a, N0, M0; BRAF V600 mutation not detected) and underwent wide local excision with clear margins. In April 2014, he presented with progressive shortness of breath and significant weight loss over the past 3–4 weeks. CT angiography of the chest showed mediastinal and hilar lymphadenopathy, along with numerous pulmonary nodules throughout both lungs ranging between 6 mm and 3.5 cm. CT abdomen and MRI brain were done which ruled out any liver lesion or brain metastasis. Biopsy of the lung nodules confirmed metastatic melanoma (BRAF V600 mutation not detected), and treatment with anti-CTLA-4 antibody, ipilimumab (3 mg/kg), was initiated. The patient received this treatment regimen for 3 months but then was lost to follow-up. In November 2014, he agreed to start therapy with nivolumab, an anti-PD- L1 antibody. Ten months later, he presented with progressive quadriplegia, lower extremity weakness worse than upper extremity weakness, developing over a few days. He reported that, due to the weakness, he fell and was unable to get up on his own. His home medication list included only nivolumab. Routine blood test in ED revealed potassium of 1.7 mEq/L, bicarbonate of 9 mEq/L, chloride of 116 mEq/L, sodium of 139 mEq/L (anion gap 14, delta ratio of 2), serum creatinine of 2.64 mg/dL (baseline of 0.91 mg/dL 3 weeks prior), and elevated eosinophils of 6%. Admission diagnosis included hypokalemia, hyperchloremic normal anion gap metabolic acidosis, acute kidney injury (AKI), and eosinophilia. Urinalysis revealed 1+ protein (urine protein/creatinine ratio of 1.42), fractional excretion of sodium of 1.9%, amorphous urine sediment, and 24-hour urine potassium of 159 mEq/L, hence indicating intrinsic kidney injury such as acute interstitial nephritis, acute tubular necrosis, or glomerulonephritis. Pertinent negatives in his blood work included normal thyroid-stimulating hormone levels. Retroperitoneal ultrasound showed normal kidneys with no solid mass, stone, or obstruction. Urinary bladder also appeared normal. There was no history suggestive of previous kidney disease; autoimmune diseases such as sjögrens, lupus nephritis, or rheumatoid arthritis (RA); thyroid disorders; diabetes; vomiting; excessive alcohol use; dehydration; or exposure to nephrotoxic agents such as antibiotics, contrast, or analgesics. Based on these findings, progressive quadriplegia was secondary to hypokalemia which was due to type 1 RTA, most likely irAE secondary to anti-PD-1 antibody therapy. The offending drug was discontinued, and the patient was started on intravenous hydrocortisone 100 mg every 6 hours for 2 days, followed by a tapering dose lasting 4 weeks. IV replacement therapy with potassium and bicarbonate was also initiated. Renal biopsy was considered but was not done as the patient responded well to steroids with return of renal function to normal. Quadriplegia gradually improved which correlated to improvement in serum potassium levels. By day 3 of hospitalization, the quadriplegia had resolved. Serum creatinine, hypokalemia, and other electrolyte imbalance improved. On discharge, renal function, potassium, and bicarbonate were normal. Subsequently, he was started on pembrolizumab, another anti-PD-1 antibody, which the patient has tolerated well.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [58, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 58 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
775,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-1166,Extracted,"A 78-year-old man is brought to the emergency department because of a 1-day history of painful enlarging bruises and skin ulceration over his thighs and external genitalia. He has type 2 diabetes mellitus, mitral regurgitation, and atrial fibrillation. Three days ago, he was started on treatment with warfarin. His only other medications are metformin and lisinopril. His temperature is 37.8°C (100.0°F), pulse is 108/min and irregularly irregular, and blood pressure is 155/89 mm Hg. Examination of the skin shows large purpura, hemorrhagic bullae, and areas of skin necrosis over his anterior legs, gluteal region, and penis.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [78, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 78 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
776,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3890736-1,Extracted,"A 67-year-old man, who was undergoing treatment for a bleeding duodenal ulcer, was admitted to our hospital for evaluation of a liver mass incidentally found on abdominal ultrasonography. The patient had a past medical history of angina pectoris, drug induced hepatitis, myocardial infarction, congestive heart failure and old pulmonary tuberculosis. The family history was none contributory. The patient complained of general weakness, easy fatigability and anorexia. He had no complaints of abdominal pain, weight loss, fever or night sweats. The blood pressure was 125/90 mmHg, pulse rate 90/min and body temperature 36℃. He appeared chronically ill and had an alert mental status. There was no tenderness on abdominal examination. Hepatomegaly of two fingers breadth was noted below the right costal margin; there was no ascites. His spleen and lymph nodes were not enlarged. Laboratory blood tests showed a hemoglobin of 12.8 g/dL, hematocrit 37%, white blood cell 5,400/µL with 42.8% neutrophils, platelet count 122,000/µL, blood urea nitrogen 14.2 mg/dL, creatinine 1.4 mg/dL, total protein 7.8 g/dL, albumin 3.8 g/dL, total bilirubin 0.8 mg/dL, alkaline phosphatase 53 IU/L, alanine aminotransferase (ALT) 30 IU/L, aspartate aminotransferase (AST) 35 IU/L, gamma glutamyl transferase (r-GT) 53 IU/L, lactate dehydrogenase (LDH) 250 IU/L (within normal range), prothrombin time 23 sec (98% of normal) and alpha-fetoprotein 3.5 ng/mL (within normal range). Hepatitis B surface antigen (HBsAg), antibody against hepatitis B surface antigen (anti-HBs) and antibody against hepatitis C (anti-HCV) were all negative. Abdominal magnetic resonance imaging (MRI) showed a well defined homogeneous mass 5.7×4.8 cm in size at segment 5 (). The following neck and chest computerized tomography (CT) scan showed no sign of other organ involvement or lymphadenopathy. Abdomen-pelvic CT scan showed no evidence of splenomegaly or lymphadenopathy. The whole body bone scan (WBBS) had no evidence of bone involvement. Gallium scan also showed no abnormal radioactivity. There were no malignant infiltrations noted on the bone marrow biopsy. Additional diagnostic evaluation included hepatic angiography and ultrasonograpy guided liver needle aspiration biopsy, using the gun shot approach, of the hypoechoic lesion in the right liver lobe. Hepatic angiography did not show any stained tumor, and lipiodol injection failed. Liver biopsy histology showed a severely distorted architecture due to lymphoreticular cell infiltration of the portal tract (). The cells had the following features: they were uniform in size, had a slightly irregular outline and showed an increased nuclear-cytoplasmic ratio. They showed no particular arrangement representative of a specific organ. The cells expressed CD20 () with a low Ki-67 labeling index supporting the diagnosis of a low grade tumor (). The cells had no immunoreactivity for CD5 and CD23 (, ). The final pathologic diagnosis was an extranodal marginal zone B-cell lymphoma of MALT according to the WHO classification. The patient underwent radiotherapy with a total dose of 4,140 cGy (1,980 cGy on the entire liver and an additional 2,160 cGy focused on the tumor area).
Abdominal ultrasonography, performed 5 years after radiotherapy, revealed complete remission of the lymphoma in the liver. In addition, the liver MRI, studied 5 years after radiotherapy, showed fibrous contraction due to post radiation change of right lobe of the liver. There was no evidence of tumor recurrence in the liver parenchyma (). However, a newly developed well-enhancing solid mass, highly suggestive of a malignancy, at the posterior basal segment of right lower lobe of lung, was incidentally discovered by MRI at this time.
Six years after diagnosis, he was readmitted due to complaints of dyspnea. The chest X-ray, chest CT scan and Whole body bone scan showed progression of the mass from the right lower lobe of the lung, pleural effusion, and multiple bone metastases. The patient refused additional diagnosis and treatment, and died as result of an undefined disease of the lung.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [67, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 67 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
777,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6289221-1,Extracted,"An 81-year-old female with a medical history of CAD with stents, hyperlipidemia, hypothyroidism, GERD, recent UTI, pancreatic cyst, constipation, anemia and leukopenia presented to the ED with a 1 day history of mild, diffuse and cramping abdominal pain. The patient was unable to give an accurate history, but the son at bedside supplemented this reporting that for several years the patient had been experiencing ill-defined abdominal discomfort. Physical exam showed a soft abdomen with mild tenderness and no evidence of peritonitis. A CT scan of the abdomen and pelvis with IV and PO contrast (Fig. ) showed edematous changes to the mesentery of the small and large bowel with swirling of vessels indicative of internal hernia. The stomach was also noted to be distended with both air and fluid as a consequence of posterior compression by the hernia contents (Fig. ). A surgical consult was obtained, a nasogastric tube and Foley catheter were placed, antibiotics were started, and the patient was taken for an exploratory laparotomy. Upon entering the abdomen through a vertical midline incision, 1.5 l of ascites was drained revealing a diffusely edematous mesentery. A large portion of the small bowel was seen to be herniated through the Foramen of Winslow (Fig. ). A Kocher maneuver and division of the gastrocolic ligament were then performed to allow release of the herniated small bowel. It was at this time that, in addition to small bowel, a large portion of the ascending and transverse colon was noted to be herniated through the foramen of Winslow. The small bowel was also seen to be torsed about its own mesentery. Normal anatomy was restored and the bowel noted to be healthy and viable with peristalsis (Fig. ). Due to the large size of the foramen after reduction and enlargement, it was deemed best to leave it open to prevent any further incarceration or strangulation. The abdomen was closed and the patient tolerated the procedure well. At a follow-up visit 2 months later, the patient had well-healed incisions, was doing well, tolerating a diet, and gaining weight appropriately.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [81, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 81 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
778,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4560315-3,Extracted,"A 67-year-old female with a past medical history significant of mucocutaneous LP diagnosed 2 years prior presented for an evaluation of dysphagia and intermittent ‘choking spells’. She was on prednisone 5 mg/day, omeprazole 20 mg/day, and topical triamcinolone (0.1%percnt; twice a day). She had undergone an esophageal dilation approximately 1 year ago. EGD at our institution revealed inflammation and a stricture in the proximal esophagus. Biopsies revealed diffuse, acute chronic inflammation and focal individual cell keratinization with lymphocytes, consistent with LP. Intralesional injection of triamcinolone and dilation was performed. The patient remained asymptomatic for a period of 2 years, but subsequently required 5 additional dilations and a steroid injection into the proximal esophageal stricture of 20 ml triamcinolone (10 mg/ml). She did not receive medical therapy. She was diagnosed with a squamous papilloma of the midesophagus 11 years after the initial diagnosis of ELP, but did not develop esophageal malignancy.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [67, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Thromboembolism history': False, 'Vascular disease history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 67 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
779,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6343859-1,Extracted,"An 80-year-old African-American man, with the history of myocardial infarction in November 2000 with two-vessel CABG (coronary artery bypass grafting) performed at that time, now presented to the outpatient radiology suite for a chest X-ray, to follow up on recent pneumonia. An X-ray revealed an abnormal contour of the right heart border (Figure ).
In order to further investigate the abnormal contouring of the right heart border, a CAT (computed tomography) scan of the chest was performed. Upon checking CAT scan results, the patient was found to have a partially thrombosed aneurysm arising from the native right coronary artery (RCA) measuring approximately 6.9 cm that was also compressing the right atrium (Figure ).
The patient did not report any symptoms of chest pain, shortness of breath and dizziness. He stated that he was in his usual state of health. He presented with baseline bradycardia with heart rate in the 40s, however, since he was asymptomatic, no further treatment was performed for the bradycardia. Electrocardiogram revealed a bi-fascicular block with Wenckebach. Other labs were normal except for the leucocytosis due to pneumonia (Figure ).
Upon initial evaluation and the echocardiography (Figure ), it was uncertain whether the aneurysm was from the venous graft or the native coronary artery. Thus, it was decided to proceed with the cardiac catheterization to further evaluate the nature of the aneurysm. Catheterization revealed patent LIMA (left internal mammary artery) and RCA grafts along with a native RCA aneurysm (Figure ).
The case was discussed with cardiothoracic surgeons for interdepartmental consultation and the consensus was that the patient will need a cardiac MRI (magnetic resonance imaging) for the imaging of RCA anatomy prior to intervention. They planned to consult with interventional cardiology for possible covered stent vs. ostial coiling. During the entire eight-day hospital stay, the patient remained completely asymptomatic. He was performing his activities of daily life without any difficulty. Upon discharge, the patient was counseled about the follow-up for outpatient cardiac MRI and to report to the ER if he feels any kind of symptoms including chest pain, dizziness or shortness of breath.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [80, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 80 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
780,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8212687-1,Extracted,"An 88-year-old male presented to our emergency department (ED) with an acute onset of a painless loss of vision to his right eye. His past medical history was significant for hypertension, coronary artery disease and atrial fibrillation (on apixaban). He stated he was lying in bed reading when he had a sudden painless loss of vision to his right eye, described as a curtain closing, for which he presented to our ED ~24 h later. He denied any other symptoms including headache, scalp pain, jaw claudication, focal weakness, numbness, angina or shortness of breath.
Vitals on arrival to the ED were as follows: 36.9°C, heart rate of 62 beats/min, respiratory rate of 16 breaths/min, blood pressure of 123/53 mmHg and pulse oximetry of 99% on room air. His cardiopulmonary exam was unremarkable. His neurologic exam was notable for a National Institute of Health Stroke Scale score of +2 for complete unilateral vision loss to the right eye. Intraocular pressures were 14 mmHg bilaterally. His remaining physical exam was notable for a right afferent pupillary defect (APD). To further assess the eye and its structures, a point-of-care ultrasound (POCUS) was then performed. Utilizing the high-frequency linear probe to the right eye, a transverse view demonstrated a retrobulbar spot sign (RBSS) in the distal portion of the central retinal artery within the optic nerve sheath (, red arrow). He had normal blood flow in his left eye (), and no blood flow was seen to the central retinal artery of the right eye, with the yellow arrow pointing to the RBSS (). The patient was then transferred to our tertiary referral center (TRC) for specialist consultation.
Ophthalmology visualized a plaque on the dilated fundoscopic exam with associated retinal ischemia. Given the onset of ~24 h prior to arrival, the risks of tissue plasminogen activator (tPA) outweighed the benefits, as such, the patient was medically managed. His head computed tomography (CT) was unremarkable for acute changes. A magnetic resonance imaging MRI could not be done, secondary to his pacemaker not being compatible. His carotid duplex was without severe stenosis or thrombus. His echocardiography showed left ventricular diastolic dysfunction with an ejection fraction of 40%, which was similar to previous studies.
Overall, his workup was without evidence of carotid artery disease or vasculitis and it was suspected to be cardioembolic in origin related to his atrial fibrillation. On further questioning, it was found that the patient’s family member had passed away 2 weeks prior, leading to depression and multiple missed doses of his anticoagulation. Compliance of his anticoagulation was stressed on discharge. At his 1-month follow-up after his hospital admission, he has regained light perception and 15% of his vision.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [88, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 88 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
781,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8428626-1,Extracted,"A 74-year-old male with remote history of left frontal lobe stroke, uncontrolled insulin-dependent diabetes mellitus, coronary artery disease, atrial fibrillation, congestive heart failure, and pseudogout presented for evaluation of waxing and waning confusion that began 24 hours prior to arrival. Prior to evaluation by our Neurology service, he was found to have a urinary tract infection (UTI) and started on Levaquin. A non-contrast computed tomography (NCCT) scan of the head revealed chronic left frontal encephalomalacia (Figure ).
Subsequent MRI brain showed an acute infarct in the right splenial region of the corpus callosum on diffusion-weighted imaging (Figure ).
This infarct was new when compared to an MRI brain that was performed outpatient one week prior to presentation to our emergency department (image unavailable). He had reportedly experienced progressive cognitive decline over the six months preceding presentation.
The finding in Figure was also confirmed via MRI fluid-attenuated inversion recovery (FLAIR) sequence (Figure ).
Additional tests were performed to further characterize his persistent stupor. Conventional angiogram was without evidence of vasculitis. Contrast-enhanced CT of the chest showed asymmetric enlargement of the thyroid with leftward sub-sternal extension; there was no sign of malignancy. Contrast-enhanced CT of the abdomen and pelvis was also negative for malignancy. Electroencephalogram was without evidence of epileptiform discharge or seizure activity. A lumbar puncture showed no evidence of pleocytosis but did reveal elevated protein (63mg/dL; normal range 15-45) and IgG index (6.4mg/dL; normal 0.0-6.0). Due to findings on CT chest, NCCT of the soft tissues of the neck was performed which revealed enlarged left thyroid lobe (Figure ).
Other notable labs during hospitalization included persistently elevated sedimentation rate with a peak of 127 mm/hr (normal range 0-20), white blood cell count with a peak of 16.3K/µL (normal range 4.5-11.0), C-reactive protein of 10 mg/L (normal range <10), negative blood cultures, total T3 0.3 ng/mL (normal range 0.9-2.44), free T3 1.2 pg/ml (normal range 3.7-4.2), free T4 0.9 ng/dl (normal range 1.3-2.8), thyroid stimulating hormone (TSH) 0.233 mIU/ml (normal range 0.5-1.5), thyroid peroxidase antibody titer 20.1 lU/ml (normal range <2). A paraneoplastic panel and encephalitis screen for herpes simplex virus (HSV) and cytomegalovirus (CMV) were unremarkable.
The elevated thyroid peroxidase antibody titer with concomitant elevation of inflammatory markers suggested a probable diagnosis of HE.
High-dose steroid infusion was initiated via intravenous solumedrol, 500mg, twice daily for three days. He also received IVIg infusion (0.4mg/kg) once daily for five days.
Following treatment, his mental status improved rapidly with eventual return to baseline.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [74, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Thromboembolism history': True, 'Vascular disease history': True, 'Stroke': True, 'Diabetes history': True, 'Transient Ischemic Attacks History': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 74 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 6 + 1 = 7.
The patient's CHA2DS2-VASc Score is 7."
782,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6058415-1,Extracted,"An 84-year-old woman with hypertension presented to the emergency department with epigastric pain, nausea, and dizziness for 3 hours. A 12-lead electrocardiogram showed a junctional rhythm at rate of 40 and 2 mm inferior ST-elevations with lateral ST depressions. High-sensitivity troponin-I level was 0.01 ng/mL. Initial management included aspirin, clopidogrel, and intravenous heparin, and she was subsequently taken emergently to the catheterization laboratory. Attempts to engage the right coronary artery (RCA) were unsuccessful despite using multiple guide catheters. The left coronary system showed no angiographic evidence of coronary artery disease with left to right collaterals. Contrast injection in the right coronary sinus suggested ostial total occlusion of the RCA (). Probing with a coronary wire near where the RCA ostium was presumed to be located was associated with an increase in the heart rate with an idioventricular rhythm and resolution of inferior ST-elevation. The RCA was then easily engaged with a guide catheter. Angiographic evaluation of the RCA showed a smooth vessel with no evidence of coronary artery disease except for abrupt termination of the distal PL2 branch (). A computed tomography angiogram was then done to explore the cause of the right ostial occlusion and revealed an aortic root thrombus (21 × 16 mm) with extension into the right coronary sinus, together with near complete obliteration of the left atrial appendage with another large thrombus ( and ). Serial electrocardiograms demonstrated paroxysmal atrial fibrillation with complete resolution of inferior ST-segment elevation. Subsequent troponin-I levels peaked at 74 ng/mL. A transthoracic echocardiogram showed inferobasal septal hypokinesis and ejection fraction of 45%. A brain magnetic resonance imaging obtained secondary to mental status changes that occurred a few hours after the procedure showed multiple embolic cerebral infarcts and complete occlusion of the left internal carotid artery. The patient was treated with intravenous heparin and bridged to warfarin therapy. She was discharged home in good condition on hospital day 5. Follow-up 6 months after the index hospitalization revealed no symptoms or signs of disease recurrence.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [84, 'years'], 'Hypertension history': True, 'Stroke': True, 'Thromboembolism history': True, 'Vascular disease history': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 84 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
783,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7559674-1,Extracted,"An 84-year-old Chinese woman was admitted to our hospital with persistent nausea and vomiting for 2 mo after an episode of community-acquired pneumonia (CAP).
Two months before admission, the patient had CAP. During treatment with intravenous moxifloxacin, she developed progressive nausea, vomiting, and constipation without hematemesis, heartburn or abdominal pain. Upper gastrointestinal (GI) radiography demonstrated decreased GI motility without obstruction. Gastroscopy at that time was normal. Positron emission tomography/computed tomography (PET/CT) showed no abnormalities. She was treated with nasogastric decompression and total parenteral nutrition. However, her condition deteriorated, with immediate postprandial vomiting, persistent low-grade fever, and dyspnea. She was then referred to our hospital.
Her previous medical history was notable for renal transplantation, hypertension, and paroxysmal atrial fibrillation, all of which were well controlled with cyclosporin A, mycophenolate mofetil, amlodipine and amiodarone.
The patient appeared weak. Vital signs were normal except for a low fever of 37.5°C. She had normal sinus rhythm and clear respiratory sounds. The abdomen was flat and soft and no GI pattern or peristaltic wave or mass was observed. Active bowel sound was auscultated.
Complete blood cell count, coagulation, liver and renal functions, as well as thyroid function were normal. Serum pH and electrolytes, including Na, K, Ca, Mg, Cl, and P, were well monitored during the entire disease course. C-reactive protein level was 19 mg/L (normal 0-8 mg/L). Serum carbohydrate antigen 19-9 (CA19-9) was elevated to 119 U/mL, but was gradually decreased to normal level during follow-up. Sputum cultures showed Pseudomonas aeruginosa. Other sputum pathogens, including fungi, mycobacteria and viruses, were negative. Repeated cultures of peripheral blood, stools, gastric drainage and urine, as well as serum pathogenic antibodies were also negative.
Upper GI radiography in our hospital showed intestinal stricture in the descending duodenum, which merely allowed the passage of a nasojejunal tube (Figure ). Axial CT with intravenous contrast demonstrated postbulbar stenosis (Figure ) and a thin-walled extraluminal diverticulum distal to the stenosis, with surrounding mesenteric fat stranding (Figure ). Other features on axial CT included hiatal hernia and a slightly dilated main pancreatic duct without mass or edema (Figure ). Gastroscopy revealed annular stenosis in the descending duodenum that did not allow the passage of an endoscope. The mucosa around the stenosis was edematous without signs of ulceration, hyperplasia or other abnormalities (Figure ). Endoscopic ultrasound revealed diffuse thickening of the mucosal layer but normal submucosal muscular layer (Figure ). Biopsy and histopathological examination of the swollen mucosa around the stenotic area revealed infiltration of nonspecific inflammatory cells. Chest CT revealed bilateral pulmonary infiltration (Figure and ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [84, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 84 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
784,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8208334-1,Extracted,"A 62-year-old male with a history of hepatitis C cirrhosis complicated by HCC and portal vein thrombosis on rivaroxaban presented to the hospital with melena for three days. The patient endorsed some mild generalized cramping abdominal pain, and denied any dizziness, syncope, nausea, vomiting, or hematemesis. The patient had a history of esophageal varices that were banded six years ago. He was diagnosed with HCC a year ago and was first started on levatinib; however, it was stopped since the patient developed neuropathy. The patient was initiated on atezolizumab and had received two doses with the last dose given three weeks before presentation. On presentation, the patient was tachycardic in 110s, hemoglobin was 8.4 g/dL (from baseline of 14-15), international normalized ratio 1.32, prothrombin time 13.9, and platelet count was 79,000. CT of the abdomen and pelvis showed a stable left hepatic mass. EGD showed four columns of large non-bleeding esophageal varices that were banded. Multiple gastric antral ulcers and prepyloric ulcer with dark spots were noted, with the largest ulcer measuring up to 2 cm (Figure ). Multiple clean-based duodenal ulcers were also noted.
He was not on non-steroidal anti-inflammatory drugs (NSAIDS), steroids, or any other drugs that can cause gastric ulcer. The patient’s GI bleed was attributed to the gastric ulcers, which were thought to be secondary to the immunotherapy agent, atezolizumab. The patient was continued on proton pump inhibitors (PPIs), and octreotide drips for a total of 72 hours and later switched to PPI 40 mg BID. Rivaroxaban was held for a week due to the findings of extensive gastric ulceration on EGD. The patient was seen in the oncology clinic a week later with no recurrence of bleeding, and his anticoagulation was restarted. Patient was restarted on atezolizumab three weeks later and continued on PPI twice a day without any evidence of further GI bleed.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [62, 'years'], 'Congestive Heart Failure': False, 'Thromboembolism history': True, 'Vascular disease history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 62 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 0 + 2 = 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
785,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7567319-1,Extracted,"A 72-year-old male with a medical history of peripheral arterial disease (PAD), mesenteric ischemia status post superior mesenteric and celiac artery stents, gastroesophageal reflux disease, hypertension, diabetes, chronic kidney disease, hypothyroidism and chronic obstructive pulmonary disease, presented with one-day history of epigastric pain, nausea and hematemesis. The patient denied any prior episodes of melena or bright red blood per rectum and reported no personal history of rectal or colon cancer. He also denied the use of nonsteroidal anti-inflammatory drugs, iron supplements or bismuth subsalicylate. He denied the use of alcohol, tobacco or recreational drugs. His medications included aspirin, clopidogrel, amlodipine, hydralazine, hydrochlorothiazide, atorvastatin, levothyroxine, furosemide and baclofen.
On admission, the patient was hemodynamically stable, his hemoglobin (HgB) was 9.2 with mean corpuscular volume (MCV) of 93.2. Eight months ago, his HgB was 11.4 with MCV of 89.9. Iron studies, level of folate and vitamin B12 were all within normal limits. Digital rectal exam showed dark stool. His aspirin and clopidogrel were held and he was started on intravenous pantoprazole 40 mg twice daily. Patient underwent upper endoscopy to identify the source of his gastrointestinal bleeding. It was unremarkable with no blood seen or identifiable source of bleeding. The esophagus, gastric mucosa and gastroesophageal junction were all normal in appearance. Dark pigmentation of the duodenal mucosa was noted and subsequently biopsied (Figure ). Evaluation of the biopsied sample was consistent with intestinal PM (Figure ) with no evidence of dysplasia or malignancy. Patient’s initial complains of nausea and hematemesis resolved without any additional intervention. He was transitioned to oral proton-pump inhibitor. Given his history of PAD, he was continued on aspirin, but his clopidogrel was discontinued upon discharge.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': True, 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
786,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7505381-1,Extracted,"A 77-year-old man, weighing 67 kg (body mass index: 23), was diagnosed with retinal detachment and scheduled for right total vitrectomy. He had a medical history of hypertension and non-insulin-dependent diabetes with unspecified, variant angina. He also reported a 55-pack-year smoking history. Percutaneous coronary intervention (PCI) was performed ∼10 years prior to this surgery due to acute myocardial infarction; he had also experienced an episode of acute congestive heart failure (HF) with preserved ejection fraction (EF) 2 years before this surgery. The patient had a physical status score of III according to the American Society of Anesthesiologists. During preoperative evaluation, the patient described his functional capacity as good and denied experiencing any symptoms of HF. Physical examination did not reveal any signs of congestive HF. The electrocardiograph (ECG) showed non-specific T wave abnormalities with LV hypertrophy (Fig. A). The transthoracic echocardiogram (TTE) revealed ischemic heart disease with normal LV size and function (EF: 67%), grade 2 diastolic dysfunction with left atrial enlargement, regional wall motion abnormalities (inferior wall hypokinesia and inferolateral wall hypokinesia), and no significant valvular pathology. In the preoperative TTE, left ventricular ejection fraction (LVEF) was 67%, the ratio of peak early to late flow of mitral inflow (E/A) was 1.02, and the ratio of LV early diastolic filling velocity to the peak diastolic velocity of the medial mitral annulus (E/e′) was 22.18 (Fig. A). The patient was taking clopidogrel 75 mg, atorvastatin 20 mg, and nicorandil 5 mg for treatment of cardiac disease. The preoperative cardiology consultation assessed the surgical risk of the patient to be low (<1%) given his stable control of blood pressure and a good functional capacity.
Upon the patient's arrival in the operating room, routine monitoring including noninvasive automated blood pressure, pulse oximetry, and electrocardiography was begun prior to premedication. Furthermore, the bispectral index (BIS) was monitored using VISTA (Aspect Medical Systems; MA); sensors were placed on the frontotemporal regions of the cranium, as recommended by the manufacturer, and were connected to an electroencephalogram monitor. The values of BIS were maintained between 40 and 60 during the intraoperative period. General anesthesia was induced using propofol, and tracheal intubation was performed following rocuronium-induced muscular relaxation. Anesthesia was maintained using sevoflurane (1.5–2.0 vol%) and an air–oxygen mixture (FiO2 0.5). Muscle relaxation was maintained using intermittent doses of intravenous rocuronium titrated to keep the train of 4 to <2 twitches.
Blood pressure, heart rate, and peripheral oxygen saturation (SpO2) were 100 to 120/76 to 86 mmHg, 70 to 86 beats/min, and 99%, respectively. Blood pressure was stable at the beginning of the surgery; however, 40 minutes after anesthetic induction, it declined to a low of 80 mmHg systolic pressure. This was managed using 5 to 10 mg ephedrine and 50 μg phenylephrine, injected thrice over 30 minutes. At 30 minutes after the onset of hypotension, a radial artery catheter was placed to measure the arterial blood pressure, and a continuous intravenous infusion of 5 μg/kg/min dobutamine was initiated. Following this, the systolic blood pressure and heart rate were 100 to 120 mmHg and 80 to 100 beats/min, respectively. The patient did not have any significant electrolyte abnormalities, as determined by arterial blood gas (ABG) investigation.
The surgery lasted approximately 2 hours. The patient experienced mild bleeding and fluid replacement was performed using 300 mL of normal saline. Postoperatively, all anesthetic agents were discontinued, and the residual neuromuscular block was reversed using 15 mg pyridostigmine and 0.4 mg glycopyrrolate. The patient was responsive to verbal commands, and was extubated immediately after adequate spontaneous ventilation was ensured. He was then transferred to the post-anesthetic care unit (PACU). On arrival in the PACU, the SpO2 was evaluated and found to be 60%; therefore, the patient was reintubated. Suctioning of the trachea revealed pink frothy sputum. At 5 minutes after tracheal intubation, the SpO2 gradually increased to 90%. The patient was transferred to the surgical intensive care unit (SICU) without extubation, for further management. In the SICU, intravenous injection of 20 mg furosemide was administered, and infusion of 10 μg/kg/min dobutamine was continued. He received an additional dose of furosemide and his respiratory status improved over the next 12 hours. The immediate postoperative chest x-ray scan revealed bilateral vascular congestion (Fig. ). The ECG showed ST depression in leads V4 to V6 (Fig. B). Computed tomography (CT) examination revealed multiple patchy densities throughout both lungs (Fig. ). Postoperative TTE, revealed an EF of 39% and moderate systolic dysfunction of the mid to apical LV wall segments; diastolic dysfunction was indeterminate due to E/A summation (Fig. B).
On postoperative day 1, his vital signs were stable and there were no signs of respiratory disturbance. Follow-up chest radiography showed a decrease in pulmonary congestion. Therefore, extubation was performed, and diuretic (furosemide) and inotropic (dobutamine) treatment was discontinued. On postoperative day 3, he was transferred to the general ward in an overall stable condition and was discharged 5 days later without any complications. No abnormalities were observed during the follow-up period of 4 weeks.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [77, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
787,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8207367-1,Extracted,"In our case, a 68-year-old man with a past medical history of end-stage renal disease, atrial flutter, and peripheral vascular disease presented to the hospital with severe, pressure-like chest pain. The initial electrocardiogram (ECG) was abnormal as shown in Figure . Initial laboratory workups, including electrolytes and cardiac enzymes, were within normal limits. The ECG in Figure demonstrates a narrow QRS complex tachycardia with normal axis. Borderline low voltage QRS complexes along with elevated ST-segments in leads II, III, and aVF are also apparent. The patient's ECG and presentation was concerning for an inferior ST-segment elevation myocardial infarction (STEMI). However, careful inspection of the ECG will reveal that the rhythm is in fact atrial flutter with 2:1 conduction to the ventricles at a rate of 106 beats per minute, and the flutter waves (tachycardia cycle length 289 ms) are falling on the ST segment of the ECG. This is best seen in lead V
1, where the flutter waves are positive.
In the index case, however, the patient was taken to the cardiac catheterization lab given high pretest probability of ischemic disease, and no evidence of coronary artery disease was found. During the cardiac catheterization, the patient spontaneously converted to sinus rhythm with resolution of ST segment changes. A previous ECG (Figure ) demonstrates atrial flutter with slow ventricular response. On this tracing, flutter waves are intermittently superimposed on the ST segments (thick arrows), and when not overlapped, clearly demonstrates the ST segment is normal (thin arrows).
Previous cases have been reported where the timing of the flutter waves raise the suspicion for ST-segment elevation, mimicking a STEMI. In these cases, reciprocal changes should be carefully evaluated, and patient history may also provide a diagnostic clue. Whenever the diagnosis of myocardial injury is unclear due to the possibility of an artifact or atrial flutter, simply repeating the ECG during carotid sinus massage or administering AV blocking agents may fortuitously dissociate the ST segments from flutter waves just briefly enough to elucidate the correct diagnosis as shown in Figure . Our case illustrates how striking the elevation of ST segments can appear when atrial flutter waves are incidentally superimposed upon the ST segments.
Recognition of this arrhythmia can potentially expedite treatment (rate control and/or cardioversion) and spare the patient invasive studies.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [68, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 68 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
788,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3303027-1,Extracted,"A 42-year-old man with drug-refractory AF was referred to our cardiology outpatient clinic to discuss treatment options. Echocardiography and magnetic resonance imaging (MRI) had been performed in the referring hospital which had revealed a giant LAA. No other abnormalities were reported.
The main complaint of the patient was recurrent, nocturnal episodes of AF once a week. His medical history was unremarkable. Physical examination revealed no abnormalities and electrocardiography showed sinus rhythm without signs of left atrial enlargement. The chest radiograph showed a prominent left upper cardiac border but with a normal cardiothoracic ratio. Sotalol, and later amiodarone, flecainide and disopyramide were tried but were ineffective or resulted in unpleasant side effects.
Since medical therapy was no option, alternative treatments were discussed. The role of the giant LAA in the pathophysiology of AF is unclear. Therefore, we proposed to perform PVAI by radiofrequency catheter ablation leaving the giant LAA in situ. The patient gave his consent.
In preparation for PVAI, transoesophageal echocardiography was performed which showed a giant LAA with good flow velocity of >40 cm/s (Fig. ). No thrombi were seen. MRI was repeated and revealed the giant LAA with a length of 7 cm in the coronal view (Figs. and ).
PVAI was performed by encircling right and left pulmonary vein antrums in pairs using an irrigated 4 mm electrode with a maximum electrode temperature of 43°C and a power of 30–40 W. The procedure lasted 240 min and the endpoint was successful electrical isolation of all pulmonary veins. Total fluoroscopy dose was 104 mGy and total fluoroscopy time was 27 min. The course of the procedure was uneventful.
After PVAI the patient was seen at the outpatient clinic. Antiarrhythmic medication was discontinued after 3 months. Six months after ablation the patient experienced a single episode of AF, treated with electrical cardioversion. With the exception of this event no recurrences of AF were seen, confirmed by four 48-hour Holter recordings (5, 7, 12, and 16 months following PVAI). Seventeen months after PVAI the patient is still in sinus rhythm and asymptomatic. He will continue to take oral anticoagulation.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [42, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 42 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
789,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7360421-1,Extracted,"On February 18, 2019, a 60-year-old woman with severe dyspnea, fine rales in the lung, tachycardia, and tachypnea was admitted at the emergency department of Heart Center of Mazandaran University of Medical Sciences, Sari, northern Iran. She suffered from multiple comorbidities, including diabetes mellitus, obesity (BMI 36.1 kg/m2), hypertension, and hypercholesterolemia. Her medical history revealed that she had been operated on 5 years ago for mitral valve (MV) replacement due to rheumatic heart disease. Laboratory data showed prothrombin time 18 seconds, international normalised ratio 2, white blood cells 4,000 /µL, and hemoglobin 12g/dL. Fluoroscopy evaluation showed that the motion of one leaflet of the prosthetic MV was fixed, while the other had severely restricted motion (). Transesophageal echocardiography demonstrated a mechanical prosthetic bileaflet MV, fixed medial leaflet MV, elevated MV mean pressure gradient (22 mmHg), pressure half-time (225 mL/s), MV left ventricular–outflow tract velocity time integral(48%), and a large obstructive mass (1.5×2 cm) on the prosthetic MV medial leaflet, which was highly suggestive of a large thrombus. Severe tricuspid regurgitation, mild–moderate aortic insufficiency, and severe pulmonary hypertension (pulmonary artery pressure 80 mmHg) was also present. Coronary angiography revealed normal arteries. Based on the hemodynamic condition of the patient (functional class IV) and large thrombus, urgent cardiothoracic surgery consultation took place, and she was a candidate for surgery. The thrombotic prosthetic MV was removed and replaced with another mechanical prosthetic MV (21 mm; CarboMedics, Austin, TX, USA) and tricuspid valve repair performed. Gross pathology showed a severe thick pannus formation with large thrombus on the prosthetic MV that caused malfunction (). Operation accomplished successfully and patient was discharged from the hospital with good condition.
On April 13, 2019, about 2 months after discharge, she went back to the emergency department with acute pulmonary edema refractory to vasodilator and diuretic therapy (). She also complained of fever and weakness for 2 weeks. Fluoroscopy showed normal leaflet motion. Chest X-ray revealed severe pulmonary venous congestion throughout the lungs, alveolar edema, and consolidation. She underwent transesophageal echocardiography (TEE). Upon reaching the TEE room, she complained of sudden vision loss in her right eye. TEE was done, and data revealed severe left ventricular systolic dysfunction (ejection fraction 30%), a bileaflet mechanical prosthetic MV, normal leaflet motion, a small mobile mass on the anteromedial swing ring, and severe aortic insufficiency. Due to destruction of the left coronary cusp of the aorta, the large size mobile mass (2.2×2 cm) protruded to the left ventricular outflow tract (vegetation mostly). Periaortic thickening with echo-free space around aorta (abscess) extended to the intervalvular fibrosa ( and ). Noncontrast brain computed tomography showed hyperdense intracranial hemorrhage in the left parietal lobe. On the second day of admission (April 15, 2019), due to prosthetic MV and native aortic valve infective endocarditis with decompensated heart failure and after consultation with a neurologist, she underwent second emergency redo surgical MV repair in combination with mechanical aortic valve replacement and aortoplasties.
The explanted valve and vegetation were sent to the laboratory for further evaluation. Direct microscopic examination (KOH preparation, 20%) of tissue biopsies showed a mass of dichotomous branching hyphae (), which was confirmed by histopathology (periodic acid–Schiff staining, ). Culture of biopsied tissue onto Sabouraud dextrose agar medium after a 24-hour incubation at 27°C yielded Aspergillus spp. On slide culture, the grown Aspergillus showed echinulate and hyaline conidiophores with globose to subglobose vesicles and uniseriate phialides. Conidia were globose to subglobose and echinulate (). On the basis of microscopic and macroscopic characteristics, the fungus was identified as Aspergillus section Flavi. Accurate identification of grown Aspergillus colonies was performed by polymerase chain reaction (PCR) assay using the two universal fungal primers Bt2a and Bt2b targeting the β-tubulin gene (). Amplicons were sequenced and compared with the GenBank database () for final identification at species level. The isolate was assigned to A. flavus based on the complete identity with corresponding sequences of the A. flavus strain CBS 816.96. Then, they were submitted to GenBank and received the accession number MN097724. Prior to antifungal therapy, three consecutive blood samples were taken and inoculated with blood cultures containing brain–heart infusion (BHI) broth and BHI agar and processed. The blood cultures had no microbial growth after 2 weeks of incubation at 37°C. DNA was extracted from negative blood culture bottles using a QIAmp DNA blood minikit and subjected to β-tubulin gene amplification. The β-tubulin amplicon from the negative blood culture sequenced and its DNA-sequence data were in complete agreement with the DNA sequences of A. flavus strain CBS 816.96, similar to the aforementioned finding regarding the colony grown from the explanted valve (). Liposomal amphotericin B at a dose of 5 mg/kg body weight/day (350 mg) together with broad-spectrum antibiotics (ciprofloxacin, meropenem, and vancomycin) were administered via a peripherally inserted venous catheter. On day 11 of admission, after 7 days’ antifungal therapy, the patient expired from presumed severe sepsis, probably related to progressive AE.
In our institution, antifungal susceptibility testing is not a routine workup; however, in vitro antifungal-susceptibility testing was performed according to document M38-A2 of the Clinical and Laboratory Standards Institute (CLSI) on Aspergillus isolates after the patient had died. Minimum inhibitory concentrations were obtained for amphotericin B(2 μg/mL), fluconazole (16 μg/mL), itraconazole (0.016 μg/mL), voriconazole (0.25 μg/mL), posaconazole (0.032 μg/mL), and minimum effective concentrations for caspofungin; (0.008 μg/mL, anidulafungin; (0.008 μg/mL and micafungin (0.008 μg/mL).This case report was performed in compliance with the Declaration of Helsinki, and written informed consent was obtained from the legal guardian for its details to be included in the manuscript and for publication. No institutional approval was required to publish the case details.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [60, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Vascular disease history': True, 'Diabetes history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 60 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
790,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8388320-1,Extracted,"A 70-year-old male, with arterial hypertension, previous paroxysmal atrial fibrillation (AF) episodes, and heavy smoker for 40 years, was admitted to the emergency department with the primary symptom of mental confusion and postural instability. Current medications included apixaban 5 mg bid and bisoprolol 2, 5 mg od. Neurologic examination was unremarkable, and a brain computed tomography scan performed immediately after admission showed no significant abnormalities. Electrocardiogram showed AF with rapid ventricular response and nonspecific ST changes []; a focused cardiac ultrasound demonstrated concomitant de novo LV dysfunction. Chest X-ray showed left basal pneumonia with parapneumonic effusion. The patient was then referred to our cardiology department.
Upon admission (day 1), transthoracic echocardiography (TTE) showed eccentric LV hypertrophy (LV end-diastolic diameter = 58 mm, interventricular septum = 13 mm) with inferolateral hypo/akinesia and reduced LV ejection fraction (Simpson's biplane rule 35%); there was no pericardial effusion. Laboratory test [] revealed increased high-sensitivity troponin I (1253 ng/L), increased NT-proBNP (8650 pg/ml), leukocytosis with neutrophilia (white blood cell count, 8.36 × 103/μL 89.6%), increased C-reactive protein and procalcitonin (29.2 mg/dL and 9.44, respectively), increased serum creatinine (2.13 mg/dl), and mild hyponatremia (Na 133 mEq/L). Empirical antibiotic therapy for community-acquired pneumonia (with ceftriaxone 2 g od and clarithromycin 250 mg bid) was immediately started. Intravenous amiodarone restored sinus rhythm a few hours after admission; additionally, ramipril was added to background therapy (i.e., apixaban and bisoprolol). Initial tentative diagnosis was tachycardiomyopathy. Given the atypical clinical presentation of pneumonia (mental confusion without cough), urinary antigen testing for atypical pathogens was performed on day 2, which resulted positive for (LP); serology for the most common viral infections was negative. Then, specific intravenous antibiotic treatment with levofloxacin 500 mg od was started. Global LV function progressively improved till 50% on day 4. On day 7, the patient underwent CMR that showed findings highly suggestive of myocarditis: Myocardial edema was demonstrated as an area of high signal intensity in T2-weighted imaging of inferolateral wall at midventricular wall, with mesocardial pattern []. Myocardial necrosis was visualized as subepicardial late gadolinium enhancement of the septal, inferior, and inferolateral walls at basal and midventricular level, with nonischemic pattern [].
The same day TTE was repeated. Global peak longitudinal strain (2D speckle tracking) was slightly reduced (i.e.,−15.9%). Bull's eye representation of the multilayer (subendocardium, midmyocardium, and subepicardium) 2D speckle-tracking analysis showed alteration of subepicardial layer of the posterolateral and anterior wall [].
The patient was discharged with a diagnosis of acute infectious myocarditis caused by LP pneumonia. The following therapy was prescribed: ramipril 2.5 mg bid, apixaban 5 mg bid, bisoprolol 5 mg od, and levofloxacin 500 mg od (for another 7 days).
The patient had a follow-up visit at 40 days; he was asymptomatic and physical examination was unremarkable. A CMR was performed the same day, showing no signs of myocardial edema in T2-weighted imaging, and slight subepicardial late gadolinium enhancement of the inferior wall at basal and midventricular level []. The TTE, acquired on the same day, showed improvement of LV ejection fraction and global longitudinal strain (57% and 18.6%, respectively); namely, layer-specific 2D speckle tracking showed impairment of the same segments as observed at baseline, whose parameters were improved with respect to the previous examination [].",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [70, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 70 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
791,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8299425-1,Extracted,"A 56-year-old El-Salvadorian male with no past medical history presented to our hospital with new-onset left-sided weakness involving the upper and lower extremities with difficulty speaking of 2 h duration. Upon arrival at the hospital, his vital signs were unremarkable. On physical examination, he scored 9 points on the NIH stroke scale (left facial droop, left upper extremity weakness, left lower extremity weakness, left-sided paresthesia, dysarthria, and extinction to bilateral simultaneous stimulation). Laboratory investigations showed LDL of 115 mg/dL and a normal hemoglobin A1C. Brain magnetic resonance imaging (MRI) with gadolinium showed an acute infarct in the right middle cerebral artery territory (shown in Fig. ) along with old cortical infarcts in the left frontal, parietal, and occipital lobes and an old left cerebellar infarct (shown in Fig. ). Brain magnetic resonance arteriogram without contrast showed no large vessel occlusion/stenosis or aneurysmal changes. The patient subsequently received intravenous alteplase and was admitted to the hospital for monitoring and further stroke workup. His electrocardiogram (ECG) showed normal sinus rhythm with bifascicular block. Carotid duplex was unremarkable. A 2D echocardiogram was obtained and demonstrated borderline reduced left ventricular ejection fraction of 50–55%; the apex was not well imaged, and no signs for left ventricular hypertrophy were seen. Repeat echocardiogram with contrast suggested a possible focal apical aneurysm, but the study was suboptimal to assess. Because of the suboptimal apical imaging by echocardiogram, cardiac MRI with gadolinium was obtained and showed near transmural late gadolinium enhancement of the lateral wall with a focal apical aneurysm (shown in Fig. ). Laboratory assessment for thrombophilia was negative, and an implantable loop recorder was placed to assess for occult atrial fibrillation. Upon review of his clinical picture, country of origin, and imaging studies, his risk for CCC became apparent, and Trypanosoma cruzi IgG testing was performed. Both commercial serologic testing and CDC confirmation with ELISA and TESA blot assays confirmed this diagnosis. By the end of his hospitalization, his neurological symptoms resolved except for a mild left facial droop.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [56, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 56 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 0 + 2 = 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
792,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8665735-1,Extracted,"A 54-year-old, Hispanic male with no known past medical history presented to the emergency room with a chief complaint of sudden-onset right-sided weakness over the past 24 hours. The patient denied any associated dizziness, visual disturbance, or reduced level of consciousness. He had not seen a physician in over 20 years. His social history was significant for chronic alcohol abuse with consumption of at least one pint of tequila or beer per day for at least 35 years. The patient was tachycardic to 101/min with a physical exam that was remarkable for right-sided facial droop as well as 1/5 strength in the right upper and lower extremities. He was noted to have a National Institutes of Health stroke scale of 17.
A stat computed tomography (CT) of the head without contrast as well as magnetic resonance imaging (MRI) without contrast were negative for acute stroke. The patient's urine drug screen and alcohol level was unremarkable. His labs were significant for an ALT of 70, AST 251, direct bilirubin 0.4, INR 1.1, platelets 79 x 10^3 (Table ). All of his other labs were normal. Further investigation with right upper quadrant ultrasound suggested possible liver cirrhosis. Computed tomography of the abdomen and pelvis revealed a micronodular appearance of the liver with numerous scattered hypodensities (Figure ). A hepatitis A, B, C panel, autoimmune panel, alpha-1 antitrypsin deficiency panel and iron panel were all negative. Our patient was suspected to have alcohol-induced cirrhosis due to his extensive alcohol history.
A lipid panel and Doppler of the neck were obtained which were found to be normal. Once an ammonia level was found to be 140 micro mol/L, the patient was started on lactulose and rifaximin. The patient opted out of physical therapy the first two days of admission; however, his neurological symptoms resolved without residual neurological deficits about 36 hours after treatment of lactulose and rifaximin. We discharged our patient with close follow-up at a GI clinic and repeat labs one month after discharge (Table ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Vascular disease history': False, 'age': [54, 'years'], 'Stroke': False, 'Diabetes history': False, 'Transient Ischemic Attacks History': False, 'sex': 'Male'}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 54 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
793,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4906173-1,Extracted,"A 75-year-old man with sudden melena was referred to our hospital. He had a history of cardiac infarction, atrial fibrillation, high blood pressure, diabetes mellitus, and Parkinson's disease. The patient always took Bayaspirin (100 mg/day) and Xarelto (15 mg/day). The patient's systolic blood pressure was 84 mmHg, and heart rate was elevated at 105 beats/min. Physical examination showed eyelid anemia, and digital rectal examination revealed attachment of bloody stool. A blood test revealed anemia with a hemoglobin level of 10.7 g/dL. In coagulation tests, prolonged coagulation time was noted, with a prothrombin time percentage (PT%) of 68%, activated partial thromboplastin time of 42.4 s, fibrin degradation product level of 6.7 μg/mL, and D-dimer level of 4.7 μg/mL. Helical computed tomographic angiography (CTA) revealed an abnormal vessel in the wall of the sigmoid colon, which was visualized as a high-density area, and a hematoma in the sigmoid colon, which was visualized as a low-density area (). Colonoscopy revealed a huge hematoma with active bleeding in the submucosal area of the sigmoid colon (). Endoscopic hemostasis procedures, such as clipping and coagulation, could not be performed, because a huge hematoma obscured the bleed point. As blood pressure did not respond to fluid administration, an emergency sigmoidectomy was performed. During the procedure, a huge submucosal hematoma was seen through the wall of the sigmoid colon. The resected specimen showed a huge submucosal hematoma, which was 180 × 70 mm in size (). Histopathological examination showed a submucosal extended vessel without elastic fibers in the hematoma (Figures and ). Therefore, he was diagnosed with colonic AD. On postoperative day 7, Hartmann's operation was performed owing to an anastomotic leak. He was discharged on postoperative day 70.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [75, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Thromboembolism history': True, 'Vascular disease history': True, 'Diabetes history': True}",8,8,8,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 75 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 7 + 1 = 8.
The patient's CHA2DS2-VASc Score is 8."
794,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3262495-1,Extracted,"An almost asymptomatic 41-year-old woman suffering from mild dyspnoea on exertion consulted her physician for the yearly checkup. The physical examination was completely unremarkable, all laboratory testings were within normal limits, and the ECG showed sinus rhythm; only the chest X-ray revealed an enlargement of the cardiac silhouette ().
Following echocardiographic examination and contrast-enhanced CT scan of the thorax revealed a lipomatous mass, measuring 16 × 14 × 12 cm, located on the left side of the heart with blood supply from the left coronary artery, highly suspective of a lipoma (). Within this mass, a dense calcification (3.5 × 1.5 cm in diameter) in the cranioventral part of the tumour was seen. This large mass caused a marked shift in the midline structures, displacing the heart to the right hemithorax.
In October 2010, the patient underwent open heart surgery via median sternotomy without cardiopulmonary support. The pericardium was opened on the left side and revealed the left atrium and ventricle pushed to the right side by a lipomatous tumor. The lipoma had a stalk measuring about 5 cm in diameter connected to the diaphragmatic surface of the left ventricle, but it did not adhere to the pericardium. The tumour mass was completely removed, hemostasis was achieved, and the chest was closed after placing one chest tube in the pericardium. The postoperative course was uneventful and the patient was discharged from hospital on the 6th postoperative day. The patient is currently asymptomatic and has not presented with evidence of recurrence at the 6-month followup.
Gross examination revealed a homogenous yellowish vascularized tumour mass with a smooth lobulated surface limited by a fibrous capsule (). Histologically, the excised specimen showed a fatty structure of mature benign fat with some areas of increased vascularity ().",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [41, 'years'], 'Congestive Heart Failure': False, 'Vascular disease history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 41 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
795,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7891243-1,Extracted,"A 79-year-old woman was referred to our hospital for recurrent paroxysmal AF with palpitation. She had a history of transient ischaemic attack and hypertension. She was on candesartan (8 mg once daily), amlodipine (2.5 mg once daily), and apixaban (2.5 mg twice daily). Her body weight was 39 kg, and height was 159 cm. All laboratory findings were within normal range. Electrocardiogram showed normal sinus rhythm and no evidence of ischaemic changes or ST elevation. Chest X-ray was unremarkable. She showed a dilated left atrium (LA diameter: 31 mm, LA volume index: 35 mL/m2) and normal left ventricular systolic function (left ventricular ejection fraction: 76%). Pre-procedural cardiac computed tomography (CT) showed four pulmonary veins, and slight dilated ascending aorta (maximum diameter: 40 mm, ) with mild calcific plaques. We decided to perform CA for AF, and recommended TOE before the CA to assess the presence or absence of left atrial appendage thrombus (LAAT) because she had a CHADS2 score of 4.
On the day before the CA, TOE was performed with an iE33 (Philips Medical System, Andover, MA, USA) with a 4-MHz OmniPlane probe. After local pharyngeal anaesthesia with lidocaine spray, the patient was placed in the left lateral position and midazolam (3 mg) was administered for mild sedation. Her physical examination showed a regular pulse rate (PR) of 62 b.p.m., a blood pressure (BP) of 117/84 mmHg, and a normal temperature. Her physical examinations at the time of TOE procedure were unremarkable. At 3 min after probe insertion, she had a BP of 117/84 mmHg, PR of 62 b.p.m., and there was no abnormal finding of the ascending aorta at that time (). We then administered additional midazolam (2 mg) due to body movement. At 5 min after the insertion, we confirmed that the absence of LAAT (BP: 95/40 mmHg, PR: 76 b.p.m.). However, TOE showed ascending aortic dissection without pericardial effusion (). The probe was removed at the end of anaesthesia after flumazenil (0.2 mg) infusion. After waking, she had severe back pain, and underwent a contrast-enhanced cardiac CT. Cardiac CT demonstrated Stanford type A aortic dissection extending from the aortic root to the bifurcation of common iliac arteries, and tight stenosis in the right coronary artery (maximum diameter; 49 mm, ). An electrocardiogram showed a normal sinus rhythm and no ST-segment abnormalities. The patient underwent a replacement of the ascending aorta, and a coronary artery bypass graft surgery for the right coronary artery. After surgery, the patient gradually stabilized, and she was transferred to a rehabilitation hospital on the 60th postoperative day. After 9 months of follow-up, the patient is doing well.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [79, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': True, 'Vascular disease history': True, 'Diabetes history': False}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 79 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
796,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4377793-1,Extracted,"A 44-year-old female presented to the ophthalmology service with bilateral severe visual loss of 1-month duration. She had a past history of protein C, protein S and anti-thrombin III deficiency, complicated by superior mesenteric and portal vein thrombosis for which she was on warfarin therapy. She had previously been investigated for autoimmune vasculitis as a possible cause of Raynaud's phenomenon.
Her vision was 6/120 in the right eye and light perception in the left. There was a right inferior quadrant and left total ERD associated with vitreous haemorrhage.
Ocular ultrasonography (B scan) did not reveal any underlying posterior scleritis or choroidal tumour. Fundal fluorescein (FA) and indocyanine-green angiography (Figure ) to visualize the retinal and choroidal vasculature, respectively, for coexistent vasculitis and leakage showed no evidence of any intraocular mass or ocular inflammatory condition causing vasculitis.
During a visit to the ophthalmologist, she was admitted to the medical ward when she was noted to have severe breathlessness from a right-sided pleural effusion and had abdominal distension from portal and superior mesenteric vein thrombosis leading to ascites. Systemic investigations revealed severe hypoalbuminaemia (albumin 10 G/L), elevated serum alkaline phosphatase 124 U/L (32–103 U/L) and gamma-glutamyl transferase 226 U/L (7–39 U/L) levels and total urine protein 0.20 G/day. The gastroenterologist made a diagnosis of protein-losing enteropathy based on the presence of intestinal oedema, which developed secondary to superior mesenteric and portal vein thrombosis.
The vision in her right eye dropped to hand movements progressively over the next 3 months due to rapid progression of ERD, which was treated conservatively in view of her underlying medical condition. The patient became increasingly unwell and defaulted follow-up. In this patient, multiple systemic complications occurred due to venous thrombosis, which eventually led to protein losing enteropathy and rapidly progress to blindness. She subsequently passed away from multi-system organ failure during one of her hospital admissions.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [44, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 44 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
797,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6703128-1,Extracted,"A 47-year-old man developed chest pain and low-grade fever. He was diagnosed with pneumonia with parapneumonic pleural effusion using a chest X-ray image () and CT without contrast (). Although he received azithromycin, followed by garenoxacin, imaging indicated worsening of the condition (). As haemoptysis was observed, he was referred to our hospital.
He had never smoked and had been previously healthy except for atrial fibrillation that had been successfully treated via catheter ablation, without complications, 5 months previously. Physical examination revealed normal percussion and auscultation findings for both lungs, a blood pressure of 110/60 mm Hg, peripheral oxygen saturation of 97% at room air, a heart rate of 88/min without arrhythmia, a respiratory rate of 18 breaths/min and a body temperature of 36.8℃. Routine blood tests yielded no remarkable finding except a C reactive protein level of 30.2 mg/L. Bronchoalveolar lavage and transbronchial lung biopsy of the apicoposterior segment of the left upper lobe () were performed. The lavage fluid was clear and the cells included macrophages (90.2%), neutrophils (5.8%), eosinophils (0.2%) and lymphocytes (3.8%). Histological examination revealed some tissue plugs within the lumina of the small airways, part-extending into the alveolar ducts and alveoli. Two weeks after bronchoscopic examination, we prescribed prednisolone (0.5 mg/kg/day) because the infiltration had progressed to the left lower lung field. Although the consolidation transiently regressed, it became slightly worse 2 weeks after treatment (). Although we increased prednisolone (to 1 mg/kg/day), opacities in the left upper lobe migrated ().",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [47, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 47 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
798,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7949244-1,Extracted,"A 73-year-old right-handed Taiwanese man was admitted to our hospital after suffering syncope. On the day of admission, he had been well until 7:00 in the morning, when he was playing tennis. Specifically, he suddenly lost consciousness and fell to the ground. The patient promptly regained consciousness, but his verbal output was limited to saying the word “hao” (meaning “yes” in English). His friends took him to our emergency department at 8:39 am.
On arrival, the patient was E2VaM4. On examination, he was alert. He had impairments in speech fluency, comprehension and repetition. His only verbal output was the sound “hao” or “hum”. Gait, extraocular motion, motor, and sensory functions were all normal. He showed no eye ptosis nor facial palsy. Blood parameters, including homocysteine levels, lipid profile, diabetes, oncology and endocrine measures, were unremarkable. Brain CT with contrast revealed no apparent intracranial haemorrhage or mass. However, CT perfusion indicated poor perfusion over the left middle cerebral territory (Fig. ).
Tracing back his medical history, the patient was normostenic (body mass index was 18). He had hypertension for more than twenty years. He also suffered from hyperlipidaemia and coronary artery disease, and 7 months previously, he had received one drug-eluting stent. His daily medications included amlodipine 5 mg, aspirin 100 mg and rosuvastatin 5 mg. He played tennis twice a day and never smoked or drank alcohol. His highest education was senior high school and was fluent in Chinese, Taiwanese and Japanese. He used to work at an international trading company but had been retired for two years.
Under the impression of acute cerebral infarction with global aphasia, he then received a recombinant tissue plasminogen activator (rtPA) injection at 9:26 am and was switched to our intensive care unit for further management. Brain non-contrast magnetic resonance imaging (MRI; Fig. ) was conducted on day 5, disclosing an acute infarction in the territory of the left middle cerebral artery (MCA), just in the perisylvian gyri, the classic areas of Wernicke and Broca. After 12 days of inpatient treatment, the patient was later discharged under stable conditions with global aphasia status and no focal neurologic signs. He was able to resume playing tennis on a daily basis soon after discharge.
The patient then received speech rehabilitation, including verbal production, auditory comprehension training, augmentative communication training, phonetic placement and high-level cognitive function training at our hospital and another hospital. His language expression gradually recovered. The CCAT was then performed 14 months after the initial stroke. His average CCAT score was 5.6, indicating moderate to severe aphasia (Fig. ). Detailed analyses of his spoken language characteristics showed subnormal performances for both sentence intonation and sentence length (Fig. ), indicating he had fluent aphasia.
We subsequently checked is cerebral blood flow using regional brain single photon emission computed tomography (SPECT; Fig. ). No radioactivity was found in the left frontal and left parietotemporal regions, and instead, a relatively high level of radioactivity uptake was noted over the right thalamus, frontal and occipital lobes.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [73, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Vascular disease history': True, 'Diabetes history': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 73 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
799,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-5106,Extracted,"An 84-year-old man presents to the emergency department for a loss of consciousness. The patient states that he was using the bathroom when he lost consciousness and fell, hitting his head on the counter. The patient has a past medical history of diabetes, hypertension, obesity, factor V leiden, constipation, myocardial infarction, and vascular claudication. His current medications include lisinopril, atorvastatin, valproic acid, propranolol, insulin, metformin, and sodium docusate. The patient denies use of illicit substances. His temperature is 99.5°F (37.5°C), blood pressure is 167/98 mmHg, pulse is 90/min, respirations are 15/min, and oxygen saturation is 98% on room air. Physical exam reveals an elderly man sitting comfortably in his stretcher. Cardiac exam reveals a systolic murmur heard at the right upper sternal border that radiates to the carotids. Pulmonary exam reveals mild bibasilar crackles. Neurological exam reveals 5/5 strength in his upper and lower extremities with normal sensation. The patient's gait is mildly unstable. The patient is unable to give a urine sample in the emergency department and states that he almost fainted again when he tried to.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [84, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 84 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
800,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4790420-1,Extracted,"A 34-year-old man with a history of recurrent epistaxis presented with a sudden fall associated with seizure-like activity. He was brought to our trauma center and was found to have a large subdural hematoma. The patient did not have any medical history except for intermittent nosebleeds since childhood. He smoked a pack of cigarettes daily, drank alcoholic beverages socially, and used marijuana. Family history revealed that his twin brother also suffered from nosebleeds, and the patient’s mother had a transient ischemic attack of unknown etiology at the age of 32.
On admission, vital signs were significant for a heart rate of 47 beats per minute and a respiratory rate of 40 breaths per minute with a Glasgow Coma Scale (GCS) score of 6. The patient was immediately intubated. He had a fixed, dilated 7-mm right pupil on examination. Preliminary blood work showed an elevated total leukocyte count (12 × 109/L) with an otherwise normal complete blood count and coagulation profile. A blood ethanol level was markedly elevated at 56.88 mmol/L. A computed tomography (CT) scan of the head revealed a large, right subdural hematoma with 1.6-mm leftward midline shift, uncal herniation, and obstructive hydrocephalus. Emergent craniotomy with evacuation of the subdural hematoma was performed. Subsequently, a brain CT venogram demonstrated 3 sites of nonocclusive thrombus within the superior sagittal sinus and the right transverse sinus. There were no cerebral arteriovenous malformations identified on imaging.
Incidentally, trauma imaging showed a serpiginous focus within the right upper lobe with a prominent feeding artery and vein arising from the pulmonary artery and pulmonary veins, respectively, consistent with a pulmonary arteriovenous malformation (PAVM; ). The feeding artery measured 2.9 mm in diameter (). The patient did not have any hemoptysis or cyanosis. The trauma imaging protocol at our institution consists of a CT head without contrast and a CT chest, abdomen, and pelvis with contrast using a 64-slice multidetector CT scan. A case-matched series has found that patients who underwent immediate total-body CT scanning had a significantly lower 30-day mortality rate as patients who underwent conventional imaging and selective CT scanning after correcting for in-hospital GCS score. Given the traumatic head injury in our patient and resulting low GCS score, he was not able to localize symptoms or provide a history related to the trauma. A multicenter randomized clinical trial is currently underway to determine the value of immediate total-body CT scanning in trauma patients (REACT-2).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [34, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 34 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
801,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2553053-1,Extracted,"A 60-year-old female with a history of hypertension and dyslipidemia visited the emergency department due to recurrent episodes of progressive, effort-related angina for the past two months. Physical examination revealed a mild systolic murmur best heart at the apex and her blood pressure was 150/85 mm Hg. Electrocardiogram (ECG) showed T wave inversion in leads I, AVL, V4–V6. The levels of cardiac enzymes were between normal ranges. Two-dimensional echocardiography showed hypokinesis of the inferoposterior and lateral wall with ejection fraction of 50% and mitral regurgitation (grade I/IV). The patient was admitted in hospital and treated with aspirin 325 mg, oral nitrates and clopidogrel 75 mg × 1.
A non-elective diagnostic coronary angiogram (CAG) was performed with standard 6 F 4 Judkins (Cordis, Johnson&Johnson, Miami, FL, USA) catheters via a right femoral approach. Contrast injection revealed two stenotic lesions of 70% and 80%, at the proximal and middle segment respectively, of a right coronary artery (RCA), with significant tortuosity (Figure ). Coronary angioplasty of the right coronary artery was decided. After an unsuccessful attempt with a 0.014-inch Hi-torque Extra Suport (Guidant Corporation; Santa Clara, USA) guidewire to cross the lesions, a 0.014-inch Hi-torque Cross-IT (Guidant Corporation; Santa Clara, CA, USA), intermediate guidewire was advanced across the stenoses and balloon dilatation was performed with a 2 × 10 mm balloon (Flash, Bolton Medical, USA) at 12 atm. The tortuous proximal segments were completely straightened by this technique and after the balloon was removed, angiographic control exposed slit like multiple filling defects along the longitudinal axis of the RCA, an appearance of stenoses strongly suggesting the accordion effect or dissection, and vasospasm (Figure ). Isosorbide dinitrate was administrated intracoronary in order to clarify the possibility of coronary spasm but the angiographic appearance of the RCA did not change. The patient had severe chest pain with ECG changes (ST elevation on leads II, III, aVF) and a drop of blood pressure at critical levels (90/60 mmHg). As the deformity of the artery persisted and in view of patient's symptoms stenting was performed. A 2.75 mm × 14 mm stent (Apollo Cordynamic, Bionert, Barcelona, Spain) was delivered with little resistance at the middle segment lesion expanded at 16 atm. A second 3 mm × 14 mm stent (Apollo, Cordynamic, Bionert, Barcelona, Spain) was deployed at the proximal lesion which was expanded at 18 Atm (Figure and ). Angiography following stenting showed residual stenosis at the edges of both stents (Figure ). Although coronary spasm was highly suspected, several intracoronary administrations of isosorbide dinitrate could not relieve of this narrowing. The appearance of newly developed lesion was thought as a repeated accordion phenomenon. Thus, the guidewire was withdrawn and this resulted in resolution of the new stenosis and resumption of previous proximal tortuosity of the artery (Figure ). The final outcome was excellent. The patient had an uneventful recovery and was discharged after 24 hours.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Hypertension history': True, 'age': [60, 'years'], 'Stroke': False, 'Transient Ischemic Attacks History': False, 'sex': 'Female'}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 60 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
802,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3999682-1,Extracted,"A 70-year-old female patient presented to us in the early morning of January 1, 2011 with massive haemoptysis. The patient was a known case of hypothyroidism and hypertension and on regular treatment. She had been complaining of cough with expectoration and mild streaking of blood in sputum for about 3 days. On examination the pulse rate was 96/min, BP 134/76 mm Hg, RR 25/min, and SPO2 94% on 2 l of O2. Chest examination revealed bilateral vesicular breath sounds with crepts in right infrascapular and infra-axillary regions. There was no history of dental manipulation, facial lesions or trauma to mouth, aspiration, or alcoholism. Her cardiovascular, GIT, and central nervous system examinations revealed no abnormality. She was admitted in the intensive care unit and her initial investigations including ECG, ABG, CBC, KFT, LFT, and RBS were within the normal range. Her sputum was sent for AFB, gram's stain, and fungal stain along with culture and sensitivity for pyogenic organisms. Her chest X-ray revealed right mid zone homogenous opacity along with the obliteration of both right costophrenic and cardiophrenic angles []. She was started on piperacillin + tazobactum along with IV haemostatics, IV fluids, and cough suppressants. Once stabilized, she was taken for diagnostic fibreoptic bronchoscopy that revealed a cauliflower-like growth in RUL bronchus [] raising a high suspicion of malignancy. BAL was taken and bronchial biopsy for histopathology was obtained from the lesion and sent for histopathological examination. She was continued on conservative treatment and the haemoptysis stopped. BAL was negative for AFB; no organisms were seen on gram's stain and fungal stain. Pyogenic culture also did not grow any organisms. Her chest X-ray after the antibiotics showed an increase in the size of the homogenous opacity abutting the heart []. CECT thorax revealed a large heterogenous soft tissue mass measuring 7 × 5.9 × 6 cm with surrounding parenchymal infiltrates in anterior segment of upper-right lobe and medial segment of middle-right lobe. The mass was abutting the anterior segmental bronchus of upper-right lobe, medial segmental bronchus of the middle-right lobe, costal and mediastinal pleura; the patchy area of consolidation was seen in lower-right lobe limited by oblique fissure with bilateral pleural effusions, which were more on the right side []. Diagnostic pleural aspiration was done. Pleural fluid did not show any organisms on gram stain, AFB stain, and fungal stain. Pyogenic culture was sterile and malignant cells were not seen. The ADA level was 4.76 IU, thus almost ruling out TB. Bronchial biopsy showed markedly inflamed bronchial mucosa with granulation tissue and sheets of inflammatory cells, predominantly neutrophils. Bronchial biopsy was also sent for culture where occasional colonies of gram positive filamentous bacteria surrounded by neutrophils were seen. CT-guided FNAC and Trucut biopsy were done for better understanding of the lesion. On performing FNAC thick pus was aspirated out. FNAC showed sheets of neutrophils and occasional branches of filamentous bacteria with impression of suppurative pathology. Trucut biopsy showed sheets of neutrophils with colonies of filamentous bacteria and sulphur granules [] consistent with actinomycotic infection. She was started on Benzyl penicillin 20 lac units IV 6 hourly and had a dramatic response. Her symptoms disappeared and chest X-ray almost cleared []. Finally, she was discharged in a stable condition on oral amoxicillin + clavulanic acid combination. She is under regular follow up and has continued to be in a stable condition for more than a year.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [70, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': False, 'Stroke': False, 'Diabetes history': False, 'Transient Ischemic Attacks History': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 70 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
803,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7709074-1,Extracted,"A 61-year-old male presented to the emergency department with a 2-h history of new alexia, intermittent expressive dysphasia and right upper limb ataxia. He had a National Institutes for Health Stroke Scale (NIHSS) score of 6 and modified Rankin Score (mRS) for neurological disability of 4. His vision assessed by confrontation remained intact. He had a past medical history of diet controlled type 2 diabetes mellitus and hypertension controlled with Ramipril and Amlodipine 5 mg.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [61, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Vascular disease history': False, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 61 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
804,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4532946-1,Extracted,"Our patient is a 54-year-old male with a past medical history of end stage renal disease on hemodialysis, diabetes mellitus type 2, hypertension, and hepatitis C who presented for altered mental status. The patient had a recent internal medicine clinic visit with concern for pain due to paraspinal muscle spasm. The patient was started on baclofen 10 mg b.i.d. and tramadol 50 mg b.i.d. On the day of admission, the patient was found to be lying on the ground and speaking incoherently by an acquaintance. He was brought to the hospital and admitted to the intensive care unit for altered mental status.
The vital signs were the following: temperature 99.1°F, respiratory rate 21 breaths/minute, pulse 83 beats/minute, blood pressure 138/64 mmhg, and pulse oxygenation 99% on room air. On initial presentation, the patient was lethargic but arousable and unable to answer questions. The remainder of the exam was consistent with his known comorbidities including a left upper extremity arteriovenous fistula and right lower extremity transmetatarsal amputation. Laboratory tests showed the following: sodium 141 mEq/L, potassium 5.2 mEq/L, chloride 101 mEq/L, bicarbonate 26 mEq/L, blood urea nitrogen 55 mg/dL, creatinine 10.98 mg/dL. A white blood cell count was 12.4 mg/dL, hemoglobin 11.3 mg/dL, and platelet count 155/mm3. A venous blood gas included a pH of 7.41 and carbon dioxide 44 mmHg. A hepatic function panel had a total bilirubin of 0.8 mg/dL, AST 45 u/L, ALT 26 u/L, alkaline phosphatase 52 u/L, creatine kinase 1738 u/L, and ammonia 52 u/L. A head computed tomography was performed with no acute intracranial abnormalities. An abdominal ultrasound found hepatomegaly with fatty infiltration. A urine toxicology screen was negative. The patient's pharmacy confirmed fulfillment of the baclofen and tramadol prescription 3 days prior to admission. Compliance with his last hemodialysis session was confirmed. With high suspicion for baclofen-induced encephalopathy, the patient was immediately dialyzed. He received hemodialysis for two sessions with significant improvement in mental status without any residual symptoms. Upon discharge, the patient had baclofen discontinued with no similar episodes since the present hospitalization.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [54, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 54 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
805,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4173472-2,Extracted,"A 60-year-old man with a history of diabetes mellitus, coronary artery disease, ischemic cardiomyopathy, moderate left ventricular dysfunction, severe right ventricular dysfunction, and severe pulmonary artery hypertension had presented to orthopedic department following trauma sustained over the left leg 1 week back, which had progressed to gangrene and was planned for above knee amputation. Patient had four episodes of angina over the period of last 2 years of which the last attack was 4 weeks back, and was on tablet aspirin 75 mg OD. He was classified under American Society of Anesthesiologist (ASA) III, New York Heart Association (NYHA) grade III with MPC III. He was a chronic smoker with 40 pack years.
Laboratory parameters were within normal limits. Chest X-ray revealed bilateral nonhomogeneous opacities with enlarged cardiac shadow. Two D ECHO revealed regional wall motion abnormality along with global hypokinesia and ejection fraction of 25%, and Grade II diastolic dysfunction. Patient was started on injection furosemide 40 mg BD, tablet amiodarone 6.25 mg BD, tablet digoxin 0.25 mg BD, tablet spironolactone 25 mg OD, and injection human albumin 20%.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [60, 'years'], 'Congestive Heart Failure': True, 'Vascular disease history': True, 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 60 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
806,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5667699-1,Extracted,"The patient, a 81-year-old Caucasian male with past medical history of chronic obstructive disease, coronary artery disease, subarachnoid hemorrhage secondary to a fall about 3 years ago, benign prostatic hypertrophy, balder diverticula, sick sinus syndrome with a pacemaker placement, ischemic cardiomyopathy, atrial fibrillation, hypertension, gastroesophageal reflux disease, and anxiety disorder, presented to the emergency department with complaints of gradually worsening generalized abdominal pain that was dull and crampy in nature, 7-8/10 intensity since the last 2 days. Pain was intermittent and was aggravated by moving and consuming food, partially relived with rest and over-the-counter pain analgesics. It was associated with abdominal distention, nausea and one episode of non-bloody, non-bilious vomiting. He did not notice any changes in his bowel habits. He denied any sick contacts or recent history of travel. His last bowel movement was 2 days prior to the presentation. He noted he was not able to pass gas since then as well. He denied any hematochezia, melena or hematemesis. He denied any dysuria, fevers, chest pain, and shortness of breath or palpitations. Patient reported that for the last 2 months, he was having unintentional weight loss but failed to quantify it. Patient reported that his last colonoscopy was about 8 years ago and was normal. Past surgical history was significant for laparoscopic cholecystectomy and cervical laminectomy. Family history was pertinent for colon cancer in mother and brother, and diabetes in father. Patient was a resident of a nursing home and he denied active tobacco, alcohol or illegal drug use. He was allergic to tetracyclines. Patient’s home medications included: Advair Diskus - 250/50 µg - one puff by inhalation twice daily; amiodarone 200 mg daily; warfarin 7.5 mg daily; escitalopram 20 mg once daily; iron sulfate (Feosol) 325 mg daily; furosemide 20 mg once daily; potassium chloride 10 mEq daily; Mucinex (Guafenesin) 600 mg twice daily; Montelukast 10 mg once daily; bupropion 15 mg daily; cetrizine 10 mg daily; over-the-counter multi-vitamin tablets - one daily; and over-the-counter vitamin C tablet once daily.
Review of systems was positive for unquantified weight loss, anorexia, constipation, abdominal discomfort, and bilateral leg swelling. On physical examination, vitals at the time of presentation to the emergency department showed temperature of 98.1 °F (36.7 °C), respiratory rate of 19 breaths/min, regular, unlabored, pulse rate of 67 beats/min, regular rate and rhythm, blood pressure of 118/62 mm Hg, and oxygen saturation of 100% on room air. Patient was an alert, oriented male who was anxious and in some distress. There was no jaundice. His conjunctivae and eyelids were normal. He had full extraocular movements. His oral cavity showed dry oral mucosa. There was no evidence of adenopathy in his head, neck or supraclavicular regions. Trachea was midline. Thyroid was not enlarged. The lungs fields were clear, symmetrical air entry. His heart exam was normal without murmurs, rubs or bruits. Abdominal examination revealed a distended, form abdomen with generalized tenderness on palpation. Percussion revealed a tympanic note. Examination was negative for guarding, rebound tenderness, organomegaly, shifting dullness, Rovsing’s sign, Murphy’s sign, and costo-vertebral angle tenderness. Hyperactive bowel sounds were appreciated in all the four quadrants. Patient refused a rectal examination. Neurological examination was normal. There was 1+ pitting pedal edema in the bilateral lower extremities. Computerized tomography (CT) of the abdomen was performed. It showed apparent transition zone at the rectosigmoid junction with marked dilatation of the large bowel proximal, elevated left hemi-diaphragm with interposition of large bowel underneath and signs of compressive atelectasis of the left upper lobe. Bladder stones were evident in a right-sided bladder diverticulum. The small bowel was not dilated. Patient was admitted to the general medical floor with a provisional diagnosis of bowel obstruction, ruling out colorectal carcinoma. Advanced imaging with a CT scan further solidified the suspicion of bowel obstruction and probable mass. Surgery and gastroenterology consultations were requested. The initial plan was to get a colonoscopy or a sigmoidoscopy to further characterize any suspected mass and then proceed with a colectomy - Hartmann procedure with a diverting colostomy. Patient was put nil per oral and supportive intravenous hydration was provided. A colonoscopy was ordered in the anticipation of a colonoscopy. Patient however did not have any bowel movement after this. A decision was taken to proceed to colonoscopy anyway. Colonoscopy revealed partially dissolved pills that were clumped together in the sigmoid colon with a questionable component of sigmoid volvulus. Pill bezoar was removed carefully and on visual inspection demonstrated multiple aggregated pills that were causing obstruction. Additional inspection of the colon was normal with no ulceration, masses or polyps. Patient’s LBO resolved completely after this and he recovered well tolerating diet with no additional symptoms.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [81, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': True, 'Diabetes history': False}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 81 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
807,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8002862-1,Extracted,"A 74-year-old male was admitted to the Department of Cardiology, Daejeon St. Mary’s Hospital (Daejeon, Korea), for the evaluation of exertional dyspnea (New York Heart Association (NYHA) functional class III), palpitations, and bilateral leg pitting edema for several months. His electrocardiography and Holter monitoring showed atrial fibrillation and rare premature ventricular complexes. He underwent transthoracic echocardiography (TTE), which showed RCM with biatrial enlargement and small pericardial effusion (A–D). His coronary artery angiogram was normal and other secondary causes of RCM were not found. Cardiac magnetic resonance (CMR) images revealed normal left ventricle (LV) chamber size, borderline diffuse left ventricular hypertrophy and very large atria. Contrast enhanced CMR images demonstrated extensive transmural late gadolinium enhancement (LGE) in the apical wall and mid myocardial patchy LGE in the ventricular septum (E–H).
We recommended clinical evaluation and genetic counseling for his family members because he presented a family history of heart disease, with two affected daughters. The proband’s second daughter had mild exertional chest discomfort. Her TTE showed asymmetric septal hypertrophy of the LV and a mildly dilated left atrium (LA) (A–D). Her diastolic dysfunction was grade I according to the American Society of Echocardiography and the European Association of Cardiovascular Imaging criteria []. The proband’s fourth daughter also had asymmetric septal hypertrophy of the LV, with mild enlargement of the LA (E–H). CMR images of the two daughters showed asymmetric septal hypertrophy of the LV, consistent with a diagnosis of HCM. LGE was not found in either daughter.
To resolve the potential genetic cause of cardiomyopathy in a Korean family (I-1, II-2, and II-4 in A), the proband’s genomic DNA was analyzed by whole exome sequencing (WES). The exomic DNA of the proband was enriched using Agilent’s SureSelect XT Human All Exon v5 (Agilent Technologies, Santa Clara, CA, USA), and paired-end sequencing was conducted on an Illumina HiSeq2500 (Illumina, San Diego, CA, USA) for the detection of variants, given the suspicion of familial disease. Base calling, alignment, variant calling, annotation, and quality control reporting were performed using a GATK Best Practices workflow for germline short variant discovery and were manually reviewed by medical laboratory geneticists. In particular, the annotation of the identified variants with respect to the results of their mutation in the reported genes was estimated using the dbNSFP [] and Ensembl Variant Effect Predictor []. By estimating sequence quality along all sequences, 5973 million reads were generated from the proband. A percentage of bases above the average of 30× was achieved for 92.3% of the target region, and the mean read depth (×) was 110. WES of the proband identified five heterozygous variants within the coding region of each gene as candidate causes of autosomal dominant inherited heart diseases with a population allele frequency within the Genome Aggregation Database < 0.001. To determine which variant was the cause of cardiomyopathy in the affected family members, Sanger sequencing was performed additionally. As a result, Sanger sequencing confirmed the presence of a heterozygous frameshift mutation (NM_000256.3:c.3313_3314insGG; p.Ala1105Glyfs*85) in MYBPC3 in the proband (I-1) and his affected daughters (second (II-2) and fourth (II-4)), but not in his unaffected granddaughter (III-3) (B). The variant is not listed in public genome databases from gnomAD (; accessed on 8 November 2020) and the Korean Reference Genome Database (; accessed on 8 November 2020). Although the four remaining variants (KALRN: NM_007064.5: c.1702C>T, p.Pro568Ser; KCNH2: NM_000238.4:c.442C>T, p.Arg148Trp; SKI: NM_003036.4: c.30T>G, p.Cys10Trp; TTN: NM_133378.4: c.54293T>C, p.Ile18098Thr) were the likely candidates, there was no exact correlation between the genotype of these variants and the clinical phenotype in the proband and his family members as determined by Sanger sequencing. Therefore, the MYBPC3 frameshift mutation seemed to be the pathogenic variant.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [74, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 74 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
808,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8088400-1,Extracted,"A 41-year-old female with a past medical history of hypertension, type 2 diabetes mellitus, and previous non-ST-elevation myocardial infarction with normal coronary arteries (MINOCA) three years prior presented with symptoms of sharp chest pain, dry cough, and shortness of breath, which had started two days prior to the presentation. Her vital signs were remarkable for a blood pressure of 122/91 mmHg, heart rate of 180 beats per minute with an irregular rate, a temperature of 36.4 °C, respiratory rate of 24 breaths per minute, and an oxygen saturation of 98% on 5 L nasal cannula. On examination, the patient appeared to be in mild distress. No jugular venous distention was appreciated. Her chest auscultation revealed bilateral crackles.
The patient's laboratory workup is summarized in Table . A nasopharyngeal swab polymerase chain reaction (PCR) was positive for COVID-19 and blood cultures showed no growth. Chest X-ray revealed patchy bilateral peripheral lung infiltrates (Figure ), and CT angiography of the chest showed no pulmonary embolism but revealed bilateral patchy ground-glass lung infiltrates consistent with COVID-19 pneumonia (Figure ). EKG showed a new atrial flutter with a rapid ventricular response (Figure ). Transthoracic echocardiogram revealed a new low left ventricular (LV) ejection fraction of 35-40%, with LV hypertrophy, as well as a granular appearance of LV myocardium suspicious for infiltrative cardiomyopathy (Figure ). Echocardiogram obtained one year prior had shown LV ejection fraction of 50-55% with LV hypertrophy.
The patient was started on intravenous (IV) diltiazem drip, but her heart rate was difficult to control; hence she was started on IV amiodarone and eventually converted to sinus rhythm. She was started on IV heparin for anticoagulation. Her respiratory status deteriorated, and she was subsequently intubated and mechanically ventilated. The COVID-19 pneumonia was treated with a combination of steroids, antibiotics, remdesivir, and convalescence plasma. She improved clinically and was discharged home on oral amiodarone, metoprolol succinate, and warfarin.
CMR obtained about two months from the date of admission showed extensive myocarditis with a typical pattern of sub-epicardial and mid-wall delayed enhancement (Figure ). There was no edema to indicate the acuteness of the disease. LV systolic function was normal with an ejection fraction of 60-65%. These findings confirmed that the patient had suffered from an acute illness at the time of her initial presentation, causing acute symptoms, a drop in LV ejection fraction, and the development of new arrhythmia, which had all resolved by the time of CMR acquisition.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [41, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 41 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
809,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6758983-1,Extracted,"A 61-year-old Caucasian male was referred by his primary care physician (PCP) for having complaints of elevated creatinine associated with hematuria for one month. His other co-morbid conditions were coronary artery disease, atrial fibrillation, hypertension, CKD, iron deficiency anemia, osteoarthritis, mitral valve replacement, and newly diagnosed benign prostate hypertrophy.
He had been to another hospital twice before presenting to the emergency department (ED) where he had been evaluated with cystoscopy that had ruled out any bladder pathology. On evaluation with computed tomography (CT) of the abdomen/pelvis, it was revealed that he had small non-obstructing stones and was told to follow up as an outpatient. He did follow up with his PCP who saw that his creatinine had increased from a baseline of 2.03 mg/dl to 6.8 mg/dl. On initial evaluation at our institution's ED, his creatinine was 6.8 mg/dl, Hb had decreased from a baseline of 12.8 gm/dl to 8.1 gm/dl, the INR was 3.52. CT abdomen/pelvis demonstrated no evidence of acute pathology, negative for obstructive uropathy, crossed unfused renal ectopia, and left kidney is in the abdomen.
Based on laboratory/imaging data, it was thought that the hematuria and AKI were secondary to kidney stones that the patient had passed. On subsequent days, the patient's renal function did not improve with fluids and supportive measures. Workup for vasculitis, infection, and protein electrophoresis were negative; it was decided to proceed with a renal biopsy. The biopsy specimen revealed minimal immunoglobulin A (IgA) deposition, as seen in Figure , and focal crescentic glomerulonephritis, as seen in Figure , with diffuse tubular injury and red blood cells (RBC) cast formation ultimately concluding the diagnosis of WRN (Figure ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [61, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 61 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
810,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7970082-1,Extracted,"A 72-year-old female patient was admitted to our clinic with dyspnea and palpitation. Transthoracic echocardiography revealed a mass which was compatible with a myxoma originating from the left atrium and interatrial septum (about 3.4x5.3 cm in size) (Figure ) which caused stenosis and insufficiency of the mitral valve. Therefore, the patient was taken to operation for the purpose of myxoma resection. A written informed consent was obtained from the patient.
Median sternotomy and standard aortobicaval cannulation were performed. Cardiopulmonary bypass was initiated to evaluate the left atrium. Left atriotomy was performed and myxoma attached to the interatrial septum by a stem was excised (Figure ). When the mitral valve was evaluated, a solid tumor which was incompatible with a myxoma, was observed above the anterior leaflet. The mitral valve, whose leaflet movements were restricted due to this mass, was excised and sent to pathology for frozen-section examination. The result was reported as a stable sarcoma-like mass which was incompatible with a myxoma. Then, the mitral valve was re-evaluated, and the operation was terminated by replacing with the mechanical prosthesis valve, since it was not suitable for repair. Mechanical valve was favored, as the patient had to use warfarin anyway as a result of valvular atrial fibrillation. The patient was followed in the intensive care unit for two days and was discharged on Day 7 of operation. No residual mass was detected in the imaging studies at 6 and 12 months after the operation.
The following results were obtained in the postoperative immunohistochemical examination: Anti-cytokeratin clone, focal positive staining in a small number of cells; CD34, focal positive staining; CD68, negative staining; protein S100, negative staining; desmin, negative staining (Figure ); actin, negative staining. The diagnosis of myxoma was excluded based on these results. Also, the sample was interpreted as a low-grade vascular fibromyxoid mesenchymal heart tumor due to the positivity of CD31 (Figure ) and vimentin (Figure ). The patient was diagnosed with a primary cardiac EHE after positivity of Friend leukemia integration 1 transcription factor (FLI-1) (Figure ) and moderate pleomorphism (Figure ) were detected in the specimens.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
811,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5414512-1,Extracted,"We present below a brief description of our experience in 2012 of a then 73-year old obese hypertensive diabetic CKD stage III Caucasian male patient seen at the Renal Unit of the Mayo Clinic Health System, Eau Claire, in Northwestern Wisconsin, USA, who developed acute yet irreversible AKI in March 2012 following a minimally invasive AVR for symptomatic AS and where IOH played a crucial instrumental role in precipitating AKI. The patient, now 77 years old, remains on maintenance in-center outpatient hemodialysis, three times a week, for ESRD. We would argue that whereas if IOH was prevented here, the patient plausibly would have only experienced mild AKI, would not have needed renal replacement therapy (RRT) and would not be on maintenance hemodialysis four long years later, in March 2016.
A 73-year-old Caucasian man, nonsmoker with past medical history for hypertension, type II diabetes mellitus, obesity, sleep apnea, dyslipidemia, atrial fibrillation, osteoarthritis, a remote history of temporary need for hemodialysis in 2004 for AKI secondary to autoimmune hepatitis, with baseline serum creatinine of 1.5-1.90 mg/dL between November 2004 and February 2012 was evaluated for dyspnea in February 2012 (). Outpatient medications included amlodipine 10 mg/d, atenolol-chlorthalidone 100/25 daily, atorvastatin 80 mg/d, insulin, lisinopril 40 mg/d and multivitamins with minerals daily. He was admitted to the CCU late in February 2012 with acutely worsening heart failure, severe dyspnea and chest pressure. Temperature 36.6, pulse 57 BPM, respiratory rate 35/min, BP 147/76 mm Hg, and pulse oximetry 93% on 3 liters nasal cannula. HEENT; he had bilateral basal inspiratory crackles and a 3/6 ejection systolic ejection murmur predominantly in the aortic region. Hemoglobin was 10.7 g/dL with otherwise normal CBC. Electrolytes were normal and serum creatinine was stable at 1.7 mg/dL. BNP was 1314 ρg/mL (0-100). Urinalysis was unremarkable, without dipstick proteinuria. His initial electrocardiogram (ECG) in the ED showed regular wide complex tachycardia of 120 BPM, in atrial flutter with left bundle branch block (LBBB). His chest x-ray showed pulmonary edema. The patient’s chest pressure resolved following intravenous Furosemide and nitroglycerin 0.1 mcg/kg/min infusion. He subsequently ruled out for acute Myocardial infarction (MI) by ECG and cardiac enzymes. Echocardiogram demonstrated a left ventricular ejection fraction (LVEF) of 50%, paradoxical septal motion consistent with LBBB, grade 2/4 diastolic dysfunction with increased filling pressures, and severe AS with mean gradient of 48 mm Hg, peak gradient of 73.6 mm Hg, peak velocity of 4.3 m/s, dimensionless index (LVOT/AV VTI ratio) of 0.25, and valve area of 1 cm2 (3-4 cm2, normal).
He underwent coronary angiogram which did not show significant coronary artery disease. He underwent prophylactic dental extraction for severe caries and subsequently on March 2, 2012 a minimally invasive surgical AVR with a 25 mm St. Jude Epic stented tissue valve was performed with temporary pacing wires, right femoral venous percutaneous cannulation for cardiopulmonary bypass.
The AVR procedure was carried out through an 8 cm right anterior chest mid-third intercostal space incision, made directly over the fourth rib. One unit of packed red blood cells was given. The postoperative transesophageal echocardiogram demonstrated an LV of 50% with a normal functioning aortic valve prosthesis. The bypass time was 150 minutes. The cross clamp time was 101 minutes. Intraoperative continuous blood pressure recordings during the nearly 8-hour long procedure demonstrated significant episodes of IOH, with systolic blood pressure values as low as 50 mm Hg, MAP as low as 50 mm Hg, and diastolic blood pressure values as low as 44 mm Hg repeatedly recorded during the operation ( and ).
Because of post-operative AKI, progressive volume overload and oligoanuria despite high-dose continuous intravenous furosemide infusion, he needed RRT to be initiated within 24 hours of the AVR. He had been on chronic ACE inhibition for many years with Lisinopril 40 mg daily immediately prior to the AVR procedure; last dose of Lisinopril documented was on February 26, 2012 as an inpatient. Serum creatinine rose very quickly and has since remained elevated ( and ). His initial hemodialysis vascular access was a temporary right femoral vein dialysis catheter, on March 3, 2012. The right femoral dialysis catheter was subsequently replaced by a left internal jugular vein tunneled Palindrome dialysis catheter (Permcath) for dialysis access on March 15, 2012. Four months later, when it became clear that there was no renal recovery, his status was converted to ESRD, and a transposed cephalic vein AV fistula was created in the left upper arm on July 10, 2012. This was converted in January 2013 to a left upper arm loop graft die to poor maturation of the prior placed AVF. He has since then continued his hemodialysis treatments using this AVF graft to date. He remains an anuric ESRD patient, with a serum creatinine of 8.85 mg/dL as at March 2, 2016, exactly four years after the minimally invasive AVR procedure ().",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [77, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
812,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7784118-1,Extracted,"A 25-year-old female presented with fever, breathlessness, palpitation and rapidly progressive generalised body weakness rendering her bedridden over a period of 3 days. She has a background of Graves’ disease, diagnosed 6 months earlier when she presented with weight loss, palpitation and heat intolerance. Initial investigation revealed severe thyrotoxicosis with thyroid stimulating hormone (TSH) level of <0.008 mIU/L (normal range: 0.35–4.94), free thyroxine (FT4) level of >75 pmol/L (9.01-19.05) and TSH receptor antibody (TRAb) level of 19.3 IU/L (<1.0). She was started on oral carbimazole but her thyrotoxicosis was suboptimally controlled due to poor compliance. She was otherwise well and did not have any previous muscle weakness.
Upon assessment, she appeared agitated with a blood pressure of 102/50 mmHg and respiratory rate of 32/min. She was also febrile at 38°C and had an irregular pulse rate of 150 beats/min. Clinical examination revealed a diffuse grade 3 goiter with thyroid bruit and bilateral exophthalmos with inactive thyroid eye disease. She also had generalised hypotonia, areflexia and diminished power of Medical Research Council (MRC) grade 2/5 in her upper limbs and 1/5 in her lower limbs both proximally and distally. Her cranial nerve examination and pinprick sensation were normal. Her condition was further complicated by decompensated cardiac failure with poor peripheral perfusion, raised jugular venous pressure, bibasal lung crepitations and gallop rhythm. Electrocardiography showed atrial fibrillation and chest X-ray revealed signs of pulmonary congestion and cardiomegaly.
Her thyroid function test (TFT) demonstrated overt hyperthyroidism with TSH level of <0.01 mIU/L and FT4 level of 43.56 pmol/L. Her serum potassium level was normal, 4 mmol/L (3.5- 5.1). Her serum bilirubin level was elevated at 53.5 umol/L (3.4–17.1) and she had severe transaminitis with alanine aminotransferase of 748 U/L (0-55) and aspartate aminotransferase of 1755 U/L (5-34). t Subsequent investigations including blood culture, lumbar puncture and antiganglioside antibodies were normal. Her nerve conduction study (NCS) showed reduced compound motor action potential (CMAP) amplitudes with normal conduction velocities and distal motor latencies (). Her sensory nerve action potentials (SNAP) were within normal limits and this relative sparing of SNAP was suggestive of underlying myopathy. Her electromyography (EMG) showed small amplitudes, short duration motor unit action potential with early recruitment. There were also increased insertional activities with complex repetitive discharges, in keeping with recent onset generalized myopathy (). Repetitive nerve stimulation was not performed in view of the positive EMG findings.
Her Burch-Wartofsky score was 85, highly suggestive of thyroid storm (). A diagnosis of thyroid storm complicated with decompensated cardiac failure, severe hepatitis and acute thyrotoxic myopathy was made. She was intubated for type 1 respiratory failure and was started on intravenous hydrocortisone 100 mg three times daily, oral Lugol’s iodine 8 drops three times daily, oral cholestyramine 4 g four times daily and oral propranolol 40 mg four times daily. Oral carbimazole 20 mg twice daily was subsequently started after 3 days when the liver function tests (LFT) improved. Within 3 days, her condition improved tremendously and she was extubated. Following one week of treatment, her muscle power improved partially to MRC grade 3/5 coinciding with an improvement in her TFT with FT4 of 15.32 pmol/L and TSH <0.01 mIU/L. Total thyroidectomy was performed during the same admission and she was then started on thyroxine replacement. She required assisted ambulation with walking frame initially upon discharge but gradually regained full muscle power over three months following biochemical remission.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [25, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 25 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
813,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3836471-1,Extracted,"A 52-year-old right-handed man, who suffered from hypertension for 5 years without regular medicine and followup, was admitted to our facility after acute loss of consciousness. The patient exhibited left hemiplegia secondary to right putaminal hemorrhage (3 × 5 cm in size) extending into the posterior portion of the internal capsule with the mass effect. On neurological examination, the patient had weak muscle power (1/5 in the left upper limb and 2/5 in the left lower limb) and positive Babinski sign on the left side. An emergent craniotomy for removal of a hematoma was performed; however, the patient demonstrated no significant recovery in his left hemiplegia after the operation. Results of a Romberg test and dynamic testing were poor. The patient's Functional Independence Measurement (FIM) score was 50, and his Barthel index (BI) was 25. Amlodipine besylate 5 mg qd, valsartan 80 mg qd, and atorvastatin 10 mg qd were prescribed for secondary prevention of cerebrovascular disease. Color Doppler sonography showed only mild degree of intimal thickening and sparse mural calcified plaques along the course of bilateral extracranial common and internal carotid and vertebral arteries as well without significant stenosis. MR angiography of the circle of Willis shows decreased signal intensity and number of branches of right middle cerebral artery.
After intensive rehabilitation, the patient's hemiplegia remained, but his gait improved gradually. Two months after the stroke, muscle power was reevaluated in the left upper and lower limbs and was 2/5 and 3/5, respectively. Single photon emission computed tomography (SPECT) showed decreased perfusion in the right cerebral cortex and in the left cerebellum. CCD on the left side was confirmed (). Four months after the stroke, the patient noticed that he involuntarily stretched his hemiplegic arm when yawning in bed. The movement consisted of a progressive abduction, anteroflexion, and mild internal rotation of the shoulder, followed by arm lifting with a flexion of the elbow. The movement lasted for a few seconds. The involuntary activity was absent when the patient was in a sitting position. Repeated attempts to induce yawning by imitation were unsuccessful.
Eight months after the stroke, a follow-up SPECT showed persistent CCD (). The patient's arm was still plegic, but he could walk slowly using a cane with the assistance of an ankle-foot orthosis. The follow-up FIM score and BI were 102 and 70, respectively. The patient continues to experience persistent hemiplegia and CCD, and his functional index has improved only gradually. The frequency and intensity of the phenomenon increased steadily with time after the stroke and also occured when sitting.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [52, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 52 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
814,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-478,Extracted,"A 50-year-old man comes to the emergency department for evaluation of right-sided facial weakness that he noticed after waking up. One month ago, he also experienced right-sided neck pain and headache that began after returning from a hunting trip to New Hampshire the week before. He took ibuprofen to relieve symptoms, which subsided a week later. He has a 5-year history of hypertension controlled with drug therapy. He has smoked one pack of cigarettes daily for 35 years and he drinks two beers daily. His vital signs are within the normal range. Physical examination shows right-sided drooping of the upper and lower half of the face. The patient has difficulties smiling and he is unable to close his right eye. The remainder of the examination shows no abnormalities.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [50, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 50 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
815,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7608498-1,Extracted,"A 59-year-old right-handed Caucasian lady, known to have migraine with aura and type-2 diabetes mellitus presented to our emergency department center with dysarthria, left upper motor neuron facial weakness and left-sided hemiparesis affecting the upper limb more than the lower limb. The patient presented with signs of a right middle cerebral artery (MCA) stroke with an National Institute of Health Stroke Scale (NIHSS) of 10 and unfortunately was out of the window period for intravenous thrombolysis as it was a wake-up stroke and last seen well (LSW) was unknown. A MRI of the brain was obtained on an urgent basis which showed an established infarction in the anterior third of the right MCA territory secondary to the occlusion of the superior M2 branch of the right MCA ().
Upon further workup, CTA showed a filling defect in the right V4 segment of the right vertebral artery which was suspected of being a dissection or a FFT, with normal flow in the left vertebral artery and the basilar artery and its distal branches ().
The attending neurologist in the referring hospital discussed the case with our neurovascular on-call team and the patient was then transferred urgently to our hospital for emergent endovascular therapy (EVT).
The patient was transferred to King Fahad hospital of the university the same night. An urgent angiogram was performed through a 5-F femoral sheath and a diagnostic catheter, under local anesthesia. The left ICA injection showed a normal flow into the MCA territory as well as the anterior cerebral artery (ACA) territory, with no cross flow to the right hemisphere. The right ICA injection showed the previously mentioned occlusion of the superior M2 branch with deficient collaterals to central MCA core territory. The left vertebral injection showed normal flow in its intracranial segment with no reflux into the right vertebral artery with normal flow into the basilar artery and its distal branches (). The right vertebral artery was accessed just at its origin and a slow injection of contrast was administered in fear of dislodging any parts of the suspected thrombus. This injection confirmed the presence of the FFT in the V4 segment of the right vertebral artery with non-visualization of the right posterior-inferior cerebellar artery (PICA) or the distal flow into the basilar artery despite minimal filling of the contrast around the clot ().
Using an exchange wire, The vertebral catheter was exchanged into a 5-F intermediate catheter (Sofia; Microvention, Aliso Viejo, CA, USA). The intermediate catheter, under road map guidance; was advanced with limited wire excursion into the area of the clot. This was followed by manual aspiration that yielded a multiple clot fragments (). Post aspiration angiogram showed complete revascularization of the right vertebral artery with a slight delay in the right PICA with mild stenosis in the V3-4 junction (). The patient tolerated the procedure well and remained stable neurologically.
Immediately after the compilation of the procedure, the patient was transferred uneventfully back to her referring hospital. The MRI obtained 24-hours post thrombectomy showed no new strokes in the posterior circulation territory (). Her stroke workup revealed the significant finding of a left atrial appendage with a thrombus which was discovered through transesophageal echocardiogram (TEE). In addition, she was found to have paroxysmal atrial fibrillation (AF). Given the presence of these 2 risk factors for cardioembolic strokes, the patient was started on anticoagulation in the form of vitamin K antagonist (VKA) warfarin for secondary stroke prevention. A follow-up echocardiogram and TEE were to be done in 3 months to assess the status of the left atrial appendage thrombus but unfortunately, the patient failed to follow up.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [59, 'years'], 'Congestive Heart Failure': False, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 59 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
816,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8221677-1,Extracted,"An 81-year-old male with a past medical history of hypertension, diabetes mellitus type 2, coronary artery disease, atrial fibrillation, and myasthenia gravis presented to the hospital with complaints of left-sided abdominal pain for few hours. He denied any trauma or fall. The abdominal pain had an intensity of 6 out of 10 on the pain scale, with no aggravating or relieving factors. It was associated with dry cough without any fever. He underwent left main coronary artery stenting 60 days prior to the presentation and was taking apixaban, clopidogrel, and aspirin for the management of the atrial fibrillation and coronary artery disease. He had minimal left upper quadrant tenderness on palpation without any guarding or rigidity. A CT of the abdomen () revealed splenic laceration, hemoperitoneum, and grade 2 perisplenic hematoma according to the American Association for the Surgery of Trauma splenic injury scale. Serum hemoglobin ranged from 8.1 to 9.3 g/dL throughout the hospital stay. He was monitored in the critical care unit for hemodynamic instability and surgical intervention was deferred due to stable hematoma. The patient’s apixaban, aspirin, and clopidogrel were held during the hospital stay. Repeat CT of the abdomen showed interval resolution of the perisplenic hematoma. At discharge, only clopidogrel was resumed.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [81, 'years'], 'Hypertension history': True, 'Stroke': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 81 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
817,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7785501-1,Extracted,"A 79-year-old male patient presented to the ED complaining of abdominal pain, nausea, and vomiting. Medical history includes type-2 diabetes mellitus, hypertension, dyslipidemia, atrial fibrillation, and aortic dissection. Additionally, surgical history was remarkable for thoracic endovascular aortic repair (TEVAR) that was done five years ago.
During physical examination, the patient was found to be hemodynamically stable and his abdomen was soft and lax with mild tenderness on the left flank. Laboratory tests showed significant elevation of lactic acid (4.16 mmol/L) and white blood cells (WBC) (13.4 K/uL) with neutrophils 80.8%. CT angiography showed occlusive thrombus at distal superior mesenteric artery (SMA) (measuring about 2 cm) and obliterated origin of both celiac trunk and SMA with collateral from inferior mesenteric artery (Figure ). In addition, thrombus at the proximal part of the abdominal aorta (Figure ).
The patient was admitted as a case of superior mesenteric artery (SMA) ischemia, and managed by thrombolytic therapy using tissue plasminogen activator (tPA) (alteplase 0.05 mg/kg/h for 12 hours) with stent on the same day through inferior mesenteric artery. There were no complications from the procedure. However, SMA stenting failed. The patient was improving and was discharged home on apixaban 2.5 mg.
Four days later, the patient presented to the ED with diffused sharp abdominal pain. The physical examination is unremarkable except for a mild central abdominal tenderness. Laboratory findings revealed lactic acid to be 2.19 mmol/L. CT angiography showed re-demonstration of near occlusion thrombus at distal SMA with a refill of distal branches from collaterals at the portal venous phase with no frank signs of bowel ischemia. The patient stayed in a regular ward and received heparin 1200 U/h; five days later the patient recovered and was discharged in good condition.
Six days later, the patient returned to the ED with the same complaint and diagnosed with MI; he was vitally stable and afebrile; the abdomen is soft and lax with no tenderness. Laboratory tests revealed high lactic acid (2.94 mmol/L), lipase (48 U/L), and erythrocyte sedimentation rate (ESR) (28 mm/h). Angiography confirmed the presence of occlusive thrombus at distal SMA. The patient underwent a retrograde right common ilio-mesenteric artery bypass (Figure ). He made an uneventful recovery and was discharged in a good condition.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [79, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': True, 'Vascular disease history': True, 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 79 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 6 + 1 = 7.
The patient's CHA2DS2-VASc Score is 7."
818,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2944190-1,Extracted,"A 66-year-old, non-smoking Caucasian woman was transferred to our emergency department after she had presented to a community health clinic with nausea, vomiting, and worsening malaise that had been present for less than a day. An electrocardiogram (EKG) performed at the clinic showed bradycardia, and periods of asystole. Our patient denied any other symptoms, including chest pain, shortness of breath, and syncope. The only recent change that she could recount was that she had consumed approximately 200 g of dulse the previous day (Figure ).
Our patient's medical history included type 2 diabetes mellitus, hypertension, hypercholesterolemia, gout, anxiety, and chronic renal disease. Her medications on presentation included omeprazole, allopurinol, lorazepam, rosuvastatin, ezetimibe, losartan, metformin, pioglitazone, amlodipine, acebutolol, famciclovir, nortriptyline, hydroxyzine, and hydrocortisone acetate cream. None of the medications were new to the patient.
On physical examination, we found our patient to be an alert, and oriented, obese woman of stated age, with a Glasgow coma scale score of 15. Her heart rate was irregularly irregular, and bradycardic at 30 beats per minute, blood pressure was 124/82 mmHg, and respirations were tachypnic at 28 breaths per minute, with an oxygen saturation of 98% on 100% oxygen administered by facemask. The remainder of the physical examination was unremarkable.
Laboratory investigation revealed an elevated white blood cell count, normal hemoglobin, normal platelets, and a random glucose level of 10.2 mmol/L (reference range 3.0 to 6.0 mmol/L). Testing for cardiac enzymes was negative. Arterial blood gas revealed a compensated respiratory alkalosis, with a pH of 7.40, PaCO2 of 33 mmHg, PaO2 of 80 mmHg, and a HCO3 of 21 mEq/L. Renal function was impaired, with elevated serum urea (11.9 mmol/L; normal range 2.5 to 7.5 mmol/L), and creatinine (168 μmol/L; 60 to 110 μmol/L). Estimation of the patient's glomerular filtration rate revealed a creatinine clearance (CrCl) rate of 37 ml/min (normal range 88 to 128 ml/min), which placed her chronic kidney disease at stage 3b by the National Kidney Foundation criteria []. Our patient was also found to be severely hyperkalemic, with a serum potassium concentration of 8.6 mmol/L (normal range 3.5 to 4.9 mmol/L). Her EKG rhythm on presentation to the emergency department showed an irregularly irregular bradycardic rhythm with periods of asystole, absent P waves, widened QRS complex, and peaked t waves (Figure ).
We diagnosed our patient with hyperkalemia secondary to acute on chronic renal failure, precipitated by the consumption of a large amount of potassium-rich dulse. She was admitted to the intensive care unit, and started on a treatment regimen that included insulin, bicarbonate, calcium gluconate, and sodium polystyrene sulfonate (Kayexalate - Sanofi-Aventis, Laval, Quebec, Canada). Our patient's usual doses of allopurinol, metformin, and losartan were withdrawn, and ultimately discontinued.
Our patient showed marked improvement overnight, and was discharged to the ward. Within a few hours of treatment initiation, her serum potassium had almost completely normalized (5.5 mmol/L), as did the EKG changes (Figure , and ). By the next morning, she was eukalemic (4.1 mmol/L), with a normal sinus rhythm (Figure ). Her serum creatinine level also improved, and at discharge was close to the patient's pre-admission baseline (93 μmol/L), with an estimated CrCl of 66 ml/min, indicating stage 2 chronic kidney disease []. She remained stable with a normal potassium, and cardiac rhythm, and was discharged on hospital day seven (Figure ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [66, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 66 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
819,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7322736-1,Extracted,"A 58 year-old gentleman presented to the hospital with worsening bloating and a gradual increase in his abdominal girth. He had also noted a loss of weight of more than 10 kg over the last 2 years. The patient otherwise denied any abdominal pain or change in his bowel habit. He was known to have a history of well-controlled diabetes mellitus, hypertension, hyperlipidaemia and atrial fibrillation. There was no previous history of pancreatitis or abdominal surgery. The patient had recently undergone a gastroscopy and colonoscopy the previous year for iron deficiency anaemia. This had shown gastritis as well as the presence of pandiverticular disease and a sub-centimeter colonic polyp. Histology showed the polyp to be a tubular adenoma with low-grade dysplasia (, , , , , ).
Clinical examination showed an adequately nourished gentleman but with a large abdominal mass occupying most of his abdomen. It was possible to feel over the superior edge but the inferior edge extended into the pelvis. The mass was non-tender on palpation. Digital rectal examination was unremarkable.
In view of the above findings, the patient underwent a computed tomography (CT) of the abdomen and pelvis. This showed a large 25 × 17 × 22 cm cystic lesion extending from the mid-abdomen to the pelvis. The lesion was thin walled and contained homogenous low density fluid (14 Hounsfield unit). There was no septations, irregularity or abnormal thickening of the cyst wall. The cyst was noted to have a mass effect but not invading the surrounding bowel loops and the urinary bladder. It was found to be separate from the liver and the kidneys. The pancreas was normal in appearance. The CT scan was otherwise unable to identify the origin of the giant cyst.
As this was a thin walled cyst with no irregular or solid component, a fine needle aspiration (FNA) was not suitable as there was no specific area to target. Aspiration of the fluid was also unlikely to yield any meaningful finding for diagnosis. Further imaging such as a MRI would also not help in identifying the origin or the diagnosis of the cyst. The possibility of a mesenteric or omental cyst was therefore discussed and surgical excision was offered to the patient. Tumour markers were not performed as it would not have affected the management.
An elective exploratory laparotomy was performed via a midline incision. A giant cyst was immediately identified but was found to have multiple adhesions to the peritoneum, omentum, mesentery, urinary bladder as well as the small and large intestines. However, the cyst was not found to be originating from any of the above organs or the vas deferens. The cyst was entirely within the abdominal cavity and did not originate from within the mesentery. A controlled decompression of the cyst was made through a purse-string encircled incision in the anterior wall. This was performed to aid with retraction and visualization of the posterior surface. Thick purulent fluid was aspirated until dry. The cyst was subsequently excised in whole.
The patient underwent an uneventful recovery with a brief period of expected post-operative ileus. He was discharged on post-operative day 6. Follow-up visits showed complete resolution of his initial symptoms and a vast improvement in his appetite.
Culture of the fluid was positive for Streptococcus agalactiae. Fungal culture and tuberculosis polymerase chain reaction (TB PCR) tests were negative. Cytology of the fluid showed mainly neutrophils.
Histological examination of the cyst showed thick fibrous walls covered with coarse fibrillary strands admixed with fibrin. There were also large numbers of mature IgG plasma cells with aggregates of neutrophils and scattered lymphocytes. No viable epithelial lining was identified. The walls stained positive for AE1/3 suggesting myofibroblasts. They were negative for CD117 and DOG-1 and therefore not suggestive of a gastrointestinal stromal tumour.
This was therefore treated as a benign cyst of an undetermined origin.
The patient was last seen in clinic two months after his surgery with a significant improvement in his appetite and oral intake. He was thereafter discharged from follow-up as the likelihood of recurrence was low considering that the cyst had been excised entirely with no remnant wall left behind.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [58, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 58 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 1 + 1 = 2.
The patient's CHA2DS2-VASc Score is 2."
820,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6200621-1,Extracted,"A 74-year-old man presented to the emergency department after a motorcycle accident. He had a deformity in the right leg. His comorbidities were chronic obstructive pulmonary disease, ischemic cardiomyopathy due to myocardial infarction, atrial fibrillation, hypertension, and dyslipidemia. His medications included aspirin and clopidogrel. Following investigations in this admission, a brain computed tomography (CT) revealed that he had acute traumatic subdural hematoma that was managed with nonoperative treatment. His right leg was broken, which was diagnosed as a closed fracture of the tibia and fibula, and was managed conservatively. He had fractures at the left iliac crest and the left superior pubic rami. The neurovascular conditions were normal. During admission, he had acute dyspnea with desaturation but no chest pain at ten days after admission. On examination, his blood pressure was 102/78 mmHg, pulse rate was 100/min, respiratory rate was 24/min, and blood oxygen saturation (SpO2) was 90% in room air, which was not corrected with oxygen supplement. He had crepitation at his left lower lung but no wheezing. CT angiography of the chest was performed and showed acute PEs at the right superior and inferior trunk. He was found to have acute respiratory failure and hypotension after the chest CT angiography was finished. He was scheduled for an emergency operation for surgical pulmonary embolectomy.
On the next day at the surgical intensive care unit (ICU), he developed progressive left leg edema with cyanosis. He had no fever and he could still move his leg, but his pain could not be evaluated since he was delirious. On examination, his left lower limb exhibited discoloration at his left foot without any ulcer or bleb, moist skin, or pitting edema, and the left dorsalis pedis and posterior tibial pulse could be palpated (1+) but were diminished (). The motor functions remained intact. Doppler ultrasonography was performed and revealed an uncompressible vein along the midsuperior femoral vein to the popliteal vein. His laboratory investigation showed that the leukocytosis and creatinine level rose from 1.04 mg% to 1.62 mg% and creatinine phosphokinase (CPK) was 322 U/L. He was diagnosed with PCD at the left femoral vein. The intervention radiologist attempted a catheter-directed thrombectomy, but it failed because the guider could not pass through the intraluminal clot. The patient was scheduled for emergency operation again for surgical thrombectomy with fasciotomy of the left leg (). The operative finding was a thrombus in the femoral vein that was 10 cm in length (). The compartment pressures before performing the fasciotomy at the anterior, lateral, and superficial posterior compartments were 43 mmHg, 37 mmHg, and 47 mmHg, respectively. The deep posterior compartment pressure was not measured. After the operation, his pain was relieved and the left dorsalis pedis and posterior tibial pulse were normal. He continued on wound dressings and the fasciotomy was closed by split-thickness skin graft. He continued on oral anticoagulant drugs for six months and underwent elective ray amputation at five months after the PCD for a dry gangrenous left big toe.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [74, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Thromboembolism history': True, 'Vascular disease history': True, 'Diabetes history': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 74 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
821,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5610138-1,Extracted,"An 83-year-old man without trauma and surgical history was admitted to our hospital with a dull ache in the chest and dyspnea for 10 days. He had a known diagnosis of hypertension, hyperlipidemia, nonvalvular atrial fibrillation, chronic obstructive pulmonary disease and chronic renal disease, with a past medication history of long-term use of amlodipine besylate (5 mg daily), benazepril (10 mg daily), atorvastatin (20 mg daily) and 7 months administration of dabigatran (110 mg twice daily).
Respiratory and heart examination revealed reduced breath sounds and dullness to percussion at the left low base, with irregular heart sounds, but no pathological murmur.
As shown in Fig. a, chest computed tomography (CT) scan revealed a massive pleural effusion in the left hemithorax with atelectasis. Vascular structures were normal, and no pulmonary emboli or obvious pericardial effusion was detected. Laboratory results included white blood cell (WBC) count (10,100/μL), neutrophil count (83.7%), red blood cell (RBC) count (3,820,000/μL), hemoglobin (123 g/L), hematocrit (0.38), blood platelet count (201,000/μL), C-reactive protein (61.1 mg/L), and procalcitonin < 0.05 μg/L. In addition, serum B-type natriuretic peptide (BNP) was 46.8 ng/L, and cardiac troponin I was below 0.01 ng/mL. Coagulation parameters of prothrombin time, international normalized ratio, activated partial thromboplastin time, thromboplastin time, and D-dimer were 15.6, 1.35, 73.3 s, out of detection, and 483 μg/L, respectively. Serum tumor markers (NSE, CEA and CYFRA-21) were normal.
Acute renal failure was observed within 4 days after admission; the patient’s serum creatinine was 159 μmol/L on the first day, 195.1 μmol/L on the second day and 329.6 μmol/L on the fourth day after admission. According to the Cockcroft–Gault formula, the creatinine clearance (CrCl) of the patient quickly decreased from 32.9 mL/min (first day) to 15.9 mL/min.
Ultrasound-guided thoracocentesis was performed. The parameters of the pleural fluid included positive Rivalta test, WBC count of 2800/μL (neutrophils 36%, lymphocytes 56% and monocyte 8%), total protein of 51.8 g/L, lactate dehydrogenase (LDH) of 377 U/L, RBC count of 1,150,000/μL, adenosine deaminase (ADA) of 9 U/L and glucose of 6.57 mmol/L. Data regarding the hematocrit of the effusion were not collected. The thinprep cytologic test (TCT) of the fluid revealed no malignancy. Bacterial smears and cultures of the drainage were negative (Table ).
The patient’s serum RBC count, hemoglobin and hematocrit dramatically dropped from 3,820,000/μL, 123 g/L and 0.38 to 2,530,000/μL, 80 g/L and 0.24, respectively, after almost 2500 mL of blood and turbid pleural fluid was aspired from the left hemithorax. Plasma transfusion was conducted to supply the lost blood volume. Diagnostic withdrawal was performed for dabigatran (day 5). The discontinuation of dabigatran led to the resolution of symptoms. Patient renal function was gradually improved after dabigatran was discontinued (Table ), and no further pleural effusion developed (Fig. b). Pleural effusion with moderate visceral (V) and parietal (P) thickening was observed on the left side after conservative treatment (Fig. c).
Our patient was later stabilized and dismissed home. Unfortunately, on a visit, he died of sudden cardiac death 6 months after his discharge from our hospital.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [83, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 83 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
822,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6671888-1,Extracted,"A 47-year-old male patient was admitted complaining of macroscopic hematuria and weight loss of 20 kg over the last two months. On physical examination bilateral massive abdominal masses were palpable extending from the flanks to the iliac fossae bilaterally. Laboratory tests showed marked metabolic acidosis, hyperkalemia and electrocardiographic alterations, which required prompt intravenous infusion of calcium gluconate and hemodialysis. Urinalysis showed pyuria. Abdominal ultrasound imaging and computed tomography scan revealed hepatic and renal polycystic disease. The kidneys were markedly enlarged extending from their original site until the iliac fossae and their architecture was effaced by multiple cysts. On the following days the patient suffered an ischemic stroke and a pulmonary thromboembolism. Outcome was characterized by daily fever despite of the use of broad-spectrum antibiotics and negative blood and urine cultures. A PET SCAN was performed which was compatible with infection of multiple and bilateral renal cysts. Therefore bilateral nephrectomy was performed, and because of technical difficulties adrenals were also excised. Surgery was technically challenging, the patient remained hypotensive and required packed red blood-cell transfusion. After ICU discharge the patient started experiencing epigastric pain and heartburn. Esophagogastroduodenoscopy (EGD) () revealed necrotizing esophagitis compatible with the endoscopic diagnosis of “black esophagus”. The duodenal bulb was deformed by scarred ulcers and a small ulcer was visible in the anterior wall. Enteral nutrition, a proton pump inhibitor, a prokinetic drug and sucralfate were prescribed. A week later, control EGD showed an effacement of the blackened areas, which had been replaced by a diffuse fibrinous esophagitis. Recovery was uneventful since then. The patient went on hemodialysis and resumed oral feeding.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [47, 'years'], 'Congestive Heart Failure': False, 'Thromboembolism history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 47 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 0 + 2 = 2.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
823,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2652426-1,Extracted,"A 72-year-old man with known history of stage 3 chronic kidney disease, hypertension, coronary artery disease, hyperlipidemia presented with a 3-days history of low-grade fever, productive cough, dyspnea, night sweats and fatigue. Patient was a non-smoker and did not consume alcohol. His kidney disease was likely due to renovascular or/and chronic atheroembolic disease with baseline serum creatinine level of 1.7 mg/dl, giving him an estimated glomerular filtration rate of 50 mL/min/1.73 m2. His medications included metoprolol, isosorbide mononitrate, gabapentin, aspirin, candesartan, tamsulosin, atorvastatin. On examination, he was alert, and not in distress. His blood pressure was 140/80 mm Hg without orthostatic changes and temperature 100.3°F. The remainder of the examination was unremarkable except of few wheezes over both lung fields. He did not have pedal edema. Serum sodium was 145 mEq/L, potassium 4.8 mEq/L, urea nitrogen 34 mg/dl, creatinine 1.7 mg/dl and glucose 130 mg/dl. Hemoglobin was 12.1 g/dL, white blood cells 5.2 × 109/L and platelets 208 × 109/L. Treatment with 250 mg of azithromycin daily was given for six days without clinical improvement. A chest radiograph showed small left apical nodules and computed tomography (CT) scan of the chest demonstrated right lower lobe scarring and left upper lobe small nodules with focal pleural thickening (Figure ). Three weeks later, serum creatinine rose to 2.6 mg/dl and urea to 48 mg/dl. Urine volume never decreased; urinalysis showed trace proteinuria, without glucose or blood. Urine sediment did not show red blood cells, white blood cells or casts. Urine sodium was 35 mmol/L. Patient completed 2 weeks treatment with 500 mg of levofloxacin, with some clinical improvement. Six weeks after initial presentation, cultures of two sputum samples were reported to be positive for Mycobacterium gordonae and Mycobacterium avium complex (MAC) by DNA probe and subsequently the positive diagnosis of pulmonary nontuberculous mycobacterial infection was made. The patient rejected long-term triple therapy, given his mild symptoms and a concern about treatment adverse effects. The patient has remained well throughout a 2 months period of close clinical observation; he has been afebrile and his serum creatinine level returned to baseline of 1.7 mg/dl.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
824,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-318,Extracted,"A 65-year-old man comes to the physician because of a 10-day history of episodic retrosternal pain, shortness of breath, and palpitations. The episodes occur when he climbs stairs or tries to walk briskly on his treadmill. The symptoms resolve when he stops walking. The previous evening he felt dizzy and weak during such an episode. He also reports that he had a cold 2 weeks ago. He was diagnosed with type 2 diabetes mellitus four years ago but is otherwise healthy. His only medication is glyburide. He appears well. His pulse is 62/min and is weak, respirations are 20/min, and blood pressure is 134/90 mmHg. Cardiovascular examination shows a late systolic ejection murmur that is best heard in the second right intercostal space. The lungs are clear to auscultation.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [65, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
825,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-5763,Extracted,"A 70-year-old man presents to his primary care physician for a general checkup. He states that he has been doing well and taking his medications as prescribed. He recently started a new diet and supplement to improve his health and has started exercising. The patient has a past medical history of diabetes, a myocardial infarction, and hypertension. He denies any shortness of breath at rest or with exertion. An ECG is performed and is within normal limits.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [70, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': True, 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 70 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
826,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-1549,Extracted,"An 84-year-old woman with Alzheimer's disease is brought to the physician by her son for a follow-up examination. The patient lives with her son, who is her primary caregiver. He reports that it is becoming gradually more difficult to care for her. She occasionally has tantrums and there are times when she does not recognize him. She sleeps 6–8 hours throughout the day and is increasingly agitated and confused at night. When the phone, television, or oven beeps she thinks she is at the dentist's office and becomes very anxious. She eats 2–3 meals a day and has a good appetite. She has not fallen. She has not left the home in weeks except for short walks. She has a history of hypertension, hyperlipidemia, atrial fibrillation, and hypothyroidism. She takes levothyroxine, aspirin, warfarin, donepezil, verapamil, lisinopril, atorvastatin, and a multivitamin daily. Her temperature is 37°C (98.4°F), pulse is 66/min, respirations are 13/min, and blood pressure is 126/82 mm Hg. Physical examination shows no abnormalities. It is important to the family that the patient continues her care in the home.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [84, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 84 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
827,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7861066-1,Extracted,"The patient is a 56-year-old Caucasian male who presented to the family medicine clinic for a general check-up for health maintenance. He has a past medical history of obstructive sleep apnea (OSA), pituitary adenoma which was successfully treated with cabergoline, and extensive anabolic steroid use. He had no immediate medical or social concerns and he also denied any exertional chest pain or dyspnea. He was not on any prescription medications but did endorse recreational use of testosterone cypionate at 125 mg per week. Supplement use was significant for garlic tablets, tauroursodeoxycholic acid (TUDCA) at 500 mg daily, resveratrol, alpha-lipoic acid (ALA) at 600 mg daily, turmeric, vitamin C, fish oil at 3 grams daily, vitamin D at 5000 IU daily, coenzyme Q10, and n-acetyl cysteine (NAC) 1200 mg daily. He did not smoke tobacco and only drank alcohol socially. The patient had a blood pressure of 136/80. Body mass index was 35.6 kg/m2. Vital signs were otherwise normal. He had no abnormal physical exam findings and was in a low body fat percentage range on visual examination.
His anabolic steroid history was quite significant. He first began using anabolic steroids over thirty years ago and has used these agents in cycles up until the present day. This included a broad range of injectable and oral anabolic steroids. He had used various esters of injectable testosterone consistently since starting this regime. Other examples of anabolic steroids used included trenbolone, nandrolone decanoate, methenolone, stanozolol (Winstrol), boldenone undecylenate (Equipoise), oxymetholone (Anadrol), metandienone (Dianabol), and fluoxymesterone (Halotesin). These compounds were used sporadically in various cycles over the years.
Lab workup was obtained which included a complete blood count (CBC), creatinine, electrolyte panel, hemoglobin A1C, total prostate-specific antigen (PSA), lipid panel, and a basic liver function panel. The patient’s hemoglobin was elevated at 18.0 g/dl but his CBC was otherwise unremarkable. Creatinine was elevated at 1.4 mg/dl, likely due to high levels of muscle mass. Cystatin C levels were within normal limits which made kidney disease unlikely. Electrolyte panel along with liver enzymes and other liver function tests were normal, as was the patient’s PSA. Surprisingly, the patient’s hemoglobin A1C was elevated at 6.4%. Upon further inquiry, he had a prior hemoglobin A1C of 6.9% in the recent past which was never followed upon. His result was fully diagnostic for diabetes mellitus. What was surprising about this result, was the diagnosis of diabetes mellitus despite his low-body fat levels and very high levels of physical activity throughout his life. Lipid panel returned significant for low-density lipoprotein (LDL) level of 168 mg/dl, high-density lipoprotein (HDL) level of 52 mg/dl, and triglyceride level of 78 mg/dl.
Urine studies obtained included a urinalysis and urine protein: creatinine ratio, both of which were normal. More specialized tests were done to further risk stratify this patient and included apolipoprotein A-1 (159 mg/dl), apolipoprotein B100 (137 mg/dl) and high-sensitivity C-reactive protein levels (hs-CRP) (1.5 mg/dl).
Electrocardiogram was obtained and was significant for left axis deviation but otherwise no other significant findings (Figure ). An echocardiogram was done on a subsequent visit and revealed mild left ventricular hypertrophy and mildly decreased right ventricular function. The patient’s ejection fraction (EF) was 50%-55%. Of important note, he never had any significant hypertension documented throughout his life. These echocardiogram findings were suggestive of direct AAS induced biventricular effects.
On further follow up, there was a further inquiry made in regards to his hemoglobin A1C and his unexpected diagnosis of diabetes mellitus. The patient had a vague and possible family history of type 1 diabetes mellitus and had previously been evaluated for this at a younger age but never had a formal diagnosis made. This prompted an evaluation for possible latent autoimmune diabetes in adults (LADA). Fasting C-peptide levels were obtained and were 1.7 ng/ml. Insulin antibodies, Islet cell antibodies, and glutamic acid decarboxylase antibody (GAD) were obtained and negative. An autoimmune component was ruled out and his overall diagnosis was consistent with type 2 diabetes mellitus (T2DM).
The combination of this patient’s T2DM diagnosis, hyperlipidemia, borderline elevated blood pressure, and moderately elevated hs-CRP was consistent with metabolic derangements that are generally not seen in athletes who maintain lower body fat levels and engage in rigorous exercise. His echocardiogram findings were also abnormal for an athlete without chronic hypertension. The patient was placed on aspirin 81 mg daily. He was not amenable to statin therapy and opted for major lifestyle modification and niacin therapy for his dyslipidemia, though his LDL goal given his T2DM diagnosis would be <70 mg/dl. He was also started on an angiotensin-converting enzyme (ACE) inhibitor at a low dose to aid in his left ventricular remodeling and better optimize his hypertension.
This case highlights the potential need for extensive metabolic and cardiac evaluation in anabolic steroid users due to various unknown risks associated with long term AAS use. While there is some reasonable understanding of the effects of testosterone use alone, most anabolic steroids that are very commonly used are poorly studied and hence not well understood.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [56, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 56 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 1 + 1 = 2.
The patient's CHA2DS2-VASc Score is 2."
828,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4603769-1,Extracted,"A fifty-nine-year-old right-handed man, former smoker, with history of chronic alcohol intake, arterial hypertension, mixed hyperlipidemia, two recent left middle cerebral artery ischemic strokes (left temporo-insular and left frontal lacunar infarcts) manifested as right hemiparesis and aphasia, right focal motor seizures, gastric ulcer secondary to excessive use of nonsteroidal anti-inflammatory drugs for occipital headache was admitted for episodes of PLC started 6 h before admission. The episodes lasted approximately 2 min, consisting of accelerated breathing, emission of guttural, snoring sounds, frowning of the eyebrows, followed by laughter accompanied by motor restlessness of all four limbs; the patient was able to walk with assistance but was unresponsive during these episodes. An additional movie file shows this in more detail [see Additional file ]. The patient denied any automatisms, loss of consciousness, loss of memory, or altered mental status. He also denies any sense of mirth during these episodes. On admission the patient’s home medication were clopidogrel, carbamazepin, gabapentin, pantoprazole, and quinapril. Initial examination was notable for confusion, right upper motor neuron facial weakness, 4/5 right hemiparesis, and a mixed aphasia. Between episodes of PLC there were pauses of about 10 min.
The differential diagnosis was made between gelastic seizures and episodes of pathological laughter as manifestation of repeated transient ischemic attacks (TIA’s). The pseudobulbar laughter was excluded because the patient didn’t present any emotional incontinence outside the pathological laughter episodes. Brain scan showed left temporo-insular and left frontal chronic lacunar infarcts. Electroencephalography (EEG) performed during and after laughter episodes revealed no spike-wave activity (Fig. ). Analysis of the cerebrospinal fluid specimen revealed a protein level of 0.3 g per liter, a glucose concentration of 72.8 mg per deciliter, a white blood cells count of 5 per cubic millimeter, polymorphonuclears of 2 per cubic millimeter, monocytes of 3 per cubic millimeter, no red blood cells. Routine laboratory blood test showed elevated uric acid of 8 mg per deciliter, slightly elevated gamma-glutamyl transferase of 57 U per liter, increased glucose level of 136 mmol per liter, increased lactate dehydrogenase of 236 mmol per liter, increased triglycerides of 152.3 mg per deciliter, increase white blood cells count of 10 790 per cubic millimeter with increased neutrophils blood count of 8 150 per cubic millimeter, all the other blood tests were normal. The patient was treated initially with clopidogrel, atorvastatin, diazepam and phenytoin during acute PLC episodes and clopidogrel, atorvastatin, carbamazepine 600 mg/day and levetiracetam 1000 mg/day as maintenance treatment, but the PLC episodes continued for 3 days with a shorter duration and a longer period between them. Brain magnetic resonance imaging (MRI), performed 5 days after symptoms onset, showed lacunar infarcts localized in the left lenticular-capsular-thalamic area associated with gliotic changes; multiple round lesions in the cortical-subcortical and in the deep white matter bilateral frontal-parietal-occipital, with T2 hyperintensity, T1 isointensity and no diffusion changes (Figs. and ). Based on symptoms, neurological examination and investigations the diagnosis of PLC as prodromal manifestation of TIA’s was made, heparin treatment was started and subsequently PLC episodes disappeared. However the gelastic seizures hypothesis could not be ruled out since EEG may not show spike-wave activity if the lesion is subcortical. Therefore the authors decided that antiepileptic treatment should be continued. The patient underwent a cognitive and psychological examination that did not reveal a cognitive dysfunction or a mood disorder. Carotid ultrasound showed non-hemodynamically significant plaque in the left carotid bulb. Transthoracic echocardiography showed moderate degenerative mitral stenosis (mitral valve area = 1.3 cm2, mean gradient 8 mmHg), mild mitral regurgitation, dilated left atrium, mild pulmonary hypertension and normal systolic left ventricular function and dimensions. Transesophageal echocardiography revealed, in addition to transthoracic echocardiography, left atrial spontaneous echo contrast (grade 3+), but no thrombus in left atrial appendage. Intra-cardiac defects with right-to-left shunt were also excluded. Some mobile atherosclerotic plaques on ascending aorta and initial part of the aortic arch were present, but no clear arguments for potential embolisation could be sustained. Given the degree of mitral stenosis, anticoagulation with acenocumarol was started, and clopidogrel was continued. Some concerns about this association were raised related to history of superior digestive hemorrhage of the patient, so clopidogrel 75 mg daily was preferred to low dose aspirin. The patient continued treatment with acenocumarol (INR = 2-3), clopidogrel 75 mg/day, atorvastatin 20 mg/day, carbamazepin 600 mg/day, gabapentin 900 mg/day and was discharged fully recovered. A video EEG was performed that showed no spike-waves only slow waves on the right side derivations (Fig. ). A month later the patient started to present multiple left carotid and vertebrobasilar TIA’s despite correct anticoagulant treatment (INR in the therapeutic range). These ongoing embolic events led to treatment with mechanical valve replacement, afterwards the patient was completely asymptomatic.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': True, 'age': [59, 'years'], 'Stroke': True, 'Transient Ischemic Attacks History': True, 'sex': 'Male'}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 59 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
829,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3656689-1,Extracted,"A 74-year-old Japanese man with hypertension, type 2 diabetes mellitus, ischemic heart failure, and nonvalvular atrial fibrillation (NVAF) presented at our hospital after the sudden onset of right hemiplasia and dysarthria. On admission, his National Institutes of Health Stroke Scale (NIHSS) score was three. The plasma level of the thrombin-antithrombin complex was 21.7 ng/ml (normal range: 0-3.0 ng/ml). Axial diffusion-weighted magnetic resonance images and magnetic resonance angiography images showed hyperintense signals in the left front-parietal cerebral cortex without any intracranial stenotic lesions, and acute cardioembolic stroke associated with NVAF was diagnosed.
Transesophageal echocardiography (TEE) performed on day 3 after admission revealed a mobile thrombus (1.0 × 2.2 cm) in the left atrial appendage (fig. ), and dabigatran therapy (110 mg b.i.d.) was initiated to prevent stroke recurrence. Activated partial thromboplastin time (APTT) was 31 s before dabigatran and 33 s 3 h after 110 mg dabigatran. TEE performed on day 9 after admission revealed that the size of the thrombus had increased to 1.5 × 3.0 cm (fig. ). Medication was changed from dabigatran to warfarin with a target prothrombin time/international normalized ratio of between 2.0 and 3.0. TEE performed on day 23 after admission revealed that the size of the thrombus had decreased (fig. ), and TEE performed on day 42 after admission revealed that the thrombus had disappeared (fig. ). The patient did not have a recurrent stroke and was discharged from hospital on day 43 with an NIHSS score of zero and a modified Rankin Scale grade of zero.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [74, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': True, 'Diabetes history': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 74 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 6 + 1 = 7.
The patient's CHA2DS2-VASc Score is 7."
830,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5023919-1,Extracted,"A 59-year-old woman was admitted to the department of Neurology for a sudden confusion with loss of vision. Her past medical history comprised of a total hysterectomy twenty-five years earlier (fibroma). She also complained of headaches and chronic asthenia for 5 years: at that time, medical investigations only found a chronic seromucous maxillary sinusitis treated by antibiotherapy, then endoscopic sinus surgery (the pathological study objective a nonspecific inflammation); however, she still complained of chronic headaches despite this treatment. At the age of 55, she had also developed refractory arterial hypertension and renal failure leading to the diagnosis of right renal artery stenosis and left renal artery occlusion: she was treated by surgery (stenting of the left renal artery, then right aortorenal bypass).
On clinical examination, there was cortical blindness, anosognosia for blindness, amnesia, and topographical disorientation suggestive of a Dide-Botcazo syndrome. There was no pyramidal sign nor cerebellar ataxia or cranial nerves involvement. No other clinical abnormality was reported. She still complained of chronic headaches.
Bilateral cerebral posterior infarction and hypodensity in the territory of the right postero-inferior cerebellar artery have been observed on brain magnetic resonance imaging (MRI) (and magnetic resonance angiography), with a severe narrowing of the basilar artery (closed to 90%) and a mild stenosis of the M1 and M2 segments of the left middle cerebral artery (Fig. A and 1B). Transcranial Doppler confirmed a severe stenosis of the basilar artery. Electrocardiogram and 24 hours electrocardiography were normal. Echocardiography (transthoracic and transesophageal) demonstrated a hypertrophic cardiopathy (with severe left ventricular hypertrophy and circumferential dilatation of the left atrium). No valvulopathy was observed, but there was a heterogeneous thickening of the interatrial septum (1.5 cm) and a hyperechogeneous thickening next to the right atrium (1.9 × 1.3 cm). Cardiac computed tomography angiography (and cardiac MRI) confirmed a right periatrial infiltration, and also found thickening of the wall of the whole aortic arch (with tardive enhancement of media) and pericardial effusion (Fig. ). Whole-body 18fluorodeoxyglucose positron emission tomography (18FDG PET) found contrast-enhancement on the right and left atria, whole aorta, iliac arteries, and femoral arteries (Fig. E). Ophthalmological examination was normal, except a grade I hypertensive retinopathy.
Ancillary tests found hyperleukocytosis (13,000/mm3, with 8890 neutrophils/mm3), biological inflammation (C-reactive protein was 24 mg/L), with no monoclonal gammopathy. Viral and bacterial serologies, immunological (antinuclear, anticardiolipin, and anti-β2-glycoprotein 1 antibodies) and metabolic (cholesterol, triglyceride, glycosylated hemoglobin, homocysteine, thyroid stimulating hormone, and transaminases) tests were unremarkable. Cerebrospinal fluid analysis was normal (1 white cells/mm3; protein level at 46 mg/dL, for a normal value <45 mg/dL; normal glucose level). A bone marrow biopsy showed no abnormality.
Plain radiographs showed bilateral and symmetric cortical osteosclerosis of the diaphyseal and metaphyseal regions of the lower limbs; 99Technetium bone scintigraphy revealed a symmetric tracer uptake by the long bone of lower extremities (and also in maxillary and frontal bones) suggestive of the diagnosis of ECD (Fig. ). After a second biopsy of the maxillary sinus, pathological study finally demonstrated a xanthogranulomatous infiltrate mainly composed by foamy histiocytes accompanied by fibrosis (stains for CD1a and S-100 were negative), confirming the diagnosis of ECD.
She was treated with interferon-α (3 million IU 3 times weekly, then a gradual increase of the dose up to 9 million IU 3 times weekly over the following months), with not only an improvement of the cognitive function (particularly visual function and memory) but also of headaches. A treatment by clopidogrel (75 mg/d) was proposed for stroke. After 3 months of treatment with interferon-α, we observed reduction of the stenosis of the basilar artery (50%) on MR-angiography (with a quite total recanalization 2 years after the onset of the treatment; Fig. ). After 4 years, the neurological examination was still stable, but she developed insipidus diabetes (successfully treated with desmopressin).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [59, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Vascular disease history': True, 'Diabetes history': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 59 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 6 + 1 = 7.
The patient's CHA2DS2-VASc Score is 7."
831,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8238100-1,Extracted,"A 65-year-old male was evaluated for mitral valve bioprosthetic replacement and coronary artery bypass graft (CABG) surgery in a setting of multivessel coronary artery disease and severe mitral regurgitation. His medical history was significant for ischemic cardiomyopathy, prior percutaneous intervention, hypertension, and hyperlipidemia.
Cardiac catherization revealed complete occlusion of the left circumflex artery, 90% occlusion of the right coronary artery, and 95% occlusion of the diagonal branch of the left anterior descending artery. The patient received 11,750 U of UFH without complication. Two-dimensional echocardiography revealed 0.3 cm effective regurgitant orifice area across the mitral valve, 60 mL regurgitant volume, and regurgitant fraction of 54% consistent with severe mitral regurgitation (). The patient also had a severely depressed preoperative ejection fraction of 20% to 25% and severe left ventricular enlargement. Preoperative platelet count was 164 K/μL.
The patient underwent CABG and mitral valve replacement utilizing 52,000 U of UFH for CPB. Cross-clamp time was 67 minutes, and the patient's immediate postoperative platelet count was 108 K/μL. The patient remained intubated and sedated postoperatively because he did not tolerate spontaneous breathing trials. Heparin infusion of 500 U/h was started on postoperative day (POD) 1. Postoperative prolonged mechanical ventilation and small bowel ileus necessitated maintenance of nothing-by-mouth status, thus delaying initiation of oral anticoagulation with warfarin. The patient's platelet count declined sharply on POD 2 (66 K/μL) before trending upward on POD 3 (82 K/μL) and POD 4 (97 K/μL). The patient was extubated on POD 6. Platelet counts continued trending upward and were stable by POD 7 (242 K/μL) and POD 8 (230 K/μL). On POD 9, the patient developed atrial fibrillation with rapid ventricular response and underwent successful electrical cardioversion.
On POD 10, the patient's platelet count acutely decreased to <100 K/μL from 149 K/μL the previous day, and the patient was reintubated because of respiratory failure. His platelet counts continued to trend downward and reached a nadir of 70 K/μL on POD 13 when physical examination noted the absence of left lower extremity pulses. Arterial duplex ultrasound revealed acute common femoral artery occlusion, and emergent embolectomy was performed. Heparin was discontinued, and argatroban 2.5 μg/kg/min was initiated. Intraoperative transesophageal echocardiography revealed heavy thrombus burden across the mitral bioprosthesis, causing severe mitral stenosis. Repeat echocardiography on POD 14 showed persistence of thrombus with a mean gradient of 20 mmHg across the mitral valve. Detection of heparin-induced antiplatelet antibody from enzyme immunoassay and positive serotonin release assay (SRA) confirmed the diagnosis of HIT.
Because of respiratory failure and severely thrombosed mitral valve, the patient underwent reoperative bioprosthetic mitral valve replacement on POD 18, with bivalirudin anticoagulation used continuously throughout the procedure. A loading dose of 120 mg bivalirudin was delivered upon initiating CPB to achieve an activated clot time 2 to 2.5 times baseline, followed by continuous infusion dosed at 2.5 mg/kg/h. The procedural approach was transseptal, and access was gained through the previous incision. Upon visualization, the mitral valve prosthetic showed dense adhesions and rigid white clots on both sides of the leaflets (). The adherent clots effectively occluded the mitral valve orifice. All debris was debrided and pledgeted sutures were removed, followed by retrieval of the prosthetic valve. The posterior leaflet was almost completely resected and copious irrigation applied. No thrombus formation in either the operative field or the CPB circuit was encountered during the operation. A 31-mm Mosaic bioprosthetic valve (Medtronic) was implanted. Intraoperative echocardiography showed improved mitral valve function with a 1- to 2-mmHg gradient. Postoperatively, the patient's platelet counts were stable and remained >150 K/μL on argatroban 1 μg/kg/min.
Despite resolution of HIT, the patient's renal function worsened postoperatively, and he developed acute kidney injury, believed to be secondary to ischemic acute tubular necrosis from multiple hypotensive episodes intraoperatively (systolic blood pressures in the 70s and 80s mmHg) and requiring pressor support. Respiratory function also deteriorated postoperatively, and despite extubation on POD 6 after his second surgery, the patient was reintubated on POD 12. The patient could not be weaned from the ventilator and had a percutaneous tracheostomy tube inserted on POD 21. The patient developed sepsis on POD 30 with multiorgan system failure. Because of the patient's respiratory and renal failure, unremitting sepsis, and low chance of meaningful recovery, the family withdrew care on POD 41 after the second surgery, approximately 2 months (POD 59) from the primary mitral valve replacement procedure. The patient died on POD 59.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [65, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
832,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-4545,Extracted,"A 71-year-old woman presents with a transient episode of right arm and hand weakness that resolved in approximately one hour. Her symptoms started while she was gardening. Her past medical history is notable for hypertension, diabetes, anxiety, and dyslipidemia. Her current medications include insulin, metformin, and fluoxetine. Examination reveals a left carotid bruit. Ultrasound duplex of her carotid arteries demonstrates right and left carotid stenosis of 35% and 50%, respectively.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [71, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': True, 'Vascular disease history': True, 'Diabetes history': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 71 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 6 + 1 = 7.
The patient's CHA2DS2-VASc Score is 7."
833,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4673320-1,Extracted,"A 38-year-old male was admitted to the Neurology Department at the Hillel Yaffe Medical Center due to severe headache of two days duration, dizziness, and confusion. Complete physical and neurological examination was normal. Brain CT scan was normal. CSF showed a protein level of 110 mg/dL, glucose level of 66 mg/dL, 2 lymphocytes, and negative test for oligoclonal bands. EEG showed slight symmetric slowing of background activity. The initial clinical diagnosis was encephalitis. He was treated with IV acyclovir. Two days after admission, a persistent bradycardia was noted with P wave EKG changes which lasted about two weeks (). Cardiac transesophageal echocardiography was normal. Three days after admission, mild right lateralizing signs were noted, with very mild speech disturbance and reduced fluency. Brain CT angiography was normal. Five days later, the patient complained about blurred right eye vision. Fundoscopy did not show arterial wall plaques. Visual field examination showed a right eye small central scotoma and ocular coherence tomography study demonstrated inner retinal layer edema inferior to the fovea (). Fluorescein angiography of the right eye disclosed central retinal artery branch occlusion. The patient was treated with Aspirin. At this point of time, workup also included negative studies for hypercoagulopathy, negative serological studies for antinuclear factor, anti DNA antibodies, and antineutrophil cytoplasmic antibodies. HLA-B51 antigen study was negative. Serologies for EBV, CMV, WNV, HSV-1, VZV, HIV, and Enterovirus were all negative.
Ten days after his admission, the patient reported intense right ear tinnitus with hearing loss, and this was followed, 24 hours later, by true vertigo and the illusion of whole body levitation. A formal audiogram 14 days after admission showed right flat sensorineural hearing loss (SNHL) of 50 Db threshold. A repeated audiogram three days later showed deterioration of the SNHL to 85 Db. Left side hearing was normal with SRT of 5 Db. Videonystagmography (VNG) showed upbeat vertical nystagmus, and right caloric weakness of 56% was demonstrated. Cochlear emissions were not demonstrated from both ears in TEOAE protocol. Brainstem evoked potential study showed normal I–IV wave patterns with interaural central conduction time asymmetry of 0.25 msec (longer right central conduction time). He was treated with Pulse methylprednisolone 1 gr per day for five days with concomitant IV immunoglobulin (IVIG) (2 gr/Kg). Brain MRI performed three weeks after admission was normal. Following treatment his condition remained stable with the disappearance of bradycardia and nystagmus. He was treated with a monthly dose of IVIG (0.4 gr/Kg). Six months later, a relapse with dizziness and blurred vision occurred. Examination showed left hand drift and dysdiadochokinesia with mild gait ataxia and positive left Fukuda test, repeated MRI showed an ill-defined T2 hyperintense signal of the left hemisphere without the typical MRI findings of Susac's syndrome (). The steroid dose was increased to prednisone 60 mg/day with the resolution of symptoms in four days. Monthly 0.4 gr/Kg IV immunoglobulin was continued for 14 months after the initial presentation.
20 months after the initial presentation, a relapse occurred with visual disturbance without other manifestations. Fluorescein angiography disclosed left eye central retinal artery branch occlusion. Brain MRI was normal. He was treated with pulse Methylprednisolone 1 gr per day for five days with concomitant 2 gr/Kg IV immunoglobulin.
His condition remained stable for further 8 months with monthly IV immunoglobulin treatment.
28 months after presentation the patient developed right eye blurred vision. Workup was positive for a new right eye lower nasal scotoma with concomitant right eye temporal retina ischemic changes. He was treated with pulse Methylprednisolone 1 gr per day for five days and then he was started on Azathioprine 50 mg per day. Azathioprine was stopped after a few weeks because of severe diarrhea and the patient was started on Mycophenolate 2 gr per day with concomitant monthly 0.4 gr/Kg IV immunoglobulin. The patient has been clinically stable for the last 13 months with monthly IV immunoglobulin and daily Mycophenolate treatment.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [38, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 38 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
834,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6332952-1,Extracted,"A 31-year-old Japanese male patient visited our clinic to seek an expert opinion from a thyroidologist. His medical history includes atopic dermatitis and atrial fibrillation, for which he had received cardiac catheter ablation when he was 21 and 25 years old. Although his elevated serum levels of thyroid hormones were apparent at the age of 27, the precise cause had not been identified. The patient was 168 cm tall and weighed 64.8 kg (body mass index was 23.0 kg/m2; the ideal body weight for his height is 62.1 kg). His blood pressure was 137/79 mmHg and pulse rate was 115/min, which were regular. His laboratory data showed elevated serum levels of free T4 and free T3 and a normal level of TSH. Autoantibodies for thyroglobulin and TSH receptor were negative. Ultrasonography revealed diffuse goiter (28 ml in volume), which shows homogeneous isoechogenicity. In routine blood tests, serum levels of lipid, protein, and electrolytes were within normal ranges ().
Because his 33-month-old son also showed elevated serum levels of free T4 and free T3 and a normal level of TSH (), we suspected that they had RTH; therefore, we examined sequences of their THRB genes. Both the index patient and his son presented with the same heterozygous germline mutation in the THRB gene: the 1244th guanine was changed to cytosine (). This point mutation results in the substitution of the 320th wild-type amino acid residue arginine to proline. We could not further examine other family members, because the parents of the index patient had died and his brother and sister could not be contacted.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [31, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 31 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
835,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3021896-1,Extracted,"A 63-year-old female was presented to emergency room with an abdominal pain. The patient had moderate mitral valve stenosis and atrial fibrillation since one year ago. She has been treated with warfarin but she often skipped her medication. Blood pressure was 120/80 mmHg and pulse rate was 72 min. The 12-lead electrocardiogram revealed atrial fibrillation with normal ventricular response. Her international normalized ratio (INR) was 1.11. Abdominal computed tomography (CT) revealed right renal infarction. Two-dimensional transthoracic echocardiography (TTE) showed moderate mitral valve stenosis with valve area of 1.2 cm2 and an enlarged left atrium. A large mobile round mass (2-3 cm in size) was seen in the left atrium (). It was unclear whether the mass had any attachment to the interatrial septum. The mean pressure gradient across the mitral valve on Doppler was 6 mmHg. To confirm a diagnosis, a transesophageal two-and three-dimensional echocardiography (TEE) was performed. A large (4 cm × 2.5 cm), ovoid and heterogeneous mass was observed in the left atrium attached with a narrow stalk to the left atrial septum (). Three-dimensional TEE showed a more definite connection with a long stalk between the mass and atrial septum. It showed tumor-like movement with cardiac cycle (). There was no mass in the left atrial appendage. Because it was thought to be a myxoma rather than thrombus, surgery with mass removal and mitral valve replacement was planed. Anticoagulation with heparin was continued for 12 days because of delayed surgery. Follow-up echocardiogram could not be done before surgery. When the operation was performed, surprisingly, there was no mass in the left atrium. We concluded that the mass must be thrombus and melt away. There was no remnant structure in the left atrium. Mitral valve replacement was done ().",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [63, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 63 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
836,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4217304-1,Extracted,"An 87 year old man with longstanding persistent atrial fibrillation and elevated stroke risk (CHADSVASC score = 3, HASBLED = 2) was felt not to be candidate for chronic oral anticoagulation due to repeated falls associated with orthopedic injury. He was referred to our Electrophysiology Laboratory for percutaneous suture ligation of the left atrial appendage.
A pre-operative CT angiogram was performed to determine the patient's left atrial appendage anatomy. This showed a single lobed appendage 3.3cm in length with a trabeculated distal portion and was deemed suitable for the exclusion procedure. Under general anesthesia, intra-operative 3D transesophageal echocardiography (TEE) demonstrated no left atrial thrombus. A Tuohy needle was used to enter the pericardial space via a subxiphoid approach under fluoroscopic guidance. Entry into the pericardial space was anterior-lateral, using contrast and a lateral fluoroscopic view. The access site was sequentially dilated and a 13Fr sheath was placed into the pericardial space. Next, trans-septal puncture was performed using an 8.5 Fr SL-1 sheath and an Extra Sharp Brokenbrough needle, via the right femoral vein. A Heparin drip was initiated to maintain adequate activated clotting time (250-300 sec).
A left atrial angiogram with an occlusive balloon (SentreHeart Endocath) confirmed the LAA size, shape and orientation, consistent with CTA findings. A magnet-tipped guidewire (Sentreheart FindrWIRZ) wire was advanced into the distal portion of left atrial appendage. A second magnet-tipped guidewire was advanced into the subxiphoid space and coupled magnetically to the LAA wire, in the end-to-end configuration. The Lariat suture loop was then advanced into the pericardial space over the magnet guidewire. The suture loop could not be advanced to the base of the appendage due to separation of the guidewire magnets. After manipulation of the suture loop the magnets were often noted to be in the end-to-side configuration, preventing successful positioning of the suture loop.
During manipulation of the magnet-tipped guidewires, the patient became hypotensive to a systolic pressure of 55 mmHg and a new pericardial effusion was noticed on TEE (). Approximately 200cc of blood was drained from the side arm of the epicardial sheath with some initial improvement in hemodynamics. The effusion reaccumulated and the blood pressure dropped. A pigtail catheter was emergently placed in the pericardial space. A total of 800cc was drained and autotransfused back to the patient. The patient's hemodynamic condition stabilized and the decision was made to continue the case. Hemostasis of the LAA would likely be achieved with successful application of the closure device.
With the pigtail catheter in place, a second subxiphoid epicardial access was obtained, directed more laterally from the first. The epicardial needle was directed towards the magnet tipped wire already in the LAA. The new orientation of the epicardial sheath was felt to improve access to the left atrial appendage.
The Lariat was advanced into the subxiphoid space through a second 13Fr sheath and easily tracked over the guidewire around the base of left atrial appendage. Appropriate position of the suture was confirmed with balloon inflation, atrial angiography, and color Doppler and 3D TEE ().
The suture loop was successfully deployed and there was no further accumulation of the effusion. Intra-op TEE showed no residual flow in the appendage. The pigtail catheter was left in place. Protamine was administered to partially reverse anticoagulation.
Follow-up transthoracic echocardiography 12 hours later showed no pericardial effusion and the pigtail catheter was removed. The patient was later discharged home.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [87, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 87 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
837,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2822321-1,Extracted,"A 53-yr-old man was hospitalized in April 2002 because of a sudden motor weakness in his left extremities, dysarthria, right eye visual disturbance, and headache. A diagnosis of nephrotic syndrome had been made elsewhere in 3 weeks before admission, based on clinical manifestation, blood, and urinary abnormalities and focal segmental glomerulosclerosis was confirmed by percutaneous renal biopsy. Also he had been diagnosed with alcohol-associated liver cirrhosis (Child-Pugh Classification A) from abdominal ultrasonography and healthy HBV carrier in 7 months before admission. After diagnosis of focal segmental glomerulosclerosis, he had been treated with diuretics, angiotensin converting enzyme (ACE) inhibitor, prednisolone 1 mg/kg/day, and lamivudine with a dosage of 100 mg/day for the prevention of flare up of viral hepatitis. He had no history of hypertension or diabetes. He had been a 30-pack year smoker and a heavy alcoholic, but quitted smoking and alcohol several months before. On admission, his general appearance revealed that he was acutely ill with bilateral pedal edema. His blood pressure was 120/80 mmHg, pulse rate 120/min, respiratory rate 24/min, and body temperature 37℃. Cardic examination showed normal findings. He had no evidence of systemic thromboembolism, deep vein thrombosis, or cervical bruit. Neurological examination revealed drowsy mentality with a left-side motor weakness, and decreased sensory perception on the left side. He was also exhibited dysarthria and right eye visual disturbance. However, the high cortical function was normal.
The initial MR and MR angiography of the brain showed a recent infarction in the right middle cerebral artery territory and the head of the caudate nucleus, no blood flow signal intensity in the right internal carotid artery (, ).
Laboratory data showed leukocytosis (2.49×103/µL) and hematocrit of 31.9% with hemoglobin of 10.9 g/dL, and platelet of 230×103/µL. The serum sodium level was 136 mEq/L, potassium 4.1 mEq/L, blood urea nitrogen 33 mg/L, serum creatinine 1.0 mg/L, and total serum protein 3.3 g/dL with albumin 1.2 g/dL. Urinalysis revealed 4+ albuminuria and 24-hr urine protein over 7.8 g/day. The serum cholesterol level was elevated at 539 mg/dL. The liver function tests, prothrombin time, and activated partial thromboplastin time were normal. The fibrinogen concentration and antithrombin III level were normal. The concentration of free protein S was 35.0% (normal 70-140%). Plasminogen and platelet aggregation test were not performed. The negative HBe Ag, undetectable HBV DNA, and HBs Ag seroconversion after lamivudine therapy were demonstrated. The C3 and C4 were in normal ranges. Anticardiolipin (IgM) was 4.9 MPL unit/mL (normal <12 MPL unit/mL). After the admission, supportive care for the cerebral infarction was initiated and he received anticoagulation therapy later. Hospital course was uneventful with a mild degree of residual left-side motor weakness at discharge. Two months after discharge, remission of nephrotic syndrome occurred on medication with steroid, angiotensin II receptor blocking agent. At present, 1 yr after discharge, serum albumin level is 4.6 g/dL with serum cholesterol 158 mg/dL and negative albuminuria on tapered dose of prednisolone 7.5 mg every other day (QOD).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [53, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Stroke': True, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 53 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 0 + 2 = 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
838,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5965084-1,Extracted,"A 65-year-old Caucasian male with a history of poorly controlled hypertension and hyperlipidemia presented to the emergency room for evaluation of near syncope. He complained 1 week history of dizziness and near syncopal events but denied any chest pain, shortness of breath or palpitations. He was taking 10 mg of amlodipine, 50 mg of atenolol and 81 mg of aspirin on a daily basis. During his recent office visit, he was found to have an elevated blood pressure of 165/90 mmHg and the atenolol dose was increased to 75 mg for better blood pressure control.
On admission, he was registering a temperature of 98.4°F, a blood pressure of 80/40 mmHg without orthostatic hypotension, a pulse rate of 40 beats/min, respiratory rate of 16/min and oxygen saturation of 96% on room air. Physical examination was unremarkable. During his physical exam, he experienced another near syncopal event. Electrocardiogram obtained showed repetitive group beating in a bigeminal pattern. The 12-lead ECG (Fig. ) shows sinus bradycardia at a rate of 36 beats/min with a P–P interval of 1840 ms. Each P wave is followed by a QRS complex with a PR interval of 200 ms. The P waves (green arrows) are best seen in lead II. A junctional escape rhythm is seen interrupting each sinus cycle at a constant escape interval of 1360 ms.The junctional escape beats are followed by regular sinus beats at intervals of 480 ms. Laboratory data including thyroid stimulating hormone, electrolytes and serial cardiac markers (troponin I) were within normal range. Transthoracic echocardiogram did not reveal any abnormalities. He had no signs or symptoms of extra cardiac sarcoidosis and did not meet the criteria for advanced cardiac imaging to look for cardiac sarcoidosis. His recent coronary angiogram a month ago showed normal coronaries.
Since beta blockers can suppress the sinus node function, we discontinued atenolol. The patient underwent temporary transvenous pacemaker placement (demand pacing at 80 beats/minute) because of symptomatic bradycardia and hemodynamic instability (Fig. ).
After 36 hours, his intrinsic sinus rate significantly improved and the temporary pacemaker was removed. The junctional escape rhythm and the escape-capture bigeminy also disappeared with improvement of the sinus rate (Fig. ). Telemetry monitoring for the next 48 hours was uneventful and he was discharged on mobile cardiac outpatient telemetry. He was also started on 10 mg of Lisinopril before discharge. On 1-month follow-up, he was asymptomatic with a blood pressure of 124/68 mmHg and no abnormal rhythms were recorded on the cardiac monitor. Atenolol-induced suppression of sinus automaticity or sinoatrial exit block is the most likely cause of dizziness and near syncope in our patient. As calcium channel blockers can also suppress the sinus node function, one cannot rule out the role of amlodipine in the contribution of the patient symptoms without rechallenging him with atenolol in the absence of amlodipine. However, he did not report any symptoms thus far while he continued to take amlodipine for hypertension.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [65, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
839,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3874350-1,Extracted,"The patient was an 87-year-old female who initially presented to her primary care provider in May 2010 complaining of increasing abdominal pain and tightness in the central abdomen for two days with associated nausea, vomiting, and anorexia. Her physician sent her to the emergency department for further evaluation. The patient's surgical history included an open appendectomy in 1960 and her past medical history was significant for hypertension, atrial fibrillation, polycythemia rubra vera, and epilepsy. Her urological history was unremarkable. According to the patient, she had similar episodes in the past few years where she felt occasional bloating and the feeling that something was protruding into her scar, but that pain usually passed within a day.
Upon evaluation in the emergency department, the emergency medicine resident noted a “soft, midline mass, which is tender and is incompletely reducible with moderate increase in discomfort.” A healed 5 cm scar was present in the right abdomen. Bowel sounds were increased, and the mass was initially attributed to a ventral hernia causing the patient's symptoms. An acute abdominal series showed no clear signs of obstruction. A CT scan (Figures and ) of the abdomen was obtained due to her age and severity of pain and the report from the on-call radiologist noted the following.
“The right kidney is no longer within the renal fossa as seen in 2006, but has changed position and is now anterior to the liver. There is resultant severe hydronephrosis involving the renal pelvis and proximal ureter. This abruptly changes caliber on axial image 38 and the ureter is not well seen inferior to this level. There is symmetric renal perfusion. High attenuation material is seen dependently within the dilated renal pelvis, this could reflect blood products or stone material.” Additionally, there was no diaphragmatic hernia noted.
The urologist on call was then called at approximately two thirty in the morning to assess the patient, and noted in the documentation the following. “A patient with what appears to be UPJ obstruction on the right side that has developed since 2006 when she had a CT scan demonstrating what looks to be a lower pole crossing the arterial vessel. She has since had progressive obstruction that has pushed her renal pelvis posteriorly and her kidney anteriorly up in front of her liver and has displaced her colon. I am concerned that a full surgical repair would require open surgery in this delicate 88 year old and would suggest that she undergo a cystoscopy and right double-J stent placement to assess how she tolerates that.” Approximately 6 weeks following the emergency department visit, a cystoscopy, bilateral retrograde pyelograms, and right double-J stent placement were performed. This ameliorated her symptoms and the stents were removed in a timely fashion.
The patient was seen recently in followup in June 2013 and she stated that she had an additional episode of abdominal pain similar to her presentation to the emergency department and that manual pressure on her right upper quadrant was successful in reducing the mass and relieving the pain. In followup, the right kidney was palpable but nontender. The patient was scheduled for a routine six-month followup to track her progress. Since then, she endorsed self-treating with manual manipulation of the kidney when it has been painful.
In November 2013, however, the patient again presented to the emergency department with the same abdominal pain. A noncontrast CT scan was performed and the patient's right kidney had now translocated across the midline to a position anterior to her left kidney with extreme hydronephrosis present (). The following day, a retrograde pyelogram () was performed showing that the right kidney had moved back to the right lower quadrant. A double-J stent was placed to reduce the hydronephrosis and subsequently her symptoms resolved. She is expected to follow up for repeated imaging and stent removal.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': False, 'age': [87, 'years'], 'Stroke': False, 'Diabetes history': False, 'Transient Ischemic Attacks History': False, 'sex': 'Female'}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 87 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
840,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8233487-1,Extracted,"A 64-year-old Caucasian female presented with dizziness, pre-syncope, and progressive decline in functional capacity, with New York Heart Association (NYHA) class III symptoms. Her past medical history was significant for atrial fibrillation, type II diabetes mellitus, hypertension, hyperlipidaemia, prior tobacco use, chronic obstructive pulmonary disease, and idiopathic thrombocytopenia. She also had been previously diagnosed with aortic stenosis, which prompted admission for further evaluation of progression. Family history was significant for coronary artery disease in her parents and brother, and colon cancer in the mother. Physical exam was significant for a holosystolic murmur radiating to the axilla, and bilateral lower extremity oedema, otherwise unremarkable. Initial electrocardiogram (ECG) showed normal sinus rhythm without LV hypertrophy or significant ST/T wave abnormalities (). Echocardiography showed normal LV systolic function, Grade II LV diastolic dysfunction, and moderate septal LV hypertrophy (1.7 cm at the level of mitral leaflet tips) (, Videos 1 and 2). At rest, there was mitral valve SAM with near septal contact and a peak LVOT gradient of 48 mmHg, with resultant moderate, posteriorly directed mitral regurgitation, which increased to SAM with septal contact after provocation with Valsalva manoeuvre, showing an increase in the peak LVOT gradient to 82 mmHg (). She underwent CMR imaging, which showed again septal hypertrophy, mitral valve SAM with moderately severe mitral regurgitation, and flow acceleration in the LVOT, suggestive of a haemodynamically significant obstruction (Video 3 and ). Interestingly, the septal thickness was less prominent by CMR (1.5 cm in the mid-inferoseptum), likely due to the inclusion of right ventricular septal trabeculation on echo and resultant overestimation of septal thickness. Cardiac magnetic resonance also defined abnormal chordal attachments from the posterior medial papillary muscle to the base of the anterior mitral valve leaflet, which were also likely contributing to LVOT obstruction (). Mild delayed gadolinium enhancement was noted within the mid-myocardium of the thickened anteroseptum, as well as at the inferior right ventricle insertion point into the inter-ventricular septum (). This constellation of imaging findings was most likely consistent with hypertrophic obstructive cardiomyopathy (HOCM). Surgery was indicated because of the haemodynamically significant LVOT obstruction in the setting of her NYHA Class III symptoms despite optimal beta-blocker therapy, in line with current guideline recommendations.
Because of her relatively thin upper septum and the abnormal chordal attachments seen on imaging, and also possible need for mitral valve repair, septal myectomy was favoured instead of alcohol ablation. She underwent septal myectomy with left-sided Cox–MAZE IV procedure, with left atrial appendage ligation, and intraoperative findings were consistent with concentric left ventricular hypertrophy. Despite her multimodality imaging findings being consistent with HOCM, histopathology of the myectomy did not show the classic histopathology of hypertrophic cardiomyopathy. Instead, it showed non-caseating granulomatous myocarditis () (). Therefore, she was initiated on prednisone and referred for ICD implantation.
A month later, cardiac and whole-body FDG-PET were performed, with adequate preparation, and showed no FDG avid process except for left lower lobe ground-glass opacification with minimal uptake, not typical for pulmonary sarcoidosis. A year and a half after the myectomy, during admission for decompensated heart failure, work-up with repeat echocardiogram showed mildly decreased LV systolic function and moderate mitral regurgitation, and N-terminal pro-B-type natriuretic peptide of 2175 pg/mL. Repeat cardiac FDG-PET was done, at this time showing a diffuse myocardial FDG uptake despite a good diet preparation, suggestive of active inflammation (large, more than five segments of inflamed myocardium), with no perfusion defects. Repeat whole-body PET showed no abnormal FDG avid processes in the remainder of the body, and ophthalmologic evaluation also ruled out eye involvement, suggesting a diagnosis of isolated cardiac sarcoidosis (CS). She was initiated on methotrexate with a plan to progressively taper corticosteroids.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [64, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Vascular disease history': True, 'Diabetes history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 64 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
841,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6159658-1,Extracted,"A 74-year-old retired white female accountant was admitted to our neurology department for progressive cognitive decline, which had started insidiously, about four years prior to admission. Her symptoms were difficulty with language, sensory dysphasia, impairment of memory, and overall disorientation. According to her husband, her first symptom was the inability to form uncommon and complex words, so aphasia was the most prominent deficit at symptom onset leading to impaired daily living activities. Her condition slowly deteriorated leading to a loss of everyday activities, becoming unable to perform simple tasks related to household, then to her personal hygiene. Her husband reported that the executive performance as well as her spatial and temporal orientation varied over time and showed frequent daily alterations. She had type-2 diabetes for 4 years well controlled with diet and metformin. She had atrial fibrillation necessitating preventive apixaban treatment. She has had hypertension and hypercholesterinemia for 5 years treated with the combination of simvastatin, betaxolol, valsartan, furosemide, and digoxin. She was taking paroxetin for depression. Her body mass index was 25 with normal vital parameters apart from arrhythmia. She was passive and apathic while in hospital; lying inactively in bed the whole time, often in a sleep-like state during the day and apparently remaining so in the night. She was sometimes cheerful, tolerating and cooperating reasonably well with any queries or interventions; she seemed friendly and quiet with no interest, motivations, or denial.
Her blood screen, TSH, and coagulation parameters were normal. Her cerebrospinal fluid (CSF) tau-level was 239 pg/ml (normal range: 341±171 pg/ml), p-tau level was 24 pg/ml (normal range: 35.84–66.26 pg/ml), amyloid-β (Aβ) level was 717 pg/ml (normal range: 797±230 pg/ml), the Aβ/tau ratio was 3, while the Aβ/p-tau ratio was 29.88. Thus, the amyloid and tau levels in the CSF were in the normal range excluding AD. CSF ubiquitin or TDP-43 testing could not be performed.
The MRI brain scan revealed moderate small vessel disease with important diffuse cerebral atrophy, mainly affecting the frontal and temporal lobes with left side dominance ().
To analyze structural results more precisely, hippocampal volumes and cortical thickness were calculated with FreeSurfer5.3 image analysis suite (freely available for download: ). The technical details are demonstrated in previous reports, no changes were made to the pipeline. The image process contains motion correction, removal of non-brain tissue, automated Talairach transformation, segmentation of deep gray matter structures and subcortical white matter, intensity normalization, tessellation of white-gray matter boundary, automated topology correction and surface deformation following intensity gradients. Following the cortical models, Freesurfer managed deformable procedures such as surface inflation, registration to spherical atlas, parcellation of cerebral cortex into units and creation of different surface based data. Cortical models and results of segmentation were quality controlled.
Average left frontal thickness (in mm) was 1.79±0.16, right frontal thickness was 2.01±0.21, left temporal thickness was 2.33±0.32, right temporal thickness was 2.45±0.36, left parietal thickness was 2.01±0.2 and right parietal thickness was 2.18±0.29. The temporal and frontal values are below the normal ranges if we compare it to data from the literature, especially on the left side, while the parietals are relatively preserved, being in line with the previous reports on FTD []. The volume of the left hippocampus was 3301 mm3, and of the right was 3997 mm3. These values are in the normal range based on our previous study with the same analysis method []. However, the left hippocampus was significantly smaller showing 17.5% asymmetry which suggests pathological changes in the volume of left hippocampus besides the normal values. Volumetric asymmetry could be considered significant above 10%. The volume of the left entorhinal cortex was 1881 mm3, while that of the right was 1811 mm3. These values and the disappearance of the difference between the two sides indicate Alzheimer or frontotemporal pathology based on previous data []. Altogether, the left dominant frontotemporal thinning and normal parietal thickness, and the involvement of the entorhinal cortex suggested the morphometry of FTD []. The routine EEG showed 20–40 uV, 9-10 Hz alpha background with frontal beta activity. We detected occasional left temporal focal slowing. No specific epileptiform activity were seen. Detailed neuropsychological analysis including Addenbrooke’s Cognitive Examination (ACE) was performed. This test has a high sensitivity (0.9) and specificity (0.93) in the differentiation of cognitive disorders, especially in the diagnosis of AD and FTD []. Her ACE score was 32/100. The Verbal-Language/Orientation-Memory ratio of ACE, which sensitively discriminates AD and FTD [], scored 1.9 suggesting FTD. The Mini-Mental State Examination score extracted from ACE [] was 16/30. The neuropsychological results were consistent with a moderate cognitive decline. The most impaired cognitive domains were single-word retrieval in spontaneous speech and naming, reading, verbal short-term memory; whereas repetition, spatial orientation and grammar were relatively preserved. No early behavioral disinhibition, apathy/inertia, early loss of sympathy/empathy, presence of perseverative behavior and hyperorality were reported, so the diagnosis of behavior variant FTD was improbable []. Based on current diagnostic recommendations, we diagnosed primary progressive aphasia related to FTD []. Based on the caregiver’s report on the significant daily variability of her cognitive functions the presence of diffuse Lewy-body dementia was also considered. However, its core criteria as Parkinsonism or visual hallucinations were not present, therefore it was excluded. To assess the severity of cognitive fluctuation we used an easily applicable, bed-side test with high sensitivity in measuring visuo-spatial performance, the Corsi Block-Tapping Task (CBTT) []. We carried out CBTT with 2-3 items four times in one day; in better and worse cognitive periods (reported by the medical staff and her husband) and compared the number of correct answers with ANOVA analysis using the IBM SPSS20 software. We revealed significant differences in the results of the four trials (df: 3; Mean Square: 1.098; F: 4.567; p: 0.004). Based on both the neuropsychology scores and the history suggesting the possibility of non-convulsive seizure-episodes, we suspected concomitant epilepsy. Risk factors for developing epileptic seizures including definitive structural lesions on MRI, previous history of head trauma, childhood seizures, CNS infection, drug or alcohol dependency or electroconvulsive therapy were absent.
To disclose the potential epileptiform activity, we performed a 24-h Holter-EEG, followed by a 3-day-long continuous scalp video-EEG monitoring. We recorded one episode of slightly irregular rhythmic theta activity lasting for 20 s during light sleep in the right temporal leads. We also detected very rare bitemporal independent sharp waves with slight right dominance, possibly consistent with epileptiform activity []. The long-term EEG revealed disturbed sleep macrostructure with superficial night sleep, no deep sleep and very short REM sleep episodes; no sleep spindles or K complexes were found.
The EEG changes supported our suspicion that the significant fluctuations of her cognitive performance might be related to temporal lobe epileptic activity. Therefore, FO electrodes were surgically implanted () under general anesthesia; and continuous video-EEG recording using both FO and scalp electrodes were performed for 4 days.
The national and institutional ethic committees approved the FO electrode implantations and the recording; the family of the patient gave written informed consent to the procedure. The FO electrode implantation and the video-EEG monitoring period were uneventful, no surgical complications, behavioral or cooperation issues occurred. Frequent neuropsychological testing with CBTT was carried out during monitoring. The patient perfectly complied so we could perform clean, artefact-free EEG recordings. The recordings revealed bilateral independent spikes on the FO leads; in average, 30 unambiguous single spikes on the right side and 4 on the left per day (). We considered these graphoelements interictal spikes because of their paroxysmal appearance, the abrupt change in polarity, the typical spike duration (less than 70 ms) and because of their consistent temporal field distribution []. The spike activity occurred mainly during superficial NREM sleep, similarly to typical temporal epileptiform activity. We recorded runs of 11-12 Hz beta waves with or without 5 Hz theta elements and spike-like components, mostly during light NREM sleep, much less during wakefulness and none during the short REM periods, as well as >1 s long runs of sharp waves more often on the left side ( and ).
None of the epileptiform EEG events propagated onto the scalp electrodes. The spikes and sharp waves had an amplitude <l00 μV, and occurred frequently in the FO electrodes. The FO revealed 15-16 Hz, crescendo-decrescendo beta spindles during wakefulness, frequently preceding movements ().
Because of the occurrence of epileptiform discharges, we initiated clobazam treatment during the monitoring period, however there were no changes in the occurrence of epileptiform potentials and the neuropsychological performance following the drug administration in the next 2 days. According to some data, levetiracetam might be effective in AD-related epilepsy and it is easier to reach a steady state much earlier than clobazam [], therefore we started levetiracetam and we plan close follow-up.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [74, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 74 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
842,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5222999-1,Extracted,"A Caucasian man aged 75 years presented to the Emergency Department at the National Hospital, Faroe Islands, with complaints of a two-week history of progressively severe diffuse myalgia, confined to the lower back and proximal lower muscles, reduced power in all four extremities, and generalized weakness, and he was immobile and bedridden. He was neurologically sound and there was no complaint regarding headache, numbness, tingling, or paraesthesia. He denied indulgence in any kind of vigorous physical exercise and over consumption of alcohol. He was already under medication for hypertension and in treatment with rivaroxaban due to atrial fibrillation and atorvastatin 80 mg daily for hyperlipidaemia and on lifelong prophylactic empirical antibiotic treatment with oral fusidic acid 500 mg twice a day combined with oral moxifloxacin 400 mg daily and for an infected aortic aneurysm, with an infected endovascular aortic stent and para-aortic abscesses. He had no familial or prior personal history of muscle disorder and no past history of muscular toxicity with statin or fibrate use. He had been in treatment with atorvastatin for several years. He had been treated with fusidic acid and moxifloxacin for 6 days before the day of admission.
He was afebrile with heart rate 75 beats/minute but hypotensive (103/42 mmHg). The cardiovascular, respiratory, and gastrointestinal tract examination was normal. He complained of moderate discomfort due to myalgia. The quadriceps muscles were tender to palpation and he had reduced power bilaterally. The cranial nerves 2–12 examination was normal. The power 5/5 strength in all the muscle groups was observed, except for the hip flexors and quadriceps which rated 3/5 bilaterally. He was immobile due to weakness. He had normal sensory examinations to light touch, pin prick, and proprioception.
On admission the laboratory measurements revealed the following: hemoglobin 6.4 mmol/L, total leukocyte count 7.8 × 109/L, potassium 4.4 mmol/L, sodium 140 mmol/L, urea 16.8 mmol/L, creatinine 128 micromol/L, and blood glucose 6.5 mmol/L. Serum muscle enzymes were markedly elevated: creatinine kinase (CK) 328 U/L (reference values: 40–208), LDH 266 U/L (reference values: 115–255), BNP 607 pmol/L (normal up to 28.9), elevated liver function test with ALAT 125 U/L (reference values: 10–70), alkaline phosphatases 232 U/L (reference values: 35–105), and normal bilirubin 9 U/L (reference values: 5–25). describes the levels of CK, myoglobin, creatinine, and urea (the combination was stopped on 6th day after admission). Urine analysis showed no significant microscopic hematuria or proteinuria. The patient was also screened for autoimmune diseases: autoantibody p-ANCA (IgG) with medium positive result (nonconclusive), autoantibody c-ANCA (IgG) negative, and autoantibody ANA negative. These results made the differential diagnoses immunological vasculitis, granulomatosis with polyangiitis, and systemic lupus erythematosus (SLE) unlikely. The rheumatological differential diagnoses polymyositis and dermatomyositis were unlikely because of negative autoantibodies known to be associated to polymyositis and dermatomyositis (). A spinal tap was performed to rule out Guillain-Barré syndrome as differential diagnosis. The spinal tap showed no pleocytosis, normal protein, and normal glucose level in the cerebrospinal fluid. An MRI of the cervical spine showed a nonsignificant spinal stenosis at the C5/C6 level, which did not explain the symptomatology of the patient. Finally because of negative HMG-CoA reductase antibodies (IgG), associated to autoimmune statin induced rhabdomyolysis, this differential diagnosis was unlikely in our patient (). Therefore, considering the clinical development, the kinetics of the biochemical markers, and the medication history, we assume that the diagnosis of rhabdomyolysis as a consequence to combination therapy with atorvastatin and fusidic acid is highly likely. Treatment with atorvastatin and fusidic acid was halted on 6th day after admission and approximately 12th day since the combination started. Fusidic acid was changed to oral Co-amoxiclav 500/125 mg tid and the patient continued on atorvastatin and oral moxifloxacin 400 mg daily. The patient was treated with intravenous fluid and physiotherapy.
The patient was discharged after 5 weeks with remarkable improvement of symptoms. When he left hospital the biochemical markers revealed normal muscle enzymes with CK 71 U/L, myoglobin 94 ng/L, and normal transaminases ( and ). It was decided not to treat the patient with fusidic acid in the future.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [75, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': True, 'Stroke': False, 'Diabetes history': False, 'Transient Ischemic Attacks History': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 75 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
843,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-5128,Extracted,"A 57-year-old man presents to the emergency department for shortness of breath. He was riding the train home from a business conference when his symptoms began. The patient has a past medical history of obesity, diabetes, diabetic nephropathy, hypertension, and a 40 pack-year smoking history. His current medications include atorvastatin, lisinopril, insulin, metformin, and nicotine gum. His temperature is 99.5°F (37.5°C), blood pressure is 130/87 mmHg, pulse is 120/min, respirations are 15/min, and oxygen saturation is 93% on room air. An EKG is ordered as seen in Figure A. A chest radiograph is ordered as seen in Figure B. Laboratory values are ordered as seen below:

Serum:
Na+: 137 mEq/L
Cl-: 105 mEq/L
K+: 4.1 mEq/L
HCO3-: 24 mEq/L
BUN: 22 mg/dL
Glucose: 129 mg/dL
Creatinine: 1.2 mg/dL
Ca2+: 10.1 mg/dL
AST: 11 U/L
ALT: 12 U/L

On physical exam you note a patient who seems in distress. His cardiac exam is notable for tachycardia. Pulmonary exam reveals bilateral air movement without any wheezes or crackles. The patient's right lower extremity appears mildly inflamed, and palpation of the calf elicits pain.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [57, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': False, 'Diabetes history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 57 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 1 + 1 = 2.
The patient's CHA2DS2-VASc Score is 2."
844,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6280337-1,Extracted,"A 76-year-old Caucasian female attended our pulmonology outpatient clinic with a four-week history of cough with mucous-purulent sputum and dyspnea. The patient was a nonsmoker and had worked for a few years in a cotton factory. Her past medical history was negative for any contact with substances known to be associated with lipoid pneumonia. She had not travelled recently and had no pets. She had been treated for atrial fibrillation with amiodarone (200 mg OD) for 30 years, systemic hypertension, diabetes mellitus type II and hypothyroidism. Physical examination revealed a well built and nourished patient with pulse rate 69 per minute and blood pressure 110/70 mmHg. Vital signs were within normal range with SpO2 of 95% in room air. Her physical examination revealed bibasal lung crackles, but no evidence of pallor, icterus, cyanosis, clubbing or lymphadenopathy. Her blood work-up was within normal range. Pulmonary function testing demonstrated moderate restrictive lung disease and a decreased diffusion capacity. (see Table ).
Since chest X-ray showed bilateral infiltrates, a high resolution computed tomography (HRCT) was conducted. The latter revealed areas of ground glass appearance significantly in the lower lobes of both lungs and airspace consolidations were seen as well (Fig., [a], [b]). The shadows improved 2 years later (Fig. , [c]).
Radiologically, differential diagnosis included atypical pneumonia, interstitial lung disease and tuberculosis was ruled out. The patient underwent fiberoptic bronchoscopy for bronchial wash and bronchoalveolar lavage (BALF) was collected for immunological studies as well. The bronchial washings were sent for smear for acid fast bacilli and cytological examination. No microorganisms were isolated by 48bacteriological examination and no malignant cells were found.
The total cell count of the BALF was 287,500/ml. The cells consisted of macrophages (64%), lymphocytes (31%), neutrophils (3%), and eosinophils (2%). The evaluation of BALF with specific staining and coloration showed the presence of fat-laden macrophages (oil red O stain). Figure [a], [b] Extracellular oily droplets were found on a sputum cytology examination. These findings were suggestive of lipoid pneumonia.
The patient had never aspirated or inhaled mineral or vegetable oils and she had never used petroleum jelly intranasally or extra-nasally as a decongestant. However, it is described in the literature that chronic use of amiodarone can cause endogenous lipoid pneumonia (phospholipidosis) []. Amiodarone, as an amphiphilic cationic compound, interferes with the movement of phospholipids across intracellular membranes and inhibits phospholipid catabolism through its potent inhibitory effect on lysosomal phospholipase 2. Drug-induced phospholipidosis assumes the form of a ‘foamy cell ‘response.
In our case, the patient had been taking amiodarone (200 mg OD) for 30 years which was considered the most likely cause. It was therefore discontinued and replaced with digoxin (0.25 mg OD) for the treatment of atrial fibrillation. She was also started on oral prednisolone (20 mg OD) which was gradually tapered over a period of six months.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [76, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Vascular disease history': False, 'Diabetes history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
845,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5817267-1,Extracted,"An 81-year-old man presented to the emergency department (ED) with shortness of breath and nonproductive cough. He denied fever, chills, or chest pain. He was afebrile with blood pressure 127/68 mmHg, pulse rate 63/min, and respiratory rate 22/min. The patient's saturation was 89% in room air which improved to 97% with 2L of oxygen. He had decreased breath sounds with crackles over the right lung field. The remainder of the physical exam was unremarkable. The patient had been admitted 2 weeks before with lower extremity weakness which was thought to be secondary to deconditioning from a recent upper respiratory tract infection for which he was treated with amoxicillin by his primary care physician. At that time, he was discharged with provisions for physical therapy. The patient had a past medical history of paroxysmal atrial fibrillation on amiodarone but not on anticoagulation, hypertension, and chronic kidney disease stage III. He had a 20 pack-year smoking history and had quit 57 years ago.
On arrival, the patient's WBC count was 12,500/µl with 85.9% neutrophils. ABG showed pH of 7.496 with pCO2 33.9 mmHg, pO2 80.2 mmHg, and bicarbonate 26.4 meq/l. Chest X-ray revealed new, moderately extensive, multifocal right lung pneumonia with small associated parapneumonic effusion (). CT chest further detailed a right basilar opacification with right pleural effusion and small amount of pleural gas (). The patient was started on IV vancomycin, piperacillin-tazobactam, and oral azithromycin in the ED. Azithromycin was discontinued a day later after recommendations from Infectious Disease. Blood, sputum, and pleural fluid studies were ordered. Thoracocentesis showed pH 6.9, protein 4.6 g/dl (serum protein 5.7 g/dl; reference range: 6.4–8.9 g/dl), albumin 2.1 g/dl (serum albumin 2.2 g/dl), and lactate dehydrogenase (LDH) 4844 IU/L (serum LDH: 273 IU/L), suggestive of empyema. A 12 Fr chest tube was placed under CT guidance by interventional radiology which yielded foul-smelling, dark burgundy fluid. Pleural fluid culture was positive for pansensitive C. perfringens. Surprisingly, sputum culture grew Pseudomonas aeruginosa and Citrobacter koseri, both of which were sensitive to piperacillin-tazobactam. We did not order a quantitative culture to differentiate between pulmonary colonization and infection. We also did not perform bronchoscopy to rule out any mass or foreign body associated with the empyema. IV vancomycin was discontinued. IV clindamycin was added but was later discontinued after stool was positive for Clostridium difficile. The patient was planned for a 4-week course of IV piperacillin-tazobactam. On day 8, the patient was noted to have right lower extremity swelling which led to the discovery of extensive DVT and submassive PE, which was treated with Eliquis. Due to bleeding risk, decortication was deferred and the patient was instead treated with intrapleural tPA and dornase alpha.
With further questioning during hospital stay, the patient mentioned that he had difficulty swallowing food due to the sensation that something was stuck in his throat. He had resting tremor of the left hand and subtle cogwheeling of the right upper extremity. The swallowing function study was positive for aspiration. MRI brain to rule out any intracranial pathology was done which showed focal acute/subacute infarction. Echocardiogram with double bubble study revealed a patent foramen ovale. For this, cardiology advised anticoagulation with consideration for closure in the event of a stroke while on Eliquis. Neurology suspected that dysphagia was due to Parkinson's disease and recommended starting Sinemet in the near future. The patient was discharged to acute rehab with a chest tube to water seal. Chest CT done a month later showed improvement of the effusion with minimal drainage from the tube. The chest tube was removed. Repeat pleural fluid cultures were negative for infection. The patient did not show any fluid reaccumulation on subsequent imaging studies (Figures and ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [81, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Vascular disease history': False, 'Diabetes history': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 81 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
846,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6955118-1,Extracted,"An 88-year-old-female presented to our emergency department with complaints of abdominal discomfort associated with nausea and vomiting for one day. Upon arrival, she was afebrile with a blood pressure of 120/54 mmHg, a pulse rate of 40 beats per minute (bpm) (), and a respiratory rate of 18 breaths per minute. She denied any chest pain, dyspnea, or palpitations. She denied any recent illnesses, had no history of recent travel, and denied any sick contacts, or recent change in medications. Her medical comorbidities included hypertension (HTN), diabetes, CAD, heart failure with preserved ejection fraction, paroxysmal atrial fibrillation, hypothyroidism, and a history of cerebrovascular accident (CVA) without any residual deficits. Her prescription regimen included amlodipine (10 mg), furosemide (20 mg OD, same dose for past 1 year), isosorbide mononitrate (30 mg OD), levothyroxine (37.5 mcg OD), metformin (500 mg BID), omeprazole (20 mg OD), and ranolazine (500 mg BID, same dose for the past 1 year). Physical examination was remarkable for bradycardia and decreased breath sounds in the left lower lung field, and she was euvolemic on exam. Laboratory studies were significant for a serum potassium level of 6.8 mEq/L and a serum creatinine level of 1.6 mg/dL and eGFR of 32 ml/min/m2 (increased from baseline creatinine of 0.9 mg/dl, eGFR 68 ml/min/m2). Thyroid studies were within the normal range. Chest radiography revealed minimal left pleural effusion. She received an intravenous fluid bolus for her acute renal injury and was administered sodium polystyrene sulfate, calcium gluconate, albuterol, intravenous insulin, and a dextrose injection to treat the hyperkalemia. Over the next few hours, her bradycardia worsened despite correction of the hyperkalemia. A 12-lead electrocardiography (ECG) showed junctional bradycardia at 32 bpm, a normal QRS complex, and a prolonged QTc of 532 milliseconds. There was no demonstrable peaking of the T waves. Atropine was administered without any significant chronotropic response. She was admitted to the cardiac care unit for close monitoring. The following day, her serum creatinine reached a maximum of 2.2 mg/dL. Ranolazine was discontinued. Metabolic derangements were treated appropriately. After 48 hours from presentation, potassium and renal function returned to baseline and her heart rate improved to a range of 60–100 bpm. She was discharged the next day with an outpatient cardiology follow-up. Ranolazine treatment was not continued upon discharge.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [88, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': True, 'Vascular disease history': True, 'Diabetes history': True}",9,9,9,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 88 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 5 + 2 = 7.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 7 + 1 = 8. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 8 + 1 = 9.
The patient's CHA2DS2-VASc Score is 9."
847,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6503592-1,Extracted,"An 86-year-old gentleman presented to the emergency department for abrasions and
right leg pain. Immediately prior to arrival, he had experienced a mechanical fall
onto concrete. His medical history consisted of atrial fibrillation for which he
took daily anticoagulation medication (rivaroxaban). On arrival, he reported
posterior right thigh discomfort that was constant, described as “tightness,” worse
with movement of the right leg, and associated with mild, vague paresthesias of the
right foot. His vital signs were within normal limits including a pulse rate of 65
beats/min and a blood pressure of 129/96. The physical exam was notable for focal
tenderness to palpation over the posterior right thigh with a compartment that felt
mildly firm to palpation. There was no overlying rash or ecchymosis. There was
decreased sensation to light touch in the right foot with fully intact motor
function. Distal pulses in the right leg were intact. The bilateral feet appeared
symmetric and well perfused and were both warm to touch.
Bedside ultrasound of the posterior right thigh was performed and revealed an area of
hypoechogencity without Doppler color flow concerning for a fluid collection ( and ). This finding raised the
provider’s concern for a traumatic hematoma in the setting of anticoagulant use and
an expedited computed tomography (CT) scan with intravenous (IV) contrast of the
right leg was obtained, which revealed an 8-cm hematoma in the right posterior thigh
with active extravasation (). Immediate specialty consultation was obtained for further management.
During the patient’s emergency department course (after acquisition of focused
advanced imaging and initial specialty consultation), he developed hypotension
requiring bolus intravenous fluids as well as progression of right foot paresthesias
and interval development of motor weakness in the right foot concerning for sciatic
nerve palsy. The patient was taken in an emergent manner to the operating room and
underwent a fasciotomy of the right posterior thigh followed by interventional
radiology embolization of a profunda femoral vessel. Following the above
interventions, the patient’s symptoms gradually improved and at his 1-month
follow-up appointment, he did not have any significant morbidity related to his
compartment syndrome.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [86, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 86 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
848,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4008350-1,Extracted,"We present a 77-year-old Caucasian man with history of multiple comorbidities including coronary artery disease, diabetes mellitus, atrial fibrillation, pacemaker placement, and 40-pack-years of smoking who presented with complaints of speech disturbance and left-sided numbness and tingling which resolved within couple of hours of the hospitalization. He was diagnosed with transient ischemic attack (TIA). His pacemaker had been implanted for tachy-brady syndrome 36 months prior to this presentation. He was on warfarin, aspirin, and beta blocker for atrial fibrillation. His pulse rate was 105 beats/min, blood pressure 121/51 mmHg, respiratory rate 20/min, and oxygen saturation 96% on 3 L of oxygen. Physical examination revealed irregularly irregular tachycardia, bilateral rhonchi, wheezes, and mild pedal edema. His international normalized ratio (INR) was subtherapeutic at 1.2. Computer tomographic scan of the head was negative for acute process. His electrocardiogram (ECG) showed paced rhythm with right bundle-branch block, rather than the typical pattern of left bundle-branch block (). His chest X-ray in lateral projection showed ventricular lead with an abnormal turn (). Given the abnormal ECG and chest X-ray findings, pacemaker lead malposition was suspected. Transthoracic echocardiogram confirmed the pacemaker lead position in the left ventricle apex instead of right ventricle, passing through the interatrial septal defect (). Cardiac chambers were nondilated with ejection fraction of 65%. There was no associated thrombus. Doppler color-flow showed normal peak flows along with mild mitral regurgitation. Carotid ultrasound did not reveal any significant stenosis. Neurology service was on board and did the standard workup for TIA/stroke, which was negative.
We explained the possibility of recurrence of stroke/TIA in the setting of the malpositioned pacemaker lead to him. In view of his multiple co-morbidities, he refused surgical removal of the lead or any invasive procedures, including transesophageal echocardiogram. We increased his warfarin dose and educated him to maintain his INR between 2.5 and 3.5. Two years after the clinical follow-up, there was no evidence of further thromboembolic phenomenon.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [77, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': True, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
849,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7333338-4,Extracted,"The patient was a 72-year-old man with lung cancer taking oral PSL (5 mg/day) for radiation pneumonitis. His medical history included steroid diabetes and atrial fibrillation, and his drug history included sulfamethoxazole/trimethoprim, teneligliptin hydrobromide hydrate, rivaroxaban, digoxin, and febuxostat (all oral). On Day 0, he was admitted for effusion drainage to treat recurrent chylothorax following chemoradiation therapy for lung cancer. A drainage tube was inserted on the same day and yielded 1270 mL of fluid. Talc pleurodesis was performed on Day 2, and chylous pleural effusion was managed by maintaining him on a fat-restricted diet. By Day 14, only 5 mL of fluid was collected and the drainage tube was removed on Day 15.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 1 + 1 = 2.
The patient's CHA2DS2-VASc Score is 2."
850,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2803844-1,Extracted,"A 70-year-old Caucasian man with end stage renal failure (ESRF) secondary to hypertensive nephrosclerosis on PD for one year presented with a one-day history of lower abdominal pain in November 2007. There was no history of altered bowel habits or features of sepsis. There were no other co-morbidities or any history of alcohol abuse or use of recreational drugs. His dialysis adequacy was reported as a Kt/V of 2.2/week, blood pressure (BP) was well controlled at 135/75 mmHg and residual urine output was about 0.7 l/day.
On examination he looked clinically well. His abdomen was soft without any other physical signs of any note.
His medication included Allopurinol, Atorvastatin, Sodium Valproate, Aspirin, Alphacalcidol, Omeprazole, Irbesartan, laxatives and Aranesp. La was added as a first-line phosphate binder about 2 weeks prior to admission at 750 mg thrice daily, the recommended starting dose of this binder instead of Sevelamer which he was taking at 2.4 g thrice daily. The rest of his medication had remained unchanged for several years.
He had a normal full blood count (FBC), bilirubin 16 micromol/L (normal 3-17 μmol/L), alkaline phosphatase (ALP) 574 IU/L (normal 40-129 iu/L), alanine transaminase (ALT) 301 IU/L (normal 8-45 iu/L), gamma-glutamyl transferase (GGT) 185 IU/L (normal 8-50 iu/L). Ferritin was 236 microgram/L (normal 22-322 μg/L) and C-reactive protein (CRP) was 2 mg/L (normal 1-10 mg/L). Routine liver function tests four weeks previously were normal with bilirubin 9 mmol/L, ALP 90 iu/L, ALT 9 iu/L, GGT 7 iu/L. Peritoneal fluid appeared clear. Gram staining and peritoneal fluid cultures were negative. His clotting parameters were normal.
A liver virology screen including hepatitis A, B, C was negative. Epstein - Barr virus (EBV) and cytomegalovirus (CMV) serology were negative. An ultrasound scan of his liver was reported as normal liver parenchyma texture. There was no evidence of gall-bladder calculi. An abdominal X-ray revealed some evidence of faecal overload and the pain was felt related to constipation. Treatment with additional laxatives had good effect.
La was stopped and Sevelamer restarted. His LFTs started improving within a week and were back to normal within 4 weeks of stopping La and blood results from December 2007 showed a bilirubin of 1 mmol/L, ALP 87 iu/L, GGT 16 iu/L, ALT 21 iu/L. Table summarizes his blood test results.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [70, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 70 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
851,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3983423-1,Extracted,"A 52-year-old woman (height 160 cm, weight 47 kg) with a history of hyperthyroidism was scheduled for total radical thyroidectomy because of a gradual increase in the size of the thyroid nodules. The patient's previous medical history was unremarkable. Preoperative laboratory tests, including thyroid function test, and chest x-ray were unremarkable. An electrocardiogram (ECG) taken 1 month prior to surgery showed atrial fibrillation, and transthoracic echocardiography revealed normal left ventricular ejection fraction without regional wall motion abnormalities. She was not given premedication before surgery. In the operating room, non-invasive blood pressure monitoring, ECG (lead II) and a pulse oximetry monitoring were placed. Pre-anesthetic blood pressure was 120/70 mmHg, heart rate was 70 beats/min, and oxygen saturation was 95%. The ECG rhythm was same as preoperative state, suggesting atrial fibrillation is chronic. After preoxygenation, anesthesia was induced with propofol (3.5 µg/ml) and remifentanil (0.1 µg/kg/min) using target controlled infusion (TCI) pump (Orchestra® Base Primea, Fresenius Vial, Brezins, France) and she was intravenously given rocuronium 50 mg. After tracheal intubation, anesthesia was maintained using propofol and remifentanil TCI in an oxygen-air mixture (FiO2 = 0.5). After about 40 minutes, atrial fibrillation converted to the NSR (heart rate, 70 or so), which persisted. On postoperative day 4, the patient was discharged with NSR. One month later, the patient was still having NSR. The patient was lost to follow-up afterwards.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [52, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 52 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
852,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8364690-1,Extracted,"A 78-year-old man diagnosed with sick sinus syndrome received a permanent pacemaker (DDDR-MRI Medtronic [ventricular lead (MEDTRONIC cistofix 5076–58 cm); atrial lead (MEDTRONIC cistofix 5076–52 cm)]). The procedure itself and the post-procedure screening were both uneventful. The wound was clean, and there was no evidence of pneumothorax or hemothorax on the chest X radiography (CXR). The patient was discharged on the second day after the procedure.
However, the patient complained of a productive cough during a routine outpatient clinic follow-up visit conducted a week after the procedure. Laboratory findings showed a decrease in hemoglobin level from 10.9 to 8.9 mg/dL. A CXR revealed newly developed borderline cardiomegaly and bilateral blunting of the diaphragmatic angle. Pacemaker interrogation results showed normal threshold and impedance of both leads. An evaluation performed at fourteen days after the procedure showed evidence of orthopnea, dyspnea upon exertion, and a minor fever (38 °C). Physical examination showed engorgement of the jugular vein, basal crackles over the bilateral lower lung fields, and pitting edema in both legs. Laboratory data revealed worsening anemia (decrease in hemoglobin level from 8.9 to 7.7 mg/dL), high NT-proBNP (1610 pg/ml), and hyponatremia (Na: 115 meq/L, Osmo: 267), but no leukocytosis or worsening of renal function. An echocardiography revealed moderate pericardial effusion (maximal thickness 1.5 cm) without dynamic diastolic collapse of the right ventricle (RV).
The patient was treated for congestion, and administered a nitrate infusion. The patient also received empirical treatment with antibiotics since the low-grade fever was suggestive of an infection. The workup for pleural effusion showed evidence of transudate, and culture results for microorganisms tested were negative, including common aerobic and anaerobic bacterium as well as mycobacterium tuberculosis. Based on concerns about lead migration or protrusion-induced hemopericardium, the patient was subjected to chest computed tomography (CT), and no protrusion was detected (Fig. ). Additionally, the density of pericardial effusion was 20 Hounsfield unit (HU), which also did not support the possibility of hemopericardium. There was a limited improvement in the patient’s condition following several days of treatment, and echocardiography showed no worsening of pericardial effusion (thickness around 1.1 cm). Based on a suspicion of PCIS, the patient was prescribed prednisolone (30 mg/day initially), after which there was a dramatic improvement of his condition. The dosage of prednisolone was gradually tapered off to 20 mg/day after a week, 20 mg to 10 mg/day after two weeks, and the patient was maintained on 10 mg/day for 8 weeks. Although the CXR returned to baseline after completion of the steroid treatment (Fig. ), there was a recurrence of pleural effusion, leading to the resumption of low dose prednisolone treatment in addition to colchicine treatment. The patient recovered well after this treatment.
An 82-year-old male with a history of chronic atrial fibrillation (CHADS2: 3) was treated with rivaroxaban. The patient presented at the cardiology clinic with crescendo angina, and was reviewed with a coronary angiography examination, which showed significant focal stenosis at the orifice of the right coronary artery (RCA) (Fig. ). The patient was subjected to percutaneous coronary intervention (PCI), where a Xience Xpedition stent (3.5/15 mm) was deployed at the orifice. The procedure was uneventful, and the final angiogram showed good RCA flow, and no evidence of perforation, dissection, or extravasations (Fig. ).
However, two hours after the procedure, the patient developed cold sweats, tightness in the chest, and hemodynamic compromise along with bradycardia (50 bpm) and hypotension (systolic blood pressure: 70–80 mm Hg). Although a complete electrocardiography (ECG) showed no abnormalities, echocardiography showed new pericardial effusion (thickness 1.1–1.5 cm) with RV early diastolic collapse. This was immediately followed by a repeat coronary angiography, which showed good RCA flow without any extravasation, perforation or thrombosis. A chest CT scan with contrast showed no aortic dissection, and the density of pericardial effusion suggested hemopericardium (HU: 40) (Fig. ). In addition to vasopressors which were administered to stabilize the hemodynamics, the patient was also prescribed a 50 mg dose of hydrocortisone for PCIS. There was an improvement in the patient’s condition on the second day and all vasopressors was discontinued in 18 h. The patient was discharged to the outpatient department with a prescription for 20 mg prednisolone, and remained stable at his follow-up visits. However, 9 months later, after we tapered off prednisolone, the patient had increased discomfort of dyspnea on exertion and the echocardiography showed pericardial effusion recurred. We prescribed colchicine and low dose prednisolone for its control and patient’s discomfort improved.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [82, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 82 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
853,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-1451,Extracted,"A 50-year-old woman comes to the physician for a follow-up examination. Two weeks ago she was seen for adjustment of her antihypertensive regimen and prescribed lisinopril because of persistently high blood pressure readings. A complete blood count and renal function checked at her last visit were within the normal limits. On questioning, she has had fatigue and frequent headaches over the last month. She has hypertension, type 2 diabetes mellitus, polycystic ovarian disease, and hyperlipidemia. Her mother has hyperthyroidism and hypertension. Current medications include amlodipine and hydrochlorothiazide at maximum doses, lisinopril, metformin, glimepiride, and atorvastatin. She has never smoked and drinks 1–2 glasses of wine with dinner every night. She is 167 cm (5 ft 5 inches) and weighs 81.6 kg (180 lbs); BMI is 30 kg/m2. Her blood pressure is 170/110 mm Hg in both arms, heart rate is 90/min, and respirations are 12/min. Examination shows an obese patient and no other abnormalities.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [50, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': False, 'Diabetes history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 50 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
854,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7469751-1,Extracted,"A 79-year-old man of German descent was brought to the hospital by ambulance after he had developed sudden-onset abdominal pain and collapsed at a local shop. He was found pale and hypotensive on site (blood pressure of 65/40 mmHg) and bradycardic with a heart rate of 40 to 50 beats/minute (slow atrial fibrillation). The patient was rushed to the operating room for open exploratory laparotomy, which revealed a ruptured infrarenal abdominal aortic aneurysm. Open repair of the aneurysm was successfully performed. During the procedure, the patient had significant blood loss with the cell saver returning 5.5 L of blood. He received 6 units of packed cells, 4 units of fresh-frozen plasma, 6 units of cryoprecipitate, 1 pooled bag of platelets, and 4 L of crystalloids. Postoperatively, the patient was brought to the intensive care unit (ICU) intubated and requiring a high dose of vasopressors. Repeated bedside transthoracic echocardiography revealed a normally functioning heart with no significant ventricular or valvular abnormality.
The patient had a medical history of hypertension and benign prostatic hypertrophy. His preadmission regular medications were atorvastatin, amlodipine, and dutasteride-tamsulosin. The patient had a documented allergy to penicillin in the form of a rash.
The patient remained unstable postoperatively. He developed acute kidney injury and mild abdominal hypertension requiring sedation and paralysis. He did not tolerate enteral feeding and received full total parenteral nutrition. He was extubated on postoperative day 10; however, he was re-intubated a few hours later because of worsening respiratory failure. On the same day, the patient developed signs of sepsis including fever and leukocytosis, and he later became unstable and required vasopressors. Because the source of infection was unclear, meropenem and vancomycin were commenced, and Serratia marcescens was subsequently isolated in several consecutive blood cultures. The bacterium was sensitive to meropenem, ciprofloxacin, and co-trimoxazole and resistant to penicillins and cephalosporins. The same pathogen was also isolated in urine and sputum cultures. The same pathogen further grew in a wound swab culture taken 2 days later. The patient’s hemodynamic and renal function eventually improved; however, he remained ventilator-dependent and was encephalopathic. Therefore, he underwent a tracheostomy on postoperative day 14.
The patient thereafter developed hyperbilirubinemia as well as mildly deranged liver transaminase levels and biochemical markers of cholestasis. These abnormalities were attributed to bile duct obstruction despite lack of evidence of cholelithiasis or dilation of the biliary ducts on abdominal computed tomography () or ultrasound imaging. The bilirubin continued to rapidly increase to 200 µmol/L. Endoscopic retrograde cholangiopancreatography (ERCP) and subsequent transcutaneous hepatic cholangiography were performed. The imaging and ERCP () demonstrated widely patent right and left hepatic and common biliary ducts with smooth tapering toward the ampulla. The cystic duct was also patent. Nevertheless, a stent was inserted in the common bile duct during ERCP, and an 8.5-French external biliary drain was also inserted under fluoroscopic guidance by an interventional radiologist ().
The patient did not improve following cholangiography and insertion of the external biliary drain, and his bilirubin level continued to rise despite the biliary drain producing up to 600 mL of bile. The patient’s direct bilirubin level reached 300 µmol/L with a conjugated bilirubin level of 169 µmol/L by postoperative day 18. Repeated abdominal computed tomography showed no evidence of an intra-abdominal collection, bleeding, or other new pathology. A subsequent cholangiogram demonstrated that the stent and bile ducts remained widely patent. On postoperative day 18, the meropenem was changed to ciprofloxacin because of suspicion of VBDS (). This was followed by a decrease in the bilirubin level during the following few days. However, meropenem was restarted 3 days later because of clinical concern regarding worsening fever and sepsis, and this therapy was associated with an immediate increase in the serum bilirubin level. This association of a further increase in the bilirubin level after re-introduction of meropenem () was strongly suggestive of meropenem-induced VBDS. The antibiotic therapy was changed to ciprofloxacin and metronidazole, leading to a dramatic decrease in the bilirubin level, which eventually normalized. Other medications that the patient received are summarized in . Changes associated with other liver enzymes are presented in and .
The biliary drain was plugged and removed with time. The patient had a prolonged ICU stay, remaining ventilator-dependent for a long period. However, he gradually improved and was decannulated and discharged from the ICU after a 3-month stay without significant organ dysfunction. The patient was treated in the general ward and ultimately discharged from the hospital.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [79, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 79 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
855,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3271685-1,Extracted,"The patient was a 63-year-old white Turkish male living in Istanbul, Turkey who presented to the clinic with increasing chest pain on exertion, which had progressed in the last six months. He was 169 cm tall and weighed 74 kg. He had been a smoker for more than 45 years, and on an average smoked 1-1.5 packs per day. His family history was negative for cardiovascular disorders. He was not hypertensive (blood pressure of 128/76 mmHg on left arm and 132/77 mmHg on right arm at rest) and did not have diabetes mellitus (overnight fasting blood glucose of 98 mg/dL, normal range: < 100 mg/dL). Blood lipid profile indicated total cholesterol and low density lipoprotein levels of 193 mg/dL (normal range: < 200 mg/dL) and 124 mg/dL (normal range: < 130mg/dL), respectively. Cardiologic check up protocol was considered and the patient underwent stress electrocardiography which resulted positive. Myocardial thallium perfusion scintigraphy indicated ischemic zones at the inferior, inferolateral and inferoapical zones of the heart. According to the results, coronary angiography was performed and it revealed triple vessel disease with subtotal occlusion of left anterior descending artery (LAD) at the midportion, midportion 80% stenosis at the circumflex coronary artery (Cx) and 70% stenosis at the right coronary artery (RCA). Echocardiography was normal with preserved left ventricular functions (65% ejection fraction) and left ventricular hypertrophy. Following the consent of the patient, coronary artery bypass grafting (CABG) was planned.
During the preparatory phase for surgery, the patient complained of acute first toe pain. The first toe looked swollen, hyperemic and painful on palpation. Laboratory findings including complete blood count, blood lipid profile, renal and hepatic enzymes, clotting times, were normal except increased serum uric acid levels (10.74 mg/dl, Normal: 3.4-7 mg/dl) and slighly elevated C-reactive protein (6.72 mg/L, Normal: 0-5 mg/L). He was consulted with internal medicine department and diagnosed as Gout arthritis. He was prescribed allopurinol 300 mg twice daily and scheduled for surgery when the circulating uric acid levels returned to normal. Following four days of treatment, uric acid levels returned to normal limits, and he underwent triple vessel CABG (Left internal mammarian artery to LAD, aorta-first obtuse marginal artery and aorta-posterior descending branch of the right coronary artery bypasses with separate saphenous veins) with the use of cardiopulmonary bypass on arrested heart at 33-34°C. Cross clamp and cardiopulmonary bypasses were 35 minutes and 47 minutes, respectively. After the operation, the patient was transferred to the intensive care unit and extubated there on the post-operative 4th hour. He was taken to the ward the next day and discharged on the 6th day. Blood and blood product usage was 1 units of erythrocyte suspension and 2 units of fresh frozen plasma in total.
Immediately after the surgery, there was a slight increase in serum uric acid levels (7.4 mg/dl) detected in the blood drawn in the intensive care unit. As soon as the patient was extubated and oral intake was started, allopurinol was initiated at the same pre-operative dosage, and this returned the serum uric acid levels to normal. Post-operative course was otherwise uneventful. He has been followed symptom free for more than 9 months and is on allopurinol treatment in addition to anti-aggregant (aspirin, 100mg daily), anti-lipidemic (atorvastatin, 20mg daily) and low dose beta-blocker (metoprolol 25 mg daily) medications and a low calori diet.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [63, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Vascular disease history': True, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 63 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 0 + 1 = 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
856,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6562171-1,Extracted,"A Thai female, aged 48 at the start of the event, had a normal body mass index (23.4 kg/m2), good health, and no history of alcohol or smoking. The patient had no cardiovascular history, and the annual gynecological and internist checkups have been always insignificant. She had a normal to hypotensive blood pressure. She underwent total thyroidectomy in June 2007 for hyperthyroidism. Since then, she has been under continuous daily medication with thyroxin 100 μg, calcium carbonate 1.6 g, and alfacalcidol μg.
After surgery, the patient started halfyearly checkups by internists and endocrinologists. Her clinical condition and laboratory status, including hemogram, were always normal. The level of serum calcium was always within the lowest normal range or slightly below. She was consistently normo-//hypotensive. She had an academic full-time job, and her physical fitness was normal.
In April 2017, the results of routine checkup showed normal values of blood pressure, serum creatinine, serum calcium, hemoglobin concentration, and thyroidal hormones. The level of Vitamin D was also normal (). Overall, there were no subjective complaints.
Day 0: September 4, 2017. Auxiliary finding during a routine blood pressure control at the dentist: massive hypertension 165/120 mmHg.
Day 1: consultation with a cardiologist. Cardiac function, including ECG, was normal, and the blood pressure still high with 160/125 mmHg; the laboratory test results revealed several pathologic findings, such as calcium serum level 16.7 mg/dL, serum creatinine 2.48 mg/dL (glomerular filtration rate: 24 mL/min), and hemoglobin concentration (cHb) 10.2 g/dL. Plasma parathyroid hormone was found to be low; and the level of vitamin D was normal. Urine status was normal with no dysuria, and stool had no occult blood. There was no bleeding, such as abnormal menstrual flow, and the patient had a usual diet. The patient did not report to suffer from any subjective symptoms.
Day 2: consultation with nephrologist and endocrinologist. The results of the nephrological inspection, including sonography, were unremarkable. The suspected diagnosis was consistent with acute kidney injury (AKI) caused by calcium intoxication. The therapy was continued by an endocrinologist.
Upon checking her schedule the same day, the patient noticed that at least four weeks before the event she accidentally took 4 alfacalcidol tablets of 1.0 μg instead of 4×0.25 μg, resulting in a daily dose of 4.0 instead of 1.0 μg.
Sole therapeutic measure is the complete cessation of calcium and alfacalcidol medication; hyperhydration and forced diuresis, as stated elsewhere, were not applied. During this period, the patient was free of complaints, and there were no symptoms of hypocalcemia. On day 10, the patient re-started the calcium + alfacalcidol medication at a dose of 800 mg and 0.5 μg per day, respectively, which was half of the scheduled medication before the event. On that day blood pressure was already normal, level of creatinine decreasing but still elevated (1.65 mg/dL), and anemia persistent (cHb 10.1 g/dL).
On day 15, all parameters were normal, except cHb 10.3 g/dL.
Not until day 66 (November 9), cHb returned to normal 12.6 g/dL.
Ten months after the event, the patient was free of complaints, and the lab results were completely normal. However, the patient was still taking the calcium 800 mg and alfacalcidol 0.5 μg medication.
The work was performed at the Boromarajonani College of Nursing, Nonthaburi, Thailand; Patient’s consent was obtained.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [48, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 48 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
857,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5385863-1,Extracted,"A 78-year-old male with hemochromatosis complicated by locally advanced HCC was admitted to our hospital from a skilled nursing facility with new-onset bilateral lower extremity edema. His comorbidities included atrial fibrillation and hypertension, but he had never suffered from significant edema or symptoms of congestive heart failure previously. He was at the skilled nursing facility for rehabilitation after a prolonged hospitalization during which he suffered from postembolization syndrome after his fourth round of transarterial chemoembolization (TACE).
On questioning, he complained primarily of discomfort in his legs related to edema but also endorsed fatigue and progressive dyspnea on exertion. On presentation, his vital signs were within the normal limits. Physical exam was notable for moderate jugular venous distension and an expectedly irregularly irregular cardiac rhythm without audible murmurs. His lungs were clear to auscultation, and his extremities had 4+ pitting edema to the sacrum. Laboratory evaluation revealed a mildly elevated BNP of 236 pg/mL, a slightly low serum sodium of 133 mmol/L, and normal kidney function. Small bilateral effusions were seen on chest X-ray.
The patient underwent transthoracic echocardiography, which revealed a 6.4 × 4.3 cm mass occupying nearly the entire right atrium, and extending to the inferior vena cava (IVC) (Fig. ). Angiography was then pursued and showed subtotal occlusion of the IVC by a mass extending from the hepatic veins into the right atrium (Fig. ). Biopsy of the cardiac mass confirmed poorly differentiated HCC. Unfortunately, the patient was not a candidate for surgical resection or chemotherapy due to his comorbidities. Palliative radiation was considered, but the patient's symptoms progressed to the point of dyspnea at rest and anasarca before it could be initiated. Given his rapid decompensation, the patient elected to pursue hospice care. He was transitioned to a local hospice care facility and died 12 days later.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [78, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 78 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
858,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3439305-2,Extracted,"The patient was a 71 year-old female referred for inpatient rehabilitation following a right total hip replacement (THR). Post-operatively she developed a deep vein thrombosis in the left posterior tibial vein for which she received anti-coagulation therapy. Her medical history was significant for mild hypertension, atrial fibrillation, hysterectomy following uterine cancer, and right THR due to osteoarthritis. Once she was cleared for rehabilitation, she presented with a lack of active right ankle dorsiflexion and given a standard plastic ankle foot orthosis (AFO) to prevent foot drag during ambulation. She began physical rehabilitation to increase mobility and strength in both lower extremities and achieve independence in activities of daily living, while maintaining total hip replacement precautions.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [71, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Thromboembolism history': True, 'Vascular disease history': False, 'Diabetes history': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 71 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
859,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-8396,Extracted,"A 61-year-old white man presents to the emergency department because of progressive fatigue and shortness of breath on exertion and while lying down. He has had type 2 diabetes mellitus for 25 years and hypertension for 15 years. He is taking metformin and captopril for his diabetes and hypertension. He has smoked 10 cigarettes per day for the past 12 years and drinks alcohol occasionally. His temperature is 36.7°C (98.0°F) and blood pressure is 130/60 mm Hg. On physical examination, his arterial pulse shows a rapid rise and a quick collapse. An early diastolic murmur is audible over the left upper sternal border. Echocardiography shows severe chronic aortic regurgitation with a left ventricular ejection fraction of 55%–60% and mild left ventricular hypertrophy.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [61, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Vascular disease history': True, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 61 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
860,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3283759-1,Extracted,"A 74-year-old woman was admitted to the hospital for diarrhea and epigastric pain. She had a history of hypertension, diabetes mellitus, chronic kidney disease, dilated cardiomyopathy, and permanent AF for 5 years (). Echocardiography performed 3 months before admission revealed severe global left ventricular hypokinesia (ejection fraction=19% by Simpson's method) and an enlarged left atrium (left atrial volume index=40 mL/m2). Her medications included digoxin (0.125 mg daily), warfarin (2 mg daily), ramipril (10 mg daily), furosemide (40 mg daily), spinolactone (25 mg daily), and carvedilol (25 mg daily).
On examination, her heart rate was 41 bpm, and blood pressure was 110/70 mm Hg. Heart sounds were regular, and there were no murmurs or thrills. An electrocardiogram (ECG) revealed junctional rhythm at a rate of 35 bpm and a QRS duration of 136 msec (). Admission laboratory results showed severe hyperkalemia (serum potassium 8.3 mEq/L), high blood urea nitrogen (62.4 mg/dL), creatinine of 4.0 mg/dL, glucose of 248 mg/dL, and low sodium (131 mM) and hemoglobin (7.2 g/dL) levels. Arterial blood gas analysis on room air showed a pH of 7.400, pCO2 of 41.6 mm Hg, pO2 of 102.8 mm Hg, and HCO3- of 26.0 mmol/L.
The patient was immediately treated with intravenous calcium chloride, followed by intravenous glucose/insulin and a sodium bicarbonate infusion. On hospital day 2, the serum potassium level was 5.3 mEq/L and the ECG showed sinus bradycardia at a rate of 53 bpm with an 80 ms QRS duration (). On hospital day 3, the ECG revealed a normal sinus rhythm at a rate of 67 bpm, and the serum potassium level was within normal limits (4.3 mEq/L). The patient was discharged 6 days after admission, and the ECG at discharge showed normal sinus rhythm at a rate of 65 bpm with occasional premature ventricular complexes. At the 10 day and 1 month follow-ups, the ECG at an outpatient clinic had returned to AF and serum potassium levels were within the normal range.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': True, 'Hypertension history': True, 'age': [74, 'years'], 'Stroke': True, 'Diabetes history': True, 'sex': 'Female'}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 74 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 6. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 6 + 1 = 7.
The patient's CHA2DS2-VASc Score is 7."
861,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3383153-1,Extracted,"A 69-year-old woman was admitted to the Department of Family Medicine at our hospital with sudden onset of right calf muscle pain and paresthesia that started 6 days ago. At the moment, she had one episode of dizziness with black out vision of 2-3 seconds. Additionally, she had complained of pain at the low back and bilateral knee.
Her medical history showed significant diabetes with retinopathy of 35 years and hypertension of 15 years. But she had no history of peripheral vascular disease, intermittent claudication, valvular heart disease, AF, hypercoagulable disorder, or smoking. Family history did not yield any remarkable findings.
On physical examination, the patient's blood pressure was 130/90 mm Hg; pulse, 76 beats per minute; temperature, 36.8℃; and respiratory rate, 20 breaths per minute. Her weight was 57.2 kg, and her body mass index was 25.4 kg/m2. She had normal heart sound with no murmurs. Her right feet had weak pulsation on popliteal artery and dorsalis pedis, cold mottled skin and smaller circumference of calf muscle than left one.
A normal complete blood cell was obtained during further examination. The levels of lipid profile and blood chemical panel except blood sugar were also in reference scale. Thyroid function was normal and HbA1c was 7.3%. The most of profiles of coagulation test were in reference range except that D-dimer level showed small elevation and that antithrombin III and protein-S activity in serum was low with 0.55 µg/mL, 32.7%, and 54%, respectively. The lupus anticoagulant and anticardiolipin antibody (IgM and IgG) were negative. The chest X-ray revealed mild cardiomegaly without active lung lesions. The sinus bradycardia was documented initially and the heart rate was 56 beats per minutes. The finding on echocardiography was normal that left atrial diameter was 32 mm, left ventricular systolic diameter 26 mm, left ventricular diastolic diameter 47 mm, left ventricular ejection fraction 69%, normal valvular morphology and function.
At the department of family medicine, the ankle and brachial systolic pressure index (ABI) doppler test was done and ABI of the right ankle was lower (0.56) than ABI of the left one (1.1). In order to find vascular lesions of the affected limb, we performed the contrast-enhanced computer tomographic angiography, which showed acute embolic occlusion of right popliteal artery (). We decided to refer to cardiovascular division of the internal medicine department for removing her thrombus. And then, femoral arteriogram confirmed the total occlusion of popliteal artery on the right side (). The thrombi were successfully removed by thombosuction at the same time. After procedure, blood flow of the right popliteal artery had been normally restored (). Anticoagulation was started immediately after eliminating emboli and transitioned to oral vitamin K antagonist. ABI follow up showed normal result (right, 1.04; left, 1.02) at 4th days after procedure. The myocardial thallium spect was performed to reveal the cause of acute embolic episode, and the result was within a normal range. When palpitating, she was tested with several times of the Holter monitorings and EKG. The PAF was recorded on the sixth holter monitoring and the EKG was performed on seven o'clock in the morning () and the rhythm was restored to normal sinus rhythm on seven o'clock in the evening (), when she visited an emergency room with palpitation. The cause of ischemic foot of the patient proved an embolic episode by PAF. The patient has been treated with oral vitamin K antagonist to prevent embolic episodes from recurring.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [69, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': True, 'Vascular disease history': False, 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 69 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
862,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4007789-1,Extracted,"A 90-year-old man presented for evaluation of a one-month history of fatigue and progressive abdominal and lower extremity edema. His history was notable for ischemic cardiomyopathy with a left ventricular ejection fraction (LVEF) of 15% with a dual-chamber pacemaker for cardiac resynchronization; paroxysmal atrial fibrillation and frequent ventricular ectopy requiring initiation of amiodarone 6 months prior (200 mcg/day); stage IV chronic kidney disease, not on dialysis. The patient reported full compliance with his medical heart failure regimen and denied any dietary indiscretion, alcohol intake, or anginal symptoms. His vital signs were unremarkable but his weight had increased by 4.6 kg. Examination revealed a regular heart rate of 60 beats/minute, jugular venous distension, a hepatojugular reflex, inspiratory crackles in the lung bases, and significant lower extremity pitting edema to mid-thigh level. The skin was notably dry. Thyroid exam was unremarkable. A chest X-ray revealed pulmonary edema and cardiomegaly (). Electrocardiography revealed a paced rhythm at 62 beats/minute and cardiac biomarkers revealed no evidence of myocardial infarction. Laboratory studies included an N-terminal pro-B-type natriuretic peptide of 10,644 pg/mL (normal < 180) and serum creatinine of 3.7 mg/dL (GFR 16 mL/min), significantly worse than his baseline creatinine of 2.3 mg/dL. A transthoracic echocardiogram revealed an LVEF of 12% with global hypokinesis, a right ventricular (RV) systolic pressure of 44 mmHg, and a moderate-sized concentric pericardial effusion ().
For treatment of decompensated heart failure, he was cautiously diuresed with furosemide. With this his pulmonary, abdominal, and peripheral edema improved, and his serum creatinine trended down to 3.2 mg/dL. However, he remained severely fatigued. Given this and the new pericardial effusion, serum thyroid studies were obtained, revealing a dramatically elevated thyroid-stimulating hormone of 187 mIU/L (normal 0.3 to 5.0), free thyroxine of 0.4 ng/dL (normal 0.8 to 1.8), and negative antithyroperoxidase antibodies. By contrast, his thyroid-stimulating hormone level was normal at 2.0 mIU/L immediately prior to initiation of amiodarone several months prior. He was diagnosed with amiodarone-induced hypothyroidism and started on low-dose oral levothyroxine (25 mcg/day), given his age, systolic heart failure, and history of ventricular dysrhythmias. His amiodarone was continued for the purpose of rhythm control. His fatigue and fluid status improved gradually over the next 4 days, and he was dismissed from the hospital.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': True, 'Vascular disease history': True, 'age': [90, 'years'], 'Stroke': False, 'Transient Ischemic Attacks History': False, 'sex': 'Male'}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 90 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
863,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3273953-1,Extracted,"A 76-year old obese woman presented to the intensive care unit for acute NSTEMI. Her medical history included poorly-controlled insulin-dependent diabetes and systemic hypertension. Two hours before the admission, pain in the substernal area developed suddenly. The first electrocardiogram obtained showed normal sinus rhythm with a rate of 85 beats per minute and ST-segment depression of 3 mm in the inferior leads. Serum levels of hematocrit, creatinine and electrolytes were all within the normal range. The troponin I level was 6.4 ng per milliliter (normal range < 0.05 ng per milliliter). Nitroglycerin, morphine, loop diuretics, unfractioned heparin and tirofiban IV were administered and the patient became asymptomatic shortly thereafter. Oral therapy with clopidogrel 75 mg, simvastatin 20 mg and metoprolol 50 mg bid was added.
Trans-thoracic echocardiography showed a normal left ventricular ejection fraction of 55% in the absence of segmental wall motion abnormalities, mild hypertrophy of the left ventricle, mild left atrial enlargement (transverse diameter 4.4 cm) and moderate mitral regurgitation.
Continuous ECG monitoring showed multiple episodes of sustained, self-terminating paroxysmal AF () symptomatic for dizziness, hypotension and palpitations. All AF episodes were triggered by short-coupled (280 msec coupling interval) ventricular monomorphic couplets with 1:1 ventriculo-atrial (VA) retrograde conduction. The ventricular ectopic beats showed left bundle-branch block (LBBB) morphology with inferior axis (, arrows) and retro-conducted P waves were detectable in aVL and inferior leads (, arrows). Intravenous metoprolol (5 mg) and amiodarone (900 mg) were administered and in one hour stable sinus rhythm was achieved.
The day after a coronary angiography was performed, which showed severe right coronary ostial stenosis. Balloon angioplasty of the lesion was performed and a bare-metal stent was successfully deployed.
The patient was discharged home four days later in therapy with acetyl-salicylic acid 100 mg, clopidogrel 75 mg, furosemide 25 mg, metoprolol 50 mg bid, enalapril 20 mg, atorvastatin 80 mg and insulin. A pre-discharge echocardiography was unchanged. At 1 month follow-up visit she was in stable NYHA functional class II, asymptomatic for angina and palpitations and in sinus rhythm.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [76, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
864,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2916002-1,Extracted,"A 94-year-old female was admitted to our hospital after she fell and sustained an anterior pelvic ring fracture (Figure ). She was hospitalized for mobilization. Over the past 18 years she had been treated with anticoagulation therapy with marcumar due to atrial fibrillation, 13 years ago subsequently a cardiac pacemaker was implanted. In the first days in hospital mobilisation was painful but with a walker possible. In the early morning of the fourth day after admission she developed severe pain in the thigh. Clinically the thigh was swollen but the foot pulses were well palpable. Because of persisting severe pain and the suspicion of a deep vein thrombosis a CT-scan of the thigh and the pelvis was performed. In the further course the patient complained of a partial loss of sensation of her left leg and weakness of her shank muscles, following the innervation area of the ishiadic nerve. The CT-scan showed an extensive haematoma expanding abroad the adductor muscles in the medial compartment and in the posterior compartment (Figure &). The compartment of the M. rectus femoris was not involved. Immediate surgery was performed with a complete decompression of the compartments of the thigh as well as the draining of the haematoma and wound covering with epigard (Othomed, Vienna, Austria) (Figure &). On the second postoperative day a revision for draining of the refilled haematoma was performed. Finally five days after the initial treatment during the second revision complete skin-closure was performed strainless. In the postoperative course the patient recovered quickly and the sensomotor deficits resolved completely however she developed partial skin necrosis along the approach in particular in the popliteal fossa. Subsequently these necrosis were resected and the skin was closed again strainless. Only in the popliteal foassa a skin graft from the ipsilateral posterior thigh was needed. The skin graft healed. In the further course of the hospital stay the patient again recovered quickly and was mobilized under physiotherapy control. Fifty-seven days after the initial trauma the patient was dismissed and transferred to rehabilitation center for further mobilization. At the latest follow up one year post operatively the patient is mobile with full weight-bearing and regular soft tissue condition.
A full-blown compartment syndrome in the thigh is a rare clinical occurrence. This is mainly due to the fact that the three muscle compartments (Figure ) in the thigh can compensate much higher volumes than the four compartments below the knee []. Not only the fascia seems to be more dilative also the thigh compartments are partly open to the pelvis explaining the higher compensation rate for increasing intracompartmental volume [,]. The small number of occurring cases makes scientific randomized prospective studies with bigger numbers difficult. However the spectrum of reported cases with different etiologies is wide: Deep venous thrombosis [], vein catheriztion [], vessel aneurysm [] the complete spectrum of femoral fractures [], total hip and knee replacement surgery, intramedullary nailing [,], gunshot and stab wounds [], sport trauma [,,-], traffic accidents [,,], external compression of the thigh [,], crush injuries [,], as well as severe blunt tissue trauma []. Mithoefer [] declares that in 46% of the cases a traffic accident is the cause for a thigh compartment syndrome. Holbein [] proclaims that regarding the literature the femur fracture is the most common cause for a thigh compartment syndrome. Kladny [] numbers this risk with 1-2%. An open fracture or wound will not safely secure the leg from a compartment syndrome [,]. Multiple trauma patients seem to have a higher risk to develope a compartment syndrome because of the concurrence of different clinical conditions. High-energy blunt trauma, external compression, systemic hypotension, vascular injury, and coagulopathy in those patients may assimilate and thus lead to a compartment syndrome []. According to Schwartz a patient with an isolated injury to the thigh without any of the above mentioned risk factors has therefore a lower risk for the development of a compartment syndrome [].
In cases were the patient is unconscious at the intensive care unit a compartment syndrome can stay unrecognized possibly causing devastating outcome [], as the patient can not express main symptoms like disproportional pain, paraesthesia or even paralysis. Only the palpatoric tension of the affected muscle is detectable. These cases must be taken into special account and the measurement of the compartment pressure has an important role in those cases for the diagnostic. Regarding the common literature addressing this topic the measurement of the intracompartmental pressure is the gold standard for the diagnosis []. However the reliability of these measurements is questionable, as especially in multiple traumatized patients the systolic blood pressure supported by catecholamines can pretend a stable hemodynamic situation neglecting a possibly severe disregulated microcirculation []. In addition there is no consensus in the literature about a specific intracompartmental point pressure or a rule regarding the diastolic blood pressure or the arterial middle pressure, clearly indicating the need of fasciotomy []. In our case we initially suspected a deep vein thrombosis and not a compartment syndrome. Therefore we decided for a CT scan. After the diagnosis surgery was performed immediatly and no further diagnostic was performed. Usually suspecting a compartment syndrome calculating the local perfusion pressure by measuring the the mean arterial pressure and the intramascular pressure is the gold standard.
Because of the wide variety of conditions in patients with huge differences in the physiological strength (young men in a car accident versus a 94-year-old women with a stable pelvic fracture) and the very limited numbers of cases with a compartment syndrome of the thigh explains why it is impossible to identify strict criteria for the need of a fascitomy. However the literature agrees that the damage caused by fasciotomy in a patient in which the tissue would not have become necrotic is far outweighed by the morbidity possibly associated by a full-blown compartment syndrome []. In a borderline compartment syndrome not only the intracompartmental pressure but close meshed checks of the sensormotor function of the affected leg as well as the typical clinical symptoms are essential for the indication of a fasciotomy.
In our patient the compartment syndrome developed with several days delay. This we hypothezised might be explained by the patient's clinical course. During the first days the patient was immobilized with bed rest. During remobilisation the vessels injured by the initial trauma started to bleed again, thereby creating a haematoma which followed gravity into the thigh. In our case the neurological symptoms resolved quickly after the decompression and no muscle necrosis were detected. However in this case the morbidity was caused by the high age of the patient resulting in multiple complications through a prolonged wound healing. Schwartz has already emphasized that infection is a further problem in the postoperative course in patients with a compartment syndrome. He reports local infection rate of 66% []. Although we were not able to detect any significant tissue necrosis in our patient we suppose that prolonged ischemia may have further compromised the microvascular perfusion in this old patient with already existing vascular sclerosis thus drastically increasing the risk of wound infection.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [94, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 94 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 6. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
865,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7554274-1,Extracted,"We present a 45 years old woman with known congenital heart defect, who was transferred to our hospital with right atrial tumour suspicion and an unrecognized BCS.
A surgical closure of an atrial septal defect (ASD) was performed when she was 8 years old. After childbirth in 2008, she was treated with heparin for pulmonary embolism, followed by a short period of warfarin therapy (a few months). An echocardiographic examination (ECHO) was performed in 2009, after the patient complained of a certain effort intolerance, and a discrete leg edema. A recanalization of ASD was excluded, and the finding was described as within normal limits.
During the preceding 6 months, she had some serious clinical symptoms: a more severe dyspnea, cough, effort intolerance, ascites and leg swelling. She was admitted to a county hospital. The differential diagnosis was focused on heart failure, lung disease, and occult neoplasm. ECHO revealed a tumorous process in the right atrium 2.7 × 1.7 cm attached to the atrial septum (Fig. ). She was transferred to our institution for further investigation and treatment.
At admission, the patient’s clinical examination revealed a markedly distended abdomen with prominent superficial veins, bilateral pedal edema and hepato-splenomegaly. There was no jaundice. Clinical presentation was highly suspicious for BCS. ECHO (transthoracic and trans-esophageal), followed by MRI, revealed a membrane, dividing IVC inflow and right atrium, without communication (Fig. ).
Percutaneous intervention was indicated. The patient was primed with 300 mg of Clopidogrel and 325 mg of Aspirin. Venous access was obtained via 6 French sheaths in the right femoral vein. Unfractionated heparin (5.000 units) was given. Venography was performed via pigtail catheter. It revealed a short, completely occluded segment (thick web) between the right atrium (RA) and IVC. After an unsuccessful attempt to puncture the membrane with a distal tip of an Amplatz stiff wire (J curve, 0,035 Cook Medical, Bloomington, IN, USA), the thick web was punctured with a curved needle through a transseptal introducer sheath (Mullins Sheath 8 Fr and Brokenborough needle 18 gauge, Medtronic, Minneapolis, MN, USA), in the same manner as we would puncture the interatrial septum. After confirming the position of the needle by contrast injection, the sheath was advanced over the needle into the RA, beyond the occlusion. Then a 0.032 J-tip wire was negotiated across the web and was parked in the right subclavian vein. The membrane was first dilated with an available 6,0/20 mm non compliant coronary balloon (NC Emerge, Boston Scientific, Boston MA, USA), with 16 atm, followed by dilatation with a bigger non-complined peripheral balloon16/20 mm with 20 atm (Atlas Gold, Bard Vascular, Tempe AZ USA), with poor result. Sequentially, several balloon dilatations with 30/40 mm semi-compliant balloon (Z-med II, Numed-Braun, Bethlehem, PA, USA), with 4 atm pressure was performed, resulting in immediate recoil. Satisfactory result was achieved after the inflated big balloon was sharply withdrawn through the membrane (a “Rashkind-like” manoeuvre). Stenting was not possible, due to the membrane position (Fig. ).
There was no procedural or late complication. The patient recovered very well, and a permanent anticoagulation therapy with warfarin was introduced. The first follow-up was done three months afterwards. Clinically, the patient felt well, there was no evidence of ascites or a peripheral edema. A reduction of collaterals, and only a discrete hepatomegaly was found. An invasive venography was performed, with a planned repeated intervention, if necessary. The result was considered good, with even improved communication throughout the membrane, in comparison with the post-intervention result, so the re-intervention was not performed (Fig. ). A permanent anticoagulation therapy was recommended to the patient and at the 12-month follow up, she was without any problems.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [45, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 45 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
866,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6675968-1,Extracted,"A 61-year-old lady presented to us with a four days history of left-sided neck swelling associated with odynophagia. She has pre-existing atrial fibrillation since ten years back and she is on non-Vitamin K antagonist oral anticoagulant (NOAC). Before this presentation, she had undergone unsuccessful transoesophageal echocardiography (TOE) at a heart centre to investigate her mitral valve prolapse. The TOE was abandoned as they had difficulty inserting the TOE probe. At the heart centre, she was monitored for a day post procedure and was discharged well.
Upon further history, she denies having upper gastrointestinal symptoms prior to this. On clinical examination, she appears well and afebrile. There was a left anterior neck swelling measuring 4 cm x 4 cm which was tender on palpation. There were no skin changes and no cervical lymph nodes palpable. All other systemic examinations were unremarkable. Initial blood investigation showed mild leukocytosis (11.4 × 109/L), but the rest of her blood investigations were normal. We suspected a delayed iatrogenic upper oesophageal perforation secondary to her recent TOE.
We proceeded with an upper endoscopic examination, but unfortunately, we were unable to visualize any mucosal abnormalities over the oesophagus (). She did, however, have an associated sliding hiatus hernia. A contrasted computed tomography (CECT) of the neck was performed. It showed a prevertebral soft tissue swelling with a maximal thickness measuring 2.2 cm and the presence of air pockets at the level of C7 (). A semilunar hypodense collection with rim-esnhancing wall is seen from the left submandibular space superiorly to the suprasternal region inferiorly ( ). Subsequently, we performed a targeted upper gastrointestinal study with gastrograffin with a complementary plain CT of the neck. Contrast leakage was seen within the previously hypodense collection at the left paravertebral region, and the contrast media is seen tracking into the left submandibular space superiorly and inferiorly, until the level of T1 ( ). A diagnosis of oesophageal perforation is thus confirmed, although the defect is likely small, as no contrast leakage was seen during the dynamic study.
As the patient was clinically well, and the upper endoscopy examination did not show any apparent mucosal defect, we elect to manage her conservatively. She was kept nil-by-mouth for a week, and total parenteral nutrition was initiated. She was also empirically started on broad-spectrum intravenous antibiotics. Her clinical condition improved with resolution of the neck swelling as well as the odynophagia. She was started on oral feeding after a week and subsequently discharged well. She was seen in our clinic four weeks after discharge, and she remains well. A repeated upper gastrointestinal study performed six months later showed smooth contrast flow though the oesophagus with no contrast extravasation.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [61, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 61 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
867,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6349972-2,Extracted,"An 83-year-old woman with a history of autoimmune thrombocytopenia, arterial hypertension and type II diabetes mellitus was admitted to the hospital with extensive hematoma of the left hemithorax following trauma. Blood tests revealed anemia (Hbg: 10 g/dL) and thrombocytopenia (PLT: 24 × 10³ µL). A computed tomographic (CT) scan of the thorax proved contrast blush in the region of left pectoralis major muscle; hence, an urgent angiography and embolization were requested.
Because of thrombocytopenia, the patient had a high risk of bleeding and vascular complications related to the FA, so we decided to perform a TRA, but the Barbeau test showed a type D waveform. DRA diameter (2 mm) was suitable for puncture at US examination. The patient gave her informed consent before the interventional procedures.
The DRA access was obtained with the same technique already described. A diagnostic angiography of left axillary and subclavian arteries was performed using a 100-cm 4-French Berenstein catheter. It showed contrast extravasation of left lateral thoracic artery (LLTA). A microcatheter was introduced for a superselective angiography of the LLTA and we used Spongostan to embolize the LLTA. A final diagnostic angiogram demonstrated the success of the procedure. An occlusive pressure of the DRA was obtained in the same way as described. The evaluation of the RA patency, using a color Doppler examination, was performed in the same way as in case 1, which gave similar results.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': True, 'age': [83, 'years'], 'Diabetes history': True, 'sex': 'Female'}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 83 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 6. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 6 + 1 = 7.
The patient's CHA2DS2-VASc Score is 7."
868,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8641495-1,Extracted,"An 82-year-old woman with chronic coronary syndrome was admitted for elective percutaneous coronary intervention (PCI) of a significant stenosis in the left anterior descending (LAD) artery with severe calcifications, without significant lesions in other coronary vessels (). The patient presented with anginal pain at minimal exertion (Canadian Cardiovascular Society class 3). Medical history included an unsuccessful attempt of PCI of LAD (2019) and permanent atrial fibrillation with percutaneous left atrial appendage closure due to recurrent bleeding episodes. Considering one-vessel disease with low lesion complexity (Syntax score 7) and intermediate risk of perioperative mortality in the EuroScore II (6.67%), despite the low risk in the STS score (2.73%), the Heart Team opted for percutaneous revascularization. Since the previous PCI attempt was unsuccessful due to severe calcifications, the use of rotational atherectomy was advocated [, ].
The procedure was performed through the right femoral access, with the use of 7 French Judkins left guiding 4.5 catheters and BMW guidewire. The rotational atherectomy was conducted with the 1.5 mm burr at a pace of 160,000 rounds per minute. Subsequently, multiple inflations with non-compliant balloons were performed (2.75 × 15 mm, 3.0 × 15 mm, 3.5 × 15 mm, 3.75 × 21 mm) at a pressure of 12–20 atmospheres (atm). The final balloon inflation was complicated by the LAD perforation, indicated by contrast extravasation in the middle segment (Ellis type III; ). This was immediately managed with prolonged balloon inflation (3.0 × 15 mm, 12 atm) with subsequent insertion of another guiding catheter to minimize the time between deflation of a balloon inserted via the first catheter and implantation of a stent-graft via the second catheter (double-guiding catheter technique; ). A stent-graft (PK Papyrus, Biotronik, Germany; 3.0 × 20 mm at 16 atm) was implanted and post-dilated with 3.0 × 25 mm (16 atm) and 3.5 × 12 mm (16 atm) balloons (). Bedside echocardiography showed features of cardiac tamponade, thus an emergency pericardial drainage was executed () with absorption of 700 ml of blood. In addition, dobutamine (10 μg/kg/min) infusion and intravenous fluid supplementation was started, 50 mg protamine sulfate was administered intravenously for heparin effect reversal and one unit of red blood cells was transfused due to hemoglobin decrease from 9.5 g/dl to 7.0 g/dl on blood gas analysis. Following stent-graft implantation and pericardial drainage, the control angiography showed minimal extravasation in the middle segment of LAD (). The patient was hemodynamically stable, with systemic blood pressure of 120/60 mm Hg. The follow-up echocardiography showed no signs of active pericardial effusion and left ventricle ejection fraction of 40%. Laboratory tests revealed a stable hemoglobin value. The patient received dual antiplatelet therapy including acetylsalicylic acid (75 mg once daily) and clopidogrel (75 mg once daily) for 12 months. She was discharged home on postprocedural day 15.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [82, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 82 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
869,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5615275-1,Extracted,"In early March 2017, the Nephrology service was consulted to see an overweight 83-year-old female patient admitted to the Hospitalist service a week earlier with dyspnea and volume overload from symptomatic heart failure complicated by rapid ventricular response atrial fibrillation, against a background history of hypertension and stage 3 CKD. Other pertinent past medical history include hypertension, sarcoidosis, COPD, atrial fibrillation and type 2 diabetes mellitus. A month earlier, she was discharged after 5 days with symptomatic hypotension and dizziness associated acute kidney injury with peak creatinine of 2.21 mg/dL, and then associated with UTI that was treated with Bactrim. At the time she was also on Lisinopril, which was then discontinued. Subsequently following conservative management in the hospital, kidney function as measured by the serum creatinine had returned to near baseline of 0.96 mg/dL at discharge.
This time in March 2017, she had become increasingly short of breath and hypotensive as well and serum creatinine had risen back up again to as high as 1.79 mg/dL at the time of the Nephrology consultation. Temperature was 36.9 °C, heart rate 67 per/min, respiratory rate 18 per/min, oxygen saturation 90% on room air, and blood pressure was 106/60. She weighed up to 75.4 kg, height was 163 cm, with a BMI of 28.4 kg/m2. She was dyspneic, JVD was elevated, with 2+ bilateral extremity edema and reduced breath sounds in both lung bases bilaterally, with bibasilar inspiratory rales evident posteriorly. Admission chest radiograph showed cardiomegaly, new bilateral pleural effusions, pulmonary vascular congestion and hypoventilation. Echocardiogram revealed normal left ventricular systolic function with ejection fraction of 64%, mild mitral valve regurgitation, bi-atrial enlargement, normal right ventricular function with right ventricular systolic pressure of 29 mmHg. At the time of this consultation, serum albumin was 2.8 g/dL, sodium was 134 mmol/L, potassium 3.6 mmol/L, chloride 94 mmol/L, bicarbonate 24 mmol/L, calcium 8.9 g/dL, hematocrit 24.9%, WBC, platelets, TSH, Free T4, AST, ALT and total bilirubin were all normal. Pro Pro B Naturetic Peptide level that was elevated at 581 pg/mL on 2 February 2017 had rapidly escalated to 4907 pg/mL by 23 February 2017, three weeks later, just prior to this admission (Pro Pro B Naturetic Peptide reference range ≤ 450 pg/mL).
Earlier in the admission, she was started on intravenous amiodarone for rate control of atrial fibrillation. Furthermore, oral Diltiazem, 120 mg three times a day, was subsequently discontinued when she became hypotensive. She had been started on continuous intravenous Furosemide infusion at 10 mg/h but the previous 24-h urine output was only 1500 cc.
We doubled the dose of intravenous continuous infusion of Furosemide to 20 mg/h and added intravenous Chlorothiazide 500 mg every 12 h. The chlorothiazide was discontinued after one dose when the patient raised concerns for a history of drug-induced pancreatitis. We then increased the dose of intravenous Furosemide to 25 mg/h, added daily intravenous Albumin 25 gm infusion to run concurrently with the continuous Furosemide infusion because of severe hypoalbuminemia. The edematous legs and feet were elevated and wrapped with ACE wraps. Overnight, urine output had more than doubled to 3450 cc (). Subsequently, twenty-four urine output increased to over 3–4 L (). After 5 days of the Furosemide infusion, she was switched to oral Bumetanide 2 mg twice daily. She continued to make urine in excess of 2.5 L an day and was discharged after another two days, much improved with edema, dyspnea and orthopnea resolved, together with significant weight loss (). She had achieved a weight loss of 12 kg during the last nine days of the admission. Her serum creatinine trajectory also improved during the second half of this admission and serum creatinine at discharge was 1.29 mg/dL ( and ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [83, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 83 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
870,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7649516-1,Extracted,"An 88-year-old man with symptomatic severe aortic stenosis, chronic obstructive pulmonary disease, and extensive peripheral artery disease was referred to our cardiovascular department for elective valvular treatment. He reported a progressive worsening of his exercise tolerance (effort dyspnoea) in the last 6 months leading to a significant limitation in daily life activity in the last month (NYHA Class III).
Physical examination at admission revealed mild systolic hypertension (140/85 mmHg), rough systolic murmur radiating to both the carotid arteries, with no signs of peripheral or pulmonary oedema. Electrocardiogram showed sinus rhythm (60 b.p.m.) with left axis deviation and moderate ST-segment depression in lateral leads. Medical therapy at the time of admission included furosemide 50 mg/die, cordarone 200 mg/die, bisoprolol 2.5 mg/die (maximum tolerated dose), ramipril 2.5 mg/die, and apixaban 5 mg/die (paroxysmal atrial fibrillation).
Transthoracic echocardiogram showed left ventricle hypertrophy with normal systolic contractility (EF 60%) but moderate diastolic dysfunction (E/E′ 28), left atrial enlargement with mild mitral regurgitation, and calcified severe aortic stenosis (valve area of 0.5 cm2 with mean gradient of 52 mmHg, VTIr 0.16). Coronary angiography excluded the presence of concomitant coronary artery disease.
Due to his advanced age and multiple co-morbidities, the patient was judged not suitable for traditional surgical valve replacement (Society of Thoracic Surgeons mortality 7.9%) and scheduled to TAVI (TAVI Score 6.42%).
Pre-procedural multislice computed tomography confirmed a bilateral calcific disease of both iliac-femoral axes with tortuosity and inadequate lumen diameters (). Conversely, the subclavian-axillary axes showed adequate dimensions (i.e. diameters 5.1 mm) and an acceptable degree of kinking and calcification (). Thus, to minimize access-related complications and facilitate peri-procedural management, a completely percutaneous TAVI was planned using an angio-guidewire-ultrasound (AGU) technique by both arms.
Transcatheter aortic valve implantation procedure was performed under conscious sedation, in a hybrid operating suite by a multidisciplinary team including cardiologists, cardiac surgeons, and anaesthesiologists. After local anaesthesia of both wrists, left and right radial arteries were cannulated with 6-Fr glide sheath (Terumo) introducers. By means of a multipurpose 6-Fr diagnostic catheter, a 0.35″ guidewire was retrogradely advanced from the left radial artery into the left axillary artery up to an angiographically ideal point (i.e. adequately large extra-thoracic segment). Ultrasound guidance was then used to scan the vessel wall and exclude the presence of any calcific plaque. Merging data from both imaging techniques, the optimal axillary access point was identified and flagged by the J-tip of the guidewire ( and ).
After local anaesthesia of the left delto-pectoral groove, puncture of the anterior surface of the left axillary artery was assured by AGU technique and a 9-Fr sheath was inserted with a standard Seldinger technique. Two Perclose ProGlide™ (Abbott Vascular Devices) were implanted immediately before sheath introduction according to the pre-close technique.
From the right radial access, a left Judkins 6-Fr diagnostic catheter was used to obtain selective antegrade left subclavian cannulation, and a 0.14″ guidewire 300 cm in length (ChoiceTM extra-support, Boston Scientific Corp., Natick, MA, USA) was positioned distally in the left forearm to ensure axillary artery access in case of acute vascular complication (i.e. vessel rupture) () and to facilitate end-procedural haemostasis.
Using the left radial access, a second 0.14″ guidewire 300 cm in length (ChoiceTM extra-support, Boston Scientific Corp., Natick, MA, USA) was then positioned distally up to ascending aorta to ensure also homolateral rescue axillary artery access.
At this point, heparin was administered intravenously to achieve an activated clotting time >250 s, a stiff guidewire (Innowi®, Symedrix GmbH, Deisenhofen) was positioned into the left ventricle and used to obtain a rapid pacing during preliminary valvuloplasty with 18 mm balloon diameter (True Balloon BARD peripheral vascular, Inc., Tempe, AZ, USA) ().
Finally, a 14-Fr equivalent 29 mm self-expanding Evolut R transcatheter aortic valve (Medtronic, Minneapolis, MN, USA) was successfully implanted with trivial residual para-valvular regurgitation ().
During valve introducer pulling out, a percutaneous transluminal angioplasty balloon (6.0 mm × 20 mm) was simultaneously advanced into the subclavian artery via the right radial access. This assured a temporary blood flow blockade during percutaneous vessel closure manoeuvres (). Finally, anticoagulation was reversed with protamine infusion, the introducer device was removed, and axillary haemostasis was immediately obtained with the vascular closure systems.
The Choice ES guidewires remained in situ to secure access into the vessel at any procedural phase. The final angiography check of the puncture site from the right radial route revealed a complete haemostasis but with a significant pinching of the lumen artery at the site of vascular sutures (). After a failed first attempt to cross the iatrogenic stenosis antegradely due to low support, the suture-caused pinching was successfully crossed retrogradely by left radial access and corrected by a gentle prolonged angioplasty (). The final angiographic check excluded residual bleeding or major vessel injury ().
Post-procedural course was uneventful (); the patient was mobilized after 24 h and transthoracic echocardiography showed a transvalvular gradient of 5 mmHg with trivial para-valvular regurgitation. At 1-month follow-up, the patient described a sensible subjective improvement in activity tolerance and echocardiogram re-evaluation confirmed the pre-discharge findings.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [88, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 88 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
871,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5618394-1,Extracted,"A previously healthy, 61-year-old right-handed woman without history of epilepsy was transferred to our hospital for further evaluation and treatment of hypokalemia, hypercalcemia, confusion, and a brief seizure. Initial magnetic resonance imaging (MRI) revealed a 3.5 × 3.3 × 2.8 cm right frontotemporal meningioma with an accompanying midline shift of 3 mm (Fig. ).
Upon arrival, her neurological exam was notable for confusion and otherwise was nonfocal. Two clinical seizures with semiology of lip smacking, left head and eye deviation, and altered awareness were also observed. Both seizures ceased following intravenous lorazepam 2 mg without any improvement in mental status. Electroencephalography (EEG) revealed two right temporoparietal seizures with frequent T8/P4 sharp waves. She was treated with intravenous fosphenytoin 15 mg/kg. Continuous video-EEG monitoring showed nonconvulsive SE (NCSE). The patient was intubated and admitted to the neuro-intensive care unit. Stepwise treatment with propofol, midazolam, and ketamine was started, with burst suppression achieved in less than 24 h. Her antiepileptic drug (AED) management consisted of levetiracetam, lacosamide, and phenobarbital. Unfortunately NCSE recurred each time with weaning of general anesthesia. Three days after admission, she underwent resection of the right frontotemporal mass which was consistent with a WHO grade I meningioma (Fig. ). During her hospital stay, she was also treated for hyperparathyroidism secondary to a parathyroid adenoma that was treated medically and then surgically. Postoperatively, she remained seizure free, but her mental status did not improve. Intermittent EEGs showed diffuse slowing with focal right hemispheric arrhythmic delta slowing and continued right T8/P4 sharp waves. She was discharged to a long-term care facility in a minimally responsive state with tracheostomy and percutaneous endoscopic gastrostomy. Her mental status improved after discharge, but she had persistent generalized weakness due to critical illness myopathy from her prolonged intensive care unit stay. At 2-month follow-up, she had normal memory, attention, and language functions.
Two weeks later, she presented with confusion and left face twitching. EEG showed continuous right hemispheric spike and wave activity consistent with focal NCSE. Her preadmission AEDs were continued with the addition of valproic acid without subsequent improvement. EEG burst suppression was achieved with propofol, ketamine, midazolam, and pentobarbital. Brain MRI showed right superior temporal encephalomalacia and gliosis (Fig. ). NCSE emerged each time anesthetic medication was lowered despite four antiepileptic medications. Due to her previous SRSE with prolonged recovery phase and current poor prognosis, the family agreed for recurrent surgical treatment. She underwent tailored right temporal lobectomy 8 days after admission with removal of the superior, middle, and inferior temporal gyri (6 cm from the tip). Hippocampectomy was guided by intraoperative electrocorticography with resultant cessation of epileptiform activity along the margin of the resections (Fig. ). Postoperative EEG continued to show frequent right posterior temporal periodic epileptiform discharges for another 15 days without clinical improvement. Topiramate was added to her AED regimen, and propofol and midazolam was again titrated to EEG burst suppression for 2 days. As general anesthesia was weaned, the EEG slowly improved to diffuse theta and delta range slowing. Surgical pathology showed nonspecific leptomeningeal necrotizing inflammation in medium-sized arteries, focal cortical neuronal loss, and gliosis. The patient received high-dose fosphenytoin steroids for 5 days for possible autoimmune encephalitis. Tests for autoimmune markers and paraneoplastic antibodies as well as imaging studies for neoplasia in any other part of the body were negative except for a nonspecific elevated antinuclear antibody. She was transferred to a long-term care facility on topiramate 400 mg/day, valproic acid 3,000 mg/day, phenobarbital 300 mg/day, lacosamide 400 mg/day, and levetiracetam 5,000 mg/day.
At 9-month follow-up, neuropsychological testing could not be performed due to somnolence and lack of cooperation. Over 3 years the patient gradually improved her interaction and alertness, with concomitant decrease in her AEDs. As her cognitive status improved, a clinical picture of sensory aphasia was revealed. This manifested as relatively fluent and articulate speech with notable paraphasic errors, verbal perseveration, word salad, and alexia. Neuropsychological testing 34 months postoperatively could not be completed due to her dense sensory aphasia. The Mississippi Aphasia Screening Test showed an improving Wernicke-type aphasia that was evolving into a transcortical sensory aphasia profile with relatively fluent and articulate speech, paraphasic errors, poor comprehension, inconsistent response to questions and command following, restricted repetition of single words only, agraphia, and inability to read complex sentences.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [61, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 61 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
872,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7509890-1,Extracted,"A 65-years-old right-hand dominant woman presented to our unit with a 24-h history of a progressively worsening discoloration and swelling to her left index finger (LIF) associated with generalized swelling and tenderness of the left hand. She denied any recent trauma to her left hand. She gave a history of epilepsy due to multiple meningiomas for which she was maintained on dexamethasone treatment (4 mg/day) for 6 months.
Clinical examination revealed an afebrile, relatively well-looking woman, with classic cushingnoid appearance and a grossly normal neurological examination. Gross swelling to her left hand, most markedly to the LIF, was noted. Her LIF was cold, insensate and dusky with epidermolysis of the dorsal skin (). She also had ascending cellulitis extending to her elbow and palpable lymph nodes on her axilla. X-ray demonstrated gross soft tissue swelling but was otherwise unremarkable, with no signs of gas within the tissues. A clinical diagnosis of fulminant NF was made; she was admitted and empirically commenced on intravenous penicillin and booked emergently for debridement of her left hand. Her laboratory analysis revealed elevated C-reactive protein 560 mg/L and white blood cell count 24 × 109U/L and hyponatremia 128 mmol/L with a LRINEC score of 7.
Intraoperatively, the clinical diagnosis of NF was confirmed with circumferential necrosis of her LIF. The LIF was amputated at the metacarpophalangeal joint () and radical debridement was performed of nonviable skin and subcutaneous tissue on the dorsum of her left hand and distal forearm. The volar tissues and the proximal forearm demonstrated healthy bleeding skin and normal looking fascia. Postoperatively, she was managed in our high dependency unit for close monitoring. A second washout was performed 24 h later not revealing any further signs of infection. Microbiology cultures later revealed penicillin sensitive Streptococcus pyogenes species. Her wounds were resurfaced with a split thickness skin graft 2 days later (). She was subsequently discharged on Day 7 post presentation.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [65, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Diabetes history': False, 'Transient Ischemic Attacks History': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
873,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8335949-1,Extracted,"A 56-year-old woman was first admitted to our hospital in January 1990, complaining of loss
of appetite, body aches, and palpitations. Past medical history included hypertension and
dyslipidaemia. Clinical examination revealed a blood pressure of 200/100 mmHg, a heart rate
88 b.p.m., temperature 37°C, and a respiratory rate 20 breaths per minute. She had normal
heart sounds on auscultation, with regular rate and rhythm. Jugulovenous pressure was not
elevated. There was no pedal oedema, and her lungs were clear to auscultation bilaterally.
Home medications included nifedipine 10 mg three times a day.
Urinalysis showed few pus cells. She was given amoxicillin/clavulanic acid 500 mg/125 mg
three times a day for 7 days.
Electrocardiogram showed normal sinus rhythm, and a chest X-ray was normal. Transthoracic
echocardiography which showed a left atrial mass measuring 3.6 × 2.9 cm, attached to the
interatrial septum, highly suggestive of left atrial myxoma. There was trace tricuspid
regurgitation, normal right ventricular function, and systolic pressure. Left ventricular
function was normal. The mitral valve was not obstructed by the left atrial myxoma, and
there is normal mitral valve gradient and only trace mitral regurgitation. Transoesophageal
echocardiography on 17 February 1990 was also highly suggestive of left atrial myxoma.
Surgical removal of her left atrial mass was recommended. However, she was reluctant to
undergo surgery, as she felt better by then. Nifedipine was changed to verapamil 40 mg twice
a day plus enalapril 10 mg twice a day. She was discharged home with blood pressure
145/80 mmHg. The patient had been noncompliant with her antihypertensive medications. She
also had a minimal access to health care resources, including international normalised ratio
(INR) checks and follow-up, limiting warfarin use as an option for anticoagulation.
Therefore, she was discharged on aspirin 81 mg once a day. She was advised to comply with
her medications and diet, and strongly advised to reconsider surgical resection for her left
atrial myxoma.
Thereafter, the patient lost to follow-up for 10 years and did not visit any outpatient
clinics until 2004. Unfortunately, most of the old echocardiography videos from the 1990s
were lost when the echocardiography system was changed to a digital archiving system.
However, a printed transthoracic echocardiography from 29 March 1994 that was attached to
her paper file clearly showed the left atrial mass suggestive of left atrial myxoma
().
The patient was later admitted in 2008 with bronchiectasis, type 2 respiratory failure and
grade 3 chronic kidney disease. She was again admitted in 2009 with a stroke resulting in
left-sided weakness, but she recovered. Workup during that admission showed significant
bilateral carotid artery stenosis, and echocardiography showed the same left atrial mass,
although it was smaller and more calcified ().
Surgery was recommended for the carotid stenosis and the left atrial myxoma. However, due
to her bronchiectasis, type 2 respiratory failure and moderate renal impairment, she was
informed of the high risk of complications, therefore she refused both surgeries due to the
high surgical risk. Clopidogrel 75 mg once a day was added to her home aspirin dose. She
then had recurrent strokes in 2013 and 2014.
During admission for the stroke in 2014, she underwent transoesophageal echocardiography
(), followed by
cardiac magnetic resonance imaging (MRI) in October 2014, which showed 2.9 × 2.4 cm atrial
mass attached to the fossa ovalis, mildly heterogeneous on steady state free precession MRI,
bright on T2 weighted images, and partially enhanced on late gadolinium enhancement. There
was no evidence of fatty contents and the mass was minimally perfused on the first pass
().
She was rehospitalized with another stroke in 2015, with worsening memory. During this
admission, she underwent carotid stenting with no further clinically detectable strokes
since then.
The patient was followed-up until November 2019, with last transthoracic echocardiography
being performed on 26 November 2019 (). During the last 16 years, the patient underwent 13
transthoracic echocardiograms, showing that the left atrium had gradually increased in size,
diastolic parameters worsened gradually, the right ventricular systolic pressure increased
to approximately 50–60 mmHg, and the left atrial myxoma became smaller and more calcified
(). She had
worsening renal impairment, and atrial fibrillation, but due to her increased risk of
bleeding, warfarin was not considered appropriate and she continued on a combination of
aspirin and clopidogrel. Unfortunately, vascular dementia developed and eventually she
became bedridden.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [56, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 56 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
874,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6966369-1,Extracted,"A 70 year-old female with a prior history of a right carotid artery stenosis status post carotid endartectomy, hypertension, and dyslipidemia presented with severe lifestyle-limiting left-sided claudication (Rutherford class 3). The ankle-brachial index (ABI) was 0.60 and 1.02 on the left and right lower extremities, respectively. The patient’s symptoms persisted despite conservative therapy which included supervised exercise, aspirin, atorvastatin, and cilostazol. Following discussion of possible treatment options, including vascular bypass, a collective decision was made to proceed with a diagnostic peripheral angiogram and percutaneous endovascular intervention, if needed.
The patient was brought to the catheterization laboratory and prepped in a sterile fashion. Ultrasound was used to confirm patency of the left dorsalis pedis artery (DPA) and anterior tibial (ATA) and guide cannulation of the DPA with a 21-gauge echogenic needle, followed by introduction of a 4-Fr Pinnacle Precision Glidesheath (Terumo) into the ATA. After confirming flow, nitroglycerin 200 mcg, verapamil 1 mg, and heparin 5000 IU were administered intra-arterially. To achieve an activated clotting time (ACT) > 300 s, additional heparin was given if needed. A tibial angiogram was performed to assess size and disease burden of the anterior tibial artery (Fig. ). A 125 cm, 4-Fr Tempo Aqua Vertebral catheter (Cordis) was advanced over a 0.014-in., 300 cm Runthrough wire (Terumo) to perform a diagnostic angiogram of the left lower extremity, which showed the distal cap of a CTO of the distal left external iliac artery (EIA). To localize the proximal cap of the stenotic lesion, left radial access was obtained and a 4-Fr Multicurve 150 cm catheter (Terumo) was advanced into the left common iliac artery (CIA). Dual injections revealed CTO throughout the entire length of the left EIA (Fig. ).
The transpedal 4-Fr Glidesheath was upsized to a 6-Fr Slender Glidesheath (Terumo) in anticipation for retrograde intervention given the extent and complexity of the CTO. This Slender Glidesheath has an outside diameter equivalent to a 5-Fr sheath, but can accommodate 6-Fr equipment. We initially attempted antegrade recanalization, however, we were unsuccessful in breaking the proximal cap likely due to lack of support from radial access. Next, retrograde wire escalation attempts were made with a 0.018-in. Glidewire Gold (Terumo) and 0.035-in. Glidewire Advantage (Terumo) with entry into a dissection plane close to the true lumen of the CIA. In order to refrain from direct entry into the aorta and compromise the contralateral limb, the decision was made to directly reenter into the CIA. The wire was exchanged with a hydrophobic 0.014-in. Granslam wire (ASAHI) and an Outback Elite re-entry device (Cordis) was advanced into the dissection plane adjacent to the CIA (Fig. ). Successful reentry was achieved and the wire was exchanged with a 0.035-in. Three hundred centimeter Supracore (Abbott), followed by balloon dilation of the stenosis and deployment of an 8 mm x100mm Absolute Pro self-expanding stent (Abbott) with excellent post-intervention results and retained patency of the ostial internal iliac artery (Fig. ). Post-intervention tibial angiogram did not reveal any damage to the vessel access site and showed good patency of the DPA and ATA. The left radial artery and left DPA introducer sheaths were removed without complications. A TR Band (Terumo) was placed on the left radial artery puncture site and a VasoStat (Forge Medical, Inc.) was placed on the left DPA puncture site to achieve hemostasis. Once the Vasostat was placed over the DPA a vascular ultrasound was used distally to ensure vessel patency. The patient was discharged home 2 h after the procedure on atorvastatin 80 mg daily, and dual antiplatelet therapy with daily aspirin 81 mg and clopidogrel 75 mg for at least 1 month. Detailed clinical follow-up was performed at 6 and 12 months after procedure, during which the patient reported significant symptom improvement (Rutherford class 1) and had normal repeat left ABI and duplex ultrasound.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [70, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 70 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
875,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3350016-1,Extracted,"A 71-year-old Nigerian female, with past medical history of rheumatic valvular disease with mitral stenosis, and atrial fibrillation, presented for routine preoperative chest X-ray for cataract surgery. The patient was asymptomatic, and otherwise in reasonably good health. A recent echocardiogram confirmed severe left atrial and left ventricular enlargement; the mitral valve area was found to be 0.7 cm2 (normal 3-4 cm2), consistent with mitral valve stenosis. Incidental findings on the chest X-ray revealed an unusual pattern of curvilinear cardiac calcification (Figures and ). Subsequently, a noncontrast CT scan of the thorax was obtained for further characterization and anatomical localization (Figures , , , and ). Surgical intervention was offered in years past, though did not occur for unknown reason(s).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [71, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 71 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
876,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3914332-1,Extracted,"An 89-year-old lady presented to the medical assessment unit with a four-day history of melaena associated with shortness of breath on exertion, postural dizziness, and lethargy. This was secondary to esophagitis and gastric erosions. During her hospital stay she developed a rapid onset, painful swelling of her right shoulder with a limited range of movement. There was no history of recent trauma to the right shoulder. This was her third presentation; previous ones had been followed up by her general practitioner.
Past medical history included well-controlled asthma, hypertension, and atrial fibrillation. There was no history of diabetes, hyperparathyroidism, or syphilis. She was an ex-smoker with a 10-pack-year history and consumed minimal amounts of alcohol only.
On examination, she was pale, with no rashes or bruises. There was a large right shoulder effusion. Both active and passive movements were limited. shows the patient's large right shoulder swelling which was warm to touch and tender with no erythema.
Plain radiograph of the affected shoulder showed joint space narrowing, subchondral sclerosis, destruction of subchondral bone, soft-tissue swelling, capsular calcifications, and intra-articular loose bodies ().
Arthrocentesis was performed and 250 mLs of haemorrhagic fluid was aspirated. Analysis of the synovial fluid showed a noninflammatory cell count with leukocytes 721/mm3 which were predominantly neutrophils. Gram stain was negative; no organisms were cultured and cytology analysis was negative, as was VDRL on the synovial fluid. The aspirate stained bright orange-red with alizarin red S, indicating the presence of calcium hydroxyapatite crystals. The diagnosis of Milwaukee shoulder syndrome was made and she was treated conservatively with colchicine and physiotherapy with a good outcome.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [89, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 89 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
877,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-5815,Extracted,"A 55-year-old woman presents to a primary care clinic for a physical evaluation. She works as a software engineer, travels frequently, is married with 2 kids, and drinks alcohol occasionally. She does not exercise regularly. She currently does not take any medications except for occasional ibuprofen or acetaminophen. She is currently undergoing menopause. Her initial vital signs reveal that her blood pressure is 140/95 mmHg and heart rate is 75/min. She weighs 65 kg (143 lb) and is 160 cm (63 in) tall. Her physical exam is unremarkable. A repeat measurement of her blood pressure is the same as before. Among various laboratory tests for hypertension evaluation, the physician requests fasting glucose and hemoglobin A1c levels.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [55, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 55 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
878,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4596111-1,Extracted,"An 87-year-old woman was admitted to the emergency room for altered mental status and left-side weakness. She had been treated with warfarin and aspirin for 2 years due to AF, ischemic stroke, and myocardial infarction. She had also been diagnosed and managed for hypertension, diabetes mellitus, dyslipidemia, and ischemic cardiomyopathy. A neurologic examination revealed a stuporous mental status, unresponsiveness to visual threatening, gaze preponderance to the right side, and left-sided hemiparesis. Magnetic resonance imaging revealed acute ischemic infarction in the right middle cerebral artery (MCA) territory and chronic infarction in the left MCA territory. The transthoracic echocardiogram findings were consistent with ischemic heart disease with moderate left-ventricular systolic dysfunction (left-ventricular ejection fraction, 30-35%), AF with enlargement of both atria, and moderate tricuspid regurgitation with borderline pulmonary hypertension. Coagulation assays were performed with a Stago STA-R device. The activated partial thromboplastin time (aPTT) was 30.8 sec (reference, 29.1-41.9 sec) and the international normalized ratio (INR) was 1.24 (reference, 0.90-1.10).
The decision was made to change from warfarin to dabigatran because the patient suffered a recurrent stroke despite receiving warfarin treatment. In addition, frequent measurement of INR could not be performed after discharge due to severe neurologic deficits. A baseline assessment revealed that she had a serum creatinine concentration of 1.29 mg/dL, an estimated glomerular filtration rate of 38.7 mL/min/1.73 m2, and a CrCL of 27.2 mL/min. Dabigatran was started at a dosage of 110 mg twice daily, 2 days after cessation of warfarin. The patient developed multiple bruises after 2 days of dabigatran use, and small old blood clot was observed in her nasogastric tube. Blood sampling revealed severe coagulopathy (), with a PT of 65.4 sec (reference, 12.6-14.9 sec), an INR of 7.99, and an aPTT of 99.7 sec. A repeat assessment performed 4 hours later revealed that the PT and aPTT were further prolonged (to 85.9 and 119.2 sec, respectively), the INR had increased (11.36), and she had a prolonged thrombin time of 230.8 sec (reference, 14.2-16.5 sec). The patient received a vitamin K injection and dabigatran was discontinued; 7 days later the PT was normalized, with an INR of 1.09 and an aPTT of 34.8 sec, but the thrombin time was still prolonged at 61.5 sec. Serial assessment of renal function revealed substantial fluctuation in the CrCL (range, 17.9-26.5 mL/min) ().",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': True, 'Hypertension history': True, 'Thromboembolism history': True, 'Vascular disease history': True, 'age': [87, 'years'], 'Stroke': True, 'Diabetes history': True, 'Transient Ischemic Attacks History': True, 'sex': 'Female'}",9,9,9,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 87 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 5 + 2 = 7.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 7 + 1 = 8. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 8 + 1 = 9.
The patient's CHA2DS2-VASc Score is 9."
879,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4302357-1,Extracted,"An 87-year-old lady was admitted to the ENT ward of a district general hospital with brisk, bright red haemoptysis. Subjectively, the patient felt the blood originated in her mouth and denied any coughing or vomiting, although she did complain of a sore throat.
She had been suffering intermittent haemoptysis for the past four months and had been investigated by multiple specialists who had not identified the source of the bleeding. She had been seen in ENT clinic, where serial nasendoscopy was normal. An oesophagogastroscopy failed to identify a cause for the bleeding. A subsequent CT of the thorax and abdomen was performed which only showed emphysematous lung changes without identifying a clear source to explain the haemorrhage. She also complained of a spreading, pruritic, blistering rash which had begun three weeks prior to presentation. She was on warfarin for atrial fibrillation, but on admission her INR was within therapeutic range (INR = 2.0).
On examination, the patient was seen spitting out bright red blood and a large deroofed blister was observed on the soft palate (). Nasendoscopy revealed normal nasal mucosa and a normal postnasal space. Examination of her abdomen and respiratory systems was normal and there was no calf swelling or tenderness. She was noted to have multiple, annular ulcerated lesions on her back which the patient reported began as pruritic blisters which then ruptured. There were also some intact, tense blisters, overlying erythematous skin predominantly on the groins, but also on the arms, the inner aspect of left thigh, and right shin.
Blood tests demonstrated the presence of a mild microcytic anaemia and the persistence of a raised urea in keeping with swallowing of blood but were otherwise unremarkable.
The patient was subsequently referred to and reviewed by the Dermatology Team on the day of her admission. They felt that given her age and the presence of intact blisters that developed from pruritic lesions, this was clinically in keeping with bullous pemphigoid with mucous membrane involvement. The deroofing of blisters in the oropharynx could account for the intermittent haemoptysis and subsequent raised urea secondary to continuous ingestion of blood. Punch biopsies of perilesional skin were sent for histopathology, which confirmed the diagnosis of bullous pemphigoid, and the patient was commenced on both topical and systemic steroid therapies.
Histology demonstrated a subepidermal bulla containing fibrin and eosinophils, consistent with bullous pemphigoid (). This diagnosis was supported by direct immunofluorescence, which showed linear homogenous deposition of IgG, C3, and IgA along the basement membrane zone (BMZ). IgM staining was negative. This pattern of linear staining is entirely in keeping with bullous pemphigoid.
The patient was commenced on systemic steroids, while awaiting biopsy reports, with prednisolone 30 mg once daily. This was a somewhat conservative dose prescribed in light of her comorbidities including congestive cardiac failure and ischaemic heart disease, compounded by mild anaemia, which at this point in her admission had decompensated to some extent, rendering her breathless. Potent topical steroids were applied to affected areas of skin and a steroid mouthwash was given. A daily blister chart was started to monitor the progress of therapy. Warfarin was withheld until her condition had improved.
Following one week of treatment, the disease activity appeared halted in its progression. After 2 weeks the systemic steroids were gradually tapered: the dose of prednisolone was reduced by 5 mg each week until a dose of 10 mg once daily was reached and thereafter weaned by 1 mg per week. Topical steroids were also reduced in strength gradually and were eventually stopped when no new blisters were reported.
The patient was followed up in outpatients clinic for several months, following the cessation of formation of new blisters at discharge. She had continued to complain of a sore mouth and was ultimately treated with a prolonged course of nystatin for oral, and probably oesophageal, candidiasis that occurred secondary to the long course of steroid therapy.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [87, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 87 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
880,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8254163-1,Extracted,"A 70-year-old lady, presented to the cardiology outpatient department with complaints of effort dyspnea and palpitations for the past 2 years and pedal edema for the past 6–8 months.
She was a known case of hypertension, and a known case of coronary artery disease for 8 years and had undergone coronary angioplasty with stent implantation to the left anterior descending artery. She also had history of carcinoma left breast which was diagnosed about 30 years back and treated with mastectomy, followed by RT and chemotherapy. There was no recurrence of carcinoma breast, but she had recently developed carcinoma esophagus for which surgical management was planned.
She underwent evaluation for the above complaints. Chest X-ray showed right ventricular enlargement. A transthoracic echocardiogram was performed, which showed evidence of multivalvular heart disease. The anterior mitral leaflet was thickened and calcified with mild mitral regurgitation. The aortic valve was trileaflet with thickened leaflets and calcification of right coronary cusp with no commissural fusion and mild aortic regurgitation []. The aortomitral continuity region was also calcified, and the wall of the aortic root was thickened []. The tricuspid valve leaflets were thickened and densely fibrosed, with rolled out edges and severe low-pressure tricuspid regurgitation due to non-coaptation of the leaflets []. Pulmonary valve leaflets were also thickened with moderate pulmonary regurgitation []. Left and right ventricular systolic function was normal but right ventricle and right atrium were significantly dilated secondary to pulmonary and tricuspid regurgitation. Inferior vena cava was dilated in size with normal inspiratory collapse. There was no pericardial thickening and no pericardial effusion.
Since this patient was seen in the OPD, nothing was done and is being reported mainly as a case of interest.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [70, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': True, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 70 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
881,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4710900-1,Extracted,"A 70-year-old male was admitted with skin rash on the trunk, back, and limbs (). He suffered from nonvalvular atrial fibrillation. The patient did not report any allergies from the past. He took diltiazem 60 mg × 2 in order to lower his heart rate, alprazolam 0,25 mg at bedtime, and dabigatran 150 mg × 2. He was starting taking dabigatran in the previous week. The skin rash developed during the last three days on the trunk and limbs with no response to levocetirizine dihydrochloride which was prescribed by his doctor. He suffered from itching and burning. Conjunctiva, mouth, and genital regions were not involved. On clinical examination, he was found to have arterial pressure 125/85 mmHg, oxygen saturation 95%, heart rate 76 bpm, and normal heart lung auscultation. He did not have fever and his general condition was good. His electrocardiogram showed atrial fibrillation, X-ray was normal, and his hematological and biochemical results were normal. The patient was transferred to the internal medicine department in order to be treated with methylprednisolon 80 mg × 2, dimethindene maleate iv, and H2 antagonists. The eruption was resistant to our therapeutic choices. Immunologic tests were ordered to rule out autoimmune disorders. On the third day of hospitalization skin biopsy was performed, which revealed neutrophilic infiltrates and leukocytoclastic vasculitis. Prednisolon was given 1 mg/kgr as well as colchicine 1 mg/day. On the fifth day of hospitalization the rash was diminished. He was able to leave our clinic two days later. Dabigatran was replaced with enoxaparin 0,6 mL/kgr/12 hours on hospitalization day 1.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [70, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 70 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
882,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-4881,Extracted,"A 67-year-old man presents to the emergency department for a headache. The patient states his symptoms started thirty minutes ago. He states he experienced a sudden and severe headache while painting his house, causing him to fall of the ladder and hit his head. He has also experienced two episodes of vomiting and difficulty walking since the fall. The patient has a past medical history of hypertension, obesity, and atrial fibrillation. His current medications include lisinopril, rivaroxaban, atorvastatin, and metformin. His temperature is 99.5°F (37.5°C), blood pressure is 150/105 mmHg, pulse is 90/min, respirations are 15/min, and oxygen saturation is 98% on room air. On physical exam, the patient localizes his headache to the back of his head. Cardiac exam reveals a normal rate and rhythm. Pulmonary exam reveals minor bibasilar crackles. Neurological exam is notable for minor weakness of the muscles of facial expression. Examination of cranial nerve three reveals a notable nystagmus. Heel to shin exam is abnormal bilaterally. The patient's gait is notably ataxic. A non-contrast CT scan of the head is currently pending.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [67, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 67 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
883,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5484601-1,Extracted,"The patient is a 72-year-old Caucasian male who presented to the emergency department with one-week history of productive cough with yellow-green sputum, general malaise, palpitations, and progressively worsening dyspnea. He had a past history of chronic obstructive pulmonary disease (COPD), and both pneumonia and a leukemoid reaction three months ago. On admission, he was found to have increased white blood cell count in the range of 70 x 109/l. He was complaining of shortness of breath and palpitations, thus an electrocardiogram (EKG) and chest radiograph (CXR) were ordered. His EKG revealed an irregular rapid heart rate around 150-200 bpm, irregular rhythm and absent p-waves that were consistent with atrial fibrillation (a-fib) with rapid ventricular rate (RVR). Additionally, his CXR showed right lower lobe consolidation consistent with bacterial pneumonia. Sputum cultures were ordered, and it grew the bacteria H. influenzae.
A physical examination revealed tachycardia with irregularly irregular rhythm, loud expiratory wheezes, moderate respiratory distress, scattered ecchymosis, but no splenomegaly. The patient's symptoms of shortness of breath and physical exam findings were consistent with severe COPD exacerbation. He was treated with intravenous steroids and nebulized bronchodilators with minimal improvement of his respiratory distress. Furthermore, his atrial fibrillation was equally challenging to manage; he was initially converted to sinus rhythm on amiodarone but had to be trialed with other treatments after his aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were elevated on his liver function tests. He had an echocardiogram and cardiac stress test that showed reversible ischemia in the apical septum and an ejection fraction of 25%. He had a cardiac catheterization that was relatively unremarkable, and he was placed on sotalol to control his atrial fibrillation. On day 3 of his admission, his white count was elevated to 155.83 x 109/l with 20% band neutrophils, 5% lymphocytes, 14% myelocytes, 2% promyelocytes and 1% blast cells. A peripheral blood smear revealed that he had an increased number of immature myeloid cells, metamyelocytes and myelocytes, basophils and eosinophils that were consistent with CML; however, a bone marrow biopsy was needed for confirmation. The patient’s bone marrow aspiration was postponed for several days until he was cleared by cardiology for the procedure. After he was cleared, his bone marrow biopsy revealed markedly hypercellular bone marrow (>80%) with granulocytic hyperplasia and positive BCR-ABL testing. The patient was subsequently started on dasatinib, a second generation tyrosine kinase inhibitor that exhibits activity against many clinically relevant BCR-ABL mutant forms []. The patient improved clinically after his white count began to trend down and stabilize in the range of 40 x 109/l.
The patient was evaluated previously three months ago for leukocytosis (range in 40 x 109/l) by a hematologist who did not determine any findings that were suggestive of leukemia on smear analysis and flow cytometry. The patient was lost to follow-up and did not have further testing.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
884,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3541576-1,Extracted,"We report the case of a 56-years-old Caucasian male a histoty of clear cell renal carcinoma status post right nephrectomy 2 years prior, and who subsequently developed lung metastasis. The patient had progression of disease after several lines of treatment including to sutent, pazopanib and temsirolimus, and he was ultimately started on axitinib 5 mg by mouth twice a day with good initial clinical and radiological response after 1 one month of treatment.He presented to the emergency department of our institution complaining of 3-day-progressive dyspnea on minimal exertion, associated to dry cough and difficulty to speak. Vital signs on admission revealed a blood pressure of 93/59 mmHg, tachycardia, tachypnea, and hypoxemia with oxygen saturation of 90% on room air. Chest examination showed absent breath sounds in the left side of his chest. Chest X-ray (CXR) revealed a left-sided tension pneumothorax, which required thoracostomy by cardiothoracic surgery in an emergent fashion; a new CXR showed complete resolution of left pneumothorax, and for that reason after 3 days the chest tube was removed and the patient was discharged home. Unfortunately the next day he returned to the emergency department with a new onset of shortness of breath and left-sided chest pain; a new CXR showed left recurrent pneumothorax; thus chest tube was inserted again. High resolution CT scan showed biapical bullae and blebs, a small left pneumothorax, subcutaneous emphysema, and a 4.3 × 2.6 cm pneumatocele within the anterior segment of the left upper lobe.
Cardiothoracic surgery decided to perform a left video assisted thoracoscopy with apical blebs resection as a definitive treatment. In the operation room, and after performing a left upper lobe wedge resection of the blebs, reexpansion of the left lung was achieved and it revealed a large left upper lobe air leaking caused by 4 × 3 cm cavitated necrotic tumor at the level of the main pulmonary artery, so the decision was made to proceed with a left thoracotomy. During the procedure it was found that the necrotic mass was not resectable, and for that reason the lesion was covered and repaired via pericardial fat flap placement. Multiple biopsies were taken from this mass, with a final pathology report of a lesion consistent with mRCC with extensive associated necrosis (Figures and ). Postoperative course was also complicated with a left side empyema and new onset atrial fibrillation that were successfully treated and the patient eventually was discharged home. A comparative review of interval imaging studies before- and afteraxitinib use showed an initial 4 × 3 cm mass seen in the same location of this large cavitated necrotic tumor (Figures and ). Apparently this mass transformed into a cavitated tumor after one month of axitinib treatment and caused the recurrent pneumothorax.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [56, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 56 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 0 + 1 = 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
885,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6530233-1,Extracted,"A 73-year-old woman presented with right hip pain and inability to ambulate after a mechanical fall in her home. The patient had a past medical history of congestive heart failure, atrial fibrillation, and hyperlipidemia. Three months prior to the fall, the patient had been hospitalized for 10 days due to a polymicrobial (Pseudomonas aeruginosa, Proteus vulgaris, non-beta-hemolytic streptococci, and Escherichia coli) urinary tract infection, was subsequently treated at a rehabilitation facility for a 6-week period, and was ultimately discharged home. Two days following discharge, she sustained a mechanical fall and presented to the emergency department. Prior to her fall, she was minimally ambulatory with a walker due to deconditioning from the recent hospitalization as well as a remote history of bilateral Achilles tendon injuries resulting in equinus contractures. The patient denied antecedent hip pain or pain in other joints on presentation. On physical exam, she was noted to be obese with a BMI of 36.56, her right lower extremity was shortened and externally rotated, and she had diffuse tenderness about the hip. She was neurovascularly intact distally. Radiographs including an anteroposterior (AP) pelvis and AP and lateral view of the hip demonstrated a displaced femoral neck fracture (). Due to medical comorbidities and limited functional status prior to the injury, the plan was made to proceed with a hemiarthroplasty as opposed to total hip arthroplasty. Two days following admission, the patient underwent a cemented hemiarthroplasty via the posterior approach to the hip without complication (). During her hospitalization, complete blood count and basic metabolic panel were monitored and within normal limits by discharge. She was diagnosed with osteoporosis on admission (left femoral neck T score of -2.8 on dual-energy X-ray absorptiometry [DEXA] scan). Her PTH level was slightly elevated (97.8 pg/mL), but both calcium and vitamin D levels were within normal limits (9.2 mg/dL and 41.8 ng/mL, respectively). An immunofixation test to detect multiple myeloma was unremarkable. She was ultimately discharged to a skilled nursing facility on postoperative day 4 with prescriptions for low molecular weight heparin for deep vein thrombosis (DVT) prophylaxis, narcotics for pain control, and vitamin D. She was also instructed to follow up with a metabolic bone disease specialist for further management of osteoporosis.
Two weeks after discharge, she presented with right posterior thigh and groin pain, which she reported had been constant since surgery and had prevented progress with physical therapy. She denied a new traumatic event. Physical exam was notable for tenderness over the proximal hamstring but was otherwise normal. Radiographs () and computed tomography (CT) scan demonstrated increased medialization of the femoral component into the acetabulum without evidence of loosening or hardware complications. Bilateral lower extremity duplex was negative for DVT. Infection workup revealed CRP 6 mg/L, WBC 11 (103/μL), and ESR 75 mm/hr, and it was determined that she did not have a periprosthetic joint infection (PJI) at that time. She was admitted overnight for pain management and discharged back to the skilled nursing facility the next day with a plan for restricted weight bearing with a walker.
At the 6-week postoperative visit, she continued to have limited progress with physical therapy, which she attributed to ongoing groin pain and weakness. Exam was within normal limits. Radiographs () and CT again demonstrated increased medialization of the femoral head, now with a fracture of the medial wall of the acetabulum. Infection workup revealed CRP < 5 mg/L, WBC 9.7 (103/μL), and ESR 71 mm/hr, and it was again determined that she did not have PJI at that time. She underwent conversion to a right total hip arthroplasty the next day () via a posterior approach. The fracture was treated with a jumbo cup and screws with impaction grafting technique utilized to restore medial bone loss. There were no complications. She was made partial weight bearing with instructions for walker-assisted ambulation at all times and discharged on postoperative day 4.
Two weeks after discharge, she presented with a 1-day history of incisional drainage. Her exam was significant for a fever of 101°F and an erythematous indurated incision with serous drainage. Infection workup revealed WBC 13.9 (103/μL), ESR 110 mm/hr, and CRP 89 mg/L. Radiographs did not demonstrate evidence of component loosening or fracture displacement (). She underwent right hip irrigation and debridement and revision arthroplasty the next day (). A cemented all-polyethylene cup was used in order to remove the bone graft and allow for the use of antibiotic cement. Intraoperative cultures grew Enterobacter cloacae, which was not one of the organisms of her previous UTI. The infection was treated with vancomycin and cefepime with a planned 6-week course as recommended by infectious disease, given that gram-positive involvement had not been entirely ruled out. She maintained partial weight bearing status and was discharged to subacute rehab on postoperative day 3.
She reported to the outpatient clinic for follow-up 3 weeks later. She continued to progress with physical therapy. Physical exam and imaging () were normal, and she was transitioned to weight bearing as tolerated.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [73, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 73 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
886,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6417354-1,Extracted,"A 36-year-old male presented with pain and progressive paresthesia in right-sided limbs for 3 years without sphincter dysfunction. Examination revealed spastic weakness (Medical Research Council Grade 4/5) in both upper limbs and right lower limb with modified McCormick Grade 2 disability. He also had 30%–40% sensory loss to touch and pain below C5 with impaired posterior column sensations. Magnetic resonance imaging (MRI) showed a well-defined mass lesion extending from cervicomedullary junction to C5, causing expansion of the cord without syrinx formation or tumor cysts. Tumor was eccentrically placed, anterolaterally on right side pushing the spinal cord toward left. It was T1 hypo to isointense, T2 hyperintense without significant contrast enhancement []. Common intramedullary lesions such as astrocytoma and ependymoma were considered among the differential diagnoses.
C1–C5 laminectomy for tumor excision was done. Intraoperatively, tumor was greyish, soft, moderately vascular lesion extending along subpial plane on the right side, without distinct planes at either end. Upper half of the tumor was found anterolateral to the cord on right side, and lower part was seen extending ventral to the cord. No myelotomy was required for tumor excision.
Histopathologically, tumor cells with mildly enlarged anisomorphic nuclei were seen clustered in the acellular fibrillary matrix. Mitotic activity and necrosis were absent. These features were consistent with subependymoma. Immunohistochemistry showed weak tumor cell positivity for glial fibrillary acidic protein (GFAP) and S-100, and negative for neuron-specific enolase and epithelial membrane antigen (EMA) with low Ki-67 index (1%) [].
Postoperatively, motor power in all four limbs worsened by one grade compared to the baseline. We planned for radiological follow-up without any adjuvant therapy. At 2-month follow-up, motor power and spasticity improved with functional recovery.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [36, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 36 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
887,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7413206-1,Extracted,"A 71-year-old female with a past medical history of smoking, hypertension, hyperlipidemia, and type 2 diabetes mellitus (T2DM) controlled on oral medications presented to the surgery clinic for evaluation of a pancreatic mass with new onset cough with hemoptysis. Previous chest computerized tomography (CT) ordered by her primary care physician for cancer screening revealed pulmonary nodules and an incidental mass in the tail of the pancreas. The patient also reported a 12-pound weight loss over the last 6 months, including five pounds in the last month, as well as frequent night sweats. She denied other constitutional symptoms such as fever, malaise, chest pain, shortness of breath, or abdominal pain.
The patient’s past surgical history was significant for hysterectomy, lithotripsy, and laparoscopic cholecystectomy. Home medications included ramipril, torsemide, atenolol, amlodipine, hydralazine, rosuvastatin, glipizide, mirtazapine, and oxycodone/acetaminophen.
The patient had a 58 pack-year smoking history with occasional alcohol and marijuana use. She described herself as “functional”, but she was not able to walk long distances, carry heavy bags, or perform strenuous house-work. The patient was able to climb four flights of stairs but was limited by bilateral thigh and knee pain. She had never performed a cardiac stress test.
On physical examination, the patient’s BMI was 22.7 kg/m2. Vitals were significant for hypertension at 177/110 mmHg and tachypnea at 27 breaths/minute. Pulse oximetry revealed oxygen saturation of 98% on room air. The patient was afebrile with a temperature of 98.2° F and had a heart rate of 70 beats/minute. Her examination also revealed well healed Pfannensteil and laparoscopic scars. The abdomen was soft and nontender. She was admitted for a pancreatic mass with new onset hemoptysis.
Laboratory values are in . Bloodwork was significant for brain natriuretic peptide (BNP) of 91 pg/mL, Carbohydrate Antigen 19–9 of 2572 U/mL and Calcium of 11.8 mg/dL. Pulmonary was consulted for hemoptysis and the patient underwent bronchoscopy with bronchioalveolar lavage which revealed normal vocal cords and no endobronchial lesions or masses. She also underwent CT of the chest, which revealed stable pulmonary nodules within the bilateral apical regions, as well as persistent scarring, mild fibrosis at the right lung base with mild paraseptal and mild/moderate centrilobular emphysematous changes. Evidence of dilation of the main pulmonary artery was also observed, suggestive of pulmonary arterial hypertension. Abdominal CT revealed a non-contrasting pancreatic mass at the tail of the pancreas with solid and cystic components, as well as nephrolithiasis.
On hospital day 2, subsequent fine needle aspiration of the pancreatic mass revealed pancreatic adenocarcinoma. Upper endoscopic ultrasound of the pancreatic mass revealed a hypoechoic homogenous lesion in the tail of the pancreas that was invading the spleen. The surgical service kept the patient informed of the results of the work-up and extent of the disease. Consults were placed to the Oncology, Cardiology and Medicine services. A decision was made for distal subtotal pancreatectomy, possible splenectomy, left nephrectomy, and left adrenalectomy.
As part of the pre-operative risk assessment an electrocardiogram (ECG) was obtained which revealed sinus bradycardia, possible left atrial enlargement, left ventricular hypertrophy, and T-wave abnormality consistent with anterolateral ischemia (inverted T waves on leads V3-V6, flattened T waves in V1–2). 2D-echocardiogram revealed a left ventricular ejection fraction 65%, grade 1 diastolic dysfunction, trivial mitral valve regurgitation, aortic valve calcification, and pulmonary artery hypertension at 25 mm-Hg.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [71, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 71 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
888,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6592466-1,Extracted,"A 65-year-old male with end-stage heart failure presented with worsening shortness of breath for the past month. He had a history of atrial fibrillation and ischemic cardiomyopathy and was currently on milrinone infusion and post-CRT-D placement. At the time of admission, his vital signs were within normal limits. The physical exam was most notable for an elevated jugular venous pressure (JVP) up to the angle of the jaw and decreased breath sounds on the left side of the chest. A chest x-ray showed a large left-sided pleural effusion as shown in Figure . Initial escalation of diuretic therapy led to acute kidney injury. During right heart catheterization (RHC), the operator reported apparent right internal jugular vein (IJV) thrombosis based on an ultrasound exam. After cannulation of the left IJV and upon contrast injection, complete occlusion of the left subclavian vein was noted. RHC via femoral access revealed normal right heart filling pressure (right atrial pressure 6 mmHg), normal pulmonary capillary wedge pressure (10 mmHg), and decreased cardiac index (1.94 L/min/m2). Next, ultrasound evaluation of the right subclavian vein showed partial thrombosis. The patient was already on therapeutic anticoagulation for atrial fibrillation, so this treatment was continued to treat the subclavian deep vein thrombosis.
The left-sided pleural effusion noted at admission was evaluated via diagnostic thoracentesis; this yielded 2 L of cloudy fluid, so a pigtail catheter for continuous drainage was placed. The pleural fluid studies were normal with the exception of triglycerides (1177 mg/dL), which was consistent with chylothorax. Because of continued high output (1-2 L/day) from the chest tube, the patient was started on a low-fat diet.
Next, a venogram was used to assess for venous obstruction as a possible cause of the chylothorax. The venogram revealed occlusion of bilateral brachiocephalic veins as shown in Figures -. The occluded right brachiocephalic vein was successfully recanalized after angioplasty using a 12 mm balloon as shown in Figure . However, CRT-D wires prevented intervention on the left brachiocephalic vein. After this intervention, chest tube output decreased to a negligible amount, so the tube was removed.
For the next five days, the patient was monitored with serial chest x-rays, but there was no reaccumulation of pleural effusion as shown in Figure . Therefore, we decided not to intervene upon the left brachiocephalic vein thrombosis. The patient was eventually discharged home on apixaban.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [65, 'years'], 'Congestive Heart Failure': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
889,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8445045-1,Extracted,"A 76-year-old man with a history of atrial fibrillation and age-related macular degeneration treated with intravitreal injection of angiogenesis inhibitors was diagnosed with disseminated colorectal adenocarcinoma. During the course of the disease, he attended the emergency department due to an episode of acute pain, with loss of vision in his left eye. The eye examination revealed a narrow anterior chamber angle with irido-trabecular apposition and an intraocular pressure of 34 mm Hg. A diagnosis was made of acute glaucoma and an MRI was requested, this revealing retinal detachment with subretinal haemorrhage and a nodular image in the temporal field that suggested that the differential diagnosis should include haemorrhagic metastasis, choroidal melanoma and blood clot.
The patient finally died and a post mortem examination of the left eye was performed.
The eye was enucleated and fixed in 4% formaldehyde. Then a first cut was made sagittally from the anterior pole to the optic nerve, revealing a heterogeneous lesion that occupied the entire volume of the vitreous body, composed of tissue with a devitalised fibrous appearance and haemorrhagic content (Figure A). Subsequently, several cuts were made parallel to the first; the tissue was embedded in paraffin and histological sections were taken with a microtome. These sections were stained histochemically (haematoxylin-eosin, PAS and Masson's trichrome stain) and immunohistochemically for analysis of stem cells (Sox-2), cellular senescence (p16), inflammatory cells (CD-68), vascular endothelium (CD-31) and glial cells (GFAP).
The choroid, below the sclera, did not show any significant lesions except near the optic papilla or blind spot, where some signs of fibrosis were observed. On the other hand, the histological structure of the retina had mostly disappeared except at certain points on the periphery (ora serrata), where there were still some cells. Only the retinal pigment epithelium was almost fully intact. Between this structure and Bruch's membrane, staining (PAS positive) revealed abundant drusen (Figure B). There was even dense collagenous connective tissue extending along the curvature of the retina seeming to take its place (Figure C). In several places, the retina had detached from the choroid and adhered through the pigment epithelium to loose connective tissue with abundant capillary vascularisation and extensive haemorrhage (Figure D). In these tissues, there was notable expression of the marker of cellular senescence p16INK4 (Figure E), both in the fibroblastic and the endothelial components of the neoformed capillaries. Along with these lesions, there was an inflammatory exudate which mainly contained macrophages, many of which were loaded with haemosiderin (Figure F).
At the level of the optic papilla, we found a glial scar (Figure G) in highly vascularised connective tissue. Its cells expressed a marker of neural stem cells, Sox-2, which was also observed in the peripheral retinal remanent. This was not observed, however, in the rest of the tissue with fibrosis and haemorrhage (Figure H).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [76, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
890,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3766558-1,Extracted,"A 48 years old woman, mother of two children with normal menstruation and insignificant prior history, presented with abdominal pain. Ultrasound examination and MRI of the abdomen revealed a solid mass, 20 cm of maximum diameter in the pelvis (), with no sign of peritoneal or nodal metastasis. Tumor markers were negative. The patient underwent laparotomy, and intraoperative gross inspection confirmed the presence of a solid mass originating from the mesentery. A uterine tumor with maximum diameter of 6 cm was also inspected. The mesenteric tumor was completely excised and was followed by frozen section examination which revealed a spindle cell neoplasm. Nuclear atypia, increased mitotic index, or tumor cell necroses were not observed. Because of the coexistence of the uterine tumor, hysterectomy with bilateral adnexectomy was performed. Infracolic omentectomy was also performed, and peritoneal biopsies were taken. Thorough counseling was made, and informed consent was taken preoperatively from the patient concerning the possibility of hysterectomy.
Paraffin-embedded sections of the mesenteric tumor revealed that it was a smooth muscle tumor, composed of anastomosing fascicles of smooth muscle cells with no atypia, mitosis, or tumor cell necrosis. Immunohistochemically, the smooth muscle cells were positive for SMA and desmin and negative for CD117 (Figures and ). Peritoneal biopsies and omentum were disease free. The uterine tumor was a typical benign leiomyoma.
The patient was discharged four days later. The postoperative course was uneventful. Because of the dilemma regarding the biologic behavior of the mesenteric tumor, long-term close followup was decided. Nine months after surgery, no recurrent disease has been noted.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [48, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 48 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
891,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5682885-1,Extracted,"A 55-year-old man with known longstanding hypertension and diabetes mellitus type 2 presented with acute onset of dizziness, slurred speech, and unsteady gait. On admission, his blood pressure was 178/100 mmHg and heart rate was 92 beats/min. He was dispirited but oriented. Additionally, he did not take the initiative to speak but could answer simple questions in a whisper with a few words. Neurological examination revealed severe dysphagia, dysarthria, mild tetraplegia (Medical Research Council Grade 4-5), and ataxia of the trunk and all four limbs. Pupillary reflexes and extraocular movements (both vertical and horizontal) were intact. Bilateral Babinski signs were positive. Meanwhile, he also showed spasmodic crying and laughing on examination. Magnetic resonance imaging (MRI) of the brain performed 36 hours after the onset of symptoms revealed acute, bilateral, symmetric, cerebral peduncular infarcts (BCPI), which showed increased signal intensity on diffusion-weighted imaging (DWI) with low values on apparent diffusion coefficient (ADC) map (Figures and ), in line with acute infarction. T1-weighted images (T1WI) demonstrated the lesion mainly involving the central portion of the cerebral peduncle with low signal intensity (). Magnetic resonance angiography (MRA) disclosed the vertebrobasilar artery occlusion and the absence of flow signals of bilateral PCA without collateral patency of the posterior communicating artery (). The patient was given antiplatelet and hypervolemic therapy, with no further deterioration of his condition. He was transferred to the rehabilitation ward for rehabilitation treatment of swallowing function twenty days after his admission.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [55, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 55 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
892,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5070336-1,Extracted,"A 44-year-old male patient presented with weakness of the left upper limb which improved over 24 h. There was no history of weakness of other limbs, speech disturbance, seizures, or loss of consciousness. No history of any other comorbid illness. Three months back, he gave a history of similar left hand weakness which had improved spontaneously. He has been a chronic smoker for last 15 years. No history of drug abuse. On examination, pulse rate - 88/min; blood pressure - 114/70 mm of Hg; cardiovascular system - S1 and S2 well-heard, and no murmur; central nervous system - no focal neurological deficit; electrocardiogram (ECG) T-wave inversion with downward ST sloping in V1–V4 suggestive of old anterolateral myocardial infarction (MI); two-dimensional echo - ejection fraction - 50%, apical septum and apex hypokinetic. Left ventricular (LV) mass one attached to the apex and another in the LV outflow tract (LVOT) were seen. Computed tomography brain revealed acute on chronic infarct in the temporal lobe. Ultrasonography abdomen was normal. Carotid Doppler was normal bilaterally. The rest of the routine investigations were within normal limit. Tumor markers such as carcinoembryonic antigen and others were negative. In view of transient ischemic attacks (TIAs) and free-floating LV mass, it was decided to excise the mass to prevent any catastrophic stroke. Intraoperative transesophageal echocardiography (TEE) Midesophageal four-chamber view showed two LV mass (a) measuring 3.8 cm × 1.9 cm attached to the left ventricle apex resembled a pedunculated tumor and (b) measuring 2.4 cm × 1.8 cm attached to the chordae of anterior mitral leaflet (AML) resembled a thrombus or an embolized tumor entangled between the chordae of the mitral valve. Both of them were homogenous, noncalcified, noncavitated, mobile; echodensity was similar to the myocardium. Apex was hypokinetic [ and ]. Midesophageal aortic valve long-axis view showed the mass attached to the AML was moving into the LVOT and obstructing the aortic valve [ and ]. The Continuous wave Doppler across the LVOT peak gradient - 7.5 mm of Hg and mean gradient - 3 mm of Hg showed there was no obstruction of the aortic valve []. Transgastric two-chamber and deep transgastric aortic valve long-axis view showed LV mass (a) attached to the apex and anterior wall and (b) attached to the AML extending into LVOT and obstructing the aortic valve [Figures and , Videos and ].
Surgical approach was through a midline sternotomy, cannulation was standard ascending aortic with bicaval venous cannulation, the minimum temperature was 32°C and using trans-left atrial approach masses were excised. Intraoperative findings were reddish white mass (a) measuring 4 cm × 2 cm × 1 cm attached to the LV apex and the anterior lateral wall and (b) measuring 3 cm × 1.5 cm × 1 cm attached to the primary chordae of the mitral valve []. Grossly, they resembled a benign tumor. Cardiopulmonary bypass (CPB) time was 48 min and aortic cross- clamp time was 32 min. Came off CPB without inotropes. Postexcision TEE showed a small residue attached to LV apex and the AML chordae. There was no injury to any of the chordae [Figures and , Videos and ]. Mitral valve was coapting well. The postoperative histopathological examination was suggestive of thrombi [].
Features favoring tumor are no history suggestive of coronary artery disease, normal angiogram; on echocardiography, echodensity similar to the myocardium, attachment to anterior wall, and gross appearance was similar to tumor probably due to fibrin deposition on the thrombus. Features favoring thrombus are history of smoking, ECG suggestive of old anterior wall MI, presence of wall motion abnormality on echo, and histopathological examination confirmed it as thrombi. Coronaries probably have recanalized after an MI 3 months back, during which he had the first episode of TIA. Postoperative patient recovery was uneventful and did not have any neurological deficit. He was discharged on the 6th postoperative day on oral anticoagulants and antiplatelet therapy.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [44, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': True, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 44 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 0 + 2 = 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
893,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4531953-1,Extracted,"A 54-year-old woman was admitted to our hospital complaining of intermittent palpitation which began 6 years ago and aggravated during the last 2 months. After the first symptom, she visited a local clinic and her symptom was managed under the impression of cardiac arrhythmia. But one year later, she discontinued anti-arrhythmic medication on her own. Until two months before admission, she had experienced intermittent palpitation again but it did not interfere with her life. Afterwards, palpitation became more severe suddenly and squeezing anterior chest tightness radiating to the left axilla developed and continued for about 10 minutes.
The patient was a housewife and had no history of smoking or alcohol consumption. There was no specific problem in her past medical and family history. The body temperature was 36.5°C and the heart beats were irregularr and rated over 140/min. On physical examination, mild moist crackling sounds were heard below a third on the back bilaterally. Neck vein engorgement was also seen. Considering the chest pain as ischemic in nature, nitroglycerin was given sublingually and the pain subsided. ECG showed atrial fibrillation with rapid ventricular response. Cardiomegaly with pulmonary vascular blurring and redistribution was seen on chest X-rays (). Other laboratory data, including cardiac enzymes and thyroid function tests, were within normal limits. Initially, cardiac tumor was not considered as the differential diagnosis. Transthoracic echocardiography, which was performed after her symptom had disappeared, showed normal global left ventricular systolic function (ejection fraction: 63%) with left ventricular enlargement and hypertrophy, and also showed trivial mitral regurgitation. On coronary angiogram, the left coronary arteries showed normal findings. But in the right coronary artery, we could find two tumor blushings which were supplied by a conus branch (). The one was on the right atrial side of the interatrial septum draining directly to the right atrium and the other was on the interventricular septum communicating with the coronary sinus via a large vein. The venous drainages of the tumor blushings could be seen simultaneously during the arterial phase. These two tumor blushings were measured about 18×10mm and 44×9.8 mm in length, respectively. These angiographic findings were compatible with the arteriovenous type of cardiac hemangioma. Left ventriculography and MRI failed to define the tumor masses. Retrospective video review of transthoracic echocardiography revealed no echogenic mass around the interatrial septum. We concluded that the patient had cardiac hemangiomas associated with atrial fibrillation",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [54, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 54 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
894,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6854615-1,Extracted,"A 41-year-old male was in good health until 2 weeks ago when he developed a left-sided renal colicky type pain and was diagnosed to have a left mid ureteric calculus by radiography. He was reassured and requested to consume plenty of water. Two days before, he had consumed excessive amount of water, about 10 l per day, and developed polyuria. During these 2 days, he has had fever, dark urine, generalized weakness and altered level of consciousness. On the day of admission, he developed a single episode of self-terminating generalized tonic-clonic seizure lasting for 5 min followed by reduced level of consciousness. There was no previous history or family history of adult-onset seizures. There were no features suggestive of psychiatric illness like low mood, reduced sleep or overtalkative behaviour. The patient was never transfused with blood or blood products. There was no recent travel history. He is married and has a 10-year-old child. He is an accountant by profession. The patient has had good income and family support. He occasionally consumed alcohol and smoked cigarette, but denied any drug abuse. He was not on any long-term medication. On examination, he was disoriented in place, person and time. The Glasgow coma scale (GCS) score was 9 on admission (motor—5, verbal—2, eye—2). Except for a temperature of 101 °F and the generalized diminished reflexes, other vital signs and cardiovascular, respiratory, abdominal and neurological examinations were normal. Table outlines the timeline of this case report.
This is a previously healthy male who presented with fever for 2 days complicated with generalized tonic-clonic seizure and reduced level of consciousness. In the acute setting, the first working diagnosis was meningoencephalitis. It could be due to viral or bacterial aetiology. Moreover, he had dark coloured urine; therefore, falciparum malaria which can led to cerebral malaria was also suspected. Collateral history from the patient’s family revealed an excessive water intake of about 10 l per day for 2 days which led to an additional differential diagnosis. One possibility is psychogenic polydipsia which is the most common cause for excessive water intake. However, there was no history of psychiatric illness or any long-term drug history which can lead to polydipsia. The reason for his excessive water intake was to get rid of the unpleasant pain due to the ureteric calculus.
On admission, he was found to have hypoosmolar (242 mOsm/kg of water), hyponatraemia (119 mmol/L), hypokalaemia (2.9 mmol/L), hypoosmolar urine (195 mOsm/kg of water), mild leucocytosis (12.7 × 103 per microliter) with neutrophilia and myoglobinuria. His serum creatinine phosphokinase (10,000 U/L) was markedly elevated with a rise in aspartate aminotransferase (AST) (2316 U/L) and alanine aminotransferase (ALT) (463 U/L) levels. Renal functions were within normal ranges. Blood for malaria parasite was negative. Non-contrast computed tomography scan of the brain was normal. Electroencephalogram done on the 5th day revealed generalized, continuous, slow activity suggestive of diffuse cortical dysfunction. This could be due to an encephalopathy preceded by hyponatraemia.
Hyponatraemia-induced generalized tonic-clonic seizure, altered level of consciousness and rhabdomyolysis were diagnosed in our patient. His hyponatraemia was most probably due to excess water intake. The patient was given a bolus of 3% hypertonic saline (100 mL over 20 min) for symptomatic severe hyponatraemia []. The diagnosis of rhabdomyolysis was made because he had body aches, dark urine, elevated levels of creatine kinase and urinary myoglobin. His serum creatinine phosphokinase peaked to the highest level (54,841 U/L) by the 7th day. Also, the patient’s elevated AST and ALT could be due to the muscle damage. As there was rhabdomyolysis, hypokalaemia correction was done once (KCl 40 mmol over 12 h) and serum potassium level was assessed regularly. Further doses of potassium were not required. A strict fluid restriction was not followed as there was a high risk of developing acute renal failure due to rhabdomyolysis. The input per hour was decided by measuring the previous hours’ output and adding 20 mL for the first 5 days. He did not develop oliguria or features of acute renal failure. Considering the history of fever and seizure with altered level of consciousness, he was started on intravenous cefotaxime (2 g 6 hourly), intravenous acyclovir (500 mg 8 hourly) and intravenous dexamethasone (2 mg 6 hourly) after collecting blood and urine for culture. However, the patient’s family denied consent for lumbar puncture. Blood and urine culture revealed no growth, but the antibiotics were continued for a total of 10 days as we could not exclude central nervous system infection without a lumbar puncture. The magnetic resonance imaging of the brain was normal on the 11th day of admission.
GCS score improved gradually to 15, and serum sodium and potassium were normalized by the 3rd day of admission. The patient did not have any further episode of seizure. His fever settled, and serum and urine osmolality were normalized by the 5th day. He responded to the above management and did not develop any complications of rhabdomyolysis. On discharge, his serum creatinine phosphokinase (49 U/L), AST (66 U/L) and ALT (78 U/L) levels were near normal. He was discharged on the 15th day of admission with appropriate medical advice to prevent similar complications.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [41, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 41 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
895,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8182662-1,Extracted,"A 79-year-old woman sought treatment at the emergency room for fever and fast-onset hip pain. She had full autonomy, and her medical history included
well-controlled non-insulin-dependent diabetes, hypertension, atrial
fibrillation, and a right hip fracture treated by total joint arthroplasty
10 years ago. Interrogation revealed no uptake of non-steroid anti-inflammatories or immunosuppressors and no alcohol abuse. Clinical examination revealed fever (38.5 C) and mild right hip pain without
limitation of the joint range of motion without erythema or swelling and with no sign of other arthritis. Cardiopulmonary auscultation, ear, nose and
throat (ENT) area, neurological testing, and the rest of the examination
were normal. Blood tests showed an increased neutrophil count (11.300 mm), decreased lymphocyte count (600 mm), and increased CRP
(90 mg L) without renal or hepatic dysfunction.
The patient was first admitted to the orthopedic department and later on to
the infectious diseases unit of a reference center since blood cultures were
positive for NTHi after matrix-assisted laser desorption ionization–time of flight (MALDI-TOF) analysis on bacterial isolates. The strain showed
susceptibility to ciprofloxacin with a minimum inhibitory concentration (MIC) of 0.380 mg L, amoxicillin (MIC of 0.750 mg L), and cefotaxime (0.008 mg L). Two grams of cefotaxime every 8 h was initiated intravenously, with a good clinical and biological response. Joint aspiration of the right hip prosthesis was
unfortunately performed after the initiation of cefotaxime therapy, with 5 mL of a cloudy liquid showing visually increased neutrophil count (without
formula because of too many red cells) and sterile 14 d culture in solid and broth aerobic and anaerobic media. Polymerase chain reaction (PCR) could not performed because no liquid was kept after the patient transfer.
A plain X-ray of the right hip and tomodensitometry showed no sign of prosthetic infection or fracture. Transthoracic and transesophageal
echocardiography ruled out endocarditis. Nevertheless,
fluorine-18fluorodeoxyglucose positron emission tomography/computed
tomography (PET) scan showed intense fixations of the L4–L5 vertebras, the right iliopsoas (continuously as shown in other images), and right periprosthetic tissues (Fig. 1a), consistent with magnetic resonance imaging (MRI), which
showed an iliopsoas infiltration and epidural abscess-associated
spondylodiscitis (Fig. 1b and c).
Advanced interview revealed that right-eye conjunctivitis had occurred 2 weeks before this episode. Sinus computerized tomography (CT) and MRI revealed a
right ethmoido-orbital mucocele responsible for lysis of the medial orbital
wall but not the anterior cranial fossa (Fig. 1d). To release the
osteolytic pressure, allow bone reconstruction, and avoid further
complications, naso-endoscopic surgery was performed (after a normal
ophthalmologic examination was confirmed) through a mid-turbinate and opened mucocele (Fig. 1e). It released a clear mucoid content on which
specific Haemophilus spp. PCR revealed a non-typeable strain. No sign of malignancy was
found on pathologic analysis.
Surgery was delayed due to the altered general state at the time of transfer. Prosthetic hip replacement following the antibiotic treatment was thus
decided on to ensure a fast rehabilitation after prolonged bed rest. The patient was treated with 12-week-duration antibiotic therapy of intravenous cefotaxime for 21 d followed by oral ciprofloxacin 750 mg
twice a day. The patient displayed full recovery, and no adverse event was noted.
No additional immunodeficiency other than a mild lymphopenia was found: abdominal CT showed full hepato-splenic integrity, no Howell–Jolly bodies
were found, and complement exploration, lymphocyte immunophenotyping, serum protein electrophoresis, quantitative immunoglobulin assay, and IgG
subclasses showed no other abnormalities.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [79, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': False, 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 79 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
896,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7717027-1,Extracted,"A sixty-one year old man, came to our emergency department because of a long episode of chest pain. He had a story of hypertension, hyperlipidaemia under statin therapy, type II diabetes mellitus treated with oral hypoglycaemic therapy, and he was a smoker in the past. He referred previous saphenectomy and haemorrhoidectomy operations, no other comorbidities.
He reported, for several days, the appearance of episodes of chest pain in the back that occur at rest for about five to ten minutes each
The first ECG showed sinus rhythm with ST segment depression in leads V2-V6, not evident at the repeated ECGs done in the absence of chest pain.
Repeated cardiac enzymes (CK-MB fraction and Troponin I) were slightly elevated with a typical trend (peak values CK-MB 23,7 ng/dl; Troponin I 4,83 ng/dl).
Echocardiographic (ECO) evaluation showed good right and left ventricular global function with ipo-akinesia of postero-lateral medium-basal wall. Non valvular diseases.
After the diagnosis of acute coronary syndromes (NSTE-ACS) non-ST-Segment Elevation the patient was admitted to hospital for the evaluation of suspected coronary artery disease and began a pharmacological anti-ischemic therapy complete with Ticagrelor 180 mg loading dose e, second ischemic and bleeding risks, fondaparinux (2.5 mg sc per day).
Twenty hours from hospital admission, the patient was referred to the haemodynamic laboratory and a coronarography was performed via right radial artery approach. Angiography revealed small left anterior descending with diffused luminal irregularities, not significant stenosis, intermediate artery of small calibre, with 99% proximal stenosis; normal Circumflex artery; right coronary artery, dominant, without stenosis.
In view of this and in agreement with the patient, it was decided to attempt interventional revascularization and stenting of the intermediate artery. An Ipercoat run-through guide wire was chosen for revascularization.
Pre-dilatation with Maverick 2 x 20 mm (8 ATM) balloon was done and the artery was stented with Supraflex 2 x 16 mm (14 ATM).
Finally post-dilation with Hiryu 2,25 x 10 mm balloon was done.
Angiography after wire retraction demonstrated a small depot of contrast evolving around the stented vessel segment, referred to coronary perforation of distal tract of third branch of intermediate artery.
The operator decided to achieve the haemostasis by sealing the coronary artery perforation with repeated balloon inflations lasting 5 minutes for each one. Administration of protamine for heparin neutralization, was prescribed. A later angiographic control displayed disappearance of images related to perforation, TIMI 3 flow.
ECG did n’t shows new ischemic changes
An echocardiography exam showed slight, stable, pericardial effusion.
Due to stable haemodynamic condition the patient was transferred to the coronary care unit, but the following hours the patient had a sudden haemodynamic evolution with a drop of blood pressure and increase of heart rate. An echocardiography exam revealed a severe pericardial effusion with compression of the right ventricle.
This situation was initially managed with rapid volume supply and vasopressor to maintain sufficient end-diastolic right atrial and ventricular pressure.
During the pericardiocentesis, sudden cardiac arrest occurred due to asystole, which required cardiopulmonary resuscitation. The ACLS protocol was performed for 15 minutes, with the administration of Epinephrine 3 mg which involved ROSC.
Pericardiocentesis, by a subxyphoid approach, was then performed emergently at patient’s bed and 500 ml of blood was removed from the pericardial space. Echocardiography was repeated 10 minutes later, having found a new pericardial effusion despite pericardial drainage. Due to persistent haemorrhage and progressive hemodynamic collapse an urgent surgery management was required .The pericardium was opened via median sternotomy and a significant amount of clot and blood was removed (about 1,5 L) with immediate hemodynamic benefit. Exploration showed an intramural ventricular haematoma of the inferior-lateral wall (site of coronary perforation) of the left ventricle with parietal haemorrhagic infarction.
Extracorporeal circulation (CEC) and cardioplegic arrest with ante-grade hot blood cardioplegia was done.
A composite Dacron with autologous pericardium patch (Resorcinol-Formol type glue) was used for left ventricular free wall rupture repair and the geometry of the left ventricle was restored. Subsequently aorta was declamped; the patient was weaned from CEC with a good haemodynamic recovery.
The postoperative evolution was characterized by bilateral decline of visual acuity. Angio-CT cerebri was negative for alteration of intracranial vessels. Retinal fluoroangiography and computerized optical tomography (OCT) were also negative for retinal ischemia and other alterations. Encephalic RMN didn’t detect significant changes. In the following days the patient showed progressive improvement and slow recovery of visual capacity. No complex arrhythmic events have been recorded and good ventricular global function was maintained. The patient was then discharged after twenty days of hospitalization and started cardiovascular rehabilitation.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [61, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': True, 'Diabetes history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 61 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
897,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8565713-1,Extracted,"We present the case of a 65-year-old male patient, with ESRD, chronically dialyzed for 13 years; initially peritoneal dialyzed for 10 years, then, for the last 3 years, hemodialyzed on arterio-venous fistula, which presented a lipothymic episode, accompanied by palpitations and dyspnea. He was then diagnosed with newly installed atrial fibrillation (AF) that occurred intradialytic (K = 3.2mEq / l) and medium quantity pericarditis. The treatment was initiated for the rhythm disorder (antiarrhythmic, beta-blocker, oral anticoagulation - antivitamin K) and for the pericardial disease (anti-inflammatory - Ibuprofen). The patient has a background of cardiovascular pathology (old anterior myocardial infarction treated with revascularization of the anterior descending coronary artery for which he received antiplatelet therapy that was interrupted right after the initiation of Ibuprofen).
Five days after discharge, the patient has a new lipothymic episode, associated with hypotension: systolic blood pressure (SBP) =50 mmHg. On admission, the patient was anxious, he had regular heart beats, systolic murmur in the mitral position, breath sounds were soft on the inferior half of the left hemithorax, SaO2 (arterial oxygen saturation) = 95% with oxygen therapy on the nasal cannula, he had abdominal-type respirations, congestive hepatomegaly, grade 3 turgid jugular veins, pale teguments, and no lower limbs edema. Vasopressor therapy (positive inotropic agent - Dobutamine) was initiated and the SBP increased to 100 mmHg.
Laboratory findings revealed: RBC (red blood cells) = 2.00 10*12/L, Hb (hemoglobin) = 6.4 g/dL HCT (hematocrit) = 20.9%, WBC (white blood cells) = 5.82 10 * 9/L, PLT (platelets) = 263 10*9/L, INR = 16.6. Myocardial cytolysis and hepatocytolysis enzymes were initially within normal limits, subsequently TGO = 1459 U/L, TGP = 669 U/L, Creatinine clearance = 5ml/min/1.73m2 CKD-EPI.
The chest radiography showed medium left pleurisy, cardiomegaly and absence of pulmonary congestion.
The echocardiography shows a normal left ventricular cavity with moderate systolic dysfunction because of the akinesia of the apical 1/2 of the septum, anterolateral wall, anterior wall and apex, associated with moderate mitral regurgitation. The pericardial effusion was circumferentially distributed (25.3 mm anterior to the right chambers, 11 mm posterior to the left ventricle), and it determined compression of the right atrium. ( and )
Diagnostic and evacuation pericardiocentesis was performed and 600 ml of hemorrhagic fluid was evacuated. Post-puncture, the effusion decreased by 10 mm and the patient’s condition enhanced, so the vasopressor therapy was stopped. The pericardial fluid was hemorrhagic with abundant blood mass and cells of venous origin, isolated and agglutinated platelet, Ht = 30%; proteins = 57 g/L, glucose = 49 mg/dL, amylase = 37 U/L, LDH = 2374 U/L, ADA (adenozin deaminaza) = 38 U/L.
Diagnostic and evacuation thoracocentesis was also performed, 900 ml of hemorrhagic fluid was evacuated (proteins - 38g/L, glucose = 120 mg/dL, amylase - 37U/L, LDH = 486 U/L, ADA = 25 U/L, cellularity - 3080 elements/mm3, tumor cells were absent).
The patient’s evolution was favorable giving the positive inotropic therapy, oxygen therapy, hemodialysis (HD) with ideal weight loss, blood transfusions, pericardium and pleurocentesis, which led to hemodynamic stabilization, anemic syndrome correction, and remission of pleural-pericardial fluid and hepatocytolysis",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [65, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': True, 'Stroke': False, 'Diabetes history': False, 'Transient Ischemic Attacks History': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
898,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2726533-4,Extracted,"A 67-years-old Caucasian man presented for refashioning of a left below-knee amputation stump. His co-morbidities included diabetes, cardiovascular disease, peripheral neuropathy, obesity and asthma. Medications included insulin, amlodipine, lisinopril, gabapentin and salbutamol. Previous regional block and general anaesthesia were uneventful. The patient made an informed choice of spinal anaesthesia. Standard perioperative monitoring was used. Spinal block was performed aseptically at the L4/5 spinal space with a 25 G Whitacre needle and 2.5 ml of heavy 0.5% bupivacaine plus diamorphine 300 mcg. The spinal block procedure was uneventful. Adequate motor and sensory block was achieved at five minutes. Adequate sensory block up to the T8 dermatome was confirmed by loss of cold sensation. The intraoperative course was uneventful. However, at the end of surgery, about 60 minutes after the spinal blockade, the patient complained of repetitive muscle spasm in the absent amputated limb. The phantom spasm was distressful to the patient and was promptly treated with intravenous midazolam 5 mg. There was no recurrence of myoclonus and no sequelae.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [67, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Vascular disease history': True, 'Diabetes history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 67 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
899,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6293186-1,Extracted,"An 85-year-old Caucasian male was admitted after sudden onset of expressive aphasia and weakness in both legs lasting 20 seconds. He was athletic, self-reliant and had no cognitive impairment. During the last 28 years, he had experienced 8-10 heterogeneous episodes of acute neurological symptoms, such as central facial palsy, hemiparesis, and non-fluent aphasia, lasting from seconds to 3-4 hours. Precerebral duplex and electrocardiography (ECG) were performed several times with normal results, and EEG registration and 24-hour Holter monitoring had been normal. Previous MRI scans showed no abnormal restricted diffusion, as seen in acute cerebral infarcts, but infarct sequelae in the left temporal lobe and both thalami. Several years later, three additional infarct sequelae were detected in the cerebellum. The patient was treated with platelet inhibitors, and medications and dosages were adjusted after new episodes. There was no suspicion of lack of compliance. Except from age, migraine, and previous smoking, with cessation 35 years ago, he had no known risk factors for cerebrovascular disease. On the current admission, he presented with reduced motor speed in his left arm and leg. Electrocardiography and Holter monitoring showed no signs of atrial fibrillation. CT and MRI revealed multiple, cortical infarct sequelae in the anterior and posterior circulation territories of both hemispheres, and MRI also detected two acute embolic infarcts in the right occipital lobe and one in the left parietal lobe (Figure ). CT and MRI angiograms and duplex sonography did not show significant plaques or stenoses, and pre- and intracerebral flow were normal with asymmetrical vertebral arteries, which were considered a normal anatomical variant. Cortical infarcts in several vascular territories strongly suggest cardioembolic etiology, but transthoracic echocardiogram showed no cardiac sources of emboli, and there was no sign of left atrial enlargement, which may be seen in the presence of atrial fibrillation. The patient concurred to further diagnostic tests aiming to determine the cause of recurrent cerebral emboli, although he was informed that the results would not necessarily alter treatment recommendations. We performed a transcranial Doppler (TCD) bubble test with 10 mL air-mixed saline injected into the left cubital vein while the left middle cerebral artery was insonated with a 2-MHz probe. Injection at resting state produced no microembolic signals, while injection after Valsalva maneuver resulted in a shower of microembolic signals followed by single signals persisting for over 30 seconds. The result implied the presence of a latent right-to-left shunt, and transesophageal echocardiography verified a large patent foramen ovale (PFO; Figure ). In agreement with the patient, we decided on non-operative treatment. Due to previous failure of antiplatelet treatment, we changed to a direct oral anticoagulant (dabigatran 110 mg twice daily), intended as a lifelong treatment. He had no subjective complaints at discharge.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [85, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': True, 'Transient Ischemic Attacks History': True, 'Vascular disease history': False, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 85 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
900,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6473795-1,Extracted,"The subject of the study was a 68-year-old male, left-handed and a native of a rural area in Lugo (Galicia, NW Spain). He was single and used to live with his mother until she passed away; he then lived alone until 2014, when he was admitted to a geriatric center close to his town. He has two brothers, a basic level of education, and his profession was agricultural worker.
The study was conducted in accordance with the Declaration of Helsinki. Written informed consent was obtained from the participant and the legal responsible.
According to the medical records, the patient presented arterial hypertension, hypertensive heart disease, paroxysmal atrial fibrillation, mild kidney failure, diabetes mellitus—type II, cholecystitis, confusional syndrome, dyslipidemia, anxiety disorder, inguinal hernia, and diffuse Lewy bodies dementia (LBD). The patient did not present toxic habits.
The documentation provided by the family in reference to the development, prior to being admitted into our gerontological center, shows an oscillating clinical course, with crisis and a negative development, with difficulties for a neuropsychiatric differential diagnosis and a clear therapeutic approach. In particular, the medical records from December 2014 show admissions in August and November of the same year in relation to “disorientation and behavioral disturbances evolving during these months”, with a hypothetic diagnose of VD vs. Parkinson disease (PD) and treatment with levodopa/carbidopa. During the same month, he showed extreme agitation and escaped from the geriatric center where he used to live. He was, therefore, examined by the Emergency Service of the Hospital Universitario de Lugo (HULA). The examination upon admission suggests that “he is disoriented in time and space, person oriented, hardly cooperative, he employs circumlocutions with partially incoherent speech, irritable, shaky, anxious and presents visual hallucinations”. Admitted in the Psychiatry Service of the same hospital, the examination shows “amnesia about his stay in the institution and about his hospital admission, incoherent speech. Lack of data about hallucinatory—delirious symptomatology. Sleeping and eating disorders. General sense of wellbeing, he ignores the reason for his admission. Unawareness of the disease”. Regarding the evolution in the hospital, the level of consciousness tends to fluctuate, with episodes of visual hallucinations without emotional response, relating situations and images with a high level of detail during periods of a few short minutes. These symptoms are presented without structured delusional ideation.
Following pharmacological adjustment, there is a gradual improvement of the visual hallucinations, but the patient still shows episodes of isolated irritability related to brief confusional states. The patient’s sleep pattern improves, but the noticeable cognitive impairment and functional dependency persists. Following pharmacological adjustment with quetiapine, 150 mg/day, there is a notable worsening of the symptoms of confusion and treatment is therefore suspended, maintaining olanzapine and tiapride.
The patient remains at the hospital for 24 days and, during that time, he is explored using additional tests. New pharmacological adjustment is done with the aim of decreasing the fluctuations in the level of consciousness, a remission of the visual hallucinations, and a decline in behavior alterations. He is referred to the primary-care center for follow-up, and it is recommended that he be re-admitted to a geriatric center, with a diagnosis of LDB in the presence of a progressive cognitive decline, consciousness fluctuations, visual hallucinations, and parkinsonism. Treatment using olanzapine is suggested, 5 mg/night/24 h, and tiapride, 100 mg/8 h. Lorazepam 1 mg is also prescribed, without signs of anxiety or insomnia. The following medications are kept: omeprazole 20, simvastatin 20, acetylsalicylic acid 100, bisoprolol 2.5, doxazosin 4, and insulin Lantus.
Consultation with the Neurology Service for physical examination, concludes that there are signs of rigid-akinetic parkinsonism and risk of falling. Blood test: dementia screening showed normal parameters in hematimetry and biochemistry. Human immunodeficiency virus (HIV) serology, syphilis, hepatitis B & C are negative. Electroencephalography with frequency analysis shows a “daytime NREM I wakefulness and sleep pattern with well-configured, symmetric, normoreactive, with no appreciable anomalies, neither under resting conditions nor during the activations performed. Signs of drowsiness”. Magnetic resonance imaging (MRI) scan includes “exploration performed in sagittal and axial planes in habitual sequences. There is a small spot of increased signal in T2 and flair in the subcortical white matter compatible with small vessel ischemic pathology. No recent ischemic pathology or other significant findings are evident”.
The patient is institutionalized and followed by external consultations with the Psychiatry Service, making adjustments to pharmacological treatment in accordance with the symptomatology. He visits the HULA emergency department as a result of behavioral changes and aggressive behaviors. At that time, he was treated with lorazepam 1 mg/24 h, olanzapine 15 mg/24 h, and clonazepam 1.5 mg/24 h. Tiapride solution is added in case of agitation.
Re-admitted to the Psychiatry Service due to an episode of agitation and aggression in the institutional environment. At that time, he was treated with rivastigmine 4.6 mg/24 h, clonazepam 4.5 mg/24 h, and clozapine 100 mg/24 h, given the therapeutic failure and the apparent paradoxical response with quetiapine, olanzapine, risperidone, haloperidol, and tiapride, in addition to the treatment for heart diseases and diabetes. During the hospitalization, the patient lacks awareness of the disease. He is restless, requiring physical restrictions and also hypoprosexic. No alterations are detected in the course or content of thought, although his spontaneous speech is not very fluid and is of a repetitive nature.
The pharmacological adjustment with rivastigmine 9.5 mg/24 h and the decrease in clonazepam due to somnolence, associated with clozapine up to 150 mg/24 h, seems to partially improve the BPSD, although the presence of low-grade fever and leukocytosis suggest the progressive withdrawal of clozapine. Gabapentin 400 mg/24 h is introduced in order to mitigate the psychomotor restlessness and behavioral alterations, with an excellent response, leading to a referral to the geriatric center where he remained until his transfer to the current gerontological center. On the day of his referral, the treatment continued with rivastigmine 9.5 mg/24 h, lorazepam 3 mg/24 h, trazodone 100 mg/24 h, clonazepam 1 mg/24 h, and gabapentin 400 mg/24 h.
During the following 6 months, there are oscillations in his cognitive functions and in his CBs, presenting nocturnal agitation, wandering, and disorganized motor behaviors, hostility, insomnia, anxiety, as well as hyperorality, constant verbalization related to food and sexual disinhibition. This symptomatology demands modifications in the pharmacological treatment with variable responses. At the end of November, he is evaluated by the Psychiatry Service, which prescribe rivastigmine 9.5 mg/24 h, trazodone 100 mg/24 h, clonazepam 1 mg/24 h, olanzapine 10 mg/42 h, and quetiapine 100 mg/24 h, withdrawing lorazepam and gabapentin.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [68, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': False, 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 68 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
901,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8269993-1,Extracted,"A 57-year-old female admitted with a history of difficulty in swallowing, shortness of breath, and hoarseness. Her personal medical history has included diabetes mellitus, hypertension, hyperlipidemia, atrial fibrillation, and familial mediterranean fever while her family history, her sister, who was comprising differentiated thyroid carcinoma, papillary thyroid carcinoma, underwent total thyroidectomy with a subsequent RAI ablation. Her vital signs were recorded within normal limits and she had no history of radiation exposure in the first two decades of her life. She was in a euthyroid hormonal status with chronic lymphocytic thyroiditis, compatible with the relevant levels of thyroid antibodies. A physical examination at the time of admission revealed a multinodular goiter with a prominent palpable firm nodule of 25 x 20 mm at the left lobe inferior.
Diagnostic imaging
Her neck B-Mode sonography exposed the multiple nodules, the larger of which in the left lobe inferior, hyperechoic solid nodule of 26 x 20 mm in diameter with well-demarcated hypoechoic halo, without able to detect its most proximal border. The neck magnetic resonance imaging (MRI) revealed a multinodular goiter with the largest nodule, 24 x 20 mm in diameter, in the left lobe inferior, expanding retrosternally while her thorax MRI put forward the left lobe was descending to the left brachiocephalic vein and the trachea was displaced to the right. Her video laryngoscopy revealed no pathologic finding (Figures , ).
Surgical procedures
A total thyroidectomy by the collar incision without a median sternotomy with I-IONM and the energy-based device was decided in order of facing with symptomatic substernal goiter, including the bilateral multiple nodules, that did not extend beyond the left innominate vein proximally, such the vital organs like as the arcus aorta. The informed consent was received for both her treatment and the present article, preoperatively. To this end, it was practiced on the ‘Iowa Head and Neck Protocols for Thyroidectomy and Thyroid, Iowa, the US' [] for most of the surgical procedures. For these purposes, she was brought to the operating room and placed on the operating table in the supine position. She was then transorally intubated and a skin crease incision was designed and drawn at one fingerbreadth above her clavicles. Thereafter, a shoulder roll was placed behind the scapulae and a mini roll behind the posterior aspect of the neck, then her hyperextended neck was prepared with chlorhexidine and draped in a sterile fashion. A 15-blade scalpel was used to perform the planned and drawn beforehand Kocher's transverse collar incision, which was carried down through the platysma to the level of the strap muscles of the neck, after administrating the agents of lidocaine 1% and epinephrine 1:100,000 into the incision line. The subplatysmal flaps were subsequently elevated through accessing its avascular space and underlying areolar tissue plan. Paying attention to the preservation of the anterior jugular veins, the strap muscles were split in the midline raphae, the linea alba cervicalis, the fascia of sternothyroid muscle was divided, and the capsular blood vessels of the gland were pointed out. After constituting a proper cleavage plan, the sternothyroid and sternothyroid muscles were retracted laterally to the gland, leading to the thyroid were explored without being supposed to dissection of the strap muscles. Firstly, the left middle vein was explored and divided to be able to provide safe and bloodless maneuvers of the left lobe of the gland. In dissecting around the left superior pole of the thyroid, the branches of the left superior thyroid artery and left superior thyroid vein were dissected separately in order not to harm the left superior laryngeal nerve, and the left superior parathyroid gland was revealed and was dissected away from the lobe. The thyroid gland was then retracted anteriorly and medially in order of facilitating the exposure of the left tracheoesophageal groove. The left inferior thyroid artery was exposed and the left recurrent laryngeal nerve (RLN) was identified and preserved by using its present anatomic association, i.e. crossing it posteriorly. The mentioned situation was also confirmed by I-IONM. The gland was then retracted superiorly and laterally in order of releasing the left inferior pole. Charles Proye’s Toboggan Technique was used to facilitate the dissection and retraction out of the left inferior lobe from the surgical bed by slackening its remaining attachments and division of the left inferior thyroid veins. Herewith, the left inferior parathyroid gland was exposed and preserved. The thyroid was carefully examined after the removal process with LigaSure Small Jaw (LSJ) (LF1212A) in order of being convinced for not harboring any evidence of parathyroid tissue on it. Afterwards, the right side was dissected and spared in a similar fashion with the relevant exposures of the branches of right superior thyroid artery and right superior thyroid vein, right superior laryngeal nerve, right superior and inferior parathyroid glands, right inferior thyroid artery and vein, and right recurrent laryngeal nerve (RLN) by using LSJ (LF1212A) and I-IONM. Both the RLNs, per se, were not lying over the enlarged gland as being possible in case of a substernal goiter. What follows both thyroid lobes with the isthmus and pyramidal lobe were resected with the aid of the I-IONM and energy-based device, the mini roll behind the posterior aspect of the neck was removed in order to attenuate the collar tension, then the wound was profusely and meticulously irrigated with the sterile saline and the relevant haemostasis was provided. The mentioned field of the surgical procedure had preserved till the anesthesiologist recognized the positions of the vocal cords. Meanwhile, the entire gland was examined carefully, particularly whether harboring any parathyroid gland/tissue or not. While no evidence of any parathyroid gland/tissue and lymphadenopathy in the level VI, cervical compartment, was notified, a 15-French Jackson-Pratt drain was inserted and secured to the skin with 3-0 non-absorbable suture. The wound was closed by reapproximating the strap muscles and platysma with deep 3-0 vicryl stitches while the skin by a running 5-0 monocryl subcuticular continuous stitch with the benzoin and steri-strips, placing over the collar incision. Eventually, she had tolerated the procedure well and extubated in the operating room uneventfully. Herein, she transferred to the post-anesthesia care unit, subsequently. No intra-, peri-, and postoperative complications and/or morbidity have developed. Ultimately, she demonstrated improved symptoms and discharged home on the hospital day one.
Histopathologic evaluations
Macroscopically, the three colloid-rich nodules, 24 x 20 x 20 mm in diameters, at the right lobe and one colloid-rich nodule, 38x26x24 mm in diameter at the left lobe of the gland were exhibited. Microscopically, the nodular architecture, entirely enveloped by thin fibrous capsule including the pale staining cuboidal cells with round inconspicuous nucleoli and in micro- and macrofollicular patterns without mitose and the extensive lymphocytic infiltrate with germinal center formation, atrophic follicles together with Hürthle cells, fibrosis, not extending beyond the capsule were revealed. Immunohistochemically, Hector Battifora Mesothelial-1 (HBME-1), Cytokeratin-19 (CK-19), and Galectin-3 negativity emerged. Herein, the ultimate histopathological diagnoses of the case revealed Hashimoto’s thyroiditis, adenomatous hyperplasia, and two reactive lymph nodes at the central compartment, VIth cervical compartment.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [57, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 57 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
902,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8230156-3,Extracted,"A 83-year-old woman underwent mitral and aortic valve replacement in 2014, for severe mitral regurgitation and concomitant moderate aortic stenosis; She received an Epic(St Jude) n.31 bioprosthesis in mitral position and an aortic Mitroflow n.21. She suffered also from Stage IV chronic kidney disease and paroxysmal AF. Initial Mitroflow degeneration was noted at first during ambulatory TTE in March 2019, showing mild-to-moderate intraprosthetic regurgitation, and normal LV EF. The patient was admitted to our cardiac intensive care unit for acute heart failure in October 2019. Blood pressure was 110/45 mmHg, electrocardiography showed atrial flutter with ventricular heart rate of 110 bpm. She had severe leg swelling, right pleural effusion, and respiratory failure. Blood tests documented worsening of renal impairment and mild anemia. Noninvasive ventilation and extracorporeal ultrafiltration were required. Sinus rhythm was restored through electrical cardioversion. TTE and TOE showed severe aortic intraprosthetic regurgitation due to prolapse of the anterior cusp (aortic peak and mean gradients: 20/10 mmHg; vena contracta: 6 mm; holodiastolic flow reversal in the distal aortic arch); severely dilated LV with severely reduced EF (31%); and normal function of the mitral biological valve. Five days later, clinical conditions were improved, but the patient was still oliguric and dependent on UFH. A new TTE confirmed severe AR and severely reduced LV EF. Surgical re-operation was judged at high risk. CTA showed the feasibility of ViV TAVI through the right femoral artery. The procedure was successfully performed (with a Medtronic Evolut R 23 mm device), without major complications, and no significant peri-prosthetic leaks []. Coronary angiography performed just before valve delivery showed no significant stenoses. The patient had immediate improvement of hemodynamics, and restart of effective diuresis was achieved. At 3-month follow-up, she was in good general conditions; TTE showed no significant aortic stenosis (peak and mean gradients: 21 and 11 mmHg), decrease in LV volumes, and improvement of EF (to 48%).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [83, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 83 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
903,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6182280-1,Extracted,"A 68-year-old woman with a history of diabetes mellitus, living-donor renal transplant on current immunosuppression, and compensated cirrhosis secondary to hepatitis C genotype 1a presented for esophageal variceal surveillance. The patient had no history of variceal bleeding, encephalopathy, or ascites. Liver function indices were unremarkable. Upon her first endoscopy [], large columns of varices were found with high-risk stigmata of a red wale sign, and 5 bands were applied successfully. She presented to us for her third session of surveillance and 3 additional variceal bands were applied (, ; before and after banding). Immediately after the procedure the patient could not swallow any liquids or secretions, with persistent spitting up of saliva admixed with small streaks of blood. Viscous lidocaine mixed with water failed to provide any relief. The patient was admitted for observation with nothing by mouth. Sucralfate was started along with proton-pump inhibitor therapy. By the second day, the patient was still unable to swallow any liquids including her own saliva. A barium esophagram showed complete obstruction of the distal esophagus (). Repeat esophagogastroduodenoscopy (EGD) the following day showed pooling of saliva in the distal esophagus, which was suctioned, along with necrotic and ulcerated esophageal mucosa at the base of the banded varices causing complete luminal obstruction (, ). We grasped the 3 bands with the hook of an endoloop cutter (Olympus America, Melville, NY, USA) (, ), and the bands were removed intact from the base of necrotic varices one-by-one without any bleeding. This restored the esophageal lumen () and led to resolution of symptoms. The patient was discharged home the following day tolerating a regular diet. Upon follow-up endoscopy, scars were seen in the area without any varices.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'age': [68, 'years'], 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False, 'sex': 'Female'}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 68 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
904,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8489795-1,Extracted,"A 78-year-old Caucasian woman presented with acute-onset dysarthria for 2-3 hours. Physical examination was unremarkable except for dysarthria. Vitals signs were normal. She had a past medical history of type 2 diabetes, coronary artery disease, chronic kidney disease, hypertension, and hyperlipidemia. She was admitted four months ago with symptoms of perioral numbness and underwent a full neurologic and cardiologic workup for stroke, which was negative for any significant findings. Subsequent transesophageal echocardiogram (TEE) revealed two MV pedunculated masses, clinically labeled as fibroelastomas. The patient was started on medical management with dual antiplatelet therapy (DAPT) instead of surgery. ECG obtained revealed normal sinus rhythm. The CT scan with and without contrast was negative for acute mass effect or bleeding. The TEE revealed two pedunculated masses that arise from the annulus by the medial side of P2. The larger mass measured 1.0 x 0.7 cm and the smaller one measured 0.5 x 0.5 cm (Figure ). The MV masses were again suspected to be fibroelastomas with no changes since the last visit. The MRI of the brain found several punctate acute microinfarcts within the left frontal lobe and the bilateral occipital lobes without large territorial infarct, mild-moderate small vessel ischemic degenerative changes, and parenchymal volume loss (Figure ). The magnetic resonance angiogram (MRA) of the brain and carotid arteries did not demonstrate any large vessel occlusion, flow-limiting stenosis, or aneurysm. The patient did not have any cardiac telemetry events during the hospital stay. The differential diagnoses after the initial workup included benign papillary fibroelastomas, myxomas, and vegetations secondary to infective endocarditis.
The patient underwent open thoracotomy for resection of MV masses. During surgery, an inspection of the MV showed 1.5 x 0.5 cm and 0.5 x 0.5 cm calcified lesions along the annulus. These lesions were excised and sent for pathology. Interestingly, the histopathology examination reported it as a cavernous hemangioma (Figure ). The patient was discharged home without any postoperative complications. Follow-up TEE in six months showed no regrowth of tumors.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [78, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 78 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
905,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6919405-1,Extracted,"A 59-year-old female presented our hospital for investigation and treatment of a sudden onset of syncope lasted about 2 minutes. She did not have significant past medical history and had taken no medication, and her physical examination was unremarkable. The head computed tomography scan revealed lacunar infarcts, and magnetic resonance imaging showed no evidence of severe stenosis or occlusion in intracranial and carotid arteries. Electrocardiogram showed normal sinus rhythm, and laboratory results were almost within normal limits. Transthoracic echocardiogram revealed a hyperechoic irregular solid structure arising from the opening of the left inferior pulmonary vein and protruding into the left atrium, and the cardiac structure and function were otherwise almost normal (Fig. ).
She was scheduled for elective resection of this mass. Median sternotomy was performed and cardiopulmonary bypass was established via aorto-bicaval cannulation. The left atrium was incised and a 10 × 15 mm mobile, gelatinous mass was found. The mass was resected en bloc along with the stalk and surrounding tissue of the left atrial wall. On gross examination, the tumor was grey-white and soft, and appeared frond-like and translucent when submerged in liquid. Postoperative histopathologic examination showed that the mass was composed of branching avascular papillary fronds lined by a layer of endothelial cells with variable amount myxoid change, collagen, smooth muscle cells and elastic fibers, leading to the definite diagnosis of papillary fibroelastoma (Fig. ). The patient's postoperative course was uneventful, and she was discharged 10 days after surgery. The patient remained free of neurologic deficits and had no evidence of residual or recurrence of tumor with echocardiography during 1 year of follow-up.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [59, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 59 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
906,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8093088-2,Extracted,"A 62-year-old male patient was admitted to the hospital with complaints of aggravated dyspnea during exercise and dizziness. Three years before his admission, he received an artificial pacemaker because he was suffering from sick sinus syndrome. A physical exam noted pitting edema on both of his legs. He weighed 80.45 kg at admission while his healthy body weight was 74.5 kg. Echocardiographic assessment revealed regional wall motion abnormality (RWMA) and an enlarged LA and LV and decreased LV systolic function with an EF of 47%. He was diagnosed with dilated cardiomyopathy. A cardiac positron emission tomography-computed tomography scan confirmed that he had cardiac sarcoidosis, so he was prescribed steroids. He was discharged from the hospital on day (HOD) #10 with plans to titrate steroid doses in an outpatient clinic.
He attended the group session for HF patients before being discharged and revisited the clinical dietitian twice after being discharged. His usual nutritional intake and anthropometric measurements are presented in and . He usually ate 3 meals regularly throughout the day but ate a large amount of food. His NQ score was 61.1, which was in the good range and his diversity score was 88.4, which was in the high range. He said that as much as he wanted of a variety of foods and did not consider his health when making eating choices. He usually ate 2,175 kcal/day and 85 g of protein/day, which were 128% and 113% of the recommended amounts, respectively. He selected 8 out of 10 in the checklist to assess his sodium intake patterns, which showed that he was at high risk of consuming a high amount of sodium. He was obese with a BMI of 26.8 kg/m2 based on his healthy body weight. His nutritional diagnoses were excessive food and beverage intake and excessive sodium intake.
At his first follow-up session, his food diary showed that he had reduced his food intake after discharge, but he still frequently ate kimchi stew and soybean paste stew, which are high-sodium foods. He ate more vegetables and nuts and less fruit; protein-dense foods, such as meat, eggs, and beans; and ramen and other instant foods. Analysis of his 3-day food diary revealed that he consumed 97% of the recommended amount of calories and 87% of the recommended amount of protein. The clinical dietitian instructed him to consume an adequate amount of lean meat and meat substitutes because the patient's protein intake decreased to less than 90% of the recommended amount as a result of the fact that he avoided most protein-dense foods. A clinical dietitian gave him individualized nutrition education and counseling to teach him how to choose foods and plan meals to reduce his sodium intake. The second follow-up session took place 4 months after the first follow-up session. He selected 4 out of 10 in the checklist to assess his sodium intake patterns, which showed that he was at moderate risk of consuming a high amount of sodium. He said that he was not adding table salt or extra sauces to foods and reduced his consumption of delivery food. His overall NQ score and each of his category scores had increased, but his food intake moderation score had increased the most. He consumed 103% of the recommended amount of calories and 96% of the recommended amount of protein. His BMI had decreased to 24.5 kg/m2, which was lower than the cutoff for obesity diagnosis as defined by the Korean Society for the Study of Obesity.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [62, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 62 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
907,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7682511-1,Extracted,"History of present illness and past medical history
A 65-year-old woman presented to the emergency department complaining of double vision: she had woken up at 8 am and noticed the problem right away but waited until noon that day to seek medical care. She recalled going to bed at 1 am, having no symptoms at the time. The patient reported feeling slightly dizzy and having mild difficulty walking but denied headache, paresthesia, muscle weakness, or recent trauma.
Past medical history was significant for three previous ischemic strokes, the earliest one at the age of 50 years and a second one at the age of 54. The patient was prescribed a coumarin-derivative (acenocoumarol) at the time of her first stroke, which she used for nearly 15 consecutive years until an episode of lower gastrointestinal bleeding prompted its substitution by clopidogrel. Six days after this event, the patient suffered her third stroke and four months later, the events described in this report took place. By this time, the patient was also being treated with 10 mg lisinopril daily for hypertension, 8 mg prednisone daily for long-standing rheumatoid arthritis, 40 mg atorvastatin daily, and 300 mg ranitidine daily. None of her previous cerebrovascular accidents had caused her lasting disability.
Physical examination
On physical examination, the patient’s vital signs were stable with blood pressure measuring 140/80 mmHg on both arms. She was oriented to person, place, and time. No dysphasias were present. Confrontation visual field assessment revealed no quadrantanopias, and there was no change in visual acuity as reported by the patient. She was found to have mild primary gaze exotropia (Figure ) along with painless, horizontal diplopia that was attenuated by levoversion. There was left internuclear ophthalmoplegia (INO): adduction impairment of the left eye with abduction nystagmus of the right eye, triggered by dextroversion. The left eye also failed to adduct during attempted convergence. Downbeat nystagmus (DBN) was observed on the left eye: it was present during downgaze alone and its amplitude varied in accordance with Alexander’s law. Lateral version of the eyes while gazing down did not affect vertical nystagmus. The patient further showed truncal ataxia with right lateralization during Romberg’s test and oscillation to the right while sitting. Pupils were symmetric in the well-lit examination room but their reactivity to light was not assessed. The exam was negative for limb ataxia, dysarthria, and dysdiadochokinesia. Muscle strength was 5/5 on shoulder abductors, elbow extensors/flexors, and knee extensors/flexors bilaterally. There was no paresthesia.
Workup and outcome
The patient was admitted to the intensive care unit (ICU). The time elapsed between ischemia onset and hospital arrival was judged to be ~11 hours based on the time she reported having gone to sleep. Once it was decided she was not a candidate for thrombolysis, treatment with prasugrel plus aspirin was initiated and a patch was placed on her left eye.
Lab testing showed microcytic, hypochromic anemia, an international normalized ratio (INR) of 1.3, and normal platelet count. The plasma glucose concentration was normal, as was electrolyte concentration (Na+, K+, Cl-). Serum total and ionized calcium were within reference ranges.
Diffusion-weighted imaging (DWI) showed hyperintense lesions in the tegmentum of the mid and rostral pons, left of the midline (Figure ), as well as a lesion in the right posterior lobe of the cerebellum that coincided with the horizontal fissure (Figure ). DWI and fluid-attenuated inversion recovery (FLAIR) sequences had thick interslice gaps; T1 images with smaller slice increments provided a clearer picture of the extent of the lesions (Figure ). Magnetic resonance angiography showed a left fetal posterior cerebral artery (PCA), hypoplasia/aplasia of the right posterior communicating artery (PComm), and stenoses along the left superior cerebellar artery (Figure ). Carotid Doppler ultrasound displayed normal waveforms and anterograde flow. Echocardiogram was positive for a patent foramen ovale; transesophageal echocardiography was advised, but the patient refused the procedure.
The patient’s symptoms improved over the next day; she was transferred from the ICU to the general ward ~36 hours after admission. On Day 5, upon examination by the neurologist, ataxia had resolved completely and only mild diplopia was present with an eccentric right gaze. She was discharged home the same day, with a modified Rankin Scale (mRS) of 1, and advised outpatient follow-up for her anemia.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [65, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': True, 'Thromboembolism history': True, 'Diabetes history': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
908,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8466326-1,Extracted,"An 85-year-old woman with a past medical history of hypertension, hyperlipidemia, cerebrovascular accident (CVA), and left lower lung lobectomy presented to the ER due to intermittent abdominal pain, dysuria, and nausea for one day. Physical exam was significant for diffuse tenderness to palpation, worse in the suprapubic region. Her vitals were blood pressure of 167/78 mm Hg, respiratory rate of 16 per minute, pulse rate 87 beats per minute, and temperature of 95.9 °F. Relevant laboratory workup is mentioned in Table .
CT scan of the abdomen and pelvis with intravenous (IV) contrast was suggestive of proximal ureteral/ureteropelvic junction rupture and a large amount of fluid in the left retroperitoneum and surrounding the left kidney in the pelvis (Figure ). No clear obstructive etiology was identified on the CT scan. There was no evidence of stone or mass on the CT scan.
The patient received broad-spectrum antibiotics in ER. While the patient was in the ER, she was noted to have an atrial flutter with rapid ventricular rate and systolic blood pressure dropped to 89 mm Hg. She was given an amiodarone bolus and she reverted to normal sinus rhythm. Norepinephrine infusion was also planned to be given but once she reverted to sinus rhythm, her blood pressure was noted to improve. She was also noted to drop her oxygen saturation to 70% and was placed on two liters of oxygen through a nasal cannula.
Urology consultants were consulted and the recommendations were to admit the patient to the intensive care unit (ICU) and placement of percutaneous nephroureteral catheter tube (PNCT). This was done successfully (Figure ). The patient was monitored in ICU and continued on antibiotics.
Over the course of her stay, the patient clinically improved, and she was transferred out of ICU to medicine service. Due to persistent leukocytosis, a CT scan abdomen and pelvis with IV contrast was repeated, which did not show any clear infectious etiology (Figure ). The infectious disease was also evaluated and antibiotics were switched to ceftriaxone as per blood culture sensitivities.
Eventually, the patient's leukocyte count down trended. Clinically she was noted to improve significantly. Urology recommended that PNCT should be kept in place for at least three weeks. She was discharged on oral antibiotics and recommendations were given to follow-up outpatient with urology and IR specialists.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [85, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Vascular disease history': False, 'Diabetes history': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 85 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 6. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
909,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7685016-1,Extracted,"An 89-year-old male presented with a 5-day history of worsening dyspnoea and cough. Past history included hypertension, ischaemic heart disease, permanent pacemaker implantation for complete heart block, chronic kidney disease stage 3 and atrial fibrillation. He was taking long-term Rivaroxaban therapy for stroke and systemic embolism prophylaxis. No compliance issues were reported. No antiplatelet or additional antithrombotic medication was being taken prior to hospital admission. Despite advanced age, the gentleman was fully independent with activities of daily living. Hospital admission was required due to hypoxia. Maximal oxygen requirements during the course of admission were 4 l/min. Reverse transcriptase viral polymerase chain reaction testing subsequently confirmed COVID-19 infection.
Admission blood testing demonstrated lymphopenia (0.82 × 109/l) and a markedly elevated C-reactive protein of 345 mg/l. Coagulation studies were prolonged (activated partial thromboplastin time 31.7 s, prothrombin time 14.4 s) due to concurrent anticoagulation with Rivaroxaban. Fibrinogen level was markedly elevated at 9 g/l. Creatinine (106 μmol/l) and estimated glomerular filtration rate (52 ml/min) were at the patient’s baseline level. Remaining biochemistry results returned within normal limits. Chest radiography confirmed new bi-basal and peripheral left mid zone pulmonary infiltrates suggestive of COVID-19 pneumonitis (). Oral doxycycline was commenced to cover for possible secondary superadded bacterial infection, in line with local institutional protocols during the early period of the COVID-19 pandemic.
On Day 4 of his hospital stay, and despite an improvement in COVID-19 symptoms with reducing oxygen requirements, the patient developed a rapid and dense left-sided hemiplegia with dysarthria, alongside clinical signs of left gaze palsy and left homonymous hemianopia. National Institutes of Health Stroke Scale was 21, signifying symptoms suggestive of acute severe stroke. Within 1 h of onset of neurological symptoms (Day 4 of hospital admission), computed tomography imaging of the brain was performed. This showed a region of low attenuation in the right basal ganglia and high density in the right M1 segment of the middle cerebral artery consistent with an acute infarct due to large-vessel occlusion (). Computed tomography angiography was requested to evaluate a potential target for mechanical thrombectomy. This demonstrated extensive thrombus occluding the right cervical internal carotid artery and a T occlusion affecting the right anterior and middle cerebral arteries ().
The patient was not a candidate for thrombolytic therapy due to concurrent anticoagulation with Rivaroxaban. Mechanical thrombectomy was discussed with interventional radiology colleagues, but it was decided that this would offer little clinical benefit given the patient’s age and comorbid status. Unfortunately, despite maximal ward-based medical treatment, the patient deteriorated and passed away 5 days later.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [89, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 89 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
910,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7755066-1,Extracted,"The first patient was an 86-year-old woman with a history of hypertensive cardiomyopathy with severe mitral regurgitation and atrial fibrillation on anticoagulant therapy with warfarin. She presented to the Emergency Department after experiencing a sudden onset of shortness of breath on mild exertion and peripheral edema.
At admission, the patient was afebrile, eupneic in oxygen therapy at rest. Thoracic physical examination revealed decreased breath sounds and crackles in the lower lung lobes, bilaterally.
Blood investigations revealed a total leucocyte count of 9140/mcL (normal 4000–11,000/mcL), Hb 11 g/dL (normal 13–18 g/dL), C-reactive protein (CRP) 15.8 mg/dL (normal < 0.50 mg/dL), Procalcitonin (PCT) 0.32 ng/L (normal < 0.5 ng/L), fibrinogen 707 mg/dL (normal 200–400 mg/dL), creatinine 1.23 mg/dL (normal 0.7–1.20 mg/dL), INR 2.36 (normal 0.82–1.19). Chest CT revealed bilateral pleural effusion with passive atelectasis of the lower lobes. Patient was diagnosed with COVID-19 on April the 8th, 2020, on the basis of RT-PCR testing that detected SARS-CoV-2. The patient was admitted to our Geriatric department and began to receive hydroxychloroquine, intravenous ceftriaxone and doxycycline, as per local protocol, observing a good clinical response and the decrease of inflammation markers. Weaning and discontinuation of oxygen therapy was possible once the patient was stable with satisfactory oxygen saturation. The anticoagulation (AC) therapy was maintained, however, we decided to switch AC therapy from warfarin to low molecular-weight heparin (LMWH) enoxaparin 6000 U BID.
Suddenly, 5 days after admission, she started complaining of pain and loss of movement of her left leg, which appeared swollen. Venous compression ultrasound (CUS) and evaluation of D-dimer excluded deep vein thrombosis, but a Chest computed tomography (CT) scan with contrast revealed an 11 × 8 × 14 cm hematoma in the left thigh (Fig. ). Laboratory tests showed a fall in hemoglobin from 11 g/dL to 7.8 g/dL and, despite the absence of active arterial extravasation, prophylactic embolization of small branches of superficial and deep femoral artery was performed. Blood tests at that time also showed alterations of coagulation system, with reduced prothrombin time, increased fibrinogen and international normalized ratio (INR), despite a platelet count within normal limits. Interleukin-6 levels were 67,9 pg/mL (normal < 12.7 pg/mL). Overall, the patient was transfused 3 unit of packed blood cells, which raised her hemoglobin to 10.1 g/dL. Table shows the patient’s routine blood test during the hospitalization. In the following days, the patient’s hemoglobin remained stable and the hematoma showed no evidence of further expansion. The patient recovered completely and was discharged shortly after the event.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [86, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 86 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
911,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4580702-1,Extracted,"A 64-year-old male presented with a 6-month history of symptomatic drug refractory PeAF. The patient was admitted for catheter ablation of AF. Transthoracic echocardiogram revealed normal ejection fraction of 55-60% with mildly enlarged LA of 43.8 mm in the anterior-posterior diameter. A transesophageal echocardiogram prior to ablation showed no visible intracardiac thrombus or shunt. Cardiac magnetic resonance (CMR) imaging revealed late gadolinium enhancement (LGE) in 20% of the LA surface including the anterior and posterior wall.
After PVI, AF was still sustained. CFAEs in the LA were mapped for 6 seconds using EnSite NavX® system three-dimensional automated software (Endocardial Solutions, St. Jude Medical, St. Paul, MN, USA). The CFAEs were predominantly located at perimitral, septal area and left atrial appendage base (). Activation pattern at the high clustering of CFAE was mapped using high density 20-pole catheters (AFocus II; St. Jude Medical, St. Paul, MN, USA). The activation patterns obtained from three AF beats of unipolar recordings at each CFAE site were classified into four categories: 1)complete reentry, 2) incomplete reentry, 3) wave collision, and 4) wave breakup with conduction block. We preferentially targeted CFAE areas with complete or incomplete reentry pattern because these sites might play an important role as rotor. In this case, only the perimitral area had re-entrant, rotor-like electrical activity (). Based on the activation pattern, we assumed that the perimitral area could be the critical site for AF perpetuation. Therefore, we decided to infuse ethanol into the VOM as an add-on to radiofrequency ablation.
At first, cannulation into coronary sinus was performed by ablation catheter (Therapy CoolFlex; St. Jude Medical, St. Paul, MN, USA) and 8 Fr sheath (SL1 sheath; St. Jude Medical, St. Paul, MN, USA). To confirm the existence and feasibility of VOM, occlusive coronary sinus (CS) venogram was done (). A multipurpose A-1 guiding catheter (7 Fr; Cordis, Miami, FL, USA) was subselectively engaged into the VOM and then a Hi-Torque Floppy II angioplastic guidewire 0.014 (Abbott, Santa Clara, CA, USA) was advanced into the VOM as far as possible. A Ryujin Plus OTW 2.0×20 mm angioplasty balloon catheter (Terumo, Tokyo, Japan) was advanced into the VOM over the angioplastic wire and inflated at the ostium of VOM. Engagement of the balloon catheter into the VOM was confirmed by injecting contrast medium into the VOM (), and 1 cc of 100% ethanol was injected into the VOM three times (). Each injection was delivered over 1 minute through a balloon lumen and flushed with normal saline. Within 30 seconds after the first ethanol injection, AF was organized to AT (). LA local activation time mapping demonstrated macro-reentrant AT, the circuit of which involved reentry around the mitral annulus in a counterclockwise fashion (). Radiofrequency ablation at PMI for only 40 seconds terminated AT (). Bidirectional block of PMI line was achieved after ablation within CS adjunct to PMI ablation (). The repeated induction test confirmed no inducibility. The patient has been followed at outpatient clinic without recurrence of AF/AT.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [64, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 64 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
912,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3008834-1,Extracted,"A 52-year-old woman was hospitalized for evaluation of a 2-day-history of chest discomfort. She had rheumatoid arthritis for 13 years and had been treated with hydroxychloroquine for >12 years (total dose, 1,898 grams). In the emergency department, she had a generalized tonic-clonic seizure caused by sinus arrest (). The initial vital signs were as follows: blood pressure, 130/80 mmHg; heart rate, 38 beats/minute; body temperature, 36.4℃; and respiratory rate, 20/minute. The physical examination revealed a mild degree of jugular venous distention, a regular, slow cardiac beat without murmurs, clear lung sounds, and no pitting edema in the extremities. The 12-lead ECG showed a junctional rhythm with sinus arrest (). The laboratory findings included a hemoglobin level of 13.1 g/dL and a normal white blood cell count with a normal differential cell count. The blood urea nitrogen was 27 mmol/L, the serum creatinine was 2.02 mg/dL and the C-reactive protein was 0.94 mg/L. The antinuclear and anti-double stranded deoxyribonucleic acid (DNA) antibodies were negative, while the rheumatoid factor was positive. The creatine kinase was 294 UI/L with a normal myocardial band fraction. The aspartate aminotransferase level was 57 U/L, the alanine aminotransferase level was 48 U/L, and the alkaline phosphatase level was 49 UI/L. Chest radiography demonstrated marked cardiomegaly without pulmonary congestion (). Transthoracic echocardiography (TTE) revealed a markedly thickened left ventricular (LV) septum and posterior wall thickness, measuring 17.7 mm and 18.8 mm, respectively, with mild LV systolic dysfunction (ejection fraction, 44%). A slightly thickened RV free wall with mild RV systolic dysfunction was also noted. Both atria were enlarged and a mild degree of mitral regurgitation was present. The mitral inflow pattern was consistent with restrictive physiology. The early mitral inflow (E) velocity was 90.28 cm/s, the late mitral inflow (A) velocity was 36.77 cm/s, and the deceleration time was 216.64 milliseconds. The E/E' was 33.4, suggesting a high left ventricular end diastolic pressure (). Magnetic resonance imaging (MRI) showed diffuse wall thickening of the LV (septal wall thickness at the end-diastolic phase, 19 mm) and the RV free wall, suggesting hypertrophic cardiomyopathy. There was a small pericardial effusion. On delayed enhancement, multifocal patchy myocardial enhancement was noted in the lateral and septal walls (). The patient underwent myocardial biopsy to determine the underlying cause of the cardiomyopathy. Light microscopy showed vacuolated myocytes (). Electron microscopy revealed abundant intra-myocyte lysosomes with numerous large, dense myelin figures occupying large portions of the myocyte sarcoplasm. Lysosomal inclusions with curvilinear substructures were also noted (). There was no evidence of amyloid deposition, myocarditis, or an acute vasculitic process. Chloroquine toxicity was diagnosed based on the pathologic findings and the hydroxychloroquine was promptly discontinued. A permanent pacemaker was inserted for management of sick sinus syndrome. Four months later, the follow-up TTE demonstrated no significant interval change in LV systolic function or the LV wall thickness compared with the previous examination. However, LV diastolic function improved from restrictive physiology to pseudonormal relaxation. The patient's rheumatoid arthritis was subsequently controlled with low-dose prednisolone and analgesics.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [52, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': True, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 52 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
913,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5458023-1,Extracted,"Question 1: What is the diagnosis when a patient develops a rash as shown in Figure A and B?
Answer 1: A 67-year-old male with a history of hypertension, diabetes mellitus, atrial fibrillation, and right total knee arthroplasty presented with a progressive rash in the lower extremities. Two weeks earlier, he had right knee debridement for septic arthritis caused by methicillin-sensitive Staphylococcus aureus for which cefazolin was initiated for 6 weeks. Upon presentation, his vital signs were within normal limits. Examination demonstrated clusters of palpable, purplish purpurae with associated intact and ruptured blisters scattered over anterior, medial, and lateral aspects of the legs bilaterally below the knees. Laboratory investigations revealed urea of 17 mg/dL, creatinine of 0.89 mg/dL, ESR of 117 mm/h, CRP of 88.14 mg/L, WBC count of 10.6 k/μL without peripheral eosinophilia, hemoglobin of 8.1 g/dL, and platelet count of 312 k/μL. Urinalysis was significant for 2+ proteinuria and microhematuria. Investigations for hepatitis B, hepatitis C, ANA, ANCA, and cryoglobulins were negative. Biopsy of the rash showed perivascular papillary dermal infiltration of polymorphonuclear leukocytes and eosinophils with prominent foci of leukocytoclasis and extravasated RBCs along with a spongiotic intraepidermal and subepidermal bullous change. Based on the clinical presentation, characteristic rash and biopsy results, he was diagnosed with leukocytoclastic vasculitis (LCV) secondary to cefazolin with cutaneous and renal involvement.
Corticosteroids were deferred in light of an ongoing infection and normal renal functions in this patient. Cefazolin was switched to vancomycin and colchicine was commenced with resultant improvement in the rash. When encountered with drug-induced leukocytoclastic vasculitis, a thorough review of medications should be made to identify the implicated drug and should be discontinued promptly. In the absence of overt organ damage, discontinuation of the offending drug is usually sufficient and immunosuppressive therapy may not be necessary as demonstrated by this case.
Most cases of leukocytoclastic vasculitis are idiopathic; however, drugs, bacterial, or viral infections, sepsis, connective tissue diseases, and underlying malignancies are associated in the rest . Histopathologically, the hallmark of diagnosis is perivascular polymorphonuclear infiltration, leukocytoclasia (degranulation and nuclear fragmentation, also known as karyorrhexis) of the neutrophils, and fibrinoid necrosis .",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [67, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': False, 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 67 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
914,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6745338-1,Extracted,"A 66-year-old man presented with intermittent dizziness for two years and aggravation for 10 d.
The patient have been smoking for more than 30 years, with more than 20 cigarettes a day. He had drunk for more than 40 years and has stopped drinking now.
The patient had a more than 10-year history of type 2 diabetes and severe diabetic eye disease with blindness in the left eye. The patient self-injected long-acting insulin subcutaneously, 12 units per day. The patient denied having other diseases.
His father died of heart disease at the age of 72 years. His mother and children are healthy.
First admission to hospital in March 2018: On physical examination, the patient’s blood pressure in the left upper limb was 120/70 mmHg, and blood pressure was not detected in the right upper limb. The patient was conscious and able to answer questions fluently, no abnormalities were detected on a nervous system examination, and the right brachial artery and radial artery pulsations were not detected.
Second admission in October 2018: The pressures in the left and right upper limbs were 140/68 mm and 85/60 mmHg, respectively. The results of a nervous system examination were normal. The right radial artery pulsation could not be detected, but the left radial artery pulsation was accessible. The patient was conscious and could carry on a normal conversation but had slightly slurred speech.
Imaging studies including a computed tomography (CT) scan of the head, computerized tomography angiography (CTA) of the vessels of the head and neck, and cerebral angiography. Upon the first admission to hospital in March 2018, CTA of the vessels of the head and neck showed severe stenosis at the beginning of the brachiocephalic artery. A CT scan of the head showed no obvious abnormalities. Cerebral angiography showed that the stenosis of brachiocephalic artery had almost occluded it (Figure ). Upon the second admission in October 2018, a CT scan of the head revealed multiple cerebral infarctions in bilateral basal ganglia and the right lateral ventricle. CTA of the vessels of the head and cerebral angiography both showed severe stenosis in the brachiocephalic artery stent. Reverse blood flow through the right vertebral artery compensated for the right subclavian artery, and the left internal carotid artery was occluded.
Laboratory examinations included routine blood tests, liver function, kidney function, electrolytes, coagulation function, routine stool, and urine tests and relevant immune factor tests, and no obvious abnormalities were found. Only blood lipid examination was abnormal (Table ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [66, 'years'], 'Hypertension history': True, 'Stroke': True, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 66 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
915,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3259548-1,Extracted,"A 42-year-old male was admitted for radiofrequency ablation of atrial fibrillation (AF). He was diagnosed as AF 4 years ago and took anti-arrhythmic agent, beta blocker and anticoagulant. He had left side weakness due to cerebral infarction of right middle cerebral artery territory 3 years ago. He had a history of hypertension. His family had no history of diseases or congenital abnormality. He had no other symptoms but intermittent palpitation. His heart sound was irregular, but nothing particular was revealed on other physical and laboratory examinations. Double the shadow of thoracic aorta and widening state of superior mediastinum were shown in chest X-ray, but there were no other remarkable matters (). Initial electrocardiogram showed AF with moderate ventricular response (average 60-80 beats/min). On transthoracic and transesophageal echocardiography, no structural cardiac abnormalities were revealed. It seemed that hepatic vein was connected to right atrium through inferior vena cava (IVC) as usual. There was no pulmonary hypertension. We checked coronary multidirectional computed tomography (MDCT) to identify the anatomical variations of the patient's coronary vessels and heart before the ablation procedure. There was a tubular structure which was paralleling with descending thoracic aorta. It was supposed to be an IVC interruption with hemiazygos continuation (). Hepatic veins were drained to right atrium. Abdomen computed tomography (CT) was performed to evaluate other combined abnormality. Multiple
and round soft tissue densities were detected around the spleen, which were enhanced at the same degree of the spleen. Left-sided colon and right-sided small bowels indicated intestinal malrotation. IVC was located at the left side of aorta, and the hepatic segment of IVC was absent (). By means of venography of IVC through right femoral vein, the interruption of the thoracic IVC with hemiazygos continuation along with aortic arch was confirmed (). All those findings were compatible with SAP.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [42, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 42 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
916,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4697919-1,Extracted,"A 79-year-old male presented to the emergency department with a 3-day history of worsening left-sided and lower abdominal pain that peaked over the last 24 h preceding admission. The pain was made worse with movement and straining; he also experienced some nausea. He did not report any rectal bleeding, change in bowel habits or urinary symptoms, and there was no history of trauma. The patient was found collapsed at home by his daughter on the day of admission.
His past medical history included hypertension, atrial fibrillation (for which he was on warfarin), gout, and bilateral inguinal hernia repair. His regular medications included atenolol, allopurinol, amlodipine, and warfarin. He smokes a pipe, indulges on occasional alcohol at the weekend and is a retired driver.
On examination, he was hypotensive with a blood pressure of 95/60, but all of his other vital signs were within normal range. Abdominal examination showed mild distension and guarding over the left iliac fossa with some percussion tenderness over the suprapubic region. No masses or enlarged organs were felt, and bowel sounds were present but sluggish. Both his femoral pulses were strong and equal, and PR examination was unremarkable. Initial blood tests showed WCC 15.7, CRP 10, haemoglobin 134 and of lactate 3.4.
After initial resuscitation with intravenous fluids and starting of empirical antibiotics, an urgent CT scan of his abdomen and pelvis was obtained, which showed an abnormal spleen with signs of rupture and free intraperitoneal blood (Figs and ). On the basis of these findings, he was taken immediately to theatre after correction of his coagulation with 5 mg of vitamin K and 2000 units of Human Prothrombin Complex (Octaplex).
During the surgery, 3500 mls of blood and clots were found in the abdomen. The spleen was of moderate size with a 3 × 2 cm area of induration on its superoposterior aspect that was considered to be most likely neoplastic (Figs and ). The abnormal area included a 5 cm laceration, which was the source of bleeding. It was sent to the histology lab for further analysis. A total of 4 units of RBC and 380 mls of cell salvaged blood were given during the surgery.
He stayed in the ITU for post-operative care and made a good recovery without requiring any organ support. He was discharged with post-splenectomy prophylactic vaccinations and haematology follow-up.
The histology report confirmed a diffuse large B cell lymphoma. Immunohistochemical staining showed the cells to be positive to CD20, CD79a, BCL-6, MUM-1, FOX P-1 and P53 (some cells), and negative to CD3, CD10 and BCL-2. The histology also confirmed a high proliferative index of over 90%.
Staging CT scan of the chest/abdomen/pelvis did not detect any additional disease.
PET scan showed no definite evidence of residual lymphoma.
It was decided during his haematology appointment that although surgery had been a definitive treatment, a combination chemotherapy including rituximab and possibly radiotherapy to the splenic bed would be beneficial. He was consented for chemotherapy with R-GCVP, which is a 3 weekly cycle of rituximab monoclonal antibody along with IV gemcitabine (at 75% dose), cyclophosphamide, vincristine and prednisolone. He tolerated this well, and the haematology plan is to continue with chemotherapy with a view to increasing the dose of gemcitabine if there is no excessive haematological toxicity.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [79, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 79 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
917,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8218827-2,Extracted,"The patient was a 65-year-old man, with diabetes mellitus, hyperuricemia, chronic obstructive pulmonary disease, and atrial fibrillation on oral anticoagulant (edoxaban 60 mg once a day). He described a 2-day history of right lower limb pain and coldness.
His physical examination revealed a pale and cool right leg, with dependent distal rubor. He presented femoral pulse with audible arterial Doppler signals at popliteal and distal level. He did not show any impairment of sensitivity or motility.
Duplex scan examination showed occlusion of the right superficial femoral and popliteal arteries.
The patient denied any history of cough, fever, palpitation, or shortness of breath, but chest X-ray revealed peripheral ground-glass lung opacities and multifocal air-space disease ().
Laboratory results on admission are summarized in . The blood counts showed 9,200 white blood cells (88% neutrophils and 8.7% lymphocytes).
DD was extremely high (24.5196 ng/ml); CRP: 393 mg/L, CK: 329 IU/L, and LDH: 869 IU/L, all elevated.
The physical examination revealed irregular heart rate (102 beats/min), blood pressure of 133/81 mmHg, temperature of 35.9 °C, and oxygen saturation of 91%.
The COVID-19 nucleic acid detection test was negative. The following day, the patient’s state became aggravated despite active treatment. His right foot was cold and pale with cyanosis and paresthesia (). The patient noted difficulties in wiggling the toes. His right femoral pulse was faintly palpable and no distal Doppler signals were detected.
The patient was taken to the operating room to perform an urgent thrombectomy. Subcutaneous enoxaparin sodium, 1 mg/kg every 12 hours was started. The clinical condition of the leg improved, but unfortunately the patient died 12 hours later. Serologic testing detected IgG-IgM antibodies to SARS-CoV-2.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [65, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
918,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7793217-2,Extracted,"A 70-year-old man with ischaemic cardiomyopathy was referred to our institution for catheter ablation of ventricular tachycardia (VT) storm. Eight years prior to his presentation, he had undergone coronary artery bypass grafting, endoventricular circular patch plasty, mitral valve plasty, tricuspid annuloplasty, and CRT-D implantation with an LV lead also surgically implanted for NYHA Class IV HF, reduced LVEF of 24%, and QRS width of 154 ms. He has also suffered from chronic obstructive pulmonary disease and chronic kidney disease (serum creatinine level, 1.99 mg/dL). Physical examination revealed a pansystolic murmur (IV/VI) over the apex and no lower-limb oedema. His BNP level was elevated to 500 pg/mL. Echocardiography revealed an LVEF of 20% and pulmonary hypertension [tricuspid regurgitation pressure gradient (TRPG) of 43 mmHg].
One day after admission, catheter ablation was performed under CARTO guidance (Biosense Webster Inc., Diamond Bar, CA, USA). CARTO mapping revealed a low-voltage area in the anterior and septal walls (). After elimination of all abnormal potentials within the low-voltage area, no VT could be induced.
However, the patient developed progressively worsening dyspnoea and hypotension even under optimized medical therapies including oral intake of carvedilol of 10 mg, spironolactone of 50 mg, furosemide of 40 mg, tolvaptan of 15 mg, and amiodarone of 200 mg and intravenous infusion of dobutamine at 5 μg/min/kg. Despite an improved LVEF of 35%, TRPG elevation to 90 mmHg was observed on echocardiography and respirator support was required. We were aware of the development of CAVB and a change in the QRS morphology during junctional escape rhythm that suggested injury to the left posterior fascicle (). We thought his haemodynamic deterioration was induced by RV and LV dyssynchrony due to CAVB caused by catheter ablation because the VT episodes were completely eliminated. We therefore decided to add a pacing lead (Model 3830, Medtronic, Inc.) at the HB region (). Although we initially placed the lead at the site where a HB potential was recorded, the pacing threshold at that site was too high to obtain stable permanent pacing. Alternatively, the lead was implanted at a more distal (ventricular) site where a possible right bundle branch potential was recorded (). During HBP, the QRS duration was not significantly shortened (186 ms, ), so we applied BiVHB+LV pacing. Fortunately, because a DF-1 lead was originally used as a defibrillator lead, we could connect the HBP lead to the RV pacing port. The pin of the original RV pacing lead was covered with a silicon cap and abandoned. Following the application of BiVHB+LV pacing, the QRS narrowed from 167 to 127 ms with an optimized AV delay (atrial-HB delay: 140 ms) and VV delay (HB-LV delay: 40 ms) (). Over the week following the upgrade to BiVHB+LV, his haemodynamics improved dramatically. Although RV-SD and LV-SD had worsened from 52 to 82 ms and 75 to 189 ms after ablation, respectively, BiVHB+LV reversed the RV-SD to 53 ms and LV-SD to 82 ms (). Unfortunately, he died from a non-cardiac cause, acute non-occlusive mesenteric infarction, 4 months after the upgrade although he had remained free from HF until that time.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [70, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 70 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
919,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5438524-1,Extracted,"A 75-year-old Caucasian woman with past medical history of atrial fibrillation, hypertension, and remotely treated breast cancer presented with dyspnea, non-productive cough, subjective fevers, polyarthralgias, myalgias, and consequent sleep disturbance of 10 days’ duration. Her medications were hydrochlorothiazide, losartan and simvastatin. Eighteen days earlier she had been seen for a routine health-care visit and received PCV13. Soon thereafter she developed a large, erythematous, warm local reaction to the vaccine, which was still present. Her vital signs included a pulse rate of 126 beats/minute, blood pressure of 99/63 mmHg, a maximum temperature of 36.6 degrees Celsius, and oxygen saturation of 83% on room air requiring bilevel positive airway pressure therapy. She had reduced breath sounds in the left lung field. Her white blood cell (WBC) count was 19.1 (normal 4–11 K/uL), creatinine level was 1.5 (normal 0.52–1.04 mg/dL), and B-type natriuretic peptide level was 1670 (normal 0–900 pg/mL). All blood bacterial cultures, urine streptococcus pneumonia and legionella antigens, mycoplasma titers, and Lyme antibody test results were negative. A chest X-ray and computed tomography (CT) scan showed a large left pleural effusion and a large pericardial effusion. An echocardiogram confirmed the pericardial effusion. Her erythrocyte sedimentation rate (ESR) was 59 (normal 0–20 mm/hour), C-reactive protein (CRP) level was 62.7 (normal 0–0.9 mg/dL), and her rheumatoid factor was 15 (normal 0–11 IU/mL). Her antinuclear antibody test result was negative. Test results for anti-Sm, -double stranded deoxyribonucleic acid (dsDNA), -histone, -cardiolipin, -ribonucleoprotein, -centromere, -topoisomerase I, -Ro, -La, -thyroid, -neutrophil cytoplasmic (-myeloperoxidase and -proteinase 3) antibodies were all negative. Her complement levels were normal.
Thoracentesis and pericardial window were required. Pleural fluid appeared bloody and was exudative by Light’s criteria (serum lactate dehydrogenase [LDH] 765 U/L, serum total protein 7.7 g/dL; pleural LDH 749 U/L, red blood cells 320,000/uL, nucleated cells 3368/uL [PMN 62%, lymphocytes 22%, macrophages/histiocytes 14%, mesothelial cells 2%], glucose 97 mg/dL) []. Cytology test results of the pleural fluid were negative. The pericardial fluid was exudative and hemorrhagic and cultures and cytology test results were negative. A pericardial biopsy showed organizing effusion containing hemorrhage and acute inflammation with reactive changes and mesothelial hyperplasia. Cultures of the pericardial biopsy were negative.
The pleural fluid re-accumulated so a chest tube was placed. Repeat fluid analysis was similar and cultures were negative. Given the severity of her illness, her serositis was treated with corticosteroids rather than nonsteroidal anti-inflammatory medications []. She received 40 mg of prednisone daily for 2 weeks with a good initial response and tapered off steroids over the next 3 months. Her vital signs recovered to normal range throughout the admission. The chest tube and pericardial drain were removed prior to discharge. A follow-up chest X-ray one year after discharge revealed no recurring pleural effusions. She has remained asymptomatic now for one and a half years since discharge.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [75, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Thromboembolism history': False, 'Vascular disease history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 75 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
920,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4375114-1,Extracted,"We present a 76-year-old man who was referred to colorectal clinic with an unusual perianal lesion. A past medical history included sarcoidosis, atrial fibrillation, hypertension, chronic kidney disease and clear cell carcinoma of the right kidney, for which he underwent right-sided nephroureterectomy 7 years previously.
Histology at that time revealed a 34-mm diameter RCC with a 10-mm satellite focus in the adjacent cortex. There was invasion of the renal vein with extension into the perinephric tissue, and Furhman grade was 4.
The patient received a regular urological follow-up and surveillance imaging. In 2011, a CT thorax noted lung nodules suspicious for metastatic disease that were kept under surveillance. In 2013, it was noted that there was a soft tissue mass in the small bowel mesentry.
The perianal lesion was removed under general anaesthetic. At time of surgery, the lesion was clearly not a haemorrhoid, although there were grade III haemorrhoids present, and on its cut surface had the appearance of renal tissue. The pedunculated appearance (B) and cut surface (C) are evident in Fig. .
On histological examination, the sections revealed a covering of hyperplastic squamous epithelium which was focally ulcerated. The core of the nodule consisted of epithelial tumour cells with moderately hyperchromatic nuclei and abundant clear cytoplasm, forming nests and tubules with intervening congested thin-walled vessels.
On immunohistochemistry, testing the tumour cells was positive for CK8/18, EMA, CD10 and vimentin, and negative for CK7. These findings were in keeping with the diagnosis of metastatic RCC of conventional clear cell type.
Given the above findings, the patient underwent full imaging again. Unfortunately, CT head and subsequent MRI revealed a 1.2-cm lesion adjacent to the occipital horn of the left lateral ventricle, with surrounding oedema, suggestive of metastasis. He continues to receive ongoing multidisciplinary team follow-up and management.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [76, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
921,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4086376-1,Extracted,"A 65-year-old female presented to the Ophthalmology Clinic complaining of deterioration and distortion of vision in her right eye over the last 2 months. She was referred by a Speciality Doctor in Ophthalmology who noted a previous diagnosis of an epiretinal membrane in the right eye and vitreomacular traction. The left eye had stable findings for dry age-related macular degeneration. There was no other ocular history. Systemic history included high cholesterol level, hypertension, fibromyalgia, hypothyroidism, atrial fibrillation, and 8 occurrences of transient ischaemic attacks in the past 9 years. Regular medication included warfarin, simvastatin 80 mg, perindopril 2 mg, bisoprolol 10 mg, amitriptyline 30 mg, levothyroxine 75 mg, and fluoxetine 40 mg. The patient was noted to be allergic to penicillin and septrin. There was no relevant family history of note.
On her first clinic visit, best corrected visual acuity (BCVA) was logMAR 0.30 for the right and 0.00 for left eye. Slit lamp biomicroscopy of the anterior segment was normal. Fundus exam of the right eye revealed cystoid macular oedema which was confirmed on ocular coherence tomography (OCT) (). Central macular thickness (CMT) was measured to be 353 μm (). Fundus fluorescein angiography (FFA) was performed showing evidence of macular teleangiectasia type 1 in the right eye ().
Initial treatment included a course of 3 intravitreal bevacizumab (IVB) (Avastin) injections (one each consecutive month). Six weeks posttreatment with IVB, BCVA of her right eye was logMAR 0.18. OCT of the right eye showed increase in CMO, CMT recorded as 401 μm () (). As the response to anti-VEGF treatment was poor, the decision was made to treat with a single intravitreal triamcinolone injection (IVTA) [].
Two weeks posttreatment with IVTA, there was deterioration in vision of the right eye, BCVA being logMAR 0.48. However, there was a reduction in CMT (recorded as 282 μm) (). No further treatment was decided at the time. At 6 weeks posttreatment with IVTA, there was no improvement in BCVA and there was a recurrence in CMO, CMT recorded as 397 μm () (). The patient was then recommended to have treatment with a single intravitreal dexamethasone implant (Ozurdex).
A standard protocol was followed for the intravitreal injection of Ozurdex 700 mcg, including topical anaesthesia, installation of povidone iodine 5%, sterile drape, and lid speculum. No peri- or postoperative complications were observed. Six weeks posttreatment with the Ozurdex implant, BCVA of the right eye deteriorated to logMAR 0.59. However, OCT scan showed decreased CMT of 286 μm (). No further treatment was decided at the time.
Fourteen weeks posttreatment with Ozurdex, a further decrease in visual acuity was found; logMAR was 0.7. OCT demonstrated new occurrence of CMO, CMT recorded as 349 μm () (). Patient was listed for a second intravitreal injection of Ozurdex.
Six weeks posttreatment with the second Ozurdex, BCVA of the right eye improved to logMAR 0.64. OCT showed a decrease of CMO, CMT recorded as 279 μm () (). Eighteen weeks posttreatment with the second Ozurdex, BCVA deteriorated to logMAR 0.74, BCVA deteriorated to logMAR 0.74. There was a recurrence of CMO, CMT recorded as 332 μm (). Patient was listed for a third Ozurdex injection. Two weeks posttreatment with the third Ozurdex injection, the patients' visual acuity was recorded as 0.78; CMT decreased to 279 μm ().
During the whole period of follow-up, no ocular adverse events were established. No cataract progression was noted and intraocular pressure remained within normal limits.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [65, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': True, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
922,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6726817-1,Extracted,"A 59-year-old man with a 40-year history of smoking and 2-year history of hypertension presented to his local hospital with severe chest pain and dyspnea. Electrocardiogram (ECG) results suggested extensive anterior AMI. Dual antiplatelet therapy, anticoagulation, and statins were administered, but he refused further invasive treatment. His symptoms were slightly relieved but he continued to experience repeated chest pain attacks. He was referred to our hospital on the 8th day. His vital signs on admission were a heart rate of 108 beats/minute and blood pressure of 86/66 mmHg. The ECG showed ST-segment elevation in leads aVL and V1-V6, with significant ST depression in leads II, III, and aVF (). An echocardiogram displayed anterior, septal, lateral, and inferior akinesia and severely impaired left ventricular function with an ejection fraction (EF) of 18%. Extensive anterior AMI (Killip Class IV) and cardiogenic shock were diagnosed. The patient was transferred immediately to the catheterization laboratory and an intra-aortic balloon pump (IABP) was placed via the right femoral artery (). Diagnostic coronary angiography revealed a dominant right coronary artery (RCA) and acute total occlusion of the distal LMS with no anterograde flow (). There was no significant stenosis in the RCA and the posterior descending and posterolateral ventricular branches were also normal (). He was treated with implantation of a paclitaxel-eluting stent in the proximal left anterior descending artery and distal LMS (). There was no residual stenosis, thrombus, or dissection after stent implantation, with TIMI 3 flow. However, he developed atrial tachycardia and was treated with amiodarone. The IABP was successfully removed 10 days after PCI. The patient subsequently made satisfactory progress and was discharged 23 days after hospital admission, with an EF of 41%. Angiography showed unobstructed stents 1 year later () and an EF of 37% (NYHA Class II). The patient remained alive after 3 years of follow-up, with whole-heart enlargement and severe mitral regurgitation, and an EF of 32% (NYHA Class III) ().
The study protocol was approved by the institutional review board and Ethics Committee of The First Affiliated Hospital of Guangdong Pharmaceutical University. Written informed consent was obtained from the patient.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [59, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 59 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
923,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5353425-1,Extracted,"An 84-year-old woman was referred to our institution because of palpitations and dyspnea started 1 week before. In her medical history there were hypertension, dyslipidemia and a previous pulmonary embolism (PE). For this reason she was taking warfarin at time of our evaluation. A nonvalvular atrial fibrillation (AF) with HR 96/m was found. At clinical examination there were signs of heart failure (rales and peripheral edema), functional NYHA class III and high BP (170/110).
Because of a previous pulmonary embolism in her clinical history a trans-esophageal echocardiography (TEE) was performed. TEE revealed a left atrial appendage (LAA) roundish mass, sizing 1.2 × 1.2 cm that seemed a thrombus []. Regarding echocardiographic features, the mass was hyperechogenic and calcified, suggesting it was an old formation, consistent with an organized thrombus. Dense left atrial spontaneous echo-contrast (SEC) was found. Left atrium was dilated and LVEF% was normal.[] International normalized ratio (INR) at presentation was 1.95.
Together with heart failure treatment, intravenous anticoagulation with unfractionated heparin was initiated. The value of aPTT during treatment was 1.9 times. Treatment was complicated by an additional right lower limb embolic event treated by Fogarty arterial embolectomy catheter. In addition, after 7 days of therapy, the LAA thrombus remained unchanged [].
A previous testing revealed heterozygosity for both the factor V Leiden and the methylenetetrahydrofolate reductase C677T mutations inducing resistance activated protein C. The test was performed 5 years before and after PE event. The combination of these thrombophilic factors can probably explain the poor anticoagulant response, additional embolic events and the failure of resolution of the LAA thrombus.[] Patient refused transcatheter closure of the LAA and was chronically treated with Novel Oral AntiCoagulant (NOAC), specifically with rivaroxaban, 20 mg OD.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': True, 'Hypertension history': True, 'Thromboembolism history': True, 'age': [84, 'years'], 'Stroke': False, 'sex': 'Female'}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 84 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 5 + 2 = 7.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 7. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
924,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4405015-1,Extracted,"Our patient was a 73-year-old female with history of Ebstein anomaly, Wolff-Parkinson-White syndrome, atrial fibrillation, hypertension, and chronic obstructive pulmonary disease on home oxygen, presented to the hospital with 1-week history of progressive shortness of breath on exertion and peripheral edema. Transthoracic echocardiography performed 2 years ago revealed mild tricuspid regurgitation and a suspected patent foramen ovale with left-to-right shunt by color Doppler.
On presentation, she had severe hypoxemia with room air oxygen saturation of 66% and partial pressure oxygen of 33 mmHg. A trial of bilevel positive airway pressure led to no improvement. She was started on empiric anticoagulation for suspected pulmonary embolism until a CT scan ruled it out. After a trial of diuretics without improvement in oxygenation, the patient was intubated and nitric oxide was initiated to facilitate transfer to a tertiary care hospital.
Postintubation transthoracic echocardiography revealed normal left ventricular systolic function, severely enlarged right ventricle with apical displacement of the tricuspid valve leaflets (consistent with Ebstein anomaly) (), severe tricuspid regurgitation, and a patent foramen ovale with right-to-left shunt at rest. Examination revealed an oxygen saturation of 80% on 100% fraction of inspired oxygen and high dose nitric oxide with evidence of peripheral cyanosis.
The patient underwent right heart catheterization demonstrating marginally elevated pulmonary artery pressure (mean pulmonary artery pressure 23 mmHg), elevated right atrial pressure (mean right atrial pressure 12 mmHg), and an oxygen step-down from the pulmonary veins to left ventricle. Transesophageal echocardiography confirmed significant flow of the tricuspid regurgitation jet through the patent foramen ovale (Figures 
, video).
Percutaneous closure of the patent foramen ovale was undertaken with a 30 mm Gore Septal Occluder device. The defect was not measured with a sizing balloon and the 30 mm device was selected to ensure complete defect coverage. This led to resolution of shunting and instantaneously improved arterial saturations (); however, the patient had significant deterioration in overall hemodynamics (20 mmHg systolic drop in systemic pressure, central venous pressure increase from 11 to 17, and mixed venous oxygen saturation of 35%). A 10 mm smaller device (20 mm Gore Septal Occluder) was selected for partial closure of the patent foramen ovale resulting in acceptable hemodynamics and reduction in right-to-left shunting (). The patient recovered, had no evidence of worsening right heart failure or peripheral edema, and was discharged home. Transthoracic echocardiography performed 3 months after patent foramen ovale closure demonstrated a moderate residual shunt present with right-to-left passage of saline contrast at rest.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [73, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 73 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
925,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-8729,Extracted,"A 57-year-old man presents to his family physician for a checkup. He has had type 2 diabetes mellitus for 13 years, for which he has been taking metformin and vildagliptin. He has smoked 10–15 cigarettes daily for 29 years. Family history is irrelevant. Vital signs include: temperature 36.6°C (97.8°F), blood pressure 152/87 mm Hg and pulse 88/min. Examination reveals moderate abdominal obesity with a body mass index of 32 kg/m². The remainder of the examination is unremarkable.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [57, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 57 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 1 + 1 = 2.
The patient's CHA2DS2-VASc Score is 2."
926,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6967264-1,Extracted,"Written informed consent was obtained from the patient and his family for publication of this case report and accompanying images.
An 81-year-old man (height, 175 cm; weight, 85 kg) visited the emergency department with bilateral leg weakness, which led to difficulty in knee flexion 3 days before. He also developed fever and experienced back pain for approximately 1 week. Earlier, he had been walking with the assistance of a walker. He reported a history of aortic valve replacement surgery, mitral valvuloplasty, and tricuspid valvuloplasty, in addition to a history of heart failure, atrial fibrillation, obstructive arteriosclerosis, diabetes, chronic obstructive pulmonary disease, spinal canal stenosis, and dementia. Therefore, his general health condition was deemed poor. He was taking aspirin, apixaban, furosemide, spironolactone, and insulin. Echocardiography showed poor wall motion with an ejection fraction of 41% and pulmonary hypertension (65/13 mmHg).
We were unable to obtain detailed information regarding neurological symptoms such as sensory disturbance and movement disorder because of the severe dementia. He could not flex his right knee, although he could briefly flex his left knee in the supine position. He also complained of severe back pain (face rating scale [FRS] = 4) at rest, which increased with body movement (FRS = 5). Except for an elevated temperature (38.0 °C), his vital signs were stable. Blood examination revealed a slight increase in C-reactive protein (3.64 mg/dl) and white blood cell count (10,300/μl).
Magnetic resonance imaging (MRI) showed extensive fluid retention in the spinal epidural space (Th6 to L3) and compression of the spinal cord (Th6/7, Th11/12, L2/3) (Fig. ). The latter suggested paraplegia due to an epidural abscess. We performed emergency drainage using fluoroscopy-guided percutaneous puncture. The patient was placed in the prone position and received local anesthesia, following which any abscess near Th6/7, Th11/12, and L2/3 was punctured using a 14 G Tuohy needle under fluoroscopic guidance. Approximately 3 ml of purulent discharge was drained from the Th6/7 and L2/3 levels, and approximately 4 ml of a clear, light-yellow colored discharge was drained from the Th11/12 level. For involved areas near Th6/7, two needles were placed at the Th6/7 and Th8/9 levels, respectively. A 5-Fr catheter was placed under fluoroscopic guidance using a guide wire, followed by perfusion with saline until apparent removal of the corpuscles. MRI performed 1 day later showed relief from the compression due to the abscess. Three weeks later, the abscess had completely disappeared (Fig. ).
At the time of admission, provisional treatment with meropenem, clindamycin, and vancomycin was initiated and continued for 3 days. The prescription was de-escalated to cefazolin and clindamycin after group G streptococcus was detected in the abscess, and the treatment was continued for 28 days. Blood cultures were negative. Pain on movement (FRS = 2) reduced after the drainage procedure, while pain at rest also improved (FRS = 1) after 3 days. The muscle weakness gradually resolved, and he could walk to a portable toilet without assistance 20 days after the procedure. He was discharged to a nursing home for the elderly on the 57th day.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [81, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Vascular disease history': True, 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 81 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
927,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6371059-1,Extracted,"76-year-old female with a past medical history significant for Paroxysmal Afib with Tachy-Brady Syndrome, hyperlipidemia and muscle spasms who presented to the emergency room (ER) with dizziness, chest discomfort and presyncope. The patient underwent uneventful placement of a dual chamber permanent pace maker (PPM) placed 3 weeks before the ER visit being described. Rivaroxaban 20 mg PO daily was started as a new medication 3 days after placement of the PPM. Blood work confirmed no renal or hepatic impairment. Her CHADS2VAsc score at time of initiating rivaroxaban was 3.
Her home medicine consisted of Flecainide, Pravastatin, Cyclobenzaprine and a Multivitamin complex. These were also continued post procedure. Patient’s past surgical and family history were unremarkable.
In the ED, her systolic blood pressure was 70, Heart rate of 74. Physical exam revealed an alert and oriented patient. Normal jugular venous pressure and normal intensity heart sounds with no friction rub. Her lungs were clear on auscultation and abdomen was soft without tenderness.
An echocardiogram revealed a moderate- large Pericardial Effusion with early tamponade physiology. Her lab investigations were significant for an INR (International Normalized Ratio) of 1.7 with a PTT (PLEASE EXPLAIN THE ABBREVIATION) of 39 seconds, platelet count was 216, creatinine of 0.89 mg/dL and creatinine Clearance of 64.7 mL/min based on Cockcroft-Gault equation. ECG revealed sinus rhythm at a rate of 74 bpm with normal QRS amplitude. There was no evidence of ST segment abnormalities or electrical alternans.
The patient was stabilized with intravenous fluid and vasopressors and taken to the cath lab for pericardiocentesis.A total of 350 cc of gross bloody fluid was removed. Post-procedure, drains were placed and removed 48 hours thereafter with no evidence of reaccumulation. Evaluation of the fluid confirmed a haemopericardium (RBC (red blood cell) count of 472,000 cells/microliter) with gram stain and culture negative for microbes.
On interrogation, the PPM had no changes in the lead parameters (threshold, impedance or sensing). Post-pericardiocentesis, a CT-angiogram protocoled for both pulmonary and aortic vasculature was negative for pulmonary embolism and aortic dissection. Furthermore, CT images showed well-placed PPM leads with no evidence of perforation or migration.
The patient was discharged on Aspirin 81mg given concern for DOAC after recent pericardial effusion. She had an interval echocardiogram with her primary cardiologist that confirmed no recurrence of the pericardial effusion. Patient was noted to have recurrent atrial fibrillation 1 year later and Apixaban was initiated without complication.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [76, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
928,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2627818-1,Extracted,"A 72-year-old asymptomatic woman presented to the clinic for a checkup. She had a history of cholecystectomy, hypothyroidism, and hypertension. She had been treated with thyroid hormone (Puran® T4, 75 μg), an anti-hypertensive agent (the angiotensin-converting enzyme inhibitor Enalapril®, 20 mg), an antiarrhythmic drug (Diltiazem®, 90 mg), and acetylsalicylic acid (200 mg). She reported use of oral contraceptives for over 30 years. She had no history of smoking, drinking, drug abuse or family history of liver disease.
On physical examination, the liver was palpable to 6.5 cm from the right costal, and 10 cm from the appendix xiphoid; it was painless, and had a rugged and hard consistency. Laboratory studies revealed the following: red blood cells, 3,690,000/mm3; hemoglobin, 11.7 g/dL; hematocrit, 35%; platelets, 278,000/mm3; cholesterol, 186 mg/dL; triglycerides, 70 mg/dL; glucose, 85 mg/dL; TSH, 2.8 U/mL; serum creatinine, 0.7 mg/dL; ALT, 47 U/L; AST, 29 U/L; GGT, 23 U/L; alkaline phosphatase, 138 U/L; TB, 0.8 mg/dL; DB, 0.4 mg/dL; PT, 12 s; INR, 1.0; PTT, 29 s; folic acid, 11 mg/mL; alpha-fetoprotein, 2.08 ng/mL; iron, 106 μg/dL; vitamin B12, 210 pg/mL; ferritin, 170 mg/L; LDH, 384 IU/L; and CEA 2.4 ng/mL.
Abdominal ultrasound revealed an enlarged and heterogeneous liver that contained an expansive and heterogeneous lesion measuring 14 × 9.4 cm with poorly defined limits, including two echogenic nodular areas, measuring 6.3 and 3.2 cm, respectively. The gallbladder was not visualized.
Computed tomography (CT) of the upper abdomen (Figure ) showed a heterogeneous lesion – measuring 15 × 14 × 10 cm – with a partially well-defined margin and hypodense permeating areas, some with attenuation values compatible with soft parts, and others with liquefaction located in the left liver lobe. After endovenous contrast injection, the lesion showed intense and non-homogeneous impregnation in the arterial and portal phases, with hypodense permeated areas located in the left lobe, notably parts II and III; these areas determined recoil and reduced the size of vascular structures adjacent to the liver. The injury also caused bulging of the border of adjacent liver tissue, causing a compressive effect on other abdominal structures, especially the stomach and pancreas.
Magnetic resonance (MR) imaging of the upper abdomen showed different components within the lesion. T2-weighted images in the peripheral region showed a discrete heterogeneous hyperintense signal, while the central portion was hypointense. In T1-weighted images, the signal in the periphery of the mass was similar to the muscle signal and the center of the lesion showed a signal that was clearly hypointense. Although impregnation of both components began in the arterial phase, the peripheral region showed a stronger signal during the arterial and portal phases, followed by signal decay in the late phase due to relatively rapid washout, indicative of hypervascularization. The center of the mass was far more intense in the late phase, probably due to slow flow through the vascular components (Figures and ).
Surgery and pathological analysis revealed a hepatic segment measuring 17.5 × 14 × 8 cm and weighing 1200 g that contained a 15 × 9 cm brown tumor with ill-defined limits. The tumor had a gelatinous component and showed hemorrhaged, necrotic, and cystic areas. The final diagnosis was TA. The patient progressed well and she remains asymptomatic after one year of follow up.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Hypertension history': True, 'age': [72, 'years'], 'Stroke': False, 'Transient Ischemic Attacks History': False, 'sex': 'Female'}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
929,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8312207-2,Extracted,"Patient 2 was an 80-year-old male, diabetic, hypertensive, with history of operated cancer colon in 2011 and chronic renal impairment. COVID-19 for this patient was in April 2021 for which he received corticosteroids. The patient presented 30 days later in May 2021 with hard palate sluggish ulcer 1 cm diameter, blackish, and painless not communicating with nasal cavity, with accompanied decrease in visual acuity in the right eye to the degree of seeing objects at 2 m.
PCR for COVID-19 was negative; CBC showed normal leukocyte count 8.2 × 103/mm3 with relative neutrophilia 84.1% (range 40.0–80.0) and relative lymphopenia 6.7% (range 20–40), CRP 35 (negative < 6.0), HbA1C 9.5, serum creatinine 2.1, and Na 117 mmol/L (range 136–145).
MRI paranasal sinuses performed prior admission at 3 Tesla high field MRI unit revealed near pan sinusitis especially along bilateral frontal, ethmoidal, maxillary sinuses, and left sphenoid. Both ethmoid sinuses show predominantly fungal sinusitis with bacterial sinusitis, while the left maxillary show more bacterial but with fungal component. No abnormal extension of the inflammatory process towards the cavernous sinus regions was noted. Both orbits had normal appearance except for mild form of the left optic neuritis that needed post intravenous contrast study that was inapplicable secondary to renal impairment (Figs. and ).
The patient was planned for evacuation and drainage of the sinuses under general anesthesia after correcting his hyponatremia.
Broad spectrum antibiotics and systemic amphotericin B were administered. Steroid therapy for optic neuritis was considered yet not initiated upon relative request, and the patient was discharged against medical will.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [80, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 80 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
930,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3742775-1,Extracted,"A 63-year-old female patient was admitted to the Galactophore Department, Bao Ji Central Hospital with a huge lump in the left breast. The patient stated that they had identified a thumb-sized lump two years earlier, but that they had ignored it. From July 2011, the patient observed that the lump was growing rapidly; in February 2012 the lump had become so large that the patient’s left chest was entirely covered with a solid, irregularly-shaped, somewhat moveable mass of tremendous size and the patient was barely able to lie in the prone position. Family members then finally convinced the patient to seek medical attention. Upon physical examination, the patient presented with an elastic hard mass in the left breast that was 45 cm in diameter, with a circumference of 97 cm (). Rapid growth had resulted in shiny stretched skin that was translucent, showing underlying extremely enlarged veins with sections of the circuitous veins about to undergo ulceration, although no bleeding or discharge was noted. The lymph nodes in the axillary and other superficial areas were not palpable. The patient’s previous medical history revealed that they had high blood pressure, diabetes and atrial fibrillation. Moreover, the patient had suffered from a cerebral infarction; the patient’s right side was paralyzed and communicative disorders had appeared two years previously. The patient was unable to care for herself due to the cerebral infarction. The patient’s medical history was negative for allergies, smoking, drinking, contagions and serious addiction. Furthermore, there was no family history of breast cancer on either side of the patient’s family.
Due to the non-compressible nature of the mass and the size of the tumor, regular breast examinations, including mammography and ultrasound studies, could not be used, while a computed tomography (CT) scan of the chest revealed a solid mass. Total body scintigraphy was negative. Comprehensive examinations and detailed assessments were additionally performed on the patient due to the presence of high blood pressure, diabetes, atrial fibrillation and cerebral infarction. In order to ensure the long-term success of the treatment, a consultation with the Respiratory Medicine, Vasculocardiology, Neurology and Anesthesiology departments was organized. Antihypertensive, glycemic control, oxygen uptake and antiarrhythmic therapies were administered prior to surgery. The pectoris major and minor had atrophied and were tightly adhered to the tumor due to long-term compression, so the surgeon decided to resect the mass along with these muscles. The mass was resected subsequent to 3 hours of surgery (). The post-operative pathology report showed an extremely large grey mass, weighing 11 kg and measuring 36×40×18 cm, which was covered by ∼32×35 cm of skin tissue. When the tumor was cut into halves along the nipple, it was observed that the majority of the tumor tissue was a myxoid, lobulated mass with multiple hollow cavities, thick, yellow, viscous fluid and certain necrotic areas. The microscopy findings showed extensive necrosis and the majority of the tumor tissue exhibited an epithelial component with a leaf-like pattern, but no cellular atypia. The final histopathological diagnosis was PT of the benign type ().
In view of the benign nature of this tumor, no chemotherapy or radiotherapy was administered following surgery. The patient recovered well and to date there has been no evidence of local recurrence or distant metastasis.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [63, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': False, 'Diabetes history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 63 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
931,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6796756-1,Extracted,"A 54 years old Saudi man, known case of Hypertension, Diabetes Miletus type II for 6 years with history of percutaneous coronary intervention which has been done 2016, due to Ischemic heart disease, atrial fibrillation and old stroke. He presented to emergency department with history of acute confessional state for 1-day duration. He was in his usual state of health till 1 days prior to admission when he presented with symptoms including fever, confusion and decrease oral intake associated with right leg pain. He was discharged recently from the hospital – 2 weeks back – when he was complaining of obvious swollen and erythematous on the right leg below the knee a diagnosis of Right lower limb cellulitis was established, he was vitally stable and treated by antibiotics (clindamycin, ciprofloxacin, meropenem). There was no history of limbs weakness, loss of consciences, seizure, trauma nor facial asymmetry. Furthermore, He denied a recent travel and ingestion of raw seafood. On physical examination, the patient was moderately obese, appeared very ill and agitated. Had temperature of 37.6 °C heart rate of 112 beats per min, respiratory rate of 20 breaths per min, blood pressure of 150/93 mm of mercury, and normal oxygen saturation while breathing room air as measured by pulse oximetry, Glasgow coma scale 14 out of 15. His lungs were clear, he was tachycardic, and the abdomen was normal without organomegaly. The right lower extremity showed gross swelling of the right lower limb up to the level of the thighs with tense right calf muscles, evident bullae and pus discharge from the sole of the right foot. Laboratory tests () revealed a leukocytosis of 16.3 × 109/L, elevation of C-Reactive Protein (15.30 mg/dL) and liver enzymes.
The patient was diagnosed to have infected right foot and impending sepsis. Sepsis protocol was initiated including cultures of blood and wounds. He was admitted on 27/07/2018 to the surgical intensive care unit and underwent surgical debridement of the right foot ulcer with right calf fasciotomy on 28/07/2018 ().
He remained in the surgical intensive care unit for 16 days for further resuscitation. The initial blood culture taken on 27/07/2018 flagged positive for Vibrio cholerae after 8.5 h of incubation in the BACT/ALERT® VIRTUO® (bioMérieux, US). Microscopic examination showed short Gram negative, slightly curved rods (image). As per the lab protocol, it was subcultured on blood, chocolate and Macconkey agar plates. 18 h later, pure growth of non-lactose fermneters was noted which gave positive oxidase and catalase reactions. Vitek MS (matrix-assisted laser desorption ionization-time of flight MS) gave the identity as V. cholerae.
Manual testing confirmed it showing it as Non O1, Non O139 serotype. The organism was grown in TCBS Selective medium (SPML, Saudi Arabia) at 42 C as yellow colonies.
Biochemical reactions, nitrite negative, lysine negative, VP positive and ONPG positive) were illustrated using Vitek II (bioMérieux, US) using the VITEK®2 GN ID card. Non-halophilic nature of the spp. was shown by ability to grow on specialized low salt medium, CLED (SPML, Saudi Arabia).
The initial antimicrobial therapy was of 1 mg IVP of Meropenem, Vancomycin and Tigacyclin 50 mg IVP. The Vibrio cholerae showed antibiotic-resistant to ampicillin. He also received further medications during his Hospital stay. He was moved to surgical ward on 06/08/2018. The right foot wound has improved with healthy granulation tissue on the right leg wound, however, right foot still has some slough along granulation tissue. Therefore, the patient was vitally stable, ready for discharge on 02/09/2018 and to continue daily dressings as an out-patient. The next day 03/09/2018 patient readmitted with urosepsis to medical word. The Surgical team of the hospital followed up as consultation for the progress of the wound and dressings continued. The calf wound was very clean however, the foot wound has minimal slough that needed daily dressings and occasionally bed side debridement. On 03/10/2018 he intubated again due to overwhelming sepsis and set on inotropic support and transferred to medical ICU. Due to the vasopressor effects the whole right leg to the level of the knee became ischemic and black with evidence of wet gangrene ().
Guillotine above knee amputation was done on 07/10/2018 and then patient returned to the medical ICU and continued on inotropic support. Eventually, he passed away at 2:00 am on 09/10/2018.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': True, 'age': [54, 'years'], 'Stroke': True, 'Diabetes history': True, 'Transient Ischemic Attacks History': False, 'sex': 'Male'}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 54 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
932,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5742444-1,Extracted,"This is an 87-year-old African male who presented to the Emergency Department complaining of increase shortness of breath after missing 2 sessions of hemodialysis. Past medical history includes end stage renal disease on hemodialysis therapy, heart failure with preserved ejection fraction, permanent atrial fibrillation, severe pulmonary hypertension, and pericardial effusion with placement of pericardial window. Physical examination revealed blood pressure of 117/59 mmHg, heart rate of 91 bpm, respiratory rate of 18 per minute, O2 sat of 96% on room air, and temperature of 37°C. There were internal jugular vein distention, irregular heart sounds, and basilar lung crackles bilaterally. Electrocardiogram (EKG) confirmed atrial fibrillation and right ventricle hypertrophy with right axis deviation. There were normal QRS voltage and complexes, T waves, and ST segments. Laboratory data were remarkable for troponin I 0.04 ng/ml (normal < 0.02 ng/ml), pro-brain natriuretic peptide 108,187 pg/ml, potassium 3.4 mmol/Lt, creatinine 2.8 mg/dl, hemoglobin 11.4 g/dl, total bilirubin 1.41 mg/dl, and albumin 3.1 gr/dl. Cardiomegaly and blunting of the right and left cost phrenic angles were evident on chest X-ray.
Patient was admitted to medical intensive care unit (MICU) for fluid overload secondary to missing hemodialysis therapy and severe pulmonary hypertension. While in MICU, transthoracic echocardiogram was done, which revealed normal left ventricular (LV) systolic function (ejection fraction > 55%) and severe tricuspid regurgitation (coronary sinus and right atrium were noted to be dilated, and a small loculated pericardial effusion was seen behind the right atrium, with no evidence of cardiac tamponade. Right ventricular systolic pressure was elevated at >60 mm Hg, consistent with severe pulmonary hypertension, and flattening of the interventricular septum (D-shaped left ventricle) with RV overload ().
Shortly thereafter, renal service was consulted and hemodialysis was initiated. Vital signs were recorded and reviewed, while the patient was undergoing hemodialysis therapy, as is illustrated on , the blood pressure trended up continuously as volume was being removed.
After hemodialysis session, the patient's shortness of breath improved and blood pressure trended up instead down as we may expect in normal individuals after removing intravascular volume. Transthoracic echocardiogram was repeated and demonstrated less left deviation of interventricular septum compared with previous echocardiogram ().
Upon discharge, the patient was seen in pulmonary clinic and cardiology clinic as an outpatient at one week and two-month follow-up. He was doing well with improvement of baseline shortness breath and adherence with hemodialysis therapy.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [87, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 87 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
933,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7768527-1,Extracted,"We present the case of a 74-year-old male who was admitted to the hospital after presenting to the emergency department (ED) with the chief complaint of right arm weakness and difficulty in speaking. His past medical history included diabetes mellitus, hypertension, persistent atrial fibrillation on long-term anticoagulation with rivaroxaban, heart failure with reduced ejection fraction of 30% and aortic stenosis with two previous bioprosthetic surgical aortic valve replacements in 2004 and 2014. Two months prior to admission, he was diagnosed with IE caused by Group B Streptococcus involving the aortic bioprosthetic valve. Initially, he presented with complaints of intermittent febrile episodes and night diaphoresis for approximately 8 weeks. At that time, the decision was made to treat him conservatively with oral antibiotics and close clinical monitoring. Blood cultures were negative in two different occasions, and the patient was discharged on stable conditions. However, a day prior to his second hospital admission, the patient noted sudden onset right upper extremity weakness (MRC power grade 3) and dysarthria. Upon further evaluation in the ED, a magnetic resonance imaging (MRI) of the brain revealed multiple embolic strokes ().
Transthoracic echocardiography and computed tomography angiography (CTA) of the chest revealed nonspecific structural changes with images compatible with a possible aortic perivalvular abscess/pseudoaneurysm (). Transesophageal echocardiography (TEE) confirmed a perivalvular cavity around the aortic root, and this cavity was communicating with the aorta. Furthermore, the cavity was also in communication with the left ventricle (LV), creating a dynamic of retrograde flow, with blood passing from the aorta to the LV through the fistulous tract (). As a result, the patient developed an ACF due to perivalvular endocarditis, which resulted in symptomatic severe aortic valve regurgitation.
The patient was transferred to a tertiary care center for further surgical evaluation. His physical examination was unremarkable, except for a slight right facial droop and mild dysarthria. All initial laboratory including new sets of blood cultures were unremarkable. He continued empiric antibiotic therapy with ceftriaxone. Sacubitril/valsartan and metoprolol were discontinued due to concerns of rapid progression to complete heart block in the setting of a perivalvular cavity.
He was evaluated by a multidisciplinary team including specialists in cardiology, cardiothoracic surgery, neurology and infectious disease. The consensus was that patient’s presentation was likely caused by a perivalvular abscess/pseudoaneurysm, which was further complicated by the formation of an ACF, requiring rapid surgical intervention. Coronary angiogram was performed as part of the preoperative evaluation, revealing smooth eccentric narrowing (50–60%) of the ostial/proximal left circumflex (LCx), which raised the suspicion of possible external compression from the known aortic root pseudoaneurysm/perivalvular abscess seen on CTA ().
TEE in the operating room evidenced a large posterior aortic pseudoaneurysm underneath the left coronary artery, corresponding to the narrowing of the LCx. This was then confirmed by surgical exploration and visual inspection. Active infection with pus secretion was noticed around the aortic annulus, with small vegetations on the prosthesis. The surgical procedure consisted of a third cardiac redo surgery with full sternotomy, explantation of previous prosthetic aortic valve and exclusion of the ACF. The aortic root and valve were replaced with a 24 mm homograft, and the LCx was reimplanted.
The patient recovered without significant complications, and he went home with intravenous ceftriaxone through a peripherally inserted central catheter for a total of 6 weeks, and any further oral antibiotic therapy was not required. Close outpatient monitoring with follow-up with cardiology, neurology, infectious disease and primary care provider was arranged in the next week. All neurological manifestations were entirely resolved with treatment and rehabilitation.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [74, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Vascular disease history': True, 'Stroke': True, 'Diabetes history': True, 'Transient Ischemic Attacks History': False}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 74 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 6 + 1 = 7.
The patient's CHA2DS2-VASc Score is 7."
934,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7693558-1,Extracted,"A 77-year-old man with high blood pressure, diabetes, coronary artery disease, and permanent atrial fibrillation was referred to our Heart-Brain Outpatient Clinic for a second opinion on the best secondary prevention therapy after two previous ischemic strokes.
The first event was characterized by right-sided hemiparesis affecting mainly the arm associated with right hemianopia and hypoesthesia. Neuroimaging revealed a left temporo-parieto-insular cortico-subcortical ischemic lesion ().
At the time of the event the patient was taking apixaban 2.5 mg twice daily even though he had normal kidney function and a body weight of 85 kg. Therapy was then changed to dabigatran 150 mg twice daily. Two months later the patient had another ischemic stroke characterized by motor impairment in the left hand associated with a right cortico-subcortical parietal ischemic lesion ().
Based on the results of thorough stroke work-up, excluding among others atherosclerotic plaques in cervical and intracranial arteries, aortic-arch atherosclerosis, and occult cancer, atrial fibrillation was considered to be the most likely etiology of patient's recurrent stroke.
Patient reported excellent adherent to anticoagulation therapy. Trough and peak dabigatran plasma levels were within the expected therapeutic range (71 ng/ml, range 61–143; 134 ng/ml, range 117–275, respectively).
The use of concomitant medications that may have altered the dabigatran effect was excluded.
The event was therefore classified as “resistant stroke.”
The patient underwent a thorough cardiological study. Cardiac computed tomography (CT) scan was performed to assess the left atrial appendage (LAA). It revealed an oval-shaped LAA with windsock-like morphology in the proximal part (ostium and landing zone) while distally the LAA presented multi-lobated with a large amount of pectinate muscles and a small retro-verse distal lobe with a small amount of blood stagnation (), configuring a cauliflower morphology according to Di Biase criteria () (). The mean diameter of the landing zone was 21 mm. The morphology of this LAA was considered to be at high risk for thrombus formation due to its dimensions, distal fragmentation and presence of small lobatures, favoring blood stagnation.
Taking into account the patient's clinical history, the occlusion of LAA as an adjunct therapy to oral anticoagulants was considered and proposed to the patient who, after adequate information, gave his consent.
Transesophageal echocardiography was performed prior to the procedure revealing a “plus” image in the distal part of the appendage suspected of being a clot (). Selective angiography showed stagnation of contrast in the distal lobe, with a slow wash out (). The integrated evaluation of the three imaging modalities allowed to attribute the anomalies to a prominent pectinate muscle.
LAA-occlusion was successfully performed with a 25 mm Amplatzer Amulet occluder (Abbott, Chicago, IL, USA) () and subsequent recovery was uneventful. Patient was discharged with dabigatran 150 mg twice daily and an indication to maintain it lifelong.
The patient was asymptomatic at 6-months follow-up.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [77, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': True, 'Stroke': True, 'Diabetes history': True, 'Transient Ischemic Attacks History': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 6 + 1 = 7.
The patient's CHA2DS2-VASc Score is 7."
935,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7676954-1,Extracted,"A 76-year-old female was referred to our unit for surgical management of upper gastrointestinal bleeding after unsuccessful endoscopic therapy. She had undergone a stomach partitioning gastrojejunostomy 20 years prior which made access with endoscopy difficult (Figure ).
Relevant other medical history included morbid obesity (BMI 62.5 kg/m2), atrial fibrillation, insulin-dependent diabetes mellitus, and obstructive sleep apnoea and iron deficiency anaemia. She was a non-smoker and was not on any regular non-steroidal anti-inflammatory drugs (NSAIDs) or regular proton pump inhibitors. There was no prior history of fever, abdominal discomfort/pain or vomiting but only melena. Her vital signs were within the normal range, and her abdominal examination revealed mild tenderness in the epigastrium. Her blood results showed haemoglobin 75 g/L, white cell count of 7.32x109/L, urea 14 mmol/L and creatinine 100 micromole/L. An abdominal CT scan showed mild distension of the stapled stomach, measuring up to 10 cm in diameter (Figure ) with a mixture of gas and high-density material, suspicious for blood clot but no evidence of active bleeding. Her initial gastroscopy showed normal proximal gastric pouch but mucosal necrosis in the excluded stomach pouch adjacent to the pylorus, which was biopsied (Figure ).
She was managed conservatively with high dose proton pump inhibitors (PPIs). However, she still experienced ongoing melena and required daily blood transfusions which prompted a surgical referral. She was taken to the operating theatre for an exploratory laparotomy which revealed a distended excluded stomach with full-thickness ischemia of the posterior wall with perforation into the lesser sac. Duodenum, jejunum and colon appeared healthy and viable. Due to concern of possible gastro-gastric fistula, the gastrojejunostomy was excised with the excluded stomach portion. A new Roux-en-Y reconstruction was performed subsequently. Histopathology showed tissue necrosis, and a dense mixed inflammatory cell infiltrates with fat necrosis and suppuration with the presence of Helicobacter pylori (Figure ).
There was no evidence of neoplasia. Postoperatively, she failed to improve, developing pneumonia and intra-abdominal collections which were managed with antibiotics and percutaneous drainage. She subsequently developed multi-organ failure and unfortunately passed away three weeks after her operation.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [76, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
936,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7500746-1,Extracted,"A 79-year-old male patient with a past medical history of hypertension, hyperlipidemia, type II diabetes, and a previous deep venous thrombosis (DVT) experienced a syncopal episode while at home. In the emergency room of an outside hospital, he was found to have right-sided weakness, gaze deviation, and altered mental status consistent with a left middle cerebral artery stroke. A CT scan of his head was negative for a bleed. The patient was administered tissue plasminogen activator (tPA) 173 minutes after he was last known to be without symptoms. Following the treatment, his neurological symptoms improved. A subsequent CT angiogram of the patient’s head and neck showed normal cerebral vasculature without occlusive thrombus or dissection. After his stroke symptoms largely abated, the patient developed respiratory distress. He was intubated and started on vasopressors, but he remained persistently hypoxic. Initially, the patient was believed to have aspirated. As his clinical picture worsened, the differential was broadened to include septic, cardiogenic, and obstructive shock. The patient’s history of a DVT suggested a potential massive PE which could result in obstructive shock. His prior DVT occurred over 10 years ago, and he completed an unspecified anticoagulation regimen at that time. The patient was transferred to Rush University Medical Center (RUMC) for escalation of care.
A transthoracic echocardiogram (TTE) showed a severely dilated right ventricle consistent with McConnell’s sign (Figure ). Lower extremity ultrasound showed an extensive DVT in the right leg. These findings strongly suggested a PE as the cause for the patient’s instability. A subsequent CT pulmonary angiogram confirmed this suspicion by revealing a large clot burden in the right pulmonary artery (Figure ). It also showed chronic emboli in the left main pulmonary artery. The patient was started on a heparin infusion within 24 hours of receiving tPA. Once the heparin was at a therapeutic level, a repeat head CT was obtained and, again, was negative for bleeding. Despite initiation of heparin, he remained hypoxic and hypotensive.
The patient developed new-onset atrial fibrillation after arriving at RUMC. This arrhythmia likely resulted from the increased demand on the heart from the extensive clot burden in the lungs. The patient experienced multiple episodes of rapid ventricular response that were unsuccessfully treated with digoxin. He was started on an amiodarone infusion that better controlled the rate.
To resolve the PE, mechanical thrombectomy was considered, but at the advice of the stroke team, it was deemed too risky; the patient could not safely tolerate the usual therapeutic dosage of heparin needed to perform the procedure with the traditional devices. Thus, the Penumbra Indigo® system (Alameda, CA, USA).was chosen for its ability to achieve thrombus aspiration within a lower therapeutic heparin range. Additionally, the device was of a small enough caliber to operate within the pulmonary arteries.
Percutaneous pulmonary artery aspiration thrombectomy was done via the right internal jugular vein using the Penumbra device. An inferior vena cava (IVC) filter was also placed during the procedure. By the next day, TTE showed that the patient’s right ventricle had already significantly decreased in size (Figure ). Three days following the procedure, he was extubated and weaned completely off vasopressors.
As the patient continued to improve, a transesophageal echocardiogram (TEE) was obtained that showed evidence of a patent foramen ovale (PFO). No evidence of left atrial appendage thrombus was seen on the TEE. Direct current cardioversion (DCCV) was done to treat his atrial fibrillation, and he was successfully converted into sinus rhythm. In an attempt to determine the cause of the DVT, a CT scan of his abdomen and pelvis was obtained. The imaging did not reveal any specific malignant or metastatic processes to explain his hypercoagulable state. Further investigation into his DVT was deferred as the findings would not change his coagulation management: life-long anticoagulation therapy. Prior to discharge, the patient was taken off of the heparin infusion and he was started on oral apixaban to be taken indefinitely.
Ultimately, the etiology of the patient’s stroke was not determined. One potential etiology was a cardioembolic stroke brought on by the new-onset atrial fibrillation. Alternatively, the stroke could have been due to a venous thromboembolism which traveled through his pre-existing PFO.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [79, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': False, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 79 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
937,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3491208-2,Extracted,"A 64-year old female patient presented with transient dizziness and memory impairment. She had a history of previous ischemic stroke with a 10-year medical history of diabetes mellitus and hypertension. Findings on MRI revealed an old border zone infarct at the right fronto-parietal lobe, and old small infarctions at the basal ganglia and the right paramedian pons. Cerebral angiography indicated right cavernous ICA stenosis of approximately 75%. During insertion of guiding catheter, acute thrombosis occurred and the patient developed left hemiparesis (motor grade 2). After thrombolysis with 300,000 IU urokinase, the occluded artery was recanalized and the left hemiparesis showed improvement, allowing us to perform balloon angioplasty using a Gateway balloon (2.5 × 15 mm) with successful placement of a 4 × 20 mm Wingspan stent. We obtained post-procedure images indicating reduction of stenosis (stenosis 25%). However, cerebral angiography revealed CCF at the stent implantation site. Transvenous coil embolization was performed successfully through the right inferior petrosal sinus. After three days, the patient developed third nerve palsy, including ptosis and paralysis of extraocular movement, however, diffusion MRI did not reveal any abnormalities. The third nerve palsy showed gradual improvement, and showed complete resolution within three months.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [64, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': True, 'Vascular disease history': False, 'Diabetes history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 64 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
938,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3859204-1,Extracted,"A 63-year-old male with a history of HIV/AIDS (last known CD4 count of 279 CMM) and disseminated Cryptococcus presented to the emergency department with a painful protuberant left lower extremity cutaneous mass. He initially experienced symptoms of bilateral lower extremity lesions four months prior to presentation, during which surgical biopsy of a left lateral calf mass yielded necrotizing granulomatous inflammation with Cryptococcus. During that admission, he was treated with amphotericin and flucytosine and discharged home on oral fluconazole. These cutaneous lesions persisted and he was treated with periodic incision and drainage of these areas; however, this new lesion on his left lower extremity appeared over several weeks prior to this admission and brought him to the emergency room. His physical exam was remarkable for the following skin findings: (1) the anterolateral aspect of his right thigh had two fluctuant, well-circumscribed, circular lesions approximately 3 cm in diameter that were tender to palpation and nonmobile and (2) his left lower extremity had a fleshy-appearing, pinkish, ovular exophytic mass approximately 5 cm in diameter that was tender to palpation and appeared to be growing over an area of previous Cryptococcus infection ().
His laboratories showed a repeat absolute CD4 count of 93 CMM, HIV RNA PCR of 117 copies/mL, and CBC significant for a normocytic, normochromic anemia (with an otherwise unremarkable differential). Given the different appearance of his new left lower extremity lesion, a repeat biopsy was performed. The biopsy of the cutaneous lesion revealed sheets of large cells with an abundant amount of cytoplasm with plasmacytoid features and increased mitosis (). In some areas, there was an increased number of tingible body macrophages noted. Immunohistochemical analysis identified malignant lymphoid cells that expressed CD138, CD79a, OCT-2, BOB-1, and MUM-1 with high mitotic rate as noted by Ki67, while the lymphoma cells were negative for CD20, CD30, and HHV-8. A cMYC rearrangement was detected by FISH. Flow cytometric analysis also supported the virtual absence of B-cell markers in the tumor cells. These findings were consistent with plasmablastic lymphoma. A bone marrow biopsy was performed which was negative for any bone marrow involvement, and a staging CT scan showed a pulmonary nodule identified in the left lower lobe which is 1.8 × 1.8 cm in diameter (), a left perirectal soft tissue mass 2.0 × 2.2 cm in diameter (), and a focal area of left anal wall thickening 2.4 × 1.6 cm in diameter. Further biopsies were not pursued, and the patient was subsequently started on his first cycle of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP). The patient was recovering from his first cycle and awaiting his second cycle of CHOP at the time of this report.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [63, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 63 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
939,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8345899-1,Extracted,"A 70-year-old male was presented to our hospital complaining of on and off chest pain for five days. The pain was over the epigastrium and the left side of the chest with no radiation. It was burning in character and associated with epigastric discomfort and belching. There was no associated sweating, breathing difficulty, abdominal pain, headache, fever, swelling of legs, and any changes in appetite and weight. There were histories of hypertension and hyperlipidemia for which he was on amlodipine 5 mg daily and atorvastatin 20 mg daily, respectively. He had a history of gastroesophageal reflux disease. There was a 30-pack-year of smoking history, and he denied intake of alcohol or any illicit drugs.
For these complaints, he had initially visited the local health center. Antacid syrup and intravenous (IV) pantoprazole were given, and an ECG was done. The initial ECG done in the local health center is as shown in Figure .
With these complaints and ECG findings, he was referred to our hospital. At presentation, his vitals were stable, and saturation was normal on room air. The lab results revealed a normal complete blood count and comprehensive metabolic panel with negative troponin-T, CK-MB 15 U/L (reference range 0-24 U/L), and troponin-I 0.009 ng/mL (reference range < 0.03). The chest x-ray was normal, and the ECG taken at our hospital showed deeply inverted T-waves in anterior chest leads (V2-V4), as shown in Figure suggesting Wellens syndrome type II.
He was treated medically with one dose of 300 mg aspirin followed by 75 mg aspirin daily, atorvastatin 40 mg daily, and started on a heparin drip. A transthoracic echocardiogram of the heart was done, and he underwent cardiac catheterization. He was found to have a clot in the proximal LADCA, which required catheter-directed thrombectomy and drug-eluting stent placement. He did well throughout the procedure, and his vitals were stable after the procedure.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [70, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 70 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
940,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7749959-1,Extracted,"A 57-year-old Caucasian male with atrial fibrillation (not on anticoagulation), hypertension, monoclonal gammopathy of undetermined significance, and AL amyloidosis with known liver involvement leading to cirrhosis initially presented to his local emergency department with right-sided weakness and headache. His blood pressure on presentation was 164/78 mmHg, and he was found to have a left parietal intraparenchymal hemorrhage and an incidental right parietal arteriovenous malformation []. He was medically managed with aggressive antihypertensive therapy and was discharged to an acute rehabilitation center with stable right-sided weakness (strength diffusely 4/5) within a few days.
He was readmitted 1 month later with severe headaches and worsening right-sided weakness (3-/5 strength) with a blood pressure of 148/73 mmHg. A head computed tomography (CT) revealed an increase in size of the left parietal hemorrhage. At that time, he also experienced epistaxis as well as catheter site bleeding that resolved spontaneously. Laboratory workup showed a stable platelet count of 127 × 109/L, normal factor X activity (338%), normal von Willebrand factor activity (736%), and a mildly elevated international normalized ratio (INR) of 1.4 for which he was given intravenous (IV) Vitamin K (phytonadione). Interval imaging demonstrated stability of the intraparenchymal hemorrhage; however, due to concern for seizures and altered mental status, he had a prolonged hospitalization on the neurology service. He was subsequently discharged back to rehabilitation with an antiepileptic drug regimen of levetiracetam (2000 mg twice daily), clobazam (20 mg twice daily), and lacosamide (50 mg daily).
The patient was readmitted 2 months later to our institution for worsening encephalopathy. A head CT showed a mild increase in ventricular size in addition to the resolving left parietal intraparenchymal hemorrhage. An electroencephalogram and extensive metabolic and infectious workup were unremarkable. Given the possibility of delayed hydrocephalus as explanation for his worsening encephalopathy, the patient was trialed on cerebrospinal fluid diversion with an EVD []. However, 5 days after EVD placement, routine interval imaging revealed a hemorrhage along the tract of the EVD. The tract hemorrhage continued to increase in size over the next few days [-]. Laboratory workup revealed mildly low platelets to 110 × 109/L, a normal partial thromboplastin time (PTT) of 30.8, and an INR of 1.4. He was given 3 days of IV phytonadione; however, his INR did not normalize. Given the expansion of the tract hemorrhage and his underlying AL amyloidosis with cirrhosis, further coagulopathy testing was pursued. This revealed a low factor VII level (38%), a normal factor II level (69%), a normal factor IX level (69%), a normal factor X level (65%), and elevated factor VIII (166%) and von Willebrand factor (421%) levels. Recombinant activated factor VII (rFVIIa) (20 mcg/kg every 2 h for 3 doses) was administered to promote clot formation and achieve hemostasis. He also had normalization of factor VII levels to 122%. A head CT performed a day later revealed stability of the tract hemorrhage [ and ]. Two days later, he developed an acute worsening of examination with fixed pupils and extensor posturing. Repeat imaging revealed development of a new acute subdural hemorrhage []. He was found to have low factor VII level to 31%. He underwent a left hemicraniectomy and was given rFVII (20 mcg/kg every 2 h for 3 doses) and placed on a continuous infusion of aminocaproic acid at 1 g/h intraoperatively which stabilized the bleeding. He was continued on the aminocaproic acid infusion postoperatively throughout his hospital stay. Despite evacuation of the hematoma and bleeding stabilization, his mental status did not improve. He was transitioned to comfort care measures and passed away within a few days.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [57, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Diabetes history': False, 'Transient Ischemic Attacks History': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 57 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
941,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8510667-1,Extracted,"We present a case of a 79-year-old African American male with a past medical history of diabetes mellitus type II, essential hypertension, and atrial fibrillation with symptomatic normocytic anemia resulting from three distinct GI cancers. The patient was treated with gastroduodenectomy with Billroth II anastomosis, gastric fundus resection, and distal pancreatectomy. The patient initially presented to the emergency department (ED) with syncope and tachycardia. He reported experiencing symptoms of fatigue, abdominal pain, and lightheadedness for 2 months. Complete blood count revealed a hemoglobin level of 4.9 g/dL requiring three packed red blood cell transfusions.
On the following day, due to his symptoms and concurrent severe anemia, the GI mass was suspected, and a CT of the abdomen and pelvis with contrast was promptly ordered. The findings of the CT report demonstrated a 1.3-cm ovoid filling defect in duodenal bulb () and a 1.5-cm cystic lesion in the pancreatic tail (). Furthermore, the patient completed an esophagogastroduodenoscopy (EGD) which exhibited a mass in the duodenal bulb that was partially resected for biopsy. The biopsy confirmed invasive adenocarcinoma of gastroduodenal origin with a histological grade of III/III under World Health Organization (WHO) classification.
The patient underwent exploratory laparoscopic resection of the duodenal bulb mass and pancreatic tail mass. During the surgical removal of the duodenal bulb tumor, the examination of the stomach showcased a pedunculated mass near the fundus on the posterior wall of the stomach. The posterior wall mass was excised with duodenal and pancreatic masses and all samples were sent to pathology.
The pathological report for proximal duodenum mass showed an in situ and invasive well to moderately differentiated adenocarcinoma measuring 4.5 × 2.3 × 2.3 cm with infiltration into the submucosa (). The posterior gastric wall mass was reported to be a GIST, 1.3 × 1.1 × 0.8 cm in size. This tumor was of low grade, spindle cell type, with dystrophic microcalcifications (). The cells stained positive with Dog1, CD34, and c-KIT. The mass on the tail of the pancreas was shown as a well differentiated neuroendocrine tumor measuring 0.8 × 0.5 × 0.5 cm. The tumor stained positive for AE1/AE3, CAM5.2, and diffusely strong staining with neuroendocrine markers (synaptophysin, chromogranin (CGA), neuron-specific enolase (NSE), and CD56) (). The oncology report demonstrated that all of the cancers were excised completely with clean margins and therefore, no chemotherapy treatment was planned.
The patient’s postoperative course revolved around management of any complications related to surgery and maintaining the hemoglobin levels. The patient’s postoperation day (POD) 1 hemoglobin/hematocrit (H&H) levels were 10.2/35.1. The H&H levels on POD 7 were 8.9/29.8 and POD 14 were 9.1/31.7. The patient did not report further abdominal pain and was no longer having episodes of syncope. The patient is currently recovering well.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [79, 'years'], 'sex': 'Male', 'Diabetes history': True, 'Hypertension history': True, 'Congestive Heart Failure': False, 'Vascular disease history': False, 'Thromboembolism history': False, 'Transient Ischemic Attacks History': False, 'Stroke': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 79 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
942,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4683789-1,Extracted,"A 50-year-old male presented to the Cardiology department due to edema of the legs, erythema, pain, abdominal swelling, and was hospitalized with pulmonary hypertension, right heart failure, atrial fibrillation, chronic obstructive pulmonary disease, and cellulitis. The patient had a history of appendectomy when he was 20 years old and had been stabbed in the abdomen when he was 35 years old. He had been stabbed twice, and 1 h after the stabbing, he had been successfully treated by general surgery. The patient had been discharged 1 week postoperatively. The patient also had a 4-year history of smoking during his adolescent period. Five years earlier, the patient (age 45 years) had presented to the Cardiology outpatient service and was diagnosed with New York Heart Association (NYHA) Class II shortness of breath. On echocardiography (echo), his right heart cavity dimensions were mildly increased and pulmonary artery systolic pressure was found to be 45 mmHg. After treatment, his complaints regressed completely. Three years earlier (age 47 years), he had been admitted to the Pulmonology department with abdominal and bilateral leg swelling, and shortness of breath (NYHA Class III) complaints. CT thorax was performed and he was diagnosed with right heart failure. But dilated IVC was missed or might have been accepted as secondary dilatation to pulmonary hypertension and right heart failure. Intravenous diuretics, steroids, teophylline, and inhaled bronchodilator treatment had been administered. Subsequently, his complaints regressed. His echo findings at that period of time were as follows: Left ventricular ejection fraction 65%, Grade I diastolic dysfunction, normal left heart cavities, significantly enlarged right heart cavities, pulmonary artery systolic pressure 70 mmHg, and Grade 2–3 tricuspid failure. He was being closely monitored by the pulmonologist for pulmonary hypertension. One year earlier (age 49 years), he had been admitted to the Pulmonology department due to newly developed high ventricular rate atrial fibrillation (168 bpm) resulting in significant abdominal ascites, diffuse edema of the lower extremities, and crackles in the middle and lower lung zones (NYHA functional Class IV). At that period of time, the echo had shown normal left heart cavity dimensions, left ventricular ejection fraction 50%, paradoxical interventricular septal motion, significantly enlarged right heart cavities, pulmonary artery systolic pressure 95 mmHg, and Grade 3 tricuspid insufficiency. The patient was started on digoxin 1 × 1 tb, diltiazem 2 × 120 mg, and warfarin by the cardiologist. In 1 week, his symptoms regressed to NYHA Class III and he was discharged from the hospital. Fifteen days later, the patient was admitted to Emergency department with symptoms of worsening right heart failure and shortness of breath; therefore, he was moved to the Cardiology department and started on intravenous furosemide, spironolactone 25 mg, clexane 2 × 0.6 cc (because of subtherapeutic international normalized ratio), and continued on diltiazem and digoxin. According to the dermatologist's recommendation, he was also started on ampicillin/sulbactam 4 × 1 g IV. Laboratory findings were as follows: Blood urea nitrogen 60 mg/dl (normal range 7–22 mg/dl), creatinine 1.2 mg/dl (normal range 0.8–1.3 mg/dl), aspartate aminotransferase 40 U/l (normal range 0–35 U/l), alanine aminotransferase 45 U/l (normal range 0 –35 U/l), hemoglobin 12.8 g/dl (14.0–17.4 g/dl), white blood cells 14,500/µl (normal range 3,500–10,500 µl). On the second day of admission, the patient first developed respiratory arrest and then cardiac arrest. Cardiopulmonary resuscitation (CPR) was initiated, the patient was intubated, and on the 5th minute of CPR, he gained basal rhythm of atrial fibrillation and a blood pressure of 100/60 mmHg. The patient was then transferred to the intensive care unit and placed on a mechanic ventilator. With an initial diagnosis of pulmonary embolism, the patient had undergone pulmonary CT angiography; however, no thrombi were detected. Deep vein thrombosis (DVT) protocol CT was not performed. Only thorax CT angiography and lower extremity venous Doppler ultrasonography were performed. But no thrombotic formation was detected at Doppler examination. The diagnosis was missed by physicians. But simple abdominal auscultation revealed the diagnosis. The IVC diameter was found to be 19 cm. On cardiologic evaluation, at the tricuspid focus, on the left and right corners, a harsh pansystolic murmur at 4–5/6 intensity was heard. The liver was palpable 7–8 cm under the costal arch, and diffuse ascites was detected in the abdomen. Edema of the legs was 3+. On the umbilical region of the abdomen, a continuous thrill and a machine-like murmur were detected []. On echo, right cardiac cavities were severely enlarged, and 3–4 degree of tricuspid failure, pulmonary artery pressure of 75–80 mmHg, and normal left heart cavities were detected. IVC was measured and found to be 18 cm. On the region of abdominal murmur, the echo probe showed fistula between the abdominal aorta and the IVC on transverse plane [Figure and ]. Transesophageal echocardiography showed intact interventricular septum and patent foramen ovale of the interatrial septum. Right to left shunt of the patent foramen ovale was seen. CT angiography was performed in order to confirm the ACP and to determine its dimensions. Right at the lower level of renal artery and bifurcation of the aorta, between IVC and abdominal aorta, a fistula was detected. At the localization of fistula on the lower level of the renal artery [], the diameter of the aorta was 22 mm, IVC diameter was 99 mm, and the diameter of the fistula tract was 11 mm. At the localization of fistula on the abdominal aortic bifurcation [], the aortic diameter was 25 mm, IVC diameter was 169 mm, and fistula tract diameter was 17 mm. Hemodynamic work-up and shunt measurements were planned. On abdominal aortography, findings consistent with CT angiography (two fistulas from the abdominal aorta to the IVC) were found []. Oxymetrically calculated left-to-right shunt was 2.8. On coronary angiography, the coronary arteries were normal and systolic pulmonary artery pressure was 75 mmHg []. The patient's condition was hemodynamically stabile; however, considering the possible complications, the ACP was decided to be closed percutaneously. The procedure was to be performed after the pneumonia secondary to intubation had resolved. Despite the antibiotic therapy, the pneumonia did not resolve. The patient developed sepsis and died of septic shock in the intensive care unit.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [50, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 50 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
943,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5353448-1,Extracted,"A 67-year-old male presented to the emergency room because of a transient confusion episode one week before. He had a silent past personal medical history. Physical examination was negligible, whilst the electrocardiogram showed the presence of atrial fibrillation and T wave inversion in V3-V6 leads. Non-contrast-enhanced computed tomography (CT) scanning of the brain detected a hypodense area within left insular cortex. Doppler echography of supra-aortic arteries was unremarkable. Transthoracic echocardiogram demonstrated a 18 × 10 mm oval-shaped, homogeneous, echo dense, highly mobile mass floating in left ventricular apex [Figure and ]. Concomitant findings were dilated left atrium without a significant mitral regurgitation, and dilated left ventricle with severely depressed global function (EF = 25%) in presence of akinetic apex. The intracardiac mass was characterized by pronounced mobility, lack of an identifiable peduncle (thus supposed to be faint), regular borders without capsule and homogeneous texture similar to myocardium (closer to the texture of vascularized tissues than to that of fibrotic or thrombotic structures). Coronary angiography showed no significant stenosis. Cardiac magnetic resonance imaging (MRI) excluded contrast enhancement of the mass, anyway its accuracy was limited by reduced temporal resolution in presence of atrial fibrillation and pronounced mass mobility. Owing to the embolic risk and the unaltered aspect after seven days of anticoagulant therapy, the patient underwent successful surgical excision through a video assisted Port Access approach [Figure and ].
Histopathologic examination identified organized hematic material configuring a white thrombus. Recovery was rapid and uncomplicated, optimal medical treatment for heart failure together with oral anticoagulant therapy was administered and well tolerated. Pre-discharge control echocardiography on the sixth day revealed a mild recovery in left ventricular function with a 35% ejection fraction, in the absence of apical thrombus recurrence.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [67, 'years'], 'Congestive Heart Failure': True, 'Stroke': True, 'Transient Ischemic Attacks History': True, 'Vascular disease history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 67 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
944,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4119906-1,Extracted,"This case is about a 40-year-old man who was presented to emergency with syncope that happened at work. He had no prior history of cardiac disease. The physical examination was normal. The ECG showed a regular sinus rhythm at 70 beats per minute, a complete right branch block, and posterior left hemiblock (), and PR interval was 120 ms. Transthoracic echocardiography revealed normal echocardiographic findings with normal left ventricular systolic function.
Electrophysiological study (EPS) was performed by intracardiac route in this patient with unexplained syncope and atypical ECG. We recorded a regular sinus rhythm, an AH interval was 150 ms, and HV interval was −24 ms. Programmed atrial stimulation was performed in the basal state and showed an effective atrial refractory period of right atrium at 200 ms and effective refractory period of accessory tract was 300 ms (). The QRS had the same morphology during atrial pacing. We found a dissociation atrioventricular conduction in retrograde. We inserted a catheter of exploration in coronary sinus; we recorded a shorter AV at the distal electrode of decapolar that confirmed the diagnosis of a left accessory bypass (). The use of isoproterenol (isuprel) showed a classic Wolff-Parkinson-White syndrome with slurred initial QRS. This ECG showed fusion of antergrade conduction from both the left sided accessory pathway (AP) and AV node (). AH interval with isuprel was 100 ms and HV interval was 42 ms. This was explicated by an accelerated atrioventricular conduction with isuprel in addition to accessory pathway (). The effective refractory period of accessory pathway was 210 ms with isuprel (). We supposed that atrial fibrillation caused ventricular fibrillation responsible for syncope. Thus, we had decided to ablate the accessory pathway ().
After accessory pathway ablation, the patient was in nodal AV block with QRS complexes of normal duration (0.10 s). In Atrial pacing, an anterograde Wenckebach cycle length was 130/BAT (suprahisian AV block). The patient became asymptomatic.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [40, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 40 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
945,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7724407-1,Extracted,"A 58-year-old man was referred to a pulmonary hypertension clinic with a progressive
history of heart failure (III functional class NYHA) with orthopnea, peripheral edema, and
the presence of severe pulmonary hypertension (PH) according to a transthoracic
echocardiographic evaluation (TTE). The history included radiofrequency catheter ablation of
atrial fibrillation incorporating pulmonary vein (PV) isolation 10 months ago in a different
hospital. One month after ablation the patient reported shortness of breath, which was
explained by the recurrence of persistent atrial fibrillation. Contrast-enhanced chest CT
was performed at a local hospital and revealed lung interstitial changes and lymphadenopathy
and signs of PH. There was no evidence of both acute and chronic pulmonary embolism
(PE).
At admission, TTE showed left atrial dilatation (left atrial volume index
42 ml/m2), preserved right ventricle size and function (4-chamber basal size
38 mm; tricuspid annular plane systolic excursion 1.7 cm), and preserved left ventricle
systolic function (left ventricular ejection fraction 55%). The pulmonary artery was dilated
(26 mm), and the estimated pulmonary artery systolic pressure was 70 mmHg.
Chest dual-energy CT-angiography (tube A—140 kV, 47 mAs; tube B—80 kV 80, 235 mAs) was
performed and revealed multiple PV stenosis (). A detailed analysis demonstrated the following
PV inflow variant: R 4b and L 2a in Marom classification. There are four separate ostia of the right PVs
(right upper lobe pulmonary vein (RUL), right middle lobe pulmonary vein (RML), superior
segment right lower lobe pulmonary vein (SSRLL), right lower lobe pulmonary vein (RLL); two
separate left PV ostia (left upper lobe pulmonary vein (LUL), and left lower lobe pulmonary
vein (LLL)). LLL pulmonary vein was present as a confluence of superior segment left lower
lobe (SSLLL) and basal pyramid veins (5 mm distal to the PV ostium). Three right PVs were
stenotic: there was a sub-occlusion of RUL, sub-occlusion of SSRLL, 70% stenosis of RLL. Two
left PVs were stenotic: 35% stenosis of LUL; total occlusion of SSLLL, and 75% stenosis of
the basal pyramid PV branch. Dual-energy CT iodine maps showed the following “perfusion”
defects: a large irregular defect in the right upper lobe, segmental defects in the right
S6, in the left S3, S6, S8, subsegmental in the left and right S10. A moderate
“hyperperfusion” of the right middle lobe was determined.
PV angioplasty was indicated, and the heart team suggested right heart catheterization
(RHC) with percutaneous PV ballooning and stenting as the first-line approach.
Under light sedation, right femoral cannulation was performed using the Seldinger
technique. RHC defined severe postcapillary PH: mean pulmonary artery pressure (PAP)
30 mmHg, pulmonary artery wedge pressure (PAWP) 29 mmHg. An antegrade transseptal access was
performed using a Brokenbrough needle, and a steerable 8F transseptal sheath (Direx, Boston
Scientific, USA) was introduced into the left atrium. Selective PV angiography using a 6F
multipurpose catheter (Cordis, Johnson and Johnson, USA) confirmed the presence of two PV
occlusion (SSRLL and SSLLL brunch), sub-occlusion of RUL, RLL and stenosis of LUL about
50%.
Considering the number of severely stenotic PVs, a decision on a two-stage angioplasty
approach was made. Since the right lung was more “hypoperfused” according to the CT iodine
maps, the right PVs were targeted first. The right upper lobe PV was dilated and stented
with the balloon-expandable stent Renal Dynamic 7 × 19 mm (Biotronik, Germany). The lower
lobe PV was stented with the Epic stent 10 × 30 mm (Boston Scientific). Cannulation of SSRLL
was unsuccessful during the first procedure. A slight decrease in PAP was noted: from
51/20/30 to 45/18/27 mm Hg. The patient was discharged with clinical improvement on triple
antithrombotic therapy.
A second angioplasty was performed after one month. The previously stented PVs showed no
restenosis. A second successful SSRLL cannulation attempt was performed, and the Promus
3.5 × 24 (Boston Scientific) stent was implanted. A Dynamic Renal 6 × 15 stent (Biotronik)
was implanted into LLL. Balloon angioplasty of LUL was performed. Multiple attempts for
cannulation of SSLLL brunch were unsuccessful. The control RHC showed reduction of mean PAP
to 21 mm Hg and PAWP to 17 mm Hg. There were no complications during and following the
interventions.
Control CT-angiography at discharge demonstrated restored lumen of all PVs with
angioplasty, and slight residual narrowing of LUL. Triple antithrombotic therapy with
aspirin, clopidogrel, and dabigatran 150 mg BID was prescribed for one month and then
changed to a combination of dabigatran and clopidogrel. The patient significantly improved
and had no dyspnea at three months of follow-up.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': True, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': False, 'age': [58, 'years'], 'Stroke': False, 'Transient Ischemic Attacks History': False, 'sex': 'Male'}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 58 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
946,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6709124-1,Extracted,"A 54-year-old right-handed woman was admitted to our hospital presenting with diplopia, slurred speech, and slightly distal numbness of the left upper limb for four days. Her medical history was notable for hypertension, type 2 diabetes mellitus, hysteromyomectomy and ischemic stroke without significant consequences. In the neurological examination, the following symptoms were found: dysarthria, bilateral seventh nerve palsy, right conjugate gaze palsy, loss of adduction of the right eye. Besides, horizontal nystagmus on abduction of the left eye was also observed. In addition, the patient showed slightly limited abduction of left eye (Fig. A). Brain MRI showed the infarctions including the bilateral pontine tegmentum and a narrow lesion along the midline in the right of the pons, which run through the pontine tegmentum to the ventral side (Fig. ). After admission, the patient received treatments such as antiplatelet aggregation, plaque stabilization, free radicals elimination, circulation improvement, nerves nourishment, and other symptomatic treatments.
In the period of 2 months of follow-up, the patient's slurred speech improved definitely. And her ocular movement recovered basically. Besides the bilateral facial paresis was also improved (Fig. H).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [54, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Diabetes history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 54 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
947,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6942334-1,Extracted,"In June 2018, a 38-year-old female patient was admitted to our hospital with anemic uterine bleeding and fever of 38.3 °C (Fig. ). Her personal history was remarkable for diabetes mellitus type I, a combined kidney and pancreas transplantation in 2016 and known uterine myomas, which were the origin of several episodes of hemorrhagic bleeding within the last 2 years. The nulliparous patient was in regular gynecological examination without surgical interventions. She was denied implantation of any levonorgestrel containing intrauterine device because of concerns about elevated risk of foreign-body associated infection in her immunocompromised state (dual immunosuppression with tacrolimus and mycophenolate mofetil; both with stable drug levels).
Upon admission at our university hospital, the patient complained about fatigue, dizziness and ongoing vaginal bleeding. Several hours before admission, a latex bladder catheter was inserted into her uterus, and she received an intravenous hemostatic treatment with tranexamic acid and fibrinogen in another hospital. On examination, the patient was in a reduced general condition but alert and fully oriented. The temperature was 38.3 °C, the blood pressure 107/45 mmHg, the pulse 90 beats per minute, and the respiratory rate and oxygen saturation were in normal range.
Laboratory examination showed severe anemia (hemoglobin 40 g/L, hematocrit 0.137 L/L, erythrocyte count [1.37 × 1012/L]) but normal leucocyte (4.38 × 109/L) and thrombocyte counts (193 × 109/L). C-reactive protein was in a normal range (3.3 mg/L).
A microbiological diagnostic workup was undertaken. The vaginal smear grew normal flora and Staphylococcus aureus. The cervical smear was PCR-negative for Neisseria gonorrhoeae and Chlamydia trachomatis. Two out of four blood culture bottles turned positive after 5 h (Bact/Alert® Virtuo, BioMérieux, Marcy-l’Etoile, France). However, microscopy with Gram stain showed no microorganisms, and subcultures on different agar media (i.e. Columbia sheep blood agar, colistin-nalidixic acid agar, chocolate agar, MacConkey agar, brucella agar, phenylethyl alcohol agar [all BioMérieux] and a modified Shepard agar medium [A7; ELITech, Puteaux, France] remained without growth. In the effort to identify the cause of the positive growth signal in the blood culture, 5 ml of the blood culture was used for metagenomic sequencing on an Illumina MiSeq platform. In detail, 2 ml erythrocyte lysis buffer (Qiagen, Hilden, Germany) was added to 5 ml of negative blood culture. It was vortexed at maximum speed for 15 s and afterwards incubated for 5 min at room temperature, followed by addition of 0.1 volume of 10X Turbo DNAse buffer and 3 μl of Turbo DNAse (Thermo Fischer Scientific Inc.). The sample was gently mixed and incubated at 37 °C for 30 min. Afterwards, it was centrifuged at maximum speed for 10 min, and the supernatant was removed. The pellet was resuspended in 650 μl of pre-warmed PM1 buffer from the AllPrep® PowerFecal® DNA/RNA Kit (Qiagen). DNA extraction from bacterial cells was performed according to the manufactures’ instructions. Library preparation was done using the Qiagen® QIAseq FX DNA Library Kit (Qiagen, Hilden, Germany), according to the producers’ recommendations. Sequencing library quality and size distribution were analyzed on a Fragment analyzer automated CE system (Advanced Analytical Technologies Inc., Heidelberg, Germany), according to the manufacturer’s instructions using the Fragment Analyzer 474 HS NGS Fragment Kit. Sequencing libraries were paired-end sequenced (2 × 150 bp) on an Illumina MiSeq platform (Illumina®, San Diego CA, USA).
Raw sequencing reads (FASTQ) were filtered and trimmed using TRIMMOMATIC [], applying a threshold PHRED score of 25. Phylogenetic analysis was done by using the full length 16S rRNA, rpoB and recA gene sequences of the following Mycoplasma spp.: M. penetrans HF-2 (NCBI accession number: BA000026.2), M. genitalium G37 (NCBI accession number: NC_000908.2), M. pneumoniae M129 (NCBI accession number: NC_000912.1), Mycoplasma fermentans M64 (NCBI accession number: NC_014921.1), Mycoplasma salivarium ATCC_23064 (NCBI accession number: NZ_AXZE01000009.1), M. hominis ATCC_23114 (NCBI accession number: NC_013511.1), and as outlier U. urealyticum serovar 10 ATCC 33699 (NCBI accession number: NC_011374.1) was included in the phylogenetic analysis. Phylogenetic trees were generated with the FastTree MP software [] (bootstrap 1000 option, maximum likelihood GTR [generalized time-reversible model] option). The metagenomic sequence reads covered 99.2% of the published reference sequence of 1.35862 Mb []. In the 16S rRNA gene, two mismatches were found at nucleotide positions C98T and T221C compared to the reference strain sequence. This combined genetic information points towards the presence of M. penetrans in the blood cultures (Fig. ). In order to confirm the phylogenetic analysis, metagenomic sequences of the negative blood culture from the patient with a growth signal in the BacT/ALERT system were classified using Kaiju [] and yielded 363′851 reads, of which 78% were annotated as M. penetrans (Additional file : Table S1, Additional file : Figure S1). An inoculated blood culture without a growth signal in the BacT/ALERT system and the non-inoculated blood culture growth medium were sequenced as negative controls for the meta-genomic sequencing approach (Additional file : Table S2, Additional file : Table S3). While no M. penetrans reads were identified in both negative controls, the most frequently detected reads assigned to Enterococcus sp., Streptococcus sp. and Staphylococcus sp. (Additional file : Figure S1).
The patient was taken to the operating theatre for diagnostic hysteroscopy and endometrial ablation. She received a preoperative single shot dose of cefazolin (2 g) intravenously. Since the postoperative course was without complications, the patient remained afebrile and the uterine bleeding stopped after the removal of intrauterine catheter. The M. penetrans bacteremia was self-limiting, requiring no further antibiotic treatment, and the patient was discharged in stable general condition.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [38, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 38 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 1 + 1 = 2.
The patient's CHA2DS2-VASc Score is 2."
948,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5337863-1,Extracted,"An 84-year-old Japanese man was admitted to our hospital for a detailed examination of an indolent swelling on his right back. He had noticed the swelling on the day of admission; its onset was unknown. He had a 9-year history of treatment with candesartan (4 mg/day), furosemide (20 mg/day), and warfarin (2 mg/day) for hypertension, chronic kidney disease, and atrial fibrillation, but he had no other remarkable medical history or family history. He was a nonsmoker and did not consume alcohol. Prior to admission, he had never presented with pain, fever, or night sweats.
On admission, his height was 159 cm, weight was 71 kg, body temperature was 36.8°C, and blood pressure was 132/76 mmHg. His heart rate was 66 beats/min and irregular. Physical examination revealed no significant abnormalities except for a painless elastic hard subcutaneous lump adjacent to the right side of the lumbar vertebrae. The lump was oval in shape and vertically long, measuring about 3 × 10 cm. His arterial blood oxygen saturation was normal at 98%. Both chest and abdominal radiographs showed normal findings. An electrocardiogram showed atrial fibrillation but no other abnormalities. Laboratory tests showed a low blood hemoglobin concentration of 12.7 g/dl (reference range, 13.5–18.0 g/dl), high international normalized ratio-prothrombin time of 1.73 (reference range, 0.85–1.15), high serum lactate dehydrogenase concentration of 270 U/L (reference range, 120–230 U/L), high C-reactive protein concentration of 0.66 mg/dl (reference range, 0.00–0.30 mg/dl), high blood urea nitrogen concentration of 34.8 mg/dl (reference range, 8.0–22.0 mg/dl), and high creatinine concentration of 2.35 mg/dl (reference range, 0.60–1.10 mg/dl). Because his renal dysfunction imposed a restriction upon the use of contrast agent, plain 3 T MRI of the abdomen, including the lumbar region, was performed. MRI of the abdomen revealed an oval-shaped lesion in the right psoas major muscle measuring 4 × 11 cm and exhibiting homogenous internal intensity (). This mass showed mildly high intensity on both T1- and T2-weighted imaging compared with the adjacent muscle, but its intensity on T2-weighted imaging was lower than that of water. The mass also showed high intensity on diffusion-weighted imaging, corresponding to the characteristics of an acute-phase hematoma, although the patient had no history of trauma that might have caused an intramuscular hematoma. Based on these findings, the oral warfarin administration was temporarily stopped on day 2 after providing the patient with information regarding the increased risk of cerebral infarction and obtaining his consent.
The patient underwent follow-up MRI on day 7 to ascertain whether this oval-shaped mass had changed with time, which is typically observed in hematomas. However, the internal intensity of the lesion was almost identical to that on admission, and the size of the lesion had slightly increased. Accordingly, a CT-guided needle biopsy was performed on day 9. Blood was not aspirated during the biopsy procedure, and a solid tissue specimen was obtained. Histopathological examination revealed diffuse infiltration of large, atypical cells with irregularly shaped nuclei among the striate muscle fibers (). These atypical cells lacked abnormal lymphoid follicle formation and were predominantly CD20-positive on immunostaining. These cells were also weakly BCL-2–positive but CD3-, CD5-, and CD10-negative. The pathological diagnosis was DLBCL. Plain CT of the neck, chest, and abdomen on day 15 showed no significant lymphadenopathy. We consulted with the hematologists of our institution regarding curative treatment, but they discouraged immunochemotherapy because of the patient's renal dysfunction. We proposed additional examinations including detailed analysis of the lymphoma tissue using flow cytometry and 18F-fluorodeoxyglucose positron emission tomography (F-FDG-PET), but the patient refused. He was discharged from our hospital on day 16 and lost to follow-up.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [84, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 84 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
949,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-6220,Extracted,"A 67-year-old man presents to the emergency department after an episode of syncope. It happened when he was doing yard work while lifting a heavy bag. Similar episodes have occurred in the past when he exerts himself. The patient is otherwise healthy and is not currently on any medications. His temperature is 98.3°F (36.8°C), blood pressure is 137/89 mmHg, pulse is 88/min, respirations are 14/min, and oxygen saturation is 99% on room air. Physical exam is notable for a delayed carotid pulse but is otherwise unremarkable. The patient is asked to walk around the emergency department, and after doing so he states he feels a little short of breath and dizzy. The patient’s initial ECG is seen in Figure A, and 2 sets of troponins are unremarkable.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [67, 'years'], 'Congestive Heart Failure': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Stroke': False, 'Diabetes history': False, 'Transient Ischemic Attacks History': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 67 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
950,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7451141-1,Extracted,"This is a 66-year-old male with a medical history significant for hypertension, hyperlipidemia, hepatitis C virus infection, and atrial fibrillation chronically anticoagulated with apixaban. He was brought in by emergency services after a fall. The patient reported dizziness, then lost consciousness, and was found down by a family member. Primary trauma survey was negative with a Glasgow Coma Score of 15 no focal neurological deficits. Noncontrast CT of the head [] was significant for a 6 mm right frontal SDH with no shift, as well as a right medial orbital wall fracture. As the patient was neurologically intact, had minimal mass effect, there was no operative intervention recommended.
The patient was admitted to the surgical intensive care unit for serial checks. On the 2nd hospital day, he developed severe headache, and the head CT was repeated [], which showed worsening of the SDH with associated mass effect and 2 mm midline shift. The patient remained neurologically intact; therefore, no surgical intervention was recommended. The patient was discharged to acute inpatient rehabilitation on the 6th hospital day with instructions to repeat the head CT in 2 weeks.
In rehabilitation, 6 days after discharge, the patient experienced a terrible headache for 3 days, which prompted a repeat neurosurgical evaluation. The patient was still neurologically intact at this time, and repeat CT head [] showed expansion of the hematoma to 15 mm, with increased mass effect and 8 mm midline shift. The patient underwent burr holes for evacuation of the SDH and placement of subdural drain. Following hematoma evacuation, the patient’s headache improved, and the SDH decreased in size on repeat CT head []. His postoperative course was without complication. The drain was removed and the patient was discharged home on the 2nd postoperative day with levetiracetam for seizure prophylaxis.
On the 14th postoperative day, the patient was seen in the office for follow-up. The patient described a strange sensation in the right arm, as well as the feeling that he could not control the arm. Based on these symptoms, he was sent directly to the emergency room for further evaluation. In the emergency room, the patient developed a focal left arm seizure. He was treated for this seizure and started on electroencephalography (EEG) monitoring. He was then admitted. That night, the patient was found to be unresponsive; CT head showed no acute hemorrhage and EEG indicated status epilepticus. The patient was intubated for airway protection and transferred to the medical intensive care unit for further management.
As the patient’s initial presentation was hemorrhagic but thought to be traumatic, dedicated vascular imaging had not been obtained previously. During this third admission, cerebral CTA was obtained as his clinical course became suspicious for either an underlying lesion or vascular issue. The studies were negative for any pathology. This admission was complicated by ventilator-dependent respiratory failure, septic shock secondary to Pseudomonas bacteremia, and the patient received a tracheostomy and gastrostomy. The patient was eventually stabilized and discharged to long-term acute care hospital on day 29 with levetiracetam and oxcarbazepine for seizure control.
Four days after discharge, the patient was found to be less responsive and was transferred back for neurosurgical evaluation. The patient opened eyes to stimulation, localized with the right upper extremity, and had minimal movement of left upper and bilateral lower extremities, and cough, gag, corneal, and pupillary reflexes were all present. CT and CTA head [] showed right frontal intraparenchymal hemorrhage measuring 5.2 cm×3.3 cm but no vascular lesion or anomaly. Cerebral catheter angiography was then performed and [ and b] showed prominence of the anterior temporal branch of the right middle cerebral artery with early, rapid, shunting of blood through a cortical vein to the superior sagittal sinus. There was opacification of a capillary-like serpiginous tangle of vessels connecting the anterior temporal artery with the early draining vein, representing an AVM, which was Spetzler-Martin Grade 1 (Spetzler-Ponce Grade A). On the second postangiogram day, embolization of the AVM was performed using N-butyl- cyanoacrylate glue. The embolization was successful and no opacification of the early draining vein or AVM nidus were seen [ and d].
On the 8th day postembolization, the patient was taken to the operating room for resection of the AVM. The right pterional craniotomy was performed to access the AVM, which was separated from surrounding brain parenchyma using microdissection techniques. The feeding arteries, followed by the draining vein, were coagulated using bipolar electrocautery and resected. Following resection, intraoperative Doppler ultrasound indicated no arterial flow in the draining vein. The associated intraparenchymal hematoma was also evacuated. Postoperative angiography showed no residual AVM.
Postoperatively, the patient’s mental status progressively improved. On the 3rd postoperative day, the patient followed commands and tracked with his eyes. There was spontaneous antigravity movement of the right upper extremity, but still no movement of the left upper or bilateral lower extremities. The postoperative course was complicated by pseudomonas sepsis, which was treated in consultation with infectious disease. The patient was eventually discharged to long-term acute care on the 15th postoperative day.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [66, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 66 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
951,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7362666-1,Extracted,"A 76-year-old man with a past medical history of chronic obstructive pulmonary disease (with history of second-hand smoke exposure and ex-cigar smoker), congestive heart failure, coronary artery disease, tachycardia-bradycardia syndrome following pacemaker placement, chronic kidney disease, atrial fibrillation (on rivaroxaban), right-sided nephrectomy (likely for renal cell carcinoma, however, the patient was unable to confirm it), hypertension, iron-deficiency anemia, and diabetes mellitus presented to our hospital for progressive worsening of shortness of breath. The patient had been admitted for monitoring and medical management of acute congestive heart failure exacerbation. Urine dipstick obtained at the time of admission showed large blood in the urine. A urinalysis, renal ultrasound, and cystoscopy were obtained for further evaluation of the hematuria, and urology service was consulted. Urinalysis showed microscopic hematuria, leukocyte esterase, white blood cells, and bacteria. Urine culture showed growth of gram-negative bacilli, and the patient was started on ceftriaxone for urinary tract infection. Histological evaluation of the urine specimen showed few atypical single and clusters of small cells present in the background with marked acute inflammation, consistent with small cell carcinoma. Renal and bladder ultrasound revealed absent right kidney and new mild left hydronephrosis, mild thickening of the bladder wall, and a small amount of debris in the bladder. Cystoscopy revealed moderate enlargement of the prostate, a significant amount of bleeding in the bladder, inability to locate the left ureteral orifice, and a significant amount of mucosal irregularity at the base of the bladder. Histologic evaluation of biopsy specimen obtained from right bladder base revealed small cell carcinoma: immunohistochemical stains were performed on block A1 and showed tumor cells positive for thyroid transcription factor 1 (TTF1), chromogranin (focal), and synaptophysin (focal), while CK7, CK20, CD56, and GATA3 were negative (Figures -).
Computed tomography (CT) revealed an enlarged irregular appearing prostate gland protruding into the bladder base (site of biopsy-proven small cell carcinoma), bladder outlet obstruction with circumferential thickening of the urinary bladder wall, and a questionable invasion of the anterior wall of the rectum (Figure ).
CT imaging also revealed tumor invasion of the left ureterovesical junction with resultant left hydroureteronephrosis, in addition to lytic lesions (likely metastatic foci) in L3 and right iliac bone. On positron emission tomography-CT (PET-CT), biopsy-proven bladder mass was not visualized and intensely F-fluorodeoxyglucose (FDG) avid urine was visualized in the urinary bladder. A 1.5-cm focus of FDG uptake noted in the right psoas muscle with a standard uptake value (SUV) max of 9.1 compatible with metastatic disease (Figure ). Lytic lesions in L3 and right iliac bone were non-FDG avid, and therefore likely to be benign lesions. Additionally, there was non-specific focal FDG uptake in the right nasopharyngeal area without corresponding mass on CT scan. The patient underwent placement of port-a-cath and was discharged with a Foley catheter for urinary retention. Two months following initial diagnosis, the patient was started on a chemotherapy and immunotherapy regimen, which included atezolizumab, etoposide, and carboplatin. Repeat cystoscopy performed four months following initial diagnosis revealed no lesions or masses.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [76, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
952,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7930644-1,Extracted,"A 54-year-old African American male was evaluated in the emergency department (ED) after a 5-minute episode of loss of consciousness without convulsion preceded by sudden onset of a nonradiating pressure type holocranial headache along with diaphoresis, palpitation, and nausea. He was then working in his normal state of health at the hospital cafeteria and the event was witnessed by his coworkers. He regained consciousness without confusion. Fifteen minutes later, he had a generalized convulsion lasting 1 minute followed by 15 minutes of post-ictal confusion as described by the nurse. The patient could not recall any aura before seizure. He did not bite his tongue or become incontinent in either of the events. His past medical history included paroxysmal atrial fibrillation (PAF), hypertension, glucose-6-phosphate dehydrogenase deficiency, and hepatosteatosis. He did not report any past or family history of seizures and no risk factors for these. He was compliant on apixaban 5 mg 2 times daily as his home medication for PAF. He was afebrile, normotensive, and had an irregularly irregular pulse rate of 110 beats per minute. During the initial neurological examination, he was drowsy, oriented to time, place, and person with intact language, cranial nerves, motor, sensory, and cerebellar functions. He had no neck rigidity. He was treated with 2 mg of intravenous (IV) lorazepam and 1-g loading dose of IV levetiracetam in the ED.
The patient tested positive for SARS-CoV-2 infection in real-time reverse transcription polymerase chain reaction analysis taken from nasopharyngeal swab. Chest X-ray was unremarkable. Arterial blood gas analysis showed respiratory acidosis (pH 7.21, pCO2 [partial pressure of carbon dioxide] 69.8, pO2 [partial pressure of oxygen] 84.2, bicarb 28, and FIO2 [fraction of inspired oxygen] 32%). Blood work-up revealed sodium 137 mmol/L (ref = 135-144), potassium 3.6 mmol/L (ref = 3.7-5.0), glucose 115 mg/dL (ref = 70-110), calcium 9 mg/dL (ref = 8.9-10.3), magnesium 1.47 mEq/L (Ref = 1.4-1.9), hemoglobin 11.5 g/dL (ref = 13.7-17.5), white cell count 4.9 × 103/µL (ref = 4.1-10.8), total bilirubin 0.9 mg/dL (ref = 0.4-1.3), aspartate transaminase 30 U/L (ref = 12-38), alanine transaminase 22 U/L (ref = 8-60), ammonia 9 µmol/L (ref = 9-55), urea nitrogen 13 mg/dL (ref = 6-20), creatinine 1.2 mg/dL (ref = 0.64-1.27), vitamin B12 582 pg/mL (ref = 180-914), C-reactive protein 4.96 mg/L (ref = 0.0-4.0), and d-dimer <150 ng/mL (ref = 21-230). Thyroid function test, serum angiotensin-converting enzyme, cardiac troponins, urine toxicology, and analysis were unremarkable.
Magnetic resonance imaging (MRI) of the brain showed increased signal in diffusion-weighted imaging (DWI) without apparent-diffusion coefficient correlation in the posterior aspect of right medial temporal lobe and para-hippocampal gyrus with associated T2-weighted-Fluid-Attenuated Inversion Recovery (T2-FLAIR) signal hyperintensity. Repeat imaging 2 days later showed persistent findings with associated contrast enhancement (). Computed tomography of the head and neck and transthoracic echocardiogram were unremarkable. Lumbar puncture was done after 24 hours before starting heparin drip without complications. Cerebrospinal fluid (CSF) analysis showed zero white blood cell and red blood cell count, protein 108 mg/dL (ref = 15-45 mg/dL), immunoglobulin G index 0.8 HI (ref = 0.0-0.7 HI), and glucose 56 mg/dL. CSF culture/stain, herpes simplex virus (HSV) 1 and 2, cryptococcal antigen, and cytology were negative. No definitive autoantibodies were detected in the CSF that included anti-amphiphysin, anti-ANNA-1/2/3, anti-AGNA-1, anti-CASPR2, anti-CRMP-5, anti-GAD-65, anti-GRAF1, anti-IgLON5, anti-MPR1, anti-LGI1, anti-mGluR1, anti-NIF, anti-NMDA-A, anti-PCA-Tr, anti-PCA-1, and anti-PCA-2. Electroencephalogram (EEG) showed right posterior quadrant lateralized periodic discharges with a frequency of 0.5 to 1 Hz, accompanied by focal delta slowing, but no electrographic seizures for the 1 hour duration of the study ().
During 4 days of hospitalization, the patient was initially treated with high-flow oxygen for hypoxia in the intensive care unit and was later transitioned to room air by maintaining his oxygen saturation above 93%. Atrial fibrillation with rapid ventricular rate was treated with an amiodarone drip and a heparin drip, which was later transitioned to oral diltiazem and apixaban. Levetiracetam was continued for seizure prophylaxis. He remained afebrile, normotensive, and had no further seizure. He had no cognitive or neurological deficits at the discharge.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [54, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 54 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
953,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8018723-1,Extracted,"A 51-year-old, Middle-Eastern male diabetic patient presented to the emergency room with complaints of sudden onset left leg pain, paresthesia, and swelling for one day. The patient denied any fever, chills, body aches, cough, or chest pain. No personal history of surgery, allergies, or malignancy was reported. The patient was a nonsmoker, denied the use of alcohol and illicit drugs. He lived with his wife and children, none of whom have exhibited COVID symptoms. His vital signs included a blood pressure of 134/86 mmHg, pulse rate of 117 beats/min, respiratory rate of 20/min, oximetry 97% on room air, and a temperature of 36.5°C (98.1°F). Physical examination was normal in the right leg, but the left leg was cool to touch from forefoot to mid-calf, with noticeable mottling over the forefoot and a nonpalpable dorsalis pedis. The patient was started on therapeutic enoxaparin and diltiazem in the ED. An electrocardiogram (EKG) completed in the emergency room was consistent with atrial fibrillation.
Chest X-ray showed bilateral pulmonary infiltrates beginning peripherally and COVID pneumonitis (Figures -). Considering the patient’s status, we had to follow strict triage and committee approval to perform any procedures. Abnormal laboratory findings included elevated erythrocyte sedimentation rate (ESR)/C-reactive protein (CRP), blood sugar of 260 mg/dL, D-dimer at 3600, and brain natriuretic peptide (BNP) levels of 2750. Troponin was 0.0250 ng/mL. A CT of the left lower extremity was performed, which showed an abrupt cutoff at the left common femoral artery, indicating a poor prognosis (Figure ). Clot removal was done in the catheter lab. An ekosonic endovascular system (EKOS) catheter with repeat thrombectomy plans was placed, aiding in deeper penetration of thrombolytic agents and decreasing the dose of tissue plasminogen activator (tPA) required and the likelihood of bleeding. Intravenous heparin infusion was continued overnight via tPA catheter with EKOS to see if flow in the left lower extremity can be re-established. On examination, no pulses were palpable, and only femoral flow could be appreciated on Doppler Ultrasonography. The patient underwent a mechanical thrombectomy and was loaded with aspirin/clopidogrel, heparin drip, and enoxaparin. Despite being on triple anticoagulation, the patient had new-onset ST elevations in V3 on 12 lead EKG, and troponin level was elevated at 12.4 (Figure ). On angiography, the patient was found to have MI with occluded mid-left anterior descending, most likely from acute on chronic thrombosis related to the patient’s COVID-19 status. Despite ballooning, the flow could not be re-established. The patient was clinically stable, so the intervention had to be stopped as there was a high risk of bleeding because of tPA. He was kept on long-term protective anticoagulation-triple therapy (an oral anticoagulant and dual antiplatelet therapy) and received pulmonary care for COVID infection. The patient was discharged on long-term triple anticoagulation and COVID precautions with scheduled retesting and follow-up.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [51, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Thromboembolism history': True, 'Vascular disease history': True, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 51 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 0 + 2 = 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
954,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8281407-1,Extracted,"Patient complained of a 20-year history of fatigue after activities, which was aggravated over the previous 2 mo.
A 53-year-old male was admitted to hospital with complaints of a 20-year history of fatigue after activities, which was aggravated over the previous 2 mo.
He had a more than 2-year history of diabetes.
There was no history of rheumatic fever and family history of cardiac tumor or sudden death.
On admission, there was a diastolic rumbling pathological murmur of grade III/VI in the apical region. Grade IV/VI systolic ejection murmur and III/VI diastolic sighing murmur in the second intercostal space near the right margin of sternum were heard. Electrocardiogram showed atrial fibrillation with rapid ventricular rate.
Laboratory data revealed slightly elevated glutamic oxaloacetic transaminase (45 U/L, normal level < 40 U/L) and total bilirubin (56 μmol/L, normal range < 23 μmol/L) and remarkably increased brain natriuretic peptide (692.7 pg/mL, normal range 0-100 pg/mL). Erythrocyte sedimentation rate was 6 mm/h. There were unremarkable abnormalities in circulation levels of serum tumor markers.
Chest computed tomography revealed bilateral emphysema with mild pulmonary edema, generally enlarged heart, and calcification of the aortic and mitral valves. Transesophageal echocardiography (TEE) demonstrated enlarged left atrium (50 mm), left ventricle (60 mm), and right atrium (64 mm × 57 mm). Mitral, aortic, and tricuspid valves were thickened and adhered, similar to rheumatic valve lesions. The mitral and aortic valve orifices exhibited severe stenosis, and the areas were 0.64 cm2 and 0.87 cm2, respectively. Multiple abnormal echo masses were found in the left ventricle (Figure ), with the largest mass (about 23 mm × 15 mm in diameter) located in the left ventricular cavity at the junction of the anterior septum and the posterior papillary muscle.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Vascular disease history': True, 'age': [53, 'years'], 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False, 'sex': 'Male'}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 53 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 0 + 1 = 1. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 1 + 1 = 2.
The patient's CHA2DS2-VASc Score is 2."
955,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7192559-1,Extracted,"An 84-year-old Caucasian male presented to the emergency room with one day history of abdominal pain, more localized to epigastric and right upper quadrant area. Pain is sharp in intensity, radiating to substernal area. Pain was associated with few episodes of nausea and vomiting. He denied any hematemesis, diarrhea, shortness of breath, wheezing, fever and chills. He never had any similar complaints in the past. He denied any weight loss or loss of appetite. His pain slightly got better in the emergency room with intravenous opiates. His past medical history was significant for essential hypertension, Alzheimer’s dementia, coronary artery disease, atrial fibrillation and stroke. Past surgical history was significant for appendectomy, coronary artery by-pass grafting and joint surgeries.
His initial vitals were within normal limits. On physical exam he had irregularly irregular rhythm with good breath sounds bilaterally. Abdomen examination was significant for right upper quadrant tenderness with positive murphy sign (tenderness and guarding in the right upper quadrant of abdomen on palpation and exacerbated by inspiration).
Significant initial laboratory findings on initial presentation include elevated alkaline phosphate 273 IU/ml (reference range: 40-150 IU/ml), elevated aspartate aminotransferase (AST) -63 IU/ml (reference range: 5-34 IU/ml), elevated total bilirubin of 1.4 mg/dl (reference range: 0.2-1.2 mg/dl), mildly elevated lipase of 101 IU/ml (reference range: 8-78 IU/ml), normal alanine transaminase (ALT) 44 IU/ml (reference range: 0-55 IU/ml), and normal white blood cell count 5.9 k/cmm (reference range: 5-10 k/cmm).
Because of clinical suspicion of acute cholecystitis, the patient had an ultrasound of gallbladder which showed cholelithiasis, and sludge/inspissated gall bladder (Figure ) with no radiographic evidence of acute cholecystitis, non-specific, soft, non-dependent tissue along the gall bladder wall (Figure ).
The patient was started on intravenous Levofloxacin and admitted to the hospital with a surgical consultation.
The patient had a laparoscopic cholecystectomy with normal intra-operative cholangiogram during that hospitalization. He was found to have a gangrenous gallbladder with a large Calot node (sentinel lymph node of gall bladder) and nodule on the wall of gallbladder and it was sent for biopsy after removal. He had an uneventful postoperative state and was discharged home the next day.
Biopsy results showed high-grade neuroendocrine carcinoma of gallbladder with predominantly small cell cancer. It was poorly differentiated, invading lymphovascular structures, perimuscular fat and serosa. Unfortunately, lymph nodes were not sampled during the surgery as the suspicion for malignancy was low.
Pathological staging showed pT3, pNx. Sections showed abundant neuroendocrine tumor with associated necrosis. Most of the cells were small in size with few intermediate to large cells (Figures , ).
Immunohistochemistry reveals that malignant cells are positive for pan keratin, low molecular weight keratin, synaptophysin, TTF1, CK7 and CA19-9. Cells are negative for CD20, CD3, CK20 and p63.
His staging studies including computerized tomography (CT) scanning of chest, abdomen, pelvis, head, and nuclear medicine whole body bone scan were negative for any metastatic lesions. Oncologist diagnosed him with Stage IIIA (pT3, Nx Mx) small cell carcinoma of the gallbladder and arranged for adjuvant chemoradiation with Capecitabine as radio sensitizing agent. The patient was supposed to be started on a small cell cancer chemotherapy regimen, however he decompensated in the next few days and died after family has opted for comfort care measures only.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [84, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 84 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
956,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7723721-1,Extracted,"A 77-year-old male was admitted to our hospital with blood with his stool for over 1 mo and a change in bowel habits for the 15 d prior.
The patient noted alteration of blood with his stool a month ago, a change in bowel habit with increased stool frequency (6-8 times a day), a progressive diminution in size of stools, anal discomfort and a weight of loss of 4 kg. There was no abdominal pain, bloating, nausea and vomiting.
The patient’s history included hypertension for over 10 years and early-stage hypertensive nephropathy and atrial fibrillation for 2 years. The noted conditions had been controlled with daily medications, including amlodipine (2.5 mg), valsartan (80 mg), metoprolol (47.5 mg) and aspirin (40 mg).
The patient’s family history was ordinary, and there was no history of genetic heritability of colorectal cancer. The patient had no prior endoscopic examinations.
There were no pertinent findings upon physical examination, and the digital rectal examination did not detect the tumor.
Laboratory tests revealed mild renal insufficiency. Creatinine levels were 113 µmol/L (normal range: 54-106 µmol/L), and uric acid levels were 445 µmol/L (normal range: 149-416 µmol/L). Neuron-specific enolase (NSE) levels were 20.2 U/mL (normal range: < 12.5 U/mL). There were no other hematological or biochemical abnormalities.
A colonoscopy revealed a cauliflower-like neoplasm located in the upper rectum, which invaded most of the intestinal wall. The intestinal surface also displayed a bleeding lesion and abundant necrotic tissue (Figure ). The colonoscopy with biopsy determined that the tissue was a malignant tumor. The expression of multiple immunohistochemical markers used to determine the cells of origin, including LCA (-), CK (±), EMA (-), TIF (-), Syn (-), CgA (-), CD56 (+), Ki-67 70% (+),CKL (-), CKH (-), CD68 (-), TIA (-),GRB (-), CD3 (-), CD5 (-), CD7 (-), CD2 (-), CD20 (-), CD79a (-), PAX-5 (+), S100 (-), SOX (-), MelanA (-), MUM-1 (-), CD138 (+), HMB45 (-), Myogenin (-), ERG (-), CD31 (+) and CD34 (-), were negative. Therefore, the tumor type could not be determined.
Contrast-enhanced computed tomography scans of the chest, abdomen and pelvis showed that the wall of the upper rectum was unevenly thickened. The lesion was very likely a rectal carcinoma, which broke through the adventitia and involved the mesentery. Multiple surrounding lymph nodes and the adjacent superior rectal artery were positive (Figure ).
A magnetic resonance image (MRI) of the pelvis revealed the lesion in the upper rectum. The MR stage was T3N2, the circumferential resection margin was positive, and the extramural venous invasion was positive (Figure ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [77, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
957,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-8790,Extracted,"A 72-year-old man presents with a recent episode of slurred speech and numbness in his left arm and left leg 2 hours ago that resolved completely within 45 minutes. He says he was having breakfast when he noticed that he had difficulty talking and the left side of his body was numb. The patient denies any past similar symptoms. Past medical history is significant for type 2 diabetes mellitus, hypertension, and ischemic heart disease. He had a coronary artery bypass graft 12 years ago and a percutaneous intervention 3 years ago. Current medications are aspirin, metformin, nitrates, and rosuvastatin. His vital signs include: blood pressure 143/97 mm Hg, pulse 80/min, oxygen saturation 98% on room air. On physical examination, the patient is alert and oriented. Higher mental functions are intact. Muscle strength is 5 out of 5l in both upper and lower limbs bilaterally. The sensation is intact. Cerebellar signs are absent and his gait is normal.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': True, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
958,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3194783-2,Extracted,"A 68-year-old woman underwent LADG with partial omentectomy and D1+ β lymph node dissection for early gastric cancer localized in the submucosa (T1bN1M0). Her past medical history was atrial fibrillation and Parkinson's disease for several years and these maladies were controlled with medication. This patient was thin with a BMI 19.7 kg/m2 (the initial weight of 50.4 kg and a height of 160 cm). On postoperative day 10, she developed localized right upper quadrant pain with leukocytosis of 17,090/mm3. She had no fever, chills or gastrointestinal symptoms such as nausea, vomiting or diarrhea other than the right upper quadrant pain.
Contrast enhanced abdominal CT was performed to differentiate the causes of her acute abdominal pain. The enhanced CT scan revealed a 4 cm sized heterogeneous fat density mass with a peripheral enhancing rim and streaky infiltration in the omentum at the anterior to the pancreas head, which was a reasonable finding of omental infarction (). She improved after administration of anti-inflammatory agents and analgesics. After five days, her symptoms disappeared completely and she was discharged from the hospital.
After five months, she was followed up with CT and F18-FDG PET-CT. The previously noted lesions had almost resolved and there was no abnormal FDG uptake except only mild omental haziness ().",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [68, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 68 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
959,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-1523371-2,Extracted,"An eighty-six year old female presented to the Accident and Emergency department. She tripped and fell at home three days prior to admission, landing on her left side. On admission she complained of left sided abdominal and chest pain. She was known to have atrial fibrillation, congestive cardiac failure and rheumatoid arthritis. In the past, she had received a short course of corticosteroids for her rheumatoid disease. She denied any history of immunosuppressive therapy.
Examination revealed a localised area of peritonism in her left upper quadrant. She was haemodynamically stable with a blood pressure of 124/74 and a pulse of 76. Her haematological profile revealed a total white cell count of 11.9 (4 – 11 × 109/l), haemoglobin of 10.1 (11.5 – 15.5 g/dl) with a normal mean corpuscular volume. Biochemical analysis revealed a creatinine of 111 μmol/l (54 – 84) but was otherwise unremarkable. Her INR was 1.2. Liver function was within normal limits.
An urgent abdominal CT scan was requested. This demonstrated a complex laceration through the anterosuperior portion of the spleen extending to its lateral margin with perisplenic haematoma free intraperitoneal blood (Fig ). More inferiorly the splenic parenchyma demonstrated foci of contrast enhancement adjacent to a hypodense cyst-like lesion and further lacerations, with disruption of the splenic capsule anteriorly (Fig )
She was initially managed conservatively on the ward but became haemodynamically unstable. In addition her haemoglobin was found to have dropped from 10.1 to 6.8. She subsequently underwent emergency splenectomy via midline laparotomy without complication. She went on to make a full recovery.
Macroscopic examination showed a spleen measuring 110 × 85 × 40 mm weighing 215 g. Subcapsular haemorrhagic nodules were noted, one of which was associated with an 80 mm capsular tear (Fig ). Sectioning revealed multiple blood-filled spaces up to 15 mm in diameter throughout the parenchyma. Histology showed unlined cystic spaces filled with blood (Figs and ). Many of these showed a parafollicular distribution. The features were consistent with splenic peliosis.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [86, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 86 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
960,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4007801-1,Extracted,"An 80-year-old woman was transferred to our institution with hematemesis. She had a history of congestive heart failure, atrial fibrillation, and hypertension; moreover, she had a history of hepatocellular carcinoma at the segment S5 caused by chronic hepatitis C, which was treated by transcatheter embolism. She underwent treatment for congestive heart failure and was prescribed warfarin potassium at a dose of 2 mg/day to prevent thromboembolic events. Transthoracic echocardiography (TTE) performed at 78 years of age revealed a 7 mm small, mobile, string-like mass attached to the noncoronary cusp (). Infective endocarditis was excluded on the basis of the following findings: blood chemical analyses revealed no elevation of inflammation markers, blood cultures were negative for microorganisms, and the patient's body temperature was within the normal range. A cardiac tumor, including metastasis of the hepatocellular carcinoma, was suspected, and surgical treatment was recommended to prevent thromboembolic events. However, the patient declined surgery; thus, she was carefully followed up with periodic TTE.
Thereafter, the patient was transferred to our institution with complaints of upper abdominal pain and hematemesis. Her blood pressure was 130/90 mmHg, and heart rate was 130 beats/min. Physical examination revealed mild anemia, a soft, flat abdomen with no palpable masses, and normal bowel sounds. On auscultation, her chest was clear and no abnormal murmurs could be heard. Chest radiography did not present any signs of cardiomegaly or pulmonary congestion. Electrocardiography revealed atrial fibrillation. Blood chemical analyses revealed mild anemia (red blood cell count: 255 × 104/μL; hemoglobin levels: 8.2 g/dL), slightly low platelet count (12.5 × 104/μL), slightly elevated serum urea nitrogen levels (29.6 mg/dL), mild hypoproteinemia (6.1 g/dL), mild hypoalbuminemia (2.3 g/dL), slightly elevated C-reactive protein levels (1.3 mg/dL), and coagulation dysfunction (prothrombin time, 49%; fibrin/fibrinogen degradation products, 27.9 μg/mL; and D-dimer, 14.7 μg/mL). Upper gastroendoscopy revealed a gastric ulcer with an exposed blood vessel situated posteriorly in the body of the stomach. Anticoagulant therapy was ceased, and a proton pump inhibitor was administered.
On day 15 of admission, the patient experienced mild impairment of consciousness, disturbance of speech articulation, and left facial paralysis. Magnetic resonance imaging of the brain revealed high-intensity signal lesions in the right insular cortex and right corona radiate (). Acute cerebral infarction was diagnosed and heparin sodium and warfarin potassium were administered; subsequently her symptoms improved. TTE revealed no alteration of mobile, string-like mass attached to the noncoronary cusp. Moreover, moderate mitral and mild aortic regurgitations were evident, although ejection fraction was unaffected. We considered the tumor to be the cause of acute cerebral infarction, although the possibility of atrial fibrillation causing the infarction could not be excluded. The patient consented to surgical therapy, and surgery was performed 1.5 months after the cerebral infarction occurred. Cardiopulmonary bypass was established and the ascending aorta was opened by median sternotomy. The tumor revealed attachments to the noncoronary, left, and right coronary cusps; eventually tumor resection was performed. Furthermore, after resection, the maze procedure was performed for atrial fibrillation.
Pathological examination of the resected specimen revealed that it is comprised of a core of aggregated elastic fibers and hyaline material covered with a single squamous cell layer (). There was no evidence of metastatic hepatocellular carcinoma; however, the pathologic findings were consistent with PFE. Atrial fibrillation was restored to sinus rhythm, and the postoperative course was uneventful.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [80, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Thromboembolism history': True, 'Vascular disease history': False, 'Stroke': True, 'Transient Ischemic Attacks History': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 80 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 5 + 2 = 7.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 7. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
961,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5389436-1,Extracted,"A 91-year-old Japanese woman presented to our hospital with hypoxia of unknown origin. She had a medical history of hypertension and atrial fibrillation. Eight years before, when she was 82, an advanced atrioventricular block was diagnosed after a syncopal episode and she received a permanent dual chamber pacemaker implantation. She underwent coronary computed tomography (CT) and radioisotope examination at this time, but there was no evidence of cardiomyopathy or of ischemic heart disease. The tip of the pacemaker lead was observed to pass through a PFO at the left ventricular apex; she received a follow-up examination because of no serious adverse event. She had no history of lung disease or tobacco smoking. She had no subjective symptoms associated with cardiovascular disease after pacemaker implantation. There was no evidence of a decline in oxygen saturation levels at that time, which were measured by pulse oximetry.
Her physical examination findings on admission were as follows: clear level of consciousness and severe hypoxia and cyanosis observed only in the right lateral decubitus position. These symptoms were immediately improved in the left lateral decubitus, the supine, and the upright position. Arterial blood gas values were consistent with her symptoms. Partial arterial oxygen pressure (PaO2) and arterial oxygen saturation (SaO2) decreased only in the right lateral decubitus position (Table ). These observations were reproducible. There was no evidence of lung rales or cardiac murmur.
Laboratory tests, including complete blood count, thyroid function tests, and D-dimers were almost normal. A chest X-ray showed a significant elevation of her right diaphragmatic dome.
An electrocardiogram (ECG) showed an atrium-sensing, ventricular-pacing rhythm with a complete right bundle branch block (RBBB) pattern (Fig. ). In general, when the pacemaker lead is set on the right ventricle correctly, the pacemaker first stimulates the right ventricle, and next the left ventricle. Because of this, the expected ECG pattern with right ventricle pacing should show a left bundle branch block (LBBB) pattern. A RBBB pattern suggests that the pacemaker first stimulates the left ventricle, and next the right one. Only this ECG pattern could indicate the possibility of inadvertent left ventricle pacing. This patient’s ECG pattern also suggested left ventricle pacing. However, we could not assess a malposition of the pacemaker lead from only an ECG pattern because sometimes we find a RBBB pattern although the pacemaker lead is set correctly. Contrast-enhanced CT excluded the diagnosis of cerebral infarction, pulmonary embolism, pneumonia, and lung parenchymal abnormalities and revealed giant liver cysts and compression of the right atrium by one of cysts (Fig. ). A chest X-ray and CT scan revealed right hemidiaphragmatic elevation that was probably compressing the right atrium. This finding was suspected in the case of right hemidiaphragmatic paralysis []. A transthoracic echocardiogram (TTE) revealed concentric left ventricular hypertrophy, left atrial dilatation, and compression of the right atrium due to the giant liver cyst. In addition, the pacemaker lead probably ran abnormally to the left atrium and ventricle through PFO, but shunt flow across the PFO on color Doppler image was not apparently observed. Pulmonary perfusion imaging with 99mTc-macroaggregated albumin (MAA) was performed in the right lateral decubitus position. MAA accumulated in her kidneys and brain, which suggested the presence of a right-to-left shunt. The estimated shunt ratio was 26.3%.
A transesophageal echocardiogram (TEE) with intravenously administered agitated saline contrast solution was performed in both right and left lateral decubitus (Fig. ). TEE showed a compressed right atrium and shunt blood flow in both directions: from the left to the right atrium and vice versa. The shunt flow was exacerbated by postural changes from the left to the right lateral decubitus (Fig. ). TEE also confirmed that the giant liver cyst was compressing the right atrium and the pacemaker lead was abnormally running to the left atrium through PFO (Fig. ).
Considering these results, we concluded that the cause of hypoxia was POS with right-to-left interatrial shunt through PFO. POS can be treated with the closure of the interatrial shunt by thoracotomy or percutaneous cardiac catheterization []. Surgical closure of PFO was not performed due to the age of our patient, surgical difficulties, and failure to obtain informed consent. For these reasons she was discharged after receiving medical advice about her posture.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [91, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 91 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
962,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7285430-1,Extracted,"A 39-year-old man – with a negative personal history for cardiovascular disorders and previous surgery – presented with cardiogenic shock following an out-of-hospital cardiac arrest. Resuscitation and emergency coronary angioplasty were successfully implemented, followed by admission to the intensive care unit. Antiplatelet therapy was started with aspirin 75 mg per day. Because of tachyarrhythmia-related cardiovascular compromise, the patient was placed on veno-arterial extracorporeal life support (VA-ECLS). However, the acute onset of pulmonary edema required placement of a LAVD (Impella® 5.0; Abiomed Inc.; Danvers, MA, USA). A brain computed tomography (CT) scan following left-sided seizure onset revealed a right cerebellar infarct. After approximately two weeks, Impella® 5.0 was removed and successfully replaced by a centrifugal continuous-flow ventricular assist device (HVAD®; HeartWare®, Medtronic, Minneapolis, MN, USA). Aspirin dosing was not tapered off because of the previous coronary angioplasty. Seven hours after recovery from anesthesia, acute neurological deficits suggestive of IS (left hemiparesis; Glasgow Coma Scale score: 10) were evident. The patient was intubated and verbal responses were not assessable. After consultation with neurologists, endovascular treatment was deemed unfeasible because of delayed discovery of the neurological presentation. A CT scan performed at 20 h post-admission revealed a complete right sylvian IS with significant mass effect resulting in a midline shift of 4.8 mm in the absence of haemorrhagic transformation (Fig. ). In light of the rapidly deteriorating neurological conditions and imaging evidence of IS, emergency DHC was performed after weighing surgical-related risks against potential benefits (Figs. and ). Aspirin 75 mg/day was stopped the day before surgery and no intraoperative prothrombotic medication was given. The pre-operative laboratory coagulation status was as follows: international normalized ratio (INR), 1.34; activated partial thromboplastin time (aPTT) ratio, 1.2; platelet count: 367,000/μL. Platelet function tests were not performed albeit expected to be impaired. Previous antiplatelet therapy did not technically affect emergency DHC. Anticoagulation (continuous infusion of unfractionated heparin at a dose of 25,000 UI/mL) was started by consensus of neurosurgeons and cardiac surgeons on the second post-DHC day. Unfractionated heparin infusion was titrated to achieve a target aPTT ratio of 1.2 for the first week and 1.8–2 for two subsequent weeks. Antiplatelet treatment was reintroduced two weeks after emergency DHC. Finally, unfractionated heparin infusion was titrated up to obtain an optimal aPTT ratio of 2.5–3. On the third post-DHC week, the patient was switched to oral anticoagulation. During the first two post-DHC weeks, the patient received empirical therapy with levetiracetam to prevent potential seizures elicited by brain edema.
Upon recovery from anesthesia after DHC, the patient was conscious and responsive to commands. Although left-side paralysis initially persisted, there was a gradual recovery in neurological symptoms that allowed transfer to a multidisciplinary rehabilitation center. Cardiac flows remained stable under control of the HVAD® device. The patient was referred for HT at five months from DHC, followed by cranioplasty one month thereafter. Both intra- and post-operative courses were uneventful.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [39, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 39 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 0 + 2 = 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
963,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5516052-1,Extracted,"A 71-year-old female presented to her primary care physician with complaints of lightheadedness. She had no other symptoms and her physical examination was unremarkable. A non-contrast head computed tomography scan was negative for any abnormalities. This prompted a cardiac work up for her symptoms. An electrocardiogram revealed premature ventricular contractions that led to a transthoracic echocardiogram (TTE). This showed a 1 cm mass within the left atrium, concerning for a thrombus. A transesophageal echocardiogram () with subsequent cardiac magnetic resonance imaging, was performed to better characterize the mass. This revealed a mass attached to the ridge between the left atrial appendage and superior pulmonary vein by a discrete stalk, measuring 1.4 x 1.1 x 1.0 cm. The mass appeared hypovascular on perfusion imaging, with no specific enhancement with delayed enhancement imaging (Figure 2). Her preoperative workup was completed with a left heart catheterization that did showed nonobstructive coronary anatomy. She was scheduled for elective resection of this mass.
The procedure was performed via median sternotomy with the aid of cardiopulmonary bypass. Central aortic arterial cannulation with bicaval venous cannulation was performed. The heart was arrested with aid of antegrade cardioplegia. For surgical exposure, Sondergaard’s groove was dissected and a left atriotomy performed. A 1 cm mobile, gelatinous mass on the left atrial wall was found (). This arose between the left atrial appendage and the left superior pulmonary vein. The lesion was resected en bloc, along with the stalk and a margin of the left atrial wall. The defect was closed using a 4-0 monofilament suture. The immediate post-operative course was uneventful and the patient was discharged home on post-operative day 4. On outpatient follow up she has been doing well and has remained asymptomatic. A repeat echocardiogram is scheduled to be performed at one year follow up.
On gross examination, the tumor was soft and grey-white, that appeared frond-like and translucent when submerged in liquid. Histologically, it was composed of branching avascular papillae with variable amount collagen and myxoid change consistent with papillary fibroelastoma, with no evidence of extension into the left atrial wall ().",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [71, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 71 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
964,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6534894-1,Extracted,"We describe the case of a 63-year-old man, Caucasian, affected by non-ischemic dilated cardiomyopathy who did not drink alcohol, did not smoke tobacco, and did not have diabetes. He had an implantable cardioverter defibrillator implanted, in New York Heart Association (NYHA) IV class, and left bundle branch block (LBBB; QRS duration of 145 ms). He was referred for CRT-D upgrade, awaiting cardiac transplantation, despite optimal medical therapy: b-Blockade, loop-diuretic, angiotensin-converting enzyme (ACE) inhibitor, K-sparing agent, and ivabradine. Standard clinical imaging protocol revealed a dilated left ventricle with an end-systolic volume (ESV) of 380 ml, an ejection fraction (EF) of 4.8% as measured by the modified Simpson’s method, and severe FMR, assessed by qualitative estimation with two-dimensional color flow Doppler approach, showing a very large central jet and reaching the posterior wall of the left atrium (see Fig. and Additional file 1: Video S1).
He underwent the implant of a CRT-D device with a quadripolar left ventricular (LV) lead placed in the posterolateral branch of the coronary sinus. After recording the right ventricle (RV)-to-LV electrical delay at each of the four LV rings, we chose the A1 unipolar vector for LV pacing (greatest electrical delay 80 ms).
At 13-day post-implant follow-up, he showed worsening heart failure (HF) symptoms and only A2 unipolar LV vector configuration, with interventricular (VV) interval of 0 ms, was suitable for simultaneous biventricular activation (Fig. ).
Echo-PIV was then used, during the acute study with contrast agent bubbles, to evaluate the orientation and relative magnitude of blood-induced intraventricular forces in correspondence of different pacing settings.
Without pacing stimulation (CRT OFF, Fig. a, and Additional file 2: Video S2) the intraventricular flow was dominated by rotation without evident inflow–outflow dynamics. As a result the intraventricular forces were predominantly transverse and not aligned along the LV axis (Fig. a1) as quantified by the large value of their mean angle φ (φ = 55.6°, this angle ranges from 0°, when forces are aligned with the LV axis, to 90°). A first setting option (CRT ON, VV delay 0 ms, Fig. b and Additional file 3: Video S3) changed the orientation of intraventricular forces (Fig. b1) reducing the angle (φ = 45°), and increasing the delay (CRT ON, VV delay − 30 ms, Fig. c and Additional file 4: Video S4) improved the alignment (Fig. c1) reducing the angle (φ = 40.3°). Eventually, the sequential biventricular activation with delay − 50 ms (Fig. d and Additional file 5: Video S5) provided the best alignment of intraventricular forces (Fig. d1, φ = 38.8°).
No reduction of FMR by three-dimensional FVCD, during the same acute study with shutdown versus reactivation of device, was demonstrated, as shown in Figure and by comparing Additional file 6: Video S6 and Additional file 7: Video S7.
The data acquisition time, by three-chamber apical view, for each three-dimensional color Doppler data set was approximately 5 seconds, and it took less than 3 minutes to analyze the average regurgitation volume, with automated anatomy detection of the LV endocardial border, mitral annulus (MA), LV outflow (LVOT), and placement of three-dimensional hemispheric flow sampling planes in the MA and LVOT. The software of three-dimensional FVCD computed the flow volumes as the area under the curve of both the MA and LVOT flow in three cardiac cycles, and FMR volume was calculated by subtracting LVOT stroke volume from MA stroke volume.
Our patient showed an improvement of NYHA class (III versus IV) and LV EF (26.6% versus 4.8%). Significant reduction of ESV (288 ml versus 380 ml) and persistent improvement of diastolic function were obtained. The regularized function is noticeable in Additional file 8: Video S8 (to be compared with Additional file 1: Video S1) and it is summarized in Fig. . At follow-up, a significant reduction of FMR (mean value regurgitant volume, 42.2 ml versus 65.3 ml) was estimated (Fig. , Additional file 9: Video S9, Table ).
The intraventricular forces estimated by echo-PIV were still partially dominated by the longitudinal path of pressure gradient (Fig. and Additional file 10: Video S10) with φ = 43.1°.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [63, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 63 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
965,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7358062-1,Extracted,"A 60-years-old male visited the emergency room for general weakness and poor oral intake for 10 days on March 18, 2020. He had a history of type 2 diabetes mellitus, hypertension for 20 years, and dyslipidemia for 10 years. Initially, he did not complain of respiratory symptoms such as cough, sputum, dyspnea, or febrile chilling sensation. His initial vital signs were pertinent for a blood pressure of 160/100 mmHg, a heart rate of 90 beats/min, a body temperature 36.8°C, a respiratory rate of 20 breaths/min, and peripheral O2 saturation of 94% on room air. However, the chest X-ray demonstrated bilateral patchy infiltration (). He had a history of close contact with a COVID-19 patient during medical practice as a physician on February 25, 2020. Accordingly, a real-time reverse transcriptase polymerase chain reaction test for COVID-19 was done and confirmed COVID-19 positive on March 19, 2020. Although an anti-viral agent (lopinavir/ritonavir) and antibiotics were administered immediate after admission, his condition continued to deteriorate during hospitalization. Intubation and mechanical ventilation was applied on the 5th day of admission. Continuous renal replacement therapy was started on the 6th day of admission and veno-venous extracorporeal membrane oxygenation (V-V ECMO) was applied on the 13th day of admission. On the 14th day of hospitalization, his vital signs became unstable. Chest X-ray revealed peribronchial ground glass opacities and nodular opacities in both lung fields (). On the electrocardiogram (ECG), ST elevation in V1–V2 leads and T wave inversion in V3–V6 leads were newly observed (). Laboratory testing demonstrated elevated cardiac troponin I of 46.1 ng/mL (reference range ≤ 0.045 ng/mL) and N-terminal pro-B-type natriuretic peptide of 1,971.5 pg/mL (reference range ≤ 125.0 pg/mL). Transthoracic two-D echocardiogram (TTE) revealed severe decreased left ventricular ejection fraction of 30%, and regional wall motion abnormalities at apex and apical septal segments.
Despite the use of inotropes and V-V ECMO, blood pressure and peripheral O2 saturation gradually decreased. Therefore, we decided to perform urgent coronary angiography (CAG). A negative pressure isolation chamber was used to minimize possible infection in the patient transfer process. A minimum number of staffs including three cardiologists, a nurse, and an X-ray technician was allowed to participate in procedure. Before the patient entered the catheterization room, medical personnel entered the room first wearing level D personal protective equipment including powered air purifying respirators (). Baseline CAG revealed multivessel disease. There was 80% diameter stenosis in the mid and distal portion of the left anterior descending artery (LAD), 90% diameter stenosis in the proximal ramus intermedius coronary artery (pRI), 90% diameter stenosis in the proximal left circumflex artery (pLCX), and 95% diameter stenosis in the proximal and distal right coronary artery (RCA) (). It was difficult to distinguish the culprit lesion by ECG, TTE, and CAG. We decided to perform complete revascularization for multivessel coronary lesions because his vital signs were unstable. First, pre-balloon angioplasty using a 2.5 × 20 mm balloon was done and drug eluting stent (3.5 × 32 mm) was implanted in the proximal RCA lesion. Second, plain old balloon angioplasty (POBA) using a 2.5 × 20 mm balloon on the pLCX lesion was done. Third, POBA using a 2.5 × 20 mm balloon was done at the pRI lesion. Fourth, pre-balloon angioplasty using a 2.5 × 20 mm balloon was done and a drug eluting stent (3.0 × 28 mm) was implanted in the mid LAD lesion. Finally, we obtained Thrombolysis In Myocardial Infarction (TIMI) grade 3 flow in LAD, LCX, and RI, separately, and TIMI grade 2 flow in RCA (). The total amount of contrast media used was 150 cc and total procedural time was 72 minutes. There were no specific complications during the procedure.
Immediately after PCI, V-V ECMO was converted to veno-arterial ECMO for hemodynamic support. Despite maximum medical therapy, the patient's condition gradually deteriorated and he did not recover from the cardiogenic shock. One day after the PCI, an intra-aortic balloon pump was applied in anticipation of improvement of cardiogenic shock. However, unfortunately, he expired the next day (16th day of admission) because of cardiogenic shock and multi-organ failure.
The study protocol was reviewed and approved by the Institutional Review Board of School of Medicine, Kyungpook National University (IRB No. 2020-06-034).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [60, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Vascular disease history': True, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 60 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
966,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8711789-1,Extracted,"An 86-year-old Jordanian woman presented to the emergency department with a one-day history of fever, increased rash, and bilateral lower limb edema. The patient reported concerns of itchy skin lesions that first appeared three months ago on her thighs and then progressed to involve the whole body, including the intertriginous areas (i.e., the axillae, inframammary, and groin areas). The patient was diagnosed with scabies in another hospital, and she and other family members were treated topically with permethrin cream (Figure ). She and her family members improved after the anti-scabietic treatment (Figure ). Her medical history included hypertension, type 2 diabetes, dyslipidemia, heart failure, atrial fibrillation, bronchial asthma, and major neurocognitive disorder due to Alzheimer’s disease.
In the emergency room, the patient became hypotensive, and the team started her on intravenous normal saline (500 cc). Her laboratory investigations revealed high creatinine, potassium, and lactic acid levels. Other results from her laboratory investigations were unremarkable. The patient did not respond to fluid management, leading the treating team to suspect septic shock. After consulting with the intensive care unit (ICU) team, her care team admitted her to the ICU.
Her care team consulted with the dermatology team because she had multiple nonblanchable purpuric lesions and an erythematous papular rash on her trunk and upper and lower limbs with facial sparing. This rash was different from the rash for which the patient was diagnosed with scabies based on the history provided by the patient’s caregiver.
Biopsies of the lesion revealed parakeratosis and neutrophil collection in the stratum corneum of the epidermis and superficial neutrophilic infiltrate in the dermis. In addition, we noted fragmented neutrophils surrounding the blood vessels with red blood cell extravasation. There were no eggs, mites, or scybala visible. This was consistent with LCV. The patient was treated with topical corticosteroid creams after finishing two applications of permethrin cream, following which all her lesions resolved. Her caretaker provided consent to publish this case report, and identifying information has been kept confidential.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [86, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 86 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 5.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
967,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4644007-1,Extracted,"An 80-year-old woman of Caribbean descent with a history of type 2 diabetes mellitus, gout, osteoarthritis, gastrointestinal reflux and atrial fibrillation, presented with a 12 h history of left-sided shoulder, neck and back pain. Her temperature was 38.0°C and her white blood cell count was 15×109 cells/L. She experienced tenderness in the left sternoclavicular and sternomanubrial regions associated with warmth and erythema, but without an effusion. Her neck range of motion was restricted by pain on the left side, including neck deviation to the right, which was compatible with torticollis. She could not abduct her shoulder beyond 60 degrees. She had a III/VI systolic ejection murmur at the left upper sternal border, but no stigmata of infectious endocarditis. Her gastrointestinal, dermatological and respiratory examinations were within normal limits.
On admission, she was empirically started on ceftriaxone for suspected shoulder joint septic arthritis. An unsuccessful attempt was made to aspirate the left shoulder joint. The pain progressed toward her anterior chest wall and within 72 h C-reactive protein levels had increased from 11 mg/L to 240 mg/L. Blood cultures were positive in three of three sets for penicillin-susceptible Streptococcus pneumoniae.
Aspiration of the sternoclavicular joint (SCJ) was unsuccessful. Transesophageal echocardiography did not reveal evidence of endocarditis. The chest radiograph did not reveal evidence of pneumonia.
Despite prolonged antibiotic therapy, the patient never experienced full recovery of function, primarily with respect to arm adduction, which was limited by pain at the SCJ. Repeat computed tomography (CT) scan after therapy revealed arthritic changes related to her treated infection. Avoidance of pain led to the patient’s torticollis, which was the most distressing clinical feature for her. This persisted for months despite regular physiotherapy sessions.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [80, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 80 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
968,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6427965-1,Extracted,"A 63-year-old right handed man was admitted because of memory impairment. His past medical history included hypertension and angina of ten years duration, for which he had been placed on regular antihypertensive medication. The patient denied a history of diabetes mellitus, episodes of stroke, or neuropsychological symptoms. He had been educated for 12 years and had learned Hanja at school. His wife said he had no problems reading or writing Hanja before admission. During neurological examinations, he was fully conscious and had a Korean Mini-Mental State Examination score of 22/30. Deficits were observed mainly in the domains of attention, calculation, and immediate memory recall. Interestingly, we found that he was unable to read or write Hanja, but could read Hangul. Hangul writing was partially impaired. In his wife's statement, he did not have any problems reading Hanja and Hangul before this stroke event. Conventional brain MRI revealed an infarct involving the left frontal and parietal lobe including the angular gyrus. Fluorodeoxyglucose positron emission tomography scans showed decrease uptake in these infarcted regions (). There were no additional hypometabolic regions. fMRI and simple language tests were performed two weeks, six weeks, and six months after stroke onset to identify activated brain regions associated with Hanja and Hangul reading in each scan. An implicit reading task was performed during each fMRI scan. Three sets of test were prepared for the fMRI experiment. Each set included ten two-syllable Hanja and Hangul words and each test included 20 words: 10 Hanja and 10 Hangul words, and a total of 30 Hanja and Hangul words were tested in one visit (Supplementary Table 1 in the onlineonly Data Supplement). After the fMRI, an independent reading and writing task was performed to obtain response times and hit-rates. Written consent was obtained from the study subject, and the study protocol was approved by the Institutional Review Board (GIRBD 0024-2012) of Gil Medical Center. Detailed fMRI scan protocol and analysis method are described in the Supplementary data (Supplementary data in the online-only Data Supplement).
Hit-rates for Hangul reading were perfect (30/30) at every session for language tasks. The mean response time for Hangul reading improved from 2.8 seconds per letter [standard deviation (SD) 2.1 sec] to 1.03 seconds per letter (SD 0.2 sec) over the 6-month experimental period. In contrast, Hanja reading, Hanja writing and Hangul writing was markedly impaired initially. However, the number of correct hits increased from 8 to 28, and the mean response time for Hanja reading shortened from 3.3 to 1.5 seconds after six months. Hangul agraphia also improved to almost normal; however, Hanja agraphia persisted. The overall results are provided in .
fMRI scans during Hanja reading showed activation of the occipital regions bilaterally including the lingual gyrus, extending to the parietal cortex bilaterally from the prefrontal area, and both insula at the initial time point and six months after the onset of symptoms (, and ). Although the fusiform gyrus was partially activated bilaterally (, Supplementary Table 2 in the online-only Data Supplement), the patient could not read Hanja. At six months after symptom onset, his ability to read Hanja greatly improved; however fMRI revealed no significant changes in the fusiform gyrus region (). Instead, both middle frontal gyri showed significantly greater activation after six months (, ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [63, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 63 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
969,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7758994-1,Extracted,"The patient is a 61-year-old male with a history significant for NF-1, hypertension, esophagitis and intermittent gastrointestinal bleeding, who initially presented to an outside institution for acute onset of bleeding per rectum. The patient noted bloody bowel movements with diarrhea for several days, which had increased in frequency over the past 24 hours. The patient reported mild abdominal pain and denied nausea, emesis, chest pain, shortness of breath, syncope or other symptoms at the time. He was not on anticoagulation and denied excessive alcohol or nonsteroidal anti-inflammatory drug (NSAID) use. His family history was significant for NF-1 diagnosed in his mother and brother. He had no significant surgical history other than a total hip replacement.
On admission at the outside hospital, the patient’s hemoglobin was 6.6 g/dl, with normal platelets, partial thromboplastin time and prothrombin time. Diagnostic workup at the outside institution included a nuclear medicine gastrointestinal scan (mTc-labeled RBCs), which was negative for abnormal bleeding. On hospital Day 2, his hemoglobin failed to respond appropriately to transfusions and a computed tomography angiogram (CTA) was completed, which showed a 6.9 × 5.8 × 6.8 cm hyper-vascular mass in the left pelvis; abutting the left border of the bladder medially, iliac arteries and veins posteriorly, rectus sheath anteriorly and the small and large bowel (). Vascular supply of the mass was identified to originate from branches of the superior mesenteric artery (SMA) and appeared to be contiguous with the adjacent jejunum. The mass was noted to also abut, but not involve, the sigmoid colon. The CT scan further noted a 9 mm enhancing tumor in the second portion of the duodenum anteriorly (). After administration of five total units of packed red blood cells with limited improvement in hemoglobin, the patient was transferred to our institutions for further management.
The patient arrived hemodynamically stable and underwent esophagogastroduodenoscopy (EGD). The EGD was unremarkable with no visualization of the previously mentioned duodenal mass. Colonoscopy was performed, which was notable for bright red blood present throughout the entire colon as well as blood 5 cm proximal to the ileocecal valve (). As the patient continued to have bloody output per rectum, with insufficient response to transfusion, interventional radiology was consulted and proceeded with mesenteric angiography with intervention (). The hyper-vascular mass was found to be supplied by ileal branches of the SMA, which were successfully embolized (). After conversations with the interventional radiology team and the patient, the decision was made to proceed with an exploratory laparotomy and resection of the identified mass.
Exploratory laparotomy was notable for a 7 cm mass originating from the distal jejunum (). This mass was mostly exophytic and a single firing of a GIA load was used to excise the mass with preserved adjacent normal wall of the jejunum. Kocherization of the duodenum revealed a single sub-centimeter duodenal mass at D2. The mass was excised with subsequent primary closure of the defect. Taking down the Ligament of Treitz allowed us to identify two additional proximal jejunal lesions that were resected and resulting defects were primarily closed. The remainder of the jejunum was evaluated and a stretch of proximal jejunum, about 10 cm from Treitz, containing 10 small (0.5 to 2 cm) lesions was identified (). The decision was made to resect a 30 cm segment of jejunum with creation of a side-to-side functional end-to-end anastomosis using a linear stapler. This allowed complete resection of macroscopic disease. The mesenteric defect was closed using multiple interrupted silk sutures. The remainder of the bowel was examined and found to be normal. The patient returned to the intensive care unit and recovered over the course of the coming days without immediate complications and without requiring additional transfusions.
Five surgical specimens were sent to pathology, including the large intra-abdominal mass, a segment of proximal jejunum (30 cm), the duodenal lesion and two proximal jejunal lesions. Microscopic examination revealed a total of 13 foci of tumor. All tumor margins were negative and 12 regional lymph nodes were examined and revealed no evidence of nodal metastases. All tumors underwent H&E staining () and immunohistochemical staining for DOG-1 (), which was strongly positive, confirming a diagnosis of GIST for all tumors.
Genetic analysis of the tumors samples was performed on paraffin-embedded tissue using the Tempus XT next generation sequencing (NGS) platform, which includes 648 cancer-related genes. No KIT or PDGFRA mutations were detected (both were wild type). Instead, NF-1 was found to harbor a loss-of-function single nucleotide alteration (c.654 + 1G > T splice region variant).
The patient recovered appropriately from his surgery and was discharged one week after the operation. He continues to do well and has returned to full-time work.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [61, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 61 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
970,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-1047,Extracted,"A 58-year-old woman comes to the physician because of intermittent painful retrosternal dullness for 4 weeks. The pain is recurrent and occurs when she exerts herself or when she is outside during cold weather. She also experiences shortness of breath and palpitations during these episodes. The symptoms resolve spontaneously when she stops or sits down for a while. Over the past few days, the episodes have increased in frequency. She has hypertension, type 2 diabetes mellitus, and osteoarthritis. Her left leg was amputated below the knee after a motorcycle accident 25 years ago. She is currently waiting for a new prosthesis and walks with crutches. Current medications include captopril, glyburide, and ibuprofen. She does not smoke or drink alcohol. Her pulse is 88/min, respirations are 20/min, and blood pressure is 144/90 mm Hg. Cardiac examination shows no abnormalities. An x-ray of the chest shows no abnormalities. An ECG shows a normal sinus rhythm without any signs of ischemia. Serum cardiac markers are within the reference range.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [58, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 58 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
971,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7769750-1,Extracted,"A 43-year-old male presented with palpitations that started three hours prior to presentation. He had a similar episode three years ago at which time he was diagnosed with AF with RVR. During that episode, he was treated with diltiazem 10 mg and the rhythm converted to sinus rhythm. After that episode, he was taking metoprolol, but had stopped taking it about two years ago. He had not followed up with a cardiologist and had not had another episode in the prior two years.
The patient was alert and oriented but complained of palpitations associated with mild nausea. The patient had been generally healthy and did not take any medication. He was diagnosed with influenza A one week prior to presentation and finished a five-day course of oseltamivir. He denied illegal drug use and endorsed occasional coffee consumption. Physical examination was unremarkable except for an irregularly irregular rhythm and tachycardia. His laboratory evaluation was also unremarkable, including a complete blood count, chemistry panel, and thyroid-stimulating hormone level.
Upon arrival to the ED, his vital signs were as follows: blood pressure of 124/89 mmHg, pulse of 119 beats per minute (bpm), respirations of 18 breaths per minute, and saturation of 98% on room air (SpO2). Electrocardiogram (ECG) revealed AF with RVR (Figure ).
Diltiazem 10 mg was ordered, and the patient was placed under telemonitoring. The second ECG was obtained, at which time vital signs were as follows: blood pressure of 103/69 mmHg, pulse of 80 bpm, SpO2 of 98% (Figure ).
The heart rate then decreased to less than 30 bpm, and the rhythm showed a complete atrioventricular (AV) block. The patient subsequently became asystolic and unresponsive (Figure ).
Chest compressions were started, and rhythm subsequently changed from asystole to ventricular tachycardia (Figure ).
The patient had return of spontaneous circulation (ROSC) within a minute without interventions such as epinephrine or defibrillation (Figure ).
Vitals at that time showed blood pressure of 124/82 mmHg, heart rate of 99 bpm, and SpO2 of 99%. The patient then woke up and was alert and oriented without any neurologic deficits, but he was unable to remember what had happened. After the rhythm was stabilized, the ECG showed a heart rate of 67 bpm and AF (Figure ).
Electrophysiology service was consulted, and the patient was admitted to the hospital for further evaluation. Two-dimensional echocardiography was performed which showed normal systolic function (50-60% ejection fraction), normal diastolic function, no valve abnormalities, and no pericardial effusion. The patient had a CHADS-VASc score of 0, but given that he was in AF for several hours, he would need anticoagulation for at least 30 days to reduce his risk of thromboembolism. The patient was thus discharged home the next day with apixaban 5 mg and propafenone 150 mg both twice daily.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [43, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 43 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
972,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8489597-1,Extracted,"A 71-year-old Chinese male with recurrent bilateral lower limb venous ulcers since 2018 and a background of chronic venous insufficiency. He has a past medical history of hypertension, atrial fibrillation, cervical spondylosis and left-sided deep vein thrombosis. Prior to blue light therapy, the patient underwent bilateral great saphenous vein ablation with cyanoacrylate glue in March 2019 and left Iliac vein venoplasty and stenting in April 2020 for his recurrent ulcers. The recurrent ulcers were also typically treated with weekly four-layer compression dressing (average duration of treatment until wound closure, 10-12 weeks for each recurrence). He developed a new ulcer on his left lateral shin eight months after, requiring further surgical debridement. Post-debridement, he was placed on weekly two-layer compression dressing. Prior to the administration of blue light therapy, his ulcer had already recurred for four weeks. Blue light therapy was administered seven times across 8 weeks, as an adjunct to the patient’s weekly two-layer compression dressing. Each dose of blue light therapy was administered at a height of 4 cm from the wound for 120 seconds, with an irradiated area of 20 cm²​​​​​​​. The baseline measurement of the wound size was 3cm² (1.5 cm x 2 cm, Figure ). By week 5, there was a total reduction of 67% of wound size (week 4; 1 cm², 1 cm x 1 cm). The patient also reported a reduction in wound-pain experienced while performing activities of daily living. Complete wound closure was observed at week 8. No wound recurrence was reported at up to four-month follow-up post-wound closure.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [71, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': True, 'Diabetes history': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 71 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
973,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5954448-2,Extracted,"A 65-year-old white man waiting for heart transplantation because of end-stage heart failure was under treatment with apixaban 5 mg twice daily because of atrial fibrillation. He had no other comorbidities and had no previous history of bleeding disorders. On the day a heart from a deceased donor was available, he had taken his morning dose of apixaban. Heart transplantation surgery was coordinated the same evening. His blood test results at the time of admission showed normal blood counts, creatinine level of 156 μmol/L, estimated GFR 40 ml/minute, PT 26 seconds and aPTT 33 seconds. The apixaban concentration was 152 μg/L. Because of the recent tablet intake and the great bleeding risk during and after the procedure, it was decided to administer aPCC 3000 IU immediately before surgery. His body weight was 108 kg, which means that the dose administered was 28 IU/kg. The surgery was uncomplicated, and so was the postoperative period. No bleeding complications or thromboembolic events were seen. CT was reduced by more than 50% (from 1482 seconds to 807 seconds), and CFT was reduced accordingly (Fig. ). PT and aPTT were also reduced after aPCC treatment (Table ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': True, 'Hypertension history': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'age': [65, 'years'], 'Stroke': False, 'Diabetes history': False, 'Transient Ischemic Attacks History': False, 'sex': 'Male'}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
974,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7069868-1,Extracted,"A 72-year-old woman with a medical history significant for sarcoidosis, paroxysmal atrial fibrillation, on apixaban, obstructive sleep apnea, hypertension, hyperlipidemia, and non-insulin–dependent type 2 diabetes mellitus, presented to the emergency department with sudden onset involuntary movements of her right arm and hand, which was followed by acute onset left-sided facial droop, dysarthria, and expressive aphasia.
Initially, stroke was suspected; therefore, she underwent computed tomography (CT) imaging of the head without contrast. This showed a curvilinear hyperdensity in the left central sulcus region, left subinsular region, and inferior frontal operculum worrisome for an acute subarachnoid hemorrhage (SAH). CT angiography of the head and neck did not reveal overt vascular abnormalities. Further investigation with angiograms of the carotid and vertebral arteries successfully confirmed the absence of vascular lesions or aneurysms that may have accounted for hemorrhage. Noted in particular, there was no active extravasation of contrast evident during the study. Magnetic resonance imaging (MRI) of the brain showed curvilinear hyperintensity filling along the left central sulcus without evidence of acute blood within the sulcus (Figure ). The MRI also revealed a second area of focal parenchymal abnormality located anterior to the left frontal horn, with subtle mass effect and associated vasogenic edema. Cerebrospinal fluid (CSF) analysis from lumbar puncture did not reveal overt xanthochromia. Given these findings, intracerebral hemorrhage was felt less likely to be the cause of the patient's presentation, thus raising concern for an underlying inflammatory or neoplastic process.
Due to concerns of an underlying malignancy, the decision was made to pursue a left frontal craniectomy with stereotactic biopsy of the abnormal leptomeningeal region within the left frontal lobe. Preliminary results from pathology revealed lymphocytic infiltration of the meninges, suggestive of either a lymphoma or inflammatory process. Final pathological results with molecular analysis supported a diagnosis of B-cell lymphoma. The lymphocyte population was comprised of mainly of CD20 + B cells (Figure ) and few scattered CD3 + T cells (Figure ). The B cells had no co-expression of CD5, CD10, nor BCL6. Studies also showed that they were negative for CD43 and TdT. The proliferation marker MIB1 was positive in <10% of lymphocytes, which was indicative of a low proliferation index. Cyclin D1 and in situ hybridization for EBER were negative, while PCR studies were positive for clonal rearrangement of IgH and Kappa light chain.
After medical optimization, the patient was discharged home on dexamethasone and antiseizure prophylaxis, with instructions to continue care for her lymphoma with hematology/oncology as an outpatient. During follow-up, a whole-body fludeoxyglucose positron emission tomography (FDG PET) scan showed no evidence of FDG avidity nor pathologic lymphadenopathy outside of the CNS. The patient also underwent bone marrow aspirate and biopsy which effectively ruled out bone marrow involvement from her lymphoma. She then began treatment with whole brain radiation therapy (WBRT), completing a total dose of 2400 cGy over 12 fractions. Radiation therapy was well tolerated and was accompanied by several doses of memantine to mitigate possible neurocognitive effects. Following WBRT, the patient developed significant fatigue, ageusia, and episodic headaches without neurological deficits. Nevertheless, she subsequently began systemic treatment with single-agent rituximab, 375 mg/m2 once weekly, for a total duration of 4 weeks.
Surveillance brain MRI demonstrated persistent enhancement of the central sulcus as well as FLAIR hyperintensity of the orbitofrontal region, despite unequivocal improvement. Findings suggested a low level of residual disease. White matter FLAIR hyperintensities that were new were thought to be radiation induced.
A few months after completing treatment, the patient returned to the hospital with confusion, weakness, and malaise. She underwent initial evaluation with CT of the head which showed no acute intracranial abnormalities to explain her symptoms. An electroencephalogram showed absence of seizure-like activity. After an extensive workup, her symptoms were ultimately believed to be attributable to polypharmacy from her multitude of home medications.
A repeat MRI of the brain performed 10 months after completion of systemic treatment remained unchanged as compared to prior MRI, and with no evidence of active intracranial disease.
The patient continues to be followed regularly in the outpatient setting with medical oncology and neurosurgery. She has shown no clinical evidence of disease recurrence to date, having completed therapy greater than 12 months ago.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
975,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7212745-1,Extracted,"Clinical Presentation and Assessment
A 57-year-old male was admitted to the emergency department 12 hours after sudden onset of left lower extremity weakness. Past medical history was relevant for ischemic stroke six months prior to admission with residual left upper extremity weakness, deep vein thrombosis and inferior vena cava filter placement. Baseline modified Rankin score (mRs) was 1. At examination, there was complete hemianopia, facial droop, left lower extremity decreased sensation and weakness. National Institutes of Health Stroke Scale (NIHSS) was 6. He was supposed to be on anticoagulation therapy but had not been taking warfarin for the past two weeks.
Initial assessment confirmed that he was out of therapeutic window (international normalized ratio [INR] was 1.1). Computerized tomography perfusion (CTP) was positive for a small acute cerebral infarction of middle cerebral artery cerebral artery territory (Figure ). Cardiac source of embolism was unlikely after negative ECG for atrial fibrillation and no obvious thrombus displayed on echocardiogram.
Computerized tomography angiography (CTA) of the head and neck revealed an intraluminal thrombus arising from a hypodense plaque in the proximal segment of the right ICA, resulting in 54% of lumen stenosis, according to the NASCET criteria (Figure ). Low attenuation of the plaque imaging was suggestive of soft lipid-rich material, which is known to be an unstable feature. Final diagnosis was acute ischemic stroke and symptomatic moderate carotid stenosis of atherosclerotic etiology.
Management and Outcome
The patient was out of time window to benefit from intravenous tissue plasminogen activator administration. Endovascular or surgical intervention at this point was not considered due to the nonocclusive nature of the thrombus, as well as a high risk of further distal embolization. Decision was then made to manage the case conservatively. He was started on heparin drip, warfarin and aspirin, and was admitted to the neurocritical care unit for close monitoring. Within three days from presentation, the patient’s symptoms gradually improved. Repeated CTA five days after admission revealed residual right ICA stenosis and partial resolution of the intraluminal thrombus.
The patient was discharged home 10 days after being admitted. He had mild left lower extremity weakness and residual neurological deficits that were already present prior to this ischemic event. Discharge NIHSS and mRs were both 2. On the last day of his hospital stay, his INR was 2.4 and he was sent home on warfarin 15 mg and aspirin 325 mg daily. CTA performed 24 days after initial presentation revealed no significant degree of stenosis and complete resolution of intraluminal thrombus in the right ICA (Figure ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [57, 'years'], 'Congestive Heart Failure': False, 'Stroke': True, 'Transient Ischemic Attacks History': True, 'Thromboembolism history': True, 'Vascular disease history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 57 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 0 + 2 = 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
976,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-452,Extracted,"A 71-year-old man comes to the physician for a health maintenance examination. Aside from occasional lower back pain in the last couple of years, he feels well. He had a right-sided myocardial infarction 4 years ago. Currently, he has no shortness of breath and has no anginal symptoms. He has a 30 pack-year history of smoking but stopped smoking 10 years ago and does not drink alcohol. His pulse is 59/min, and his blood pressure is 135/75 mm Hg. Physical examination reveals 1+ lower extremity edema. Cardiac and pulmonary auscultation show no abnormalities. There is no lymphadenopathy. His laboratory studies show a hemoglobin of 13.2 g/dL and serum protein of 10.1 g/dL. ECG shows known Q wave abnormalities unchanged since the last ECG one year ago. A serum protein electrophoresis with immunofixation is shown.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [71, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 71 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
977,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5819634-1,Extracted,"An 81-year-old female presented to the emergency department (ED) complaining of progressive shortness of breath over the preceding few weeks. Other symptoms include weight loss of 30 lb over 5 months, pain in both knees and hips, as well as swelling and numbness in her right-hand fingers. Patient had been following regularly at the cardiology clinic. She had extensive past medical history significant for chronic kidney disease (CKD) stage III, hypertension, coronary artery disease and history of remote myocardial infarction complicated by right ventricular (RV) aneurysm with mural thrombus treated with warfarin therapy, and sick sinus syndrome managed with a pacemaker. She also had remote colon cancer treated with partial colectomy.
On arrival to the ED, she was afebrile, had tachypnea and tachycardia with stable blood pressure. Physical exam revealed fine crackles along the bases and absent pedal edema. She had wide spread hyper pigmented macules and papules over the back and extremities. Initial laboratory workup showed creatinine 2.84 mg/dL, hemoglobin (Hb) 8.2 g/dL, brain natriuretic peptide (BNP) 317 pg/mL and normal troponin level. Electrocardiogram (EKG) showed ST changes along the inferior leads with low voltage QRS (). Transthoracic echocardiography (TTE) revealed a large circumferential pericardial effusion with tamponade physiology (). Previously seen RV mural thrombus was not identified. Pericardiocentesis was performed with 700 mL of frankly bloody pericardial fluid drained, and a pigtail catheter was left in place for passive dependent drainage (). Pericardial fluid analysis showed a hemorrhagic exudate without evidence of infection or malignancy based on normal microbiology studies and cytology results.
Further tests showed an erythrocyte sedimentation rate (ESR) 109 mm/h, C-reactive protein (CRP) 10.5 mg/L and normal thyroid function test. She had positive serology for ribonucleoprotein antibodies at 1.9 consistent with a diagnosis of MCTD. Further serology tests were negative for anti-dsDNA, ribosomal P protein, anticentromere Ab, Sjogren’s syndrome A and B, Jo1 Ab and Scl-70 Ab.
Computed tomography (CT) scan of the chest, abdomen, and pelvis showed no evidence of malignancy, and tumor markers including CA19-9, CA125 and CEA were negative. Follow-up echocardiogram during admission showed rapidly re-accumulating pericardial effusion. Accordingly, she had a sub-xiphoid pericardial window placed and pericardial tissue biopsy revealed acute and chronic fibrinous pericarditis (). Patient responded to empiric therapy with intravenous prednisone. Prior to discharge, echocardiography showed left ventricular ejection fraction (LVEF) of 30-35% with only a trivial pericardial effusion. Given the high risk for recurrence of a pericardial effusion and lack of a mural thrombus, warfarin was held.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [81, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': True}",8,8,8,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 81 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 5 + 2 = 7.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 7 + 1 = 8. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 8.
The patient's CHA2DS2-VASc Score is 8."
978,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8460889-1,Extracted,"A 72-year-old male patient presented as an outpatient for a routine checkup and was admitted due to acute kidney failure. He had been diagnosed with ulcerate nodular melanoma 10 months earlier. His further medical history included atrial fibrillation and prostatic hyperplasia. At the time of admission, his medication consisted of methylprednisolone (16 mg daily), bisoprolol, and pantoprazole. In June 2020, he had received double immunotherapy with nivolumab (1 mg/kg) plus ipilimumab (3 mg/kg). Fourteen days later, the patient was admitted with high fever (39°C) that was accompanied by mild prerenal AKI or hemoconcentration (fractional sodium excretion <0.1%, otherwise normal urinalysis, and SCr max 1.4 mg/dL). Renal function recovered within 4 days (SCr 1.1 mg/dL) upon volume expansion (Fig. ) before steroid exposure. Three days later, the patient developed grade 3 autoimmune colitis. In accordance with the recommendations of the “American Society of Clinical Oncology (ASCO),” steroid therapy was initiated at 1 mg/kg/day methylprednisolone for the colitis, which was tapered over 5 weeks []. After clinical stabilization, the therapy was resumed with a single dose of 480 mg nivolumab. The asymptomatic patient presented for a routine follow-up after 2 weeks. As SCr had drastically increased from 1.01 mg/dL to 4.93 mg/dL, he was immediately admitted to the hospital. Mildly elevated urinary protein excretion (protein to creatinine ratio 0.22 mg/mg) as well as mild hematuria was observed. The urinary sediment revealed sparse leukocyturia without cylinders or signs of acute tubular necrosis, while fractional excretion of sodium now indicated renal AKI (4.4%). In face of the rapid and unexplained AKI, a percutaneous renal biopsy was performed that revealed a severe, acute, and partly granulomatous tubule-interstitial nephritis with signs of a parenchyma destruction, while there were no signs of glomerular damage (shown in Fig. ). A CD3-positive T-cell infiltrate was found interstitially. CD4-positive cells predominated over CD8-positive cells, being accompanied by sparse B lymphocytes (shown in Fig. ). We escalated steroid therapy to 250 mg methylprednisolone intravenously over 2 days. However, kidney function continued to decline, with an SCr of 5.7 mg/dL. A significant improvement in kidney function was only achieved after further escalation to 500 mg intravenous methylprednisolone for 1 day. The steroid therapy was switched to oral prednisone, and treatment with nivolumab/ipilimumab was discontinued. In a follow-up visit 5 weeks after discharge, a gradual decline of the SCr to 2.23 mg/dL was recorded. Over the course of 3 months under steroids, a continuous decline of SCr levels to 1.74 mg/dL was noted. After 5 weeks during steroid tapering to 40 mg/day, an acute elevation of alanine transaminase (AST) to 474 U/L was observed, suggesting grade 3 autoimmune hepatitis. AST rapidly fell to 83 U/L upon transient steroid escalation to 80 mg. Steroid tapering was resumed and the regime switched to hydrocortisone for this purpose. However, a dose of 30 mg hydrocortisone was maintained. Seven months after the renal biopsy, the patient was readmitted due to progressive disease with disseminated metastatic spread, and therapy was limited to palliative care. In contrast, a decrease of SCr to 1.38 mg/dL indicated further recovery of renal function.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
979,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5066018-1,Extracted,"A 58-year-old homeless male with a history of hypertension and prior venous thromboembolism presented to the emergency department (ED) for 1 week of weakness and fatigue. He denied any hemoptysis, dyspnea, chest pain, headache, nausea, and vomiting. Besides a heart rate of 113 bpm his physical exam was normal. His past medical history included type II diabetes. His past surgical history was significant for an infrarenal IVC filter placement 15 years ago that was still in place. He was unsure as to why it was initially placed. He had no known allergies and took atenolol, lisinopril, and metformin at home. He was not taking any oral anticoagulants. He had no family history of malignancies and bleeding disorders.
While in the ED the patient became unresponsive and ACLS was initiated and lasted for 11 minutes. The patient was intubated, resuscitated, and transferred to the intensive care unit. While in the ICU it was noted that the patient's hemoglobin dropped from 12.3 gm/dL to 6.8 gm/dL.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [58, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': True, 'Vascular disease history': True, 'Diabetes history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 58 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
980,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5337234-11,Extracted,"A 68-year-old man present at hospital after a sudden onset of visual disturbances, dizziness and slight headache. Neurological examination 25 min later revealed right-sided homonymous hemianopsia and marginal evidence of non-fluent aphasia from a stroke 20 months earlier. Brain MRI revealed restricted diffusion on diffusion-weighted imaging in the medial part of the left occipital lobe without demarcation in FLAIR.
The patient’s medical history included recurrent transient ischemic attacks. He had been taking dabigatran 110 mg b.i.d. for NVAF. At the time of treatment initiation, his renal function was slightly impaired; however, the prescribed dose regimen may have been inappropriate given the patient’s age and medical history. Laboratory examinations revealed an eGFR of 102 mL/min, a dTT of 34 ng/mL and an aPTT of 34 s. It was decided to neutralize the anticoagulant activity of dabigatran and to perform thrombolysis with rt-PA, considering hemianopsia as a functionally relevant deficit (mRS of 3).
The patient received a rapid i.v infusion of idarucizumab (5 g), which was followed, after 10 min (and a total of 110 min from symptom onset), by intravenous thrombolysis with rt-PA (70 mg). Transcranial Doppler sonography shortly after rt-PA infusion showed regular blood flow in both posterior cerebral arteries. Transthoracic echocardiography on day 2 did not reveal cardiac thrombi or structural heart disease. The patient was discharged on day 3 with slightly improved hemianopsia (NIHSS 3, mRS 2). Dabigatran treatment was resumed at the higher dosage (150 mg b.i.d.) as renal function tests were normal.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [68, 'years'], 'Congestive Heart Failure': False, 'Stroke': True, 'Transient Ischemic Attacks History': True, 'Vascular disease history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 68 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
981,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6592840-2,Extracted,"A 50-year-old female with a history of HIV and non compliance with highly active antiretroviral therapy (HAART) presented with one month of confusion, fevers, fatigue, and night sweats. Laboratory findings on admission were significant for hemoglobin of 4.6 g/dL, lactate of 2.8, and INR of 3.9 with normal liver function tests (LFTs). Her CD4 count was 51/mm3, HIV viral load less than 20 and leukocyte count otherwise normal. Hemoglobin and hematocrit responded to blood transfusions but no source of bleeding was identified. The patient remained febrile and hypotensive despite coverage with piperacillin-tazobactam, vancomycin, trimethoprim-sulfamethoxazole and acyclovir. Cultures remained unrevealing but her course was complicated by Clostridium difficile infection on day 4. On day 6 of hospitalization, she was transferred to the medical ICU requiring vasopressors and was intubated for worsening encephalopathy. MRI of the brain at this time suggested HIV encephalitis and abdominal CT showed splenomegaly and multiple hypodense lesions in the liver and spleen. She developed progressive oliguric renal failure for which hemodialysis was initiated on hospital day 9. Testing for viral pathogens revealed 64,000 copies of EBV DNA per mL, and serum ferritin was elevated at 2,512 ng/mL. Her platelet counts also fell gradually to 17,000/uL from normal levels on admission. HLH was suspected but treatment was not initiated as she only met four of the eight criteria for diagnosis. A bone marrow biopsy resulted on day 11 of hospitalization, confirming the presence of hemophagocytic cells. She was immediately started on HLH-94 protocol with etoposide and dexamethasone. Despite treatment, the patient’s hypotension, acidosis, and renal failure worsened. She did not tolerate hemodialysis despite vasopressor support and the family agreed to withdraw care. The patient passed away on day 12. Her autopsy report also showed evidence of Hodgkin’s lymphoma in her liver and spleen, which was a new diagnosis.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [50, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 50 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
982,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3680611-1,Extracted,"A 76-year-old female patient presented at the emergency department with dyspnea, a productive cough, and a fever for several days. She had experienced exacerbations of congestive heart failure for the previous 20 years and had a permanent cardiac pacemaker that had also been initially inserted about 20 years earlier due to sick sinus syndrome with atrial fibrillation. She also had dementia, and a history of multiple incidents of cerebral infarction and its complications.
At the emergency department, her blood pressure was 112/72 mmHg, pulse rate was 101/min with an irregular rhythm, and body temperature was 36.5℃. On examination, she appeared tachypneic (respiratory rate, 28/min) and her breathing sounds were reduced over the left lung field. The arterial oxygen saturation in room air was 92%. The other laboratory findings were not notable. Chest radiography revealed opacification of the whole left lung field, thought by a physician of the emergency department to be unilateral pleural effusion (). Therefore, after local anesthesia and under sterile conditions, a 16F catheter (Prime-S; Sungwon Medical, Cheongju, Korea) was inserted into the 6th left intercostal space in the anterior axillary line without image guidance.
Shortly after insertion, blood was draining in a pulsatile way from the catheter. However, she was hemodynamically stable with a blood pressure of 132/78 mmHg and a heart rate of 98/min. After clamping the catheter, contrast-enhanced computed tomography (CT) of the chest was performed () and showed that severe cardiomegaly with displacement of the heart to the left with atelectasis (originally thought to be massive pleural effusion). The catheter had been inserted anterolaterally into the sixth intercostal space on the left and was within the left ventricle, exiting the ventricle through the aortic valve with the tip of the catheter located in the ascending aorta. Transthoracic echocardiography revealed mild aortic regurgitation with a small amount of pericardial effusion without hemodynamic significance.
Open mini-thoracotomy with chest tube insertion was performed under general anesthesia the next day. The previous catheter was carefully pulled out without myocardial repair. Although the removal of the catheter was successful and well tolerated by the patient, the hospital course was complicated by pneumonia and long-term mechanical ventilation. About a month after the complication, the patient died from pneumonia with septic shock.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [76, 'years'], 'Congestive Heart Failure': True, 'Stroke': True, 'Transient Ischemic Attacks History': True, 'Vascular disease history': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 6. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
983,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8464218-1,Extracted,"A 41-year-old African-American gentleman with a history of uncontrolled type 2 diabetes mellitus, and hypertension presented to the emergency room complaining of sudden onset severe chest pain that started immediately after having sexual intercourse with his partner. His symptoms were associated with nausea and sweating. It was the first time he experienced such pain in his life. The pain started one hour prior to the presentation. His home medications were metformin 1,000mg orally twice daily and lisinopril 10mg orally once daily. He has a 10-pack-year smoking history but denied any alcohol or illicit drug abuse. On presentation he was afebrile, heart rate of 74 beats/minute, respiratory rate of 18/minute, and oxygen saturation of 100% on room air. Physical exam was within normal limits, normal S1/S2 on cardiac auscultation without any murmur or extra heart sounds, no jugular venous distension on neck inspection, no crepitation on chest exam, and no lower limb swelling. Initial electrocardiogram (EKG) was significant for ST elevation in anterolateral leads (Figure ).
He has loaded with aspirin 325mg, ticagrelor 180mg, heparin 5,000 IU IV, and was immediately brought to the catheterization lab. The procedure was done through the right radial artery and the coronary angiogram was significant for proximal left anterior descending (LAD) stenosis of 80% secondary to local spontaneous dissection and thrombus formation with a 100% thrombus occlusion of the distal LAD artery (Figure ).
A 3.5 x 15mm drug-eluting stent was successfully placed in the proximal LAD, however unsuccessful PCI for the distal LAD with no-reflow phenomenon due to heavy intracoronary clot burden resistant to several attempts of aspiration and local vasodilator injection. After the procedure, the patient was transferred to the cardiac intensive care unit in a stable condition and was continued on tirofiban infusion for 24hrs after the procedure. The patient was started on metoprolol succinate 25mg orally once daily and atorvastatin 80mg orally once daily. His transthoracic echocardiogram showed an ejection fraction of 60% with small apical and apical septal hypokinesis. No evidence of valvular disease was seen on the echocardiogram. Complete blood count and complete metabolic panel were within normal limits. His troponin peak level was 33.8ng/mL. His LDL was 74mg/dL, HDL 44mg/dL, and triglycerides 132mg/dL. The patient was counseled on smoking cessation and discharged home one day after in a stable condition on ticagrelor 90mg orally twice daily and aspirin 81mg orally once daily in addition to metoprolol succinate 25mg orally once daily, lisinopril 10mg orally once daily and atorvastatin 80mg orally once daily. The patient was also started on a basal-bolus insulin regimen, Insulin glargine 10 units at bedtime, and Insulin lispro 10 units subcutaneous three times a day.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': True, 'age': [41, 'years'], 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False, 'sex': 'Male'}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 41 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
984,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7233937-1,Extracted,"A 66-year-old female presented to the emergency department (ED) via emergency medical services (EMS) with a chief complaint of abdominal pain and syncope. Per EMS, the patient syncopized upon their arrival but regained consciousness shortly thereafter. Pre-hospital management included 250 cc of normal saline (NS) and 2 L of oxygen via nasal cannula. For EMS, glucose was 108 mg/dL, respiratory rate 22 breaths/minute, oxygen saturation 94% on room air, and blood pressure 127/72 mmHg. The patient was not able to communicate her full history at the time as her mental status waxed and waned. Per the daughter, the patient started complaining of abdominal pain 12 hours prior to arrival. The pain became progressively worse and was described as sharp, constant, diffuse, and rated 10/10. The daughter called 911 upon arriving home from work and finding her mother weak and pale. Medical history per daughter included repair of a dissecting Type A thoracic aneurysm (TEVAR with Gore thoracic endograft 40 x 15) 4 months prior, descending aortic dissection (from graft to celiac artery), infrarenal aortic aneursym, L internal iliac artery aneursym, congestive heart failure, chronic obstructive pulmonary disease, hypertension, diabetes mellitus type II, and atrial fibrillation on warfarin. Other medications included lisinopril, metoprolol, amiodarone, furosemide, metformin, potassium, atorvastatin, and flucticasone/salmeterol.
Upon arrival to the ED, the patient was cool, pale, diaphoretic, and soporific, however, oriented x3 when aroused. The Glasgow coma score (GCS) was 14 (E3V5M6). She was mildly hypotensive with a blood pressure of 101/59 mmHg, afebrile, tachypneic, and with a normal pulse rate of 80 beats per minute. The patient's physical exam findings were remarkable for an abdomen that was soft, diffusely tender, without rebound, guarding or palpable mass, and decreased bowel sounds.
After establishing intravenous (IV) access and initiating fluid resuscitation with NS, the rapid ultrasound for shock and hypotension (RUSH) exam was performed within minutes of the patient's arrival [-]. A large hypoechoic infra-umbilical fluid collection was revealed upon visualization of the suprapubic window. The aorta views were inadequate secondary to a technically difficult examination, but the patient's splenorenal and Morrison's pouch views were negative for acute findings.
Given the initial presentation of syncope, worsening hypotension (90/61 on repeat), diaphoresis, conjunctival pallor, and delayed capillary refill, our biggest concern was for hemorrhagic shock. Although unsure of the source, the differential included but was not limited to AAA rupture, aortic dissection, aortoenteric fistula, compromise of the ascending aorta elephant trunk graft, diverticulitis, perforated ulcer, perforated diverticulitis, mesenteric ischemia, perforated gallbladder, sepsis, volvulus, and any other state which causes vascular compromise. We could not rule out sepsis, and so the patient was concurrently started on 2L normal saline, vancomycin, and cefepime.
As the patient became progressively more hypotensive (80s/60s) and multiple attempts at second peripheral IV access failed, a central line was placed for emergency release blood. A chest radiograph and CTA of the chest, abdomen, and pelvis were obtained. The patient was found to have supra- and infrarenal abdominal aortic aneurysms, the infrarenal aneurysm measuring 3.5 cm x 3.4 cm with intimal dissection and extension into the common iliac arteries. There was also a dissection of the abdominal aorta extending from the aortic graft into the celiac, superior mesenteric, and renal arteries, with the false lumen feeding the celiac artery. Finally, CTA showed a complex infraumbilical ascites or blood collection, measuring 8 cm x 10 cm x 7 cm. No artery aneurysm rupture or active extravasation was seen (Figures -). The suprarenal aneursym, measuring 5.4 cm x 5.1 cm, was new compared to her imaging 4 months prior, as was the fluid collection (Figure ).
Abnormal labs were as follows: international normalized ratio (INR) 2, point of care (POC) lactic acid 7.9 mmol/L, hemoglobin 9.9 gm/dL, hematocrit 30%, calcium 7.9 mg/dL, potassium 2.9 mmol/L, and CO2 20 mmol/L.
Surgical consultation was obtained. Although the CTA abdomen/pelvis could not clearly show the HAA, our general surgeon noted blood in the hepatic capsule, and in the pelvis (Figure ), which was concerning to him. Given the extensive aneurysms and dissections of the thoracic, abdominal, and pelvic arterial systems, the suspicion was still very high for a vascular rupture. In the ED, the patient received 4 units of packed red blood cells, 2 units of fresh frozen plasma, 1 dose of anti-inhibitor coagulant complex (FEIBA), 10 mg of vitamin K (phytonadione), and 10 mg of metoprolol IV. After examining the patient, reviewing labs and imaging, and seeing the trended vitals, general surgery agreed to take the patient to the OR, with vascular surgery on stand-by.
In the operating room, general surgery and vascular surgery found a ruptured hepatic artery aneursym with approximately 2 L of hemoperitoneum. The proper hepatic artery was ligated proximally, excised, and abdomen packed. The patient received an additional unit packed red blood cells and unit of platelets, for a total of 5 units packed RBCs, 2 units of FFP, and 1 unit of platelets. The abdomen was temporarily closed with a wound vac for further resuscitation and planned second surgery for celiac artery bypass. The following day, she was taken back to the OR for the vascular procedure; however, marked ischemia was noted to the gallbladder and hepatic segments 2, 3, 4a, and 4b. The patient underwent emergent cholecystectomy but was not able to undergo a celiac artery bypass. The abdomen was temporarily closed with a wound vac for further resuscitation and planned third look surgery. On day 3, the patient was again taken back to the operating room but hepatic segments 2 and 3 had infarcted; non-anatomical left partial hepatectomy including segments 2 and 3 was performed. The abdomen was temporarily closed with a wound vac for further resuscitation and planned fourth look surgery. On day 4, the patient returned to the operating room and underwent splenectomy secondary to ruptured splenic hematoma and splenic necrosis along with fascial closure and incisional wound vacuum. The patient was extubated on hospital day 7. On day 19, the patient was ambulatory and discharged to rehab. Complications in the hospital included hospital-acquired pneumonia, acute kidney injury, deep vein thromboses in the right upper extremity, and a poorly-healing surgical wound. She was sent home with a wound vacuum, IV antibiotics. and oxygen (a new requirement). The patient was started on Eliquis at discharge, replacing her warfarin. No blood pressure targets were listed in the discharge summary; however, the patient was to follow up with cardiology, vascular surgery, and general surgery outpatient. She was able to see general surgery 2 weeks after discharge but was in guarded condition. The aneursyms and dissections were being managed medically. The patient was seen in the clinic after 3 months with healed wounds and is back to her usual activities.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [66, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 66 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
985,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3888697-1,Extracted,"A 72-year-old male with a remote history of splenectomy secondary to Hodgkin's lymphoma, paroxysmal atrial fibrillation (on anticoagulation), coronary artery disease status after coronary artery bypass graft (X1 vessel), and hypertension presented with high-grade fever and confusion for 3 days. He had similar complaints 9 months prior, at which time he was diagnosed with pneumococcal meningitis and pneumococcal mitral valve endocarditis (often referred to as Austrian syndrome). During that time, a transesophageal echocardiogram (TEE) showed mitral valve vegetation and posterior annular abscess. Blood cultures grew penicillin-sensitive Streptococcus pneumoniae. He underwent mitral valve repair, which consisted of P2 resection with the vegetation and repair of the posterior annular abscess at the hospital of the University of Pennsylvania (HUP). Five months later, he was again diagnosed with penicillin-sensitive pneumococcal mitral valve endocarditis; however, he responded promptly to medical therapy with ceftriaxone given intravenously over a 6-week period. He had received a pneumococcal vaccination 2 years prior to this presentation. On physical examination during this admission, he was alert but disoriented to time, place and person. The temperature was 104.3°F, blood pressure 120/74 mm Hg, heart rate 87/minute, and respiratory rate 22/minute. Cardiac auscultation revealed a soft S1 and grade 2/6 systolic murmur at the mitral area without any radiation. There were no meningeal signs, focal neurological deficits, or peripheral stigmata of infective endocarditis. Laboratory data is shown in . Chest X-ray and urinalysis were normal. Electrocardiogram showed an old left bundle branch block. Computed tomography of head was normal. The patient was initially started on intravenous ampicillin, ceftriaxone, and vancomycin while waiting for blood cultures. Lumbar puncture was not performed on admission due to the risk of bleeding as the patient was on coumadin (INR-2.3). Blood cultures (4/4 cultures) grew penicillin-sensitive Streptococcus pneumoniae. Ampicillin and vancomycin were stopped on day 3. TEE revealed severe mitral regurgitation and a small vegetation on the posterior mitral leaflet without any evidence of abscess (). Patient clinically responded to intravenous ceftriaxone. However, due to recurrent pneumococcal mitral valve endocarditis and severe mitral regurgitation, the patient underwent mitral valve replacement. There was a vegetation on the pledgeted suture that was placed during mitral valve repair, and the whole suture line along P2 was infected. This infected area was widely debrided. A #29 St. Jude mechanical valve was placed. The patient had an uneventful postoperative recovery and was discharged home on anticoagulation for atrial fibrillation and mechanical heart valve. He finished a 6-week course of intravenous ceftriaxone therapy. During the follow-up visit at the clinic 6 weeks later, he was found to be asymptomatic and stable.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
986,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8688592-1,Extracted,"A 76-year-old woman with a history of HIT-T was admitted to our department for unstable angina pectoris (UAP); coronary artery bypass grafting (CABG) was indicated. Her first admission by the cardiologist was 7 years prior for UAP with congestive heart failure, and diagnosed with three-vessel coronary artery disease. She was mechanically ventilated; intra-aortic balloon pumping (IABP) and percutaneous coronary intervention (PCI) with a bare-metal stent to the right coronary artery (RCA) were performed. Post-intervention, continuous hemodiafiltration (CHDF) with heparin was continued. Repeated heparin use caused gangrene and amputation of four fingers; she was subsequently diagnosed with HIT-T, and a temporary tracheostomy was required. Moreover, due to her poor general condition, PCI for residual coronary disease was not performed.
Other comorbidities included insulin-dependent diabetes mellitus (hemoglobin A1c = 6.4%), chronic kidney disease (eGFR = 15 ml/min/1.73 m2), pulmonary hypertension, and peripheral artery disease (left carotid artery and left radial artery stenosis). There was no family history of coronary disease, allergy, or history of smoking.
Her left ventricular function was moderately impaired (left ventricular ejection fraction, 44%). The preoperative platelet count was 18.0 × 104/μl, and platelet factor PF4/H Ab was negative; thus, she was diagnosed with ‘‘remote’’ HIT [, ]. The estimated postoperative mortality by Japan SCORE II (which does not include entry for the thromboembolism) was 4.9%, and the estimated risk of mortality and morbidity was 28%.
On admission, aspirin and clopidogrel were substituted for argatroban, and argatroban was used during coronary angiography. Target activated partial thromboplastin time (aPTT) was twice the baseline; thus, argatroban was administered until 9 h prior to the operation. Surgery was performed under general anesthesia, and a median sternotomy approach was used. Simultaneously, the right femoral artery and vein were secured by introducing peripheral mechanical circulatory support, avoiding central cannulation for cardiopulmonary bypass establishment.
A bolus of 5000-unit unfractionated heparin was administered when anastomosis was started, and activated clotting time (ACT) was maintained between 189 s (control score) and 429 s (Fig. ). After all coronary anastomoses (RITA-LAD, LITA-LPL, SVG-4PD) were completed, 100 mg protamine was administered; however, the ACT did not normalize fully (Fig. ). The surgery was uneventful, and the patient was extubated in the operating theater. The intra and postoperative blood losses were 495 cc and 358 cc/16 h, respectively.
Furthermore, the postoperative anticoagulation regimen was based on the ACCP guideline []. Argatroban was initiated at 0.2µg/kg/min (this value is in accordance with the Japanese standard []) 3 h postoperatively and continued until postoperative day (POD) 6. (Fig. ) Warfarin was also started when platelet count exceeded 10 × 104/μl on POD 4 and continued for 3 months. The postoperative course was uneventful, and there were no signs of thromboembolism. PF4/H Ab was positive on POD 8 (examined by latex flocculation turbidimetry; 2.8 U/ml: the threshold is < 1.0) and negative by POD 91.
Informed consent was obtained from the patient for the reporting of this case.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [76, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 6 + 1 = 7.
The patient's CHA2DS2-VASc Score is 7."
987,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3668300-1,Extracted,"A 69-year-old Caucasian woman with a past medical history of atrial fibrillation presented to Baylor University Medical Center, Waxahachie, TX, USA after having substernal chest pain following a motor vehicle accident. Her initial electrocardiogram showed atrial fibrillation with a heart rate of 60 to 70 beats per minute with no S-T-wave changes. Her initial level of troponin was 0.85ng/mL and trended up to a peak level of 4.58ng/mL. She was loaded with clopidogrel bisulfate (Plavix®) started on a heparin drip and taken to emergent cardiac catheterization at Baylor University Medical Center, Dallas, TX, USA.
Catheterization showed her to have a depressed left ventricular ejection fraction of 40% with moderate inferior and anterolateral hypokinesis with a 30% mid stenosis of her right coronary artery but otherwise unremarkable coronaries. She was discharged home on metoprolol tartrate (Lopressor®) aspirin and ramipril. Our patient’s subsequent transthoracic echocardiogram demonstrated normal left ventricular systolic function with an estimated ejection fraction of 55%.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [69, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 69 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
988,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5798152-2,Extracted,"Case 2 was a 65-year-old male pensioner. Whilst the patient had low alcohol consumption (<14 units/week) and a moderate caffeine intake (1 cup/day), the patient was a heavy cigarette smoker (46 pack years smoked). The patient had been diagnosed with ADPKD during a routine clinical examination at the age of 55. The patient’s father died early without a diagnosis of ADPKD and their mother did not suffer from ADPKD. The patient’s sister, however, had been diagnosed with ADPKD and underwent unilateral nephrectomy at the age of 55. At the time of the patient’s presentation, their sister had not reached ESRD at the age of 64 years.
The patient’s comorbidities included hypertension, which was diagnosed in later life and treated with candesartan and bisoprolol, but with poor control. The patient had not experienced any urological complications. The patient had suffered various cardiovascular disorders, including hypertrophic obstructive cardiomyopathy [which had been treated with an automated implantable cardioverter defibrillator (AICD), subvalvular myectomy and mitral valve reconstruction], a recent transient ischaemic attack and atrial fibrillation. Extrarenal manifestations of ADPKD included sigmoid diverticulosis.
The patient’s renal function at presentation showed an eGFR (CKD-EPI) of 32 mL/min/1.73 m2, with a documented decline from 49 mL/min/1.73 m2 3.5 years prior (seven creatinine values in between documenting the slope; CKD-3b). Genetic testing had not been performed, so a PROPKD score could not be calculated. Also, due to the AICD, it had not been possible to perform an MRI; however, sonographic measurements revealed an htTKV (ellipsoid formula) that placed the patient into Mayo class 1D.
In this patient, tolvaptan was not recommended. Generally, as the patient showed a significant loss of renal function and fulfilled the criteria of Mayo class 1D, prescription of tolvaptan would have been possible. However, there were no data regarding the patient’s age group and little data regarding late CKD-3b. In addition, the patient’s late onset of hypertension, the poor control of hypertension, the patient’s other comorbidities and their sister’s clinical history (not having reached ESRD despite unilateral nephrectomy) indicated that these could have been alternative explanations for the patient’s loss of kidney function. All these aspects were discussed with the patient and they followed the recommendation not to commence tolvaptan therapy.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [65, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': True, 'Vascular disease history': True, 'Diabetes history': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
989,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5081674-1,Extracted,"A 93-year old man was brought to the emergency room for recent neurological deterioration. His past medical history was relevant for hypertension, diabetes mellitus, dyslipidemia, coronary artery disease, chronic atrial fibrillation and mild memory loss. He had no history of kidney disease. His chronic medication included clopidogrel, acenocoumarol, amlodipine, atorvastatin, molsidomine and furosemide; he was on levofloxacin since two weeks for pneumonia. On admission, the patient’s physical examination revealed obnubilation with episodes of agitation, a blood pressure of 160/80 mmHg, an irregular heart rate of 50 beats per minute (bpm), jugular venous distention, decreased bilateral basal breath sounds, no fever and no leg edema. He was not obese. Initial abnormal serum laboratory results included: white blood cell (WBC) count of 12630/mm3 (84 % neutrophils), international normalized ratio (INR) of 4.5, creatinine of 2.3 mg/dL (203 μmol/L), blood urea nitrogen (BUN) of 80 mg/dL (28.5 mmol/L), albumin of 3.2 g/dL (32 g/L), phosphorus of 5.9 mg/dL (1.96 mmol/L) and gamma glutamyl transferase of 275 UI/L. He had a positive troponin I of 0.27 ng/mL but normal CPK and CPK-MB. C-reactive protein was 19 mg/L. He had no electrolytes’ disturbance (potassium 4.9 mmol/L, sodium 144 mmol/L, chloride 110 mmol/L, bicarbonate 23 mmol/L), no hypocalcemia (corrected calcium 8.9 mg/dL) nor anemia (hemoglobin 13.4 g/dL, hematocrit 42 %). Urinalysis showed 3+ protein.
Further investigations revealed left lung basal consolidation with bilateral effusion on chest X-ray. The arterial blood gas (ABG) showed: pH 7.27, PaO2 91 mmHg, PaCO2 52 mmHg, HCO3ˉ 23 mmol/L. Electrocardiogram (ECG) on admission showed a slow atrial fibrillation of 55 bpm (Fig. ). Brain computed tomography (CT) scanning ruled out possible ischemic or hemorrhagic stroke.
The patient was admitted to the intensive care unit (ICU). An echocardiography showed a left ventricular ejection fraction (LVEF) of 40 %, ventricular hypertrophy, pulmonary arterial pressure of 40 mmHg, dilated right ventricle and slightly enlarged left atrium. Renal ultrasound was normal.
Empiric antibiotics were started combining ceftriaxone and levofloxacin; fluconazole was added at day 2 after sputum cultures grew Candida albicans. Urine culture was sterile.
During cardiac monitoring in the ICU, episodes of extreme bradycardia were noticed as low as 32 bpm with maintained systolic blood pressure at 100–120 mmHg and very low diastolic blood pressure of 30–40 mmHg.
On day 3, the patient became unconscious and developed severe respiratory acidosis with ABG showing: pH 7.16, PaCO2 64 mmHg, PaO2 75 mmHg, HCO3ˉ 22 mmol/L and he was intubated. He concomitantly became oligoanuric and serum creatinine started to increase. A spot urine test revealed a sodium (Na) of 22 mmol/L and potassium (K) of 34 mmol/L with a ratio Na/K <1. He received sodium bicarbonate whenever his bicarbonate level was less than 22.
Complete AV block was then identified on ECG. A temporary pacemaker was implanted on day 5 and the patient was extubated. Serum creatinine decreased and urine output improved considerably. Table illustrates the heart rate (HR), urine output, systolic and diastolic blood pressure values, serum creatinine and potassium variations before and after the pacemaker insertion.
The patient finally got a permanent single chamber pacemaker VVIR and improved considerably his consciousness and renal function. At discharge he had a serum creatinine of 1.6 mg/dL and he was conscious, alert and well oriented.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [93, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 93 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
990,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7824006-2,Extracted,"Prosthetic valve endocarditis was diagnosed in 72-year-old woman presented with chronic heart failure, permanent atrial fibrillation and a history of multiple heart valve interventions. She had a background of mitral commissurotomy (years ago) and surgical valves replacement in 2000 (a mechanical prosthesis in the mitral position and bioprosthesis in the tricuspid position and replaced later in 2011). Moreover, she underwent a pacemaker implantation in 2000 and combined aortic valve disease with the predominant stenosis diagnosed in mean time.
MSSA was grown in blood cultures so cloxacillin, gentamicin and rifampicin were implemented in accordance with the ESC guidelines [,,]. In the past, most likely, due to the coexistence of hepatic cirrhosis secondary to right heart failure, INR values above 3.5 were often found. Therefore, the patient had her own portable INR measuring device. To date, low doses of acenocoumarol (approximately 0.5 mg daily) have been used in chronic treatment. Anticipating difficulties in the dosage of VKA with concomitant use of rifampicin, it was decided to increase the frequency of INR measurements to two per day and the possibility of using low doses of acenocoumarol twice a day. In the following days, the INR was maintained within the therapeutic range using this strategy, despite the intake of rifampicin. Changes in the dosage of acenocoumarol along corresponding INR values on subsequent days of antibiotic therapy are presented in . As for the other blood test results, creatinine concentration was slightly alleviated at the beginning of the treatment (86 μmol/L) and normalized toward its end (75 μmol/L, GFR > 60 mL/min/1.73 m2). The concentration of haemoglibin was stable and amounted to about 9–10 g/dl (patient initially with anemia of chronic diseases). No thrombocytopenia was observed. Transient increases in the activity of transaminases were also observed, as in the first case, but were rather slight (ALT up to 46 U/L and AST up to 59 U/L).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [72, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
991,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3318881-5,Extracted,"A 67 years old woman, premorbidly bed ridden due to stroke was brought in from nursing home after complaining of left knee pain and swelling for a week. She denied any history of fever, fall or trauma. Her other medical illnesses include mixed connective tissue disease, diabetes mellitus, hypertension and chronic atrial fibrillation. She was also on long term oral prednisolone 15 mg OD for autoimmune hemolytic anemia and vasculitis.
On admission, she was septic looking and in severe pain. The left knee was swollen, tender, warm and erythematous, extending proximally to mid thigh. There were multiple inguinal lymph nodes palpable. Other systems examinations were unremarkable.
Her total WBC was 19.3 x 109/L with neutrophilia of 18.2 x 109/L. Her ESR was 86 mm/hour and C-reactive protein was 16.8 mg/dL. Ultrasound of the left knee showed hypoechoic collection at the suprapatella region with some internal echos and septation within the lesion. The collection was seen within the muscular striation and appears to be continous with the subpatellar knee joint region. Left knee x-ray showed soft tissue swelling at suprapatellar region with reduced joint space and osteophytes. Aspiration from the joint revealed thick, turbid fluid. There were more than 500 white blood cells/mm3 and more than 500 red blood cells/mm3 in the synovial fluid and culture grew Pseudomonas Species. Blood culture grew Bacillus Species and urine culture grew Klebsiella ESBL. She responded well with intravenous Meropenam and oral steroid was reintroduced slowly.
She underwent arthroscopic knee wash out at day 14 of admission and repeat synovial fluid, blood and urine culture were negative.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [67, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 67 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
992,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5944231-1,Extracted,"A 59-year-old healthy male presented for an assessment of nonhealing painful necrotic lesions of the left leg. His past medical history included anemia with intermittent pancytopenia diagnosed 10 years ago. Previous specialist hematologic assessment did not reveal an etiology. Two weeks prior, he believed that he sustained a spider bite while mowing the lawn during the month of August. The lesion began as a small papule less than 1 cm and then developed into a large blister on the left lower calf. Oral cloxacillin was initiated for one week; however, the lesion rapidly increased in size, began to ulcerate, and was extremely painful. He presented to the emergency room at a community hospital, febrile (38 degrees Celsius) with otherwise stable vitals. The documented area of necrosis measured 10 cm × 13 cm. Blood work showed ongoing pancytopenia (white blood cell count of 1.8 × 109/L, hemoglobin 100 g/L, platelets 88 × 109/L). He underwent urgent surgical debridement due to clinical concerns of a necrotizing process. Empiric ceftriaxone, metronidazole, and clindamycin were initiated. There was no intraoperative evidence of necrotizing fasciitis, purulence, or foul odour. Tissue cultures yielded methicillin-susceptible Staphylococcus aureus (MSSA), and the antibiotics were narrowed to cefazolin. Necrosis developed at the surgical margins and rapidly extended a further 3 cm over the next 3 days. A second surgical debridement was completed with the addition of a negative pressure dressing over the wound. The intraoperative tissue cultures yielded MSSA and Pseudomonas aeruginosa. Ciprofloxacin was added to cefazolin. During the subsequent three days, the patient developed severe calf pain with an expanding hematoma and required urgent surgical exploration. No significant abnormalities were noted. Tissue cultures yielded the same mixture of organisms. Further extension of necrosis again was observed at the surgical margin, and a fourth surgical debridement extended his wound up to the popliteal fossa and down to the ankle. Microbiology yielded commensal flora. Histopathology showed skin necrosis, ulceration and inflammation of subcutaneous tissues, and neutrophilic dermal infiltration with abscess formation. All bacterial and fungal stains were negative, and there was no evidence of vasculitis. New necrotic lesions developed on the left medial malleolus and the plantar aspect of his first metatarsophalangeal (MTP) joint. He was subsequently transferred to our centre for evaluation of an infectious etiology of progressive nonhealing necrotic skin lesions and assessment for potential limb amputation.
On initial assessment, the lesions were violaceous, painful, and necrotic with raised, irregular borders. The largest lesion extended circumferentially from the left tibial tuberosity to the ankle. Satellite lesions were noted at the medial and lateral malleoli and the base of the first MTP joint (). Investigations showed ongoing pancytopenia (leukocytes 2.3 × 109/L, hemoglobin 72 g/L, and platelets 64 × 109/L). His C-reactive protein level was 225 mg/L. A nuclear bone scan indicated osteomyelitis of the left first MTP joint. A bone marrow biopsy showed pancytopenia with possible hairy cells. Flow cytometry revealed a pattern consistent with hairy cell leukemia (HCL).
Based on the clinical course of leg lesions exhibiting a pathergic phenomenon in response to skin trauma and nonresponse to multiple adequate courses of antimicrobial therapy and pathology showing sterile neutrophilic infiltration, combined with diagnosis of underlying hematological malignancy, we diagnosed him clinically with pyoderma gangrenosum. All further debridement was suspended, and negative pressure dressings were stopped. Due to the open nature of the wound, imaging consistent with osteomyelitis and impending chemotherapy, empiric piperacillin-tazobactam and vancomycin were initiated. A bone biopsy of the left MTP grew E. coli (Amp C) and P. aeruginosa. Antibiotics were switched to ertapenem and ciprofloxacin. He received seven days of cladribine chemotherapy plus prednisone for HCL and continued antibiotics for osteomyelitis of his left MTP. Six months after diagnosis of PG, the lesions showed significant clinical improvement, but severe scarring ().",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [59, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 59 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
993,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5043006-2,Extracted,"A 17-year-old, otherwise healthy, male patient presented with an upper respiratory tract infection and was treated with amoxicillin (dose not available). He was admitted to a peripheral hospital when he developed skin rash and muscle pain. Physical examination revealed tonsillitis and cervical lymphadenopathy; neurological examination was normal at this time. Differential blood count showed monocytosis (18 %, normal range 1–12 %); CRP was elevated (1.21 mg/dl, normal range <0.5 mg/dl).
Within 24 h, the patient developed drowsiness and neurologic exam showed neck stiffness. CSF analysis revealed mild pleocytosis (7 cells/µl, normal range 0–4/µl) and normal glucose levels (CSF/serum glucose ratio of 0.66, normal range >0.6). Antiviral therapy with acyclovir (500 mg TID) and antimicrobial chemotherapy with ceftriaxone (2 g BID) was initiated. The patient further deteriorated and was mechanically ventilated and transferred to our unit. On arrival, neurologic exam revealed bilateral non-reactive dilated pupils, which most likely developed during the 30 min of helicopter transfer. Head CT scan demonstrated global cerebral edema (Fig. b) with transtentorial herniation. The patient immediately underwent bilateral craniectomy. Neuromonitoring probes were placed into the right frontal white matter to measure ICP, brain metabolism, CBF, and brain water content (BWC) (HEMEDEX QFlow500™ Perfusion Probe, HEMEDEX™, Cambridge, MA). A broad diagnostic workup revealed Epstein-Barr virus (EBV)-associated encephalitis confirmed by serology (IgM/IgG antibodies in CSF and serum) and PCR (EBV-DNA in CSF). Intravenous ganciclovir (300 mg BID) and doxycycline (100 mg BID) treatment was initiated.
After craniectomy, ICP was still elevated (episodes of ICP >30 mmHg) and decreased only after osmotherapy, therapeutic hypothermia (33 °C), as well as thiopental (1.7 mg/kg/h) and propofol infusion (1 %, 10 ml/h), aiming to achieve a burst-suppression pattern on surface electroencephalogram (EEG). CBF was low (median 16 ml/100 g/min, IQR 13.7–18.1) during the first 24 h of monitoring and increased thereafter. BWC started at 86 % and decreased to 82 % during repeated osmotherapy concomitant to radiologic edema regression (significantly lower BWC values around 70 % have been described in normal-appearing brain tissue on head CT scans in acutely brain-injured patients) []. As ICP normalized on day four, intravenous thiopental and propofol infusions could be gradually reduced; slow rewarming was initiated, and the patient’s body temperature reached 36 °C on day nine of monitoring (Fig. a).
During the time of hypothermia, CMD-glucose levels were low (64 % of measurements <0.7 mM/l, 4 % <0.2 mM/l), despite a liberal systemic glucose management. Overall, 80.7 % of systemic glucose measurements were >6 mM/l. Insulin application (3 U/h) was started together with parenteral amino acid supplementation after 11 h, EN (Isosource® Standard Neutral Smartflex®, Nestlé Austria, Vienna, Austria) was started after 22 h. CMD-lactate, CMD-pyruvate, and CMD-LPR were within normal range [median of 1.9 mM/l (IQR 1.7–2.2), 84 µM/l (IQR 69.3–93.7) and 23 (IQR 21.4–25.5), respectively].
After the patient’s body temperature reached 36 °C, CMD-glucose levels remained low (54 % <0.7 mM/l, 11 % <0.2 mM/l), CMD-lactate and CMD-LPR exceeded pathologic thresholds for extended periods of time (32.4 % >4 mM/l and 46.3 % >30, respectively). As CMD-pyruvate levels were at a median of 92 µM/l (IQR 71–149) and 94 % >70 µM/l, several episodes (32.7 % of measurements) of mitochondrial dysfunction were observed (Fig. b).
When neuroglucopenia was detected, ICP was within normal range (<20 mmHg) in 80.2 %, CPP was >60 mmHg in 97.7 %, and CBF was >17 ml/100 g/min in 69.2 % of time. An association between systemic and CMD-glucose levels is shown in Fig. c. Serum- and CMD-glucose levels were significantly correlated (r = 0.47, p < 0.0001); insulin-dosage was negatively associated with CMD-glucose levels, and intermittent pauses of EN and PN were associated with a decrease in CMD-glucose.
The patient gradually improved and could be extubated after 23 ventilator days. He showed an atactic-ballistic movement disorder, discrete paresis of the lower limb (especially dorsal flexors), and transient psychosis. He could be discharged to an acute rehabilitation facility after 7 weeks. Fortunately, he improved within 3 months to a normal functional level with only mild neuropsychological deficits (modified Rankin Scale Score of 1, respectively).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [17, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 17 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
994,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7188448-1,Extracted,"An 80-year-old male with a history of coronary artery disease post bypass grafting, paroxysmal atrial fibrillation (AF) on warfarin for stroke prophylaxis, acid reflux, hypertension, and chronic kidney disease presented to our emergency department with the chief complaint of fatigue, confusion, and dry cough for the last two weeks. The patient stated that the symptoms started while he was on vacation in Atlanta and he returned two days ago. The cough was described as dry with occasional greenish sputum associated with shortness of breath, sore throat, and chills but no fevers. He denied any sick contacts, hiking, backpacking, or exposure to bats. He reported to be a chronic smoker with a 40 pack-year smoking history and quit smoking a few years ago and drank alcohol socially.
On presentation, the patient was alert and oriented with no apparent confusion, and diffusely decreased breath sounds with occasional rhonchi were heard on right upper lung auscultation with irregularly irregular rhythm on cardiac auscultation. Vital signs revealed a heart rate (HR) of 110 beats per minute (BPM), a respiratory rate of 18 breaths per minute, a blood pressure of 102/45 mmHg, and an oxygen saturation of 90% on room air. Electrocardiogram showed AF with a complete right bundle branch block (Figure ).
The complete blood count was unremarkable, and metabolic profile revealed an elevated creatinine of 1.71 mg/dL (normal: 0.73-1.22 mg/dL) and magnesium level of 1 mg/dL (normal: 1.7-2.3 mg/dL). International normalized ratio was 2.8 on warfarin, brain natriuretic peptide was 1,246 pg/mL (normal: less than 450 pg/mL), and troponin T was normal. Chest X-ray showed new hazy right upper lobe lateral opacity concerning for an infiltrate with the increased prominence of right hilum indicating adenopathy or bronchiectatic inflammatory changes (Figure ).
Influenza screen was negative; nasopharyngeal swab for coronavirus 19 testing was sent, blood cultures were drawn, and the patient was commenced on intravenous doxycycline and ceftriaxone before transfer to our service on the regular medical floor (RMF).
On the RMF, the patient was initially managed as community-acquired pneumonia with a COVID-19 rule out status. All protective measures and precautions for suspected COVID-19 infection were taken, and the patient was placed in isolation. Intravenous antibiotics were continued, and bacterial pneumonia workup and procalcitonin were sent.
Overnight, the patient became tachycardiac (HR, 130 BPM) and spiked a fever of 101.5°C, with physical examination revealing worsening bilateral wheezing and intermittent delirium. Sepsis lactate was 1 mmol/L (normal: 0.5-2 mmol/L) and C-reactive protein was 6.1 mg/dL (normal: 0-1 mg/dL). Bacterial pneumonia workup came back negative and COVID testing was still pending amid severe backlog. AF with a rapid ventricular response (RVR) was deemed to be due to acute illness, and home metoprolol dose was increased. Instructions were given to avoid nebulizer treatments and oral/parenteral steroids due to the pending COVID 19 status.
On the morning of day 2 of admission, the patient became progressively hypoxic and his oxygen demands acutely increased, with worsening diffuse wheezing on examination. Attempts were made to relax the airway with ipratropium and budesonide inhalers, with minimal effect. Eventually, the rapid response team was called in the afternoon of day 2 for persistent hypoxia and AF with RVR. Arterial blood gas revealed acute hypoxic respiratory failure with a P:F of 140.
Chest X-ray this time around showed worsening infiltrates bilaterally (Figure ).
Transthoracic echocardiogram showed normal biventricular size and function (Figure ).
Intravenous steroids were administered, and the patient was transferred to the intensive care unit (ICU). En route to the ICU, the patient’s COVID 19 test came back positive, approximately 48 hours after it was ordered. The patient was intubated and put on mechanical ventilation in the ICU under airborne precautions, avoiding non-invasive ventilation and commenced on hydroxychloroquine and azithromycin, as an initial step with an aim to add on other proposed therapies (remdesivir, tocilizumab, lopinavir-ritonavir). The patient currently remains in the ICU, critically ill with a poor prognosis.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': True, 'age': [80, 'years'], 'Diabetes history': False, 'Transient Ischemic Attacks History': False, 'sex': 'Male'}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 80 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
995,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5758175-1,Extracted,"A 57-year-old woman, gestation 4, production 2, presented with irregular vaginal bleeding for 3 months, 7 months after the onset of menopause. The patient was examined in a gynecology clinic, in December 2006, she had no personal history of diabetes or cardiovascular disease and her body mass index (BMI) was within normal limits, despite having undergone subtotal thyroidectomy due to hyperthyroidism 13 months before. In addition, she had a family history of cancer and her brother died from esophageal cancer. Transvaginal B-ultrasound examination revealed irregular endometrial thickening, with a thickness of 1.1 cm, the echo was not uniform and showed abundant arteriovenous blood flow signal. Subsequently, curettage of the uterus was performed on the patient and a biopsy of the uterus revealed a moderately differentiated endometrioid adenocarcinoma. For the treatment of the EC, the patient, under general anesthesia, underwent an operation of epidural hysterectomy and bilateral salpingo-oophorectomy plus pelvic and para-aortic lymph nodes dissection. In addition the peritoneal cytology was negative. Postoperatively, the patient was diagnosed with endometrioid adenocarcinoma whose clinical FIGO stage and histological grade was IB and G2, respectively (referred to the 1988 FIGO stage of endometrial cancer at that time). The postoperative pathological report was consistent with the biopsy results, it showed that the carcinoma had a size of 2.5×0.8 cm and infiltrated the superficial muscle layer; immunohistochemical analysis was not performed during that period, however (Fig. A). Fortunately, the patient had no cervical or vaginal carcinoma invasion, no lymph node metastasis and no abnormality of double attachment. After being released from the hospital, the patient was followed-up regularly, exhibited no obvious change in tumor markers levels and on computed tomography (CT) analysis and maintained a good quality of life, without signs of tumor progression or recurrence.
The patient presented with irregular cough with no apparent cause after 54 months of remission, but appearance of pulmonary metastasis was suspected. Pulmonary CT showed multiple high-density pulmonary nodules indicating that it was likely a metastatic tumor (Fig. ). Also, lung biopsy confirmed the moderately differentiated adenocarcinoma infiltration of the lung tissue, which according to our pathologist was from EC metastasis, combined with her cancer history (Fig. B). Additionally, immunohistochemical analysis revealed the staining status of ER (++), PR (++), C-erB-2(−) (Fig. C and D). In addition, the cancer antigen 125 (CA-125) level was 24.62 U/mL (normal range, 0–35 U/mL). After explaining the patient's condition to her daughter, the family made it clear that they refused the treatment by auxiliary chemotherapy, but agreed to hormone therapy. Accordingly, the patient was treated with Megestrol Acetate Dispersible Tablets (trade name Yilizhi), 160 mg, orally, once daily, without interruption. No significant progression of the tumor was observed in pulmonary CT scans 3, 9, 22, 24, 34 and 63 months after the lung metastasis was detected (Fig. ) and corresponded with the CA-125 levels which remained steady within the normal range. To date, the patient has been treated with progesterone therapy for stable conditions and her survival time is already roughly a decade (December 2006–October 2016). This implies that rational hormone therapy is an effective means to treat EC patients postoperatively, and especially for the recurrent cases. During the treatment period with this drug, the monitoring of the patient's biochemical indices of the liver and kidney function revealed that they all were in the normal range.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [57, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 57 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
996,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6318108-2,Extracted,"A 66-year-old Caucasian male with past medical history significant for hypertension and hyperlipidemia presented with altered mental status. Symptoms at presentation included slurred speech. He was found walking around his yard and his neighbor noted his slurred speech. His last know well state was the day before in the evening hours. Upon arrival, the blood pressure was found to be at 150/70 and his laboratory workup including complete blood count, complete metabolic profile and urinalysis were normal. Urine drug screen was positive for cannabinoids and serum alcohol level was not detectable. CT of the head showed age-related atrophy and mild small vessel ischemic changes without acute intracranial bleeding (Figure ). Questionable loss of gray-white junction and edema was found in the left frontoparietal region. On physical exam, the patient was confused but had normal movements and strength. He denied use of any tobacco products. TTE showed a normal left ventricle size, thickness, and function. The ejection fraction was estimated at 60% with normal right ventricular structure and function. There was a small PFO with predominant left-to-right shunting visualized. MRI showed an acute left middle cerebral artery territory infarction without midline shift or hemorrhagic conversion (Figure ). CTA showed the right internal carotid artery with estimated stenosis of 30-50% and the left internal carotid artery with stenosis estimated at 30-50%. TEE showed the PFO previously demonstrated and an ejection fraction of approximately 60%. Ultrasound of lower extremities failed to show deep vein thrombosis. The patient continued receiving neuro checks during the length of the stay and was started on antiplatelet therapy and atorvastatin with an outpatient follow-up and discharged with an event recorder and possible percutaneous closure of PFO after conduction abnormalities were ruled out.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [66, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 66 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
997,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5652892-1,Extracted,"A 57-year-old, right-handed man presented with mild cellulitis over the dorsum of his left lower limb. He was involved in a road traffic accident a week prior to his admission, resulting in an abrasion over the dorsum of his left foot. On further questioning, the patient admitted to an episode of syncope while riding his bike, which caused him to hit a car at the traffic light. He had no prodrome and made full recovery after a brief loss of consciousness, lasting for 2-3 minutes. He did not complain of any other alarming symptoms prior to or after his accident. He did not have any significant past medical history or family history of note.
On examination, he was apyrexial and his blood pressure was 148/96 mm Hg, but this settled subsequently to less than 130/80 mm Hg. There were no focal neurological findings. However, his heart rate was irregularly irregular and his electrocardiograms (Figure , ) revealed AF, which was confirmed on a 24-hour Holter monitor. Echocardiography demonstrated normal valve morphology and no other abnormality was revealed.
All his laboratory tests were normal, including electrolytes, renal, liver, and thyroid function. Complete blood counts and inflammatory markers were within normal limits, with a slight elevation of the C-reactive protein (CRP) of 13.3 mg/L (reference range, 0.2-9.1 mg/L). A computed tomography (CT) scan of the head (Figure , ) demonstrated a suspected mass lesion centered in the left temporal lobe. Magnetic resonance imaging (MRI) (Figure , ) of the brain confirmed the presence of a well-defined, avidly enhancing extra-axial mass lesion over the left temporal lobe. This patient’s care was transferred to the neurosurgery department for further management.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [57, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 57 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
998,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6325870-1,Extracted,"A 51-year-old woman was admitted to our hospital complaining of chest tightness, palpitations and dyspnoea after activity. On admission, physical examination revealed a normal state of consciousness, an average heart rate of 76 beats per minute (bpm), and a blood pressure of 111/70 mmHg. Cardiac auscultation revealed variable first heart sound intensity and a diastolic murmur in the mitral stethoscope area. The other findings were unremarkable. The electrocardiogram showed atrial fibrillation. The echocardiogram performed by our hospital also showed rheumatic heart disease (severe mitral stenosis and regurgitation) with normal cardiac function and wall motion.
After the completion of the preoperative examination, the patient was sent to the operating room for mitral valve replacement. The operation was successful. After the aorta was reopened, ventricular fibrillation occurred. Sinus rhythm was not restored until 5 rounds of electrical defibrillation had been performed. Not long after returning to the intensive care unit (ICU), this patient developed heart failure with low blood pressure (70~85/45~50 mmHg) and tachycardia (125–135 bpm). Blood gas analysis showed progressive lactic acidosis, and blood lactate increased from 2.4 mmol/L to 15.3 mmol/L. Troponin T was slightly elevated compared to the preoperative level (1.960 ng/mL vs 0.019 ng/mL). N-terminal pro-brain natriuretic peptide levels increased markedly from 821.7 pg/mL to 21,025 pg/mL. Electrocardiogram (ECG) (Fig. ) showed that the V5–6 ST-segment depression was 0.1 mV. The bedside chest film showed a small amount of fluid in the left chest. Urgent bedside echocardiography demonstrated akinesis in the middle and apical segments of the left ventricle with depressed LV function (EF 36%),while basal segments’ movement were generally normal.
To determine the blood flow in the myocardium, myocardial contrast echocardiography (MCE) was performed immediately (Figs. a, b, and a). For the MCE examination, the ultrasound system was switched to the contrast mode, with a mechanical index of 0.1–0.5. MCE was performed using intravenous administration of 2.0 mL of SonoVue (Bracco, Milan, Italy). To achieve a balance among ultrasound intensity, penetration, and the duration of myocardial opacification, the contrast-specific imaging mode needed to be adjusted. Similar enhancement intensity was observed in the basal, middle and apical segments. Quantitative analysis also showed approximately equivalent maximum intensity values in these regions.
The diagnosis was considered TCM instead of myocardial infarction. The treatment mainly involved maintaining effective circulation and reducing the postcardiac load. After the administration of epinephrine and norepinephrine, the patient’s blood pressure was still low. Considered the patient’s condition as heart failure, an intra-aortic balloon pump was inserted. Although myocardial enzyme levels were elevated, the doctors did not perform treatment for coronary heart disease, considering the reason of tissue injury after heart surgery. The therapeutic regimen for this patient included ventilator-assisted ventilation, postoperative anticoagulation therapy, anti-infection treatment and other conservative treatments.
A week later, the patient underwent coronary angiography, and the results showed no significant narrowing of the coronary artery. This patient was extubated 13 days after surgery and was later weaned from epinephrine. Myocardial contrast echocardiography performed 2 weeks later (Figs. c, d, and b) showed that apical movement was significantly improved, with a slight decrease in interventricular septal motion. In addition, the perfusion of the myocardium was normal, with an EF (Simpson) of 52%.
The clinical evolution was favourable, and the patient was discharged 3 weeks later. Before discharge, echocardiography showed that the artificial mitral valve function and the segmental wall movement were normal, with an EF of 72%. One year later, the patient remained asymptomatic and showed normalization of ventricular wall motion in the apical segment.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [51, 'years'], 'Congestive Heart Failure': True, 'Vascular disease history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 51 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
999,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7026610-1,Extracted,"A 29-year-old woman with systemic lupus erythematosus (SLE) diagnosed at age 12 years with severe idiopathic thrombocytopaenic purpura (ITP), presented acutely while visiting her baby in the Neonatal Intensive Care Unit with sudden onset chest pain and shortness of breath. Her SLE was complicated by spontaneous deep vein thrombosis, triple positive antiphospholipid syndrome (APLS), and Class IV lupus nephritis. This triggered an emergency call to the neonatal ward, with examination notable for tachycardia, but normotensive and normal oxygen saturation initially. Her chest was clear with dual heart sounds and no oedema. Her medications at presentation were enoxaparin 100 mg and aspirin 100 mg daily, transition to warfarin was planned at 2 weeks’ postpartum. Her immunosuppression regime was hydroxychloroquine 400 mg daily, azathioprine 150 mg daily, and prednisone 5 mg daily, other medications included calcitriol 0.25 μg daily and calcium carbonate 1.25 g daily.
Electrocardiogram (ECG) showed sinus tachycardia with no ischaemic changes. Initial blood results shown in . Chest X-ray showed cardiomegaly with increased interstitial markings (). She deteriorated rapidly over the next hour with climbing oxygen requirements and hypotension and was investigated for pulmonary embolism (PE) and treated with morphine and enoxaparin. She was escorted to radiology from the neonatal ward for the CT pulmonary angiography (CTPA) which showed pulmonary oedema and no PE and was admitted to cardiovascular intensive care (CVICU). On arrival, she was intubated for respiratory distress and, as no transthoracic echocardiogram had been performed, she had a transoesophageal echocardiogram. This demonstrated the posterolateral papillary muscle rupture and flail anterior leaflet with torrential MR and preserved left ventricular (LV) function (see ).
She proceeded to emergency mitral valve (MV) replacement, on transfer to the operating table she had a pulseless electrical activity (PEA) arrest, resuscitated with adrenaline and CPR before return of circulation and the start of operative intervention. The posterolateral papillary muscle was pale and sheared directly off the ventricular wall. The MV was replaced by a 29-mm St Jude’s Mechanical valve. At the end of the procedure, VA ECMO was instituted due to persistent severe pulmonary oedema and biventricular failure despite maximal ionotropic support.
The histology of the valve revealed preserved architecture with scattered fibrinous deposits and a focal larger fibrinous vegetation with occasional inflammatory cells, with no organisms, consistent with chronic Libman -Sacks endocarditis (). The papillary muscle showed extensive central necrosis with a surrounding rim of acute inflammation consistent with infarction several days old, thrombi were seen within the intramyocardial arteries (). The endocardial surface had mixed inflammatory infiltrates and focally fibrinous material with granuloma-like appearance, in keeping with Libman–Sacks.
ECMO was required for 2 days, on decannulation and desedation, she had some abnormal movements so magnetic resonance imaging (MRI) brain was performed which showed widespread hypoxic injury. She had paroxysmal atrial fibrillation and mild LV impairment so was commenced on metoprolol CR 166.25mg and cilazapril 1 mg daily and transitioned from heparin back to warfarin and aspirin 100 mg daily. She underwent inpatient rehabilitation after 4 weeks in CVICU before discharge. At this point, her neurological function was normal.
She continued the same immunosuppression regime from admission on discharge as well as the medications mentioned above. She was planned to continue both aspirin and warfarin given the recurrent thrombosis previously.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [29, 'years'], 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 29 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
1000,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4532065-2,Extracted,"The patient was a 34-year-old woman. One year prior to admission, she had began suffer-ing from an abdominal fullness and weakness. Physical findings revealed a hard non-tender mass in the right upper quadrant.
Laboratory examinations manifested serum ALT of 391IU/L, serum AST of 341IU/L, alkaline phosphatase of 279IU/L, gamma glutamyl transferase of 298IU/L, alpha-fetoprotein of more than 7000ng/ml and alpha 1-antitypsin of 410mg/dl. Blood count was normal.
Abdominal computed tomography revealed an ill-definded large inhomogeneous mass filling the entire right lobe of the liver with underlying liver cirrhosis and tumor thrombus in the upper portion of the IVC and the right atrium (). The electrocardiogram was normal. Two-dimensional echocardiogram manifested thrombus in the right atrium(). She expired 4 months later.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [34, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 34 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1001,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8655858-1,Extracted,"A 50-year-old previously healthy female presented with dyspnea, fatigue, and 6-kg weight loss during the course of 3 months. She was found to have a giant left atrial tumor by transthoracic echocardiography (TTE). Cardiac computed tomographic angiography (CTA) () showed an 88 × 76 mm large cardiac mass with a broad base involving the atrial septum and the anterior left atrial wall, nearly filled the entire left atrium. The right pulmonary vein orifices and the mitral valve were associated with the tumor. 18F-fluorodeoxy-glucose positron emission tomography-computed tomography (PET-CT) scan demonstrated that left atrial tumor was hypermetabolic tumor activity without signs of any distant metastases (). These preoperative images studies suggested that the left atrial tumor could be malignant. To better understand the adjacent anatomic relationship between left atrial tumor and surrounding tissues, a 3D printing model () was fabricated in collaboration with Changsha Jiebo Information Technology Co., Ltd, China. It was made of photosensitive resin material by 3D printing device (Sailner J501 Series Color Multimaterial 3D printer). The duration of the print run was about 5 h. In view of the extent of the mass and the limited exposure, the conventional surgical resection approach would be difficult and risky. After careful evaluation of the 3D printed model, cardiac autotransplantation was considered to be suitable. Following median sternotomy and full heparinization, the aorta and superior vena cavae and right femoral vein were cannulated, and cavae snared, for total cardiopulmonary bypass. The heart was arrested using antegrade cardioplegic solution (Custodio HTK Solution; Dr Franz Kohler Chemie GMBH, Bensheim, Germany). The heart was excision () and the tumor were removed (). The repair of the excised septum and anterior left atrial wall was performed with two bovine pericardium patches (). Reimplantation of the heart is similar to a bicaval orthotopic cardiac transplant (). Self-constructed bovine pericardial tube has been used as a graft to complete the re-anastomosis of inferior vena cavae to alleviate tension (). Although preoperative images suggested the left atrial tumor was malignant, the final pathology confirmed atrial myxoma. The patient recovered well and was discharged on post-operative day 12. She remains well without recurrence or arrhythmias at 9 months after surgery.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [50, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 50 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1002,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5259659-1,Extracted,"A 72-year-old Caucasian male with past medical history of coronary artery disease, diabetes mellitus, hypertension, and hyperlipidemia was transferred to our facility with acute right sided facial droop and dysarthria. Initially, patient experienced gradual onset right lower extremity weakness followed by slurring of speech. Over the next day his symptoms progressed to right sided hemiplegia, dysarthria, and behavioral disturbances with emotional liability. Family reported history of cerebrovascular accidents in the past with no residual symptoms. Magnetic resonance imaging (MRI) done at outlying hospital showed old infarcts in right cerebellum, left parietal lobe, left thalamus, bilateral occipital lobes, and bilateral basal ganglia. Further workup at our facility included echocardiogram, which was normal. Cardiac telemetry monitoring revealed no arrhythmia. Prior carotid duplex from four years ago showed less than 50% stenosis of both carotid arteries and no repeat carotid duplex was done on admission. During his hospital stay, the right sided hemiplegia showed significant improvement on the next day of admission. However, on day three of hospitalization, he had an acute worsening of his right sided weakness. Stroke alert was called and emergent computed tomography angiography (CTA) of head and neck was ordered. CTA imaging showed 90% stenosis of proximal left internal carotid artery (ICA) with free floating thrombus (FFT) within the lumen along with adjacent calcified atheromatous plaque. Left paramedian pons hypodensity consistent with acute ischemia was a new finding. Occlusion of right vertebral artery at origin with collaterals from occipital artery and occluded posterior inferior cerebellar artery (PICA) were noted (Figures –).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
1003,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5642466-1,Extracted,"A 43-year-old female was admitted for perirectal abscess. Her comorbid conditions included hypertension, obstructive sleep apnea, type 2 diabetes, atrial fibrillation, morbid obesity, and rheumatoid arthritis (treated with chronic steroid therapy). The patient’s current presentation began with 1 month of reddish drainage from the right buttock. She reported no trauma, fever, or other systemic symptoms. On physical examination, she had a large perirectal abscess sized 12.24 × 8.56 cm with overlying necrosis and extensive erythema up to the lower back with discharge of brown-red material. Her creatinine was 3.7 mg/dL, which increased from her baseline of 0.8 mg/dL. She was started on intravenous cefoxitin and clindamycin. The findings revealed 10 – 12 cm of necrosis and left perirectal abscess involving the ischiorectal fossa but not extending to the rectum. Postoperatively, she was transferred to the ICU as she was hypotensive, requiring vasopressor infusion. The patient was taken to the operating room multiple times for debridement and split-thickness skin grafts from her left posterior thigh. Her condition continued to improve, and she was able to be moved out of the ICU. Her creatinine came back to 1 mg/dL.
On hospital day 17, she developed areas of numerous severely sharp, painful erythematous lesions with central dusky necrosis and subsequently ulcerated lesions ranging in size from 1 to 5 cm on the bilateral lower extremities (). Punch biopsy from these lesions was done. The final pathologic diagnosis was small-vessel vasculitis. It was thought that the lesions were pyoderma gangrenosum related to her underlying rheumatoid arthritis. Her steroid dose was increased to prednisone 30 mg daily for lesion treatment. The labs were sent off for the genetic hypercoagulable panel, including protein C, protein S, cryofibrinogen, reptilase time, DRVVT screen ratio, prothrombin G20210A mutation, lupus anticoagulant, and antithrombin III, which were all negative. The patient was discharged to a short-term rehab facility as her condition had improved. Three days later, she was readmitted again for sepsis syndrome due to infected ulcers on the bilateral lower extremities. She developed fever up to 38.2 °C and was hypotensive. Broad-spectrum antibiotic, vancomycin, and piperacillin-tazobactam were initiated again. Since the patient had numerous non-healing bilateral lesions on her lower extremities, which did not respond to steroids, skin biopsy of the same lesion was performed again and sent to a pathology laboratory in a tertiary facility. Final pathology showed extensive fat necrosis and lymphohistiocytic inflammatory cell infiltrate. Medial calcification of vessel walls was seen focally, and some pockets of neutrophils were visible. These findings were consistent with calciphylaxis. On review of the record, the patient also had secondary hyperparathyroidism due to vitamin D deficiency (). Her calcium and phosphorus were in the normal range. The intact parathyroid hormone (PTH) was mildly elevated at 88 pg/mL (14 – 72 pg/mL). Total vitamin D level was 11 ng/mL (31 – 100 ng/mL). Consequently, she was started on treatment with 15 L of oxygen by facemask for 2 hours a day, sodium thiosulfate 25 g intravenously 5 days per week, and sodium thiosulfate intralesional injections every 7 days. Daily prednisone 30 mg was maintained for rheumatoid arthritis treatment. Oxycodone, oral morphine, gabapentin, and acetaminophen were used to control the ulcer pain. Vitamin D level was repleted with cholecalciferol 1,000 µg per day.
On 6-month follow-up, the ulcerated lesions had satisfactorily improved (). Two out of four ulcer regions on her lower extremities were healed. The two remaining were in the process of healing. She has made good improvement in physical function.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [43, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Diabetes history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 43 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
1004,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6842486-1,Extracted,"A 83-year-old woman affected by Critical Limb Ischemia (CLI) developed an ulcerated cutaneous lesion of the right leg, extended to the second and third finger of the homolateral foot. Her medical history showed type II diabetes mellitus, systemic arterial hypertension, ischemic heart disease (previous coronary artery bypass surgery) and atrial fibrillation; she was also an active cigarette smoker (20 cigarettes/day for 40 years). On physical examination, the above mentioned cutaneous ulceration showed anterior and posterior necrotic eschars; moreover, acupressure provoked a lively tenderness and pain inhibited leg motility. Finally, bilateral femoral pulses were present while distal peripheral pulses were absent (popliteal, posterior tibial and pedidial artery). Ankle Brachial Index (ABI) was bilaterally not assessable.
On admission, blood exams showed C-reactive protein (CRP) 101,000 μg/L, erythrocyte sedimentation rate (ESR) 100 mm/h, hemoglobin (HGB) 8.0 g/dl, platelets count 454,000 μg/L, white blood cells count (WBC) 12,800/μl, international normalized ratio (INR) 1.87, partial thromboplastin time (PTT) ratio 2.3. Surgical management consisted of recanalization and percutaneous transluminal angioplasty (PTA) with drug eluting balloon (DEB) ranger 5 × 100 mm in superficial femoral artery (SFA) and right popliteal artery, followed by surgical curettage of necrotic forefoot injuries and amputation of the second toe of the right foot. The infectious diseases specialist recommended to start systemic antibiotic therapy with piperacillin/tazobactam 4.5 g I.V. every 8 h.
After 8 days, an improvement of inflammatory markers was observed, and antibiotic therapy was switched to oral minocycline100 mg (1 tablet every 12 h) for 15 days. The patient was discharged after a total of 21 days of hospitalization. At home, the patient underwent local dressing of wound and amputation margins with antiseptic compress solution twice a week after cleansing, furthermore a polymeric membrane (PolyMem®-Ferries Mfg) was routinely applied.
36 days after hospital discharge, given the worsening of local condition with considerable increase in exudation, despite a 4 weeks course of antibiotic therapy with Amoxicillin (500 mg orally every 12 h) empirically prescribed by the treating physician, the patient referred to our University Center. At the time of first observation, the wound appeared moist with abundant secretion and covered with fibrin. A wound swab was routinely performed and confirmed the previous evidence of positivity for MDR K. pneumoniae, E. faecalis and P. mirabilis. Although the patient was afebrile, three blood cultures, that tested negative, were performed.
Give the multiple microorganisms present on the wound and the severely prostrated general conditions of the patient, it was decided to start medications with 10% cutaneous-iodopovidone solution for topical use (Poviderm® 10% Skin Solution). After 30 days, since no improvement of the wound was observed, systemic antibiotic treatment was suspended. In reason of the previous therapeutic failures, the possibility of treating the wound with a mixture of probiotics as a rescue therapy was considered; written informed consent was obtained and subsequently a mixture of probiotic bacteria (lyophilized powder sachets, each containing 100 billion colony forming unit (CFU) of Lactobacillus plantarum NCIBMB 43029 20% in weight, Lactobacillus acidophilus NCIBMB 43030 20% in weight and Streptococcus thermophilus NCIMB 30438 40% in weight) (provided by Mendes SA, Lugano, Switzerland) was topically applied three times/week. Probiotic treatment was provided by Mendes SA, Lugano, Switzerland.
The conditions of the wound appeared stable after 1 week of probiotic treatment. Following 2 weeks of treatment a modification in microbiological results and a slowly progressive healing of the lesion were noted. The wound pad tested negative for E. faecalis at day 48 (12 days after the start of the probiotic treatment) and negative for K. pneumoniae and P. mirabilis at day 57 (after 21 days of the topical probiotic treatment). In the initial phase of treatment, an entire probiotic sachet (100 billion CFU) was applied three times/week, while in subsequent period the applied amount was proportional to the residual size of the wound. Systemic or topical antibiotic treatment was not administered during the course of probiotics. The overall duration of probiotic application was 24 days (Fig. ).
During the subsequent 90 days, a slow but complete wound healing was observed; PolyMem dressings were applied by the patient to improve comfort in reason of the fact that autonomous walking and other daily tasks were resumed. Furthermore, normalization of serum inflammatory markers (erythrocyte sedimentation rate (ESR) and CRP) was observed.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [83, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 83 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
1005,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5398301-1,Extracted,"A 76-year-old man was admitted in June 2014 due to progressive deterioration of renal function, loss of appetite, and asthenia. Nine months prior to his admission (September 2013), he was diagnosed with effort angina and infrarenal abdominal aortic aneurysm. At the beginning of October 2013, he was found to have unprovoked PE for which he had received oral warfarin, delivering a prothrombin time-international normalized ratio (PT-INR) of 1.7 to 2.1 (reference range: 0.9-1.2) with a favorable clinical course. He had no history of renal disease, and steady serum creatinine (sCr) levels ranging between 0.96 and 1.12 mg/dL (reference range: 0.63-1.03 mg/dL) were noted until mid-December 2013. His sCr level was 1.89 mg/dL in mid-March 2014 and increased to 7.33 mg/dL in early June 2014. Therefore, he was referred and admitted to our hospital for further examination. His medical history included a diagnosis of acute myocardial infarction at 58 years of age. He had been a smoker for more than 40 years but denied the use of any drugs.
At the time of admission, the patient was alert and had a temperature of 36.4°C, a heart rate of 89 beats/min, and a blood pressure of 176/94 mm Hg. His physical examination revealed livedo reticularis on the soles of his toes and a blue-purple discoloration of all toes bilaterally (), whereas his feet were warm to the touch and the peripheral pulse remained intact. Laboratory examinations revealed the following: blood urea nitrogen (BUN), 64 mg/dL (reference range: 8-20 mg/dL); sCr, 7.23 mg/dL; white blood cell count, 9800/µL (reference range: 3900-9800/µL); eosinophils, 1092/µL (reference range: 0-400/µL); platelet count, 166 × 103/µL (reference range: 130-369 × 103/µL); erythrocyte sedimentation rate (ESR), 59 mm/h (reference range: 0-10 mm/h); serum albumin, 3.5 g/dL (reference range: 6.9-8.4 g/dL); triglycerides, 203 mg/dL (reference range: 40-185 mg/dL); low-density lipoprotein (LDL) cholesterol, 129 mg/dL (reference range: <139 mg/dL), fibrinogen, 410 mg/dL (reference range: 129-271 mg/dL); fibrin/fibrinogen degradation products, 13.5 µg/mL (reference range: 0-5 µg/mL); D-dimer, 5900 µg/L (reference range: 0-1500 µg/L); PT-INR, 1.76; C3, 104 mg/dL (reference range: 86-160 mg/dL); C4, 45 mg/dL (reference range: 17-45 mg/dL); and C-reactive protein, 0.49 mg/dL (reference range: 0-0.14 mg/dL). Tests for anti-neutrophil cytoplasmic antibodies, anti-glomerular basement membrane antibodies, hepatitis B virus surface antigen (HBsAg), anti-HBsAg antibodies, and antibodies to the hepatitis C virus were all negative. His urine was trace positive for protein, 2+ for occult blood, and contained 0.09 g of protein in a 24-hour specimen, whereas his creatinine clearance was 3.9 mL/min. The urinary excretion of β2-microglobulin and N-acetyl-beta-d-glucosaminidase was 22 856 µg/L (reference range: <200 µg/L) and 5.4 U/g·Cr (reference range: 0.9-2.4 U/g·Cr), respectively. A computed tomographic scan revealed a calcified thoracic aorta without a dimensional disorder and an infrarenal aortic aneurysm with a maximum diameter of approximately 4.4 cm. Diagnostic noncontrast-enhanced T2-weighted half-fourier-acquired single-shot turbo spin ecocho (HASTE) magnetic resonance imaging subsequently revealed hypointense areas and bright signals, which were suggestive of an atheromatous plaque consisting of lipids and fibrous tissues, respectively, in the abdominal aorta (). Oral warfarin was discontinued on admission, and the patient was subjected to empirical treatment with pravastatin at a dose of 10 mg/day combined with limaprost alfadex at a dose of 30 µg/day. A 5-mm-deep punch biopsy was performed on clinical day 7 within the territory of livedo reticularis on the lateral aspect of the left first toe. Typical biconvex needle-shaped empty spaces, suggestive of cholesterol clefts, were observed within the lumen of the arteriole in the subcutis (). A diagnosis of CES was made based on pathological and imaging findings as well as clinical manifestations.
Due to the elevated D-dimer level of 10 600 µg/L confirmed on clinical day 8, the decision was made to resume anticoagulation therapy despite our failure to detect deep venous thrombotic lesions using ultrasonography. The patient was treated with intravenous heparin and then switched to warfarin 2.5 mg/day on clinical day 30. Oral prednisolone (PSL) at a dose of 20 mg/day was also initiated on clinical day 22, resulting in the amelioration of eosinophilia and cutaneous manifestations within a few days and the subsequent stabilization of sCr levels at approximately 4.3 mg/dL. His elevated blood pressure was also controlled at approximately 120-130/70-80 mm Hg with irbesartan (100 mg/day) and amlodipine besilate (5 mg/day). However, sCr levels started to increase when PSL was tapered to 5 mg/day. The patient developed general fatigue, appetite loss, decline in urine output, and progressive swelling in both legs without any calf pain at the end of September 2014, with an elevated sCr level of 8.07 mg/dL, and was readmitted for further examinations. Similar to his initial admission, a laboratory analysis at this point revealed mild hypoalbuminemia (3.6 g/dL), whereas echocardiography and chest radiograph findings did not support the concurrent presence of heart failure. The relationship between deteriorated cutaneous manifestations and recurrent eosinophilia of 1365/µL resulted in the diagnosis of relapsed CES. The patient received hemodialysis (HD). After the resumption of an increased dose of PSL (15 mg/day) and the addition of a transient session of LDL apheresis (LDL-A) to the therapeutic regimen, his cutaneous manifestations improved and eosinophilia disappeared; however, severely deteriorated renal function did not recover, and he was finally started on a periodic HD program with favorable volume control ().",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [76, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': True, 'Vascular disease history': True, 'Stroke': False, 'Diabetes history': False, 'Transient Ischemic Attacks History': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
1006,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8356265-1,Extracted,"A 71-year-old male patient presented to the emergency room (ER) with a chief complaint of dry cough for one week followed by dyspnea and febrile that had increased three days before admission. He had a fever one week prior admission that relieved with sacetaminophen, and no other complaints were reported. He had no contact history with confirmed COVID-19 patients. He has history of diabetes mellitus, hypertension, and myocardial infarction. He previously consumed aspirin, bisoprolol, lisinopril, diltiazem, atorvastatin and subcutaneous insulin.
His blood pressure (BP) was 132/75 mmHg, heart rate (HR) 79 beats per minutes (bpm) regular, and respiratory rate (RR) of 28 breaths per minute, with oxygen saturation of 85% (free air) that improved to 95% with a non-rebreathing oxygen mask (NRM) 15 Liters per minute. His physical examination showed no increased jugular venous pressure, bilateral lung crackles, pleural friction rub, and leg edema.
Comprehensive evaluations were performed, including ECG, COVID-19 antigen swab, laboratory examination, and chest radiography. His initial ECG showed normal sinus rhythm of 79 bpm, left axis deviation, with inferior OMI. Laboratory data showed increased CRP (195.3 mg/L), hypokalemia (3.2 mEq/L), respiratory failure, and respiratory acidosis. Chest radiography showed cardiomegaly and bilateral pneumonia. COVID-19 antigen swab was positive. Thus patient and family were consent for isolation and tracing procedure. As his blood gas showed respiratory failure with severe ARDS (
PaO
2/
FiO
2 82 mmHg), we planned on invasive ventilation, however the procedure was postponed due to unavailability of ventilator machine and intensive care unit overload.
He was then started on antibiotic treatment with moxifloxacin, antiviral therapy with remdesivir, dexamethasone, continuous infusion of unfractionated heparin (UFH) multivitamins and his daily medication (insulin, aspirin, lisinopril, beta-blockers, nitrates, and atorvastatin). Tocilizumab 400 mg was also given on the second day of admission and continued for 5 days. His vital signs and laboratory examinations were routinely monitored.
During the sixth day of admission, his oxygen saturation deteriorated. He was then put on non-invasive ventilation (NIV) with slightly better oxygen saturation (92-94%). His symptoms showed gradual improvement in several days. His laboratory examination on the tenth day showed leukocytosis, thrombocytopenia, increased neutrophil–lymphocyte ratio (NLR), increased D-Dimer. No prolonged hemostatic values were found. Plasma prothrombin time (PPT) was 20 sec, and activated partial thromboplastin time (APTT) was 38.6 sec.
On the ninth day of admission, the patient reported gross hematuria, at that time he was still on unfractionated heparin therapy within targeted APTT. Laboratory data showed significantly reduced thrombocytes (40,000 mg/L). Urine examination showed gross hematuria with leukocyturia (10–15 cells/field), nitrituria, and proteinuria (2+). The patient underwent ECG and chest radiography evaluation, which showed no significant changes (
).
Heparin was thought to be the underlying cause of thrombocytopenia in this patient. Since heparin antibody was not routinely checked in the developing country, we choose HIT’s scoring system as an alternative. The scoring system shows 4Ts of 6 and HEP Scoring system of 5 (
). Both 4Ts and HEP scoring indicate a high-risk probability for HIT, hence the anticoagulant was switched to rivaroxaban 20 mg twice daily. The symptoms were then improved with the absence of hematuria after 2 days. The thrombocyte evaluation showed normalization to 177,000 on the eleventh day. The patient was transferred back to the low care and discharged after 13 days.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [71, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 71 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
1007,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4978858-1,Extracted,"The 67-year-old male patient was admitted to our emergency department because of swelling in his right cheek since the previous day. He had a history of atrial fibrillation, which had been treated with dabigatran, 150 mg twice daily (last dose 15-16 hours before presentation), and suffered from chronic renal impairment due to type II diabetes mellitus and hypertension. The febrile patient was haemodynamically stable on admission. The physical examination revealed significant hot and painful right facial swelling. The laboratory results on admission were as follows: white blood count 17.7 Giga/L; C-reactive protein 234 mg/L; creatinine 165 μmol/L (GFR 36.5 mL/min); and unbound dabigatran concentration as measured with diluted thrombin time (dTT; Hyphen Hemoclot, Neuville-sur-Oise, France) 119.05 ng/mL. The activated partial thromboplastin time (aPTT) and thrombin time were prolonged (61 sec, resp., <120 sec). For a summary of coagulation tests, see . We administered 2.2 g i.v. Co-Amoxicillin and computed tomography was performed to plan abscess surgery.
As the patient was becoming increasingly septic and haemodynamically unstable despite volume substitution, emergency surgery was indicated.
We administered a 2.5 g infusion of idarucizumab, followed by a second infusion of 2.5 g idarucizumab after 10 minutes. No side effects were reported by the patient.
Immediately after the second dose, coagulation testing was repeated and aPTT as well as thrombin time were found to be normal; dabigatran concentration was below detection limit (<30 ng/mL; see ). Thirty minutes after idarucizumab application, enoral incision of the multilocular abscess was performed, with irrigation and insertion of Penrose and Easy Flow drainage. There was no relevant blood loss and no other complications. The surgical team rated the intraoperative bleeding as being “as expected.”
The patient could be managed postoperatively on an ordinary surgical ward with rapid clinical improvement. Coagulation tests were repeated 24 hours after administration of idarucizumab (). Postoperative kidney function improved after treatment of infection (creatinine 115 μmol/L, GFR 56 mL/min, day 6). As there was no postoperative bleeding, dabigatran was restarted 36 hours after surgery and administration of idarucizumab. The patient was discharged from hospital without any complications.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [67, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 67 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
1008,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7714298-1,Extracted,"A 65-year-old male visited Seoul St. Mary’s Hospital complaining of right shoulder pain over the course of 6 months. He had a history of hypertension and atrial fibrillation. He had experienced an episode of transient ischemic attack in the brain but had no sequalae of brain damage. He complained of a painful arc during forward flexion of his right shoulder, but the shoulder had nearly full range of motion. Rent sign was positive and manual muscle power testing of shoulder flexion was scored as grade 4. Tests for the impingement sign and speed were positive, which suggested the presence of subacromial bursitis and pathology of the long head of the biceps tendon. On MRI, a 2 cm medially retracted and anteroposterior 2.5 cm sized full-thickness tear of the supraspinatus tendon was noted (). No bone abnormalities were observed ().
The patient underwent ARCR. During the operation, an approximately 2.0×2.5 cm full-thickness tear of the supraspinatus tendon was found. Partial tears of the long head of the biceps tendon and the subscapularis tendon were also noted. We repaired the supraspinatus tendon with the transosseous-equivalent repair technique using two Bio-Paladin anchors (5.0 mm; CONMED, Utica, NY, USA) for medial row fixation and two Pop-Locks (3.5 mm; CONMED) for lateral row fixation (). Tenodesis of the long head of the biceps tendon was performed using a Bio-Swivelock (5.5 mm; Arthrex, Naples, FL, USA). The subscapularis tendon was repaired with a Bio-Swivelock stitch for tenodesis of the long head of the biceps.
One month post-surgery, the patient started pendulum exercises and a rehabilitation program. At two months post-operation, the Sleeper’s stretching exercise and the pulley exercise were prescribed. At three months post-operation, rubber exercises on the shoulder were begun in order to improve external rotation power. On the 3-month post-operative follow-up X-ray, an approximately 5×5 mm cyst was observed on the medial anchor site of the humeral head (B). The patient complained of mild pain during forward flexion and internal rotation, but there was no aggravation of pain compared with the previous follow-up visit. Rehabilitation exercises were continued until the next follow-up visit. Six months post-surgery, a follow-up X-ray showed that the cyst had increased in size to 7×7 mm (). In addition, MRI showed an approximately 18×16×14 mm peri-anchor cyst around the medial anchor within the humeral head and a sub-deltoid effusion on the lateral side of the humeral head (). Corticosteroid (triamcinolone, subacromial space 20 mg+glenohumeral joint 20 mg) was injected via sonographic guidance to relieve pain and improve the range of motion. At one year post-surgery, follow-up MRI showed that the size of the cystic lesion had increased to 25×18×18 mm, although the continuity of the repaired cuff was well-maintained (). Pain in the repaired shoulder was reduced, and functional scores were improved ().
Twenty months post-surgery, the patient complained of severe pain in his right shoulder with no specific cause. MRI showed extensive enlargement of the cyst and a change in the inclination of the medial anchor, which appeared to be floating. Nonetheless, the continuity of the repaired rotator cuff was maintained (). The amount of subacromial effusion had increased; therefore, aspiration of the subacromial effusion was performed under sonographic guidance (), and subacromial corticosteroid injection (triamcinolone, 40 mg) was administered. Cytological analysis indicated the presence of neutrophils and a few macrophages, but there were no infectious microbes.
A follow-up MRI was performed 3 years after the operation. On a T2-weighted image, low-signal intensity tissue was observed at the cystic lesion, and the integrity of the repaired rotator cuff was well-maintained. Also, subacromial effusion was reduced and the continuity of the repaired cuff was maintained (). Four years post-surgery, the patient visited our clinic for routine follow-up and did not complain of pain, limited range of motion, or weakness. The final follow-up MRI showed some granulation tissues that were fused with the anchors and had filled the cavity. The continuity of the repaired tendon was well-maintained ().
Four years and 3 months after the surgery, the patient underwent a procedure for cubital tunnel syndrome at the ipsilateral elbow. After receiving the patient’s consent, a second arthroscopic procedure was performed on the right shoulder, which revealed that the integrity of the repaired rotator cuff was well-maintained and that some fibrotic tissues and bursa were comingled above the repaired cuff ().",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [65, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': True, 'Vascular disease history': False, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
1009,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5728896-1,Extracted,"A 71-year-old woman presented with sudden neck pain and weakness in her right upper and lower limbs while she was having a bath at home. Her symptoms resolved spontaneously within 10 minutes. After half past 4 hours later, she had the same onset of right hemiparesis and had full recovery within 15 minutes, and then was immediately admitted to our emergency department. The patient had a 30 years history of hypertension without well-control. She had no previous history of taking any antiplatelet or anticoagulant drugs. There was no recent history of head and spinal trauma or surgery.
The initial blood pressure was 210/90 mm Hg. On neurological examination, the patient had a normal cranial nervous system and sensory system. Her muscle strength was grade 5/5 in bilateral upper and lower limbs, but the right knee reflex was hyperactive and Hoffman's sign was positive. Laboratory investigations showed that a complete blood cell count, prothrombin time, and partial thromboplastin time were within normal limits. An emergency brain computed tomography and cervical x-ray scans were unremarkable. A clinical diagnosis of TIA was considered. Then the patient was hospitalized in the neurological wards and treated with antiplatelet therapy (100 mg aspirin and 75 mg clopidogrel, once daily). She did not complain any other symptoms except a mild neck pain in the following 2 days after admission.
On the third hospital day, the brain magnetic resonance imaging (MRI) and cervical MRI were performed. The brain MRI showed no signs of acute cerebral infarction. The cervical MRI revealed a spinal epidural hematoma located in the posterior spinal epidural space extending from the C2 to C6 spinal vertebral level. The hematoma was isointense on T1-weighted images and hyperintense on T2-weighted images (Fig. ). Just after returning to the wards, the patient recurred the right hemiplegia (muscle strength was grade 3/5 in right upper and lower limbs), and developed rapidly progressive quadriplegia, loss of pain and temperature sensation, dyspnea, and uroschesis. Neurological examination revealed tetraplegia (the muscle strength was grade 2/5 in left limbs and 1/5 in right limbs) and loss of pain below the C2 level bilaterally. She had neither aphasia nor abnormal cranial nerve signs. Given her progressive symptoms and imaging findings, the diagnosis of spinal cord compression was considered. The patient was transferred to the intensive care unit immediately and treated with trachea cannula and ventilator-assisted ventilation. Her family members did not consent to emergency surgical decompression and the patient became worse in the following days. After a week later, her family members finally consented to the surgical decompression. The findings of operation confirmed a hematoma arising on the dorsal spinal epidural surface and extended from the C2 to C6 spinal vertebral level, and the right was more serious.
One week after operation, the sensory deficit above C6 level improved, but there was no improvement in her muscle strength and dyspnea. Unfortunately, she died 1 month later.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [71, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': True, 'Vascular disease history': False, 'Diabetes history': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 71 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
1010,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7350559-1,Extracted,"Our patient is a 63-year-old Caucasian man with a past medical history of recent myocardial infarction (MI) status post unsuccessful percutaneous coronary intervention, heart failure with reduced ejection fraction (25–30%), coronary artery disease, and atrial fibrillation who presented to our institution with a 3-day history of syncope without chest pain or dyspnea. Initial vital signs reveal tachycardia and hypotension (lowest recorded 85/64). Initial testing revealed new-onset atrial fibrillation with rapid ventricular response, negative troponin, chest X-ray revealing cardiomegaly, and negative computer tomography of the brain. Subsequent cardiac catheterization revealed a single ostium shared by all three coronary arteries (right coronary artery, LCX, and LAD) all originating from the right coronary cusp with the left anterior descending artery originating posteriorly and coursing between the aorta and left atrium (Figs. , and ). In addition to an occluded mid RCA, distal disease of the LAD and severe disease of the superior branch of the obtuse marginal artery of the LCX were noted. The occluded RCA appeared to have left-to-right collaterals from the septal branches of the LAD to the posterior descending artery (PDA) (Fig. ). Next, a CCTA was performed to evaluate the artery for a ‘malignant course” defined as an anomalous origin of the coronary artery with subsequent course between the aorta and pulmonary trunk. It is considered malignant as the affected coronary artery can get compressed between the aorta and pulmonary trunk, specifically during exercise, and can produce angina or in worst cases, sudden cardiac death. Our patient was found to have a non-malignant course (Fig. ). Our patient was evaluated by cardiothoracic surgeons as well as other interventionalists with the decision to treat conservatively, with the option for coronary artery bypass graft (CABG) with or without repositioning of the artery if he remained symptomatic (Table ). Our patient ultimately underwent successful dual-chamber implantable cardioverter-defibrillator (ICD) placement several months later secondary to ischemic cardiomyopathy with reduced ejection fraction (25–30%) after maximally tolerated medical therapy. Of note, our patient did experience a recent MI 23 days prior to this admission. A cardiac catheterization at that time did show a completely occluded mid RCA with unknown chronicity of the lesion. However, it appeared to be subacute or chronic as the vessel was unable to crossed by the guidewire. Anomalous origin of his coronary arteries was noted at that time. As no percutaneous coronary intervention (PCI) could be performed, our patient was treated medically and later discharged home.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [63, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 63 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
1011,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6787409-1,Extracted,"An 80-year-old female with a history of hypertension, hyperlipidemia, hypothyroidism, migraine headaches, and paroxysmal nonvalvular atrial fibrillation presented to our hospital with a 2-day history of new-onset, severe, stabbing headaches over her left frontal scalp. Three days prior to her presentation at our institution, she had presented to an outside Emergency Department (ED) with 24 h of fevers, chills, as well as a low-grade generalized headache. Physical examination at that time revealed a temperature of 100.8°F, a body weight of 72 kg, a stiff neck, and mild photophobia. Initial investigations revealed a white blood cell (WBC) count of 18.1 × 103 cells/μL, platelet count of 235 × 103 cells/μL, creatinine of 0.8 mg/dL, normal urinalysis, normal chest X-ray, negative flu swab, and normal computerized tomography (CT) imaging of the abdomen/pelvis. CT of the head was done, which revealed no signs of stroke, intracranial hemorrhage, intracranial masses, hydrocephalus, or signs of increased intracranial pressure. She had no history of central nervous system disease and did not take any immunosuppressive medication. There was no report of altered consciousness, focal neurological deficits, or papilledema on exam. As other acute causes of headache had been ruled out and due to the concern for meningitis, she immediately underwent an urgent diagnostic LP in the ED. Approximately 12–16 mL of cerebrospinal fluid (CSF) was removed for testing (4 vials of 3–4 mL each). LP was performed without complication and revealed a CSF WBC count of 2, a red blood cell count of 10, and no bacteria on Gram stain. The CSF was negative for herpes simplex virus. The patient was diagnosed with a mild systemic infection, likely viral, and discharged on oral ciprofloxacin 500 mg twice daily for 7 days.
The patient was taking apixaban 5 mg twice daily for stroke prevention and had taken her last dose on the morning of admission, approximately 7 h prior to the LP. This was reflected in the laboratory analysis showing an international normalized ratio (INR) of 1.47, a prothrombin time of 16.3 s, and activated partial thromboplastin time of 26.4 s. Anti-Xa level was not checked. Apixaban was resumed without interruption after her discharge, and she took her evening dose approximately 5 h after the LP.
On the following day (24 h post-LP), she developed a new, severe headache which was different completely in character from the one she had presented with the day prior to the outside ED. She described it as a sharp stabbing pain, located over her left frontal scalp, somewhat relieved when lying flat. She contacted the outside ED by telephone and described her symptoms to them. She was informed that she likely had developed a post-LP headache and was instructed to take acetaminophen for the pain and return to the ED if her symptoms worsened.
Her headache continued to worsen over the next 48 h. By the time she presented to our ED (72 h post-LP), she was complaining of 10/10 headache as well as interval development of gait instability, loss of balance, generalized weakness, and nausea. Upon admission, vital signs were normal. Physical exam revealed a Glasgow coma scale of 15 and no focal neurologic deficits. Laboratory analysis revealed normal WBC count; her coagulation profile was consistent with the use of apixaban, with an INR of 1.3, prothrombin time of 16.0 s, and activated partial thromboplastin time of 39.8 s. Platelet count at this time was 203 × 103 cells/μL. Creatinine remained stable at 0.8 mg/dL. Noncontrasted CT of the brain revealed bilateral subdural hematomas with features of acute bleeding. The left frontal hematoma measured approximately 14.2 mm, while the right frontal hematoma was about 11.9 mm. These findings were confirmed by MRI (Fig. ).
Initially, conservative management was attempted, with discontinuation of apixaban and symptomatic treatment with acetaminophen, gabapentin, and ondansetron. However, her headache continued to worsen, and she therefore underwent evacuation of the subdural hematomas via left burr hole on hospital day 3.
Postoperatively, the patient had remarkable improvement in her headache and associated symptoms. Serial CT scan also demonstrated interval improvement. She was discharged home on hospital day 10 with home healthcare for rehabilitation with aspirin 81 mg daily. Her aspirin dose was increased to 325 mg daily 1 month after discharge.
Four months after discharge, her case is still actively being discussed in detail amongst the neurology, cardiology, and neurosurgery services; with specific attention as to whether or not to restart anticoagulation. Ultimately, the deployment of a left atrial appendage closure (WATCHMAN) device was recommended to the patient as the preferred option; however, the patient has thus far deferred this procedure as of the time of this writing. She has a CHADS2VASC score of 4 implying a 5′ annual stroke risk, and a HASBLED score of 3 implying a 5.8′ annual bleeding risk. The current decision is to continue aspirin 325 mg and avoid anticoagulation, although this decision may continue to evolve based upon the patient's preferences.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [80, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': False, 'Stroke': False, 'Diabetes history': False, 'Transient Ischemic Attacks History': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 80 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
1012,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7178514-1,Extracted,"A 76-year-old African American lady presented to the hospital with new onset weakness and back pain. Her medical history consisted of essential hypertension, atrial fibrillation, abdominal aortic aneurysm, sick sinus syndrome, asthma, and gout. She reported that her back pain started after she came back from the bathroom at 4 : 00 a.m. while trying to sit down on the bed. The patient described the pain as shooting in nature, severe in intensity, and radiating down her left arm with no clear exacerbating or relieving factors. Over the following few minutes, she developed progressive weakness in her left lower and upper extremities and later on became unable to move her left leg which led to her being transferred to the Medical Intensive Care Unit. She also developed numbness in her left leg up to the level of the knee and in her left arm up to the level of the shoulder. There was no history of any urinary or stool incontinence or retention or any previous similar episodes.
The patient had been recently diagnosed with atrial fibrillation one month prior to presentation in an outside hospital and had since been maintained on apixaban 1 tablet 5 mg twice daily. Her other home medications included alprazolam, allopurinol, losartan, hydrochlorothiazide, and metoprolol. She reported full compliance with her medications prior to presentation. A dual chamber pacemaker was inserted 11 days before this visit in an outside hospital, and her other surgical history included a hysterectomy several years ago for uterine fibroids. She denied any history of smoking, alcohol abuse, or illicit substances usage. The patient did not have previous bleeding history.
The patient's vital signs on presentation were within normal limits, and her neurological exam showed a patient alert and oriented to time, place, and person with intact speech. Her motor power was 5/5 in her right upper extremity proximally and 4/5 distally and 3/5 in her left upper extremity proximally and 1/5 distally. In her lower extremities, the motor power was 5/5 on the right and 1/5 all over on the left. She had decreased sensation to light touch in her left upper and lower extremities. She had no clonus, and Hoffman and Babinski signs were negative bilaterally. Her reflexes were 2+ all over and symmetric.
Initial lab tests were significant for hypokalemia (3.1 mmol/L), leukocytosis (12700 WBCs per microliter), and slight anemia with a hemoglobin level of 9.3 g/dl with unknown baseline. Her other lab tests including liver function and renal function were within normal limits.
Given her presentation of acute focal neurological deficit, a noncontrast head CT scan was ordered and showed signs of chronic vascular ischemic disease only. The patient continued to have severe back pain, and having a history of abdominal aortic aneurysm, an acute aortic dissection was suspected, and hence, a CT angiogram of the abdomen, pelvis, and thorax was ordered. The CT angiogram did not show any signs of aortic dissection. A CT scan of the neck was performed to investigate the cause of the left upper extremity weakness and numbness. It showed an epidural soft tissue density extending along the left aspect of the spinal canal causing compression and marked rightward deviation of the cord concerning for an epidural hematoma extending from C2-C3 level to C6-C7 ().
As the patient was on apixaban at the time, a decision was made to delay surgical treatment for 2 days to decrease the risk of intraoperative bleeding. A C2-C7 laminectomy, hematoma exclusion, and spinal fusion were then performed. On discharge, 9 days later, her physical exam was mostly unchanged from that on presentation except for the resolution of pain and improvement in motor power in her left lower extremity from 1/5 to 2/5 distally.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [76, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
1013,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7852650-1,Extracted,"A previously healthy, 50-year-old woman was admitted to our hospital with a 2-d history of generalized abdominal pain and repeated vomiting following ingestion of two raw grass carp gallbladders.
The patient consumed two raw grass carp gallbladders (approximately 4-6 mL) for alleviation of her cough 2 d prior to presenting at our hospital. She developed diffuse abdominal pain and profuse vomiting 6 h after its ingestion, accompanied by sweating, dry mouth, heaviness in the chest, and dizziness.
She had no history of hypertension, diabetes, cardiac disease, cerebrovascular disease, allergies, or surgical interventions.
She had no relevant family history.
At admission, her temperature was 37.1 °C, pulse rate 46/min, respiratory rate 20/min, and blood pressure 108/74 mmHg. She had upper abdominal tenderness, with no rebound pain, hyperactive bowel sounds of 5-6/min, and no pain on renal percussion. The rest of her systemic examination was unremarkable.
At admission, her serum creatinine was 344 μmol/L and urea was 15.88 mmol/L (normal range being 2.5-6.4 mmol/L). On day 4, her urine output decreased drastically (< 100 mL over 24 h). Serum creatinine markedly rose to 505 μmol/L. Liver function tests revealed increased alanine aminotransferase, aspartate aminotransferase, total bilirubin, and direct bilirubin, as shown in Table .
Her echocardiogram (ECG) revealed sinus bradycardia of new onset, with a heart rate (HR) of 46/min at that time.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [50, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 50 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1014,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-1501082-1,Extracted,"An eighty-four year old Dominican man presented to the Emergency Department complaining of “dizziness”. He had a past medical history significant for aortic stenosis, status post aortic valve replacement, paroxysmal atrial fibrillation and sick sinus syndrome, for which a DDD pacemaker was placed. Two days prior to admission he noted light-headedness, which began while walking.
Initial electrocardiogram (ECG) (), revealed a wide complex tachycardia at 170 bpm with LBBB morphology. The differential diagnosis included ventricular tachycardia with exit block, atrial tachycardia, atrial flutter, and A-V nodal reentrant tachycardia. Previous tracings had shown a preexisting LBBB.
The tachycardia terminated spontaneously but recurred. After the resolution of symptoms, the ECG was repeated (). This ECG showed a QRS morphology similar to the admission tracing with a ventricular rate of 85 bpm and no clear P wave activity.
Because the follow up ECG was at a rate exactly half the initial one, an underlying atrial tachycardia was suspected. The pacemaker was interrogated to assist in analysis of the rhythm (). The interrogation revealed atrial tachycardia with 2:1 block, with an atrial rate of 170 bpm and a ventricular rate of 85 bpm. The patient was treated with metoprolol and his symptoms resolved after normalization of his rhythm.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [84, 'years'], 'sex': 'Male', 'Congestive Heart Failure': False, 'Vascular disease history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 84 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
1015,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5216231-1,Extracted,"A 71-year-old Japanese postmenopausal woman was referred to us for evaluation of a tumor in the right breast. She had suffered from malignant lymphoma (diffuse, medium to large B-cell lymphoma) treated with chemotherapy consisting of eight cycles of R-CHOP and radiotherapy (total 46 Gy) to the head for the previous 3 years. She had undergone hysterectomy for myoma of the uterus at the age of 41 years. In addition, she had a medical history of hypertension and hyperlipidemia. There was no remarkable family history.
Physical examination demonstrated an elastic hard lump on palpation located in the lower lateral quadrant of the right breast. The tumor size was 2.0 cm in diameter, and the borderline was unclear. No skin change or dimpling was seen. Nipple charge was not evident. No axillary lymph node swelling was found. All laboratory data were unremarkable, and there was no increase of tumor markers such as CEA and CA15-3.
Mammography of the right breast showed an unclear mass with accumulation of calcification (Fig ). Ultrasonography showed a hyperechoic lesion within a hypoechoic area, with rough surface (Fig ). Enhanced magnetic resonance imaging revealed a mass of high intensity in the right breast (Fig ).
Histopathological evaluation of the core needle biopsy material revealed an invasive adenocarcinoma with metaplastic change, but definitive histological diagnosis could not be determined. There was no proliferation of atypical lymphocytes.
The patient underwent right mastectomy and sentinel lymph node biopsy. The frozen section of the sentinel lymph node was found to be free of disease by intraoperative diagnosis.
Macroscopically, cut sections revealed a white, solid, and well-circumscribed tumor measuring approximately 17 × 15 mm (Fig ). Histopathologically, the tumor was composed of cancer cells forming papillary or tubular structures with an abundant mucus cytoplasm, which was positive for periodic acid-Schiff staining, and accompanied by psammoma bodies (Fig , Fig ). Squamoid cancer cells proliferated in sheet-like patterns, but intracellular bridges or keratinization were not seen (Fig ). Intermediate cells were also seen (Fig ). In the stroma, many inflammatory cells proliferated around the tumor.
Immunohistochemical findings showed that the tumor cells were positive for cytokeratin 7, cytokeratin 5/6, cytokeratin 14, epidermal growth factor receptor, p63, and MUC-1, and negative for gross cystic disease fluid protein-15, estrogen receptor, progesterone receptor, and human epidermal growth factor receptor-2. Ki-67 labeling index was 22%. The mitotic index was one mitosis per 10 high-magnification fields. No vascular or perineural invasions were observed. Histological examination determined MEC of the breast, intermediate histological grade.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [71, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 71 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
1016,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5260602-1,Extracted,"A 63-year-old African American man was transferred to the neurological intensive care unit from a nearby hospital after presenting with an acute history of multiple falls. Earlier that day, he had fallen once while walking to the bathroom from his bed and had fallen again shortly thereafter while walking through his living room. The patient's family decided at that time to bring him to the nearby hospital for treatment. At that hospital, no focal findings were discovered, but his blood pressure was noted to be elevated at 272/139 mm Hg. At that point, the original hospital placed the patient on a nicardipine drip to treat his hypertension and transferred the patient to our medical center, where he arrived late that night.
The patient presented to the medical center complaining of dizziness and agonizing headache. He was also noted to be somnolent and experiencing some dysarthria. The family at the bedside reported that the patient's past medical history was significant for hypertension, diabetes mellitus type II, and hyperlipidemia. It was also determined that the patient was a former chronic smoker, did not consume alcohol, and used marijuana occasionally. Physical exam showed some lethargy, dysarthria, right gaze paresis and nystagmus, vertical gaze weakness, and dysmetria on the right side more so than on the left. There was no hemiparesis, and visual fields were normal to confrontation. The patient had 5/5 strength, intact sensation, and 2+ reflexes of the upper and lower extremities bilaterally. It was determined that the patient had 4 points on both the NIH Stroke Scale and the Modified Rankin Scale for Neurologic Disability at admission. Computed tomography (CT) of the head and neck revealed decreased attenuation throughout most of the cerebellar hemispheres suggestive of ischemic injury (Fig ), diminished caliber of the fourth ventricle indicating increased pressure, and an old watershed infarct on the right side between the territories of the middle cerebral artery and the posterior cerebral artery (PCA). The area of the brain that is perfused by the PCA was surprisingly completely spared from infarct. CT angiography of the head revealed diffuse abnormally decreased attenuation of the cerebellar hemispheres with sparing of the vermis, suggesting infarction of both SCAs, and a narrow irregular left vertebral artery with a risk for subtotal thrombosis. There was no evidence of stenosis or a blood clot in the basilar artery or either SCA at the time of the CT angiography. Furthermore, it was discovered that the patient had a partial fetal-type PCA (fPCA) originating from the internal carotid artery (ICA) on the right side as seen in Figure .
Due to the fact that the patient was well out of the window for thrombolytic therapy, he was initially treated with aspirin. Neurosurgery was consulted because of the patient's declining mental status caused by a mass effect in the posterior fossa. They elected to immediately take the patient in for a decompressive craniotomy. During the procedure, the dura overlying the cerebellum was noted to be very taut and to have a blue discoloration. Upon incision of the dura, there was spontaneous protrusion of necrotic brain matter. Much of the left and right cerebellum hemispheres were necrotic, but the vermis appeared to be spared from damage. The necrotic tissue was cleared, and the patient's cranium was closed.
Over the next 24 h after the operation, the patient was extubated and remained lethargic but arousable. He responded to verbal commands, and facial movements were symmetrical. His right lateral gaze weakness persisted, and movement was diminished somewhat in the left extremities. Additionally, CT of the head showed new hydrocephalus, and electrocardiogram monitoring revealed intermittent atrial fibrillation throughout the day. Transthoracic echocardiogram was performed after discovery of the patient's arrhythmia, and it showed an ejection fraction of 55–60% as well as no evidence of residual thrombus. An amiodarone drip was administered in an effort to normalize the patient's heart rhythm. Anticoagulation with warfarin was not prescribed for another 3 weeks, as the patient experienced some bleeding in the posterior fossa after surgery. Neurosurgery placed an external ventricular drain to help decrease the intracranial pressure.
Prior to the discovery of this patient's atrial fibrillation, the intensive care team had proposed that the cause of the stroke might have been an embolism from the diseased left vertebral artery. However, knowing that this patient was experiencing intermittent atrial fibrillation led the team to assess that the cause was more likely an embolism from the left atrium. Because it is unlikely that 2 separate emboli occluded both SCAs simultaneously, it was postulated that this was a single top of the basilar artery embolism that was large enough to occlude both SCAs. Such an occlusion should have led to ischemic injury of the regions of the brain perfused by the PCAs. Given this, the team determined that the bilateral PCA sparing may have been due to collateral perfusion supplied by the fetal origin of the PCA on the right side.
The patient remained lethargic over the next 24 h despite the placement of the external ventricular drain. The next morning, however, the patient woke up with markedly improved symptomatology. He was oriented to person and place, followed commands appropriately, and had 5/5 strength in all extremities along with intact sensation. Dysarthria and dysmetria of both upper extremities were noted, but overall the patient made a remarkable recovery from his condition the day before. The team continued to monitor and treat the patient over the next 3 weeks, and the patient was discharged for rehabilitation. At discharge, it was determined that the patient once again had 4 points on both the NIH Stroke Scale and the Modified Rankin Scale for Neurologic Disability.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [63, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 63 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
1017,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5740188-1,Extracted,"In March 2016 a 77-year-old Italian man attended the Emergency Room of San Giuseppe Hospital in Empoli. He was a retired farmer, who had been suffering from hematochezia together with melena for two weeks. His vital parameters were normal. In his medical history there was chronic atrial fibrillation, for which he was taking rivaroxaban 20 mg/d and digoxin 0.125 mg/d, and prior cholecystectomy. He weighed 68 kg, was 170 cm tall (body mass index 23.5). Digital rectal examination revealed the presence of melena. A nasogastric tube was inserted, with no evidence of gastric blood traces. Laboratory tests showed anemia (Hb 5.1 g/dL). The patient underwent blood transfusions and esophagogastroduodenoscopy (EGD), which showed a small hiatal hernia, bile in the stomach and a 10 mm duodenal fibrinous ulcer. We decided to suspend rivaroxaban and start low molecular weight heparin. Continuous intravenous infusion of pantoprazole was administered and the patient was admitted to the Gastroenterology Department.
In the following days he continued to bleed and required further blood transfusions. He also underwent several EGDs, which confirmed the previous findings and allowed us to get biopsies in the antrum for rapid urease test and on the ulcer margins for histology assessment. We also used argon plasma coagulation on the oozing borders of the ulcer, with consequent bleeding cessation. The rapid urease test was positive for H. pylori and the patient started eradication treatment. The biopsies of the ulcer margins demonstrated regenerative hyperplasia on productive inflammation.
Despite endoscopic therapy, the patient still complained of melena and hematochezia. He underwent ileocolonoscopy, which showed bright red blood in ileum and colon, without identification of the bleeding source. We performed a contrast-enhanced computed tomography (CT) scan of the abdomen and of the abdominal aorta, which showed no bleeding cause and only minor findings like parietal calcifications of blood vessels, a small hepatic cyst, diffuse moderate intra- and extrahepatic biliary ducts dilation and benign prostatic hyperplasia. We then decided to use wireless capsule endoscopy (WCE), which described two duodenal fibrinous ulcers (5 and 10 mm) without signs of recent bleeding, the presence of a tapeworm, starting from 1 h 45 min until 4 h 28 min after WCE ingestion (Figures and ) and plentiful dark red blood in the colon, lighter in the proximal regions.
The patient reported only then, that he had occasionally eaten raw beef and that he had taken mebendazole 5 mo before, because of suspected oxyuriasis. The patient received albendazole 400 mg/d for five days, since this drug was suitable for taeniasis and already available in the department.
While on albendazole, he still complained about melena and iron-deficiency anemia (IDA) (Hb 9 g/dL, Hct 27%, RDW-CV 17%, iron 27 μg/dL, ferritin 53 ng/mL), with constant need of blood transfusions. He also stated he had not discharged the head of the tapeworm yet. We performed the last EGD, which demonstrated healing of the ulcers, with no bleeding signs. The second ileocolonoscopy was comparable to the first one, hence we decided to give him a second WCE after discontinuation of albendazole, which demonstrated persistence of the tapeworm starting from jejunum to the whole ileum (last visualization at 4 h 25 min) and plentiful dark red blood in the colon, lighter in the proximal regions (Figures and ).
We consulted an infectious disease specialist for a change of therapy after albendazole failure. He advised to give the patient niclosamide 2 g in a single administration and then to initiate bowel preparation with macrogol. After niclosamide and bowel preparation we performed the last ileocolonoscopy, which displayed no blood in ileum or colon and 2 non polypoid lesions in the caecum that we removed via loop electrosurgical excision procedure. Histology revealed those lesions to be intestinal tubular adenomas with low grade dysplasia.
The day after niclosamide administration, the patient felt a lot better. Melena and rectal bleeding had finally stopped and after two more days he noticed the complete excretion of the tapeworm head. Since his condition was improving, we decided to dismiss him.
He was seen at follow-up visit in mid-June 2016, where he stated he was feeling good and had no more rectal bleeding. He performed fecal obscure blood test and H. pylori stool antigen test, both showing negative results. His hemoglobin had reached 11.3 g/dL by then, with a positive trend. He underwent ova and parasite fecal exams at 2, 4 and 6 mo after dismission, none of which showed relapse of the infestation.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [77, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
1018,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7891233-1,Extracted,"An 80-year-old obese man with a past history of smoking, diabetes mellitus, hypertension, colon, and prostate carcinoma (which were curatively treated with surgery and radiation therapy in 2004 and 2017 successively) was presented in our emergency department (ED) with complaints of progressive dyspnoea and bilateral lower extremity oedema, as well as a weight gain of 10 kg in a few weeks. Medication used by the patient upon admission is listed in , the dosage of the medication had not been changed recently. Vital signs were normal. Cardiac examination was normal, no additional heart sounds were heard and the jugular veins could not be visualized due to severe obesity. With pulmonary auscultation mildly decreased breath sounds in the lower region bilaterally were heard. Abdominal examination revealed a distended abdomen with tympanitic percussion on the left and right side suspect for ascites. In the lower extremities, extensive bilateral oedema was found.
An electrocardiogram showed new-onset atrial fibrillation with normal ventricular response, there were no signs of ischaemia. Laboratory tests revealed normocytic anaemia (haemoglobin level 7.6 mmol/L, normal 8.5–11.0 mmol/L), elevated D-dimer levels (3.17 mg/L, normal −0.50 mg/L), elevated gamma-glutamyl transferase (GGT 89 IU/L, normal −55 IU/L), and decreased renal function (creatinine 233 μmol/L, normal 59–104 μmol/L). For additional laboratory values at the time of presentation, see . A transthoracic echocardiogram performed at the ED showed a left ventricle with normal dimensions and a preserved left heart function (ejection fraction 60%), a D-shaped left ventricle in both systole and diastole suggesting increased right-sided pressure, mitral annular calcification without valve dysfunction and left atrial dilatation. In the IVC, a ‘snake thrombus’ was seen, visible up to the right atrium (Figure and B, Movies 1 and 2). Patient underwent computed tomography (CT) of the abdomen to screen for possible causes of IVCT which revealed a large mass (9 cm × 10 cm × 8 cm) in the right kidney with growth into the IVC, highly suspect for an RCC (Figure and B). A CT-thorax showed no metastases. The patient was diagnosed with a right-sided T3bN0Mx RCC.
According to current guidelines anticoagulant therapy was initiated with low-molecular-weight heparin (LMWH). Due to the reduced glomerular filtration rate (GFR) a reduced dose of tinzaparin was administered. After 3 days factor Xa levels were checked and revealed a level of 0.33 U/mL (normal 0.5–1.2 IU/mL), which was considered inadequate and the patient was switched to heparin intravenous. The possibility of neo-adjuvant chemotherapy and surgical therapy were considered in a multidisciplinary team. However, the clinical condition of the patient deteriorated significantly over the next few days with progressive dyspnoea, oedema, and kidney failure. The patient deceased on day 12 of admission, after initiating palliative care.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [80, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 80 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
1019,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5313451-2,Extracted,"The second patient is a 60-year-old woman, in whom mild asymmetrical hypertrophy was observed during a routine occupational check-up at age 39 (Fig. ). Echocardiography showed a high LVEF (78%) and an MWT of 20 mm (stage II). She was followed-up yearly at a peripheral hospital. Echocardiography showed no LVOTO at rest, and provocation with Valsalva or exercise was never performed. Treatment with disopyramide and verapamil was started. From the age of 46 she had experienced recurrent chest pain. At age 50 the LV anterior wall was described as akinetic (stage II–III), and over subsequent years there was a gradual decrease of LVEF coupled with progressive dilatation of the LV and LA (stage III). At age 58 the patient was admitted to the emergency department with AF and a coronary angiogram was performed which excluded coronary artery disease as the cause of LVEF deterioration.
At age 58 the patient was seen at the outpatient clinic of the UMC Utrecht. CMR showed an LVEF of 32% and extensive LGE (Fig. e), suggesting replacement fibrosis and stage IV disease. Genetic testing identified a pathogenic splice-site mutation in the gene encoding myosin-binding protein C (MYBPC3; c.654 + 1G > A). This led to the conclusion that the patient had HCM, with LV dysfunction in the context of end-stage progression. The diagnosis was supported by residual mild, but significant LV hypertrophy (MWT 13 mm). The pattern of LGE together with a history of angina supported the presence of progressive ischaemic damage caused by microvascular dysfunction [, ] leading to replacement fibrosis.
These two cases illustrate how individual patients may progress through different stages of HCM during their lifetime, with profoundly different clinical profiles, risks and therapeutic needs. Unless all these stages are familiar to cardiologists, there is a substantial possibility that the disease will be misinterpreted and mismanaged over time.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [60, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 60 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
1020,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4983343-1,Extracted,"An 88-year-old Caucasian female was referred from the emergency department with lower gastrointestinal bleeding. She gave a history of five episodes of fresh rectal bleeding with blood separate from the stools, of one day's duration. This was preceded by one day of loose stools and a constant low grade central abdominal pain. There were no other associated upper or lower gastrointestinal symptoms and no systemic disturbance. Past medical history included atrial fibrillation for which she was prescribed warfarin. She was a nonsmoker with minimal alcohol intake.
On examination, body mass index was 23 and blood pressure 140/70 with an irregular heart rate of 80 bpm, a respiratory rate of 18, and oxygen saturation 100% on room air. Examination of the abdomen elicited tenderness in the periumbilical region with no peritonism. On digital rectal examination the rectum was empty with no masses and no perianal disease. Dark blood was noted on the glove with no clots. Haematological and biochemical investigation revealed haemoglobin was 103 g/L (normal range 115–160 g/L), C-reactive protein 210 mg/L (<10 mg/L), and international normalised ratio 4.47 (target 2.5). Urea and electrolytes, liver function, and serum amylase were normal. Electrocardiogram confirmed atrial fibrillation.
The patient was managed with intravenous fluid replacement and 10 mg vitamin K. Warfarin was stopped. A flexible sigmoidoscopy was performed with no polyps or masses identified and fresh blood and clots seen throughout the sigmoid colon. The patient continued to report bleeding and repeat haemoglobin had decreased to 81 g/L. Two units of packed red cells were transfused and an oesophagogastroduodenoscopy revealed atrophic gastritis and a prepyloric erosion unlikely to be the source of bleeding. Following this computed tomography (CT) angiography showed a splenic artery pseudoaneurysm with associated collection and fistula to the transverse colon at the level of the splenic flexure ().
Radiology consult was obtained and the pseudoaneurysm embolised via catheter directed metallic microcoils. Upon completion no further contrast extravasation was seen, with cessation of flow through the fistula (). Rectal bleeding ceased and there were no complications. The patient recovered well and was discharged. A follow-up CT angiography at 6 weeks after embolisation revealed no persistence of the splenic artery pseudoaneurysm.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [88, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 88 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
1021,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6936742-1,Extracted,"An 83-year-old-woman presented with a subcarinal mass detected by a precise examination of upper abdominal pain worsening after meals. Magnetic resonance imaging revealed a well-circumscribed cystic mass in the subcarinal area compressing the surrounding organs and suggested a BC as the most likely diagnosis (). She had poorly controlled type 2 diabetes mellitus (A1c level 9.1%), hypertension, and also noted worsening paroxysmal atrial fibrillation (CHADS2 score3) and was receiving dabigatran etexilate over the last several months. A surgical resection of the cyst was recommended. With the patient in the prone position, two 5-mm ports in the third and fifth inter costal spaces (ICSs) and a 12-mm port in in the seventh ICS on the mid-axillary line were made, respectively. An additional 5-mm port was inserted into the eighth ICS on the scapular line and used as a camera port (). Carbon dioxide (CO2) was insufflated at a pressure of 8–mm Hg and then a tense mass was clearly visualized in the subcarinal area (). The cyst wall was found to have strictly adhered to the adjacent organs suggestive of past inflammatory events. Because an attempt to dissect between the cyst and lung resulted in parenchymal injury with alveolar leakage, we considered that the lesion was not amenable to a complete excision. After
the fenestration of the cyst wall with the aspiration of an yellowish mucus content, a large proportion of the thickened wall was removed to open the cavity wide enough. The remnant luminal epithelium was ablated by electrocautery. The operative time was 117 minutes and the bleeding amount was 5 g. The postoperative course was uneventful, and she was discharged on the second postoperative day. A histopathological examination revealed a ciliated epithelium, hyaline cartilage and bronchial mucus glands consistent with a BC. Her digestive problem and palpitations disappeared immediately after the surgery, and she is currently symptom free at 18 months.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': False, 'age': [83, 'years'], 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False, 'sex': 'Female'}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 83 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
1022,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6855040-1,Extracted,"A right-handed 81-year-old man with a past medical history of ischemic stroke, hypertension, hyperlipidemia, type-II diabetes mellitus, and paroxysmal atrial fibrillation presented to the hospital with symptoms of unsteadiness, mild dysphagia, and sharp stabbing right-sided facial pain. Neurological examination revealed decreased pin-prick sensation on the right side of the face. The patient had normal strength bilaterally. Coordination examination showed finger-to-nose dysmetria bilaterally, but more pronounced on the right. Ataxia with swaying to the right was observed on gait examination.
MRI of the brain revealed an area of restricted diffusion within the right posterior lateral medulla consistent with an acute or subacute infarction (). Coagulation studies revealed an international normalized ratio of 2 while on warfarin; the patient endorsed some noncompliance with the recommended regimen.
The patient noted the concomitant onset of right “sharp-stabbing” intermittent pain merely hours after the onset of unsteadiness. The pain occurred in the ophthalmic and maxillary distribution of the trigeminal nerve and was acutely worsened by cold temperature. He was diagnosed with central facial pain secondary to lateral medullary infarct. The pain initially improved with the administration of carbamazepine, which was discontinued after hospital discharge due to adverse reactions. He was subsequently started on gabapentin 100 mg by mouth three times a day with some relief, but stopped the medication secondary to an adverse reaction of dizziness. The patient still experienced recurrent episodes of right-sided facial pain. Several months after the initial event, he was evaluated in the office and was found to have a nonfocal examination. He continues to complain of brief episodes of right-sided lancinating pain in the forehead, cheek, nose, and periorbital region occurring on average three times a day. Symptoms were aggravated by cold temperature. The patient denied any associated symptoms of lacrimation or sweating.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [81, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': True, 'Stroke': True, 'Diabetes history': True, 'Transient Ischemic Attacks History': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 81 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
1023,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8191279-1,Extracted,"A 52-year-old male obese patient (weight 115 kg, height 181 cm), with history of hypertension, analgesics abuse due to chronic back pain, came to Emergency Department for repeated massive hematemesis episodes. Upon arrival, the patient was conscious, with slightly reduced response to painful stimulation and regularly reflexive pupils; vital signs were recorded: heart rate was 145 bpm, non-invasive blood pressure 80/45 mmHg, SpO2 86% in room air. Blood tests were performed, urinary catheter and indwelling arterial line for blood pressure monitoring and serial blood gas measurements were placed. After anamnesis excluded presence of active liver disease and esophageal varices, the patients signed the informed consent so that a gastric tube was gently positioned to drain blood from stomach, and immediately after a Sengstaken Blackmore tube to in an attempt to stop bleeding.
Emergency endoscopy was arranged and performed with locally sprayed 10% lidocaine and minimal sedation with midazolam 1 mg, resulting in failure to identify and control active source of bleeding with endoscopic treatment. Following the worsening of hemodynamic conditions and impossibility to stop bleeding, immediate surgical access was scheduled. Patient was moved to operatory room and, under vital parameters monitoring and 3 minutes preoxygenation in 100% oxygen, a rapid sequence induction was performed with etomidate 0.2 mg*kg-1, suxamethonium 1 mg*kg-1, and fentanil 100 mcg. Cricoid pressure (CP) was applied in order to decrease the risk of regurgitation. Before the procedure, patient was not carefully studied for airway management, due to urgent setting, but a Mallampati 3 score and slightly reduced neck movement were recorded. At a first direct laryngoscopy, no glottic structures were visible; a second attempt, after aspiration of blood and releasing of CP, showed a Cormack-Lehane 3 grade with partial view of lingual border of epiglottis.
Intubation was attempted blindly twice with styletted tube, unsuccessfully, whereas ventilation by face-mask was getting quickly worse. As the oxygen saturation was descending rapidly (spO2 60%), a number 4 classic LMA was placed after repeated mouth aspiration. Mask was inflated accordingly to manufacturers' instruction (25 ml of air) and manual ventilation was obtained via gentle but frequent insufflation with 100% Oxygen. Once saturation was fully recovered, considering emergency surgery and aspiration risk, the decision to intubate through LMA was taken.
Optical instruments (video/fiberoptical) were not available. We then inserted a 16 Fr standard nasogastric tube (NGT) blindly through LMA, finding indirect sign of passage in trachea in easy advancement without resistance and repeated free air aspiration. Then, we cut proximal tip of NGT and kept granting ventilation passing proximal end of NGT via holed catheter mount. Next, proximal part of LMA with glued connector was cut and removed to allow passage of a 7,5 mm endotracheal tube (ET) through LMA by railroading on NGT [].
Before removing the LMA, the ET cuff was inflated and position confirmed by capnography.
After successful intubation, surgery started and patient was successfully treated for duodenal ulcer. Vital parameters were stable throughout the operation, but blood and plasma transfusion were necessary according to blood test results. At the end of the surgery, the patient was moved to intensive care unit for postoperative monitoring and uneventfully extubated the day after using a safe extubation technique.[]",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [52, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 52 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1024,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-5354,Extracted,"A 55-year-old man presents to his primary care physician for a general checkup. The patient has a past medical history of diabetes, hypertension, and atrial fibrillation and is currently taking warfarin, insulin, lisinopril, and metoprolol. The patient’s brother recently died from a heart attack and he has switched to an all vegetarian diet in order to improve his health. His temperature is 98.6°F (37.0°C), blood pressure is 167/108 mmHg, pulse is 90/min, respirations are 17/min, and oxygen saturation is 98% on room air. The patient’s physical exam is unremarkable.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [55, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 55 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 1 + 1 = 2.
The patient's CHA2DS2-VASc Score is 2."
1025,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3092967-1,Extracted,"A 53-year-old male (height 169.4 cm, weight 68.2 kg) was scheduled for an emergency laparoscopic appendectomy due to acute appendicitis. A week before, he had undergone a mitral valvuloplasty and Maze operation for severe mitral regurgitation and atrial fibrillation. The patient had a history of hypertension and bronchial asthma. A follow-up ECG after the open heart surgery showed a sinus rhythm with a normal QTc interval (). Postoperative follow-up echocardiography showed mild mitral regurgitation and an ejection fraction of 49%. Laboratory studies returned normal findings except for a prothrombin time of 2.20 international normalized ratio (INR) due to warfarin therapy. Electrolytes including potassium (4.2 mmol/L), magnesium (1.9 mg/dl) and ionized calcium (0.95 mmol/L) were within normal limits. No preoperative antibiotics were given.
For the emergency appendectomy, the patient was not premedicated. Monitoring included non-invasive blood pressure determination, ECG (lead II), pulse oximetry, and end-tidal carbon dioxide concentration (ETCO2) measurement. The vital signs included a blood pressure (BP) of 125/75 mmHg, a regular sinus rhythm heart rate (HR) of 85 beats/min, and peripheral oxygen saturation (SpO2) of 98%. Anesthesia was induced using mask administration of 100% oxygen. Etomidate (12 mg) and rocuronium (40 mg) were administered intravenously, and the trachea was intubated using an 8.0 mm cuffed endotracheal tube.
Anesthesia was maintained using 1 L/min O2, 1 L/min N2O, and 1.5-2.0 vol% sevoflurane. Ventilation was mechanically performed at a tidal volume of 600 ml and a rate of 12 breath/min. The ETCO2 was maintained between 31-35 mmHg. At the commencement of surgery, the patient had a BP of 100/65 mmHg, a regular sinus rhythm HR of 95 beats/min and 100% SpO2. The operation took approximately 1 hour, and proceeded unremarkably. The neuromuscular blocker was then reversed using 15 mg pyridostigmine and 0.4 mg glycopyrrolate. Extubation was performed without complications. At that time, the patient had a BP of 140/100 mmHg, 100% SpO2, and the ECG showed sinus tachycardia with a HR of 160 beats/min. As the patient recovered from anesthesia completely including alert mentation, spontaneous breathing, reversal of muscle tone, he was transferred to the PACU.
While applying the monitoring instrument immediately after entering the PACU, the patient lost consciousness, ceased spontaneous breathing and a carotid pulse could not be palpated. BP was unmeasurable, the SpO2 was 36% and the ECG showed ventricular fibrillation. Mask ventilation was promptly initiated using an ambu-bag, chest compression was performed, and a direct current of 360 J was applied 3 times using a monophasic defibrillator. The ECG showed resolution of the ventricular fibrillation and appearance of a sinus rhythm. However, shortly thereafter TdP-type polymorphic ventricular tachycardia developed (). Defibrillation was performed 3 times, and 1 mg epinephrine and 110 mg lidocaine were intravenously administered. Additionally, magnesium sulfate 2 g was given intravenously over 10 min. The sinus rhythm returned with a HR of 80 beats/min, the BP increased to 166/80 mmHg and the SpO2 to 95%. The patient was moved to the intensive care unit (ICU) with endotracheal intubation in a stable condition. The BP was 110/67 mmHg, the SpO2 was 98%, and an ECG showed QTc interval prolongation (617 ms) and a HR of 111 beats/min on arrival at the ICU. Norepinephrine (0.04 µg/kg/min), isosorbide dinitrate (1 µg/kg/min) and magnesium sulfate (2 g) were administered intravenously. The vital signs stabilized and norepinephrine infusion was ceased at 3 hours after ICU arrival. There was no necessity for supplement of electrolytes during ICU care, because all electrolytes were within normal limits including potassium (4.1 mmol/L), magnesium (2.2 mg/dl) and ionized calcium (0.9 mmol/L). In addition, no other drugs known to prolong QTc interval were administered. The patient was moved to the general ward on the 3rd postoperative day without relapse of TdP.
We retrospectively investigated the QTc interval and Tpeak-Tend interval (Tpe interval) identified on the ECG data (). The ECG showed QTc interval prolongation after the open heart surgery, although it had normalized by the day of the emergency appendectomy. The patient was discharged without relapse of TdP.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [53, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': True, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 53 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
1026,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6304699-1,Extracted,"Our patient was an 83-year-old male with past medical history of hypertension,
hyperlipidemia, atrial fibrillation, cerebrovascular accident, and end-stage renal
disease. He was on scheduled hemodialysis treatment through a catheter on his right
chest. He was brought to the emergency department for fever and rigors of 1-day
duration, with a recorded body temperature of 101.8°F. There was no cough, chest
pain, shortness of breath, abdominal pain, diarrhea, vomiting, headache, altered
mental status, and pain or burning on urination. Physical examination and the
initial investigations failed to elucidate any obvious focus of infection. The
patient was admitted for possible sepsis associated with infected dialysis catheter,
and treated empirically with intravenous cefepime 1 g every 24 hours, intravenous
vancomycin 15 mg/kg body weight every 24 hours, and intravenous metronidazole 500 mg
every 8 hours. The dose of vancomycin was altered as needed to maintain the
vancomycin trough level between 15 µg/mL and 20 µg/mL. Two sets of initial blood
culture and subsequent dialysis catheter tip culture grew Staphylococcus
aureus resistant to methicillin but sensitive to vancomycin,
daptomycin, rifampin, and tetracycline, while a transthoracic echocardiography
revealed right atrium mass, suggestive of endocarditis. The patient was therefore
continued only on intravenous vancomycin for MRSA endocarditis.
On the 11th day of admission, the patient developed palpable purpura on his both
lower limbs (). He
denied any pain or itching. While the erythrocyte sedimentation rate was elevated to
45 mm/h (normal = 0-30 mm/h), rest of his immunological workup including c-ANCA,
p-ANCA, and atypical ANCA were negative, and C3, C4 levels were normal. Skin biopsy
was done, which revealed severe leukocytoclastic necrotizing small cell vasculitis
consistent with hypersensitivity vasculitis related to drug therapy (). So his vancomycin
was switched to daptomycin. The purpura started to resolve within 3 days of
discontinuing vancomycin. Both his vasculitis and initial clinical condition
continued to resolve during the rest of his hospitalization, and he was successfully
discharged after 22 days of hospital stay.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [83, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False, 'Diabetes history': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 83 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
1027,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7385892-1,Extracted,"A 97-year-old Caucasian woman presented to the emergency department of our institution with a painful, malodorous, necrotic right submandibular mass (Fig. ). A solitary enlarged lymph node had been identified in this region on computed tomography two months prior. She gave no history of B-symptoms, immunodeficiency or immunosuppression.
She lived at home alone with support from a carer who visited twice daily. She did not smoke tobacco or consume alcohol. Her comorbidities included dementia, congestive cardiac failure, paroxysmal atrial fibrillation, a previous above-knee deep vein thrombosis and early-stage breast cancer diagnosed 17 years earlier, managed surgically and considered to be in remission. Her regular medications included bisoprolol 2.5 mg daily, ramipril 1.25 mg daily, aspirin 100 mg daily, digoxin 62.5 μg daily and periciazine 2.5 mg daily.
She was afebrile and hemodynamically normal at presentation and other than the right neck mass, her physical examination was unremarkable. Blood work showed a white cell count of 10.87 × 109/L (normal range, 4–11) with slight neutrophilia at 9.05 × 109/L (normal range, 1.8–7.5) and lymphopenia at 1.01 × 109/L (normal range, 1.5–3.5). Her hemoglobin was normal at 137 g/L, as was her platelet count of 197 × 109/L. Her potassium was measured as 3.3 mmol/L (normal range, 3.5–4.9) but all other electrolytes were within the normal range. Her creatinine measured 69 μmol/L with an estimated glomerular filtration rate of 64 ml/minute/1.73 m2. Her lactate dehydrogenase was elevated at 267 U/L (normal range, 110–230) but her liver enzymes were all within the normal range.
Following non-diagnostic fine needle aspiration of the mass, core biopsy revealed DLBCL with a non-germinal center immunophenotype using the Han's algorithm, and Epstein Barr encoded ribonucleic acid (RNA) in situ hybridization positivity (Figs. and ).
Computed tomography and 18-fluorodeoxyglucose (FDG) positron emission tomography (Fig. ) revealed this to be the only site of disease, consistent with stage 1A.
Given her age, frailty, performance status and multiple comorbidities, she was deemed unfit for systemic therapy and palliative radiotherapy was recommended.
She received a dose of 25 Gy delivered over five fractions on alternate days over a two-week period. Treatment was delivered using a four-beam three-dimensional conformal technique with 6-megavoltage photons and daily image guidance. The treatment incorporated the use of bolus material placed over the surface of the mass to optimize the radiation dose delivered superficially to the skin.
The patient was followed up monthly and after four months the mass completely resolved (Fig. ). The overlying skin on the right neck had healed to cover the previous necrotic deficit and no mass was palpable. She was asymptomatic with no observable toxicity at the latest review at four months.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': True, 'Thromboembolism history': True, 'Vascular disease history': False, 'age': [97, 'years'], 'Stroke': False, 'Diabetes history': False, 'Transient Ischemic Attacks History': False, 'sex': 'Female'}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 97 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 6. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
1028,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6426109-1,Extracted,"A 64-year-old woman who had been diagnosed with pulmonary valve stenosis (PVS) in childhood underwent open surgical commissurotomy and infundibulectomy at the age of 35. Significant residual pulmonary regurgitation (PR) was documented at follow-up. After remaining asymptomatic for years, she was referred to our centre following rapid progression of exertional dyspnoea and recent onset of effort-related chest pain.
Physical examination revealed good general condition, mild hypertension (147/81 mmHg), heart rate of 80 b.p.m., and oxygen saturation of 98%. There were no signs of heart failure and the cardiovascular examination showed a short, low-pitched diastolic murmur over the left upper sternal border.
An electrocardiogram showed sinus rhythm, right bundle branch block, and frequent supraventricular premature complexes. A chest X-ray revealed signs of dilated right heart and a prominent PA (Figure ).
Our differential diagnosis included progressive PR with right ventricular (RV) failure, RV restrictive physiology with diastolic dysfunction, exercise desaturation in the presence of a patent foramen ovale, progressive PH with RV failure, and LMCA or compression of the left mainstem bronchus by PA dilatation.
To evaluate these potential diagnoses, we first performed an echocardiogram that showed moderate right ventricle and atrial dilatation with normal RV systolic function (TAPSE of 19 mm and fractional area change of 43%), significant PR with diastolic retrograde flow from the main PA, pressure half-time of 209 ms and a PR index (ratio of PR duration/diastole duration) of 80%, normal RV outflow gradient (see , Videos S1 and S2), mild tricuspid regurgitation with an estimated RV systolic pressure of 34 mmHg, and a normal-sized inferior vena cava. No evidence of RV restrictive physiology was observed.
We then performed cardiopulmonary exercise testing. The patient did not develop any symptoms and oxygen saturation remained constant throughout the test, but functional capacity was poor, achieving 1.2 METS. Age-predicted maximal heart rate attained was 65%, and percent-predicted peak oxygen consumption was 23%. During the test, she developed frequent exercise-induced ventricular premature beats. Consequently, we performed a 24-h Holter monitor, which showed frequent atrial and ventricular premature beats and a short run of non-sustained ventricular tachycardia (NSVT) (Figure ).
We next performed a coronary computed tomography angiography (CCTA) to evaluate potential mechanical complications caused by PA dilatation. No compression of the left main bronchus was seen. Coronary artery anomalies and significant coronary artery disease were ruled out. However, the CCTA showed extrinsic compression of the proximal segment of LMCA caused by an enlarged PA (60 mm diameter in systole) (Figure ), and a takeoff angle of the LMCA of 26° (defined by a line parallel to the border of the left coronary sinus and a line parallel to the LMCA) (Figure ). A coronary angiogram confirmed the diagnosis and the right-sided heart catheterization showed normal PA pressure (see , Video S3).
The patient underwent surgical PAA repair along with pulmonary valve replacement with a conduit constructed intraoperatively composed of a 25 mm bioprosthetic Carpentier-Edwards valve within a Dacron tube graft. As complete decompression of LMCA was visually documented intraoperatively, coronary revascularization surgery was unnecessary. Intraoperative findings showed a thickened, trileaflet pulmonary valve, and the anatomopathological examination of the PA wall showed changes suggestive of cystic medial necrosis.
A second CCTA, performed 2 weeks after surgery, showed the PAA had decreased in size (Figure ) and LMCA compression had disappeared (Figure ). An exercise stress test performed 4 months after surgery showed functional capacity had improved, and no ventricular premature beats were observed. Over a 9-year follow-up, the patient has remained asymptomatic and functional capacity is good.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [64, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 64 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
1029,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-8880,Extracted,"A 60-year-old man comes to the clinic with the complaint of knee pain for the past few weeks. The pain is located in the left knee, associated with morning stiffness for about an hour, and improves with activities throughout the day. He also has a history of diabetes mellitus, hypertension, peptic ulcer disease, and ischemic heart disease. He underwent angioplasty last year for a STEMI. The patient takes metformin, aspirin, clopidogrel, atorvastatin, ramipril, omeprazole, and bisoprolol. He used to smoke one pack of cigarettes a day for the last 45 years but stopped smoking for the past one year following his heart attack. He drinks alcohol socially. His father has Alzheimer’s disease and is in adult home care, and his mother died of breast cancer when she was 55. His temperature is 37.6°C (99.8°F), blood pressure is 132/65 mm Hg, pulse is 90/min, respirations are 14/min, and BMI is 22 kg/m2. On examination, his left knee is swollen, warm, tender to touch, and has decreased range of movement due to pain. Cardiopulmonary and abdominal examinations are negative.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [60, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 60 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
1030,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7219988-1,Extracted,"A 72 year-old-male with known past medical history inclusive of right lower extremity deep vein thrombosis currently on the DOAC rivaroxaban, myelodysplastic syndrome status post stem cell transplant complicated by graft versus host disease (GVHD), hyperlipidemia, stage three chronic kidney disease, and type II non-insulin dependent diabetes mellitus presented to the ED with right buccal mucosa bleed after undergoing punch biopsy by dermatology six hours prior. The last administered dose of rivaroxaban was earlier the same morning, as he was not instructed to hold the dose because the diagnostic punch biopsy for GVHD workup was scheduled ad hoc while he was in the hospital for routine follow-up. Despite manually holding direct pressure with a paper towel over the bleeding site, the patient stated that he had been unable to achieve hemostasis, which was affecting his ability to speak and sleep due to the continuous need to spit out blood, prompting his visit to the ED. A single, folded, paper towel sheet became saturated and required exchange every 15 minutes.
Review of systems was notable for oral bleeding, minor post-procedural pain (2/10 in severity) at the biopsy site, and three days of acute on chronic constipation, believed to be unrelated to his chief complaint. The patient denied shortness of breath, cough, hemoptysis, and dysphagia. On physical examination, the airway was intact, and there was an active, continual oozing of dark blood from a five-millimeter biopsy site along the right buccal mucosa. Due to the duration of bleeding and reported amount of saturated dressings, a complete blood count, general chemistry panel, and coagulation panel were drawn, which was notable for a hemoglobin and hematocrit of 12.9 grams per deciliter (g/dL) [14–17.4g/dL] and 37.6% [42–54%], respectively, with prothrombin time and international normalized ratio of 10.1 seconds [9.2–11.9 seconds] and 0.91 [0.8–1.2], respectively. The patient was placed in an examination room with continuous wall suctioning and given a Yankauer suction tip to clear his oropharynx.
Given the wide base of the biopsy site and lack of overlapping tissue, the wound was not amenable to hemostasis through placement of sutures. Thus, along with emergency pharmacy guidance and approval, a sterile 4-inch × 4-inch gauze dressing was soaked with 500 mg [5 milliliter (mL)] of 100 mg/mL TXA and placed over the bleeding site. The soaked gauze was held in place with pressure applied by two tongue depressors taped on one end with medical tape and held to the patient’s cheek with an adhesive dressing (). After 30 minutes, the device and gauze were removed, and a clot was visualized (). Due to the possibility of recurrent bleeding and impending airway compromise, the patient was admitted under the otolaryngology service for observation and was discharged from the hospital eight hours later without any significant rebleeding events. There was no 72-hour ED return visit noted within the health system’s electronic health records.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
1031,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4766148-1,Extracted,"We present a case of a healthy 63-year-old Caucasian man who had simultaneous onset of skin lesions, joint pain, and morning stiffness of up to 2 h duration. He also reported a subjective fever, weight loss (10 lbs.), and weakness. On clinical exam, the patient had red-brown macules and papules symmetrically distributed on the dorsum of hands, elbows, periocularly, and periauricularly (Figs. , ). Yellow translucent firm papules were noted on the helix of the left ear, glabella, and bilateral eyebrows. There was no lymphadenopathy. Joint examination revealed swelling and tenderness in proximal and distal interphalangeal joints (PIPs, DIPs), metacarpophalangeal joints (MCPs), elbows, shoulders, and knees.
An aspirate from his knee effusion revealed a total nucleated count of 5540/mm3 with 16 % neutrophils, 54 % lymphocytes, and 30 % monocytes. Synovial fluid analysis did not reveal crystals and cultures were negative. Serum laboratory studies were unremarkable, including erythrocyte sedimentation rate (ESR), complete blood cell counts, liver and renal function tests. His antinuclear antibody (ANA) and rheumatoid factor were negative.
Initial clinical differential diagnosis included dermatomyositis, rheumatoid arthritis, and psoriatic arthritis. A skin biopsy demonstrated numerous multinucleated histiocytes infiltrating between the collagen bundles in the superficial dermis (Fig. ). There is a Grenz zone separating the epidermis from the dermal tumor. The multinucleated histiocytes are large with an eosinophilic and finely granular “ground-glass” cytoplasm. The nuclei are haphazardly arranged, but tend to favor the center of the cells (Fig. ). Additionally, there are an increased number of blood vessels amongst the histiocytes, as well as scattered lymphocytes. A CD163 stain was diffusely positive and the cells were focally PAS-positive diastase-resistant. The cells were negative for S100. Polarization did not reveal and polarizable material. These findings are diagnostic of MRH.
Radiographs of the hands showed erosions in the left third DIP and right second DIP, in addition to mild joint space narrowing with mild diffuse osteopenia. There were also erosions seen in the scaphoid bone with surrounding soft tissue swelling (Fig. ). Given the age of the patient concomitant osteoarthritis is the most likely cause of joint space narrowing. The patient’s left shoulder X-ray showed marked glenohumeral joint space narrowing, small humeral head osteophytes, subchondral sclerosis, subchondral cysts (Fig. ), and large erosions of the humeral head. The bones were diffusely demineralized. Magnetic resonance imaging (MRI) of the shoulder showed moderate glenohumeral joint effusion with synovitis and well-demarcated erosions of the humeral head (Fig. ). We performed an ultrasound on the second right MCP (Fig. ) and first Interphalangeal joint which showed minimal effusion but marked synovial proliferation with moderate Doppler flow, suggesting disease activity. An ultrasound of the knee showed a large anechoic effusion, echogenic synovial proliferation with grade 2 Doppler flow (Fig. ).
Given the association of MRH with internal malignancy (Trotta et al. ), the patient underwent cancer screening. This screening included colonoscopy and chest/abdominal computed tomography (CT). Purified protein derivative (PPD) skin test was negative. He was initially started on prednisone and methotrexate 20 mg/week with subsequent improvement in the appearance of his cutaneous disease. Due to continued pain and joint swelling after 3 months of treatment, he was started on adalimumab 40 mg subcutaneously every other week which was eventually increased to weekly dosing. Alendronate (70 mg weekly) was also started because of evidence in the literature of benefit in patients with MRH.
Over a follow-up period of 4 years the patient’s disease symptoms were largely controlled on the above medication regimen. However, imaging continued to show effusions in the hand joints and marked synovial proliferation in multiple MCPs, PIPs, and DIPs. Also, despite most of his symptoms improving, he had continued prominent right shoulder pain, with progressive disease shown on MRI, requiring joint replacement. He continued the use of the above medication regimen, and was able to taper his prednisone to 3 mg daily. Throughout his course, he continued to have radiologic evidence of disease despite relatively good symptom control.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [63, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 63 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
1032,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4234524-1,Extracted,"A 90-year-old Caucasian woman with a past medical history significant for provoked upper extremity deep venous thrombosis and Clostridium difficile colitis with subsequent ileostomy was admitted to our orthopedic service for a planned left hip arthroplasty revision and correction of acetabular protrusion. Preoperatively our patient denied chest pain or shortness of breath. She was unable to achieve four metabolic equivalents secondary to hip pain. Past surgeries included left hip arthroplasty, bilateral total knee replacement, hysterectomy, appendectomy, and cholecystectomy without any cardiopulmonary complications. A preoperative examination was unremarkable with all vital signs within normal limits and no murmurs, gallops or rubs on cardiac auscultation. Her only medications were omeprazole and vitamin B12. Patient risk was stratified as average risk for an intermediate risk procedure. Intraoperatively our patient was given regional, spinal, and monitored anesthetic care (MAC), which were well tolerated. She initially received midazolam prior to morphine spinal anesthetic. Due to the procedure length, she was converted to general anesthesia using a laryngeal mask airway. Fentanyl, midazolam, and propofol were used to convert to general anesthesia. Shortly after the transition to general anesthesia, she converted from normal sinus rhythm to sinus tachycardia. Unexpected hypotension near the end of operation required 3200cc of crystalloid fluids, 500cc albumin, and two units of packed red blood cells. Postoperatively she was transferred to our surgical intensive care unit.On postoperative evaluation, our patient was alert, comfortable, and without any complaints. Her vital signs revealed a blood pressure of 89/46mmHg and a heart rate of 95 beats per minute on a phenylephrine drip. A physical examination was significant for a new-onset grade 4/6 systolic murmur at the apical area radiating to the axilla. She was breathing comfortably without accessory muscle use and her extremities were warm with 2+ pulses. Her postoperative hemoglobin dropped to 7mg/dL from 12mg/dL preoperatively; her electrocardiogram, renal function, and troponin results were negative. An emergent transthoracic echocardiogram (TTE) revealed dynamic LVOT obstruction with peak velocity of 4.2L/m/s and moderate to severe mitral regurgitation due to SAM of the anterior MV leaflet (Figure ). Her LV outflow gradient was 65 to 70mmHg (normal <30mmHg). By the end of postoperative day 1, our patient was weaned off the phenylephrine. On postoperative day 2, she no longer had a cardiac murmur on auscultation. A follow-up echocardiogram three days later revealed resolution of outflow obstruction and resolution of mitral regurgitation (Figure and Figure ).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [90, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': False, 'Diabetes history': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 90 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
1033,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7874282-1,Extracted,"A 39-year-old woman with no other comorbidities presented with left-sided numbness and weakness, facial asymmetry, and difficulty in speech for one hour. She delivered two months back her fourth live child. On neurological examination, she had dysarthria, left-sided hypoesthesia, upper motor neuron seventh nerve palsy, and left hemiparesis; National Institutes of Health Stroke Scale (NIHSS) score 8. On examination, she was dyspneic, tachypnea (respiratory rate 24/minute), pulse 104/minute, SpO2 89%, respiratory examination showed bilateral crepitations. Her bedside transthoracic echocardiography (TTE) showed global hypokinesia of left ventricle (LV) with ejection fraction (EF) 30%, mild-to-moderate mitral regurgitation. She was started on noninvasive ventilation and oxygen for acute heart failure. Her other laboratory investigations are in . The computed tomography (CT) brain showed no abnormality and she was thrombolyzed with intravenous alteplase. Her transesophageal echocardiography showed no intracardiac thrombus (). She was started on other anti-heart failure medications, candesartan, bisoprolol, and aldactone in the next 72 hours. The enoxaparin at 1 mg/kg body weight 12 hourly was started after 24 hours of thrombolysis and repeat CT scan showed no hemorrhage. The magnetic resonance imaging (MRI) brain after 72 hours of thrombolysis showed multiple focal areas of acute ischemic infarct in the right centrum semiovale and frontal parieto-temporal region with normal carotid and cerebral vessels Doppler ( and ). Her thrombophilia profile was normal. She was started on warfarin after 5 days and enoxaparin was stopped after International Normalized Ratio (INR) increased above 2. She was discharged on the 8th day with warfarin, candesartan, bisoprolol, and aldactone and necessary education on INR monitoring. She was followed for 5 months and warfarin was stopped after 4 months and serial TTE showed resolution of cardiomyopathy.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [39, 'years'], 'Congestive Heart Failure': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 39 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
1034,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6867717-1,Extracted,"A 56-year-old man with metastatic GC and was admitted to our hospital due to “dizziness and bilateral lower limb weakness.”
The patient had a history of type 2 diabetes for 6 years and had no history of other chronic diseases such as hypertension. He was initially diagnosed with stage IV GC in April 2012. He underwent several many cycles of chemotherapy due to disease progression. The last cycle of chemotherapy (paclitaxel liposome combined with epirubicin) was performed on May 10, 2018. The patient underwent palliative radiotherapy due to right scapular metastasis and right adrenal metastasis in April 2016 and March 2017, respectively, with no apparent discomfort. From the date of diagnosis of GC until June 2018, the patient had not used any targeted drugs and had normal blood pressure.
The patient was admitted to our department for review on July 16, 2018. A CT scan showed that the left adrenal metastasis was significantly greater than before. The patient refused to undergo chemotherapy. He had a Karnofsky (KPS) score of 100. Hematological indicators, including liver function, kidney function, blood cell analysis, electrolytes, and coagulation index were normal. Blood pressure was also in normal range. He was advised to use apatinib (750 mg p.o. q.d.) on July 19, 2018. He had no obvious discomforts for 7 days after oral apatinib administration, and he was discharged. Blood pressure was normal during hospitalization. The patient was advised to monitor blood pressure by daily at home, but he did not perform it. He had dizziness accompanied by weakness in both lower limbs on the evening of July 31, 2018 (12 days after oral apatinib administration). Blood pressure was 185/110 mm Hg. He was administered valsartan 80 mg. There were no any changes in his blood pressure measured 2 hours after administration of this drug, and he went to sleep. The patient was admitted in our department on the morning of August 1, 2018. Blood pressure after admission was 198/111 mm Hg. He did not use any other drugs that may cause an increase in blood pressure at home. He was instructed to discontinue apatinib use. Nifedipine controlled-release tablet 20 mg and furosemide 20 mg were administered immediately. Blood pressure was reduced to the normal range in 4 hours after drug administration. Hematological indicators, such as liver function, kidney function, blood cell analysis, electrolytes, etc were normal. Seizures, however, occurred twice during this period, and his consciousness improved after using diazepam. The patient reported vision loss on both eyes after the second seizure occurrence. Physical examination revealed that the bilateral eyeballs squinted to the left side, the size of both pupils were normal, and light reflection on both eyes was slightly dull. Brain CT scan on the afternoon of August 1 revealed bilateral basal ganglia, radial crown, frontal lobe, parietal lobe, and occipital lobe with patchy low-density areas (Fig. ). On August 2, cranial T2-weighted MRI revealed symmetrical increased signal intensity in bilateral areas of the basal ganglia, radiation crown, frontal lobe, parietal lobe, and occipital lobe, which was suggestive of RPLS (Fig. -I). Diffusion-weighted imaging showed no obvious abnormal signal (Fig. -ID). Mannitol [150 mL intravenous (i.v.) drip q12 h], dexamethasone (5 mg i.v. q.d.), and phenobarbital sodium (0.1 g i.m. q8h) were administered to him. Blood pressure was maintained at 97 to 126/59 to 75 mm Hg, and antihypertensive drugs were discontinued. No seizure occurred, vision returned to normal, and bilateral lower limb weakness improved 3 days after treatment. A repeat MRI scan of the brain on 13th August showed partial resolution of previous the abnormalities (Fig. -II). The patient was discharged on 20th August. A brain MRI scan on 5th September showed complete resolution of previous changes (Fig. -II). Without using any antihypertensive drugs anymore, his blood pressure remained normal until now (April 25, 2019). Moreover, the patient has no obvious signs of discomfort and can take care of himself until the follow-up (by phone on April 25, 2019).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [56, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 56 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 0 + 1 = 1.
The patient's CHA2DS2-VASc Score is 1."
1035,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7317131-1,Extracted,"A 79-year-old male with a past history of nonischemic cardiomyopathy requiring implantable cardioverter-defibrillator (ICD), atrial fibrillation, hypertension, end-stage renal disease, and mild to moderate aortic stenosis now presented with lightheadedness and shortness of breath on mild exertion. The patient also had a history of atrial fibrillation for more than 15 years and developed intermittent episodes of GI bleeding requiring discontinuing and switching of different anticoagulation treatments. He was taking a reduced dose of apixaban with intermittent compliance before his current presentation. On admission, his vital signs were stable with a heart rate of 90 beats per minute and blood pressure of 110/83 mmHg. The cardiac exam revealed a late peaking systolic murmur at the aortic area with a soft second heart sound. No crackles, jugular venous distension, or pedal edema was noticed. Electrocardiogram revealed atrial fibrillation with slow ventricular response and occasional demand pacing (Figure ).
Cardiac troponin was normal. Hemoglobin was 9 g/dl (baseline anemic with a range of 8-10 g/dl). Echocardiogram revealed severe aortic stenosis with a valve area of 0.9 cm2 and mean and peak gradients of 37 and 72 mmHg, respectively, that were consistent with severe aortic stenosis (Figure ).
On further history, he did endorse hospitalization for episodes of GI bleeding earlier the same month when a colonoscopy, esophagogastroduodenoscopy, and capsule enteroscopy were nondiagnostic. Due to persistent GI bleeding, his apixaban was discontinued despite having a CHADS2-VASc score of 5 but with a HAS-BLED score of 6 at that visit. The severe symptomatic aortic stenosis causing dizziness and lightheadedness combined with recurrent GI bleeding presumed to be related to the aortic stenosis leads to a decision of valve replacement procedure during the same hospital visit. Considering the patient’s age and high surgical risks (society of thoracic surgeons/STS score predicting a 13.3% risk of operative mortality), a transcatheter aortic valve replacement (TAVR) procedure was performed. Post-TAVR bioprosthetic valve replacement, gradients across the valve improved to mean and peak gradients of 6 and 14 mmHg, respectively (Figure ).
This was followed by plans for placement of the Watchman device during the follow-up visit due to high bleeding risk and recurrent GI bleeds as well as high thrombotic risk and need for stroke prophylaxis.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [79, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Vascular disease history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 79 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
1036,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-9838,Extracted,"A 77-year-old woman is brought by ambulance to the emergency department after she developed weakness of her right arm along with a right-sided facial droop.  By the time the ambulance arrived, she was having difficulty speaking. Past medical history is significant for hypertension, diabetes mellitus type II, and hyperlipidemia. She takes lisinopril, hydrochlorothiazide, metformin, and atorvastatin. On arrival to the emergency department, her vital signs are within normal limits.  On physical examination, she is awake and alert but the right side of her mouth is dropping, making it difficult for her to speak clearly. Her heart has a regular rate and rhythm and her lungs are clear to auscultation bilaterally. Fingerstick glucose is 85 mg/dL. Her right upper extremity strength is 2/5 and her left upper extremity strength is 5/5.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [77, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Vascular disease history': False, 'Diabetes history': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 77 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 6. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 6 + 1 = 7.
The patient's CHA2DS2-VASc Score is 7."
1037,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4252351-1,Extracted,"A 74-year-old man with diabetes mellitus (DM), hypertension (HTN), and atrial fibrillation (AF) presented to the emergency room with sudden onset of left leg pain due to superficial femoral artery (SFA) thrombosis. Soon after arrival, he was scheduled to undergo emergency thrombectomy. He had been receiving metformin (850 mg/day) for DM, olmesartan (40 mg/day) for HTN, and warfarin (3 mg/day) and digoxin (0.25 mg/day) for AF. In the preoperative evaluation, chest radiography showed cardiomegaly, while electrocardiogram showed the presence of atrial fibrillation. Laboratory investigations showed no remarkable findings. Prothrombin time (PT) and international normalized ratio (INR) were within the normal range (PT, 10.5 sec; INR, 0.92), even though the patient was on warfarin therapy. A central venous catheter (CVC, 7-Fr double lumen catheter) was inserted via the left subclavian vein using the landmark technique under general anesthesia. In the first attempt, the needle was passaged twice without aspiration of blood. In the second attempt, after positioning the needle tip, blood was successfully aspirated through the needle in the third passage to confirm its location, followed by successful insertion of the CVC.
Subsequently, 5,000 U of heparin was administered 5 minutes before incision of the femoral artery for thrombectomy. The thrombectomy was performed uneventfully with an operative time of 90 minutes. The arterial blood gas analysis (ABGA) during surgery showed the following: pH, 7.337; PaCO2, 43.4 mmHg; PaO2, 112 mmHg; and oxygen saturation, 98%. Additionally, the hemoglobin (Hb) level was 15.6 g/dl. The estimated blood loss and urine output were approximately 100 ml and 300 ml, respectively. A total of 1,250 ml of Hartmann's solution was administered during surgery.
The patient was then transferred to intensive care unit (ICU) for close monitoring. Postoperatively, continuous infusion of heparin (1,000 U/hr) via CVC was maintained. The infusion rate was adjusted under the activated partial thromboplastin time of 80-120 sec. A portable chest radiograph showed proper position of the CVC in the superior vena cava and no interval changes (). At 6 hr postoperation, a small swelling and oozing were observed at the insertion site of the CVC. Consequently, CVC was removed and compressed for 30 minutes. At 15 hr postoperation, when the patient's hemodynamic values were stable and the dorsalis pedis artery was palpable, he was transferred to the general ward. On the first postoperative day (POD), the patient was started on warfarin (4 mg/day). A chest radiograph at this point showed no remarkable findings except a slightly increased opacity in the left anterior chest wall (). In addition, there were no remarkable findings from the laboratory examinations. However, 10 mg of furosemide was administered when the urine output decreased, even though the fluid intake was adequate.
On POD 2, the patient experienced syncope on his way to bathroom, possibly due to orthostatic hypotension. His vital signs were as follows: blood pressure (BP), 80/50 mmHg; heart rate (HR), 142 bpm; and SpO2, 85%. Subsequently, the patient was transferred to the ICU and a diagnostic workup was performed. The ABGA revealed severe metabolic acidosis (pH, 6.93; PaCO2, 28 mmHg; PaO2, 164 mmHg; HCO3, 5.9 mM; oxygen saturation, 98%), and the patient received 15 L/min oxygen via a reservoir mask. His Hb level decreased from 14.3 g/dl to 9.6 g/dl. After transferring him to the ICU, his BP was 61/44 mmHg. Volume resuscitation was initiated with normal saline and packed red blood cells (RBCs). However, inotropes were not administered to the patient, because his BP increased to 90/50 mmHg after volume resuscitation. His hemodynamic values returned to normal with fluid therapy (4,300 ml of normal saline) and transfusion (3 units of packed RBC). In addition, sodium bicarbonate was administered to cure the severe acidosis. A computed tomography (CT) revealed a huge hematoma between the pectoralis major and minor muscles on the left chest wall (). However, an angiogram showed no detectable extravasations from the branches of the left subclavian artery. Laboratory tests revealed multiple organ dysfunction syndrome including respiratory failure, ischemic hepatitis, and acute kidney injury due to hemorrhagic shock. The levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and creatinine (Cr) were remarkably elevated: AST, 2,800 IU/L; ALT, 2,100 IU/L; LDH, 6,000 IU/L; Cr, 3.40 mg/dl. Continuous renal replacement therapy (CRRT) was started on POD 2, and tracheal intubation was performed on POD 3 when an ineffective breathing pattern was observed and the SpO2 decreased to 90%. Mechanical ventilation was applied without any intervention to the hematoma, such as insertion of the wound, use of a suction tube, or surgical removal. The patient was extubated on POD 12, and CRRT was stopped on POD 13. The patient was transferred to the general ward on POD 20, and the hospital course was uneventful thereafter.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [74, 'years'], 'Hypertension history': True, 'Thromboembolism history': True, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 74 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
Because the congestive heart failure history is not specified in the patient note, we assume it is absent from the patient. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
1038,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7171631-1,Extracted,"A 44-year-old Japanese woman presented with postprandial abdominal pain since 2 months. She had been diagnosed with SLE at the age of 37 years. The patient also had lupus nephritis, Basedow's disease, steroid diabetes, idiopathic thrombocytopenic purpura, and hypertension, for which she had been taking tacrolimus, azathioprine, hydroxychloroquine, prednisolone (10 mg/day), nifedipine, eplerenone, hydralazine, lansoprazole, propylthiouracil, alfacalcidol, and sodium ferrous citrate. She was a social drinker and an ex-smoker who smoked 30 cigarettes/day for 10 years. On examination, her body temperature was 36.7°C, blood pressure was 123/80 mmHg, and pulse rate was 103 bpm. Her height was 148.5 cm and weight was 42.4 kg. Physical examination revealed conjunctival anemia, exophthalmos, enlarged thyroid, and distended abdomen with hyperactive bowel sounds, but there was no palpable mass or tenderness in her abdomen. Laboratory tests showed decreased values for hemoglobin concentration (9.0 g/dL) and hematocrit (28.3%). The C-reactive protein (4.11 mg/dL), erythrocyte sedimentation rate (104 mm/h), and soluble interleukin-2 receptor (779 U/mL) levels were elevated. The white blood cells, platelets, lactate dehydrogenase, creatine phosphokinase, anti-double stranded DNA IgG antibody, complements, carcinoembryonic antigen, and carbohydrate antigen 19–9 were within the normal range. Urinalysis revealed proteinuria, leukocytes (20–29 cells/high power field), and tubular epithelium. Hematuria was absent.
Computed tomography scanning showed whole circumferential thickening of the jejunum with aneurysmal dilatation, which is a typical feature of malignant lymphomas of the intestine (). On positron emission tomography scanning, tracer uptake was observed in the thickened intestinal wall (). Double balloon enteroscopy revealed circumferential ulcer and necrotic debris in the jejunum (). A contrast study during enteroscopy showed dilated jejunal lumen (). Based on the morphology of the jejunal lesion, we suspected small intestinal lymphoma rather than cancer. Thus, we performed flow cytometry analysis with 2 endoscopically biopsied fragments, as described previously () []. The κ/λ ratio of CD19 + CD20+ cells was 3.3 (53.36/16.39), indicating monoclonal proliferation of the B cells producing the κ light chain. The isolated cells were negative for CD5 and CD10 on flow cytometry analysis. Bone marrow biopsy and cytology revealed no lymphoma cell invasion. Biopsy of the jejunal lesion showed infiltration of atypical, large lymphoid cells that were positive for CD20 and BCL2 and negative for CD3, CD5, CD10, and cMYC (). The cells were diffusely positive for Ki-67. The results of in situ hybridization for Epstein–Barr virus-encoded small RNA-1 were also positive. The jejunal tumor, which had invaded the transverse colon, was surgically resected. Lymphadenopathies of the mesentery were observed intraoperatively. Consequently, a diagnosis of diffuse large B-cell lymphoma in the jejunum at stage II1E (large intestine) was made. Chemotherapy with cyclophosphamide, adriamycin, vincristine, and prednisone plus rituximab was administered postoperatively.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [44, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': False, 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 44 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
1039,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7821107-2,Extracted,"The second patient was an 85-year-old man who was referred to our hospital as an outpatient with symptomatic, severe aortic stenosis (AVA 0.8 cm2) and preserved LVEF of more than 50%. His medical history included permanent atrial fibrillation and bilateral hip replacement. His symptoms were graded as NYHA II, with dyspnea on exertion and fatigue being his main symptoms. This patient was triaged as urgency Level 2.
Using conscious sedation, TAVR was successfully performed through transfemoral approach, with no valvular and paravalvular regurgitation. However, the procedure was complicated by bleeding of the right femoral artery due to unsuccessful placement of the closure device, necessitating surgical repair under general anesthesia and admission to the ICU. The same evening of the TAVR procedure, the patient was transferred to the CCU. The patient was discharged to the cardiology ward of the referring hospital for further rehabilitation the following day, and discharged home 4 days after TAVR.
Seven days after discharge (and 11 days after TAVR), the patient presented to the emergency department with a 2-day history of fever, dyspnea and orthopnea. Chest CT showed bilateral ground-glass opacities and possible peribronchial infection in the left lower lobe. Subsequent PCR testing was positive for COVID-19. Patient was admitted to the COVID-19 ward and died 5 days later due to respiratory failure.
Contact tracing revealed hospital visits from only one visitor for this patient. This person exhibited COVID-19 related symptoms after the patient's readmission to the hospital (4 days after the patient exhibited symptoms), with PCR confirming COVID-19 five days after the patient's death. Other visitors outside the hospital never exhibited any COVID-19 related symptoms. In both the TAVR-center and the referring hospital, no COVID-19 cases were reported among the hospital personnel during that period.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [85, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 85 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
1040,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7198086-1,Extracted,"A 68-year-old male presented with a two-year history of a cystic nodule on the radial aspect of the P1 (proximal) phalanx of the left third finger. The cyst had been progressively increasing in size over the last two years and became painful a few months prior to the presentation. He had no other associated symptoms. His past medical history was significant for HIV (well controlled, last CD4 700-900), chronic atrial fibrillation on dabigatran, diabetes mellitus type 2, essential hypertension and hyperlipidemia. Physical exam showed a 12 mm x 11 mm, nontender, mobile subcutaneous cystic lesion at the dorsal aspect of the left distal phalanx of the third finger. Complete blood counts, renal function, basic electrolytes and liver function were unremarkable. Given the location and clinical characteristics of the lesion, ganglion cyst, arteriovenous malformation, hemangioma, lipoma and fibroma were initially considered in the differential diagnosis. The patient opted for excision of the nodule. On macroscopic examination, the tumor was a well-circumscribed tan-pink nodular mass measuring 0.7 x 0.7 x 0.5 cm. Microscopic examination showed a solid type tumor with well-circumscribed closely packed smooth muscle fascicles with moderately low cellularity surrounding vascular lumina (Figures , ).
There was no evidence of atypia, hemorrhage, necrosis, mitosis or calcifications. Immunohistochemical staining with CD34 and smooth muscle actin were positive (Figures , ). Testing for S100 (a neural tissue marker) was negative and desmin (a myogenic marker) was noncontributory. Diagnosis of angioleiomyoma was made after the histopathological exam. The patient recovered well from the procedure, and there was no recurrence after nine months of follow-up.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [68, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 68 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
1041,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5960533-1,Extracted,"A 50-year-old man with a past history of hypertension and diabetes was referred to our hospital after the onset of left-sided numbness and weakness for 5 hours. The patient had not any other past medical history other than hypertension and diabetes, and there was no family history of similar diseases. A preoperative computed tomography (CT) of the head and CT angiogram of the brain (CTA) scan on admission showed no abnormalities and vascular malformations (Figures and ). He was transferred to the intensive care unit (ICU) for further investigations and treatment. He was given an intensive care such as oxygen therapy and lipid-lowering.
Initial examination at the time of admission showed a temperature of 39°C, blood pressure of 140/92 mmHg, and a regular heart rate of 78/minute. His Glasgow coma scale (GCS) score was 7, pupils were equal and reacting, and there was grade 3 power in the left limb and grade 5 in the right limb. Further laboratory examination showed a leukocyte count of 16.5 × 109/L, a hemoglobin level of 129 g/L, neutrophil count of 83.4%, blood gas of pH 7.463, PO2 88.4, PCO2 26.8, and glucose in urine 4+; his hypersensitive c-reactive protein was 497.4 mg/L (normal < 3 mg/L). Echocardiography was performed showing a reduced compliance of left ventricle; the E-F slope of anterior mitral valve leaflet was decreased; otherwise, the size, structure, and movement of the heart were normal.
The patient was diagnosed with liver abscess, perisplenic and intracranial infection, and septicemia; a contrast-enhanced CT scan of the abdomen showed rounded hypodense lesion with central low attenuation in the right lobe of the liver and a hypodense splenic air-filled lesion with an irregular wall (). Ultrasonically guided percutaneous drainage of the splenic cyst fluid was performed; approximately 65 ml of light yellow, murky fluid was removed. The blood cultures and splenic cyst drainage were positive with Klebsiella pneumoniae which were the primary source of septicemia.
On the third day in the hospital, magnetic resonance imaging (MRI) of the head showed high signal intensity on DW image and well-defined rounded cystic lesion on the T2-weighted and T1-weighted images involving in the right corona radiata and basal ganglia (), although the lesion looks like that of an acute stroke but lately was confirmed to be early stage of cerebral abscess. On the seventh day, the patient was noted to have worsening neurological status and left extremity weakness and a repeat computed tomography (CT) scan revealed a right occipital lobe hematoma with blood loss of 40 ml (). He was immediately admitted to the surgical ward to undergo an urgent intracranial hematoma evacuation surgery. During the first three postoperative days the patient was delirious; further MRI of the brain three days after operation showed multiple hemorrhagic lesions involving both cerebral hemispheres and cerebellum and a cystic lesion in the basal ganglia region ().
On hospital day 34, the patient developed high-grade fevers accompanied by worsening neurological status. Contrast-enhanced CT of the head showed a well-defined lesion, with thin, ring-like enhancement pattern in the right basal ganglia with perilesional edema, which compressed right lateral ventricle with midline shift towards left and was given the possibility of brain abscess (). The patient was treated conservatively with supportive care; he was given an antiplatelet and anti-infective therapy; the antibiotic drugs that he was given were included imipenem, linezolid, and vancomycin. He was discharged to home after two months in stable condition and slow improvement in his mental status but he still had some weakness on the left side of his body.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [50, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 50 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
1042,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4528881-1,Extracted,"A 55-year-old male with history of atrial fibrillation, HHT, hyperlipidemia, hypertension, prostate cancer status post prostatectomy, remote smoking, and obesity was scheduled for a Maze procedure for treatment of atrial fibrillation. Medications for this patient included estradiol TD nasal spray, cromolyn sodium nasal spray, mupirocin 2% nasal ointment, aspirin, digoxin, metoprolol, and pravastatin.
Preoperatively he was seen by Hematology for assessment of the use of anticoagulation therapy for atrial fibrillation in the setting of HHT. As mentioned, this patient was currently on only aspirin for anticoagulation given the risk of bleeding with HHT. After consultation, recommendations were to avoid further anticoagulation unless proved to be medically necessary in the setting of his cardiac pathology. Further recommendations revealed close follow-up with his physician as well as ongoing laboratory markers to evaluate for anemia.
The patient was also seen preoperatively in the Outpatient Preoperative Assessment Center in preparation for his surgery. Pertinent physical exam findings at that time revealed several telangiectasias on the tongue, lips, and right cheek. Exam of the airway revealed a mallampati class II, full cervical range of motion in all planes, and aforementioned small focal telangiectasias of the tongue but none noted in the posterior oropharynx. The patient was determined to be an ASA physical status 3 with good cardiac functional capacity. He also was determined to be high risk for obstructive sleep apnea as determined by the STOP BANG questionnaire.
Laboratory data included a hemoglobin of 15.1 g/dL, hematocrit of 43.6%, and electrocardiogram showing atrial fibrillation with a rate of 68. A chest x-ray reviled no cardiopulmonary pathology. There was a recent transthoracic echocardiogram completed revealing an ejection fraction of 59% with left ventricular hypertrophy and a mildly dilated left atrium. There were no signs of diastolic dysfunction, and the heart was otherwise structurally normal. Furthermore, there was also documented evidence of a negative lexiscan cardiolyte stress test preformed 3 months prior.
The patient was originally diagnosed with atrial fibrillation 8 years ago and had undergone successful cardioversion to normal sinus rhythm after his initial presentation. He had spontaneously converted back to atrial fibrillation approximately 5 months prior to his planned surgery and had since been experiencing ongoing dyspnea on exertion and palpitations.
Significant to his history of HHT, he previously had experienced frequent episodes of epistaxis and does follow with an otolaryngologist. His epistaxis was complicated by a deviated septum in the setting of HHT, and he subsequently underwent septoplasty for surgical repair. After this nasal surgery he was started on a nasal estrogen for treatment of his epistaxis. Estrogens have been shown to be beneficial in the treatment of epistaxis secondary to HHT. It is postulated that estrogens may improve the integrity of the vascular endothelium or cause microhemostasis in the microcirculation. Since initiation of treatment and nasal surgery the patient’s episodes of epistaxis have been rare.
On arrival in the preoperative holding area, an 18 gauge IV was started and a right radial arterial line was inserted for hemodynamic monitoring. The patient was transferred to the operating room where standard ASA monitors were applied and pre-oxygenation commenced. General anesthesia was induced with fentanyl, midazolam, lidocaine, propofol, and rocuronium. The patient was intubated with a left double lumen endotracheal tube (ETT) using a MAC 3 blade revealing a Cormack-Lehane grade I view. Careful attention with gentle manipulation was used during direct laryngoscopy and no telangiectasias were appreciated in the posterior oropharynx. The ETT was pretreated by soaking in warm sterile normal saline to allow pliability and lubricated to facilitate smooth intubation and avoid airway trauma and rupture of any possible oropharyngeal telangiectasias. After successful intubation, correct positioning of the ETT was confirmed by bronchoscopy. After induction of general anesthesia, a cordis centeral venous catheter was inserted in the right internal jugular vein for central venous pressure monitoring and access for fluid and blood resuscitation if needed. A transesophageal echocardiogram (TEE) was performed ruling out an intracardiac thrombus or any significant structural heart disease. General anesthesia was maintained with isoflurane, oxygen, fentanyl, and vecuronium. Single lung ventilation ensued on the left for access to the heart via thoracotomy on the right chest wall. Prior to induction, the patient was in atrial fibrillation with a rate of 111. Intraoperatively successful cardioversion was performed 3 times for rates in the 160s. The surgery was successful without complication, and the patient remained in normal sinus rhythm with a rate of 70 at the conclusion of the procedure. Near the end of the procedure 2 lung ventilation resumed and the patient was treated with ondansetron for prevention of postoperative nausea and vomiting. The patient’s neuromuscular blockade was reversed with neostigmine and glycopyrolate. The double lumen ETT was exchanged for an 8.0 single lumen ETT under direct visualization with a size 4 McGrath video laryngoscope. Due to the high risk for obstructive sleep apnea (OSA) the decision was made to transfer the patient to the intensive care unit intubated where he was able to recover from anesthesia and was successfully extubated later in the day. Estimated blood loss from the case was 50 cc, urine output was determined to be 200 cc, and the patient received a total of 2700 cc of crystalloid throughout the procedure.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [55, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 55 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1043,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5716652-1,Extracted,"A 52-year-old man presented to Asan Medical Center with a recurrent mediastinal mass incidentally found on follow-up chest computed tomography (CT) (). The patient had undergone the excision of an anterior mediastinal sarcoma 6 years ago at another hospital. That mass measured 150 mm×100 mm, and was completely removed through a median sternotomy combined with a left thoracotomy. His past medical history revealed total thyroidectomy due to thyroid cancer and paroxysmal atrial fibrillation that had persisted for the previous 6 years.
Preoperative transthoracic echocardiography (TTE) revealed severe left ventricular (LV) dysfunction with an ejection fraction (EF) of 22% accompanied by mild mitral and tricuspid insufficiency. In addition, a newly developed anterior mediastinal mass measuring 35 mm×30 mm abutting the aortic arch was observed. The mass, which had abroad base attached to the right brachiocephalic vein, encircled both the right brachiocephalic and left common carotid arteries.
We planned complete en bloc excision of the invaded tissue, followed by reconstruction of the aortic arch and superior vena cava (SVC). After a redo median sternotomy, cardiopulmonary bypass (CPB) was established by cannulating the ascending aorta and right atrium. The aorta was cross-clamped, and then 1 L of cold del Nido cardioplegic solution was administered via the aortic root. A left-sided Maze procedure with cryoablation was performed through a left atriotomy. After closure of the left atriotomy, the entire tumor, including the invaded SVC, right brachiocephalic vein, and aortic arch, was resected en bloc under total circulatory arrest at a nasopharyngeal temperature of 21°C (). First, the right brachiocephalic artery was anastomosed to a 4-branched vascular graft (Hemashield Platinum Woven Double Velour Vascular Grafts 24 mm; Maquet Holding BV & Co. KG, Rastatt, Germany) to secure immediate unilateral antegrade cerebral perfusion. Then, anastomoses of the descending thoracic aorta, left common carotid artery, and proximal ascending aorta were performed, in order. The left subclavian artery was anastomosed under beating-heart CPB after the release of aortic cross-clamping (ACC). The SVC was then reconstructed using a bovine pericardial patch tailored in a tubular shape. Weaning from CPB was smooth, and normal sinus rhythm was restored. The intraoperative frozen biopsy revealed a negative resection margin, free of tumor cells.
The total circulatory arrest time, lower body ischemic time, ACC time, and CPB time were 13 minutes, 23 minutes, 78 minutes, and 132 minutes, respectively. The patient was transferred to the intensive care unit and extubated after 12 hours. The patient was transferred to the general ward on postoperative day (POD) 2 and was discharged on POD 9 without complications. Postoperative TTE showed no changes in overall cardiac function compared to the preoperative exam, except for slightly alleviated LV dysfunction, with an EF of 28%. Postoperative CT showed no evidence of a residual tumor, and confirmed the presence of a well-reconstructed arch, arch vessels, and SVC without architectural distortions ( ). The pathologic examination revealed a myxofibrosarcoma with resection margins free of tumor cells (pT1bN0M0, stage IA according to the American Joint Committee on Cancer seventh edition). The patient has been followed up a tour outpatient clinic for the last 9 months, and no evidence of tumor recurrence has been found. Recent follow-up TTE revealed normalized LV systolic function, with an EF of 63% and sinus rhythm. The patient’s resting pulmonary hypertension was relieved, and the extent of mitral and tricuspid insufficiency was reduced.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [52, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 52 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
1044,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3276803-3,Extracted,"A 23 year-old woman presented with a round shaped hyperpigmented patch, 12 cm in diameter on the left buttock, on exactly the same site as in an episode 3 months previously (). Histopathological examination was consistent with a diagnosis of FDE. Cefotetan and doxycycline were the drugs she had taken occasionally during the last 5 months because of chronic pelvic inflammatory disease. Within 5 days of withdrawal of the suspected drugs, the lesion cleared, leaving residual hyperpigmentation. Three months later, she was treated with doxycyline to control rosacea on her face that led to reactivation of the previous lesion. The case was diagnosed as doxycycline-induced FDE. The location of the lesion on the right buttock area was consistent with the L2-maximal point, the known projection point of the uterus and adnexes,.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [23, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 23 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1045,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-1608,Extracted,"Nine days after being treated for a perforated gastric ulcer and sepsis, a 78-year-old woman develops decreased urinary output and malaise. She required emergency laparotomy and was subsequently treated in the intensive care unit for sepsis. Blood cultures grew Pseudomonas aeruginosa. The patient was treated with ceftazidime and gentamicin. She has type 2 diabetes mellitus, arterial hypertension, and osteoarthritis of the hips. Prior to admission, her medications were insulin, ramipril, and ibuprofen. Her temperature is 37.3°C (99.1°F), pulse is 80/min, and blood pressure is 115/75 mm Hg. Examination shows a healing surgical incision in the upper abdomen. Laboratory studies show:
Hemoglobin count 14 g/dL
Leukocyte count 16,400 mm3
Segmented neutrophils 60%
Eosinophils 2%
Lymphocytes 30%
Monocytes 6%
Platelet count 260,000 mm3
Serum
Na+ 137 mEq/L
Cl- 102 mEq/L
K+ 5.1 mEq/L
Urea nitrogen 25 mg/dL
Creatinine 4.2 mg/dL
Fractional excretion of sodium is 2.1%.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [78, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': False, 'Diabetes history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 78 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
1046,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8289619-1,Extracted,"A 78-year-old man who presented with a one-day history of fever, chills, and altered mental status (AMS) preceded by 7 days of malaise and anorexia. At the emergency room (ER), he was found normotensive (107/67 mmHg), afebrile (37.1°C), not hypoxic (98%), and without tachypnea (19 rpm), yet tachycardia (131 bpm) was present. He was disoriented and lethargic but showed no focal neurological deficit nor signs of meningeal irritation. His heart rhythm was irregular, and a systolic ejection murmur (II/VI) was present at the right upper sternal border. Jugular venous distension was not evident, and his extremities were warm and without edema. His abdomen was nontender. Lungs were clear to auscultation, and no skin stigmata for endocarditis was appreciated (splinter hemorrhages, Osler, and Janeway lesions). Recent surgeries, new medications, travels, and toxic habits were all denied.
His medical history was remarkable for essential hypertension, dyslipidemia, GERD, atrial fibrillation (afib) on chronic anticoagulation (apixaban 5 mg twice per day), and a bioprosthetic surgical aortic valve replacement (SAVR) in 2008 followed by valve-in-valve TAVR (2017) two years prior to presentation. Dietary habits included regular consumption of raw salmon.
Initial electrocardiogram () showed afib with a fast ventricular response (FVR), without chest pain or new ST-segment changes compelling for an acute coronary syndrome. Chest X-ray () and head CT scan were negative for acute pathologies. However, mild leukocytosis (11.3 × 103/μL) with neutrophilia, elevated ESR (72 mm/1Hr), CRP (214.7 mg/L), and procalcitonin levels (0.20 ng/mL) were present, all suggestive of an underlying bacterial infection. His toxicology, urinalysis, and HIV tests were unremarkable.
His encephalopathy in the context of afib was worrisome for stroke; however, no focal neurological deficits were found, plus his head CT scan was negative, and he had been compliant with anticoagulation therapy. His laboratories and tachycardia suggested an underlying bacterial infection of unclear foci. At first, meningoencephalitis was contemplated although meningeal irritation signs were missing. A lumbar puncture was attempted but ultimately deferred as the patient became aggressive and uncooperative with the procedure. As per the sepsis protocol, the patient was pan-cultured, resuscitated with intravenous (IV) fluids, and started on broad-spectrum IV antibiotics (vancomycin and cefepime). Acyclovir was added given the possibility of herpetic meningoencephalitis.
Subsequently, blood cultures (4/4) grew Lactococcus garvieae (). Transthoracic echocardiogram (TTE) revealed no prosthetic aortic valve dysfunction nor large vegetations (). Nonetheless, a transesophageal echocardiogram (TEE) showed a pedunculated/oscillating echo-dense structure measuring 0.7 cm in its largest dimension attached to the right coronary cusp of the TAVR consistent with vegetation (, Video ). There were no cusp perforations, significant valvular insufficiencies, paravalvular abscess or leaks, nor evidence of valve thrombosis (normal valve hemodynamics by Doppler, plus valve was bioprosthetic and not mechanical, and patient was compliant with chronic anticoagulation).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [78, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 78 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
1047,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8702428-1,Extracted,"In April 2016, a 51-year old male patient complained of consistent cough for 2 months and was admitted to our center for a diagnosis of poorly differentiated lung adenocarcinoma [PCK(+), CK7 (focally +), TTF-1(+), CK18(+), CK5/6(-), P63(scattered +), CK14(-), CDX-2(-), CD56(+), CgA(-), Sgn(-), Ki-67(~50%)] in the right upper lobe with enlarged ipsilateral mediastinal lymph node and MPE confirmed by cytological examination of the fluid via both cell block and smear from the collected sample by thoracentesis, which was not further confirmed by pleural biopsy (cT3N2M1a, IVa) (). The patient was generally in normal condition but was found to have type two diabetes mellitus with an Eastern Cooperative Oncology Group score of 1. With the primary tumor extracted via percutaneous needle biopsy for next-generation sequencing, it was confirmed to have epidermal growth factor receptor (EGFR) gene mutation (exon 21 L858R) and the patient was advised to receive gefitinib (250 mg, QD) for treatment. After taking gefitinib for 4 months, the patient was re-evaluated comprehensively and an excellent radiographic response to gefitinib was found on his chest computed tomography scan (). Therefore, the patient was discussed in a multidisciplinary meeting in our center, and salvage surgery was recommended for him. In August 2016, after providing signed informed consent, the patient received lobectomy and systematic lymph node dissection under video-assisted thoracoscopic surgery (VATS) successfully and intraoperative findings did not reveal any pleural involvement, which was further confirmed by pleural biopsy. The patient was discharged on postoperative day 5 uneventfully and his postoperative pathological finding revealed no residual tumor neither in the right upper lobe nor in the mediastinal lymph node and pathological complete response to gefitinib was confirmed in the patient (ypT0N0M0) as shown in his pathological report that numerous chronic inflammatory cells, foamy histiocytes, and dense fibrosis were observed and no viable tumor was seen [PCK(-), EMA(-), CK7(-), TTF-1(-), NapsinA(-), CK5/6(-), P63(-), PGM-1 (inflammatory cells+), complete pathologic response]. As usual, after surgery, the patient discontinued gefitinib and underwent four cycles of adjuvant chemotherapy (cisplatinum 40 mg on day 1 to 3 and pemetrexed 800 mg on day 1) instead because chemotherapy was the regular regimen for postoperative adjuvant therapy then and finished his last course of adjuvant chemotherapy in December 2016 with only grade 2 of leukopenia without any drug-related grade 3 to 4 adverse events. Since then, the patient received no additional treatment (such as targeted therapy, chemotherapy, or radiotherapy) and was followed up regularly every 3–4 months with chest and abdominal CT scans and tumor biomarkers and annual positron emission tomography (PET)/CT scan. The patient's recent PET/CT scan (October 2021) still revealed no sign of recurrence (), and he is still alive without disease for 62 months after surgery (disease-free survival: 62 months). The whole treatment timeline of the patient in our case was summarized in .",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [51, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 51 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 0 + 1 = 1.
The patient's CHA2DS2-VASc Score is 1."
1048,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5827887-1,Extracted,"An 80-year-old male with hypertension and coronary artery disease presented with a three-day history of emesis and diarrhea, diagnosed as gastroenteritis. He endorsed dizziness and weakness but did not report any headache, blurry vision, paresthesias, or syncope. The patient also described a three-day history of complex visualizations involving a moving car. The car had color and appeared life-like. It was not distorted and seemed to be driving in a realistic manner in front of him. This occurred exclusive when his eyes were closed and immediately resolved upon opening his eyes. It was present for the majority of the time his eyes were closed and made it difficult for him to sleep.
He denied any prior hallucinations and had insight that the car was not real. He had no history of head trauma, cerebrovascular disease, or personal or familial history of psychosis or dementia. Ophthalmologic history was unremarkable and he used glasses only for reading. He was not experiencing any other sensory hallucinations or illusions at this time.
The patient was hemodynamically stable and afebrile, and physical examination was significant only for mild abdominal tenderness. There were no signs of cognitive impairment. Fundoscopic examination did not reveal any abnormalities. Laboratory analysis showed white blood cell count 4.6 billion cells/L, sodium 119 mEq/L, potassium 3.2 mEq/L, carbon dioxide 24.6 mEq/L, anion gap 10, glucose 186 mg/dL, and lactate 2.1 mmol/L. Urine drug screen was negative. Chest X-ray was normal, and electrocardiogram showed normal sinus rhythm.
Fluid resuscitation with normal saline and electrolyte replenishment was initiated. The visualizations decreased in frequency over the next two days and were completely absent by the third day after admission, which was the sixth day since they first began. Serum sodium increased during treatment and was 130 mEq/L on the day the hallucinations subsided. The patient was discharged the next day and has not experienced any recurrence of closed-eye visualizations or other hallucinations in the eight months since.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [80, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 80 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
1049,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7501890-1,Extracted,"A 40-year-old man presented with palpitations 2 years ago and was diagnosed with paroxysmal atrial fibrillation 5 months ago. He was receiving anticoagulation treatment with edoxaban.
On admission, the examinations showed that he was haemodynamically stable. Surface 12-lead electrocardiography revealed sinus rhythm. Laboratory investigations revealed no notable findings. Physical examination, chest X-ray, and echocardiography did not yield evidence of clinically overt structural and/or organic heart disease.
Catheter ablation using the CBA system was performed under sedation with dexmedetomidine. A transseptal puncture was performed without any complication, and angiography of the left atrium (LA) showed four independent PVs. Heparin was administered to maintain an activated clotting time >300 s. A 20-mm circular mapping catheter (Achieve™; Medtronic, Minneapolis, MN, USA) and a 28-mm cryoballoon catheter (Arctic Front™; Medtronic) were advanced into the LA via a steerable sheath. Firstly, we targeted the two left PVs with single freeze, under observation of the oesophageal temperature using an internal oesophageal probe. Afterwards, a circular mapping catheter was advanced in the right inferior pulmonary vein (RIPV), and single freeze was performed along with phrenic nerve capture (Figure ). After isolation of the PV, an attempt was made to withdraw the catheter from the PV. However, the catheter tip was immobile and could not be withdrawn with significant resistance. Repeated attempts to withdraw the catheter by rotational traction were not effective (Figure ). Computed tomography showed that the catheter tip perforated the posterior basal vein (V10: posterior basal vein) of the RIPV and was stuck in the right lower lobe, along with intrapulmonary haemorrhage (Figure and B). Considering that strong traction could cause major bleeding and breakage of the catheter, surgical removal was performed after obtaining informed consent from the patient.
Surgery was performed via right 7th intercostal lateral thoracotomy. The right lung (mainly S10: posterior basal segment) was congested due to intrapulmonary haemorrhage. The RIPV was peeled to the periphery to expose the posterior basal vein (V10). The catheter perforated the vessel wall in the middle of V10 and entered the pulmonary parenchyma (Figure ). The catheter could not be removed even through direct traction. A microincision on the lung parenchyma covering the surface of the catheter tip was performed, and the circular distal portion of the catheter was cut (Figure ). The entire catheter (i.e. shaft and proximal portion) was successfully removed from the transseptal catheter, and the V10 was repaired using suture. The removed catheter had a fracture at the junction of the distal portion and the shaft due to repeated traction (Figure ). After surgery, the patient had an uneventful course without evidence of complications.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [40, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 40 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
1050,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5770006-1,Extracted,"JE, a 68-year-old right-handed male with 10th-grade education was referred by a neurologist for neuropsychological evaluation in December 2016 due to forgetfulness which emerged after January of the same year. In January 2016, he had suffered an ischemic stroke of cardioembolic etiology. JE had a medical history of hypertension and chronic atrial fibrillation. According to JE and his wife, before the stroke he was normally able to manage his home activities and job tasks as a machine mechanic. However, after the stroke, the patient had severe difficulty organizing his finances and could no longer work or drive. His family perceived memory deficits such as forgetting new events, commitments, asking about people who died recently, and repeatedly asking the same question. JE also presented disorientation in time and new places.
On medical evaluation, laboratory test results were within normal ranges (including blood count, comprehensive metabolic panel, thyroid-stimulating hormone, vitamin B12 and venereal disease research laboratory). A magnetic resonance imaging scan of the brain performed in January 2016 indicated an ischemic lesion affecting the left parahippocampal gyrus, hippocampus, and anterior portion of the middle and inferior temporal gyrus. There were some additional tiny lesions of the white matter not exceeding possible typical age-related changes (). At the time of the neurologist's observation, JE scored 23/30 on the Mini-Mental State Examination (MMSE), with deficits mainly on the subitems of time, place, and delayed recall. This demonstrated a marked decline of orientation and EM. On the Montreal Cognitive Assessment (MoCA), JE's score (18/30) was mainly attributed to errors in memory and orientation subtests. A diagnostic hypothesis of neurodegenerative dementia (e.g., Alzheimer's disease dementia) was excluded. There was evidence of a stroke temporally related to the onset of memory impairment, as well as lack of insidious onset of the decline. Therefore, the diagnosis of probable Alzheimer's disease dementia and other neurodegenerative dementias was not applicable.
The patient underwent a comprehensive neuropsychological assessment to evaluate memory impairment and other functions (). Overall, JE's performance showed severe EM impairment in verbal and visual modalities indicated by delayed recall measures of the Rey Auditory Verbal Learning Test (RAVLT) (0/15) and the Rey-Osterrieth Complex Figure Test (RCFT) (3/36) with scores below the 5th percentile. The Memory Subscale from the Dementia Rating Scale (DRS – 2) also indicated impaired performance (10/25, < 5th percentile). He underperformed on the RAVLT Word Recognition list, which may indicate an inability to encode and consolidate new episodic contents. Category fluency (animals form) and Vocabulary (WAIS III) tests indicated preserved semantic memory (50th percentile). JE had an appropriate strategy for visuospatial construction, making few mistakes on the ROCF Copy test. Regarding language processes such as naming and comprehension, there were no indications of impairment according to results on the Boston Naming Test (short version) and Token Test, respectively.
There was no evidence of executive impairment in general. On the Five Digit Test, which is a numeric-Stroop paradigm applying four steps (Reading, Counting, Choosing and Shifting) that evaluates processes such as processing speed, selective attention, inhibitory control and cognitive flexibility, JE had scores indicative of clinical impairment (< 5th percentile). However, considering the indices of Inhibition and Flexibility (interference scores that subtract Reading time from Choosing and Shifting time, which minimize the influence of processing speed on executive performance), there was no indication of impairment in these measures (50th percentile). This discrepancy can be explained by the decreased processing speed observed in the patient, and not by a deficit in superior/executive functioning. This is corroborated by the fact that the patient was slow to perform the tests, but did so without errors, and due to the fact that he had adequate performance in all other tests of executive functioning.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [68, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Thromboembolism history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 68 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
1051,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6456878-1,Extracted,"An 83-year-old Caucasian man has history of smoking habit, hypertension, dyslipidaemia, COPD with moderate obstructive deficit and chronic kidney disease (CKD) and moderate reduction of glomerular filtration rate (GFR = 45 mL/min).
In 1998, the patient was hospitalized for a non-ST elevated myocardial infarction with documentation of severe three vessel coronary diseases. Echocardiography showed hypertrophic left ventricle with anterior and lateral hypokinesia and slightly reduced ejection fraction (50%). The patient underwent coronary artery bypass grafts with left internal mammary artery (LIMA) on left anterior descending (LAD), and saphenous vein graft (SVG) on obtuse marginal (OM)1 and on right coronary artery (RCA). Follow-up was uneventful until 2013, when the patient was again hospitalized for unstable angina. On this occasion, he reported classical symptoms of angina [Canadian Cardiovascular Society (CCS) Class III] in the last 6 months and more recently typical chest pain episodes at rest lasting 15 min and responsive to nitrates. Echocardiography was slightly worsened with akinesia of the anterior apex and hypokinesia of the anterolateral wall. Considering the high-risk profile and the symptoms, we decided to perform coronary artery angiography that showed: functional LIMA occlusion, occlusion of the SVG for RCA, and critical stenosis of the SVG for OM1 with LAD, RCA, and OM1 occlusion (Figure ). Percutaneous coronary intervention (PCI) on LAD was performed with single drug-eluting stent (DES) implantation and on SVG for OM1 with DES implantation (Figure ). Patient was discharged on dual antiplatelet therapy (aspirin and clopidogrel), perindopril 5 mg, amlodipine 10 mg, doxazosin 2 mg, and atorvastatin 80 mg. A low dosage of selective β-blocker (bisoprolol 1.25 mg) was added [blood pressure (BP) 120/80 mmHg, heart rate (HR) 86 b.p.m.]. The patient was already on tiotropium 18 mcg for his COPD. After 5 years, the patient came to our attention for worsening effort angina (CCS III). A myocardial perfusion scintigraphy showed anterior and lateral ischaemia involving 18–20% of the left ventricular mass. In the meanwhile, diabetes mellitus type II was diagnosed and CKD worsened becoming severe (GFR 28 mL/min). Thus, perindopril was withdrawn and doxazosin was uptitrated to 4 mg as well as bisoprolol to 2.5 mg (BP 110/70 mmHg, HR 82 b.p.m.). Coronary artery angiography showed in-stent occlusive restenosis of LAD, critical stenosis of the SVG for OM1 due to distal progression of the disease (Figure ). Saphenous vein graft for OM1 was treated with another DES (Figure ), while an unsuccessful attempt of PCI was performed on LAD. We uptitrated bisoprolol to 5 mg (BP 120/70 mmHg, HR 80 b.p.m.). After 2 months, the patient underwent his scheduled pneumology follow-up that with spirometry that showed worsening of forced expiratory volume (FEV)1 (0.69 L, 55% of the predicted value) and of FEV1/forced vital capacity (66% of the predicted, Figure ) with overall severe obstructive deficit. Salmeterol/Fluticasone 50/500 mcg was added to tiotropium, and a cardiology evaluation was suggested to re-evaluate therapy (in particular the need of β-blocker). The patient referred slight amelioration of symptoms after PCI with residual CCS II angina. Electrocardiogram (ECG) showed sinus rhythm with 78 b.p.m. (Figure ). We decided not to withdraw bisoprolol but to add ivabradine 5 mg b.i.d. in order to control symptoms. The patient is actually in CCS Class I and the control spirometry showed moderate obstruction comparable to his chronic situation.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': True, 'age': [83, 'years'], 'Diabetes history': True, 'sex': 'Male'}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 83 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
1052,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4358708-1,Extracted,"A 56-year-old male electrician, with treated hypertension (reported mean values of blood pressure: 130/95 mm Hg), was admitted with chest pain lasting for about 60 minutes. He was journeymen electrician specialized in commercial, residential and low-voltage wiring.
He gave a history that on the morning he had working for almost 4 hours carrying out various activities such as manipulate cables and wires through cavities or carry boxes of electrical equipment weighing about 20 kilos, with considerable physical effort.
In his clinical history he reported to have had occasional atypical chest pain for which he submitted two years ago to exercise stress testing, which resulted maximal for age and negative for ischaemia induced by stress. The patient on admission had tachypnoea at rest with oxygen saturation of 93%. Electrocardiogram (ECG) showed atrial fibrillation with a heart rate of 90 beats/min. Blood pressure was 175/95 mm Hg. Cardiac auscultation was normal but at pulmonary level bilateral basal crackles were present. Cardiac enzymes were slightly elevated: Troponin T (TnT): 0,033 ng/l [norm: <0.03] and Creatine Kinase (CK): 260 U/l [norm: 47–220]. Regional left ventricular wall motion and ejection fraction was normal (Ejection Fraction EF 60%). After cardioversion with DC shock (3 J/Kg body weight), considering TnT and CK levels [] a CAG was performed to exclude coronary disease. It revealed a suspect of single coronary vessel arising from the right sinus of Valsalva. The right coronary artery (RCA) showed a normal course (Figure : panel A). Stenoses of the coronary arteries were not present. In order to better define the origin and course of the single vessel, we performed a Multi Slices Computed Tomography (MSCT) (Figure : panels B, C and D) using a 64-detector-row scanner (Aquilion 64; Toshiba Medical System, Tokyo, Japan).
MSCT showed a SCA arising from the right sinus Valsalva and dividing in RCA and Left Main (LM) (Figure : panel B,C and D). The LM showed an acute take-off angle, turned posteriorly behind the aorta, reaching the atrio-ventricular groove where it divides into left anterior descending (LAD) and left circumflex (CX) arteries. No atherosclerotic plaque were present. The patient was discharged with only antihypertensive drug therapy. After 2 month, at follow up medical check, he reported no angina and no exertional dyspnea. His left ventricular ejection fraction was normal and exercise tolerance >12 METs. He returned to his full work duties, although we recommended him to avoiding strenuous work (under 6 METs) and work on overhead lines too.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [56, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 56 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1053,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7989724-1,Extracted,"A 62-year-old right-handed male with a longstanding history of diabetes mellitus and hypertension presented with sudden-onset left-sided body weakness as well as a loss of feeling over the left side of his body. These symptoms started approximately 3 days before the presentation to the hospital. He gave a history of difficulty looking to the left side as well. There was no history of loss of consciousness, speech difficulties, seizures, headaches, or vomiting. His neurologic examination showed an intact level of consciousness, normal higher mental functions as well as normal speech. The examination of vision showed conjugate horizontal left gaze palsy. He could maintain gaze near mid-position but could not cross the midline to the left side. Doll's head maneuver brought the eyes past the midline to the left. Visual acuity was normal at the bedside near-fixation test. Visual fields were assessed by bedside confrontation methods and did not show clear defects. Examination of facial nerves showed weakness of the upper motor neuron type on the left side, and the remainder of cranial nerves was intact.
Motor system examination showed hypotonia, hemiplegia, hyporeflexia as well as extensor plantar response on the left side of the body. Sensory system examination showed left hemisensory loss of pain and temperature sensations.
Computed tomography scan of the brain showed an area of infarction over the right subcortical corona radiata region (Fig. ). He received inpatient stroke care and then was discharged home.
He was re-assessed in the neurology outpatient clinic (OPD) at 1, 3, and 6-month intervals after discharge. Neurologic examination on the first visit to the neurology clinic showed some improvement in the range of eye movements; however, he had residual partial defects of both saccadic and pursuit functions on horizontal gaze. His motor power over the left side of his body was better as compared to his baseline. Tone and deep tendon reflexes were increased over the left side as well, and the other neurologic findings were the same as his baseline.
His neurologic assessment on the second visit to the neurology OPD did not show significant changes from the first visit. However, re-assessment on the third visit (i.e., 6 months after discharge) showed complete recovery of gaze palsy, better motor power on the left side of his body with otherwise similar findings as before.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [62, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 62 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
1054,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3118206-1,Extracted,"A 69-year-old Italian Caucasian woman arrived at the emergency department presenting with sudden onset of lower left limb pain. The patient reported no dyspnea, chest pain, weight loss, nausea, abdominal pain, hematuria, myalgias, or arthralgias. Her medical history was notable for type 2 diabetes mellitus and chronic atrial fibrillation. She had no history of coronary heart disease, hypertension, or dyslipidemia, and she did not smoke. Her medications included digoxin and repaglinide, but not anti-thrombotic drugs.
The patient's physical examination revealed that she appeared to be in good condition, but she reported discomfort due to pain in the left leg. The patient's blood pressure was 125/85 mmHg, and her heart rate was 80 beats/minute and irregularly irregular. Her respiratory rate was 22 breaths/minute, her oxygen saturation was 98% while the patient was breathing ambient air, and her body temperature was 36°C.
In her left leg, femoral, popliteal, and tibial pulses were absent, with pale and cool feet and with slow capillary return. Her right leg was absent of tibial pulse. Her Ankle Brachial Pressure Index was 0 on the left and 0.4 on the right. The motor and sensory functions of the legs were preserved.
A transesophageal echocardiogram revealed enlargement of the left atrium with a thrombus in its appendange and enlargement of the right atrium. She had no signs of atrial shunt or detectable atherosclerosis in the proximal aorta. A diagnosis of embolizing non-valvular atrial fibrillation was confirmed, and the patient underwent lower left limb Fogarty thromboembolectomy, that successfully restored distal blood flow. The patient was discharged after two days to a low molecular weight heparin regimen as bridging therapy for a warfarin regimen.
After one week, the patient returned to the emergency department with acute ischemic symptoms in her left leg. Angiography was performed, which showed an apparently normal wall of the abdominal aorta, right iliac and femoral artery branches, obstruction of the left external iliac artery and total obstruction of the left femoral artery branches, and obstruction of the right popliteal artery and of the tibial-peroneal axes on both sides. Urgent embolectomy was again performed with subsequent restoration of blood flow, and the patient was discharged under warfarin therapy.
After four weeks, the patient returned with left leg pain at rest. A search for a hypercoagulable state revealed normal thrombin, pro-thrombin, and partial thromboplastin times; normal anti-thrombin III, protein S, and protein C antigens; and a normal protein C pathway, activated protein C resistance, and homocysteine level. Screening for anti-cardiolipin antibodies and lupus anti-coagulant were negative, and her anti-nuclear antibody test was negative. Her erythrocyte sedimentation rate was 8 mm/hour. Her blood cell count revealed normal amounts of red and white cells, and her platelet count was 850,000/μl.
Transesophageal echocardiography showed resolution of the atrial thrombus; however, an intra-luminal pyramidal lesion (1.4 cm×1.5 cm in size) with an irregular surface was seen on the anterior wall of the descending aorta (Figure ). Computed tomography (Figure ) with contrast medium confirmed the presence of a mural aortic thrombus in the anterior wall of the descending aorta extending 1.5 cm distally, a mural thrombus in the left pulmonary artery localized in close proximity to the aortic thrombus, a lung infarction in the inferior left lobe, an infarction in the spleen, sparse atherosclerotic plaques in the abdominal aorta and the right femoral artery, occlusion of the left external iliac artery, and occlusion of the right internal iliac artery. There were no signs of venous thrombosis.
The patient underwent surgical treatment consisting of an endovascular exclusion of thrombus with a Zenith 32 mm×80 mm endoprosthesis (Cook, Inc., Bloomington, IN) implanted just after the emergence of the left anonym subclavian artery, a subsequent thromboembolectomy of the left external iliac artery, and a femoro-popliteal bypass. The patient was discharged after a few days under a low molecular weight heparin regimen as bridging therapy for a warfarin regimen, as well as aspirin. Additional therapy included β-blockers and hydroxyurea, an anti-neoplastic drug acting on nucleic acid synthesis to reduce her platelet count. Her platelet count decreased to 300,000/μl.
Two months later an echocardiographic Doppler study revealed the patency of the bypass and the left femoral axis, which previously had been treated by embolectomy. Two months later the patient presented with left leg pain while she was being treated with warfarin. An echocardiographic Doppler scan showed obstruction of the popliteal bypass. Therapy with aspirin, clopidogrel, and warfarin was initiated. Out-patient follow-up was arranged, and eight months later the patient did not report any further embolization.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [69, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Thromboembolism history': True, 'Vascular disease history': False, 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 69 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
1055,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6439362-2,Extracted,"An 81-year-old man (body mass index: 22.9 kg/m2) underwent permanent pacemaker implantation with epicardial leads in 1988 for atrial fibrillation with bradycardia during aortic valve replacement. At our outpatient clinic, we observed battery depletion, with a significant increase in pacing threshold and resistance at the epicardial leads. Due to mobility limitations due to knee joint pain, the patient had restricted mobility. Therefore, we implanted an LTP and removed the old battery in February. The LTP was successfully implanted at the first attempt without any technical difficulty at the mid-right ventricular septum. We confirmed fixation of three tines under fluoroscopy. The pacing threshold at implantation in supine position was 0.63 V at 0.24 ms, sensitivity was 4.4 mV, and impedance was 510 Ω, with stability maintained at 5 min and 10 min after implantation. When the device was interrogated 1 week later, the pacing threshold had increased to 2.38 V at 0.24 ms, and impedance had decreased to 370 Ω in supine position. We investigated the trend data for the week and observed significant daily fluctuation of the threshold from 0.38 V to 2.5 V at 0.24 ms (Figure ). We confirmed the absence of acute febrile illness during the week of examination (C-reactive protein: 0.6 mg/dL) and electrolytes abnormalities (Na: 139, K: 4.2, and Cl: 108 mEq/L) and stable LTP position on chest X-ray (Figure ) at this point. We also found variation in pacing threshold according to body position, with the lowest value of 0.5 V at 0.24 ms in sitting position and the highest value of 2.38 V at 0.24 ms in supine position (Table ). Impedance did not change with body position, and remained between 370 Ω and 400 Ω. We again measured the pacing threshold in different body positions 1 month later and observed the same results.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [81, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 81 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
1056,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5994706-1,Extracted,"An 85-year-old woman presented to hospital on 10 July with shortness of breath, fever and raised inflammatory markers and she was treated with levofloxacin for possible pneumonia. Her past medical history was notable for a tissue aortic valve replacement 11 years prior to this event, she had atrial fibrillation and was on apixaban and had hypertension and hypothyroidism.
Blood cultures taken 2 days after admission were negative and a computed tomography pulmonary angiogram showed bibasal pleural effusions thought to be parapneumonic in nature. Deterioration in her clinical condition and new febrile episodes prompted repeat blood cultures to be taken on 28 July and these were positive for Campylobacter fetus identified by matrix-assisted laser desorption ionization time-of-flight analysis after 3 days of incubation. She did not have any loose stools during her admission at any point and had no known contact with animals. She was treated with 3 days of azithromycin. A transthoracic echocardiogram (TTE) was done and was reported as showing the prosthetic aortic valve was well seated with a preserved ejection fraction and mild diastolic dysfunction. She was discussed with the Cardiology team who felt that she did not warrant any further investigation as she did not display any features of endocarditis and her inflammatory markers had normalized, and she was discharged on 25 August.
She was then re-admitted on 6 September with multiple tonic-clonic seizures. In between episodes it was noticed she had a unilateral facial droop and had developed a fixed gaze. She was afebrile with a heart rate of 116 bpm and a blood pressure of 127/80 mmHg, and on examination it was noted that she had an audible ejection systolic murmur. Her C-reactive protein (CRP) level was 23 mg l−1 on admission and she had a white cell count of 13.0 g l−1 in the context of recurrent seizures.
She was initially started on ceftriaxone 2 g twice daily and acyclovir as there were concerns regarding central nervous system infection. However, as she slowly began to recover it became evident that she had a persistent right-sided facial droop, hemianopia and right-sided hemiparesis. An electroencephalogram done on admission was consistent with a vascular insult in the left hemisphere and not encephalitis and ceftriaxone and acyclovir were stopped. An initial computed tomography (CT) scan showed severe small vessel disease and a magnetic resonance imaging (MRI) scan done on 10 September showed bilateral emboli in both cerebral hemispheres. The working diagnosis at this point was that the patient had a cerebrovascular event secondary to her atrial fibrillation and she was transferred to the stroke team.
Over the next 2 weeks her inflammatory markers started to climb and she started spiking temperatures to over 38 °C on 22 September and became less rousable. Aspiration pneumonia was suspected clinically and she was started on co-amoxiclav. Blood cultures were taken and were again positive 2 days later with C. fetus. As previously, the patient had no gastrointestinal symptoms. At this point clarithromycin was added pending MICs.
Given the repeatedly positive blood cultures, possibly septic emboli seen on MRI scan and prosthetic heart valve, endocarditis was strongly suspected. A repeat TTE on 26 September showed a significant change in the aortic valve appearance compared to the previous imaging, with thickening and restricted movement with possible thickening of the aortic root and an increase in the peak gradient to 67 mmHg although systolic function was maintained. It was felt that this warranted treatment for infective endocarditis due to C. fetus. A CT angiogram showed no evidence of aortitis but a possible wedge perfusion defect was noted in the spleen. She was not considered a surgical candidate and given her age, frailty and co-morbidities a transoesophageal echo was not performed.
MICs were determined and were as follows: amoxicillin 0.50 µg ml−1, meropenem 0.016 µg ml−1, azithromycin 0.125 µg ml−1, gentamicin 0.38 µg ml−1, tetracycline 0.75 µg ml−1 and ceftriaxone 3 µg ml−1. Based on this information the antibiotics were switched to intravenous (IV) amoxicillin 2 g every 4 h to complete 6 weeks for prosthetic valve endocarditis along with 2 weeks of synergistic gentamicin at 1 mg kg−1 twice daily. Repeat blood cultures taken on antibiotic treatment were negative.
The patient gradually improved, her temperatures normalized and her CRP dropped to 7mg l−1 . She remained in hospital to complete her antibiotic treatment and multiple repeat blood cultures were negative. She remained afebrile with normal inflammatory markers while in hospital for 3 weeks after completing her treatment and was discharged to a rehabilitation facility on 28 November. There was no evidence of relapse of infection 2 months after discharge.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [85, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': True, 'Stroke': True, 'Diabetes history': False, 'Transient Ischemic Attacks History': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 85 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
1057,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8440084-1,Extracted,"An 80-year-old woman was followed up in the outpatient nephrology clinic for the management of Stage 4 CKD and proteinuria. Other significant medical history included type 2 diabetes (T2D), hypertension, obesity, and heart failure with reduced ejection fraction (HFrEF). Her medications included irbesartan 150 mg daily, carvedilol 25 mg twice daily, torsemide 40 mg daily, and insulin. The patient's CKD and proteinuria were secondary to diabetes and had been diagnosed 5 years previously. Proteinuria was in the subnephrotic range, with a urine albumin-to-creatinine ratio (ACR) of 113–169.5 mg/mmol. She had a serum creatinine level of 221 μmol/L and an eGFR of 20–25 mL/min/1.73 m2.
The dose of irbesartan was increased to reduce proteinuria, conserve renal function, and maximize the benefit of RAASi therapy for the management of her CHF. When irbesartan was increased to its maximum dose of 300 mg daily, K+ levels increased from 4.5 mmol/L to 5.7 mmol/L. The K+ level remained elevated between 5.5 mmol/L and 6.0 mmol/L on repeated testing. Patiromer 8.4 g/day was subsequently initiated, enabling the patient to continue taking the maximum dose of irbesartan (300 mg daily) without recurrence of hyperkalemia. Within a year, her urine ACR had decreased to 79.1 mg/mmol and showed further improvement, remaining around 11.3–22.6 mg/mmol.
The patient subsequently developed metastatic lung cancer and chose to spend her remaining days at home with family and under the care of home hospice services. She opted to withdraw from the management of her chronic medical conditions but remained on patiromer 8.4 g daily, with control of hyperkalemia for 3 years after the initiation of therapy. Renal function had been unchanged from the initial baseline visit when irbesartan was initially maximized, and proteinuria had remained controlled. The patient's CHF had remained stable with no HF-related hospital admissions while receiving the maximum dose of irbesartan (300 mg daily). Her serum potassium was 4.6, sodium 137 mmol/L, chloride 96 mmol/L, bicarbonate 24 mmol/L, calcium 9.3 mg/dL, phosphorus 4.3 mg/dL, and Mg 2.0 mg/dL during patiromer therapy. There were no reported complications with patiromer, such as constipation or other gastrointestinal side effects, hypokalemia, or hypomagnesemia.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [80, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 80 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
1058,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8646198-1,Extracted,"The present report describes the case of a 92-year-old female patient who was diagnosed with atrial fibrillation in 2009 and was being treated with phenprocoumon (Marcumar®) for stroke prevention. Pre-existing comorbidities were arterial hypertension, coronary heart disease, diabetes mellitus type 2, mild senile dementia and renal insufficiency. Ongoing treatment of comorbidities comprised the following: 95 mg metoprolol succinate, twice daily; 10 mg torasemide, once daily; 20 mg omeprazole, once daily; 2 mg glimepiride, once daily; 20 mg furosemide, once daily; and 80 mg febuxostat, once daily; combined with speech therapy and physiotherapy. Despite being treated with phenprocoumon (Marcumar®), the patient experienced an ischaemic stroke in 2016. The patient presented at Philippusstift Hospital, Hülsmannstrasse 17, 45355 Essen, Germany in August 2016 with the first clinical signs of stroke (hemiplegia, gaze turn to the right, anarthria, and National Institutes of Health Stroke Scale score of 13). Cranial computed tomography confirmed occlusion of the right middle cerebral artery in the distal M1 segment. Lysis of the thrombus using systematic treatment was not performed. Her measured international normalized ratio (INR) values during the months prior to stroke were within the therapeutic range of 2–3, but on the first day of hospitalisation due to stroke, her INR was found to have decreased to 1.25. During hospitalization, the patient’s INR values normalized ().
The patient’s sodium and potassium levels were within normal range throughout the hospital stay (sodium, 137–145 mmol/l; potassium, 3.92–4.82 mmol/l), and renal parameters were elevated but consistent with her present diagnosis of renal insufficiency. These values improved during hospitalization, and at discharge they matched those recorded at an outpatient appointment prior to the drop in INR and ischaemic stroke. Liver parameters were slightly pathological, but stable during hospitalization and consistent with the patient's previous morbidities (). Phenprocoumon (Marcumar®) treatment, together with physiotherapy and speech therapy, were maintained during hospital stay and continued following hospital discharge. At the latest follow-up, the patient was able to walk a distance of 80 m, had no further speech or swallowing difficulties, and had no further stroke symptoms.
A retrospective inquiry revealed that the patient received daily personal care from her daughter, and thus had a controlled daily routine, and did not reveal any significant changes in the personal behaviour of the patient or to therapy adherence that may have led to an ischaemic stroke, other than the consumption of 1.5 kg (3.3 lb) of hard-boiled candy liquorice in the days leading up to the stroke. In the present case, the liquorice candy contained liquorice extract, as well as ammonium chloride, sugar, flavouring, and colourant E153. As a result, an intensive literature review was performed to investigate whether the consumption of liquorice candy may explain a sudden fall in INR values prior to the stroke. The PubMed and Ovid Medline databases were searched for articles published between 2001 and 2021 using the terms ‘Liquorice’ AND/OR ‘phenprocoumon’ AND/OR ‘ischaemic stroke’ AND/OR ‘herbal substances’ AND/OR ‘cytochrome P450’ AND/OR ‘vitamin K antagonists’ AND/OR ‘PPARα’. Articles that focused on interactions between phenprocoumon and herbal substances in patients and animals were selected from the search results. Following review, articles that were most relevant in terms of quality and mechanistic insight into the interaction between phenprocoumon and liquorice were selected for discussion. The search was conducted by two independent investigators (HCR and SB).
The University Hospital Essen does not require institutional ethics review board approval for reporting individual cases or case series, thus ethics approval was not obtained. Written informed consent was obtained from the patient for publication of the case report, and the reporting of this study conforms to CARE guidelines.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [92, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Vascular disease history': True, 'Diabetes history': True}",8,8,8,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 92 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 7 + 1 = 8.
The patient's CHA2DS2-VASc Score is 8."
1059,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7938212-1,Extracted,"A 67-year-old Japanese male and current smoker had hypertension, diabetes mellitus, and old myocardial infarction, which was treated by percutaneous coronary intervention and anticoagulant therapy. He presented to our hospital with a complaint of sputum. The patient's chest X-ray showed consolidation in the left middle lower lung field. CT scans revealed consolidation with CT angiogram in the S3 and lingular segments of the left lung (Fig. ), and positron emission tomography-CT demonstrated abnormal accumulation at the same site. Sputum culture and sputum cytology were both negative. The serum levels of carcinoembryonic antigen and Sialyl Lewis X-i were slightly elevated to 9.4 ng/mL (normal range: 0–5.0 ng/mL) and 52 U/mL (normal value: ≤38 U/mL), respectively. The serum levels of squamous cell carcinoma antigen and cytokeratin 19 fragment (CYFRA) were normal. Then, either lung cancer including IMA or bacterial pneumonia or organizing pneumonia was suspected. On flexible bronchoscopy, radial EBUS performed in the B4 bronchus of the left lung showed an unusual finding: snowball-like hyperechoic nodules floating on a hypoechoic background (Fig. ). We performed bronchial wash and bronchial brushing within the lesion. The cytological specimens were not malignant. Then, the left upper lobe was surgically resected and ND2a-1 was performed. The section contained many various-sized cancer foci in the entire lobe. Thin mucinous and fibrinous exudates were seen in the alveolar spaces (Fig. ). Microscopic findings showed cancer cells with large columnar cytoplasm containing abundant intracytoplasmic mucin and proliferation of cells with small round-to-oval basal nuclei in a lepidic pattern (Fig. ). Periodic acid–Schiff (PAS)–Alcian blue staining showed neutral mucin in their cytoplasm (Fig. ). Immunohistochemically, cancer cells were positive for cytokeratin-7 (CK7) and MUC5AC; weakly positive for CK20 and MUC6; and negative for thyroid transcription factor 1, Napsin A, and p53 (Fig. ). The patient was diagnosed with primary pulmonary IMA (left upper lobe, 15 × 6 cm, T3N0M0 stage IIB). Molecular analysis of the tumour for epidermal growth factor receptor (EGFR) mutation, anaplastic lymphoma kinase (ALK) rearrangement, and PD-L1 expression was negative. Molecular analysis for KRAS mutation was not performed. After post-operative adjuvant chemotherapy, the disease recurred two years later, and although the patient was administered additional chemotherapy, he died.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [67, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 67 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
1060,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7346111-1,Extracted,"An 85-year-old man presented to our institution complaining of recurrent fever and a mitral regurgitation murmur. He has a past history significant for atrial fibrillation being treated with apixaban status post leadless pacemaker implantation and AV nodal ablation 15 days ago, hypertension, hyperlipidemia, obstructive sleep apnea on continuous positive airway pressure, diverticulosis and diverticulitis, dental caries, melanoma in situ, and persistent pulmonary coccidioidomycosis on fluconazole.
He underwent a transthoracic echocardiogram which showed normal left ventricular size and no wall motion abnormalities, LVEF of 56%, severe mitral regurgitation due to incomplete coaptation of the mitral valve leaflets (Figures and ), mild right ventricular enlargement, systolic dysfunction with visible apical right ventricular lead, mild tricuspid regurgitation, and no pericardial effusion. A transesophageal echocardiogram confirmed restricted mitral valve leaflets resulting in incomplete coaptation and severe mitral regurgitation (Figures and ). No vegetations were seen. Blood cultures ruled out endocarditis as the cause of fever, and he was later found to have non-Hodgkin's lymphoma.
His cardiac history is notable for atrial fibrillation diagnosed 10 years ago which was treated with atenolol and warfarin. Despite this treatment, he had recurrent episodes of paroxysmal symptomatic atrial fibrillation with a rapid rate requiring multiple emergency department visits and hospital admissions (). Given difficulty to control the rate, he underwent AV nodal ablation and leadless pacemaker insertion 15 days prior to current presentation with resultant LBBB on his electrocardiogram (ECG) post implantation (). His echocardiogram days before pacemaker insertion revealed only mild mitral regurgitation and normal coaptation of the mitral valve leaflets ().
Given the absence of degenerative mitral valve abnormality and no evidence of cardiomyopathy, his diagnosis of new-onset severe mitral regurgitation is the direct result of abnormal electrical conduction related to iatrogenic LBBB due to AV nodal ablation and single-chamber paced rhythm.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': False, 'age': [85, 'years'], 'Stroke': False, 'Diabetes history': False, 'Transient Ischemic Attacks History': False, 'sex': 'Male'}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 85 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
1061,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7206957-1,Extracted,"The patient was a 73 years old female who was leucodermic and who had a known personal history of arterial hypertension, type 2 diabetes mellitus treated with insulin, dyslipidemia, and cerebrovascular disease. The patient denied known drug allergies. She visited the emergency department for productive cough with purulent sputum and fever (38.1°C) with 5 days of evolution. The increase in inflammatory parameters determined analytically and the condensation of the left lower lobe determined by radiology favored the diagnosis of community-acquired pneumonia. She was prescribed amoxicillin/clavulanic acid, and the first administration was by the intravenous route in the emergency department. Approximately one minute after the drug was injected, the patient exhibited a generalized skin rash and an altered state of consciousness, with peripheral oxygen saturation in room air of 67%, blood pressure 87×50 mmHg, and heart rate of 110bpm. She was treated with 2mg clemastine and 200mg hydrocortisone and unfavorably progressed to cardiorespiratory arrest, with subsequent pulse recovery after advanced life support, orotracheal intubation and mechanical ventilation. Electrocardiography showed evidence of ST segment elevation in the inferior territory (). Urgent coronarography was performed, revealing diffuse atherosclerotic disease, with the absence of obstructive lesions (). Spontaneous resolution of ST-T segment elevation was also observed in the hemodynamic room. The following laboratory results were obtained: troponin I peak, 2,046µg/L; total creatine kinase (CK), 647U/L; and CK-MB, 55U/L. After contact, the family mentioned a previous allergy to penicillin, which the patient was unaware of. In the first 6 hours after shock, the tryptase level was 132ng/mL (strongly positive). Considering the context of being administered amoxicillin/clavulanic acid, the patient was diagnosed with Kounis syndrome type 2. The patient remained under mechanical ventilation for 29 hours, with good subsequent clinical evolution. She was discharged with a recommendation to avoid beta-lactam antibiotics and was referred for immunotherapy.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [73, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Vascular disease history': True, 'Diabetes history': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 73 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 6 + 1 = 7.
The patient's CHA2DS2-VASc Score is 7."
1062,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6515634-1,Extracted,"The patient was a 76-year-old woman with a history of left renal thromboembolism, hypertension, atrial fibrillation, hyperthyroidism, stroke, and AAA. Two years before admission, she had undergone EVAR with a stent graft for infrarenal aortic aneurysm, which led to right ostial RAO. Her left kidney was already atrophic due to previous renal thromboembolism, causing her to develop dialysis-dependent renal failure immediately after EVAR. Twenty-two days after EVAR, she underwent successful PTRA and stenting, and hemodialysis was discontinued (Fig. a). However, 2 years after EVAR, she developed acute onset of leg edema, anuria, and hypertension for 2 days, and thus went to the hospital. She was found to have significant worsening of renal function, with a serum creatinine level of 2.4 mg/dL, which had increased from a recent baseline level of 1.0 mg/dL. Acute kidney injury (AKI) due to renal artery in-stent restenosis was suspected, and she was admitted to the hospital. On day 2 of hospitalization, renal artery angiography demonstrated that the right renal artery could not be visualized, thereby confirming the diagnosis of AKI due to right renal artery in-stent occlusion. On the same day, PTRA for the right renal artery was attempted; however, it was unsuccessful as the guide wire could not pass through the ostium of the renal artery (Fig. b). Given that her renal function did not improve and anuria persisted, hemodialysis was initiated on the same day. She was transferred to our hospital for preparation of regular hemodialysis on day 9 of hospitalization.
On admission, she had a blood pressure of 202/109 mmHg, heart rate of 76 beats/min, and respiratory rate of 16 breaths/min. During examination, no extremity edema was noted, and no bruit was detected on abdominal auscultation. Her laboratory results at the time of admission were as follows: serum creatinine level, 9.5 mg/dL; estimated glomerular filtration rate (eGFR), 3.5 mL/min/1.73 m2; serum albumin level, 3.2 g/dL; serum potassium level, 3.8 mEq/L; serum calcium level, 8.6 mg/dL; serum phosphate level, 4.7 mg/dL; and hemoglobin level, 10.1 g/dL.
Anuric AKI persisted after she was transferred to our hospital. In addition to RAO, we suspected contrast-induced nephropathy or cholesterol emboli as a differential diagnosis. However, these were unlikely as she developed AKI before contrast medium was administered and before the intravascular catheter procedure was performed; moreover, there were no signs of peripheral atheroembolism. Her high plasma renin activity (10.7 ng/mL/h, with a plasma aldosterone level of 140 pg/mL), which was tested to determine the cause of hypertension, raised the suspicion that she had a minimally but significantly perfused right kidney. Doppler ultrasonography revealed a renal interlobular artery flow inside the right kidney, indicating that the perfusion of the kidney was sustained, at least at a low level. Renal mercaptoacetyltriglycine (MAG-3) scintigraphy revealed that the right kidney had stained slowly and MAG-3 had not washed out even at 66 min post-injection. The absence of MAG-3 washout meant that the function of the kidney decreased severely, which did not rule out contrast induced AKI, but at least indicated that while renal perfusion was sustained, it was not sufficient to sustain the GFR (Fig. a). Although we initially planned to create an arteriovenous fistula for vascular access for permanent hemodialysis, the results of these renal imaging studies led us to reconsider that the AKI may be reversible if the renal artery was revascularized. However, a second attempt of PTRA was considered challenging, given that the renal artery was almost completely occluded. With no prior experience performing hepatorenal bypass, a transplant surgeon on our team considered kidney AutoTx to be a feasible alternative; therefore, kidney AutoTx was performed on day 25 of hospitalization. The renal artery and vein were anastomosed to the external iliac artery and vein, respectively. Cold and warm ischemia time of the right kidney were 84 and 7 min, respectively. After declamping the external iliac artery, the kidney perfused well, except for the upper one-fifth portion, which appeared to be perfused by an upper polar renal artery. Hence, we decided to anastomose the upper polar renal artery to the inferior epigastric artery; this successfully perfused the upper kidney region. Intraoperatively, the patient started passing urine. For the first 24 h postoperatively, her urine output was 2.2 L, and hemodialysis was discontinued (Fig. ). Her serum creatinine level decreased to 1.02 mg/dL by postoperative day 22, which was almost equivalent to her baseline creatinine level. Her hypertension improved, and the dose of nifedipine was successfully reduced. Her 0-h kidney biopsy during the surgery showed only mild tubular injury and no tubular necrosis. Of 24 glomeruli, 11 showed global glomerular sclerosis, and the remaining 13 exhibited no acute changes. Mild arteriosclerosis with only one cholesterol embolism was observed. Thus, no histological changes were noted that could account for prolonged ischemia leading to anuric AKI (Fig. ). The patient was discharged on day 42 of hospitalization, and her kidney function remained stable for 2 years, with a creatinine level of 1.03 mg/dL. Four months after surgery, a repeat renal MAG-3 scintigraphy showed that the transplanted right kidney at the right iliac fossa stained smoothly, and MAG-3 washed out 15 min after injection, indicating that renal perfusion and glomerular filtration has recovered (Fig. b).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [76, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': True, 'Vascular disease history': True, 'Stroke': True, 'Diabetes history': False, 'Transient Ischemic Attacks History': False}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
1063,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-41,Extracted,"A 73-year-old woman is brought to the physician by her son because of increasing forgetfulness over the past 2 years. Initially, she used to misplace keys and forget her dog's name or her phone number. Now, she often forgets about what she has seen on television or read about the day before. She used to go for a walk every morning but stopped one month ago after she became lost on her way back home. Her son has prevented her from cooking because she has had episodes of leaving the gas stove oven on after making a meal. She becomes agitated when asked questions directly but is unconcerned when her son reports her history and says he is overprotective of her. She has hypertension, coronary artery disease, and hypercholesterolemia. Current medications include aspirin, enalapril, carvedilol, and atorvastatin. She is alert and oriented to place and person but not to time. Vital signs are within normal limits. Short- and long-term memory deficits are present. Her speech rhythm is normal but is frequently interrupted as she thinks of words to frame her sentences. She makes multiple errors while performing serial sevens. Her clock drawing is impaired and she draws 14 numbers.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [73, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 73 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
1064,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-8957,Extracted,"A 62-year-old man presents to the emergency department with a 2-day history of fatigue, exertional dyspnea, and the sensation of his heartbeat roaring in the ears. He informs you that he recently had an acute upper respiratory infection. He is a retired car salesman, and he informs you that he and his partner enjoy traveling to the tropics. His medical history is significant for gout, hypertension, hypercholesterolemia, diabetes mellitus type II, and multiple basal cell carcinomas on his face and neck. He currently smokes 1 pack of cigarettes per day, drinks a 6-pack of beer per day, and denies any illicit drug use. His vital signs include: temperature 36.7°C (98.0°F), blood pressure 126/74 mm Hg, heart rate 111/min, and respiratory rate 23/min. On physical examination, his pulses are bounding, his complexion is pale, and scleral icterus is apparent. The spleen is moderately enlarged. Oxygen saturation was initially 81% on room air, with a new oxygen requirement of 8 L by face mask. Laboratory analysis results show a hemoglobin level of 7.1 g/dL and elevated total bilirubin.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [62, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': False, 'Diabetes history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 62 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 1 + 1 = 2.
The patient's CHA2DS2-VASc Score is 2."
1065,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4793099-1,Extracted,"A 64-year-old woman was brought to ED by a family member for generalized weakness for 10 days associated with epigastric pain and discomfort. Patient also reported having a fall one week prior to her presentation to ED. She noticed to have dark stools and red urine within few days of the fall.
Her medical history was significant for atrial fibrillation on warfarin, COPD, active smoking, and hypertension. Additional history of laryngeal cancer was present, which was treated with radiotherapy and chemotherapy four years ago. As a followup after presenting with hoarseness of voice three years ago, recurrent malignancy was ruled out with vocal cord biopsy. No personal or family history of liver disease was identified. There were no changes to her medications, which included warfarin, amlodipine, metoprolol, aspirin, and atorvastatin.
In ED, patient was tachycardic with a pulse of 160/min, afebrile, and normotensive. The patient had no evidence of acute distress or external injury. She had right subconjunctival hemorrhage, and mucous membranes were dry. Heart examination was significant for tachycardia with no murmurs, rubs, or gallops. Lungs had good bilateral air entry with no wheezing, crackles, or crepitations. Abdominal examination revealed soft but mildly tender epigastrium with normal bowel sounds, whereas rectal examination showed stool mixed with dark blood. She was alert and oriented to time/place/person but appeared slightly lethargic, no focal neurological deficits on neuro examination were found.
Laboratory studies revealed anemia with hemoglobin concentration of 7.2 mg/dL with baseline values around 12 mg/dL less than 3 months ago, leukocytosis with white blood cell count of 15 k/uL, normal platelet count of 232 k/uL, prothrombin time (PT) of 169 seconds, partial thromboplastin time (PTT) of 92 seconds, and unrecordable INR. Chemistry showed prerenal azotemia with blood urea nitrogen levels of 54 mg/dL, creatinine of 1.3 mg/dL, bicarbonate of 10 mEq/L, and normal serum electrolytes. Liver function tests (LFTs) showed hypoalbuminemia with albumin of 2.8 g/dL, transaminitis with alanine aminotransferase (ALT) of 420 U/L, aspartate transaminase (AST) of 973 unit/L, and alkaline phosphatase (ALP) of 435 unit/L. Other significant laboratory values were elevated lactic acid to 13.3 mmoles/L, lactate dehydrogenase (LDH) level of 8003 unit/L, elevated troponin of 0.206 ng/mL, creatine kinase (CK) of 872 unit/L, and creatine kinase MB (CKMB) of 40 ng/mL with MB% of <5. Please refer to for laboratory values during the hospitalization. Hepatitis A, B, and C serologies were negative and serum acetaminophen level was <15 ng/dL.
Her INR two weeks prior to her presentation was 2.8 with normal LFTs four weeks prior to admission. She had been on stable dose of warfarin for the past 1.5 years. Please refer to for warfarin dosage and INR levels in the past one year.
Initial chest X-ray () did not show any evidence of an acute pulmonary edema or pneumonia. Computed Tomography (CT) scan of the abdomen () showed markedly enlarged abnormal heterogeneous liver suggestive of an infiltrative process with no obvious free fluid or evidence of significant bleeding. CT scan of the head was negative for acute intracranial hemorrhage, infarction, or masses.
The patient had been given vitamin K and multiple transfusions of Fresh Frozen Plasma (FFP) to reverse coagulopathy.
After admission to intensive care unit (ICU), there was a rapidly progressive decline in the patient's clinical status. She developed acute respiratory failure requiring mechanical ventilation, hypotension necessitating vasoactive agents, and liver failure with worsening LFTs. In addition, she progressed to worsening of coagulopathy, elevated cardiac markers, and lactic acidosis. Her multiorgan failure did not improve with aggressive resuscitative measures, culminating in cardiac arrest and death.
Autopsy revealed that patient's liver weighed 4950 grams (Figures and ), and it was enlarged with intact smooth capsule with soft tan brown parenchyma which was nearly completely replaced by multiple discrete and near-confluent sheets of white masses, some with central punctate hemorrhage, ranging in size from approximately 0.3 to 3 cm in the greatest dimension. These tumor masses replaced nearly 90% of the total liver volume. Histopathology (Figures and ) showed poorly differentiated squamous cell carcinoma secondary to metastasis. Review of prior pathology from the time of LC surgery (Figures and ) showed moderately differentiated squamous cell carcinoma, which was histopathologically consistent with the observed metastasis in the liver.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [64, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 64 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
1066,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4370301-1,Extracted,"A 74-year-old man was presented to the emergency department with epigastric pain, asthaenia and drowsiness. He had a past medical history of chronic heart failure, chronic subdural haematoma, atrial fibrillation and chronic kidney disease stage 3b and received dabigatran 75 mg twice daily. He took his last dose of dabigatran 7 h before the admission. He was somnolent but arousable, confused with Glasgow Coma Scale 14, haemodynamically unstable with hypotension (95/51 mmHg), mottled skin and tachycardia (100 bpm). Mucocutaneous pallor was noted but without external bleeding. First biology results found anaemia with haemoglobin 7 g/dL (versus 11.5 g/dL two weeks before) and creatinine 276 µmol/L (versus 150 µmol/L usually) i.e. acute kidney injury stage 1 KDIGO. Plasma coagulation was abnormal with prothrombin ratio (PR) 28% and activated partial thromboplastin time (aPTT) 66 s. Blood dabigatran level was 534.9 ng/mL. Brain computed tomography found chronic subdural haematoma without acute bleeding. The patient received 3 packed red blood cells and 1000 mL of intravenous fluids (sodium chloride 0.9%). Upper gastrointestinal endoscopy was realized, finding stomach ulcer with acute bleeding. He was treated by local epinephrine injection and clipping with good efficiency. Continuous infusion by proton pump inhibitor was started (omeprazole 8 mg/h). He did not receive procoagulants drugs. The patient was hospitalized in ICU for RRT.
In ICU, a dialysis catheter (Blue FlexTip Catheter, 2 lumen, 16 cm, 12 Fr - ARROW®) was inserted in the right internal jugular vein. The patient was started on 4 h of HDF on PRISMA FLEX System (GAMBRO®) with a high-flux dialysis filter (Multiflow 60 AN69HF 0.60 m2 polyacrylonitrile hollow-fibre membrane). The blood (Qb), dialysate (Qd) and ultrafiltration (Quf) flow rates were 200 mL/min, 1 L/h and 3 L/h, respectively. Substitution fluids were delivered in predilution (1 L/h) and in postdilution (2 L/h) with zero net ultrafiltration. Dabigatran levels were sampled every 20 min in blood (inlet line) and effluent (ultrafiltration and dialysate volume collected every 20 min). Dabigatran level was measured by validated liquid chromatography tandem mass spectrometry method. The patient remained awake and alert for the entire session, without external bleeding. Diuresis was 250 mL on 8 h with residual clearance of creatinine measured at 14 mL/min. Dabigatran plasma concentration was 325.3 ng/mL at the beginning of RRT. It decreased gradually during the session to reach 160.5 ng/mL after 4 h (Figure ). Decrease of dabigatran during HDF was of 25% at 2 h and 51% at 4 h. Conversely, the effluent level of dabigatran increased to reach 138.5 ng/mL at the end of the session. In parallel, aPTT decreased from 180 s at the initiation of HDF to 57.8 s 4 h after the session and PR increased from 30 to 41%. The patient did not receive any drugs that could have interfered with clotting time.
Mean haemodiafiltration clearance of dabigatran (Cl(hdf)) was 48 mL/min. Cl(hdf) was measured every 20 min using the recovery method according to the following equation Cl(hdf) = EV/P where E = effluent concentration of dabigatran, V = effluent rate and P = dabigatran plasma concentration. The half-life of dabigatran was 4.8 h. Only the terminal half-life was determined according to the following equation T1/2 = ln(2)/lambda(z) where lambda(z) is the slope of the terminal portion of the log transform concentrations versus time. This was obtained by unweighted linear regression of at least three concentrations.
A rebound of concentrations of dabigatran was observed with a plasma level at 195.7 ng/mL 2 h after the end of the HDF session. Six hours after the HDF session, dabigatran concentration decreases to reach 11 ng/mL probably due to renal recovery. Because of renal recovery, clotting time improvement and decrease of dabigatran levels, no other dialysis session was realized.
The following day, haemoglobin was 8.6 g/dL. Control endoscopy was realized with a new clipping because of minimal bleeding. Renal function recovered with serum creatinine 168 µmol/L. Coagulation parameters continued to improve with PR 76% and aPTT 37 s at the patient's discharge. After cardiologic consultation, dabigatran was discontinued, replaced by aspirin because of a major risk of bleeding compared with the thromboembolic risk. The patient was discharged to home after 8 days.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [74, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 74 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
1067,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4674994-1,Extracted,"During an outpatient cosmetic procedure a 60-year-old male developed the sudden onset of confusion, rigors, tachypnea, and hypotension. The procedure, liposuction of the neck, lasted approximately 1 hour and was performed without generalized anesthesia. The only medications administered were local anesthesia with lidocaine, intravenous fluids, and 2 days of preoperative oral cephalexin. Immediately following the procedure, the patient developed rigors, chills, and nausea prompting concern of an adverse reaction or complication. The outpatient clinic transferred him to our emergency department via ambulance where he was found to be encephalopathic and hypotensive. His medical history indicated paroxysmal atrial fibrillation, cerebrovascular accident with mild dysarthria, and a bicuspid aortic valve. The patient’s medications included weekly testosterone injections, pregabalin, sildenafil, celecoxib, diazepam, esomeprazole, atorvastatin, dabigatran, and escitalopram. He had no reported drug allergies. Review of systems was negative for neck and chin pain, pruritus, or dyspnea. On examination, the patient was tachycardic, tachypneic, febrile, and diaphoretic. The chin and neck area exhibited a submental incision. Incisional edema, erythema, and tenderness were deemed appropriate for the immediate postprocedural time frame. Pulmonary auscultation revealed no abnormalities, and skin and mucosal exam revealed no rashes. Essential laboratory values () were consistent with severe sepsis and multiorgan dysfunction. Initial electrocardiogram revealed atrial fibrillation with rapid ventricular response, which converted to sinus tachycardia following initial resuscitation. Computed tomography of the neck revealed small subcutaneous air collections without focal abscess. Computed tomography pulmonary angiography did not reveal evidence of pulmonary emboli. He was treated for presumed septic shock with 4 liters of normal saline. Central venous access was established and a norepinephrine infusion was initiated. Vancomycin and meropenem were administered empirically after blood and urine cultures were drawn. On transfer to the intensive care unit, his mentation improved and he was able to confirm that he had been asymptomatic prior to the procedure. Partial lactic acid clearance was documented after initial resuscitation (). Aspirin therapy was continued and stress dose corticosteroids were administered.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [60, 'years'], 'Congestive Heart Failure': False, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 60 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 0 + 2 = 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
1068,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4192411-1,Extracted,"A 76-year-old male (preoperative logistic EuroSCORE 9.92%) underwent an uneventful TAVR with a 29 mm CoreValve for severe symptomatic AS in January 2012 ( and , , , , ). He had hypertension and atrial fibrillation. He also had a VVI pacemaker implanted for sick sinus syndrome in 2002. Furthermore, he suffered from ischemic heart disease which had been treated by percutaneous coronary intervention to mid-left anterior descending coronary artery 7 years before. Although the patient's logistic EuroSCORE was relatively low, he and his family strongly preferred TAVR than SAVR. Before the procedure, transthoracic echocardiography demonstrated severe AS (peak/mean gradient 90/55 mmHg, aortic valve peak velocity 4.74 m/s, aortic valve area 0.73 cm2 by continuity equation) with normal left ventricle (LV) function (ejection fraction 69%) and there was no pulmonary hypertension. He was discharged 7 days after the procedure with only mild paravalvular aortic regurgitation (AR).
He was readmitted 2 months after TAVR for fever, dyspnea and mild confusion. On meticulous history taking, he had periodontitis, for which incision and drainage of the abscess was performed 1 month prior to admission at a nearby hospital.
Inflammatory markers including white blood cell count (19700/mm3) and C-reactive protein level (11.54 mg/dL) were markedly elevated. Simple chest X-ray revealed bilateral pleural effusion () and electrocardiogram showed atrial fibrillation with rapid ventricular response and left bundle branch block (). Transthoracic echocardiography showed a normal sized LV with normal systolic function. However, severe mitral regurgitation was noted just beneath the strut of the bioprosthesis (, ). Transesophageal echocardiography was performed without delay, which demonstrated a large mobile vegetation attached to the anterior mitral leaflet and severe mitral regurgitation due to multiple perforations of the mitral valve leaflet. Abscess was also noted at the aortomitral continuity (, ). The bioprosthetic aortic valve function was normal.
We performed brain imaging studies for evaluation of altered mentality. Both intracerebral and subarachnoid hemorrhage was detected on brain computed tomography imaging (). Vancomycin, gentamicin and rifampin were started without delay under the diagnosis of IE. Streptococcus anginosus was identified on all three separate blood cultures.
The patient and his family members refused surgical intervention because of the high risk. The patient died 4 days after hospital admission due to refractory sepsis. The autopsy was refused.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [76, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
1069,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7065311-1,Extracted,"A 43 years old man was admitted to our Internal Medicine Unit on April 2018 with a 7 days history of low-grade fever, bilateral epistaxis and abdominal pain.
His personal medical history showed that 9 years earlier he was hospitalized for subjective dizziness and syncope. Brain MRI showed multiple bilateral posterior parietal hyperintense gliotic lesions, while transthoracic echocardiogram revealed a free floating mass attached to the cusp of the mitral valve with moderate mitral regurgitation. A subsequent transesophageal echocardiogram confirmed the presence of vegetation on mitral valve; a mechanical valve replacement was then performed and a long-term anticoagulant therapy with Acenocoumarol was started with INR target between 2.5–3.5 and TTR target of 70%. The histological analysis of the native valve showed a non-bacterial thrombotic endocarditis. During the recovery, a thrombocytopenia (97,000/mm3—n.v. 179–373) was found but no other diagnostic investigation was carried out.
At the age of 41 years, he was admitted to a Neurosurgery Unit for generalized seizures and subsequent head injury. Brain computed tomography (CT) showed a right subdural hematoma and electroencephalography (EEG) background activity was rather irregular, but did not reveal any epileptic abnormalities during wakefulness. The patient was only managed with antiepileptic drugs (phenobarbital). During the hospitalization, a low count of platelet (57,000/mm3) was observed and, after haematological evaluation, immune thrombocytopenia (ITP) was diagnosed and steroid therapy (methylprednisolone) was started and extended for 10 days with satisfactory clinical outcome. During the haematological follow-up, courses of therapy with methylprednisolone lasting 7–10 days were administered, taking into account the platelet count.
He had a family history of diabetes and hypertension, he was allergic to aspirin and at admission to our clinical unit he was taking therapy with ramipril, carvedilol, phenobarbital and acenocumarol.
At admission to our clinical unit the physical examination revealed a diffused reduction of vesicular murmur with right basal crackles, ache and pain in the upper abdominal quadrants and splenomegaly.
Laboratory findings were as follows: platelets (PLT) 25 × 103/mm3 (n.v. 179–373), prothrombin time (PT)—INR 4,58 (n.v. < 1.2), activated Partial Thromboplastin Time (aPTT) ratio 2.54 (n.v. < 1.20), Amylase 104 U/L (n.v. 8–53), Lipase 1399 U/L (n.v. 73–393), gamma glutamyl transferase (GGT) 393 mU/mL (n.v. 15–85), C-Reactive-Protein (CRP) 149 mg/L (n.v. < 2.9), Lactate Dehydrogenase (LDH) 333 mU/mL (n.v. 87–241); haemoglobin, white blood cell (WBC), serum urea, creatinine, electrolytes, glycaemia, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and bilirubin levels were all within the normal range. Microbiological tests (i.e. Toxoplasma, CMV, HSV, EBV, HIV, HBV, HCV) were all negative and neoplastic markers were within the normal values. Peripheral blood smear showed only megaplatelets.
Workup for autoimmune disorder revealed high titre of anti-β2 glycoprotein I (β2GPI) IgG (113.4 U/mL) and anti-Cardiolipin (aCL) IgG (> 640 U/mL) antibodies, and a low titre of anti-β2GPI and anti-aCL IgM (26.7 U/mL and 24.3 U/mL, respectively); whereas, antiplatelets antibody, Antinuclear antibody, anti ds-DNA, Anti-Mitochondrial antibody (AMA), Antineutrophil cytoplasmic antibody (ANCA), Anti-Liver-Kidney Microsomal Antibody (LKM) and Anti-Smooth Muscle Antibody (ASMA) were negative.
Lupus Anticoagulant (LAC) was performed using Silica Clotting Time (SCT) and Diluted Russell Viper Venom Time (dRVVT) test in three steps (screening, mixing and confirmatory); positive results confirmed the presence of inhibitors of hemostasis, although false positive test may result from interference by concurrent anticoagulant therapy. Anyway, given the presence of both aCL and a β2GPI antibodies, the test was not retested during anticoagulation suspension.
The ultrasound abdomen exam was normal, except of splenomegaly (14 cm). Total body CT confirmed splenomegaly and showed right lower and middle lobe pneumonia; pelvic and other abdominal organs were normal.
Based on the multiple previous courses of therapy with steroid that may facilitate pseudomonas lung infection, a dual antibiotic therapy with piperacillin/tazobactam and levofloxacin was given with sudsequent pneumonia resolution.
The anticoagulation therapy was carried on and steroid therapy with methylprednisolone was set up with increase of platelet count (61 × 103/mm3). Supported therapy for the pancreatic insult was also administrated with subsequent normalization of pancreatic enzymes.
On the basis of medical history, clinical and laboratory features, despite the lack of confirmed clinical criteria, and ruling out associated autoimmune diseases, diagnosis of primary antiphospholipid syndrome was made.
At 3 month follow-up, the patients was free of symptoms; CRP, LDH, GGT were restored at normal range; platelet count was 57 × 103/mm3; the presence of Anti-β2GPI antibodies IgG (63.7 U/mL—middle titre) and IgM (20.5 U/mL—low titre), aCL antibodies IgG (> 640 U/mL—high titre) and IgM (26.7 U/mL—low titre) was confirmed.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [43, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': True, 'Thromboembolism history': True, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 43 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
1070,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6732194-1,Extracted,"A 75-year-old Hispanic woman with extensive comorbidities including coronary artery disease, end-stage renal disease on dialysis, paroxysmal atrial fibrillation on warfarin therapy, presented with exertional chest pain for 1 month. Her chest pain was episodic, lasted for a few minutes, was triggered by activities, and alleviated by resting; it was associated with shortness of breath and leg swelling. She takes amlodipine 5 mg daily, losartan 25 mg daily for her hypertension, carvedilol 25 mg twice daily, aspirin 81 mg and atorvastatin 80 mg daily for coronary artery disease, as well as warfarin 6 mg daily for atrial fibrillation. She has a surgical history of abdominal aortic aneurysm repair, cholecystectomy, and arteriovenous fistula on her left arm. Her family history is positive for hypertension and diabetes. She was a former smoker of tobacco of half a pack a day for 30 years. She drinks alcohol occasionally. She was a housewife and lives with her son.
On admission, she had normal temperature of 36.89 ºC (98.4 ºF), elevated blood pressure of 155/75 mmHg, pulse rate of 73 per minute, respiratory rate of 19 per minute, and saturation of 95% on room air. A physical examination was significant for bibasilar lung crackles and bilateral lower extremity pitting edema. A neurologic examination was unremarkable. A complete blood count showed hemoglobin of 6.9 g/dL with normal white cell count and platelets. A basic metabolic panel revealed elevated creatinine of 3.78 and was otherwise unremarkable. Troponin was noted to be mildly elevated at 0.051 ng/mL, which normalized the next day. Brain natriuretic peptide (BNP) was also elevated at 1908.7 pg/mL. An electrocardiogram demonstrated normal sinus rhythm with a rate of 70 beats per minute. A chest X-ray showed mild pulmonary vascular congestion with no focal consolidation (Fig. ). A transthoracic echocardiogram was performed which revealed an ejection fraction of 55% with no evidence of focal wall motion abnormality.
A presumptive diagnosis of unstable angina was made and a transradial cardiac catheterization was planned. Warfarin was held before the catheterization and pre-procedure international normalized ratio (INR) was found to be 1.7. Establishment of access to her right radial artery was attempted with the use of ultrasound guidance and was successfully performed on the first attempt. However, she was noted to have a slight radial artery spasm during catheter manipulation. She was found to have 70–80% stenosis in distal left coronary circumflex artery and percutaneous transluminal coronary angioplasty using Guidezilla™ (Boston Scientific) 5 French catheter was performed. A Synergy™ (Boston Scientific) drug-eluting stent was then successfully placed. The procedure was not complicated by any difficult access or accidental catheter advances. A TR band (Terumo Corporation) was applied at the puncture site for 5 hours after the procedure and was then removed. Warfarin was resumed after the procedure and dual antiplatelet therapy of aspirin 81 mg daily and clopidogrel 75 mg daily was also started.
No sign of bleeding or swelling was noticed during the first day after the procedure. On the second day after the procedure, our patient developed significant right forearm swelling (Fig. ). An examination revealed a hard swollen mass that was tender to palpation. No bruits were appreciated. The swelling was initially treated with bandage compression, but there was no improvement. Doppler ultrasound was then performed which demonstrated a pseudoaneurysm from the radial artery located at the puncture site. The pseudoaneurysm measured 2.05 × 0.68 cm, with a neck size of 0.25 cm (Fig. a). A second more proximal pseudoaneurysm at the mid-forearm was also noted with a size of 0.70 × 0.60 cm and a neck size of 0.09 cm (Fig. b).
Vascular surgery was consulted for possible surgical intervention. Our patient was deemed to be a poor surgical candidate for surgical repair due to her comorbidities. A trial of compression therapy was recommended. Starting the second day after percutaneous coronary intervention (PCI), TR band compression was reapplied daily with the guidance of ultrasound. Each session lasted 2 hours and TR band was then removed. Distal pulse oximetry and Doppler ultrasound were obtained to ensure the patency of the radial artery during compression. Warfarin was held after the discovery of the pseudoaneurysms. Dual antiplatelet therapy was continued given the presence of coronary drug-eluting stent. A series of vascular Doppler ultrasounds were performed to evaluate if the pseudoaneurysm was still present. The treatment was well tolerated by our patient. After 2 days of TR band compression, the distal pseudoaneurysm thrombosed completely (Fig. c). After 4 days of daily TR band compression, the proximal pseudoaneurysm was noted to be partially thrombosed. She was discharged with a plan of out-patient follow-up with vascular surgery. Four days after discharge, the proximal pseudoaneurysm was found to have spontaneously thrombosed during the out-patient visit (Fig. d). No surgical intervention was required or performed. Warfarin was eventually resumed after closure of both pseudoaneurysms. A follow-up visit 7 months after discharge showed no recurrence of pseudoaneurysm. A timeline of the events is shown in Figure .",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [75, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 75 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
1071,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5562676-1,Extracted,"A 56-year-old woman with a history of atrial fibrillation, hypertension, congestive heart failure, and mechanical mitral valve repair following rheumatic heart disease on warfarin was transferred to our hospital after being found unresponsive. On arrival, her blood pressure was 141/66. She was awake and able to move all four extremities to command; however, she had no verbal output, and her Glasgow Coma Scale (GCS) was 10 (E = eye opening 3, V = verbal response 1, and M = motor response 6).
A head CT (Figure A) demonstrated a small ICH in the left periventricular white matter with significant intraventricular blood. CT angiogram of the head (Figure B) was suggestive of Moyamoya-like vasculopathy involving the left internal carotid artery (ICA) summit. Laboratory testing showed an INR of 3.6. She received intravenous vitamin K and prothrombin complex concentrate for INR reversal.
Following intubation for airway protection due to declining mental status, an EVD was placed; however, drainage ceased within 1 h of placement due to obstruction of the catheter with blood. On repeat clinical exam off sedation, the patient was not following commands with a GCS of 4T. She had fixed, non-reactive pupils at 3 mm; absent corneal, oculocephalic, cough, and gag reflexes; no spontaneous breaths; and slight flexion to painful stimuli in the upper extremities. Repeat head CT showed worsened IVH (Figure C) with hydrocephalus and apparent compression of the midbrain (Figure D).
The patient’s husband was immediately informed that these developments were concerning for a devastating functional outcome, if she were to survive. Consequently, no further attempt was made to adjust the EVD for improved drainage or place a second EVD. Her code status was changed to “do not resuscitate” in the evening of admission. Her husband requested time to consider full comfort measures as goals of care, while continued routine ICU care would be pursued. Given the non-functioning EVD, obtained ICP readings were deemed inaccurate and thus not further acted upon through EVD manipulation or osmotherapy.
However, the patient’s clinical exam spontaneously improved over the following 48 h, while supportive ICU care was continued. She began overbreathing the ventilator and regained reactive pupils, cough, and gag reflexes, with absent, but eventual return of corneal and oculocephalic reflexes. On motor exam, she extended in the right arm and leg, but moved the left arm spontaneously and withdrew in both left arm and leg.
Shortly after these observations, her EVD then started to drain spontaneously, without intervention, again approximately 48 h after initial placement. Based on this clinical improvement, the patient’s husband requested that her code status be changed back to “full resuscitation.” Repeat head CT on postbleed day 4 (Figure E) showed improved hydrocephalus, although still with ventricles “casted” from IVH. A more aggressive care approach was pursued at that time, and a left-sided EVD was placed.
A diagnostic cerebral angiogram confirmed a Moyamoya syndrome characterized by (1) chronic occlusion of the left supraclinoid ICA above the origin of the anterior choroidal artery, (2) a meshwork of small vessels replacing the ICA summit, proximal ACA, and proximal MCA, and (3) robust collaterals supplying the L MCA vascular territory via a widely patent anterior communicating artery and leptomeningeal collaterals derived from the distal L PCA (Figures F,G). No definite, angiographically demonstrable culprit lesion was demonstrated. However, in light of these findings, empiric administration of intraventricular tissue plasminogen activator was deferred, given an unknown further risk of intracranial hemorrhage in the setting of the patient’s unique cerebrovascular anatomy. The patient was extubated safely 1 week after admission.
At the time of discharge to inpatient rehabilitation, 3 weeks posthemorrhage, the patient was able to follow commands intermittently and could move the right arm in the plane, the right leg with flicker movement, and the left arm and leg antigravity.
Figure H shows a surveillance head CT at 3 weeks without residual intraventricular blood.
At the time of outpatient follow-up at 12 weeks, the patient was alert, communicated well, was able to eat by herself, and required two-person assist for walking. Neurologic examination showed her to be partly oriented, with full ability to follow commands and no evidence of aphasia. On cranial nerve testing, she could count fingers in central visual fields only. Gaze was dysconjugate with a right third nerve palsy and bilateral restricted upgaze. The remaining cranial nerves were intact. Motor exam showed near full strength in the upper extremities and strength of 4 of 5 in the lower extremities. Sensory and cerebellar functions were intact. Her mobility had further improved, and at 9 months, she is able to ambulate with a rolling walker and requires one-person assist at times.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [56, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Diabetes history': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 56 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
1072,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4438392-1,Extracted,"A 67-year-old Caucasian male, with previously normal kidney function [serum creatinine concentration (sCr) 1.0 mg/dL (88 μmol/L), eGFR 78 mL/min/1.73 m2 using the CKD-EPI equation, and no proteinuria on urinalysis], presented with AKI and 1 week of gross hematuria. The past medical history included coronary disease and atrial fibrillation. He denied family history of kidney disease, but did have one previous episode of ‘dark-colored urine’ 2 months prior that resolved spontaneously.
Medications included aspirin 81 mg daily, sotalol, omeprazole, lisinopril and dabigatran 150 mg twice daily. One week prior to presentation, warfarin had been held for 3 days and then dabigatran initiated, at request of the patient. Aspirin was continued for cardioprotection. His blood pressure was 140/76 mmHg. Physical examination was unremarkable. SCr was 5.5 mg/dL (420 μmol/L) with no evidence for systemic hemolysis. The international normalized ratio (INR) was 1.6 with a prothromboplastin time of 62 s. He was initially managed with i.v. fluids, and anticoagulants were held. A serological workup, including antineutrophilic cytoplasmic antibody (ANCA), cryoglobulins, C3/C4, serum/urine protein electrophoresis, and viral serologies, was negative. Because hematuria persisted and creatinine continued to rise, he underwent kidney biopsy.
The biopsy showed extensive, diffuse tubular injury with nuclear dropout, sloughing of brush border membrane and cytoplasmic reabsorption droplets containing eosinophilic proteinaceous material (A). There were also several, large intratubular RBC casts. The glomeruli showed capillary congestion and mesangial matrix expansion and hypercellularity (B). The vessels were unremarkable and a Prussian-Blue stain showed focal positivity in 1–2% of tubular profiles. Immunofluorescence studies showed 2–3+ mesangial positivity for IgA (C) and 1+ mesangial positivity for C3. IgG, IgM and C1q stains were negative. There was no significant interstitial infiltrate. Ultrastructural evaluation showed segmental foot process effacement and large mesangial immune complex deposits (D). The proximal tubular epithelial cells showed cytoplasmic reabsorption droplets containing heme-proteins and intratubular granular casts (E). Immunohistochemistry revealed strong, diffuse positivity for CD163 (F).
The patient had previously had mild undiagnosed IgA nephropathy that was found on biopsy but in the setting of a high dose of dabigatran and aspirin he developed massive hematuria (likely predisposed by IgA nephropathy) and acute tubular necrosis from the direct toxic effect of heme pigment in the proximal tubular cells. The patient's creatinine stabilized at 6.0 mg/dL (530 μmol/L), and he was treated with normal saline to encourage diuresis. He was discharged home and his creatinine improved over a 3-month period to 1.8 mg/dL (160 μmol/L). He eventually resumed warfarin without evidence of hematuria or AKI.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [67, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False, 'Transient Ischemic Attacks History': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 67 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
1073,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6882214-1,Extracted,"A 66-year-old Caucasian male was referred for colonoscopy having had a positive faecal occult blood test (FOBT) as part of the national bowel cancer screening programme performed in the UK. At screening the patient was asymptomatic and denied rectal bleeding. He was not anaemic.
The endoscopist noted a past medical history of ischaemic heart disease, systemic lupus erythematosus, atrial fibrillation and hypercholesterolaemia, for which his medication included Dabigatran. The patient was a retired labourer, normally fit and well with a performance status of 1.
Colonoscopy was carried out using Olympus standard colonoscope with CO2 insufflation and pump irrigation containing simethicone, under Entonox gas. At intubation an unusual vascular pattern encompassing the entire rectum up to the rectosigmoid junction was noted. At this point a decision was taken with the patient to proceed with full colonoscopy. The lesion was characterised by confluent circumferential purple discolouration indicating venous blood supply, with heaping up of the mucosa involving the entire rectum (see Figs. & ) and rectosigmoid junction. There was a well demarcated border with normal mucosa in the distal sigmoid colon (see Fig. ). No mucosal ulceration or active bleeding was seen.
Macroscopically, the pattern within the rectum resembled extensive rectal varices, although the patient did not have liver disease or venothromboembolic disease and was not known to have any cutaneous or visceral vascular malformation.
The patient proceeded to axial imaging with computed tomography (CT) to further evaluate this abnormality. The CT demonstrated a considerably thickened rectosigmoid wall with multiple small rounded punctate calcifications seen within it (see Fig. ). There was no evidence of other visceral involvement or cutaneous lesions.
To further characterise the CT findings a magnetic resonance (MR) scan of the pelvis was performed which demonstrated extensive diffuse thickening of the rectum and lower sigmoid with intermediate to high T2 signal, and an internal architecture of multiple ‘grapelike’ lobulations. The outer margin was well-defined, largely with a low signal wall indicating that the pathology was confined by the muscularis propria. Incidentally, the abnormality extended inferiorly, into the right side of the anal canal posteriorly, between the internal and external sphincter. Following enhancement, there was initially some nodular mucosal enhancement followed by progressive enhancement of the multiple discrete lobulations with infilling (see Figs. and ). Incidentally there was also a patchy intermediate signal in the prostate with avid peripheral zone enhancement. His prostate specific antigen was normal.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [66, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 66 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
1074,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3789080-1,Extracted,"A 24-year-old Mongolian female was referred to the outpatient clinic at Huashan Hospital (Shanghai, China) with mild sacrococcygeal pain that had been present for two months with no obvious causation. The individual had no fever, abdominal pain or changes in habitual normal bowel movement and urination. Magnetic resonance imaging (MRI) of the patient’s pelvis revealed a 53×40×33-mm pelvic mass, posterior to the sacrum and at the right side of the rectum (). An enhanced MRI showed that the mass, a possible teratoma, was under the sacrum (). Based on the radiological features, the mass was located at the posterior of the rectum towards the right side and was extended near the sacrum with clear boundaries without evidence of sacral invasion. A laboratory examination of the tumor section, including an analysis for tumor markers CA 19-9 and CA 125, revealed results within the normal ranges. The patient’s medical history included a coccyx fracture in 2002 and a sacral epidermal cystectomy in 2004.
Upon admission to the hospital, no abdominal tenderness, rebound pain or palpable masses were identified by a physical examination. The initial rectal exam detected the inferior end of a non-mobile, non-tender and smooth-edged mass attached to the right posterior side of the rectum.
The patient was scheduled for surgical treatment under general anesthesia two days after admission. Intraoperatively, the patient was placed in the prone jack-knife position. The surgery was performed with a 10-cm incision at the inferior margin of the fifth sacrum. The coccyx and the inferior margin of the fifth sacrum were removed. The right side of the wall of the rectum was dissociated from the presacral rectum by an incision into the gorge of the sacrum. No tumor mass was located by laparotomy or the initial examination during surgery. Next, an ultrasound examination was performed and the mass was visualized at the right side of rectum, posterior to the uterus. The right ovary was not located at its normal anatomical site. The peritoneum was opened and the enlarged right ovary was identified as a presacral mass with an irregular appearance. The mass had a diameter of 5 cm and its outer boundary was smooth with no feeding vessel or ligamentous connection to the surrounding organs, including the rectum, uterus, cervix and vagina. The sacrum and coccyx were unaffected (). The left ovary was normal in appearance and located at its usual anatomical site.
The right ovary tumor mass was resected and removed from the normal ovarian tissue by a gynecologist. The examination of an intraoperative frozen section indicated a possible diagnosis of a presacral MCT (dermoid cyst). A further pathological examination confirmed the diagnosis of a presacral MCT. The patient recovered uneventfully and was discharged 6 days after the surgery. Written informed consent was obtained from the patient for the publication of this case report.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [24, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 24 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1075,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2823679-1,Extracted,"A 66-year-old man, who had received a renal transplant 5 months before, and was on tritherapy [prednisolone (1 mg/kg/day); cyclosporine A (7 mg/kg/day); azathioprine (1 mg/kg/day)], was admitted to the hospital with hemoptysia. A computed tomographic scan of the chest showed a not well-circumscribed and excavated mass mass involving the pulmonary inferior left lobe, bilateral pleural effusions, and a small parenchyma nodule in the pulmonary inferior right lobe (Fig. et ). An analysis of the BAL was quickly performed due to the presence of Aspergillus fumigatus in sputum: cytopathological examination showed filamentous hyphae corresponding to aspergillosis (Fig. ). These filaments were subsequently identified by culture as A. fumigatus. In addition, pyocyanic bacteria were isolated from the BAL. Treatment associating voriconazole, ceftazidime and ciprofloxacine was started. However, the absence of a clinically improved status and repeated massive hemoptysia, led to surgical resection of the pulmonary left inferior lobe one week later. Gross macroscopy demonstrated a diffuse hemorrhagic infarct of the lung (Fig. ). A specimen of lung tissue was sent to the mycology laboratory. The patients died of cardio-pulmonary failure two days after surgery.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [66, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 66 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1076,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3549390-1,Extracted,"A 40-year-old woman presented for cesarean delivery for fetal breech presentation at 39 weeks' gestation under spinal anesthesia. Her previous obstetrical history included two previous first trimester abortions and a full-term pregnancy delivered by cesarean section due to breech presentation. Her present antenatal course was smooth, except for a progressive painless swelling in the right flank noticed at 20 weeks' gestation. Multiple ultrasound examinations were done at different intervals during the course of pregnancy. They demonstrated a rapidly growing sharply defined abdominal mass, heterogeneous in echogenicity and smooth in contour, highly suggestive of a subserosal uterine leiomyoma. No other signs and/or symptoms were reported. The patient denied smoking, drinking alcohol, or taking any medications besides her prenatal vitamins.
Intraoperatively, the tumor was found to be extra-peritoneal originating from the right abdominal wall. It was whitish in color, hard in consistency, and fixed to its surroundings. It was arising from the lateral wall (rectus and external oblique muscles) reaching the vicinity of the anterior superior iliac spine. Following the delivery of a live male newborn (Birthweight: 3560 g; Apgar score 9 at 5 min) through a lower segment transverse uterine incision, a general surgeon was called in for an intraoperative consultation. Frozen sections revealed benign spindle cells suggestive of a desmoid tumor (), although a sarcoma could not be ruled out in view of the tumor rapid growth. The patient consented to a wide surgical excision of the mass within the same surgery. Radical resection of the tumor was performed including affected abdominal wall muscle and a peripheral margin of healthy tissues surrounding it. The patient tolerated the procedure well. She developed right femoral lateral cutaneous neuralgia that resolved spontaneously a few weeks later.
Grossly, the tumor was a 12 × 9.5 × 7 cm mass weighing 457 g, ovoid in shape, firm in consistency, covered by a smooth glistening layer with some attached adipose tissue in areas. Cut sections showed tan fleshy softer tissue in the inside. This was surrounded by a capsule and an inner rim of brown gray firm tissue measuring 0.6 cm in average thickness. The final diagnosis of musculoaponeurotic fibromatosis/desmoid tumor was made.
Two years later, the same women gave birth to her third child by cesarean section. Surgical inspection of the previous resection site was unremarkable. There was no evidence of tumor recurrence.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [40, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 40 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1077,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5415351-1,Extracted,"A 76-year-old El Salvadorian woman presented with warfarin-associated supratherapeutic international normalized ratio (INR) from nursing home. She was on warfarin for pulmonary embolism (PE) diagnosed 3 weeks earlier after presenting with acute shortness of breath. A filling defect in the right upper lobar artery was shown on computed tomographic (CT) angiography performed at that time with a normal venous duplex ultrasound of lower extremities for deep vein thrombosis. Hence, the initial CT angiography, which was done for pulmonary emboli thrombosis, showed an intracardiac lesion, but unfortunately radiologist did not report such lesion in the heart, probably because the focus was only on lungs. On her second admission, she was found to have an INR of 9.9. She was only on Coumadin as an anticoagulant, and because of the lack of follow-up of INR in the nursing facility, she was admitted with such high number. She was otherwise asymptomatic. Her medical history was significant for permanent cardiac pacemaker insertion 4 years ago due to sick sinus syndrome. She had low risk of developing PE. Her vital signs were stable. Physical examination revealed decreased breath sounds in the lower region of her right lung. On initial investigations, she had a moderate-sized right pleural effusion with bibasilar atelectasis. Warfarin was discontinued and vitamin K was administered. The electrocardiogram revealed an atrial paced rhythm. Further workup for right-sided pleural effusion included a transthoracic echocardiography (TTE) which showed normal left ventricular function with a 2.5-cm2 sessile mass in the RA cavity above the tricuspid valve attached to the septum (). Patient did not have any recent TTE for comparison. Transesophageal echocardiogram was then ordered, which revealed a 2.5-cm2 sessile mass attached to the inferolateral wall of the RA with no vegetative lesion. A pacer wire was noted traversing the tricuspid valve. Magnetic resonance imaging would be a very good next step after TTE in such patients, but as the mass was very similar to a cardiac myxoma, the surgeon and cardiologist decided to pursue with resection. The patient was scheduled for removal of the atrial mass with an impression of possible myxoma 5 days later. Because she was on anticoagulant for 3 weeks prior to the surgery and it did not affect the mass, and we initially thought it was a myxoma, we decided to proceed with the surgery soon. Her preoperative cardiac catheterization showed minimal coronary artery disease. During operation, the mass was identified near the annulus of the tricuspid valve with a small stalk and it was excised completely, including the stalk involving the endocardium of the heart (). Histopathologic examination revealed a smooth red-tan to dark red-tan surface. Microscopic views showed significant deposit of fibrin and proliferation of the blood vessels and fibroblasts. Focal accumulation of hemosiderin-containing histiocytes was also noted (). Three pathologists evaluated the samples, and the mass was reported as a cardiac thrombus. They all agreed that this mass was not a myxoma because it did not have typical features of myxoma, such as hypocellularity, bland cells, collagenized capsule at periphery, with basophilic matrix, and few spindle cells.
The patient had an uneventful hospital course. She had the thrombus in both lung and heart initially before starting any warfarin. She did not have a positive family history of thrombophilia. The only reliable tests of hypercoagulable disorder during an acute thromboembolism, such as antithrombin, protein C, and protein S, were measured which were negative. The rest of the tests were deferred to later in follow-up course. Also, a basic workup, including pan-CT scan of body cavities, was done to look for malignant lesions, which were all unremarkable. She was restarted on warfarin for at least 6 months and discharged to a rehab facility for postoperative recovery. The patient was followed up by the oncologist and her primary care physician in the 6 months with improvement of her chest imaging and resolution of PE on warfarin treatment.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [76, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': False}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 5.
The patient's CHA2DS2-VASc Score is 5."
1078,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7384735-1,Extracted,"A 71-year-old woman presented to the emergency department with symptoms of dizziness, fatigue, and bright red bleeding per rectum. She has a past medical history of atrial fibrillation and hypertension. She started having six to seven bright red colored stools for about one week, unassociated with mucus. She reported concerns of constant right upper quadrant pain that started approximately two days before the presentation. She denied any nausea, vomiting, or subjective fever, and she had no recent travel or exposure to sick contacts and no history of hemorrhoids.
On examination, she was found to be tachycardic with a heart rate of 130 beats per minute. Her blood pressure was 98/50 mmHg, and her body temperature was 100.2°F. Her oxygen saturation was 93% on room air. She appeared thin, cachectic, and had no scleral icterus. Her lungs were clear on auscultation, and her cardiovascular examination revealed no significant murmurs.
Her laboratory investigation showed leukocytosis with white blood cell count of 29,000 per microliter (neutrophils, 88%; lymphocytes, 3.5%; monocytes, 3.7%; eosinophils, 1.2%; basophils, 0.3%). Her hemoglobin was 9 g/dl (reference range: 11.2-15.7 g/dl), and her mean corpuscular volume was 77. Urine analysis was negative for infection. Chest X-ray did not show any active consolidation (Figure ).
Her Clostridium difficile screening was negative. Right upper quadrant ultrasound showed several indeterminate hypoechoic solid masses, and both lobes of the liver had several indeterminate hypoechoic solid masses. A slight gall bladder wall thickening with no surrounding inflammatory signs was noted. MRI of the abdomen showed multiple circumscribed lesions throughout the liver compatible with metastasis (Figure ).
The patient was started on empiric antibiotics with vancomycin and cefepime for possible infection. Her blood cultures grew S. anginosus, and her antibiotic regimen was changed to ceftriaxone.
As the source of the bacteremia was unknown, and because of her microcytic anemia with a recent change in bowel habits, she underwent a colonoscopy and transthoracic echocardiogram (TTE). The colonoscopy revealed a fungating infiltrative, ulcerated, partially obstructing mass in the sigmoid colon. The biopsy results are positive for moderately differentiated adenocarcinoma of the colon (Figure ).
TTE showed thickening and possible vegetation involving the aortic and mitral valves. Subsequent transesophageal echocardiogram revealed vegetation (approximately 0.2 cm) on the aortic and mitral valves (Figures , ).
She had no signs of a perivalvular abscess, and her ejection fraction was within reference range at 55% to 60%. Her care team decided to continue treatment with antibiotics for at least six weeks. Her anticoagulation for atrial fibrillation was halted due to active gastrointestinal (GI) bleeding. The patient died several days later as her family focused on comfort care measures based on the patient's wishes.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [71, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 71 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
1079,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6796715-1,Extracted,"A 78-year-old female presented to an outside hospital with one-week history of diffuse abdominal pain with associated nausea, vomiting, and diarrhea. Her past medical history was significant for factor V Leiden, deep vein thrombosis, pulmonary embolism, hypertension, diabetes mellitus, morbid obesity, atrial fibrillation, heart failure with preserved ejection fraction, and chronic obstructive pulmonary disease on 2 liters home oxygen. She was on warfarin and had an inferior vena cava filter in place for her history of venous thromboembolic disease and thrombophilia. Her vital signs were significant for tachycardia. Abdominal examination was soft, non-distended, minimally tender to palpation in the epigastrium without rebound or guarding. Initial laboratory studies were significant for a white blood cell count (WBC) of 21,600 cells/μL, serum creatinine of 2.18 mg/dL, lactate of 2.7 mmol/L, and international normalized ratio (INR) of 5.36. Her INR was corrected with vitamin K and fresh frozen plasma and the patient was transitioned to an intravenous unfractionated heparin infusion. CT scan of the abdomen without contrast was obtained to evaluate her abdominal pain and revealed gastric distension with gastric pneumatosis (). She was treated for EG with nasogastric tube (NGT) decompression, intravenous fluid resuscitation, nil per os (NPO), antibiotics (vancomycin, cefepime, metronidazole, and fluconazole), and proton pump inhibitor (PPI). Two days after admission, she developed bloody output through her NGT and dropped her hemoglobin from 11.2 to 7.8 g/dL. Her heparin infusion was stopped. At this point, she was transferred to our medical intensive care unit for escalation of care. On arrival the patient was hemodynamically stable with coffee-ground output from her NGT. She reported that her abdominal pain had improved significantly. Laboratory studies eventually revealed a normalization of her WBC count, serum creatinine, and lactic acid. Her hemoglobin stabilized without further need for transfusion. Decision was made to not pursue an esophagogastroduodenoscopy (EGD) given no further evidence of bleeding and improvement in her pain. General surgery was consulted and recommended non-operative management. After four days from the first CT scan, a CT angiography of the abdomen with contrast was obtained to evaluate for vascular patency which revealed patent celiac trunk and resolution of her gastric pneumatosis (). The NGT was then removed and the patient tolerated an oral diet. She completed a total of seven days of antibiotics. She was discharged home on PPI therapy and warfarin was restarted.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [78, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Thromboembolism history': True, 'Diabetes history': True}",8,8,8,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 78 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 5 + 2 = 7.
Because vascular disease history is not specified in the patient note, we assume it to be absent.
Because the patient does not have vascular disease, no points are added to score, keeping the score at 7. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 7 + 1 = 8.
The patient's CHA2DS2-VASc Score is 8."
1080,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,usmle-1611,Extracted,"A 69-year-old man comes to the physician with a 9-month history of worsening shortness of breath on exertion and need to urinate at night. He occasionally has palpitations but does not have chest pain. The patient had a transient ischemic attack 5 years ago for which he underwent right-sided carotid endarterectomy. He has hypertension and type 2 diabetes mellitus. Current medications include metformin, lisinopril, aspirin, and simvastatin. He appears fatigued. His pulse is 61/min, blood pressure is 120/75 mmHg, and respirations are 25/min. Pulse oximetry shows an oxygen saturation of 96%. Examination shows cold extremities. There are no murmurs or rubs on cardiac auscultation. Fine, bilateral crackles are heard at the lung bases. There is 2+ lower extremity edema. An ECG shows sinus rhythm and known T wave inversions in leads V1 to V4.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [69, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': True, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 69 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
1081,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5036825-1,Extracted,"A 52-year-old male with no previous history of gastrointestinal bleeding presented to the emergency department with chest pain and solid food dysphagia. His medical history included atrial fibrillation, hypertension, obstructive sleep apnea, asthma, and splenectomy at age 14 following a traumatic splenic rupture after being kicked by a horse. Initial cardiac workup was negative and he was discharged home with an outpatient follow-up appointment with gastroenterology.
His medications included dabigatran, diltiazem, irbesartan, montelukast, budesonide/formeterol, fluticasone/salmeterol, and salbutamol.
Outpatient upper endoscopy identified a Schatzki’s ring at the esophageal–gastric junction as well as several small clean-based ulcers at the prepyloric region on a duodenum hiatus hernia. Biopsies were obtained from the gastric mucosa to rule out Helicobacter pylori. He was placed on a proton-pump inhibitor and sent home following the procedure.
Four days later he re-presented to the emergency department with multiple episodes of melena, light-headedness, progressive shortness of breath on exertion, and rapid atrial fibrillation (heart rate ~130 bpm, normotensive). Bloodwork revealed: hemoglobin 112 g/L (baseline ~150 g/L), mean corpuscular volume 83.8 fL, platelets 312×109/L, creatinine 79 μmol/L, urea 10.8 mmol/L, international normalized ratio 1.2, partial thromboplastin time 28, and normal liver function tests. He was given 1 L of crystalloid, placed on a pantoprazole infusion, and his dabigatran was held.
Urgent upper endoscopy revealed stigmata of recent hemorrhage from recent biopsy sites, the previously observed clean-based ulcers, and a submucosal lesion in the third part of the duodenum, which was not bleeding. The biopsy sites were cauterized with a gold-probe and he was admitted for observation.
On post-admit day 2, the patient had a syncopal episode associated with melena and a hemoglobin decline of 30 g/L. Repeat endoscopy revealed only a large adherent clot in the fundus, which could not be aspirated. The patient’s melena persisted and hemoglobin continued to fall prompting another upper endoscopy that demonstrated a small pouch in the gastric fundus without any stigmata of recent hemorrhage, but concerning for either a diverticulum or fistula. A subsequent upper gastrointestinal series confirmed a mild focal out-pouching of the gastric fundus without any evidence of a fistula or leak. A computed tomography (CT) scan was performed and revealed replacement of the spleen by multiple soft tissue nodules consistent with splenosis, but could not identify a clear source of bleeding due to retained oral contrast within the stomach from the prior upper gastrointestinal series. On post-admit day 8, the patient had a repeat CT scan which revealed a previously unidentified 1.3 cm perigastric lesion with moderate vascularity within the gastric fundus. The possibility of a gastric varix was raised. An endoscopic ultrasound was performed, which did not reveal any large varices, but did confirm a number of smaller perforating vessels within the fundal lesion, as well as several perigastric lesions, which were later identified as perigastric splenosis. Endoscopic ultrasound-assisted fine-needle aspiration of one of the perigastric lesions revealed a mixed population of lymphocytes, plasma cells, neutrophils, and eosinophils favoring a reactive lymph node, thus, nondiagnostic.
The patient continued to have melena stool and a subsequent CT angiogram was acquired revealing an extensive network of enlarged arteries within the wall of the gastric fundus that were supplying a grouping of splenosis along the posterior aspect of the gastric fundus (). The dominant arterial supply was localized to a branch of the left inferior phrenic artery, which underwent successful transarterial coil embolization that was confirmed on a follow-up CT scan ( and ). The patient clinically improved, his hemoglobin stabilized, and he was ultimately discharged home.
Follow-up imaging 2 months later revealed further interval decrease in the size of the intramural gastric arterial collaterals perfusing the perigastric splenules. As of the most recent follow-up appointment 8 months following the patients’ initial presentation, there was no further bleeding. Verbal consent was provided by the patient to have his data used in this study.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [52, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': False, 'Stroke': False, 'Diabetes history': False, 'Transient Ischemic Attacks History': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 52 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1082,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2966711-1,Extracted,"A 70-year-old woman (height: 156 cm, body weight: 48 kg) with lower abdominal pain was admitted and associated symptoms were fever, nausea, vomiting and diaphoresis which started from the day previous to her admission. On abdominal computed tomography (CT), right ovarian cyst in size of 2.5 cm was found, and an acute appendicitis was diagnosed by an abdominal ultrasonography. An elective operation was scheduled under the collaboration of gynecology and general surgery.
In the patient's past medical history, she had taken digoxin, dilatrend, nitrate, telmisartan, and thiazide for 5 years because of hypertension, congestive heart failure, AF, and right coronary artery 90% stenosis on coronary angiography. An electrocardiogram before operation showed AF with ventricular response 90-100 times/min, left ventricular hypertrophy. Cardiomegaly and pleural effusion were found on chest X-ray. On transthoracic echocardiography (TTE), ejection fraction was 55% and left atrial enlargement, right atrial enlargement and eccentric hypertrophy with decreased mobility of the inferior wall of the left ventricle were shown. A moderate aortic valve insufficiency, aortic valve sclerosis, mild aortic stenosis, and severe posterior mitral valve leaflet calcification were also found and the width of mitral valve measured by pressure half-time was 1.92 cm2. A chronic cerebral infarction in the right posterior cerebral artery was found on brain CT with symptoms of dysarthria. Signs of dehydration on physical examinations with prerenal azotemia of FeNa 0.1% and serum creatinine of 1.7 mg/dl on blood test led us to start an fluid therapy. The serum creatinine was decreased to 1.3 mg/dl after the fluid therapy.
Glycopyrrolate 0.2 mg IM was premedicated at 30 minutes pre-operation. The patient's blood pressure (BP) was 130/50 mmHg, ventricular response 90-100 times/min, and arterial oxygen saturation 97% when she arrived at the operation room. A right radial artery was cannulated with great caution before the induction of anesthesia. The induction of anesthesia was initiated with injecting 2 ml of 2% lidocaine to reduce injection pain and propofol (Diprivan® AstraZeneca, UK) and remifentanil (Ultiva® GlaxoSmithKline, UK) were injected using a target-controlled infuser (Orchestra® Fresenius Vial, France). After confirming the patient's being unconscious, rocuronium 40 mg was injected and then endotracheal intubation was performed with close monitoring of arterial blood pressure. Ventilation with 100% O2 was given while central venous catheterization was placed in right jugular vein. After the induction of anesthesia, the patient's vital sign showed no hemodynamic disorder with systolic BP 130-150 mmHg, diastolic BP 40-60 mmHg, ventricular response approximately 100-110 times/min, and central venous pressure (CVP) 8-9 mmHg. The effect site concentration was injected as 2.5-3.0 µg/ml of propofol and and 2.0 ng/ml of remifentanil.
After the lower abdomen laparotomy at obstetrics and gynecology for the right ovary cystectomy, a small bowel infarction from jejunum to ileum was detected. The authors suspected a mesenteric arterial embolism based on the patient's previous medical history. A transesophageal echocardiology (SonoSite MicroMaxx, Bothell, USA) probe was immediately inserted and a spontaneous echo contrast (SEC or ""smoke"") in the left atrium (LA) and a 13 × 18 mm size thrombus in the LAA was detected (). The findings in TEE made a mesenteric arterial embolism highly suspicious for the cause of the small bowel infarction. A segmental resection and intestinal anastomosis were performed by the department of general surgery. No hemodynamic instability was observed through whole procedure of operation and the patient was transferred to the intensive care unit with endotracheal tube inserted. After confirming her awareness and the absence of any neurologic disorder, extubation was performed in intensive care unit. To minimize the risk of hemorrhage of the anastomosis site, anticoagulation was performed with caution under the collaboration of general surgery and cardiology. It was started with low molecular weight heparin 3 days after the operation and oral warfarin was added 5 days after the operation. After 4 weeks, cardioversion was successfully performed to turn into normal sinus rhythm.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [70, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': True, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': True, 'Diabetes history': False}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 70 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
1083,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4735536-1,Extracted,"A 54-year-old male patient with main pulmonary artery (MPA) dilatation detected in out-clinically performed computed tomography (CT) and with well controlled arterial systemic hypertension was referred to our department for advanced diagnostics and for a further therapy decision to be made. His first hospitalisation due to congenital heart disease suspicion was at the age of 18. At that time there were no clinical symptoms besides the presence of protomezosystolic murmur over the left sternal edge and cardiac apex. In chest X-ray tomography performed at that time enlargement of the left pulmonary artery was found. In those days – in 1976 – atrial septal defect was suspected and the patient was referred for haemodynamic and angiographic studies. However, it was abandoned due to lack of compliance. In 2003 diagnostic procedures were restarted, and CT revealed MPA dilatation to 40 mm.
During the present hospitalisation the patient denied the presence of any cardiovascular symptoms and confirmed regular physical activity. Examination revealed only slight systolic murmur (Levine 1/6) over the left sternal edge. Electrocardiography (ECG) study was normal. Chest X-ray revealed enlargement of the left hilum probably due to enlargement of the main pulmonary artery (). Echocardiography showed proximal MPA diameter of 29 mm distally exceeding to 45 mm. The right pulmonary artery (RPA) was enlarged up to 29 mm, and the left one was not precisely visible. Blood flow profile was normal. No signs of intracardiac or extracardiac shunting were found. Right ventricule diameter and contractility were normal (RVdD – 29 mm) without symptoms of pulmonary hypertension (TRPG – 20 mmHg). Cardiac CT revealed MPA aneurysm (47 × 40 mm in diameter) with significant enlargement of the left (37 × 35 mm) and right pulmonary artery (24 × 27 mm; and ). Potential primary causes of MPA dilatation were eliminated, such as: distal MPA stenosis, pulmonary embolism, and the presence of any pulmonary disease. Coronary arteries CT scan was performed and showed no signs of left coronary artery compression with MPA aneurysm (, ). Additional laboratory studies excluded inflammatory and collagen disorders. According to the gathered data a diagnosis of idiopathic dilatation of the main pulmonary artery (IDPA) was stated. At that time the patient was disqualified from surgical intervention. The following therapy was targeted at optimal medical management of arterial systemic hypertension. Future control tests after 6 and 10 months were planned.
After six months control echocardiography showed a proximal MPA diameter of 28 mm with enlargement progression of the distal segment to 51 mm and RPA to 31 mm. Right ventricule diastolic diameter was also enlarged to 41 mm with preserved contractility. Computed tomography study revealed progression of MPA diameters to 52 × 45 mm, LPA diameter to 36 × 27 mm, and RPA diameter to 30 × 26 mm. After the next four months an echocardiography study showed stable parameters of pulmonary arteries with MPA enlargement progression to 57 mm. The patient was continuously disqualified from surgical treatment due to asymptomatic course. Continuation of optimal medical therapy of arterial hypertension was administered.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [54, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 54 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1084,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4826711-1,Extracted,"A 72-year-old woman was admitted to our department due to acute ischemia of the right leg. She was diagnosed with persistent nonvalvular atrial fibrillation 7 days ago, and it was decided that she would benefit from warfarin for stroke prophylaxis. Warfarin was prescribed at 2 mg daily as a slow loading dose and on the fifth day the primary care physician increased the dose to 5 mg, due to the low value of the international normalized ratio [INR = 1.5]. Moreover, the patient had a history of hypertension and diabetes mellitus and there was no history of any trauma or local/systemic infection.
On physical examination, the right leg of the patient was found to be pale and cold with the sign of developing mottling and cyanosis from knee level down. The calf muscles were also tender on examination. She had no detectable arterial pulses below her right knee by palpation, which was confirmed by an emergency Doppler examination revealing the complete lack of blood flow in both dorsalis pedis and posterior tibial arteries. Furthermore, a necrotic lesion was revealed measuring 5 cm in diameter on the lateral aspect of lower right leg [].
The diagnosis of acute right leg ischemia due to the acute occlusion of the 3-infrapopliteal arteries was considered. A dose of intravenous (IV) heparin was chosen and lower limb thromboembolectomy (TE) was immediately performed via the right femoral artery. The patient's postoperative course was uncomplicated, and the extremity tenderness and mottled skin were improved. Moreover, dermatology consults and skin biopsy revealed noninflammatory thrombosis with focal necrosis in the leg lesion. Warfarin therapy was discontinued and the patient was started on dabigatran 150 mg twice daily. Skin lesion was followed with conventional surgical debridement and was seen to improve [] in a few days, without any recurrence under dabigatran therapy.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': False, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 3 + 2 = 5.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
1085,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4507383-1,Extracted,"A 50-year-old woman was admitted to our emergency room with left-sided weakness of 5 hours and 45 minutes duration. She had been taking warfarin due to chronic atrial fibrillation for 10 years (CHA2DS2 VASc score=2). An initial neurologic examination revealed dysarthria, left visual field defect, and face and limb weakness on the left side. Visuospatial neglect on the left side was also noted. Electrocardiography revealed an atrial fibrillation. Her international normalized ratio (INR) was 1.74. Brain computed tomography (CT) angiography revealed tandem occlusion of the right distal internal carotid artery (ICA) and right proximal middle cerebral artery (MCA) along with low densities in the right insula and the basal ganglia. Emergent mechanical thrombectomy was performed (). A 0.58 mm microcatheter was navigated across the occlusion site to the M2 portion of the right MCA using a 0.36 mm microwire. After removing the microwire, a Solitaire (ev3 Inc., Irvine, CA, USA) 4/20 stent was introduced and placed spanning the entire length of the thrombus. The Solitaire stent was retrieved during compression of the right common carotid artery, 5 minutes after deployment. After four attempts using this procedure, recanalization of the right ICA and MCA was achieved with capturing of the occluding thrombus, but the M2 superior division remained occluded. Another attempt at mechanical thrombectomy of the right M2 was conducted and complete recanalization (thrombolysis in cerebral infarction score, 3) was achieved at 8 hours and 15 minutes after symptom onset. A delayed angiogram revealed complete recanalization without residual stenosis (). Brain magnetic resonance imaging (MRI) performed on the next day revealed an acute infarction in the right insula and basal ganglia with patent flows in the right ICA and MCA (). The patient had no neurologic sequelae on day 3 after stroke onset. She had been administered intravenous heparin, and switching to warfarin was attempted.
Transthoracic echocardiography performed 5 days after the stroke onset demonstrated the presence of a thrombus, severe spontaneous echo contrast in the left atrium with left-atrium enlargement (volume of 142.6 mL), and decreased left atrial appendage (LAA) emptying velocity (0.087 m/sec). On day 6 after symptom onset, a 22-mm-sized thrombus with marked left atrial enlargement was noted in the LAA on multichannel cardiac CT (). Aphasia and right-sided hemiplegia developed 2 hours and 45 minutes after cardiac CT was performed. The patient's INR was 2.34. Brain CT angiography revealed a newly developed occlusion on the M1 segment of the left MCA. Endovascular thrombectomy was attempted again (). Complete recanalization was achieved at 2 hours after symptom onset with the first attempt at suction thrombectomy and one trial mechanical thrombectomy with the Solitaire (ev3 Inc.) device for left M1 occlusion (). The patient's neurologic symptoms again completely resolved immediately after successful thrombectomy. Diffusion-weighted MRI conducted the next day revealed a slightly high signal intensity in the left basal ganglia (). Follow-up multichannel cardiac CT performed 3 days after the second event confirmed the disappearance of the previously observed thrombus in the left atrium, but a small residual thrombus was suspected in the LAA (). The patient was discharged to home 10 days later.
Histologic studies were performed to investigate the nature of the thromboemboli that had been retrieved during the endovascular treatments for this patient. Hematoxylin and eosin (H&E) staining of the extracted thromboembolus of the index stroke revealed a large amount of fresh red blood cells (RBCs) and intact granulocytes (), while the clot of the second stroke contained few intact RBCs and granulocyte apoptosis (). However, antiglycophorin-A staining, which is used for highly selective detection of RBCs, revealed that both thrombi were mostly composed of RBCs ().",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [50, 'years'], 'Congestive Heart Failure': False, 'Stroke': True, 'Transient Ischemic Attacks History': True, 'Thromboembolism history': True, 'Vascular disease history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 50 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 1 + 2 = 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
1086,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4712376-1,Extracted,"A 68-year-old man presented with progressive dyspnea and cough with blood-stained sputum for five days. He underwent surgery for mitral valve replacement with a 31 mm Carpentier-Edwards bovine pericardial valve and coronary artery bypass grafting with a great saphenous venous graft to the left anterior descending artery three months ago. He had permanent atrial fibrillation, rheumatoid arthritis and chronic obstructive airway disease, and received regular medical follow up. Five weeks after the surgery, he presented with an episode of acute pulmonary edema and bilateral pleural effusion, and was admitted. During admission, transthoracic echocardiography revealed normal ejection fraction of both ventricles and a mitral PVL that caused severe mitral regurgitation. Transesophageal echocardiography (TEE) was then performed and revealed that the mitral PVL was approximately 6 × 3 mm in diameter and was in one o'clock position (). He was treated with diuretics and was discharged from the hospital after one week as the pulmonary edema and pleural effusion gradually subsided. After discharge, he experienced dyspnea with mild activity and developed repeated episodes of acute pulmonary edema and pleural effusion which required intermittent injection of loop diuretic in the following two months (New York Heart Association functional class III-IV). After we had explained the treatment options, including re-operation and transcatheter intervention, he agreed to undergo transcatheter closure of the defect. Because he declined the transapical approach and the defect would be difficult to approach through the antegrade transseptal approach, the retrograde transfemoral arterial approach was chosen.
Under general anesthesia, a 7F sheath was placed in the left common femoral artery. After heparinization, we used a 0.025-inch J-tipped guidewire (Terumo Glidewire®, Terumo Medical Corp., Somerset, NJ, USA) to cross the defect with the support of a 5F Judkins right 4.0 (JR4) diagnostic catheter via the retrograde approach through the left femoral artery into the left atrium under the guidance of TEE and fluoroscopy. The diagnostic catheter was then exchanged with a 6F JR4 guiding catheter but it failed to cross the defect. Therefore, we introduced another 0.035-inch guidewire into the left atrial cavity, but the guiding catheter still failed to cross the defect despite the support with double wires (). To provide more support, the standard 0.035-inch guidewire was replaced with a 260-cm long 0.035-inch J-tipped Amplatzer® Super Stiff guidewire (AGA Medical Corp., Plymouth, MN, USA) and we introduced a 5F multipurpose guiding catheter inside the 6F JR4 guiding catheter over the guidewire as a mother-in-child catheter technique (). Finally, the 6F JR4 guiding catheter crossed the defect. An Amplatzer® Duct Occluder II (AGA Medical Corp., Plymouth, MN, USA) (waist diameter, 6 mm; length, 4 mm; disc diameter, 12 mm) was advanced through the 6F JR4 guiding catheter and deployed after confirmation of proper device positioning by TEE (). Subsequent TEE showed that the paravalvular leak was sealed and only minimal residual leak was observed (). The patient was discharged 5 days after the procedure and the post-procedural course was uneventful during six months of follow-up.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [68, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 68 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
1087,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8275069-1,Extracted,"An 81-year-old Caucasian man presented to our hospital after a mechanical fall resulting in a right femur periprosthetic fracture. His past medical history was pertinent for coronary artery bypass grafting (CABG) and aortic valve replacement with a 27-mm Saint Jude Biocor bioprosthetic valve due to severe aortic insufficiency in 2007, paroxysmal atrial fibrillation, hypertension, hyperlipidemia, diabetes mellitus, former tobacco abuse, right popliteal aneurysm, and abdominal aortic aneurysm measuring up to 12 cm x 12 cm status post-endovascular aortic repair in 2011 (Figure ).
He reported intermittent chest pressure and dyspnea with mild exertion. He can walk about half of a block before stopping to rest due to dyspnea. Transthoracic echocardiogram showed preserved ejection fraction of 60-65%, stage 1 diastolic dysfunction, well-seated bioprosthetic aortic valve with normal gradients, and no other major valvular abnormalities. A regadenason nuclear stress test was performed and it revealed a fixed inferior wall defect and significant transient ischemic dilation, prompting further investigation with coronary and bypass angiography. Coronary angiography revealed numerous aneurysmal dilations, most notably the proximal left anterior descending artery (LAD), as well as severe atherosclerosis lesions (Figure ).
The left circumflex artery (LCX) was occluded proximally (Figure ).
Bypass angiography revealed patent grafts to the LAD, obtuse marginal branch, and right coronary artery (RCA) (Figure ).
Given his age, underlying comorbidities, and patent bypass grafts, we opted to treat him medically with optimization of medical therapy, which included anti-platelet, angiotensin receptor antagonists, and statins.
He proceeded with open reduction internal fixation of the right periprosthetic femur fracture. The surgery was uncomplicated, and his post-operative course was relatively unremarkable. He was discharged to an inpatient rehabilitation facility to continue recovery.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [81, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 81 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
1088,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7202050-1,Extracted,"A 63-year-old male presented with a 2-day history of a widespread, erythematous rash covering all surfaces of his body. The rash appeared 2 days prior to admission with associated prodromal malaise and anorexia. His medical history was significant for a cellulitis of his left lower limb for which he was prescribed oral clindamycin 5 days prior. Two days before admission, the patient noted a pruritic rash on his abdomen which subsequently became erythematous. The rash then migrated to his face and the rest of his torso. Within the next 48 h, it spread to involve his back and upper and lower limbs. The patient then began experiencing subjective fever and presented to his general practitioner before being referred to hospital. On hospital presentation he was apyrexic, tachycardic (irregularly irregular pulse rate of 170 beats per min) and was tachypneoic (respiratory rate of 28). He was normotensive (126/84 mmHg) and remained alert and interactive clinical examination was remarkable for an oatmeal dermatitis of the face and perioral area ( and ) and an erythematous, blistering rash covering 80% of his total body surface area. Nikolosky sign was positive. Oral involvement was noted. The palms of his hands and the soles of his feet were spared.
Potentially causative medications (including clindamycin) were stopped. Electrocardiogram confirmed atrial fibrillation. The patient was immediately isolated from other patients and increased contact precautions were taken. Fluid resuscitation was commenced as per local hospital sepsis guidelines and urinary output monitored. Paraffin gel was applied liberally two hourly and potent topical corticosteroids twice daily. Intravenous hydrocortisone (100 mg) was given four times daily. Laboratory investigations on admission were significant for a moderate leucocytosis of 15.5 × 109/l and a neutrophilia of 14.5 × 109/l. C-reactive protein levels were 123 mg/l and venous lactate was markedly elevated at 6.5 mg/dl. Blood, urine and wound site cultures were sent for culture and sensitivity. Autoimmune and viral screens were taken. Skin biopsies were performed on two occasions: A 4 mm punch biopsy of affected skin was taken from the anterolateral left forearm and a repeat punch biopsy was taken from the sacral area on Day 2 of admission. The patient’s chest X-ray revealed no abnormality.
A marked improvement in the patient’s rash was seen on admission Days 3 and 4, and his clinical condition gradually improved. The patient remained apyrexic. A switch from intravenous hydrocortisone to 30 mg of oral prednisolone was made on Day 7. The patient evidenced impressive regeneration of the affected skin and corticosteroids were tapered prior to discharge 21 days after admission.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [63, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 63 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
1089,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3652758-1,Extracted,"A 62-year-old Chinese man who had myocardial infarction on anterior wall was recommended for cardiac surgery after diagnosed with unstable angina. His cardiac function was grade III according to the New York Heart Association classification. Coronary angiography showed triple-vessel lesions. Echocardiography revealed paradoxical cardiac movements in the apex of the left ventricle in the systolic phase without mural thrombosis. The left ventricular ejection fraction was 0.40 and the left ventricular end-diastolic diameter was 55 mm. Preoperative 12-lead electrocardiography (ECG) showed premature ventricular contractions (PVC). 12-lead Holter monitoring confirmed the presence of frequent multifocal VA (26400/24 h) and paroxysmal ventricular tachycardia. The patient had non-sustained ventricular tachycardia, and did not show mural thrombi. The patient took at least three kinds of anti-arrhythmic drugs including beta-blocker, lidocaine, and amiodarone to reduce the occurrence of VA before the operation. However, those anti-arrhythmic drugs did not seem effective for the patient.
Standard median sternotomy incision was used to expose the heart. Off-pump coronary artery bypass (OPCAB) grafting was performed. A left internal mammary artery was grafted to the left anterior descending artery and a saphenous vein was anastomosed to the diagonal branch, the obtuse marginal artery, and the right coronary post-descending artery sequentially. The border of the aneurysm wall was clear on the beating heart.
A bipolar intramural electrode placed at the base of right ventricle via right femoral vein was used to record a reference electrogram. Ventricular tachycardia appeared spontaneously during the operation. We used more than 40 predetermined locations on the left ventricle to record bipolar potential to construct ventricular epicardial depolarization map. The time point when the epicardial spike moved the most rapidly, approximately 7 ms, represented the moment at which electrical force passed between the bipolar references. The locations where the rapid spike movement occurred were marked. Connecting these locations resulted in a circular area along the border between the aneurysm wall and the surrounding normal myocardial tissue. The circular area was the target for radiofrequency ablation. Other locations showed a spiking time longer than 7 ms. Unipolar radiofrequency ablation was performed by using a Medtronic system, which consisted of a Cardioblate 68000 ablation host and a Cardioblate unipolar pen. The ablation energy was set at 30w without temperature control, and the duration of radiofrequency discharge was set at 20–30s. We first performed a circular epicardial ablation along the borderline using the unipolar ablation pen (Figure ).
The left ventricular aneurysm was then repaired by linear closure []. The edges were readapted with two strips of felt for reinforcement, parallel to the long axis of the left ventricle. Interrupted mattress stitches were used with Surgipro-843 sutures (Figure ). Sutures were placed further apart on the tissue edges rather than on the felt strips. This strategy improved the restoration of the normal shape of ventricle. Finally, we performed cross-shaped ablation on the epicardium at the central zone of the aneurysm (Figure ).
In this case, we found that radiofrequency ablation significantly reduced the frequency of accidental premature ventricular contraction to less than one per minute, and the same type of preoperative arrhythmia did not occur within 30 min after the operation. In addition, we compared the effect of overdrive pacing on the patient’s cardiac rhythm before and after radiofrequency ablation. We found that before the ablation, overdrive pacing accelerated the patient’s cardiac rhythm; while after the ablation, overdrive pacing did not have any effect on the patient’s cardiac rhythm. This observation indicates that the radiofrequency ablation procedure could affect the reentrant mechanism underlying the VA in this patient. VA did not occur when sinus rhythm reached 120–130 beats per min responding to intravenous perfusion of isoprenaline []. Incision was carefully washed before the chest was closed. An accurate assessment of the effectiveness of radiofrequency ablation would be a re-induction of reentry via burst pacing or programmed stimulation after the operation. We did not perform this test in this case because the patient had spontaneous ventricular arrhythmia. We will include this test in our future investigation.
The patient recovered well without postoperative complications and was discharged at day 7 after the operation. He has not taken any anti-arrhythmic medicine since the operation. Holter monitoring at the seventh day after the operation showed no recurrence of the same VA and the amount of arrhythmia decreased to 120/24 h. The patient came back to follow-up visit six months after the operation and had no complaints for heart symptoms. His cardiac function was improved to grade II. Holter monitoring at the six-month follow-up visit showed occasional arrhythmia. We did not perform additional Holter monitoring test on the patient beyond six-month follow-up, because we think that the test might provide limited information regarding the correlation between the incidence of VA and LVA repair, although the test result reflects how well the VA condition has been improved by the operation. Currently, we are still exploring new electrophysiological approaches that can accurately identify the association between the incidence of VA and the location of aneurysm. In addition to the electrophysiological test, we performed other examination to assess the overall postoperative outcome of the patient. Echocardiography revealed ejection fraction of 0.50 and left ventricular end-diastolic diameter of 50 mm at the six-month follow-up visit. The patient has been angina-free for 25 months since the operation and showed increasing exercise tolerance.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [62, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Thromboembolism history': False, 'Vascular disease history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 62 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 1 + 1 = 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
1090,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7387073-1,Extracted,"An 89-year-old male presented to the ED with abdominal pain, nausea, vomiting, and constipation of four days duration. His past medical history included hypertension, hyperlipidemia, type 2 diabetes mellitus, stage 3 chronic kidney disease, atrial fibrillation, and coronary artery disease with a prior coronary artery bypass graft. On exam, he was hypotensive and tachycardic with diffuse rebound tenderness and muscle guarding. Cardiopulmonary exam was otherwise benign. The patient was admitted to the hospital and received conservative treatment for bowel obstruction. His atrial fibrillation was treated with diltiazem 10 mg and metoprolol 5 mg. However, conservative management did not relieve his bowel obstruction, and exploratory laparotomy was scheduled. His preoperative cardiac work-up revealed an ejection fraction of 35%, and his pre-operative labs were significant for a hemoglobin of 9.7 g/dL (13.5-17.5 g/dL), but otherwise within normal limits. The patient was categorized as American Society of Anesthesiology Class IV.
The patient’s preoperative blood pressure was 130/75 mmHg, and his atrial fibrillation was under control with a heart rate of 89 beats per minute. The patient was brought to the operating room with standard monitors applied, and anesthesia was induced in the supine position with etomidate, fentanyl, and rocuronium. After intubation, anesthesia was maintained with sevoflurane in 100% oxygen. Left radial artery was cannulated with 20G cannula. The patient remained hemodynamically stable until three hours post-induction, when he became hypotensive at 65/40 mmHg. Intravenous (IV) normal saline and intermittent phenylephrine were administered. Subsequently, a central venous catheter was placed in the right internal jugular vein under ultrasonic guidance for additional IV access and central venous pressure (CVP) monitoring. After 5,000 mL of IV isotonic fluid, his CVP was elevated at 10 mmHg (2-8 mmHg) and his blood pressure remained low. Arterial blood gas analysis showed pH of 7.4, PaCO2 of 42 mmHg, PaO2 of 272 mmHg (80-100 mmHg), and HCO3 of 26.3 mEq/L (22-28 mEq/L). His hemoglobin was 9.7 g/dL. Electrocardiogram (ECG) showed atrial fibrillation with rapid ventricular response at 120-140 beats per minute (Figure ). The patient also received additional IV fentanyl to treat possible surgical pain.
To provide the best care to the patient, the attending physician and senior resident used the Stanford Anesthesia Emergency Manual checklist on the management of supraventricular tachycardia to guide the treatment. Multiple doses of 100 mcg bolus of phenylephrine were administered. The anesthesiologist then administered 20 mg of esmolol to temporarily control the tachycardia, with continued intermittent phenylephrine, which resulted in blood pressure stabilization with the mean arterial pressure (MAP) restored to greater than 65 mmHg. The patient was placed on an esmolol infusion at 50 μg/kg/min to maintain MAP for the remaining intraoperative time. During the operation, the patient was given total of 7,000 mL of IV normal saline. The patient was transferred to the post-anesthesia care unit with an endotracheal tube in place. His postoperative vital signs were significant for hypotension (102/63 mmHg) and tachycardia (138 bpm). Cardiology was consulted. The patient required continuous diltiazem for hemodynamic stability in the post-anesthesia care unit, where he was eventually transferred to the ICU. His remaining post-operative course was uneventful with no post-operative complications.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': True, 'age': [89, 'years'], 'Stroke': False, 'Diabetes history': True, 'sex': 'Male'}",5,5,5,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 89 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 4 + 1 = 5.
The patient's CHA2DS2-VASc Score is 5."
1091,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5753882-1,Extracted,"We present the case of a 78-year-old male who had a few months history of mild dysphagia. He had been investigated at his local hospital with an oesophagoduodenoscopy (OGD), that had revealed mild extrinsic compression of the oesophagus and a computed tomography (CT) ( and ) scan that revealed a right-sided arch with an aberrant left subclavian artery passing posterior to the oesophagus. A Kommerell’s diverticulum was identified with both the origin of the left subclavian artery and the aorta at that level being aneurysmal, measuring 4 and 5.2 cm, respectively. The CT scan measurements were taken in corrected plan to the centreline. His past medical history included paroxysmal atrial fibrillation, hypertension, hypothyroidism and hypercholesterolaemia. Pre-operative work up with echocardiogram; lung function tests did not reveal significant impairment. He refused an open repair with potential prolonged recovery, as he was the single carer of his disabled wife.
Following multi-disciplinary discussion and after full consent, the patient underwent a bespoke hybrid endovascular repair, incorporating bilateral carotid–subclavian bypasses and branched thoracic endograft placement (branches for both common carotid arteries). A dual branch custom-made endograft (Bolton Medical, Inc., Sunrise, FL, USA) was manufactured with the following features: proximal diameter of 40 mm, distal diameter of 36 mm, total length of 270 mm and tunnel length and diameter of 45 and 10 mm, respectively. Those measurements ensure 20% oversizing for the landing zones.
The patient was positioned supine, sat up at 45°. Bilateral carotid–subclavian bypasses were fashioned sequentially through transverse supraclavicular incisions using 6-mm Dacron grafts. Both the left and right subclavian arteries were ligated proximal to the origin of the vertebral arteries. The justification of this bilateral bypass approach and ligation of native subclavian artery is the fact that stent graft implantation in the aortic arch, even with two branches for the two common carotid arteries, will cover the origin of both subclavian arteries including the antegrade flow to the vertebral arteries. Therefore, revascularisation of both subclavian arteries with preservation of flow to the vertebral arteries is strongly recommended to prevent posterior cerebral infarction. Right ventricular pacing lead inserted via right groin access was positioned and tested. The left common femoral artery (CFA) was accessed via a formal cut-down. The dual branch endograft was introduced over a stiff wire. Angiographic imaging was performed in the 30° right anterior oblique (RAO) projection for optimum visualisation of the origins of the carotid arteries, utilising an imaging catheter placed percutaneously through the right CFA. The endograft was then positioned in the thoracic aorta ().
Rapid cardiac pacing was commenced (target 200 beats per minute), and cessation of cardiac output was confirmed. The graft was then deployed under fluoroscopic guidance before return of normal rhythm and cardiac function.
The cannulation of the two tunnels of the stent graft was expected to be challenging due to unusual anatomy and orientation of the great vessels. Therefore, meticulous pre-procedure planning using the CT scan identified the best image angulation and tube position that unravel the origin of the tunnels in relation to the carotid arteries. Right and the left common carotid artery approaches were utilised sequentially to cannulate the tunnels in thoracic endograft. This approach was chosen because the carotid retrograde approach had a straight angle. Lifestream© (Bard Medical, Covington, GA, USA) (8 mm × 58 mm) balloon expandable covered stent was introduced first and followed by VIABHAN © (W.L. Gore & Associates, Inc., Newark, DE, USA) (13 mm × 50 mm) in each side and deployed in telescopic fashion. The left and right common carotid arteries measure 6.8 and 6.6 mm, respectively. The stent graft tunnels measure 10 mm each. It was the operator’s choice to use higher radial force balloon expandable covered stent first to strengthen the stented segment of the artery as it comes off the native aortic arch and courses through the thoracic inlet while leaving the lower profile covered stent to overlap with the tunnel and match up the needed oversizing.
No balloon expandable or self expandable bare stent was used to strengthen the Viabhan stent because the course of the stent was quite straight and not compromised. This is different from chimney technique where the bridging stent is competing with the main stent graft for space.
No kissing balloon was used in this case as the adjacent tunnels of the branch graft are close but separate from each other.
Post-operatively, the patient was managed on the intensive care unit for 24 h and then in an intermediate care unit for another 48 h. His post-operative recovery was complicated with a chest infection that required treatment with intravenous antibiotics. A CT scan performed on post-operative day 5 revealed good position of the thoracic endograft and carotid stents () with no endoleak or graft kinking. He was subsequently discharged home on post-operative day 7. The patient demonstrated no clinical or radiological evidence of stroke. He remains well on 18-month follow-up with significant improvement in the presenting complain of mild dysphagia. The 18-months’ CT angiography that covers the head, neck and chest shows complete aneurysm seal, patent branches, patent vertebral arteries with intact circle of Willis and slight shrinkage in the Kommerell’s diverticulum and arch aneurysms, measuring 3.6 and 4.8 cm, respectively. There was no evidence of brain infarct.
Ethical approval was waived according to our institutional ethics committee rules.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [78, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 78 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 2 + 1 = 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
1092,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7444743-1,Extracted,"A 78-year-old gentleman with a past medical history of diabetes mellitus, coronary artery disease status post coronary artery bypass graft, peripheral vascular disease, atrial fibrillation on warfarin, chronic obstructive pulmonary disease, chronic kidney disease stage 3, and bipolar disorder was brought to the ER after a mechanical fall. He denied any typical symptoms associated with SARS-CoV-2 including cough, fever, chills, shortness of breath, sore throat, or gastrointestinal symptoms. As he resided in a nursing facility, he was tested for SARS-CoV-2 (polymerase chain reaction, PCR testing) on admission which resulted positive. On physical exam, there was an erythematous, diffuse morbilliform rash without scale, most prominent on the back and the neck (Figures -). The rash was maculopapular, blanchable, and with large areas of confluence. It was nontender and nonindurated on palpation. He had noticed the rash a day prior and complained of pruritis. He denied the usage of any new medications, foods, clothes, or skin products in the preceding weeks. He denied any recent travel or sick contacts. There was no significant occupational exposure as he was retired. He denied long hours of sun exposure. The patient had no other signs or symptoms of an infectious process on admission. He had no prior history of HIV, infective endocarditis, or injectable drug use. Vital signs were normal and the patient was saturating well on room air. Laboratory testing revealed a chronic normocytic, normochromic anemia (Hgb 10g/dL), mild thrombocytopenia (118,000/microliter), and chronic lymphocytopenia (absolute lymphocyte count 0.7 10*3/microliter). No abnormalities were noted on the liver panel. He had an acute kidney injury on chronic kidney disease which improved during the hospitalization. The initial chest X-ray did not show any abnormalities. A biopsy of the rash was not pursued due to the patient being on oral anticoagulants. The rash was treated with oral diphenhydramine and topical triamcinolone 0.1% cream. He later developed fever up to 101 degrees Fahrenheit, which resolved prior to discharge with no further signs of an infectious syndrome.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [78, 'years'], 'sex': 'Male', 'Congestive Heart Failure': False, 'Vascular disease history': True, 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 78 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 3 + 1 = 4.
The patient's CHA2DS2-VASc Score is 4."
1093,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7714747-1,Extracted,"A 54-year-old male landscaper with no significant past medical or surgical history presented to the hospital with fatigue, lightheadedness, decreased appetite, nausea, vomiting, dark stool, and significant weight loss for the one-month duration. He denied headaches, dizziness, night sweats, hemoptysis, shortness of breath, chest pain, constipation, diarrhea, abdominal pain, dysuria, and hematuria in the recent past. The patient denied taking any home medications, including over-the-counter medications, and he denied any history of tobacco, alcohol, or recreational drug use.
He appeared cachectic, fatigued, and was cooperative but in no acute distress. He was conscious, alert, and oriented to person, place, and time. The physical exam was significant for cachexia and abdominal distention but otherwise unremarkable, including a benign cardiovascular, respiratory, abdominal, neurological, and skin exam. His initial vitals were notable for elevated heart rate at 110 beats/minute and body mass index (BMI) of 17.1 kg/m2 but were otherwise within normal limits. Pertinent lab results on admission are listed in Table . He met systemic inflammatory response syndrome (SIRS) criteria on admission with elevated white blood cell (WBC), elevated heart rate, and elevated lactate. Urinalysis and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Abbott (dry swab) were negative.
CT of abdomen and pelvis with contrast was done, and pertaining results are depicted in Videos - and Figures -.
According to the radiology report, the right kidney was markedly abnormal, demonstrating features suggestive of xanthogranulomatous pyelonephritis, including a large staghorn calculus at the lower pole and diffuse cortical thinning consistent with ""bear paw sign"" (Figure ). The right renal cortex was diffusely infiltrated by a heterogenous complex mass, suggestive of possible neoplasm. There was marked hydronephrosis containing locules of air, which appeared to be related to a fistula from the antrum of the stomach to a superior right renal calyx (Figure ). There was no hydroureteronephrosis and no air seen in the right renal collecting system. Inflammation surrounded the right kidney, and there were some ill-defined, enlarged lymph nodes in the upper right quadrant. Nodular densities suspicious for implants were seen posterior and lateral to the right kidney and along the paracolic gutter, the largest along the facia posterior to the right kidney, and measured up to 1.8 centimeters (Figures -). Additional nodular implants were seen inferior to the right hepatic lobe (Figure ) with some perihepatic ascites. The nodular implants may be related to the extension of the process in the right kidney. The left kidney appeared within normal limits with no hydronephrosis (Figure ). The stomach was markedly dilated to the level of the gastric antrum with likely gastric outlet obstruction (Figure ). The duodenum and small bowel were essentially collapsed. The infrarenal inferior vena cava were not seen, suggesting chronic thrombosis, possibly may be secondary to extension of the mass. The mass was seen encasing and narrowing the superior mesenteric artery and partially encasing the abdominal aorta. The right renal vein and artery were also not readily visualized, presumably thrombosed/obliterated. The portal vein, splenic vein, and superior mesenteric vein were patent, and a prominent azygous vein was noted. A nodular right adrenal gland was seen as well. Moderate pleural effusions could be seen in both lungs (Figure ).
The patient was given two units of packed red blood cells on admission with intravenous 1 liter sodium chloride 0.9% for over 30 minutes. All electrolytes were repleted as needed. He was put on nil per os (NPO) with intravenous total parenteral nutrition due to gastric outlet obstruction. The patient was transferred to a tertiary care center for further evaluation and treatment. Endoscopy was performed, and the antral and duodenal mucosa biopsy revealed well-differentiated, keratinizing squamous cell carcinoma pathology. The mass involved the antrum and proximal duodenum, adjacent to the fistulous communication area between the right renal collecting system and the gastric antrum. The patient was scheduled for palliative gastrojejunostomy. Unfortunately, the patient decompensated in the following days from complications of the carcinoma and was placed on comfort measures only. The patient expired shortly afterward.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [54, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",0,0,0,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 54 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 0. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 0.
The patient's CHA2DS2-VASc Score is 0."
1094,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6823064-1,Extracted,"A 47-year-old Caucasian female with a known medical history of essential hypertension being treated with labetalol came to the emergency department (ED) with complaints of non-exertional, intermittent (lasting one to two minutes), 3/10, left-sided chest pain which started three days ago. At the time of presentation, the patient was asymptomatic. She was afebrile with a blood pressure of 188/90 mmHg, heart rate of 73 beats per minute, respiratory rate of 16 per minute and normal oxygen saturation levels. Physical examination revealed a faint 1/6 systolic murmur which accentuated to 2/6 in intensity when she was made to go from crouching to standing. The remainder of the physical exam was unremarkable. The patient denied any pertinent family history. She was a former smoker and reported no allergies. Laboratory studies disclosed normal serum chemistry with normal troponin and brain natriuretic peptide (BNP) levels. Electrocardiogram (EKG) showed normal sinus rhythm with no ST-T wave changes. A chest radiograph identified borderline cardiomegaly with no evidence of infection or pulmonary vascular congestion.
A transthoracic echocardiogram (TTE) was pursued, which revealed normal left ventricular (LV) size and function. LVOT appeared normal without sub-valvular ridge or asymmetric septal hypertrophy. Mitral valve demonstrated normal-appearing leaflets; however, there was a large centrally echolucent sub-valvular chordal cyst greater than 1 cm in the largest diameter (Figure ). Due to concerns of possible exertional LVOT obstruction, an exercise stress echocardiography was scheduled. Labetalol was switched to carvedilol due to the latter’s negative inotropy and better heart rate control. During exercise stress echocardiography, the patient exercised to stage five Bruce protocol achieving 14.5 metabolic equivalents (METs). There was no suggestion of obstruction on doppler at rest however, transient LVOT obstruction was noted with exercise. The patient had an appropriate heart rate and blood pressure response to stress with no signs of coronary ischemia or regional wall motion abnormalities. (Figures -).
A cardiac magnetic resonance imaging (MRI) showed no evidence of increased enhancement confirming the diagnosis of a benign subvalvular blood cyst of the mitral apparatus. In light of asymptomatic nature of the condition, mild to moderate LVOT obstruction at peak exertion in a beta-blocker deprived state, a conservative strategy was opted after multidisciplinary discussion with cardiothoracic surgery. The patient was resumed on carvedilol and was advised to maintain adequate hydration to avoid worsening of LVOT obstruction due to dehydration. A surveillance stress echocardiogram done during six months follow-up visit showed stable exertional hemodynamics.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [47, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 47 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
1095,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8188873-1,Extracted,"In 2010, a 49-year-old asymptomatic woman was referred to our hospital because a chest radiograph revealed an abnormality in the left cardiophrenic angle. She had no particular medical or medication history. Cardiopulmonary examination and vital signs were normal, and electrocardiogram (ECG) revealed normal sinus rhythm. The chest radiograph showed a homogenous density (). She was ultimately diagnosed with a benign pericardial cyst via contrast-enhanced chest CT () and MRI. The attenuation of the cyst on CT was 5–10 Hounsfield units. Neither pleural effusions nor mediastinal lymphadenopathy was evident on CT. Given that she was asymptomatic at the initial diagnosis, our team decided to pursue conservative management with regular follow-up. As time passed, although the cyst increased in size, the patient remained asymptomatic. It was not until 2020 that she began to experience palpitations and shortness of breath with exertion. Follow-up CT () and MRI revealed a 12 cm (major axis) pericardial cyst in the left cardiophrenic angle associated with left ventricular compression and new-onset atrial fibrillation on ECG. T1-weighted MR image showed a round low-signal intensity cyst with a regular thin wall. Axial and sagittal T2-weighted MR image showed a well-circumscribed high-attenuated cyst in contact with the left cardiac margin (). The patient was scheduled for thoracoscopic resection of the pericardial cyst per our cardiac team’s recommendations. Pre-operative transthoracic echocardiography revealed a large, fluid-filled, echolucent space in the left hemithorax. Left ventricular size was decreased, with normal systolic function and moderate mitral regurgitation with a left atrial enlargement (Video 1). The left atrium diameter was 40 mm. Operative visualization was provided by 3D VATS. Three small incisions about 1 cm in length for trocar insertion were made in the fourth, fifth, and sixth intercostal spaces. Ports facilitated the introduction of a camera and left- and right-hand instruments. Surgeons carefully peeled away the cyst, which contained clear water-like fluid ( and ). Histopathological findings revealed a cyst wall composed of a thin layer of fibrous tissue lined with a single layer of mesothelial cells (). The patient’s post-operative course was uneventful. We performed cardioversion for her atrial fibrillation on post-operative Day 7, and the patient maintained normal sinus rhythm afterwards. Post-operative echocardiography showed mild mitral regurgitation (Video 2). The patient is doing well and has no post-operative symptoms.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [49, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 49 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1096,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4520885-1,Extracted,"A 44-year-old woman was admitted to our hospital with a drowsy mental status since a few days ago. She had a history of ulcerative colitis that was treated with medication (oral prednisolone 35mg/day, mesalazine 3,000 mg/day). Two weeks prior to admission, she had discontinued the steroid treatment and wanted to be treated with alternative medicine that included sodium chloride, multivitamin, and selenium with discontinuation of her regular diet.
Clinically, she was severely dehydrated due to frequent watery diarrhea. She was hypotensive and her blood pressure was 80/50mmHg. On initial examination, she was stuporous and slightly confused, and she responded only to painful stimuli and had weakness in both arms and legs. A hypoactive deep tendon reflex was present, but there were no other focal neurological deficits or neck stiffness.
Initial blood laboratory test results showed a sodium level of 197mEq/L (range, 135-146mEq/L), potassium level of 2.9mEq/L (range, 3.5-5.3mEq/L), chloride level of 159mEq/L (range, 99-108mEq/L), blood urea nitrogen level of 96mg/dL (range, 8-19mg/dL), creatinine level of 1.56mg/dL (range, 0.67-1.17mg/dL), serum osmolality of 415mOsm/kgH2O(range, 280-300mOsm/kgH2O), ACTH level of 3.99 pg/mL (range, 7.2-63.3 pg/mL), and serum cortisol level of 30.84 ug/dL (range, 4.3-22.4 ug/dL). Urinalysis showed a specific gravity of 1.030, osmolality of 885mOsm/kgH2O, urine sodium level of 12.0mEq/L, and urine creatinine level of 128.1mg/dL.
The patient was admitted to the medical intensive care unit where intravenous fluids were rapidly administered and serial monitoring of electrolytes and osmolality was started. There was no evidence of adrenal insufficiency, but we intravenously administered dexamethasone 5mg and hydrocortisone 100mg/day considering her history of steroid use for protection from adrenal insufficiency. Immediate treatment with 0.45% saline and 5% dextrose water was started along with modification of the rate and concentration so that the fall in serum sodium level did not exceed 0.5mEq/L/hour. Despite our effort to avoid very rapid correction of hypernatremia, the correction rate exceeded 1mEq/L/hour (, ).
Six days after admission, the serum sodium level was 149mEq/L and she had partially recovered her mental status, especially her early depression of consciousness level; however, weakness in all extremities persisted. Diffusion-weighted (DW) magnetic resonance imaging (MRI) performed on hospital day 6 revealed multifocal, symmetric, diffusion restriction within the lateral pons, thalami, and splenium of the corpus callosum(). However, there were no abnormal signal intensity changes on fluid-attenuated inversion recovery (FLAIR) images. Considering the clinical and radiologic findings, despite the unusual pattern in the pons, our diagnosis was osmotic demyelination syndrome involving both the lateral pontine and extrapontine sites associated with rapid correction of hypernatremia. The patient was closely observed and was treated with corticosteroid therapy and conservative management including nutritional support.
Follow-up MRI performed on hospital day 30 revealed high signal intensity changes in the lateral pons and bilateral thalami on FLAIR images, which were pseudonormalized on DW images (). The previously noted corpus callosum lesion had resolved on FLAIR and DW images. The patient's mental status and motor weakness were improved, and she was discharged to a rehabilitation hospital at hospital day 49. She remained free of neurologic symptoms during the 6-month follow-up period, and the serum sodium concentration had stabilized.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [44, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 44 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1097,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-8256405-1,Extracted,"We report of a 58-year-old woman, who did not suffer from any pre-existing medical conditions, with the only exception of being mildly overweight (BMI 31.25). In particular, she did not smoke, she had no history of migraine, and she did not receive any hormone replacement therapy after menopause, that occurred at age 51. One hour after the execution of her first-time (later revealing as negative) nasopharyngeal swab, while driving home, she likely experienced amnesia: the bystanders reported that the woman pulled over the car, lowered the window and called for rescue, telling she was unable to find the right direction; when she was asked where she was going, she answered she did not remember and began to behave anxiously. The bystanders reported that she could tell her name and other personal information, and that she could herself remember the unlock code of her phone and call her husband. The husband noticed she was disoriented, repeatedly asking the same questions about where she was and what she was doing. This episode lasted for about two hours then reverted; the day after, she was conducted to our attention for evaluation. A memory gap for the episode persisted: she could remember having had the swab tested, then having paid for the test, having left the hospital, and reached the car after the procedure, but she could not remember the following events, including those witnessed by the by-standers and including the call to her husband and its arrival on the place where she had left her car.
Neurological examination was normal. Brain MRI, performed one day after TGA, revealed a hippocampal punctate area of DWI restriction (Fig. ), confirming the clinical suspect. Supra-aortic vessels Duplex ultrasonography and EEG were negative, ruling out mimics. The strict temporal relationship between nasopharyngeal swab and TGA may have been simply coincidental, but we are usually prone to investigate each time carefully the triggers for TGA, since TGA recent anamnesis is often full of peculiar, even bizarre, but usually biologically fitting antecedents.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [58, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 58 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1098,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7219983-1,Extracted,"A 55-year-old man presented to the emergency department (ED) of an urban, academic, medical center with intermittent palpitations (fast beats accompanied by a “pounding” sensation in the chest) for the prior month. Palpitations were most noticeable at night but had become more severe and constant over the preceding three days. He also reported shortness of breath while supine in bed and lightheadedness with exertion. The patient is an avid hiker, so he only presented once his dyspnea prevented him from completing a typical family hike. He denied any chest pain, fevers, weight loss, syncope, leg swelling, cough, nausea, vomiting, or rashes.
The patient was diagnosed with type 1 diabetes mellitus when he was 30 and has a history of hypertension. He was taking insulin glargine nightly with sliding-scale insulin aspart during meals and had recently switched from ramipril to losartan 50 milligrams (mg) daily due to nocturnal cough. He denied any drug, alcohol, or tobacco use. His father died suddenly at age 42 due to a heart attack. He denied any allergies.
The patient’s vital signs on presentation were as follows: temperature 97.2 degrees Fahrenheit; blood pressure 131/83 millimeters of mercury (mm Hg); pulse 55 beats per minute, respiratory rate 18 breaths per minute; and oxygen saturation 99% on room air, with a body mass index of 28.6 kilograms per meters squared. Physical exam revealed a well-developed and well-nourished male patient in no acute distress. His head was normocephalic and atraumatic. His eye exam was normal with pupils that were equal, round, and reactive to light. No scleral icterus was seen. His neck was supple and had normal range of motion. There was no jugular venous distension seen. The patient’s cardiac exam was notable for a bradycardic and irregularly irregular heartbeat without a murmur. His lungs were clear to auscultation bilaterally, and no wheezes or rales were heard. The patient’s abdomen was soft, non-tender, and non-distended. His extremities were warm and well perfused, and without edema. The patient’s cranial nerves II–XII were intact, and gait and strength assessments were unremarkable. No pronator drift was seen. Skin was normal in appearance, without any lesions or rashes. The patient demonstrated a normal mood and affect throughout the history and exam.
A chest radiograph (CXR) and electrocardiogram (ECG) were obtained ( and , respectively). Laboratory studies () were notable for a white blood cell count of 6.2 thousand per microliter, hemoglobin of 15.1 grams per deciliter, platelets of 190,000 per microliter, glucose 250 milligrams per deciliter, negative troponin, B-type natriuretic peptide (BNP) of 502 picograms per deciliter, a thyroid stimulating hormone level of 1.2 milli-international units per liter with free thyroxine of 1.4 nanomoles per liter, and a Borrelia Burgdorferi IgM/IgG (immunoglobulin) titer of 0.28, negative antinuclear antibody test. (The latter test resulted after the patient was admitted.) While in the ED the patient experienced an acute episode of palpitations. His rhythm, as recorded by telemetry, is shown in . An echocardiograph was performed, which showed severe global hypokinesis with a left ventricular ejection fraction (LVEF) of 15%, mild dilation, biatrial enlargement, and no pericardial effusion.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [55, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 55 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 0 + 1 = 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 1 + 1 = 2.
The patient's CHA2DS2-VASc Score is 2."
1099,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2254639-3,Extracted,"A 76 years old woman presented to the Emergency Department with complaints of abdominal pain, and an abdominal mass in the right upper quadrant. She had a history of congestive heart failure, chronic atrial fibrillation, chronic obstructive lung disease, ischemic cerebrovascular disease and myocardial infarction. The patient had been taking warfarin sodium 5 mg/day for atrial fibrillation for 2 years without medical supervision. On physical examination painful mass in the left lower quadrant and suprapubic region of the abdomen was observed. Ausculatation of the abdomen revealed hypoactive bowel sound. Mean arterial pressure was 140/80 mmHg, pulse rate 118/min, hemoglobin level 13.32 g/dL, hematocrit 30.26%, platelet 199000/UL, PT: 79.2 sec, aPTT: 56 sec, INR: 6.68. The other biochemical tests were normal. Abdominal CT revealed rectus sheath hematoma (Figure ). During the follow up period 6 units of fresh frozen plasma was administered. Due to the hemodynamic stability patient was referred to the Internal Medicine Department.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [76, 'years'], 'Congestive Heart Failure': True, 'Stroke': True, 'Transient Ischemic Attacks History': True, 'Vascular disease history': True}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 76 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
1100,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7649495-1,Extracted,"A 57-year-old Caucasian man diagnosed with HF due to hypertensive dilated cardiomyopathy associated with permanent AF was referred to an exercise training program. He had non-insulin-dependent diabetes mellitus and LVEF was 35%. The functional class was III [(New York Heart Association (NYHA)] and drug therapy was according to the III Brazilian Guideline on Heart Failure and II Brazilian Guideline on Atrial Fibrillation: Losartan 100 mg, Furosemide 40 mg, Carvedilol 150 mg, Warfarin 5 mg, Simvastatin 20 mg, Metformin 1700 mg, and Omeprazole 20 mg. Because of a long history of AF, rate control strategy was implemented. The patient did not have a history of neuromuscular or pulmonary disease. He never smoke and did not drink alcohol. According to his level of physical activity, he led a sedentary life, defined as self-reported less than 1 day/week of planned, structured, and repetitive exercise. His body mass index was 36.8 kg/m2 and resting blood pressure was 115/80 mmHg. Resting electrocardiogram showed AF with an average heart rate of 75 b.p.m.
The supervised exercise training program was carried out three times a week, for a period of 12 weeks in a closed environment, with a controlled temperature between 21°C and 24°C in the afternoon (3:30 pm to 4:30 pm). The exercise training protocol consisted of 5 min of warm-up exercises, 30 min of aerobic training performed on a cycle ergometer at 60 rpm, 20 min of resistance exercises with lower and upper limbs and 5 min of relaxation exercises. The workload was adjusted during the stimulus phase of the aerobic training to keep the perceived effort intensity between 11 (relatively easy) and 13 (slightly tiring) of the Borg Scale. Resistance training was performed in a weight training station and consisted of 2 sets of 10 repetitions, and the following sequence of exercises: leg extension, leg curl, lat pull-down, peck deck, and press chest. The initial workload was set at 60% of 1 repetition maximum. He was encouraged to complete the sets of 10 prescribed repetitions, performing the appropriate movement and avoiding Valsalva manoeuvre. He was instructed to rest for 30–60 s between sets. The intensity of the exercise was increased from 5% to 10% whenever the patient adapted to the exercise workload thorough the 12 weeks of training.
After 12 weeks of supervised sessions, the patient became asymptomatic (NYHA I) and was instructed to continue exercising at home.
displays the results of the cardiopulmonary exercise test before and after 12 weeks of exercise training, performed on a cycle ergometer, using the modified Balke protocol (25 w/min). Comparing the exercise test before and after 12 weeks, we observed that the rest HR reduced and the peak HR increased, and that systolic blood pressure increased, and diastolic blood pressure decreased at the peak of exercise. Peak oxygen consumption (VO2peak) increased and VE/VCO2 slope decreased after training. shows data on muscle sympathetic nerve activity (NMSA) before and after the intervention, obtained by a microelectrode implanted in the fibular nerve and recorded by the shots per minute and every 100 b.p.m. We observed that the shots decreased in both registers, indicating a reduction in NMSA. The muscle blood flow (MBF), obtained by plethysmography venous occlusion, increased after exercise intervention as shown in .",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [57, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False, 'Diabetes history': True}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 57 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 0 + 1 = 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 2 + 1 = 3.
The patient's CHA2DS2-VASc Score is 3."
1101,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5749288-1,Extracted,"The patient is an 80-year-old female with a history of recurrent abdominal pain. Permission was obtained from the patient to allow discussion and publication of his case. The patient had a history of coronary artery disease, atrial fibrillation (on anticoagulation), multiple cerebral vascular accidents, chronic obstructive pulmonary disease, an aortic and mitral valve replacement, and a prior hysterectomy. The patient was noted to have presented to the hospital three times in the prior month with similar complaints of vague, diffuse abdominal pain that would last a few hours and resolve. The patient did note nausea and vomiting with these episodes. The patient re-presented to the emergency room, where a CAT scan was performed () which showed mesenteric swirling secondary to possible internal hernia. The patient underwent a small bowel follow through with gastrografin, which demonstrated no abnormalities. The patient then underwent an obstructive series that was also noted to be normal. The patient's symptoms, however, did not subside. Due to the chronicity and the unresolving symptoms, the patient was brought to the operating room after a long discussion of possible outcomes with the patient.
The operation was started laparoscopically but was soon converted to an open laparotomy due to a large mass of small bowel swirled onto itself that was adhered together (). In mobilizing the small bowel, blunt dissection was used to lyse adhesions and untwist the mesentery. The small bowel mesentery was observed, and no mesenteric defects were noted. It was seen that the mesentery had swirled and twisted upon itself (). While running the bowel, a large, proximal jejunal diverticulum was present. The diverticulum was excised using a 60 mm stapler. The bowel was run from the ligament of Treitz down to the ileocecal valve with no mesenteric defects noted, and all bowel was viable. The small bowel was returned to the abdomen. The patient did well postoperatively and was seen in follow-up without complication.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': True, 'age': [80, 'years'], 'Stroke': True, 'Transient Ischemic Attacks History': True, 'sex': 'Female'}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 80 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is present. Based on the patient note, the patient history for thromboembolism is absent. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 6 + 1 = 7. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 7.
The patient's CHA2DS2-VASc Score is 7."
1102,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-1192795-1,Extracted,"A 70 year old man was admitted with more than one year history of abdominal distension and a weight gain of 10 kilograms. He was evaluated in another center and was given the diagnosis of ascites associated with cirrhosis.
His past medical history was significant due to acute myocardial infarction in 1974, mild asthma and paroxysmal atrial fibrillation. Since his last evaluation, he has been receiving diltiazem 180 mg/day, aspirin 100 mg/day, digoxin 0,750 mg/week and spironalactone 50 mg/day. He is asymptomatic and walks 2000–3000 meters a day without angor or dyspnea.
The physical examination shows moderate abdominal distension, with no hepatosplenomegaly or edema, and there is mild jugular vein distension (1/3). The hepatojugular reflux was negative. His blood pressure is 130/70 mmHg, pulse 70/ min and regular. The cardiac auscultation is normal and his lungs are clear. His current weight is 78.8 kg. One year before this admission he weighted 70 kg and before starting diuretics he was weighting 81 kg.
The blood laboratory was normal, except for a slightly increase in gamma-glutamyltransferase and 5'nucleotidase (Table ). A paracentesis was performed which showed a milky fluid with a high albumin gradient showing portal hypertension (Table ), all cultures and cytological studies were negative. Other studies showed normal iron values; antiHIV, HBsAg, antiHBs, antiHBc IgM and antiHCV negative, antiHBc IgG positive; ANA, AMA, SMA y ANCA negative.
A helical CT scan of the abdomen showed mild hepatomegaly, mild enlargement of caudate lobe and ascites. An upper endoscopy ruled out esophageal varices and portal hypertensive gastropathy. A Doppler ultrasound showed a patent portal vein, with a normal diameter (6.6 mm) without alterations in the flow. A cardiac ultrasound showed moderate to severe systolic left ventricle dysfunction with global hypokinesia and the inferolateral wall was akinesic. The left ventricle diameters were normal and the left atria was enlarged (52 mm). The estimated left ventricular ejection fraction was 35%. There were no relevant valve signs, nor mitral or tricuspid regurgitation, nor pericardial disease.
A liver biopsy showed engrossment of centrilobular veins walls and fibrosis, with centrilobular hemorrhage and marked sinusoidal dilatation in acinar zone 3, suggesting increased intrahepatic venous pressure. An angiogram showed dilated but patent suprahepatic and portal veins and inferior vena cava, with slow flow. The measure of free suprahepatic, wedge suprahepatic, pulmonary capillary wedge, pulmonary artery, right ventricle and right atrial pressures confirmed the diagnosis of portal hypertension related to heart failure (Table ). He began treatment with furosemide 40 mg/day and spironalactone 100 mg/day; he continued treatment with aspirin, digoxin and diltiazem. The patient lost 8 kg and the abdominal distension was resolved approximately 2 month after the beginning of the treatment. Given the good response to treatment we decided to withhold other possible treatments (i.e. angiotensin-converting enzyme inhibitors).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [70, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 70 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
1103,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5358179-1,Extracted,"A 65-year-old woman with type 2 diabetes mellitus was admitted with left ventricular failure and accelerated hypertension (blood pressure of 180/100). She was a known case of ischemic dilated cardiomyopathy (DCM) with severe left ventricular (LV) dysfunction and long standing AF with fast ventricular rate (). Chest film showed pulmonary venous hypertension; two-dimensional transthoracic echocardiography showed dilated chambers with global systolic dysfunction with ejection fraction (EF) of 30%. Treatment was initiated with intravenous nitroglycerine infusion and frusemide. Subsequently, her blood pressure and failure symptoms were brought under control. During hospital stay, she developed profuse diarrhoea followed by severe hyperkalemia (serum potassium 8.3 mEq/L). Her complete blood count, renal and liver parameters were normal. Arterial blood gas analysis showed compensated metabolic acidosis.
She was promptly treated with intravenous calcium gluconate, insulin dextrose infusion and salbutamol nebulisation. Serum potassium levels normalized to 5.4 mEq/L. ECG was repeated the next day, which showed sinus rhythm at 64 beats per minute. The patient was discharged on control of her failure symptoms after 5 days of hospital stay with aspirin, ACE inhibitors, low dose loop diuretics, beta blockers, digoxin and eplerenone. She had a CHADS-VASc score of 3 and was started on lifelong oral anticoagulation with warfarin to maintain INR of 2-3. ECG done at discharge and at 1 month follow-up revealed that the patient maintained normal sinus rhythm ().",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [65, 'years'], 'Congestive Heart Failure': True, 'Hypertension history': True, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 65 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is female and so one point is added to the score, making the current total 1 + 1 = 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
1104,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2646693-1,Extracted,"A 30-year-old male patient presented to the emergency with severe pain with an onset at the front part of the chest followed by spreading to the back and arms, nausea and excessive sweating developing during a football match. The investigations performed revealed anterior wall infraction and thus he was admitted to coronary intensive care unit. Thrombolytic treatment (streptokinase, 1.5 million IU/1 hour) and metoprolol 50 mg 1 × 1 and ASA 300 mg 1 × 1 were administered. The patient, who recovered from chest pain following thrombolytic treatment, was referred to our center to undergo coronary angiography at Day 3. Patient's history was normal except for smoking (1 packet/day/10 years). The patient was detected to play football occasionally since his childhood; however, we learnt that he had started playing without warm-up exercises at the last football match. His family history included no risk factors regarding coronary artery disease. On physical examination, arterial blood pressure was 120/70 mmHg, pulse was 88 beats/min and the other findings were normal. Electrocardiography revealed ST segment elevation on anterior leads (V2-5) and T negativeness (Figure ). Troponin I was measured to be 4.54 ng/mL (0.0 – 0.04), blood glucose and lipid panel were within normal limits. Echocardiography detected minor aneurysm in the left ventricular apex. Coronary angiography detected a lesion with an onset in the left anterior descending artery following the 1st diagonal and extending to the 2nd diagonal and exhibiting a significant contraction during systole, which returned to normal during diastole (Figure , ). The right and circumflex artery was normal and ventriculography revealed normal findings except for mild dyskinesia in the apex (Figure ). Sports requiring heavy effort were prohibited and the patient was discharged with prescriptions of acetyl salicylic acid 300 mg 1 × 1, metoprolol 50 mg 1 × 1. At the follow-up visit taking place 3 months later, he had no complaint.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [30, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True, 'Diabetes history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 30 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is male and so no points are added to the current total, keeping the total at 0.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 0.
The patient history for hypertension is absent. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 0.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 0.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 0 + 1 = 1. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1105,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-7243931-1,Extracted,"An 85-year-old female patient presented to the emergency department 3 h after receiving hemodialysis, with severe left loin pain and dizziness. Her blood pressure was 70/40 and pulse was 110 not responding to bolus infusions of normal saline. Serum hemoglobin was 60 g/L. Examination revealed a left hypochondrial tender mass, with clinical evidence of hemorrhagic shock. An emergent CT of the abdomen and pelvis was done and showed extensive left retroperitoneal hemorrhage and heterogeneous left kidney. The patient was on warfarin and had end-stage renal disease (ESRD) secondary to diabetes mellitus, atrial fibrillation, congestive heart failure, diastolic dysfunction, coronary artery bypass grafting, and hypertension.
She was positioned with left flank elevated 45° and left retroperitoneal subcostal transverse lateral lumbotomy was done. The retroperitoneal cavity was full of blood clots that were removed; this was rapidly followed by kidney dissection using blunt dissection and Ligasure vascular control. The renal pedicle was soon accessible and Hem-o-lok clips were used for pedicle control. The kidney was safely removed and the whole procedure was completed in 35 min. The patient vitals were stabilized and she was transferred to ICU for 24 h observation.
Pathology showed extensive sclerosed glomeruli, marked interstitial inflammation, severe arteriosclerosis, perirenal and renal parenchymal hemorrhage, severe renal artery atherosclerosis, and ACKD. and show the enlarged left kidney with massive retroperitoneal hemorrhage on CT scan.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': True, 'Hypertension history': True, 'Thromboembolism history': False, 'Vascular disease history': True, 'age': [85, 'years'], 'Stroke': False, 'Diabetes history': True, 'Transient Ischemic Attacks History': False, 'sex': 'Female'}",7,7,7,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 85 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 3 + 1 = 4.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 4 + 1 = 5.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 5.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 5 + 1 = 6. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 6 + 1 = 7.
The patient's CHA2DS2-VASc Score is 7."
1106,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2572024-1,Extracted,"A 72-year-old man presented to the emergency department with the complaint of palpitation, progressive dyspnea and mental status deterioration present for four days. Physical examination revealed a blood pressure of 70/40 mmHg and an irregular heart rate of 190-240 beats per minute. The 12 lead- electrocardiogram showed preexcited atrial fibrillation (). Urgent cardioversion was required. So transesophageal echocardiography was performed to rule out the presence of left atrial thrombus. Echocardiography revealed a mitral valve area of 1.19 cm2 with a gradient of 20/10 mmHg, moderate tricuspid regurgitation and no left atrial thrombus. A biochemical profile obtained on admission revealed high levels of serum glutamic-oxaloacetic acid transferase (SGOT), serum glutamic pyruvic transaminase (SGPT), international normalized ratio (INR) and creatinine (CR) (SGOT 1800 IU/L, SGPT 3600 IU/L, INR 6.3 CR: 2.8 mg/dl) indicating hepatic and renal failure. Because of hemodynamic instability, immediate cardioversion was performed. But multiple attempts of electrical cardioversion using biphasic energy failed to restore normal sinus rhythm. Also it was not possible to control the ventricular rate medically. Because of hepatic failure, amiodarone couldn't be given to control the ventricular rate. After obtaining informed consent the patient was transferred to the electrophysiology laboratory. Because stable cannulation of coronary sinus was not possible due to anatomical reasons, two electrode catheters, one 6-French Josephson catheter, and one 7-French ablation catheter (Medtronic, Minneapolis, MN), were advanced through both femoral veins and placed at right ventricular apex, and tricuspid annulus positions. During AF, full preexcitation was present in 12-lead ECG. According to 12-lead ECG, accessory pathway was right paraseptal in location. But to exclude the possiblity of a left-sided paraseptal accessory pathway, coronary sinus was mapped by the ablation catheter. Mapping of coronary sinus revealed that earliest ventricular activation in coronary sinus was located in the ostium. Then, endocardial mapping of the tricuspid annulus during preexcited AF showed the area of earliest ventricular activation at the level of the right midseptal region (: ). Current was delivered at this site using automatic temperature control with a maximum power setting of 30 watt and a target temperature of 50ºC. Because it was impossible to follow 1:1 AV conduction during ablation, we only observed bradycardia and regularity of the rhythm to follow AV conduction. Radiofrequency current was then applied abolishing the preexcitation in the first second of the application without bradycardia and regularity of AF (). Then after 20 seconds, setting of the generator was changed to a maximum of 50 watt and a target temperature of 60ºC. Ablation was performed for total of 60 seconds. After ablation, AF was still present, but the rate was less than 100 bpm and QRS complexes were narrowed. No preexcitation was seen and there was no AV block. After ablation procedure, electrical cardioversion was reattempted and sinus rhythm was restored. But after 1 hour, atrial fibrillation resumed again. Because mitral stenosis was present and the recurrence risk of AF was high after even a successful cardioversion and rate control was perfect after ablation of accessory pathway, cardioversion was not considered. After ablation, rate control was obtained by AV nodal blocking agents easily. SGOT, SGPT, INR and CR levels reduced to normal range after sixth day of ablation.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [72, 'years'], 'Congestive Heart Failure': False, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",1,1,1,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 1.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 1.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 1. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 1.
The patient's CHA2DS2-VASc Score is 1."
1107,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-3539102-1,Extracted,"A 72-year-old man presented with exertional chest pain. He was an ex-smoker and had diabetes mellitus. He visited the department of chest surgery for a palpable abdominal mass. The diagnostic work-up showed ascending and abdominal aortic aneurysm, aortic stenosis, and severe discrete concentric stenosis in the mid portion of the right coronary artery (RCA) with mild ectatic change (). Aortic valve replacement (AVR; with a Carpentier-Edwards Perimount Magna 23-mm valve), reduction aortoplasty of the ascending aorta (with the suture plication technique and external wrapping with a 26-mm vascular graft), and coronary artery bypass graft (CABG; left great saphenous vein from aorta to distal RCA) was done. After 6 months, replacement of the abdominal aorta with a Hemashield 20-mm straight graft was done.
At 7 months after the last surgery, the patient developed exertional chest pain. Coronary computed tomography (CT) angiography showed two focal sites of significant, eccentric stenosis in the mid RCA and total occlusion of the LGSV to RCA. (). Echocardiography showed acceptable bioprosthetic aortic valve function and no regional wall motion abnormalities.
CAG through the right femoral artery was performed. The angiographic findings showed moderate tubular concentric stenosis in the proximal RCA and severe discrete concentric stenosis in the mid RCA with ectatic changes. However, blood flow from the LGSV to RCA was not shown, which suggested total occlusion ().
Because of the larger size of the stenotic CAE, balloon angioplasty with parallel stenting was considered. However, balloon angioplasty alone without stenting was planned initially because of the possibility of early discontinuation of dual anti-platelet agents because of the chance of additional surgery for underlying valvular heart disease and aortic disease. The patient had previously undergone major cardiac surgery twice before owing to aortic stenosis and aortic aneurysm. Although the prosthetic aortic valve was intact, the aortic aneurysm was repaired through a staged operation and the graft did not entirely cover the aneurysm. Thus, we considered the possibility of future additional operative repair.
With a 7F AR2 catheter as a guide (Medtronic Inc., Minneapolis, MN,USA), balloon dilation was done with an Avita 3.0×15-mm balloon (Orbusneich, Wanchai, Hong Kong) and residual stenosis was more than 70%. Further ballooning was done with a Mercury 4.5×20-mm balloon (Abbott Vascular, Illinois, USA) and residual stenosis was less than 30% ().
The patient was on the dual antiplatelet agents (aspirin and clopidogrel), a lipid-lowering agent (simvastatin), a calcium channel blocker (diltiazem), and a beta-blocker (carvedilol) after the percutaneous coronary intervention. He was safely discharged without chest pain or any other cardiovascular events. Routine follow-up CAG at 6 months showed no significant restenosis at the previous balloon angioplasty site (). Dual antiplatelet agents were maintained for 2 years because of his history of diabetes and restenosis after CABG.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [72, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': True, 'Vascular disease history': True, 'Diabetes history': True}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 72 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 2 + 2 = 4.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 4 + 1 = 5. Based on the patient note, the patient history for diabetes is present. Because the patient has diabetes, one point is added to the score, making the current total 5 + 1 = 6.
The patient's CHA2DS2-VASc Score is 6."
1108,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-2654444-1,Extracted,"B. A., a 71-year-old man, presented with dyspnoea under moderate exercise, without angina. His clinical history was characterized by a silent inferior-basal myocardial infarction detected by a control ECG that presented inferior Q waves, and he had not previously presented symptoms. The infarct was referable to maximum a couple of months before especially basing on symptoms worsening. So he had not any previous diagnosis or treatment of the acute event.
Functional NYHA Class was III, but it was I two months before, and symptoms were rapidly worsening in the last 20 days.
The patient was a smoker, affected by chronic obstructive pulmonary disease (COPD), hypertension, and peripheral vascular disease, presented in sinus rhythm. Medical therapy was based beta blockers, ASA, and a diuretic with some relief of symptoms.
A transthoracic echocardiogram (TTE) showed a dyskinetic posterior wall of the left ventricle, mild mitral regurgitation, with moderate reduction of the ejection fraction (EF = 44%). An aneurysmatic enlargement was noted in the posterior wall, but with few signs to distinguish a true aneurysm from a pseudo-aneurysm. The patient underwent a coronary angiographic examination that revealed patent anterior descending and circumflex arteries and a right coronary artery that was completely closed and perfused by hetero-coronaric circulation. Contrast ventriculography showed an enlargement of the left ventricle with a large dyskinetic cavity localized in the diaphragmatic region, suggesting the presence of a pseudo-aneurysm. (Fig. )
A second TTE was done, with results similar to the first one, but a thrombus in the posterior wall was also disclosed.
At the time of surgery a large true aneurysm of the posterior wall of the left ventricle was found (Fig. , ). The aneurysm consisted of a very thin myocardium layer; inside there was a thrombus about 6 cm × 4.5 cm. (Fig. )
Surgery was performed via medial sternotomy. A normothermic cardiopulmonary by-pass (CPB) was carried out with cannulation of the aorta and the right atrium, on a beating heart without cardioplegic arrest and without clamping of the aorta. We performed the Dor repair, as described by Dor et al. [], after creating a neck of healthy muscle with 2/0 Prolene suture. The defect was closed, using the thin autologous aneurysmatic excised myocardium layer as patch. It was sutured with 3/0 continuous Prolene.(Fig. ) Two Teflon pledgets were used to reinforce the ventricle suture on the outside.(Fig. ) The CPB was 78 minutes long. Intra-operative TEE showed no mitral regurgitation (MR) and satisfactory post-surgical remodelling.
The patient was discharged 6 days after surgery without complications. At his 3 month control, the patient was completely restored to a normal life, an echocardiography showed good results in left ventricular remodelling with mild mitral regurgitation and an improved ejection fraction (EF = 55%).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Congestive Heart Failure': False, 'Hypertension history': True, 'Vascular disease history': True, 'age': [71, 'years'], 'Diabetes history': False, 'sex': 'Male'}",3,3,3,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 71 years old. Because the age is between 65 and 74, one point added to the score, making the current total 0 + 1 = 1.
The patient's gender is male and so no points are added to the current total, keeping the total at 1.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 1.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 1 + 1 = 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Because stroke history is not specified in the patient note, we assume that it is absent from the patient. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 2 + 1 = 3. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 3.
The patient's CHA2DS2-VASc Score is 3."
1109,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6563334-1,Extracted,"A 79-year-old Caucasian male, with a past medical history of atrial fibrillation on warfarin and metoprolol, and coronary artery disease on atorvastatin with previous coronary artery bypass grafting and placement of a dual-function pacemaker/ implantable cardioverter defibrillator (ICD), was on a motor boat in a remote location. The patient’s boat went over a wake of a larger boat passing by. He bounced off his seat in a vertical direction and subsequently landed on his tailbone. After the high impact fall, he complained of both immediate lower back and diffuse abdominal pain but did not seek out urgent medical help.
Two days after the initial incident, he started to become pale and diaphoretic; additionally, his ICD delivered three shocks over a 30-min period. He presented via ambulance service to a local community hospital in hemorrhagic shock with a blood pressure of 63/22 and heart rate of 118 beats/min. A primary survey was pertinently positive for hemodynamic instability and diffuse abdominal and lower thoracic spine tenderness.
He was resuscitated with 1 L of normal saline leading to an improvement of his pressure to 106/88. Initial laboratory investigations included a hemoglobin of 95 g/L, lactate of 6.1 mmol/L, creatinine of 129, and a supratherapeutic INR of 8.8. An initial non-contrast CT abdomen and pelvis showed moderate hemoperitoneum with sentinel clot in the left upper quadrant and pericolic gutter, as well as the area adjacent to the posterior wall of the stomach. An additional finding of a severely comminuted, minimally displaced burst fracture of the T10 vertebral body was noted (). Further interventions included INR reversal with 3 mg of Vitamin K and 3000 units of prothrombin complex concentrate, and administration of 2 units of packed red blood cells and 2 L of normal saline. Based on clinical severity, the patient was transferred to the trauma service at a tertiary-care Level 1 trauma center.
Primary survey revealed a protected airway, spontaneous and bilateral air entry, and hemodynamic stability with a blood pressure of 100/60 and a heart rate of 88 beats/min. His abdomen continued to be mildly distended and tender without peritoneal signs, however the patient reported it had improved since his original presentation to the local hospital. Repeat laboratory investigations revealed a stable hemoglobin of 94 g/L, and correction of his INR to 1.2. Given his stable condition, he underwent a CT RIPIT (Rapid Imaging Protocol in Trauma) [] and CT angiogram (CTA) of the abdomen and pelvis. His imaging revealed pseudoaneurysms of the left gastric artery measuring up to 6 mm with another 9 mm rounded area of increased attenuation along the lesser curve of the stomach (, ). No extravasation was seen. Decision was made to monitor the patient closely with serial abdominal exams and repeat imaging in 72 h, or sooner if the patient exhibited any signs of deterioration.
Over the next 72 h, the patient’s vital signs and abdominal exams, improved and his hematological profile remained stable. Given the patient’s CHADS score of 2, it was decided to hold therapeutic anticoagulation until the patient’s bleeding risk decreased, however deep venous thrombosis prophylaxis was initiated. A repeat CTA was performed to follow the evolution of the two pseudoaneurysms. The imaging study revealed unchanged pseudoaneurysms but noted the distal aspect of the left gastric artery was attenuated in keeping with a focal dissection and intramural thrombus. Secondary to the dissection, the patient was started on 81 mg of aspirin daily. Over the next few days the patient continued to improve clinically, and was discharged home. The patient lived outside of the local area, and arrangements for close follow up were made.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [79, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': True}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 79 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is male and so no points are added to the current total, keeping the total at 2.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 2 + 1 = 3.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 3.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 3.
Based on the patient note, the patient history for vascular disease is present. Because the patient has vascular disease, one point is added to the score, making the current total 3 + 1 = 4. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
1110,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-6489390-1,Extracted,"36 year old female patient weighing 36 kgs, height 152 cm, admitted to our hospital with diagnosis of rheumatic heart disease, severe mitral stenosis (MS), severe aortic stenosis (AS), and severe tricuspid regurgitation (TR). The patient had dyspnea on exertion for the last 1½ years, with recent deterioration to dyspnea of New York Heart Association Class III. She was admitted with CHF 7 months back and managed conservatively. On examination, the patient had a pulse rate of 100 beats/min (bpm) in atrial fibrillation rhythm, mild pallor, and icterus, and pedal edema was present. Cardiovascular examination findings were suggestive of MS and AS. Hepatomegaly was present.
She was started on tablet furosemide 40 mg once daily (OD) along with tablet metoprolol 25 mg twice a day.
She was operated and mitral valve was replaced with size 27 St. Jude's mechanical valve and aortic valve with size 17 regent mechanical valve. Tricuspid commissurotomy was performed. Immediate postoperative period was uneventful and all predischarge investigations were within normal range. She was discharged on the postoperative day (POD) 9 with prescription of tablet furosemide 40 mg OD, tablet aldactone 100 mg OD, tablet ramipril 5 mg HS, and tablet amiodarone 200 mg OD, and ecosprin 150 mg OD. On discharge, the patient did not have pedal edema or hepatomegaly.
On POD 28, her medication was changed to furosemide with spironolactone 40/25 mg BD, tablet acenocoumarol, tablet aldactone 100 mg OD, and tablet digoxin 0.25 mg OD. High dose of diuretics was used for a short while as the patient still had features of fluid overload. Postoperative echocardiography showed normal prosthetic valve function with normal biventricular function and moderate TR.
On POD 33, she presented in the emergency department with complaints of loose stool and vomiting (3 episodes) with severe muscular weakness. On examination, pulse was 36 bpm, irregular, systolic BP 60 mmHg, extremities were cold and clammy, signs of dehydration present, peripheral pulses not palpable, valve click present, and tender hepatomegaly present. Serum electrolytes showed hyperkalemia with serum potassium of 7.87 meq/L, hyponatremia with serum sodium 129 mmol/L and hypocalcemia, hemoglobin 9.6 gm% and hematocrit 38%, pH 7.28, base deficit-11, serum osmolality 252 mmol/L, serum creatinine 1.1 mg%, and blood urea nitrogen (BUN) 17 mg/dl. Electrocardiograph (ECG) showed heart rate of 30 beats/min, broad QRS complex, tented T-wave, and impending sine wave pattern. When detailed history was elicited from her husband, he revealed that apart from her medication, she was taking 7–8 bananas every day as part of her regular diet for the last 3 weeks.
She was managed with aggressive antihyperkalemic treatment with intravenous (IV) calcium gluconate, glucose-insulin drip, soda-bicarbonate, loop diuretics, K+ binding resins, and IV fluids. Over 24 h, she was stabilized in the intensive care unit (ICU) with same treatment. Hemodialysis was not required, she recovered hemodynamically and maintained good urine output. Potassium levels were serially monitored and were on a decreasing trend and finally levels decreased to 4.5 meq/L. ECG showed normal sinus rhythm, rate of 80–90 bpm. She was discharged from ICU after 2 days. She was advised to eat 1–2 bananas every day and the dose of potassium-sparing diuretics was reduced. She remained in a regular follow-up and no such incidence recurred.
8 years old child weighing 21 kgs, height 130 cm, admitted to our hospital with diagnosis of tetralogy of Fallot physiology for intracardiac repair. Examination showed a cyanotic child with pulse rate of 78 bpm in sinus rhythm and blood pressure of 100/70 mmHg. Preoperatively, the patient was continued on tablet propranolol 10 mg 8th hourly.
Perioperatively, dacron patch closure of ventricular septal defect, infundibular resection done, and transannular bovine pericardial patch placed. On POD 1, the patient developed complete heart block and was treated with temporary pacing, and injection dexamethasone was started, which was tapered off gradually and stopped on POD 10. Other medications included tablet furosemide 20 mg OD and tablet captopril 12.5 Mg 8th hourly. For nutrition, he was adviced to include banana in the diet. Gradually over next week, the patient developed hepatomegaly and weight gain of 4 kg and was started on tablet aldactone 25 mg BD. The patient was then discharged on POD 15 after features of CHF were relieved.
On POD 21, he presented in the emergency department with nausea and vomiting, electrolytes showed K+ of 7.12 meq/L, Na+ 121 meq/L, serum creatinine 1.2 mg%, and BUN 15 mg%. ECG showed hyperkalemic changes. He was shifted to ICU and antihyperkalemic treatment started that included IV calcium gluconate, sodium bicarbonate, glucose-insulin drip, and potassium-binding resin. He was maintaining good hemodynamics with adequate urine output. Potassium levels were serially monitored and after 24 h of aggressive management, his K+ level was 4 meq/l. Dialysis was not required. He was discharged from ICU after 2 days. Retrospectively on interrogating further his father said that the boy was eating at least 6–7 bananas every day for the last 15 days. He was advised to eat a single banana every day and he remained in regular follow-up and had no such episode again.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [36, 'years'], 'Congestive Heart Failure': True, 'Stroke': False, 'Transient Ischemic Attacks History': False, 'Thromboembolism history': False, 'Vascular disease history': False}",2,2,2,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 36 years old. Because the age is less than 65 years, no points are added to the current total, keeping the total at 0.
The patient's gender is female and so one point is added to the score, making the current total 0 + 1 = 1.
The patient history for congestive heart failure is present. Because the patient has congestive heart failure, one point is added to the score, making the current total 1 + 1 = 2.
Because hypertension history is not specified in the patient note, we assume that it is absent from the patient. Because the patient does not have hypertension, no points are added to the current total, keeping the total at 2.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 2.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 2. Because diabetes history is not specified in the patient note, we assume it's value as 'absent'. Because the patient does not have diabetes, no points are added to score, keeping the score at 2.
The patient's CHA2DS2-VASc Score is 2."
1111,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-5385244-1,Extracted,"An 84-year-old Italian woman presented to our hospital with a stroke and was referred to our cardiology unit for cardiologic evaluation. She had a history of hypertension, dyslipidemia, and pulmonary embolism and was using warfarin for pulmonary embolism during our evaluation: international normalized ratio (INR) 2.3; time in therapeutic range (TTR) >63%. She reported palpitations and dyspnea that started 1 week before our evaluation. An electrocardiogram showed AF with a heart rate of 96 beats per minute. Transthoracic echocardiography revealed normal left ventricle (LV) diameters and volume, left ventricular ejection fraction of approximately 60%, and a dilated left atrium (LA) with dense spontaneous echo contrast. Transesophageal echocardiography (TEE) showed a round, partially mobile, disorganized and weakly hypoechogenic mass (12 × 12 mm) that resembled a thrombus in the LAA (Fig. a). We examined the following in regard to thrombophilia: prothrombin time, activated partial thromboplastin time, fibrinogen, activated protein C resistance, factor V Leiden, prothrombin G20210A mutation, homocysteine, ATIII, protein C, protein S, antiphospholipid antibodies (lupus-like anticoagulant), anti-beta 2 glycoprotein I antibodies, anti-cardiolipin antibodies, factor VIII, and methylenetetrahydrofolate reductase C677T mutation. Testing revealed heterozygosity for both factor V Leiden and methylenetetrahydrofolate reductase C677T mutation, which created resistance to activated protein C [].
We started anticoagulant treatment with unfractionated heparin administered intravenously. After 1 week of therapy, we performed a second TEE that showed that the LAA thrombus remained unchanged (Fig. b). Her treatment was then switched to rivaroxaban 20 mg once daily for long-term treatment and stroke prevention []. A third TEE performed at the 3-month follow-up visit revealed no thrombotic mass (Fig. c). No major or clinically relevant bleeding occurred during follow-up. At the 6-month and 12-month follow-up visits, she continued to be in good clinical condition. After thrombus resolution, because our patient was at high risk for thromboembolism and had a history of pulmonary embolism, we recommended LAA percutaneous occlusion; however, she refused this option.
For rate control, because our patient had a first diagnosed AF with mean ventricular response, we treated her with a beta blocker (bisoprolol) at low dosages (1.25 mg twice daily).",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [84, 'years'], 'sex': 'Female', 'Stroke': True, 'Hypertension history': True, 'Congestive Heart Failure': False, 'Thromboembolism history': True, 'Transient Ischemic Attacks History': False, 'Vascular disease history': False, 'Diabetes history': False}",6,6,6,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 84 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is present. Based on the patient note, the patient history for tia is absent. Based on the patient note, the patient history for thromboembolism is present. Because at least one of stroke, tia, or thromboembolism is present, two points are added to the score, making the current total 4 + 2 = 6.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 6. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 6.
The patient's CHA2DS2-VASc Score is 6."
1112,4,CHA2DS2-VASc Score for Atrial Fibrillation Stroke Risk,risk,integer,pmc-4137599-1,Extracted,"A 75-year-old female presented to our hospital with malaise, palpitations, and mild fine tremors. She had felt ambiguous chest discomfort for a long period of time. In addition, she was anxious about her unintentional weight loss. Her past medical history was unremarkable except for untreated hepatitis C virus infection. Mild hyperthyroidism had been detected; however, the accurate diagnosis was not confirmed for at least two years at another hospital. Her family history was negative for endocrinopathy, including thyroid disease. She was currently receiving treatment with amlodipine for hypertension and rivaroxaban for paroxysmal atrial fibrillation. She was thin and appeared tired on general inspection. On a physical examination, she was found to be 156 cm in height and 46 kg in weight (body mass index: 18.9 kg/m2). Her blood pressure was 140/80 mmHg and her heart rate was 104 beats per minute. No diffuse goiters were apparent on inspection, and no abnormal masses were palpable in the thyroid gland. She did not exhibit any signs suggestive of Graves' ophthalmopathy, including conjunctival injection, periorbital edema, or proptosis.
The laboratory data were as follows: AST = 46 IU/L (range, 11–28), ALT = 54 IU/L (range, 7–23), ALP = 352 IU/L (range, 115–330), γGTP = 18 IU/L (range, 9–27), TSH = <0.005 μIU/mL (range, 0.2–4.0), free thyroxine = 2.66 ng/dL (range, 1.00–2.00), free triiodothyronine = 11.35 pg/mL (range, 2.30–4.00), and negative thyroid autoantibodies, including negative TRAb, negative anti-thyroglobulin antibodies (TGAb), and negative anti-thyroid peroxidase antibodies (TPOAb). Thyroid autoantibodies were tested twice, with negative results both times. TSH receptor stimulating antibodies (TSAb), as assessed on a bioassay, were also negative.
Ultrasonography of the thyroid gland revealed a tumor in the right lobe () measuring 21.5 mm × 19.4 mm × 36.3 mm in diameter. The lesion had a relatively low echoic appearance and sharp border. No areas of microcalcification were detected in the tumor, although areas of macrocalcification were present. The remaining thyroid gland had an inhomogeneous, rough texture with a high color Doppler flow (). I123 scintigraphy was performed following iodine restriction for one week prior to the study, revealing a hot nodule in the lower right thyroid gland corresponding to the tumor detected on ultrasonography (). The total uptake percentage of I123 for four hours was approximately 24% (range: 4–16%). Surprisingly, there was an increased uptake of radionuclide in the remaining thyroid gland despite the suppressed level of TSH and negative TRAb titer, suggesting underlying Graves' disease.
Thioamides, which are commonly used to treat Graves' disease in Japan, have the well-known side effect of hepatotoxicity [, ]. Because the patient displayed elevated liver enzymes due to her untreated hepatitis C, we administered 10 mCi of radioiodine instead of thioamides. After the treatment, her subjective ambiguous chest discomfort, possibly due to paroxysmal atrial fibrillation, was ameliorated. Thyroid function test results on a regular visit conducted one month after the radioiodine treatment were as follows: TSH = <0.005 μIU/mL (range, 0.2–4.0), free thyroxine = 1.40 ng/dL (range, 1.00–2.00), and free triiodothyronine = 4.91 pg/mL (range, 2.30–4.00). Her hyperthyroidism was successfully improved one month after the administration of the radioisotope and no episodes of recurrence have since been observed.",What is the patient's CHA2DS2-VASc Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [75, 'years'], 'Congestive Heart Failure': False, 'Hypertension history': True, 'Stroke': False, 'Vascular disease history': False, 'Diabetes history': False}",4,4,4,"The criteria for the CHA2DS2-VASc score are listed below:

1. Age: < 65 years = 0 points, 65-74 years = +1 point, ≥ 75 years = +2 points
2. Sex: Female = +1 point, Male = 0 points
3. Congestive Heart Failure (CHF) history: No = 0 points, Yes = +1 point
4. Hypertension history: No = 0 points, Yes = +1 point
5. Stroke, Transient Ischemic Attack (TIA), or Thromboembolism history: No = 0 points, Yes = +2 points
6. Vascular disease history (previous myocardial infarction, peripheral artery disease, or aortic plaque): No = 0 points, Yes = +1 point
7. Diabetes history: No = 0 points, Yes = +1 point

The CHA2DS2-VASc score is calculated by summing the points for each criterion.
    
The current CHA2DS2-VASc score is 0.
The patient is 75 years old. Because the age is greater than 74, two points added to the score, making the current total 0 + 2 = 2.
The patient's gender is female and so one point is added to the score, making the current total 2 + 1 = 3.
The patient history for congestive heart failure is absent. Because the patient does not have congestive heart failure, no points are added to the current total, keeping the total at 3.
The patient history for hypertension is present. Because the patient has hypertension, one point is added to the score, making the current total 3 + 1 = 4.
One criteria of the CHA2DS2-VASc score is to check if the patient has had any history of stroke, transient ischemic attacks (TIA), or thromboembolism. Based on the patient note, the patient history for stroke is absent. Because tia history is not specified in the patient note, we assume that it is absent from the patient. Because thromboembolism history is not specified in the patient note, we assume it to be absent. Because all of stroke, tia, or thromboembolism are absent, no points are added to score, keeping the score at 4.
Based on the patient note, the patient history for vascular disease is absent. Because the patient does not have vascular disease, no points are added to score, keeping the score at 4. Based on the patient note, the patient history for diabetes is absent. Because the patient does not have diabetes, no points are added to score, keeping the score at 4.
The patient's CHA2DS2-VASc Score is 4."
1113,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7729,Extracted,"A 34-year-old poultry worker presents to his physician with a sore throat and a non-productive cough for 2 weeks. His cough is associated with fever. The vital signs include: blood pressure 120/80 mm Hg, heart rate 67/min, respiratory rate 18/min, and temperature 37.6°C (98.0°F). Physical examination shows oropharyngeal erythema and scattered, moist rales on lung auscultation. The patient’s X-ray demonstrates patchy reticular opacities in the perihilar regions of both lungs. After some additional tests, he is diagnosed with community-acquired pneumonia and is treated with cephalexin with modest improvement.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1114,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-6300,Extracted,"A 65-year-old man presents to the emergency department with a strange sensation in his chest. He states that it started this morning and has not been improving. The patient works as a farmer and has never seen a physician. He drinks alcohol regularly and smokes a pipe. He was working in the field when his symptoms began. His temperature is 98.6°F (37.0°C), blood pressure is 85/58 mmHg, pulse is 140/min, respirations are 18/min, and oxygen saturation is 95% on room air. An ECG is performed as seen in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [58.0, 'mm hg'], 'Systolic Blood Pressure': [85.0, 'mm hg']}",67,63.65,70.35,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 85.0 mm Hg + 2/3 * 58.0 mm Hg = 67.0 mm Hg.
Hence, the patient's mean arterial pressure is 67.0 mm Hg."
1115,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2941600-1,Extracted,"A 55-year-old male presented in the medicine outpatient department with complaints of multiple swellings on the chest wall since 2 months. There was no history of trauma, Ischemic heart disease, hypertension or diabetes. On examination, there were three cystic swellings on the anterior chest. The swelling was small to start with and increased up to 6.5 cm in 2 months []. It was firm, cystic and variegated in consistency and nontender on palpation. The liver was enlarged by 2 cm. Other examinations were unremarkable. His blood pressure was 130/80 mmHg. The hemoglobin was 9.6 g%, total leucocyte count was 6,300/cmm with a differential of 45% neutrophils, 37% lymphocytes, 17% monocytes and 1% eosinophils, with no myeloma cells in the peripheral smear. The erythrocyte sedimentation rate was 110 mm 1st hour (Westergren). Bence-Jones proteins was absent in the urine. Serum electophoresis shows a very thick Beta band. Serum proteins were 8.2 g%, with albumin 2.9% and globulin 4.3 g%. Blood urea and blood sugar were normal. Serum calcium, phosphorus and alkaline phosphatase were 13.2 mg%, 4.0 mg% and 7.2 Bodansky unit, respectively. Serum bilirubin was 0.3 mg%. Electrocardiogram was normal. Fine needle aspiration cytology cytology of the swelling shows plasmacytoma. The cells bear characteristic morphologic features of plasma cells, round or oval cells with an eccentric nucleus composed of coarsely clumped chromatin, and a densely basophilic cytoplasm. Binucleate and multinucleate malignant plasma cells can be seen []. X-ray skull showed multiple punched-out osteolytic lesions []. Bone marrow biopsy revealed myeloma cells and was diagnostic of multiple myeloma. The patient was started on thalidomide and corticosteroids. He also received radiotherapy for the local swelling, which was reduced on the subsequent day. He is doing well on follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1116,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3830321-1,Extracted,"A 40-year-old man referred to department of endocrinology with adrenal mass and hypertension. He was diagnosed with hypertension 3 years back, initial BP was 180/110 mm Hg, was started on anti-hypertensive treatment. On examination, there were no neurocutaneous markers or marfanoid habitus, no features of Cushing's syndrome, 24-hour urine metanephrines level was 3000 micrograms/day (normal < 900 micrograms/day, the test was done after stopping all interfering drugs). Ultrasonography revealed 9.8 × 8.5 cms well-defined predominantly hyperechoic lesion, faint hypoechogenicity originating from right suprarenal region abutting the upper pole of right kidney and lower surface of right lobe of liver suggestive of right adrenal mass. CECT of abdomen showed 9.8 × 8.5 cm well-defined, well-circumscribed heterogenous hypoattenuated mass lesion noted in right suprarenal region and minimal enhancement on contrast with −80 to −100 HF units of attenuation suggestive of myelolipoma of right adrenal gland []. Baseline hematological and biochemical investigations and urinalysis were normal. Low-dose dexamethasone suppression test was normal.
In view of hypertension, adrenal mass, and elevated 24-hour urine metanephrines (>3 times), possibility of pheochromocytoma was considered. Hypertension was brought under control. Patient underwent surgery, and well encapsulated right adrenal tumor (weight: 500 gm) was excised []. Biopsy of specimen was suggestive of adrenal myelolipoma []. Immuno-histochemistry of specimen revealed positive for chromogranin A, suggestive of catecholamine-secreting granules in the tissue [].
The patient had remission in hypertension. Metanephrine levels became normal after surgery. The patient is normal at the 3-month follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [180.0, 'mm hg'], 'Diastolic Blood Pressure': [110.0, 'mm hg']}",133.33333,126.66666,140,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 180.0 mm Hg + 2/3 * 110.0 mm Hg = 133.33333 mm Hg.
Hence, the patient's mean arterial pressure is 133.33333 mm Hg."
1117,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5634588-1,Extracted,"A 42-year-old healthy man with a long history of left nasal obstruction attempted to relieve his stuffy nose by inserting a 6–8 cm long metal stick into his left nostril. He reported hearing a click sound followed by bleeding from the left nasal cavity. The epistaxis stopped shortly after local compression, and the patient blew his nose to clear the residual blood clots. He then noticed a clear, watery discharge from the left nostril. Six hours later, diffuse headache developed. The watery rhinorrhea persisted for the next 2 days, and the headache became intolerable. So he visited the emergency department of our hospital. Computed tomography (CT) scan revealed left maxillary and ethmoid sinuses opacification and the possible site of breach in the lateral lamella of cribriform plate on patient's left side (). CT also showed multiple air formation in the subarachnoid spaces, suggesting pneumocephalus (). On examination, he had signs of meningeal irritation, including nuchal rigidity, but no other focal neurological signs or symptoms. His body temperature was 38.0°C, blood pressure was 133/68 mm Hg, pulse rate was 104 beats per minute, and respiratory rate was 20 breaths per minute. His laboratory parameters showed elevated white blood cell count (11,100/mm3; neutrophils, 87%, and lymphocytes, 7.2%) and C-reactive protein (CRP; 63.5 mg/L). Through sinuscopy, neither CSF leakage nor gross destruction of nasal structures could be detected. The patient was admitted and was advised bed rest for 6 days and to avoid coughing, sneezing, nose blowing, and anything strenuous. Empiric antibiotics, such as vancomycin, ceftriaxone, and metronidazole, were intravenously administered to treat meningitis. His fever subsided, and the headache and meningeal signs gradually resolved. The follow-up blood test revealed no leukocytosis, and CRP was in the reference range of 3.97 mg/L. The patient was discharged after 6 days of supportive treatment without surgical intervention.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [68.0, 'mm hg'], 'Systolic Blood Pressure': [133.0, 'mm hg']}",89.66667,85.18334,94.15,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 133.0 mm Hg + 2/3 * 68.0 mm Hg = 89.66667 mm Hg.
Hence, the patient's mean arterial pressure is 89.66667 mm Hg."
1118,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8039083-1,Extracted,"A 12-year-old girl presented to emergency department of Shahid Rajaei Hospital in Ghazvin, Iran, with headache, drowsiness, mild fever, nausea, vomiting, and lethargy form two day before admission. The patient had a history of head trauma in a driving accident six weeks before and had been hospitalized in Hamedan city, where she had undergone spiral brain computed tomography (CT) scan without contrast due to reduced consciousness. Brain CT scan reported right frontal contusion, right frontal bone fracture involving frontal sinus and filling of ethmoid sinuses. The patient had received treatment in that centre for one week and was discharged in good general condition. The patient did not report any history of seizures, otorrhoea, or rhinorrhoea during these six weeks.
The presenting vital signs of the patient were as follows: pulse rate: 88/minute, respiratory rate: 18/minute, blood pressure: 105/75 mmHg, axillary Temperature: 37.8°C, Glasgow coma scale (GCS): 13/15 (eye response = 3, motor response = 6, verbal response = 4). Pupils were symmetrical of 3 millimetres and reduced response to light was detected in the right pupil. The four limbs had equal force of 5/5. Deep tendon reflexes (DTRs) were 2+ and symmetrical, and bilateral plantar reflex was symmetrical and downward. Other clinical examination findings were unremarkable.
The patient underwent brain CT scan again in our centre, which revealed hydropneumocephalus in the frontal parenchyma with midline shift and compression effect on the anterior horn of the lateral ventricles in the right frontal lobe (). Thus, the patient underwent treatment with phenytoin and 100% concentration oxygen. Moreover, given her mild fever and likelihood of brain abscess, a broad-spectrum antibiotic (Vancomycin) was administered until magnetic resonance imaging (MRI) was done. Neurosurgery emergency consultation was requested, and the patient was admitted to the Intensive care unit for further treatments. Considering the trend of recovery and at the neurosurgeon’s discretion, the patient was a candidate for conservative non-surgical therapy. MRI with contrast on the third day of admission revealed no rim enhancement around the lesion, and confirmed the diagnosis of tension hydropneumocephalus (). Therefore, antibiotic was discontinued. On the seventh day, the patient was advised to continue taking oral phenytoin, and was discharged in good general condition. The patient reported no complications during the six-month follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [75.0, 'mm hg'], 'Systolic Blood Pressure': [105.0, 'mm hg']}",85,80.75,89.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 105.0 mm Hg + 2/3 * 75.0 mm Hg = 85.0 mm Hg.
Hence, the patient's mean arterial pressure is 85.0 mm Hg."
1119,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7671081-1,Extracted,"A 28-year-old sporty (martial arts practitioner) woman, without relevant medical history, activated the national emergency system because of two episodes of pre-syncope at home. Shortly after arrival of the medical team, she collapsed, and the cardiac monitorization showed ventricular fibrillation (VF) from which she was promptly defibrillated, and return of spontaneous circulation ensued. The electrocardiogram (ECG) after defibrillation showed sinus tachycardia with voltage criteria for left ventricular (LV) hypertrophy.
At the emergency room, blood pressure was 105/72 mmHg and a grade II/VI holosystolic murmur was heard at the left sternal border on cardiac auscultation. High-sensitivity cardiac troponin showed a slight elevation (0.045 ng/mL).
Transthoracic echocardiographic evaluation revealed LV enlargement (112 mL/m2), mild LV hypertrophy (maximal wall thickness 12 mm), hypokinesia of the basal and mid segments of the anterior and anteroseptal walls, as well as of all distal segments, and moderately depressed LV function.
The patient underwent coronary CT angiography that showed an anomalous origin of the left coronary artery (LCA) from the pulmonary artery (ALCAPA). This was associated with a dilated right coronary artery (RCA) with extensive collateral network (Figure ). Cardiac magnetic resonance (CMR) imaging demonstrated subendocardial late gadolinium enhancement in the anterior wall and mid-distal anteroseptum, with transmural extension in the medium segment of anterior wall (Figure ). Furthermore, cardiovascular magnetic resonance imaging (CMR) showed extensive peri-infarct ischemia involving anterolateral wall, middle segment of inferoseptal wall and distal segment of the inferior wall (Figure ).
An invasive coronary angiography was performed, and retrograde filling of the LCA territory through collaterals arising from an enlarged RCA was apparent (Figure ).
During hospitalization the patient remained hemodynamically stable. She underwent surgical treatment by the creation of a poly-tetrahydrofuran (pTHF) conduct connecting the aorta and left coronary artery (Figure ). Communication between the main pulmonary artery and left coronary artery was closed with bovine pericardial patch. A transvenous implantable cardioverter defibrillator (ICD) was implanted, for secondary prevention of SCD. She was discharged five days after surgery.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [105.0, 'mm hg'], 'Diastolic Blood Pressure': [72.0, 'mm hg']}",83,78.85,87.15,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 105.0 mm Hg + 2/3 * 72.0 mm Hg = 83.0 mm Hg.
Hence, the patient's mean arterial pressure is 83.0 mm Hg."
1120,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3727983-1,Extracted,"A 34-year-old woman presented with insidiously progressing abdominal distension of one year’s duration. Review of systems was significant for colicky abdominal pain, fatigue, night sweating and anorexia. The woman had no history of fever, jaundice, tuberculosis contact, weight loss or lower limb swelling. She was not on any medications. Her surgical history included laparoscopic gastric banding surgery for obesity (body mass index = 50; weight, 120 kg) 4 years earlier without complications. The patient had received normal saline injections through an injection port underneath the skin in the first 2 years after surgery to tighten the band. She had lost 50 kg since surgery. She was single, a graphic designer, and a smoker. Her menses were regular and there was no family history of malignancy. The patient’s blood pressure on admission was 110/78 mmHg, her pulse was 82 bpm, her respiratory rate was 18 breaths per minute, and her temperature was 36.8°C. There were no palpable lymph nodes, pallor, jaundice, or other stigmata of chronic liver disease. Abdominal examination revealed a distended soft lax abdomen, a tender epigastrium on deep palpation with no guarding or rigidity, positive shifting dullness, and otherwise normal findings. Complete blood count and hepatic, coagulation and renal profiles were within normal limits and there was no proteinuria. Abdominal ultrasound showed moderate to severe ascites and normal liver size and echogenicity with a patent portal vein. Tumor marker CA 125 was high. Abdominal computed tomography showed large ascites with prominent ovaries bilaterally but no definitive mass or lymphadenopathy. Diagnostic and therapeutic paracentesis was performed, draining 7 l. Fluid analysis showed low serum ascites albumin gradient. Cytology was negative for malignant cells. Laparoscopic peritoneal and ovarian biopsies showed caseating granulomata without malignant cells or acid-fast bacilli. Acid-fast bacilli culture of the ascitic fluid and of peritoneal and ovarian biopsies grew Mycobacterium species in both Middlebrook 7H9 Broth (BACTEC MGIT 960 system) and Lowenstein-Jensen after one week of incubation. Colonies appeared smooth and greyish in Lowenstein-Jensen at a temperature of 28°C and 36°C with positive arylsulfatase test and negative ProbeTec ET test. The patient began treatment for rapidly growing Mycobacterium infection with clarithromycin, rifampicin, moxifloxacin and ethambutol. The isolate was identified by Line Probe Assay INNO-LiPA MYCOBACTERIA V2 (Innogenetics, Ghent, Belgium) as M. chelonae complex /abscessus. The Clinical Microbiology Laboratory at Mayo Clinic used DNA sequencing and real-time PCR, per the Clinical and Laboratory Standards Institute (CLSI)
[],to confirm that the isolate was M. abscessus, subspecies abscessus. Breakpoint susceptibility testing was performed using the CLSI recommended broth microdilution MIC method with nine drugs (amikacin, tobramycin, trimethoprim-sulfamethoxazole, cefoxitin, imipenem, linezolid, doxycycline/minocycline, clarithromycin and ciprofloxacin) [Table 
]. Breakpoints for tigecycline have not been evaluated by the CLSI for mycobacteria
[]. The isolate was resistant to quinolones and rifampicin, and was susceptible to clarithromycin and amikacin. Rifampicin and moxifloxacin were discontinued and amikacin was started along with ethambutol and clarithromycin. Laparoscopic surgery for gastric band removal was performed. Significant inflammation with dense adhesions surrounding the entire band and black discoloration of the gastric band were noted during the procedure (Figure 
). Adhesiolysiswas performed and the band was removed. Tissue from the inflammation around the band showed granulomata and culture was positive for M. abscessus. Additional antimicrobials with potential activity against M. abscessus were added sequentially (imipenem, tigecycline and linezolid), but the patient could not tolerate them for various reasons. After 5 months of clarithromycin and ethambutol treatment supplemented with amikacin for the first 2 months, the patient had an excellent recovery and become completely asymptomatic.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",88.66667,84.23334,93.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 78.0 mm Hg = 88.66667 mm Hg.
Hence, the patient's mean arterial pressure is 88.66667 mm Hg."
1121,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6230344-1,Extracted,"A 67-year-old man presented to the emergency department (ED) complaining of sudden onset atraumatic right lower extremity pain shortly after using crack cocaine. He described the pain as sharp and burning throughout his entire leg. The patient denied chest pain, shortness of breath, abdominal pain, and focal neurologic symptoms. His past medical history was otherwise unremarkable.
On examination, the patient was alert and oriented but in obvious distress. Vital signs were within normal limits excluding a blood pressure of 180/100 millimeters of mercury (mmHg). The cardiopulmonary and abdominal examinations were benign with notably equal radial pulses. The patient’s right lower extremity was cool to touch without palpable pulses distal to and including the common femoral artery. The left lower extremity was warm with bounding pulses. On neurologic exam, the patient had normal and symmetric strength in his bilateral upper and lower extremities without apparent sensory deficits.
Based upon the patient’s acute presentation a POCUS was performed immediately in the ED. Our emergency ultrasound division has developed a protocol combining transthoracic echocardiography (TTE) and abdominal aorta ultrasound to evaluate for aortic pathology. POCUS demonstrated a large, undulating intimal flap within the abdominal aorta (). TTE did not reveal evidence of a Stanford Type A dissection. Immediate aggressive blood pressure control was initiated, and the patient was taken emergently for computed tomography (CT), which confirmed a Stanford Type B dissection (). Ultimately, the patient underwent thoracic endovascular aortic repair without complications.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [180.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",126.66667,120.33334,133,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 180.0 mm Hg + 2/3 * 100.0 mm Hg = 126.66667 mm Hg.
Hence, the patient's mean arterial pressure is 126.66667 mm Hg."
1122,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4350223-1,Extracted,"At 38-weeks gestation a 31-year-old primigravida presented with diplopia on left gaze of 1- day duration. The diplopia was worse for far objects. She had unilateral throbbing headache similar to her previous migraines for 3 days prior to admission, associated with two to three episodes of vomitting per day, which were similar to her previous migraine attacks. There was no history of fever, photophobia or phonophobia.
She had an uneventful follow-up in antenatal clinic throughout the pregnancy. Her blood pressure was normal at the 13 week, 20 week and 33 week follow up visits. Her urinalysis was normal and she was not diabetic. There was no significant past medical or family history. She was non-smoker, non-alcoholic and there was no history of substance abuse. Preeclampsia was ruled out and she was referred to neurology with above history on the same day of admission.
On examination, she was alert and oriented. Her blood pressure was 106/65. There was complete paralysis of the left lateral rectus muscle. She had hyper-reflexia in all four limbs (Deep tendon reflexes were 3+). Rest of the neurologic examination was normal. MRI brain showed a non-enhancing, central, symmetrical, pontine T2 hyper-intensity which also showed evidence of restricted diffusion [Figure and ] consistent with central pontine myelinolysis (CPM). The MRI of orbits, MR angiogram and MR venogram were unremarkable.
Blood investigations including full blood count, ESR, renal, liver and thyroid function tests, folate, Vitamin B12, calcium and phosphate were normal. Serial daily electrolytes did not reveal any derangement. Toxicology and autoimmune workup included were negative.
Lumbar puncture opening pressure was normal and CSF was unremarkable. (WBC = 0; Proteins = 0.24g/; Glucose normal; Gram stain, bacterial culture, fungal smear and culture, TB-PCR and TB-culture negative, oligoclonal bands negative).
Patient underwent Caesarean section. A healthy baby weighing 3180 g was delivered. Considering the diagnosis of CPM due to typical lesion, absence of obvious secondary cause and mild symptoms and signs, she was observed without any specific treatment. She gradually improved and the left eye abduction movement had recovered to about 50% at the time of discharge 4 days after the delivery. At 2-week follow-up after discharge, she was asymptomatic and her VI nerve palsy had fully recovered. A repeated MRI at this time showed complete resolution of the previous changes. []",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [65.0, 'mm hg'], 'Systolic Blood Pressure': [106.0, 'mm hg']}",78.66667,74.73334,82.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 106.0 mm Hg + 2/3 * 65.0 mm Hg = 78.66667 mm Hg.
Hence, the patient's mean arterial pressure is 78.66667 mm Hg."
1123,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-568,Extracted,"A 52-year-old woman comes to the physician because of vaginal itchiness and urinary frequency for the past 1 year. She stopped having vaginal intercourse with her husband because it became painful and occasionally resulted in vaginal spotting. Her last menstrual cycle was 14 months ago. She has vitiligo. Her only medication is a topical tacrolimus ointment. Her temperature is 37.1°C (98.8°F), pulse is 85/min, and blood pressure is 135/82 mm Hg. Examination shows multiple white maculae on her forearms, abdomen, and feet. Pelvic examination shows scarce pubic hair, vulvar pallor, and narrowing of the vaginal introitus.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [82.0, 'mm hg'], 'Systolic Blood Pressure': [135.0, 'mm hg']}",99.66667,94.68334,104.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 82.0 mm Hg = 99.66667 mm Hg.
Hence, the patient's mean arterial pressure is 99.66667 mm Hg."
1124,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2494987-1,Extracted,"A previously healthy 26-year-old woman was referred to the Emergency Department with an influenza-like illness, which had started 2 days previously, and was associated with progressive disturbance of consciousness. Clinical examination was normal except for a blood pressure of 70/30 mmHg and a tachycardia of 120 beats/min. There was no response to a fluid challenge (1 L of colloid over 30 min). Central nervous system infection was ruled out by lumbar puncture and cerebral tomodensitometry. Her white blood cell count was 7,000 per μl and the procalcitonin concentration was not raised. EKG and chest radiography were normal. The first troponin measurement was 0.02 ng/mL.
The patient was transferred in a medical Intensive Care Unit (ICU) under the diagnosis of probable septic shock. Fluid resuscitation (4 L of cristalloids during the 6 first hours) was followed by a daily continuous infusion of 3 L of cristalloids and norepinephrine infusion. Antibiotics were given: cefotaxime (4 × 2 g/day, erythromycin 3 × 1 g/day and gentamycin 1 × 400 mg/day), plus intravenous hydrocortisone (200 mg per day).
Fluid resuscitation produced no improvement in blood pressure. Degradation of the oxygenation (PaO2/FiO2 < 120) requiring mechanical ventilation was observed. Her hemodynamic status rapidly deteriorated during the subsequent hours despite high doses of vasopressor (norepinephrine 5 mg/h). Diagnosis of cardiogenic shock was established by the association of severe hemodynamic compromise requiring high-dose of vasopressor, low right atrial oxygen saturation (45%) and transthoracic echocardiography showing a diffuse hypokinesia with an estimated left ventricular ejection fraction (LVEF) of 20%, elevated right and left filling pressures. Left ventricle diastolic dimensions were however normal (44 mm) as was septal thickness (8 mm). The troponin I concentration was 28 ng/mL. Monitoring by pulse contour analysis and thermodilution showed a cardiac index of 2.4 L/min/m2. Restriction of parenteral fluids and continuous veno-venous hemofiltration with fluid removal at an average rate of 300 ml/h substantially improved gas exchange. However, despite increased inotropic support (epinephrine 2 to 25 mg/h and dobutamine 12 μg/kg/min), the hemodynamic status further worsened and the multi-organ dysfunction syndrome became obvious (arterial lactate level at 10 mmol/L, alanine aminotransferase level of 293 IU/L, aspartate aminotransferase level of 587 IU/L, bilirubin level of 21 mg/dL and progressive oliguria) (Table ).
A circulatory support device was connected by percutaneous femoral vein and artery cannulation. Pump flow of 3500 rpm generated an output of 4 L/min and a non pulsatile systemic pressure of 80 mmHg. Intravenous heparin was given, aiming at an activated cephalin time of 60–80 secs. This procedure allowed rapid weaning of the inotropic support, and led to urine production and decreased lactacidemia (Table ).
The patient was transferred to a Cardiac ICU 24 hours later. Echocardiography showed lower left and right heart pressures, but the LVEF was persistently low at 20%. Multiple biopsies of the myocardium were performed. These latter, using routine staining, revealed interstitial inflammation and tissue destruction, but bacterial cultures remained negative. Real time polymerase chain reaction showed the presence of Influenza A RNA in the biopsy. Influenza A infection was confirmed by serologic tests and positive culture of the endotracheal aspirate. Liver function tests improved during circulatory support but there was anuric renal failure. On the 5th day of mechanical circulatory support, echocardiography showed improved diastolic and systolic function (LVEF of 50%) which allowed the progressive withdrawal of inotropic support. Mechanical circulatory support was reduced on the 6th day, and was withdrawn 24 hours later. The empiric antibiotherapy was stopped on the 7th day; she was extubated on the 13th, and vasopressor support was withdrawn on the 15th. Renal function recovered after 20 days of continuous veno-venous hemofiltration. She was discharged on the 26th day with an LVEF of 70%, good diastolic function and no ventricular dilatation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [30.0, 'mm hg'], 'Systolic Blood Pressure': [70.0, 'mm hg']}",43.33333,41.16666,45.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 70.0 mm Hg + 2/3 * 30.0 mm Hg = 43.33333 mm Hg.
Hence, the patient's mean arterial pressure is 43.33333 mm Hg."
1125,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8330459-1,Extracted,"A 15-year-old Caucasian male presented to the pediatrician’s office with a 1-day history of intermittent suprapubic abdominal pain. The pain was described as 7/10 maximum severity but, after a single dose of acetaminophen, significantly improved (1/10 in severity). There was no fever, vomiting, weight loss, constipation, or diarrhea. The patient recalled passage of a normal soft bowel movement without blood or mucus the day prior. There were no recent sick contacts or dietary changes. He was afebrile and vital signs were normal. Physical exam revealed a well-appearing male with a soft, non-tender, and non-distended abdomen. Bowel sounds were hyperactive. Testicular exam was normal and the patient was able to maneuver on and off the exam table without significant discomfort. Urinalysis revealed ketones 40 mg/dL but was otherwise unremarkable. The patient was sent home with presumed acute viral gastroenteritis and instructions to take acetaminophen every 4 hours as needed and to seek medical care for persistent or worsening symptoms.
Two days later he reported to the pediatric emergency department with moderate suprapubic cramping abdominal pain with radiation to the bilateral flanks. There was associated nausea and 1 episode of non-bloody and non-bilious emesis. The patient had not had a bowel movement in 3 days. Vital signs included a blood pressure of 132/87, temperature 36.6°C (97.9°F), heart rate 87, and respiratory rate 16. Physical exam revealed an uncomfortable-appearing child with moderate tenderness in all 4 abdominal quadrants. Bowel sounds were hypoactive and there was moderate abdominal distention. A complete blood count, urinalysis, C-reactive protein, lipase, coagulation studies, and lactic acid were unremarkable. Complete metabolic panel was normal except for hyperglycemia (156 mg/dL). SARS-COV-2 by NAA was not detected. Abdominal radiograph revealed a markedly distended inverted U-shaped bowel loop sigmoid colon or “coffee bean sign” (). Computed tomography with 100 cc of Omnipaque 350 intravenous contrast revealed marked gas distention of the sigmoid colon and a “whirlpool sign” in the lower abdomen consistent with sigmoid volvulus ().
A pediatric surgeon and pediatric gastroenterologist were consulted and jointly decided to attempt endoscopic reduction of the sigmoid volvulus with, should it become necessary, subsequent exploratory laparotomy. After obtaining informed consent and induction of general anesthesia, an Olympus PCF-H190DL colonoscope was passed under direct visualization through the anus to the sigmoid colon where the colonic mucosa demonstrated a twisted appearance (). Detorsion of the volvulus was achieved with careful insufflation and gentle pushing, and confirmed by passage of stool along with visualization of grossly dilated descending colon. Further inspection revealed normal mucosa; due to presence of stool, the colonoscopy was limited to the splenic flexure. A rectal tube was not placed during the procedure. The child was returned to the hospital ward in stable condition, tolerated standard advancement of the diet, and was discharged home the following day.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [87.0, 'mm hg'], 'Systolic Blood Pressure': [132.0, 'mm hg']}",102,96.9,107.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 132.0 mm Hg + 2/3 * 87.0 mm Hg = 102.0 mm Hg.
Hence, the patient's mean arterial pressure is 102.0 mm Hg."
1126,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8511675-1,Extracted,"A 44-year-old man, working in a chemical plant, was accidentally exposed to bromine gas (Br2). The worker became unconscious for 15 min and was transferred to an open-air setting by the colleagues, where the man gained consciousness after 10 min.
Upon admission to a local hospital, the man presented with several symptoms, such as dyspnea, vomit, fatigue, cough, pharyngalgia, and mental confusion. The patient remained conscious with the following vital signs: blood pressure 92/63 mmHg, pulse rate 94 beats/min, respiratory rate 22 breaths/min, temperature 36°C, oxygen saturation (80–85%) supported by mask ventilator assisted ventilation with inhaled 100% oxygen concentration. Arterial blood gases obtained before intubation were: pH 7.309, partial pressure of oxygen (PaO2) 8.18 kpa, partial pressure of carbon dioxide (PaCO2) 6.73 kpa, and bicarbonate concentration −0.9 mmol/L (P/F oxygen ratio was 61.5 mmHg). Despite inhaling 100% oxygen, the status of dyspnea did not improve but progressively worsened accompanied with profuse sweating and irritability. Moreover, a pronounced stridor could be heard. The physical examination revealed cyanosis of the lips and mouth, shortness of breath, three concave signs, and increased bilateral vesicular sounds. Because of laryngeal edema caused by Br2 irritation and potential retention of secretions in the lower respiratory tract with a probable need for more than a week of respiratory support, a tracheotomy was performed immediately. A large amount of pinkish foamy secretions was discharged from the patient's mouth after tracheotomy. The clinical and laboratory investigations indicated that the pulse oxygen saturation (SpO2) was less than 90% after assisted mechanical ventilation. A chest x-ray showed pulmonary edema with fluid-filled bilateral lungs (). Subsequently, a single dose of methylprednisolone (80 mg) was administered intravenously. Considering the severity of the Br2-induced injury, the patient was transferred to critical care center 4 h after Br2 inhalation for definitive treatment.
At the critical care center, the patient received synchronized intermittent mandatory ventilation (SIMV), with initial settings of positive end-expiratory pressure (PEEP) of 12 cmH2O, fraction of inspired oxygen (FiO2) of 1.0, respiratory rate (RR) of 16 bpm, tidal volume (VT) of 4 ml/kg, and plateau pressure (Pplat) ≤ 25 cmH2O. In addition to the routine critical care, initial management included absolute bed rest, intravenous methylprednisolone, anticoagulation, energy and vitamin supplements, maintenance of water, electrolytes, and acid-base balance. However, the condition of the patient worsened. Arterial blood gases recorded 48 h after mechanical ventilation were: pH 7.26, PaO2 6.13 kpa, PaCO2 4.97 kpa, and bicarbonate concentration 2.4 mmol/L (P/F oxygen ratio was 46 mmHg). Thereafter, the patient was initiated on ECMO. Two cannulas were placed percutaneously by vessel puncture, guidewire placement, and serial dilation. One cannula (Edward 24F, Edwards Lifesciences Corp., CA, USA) was advanced into the right femoral vein; another (Edward 16F) into the right internal jugular vein. The assembled circuit (PLS heparin-coated ECMO kit, Edward) was primed. Initial ECMO flow settings were: blood flow of 4 L/min, sweep gas flow of 2 L/min, FiO2 of 1.0, and temperature of the water bath was set at 36.8°C (adjusted according to arterial blood gas). The ventilator settings immediately pre-ECMO were: P-SIMV, PEEP 12 cmH2O, FiO2 0.5, RR 8 bpm, VT 4 ml/kg, Pplat ≤ 25 cmH2O. The patient was sedated with fentanyl and midazolam during cannulation and management for the first 12–24 h. Richmond Agitation-Sedation Scale (RASS) was −5. The neurologic examination was performed daily to ensure that the sedation was sufficient. Once the patient had stabilized on ECMO, all the sedatives and narcotics were stopped and resumed depending on the levels of anxiety and discomfort of the patient. Heparin (50–100 units per kg) was administered at the time of cannulation and continuously infused during ECMO. Heparin infusion was regulated to keep the activated partial thromboplastin time (APTT) at designated levels (usually 1.5 times the normal values for the APTT measurement system). Hemoglobin levels, blood platelet counts, and lactic acid accumulation were regularly detected to monitor the development of complications. The rest settings during ECMO support were: Ppeak 20–25 cmH2O, PEEP 10–15 cmH2O, RR 10 bpm, and FiO2 0.4.
In addition to ECMO support, the pharmacologic diuresis and antibiotic treatment were administered. Respiratory parameters of the patient improved and the chest CT images showed that the bilateral infiltrations had regressed after 7 days of therapy. The patient was weaned off ECMO upon shock reversal and attaining stable condition. The arterial blood gases were analyzed when the patient was extubated: pH 7.47, PaO2 98.3 mmHg, PaCO2 38.7 mmHg, and SpO2 99%. The chest CT was performed on 2nd and 7th day after weaning (). It was found that the lung edema had resolved. Follow-up chest CT after discharge from the hospital showed progressive improvement in the affected lung regions.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [92.0, 'mm hg'], 'Diastolic Blood Pressure': [63.0, 'mm hg']}",72.66667,69.03334,76.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 92.0 mm Hg + 2/3 * 63.0 mm Hg = 72.66667 mm Hg.
Hence, the patient's mean arterial pressure is 72.66667 mm Hg."
1127,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5877,Extracted,"A patient is brought to the emergency department by his spouse. The patient is admitted, treated, and transferred to the floor. The patient has a past medical history of obesity, type II diabetes mellitus, asthma, depression, and multiple suicide attempts. His current medications include pantoprazole, insulin, metformin, albuterol, fluticasone, lithium, levothyroxine, and fluoxetine. The patient has a 20 pack-year smoking history. On the floor, his temperature is 99.5°F (37.5°C), blood pressure is 140/85 mmHg, pulse is 70/min, respirations are 13/min, and oxygen saturation is 98% on room air. The patient's initial radiograph is reviewed as seen in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [85.0, 'mm hg'], 'Systolic Blood Pressure': [140.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 85.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
1128,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5633098-1,Extracted,"A 76-year-old Japanese man suffered from fever in April 2014. He had been receiving insulin therapy for diabetes mellitus and had been administered antiplatelet agent since the onset of cerebral infarction at age 60. On physical examination, his superficial lymph nodes, liver, and spleen were not palpable. Laboratory findings were as follows: white blood cell (WBC) count, 8.5 × 109/L with 0.5% abnormal lymphocytes; hemoglobin, 7.8 g/dL; platelet count, 79 × 109/L; lactate dehydrogenase (LDH), 1,004 U/L (normal range, 124 - 226 IU/L); C-reactive protein (CRP), 19.02 mg/dL; and soluble interleukin-2 receptor (sIL-2R) level, 11,400 IU/mL. Bone marrow aspiration revealed proliferation of large abnormal lymphocytes with vacuoles. These cells were positive for CD19, CD20, and kappa and were negative for CD5, CD10, and lambda, as determined by flow cytometric analysis. Positron emission tomography-computed tomography (PET/CT) scans revealed abnormal accumulations in the spleen and bone marrow. He was diagnosed with B-cell non-Hodgkin’s lymphoma. Because of acute deterioration, chemotherapy had to be initiated despite the absence of a pathological definitive diagnosis with bone marrow biopsy. Eight courses of reduced-dose R-CHOP therapy, which consisted of rituximab (375 mg/m2 on day 1), doxorubicin (25 mg/m2 on day 2), cyclophosphamide (375 mg/m2 on day 2), vincristine (0.7 mg/m2 on day 2), and prednisone (50 mg/body on days 1 - 5), were administered every 3 weeks. CNS prophylaxis was not performed. Complete remission was confirmed by laboratory findings and PET/CT. Until April 2015, there were no findings that actively suggested relapse. His sIL-2R level had remained approximately 700 - 900 IU/mL and was 876 IU/mL at that time.
In May 2015, 3 days before admission, he could not recognize cards in a deck when playing by himself. Additionally, behaviors that his family could not understand became increasingly evident. On the day of admission, he moaned in the bedroom and then had generalized convulsions. He was transferred to our hospital in an ambulance while the convulsion persisted. On physical examination at emergency visits, tonic-clonic convulsions continued. His temperature was 40.5 °C, heart rate was 157 beats per minute, blood pressure was 187/79 mm Hg, and respiratory rate was 20 breaths per minute. His Glasgow coma scale score was E1V1M4. His pupils were round and equal with a slow light reflex. There was right conjugate deviation but no neck stiffness. The liver, spleen, and superficial lymph nodes were not palpable. The laboratory findings were as follows: WBC count, 15.1 × 109/L with no abnormal cells; hemoglobin, 9.9 g/dL; platelet count, 188 × 109/L; prothrombin time, 13.2 s; activated partial thromboplastin time, 27.2 s; fibrinogen, 417 mg/dL; D-dimer, 2.5 µg/mL; total protein, 7.0 g/dL; albumin, 4.5 g/dL; aspartate aminotransferase, 24 U/L; alanine aminotransferase, 11 U/L; LDH, 313 U/L; total bilirubin, 0.5 mg/dL; serum creatinine, 1.36 mg/dL; CRP, 0.75 mg/dL; HbA1c, 8.3%; and electrolytes and blood glucose levels were normal. Brain CT scan revealed a high-density tumor with edema and intratumoral hemorrhage in the left temporal lobes (). The tumor was iso- to hypointense on T1-weighted magnetic resonance imaging (MRI) and hypointense on T2-weighted MRI and diffusion-weighted MRI (). In addition, gadolinium-enhanced T1-weighted imaging showed heterogeneous enhancement ().
For convulsion, diazepam and levetiracetam were initiated. Brain biopsy for definitive diagnosis was scheduled. However, convulsion frequently developed despite increased amounts of levetiracetam. His urinary tract infection was complicated, so antibiotics were started; however, his fever worsened. On the 24th hospital day, his LDH level drastically increased to 1,792 U/L and his CRP increased to 23.5 mg/dL. A few lymphoma cells were detected in the peripheral blood. Respiratory failure and disseminated intravascular coagulation (DIC) developed. He died on the 27th hospital day.
Autopsy was performed with the consent of his family and revealed DLBCL, which had infiltrated the brain, meninges, bone marrow, spleen, lung, retroperitoneum, adrenal gland, and lymph nodes. However, there was no macroscopically enlarged lymph node. Focal hemorrhage was observed in the left temporal lobe in which lymphoma cells had diffusely infiltrated with hemorrhage (). Lymphoma cells were observed in parts of the lung lesions within the lumina of vessels (). Lymphoma cells in the brain lesion were positive for CD20, CD79a, and PAX5 (), and those of other organs were negative for CD20 but positive for PAX5 ().",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [187.0, 'mm hg'], 'Diastolic Blood Pressure': [79.0, 'mm hg']}",115,109.25,120.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 187.0 mm Hg + 2/3 * 79.0 mm Hg = 115.0 mm Hg.
Hence, the patient's mean arterial pressure is 115.0 mm Hg."
1129,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8530503-1,Extracted,"A 56-year-old man presented to the emergency department with pelvic pain, rectal tenesmus, and fatigue. In the past four months, he experienced some episodes of low urinary tract symptoms and initiated treatment for hypertension.
Computed tomography (CT) documented a large heterogenic prostatic mass (59 x 35 x 33 mm) with loss of cleavage planes, numerous adenomegalies, multiple pericentimetric hepatic hypocaptating lesions, suggestive of secondary lesions, and evidence of bone involvement (Figures , ).
A urinary catheter was placed due to urinary retention. PSA was elevated with 223 ng/ml (normal <4 ng/ml) and the patient was admitted for pain control and investigation.
At admission, the patient was hypertensive (165/89 mmHg). Laboratory tests evidenced metabolic alkalosis (pH 7.58; HCO3 42 mEq/L), normal sodium of 140 mEq/L, and severe hypokalemia (2.1 mEq/L; normal 3.5-4.5 mEq/L), that showed to be refractory to adequate replacement measures. Hypokalemia investigation showed high levels of morning plasma cortisol (58 𝜇g/L; normal 3.7-19.4 𝜇g/L), high levels of 24 h urinary cortisol (12,333 𝜇g/24 h; normal range 4.3-176) with a negative overnight 8 mg dexamethasone suppression test (81 𝜇g/L; normal <19 𝜇g/L) and elevated levels of plasma ACTH (253 pg/mL; normal 7.2-63.3 pg/mL). A diagnosis of paraneoplastic ACTH-dependent CS was made. The patient was initiated on 250 mg metyrapone daily. The patient's potassium levels increased and 24 h urinary cortisol, after one week on metyrapone, decreased to 3254 𝜇g/24 h. A brain magnetic resonance imaging confirmed the absence of any pituitary abnormality and CT excluded nodules on the thyroid or adrenal gland, confirming ectopic ACTH production.
A prostatic biopsy revealed a small cell neuroendocrine carcinoma, positive for synaptophysin and focally for CAM5.2 and PSA, and negative for chromogranin A with a very high Ki67 expression (90%-100%) (Figures -).
Bone scintigraphy showed foci of hyperfixation, suggestive of osteoblastic metastization pattern dispersed along the axial and appendicular skeleton.
Diagnosis of stage IV (cT4N1M1b) NEPC was made. Fluorodeoxyglucose (FDG) positron emission tomography (PET) and 68Ga-DOTA-(Nal3)-octreotide (DOTA-NOC) PET were planned to complete the investigation and palliative chemotherapy was scheduled.
Days after diagnosis, the patient’s condition started to decline and repeated CT scans showed the disease’s progression. The patient developed a nosocomial urinary tract infection with Escherichia coli bacteremia that failed to respond to therapy and died within days with multiple organ dysfunctions.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [89.0, 'mm hg'], 'Systolic Blood Pressure': [165.0, 'mm hg']}",114.33333,108.61666,120.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 165.0 mm Hg + 2/3 * 89.0 mm Hg = 114.33333 mm Hg.
Hence, the patient's mean arterial pressure is 114.33333 mm Hg."
1130,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9886,Extracted,"A 10-year-old girl with a rash is brought to the clinic by her mother. The patient’s mother says that the onset of the rash occurred 2 days ago. The rash was itchy, red, and initially localized to the cheeks with circumoral pallor, and it gradually spread to the arms and trunk. The patient’s mother also says her daughter had been reporting a high fever of 39.4°C (102.9°F), headaches, myalgia, and flu-like symptoms about a week ago, which resolved in 2 days with acetaminophen. The patient has no significant past medical history. Her vital signs include: temperature 37.0°C (98.6°F), pulse 90/min, blood pressure 125/85 mm Hg, respiratory rate 20/min. Physical examination shows a symmetric erythematous maculopapular rash on both cheeks with circumoral pallor, which extends to the patient’s trunk, arms, and buttocks. The remainder of the exam is unremarkable. Laboratory findings are significant for a leukocyte count of 7,100/mm3 and platelet count of 325,000/mm3.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [85.0, 'mm hg'], 'Systolic Blood Pressure': [125.0, 'mm hg']}",98.33333,93.41666,103.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 85.0 mm Hg = 98.33333 mm Hg.
Hence, the patient's mean arterial pressure is 98.33333 mm Hg."
1131,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7958,Extracted,"A 70-year-old Caucasian woman presents with a 2-week history of blood-tinged sputum. Her past medical history is significant for peptic ulcer disease for which she underwent triple-drug therapy. She is a lifetime non-smoker and worked as a teacher before retiring at the age of 60 years. A review of systems is significant for a weight loss of 6.8 kg (15 lb) over the last 5 months. Her vitals include: blood pressure 135/85 mm Hg, temperature 37.7°C (99.9°F), pulse 95/min, and respiratory rate 18/min. Physical examination is unremarkable. A contrast CT scan of the chest shows an irregular mass in the peripheral region of the inferior lobe of the right lung. A CT-guided biopsy is performed and reveals malignant tissue architecture and gland formation with a significant amount of mucus.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [135.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",101.66667,96.58334,106.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 85.0 mm Hg = 101.66667 mm Hg.
Hence, the patient's mean arterial pressure is 101.66667 mm Hg."
1132,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-12367,Extracted,"A 24-year-old Turkish female presents to your office for a routine examination. She recently started a new job and has been tired most of the time. She does not have any dizziness and has not lost consciousness. She follows a well-balanced diet and is not vegetarian. She recalls that other family members have had similar symptoms in the past. On physical exam her temperature is 99°F (37.2°C), blood pressure is 115/78 mmHg, pulse is 100/min, respirations are 22/min, and pulse oximetry is 99% on room air. On physical exam, you notice conjunctival pallor. Labs are obtained and the results are shown below:

Hemoglobin: 10.2 g/dL
Hematocrit: 34%
Leukocyte count: 5,000 cells/mm^3 with normal differential
Platelet count: 252,000/mm^3
Mean corpuscular hemoglobin concentration: 20.4%
Mean corpuscular volume: 65 µm^3

Peripheral blood smear is shown in the image provided.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [115.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",90.33333,85.81666,94.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 78.0 mm Hg = 90.33333 mm Hg.
Hence, the patient's mean arterial pressure is 90.33333 mm Hg."
1133,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8265184-1,Extracted,"A 23-year-old female was brought to the emergency department with complaints of recurrent high-grade fever, seizures and, altered mental state (AMS). She had been seeking treatment from a local practitioner for a previously diagnosed tuberculous pericardial effusion, which had not yet resolved. Her past medical history included iron deficiency anemia, stomatitis, right mastitis, and she had been on anti-tubercular treatment (ATT) for the past 45 days. She had a family history of tuberculosis but denied having diabetes, hypertension, or asthma. She had suffered five to six episodes of abnormal body movements and altered sensorium before being admitted to the hospital. On admission, she had a fever of 101 ℉, tachycardia with 180 beats/minute, respiratory rate of 24 breaths/minute, blood pressure of 110/70 mmHg, and low oxygen saturation of 85% on ambient air. The patient's hematological and biochemical parameters are shown in Table and Table respectively.
On physical examination, her lymph nodes were found to be tender and painful, and she had generalized LAP, involving the right-sided cervical, axillary, bilateral inguinal, and inter-trochanteric lymph nodes. The LAP had started as a swelling below the medial aspect of the right chin; the swelling had then progressed to the medial aspect of the right elbow and finally evolved to be generalized LAP. She also presented alopecia and malar rash. Her respiratory examination revealed the presence of bilateral crepitus. Her deep tendon reflexes were present but were depressed. Her CNS examination revealed a Glasgow Coma Scale (GCS) score of 8 (eye: 2, verbal: 2, motor: 4). Neck rigidity was also present. She was administered IV methylprednisolone. However, the LAP did not resolve. Later on, she was started on IV glucocorticoids and phenytoin, along with the continuation of ATT.
The patient's urine examination revealed proteinuria (total protein: 226.90 mg/dL; creatinine: 86.96 mg/dL; protein-creatinine ratio: 2.61), macroscopic hematuria with 15-20 red blood cells/high power field, and was indicative of lupus nephritis. Her cerebrospinal fluid (CSF) examination was suggestive of meningitis (total protein: 270.40 mg/dL; cell count: 10/mm3; all mononuclear and glucose: 56.21 mg/dL). Her MRI scan of the head revealed enhancements in the brain parenchyma, signifying inflammation and indicating lupus cerebritis (Figure ).
Her chest X-ray revealed a bilaterally enlarged cardiac silhouette (Figure ), which raised suspicion for pericardial effusion. Her subsequent echocardiography confirmed our suspicion. Her anti-double stranded DNA (anti-dsDNA) was positive, and the anti-smooth muscle antibody (ASMA) was negative. Her immunofluorescence assay of pericardial fluid was positive for anti-nuclear antibodies (ANAs) with cytoplasmic dense fine-speckled pattern and intensity of 2+ (mildly positive) with a dilution of 1:80. In light of these findings, we concluded that her pericardial effusion was a complication of SLE rather than one caused by tuberculosis as diagnosed earlier by her local practitioner. According to the European League Against Rheumatism (EULAR) and the American College of Rheumatology (ACR) 2019 diagnostic criteria for SLE, a score of 10 or more must be considered as indicative of SLE. In our case, the score was 37, which is much more than what is needed to satisfy the criteria.
Even though the patient responded well to the treatment initially, she succumbed to the disease after one week of treatment.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1134,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6205061-1,Extracted,"A 27-year-old man without any significant medical history, presented to the emergency department (ED) with right lower abdominal pain and a fever of 38.7 °C A computed tomography (CT) scan of abdomen and pelvis showed a perforated appendix (). Emergency laparotomy was performed and the patient underwent appendectomy and washout. He was discharged home three days later.
On postoperative day 12, the patient was presented again to the ED with a septic shock with a pain of right flank. The vital signs at presentation were as follows: GCS 11/15; blood pressure 110/65 mmHg; pulse 110–120 beats/min; respiratory rate 25 breaths/min and body temperature 39 °C. Physical examination showed right thigh tenderness with a moderately erythematous abdomen and subcutaneous emphysema. Laboratory evaluation revealed a white blood cell count of 25000/mm³ with 90% neutrophil forms; hemoglobin 13 g/dL; Creatinine 65 μmol/L; C-reactive protein was 200 mg/dL and serum lactate level 4.9 mmol/L
A new surgical exploration was performed after appropriate resuscitation with intravenous fluids and antibiotic, revealed a purulent peritonitis with necrotizing fasciitis involving the right lower abdomen, right psoas muscle and right retroperitoneum. Culture of the necrotic tissues revealed polymicrobial infection consisting of Escherichia coli and Pseudomonas aeruginosa.
Postoperatively, the patient stayed intubated in the surgical intensive care unit and had mild hemodynamic instability requiring low-dose of noradrenaline. Antibiotics (Vancomycin 20 mg/kg/24 h, Tazobactam-Piperacillin 80 mg/kg every 6 h, Amikacin 15 mg/kg/24 h, metronidazole 40 mg/kg) were administered and the patient received repeated debridement for the unhealed abdominal wound. In addition, incision, drainage and hyperbaric treatments were performed three times for the necrotizing soft tissue infections over the retroperitoneal region of the right flank and also over the scrotal region and the external genital organ because of the extension of the necrosis. One week later, the patient developed another septic shock due to the extension of the necrosis to the right chest wall. A CT scan of the chest showed right-sided pleural effusion with erosive aspect of the ribs (). Necrotic tissues were debrided and antibiotic was changed due to wound superinfection with Acinetobacter Baumannii (Coli-mycin 100,000 UI/kg/24 h, rifampicin 30 mg/kg/24 h). After the improvement of his general health, skin flaps were putted by plastic surgeon to cover the exposed ribs ().
On the sixty postoperative day, the patient developed a mitral valve infective endocarditis with negative blood culture. Three days later, he died of septic shock and multiple organ failure.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 65.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1135,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4391523-1,Extracted,"A confused 41-year-old male was found in a park and brought to emergency department by the paramedics. During transit he had two generalized seizures. On the admission the patient appeared confused but conscious with a Glasgow Coma Scale of 13. He behaved aggressively and spoke neither English nor a local language. An interpreter was consulted, but the patient showed aggressive behaviour, therefore making it impossible to take a history. The physical examination was unremarkable except for a tongue bite and several bruises and scratches over the whole body. The pupils were moderately dilated and sluggishly reactive. All vital signs were stable (heart rate: 108 beats per minute, blood pressure: 123/80 mmHg, oxygen saturation: 98% at room air with a normal respiratory rate, and a body core temperature of 37.2°C). Laboratory tests revealed a leukocytosis of 25.1 G/L, elevated values for C-reactive protein (12 mg/L), creatinine kinase (2185 U/L), myoglobin (618 μg/L), creatinine (143 mmol/L), and uric acid (1344 mmol/L) suggesting renal insufficiency. Electrolytes, liver enzymes, troponin I, coagulation, and haematology were in the normal range. An electrocardiogram showed a sinus tachycardia. Neurology service was consulted because of ongoing confusion and for assessment of epilepsy. A cranial CT scan ruled out haemorrhage or other focal lesions. Lorazepam (2 mg, IV) was administered twice with no effect on his neurological status. The patient started to sweat and became hypertensive (systolic blood pressure of 180 mmHg) and more tachycardic (heart rate of 140/min). A drug screening (Triage 8) was performed, which was positive for cocaine. Finally he admitted the cocaine consumption but refused to give further information. Benzodiazepines as well as phentolamine were given. In order to further investigate the drug intoxication a plain abdominal dual-energy CT scan was requested. Four round, hyperdense, foreign bodies were found in the transverse colon ().
An emergency laparotomy was indicated and carried out immediately. Following colotomy four packages () were removed. Thorough exploration revealed no further packages. The procedure took 60 minutes and postoperatively the patient was on observation for 24 h in the intensive care unit. The neurological signs as well as the renal insufficiency improved rapidly under conservative therapy. The further clinical course was unremarkable, and the patient was discharged six days after surgery.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [123.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",94.33333,89.61666,99.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 123.0 mm Hg + 2/3 * 80.0 mm Hg = 94.33333 mm Hg.
Hence, the patient's mean arterial pressure is 94.33333 mm Hg."
1136,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5796,Extracted,"A 23-year-old woman is admitted to the inpatient psychiatry unit after her boyfriend reported she was “acting funny and refusing to talk.” The patient’s boyfriend states that he came home from work and found the patient sitting up in bed staring at the wall. When he said her name or waved his hand in front of her, she did not respond. When he tried to move her, she would remain in whatever position she was placed. The patient’s temperature is 99°F (37.2°C), blood pressure is 122/79 mmHg, pulse is 68/min, and respirations are 12/min with an oxygen saturation of 98% O2 on room air. During the physical exam, the patient is lying on the bed with her left arm raised and pointing at the ceiling. She resists any attempt to change her position. The patient remains mute and ignores any external stimuli. The patient’s medical history is significant for depression. She was recently switched from phenelzine to fluoxetine.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [122.0, 'mm hg'], 'Diastolic Blood Pressure': [79.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 122.0 mm Hg + 2/3 * 79.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1137,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7769789-1,Extracted,"A 92-year-old female with a medical history notable for hypertension, hyperlipidemia, atrial fibrillation on anticoagulation, diabetes mellitus, and chronic kidney disease who presented to the ED with altered mental status, shortness of breath, and abdominal pain of one-day duration. She described diffuse, nonradiating abdominal pain that was crampy in nature, rated 5/10 in intensity, and associated with two episodes of nonbloody and nonbilious emesis. On admission, physical examination was remarkable for elevated blood pressure (188/79 mmHg), but an otherwise preserved heart rate and oxygen saturation. The abdominal examination demonstrated mild discomfort on palpation of the lower abdomen, but no evidence of rebound or guarding. Laboratory workup (Table ) was remarkable for leukocytosis (19.2 k/uL), an elevated lactate (4.7 mmol/L), elevated C-reactive protein (CRP) (79 mg/L), erythrocyte sedimentation rate (ESR) (60 mm/hour), lactate dehydrogenase (LDH) (281 U/L), creatine kinase (CK) (738 U/L). CT scan of the head and chest radiograph demonstrated no acute abnormalities. CT scan of the chest was subsequently performed and revealed an irregular mass-like area of ground-glass density in the left upper lobe (Figure ). Given the patient’s overall clinical presentation and elevated inflammatory markers, a nasopharyngeal swab specimen was collected to rule out COVID-19, which ultimately demonstrated SARS-CoV-2 positivity. The patient’s hospital course was complicated by multiple episodes of watery diarrhea for which additional diagnostic workup - stool ova and parasites, stool culture, and Clostridium difficile - was ordered and found negative. The patient was treated with supportive care (IV hydration, electrolytes monitoring) and antibiotics which resulted in symptomatic improvement 16 days following presentation and 17 days following onset of symptoms.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [79.0, 'mm hg'], 'Systolic Blood Pressure': [188.0, 'mm hg']}",115.33333,109.56666,121.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 188.0 mm Hg + 2/3 * 79.0 mm Hg = 115.33333 mm Hg.
Hence, the patient's mean arterial pressure is 115.33333 mm Hg."
1138,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4763642-1,Extracted,"A 32-year-old male patient was admitted to the outpatient clinic with complaints of weight gain, dry mouth, and fatigue. In 2002, some eruptions appeared on the skull. Two (2) years later, skin eruptions spread all over his body. At that time, he was diagnosed with psoriasis and prescribed topical clobetasol propionate. He had not been reexamined after that and has been using clobetasol propionate 0.005% routinely for 10 years. He has applied the drug to his arms, legs, and all over the trunk. Over the past year, he put on weight obviously (8 kg). He stopped the treatment 1 month ago, at the time of writing. He has been complaining of dry mouth and fatigue for the last month. On his physical examination, moon face, central adiposity, and purple-red striae on the abdomen under umbilicus were observed. There were scaly patches and erythematous plaques on the skull, interscapular area, sacrum, arms, legs, knees, and elbows []. Other systemic examinations were all normal. Blood pressure was 130/90 mmHg, pulse 75/min, height 1.76 m, weight 77 kg, and body mass index 24.8 kg/m2. On laboratory examination, fasting blood glucose: 152 mg/dL (N: 70-105), creatinine: 1 mg/dL (N: 0.72-1.25), triglyceride: 160 mg/dL (N: 0-200), total cholesterol: 240 mg/dL (N: 0-200), high-density-lipoprotein (HDL)-cholesterol: 44 mg/dL (N: 45-55), low-density-lipoprotein (LDL)-cholesterol: 164 mg/dL (N: 0-130), ALT: 42 u/L (N: 0-55); AST: 27 u/L (N: 0-34); sodium: 140 mmol/L (N: 136-145); potassium: 4.6 mmol/L (N: 3.5-5.1); calcium: 9.9 mg/dL (N: 8.4-10.2); phosphorus: 3.5 mg/dL (N: 2.3-4.7); albumin: 4.6 g/dL (N: 3.2-5.2); intact-parathyroid hormone (iPTH): 38 pg/mL (N: 14-72); 25-OH Vitamin D: 4.9 ng/mL (N: 24-50); white blood cell (WBC) count: 12.76-103 /uL (N: 4.23-9.07); hemoglobin (Hb) count: 14.7 gr/dL (N: 13.7-17.5); platelet: 217-103 /uL (N: 150-400); morning (8 AM) adrenocorticotropic hormone (ACTH): 5.6 pg/mL (N: 0-46); morning (8 AM) serum cortisol: <0.2 μg/dL (5.5 nmol/L) (N: 4.3-22.4). According to these findings, the patient was diagnosed with iatrogenic Cushing's syndrome secondary to topical steroid use. For adrenal insufficiency, 20 mg/day hydrocortisone treatment was commenced, and for vitamin D deficiency, vitamin D replacement. As the patient had high blood glucose levels, dyslipidemia, and large waist circumference (101 cm), he was diagnosed with metabolic syndrome, and a low-calorie diet and exercise were advised. Metformin treatment at a dose of 2000 mg/day was commenced for glucose regulation. The patient consulted at the dermatology department for his psoriasis, and calcipotriol pomade and emollients were prescribed. One (1) month after that, 1 μg tetracosactide i.v. was applied and cortisol levels were measured at 30 min and at 60 min. As both measured levels were below 3 μg/dL, glucocorticoid maintenance treatment was continued.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 90.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
1139,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5058839-1,Extracted,"A 62-year-old man presented to his local hospital after 1 month of mucous and bloody stool and 2 weeks of worsening abdominal pain. He had leukocytosis (1.4 × 104/μL), thrombocytopenia (6.4 × 104/μL), and elevated blood urea nitrogen (BUN; 71 mg/dL) and serum creatinine (2.56 mg/dL) levels. The patient was admitted with a suspicion of sepsis secondary to intraabdominal infection, and broad-spectrum antimicrobial therapy was initiated. However, his condition deteriorated, and after 7 days, he was transferred to the intensive care unit (ICU) at Chiba University Hospital.
On admission to the ICU, the 165.3 cm tall patient weighing 99.3 kg was fully conscious (Glasgow Coma Scale E4V5M6), but he had a tendency to somnolence. His blood pressure was 154/103 mm Hg, heart rate 115/minutes, respiratory rate 30/minutes, body temperature 37.9 °C, and SpO2 96% on room air. The conjunctiva and skin were icteric. The chest was clear to auscultation. There was abdominal distention with mild hypogastric tenderness but no sign of peritoneal irritation. There was pitting edema in the upper and lower extremities. The white blood cell count was 1.2 × 104/μL, C-reactive protein level was 23.9 mg/dL, and procalcitonin level was 8.92 ng/mL, which were consistent with a diagnosis of bacterial infection. The platelet count had dropped to 3.8 × 104/μL, and the prothrombin time was 41% with a fibrin degradation product level of 53.1 μg/mL, indicative of coagulopathy. The lactate dehydrogenase level was 392 IU/L, aspartate transaminase and alanine transaminase levels were 50 and 17 IU/L, respectively, and also total and direct bilirubin levels were 6.2 and 4.6 mg/dL, respectively; however, other indicators of hemolysis, including anemia and schistocytosis, were absent. The BUN had increased to 92 mg/dL and the creatinine level was stable at 2.09 mg/dL. The CH50 level was 40.6 U/mL (normal range: 30–50 U/mL), the C3 level was 85 mg/dL (normal range: 65–135 mg/dL), and the C4 level was 23 mg/dL (normal range: 13–35 mg/dL).
The patient's clinical course is summarized in the Fig. . Since a stool culture test on ICU admission identified Enterococcus species and Corynebacterium striatum, a diagnosis of severe sepsis derived from bacterial enteritis was established and wide-spectrum antimicrobial therapy was initiated. Continuous hemodiafiltration was initiated on ICU day 3 but oliguria progressed to anuria, thrombocytopenia persisted, and laboratory values did not improve. Blood, urine, and spinal fluid cultures taken on admission to the ICU were all negative, which eliminated the possibility of additional foci of infection. Two polyps (one each in the sigmoid colon and the rectum) were discovered on lower gastrointestinal endoscopy, which were diagnosed at histopathology as early-stage nonhemorrhagic adenocarcinoma. The polyps did not appear to be the cause of the bloody stool. Additional laboratory evaluations were negative for other hematological disorders or connective tissue diseases. On ICU day 9, schistocytosis (0.5%) was noted on the peripheral blood smear, and a diagnosis of TMA was established. The Hct level also had dropped to 23.5% on the same day and the declining trend continued, therefore red blood cell transfusion was performed days later when he complained dyspnea. Plasma exchange (PE) therapy was initiated on ICU day 11. The patient had only a slight remission of thrombocytopenia after a total of 8 PE sessions (2.1 × 104/μL before the 1st PE and 5.9 × 104/μL after the 8th PE), but there was no notable clinical improvement and the anuria persisted (Fig. ). The level of ADAMTS13 activity in a plasma sample collected from the patient prior to initiation of PE was 25.1%, and the sample was negative for ADAMTS13 inhibitor. These findings eliminated the possibility of TTP. Furthermore, the stool was negative for Shiga toxin-producing-strains of Escherichia coli, and the serum titer for anti-Shiga-toxin antibody was also negative, eliminating the possibility of HUS. Although we considered TMA secondary to colorectal cancer in the differential diagnosis, the endoscopic findings of intramucosal carcinoma and negativity for tumor markers eliminated this possibility. Careful consideration of other possible causes, previous history, and drug history failed to identify an extrinsic etiology of TMA in this patient, and we ultimately suspected aHUS as the cause. Accordingly, intravenous eculizumab treatment (900 mg, once a week) was initiated on ICU day 26. An increase in urine output was observed on the next day, and renal support was successfully discontinued on the same day. And also marked recovery of the platelet count was obtained in combination with the effectiveness of supportive therapy including PE. Biweekly eculizumab infusion was repeated 4 times and then discontinued.
After approval by the institutional review boards of Chiba University, the University of Tokyo, and National Cerebral and Cardiovascular Center, an anticomplement factor H (CFH) antibody assay and an analysis of complement factor H-related (CFHR) genes were performed using a blood sample collected from the patient prior to initiation of PE. Also written informed consent was obtained from the patient before the assays. The anti-CFH antibody level was 6.16 AU/mL, which indicated negativity for anti-CFH antibody. We performed the multiplex ligation-dependent probe amplification (MLPA) analysis to screen the copy numbers of CFHR1/3 on chromosome 1q32 using a commercially available kit (MLPA kit P236-A2; MRC-Holland, The Netherlands),[ and found that CFHR1/3 did not show gene deletions. However, moderate hemolysis was induced in concomitant hemolytic assays using sheep red blood cells (RBCs), and analysis for mutations potentially associated with aHUS identified a nonsynonymous mutation (p.Ala311Val) in the gene encoding membrane cofactor protein (MCP). All screened genes are presented in the Table .
The patient was discharged from the ICU on day 37 and was discharged to home on day 58. He was followed up regularly as an outpatient and was receiving 40 mg/day of prednisolone. At approximately 1 year after discharge, the patient remained in stable condition without relapse or resumption of eculizumab therapy.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [154.0, 'mm hg'], 'Diastolic Blood Pressure': [103.0, 'mm hg']}",120,114,126,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 154.0 mm Hg + 2/3 * 103.0 mm Hg = 120.0 mm Hg.
Hence, the patient's mean arterial pressure is 120.0 mm Hg."
1140,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7477526-1,Extracted,"A three-year-old female with a history of complex congenital heart disease and previous cardiac surgeries was admitted to the pediatric intensive care unit (PICU) in shock that progressed to cardiopulmonary arrest requiring resuscitation due to thrombosis in her right ventricle-to-pulmonary artery conduit. She subsequently demonstrated evidence of severe hypoxic-ischemic encephalopathy and acute kidney injury (AKI), of which the latter resolved.
The main reason for her subsequent PICU stay was for neurological rehabilitation and transition to home ventilation. She was receiving treatment for dystonia, heart failure, endocarditis, and pulmonary embolism. At the request of the parents, stem cell therapy for neurological dysfunction was investigated. As metformin has shown properties to recruit existing neural stem cells and enhance neural functions, a trial of therapy was initiated. The patient was placed on metformin (20 mg/kg) 17 days before the event, which was increased to 40 mg/kg (250 mg twice-daily) six days prior to the event.
On the day of the event, the patient acutely presented with a new wide complex bradycardia 70–80 beats per minute (bpm) from a baseline of 110–120 bpm and peaked T waves. The other vital signs were blood pressure = 90/40 mmHg, respiratory rate = 26 breaths per minute, temperature = 37.2 °C, and oxygen saturation = 87% on her baseline ventilation settings. She was poorly perfused with prolonged capillary refill time and lethargic. Immediate and subsequent venous blood sampling showed severe lactic acidosis and hyperkalemia [].
She was managed for hyperkalemia, and propranolol was discontinued. She became hypotensive, requiring dopamine and norepinephrine infusions, and higher ventilator support. The patient’s clinical status improved within three hours, and support therapies were weaned towards the baseline. Twelve hours after the initial event, a similar episode recurred with a rise in serum lactate and hyperkalemia, which was treated similarly and resolved. A detailed review of both events demonstrated that they occurred 1 to 2 hours after the administration of metformin. In addition, her creatinine levels had doubled five days prior to the event with a recent increment in metformin dose six days before.
At this point, metformin was discontinued. No further episodes were noted, and her clinical status returned to baseline [].",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [40.0, 'mm hg']}",56.66667,53.83334,59.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 40.0 mm Hg = 56.66667 mm Hg.
Hence, the patient's mean arterial pressure is 56.66667 mm Hg."
1141,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4010031-1,Extracted,"A 38-year-old woman presented to the emergency department with a two-day history of confusion, agitation, and “restless, swollen legs.” Her past medical history included gastric bypass surgery, depression, and previous alcohol abuse. Regular medications were fluoxetine, omeprazole, and cetirizine. On initial assessment in the emergency room she was tachycardic at 102 beats per minute, her blood pressure was 130/70 mmHg, and her chest was clear to auscultation with an SpO2 of 100% on room air. She was confused, with a GCS score of 10 (E3V2 M5), but with no focal neurological abnormalities or rash. Her temperature was 37.5°C and blood sugar was 5.6 mmol/L. Due to her confusion and agitation, sedation was given and a CT brain scan performed. This demonstrated no acute abnormality. A lumbar puncture was performed and treatment for CNS infection instituted with ceftriaxone and acyclovir. Her potassium was 1.9 mmol/L (3.6–5.0 mmol/L), sodium 146 mmol/L (136–145 mmol/L), phosphate 0.57 mmol/L (0.8–1.4 mmol/L), and chloride 122 mmol/L (96–106 mmol/L). Her renal function was otherwise normal with a urea of 2.7 mmol/L (2.5–6.6 mmol/L) and creatinine 56 μmol/L (60–120 μmol/L). An arterial blood gas (FiO2 0.40) demonstrated a compensated metabolic acidosis: H+ 38.6 nmol/L, PaCO2 3.5 kPa, PaO2 24.44 kPa, HCO3 18.8 mmol/L, BE 8.2 mmol/L, Lactate 1.13 mmol/L. An ECG showed ST segment depression and U-waves but no ectopic beats or arrhythmias.
On further questioning, the patient's family suggested that she may have been taking large amounts of Nurofen Plus, as this had been an issue previously.
Due to her confusion and profound biochemical abnormalities she was admitted to the intensive care unit for further management.
Her management on ITU involved invasive monitoring and correction of the biochemical abnormalities. During the initial 48 hours in hospital she received 509.5 mmol of intravenous potassium replacement, which increased the serum potassium to 4.8 mmol/L. Phosphate replacement was given and once the serum potassium level had improved, 1.26% sodium bicarbonate was used as maintenance intravenous fluid. With the correction of her biochemical abnormalities (), her neurological function improved to GCS 15 (E4V5 M6). The biochemical abnormalities in the serum and urine suggested a diagnosis of renal tubular acidosis with a serum anion gap of 9 mmol/L, urinary anion gap of 20 mmol/L, and transtubular potassium gradient of 11.37. On improvement of her symptoms and conscious level, the patient admitted to taking large amounts of Nurofen Plus tablets (20–40 per day) during the preceding weeks.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 70.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1142,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5360,Extracted,"A 16-year-old female presents to her primary care physician with worsening facial acne over the last several months. She states that she first developed sparse pimples around age 12, and she used over-the-counter face cleansers containing salicylic acid with moderate improvement. She was prescribed a topical retinoid two months ago when her acne first started to worsen, but she has been unable to use it consistently due to excessive skin drying. She still feels that her acne is poorly controlled. She states that her skin seems to break out more around her menstrual period, which occurs every 28 days. The patient has a past medical history of migraines with aura, for which she sometimes takes sumatriptan. Her mother has a history of hypertension, and her father died of a myocardial infarction at age 51. The patient is a junior in high school and plays varsity soccer. She denies use of alcohol, tobacco, and drugs and has never been sexually active. Her temperature is 98.2°F (36.7°C), pulse is 70/min, blood pressure is 117/61 mmHg, respirations are 14/min, and oxygen saturation is 99% on room air. Cardiopulmonary exam is unremarkable. A representative portion of her facial skin exam is shown in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [117.0, 'mm hg'], 'Diastolic Blood Pressure': [61.0, 'mm hg']}",79.66667,75.68334,83.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 117.0 mm Hg + 2/3 * 61.0 mm Hg = 79.66667 mm Hg.
Hence, the patient's mean arterial pressure is 79.66667 mm Hg."
1143,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3771485-1,Extracted,"A 10-year-old African American girl was admitted to our hospital with chief complaints of fever and abnormal movements.
The patient is a previously healthy, a 10-year-old girl who two weeks prior to admission started having episodes of headache on and off controlled with Tylenol. Headache was generalized, not associated with nausea or vomiting. Three days prior to admission, the patient had low grade fevers, and mom noticed some abnormal movements of the extremities which progressed over the next 2 days to the point where she cannot eat or dress on her own. She also had difficulty in walking and holding on to objects. H/o lip smacking and slurred speech are present for the past 3 days. H/o rash in the lower extremities which looked like hives is present for the past 2 days.
H/o decreased appetite with loss of weight is present. The day prior to admission the patient had fevers with temperature up to 101 F, and with progression of involuntary movements the patient was taken to her PCP who started her on Acyclovir. With the symptoms getting worser, the patient was taken to an emergency center that evening before being transferred to our hospital for further care and management.
No H/o any prior hospitalization. Past H/o sore throat about a month ago which lasted for 2 days. At that time the child did not receive any medical attention, and sore throat went away on its own.
The child was adopted, and not much is known about the birth and family history. As per adoptive parents biological mom might have been worked up for some autoimmune diseases, the specificity of which is unknown.
On admission, the patient had a temperature of 99.5 F, weight of 55.5 kg (lost 10 pounds over the past 2 to 3 weeks), blood pressure of 99/77, heart rate of 129, and respiratory rate of 20.
On Neurological exam, the patient was awake, alert and cooperative. Involuntary lip smacking with tongue protrusion and slurred speech were present. Pronounced choreoathetoid movements of the upper and lower extremities were present. Milkmaid grip was positive. With arms outstretched above the head noticeable chorea with pronation of forearm was present.
On Motor exam Tone and reflexes were equal and normal in all 4 limbs. Strength was decreased in the lower extremities and choreiform movements were present.
Sensation was intact. She had trouble with walking without support.
She had a diffuse macular rash involving the lower extremities which is erythematous and confluent in some areas. The rest of her physical exam including her thyroid, cardiovascular, respiratory, and abdominal exam was normal.
Lab values from the outlying ER include a CBC which showed anemia with a Hb of 10.8 g/dL, hematocrit of 32.5%, MCV of 76.5, and thrombocytopenia with platelet count of 89000/mm3. CT scan and a spinal tap were done which were essentially normal. CSF studies showed no pleocytosis with normal protein and glucose. A gram stain of the CSF was negative. Bacterial culture and HSV PCR were pending at the time of admission.
The patient was worked up for the differential of choreiform movements. High on the list of our suspicion was sydenham's chorea secondary to rheumatic fever. ASO titre was elevated at 215 IU/ML (<150), ESR was elevated at 55 mm/hr (0–10), and urine analysis was positive for proteins at 25 mg/dL (neg), ketones at 50 mg/dL, and small blood. The patient was initially started on penicillin.
An echocardiogram of the heart was done () which showed 9 mm × 8 mm echogenic, nonmobile area on the posterior mitral valve leaflet suspicious for thrombus versus vegetation with normal function, and anatomy of the valves.
MRI of the brain was done which was normal except for nonspecific small white matter hyperintensities in the left frontal lobe.
With the patient's history of fever, and possible thrombus versus vegetation on echocardiogram, thought of infective endocarditis was entertained. Blood cultures were sent, and the patient started on Lovenox and ceftriaxone pending culture results. For the possible thrombus, coagulation workups were done including a prothrombin time which was normal. Test for Cardiolipin IgG was negative at 8.3 GPL (Neg < 10.0 GPL) and Borderline positive for Cardiolipin IgM at 14.5 GPL (Borderline 10.0–14.9 GPL).
Next on the list of our differential was systemic lupus erythematosus. With Biologic mom's possible workup for autoimmune disease and the fact that chorea even though is a rare complication for SLE can be a presenting feature especially in pediatric SLE, a blood analysis for ANA was sent. Other labs that were done to rule out other causes of chorea including urine and serum toxicology screen, thyroid panel, and lyme titres which came back negative.
On day 2 of the hospital course ANA titres came back positive at 1 : 1280 with a homogenous pattern. Further testing for SLE revealed positive results for anti-DS DNA at 473 IU/ML (Neg < 100), anti-Smith antibodies at 177AU/mL (Neg < 100), Sjogren's anti-SS-A at 937 AU/mL (Neg < 100), Sjogren's anti-SS-B at 118 (Neg < 100), and antihistone abs at 330 AU/mL (Neg < 100), and complement levels for C3 was low at 55 mg/dL (86–184). CPK levels were also abnormally elevated.
Blood cultures and HSV PCR from the outlying hospital came back negative. Ceftriaxone and acyclovir were stopped and patient was started on IV steroids for SLE.
The patient's chorea dramatically improved after starting steroids. She received Solu-Medrol at 500 mg daily for 3 days and slowly tapered over to oral steroids over a course of 2 weeks. The patient was discharged home on oral steroids and Lovenox with follow-up appointments scheduled with rheumatology and cardiology.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [99.0, 'mm hg'], 'Diastolic Blood Pressure': [77.0, 'mm hg']}",84.33333,80.11666,88.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 99.0 mm Hg + 2/3 * 77.0 mm Hg = 84.33333 mm Hg.
Hence, the patient's mean arterial pressure is 84.33333 mm Hg."
1144,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3811697-2,Extracted,"A 35-year-old female came to the Department of Obstetrics and Gynecology at Cheil General Hospital & Women's Healthcare Center with sterility 6 months ago. In the past medical history, she had been treated with medication for hyperthyroidism and had underwent surgery for endometriosis. She had received subcutaneous injections of leuprorelin acetate of 3.75 mg per month, three times in all, as a pretreatment for in vitro fertilization from 2 months ago. Since she had a past history of hyperthyroidism, she was refered to the Department of Internal Medicine for further evaluation.
Her blood pressure was 118/79 mm Hg, pulse was 79 per minute, and BMI was 18.6 kg/m2 (159 cm/47 kg). She had been diagnosed with hyperthyroidism a decade ago and had taken methimazole 10 to 2.5 mg until 3 months before she came to our hospital because her thyroid function was normalized. She also underwent surgery for endometriosis at another hospital 1 year ago. Nothing was noteworthy in her family history.
She complained of sweating, heat sensation intolerance, and facial flushing. On physical examination, she had slightly diffuse thyroid enlargement and the ECG was normal.
Serum T3 (120.6 ng/dL), fT4 (21.8 pmol/L), and TSH (0.51 µU/mL) were all whinin the normal range, but anti-TG Ab (13 U/mL), anti-TPO Ab (>100 U/mL), and TBII (22%) were all positive. Thus, further observation was required.
One month later, she complained of palpitation and fatigue, while T3 (259.5 ng/dL) and fT4 (60.6 pmol/L) were elevated, TSH (<0.01 µU/mL) was suppressed, and anti-TG Ab (17 U/mL), anti-TPO Ab (>100 U/mL), and TBII was elevated to 27%. Thus, she was diagnosed with hyperthyroidism and started taking methimazole 10 mg. Two months later, T3 (304.0 ng/dL), fT4 (57.0 pmol/L), TSH (<0.01 µU/mL), and TBII was elevated to 37% and medication was changed to propylthiouracil 200 mg. Three months later, she is currently maintaining propylthiouracil 100 mg under serial assessment by the Department of Internal Medicine ().",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [118.0, 'mm hg'], 'Diastolic Blood Pressure': [79.0, 'mm hg']}",92,87.4,96.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 118.0 mm Hg + 2/3 * 79.0 mm Hg = 92.0 mm Hg.
Hence, the patient's mean arterial pressure is 92.0 mm Hg."
1145,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2556315-1,Extracted,"A 65 year old white male presented with signs of increasingly severe dysphagia of four months duration. He stated that foods become impacted in his throat shortly after eating, with resultant vomiting and regurgitation. This is worse with solids as opposed to liquids and resulted in the loss of 10–15 pounds over the last several months. He noted these symptoms only in association with meals and not with any changes in position. The patient denied having odynophagia, chest pain, abdominal pain, or constitutional symptoms. He was transferred from an outside hospital with an additional diagnosis of aspiration pneumonia, his third episode in recent months. The patient's past medical history was significant for small cell carcinoma of the right lung, treated with 4 cycles Cisplatin, Etoposide and radiation therapy in 2004 and 2005, and GERD. His list of medications included moxifloxacin, omeprazole, simvastatin, loratadine, and albuterol and flunisolide inhalers. The patient also had a 60 pack year history of smoking.
On admission, the patient's vital signs were a temperature of 97.8, a pulse of 98, a respiratory rate of 16, a blood pressure of 90/50, and 95% hemoglobin saturation on 3 L of oxygen. Physical examination was completely unremarkable, with a non-tender, non-swollen neck, an intact gag reflex, and no epigastric tenderness. Laboratory data revealed an elevated WBC of 12.07 k/cmm with an increased ANC of 10.54 k/cmm and 87.3% bands, a decreased hemoglobin of 10.9 g/dL and a hematocrit of 33.4%. The patient's calcium was slightly lowered at 8.1 mg/dL. Urine specific gravity was 1.006. Other labs were within normal limits. An MBS was performed which was nondiagnostic. Chest x-ray revealed a left apical mass-like consolidation with a mild perihilar infiltrate. Although these findings could simply be due to the patient's pneumonia, the history of dysphagia and weight loss prompted further investigation with a CT scan. While no malignancy was detected, there was evidence of chronic aspiration pneumonitis. The patient was placed on ceftriaxone (1 gm IV) and azithromycin (500 mg IV) and was switched to PO Augmentin at 875 mg/day after 3 days on improvement of his pulmonary symptoms. Because it was known that esophageal dysfunction predisposes patients to repeated episodes of aspiration pneumonia, an EGD was performed for further workup. The EGD demonstrated a tortuous esophagus with pooling of secretions. There was mild increased resistance of LES on passage of the scope. This stricture did not appear inflammatory or malignant and was located adjacent to the area previously irradiated four years ago during treatment for the patient's small cell lung carcinoma.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [50.0, 'mm hg']}",63.33333,60.16666,66.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 50.0 mm Hg = 63.33333 mm Hg.
Hence, the patient's mean arterial pressure is 63.33333 mm Hg."
1146,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1644,Extracted,"A 68-year-old man comes to the emergency department because of a 1-week history of difficulty breathing. He has had recurrent palpitations over the past 2 years. During this time, he has also had several episodes of anxiety despite no change in his daily life. He has occasional sharp chest pain localized to the left upper sternal border. He has no abdominal pain or leg swelling. Two years ago, he had streptococcal pharyngitis, which was promptly treated with a 10-day course of penicillin. He has never traveled outside of the country. His temperature is 36.5°C (97.7°F), pulse is 82/min, and blood pressure is 140/85 mm Hg. Physical examination shows a 3/6 holosystolic murmur that is loudest at the apex and radiates to the axilla with a mid-systolic click. Bilateral fine crackles are heard on lung auscultation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 85.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
1147,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3970460-1,Extracted,"A 23-year-old female patient admitted to endocrinology outpatient clinic with the complaint of hirsutism for the last year. Excessive hair growth was identified to originate from facial and mandibular areas initially and then to spread to abdominal and thoracic regions. She had regular menstrual cycles since her first period by the age of 12. Medical background and family history were unremarkable. Physical examination revealed that body temperature was 37°C, pulse rate was 80 beats/min, height was 156 cm, weight was 61 kg, BMI was 25.4 kg/m2, and the blood pressure was 120/80 mm Hg. She had acnes on her face while showed no signs of moon face or facial plethora. Thyroid gland was nonpalpable and abdominal examination was normal in superficial and deep palpation. No organomegaly or mass was detected. Examination of the urogenital system revealed normal findings with feminine type of hair growth and normal breast development. Absence of ecchymosis, normal turgor and tonus, and normal skin thickness were noted in the examination of the skin. There were no findings of purple stria and acanthosis nigricans, whereas hirsutism was remarkable. Ferriman Gallwey score was 23. There were no signs of virilization including vocal changes, muscular hypertrophy, breast atrophy, and hypertrophy of clitoris.
Given the findings of marked hirsutism and facial acne, laboratory tests were performed for the differential diagnosis of hirsutism which revealed total testosterone level of 4.2 ng/mL, free testosterone of >100 pg/mL, and DHEAS level of 574 μg/dL (). Pelvic USG revealed normal endometrial thickness besides normal size of uterus and normal size and appearance of ovaries. Based on these findings, the likelihood of an androgen-secreting adrenal tumor was considered in the initial diagnosis and, therefore, the adrenal MRI was performed. MRI revealed a 27 × 25 mm isointense solid mass lesion in the left adrenal gland in T1A and T2A series (). Afterwards, functional screening for adenoma was performed which revealed normal findings on a 24-hour urine test for metanephrine (73.91 mcg/day) and normetanephrine (133.95 mcg/day) besides normal levels for aldosterone (65 pg/mL) and renin (2.1 ng/mL). Lacking findings related to Cushing syndrome in the physical examination, our patient had basal ACTH levels of <5 pg/mL twice. Dexamethasone (1 mg) suppression test (DST) was 4.7 μg/dL and there was no suppression in cortisol levels also with 2 mg DST (5.4 μg/dL). Urinary cortisol level was normal (75 mcg/day), while the physiological cortisol circadian rhythm was determined to be disturbed.
Based on consideration of overall findings, with the initial diagnosis of testosterone- and cortisol-secreting tumor in the left adrenal gland, the patient underwent laparoscopic left adrenalectomy with perioperative steroid replacement. Pathological examination confirmed the diagnosis of benign adrenocortical oncocytoma. Macroscopically, the tumor was a rounded, encapsulated, and well-circumscribed mass, with an average diameter of 2.2 × 2 cm. The microscopic appearance of oncocytic neoplasm included cells with eosinophilic cytoplasm arranged in solid pattern (). Immunohistochemical studies revealed that the case was positive for CD56, synaptophysin (), and vimentin and negative for chromogranin. Ki-67 proliferation index was found 3% in the tumor. Capsular and venous invasion, high mitotic rate, and atypical mitoses were not observed, so it was considered as benign according to the Lin-Weiss-Bisceglia criteria []. At the postoperative 72nd hour, cortisol level was 15.7 mcg/dL at 08:00 a.m., while ACTH level was 7.66 pg/mL. There was no need for postoperative steroid treatment. Postoperative total testosterone level was determined to regress to 1.05 ng/mL, free testosterone to 2.26 pg/mL, and DHEAS to 345.6 mcg/dL.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1148,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2775877-1,Extracted,"34-yr-old man was admitted to the hospital because of a sudden development of headache, sweating and vomiting. He had a history of hypertension and chronic renal failure due to IgA nephropathy. After 3 yr of peritoneal dialysis (one and a half years before the current admission), hemodialysis was initiated. At the time of the patient's visit to the emergency room, his temperature was 37℃, the pulse was 95 beats per minute, the respiratory rate was 25 breaths per minute and the blood pressure was 162/86 mmHg. Brain computed tomography (CT) revealed intracerebral hemorrhage in the left thalamus and intraventricular hemorrhages in both lateral ventricles, and the third and fourth ventricles. Burr hole operation with external ventricular drainage (EVD) was performed. Laboratory test performed on the admission day showed uremia, creatinemia and hyperkalemia. Intermittent hemodialysis was done and Kalimate (Kunwha Pharmaceutical Co. Ltd., Korea, 10 g, b.i.d.) was administered orally. On the ninth day of admission, the level of potassium was highly elevated (8.0 mEq/L) and an electrocardiogram showed ST-segment depressions and poor R wave progression. For the management of hyperkalemia, two enemas with Kalimate preparation (30 g of Kalimate in 200 mL of 20% DW each) were performed, and oral Kalimate (15 g, t.i.d.) had been given for three days. Two days later, profuse hematochezia developed. A sigmoidoscopy was performed, revealing diffuse active ulceration with mucosal necrosis and hemorrhage from the rectum to beyond the reach of an endoscope (). Multifocal pseudomembrane formations were found. Random biopsies from multiple ulcerative areas were performed.
Histologically, the colonic mucosa showed active colitis with mucosal necrosis or ulceration. There were irregular shaped and sized, angulated crystals with a characteristic crystalline mosaic pattern on the mucosa and ulcer bed tissue and within the necroinflammatory debris (). They were basophilic on H&E stain (), blue on Diff-Quik stain () features of viral infection or acute ischemic colitis, such as withering crypts, stromal hyalinization or fibrin thrombi in the vessels. Also there were no features of chronic colitis, including inflammatory bowel disease, chronic diverticular disease-associated colitis or chronic ischemic colitis. After the discontinuance of Kalimate, conservative treatment was initiated. One week after the initial sigmoidoscopy, a follow-up sigmoidoscopy was performed, showing multiple scattered ulcers with slight improvement. Random biopsies were obtained from the different levels of the rectum, sigmoid and lower descending colon, showing healing ulcerations with the presence of a few remaining crystals (). Clostridium difficile (C. difficile) toxin assays had been performed four times during the period between endoscopic examinations and 2 weeks after the second endoscopy, and all were negative. Hematochezia gradually subsided and disappeared, however the patient died of cardiovascular problems on the forty fifth day of admission.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [162.0, 'mm hg'], 'Diastolic Blood Pressure': [86.0, 'mm hg']}",111.33333,105.76666,116.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 162.0 mm Hg + 2/3 * 86.0 mm Hg = 111.33333 mm Hg.
Hence, the patient's mean arterial pressure is 111.33333 mm Hg."
1149,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8459915-1,Extracted,"A 17-year-old female presented to the emergency room with an alleged history of ingestion of multiple drugs, including 38 tablets of MMF 500 mg and five tablets of phenobarbital 60 mg four hours earlier. She consumed her mother’s medicines with suicidal intention. According to her mother, she was found in an intoxicated and ataxic state with slurring of speech two hours before the presentation at the emergency room. After that, she developed drowsiness and was brought to the hospital. Her past medical and psychiatric history were unremarkable. Upon arrival, she was in a drowsy state. Her heart rate was 115 beats per minute (bpm) and her blood pressure (BP) was 110/70 millimeters of mercury. Her respiratory rate was 18 per minute with symmetrical chest rise and oxygen saturation was 97%. Neurological examination revealed ataxia and slurred speech but she could follow commands. She had grossly intact cranial nerve functions, normal motor strength, and reflexes. Other systemic examination findings were unremarkable. Her body mass index (BMI) was 34.8 kg/m2. Her management in the emergency room consisted of intravenous hydration; continuous monitoring of her condition and vital signs. She was fully alert, her heart rate was 80 bpm, and her BP was 120/70 mmHg within four hours of arrival. After that, she did not complain of any other symptoms.
On admission, her laboratory studies showed a white blood cell (WBC) count of 7,800/mm3, hemoglobin of 12.2 g/dL, and platelet count of 287,000/mm3. Blood chemistry revealed serum creatinine of 1.2 mg/dL, aspartate aminotransferase of 21 IU/L, alanine aminotransferase of 19 IU/L, and glucose of 80 mg/dL. She had normal urinalysis, prothrombin time-international normalized ratio (PT-INR), electrolytes, and arterial blood gases. Chest x-ray and electrocardiogram were unremarkable. Ultrasonography of the abdomen did not reveal any significant abnormalities except fatty liver. From day 2 of hospitalization, she reported occasional mild headaches relieved by acetaminophen. Otherwise, her hospital stay was uneventful. She was monitored and managed conservatively in the Intensive Care Unit (ICU) for two days and later in the general medical ward for the next three days. After a psychiatric evaluation, she was diagnosed with an unspecified mood disorder with suicidal ideation. She was prescribed aripiprazole and advised for a regular follow-up. She was discharged on the fifth day of admission. Her laboratory studies were last done on day 4, which demonstrated a WBC count of 6,500/mm3, hemoglobin of 12.5 g/dL, platelet count of 263,000/mm3, serum creatinine of 0.9 mg/dL, aspartate aminotransferase of 13 IU/L, alanine aminotransferase of 15 IU/L, and glucose of 95 mg/dL. The electrolyte levels, PT-INR, and urinalysis were within normal parameters. Her laboratory studies during the time of admission and before discharge are summarized in Table .",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1150,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6935339-1,Extracted,"A 15-year-old previously healthy female was admitted to our tertiary care pediatric intensive care unit (PICU) from a community emergency room with unresponsiveness. She was found by her parents in an unresponsive and tremulous state on the morning of admission. Emergency rescue was called and upon their arrival, the patient was intubated at the scene for significant respiratory depression. The patient was then transported to a local emergency department, and en route she was given one dose 1 mg lorazepam (0.02 mg/kg) for tremulousness, suspected to be seizure-related, with no response. Upon arrival to the outside emergency room, she was unresponsive, normothermic, tachycardic with a heart rate of 150 bpm and with mild hypertension and the blood pressure of 130/84 mmHg. She had symmetric and reactive pupils on examination. She received an additional 1 mg of lorazepam for ongoing tremulous movements with no response. She had an unremarkable brain computerized tomography scan and cerebrospinal fluid studies. She had normal electrolytes and liver function test. In addition, urine toxicology screen, blood alcohol, acetaminophen, and aspirin level were negative. She received a normal saline bolus, and a dose of ceftriaxone was then transferred to our PICU with a diagnosis of status epilepticus and possible meningitis. Just prior to transport, she was started on propofol infusion at 20 mcg/kg/min. At admission to the PICU, her physical examination was notable for normothermia, normotension, and tremulous motor activity. She had no response to painful stimuli but had a normal pupillary examination. Her propofol infusion was discontinued immediately and on follow-up assessment, she was able to localize to pain. Her repeat electrolytes, blood gas, chest X-ray, and electroencephalogram were normal, and electrocardiogram revealed sinus tachycardia with normal PR or QTc intervals. Over the next 10 hours, her neurological status remained unchanged. She was continued on invasive mechanical ventilation and intravenous fluids. Despite her negative toxicology screen, and her family’s denial of any history drug use in the past or significant potential sources of mood-altering drugs in the house, we considered a trial of ILE therapy secondary to the possibility of a drug overdose. She was started on intravenous 20% lipid emulsion at a dose of 1 mL/kg over one hour. By the end of lipid infusion, the patient had such a dramatic improvement in her sensorium, she was extubated, and became quite verbal admitting that she ingested about forty 350 mg of each tablet of carisoprodol (14 gm), which was used by her father for chronic lower back pain.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [84.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",99.33333,94.36666,104.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 84.0 mm Hg = 99.33333 mm Hg.
Hence, the patient's mean arterial pressure is 99.33333 mm Hg."
1151,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6893042-2,Extracted,"A 58-year-old man came to the emergency department in our hospital because of the sudden onset of severe back pain. He was alert, his blood pressure was 93/70 mmHg and his heart rate was 102 bpm. Transthoracic echocardiography revealed pericardial effusion. Pericardiocentesis was performed, and it showed bloody fluid. Contrast-enhanced computed tomography showed a distal aortic arch aneurysm and pericardial effusion (), so the diagnosis was intrapericardial rupture of an aortic arch aneurysm, and emergent surgery was performed. At the operation, the heart was covered with coagulation, and we found the foramen lacerum at the aneurysm that penetrated the precardium (). We performed total arch replacement using the same method as described in the first case. The CPB time, aortic clamp time and total circulatory arrest times were 177, 83 and 56 minutes, respectively. The patient recovered well and discharged from the hospital without complication. He was alive and had no complications at 26 months, the time of his last appointment.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [93.0, 'mm hg']}",77.66667,73.78334,81.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 93.0 mm Hg + 2/3 * 70.0 mm Hg = 77.66667 mm Hg.
Hence, the patient's mean arterial pressure is 77.66667 mm Hg."
1152,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4481,Extracted,"A 15-year-old boy presents to the emergency room with severe lower abdominal pain that awoke him from sleep about 3 hours ago. The pain is sharp and radiates to his left thigh. While in the emergency room, the patient experiences one episode of vomiting. His temperature is 99.3°F (37.4°C), blood pressure is 126/81 mmHg, pulse is 119/min, respirations are 14/min, and oxygen saturation is 99% on room air. Abdominal examination reveals no tenderness in all 4 quadrants. Scrotal examination reveals an elevated left testicle that is diffusely tender. Stroking of the patient's inner thigh on the left side does not result in elevation of the testicle.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [126.0, 'mm hg'], 'Diastolic Blood Pressure': [81.0, 'mm hg']}",96,91.2,100.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 126.0 mm Hg + 2/3 * 81.0 mm Hg = 96.0 mm Hg.
Hence, the patient's mean arterial pressure is 96.0 mm Hg."
1153,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3784139-1,Extracted,"A 33-year-old primigravida was transferred to the Kyung Hee University Medical Center for preterm labor and pre-eclampsia at 36+4 weeks gestation. She had a twin pregnancy after in vitro fertilization-embryo transfer. Her blood pressure measured 140/100 mm Hg. Her urine protein was 4+ and 24-hour urinary protein excretion was 2,333 mg/day. She did not have headache, visual disturbances, or pitting edema. She had regular uterine contractions and a cervix dilated about 2 cm. An emergency cesarean section was performed uneventfully, and healthy twin babies were born.
On the second postoperative day, the patient had abdominal distension, steady epigastric and whole abdominal pain. An abdominal X-ray examination showed paralytic ileus. Laboratory examination showed white blood cell (WBC) count of 11,890, low Ca+ of 6.4 mg/dL, elevated blood urea nitrogen (BUN) of 64 mg/dL, serum creatinine of 1.5 mg/dL, aspartate transaminase (AST) of 52 IU/L, alanine aminotransferase (ALT) of 21 IU/L, elevated C-reactive protein (CRP) of 20.74 mg/dL, triglyceride 1,080 mg/dL and otherwise non-specific. At that time, she started complaining of blurry vision. Because pre-eclampsia-related visual disturbances are common, we did not perform a formal ophthalmic examination. We decided on conservative management including nasogastric drainage, parenteral nutrition, non per os, pain control, and avoidance of toxic renal medications.
On the fifth postoperative day, the patient had flank pain, diarrhea, tachycardia (pulse 112 per minutes) and fever (38℃). Laboratory examination showed WBC count of 14,900, low Ca+ of 5.6 mg/dL, AST of 61 IU/L, ALT of 33 IU/L, elevated CRP of 8.56 mg/dL, and normalized BUN and serum creatinine. Bacterial cultures were taken from blood and urine, and antibiotics were started. Her visual loss was equivocal.
The patient still had epigastric pain, a fever (38.3℃) and visual loss in both eyes until eight days after operation. At this point, we therefore decided to do an abdominal computed tomography (CT) scan and an ophthalmology consultation. The abdominal CT scan showed enlargement of pancreas with fat infiltration, fluid collection in the pancreatic area and no other abnormal findings. Serum amylase and lipase levels were elevated at 149 U/L (normal range, 25 to 125 U/L), and 128 U/L (normal range, 5.5 to 58 U/L) respectively, on the day of CT scan. The patient was diagnosed as having acute pancreatitis based on her steady epigastric pain and abdominal CT scan. She recovered fully upon resolution of pancreatic necrosis with conservative management and drainage of the underlying fluid collection.
On the same day, the patient underwent an ophthalmologic examination, and her visual acuity test was 0.02 (right) and finger count 30 cm (left). There were multiple discrete retinal changes, and macular yellow patches, known as Purtscher flecken, in both eyes. A retinal splinter hemorrhage was seen in the right eye upon retinal photography (). A fluorescein angiogram showed arteriolar occlusion, and retinal ischemia, typical signs of Purtscher-like retinopathy. She was diagnosed with Purtscher-like retinopathy based on her symptoms and the results of the ophthalmologic examinations. Because there are no definite guidelines for the treatment of this condition, her visual acuity was closely monitored with conservative management. We also performed a brain magnetic resonance imaging (MRI) to rule out cortical blindness. The brain MRI showed unremarkable findings (). Two months after onset of visual loss, her visual acuity test was 0.08 (right) and 0.01 (left) and the multiple yellowish patches had decreased in both eyes on retinal photographs. At a recent follow-up (two years after the onset of her visual symptoms), her corrected visual acuity was 0.2 (right) and 0.1 (left). There was gradual improvement in the visual functions of both eyes, but she still had visual impairment.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",113.33333,107.66666,119,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 100.0 mm Hg = 113.33333 mm Hg.
Hence, the patient's mean arterial pressure is 113.33333 mm Hg."
1154,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4958,Extracted,"A 37-year-old African American man is brought to the emergency department by police. The patient refused to leave a petting zoo after closing. He states that he has unique ideas to revolutionize the petting zoo experience. The patient has a past medical history of multiple suicide attempts. His temperature is 99.5°F (37.5°C), blood pressure is 130/85 mmHg, pulse is 100/min, respirations are 16/min, and oxygen saturation is 99% on room air. The patient's cardiac and pulmonary exams are within normal limits. He denies any nausea, vomiting, shortness of breath, or systemic symptoms. The patient struggles to answer questions, as he is constantly changing the subject and speaking at a very rapid rate. The patient is kept in the emergency department overnight and is observed to not sleep and is very talkative with the nurses.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [85.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 85.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1155,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8543969-1,Extracted,"A 67-year-old male was admitted for exertional dyspnea and fatigue. He was diagnosed with MM one year earlier. He had received chemotherapy with bortezomib, cyclophosphamide, and dexamethasone, achieving nearly complete remission without maintenance therapy. Two months earlier, he was diagnosed with sick sinus syndrome due to syncope and was implanted with a permanent pacemaker. After this admission, the patient had a body temperature of 36 °C, blood pressure of 119/72 mmHg, pulse rate of 74 beats per min, and respiratory rate of 20 beats per min. Physical examination revealed mild edema on his face and lower extremity. Slightly distended jugular veins were observed. The electrocardiogram revealed atrial fibrillation. Transthoracic echocardiography (TTE) showed a significant and irregularly shaped mass filling the right atrium (RA) (Fig. a) and obstructing the right ventricular inflow tract. The mass also extended into the superior vena cava (SVC) and inferior vena cava (IVC), resulting in almost complete occlusion of the SVC and partial obstruction of the IVC (Fig. b and c). A computed tomography (CT) scan also demonstrated a large mass in the RA extending to the SVC and IVC (Fig. d–f). The large mass surrounded the pacemaker lead (Fig. d). Bilateral pleural effusions were also observed. Angiography was negative for pulmonary embolism. The laboratory test showed a white blood cell count of 4.5 × 109/L, hemoglobin level of 127 g/L, platelet count of 119 × 109/L, creatinine level of 108 μmol/L, and alanine aminotransferase level of 57.7 U/L.
Because the patient was in a stable course of MM and the pacemaker led through his SVC and RA, we initially considered the mass to be a right atrial thrombus. The patient underwent right atrial mass resection under cardiopulmonary bypass. Intraoperative findings revealed multiple lobulated masses occupying most of the RA (Fig. a), extending to the SVC and IVC. The mass also infiltrated the free wall of the RA, especially “freezing” the anterolateral wall of the RA. Intraoperative rapid pathological examination of the mass indicated a malignant tumor. The large mass in the RA could not be completely removed due to infiltration of the atrial wall. Therefore, a partial tumor and the anterolateral wall of the RA were resected to relieve the obstruction of the SVC, IVC, and right ventricular inflow tract. Then, the incision of the RA was reconstructed with a pericardial patch. The patient recovered uneventfully after the surgery. One month later, he received one cycle of chemotherapy with bortezomib, cyclophosphamide, and dexamethasone.
Postoperative pathological examination of the right atrial mass suggested malignant plasmacytoma associated with MM. Immunocytochemical staining of the tumor sections indicated atypical immature plasma cells positive for CD138, CD38, CyclinD1, and λ, and negative for CD20, CD79a, and CD10 (Fig. b).
After follow-up for seven months, our patient was still alive with a considerably good health condition after surgery. His echocardiography showed no intracardiac relapse of MM.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [119.0, 'mm hg'], 'Diastolic Blood Pressure': [72.0, 'mm hg']}",87.66667,83.28334,92.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 119.0 mm Hg + 2/3 * 72.0 mm Hg = 87.66667 mm Hg.
Hence, the patient's mean arterial pressure is 87.66667 mm Hg."
1156,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4593889-1,Extracted,"A 68-year-old man with a history of HCV and alcohol-related cirrhosis (Child-Pugh stage C) was admitted for confused mental state, increased abdominal volume, edema of the lower limbs, and deterioration of general conditions lasting for several days. The patient had been hospitalized the previous month for ascites and decompensated cirrhosis, and had undergone paracentesis. Up to two weeks prior to the last hospitalization he was on ciprofloxacin 500 mg BID. Allergy to tetracycline was documented.
Upon admission the patient was in poor clinical conditions: blood pressure 100/50 mmHg, heart rate 100 beats per minute, respiratory rate 20 breaths per minute, with stupor, flapping tremor, significant bilateral ankle edema with positive fovea sign, and jaundice. There was abdominal distension, pain on deep palpation on the lower and lateral quadrants, and negative Blumberg’s sign. Blood gas analysis revealed respiratory and metabolic alkalosis; laboratory analysis showed total leukocytes of 11.7×109/L with neutrophilia, and thrombocytopenia (platelet count of 39×109/L); creatinine was 1.8 mg/dL (estimated creatinine clearance of 48 mL/min), hyperbilirubinemia (total 5.2 mg/dL, direct 2.9 mg/dL), increased INR (1.7), and hyperammonemia. The patient was treated with diuretics and ceftriaxone (2 g IV OD), and admitted to the internal medicine department.
After admission the patient’s conditions worsened with deterioration of encephalopathy, fever of 38°C, and an increase in creatinine (2.5 mg/dL) and C-reactive protein (120 mg/L; normal value <5 g/L). Blood and urine cultures were initiated. Explorative paracentesis detected the presence of polymorphonuclear neutrophils (910/mm3). Ceftriaxone therapy was replaced with meropenem (1 g IV BID; dose adjusted for creatinine clearance). Despite antibiotic therapy, fever persisted with hypotension and signs of sepsis. On day 4 after admission microbiological results of ascites fluid showed MRSA. The complete antibiogram of the isolate is shown in . After infectious disease consultation, daptomycin 6 mg/kg/day was initiated, considering the high MIC of vancomycin and the concomitant presence of renal insufficiency and thrombocytopenia. The informed consent was obtained from the patient.
After initiation of anti-MRSA therapy there was progressive clinical improvement with defervescence, reduction of ammonemia, improvement of encephalopathy, and a decrease in abdominal volume and peripheral edema. The patient was treated with daptomycin for 12 days with progressive normalization of C-reactive protein; an increase of CPK and/or impairment of renal function were not recorded during the treatment. The patient was then discharged and referred to an ambulatory clinic.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [50.0, 'mm hg'], 'Systolic Blood Pressure': [100.0, 'mm hg']}",66.66667,63.33334,70,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 50.0 mm Hg = 66.66667 mm Hg.
Hence, the patient's mean arterial pressure is 66.66667 mm Hg."
1157,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-11609,Extracted,"A 44-year-old obese woman presents with abdominal pain. She says the pain started while she was having lunch at a fast-food restaurant with her children. The pain began shortly after eating and has persisted for 6 hours. She has vomited once. Her vital signs are as follows: HR 88, BP 110/70 mmHg, T 38.5°C (101.3°F). On physical exam, she is tender to palpation in the right upper quadrant of her abdomen. Her skin appears normal. Her liver function tests, amylase, and lipase levels are normal. A right upper quadrant abdominal ultrasound is challenged by her body habitus and is not able to visualize any gallstones.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1158,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6661044-2,Extracted,"A 73-year-old woman (height 155 cm, weight 49 kg) had right renal arterial embolism, chronic kidney disease, and pleurisy in her past history.
Preoperatively, her upper arm blood pressure exhibited no laterality (HR 76/min, BP right 120/80 mmHg, BP left 123/75 mmHg).
Preoperative enhanced computed tomography (CT) imaging revealed a thoracic aortic aneurysm with a maximum diameter of 52 × 50 mm, but the left AAO was not obvious because the left innominate vein’s enhancement concealed LSAO findings.
We planned zone 2 thoracic endovascular aneurysm repair (TEVAR) for thoracic aortic aneurysm and embolization of the left subclavian artery via the left brachial artery, but we failed to pass through the left subclavian artery because of AAO, and therefore, we simply covered the orifice of the left subclavian artery using a stent graft without embolization. No endoleak was observed postoperatively.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1159,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-358,Extracted,"A 61-year-old woman with a history of stage IV pancreatic cancer comes to the emergency department with insomnia due to intractable midepigastric pain. The pain had been constant for months but has worsened over the past few weeks despite the fact that she is already taking hydrocodone 10 mg and ibuprofen 400 mg. She has a past medical history of chronic pain and major depressive disorder. In the past month, she has been taking her pain medications with increasing frequency, going from twice a day to four times a day. Her other medications include venlafaxine and eszopiclone. She describes her mood as low, but states she does not have any suicidal thoughts. She appears fatigued and slightly cachectic. Her temperature is 36°C (96.8°F), pulse is 100/min, and blood pressure is 128/65 mm Hg. Physical examination shows a mass in the midepigastric region.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [128.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",86,81.7,90.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 128.0 mm Hg + 2/3 * 65.0 mm Hg = 86.0 mm Hg.
Hence, the patient's mean arterial pressure is 86.0 mm Hg."
1160,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9892,Extracted,"A 55-year-old woman seeks evaluation of difficult and incomplete voiding and spontaneous urine leakage that occurs continuously during the day and night. The symptoms are not associated with physical exertion. She denies any urethral or vaginal discharge. She is menopausal and does not take hormone replacement therapy. At 33 years of age, she had a right salpingectomy as treatment for an ectopic pregnancy. She has a 2-year history of a major depressive disorder and takes amitriptyline (100 mg before the bedtime). She was also diagnosed 5 years ago with arterial hypertension, which is controlled with enalapril (20 mg daily) and metoprolol (50 mg daily). The weight is 71 kg (156.5 lb) and the height is 155 cm (5 ft). The vital signs are as follows: blood pressure 135/80 mm Hg, heart rate 67/min, respiratory rate 13/min, and temperature 36.4℃ (97.5℉). The physical examination is significant for a palpable urinary bladder. The neurologic examination is within normal limits. The gynecologic examination shows grade 1 uterine prolapse.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [135.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",98.33333,93.41666,103.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 80.0 mm Hg = 98.33333 mm Hg.
Hence, the patient's mean arterial pressure is 98.33333 mm Hg."
1161,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-10318,Extracted,"A 19-year-old college student is brought to the emergency department by her roommate. Her roommate reports that the patient was complaining of a headache this morning. A few hours later, the patient seemed lethargic and confused. In the emergency department, the patient's vital signs are as follows: HR 98, BP 110/70, T 38.7 degrees Celsius. Her neurological exam is notable for flexion at the hips when her neck is passively flexed. A lumbar puncture is performed, and Gram stain results are shown in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1162,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8559,Extracted,"A 30-year-old woman who is 24-weeks pregnant presents to the emergency department with fever, painful urination, and headache. The patient's blood pressure is 111/67 mm Hg, the pulse is 95/min, the respiratory rate is 16/min, and the temperature is 38.3°C (101.1°F). Physical examination reveals bilateral tender inguinal lymphadenopathy and painful genital lesions. On closer inspection, the patient’s genital lesions contain clear fluid and measure 5–6 mm in diameter.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [67.0, 'mm hg'], 'Systolic Blood Pressure': [111.0, 'mm hg']}",81.66667,77.58334,85.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 111.0 mm Hg + 2/3 * 67.0 mm Hg = 81.66667 mm Hg.
Hence, the patient's mean arterial pressure is 81.66667 mm Hg."
1163,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3612464-1,Extracted,"A previously healthy 29-year-old man with no family history of cardiovascular disease was admitted to the emergency room due to palpitations, dizziness, and near-syncope during weightlifting. Three days prior to admission, an episode of less severe but similar symptoms was reported. The patient appeared clinically stable on physical examination, and vital signs were reported as a blood pressure of 135/75 mmHg, pulse 121 beats per minute, oxygen saturation 94%, respiratory rate 20 per minute, and central body temperature of 37.4°C.
The initial electrocardiogram (ECG) showed sinus tachycardia with a rate of 147 beats per minute and an episode of non-sustained, monomorphic VT. Consequently, the patient was transferred to the department of cardiology for ECG-monitoring and further evaluation. An ECG () confirmed the presence of sinus tachycardia and non-sustained VT, and an echocardiogram showed a structurally normal heart with a normal left ventricular ejection fraction. Initial blood tests, including electrolytes and high-sensitivity cardiac troponin T (hs-cTnT), were within the reference range. Due to multiple paroxysms of non-sustained monomorphic VT (), the patient was given a 300 mg bolus of amiodarone intravenously over 20 minutes, which rapidly led to stabilization of the heart rhythm. The VT resolved completely within three hours.
The patient did not take any prescription drugs. However, he was taking one capsule of weight loss pills daily, initiated one week prior to admission. He had purchased the product, which contains ephedrine, caffeine, and aspirin, on the internet. Since no other risk factors for VT were present, these capsules were the most likely cause of arrhythmia.
The patient was monitored for another 24 hours without recurring episodes of VT. The corrected QT-interval (QTc) was normal during the entire admission, and hs-cTnT values remained within the reference range during serial measurements. The patient was discharged without further evaluation or follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [135.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",95,90.25,99.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 75.0 mm Hg = 95.0 mm Hg.
Hence, the patient's mean arterial pressure is 95.0 mm Hg."
1164,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4532120-1,Extracted,"A 31-year-old Korean male patient was transferred to our hospital from a local hospital because of persistent melena of undetermined origin. Four months ago, the patient visited the hospital with complaints of chest tightness and productive cough. An X-ray film of the chest at that time showed a patch infiltration in the right lower lung field. Studies of the sputum for acid fast bacilli were negative but anti-tuberculosis medications were started under the impression of pulmonary tuberculosis. Three months later, he was admitted to the same hospital because of melena and underwent extensive work-ups including gastroscopic examination, barium studies of the colon and small bowels, and a gastric mucosa scan for Meckel’s diverticulum, but no bleeding focus was found. During the stay in that hospital, the melena improved spontaneously and he was discharged. He did fairly well until 10 days prior to this admission when recurrent melena developed. Additional studies including 99mTC-sulfur colloid scintigraphy were carried out, but no bleeding focus was found.
On admission, the patient appeared pale and acutely ill. The blood pressure was 130/70 mm/Hg, pulse rate 120/min, respiratory rate 20/min, and the temperature 36.5°C. The heart sound was normal without murmur. Breathing sound was decreased at the right lower lung field. No lymphadenopathy was found in the neck or axilla. No palpable abdominal mass was felt. Rectal examination revealed internal hemorrhoid and hematochezia.
The hemoglobin was 4.6 g/dl and the hematocrit was 14%. The white blood cell count was 6300/mm3 and the platelet 203,000/mm3. The urea nitrogen was 22.4 mg/dl, the creatinine 1.5 mg/dl, the protein 2.5 g/dl (the albumin 1.3 g/dl and the globulin 1.2 g/dl), the bilirubin 0.4 mg/dl, the alkaline phosphatase 53 IU, the aspartate aminotransferase (AST) 10 IU, and the alanine aminotransferase (ALT) 10 IU. The serum sodium was 127 mEq/L and the potassium 4.1 mEq/L. Chest X-ray film revealed an ill defined dense infiltrate with air bronchogram in the right lower lung field (). Mesenteric arteriography was performed but could not find any bleeding focus. Because of severe hematochezia, the flexible sigmoidoscopy was not available. The hemorrhoid with massive bleeding was found by anoscopy. An emergency hemorrhoidectomy was carried out on the second hospital day. However, a large amount of hematochezia persisted even after the operation and signs of serious disseminated intravascular coagulopathy (DIC) follwed. On the 10th hospital day while the DIC improved, the patient complained of abdominal distension and pain. Ascites was suspected.
An abdominal paracentesis revealed intraabdominal bleeding. An emergency exploratory laparotomy was perfomed. On operation, multiple polypoid masses of various sizes were palpated intraluminally in the jejunum from 10 cm below the Treitz ligament to the 120 cm distally. A large perforation of the jejunum (8 cm in diameter) probably caused by necrosis of the bowel wall was found on the antemesenteric border of the jejunum 20–25 cm below the Treitz ligament. Multiple mass lesions including hematomes were also found in the mesenteric root of the small intestine. Small bowel resection and end-to-end anastomosis were performed. On section, 36 polypoid masses were scattered grossly along the full length of the resected jejunum. The largest mass was 5.0×8.0×4.0 cm in size and composed of brownish homogeneous materials. Similar materials were filled in the mesenteric arteries and veins ().
Mlicroscopically, numerous hemosiderin pigments were scattered throughout the fields. The cells in the polypoid mass lesion were consistent with large round cells of undetermined origin. Each cell had a round nucleus containing prominent nucleoli. The cytoplasm was homogenous and clear (). The immunohistochemical study for S-100 protein was negative. Electron microscopically, obvious desmosomes were identified as convincing evidence of carcinoma (). Bronchoscopic examination, which was done on the 10th postoperative day, revealed an obstructing round mass at the entrance of the right main bronchus (). Histologically, this lesion was diagnosed as large cell carcinoma of the lung ().
On the 27th postoperative day, massive amounts of hematemesis and hematochezia developed again. The patient died on the 31st postoperative day due to hypovolemic shock.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 70.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1165,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3082123-1,Extracted,"The subject was a 24-yr-old female nurse who worked in the intensive care unit at a University Hospital. She had handled piperacillin/tazobactam without gloves or a mask since March 2003. Eighteen months later (October 2004), she experienced generalized urticaria with onset immediately and repeatedly after she had administered piperacillin. Nevertheless, she continued to work and finally experienced chest tightness, dizziness, sweating, generalized urticaria, abdominal pain, and diarrhea 10 min after giving a piperacillin injection in April 2005. Her blood pressure was 80/50 mmHg with a pulse rate of 104 beats/min. Her breath sounds were clear. The symptoms resolved completely after treatment with epinephrine, diphenhydramine, and methylprednisolone. She had a previous history of atopic dermatitis, and her hand eczema had become exacerbated after she had begun to work at the hospital.
Skin prick tests using 80 common inhalant and food allergens (Bencard, Brentford, UK) were all negative. We did not perform a skin prick test with piperacillin/tazobactam because of the risk of anaphylaxis (). Serum total IgE, measured using an immuno-CAP® system (Phadia, Uppsala, Sweden), was 283 IU/mL.
To assay piperacillin-specific serum IgE and IgG, we prepared piperacillin-human serum albumin (HSA) conjugates in our laboratory and performed an ELISA as described previously (). Piperacillin-specific IgE and IgG levels in an initial serum sample and the IgE level in a serum sample obtained 5 yr later (May 2010) were measured. In brief, the wells of a 96-well ELISA microplate (Corning, New York, NY, USA) were coated by incubation with piperacillin-HSA conjugate at 10 µg/mL in phosphate-buffered saline (PBS) overnight at 4℃. After the wells were washed four times with 350 µL of PBS containing 0.05% Tween 20 (PBS-T; Sigma-Aldrich, St. Louis, MO, USA), nonspecific binding sites were blocked by incubation with 200 µL of 10% fetal bovine serum (FBS; GIBCO/Invitrogen, Carlsbad, CA, USA) in PBS at room temperature for 2 hr. After washing four times with 0.05% PBS-T, 50 µL of diluted serum (1:3) were added to each well, followed by incubation for 2 hr at 37℃. The plate was washed four times with 0.05% PBS-T, then 100 µL of goat anti-human IgE antibody (Kirkegaard & Perry Laboratories, Inc., Gaithersburg, MD, USA) diluted 1:1,000 with 10% FBS-PBS were added to each well, and the plate was incubated for 1 hr at room temperature. After washing four times with 0.05% PBS-T, 100 µL of alkaline phosphate-conjugated rabbit anti-goat IgG antibody (ReserveAPTM; Kirkegaard & Perry Laboratories) diluted 1:500 with 10% FBS-PBS were added to each well, and the plate was incubated for 1 hr at room temperature. PNPP (p-nitro-phenyl phosphate; Sigma-Aldrich) substrate was added, and the reaction was stopped by the addition of 1 N NaOH. The optical density of the solution in each well was measured at 405 nm using a microplate reader (Synergy HT; Bio-Tek, Winooski, VT, USA). The final absorbance value of piperacillin was determined by subtracting the absorbance value of a control crosslinker-HSA conjugate, which was obtained using a procedure identical to that described above, except that a crosslinker-HSA conjugate was used in place of piperacillin-HSA conjugate. The positive cutoff value was determined as the mean plus three standard deviations of the absorbance values in serum samples from 11 unexposed, non-atopic healthy controls. For the inhibition ELISA, increasing amounts (1-100 µg/mL) of free piperacillin, piperacillin-HSA conjugate, and HSA alone, dissolved in 10% FBS-PBS, were incubated with serum overnight, and an ELISA was performed as described above. The percentage inhibition was calculated as follows: % inhibition = (1 - absorbance with inhibitor/absorbance without inhibitor) × 100. For the ELISA of piperacillin-specific serum IgG levels, alkaline phosphate-conjugated rabbit anti-human IgG antibody (Kirkegaard & Perry Laboratories) was used instead of goat anti-human IgE antibody and alkaline phosphate-conjugated rabbit anti-goat IgG antibody. A high level of specific IgE antibody to piperacillin-HSA conjugate was detected in the initial serum sample from the subject; however, this had decreased markedly after 5 yr (). Significant inhibition by both free piperacillin and piperacillin-HSA conjugate occurred in a dose-dependent manner, with minimal inhibition by HSA alone (). High levels of piperacillin-HSA conjugate-specific IgG were also detected in the initial serum sample (data not shown).
Based on these findings, the subject was diagnosed with occupational anaphylaxis and urticaria caused by piperacillin. The subject was transferred to a different department and has not again experienced anaphylaxis or urticaria.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [80.0, 'mm hg'], 'Diastolic Blood Pressure': [50.0, 'mm hg']}",60,57,63,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 80.0 mm Hg + 2/3 * 50.0 mm Hg = 60.0 mm Hg.
Hence, the patient's mean arterial pressure is 60.0 mm Hg."
1166,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4624913-1,Extracted,"A 15-year-old female student with no relevant medical history was admitted to the emergency department with dizziness, nausea, and progressive weakness over the last 24 hours. She denied smoking, alcohol consumption, or diuretic use but recognized practicing aerobic exercise every day. Her familial medical history was unremarkable. She had not had dyspnoea, fever, vomiting, or diarrhea in the last days. Physical examination showed a blood pressure of 135/80 mmHg and heart rate of 75 beats per minute. Chest auscultation revealed regular heart sounds with no murmurs, and abdominal exam did not reveal tenderness, hepatomegaly, or masses. In the electrocardiogram sinus rhythm was described, with prolonged QT interval of 600 milliseconds ().
The initial laboratory data showed severe hypokalemia of 1.8 mmol/L and metabolic alkalosis with pH 7.6, pCO2 48 mmHg, and HCO3 47 mmol/L. Serum creatinine, sodium, calcium, phosphate, magnesium, and uric acid were within the normal range. Mild elevation of creatine kinase of 321 U/L was observed. A urine sample analysis showed urinary sodium of 50 mmol/L and potassium of 65 mmol/L, with a transtubular potassium gradient of 16.
Over the next six days, the patient received high doses of intravenous and oral potassium chloride, with slow progressive correction, and further studies were performed in order to exclude other potential causes. Low plasma renin concentration [<0.3 ng/mL/h (normal values 0.3–7 ng/mL/h)], low plasma aldosterone [3.4 ng/dL (normal 5–40 ng/dL)], normal cortisol concentration [10.5 mcg/dL (normal 3–20 mcg/dL)], and normal adrenocorticotropic hormone levels [15 pg/mL (normal 5–45 pg/mL)] were found on specific hormonal analysis. Abdominal computed-tomography findings were unremarkable. Although a primary hereditary tubular disorder was the first clinical suspicion, after detailed anamnesis the patient confessed regular consumption of licorice roots over the last two weeks. The clinical course was favourable and the patient was discharged ten days after, with complete correction of these biochemical abnormalities, correction of electrocardiographic changes, and a clear advice of not taking licorice again.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [135.0, 'mm hg']}",98.33333,93.41666,103.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 80.0 mm Hg = 98.33333 mm Hg.
Hence, the patient's mean arterial pressure is 98.33333 mm Hg."
1167,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6737861-1,Extracted,"A 58-year-old female with no previously known medical history was brought in by her daughter due to unsteady gait for the past 6 weeks and unable to ambulate without assistance. For the past week, the patient’s mental status was declining with increased forgetfulness and disorganized speech. The patient had no history of falls or head trauma, headache, dizziness, fever, cough, night sweats, animal bite, or recent exposure to ill contacts. She has no history of tobacco, alcohol consumption, or use of illicit drugs. She was born and raised in Ghana and moved to the United States many years ago. Her last visit to Ghana was 2 years prior to hospitalization. Her vaccination history was unknown.
On presentation her temperature was 99.0° Fahrenheit (F), heart rate of 70 beats per minute (bpm), respiratory rate of 20 breaths per minute, blood pressure (BP) of 123/66 mmHg, and 97% oxygen saturation breathing ambient air. Her physical exam showed a well-groomed woman who was in no acute distress. There were no cranial nerve abnormalities. Her oropharynx was clear, moist, without oral thrush, and her neck was supple, without thyromegaly or lymphadenopathy. There was no nuchal rigidity. Her cardiovascular and pulmonary exams were normal. She had normal sensation, muscle tone, strength, and symmetric reflexes. She had a negative Romberg test. Brudzinski and Kernig signs were absent. She was noted to have positive dysdiadochokinesia and an ataxic shuffling gait. She was oriented to her name and that she was in a hospital but did not know the hospital name. She knew the year and month but not the day of the month. She could not understand why she was there and her affect was flat with dull mood. Mini-Mental State Examination (MMSE) score was 23/30.
Computed tomography (CT) scan of the head without contrast ruled out acute hemorrhage and showed an age-indeterminate left cerebellar lacunar infarct. She was treated for a possible cerebrovascular accident and placed on telemetry. However, the findings did not account for the acuity of change in mental status. Carotid Doppler ultrasound and echocardiogram were normal. Thyroid-stimulating hormone (TSH), vitamin B12, and folate levels were within normal limits and rapid plasma reagin (RPR) test was nonreactive. Urinalysis and urine drug screen were negative and blood work did not show any electrolyte abnormalities, renal dysfunction, or anemia. She had a reactive HIV-1 antibody test. This was determined to be a false positive after further testing confirmed by undetectable HIV RNA viral load and a CD4T-Cell count of 1449 cells/µL. Cryptococcal antigen was negative.
Due to the rapid decline in her mental function in the last 2 months, a lumbar puncture was performed to rule out infectious causes. Empiric intravenous acyclovir was begun to treat possible herpes simplex meningoencephalitis pending results. Cerebrospinal fluid (CSF) testing was performed for gram stain, culture, cell count, protein and differential, India ink stain, glucose, protein, herpes simplex virus (HSV) polymerase chain reaction (PCR), Venereal Disease Research Laboratory (VDRL), fluorescent treponemal antibody absorption (FTA-Abs), anti-N-methyl-d-aspartate (NMDA) receptor antibodies, and 14-3-3 proteins. The CSF was clear and colorless, and a total of 3 cells/µL were present, with 1 WBC cell/µL, 1 RBC cell/µL, and a differential of 100% lymphocytes. Cerebrospinal fluid protein was 40.7 mg/dL and glucose 71 mg/dL. Gram stain, culture, VDRL, and HSV PCR were negative. All serology, paraneoplastic, and vasculitis biomarkers returned negative and acyclovir was discontinued.
Fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI) sequence showed high intensity involvement of the caudate nucleus and putamen. Diffusion-weighted imaging (DWI) of MRI showed apparent increased signals of the bilateral supratentorial cortical ribbon and caudate nucleus (). An electroencephalogram demonstrated diffuse slow wave activity. She was given supportive treatment for dementia. She was later discharged home on her daughter’s request with home services and physical therapy. The 14-3-3 proteins CSF test result was pending.
Two weeks later, she was brought to the hospital and readmitted due to further worsening of her mental status. She had fallen 3 times in the last 3 days without any head trauma. Although her vitals and chemistry panel were unchanged, she was more somnolent and had periodic myoclonic jerks of her extremities at irregular intervals. She developed severe bruxism and spasticity. She was not oriented to self, place, or time. Repeat CT and MRI imaging of the brain did not show any new changes. A repeat electroencephalography (EEG) was consistent with severe diffuse cerebral disease with 3 to 4 Hz triphasic waves seen throughout ().
The 14-3-3 proteins study of the CSF sent out in her first admission returned positive. The National Prion Disease Pathology Surveillance Center reported a positive result of the Real-time Quaking-induced Conversion (RT-QuIC) assay and elevated T-tau protein levels. The diagnosis of sporadic form Creutzfeldt-Jakob disease (sCJD) was made and the Centers for Disease Control and Prevention (CDC) was notified. No brain biopsy was required for clinical management. The results and prognosis were discussed with her daughter and the patient was given supportive management and discharged to a long-term care facility.
The patient was readmitted 36 weeks later after diagnosis due to a percutaneous endoscopic gastrostomy (PEG) tube malfunction that required replacement. The infection had rendered her nonverbal and unable to consume adequate oral intake due to progressive spasticity and myoclonus. Although she was awake, there was deterioration in her mental status. Vital signs showed temperature of 98.7°F, heart rate of 73 bpm, respiratory rate of 18 breaths per minute, BP of 131/71 mmHg, and 99% oxygen saturation on room air. Her serum chemistry panel, complete blood count (CBC), and other routine labs were unremarkable. Due to her severe bruxism, a PEG tube placement could not safely be performed, even with deep sedation and general anesthesia. Discharge to hospice care was deemed appropriate and comfort measures were recommended to her family. Unfortunately, the patient was lost to follow-up. Results of an autopsy and postmortem testing, if performed, could not be obtained.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [123.0, 'mmhg'], 'Diastolic Blood Pressure': [66.0, 'mmhg']}",85,80.75,89.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 123.0 mm Hg + 2/3 * 66.0 mm Hg = 85.0 mm Hg.
Hence, the patient's mean arterial pressure is 85.0 mm Hg."
1168,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8116089-1,Extracted,"We present a case of female Bosnian patient 50 years old who lives in Belgium for 20 years ago and during her visit to Bosnia she came to our polyclinic for cardiological exam. In the last 4 years ago, she complained of cardiac arrhythmia, palpitations, anaemia and iron deficiency and high blood pressure. During physical exam she was acyanotic, BP 150/100 mmHg, HR 83/min, Spo2 96%, respiratory rate 15 breaths/min. and BMI 30. The cardiovascular examinations revealed regular heartbeat with rumbling middiastolic murmur at the lower left sternal border. ECG showed sinus rhythm, RBBB with rSR1 in V1 lead. Transthoracic echocardiographic showed enlargement of left atrium (LAD 51mm), right atrium and ventricle (RAD 46mm, RVd 33mm), atrial septal defect with left right shunt and mild mitral regurgitation, mild pulmonary hypertension and Qp:Qs 2,3:1. Blood lab analysis showed anaemia with low Hb 91 g/L, low HcT 28%, low Iron 8 μmol/L and high lipids. Next day the 2D and 3D Transesophageal (TEE) exam confirmed the existence of secundum atrial septal defect 9mm diameter size with left right shunt and mild mitral regurgitation, no signs of pulmonary hypertension. Several months later transcatheter device closure with Amplatzer occluder was performed and subsequent symptomatic improvement reported after closure (Panels A, B, C, D).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [100.0, 'mm hg'], 'Systolic Blood Pressure': [150.0, 'mm hg']}",116.66667,110.83334,122.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 100.0 mm Hg = 116.66667 mm Hg.
Hence, the patient's mean arterial pressure is 116.66667 mm Hg."
1169,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5932,Extracted,"A 62-year-old man presents to the emergency department with confusion. The patient’s wife states that her husband has become more somnolent over the past several days and now is very confused. The patient has no complaints himself, but is answering questions inappropriately. The patient has a past medical history of diabetes and hypertension. His temperature is 98.3°F (36.8°C), blood pressure is 127/85 mmHg, pulse is 138/min, respirations are 14/min, and oxygen saturation is 99% on room air. Physical exam is notable for a confused man with dry mucous membranes.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [85.0, 'mm hg'], 'Systolic Blood Pressure': [127.0, 'mm hg']}",99,94.05,103.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 127.0 mm Hg + 2/3 * 85.0 mm Hg = 99.0 mm Hg.
Hence, the patient's mean arterial pressure is 99.0 mm Hg."
1170,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7422689-1,Extracted,"A 56-year-old woman with a history of DM, gastroesophageal reflux disease (GERD), and alcohol abuse presented to the emergency room with a 2-day history of abdominal pain and intractable nausea and vomiting for 24 hours. The abdominal pain was sharp epigastric, 10/10 in severity, and non-radiating, precipitated with ingestion of oral intake, without alleviating factors. Prior to presentation, she had more than 30 episodes of vomiting, which was initially clear, but progressed to coffee ground emesis. She had no melena or hematochezia. Her social history was consistent with alcohol abuse (8–10 beers per day), without history of smoking, or substance or domestic abuse. On examination, she was tachycardic (120 per minute) and hypotensive (80/50 mm Hg), had oropharyngeal erythema with white spots on its posterior wall, and significant ptyalism. She had epigastric tenderness and unremarkable digital rectal examination. Laboratory work-up revealed lactic acidosis (>15 mmol/L), acute kidney injury with creatinine 2.21 mg/dL, leukocytosis (18 ×109/L), transaminitis with aspartate aminotransferase 175 U/L, alanine aminotransferase 121 U/L, alkaline phosphate 84 U/L, and a total bilirubin of 1.2 mg/dL. A CT of the abdomen and pelvis without contrast was unremarkable except for paraesophageal hernia. The hospital course was complicated by hematemesis, dysphagia and melena. She was resuscitated with intravenous fluids and initially started on proton pump inhibitor (PPI), antiemetics, antibiotics and analgesics. After initial resuscitation, esophagogastroduodenoscopy (EGD) was performed which showed inflammation of the epiglottis, arytenoid cartilages, and dark mucosal pigmentation of the distal two-thirds of the esophagus with associated hiatus hernia ( and ). A biopsy of the esophageal mucosa demonstrated fragments of fibrinopurulent exudate, and necrotic tissue with predominant neutrophil infiltration indicating severe inflammation (). A periodic acid Schiff stain was negative for fungal organisms. There was no evidence of Helicobacter pylori, cytomegalovirus (CMV), herpes simplex virus (HSV), Candida albicans infections and malignancy on further testing of biopsy specimen. She was managed with strict restrictions of oral intake, total parenteral nutrition, PPI, pain control with analgesic, and serial EGDs at 2 weeks () and 3 weeks () to assess for inflammation and improvement in necrosis. Complete resolution of esophageal necrosis was noted at 8-week EGD follow-up (). She was transitioned to oral diet, which she tolerated well.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [80.0, 'mm hg'], 'Diastolic Blood Pressure': [50.0, 'mm hg']}",60,57,63,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 80.0 mm Hg + 2/3 * 50.0 mm Hg = 60.0 mm Hg.
Hence, the patient's mean arterial pressure is 60.0 mm Hg."
1171,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8127745-1,Extracted,"A 69-year-old male with a history of Stage III immunoglobulin G Lambda multiple myeloma. He had been treated with bortezomib, lenalidomide, and dexamethasone. He had completed 5 cycles of cyclophosphamide, bortezomib, and dexamethasone. Due to the coronavirus disease-2019 pandemic and to prevent exposure to hospital for chemotherapy infusions, he was transitioned to an oral chemotherapy regimen. He was initiated on ixazomib 3 mg, dexamethasone 36 mg, and lenalidomide 25 mg. He was started on a regimen of ixazomib 3 mg to be taken on days 1, 8, and 15; dexamethasone 36 mg on days 1, 8, 15, and 22; and lenalidomide 25 mg on days 1 to 22. The patient, instead of taking ixazomib weekly, took the ixazomib daily for 3 days.
He was admitted with nausea, fatigue, and profuse watery diarrhea. He also had developed a diffuse macular rash in his lower extremities extending to the part of his lower abdomen, which was non-pruritic. Initial blood pressure on arrival was 79/51 mm Hg. He was afebrile, and his pulse was 84 beats per minute. Laboratory studies throughout the hospital course are listed in . He was initiated on a fluid bolus with 2 L and was started on maintenance fluids. His blood pressure improved initially; however, due to worsening of blood pressure, he required transfer to the medical intensive care unit. He was initiated on norepinephrine infusions to maintain mean arterial blood pressure above 65 mm Hg. He was empirically initiated on vancomycin, cefazolin, and metronidazole. A diarrhea panel obtained for several common gastrointestinal pathogens () was negative. A computed tomography image of the abdomen was obtained, which showed scattered regions of mild mural thickening and the presence of mild inflammation in the small bowel loops suggesting possible enteritis. One out of the 2 blood cultures collected at the time of admission returned positive for methicillin-resistant Staphylococcus aureus (MRSA) from the port site. His antibiotics were ultimately changed to daptomycin. He underwent transthoracic and transesophageal echocardiography, which did not show any evidence of vegetation and he completed a course of 2 weeks of intravenous daptomycin for MRSA along with the removal of the port.
Hemodynamic and laboratory parameters improved over the first week of admission; however, the patient continued to have ongoing diarrhea. He initiated on loperamide and diphenoxylate without improvement. General surgery was consulted and determined no surgical intervention was deemed necessary. He was then started on octreotide with improvement in diarrhea. He was ultimately discharged in stable condition to a subacute rehabilitation center. His chemotherapy was not initiated on discharge. His chemotherapy was then initiated 2 months post-discharge and was changed to carfilzomib and dexamethasone and he currently is in stable condition.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [51.0, 'mm hg'], 'Systolic Blood Pressure': [79.0, 'mm hg']}",60.33333,57.31666,63.35,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 79.0 mm Hg + 2/3 * 51.0 mm Hg = 60.33333 mm Hg.
Hence, the patient's mean arterial pressure is 60.33333 mm Hg."
1172,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-622,Extracted,"A 65-year-old woman is brought to the emergency department by her husband after he found her with nausea, headache, and agitation 1 hour ago. When he left their lakeside cabin 6 hours before to go ice fishing and get more firewood, she did not have any symptoms. She has chronic migraines, hypertension, and type 2 diabetes mellitus. Her medications include lisinopril and metformin, but she ran out of her anti-hypertensive medications over the weekend. Her temperature is 37.1°C (98.8°F), pulse is 110/min, respirations are 21/min, and blood pressure is 154/92 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 98%. She is confused and oriented only to person and place. She recalls only one of three objects after 5 minutes. Her gait is unsteady. Physical examination shows no abnormalities.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [154.0, 'mm hg'], 'Diastolic Blood Pressure': [92.0, 'mm hg']}",112.66667,107.03334,118.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 154.0 mm Hg + 2/3 * 92.0 mm Hg = 112.66667 mm Hg.
Hence, the patient's mean arterial pressure is 112.66667 mm Hg."
1173,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6942747-1,Extracted,"A 56-year-old female presented to the Emergency Department after a fall. The patient reported that she had been having a fever for the last 2 days and there was associated dizziness which led to the fall. There was no loss of consciousness or head injury secondary to the fall. She also reported a non-productive cough, several episodes of non-bilious, non-bloody vomiting, and two episodes of diarrhea.
The patient's past medical history was that of chronic ischemic heart disease; type two diabetes mellitus, hyperlipidemia and hypertension. She did not have any known drug allergies. She denied drinking alcohol, smoking or use of any illicit drugs. Her travel history including traveling to India three months ago. On physical examination she looked diaphoretic, lethargic and in pain, with a blood pressure of 125/95 mmHg, pulse rate of 127 beats per minute, respiratory rate of 20 per minute, oxygen saturation of 97% on room air and a temperature of 39.7°C. An abdominal examination revealed that she was tender in the right lower quadrant and right upper quadrant with no rebound tenderness or guarding, and Murphy's sign was negative. Examination of the other systems did not reveal any abnormalities.
Based on the clinical history and examination the working diagnosis of pneumonia and possible acute appendicitis or diverticulitis was made. She was given intravenous normal saline fluid, intravenous antibiotics and analgesia. The electrocardiogram showed sinus tachycardia with nonspecific T wave inversion. The chest X-ray showed clear lungs fields and the heart size was normal. A renal panel, liver panel, full blood count, C-reactive protein, prolactin, and urine analysis were ordered. The patient had transaminitis, markedly raised inflammatory markers, and thrombocytopenia. The patient's lab results are shown in .
Patient was sent for a computed tomography (CT) of the abdomen and pelvis with intravenous contrast to rule out appendicitis or diverticulitis. shows the CT findings for this patient. The results showed a linear radio dense foreign body within the hepatic segment, most likely a fishbone with the site of perforation possibly being the distal stomach. Surrounding the foreign body there is a well-defined hypodense region suggestive of a phlegmonous area of inflammation measuring 9.4 × 7.0 cm. No subcapsular hematoma, intra-abdominal free fluid or pneumoperitoneum was present.
The patient was then admitted to the general ward and was treated conservatively with intravenous antibiotics for 15 days. She was initially started on Ceftriaxone and Metronidazole and subsequently switched to Piperacillin/Tazobactam on Day 4 of illness. On day 10 of admission, the patient went for a repeat CT of the abdomen and pelvis and it was found that the abscess had significantly increased in size and a percutaneous catheter was inserted at this time. On day 18 the abscess was still the same size and the patient continued to spike fevers so the patient underwent open liver abscess drainage which showed a heterogeneous abscess in segment 4 extending to segment 8, but no liquid abscess was seen and no foreign body could be found. On day 27 a repeat CT of the abdomen and pelvis was done, because the patient was still spiking fevers, showing pockets of residual collection in right lobe of the liver with a foreign body still present and then a new percutaneous drain was placed. On day 29 the drain was removed because the drain output had dropped. An ultrasound was performed of the liver on day 34 and there was an ill-defined heterogenous hypoechoic area noted in the liver extending from segment 4 to 8. There was no new focal hepatic lesion. The repeat ultrasound on day 44 was done and the abscess cavity was now smaller and there was still a remnant foreign body.
The patient was successfully discharged asymptomatic on day 55. The patient remained well on follow up. She had repeat ultrasounds done at 1 month and 3 months post discharge which showed a heterogeneously hypoechoic area which had decreased in size but still had the fishbone present.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [95.0, 'mm hg']}",105,99.75,110.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 95.0 mm Hg = 105.0 mm Hg.
Hence, the patient's mean arterial pressure is 105.0 mm Hg."
1174,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7557910-1,Extracted,"A 34-years-old Caucasian female presented with left upper arm weakness associated with paresthesia. The symptoms had started about 24 hours before, on waking.
Physical examination revealed left hemiparesis, with diminished left upper (2/5) and lower (3/5) strength, and extensor plantar response on the left side. There were no cerebellar signs, and the cranial nerve examination was normal. The electrocardiogram showed normal sinus rhythm at 70 beats per minute, and blood pressure values were 160/90 mmHg. No other remarkable signs were present.
Cranial multimodal computed tomography (CT) imaging was performed, showing no sign of cerebral hemorrhage and hypodensity on cortical and subcortical right frontoparietal regions, compatible with ischemic stroke. Thrombolysis was not performed because of the remote onset of the symptoms. Cranial Magnetic Resonance Imaging (MRI) showed an area of ischemia in the acute/subacute phase, without hemorrhagic infarction, with occlusion of the M2 segment of the middle cerebral artery. She was given a loading dose of acetylsalicylic acid and transferred to our division.
Collecting a complete medical history, the patient revealed to be a habitual consumer of substances like heroine, methadone, cocaine, and alcohol; moreover, in the night before the episode, she had smoked crack cocaine. A toxicological screen resulted positive for cocaine and opioids. ECG and cardiac ultrasound were normal.
Carotid ultrasound (CU) showed a huge homogeneous soft plaque with an irregular surface, protrusive morphology, and circumferential blood flow at the distal end, inside the internal carotid artery ().
Enoxaparin at the dosage of 100 U/kg twice/day was started, followed by warfarin therapy. Seriated CUs showed gradual dissolution of the thrombus (). Her symptoms gradually improved during the next weeks, and she was discharged from the hospital in good general conditions. However, the patient continued drug abusing, and a new cerebral stroke occurred the year after.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [160.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",113.33333,107.66666,119,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 90.0 mm Hg = 113.33333 mm Hg.
Hence, the patient's mean arterial pressure is 113.33333 mm Hg."
1175,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4532066-1,Extracted,"A 33 year old man was admitted to the hospital with fever and decreased urine output. Thirty six days prior to admission, renal transplantation was performed in this hospital. He was placed on intravenous solumedrol pulse followed by maintenance oral prednisone and intravenous cyclosporin for 2 weeks. He complained of mild epigastric discomfort and nausea. His blood pressure was 140/90 mmHg, body temperature 37.5 °C, pulse 88, and respirations 22. On physical examination the lungs were clear with a normal regular heart beats with out murmur. There was no organo-megaly, but mild tenderness and swelling of the operation site was noted.
Laboratory analysis revealed hemoglobin 9.9 gm/dl, hematocrit 29.4%, white blood cell 10,500/mm3 with normal differential and platelets 207,000/mm3. Blood chemistry showed FBS 125mg/dl, BUN 79.9mg/dl, Cr 7.1mg/dl, Na 129mM/L, K6.2mM/L, Ca 8.1 mg/dl, P 2.7mg/dl, Cl 92mM/L, total protein 5.0gm/dl, albumin 3.0gm/dl, total bilirubin 0.2gm/dl, AST 10 IU/L, ALT 22IU/L, alkaline phosphatase 77IU/L, total cholesterol 188mg/dl, and prothrombin time 11 sec. Urinalysis revealed protein+4 with many red blood cells under microscopy.
An endoscopic examination was performed on the 11th hospital day. There were multiple dark red, grouped and discrete vesicles of 3 to 5mm in diameter along the entire esophagus (,). The stomach showed several flat erosions confined to the antrum, but the duodenum was normal. All vesicular lesions were easily removed from the esophagus with biopsy forceps. Light microscopy showed characteristic intranuclear inclusions and multi-nucleated giant cells (). The patient was placed on acyclovir from the 14th hospital day. Follow up endoscopy 11 days later revealed a complete absence of vesicles and the presence of faint scars in the esophagus. Renal impairment was also improved. For the confirmation of herpes esophagitis, in situ hybridization of herpes viral DNA was performed, resulting in a positive test for type 1 herpes simplex ().",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1176,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2803826-1,Extracted,"A 59-year-old Caucasian man was admitted with lethargy and progressive weight loss for 6 to 8 months prior to presentation. He had no history of loss of appetite, diarrhoea, excessive sweating, heat intolerance or visual disturbances. His medical history included ankylosing spondylosis with previous prosthetic aortic valve replacement for aortic regurgitation 20 years before presentation. Physical examination revealed an emaciated and lethargic man with a body mass index of 16. He was slightly pale, jaundiced and febrile with a diffused non-tender multinodular goiter with tremor on upper extremities. His pulse rate was 40/minute with a blood pressure of 110/70 mmHg. Examination of his cardiovascular system revealed prosthetic S2 without any evidence of aortic regurgitation. There were no signs of heart failure or infective endocarditis. His lungs were clear and his abdomen revealed two-finger breath tender hepatomegaly with smooth edges without any ascites or splenomegaly. Investigations revealed the following: haemoglobin 9.8 gm/dl, mean cell volume 88.6 fl, white cells 5.2 × 109/L, platelets 80 × 109/L, potassium 5.6 mmol/L, urea 18 mmol/L, creatinine 250 μmol/L, blood glucose 8.9 mmol/L, C-reative protein 66 mg/L, magnesium 0.94 mmol/L, bilirubin 54 μmol/L, alkaline phosphatase 187 μ/L, alanine aminotransferase 80 μ/L, gamma glutamyl transferase 184 μ/L, total protein 82 gm/L, albumin 34 gm/L and adjusted calcium 2.77 mmol/L. On top three sets of blood cultures were negative of bacterial aerobic and anaerobic growths. His chest X-ray showed cardiomegaly but no pulmonary oedema. However his 12-lead electrocardiogram showed complete heart block with underlying atrial fibrillation (Figure ). Interestingly his thyroid function confirmed a toxic state with thyroid stimulating hormone of < 0.03 mU/L, tri-iodothyronine (T3) at 24.1 pmol/L, and free thyroxine (T4) at > 100 pmol/L. Of note, the autoimmune thyroid antibodies were negative for both thyrotropin receptors and microsomes. A transthoracic echocardiogram revealed stable aortic valve prosthesis without any regurgitation. His left ventricle was notably dilated but did have a preserved good systolic function and no other valvular abnormalities were seen. However the ultrasonogram (USG) of his abdomen revealed a smoothly enlarged liver without any evidence of focal lesions or biliary obstruction. Similarly USG his neck confirmed enlarged thyroid gland with multiple nodules.
The patient was briefly managed with temporary pacing during the period of the hemodynamic instability. He was treated with 40 mg of carbimazole once daily for 3 weeks, subsequently achieving both clinical and biochemical euthyroid state with improvement in his renal functions. Similarly his heart rhythm was stabilised restoring sinus rhythm with PR interval of 180 msec with normal QRS complexes (Figure ). His subsequent prolonged cardiac monitoring showed sinus rhythm without any evidence of bradycardia or heart blocks. Subsequently, the patient underwent an uncomplicated subtotal thyroidectomy.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1177,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3303746-1,Extracted,"A 78-year-old retired male mechanical engineer from Arkansas presented with 3-month history of low-grade fever, rigors, and confusion, associated with poor appetite, 15-pound unintentional weight loss, abdominal discomfort, and increased frequency of urination. He denied having nausea, vomiting, or changes in bowel habits. The patient had no significant past medical history, and had no history of sick contacts, recent travel, ingestion of raw food or milk, or known exposures to animals. Urinalysis showed microscopic hematuria, but no pyuria. Although urine culture was negative, he was treated for presumed urinary tract infection with a 7-day course of oral ciprofloxacin without significant improvement, followed by a 14-day course of doxycycline for presumed prostatitis. He was afebrile while taking doxycycline, but fever recurred 3 days after completion of the antibiotic. He was noted by his wife to be confused and found to have blood pressure (90/60 mmHg) on the day of admission.
On admission, he had a temperature of 37.3°C, a heart rate of 130 beats/minute, and a blood pressure of 118/72 mmHg. A complete physical examination, including neurological evaluation, was within normal limit. Laboratory results were notable for neutrophilic leukocytosis (white blood cell count of 28.0 × 109/L, absolute neutrophil count of 26 × 109/L), anemia (hemoglobin of 111 g/L), elevated C-reactive protein (31.1 mg/L), and mild hyponatremia (128 mmol/L). His liver and kidney functions were normal, and chest X-ray was unremarkable. Computed tomography (CT) of the head showed mild cerebral degenerative changes. Abdominal CT was significant for three large thick-walled low-density lesions in the right hepatic lobe, with the largest measuring 75 × 55 × 58 mm and multiple smaller low-attenuation lesions within the liver, likely representing multiple hepatic abscesses (). Ultrasound-guided aspiration yielded 25 mL of purulent fluid with subsequent placement of two drainage catheters. Gram stain of the purulent fluid showed many white blood cells but no organisms. Fungal and acid-fast smear were negative as well. Intravenous meropenem and vancomycin were empirically begun while awaiting culture results.
Although the patient responded promptly to antimicrobial therapy with resolving confusion, fever, and leukocytosis, his cultures, including blood cultures remained negative. The negative cultures were possibly attributed to the demeclocycline, a tetracycline with some antibacterial properties [], that the patient received for the treatment of hyponatremia. The patient underwent transesophageal echocardiography to evaluate for endocarditis given concern for septic hepatic emboli from occult source, and it was negative for signs of endocarditis. Due to good clinical response, the patient was discharged on hospital day 7 on ertapenem administered via a peripherally inserted central catheter line, despite negative cultures. Following discharge, the liver aspirate was later reported to be growing a gram-positive bacillus in the anaerobic plate (CDC blood sheep agar) after 6 days of incubation. Identification via PCR-amplified 16S rRNA sequencing technique revealed Eggerthella lenta (Eggerthella lenta strain SECO-Mt75m2 16S ribosome RNA gene sequence: GGATGAACGCTGGCGGCGTGCCTAACACATGCAAGTCGAACGATGAAACCGCCCTCGGGCGGACATGAAGTGGCGAACGGGTGAGTAACACGTGACCAACCTGCCCCCCTCTCCGGGACAACCTTGGGAAACCGAGGCTAATACCGGATACTCCCTCCCCTGCTCCTGCAGGGGTCGGGAAAGCCCAGGCGGAGGGGGATGGGGTCGCGGCCCATTAGGTAGTAGGCGGGGTAACGGCCCACCTAGCCCGCGATGGGTAGCCGGGTTGAGAGACCGACCGGCCACATTGGGACTGAGATACGGCCCAGACTCCTACGGGAGGCAGCAGTGGGGAATTTTGCGCAATGGGGGCAACCCTGACGCAGCAACGCCGCGTGCGGGACGACGGCCTTCGGGTTGTAAACCGCTTTCAGCAGGGAAGAAATTCGACGGTACCTGCAGAAGAAGCTCCGGCTAACTACGT, GenBank # AY937380.1, National Center for Biotechnology Information, U.S. National Library of Medicine). Antimicrobial susceptibility testing was not performed because of inadequate growth. At followup, the patient was doing well clinically with radiographic resolution of the hepatic abscesses after a 6-week course of ertapenem (). Colonoscopy after resolution of infection showed extensive diverticulosis distal to the hepatic flexure.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [118.0, 'mm hg'], 'Diastolic Blood Pressure': [72.0, 'mm hg']}",87.33333,82.96666,91.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 118.0 mm Hg + 2/3 * 72.0 mm Hg = 87.33333 mm Hg.
Hence, the patient's mean arterial pressure is 87.33333 mm Hg."
1178,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7066031-1,Extracted,"We report the case of a mesenteric vessel thrombosis in a 30 year old female, G5 P3, eight days after caesarean section. She also had history of two spontaneous abortions between P2 and P3. She had undergone uneventful caesarean section in view of fetal distress with meconium stained liquor, delivered a healthy female baby and was discharged on fifth post-operative day. Patient developed fever with rigors & chills and respiratory distress on sixth post-operative day. Also had repeated episodes of vomiting which were non-bilious, non-projectile in nature. Patient had normal bowel and bladder habits till 8th post-operative day.
Eight days after her caesarean section, she presented to emergency department with respiratory distress. On examination, she was afebrile and her abdomen was soft. On auscultation there was decreased air entry in bilateral lungs. Her blood pressure on arrival was 156/110 mm of Hg and pulse 102/min. Patient was nebulized and put on antibiotics, oral Labetalol 20 mg, injection Amlodipine10 mg stat, injection MgSO4 loading followed by maintenance. Vital charting was done; patient had persistent tachycardia during next 4 days. All baseline investigations were sent. Subsequently, on Day 5 of admission patient developed abdominal distension with absence of bowel sounds and also complained of numbness in left arm. On examination of pulses: right sided radial artery volume was good but low volume was noticed in left sided radial, brachial, bilateral dorsalis paedis and posterior tibial artery. Right arm B.P – 128/70 mm of Hg, Left arm B.P – 80/60 mm of Hg. Abdomen was diffusely tender. Probable diagnosis of sepsis with intestinal obstruction was made.
Investigations: ()# Hb 10.0 g/dL, platelets 2.8 lakh/mm3, total leucocyte count 18,500/mm3 with neutrophilia, serum creatinine 1.3 mg/dL, serum uric acid 7.7 mg/dL, electrocardiogram normal, chest X-ray- prominent vascular markings, abdominal X-Ray - dilated bowel loops (). USG whole abdomen showed prominent bowel loops and sluggish peristalsis. Color Doppler – No significant vascular abnormality, no obvious thrombosis/stenosis noted. CT – Angiography revealed complete occlusion of superior mesenteric artery (a and b), and saddle shaped thrombus in right and left pulmonary artery extending into bilateral upper and lower lobe segmental branches suggestive of pulmonary thromboembolism (c). CECT abdomen showed dilation of jejunal and ileal loops, likely small bowel ischemia.
Emergency exploratory laparotomy was performed with resection of gangrenous bowel with end to end anastomosis. Unfortunately, patient did not recover from shock and died on post-operative day 1 after laparotomy.
Gangrenous segment of bowel was received in pathology department. Specimen was 60 cm in length and included jejunum and ileum. Grossly there was marked blackening and thinning out of areas in bowel wall (a and b). Microscopic sections examined showed features of mesenteric vessel thrombosis leading to infarction of segment of gut. Changes were typical of ischaemic damage comprising of necrosis and sloughing of mucosa, marked edema and haemorrhage in interstitium. Cut ends were viable. Sections examined from mesenteric vessels traced from the specimen show a fresh thrombus of 24 hour duration in mesenteric vein occluding upto 80 % of lumen (). This case is reported in line with the SCARE criteria [].",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [156.0, 'mm hg'], 'Diastolic Blood Pressure': [110.0, 'mm hg']}",125.33333,119.06666,131.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 156.0 mm Hg + 2/3 * 110.0 mm Hg = 125.33333 mm Hg.
Hence, the patient's mean arterial pressure is 125.33333 mm Hg."
1179,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3079140-1,Extracted,"A 70-year-old man presented to our hospital with a two-week history of fever associated with lower back pain. He had a past history of recurrent infective endocarditis, for which he was admitted to our hospital in 2005 and in 2009. Streptococcus bovis was isolated during the first visit in 2005 as the causative organism of infective endocarditis. In addition, vegetation was found on the posterior leaflet of the mitral valve. During the second admission, blood culture showed the growth of a Streptococcus species. However, specific culture results were not reported. Similar to the first admission, vegetation growth was again found on the posterior leaflet of the mitral valve. On both admissions, the patient successfully recovered following the appropriate antibiotic treatment with reduction of vegetation.
On admission, the patient's core body temperature was 39.0℃, blood pressure 130/80 mmHg, and pulse rate was 88 beats/minute. Auscultation revealed a regular heart beat with an early systolic murmur was found at the left lower sternal border (grade III/VI). Neurological examination was unremarkable. No peripheral stigmata of infective endocarditis were noted.
Laboratory tests showed absence of leukocytosis (white blood cell 7,400/mm3), but mild anemia (hemoglobin 8.5 mg/dL), and thrombocytopenia (platelets 120,000/mm3) was noted. Except for a C-reactive protein (CRP) value of 4.17 mg/dL (0.1-0.8 mg/dL), no other laboratory tests showed significant abnormalities (blood urea nitrogen 15 mg/dL, creatinine 0.8 mg/dL, total protein 6.9 g/dL, albumin 3.4 g/dL, aspartate aminotransferase 27 IU/L, alanine aminotransferase 14 IU/L).
Chest radiography showed no pulmonary edema or active lesions in the lungs. In transthoracic echocardiography, a 2.7×1.4 cm sized vegetation on the posterior leaflet of the mitral valve () was noted. Furthermore, moderately severe mitral regurgitation, trivial aortic regurgitation, and moderate tricuspid regurgitation was also noted. Other findings included left ventricular (LV) hypertrophy (LV mass 270.5 gm), LV enlargement (LV end diastolic dimension 61 mm, LV end systolic dimension 41 mm), left atrial (LA) enlargement (LA dimension size 40.1 mm), and mild pulmonary hypertension (pulmonary arterial pressure 37 mmHg).
After diagnosis of infective endocarditis was confirmed, treatment was immediately started with intravenous ceftriaxone and gentamycin, on suspicion of recurrent infective endocarditis.
On the second day of antibiotic therapy, fever and other signs of infection resolved. We continued antibiotic treatment for four weeks. However, blood culture demonstrated no growth of bacteria and fungi. Although his clinical signs and symptoms related to infective endocarditis improved, and CRP level decreased, his back pain did not completely resolve. Consequently, we decided to order a plain lumbar spine radiograph to evaluate the lower back pain, which showed disc space narrowing and endplate erosion of the L3 and L4 vertebral bodies (). Magnetic resonance imaging of the lumbar spine was performed to further evaluate the erosive lesions, which confirmed acute spondylodiskitis of L3, L4 vertebrae and L3-4 disc space (). Pyogenic spondylodiskitis was highly suspicious to be associated with infective endocarditis according to the clinical course and patient's history. The patient was discharged after four weeks of intravenous antibiotic treatment without complication. We decided to conduct follow-up evaluation of the patient's spinal lesions at the orthopedic outpatient clinic.
During follow-up at the outpatient clinic, the size of mitral valve vegetation was shown to be reduced on echocardiography (1.35×0.67 cm). There were no symptoms of infective endocarditis or pyogenic spondylodiskitis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1180,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4544255-1,Extracted,"A 19-year-old man complained of recurrent fever and lower back pain for a month. He had
a history of scalded mouth syndrome with no regular antibiotic or antifungal drug
treatment six months prior to hospitalization. He had neither history of taking
immunosuppressors, nor of any disease indicative of immunodeficiency. He had, however,
received the Bacillus Calmette-Guérin (BCG) vaccine during childhood. On admission, his
vital signs included an oral temperature of 39 ºC, heart rate of 92 beats per minute,
respiratory rate of 20 breaths per minute and blood pressure of 130/80 mmHg. Physical
examination revealed a 9×8cm mass in the right of the patient's neck, but no lesions
were found on the oral mucosa. The remainder of the systemic examination was
unremarkable.
Laboratory results included a leukocyte count of 14800×103/mm3,
serum glucose level of 143 mg/dL, blood urea nitrogen of 40 mg/dL and creatinine level
of 1.7 mg/dL. Inflammatory markers were elevated with an erythrocyte sedimentation rate
(ESR) of 120 mm/h and C-reactive protein (CRP) level of 11.1 mg/L. Both a tuberculin
skin test and human immunodeficiency virus (HIV) antibody exam were negative.
Comprehensive immunological studies, including serum immunoglobulins and complement
levels, tests for cell-mediated immunity (NK, CD3, CD4, CD8, CD4/CD8 and CD19) and
autoantibody tests, were normal. 1, 3-β-D-glucan assay levels and the galactomannan test
were normal. Blood cultures were also negative. Whole-body positron emission
tomography/computed tomography (PET/CT) revealed multiple abscesses in the right of the
patient's neck, liver and right psoas major area respectively (); and there was a raised uptake of [18F] FDG in
vertebral bodies of T11, T12 and L1. Consequently, percutaneous abscess drainage was
conducted on the upper body using B-mode ultrasonography and drained brown fluids (30
mL, 280 mL and 130 mL, respectively, ) were
sent to the microbiology lab. Also, drainage tubes were inserted into abscesses in the
liver and psoas major, but were removed after no drainage took place. Results of the
Chromagar Candida Medium (Chromagar, France) cultures were positive for Candida
albicans (), but no acid-fast
bacilli were detected. The germ tube test was positive and the documented diagnosis
using API 20C Aux systems (BioMeriux, France) was Candida albicans,
which was sensitive to amphotericin B, fluconazole, itraconazole, voriconazole,
caspofungin and 5-fluorocytosine. Based on antifungal guidelines and susceptibility
tests, he was treated with intravenous 35 mg amphotericin B daily (0.5 mg/kg per day).
The patient responded to antifungal therapy and his fever abated after ten days of
treatment. Abscess detection using B-mode ultrasonography revealed that the extent of
infection in the upper body had greatly decreased at the end of three-week antifungal
therapy.
However, there was no improvement in the patient's lower back pain. Spinal magnetic
resonance imaging (MRI) showed altered signal intensity in T11, T12, L1 and unique
osteolytic lesions in upper vertebral bodies (). Subsequently, computed tomography (CT) guided percutaneous vertebral
biopsy specimens from the T12 vertebrae revealed caseous material and the acid fast
bacilli were identified (, ). Also, the aspirate culture showed growth of the
M. tuberculosis. Chest CT, urine and sputum examinations were
normal. Taking histological and microbiological findings into consideration, the patient
was treated with antitubercular therapy (rifampicin, isoniazid, pyrazinamide,
ethambutol) for 12 months. In addition, he was treated with a total dose of 1500 mg of
amphotericin B, while oral fluconazole and 5-flucytosine were subsequently prescribed
for six months. By his 2-year follow up, there were complete resolutions of the lesions
in the upper vertebral bodies and no evidence of new abscesses.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1181,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5899341-1,Extracted,"A fourty-year-old man with DEB diagnosed at the age of eight was admitted to the department of gastroenterology because of the dysphagia for two previous months. The diagnosis of DEB was established due to the presence of single blisters on the whole body since the sixth month of life. His sister was also diagnosed with DEB and had similar symptoms of the disease. To our knowledge, the presented patient and his sister are the oldest diagnosed with EB living in Poland. At the age of four the patient started experiencing heartburn occasionally. Five years later dysphagia appeared for the first time. It was an episodal and periodical ailment. He reported a deterioration of dysphagia at the age of nineteen; he mostly consumed liquids and soft consistency meals during that time. Nonetheless, the patient admitted that this esophageal discomfort still was not a constant one and there were time intervals without this ailment. In the past there were also episodes of mild esophageal bleeding. The only one endoscopic esophageal dilatation in this patient took place in 1997; a stenosis was located then approximately 18 cm from incisors. The performed procedure ameliorated swallowing difficulty. A barium swallow test obtained one year after the endoscopic dilatation of the esophagus also revealed esophageal constriction on the same level. In 2014 the patient was diagnosed because of hematochezia and pain in hypogastrium. Tissue samples obtained in colonoscopy revealed the presence of nonspecific inflammatory infiltration in the ascending colon and terminal part of the ileum. Interestingly, 3 years ago he complained of hemoptysis and there was a suspicion of bleeding to pulmonary alveoli in the course of DEB. However, a CT scan did not confirm bleeding. On admission to our department the patient was complaining of painful swallowing of solids. Two months earlier he was diagnosed in the cardiology unit because of the chest pain and elevated level of troponin I. An electrocardiogram did not show any abnormalities. The patient refused to undergo coronarography and no more cardiological diagnostic procedures were performed Additional file . On admission to our unit he did not complain of the chest pain. On physical examination he appeared comfortable, afebrile with pulse 90 beats per minute, blood pressure 125/90 mmHg, respiratory rate 19 per minute and the body mass index (BMI) was 24.7 kg/m2. The patient presented blisters, skin reddening and crust formation on the upper and lower limbs. There were also contractures and disabled movement in his hand joints together with a loss of a finger and toenails (Fig. ). The apex of the tongue and left palatine arch were covered by superficial ulcerations. During his hospital stay, performed laboratory tests did not reveal any abnormalities. A CT scan of the chest and abdomen showed a thickening of the esophageal wall at maximum to 7 mm on the level from the fourth cervical vertebra to the fourth thoracic vertebra (Fig. ). A probe of gastroscopy under sedation with benzodiazepine failed due to an esophageal stenosis. An attempt of examination with paediatric endoscope was also unsuccessful. A barium swallow test revealed a narrowing of upper esophageal lumen to 7 mm along the length of 4 cm together with two diverticula on the right side not emptying of contrast. During swallowing other two diverticula appeared which were emptying of contrast (Fig. ). A barium swallow test also showed a noticeable weakening of the esophageal mucous membrane. After the performed investigation the patient was qualified to endoscopic dilatation of esophageal stenosis and endoscopic management of diverticula. However, he did not agree to undergo this procedure during current hospital stay. In our unit the patient was treated with proton pump inhibitor (PPI) and prokinetic drugs administered intravenously, which caused an amelioration of esophageal discomfort. He was discharged in a good general condition with a recommendation of a diet based on soft consistency meals, oral PPI and prokinetic drugs administration and the next follow-up in a month.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",101.66667,96.58334,106.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 90.0 mm Hg = 101.66667 mm Hg.
Hence, the patient's mean arterial pressure is 101.66667 mm Hg."
1182,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6136232-1,Extracted,"A 66 year old Caucasian woman, was admitted to hospital with malaise, macroscopic haematuria and a petechial rash on both thighs. Her past medical history included seronegative rheumatoid arthritis and hypertension. Her kidney function at that point was normal, with a creatinine of 73 μmol/l (eGFR > 60 mls/min/1.73m2, MDRD formula), and there was no proteinuria. Investigations revealed negative ANA, ANCA, anti-GBM antibodies as well as hepatitis B and C serology. A kidney biopsy showed mild focal tubular and interstitial scarring, suggestive of modest chronic ischaemic damage, but no significant glomerular lesion and negative immunoperoxidase staining on formalin fixed tissue for all immunoproteins. Rapid resolution of the rash was seen following a course of high-dose prednisolone.
Four months following the discontinuation of prednisolone and after a flu like illness, the rash recurred, along with macroscopic haematuria, malaise and anorexia. On admission, she had a blood pressure of 162/90 and a purpuric rash over both thighs. Creatinine had risen to 241 μmol/L (eGFR 18 mls/min/1.73m2). Haemoglobin 10.9 g/dL, CRP 138 mg/L. Urine protein: creatinine ratio (PCR) was elevated at 150 mg/mmol; Tests revealed negative ANCA, ANA and rheumatoid factor, normal levels of immunoglobulins and complement. No anti-GBM antibody was obtained at this time. A repeat kidney biopsy demonstrated a severe, acute crescentic pauci-immune glomerulonephritis, with evidence of moderate chronic kidney damage. 13/22 glomeruli showed evidence of vasculitic lesions, 3 were globally sclerosed and 6 were normal. Immunoperoxidase and immunofluorescence were negative for IgG, IgM and IgA and C3 (Fig. ).
Treatment with intravenous methylprednisolone and cyclophosphamide was commenced. An anti-GBM antibody titre, obtained 2 weeks post-discharge, was significantly elevated at 359 IU/ml (NR 0–10, ELiA, Phadia systems, Thermo Scientific). This elevation was confirmed on repeat testing. 14 cycles of plasma exchange were performed with 6 doses of pulsed cyclophosphamide. At four months creatinine was 130 μmol/l and at 4 years 105 μmol/l (eGFR 37 and 47 mls/min respectively)while ANCA and anti-GBM have remained negative (Table ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [162.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",114,108.3,119.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 162.0 mm Hg + 2/3 * 90.0 mm Hg = 114.0 mm Hg.
Hence, the patient's mean arterial pressure is 114.0 mm Hg."
1183,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5097346-1,Extracted,"A-70-year-old man with symptomatic osteoarthritis of the right hip, weighing 79 kg, tall 177 cm was presenting for a primary THA. He was recently diagnosed with systemic indolent mastocytosis with multiple sclerotic and osteolytic laesions. History showed no allergic reactions in the past. In 1998 cannulated hip screws were used to treat a left proximal transcervical femur fracture successfully. Multiple insufficiency vertebra fractures were treated non-operative in 2015. A multimodal oral analgesic regime consisting of paracetamol 1 g, naproxen 500 mg and gabapentin 600 mg was administered 1–2 h pre-operatively. On the pre-anesthetic care unit the blood pressure was 150/95 mmHg with a saturation of 95 % and 11,85 mg Dexamethasone and Cefazoline 2000 mg soluted in 20 ml Sodiumchloride (NaCl) 0.9 % was administered intravenously. In the operating room spinal anesthesia with 7.5 mg bupivacaine 0,5 % plain via the L2/3 vertebral interspace with a standardized intraoperative regime for fluid administration, consisting of 0,9 % saline (500 ml) was given. After spinal anesthesia the patient received sedation with propofol TCI 0,8 ug/ml (0,1–2.0 ug/ml). To reduce blood loss, tranexamic acid 1000 mg was given at the beginning of surgery. To reduce nausea and vomiting ondansteron 4 mg IV is added in this multimodal regimen. To reduce chronic pain, ketamine 15 mg IV is titrated after starting the sedation. The blood pressure was 120/70 mmHg after spinal anesthesia and starting the sedation. Three liter of Oxygen was added during sedation. Thirty minutes after induction the orthopedic surgeon inserted a cemented acetabular component. Blood pressure dropped from 90/50 to 60/40 mmHg. Saturation dropped from 95 to 80 %. Oxygen 100 % with a Ventimask was administered and rapid infusion of NaCl 0.9 % 1000 ml as well as Phenylephrine 4 × 100 ug, phenypephrine 2 × 200 ug and 10 mg ephedrine was given intravenously. Phenylephrine infusion was started and replaced by Noradrenaline 5 mg/50 ml NaCl 0.9 % 2.0–9.0 ml/h. The breath sounds remained normal, and no angioedema, urticaria or rash occurred. All the time, the patient was conscious and able to respond questions. With rapid infusion and finally Noradrenaline he recovered hemodynamically within 15 min, blood pressure 100/50 mmHg with 95 % saturation. Forty-five minutes after onset of the symptoms, the surgical procedure was completed after inserting a press fitted uncemented femoral stem component. The patient was transported to the Intensive Care Unit (ICU) for optimal postoperative treatment and monitoring. Biochemistry showed stable hemoglobin levels (8.3 mmol/l on ICU arrival and 8.4 mmol/l after 4 h), elevated white blood cell count (19.3 × 109/l), normal levels of electrolytes, liver enzymes, creatine kinase and troponin, and an arterial blood sample of pH 7.36 pCO2 6.1 kPa; pO2 14.4 kPa; HCO3 26 mmol/l; Base excess 0.4 mmol/l; Fys. O2 sat 98.7 %; FiO2 30 %; lactic acid 1.0 mmol/l. Electrocardiography (on ICU arrival and after 24 h) remained normal, and echocardiography showed no left or right ventricular disfunctioning or elevation of the right atrial pressure. Within six hours after surgery the patient started to ambulate following our standard fast-track rehabilitation regime. Post-operative day one he was discharged according strict functional criteria to the specialized Orthopedic Department. After 5 hospital days the patient was discharged to his home.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [95.0, 'mm hg']}",113.33333,107.66666,119,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 95.0 mm Hg = 113.33333 mm Hg.
Hence, the patient's mean arterial pressure is 113.33333 mm Hg."
1184,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4258988-1,Extracted,"A 12-year-old boy weighing 25 kg was admitted to our hospital with severe colicky periumbilical pain associated with recurrent bilious vomiting. He had a history of cough and fever since 1 month, which was treated. He developed a palpable purpura over legs and buttocks for which he was put on topical betamethasone cream. He also developed bilateral knee joint pain since 15 days [].
He appeared poorly built and pale. There was a diffuse, nonblanching palpable purpura over buttocks and both lower limbs. Pulse rate (PR) was 80/min and regular. Blood pressure (BP) was 100/60 mm Hg in the upper limb. Abdominal examination showed diffuse tenderness and no organomegaly. Respiratory and cardiovascular systems were normal.
Laboratory investigations revealed a hemoglobin of 12 mg/dl, normal renal and liver function tests, prothrombin time and serum electrolytes. Urine examination revealed 6-8 pus cells and 8-10 red blood cells/high power f ield (HPF) and protein++; 24 h urine protein was 234 mg/dl. Ultrasonography of abdomen and pelvis showed left kidney size 9 × 4 × 13 cm, ectopic and fused with the lower part of right kidney. Left renal fossa was empty. Other organs were normal. A provisional diagnosis of HSP was made. Laboratory facilities for immunoglobulin examinations were not available and were hence not done.
The patient was posted for elective diagnostic laparoscopy for recurrent abdominal pain. After premedication with injections ondansetron 2 mg, glycopyrronium 0.1 mg, midazolam 1 mg and fentanyl 50 μg intravenously, he was induced with intravenous propofol 50 mg and atracurium 12 mg. Tracheal intubation was performed with 6 mm internal diameter endotracheal tube. Anesthesia was maintained with oxygen, nitrous oxide (3:5) and injection atracurium. Positioning was carefully done to prevent injury and skin necrosis. Intraabdominal pressure monitoring was done. End tidal carbon dioxide level was maintained at 25-30 cm H2O, BP at 100/60 mm Hg, PR at 80/min and SpO2 100%. The surgeons performed a laparoscopic appendectomy. The trachea was extubated after reversal. Patient was shifted to the pediatric intensive care unit for observation.
The patient continued to have abdominal pain even on the second postoperative day. The palpable purpura soon extended up to the trunk and upper extremities. He developed hematuria, scrotal swelling, facial puffiness with periorbital edema and bilateral pedal edema up to the knee. He was in agony with a with a bradycardia (PR of 54/min) and an irregular rhythm. BP was 120/70 mm Hg and SpO2 100%. Abdominal examination revealed signs of minimal free fluid, an increased abdominal girth with bowel sounds present. Urine examination showed protein 3+, 8-12 red blood cells/HPF. An electrocardiogram showed bradycardia and two-dimensional-echocardiography revealed normal findings. Serum electrolytes including sodium and potassium levels, serum creatinine and other investigations were within the normal limits.
He was started on intravenous dexamethasone 0.15 mg/kg for 3 days and then changed over to oral prednisolone 10 mg once daily. Intravenous fluids, antibiotics, oral paracetamol 250 mg twice daily were given. The bradycardia and irregularity of PR continued up to the sixth postoperative day. He improved by the seventh postoperative day and was shifted to the ward. Renal biopsy was done, which showed features suggestive of glomerulonephritis with <50% crescents. He was discharged with advice of regular follow-up, oral prednisolone 10 mg twice daily with tapering after 1 week and tablet enalapril 2.5 mg once a day. He is now being followed up regularly in our hospital every 15 days [].",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",73.33333,69.66666,77,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 60.0 mm Hg = 73.33333 mm Hg.
Hence, the patient's mean arterial pressure is 73.33333 mm Hg."
1185,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3026341-8,Extracted,"A 21-year-old male farmer was admitted because of suicidal ingestion of organophosphate toxin. His symptoms started with sweating, headache, nausea and vomiting, muscular weakness, and dizziness. Upon admission, he had pin-point pupils which followed by loss of consciousness, urinary incontinence and finally seizure. His vital signs were as follows: BP=90/60, PR=50/min, RR=12/min. Brain CT scan showed bilateral hypodensity lesions of the basal ganglia indicative of infarctions (Figs. ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [60.0, 'mm hg'], 'Systolic Blood Pressure': [90.0, 'mm hg']}",70,66.5,73.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 60.0 mm Hg = 70.0 mm Hg.
Hence, the patient's mean arterial pressure is 70.0 mm Hg."
1186,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5988205-1,Extracted,"A 42-year-old lady of South African origin without any significant past medical history presented to the emergency department with a complaint of sudden onset epigastric and left upper quadrant abdominal pain for the past few hours. She described the pain as sharp in character, severe in intensity, and continuous and radiating to the left shoulder and back. This pain started while she was working out in her regular Zumba dance session and had remained constant since then. The abdominal pain was associated with a sensation of dizziness and shortness of breath. She felt nauseated but did not have any vomiting. She denied any previous history of similar abdominal pain, altered bowel habits, abdominal distension, urinary complaints, or menstrual complaints. She did not report any history of palpitations, chest pain, cough, or fever. She was not taking any regular medications and did not have a history of any previous surgery. She had no significant past medical history. She denied any history of trauma.
Upon arrival to the emergency department, her vital signs were: pulse rate 96 beats per minute (regular), blood pressure 129/79 mm Hg (left arm), temperature 36.8°C (oral), and respiratory rate 19 breaths/min. On physical examination, abdominal examination revealed epigastric and left upper quadrant tenderness with guarding. No rebound tenderness or other peritoneal signs were noted. Bowel sounds were audible and normo-active. Laboratory investigations were within normal limits, except for a mild neutrophilic leukocytosis (white cell count of 13.6 × 109/L with 85% neutrophils). Serum beta-human chorionic gonadotropin (β-hCG) was within normal limits. Her plain chest radiograph (Figure -A) showed an elevated left hemi-diaphragm with visualization of a gastric bubble (fundus of the stomach) within the left hemi-thorax. Her electrocardiogram showed a normal sinus rhythm with no ST segment or T-wave abnormalities. A computed tomography (CT) scan of the chest, abdomen, and pelvis was performed, which revealed a defect in the posterolateral aspect of the left hemi-diaphragm with herniation of the entire stomach, spleen, tail of pancreas, and part of the splenic flexure into the thoracic cavity. These findings were concerning for an obstructed diaphragmatic hernia (Figure ).
The patient was kept nil by mouth and she was administered intravenous hydration and analgesia. A nasogastric tube was inserted for gastric decompression (after CT scanning had been performed). The general surgery team was consulted and the patient was taken to the operating room for diagnostic laparoscopy. Perioperatively, a large posterolateral Bochdalek hernia was identified with strangulation of the stomach. Abdominal viscera were reduced to the abdominal cavity and the diaphragmatic defect was closed (from below) using a synthetic biodegradable mesh (Gore Bio-A; W.L. Gore and Associates, Inc., Flagstaff, AZ) secured with non-absorbable sutures (see Figure ). A small perforation was noted in the anterior wall of the stomach, which was repaired with absorbable sutures. Methylene blue was then injected through a nasogastric tube to ensure that there was no gastric leak. A Jackson-Pratt drain was left in place and abdominal port sites were closed. Postoperatively, the patient’s abdominal pain improved and she remained stable. Her postoperative chest radiograph is shown in Figure -B. Her drain was removed and she was discharged home after three days. She remained healthy at a one-month follow-up visit.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [79.0, 'mm hg'], 'Systolic Blood Pressure': [129.0, 'mm hg']}",95.66667,90.88334,100.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 129.0 mm Hg + 2/3 * 79.0 mm Hg = 95.66667 mm Hg.
Hence, the patient's mean arterial pressure is 95.66667 mm Hg."
1187,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-969,Extracted,"A 75-year-old man is brought to the emergency department because of a 5-hour history of worsening chest pain and dyspnea. Six days ago, he fell in the shower and since then has had mild pain in his left chest. He appears pale and anxious. His temperature is 36.5°C (97.7°F), pulse is 108/min, respirations are 30/min, and blood pressure is 115/58 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 88%. Examination shows decreased breath sounds and dullness to percussion over the left lung base. There is a 3-cm (1.2-in) hematoma over the left lower chest. An x-ray of the chest shows fractures of the left 8th and 9th rib, increased opacity of the left lung, and mild tracheal deviation to the right.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [58.0, 'mm hg'], 'Systolic Blood Pressure': [115.0, 'mm hg']}",77,73.15,80.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 58.0 mm Hg = 77.0 mm Hg.
Hence, the patient's mean arterial pressure is 77.0 mm Hg."
1188,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3874924-1,Extracted,"A 43-year-old man presented with a 2-day history of dyspnea and chest pain after shouting in a quarrel with his wife. He had presented to a local clinic with fever, cough, sputum, and odynophagia 3 days previously, and was treated for acute pharyngitis. Before the onset of symptoms, he was in good health and had no significant past medical history except for 50 pack-years smoking history. Vital signs on admission were blood pressure 120/70 mm Hg, heart rate 100/min, respiration rate 28/min, and body temperature 38.7℃. On physical examination, there was swelling and tenderness in the left cervical area. Crackles were noted in both cervical areas. Coarse breath sounds were noted in both lung fields, and crackles were noted in the left lower lung field.
Leukocyte count was 13000/mm3 (85.2% neutrophils, 9.4% lymphocytes, 4.7% monocytes, 0.2% eosinophils), hemoglobin 13.0 g/dL, and platelet count 229000/mm3. The results of arterial blood gas analysis in room air were pH 7.491, PaCO2 25.2 mm Hg, PaO2 62.4 mm Hg, HCO3- 21.8 mmol/L, and SaO2 94.2%. Liver function tests were normal. Serum total protein was 6.5 g/dL, albumin 3.5 g/dL, blood urea nitrogen 20.0 mg/dL, creatinine 1.2 mg/dL, sodium 135 mmol/L, potassium 4.2 mmol/L, creatine phosphokinase 431 IU/L, lactate dehydrogenase 658 IU/L, and high sensitivity C-reactive protein 30.7 mg/dL. Urinalysis was normal.
An initial chest radiography showed linear air trapping parallel to the border of the trachea, bilateral pleural effusion that was more severe on the left side, and consolidations in both lower lungs (). A chest computed tomography (CT) scan revealed air collection around the airway and mediastinum, infiltration around the mediastinum, and bilateral pleural effusions ().
Laryngoscopy was performed by an otolaryngologist, and a small pharyngeal perforation in the right side of the vallecula was seen. A cervical CT scan also showed lacerations in the same area (). Analysis of the pleural fluid on the left side was consistent with parapneumonic effusions (pH 8.0, red blood cell count 3840/mm3, white blood cell count 2880/mm3, neutrophils 95%, total protein 4.6 g/dL, albumin 2.5 g/dL, lactate dehydrogenase 27198 IU/L, glucose 27 mg/dL). Intravenous moxifloxacin was started. In addition, chest tubes were inserted on both sides and supplemental oxygen was administered. Laryngoscopy was repeated 2 days later, and the previously-noted small pharyngeal perforation was not seen. Blood and pleural fluid cultures were negative, but fever and leukocytosis persisted. Antibiotics were broadened to piperacillin-tazobactam and amikacin. Fifteen days after admission, a follow-up chest radiography showed resolution of air trapping around the mediastinum and regression of parapneumonic effusions. The patient's symptoms and laboratory results continuously improved, and the patient was discharged 29 days after admission.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1189,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5687,Extracted,"A 33-year-old man presents to his primary care physician for left-sided knee pain. The patient has a history of osteoarthritis but states that he has been unable to control his pain with escalating doses of ibuprofen and naproxen. His past medical history includes diabetes mellitus and hypertension. His temperature is 102.0°F (38.9°C), blood pressure is 167/108 mmHg, pulse is 100/min, respirations are 14/min, and oxygen saturation is 98% on room air. Physical exam reveals a warm and tender joint that is very tender to the touch and with passive range of motion. The patient declines a gait examination secondary to pain.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [108.0, 'mm hg'], 'Systolic Blood Pressure': [167.0, 'mm hg']}",127.66667,121.28334,134.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 167.0 mm Hg + 2/3 * 108.0 mm Hg = 127.66667 mm Hg.
Hence, the patient's mean arterial pressure is 127.66667 mm Hg."
1190,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4750,Extracted,"A 14-year-old girl presents to the pediatrician for behavior issues. The girl has been having difficulty in school as a result. Every time the girl enters her classroom, she feels the urge to touch every wall before heading to her seat. When asked why she does this, she responds, ""I'm not really sure. I just can't stop thinking about it until I have touched each wall."" The parents have noticed this behavior occasionally at home but were not concerned. The girl is otherwise healthy, has many friends, eats a balanced diet, does not smoke, and is not sexually active. Her temperature is 98.2°F (36.8°C), blood pressure is 117/74 mmHg, pulse is 80/min, respirations are 15/min, and oxygen saturation is 98% on room air. Physical exam is notable for a healthy young girl. Neurologic exam is unremarkable. There is no observed abnormalities in behavior while the girl is in the office.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [74.0, 'mm hg'], 'Systolic Blood Pressure': [117.0, 'mm hg']}",88.33333,83.91666,92.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 117.0 mm Hg + 2/3 * 74.0 mm Hg = 88.33333 mm Hg.
Hence, the patient's mean arterial pressure is 88.33333 mm Hg."
1191,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3502769-1,Extracted,"A 77-year-old woman was admitted to the Emergency Department of Abant Izzet Baysal University Hospital with complaints of fever, chills, nausea, vomiting, loss of appetite and abdominal pain located in the right-upper quadrant. She described fever and chills, especially in the night time for the last two weeks before admission. Her history was positive for hepatic hydatid cyst ten years ago. Physical examination revealed a mild, confused, and sick appeared woman. Vital signs were as follows: temperature 39.2°C, pulse rate 122 beats/min, respiration rate 20 breaths/min, and blood pressure 95/50 mmHg. Abdominal examination revealed a painful mass filling the right-upper quadrant and extending down to umbilicus. Laboratory findings were as follows: total white cell count 7.6 × 109/L (90% neutrophil), hemoglobin 10.9 g/dL, platelet 121000/mm3, blood urea 77 mg/dL, creatinine 0.7 mg/dL, aspartate aminotransferase 47 U/L, alanine aminotransferase 19 U/L, alkaline phosphatase 76 U/L, and C-reactive protein (CRP) 265 mg/dL. Indirect hemagglutination (IHA; Fumouze Diagnostics, France) test for hydatid cyst was positive at a titer of 1/320. Ultrasonography (US) of the abdomen revealed a hyperechogenic lesion filling the right-upper quadrant with a dimension of 19 cm × 19 cm × 20 cm. The lesion included more than 10 cysts in it, and the largest cyst was with an 80 mm diameter. Complicated, thick-walled multicystic lesions with different dimensions and with air-fluid levels located in right-upper quadrant of the abdomen were determined in abdominal computed tomography (CT) (). The patient was diagnosed with PLA secondary to the infection of hepatic hydatid cysts. Surgeons performed cystectomy and cholecystectomy. Abscess material was cultured into microbial broth. Intravenous cefazolin 3 × 1 g and 3 × 500 mg metronidazole were empirically administered, and cefazolin was replaced with 2 × 750 mg intravenous cefuroxime because no clinical improvements were achieved. Gram staining of the abscess material revealed 5-6 leukocytes and Gram-negative bacilli. Gram-negative growth in the culture was identified as M. morganii by conventional methods and by VITEK 2 automated system (bioMerieux Inc., Marcy L'etoil, France). Antibiotic susceptibility tests were done with VITEK 2 (bioMerieux Inc., Marcy L'etoil, France) automated system. The bacilli were susceptible to ceftriaxone, ceftazidime, ertapenem, imipenem, meropenem, tetracycline, aztreonam and trimetoprim/sulphametoksazol. The patient was consulted to infectious diseases specialists in the 7th day and according to their advice, antibiotherapy was switched to ceftriaxone 2 × 1 gram daily. Clinical signs of the patient resolved at the second week of treatment and she was discharged from hospital.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [95.0, 'mm hg'], 'Diastolic Blood Pressure': [50.0, 'mm hg']}",65,61.75,68.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 95.0 mm Hg + 2/3 * 50.0 mm Hg = 65.0 mm Hg.
Hence, the patient's mean arterial pressure is 65.0 mm Hg."
1192,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-11909,Extracted,"A 33-year-old man presents to the emergency department with a rash. The patient is homeless and is a known IV drug abuser. His temperature is 99.5°F (37.5°C), blood pressure is 127/68 mm Hg, pulse is 100/min, respiratory rate is 24/min, and oxygen saturation is 98% on room air. Physical exam reveals the finding in Figure A and a red rash on the skin.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [127.0, 'mm hg'], 'Diastolic Blood Pressure': [68.0, 'mm hg']}",87.66667,83.28334,92.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 127.0 mm Hg + 2/3 * 68.0 mm Hg = 87.66667 mm Hg.
Hence, the patient's mean arterial pressure is 87.66667 mm Hg."
1193,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1995,Extracted,"A 56-year-old man is brought to the emergency department after falling 16 feet from a ladder. He has severe pain in both his legs and his right arm. He appears pale and diaphoretic. His temperature is 37.5°C (99.5°F), pulse is 120/min and weak, respirations are 26/min, and blood pressure is 80/50 mm Hg. He opens his eyes and withdraws in response to painful stimuli and makes incomprehensible sounds. The abdomen is soft and nontender. All extremities are cold, with 1+ pulses distally. Arterial blood gas analysis on room air shows:
pH 7.29
PCO2 33 mm Hg
PO2 65 mm Hg
HCO3- 15 mEq/L
A CT scan shows displaced fractures of the pelvic ring, as well as fractures of both tibiae, the right distal radius, and right proximal humerus. The patient undergoes emergent open reduction and is admitted to the intensive care unit.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [50.0, 'mm hg'], 'Systolic Blood Pressure': [80.0, 'mm hg']}",60,57,63,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 80.0 mm Hg + 2/3 * 50.0 mm Hg = 60.0 mm Hg.
Hence, the patient's mean arterial pressure is 60.0 mm Hg."
1194,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2829597-1,Extracted,"A 28-year-old Polish woman who has been residing in the United Kingdom for four years presented to the accident and emergency department of a district general hospital with severe ulceration of the perineal area, dysuria, soreness of the mouth, fever, non-productive cough, and a facial rash. Her illness started two weeks prior to presentation with a flu-like illness and sore throat for which she was prescribed with antibiotics. Three days into the illness, she developed severe burning and itching of her genital region. Antifungal topical treatment and appropriate antibiotic therapy for a concurrent urinary tract infection provided minimal relief. She further developed high fever, vomiting, and a facial rash.
Her medical history included von Willibrand's disease and a caesarean section two years prior to presentation. She had no relevant drug history or sexual history.
On examination our patient was unwell with a temperature of 38°C, heart rate of 110 beats per minute, blood pressure of 105/60, and initial oxygen saturations of 100% on air.
She had crepitations at the base of her left lung, tenderness on palpation at the right upper quadrant of her abdomen, and an ill-defined rash over her face and neck. There was some erythema at the back of her mouth and a white coating resembling candida. She had mild injection of both eyes.
The most marked findings were of vulval and perineal erythema and excoriations with discrete ulceration. The associated pain was so severe it prevented her from moving her legs freely.
Further investigations revealed that she had a lymphopenia of 0.26 × 109/L (NR = 1.10 to 4.80) and a C-reactive protein (CRP) level of 49 (NR = <5). Meanwhile, abnormal liver function tests revealed an alanine transaminase (ALT) level of 342I U/L (NR = 0 to 55) and alkaline phosphatase (ALP) level of 185 IU/L (NR = 40 to 150).
With these initial findings of genital ulceration, oral soreness and candidiasis, fever, and rash, we sought an infectious disease opinion. The differential diagnosis at this stage included human immunodeficiency virus (HIV), herpes simplex virus, and noninfective causes such as Bechet's, systemic lupus erythematosus, and systemic vasculitis. Reiter's syndrome was also considered as it can present without arthritis in women.
Tests for viral screen (including measles IgM and IgG), anti-streptolysin O (ASO) titre, HIV, PCR, complement levels, autoimmune screen, and immunoglobulin levels were requested. Our patient, meanwhile, was initially treated with intravenous acyclovir and high-dose prednisolone.
Within 20 hours of presentation she developed type 1 respiratory failure with a pO2 of 9.5 KPa on 10 liters of oxygen. She began to tire and required noninvasive ventilation. Her respiratory symptoms were out of proportion to the changes exhibited in her chest X-ray (minimal consolidation at her left lung base, see Figure ), although clinically she began to develop bronchial breathing at her left lung base.
The most likely diagnosis at this stage was HIV seroconversion complicated by Pnemocystis carinii pneumonia. Another possibility was of an atypical but severe bacterial infection. She was treated with intravenous broad spectrum antibiotics (imipenem and teicoplanin) and treatment doses of cotrimoxazole. Her steroids were also changed to high-dose methylprednisolone.
On day 4 of admission her facial rash had resolved and her oxygenation began to improve (PO2 13.1 Kpa, Fio2 at 40%). Meanwhile, her blood tests revealed negative HIV PCR, negative ASO titre, normal complement levels, normal immunoglobulin levels, and negative autoimmune screen. Her steroid medication was slowly weaned and the antibiotics, including cotrimoxazole, were stopped.
Her symptoms had completely resolved by day 10 of admission. It seemed likely that she had an atypical viral infection. Elevated serum titres of IgM and IgG antibodies to measles were subsequently demonstrated, thus confirming a diagnosis of acute measles. The patient is now well.
A vaccination history of our patient revealed that she had completed all her childhood vaccines in Poland.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [105.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",75,71.25,78.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 105.0 mm Hg + 2/3 * 60.0 mm Hg = 75.0 mm Hg.
Hence, the patient's mean arterial pressure is 75.0 mm Hg."
1195,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8335880-1,Extracted,"A 60-year-old female patient was admitted to our hospital with a complaint of complex aneurysm of the entire thoracic–abdominal aorta. Two month ago, the patient’s routine chest x-ray revealed a huge mass in the upper mediastinum (Fig. A), and further chest CT revealed an aneurysm of the total thoracic–abdominal aorta (Fig. B). For further surgical treatment, she was transferred to our hospital.
On admission, his vital signs were stable, no fever, no chest and abdominal pain. Blood pressure, 132/78 mmHg; heart rate, 80 beats/min; body temperature, 36.4℃; respiratory rate, 16 beats/min; arterial oxygen saturation on room air, 97%. The height is 162 cm, the weight is 65 kg, and the body mass index is 24.8 kg/m2. The patient's eye vision is normal. There was no abnormal growth in the bones of her limbs. She has a history of hypertension with well controlled. She denies that there are genetic diseases such as Marfan syndrome in her family, and she denies her personal history of drug abuse and promiscuity.
The laboratory test results are as follows: total cholesterol 5.8 mmol/L, triglyceride 2.09 mmol/L, uric acid 426umol/L. Transthoracic echocardiography showed that the patient’s aortic sinus was widened (maximum diameter 50 mm), and the aortic valve had moderate to severe regurgitation. Aortic CTA indicates aortic aneurysm, lesions involving the ascending aorta, aortic arch, thoracic–abdominal aorta, aortic arch and abdominal aortic wall thrombus, multiple penetrating ulcers in the thoracic–abdominal aorta, 58 mm at the widest part of the ascending aorta, diameter of the aortic arch 59 mm, 72 mm at the widest part of the thoracic aorta, and 57 mm at the widest part of the subrenal abdominal aorta (Fig. B).
Given that the patient’s entire thoracic–abdominal aortic aneurysm is very complex and older, after thorough discussion and full communication with the patient and family members, our team believes that the risk of two-staged total thoracic–abdominal aortic replacement surgery is less than of the one-staged total thoracoabdominal aortic replacement. We finally decided to implement two-staged surgery, namely Bentall procedure and Sun’s operation in the first-stage and thoracoabdominal aortic replacement in the second-stage.
During the first-stage of Bentall + Sun’s operation, we routinely use median sternotomy, right axillary artery and right atrium cannulation to establish cardiopulmonary bypass, and blow CO2 into the surgical field. After blocking the ascending aorta, the cardioplegia was perfused directly through the opening of the left and right coronary arteries. During the cooling process, the Bentall procedure of the aortic root was completed. When the nasopharyngeal temperature drops to 24–25 °C and the rectal temperature drops to 26–28 °C, the patient’s head was lowered by 20°–30°. The innominate artery, left common carotid artery and left subclavian artery were blocked respectively, and selective cerebral perfusion was performed, and the perfusion flow rate was reduced to 5 mL/kg min. During the operation, according to the monitoring of bilateral cerebral oxygen or the amount of blood returned to the left common carotid artery, decide whether to choose bilateral cerebral perfusion. Most patients with good collateral circulation in the basilar artery ring (Williams) can tolerate unilateral cerebral perfusion. After placing a suitable elephant trunk stent during the operation, the distal aortic anastomosis was quickly completed. After the left common carotid artery anastomosis is completed, the perfusion flow is gradually restored through one of the 4-branch artificial blood vessel, and bilateral cerebral perfusion and systemic perfusion are performed, and the temperature is slowly rewarmed. Then anastomose the left subclavian artery, the proximal end of the artificial blood vessel, and finally the innominate artery to complete the Bentall + Sun’s operation (Fig. A). After the first-stage of Bentall procedure and Sun’s operation was successfully performed, a re-examination of CTA showed that the lesions of aneurysm in the aortic root, ascending aorta, and aortic arch were well treated (Fig. B).
One month after the patient was discharged from our hospital, in order to avoid the residual thoracic–abdominal aortic aneurysm from rupturing, we performed the second-stage of surgery, that is, the patient underwent thoracoabdominal aortic replacement. A combined thoracic–abdominal incision was used, a double-lumen endotracheal tube was used during anesthesia, and a cerebrospinal fluid drainage tube was routinely inserted. The incision is made between the left scapula and the spine, bypassing the subscapular corner, along the posterolateral fifth intercostal space to the lower edge of the costal arch, and continuing to the rectus abdominis muscle and down to the iliac fossa. Enter the chest through the fifth intercostal space, traverse the costal arch, and cut off the diaphragm from the front to the posterior side at a distance of 3–4 cm from the chest wall along the edge of the diaphragm to reach the aortic hiatus. We used a total extraperitoneal approach to expose the abdominal aorta and its branch arteries, and performed thoracoabdominal aortic replacement surgery with a normal temperature (nasopharyngeal temperature 34–36℃) left heart bypass technique. After systemic heparinization, cardiopulmonary bypass was established through cannulation of the left inferior pulmonary vein, left femoral vein, and left femoral artery. Block the thoracic–abdominal aortic aneurysm at a distance of 2–3 cm from the distal end of the elephant trunk stent, transcribe the descending aorta, cut the aneurysm longitudinally, and suture the open intercostal artery. The proximal end of a suitable type of the 4-branch artificial blood vessel was anastomosed with the distal end of elephant trunk stent. After wrapping the lower intercostal artery into a vessel island, it was anastomosed end-to-side with the 4-branch artificial blood vessel to complete the reconstruction of the intercostal artery. Reduce the extracorporeal circulation flow to 1/2 of the full flow, block the external iliac artery cannulation, stop the circulation in the lower body, and complete the reconstruction of the abdominal aortic branch artery in turn. We usually use the superior mesenteric artery, celiac artery, right renal artery and left renal artery anastomosis sequence. After anastomosis of a blood vessel, immediately open a blood vessel to reduce ischemia time. Finally, the distal end of the abdominal aorta was anastomosed, and the thoracic–abdominal aorta replacement operation was completed (Fig. A). Fortunately, this female patient tolerated the operation well, without complications such as paraplegia, renal failure, or infection. The postoperative CT scan revealed that the thoracic–abdominal aortic aneurysm was completely treated with satisfactory results (Fig. B).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [132.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",96,91.2,100.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 132.0 mm Hg + 2/3 * 78.0 mm Hg = 96.0 mm Hg.
Hence, the patient's mean arterial pressure is 96.0 mm Hg."
1196,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6198702-1,Extracted,"A 27-year-old male presented with history of fall from 10 feet height, 4 h earlier. He sustained injuries over his chest and abdomen. He complained of pain in the right chest and right side of abdomen. His management was started as per the ATLS protocol. He was conscious, oriented. His air entry was bilaterally normal. He had a tachycardia of 90–100 beats/min. His blood pressure at presentation was 100/80mm Hg. There were no other external injuries. The patient was reassessed every hour to look for any hemodynamic deterioration.
Ultrasound showed free fluid in the peritoneal cavity. computed tomography (ACT) showed a pseudoaneurysm of hepatic artery proper (HA) just proximal to its bifurcation into right and left hepatic arteries []. There was a hematoma in the peri-hepatic space with a mild hemoperitoneum.
A digital subtraction angiography showed a 2-cm aneurysm at junction of right and left hepatic arteries [] with no active bleeding. Endovascular intervention was considered but was not attempted due to the difficult location of aneurysm and a higher risk of failure.
While an elective intervention was being planned, the patient developed sudden hypotension (BP 60/40 mmHg) and disorientation. Decision to perform an emergency laparotomy was taken.
On exploratory laparotomy, there was about 500 mL of blood in the peritoneal cavity. There was a contusion in the hepatoduodenal ligament. An actively bleeding aneurysm of size 2 × 2 cm was identified proximal to the bifurcation of hepatic artery proper (HA). Double ligation of HA and right and left hepatic arteries was done. However, bleeding continued through retrograde flow from gastroduodenal artery, and hence ligation of gastrodudenal artery was also done. There was no immediate discoloration of the liver. Two units of packed cells were transfused intraoperatively. There were no associated injuries to the adjacent organs.
Postoperative recovery was uneventful. His transaminases were 350 and 370 U/L (AST and ALT) on day 1 which reduced to 100 and 120 U/L by day 5. He was discharged from the hospital on day 8. At follow-up of 10 months, he is symptom-free.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 80.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1197,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7648702-1,Extracted,"A 54-year-old man was hospitalized with diffuse abdominal pain and abdominal distention. The pain occurred 4 days prior to admission and was gradually increasing. At first, the pain was localized in the epigastric region, then radiating throughout the abdomen. The patient reported nausea but no vomiting nor jaundice. He was normotensive with a blood pressure of 120/60 mmHg, pulse rate 75 bpm, respiratory rate 21 per minute, and temperature 37.7°C. He noticed recent weight loss of 4 kg over 3 months. He reported rare alcohol consumption, no smoking, and noncontributing family history. Examination showed no symptoms of biliary obstruction but diffuse abdominal tenderness on palpation. Serum amylase, lipase, and IgG4 were within normal ranges, and CA19-9 and CA242 were 69.6 U/mL (normal value ≤ 37 U/mL) and 82.1 U/mL (normal value ≤ 20 U/mL), respectively. Bilirubin, alpha-fetoprotein, and HBsAg were normal.
Abdominal ultrasound revealed a diffusely enlarged and heterogeneous hypoechoic pancreas. Slightly infiltrated fat layer was found around the pancreas without associated fluid. Simultaneously, the liver also showed multiple solid hypoechoic or hyperechoic masses. CT scan confirmed enlargement of the pancreas with relatively homogenous enhancement remarkably in the arterial phase and washout in the delayed phase (). Multiple liver lesions showed early arterial enhancement with washout in the delayed phase suggesting hypervascular metastases (). The pancreatic duct and biliary tract did not dilate; there was no presence of pathological lymph nodes. The patient subsequently underwent MRI that showed characteristics similar to ultrasound and CT with a diffusely enlarged pancreas with low signal intensity on T1-weighted, high signal intensity heterogeneous on T2-weighted, restricted diffusion on diffusion-weighted imaging, and relatively homogenous enhancement on postcontrast T1-weighted images ().
According to the clinical presentation, laboratory results, and radiological findings, we had a provisional diagnosis of diffuse pancreatic carcinoma with liver metastasis. We performed pancreatic FNA under ultrasound guidance; cytology revealed suspected carcinoma. The patient then underwent ultrasound-guided biopsy of liver lesions; histopathological findings confirmed metastases from carcinoma. He received conservative treatment, and after 2 weeks, the symptoms were much improved. We offered chemoradiotherapy and palliative care, but he refused and requested to be discharged 1 week later. We contacted the patient after 2 months, but family members said his conditions were getting worse.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 60.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1198,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3008834-1,Extracted,"A 52-year-old woman was hospitalized for evaluation of a 2-day-history of chest discomfort. She had rheumatoid arthritis for 13 years and had been treated with hydroxychloroquine for >12 years (total dose, 1,898 grams). In the emergency department, she had a generalized tonic-clonic seizure caused by sinus arrest (). The initial vital signs were as follows: blood pressure, 130/80 mmHg; heart rate, 38 beats/minute; body temperature, 36.4℃; and respiratory rate, 20/minute. The physical examination revealed a mild degree of jugular venous distention, a regular, slow cardiac beat without murmurs, clear lung sounds, and no pitting edema in the extremities. The 12-lead ECG showed a junctional rhythm with sinus arrest (). The laboratory findings included a hemoglobin level of 13.1 g/dL and a normal white blood cell count with a normal differential cell count. The blood urea nitrogen was 27 mmol/L, the serum creatinine was 2.02 mg/dL and the C-reactive protein was 0.94 mg/L. The antinuclear and anti-double stranded deoxyribonucleic acid (DNA) antibodies were negative, while the rheumatoid factor was positive. The creatine kinase was 294 UI/L with a normal myocardial band fraction. The aspartate aminotransferase level was 57 U/L, the alanine aminotransferase level was 48 U/L, and the alkaline phosphatase level was 49 UI/L. Chest radiography demonstrated marked cardiomegaly without pulmonary congestion (). Transthoracic echocardiography (TTE) revealed a markedly thickened left ventricular (LV) septum and posterior wall thickness, measuring 17.7 mm and 18.8 mm, respectively, with mild LV systolic dysfunction (ejection fraction, 44%). A slightly thickened RV free wall with mild RV systolic dysfunction was also noted. Both atria were enlarged and a mild degree of mitral regurgitation was present. The mitral inflow pattern was consistent with restrictive physiology. The early mitral inflow (E) velocity was 90.28 cm/s, the late mitral inflow (A) velocity was 36.77 cm/s, and the deceleration time was 216.64 milliseconds. The E/E' was 33.4, suggesting a high left ventricular end diastolic pressure (). Magnetic resonance imaging (MRI) showed diffuse wall thickening of the LV (septal wall thickness at the end-diastolic phase, 19 mm) and the RV free wall, suggesting hypertrophic cardiomyopathy. There was a small pericardial effusion. On delayed enhancement, multifocal patchy myocardial enhancement was noted in the lateral and septal walls (). The patient underwent myocardial biopsy to determine the underlying cause of the cardiomyopathy. Light microscopy showed vacuolated myocytes (). Electron microscopy revealed abundant intra-myocyte lysosomes with numerous large, dense myelin figures occupying large portions of the myocyte sarcoplasm. Lysosomal inclusions with curvilinear substructures were also noted (). There was no evidence of amyloid deposition, myocarditis, or an acute vasculitic process. Chloroquine toxicity was diagnosed based on the pathologic findings and the hydroxychloroquine was promptly discontinued. A permanent pacemaker was inserted for management of sick sinus syndrome. Four months later, the follow-up TTE demonstrated no significant interval change in LV systolic function or the LV wall thickness compared with the previous examination. However, LV diastolic function improved from restrictive physiology to pseudonormal relaxation. The patient's rheumatoid arthritis was subsequently controlled with low-dose prednisolone and analgesics.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1199,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6194182-1,Extracted,"A 45-year-old male hailing from Dhanbad district of Jharkhand state working as a staff in a courier service reported to medicine OPD of Patliputra Medical College and Hospital (PMCH), Dhanbad with the chief complain of—soreness of mouth and difficulty in swallowing both solid and liquid since past 1 month, multiple episodes of fever on and off for one and a half months, mild cough with scanty expectoration and weight loss (not documented) since past 2 months.
Patient was apparently asymptomatic 2 months ago when his complaints started in the form of mild cough with scanty expectorations. It was gradual in onset, non-progressive, no diurnal variation. Symptoms sometimes showed relief on taking cough syrup containing codeine and dextromethorphan. The sputum was white in colour, non-blood tinged and mucoid in consistency. Patient also complained of loosening of clothes which used to fit him earlier.
Since past one and a half months, he complained of multiple episodes of fever on and off with no particular pattern. It was gradual in onset, non-progressive though little relief was seen on taking paracetamol. Gradually, the patient developed soreness of mouth and difficulty in swallowing both solid and liquid food items. It was gradual in onset with no complaint of burning sensation in mouth or heart burn.
Before the start of these complains or during this period, he was not on any drug (except for cough syrup and paracetamol).
On general physical examination, he was thin built, febrile, weighed 42 kg, BP 120/80 mmHg, pulse 96/min. Pallor was present. No icterus, clubbing, cyanosis, lymphadenopathy, oedema. On the examination of oral cavity, white keratotic lesions were seen over vestibular and buccal mucosa, suspected to be verrucous leukoplakia.
On systemic examination, no abnormalities were detected. Laboratory data revealed Hb 9.2 gm%, TC 2700/mm3, neutrophil 79% and lymphocyte 21%. Ultrasonography (USG) of whole abdomen showed multiple retroperitoneal and mesenteric lymph nodes (largest being 28 mm).This made us think that the patient was suffering from abdominal tuberculosis which might have disseminated from the lungs. So, now sputum was analysed for acid-fast Bacilli which was negative. Rest all investigations like chest X-ray, electrolytes, kidney function test, random sugar, routine urine, liver function test and lipid profile were within normal limit. Then blood was tested for HIV I and II and was found to be positive for HIV I. Therefore, he was now registered at the Anti Retroviral Therapy centre of PMCH Dhanbad on 28-03-2017. CD4 count was 58/mm3 which signifies stage 4 of the disease.
Based on high clinical suspicion and the epidemiological data, his treatment was started with antitubercular therapy (ATT) Cat-I on 30-03-2017 (consisting of Isoniazid, Rifampicin, Pyrazinamide and Ethambutol) and HAART (consisting of Zidovudine, Lamivudine and Efavirenz) after 2 weeks on 14 April 2017 to avoid immune reconstitution inflammatory syndrome. Even after 2 weeks, no clinical improvement was seen in the patient which according to the literature is one of the criteria to state that the patient had tuberculosis and get cured following ATT administration. Failure of above treatment advised us to do USG guided fine-needle aspiration cytology (FNAC) of the retroperitoneal and mesenteric lymph nodes. Cytological reports showed large masses of round yeast like structure with negatively stained capsule admixed with lymphoid cells, plasma cells, foamy macrophages, epitheloid cells in the background of necrotic debris. These suggested a possibility of fungal (Cryptococcus) necrotizing granuloma involving the lymph nodes. No acid-fast bacilli were seen.
Following this report, ATT was stopped on 27 April 2017 and patient was referred to Rajendra Institute of Medical Science, Ranchi where he was treated with injection amphotericin B for 7 days followed by oral fluconazole and flucytosine. Flucytosine could not be continued after discharge from hospital due to financial constraints. After 15 days, patient came for follow-up and there was improvement in clinical symptoms and with the gain of 2 kg weight. The USG showed a decrease in size of the lymph nodes.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1200,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1811,Extracted,"A 30-year-old woman comes to the physician because of a swelling on her neck for 5 months. It has gradually enlarged in size and is mildly painful. She has also had intermittent episodes of throbbing headache, sweating, and palpitations over the past 3 months. Menses occur at regular 28-day intervals and last for 4–5 days. She does not smoke, occasionally consumes alcohol on weekends. She appears thin and pale. Her temperature is 38.7°C (101.7°F), pulse is 112/min, and blood pressure is 140/90 mm Hg. Examination shows a firm, 3-cm swelling on the neck that moves with swallowing; there is no lymphadenopathy. Cardiopulmonary examination shows no abnormalities. Laboratory studies show:
Hemoglobin 13 g/dL
Leukocyte count 9500/mm3
Platelet count 230,000/mm3
Serum
Na+ 136 mEq/L
K+ 3.5 mEq/L
Cl- 104 mEq/L
TSH 2.3 μU/mL
Calcitonin 300 ng/dL (Normal < 5 ng/dL)
An electrocardiogram shows sinus tachycardia.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1201,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5992108-1,Extracted,"A 28-year-old Pakistani male presented to the emergency department (ED) complaining of a severe headache. The headache had started 7 days prior to presentation and was localized to the left side of the head with no radiation. The pain was pulsatile and throbbing in nature. The patient rated the pain 9/10 on the visual analog scale. His headache was associated with unilateral photophobia and denied any visual impairment. There were no other associated symptoms and no focal neurological abnormality. The patient had a long-standing history of migraines that started around 2 years ago, experiencing an episode once every 2 weeks. Usually, those episodes subsided with paracetamol and Ibuprofen; on the rare occasion, the patient has had to present to the ED for further management.
Along with his migraine, our patient developed cutaneous markings (Figs. and ). There were multiple, 1–2-cm non-blanching linear erythematous lesions that appeared on his forehead and disappeared a few days after the headache subsided (Fig. ). These markings, first appeared in 2014, then reappeared in April 2017 and had been reoccurring with each migraine attack until he visited our ED. The patient correlated the severity of the pain with the size and number of markings. He reported that as his pain increased, the marks would get more intense in color, they started off as red but then eventually would turn blue/black resembling a bruise.
The patient’s past medical history was only significant for dyslipidemia, for which he was on a statin. Of note, the patient has a positive family history for migraines, but denies any migraine-associated cutaneous manifestation in the family. On presentation to the emergency department, the patient vitals were as follows: temperature 36.8 °C, a pulse rate of 118 bpm, a respiratory rate of 18 bpm, and a blood pressure of 148/91 mmHg. On examination, he was alert, oriented to time and place. On further examination, his chest and lungs were clear and he had no focal neurological deficits. His pupils were reactive and his GCS was 15. His forehead showed multiple 1–2-cm erythematous markings that were purple in color and non-tender (as shown in pictures 1 and 2 below). We put the patient on an oxygen mask and gave him 20 mg of metoclopramide IM. The patient was then kept in a dark room to rest, and within 30 min, the patients pain decreased from a severity of 9/10 to a 4/10. Laboratory investigations were not sent in this visit as the patient felt significantly better and had had prior workup done, including an MRI, which were all unremarkable. Although the patient’s pain had significantly improved, the markings were the same. They remained the same size and shape upon discharge. The patient was advised to follow up with a neurologist for further management. When the patient was then later contacted, the markings had disappeared on their own a few days later (Fig. ).
Our top differential diagnosis was migraines, as the patient’s history was classic of migraines. But we also thought about the possibility of a brain tumor, tension headaches, cluster headaches, and even possibly a vascular disorder. Acute headache causes were ruled out due to the patient’s history of frequent similar episodes of headaches. As the patient has been fully worked up, we ruled out most pathologies including a brain tumor as the MRI was reported normal.
The clinical diagnosis was migraines with cutaneous manifestations.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [148.0, 'mm hg'], 'Diastolic Blood Pressure': [91.0, 'mm hg']}",110,104.5,115.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 148.0 mm Hg + 2/3 * 91.0 mm Hg = 110.0 mm Hg.
Hence, the patient's mean arterial pressure is 110.0 mm Hg."
1202,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5122644-1,Extracted,"A 73-year-old woman with long-standing ankylosing spondylitis treated with adalimumab presented to an emergency department complaining of chest pain and dyspnea for 5 days. Her husband had died 10 days previously, causing her severe emotional stress. Her heart rate was 112 beats/min, and blood pressure was 102/68 mm Hg. A grade 4/6 holosystolic murmur was audible at the apex. An electrocardiography showed prominent ST-segment elevation in leads V2–5 (). Troponin I was 1.3 ng/mL (reference range, <0.12 ng/mL) and creatine kinase was 141 U/L (reference range, 55–170 U/L). Bedside echocardiography showed an akinesis from the mid to apical left ventricle, but preserved systolic function within the basal segment (). Left ventricular ejection fraction was 58% and flow acceleration in left ventricular outflow tract was not noted by color Doppler. Right ventricular systolic function was also reduced, particularly within the mid to apical segments. Estimated pulmonary artery systolic pressure was 59 mm Hg. In addition, a ventricular septal defect resulting from apical septal rupture with a left-to-right shunt was noted (). Pericardial effusion was not present in the initial echocardiographic assessment. Angiography demonstrated no significant stenosis of the epicardial coronary arteries (), suggesting the diagnosis of ventricular septal rupture complicated by takotsubo cardiomyopathy with right ventricular involvement.
The patient was taken to the operating room 3 hours after admission for emergency repair of the ventricular septal rupture. However, immediately before induction of anesthesia, her blood pressure suddenly collapsed with pulseless electrical activity. After 5 minutes of resuscitation, cardiac activity was restored. Sternotomy was done, and the pericardium full of fresh blood was found. Both left and right ventricles had necrotic changes with hemorrhage (). Cardiopulmonary bypass was established and the apex was incised. Ventricular septal wall rupture was confirmed (). Also, another rupture within the right ventricular free wall measuring 20×18 mm was noted (), which had led to the cardiac tamponade that presented in the operating room. Patch closure of the ventricular septal rupture with right ventriculoplasty was performed. Pathological examination of the ruptured ventricular septum revealed disrupted myocytic integrity in multiple foci with lymphohistiocytic infiltrate and myocytic necrosis (). Although she was sent to the intensive care unit after weaning of the cardiopulmonary bypass, extracorporeal membrane oxygenation support was required because of refractory shock 4 hours after surgery. The patient died 5 days after admission.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [68.0, 'mm hg'], 'Systolic Blood Pressure': [102.0, 'mm hg']}",79.33333,75.36666,83.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 102.0 mm Hg + 2/3 * 68.0 mm Hg = 79.33333 mm Hg.
Hence, the patient's mean arterial pressure is 79.33333 mm Hg."
1203,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5136770-1,Extracted,"A previously healthy 2-year-old Caucasian boy was brought to the Emergency Room (ER) of a local hospital because of few hour history of high fever, not relieved by antipyretic treatment. Physical examination revealed a febrile [body temperature (BT) of 39.2°C], severely ill, extremely irritable child with heart rate of 170/min, blood pressure of 98/51 mmHg and petechial lesions disseminated on the torso and limbs. Suspecting meningococcemia, intravenous (IV) fluids and ceftriaxone had been immediately administered. Due to hypotension, despite massive IV fluids resuscitation, after neurological deterioration the child required inotropic support, intubation and mechanical ventilation before being transferred to the pediatric Intensive Care Unit (PICU) of our Pediatrics Department. Neisseria meningitidis serogroup B was isolated from the blood culture drawn in the ER while a cerebrospinal fluid sample was normal on biochemistry, microscopy and culture.
After PICU admission antibiotic therapy with ceftriaxone was continued with gradual improvement of the patient’s general conditions and inflammatory markers levels [C-reactive protein (CRP) decreased from 345 mg/L after admission to 48.4 mg/L on day 9 (normal value up to 6 mg/L)]. On day 5 inotropic agents were stopped and on day 7 the child was extubated. Despite the general improvement, he continued to present spikes of fever (BT of 38.5°C). Suspecting a hospital acquired infection, a broader antibiotic therapy with ceftriaxone, gentamicin and teicoplanin was started. Blood and urine cultures and a lumbar puncture yielded negative results. Chest X-ray and brain magnetic resonance imaging (MRI) didn’t show any sign of an ongoing infection. On his transfer to the General Pediatrics Unit (GPU) on day 13, he was stable but still febrile (BT of 38.5°C). Physical examination was unremarkable except for the presence of numerous cutaneous ulcers in different stages of scarring. Blood tests showed: hemoglobin (HB) 8.1 g/L, red blood cells 3,050,000/mm, mean corpuscular volume (MCV) 80.6 fl, white blood cell (WBC) count 25,830/mm [polymorphonuclear leucocytes (PMN) 16,140/mm], Platelets (PLT) count 1.090.000/mm and stable CRP (44.80 mg/L). During the first week (days 13-20) in the GPU child remained febrile with BTs always <39°C with one or two spikes per day. On day 21 his conditions worsened despite broad-spectrum antibiotic treatment. He became extremely irritable with more frequent (every 6-8 hours) fever spikes that reached higher temperatures (BT>39°C). CRP (89.70 mg/L), erythrocyte sedimentation rate (ESR) (36 mm/h with normal value 0-15), Ferritin (173 ug/L with normal value 7–140), neopterine (31.0 nmol/L with normal up to 10 nmol/L) and TNF (29.8 ng/L with normal value up to 8.1 ng/L) confirmed the persistence of the inflammatory state. Due to the worsening of general conditions antibiotic therapy was broadened with meropenem and teicoplanin and a new set of cultures was collected. All the cultures collected resulted negative and gradually, from day 22, the child developed erythematouspapular rash, hepatomegaly, and remarkable bilateral cervical lymphadenopathy. Suspecting a viral infection, serological tests for Adenovirus, EBV, CMV and Parvovirus B19 were performed and came back negative on day 25. Neck ultrasound showed only the presence of reactive lymph nodes. Considering the high suspicion of a vasculitis as atypical Kawasaki, an electrocardiogram and echocardiography were performed. The first was normal and the second showed: No atrial shunt, no mitral or tricuspid regurgitation, good biventricular contractility. Hyper echogenicity of mitral papillary muscles, outflows free, normal coronaries. On day 26 one dose IVIG was administered at a dose of 2 g/kg with no effect on the fever spikes. So on day 28 IVIG administration had been repeated still with poor clinical improvement. On day 29 his blood tests showed: HB 7.4 g/dL, RBC 3,050,000/mm, MCV 76.4 fl, WBC count 23,470/mm, PMN 11,050/mm, PLT count 98,000/mm, LDH 1091 U/L, normal renal function, albumin 31 g/L, AST 86 IU/L, ALT 117 IU/L, GGT 300 U/L, sodium 135 mmol/L, triglycerides 361 mg/dL (normal value <150 mg/dL) with coagulation pattern compatible with severe discoagulopathy with prolongation of prothrombin (15%) and activated partial thromboplastin time (45 sec), fibrinogen 1 g/L (normal value 1.5-4.5 g/L). Fever remained high (BT>39°C) and CRP elevated (64.70 mg/L). Vitamin K and fresh frozen plasma were administered with normalization of coagulation pattern. Bone marrow aspirate showed no signs of hemophagocytic lymphohistiocytosis. Furthermore, from day 30 the child gradually presented conjunctival injection, fissured dry lips and facial and feet edema, matching all criteria for KD. Suspecting KD unresponsive to IVIG complicated by MAS on day 32 IVMP at a dose of 30 mg/kg for 2 consecutive days was administered.
In the following days inflammatory markers gradually decreased (CRP 3.36 mg/L on day 35) and fever spikes reduced. On day 37 the child finally remained afebrile. Before discharge no cardiac worsening on follow-up echocardiogram was documented.
Follow up at 3 months after the onset of his illness showed a healthy child with normal physical examination, laboratory tests, inflammatory markers and ECG were normal and follow-up echocardiogram confirmed no cardiac worsening.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [98.0, 'mm hg'], 'Diastolic Blood Pressure': [51.0, 'mm hg']}",66.66667,63.33334,70,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 98.0 mm Hg + 2/3 * 51.0 mm Hg = 66.66667 mm Hg.
Hence, the patient's mean arterial pressure is 66.66667 mm Hg."
1204,5,Mean Arterial Pressure (MAP),physical,decimal,trec-cds-2015-4,Extracted,"An 82-year-old woman comes to the emergency department because of chest pain and shortness of breath after being awakened in the morning by stabbing substernal chest pain radiating to the left shoulder and jaw. The patient had hypertension, renal-artery stenosis with chronic renal insufficiency, hypercholesterolemia, osteoporosis and dementia. Blood pressure was 199/108 mm Hg, respiratory rate 18 bpm, oxygen saturation 98% on ambient air. The heart sounds were rapid and with no murmurs. CK-MB was 10.9 ng/ml, CK was 89 U/l, CK index was 12.2% and Troponin T was 0.40 ng/ml. An EKG showed sinus regular tachycardia of 119 bpm, with ST-segment elevations up to 3 mm in V1, V2, and V3. A chest radiograph showed low lung volumes and right basilar subsegmental atelectasis. Coronary angiography showed no stenosis or clinically significant disease. Left ventriculography revealed akinesis of the anterior wall, hypokinesis of the apical and distal inferior walls, and compensatory hyperkinesis of the basal anterior and basal inferior walls. A transthoracic echocardiogram showed severe segmental left ventricular dysfunction involving the septum, anteroseptal territory, and apex. The overall left ventricular systolic function was mildly impaired and there was mild mitral regurgitation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [199.0, 'mm hg'], 'Diastolic Blood Pressure': [108.0, 'mm hg']}",138.33333,131.41666,145.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 199.0 mm Hg + 2/3 * 108.0 mm Hg = 138.33333 mm Hg.
Hence, the patient's mean arterial pressure is 138.33333 mm Hg."
1205,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8537463-1,Extracted,"PCM, 18 years old, female, from the Gorj County, was admitted on 21 September 2019 to the Infectious Diseases Department with high fever (39–40 °C), chills, intense sore throat and headache. The onset of the disease was two weeks earlier with fever and sore throat. She had consulted the general practitioner who established the diagnosis of exudative tonsillitis and recommended treatment with 625 mg amoxicillin/clavulanate three times per day and 200 mg ibuprofen two times per day. The patient followed the treatment for 12 days, but the condition worsened, the fever gradually went up and a bulge appeared on the left side of the neck.
Her past medical history was inconspicuous; the patient denied consumption of tobacco, alcohol, recreational drugs or oral birth control drugs. She had received all the mandatory immunization (according to the Romanian national program).
There was no contact with other sick persons with similar symptoms.
When she was admitted to the hospital, her general condition was consistent with moderate sepsis; she had fever (38.9 °C), elevated pulse rate (137 bpm), normal blood pressure (116/74 mm Hg) and normal oxygen saturation (97%). A significant lymph nodes enlargement (about 6 cm in diameter) was noted on the left side of the neck, in front and behind the sternocleidomastoid muscle, and left supraclavicular adenopathy; there was limited movement of the enlarged lymph nodes and they were hard on palpation. Both tonsils showed white exudate on their surface. There was no abnormal lung or heart sounds, no liver or spleen enlargement and no neurological abnormalities. The urine output was normal.
The initial laboratory tests are shown in .
The chest X-ray showed consolidation on the lower right lobe. An ultrasound of the left side of the neck highlighted the lymph nodes enlargement, intense vascularization and a deep edema. A computed tomography (CT) of the neck (see and ) and the upper thorax showed segmental partial thrombosis of the left internal jugular vein. The Ear-Nose-Throat (ENT) examination established the diagnosis of cryptic tonsillitis and cervical adenitis.
The throat swab culture on blood agar media and blood culture using BACTEC vials for aerobic germs were negative. An enzyme-linked immunosorbent assay (ELISA) test for HIV was also negative.
The diagnosis of Lemierre’s syndrome was established and the initial prognosis was reserved (the patient met the old criteria for sepsis); she started antimicrobial treatment with penicillin G, 4 international megaunits (MUI)/day, intravenous (i.v.), and metronidazole, 1.5 g/day, per os (p.o.). She also received enoxaparin, 0.6 mL twice a day, s.c., and diclofenac, 100 mg/day, p.o.
The fever gradually decreased, the patient returned to normal temperature after 6 days of treatment, and the general condition improved; however, the lymph nodes remained enlarged throughout the period of hospital admission.
The follow-up laboratory tests are shown in .
The patient was discharged after 16 days; she received a prescription for metronidazole, 1.5 g/day, p.o., for another 14 days and for rivaroxaban, 20 mg/day, p.o., for 30 days; she continued with this regimen at home as recommended.
A month later, she was seen in our department: she was in good condition, there were no signs of infection, but the ultrasound still showed signs of thrombosis of the jugular vein. She refused the surgical intervention to remove the thrombus.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [116.0, 'mm hg'], 'Diastolic Blood Pressure': [74.0, 'mm hg']}",88,83.6,92.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 116.0 mm Hg + 2/3 * 74.0 mm Hg = 88.0 mm Hg.
Hence, the patient's mean arterial pressure is 88.0 mm Hg."
1206,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-2881,Extracted,A 25-year-old man comes to the emergency department because of a 1-week-history of progressively worsening dyspnea and intermittent chest pain that increases on inspiration. He had an upper respiratory tract infection 2 weeks ago. His pulse is 115/min and blood pressure is 100/65 mm Hg. Examination shows inspiratory crackles bilaterally. His serum troponin I is 0.21 ng/mL (N < 0.1). An x-ray of the chest shows an enlarged cardiac silhouette and prominent vascular markings in both lung fields; costophrenic angles are blunted. A rhythm strip shows inverted T waves.,What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",76.66667,72.83334,80.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 65.0 mm Hg = 76.66667 mm Hg.
Hence, the patient's mean arterial pressure is 76.66667 mm Hg."
1207,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8289678-1,Extracted,"We report a case of a 30-year-old male with a history of hidradenitis suppurativa presented to our clinics with flare up of his disease with perineal and bilateral axillary ulcerative and purulent lesions. The history of his disease dates back to the age of 18 when he was treated medically with Etanercept and kept off symptoms for 10 years, after which he was treated surgically with repetitive incisions and debridement of recurrent small abscesses until this presentation.
On physical examination, the patient was febrile (temperature = 40.1°C), tachycardic (110 beats per minute), normotensive (blood pressure = 120/80 mmHg), and he had normal oxygen saturation (SpO
2
 = 97%). Multiple scares were noted over all his body, large bilateral axillary Hurley stage 2 abscesses, and perineal Hurley stage 3 lesions were noted. They were hot and tender to touch and with purulent secretions.
Moreover, the patient's laboratory studies revealed leukocytosis (white blood cell = 21,200/μL) and CRP (220 mg/L). Interestingly, Magnetic resonance imaging of the pelvis showed complex trans-sphincteric fistula at 12 o'clock with the presence of intersphincteric, anterior perirectal, and right ischial anal fossa abscesses as well as a fistulous tract within the right perineum, right buttocks, and extending from the perineum anteriorly to the intergluteal cleft posteriorly (
). Computed tomography of the chest showed cutaneous thickening associated with multiple air pockets bilaterally and almost symmetrically, with evidence of well circumscribed collections.
Broad spectrum antibiotherapy was started as well as multiple attempts of debridement, within few days interval, as a primary treatment of sepsis. Culture samples were in favor of carbapenem-resistant Enterobacteriaceae growth.
After a 6-week regimen of antibiotics, a radical excision of the lesions was done, keeping behind a wide open wound of perineum (
) and bilateral wounds of axillae (
). On day 2, a protective side colostomy was done at the level of the descending colon to divert feces.
Negative pressure wound therapy (Genadyne's NPWT) was initiated over the three open wounds and continued for 2 months after surgery until the granulation tissue formation was noted (
).
The patient then benefited from intraoperative skin substitutes (Integra Dermal Regeneration template) placement over the open wounds and fixation with staples (
and
).
About 3 weeks postinsertion, the follow-up demonstrated good uptake of the graft without breakdown. Surgical staples were removed and patient was discharged home with instruction of wet to dry dressing with active Leptospermum honey (MEDIHONEY Gel) (
and
).
Moreover, 1-year follow-up showed no recurrence and preservation of patient functionality (
). Re-establishment of continuity of bowels done and patient discharged home without complications.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1208,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7105261-1,Extracted,"A 28-year-old female, with no known comorbidities, presented to the outpatient department with complaints of left upper abdominal pain and swelling for four to five years. The pain was spontaneous in onset, severe in intensity, radiating to the back and relieved on rest. It was not associated with food intake. The abdominal distension was gradually increasing in size. There was no history of fever or bleeding per rectum. Later she developed shortness of breath, nausea, and early satiety. Her past history was insignificant.
On examination, her blood pressure was 130/85 mm Hg, respiratory rate was 18 breaths per minute, and heart rate was 75 beats per minute. Abdominal examination revealed a soft, non-tender, grossly distended abdomen with centrally placed umbilicus. Splenic notch was palpable up to the umbilicus, firm and smooth in contour with regular margins. Bowel sounds were resonant. Neurological examination showed no focal neurological deficits with a Glasgow Coma Score of 15/15. Rest of the systemic examination was insignificant.
Laboratory evaluation on admission revealed hemoglobin (Hb) of 7.8 g/dL [normal (N)=12-15.5], hematocrit of 26% (N=36-46), mean corpuscular volume of 74 fL (N=80-100), mean corpuscular hemoglobin (MCH) of 22 pg (N=27-32), MCH concentration of 30 g/dL (N=31.5-34.5), total leukocyte count of 2.4x109/L (N=4-10), and platelet count of 22x109/L (N=150-400). Peripheral blood film depicted anisocytosis, poikilocytosis, hypochromia, and pancytopenia with teardrop cells. Considering the history of anemia, serum iron, red blood cell folate, and vitamin B12 were checked, which were found as 26 ug/dL (N=26-170), 1600.3 ng/mL (N=499-1504), and 294 pg/mL (N=206-678), respectively. The direct and indirect Coombs tests were negative. Serum electrolytes were also within normal ranges.
The AUS report showed altered echotexture of the liver, grossly enlarged spleen measuring about 23 cm with dilated SV (1.2 cm) and mild ascites. In addition, chronic thrombosis with CTPV and few splenic varices at splenic hilum were observed in the Doppler study (Figures , ).
Liver function tests (LFTs) showed total bilirubin of 0.9 mg/dL (N≤1.2), serum glutamic oxaloacetic transaminase of 20 U/L (N≤31), and alkaline phosphatase (ALP) of 26 IU/L (N=44-147), and gamma-glutamyl transferase of 16 U/L (N≤38). Viral markers were absent.
Keeping in view the abnormal Doppler study directed towards a procoagulant state, the patient was further considered for a detailed coagulation profile (Table ).
Multiple axial sections of CT scan of the abdomen and pelvis were carried out after non-ionic intravascular contrast enhancement. The liver with slight undulating margins and markedly attenuated caliber of PV up to the portosplenic confluence (6 mm approximately) with chronic intraluminal thrombus were observed. Multiple collaterals were formed at porta hepatis in keeping with the cavernous transformation (Figures , ).
This caused compression over the common bile duct at the porta hepatis resulting in mild prominence of intrahepatic biliary ducts. The spleen was markedly enlarged measuring approximately 21 cm. Extensive collateral vessels were seen at the splenic hilum in the peripancreatic and perirectal regions. A significant fat stranding was identified in the region of porta hepatis and in the root of mesentery with multiple prominent mesenteric lymph nodes. Upper gastrointestinal endoscopy revealed grade II esophageal varices (Figure ). A final diagnosis of chronic non-cirrhotic PVT leading to massive splenomegaly with esophageal varices secondary to protein C and S deficiency was established.
As the thrombus in the PV was organized, thrombectomy could not be performed. A decision of splenectomy with end-to-side surgical shunting via SRS was made. Considering the patient was severely anemic and predisposed to several infections post-splenectomy, the Hb was initially improved to 10 g/dL along with vaccination against encapsulated organisms. Five pints of human blood was arranged before surgery to compensate for the blood loss during splenectomy.
Two weeks later, the patient underwent splenectomy with end-to-side SRS construction. The splenic artery was ligated, and the SV was clamped and divided. The remaining attachments of spleen were then divided, and spleen was removed en bloc. The SV was freed up to its confluence with the inferior mesenteric vein. The left renal vein (RV) was isolated through an incision over the renal hilum. The renal artery was clamped, and the SV was brought to the RV. An end-to-side splenorenal anastomosis was performed once an optimal length of the SV was obtained. Due to extensive bleeding, the patient was transfused with four pints of blood. Post-operatively, the patient was maintained on life-long anticoagulant therapy with frequent follow-ups.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 85.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1209,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4636106-1,Extracted,"A 48-year-old man was brought to the emergency care unit with a 2-week history of malaise and headache followed by abnormal behavior over the last week, when he presented a depressed mood and an alteration in his mental status with disorientation, uncooperativeness, and self-aggressiveness. Indeed, the patient attempted suicide by trying to hang himself. There was no history of any previous similar episodes, psychiatric diseases, fever, other signs of infection, head trauma, or abuse of illegal substances.
The patient was previously diagnosed with hypertension and diabetes mellitus, and was taking enalapril, metformin and glicazide. There were no reports of tobacco or alcohol consumption, nor any familial history of psychiatric diseases.
On the initial examination, the patient was ruddy, afebrile, and hydrated. His heart rate was 87 beats per minute; arterial pressure was 140/110 mmHg, respiratory rate was 14 breaths per minute; and capillary glycemia was 237 mg/dL.
The cardiovascular, pulmonary, abdominal, and skin examination was normal. The mental status on admission showed a Glasgow Coma Scale (GCS) of 10, and he was uncooperative, inattentive, and disorientated. His pupils were normal and no motor deficit was detected.
The initial laboratory work-up and the brain computerized tomography were normal. A cerebrospinal fluid (CSF) examination (lumbar puncture) was performed and the results are presented in . The diagnosis of encephalitis due to the herpes simplex virus (HSV) was suspected and intravenous acyclovir was promptly prescribed, as recommended by Studahl et al.. Polymerase chain reaction for HSV was not requested due to its unavailability. The electroencephalogram was normal.
After 7 days of anti-viral therapy (acyclovir, 10 mg/kg, tree times daily), no clinical improvement was observed, and indeed a new CSF examination resulted in worsened cytological and biochemical parameters (). Therefore, serum fluorescent treponemal antibody and the Venereal Disease Research Laboratory (VDRL) were requested that resulted positive. The VDRL title was 1/128. The VDRL in the CSF also resulted in the same title (1/128). shows the electrophorectic profile of the CSF proteins. Intravenous crystalline G penicillin at a dosage of 24 million units per day in six divided doses over 14 days was prescribed and acyclovir was discontinued on the eighth day. The magnetic resonance imaging (MRI) of the brain revealed oval spots of hyperintensity on T2-weighted and fluid attenuated inversion recovery (FLAIR) sequences involving subcortical white matter of the superior frontal gyri.
Marked clinical improvement was observed after 30 hours of antibiotic therapy. The patient achieved a GCS of 15 and started managing his basic daily living activities. However, he started complaining of visual and auditory hallucinations with persecutory content that were controlled after the administration of risperidone.
At the end of the penicillin therapy, the patient’s wife reported his normal behavior. He was discharged to continue medical monitoring in the outpatient clinic.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [110.0, 'mm hg'], 'Systolic Blood Pressure': [140.0, 'mm hg']}",120,114,126,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 110.0 mm Hg = 120.0 mm Hg.
Hence, the patient's mean arterial pressure is 120.0 mm Hg."
1210,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4416286-1,Extracted,"A 52-year old Cameroonian male patient with history of HIV infection diagnosed four years earlier, current cigarette smoking and heavy alcohol consumption for more than ten years was referred to the cardiology department of the Yaounde Central hospital for gradually worsening shortness of breath on minimal exertion, fatigue, persistent dry cough, lower extremity swelling of about two weeks duration. He did not have any history of hypertension or family history of heart disease. His HIV treatment regimen consisted of zidovudine, nevirapine and efavirenz. On admission he was alert and awake, but complained of mild respiratory distress. His vital parameters were: heart rate at 110 beats per minute and a blood pressure of 102/83 mmHg. There was elevated jugular venous pressure, displaced apex beat to the 6th intercostal space, bilateral basal rales, and lower extremity edema. The heart sounds were faint, with frequent premature beats; there was no S3 and no murmurs. Relevant laboratory tests were within normal limits.
Chest x-ray showed cardiomegaly, bilateral interstitial infiltrates. Serologies for hepatitis B and C were negative. He had a CD4 count of 135/mm3. The electrocardiogram showed sinus rhythm, poor R wave progression in precordials, with pathological Q waves in leads V1, V2, V3, V4, V5, leads I and aVL. Two-dimensional Echocardiography demonstrated a dilated left ventricle (Figure ) with severe left ventricular systolic dysfunction (ejection fraction = 20%), with akinesis of the apex and, hypokinesis of the other segments of the left ventricle. There was mild mitral and severe tricuspid regurgitation, dilatation of the inferior vena cava as well as right and left ventricular masses (Figures and ). Both masses were dense than myocardium, acoustically distinct from underlying myocardium, well circumscribed, filling the apex of the left ventricle and the right ventricle. The right ventricular mass measured 28.7 mm × 33.9 mm while the left ventricular mass measured 29.5 mm × 45 mm. The masses were not mobile and prominent in the apical four chamber view. Bilateral ventricular thrombi were diagnosed. Cardiac catherization was not performed to explore the coronary anatomy. The diagnosis of dilated cardiomyopathy was made, complicated with biventricular thrombi in an HIV infected patient. There was no clinical evidence of thrombosis at other sites. Conventional treatment for congestive heart failure was started with loop diuretics and angiotensin converting enzyme inhibitors and he showed significant improvement of symptoms. Low molecular weight heparin was administered for the biventricular thrombi which was later on substituted with oral vitamin K antagonist (acenocoumarol) after overlapping with a target international normalized ratio (INR) between 2 and 3. The patient was discharged on day 12 on oral anticoagulation after he was reviewed by the HIV specialist. Six months later, a control echocardiography showed a near complete dissolution of the right ventricular thrombus and a marked decrease in the left ventricular thrombus (Figure ); there was no evidence of neither pulmonary nor systemic embolization. Follow up INR were sub-therapeutic and the patient did not turn up for regular scheduled follow up visits to assess efficacy of anticoagulation and dose adjustments. There was no bleeding related to oral anticoagulation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [102.0, 'mm hg'], 'Diastolic Blood Pressure': [83.0, 'mm hg']}",89.33333,84.86666,93.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 102.0 mm Hg + 2/3 * 83.0 mm Hg = 89.33333 mm Hg.
Hence, the patient's mean arterial pressure is 89.33333 mm Hg."
1211,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7385607-1,Extracted,"A 58-year-old woman presented with lower abdominal pain from the deep pelvis and frequent failure of flatulence for 4 mo.
She was referred from a department of gynecology and diagnosed with a suspicious leiomyosarcoma of the rectum or a pedunculated myoma of the uterus after colonoscopy and abdominopelvic computed tomography (CT) in a previous hospital. She visited the outpatient clinic after 10 d and was transferred to the emergency center because of severe lower left abdominal pain on 2 d before her scheduled admission. She had nausea, vomiting, and non-whirling dizziness. She was diagnosed with colonic cancer perforation with an abscess and was admitted for antibiotic treatment. We ensured that the acute septic condition was stabilized, and the patient underwent operation.
She had no co-morbid disease.
On digital rectal examination, a circumferential fungating mass with a central ulceration was palpated 8 cm from the anal verge, and it was fixed in the pelvic cavity. In the emergency center, the patient’s body temperature was 38.9 °C. The systolic and diastolic blood pressures were 110 mmHg and 70 mmHg respectively, pulse rate was 78 beats per minute, and respiratory rate was 20 breaths per minute.
Laboratory results were as follows: White blood cell count (23900/µL; 93.9% of neutrophil), hemoglobin (11.6 g/dL), platelet count (416000/µL), C-reactive protein (16.14 mg/dL), lipase (9 IU/L), albumin (3.2 g/dL), alkaline phosphatase (265 IU/L), sodium (132 mEq/L), chloride (93 mEq/L), and prothrombin time percentage (73.2%).
Chest X-ray showed a nodule in the right upper lung field. Besides this, there was no active lesion in the lungs. Colonoscopy revealed a huge submucosal mass-like lesion with focal ulceration located 8 to 15 cm from the anal verge. Abdominopelvic CT showed a poorly marginated mass measuring 7.4 cm × 6.3 cm × 5.5 cm in size located between the rectum and uterus and separated from the uterus by fat tissues. The mass had focal non-enhancing lesions without lymph node enlargement. To rule out the origin of the mass, the patient underwent pelvic magnetic resonance imaging (MRI) before the operation. MRI revealed an exophytic growing mass with a maximum diameter of 7.2 cm at the right lateral wall of the rectum with an internal cystic portion and hemorrhage, multiple lymph node enlargement at the iliac bifurcations, obturator, and presacral areas, and a 2.2-cm-sized multiseptated cystic mass in the fundus of uterus (Figure ). Positron emission tomography-CT revealed a high possibility of a malignant tissue with a hypermetabolic mass (SUVmax = 15.1) and cystic changes in the rectum, and this lesion was considered to directly invade the adjacent uterus. Multifocal FDG uptake (SUVmax = 4.0) was observed in the left common iliac, perirectal area, and presacral area (Figure ).
The tumor was a polypoid mass measuring 10 cm × 4 cm × 4 cm in size, and it invaded left ovary and salpinx via the serosal membrane (Figure ). No lymph node metastasis, lymphovascular invasion, or perineural invasion was observed. Microscopically, the tumor was a cellular mass that had a solid growth pattern with few glandular structures and many foci of intratumoral necrosis. Tumor cells had elongated nuclei and scant cytoplasm. Mitotic figures, including atypical ones, were also frequently observed. At the boundary between the tumor and normal tissue, tumor cells were arranged in a palisading pattern, resembling basal cell carcinomas of the skin (Figure ). Immunohistochemical examinations revealed that the tumor cells were focally positive for cytokeratin (CK) 7, p63, and Pan-CK and were negative for CK20; neuroendocrine markers, such as synaptophysin and CD56; and mesenchymal cell markers, including CD34, CD117, desmin, S100 protein, and α-smooth muscle actin. Additionally, the tumor cells were negative for vimentin, WT-1, calretinin, CD99, TTF-1, and CDX2.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1212,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7584818-1,Extracted,"A 70-year-old female was brought with history of one episode of generalized tonic–clonic seizure lasting for less than 1 minute. The episode was associated with frothing from mouth, with no tongue bite or bowel and bladder incontinence. She had a post-ictal phase lasting for about 15 minutes. There were no seizure episodes in the past. She also complained of frequent muscle cramps for the past 3 months. She was diagnosed to have coronary artery disease (triple-vessel disease) about 1 month ago and advised coronary artery bypass graft (CABG). Her oral medication list comprised of aspirin (75 mg once daily), clopidogrel (75 mg once daily), atorvastatin (40 mg once daily), glyceryl trinitrate sustained release (2.6 mg twice daily), torsemide (5 mg once daily), and metoprolol (25 mg twice daily). She was mainly confined to her house, and her diet was devoid of milk and milk products for many years.
On presentation, she was conscious and oriented. She was afebrile, with pulse rate of 80/minutes, blood pressure 130/80 mm Hg, and respiratory rate 20/minutes (with saturation 94% rom air). Her systemic examinations were normal, with no signs of meningeal irritation. Trousseau sign was positive but Chvostek sign was negative.
Her blood investigations such as complete blood counts, renal and liver functions, electrolytes, random blood glucose, HbA1c, TSH, and plasma ammonia were normal. Serum calcium was 6.4 mg/dL, serum albumin was 2.9 mg/dL, and corrected calcium was 6.9 mg/dL (8.7–10.2). Serum magnesium and phosphorus were normal. Vitamin D3 level was 7 ng/mL (30–100), and PTH levels were 324 ng/L (8–51). Computed tomography of the brain showed diffuse age-related atrophic changes, electroencephalogram was suggestive of diffuse cerebral dysfunction (high amplitude activity with slow waves in the posterior head regions which were bilaterally responsive to eye opening; no epileptiform activities were seen), and cerebrospinal fluid analysis was normal. Electrocardiography showed mild ST-segment depression in anterolateral leads with T-wave inversion in V1-4, T-wave flattening in V5-6 with QT prolonged (), and echocardiography had regional wall motion abnormality, mild mitral regurgitation, and moderate left ventricular systolic and diastolic dysfunction with 35% ejection fraction. Ultrasound of her neck did not show any thyroid or parathyroid abnormality. Ultrasound of abdomen and chest X-ray were normal. Her 24-hour urinary calcium was normal (100 mg).
She was given single bolus dose of intramuscular cholecalciferol (3 lakh IU) and intravenous 10% calcium gluconate (20 mL), followed by 10% calcium gluconate infusion (1.5 mg/kg/hour). Oral sodium valproate (300 mg twice daily) was started in view of possibility of recurrence of seizure. Her serial calcium levels started showing an increasing trend and got normalized (9.3 mg/dL) by day 4 of admission. Calcium infusion was stopped and changed to combination tablet of calcium carbonate (500 mg elemental calcium) with vitamin D3 (250 IU) thrice daily, along with oral calcitriol (0.25 μg twice daily). Following normalization of calcium levels, she was taken up for CABG. Her postoperative period was uneventful and was discharged on day 10 of admission on oral calcium with vitamin D3 (500 mg/250 IU once daily), calcitriol (0.25 mg once daily), sodium valproate (300 mg twice daily), aspirin (75 mg once daily), clopidogrel (75 mg once daily), atorvastatin (40 mg once daily), glyceryl trinitrate sustained release (6.4 mg twice daily), torsemide (10 mg once daily), and metoprolol (25 mg twice daily). On review after 2 weeks, her calcium levels were normal. Calcitriol was stopped, and oral calcium with vitamin D3 (500 mg/250 IU once daily) was continued. Her calcium, parathyroid hormone, and vitamin D3 levels after 1 month of CABG were 9.2 mg/dL, 34 ng/L, and 47 ng/mL, respectively. She did not have any further episodes of seizure. Sodium valproate was tapered and stopped, with continuation of oral calcium with vitamin D3 (500 mg/250 IU once daily) along with routine cardiac medications. She was advised milk and milk products in her diet and regular monthly monitoring of calcium and vitamin D3 levels. The course of her calcium levels is depicted in .",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1213,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7891267-1,Extracted,"A 54-year-old woman presented to the emergency department with abdominal pain and bilateral lower limb swelling. She had a 1-year history of recurrent episodes of dyspnoea with dry cough and was managed as bronchial asthma. Despite appropriate treatment, her symptoms persisted. She also complained of dysphagia, palpitations without noticeable chest pain and feeling dizzy when leaning forward. On admission, she was haemodynamically stable, with normal blood pressure (120/78 mmHg) and pulse (72 beats/min). Examination revealed normal heart sounds, no murmurs, bilateral peripheral pitting oedema, and no other remarkable findings.
Electrocardiogram showed normal regular sinus rhythm, bifid P waves, and no ischaemic changes (). Laboratory findings, including blood culture, were normal. Chest X-ray showed accentuated vascular markings bilaterally with diffuse reticular peripheral and basal lines, suggestive of pulmonary congestion (). Consequently, a transthoracic echocardiography (TTE) was done which revealed a Grade III diastolic dysfunction with normal left ventricular systolic function. No regional wall motion abnormality was noted; however, moderate mitral and tricuspid regurgitations were observed on Doppler ultrasound. Additionally, it showed a large pedunculated mass (Video 1), approximately 9 × 7 cm attached to the upper third of the atrial septum, as well as severe pulmonary arterial hypertension (PAH) (84 mmHg) with a competent pulmonary valve.
Preoperative transoesophageal echocardiography (TOE) () was performed and confirmed the presence of a huge mobile mass filling the LA. It had a heterogenic core of multiple lucent areas and a smooth outer surface. On Doppler scan, a moderate degree of mitral and tricuspid regurgitation was evident by the presence of mosaic blood flow. Subsequently, a surgical excision was performed via conventional median sternotomy. In order to surgically approach such a huge tumour, it was decided to use the inverted T-shaped bi-atrial technique. A 3 cm incision was made in the LA parallel to the interatrial groove and anterior to the right superior pulmonary vein. Then, a second incision perpendicular to the first was made in the right atrium about 4 cm posterior to the interatrial groove towards the sulcus terminalis. The second incision met the first one near to its middle, forming an inverted T-shaped opening. At this point, the interatrial septum was divided towards the fossa ovalis. This revealed a pedunculated mass with a short stalk (about 1 cm in length), arising from the interatrial septum (IAS), at the fossa ovalis. The tumour, its stalk and part of the IAS were resected, followed by closure of the defect using a suture line without a pericardial patch. Due to presence of mitral regurgitation on TOE, two sutures were used opposite to the middle of the posterior mitral leaflet to reduce the size of the mitral ring, minimizing the leak (). Since the tricuspid valve showed mild regurgitation and intact anatomy, no intervention was required.
Macroscopically, the specimen measured 10 × 8 × 6 cm () and weighed 119 g (). The outer surface was smooth with punctate haemorrhage, whereas a cut surface showed a yellow-to-brown gelatinous material (). Microscopically, a low cellular myxoid growth with numerous cords, nests, and glandular pattern of stellate to spindled cells surrounded by eosinophilic to bluish matrix were observed. No mitotic figures or malignant features were seen. Additionally, there were cystic formations and vascular differentiation with occasional calcifications (). Five days after the operation, the patient’s condition improved uneventfully with complete resolution of her presenting symptoms. One week later, a follow-up echocardiography showed improvement of her heart function and normalization of PAH.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",92,87.4,96.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 78.0 mm Hg = 92.0 mm Hg.
Hence, the patient's mean arterial pressure is 92.0 mm Hg."
1214,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2639565-1,Extracted,"A 20 years old male patient admitted to our clinic complaining of fever, sweating, fatigue and lost of weight. He was referred by the secondary health centre in Gjakova, after ten days hospitalization for suspicious endocarditis. Four years ago he underwent atrial septal defect correction and implantation of pulmonary valve with Contegra® Pulmonary Valved Conduit in Lausanne, Switzerland. A murmur on the precordium was prescribed on his third month of life. During all his life he was enabled for enforced physical activity. He periodically complained of fatigue, dispnea and later on the cyanosis appeared. These signs and symptoms were aggravated on his age of 15th. At that time (four years ago) he was diagnosed and successfully operated for dysplastic pulmonary valve with its severe stenosis and severe regurgitation, severe dilatation of the right ventricle, pulmonary trunk and right pulmonary artery, as well as the type II atrial sepal defect.
On admission the blood pressure was 130/80 mmHg, pulse rate 100 beats/min., and body temperature 39°C. Heart auscultation revealed regular heart rhythm, clear sounds and systolic murmur 5/6 on the precordium with punctum maximum on the second right intercostal space. On lung auscultation there was normal findings. ECG showed normal sinus rhythm, heart rate of 100 beats/min., and right axis deviation.
Laboratory data showed: high erythrocite sedimentation (132 mm/h), low number of erythrocites (2.94 × 1012/mm3); low hemoglobin rate (8 g/dL), low hematocrite (24%), high number of leucocytes (19.7 × 103/mm3, high percentage of granylocites (82.7%), high urea (27 mmol/L) and creatinine (860 mmol/L) concentrations. All other laboratory findings were within normal reference range. Blood cultures revealed the MRSA infection.
Chest X-ray showed mild pleural adhesions in right diaphragmal localization, and the triangled heart shadow. The abdominal ultrasonographic examination showed splenomegaly and signs of diffuse glomerulonephritis.
Transthoracic echocardiography demonstrated the presence of the huge vegetation on the Contegra bovine leaflet, with dimensions 0.56 × 0.75 cm (Fig. ). Continuous wave Doppler assessment of the Contegra valve showed increased pressure gradient (maximal pressure gradient of 80 mmHg, Fig. ). Tricuspid valve was thickened, with its important prolapse (Fig. ). Severe tricuspid regurgitation, high trans-tricuspid pressure gradient (93 mmHg, Fig. ) and enlarged right heart chambers (right ventricle = 5.2 cm, right atrium = 6.9 cm) were registered.
The left atrium (3.6 cm), aortic root (3.1 cm), left ventricular dimensions (end systolic = 5.4 cm, end-systolic = 3.7 cm), thickens (interventricular septum = 0.9 cm, left ventricular posterior wall = 0.8 cm) and left ventricular systolic function (shortening function = 31%, ejection fraction = 59%) were within normal range. It was registered mild mitral regurgitation through mildly thickened mitral valve leaflets.
The patient was treated with beta-blockers, salycilates, antibiotics (Vancomycin and Gentamycin, which was reduced and stopped, because of renal failure that was aggravated during the hospitalization). Also, the transfusions with red blood cells were administrated for the anemia correction.
After three weeks of the intensive treatment, the patient was transferred to the cardiovascular center that performed the operation four years ago, for the re-correction of the pulmonary artery valve, in general stable conditions.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1215,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1635,Extracted,"A 27-year-old man comes to the physician because of worsening abdominal pain over the last several months. He has also had recent feelings of sadness and a lack of motivation at work, where he is employed as a computer programmer. He denies suicidal thoughts. He has a history of multiple kidney stones. He has a family history of thyroid cancer in his father and uncle, who both underwent thyroidectomy before age 30. His temperature is 37°C (98°F), blood pressure is 138/86 mm Hg, and pulse is 87/min. Physical examination shows diffuse tenderness over the abdomen and obesity but is otherwise unremarkable. Serum studies show:
Na+ 141 mEq/L
K+ 3.6 mEq/L
Glucose 144 mg/dL
Ca2+ 12.1 mg/dL
Albumin 4.1 g/dL
PTH 226 pg/mL (normal range 12–88 pg/mL)
Results of a RET gene test return abnormal. The physician refers him to an endocrine surgeon.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [86.0, 'mm hg'], 'Systolic Blood Pressure': [138.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 138.0 mm Hg + 2/3 * 86.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
1216,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7378,Extracted,"A 60-year-old man presents with breathlessness for the past 3 months. His symptoms have been getting progressively worse during this time. He denies any history of cough, fever, or chest pain. He works at a local shipyard and is responsible for installing the plumbing aboard the vessels. His past medical history is significant for hypertension for which he takes metoprolol every day. He denies smoking and any illicit drug use. His pulse is 74/min, respiratory rate is 14/min, blood pressure is 130/76 mm Hg, and temperature is 36.8°C (98.2°F). Physical examination is significant for fine bibasilar crackles at the end of inspiration without digital clubbing.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [76.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",94,89.3,98.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 76.0 mm Hg = 94.0 mm Hg.
Hence, the patient's mean arterial pressure is 94.0 mm Hg."
1217,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7463145-5,Extracted,"A girl named T, 5 years old, with acute lymphoblastic leukemia, 5th day of care. According to the mother, the child had complained of fever for five days. The peak fever was 39°C, Hb: 10.8 gr/dL, Ht: 30.4%, leukocytes: 8080/mm3, platelets: 25,000/mm3, ANC: 424/mm3, warmed acral, petechiae on both legs, BP: 90/60 mmHg, HR: 100 x/minute, RR: 25 x/minute, body temperature: 38.6°C, SpO2: 99%, BW: 16 kg, BH: 94 cm, LLA: 16 cm. The child had good nutritional status and ate half portions. The child’s hydration status was adequate, with a positive fluid balance and without any signs of overload. The child’s rest and sleep statuses were adequate.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [60.0, 'mm hg'], 'Systolic Blood Pressure': [90.0, 'mm hg']}",70,66.5,73.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 60.0 mm Hg = 70.0 mm Hg.
Hence, the patient's mean arterial pressure is 70.0 mm Hg."
1218,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3862585-2,Extracted,"A 17-year-old, 47 kg female patient with a diagnosis of FMF was admitted to a local hospital with the complaints of nausea and vomiting after taking 9.5 mg or 0.2 mg/kg (19 tablets of 0.5 mg) colchicine for suicide attempt. She underwent stomach lavage and treatment with activated charcoal at that facility, and was transferred to our hospital an hour after ingestion. She was conscious, responsive, and cooperative, and she had diarrhea. On physical examination she had a blood pressure of 125/55 mmHg, body temperature 36.5°C, respiratory rate 15 breaths/minute, and heart rate 70 beats/minute. The patient was pale and cold, and she had abdominal tenderness on palpation. Other system examinations were unremarkable. She was admitted to the intensive care unit. Her initial laboratory findings in the intensive care unit were WBC, 6.640 (103 μL); hemoglobin, 13 gr/dL; hematocrit, 40.3%; PLTs, 428,000/mm3; AST, 32 U/L; ALT, 21 U/L; sodium, 139 mmol/L; K, 4.1 mmol/L; Ca, 9.5 mmol/L; Total-CK, 112 U/L; CK-MB, 25 U/L; LDH, 156 U/L; troponin I, 0.00 ng/ml; D-dimer, 1,833.78 ng/L; INR, 1.14; BUN, 13 mg/dL; Cr, 0.7 mg/dL. Blood gas values were: pH, 7.48; pCO2, 21.2 mmHg; HCO3, 20.0 mmol/L; BE, −5.9 mmol/L. Following the recommendation of the contacted poison control center, gastric lavage was performed again and activated charcoal was given every hour for 6 hours (0.25 g/kg per hour) to reduce the intestinal colchicine absorption. Blood gas analyses were performed every 12 hours (). On follow-up of the patient, AST, ALT, Total-CK, CK-MB, troponin I, LDH, and INR remained normal (). Normal sinus rhythm was determined by electrocardiography, and echocardiography revealed the left ventricle had normal systolic function and an ejection fraction of 60%. She did not need hemodialysis and was transferred to the internal medicine service on the fifth day of her admission. The consultant psychiatrist diagnosed a depressive episode as the underlying cause for her suicide attempt. She recovered without sequelae and was discharged on the seventh day of her follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [55.0, 'mm hg']}",78.33333,74.41666,82.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 55.0 mm Hg = 78.33333 mm Hg.
Hence, the patient's mean arterial pressure is 78.33333 mm Hg."
1219,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4293,Extracted,"A 64-year-old man presents to his primary care physician's office for a routine check-up. His past medical history is significant for type 2 diabetes mellitus, hypertension, chronic atrial fibrillation, and ischemic cardiomyopathy. On his last visit three months ago, he was found to have hyperkalemia, at which time lisinopril and spironolactone were removed from his medication regimen. Currently, his medications include coumadin, aspirin, metformin, glyburide, metoprolol, furosemide, and amlodipine. His T is 37 C (98.6 F), BP 154/92 mm Hg, HR 80/min, and RR 16/min. His physical exam is notable for elevated jugular venous pressure, an S3 heart sound, and 1+ pitting pedal edema.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [154.0, 'mm hg'], 'Diastolic Blood Pressure': [92.0, 'mm hg']}",112.66667,107.03334,118.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 154.0 mm Hg + 2/3 * 92.0 mm Hg = 112.66667 mm Hg.
Hence, the patient's mean arterial pressure is 112.66667 mm Hg."
1220,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6820669-1,Extracted,"A 15-year-old girl from rural area was admitted with a history of fever with chills, headache, cough with scanty expectoration, and myalgia for five days duration. On examination, she was febrile (temperature 101°F), dehydrated and toxic appearing, tachypnoeic (26 breaths/min), and had pulse rate of 102/min and blood pressure of 100/60 mmHg with no skin rashes, eschar, and lymphadenopathy. Her systemic examination revealed tubular bronchial breathing in the left supraclavicular, infraclavicular, axillary, and suprascapular areas along with fine crepitations with SpO2 of 85%-90% in room air with normal cardiovascular status. Her abdominal and neurological examination was normal. The patient was diagnosed clinically to have left upper lobe consolidation with respiratory failure due to community-acquired pneumonia and started on injection ceftriaxone suspecting bacterial etiology along with oxygen after sending relevant investigations. Arterial blood gas analysis showed hypoxemia with respiratory alkalosis. Chest radiograph on admission revealed left upper and mid-zone heterogenous opacities with air bronchogram (Figure ). Her investigations are summarized in Table .
Contrary to our expectation, investigations revealed a normal white blood cell count with sputum negative for Gram stain and no growth in culture which is unusual in a case of bacterial pneumonia. Because of upper lobe involvement investigations for pulmonary tuberculosis were done which turned out to be negative. Even after two days of antibiotics the patient’s fever persisted and tachypnoea worsened and she became hypotensive (80/60 mmHg) and she was started on noninvasive ventilation and vasopressor. Computed tomography of the chest showed left upper and lingular lobe consolidation with air bronchogram with no pleural effusion (Figure ).
As the patient is immunocompetent with normal white blood cell count and mild thrombocytopenia, our locality being a high prevalence area, scrub typhus was suspected and enzyme-linked immunosorbent assay (ELISA) for scrub typhus was done which came out to be positive. Oral doxycycline was added to the treatment regime and treated as scrub typhus pneumonia. Within 24 hours of adding doxycycline, fever spikes reduced and respiratory distress started improving. The patient was weaned of noninvasive ventilation on the seventh day and chest radiograph before discharge showed complete resolution of opacities which is unusual as radiological findings due to pneumonia lag behind the clinical improvement by few weeks (Figure ). She was discharged home on the 10th day of admission on oral doxycycline for four more days and on follow-up visit after a week, she was asymptomatic.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",73.33333,69.66666,77,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 60.0 mm Hg = 73.33333 mm Hg.
Hence, the patient's mean arterial pressure is 73.33333 mm Hg."
1221,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7783285-1,Extracted,"A 54-year-old man was admitted to the Emergency Department with a 1-week history of
abdominal fullness and obstipation. He had no history of anticholinergic
medications, trauma, or abdominal surgery, but had an upper respiratory infection 3
weeks previously.
On arrival, his vital signs were as follows: temperature, 36.8°C; pulse rate, 104
beats/minute; respiratory rate, 20 breaths/minute; and blood pressure, 138/81 mm Hg.
His abdomen was distended, nontender, and tympanitic, without bowel sounds or signs
of peritoneal irritation or hepatosplenomegaly. No urinary retention was observed. A
neurological examination showed intact muscle strength and normal tendon tap test
results. Routine blood and biochemical analyses were unremarkable. Abdominal
contrast-enhanced computed tomography (CT) () showed a dilated small intestine
and colon with multiple air–fluid levels. Gadolinium-enhanced magnetic resonance
imaging of the thoracolumbar spinal cord was performed to rule out the possibility
of multiple sclerosis or myelopathies, and it showed no anomalies. No contrast
passed through the duodenum during a 6-hour small bowel series examination (). Gastric emptying
scintigraphy ()
showed markedly delayed radiotracer emptying, which suggested paralytic ileus.
Over 3 days of total parenteral feeding and prokinetic use, the patient showed
persistent severe ileus. Development of symmetrical mild paraparesis with medical
research council (MRC) grade 4/5, in combination with hypoesthesia (with an
impairment of light touch and pinprick over distal limbs, but no sensory level) and
loss of deep tendon reflexes in the lower limbs, were observed on hospital day 2. A
nerve conduction study on the same day showed demyelinating sensorimotor
polyneuropathy, and cerebrospinal fluid analysis showed a normal white blood cell
count (3/µL; reference: 0–5/µL), and high protein (2030 mg/L; reference: 150–450
mg/L) and glucose levels (7.77 mmol/L; reference: 2.22–3.89 mmol/L). Because of the
clinical presentation and context, and the lack of electrolyte or acid–base balance
abnormalities or other causes for the patient’s condition, we diagnosed him with
paralytic ileus secondary to GBS. Immediate treatment with intravenous
immunoglobulin (IVIG) 0.4 g/kg daily (from hospital days 2–6) was initiated.
On hospital day 3, the patient’s condition rapidly progressed to involvement of the
upper extremities (MRC grade: 4/5) and flaccid quadriplegia (MRC grade: 2/5) was
observed on day 4. On day 5, the patient’s condition was ultimately determined to be
respiratory muscle failure requiring mechanical ventilation and admission to the
intensive care unit. After 5 days of treatment, his muscle strength of the
extremities partially improved. The best recovery performance was achieved with an
MRC grade of 3/5 on the next day after the IVIG therapeutic course had finished.
However, enteral feeding was undesirable because of persistent gastroparesis
complicated by fungemia and profound sepsis throughout the hospital course. Finally,
he died 1 month after admission.
Local Ethics Committee approval was not necessary because this was a case report
and specific information about the patient was not included in the report.
Written consent for publication was obtained from the patient’s parents.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [138.0, 'mm hg'], 'Diastolic Blood Pressure': [81.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 138.0 mm Hg + 2/3 * 81.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1222,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4161720-1,Extracted,"A 38-year-old primiparous pregnant Japanese woman was transferred to our hospital because of pregnancy-induced hypertension at 37 + 0 weeks’ gestation. Until that time, her pregnancy had been uneventful. On admission, the patient’s height was 156 cm, her body weight was 66 kg, and her blood pressure was 144/67 mmHg. Proteinuria was negative. The patient’s labor progressed rapidly on the day of admission, with full dilation of the cervix 8 hours after the onset of labor. Because of prolonged deceleration on cardiotocogram, vacuum extraction was performed when the fetal head reached the +2 station. The 2,405 g male neonate had an Apgar score of 8 at 1 min and 9 at 5 min after delivery. A vaginal laceration extending 5 cm from the introitus at the 6 o’clock position was repaired. Two hours after delivery, massive bleeding from the vaginal sutures was found. When all sutures were released, pulsatile bleeding was confirmed, necessitating a second repair.Two hours after the second repair, transvaginal ultrasonography showed a hyperechoic 18 × 20 mm mass at the 5 o’clock position on the vaginal wall, suggestive of a hematoma, within which a 6 × 7 mm anechoic mass with pulsation was described (Figure 
A). Power-Doppler ultrasonography showed blood flow signals in the anechoic mass (Figure 
B), and arterial waveforms were detected in pulsed-Doppler mode. Contrast-enhanced CT revealed an 8 mm diameter pooling of contrast adjacent to an 18 × 32 mm mass in the pelvis (Figure 
C, D).
By the fourth postpartum day, the pseudoaneurysm had grown to 10 mm in diameter (Figure 
A). Because of the risk of rupture, elective embolization was planned. On the sixth postpartum day, the patient experienced abdominal pain and massive vaginal bleeding of 260 ml. Contrast-enhanced CT showed that the pseudoaneurysm had grown to 14 mm (Figure 
B). Emergency selective angiography showed strong staining with extravasation from a peripheral branching vessel of the left vaginal artery, indicating ruptured pseudoaneurysm (Figure 
). Selective embolization was performed using n-butyl-2-cyanoacryate. No blood transfusion was necessary. The patient was discharged without further complications on the 13th postpartum day.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [144.0, 'mm hg'], 'Diastolic Blood Pressure': [67.0, 'mm hg']}",92.66667,88.03334,97.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 144.0 mm Hg + 2/3 * 67.0 mm Hg = 92.66667 mm Hg.
Hence, the patient's mean arterial pressure is 92.66667 mm Hg."
1223,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8666465-1,Extracted,"A 22-year-old woman of Middle Eastern origin, born in Iran and recently living in Western Europe, presented to a UK hospital with a three-week history of intermittent frontal headache and fatigue a few days after she received her second dose of AstraZeneca ChAdOx1 nCoV-19 vaccine. These symptoms did not respond to paracetamol and progressed on to an acute two-day history of confusion and hallucinations (visual and tactile). She reported seeing “disco balls” and experiencing someone touching her skin. She had non-syndromic retinitis pigmentosa but no other medical co-morbidities, and there was no personal or family history of psychiatric illness. She was a non-smoker and non-drinker, and enjoying undergraduate studies at university.
On admission, she had one recorded fever of 38ºC, but otherwise-normal observations (HR 91, BP 123/81, RR 18, O2 saturations 100% on air). She was alert but disorientated to time, person and place, and agitated with a labile affect; she complained of auditory and visual hallucinations – for example, that the room was on fire – and delusions that were often hyper-religious in nature. She was also seen to be gesturing to the air as if responding to unseen stimuli. On examination, excepting very restricted visual fields, there was no focal neurology, meningism or photophobia, and cardio-respiratory and abdominal examination was normal. Initial investigations revealed Hb 126 g/L, WCC 6.6 × 109/L (neutrophils 4.6 × 109/L), CRP 1.1 mg/L (reference range < 5 mg/L), normal renal and liver function, platelets 275 × 109/L, and D-dimer of 1,240 ng/mL (reference range < 500 ng/mL). Chest X-ray was unremarkable, urine microscopy and culture negative, and PCR for SARS-CoV-2 and other respiratory viruses was negative (see Table ). She was empirically commenced on intravenous ceftriaxone 2 g BD and acyclovir 800 mg TDS for possible meningo-encephalitis pending lumbar puncture (LP). She was transferred to the Infectious Diseases ward.
Initially she required rapid pharmacological tranquilisation with lorazepam and haloperidol to manage extreme agitation. CT head and CT venogram were unremarkable. Initial LP, performed 2 days after the fever, revealed an opening pressure of 30 cm H2O and WCC 6 cells/µL (100% lymphocytes) with negative microbiology and virology (see Table ) on cerebrospinal fluid (CSF) analysis. She had no further recorded fevers throughout her admission and antibiotics and antivirals were stopped.
Her psychotic symptoms continued in the second week, and due to dystonia, the haloperidol was switched to regular olanzapine, titrated to a maximum of 7.5 mg/day, and PRN promethazine. MRI brain on day 7 was normal, and EEG on day 8 was also normal with no evidence of seizure activity or encephalopathy. CT imaging of the abdomen was not performed due to the patient’s age. Abdominal and pelvic ultrasound was therefore conducted to exclude ovarian teratoma as a secondary cause of autoimmune encephalopathy, and this was also normal. A second LP on day 7 showed abnormal WCC of 18 cells/µL (100% lymphocytes) and her CSF was positive for IgG oligoclonal bands (with negative paired serum oligoclonal bands). Serum and CSF was sent to UK national neuro-immunology and infection reference laboratories in Oxford and London, and Porton Down, respectively, with a variety of specialist tests undertaken (Table ) based on the clinical history. Cell surface antibodies were tested using commercial kit-based assays. Her case was discussed in the encephalitis multidisciplinary team (MDT) meeting at the National Hospital for Neurology & Neurosurgery, UK, and a possibility of autoimmune encephalitis secondary to the COVID-19 vaccine was considered given the temporal association and CSF pleocytosis (possible autoimmune encephalitis by Graus criteria []). However, a decision was made to avoid giving any steroids or other immunomodulatory therapy given the possibility of an infective cause pending repeat LP and given early improvements in her clinical state.
In the third week her symptoms improved with no further hallucinations and a Montreal Cognitive Assessment (MoCA) score of 22/30, and she was weaned off olanzapine. She had a third lumbar puncture on day 14, second EEG on day 22, and a second MRI on day 23, which were all normal. Other investigations were undertaken (see Table ). She had a mild relapse in her delirium with psychotic symptoms, with simple auditory and visual hallucinations (seeing “green lights” and hearing “the sound of coins pouring into a dish”, hyper-religiosity, continuous praying and labile mood). Neurological examination remained normal, with no unresponsive episodes, witnessed involuntary movements, seizure activity, or evidence of aura. These features stabilised with resumption of olanzapine (titrated to 5 mg twice-daily), and she was successfully discharged with ongoing follow-up with Neurology and Psychiatry. The case was notified to the national COVID-19 vaccine adverse event reporting scheme.
One month after discharge she remains on low dose olanzapine and is functionally well with independent activities of daily living. However, her family report that she has not recovered back to her pre-morbid state. She is quieter and more withdrawn now, and still has residual psychotic symptoms of occasionally seeing green lights and praying more than before.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [123.0, 'mm hg'], 'Diastolic Blood Pressure': [81.0, 'mm hg']}",95,90.25,99.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 123.0 mm Hg + 2/3 * 81.0 mm Hg = 95.0 mm Hg.
Hence, the patient's mean arterial pressure is 95.0 mm Hg."
1224,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7676219-1,Extracted,"On August 23, 2018, an 84-year-old man, who had suffered from skin ulcer and soft-tissue necrosis at multiple sites of limbs for three months, was admitted to the First People's Hospital of Wenling. Three months ago, he had skin edema under no apparent predisposing cause. The edema was initially single and limited at his right ankle alone, while was gradually developed to be multiple, and then was aggravated to necrosis ulcers within 2 weeks. He was diagnosed as a soft-tissue infection (bacteria being considered firstly) at Sir Run Run Shaw Hospital, and received both surgical debridement and irrigation, and antibiotics treatment (Rocephin®, ceftriaxone sodium, 2 g, qd) for 3 days. He did not test any laboratory examinations and went back home after treatment. However, the skin lesions did not recover but disseminated to the right arm at the follow-up 2 months. To get further treatment, he visited the First People's Hospital of Wenling and was admitted to the Department of Burns with the impression of soft-tissue infection (unknown reason).
The patient's body temperature was normal (37℃), and blood pressure was 130/70 mm Hg at the admission day. Blood laboratory tests, including white blood count (6.33 + E9/L, neutrophil percentage 73.1%), and glucose level (5.3-5.6 mmol/L), were not abnormal except for C-reactive protein (CRP, 103.14 mg/L). Body examination showed cutaneous necrosis, and necrotic ulcers were presenting at both the right ankle and the right arm with the largest ulcer size over 6 × 10 × 0.1 cm. The damaged skins were red with high temperature. Thickening and subcutaneous soft-tissue edema expanded to the whole right leg and arm (Figure ). No other positive physical signs were observed. The patient had had comorbidities of type II diabetes mellitus for 4 years and gout for 6 years. He had received insulin therapy subcutaneously for four years. He is a farmer who is engaged in agriculture.
Tissue samples were collected from the right arm's damaged skin after debriding with 0.9% sodium chloride and sent to the clinical microbiology laboratory. It was used for both direct microscopic examination and further microbial culture after being digested with 3% sodium hydroxide.
Staining methods of lactophenol cotton blue (Baso) and fungus fluorescence (Jiangsu Lifetime Biological Technology) were completed. Two plates of Columbia agar with 5% defibrinated sheep blood and Sabouraud agar were used for further culture under 37℃ and 5% CO2 condition. To identify the species of the colonies growing on the plate, the VITEK system (bioMérieux) based on biochemical reaction method with YSD card was utilized according to the manufacturers' instructions. Molecular method based on partial mitochondrion-encoded cytochrome b (cytb) gene sequencing was involved for further species confirmation, as previously reported. To compete with the cytb gene sequencing, genomic DNA was first extracted using ZR Fungal/Bacterial DNA MiniPrep Kit (ZYMO research) and then PCR was performed to amplify the cytb gene following-up Sanger sequencing at Biosum company. The sequence was then submitted to NCBI database () for alignment.
In vitro antifungal susceptibility testing was detected using YeastOne plate (Thermo Fisher Scientific) according to standard detecting procedure.
Round, grape-like, and scattered morula forms were observed under the microscope in bright blue and green fluorescence dying with lactophenol cotton blue and fungus fluorescence. Moruloid sporangia were composed of two to eight small sporangiospores and had a thick and highly refractile wall (Figure ).
After 48 hours of incubation, yeast-like colonies were grown on both plates, which were white, mid-sized, rough, round or corrugated margin, undulate and rough in morphology (Figure ). Both the VITEK system and the sequence of cytb gene showed P wichehamii with 100% similarity.
P wichehamii showed resistance to three echinocandins (anidulafungin, micafungin, and caspofungin), fluconazole, and 5-fluorocytosine, while was susceptible to amphotericin B, posaconazole, itraconazole, and voriconazole (Table ).
The clinical diagnosis was then revised to tissue-skin infection (human protothecosis) when the identification of P wichehamii was confirmed. The patient was advised to immediately treat with antifungal drugs, including fluconazole (200 mg, iv, q 12 h) and compound econazole nitrate cream on the damaged skin after debridement and irrigation (0.5 g, bid). Besides, regular insulin kept on using to control the level of blood glucose. Skin ulcers recovered within two weeks of therapy, and no more skin damage appeared. (Figure ) The patient was fully recovered and discharged one month later when C-reactive protein was decreased to less than 0.8 mg/L.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 70.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1225,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5926487-1,Extracted,"A 54-year-old man presented with worsening sharp pain over his right upper back. The pain had started two weeks back immediately after getting a flu vaccination in his right shoulder. There was no radiation and no aggravating or relieving factors. It was associated with a localized sensation of warmth and occasional chills. He, however, denied any preceding trauma, fever, cough, weakness, numbness, or pain in any other part of the body. Rest of the review of symptoms was negative. His past medical history was significant for hypertension, type 2 DM, morbid obesity with a body mass index of 44 kg/m2, and depression. He was not compliant with his diet nor his medications. At presentation, he was afebrile but, subsequently, he developed a fever with a temperature of 102 F. His blood pressure was 137/75 mm Hg with a pulse rate of 113 beats per minute. His physical examination was significant for an extensive area of induration in the right upper back extending into the back of the neck, measured about 25 cm × 20 cm in size, and had a 3 cm × 4 cm × 3 cm area of fluctuation with erythema and tenderness (). His laboratory investigations were significant for leukocytosis with a white blood cell count of 26,000/μL, lactic acidosis with a serum lactic acid of 2.4 mmol/L (normal 0.5–1.9 mmol/L) and serum bicarbonate of 16 mmol/L (normal 22–32 mmol/L), and poorly controlled diabetes with serum glucose of 291 mg/dL (normal 74–118 mg/dL) and subsequent hemoglobin A1C of 10.3% (normal 4.8%–5.6%). Erythrocyte sedimentation rate was 104 mm/hr (normal 0–20 mm/hr), C-reactive protein was 345.7 mg/L (normal 0–4.9 mg/L), thyroid stimulating hormone level was 1.360 μIU/mL (normal 0.450–4.50 uIU/mL), and free thyroxine level was 5.1 μg/dL (normal 4.5–12 ug/dL). Serum protein electrophoresis (SPEP) showed a normal pattern with no monoclonal protein, and antistreptolysin O (ASO) titer was negative. Chest imaging showed bullous changes in the upper lobes of the lung, a large area of soft tissue density in the subcutaneous tissue of right upper back, and enlarged right trapezius muscle (). In this setting of fever, tachycardia, leukocytosis, and lactic acidosis, a presumptive diagnosis of sepsis likely due to cellulitis of the back with abscess formation was made. The patient was then started on broad-spectrum intravenous antibiotics and taken to the operative room for incision and drainage. His deep-seated abscess was drained and cultured, which subsequently grew Staphylococcus lugdunensis sensitive to methicillin, so the patient was started on intravenous Nafcillin. A skin biopsy taken from the back was sent for histopathology and showed fibroadipose tissue and skeletal muscle with focal acute and chronic inflammation with granulation tissue (). These histopathological findings were consistent with scleredema diabeticorum and was thought to have resulted from his longstanding, poorly controlled diabetes. However, he denied prior symptoms of tightness or discomfort over the shoulders and upper back. The patient was counseled extensively and started on insulin and metformin, and the dosage was optimized during hospitalization. He was also informed about the treatment options for scleredema diabeticorum including immunosuppressants and phototherapies, but he declined any treatment for the time being. And with the sepsis resolved, blood glucose better controlled, and his surgical wound healing, he was discharged home to follow up as an outpatient.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [137.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",95.66667,90.88334,100.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 137.0 mm Hg + 2/3 * 75.0 mm Hg = 95.66667 mm Hg.
Hence, the patient's mean arterial pressure is 95.66667 mm Hg."
1226,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8246,Extracted,"A 28-year-old man is brought in by ambulance to the ER, barely conscious, after feeling drowsy and falling to the floor during a presentation several hours ago. His colleague who accompanied him says he has had similar episodes 5 times in the past 3 months. No significant past medical history. His blood pressure is 110/80 mm Hg and pulse is 114/min. His capillary blood glucose is 15 mg/dL. Immediate IV dextrose with thiamine is started, and he rapidly regains consciousness. A contrast CT of the abdomen is performed which reveals a tumor in the pancreas.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 80.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1227,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6964363-1,Extracted,"The patient was an 82-year-old white male with a history of ischemic cardiomyopathy status postcardiac stenting, history of heart failure with reduced ejection fraction (HFrEF with ejection fraction (EF): 20–25%) with implantable cardiac defibrillator (ICD), chronic atrial fibrillation on dabigatran, obstructive sleep apnea (OSA), chronic kidney disease (CKD) stage III, carpal tunnel syndrome, and gout who presented with fatigue, acute hematuria, and urinary retention. He was a nonsmoker, did not endorse regular alcohol use, and denied any illicit drug use. His family history was noncontributory. His vitals at presentation were temperature 36.3°C, heart rate 80 beats per minute, blood pressure 100/70 mm Hg, and oxygen Saturation 93% on room air. Home medications included bumetanide 1 mg daily, metolazone 1.25 mg twice a week, carvedilol 12.5 mg daily, and dabigatran 75 mg twice a day. Complete blood count (CBC) was unremarkable, and basic metabolic panel (BMP) showed creatinine of 2.2 mg/dl (near baseline). NT-pro-BNP was elevated at 18,500 pg/ml (baseline 2000s). Troponin was elevated at 0.36 ng/ml.
Urology was consulted, and patient underwent cystoscopic evaluation for hematuria. Clot evacuation and fulguration of diffuse bladder lesions were performed. Bladder biopsy was also obtained, and subepithelial amyloid deposits were identified based on Congo-red stain.
In the following days, the patient developed intermittent episodes of atrial fibrillation with rapid ventricular rate, hypotension, liver dysfunction, and acute kidney injury secondary to acute tubular necrosis. Aspartate aminotransferase (AST) peaked at 3000 (U/L) and alanine aminotransaminase (ALT) at 2000 (U/L). Remaining liver function tests showed alkaline phosphatase 50 (U/L), bilirubin 3-4 mg/dl, hyperammonemia (72 mcmol/L) and elevated international normalized ration (INR) around 4. Computed tomography imaging of chest, abdomen, and pelvis was negative for any acute process but showed cardiomegaly that was seen in the plain chest radiography as well. Workup for any acute infectious or inflammatory processes (viral markers, acetaminophen levels, and autoimmune markers) for evaluation of acute liver dysfunction did not reveal any alternate diagnosis, thereby suggesting acute decompensation from shock liver.
Echocardiogram demonstrated worsening of ejection fraction (EF) to 10–15% with concentric left ventricle hypertrophy, impaired left ventricular diastolic dysfunction, thickened interventricular septum more than 12 mm, normal biventricular dimensions, biatrial dilation with no significant valvular abnormalities (findings compatible with cardiac amyloidosis) (). Magnetic Resonance Imaging (MRI) was not performed due to underlying CKD. His condition continued to deteriorate, and he was transferred to the cardiac care unit for acute decompensated heart failure. He was started on milrinone infusion with transient improvement in his cardiac function and end organ perfusion.
He was evaluated for cardiac resynchronization therapy upgrade but deemed unstable from medical standpoint to undergo the procedure.
Hematology team was consulted and performed biochemical workup for amyloidosis. Serum protein electrophoresis (SPEP) did not show an M-spike. Serum-free light analysis (kappa/lambda ratio 2.9) and urine immunofixation studies were not significant ruling out evidence for plasma cell dyscrasias. Meanwhile, the mass spectrometry analysis of the bladder biopsy specimen confirmed wild-type transthyretin (ATTRwt) consistent with senile systemic amyloidosis. Immunohistochemical analysis was not performed as mass spectrometry has been demonstrated to be a well-validated technique to diagnose and classify amyloidosis [, ]. Genetic testing can help clarify if the disease was hereditary or not but was not performed in this case and remains a limitation.
Multiple specialties including internal medicine, hematology, cardiology, and critical care were involved in the patient care, but despite aggressive management, patient's condition gradually deteriorated. Due to the poor prognosis in the setting of multiple comorbidities and decompensated heart failure, the patients' family decided to stop further treatment and focus on patients comfort only which was facilitated by the palliative care team. The patient passed away shortly thereafter from cardiac arrest, and the diagnosis was acute on chronic cardiac failure from senile systemic amyloidosis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 70.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1228,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4010013-1,Extracted,"A 36-year-old Japanese woman was referred to our critical care and emergency center with mild abdominal distention and epigastric pain of about 10 days duration. She gave a history of having been diagnosed as having bilateral uveitis and erythema nodosum in the lower extremities six months previously. The patient was diagnosed as having Sjogren's syndrome based on a positive Schirmer's test and reduced amount of saliva. During the 2 months prior to hospitalization, the patient suffered from loss of vision, ophthalmoplegia, and painful erythema nodosum nodules in the lower extremities. She had taken prednisolone at the dose of 20 mg/day. The serum albumin and calcium levels were reduced (2.4 mg/dL and 6.7 mg/dL). The serum angiotensin-converting enzyme (ACE) and lysozyme levels were slightly elevated (38.4 IU/l and 23.2 ug/mL, resp.). The tuberculin skin test was the reaction with induration of less than 5 mm in size. Bronchoalveolar lavage contained 61% lymphocytes, with a CD4/CD8 ratio of 4.9, and examination of transbronchial lung biopsy (right B8) specimens revealed the presence of noncaseating epithelioid cell granulomas. Microscopic examination of PAS- and acid-fast stained specimens revealed no acid-fast bacilli. Based on these findings, except for the low serum levels of calcium, sarcoidosis had been diagnosed about 4 months previously. She had suffered from pain of progressively increasing severity because of uveitis and erythema nodosum during the 10 days prior to admission. She had been prescribed 75 mg/day of slow-release diclofenac sodium and prednisolone in slowly tapering doses (current dose, 5 mg/day).
At the time of admission to our hospital, her vital signs were as follows: body temperature 36 degrees Celsius, heart rate 81 beats/min, blood pressure 102/45 mm Hg, and respiratory rate 20/min. Physical examination revealed marked abdominal distention, with slight guarding and rebound tenderness. No bowel sounds could be heard on auscultation. She had no history of consumption of contaminated foods or water. There were no clinical features, such as rose spots, tenesmus, mucous/bloody diarrhea, or joint pain. She had sicca syndrome and dry eye, but no oral aphthae or genital ulcers. She had never visited any countries with poor sanitary conditions or tropical areas and had no history of venereal diseases. The pathergy test was negative. The results of blood investigations were as follows: white blood cells 3950/mm3, hemoglobin 10.3 g/dL, and platelet count 73,000/mm3. The serum C-reactive protein level was 3.7 mg/dL. Renal function, hepatobiliary function, serum electrolytes, and the coagulation profile were within normal limits. Radioimmunoassay for hepatitis virus markers in the serum revealed a positive test for hepatitis B surface antigen (HBs Ag) and negative tests for both hepatitis B surface antibody (HBs Ab) and anti-hepatitis C antibody. Serum tests for rheumatoid factor and HLA-B51 were negative. Both proteinase-3-antineutrophil cytoplasmic antibody (PR3-ANCA) and myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA) titers were within normal limits (<10 EU). A chest X-ray obtained with the patient upright demonstrated free air under the diaphragm bilaterally (). An emergency laparotomy was performed because of suspected panperitonitis caused by intestinal perforation. The abdominal cavity contained approximately 400 mL of fetid fluid. The stomach, duodenum, and small intestine were normal on exploration. There were several perforations on the antimesenteric aspect of the transverse colon. Therefore, a transverse colectomy and loop colostomy were performed. The resected specimen contained a large amount of soft stool and exhibited 11 punched-out ulcerations, many of which measured up to 10 mm in diameter (). Microscopic examination revealed nonspecific findings and showed perforation of the intestinal wall with infiltration of the ulcer bed with leukocytes ().
Slow-release diclofenac sodium had been discontinued since the time of admission and, subsequently, the corticosteroid was also tapered off and discontinued. On day 14, colonoscopy revealed mild aphthoid ulcers at the anastomotic site, but no evidence of perforation. The patient made good postoperative recovery. Colostomy closure was performed on day 42 without any complications, and the patient was discharged on day 73 of hospitalization.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [102.0, 'mm hg'], 'Diastolic Blood Pressure': [45.0, 'mm hg']}",64,60.8,67.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 102.0 mm Hg + 2/3 * 45.0 mm Hg = 64.0 mm Hg.
Hence, the patient's mean arterial pressure is 64.0 mm Hg."
1229,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-743,Extracted,"A 29-year-old woman comes to the emergency department because of progressive numbness and weakness in her right arm and right leg for 1 day. Two months ago, she had blurry vision and headache for a week, which resolved without treatment. She does not smoke or drink alcohol. Her temperature is 37°C (98.6°F), pulse is 78/min, respirations are 14/min, and blood pressure is 115/71 mm Hg. Muscle strength is 3/5 in the right arm and leg and 5/5 on the left side. MRI of the brain shows gadolinium-enhancing lesions in the left central sulcus, cervical spinal cord, and optic nerve. Intravenous methylprednisolone therapy is started.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [71.0, 'mm hg'], 'Systolic Blood Pressure': [115.0, 'mm hg']}",85.66667,81.38334,89.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 71.0 mm Hg = 85.66667 mm Hg.
Hence, the patient's mean arterial pressure is 85.66667 mm Hg."
1230,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8213488-1,Extracted,"A 78-year-old Arabic female with a history of lymphoma in 2015 presented to our institution in July 2020 with dyspnea and cough. Prior to this presentation, nasopharyngeal swab polymerase chain reaction (PCR) for SARS-CoV-2 was positive in April 2020, at which time the patient was admitted to a different hospital. During this initial hospitalization, the patient's temperature was 37.3 °C, heart rate was 94 beats/min, respiratory rate was 23 breaths/min, blood pressure (BP) was 146/74 mmHg, and oxygen saturation was 83% on room air, which improved to 94% with supplemental oxygen. Lung examination was notable for bilateral coarse breath sounds. The patient was hypoxic and required supplemental oxygen. The white blood cell (WBC) count was 3,100/mL, with an absolute lymphocyte count of 400/mL, hemoglobin level was 10.2 g/dL, and platelet count was 250,000/mL, with a total protein of 6.2 g/dL. Nasopharyngeal PCR testing for COVID-19 was positive. Computed tomography (CT) chest with contrast (Figure ) demonstrated diffuse peripheral interstitial and alveolar airspace opacities most prominent at the lung bases and testing for SARS-CoV-2 was again positive. She received supportive care, dexamethasone with prednisone taper upon discharge. After her discharge, her condition improved temporarily; however, she continued to require multiple hospital admissions at different facilities between August and October for similar complaints. During one of the hospitalizations, she was found to be severely immunocompromised, with critically low immunoglobulin G (IgG) levels with a cluster of differentiation 4 (CD4) lymphocyte count of less than 50, human immunodeficiency virus (HIV) antigen/antibody screen negative. Though she received a course of intravenous immunoglobulin (IVIG) afterward, she experienced a gradual decline in her functional capacity between July and October due to her illness. Late in October, she was admitted again to our institution; however, now in the intensive care unit (ICU) requiring mechanical ventilation for hypoxemic respiratory failure. The WBC count was 16,800/mL with an absolute lymphocyte count of 100/mL, hemoglobin level was 9.6 g/dL, and platelet count was 206,000/mL, and total protein of 5.3 g/dL. Nasopharyngeal polymerase chain reaction (PCR) testing for COVID-19 was positive again.
Repeat CT scan of the chest (Figure ) showed significant improvement but residual consolidations with surrounding ground-glass opacities predominantly involving bilateral lung bases. Testing for SARS-CoV-2 was again positive on this admission. Bronchoscopy with bronchoalveolar lavage was performed that revealed inoculation of aspergillus species. Her condition continued to deteriorate, and she subsequently expired. Her clinical course lasted approximately seven months, requiring multiple admissions to different hospitals with multiple courses of corticosteroid therapy in the form of dexamethasone, hydrocortisone, and prednisone.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [146.0, 'mm hg'], 'Diastolic Blood Pressure': [74.0, 'mm hg']}",98,93.1,102.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 146.0 mm Hg + 2/3 * 74.0 mm Hg = 98.0 mm Hg.
Hence, the patient's mean arterial pressure is 98.0 mm Hg."
1231,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3259520-1,Extracted,"A 47-year-old woman visited our emergency room (ER) because of a persistent headache, chills, acute cough, and a mild fever for 5 days. Initial examination showed: blood pressure, 114/59 mmHg; body temperature, 37.7℃; pulse rate, 102/min; and breathing rate, 20/min. She appeared pale and chronically ill. On physical examination, there was no specific finding except a palpable spleen in the left upper quadrant (LUQ) of the abdomen. She had no notable previous medical history except iron deficiency anemia (IDA) due to severe menorrhagia, for which she took iron supplements for 6 months. Chest X-ray showed mild cardiomegaly, and her EKG was normal. The blood tests showed: Hb, 3.2 g/dL; Hct, 13.4%; WBCs, 2.4×109/L; platelets (PLTs), 93×109/L; RDW, 21.3%; MCV, 57.3 fL; MCH, 13.7 pg; reticulocytes, 0.17%; and LDH, 152 IU/L. Iron profiling showed a serum ferritin level of 3 ng/mL, a serum iron level of 22 µg/dL, and a UIBC of 325 µg/dL. After 2 packs of RBCs were transfused in the ER, her Hb increased to 6.3 g/dL, and her general condition improved. She was admitted to our hospital for further examination and treatment. Peripheral blood (PB) smear showed microcytic hypochromic dysmorphic RBCs, including many elliptocytes, schistocytes, and teardrop cells. Biochemical tests found: total billirubin, 1 mg/dL; indirect bilirubin, 0.3 mg/dL; AST, 24 IU/dL; ALT, 6 IU/dL; BUN, 9 mg/dL; creatinine, 0.5 mg/dL; Na, 143 mEq/L; K, 3.3 mEq/L; and Cl, 109 mEq/L (). Two blood cultures showed no microorganism growth for 5 days. Serological testing for Parvovirus was positive for IgG and negative for IgM. Tests for antinuclear antibody (ANA) and rheumatoid factor (RF) were negative. The stool occult blood test was negative, and there was no evidence of blood loss except hypermenorrhea. Abdominal CT was performed to rule out gastrointestinal malignancy. Abdominal CT showed that spleen was enlarged to approximately 17 cm in length of the long axis (). A bone marrow biopsy was performed to find other causes for pancytopenia and iron-refractory IDA. Bone marrow aspiration showed hypercellular marrow with an increased M:E ratio (0.7:1). The cellularity of the bone marrow was up to 80%. Both erythropoiesis and the number of megakaryocytes increased. However, iron storage decreased. There were no dysplastic marrow cells or abnormal cell infiltration. On the 12th hospital day, the patient was discharged with the Hb level of 7.2 g/dL.
Five days later, the patient revisited the ER due to severe abdominal pain in the LUQ. She suffered from acute abdominal pain after she was discharged, and the pain was aggravated. Her blood pressure was 160/80 mmHg, pulse rate was 120/min, and breathing rate was 30/min. She was not febrile. Physical examination showed that she had direct tenderness in the left upper abdomen. Blood tests revealed: Hb, 7.4 g/dL; Hct, 26.5%; WBC, 5.4×109/L; PLTs, 87×109/L; MCV, 73.4 fL; and MCH, 20.5 pg. These were nearly identical as those at first admittance. However, LDH increased to 711 IU/L from 152 IU/L, and reticulocytes increased to 3.53% from 0.17%. Biochemical testing showed: total billirubin, 2.6 mg/dL; indirect billirubin, 0.7 mg/dL; AST, 32 IU/L; and ALT, 3 IU/L (). Both PT and aPTT were within the normal range. A PB smear showed normocytic normochromic RBCs with spherocytes, elliptocytes, and teardrop cells. Haptoglobin decreased to 1 mg/dL (30-200 mg/dL) and D-dimer increased to 2,743 ng/mL (0-500 ng/mL). Under suspicion of hemolytic anemia, direct antiglobulin tests (DAT) and indirect antiglobulin tests (IAT) were performed. The DAT for IgG and C3d and the IAT for IgG were positive, but the IAT for C3d was negative. Flow cytometry for paroxysmal nocturnal hemoglobinuria (PNH) was within the normal range. She was diagnosed with AIHA. EKG showed sinus tachycardia. Abdominal CT showed that the spleen had increased to 20 cm and new multiple splenic infarctions were observed compared with the previous CT. However, thrombosis of blood vessels, including the splenic artery, was not observed (). Transthoracic echocardiography showed no intracardiac vegetation or thrombus.
To rule out a hypercoagulable status, the activity of protein C and S and antigen level were measured. Protein C activity and antigen level decreased to 44.0% (60-140%) and 42.0% (65-140%), respectively, and protein S activity and antigen level were within the normal range. Antithrombin was within the normal range at 21.8 mg/dL (22-39 mg/dL). No Factor V Leiden mutation or lupus anticoagulant antibody was present. Anticardiolipin antibody IgG was negative, but IgM was positive. Serologic tests for cytomegalovirus, Epstein-Barr virus, HIV, and hepatitis B and C virus were performed. Anti-EBV viral capsid IgM (anti-EBV-VCA IgM) was equivocal, and all others were negative. Anti EBV-VCA IgG was negative, and EBNA was not checked.
On the second hospital day, a splenectomy was performed due to the uncontrolled, severe left upper abdominal pain. On the cross section, the spleen showed multifocal wedge-shaped subcapsular infarcts. On microscopic examination, there was no evidence of lymphoma or leukemic infiltration (). After splenectomy, her symptoms and pancytopenia improved. Two weeks later, complete blood counts showed a full recovery: Hb, 12.1 g/dL; WBCs, 6.9×109/L; PLTs, 629×109/L; and reticulocytes, 1.37%.
After discharge, her protein C activity was 109.0% (60-140%) and antigen level was 132% (65-140%). The patient has been under observation at the outpatient center.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [160.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 80.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1232,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3152183-3,Extracted,"A 45-year-old female presented with complaints of insidious onset pain over lower part of right thigh She gave history of diabetes for 4 years and was on oral hypoglycemics very irregularly. She had hypertension (BP 160/90 mm Hg), distal symmetrical mixed sensorimotor polyneuropathy, and nonproliferative diabetic retinopathy. There was a localized tender and firm oval-shaped lump (5 × 4 cm) on the medial aspect of the right thigh. Glycemic status was poor (RBS at admission 523 mg/dl, HbA1c 12.6%), serum creatinine 1.4 mg/dl, and her 24 hrs urinary albumin was 734 mg. Ultrasonography of the thigh showed ill-defined hypoechoeic areas involving vastus group of muscles and there was increased vascularity around the hypoechoeic areas []. She was treated with insulin, analgesics, and antihypertensives. She responded well and was discharged after 3 weeks.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [160.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",113.33333,107.66666,119,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 90.0 mm Hg = 113.33333 mm Hg.
Hence, the patient's mean arterial pressure is 113.33333 mm Hg."
1233,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2878426-1,Extracted,"A 5-year-old female presented with continuous dribbling of urine without any voiding stream since birth. Because of poor socioeconomic status and an illiterate rural background, the parents consulted a specialist only when the child reached a school-going age. There was no history of any bowel complaints. On general examination, her blood pressure was 140/74 mmHg in the left forearm. There were no skeletal defects, anal tone and neurological examination were normal. The external genitalia was of the female phenotype and on separating the labia majora, a single opening with a continuous urine leak was seen. All routine investigations such as hemoglobin, total leucocyte count, renal function tests, and urine microscopic examination were within the normal range. On abdominal sonography, bilateral moderate hydronephrosis and hydroureters were seen. Renal parenchymal thickness, echogenicity, and corticomedullary differentiation were normal on both sides. The uterus and fallopian tubes were normal but the ovaries could not be seen. On micturating cystourethrogram catheter went into the left ureter, which was dilated; however, there was contrast overspill into the bladder and reflux was seen into the right ureter, which was also dilated []. An intravenous pyelography showed good contrast excretion on both sides and dilated ureters were seen up to the lower part of the bladder, which was faintly visualized with the contrast []. A computed tomography (CT) scan showed a low capacity bladder with urogenital sinus []. On urogenital sinus scopy and cystoscopy [], both dilated ureteric orifices were found to open into vaginalized urogenital sinus by the side of the bladder neck. The bladder neck was wide open and incompetent. The bladder had a smooth lining without identifiable trigone. The cystometric capacity was 20 cc. Karyotype by fluorescence in-situ hybridization was 46 XX. Because of high blood pressure, two dimensional echocardiography was done that revealed coarctation of the aorta distal to the left subclavian artery.
We plan for continent diversion with cutaneous stoma in this case once the patient undergoes surgery for coarctation of the aorta.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [74.0, 'mm hg']}",96,91.2,100.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 74.0 mm Hg = 96.0 mm Hg.
Hence, the patient's mean arterial pressure is 96.0 mm Hg."
1234,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5776,Extracted,"A 24-year-old man presents to the emergency department after a motor vehicle collision. He was the front seat and unrestrained driver in a head on collision. His temperature is 99.2°F (37.3°C), blood pressure is 90/65 mmHg, pulse is 152/min, respirations are 16/min, and oxygen saturation is 100% on room air. Physical exam is notable for a young man who opens his eyes spontaneously and is looking around. He answers questions with inappropriate responses but discernible words. He withdraws from pain but does not have purposeful movement.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",73.33333,69.66666,77,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 65.0 mm Hg = 73.33333 mm Hg.
Hence, the patient's mean arterial pressure is 73.33333 mm Hg."
1235,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3880742-1,Extracted,"A 26-year-old nulliparous woman with a dichorionic-diamniotic twin pregnancy achieved by assisted reproductive techniques was admitted at 32 weeks of gestation. At admission, her complaints were epigastric pain and flank pain. Until that time, the patient had an uneventful pregnancy without history of vaginal bleeding, abdominal trauma, uterine contraction, or recent sexual intercourse. Her past medical history included neither abdominal surgery nor myoma uteri. On physical examination, the temperature was 36°C, the blood pressure was 110/70 mm Hg, the pulse was 92 beats per minute, and respiratory rate was 24 beats per minute and vital parameters were normal. At initial abdominal examination, she had no rebound tenderness. Pelvic examination was one cm dilated with a soft cervix. Cardiotocography showed irregular contractions with reactive fetal heart rate tracing. Hemoglobin (Hb) was 10.3 g/dL, hemotocrit level (Hct) was 31.4%, white blood cell count (WBC), C-reactive protein (CRP) level and other laboratory results were normal. Urinalysis revealed 100 mg/mL protein and leucocyte (++). Obstetrical ultrasonography examination revealed two otherwise healthy fetuses with apppropriate biometrical calculations and with normal amniotic fluid, Doppler flow velocimetry indices. Maternal abdominal ultrasound examination revealed minimal anechoic free fluid in the right lower quadrant but appendix was not observed. Transvaginal ultrasound examination revealed a 26 mm cervical length.
After hospitalisation, steroid therapy betamethasone (Celestone Chronodose, 1 ml, Schering Plough, Germany) was performed for lung maturation. Nifedipine 10 mg 6 times a day (Nidilat, Sanofi Aventis, France) and then beta-agonists was administered for 24 hours for accelerated uterine contractions. Within 24 hours of admission the patient gradually complained of progressive nausea and vomiting. The patient was consulted to general surgery department, and oral intake was stopped, a nasogastric catheter was placed, a proton pump inhibitor was started intravenously, and an antibiotic regimen was administered (ceftriaxone 2 gr/day (Rocephine, Saba, Turkey)) and metronidazole 1 gr/day (Flagyl, Ecz.Baxter, Turkey) for suspicion of appendicitis. Whole abdominal and pelvic magnetic resonance (MR) imagings were performed and revealed a minimal intra-abdominal free fluid without any pathological signs. On the second day, abdominal pain with nausea and vomiting gradually increased but no rebound tenderness was experienced. Hg level decreased to 9.53 g/dL, htc level decreased to 29.4%, and WBC increased in value of 19.4 × 103/UL. Since leucocyte counts increased gradually and symptoms became more obscure, surgery had been decided with the diagnosis of acute abdomen. Under spinal anesthesia, laparotomy was extended through pfannenstiel incision and 300–400 mL hemoperitoneum was observed in the peritoneal cavity. Pelvic exploration revealed blurish color on the posterior right side of the uterus, active bleeding from right uterine vessel, and a torn uterine serosa (). A 8-9 apgar, 1760 gr, female fetus and a 8-9 apgar, 1730 gr, male fetus were born by a Cesarean section. The placenta was normal in appearance without retroplacental hematoma, ablation, or previa. Uterine vein branch was sutured with polyglactin 910 number 1.0. (Ethicon,Johnson & Johnson) (). Postoperative period was uneventful without any necessity of blood transfusion, and the patient was discharged home on the second postoperative day.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1236,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4935817-1,Extracted,"A 78-year-old right-handed lady was referred to elective cardiac surgery department for coronary artery bypass graft (CABG) surgery. She was hospitalized for conducting the pre-operation investigations. On the second day of admission, she developed sudden onset weakness of left upper and lower limbs and dropping of left side of the face. She has had a past history of hypertension, which was controlled by taking 50 mg atenolol twice a day. She has had angina pectoris but not any history of myocardial infarction. According to her coronary angiography, she was candidate for CABG surgery due to coronary artery stenosis.
The vital signs at the onset of left side hemiparesis included pulse rate of 74/min with regular rhythm, respiratory rate of 16/min, blood pressure of 160/100 mm Hg and normal body temperature. Her baseline electrocardiogram showed evidences of left ventricular hypertrophy (LVH) and there was no evidence of acute cardiac ischemia.
Axial brain computed tomography (CT) scan without contrast, which has been done after 30 minutes of hemiparesis, showed no evidence of hemorrhage, no new parenchymal hypodensity and no dense clot sign. Although, the brain CT scan showed an old stroke in left hemisphere which was not compatible with the symptoms of the patient. Due to acute left hemiparesis and no evidence of hemorrhage on brain CT scan, the diagnosis of ischemic stroke with unclear mechanism was made. The National Institutes of Health Stroke Scale (NIHSS) was 10 out of 42, composed of 2 score for partial paralysis of lower face, 3 score for left arm motor weakness, 3 score for left leg motor weakness, 1 score for sensory disturbances and 1 score for language problem. Next decision was to administer the intravenous thrombolytic. Intravenous rTPA was started after 120 minutes of the event onset. The bolus dosage of rTPA was 8 mg, followed by infusion of 58 mg in the next 60 minutes.
Approximately three hours later, the patient complained of chest pain and palpitation. The immediate electrocardiogram (ECG) showed ST-segment elevations in the inferior leads (II, III, aVF), and ST-segment depressions in the anterolateral leads (I, aVL) (). The patient was emergently transferred to the cardiac catheterization laboratory for rescue percutaneous coronary intervention (PCI). On angiography, the occlusion of right coronary artery was detected. Thrombectomy via an aspiration catheter was performed and normal coronary blood flow was restored. Then PCI was conducted on right coronary artery and posterior descending artery bifurcation with two bare metal stents. After revascularization, the patient’s heart rhythm returned to normal sinus and hypotension was resolved. The brain CT scan was repeated and showed a new hypodensity in right parietal lobe. Brain MRI with diffusion-weighted sequence (DW) revealed a watershed ischemic infarction between anterior cerebral artery (ACA)-multiple correspondence analysis (MCA) and MCA-principal component analysis (PCA) territories in right side, which was hyposignal in equivalent Apparent Diffusion Coefficient (ADC) sequence that means an acute stroke occurred (). The echocardiography revealed a left-ventricular ejection fraction of 50% with inferior hypokinesia and without evidence of intracardiac thrombus or intracardiac right-to-left shunt.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [160.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",120,114,126,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 100.0 mm Hg = 120.0 mm Hg.
Hence, the patient's mean arterial pressure is 120.0 mm Hg."
1237,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5763093-1,Extracted,"A 30-year-old male with no past medical history presented to the emergency department reporting three weeks of progressively worsening cough producing yellow sputum, pleuritic right scapular pain, four days of fever (to 38.9°C), and one episode of night sweats. Additionally, he noted a ten-pound weight loss, which he attributed to decreased appetite. He denied hemoptysis, shortness of breath, diarrhea, or dysuria. The patient had recently completed a five-day course of azithromycin and had been using benzonatate without relief.
In the two months prior to his presentation, he traveled through Japan, Cambodia, Thailand, Laos, and Israel. He took antimalarial medications when appropriate and had received all required travel vaccinations prior to departing. Additionally, one month before presentation, he had attended Burning Man, an artistic gathering in the middle of the Black Rock Desert in Nevada. His fiancée had traveled with him and was also experiencing a similar but less severe cough. They used a single-room humidifier nightly while sleeping. He had no history of recurrent or severe infections. He denied tobacco or alcohol use. He had a history of occasional marijuana use but denied any intravenous drug use. He worked as a teacher.
On physical exam, his blood pressure was 140/69 mmHg with a pulse rate of 84/min. His tympanic temperature was 36.5°C. His respiratory rate was 18/min, and oxygen saturation on room air was 99%. He was in no acute distress, and examination of his chest was clear to auscultation bilaterally. Laboratory results showed a leukocytosis (WBC 11.3 × 103/μL, 11.2%) without eosinophilia, an elevated venous blood lactate (3.3 mmol/L), and anemia (hemoglobin 12.9 g/dL). His initial chest x-ray was abnormal, so a CT chest with contrast was obtained, which demonstrated a 2.9 cm right upper lobe cavitary lesion (). A brief workup for immunodeficiency was then performed. The patient had a negative 4th generation HIV antigen-antibody test as well as a negative HIV RNA PCR. His CD4 count was not measured, but quantitative immunoglobulin analysis was within normal limits (IgG 875 mg/dL, IgA 186 mg/dL, and IgM 76 mg/dL). Quantiferon TB Gold was negative.
Given his clinical stability, failure of outpatient antibiotics, and inability to produce an adequate sputum sample for Gram stain, the decision was made to proceed with bronchoscopy. Bronchoscopy showed diffuse inflammation with mild thick yellow secretions. Cultures of bronchoalveolar lavage, washings, and tissue culture performed during bronchoscopy resulted with heavy growth of P. aeruginosa (). No other pathogens were identified. Fungal culture showed no growth after four weeks. Blood cultures, three Kinyon smears of sputum, and urine Legionella antigen were also negative. Aspergillus galactomannan antigen and (1-3)-β-D-glucan assay (Fungitell) were negative. Histoplasma urine antigen, serum cryptococcal antigen, and serum coccidioides antigens were not detected. Echinococcus antibody was not detected. Once Gram-negative bacilli were identified on cultures, he was treated with ceftazidime (1g q8h IV). The dose was increased to 2g q8h IV after speciation, and sensitivities became available. On this regimen, his condition steadily improved. He was subsequently transitioned to oral ciprofloxacin (750 mg BID for 14 days) and discharged with outpatient follow-up. He completed a 21-day antibiotic course in total.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [69.0, 'mm hg']}",92.66667,88.03334,97.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 69.0 mm Hg = 92.66667 mm Hg.
Hence, the patient's mean arterial pressure is 92.66667 mm Hg."
1238,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-450,Extracted,"A 60-year-old man comes to the physician because of recurrent nose bleeds that occur with light trauma or at random times during the day. Over the past 6 months, the patient has felt weak and fatigued and has had a 10-kg (22-lb) weight loss. He has poor appetite and describes abdominal discomfort. He does not have night sweats. His pulse is 72/min, blood pressure is 130/70 mm Hg, and his temperature is 37.5°C (99.5°F). The spleen is palpated 10 cm below the left costal margin. Multiple bruises are noted on both upper extremities. Laboratory studies show.
Hemoglobin 9.8 g/dL
Hematocrit 29.9%
Leukocyte count 4,500/mm3
Neutrophils 30%
Platelet count 74,000/mm3
Serum
Lactate dehydrogenase 410 IU/L
A peripheral blood smear detects tartrate-resistant acid phosphatase activity.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 70.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1239,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6392811-1,Extracted,"A 47-year-old male patient presented in our inpatient department with epigastric pain, high fever, and vomiting for 4 days, with aggravation for 24 hours. Four days prior, the patient complained of severe epigastric pain with high fever (highest temperature was 39.2 °C) and vomited. The patient also reported that he had a respiratory infection about 2 weeks ago, which improved after taking an oral anti-inflammatory drug, but he did not recover completely. The patient was sent to the local hospital and received the second-generation antibiotic cefuroxime, but the condition was not improved. Twenty-four hours ago, the condition progressed, and he was sent to our hospital. The patient had a history of 30 years of alcohol intake of 250 g/d and had a gastric ulcer for many years without regular treatment.
Upon admission, the temperature was 39.0 °C, P was 136 times/min, and blood pressure was 136/85 mmHg. Physical examination revealed difficult abdominal breathing, epigastric pain, rebound pain, abdominal wall tightness, and weak bowel movement (0–1 times/min). Blood biochemical tests showed that the white blood cell count was 6.41 G/L and the Neut% was 87.1%. Contrast-enhanced computed tomography (CT) indicated that the whole gastric wall was edematous and thickened, but no sign of perforation was observed (Fig. ).
After admission, we administered Cefperazone–Sulbactam and tinidazole anti-infection, PPI acid suppression therapy, and rehydration treatment. However, we decided to operate because abdominal pain intensified, vomiting occurred repeatedly, and the vomitus contained fester during the treatment. The operation revealed more abscess fluid surrounding the stomach wall. The anterior, side, and posterior wall of the stomach were nigrescent necrotic (Fig. ). Hence, total gastrectomy was performed followed by reconstruction (roux-en-y). The specimen showed a considerable amount of pus accumulated in the stomach wall, and we sent the pus to culture (Fig. ). The patient was sent to the intensive care unit, given Cefperazone–Sulbactam and tinidazole for anti-infection, nutrition support, and rehydration treatment. After 24 days of treatment, the patient was transferred back to the ordinary ward to continue treatment and at last recovered.
Biopsy showed gastric mucosal necrosis, and necrosis was found on areas of the mucosal muscularis, muscularis, and serosa layer, where extensive neutrophil infiltration was present. Abscess formations were also found in the said areas, and the stomach and the greater omentum were phlegmonous (Fig. ). Tissue culture specimens were positive for hemolytic streptococcus.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [136.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",102,96.9,107.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 136.0 mm Hg + 2/3 * 85.0 mm Hg = 102.0 mm Hg.
Hence, the patient's mean arterial pressure is 102.0 mm Hg."
1240,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7599039-1,Extracted,"A 60-year-old male patient was admitted with a three-day history of severe breathlessness, pyrexia, tachypnea, and generalized malaise. He was a longstanding diabetic (> 10 years) on oral antihypoglycemic tablets. On examination, his pulse rate was 80/minute, blood pressure was 150/90 mmHg, he was afebrile on admission, respiratory rate was 26/minute, with a specific oxygen saturation of 86% on oxygen supplementation (10 liters/min). The relevant physical examination revealed bilateral crepts at the lung bases with a normal cardiovascular and neurological exam. A non-healing ulcer consistent with the diabetic peripheral vascular disease was seen on his right foot.
A reverse-transcriptase polymerase chain reaction (RT-PCR) from a nasopharyngeal swab was positive for the SARS-CoV-2 virus. A computed tomography (CT) scan of the chest showed multiple patchy ground-glass opacities in both lungs involving both upper lobes, the right middle lobe, and the lingula predominantly in a peripheral distribution strongly suggestive of COVID-19 infection (Figure ).
He was started on intravenous meropenem (1 gm thrice daily), oral oseltamivir (75 mg twice daily), with intravenous methylprednisolone (40 mg twice daily) and dexamethasone (4 mg twice daily), in conformity with the local protocol, along with general supportive care. His diabetes mellitus was managed with insulin adjusted as per a sliding scale based on his premeal blood sugar levels adjusted to maintain 180-200 mg/dl. He also received subcutaneous enoxaparin (40mg/0.4 ml) twice daily.
He gradually deteriorated with the onset of acute respiratory distress syndrome over the next few days. On day three, he was shifted to non-invasive ventilation to maintain his oxygen saturation. On day four, he received a single dose of injectable tocilizumab (400 mg) and was started on an oral combination of sitagliptin/metformin (50/500) twice daily and oral metformin (500 mg) thrice daily with subcutaneous insulin glargine (20 units) at night with regular insulin as needed to continue to maintain a blood sugar level of 180-200 mg/dl.
On day 10, bilateral lid edema with right eye prominence was noted and topical moxifloxacin was prescribed. The next day, on MRI of the brain, orbits, and paranasal sinuses, a soft tissue swelling was noted in the right preseptal, malar, premaxillary, and retrobulbar regions, which appeared hyperintense on T2 and fluid-attenuated inversion recovery (FLAIR). The right extraocular muscles were bulky and mild right proptosis was noted. Sinusitis in the form of significant mucosal thickening in the right frontal, maxillary, and ethmoidal sinus was also seen (Figure ).
A preliminary diagnosis of right orbital cellulitis was made and he was transferred to a tertiary care center. On admission, he was afebrile, breathless, and hypoxic. He underwent a complete systemic and laboratory evaluation. Relevant baseline investigations revealed a hemoglobin value of 10.40 gm/dl (normal 13-17 gm/dl), mild lymphopenia (9.60%; normal 20-40%), elevated serum creatinine (1.57 mg/dl; normal 0.70-1.20). C-reactive protein (CRP) was 29.53 mg/l (normal <5.0), procalcitonin (PCT) was 0.34 ng/ml (normal <0.5), with a D-dimer assay of 1547 ng/ml (normal 0-243) and an IL6 level of 3439 micrograms/ml (normal 0-7.0), suggestive of a severe cytokine storm.
He was continued on intravenous meropenem (1 gm thrice daily) and vancomycin (1 gram twice daily) with the addition of amphotericin B (0.5 mg/kg/day) and the cessation of steroid therapy.
An ophthalmic evaluation was requested the next day. On examination, the right eye was mildly proptotic with extensive areas of edema in the periorbital region with soft tissue necrosis along the medial half of the upper and lower lids. The right eye was congested with conjunctival edema and signs of exposure keratitis. The left eye appeared fixed and had a dilated non-reactive pupil (to light) either due to extension of infection to the other cavernous sinus or due to COVID-19 coagulopathy. Visual acuity and detailed ocular movements could not be assessed, as the patient was drowsy and not responsive. The clinical picture and MRI picture strongly suggested invasive fungal infection likely mucormycosis. A nasal swab was non-contributory but a nasal biopsy from the middle turbinate revealed broad aseptate filamentous fungal hyphae suggestive of mucormycosis, which was confirmed on a Sabourauds Dextrose Agar culture.
The patient continued to deteriorate, was ventilated, and eventually required inotropic support. Due to persistent hypotension, we were unable to carry out repeat imaging or any debridement measures. Despite all measures, he died on day six of this admission.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",110,104.5,115.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 90.0 mm Hg = 110.0 mm Hg.
Hence, the patient's mean arterial pressure is 110.0 mm Hg."
1241,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3943460-1,Extracted,"A 25-year-old Caucasian woman was brought to our emergency department after a single, high velocity projectile penetrated her vehicle windshield and struck her in the head. The vehicle was found pulled to the side of the road with transmission in park; there was no evidence of vehicular damage apart from the windshield damage. It was presumed by emergency responders that the patient had pulled over and stopped the car. The patient had been wearing a seatbelt. On presentation to our emergency department, our patient had a Glasgow Coma Scale score of 3, and was subsequently intubated for airway protection. A physical examination revealed a blood pressure of 111/87mmHg and her heart rate ranged from 100 to 150 beats per minute. A neurological examination revealed fixed and dilated pupils, as well as decerebrate posturing. She had a large, bleeding scalp laceration but no foreign material was noted. The remainder of the physical examination was normal. No other contusions or lacerations of her neck, chest or abdomen were identified. Of note, there was absence of a lap belt sign.
Initial laboratory results showed a normal hemoglobin level of 130g/dL and hematocrit of 0.40. A toxicology screen, including alcohol, was negative. A subsequent total body computed tomography (CT) scan, performed approximately 1 hour 15 minutes after the accident, revealed extensive intracranial injuries, including acute subdural hematoma, subarachnoid hemorrhage and cerebral edema, with loss of gray-white matter differentiation (Figure ). Transtentorial and cerebellar tonsillar herniation were also present. There were numerous skull fractures, including splitting and diastasis of her skull through the sagittal suture and the left lambdoidal suture (Figure ). A depressed fracture of the frontal bone, with associated pneumocephalus, was also present, in addition to a fracture through her planum sphenoidale.
CT of her abdomen and pelvis with intravenous contrast demonstrated an abnormal pancreas, which appeared diffusely enlarged (Figure ). Multiple linear hypodensities were seen throughout her pancreas, which had the appearance of prominent pancreatic folds. No pancreatic laceration was identified. A small to moderate amount of simple fluid was present in her abdomen, but localized to her retroperitoneum; specifically, the peripancreatic region. Overall, the findings simulated the CT appearance of early acute pancreatitis or low-grade pancreatic injury, which have overlapping imaging characteristics. However, no other abnormalities, or other findings of traumatic injury, were seen within the remainder of her chest, abdomen or pelvis. In particular, the structures adjacent to her pancreas, including her liver, duodenum, spleen and aorta, were normal. There were no gallstones seen on CT, and there was no intrahepatic biliary duct or common bile duct dilation. The mechanism of our patient’s injury, a single penetrating injury to her head, could not account for the finding.
Our patient was subsequently admitted to our intensive care unit. Her serum lipase levels obtained during this time were within normal limits, at 14U/L (normal range: 0 to 60 U/L), and her amylase levels were elevated at 248U/L (normal range: 30 to 110U/L). A repeat amylase level was not obtained, but a repeat lipase level (obtained approximately six hours later) remained within normal limits at 10U/L. Her neurological status failed to improve and a subsequent perfusion nuclear medicine study showed findings consistent with brain death. Consent was obtained from the patient’s family for organ donation.
During a laparotomy for organ donation, approximately 28 hours from the time of the initial trauma, the transplant surgeon observed marked pancreatic and peripancreatic edema, but no findings consistent with traumatic injury, such as laceration, pancreatic duct injury or regional hemorrhage. This was an isolated finding at surgery, with no other findings of traumatic injury identified in the remainder of her abdomen. Her pancreas was not removed for organ transplant, given its edematous appearance.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [87.0, 'mm hg'], 'Systolic Blood Pressure': [111.0, 'mm hg']}",95,90.25,99.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 111.0 mm Hg + 2/3 * 87.0 mm Hg = 95.0 mm Hg.
Hence, the patient's mean arterial pressure is 95.0 mm Hg."
1242,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7901359-1,Extracted,"A 75-year-old man presented to the emergency department of Klinikum Coburg after falling on his head while using a walker in the nursing home. He had been residing at that facility for ~ 3 weeks following a hospitalization in the surgical service of Klinikum Coburg for a traumatic right-sided parietal skull impression fracture. The head injury had resulted from a fall on the occipital area of the head with loss of consciousness, while the patient was still living independently in his own home. Although hyponatremia had been noted during that hospitalization (see below), the nephrology service was not consulted and no specific treatment was prescribed.
At the time of the current presentation, the patient reported dizziness but denied loss of consciousness; he also had no shortness of breath, chest pain, diarrhea, vomiting, or fever. The initial blood pressure in the emergency room was 98/50 mmHg with a heart rate of 82/min. The Glasgow Coma Scale was 15, and there were no focal neurological deficits. A fresh, bleeding laceration of the skin at the right temple was present. The mucous membranes were dry, and no jugular venous distention was noted; lungs were clear to auscultation bilaterally, skin turgor was reduced, and there was no peripheral edema. The remainder of the physical examination was normal. The skin laceration required suturing for hemostasis and wound closure. On questioning, the patient described that he had fallen several times bumping his head, even sustaining a bleeding head wound, in the days leading up to his first hospitalization, and that he had increased his fluid intake to counteract orthostatic dizziness. Past medical history included arterial hypertension and type 2 diabetes mellitus for which the patient was taking candesartan and metformin. He had no history of chronic renal disease and denied use of diuretics.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [98.0, 'mm hg'], 'Diastolic Blood Pressure': [50.0, 'mm hg']}",66,62.7,69.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 98.0 mm Hg + 2/3 * 50.0 mm Hg = 66.0 mm Hg.
Hence, the patient's mean arterial pressure is 66.0 mm Hg."
1243,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6862831-1,Extracted,"A 28-year-old woman visited the emergency room with confused mental status after a few generalized tonic-clonic seizure attacks. She had been treated for spinal cord glioblastoma for 4 years. She had undergone surgical removal of a spinal cord tumour and had been on concomitant chemoradiation therapy, which was terminated 2 weeks before the visit. CSF tap was not performed due to an intracranial space occupying lesion.
Brain MRI performed 3 months before the visit showed extension of the tumour from the brainstem to the upper thoracic spinal cord and another lesion at the right temporal pole.
Figure on presentation, she was drowsy and vital signs were as follows: blood pressure, 125/65 mmHg; body temperature, 36.4 °C; pulse rate, 100 per minute; respiratory rate, 19/min. The emergency medical faculty immediately gave her intravenous LEV 1000 mg; however, there was one more generalised tonic-clonic seizure without mental recovery. Video-EEG monitoring was initiated 2 h after the end of LEV loading; at that time, she started to show choreoathetoid movements in her face and bilateral limbs (see Additional file ), but no epileptiform discharges were noted on concomitant electroencephalography (EEG) as seen in Fig. . Laboratory findings including complete blood counts, electrolytes, blood urea nitrogen, creatinine, and arterial ammonia levels were normal. Review of her medical history revealed that she had been treated with solifenacin, esomeprazole, baclofen, and escitalopram for more than 3 months. She was not on concomitant drugs such as dopamine receptor blockers or antipsychotic agents. Considering the temporal relationship between the onset of involuntary movements and administration of LEV, further treatment with LEV was withheld. Chorea movement continued for about 30 min. She could communicate with her caregiver and physician until the end. After administration of 4 mg of lorazepam and 1200 mg of phenytoin, the involuntary movements ceased gradually. The next day her mental status gradually improved and no more involuntary movements were observed.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",85,80.75,89.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 65.0 mm Hg = 85.0 mm Hg.
Hence, the patient's mean arterial pressure is 85.0 mm Hg."
1244,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-6854,Extracted,"А 55-уеаr-old mаn рrеѕеntѕ to hіѕ рrіmаrу саrе рhуѕісіаn wіth a сomрlаіnt of fatigue for a couple of months. He was feeling well during his last visit 6 months ago. He has a history of hypertension for the past 8 years, diabetes mellitus for the past 5 years, and chronic kidney disease (CKD) for a year. The vіtаl ѕіgnѕ include: blood рrеѕѕurе 138/84 mm Нg, рulѕе 81/mіn, tеmреrаturе 36.8°C (98.2°F), аnd rеѕріrаtorу rаtе 9/mіn.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [84.0, 'mm hg'], 'Systolic Blood Pressure': [138.0, 'mm hg']}",102,96.9,107.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 138.0 mm Hg + 2/3 * 84.0 mm Hg = 102.0 mm Hg.
Hence, the patient's mean arterial pressure is 102.0 mm Hg."
1245,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8565698-1,Extracted,"A 44-year-old Hispanic woman with type II diabetes mellitus and no prior history of tobacco use was admitted to the hospital after being found unresponsive in her home. On arrival she had a temperature of 36.6 C degrees, heart rate of 126 bpm, respiratory rate of 26, blood pressure of 160/90, and an oxygen saturation of 78% on room air. Her physical exam was remarkable for a Glasgow coma score of 3, dry mucous membranes, and clear lung sounds to auscultation bilaterally. She was intubated upon arrival. Laboratory studies revealed a white blood cell count of 13000, CRP 412, blood glucose 997 mg/dl, serum sodium 160 mmol/L, serum creatinine of 3.72 mg/dL, and serum bicarbonate 11. Her arterial blood gas showed pH of 7.08, PaCO2 37.1, and PaO2 of 96 on 60% fraction of inspired O2 (FiO2) and she tested positive for SARS-CoV-2 by RT-PCR. COVID-19 specific labs were drawn and revealed elevated D-dimer to 1393 and normal values for troponin, BNP, procalcitonin, INR, AST/ALT, and ferritin. The patient was started on an insulin drip for her hyperglycemic syndrome. Her COVID-19 pneumonia was treated with 5 days of both remdesivir 100 mg IV daily and methylprednisolone 30 mg IV twice a day. Due to the critical presentation of the patient, empiric treatment for a possible superimposed bacterial pneumonia was also initiated on hospital day 1 with the broad-spectrum antibiotics cefepime and vancomycin.
The patient’s metabolic derangements improved during the first 3 days of her ICU stay, however her respiratory status worsened and she developed acute respiratory distress syndrome associated with her COVID-19 pneumonia. She required optimization of her ventilatory parameters along with rescue therapies including neuromuscular blockade and prone positioning by hospital day 4. Tracheal aspirate cultures were drawn at this time and revealed Pseudomonas aeruginosa and Aspergillus flavus. The patient was started on voriconazole 250 mg IV twice daily and switched to piperacillin/tazobactam 4.5 g IV every eight hours based on susceptibilities.
Computed tomography of the chest was obtained on hospital day 8 due to worsening hypoxemia and revealed diffuse ground glass opacities (GGO) and multiple cavitary lesions measuring up to 2.1 cm in the right middle and upper lobes ( and ). Micafungin 150 mg IV daily was added to the patient’s treatment regimen on hospital day 9 for invasive pulmonary aspergillosis given her poor response to treatment.
Bronchoscopy was performed on hospital day 13 due to worsening ventilation/perfusion ratio to less than 100 and lack of response to treatment. Multiple gray necrotic-appearing mucosal lesions were visualized bilaterally with near complete destruction of the left upper lobe and lingula. The lesions could be easily detached from the endobronchial wall and were non-friable. Endobronchial biopsy and bronchoalveolar lavage (BAL) were performed on the necrotic appearing lingula and Grocott’s methenamine silver stain on the sample revealed pauciseptated hyphae consistent with zygomycetes. Culture results were significant for isolated Candida albicans, glabrata, and krusei along with Aspergillus flavus and niger. The patient’s hemoglobin A1c was then checked and found to be 13. Given the endobronchial destruction on bronchoscopy, the histopathologic findings, and evidence of poorly controlled diabetes, a clinical diagnosis of pulmonary mucormycosis was made and the patient was then started on treatment with liposomal amphotericin B 5 mg/kg/day.
Despite aggressive therapy, the patient’s condition continued to decline. She required continuous renal replacement therapy and was deemed not to be a candidate for extracorporeal membrane oxygenation given her devastating pulmonary disease and multi-organ dysfunction. The patient expired on hospital day seventeen.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [160.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",113.33333,107.66666,119,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 90.0 mm Hg = 113.33333 mm Hg.
Hence, the patient's mean arterial pressure is 113.33333 mm Hg."
1246,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8429817-1,Extracted,"An 11-year-old Chinese girl was admitted to our hospital who presented with nephrotic syndrome. She weighed 49 kg and her blood pressure was 120/80 mmHg. Physical examination at admission revealed mild edema of the lower limbs with no associated corneal arcus or xanthoma. Laboratory investigations showed anemia (98 g/L), elevated serum urea (6.7 mmol/L) and creatinine (58 μmol/L), and decreased albumin (21 g/L). Urinalysis revealed proteinuria (4+) and microscopic hematuria (3+). Urinary protein was 2.06 g/24 h. Lipid profile showed elevated total cholesterol (5.04 mmol/L), elevated triglyceride (2.18 mmol/L), and normal LDL-cholesterol (2.24 mmol/L).
Based on laboratory findings, secondary causes of NS were excluded. Anti-nuclear, anti-cardiolipin, anti-neutrophil cytoplasmic, and anti-glomerular basement membrane antibodies were negative. Rheumatoid factor was also negative. Hepatitis B and C serology were negative. In addition, complement C3 and C4 levels were normal. Renal ultrasonography revealed normal-sized kidneys. These findings were consistent with the diagnosis of primary NS.
Despite treatment with prednisone (60 mg/day) and captopril (60 mg/day) for 2 months, her massive proteinuria and microscopic hematuria persisted, thereby prompting further evaluation via percutaneous renal biopsy. Light microscopy showed segmental glomerulosclerosis in three out of nine samples and mild-to-moderate proliferation of the mesangial cells and matrix (). The capillary lumina were dilated due to the presence of lipoprotein thrombi with pale staining on periodic acid-methenamine silver (). Oil red O staining confirmed the presence of intraluminal lipid droplets (). Immunofluorescence microscopy revealed that immunoglobulins (i.e., IgG, IgA, and IgM) and complement factor 1q (C1q) were negative. These findings were highly suggestive of LPG.
Genetic testing confirmed the presence of the c.127C>T (p.R43C) or Kyoto mutation of the APOE gene (). Her parents refused to undergo genetic screening. Therefore, her grandparents were investigated and underwent genetic screening. Her grandfather was asymptomatic and her grandmother was otherwise healthy. The APOE mutation in the patient and her grandfather were heterozygous (). In addition, the patient did not have any siblings.
All of these findings were consistent with the diagnosis of LPG. Prednisone was gradually tapered. Ideally, the patient should have been given captopril and a lipid-lowering agent. However, her grandfather refused the latter.
A 2-year follow-up revealed that her serum creatinine (102 μmol/L) and urine protein levels (3.2 g/24 h) were elevated. Moreover, her lipid profile showed elevated total cholesterol 6.56 mmol/L, triglyceride (2.82 mmol/L), and LDL-cholesterol (3.87 mmol/L).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [120.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1247,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8297213-1,Extracted,"On 1 March 2021, a 14-year-old boy was admitted to the Pediatric Emergency Department with compromised general status. He was found to be alert and oriented, febrile with 38.2 °C, tachycardic (118/beats/min), hypotensive (60/40 mmHg), saturating 100% on room air breathing 42 breaths per minute. Upon clinical examination, he was found to be dehydrated, with jaundiced skin, capillary refill 3–4 s, cold extremities with feeble peripheral pulses, palmoplantar erythema and edema, diffusely painful abdomen and palpable hepatosplenomegaly. He was in a condition of multiorgan failure: acute kidney injury, hepatosplenomegaly with increased inflammatory markers, in particular of IL-6 (144.6 pg/mL) and compromised hemodynamic status with reduction of left ventricular ejection fraction. We also noticed elevated values of alanine aminotransferase (ALT) (139 UI/L), aspartate aminotransferase (AST) (102 UI/L) and indices of cholestasis. Given the family history of SARS-CoV-2 infection and the positivity of SARS-CoV-2 IgG from serum, he was diagnosed with MIS-C. The patient’s compromised hemodynamic status required vasoactive support at the Cardiac Intensive Care Unit for the first 3–4 days of hospitalization. He was treated with intravenous immunoglobulin (2g/kg over 48 h) and pulse Methylprednisolone (10 mg/kg a bolus twice a day for 3 days and then progressively reduced). In consideration of the elevation of D-dimer (5734 ng/mL), a prophylactic antithrombotic therapy was started with low-molecular-weight heparin and aspirin (3 mg/kg/day). During hospital course, we noticed an improvement of his general conditions, with return to clinical baseline and progressive normalization of laboratory alterations, particularly of ALT and cholestatic indices. Ultrasonography of the abdomen was performed prior to discharge, and we found no abnormalities (). He was discharged at day 14 with indication to continue therapy with Aspirin and Prednisone per os, in progressive decalage according to the tapering strategy.
Following discharge, the patient was re-evaluated in a follow-up visit program (physical examination, laboratory tests and echocardiography) during which we started to taper off prednisone (until 1 mg/Kg/day). On 23 March, at the first follow-up visit, the patient was found to be in good conditions, without particular findings on the physical examination. The laboratory tests were normal except for the elevation of ALT (122 UI/L). On the second follow-up visit, 30 days following the onset of MIS-C, the patient was completely asymptomatic but clinical assessment revealed palpable hepatomegaly (2 cm below the costal margin) and further elevation of ALT (143 UI/L) on laboratory testing. AST, serum bilirubin and all the other lab parameters were normal. Ultrasonography of the abdomen was performed and revealed that hepatomegaly was secondary to hepatic steatosis (), with absence of pre-existing obesity (BMI 19.2) and signs of Nonalcoholic Fatty Liver Disease (NAFLD). Moreover, any other existing or previous inflammatory pathology was excluded. The following follow-up visits, laboratory tests () and ultrasonographies of the abdomen showed data suggesting hepatic steatosis as well. We did not introduce a drug therapy but we started a lifestyle approach including dietary improvements and increasing physical activity. Our patient was referred to a Pediatric Gastroenterologist. Currently, the patient is in good general clinical condition, with an optimal recovery of cardiac and renal function and not on drug therapy, as steroid therapy was withdrawn during the follow-up visit program. Nevertheless, our patient still has hepatic steatosis which was also confirmed by ultrasonography of the abdomen performed during the most recent follow-up visit on 27 May.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [60.0, 'mm hg'], 'Diastolic Blood Pressure': [40.0, 'mm hg']}",46.66667,44.33334,49,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 60.0 mm Hg + 2/3 * 40.0 mm Hg = 46.66667 mm Hg.
Hence, the patient's mean arterial pressure is 46.66667 mm Hg."
1248,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-6928,Extracted,"A 55-year-old woman with diabetes presents to the emergency department due to swelling of her left leg, fever, and chills for the past 2 days. The woman’s maximum recorded temperature at home was 38.3°C (101.0°F). Her left leg is red and swollen from her ankle to the calf, with an ill-defined edge. Her vital signs include: blood pressure 120/78 mm Hg, pulse rate 94/min, temperature 38.3°C (101.0°F), and respiratory rate 16/min. On physical examination, her left leg shows marked tenderness and warmth compared with her right leg. The left inguinal lymph node is enlarged to 3 x 3 cm.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",92,87.4,96.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 78.0 mm Hg = 92.0 mm Hg.
Hence, the patient's mean arterial pressure is 92.0 mm Hg."
1249,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-6056,Extracted,"A 67-year-old man presents to his primary care physician for abdominal pain. The patient states that he has had abdominal pain for the past month that has been steadily worsening. In addition, he endorses weight loss and general fatigue. The patient has a past medical history of obesity, diabetes, and hypertension. His current medications include metformin, insulin, and lisinopril. The patient is a current smoker and drinks roughly 3 drinks per day. His temperature is 99.5°F (37.5°C), blood pressure is 139/79 mmHg, pulse is 95/min, respirations are 17/min, and oxygen saturation is 98% on room air. The patient's cardiac and pulmonary exams are within normal limits. Examination of the patient's lower extremity reveals multiple tender palpable masses bilaterally that track linearly along the patient's lower extremity.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [139.0, 'mm hg'], 'Diastolic Blood Pressure': [79.0, 'mm hg']}",99,94.05,103.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 139.0 mm Hg + 2/3 * 79.0 mm Hg = 99.0 mm Hg.
Hence, the patient's mean arterial pressure is 99.0 mm Hg."
1250,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6150772-1,Extracted,"A 40-year-old man with a history of end-stage renal disease on hemodialysis, hypertensive cardiomyopathy, and poorly controlled hypertension presented to the emergency department with a sudden onset of 48-hour right visual blurring and headache. On physical examination, he was alert, oriented to time, place and person, with a blood pressure of 200/124 mmHg, and a heart rate of 88 beats/minute. Neurologic examination was only significant for decreased right visual acuity. The electrocardiogram revealed normal sinus rhythm.
Computed tomography of the head revealed focal area of hypoattenuation in the left cerebellar hemisphere (Figure ).
Magnetic resonance imaging of the brain revealed multiple new regions of restricted diffusion within the left frontal, parietal and occipital lobes, consistent with an embolic stroke (Figure ).
A carotid duplex ultrasound was unremarkable for carotid artery stenosis. A two-dimensional transthoracic echocardiography revealed a large calcified mass measuring 24.5 mm x 16.0 mm (Figure , asterisks; Video ).
A three-dimensional transesophageal echocardiogram of the mitral valve revealed two discrete nonmobile calcified masses, with central areas of echolucency consistent with CCMA (Figure , asterisks; Video ).
As no other potential sources of embolism were identified, CCMA lesion was postulated as the possible source of embolism. Dual antiplatelet therapy (aspirin 81 mg daily and clopidogrel 75 mg daily) and high-intensity atorvastatin 80 mg daily were initiated. Surgical excision of the CCMA lesion was considered but not performed immediately due to the potential risk of hemorrhagic conversion of the ischemic stroke.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [200.0, 'mm hg'], 'Diastolic Blood Pressure': [124.0, 'mm hg']}",149.33333,141.86666,156.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 200.0 mm Hg + 2/3 * 124.0 mm Hg = 149.33333 mm Hg.
Hence, the patient's mean arterial pressure is 149.33333 mm Hg."
1251,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6650453-1,Extracted,"A 48-year-old female patient presented to the emergency department (ED) after CPR due to VF that occurred after a seizure. Four years prior, she presented to other hospital ED and discharged after observation for a condition where her arms were raised and her limbs were stretched continually for approximately 1 min while sleeping after an episode of alcohol intake. She did not undergo any particular tests and neither was she administered any drugs, under the assumption that these symptoms were temporary and had been caused by alcohol intake. Three years prior, a similar episode occurred during sleep, for which some medical tests were conducted such as electrocardiogram (ECG), brain MRI, and electroencephalogram (EEG), but no conclusive results were reported. Drugs were also prescribed but not taken by the patient. One and a half year prior, the patient experienced another relapse again during sleep at dawn. According to the statement given by her husband who witnessed the episode at the time, for approximately 1 min while sleeping, the patient groaned with her mouth shut tightly, her arms raised, limbs stretched, and did not respond when called. Subsequently, her body collapsed, she stopped breathing for approximately 30–40 s, and then she breathed in a concentrated manner. Urination and post-ictal confusion were also noted. The patient had no family history of epilepsy or no medical history of febrile convulsion in the past, and only reported of the inability to sleep well and waking up frequently due to a burning sensation in the foot. In the previous hospital, the patient underwent video-EEG and polysomnography in an epilepsy monitoring unit (EMU) for two days to investigate the cause under the putative diagnosis of restless legs syndrome and nocturnal bilateral tonic seizure – frontal lobe epilepsy. Based on EEG findings, there was no inter-ictal epileptiform discharge and an intermittent slow wave was observed in the right frontotemporal area, but it was equivocal, and therefore, no clear abnormality was reported. Subsequently, administration of pramipexole and pregabalin was started to control the rare nocturnal seizures and symptoms of the restless legs syndrome under the putative diagnosis of restless legs syndrome and unknown etiologic epilepsy – bilateral tonic seizure.
On the day before current admission, her epileptic seizure relapsed during sleep but she recovered consciousness immediately; thus, she did not come to the hospital. In the evening of the admission day, while conversing with her children, she suddenly had a general tonic-clonic type seizure for 2–3 mins and emergency medical services (EMS) were informed as she did not recover consciousness immediately after the seizure like in previous episodes and her breathing was almost negligible. Following the instructions of the EMS center, her family started CPR. After the paramedics arrived, spontaneous circulation was restored after CPR and 2 times of defibrillation as VF was indicated by the AED findings (). At the time of ED arrival, the patient was stupor and her vital signs and oxygen saturation were normal with a blood pressure of 121/82 mmHg, pulse rate of 80 beats per minute, respiratory rate of 16 breathes per minute, and body temperature of 36.2°C. ECG performed immediately after arrival showed a sinus rhythm with a heart rate of 78 beats per minute and QTc duration of 401 ms (). The initial arterial blood gas analysis (ABGA) showed a pH of 7.35, PCO2 21 mmHg, PO2 134 mmHg, HCO3 11.6 mEq/L, and a lactate level of 6.1 mg/dL. Approximately 10 min after arrival, she regained consciousness but Todd’s paralysis in the right limbs and global aphasia were shown. The repeat ABGA showed that all values had recovered to normal levels. All other blood test results were normal, including electrolyte and myocardial enzyme levels. Levetiracetam was administered intravenously in the ED. Brain diffusion MRI showed no abnormality. Thereafter, the patient was admitted to the cardiology intensive care unit (ICU) and received a full cardiologic work-up. After admission to the ICU, her consciousness was maintained in an alert state, the paralysis in the right limbs and aphasia resolved completely, and the EEG showed normal results. Transthoracic echocardiography performed on the day after admission showed that the left ventricle ejection fraction (LVEF) was reduced to 44%, and left ventricle global hypokinesia and moderate systolic dysfunction were observed. After that, consecutively performed coronary angiography (CAG), spasm provocation test, cardiac MRI, and 24-hr Holter monitoring showed normal results. For the purpose of preventing sudden cardiac death (SCD), the insertion of an implantable cardiac defibrillator (ICD) was recommended. The patient was discharged without any complications 6 days after the procedure. Currently, levetiracetam administration is being maintained by the neurology department and her condition is being periodically followed by the cardiology department under the diagnosis of aborted SCD due to VF and heart failure with mid-range ejection fraction.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [121.0, 'mm hg'], 'Diastolic Blood Pressure': [82.0, 'mm hg']}",95,90.25,99.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 121.0 mm Hg + 2/3 * 82.0 mm Hg = 95.0 mm Hg.
Hence, the patient's mean arterial pressure is 95.0 mm Hg."
1252,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5674467-1,Extracted,"A 65-year-old man was brought to hospital by ambulance and admitted to our emergency department with fever and brief impairment of consciousness. This condition followed 4 days of general fatigue and appetite loss. The patient had a history of lumbar canal stenosis and had undergone sacral epidural block 2 weeks previously. He had no other predisposing factors for infection, such as diabetes, alcoholism, or i.v. drug use. On arrival, the patient's vital signs were as follows: Glasgow Coma Scale, E4V5M6; blood pressure, 134/80 mmHg; pulse rate, 136 b.p.m.; body temperature, 38.6°C; respiration rate, 25 breaths/min; and oxygen saturation, 100% in room air. On physical examination, the patient presented with neck stiffness. A knock pain was positive in the right lumbar region. He showed no radiculopathy or neurological deficits. Laboratory testing revealed a white blood cell count of 8500/μL and C-reactive protein level of 24 mg/dL. Cranial computed tomography was unremarkable. Cerebrospinal fluid (CSF) was sampled at the L2–3 level to avoid the region of lumbar canal stenosis and epidural block. Blood culture was also carried out. The CSF was xanthochromic with elevated protein (948 mg/dL), polymorphonuclear pleocytosis (282/μL), and low glucose (72 mg/dL; plasma glucose, 176 mg/dL). We diagnosed bacterial meningitis on the basis of fever, meningeal irritation, and polycytosis in the CSF. We administered meropenem and vancomycin. Blood culture revealed that the pathogen was methicillin-sensitive Staphylococcus aureus. We changed antibiotics to ceftriaxone on day 2. Blood culture on day 4 remained positive. Spinal epidural abscess or pyogenic spondylitis was suspected because of the patient's recent sacral epidural block. Magnetic resonance imaging showed a dorsal epidural abscess extending from C6 to S1 (Fig. ). Spondylitis was also present from L1 to S1 (Fig. A). Inflammation was observed in the connective tissue in the dorsal lumbar region (Fig. B). We informed the patient that the sacral epidural block was the likely cause of SEA. Initially, we planned conservative therapy because the patient had no neurological deficits. However, fever had been present for 7 days, the white blood cell count had increased, and blood culture remained positive on days 5 and 7. Furthermore, computed tomography with contrast confirmed abscesses in the mediastinum (Fig. A) and bilateral psoas muscles on day 6 (Fig. B, C). Medical management was thus considered to be ineffective. Therefore, on day 8, the patient underwent epidural drainage by laminectomy at T2–T3, T10–T11, and L4–5, followed by mediastinal abscess drainage with video-assisted thoracoscopy. The drainage was purulent. The postoperative diagnosis was panspinal epidural abscess, pyogenic spondylitis at L4–5, and mediastinal abscess. The patient's postoperative course was satisfactory. The patient received i.v. antibiotics for 8 weeks and was transferred to another hospital on day 61.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [134.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",98,93.1,102.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 134.0 mm Hg + 2/3 * 80.0 mm Hg = 98.0 mm Hg.
Hence, the patient's mean arterial pressure is 98.0 mm Hg."
1253,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8204668-1,Extracted,"A 23-year-old Caucasian female presented with right-sided pulsatile tinnitus of 9 months duration. She described hearing a whooshing noise. She did not have any hearing loss or dizziness. The patient struggled to focus while studying because of the intrusive tinnitus.
The patient was initially seen in an otology clinic where she did not have any otological, rhinological or neurological symptoms. Otoscopy revealed normal tympanic membranes; cranial nerves were intact; cerebellum function was intact and the balance tests were negative. Full examination of the nose, mouth, pharynx and larynx was normal. Fundoscopy and auscultation of her head and neck were normal. Her blood pressure was 120/64 mmHg (millimetres of mercury). She had normal hearing on pure audiogram (Figure 1 ) and normal ventilation of her middle ears on tympanogram (Figure 2 ).
All the routine blood tests including thyroid function tests were normal. MRI brain and internal auditory canals was normal. The CT scan of the petrous temporal bone showed a large high lying right-sided jugular bulb. It also showed dehiscence of right sigmoid plate with herniation of the lateral aspect of the transverse and sigmoid venous sinuses into the mastoid complex (Figure 3 ).
She was seen in a Tinnitus clinic and thorough counselling was provided by the senior audiologist. She tried environment sound therapy along with other conservative measures but continued to struggle with her intrusive right sided pulsatile tinnitus.
The patient was seen by the skull base surgeon. Clinically, there was no dehiscence of the jugular bulb and the hypotympanum was clear. The patient described hearing a whooshing noise and it was accepted as a venous hum secondary to dehiscence of the sigmoid sinus. The presence of the high lying jugular bulb on radiology added complexity to the possible aetiology of her tinnitus. It was discussed that even correction of the sigmoid sinus dehiscence may not lead to symptom resolution as high lying jugular bulb is associated with tinnitus as well. The patient accepted this possibility and it was agreed that if her symptoms fail to settle down after dehiscent sigmoid correction then she might need ligation of the right internal jugular vein at a later stage.
Surgical intervention: the patient was positioned supine with head elevation and turned to left. The skin was cleaned with betadine and standard drapes were applied. Postauricular incision was made exposing the mastoid bone. Cortical mastoidectomy was carried out to expose the sigmoid sinus, lateral semicircular canal and the jugular bulb. An example of intra-operative appearance of the cortical mastoidectomy and sigmoid sinus is shown in Figure 4 .
Intraoperatively, dehiscence was noted between the walls of the jugular bulb and floor of the middle ear. Bleeding encountered when separating the jugular bulb from the adjacent bones. The bleeding was controlled by Fibrillar and Surgicel packing. This was further supported by extraluminal packing with acellular dermal graft SureDerm. The jugular bulb was separated from the middle ear floor and packing with SureDerm continued between the sigmoid sinus and bony wall anteriorly. Multiple layers of SureDerm were used for extra luminal packing of mastoid cavity and hypotympanum along with Surgicel. Little muscle harvested from incision margin was placed on top of packing. The incision was closed with 3/0 monocryl and skin staples. Bactroban ointment was applied to the incision edges followed by gauze and crepe bandage. The microscope was used to examine the ear canal and tympanic membrane confirming absence of any haemotympanum.
The patient made a good postoperative recovery and reported resolution of tinnitus on recovering from anaesthesia. The patient was discharged home the following day and head bandage was removed.
Two days after the operation the patient noticed some bleeding from her nose and throat. On examination no active bleeding was seen from the ear and the nasal endoscopy did not show any bleeding from her nose or eustachian tube orifice. There was evidence of haemotympanum on microscopic examination of her right ear. The patient reported impaired hearing in her right ear. She was advised to avoid any physical exertion for the next few days.
At three-month follow-up the haemotympanum had resolved and her hearing had returned back to normal (Figure 5 ). The patient has remained tinnitus free 11 years following her surgery.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [64.0, 'mm hg']}",82.66667,78.53334,86.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 64.0 mm Hg = 82.66667 mm Hg.
Hence, the patient's mean arterial pressure is 82.66667 mm Hg."
1254,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4901014-1,Extracted,"A 43-year-old Korean man visited Chonnam National University Hospital due to fever and rash. The patient had history of staying and mosquito bites at Cumbuco, Ceara, Brazil for 3 weeks from 17 Feb 2016 to 9 Mar 2016, and returned to Republic of Korea on 11 Mar 2016. He had fever, chill, myalgia, and eyeball pain on 6 days after return from Brazil. Three days later, rash also developed. The patient visited nearby clinic and the blood was sampled for Zika virus reverse-transcriptase polymerase chain reaction (RT-PCR) on the 6th day of illness. The RT-PCR result was reported to be positive by the Korea Center for Disease Control and Prevention. The patient was admitted to Chonnam National University Hospital for further evaluation and management on the 7th day of illness.
Upon admission, he had a blood pressure of 110/70 mmHg, pulse rate of 80 beats/min, respiratory rate of 20/min, and a body temperature of 36.3°C. Painless multiple erythematous maculopapular rash with itching was observed in trunk and both upper and lower extremity (). Hyperemia was present in both eyes and the patient complained of feeling of dryness in both eyes. Enlarged lymph node was not observed. Neurologic symptoms or signs including headache, vomiting, decrease in motor power, or abnormal sensation were absent. Initial laboratory findings performed on the day of admission were as follows: white blood cell count 4,900/µL (neutrophils 55%, lymphocytes 29%, monocytes 15%), hemoglobin level 16.5 g/dL, platelet count 221,000/µL, erythrocyte sedimentation rate 2 mm/hr, serum C-reactive protein 0.47 mg/dL, procalcitonin 0.05 ng/mL, serum neutrophil gelatinase-associated lipocalin 89.4 ng/mL, blood urea nitrogen 12.8 mg/dL, total protein 7.4 g/dL, albumin 4.6 g/dL. Serum aspartate aminotransferase, alanine transaminase, and lactate dehydrogenase were 61 U/L, 92 U/L, and 459 U/L, respectively. Serum level of ferritin was 417 ng/mL and serum adenosine deaminase was 37 IU/L.
He was only medicated with cetirizine 10 mg/day per oral. Intravenous fluid or other medication was not prescribed during the hospital stay. The patient no longer felt myalgia or febrile sense during the hospital stay. Conjunctival hyperemia continued but maculopapular rashes were fading out. He was discharged from the hospital on 8th day of illness, and then was followed up weekly for 6 weeks. During the 6 weeks of follow-up, he did not have symptoms or signs of neurologic abnormality. Zika virus RT-PCR was positive from saliva and urine for 2 weeks after the symptom onset but became negative after 3 weeks ().
Culture isolate of Zika virus was obtained by inoculating monolayers of Vero cells with his semen sample at the 7th day of the illness and culturing the cells at 37°C in a 5% carbon dioxide atmosphere. In the culture of first passage, the serial change of cycle threshold value by RT-PCR using RealStar Zika virus RT-PCR kit 1.0 (Altona Diagnostics, Hamburg, Germany) was shown in .
For electron microscopic observation, Vero cell monolayer inoculated with culture supernatant of second passage was fixed as previously described (). It was cut on ultramicrotome (RMC MT-XL) at 65 nm. Ultrathin sections were stained with saturated 4% uranyl acetate and 4% lead citrate before examination with a transmission electron microscope (JEM-1400; JEOL Inc., Tokyo, Japan) at 80 kV. Virus particles were observed within the cytoplasm ().
Immunofluorescence staining was performed by previously described method (). Briefly, Zika virus-infected and mock-infected cells were fixed with 4% paraformaldehyde in PBS for 1h at room temperature. Slides were blocked and then incubated with the 3 weeks convalescent serum of patient (1:40 dilution) and serum of healthy control (1:40 dilution) at -4°C overnight. Cells were washed and incubated for 1 hour at room temperature with fluorescein isothiocyanate-conjugated anti-human IgG. 4',6-Diamidino-2-phenylindole dihydrochloride was used to stain the nucleus. Preparations were examined with a confocal microscope (Leica, Buffalo Grove, IL, USA). Immunofluorescence was observed in Zika virus-infected Vero cells applied with convalescent serum rather than control serum ().",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1255,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5149592-1,Extracted,"A 30-year-old previously healthy male presented to the emergency department with constitutional symptoms of weakness, fatigue, dizziness, and anorexia. A baseline EKG and chest X-ray were within normal limits. He was diagnosed with primary adrenal insufficiency presenting with biochemical evidence of high ACTH (>278 pmol/L) and low cortisol levels (32 nmol/L) and started on prednisone 5 mg po od and fludrocortisone 0.1 mg po od. Two weeks later, he presented with a 5-day history of orthopnea and increasing dyspnea on minimal exertion. On presentation, the blood pressure was 104/74 mm Hg with a heart rate of 90 beats per minute. The jugular venous pressure was elevated at the angle of the jaw with displacement of the cardiac apex and normal heart sounds. There were diminished breath sounds bilaterally in both lower lung fields without evidence of peripheral edema. The serum sodium was mildly reduced at 132 mmol/L (normal range: 135–145 mmol/L) while the potassium was increased at 5.6 mmol/L (normal range: 3.5–5.0 mmol/L). There was a markedly elevated N-terminal brain natriuretic peptide of 4515 pg/mL (normal range <125 pg/mL), consistent with clinical and biochemical evidence of acute heart failure. The serum TSH, urine toxicology, and metanephrines were within normal limits. A 12-lead EKG demonstrated poor R-wave progression across the precordial leads with evidence of a left anterior fascicular block. Chest X-ray findings were consistent with bilateral pleural effusions, vascular redistribution, and interstitial edema. Transthoracic echocardiography (TTE) confirmed a dilated left ventricle (LV), severe LV systolic dysfunction with an ejection fraction of 15%, and moderate functional mitral regurgitation. Cardiac magnetic resonance imaging with late gadolinium enhancement was normal with no evidence of a viral myocarditis nor infiltrative cardiomyopathy. Cardiac catheterization demonstrated normal coronaries consistent with the diagnosis of a nonischemic dilated cardiomyopathy. A computed tomographic scan of the abdomen revealed hyperdense adrenal glands with central necrotic areas of hypoattenuation and peripheral enhancement, consistent with the recent diagnosis of primary adrenal insufficiency. With a new diagnosis of acute heart failure due to primary Addison's disease, the patient was admitted for medical treatment with parenteral diuretics, ACE inhibition, beta blockade, and a decrease in the fludrocortisone dosage (that was started 2 weeks before). A 6-month follow-up multigated acquisition scan (MUGA) revealed an improvement in LV ejection fraction to 40–45%.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [74.0, 'mm hg'], 'Systolic Blood Pressure': [104.0, 'mm hg']}",84,79.8,88.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 104.0 mm Hg + 2/3 * 74.0 mm Hg = 84.0 mm Hg.
Hence, the patient's mean arterial pressure is 84.0 mm Hg."
1256,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8110227-1,Extracted,"An 18-year-old male with known beta-thalassemia major on chelation therapy presented to a district general hospital with a 3-day history of generalised abdominal pain. He received weekly blood transfusions from a young age and had been taking deferasirox for over 5 years. He denied any melena or hematemesis. He denied taking any non-steroidal anti-inflammatory drugs (NSAIDs) or steroid use. He denied any alcohol consumption, smoking or recreational drugs.
On admission, his temperature was 34.6 °C, blood pressure 100/60 mm Hg and heart rate 160 beats per minute. Electrocardiogram confirmed a supra-ventricular tachycardia. On examination, he had bilateral clear lung fields with a tender and distended abdomen. He appeared clammy, pale and peripherally shutdown. His blood panel is shown in . His viral polymerase chain reaction (PCR) was positive for SARS-CoV-2 infection.
His initial management included aggressive fluid resuscitation, five units of packed red blood cells, a platelet pool, fresh frozen plasma, intravenous piperacillin/tazobactam, tranexamic acid and intravenous fluids. He was cardioverted with adenosine and synchronized direct-current cardioversion (DCCV) with 180 J. Despite this, he remained hemodynamically compromised and his hemoglobin dropped to 56. His admission chest radiograph identified air under the left hemidiaphragm (). He was intubated and ventilated and transferred for a computed tomography (CT) scan. This confirmed pneumoperitoneum with a moderate degree of ascites with a likely perforated gastric ulcer (). He was taken to theatre for urgent laparotomy where a perforated gastric ulcer was confirmed and treated surgically with omental patching. Biopsy samples demonstrated ulceration with a negative Campylobacter-like organism (CLO) test.
During his intensive treatment unit (ITU) admission, he developed respiratory distress and increasing hypoxia. A repeat CT scan confirmed bilateral lung infiltrates in keeping with worsening SARS-CoV-2 pneumonia and possible aspiration pneumonia. It was noted he had increased hepatosplenomegaly in keeping with recent hemolysis. He was also identified to have a deep vein thrombosis. He was treated with a 10-day course of antibiotics, remdesivir, dexamethasone and anticoagulation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",73.33333,69.66666,77,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 60.0 mm Hg = 73.33333 mm Hg.
Hence, the patient's mean arterial pressure is 73.33333 mm Hg."
1257,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7885145-1,Extracted,"An 8-year-old boy, previously healthy, presented to the emergency department with a 3-day history of double vision and right eye squint with giddiness for 1 month. He denied any history of recent head trauma, fever or headache. On the initial presentation, blood pressure was 186/124 mmHg with a pulse rate of 83 per minute and afebrile. On examination, there was limited right eye movement on the lateral gaze. The rest of the physical examinations were normal. Computed tomography of the brain was normal. Intravenous and oral antihypertensive medications were initiated to control blood pressure. Blood investigations were normal. Special blood investigations that include antinuclear antibody, antistreptolysin O titer, C3, C4, random cortisol, aldosterone and renin level were also normal. Renal ultrasound () showed a small right kidney with multiple cystic areas and an enlarged lobulated left kidney. Given suspicion for renal mass causing the hypertensive emergency episode, magnetic resonance imaging (MRI) of the abdomen was performed. MRI () revealed a large well-circumscribed lobulated heterogeneous mass at the lower pole of the left kidney with dysplastic right kidney.
Considering suspicious MRI findings of left renal mass, a paediatric radiologist was consulted for a second opinion. Micturating cystourethrography () was then performed, which revealed right grade 5 vesicoureteric reflux, left upper pole grade 3 vesicoureteric reflux and left lower pole compensatory hypertrophy. Re-evaluation of the MRI images concludes findings of severely hydronephrotic and atrophied right kidney, atrophied upper pole and hypertrophied lower pole of the left kidney. Cystic areas in the right kidney correspond to severe hydronephrosis, while the enlarged lobulated left kidney represents hypertrophied left lower pole. At this stage, overall features were suggestive of chronic vesicoureteric reflux with bilateral reflux nephropathy. 99mTc-dimercaptosuccinic acid (DMSA) scan () carried out later has confirmed the diagnosis.
The patient was then managed in an outpatient setting under general paediatric and paediatric nephrology follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [186.0, 'mm hg'], 'Diastolic Blood Pressure': [124.0, 'mm hg']}",144.66667,137.43334,151.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 186.0 mm Hg + 2/3 * 124.0 mm Hg = 144.66667 mm Hg.
Hence, the patient's mean arterial pressure is 144.66667 mm Hg."
1258,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4024387-1,Extracted,"A 33-year-old woman from Saint Vincent Island presented to the emergency department with complaints of 6-month history of epigastric mass and pain, 15-lb weight loss, and poor appetite. She stated that she was evaluated by the local physician in the Caribbean and was told that she has a cyst. No other further work-up was done. She denied fevers, chills, change in the color of the urine or stool, nausea, or vomiting. She was an ex-smoker and quit 10 years ago. She denied alcohol intake, any prescribed or illicit drug use, drug allergy, or any significant family history.
Vital signs revealed a pulse of 82 beats/min, blood pressure of 101/62 mmHg, respiratory rate of 20 respirations/min, and normal temperature. On physical exam, the patient appeared cachectic. Rest of the physical exam was significant for jaundice, scleral icterus, and a 14 × 16 cm non-tender epigastric mass. Laboratory tests revealed the following: white blood count of 16,000/μL, hemoglobin of 9.9 g/dL, platelet count of 882,000/μL, total bilirubin of 8.7 mg/dL, alkaline phosphatase of 590 units/L, albumin of 2.2 g/dL, LDH of 374 units/L, INR of 1.5, and normal glucose, electrolytes, renal function, amylase, lipase, and rest of the liver function tests. Tests of tumor markers revealed an AFP level of 1,451 ng/dL and normal carcinoembryonic antigen, CA 19-9, and βHCG. CT scan of the abdomen with oral and intravenous contrast revealed a heterogeneous upper abdominal mass measuring 12.6 × 11.7 × 11.4 cm inseparable from the lesser curvature of the stomach, compressing the liver hilum, periportal vessels and causing mild to moderate intrahepatic biliary ductal dilatation (Fig. ). Ultrasound of the abdomen also confirmed these findings. Esophagogastroduodenoscopy revealed candidal esophagitis and a large smooth intramural or extrinsic mass arising from the lesser curvature of the stomach. Histopathological examination of the biopsy of the gastric mass was inconclusive. Histopathological examination and immunohistochemistry of CT-guided fine-needle aspiration of the abdominal mass revealed CK7+ rare positivity, CK20+, villin+, CDX-2+, and negative for CA 19-9 and CA 125. AFP stain was negative. These findings were consistent with upper gastrointestinal, pancreatobiliary, or bladder neoplasm. Ultrasound of the pelvis did not reveal any masses. Serology for Helicobacter pylori was positive, and treatment was initiated. She was also treated for candidal esophagitis. Further testing revealed sequential elevations in the total bilirubin, direct bilirubin, and the alkaline phosphatase levels. The patient became more cachectic and could not maintain adequate oral intake. Parenteral nutrition was started. She also underwent a laparoscopy and core biopsy of the abdominal mass, and the histopathological examination and immunohistochemistry revealed adenocarcinoma with extensive necrosis most consistent with upper gastrointestinal primary neoplasm. An independent external pathology laboratory also confirmed the same findings. Jejunostomy tube was also placed for feeding, and parenteral nutrition was discontinued. Due the rising bilirubin levels, a transhepatic cholangiogram was performed with placement of an internal/external biliary catheter for drainage. The bilirubin levels decreased to a nadir of 12.5 mg/dL after the placement of the biliary drainage catheter. Due to the abnormal bilirubin, the patient was not a candidate for the conventional gastric adenocarcinoma chemotherapy regimens, and the plan was to start chemotherapy consisting of weekly gemcitabine at a reduced dose to adjust for the bilirubin levels. She received gemcitabine at the reduced dose of 800 mg/m2. Pain control was achieved with intravenous hydromorphone via the patient-controlled analgesia pump. Soon after the administration of chemotherapy, there was an improvement in the clinical and laboratory parameters. However, after a few days, there was deterioration in the patient’s mental and respiratory status. CT scan of the head and the chest did not reveal metastasis or pulmonary embolism. Ammonia level was elevated, and lactulose was administered. She was not able to receive any further chemotherapy, and efforts were made to keep her on comfort care. Eventually, the patient was discharged in stable condition as per the family’s wishes to the Saint Vincent Island.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [101.0, 'mm hg'], 'Diastolic Blood Pressure': [62.0, 'mm hg']}",75,71.25,78.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 101.0 mm Hg + 2/3 * 62.0 mm Hg = 75.0 mm Hg.
Hence, the patient's mean arterial pressure is 75.0 mm Hg."
1259,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4137535-1,Extracted,"A case of 63-year-old man with complaints of severe chest pain, sweating, and nausea was investigated. Acute coronary syndrome was considered as the differential diagnosis, but the coronary angiography was normal. Abdominal ultrasound demonstrated a 15 × 14 × 13 cm mass in the left adrenal gland (), and then patient was referred to our clinic. Physical examination of the patient revealed not only nonpainful, firm, and mobile abdominal mass in left hemi-upper abdomen but also painful mass on his left 8th, 9th, and 10th ribs (). His blood pressure was 185/95 mmHg and pulse was 86 per minute. Thoracoabdominal computed tomography (CT) revealed 12.5 × 14.5 × 14 cm mass located in the left retroperitoneum. This mass appeared to be invading the left kidney and there were cystic areas and calcifications (). Also both in CT scan and PET scan, multiple metastases in both lungs, right lobe posterior-inferior subsegments of liver, and the skeletal system were detected (). The results of blood analysis (glucose, uric acid, plasmatic proteins, ions, and complete blood count) were normal. Plasma and urinary catecholamamines and metanephrines were elevated (). He received 4 mg doxazosin four times a day for 15 days prior to the surgery. Three days after blocking alpha, he also received 50 mg metoprolol twice a day and 20 mg amlodipine once a day for preoperative preparation. For 3 days prior to the operation, he received daily 3500 ml saline for hydration and blood pressure was titrated with Na-nitroprusside during the operation. During the surgical exploration with thorachoabdominal incision, 1736 grams of 20 × 17 × 9 cm fixed round well-vascularized retroperitoneal mass involving the surrenal gland () and the mass in ribs 7–10 were observed. Left surrenalectomy and excision of ribs which were surrounded with soft tissue mass were done without complication while high blood pressure attacks were normalized with Na-nitroprusside during the operation. There were no postoperative complications. Histological analysis showed a solid-cystic adrenal neuroendocrine tumor and pathology resulted as malignant pheochromocytoma () with rib metastasis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [185.0, 'mm hg'], 'Diastolic Blood Pressure': [95.0, 'mm hg']}",125,118.75,131.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 185.0 mm Hg + 2/3 * 95.0 mm Hg = 125.0 mm Hg.
Hence, the patient's mean arterial pressure is 125.0 mm Hg."
1260,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5588,Extracted,"A 42-year-old man presents to the emergency department with persistent cough. The patient states that for the past week he has been coughing. He also states that he has seen blood in his sputum and experienced shortness of breath. On review of systems, the patient endorses fever and chills as well as joint pain. His temperature is 102°F (38.9°C), blood pressure is 159/98 mmHg, pulse is 80/min, respirations are 14/min, and oxygen saturation is 98% on room air.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [159.0, 'mm hg'], 'Diastolic Blood Pressure': [98.0, 'mm hg']}",118.33333,112.41666,124.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 159.0 mm Hg + 2/3 * 98.0 mm Hg = 118.33333 mm Hg.
Hence, the patient's mean arterial pressure is 118.33333 mm Hg."
1261,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8673460-1,Extracted,"We report a case of a 16-years-old female, presented with upper central abdominal pain, associated with upper abdominal distension and multiple episodes of non-bilious, non-blood stained vomiting containing food particles since 1 day without significant past medical or surgical history. On examination, her heart rate was 120 per minute, blood pressure 120/70mmHg and respiratory rate 20 per minute. Abdominal examination revealed epigastric distension and tenderness. Blood investigations revealed leukocytosis (21100) with significantly raised levels of amylase (1180) and lipase (1680).
The patient was admitted with a provisional diagnosis of acute pancreatitis and nasogastric decompression was done. On further evaluation chest X-ray () revealed a distended stomach with air-fluid level and as she did not have significant improvement with conservative management.
Then, contrast-enhanced computed tomography (CECT) of abdomen and pelvis was done which was suggestive of gastric volvulus. Immediate open surgical exploration was done under general anaesthesia.
Mesenteroaxial gastric volvulus with gangrene over greater curvature, wandering spleen and pulled up left hemidiaphragm was noted (Figure 3 A, B). Gastric volvulus was derotated, transverse colon mobilized, spleen placed in anatomical position and phrenicocolic ligament fixed to peritoneum with polypropylene 2-0 suture. Wedge resection of greater curvature with closure in 2 layers was done with polyglactin 2-0 suture. Anterolateral gastropexy with polypropylene 3-0 suture was done. The patient had an uneventful recovery. Sips were started on 1st postoperative day and liquids by 2nd postoperative day, nasogastric (NG) tube was removed on her 4th postoperative day and was discharged on 5th postoperative day.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [120.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1262,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5899395-1,Extracted,"Patient 1 was a 62-year-old Japanese man admitted to our hospital for general malaise and systemic edema. He had been an office worker, had a history of smoking, and had no history of alcohol intake. He had no apparent family history of cardiovascular and liver diseases. He had been diagnosed with cardiac sarcoidosis complicated with ventricular tachycardia (VT) when he was 49 years old. Since then, he had been treated with corticosteroids (prednisolone 10 mg/day) and amiodarone (150 mg/day), in addition to enalapril (5 mg/day), metoprolol (20 mg/day), and lansoprazole (15 mg/day). After the initiation of amiodarone, the patient’s liver enzymes were gradually as well as intermittently exacerbated to elevated over the course of 13 years (peak aspartate aminotransferase 161 IU/L [normal range 9–32 IU/L]; peak alanine aminotransferase 106 IU/L [normal range 4–37 IU/L]); however, the treating physician decided to continue amiodarone to control the patient’s VT. During the follow-up period, the patient’s mean plasma level of amiodarone was 1.8 μg/ml and that of desethylamiodarone was 1.1 μg/ml. An abdominal plain CT scan showed diffuse high attenuation of the liver parenchyma (Fig. ). The patient had no history of hospitalization for heart failure after the introduction of amiodarone. However, general malaise and systemic edema occurred, and abdominal ultrasound showed liver cirrhosis, splenomegaly, and massive ascites.
At admission, the patient’s blood pressure was 95/66 mmHg, his heart rate was 69 beats/minute, and his body temperature was 35.6 °C. His consciousness was clear, and his respiratory sounds were normal. Marked distention of the abdomen was observed, and the liver and spleen were palpable from the abdominal wall. No abnormal neurological finding was observed.
A chest x-ray revealed mild cardiomegaly (cardiothoracic ratio 50%) without marked congestion and pleural effusion. Echocardiography showed mild left ventricular systolic dysfunction (ejection fraction 45%) and mild mitral and tricuspid regurgitation without a finding of pulmonary hypertension. Blood tests showed thrombocytopenia (81 × 103/μl), elevations of liver and ductal enzymes (aspartate aminotransferase 135 IU/L, alanine aminotransferase 91 IU/L, γ-glutamyl transpeptidase [γ-GTP] 202 IU/L, total bilirubin 2.4 md/dl), and hypoalbuminemia (serum albumin 3.1 g/dl). The patient’s brain natriuretic peptide level was mildly elevated (136 pg/ml), which showed no change during follow-up. Other serologic study results were negative for chronic viral hepatitis and other liver diseases. An abdominal plain CT scan showed massive ascites and splenomegaly, in addition to diffuse high attenuation of the liver parenchyma (Fig. ). At that time, amiodarone was discontinued because amiodarone-induced hepatotoxicity was suspected. However, the patient died of hepatic insufficiency during hospitalization. An autopsy revealed yellow liver specimens with a rough surface that suggested cirrhotic changes. Hematoxylin and eosin staining showed regenerative nodules and well-developed bridging fibrosis. Marked neutrophilic infiltrates, a remarkable amount of Mallory bodies, and hepatocellular ballooning were observed (Fig. ). Moreover, electron microscopic examination detected numerous whorled or lamellar bodies in the lysosomes (Fig. ). These findings helped diagnose amiodarone-induced hepatotoxicity associated with irreversible liver cirrhosis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [66.0, 'mm hg'], 'Systolic Blood Pressure': [95.0, 'mm hg']}",75.66667,71.88334,79.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 95.0 mm Hg + 2/3 * 66.0 mm Hg = 75.66667 mm Hg.
Hence, the patient's mean arterial pressure is 75.66667 mm Hg."
1263,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-11924,Extracted,"A 25-year-old man presents to his primary care provider complaining of several weeks of intense itching, particularly localized around his anus. Of note, the patient denies any recent travel, sexual contacts, fever, dysuria, or diarrhea. His temperature is 98.1°F (36.7°C), blood pressure is 110/70 mmHg, pulse is 65/min, and respirations are 12/min. On exam, the patient demonstrates severe excoriations in his perianal region with slight erythema over the areas that are torn. He does not have any other dermatologic findings. The scotch tape test is positive. The patient has a previous documented allergy to albendazole.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1264,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3537207-1,Extracted,"A 74-year-old female with a history of coronary artery disease was admitted to our hospital with a history of exertional dyspnea (function class II) during recent months. She had a past history of CABG and MVR surgery approximately 10 months prior to her admission.
The postoperative echocardiography, performed one week after surgery, showed mild LV hypertrophy with an ejection fraction of 50%, a prosthetic MV with an acceptable gradient, and a normal right ventricle size with a good systolic function.
On present admission, the patient’s pulse rate was 90 per minute and regular, and her blood pressure was 130/70 mm Hg. The patient had 1+ edema in her lower limbs. Auscultation revealed fine crackles in both lung bases and III/VI systolic murmur. An electrocardiogram (ECG) showed left bundle branch block and inverted T wave in V5–V6 leads.
TTE showed a large echolucent space with a narrow neck (about 1.8 - 2 cm in diameter) on the basal posterolateral portion of the LV (near the prosthetic MV) and the diameter of the cavity was about 70 mm, suggestive of a large pseudoaneurysm in the basal posterolateral portion of the LV with a to-and-fro flow on color Doppler ( and ). RT 3D TTE (Vivid 7 / GE / RT 3D probe) was performed in order to better reveal the spatial relations between the pseudoaneurysm and the adjacent cardiovascular and thoracic structures and to better delineate the pseudoaneurysm borders before surgery. RT 3D TTE showed a large pseudoaneurysm (80 × 52 mm), parallel to the free wall of the LV (). Its orifice was about 20 mm and was very close to the MV annulus.
The patient underwent urgent surgery through median sternotomy using cardiopulmonary bypass. After mid sternotomy and moderate hypothermia (28 °C), the left atrium was opened. The prosthetic MV (St Jude #27) remained intact, but the orifice of the LV pseudoaneurysm was unclear when visualized through the St Jude valve. The prosthetic MV was removed. In the posterolateral aspect of the LV just below the annulus of the MV, the large orifice of the pseudoaneurysm (about 20 mm in diameter) was found, which was closed with a pericardial patch (). After the closure of the defect,MVR with a bileaflet mechanical valve (St. Jude # 27) was performed and the patient was weaned from CPB without problems. Post-pump intraoperative transesophageal echocardiography confirmed the complete closure of the orifice of the pseudoaneurysm without a flow. The postoperative course was acceptable and the patient was discharged on 10th postoperative day. TTE was performed before discharge and showed the prosthetic MV with an acceptable gradient, without paravalvular leak and a large echomixed cavity (7 × 3.8 cm) due to a previous pseudoaneurysm posterolateral to the LV, which was filled by a clot. At one year’s follow-up, the patient was in good condition and was taking oral medications.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 70.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1265,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5093235-1,Extracted,"A 27-year-old female was brought to the hospital when she collapsed during her first marathon, an hour into the run. Her friends threw some water on her face to no avail. Emergency medical service was called and patient was immediately brought to the hospital. At presentation, she was severely encephalopathic. Her vitals were pertinent for a temperature of 40.2°C, blood pressure of 82/54 mmHg, and a heart rate of 125 bmp. Her BMI was around 23.29. Laboratory work-up revealed a creatinine of 1.6 mg/dL, potassium of 5.6 mg/dL, lactate of 2.5 mmol/L, and creatine kinase (CK) of 1825 U/L. A computed tomography (CT) scan of the head was negative for any acute disease. She was treated with intravenous (IV) infusion of cold normal saline, cooling blankets, and ice packs with improvement in her mental status. The next day, patient developed abdominal pain and bloody diarrhea with a lactate of 3.6 mmol/L. She did report general intermittent use of ibuprofen but not recently. CT scan of the abdomen revealed ascending colon wall thickening signifying ischemic colitis (). Further work-up revealed acute liver injury with elevated transaminases (ALT of 1484 U/L and AST of 1217 U/L) and worsening of rhabdomyolysis with further elevation of CK (2213 U/L). Patient's course was further complicated by disseminated intravascular coagulation (DIC) evident from a platelet count of 92000/μL, d-dimer of 4.2 mcg/mL, fibrinogen of 98 mg/d, prothrombin time of 21 seconds, and partial thromboplastin time of 48 seconds. She was managed with aggressive IV fluid resuscitation for 3 days with normalization of creatinine and lactate and significant improvement in her liver function tests and coagulation parameters. She was discharged after a 4-day hospital course and seen in clinic after 2 weeks with normalization of the rest of her lab abnormalities.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [54.0, 'mm hg'], 'Systolic Blood Pressure': [82.0, 'mm hg']}",63.33333,60.16666,66.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 82.0 mm Hg + 2/3 * 54.0 mm Hg = 63.33333 mm Hg.
Hence, the patient's mean arterial pressure is 63.33333 mm Hg."
1266,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4803109-1,Extracted,"On 19 March 2015, a 38-year-old Vietnamese woman presented to a healthcare facility in Dong Nai province in southern Vietnam (approximately 30 km east of Ho Chi Minh City) with 18 days of fever, headache, and arthralgia. She did not seek medical advice during this period but self-treated with antipyretics. She worked in a footwear factory, had given birth on 23 November 2014, and was breastfeeding a healthy infant; her past medical history was unremarkable with no known underlying medical condition. Her only account of recent travel was to Krong Pac district in Dak Lak, a rural province in Vietnam's Central Highlands, from 8 February to 2 March, to visit relatives over the lunar New Year holiday. She had never traveled outside Vietnam.
On presentation at the provincial hospital, she was treated presumptively for malaria with dihydroartemisinin-piperaquine. The following day she remained febrile and was transferred to the Hospital for Tropical Diseases (HTD) in Ho Chi Minh City. On admission at HTD, she had a severe headache but no additional neurological symptoms or signs, and her Glasgow Coma Scale score was 15/15. Her temperature was 39.5°C, respiratory rate was 22 breaths/minute, pulse was 100 beats/minute, and blood pressure was 110/70 mm Hg. Cardiorespiratory examination was normal and abdominal examination revealed nontender hepatomegaly.
Initial blood tests showed pancytopenia and mild renal impairment with raised liver aminotransferases and hypoalbuminemia (Table ); electrolytes, lactate dehydrogenase, creatine phosphokinase, and troponin I were within normal ranges. Microbiological cultures performed on blood, urine, and cerebrospinal fluid (CSF) did not produce any significant growth; CSF cell count, protein, and glucose concentrations were within normal ranges. Serological tests for hepatitis B, hepatitis C, and human immunodeficiency virus were negative. A blood film, stained with Giemsa and examined by microscopy, was negative for malaria; however, numerous unicellular flagellate protozoa, with the distinctive morphology of Trypanosoma and with an estimated concentration of >50 000 parasites/µL, were identified (Figure ). Motile parasites were also observed by direct microscopic examination of the blood (). Chest radiography and electrocardiography were normal, and abdominal ultrasound confirmed hepatomegaly (164 mm) and splenomegaly (117 mm).
First-line antitrypanosomal drugs (eg, pentamidine and suramin) are not available in Vietnam. Consequently, the patient was treated with amphotericin B (0.7 mg/kg/day) for 7 days, due to its reported trypanocidal activity []. She was afebrile after 12 hours of treatment. After 24 and 48 hours of treatment, blood films demonstrated a fall in trypanosoma parasitemia from 11 880 parasites/µL to 5900 parasites/µL, respectively. No parasites were observed in blood films by the fourth day of treatment. White blood cell and platelet counts improved, while hemoglobin dropped to 6.6 g/dL. She was discharged without symptoms and with normal blood values on the 10th day after admission (Table ). The patient was recalled for follow-up 4 weeks after discharge; she remained asymptomatic with normal blood values, and no parasites were visible upon microscopy.
Six weeks after hospital discharge (15 May), the patient returned to HTD with 2 days of fever, headaches, nausea, and vomiting. Blood tests again demonstrated pancytopenia, raised liver enzymes, and hypoalbuminemia (Table ). An ultrasound showed hepatomegaly of 167 mm and splenomegaly of 126 mm, and a peripheral blood smear identified >70 000 parasites/µL. CSF examination was normal. By this time, suramin had been sourced from the World Health Organization (WHO), and she was treated with 1 g weekly for 5 weeks. The fever resolved within 8 hours of the first dose, and the blood smear was negative within 12 hours. The patient was discharged and completed suramin treatment without complications. She was followed up monthly for 6 months with repeated clinical examination and blood films. Further investigations to identify the infecting parasite, the patient's serological responses and susceptibility, and the potential source were subsequently undertaken.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1267,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-48,Extracted,"A 63-year-old woman comes to the physician for a follow-up examination. She has had numbness and burning sensation in her feet for 4 months. The pain is worse at rest and while sleeping. She has hypercholesterolemia and type 2 diabetes mellitus. Current medications include insulin, metformin, and atorvastatin. She has smoked one pack of cigarettes daily for 33 years. Her temperature is 37°C (98.6°F), pulse is 88/min, and blood pressure is 124/88 mm Hg. Examination shows full muscle strength and normal muscle tone in all extremities. Sensation to pinprick, light touch, and vibration is decreased over the soles of both feet. Ankle jerk is 1+ bilaterally. Biceps and triceps reflexes are 2+ bilaterally. Babinski sign is negative bilaterally.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [124.0, 'mm hg'], 'Diastolic Blood Pressure': [88.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 124.0 mm Hg + 2/3 * 88.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1268,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7797464-1,Extracted,"A 59-year-old woman was admitted to the emergency department with sudden onset of chest pain for five hours. She had hypertension (treated with β-blockers) as a cardiovascular risk factor. She was diagnosed with advanced non-small-cell lung cancer with liver metastases one month previously. The patient was not considered for surgical resection, she was scheduled for chemotherapy, and, consequently, no antineoplastic treatment had been initiated yet. Prophylactic anticoagulation was not indicated On clinical examination, her blood pressure was 150/90 mmHg with a pulse of 100 beats per minute, oxygen saturation of 95%, and normal heart sounds. The 12-lead electrocardiogram showed sinus rhythm with a heart rate of 102 beats for minutes and ST-segment elevation in all leads except aVR where ST-segment depression was noted (Figure ). Her laboratory test results revealed a baseline troponin T level of 1212 ng/ml (normal range < 26 ng/ml). Also, the echocardiography findings revealed akinetic walls from the mid to apical septum and anterior and inferior walls. The ejection fraction was estimated to be 39%. Therapy was started with clopidogrel, aspirin, and low-molecular-weight heparin. The patient underwent a coronary angiogram from the right radial approach, which revealed the presence of an extended thrombus in the left anterior descending artery (LAD), and another thrombus was found in the second segment of the right coronary artery (RCA) with thrombolysis in myocardial ischemia (TIMI) III flow and without any atherosclerotic lesions in the coronary artery tree (Figure and Figure ), therefore, balloon angioplasty and/or stent placement was not considered. The patient was taken to the coronary care unit (CCU) and tirofiban infusion was administered for a period of 48 hours. In view of persistent breathlessness, pulmonary embolism was suspected. There were no symptoms or clinical signs suggestive of deep venous thrombosis. A computed tomographic pulmonary angiography was performed and showed a distal pulmonary embolism (Figure ). The patient was discharged on acenocoumarol to be followed as an outpatient. At her 45 days follow-up, she did not report any episode of chest pain, bleeding, as well as any thrombotic events.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",110,104.5,115.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 90.0 mm Hg = 110.0 mm Hg.
Hence, the patient's mean arterial pressure is 110.0 mm Hg."
1269,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8440,Extracted,"A 70-year-old man with a 2 year history of Alzheimer disease presents is brought in from his nursing facility with altered mental status and recurrent falls during the past few days. Current medications include donepezil and galantamine. His vital signs are as follows: temperature 36.0°C (96.8°F), blood pressure 90/60 mm Hg, heart rate 102/min, respiratory rate 22/min. Physical examination reveals several lacerations on his head and extremities. He is oriented only to the person. Urine and blood cultures are positive for E. coli. The patient is admitted and initial treatment with IV fluids, antibiotics, and subcutaneous prophylactic heparin. On the second day of hospitalization, diffuse bleeding from venipuncture sites and wounds is observed. His blood test results show thrombocytopenia, prolonged PT and PTT, and a positive D-dimer.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [60.0, 'mm hg'], 'Systolic Blood Pressure': [90.0, 'mm hg']}",70,66.5,73.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 60.0 mm Hg = 70.0 mm Hg.
Hence, the patient's mean arterial pressure is 70.0 mm Hg."
1270,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7750025-1,Extracted,"An 82-year-old woman presented to our hospital emergency department because of repeated vomiting that persisted for 2 days without induction. She had a history of cerebral infarction, hypertension, dementia, and surgery for a perforated sigmoid diverticulum. An upper gastrointestinal endoscopy had been performed at another hospital a month ago, but no abnormalities were noted. A physical examination revealed consciousness corresponding to the Glasgow Coma Scale score of 12 (E4V3M5), blood pressure of 98/71 mmHg, pulse of 119/min, temperature of 36.5°C, tachypnea (≥30 times/min), and 85% oxygen saturation (on room air), with diminished breath sounds on the left side. Chest X-ray revealed a large gastric bubble in the left chest cavity, with the mediastinum strongly displaced to the right side (Fig. ). Oxygen at 5 L/min improved the oxygen saturation (SpO2) to 92%, but tachypnea and tachycardia persisted. We speculated that a worsening esophageal hiatal hernia was probably responsible for the deterioration in respiration and circulation. Computed tomography (CT) performed for a definitive diagnosis showed that the entire stomach had escaped into the mediastinum and that it was craniocaudally inverted with axial torsion. In addition, the mediastinum had undergone a remarkable shift to the right owing to the presence of the dilated stomach; other structures, such as the left lung, heart, and inferior vena cava, were also highly displaced. There was no evidence of pneumonia (Fig. ). Her condition deteriorated to agonal respiration with worsening tachycardia (120–150 times/min) when she returned to the emergency room after the CT scan, and assisted ventilation was immediately initiated. Subsequently, she developed pulseless electrical activity. Cardiopulmonary resuscitation was immediately initiated. CT findings suggested that the dilated stomach, along with the esophageal hiatal hernia, was strongly pressing on the heart, thereby disrupting circulation. Therefore, a gastric tube was used to decompress the stomach through which 1,400 mL of gastric fluid was aspirated. A spontaneous heartbeat resumed immediately, with stable circulation. Chest X-ray performed after the gastric tube insertion revealed normal mediastinal structures and the absence of the previously present giant gastric bubble in the mediastinum (Fig. ). Subsequently, the correction of dehydration by infusion stabilized both the blood pressure and tachycardia; however, because she developed aspiration pneumonia, her respiratory status did not improve and she died on the fourth hospital day (Fig. ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [98.0, 'mm hg'], 'Diastolic Blood Pressure': [71.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 98.0 mm Hg + 2/3 * 71.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1271,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4006561-1,Extracted,"A 26-year-old Caucasian woman without previous medical history was referred to the emergency department for sudden headache. Arterial blood pressure was 110/60 mm Hg and heart rate was 90/min. Because of altered consciousness (Glasgow Coma Scale 6/15), orotracheal intubation was immediately performed. Brain computed tomography (CT) showed an intraparenchymal left cerebellar hemorrhage with massive subarachnoid extension, probably due to a vascular malformation. The first electrocardiogram (ECG) recording in the emergency room showed sinus rhythm with abnormal repolarisation in lateral leads (). Troponin-I (Tn-I) values and chest X-ray were normal on admission. The patient underwent immediate surgery for hematoma evacuation and ventricular drainage.
One day after admission, we observed increasing oxygen requirements and chest X-ray was consistent with pulmonary edema. The ECG at this time was unchanged and serum Tn-I concentration increased till a peak value of 8.25 ng/mL (<0.08 ng/mL). Echocardiography showed normal left ventricular internal dimensions but depressed left ventricular (LV) ejection fraction (25%). LV mid and basal segments were severely hypokinetic, whereas apical segments were hypercontractile ( and movie clip 1). The right ventricular size and systolic function, as well as valves, were normal. Nonetheless, the patient did not require hemodynamic support and did not receive catecholamines.
Systolic function steadily improved over the two following days, along with oxygenation parameters and chest X-ray. Extubation was possible on day 3. Echocardiography confirmed the improving LV function. The ECG returned to normal morphology. A control cerebral angiography performed several weeks later failed to reveal the origin of the bleeding. It was hypothesized that a minimal arteriovenous malformation had been removed during the neurosurgical procedure, together with the subsequent hematoma. The patient made a full cardiac and neurological recovery.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",76.66667,72.83334,80.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 60.0 mm Hg = 76.66667 mm Hg.
Hence, the patient's mean arterial pressure is 76.66667 mm Hg."
1272,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8530793-1,Extracted,"Case 1 (patient with hypertensive emergency)
A previously healthy 14-year-old male presented to an emergency department of a hospital in the southeastern United States with epistaxis. Six weeks prior to presentation, he was febrile with complaints of sore throat, epistaxis, petechial rash, headache, chest discomfort, and joint and back pain. Two weeks prior to presentation, he reported bleeding of his gums, gross hematuria, and decreased urine output. In the emergency department, his temperature was 38.4°C, pulse was 106 beats per minute, blood pressure was 178/109 mmHg, respiratory rate was 20 breaths per minute, and oxygen saturation was 95% at room air. Notably, on physical examination, the patient had gingival hyperplasia with mucosal bleeding and friability, injected conjunctiva, decreased airy entry on left lung fields, and bilateral lower extremity edema with diffuse purpura (Figure ). The patient also reported a recent 15lbs weight loss. He denied a history of upper respiratory or gastrointestinal symptoms, previous episodes of melena, hematochezia, or hematemesis, known sick contacts, recent travel, or trauma. The patient received vancomycin and ceftriaxone before being admitted to the pediatric intensive care unit (PICU) as sepsis was considered a differential diagnosis.
Laboratory workup included a serum creatinine (Cr) of 1.25mg/dL (normal: 0.45-0.81mg/dL), a urinalysis (UA) significant for hematuria and proteinuria with a urine protein-to-creatinine (Up/c) ratio of 2 (normal <0.2), erythrocyte sedimentation rate (ESR) 90mm/h (normal: 0-10mm/h), and CRP 15.8mg/L (normal: 0.1-1.0mg/L), serum c-ANCA of 1:640 and proteinase-3 (PR3) of 1501U/mL (Table ). Of note, the patient was negative for p-anti-neutrophilic cytoplasmic antibody/myeloperoxidase (ANCA/MPO), glomerular basement membrane (GBM), C3/C4, antisense oligonucleotide (ASO), and lupus anti-coagulants. Chest CT was significant for evidence of focal pulmonary hemorrhage. Renal biopsy showed 42% (20/47) of glomeruli had fibrocellular crescents on hematoxylin and eosin stain (H&E) and no deposits noted on electron microscopy (EM) - findings consistent with pauci-immune crescentic glomerulonephritis (Figure ).
Given serology positive for c-ANCA/PR3, abnormal UA findings, evidence of pulmonary hemorrhage, and renal biopsy consistent with pauci-immune crescentic glomerulonephritis, the patient met the European League Against Rheumatism, Pediatric Rheumatology International Trials Organization, and Pediatric Rheumatology European Society (EULAR/PRINTO/PRES) criteria for granulomatosis with polyangiitis (GPA) [].
The patient received induction therapy with intravenous (IV) methylprednisolone 1g x3 doses daily, oral (PO) prednisolone 60mg/d, IV cyclophosphamide (Cytoxan) 1000mg x6 doses (750mg/m2 per month), IV rituximab 375mg/m2 x2 doses, therapeutic plasma exchange (TPE) x5 rounds, and IVIG x1 round. Maintenance therapy included daily PO prednisolone with a tapering schedule and azathioprine (Table ).
Remission was successfully achieved in this patient; however, approximately two years after the diagnosis was made, the patient had a relapse, which was responsive to IV steroid pulse 1g x3 doses and rituximab 375mg/m2 x3 doses per institution protocol. Two years after his episode of relapse, the patient passed away from an unknown unrelated illness following the transition to adult nephrology care (Table ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [178.0, 'mm hg'], 'Diastolic Blood Pressure': [109.0, 'mm hg']}",132,125.4,138.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 178.0 mm Hg + 2/3 * 109.0 mm Hg = 132.0 mm Hg.
Hence, the patient's mean arterial pressure is 132.0 mm Hg."
1273,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4124553-1,Extracted,"A 49-year-old African-American man presented to the emergency department with sudden onset of left arm discomfort and to a much lesser extent, left-sided chest discomfort, which started about 30 minutes before presentation. This was associated with diaphoresis and it occurred at rest. Of note he had 2 similar events in the preceding month but did not seek medical intervention as symptoms resolved within 10 minutes of onset. He was an active smoker with a 35-pack-year history and also had a history of cocaine use in the past. Cardiovascular examination was unremarkable and the vital signs recorded were: blood pressure of 145/95 mmHg, a heart rate of 69 bpm, respiratory rate of 16 cpm, temperature of 98.3° F, and oxygen saturation of 98% on room air. The EKG on admission showed normal sinus rhythm, left ventricular hypertrophy and no acute ischaemic changes. He received aspirin 325 mg orally. His symptoms resolved shortly after presentation. The troponin I level was <0.015.
The patient was to be discharged but again developed left-sided arm and chest discomfort with diaphoresis while walking in the emergency department. Vital signs at this time were, a blood pressure of 153/103 mmHg, heart rate of 62 bpm, respiratory rate of 17 cpm, and oxygen saturation of 100% on room air. An EKG done immediately showed ST elevation and hyper-acute T waves in leads V2, V3, and V4 []. He was given nitroglycerin 0.4 mg sublingually twice and intravenous morphine 4 mg and his discomfort resolved. The troponin I level drawn at that time returned as 0.477. The EKG was repeated (35minutes after the preceding EKG), and it showed a resolution of ST elevation and hyper-acute T waves post treatment [].
The patient was subsequently admitted to the coronary care unit where he received clopidogrel, lovenox, simvastatin, lisinopril, and isosorbide mononitrate. Beta-blocker therapy was withheld pending urine toxicology result; his resting heart rate was between 50 bpm and 60 bpm. An echocardiogram done later revealed moderate to severely reduced left-ventricular function with an ejection fraction of 35% and severe anterior wall hypokinesis. Urine toxicology was negative for cocaine.
The troponin I peaked at 0.716 overnight and declined to 0.177 by the following morning. A diagnostic angiography done that morning revealed a 70% focal stenosis in the mid-left anterior descending artery, whose appearance was consistent with an atheromatous plaque []. Metoprolol was added on discharge for the left-ventricular dysfunction.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [153.0, 'mm hg'], 'Diastolic Blood Pressure': [103.0, 'mm hg']}",119.66667,113.68334,125.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 153.0 mm Hg + 2/3 * 103.0 mm Hg = 119.66667 mm Hg.
Hence, the patient's mean arterial pressure is 119.66667 mm Hg."
1274,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3249341-1,Extracted,"A 39-year-old woman was admitted to our hospital due to the presence of a pulsatile mass on her right inner thigh. The patient complained of tightness with distension at the inner surface of her right thigh, which was developed 2 months ago and increased in size. She had no definite history of trauma on the right lower leg, diabetes mellitus, nor hypertension, and did not smoke. On admission, her arterial pressure was 120/80 mmHg and blood analysis was within the normal range. Peripheral pulsations could be palpated well at the dorsalis pedis artery and the posterior tibial artery. Ultrasound and CT (Computed tomography) showed an isolated saccular aneurysm with thrombus and calcification measuring 6×8 cm on the right distal SFA (Superficial femoral artery). The proximal and distal walls of the aneurysm looked normal and the distal flow was preserved. The ascending aorta, aortic arch, abdominal aorta, and other major branches of the aorta were not dilated nor thickened in the CT scan (). An operation was performed under general anesthesia. A medial longitudinal incision was made over the pulsatile mass closer to the great saphenous vein (GSV) above the knee. After harvesting the GSV, we entered the deep fascia and dissected the aneurysm carefully. After controlling the vessels proximal and distal to the aneurysm, the aneurysm was resected and the GSV was continuously interposed with 6-0 Prolene (). The wall of the aneurysm was thickened and calcified, and exhibited three layers upon histological examination (). The patient had recovered uneventfully, and was discharged on the seventh day postoperatively with administration of antiplatelet agents (aspirin 100 mg and clopidogrel 75 mg daily) and a lipid-lowering agent (atorvastatin 5 mg daily). The postoperative CT showed that the aneurysm was completely resected and the graft was patent (). The patency of the graft at 12 months follow-up was satisfactory.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [120.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1275,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6225729-1,Extracted,"A 70-year-old bisexual man was admitted with generalized myalgia and abdominal pain lasting for 7 days. Three months earlier, he was diagnosed with HIV infection during the evaluation of a fever. The initial HIV RNA level was 36,500 copies/mL, with 114 CD4+ lymphocytes/μL, which were consistent with the definition of AIDS [] although the exact timing of HIV infection was unknown. At that time, abdominal and chest computed tomography (CT) showed no abnormality and an ophthalmologic examination showed no evidence of ocular disease. In addition, anti-cytomegalovirus (CMV) IgG was positive. For 3 months, he was treated with an integrase strand transfer inhibitor (INSTI)-based regimen (elvitegravir, cobicistat, tenofovir disoproxil fumarate, and emtricitabine) and showed good adherence.
At the time of the current admission, his vital signs were: blood pressure, 110/80 mmHg; pulse rate, 98/min; body temperature, 38.0 °C; and respiratory rate, 20/min. There was no localized tenderness of the abdomen on physical examination. The laboratory findings showed anemia (hemoglobin, 9.7 g/dL), thrombocytopenia (platelets, 53 × 103/mm3), acute kidney injury (creatinine, 1.8 mg/dL), and an elevated lactate dehydrogenase level (LDH; 6608 U/L). No HIV-RNA was detected (< 20 copies/mL), and there were 256 CD4+ lymphocytes/μL. Abdominal CT revealed multiple liver masses (Fig. ), and a core needle biopsy was performed to differentiate between liver abscess and malignancy. An atypical lymphocytic population composed of medium-sized basophilic cells was observed on hematoxylin and eosin staining (Fig. ). Immunohistochemistry was positive for the B cell markers CD20 (Fig. ) and CD79a (Fig. ), and the Ki-67 labelling index approached 90%. The tumor cells were also positive on EBV in situ hybridization (Fig. ). The liver lesion was diagnosed as Burkitt’s lymphoma. An additional diffuse hypermetabolic bone marrow lesion was found on positron emission tomography-CT (PET/CT), and he was confirmed to have stage IV Burkitt’s lymphoma by the Lugano classification.
Three cycles of antineoplastic chemotherapy based on rituximab plus fractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone (R-hyper-CVAD) were administered, and two cycles of methotrexate were given via an intrathecal route. The HAART was replaced with another INSTI-based regimen (raltegravir, tenofovir disoproxil fumarate, and emtricitabine) after considering potential drug interactions. Interim PET/CT showed a partial response with marked improvement of the lymphomatous involvement in the bone marrow and liver, but hypermetabolic para-aortic, aortocaval lymph nodes remained 3 months after initiating chemotherapy.
Just after the third cycle of R-hyper-CVAD, the patient suddenly complained of decreased visual acuity and an ophthalmologist diagnosed CMV retinitis. At that time, there were 56 CD4+ lymphocytes/μL, but no HIV RNA was detected (< 20 copies/mL). Intravitreal and intravenous ganciclovir were used for induction therapy, and valganciclovir maintenance therapy was continued. Chemotherapy was stopped after the third cycle of R-hyper-CVAD due to intolerance and the CMV retinitis. Four months after discontinuing the chemotherapy, PET/CT showed disease progression in the para-aortic, aortocaval lymph nodes, and newly developed lymphomatous involvement was seen in the paravertebral and cardiophrenic space.
Ten months after discontinuing systemic chemotherapy, the patient developed swelling and pain in his right thigh. CT showed edematous changes and skin thickening in this area (Fig. , arrow), but there was no remarkable size increase in the inguinal lymph nodes. There were 129 CD4+ lymphocytes/μL, and HIV RNA was undetectable. A skin punch biopsy was performed because it was unclear whether the manifestation was related to the Burkitt’s lymphoma. The biopsy specimen was composed predominantly of plump spindle cells with intervening vascular spaces (Fig. ). Despite the bland cytology of the tumor cells, frequent mitotic figures were seen and the tumor was infiltrating the dermal collagen fibers. The tumor cells were positive for CD31 (Fig. ) and HHV-8 latent nuclear antigen-1 (LNA-1) by immunohistochemistry (Fig. ). The histology was consistent with KS. Twenty Grays of radiation were given in five fractions without systemic chemotherapy. Two months after radiation therapy, multiorgan (bone, liver, and pericardium) lymphoma aggravation led to his death.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 80.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1276,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4342780-1,Extracted,"A previously healthy 13-year-old girl visited our Emergency Department due to left-sided chest pain that had occurred suddenly 10 hours ago. The pain was continuous pressing in nature without any radiation, and it improved on bending forward but worsened with deep inspiration. She had no specific past medical history such as Kawasaki disease, asthma, and no family history of heart or lung disease. She did not appear ill; and her vital signs were as follows: blood pressure was 133/79 mmHg, heart rate was 117 beats/min, and temperature was 37.6℃. Her weight was 40 kg. The physical examination did not reveal any other specific findings, especially her lung sound was normal Electrocardiogram (ECG) showed sinus tachycardia with a heart rate of 114 beats/min without ST segment changes (), and the chest x-ray was normal. We performed echocardiography that revealed normal regional wall motion and normal anatomy. However, her cardiac enzyme levels were slightly elevated; N-terminal prohormone brain natriuretic peptide was 257.6 pg/mL, troponin I was 2.138 ng/mL, and creatine kinase-myoglobin (CK-MB) was 13.02 ng/mL. The next day, she again complained of severe chest pain. Her blood pressure was 100/60 mmHg. Her ECG was taken again, and it showed marked ST elevation in the V4-V6 left precordial leads and inferior leads and ST depression in aVR lead, which was suggestive of myocardial ischemia (). Also, her cardiac enzyme levels were elevated; troponin I was 4.310 ng/mL, CK-MB was 10.78 ng/mL. Although the chest pain regressed spontaneously, further evaluation was performed.
We performed coronary angiography; left coronary artery (LCA) was bifurcated normally into left anterior descending (LAD) and left circumflex (LCX) coronary arteries, and it showed the absence of normally originating right coronary artery (RCA). An aberrant branch was extended from the distal LCX, which crossed the crux and continued to the right atrioventricular groove, covering the territory of the RCA (). There was no focal stenotic lesion in LCX including abberant branch. LAD and its branches (septal perforator branch, diagonal branch) also had no stenotic lesion. We also performed cardiac computed tomography and confirmed the absence of the RCA and the presence of a well-developed LCX coronary artery covering the right side of the heart (). A treadmill test was performed and the results were normal. She had no symptoms and electrocardiographic findings were normal during exercise. She was discharged without any medications; however, a regular follow-up was recommended.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [133.0, 'mm hg'], 'Diastolic Blood Pressure': [79.0, 'mm hg']}",97,92.15,101.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 133.0 mm Hg + 2/3 * 79.0 mm Hg = 97.0 mm Hg.
Hence, the patient's mean arterial pressure is 97.0 mm Hg."
1277,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8844,Extracted,"A 61-year-old woman presents with painless vaginal bleeding. Patient says the bleeding has been occurring occasionally for the past 3 years. Past medical history is significant for diabetes mellitus type 2 and hypertension, both managed medically. Current medications are atorvastatin, lisinopril, hydrochlorothiazide, and metformin. Patient has not been sexually active since the death of her husband 9 years ago. Menopause occurred 8 years ago, and she denies taking hormone replacement therapy or estrogen-containing oral contraceptives. Her last Pap smear 1 year ago was normal. Vital signs are temperature 37.0℃ (98.6℉), blood pressure 130/85 mm Hg, pulse 82/min, respiratory rate 13/min, and oxygen saturation 99% on room air. BMI is 33.8 kg/m2. On physical examination, patient is alert and cooperative. Cardiac exam is normal. Lungs are clear to auscultation. Abdomen is soft and non-tender with no masses or hepatosplenomegaly. Examination of the perineum shows pale, atrophic vaginal mucosa. Speculum examination shows no vaginal or cervical lesions. The cervix is movable and non-tender. There is trace blood in the vaginal vault and mild bleeding from the cervical os. The uterus is not enlarged but softened on palpation. Adnexa is non-palpable.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 85.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1278,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6327756-1,Extracted,"A 44-year-old male, hypertensive for 11 years complained of weakness and joint pain-on and -off for 2 months and was admitted with above-mentioned complaints in November 2014. On evaluation, patient was found to be anemic (hemoglobin - 7.1 mg/dL) with deranged renal parameters (blood urea - 165 mg/dL; serum creatinine - 13.8 mg/dL; serum sodium - 146 mEq/L; serum potassium - 6.1 mEq/L). On examination, blood pressure – 160/100 mmHg, pulse rate – 96/min, pallor present, itching all over the body, no pedal edema. Cardiovascular and respiratory examination revealed no abnormality. The patient was diagnosed with a case of end-stage renal disease and started on maintenance hemodialysis, and the possibility of renal transplantation was discussed with the patient. The transplant workup was started for ABO compatible living donor related renal transplantation. The patient had a history of blood transfusion 5–6 months back (3–4 units of packed red blood cells). Infectious marker screen (hepatitis b, hepatitis c, and human immunodeficiency virus) was negative. Autoimmune markers (anti-nuclear antibody, ANA; rheumatoid factor, RF; anti-double-stranded DNA, anti-dsDNA; antineutrophil cytoplasmic antibody, ANCA; anti-signal recognition particle, anti-SRP) were also negative. As per the routine departmental histocompatibility testing protocol, initial testing included CDC AHG crossmatch, HLA antibody screening and LumXm. Initial testing revealed positive CDC AHG crossmatch and negative luminex based assays (HLA antibody screening and LumXm). shows the algorithmic approach for histocompatibility workup performed for the patient. Detailed histocompatibility workup was suggestive of IgG auto-antibodies, which were complement activating and lymphocytotoxic in nature. Due to unexplained strong positivity in CDC and flow crossmatch, renal transplantation was not performed.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [160.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",120,114,126,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 100.0 mm Hg = 120.0 mm Hg.
Hence, the patient's mean arterial pressure is 120.0 mm Hg."
1279,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1838,Extracted,"A 49-year-old woman, gravida 1, para 1, comes to the physician because of shorter and less frequent menstrual periods over the past year. During this time, she has also had frequent mood swings and a 2.5-kg (5-lb) weight loss. She occasionally wakes up at night because she is too warm and sweating profusely. These episodes are followed by chills and anxiety that subside within minutes. She has no history of abnormal Pap smears. She is sexually active with her husband, who had a vasectomy 10 years prior. She is 163 cm (5 ft 3 in) tall and weighs 70 kg (154 lb); BMI is 26 kg/m2. Her temperature is 37°C (98.6°F), pulse is 103/min, respirations are 16/min, and blood pressure is 129/84 mm Hg. Abdominal and genitourinary examination shows no abnormalities.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [84.0, 'mm hg'], 'Systolic Blood Pressure': [129.0, 'mm hg']}",99,94.05,103.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 129.0 mm Hg + 2/3 * 84.0 mm Hg = 99.0 mm Hg.
Hence, the patient's mean arterial pressure is 99.0 mm Hg."
1280,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5727660-1,Extracted,"A 32-year-old woman sought care at a provincial hospital after passing loose and dark stool about 10 times in a single day. She had been healthy until the diarrhea occurred and was not taking any medications. Her past medical history was unremarkable, except that she had undergone tubal surgery for pelvic inflammatory disease three years priorly. She had one child who was born by vaginal delivery. She had never undergone an instrumental pregnancy termination or intrauterine device insertion, which might lead to uterine perforation. She had no history of amenorrhea or abnormal vaginal discharge. Her initial diagnosis was upper gastrointestinal hemorrhage, but this was changed when bile was observed in the nasogastric tube after which the patient developed exsanguinating hematochezia and severe hypotension requiring 11 units of packed red cell transfusion for stabilization. Soon after, she was transferred to a tertiary care center.
The patient's blood pressure was 70/40 mmHg, and her pulse rate was 120 beats/min. The abdominal examination was unremarkable. The per-rectal examination revealed excessive bleeding without any discernible cause. The laboratory tests showed a hemoglobin level of 6.3 g/dL and a platelet count of 28 × 103/µL. Owing to the unstable condition of the patient, an emergency exploratory laparotomy was conducted in order to localize and control the bleeding. During the laparotomy, blood was found in the peritoneal cavity and a segment of the ileum attached to the fundus of uterus (). The intraluminal content was palpated in the adhered ileal segment (). An enterotomy revealed a fetus 7.5 cm in crown-rump length and fresh blood in the ileal lumen (). The placental tissue had implanted at the fundal dome of the uterus and eroded into the small bowel (). A segmental small bowel resection was performed along with reanastomosis. The placental tissue was removed by way of a wedge resection of the uterine wall. The patient had an uneventful postoperative course and was discharged on postoperative day 7.
Histologic examination of the resected specimens later confirmed the diagnosis of an abdominal pregnancy which included a male fetus of 4 months' gestational age (), normal cord, subserous uterine myoma, and submucosal hemorrhage in the small intestine.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [40.0, 'mm hg'], 'Systolic Blood Pressure': [70.0, 'mm hg']}",50,47.5,52.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 70.0 mm Hg + 2/3 * 40.0 mm Hg = 50.0 mm Hg.
Hence, the patient's mean arterial pressure is 50.0 mm Hg."
1281,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4890486-1,Extracted,"Fifty-four year old male
The chief complaint of the patient included breathing difficulty and coughing during exercise that developed 2 months previously.
Breathing difficulty and coughing aggravated further during mountain hiking. A pulmonary disease was suspected from the findings of chest radiographs. The patient was hospitalized to obtain an accurate diagnosis and for treatment.
On a special health examination performed 5 months before admission, no unusual findings were observed on the plain chest radiography. The patient had no ophthalmologic diseases, but complained of eye dryness for several months. He frequently used artificial tears because of the eye dryness.
The patient had a history of smoking 20 cigarettes a day for 20 years and then 10 cigarettes a day for 10 years; however, he quit smoking 3 months previously. He has a history of consuming five bottles (350 mL) of soju (approximately 18 % alcohol by volume) per week. No significant family history of autoimmune diseases was noted.
On admission, the patient’s vital signs were stable with blood pressure of 140/80 mmHg, pulse rate of 86 beats/min, respiratory rate of 20 breaths/min and body temperature of 37.0 °C. Although the patient showed an acute ill-looking appearance, his consciousness was clear, cardiac sound regular, and no heart murmur was heard. Fine inspiratory crackles were heard at both lower lung fields. Finger clubbing was not observed, but fingers were swollen and skin was thickened. The findings in the abdomen, extremities, and neurological examination were normal.
In a plain chest radiograph obtained on admission, ground glass opacities (GGOs) were observed at the lower part of both lungs (Fig. ). In a chest computed tomography image, reticulation and GGOs were observed in both lungs, leading to the diagnosis of interstitial lung disease (Fig. ).
In arterial blood gas analysis performed before hospitalization, pH was 7.4; PaCO2, 38 mmHg; PaO2, 94.2 mmHg; and oxygen saturation, 97.3 %. In a peripheral blood test, the leukocyte count was 8,300/μL; hemoglobin, 5.2 g/dL; and platelet count, 436,000/μL. In a lung function test, findings of restrictive lung function disorder were obtained with forced vital capacity (FVC) 2.62 L (67 % of the predicted value), forced expiratory volume in 1 s (FEV1) 2.31 L (80 % of the predicted value), the ratio of FEV1/FVC 88 %, forced expiratory flow 25–75 % 4.76 L/sec (154 % of the predicted value), and peak expiratory flow rate 8.16 L/sec (110 % of the predicted value).
The results of bronchoscopy and a lung lavage test revealed chronic inflammation with fibrosis. The results of lung biopsy were consistent with usual interstitial pneumonitis. Breathing difficulty was alleviated with systemic steroid therapy. During admission, the patient complained of dry mouth and difficulty of swallowing dry food without liquid. Immune serologic tests were performed under suspicion of autoimmune disease. The results of serologic tests were as follows; positive for antinuclear antibody (1:2560), negative for rheumatoid factor, positive for anti-SSA (Ro) antibody, negative for anti-SSB (La) antibody and positive for anti-Scl 70 antibody. The anti-ds DNA level was 7.64 IU/mL (reference level, <7.0 IU/mL). The secretory function of the salivary gland was considered to be decreased. In a salivary gland scan, the uptake increases in the parotid gland and submandibular gland were relatively normal; however, the ejection fraction of the salivary gland after stimulation decreased by more than the moderate level. Although the results of Schirmer’s test did not satisfy the diagnostic criteria for Sjögren’s syndrome, with the right eye showing a result of 12 mm in 5 min and the left eye showing a result of 7 mm in 5 min, they were found to be lower than the normal range. Other diseases such as hepatitis C, acquired immunodeficiency syndrome, lymphoma and sarcoidosis were excluded by medical history and the results of relevant laboratory tests. Clinical findings including ocular symptom of dry eyes, oral symptom of difficulty in swallowing dry food without liquid, oral sign of abnormal salivary scintigraphy and positive autoantibody of anti-SSA (Ro) antibody were compatible with diagnostic criteria for Sjögren’s syndrome (Table ) []. In addition, there were some features of systemic sclerosis (puffy fingers, interstitial lung disease and positive for systemic sclerosis related autoantibody [anti-Scl 70]) according to the revised classification criteria of systemic sclerosis (Table ) []. The patient has been followed for the overlap syndrome with Sjögren’s syndrome and systemic sclerosis.
The patient had worked for 25 years as a worker in the large-scale rolling department of a steel-manufacturing company. He was in charge of maintenance and repairs for the roughing mill and intermediate mill. His major tasks were the management of oils, roll exchange of the rolling mill for different sizes and stand-seating manufacture. Rolling is a plastic process in which the cross-sectional thickness of a material is reduced by successively pressing while passing it between two rollers. A roughing mill is the first process where slabs coming out of the furnace are rolled, and this produces dust containing silica. Hot rolling is a rolling process performed at a temperature of between 1100 °C and 1200 °C. A large amount of fumes develops at that high temperature. Generally, the hot rolling process is a wet process. As it progresses, oxidized film on the surface of the rolled material is removed and water is jet-sprayed to prevent the high generation of fumes. The final product is a scroll-shaped intermediate processed product called a coil, after which additional processing is performed in the cold rolling process. The large-scale milling process in which he was involved is a series of operations comprising the furnace, roughing mill, intermediate mill, finishing mill and cutting. The roll was being exchanged for different sizes more than once a day, depending on the work volume. To meet the production standards when changing the roll, the process of resting the new roll on a stand, dissembling the existing roll and performing the exchange was mainly performed near the rolling mill owing to the nature of the work. According to the report of working environment measurement, noise, dust, toxic metals and heat were identified as occupational hazards. In general, workers in the milling process take 30-min rest after 30-min working because of the high-heated working condition. The patient has worked on the three-shift system. The total ventilation system was applied in the plant, and the patient has regularly used personal protective equipment including mask and ear plugs.
It was verified that standard steel products produced by a series of hot rolling processes contain a maximum of 0.4 % silicon []. However, the concentration of free silica in the air was not measured directly. Instead, type 2 dust, which contains silicon dioxide up to 30 %, was measured as mineral dust. According to the report of working environment measurement in 2008, the concentration of type 2 dust was 1.444 mg/m3 and 0.417 mg/m3 in the roughing and intermediate mills, respectively (Table ). Potential toxic substances other than silica were found in the milling process such as nickel, chromium and manganese, but the ambient concentration was very low or not detectable. For example, the highest concentration of nickel and manganese were measured at the roughing mill site, which were 0.0026 mg/m3 and 0.0051 mg/m3, respectively (Table ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 80.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1282,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7613,Extracted,"A 48-year-old woman with a history of osteoarthritis and hypertension presents to the office complaining of persistent abdominal pain for the last 2 months. She describes the pain as 'burning and achy' that is worse when she eats, which has lead to a weight loss of 4.5 kg (10.0 lb). The patient is currently taking lisinopril and atenolol for her blood pressure and ibuprofen as needed for her osteoarthritis. Her temperature is 37.1°C (98.7°F), heart rate is 75/min, and blood pressure is 120/80 mm Hg. An endoscopy is performed and a gastric ulcer is visualized and biopsied. The biopsy reveals H. pylori infection.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1283,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4607964-1,Extracted,"A 40-year-old Tunisian woman, with a history of diabetes mellitus in diet and Lofgren's syndrome (an acute presentation consisting of polyarthralgia, erythema nodosum, bilateral intrathoracic lymphadenopathies) diagnosed in February 2013, came to our department, in February 2014, for exploration of exertional dyspnea of one month evolution and progressively worsening without fever, chest pain, or syncope. The patient denied any past history of hypertension, coronary artery, or thyroid disease. She did not smoke or consume alcohol. On physical examination, she was conscious, cooperative, and afebrile. She was hemodynamically stable (blood pressure (BP) 130/70 mmHg and had a regular pulse of 88 beats /minute.). She had good color and was slightly polypneic with no peripheral cyanosis (peripheral oxygen saturation 97%). She presented no palpable adenopathy or signs of jugular distension. Cardiac auscultation revealed rhythmic sounds with no murmur or friction rub. There were no signs of peripheral edema or deep vein thrombosis. Pulmonary, abdominal, and neurological examination revealed no abnormalities. The admission electrocardiogram (ECG) was normal. On investigation, blood biochemistry, liver, renal function, thyroid function and, hemogram showed no abnormalities except lymphopenia. Her angiotensin converting enzyme (ACE) level was 132 units (normal range < 68units). The immunological markers were negative. A contrast-enhanced computed tomography (CT) chest scan showed almost complete regression of mediastinal lymphadenopathies without pleuroparenchymal lesion. Respiratory functional tests and bronchoscopy with transbronchial lung biopsy were normal. The transthoracic echocardiography with Doppler showed abnormal left ventricular relaxation and systolic dysfunction of the left ventricle with ventricular ejection fraction (EF) of 40%. In the light of these symptoms and echocardiographic abnormalities, for which other possible causes have been excluded, the diagnosis of sarcoidosis with heart involvement was suspected. Thus, more specialized cardiac evaluation was needed. 24 hour holter monitoring showed recurrent episodes of 2000 monomorphic ventricular extrasystoles. Cardiac magnetic resonance imaging (MRI) with gadolinium contrast showed evidence of delayed hyper enhancement in both the basal and inferolateral left ventricular regions, suspicious for fibrogranulomatous tissue of sarcoidosis (). The left ventricular ejection fraction was 40%. Laboratory tests confirmed negative serial markers of myocardial necrosis. Technetium99m sestamibi scintigraphy myocardial perfusion study showed decreased uptake in the inferolateral and apical ventricular myocardium, which was reversible during stress (reverse distribution) (). Coronary angiography and let ventriculography showed angiographically normal coronary arteries. Considering all these clinical and investigatioanal findings in a patient with a history of Lofgren's syndrome and in the absence of primary heart disease, the diagnosis of cardiac sarcoidosis was made. The patient started with a dose of 1mg/kg/day of corticosteroids in addition to supportive care. This dose was tapered gradually to a maintenance level of 15 mg per day over 5 months. To this day, evolution was favorable.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 70.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1284,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8435225-1,Extracted,"We report an 11-year-old boy, a known patient with SCD (HBSS type). He was referred from a peripheral hospital to the pediatric emergency Unit of Mulago National Referral Hospital with a one-week history of bilateral eyelid swelling and progressive proptosis, more marked on the left eye with associated reduction in vision. The patient also had fever and severe headache but no history of trauma, neck pain, convulsions, or loss of consciousness. He had bilateral lower limb pains but with no joint pain or swelling. He was receiving prophylactic daily folic acid and monthly sulfadoxine/pyrimethamine (fansidar) but not on hydroxyurea. He had been transfused with two units of whole blood at the peripheral hospital prior to admission.
On examination, the child was sick looking with mild pallor of mucous membranes and mild icterus but no dehydration and lymphadenopathy. He was febrile with an axillary temperature of 38.0°C. The pulse rate was 100 beats per minute, respiratory rate at 32 breaths per minute, blood pressure of 112/66 mmHg, and oxygen saturation of 98% on room air. The left eyeball was protruding and hyperemic with a pus discharge, tearing with eyelid edema without pupillary reflexes elicited (Figure ). The right eye was mildly swollen with mild hyperemia but no pus discharge or tearing. The right pupil was small and reacting poorly to light. There was a firm tender swelling measuring about 2 × 3 cm on the right parietal scalp. Per abdomen, there was a palpable spleen, about 4 cm below the costal margin in the left mid-clavicular line. Both lower limbs were tender below the knee joints but there were no swellings.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [66.0, 'mm hg'], 'Systolic Blood Pressure': [112.0, 'mm hg']}",81.33333,77.26666,85.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 112.0 mm Hg + 2/3 * 66.0 mm Hg = 81.33333 mm Hg.
Hence, the patient's mean arterial pressure is 81.33333 mm Hg."
1285,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8057905-1,Extracted,"A 79-year-old male with COPD and peripheral artery disease was transferred to our institution from a secondary hospital with the diagnosis of aortic transection, after a lone motorcyclist accident without wearing a helmet. While arriving at our emergency room, the patient was confused and complained of chest pain especially aggravated with deep breathing. Physical examinations showed stable vital signs: blood pressure (BP), 122/74 mmHg; pulse rate, 98/min; and respiratory rate, 20/min. Glasgow Coma Scale at admission was 8, so he was intubated on arrival. His injuries included subarachnoid and subdural hemorrhage, fracture of the occipital bone, mandibular fracture, rib fractures with bilateral pulmonary contusions, hemothorax in the left side, and fracture of the left femur as well. Blood loss through the chest tube at insertion was 400 ml and stabilized at 700 ml thereafter. Three-dimensional reconstruction images of contrast-enhanced computed tomographic angiography (CTA) demonstrated an intimal injury with periaortic hematoma (grade II aortic injury). It was located across the origin of the left subclavian artery (). A multidisciplinary trauma team approach was instituted.
As there is no endograft availability in our institution, orthopedists stabilized the femur, and then, we proceeded to treat the aortic injury given its severity. Fortunately, the patient was hemodynamically stable. Anti-impulse therapy was administered during the whole procedure which was held in the operating room with mobile c-arm. The patient was placed in a supine position. Aortography was performed via a catheter placed percutaneously through the brachial artery to confirm the anatomy and define the landing zones for the device. Because of multiple atherosclerotic lesions in both femoral arteries and in the left iliac artery, extraperitoneal exposure of the right iliac artery was performed. An incision was made 2 cm above and parallel to the inguinal ligament, extending from the lateral edge of the rectus sheath to a point 2 cm cephalad to the anterior superior iliac spine. After exposure of the external iliac artery, it was found that the guidewire could not be advanced in the descending thoracic aorta due to heavily calcified vessels. It was decided to proceed with partial sternotomy in order to place the stent-graft to the proper position in an antegrade fashion.
After completion of partial sternotomy, lowering the blood pressure, a partial clamp was placed on the ascending aorta and an 8 mm Goretex thin-walled, ringed graft was anastomosed in end to side fashion to the aorta (). An access sheath was placed in the ringed graft, and a guidewire is advanced through the sheath under fluoroscopic guidance from the ascending to the descending aorta. A Conformable Gore TAG stent-graft 34 mm × 10cm was positioned by advancing it over a stiff guidewire (Lunderquist). Its position was confirmed with repeated aortography especially in LAO 30 projection. Before device deployment, the patient's blood pressure was lowered again to lessen the arterial impulse and minimize the potential for misplacement during deployment. The device was then deployed, and completion aortogram was performed to confirm patency of the endograft and successful exclusion of the transection (i.e., no endoleak). However, the LSA was covered and the elimination of arterial pulse with a decrease in oxygen saturation of the left hand was noted. The limb became pale and cold, so a placement of additional Gore Viabahn Endoprosthesis 10 mm × 10cm in the covered LSA was decided (). The arterial pulse and oxygen saturation were immediately restored. The guidewires and introducer sheaths were removed, and the arteriotomies were repaired. Transesophageal echocardiography and angiography were used together to position and deploy the device precisely.
Subsequently, the patient was admitted to the ICU for deep sedation and ventilator management. Postoperative CTA disclosed appropriate position of stent-grafts and adequate flow to the left arm (). On the POD 10, the patient's oxygenation worsened, and purulent sputum with fever made an appearance. We, therefore, arrived at a diagnosis of ventilator-associated pneumonia (VAP), and his PaO2/FiO2 ratio deteriorated, and multiple organ failure was developed. He required continuous venous-venous hemofiltration for severe acute kidney injury. Finally, the patient deceased on POD 22.
In this patient, we did not administer antiplatelet drugs nor heparin during stent-graft deployment because of the traumatic brain injury.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [122.0, 'mm hg'], 'Diastolic Blood Pressure': [74.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 122.0 mm Hg + 2/3 * 74.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1286,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3686071-1,Extracted,"A 32-year-old male presented with a sudden onset of massive rectal bleeding. He had a history of KTS since childhood. He had multiple admissions for bleeding, presenting mainly as hematuria that started at the age of 11. He also had one episode of self-limited rectal bleeding four years prior to this presentation. His medications were multivitamins with iron supplement.
At the time of admission, physical examination was remarkable for blood pressure of 55/29 mm Hg, HR of 135 per minute, respiratory rate of 22 per minute, and normal temperature. He appeared pale and diaphoretic. Cardiopulmonary examination was unremarkable except for tachycardia and tachypnea. His abdomen was soft and nontender, with active red blood oozing from his rectum. He was noted to have extensive varicose veins over the right leg and scrotum and his right leg was larger than the left one.
Laboratory studies showed Hg 7.1 g/dL (normal 13–17 g/dL), hematocrit 22.9% (normal 38.6–49.2%), MCV 80.6 fl (normal 80–100 fl), MCH 24.9 pg (normal 26–34 pg), platelets 148 k/mL (normal 150–450 k/mL), AST 522 IU/L (normal 0–40 IU/L), ALT 257 IU/L (normal 0–50 IU/L), alkaline phosphatase 39 IU/L (normal 40–129 IU/L), bilirubin 1.7 mg/dL (normal 0-1 mg/dL), and INR 1.7 (normal 0.8–1.2).
Kidneys, ureters, and bladder (KUB) X-ray revealed multiple small rounded calcifications throughout the lower abdomen (). Computed tomography (CT) scan of the abdomen and pelvis showed marked wall thickening in the left colon, sigmoid colon, and the rectum (Figures and ). The patient underwent upper endoscopy which was within normal limits. Subsequent colonoscopy showed long, large, and dilated tortuous veins throughout the colon, with large amount of red and clotted blood extending to the ascending colon (Figures and ).
He underwent angiography which showed hypervascularity of one of the superior mesenteric artery branches supplying the right colon. This area was embolized, but the patient continued to bleed and subsequently underwent rectosigmoid resection.
Grossly, the resected left colon and rectum showed extensive mucosal varicoses with nodular changes (). Almost the entire mucosa was cobblestone in appearance with multiple polypoid areas. The wall was markedly thickened, and the mucosal surface was reddish-pink in color (Figures and ). The serosal surface showed markedly dilated veins with prominent varices (Figures and ). Histological examination of the resected area showed extensive venous malformations and dilated lymphatics with focal thrombosis consistent with KTS (). Postoperative course was complicated by hemoperitoneum, worsening coagulopathy, peritonitis, sepsis, and right leg deep venous thrombosis (DVT). He had an inferior vena cava (IVC) filter placed. He was sent to an operative room three times for hemoperitoneum evacuation and wound dehiscence closure. Patient required intubation, mechanical ventilation, and vasopressors multiple times during his hospitalization because of the sepsis and respiratory failure. He required transfusion of a total of 50 units of blood (33 units on the first day of presentation), 18 units of fresh frozen plasma, 26 units of platelets, and 10 units of cryoprecipitate. He expired after 2 months of hospitalization.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [55.0, 'mm hg'], 'Diastolic Blood Pressure': [29.0, 'mm hg']}",37.66667,35.78334,39.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 55.0 mm Hg + 2/3 * 29.0 mm Hg = 37.66667 mm Hg.
Hence, the patient's mean arterial pressure is 37.66667 mm Hg."
1287,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9071,Extracted,"A 57-year-old man presents to his primary care provider because of chest pain for the past 3 weeks. The chest pain occurs after climbing more than 2 flights of stairs or walking for more than 10 minutes. His symptoms remain for an average of 30 minutes despite rest, but they eventually remit. He is obese, has a history of type 2 diabetes mellitus, and has smoked 15–20 cigarettes a day for the past 25 years. His father died from a myocardial infarction at 52 years of age. His vital signs reveal a temperature of 36.7°C (98.0°F), blood pressure of 145/93 mm Hg, and a heart rate of 85/min. The physical examination is unremarkable.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [93.0, 'mm hg'], 'Systolic Blood Pressure': [145.0, 'mm hg']}",110.33333,104.81666,115.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 145.0 mm Hg + 2/3 * 93.0 mm Hg = 110.33333 mm Hg.
Hence, the patient's mean arterial pressure is 110.33333 mm Hg."
1288,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8716132-1,Extracted,"We present the case of a 61-year-old man who presented to the emergency department with a two-day history of severe abdominal pain. The pain was generalized and non-radiating. He described the pain as burning in character and was constant. The pain was aggravated by food intake and was not relieved by over-the-counter medications. He rated the pain as 8 out of 10 in severity and he could not sleep because of the pain. The pain was associated with nausea and recurrent episodes of vomiting. The patient reported that he had been having abdominal pain that was similar in quality but much milder in severity than the current episode. He reported that he usually developed abdominal pain following meal intake. He visited several outpatient clinics for his pain. He was diagnosed as having indigestion. He has been on a proton pump therapy for two years and it has provided moderate relief to his pain. He underwent upper gastrointestinal endoscopy and revealed normal findings. He reported that because of the chronic abdominal pain, he had reduced appetite and lost more than 15 kg.
In addition to the chronic abdominal pain, the past medical history was remarkable for a longstanding history of hypertension, dyslipidemia, diabetes mellitus, and chronic obstructive pulmonary disease. The patient had a history of Helicobacter pylori gastritis 15 years back that was successfully eradicated by triple therapy. The patient was on several medications for his comorbidities, including metformin 1000 mg, amlodipine 5 mg, omeprazole 40 mg, atorvastatin 20 mg, and aspirin 75 mg. His surgical history included a remote history of tonsillectomy. He was not known to have any drug or food allergies. He was a heavy smoker with a 30 pack-years smoking history. He never consumed alcohol. He was a retired school teacher. The family history was remarkable for inflammatory bowel disease.
Upon examination, the patient appeared in pain. His vital signs showed tachycardia (115 bpm), normal respiratory rate (14 bpm), normal temperature (36.8℃), and maintained blood pressure (124/91 mmHg). His oxygen saturation was normal on the room air. Abdominal examination revealed a soft abdomen with generalized tenderness. However, there was no guarding or rigidity. The bowel sounds were present and had normal intensity and frequency. Cardiovascular examination revealed a loud S2 sound with no added sounds or murmurs. The peripheral pulses were normal. The respiratory and neurological examination findings were normal. The initial laboratory findings, including hematological and biochemical investigations, were within the normal range (Table ).
Considering the cardiovascular risk factors for atherosclerosis and the severity of the pain, the initial differential diagnosis was acute mesenteric ischemia. Hence, the patient underwent a contrast-enhanced computed tomography scan of the abdomen. The scan demonstrated an acute angulation and indentation upon the celiac trunk with thickening of the median arcuate ligament (Figure ). The bowel loops had normal wall thickness and enhancement. In light of the clinical and radiological findings, the diagnosis of celiac artery compression syndrome was made.
Subsequently, the patient was prepared for surgical intervention for decompression. He underwent laparoscopic surgery. The operation was done under general anesthesia and the patient was placed in a supine position. After establishing pneumoperitoneum, diagnostic exploration was made. The thickened median arcuate ligament was appreciated. Careful dissection of the ligament was performed and the celiac artery was decompressed successfully. No complications occurred during the operation. The patient had an uneventful recovery. Postoperatively, the patient was able to tolerate oral feeding with no postprandial pain. He was discharged on the fifth postoperative day. After one year of regular follow-up visits, the patient had major satisfaction and his symptoms showed complete resolution.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [124.0, 'mm hg'], 'Diastolic Blood Pressure': [91.0, 'mm hg']}",102,96.9,107.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 124.0 mm Hg + 2/3 * 91.0 mm Hg = 102.0 mm Hg.
Hence, the patient's mean arterial pressure is 102.0 mm Hg."
1289,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-834,Extracted,"A 74-year-old Hispanic man comes to the physician because of a three-week history of dizziness upon standing and a brief loss of consciousness one hour ago. The patient suddenly collapsed on his way to the bathroom after waking up in the morning. He did not sustain any injuries from his collapse. He has a history of gastroesophageal reflux disease, benign prostatic hyperplasia, and gout. The patient's mother died of a grand mal seizure at the age of 53 years. He has smoked one pack of cigarettes daily for 55 years. He drinks three beers and two glasses of whiskey daily. Current medications include ranitidine, dutasteride, tamsulosin, and allopurinol. He is 166 cm (5 ft 5 in) tall and weighs 62 kg (137 lb); BMI is 22.5 kg/m2. He appears pale. Temperature is 36.7°C (98.0°F), pulse is 83/min, and blood pressure is 125/80 mm Hg supine and 100/70 mm Hg one minute after standing with no change in pulse rate. Physical examination shows conjunctival pallor. A plopping sound is heard on auscultation, immediately followed by a low-pitched, rumbling mid-diastolic murmur heard best at the apex. The remainder of the examination shows no abnormalities. An ECG shows regular sinus rhythm.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",95,90.25,99.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 80.0 mm Hg = 95.0 mm Hg.
Hence, the patient's mean arterial pressure is 95.0 mm Hg."
1290,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3221138-1,Extracted,"A 36-year-old woman complained of intermittent abdominal pain in the upper right quadrant of 7 days duration. The pain was associated with hematemesis and jaundice. The patient also reported weakness, light-headedness, and syncope. On examination, her vital signs showed a temperature of 37°C, blood pressure of 90/60 mm Hg, respiratory rate of 18 breaths/minute, and oxygen saturation of 98% in room air. Laboratory tests revealed a hemoglobin level of 10.0 g/dL, hematocrit of 32.4%, total bilirubin of 32.0 μmol/L (normal: 3-20 μmol/L), direct bilirubin of 21.0 μmol/L (normal: 0-6.8 μmol/L), gamma-glutamyl transferase of 1125 U/L (normal: 5-36 U/L), aspartate aminotransferase of 126.8 U/L (normal: <37 U/L), and alanine aminotransferase of 333.9 U/L (normal: <35 U/L). She had undergone MC for a gallstone 5 weeks earlier and reported no history of iatrogenic or other liver injury. Because she had recurrent symptoms of a microlithiasis before MC, a magnetic resonance cholangio-pancreatography (MRCP) was performed to exclude choledocholith and anomalies of the biliary system. Preoperative MRCP revealed a normal biliary tree structure.
Two days after admission, an axial MR image revealed hemorrhagic fluid in the gallbladder fossa and the subcapsular portion of the liver and an abnormal extrahepatic bile duct (Figures and ). An upper endoscopy revealed gastritis and blood clots at the papilla of Vater. Abdominal ultrasound revealed only fluid collection in the gallbladder fossa. Five days after admission, she developed mild epigastric pain and significant hematemesis again. The epigastric pain worsened with radiation to the right upper shoulder. In addition, hematemesis led to hemodynamic instability. After resuscitation, the patient was transferred to the Department of Interventional Radiology (The Affiliated Hospital of Inner Mongolia Medical College, Hohhot, China). Emergency angiography confirmed the formation of right HAP with active bleeding. Coil embolization was immediately performed on her to control bleeding (Figures and ). Prior to the procedure, the patient received 6 U of packed red blood cells. After hepatic artery coil embolization, the patient recovered well and was discharged without evidence of bleeding. At the 10-month follow-up, she showed satisfactory recovery, with normal liver function test results.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [60.0, 'mm hg'], 'Systolic Blood Pressure': [90.0, 'mm hg']}",70,66.5,73.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 60.0 mm Hg = 70.0 mm Hg.
Hence, the patient's mean arterial pressure is 70.0 mm Hg."
1291,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9514,Extracted,"A 50-year-old man with a history of stage 4 kidney disease was admitted to the hospital for an elective hemicolectomy. His past medical history is significant for severe diverticulitis. After the procedure he becomes septic and was placed on broad spectrum antibiotics. On morning rounds, he appear weak and complains of fatigue and nausea. His words are soft and he has difficulty answering questions. His temperature is 38.9°C (102.1°C), heart rate is 110/min, respiratory rate is 15/min, blood pressure 90/65 mm Hg, and saturation is 89% on room air. On physical exam, his mental status appears altered. He has a bruise on his left arm that spontaneously appeared overnight. His cardiac exam is positive for a weak friction rub. Blood specimens are collected and sent for evaluation. An ECG is performed (see image).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [65.0, 'mm hg'], 'Systolic Blood Pressure': [90.0, 'mm hg']}",73.33333,69.66666,77,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 65.0 mm Hg = 73.33333 mm Hg.
Hence, the patient's mean arterial pressure is 73.33333 mm Hg."
1292,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-6080,Extracted,"A 67-year-old man presents to the emergency department with a fever and altered mental status. The patient has a history of Alzheimer dementia and is typically bed bound. His son found him confused with a warm and flushed complexion thus prompting his presentation. The patient has a past medical history of dementia, diabetes, and hypertension and typically has a visiting home nurse come to administer medications. Prior to examination, he is given haloperidol and diphenhydramine as he is combative and will not allow the nurses near him. His temperature is 102.9°F (39.4°C), blood pressure is 104/64 mmHg, pulse is 170/min, respirations are 22/min, and oxygen saturation is 100% on room air. Physical exam is notable for dry and flushed skin and a confused man. There is no skin breakdown, and flexion of the patient’s neck elicits no discomfort. Laboratory studies are drawn as seen below.

Hemoglobin: 15 g/dL
Hematocrit: 45%
Leukocyte count: 4,500/mm^3 with normal differential
Platelet count: 227,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 24 mEq/L
BUN: 30 mg/dL
Glucose: 97 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 10.2 mg/dL
AST: 12 U/L
ALT: 10 U/L

Urine:
Color: Yellow
Bacteria: Absent
Nitrites: Negative
Red blood cells: Negative

An initial chest radiograph is unremarkable. The patient is given 3 liters of Ringer's lactate and an electric fan to cool off. Two hours later, his temperature is 99°F (37.2°C), blood pressure is 154/94 mmHg, pulse is 100/min, respirations are 17/min, and oxygen saturation is 100% on room air. The patient’s mental status is at the patient’s baseline according to the son.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [64.0, 'mm hg'], 'Systolic Blood Pressure': [104.0, 'mm hg']}",77.33333,73.46666,81.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 104.0 mm Hg + 2/3 * 64.0 mm Hg = 77.33333 mm Hg.
Hence, the patient's mean arterial pressure is 77.33333 mm Hg."
1293,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4848,Extracted,"A 27-year-old woman presents to her primary care physician for a follow-up appointment. At her previous visit she had missed her previous two menses and also had a blood pressure of 147/100 mmHg. The patient has a past medical history of anxiety, depression, bulimia nervosa and irritable bowel syndrome. Her physician prescribed her an exercise program as well as started her on hydrochlorothiazide and ordered lab work. The results of the patient's lab work are below:

Serum:
Na+: 145 mEq/L
K+: 2.9 mEq/L
Cl-: 100 mEq/L
HCO3-: 30 mEq/L
BUN: 18 mg/dL
Ca2+: 10.9 mg/dL
Mg2+: 2.0 mEq/L
Creatinine: 1.2 mg/dL
Glucose: 110 mg/dL

The patient's blood pressure at this visit is 145/100 mmHg and she has still not experienced her menses. Her cardiac, abdominal, and pulmonary exams are within normal limits. Inspection of the patient's oropharynx is unremarkable as is inspection of her extremities. The patient is started on furosemide and sent home.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [145.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",115,109.25,120.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 145.0 mm Hg + 2/3 * 100.0 mm Hg = 115.0 mm Hg.
Hence, the patient's mean arterial pressure is 115.0 mm Hg."
1294,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4274402-1,Extracted,"A 35-year-old male with an 8-year history of AIDS presented with a 3-day history of recurrent frontal headaches, subjective fever and altered mental status. He had a history of non-adherence to medications, but he had resumed antiretroviral drugs for about 10 weeks. Four weeks prior to presentation to our hospital, he had been diagnosed with cryptococcal meningitis (CM) in an outside hospital and had received a 7 day course of intravenous amphotericin B (lipid complex preparation). This was discontinued due to progressive acute kidney injury and he was subsequently placed on high dose (800 mg) oral fluconazole (FLU) daily.
At the antecedent hospital visit, his presenting CD4 count was 16 cells/µL and plasma HIV RNA viral load was 1970 copies/mL, a decrease from a viral load of 50,000 copies/mL at treatment re-initiation 8 weeks previously. His viral load had further declined to less than 20 copies/mL at the time of initial evaluation at our facility 4 weeks later. His nadir CD4 count was 9 cells/µL (). His antiretroviral drug regimen consisted of darunavir boosted with ritonavir, tenofovir and emtricitabine taken once daily. He reported at least 2 prior episodes of CM with the most recent and preceding episode occurring about 3 years ago. He had not been on antifungal prophylaxis prior to his current illness.
On presentation, he was cachectic, but was in no acute distress. Temperature was 36.9°C, heart rate 84 beats/minute, BP 87/65 mmHg, respiratory rate 18 cycles/minute and oxygen saturation of 100% on room air. He was alert and oriented to time, place and person; a mini mental status examination score was 25; he exhibited photophobia but no other meningeal signs. He had bilateral horizontal nystagmus and mild right upper extremity hemiparesis. Cardio-pulmonary exam was unremarkable.
Peripheral white blood cell (WBC) count was 2900 cells/µL with a normal differential. Although no formal measurements were taken, a spinal tap was consistent with elevated opening pressure as there was brisk cerebrospinal fluid (CSF) flow. CSF analysis showed a WBC count of 41 cells per high power field comprising 75% lymphocytes, protein - 800 mg/dL (<50 mg/dL - normal), and glucose level of 13 mg/dL (40-70 mg/dL - normal). CSF India Ink stain demonstrated yeast but there was no subsequent growth on culture after 4 weeks of incubation. CSF and serum cryptococcal antigen (CRAG) titers were >1:1024 and 1:512 respectively. Blood cultures showed no growth.
A brain magnetic resonance image (MRI) with gadolinium showed clusters of gelatinous cystic lesions along the periventricular white matter structures and within the lateral ventricles, basal ganglia and posterior cranial fossa. There was enlargement of the ventricular system with no evidence of structural obstruction to CSF flow to suggest communicating hydrocephalus. It also showed diffuse leptomeningeal and ependymal enhancement consistent with meningitis and ventriculitis ().The patient was started on induction therapy with liposomal amphotericin B (LAmB) 6 mg/kg/d and flucytosine (5FC) 100 mg/kg/d for 2 weeks and subsequently transitioned to 400mg oral FLU with resolution of motor deficits and improved CSF parameters (). His ART was continued and he was discharged home.
He was readmitted to the hospital 5 weeks later with recurrent headaches and fevers. MRI of his brain showed no change. Repeat CSF evaluation showed persistent lymphocytic pleocytosis, hypoglycorrhachia and an elevated opening pressure of 38 cm H2O. There were no cryptococcal organisms noted on fungal stain and culture eventually showed no growth. At this point, it was suspected that his presentation was at least in part due to IRIS. However, because of concern for his persistent cerebral mass lesions, ventriculitis and CSF abnormalities, it was decided to treat him with a prolonged induction course (8 weeks) of LAmB and 5FC followed by FLU consolidation therapy (400 mg daily oral dose). He underwent serial LPs during this course which showed persistently elevated protein, low glucose and high CRAG titers (weeks 12-20 in ).
Four months later, he required placement of a ventriculoperitoneal shunt for persistently elevated CSF pressures. A biopsy of one of his CNS cysts at the time showed an aggregation of organisms morphologically consistent with Cryptococcus species on pathologic examination. No cultures were performed. He was maintained on oral FLU 200 mg daily. On outpatient follow up 1 year later, he demonstrated severe cognitive impairment. Our patient was subsequently lost to follow up and 2 years after his initial presentation, he died. Proximate cause of death remains unknown.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [87.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",72.33333,68.71666,75.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 87.0 mm Hg + 2/3 * 65.0 mm Hg = 72.33333 mm Hg.
Hence, the patient's mean arterial pressure is 72.33333 mm Hg."
1295,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3542936-1,Extracted,"A 53-year-old man was brought in by ambulance with the chief complaint of multiple “fainting” episodes. He was reported by the paramedics to be hypotensive and tachycardic prior to arrival. His past medical history was significant for hypertension, chronic renal insufficiency, and gouty arthritis. On presentation to the emergency department, the patient appeared critically ill with generalized pallor, perioral cyanosis, with a heart rate of 133 beats per minute (bpm), blood pressure of 130/106 mm Hg, and oxygen saturation of 100% on 15 L O2 via a nonrebreather mask. His exam was significant for grunting, otherwise clear bilateral breath sounds, rapid but regular heart tones, weak femoral pulses, and symmetric, non-edematous lower extremities.
Shortly after arrival, a bedside ultrasound was performed, demonstrating a thrombus in the right ventricle (RV) and inferior vena cava (IVC) (Figures and ). The patient lost cardiac motion during the ultrasound, and cardiopulmonary resuscitation (CPR) was initiated with return of spontaneous circulation within one minute. He was emergently intubated, and his postintubation oxygen saturation was noted to be 60%, despite 100% FiO2 and confirmation of adequate tube placement. A repeat bedside ultrasound was performed with visualization of an enlarged right ventricle (), and an EKG demonstrated a new right bundle branch block (), highly suspicious for a massive pulmonary embolus. Shortly thereafter, the patient again lost pulses requiring CPR and 1 mg IV epinephrine, with subsequent return of spontaneous circulation in three minutes. The patient's blood pressure was maintained on a continuous infusion of epinephrine, and bolus dosing of alteplase (tPA) was being prepared while a CT angiogram (CTA) of the thorax was ordered. The CTA confirmed the diagnosis of bilateral massive pulmonary emboli (PE) (), and alteplase was administered at a bolus dose of 0.6 mg/kg over 2 minutes followed by a heparin infusion and admitted to the ICU without further hemodynamic decompensation.
The patient's course was complicated by bilateral pneumothoraces, acute renal failure, and subconjunctival hemorrhage. However, he was ultimately extubated and discharged home with full neurologic recovery, and a repeat CTA chest demonstrated resolution of pulmonary thrombi (). A deep venous thrombosis (DVT) in the left distal popliteal vein with an aneurismal dilation of the popliteal vein was diagnosed during his inpatient stay, thought to be related a recent flare of gouty arthritis. The patient is currently awaiting outpatient work-up for possible coagulopathy and continues on warfarin anticoagulation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [106.0, 'mm hg']}",114,108.3,119.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 106.0 mm Hg = 114.0 mm Hg.
Hence, the patient's mean arterial pressure is 114.0 mm Hg."
1296,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4332731-1,Extracted,"A 55-year-old Chinese female with a history of hypertension was evaluated by the cardiologist. She had a normal pulse rate and a regular rhythm, and her blood pressure was 150/85 mmHg. No murmur or thrill was present. The chest radiograph was normal. Echocardiogram showed a mass in the right atrial free wall, measuring around 30 mm × 15 mm in diameter (Figure A). She was admitted to our hospital for further evaluation.
To obtain better definition of the mass, a 64-slice computed tomography (CT) was performed. An evaluation by means of CT demonstrated that the mass, which contained several thin septations, was consistent with lipoma. The mass occupied a part of the right atrial free wall (Figure B). But, we were uncertain whether the fatty tumor was epicardial, intramural, or endocardial.
Surgical treatment was indicated. After routine median sternotomy, the patient was started on moderate systemic hypothermic (34°C) cardiopulmonary bypass with cannulation of the aorta ascendens and both venae cavae. The superior vena cava cannula was inserted very high in the superior vena cava so as to be away from the tumor. The inferior vena cava cannula was also inserted very low near the diaphragm. To reduce the risk of complications, the patients underwent open heart operation on beating hearts. After the right atrium was opened, there was a large, yellowish rubbery mass (32 mm × 17 mm × 7 mm) constituting part of the free wall of the right atrium (Figure A). After total tumor excision, the defect of atrial free wall was closed directly without any patch.
Gross examination revealed a 32 mm × 17 mm × 7 mm mass comprised predominantly of mature adipose tissue of an intramyocardial lipoma (Figure B). Histologically, the excised specimen showed many fatty structures lined by myocardium, suggesting that the tumor had indeed originated within the atrial wall (Figure C).
The patient recovered well on the ward and was discharged 8 days after the operation. On 1-year follow-up, the patient remained asymptomatic, with good clinical and echocardiography evaluations.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [85.0, 'mm hg'], 'Systolic Blood Pressure': [150.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 85.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1297,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4976580-1,Extracted,"A 56-year-old female patient was admitted to Hangzhou Normal University Affiliated Hospital on November 12, 2014. She had fever for 1 week with the highest temperature reaching 39°C, coughed white sputum with no blood or yellowish stuff, and complained chest tightness and dyspnea when severe coughing. She felt nausea and even vomit in the course but no coffee-like objects were vomited. She was treated with intravenous cefuroxime and levofloxacin in outpatient service for 3 days without expected improvement. She had been diagnosed as type 2 diabetes in the past and had been given metformin and acarbose treatment. Clozapine and trihexyphenidyl and other drugs were daily administrated orally to treat schizophrenia diagnosed previously. She has no smoking and drinking history, no omophagia fish, and shrimp history. No obvious abnormalities were found in the regular physical examination and chest X-ray scan [] performed a half year before. Physical examination showed body temperature of 38.2°C, pulse rate of 89/min, respiratory rate of 22 breaths/min, blood pressure of 125/70 mmHg (1 mmHg = 0.133 kPa), and pulse oxygen saturation of 85% (concentration of oxygen inhalation: 21%). Her consciousness was clear, with poor spirit and mild cyanosis. No enlarged superficial lymph nodes were found and widely moist rales could be heard in two lungs. Her heart rate was 89 beats/min with no pathological murmur. The abdomen is soft, no lower limbs dropsy. On auxiliary examination, chest CT scan [Figure –, November 12, 2014] found diffused uniform ground-glass shadow in two lungs with no enlarged mediastinal lymph nodes. On admission, preliminary diagnosis revealed: (1) diffuse lung disease of unknown origin, respiratory failure, (2) type 2 diabetes, and (3) schizophrenia. After admission, the patient presented high fever and pulmonary diffuse exudate with respiratory failure. Considering previous history of type 2 diabetes, we suspected pulmonary infection with unknown pathogen. Oxygen therapy and hypoglycemic therapy were given. In addition, 4.5 g of piperacillin-tazobactam by intravenous drip bid and 0.4 g of moxifloxacin once a day (QD) combined with anti-infection and cough expectorant were given to relieve symptoms and simultaneously improve the relevant inspection.
Laboratory examination: Routine blood test + high-sensitive C-reactive protein (hs-CRP), leukocyte 19.67 × 109/L, percentage of neutrophils 91.0%, 6.1% of lymphocyte percentage and 0 of eosinophil cell percentage, red-cell count 4.65 × 1012/L and 130 g/L of hemoglobin, platelet count of 216 × 109/L, hs-CRP 30.99 mg/L. Arterial blood gas analysis: pH 7.31, partial pressure of carbon dioxide in artery 27.10 mmHg, arterial partial pressure of oxygen 57.90 mmHg, arterial oxygen saturation 87.10%. B-type natriuretic peptide: 65.30 pg/ml. Allergen determination: total immunoglobulin E 11.50 IU/ml, no specific allergen was detected. Procalcitonin <0.5 ng/ml. Antinuclear antibodies, double-stranded-DNA, anti-Sjogren syndrome A antibody, anti-Sjogren syndrome B antibody and other autoantibodies were all negative. Perinuclear antineutrophil cytoplasmic antibody, cytoplasmic antineutrophil cytoplasmic antibodies and myeloperoxidase antibody was negative. Tumor screening: α-fetoprotein - 3.61 ng/ml, carcinoembryonic antigen (CEA) - 2.5 ng/ml, carbohydrate antigen (CA) 199-25 kU/L, CA 125-14 U/ml, all were in the normal range. Interferon gamma release test for tuberculosis infection: negative. 1,3-beta-glucan test: 300.2 pg/ml (reference value <100.5 pg/ml); galactomannan test: negative. Nucleic acid detection of influenza A virus (throat swab): negative; human immunodeficiency virus antibody: negative, urine cytomegalovirus DNA detection: negative. Acid fast bacilli is negative in 3 smear tests. Sputum cytology found no tumor cells. Electrocardiograph: sinus rhythm.
Cough, shortness of breath gradually worsened after 3 days treatment with piperacillin-tazobactam combined with moxifloxacin. Body temperature had been fluctuating between 37°C and 38°C since the admission. The patient was administered with 0.2 g voriconazole by intravenous drip q12h and 40 mg methylprednisolone by intravenous QD to inhibit fungal infections and inflammation for 4 days. Intermittent noninvasive ventilation was given as needed. On the 5th day of admission, electronic bronchoscopy was performed and showed that the trachea and bronchial lumen was smooth and the mucosa was congested. A huge amount of white foam sputum was found in the tracheal cavity to be constantly emitted after suction; no stenosis and neoformation, no cheese-like necrosis tissue was observed. Oxygen saturation increased from 70% to 80% to above 93% after foamy sputum was suctioned. Transbronchial lung biopsy (TBLB) was performed in the right lower lung and TBLB pathology reported adenocarcinoma []. Epidermal growth factor (EGFR) gene and anaplastic lymphoma kinase-echinoderm microtubule-associated protein-like (ALK-EML4) fusion gene were further analyzed, and no mutation was found. The patient was given antitumor Chinese traditional medicine, anti-infection treatment, and nutritional support together with noninvasive ventilation and other treatment to relieve symptom. The patient died of respiratory failure on the 20th day after admission.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",88.33333,83.91666,92.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 70.0 mm Hg = 88.33333 mm Hg.
Hence, the patient's mean arterial pressure is 88.33333 mm Hg."
1298,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6967041-1,Extracted,"A 59-year-old man (170 cm, 78 kg) had cerebral infarction of the right precentral gyrus 2 years prior presentation and was diagnosed with bilateral ICA stenosis. He was treated conservatively (oral cilostazol and clopidogrel) and followed up; however, the stenosis of the left ICA progressed. Therefore, he was scheduled for CEA. There were no apparent complications related to his previous cerebral infarction. He was receiving an oral treatment for hypertension and dyslipidemia and had a long history of smoking (40 cigarettes per day for 40 years). There were no other notable findings in preoperative examinations. On the day of surgery, he was admitted to the operating room without premedication. Pre-oxygenation was performed using a mask without headband. Anesthesia was induced using 200 μg fentanyl and 5 mg midazolam, and 60 mg rocuronium was given to facilitate tracheal intubation. A Macintosh laryngoscope was used to expose the larynx. The view was classified as Cormack III. We attempted a tracheal intubation with a endotracheal tube (Shiley™ Endotracheal Tube with TaperGuard™ Cuff 7.5 mm), but the esophagus was inadvertently intubated, so it was removed. The second tracheal intubation by using a Macintosh laryngoscope was successful. Wheals appeared on the upper limbs, neck, and precordium without any vital sign changes after infusion of cefazolin sodium as a preoperative antibiotic, so administration was discontinued. The skin signs were believed to be an allergic reaction to cefazolin, which was changed to fosfomycin, and the patient also received an intravenous infusion containing 200 mg of hydrocortisone sodium phosphate. During surgery, he was placed in the supine position, but the neck was slightly rotated and lateroflexed to the right to secure the surgical field. Anesthesia was maintained with 1.4% sevoflurane and remifentanil at a dose of 0.2 μg/kg/min. Mild hypotension was observed intraoperatively. This was managed with fluid infusions and continuous administration of an appropriate dose of noradrenaline. Surgery was concluded without problems, and the preoperatively observed wheals resolved. Endotracheal aspiration was performed after waking up the patient, but it triggered a strong cough reflex. The patient was then extubated. The duration of surgery was 4 h and 57 min, the duration of anesthesia was 6 h and 29 min, the volume of blood loss was negligible, the in-out balance was + 3210 mL (crystalloid fluid 4175 mL, urine volume 965 mL), and mild swelling of the face and both upper limbs was noted. The patient was admitted to the intensive care unit (ICU) in a lucid state with a blood pressure of 120/70 mmHg, a heart rate of 110 beats/min, oxygen saturation of 100% on 3 L of nasal oxygen and respiratory rate of 12 breaths/min. His arterial blood gas analysis was normal, and mild hoarseness was noted without swelling of the neck or stridor. Six hours after admission to the ICU mild bilateral neck swelling appeared. The hoarseness rapidly worsened, and tachypnea and stridor appeared 1 h later without oxygen desaturation. Emergency intubation with a tube (Shiley™ Evac Endotracheal Tube with TaperGuard™ Cuff 7.5 mm) was immediately performed with mild sedation with propofol under spontaneous breathing on suspicion of upper airway obstruction. We used a video laryngoscope (HOYA Co. Ltd., airway scope) with a gum elastic bougie tube introducer. Laryngopharyngeal findings at this time included no epiglottic edema. However, the edema of the lateral and posterior pharyngeal walls was present, and it narrowed the oral and pharyngeal cavities. The neck swelling was pronounced, and the neck circumference was 63 cm (Fig. ). A CT scan was performed to investigate the cause and to facilitate differential diagnosis of possible postoperative hemorrhage, but no bleeding was observed. The bilateral parotid and salivary glands were markedly swollen (Fig. ), and the edema of the posterior pharyngeal wall was developed (Fig. ) when compared to the preoperative state. Blood test results revealed a leukocyte count of 8000/μL (eosinophils 0%), amylase at 1790 U/L, mumps immunoglobulin G (IgG) at 16.6 (+), mumps IgM at 0.27 (−), and C-reactive protein at 0.18. Based on these findings, we concluded that the patient had previously suffered from a mumps infection, but had no active disease. Moreover, he only presented with the clinical features of sialadenitis. We commenced administration of steroids to reduce the edema. On postoperative day (POD) 2, the serum amylase decreased to 457 U/L, gradual improvement of the bilateral parotid gland swelling was observed, and the patient was extubated. The subsequent clinical course was favorable, and the neck swelling disappeared. The general condition, airways, and ability to swallow were all normal when the patient was discharged on POD 11.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1299,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7723697-1,Extracted,"A 36-year-old pregnant woman (G3P1) at 34 4/7 wk of gestation returned to Wenzhou from Wuhan on January 20, 2020. Due to her residence history in Wuhan, she was asked to self-quarantine at home. She revealed that she had run a business in Hubei Province, but said that she had not visited the Huanan Seafood wholesale market in Wuhan, which is where most experts believe the coronavirus infected humans.
On January 30, 2020, 9 d after returning to Wenzhou, the woman at 36 wk of pregnancy was hospitalized in the Yueqing People’s Hospital because of the emergence of a dry cough and fever.
No history of past illness.
No personal and family history.
The patient did not exhibit chest pain, shortness of breath, or coarse rales in either lung. Physical examination was as follows: a temperature of 38.5 °C, a pulse rate of 104 beats/min, a respiratory rate of 20 breaths/min, and a blood pressure of 101/76 mm of Hg.
Laboratory examination showed low lymphocyte counts and elevated concentrations of C-reactive protein (Table ).
Computed tomography (CT) examination indicated that both lungs possessed multiple patchy, ground-glass-like fuzzy shadows that were primarily distributed under the pleurae (multifocal ground-glass opacities bilaterally, especially in the apical posterior segment of the left-upper lobe) (Figure and ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [101.0, 'mm hg'], 'Diastolic Blood Pressure': [76.0, 'mm hg']}",84.33333,80.11666,88.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 101.0 mm Hg + 2/3 * 76.0 mm Hg = 84.33333 mm Hg.
Hence, the patient's mean arterial pressure is 84.33333 mm Hg."
1300,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3371498-1,Extracted,"A 20-year-old Gravida 2, Para 1 (G2, P1) post-partum female presented to us with headache and seizures 4 days after a caesarean section. She was normally healthy and her antenatal course was uncomplicated. She received a lumbar epidural during labour. It was noted to be a difficult procedure, but a dural puncture was not recorded as having occurred. The epidural was extended for an emergency caesarean section due to poor progress of labour, and both the procedure and the immediate post-operative period were uneventful. On the first post-operative day, she complained of a postural frontal headache, which was treated with bed rest, intravenous fluids and simple analgesics. As the symptoms improved, she was discharged home on day three.
She presented to the Emergency Department the following day with generalised tonic-clonic seizures preceded by nausea and headache. There was no history of visual disturbances, raised temperature, tinnitus or neck rigidity. Paramedics administered diazepam in the ambulance to terminate the seizures. On examination, Glasgow Coma Scale (GCS) was 8/15 with normal peripheral neurological reflexes and equally reacting pupils. She was afebrile with a pulse rate of 114 beats/min, blood pressure of 108/46 mmHg and SPO2 (oxygen saturation) of 98% on 5 L/min oxygen. Chest and abdominal examination were normal. Obstetricians treated her with magnesium sulphate and obtained a computerized tomography (CT) scan of the head, which did not reveal any abnormality. Routine investigations showed a haemoglobin of 10 g/dL, white cell count (WCC) of 15.9×109/L, platelets of 102×109/L, normal urea, electrolytes, clotting, liver function tests, uric acid and no proteinuria. GCS improved over the next few hours to 15/15, and at this point we were asked to assess and advise on her further management.
As eclampsia seemed an unlikely diagnosis, magnesium sulphate was stopped. A lumbar puncture with a 27G spinal needle revealed clear cerebrospinal fluid, raised protein of 715 mg/L (normal range: 120–600 mg/L) and no cells. A loading dose of intravenous phenytoin was administered and close Electrocardiographic (ECG) monitoring was instituted in the labour ward. This was followed by oral phenytoin and analgesics. There were no further episodes of seizures and, after 24 h, her only symptom was a severe postural headache (aggravated by upright position and relieved on lying supine). Neurologists were consulted, who requested a magnetic resonance imaging (MRI) scan and a magnetic resonance (MR) venous angiogram of the head. The scans were normal with no intracranial pathology. A consensus between the anaesthetists, neurologists, obstetricians and radiologists attributed dural puncture as the most likely cause for the headache. An epidural blood patch was discussed as a treatment option on the eighth post-partum day. After patient consent, 20 mL of sterile blood withdrawn from the ante-cubital fossa prepared with chlorhexidine solution 0.5% was injected into the epidural space aseptically without any complications. There was an almost immediate resolution of headache and the patient was discharged home the next day for further follow-up. The typical clinical features and dramatic improvement following epidural blood patch makes us confident that an unrecognised dural puncture was the cause of headache and seizures.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [108.0, 'mm hg'], 'Diastolic Blood Pressure': [46.0, 'mm hg']}",66.66667,63.33334,70,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 108.0 mm Hg + 2/3 * 46.0 mm Hg = 66.66667 mm Hg.
Hence, the patient's mean arterial pressure is 66.66667 mm Hg."
1301,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4987479-1,Extracted,"The patient was a 71-year-old woman with diabetes, hypertension, and cirrhosis, transferred to our hospital for management of acute decompensated heart failure. She was previously a highly active and independent individual until a recent tibial/fibular fracture from a mechanical fall. Her home medications were Insulin, Tramadol, and Bactrim. She presented from her rehab facility to an outside hospital with hyperglycemia (glucose greater than 700) and, on initial evaluation, was noted to have ST elevations in V3–V6, Troponin 4.46, and creatine kinase 130. She was diagnosed with a subacute myocardial infarction (MI). Transthoracic echocardiogram (TTE) revealed a left ventricular ejection fraction (EF) of 20–25%, with apical akinesia and ballooning and hyperdynamic base (, Video 1 in Supplementary Material available online at ) consistent with Takotsubo Syndrome, as well as a distal muscular ventricular septal defect (VSD) (, Video 2). She received intravenous (IV) diuresis, was initiated on IV heparin and a heart failure regimen, and was transferred to our hospital for further management.
On arrival, she was afebrile with blood pressure of 107/51 mmHg, heart rate of 97 beats per minute, and respiratory rate of 18 on 3 L of oxygen. On examination she had a 3/6 holosystolic murmur loudest at the apex and was volume overloaded with jugular venous distension to 15 cm H2O and 2+ lower extremity edema. EKG showed normal sinus rhythm, poor R-wave progression, T-wave inversions in II, III, aVF, V2–V6, and prolonged QTc of 570 ms, patterns consistent with those described with Takotsubo Syndrome [–, , ]. Repeat TTE on arrival, 11 days after the initial TTE, showed EF recovery to 75% (, Video 3), a persistent 1 cm inferior apical VSD, and right ventricular (RV) dilatation and elevated pulmonary pressures, with pulmonary artery systolic pressure (PASP) of 57 mmHg. The VSD was thought to be a major contributor to her continued decompensation. She was managed with diuresis and medical optimization and underwent evaluation for VSD repair.
Although she had no prior echocardiogram for comparison, discussion with the patient's primary care provider revealed that she had no cardiac history and no documented cardiac murmur throughout her prior history. To rule out VSD as a complication of MI, the patient underwent left heart catheterization, demonstrating completely normal coronary arteries. Ventriculography confirmed VSD. Right heart catheterization demonstrated right atrial pressure of 7 mmHg, pulmonary artery pressure of 42/14 mmHg, wedge pressure of 10 mmHg, cardiac output of 4.0 L/min, and index of 2.7 L/min/m2, with Qp : Qs ratio of 2.2 : 1, consistent with a large VSD. Given these findings, initial echocardiographic appearance of her heart, and rapid EF recovery, she was thought to have a rare case of ventricular septal perforation due to Takotsubo Syndrome. She underwent transcatheter closure of her VSD (, Video 4), was medically optimized afterwards, and was eventually discharged home after a prolonged hospitalization. Repeat echocardiography performed 2 months later demonstrated normal PASP and improvement in right heart function.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [107.0, 'mm hg'], 'Diastolic Blood Pressure': [51.0, 'mm hg']}",69.66667,66.18334,73.15,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 107.0 mm Hg + 2/3 * 51.0 mm Hg = 69.66667 mm Hg.
Hence, the patient's mean arterial pressure is 69.66667 mm Hg."
1302,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5767976-1,Extracted,"A 52-year-old white man with chronic obstructive pulmonary disease, 15 pack-years of tobacco smoking history, moderate use of alcohol, and no significant family history presented with pre-syncopal episode and was found to be pancytopenic. His vital signs were temperature 36.7 °C, pulse 93 beats/minute, respiration rate 20 breaths/minute, blood pressure 101/60 mmHg, and blood oxygen saturation (SpO2) 99% at room air. A physical examination including neurological examination was unremarkable. Comprehensive metabolic profile and urine analysis was normal. Complete blood count showed pancytopenia. A peripheral blood smear showed a myeloid left-shift with 5% blasts. Subsequent bone marrow biopsy showed erythroid dyspoiesis, left-shifted granulopoiesis, and grade 3+ fibrosis consistent with MDS with marrow fibrosis. Genetic testing revealed wild-type JAK2 and MPL, a normal male karyotype, lack of BCR-ABL1 translocation, and a negative MDS fluorescence in situ hybridization (FISH) panel. Based on the lack of cytogenic abnormalities, hemoglobin (Hgb) of 7.8 g/dL, platelets (Plt) of 32 × 109/L, absolute neutrophil count (ANC) of 11.3 × 109/L, and the presence of 5% blasts, an age-adjusted Revised International Prognostic Scoring System (IPSS-R) score of 5.1 was calculated (that is, high risk – with a median survival and time to progression to acute leukemia of 1.6 and 1.4 years, respectively) []. He received multiple blood transfusions for pancytopenia and was treated with 5 mg twice a day of the Janus kinase inhibitor, ruxolitinib.
Three months after diagnosis of MDS with fibrosis, during workup for allogenic bone marrow transplantation (BMT), a 4 cm right hepatic lesion was discovered on ultrasound. The lesion was hypoechoic (Fig. ) with internal vascularity. Hepatosplenomegaly was also noted with the spleen measuring 19 cm in the craniocaudal dimension. MRI performed with MultiHance® revealed diffuse hepatic iron deposition and a T1 hypointense (Fig. ) and T2 isointense (not shown) lesion in segment 7 showing heterogeneous mild arterial phase enhancement (Fig. ) with washout to isointensity on portal venous (Fig. ) and delayed phase images (Fig. ). Of note, the lesion was not visible on T2*-weighted GRE (Fig. f) images suggesting the presence of iron deposition within the lesion similar to that in background hepatic parenchyma. The lesion was also not visible on diffusion-weighted imaging (DWI; Fig. ). The differential diagnosis offered at this point included focal nodular hyperplasia (FNH) and adenoma, with hepatocellular carcinoma (HCC) being less likely and metastasis being unlikely. A few days later, our patient underwent ultrasound-guided core needle biopsy of the lesion, revealing marked sinusoidal EMH (Fig. ) with left-shifted granulopoiesis including increased blasts, the latter highlighted on c-KIT immunostain (Fig. ). Perls’ iron stain highlighted 4+ iron in hepatocytes and Kupffer cells (Fig. ).
After approximately 7 months of therapy with ruxolitinib, a repeat bone marrow biopsy did not show any change in the blast count but a peripheral smear showed 7% blasts, meeting criteria for refractory anemia with excess blasts-2 (RAEB-2) using the 2008 World Health Organization (WHO) classification system for MDS subtypes []. Two weeks later, while still being evaluated for BMT, pulmonary function tests revealed a poor forced expiratory volume at 1 second (FEV1) of 60% and a disproportionately reduced diffusing capacity of the lung for carbon monoxide (DLCO) of 56% predicted. This prompted a computed tomography (CT) angiogram of his chest, which showed an enhancing mass within his right main pulmonary artery suggestive of tumor thrombus (Fig. ). Bronchoscopic aspiration of the mass also showed EMH with dyspoiesis. He shortly developed hemoptysis at which point treatment with ruxolitinib was stopped and he was treated with low-dose radiotherapy to his chest (1 to 2 Gy/5 to 10 fractions) for approximately 10 days. A third bone marrow examination performed shortly afterwards showed similar findings to the previous with the additional finding of a significant peripheral monocytosis, at which point the disease was best classified as chronic myelomonocytic leukemia-2 (CMML-2) (Fig. ). Two weeks after diagnosis of CMML-2 and 3 weeks after the CT angiogram, he developed mediastinal hematoma probably due to progressive CMML-2 and radiation-induced degeneration of the pulmonary arterial EMH; he died shortly afterward, secondary to expanding mediastinal hematoma causing respiratory arrest. An autopsy was not performed to the best of our knowledge.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [101.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",73.66667,69.98334,77.35,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 101.0 mm Hg + 2/3 * 60.0 mm Hg = 73.66667 mm Hg.
Hence, the patient's mean arterial pressure is 73.66667 mm Hg."
1303,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4403,Extracted,"A 32-year-old man presents to his physician with a complaint of pain with urination that has developed and persisted over the past 8 days. Upon awakening today, he also noted a clear discharge from his urethra. The patient states he is otherwise healthy. Social history is notable for the patient working at a local farm with livestock. Review of systems is notable for left knee and ankle pain for the past week and worsening of his seasonal allergies with red and itchy eyes. His temperature is 97.7°F (36.5°C), blood pressure is 122/83 mmHg, pulse is 89/min, respirations are 14/min, and oxygen saturation is 98% on room air.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [122.0, 'mm hg'], 'Diastolic Blood Pressure': [83.0, 'mm hg']}",96,91.2,100.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 122.0 mm Hg + 2/3 * 83.0 mm Hg = 96.0 mm Hg.
Hence, the patient's mean arterial pressure is 96.0 mm Hg."
1304,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2728610-2,Extracted,"A previously healthy 68-year-old man, father of one child, presented in 1994 with fatigue and nausea. For many years he had suffered arthralgic pain and had been treated with antiflogistics. The last months he had experienced problems with nocturia and impotence. He was referred to ultrasonography of the abdomen, on which a tumor in the right adrenal was detected. An adrenal CT scan showed a 4 × 4 × 2.5 cm tumor in the right adrenal with high fat content, which was radiologically considered to be a myelolipoma. The left adrenal was evaluated as normal.
Further clinical investigation showed height 165 cm, blood pressure 140/80 mmHg, and normal male genitalia with testicular tenderness bilaterally. Biochemical investigation showed high basal level of 17-OH-progesterone, which was suppressible with dexamethasone, and an impaired cortisol response to ACTH stimulation (). Adrenal iodomethyl-19-norcholesterol scintigraphy showed high uptake in the right adrenal, which however was suppressed by dexamethasone; uptake was normal or low in the left adrenal. DNA sequencing of CYP21 revealed compound heterozygozity for the I172N mutation (c. 515T > A) and the I2 splice mutation (g.655A/C > G, I172N/I2splice).
The myelolipoma was not removed and the tumor size did not increase during a four-year observation period. The patient was started on treatment with 5 mg prednisolone daily for one year, later cortisone acetate 12.5 mg twice a day whereupon his condition improved. The patient died suddenly, 73 years old, in his home; the cause of death remains unknown.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [140.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 80.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1305,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5595,Extracted,"A 77-year-old man presents to the emergency department with a change in his mental status. The patient’s daughter states that he can cook and clean up after himself and only needs help paying bills. Yesterday the patient seemed fine; however, this morning she noticed that he struggled to perform simple tasks and was forgetful while cooking, leaving the stove on. They recently returned from a trip to Mexico and admit to drinking unfiltered water and eating local cuisines while abroad. The patient has a past medical history of hypertension and diabetes. His temperature is 97.5°F (36.4°C), blood pressure is 187/118 mmHg, pulse is 90/min, respirations are 16/min, and oxygen saturation is 100% on room air.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [187.0, 'mm hg'], 'Diastolic Blood Pressure': [118.0, 'mm hg']}",141,133.95,148.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 187.0 mm Hg + 2/3 * 118.0 mm Hg = 141.0 mm Hg.
Hence, the patient's mean arterial pressure is 141.0 mm Hg."
1306,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7229,Extracted,"A 10-year-old boy is brought to the emergency department due to vomiting and weakness. He is attending a summer camp and was on a hike with the other kids and a camp counselor. His friends say that the boy skipped breakfast, and the counselor says he forgot to pack snacks for the kids during the hike. The child’s parents are contacted and report that the child has been completely healthy since birth. They also say there is an uncle who would have to eat regularly or he would have similar symptoms. At the hospital, his heart rate is 90/min, respiratory rate is 17/min, blood pressure is 110/65 mm Hg, and temperature is 37.0°C (98.6°F). Physical examination reveals a visibly lethargic child with slight disorientation to time and place. Mild hepatosplenomegaly is observed but no signs of dehydration are noted.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 65.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1307,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7657,Extracted,"A 40-year-old man presents with problems with his vision. He says he has been experiencing blurred vision and floaters in his left eye for the past few days. He denies any ocular pain, fever, or headaches. Past medical history is significant for HIV infection a few years ago, for which he is noncompliant with his antiretroviral medications and his most recent CD4 count was 100 cells/mm3. His temperature is 36.5°C (97.7°F), the blood pressure is 110/89 mm Hg, the pulse rate is 70/min, and the respiratory rate is 14/min. Ocular exam reveals a decreased vision in the left eye, and a funduscopic examination is shown in the image. The patient is admitted and immediately started on intravenous ganciclovir. A few days after admission he is still complaining of blurry vision and floaters, so he is switched to a different medication.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [89.0, 'mm hg']}",96,91.2,100.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 89.0 mm Hg = 96.0 mm Hg.
Hence, the patient's mean arterial pressure is 96.0 mm Hg."
1308,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3862225-1,Extracted,"A 15-year-old white girl was admitted with abdominal pain and vomiting for 2 days. Two days prior, she was seen by her primary physician for vomiting. She was prescribed intravenous metoclopramide without improvement. She was referred to the pediatric emergency unit for appendicitis suspicion. The girl was febrile with a body temperature of 38 °C. On physical examination, signs of puberty were appropriate for her age (she had menarche at age 14). A mass that was painful on palpation was located in the right lower quadrant. Headache was reported without alterations in level of consciousness, or other neurologic symptoms. Her vital signs were significant with respiratory rate of 24 breaths per minute, oxygen saturation of 96%, heart rate of 120 beats per min indicating tachycardia, and blood pressure of 136/85 mm Hg. Laboratory examination showed normal urea and creatinine, but corrected serum calcium was 14.9 mg/dl (3.70 mmol/l), phosphorus 0.50 mmol/l, LDH 348 U/l, and C-reactive protein level 259 mg/l. Serum parathyroid hormone-intact (PTH-i) level was 10 pg/ml (normal 10–65). Alpha fetoprotein and beta human chorionic gonadotropin were both normal at < 10 IU/ml. Serum CA-125 was 204 (normal, 0–35) U/ml, while serum CA-15-3 was normal. Serum inhibin was not ever checked. Electrocardiograph was normal. Abdominal ultrasonography demonstrated semisolid pelvic mass measuring 125 mm × 105 mm × 65 mm. An abdominal contrast-enhanced computed tomography scan revealed a right ovarian mass with pelvic ascites, without involvement of pelvic structures (). She was referred to intensive care unit for an antihypercalcemic treatment. Isotonic saline hydration was started together with intravenous infusion of pamidronate (1 mg/kg) and furosemide. An isotopic (99 mTc-HMDP-“Osteocis”) bone scanning did not detect bone metastasis.
On the six day after starting the management of hypercalcemia, she underwent a median infraumbilical laparotomy with right salpingo-oophorectomy, omentectomy and drainage of ascites. Her serum calcium remained normal.
The tumor measured 120 mm × 90 mm × 65 mm with soft consistency. Its external surface was smooth and intact. The cut surface was heterogeneous, showing bright yellow nodular areas alternating with hemorrhagic areas and small cystic structures (Fig. 2). The right fallopian tube and the omentum were normal.
Microscopic examination revealed a solid nodular proliferation of medium-sized cells with hypocellular edematous areas, tumor cell necrosis and some pseudofollicular structures. The tumor cells had moderate to large amounts of pale or eosinophilic cytoplasm with focal features of luteinization. The nuclei were round to oval without groove. The cells were mitotically active, averaging 7 mitoses per 10 high power fields (Fig. 3A). Immunohistochemical profile was the following: the tumor cells demonstrated positive reactivity for alpha-inhibin (B) which confirms the histological suspicion of a sex-cord stromal process. The tumor also expressed reactivity to calretinin, estrogen and progesterone receptors, CD56 and smooth muscle actin. The cells were focally positive for cytokeratin KL1. The tumor was negative for TTF1, synaptophysin and chromogranin, pS100, EMA, and CD99.
These morphological and immunohistochemical features were the ones of a juvenile granulosa cell tumor, excluding the hypotheses of a neuroendocrine carcinoma or a clear cell carcinoma of the ovary which are however the most common ovarian tumors associated with hypercalcemia.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [136.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",102,96.9,107.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 136.0 mm Hg + 2/3 * 85.0 mm Hg = 102.0 mm Hg.
Hence, the patient's mean arterial pressure is 102.0 mm Hg."
1309,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3841517-1,Extracted,"A 9-year-old male child weighing 23.5 kg was admitted in December 2012 with complains of vomiting, oliguria, edema face and pallor for 4 days. There was no history of fever, diarrhea and frank hematuria, pain in abdomen, pain in chest, dyspnea, dysuria or joint pain. Child had a history of similar complains in February 2012 when he was admitted in our institute and was diagnosed to have hemolytic uremic syndrome (HUS). He had undergone six sessions of plasma exchanges and alternate day hemodialysis (HD) during his stay in hospital. He was discharged on continuous ambulatory peritoneal dialysis (CAPD) with tablet nifedipine- retard 10 mg twice-a-day, tablet clonidine (0.1 mg) half-tablet twice-a-day and tablet sodium bicarbonate (500 mg) twice-a-day. In May 2012, his CAPD catheter was removed when his urine output was increased to 1.5 L/day and he was maintaining serum creatinine of 0.6 mg/day. He was continued on anti-hypertensive medication and he was on monthly follow-up evaluation.
On examination, child was well-built, well-nourished, intelligent with normal skin texture without any bruises on joints, having a height of 130 cm, upper segment 66 cm, lower segment 64 cm with an arm span of 126 cm without any abnormal phenotypic feature. His pulse was 100 beat/minhaving bilateral symmetry, blood pressure 200/100 mm of Hg in both upper limb in a sitting position and 206/100 mm of Hg in both lower limbs in lying down position. Femoral, popliteal and dorsalis pedis arteries were equally palpable on both sides. There were no parasternal murmurs on auscultation. Respiratory system was normal on examination and fundus examination was normal. On investigation, urine examination showed albumin +2, sugar nil, 30-40 dysmorphic red blood cells/high power field, hemoglobin 13.1 g/dL, platelet-100,000/cm, peripheral smear showed many schistocytes suggestive of hemolysis. Direct Coomb's test was negative. Blood urea was 154 mg/dL, serum creatinine-5.36 mg/dL, lactate dehydrogenase (LDH) 1317 U/L, high-sensitivity C-reactive protein 2.7 μg/mL (reference range 1-3 μg/mL), serum sodium 138 meq/L, serum potassium 4.8 meq/L, serum C3 level 68 mg/dL (reference level 90-207 mg/dL) serum C4 level 30 mg/dL (reference level 17.4-52.4 mg/dL), ultrasound abdomen showed right kidney 8.4 cm × 3.1 cm and left kidney 8.7 cm × 3.1 cm with increased echogenicity without stone or hydronephrosis. Right internal double lumen catheter (DLC) was inserted for management and X-ray chest was taken to confirm the position of DLC, which showed widening of the mediastinum and well-defined soft-tissue opacity in left paratracheal and left paracardiac region and shadow of aortic knob and descending aorta was not visualized. Contour of right cardiac border was normal and catheter tip was in the right atrium. X-ray chest of previous admission was brought out and it was showing normal cardiac shadow []. Transthoracic echocardiography showed normal aortic valve, ascending aorta and cardiac chambers. Doppler of the abdominal aorta and computed tomography with contrast (CT angio) showed dissection of aorta arising distal to the left subclavian artery and extending up to bifurcation of the aorta with a diameter of descending thoracic aorta 4 cm and abdominal aorta 38 mm with central patent lumen of 2.4 cm and intimal flap within with false lumen diameter of 0.4 cm with partial peripheral thrombus in true lumen [Figures and ]. CT angio showed two left renal arteries and one right renal artery of normal caliber without any aortic branch vessel involvement []. As the child is asymptomatic and has type B dissection of the aorta with a diameter of less than 4 cm, he was started on conservative management with beta blocker and other anti-hypertensive medications along with CAPD and other supportive medications on surveillance monitoring. For his relapse of HUS child was given alternate day hemodialysis and five sessions of plasma exchange each of 1L volume when his platelet count reached 320,000/cu mm and LDH 240 U/L. His oliguria persisted to 300 mL/day and serum creatinine remained 4.28 mg/dL. Renal biopsy was performed, which showed acute on chronic HUS []. CAPD catheter was again inserted and peritoneal dialysis cycles were restarted and his anti-hypertensive requirement included tablet atenolol (50 mg/day), tablet minoxidil (2.5 mg twice a day), tablet prazosin (slow release) (5 mg/day), tablet losartan (50 mg twice a day) and he is maintaining blood pressure of 110/70 mm of Hg at the time of discharge. His father was trained to measure blood pressure at home and keeps a record of same and he has been informed about warning symptoms and child is prohibited from weight lifting.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [100.0, 'mm hg'], 'Systolic Blood Pressure': [200.0, 'mm hg']}",133.33333,126.66666,140,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 200.0 mm Hg + 2/3 * 100.0 mm Hg = 133.33333 mm Hg.
Hence, the patient's mean arterial pressure is 133.33333 mm Hg."
1310,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8511279-1,Extracted,"A 41-year-old woman visited with fever and pain in the transplant kidney. She had end-stage renal disease due to unknown cause and underwent peritoneal dialysis for 7 years. The patient was diagnosed with azotemia 14 years ago. During her first visit, both her kidneys presented with decreased size (approximately 7.8 cm) and increased echogenecity, and her serum creatinine level was 397.8 μmol/L. Considering these, we diagnosed her with end-stage renal disease and did not perform renal biopsy to confirm any underlying disease. Before dialysis, we performed autoimmune studies, checking for anti-nuclear antibodies, anti-double-strand DNA antibodies, C3, C4, anti-glomerular basement membrane antibodies, or anti-neutrophil cytoplasmic autoantibodies, but all of them showed no evidence of autoimmune disease. In addition, the patient did not present any symptoms or signs associated with coagulopathies; her bleeding time was 1.3 min (reference range: 1–4 min). Six years ago, she underwent kidney transplantation from a deceased donor. After kidney transplantation, she received 5 mg prednisolone, 4 mg tacrolimus, and 1500 mg mycophenolate mofetil as immunosuppressants and 2.5 mg amlodipine for hypertension. Her tacrolimus trough level remained stable between 6.2 and 8.7 nmol/L. There was no rejection history. Her serum creatine level was 71.6 μmol/L, and renal graft function was normal on outpatient examination.
At 6 years after the transplantation, she visited the hospital, complaining of fever and pain in the grafted kidney. Her blood pressure was 80/50 mmHg, and her body temperature was 39.5 °C. She had direct and rebound tenderness over the grafted kidney. The urine output on the first hospital day was only 100 cc/day. She was admitted to intensive care, and her electrocardiogram showed tachycardia with normal sinus rhythm. On admission, laboratory analysis showed a white blood cell (WBC) count of 1381 × 109/L, hemoglobin level of 134 g/L, platelet count of 90 × 109/L, and C-reactive protein level of 32.0 mg/dL. Her blood urea nitrogen and serum creatinine levels were 10.7 mmol/L and 435.8 μmol/L, respectively. The lactate dehydrogenase level was 607 IU/L (reference range: 150–550 IU/L). Urine microscopy showed 5–10 WBCs/high power field (HPF) and 3–5 red blood cells/HPF. Her tacrolimus level on admission was 6.2 nmol/L. BK virus were determined on admission and the virus titer then was < 100 copies/mL in her urine or whole blood. Her thyroid-stimulating hormone and free T4 levels were 1.66 mIU/L (reference range: 0.34–4.25 mIU/L) and 10.35 pmol/L (reference range: 10.3–21.9 pmol/L), respectively. Her basal adrenocorticotropin and cortisol levels were 3.5 pmol/L (reference range: < 26 pmol/L) and 423.7 nmol/L (reference range: 138–690 nmol/L), respectively. Non-enhanced computed tomography was performed immediately after admission and revealed acute pyelonephritis (APN) (Fig. A). In addition, our center performed a multiplex PCR for her using a nasal swab, which is performed for detecting respiratory virus in patients with a septic condition; the PCR kit detects respiratory viruses, including influenza virus, respiratory syncytial virus, human metapneumovirus, adenovirus, human coronavirus, human enterovirus, human bocavirus, parainfluenza virus, and human rhinovirus []. All viruses were not detected in our case.
Based on clinical and laboratory tests, we used ceftriaxone 2 g per day and inotropics for septic shock and APN. On the first hospital day (HD1), she had oliguria (100 cc/day), and we started emergency hemodialysis. We treated her with IVIG (Liv Gamma; SK Chemical Life Science, South Korea) for septic shock (300 mg/kg/day for 3 days). On HD2, her blood pressure stabilized with use of inotropic agents and fluid therapy, and urine output increased to 400 cc/day. However, on the second day (HD3) of IVIG administration, she abruptly developed gross hematuria and urine output decreased to 100 cc/day. At that time, we performed additional laboratory tests to differentiate the other causes of hematuria. Her platelet counts were normal at 174 × 109/L, and prothrombin time and activated partial thromboplastin time also showed normal values of 10.4 s and 34.1 s, respectively. On peripheral blood smear, microangiopathic hemolytic anemia finding was not seen. The patient underwent continuous electrocardiogram monitoring during IVIG infusion; however, there was no evidence of arrythmia. In addition, on HD 3, further heart problem was evaluated using electrocardiogram and echocardiogram. The electrocardiogram showed normal sinus rhythm without ST-T changes, whereas the echocardiogram revealed left ventricular ejection fraction decreased to 34%, and a borderline enlarged left ventricle. Echocardiogram also showed abnormalities in the basal to upper middle left ventricular regional wall motion, which is more likely to cause stress induced cardiomyopathy than acute coronary syndrome. Her abnormal echocardiographic findings were considered transient, caused by stress induced cardiomyopathy owing to septic shock.
IVIG treatment was terminated at HD4, but oliguria and gross hematuria persisted. We considered a kidney biopsy to evaluate oliguria and hematuria, but could not proceed because her serious condition. The fever was persisted so the antibiotic was changed to meropenem. On HD 4, vancomycin added due to persistent fever following antibiotic change. On HD7, the fever disappeared, but oliguria persisted. LDH levels on HD 9 and 14 increased to 1704 and 1258 IU/L, respectively, compared to 607 IU/L at the time of admission. Blood and urine cultures were repeatedly performed since she was admitted, but no growths were identified in the two specimens. Her first transfusion was performed due to her low hemoglobin level of 76 g/L at HD 22. On HD 14, we performed conventional kidney sonography, which showed thickening of the renal pelvis and urethral wall; it did not show abnormal focal lesions and hydronephrosis. However, on HD 29, we performed doppler ultrasonography to confirm renal infarction and observed a lack of renal parenchymal and hilar vascular flow (Fig. A). We also performed renal biopsy and reveal that renal infarction with diffuse ischemic changes in the glomeruli but no rejection or other pathology (Fig. B). In addition, we performed SV40 staining using the renal biopsy specimen, and the staining results were negative for SV40. The biopsy specimen did not include medium or large vessels, and arteriolopathies, such as hyalinosis in small arteries or arterioles, were not detected within specimens. After discharge, oliguria and azotemia persisted and she is still on hemodialysis. Follow-up echocardiogram after discharge showed normal wall motion and improved left ventricular ejection fraction (71%). Her bleeding time and autoimmune studies were performed again 2 months after discharge. Her bleeding time was 2 min, and autoimmune studies once again showed negative findings. These results also did not show any evidence of coagulopathies or any autoimmune diseases as underlying comorbidities. Contrast enhanced computed tomography showed markedly atrophied transplant kidney after 4 years of renal infarction (Fig. B).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [80.0, 'mm hg'], 'Diastolic Blood Pressure': [50.0, 'mm hg']}",60,57,63,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 80.0 mm Hg + 2/3 * 50.0 mm Hg = 60.0 mm Hg.
Hence, the patient's mean arterial pressure is 60.0 mm Hg."
1311,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6083606-1,Extracted,"A 51-year-old man with no past medical history presented to the emergency room with pressure-like chest pain of two-day duration. He had multiple episodes of pain, and each lasted for around 20 minutes. It was associated with palpitations and exacerbated by physical exertion. He was a former smoker and reportedly quit smoking 20 years back. His blood pressure was 153/95 mmHg, temperature 98.1°F, heart rate 73/min regular, and respiratory rate 18/min. Electrocardiogram (ECG) showed Type 1 Wellens' Biphasic pattern in leads V2 and V3. ().
Three sets of cardiac troponins were normal. Wellens' pattern on ECG is highly specific (89%) for critical left anterior descending artery (LAD) stenosis [, ]. Therefore, the patient was sent for emergent cardiac catheterization. Coronary angiography revealed normal left main, left circumflex, and right coronary artery. However, LAD artery showed moderate myocardial bridging.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [153.0, 'mm hg'], 'Diastolic Blood Pressure': [95.0, 'mm hg']}",114.33333,108.61666,120.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 153.0 mm Hg + 2/3 * 95.0 mm Hg = 114.33333 mm Hg.
Hence, the patient's mean arterial pressure is 114.33333 mm Hg."
1312,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6198549-1,Extracted,"A 34-year-old male presented to our Emergency Department via emergency medical services complaining of palpitations, shortness of breath, and cough with one episode of hemoptysis that started earlier that day. The patient reported that his symptoms rapidly progressed a few hours prior to arrival shortly after smoking crystal methamphetamine. The patient reported chronic methamphetamine use for 10 years, becoming an everyday user 3 years ago. He admitted to occasional polysubstance use that included ketamine, ecstasy, and alcohol, although those were limited to a few times a month. Past medical history was significant for two remote spontaneous pneumothoraces, but the patient stated that his current symptoms felt unrelated. Past surgical history was noncontributory and he denied allergies or taking any prescribed medications. Reviews of systems were positive for myalgias and fatigue. The patient denied any chest pain, chest tightness or abdominal pain.
Initial vital signs include the following: HR: 153 bpm, RR: 20, BP: 115/56 mmHg, Temp (O): 102.1 °F, and SpO2 96% (RA).
The physical exam demonstrated a well-nourished, well-kept male appearing in his stated age in good physical shape. The patient appeared anxious and diaphoretic with dry mucus membranes and labored breathing. The patient was alert and oriented but found to have mild confusion upon detailed questioning. The rest of the neurologic exam was normal and the patient did not display any meningeal signs. Auscultation of the chest revealed rales at the lung bases. Cardiac exam demonstrated a regular, tachycardic rhythm without the presence of obvious murmurs, rubs, or gallops. There was no lower extremity edema present and patient displayed normal muscle tone. The rest of the physical exam was unremarkable.
Upon the patient's initial presentation, orders for initial management were with a normal saline bolus of 2 liters, supplemental oxygen with 2 liters on nasal cannula, broad spectrum antibiotics (piperacillin/tazobactam and vancomycin), antipyretics, and multiple doses of IV lorazepam with the aim of treating his tachycardia with a mixed picture of sepsis, dehydration, and methamphetamine intoxication.
Point-of-care ultrasound (POCUS) of the inferior vena cava (IVC), heart, and lungs was obtained. The IVC diameter measured 1.85 cm (max) in inspiration and 1.71 cm (min) in expiration (Images -, ). Cardiac views demonstrated gross biatrial and biventricular dilation on visual inspection with a severely reduced left ventricular ejection fraction (LVEF) and a small pericardial effusion (Images -, Videos -). Lung ultrasound demonstrated bilateral lung sliding anteriorly and B-lines in bilateral inferolateral lung fields (Images -, Videos -). With the information obtained via US, the decision was made to consult cardiology and to restrict IVF administration by giving the patient 1 liter of normal saline over the course of two hours instead of a 2-liter bolus.
Electrocardiogram (ECG) revealed sinus tachycardia with a normal axis and without ST elevations, PR depressions, or significant T-wave inversions (). Chest X-ray demonstrated a right lower lobe consolidation with evidence of central pulmonary venous congestion and cephalization (). Significant laboratory findings included a WBC count of 21,000 with a neutrophilic predominance of 81%, lactic acid of 1.8 mmol/L, Pro-BNP of 1,741 pg/ml, and Troponin I < 0.04 ng/ml. The rest of the basic blood works including renal function and electrolytes were within normal limits for our institution. Computed tomography (CT) pulmonary angiogram was performed and demonstrated a right lower lobe consolidation and no evidence of pulmonary embolism. Also evident on CT were atrial and ventricular enlargement, central pulmonary venous congestion, and signs of early pulmonary edema (Images -).
The patient was admitted to the ICU and was continued on broad-spectrum antibiotics and a normal saline infusion of 75 ml/hr. On day two, all IV fluids were discontinued and diuresis was employed for decompensated heart failure with developing hypoxia. The patient grew 2/2 positive blood cultures for Streptococcus pneumoniae and was found to be Influenza B positive. Comprehensive 2D Echocardiogram revealed dilated cardiomyopathy with LVEF of 16%, restrictive left ventricular filling pattern, elevated filling pressures with E/e'=30, moderate/severe mitral regurgitation, and severe tricuspid regurgitation.
The patient improved during hospitalization and was discharged on day 9 with a diagnosis of severe sepsis, right lower lobe pneumonia, Streptococcus pneumoniae bacteremia, Influenza B, and Methamphetamine-Associated Cardiomyopathy.
He was discharged on antibiotic therapy and a heart failure regimen consisting of lisinopril and metoprolol.
His cardiac dysfunction improved with drug abstinence and medical therapy. A four-month echocardiogram demonstrated resolution of dilated atrial and ventricular chambers, with improvement of LVEF to 45% and improvement in valvular dysfunction to only trace mitral and tricuspid regurgitation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [115.0, 'mm hg'], 'Diastolic Blood Pressure': [56.0, 'mm hg']}",75.66667,71.88334,79.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 56.0 mm Hg = 75.66667 mm Hg.
Hence, the patient's mean arterial pressure is 75.66667 mm Hg."
1313,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4375664-1,Extracted,"It is the case of a 57-year-old female patient, with dyspnea that progressed to
orthopnea, paroxysmal nocturnal dyspnea and lower extremity edema for two months. She
had been diagnosed with rheumatic valvulopathy for seven years, permanent AF with no
anticoagulation; she was a smoker. In the physical examination, she presented with good
general status, 44 bpm heart rate, 150 x 80 mmHg blood pressure, cardiac auscultation
with hyperphonetic sound, second normophonetic sound, presence of opening snap close to
second sound, rumbling 2+/6+ diastolic murmur in the mitral area and pulmonary
auscultation with fine crepitation in both bases. The electrocardiogram presented AF
rhythm. The thoracic x-ray showed bilateral pulmonary congestion and increased
cardiothoracic index. The transthoracic echocardiogram showed mitral valve with
commissural fusion, thickened cusps and reduced valve opening, mean LA-LV diastolic
gradient of 4 mmHg and maximum of 16 mmHg, with valve area of 1.2 cm2, which
is compatible with moderate rheumatic compromise. A 51 mm LA and the presence of
hyperechoic image from the left atrial roof to its lateral wall were described,
measuring 65 x 54 mm ( and ). There was also severe pulmonary arterial
hypertension (SPAP 66 mmHg) and important increase in the left chambers, eccentric
hypertrophy and left ventricular systolic dysfunction (35% ejection fraction), with
diffuse hypokinesis.
The patient was submitted to cardiac catheterization, which excluded obstructive
coronary lesions and showed the presence of extensive vascularization of the atrial
mass, with irrigation originated from the left () and right () coronaries.
Cardiac nuclear magnetic resonance showed important LA increase, with thickened walls
and image compatible with large thrombus adhered to its walls (roof, floor and lateral
wall), besides positive parietal diffuse enhancement, compatible with hypertrophy and
atrial fibrosis, probably associated with MS. However, in the interface between the
thrombus and the lateral LA wall, there was a positive perfusion, so it was not possible
to prevent other expansive processes in the atrial wall. The late left ventricular
enhancement was negative.
By considering the presence of an image in the LA in a patient with moderate MS and no
anticoagulation for AF, there was the hypothesis of a giant thrombus. Due to the
progression of the symptoms, size of thrombus and risk of embolism or mechanical
obstruction of the mitral valve, the surgical treatment was chosen.
The patient was submitted to surgery, therefore, the mass that presented red coloration,
with soft and friable consistency was removed, which confirmed the diagnosis of left
atrial giant thrombus and impairment of the entire LA posterior wall, weighing 80 g
( and ). Anterior and posterior commissurotomy was conducted in the mitral valve.
The postoperative transthoracic echocardiogram showed mitral valve with mean LA-LV
diastolic gradient of 4 mmHg and maximum diastolic gradient of 12 mmHg, and also a 1.6
cm2 valvular area. There was still systolic dysfunction (EF 42%) resulting
from diffuse hypokinesis. The patient evolved well in the postoperative period and
received asymptomatic hospital discharge, on warfarin anticoagulant.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 80.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
1314,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7380,Extracted,"An 8-year-old African American girl is brought to the clinic by her mother for her regular blood exchange. They come in every 2–3 months for the procedure. The child is in good health with no symptoms. Her last trip to the emergency department was 6 months ago due to bone pain. She was treated with morphine and oxygen and a blood transfusion. She takes hydroxyurea and a multivitamin with iron every day. She has an uncle that also has to get blood exchanges. Today, her heart rate is 90/min, respiratory rate is 17/min, blood pressure is 110/65 mm Hg, and temperature is 37.0°C (98.6°F). She calmly waits for the machine to be set up and catheters inserted into both of her arms. She watches a movie as her blood is slowly replaced with 6 L of red blood cells.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 65.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1315,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-11386,Extracted,"A 34-year-old female comes to the ED complaining of epigastric pain and intractable nausea and vomiting for the last 24 hours. Her vitals are as follows: Temperature 38.1 C, HR 97 beats/minute, BP 90/63 mm Hg, RR 12 breaths/minute. Arterial blood gas and labs are drawn.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [63.0, 'mm hg'], 'Systolic Blood Pressure': [90.0, 'mm hg']}",72,68.4,75.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 63.0 mm Hg = 72.0 mm Hg.
Hence, the patient's mean arterial pressure is 72.0 mm Hg."
1316,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7255555-1,Extracted,"An 85-year-old male with a medical history pertinent for atrial flutter on coumadin and hypertension developed new onset of shortness of breath. At baseline he could ambulate without issues but was getting short of breath walking 150 feet. He also endorsed paroxysmal nocturnal dyspnea and orthopnea. His symptoms began a week before he was admitted to the hospital. He first went to this cardiologist who did an outpatient echocardiogram that showed severe systolic heart failure with an ejection fraction of 30%, a moderate mitral regurgitation, and a dilated left ventricle. He was referred to the hospital for a nuclear stress test. However, as his shortness of breath was worsening he instead went to the ED where he was found to be in atrial flutter with rapid ventricular response (RVR) with a heart rate of 130 in a 2:1 AV block. On presentation, vital signs were as follows: blood pressure 120/80 mmHg, heart rate 130 beats per minute (bpm), pulse ox 96% on two liters nasal cannula, respiratory rate 18, and temperature 99.8°F orally. It was thought that his newly diagnosed congestive heart failure (CHF) was tachycardia induced. In the ED his electrocardiogram (EKG) showed atrial flutter with RVR and no acute ST changes, and his troponins were mildly elevated, peaking at 0.07. He was admitted in the hospital and started on IV cardizem infusion per protocol and the patient was given a loading dose of oral amiodarone. On physical exam, the patient had jugular venous distension, normal sinus rhythm with systolic murmur, mild crackles bilaterally on auscultation of his lungs, a distended abdomen with dullness to percussion, and positive shifting fluid wave without palpable hepatosplenomegaly. He had trace lower extremity edema bilaterally and no changes on neurological exam. Laboratory investigation revealed (Table ) hyponatremia of 130 mmol/L, glomerular filtration rate (GFR) >60, mildly elevated liver function tests (LFTs) with aspartate aminotransferase (AST) of 48 iU/L and normal alanine aminotransferase (ALT) of 42 iU/L. Complete blood count (CBC) was pertinent for mild leukocytosis of 13.5 K/uL and microcytic anemia with a hemoglobin of 11.8 g/dL, which was around his baseline. He was found to have coumadin coagulopathy with an INR of 7.74. Of note, brain natriuretic peptide (BNP) was 863 on admission. His coumadin was held and he was given oral 5 mg vitamin K. Chest X-ray showed bilateral pleural effusions and some vascular congestion. He was initially watched with telemonitoring on the medical floors. He received Lasix IV after which his shortness of breath resolved, and he no longer appeared to be in CHF exacerbation. On his first day after admission his LFTs were within normal limits (AST/ALT 33/40). His second day of admission, after he had received a total of three doses of 800 mg of oral amiodarone, he began to have transaminitis, with AST/ALT of 3842/1665. He was also found to have acute renal failure with a GFR of 24. INR continued to be elevated at 8.7 and he was given another dose of oral 5 mg vitamin K. At that point, the patient was started on a N-acetylcysteine drip and transferred to the medical intensive care unit (MICU) for close monitoring. At that time, his oral amiodarone was discontinued and work-up was sent to evaluate the etiology of his fulminant hepatic failure. Gastroenterology and nephrology were consulted. Per nephrology, he was given some IV hydration due to the possibility of his acute renal failure being of pre-renal etiology. Eosinophils in the urine and blood were negative. Hepatitis panel, anti-nuclear antibodies (ANA), c-peptide, anti-double-stranded DNA, and immunoglobulin G (IgG) to glomerular basement membrane were within normal limits. Total complement level was low at 35 (normal 60-144 units). LFTs continued to rise to a maximum of AST/ALT 11675/4960 iU/L (Table ).
Within three days of discontinuing amiodarone, the patient’s liver function and renal function started to improve. Etiologies considered for the patient’s fulminant liver failure included viral hepatitis, acetaminophen toxicity, salicylate toxicity, ischemia, CHF exacerbation, Wilson’s disease, and autoimmune hepatitis. Work-up, as detailed above, for all these etiologies came back negative. Due to the timing of the patient’s fulminant liver failure, it was discussed and agreed upon by the medical, gastrointestinal, and nephrology team that the patient’s acute liver failure was most likely due to the three doses of oral amiodarone he received. His LFTs continued to downtrend and he was eventually discharged to rehab.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1317,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-10467,Extracted,"A 34-year-old female presents to the emergency room with headache and palpitations. She is sweating profusely and appears tremulous on exam. Vital signs are as follows: HR 120, BP 190/110, RR 18, O2 99% on room air, and Temp 37C. Urinary metanephrines and catechols are positive.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [110.0, 'mm hg'], 'Systolic Blood Pressure': [190.0, 'mm hg']}",136.66667,129.83334,143.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 190.0 mm Hg + 2/3 * 110.0 mm Hg = 136.66667 mm Hg.
Hence, the patient's mean arterial pressure is 136.66667 mm Hg."
1318,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7746028-1,Extracted,"The patient was a 58 year-old male with a history of hypertension, hyperlipidemia and diabetes, who initially presented to our emergency department complaining of a fever, diarrhea and fatigue. According to the patient, these symptoms had been ongoing for the past 5 days. The patient also had a non-productive cough. The patient denied any chest pain, heart palpitations, shortness of breath, syncope, dizziness, or abdominal pain. The patient denied any previous syncopal episodes or any previous cardiac history including dysrhythmias, previous myocardial infarctions, coronary artery disease, or congestive heart failure. The patient denied any family history of early cardiac deaths or family history of heart disease. Review of the patient’s current medications at the time included atorvastatin, lisinopril-hydrochlorothiazide, and metformin.
The patient was febrile on presentation with a temperature of 39.5° C. He was tachycardic with a heart rate of 110. Patient was hemodynamically stable with a blood pressure of 108/67mmHg. Crackles were heard at the bases of his lungs bilaterally. The remaining physical exam was unremarkable.
Initially there was concern for sepsis, given his history of fever for five days and diarrhea. An infectious/metabolic workup was performed, as our initial differential diagnosis included pulmonary disease (atelectasis, bronchitis, pneumonia, tuberculosis, empyema, pulmonary embolism), urinary tract infection, bacteremia, gastroenteritis, and viral syndrome. Also, as the patient was complaining of fatigue and had cardiac risk factors, it was important to expand our differential to rule out cardiac causes such as myocardial infarction, myocarditis, and life-threatening dysrthymias. A complete blood count, electrolyte panel, troponin, EKG, chest x-ray, and blood cultures were obtained. Of note, the patient had an elevated lactic acid of 3.8 mmol/l, a sodium of 128 mmol/l and a white blood cell count of 29.2 k/mm. The remaining laboratory studies were unremarkable and within normal physiologic limits, including his potassium, calcium and troponin. Surprisingly, the patient’s EKG demonstrated a type 1 Brugada pattern (Figure 1). This was a new finding, as his previous EKG had shown an incomplete right bundle branch block (Figure 2). Cardiology was consulted and it was recommended an echocardiogram and a computed tomography (CT) angiogram of the chest be obtained in order to rule out a right ventricular infarct and pulmonary embolism, respectively. Echocardiogram showed a left ventricular ejection fraction of 70% with trace mitral and tricuspid regurgitation. There was no evidence of valvular pathology, hypokinesis, or thrombus. CT angiogram of the chest demonstrated a large opacity in the left lower lobe, and infiltrates in the right upper, middle and lower lobes consistent with pneumonia. There was no evidence of pulmonary embolism. The patient was started on ceftriaxone and azithromycin and admitted to the hospital for further evaluation and treatment for community-acquired pneumonia. The patient was discharged from the hospital four days later. He was started on aspirin and metoprolol per recommendations by cardiology and was instructed to follow up with them in their office two weeks later.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [108.0, 'mm hg'], 'Diastolic Blood Pressure': [67.0, 'mm hg']}",80.66667,76.63334,84.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 108.0 mm Hg + 2/3 * 67.0 mm Hg = 80.66667 mm Hg.
Hence, the patient's mean arterial pressure is 80.66667 mm Hg."
1319,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1378,Extracted,"A 29-year-old African-American woman, gravida 4, para 0, comes to the physician for evaluation of recurrent abortions. Each pregnancy resulted in spontaneous abortion in the second trimester. The patient has a history of joint pain, chronic migraines, and recurrent poorly defined, macular skin rashes. She also reports episodes in which her fingers become pale and cold, and then redden. She is sexually active with her husband and does not use contraceptives. The patient works as a landscape architect. Her mother has a history of endometriosis. The patient takes a daily prenatal multivitamin and occasionally sumatriptan. She appears tired. Temperature is 36.5°C (97.7°F), pulse is 65/min, and blood pressure is 110/65 mm Hg. Examination of the hands shows two ulcerations on the tip of the right index finger and multiple tiny hemorrhages under the nails. There is a purple reticular rash on both calves.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [65.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 65.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1320,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4236451-1,Extracted,"A 46-year-old Chinese male with a history of hypertension presented with sudden syncope and came to his senses after ten minutes without headache. His respiratory rate was 21 breaths per min and the lungs were clear on auscultation. Cardiac examination revealed a grade II/6 diastolic murmur at the parasternal border. The pulse rate was 75 beats per min with normal sinus rhythm. The blood pressure was 109/76 mmHg in the left arm and 112/62 mmHg in the right arm. No remarkable abnormal was found in abdominal examination. Coagulation tests were normal. Arterial gas analysis on 3 L/min oxygen inspiration was pH 7.39, PaCO2 39.8 mmHg, PaO2 62.5 mmHg, SaO2 91.1%. A chest x-ray revealed widening of the mediastinum, a cardiothoracic ratio of 60%, and normal lung fields. Echocardiography revealed ascending aortic dissection and moderate aortic regurgitation with small to moderate pericardial effusion. Computed tomography scanning revealed ascending aortic to aortic arch dissecting aneurysm, in which the proximal part of right brachiocephalic trunk was also influenced. The left and right pulmonary arteries were normally enhanced with contrast medium. The patient underwent emergency operation for the thoracic aortic dissection, including Bentall procedure, interposition graft replacement of aortic arch, stented descending aorta with a shunt from a chamber around the aortic root to the right atrium. The patient was successfully weaned off bypass and transferred to the intensive care unit. The ratio of PaO2 to FiO2 after operation was 300. The haemodynamics was stable. However, the ratio of PaO2 to FiO2 fell to 150 gradually after operation. Two days after operation, the patient was conscious and cooperative, and his lung compliance and airway resistance were normal. But severe hypoxaemia ensued. In order to find out the cause of hypoxaemia, a chest computer temography was carried out but no evidence of atelectasis or pneumonia was shown. Pulmanary arteriography showed that an entire right lung field was defected without an extrinsic compression, which indicated embolism of the right pulmonary artery (Figure ). Considering the stable haemodynamics and the danger of haemorrhage, embolectomy and thrombolytic therapy were not applied in the patient. We took the anticoagulant therapy with low molecular weight heparin and warfarin, which sustained INR at 2-3. Pulmanary arteriography was reexamined every 3-4 day. The images indicated that thrombus gradually dissolved (Figure ). And the patient’s hypoxemia was improved. According to the effectiveness of treatment, we made sure that the entire right lung field defect in pulmanary arteriography was due to thromboembolism. Unfortunately, ventilator-associated pneumonia (VAP) occurred. Therefore, the tracheotomy tube was extubated until one month after operation. He survived for one year after discharging from the hospital without complications related to lung and heart.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [112.0, 'mm hg'], 'Diastolic Blood Pressure': [76.0, 'mm hg']}",88,83.6,92.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 112.0 mm Hg + 2/3 * 76.0 mm Hg = 88.0 mm Hg.
Hence, the patient's mean arterial pressure is 88.0 mm Hg."
1321,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6389028-1,Extracted,"A 31-year-old female presented to the emergency department (ED) in January 2017 with complaints of sharp epigastric pain radiating to the back associated with nausea and diarrhea. Past medical history was significant for cholecystectomy in 2010, depression, and IBS-D. She did not have a family history of pancreatitis. She did not consume alcohol or tobacco. Her medications included eluxadoline, bupropion, and oral contraceptive pills. Vital signs included blood pressure 123/78 mm Hg, heart rate 110 beats/minute, sinus tachycardia on telemetry, respiratory rate 18/minute, and oxygen saturation was 100% on room air. On examination, no jaundice or pallor was noted. The patient had epigastric tenderness without rebound. No organomegaly was noted.
She had presented with similar complaints three weeks ago to the ED when she was diagnosed with acute pancreatitis due to epigastric pain and a lipase level of 1067 U/L by Atlanta criteria at that time. There was no abnormality on computed tomography (CT) scan of the abdomen. After stabilization in hospital, she was discharged home with symptomatic management with analgesics, anti-emetics and a plan to advance diet as tolerated. Her symptoms had resolved except for vague abdominal discomfort after meals that was characteristic of her IBS-D.
Further history revealed that the patient was started on eluxadoline 75 mg BID for IBS-D three weeks before the first episode of pancreatitis. This was the reduced dose, recommended for patients without a gallbladder. Lipase level before starting the drug was 31 U/L. During this admission, her lipase level was found to be 1374 U/L. Triglyceride level was 128 mg/dl. Magnetic resonance cholangiopancreatography (MRCP) showed a normal ductal anatomy and absence of stones or tumors. The IgG4 level was normal. Lipase level decreased to 157 U/L within two days of stopping the eluxadoline. Liver function tests and blood counts were normal on both occasions. She was discharged home in a stable condition once her symptoms improved.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [123.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",93,88.35,97.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 123.0 mm Hg + 2/3 * 78.0 mm Hg = 93.0 mm Hg.
Hence, the patient's mean arterial pressure is 93.0 mm Hg."
1322,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7495169-1,Extracted,"A 60-year-old male with a history of hemochromatosis status postorthotopic liver transplant (on immunosuppression), type 2 diabetes, chronic kidney disease (baseline creatinine 1.4), and prior right common femoral deep venous thrombosis presented with non-ST-elevation myocardial infarction (NSTEMI) at an outside institution. The patient underwent coronary angiography at the outside institution and was placed on dual antiplatelet therapy. No information regarding contrast type and premedications prior to coronary angiography was available. Given liver transplant status and persistent elevations in troponin, the patient was transferred to our institution for a higher level of care. One day after coronary angiography at the outside institution, the patient underwent repeat angiography and percutaneous coronary intervention (PCI) at our institution. No premedications were administered prior to the procedure. The patient had no history of any allergies and had a baseline Cr of 1.4. Angiogram was performed with 165 ml of iodixanol 320 mg/ml (Visipaque), an iodine-containing nonionic radiocontrast agent, over a 60 min interval. The procedure was performed under conscious sedation without any manipulation of the mouth or throat. Four hours following the procedure, the patient presented with painless swelling of the floor of mouth (FOM), and otolaryngology was consulted. At the time, the patient also denied any dyspnea, dysphonia, or neck pain.
On examination, the patient was afebrile, with a pulse of 93 beats/min, blood pressure of 106/69 mm/Hg, and a respiratory rate of 20 breaths per minute. Painless swelling of the FOM consistent with swollen sublingual glands was present without any evidence of mucopurulent drainage or fluctuance (). The rest of the physical exam was unremarkable.
Differential diagnosis included allergic etiologies (angioedema), sialadenitis, acute infection (e.g. Ludwig's), and contrast-induced sialadenitis. Given history of recent contrast exposure, localized bilateral swelling, and no acute signs of infection, patient's presentation was most consistent with CIS involving the sublingual glands. The patient was administered with diphenhydramine perorally for treatment.
Overnight, the patient became febrile and septic with increasing oxygen requirements likely secondary to cardiac etiology versus pneumonia. Physical exam revealed decreased swelling of the sublingual glands. Blood cultures and labs were remarkable for elevated creatinine (2.4) consistent with acute kidney injury (AKI). Etiology of shock remained unclear but was thought to be an infectious source. Broad spectrum antibiotics were prophylactically started on the patient given immunosuppressed status. The CT of the neck and chest without contrast was also obtained by the primary team to rule out any occult deep neck space infection given immunosuppressed status. CT neck and chest was unremarkable, with no evidence of masses, infectious processes, or airway compromise. No enlargement of either the parotids or the submandibular gland was noted on imaging (Figures and ). While no sublingual swelling was visualized, the CT was performed 36 hours after contrast insult and without contrast. Subsequent physical exams revealed decreased swelling until full resolution at 3 days (Figures and ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [106.0, 'mm hg'], 'Diastolic Blood Pressure': [69.0, 'mm hg']}",81.33333,77.26666,85.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 106.0 mm Hg + 2/3 * 69.0 mm Hg = 81.33333 mm Hg.
Hence, the patient's mean arterial pressure is 81.33333 mm Hg."
1323,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8450616-1,Extracted,"A 70-year-old man (170 cm, 48 kg, American Society of Anaesthesiologists status IV) had a history of HFrEF with dilated cardiomyopathy, diabetes mellitus, and chronic obstructive pulmonary disease. He was scheduled to undergo debridement of skin necrosis in the right leg. He had developed right leg weakness 4 months previously and was diagnosed with thrombotic occlusion of the right ilio-femoral artery. Skin necrosis appeared on the anterolateral side of the lower leg (). While being treated for the skin lesion, his HF was treated with spironolactone, ivabradine, sacubitril/valsartan, and warfarin (1.5 mg) to optimise cardiopulmonary function. He had also received an implanted defibrillator 3 months previously.
Despite inotropic administration, the patient’s systolic and diastolic blood pressure was 70 and 40 mmHg, respectively. His coagulation profile showed that the activated prothrombin time was 49.4 s and the prothrombin time/international normalised ratio was 1.63. However, anticoagulation therapy was continued because of the high risk of thromboembolism. The initial BNP level was 837 pg/mL, which decreased to 216 pg/mL just before surgery after treating the HF. Chest radiography showed pneumonic infiltration in the right lung (mainly in the right lower lobe) and diffuse emphysematous changes in both lungs (). Preoperative transthoracic echocardiography revealed global hypokinesia with severe left ventricular dysfunction, an ejection fraction of 11%, an enlarged left atrium and ventricular chamber, and grade II diastolic dysfunction.
Regional anaesthesia was considered safer than general anaesthesia because of the patient’s unstable cardiopulmonary function, but a neuraxial block was contraindicated owing to anticoagulation therapy. Therefore, we used a USG sciatic nerve and fascia iliaca compartment block to cover the operative field and avoid haemodynamic instability. However, the scheduled operation was postponed because the patient strongly requested only general anaesthesia and refused regional anaesthesia using a PNB. He had previously undergone wound dressing changes with local anaesthesia, and suffered from excruciating pain. Because of this previous experience, he was afraid that he might feel severe pain during the operation because of failure of the nerve block. Several counselling sessions were held to provide sufficient information to the patient, along with emotional support to overcome his fear and optimise the anaesthesia.
Standard monitoring, including non-invasive blood pressure monitoring, three-lead electrocardiography, and pulse oximetry, were applied before the nerve block, and the left brachial artery was cannulated for continuous blood pressure monitoring. Supplemental oxygen was administered through a facial mask at 5 L/minute. The patient was positioned laterally for the popliteal sciatic nerve block. A high-frequency linear transducer (HFL38x®; SonoSite, Bothell, WA, USA) was transversely placed on the posterior aspect of the popliteal fossa, and the sciatic nerve was located. Under real-time ultrasound (M-Turbo®; SonoSite) guidance, a 25 G needle was inserted 5 cm from the popliteal crease using the in-plane approach. Once the needle tip was near the distal sciatic nerve, 40 mL of 0.375% ropivacaine was injected around the sciatic nerve after confirming negative blood aspiration. Subsequently, the patient was placed in the supine position for the fascia iliaca compartment block. Using the same ultrasound transducer, the fascia lata and fascia iliaca were checked. A 20-mL aliquot of 0.25% ropivacaine was injected into the plane between the fascia iliaca and iliopsoas muscles after checking for negative aspiration (). A loss of sensation was confirmed in the surgical area after 30 minutes. The surgery commenced after confirming adequate sensory block. During the operation, the patient did not require any analgesics or rescue block, and haemodynamic parameters were stable. The patient was transferred to the intensive care unit after surgery for close monitoring because of his severely compromised cardiopulmonary function. Haemodynamic stability was confirmed and he was transferred to the general ward the next day. Thereafter, the patient underwent wound debridement twice more and finally received a skin autograft at the defect site. All of these surgical procedures were successfully performed using the same PNB techniques. After the skin graft, the patient was discharged from the hospital without any symptoms, such as dyspnoea or surgical site pain.
The reporting of this study conforms to the CARE guidelines.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [70.0, 'mm hg'], 'Diastolic Blood Pressure': [40.0, 'mm hg']}",50,47.5,52.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 70.0 mm Hg + 2/3 * 40.0 mm Hg = 50.0 mm Hg.
Hence, the patient's mean arterial pressure is 50.0 mm Hg."
1324,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8318172-1,Extracted,"An 82-year-old woman, with a body weight of 57 kg, with a medical history of treated arterial hypertension, was admitted to our intensive care unit (ICU) with the diagnosis of septic shock. First physical examination found a heart rate at 124/min and blood pressure at 80/45 mmHg without response after 1-L crystalloid fluid expansion. The patient had a polypnea at 28 cycles/min without other respiratory distress sign. The abdomen was tense and painful to the palpation. First laboratory blood test showed a hyperlactatemia-related metabolic acidosis with a pH at 7.21, a PCO2 at 24 mmHg, a bicarbonate level at 14 mmoL/L, and a lactate level at 9 mmoL/L. Abdomen and pelvis computed tomography (CT) scan with injection of contrast material showed a voluminous liver abscess [, Panel A], consistent with the diagnosis of liver abscess-associated septic shock. Rapidly, the patient developed respiratory and hemodynamic failure with the need of mechanical ventilation, and continuous norepinephrine infusion up to 8 mg/h. An empiric broad-spectrum antimicrobial therapy consisting of piperacillin/tazobactam 4 g fourth a day and one injection of 8 mg/k of gentamicin (480 mg) was administrated for up to 3 weeks. The patient underwent an emergency laparotomy surgery for microbiological sampling and drainage of the liver abscess. In the early postoperative course, the patient demonstrated crepitation of the thoracic and cervical region consistent with the diagnosis of SE. A second CT scan confirmed the presence of massive SE extending from the abdomen to the head associated with a pneumoperitoneum [, Panels B to D]. Of note, SE was found neither during the first physical examination at ICU admission nor on the first CT scan. There were no arguments, for upper airway injuries or pneumothorax. Because of the pneumoperitoneum, an early surgical complication was suspected; thus, the patient underwent a second emergency laparotomy which revealed a perforated lesion of the transverse colon. Five centimeters of colon was removed, and a colostomy was carried out. Unfortunately, despite surgery, the patient passed away few days later due to multiorgan failure.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [45.0, 'mm hg'], 'Systolic Blood Pressure': [80.0, 'mm hg']}",56.66667,53.83334,59.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 80.0 mm Hg + 2/3 * 45.0 mm Hg = 56.66667 mm Hg.
Hence, the patient's mean arterial pressure is 56.66667 mm Hg."
1325,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7683,Extracted,"A 40-year-old man presents with acute abdominal pain. Past medical history is significant for hepatitis C, complicated by multiple recent visits with associated ascites. His temperature is 38.3°C (100.9°F), heart rate is 115/min, blood pressure is 88/48 mm Hg, and respiratory rate is 16/min. On physical examination, the patient is alert and in moderate discomfort. Cardiopulmonary examination is unremarkable. Abdominal examination reveals distant bowel sounds on auscultation. There is also mild diffuse abdominal tenderness to palpation with guarding present. The remainder of the physical examination is unremarkable. A paracentesis is performed. Laboratory results are significant for the following:
Leukocyte count 11,630/µL (with 94% neutrophils)
Platelets 24,000/µL
Hematocrit 29%
Ascitic fluid analysis:
Cell count  658 PMNs/µL
 Total protein 1.2 g/dL
 Glucose 24 mg/dL
Gram stain  Gram-negative rods
Culture Culture yields growth of E.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [88.0, 'mm hg'], 'Diastolic Blood Pressure': [48.0, 'mm hg']}",61.33333,58.26666,64.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 88.0 mm Hg + 2/3 * 48.0 mm Hg = 61.33333 mm Hg.
Hence, the patient's mean arterial pressure is 61.33333 mm Hg."
1326,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7507882-1,Extracted,"A 56-year-old man presented with an abnormal tingling sensation around the right side corner of the mouth, and in the hand, foot and lateral thoracic region (). He had a history of dyslipidemia and anxiety disorder, for which he was taking simvastatin and escitalopram. His body temperature was 36.7°C, his pulse was 90 bpm, and his blood pressure was 128/86 mmHg. Neurologic examination revealed that the patient was alert, his cranial nerves were intact, his motor power was grade V in all extremities, and his deep tendon reflexes were normal. Objective sensory deficit was not seen. We suspected COPS with additional thorax involvement. COPS is usually due to a lesion in the thalamocortical projections or thalamus and brainstem. The differential diagnosis of COPS in this patient included lacunar infarction because he had a risk factor for dyslipidemia, hemorrhagic stroke or cerebral vascular malformations such as CMs, and arteriovenous malformations were also possible differential diagnosis.
Brain magnetic resonance imaging (MRI) showed a well-defined lesion in the left side of the dorsal pons, measuring 1.2 × 1.1 cm and showing T1 hyperintensity without enhancement, T2 hyperintensity with a hemosiderin rim and surrounding edema, and an associated blooming susceptibility artifact on susceptibility weighted imaging (SWI), and was diagnosed with a bleeding CM (). Because his symptoms did not disturb his quality of life and the lesion was located in the deep pons, where the morbidity associated with the intervention is high. Observation was considered and gabapentin was prescribed at 300 mg/day. His sensory symptom was gradually decreased, and he had only mild tingling sensation with no additional symptoms after the 16-week follow-up period.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [86.0, 'mm hg'], 'Systolic Blood Pressure': [128.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 128.0 mm Hg + 2/3 * 86.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1327,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5965174-1,Extracted,"A 14-year-old female patient presented to the ED with intermittent lower abdominal pain for three weeks. Her pain was bilateral and cramping, with episodes of intense worsening that were associated with non-bloody, non-bilious emesis. She reported abdominal distension, constipation, and breast tenderness, and denied urinary changes, vaginal bleeding, or discharge. She had not yet experienced menarche and she denied sexual activity. The patient had seen her pediatrician at symptom onset, and it was documented that the patient had Tanner Stage IV development but no menstruation. No genitourinary exam had been performed. At that visit, the patient was diagnosed with constipation and counseled on diet changes. Two weeks later, the patient returned to her pediatrician for the same symptoms, and an outpatient transabdominal US was ordered to evaluate her pelvic organs. Her pain worsened prior to her scheduled US, so she presented to the ED.
The patient was afebrile with a pulse of 105 beats per minute, blood pressure of 125/91 mmHg, respiratory rate of 18 breaths per minute, and oxygen saturation of 100%. She was actively vomiting and reporting abdominal pain. Abdominal examination was notable for mild distension, suprapubic tenderness, and a palpable mass in the lower abdomen and pelvis. Bowel sounds were normal. Pelvic examination was notable for a bulging, tense, blue, imperforate hymen. Transabdominal POCUS showed a distended vaginal canal, markedly enlarged uterus, and moderate hydronephrosis bilaterally (). Renal function was normal on a chemistry panel. She was diagnosed with hematometrocolpos, and gynecology was consulted. The patient was taken to the operating room for hymenectomy, which drained 900 mL of dark brown fluid. She recovered without complication and had normal menstruation one month later.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [91.0, 'mm hg'], 'Systolic Blood Pressure': [125.0, 'mm hg']}",102.33333,97.21666,107.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 91.0 mm Hg = 102.33333 mm Hg.
Hence, the patient's mean arterial pressure is 102.33333 mm Hg."
1328,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8324358-1,Extracted,"A 51-year-old male on chronic TPN for short bowel syndrome after a colectomy was admitted for sepsis and acute kidney injury. He reported a month-long history of generalized fatigue, intermittent low-grade fevers, chills, night sweats, and unintentional weight loss. On presentation, he was febrile (101.6°F), tachycardiac (HR 106 bpm), but hemodynamically stable (BP: 130/86 mm Hg) and saturating well (96%) on room air. Physical examination revealed no erythema or tenderness at the site of his peripherally inserted central catheter (PICC), through which he had been receiving TPN. No significant cardiac murmurs or sequelae of infective endocarditis were observed, and the remainder of physical examination was benign as well. Admission laboratory workup revealed a white cell count of 12,000/mm3, elevated ESR: 99 mm/hr, CRP: 139 mg/L, and creatinine: 3.56 mg/dL (baseline: 0.9 mg/dL). Urinalysis and chest X-ray were unremarkable for infection, and standard blood cultures displayed no growth of microorganisms. Electrocardiography (EKG) showed normal sinus rhythm without any conduction system abnormalities. Broad-spectrum antibacterial coverage with vancomycin and piperacillin-tazobactam was initiated, while micafungin was added with suspicion of fungemia given the history of TPN. Extended blood cultures from admission showed growth of Candida glabrata (C. glabrata) and Candida dubliniensis (C. dubliniensis); both species were sensitive to amphotericin-B (minimum inhibitory concentration: 0.2 mcg/ml) and micafungin (minimum inhibitory concentration: 0.12 mcg/ml). The PICC was subsequently removed; cultures from the catheter tip also grew C. glabrata and C. dubliniensis. A transthoracic echocardiogram (TTE) showed an echogenic large mobile right atrial mass (4 cm × 6 cm × 2.5 cm), extending from the superior vena cava into the right atrium and prolapsing into the right ventricle and right ventricular outflow tract. There was no evidence of outflow tract obstruction. These findings were concerning for an intracardiac fungal mass versus a large thrombus. Transesophageal echocardiogram (TEE) revealed similar lesions, with an additional aortic valve vegetation (1 cm × 0.5 cm) (Figures –). EKGs remained unremarkable, and ophthalmologic exam was not concerning for endophthalmitis. A computed tomography (CT) scan of the chest showed diffuse nodular opacities in the lungs bilaterally, concerning for septic emboli. Cardiothoracic surgery was consulted for surgical intervention for the intracardiac mass. However, due to the patient's significant comorbidities and extensive size of the lesion, he was deemed a poor surgical candidate. He was, thus, treated conservatively with micafungin for 8 weeks. Following acute antifungal therapy and given the need for ongoing chronic TPN, he was started on lifelong suppressive therapy with fluconazole after sepsis resolved. Three months later, a repeat TTE showed complete resolution of the intracardiac mass without evidence of persistent vegetations, thus confirming the fungal origin of the mass ().",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [86.0, 'mm hg']}",100.66667,95.63334,105.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 86.0 mm Hg = 100.66667 mm Hg.
Hence, the patient's mean arterial pressure is 100.66667 mm Hg."
1329,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8117474-1,Extracted,"A 74-year-old man, with no relevant comorbidities, presented to the emergency department with respiratory failure. For 7 days he had been suffering from fatigue, loss of appetite, coughing and progressive shortness of breath. At presentation he was confused, although there was no loss of orientation in space and time. He had no history of smoking or drug abuse. At admission, the patient was not suffering from chest pain.
Physical examination showed a man clearly short of breath with a respiratory rate of 51/min and an oxygen saturation (SO2) of 84% on room air. On a 15 L/min non-rebreathing mask (NRM) he improved to 100% SO2. He had a blood pressure of 137/78 mm Hg with a pulse of 139 beats per minute. His temperature was 36.3°C. Auscultation revealed bilateral fine crackles. Inspection and palpation of the skin did not reveal any subcutaneous crackling bubbles at that time. Also, there was no swelling of the neck.
Bilateral patchy infiltrates were seen on his X-ray of the chest. There was no sign of a pneumomediastinum or subcutaneous emphysema at that time (). The patient’s C-reactive protein (CRP) was elevated at 245 mg/L (0–5 mg/L), as well as an elevated procalcitonin of 0.55 µg/L (0–0.50 µg/L). The polymerase chain reaction analysis for COVID-19 was positive.
The patient was started on dexamethasone 6 mg and prophylactic dalteparin 5000EH. Additionally, he received supplemental oxygen via HFNC (Optiflow) with settings flow 40 L and FiO2 60%, which resulted in a respiratory rate of 28/min and an oxygen saturation of 96%.
On day 4, there was an increase in shortness of breath. The current settings of the HFNC were flow 40 L and FiO2 70%; the FiO2 was raised over the previous days due to a persistently high respiratory rate and an oxygen saturation <94%. Another X-ray of the chest was made, and D-dimer was determined to find a cause for the increase in shortness of breath.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [137.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",97.66667,92.78334,102.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 137.0 mm Hg + 2/3 * 78.0 mm Hg = 97.66667 mm Hg.
Hence, the patient's mean arterial pressure is 97.66667 mm Hg."
1330,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6075485-1,Extracted,"A 26-year-old female presented to a Level I trauma center after a motorcycle crash in which she was the unhelmeted passenger thrown from the vehicle. The patient did lose consciousness and was noted to be briefly confused on scene. Her right shoulder had a palpable deformity and she had difficulty moving the right upper extremity, but she denied other symptoms and was transported to our facility via ground emergency medical services. Upon arrival, the patient was in no distress, alert and oriented, and reported only pain in the right shoulder.
Initial vital signs were temperature of 36.7° Celsius, heart rate 107 beats per minute, blood pressure 102/57 mmHg, respiratory rate 18 breaths per minute, and 100% oxygen saturation on room air. She was evaluated by standard trauma protocol. Computed tomography (CT) imaging of the head, cervical spine, and chest/abdomen/pelvis were significant only for a right anterior shoulder dislocation. The patient was treated symptomatically and preparations were made to perform procedural sedation to reduce the shoulder dislocation. Prior to sedation, the patient developed an abrupt change in mental status. Her right pupil became fixed and dilated. She became aphasic, and her right side became flaccid. The patient was immediately intubated based on Glasgow Coma Scale (GCS) of 7 and rapid deterioration of her clinical status.
A repeat CT head was obtained and revealed a hyperdense left middle cerebral artery (MCA). Neurosurgery and neurology were both immediately consulted. CT angiography (CTA) of the head and neck revealed a left internal carotid dissection with tandem embolus to the proximal left MCA. A tandem occlusion is defined by injury that results in cervical carotid artery dissection, as well as embolic occlusion of a large intracranial artery. This type of vascular occlusion typically does not respond well to thrombolysis. Given the confirmed presence of a tandem occlusion in our patient, a discussion regarding the utility of thrombolytics was held. Neurosurgery opted to perform endovascular mechanical thrombectomy and stenting of the internal carotid artery. Diagnostic cerebral angiogram revealed complete revascularization of the distal left MCA territory. The patient was subsequently admitted to the intensive care unit. There, her course was uncomplicated, and by discharge on hospital day 18 the patient had regained a significant amount of independent function.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [102.0, 'mm hg'], 'Diastolic Blood Pressure': [57.0, 'mm hg']}",72,68.4,75.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 102.0 mm Hg + 2/3 * 57.0 mm Hg = 72.0 mm Hg.
Hence, the patient's mean arterial pressure is 72.0 mm Hg."
1331,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1096,Extracted,"A 17-year-old girl comes to the emergency department because of a 6-day history of gradual onset abdominal pain, fever, vomiting, and decreased appetite. Her pain started as dull and diffuse over the abdomen but has progressed to a sharp pain on her right side. She has taken ibuprofen twice daily since the onset of symptoms, which has provided moderate pain relief. She has no history of serious illness. She is sexually active with one male partner and uses condoms consistently. She appears stable. Her temperature is 38.2°C (100.8°F), pulse is 88/min, respirations are 18/min, and blood pressure is 125/75 mm Hg. The abdomen is soft. There is tenderness to palpation of the right lower quadrant. Laboratory studies show:
Leukocyte count 16,500/mm3
Serum
Na+ 135
K+ 3.5
Cl- 94
HCO3- 24
Urea nitrogen 16
Creatinine 1.1
β-hCG negative
Urine
WBC 3/hpf
RBC < 3/hpf
Nitrite negative
Leukocyte esterase negative
CT scan of the abdomen shows a small (3-cm) fluid collection with an enhancing wall surrounded by bowel loops in the right pelvis. The patient is placed on bowel rest and started on IV fluids and antibiotics.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",91.66667,87.08334,96.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 75.0 mm Hg = 91.66667 mm Hg.
Hence, the patient's mean arterial pressure is 91.66667 mm Hg."
1332,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4471381-1,Extracted,"A 64-year-old man was admitted to our clinic with a 2-week history of nausea and vomiting. His past medical history included diabetes mellitus type 2 and hypertension controlled on metformin and irbesartan. He had no history of any renal disease. On physical examination the patient's blood pressure, pulse rate, respiratory rate, and body temperature were 110/70 mm Hg, 96 beats/minute, 14 breaths/minute, and 37°C, respectively. His physical examination also revealed splenomegaly with no evidence of hepatomegaly and lymphadenopathy. The fundus examination was normal. There were no other abnormal findings. Initial laboratory data showed the following values: leukocyte count was 18.6 × 109/L (lymphocytes %65), hemoglobin 78 g/L, thrombocytes 265 × 109/L, blood urea nitrogen 48 mg/dL, serum creatinine 2.2 mg/dL (estimated GFR: 38 mL/min/1.73 m2), sodium 137 mEq/L, potassium 3.2 mEq/L, lactate dehydrogenase 378 U/L, uric acid 4.5 mg/dL, albumin 3.7 g/dL, gamma globulin level 2.5 g/dL, and erythrocyte sedimentation rate 51 mm/h. Serology was negative for antinuclear antibody, antineutrophil cytoplasmic antibody (ANCA), antiglomerular basement membrane antibody, HBsAg, and anti-HCV. Serum complement (C3 and C4) levels were normal and cryoglobulin was negative. Both monoclonal immunoglobulin levels and free light chain analysis for kappa and lambda in serum and urine were normal. Urine analysis showed only mild proteinuria (24 h protein excretion was 100 mg) without dysmorphic cells or casts. Blood smear revealed mild mature lymphocytosis. Sinus rhythm was observed on electrocardiogram. An abdominal ultrasonography (USG) revealed normal kidney size. A bone marrow biopsy was consistent with CLL and these monoclonal B lymphocytes were determined by means of immunological markers: CD5, CD20, CD23, and CD79 (Figures and ). The cause of the ARF was not apparent despite numerous investigations. A fine needle aspiration of the kidney was performed, and it was suggestive of diffuse leukaemic infiltration of the renal parenchyma (). Immunohistochemistry showed these cells were positive for CD20, CD5, and CD79 (). There was no evidence of amyloid and light chain deposition. Morphological and immunohistochemical findings supported a diagnosis of ARF due to leukaemic infiltration of the kidneys in CLL. The patient was started on a combination of cyclophosphamide (50 mg/day) and methylprednisolone (48 mg/day). The followed parameters on admission and during treatment were compiled in . The patient completely recovered from renal dysfunction a month after the initiation of therapy.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1333,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8091778-1,Extracted,"A 72-year-old Japanese woman on medications for hypertension, obesity, and diabetes mellitus, was referred to our hospital with abnormal uterine bleeding. She was previously diagnosed with abnormal endometrial cytology at a previous clinic and visited our hospital for further examination and treatment. Endometrial biopsy revealed an adenocarcinoma (G2), while pelvic magnetic resonance imaging revealed a lesion mass of size 60 × 66 × 53 mm in the right side of the uterus (Fig. ), which was suspected to invade the serosal side. An enlarged lymph node measuring 18 mm was also found in the lymph node clusters in the right internal iliac artery and the obturator lymph node. Therefore, hysterectomy, bilateral adnexectomy, pelvic lymph node dissection, and para-aortic lymph node dissection were performed. A pathological examination using surgical specimen revealed endometrial serous carcinoma (Fig. ). Finally, she was diagnosed with stage III C2 endometrial cancer.
On the 6th postoperative day (POD), the patient developed abdominal bloating and nausea. Abdominal radiography revealed that the stomach and the intestine were markedly dilated with gas and air-fluid levels, indicating paralytic ileus (Fig. ). Thus, the patient was initiated on fasting and fluid replacement therapy, following which she recovered completely within 4 days. On the 27th POD, the patient received the first cycle of combination chemotherapy consisting of paclitaxel (175 mg/m2; 3-h infusion) and carboplatin (at a dose corresponding to an area under the curve [AUC] of 5 mg/mL/min).
On day 5 of chemotherapy, the patient developed a fever (38.6 °C), diarrhea, and fatigue. Her pulse rate, respiratory rate, and blood pressure were 120 beats/min, 20 breaths/min, and 88/52 mmHg, respectively. Blood examination revealed a white blood cell count, neutrophil count, and C-reactive protein (CRP) level of 270/μL, 40/μL, and 17.92 mg/dL, respectively, which were suggestive of the systemic inflammatory response syndrome including febrile neutropenia (FN) and sepsis. Therefore, an antibiotic therapy and granulocyte-colony stimulating factor therapy were initiated immediately. However, her condition worsened the next day. The body temperature, pulse rate, respiratory rate, blood pressure, white blood cell count, neutrophil count, and CRP level were 40.2 °C, 150 beats/min, 49 breaths/min, 63/42 mmHg, 150/μL, 0/μL, and 41.5 mg/dL, respectively.
Because she suffered from septic shock and DIC, she was shifted to the intensive care unit (ICU). Computed tomography (CT) of the abdomen and pelvis revealed remarkable intestinal dilation and thickening of the intestinal wall. Therefore, we considered enteritis as the origin of inflammation (Fig. ). Furthermore, we speculated that the patient’s condition was associated with toxicity due to bacterial translocation. However, no bacteria were detected in the blood and intestinal fluid. In addition to the treatment for septic shock and DIC, a long ileus tube was inserted into the stomach through the nasal cavity because she experienced a constant high-pressure feeling in the intestine and because we had to suction the extra air and fluid. Favorable outcomes were achieved, including reduced edema in the intestinal colon, improved circulation in the involved intestine, and correction of the intestinal kinking. Her condition gradually improved, and the neutrophil count and immune function improved from the 4th day of ICU admission. She was discharged alive and well from the ICU after 18 days (Fig. ). The patient’s clinical course is shown in Fig. . Written informed consent was obtained from the patient for participating in all procedures, and this work was approved by the Institutional Review Board of the Shimane University (IRB No-20200110-1).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [52.0, 'mm hg'], 'Systolic Blood Pressure': [88.0, 'mm hg']}",64,60.8,67.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 88.0 mm Hg + 2/3 * 52.0 mm Hg = 64.0 mm Hg.
Hence, the patient's mean arterial pressure is 64.0 mm Hg."
1334,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5949,Extracted,"A 72-year-old man presents to the emergency department after a fall. The patient was found lying down on the floor in his room in his retirement community. The patient has a past medical history of Alzheimer dementia and a prosthetic valve. His current medications include donepezil and warfarin. His temperature is 97.7°F (36.5°C), blood pressure is 85/50 mmHg, pulse is 160/min, respirations are 13/min, and oxygen saturation is 97% on room air. That patient is started on IV fluids and a type and screen is performed. Laboratory values are ordered as seen below.

Hemoglobin: 13 g/dL
Hematocrit: 39%
Leukocyte count: 5,500 cells/mm^3 with normal differential
Platelet count: 225,000/mm^3

INR: 2.5
AST: 10 U/L
ALT: 12 U/L

A chest radiograph and EKG are performed and are within normal limits. A full physical exam is within normal limits. The patient’s vitals are repeated. His temperature is 99.5°F (37.5°C), blood pressure is 110/70 mmHg, pulse is 90/min, respirations are 10/min, and oxygen saturation is 98% on room air.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [50.0, 'mm hg'], 'Systolic Blood Pressure': [85.0, 'mm hg']}",61.66667,58.58334,64.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 85.0 mm Hg + 2/3 * 50.0 mm Hg = 61.66667 mm Hg.
Hence, the patient's mean arterial pressure is 61.66667 mm Hg."
1335,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4415179-1,Extracted,"A 13-year-old boy without any known chronic illness was admitted to our outpatient policlinic with complaints of fatigue, fever, sputum expectoration, vomiting, loss of appetite, and acute attacks of choking cough especially at night. The complaints had not decreased over the last 20 days despite the patient using different types of antibiotics. His general physical appearance was pale and exhausted. He had subfebrile fever of 37.5℃ and blood pressure of 110/70 mmHg. Physical examination revealed bilaterally reduced pulmonary sounds at the mid and lower zones with bilateral crepitations which were heard more in the right lung. Abdominal examination was normal without hepatosplenomegaly. Laboratory findings showed leukocyte of 38,470/mm3(consisted of 92% neutrophil, 4.2% lymphocyte, 2.1% monocyte, and 1.5% eosinophil), hemoglobin of 14.3 g/dL, platelet of 437,000/µL and C-reactive protein of 120 mg/dL. Posteroanterior chest x-ray showed extensive infiltration in the mid and lower zones of the right lung with a round-shaped air-filled lesion (). Thoracic ultrasonography confirmed the presence of bronchogram in the lower zone of the right lung as a pneumonic consolidation. The possibility of abscess was excluded. Ampicillin/sulbactam in combination with amikasin was started. On the third day of treatment, the patient developed a confused state of mind together with tachypnea (60 times per minute), dyspnea, tachycardia (130 beats per minute), hypoxemia (oxygen saturation <90% under nasal oxygen flow at the rate of 6 L/min), and hypotension (75/40 mmHg). The patient was transferred to the pediatric intensive care unit. Considering possible shock status due to staphylococcal pneumonia, an aggressive intravenous fluid regimen and a change in antibiotic treatment to vancomycin and meropenem were started. Respiratory distress did not improve despite intensive application of inhaled β2 mimetic, inhaled corticosteroid and intravenous corticosteroid. The patient's immunity showed resistance to medical therapy and was clinically unstable. Since our hospital was lacking high-resolution computed tomography facility, the high resolution computed tomography (HRCT) examination could not be performed emergently.
In this case, HRCT examination was performed after stabilization of the patient, it showed a lobulated, 9 cm × 7 cm × 7-cm lesion with cavitation in the superior segment of the lower lobe of the right lung indicating a ruptured hydatid cyst (). The diagnosis of anaphylaxis due to ruptured hydatid cyst was confirmed. Medical history also showed that the patient had experienced expectoration of cystic fluid together with an acute attack of severe cough just 30 minutes before the onset of shock status. A repeated hemogram test showed hemoglobin level of 12.4 g/dL, platelet of 276,000/µL, and leukocyte of 28,440/mm3. The peripheric blood film showed an eosinophilic ratio of 45%. The diagnosis of echinococcal infection was supported with positive indirect hemagglutination (IHA) and immunofluorescence antibody technique (IFAT) results of 1/640 and 1/1,000 respectively. The patient was given albendazole with an oral dose of 15 mg/kg/day twice a day. A cystectomy and capitonage operation was performed in the patient and a postoperative chest x-ray showed sufficient expansion of the lungs (). In the follow-up, abdominal ultrasonography and chest x-rays were normal without any other pathology. The patient was discharged with albendazole treatment and a further follow-up plan was made.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1336,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2881009-1,Extracted,"A 25-year-old Caucasian female with a history of type 1 neurofibromatosis was brought to our hospital with diffuse abdominal pain, nausea, vomiting and fever following cesarean section for fetal distress. She was transferred to our institution within 18 hours of the onset of symptoms for surgical intervention in view of the ominous findings on computed tomography (CT) scan and endoscopy done at the peripheral hospital. She had not passed flatus or stool since surgery and denied hemetemesis, melena, shortness of breath, or chest pain. There was no history of tobacco or alcohol abuse, ingestion of corrosive substances or non-steroidal anti inflammatory drugs (NSAIDs).
Our patient appeared acutely ill and toxic. She had a temperature of 38.8°C, pulse of 120/min, blood pressure of 154/90 mmHg, respiratory rate of 24/min, and oxygen saturation of 97% on 2 L of oxygen. The cardiac and respiratory exams were otherwise unremarkable. Her abdomen was markedly distended. There was diffuse tenderness on palpation of the abdomen with no peritoneal signs. The cesarean section incision appeared clean with no tenderness or discharge. Bowel sounds were absent on auscultation. There were multiple neurofibromas on our patient's neck and anterior chest consistent with her diagnosis of neurofibromatosis. Her white blood cell count was 25,000/mm3, with 91% neutrophils. The initial electrolytes, amylase, lipase and liver function tests were within normal limits.
CT scan of our patient's abdomen showed marked gastric dilation and air in the wall of the stomach along the entire greater curvature and portal venous system (Figures and ). There was marked dilatation of the small and large bowel. Esophagogastroduodenoscopy (EGD) of our patient showed areas of diffuse mucosal congestion and extreme pallor as well as ulceration on the posterior wall and greater curvature of the stomach. Gastric biopsy revealed transmural necrosis. Streptococcus viridans was isolated from gastric biopsy. Blood cultures did not grow any pathogenic bacteria and nasogastric cultures were not obtained.
Our patient was diagnosed with emphysematous gastritis and promptly started on intravenous clindamycin and piperacillin/tazobactam, nasogastric decompression and intravenous hydration. Total parenteral nutrition was initiated from day two and our patient was closely monitored in the intensive care unit for three days. She improved with the above measures and tube feedings were initiated from day seven. Follow-up CT scan on day eight showed resolution of the gastric and portal venous air (Figure ). Our patient was finally discharged home on oral proton pump inhibitors on day 10. A follow-up EGD two months later showed no sequelae and our patient remained asymptomatic.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [154.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",111.33333,105.76666,116.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 154.0 mm Hg + 2/3 * 90.0 mm Hg = 111.33333 mm Hg.
Hence, the patient's mean arterial pressure is 111.33333 mm Hg."
1337,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4300147-1,Extracted,"A 53-year-old gentleman presented to the emergency department complaining of a sudden right-sided abdominal pain for one day prior to admission. He also had general fatigue, myalgia, and weight loss of 10 pounds over a period of several months. His past medical history was significant for a mechanical aortic valve that had been replaced 2 years prior to hospital admission. The patient had been compliant with his warfarin; however, his presenting international normalized ratio (INR) level was 6.4.
Physical examination on admission revealed a blood pressure of 154/74, borderline bradycardia, and tachypnea. He had a mechanical S2, a 3/6 systolic ejection murmur at the apex radiating to the axilla, and a 1/4 diastolic murmur at the left lower sternal border. Other than severe tenderness in the right lower quadrant, the rest of his physical examination was essentially benign. Of note, the patient did not have any rashes, subconjunctival hemorrhage, Janeway lesions, or Roth spots.
Pertinent laboratory data revealed hemoglobin of 7.9 gm/dL and white blood cell count of 19.8 K/mcL. Computed tomography (CT) scan of the abdomen without contrast showed a large right perirenal hemorrhage extending caudally through the retroperitoneum to the right inguinal canal with evidence of active hemorrhage. Urology and general surgery evaluated the patient and were both suspecting underlying renal malignancy because visualization was obstructed from the active hemorrhage.
Cardiology was consulted because the patient had atrioventricular dissociation on his initial electrocardiogram (). The patient was started on antibiotics and blood cultures were drawn because he met criteria for systemic inflammatory response syndrome (SIRS). The blood cultures grew Streptococcus viridans in six of the six bottles. With the patient's history of mechanical aortic valve, presumed embolic phenomenon with the renal hemorrhage, leukocytosis, and new third degree heart block the suspicion for endocarditis with periaortic abscess was high. Therefore, transthoracic echocardiogram (TTE) was performed which showed a mass that was present in the left ventricular outflow tract and transesophageal echocardiogram (TEE) was recommended for better visualization. The patient had worsening tachypnea and his oxygen requirements were increasing requiring the patient to be prophylactically intubated in anticipation of the fact that he would require surgical intervention in the near future. TEE was then performed and revealed a bileaflet mechanical aortic valve with perivalvular abscess and valvular vegetation as well as severe eccentric paravalvular aortic regurgitation (Figures and ).
The patient's surgery was scheduled but not performed until the patient had negative blood cultures with antibiotic therapy because he was relatively hemodynamically stable on the ventilator. After sterilization the patient underwent a successful redo-median sternotomy, aortic root reconstruction, and aortic valve replacement.
Postoperatively, the patient remained in complete heart block but permanent pacemaker placement was withheld until completion of several more days of antibiotic therapy could be performed. After complete sterilization, permanent pacemaker placement was performed and he tolerated the procedure well with no major postoperative complications. He was later discharged home and continues to do well.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [154.0, 'mm hg'], 'Diastolic Blood Pressure': [74.0, 'mm hg']}",100.66667,95.63334,105.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 154.0 mm Hg + 2/3 * 74.0 mm Hg = 100.66667 mm Hg.
Hence, the patient's mean arterial pressure is 100.66667 mm Hg."
1338,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3035195-1,Extracted,"We report the case of a 22-year-old Caucasian man with a 10-year history of Crohn's disease. He had recently undergone a small bowel resection and ileocecal anastomosis. On his fourth post-operative day, he experienced a breakdown of his anastomosis and underwent surgical repair. He had no other medical co-morbidities and was not being treated with immunosuppressive agents. On post-operative day three, he developed symptoms of lightheadedness, headache, and blurred vision that progressed to visual loss. An emergent ophthalmology evaluation revealed poor visual acuity (he was only able to count fingers at 3 inches bilaterally) but no fundoscopic or ocular abnormality. His neurologic examination was otherwise unremarkable. Shortly thereafter, he developed a tonic-clonic seizure that abated spontaneously after approximately one minute. His blood pressure throughout the episode was 150-160/80-90 mmHg, up from a baseline of 100-130/70-80 mmHg. His serial electrolytes (including calcium), arterial blood gas, cardiac enzymes, urine analysis, and electrocardiogram were within normal limits. A head computed tomography (CT) scan demonstrated subtle, ill-defined regions of low attenuation involving his bilateral posterior temporo-occipital lobes (Figure ). A head magnetic resonance imaging (MRI) scan confirmed patchy T2 hyperintensities in his bilateral temporo-occipital subcortical white matter, consistent with vasogenic edema (Figure ). There were no diffusion weighted imaging (DWI) or apparent diffusion coefficient (ADC) signal abnormalities to suggest an acute infarction. Given our clinical and classical radiological findings, he was diagnosed with PRES.
His symptoms and the imaging findings resolved with an aggressive blood pressure control. A subsequent ocular examination showed him to have a visual acuity of 20/40 OD and 20/30 OS. A follow-up MRI was performed three days after his symptoms had resolved. This MRI showed the complete resolution of his bilateral temporo-occipital subcortical white matter T2 signal abnormalities. He continued to do well at his two-year follow-up examination.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [8090.0, 'mm hg'], 'Systolic Blood Pressure': [150160.0, 'mm hg']}",55446.66667,52674.33334,58219,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150160.0 mm Hg + 2/3 * 8090.0 mm Hg = 55446.66667 mm Hg.
Hence, the patient's mean arterial pressure is 55446.66667 mm Hg."
1339,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7134,Extracted,"A 3-year-old boy presents with episodic diarrhea with malodorous stools, stunted growth, occasional abdominal cramps, and an itchy rash. His mother says that these symptoms developed approximately 2 years ago. The patient was exclusively breastfed up to the age of 7 months. Supplementary feeding was started with non-starchy vegetable followed by starchy vegetables, meat, fish, eggs, and bread. Bread and cookies were the last product to be introduced at the age of 12 months. The patient’s mother tried to withdraw dairy products from the patient’s diet because she heard that lactose can cause such symptoms, but it did not help. The patient’s vital signs include: blood pressure 90/55 mm Hg, heart rate 101/min, respiratory rate 19/min, and temperature 36.3℃ (97.3℉). His weight is 11 kg (24.2 lb, -2 SD) and height is 90 cm (2 ft 11 in, -1 SD). On physical examination, the patient’s skin is pale with a papulovesicular rash on his abdomen and back. There are a few aphthous ulcers in the oral cavity. The abdomen is distended but no tenderness to palpation. No hepatosplenomegaly. An immunological assay is performed and shows positive anti-transglutaminase and anti-endomysial antibodies.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [55.0, 'mm hg']}",66.66667,63.33334,70,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 55.0 mm Hg = 66.66667 mm Hg.
Hence, the patient's mean arterial pressure is 66.66667 mm Hg."
1340,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-11848,Extracted,"A 55-year-old man presents to his primary care provider with increased urinary frequency. Over the past 3 months, he has been urinating 2-3 times more often than usual. He has started to feel dehydrated and has increased his water intake to compensate. He works as a bank teller. He has a 25-pack-year smoking history and drinks 8-10 beers per week. His temperature is 98°F (36.8°C), blood pressure is 114/68 mmHg, pulse is 100/min, and respirations are 18/min. Capillary refill is 3 seconds. His mucous membranes appear dry. The patient is instructed to hold all water intake. Urine specific gravity is 1.002 after 12 hours of water deprivation. The patient is given desmopressin but his urine specific gravity remains relatively unchanged.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [68.0, 'mm hg'], 'Systolic Blood Pressure': [114.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 114.0 mm Hg + 2/3 * 68.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1341,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7338997-1,Extracted,"A 28-year-old female, non-smoker and non-alcohol drinker, was transferred from a hospital to our institution’s emergency department by an ambulance for severe, acute abdominal pain. The pain was diffuse and progressively worsening over the past few days. It was associated with nausea and one episode of non-bilious, non-bloody emesis. She denied changes in her bowel movements, fever and chills.
The patient’s past medical, surgical and family history were non-contributory, except for a history of episodic, recurrent, vague abdominal pain that occurred every few months over the past few years prior to presentation and was responsive to analgesics. The patient was not taking medications nor using illicit drugs.
On physical examination, the patient was in acute distress, screaming in pain. She had a heart rate (HR) of 126 beats per minute (bpm) and a blood pressure of 107/85. Her abdomen was diffusely tender to palpation, tense and distended.
The patient’s blood work was pertinent for metabolic and lactic acidosis: pH 7.29, bicarbonate 15 mEq L−1, and lactic acid 3.69 mmol L−1. A computed tomography (CT) scan of her abdomen and pelvis was done at a peripheral hospital 3 h prior to presentation and was reviewed by our team. It showed right-to-left inversion of superior mesenteric artery (SMA) and vein, as well as swirling intestines, consistent with malrotation and midgut volvulus (). Due to the patient’s unstable condition, we forfeited further investigations, based our judgement on the CT imaging done at the previous hospital and brought in by the patient, and rushed her for operative exploration after obtaining the patient’s consent.
Under general anesthesia, exploratory laparotomy was done by an attending general surgeon and a chief resident with 5 years of specialized training. It revealed bluish discoloration of the small bowels with areas that were significantly dark (). The mesentery was twisted, resulting in secondary ischemia (). The bowels and mesentery were untwined, which caused the intestines to resume their healthy color and peristalsis. However, a length of about 40 cm remained borderline-ischemic, marked with punctate hemorrhage, yet peristaltic with positive Doppler signal. Thus, we preferred to have a second look in 24 h.
Meanwhile, the veins along the ascending and transverse mesocolon were noted to be tortuous. We avoided ligating these tortuous veins in case they were serving as an alternate drainage for the small bowel, which instead would cause congestion and worsening of small bowel ischemia. Ladd's bands were then excised, and the abdomen was closed with Bogota bag after irrigating it with warm water.
Postoperatively, the patient was transferred to the surgical intensive care unit (SICU), where she received vasopressors and antibiotics. Her laboratory workup showed leukocytosis (WBC 11600, 85%) and persistent metabolic and lactic acidosis (HCO3− 14, lactic acid 4.7 mmol L−1). Six hours postoperatively, the patient developed decreased urinary output, worsening abdominal exam and exacerbated lactic acidosis (lactic acid 7.13 mmol L−1). Tissue reperfusion injury or necrosis of the borderline segment of the small intestines were suspected, therefore, the patient underwent emergent re-exploration.
Intraoperatively, the small intestine that showed borderline viability in the first surgery, looked viable, except for a 20 cm stretch whose viability was still questionable. The majority of the bowel resumed Its viable color, peristalsis and had palpable mesenteric pulses (). Another laparotomy was planned in 48 h.
Over the next 48 h, the patient was hemodynamically stable, and her laboratory workup normalized. In the last laparotomy, all the bowels were viable without signs of persistent ischemia. Ladd procedure was completed; small bowel mesentery was further broadened; its serosa was fixed to the retroperitoneum and the appendix was removed. The abdominal wall edges could not be fully approximated; thus, the defect was closed using 30 × 30 cm Vicryl mesh. Finally, an abdominal binder was applied postoperatively. The remaining hospital stay was noneventful; the patient was discharged home 5 days later.
The patient was initially followed-up clinically every few weeks, then every 6 months for a total of 18 months. Patient has been doing well, tolerating diet and gaining weight. She has developed, however, a small, reducible midline incisional hernia with minimal discomfort, despite adhering to the abdominal binder and avoiding heavy lifting for 6 months as we recommended. Nevertheless, the patient has been satisfied with the outcome.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [107.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",92.33333,87.71666,96.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 107.0 mm Hg + 2/3 * 85.0 mm Hg = 92.33333 mm Hg.
Hence, the patient's mean arterial pressure is 92.33333 mm Hg."
1342,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3893488-1,Extracted,"A 23-year old male with ESRD secondary to IgA nephropathy was brought to home hospital for generalized seizure activity. He was known to have poor compliance with his intermittent peritoneal dialysis (PD), administer four times per day, and had apparently missed his last two treatments. He did not have a recent peritoneal equilibrium test. On arrival to the hospital he was found to have a blood pressure exceeding 182/107 mmHg and was described as being combative and confused. Labetalol 20 mg IV, lorazepam 1 mg IV, and haloperidol 1 mg IV were administered by a nurse practitioner before being transferred to the nearest tertiary care centre. Collateral history obtained suggested that the patient was complaining of headache and blurred vision hours prior to seizing.
Other past medical history was significant for hypertension secondary to renovascular disease, as well as being a carrier of methicillin-resistant staphylococcus aureus. His medications included atenolol, amlodipine, ramipril, hydroxyzine, scheduled clonidine, erythropoetin, calcium, and Replivite tablets. There was no family history of epilepsy. Social history was significant for tobacco smoking and previous recreational cocaine use.
Examination at the tertiary centre revealed a temperature of 36.8°C and a still elevated blood pressure of 200/100 mmHg. Heart rate was recorded at 63 beats per minute and oxygen saturation was 98% on room air. General examination revealed a rousable individual who appeared somewhat confused, but was alert to person and place. The remaining neurological exam, including language assessment and fundoscopy, was normal. There was no meningismus. Cardiovascular exam was significant for a loud S2 heart sound, but no cardiac rubs or murmurs were appreciated. Respiratory and abdominal exams were non-contributory.
Admission blood work revealed a urea of 41 mmol/L, a serum creatinine of 1531 μmol/L, a WBC of 11.4, and hemoglobin of 99. Serum sodium was slightly low at 129 mol/L, and potassium was elevated at 6.3 mmol/L. Calcium was low at 1.93 mmol/L, phosphate was elevated at 3.57 mmol/L, and magnesium was 1.24 mmol/L. Liver enzymes were generally unremarkable. An EKG revealed tall peaked T-waves consistent with hyperkalemia. A CT-head showed multiple cortical and subcortical hypodensities involving the posterior parasagittal portions of both parietal lobes and the medial right occipital lobe, which was reported as being suggestive of PRES. A lumbar puncture for CSF analysis to rule out meningoencephalitis was not performed as the patient was afebrile with no signs of meningeal irritation.
The patient was admitted to hospital for further work-up and management. The hyperkalemia was medically treated. Phenytoin was initiated to prevent further seizures. An MRI brain was obtained and showed multiple regions of cortical and subcortical increased T2 signal, predominantly involving the posterior and paramedian parietal and occipital lobes with relative symmetry (Figure A). There was no diffusion restriction. On the third day after admission the patient began to have episodes of headache and blurred vision associated with increased blood pressure, despite achieving good volume control through in-hospital PD and increasing his antihypertensive regimen. These episodes continued, and thus on the fifth day after admission he was transferred to the intensive care unit to receive continuous blood pressure monitoring and control through an intravenous labetalol infusion. Blood pressure was decreased to 160/80 mmHg and he was transitioned back to oral antihypertensive medication. He was subsequently discharged from hospital and follow-up MRI brain three months later showed complete resolution of previously noted findings (Figure B).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [107.0, 'mm hg'], 'Systolic Blood Pressure': [200.0, 'mm hg']}",138,131.1,144.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 200.0 mm Hg + 2/3 * 107.0 mm Hg = 138.0 mm Hg.
Hence, the patient's mean arterial pressure is 138.0 mm Hg."
1343,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1410,Extracted,"A 58-year-old woman comes to the physician for a routine follow-up examination. She has a history of type 2 diabetes mellitus, hypertension, and asthma. Last year, she received laser photocoagulation for proliferative retinopathy. Her current medications include metformin, lisinopril, and an albuterol inhaler. Her mother died of complications from diabetes. She drinks 1 glass of wine daily with dinner and does not smoke. Her temperature is 37.2°C (99°F), pulse is 92/min, respirations are 14/min, and blood pressure is 152/98 mm Hg. Cardiopulmonary examination is unremarkable. There is decreased sensation to monofilament testing of the plantar surfaces of both feet.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [152.0, 'mm hg'], 'Diastolic Blood Pressure': [98.0, 'mm hg']}",116,110.2,121.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 152.0 mm Hg + 2/3 * 98.0 mm Hg = 116.0 mm Hg.
Hence, the patient's mean arterial pressure is 116.0 mm Hg."
1344,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5510979-1,Extracted,"A 33-year-old African-American male with past medical history significant for intravenous drug abuse presented to the emergency department (ED) with the chief complaint of bilateral eyelid swelling and loss of vision in the right eye for one day.
The patient had been seen two days prior in the ED when he had presented with right retro-orbital pain. Computed tomographic (CT) scan of the head was obtained that showed no acute intracranial process. He was treated as having cluster headache with prochlorperazine, diphenhydramine, ketorolac, and oxygen and was subsequently discharged. The very next day, the patient began to develop progressively increasing bilateral eyelid swelling, severe retro-orbital headache with subjective chills and fever. He also developed dysphagia and odynophagia, prompting him to return to the ED.
On arrival, the patient appeared sick and in distress. He had a temperature of 102.2°F, heart rate of 110 per minute, respiratory rate of 18 per minute and blood pressure of 109/69 mmHg. On examination, there was bilateral eyelid edema and swelling. He had conjunctival chemosis and bilateral proptosis. Right pupil was non-reactive to light, had complete ophthalmoplegia with visual acuity 20/400. Left pupil was reactive to light, had lateral rectus palsy with visual acuity of 20/30. There was no murmur on the cardiovascular exam and no peripheral stigmata of infective endocarditis. Oropharyngeal, respiratory and abdominal examinations were also unremarkable.
The initial complete blood count revealed a leukocytosis 19700/cmm with a left shift. The CT scan of the face was then obtained that showed bilateral proptosis with stranding of the surrounding fat concerning for orbital cellulitis. The radiology team also expressed concern about a retropharyngeal fluid collection. Blood cultures were obtained and the patient was immediately started on vancomycin and ampicillin/sulbactam. Infectious disease, otolaryngology (ENT) and ophthalmology consultation were requested. The patient underwent urgent magnetic resonance imaging (MRI) of the brain, orbits and soft tissues of the neck which showed extensive bilateral orbital cellulitis and proptosis (Figure ), enhancement of the leptomeninges concerning for basilar meningitis and retropharyngeal abscess (Figure ).
Magnetic resonance imaging (MRI) brain also showed focal areas of enhancement in the right caudate nucleus and left lateral pons concerning for cerebritis. Magnetic resonance venogram (MRV) showed bilateral cavernous sinus thrombosis (Figure ).
Magnetic resonance angiogram (MRA) of the head and neck showed normal intracranial and neck vessels.
Otorhinolaryngology (ENT) team took the patient to the operating room emergently owing to the retropharyngeal abscess and concern for airway compromise. He underwent incision and drainage of the retropharyngeal abscess. The patient was then transferred to the intensive care unit (ICU) on mechanical ventilation. He was given then three doses of intravenous (IV) 10 mg dexamethasone every eight hours to decrease orbital inflammation and started on the heparin drip for cavernous sinus thrombosis.
Due to the central nervous system (CNS) findings, lumbar puncture was performed and 20 milliliters (mL) of cloudy cerebrospinal fluid (CSF) was obtained. CSF analysis showed a white cell count of 600 cells/cmm with 94% neutrophils. CSF glucose level was 50 mg/dl and protein level of 135 mg/dl.
Patient’s ventilatory support requirements began to increase the next morning. The CT chest scan was obtained that showed multifocal cavitary lesions scattered throughout the lungs concerning for septic emboli (Figure ).
Blood cultures initially obtained in the ED, and the CSF cultures came back positive for methicillin-sensitive Staphylococcus aureus (MSSA). The transthoracic echocardiogram was obtained which showed a mobile echodensity on the anterior tricuspid leaflet (Figure ).
Antibiotics were switched to IV Nafcillin in the context of identification of the pathogen and for better central nervous system (CNS) penetration.
At this point, it was concluded by the multidisciplinary team that patient’s IV drug abuse had contributed to native tricuspid valve acute infective endocarditis. The vegetation served as the source of infection with hematogenous spread of septic emboli to the orbit, lungs, brain and retropharyngeal space hence accounting for the initial presenting symptoms. With treatment, the patient began to improve and was weaned off the ventilator after one week. Right eye visual acuity improved significantly to 20/50 with complete resolution of ophthalmoplegia. He was subsequently discharged to the long-term acute care facility on oral warfarin and a six-week course of IV Nafcillin.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [109.0, 'mm hg'], 'Diastolic Blood Pressure': [69.0, 'mm hg']}",82.33333,78.21666,86.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 109.0 mm Hg + 2/3 * 69.0 mm Hg = 82.33333 mm Hg.
Hence, the patient's mean arterial pressure is 82.33333 mm Hg."
1345,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4363686-1,Extracted,"The patient was a 76-year-old female who presented for an outpatient upper gastrointestinal endoscopy (EGD) and a colonoscopy as a work-up for iron deficiency anaemia. She had a significant past medical history with coronary artery disease and previously underwent percutaneous coronary intervention with stents 4 years prior. She was on aspirin. There was no prior history of prior abdominal surgery. She underwent bowel preparation with a polyethylene glycol solution. She underwent EGD and colonoscopy under monitored sedation. Suring colonoscopy, the bowel preparation was noted to be adequate but the colonoscopy procedure was noted to be technically difficult with looping experienced especially in the transverse colon and hepatic flexure. External manual pressure was also applied. Repeated attempts to visualize beyond the hepatic flexure were unsuccessful, after which the procedure was aborted. No lesions or polyps were visualized. She tolerated the procedure well and reported no complaints immediately after. One hour after the endoscopy, the patient complained of light-headedness when trying to get out of bed, with an episode of syncope.
She complained of shortness of breath and chest pain. Vital signs were notable for pulse of 110/min, blood pressure 110/70 mmHg, respiratory rate of 20/min. On physical examination, she appeared uncomfortable, diaphoretic and pale. The abdominal exam was benign. Laboratory work-up was remarkable for haemoglobin of 8.5 mg/dl (preoperative hemoglobin was 9.5 mg/dl). Given her prior history of coronary artery disease, she underwent an electrocardiogram and serum troponin levels were normal. A portable upright chest X-ray was found to be negative for pneumoperitoneum, effusions or infiltrates (Fig. ).
She underwent immediate CT scan of the chest, abdomen, and pelvis with oral and intravenous contrast. During the preparation for the CT scan, she began to complain diffuse of abdominal pain. Her physical examination was now remarkable for a soft but diffusely tender abdomen. The pulse remained between 110 and 120/min and the blood pressure was 90/60. After 3 h, the hemoglobin was 6.1 mg/dl.
CT scan (Figs and ) revealed a large hematoma at the lateral margin of the spleen that displaced the spleen medially and compresses its lateral margin. A moderate amount of relatively low attenuation fluid also tracked into the right paracolic gutter and perihepatic space. There also appeared to be a 3.5 × 2.5 cm broad-based mass along the wall of the right colon. The CT scan of the chest also demonstrated a pulmonary embolus in a subsegmental artery of the right upper lobe. Given these findings, the patient was aggressively resuscitated with packed red blood cells and taken emergently to the operating theatre.
At surgery, an exploratory laparotomy was performed. About 1.5 l of fresh blood and 1 l of blood clots were encountered with active bleeding around a shattered spleen. Splenectomy was performed. Further exploration revealed a large hematoma around the hepatic flexure with avulsion of mesocolon causing visible evidence of ischaemia to the right colon. A mass was palpated at the cecum. A decision was made to perform a right haemicolectomy. Since the patient was haemodynamically unstable requiring massive blood transfusion, a primary anastomosis was avoided and an end ileostomy was performed with a mucus fistula.
Following this procedure, an inferior vena cava filter was placed using fluoroscopic assistance.
Histological examination of the colon was remarkable for a 3 cm low-grade mucinous adenocarcinoma of the cecum. Mesenteric lymph nodes were negative for metastases (T2N0M0). The patient made an uneventful recovery and was discharged home on the eighth postoperative day with plans to reverse the ileostomy in about 6 weeks.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mmhg'], 'Diastolic Blood Pressure': [70.0, 'mmhg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1346,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5776002-1,Extracted,"A 38-year-old gentleman presented to us for fever and weight loss of two months duration. He had a significant background history of having multiple sex partners and had no other co-morbidities. His vitals were normal, systemic and general physical examinations were normal except for low body mass index (BMI) of 17.5 kg/m2. On subsequent evaluation, he was found to have acquired immune deficiency syndrome (AIDS) with cluster of differentiation 4 (CD4) cell count of 50 cells/mm3. He was started on highly active antiretroviral therapy (HAART) comprising of tenofovir, lamivudine, and efavirenz. His fever subsided with improvement in general well-being till one month back, when he again presented to us, this time with generalised lymphadenopathy and low-grade fever. On examination, he was febrile with the temperature of 100ºF, had normal blood pressure (112/74 mmHg) with a heart rate of 96/min and respiratory rate of 18/min. He was malnourished with body mass index (BMI) of 18 kg/m2. General physical examination showed pallor with multiple, bilateral, cervical and inguinal lymphadenopathy. The lymph nodes were non-tender, mobile, firm in consistency and maximum 3×3 cm in size. Examination of the respiratory system, cardiovascular, per-abdominal and central nervous system were within normal limits. Complete blood count showed normocytic, normochromic anaemia (10.4 g/dl) with mild neutropenia (32×109/L) and normal platelet count (180×109/L). Chest X-ray showed miliary infiltration in bilateral lung fields. Lymph nodal biopsy showed spindle-shaped histiocytes, filled with acid-fast bacilli on Ziehl-Neelsen (ZN) stain, suggestive of MSP (figures -). Immunohistochemical (IHC) stains were positive for CD68, S-100 and negative for CD31, which were consistent with MSP (figures , , and ). Polymerase chain reaction (PCR) of the biopsy tissue was positive for MTB. Subsequently, he underwent bone marrow biopsy, which also showed epitheloid granuloma suggestive of tubercular marrow infiltration. Hence, HAART was continued and anti-tubercular therapy (ATT) was started with isoniazid, rifampin, ethambutol, and pyrazinamide along with pyridoxine supplementation. Fever resolved 2 weeks after the initiation of ATT and there was a resolution of lymph nodal swelling by 6 weeks.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [74.0, 'mm hg'], 'Systolic Blood Pressure': [112.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 112.0 mm Hg + 2/3 * 74.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1347,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6855583-1,Extracted,"A 54-year-old woman with hepatitis B cirrhosis, weighing 60 kg, presented to the hospital because of fever for half a month. On examination, she was conscious, the temperature was 36.6°C (the maximum body temperature was 39.0°C during the course of fever), pulse 74 times/min, R 18 times/min, and blood pressure 125/70 mm Hg. She had no history of drug allergies or adverse drug reactions. The temperature of patient did not improve after 3 days of empirical anti-infective therapy with piperacillin/tazobactam (PT), at this time, S aureus was identified in the twice blood culture. Additional laboratory analyses revealed the following: white blood cell (WBC) count of 3770/μL, neutrophil of 2639/μL, platelet of 66,000/μL, and hemoglobin of 10.8 g/dL, serum total bilirubin was 15.3 μmol/L, direct bilirubin 5.5 μmol/L, indirect bilirubin 9.8 μmol/L, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and kidney function were normal. Under the impression of bacteremia, PT was replaced by intravenous FA (0.5 g, q8 hours). Twelve days after FA therapy, she developed nausea and jaundice. And liver function test showed serum total bilirubin was 72.6 μmol/L, direct bilirubin 39.5 μmol/L, indirect bilirubin 33.1 μmol/L, ALT, AST, and kidney function were still normal. Complete blood cell count showed aggravated thrombocytopenia with platelet count of 18,000/μL, neutropenia with neutrophil count of 619/μL, and WBC of 1360/μL, and hemoglobin of 12.8 g/dL. On suspicion of adverse drug reaction, FA was stopped immediately, reduced glutathione was prescribed for hepatoprotective therapy. Given that the patient's temperature remained normal for 10 days, other antibiotic was not used. One day after discontinuation of FA, nose bleeding occurred with a nadir of platelet count of 4000/μL. However, WBC count increased slightly to 2090/μL, neutrophil to 1831/μL. Due to the severity of low platelet count, transfusion of random-donor platelet concentrates was used, but thrombocytopenia did not improve immediately. At the same time, bone marrow aspiration showed myeloid and megakaryocytic hyperplasia, suggesting increasing peripheral destruction (Fig. ). Five days after cessation of FA, jaundice resolved and the hematologic index returned to the level before FA. Throughout the period of FA treatment and after discontinuation of FA, the other drugs she took concurrently were entecavir tablets and polyene phosphatidylcholine injection, the former had been taking for 2 months prior to this admission, the latter was administered for 22 days from this admission to discharge. The serial data of WBC, neutrophil, and platelet counts are shown in Figure . And that of bilirubin are shown in Figure . At 1-month follow-up after discharge, the patient told us that she felt normal and did not have any discomfort. Written permission to publish this case report was obtained from the patient.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [125.0, 'mm hg']}",88.33333,83.91666,92.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 70.0 mm Hg = 88.33333 mm Hg.
Hence, the patient's mean arterial pressure is 88.33333 mm Hg."
1348,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-10502,Extracted,"A 4-year-old male is accompanied by his mother to the pediatrician. His mother reports that over the past two weeks, the child has had intermittent low grade fevers and has been more lethargic than usual. The child’s past medical history is notable for myelomeningocele complicated by lower extremity weakness as well as bowel and bladder dysfunction. He has been hospitalized multiple times at an outside facility for recurrent urinary tract infections. The child is in the 15th percentile for both height and weight. His temperature is 100.7°F (38.2°C), blood pressure is 115/70 mmHg, pulse is 115/min, and respirations are 20/min. Physical examination is notable for costovertebral angle tenderness that is worse on the right.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [115.0, 'mm hg']}",85,80.75,89.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 70.0 mm Hg = 85.0 mm Hg.
Hence, the patient's mean arterial pressure is 85.0 mm Hg."
1349,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5966895-1,Extracted,"A 65-year-old Japanese man presented with increasing edema of the lower extremities, which he noted for about one year. In a routine medical check-up two years previously, no proteinuria was identified. He had no remarkable family history, and had a medical history of hypertension and hyperlipidemia which were treated with olmesartan medoxomil, amlodipine, and pravastatin sodium. His blood pressure control was good. Two weeks before presentation, he had cerebral infarction. Although the infarction was mild, general edema was exacerbated and pleural effusion appeared. Therefore, he was transported to our hospital.
On admission, his blood pressure was 162/92 mmHg and pulse rate was regular at 80 beats/min. Marked edema of the lower extremities, articular disorder and a positive Barré’s sign, a diagnostic sign indicating a disease of the pyramidal tracts, were noted on physical examination. Urinalysis showed proteinuria of 14.3 g/day and 23.8 red blood cells/high-power field with hyaline casts. Serum creatinine, blood urea nitrogen, total protein and albumin levels were 138 mmol/dL, 7.4 mmol/L, 43 g/L and, 19 g/L, respectively. Estimated glomerular filtration rate (eGFR), which was calculated by Japanese equation for eGFR [], was 36.0 ml/min/1.73 m2. Severe hypokalemia (2.43 mmol/L) was observed under the treatment with furosemide (10 mg/day) and spironolactone (50 mg/day), while the urinary potassium level was 17.6 mmol/L. Arterial gas analysis showed metabolic alkalosis (pH, 7.54; pO2, 64 mmHg; pCo2, 41 mmHg; and HCO3−, 35.1 mmol/L). Despite both hypoalbuminemia and the use of two diuretics, the plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were suppressed to undetectable levels (Table ). Urine cortisol was slightly increased, but adrenocorticotropic hormone, plasma cortisol and plasma 11-deoxycorticosterone levels were within the normal ranges (Table ).
A renal biopsy showed findings of diffuse thickening of the glomerular capillary walls with spikes and moth-eaten appearance but not mesangial or endocapillary proliferative changes (Fig. ). On immunofluorescence examination, marked IgG granular deposits were observed along the capillary walls (Fig. ). On electron microscopy, numerous subepithelial dense deposits were found. These deposits were closely approximated with intervening spikes or encircled and incorporated into the capillary walls by spikes (Fig. ). The interstitium was edematous and increased slightly. Foamy changes of paroxysmal tubules were patchy, but no remarkable changes of the distal tubules were noted. These finding were comparable to stage II to III MN.
The patient was first treated with oral prednisolone (30 mg/day) for MN, and then, triamterene (50 mg/day) was added after considering a diagnosis of Liddle’s-like syndrome. The dose of triamterene was increased to 100 mg/day 5 days after the start of administration. Although proteinuria did not decreased, blood pressure, serum potassium levels, and edema were remarkably improved. In parallel with these treatments, screening examinations for cancer as a possible cause of MN were conducted, and advanced gastric cancer (type V) was found. Although proteinuria of over 5 g/day was still observed, prednisolone was quickly tapered to 10 mg/day, and total gastrectomy was performed. Two weeks after the gastrectomy, proteinuria was decreased to approximately 2 g/day. As the patient began to display hypotension (systolic blood pressure < 100 mmHg), triamterene was discontinued. After the cessation of triamterene, neither hypotension nor hypokalemia was observed. Prednisolone at 10 mg/day was continuously administered. Proteinuria continued to decrease gradually and disappeared 8 months after the operation. Finally, nephrotic syndrome showed complete remission, and laboratory data showed normal serum levels, PRA, and PAC (Table ), and no metabolic alkalosis even without triamterene treatment.
After obtaining informed consent, genetic mutations of the β and γ subunits of ENaC were assessed using a direct sequence approach as previously described []. However, no genetic mutation was detected in either of the subunits.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [162.0, 'mm hg'], 'Diastolic Blood Pressure': [92.0, 'mm hg']}",115.33333,109.56666,121.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 162.0 mm Hg + 2/3 * 92.0 mm Hg = 115.33333 mm Hg.
Hence, the patient's mean arterial pressure is 115.33333 mm Hg."
1350,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6169071-1,Extracted,"A 46-year-old Moroccan man with a history of cocaine and alcohol abuse, former smoker of 10 packs/year, detained in a penitentiary for 3 months, presented to an emergency department because of the finding by penitentiary doctors of severe anemia: hemoglobin (Hb) 43 g/L. He did not report previous concomitant comorbidities and he did not take any medication prior to hospital admission. It was difficult to collect a detailed family history because of a language barrier; he worked as a street vendor. He complained of progressive fatigue, arthromyalgia, upper finger paresthesia, mild abdominal pain, left ear tinnitus, and recurring headache for the previous 2 months. He denied fever, bleeding, and changes in bowel habits. At admission, severe normocytic anemia with Hb of 36 g/L, mean corpuscular volume (MCV) 87 fl, hematocrit (htc) 10.8%, and random distribution of red cell width (RDW) of 27% was confirmed, with neutropenia (0.59 × 109/L) and normal platelet count (15 × 109/L). On presentation he was oriented, afebrile (axillary temperature of 36 °C), and hemodynamically stable with blood pressure of 110/70 mmHg and a heart rate of 80 per minute. A physical examination showed pale skin, slight epigastralgia, and left tympanic membrane perforation; no lymphadenopathy, purpura, or hepatosplenomegaly were detected. A neurological examination was normal without any motor, sensory, or cranial nerves dysfunction except for slight upper finger paresthesia. Initial laboratory investigations revealed renal impairment with creatinine up to 176.8 μmol/L and azotemia 24.9 mmol/L, marked anisopoikilocytosis and multiple schistocytes (10%) on peripheral smear, lactate dehydrogenase (LDH) increase (19.7 μkat/L), haptoglobin less than 1 mg/L, and normal bilirubinemia (17.1 μmol/L). Coagulation studies were normal except for slight elevation of D-dimer (2.63 nmol/L); markers of inflammation were negative; liver function was normal with aspartate aminotransferase (AST) 30 U/L and alanine aminotransferase (ALT) 18 U/L. A direct Coombs test was negative, reticulocytes count was consistent with inappropriate bone marrow response (reticulocytes production index 0.061), and ferritin was within normal range.
Hydration with normal saline and blood transfusions with packed red blood cells were started. We observed an initial improvement of renal function but anemia did not improve enough despite transfusions with five bags of packed red blood cells, and it was associated to hemolysis (schistocytes, LDH further increase and haptoglobin consumed). In parallel we observed a progressive rapid decrease of platelet count down to 46 × 109/L and severe neutropenia was persistent without peripheral blasts. A diagnosis of thrombotic thrombocytopenic purpura and hemolytic uremic syndrome was considered, but the rapid improvement of renal function with only hydration and the pancytopenia suggested a bone marrow deficiency associated to a hemolytic component of unclear origin. We decided to keep on with blood transfusion support and to strictly monitor our patient until the results of further investigations; meanwhile, we started intramuscular vitamin B12 1000 mcg daily because of extremely low, barely detectable, plasma levels (< 36.9 pmol/L). Serology for cytomegalovirus, Epstein–Barr virus, parvovirus B19, and Toxoplasma gondii were negative (past infection) as were serology for human immunodeficiency virus and hepatitis virus. Bone marrow aspirate revealed normal cellularity with different cell types at various stages of maturation and without dysplastic alterations. An abdomen ultrasound showed normal kidneys and very slight splenomegaly (bipolar diameter 12.2 cm) without hepatomegaly and lymphadenopathy. See Additional file : Figure S1 for the timeline of the diagnostic and therapeutic flow of the present case report.
A week after beginning the vitamin B12 supplement we observed a dramatic hematological improvement with simultaneous decrease of hemolysis indexes; marked anisopoikilocytosis with teardrop cells (5%) persisted on peripheral smear without schistocytes (Fig. ). Anti-parietal cell antibodies were negative; upper endoscopy showed moderate gastric corpus atrophy, without presence of Helicobacter pylori. Recovery was complicated by pneumonia and urinary tract infections which were treated with intravenously administered amoxicillin/clavulanic acid.
We discharged our asymptomatic patient 2 weeks after admission with normal renal function, moderate normocytic anemia (85 g/L), and normal platelet and neutrophil count (484 × 109/L and 2.79 × 109/L, respectively).
At a follow-up of 6 months, he was alive but it was not possible to collect further medical information because we were informed that he was a fugitive.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1351,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5102721-1,Extracted,"A previously healthy 5-year-old African American male presented to the emergency department with a 9-day history of lethargy, fever, vomiting, weight loss, and diarrhea. The week before presentation, he was diagnosed with streptococcal pharyngitis via rapid antigen testing. He was prescribed a course of oral antibiotics but was noncompliant. On presentation, he was tall and thin (BMI < 3rd percentile, height > 95 percentile) with noticeable goiter and prominent proptosis. He was agitated, restless, tachycardic, and hypertensive (heart rate: 140 beats per minute, blood pressure: 154/99 mmHg). The mother noted that he had always been tall and thin. She had not noted any symptoms of hyperthyroidism such as weight loss, increased appetite, palpitation, or diarrhea prior to this illness. Chest X-ray showed cardiomegaly. Echocardiogram revealed dilated cardiomyopathy with severely dilated left ventricle with severely decreased left ventricular systolic function. Preliminary labs showed significantly elevated pro B-type natriuretic peptide at 19,632 (reference range is <450 pg/mL), suppressed TSH <0.005 μU/mL, and elevated free T4 >7.77 ng/dL consistent with severe hyperthyroidism and cardiomyopathy. Based on his clinical presentation and his significant cardiac findings, he was diagnosed with thyroid storm and was admitted to the pediatric ICU for further monitoring and management.
In the PICU, he was started on atenolol 25 mg daily and methimazole 5 mg twice daily for hyperthyroidism and given a dose of penicillin G for treatment of his streptococcal pharyngitis. Streptozyme test was positive. He was also noted to have persistent microscopic hematuria and 30 mg/dL of protein on the urine dipstick. Pediatric nephrology was consulted. Renal workup revealed low C3 (60 mg/dL; reference range is 85–288) and normal C4 complement levels (30 mg/dL; reference range is 17–64). He had normal creatinine for his age (0.3 mg/dL). An ASO titer was elevated at 857 (reference range: 0–207 IU/mL). Given the history of recent streptococcal pharyngitis, elevated ASO and streptozyme levels, microscopic hematuria, and low C3, he was presumed to have poststreptococcal glomerulonephritis and was followed up conservatively. Because of the elevated thyroid stimulating immunoglobulin at 464%, he was diagnosed with Graves' disease. Over the next several days, his heart rate, blood pressure, and mental status improved and his thyroid function tests normalized (see ). His left ventricular function also showed significant improvement after three weeks of treatment. He was discharged home on methimazole and atenolol on hospital day 15. Hematuria slowly resolved after discharge over the next few days. Repeat labs performed 8 weeks after hospitalization showed normal electrolytes and C3 levels, confirming the diagnosis of poststreptococcal glomerulonephritis. At follow-up, he had a bone age study done that showed significant advanced age (bone age of 11 years and 6 months at a chronological age of 5 years and 11 months) consistent with history of long-standing hyperthyroidism. Atenolol was discontinued several months later. He remained on methimazole at a maintenance dose.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [99.0, 'mm hg'], 'Systolic Blood Pressure': [154.0, 'mm hg']}",117.33333,111.46666,123.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 154.0 mm Hg + 2/3 * 99.0 mm Hg = 117.33333 mm Hg.
Hence, the patient's mean arterial pressure is 117.33333 mm Hg."
1352,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7220350-2,Extracted,"Patient 2 was a 26-year-old man who visited our hospital due to the discovery of heart shadow enlargement during an orientation health check in another hospital 4 months prior. A physical examination revealed his body temperature was 36.7 °C, his pulse was 71 beats/minute, his blood pressure was 121/71 mm Hg, the heart border was enlarged bilaterally, and there was no detected cardiac murmur. ECG revealed type I atrial flutter with a ventricular rate of 77 beats/min, a regular heart rhythm, and that the cardiac electric axis was shifted leftward. Transthoracic ultrasonography (IE33, PHILIPS, Netherlands) revealed a cystic mass in the right auricle area (Fig. a) that was approximately 6.4 cm × 4.3 cm × 3.9 cm in size and was connected to the right atrium. No abnormality was observed in the bilateral ventricles or left atrial structure. Doppler ultrasonography revealed unrestricted bilateral ventricular blood filling at diastole. Transesophageal ultrasonography revealed dense spontaneous contrast agent stagnation inside the lesion, but no thrombosis was seen inside the lesion or in the left atrium. The patient was diagnosed with RAA. Chest CTA (Aquilion One, TOSHIBA, Japan) suggested that the right atrium was oval and protruded outside the cavity, and the contrast agent density inside the lesion was similar to that in the right atrium (Fig. b–d). The patient refused surgical treatment and was prescribed orally administered amiodarone and warfarin anticoagulant therapy. At present, the patient has been followed up for 4 months, and no clinical symptom has been observed.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [121.0, 'mm hg'], 'Diastolic Blood Pressure': [71.0, 'mm hg']}",87.66667,83.28334,92.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 121.0 mm Hg + 2/3 * 71.0 mm Hg = 87.66667 mm Hg.
Hence, the patient's mean arterial pressure is 87.66667 mm Hg."
1353,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6939791-1,Extracted,"A 70-year-old female patient presented to the emergency department with rapidly progressive shortness of breath over a week. Her past medical history included significant weight loss, dysphagia, and anorexia 1 year prior to admission which was diagnosed as oesophageal carcinoma which was treated by oesophageal stenting 5 months prior to admission. On admission, the patient was in moderate distress with the following vital signs: blood pressure 130/80 mmHg, pulse: 130 b.p.m., temperature 37°C, and respiratory rate 25 b.p.m. Precordial examination revealed distant heart sounds. Chest examination revealed bilateral diminished air entry over both lung bases. Electrocardiogram demonstrated sinus tachycardia with premature atrial contractions (PACs), low voltage, and subtle electrical alternans (Figure ).
As a first line imaging modality, we selected a transthoracic echocardiogram which demonstrated a metallic shadow behind the left atrium (oesophageal stent) (Figure , , Movie S1, Figure , , Movie S2). It also revealed a massive circumferential pericardial effusion (that was mainly posterior and lateral and measured 3 cm and 2.8 cm, respectively) as well as large left pleural effusion (Figure , , Movie S1).The inferior vena cava (IVC) was dilated (2.6 cm) and it did not show adequate inspiratory collapse (Figure ). Apart from significant respiratory variation in mitral and tricuspid inflow (Figures and ), the echocardiographic features of tamponade were absent. We decided to apply the triage chart proposed by the European Society of Cardiology Working Group on myocardial and pericardial diseases to calculate the pericardiocentesis score. Despite that the patient was normotensive, the pericardiocentesis score was 13.5 ().
So urgent pericardiocentesis was performed with tapping of about 500 mL haemorrhagic fluid followed by immediate and marked improvement of symptoms and tachycardia (heart rate dropped to 100). Then, the patient was referred for pleuropericardial window.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1354,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-12462,Extracted,"A 22-year-old woman presents to her primary care physician in April for seasonal allergies. She has suffered from seasonal allergies for the past 2 years and takes diphenhydramine as needed when her symptoms worsen. She has not yet seen a physician for her allergies. She reports that diphenhydramine has been helpful in controlling her symptoms, but she does not like feeling drowsy from the medication. Her past medical history is also notable for well-controlled asthma. She uses an albuterol inhaler on an as-needed basis. She smokes marijuana daily. Her temperature is 99.2°F (37.3°C), blood pressure is 120/70 mmHg, pulse is 76/min, and respirations are 16/min. She has a prominent nasal crease. Her nasal turbinates are boggy and bluish-gray. She has copious thin and watery nasal mucus. The physician suggests replacing diphenhydramine with fexofenadine to improve her drowsiness.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [120.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1355,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5330221-1,Extracted,"A woman in her early twenties with a history of asthma was ambulatory on arrival to an academic ED in 2008 complaining of sore throat for 3 days that was associated with weakness, fever, productive cough and back pressure. At triage her oral temperature was 37.8 °C (100.1 °F), heart rate was 136 beats min−1 and blood pressure was 120/60 mmHg. The shock index (heart rate divided by systolic blood pressure) was 1.13 (normal ≤0.7, ). Physical examination revealed a normal oropharynx and expiratory wheezes. During the course of her visit, a second oral temperature was measured at 39.4 °C (103.0 °F). Chest radiograph showed basilar streaky opacities in one view. No laboratory studies were sent. Vital signs were repeated 5 h after arrival and showed a heart rate of 112 beats min−1 and a blood pressure of 100/60 mmHg (shock index 1.12). The patient was discharged with a diagnosis of upper respiratory infection of likely viral aetiology.
Thirteen hours later she returned to the ED by ambulance complaining of pain and red spots on her hands and feet. Vital signs revealed an oral temperature of 37.2 °C (98.9 °F), heart rate of 120 beats min−1 and a blood pressure of 92/60 mmHg (shock index 1.3). The patient was described as tachypnoeic, with a respiratory rate of 30 breaths min−1 and hypoxic with an oxygen saturation of 90 % on room air. She also complained of a mild headache, but had no nuchal rigidity or neurological abnormality on examination. Purpura was noted on her extremities and trunk. Although she received appropriate intravenous antibiotics 2 h after triage, her condition deteriorated and she died in the intensive car unit (ICU) 6 h after her arrival. N. meningitidis was isolated from her blood cultures and autopsy showed adrenal haemorrhage, consistent with meningococcaemia.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 60.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1356,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7320661-1,Extracted,"A 22-year-old male nursing student presented to the emergency department with complaints of retrosternal pain and dyspnoea for one day. The patient also complained that he could feel some air passing through the tissues below the skin in the neck. The patient had a history of throat pain and intermittent cough for three days and a history of ingestion of hot water a day before the presentation. He denied any history of trauma to the neck or any strenuous activity over the past one week. His other medical history was unremarkable. He had no addictions and not undergone any surgeries in the past.
Physical examination revealed a healthy-looking young man with tachypnoea. His pulse rate was 112 beats/min and blood pressure was 120/70 mmHg, his respiratory rate was 24/min. Crepitations were felt in the neck region extending up to the left nipple over the chest. The breath sounds and heart sounds were normal. Other systemic examinations were within normal limits.
Laboratory values (complete blood count, renal function test, electrolytes) and arterial blood gas were within normal limits. His electrocardiogram (ECG) was normal. X-ray neck and chest showed pneumomediastinum and subcutaneous emphysema (Figures -). Laryngoscopic examination did not reveal any mucosal lesion or foreign body. Computed tomographic scan of the head, neck and chest with oral gastrograffin was done which was suggestive of pneumomediastinum (Figures -). There was no evidence of any oesophageal perforation, pneumothorax, pleural disease and lung pathology. Upper gastrointestinal endoscopy and bronchoscopy was also normal. The patient was admitted and managed conservatively. He was given oxygen by mask, analgesics, cough suppressants, and steroid nebulisation. His symptoms settled with conservative management in three days and hence the patient was discharged. The patient was followed up for six months and there was no recurrence of symptoms. Chest X-ray was repeated after three and six months and there was no evidence of pneumomediastinum (Figure ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1357,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3549770-1,Extracted,"A 26-year-old man was admitted to our Department of Nephrology for a headache and newly ascertained advanced renal insufficiency (serum creatinine level 606 μmol/L, urea nitrogen 21 mmol/L, creatinine clearance 0.29 mL/s) with blended urinalysis (proteinuria 5.6 g/day, microhematuria – 25/ μl). Any serious diseases were noted at the time of admission to the hospital in February 2001. When he was sixteen he was hospitalized for a headache and uncertain abnormality of urinalysis but after this incident the patient was not examined and followed by the doctors. The patient did not take any regular treatment or addictive drugs, he abstained from alcohol and was a nonsmoker. There was an interesting statement in his family history about his 4-year older brother, who was hemodialysed for four years due to end stage renal disease probably evoked by addictive drugs (without verification by a renal biopsy) and he died at the age of 29 years. His five brothers and two sisters had no symptoms for renal or other diseases. The patient’s father died of prostate cancer at the age of 35 and he had no cardiovascular or renal disease, the patient’s mother suffered from a heart attack and epilepsy.
Physical examination of the patient revealed arterial hypertension (blood pressure was 150/100 mmHg, pulse was 70 beats/min), body temperature was 36.1°C, BMI 25, and no other abnormalities were found by clinical examination.
The levels of renal parameters at the time of admission to the hospital are mentioned above. Ultrasound of abdomen detected bilateral smaller kidney (length 98 mm with an unclear structure). Laboratory results showed serum level of potassium 5.3 mmol/L, hyperphosphataemia 2.1 mmol/L, total protein 67 g/L, albumin 43 g/L, metabolic acidosis (pH 7.2, HCO3 16.8 mmol/L, BE – 6.8 mmol/L), mild anaemia (the level of hemoglobin 125 g/L), mild hyperuricaemia (the level of uric acid 448 mmol/L), dyslipoproteinaemia with an elevation of LDL cholesterol (total cholesterol 7.5 mmol/L, LDL cholesterol 4.8 mmol/L, triglycerides 3.11 mmol/L), results of liver function tests were negative, urinalysis showed a pH 6, microhematuria – 25/ μl, the 24-h protein excretion was 5.6 g/d). Immunology tests were normal (immunoglobulin A, immunoglobulin M, immunoglobulin G, C3 and C4 complement, antinuclear antibodies, antibodies to extractable nuclear antigens, anti-neutrophil cytoplasmic antibodies, immune complexes). The electrocardiogram revealed the signs of left ventricle hypertrophy.
The patient underwent renal biopsy. In a renal biopsy sample, immunofluorescence and light microscopy [Figure ,] showed an advanced form of mesangioproliferative IgAN with marked scarring and epithelial crescents (in two glomeruli of the 12, the remaining 10 glomeruli were completely sclerotic) and vascular changes as a part of hypertension (electron microscopy was not performed because only sclerotic glomerulus was present in the sample). FD was not identified at that time. Blood pressure was well regulated by means of antihypertensive treatment (angiotensin-converting enzyme inhibitors, beta-blockers, diuretics). The regimen with corticosteroids (Prednisone 0.5 mg/kg) was initiated because of the age of the patient and suspected signs of the disease activity in the renal biopsy sample even though the possible influence of hypertension played a role in the occurrance of epithelial crescents. Subsequently, because of his progressive renal insufficiency the patient started to be hemodialysed in August 2001 (six months after renal biopsy) and corticosteroids were discontinued.
By means of the screening method in dried blood spots in 2003 [] a diagnosis of FD was suspected. Extensive tests for FD were implemented. Deficient activity of alpha-galactosidase A in the patient’s plasma (patient 0,47 nmol.ml-1.h-1, normal range 2.4 - 11.3 nmol.ml-1.h-1) and leukocytes (patient 0.23 nmol.mg-1.h-1, normal range 30–77 nmol.mg-1.h-1) confirmed the diagnosis of FD. After the patient’s informed consent was obtained mutation analysis (Sanger sequencing and RFLP method) was performed. We identified a missense mutation c.950 T>C (p.Ile317Thr) in exon 6. This mutation was previously found in an unrelated FD patient []. With this knowledge we performed additional electron microscopy from archive paraffin embedded kidney tissue [Figure and additionally showed dense deposits in paramesangial areas as a part of IgAN, and podocytes with inclusions of so-called zebra bodies and myelin figures characteristic of FD. The enzyme replacement therapy started in July 2004 and still continues. The patient underwent kidney transplantation in November 2005. Currently, the actual serum creatinine level is 250 μmol/L without the necessity of dialysis.
Other organ damages included hypertrophic cardiomyopathy. After the diagnosis of the coincidence of FD and IgAN was assessed we asked the patient about the possible clinical symptoms in his history related to FD and we found two typical signs such as febrile crisis and neuropathic pain in the extremities. Typical symptoms of FD – angiokeratomas and corneal changes – were not observed in this patient. Nevertheless, other findings (febrile and painful crisis, neuropathy, hypertrophic cardiomyopathy and Fabry nephropathy) supported the diagnosis of FD. On enzyme replacement therapy myocardial hypertrophy has stabilised, febrile crisis and neuropathic pain in the extremities have disappeared. To date, no other progression of the disease has been noted. After the informed consent was obtained, mutation analysis of the GLA gene was performed in 12 relatives, using the direct sequencing. Other 8 relatives were newly diagnosed with FD [3 hemizygous and 5 heterozygous, Figure ].
The second, a 30-year-old woman, suffered from long-term hematuria with a good renal function. Due to increasing proteinuria (2.6 g/day) appeared and a renal biopsy was performed. Histopathology showed IgAN with remarkably enlarged podocytes. IgAN and a high suspicion of a combination with FD was diagnosed by evaluation using immunofluorescence and light microscopy [Figure , . Electron microscopy [Figure , semithin section] revealed dense deposits in paramesangial areas typical of IgAN and podocytes with inclusive zebra bodies and myelin-like bodies characteristic of FD. The activity of alpha-galactosidase A in plasma was within the range of control values (3.3 nmol.ml-1.h-1, normal range 2.4 - 11.3 nmol.ml-1.h-1) and was decreased in leukocytes (26 nmol.mg-1.h-1, normal range 30–77 nmol.mg-1.h-1). The diagnosis of FD was confirmed by the identification of the GLA gene mutation c.1085C>T (p.Pro362Leu). This mutation was previously described in an unrelated FD patient []. Mutation analysis was performed after the informed consent was obtained. The mutation analysis also revealed the diagnosis of FD in the patient’s mother and sister (both heterozygous) with the same mutation [Figure . Subsequent examination of our patient showed corneal changes (cornea verticillata). Other organ defects were not proved. Enzyme treatment was initiated recently, but we still can not assess the effect of enzyme replacement treatment (the short duration of enzyme treatment – only one month).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",116.66667,110.83334,122.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 100.0 mm Hg = 116.66667 mm Hg.
Hence, the patient's mean arterial pressure is 116.66667 mm Hg."
1358,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5343141-1,Extracted,"A 30-year-old female presented with a two week history of dyspnoea, productive cough and fatigue. Other complaints included loss of appetite and weight. She had been diagnosed with pulmonary TB and HIV infection two months prior to this presentation. Her CD4 count was 363 cells/mm3 and the viral load was 1737 copies/ml. She was not on anti-retroviral therapy. The TB diagnosis was initially based on clinical features as the Xpert MTB/RIF (Cepheid GeneXpert, Sunnyvale, Ca, USA) sputum results were negative. She was then started empirically on the standard first line TB treatment (rifampicin, isoniazid, pyrazinamide and ethambutol). However sputum culture (MGIT 960 system, BACTEC MGIT Becton Dickinson, USA) later confirmed drug susceptible Mycobacterium tuberculosis (MTB). There was no history of smoking or alcohol consumption.
Physical examination revealed that she was apyrexial with a temperature of 36.5 °C. She was in respiratory distress with pleural effusion involving the entire left lung which was confirmed on the chest X-ray. On examination of the cardiovascular system, she was pale, had a sinus tachycardia with a heart rate of 160 beats per minute and a blood pressure of 112/65 mmHg. There were no abnormal heart sounds or murmurs. Examination of the abdomen and the central nervous system was unremarkable.
Laboratory investigations showed severe anaemia with a haemoglobin of 5.4 g dL−1, a raised white cell count of 15.7×109 L−1 and thrombocytosis of 958×106 L−1. Urea and electrolytes were normal while liver function test results were as follows: total protein 90 g L−1, albumin 20 g L−1, total bilirubin 10 umol L−1, alanine transaminase 40 U L−1, aspartate transaminase 65 U L−1, alkaline phosphatise 228 U L−1 and gamma glutamyl transferase 88 U L−1. The blood cultures taken on the day of admission were negative after five days of incubation using the BacT/ALERT® automated system (bioMérieux, Marcy l'Etoile, France). The C-reactive protein and erythrocyte sedimentation rate were high at 217 mg L−1 and 105 mm h−1, respectively.
An intercostal drain was inserted into the left lung which initially drained 500 ml of pus, some of which was sent for laboratory analysis while the patient was treated empirically using ceftriaxone. First line antiretroviral treatment (tenofovir, lamivudine and efavirenz) was also initiated. No MTB was detected from the pleural fluid using Xpert MTB/RIF, unfortunately, mycobacterium culture of the fluid was not performed.
Laboratory analysis of the pleural fluid showed glucose of 0.1 mmol L−1, protein of 62 g L−1, while the lactate dehydrogenase was 20 799 U L−1. The Gram stain revealed many leukocytes with numerous Gram-positive cocci in pairs and short chains. The pus was cultured onto chocolate agar, 5 % horse blood agar, Mac-Conkey agar and colistin nalidixic acid agar (Diagnostic Media Products, National Health Laboratory Services, Sandringham South Africa). A pure heavy growth of small pin-point size, non-haemolytic colonies was observed on the blood plate after 48 h of incubation in CO2 with no growth on any of the other plates. The catalase and oxidase tests were negative.
The Satellite test was performed on both chocolate and 5 % horse blood agar using a streak of Staphylococcus aureus ATCC 25923. The organism demonstrated satellism on chocolate agar plate but normal growth was observed with no satellism on the blood plate. The VITEK 2 Gram-Positive Identification Card (bioMérieux SA, France) identified the organism as G elegans with 97 % probability identification index. This identification was later confirmed by the matrix-assisted laser desorption ionization – time of flight mass spectrometry (MALDI-TOF MS; VITEK® MS, bioMérieux)
Antimicrobial susceptibility testing was performed according to Clinical Laboratory Standards Institute (CLSI) guidelines for Streptococcus species, Viridans group, however testing was done on horse blood as isolate failed to grow on sheep blood. The penicillin Etest was susceptible at 0.023 µg mL−1. Repeated attempts on broth microdilution (Sensititre®, TREK Diagnostic Systems, USA) with cation adjusted Mueller-Hinton broth supplemented with 5 % lysed horse blood yielded no growth. The treatment was then changed to penicillin and the patient improved and was subsequently discharged after three weeks in hospital.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [112.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",80.66667,76.63334,84.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 112.0 mm Hg + 2/3 * 65.0 mm Hg = 80.66667 mm Hg.
Hence, the patient's mean arterial pressure is 80.66667 mm Hg."
1359,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6868723-1,Extracted,"A 31-year-old, gravada-three, para-two, female with two prior cesarean sections and three live births, at 22-weeks gestation presented to the Emergency Department (ED) via ambulance with a chief complaint of severe dyspnea. The patient had no other past medical history and no prior obstetric complications. She was reported to have had one episode of syncope lasting several seconds, with no head trauma. At the time of presentation, the patient did not have, or report any prior, abdominal pain. However, when obtaining additional history from the patient’s husband, it was reported that the patient had experienced a brief episode of abdominal pain prior to her syncope. There were no other pertinent findings on history of present illness or review of symptoms.
On physical exam, the patient appeared pale and her skin was cool to touch. Her pulse was 72 beats/minute and regular, blood pressure was 110/80 mmHg, oxygen saturation was 97% on room air and her oral temperature was 37 C. She had altered mental status with intermittent episodes of drowsiness and restlessness. The remainder of her exam was significant for a gravid uterus slightly above the umbilicus with no significant tenderness elicited on palpation. Vaginal exam was negative for blood in the vault. Despite the patient’s normal blood pressure, her altered mental status combined with her cold and clammy extremities were consistent with compensated shock commonly manifesting with cutaneous and neurologic findings preceding hemodynamic instability.
As part of the patient’s initial management, laboratory studies were drawn. Significant findings included a white blood cell count of 24.4 × 103/mm3. Her initial hemoglobin of 9.8 mg/dL later fell to 7.9 mg/dL. A venous blood gas included a pH of 7.295 and a lactate of 4 mmol/L. Of note, however, was that the majority of these laboratory studies had not yet resulted prior to the patient’s initial management and disposition, and were generally noncontributory to her care in the emergency department.
Due to the patient’s clinical presentation of undifferentiated shock, a point of care ultrasound (POCUS) was immediately done and revealed a significant amount of fluid in the abdominal cavity along with fetal bradycardia. Secondary to these findings, an intra-abdominal bleed was suspected and fluid resuscitation with unmatched uncrossed blood (O-negative) was initiated.
The obstetric service (OB/GYN) was urgently consulted and a repeat bedside ultrasound, performed by the OB/GYN attending, concurred with our findings of intraabdominal hemorrhage but was not diagnostic for uterine pathology or a clear source of the bleeding. It did, however, show that there was no fetal heart beat or movement, concerning for fetal demise. The patient was taken for emergent surgical exploration that showed an acute left uterine wall rupture extending into the parametrium with an invasion of the placenta. Three liters of blood were evacuated from the abdominal cavity, as well as the pre-viable pregnancy. After separating the placenta from the uterus, the uterus was surgically repaired and a surgical drain was left in place. The patient required eight units of packed red blood cells and four units of fresh frozen plasma over the course of her resuscitation. She ultimately had an uneventful medical recovery with discharge on post-operative day five.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 80.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1360,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4100825-1,Extracted,"A 63-year-old man presented with abdominal distension and shortness of breath for two days. He reported flatus and denied chest pain, anorexia, vomiting, or abdominal pain. Surgical history was notable for left hepatectomy, cholecystectomy and choledochojejunostomy with a Roux-en-Y. He was afebrile with a pulse in the 100s, blood pressure of 130/60, respiratory rate of 34, and oxygen saturation of 92% on room air. Breath sounds were decreased in the lower lung fields and bowel sounds were noted in the chest. Abdominal exam was notable for distension, tympany and normoactive bowel sounds, but no tenderness, rigidity or fluid wave.
Complete cell count, chemistry panel and lipase were normal. Bedside echocardiography was obscured by air. A computed tomography (CT) was obtained. What is the diagnosis?",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [60.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 60.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1361,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6795531-1,Extracted,"A 55-year-old male presented to the emergency department with abrupt onset of severe chest pain, radiating through to the back, which had started 12 hours earlier and remained severe. There was no associated dyspnea, presyncope, syncope, or neurologic deficit.
He had been diagnosed with mild hypertension 1 month ago but not yet started on pharmacotherapy. He was a 15 pack-year smoker. He had no known cardiac disease, no history of chest pain, no Marfanoid features, no family history of aortic disease, no prior traumatic injury, and no systemic complaints.
On examination, he was distressed and diaphoretic with ongoing pain. His blood pressure was 175/90 mm Hg, and the heart rate was 90 bpm. There were no pulse deficits. There was a 2/6 systolic ejection murmur at the base of the heart. No pericardial friction rub was present. Jugular venous pressure was normal.
The 12-lead electrocardiogram showed normal sinus rhythm. The anteroposterior chest radiograph revealed a normal-sized heart but an abnormal aortic contour in the ascending and arch locations. There was no left pleural effusion and no intimal displacement sign at the distal aortic arch.
A contrast-enhanced computed tomography scan was obtained to assess the possibility of acute aortic dissection. An intimal flap was imaged beginning in the ascending aorta, which was 45 mm in diameter, and continuing around the arch, down the descending aorta and extending into the left iliac artery (
). Transthoracic echocardiography revealed moderate aortic valve insufficiency.
The patient underwent surgical repair with graft replacement of the ascending aorta and mechanical aortic valve replacement. Intraoperative transesophageal echocardiography revealed that the aortic valve was quadricuspid, which was confirmed at surgical inspection. The intimal tear was located above the noncoronary cusp. The pattern of the quadricuspid valve was of two larger and two smaller cusps (
). Pathological examination revealed that the smaller cusps were thickened, and there were fenestrations. The patient was discharged on the 7th postoperative day, on warfarin and metoprolol, and remains well in follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [175.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",118.33333,112.41666,124.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 175.0 mm Hg + 2/3 * 90.0 mm Hg = 118.33333 mm Hg.
Hence, the patient's mean arterial pressure is 118.33333 mm Hg."
1362,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4046594-1,Extracted,"An-81- year old diabetic female presented with severe pain and swelling of left thigh in the emergency department in January, 2011. The previous night she woke up suddenly because of the severe pain in her left thigh. The pain was so severe that she couldn’t touch her thigh nor could she move it. She denied having any other symptoms. On examination, she was a febrile with pulse rate of 90 beats/min; respiratory rate of 16 breath/min and blood pressure was 160/100 mmHg. Systemic examination of chest, heart and abdomen was also normal. On local examination left thigh was swollen with difference of 12 cm between left and right, indurated and was excruciatingly tender to touch, maximum on anterolateral aspect without any erythema and cellulitis but was warmer than right thigh. Funds examination showed hypertensive along with background diabetic retinopathy changes. Peripheral pulses were symmetrical. There were no muscle fasciculations, muscle atrophy and tenderness of the spine. There was no evidence of neurovascular compromise. Neurological examination revealed absent ankle reflexes and absent vibration sensation at big toe and ankle bilaterally. Her urea was 86 mg % (10-35 mg%) and creatinine was 1.9 mg% (0.5-1.0 mg%) and rest of her routine blood tests were normal. Her random blood sugar was 320 mg% and blood ketones was negative. Twenty four hour urine revealed 800 mg of protein. D-dimer and antinuclear antigenwere negative. Creatine kinase was raised two time of the normal. Compressive Ultrasonography of left thigh was normal. MRI of pelvis and thighs showed high T2 signal and hypodense signal on T1 images of left thigh characteristic of fluid affecting subcutaneous and quadriceps with maximum involvement of vastes lateralis muscle of left thigh [Figures and ]. On i.v gadolinium there was uniform enhancement of the muscle with central non-enhanced area of necrotic muscle [ and ]. Fine needle aspiration was done which showed of muscle fibres in various stages of degeneration. Moreover, Sudden onset of excruciating pain and swelling without weakness in the thigh and with no signs of local and systemic inflammation, without any evidence of neurovascular compromise with small increase in creatine kinase, negative collagen network in a long standing diabetic woman having underlying micro vascular complications in the form of retinopathy, nephropathy and neuropathy is highly suggestive of diabetic muscle necrosis in our patient. The highly characteristic MRI findings further support the clinical diagnosis. The patient was treated conservatively with bed rest, analgesics and insulin. She starts showing improvement and was discharged after 24 days.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [160.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",120,114,126,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 100.0 mm Hg = 120.0 mm Hg.
Hence, the patient's mean arterial pressure is 120.0 mm Hg."
1363,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6580543-1,Extracted,"During a hot afternoon in July, a 48-year-old man developed symptoms, such as nausea, vomiting, headache, chest tightness, and shortness of breath, while working outdoors for 2 h in a southern city in China. The outside temperature at that time was 35 °C. Notably, the patient lived in the north part of China and had traveled to the southern part when he was sick. After 15 h, he went into coma and was then transferred to the emergency department of the hospital. The patient was in good health before the onset of the disease. Upon arrival, the temperature of the patient was 40.2 °C, blood pressure was 75/40 mmHg, and pulse rate was 100 beats/min. His blood oxygen saturation under balloon-assisted ventilation was 95%. Laboratory tests indicated rhabdomyolysis syndrome, acute kidney injury, hepatic disfunction, hyperkalemia, and metabolic acidosis. The serum D-dimer level of the patient was elevated at 1022 (normal range: 0–232) μg/L. Therefore, the patient was diagnosed with HS. He was immediately treated with a cooling blanket and plasma exchange and received assisted ventilation. Brain CT scans performed on the 3rd day of admission showed symmetrical low-density lesions in the bilateral basal ganglia. On the 7th day of admission, the patient’s state of consciousness improved. However, he experienced blurred vision. Eye examination results were normal. Brain magnetic resonance imaging (MRI) was performed 8 days after admission. Cerebral MRI revealed a slight hyperintensity in the bilateral putamen on diffusion-weighted imaging (DWI) sequence and bilateral symmetrical hypointensity in the middle of the putamen and hyperintensity around hypointensity on the apparent diffusion coefficient (ADC), fluid-attenuated inversion recovery (FLAIR), and T2-weighted imaging (T2WI) sequence. The lesions showed hyperintensity in the middle of the bilateral putamen and hypointensity around them on T1-weighted imaging (T1WI) sequence (Fig. A-E). Magnetic resonance venography (MRV) in sagittal projection performed on the 12th day of admission showed the absence of a straight sinus and vein of Galen, indicating CVT. In addition, the lack of flow signal was also found in the distal part of the superior sagittal sinus that also corresponds to CVT (Fig. F). Intravenous treatment of mannitol, subcutaneous injection of low-molecular-weight heparin calcium (5000 IU, two times/day) was initiated to reduce high intracranial pressure and to treat CVT. Cerebrospinal fluid (CSF) examination conducted on day 17 showed elevated protein levels at 1.87 (normal range: 0.15–0.45 g/L and immunoglobulin G levels at 267.0 (normal range: 0–34.0) mg/L. The CSF pressure was 210 (normal range: 80–180) mmH2O. Susceptibility-weighted imaging (SWI) obtained on the same day indicated bilateral hemosiderin deposition or hemorrhagic foci in the basal ganglia (Fig. ). Follow-up MRI obtained 25 days after admission showed symmetrical abnormal signals in the bilateral posterior limb of the internal capsule, putamen, external capsule, and insular lobe. The signals were hypointense on T1WI and hyperintense on T2WI, FLAIR, and ADC and were not limited by diffusion on DWI. Strip and dot-like signals, which were isointense and slightly hypointense on T1WI and hypointense on T2WI, can be observed in the lesions. DWI revealed bilateral hyperintensity on the frontal and occipital lobes (Fig. A1–E3). The flow signals of the superior sagittal sinus, straight sinus, and vein of Galen were significantly better on follow-up MRV (Fig. ). On the 28th day of admission, after the administration of gadolinium, MRI revealed abnormal enhancement within the bilateral basal ganglia, and the size of the lesions decreased on MRI conducted 25 days after admission (Fig. ). The patient was discharged with blurred vision on the 38th day. (Timeline of brain imaging was shown in Table ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [75.0, 'mm hg'], 'Diastolic Blood Pressure': [40.0, 'mm hg']}",51.66667,49.08334,54.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 75.0 mm Hg + 2/3 * 40.0 mm Hg = 51.66667 mm Hg.
Hence, the patient's mean arterial pressure is 51.66667 mm Hg."
1364,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5390442-1,Extracted,"A 61-year-old Caucasian man presented to our emergency department with 20 pounds of unintentional weight loss over 2 months followed by a 2-week history of worsening shortness of breath, epigastric tenderness, and bilateral pitting leg edema. He had no symptoms of fever, cough, phlegm production, diaphoresis or night sweats. He had a 40 pack-year smoking history and 40-year history of alcohol misuse, but no significant past medical history or family history of significant medical illness. Later in the course of his current presentation, he admitted to 6 months’ history of intermittent abdominal pain and diarrhea. He had attributed this to his use of alcohol and he did not seek medical care.
On physical examination, he was emaciated and afebrile with a heart rate of 118 beats per minute and a blood pressure of 103/70 mmHg. His jugular venous pressure was elevated at 5 cm above the sternal angle. His abdomen was not distended but tender to light palpation in the epigastrium. He was not jaundiced. Leg pitting edema was noted from his feet up to the distal thirds of his tibia bilaterally. Auscultation of the lung fields revealed significantly decreased air entry at the base of the right lung. His oxygen saturation on room air was found to be 85%. With supplemental oxygen delivered by nasal prongs at 2L/minute he maintained an oxygen saturation of 94%.
The admission blood work is presented in Table . Results showed an elevated leukocyte count of 24.0 × 109/L, predominately neutrophils, elevated thrombocyte count of 894 × 109/L and low hemoglobin 79 g/L with a hematocrit of 27%. Liver enzyme test results revealed elevated alkaline phosphatase 197 U/L, elevated gamma glutamyl transferase (ϒGt) 121 U/L, international normalized ratio (INR) elevated at 1.4 and C-reactive protein (CRP) elevated at 262.5 mg/L. There was a significant drop in his albumin level, at 24 g/L. Serology results did not demonstrate any evidence of hepatitis B infection. Additionally, no evidence of hepatitis B immunity was found. Hepatitis C antibodies were non-reactive.
The admission chest X-ray, Fig. , revealed a large right lung pleural effusion with near complete opacification associated with mass effect and mild mediastinal shift toward the left hemithorax. A thoracentesis removed 1.5 L of yellow cloudy fluid from the right hemithorax in the emergency room. The pleural fluid analysis revealed an exudative effusion with a fluid lactate dehydrogenase of 256 U/L, nucleated cell count of 14.3 × 109 with 86% being neutrophils, and fluid to serum amylase ratio of 1:2. Light’s criteria were assessed and consistent for exudative effusion, Table . The serum effusion albumin gradient (SEAG) was measured at 5g/L (serum albumin 24g/L – effusion albumin 19g/L), which is consistent with exudative effusion. The fluid was also sent for Gram stain and microbiological culture.
Our patient was admitted to the internal medicine ward and piperacillin-tazobactam 3.375 g intravenously every 6 hours was initiated. A right-sided Wayne catheter chest tube was inserted with ultrasound guidance the following day; however chest X-rays post chest tube insertion did not show any significant decrease in effusion size. An esophagogastroduodenoscopy (EGD) and colonoscopy were performed to help determine the cause of the patient’s anemia. The EGD did not identify a source of bleeding, but the colonoscopy revealed an impassable diverticular stricture encountered at 25 cm from the sigmoid colon.
A computed tomography (CT) scan of our patient’s thorax demonstrated a tiny gas and fluid collection in the right lobe of the liver, suggestive of decompressed hepatic abscess with extension through the right pleural space and into the right lower lobe of the lung, Fig. . A CT scan of his abdomen confirmed a ruptured intrahepatic abscess extending across the diaphragm into the right pleura and into small right lower lobe abscesses. Furthermore, a complicated sigmoid colon diverticulitis with a fistula to the rectum was also seen, Fig. .
At this time, the general and thoracic surgery services were consulted. A decision was made to request the interventional radiology service to place a percutaneous drain to clear the remaining intrahepatic abscess. During the procedure, fluoroscopic contrast was instilled into the abscess drain and was found to track through the right hemidiaphragm into the right lung pleural space and bronchi, Fig. . This resulted in a sudden drop in the patient’s oxygen saturation, which resolved when the contrast was evacuated from the bronchi. A new chest tube was inserted to drain the remaining pleural fluids. Despite the intrahepatic drain and two chest tubes in situ, the patient’s pleural effusions failed to drain completely. The thoracic surgery team subsequently decided that lung decortication and exploratory bronchoscopy was indicated for the patient. The microbiological culture of the pleural fluid grew penicillin-sensitive Streptococcus anginosus, but our patient’s antibiotic regimen was not changed in order to maintain coverage for possible anaerobic and Gram-negative enteric microbes.
Our patient was taken to the operating room, where bronchoscopy revealed clear airways with no perforations. A thoracotomy was then performed to expose the pleura, which was found to be markedly thickened. The pleura were incised and a large amount of gelatinous material was removed from the pleural cavity. Extensive decortication of the right lung resulted in significantly improved intraoperative lung inflation. A biopsy of the lung abscess was also taken. Four chest tubes were placed intraoperatively to ensure effective drainage of the pleural cavity. Our patient tolerated the procedure well and substantial lung re-expansion was observed on chest X-rays in the days following the procedure. A subsequent drain check performed by an interventional radiologist, showed a residual cavity in the right lobe of the liver and that the fistula to the pleural space was still patent. However, no continuity to the lung abscess or bronchi was observed. General surgery also opted not to surgically remove the fistula as it was felt that it would close on its own given the effective drainage that had been achieved.
Ten days following his operation, our patient was discharged home with his hepatic abscess drain still in situ and with a 21-day course of ciprofloxacin 500 mg and metronidazole 500 mg, both orally and twice daily. An abscess check performed 3 weeks later found that the abscess had resolved without complications and the percutaneous drain was removed.
The general surgery service re-assessed our patient approximately 1 month post-discharge from hospital. Our patient reported he was feeling well and denied experiencing any abdominal pain or other concerning gastrointestinal symptoms. Because of this complex diverticulitis with an increased the risk of future bacterial seeding, a lower anterior resection of the affected colon and rectum was offered to the patient. Our patient agreed to have this procedure performed laparoscopically, however significant adhesions were found intraoperatively in the pelvis preventing easy mobilization of the sigmoid colon. Subsequently, the operation was converted to an open laparatomy. The segment of colon containing the fistula was identified and resected. A tension-free end-to-end anastomosis was then created without difficulty. Our patient tolerated the procedure well and was discharged from hospital 5 days following the operation. At follow-up appointments at 1 week and 1 month following his discharge, our patient again reported that he was feeling well and denied experiencing any abdominal pain or other gastrointestinal symptoms.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [103.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",81,76.95,85.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 103.0 mm Hg + 2/3 * 70.0 mm Hg = 81.0 mm Hg.
Hence, the patient's mean arterial pressure is 81.0 mm Hg."
1365,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3467955-1,Extracted,"A 73-year-old man was admitted to our emergency department with chest pain. As he stated, he had been suffering from pain without radiation for the past 30 minutes, accompanied by nausea, vomiting, and diaphoresis. He claimed that he had had a previous similar episode the day before his admission, but the pain had resolved spontaneously after about one hour. He had a history of cigarette smoking, hypertension, and respiratory disease, for which he had received no appropriate and regular medical care. He had used Atenolol for the last three months in an irregular manner. No abnormal findings were detected on his physical examination (blood pressure = 140/80 mmHg, heart rate = 60 bpm, and normal breathing and heart sounds). His initial electrocardiogram (ECG) showed a left-axis deviation and left anterior hemiblock with ischemic changes (inverted T wave) on its pericardial leads. He had elevated cardiac troponin, and no other significant abnormalities were detected in his blood tests. He underwent medical management for acute coronary syndrome, and his pain was reduced within his first hour of admission. Echocardiography was performed for the patient and revealed a moderate left ventricular (LV) dysfunction with an LV ejection fraction of 40% and anterior and lateral wall hypokinesia. Mild LV hypertrophy was also detected. The patient was scheduled for coronary angiography on the following day. No chest pain or other symptoms were reported during the first night. The next morning, the ECG showed the evidence of a posterior (lateral) myocardial infarction (MI).
The patient underwent cardiac catheterization via the standard Judkins techniques. The selective angiography of the left coronary artery showed a critical and thrombotic stenosis on the midportion of the LAD as well as a moderate lesion on the midportion of the left circumflex (LCx) artery (). Mild stenoses were also detected at the proximal end of the LAD and high obtuse marginatus. The LAD ran through the interventricular groove but at the end of the midportion, it deviated from its usual course and transformed to a diagonal and supplied the anterolateral area of the LV. On the right side, the selective coronary artery injection revealed a dominant right coronary artery (RCA) and also an anomalous coronary artery arising just after the origin the RCA (). The accessory vessel ran into the left side and coursed into the mid and distal portions of the anterior interventricular groove and supplied the apex area. There were small septal arteries separating from it. On the left ventriculography, hypokinetic anterolateral and diaphragmatic walls were seen. The culprit lesions on the LAD were stented with a drug-eluting stent (DES), and the patient was discharged from the hospital with an acceptable condition on the fourth day of his hospitalization.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [140.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 80.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1366,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5646306-1,Extracted,"60-year-old previously healthy male presented with a progressive intermittent claudication of his right leg of 2-month duration. He is a nonsmoker and occasionally consumes alcohol. He did not have a past history of diabetes mellitus, hypertension, or dyslipidaemia. His right lower limb claudication gradually became worse over one month and he experienced right leg pain even on minimal exertion in walking few meters. For the last four months, he had an evening low grade fever, profound myalgia with loss of appetite, and a gradual weight loss of 8 kg. Two weeks before the admission he noticed a weakness of his right ankle with a rash on his right leg. He had no history of abdominal or testicular pain.
On examination he was afebrile, pale, and cachectic. There was no lymphadenopathy or organomegaly. He had a livedo reticularis rash over the right leg with polymorphic vasculitic changes (). His blood pressure was 160/100 Hg mm. The examination of peripheral pulses revealed absent femoral, popliteal, and distal pulses of the right lower limb. On the left lower limb, he had preserved popliteal and femoral pulses with absent dorsalis pedis and posterior tibial pulses. His respiratory system and abdominal examination were normal. He had a right-side foot drop with sensory impairment over the right dorsum of foot with preserved deep tendon reflexes. Fundal examination was normal.
His investigations revealed normocytic normochromic anaemia (8.4 g/dl) with an ESR of 120 mm per 1st hour. His CRP was 92 u/l (<6). Transaminases were normal and his albumin to globulin ratio was reversed. Renal functions were normal (serum creatinine 90 mmol/l) and the urine tests revealed a significant microscopic haematuria without proteinuria or dysmorphic red cells. Chest radiograph was normal. His autoimmune antibody testing including ANA and ANCA (including MPO and PR3) and rheumatoid factor was negative. His 2D echocardiogram, homocysteine level, and HbA1c and lipid profile were within normal limits and the HIV status was negative. His hepatitis B and C status was also negative. Digital subtraction angiography of aorta and lower limb revealed left side renal artery stenosis () with segmental occlusion of left iliofemoral and right femoral arteries (). There was no evidence of aneurysms in angiography. Nerve conduction study revealed right-side peroneal nerve palsy. Deep punch biopsy from vasculitic skin lesions showed segmental transmural inflammation of muscular arteries with fibrinoid necrosis with a polymorphonuclear infiltrate suggestive of a medium vessel vasculitis.
With the history of constitutional symptoms with severe myalgia, new onset hypertension, mononeuropathy together with angiographic changes, and medium vessel involvement in histology, we diagnosed PAN in our patient. After excluding viral causes such as hepatitis B, hepatitis C, and HIV, we had to start immediate immunosuppressive medication. Due to rapidly progressing limb-threatening disease, we started the patient on steroid pulses and intravenous cyclophosphamide. Subsequently, due to the disabling ischaemic rest pain we referred the patient to vascular surgical team and he underwent a successful right-side iliofemoral bypass.
After aggressive immunosuppression and bypass surgery our patient could mobilize with aid and his constitutional symptoms and the vasculitic rash improved with time. The rest of the pain of right lower limb disappeared and he could walk for 20–30 m without developing claudication. We continued giving the patient steroids tailing off gradually and planned on monthly intravenous cyclophosphamide therapy. With treatment, his constitutional symptoms and myalgia reduced and the ESR came down to 60 in 1st hour. His weight was stable. Within the next 6 months, while on immunosuppressants, he was admitted with recurrent infections to the hospital, so that we had to stop cyclophosphamide and switch to azathioprine.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [160.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",120,114,126,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 100.0 mm Hg = 120.0 mm Hg.
Hence, the patient's mean arterial pressure is 120.0 mm Hg."
1367,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4370030-1,Extracted,"A 29-year-old Hispanic male was found on the street unconscious by the police and was brought to the emergency department (ED). The patient had a medical history that included alcohol abuse with multiple ED visits for alcohol intoxication and physical trauma over a 7-year period. His social history is remarkable for recent immigration to the USA 8 years ago from Mexico, and he currently resides in a dorm with eight roommates. Further history was not obtainable from the patient due to altered mental status and there were no family members or roommates present at the time of admission.
Initial physical exam revealed vital signs that were within normal limits aside from mild tachycardia and tachypnea with a temperature of 36.7°C, heart rate of 112/min, blood pressure of 110/79 mmHg and respiratory rate of 22 breaths per minute with oxygen saturation of 98% on ambient air. The patient was a thin appearing, disheveled male in mild distress. There was no evidence of trauma to the patient's head or body. He was alert but disoriented, and was unable to follow simple commands. Lung auscultation revealed normal vesicular breath sounds bilaterally with no wheezes or crepitations. Heart and abdominal examinations were unremarkable. Laboratory tests revealed a white blood cell count of 6000/µl, hemoglobin of 12 g/dl, platelet count of 88/µl, sodium of 117 mg/dl, alkaline phosphatase of 269 U/l and total bilirubin of 1.2 mg/dl. Urine drug screen obtained upon admission was negative, and blood alcohol and ammonia levels were normal. A computed tomography (CT) of the head without contrast was negative for a subdural bleed or other intracranial abnormality.
A chest radiograph revealed diffuse ground-glass nodular opacities with a ‘tree-in-bud’ sign greatest in the left mid-lung (Fig. A). These abnormalities were not present on chest radiographs taken 3 months earlier when he presented to the ED with chest pain (Fig. B). CT of the chest with intravenous contrast revealed innumerable tiny pulmonary nodules in a random, miliary pattern (Fig. ). In addition, there were multiple enlarged mediastinal and hilar lymph nodes, the largest of which measured 12 mm in diameter. A calcified granuloma was also noted in the left upper lobe. The differential diagnosis of a relatively new-onset miliary pattern on imaging included disseminated viral, bacterial, fungal and mycobacterial infections, hypersensitivity pneumonitis or metastatic disease with either hematogenous or lymphangitic spread. In the present patient, the findings on chest radiography coupled with risk factors of travel from an endemic area, malnutrition, overcrowding and alcohol abuse made the diagnosis of post-primary miliary TB very likely.
The patient was admitted and placed in a negative pressure room with droplet and respiratory isolation precautions. Sputum samples were obtained and microscopy revealed 3+ acid-fast bacilli (AFB). Concern for tuberculous meningitis was high given the initial presentation of altered mental status. A lumbar puncture was therefore performed and examination of cerebrospinal fluid (CSF) showed 13 nucleated cells (9 lymphocytes, 3 neutrophils and 1 monocyte), protein of 85 mg/dl and glucose of 94 mg/dl. A nucleic acid amplification test (NAAT) on sputum and CSF was positive for M. tuberculosis. Additionally, microscopy of a urine sample revealed AFB. The diagnosis of disseminated TB was made, with pulmonary, renal, central nervous system (CNS) and probable hepatobiliary involvement in light of elevated alkaline phosphatase and total bilirubin.
During the first 24 h of admission the patient's respiratory status deteriorated, requiring intubation and mechanical ventilation. His respiratory failure was believed to be due to acute respiratory distress syndrome from overwhelming infection. The patient was started on parenteral isoniazid (INH) and rifampin, due to concern for poor enteral absorption, and oral ethambutol and pyrazinamide as soon as the sputum samples returned positive for AFB. He was also started on dexamethasone as adjunctive anti-inflammatory therapy for tuberculous meningitis. The patient's clinical status improved and repeat chest CT showed significant improvement in miliary nodularity within 2 weeks (Fig. ).
The patient required quadruple anti-TB therapy for 2 months followed by 7 months of INH and rifampin due to CNS disease. He suffered neurologic sequelae in the form of cognitive impairment, but made a fairly decent recovery.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [79.0, 'mm hg']}",89.33333,84.86666,93.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 79.0 mm Hg = 89.33333 mm Hg.
Hence, the patient's mean arterial pressure is 89.33333 mm Hg."
1368,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8437203-1,Extracted,"A 55-year-old female with a past medical history of hypertension, type 2 diabetes, and obesity was brought to the emergency department by her family members for concerns regarding her behavior. The patient was discharged from another hospital a week ago, where she was treated for COVID-19 infection using oxygen therapy, steroids, and remdesivir. She received dexamethasone 6 mg IV for seven days. She was discharged with no psychotic symptoms during her hospital stay and continued to receive oxygen therapy at home after steroids and remdesivir were discontinued. The patient became symptomatic with COVID-19 three weeks before her current presentation, and she tested negative on the COVID-19 RNA test performed during the current ED visit. In ED, the patient had a blood pressure of 147/119 mmHg and tachycardia (130 bpm). Her SpO2 saturation was 97%. The patient was without any fever at the presentation. Her lactate dehydrogenase levels were 825 units/L, and her white blood cell count was 4500 cells/mm3. She had non-command type auditory hallucinations and delusions of religious nature. She reported hearing God’s voice asking her to save the earth. COVID-19 was also the central theme of such hallucinations/delusions. She was agitated, screaming at staff members, and removing IV lines. She received diphenhydramine 25 mg, haloperidol 5 mg, and lorazepam 2 mg for acute management of symptoms. She was also started on metoprolol 25 mg for management of her hypertension. Infectious disease workup was negative. MRI and CT scans of the brain were unremarkable. The urine drug screen was negative for substances. All etiologies of such presentation were ruled out.
On a follow-up visit the next day, the patient continued to have grandiose delusions, her speech was pressured. She was preoccupied with God, COVID-19, and the Devil. She reported seeing God and reported that God is talking with her during the interview. It was decided to admit the patient to the inpatient psychiatric ward. She was started on haloperidol 10 mg and sodium valproate 1000 mg for treatment. She continued to show improvement in her symptoms. Considering the better side effect profile of second-generation antipsychotics regarding extrapyramidal side effects, she was discharged from the hospital on aripiprazole 10 mg and sodium valproate 1000 mg daily after two weeks of inpatient stay to follow-up at the outpatient clinic.
During her stay, we collected collateral information from multiple sources. The patient was never diagnosed with any psychiatric illness. She never visited a psychiatrist in her lifetime. Family history is positive for bipolar disorder type I in a distant cousin. Her family also has a history of developing psychiatric symptoms following steroid use. However, there is no history of her developing psychiatric symptoms following treatment with steroids in the past. The family members reported that they have never seen abnormal behavior in her before this instance.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [147.0, 'mm hg'], 'Diastolic Blood Pressure': [119.0, 'mm hg']}",128.33333,121.91666,134.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 147.0 mm Hg + 2/3 * 119.0 mm Hg = 128.33333 mm Hg.
Hence, the patient's mean arterial pressure is 128.33333 mm Hg."
1369,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4802827-2,Extracted,"A 36-year-old otherwise healthy foreign male was found wincing in the vicinity of a ladder underneath a warehouse roof (height approximately 5 meters). Upon arrival of the EMS doctor the patient was able to maintain an open airway, the chest was stable und bilateral breath sounds were present. The patient was hemodynamically stable. The vitals were: respiratory rate 18/min, oxygen saturation 100 % without oxygen supply, heart rate 95 bpm, blood pressure 180/90 mmHg, blood sugar 135 mg/dl. Because of pelvic pain and suspected pelvic instability EPS was performed with the SAM Pelvic SlingTM II (SAM Medical Products®, Wilsonville, OR, USA). The Glasgow Coma Scale (GCS) was 14 (E4/V4/M6) and a fracture of the left lower leg was clinically diagnosed. After rapid sequence induction the patient was endotracheally intubated and a total crystalloid volume of 2000 ml was administered en route to our hospital. On admission we saw an intubated and mechanically ventilated patient. The vitals were: respiratory rate 12/min, etCO2 36 mmHg, oxygen saturation 100 % with FiO2 1.0, heart rate 80 bpm, regular sinus rhythm, blood pressure 150/90 mmHg. On physical examination no injuries to the cranium, chest or abdominal cavity were clinically evident. Sonography (Focused Assessment with Sonography in Trauma (FAST)) did not reveal any fluid collections and the pelvis had been immobilized as described above. The left lower leg was evidently fractured on clinical examination. The patient underwent whole-body CT that revealed bilateral lung contusions, a fracture of the right transverse process of the 5th lumbar vertebra, a right sided sacral fracture and superior and inferior pubic rami fractures (Fig. ). The patient was taken to the operating room for supraacetabular external fixation of the pelvis and external fixation of the left lower leg. Upon arrival in the operating room provisional EPS was removed. Astonishingly, intraoperative fluoroscopy of the pelvis revealed a significantly wider pubic symphysis, suggestive of symphyseal disruption (Fig. ). In due course, internal fixation of the anterior pelvis was performed together with iliosacral screw fixation. Intraoperative complete symphyseal disruption was confirmed warranting extended plate osteosynthesis of the pubic symphysis (Fig. ). After converting the external fixation of the left lower leg to intramedullary nailing the further course of the patient was uneventful and the patient was repatriated on day eight after trauma.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [90.0, 'mm hg'], 'Systolic Blood Pressure': [180.0, 'mm hg']}",120,114,126,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 180.0 mm Hg + 2/3 * 90.0 mm Hg = 120.0 mm Hg.
Hence, the patient's mean arterial pressure is 120.0 mm Hg."
1370,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6462315-1,Extracted,"The patient is a 21-year-old African American man with a past psychiatric history of schizophrenia who was transferred from the psychiatry unit to the medical floor to rule out sepsis after the development of fever and tachycardia. The patient was reported to have decompensated on account of nonadherence with his home medications resulting in frequent hospitalizations and poor functioning. As per the patient's admission records, the patient's initial labs and urine toxicology were within normal limits. The patient had been on various antipsychotics since his diagnosis with schizophrenia at the age of 19, including haloperidol, olanzapine, and risperidone, but he continued to decompensate despite adequate medication trials. The decision was made to start the patient on clozapine due to possible failure of these previous antipsychotics. Clozapine was started at 25 mg PO twice daily and titrated up to 150 mg PO twice daily over the next 12 days. His current daily dose was 300 mg when he was transferred to the telemetry unit following a sudden development of fever and tachycardia on the psychiatric inpatient floor.
On the medical inpatient unit, the patient was mostly selectively mute and did not appear to be in any pain, was not vomiting, and had no diarrhea and no reported loss of consciousness or seizures. His admission vitals were a temperature of 102.4 degrees Fahrenheit, BP of 115/81 mmHg, HR of 114 beats per minute, and an oxygen saturation of 97% on room air. Physical examination did not reveal any significant findings other than a mild dehydration, no skin rash, no jugular venous distension, basal crepitation or pedal edema. Cardiac auscultative findings were largely normal except for a tachycardic heart rate; apex beat was in the 5th intercostal space, midclavicular line. The patient's heart sounds, S1 and S2, were normal, no rubs, or murmurs, and no obvious gallop rhythm. His peripheral extremities were warm with a normal capillary refill.
The patient was given an intravenous bolus of normal saline and a stat dose of intravenous antibiotics (vancomycin and meropenem), and full workup including 2 sets of blood cultures, urine analysis, and a chest radiograph was ordered. His complete blood count (CBC) revealed a normal leukocyte count of 7000/µl with elevated eosinophils of 500 (reference 0.0–400, see for trend) and normal platelet count. He had an elevated erythrocyte sedimentation rate (ESR) of 26 (reference 0–15 mm/Hour) and CRP was 147.4 mg/dl (reference 0.0–4.9 mg/dl).
In view of the patient's current clozapine use, a presumptive diagnosis of myocarditis was made and troponin I was requested which turns out to be markedly increased, 1.12 ng/dl (reference: 0.00–0.05 ng/dl). His NT-pro B-type natriuretic peptide (BNP), lactic acid, and creatine kinase levels were normal. His electrocardiogram (EKG) showed sinus tachycardia without specific ST-T changes ( below). His chest radiograph was unremarkable. Urinalysis and urine toxicology were negative. Initial transthoracic echocardiogram (TTE) revealed a left ventricular systolic dysfunction with apical hypokinesis (ejection fraction 45%) and mild tricuspid regurgitation. Coronary angiogram showed patent coronaries; ventilation/perfusion scan resulted as low probability for pulmonary embolism.
Clozapine was discontinued on admission to the medical unit. Subsequently, the patient's fever and tachycardia resolved. Troponin I trended down (lowest being 0.22 ng/ml). Eosinophil count initially increased but later normalized as shown in . Repeat transthoracic echo after one week of discontinuing clozapine revealed normal left ventricular systolic function with mild apical hypokinesis (ejection fraction of 60–65%). The patient was clinically stable throughout the hospital course. The psychiatry consult liaison team started the patient on aripiprazole which was well tolerated by the patient without any side effects. The patient later underwent an uneventful discharge to the community outpatient clinic.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [115.0, 'mm hg'], 'Diastolic Blood Pressure': [81.0, 'mm hg']}",92.33333,87.71666,96.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 81.0 mm Hg = 92.33333 mm Hg.
Hence, the patient's mean arterial pressure is 92.33333 mm Hg."
1371,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5830817-1,Extracted,"A 45-year-old female presented to our facility with a 3-month history of persistent headache and abdominal pain. She also complained of vertigo, blurred vision, and bilateral eye pain. She had a medical history significant for hypertension, hypothyroidism, and chronic Hepatitis B infection. Physical examination revealed blood pressure of 148/68 mmHg and pulse of 64/min, and diplopia was pronounced when looking to the right. Fundi were normal. Cardiovascular and respiratory system and abdominal examination were unremarkable. Computer tomographic (CT) scan of brain was normal. CT angiography of the head was negative for aneurysm or thrombus. Laboratory work was negative for complement levels, antinuclear antibody, anticardiolipin antibodies, and cryoglobulins. Hemoglobin and plasma biochemistry were normal. Erythrocyte sedimentation rate was elevated with a value of 60 mm/h and C-reactive protein of 15 mg/l. Urine microscopy was normal with no proteinuria. Hepatitis B surface antigen was positive and hepatitis B virus (HBV) DNA as detected by polymerase chain reaction revealed a viral load of more than 318,337 copy/ml. Renal angiogram, performed because of a suspicion of polyarteritis nodosa (PAN), showed multiple microaneurysms in the renal circulation []. The patient was started on steroid and tenofovir therapy with symptomatic improvement.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [68.0, 'mm hg'], 'Systolic Blood Pressure': [148.0, 'mm hg']}",94.66667,89.93334,99.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 148.0 mm Hg + 2/3 * 68.0 mm Hg = 94.66667 mm Hg.
Hence, the patient's mean arterial pressure is 94.66667 mm Hg."
1372,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4299690-1,Extracted,"A 70-year-old woman with severe abdominal pain and vomiting of 24-hour duration was admitted to our hospital. She had history of scleroderma and rheumatoid arthritis and had been taking steroids for 5 years. In addition, she received operations of thymoma with myasthenia gravis 31 years ago and stomach cancer (pT1AN0M0) 3 years ago. Her gynecological history was unremarkable, and there was no history of postmenopausal bleeding or vaginal discharge. On the physical examination, her abdomen was very tender and was distended and showed muscle rigidity. Rebound tenderness was absent. Bowel sounds were hypoactive. There was no palpable mass. Her blood pressure was 81/43 mmHg and pulse rate was 110 beats/min. Laboratory studies demonstrated a white blood cell count of 22,350 × 106/L and C-reactive protein at 32.39 mg/dL (normal range <0.3). Urgent computed tomography (CT) of the abdomen reported the presence of fluid and free intraperitoneal air mostly in the upper abdomen (), in addition to dilatation of upper small intestine. It was not possible to confirm the specific site of perforation accurately but it was suggestive of perforation of GI tract.
Following prompt resuscitation and intravenous antibiotics (flomoxef, 2 g/day, daily administration), laparotomy was performed, which confirmed the presence of free air and pus as well as an inflamed small intestine. Two thousand mL of pus was found to be present in peritoneal cavity. The rest of alimentary tract, gall bladder, and liver were normal. During peritoneal lavage, we found a perforation with a diameter of approximately 5 mm over fundus of the uterus. Total abdominal hysterectomy, copious saline lavage, and tube drainage were performed as a joint procedure. No colonic resection was deemed necessary. The uterus was soft and slightly enlarged. Retrospective review of the CT reported, in addition to the previously documented findings, a fluid-filled uterus with free air in the anterior wall (). Histological examination confirmed pyometra with no evidence of malignancy or cervical stenosis. Culture of the pus grew Bacteroides fragilis, Escherichia coli, and Eubacterium.
Postoperatively, intravenous antibiotics (flomoxef, 2 g/day) and sepsis treatment were continued and the patient was admitted to the intensive care unit with strict management of respiration and circulation. Her condition improved over time and she was transferred to the gynecological unit on postoperative day (POD) 4. However, she broke into decrease in blood pressure and saturation, pyrexia, and abdominal distension on POD 11. Although hepatic and renal dysfunctions were not revealed, sepsis and multiple organ failure were suspected. A contrast-enhanced CT showed the increased abdominal pus, and then vancomycin (1 g/day) and meropenem (1 g/day) were added to antibiotic therapy. Despite exhaustive clinical efforts, sepsis grew progressively worse and the patient died on POD 16.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [81.0, 'mm hg'], 'Diastolic Blood Pressure': [43.0, 'mm hg']}",55.66667,52.88334,58.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 81.0 mm Hg + 2/3 * 43.0 mm Hg = 55.66667 mm Hg.
Hence, the patient's mean arterial pressure is 55.66667 mm Hg."
1373,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7815671-1,Extracted,"A 28-year-old married housewife presented in the orthopedics outpatient department of tertiary care hospital in Central India with the chief complaints of pain in both thighs, more on the right side and difficulty in walking for the past 2 years. Pain had started spontaneously, was insidious in onset, and localized initially to both thighs. It increased with weight bearing, walking and household chores and partially got relieved on rest and medication. There was pain in elbow, wrist, and both hands for a few months initially. There was no history of fever, loss of appetite, loss of weight, or any change in menstrual cycle. Her joints’ pain and left thigh pain got completely relieved with drugs, but pain in the right thigh and hip area did not improve. She noticed progressively increasing difficulty in walking, squatting, and sitting cross-legged during the past 6 months. She started feeling rest pain in the right thigh and started taking stick support for the past 2 months. She had undergone repeated consultations, investigations, and treatment, but was not relieved of her symptoms.
Examination revealed painful gait with minimal weight bearing on the right lower limb. The patient was thin built with mild pallor and without any systemic abnormality. Her pulse was 84/minute and blood pressure 130/70 mmHg. Tenderness was present on upper one-third of right thigh and both pubic rami with adductor muscle spasm. Right hip rotations and abduction adduction were grossly restricted with flexion possible up to 70°. Left hip movements were normal except terminal restriction of flexion. There was no neurovascular deficit. Examination of other bones and spine did not reveal any abnormality.
A clinical diagnosis of Osteomalacia with Looser’s zone in pubic rami and incomplete fracture in right femur was considered. Metastatic lesions, multiple myeloma, or hyperparathyroidism with brown tumors were considered as differential diagnoses. The patient underwent X-rays of relevant areas. X-ray of pelvis with both hips ( and ) showed multiple small osteolytic lesions in both ilium and femur, thinning of cortices and uniting fractures in bilateral pubic rami. X-rays of both thighs ( and ) showed generalized osteoporosis, multiple lytic areas of 2–3 cm size separated with each other by a small zone of normal bone in upper one-third of shaft. There were two large osteolytic areas in the right shaft femur. The patient was admitted for prophylactic nailing in right femur in view of the impending fracture through the lytic areas (). She was given an above knee up to groin plaster slab and advised bed rest. In the left femur, the osteolytic areas were relatively smaller, cortices were thicker and there was no immediate risk of an impending fracture. Hence, fixation of left femur was not considered. X-rays of skull, chest, lumbar spine, feet, and hands did not show any obvious abnormality. Old magnetic resonance imaging (MRI) of thighs suspected the small lytic lesions in both femora as simple bone cyst. Fresh MRI with contrast ( and ) showed multiple intramedullary solid cystic lesions of varied size in both pubic rami, ischium, iliac blades, and upper and middle one-third of both femora probably due to browns tumor. USG of neck suggested the possibility of parathyroid adenoma of size 37 mm × 19 mm. Contrast-enhanced CT scan of neck showed well defined heterogeneously enhancing nodular mass lesion of size 33 mm × 24 mm × 23 mm just posterior to the right lobe of thyroid, suggestive of parathyroid adenoma with lytic lesions in the base of skull and in the right occipital bone. USG-guided fine-needle aspiration cytology from lytic lesion over right iliac crest showed only hemorrhagic background without any cellularity.
Patient’s complete blood count, erythrocyte sedimentation rate, C-reactive protein, rheumatoid factor, and urine examination were normal. She had hypercalcemia and hyperparathyroidism with serum calcium level of 10.78 mg/dl, PTH 1632 pg/dl, ALP 1686 IU/L, and Vitamin D3 24 ng/ml. Serum calcium, PTH, ALP, and Vitamin D3 levels done on various occasions are summarized in .
While indoor, the patient tried going to bathroom and fell down, leading to fracture through the lytic area in the right proximal femur (). The fracture was surgically stabilized with long proximal femur nail and static locking (). Open biopsy from lytic lesion was done after stabilization of fracture. The biopsy showed fibro-collagenous tissue having sheets of cells with adequate amount of eosinophilic granular cytoplasm and centrally placed nucleus without any malignant features. Per-operatively, the lytic area was very soft containing reddish brown friable tissue. Bony destruction was gross causing gap in cortical continuity at pathological fracture site despite nailing. Her post-operative period was uneventful. She was transferred to surgical unit for right parathyroid adenoma excision which was done successfully. The excised adenoma was of size 2.5 cm × 2.5 cm × 1 cm. Its histology showed typical features of adenoma without any features of malignancy and vascular or capsular invasion (). Immediately after adenoma excision she was kept on supportive intravenous calcium supplementation to avoid hypo-calcemic crisis (Hungry bone syndrome). The post-operative protocol followed was: Static quadriceps and hamstring exercises with active hip, knee, and ankle mobilization in bed for 2 weeks. After this, bedside knee mobilization and non-weight bearing mobilization with walker was started gradually. Patient was kept non-weight bearing for 12 weeks, followed by partial weight bearing with walker. Oral calcium and Vitamin D supplementation were continued. A 3 monthly follow-up was continued for clinical, radiological and serum calcium, and PTH estimation. She became asymptomatic at 6 months with near normal serum parameters and was permitted to walk with stick support. At 1 year (), her fracture had consolidated satisfactorily; lytic lesions had almost disappeared and the patient was having full range of hip movement with normal weight bearing without support. The X-ray of left femur at 1 year is shown in . Serum calcium and PTH values had returned to normal. She conceived 1 year after the surgery and delivered a full-term normal baby. At 2 years follow-up, there is no pain in any bone, the right lower limb is shorter by 0.5 cm and her gait is normal. Patient is able to squat but has difficulty in sitting cross legged due to moderate restriction of external rotation in right hip. Nail removal is planned in a few months. The serum calcium, PTH, ALP, and Vitamin D levels are normal and majority of the brown tumors had regressed. The patient is asymptomatic and leading a normal life.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 70.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1374,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7370341-2,Extracted,"A 60-year-old-male with no significant past medical history presented with an acute abdomen. His hemodynamic status was unstable; blood pressure and heart rate were 80/50 mmHg and 111 beats/minute, respectively. CT revealed possible hemorrhagic ascites mainly involving the left greater omentum and dilated, stenotic change of the left OA with the possible hematoma, which was compatible with a sentinel clot sign (Fig. a). In addition to such characteristic CT findings, taking into consideration being a middle-aged male without apparent arteriosclerosis, acute-onset symptoms and negative laboratory screening test results and clinical findings suggesting vasculitis, SAM-associated left OA bleeding was suspected, and TAE was planned after written informed consent for the embolization procedure was obtained from the patient.
Celiac artery angiography revealed dilated, stenotic change of the right and left hepatic arteries, right gastroepiploic artery, and left OA. Left OA angiography revealed proximal dilated and stenotic change with distal occlusion (Fig. b). Despite having no signs of active bleeding, review of the CT and angiography findings suggested the left OA as the bleeding site because of CT sentinel clot sign. Because left OA was considered as the most likely bleeding site based on CT sentinel clot sign and because he was hemodynamically unstable, TAE was performed. Given that proximal embolization at this point could lead to incomplete hemostasis or rebleeding via arterial collateral network between OAs, an attempt was made to navigate the microcatheter into the distal side beyond the occluded point, which was achieved without complications. The distal OA over the occluded point was intact and directly communicated with a right OA arising from right gastroepiploic artery (Fig. c). The SAM-associated lesion was successfully isolated with 13 coils (10 C-STOPPER Filling COILs, PIOLAX, Yokohama, Japan and 3 Tornade Embolisation Coil, COOK MEDICAL, Bloomington, IN, USA). Angiography of the proximal left OA and right gastroepiploic artery confirmed complete hemostasis (Fig. d). The patient’s hemodynamic status improved, with a blood pressure and heart rate of 113/75 mmHg and 93 beats/minute. During his clinical course in our hospital, he had no abdominal pain or anemia, and he was transported to another hospital on hospital day 3. Based on a follow-up phone call, he has not experienced any symptoms associated with SAM such as abdominal pain during the one-year follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [80.0, 'mm hg'], 'Diastolic Blood Pressure': [50.0, 'mm hg']}",60,57,63,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 80.0 mm Hg + 2/3 * 50.0 mm Hg = 60.0 mm Hg.
Hence, the patient's mean arterial pressure is 60.0 mm Hg."
1375,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5523346-1,Extracted,"A 71-year-old female with a history of peripheral neuropathy of unknown etiology presented with a one-year history of intermittent pallor of both hands which was precipitated with cold objects. She fell from a chair onto her elbows and hands one year earlier, but no fractures or dislocations were sustained. There was no history of rest or claudication pain and no prior instrumentation of the vessels. She had no family history of autoimmune or hypercoagulable conditions and no history of smoking, alcohol, or illicit drug use.
On examination, her blood pressure was 120/60 mmHg on the right arm and 100/50 mmHg on the left, pulse 86 beats per minute, and respiratory rate 18 breaths per minute. Her radial pulses were reduced bilaterally. There were no sensory deficits in her bilateral upper extremities and no palmar atrophy. Other aspects of her clinical examination were unremarkable. There was no pallor or cyanosis of the palms of her hand at the encounter. However, prior photos taken showed marked pallor of the distal fingers of the palms of both hands (Figures and ). Laboratory investigations including autoimmune screen, ESR, CRP, and prothrombotic panels were unremarkable. HIV testing was negative. Echocardiography was normal with an ejection fraction of 65–70%. CT angiography showed a focal right brachial artery stenosis and a short segment 2 cm occlusion of left brachial artery with distal reconstitution by muscular collateral branches. She further underwent conventional angiography which showed tapered high grade stenosis of the proximal right brachial artery () and on the left a short focal tapered occlusion, with likely dissection of the left brachial artery reconstituted with collateral muscular branches ().
Treatment was undertaken on the right with low pressure balloon angioplasty across the affected segment. After angioplasty there was modest improvement in luminal diameter with no extravasation of contrast and a 5 mm × 5 cm Viabahn covered stent was inserted and then postdilated with 4 mm mustang balloon. Repeat angiography showed excellent positioning of the stent and no residual stenosis. Runoff angiogram showed widely patent runoff arteries (). A stent was applied to the focal dissection on the left and a 5 mm mustang angioplasty balloon was advanced across the occluded segment and used for low pressure balloon angioplasty. The occluded segment was stented with 2 overlapping stents, 5 mm × 2.5 cm Viabahn stents. The stents were postdilated with a 5 mm mustang balloon. Poststent angiogram showed good poststenting positioning and no residual stenosis and unimpeded flow of contrast to the hand (). There was no evidence of embolic phenomenon. There were no postprocedural complications and dual antiplatelet therapy with aspirin and clopidogrel was commenced. Five months later the patient remained asymptomatic without further episodes of hand pallor.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [60.0, 'mm hg'], 'Systolic Blood Pressure': [120.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 60.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1376,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-6760,Extracted,"A 28-year-old woman presents to the clinic with complaints of occasional low-grade fever and joint pain for 1 month. She also complains of morning stiffness in the proximal interphalangeal joints of both hands, which lasts for 5 to 10 minutes. She recently noticed a pink rash on her nose and cheekbones. Her family history is significant for similar complaints in her mother. She is not taking any medications. On examination, her temperature is 37.6°C (99.6°F), pulse is 74/min, blood pressure is 110/70 mm Hg, and respirations are 18/min. Aphthous ulcers are noted on her oral mucosa.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1377,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5366192-1,Extracted,"A 67-year-old female with previous medical history of inactive pulmonary sarcoidosis (), hypertension, and impaired glucose tolerance, presented to emergency department with five-day history of nausea, vomiting, abdominal pain, and constipation. On physical examination she was alert, oriented, and not in acute distress. Her vital signs were as follows: Temp 36.7°C; pulse 93 bpm; respiratory rate 18 bpm; blood pressure 147/85 mmHg; and O2% of 98% on room air. Her abdomen was distended and mildly tender over the epigastric area, with no evidence of organomegaly. Her bowel sounds were hyperactive. Initial imagining studies with abdominal X-ray revealed dilated small-bowel loops with multiple scattered air fluid levels suggesting partial versus early complete small-bowel obstruction. A contrasted computed tomography (CT) scan of the abdomen and pelvis demonstrated multiple dilated loops of proximal small bowel with no definitive transition point and no intraperitoneal free air or fluid identified, a picture suggestive of a high-grade small-bowel obstruction ().
She was managed conservatively with bowel rest, nasogastric tube, and IV fluids. Her symptoms failed to improve, so gastrografin small-bowel follow-through was performed and demonstrated failure of contrast to pass into the colon ().
General surgery was consulted and diagnostic laparoscopy was performed and revealed multiple dilated bowel loops which revealed diffuse skin tag appearing lesions on the antimesenteric surface of the midjejunum causing inflammatory adhesions to the mesentery (). The bowel was completely viable with no additional lesions in the liver, stomach, or visible parts of the colon. Histopathologic examination of tissue biopsy revealed lymphohistiocytic noncaseating granulomatous inflammation with multinucleated giant cells, consistent with sarcoidosis (). Further evaluation revealed negative acid-fast bacilli and fungal and viral tissue cultures. Her postoperative course was uncomplicated and she was discharged on prednisone taper dose with close outpatient follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [85.0, 'mm hg'], 'Systolic Blood Pressure': [147.0, 'mm hg']}",105.66667,100.38334,110.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 147.0 mm Hg + 2/3 * 85.0 mm Hg = 105.66667 mm Hg.
Hence, the patient's mean arterial pressure is 105.66667 mm Hg."
1378,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6537048-1,Extracted,"A 78-year-old Hispanic female with a significant past medical history of type 2
diabetes mellitus, hypertension and hypothyroidism presented with altered mental
status. She was brought to the emergency department by her family members who
assisted with history gathering. According to her family, the patient had a cough
and worsening shortness of breath over 3 days prior to admission unrelieved by
over-the-counter antihistamine and antitussive medications. The family did not know
how long she had been diabetic or hypertensive. Nor could they list her medications.
Upon presentation she was lethargic, had labored breathing and was lying in bed
shaking. Her blood pressure was 142/67 mmHg in the supine position, heart rate
114 bpm, axillary temperature 36.7°C and she weighed 51.7 kg. On physical
examination, she was ill-appearing, obtunded, not following verbal commands and with
Glasgow coma scale of 9. She had decreased breath sounds over the left lung lower
field. The examination of the heart, abdomen and extremities was normal. On
neurological examination, she had hyperreflexia at the patellar and ankle joints, as
well as stimulated bilateral clonus and positive Babinski sign. The screening blood
tests performed upon her admission to the hospital were consistent with severe HHS.
Her initial laboratory findings revealed glucose 635 mg/dL (normal: 70–105), sodium
175 mEq/L (corrected Na: 188 mEq/L) (normal: 135–145 mEq/L), blood urea nitrogen
(BUN) 76 mg/dL (normal: 6–20 mg/dL), creatinine 1.61 mg/dL (normal: 0.5–1.2 mg/dL)
with a serum osmolality 410 mOsm/kg (normal: 280–300 mOsm/kg). Her urine ketones
were negative. On arterial blood gas her pH was 7.43, and HCO3 29 mEq/L
(normal: 22–29). Her initial hemoglobin (Hgb) was 16.8 g/dL, white blood cell count
(WBC) 18.3 × 103/µL and platelet count 194 × 103/µL. The
initial chest X-ray and noncontrast head computed tomogram (CT) were negative with
the head CT showing only mild diffuse cortical atrophy, proportional to the size of
the ventricular system. The calculated water deficit on admission was about 5.5 L.
In the emergency department, aggressive fluid resuscitation for volume replacement
was started using normal saline (NS), which initially caused worsening in sodium
values to 180 mEq/L (corrected Na: 193 mEq/L). After 2 L of NS, WBC was
23.2 × 103/µL, Hgb was 15.1 g/dL, platelet was
160 × 103/µL and her HCO3 was within normal limits in our
laboratory at 28 HCO3 mEq/L. She was admitted to the intensive care unit
(ICU), and nephrology was consulted. She was started on 0.45% NS and subsequently
switched to 5% dextrose in water. The sodium began to trend down, while maintaining
a mean steady decrease of 6 mEq/L of sodium daily, resulting in desired sodium range
within 5 days ().
An insulin drip was placed to control the severe hyperglycemia, which resolved
steadily over the first 48 h. The insulin drip was discontinued, and insulin
glargine with correctional insulin lispro was started. An abdominal pelvic CT was
negative. Due to her neurological findings, a continuous EEG (cEEG) was ordered,
which showed left frontocentral and temporal PLEDs on day 1. By day 2, the cEEG
showed only abnormal slowing without epileptiform discharges. During the
hospitalization, a nasogastric tube was placed and tube feeds were started due to
her poor mentation. Her kidney function improved and returned to baseline. She was
also found to have a left lower lobe infiltrate and was treated for community
acquired pneumonia. She was initially treated with ceftriaxone and azithromycin;
however, over the hospital course she clinically improved and was switched over to
oral cephalexin to finish the course. Her mental status improved and returned back
to baseline. In order to prevent potential aspiration, she underwent a successful
swallow study with modified barium and was started on regular diabetic diet. She
stayed in the hospital for 7 days and was diagnosed with severe hypernatremia
secondary to osmotic diuresis and dehydration from HHS. Her hemoglobin A1c was found
to be 9.9%, and upon discharge, she was placed on metformin, insulin glargine and
insulin lispro sliding scale. Due to her decline in functional status and
deconditioning, she was discharged to a skilled nursing facility. She received
diabetes teaching, which included lifestyle modifications, proper nutrition, insulin
administration and glucose checks. Unfortunately, there was no good follow-up with
the patient, because she returned to her home abroad.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [142.0, 'mm hg'], 'Diastolic Blood Pressure': [67.0, 'mm hg']}",92,87.4,96.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 142.0 mm Hg + 2/3 * 67.0 mm Hg = 92.0 mm Hg.
Hence, the patient's mean arterial pressure is 92.0 mm Hg."
1379,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-1635700-1,Extracted,"A 30-years-old woman was admitted to the emergency department with upper abdominal pain. The patient had been well until the day before, when she began to have pain in the epigastrium. A few hours before admission the pain, which was now localized to the upper right abdominal quadrant, became constant and severe. Anorexia and nausea developed, followed by vomiting.
The patient had a previous history of hepatic hydatid disease. Two months earlier she underwent an abdominal ultrasound for abdominal pain during admission in another hospital. Following that exam, the patient underwent magnetic resonance imaging (MRI) which was diagnostic for hepatic hydatid cyst. For this reason the patient was on mebendazole for about 2 weeks until the last hospital admission. She took an oral contraceptive for about six months in the past and was not on any other medication.
The temperature was 39°C, pulse 96 and blood pressure was 100/70. The oxygen saturation was 98 % while the patient was breathing ambient air. On physical examination the patient appeared in severe pain. Lungs and heart sounds were normal. The abdomen was distended, and bowel sounds were absent. There was tenderness in the right upper quadrant and epigastrium, with guarding and rebound tenderness. No abnormalities were found on rectal examination.
The hematocrit was 30%, hemoglobin 10 g/dl, red blood cells 3.3 × 103 mm3, white cell count 13.7 × 103 mm3, and neutrophils were 84.4 %. The remaining lab tests and urine were normal. Since it was an emergent setting, no further attempts were made to confirm echinococcus infestation. Abdominal ultrasound and contrast-enhanced computerized tomography (CT) scan of the abdomen showed a 9 × 11.8 × 10 cm cyst localized in the IV, VII and VIII hepatic segments, with multiple smaller cysts inside (Figure ). The cyst was located just posterior to the portal branch for the VII and VIII segments (Figure ). It compressed the inferior vena cava and the right and medial hepatic vein. The wall of the cyst was detached from the hepatic parenchyma as for hemorrhagic leak. Posteriorly to the hepatic peduncle, the wall of the cyst emerged at liver surface, just underneath the Glisson's capsule. Also, the adipose tissue between the liver on one side and the right adrenal gland and right kidney on the other showed signs of haemorrhage.
The patient was brought to the operating room in an emergent setting. Bilateral subcostal incision was performed. At the opening of the peritoneal cavity a small amount of clear fluid was found. Intra-operative liver ultrasound was employed. A voluminous hepatic cyst was found, which emerged to the liver surface at the level of caudate lobe and was extended up to the VIII segment. The cyst was evacuated of its content which was a brown-colored mucinous fluid. The intracystic fluid was sent for bacterial culture and evaluation for parasitic infestation. Hypertonic saline solution (33%) was injected into the cyst as a precaution in case of parasitic infestation. Partial pericystectomy was performed at the level of the caudate lobe. Ultrasound confirmed the complete evacuation of the cyst. Cholecystectomy was carried out due to the presence of biliary sludge. A biliary cystadenoma was confirmed at histologic evaluation. Sections 3 μm thick were cut and stained with hematoxylin and eosin. The sections were immunostained with primary antibodies directed against vimentin (1:100 dilution; Dako), muscle-specific actin (1:100 dilution; Dako, clone HHF35), and desmin (1:100 dilution; Dako, clone D33). Immunodetection was performed using Universal Dako Cytomation LSAB + KIT, Peroxidase. Section analysis revealed multiple communicating locules of different size. The locules were lined by columnar, cuboidal or even flattened epithelium (Figure ). This was surrounded by a layer of highly cellular, mesenchymal tissue resembling ovarian stroma. The stromal cells were diffusely positive for vimentin and muscle specific actin, and focally positive for desmin. Cystic fluid analysis showed elevated levels of carbohydrate antigen (CA) 19.9 (126387.10 UI/ml) while serum CA 19.9, carcinoembryogenic antigen (CEA) and α-fetoprotein were within the normal range. Cultures returned negative.
Post-operative course was uneventful and the patient was discharged on post-operative day 8. After complete recovery, the patient was admitted again to our Unit for definitive treatment. Before undergoing re-operation, the patient was re-evaluated with a new abdominal CT scan which showed the partial collapse of the cyst. Patient was brought to the operating room, where she underwent caudate lobectomy and posterior segmentectomy, including segmentectomy of segments VI and VII, and atypical segmentectomy of segment IV. Intra-operative ultrasound was used to evaluate the relationship of the cyst with adjacent structures. Since a communication between the cystadenoma and the biliary tree was found, a cholangiogram followed by a single suture closure of the biliary communication was performed. Histology confirmed the previous diagnosis of biliary cystadenoma. Postoperative course was uneventful and the patient was discharged on postoperative day 8. Follow-up abdominal CT scans showed no local recurrence and the patient is doing fine 15 months after hepatic resection.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 70.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1380,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5517,Extracted,"A 27-year-old woman presents to her primary care physician with a chief complaint of pain in her hands, shoulders, and knees. She states that the pain has lasted for several months but seems to have worsened recently. Any activity such as opening jars, walking, or brushing her teeth is painful. The patient has a past medical history of a suicide attempt in college, constipation, anxiety, depression, and a sunburn associated with surfing which was treated with aloe vera gel. Her temperature is 99.5°F (37.5°C), blood pressure is 137/78 mmHg, pulse is 92/min, respirations are 14/min, and oxygen saturation is 98% on room air.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [78.0, 'mm hg'], 'Systolic Blood Pressure': [137.0, 'mm hg']}",97.66667,92.78334,102.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 137.0 mm Hg + 2/3 * 78.0 mm Hg = 97.66667 mm Hg.
Hence, the patient's mean arterial pressure is 97.66667 mm Hg."
1381,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3910070-1,Extracted,"A 74-year-old female patient applied to our clinic with the complaints of fatigue, loss of appetite, weight loss. She had lost five kg in the last two months during which she had the complaints. In tests conducted by another center, high erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) values had been detected, and for evaluation she was referred to our hospital with malignity and infection prediagnoses. When detailed anamnesis was taken, she was found to have complaints of fever, one-sided headache, and claudication. She had no diseases other than hypertension from which she had suffered for 10 years.
Physical examination determined the following findings: body temperature, 36.8°C; heart rate, 80 beats/min and rhythmic; blood pressure, 130/80 mmHg. Left temporal artery was tender with palpation and scalp was aching. There was no pathological finding in lung and cardiac examination. In abdominal examination, there was no abnormality other than slight tenderness in right, upper quadrant upon deep palpation. Other system examinations were normal.
Laboratory test findings were as follows: ESR: 120 mm/hr, CRP: 181 mg/L (0–5), leucocyte: 10400/mm3 (4000–11000), Hgb: 9.9 g/dL (11–18), Plt: 611000/mm3 (150000–400000), MCV: 83 fL (80–100), ferritin: 473.6 ng/mL (13–150), ALT: 67 U/L (7–35), AST: 51 U/L (10–38), ALP: 307 U/L (35–270), GGT: 406 U/L (5–61), total bilirubin: 0.32 mg/dL (0.01–1.2), albumin: 2.3 gr/dL (3.4–5.5), INR: 1.23. Kidney and thyroid functions were within normal ranges and no abnormality was found in urine tests. Rheumatoid factor, anti-nuclear antibody, anti-neutrophilic cytoplasmic antibody, and brucellosis agglutination were negative. Immunoglobulin levels were normal. Hepatitis and other viral serological tests turned out to be negative. There was no characteristic in lung radiography and no pathology was detected in abdominal USG. The patient had no visual problems and fundoscopic examination did not reveal any abnormality.
The patient had high ESR and CRP values in addition to fever complaint. Procalcitonin value was 0.18 and no growth was observed in blood and urine cultures. No infection source was determined, and therefore antibiotic treatment was not started. In echocardiography of the patient, pericardial effusion was detected. Left ventricular diameter and functions were within normal limits. There was an effusion (10–12 mm) which surrounded the heart all the way but did not cause cardiac tamponade or hemodynamic instability. Electrocardiography was normal except for low voltage.
Based on the available clinical and laboratory findings, GCA was considered and temporal artery biopsy was conducted. Results of biopsy confirmed GCA (Figures and ). A 60 mg/day prednisolone treatment was started. After the treatment, clear improvements were observed in clinical conditions of the patient. A week later, ESR, CRP, and liver function tests decreased to normal levels. In the follow-up echocardiography, pericardial effusion was remarkably decreased. Steroid dose administered was gradually lowered. At the end of one year, the patient who was continuing to take 10 mg/day maintenance level of steroid was stable in terms of clinical status and laboratory values. In echocardiography, pericardial effusion was completely disappeared.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1382,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6436364-1,Extracted,"A 72-year-old woman presented to the emergency room with gastrointestinal symptoms and hypokalemia. Air in the sigmoid colon mesentery and a solid pancreatic head mass were noted on CT of the abdomen/pelvis (). Sigmoid diverticular perforation and a small pericolonic abscess were confirmed on subsequent Hartmann procedure. With cushingoid features, the Endocrinology service was consulted postoperatively. Collateral history from her family revealed a recent general decline in health and the development of signs and symptoms of hypercortisolism over the past 12 months. On exam, in addition to a cushingoid appearance, obesity (body mass index of 40) and mild hypertension (blood pressure 145/77 mmHg) were noted. Investigations were consistent with ectopic ACTH-dependent hypercortisolism from a pancreatic neuroendocrine tumor (). MRI sella was contraindicated because she had a pacemaker, but no pituitary adenoma was visible on CT of the head. Inferior petrosal sinus sampling was not completed because the patient was unstable. Treatment with metyrapone, followed later by the addition of ketoconazole was initiated with some benefit. Short-acting octreotide was added based on a positive octreotide scan (). Metyrapone and ketoconazole were discontinued several days later due to a significant drop in serum cortisol on octreotide. Given her recent Hartmann procedure and clinical instability, surgery was not an option. Almost one month after initiation of octreotide, she became hypotensive and unresponsive from a suspected intracranial hemorrhage. Her family decided against further medical intervention. A postmortem examination was not performed.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [145.0, 'mm hg'], 'Diastolic Blood Pressure': [77.0, 'mm hg']}",99.66667,94.68334,104.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 145.0 mm Hg + 2/3 * 77.0 mm Hg = 99.66667 mm Hg.
Hence, the patient's mean arterial pressure is 99.66667 mm Hg."
1383,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5397793-1,Extracted,"A 15-year-old boy presented to our University Hospital, a tertiary care neurology facility, with fever, headache, and altered sensorium of 12-day duration. At admission, he was febrile (101 °F), with a pulse rate of 110/min and a blood pressure recording of 114/74 mmHg; his Glasgow Coma Scale score was 10 (E3M4V3). There were no petechiae or signs of bleeding over the skin or any mucosal surface. There was no focal neurological deficit and neurological examination was normal, including (absence of) signs of meningeal irritation. Laboratory evaluation revealed the following estimations: hemoglobin of 11 g/dl, total leukocyte count of 3300 cells/mm3, and platelet count of 22,000 cells/mm3 which dropped to 8000 cells/mm3 on next day. His aspartate aminotransferase level was 155 U/L, alanine aminotransferase was 140 U/L and alkaline phosphatase was 56 U/L. Additional biochemical parameters, renal function tests, blood sugar, electrolytes, and arterial blood gas analysis, were normal. Malarial parasite was not detected in the peripheral blood smear. The cerebrospinal fluid examination, cytological and biochemical, was normal. IgM antibody against dengue virus was positive both in serum and cerebrospinal fluid; meanwhile, dengue NS1 antigen was negative. Electroencephalography revealed generalized slowing. On magnetic resonance imaging of the brain, signal changes were seen in bilateral parietooccipital and left frontal region (left hemisphere was more involved than the right hemisphere). There were diffuse subcortical white matter changes along with suggestion of hemorrhage on gradient echo sequence. Subtle hyperintensity on T2 W images was also noted in bilateral basal ganglia. Gadolinium-contrast study revealed a gyriform enhancement suggestive of cortical laminar necrosis (Fig. ). He was managed conservatively and given platelet transfusion. The patient responded well to management and became fully conscious in 7 days.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [114.0, 'mm hg'], 'Diastolic Blood Pressure': [74.0, 'mm hg']}",87.33333,82.96666,91.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 114.0 mm Hg + 2/3 * 74.0 mm Hg = 87.33333 mm Hg.
Hence, the patient's mean arterial pressure is 87.33333 mm Hg."
1384,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2771816-1,Extracted,"A 41-year-old male with a history of cigarette smoking sought evaluation at the emergency room due to pain in the anterior chest and epigastrium of 35 hours duration. At the time of onset of the chest pain, he was isolated on an island and unable to access transportation for transfer to the hospital. On registration in the emergency department, the patient's vital signs were as follows: temperature, 37.1℃; heart rate, 116 beats per minute; blood pressure, 130/90 mmHg; and pulse oximetry, 98% on room air. The electrocardiogram (ECG) showed marked ST segment elevation in the precordial leads (). The results of laboratory tests were notable for a white blood cell count of 1,7540/mm3 and elevated cardiac biomarkers. The C-reactive protein was elevated to 151.54 mg/dL. An echocardiographic examination revealed akinesia of the left ventricular septum and severe left ventricular dysfunction. He subsequently underwent coronary angioplasty and stenting of the left anterior descending artery using two sirolimus-eluting stents ().
One day after the PCI, the patient complained of severe pleuritic chest pain radiating to both shoulders and the lower jaw. On physical examination, pericardial friction rubs and a crunching sound were heard over the precordium. The erythrocyte sedimentation rate was elevated to 120 mm/h. A repeat echocardiogram was performed, and the results were unchanged. Computed tomography (CT) showed small gas bubbles around the aortic wall and mild pericardial thickening with subtle air densities suggesting acute mediastinitis (). Based on these results, the patient was diagnosed with PCIS and acute mediastinitis, and was given oral ibuprofen and broad-spectrum intravenous antibiotics (ceftriaxone, aminoglycoside, and lingcosimide). The patient began to feel some subjective improvement within 24 hours and the pericardial friction rub was no longer heard on physical examination. The antibiotics were terminated on the 6th day. A chest CT was repeated; the previously noted soft tissue density lesion surrounding the ascending aortic wall and the subtle streaky fatty infiltrations with small gas bubbles had resolved. However, multiple low-density nodules were noted in the apex of the left ventricle, suggesting acute thrombi (). Thus, intravenous heparin with oral warfarin treatment was started. The patient was discharged from the hospital on the day 17 with persistent apical mural thrombi.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 90.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
1385,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-3538,Extracted,"A 47-year-old woman with metastatic breast cancer who is undergoing chemotherapy comes to the physician for a follow-up exam. She reports extreme fatigue since beginning her chemotherapy regimen. Her pulse is 98/min, respirations are 16/min, and blood pressure is 132/84 mm Hg. Her hemoglobin is 10.4 g/dL, leukocyte count is 800/mm3 with 5% monocytes, and platelet count is 50,000/mm3. The patient is started on a new medication. One week later, serum studies show a hemoglobin of 10.6 g/dL, a leukocyte count of 2,000/mm3 with 2% monocytes, and a platelet count of 56,000/mm3.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [84.0, 'mm hg'], 'Systolic Blood Pressure': [132.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 132.0 mm Hg + 2/3 * 84.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1386,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3345141-1,Extracted,"A 40-year-old female presented with complaints of dyspnea and palpitation on exertion since 1 month prior to admission, which had been insidious in onset and progressive. There was no history of orthopnea or paroxysmal nocturnal dyspnea. There was a history of occasional retrosternal chest pain, nonradiating and anginal in character. On examination, she was pale, had a pulse of 88/min, which was regular, with average volume, blood pressure (BP) of 110/80 mm of Hg. Her jugular venous pulse (JVP) was normal; also, there were no signs of congestive cardiac failure (CCF). On cardiovascular examination, the apex was present in the 6th intercostal space (ICS) on the right side, lateral to mid clavicular line; right parasternal heave and diastolic shock were also present. First heart sound was loud and there was a wide, fixed split second heart sound. There was a mid diastolic murmur present at the apex and a systolic murmur present at the right parasternal area at the 3rd–4th ICS. There were no rales or wheeze on auscultation of lungs. There was no hepatomegaly or pedal edema.
A chest X-ray was done which showed a right-sided cardiac shadow with presence of cardiomegaly.
2D echocardiography revealed dextrocardia, situs inversus, concordant atrio-ventricular (AV) connection, large-size (12 mm) ostium secundum type of atrial septal defect (ASD) with bidirectional shunt []; dilated right atrium and ventricle; concordant ventriculo-arterial connection (aorta arises from the left ventricle and pulmonary artery arises from the right ventricle); intact interventricular septum; normal biventricular function; and mild to moderate tricuspid regurgitation. Mitral valve was thick, pliable with commissural fusion and doming of anterior mitral leaflet []. Moderate pulmonary regurgitation was present and mean pulmonary artery pressure was 35 mm of Hg. Mitral valve area was 1.60 cm []. Tricuspid, aortic and pulmonary valve were normal. There was no evidence of patent ductus arteriosus. Total anomalous pulmonary venous connection or coarctation of aorta. Mild to moderate pericardial effusion was present []. The patient also underwent an ultrasound examination of the abdomen which showed liver on the left side, confirming situs inversus [].
Pericardiocentensis was done. Pericardial fluid was straw colored and had a protein (albumin) content of 3.2 g/dl and showed lymphocytosis consistent with tubercular pericardial effusion. The patient was started on antitubercular treatment.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 80.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1387,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3125005-1,Extracted,"A 60-year-old woman with insignificant history, who had been taking low-dose Cabergoline 0.25 mg for hyperprolactinemia (micro prolactinoma) from last four years, presented with one and half month history of increasing ankle swelling, abdominal discomfort, and exertional breathlessness. On examination, she had a regular pulse of 88 beats per minute. Her blood pressure was 140/85 mmHg, her jugular venous pressure was elevated, and she was having pitting edema to her mid calves. Heart sounds were dual, with systolic murmurs audible along left sterna border with positive carvello's sign and she was also having tender hepatomegaly. These clinical findings were suggestive of right heart failure. ECG showed sinus rhythm with rate of 90 beats per minute. A chest X-ray showed borderline cardiomegaly with clear lung fields. There was no evidence of interstitial edema or fibrosis or pleural effusions. Blood tests were normal. Echocardiography showed moderate tricuspid regurgitation [] and mild pulmonary arterial hypertension, without any regional wall motion abnormality or dilated right ventricle, also no sign of rheumatic heart disease (RHD) and ejection fraction (EF) was 67%. Cabergoline was stopped and patient was put on furosemide and spironolactone. There was an excellent clinical response to this diuretic regimen.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 85.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
1388,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8411108-2,Extracted,"A 42-year-old man of South Asian background recently diagnosed with AKU was referred for further management at first visit (Tables and , Figure ). He has bilateral ear and eye ochronosis, nail ochronosis, previously passed renal stones at age 27 years, dyspepsia, angina, generalized spondylosis affecting, cervical, thoracic and lumber spine, with generalized joint pains. He is one of the siblings mentioned in case 1. He was 1.67 m and weighing 70 kg, with a blood pressure of 116/74 mm Hg. His medications consisted of buprenorphine patches, co-codamol, vitamin C, vitamin D, cetirizine, and beclomethasone cream. He was commenced on nitisinone 2 mg alternate days for 3 months and then the dose was increased to 2 mg daily. At the 2-year visit, an increase in skin pigmentation was noticed in the dorsal aspects of the thumb and middle finger of the right hand. At the 3-year visit, he mentioned increased discoloration of the skin in the genital region. At his 4-year visit, he was diagnosed with vitiligo affecting his scalp, periorbital regions, and groin. His sister with AKU also had systemic lupus erythematosus and has not developed vitiligo so far despite also being on nitisinone 2 mg for 5 years. Five years after the baseline visit, the vitiligo had extended to involve his trunk. He was on the following mediations at this time namely, nitisinone 2 mg, buprenorphine patches (5 mg patch), co-codamol (codeine 50 mg, paracetamol 500 mg), vitamin C (1 g), vitamin D (800 units), cetirizine 10 mg, cream containing betamethasone and clotrimazole, omeprazole 20 mg, pregabalin 75 mg, testosterone 2% gel, clenil modulite 200 mcg inhaler twice a day. At the 6-year visit, vitiligo had extended to all over his body including the covered areas, forehead, armpits, around his groin and his left hand. Topical steroid cream made no difference.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [74.0, 'mm hg'], 'Systolic Blood Pressure': [116.0, 'mm hg']}",88,83.6,92.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 116.0 mm Hg + 2/3 * 74.0 mm Hg = 88.0 mm Hg.
Hence, the patient's mean arterial pressure is 88.0 mm Hg."
1389,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3391813-1,Extracted,"A 43-year-old man, who is known to have autosomal dominant polycystic kidney disease (ADPKD), systemic hypertension, and chronic kidney disease (on conservative management) for the last five years, was admitted in our Institute with symptoms of bilateral flank pain, fever, and macrohematuria of two days duration. He had a progressive worsening of renal functions over five years. On examination, he was conscious, oriented, pale, toxic, and febrile (Temperature: 103 degree F). Pulse rate was 120/minute and regular, Blood pressure was 130/70 mmHg, and respiratory rate was 26/minute. He had bilateral enlarged kidneys, which were bimanually palpable with irregular surface and associated with tenderness on both sides.
Investigations : Urine showed bacteriuria and pyuria, and urine culture grew Escherichia coli (100,000 cfu/ ml). He had anemia (Hb: 8.2 g/dl), neutrophilic leukocytosis (15 000 cells/cu.mm with 85% neutrophils), normal blood sugars, and severe renal failure (S. creatinine: 10.4 mg/dl; B. urea: 277 mg/dl). Ultrasonogram of abdomen showed bilateral enlarged kidneys with numerous cysts, with some cysts having internal echos within. Multi detector computed tomography (MDCT) of abdomen (plain + contrast) confirmed bilaterally enlarged kidneys with numerous cysts and also showed multiple cystic lesions scattered in both lobes of liver. Both kidneys had multiple hemorrhagic cysts with a few showing multiple air pockets bilaterally [Figure and ]. Other intra-abdominal organs were normal on ultrasonogram as well as MDCT. The diagnosis of ADPKD with bilateral emphysematous pyelonephritis (EPN) class 4[] with severe renal failure was made.
Hemodialysis was initiated through a left radiocephalic areriovenous fistula (AVF) which had been created earlier. He was started on sensitive antibiotics as per urine culture report (Piparacillin-Tazobactam). As he continued to have high-grade fever after 7 days of Piparacillin-Tazobactam, this antibiotic was stopped and was started on injection Meropenem in appropriate doses. The MDCT of abdomen repeated after 2 weeks showed persistence of with air pockets in both kidneys. Patient continued to have fever and loin pain. Gastrosurgery and Urology units evaluated him and bilateral nephrectomy was advised as he did not respond to an appropriate antibiotic course. He underwent bilateral nephrectomy. Forty-eight hours after bilateral nephrectomy, he became afebrile and macrohematuria subsided. At present, he is being continued on thrice weekly hemodialysis and is planned for renal transplantation at a later date.
Macroscopic examination of kidneys showed multiple cystic spaces with necrotic areas [Figure and ]. On light microscopy, the cysts were lined by flat to cuboidal epithelium. Intercystic spaces had periglomerular fibrosis and glomerulosclerosis. Extensive necrosis with predominantly neutrophilic infiltrates was seen in the interstitium. Tubules showed dilatation and thyroidization at places. Renal pelvis showed areas of necrosis and inflammation. There was no evidence of granulomas, dysplasia, or malignancy. The above features were consistent with diagnosis of ADPKD with pyelonephritis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 70.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1390,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7083246-1,Extracted,"A 70-year-old woman underwent primary percutaneous coronary intervention of the right coronary artery for an inferoposterior myocardial infarction. The patient was reviewed 6 months later. She had no symptoms of heart failure. Blood pressure was 140/60 mm Hg, with a heart rate of 80 beats/min and an oxygen saturations of 98%. On examination, a harsh, 3/6 systolic murmur at the left lower sternal edge was noted. Transthoracic echocardiography (TTE) demonstrated a large inferobasal LV pseudoaneurysm, confirmed on computed tomography (CT) (). The maximum diameter of the pseudoaneurysm neck was 9 mm. The patient was discussed at the multidisciplinary team (MDT) meeting. Although she was asymptomatic, there was a risk of potentially fatal pseudoaneurysm rupture. The delay from the infarct also favored closure, in contrast to repair in the acute peri-infarct period, when tissue rims are often too friable to support a device.
The procedure was performed from the right femoral artery and using local anesthesia with TTE and fluoroscopy. A 5-F Judkins right 4 (JR4) diagnostic catheter was advanced into the left ventricle, and the defect was crossed with a 0.035-inch hydrophilic wire. The JR4 catheter was advanced into the pseudoaneurysm (), and the wire was exchanged for a 0.035-inch Confida wire (Medtronic, Minneapolis, Minnesota). The JR4 catheter was exchanged for a 7-F 90-cm guiding sheath. Because of the defect diameter, as well as the wall thinning of the infarcted area which necessitated a short waist length, an 11-mm Amplatzer Septal Occluder (Abbott, Abbott Park, Illinois) was deployed ( and ). The final angiographic result was satisfactory (). TTE the following day confirmed complete exclusion of the pseudoaneurysm. The patient was discharged home.
This case demonstrates the feasibility of low-risk percutaneous closure of a focal LV rupture. It is important to distinguish the subacute presentation of this patient with acute presentations in the immediate peri-infarct phase. Pre-procedure CT was valuable in delineating the anatomy and allowing selection of an appropriate device. Finally, pre-procedural imaging and favorable apical TTE windows allowed for a safe and efficient procedure using local anesthesia.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 60.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1391,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8134926-1,Extracted,"A 66-year-old Korean woman who had been hospitalized in the orthopedic department developed acute-onset whole-abdominal pain following hematochezia. She had undergone a modified radical mastectomy with axillary lymph node dissection for right breast cancer (pT2N1M0, stage IIB) 5 years previous. The patient had received six cycles of adjuvant chemotherapy with CMF (cyclophosphamide 600 mg/m2, methotrexate 40 mg/m2, and fluorouracil 600 mg/m2) regimen one month after breast surgery. Four years after surgery, bone metastasis was detected on the T8 vertebra. Three months after detection of this bone metastasis, the chemotherapy regimen was changed to everolimus (10 mg/day) with an aromatase inhibitor. Seven months after changing this chemotherapy regimen, the patient received an arthrotomy of the left wrist because of seronegative rheumatoid arthritis and then began polmacoxib medication. Seventeen days after starting polmacoxib, the patient complained of acute-onset whole-abdominal pain following hematochezia.
The patient had no other underlying disease except breast cancer and seronegative rheumatoid arthritis. She had not received any radiotherapy or steroids and had no past history of chronic intestinal ailment. On physical examination, the patient appeared acutely ill. Her body temperature was 37.5°C, pulse rate was 87 beats per minute, and blood pressure was 111/68 mmHg. Her abdomen was rigid and exhibited whole-abdomen tenderness and rebound tenderness. The maximal point of tenderness was the left upper quadrant. Rectal examination showed no active bleeding or rectal mass. Laboratory tests showed increased leukocyte count 12.44 × 103/mm3 with neutrophilia, decreased hemoglobin count 9.9 g/dL, hematocrit level 29.8%, and platelet count 332 × 103/mm3. Prothrombin time and international normalized ratio were prolonged at 14.5 and 1.36 seconds, respectively. An abdominopelvic computed tomography (APCT) scan showed multiple wall defects in the descending colon with perilesional fat infiltration and pneumoperitoneum, suggesting multiple perforations of the descending colon ().
Emergency laparoscopic exploration was performed. Intraoperative findings included diffuse inflammation and multiple abscess pockets in the mesocolon, severely inflamed left colon, and a gross perforation in the proximal descending colon measuring 2 cm that was connected to the largest abscess pocket. A left hemicolectomy with abscess drainage and irrigation of the peritoneal cavity was performed using hand-assisted laparoscopy. The severely inflamed left colon and perforation site were resected, and a transverse sigmoid anastomosis was created. The specimen obtained during the operation showed multiple transmural ulcerations adjacent to the gross perforation site (). There was no evidence of underlying gastrointestinal disease such as diverticulitis or inflammatory bowel disease. Pathological evaluation of the specimen showed chronic active transmural inflammation, vascular congestion, and acute serositis ().
After operation, the patient was treated with intravenous antibiotics for peritonitis, and all previous oral medications, including everolimus and polmacoxib, were discontinued. The patient’s abdominal pain improved on postoperative day 1. However, on postoperative day 3, fresh red blood hematochezia without abdominal pain started. Under suspicion of intraluminal bleeding at the anastomosis site, emergency sigmoidoscopy was performed, which showed that the anastomosis was clean and patent and multiple geographic ulcers existed in the remnant colon wall (). Although the range of ulceration involved the whole colon, there was no sign of additional perforation, and we chose not to return the patient to the operating room immediately.
Considering the possibility of total colectomy, we observed this patient closely. On postoperative day 5, the hematochezia stopped spontaneously after conservative management. On postoperative day 8, follow-up APCT showed diffuse edematous wall thickening from the distal transverse colon to the rectosigmoid colon. Loculated fluid appeared in the lower abdomen, and percutaneous drainage was performed. There was no evidence of newly developed colon perforation. The patient started an oral diet on postoperative day 13 and was discharged home on postoperative day 34. Colonoscopy was performed 6 months after the operation and showed that the colon ulceration had self-resolved, and the remainder of the colon was normal ().
This study was approved by the Institutional Review Board of the Kangbuk Samsung Hospital (No. 2019-05-024). Written informed consent was waived.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [111.0, 'mm hg'], 'Diastolic Blood Pressure': [68.0, 'mm hg']}",82.33333,78.21666,86.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 111.0 mm Hg + 2/3 * 68.0 mm Hg = 82.33333 mm Hg.
Hence, the patient's mean arterial pressure is 82.33333 mm Hg."
1392,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4694,Extracted,"A 66-year-old man with a past medical history of coronary artery disease and obesity complains of left great toe swelling on the second day of his hospital stay for melena due to peptic ulcer disease. He describes significant pain at the metatarsal-phalangeal joint, and the radiographic findings are shown in Figure A. He also complains of chronic bilateral hip pain that has worsened during his admission. Temperature is 99.4°F (37.4°C), blood pressure is 142/91 mmHg, pulse is 92/min, respirations are 16/min. On examination, his left great toe is red, swollen and feels hot to the touch. Palpation of the hips does not elicit tenderness but active range of motion is slightly decreased. The patient's CBC shows a hemoglobin of 11.1 g/dL, white blood cell count of 10.3 x 10^9/L, and platelet count of 200,000/mL.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [142.0, 'mm hg'], 'Diastolic Blood Pressure': [91.0, 'mm hg']}",108,102.6,113.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 142.0 mm Hg + 2/3 * 91.0 mm Hg = 108.0 mm Hg.
Hence, the patient's mean arterial pressure is 108.0 mm Hg."
1393,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7713328-1,Extracted,"A 36-year-old man was admitted to the emergency department of our university hospital with sudden onset of nausea, fever, chills and worsening general condition.
He had been diagnosed with familial mediterranean fever 10 years ago and renal biopsy was resulted with AA amyloidosis. After uremic symptoms, hemodialysis was started 3 days a week by transjugular catheter 5 months ago. Because of catheter malfunction, his catheter was replaced in the another medical center. Ten days after catheter malposition, his complaints started. On admission, the patient was good, conscious and orientated and his fever was: 38.5 °C, pulse: 104 beats/minute, respiratory rate: 26/min, blood pressure: 100/50 mmHg. During physical examination, distension, right flank pain and venous collateral development was observed in the patient’s abdomen. Laboratory studies revealed that blood urea nitrogen: 59 (6–20) mg/dl, creatinine: 4.4 (0.5–1.2) mg /dl, sodium: 137 (136–145) mmol /l, potassium: 3,9 (3.5–5.1) mmol/l, Total bilirubin: 1.1 (0–1.4) mg/dl, direct bilirubin: 1.0 (0–0.3) mg/dl, Total protein: 5.1 (6.4–8.3) gr/dL, albumin: 2.4 (3.5–5.2) gr/dl, alkaline phosphatase: 99 (44–130) u / L, − lactate dehydrogenase: 327 (135–250) u/L, aspartate aminotransferase: 142 (0–40) u/L, alanine aminotransferase: 453 (0–41) u /L, gamma glutamyl transferase:: 256, (10–71) u /L, C reactive protein: 174 (0–5) mg /L, procalcitonin: 100 (0–0.5) ng /dl, Hemoglobin: 9.5 (12–16) g /dl, platelet: 65000 (130–400) μ /L, white blood cell: 11 × 109 (4.8–10.7)(109)/liter, d dimer: 4220(0–500) ug/L. In the axial contrast enhanced venous phase CT image, a hypodense thrombus was observed in which the distal end of the catheter is at the level of drainage of the hepatic veins into the vena cava inferior and that blocked hepatic vein drainage around the catheter. Additionally, mosaic contrast pattern and perihepatic fluid is seen on computed tomography (CT) (optima CT 540, GE, USA) image (Fig. ). Thrombus around the catheter was also confirmed by Doppler US (GE Logiq Pg medical System (GE, Healthcare,Chicago,IL,USA))examination.
The sagittal reformat, in which the distal tip of the catheter was inferior to the vena cava, was also observed in the CT image (Fig. ) The patient’s diagnosis was accepted Acute Budd Chiari syndrome developed as a result of catheter malposition. Heparin and broad-spectrum antibiotic therapy (Vankomycin/meropenem) were administered for the patient immediately. The catheter was removed and a new catheter was inserted in the same session. A few days after this procedure, symptoms of liver failure regressed (Table ). Because patient’s general condition was good and without fever, he was discharged with advices on the 9th day of hospitalization.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [50.0, 'mm hg']}",66.66667,63.33334,70,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 50.0 mm Hg = 66.66667 mm Hg.
Hence, the patient's mean arterial pressure is 66.66667 mm Hg."
1394,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-489,Extracted,"A 44-year-old woman comes to the physician because of pain and swelling below her left eye for 3 days. She has also had excessive watering from her eyes during this period. She has no history of serious illness and takes no medications. Her temperature is 37°C (98.6°F), pulse is 90/min, and blood pressure is 110/70 mm Hg. Examination shows erythema, tenderness, warmth, and swelling below the medial canthus of the left eye. There is purulent discharge from the lower lacrimal punctum on palpation of the swelling. The remainder of the examination shows no abnormalities. The discharge is sent for cultures.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1395,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-3726,Extracted,"A 55-year-old man comes to the physician because of episodic retrosternal chest pain and shortness of breath for the past 6 months. His symptoms occur when he takes long walks or climbs stairs but resolve promptly with rest. He has a history of chronic obstructive pulmonary disease, for which he takes ipratropium bromide. His pulse is 81/min and blood pressure is 153/82 mm Hg. Physical examination shows mild expiratory wheezing over both lungs. Additional treatment with a beta blocker is considered.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [153.0, 'mm hg'], 'Diastolic Blood Pressure': [82.0, 'mm hg']}",105.66667,100.38334,110.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 153.0 mm Hg + 2/3 * 82.0 mm Hg = 105.66667 mm Hg.
Hence, the patient's mean arterial pressure is 105.66667 mm Hg."
1396,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5591494-1,Extracted,"This patient is a 7-year-old Bahraini boy who sustained blunt trauma to his abdomen from the bar of a football goal post. He presented with abdominal pain and vomiting. On arrival to accident and emergency department, he was conscious, alert, and oriented. His pulse was 121 beats per minute, blood pressure was 96/53 (mean 68) mmHg, and respiratory rate was 30 cycles per minute. His abdomen was distended with an epigastric bruise. On admission his hemoglobin was 9.2 g/dL (12 to 14.5), white blood cell count was 20.3×109/L (3.6 to 9.6), serum amylase was 116 U/L (30 to 118), and glucose was 26.8 mmol/L (3.6 to 8.9; Table ). Pan-CT revealed a grade III liver injury (Fig. ), grade I bilateral renal injury, and a suspicion of splenic injury was raised by the radiology registrar. The CT films were reviewed next day by a consultant radiologist and reported a grade III to IV pancreatic injury (Fig. ). Our patient was admitted to the Pediatric Intensive Care Unit (PICU) and was treated conservatively. Because he was stable, he was discharged to the surgical ward by day 3. His blood test results were monitored closely and showed a gradual rise in serum amylase level during the first week of injury (Fig. ). At day 18 he developed abdominal distension and vomiting. An abdominal examination revealed a palpable epigastric mass. A CT scan showed a pseudocyst (Fig. ) which was aspirated percutaneously under ultrasound guidance by an interventional radiologist. The cyst recurred at day 25 (Fig. ) so a pigtail catheter was inserted for continuous drainage under ultrasound guidance. Throughout his stay, he was maintained on total parenteral nutrition (TPN) through a peripherally inserted central catheter (PICC) line. The pigtail catheter was removed after ten days and a low fat diet was started by day 44 as he did not tolerate orally administered nutrition earlier. He was discharged home at day 55 in good health. Out-patient follow-up and serial ultrasound showed resolution of the cyst (Fig. ) and normalization of his blood investigations (Fig. and Table ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [53.0, 'mm hg'], 'Systolic Blood Pressure': [96.0, 'mm hg']}",67.33333,63.96666,70.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 96.0 mm Hg + 2/3 * 53.0 mm Hg = 67.33333 mm Hg.
Hence, the patient's mean arterial pressure is 67.33333 mm Hg."
1397,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7251296-1,Extracted,"A 36-year-old male patient presented to the hospital with a 1-day history of abdominal pain on the whole abdomen. Pain was initially located at the umbilical area, but then generalized and became severe every time, and was accompanied by nausea, vomiting and fever. The patient had no history of peptic disease or trauma, but he had of significant weight loss (9 Kg over 3-months) and loos of appetite. Clinical examination revealed a heart rate of 110, respiratory rate 24 times/minute, blood pressure 140/70 mmHg, temperature 38 °C. Upon abdominal exam, we found distention of the patient's abdomen, bowel sounds were reduced on auscultation, and a tender generalized pain of the abdomen accompanied with tympanic sounds on percussion. Rectal examination was normal. Other system were normal. Complete blood count with leukocytes 14.000 cell/ml with a 75,6% neutrophil composition. Patient was negative for hepatitis B and human immunodeficiency virus (HIV). An abdominal X-ray within normal limits. We diagnosed the patient with peritonitis suspected due to perforation of the hollow viscus.
An exploratory laparotomy was then performed. Immediately after the midline incision and opening of the abdomen in layers, approximately 100 ml of bowel content was revealed in the cavity. Perforation was observed on two sites within the jejunum, approximately 30 cm and 40 cm from the Treitz ligament with a size of 0,5 mm × 1 mm and 0,6 mm × 2 mm (). No abnormalities (tumour) were observed in the liver, spleen and peritoneum.
We performed resection of the jejunum segment containing the mass and the mesentery, followed by end to end anastomosis. The resected jejunum specimen was sent to the anatomical pathology laboratory. Seven days after the operation, the histopathological examination of the specimens revealed features of Malignant Non-Hodgkin Lymphoma of the diffuse large B-cell type () and Immunohistochemistry showed Leucocyte common antigen (CD45) positive and Cytokeratin (CK) negative on the tumour cell ().
The patient was discharged 8 days postoperative with a good condition, and was chemotherapy by oncology division with Cyclophosphamide-Hydroxyldaunorubicin (Doxorubicin)-VinCRIStine-Prednisone (CHOP) regimen for further management. This patients received a total of six cycles of CHOP regimen. At follow-up up to 6 months, there were no signs of recurrence on physical examination and CT scan with contrast of the chest, abdomen, and pelvis (C/A/P CT Scan) within normal limit. We doesn't performed Positron emission tomography (PET) because our institution doesn't have PET scan.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [140.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 70.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1398,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-6356,Extracted,"A 19-year-old male with a past medical history of surgical repair of a torn anterior cruciate ligament and seasonal allergies presents to the emergency department with a rash. He reports that he first noticed the rash on his torso when he woke up this morning, and it has spread down his legs over the last few hours. He also endorses fatigue, malaise, and sore throat for four days. The patient reports that he was seen yesterday at his college’s student health clinic for similar symptoms and was prescribed amoxicillin. He also reports that his younger sister was recently diagnosed with streptococcal pharyngitis, and his mother has psoriatic arthritis. He is a sophomore on the men’s soccer team, but he has had to sit out of practice for the last several days. His home medications include cetirizine and fluticasone nasal spray. He has no known drug allergies. His temperature is 100.8°F (38.2°C), blood pressure is 122/76 mmHg, pulse is 97/min, and respirations are 16/min. On physical exam, he has an erythematous oropharynx with posterior cervical lymphadenopathy. His rash can be seen in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [76.0, 'mm hg'], 'Systolic Blood Pressure': [122.0, 'mm hg']}",91.33333,86.76666,95.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 122.0 mm Hg + 2/3 * 76.0 mm Hg = 91.33333 mm Hg.
Hence, the patient's mean arterial pressure is 91.33333 mm Hg."
1399,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5986017-1,Extracted,"Mr. T.P. is a 49-year-old patient of Togolese nationality, who has been admitted to our department for throbbing, NYHA Stage II stress dyspnea and intense angular chest pain. He had no personal history of cardiovascular disease. No heart disease or sudden death in the family. The admission examination had found a conscious patient, in good general condition with a blood pressure of 122/77 mmHg, a SaO2 at 99% in ambient air, an obesity with BMI at 33 kg/m2, a regular tachycardia at 200 bpm without added noise. There were no peripheral signs of heart failure. The emergency electrocardiogram recorded a regular tachycardia at 209 bpm at wide QRS with a complete right bundle branch block and 150° right axis (Fig. ). There was complete atrioventricular dissociation. In total, the electrocardiogram recorded monomorphic ventricular tachycardia with a complete right bundle branch block aspect and posterior fascicular block. In the emergency, we had carried out an external electrical shock biphasic 150 J which allowed a return in sinus rhythm. Transthoracic echocardiography showed normal sized heart chambers with a left ventricular ejection fraction at 68%. There were no other structural anomalies objectivized (Fig. ). The diagnosis of anterior fascicular ventricular tachycardia of Belhassen was then discussed. Thirty minutes later, the patient experienced a recurrence of ventricular tachycardia with identical QRS as those on the 1st ECG. The patient was this time put on verapamil injection, which allowed to obtain a sinus rhythm at 66 bpm, an incomplete right block and an axis at −40° (Fig. ). The biological assessment performed including glycaemia, creatinine, blood ionogram, troponin I, calcium, magnesium, and blood count was normal. The 24-h ECG Holter performed the next day had noted right ventricular extrasystole with QRS identical to ventricular tachycardia.
The patient was placed on oral verapamil, followed by bisoprolol 1 month later. The evolution was marked by two recurrences. We therefore combined verapamil with bisoprolol, which allowed us to maintain a permanent sinus rhythm with a current decline of 15 months.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [77.0, 'mm hg'], 'Systolic Blood Pressure': [122.0, 'mm hg']}",92,87.4,96.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 122.0 mm Hg + 2/3 * 77.0 mm Hg = 92.0 mm Hg.
Hence, the patient's mean arterial pressure is 92.0 mm Hg."
1400,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1695,Extracted,"A 32-year-old white woman comes to the physician because of fatigue, lethargy, and swelling of the lower legs for 2 months. She reports recurrent episodes of pain in both wrists, her right knee, and her right ankle in the past year. She has had skin problems that are aggravated by exposure to sunlight for the past 18 months. She has smoked one pack of cigarettes daily for 13 years and drinks one alcoholic beverage daily. Her temperature is 37°C (98.6°F), pulse is 92/min, and blood pressure is 115/75 mm Hg. Examination shows 2+ pretibial edema bilaterally and periorbital edema. There are erythematous patches with scaling on both cheeks.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [115.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",88.33333,83.91666,92.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 75.0 mm Hg = 88.33333 mm Hg.
Hence, the patient's mean arterial pressure is 88.33333 mm Hg."
1401,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7034210-1,Extracted,"This case is of a 58-year-old male with a past medical history of hypertension and paranoid schizophrenia who presented to the emergency room with hypoxemia and right ventricle (RV) failure. The patients' vital signs are as follows: blood pressure 89/60 mmHg, pulse 120 beats/min, respiratory rate of 22, and saturation of 88% on 2 L/min nasal cannula. Computed tomography angiogram revealed a saddle embolus in the main pulmonary artery with extensive clot burden affecting all lobes and right heart strain with reverse curvature of the interventricular septum. Transthoracic echocardiogram (TTE) displayed a severely dilated RV with severely reduced systolic function. exhibits a dilated RV with a flattened interventricular septum. A mobile thrombus was seen in the right atrium that measured 2.7 × 1.2 cm.
This patient had a preinduction arterial line placed, and the patient had a standard induction with etomidate, fentanyl, lidocaine, midazolam, and rocuronium. Once the airway was secured with an 8.0 standard endotracheal tube through direct laryngoscopy, a 9 French MAC Introducer was placed through the right internal jugular vein. The surgical team, as well as the perfusionist, was on standby during induction of anesthesia in the event of hemodynamic collapse to initiate cardiopulmonary bypass. The patient underwent emergency pulmonary embolectomy for massive pulmonary embolus with hemodynamic compromise. Intraoperative transesophageal echocardiogram (TEE) demonstrated the mobile thrombus in the right atrium that was seen on TTE. demonstrates the right atrial thrombi in the mid-esophageal five-chamber view. In addition to the right atrial thrombi, TEE revealed a new finding of large thrombi in the left atrium. reveals a thrombus in the left atrium in the mid-esophageal aortic valve in long-axis view with an arrow highlighting the left atrial thrombus. The patient underwent sternotomy with cardiopulmonary bypass for embolectomy. Massive pulmonary emboli and clots were removed from both the left and right pulmonary arteries as well as the right and left atria. After removal of the thrombi, TEE demonstrated a PFO with left-to-right shunt and no residual intracardiac or pulmonary artery thrombi. shows the PFO with the left-to-right shunt after the removal of right and left atrial thrombi as well as pulmonary artery embolectomy. The patient was subsequently weaned off cardiopulmonary bypass and remained hemodynamically stable. At the end of the procedure, an inferior vena cava filter was placed to prevent further PE. The patient recovered with aggressive medical management without neurologic consequences.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [89.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",69.66667,66.18334,73.15,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 89.0 mm Hg + 2/3 * 60.0 mm Hg = 69.66667 mm Hg.
Hence, the patient's mean arterial pressure is 69.66667 mm Hg."
1402,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-11498,Extracted,"A 59-year-old man with a history of congestive heart failure presents to his cardiologist for a follow-up visit. His past medical history is notable for diabetes mellitus, hypertension, and obesity. He takes metformin, glyburide, aspirin, lisinopril, and metoprolol. He has a 40 pack-year smoking history and drinks alcohol socially. His temperature is 99.1°F (37.2°C), blood pressure is 150/65 mmHg, pulse is 75/min, and respirations are 20/min. Physical examination reveals bilateral rales at the lung bases and 1+ edema in the bilateral legs. The physician decides to start the patient on an additional diuretic but warns the patient about an increased risk of breast enlargement.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 65.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1403,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3527052-1,Extracted,"A day before being applied to us (Istinye Public Hospital, Istanbul, Turkey, 2008), the patient (6-year-old male) with his two brothers had been taken to a physician with complaints of nausea and abdominal pain. Five milligram dose of metoclopramide had been prescribed to the patient. After receiving the first dose of medication, the contraction and retention of neck, contractions of chin and arms occurred within half an hour in the patient who used metoclopramide. The patients were brought to our clinic. The patient's conscious was clear, but he was agitated and restless. Pulse was 102/min; blood pressure was 85/45 mmHg. Respiratory rate was 27/min as normal. There were speech dysfunction, trismus, and dystonic movements of sleeves. Involuntary movements gradually increased and opistotonus developed. Results of complete blood count (CBC), liver and kidney function tests and electrolytes were within normal values.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [45.0, 'mmhg'], 'Systolic Blood Pressure': [85.0, 'mmhg']}",58.33333,55.41666,61.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 85.0 mm Hg + 2/3 * 45.0 mm Hg = 58.33333 mm Hg.
Hence, the patient's mean arterial pressure is 58.33333 mm Hg."
1404,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3275640-1,Extracted,"A 71-year-old Iranian man with Persian ethnicity presented to our urology clinic complaining of recurrent episodes of gross hematuria and left-sided flank pain of one week's duration. He mentioned no history of trauma, prior disease, medication usage or significant family disorder. On physical examination, he was fully conscious with a blood pressure of 110/70 mmHg, pulse rate of 120 beats/min and temperature of 37°C. His bowel sounds were normoactive on auscultation. There were no remarkable findings on abdominal palpation, except for a non-tender, large left inguinal hernia with extension to his scrotum. Other related examinations, including a digital rectal examination, were normal. A urine analysis showed pH 5, with 10 to 15 RBCs per HPF, 10 white blood cells per HPF, with rare bacteria and yeast. A urine culture was negative.
Genitourinary ultrasonography reported a grade 2 hydroureteronephrosis on his left side. An intravenous pyelogram also revealed left hydroureteronephrosis associated with an ill-defined filling defect on the left side of his urinary bladder (Figure ). In order to rule out any intravesical lesion, a cystoscopy was performed that showed a bulging on the left side of his bladder wall due to extravesical pressure. The mucosal lining of his bladder was normal. Intravenous and oral contrast-enhanced abdominal computed tomography (spiral multislice thin section scan) showed an entrapped sigmoid colon that was herniated through his left inguinal canal. Anteromedial displacement of his bladder and left ureter were also evident due to the pressure of his sigmoid colon. His left ureter was dilated due to distal obstruction (Figure ).
A diagnosis was made of a large inguinal hernia with pressure effects on the urinary system, resulting in hematuria and obstructive hydroureteronephrosis;the abdominal wall was thus opened with a classic inguinal incision. The contents of his hernial sac, including his sigmoid colon and its mesentery, were adhered to the surrounding tissues. An attempt to reduce the content of his hernial sac was unsuccessful, so a low midline incision was made for better exposure and reduction. There was no intra-abdominal mass. A redundant sigmoid colon was found fixed at the internal ring due to severe and chronic adhesion. His proximal sigmoid colon had compressed his bladder and distal ureter at the vesicoureteral junction. After reduction of his hernial sac content, our patient underwent a successful hernia repair with mesh, leading to a quick and uneventful postoperative recovery.
Our patient's signs and symptoms subsided following surgery. On a postoperative cystogram, all signs had disappeared (Figure ). Our patient was initially followed-up with monthly visits for the next six months, and then every six months. He remained symptom free during postoperative follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1405,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8021304-1,Extracted,"A 16-month-old boy was transferred from an outside hospital because of a high fever and skin rash. He was born via normal vaginal delivery at 40 weeks of gestation, with a birth weight of 3670 g. He was previously healthy except for atopic dermatitis and a history of suspected viral meningitis at the age of 100 days, which was resolved without complication. Age-appropriate vaccination was done without specific adverse events following the administration of the vaccines, which included the Bacillus Calmette–Guérin (BCG), measles/mumps/rubella, and varicella vaccines. His language and motor development were within the normal ranges. On the day of admission, he had a weight of 11.5 kg (50th–75th percentile) and a height of 81.9 cm (50th–75th percentile).
He was admitted to the outside hospital because of a high fever of up to 40°C for 3 days. On physical examination, abnormal findings were not shown other than hand and foot swelling. The initial complete blood count (CBC), blood urea nitrogen (BUN), creatinine (Cr), and serum albumin levels were normal. However, his C-reactive protein (CRP) level was high, at 10.37 mg/dL (the normal level is < 0.5 mg/dL). He was treated with an initial empiric antibiotic of intravenous cefotaxime. On his third day of hospitalization, perioral ecchymosis and mild coagulopathy developed, with a prothrombin time (PT) international normalized ratio (INR) of 1.30, activated partial thromboplastin time (aPTT) of 67.0 seconds, and D-dimer of > 1000 ng/mL. No bacterial or viral pathogens were identified in the initial blood culture and respiratory viral polymerase chain reaction (PCR), respectively. Besides, oliguria (urination of 0.5 cc/kg/h) developed, along with persistent high fever and swollen extremities. He was transferred to our hospital on the sixth day of fever.
On the first day at our hospital, his vital signs were as follows: a blood pressure of 149/91 mm Hg (reference: 86–103/40–55); a pulse of 189 bpm (reference: 70–160); and a body temperature of 38.2°C. He appeared acutely ill. Generalized edema, oral ulcers, and multiple purpura, including perioral ecchymosis, were observed on physical examination (Fig. ). His blood count showed bicytopenia with hemoglobin of 9.5 g/dL, platelet count of 120,000/μL, and white blood cell (WBC) count of 7200/μL, of which 70.7% were neutrophils, 15.8% were lymphocytes, and 4.8% were eosinophils. Other blood laboratory findings were as follows: CRP of 11.14 mg/dL, BUN/Cr of 3 mg/dL / 0.17 mg/dL, albumin of 2.3 mg/dL, PT INR of 1.22, aPTT of 47.8 seconds, fibrinogen of 372 mg/dL, D-dimer of 5.82 μg/mL, and fibrin degradation product of 33 μg/mL. The cerebrospinal fluid profile and urinalysis were unremarkable. Under the impression of serious bacterial infection, he was given vancomycin (60 mg/kg/day, intravenous) and meropenem (60 mg/kg/day, intravenous) as empiric antibiotics. However, repeated culture studies showed no definite pathogens. On the third day, new ecchymosis around his right ear and forehead developed, and a high spiking fever persisted.
To exclude other etiology of fever of an unknown origin, a peripheral blood smear, bone marrow examination, and bone scan were done, which showed no specific abnormalities suggesting malignancies. The immunoglobulin (Ig) G, M, and A levels were normal [at 969 mg/dL (normal: 345–1236), 242 mg/dL (normal: 43–207), and 74.3 mg/dL (normal: 14–159), respectively]. However, the immunoglobulin E (IgE) level was high, at 1679 kU/L (normal: 0–230), and the complement fractions C3, C4, and CH50 were low, at 80.0 mg/dL (normal: 77–195), 6.7 mg/dL (normal: 7–40), and 13.3 U/mL, respectively. The antinuclear antibody (ANA) was positive, at 1:320 with homogenous fluorescence, and the anti-double stranded (anti-ds) DNA antibody was also positive, at 10.8 IU/mL. The tests for anti-SSA, anti-SSB, anti-ribonucleoprotein, anti-scleroderma 70, and anti Jo1 antibodies were all negative.
Two weeks after he was hospitalized, leukopenia developed, and thrombocytopenia became worse, along with the persistent fever. The complement fractions were decreased to 37.9 mg/dL of C3, < 1.5 mg/dL of C4, and under 10.0 U/mL of CH50, respectively. The ANA titer increased to 1:1280 with homogenous fluorescence, and the anti-ds DNA antibody level increased to 84.4 IU/mL. The lupus anticoagulant and anticardiolipin antibody were all positive, while other autoantibodies were all negative. To control the fever, he was started on naproxen on the 30th day of fever, and his fever subsided from 32nd day of fever. He definitively satisfied the 2015 American College of Rheumatology (ACR)/Systemic Lupus Erythematosus International Collaborating Clinics (SLICC) revised criteria for the diagnosis of SLE (7 points out of 16); therefore, he was treated with a steroid (methylprednisolone, 2 mg/kg/day, intravenous). The anti-ds DNA antibody level and complement fractions were improved after steroid therapy, and his fever did not recur.
Approximately 1 week after starting steroid treatment, his steroid dose was reduced to 1.0 mg/kg/day, orally. Two weeks after the first dose reduction, his steroid dose was again reduced to 0.5 mg/kg/day. However, at this point, his fever returned, and his anti-ds DNA antibody titer increased. Accordingly, his steroid dose was increased to 1.0 mg/kg/day, and his fever disappeared. One week later, fever, the swelling of the hand and foot, and proteinuria (Urine Protein/Creatinine ratio of 0.484 mg/mg) appeared again. A renal biopsy confirmed the diagnosis of lupus nephritis (focal lupus nephritis, class III). Transthoracic echocardiography showed vegetation in the tricuspid valve, which was thought to be indicative of Libman-Sacks endocarditis. He was treated with intravenous methylprednisolone (1.0 g/m2) for 3 days, followed by cyclophosphamide (500 mg/m2). Then, steroid (deflazacort), mycophenolate mofetil, and cyclosporin were used for his SLE, and the disease was well controlled.
Considering the early-onset SLE, partial exome sequencing for 4813 OMIM genes was performed in his peripheral leukocytes. Exomes were captured using the TruSight One Panel (Illumina Inc.), which enriches a 12 Mb region spanning 4813 genes. Sequencing was performed using the NextSeq platform (Illumina Inc.). Sequence reads were aligned to the reference genome, hg19, using a Burrows–Wheeler aligner (BWA) (v0.7.12, MEM algorithm). The mean depth of coverage was 90× (> 10× = 98%). One heterozygous missense variant, c.5536A>G (p.Lys1846Glu), was found, which was inherited from his father. This variant was not reported previously. The mutation was confirmed using in silico prediction tools, such as PolyPhen-2 (, score 1.00) and SIFT (, score 0.00). This variant has been classified as likely to be pathogenic, according to the American College of Medical Genetics and Genomics (ACMG).[ To rule out the possibility of a large exonic deletion of DOCK8, multiple ligation-dependent probe amplification (MLPA) analysis (P385-A2, MRC Holland, Amsterdam, the Netherlands) was done in the peripheral leukocytes of both the patient and his parents, which revealed a heterozygous deletion of exon 1 to 8 in the patient and his mother. Through the results of the genetic testing, he was confirmed to have DOCK8 deficiency.
At the age of 22 months, when the patient's anti-ds DNA antibody titer and complement levels were normal as a result of the use of immunosuppressants, he newly experienced skin and soft tissue infections and bacteremia caused by Pseudomonas aeruginosa and received cefepime (60 mg/kg/day, intravenous). From that point, he experienced skin and soft tissue infections several times, which is compatible with ecthyma gangrenosum.
At the age of 28 months, he received haploidentical hematopoietic stem cell transplantation (HSCT) from his mother as a donor, with a non-myeloablative conditioning regimen that included antithymocyte globulin, thiosulfan, and fludarabine. WBCs were grafted on the 10th day following HSCT, and no significant HSCT-related morbidity, including graft versus host disease (GvHD), occurred during a follow-up period of 1-year post-HSCT. At 1 month post-HSCT, the complement fractions C3, C4, and CH50 were normal, at 113.0 mg/dL, 22.7 mg/dL, and 51.2 U/mL, respectively. The ANA was positive at 1:160, with homogenous fluorescence, and the anti-ds DNA antibody level had decreased to 13.0. The IgE level was high, at 526 kU/L. However, the anti-ds DNA antibody normalized at 3 months post-HSCT, and the ANA and IgE became normal at 6 months post-HSCT. He had 20% and 33% donor T-cell chimerism at 3 months and 6 months post-HSCT, respectively. Currently, at 12 months post-HSCT, he is doing well, without any autoimmune features or recurrent infections (Fig. ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [149.0, 'mm hg'], 'Diastolic Blood Pressure': [91.0, 'mm hg']}",110.33333,104.81666,115.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 149.0 mm Hg + 2/3 * 91.0 mm Hg = 110.33333 mm Hg.
Hence, the patient's mean arterial pressure is 110.33333 mm Hg."
1406,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4350645-1,Extracted,"A 57-year old Thai man presented for HIV screening at an anonymous testing center in Bangkok where routine evaluation for AHI is performed
[]. At presentation, the patient was reactive to the HIV antigen-antibody combination 4th generation enzyme immunoassay (EIA, AxSYM, Abbott Laboratories, Wiesbaden, Germany) and the IgM-sensitive 3rd generation HIV EIA (Genscreen HIV 1/2, Bio-Rad, Marnes la Coquette, France) but was non-reactive to the IgG-sensitive 2nd generation HIV EIA (Genetic Systems rLAV EIA, BioRad Laboratories, Redmond, WA). This signified infection within the past 4 weeks
[], and consistent with his history of HIV exposure via unprotected sex with a female sex worker 30 days prior. Twelve days prior to AHI diagnosis, he experienced symptoms consistent with acute retroviral syndrome (fever, fatigue, diarrhea, nausea and vomiting) and was hospitalized for 3 days for intravenous hydration; no laboratory tests are available from that admission. At the time of presentation with AHI diagnosis, he reported only mild fatigue, and did not have oliguria or edema. Blood pressure was 174/99 mmHg, pulse rate was 62 beats/minute and temperature was 37.2 C. His HIV RNA was 81,515 copies/ml and CD4 was 313 cells/mm3. Three days later, he consented to enrollment in an AHI study, by which time his HIV RNA was 354,706 copies/ml. However the 2nd generation HIV EIA remained non-reactive. Routine clinical chemistries revealed a creatinine of 8 mg/dl and an estimated glomerular filtration rate (eGFR) of 7.8 ml/min/1.73 m2 using the Modification of Diet in Renal Disease formula corrected for Thai ethnicity
[]. Abnormalities were confirmed by subsequent sampling. Urinalysis showed a specific gravity 1.010, pH 5.0, 1+ proteinuria, 1+ leukocytes, 1+ blood, negative glucose, ketone, and bilirubin, 3–5 white blood cells/HPF, 2–3 red blood cells/HPF, 1–2 epithelial cells/HPF and no casts. Spot urine was tested for protein/creatinine ratio (0.14) and fractional excretion of sodium (2.47%). Other clinical laboratories included: hemoglobin 15.5 g/dl, alanine transaminase 81 U/l, creatine phosphokinase 54 U/L, uric acid 12 mg/dl, calcium 8.4 mg/dl, phosphate 5.5 mg/dl, albumin 3.7 g/dl, sodium 132 mmol/l, potassium 4.4 mmol/l, chloride 97 mmol/l and carbon dioxide 21 mmol/l. Fasting blood glucose (135 mg/dl) and HbA1C (8.2%) were elevated. Hepatitis B surface antigen, anti-hepatitis C antibody and rapid plasma reagent for syphilis were negative. The Epstein Barr virus (EBV) IgM was negative at time of ARF and 4 weeks later while IgG levels were 76 U/ml and 86 U/ml, respectively. Cytomegalovirus (CMV) IgM was weakly positive (level of 0.28, cut off 0.19 units) at baseline and negative 4 weeks later while IgG levels were 155 RU/ml and 191 RU/ml at these 2 time points.
His past history included hypertension and diabetes mellitus (DM) diagnosed 4 years prior, and he was treated with once daily oral metformin (500 mg), glyburide (5 mg), atenolol (100 mg), amlodipine (10 mg). Six months before AHI, his BUN and creatinine were 25 and 1.8 mg/dl with no proteinuria and trace glucosuria. The patient denied taking non-steroidal anti-inflammatory or other nephrotoxic drugs. He complained of intermittent episodes of palpitation during AHI, captured by cardiac monitoring during this hospitalization for ARF and characterized as atrial fibrillation that recovered spontaneously.
Renal ultrasonography demonstrated normal size and echogenicity of both kidneys with no apparent structural abnormalities. Renal biopsy identified tubular changes consistent with acute tubular nephropathy. By light microscopy, some tubules were dilated withfocal epithelial attenuation, blebbing, sloughing and nuclear dropout (Figure 
). Electron microscopic examination revealed attenuation and loss of nuclei are observed (Figure 
). Loss of the brush border was seen in proximal tubules. There was moderate interstitial fibrosis associated with a scattered inflammatory cell infiltration of mainly mononuclear cells and a few eosinophils. Glomeruli were normocellular. There was no evidence of immune complexes, fibrinoid necrosis or wire-loop lesions. Viral inclusions were not identified in tubular epithelium on electron microscopy. Arteries and arterioles were moderately thickened.
The patient received supportive care without dialysis in the hospital for 2 weeks and his eGFR gradually rose to 30 mg/min/1.73 m2 at week 2 following AHI diagnosis. Antiretroviral therapy (ART) was initiated on day 11 with eGFR-adjusted dosages of zidovudine and lamivudine, given in combination with standard dosage of efavirenz. His HIV RNA declined rapidly to 446 copies/ml at week 4 of ART. After 12 weeks of ART, his HIV RNA declined to 72 copies/ml, the CD4 rose to 445 cells/mm3, and his renal function had normalized with a creatinine of 1.0 mg/dl, eGFR of 85 ml/min/1.73 m2. Repeat urinalysis was normal. His fasting glucose was 144 mg/dl and blood pressure was 121/108 mmHg on the same medications for DM and hypertension. At one year following the ARF episode, he had an undetectable HIV RNA, CD4 of 618 cells/mm3, creatinine of 1.1 mg/dl, eGFR of 77 ml/min/1.73 m2 and normal urinalysis. He is currently doing well except for occasional episodes of palpitations precipitated by fatigue.
We searched the Pubmed database with the following key words: primary HIV infection, AHI, ARF, acute tubular nephropathy, acute tubular necrosis, multiple organ failure and rhabdomyolysis to identify case reports published in the English-language literature from January 1984 to July 2014. We included only cases with AHI/primary HIV infection and creatinine abnormalities of grade 2 and above (≥1.8 mg/dl) according to the US Department of Health and Human Services. AHI is defined by having a positive HIV nucleic acid and/or reactive IgM-sensitive HIV antibody testing with non-reactive IgG-sensitive HIV antibody testing and/or Western Blot
[, ]. Primary HIV infection is defined as HIV seroconversion within the past 6 months.
There were 7 reported cases (Table 
). In 4 cases, nephropathy occurred as part of rhabdomyolysis
[, –], 1 had hemolytic uremic syndrome (HUS)
[], and 2 cases had HIV-associated nephropathy (HIVAN)
[, ].Three of 4 patients with rhabdomyolysis had acute tubular necrosis by renal biopsy and 1 case had renal infarcts by CT scan. HIVAN, a sclerosing glomerulopathy, is associated with advanced HIV infection, but in both patients reported here, it occurred during the period of high HIV RNA and prior to HIV seroconversion
[, ] HUS, another complication usually seen in advanced HIV infection, was reported in a case with high HIV viremia associated with AHI
[]. The serum creatinine ranged from 2.3 to 8 mg/dl, and 4 of 7 patients required hemodialysis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [174.0, 'mm hg'], 'Diastolic Blood Pressure': [99.0, 'mm hg']}",124,117.8,130.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 174.0 mm Hg + 2/3 * 99.0 mm Hg = 124.0 mm Hg.
Hence, the patient's mean arterial pressure is 124.0 mm Hg."
1407,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1339,Extracted,"A 36-year-old man is brought to the emergency department for right upper quadrant abdominal pain that began 3 days ago. The pain is nonradiating and has no alleviating or exacerbating factors. He denies any nausea or vomiting. He immigrated from Mexico 6 months ago and currently works at a pet shop. He has been healthy except for 1 week of bloody diarrhea 5 months ago. He is 182 cm (5 ft 11 in) tall and weighs 120 kg (264 lb); BMI is 36 kg/m2. His temperature is 101.8°F (38.8°C), pulse is 85/min, respirations are 14/min, and blood pressure is 120/75 mm Hg. Lungs are clear to auscultation. He has tenderness to palpation in the right upper quadrant. Laboratory studies show:
Hemoglobin 11.7 g/dL3
Leukocyte Count 14,000/mm
Segmented neutrophils 74%
Eosinophils 2%
Lymphocytes 17%
Monocytes 7%
Platelet count 140,000/mm3
Serum
Na+ 139 mEq/L
Cl- 101 mEq/L
K+ 4.4 mEq/L
HCO3- 25 mEq/L
Urea nitrogen 8 mg/dL
Creatinine 1.6 mg/dL
Total bilirubin 0.4 mg/dL
AST 76 U/L
ALT 80 U/L
Alkaline phosphatase 103 U/L
Ultrasonography of the abdomen shows a 4-cm round, hypoechoic lesion in the right lobe of the liver with low-level internal echoes.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 75.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1408,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4062,Extracted,A 59-year-old man comes to the physician because of a 6-month history of progressive blurry vision in both eyes. His vision has not improved with the use of reading glasses. His blood pressure is 155/98 mm Hg. Physical examination shows his visual acuity to be 20/80 in the right eye and 20/60 in the left eye. A photograph of the fundoscopic examination of the right eye is shown.,What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [155.0, 'mm hg'], 'Diastolic Blood Pressure': [98.0, 'mm hg']}",117,111.15,122.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 155.0 mm Hg + 2/3 * 98.0 mm Hg = 117.0 mm Hg.
Hence, the patient's mean arterial pressure is 117.0 mm Hg."
1409,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4152689-1,Extracted,"A 47-year-old known hypertensive female with chronic kidney disease-5 [CKD-5], on thrice weekly hemodialysis (HD), presented with cough with expectoration and breathlessness for 3-4 weeks and fever for 10 days. She was managed in an outside facility for 1 week on amlodipine, erythropoietin, imipenem, HD and other supportive care for CKD. On presentation, patient was conscious, well-oriented with a heart rate of 116 beats/min regular, non-invasive blood pressure of 108/66 mmHg, temperature of 100.2°F and respiratory rate of 34/min with accessory muscles being used. On chest examination, bilateral normal vesicular breath sounds were heard with decreased air entry and occasional coarse crepts in the right lower zone. Her laboratory workup on the day of admission and subsequently is shown in . Chest X-ray showed right lower lobe consolidation/collapse with pleural effusion. Blood and urine cultures were sent, which were sterile. She was managed in the medical intensive care unit on antibiotics and non-invasive ventilation. She was continued on injection imipenem 500 mg twice daily (BID), which she had already received for 2 days prior to admission. On the 3rd day of admission, the patient's clinical condition deteriorated with a significant rise in total leukocyte count (TLC) up to 28,600/mm3. Repeat blood cultures were sent and injection teicoplanin and injection caspofungin added empirically. Next day, a provisional report of gram-negative coccobacilli in blood was received, which was later confirmed to be Acinetobacter baumannii. Injection colistin in a dose of 1 million units (MU) (80 mg colistimethate sodium) intravenous (i/v) once daily (OD) following a loading dose of 2 MU was started. Her fever and TLC started decreasing gradually from the 7th day onward. Caspofungin was de-escalated on receiving culture reports and imipenem was stopped after 10 days of therapy. Patient continued to improve clinically with off and on low-grade fever. She was continued on almost alternate day HD.
On the morning of 16th day of admission, patient had sudden onset of abnormal facial twitchings, which were mainly circumoral and initially limited to the neck. The seizures were controlled with short acting benzodiazepine in the form of injection midazolam 1 mg i/v stat. She was loaded with injection phenytoin 1 g i/v on neurologist's opinion, followed by 100 mg i/v BID. But in the same evening, patient had another episode of seizures, which were generalized tonic clonic and got relieved with injection midazolam 1 mg + 1 mg i/v bolus. Levirecetam 1 g i/v stat followed by 500 mg i/v BID was added by the neurophysician. Her laboratory workup reflected no acute metabolic derangements. Liver profile was normal. Neuroimaging of the brain (magnetic resonance imaging) and electroencephalography were normal. Nerve conduction velocity to rule out critical illness neuropathy was also done. To rule out meningitis as a cause for fever and seizures, lumbar puncture was performed and the cerebral spinal fluid (CSF) was found to be clear, with normal pressure and CSF biochemistry was within normal limits (CSF glucose = 56 mg/dl (corresponding Random Blood Sugar = 92), proteins = 37, TLC = nil).
Further search for any offending drug as a cause for seizures was made. Imipenem which is a potentially seizure inducing drug, was stopped around 1 week before the occurrence of focal seizures. Excluding all other possible causes, colistimethate which is a seizure-threshold lowering drug, was considered to be the sole possible causative agent for seizures. As the patient had improved clinically, colistin was stopped on the occurrence of seizures. Fresh blood cultures were sent after 48 h of stopping antibiotics, which were sterile. Patient had no recurrence of seizures at any point of time after stopping the drug. The antiepileptics were tapered after 1 week of starting the treatment. The patient was shifted to the ward and was finally discharged in a fair condition after 33 days of hospital stay.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [108.0, 'mmhg'], 'Diastolic Blood Pressure': [66.0, 'mmhg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 108.0 mm Hg + 2/3 * 66.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1410,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7945001-1,Extracted,"A 42-year-old male with a past medical history of type II diabetes was admitted with left shoulder pain, abdominal and back pain, and a near syncopal event. Approximately one month prior to hospitalization, the patient was in his typical state of health when he sustained a cat bite at the base of his left thumb. He later developed a fever of 102.7oF and generalized body aches. He was treated with a course of amoxicillin/clavulanic acid, but within one week he returned to the clinic for soreness in his left arm, axillary lymphadenopathy, and a small ulcer at the base of his left thumb. Surface swabs of the ulcer were sent for culture but ultimately finalized with no growth. The patient was then treated with a course of trimethoprim/sulfamethoxazole, but symptoms progressed to include recurrent fevers, myalgia, mild abdominal pain, and constipation. His regimen was transitioned to doxycycline but was hospitalized after having a near syncopal event.
On admission, the patient’s vital signs were temperature of 96.8oF, heart rate 97 bpm, blood pressure 156/94 mmHg, respiratory rate of 21 breaths/minute on room air. Initial laboratory findings are summarized below (Table ). Physical examination was notable for abdominal tenderness and left axillary lymphadenopathy. Abdominal computed tomography (CT) scan showed splenomegaly with subcapsular splenic rupture and large hematoma (Figures -). The patient ultimately required an emergent splenic angiogram with embolization (Figure ).
A broad differential was considered especially with respect to cat bites and associated diseases. The treating team later learned that the cat had succumbed to an unknown illness shortly after the bite incident. Limited testing was performed on the cat to rule out rabies, but a complete necropsy was not performed, and the remains were discarded several days prior to his hospitalization described above. The patient was vaccinated against rabies and tetanus according to guidelines. Antibiotic therapy included ampicillin/sulbactam, azithromycin, and rifampin. Because of the axillary lymphadenopathy and spontaneous splenic rupture, a broad infectious work-up was pursued but was ultimately negative in terms of Bartonella serology. Similarly, serologic work-up for Brucella, Epstein-Barr virus (EBV), and HIV were negative. Serology for endemic fungal infections including Blastomyces dermatitidis and Histoplasma capsulatum were likewise normal. The patient’s blood cultures on admission finalized without growth. Given the patient’s suboptimal response to therapy and intermittent fevers, transesophageal echocardiogram was performed but showed no radiographic evidence of endocarditis. Tularemia serology was obtained and returned positive with a titer of 1:2560. The patient’s antibiotic regimen was transitioned to doxycycline. The patient clinically improved and was eventually discharged home.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [156.0, 'mm hg'], 'Diastolic Blood Pressure': [94.0, 'mm hg']}",114.66667,108.93334,120.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 156.0 mm Hg + 2/3 * 94.0 mm Hg = 114.66667 mm Hg.
Hence, the patient's mean arterial pressure is 114.66667 mm Hg."
1411,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8062124-1,Extracted,"A 42-year-old male non-smoker and non-alcoholic presented with acute right-sided abdominal pain, vomiting, dysuria and fever. The pain was in the right lower abdomen and aggravated by movement. He had nausea and non-bilious vomiting. He had painful micturition with concentrated urine. He had no prior abdominal trauma or surgery. He had no weight loss, diabetes, hypertension, tuberculosis or pancreatitis. He worked as a construction worker for 15 years. He worked in 8-hour shifts, 6 days a week, throughout the year. His main job was to mix cement with asbestos and erect asbestos sheets. He has been handling asbestos daily for >10 years. Physical examination showed: Heart rate 120 bpm, blood pressure 110/70 mm Hg, temperature 39°C, distension and guarding in the right iliac and umbilical region.
Chest radiology and cardiogram were normal. Sputum was negative for acid-fast bacilli. Lab reports showed: haemoglobin 10.4 g/dl, white blood cell 6400 per microlitre, serum creatinine 0.9 mg/dl, alanine-aminotransferase 16 IU/L, aspartate-transferase 51 IU/L, lipase 149 IU/L, amylase 49 IU/L, serum Na + 129 mmol/L, Glucose 146 mg/dl, partial pressure of oxygen 54 mm Hg. Urine microscopy showed numerous red blood cells.
Abdominal ultrasound showed a well-defined intra-abdominal cyst with clear echoes situated in the pelvis compressing and displacing the urinary bladder to the left. The rest of the organs were normal. There was no free fluid.
Computerized tomography showed a solitary well defined intraperitoneal cyst consisting of fluid showing low attenuation. The wall of the cyst was 1 cm thick, with no contrast enhancement. It was situated in the pelvis compressing the urinary bladder. It had no communication with either the bowel or the urinary bladder. The pancreas was normal, as also the rest of the abdominal organs. There was no ascites (–). The diagnosis was a large intraperitoneal infectedcyst.
At laparotomy, a sizeable intra-abdominal cyst, free from the mesentery, omentum and mesocolon, was seen occupying the pelvis, compressing the urinary bladder’s superior aspect. There was no connection between the cyst and the anterior abdominal wall, the umbilicus or the urinary bladder (). The wall of the cyst was blackish suggestive of infarction ( and ). The fluid within the cyst was clear. Complete excision of the cyst was performed. The patient was given third-generation cephalosporins for 3 days. The fluid culture reported no growth of bacteria. The patient showed significant signs of improvement on the second postoperative day. Microscopic haematuria resolved. He was discharged on the 10th postoperative day. He showed no recurrence at 1 year of follow-up.
Histopathology showed cyst wall infarction with infiltration of inflammatory cells, blood vessels and extensive intra-mural bleeds. Few collagen fibres were seen (). Immunohistochemistry could not be done as the epithelial lining was destroyed totally.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1412,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6195710-1,Extracted,"A 43-yr-old, 66 kg, 175 cm man was to undergo gastrectomy for a tumor in the stomach. He had no history of hypertension, myocardial infarction,or angina pectoris,but with a smoking history(10 packs year).His physical examination was normal. Preoperative resting electrocardiogram (ECG) (Fig. )and echocardiogram(UCG) were within normal limits. Laboratory data revealed no abnormalities.
No premedication was given. After the patient,s arrival in the operating room, intravenous access was established. Lead II and V5 of the ECG were monitored. Blood pressure (BP) was 128/70 mmHg and heart rate(HR) 75 beats/min. An ultrasound-guided subcostal TAP block was performed bilaterally []. Each hemi abdomen was injected with 20 ml 0.3% ropivacaine to give a dual block from T6-T9. TAP block was uneventful without heart rate and blood pressure variations. After 30 min, general anesthesia was induced, then it was maintained with sevoflurane inhalation, target controlled infusion (TCI) remifentanil and given sufentanil and cisatracurium intermittently. The patient was mechanically ventilated with a tidal volume of 500 ml and respiratory rate of 10 breaths/min to maintain PetCO2 at 35–40 mmHg under end-tidal CO2 monitoring. Arterial BP was continuously monitored via a left radial artery catheter.
Two hours after start of the operation, when the surgeons were dissecting para gastric lymph node, ST segment elevation in lead II was noted (Fig. ) and lead V5 showed no abnormalities. The change recovered abruptly without treatment 30 s later. When it happened, SpO2 was 100%, end-tidal sevoflurane concentration was 1.3% and no obvious hemorrhage. Except for this, the patient,s course during 4 h of operation was uneventful: BP was about 100/70 mmHg, HR about 70 beats/min, body temperature about 36.5 °C and estimated blood loss was less than 300 ml. Four hours after start of the operation, the arterial BP was 88/55 mmHg and aramine 0.4 mg was given intravenously. The BP increased to 110/65 mmHg without HR change. Approximately 5 min later, the ECG showed premature ventricular contractions and a marked ST segment elevation again (Fig. ). Ventricular tachycardia and fibrillation were subsequently noticed with BP decreased to 32/14 mmHg, and electric defibrillation was initiated with repeated infusions of epinephrin. Within approximately 2 min, the ECG returned to sinus rhythm and BP gradually to normal. The patient remained hemodynamically stable for the remainder of the operation. Following the operation, he was transferred to the cardiac care unit (CCU) in our hospital. Serial ECGs and cardiac enzyme studies showed no abnormalities, thus ruling out myocardial infarction and CAS was diagnosed. The patient suffered no further cardiac attacks during his hospital stay. Consent was obtained from the patient to publish this case report.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [128.0, 'mm hg']}",89.33333,84.86666,93.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 128.0 mm Hg + 2/3 * 70.0 mm Hg = 89.33333 mm Hg.
Hence, the patient's mean arterial pressure is 89.33333 mm Hg."
1413,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-10983,Extracted,"A 59-year-old man presents to general medical clinic for his yearly checkup. He has no complaints except for a dry cough. He has a past medical history of type II diabetes, hypertension, hyperlipidemia, asthma, and depression. His home medications are sitagliptin/metformin, lisinopril, atorvastatin, albuterol inhaler, and citalopram. His vitals signs are stable, with blood pressure 126/79 mmHg. Hemoglobin A1C is 6.3%, and creatinine is 1.3 g/dL. The remainder of his physical exam is unremarkable.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [79.0, 'mm hg'], 'Systolic Blood Pressure': [126.0, 'mm hg']}",94.66667,89.93334,99.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 126.0 mm Hg + 2/3 * 79.0 mm Hg = 94.66667 mm Hg.
Hence, the patient's mean arterial pressure is 94.66667 mm Hg."
1414,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4900321-1,Extracted,"A 25-year-old primigravida weighting 47 Kg (height 165 cm) presented at 29+ week pregnancy with severe AS and New York Heart Association (NYHA) functional class IV. The patient responded to digoxin and furosemide, but with advancing pregnancy patient's condition worsened with episodes of arrhythmia. In view of worsening CHF and viable fetus of 33+ week's gestation, decision for LSCS with AVR was taken. Pre-anesthesia checkup revealed Mallampati class 1 airway, heart rate (HR) 120/min, blood pressure 80/50 mm Hg, respiratory rate (RR) 25/min and orthopnea. Arterial blood gas on ventimask with 0.4 FiO2 showed pH 7.42, PaO2 109 mmHg, PaCO2 24 mmHg, base deficit −6.9, and SaO2 98%. Electrocardiogram revealed sinus rhythm and left ventricular (LV) hypertrophy. Transthoracic echocardiography (TTE) showed bicuspid aortic valve with severe AS and LV ejection fraction (LVEF) 32%. Doppler across the aortic valve revealed a peak velocity of 5.1 m/s. Obstetric examination confirmed a fundal height suggesting 33+ weeks of gestation and fetal heart rate (FHR) of 140/min. An elective LSCS was planned for the delivery of the fetus. The hemodynamics were planned to be maintained close to the baseline with vasoactive agents and emergency institution of CPB if hemodynamic deteriorates.
On the day of surgery, aspiration prophylaxis was given, and furosemide and digoxin were stopped. The operating room (OR) temperature was maintained at 28°C and neonatologist was called for resuscitation. Patient was positioned supine with a left lateral tilt. After attaching routine monitors, left radial artery, a triple lumen central venous catheter and an 8.5 French sheath in right internal jugular vein were inserted under local anesthesia. The baseline hemodynamics was - HR 120/min, arterial blood pressure (ABP) 116/58 mmHg, RR 30/min, SpO2 94%. Patient was pre-oxygenated with 100% oxygen with face mask for 5 min and infusions of adrenaline (0.05 μg/kg/min) and phenylephrine (0.1 μg/kg/min) was started to maintain contractility and ABP. During pre-oxygenation urinary bladder was catheterized and cleaning and draping for AVR and LSCS was done. The cardiac surgical and obstetrics team were ready to intervene if required. Anesthesia was induced with titrated dose of thiopentone (100 mg) till eyelash reflex was lost. Cricoid pressure was applied after loss of consciousness and vecuronium 0.1 mg/kg was administered after ensuring ventilation. ABP of the patient dropped to 80/50 mmHg, which responded to increases in infusions of phenylephrine (0.3 μg/kg/min) and adrenaline (0.08 μg/kg/min) and ABP stabilized at 90–100 mmHg with mean ABP of 60–70 mmHg. Saturation remained at 99% till the delivery of the neonate. LSCS was started while cricoid pressure was maintained, and patient ventilated with sevoflurane in oxygen. Patient was intubated after 3 min with 7 mm cuffed endotracheal tube (ETT). Intermittent positive pressure ventilation was established with sevoflurane in oxygen. The MAC value varied from 0.8 to 1.2. Nasopharyngeal temperature probe and transesophageal echocardiography (TEE) probe was introduced after securing ETT. By the time TEE probe was secured, the baby was delivered. Skin incision to delivery time was 8 min. APGAR score at one and 5 min was 8 and 9 respectively. The uterus was closed and post hemostasis, abdomen was packed with sponges and skin was stapled pending final closure post CPB. Clean sheet was kept below pelvis between the thighs to monitor uterine bleeding. Oxytocin infusion was started after delivery at 20 IU/h for 1st h, followed by 10 IU/h. Intramuscular prostaglandin 250 μg was administered to facilitate uterine contraction. Post-delivery sevoflurane was stopped and breathing system was flushed till gas monitor showed absence of sevoflurane. Post-delivery anesthesia was maintained with midazolam (1 mg), morphine (0.1 mg/kg), followed by propofol infusion (25–75 μg/kg/min), intermittent boluses of vecuronium (0.2 mg/kg) and morphine (every 15 min) before going on CPB. Post-delivery ABP stabilized to 110/58 mmHg probably due to uterine contraction induced auto-transfusion. Therefore, adrenaline was stopped, and phenylephrine was decreased to 0.1 μg/kg/min. Prebypass TEE showed [] peak and mean aortic valve gradients of 126 and 82 mmHg, respectively, and LVEF of 31%. Heparin 300 IU/kg was administered before establishing CPB. Aortic valve was replaced with a 16 mm ATS aortic valve (mechanical). Patient was separated from CPB with the supports of adrenaline 0.1 μg/kg/min and milrinone 0.3 μg/kg/min, respectively. Heparin was neutralized. Sternal wound was packed, uterine contraction and intra-abdominal hemostasis was reassessed and abdominal wound was closed. Thereafter, sternal closure was done. Intra-operatively one unit of packed cell was added to the CPB prime. Two units of packed cells, 2 units of fresh frozen plasma and 2 units of platelets were administered after CPB. Total CPB and ischemia times were 100 and 62 min. Post-CPB, TEE showed peak and mean gradients of 31 and 19 mmHg, respectively. Patient was shifted to the intensive care unit for ventilation and was extubated after 9 h. The patient was transferred to ward after 5 days and healthy mother and baby were discharged after 9 days. TTE at discharge showed peak and mean gradients of 43 and 26 mmHg, pulmonary artery pressure of 44 mmHg and LVEF 25%.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [116.0, 'mm hg'], 'Diastolic Blood Pressure': [58.0, 'mm hg']}",77.33333,73.46666,81.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 116.0 mm Hg + 2/3 * 58.0 mm Hg = 77.33333 mm Hg.
Hence, the patient's mean arterial pressure is 77.33333 mm Hg."
1415,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7562,Extracted,"A 29-year-old internal medicine resident presents to the emergency department with complaints of fevers, diarrhea, abdominal pain, and skin rash for 2 days. He feels fatigued and has lost his appetite. On further questioning, he says that he returned from his missionary trip to Brazil last week. He is excited as he talks about his trip. Besides a worthy clinical experience, he also enjoyed local outdoor activities, like swimming and rafting. His past medical history is insignificant. The blood pressure is 120/70 mm Hg, the pulse is 100/min, and the temperature is 38.3°C (100.9°F). On examination, there is a rash on the legs. The rest of the examination is normal.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1416,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-12507,Extracted,"A 26-year-old female presents to your office due to one week of “feeling unwell.” She complains of a headache and non-productive cough over the last several days, which have both worsened today. She does not have any history of serious infection and is not currently taking any medication. On physical exam, her temperature is 99°F (37.2°C), blood pressure is 120/78 mmHg, pulse is 90/min, respirations are 21/min, and pulse oximetry is 98% on room air. She has diffuse rhonchi bilaterally. You decide to order a chest radiograph, shown in image A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [78.0, 'mm hg'], 'Systolic Blood Pressure': [120.0, 'mm hg']}",92,87.4,96.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 78.0 mm Hg = 92.0 mm Hg.
Hence, the patient's mean arterial pressure is 92.0 mm Hg."
1417,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8383691-1,Extracted,"A woman, 44 years old with para 3, abortion 0, came to the Prof. Dr. R.D. Kandou General Hospital with chief complaint of the discharge of a lump from the birth canal. The patient had felt a lump in her pubic area in the past 6 months, but only now did the lump come out of the birth canal. Complaints such as pain in the lump, the presence of vaginal discharge or bleeding out of the birth canal were denied. The patient also had no complaints about urinating and defecating. The patient complained of a feeling of fullness in the pubic area. Menarche was at 15 years of age with regular menstrual cycles every 28 - 30 days and a duration of 3 to 5 days. The patient had her last menstrual period in 2006. The patient has routinely used 3-month injection contraception since 2006 until now. The patient denied that she had menstrual irregularities or with profuse bleeding. At the time of examination, the patient appeared calm, with a blood pressure of 130/80 mm Hg, a pulse rate of 80 beats per minute, a respiratory rate of 20 times per minute, and a body temperature of 36.9 °C. The patient did not appear icteric or anemic. On examination of the abdomen, no abnormalities were found. On pelvic examination, a pink mass emerged from the vagina. The mass was 8 × 8 × 6 cm in size with a solid consistency (). An ultrasound examination showed that there was an adenomyosis appearance. We did biopsy of the cervical mass and the result was leiomyoma. After clinicopathological conference in our department, we decided to perform vaginal myomectomy, continued with total vaginal hysterectomy. The procedure was performed by an urogynecologist. A vaginal myomectomy was performed under general anesthesia. Intraoperatively, a leiomyoma that came out of the vagina with a hypertrophied cervix was found (). The leiomyoma was removed completely after it was clamped at the base and twisted. The base of the myoma was ligated with polyglycolic acid (PGA) No. 1 tapper. We continued with total vaginal hysterectomy. Estimated bleeding is about 200 mL. Post-operative recovery was good, and the patient was discharged on day 3. The patient came to control 3 days after going home with a good condition.
The histopathologic reports were as follow. From macroscopic appearance, the mass was well-circumscribed white-grey tissue with a glistening surface. It measured 8 × 8 × 6 cm and weighed ± 529 g (). From microscopic appearance it was consistent with leiomyoma with necrotic debris, focal edema, and focal infarction with signs of infection with neutrophil infiltrates. The final diagnosis was cervical leiomyoma.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1418,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6819294-1,Extracted,"A 65-year-old man on peritoneal dialysis was referred to our hospital in July 2018 with complaints of blisters on the left frontal area with pain, and unstable walking and hallucinations.
The patient felt severe pain in the left frontal face, with blisters for 6 d, and was diagnosed with herpes zoster. He was given antiviral treatment with intravenous acyclovir 0.5 g qd and dexamethasone 5 mg qd to relieve pain (continuous treatment for 3 d). The dermatologist prescribed oral valacyclovir 0.3 g bid after 3 d. Nonetheless, the patient misunderstood the recommendation, and received acyclovir and valacyclovir simultaneously. After 2 d of treatment, the local facial pain was relieved, and the blisters became stable, but he became with unstable walking and involuntary shaking of the limbs, accompanied by hallucinations (irregular fluttering of objects when the eyes were closed), irritability, and lethargy. He denied fever, loss of consciousness, epilepsy, suicidal or homicidal ideation, and a sudden stop of dialysis. Before onset, the patient had mild temperament and took care of himself in the daily life.
The patient had a history of hypertension for more than 10 years, under control using nifedipine controlled release tablets 30 mg bid and valsartan 80 mg bid.
He was diagnosed with idiopathic chronic renal failure (stage 5). He had been receiving peritoneal dialysis treatment for 3 years. He was anuretic at admission using peritoneal dialysis solution with 2.5% calcium glucose 2000 mL × 4 bags, continuous ambulatory peritoneal dialysis (CAPD), with an ultrafiltration of 1200 mL/d.
The patient denied any personal or family history of diseases.
On admission, the body temperature 37.2 °C, pulse 107 bpm, breathing 20/min, blood pressure 175/108 mmHg, intermittent mild disturbance of consciousness, and with visible scattered red blister rash in the left eyelid and left forehead, which was protruded and tender, but otherwise with normal superficial lymph nodes and cardiopulmonary examinations. Nervous system examination showed negative Pap's sign but normal muscle tension in limbs.
The laboratory examinations showed: White blood cells 7.8 × 109/L, hemoglobin 86 g/L, albumin 28 g/L, creatinine 1146 µmol/L, urea nitrogen 21.6 mmol/L, uric acid 277 µmol/L, potassium 4.2 mmol/L, sodium 145 mmol/ L, chlorine 100 mmol/L, PO2 43 mmHg, TCO2 24 mmol/L, glucose 4.7 mmol/L, and iPTH 313 pg/mL. Dialysis adequacy: KT/V = 1.64 (1 mo ago), Ccr= 41.4 L/wk. The electrocardiogram showed normal sinus rhythm. The lumbar puncture showed: Cerebrospinal fluid pressure 155 mmH2O, proteins 542 mg/L, glucose 4.64 mmol/L, chlorine 121.7 mmol/L (no abnormality), and negative bacteria and tuberculosis.
There were no obvious abnormalities in head and chest computed tomography (CT) as well as head magnetic resonance imaging (MRI).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [175.0, 'mm hg'], 'Diastolic Blood Pressure': [108.0, 'mm hg']}",130.33333,123.81666,136.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 175.0 mm Hg + 2/3 * 108.0 mm Hg = 130.33333 mm Hg.
Hence, the patient's mean arterial pressure is 130.33333 mm Hg."
1419,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6108301-1,Extracted,"A 40-year-old male presented to emergency room of our hospital with a history of fever, cough, severe neck pain, sore throat, and difficulty in deglutition of 1-week duration. He was a known case of diabetes mellitus following acute severe pancreatitis and pancreatic surgery 3 years back; now on mixed insulin 18 units 8 hourly and plain insulin 10 units afternoon. On examination, the patient was normal built, conscious, anxious, and febrile (temperature 39°C). His vitals include heart rate 147 beats per minute, blood pressure 92/51 mmHg, SpO295% on room air, and arterial blood gas showed mild metabolic acidosis with lactate of 2.7. A large tender midline swelling of approximately 5 cm × 4 cm, warm on touch, in the thyroid region, with erythema over the overlying skin []. The swelling moved with deglutition. The thyroid function tests showed hyperthyroidism with free T3 8.86 pg/ml (1.71–3.71), free T4 more than 5 ng/dl (0.7–1.48), and very low thyroid-stimulating hormone 0.004 μIU/ml (0.35–4.94). His other significant laboratory investigations are seen in . He was shifted to ICU and managed as per surviving sepsis guidelines with fluids, antibiotics (ceftriaxone and moxifloxacin) and other supportive management. The bedside ultrasound neck revealed diffuse hyperechoic swelling on the right side of the neck most likely originating from the right thyroid lobe with suspected air halos. After initial resuscitation patient was started on intravenous (IV) antibiotics (ceftriaxone and moxifloxacin), tablet propranolol 20 mg 8 hourly, hydrocortisone 50 mg IV 8 hourly, and carbimazole 10 mg 8 hourly. Contrast-enhanced computed tomography (CT) scan of the neck revealed a large ill-defined area of peripherally enhancing collection with multiple compartments and multiple entrapped air pockets and areas of liquefaction suggestive of abscess arising from right lobe of thyroid with left lobe of thyroid appearing normal []. The diagnosis of thyroid abscess was made, and CT-guided drainage of 25 ml of pus was done after 18 h of admission, and 8F catheter was left in situ []. The patient continued to have hoarseness of voice which on direct laryngoscopy was found to be right vocal cord paralysis. The pus showed Klebsiella pneumoniae sensitive to ceftriaxone. The urine culture also showed K. pneumoniae with similar antimicrobial sensitivity profile. Ultrasound abdomen did not show any pyelonephritis but hypoechogenicity in urinary bladder suggestive of cystitis. His final diagnosis was acute suppurative thyroiditis, thyroid abscess, and thyrotoxicosis with diffuse goiter without thyroid crisis, urinary tract infection, right vocal cord palsy, and diabetes mellitus. The moxifloxacin was stopped and ceftriaxone was continued for 8 days. The patient condition improved and was discharged after on 9th day. On 6-month follow-up, the patient continued to have mild hoarseness of voice with thyroid function recovered to normal.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [51.0, 'mm hg'], 'Systolic Blood Pressure': [92.0, 'mm hg']}",64.66667,61.43334,67.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 92.0 mm Hg + 2/3 * 51.0 mm Hg = 64.66667 mm Hg.
Hence, the patient's mean arterial pressure is 64.66667 mm Hg."
1420,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-2013,Extracted,"A 56-year-old woman is brought to the emergency department by her husband because of increasing confusion, generalized fatigue, and irritability for the past week. She has been unable to recall her husband's name or their address. She has had insomnia and daytime sleepiness during this period. Her last bowel movement was 3 days ago. One month ago, she underwent a transjugular intrahepatic portal shunt (TIPS) placement. She has alcoholic liver cirrhosis. Current medications include spironolactone and furosemide. She used to drink over a pint of vodka daily but quit 2 months ago. She is oriented to place and person. Her temperature is 37.3°C (99.1°F), pulse is 88/min, and blood pressure is 102/64 mm Hg. Examination shows scleral icterus and jaundice. There are several telangiectasias over the chest and back. Palmar erythema is present. The abdomen is mildly distended and nontender. Shifting dullness is present. There is a flapping tremor of both hands when outstretched and dorsiflexed. Neurologic examination shows no other focal findings. She completes the number connection test slower than the age-normalized standard.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [64.0, 'mm hg'], 'Systolic Blood Pressure': [102.0, 'mm hg']}",76.66667,72.83334,80.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 102.0 mm Hg + 2/3 * 64.0 mm Hg = 76.66667 mm Hg.
Hence, the patient's mean arterial pressure is 76.66667 mm Hg."
1421,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5947929-2,Extracted,"A 55-year-old female patient presented with abdominal pain, nausea, and vomiting. The patient’s medical and family history did not include any specific characteristic. Her blood pressure was 140/80 mmHg, and pulse was 85 (min) at presentation. Laboratory analysis did not indicate any significant pathology. Computerized tomography of the abdomen showed an abdominal mass of mesenteric origin sized 6.7*6*5.5 cm, with intense contrast uptake in the mesenterium in the lower abdominal quadrant. The patient had no additional morbidity, and a decision was made for surgery. Intra-abdominal exploration revealed a mass with regular margins, localized at the mesenteric root at approximately 50 cm proximal of the terminal ileum. The mesenteric mass was resected together with segmentary small intestine resection (Figure ).
Histopathological investigation of the mass revealed a giant granulomatous structure that consisted of plasma cells. In light of this information, the patient was screened for potential granulomatous diseases, such as tuberculosis and sarcoidosis. The patient was diagnosed with Castleman disease, as she was found to be negative for granulomatous diseases (Figure ). The patient is currently in the postoperative twelfth month, and she had been followed-up without any complications.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 80.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1422,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5066102-1,Extracted,"A 22-year-old non vegetarian Afro-Trinidadian female, previously well, active and working as a student nurse, presented to the emergency department of hospital with severe left sided frontal headaches and vomiting over two days. Her symptoms were associated with fever, unsteady gait and dizziness. She had no history of head trauma or use of recreational drugs, alcohol, smoking or exposure to chemicals at work. However, the patient reported a first time use of a single intramuscular dosage of 150 mg of medroxyprogesterone for contraceptive purpose two weeks before date of admission to hospital. She had no previous medical or surgical problems. Patient’s family history was unremarkable. On physical examination the patient was in no cardiorespiratory distress with a Glasgow Coma Scale of 15/15. She was oriented to time, place and person. Blood pressure was 113/69 mm of Hg, heart rate was 106 beats per minute regular, respiratory rate was 18 breaths per minute, body temperature was 36.5°C, oxygen saturation of 100% on room air and patient’s body mass index was 25. Visual acuity, visual field, pupillary reflexes, eye movements and other cranial nerves examination were initially normal. Tone and power in upper and lower limbs were normal. Deep tendon reflexes were equal and symmetrical +++ at ankles, knees, biceps and triceps bilaterally. Plantar response showed positive Babinski’s sign bilaterally. Sensory, vibration and proprioception tests were normal. Kernig’s and Brudzinski’s signs were negative. Romberg’s test was positive and associated with wide based stance and ataxic gait. The patient showed poor coordination of voluntary movements during rapid alternate movements, finger to nose and heel to shin tests. On the second day of admission to hospital, the patient developed blurred vision and diplopia bilaterally. Fundoscopic examination showed bilateral papilloedema. Full blood count report revealed that hemoglobin was 129 g/L (female 120-156 g/L), platelet count was 187×109 platelets/L (150-350×109 platelets/L), white cell count was 8.4×109/L (4.5-11.0×109/L), mean red blood cell volume was 88.8 fL (80-100 fL), hematocrit was 0.38 (female 0.36-0.46). A blood film showed normochromic and normocytic red blood cells. Renal function tests, liver function tests, thyroid function tests, C3, C4, and electrolytes were all within normal limits. C reactive protein was 1.0 mg/L. Urine beta human chorionic gonadotropin, HIV rapid, Venereal Disease Research Laboratory, Mantoux and Ebstein barr antibody tests were all negative. Autoimmune and vasculitic screen: antinuclear antibodies, DS-DNA, atrial natriuretic factor, SS-B, Scleroderma-70, PM-SCL, JO-1, centromere autoantigen B, proliferating cell nuclear antigen, antinucleosome antibodies, histone antibodies, antiribosomal P protein antibodies, AMA-M2, lupus anticoagulant, P-antineutrophil cytoplasmic antibodies (ANCA), and C-ANCA were all negative. Serum vitamin B12 was 2000 pg/mL (211-946 pg/mL). Serum methylmalonic acid was 427 nmol/L (0-378 nmol/L), serum homocysteine was 14.2 umol/L (3.4-20.4 umol/L), parietal cell antibodies were less than 2 RU/mL (Negative when less than 20) and intrinsic factor antibodies were less than 2 RU/mL (Negative when less than 20). Tissue transglutaminase antibodies (IgA, IgG) and endomysial and Anti-Saccharomyces cerevisiae antibodies were negative. A lumbar puncture done 8 days after admission showed an opening cerebrospinal fluid (CSF) pressure of 13 cm of H2O, clear CSF fluid with normal cell count, protein and glucose. CSF culture showed no bacterial growth. CSF displayed 3 unmatched oligoclonal IgG bands and one matched oligoclonal IgG band using isoelectric focusing and immunoblotting methodology.
A brain computerized axial tomography scan was normal. Brain magnetic resonance imaging (MRI) scan, magnetic resonance angiography scan and magnetic resonance venography scan were all normal (). MRI scan of the spine was normal. Visual perimetry showed enlargement of blind spot in both eyes. Optical coherence tomography of both eyes was normal. The patient was diagnosed then as suffering from possible IIH induced by medroxyprogesterone. She was treated with oral acetazolamide 300 mg three times daily in addition to a therapeutic lumbar puncture, following which there was complete resolution of patient’s headaches, vomiting and blurred vision. Due to rapid improvement repeat lumbar puncture was considered unnecessary. She had minimal improvement of gait but Romberg’s test and Babinski became negative. The patient was discharged after 15 days in hospital with continued physiotherapy, medical outpatient clinical follow up and advised on cessation of medroxyprogesterone. She developed complete ophthalmological and neurological recovery three months after administration of medroxyprogesterone. She has since returned to her job and performing normal duties as a student nurse. Brain MRI scan sequences including fluid inversion recovery images performed one year later remained the same with normal third, laterals and fourth ventricles without transependymal changes.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [113.0, 'mm hg'], 'Diastolic Blood Pressure': [69.0, 'mm hg']}",83.66667,79.48334,87.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 113.0 mm Hg + 2/3 * 69.0 mm Hg = 83.66667 mm Hg.
Hence, the patient's mean arterial pressure is 83.66667 mm Hg."
1423,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7784230-1,Extracted,"A 58-year-old Malay lady with underlying type 2 diabetes and hypertension for 2 years was admitted to a nearby hospital for lacunar stroke. During assessment, she was noted to have features of acromegaly. On further interview, she disclosed increased shoe (from 6 to 11) and ring (14 to 26) sizes. She also experienced hoarseness, increased sweating, weight gain and higher blood pressure on monitoring. She also observed an enlarging goiter but denied obstructive symptoms. She had severe sleep apnea symptoms based on the Epworth Sleepiness scale. There were no known endocrine disorders or malignancy in her family.
Physical examination revealed marked features of acromegaly: frontal bossing, prognathism, increased interdental separation, thick lips and coarsened facial features. Her blood pressure was 160/90 mmHg, with no clinical evidence of heart failure. She had a hard goiter with palpable cervical lymph nodes. She had moist palms and skin tags. Visual field was intact on confrontation test.
Initial tests showed elevated IGF-1 (703 μg/L, reference range 35-210) and fasting GH (10.3 ng/mL, reference range up to 8). GH was not suppressed by oral glucose loading, with a nadir of 12.9 μg/L. Follicle stimulating hormone (26.5 IU/L) and luteinizing hormone (8.6 IU/L) were low for age. Other parameters were within reference ranges (prolactin 150 IU/mL, thyroid stimulating hormone 1.15 μIU/mL, free thyroxine 13.8 pmol/L, corrected Ca 2.36 mmol/L, serum Na 138 mmol/L, serum K 4.0 mmol/L and serum creatinine 44.9 μmol/L). HbA1c was 6.9%. Sleep study yielded an Apnea-Hypopnea Index (AHI) of 36.5, indicative of severe OSA. Echocardiogram performed in preparation for eventual surgery showed concentric LVH and diastolic dysfunction with an ejection fraction of 65%. Magnetic resonance imaging (MRI) of the pituitary revealed a 1.5 cm x 1.8 cm x 1.1 cm macroadenoma located at the anterior pituitary invading the right cavernous sinus and encasing the right internal carotid artery. There was a clear plane separating the pituitary from the optic chiasm ().
Neck ultrasonography showed multiple mixed solid and cystic nodules in both thyroid lobes. The thyroid nodule on the right lobe appeared solid and cystic, with wall calcification and no vascularity (). There were multiple predominantly solid thyroid nodules with internal microcalcifications on the left lobe, with the largest nodule measuring 3.2 cm x 3.2 cm x 4.6 cm located at the lower pole (). Subcentimeter cervical lymph nodes were also seen. Fine needle aspiration cytology of the thyroid nodule reported neoplastic thyroid epithelial cells displaying enlarged nuclei, nuclear grooves and intranuclei inclusions suggestive of papillary thyroid cancer.
Medical therapy with subcutaneous octreotide LAR 20 mg monthly for 6 months prior to surgery was initiated to alleviate cardiovascular, metabolic and respiratory comorbidities. Recent lacunar strokes were also a contraindication to immediate surgery. After 3 months of medical therapy, clinical features of acromegaly and OSA improved, and IGF-1 became normal.
She underwent total thyroidectomy with therapeutic anterior and left lateral neck dissection. Histopathologic evaluation revealed papillary thyroid cancer measuring 5 cm x 5 cm, with involvement of 5 of the 8 resected lymph nodes. Subsequent remnant ablation with radioactive iodine 120 mCi was done. Post-treatment whole body scan (WBS) showed uptake at the area of the thyroid bed.
Follow-up MRI after 6 months of octreotide LAR revealed a residual 0.5 cm x 0.6 cm x 0.3 cm pituitary microadenoma (). Transphenoidal adenomectomy was uneventful, with no post-operative pituitary hormonal deficit and diabetes insipidus. IGF-1 remained within normal range for age and gender.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [160.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",113.33333,107.66666,119,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 90.0 mm Hg = 113.33333 mm Hg.
Hence, the patient's mean arterial pressure is 113.33333 mm Hg."
1424,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6113389-1,Extracted,"Case 1 is a 65-year-old, right-handed male with 84 cytosine-guanine-guanine (CGG) repeats, who denied tremor and ataxia. On examination his blood pressure was 177/87 mmHg and his heart rate was 62 bpm. This was consistent with reported history of and treated with metoprolol and candesartan. His body mass index (BMI) was 29.3. On neurological examination, finger-to-nose touching was without tremor and his arm movements were normal. His deep tendon reflexes were 1 to 2+ in the upper extremities, 3+ at the knees, and 2+ at the ankles. His temperature sensation was normal and his vibration sensation was absent in both great toes. Tandem walking was performed normally. No cognitive abnormalities were present on neuropsychological examination and no psychiatric symptoms were reported.
His MRI demonstrated the emergence of a faint MCP sign (Figure ). His CC was slightly thin with minimal hyperintensity of the splenium of the CC. There was no significant atrophy but there was a hint of white matter hyperintensity in the insula bilaterally.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [177.0, 'mm hg'], 'Diastolic Blood Pressure': [87.0, 'mm hg']}",117,111.15,122.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 177.0 mm Hg + 2/3 * 87.0 mm Hg = 117.0 mm Hg.
Hence, the patient's mean arterial pressure is 117.0 mm Hg."
1425,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8264243-1,Extracted,"A 63-year-old African American male with a history of hypertension and anemia presented with intractable hiccups and fevers for 2 weeks. He denied dysphagia, shortness of breath, cough, abdominal pain, nausea, vomiting, jaundice, changes in stool, and dysuria. The patient initially visited an outside hospital 1 week prior to presentation for similar symptoms and was discovered to have acute kidney injury, pneumonia, and elevated liver enzymes. He was then admitted for 3 days, treated with fluids and intravenous antibiotics prior to being discharged home on oral antibiotics. He continued to experience hiccups, which prompted him to return to the same hospital's emergency department where he was prescribed oral diazepam and discharged home. Patient now sought a second opinion for persistent hiccups and ongoing fevers. Upon arrival, vital signs were notable for blood pressure 150/110 mmHg, heart rate 101 bpm, and temperature 38.9°C. Physical examination revealed an ill-appearing, diaphoretic male with a soft, non-tender, non-distended abdomen. Laboratory studies were significant for leukocytosis with white blood cell count (WBC) of 23 400 mm3, segmented neutrophils 85%, hemoglobin 13.6 g/dL, mean corpuscular volume 84.2 fL, creatinine 1.12 mg/dL, aspartate aminotransferase 17 U/L, alanine aminotransferase 37 U/L, alkaline phosphatase 111 U/L, and total bilirubin 0.7 mg/dL. Contrast-enhanced, abdominopelvic computed tomography (CT) scan revealed acute sigmoid diverticulitis and diffuse, multiloculated hypodense lesions consistent with liver abscesses, with the largest lesions measuring 8.3 × 5.6 cm and 3.9 × 3.5 cm in size (Fig. ). Patient was started on intravenous piperacillin–tazobactam and underwent percutaneous abscess drainage. Fine needle aspiration yielded 5 mL of purulent aspirate. Bacterial culture did not show growth after 5 days. He was also started on baclofen. Patient's clinical condition subsequently improved with complete resolution of his hiccups, and he was discharged home on a 6-week course of oral antibiotics ciprofloxacin and metronidazole.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [110.0, 'mm hg'], 'Systolic Blood Pressure': [150.0, 'mm hg']}",123.33333,117.16666,129.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 110.0 mm Hg = 123.33333 mm Hg.
Hence, the patient's mean arterial pressure is 123.33333 mm Hg."
1426,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8223,Extracted,"A 41-year-old woman presents with acute onset severe epigastric pain radiating to the back that began a few hours ago. She also complains of nausea and has vomited twice in the past hour. She denies any history of similar symptoms or trauma in the past. Past medical history is significant for diabetes type 2 and HIV infection diagnosed 6 months ago long-standing mild intermittent asthma, and generalized anxiety disorder. She takes metformin for her diabetes but does not remember the names of her HIV medications. She reports moderate social alcohol use. Her vital signs include temperature 37.6°C (99.6 °F), pulse 95/min, blood pressure 110/74 mm Hg, respiratory rate 12/min Her body mass index (BMI) is 21 kg/m2. Laboratory findings are significant for the following:
Serum amylase: 415 U/L
Serum lipase: 520 U/L
A contrast CT of the abdomen reveals an edematous pancreas with peripancreatic fluid collection with a normal gallbladder.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [74.0, 'mm hg']}",86,81.7,90.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 74.0 mm Hg = 86.0 mm Hg.
Hence, the patient's mean arterial pressure is 86.0 mm Hg."
1427,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5965420-1,Extracted,"A 34-year-old woman presented to the emergency department (ED) with acute onset of severe abdominal pain and distention with associated diffuse tenderness and guarding. Her medical history was significant for a two-year history of fibroids, which contributed to mild menorrhagia. Within 30 minutes of arrival, the patient developed signs of shock with a blood pressure of 89/67 mmHg, heart rate of 115 beats per minute, and a drop in serial hemoglobin measurements from 8.4 g/dL to 6.8 g/dL. Point-of-care ultrasound showed a large amount of free fluid in the abdomen associated with a large abdominal mass originating in the pelvis. Emergent computed tomography (CT) imaging demonstrated a large amount of intra-peritoneal bleeding associated with massive fibroids as shown in –. Exploratory laparotomy discovered 3L of hemoperitoneum as well as a roughly 30-week-sized uterus with multiple fibroids, two of which were torsed and actively bleeding. The patient received four units of packed red blood cells, underwent emergent supracervical hysterectomy without additional complications, and was eventually discharged on post-operative day 3. Surgical pathology demonstrated normal endocervical and endometrial tissue, as well as multiple intramural and subserosal leiomyomas measuring up to 17.8 cm in length.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [89.0, 'mm hg'], 'Diastolic Blood Pressure': [67.0, 'mm hg']}",74.33333,70.61666,78.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 89.0 mm Hg + 2/3 * 67.0 mm Hg = 74.33333 mm Hg.
Hence, the patient's mean arterial pressure is 74.33333 mm Hg."
1428,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7883526-1,Extracted,"We present a case of a 40-year-old female who presented to the emergency department for nausea, vomiting, diarrhea, and left-sided abdominal pain. On admission, her temperature was 98.1 F (36.7 degrees C), with a blood pressure of 176/119 mmHg, heart rate of 111 bpm, tachypneic at 38 cpm, saturating 100% on room air. Initial laboratory workup showed leukocytosis of 15.2 K/uL (normal: 3.3 -8.7 K/uL) with 81% neutrophils (normal 44-73%), anemia of 10 (normal: 14-17 g/dL), thrombocytopenia of 134 K/uL (normal: 147-347 K/uL), elevated blood urea nitrogen (BUN) - 109 mg/dL (normal: 8-20 mg/dL), bicarbonate - 8 mmol/L (normal: 23-31 mmol/L), anion gap of 20 mmol/L (normal: 8-16 mmol/L), creatinine - 5.1 mg/dL (normal: 0.7-1.3 mg/dL), sodium - 139 mmol/L (normal: 136-145 mmol/L), potassium 4.8 mmol/L (normal: 3.5-5.1 mmol/L). Urinalysis showed 2+ protein, 3+ leucocyte, and negative nitrite. Urine microscopy showed >100 white blood cells (WBC), 51-100 red blood cells (RBC), and trace bacteriuria. She was started on empirical antibiotics with ceftriaxone for pyelonephritis. After 24 hours, hemoglobin dropped to 3.6 and she was admitted to the intensive care unit (ICU) for hemorrhagic shock secondary to upper gastrointestinal bleed for pressor support and acute hypoxic respiratory failure requiring intubation. She was started on hemodialysis for her acute kidney injury and later continuous renal replacement therapy (CRRT) due to shock. Ceftriaxone was escalated to cefepime 48 hours after initiation for worsening leukocytosis and preliminary blood cultures with gram-negative bacilli. She received 2 g every 12 hours of cefepime (based on dosing in hemofiltration). Urine culture later grew Escherichia coli. Upper limb extremity twitching was noted with passive movement of her upper limbs 96 hours after the commencement of cefepime. Neurology was consulted. MRI was negative for any acute intracranial process. Spot electroencephalograph (EEG) showed diffuse slowing suggestive of encephalopathy, triphasic waves with no evidence of epileptiform discharges or electrographic seizures (Figure ). Due to continued twitching involving the face and bilateral upper extremities, EEG was converted to continuous which later showed 2 Hertz sharply contoured triphasic form rhythmic wave suggestive of non-convulsive status epilepticus (Figure ). The discharges had clinical correlation with eye movements seen on the video EEG. Cefepime was discontinued and deescalated to ceftriaxone. The patient received lorazepam, loaded with levetiracetam, and started on propofol. She was later changed to midazolam drip due to concern for cefepime-induced seizures and its action on gamma-aminobutyric acid (GABA) receptors. Hemodialysis (HD) was completed to aid cefepime clearance. Following dialysis, her twitching stopped and no further electrographic seizures or triphasic waves were seen on video EEG. EEG was discontinued. The patient was weaned off sedation with improvement in neurological status. She was extubated three days after HD. Her renal function improved, and she was subsequently discharged home.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [176.0, 'mm hg'], 'Diastolic Blood Pressure': [119.0, 'mm hg']}",138,131.1,144.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 176.0 mm Hg + 2/3 * 119.0 mm Hg = 138.0 mm Hg.
Hence, the patient's mean arterial pressure is 138.0 mm Hg."
1429,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7219986-1,Extracted,"A 55-year-old woman presented to the emergency department (ED) with the chief complaint of headache for three days, associated with nausea, vomiting, and visual changes. The headache was described as being sudden in onset, constant, bilateral, retro-orbital, and throbbing. The pain was a six out of ten in intensity. The pain was not alleviated with over the counter acetaminophen use. She was not able to describe any alleviating or exacerbating factors. The visual changes were described by the patient as “blurry vision” and “double vision” affecting her left eye greater than her right. She reported photophobia and difficulty keeping the left eye open. The patient described this difficulty of keeping the eye open as a weakness and not secondary to pain. She had approximately five episodes of non-bloody and non-bilious vomiting over the past three days and reported inability to tolerate her home medications. She also reported a sore throat and cough productive of yellow sputum for the previous two to three days, but denied fever, chills, chest pain, hemoptysis, or dyspnea.
Her past medical history included essential hypertension, hyperlipidemia, and a remote history of uterine fibroids associated with iron deficiency anemia. Prescribed medications included losartan 25 milligrams (mg) and hydrochlorothiazide 12.5 mg. She had no known drug allergies, did not smoke, drink alcohol, or use illicit drugs. She was unemployed and lived alone. The patient was post-menopausal and was pregnant three times-two of which were normal spontaneous deliveries with two living children and one prior abortion.
Vital signs were: temperature 98.8° Fahrenheit, heart rate 84 beats per minute, blood pressure 135/74 millimeters of mercury, respiratory rate of 18 breaths per minute and room air oxygen saturation 97%. Her body mass index was 42 (normal 18.5–24.9). Complete physical examination was unremarkable except her left eye’s lateral gaze was restricted by approximately 25%. Her visual acuity was 20/25 and 20/30, right and left eyes, respectively. Initial laboratory testing were resulted ( and ). An electrocardiogram was performed ().",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [74.0, 'mm hg'], 'Systolic Blood Pressure': [135.0, 'mm hg']}",94.33333,89.61666,99.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 74.0 mm Hg = 94.33333 mm Hg.
Hence, the patient's mean arterial pressure is 94.33333 mm Hg."
1430,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1002,Extracted,"A 42-year-old woman comes to the physician for a routine health maintenance examination. She has generalized fatigue and has had difficulties doing her household duties for the past 3 months. She has eczema and gastroesophageal reflux disease. She has a history of using intravenous methamphetamine in her youth but has not used illicit drugs in 23 years. Her medications include topical clobetasol and pantoprazole. She is 160 cm (5 ft 3 in) tall and weighs 105 kg (231 lb); BMI is 42 kg/m2. Her temperature is 37°C (98.6°F), pulse is 95/min, and blood pressure is 145/90 mm Hg. The lungs are clear to auscultation. Cardiac examination shows no abnormalities. Pelvic examination shows a normal vagina and cervix. Laboratory studies show:
Hemoglobin 13.1 g/dL
Leukocyte count 7,800/mm3
Platelet count 312,000/mm3
Serum
Na+ 141 mEq/L
K+ 4.6 mEq/L
Cl- 98 mEq/L
Urea nitrogen 12 mg/dL
Fasting glucose 110 mg/dL
Creatinine 0.8 mg/dL
Total cholesterol 269 mg/dL
HDL-cholesterol 55 mg/dL
LDL-cholesterol 160 mg/dL
Triglycerides 320 mg/dL
Urinalysis is within normal limits. An x-ray of the chest shows no abnormalities. She has not lost any weight over the past year despite following supervised weight loss programs, including various diets and exercise regimens.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [145.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",108.33333,102.91666,113.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 145.0 mm Hg + 2/3 * 90.0 mm Hg = 108.33333 mm Hg.
Hence, the patient's mean arterial pressure is 108.33333 mm Hg."
1431,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3755407-1,Extracted,"A 72-year-old female patient presented to the emergency otolaryngology services with a huge anterior neck swelling, hoarseness of voice, and stridor. The swelling started as a painless lump in the upper part of neck which gradually increased in size over 5 years. The patient developed progressive difficulty in breathing and hoarseness of voice of one-month duration and noisy breathing (stridor) of 4-days-duration which brought her to the emergency department. There was no history of recent rapid increase in size of the swelling. The patient did not give history suggestive of any neurological illness, prior surgery, or trauma.
On examination, the patient had severe stridor and hoarseness of voice which worsened in supine position. The pulse rate was 110 per min and regular in rhythm. The blood pressure was 110/80 mm of Hg. The respiratory rate was 42 per minute. Neck examination revealed a 20 cm × 18 cm mass in the anterior neck more on the left side extending from the level of hyoid superiorly to the level of the suprasternal notch inferiorly (). The mass extended from the posterior border of left sternocleidomastoid to the anterior border of right sternocleidomastoid crossing the midline. The mass moved with deglutition but not with protrusion of tongue. The hyoid, laryngeal framework, and the trachea were pushed towards the right side (). The right carotid pulse could be felt along the lateral border of the mass (). Laryngoscopy with 70 degree 4 mm rigid endoscope (Karl Storz) revealed a distorted upper airway with folded epiglottis and a narrowed glottis pushed to the right (). The right cord was mobile and the left cord was paralysed. Based on history and clinical examination a provisional diagnosis of a malignant lesion of thyroid was made with a differential diagnosis of cystic colloid goitre and branchial cyst.
Ultrasound revealed a 14 cm cystic mass which was hypoechoic with homogenous echogenicity compressing the airway. The right carotid was found to be pushed laterally. Contrast enhanced computed tomography (CECT) showed a homogenous mass of size 14 × 10 cm on the left side extending from the hyoid to the manubrium sterni compressing the tracheal lumen to a longitudinal slit. The cyst was intimately related to the hyoid bone. There was distortion of the laryngeal framework with localized remodelling of hyoid bone (Figures and ). Baseline haematological and biochemical parameters and chest radiograph were normal.
As the airway anatomy was distorted, difficult intubation was anticipated. The airway was secured in the awake patient, with endoscopic guidance by railroading the endotracheal tube over number 14.0fr/65 cm ventilating airway exchange catheter (FROVA, COOK INCORPORATED, USA). Intraoperatively approximately 14 cm × 10 cm cystic mass was seen compressing the left lobe of thyroid gland. The left recurrent laryngeal nerve was found to be displaced from the tracheo-esophageal groove and stretched beneath the mass.
The left lamina of thyroid cartilage, the cricoid cartilage, and the tracheal rings were distorted and compressed by the mass. The cyst was partially decompressed by needle aspiration which helped to identify the tissue planes and the entire cyst was removed completely after identifying the recurrent laryngeal nerve on both sides. The patient was extubated after surgery without any need for tracheostomy.
Histopathological examination revealed a cyst with squamous epithelial lining with underlying thyroid tissue. There was no evidence of malignant foci within the cyst. The findings were consistent with a benign thyroglossal cyst. The cyst fluid was sterile with plenty of exfoliated epithelial cells and negative for malignant cytology. The postoperative period was uneventful. Post-op thyroid function tests revealed an euthyroid status. The stridor resolved completely immediately after surgery but hoarseness persisted. The patient was discharged on the 10th post-op day. No recurrence was found in the patient on followup three months after surgery.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 80.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1432,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9361,Extracted,"A 32-year-old woman presents with a severe headache and neck pain for the past 60 minutes. She says the headache was severe and onset suddenly like a ‘thunderclap’. She reports associated nausea, vomiting, neck pain, and stiffness. She denies any recent head trauma, loss of consciousness, visual disturbances, or focal neurologic deficits. Her past medical history is significant for hypertension, managed with hydrochlorothiazide. She denies any history of smoking, alcohol use, or recreational drug use. The vital signs include: temperature 37.0°C (98.6°F), blood pressure 165/95 mm Hg, pulse 92/min, and respiratory rate 15/min. On physical examination, there is mild nuchal rigidity noted with limited flexion at the neck. An ophthalmic examination of the retina shows mild papilledema. A noncontrast computed tomography (CT) scan of the head is performed and shown in the exhibit (see image).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [95.0, 'mm hg'], 'Systolic Blood Pressure': [165.0, 'mm hg']}",118.33333,112.41666,124.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 165.0 mm Hg + 2/3 * 95.0 mm Hg = 118.33333 mm Hg.
Hence, the patient's mean arterial pressure is 118.33333 mm Hg."
1433,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4683482-1,Extracted,"A 23-year-old primigravida at term, presented with grade III dyspnea (New York Heart Association grading). This case was diagnosed as a case of congenital heart disease at 9 months of pregnancy by a primary care physician and referred to our hospital for safe confinement. Patient had a history of palpitations not associated with chest pain or any syncopal attack. At 15 years of age patient had breathlessness for which she was prescribed tablet furosemide 40 mg overdose (OD) by her primary care physician. She continued the medication only for 1-year. Previous echocardiographic evaluation done 3 years prior was suggestive of congenital heart disease (large VSD with severe pulmonary hypertension, right ventricular hypertrophy, bidirectional shunt). Patient had gestational hypertension detected in the third trimester, but was not on any treatment. Patient had also been diagnosed as a case of hypothyroidism 1-year back and was on tablet eltroxin 50 µg OD. Otherwise she was asymptomatic throughout her pregnancy.
On physical examination, patient was of average body build, with weight of 48 kg, pulse rate of 80/min, good volume with blood pressure of 130/80 mmHg in supine position and 150/90 in left lateral position. There was grade II clubbing and cyanosis. Her room air SpO2 was 80–85% and increased to 92% with oxygen supplementation. There was no pedal edema. Cardiovascular system revealed apex beat shifted to 6th intercostal space lateral to mid clavicular line. S1, S2 were normally heard, there was a loud p2 and a grade III holosystolic murmur heard in the right lower sternal border radiating to axilla. Patient's respiratory rate was 20/min with bilateral vesicular breath sounds with few basal crepitations. Fundal height corresponded to 32 weeks of gestation, fetal heart sound was well heard with a heart rate of 140/min. Ultrasonography of the abdomen showed a live fetus with intrauterine growth restriction and oligohydramnios. Electrocardiography findings were sinus rhythm with first degree heart block, right bundle branch block and right ventricular hypertrophy. Echocardiography revealed a large sub-pulmonic VSD, bi-directional shunt, severe pulmonary artery hypertension (PAH) with right ventricular hypertrophy. Both the great vessels originated from the right ventricle (RV), suggestive of DORV []. Investigations showed hemoglobin of 10.2 g/dL, a platelet count of 2.2 lakhs/mm3 and an INR of 1.2. After shifting the patient to operation theater table, a wedge was kept under the right hip and oxygen supplementation was carried out by mask. After connecting all standard monitors, she was put in left lateral position and preloaded with 200 ml crystalloids slowly. Under full aseptic precautions, after local infiltration, an 18 gauge Tuohy epidural needle was used to locate the epidural space by loss of resistance to air at L2-L3 interspace and an epidural catheter was threaded 4 cm inside. Test dose was given and there was no evidence of intravascular or subarachnoid placement. Patient was turned to supine position, and a wedge placed under the right hip. Patient continued to receive supplemental oxygen by mask. As the expected duration of the surgery was <1 h, we used 2% lignocaine through the epidural catheter. After giving 5 ml of lignocaine 2% initially through the epidural catheter we waited for 5 min. Adequate level was not achieved. Additional 5 ml of lignocaine 2% was repeated and level was checked. After injecting another 3 ml of 2% lignocaine, a T6 level was achieved. A total volume of 16 ml of lignocaine was given including the test dose. During this period blood pressure was maintained within normal limits.
After delivery of the baby, patient received injection oxytocin 5 units slow intravenous (IV)[] (diluted to 10 ml) followed by another 5 units as an infusion. Uterus was well contracted. Total duration of surgery was 40 min and patient was shifted to Intensive Care Unit (ICU) for observation under continuous monitoring. Patient received epidural morphine for postoperative analgesia. Baby was observed in neonatal ICU in view of IUGR. Patient was ambulated within the next 24 h in the ICU. Her repeat echocardiography showed, DORV, Large VSD with bidirectional shunt, severe PAH with 4 mm patent ductus arteriosus. Contrast enhanced cardiac computer tomography – showed both great vessels arising from RV, sub-pulmonic VSD, large dilated pulmonary artery, suggestive of Taussig–Bing variant with TGA physiology.[] She was prescribed tablet furosemide and tablet sildenafil[] and subsequently followed-up by the cardiologist for further management. She was discharged from the hospital on the 8th day postpartum.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1434,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2584645-1,Extracted,"A 50-years-old woman was presented to the emergency department with chest pain and dyspnea. She was a case of single kidney. She had no history of systemic disease such as diabetes and hypertension. On the day of admission she collapsed and was unresponsive for a short while. She had not suffered from any episodes of syncope before. Physical examination revealed a well nourished woman with a blood pressure of 90/60 mmHg and a pulse rate of 100 beats per minutes. She had a puffy face and examination of the neck revealed no struma. The jugular venous pressure was normal. Cardiac auscultation was normal and the lungs were clear. Peripheral pulses of radial, femoral and dorsalis pedis were present. Electrocardiography (ECG) showed torsades de pointes type ventricular tachycardia (Fig ). The patient received Magnesium and transferred to cardiac care unit (CCU).
Next ECG obtained from the patient revealed T wave inversion and prolongation of QT intervals of 0.71 S (Fig ). So the patient received phenytoin as treatment for prolongation of QT intervals. At the third day of admission the patient developed positional vertigo and her blood pressure dropped to 80 mmhg (pulse). Evaluation of thyroid function was recommended after consultation with neurologist. Thyroid function test revealed profound hypothyroidism. Total T4 was 0.71 μg/dL, free T4 (FT4) was 0.1 ng/mL, total T3 was 74 μg/dL and thyroid stimulating hormone (TSH) was 36 μU/mL. Other laboratory data such as blood urea nitrogen (BUN), Creatinine and electrolytes were in normal range. So the patient received levothyroxine 100 μg/day. Two months after treatment with levothyroxine, QT intervals normalized and ventricular tachycardia was abolished. Her periorbital edema had diminished and both TSH and free T4 had normalized.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",70,66.5,73.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 60.0 mm Hg = 70.0 mm Hg.
Hence, the patient's mean arterial pressure is 70.0 mm Hg."
1435,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-941,Extracted,"A previously healthy 16-year-old boy comes to the physician because of a pruritic rash on the chest that has become progressively larger over the past 10 days. It is not painful. He is sexually active with two female partners and uses condoms inconsistently. He works part-time as a lifeguard. He has no family history of serious illness. He does not smoke. He drinks 5–6 beers on weekends. His temperature is 36.7°C (98°F), pulse is 66/min, and blood pressure is 110/70 mm Hg. A photograph of the rash is shown below.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1436,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3517949-1,Extracted,"A 73-year-old man was admitted to our hospital with a complaint of diffuse abdominal pain that had lasted for 2 days. He was diagnosed as extensive stage SCLC of the left lung with multiple metastases of brain, right adrenal gland, pancreas and lumbar spine, 2 months ago, and had received radiation therapy for the metastatic brain tumor. He had been taking hydrochlorothiazide for 5 years under the diagnosis of hypertension, and had a history of 35 pack-year smoking.
Ten days before admission, chemotherapy consisting of irinotecan 100 mg (60 mg/m2 days 1 and 8) and cisplatin 100 mg (60 mg/m2 day 1) was started. On admission day, vital signs were blood pressure 130/70 mm Hg, heart rate 76/min, respiration rate 20/min, and body temperature 36.6℃. Bowel sound was hyperactive, and there was mild tenderness on the right lower quadrant without rebound tenderness or palpable mass. Laboratory data showed white blood cell (WBC) count of 4,000/mm3 with absolute neutrophil 3,600/mm3, hemoglobin 10.6 g/dL, platelet 210,000/mm3, high sensitivity C-reactive protein was 8.10 mg/dL. His liver and renal function panel were unremarkable. Chest X-ray films showed left hilar mass without interval change compared with the one taken at the time of cancer diagnosis (). On the abdominal X-ray films, there was a nonspecific gaseous distension (). He was treated with antispasmodics, symptomatically.
On the day 3 of hospitalization (day 13 of chemotherapy), despite supportive care, he complained of aggravated abdominal pain and developed fever of 37.6℃. Laboratory data revealed a hematological toxicity, hemoglobin decreased to 9.2 mg/dL, WBC count to 1,400/mm3, absolute neutrophil count to 1,064/mm3, and platelets to 161,000/mm3. An enhanced abdomen computed tomography (CT) scan revealed bowel wall thickening in the cecum and terminal ileum, and surrounding mesenteric inflammation, consistent with typhlitis (). He was treated with empirical antibiotics and supportive therapy of bowel rest, intravenous fluids, and nutritional support.
During the next 4 days, his abdominal pain improved slowly. On the day 7 of hospitalization, oral intake was available and absolute neutrophil count increased to 1,704/mm3. Follow-up ultrasonography performed on the day 16 of hospitalization showed resolution of bowel wall thickening, and he was discharged on hospital day 29. After discharge, he refused additional chemotherapy and expired 3 months later due to progression of SCLC.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 70.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1437,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5662164-1,Extracted,"A 24-year-old male with no known comorbid was presented to the outpatient department with high-grade fever and diffuse abdominal pain since the past five days. The fever on presentation was 101 F but increased to 102.5-103.5 F which was persistent, not relieved by antipyretics, and associated with lethargy, chills, shivering and sweating. The abdominal pain was diffuse, 6/10 in intensity, relieved by defecation and associated with nausea, anorexia and bloating. There was no vomiting or changes in bowel movement.
On examination, the patient appeared ill, dehydrated, and pale. His pulse was 95 beats per minute, SpO2 was 97%, blood pressure (BP) was 110/60 mmHg, temperature was 103 F, and respiratory rate was 24 breaths per minute. Abdominal examination revealed diffuse abdominal tenderness with increased bowel sounds.
On admission, his initial workup was done and he received intravenous fluids and empirical antibiotics. Laboratory investigations are shown below in Table .
The patient was diagnosed with typhoid (enteric fever) and was started on intravenous ceftriaxone and continued intravenous fluids.
On day 2 of admission, the patient developed severe diarrhea, difficulty swallowing, pruritus and exanthematous maculopapular rash insidiously as shown in Figure and Figure . The morbilliform rash started on the face and ultimately spread centrifugally towards the limbs from the trunk. In addition to the rash, the patient developed Koplik’s spots and conjunctivitis.
Further laboratory investigations are shown in Table .
The patient was eventually diagnosed with measles superimposed over typhoid. Besides continuing previous management, he also received intravenous metronidazole, oral antipyretics, antihistamine and vitamin A supplements. After seven days of intensive therapy, the patient’s symptoms were relieved, and he was discharged in a stable condition with a follow-up plan of care.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [60.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",76.66667,72.83334,80.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 60.0 mm Hg = 76.66667 mm Hg.
Hence, the patient's mean arterial pressure is 76.66667 mm Hg."
1438,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8526441-1,Extracted,"Case Presentation: A 30-years-old gentleman of middle socio-economic class, living in an apartment with his wife and had no travel history within the last 14 days, presented at the Dhaka Hospital of icddr,b's (formerly known as the International Centre for Diarrhoeal Disease Research, Bangladesh) COVID-19 emergency response provisional tent hospital on 19 June 2020. Since 15 June 2020 (4 days before hospital admission), the patient was found to have COVID-19 confirmed by reverse-transcription polymerase chain reaction (RT-PCR) tested at icddr,b. The patient was receiving medicine after being positive for SARS-CoV-2 according to the COVID-19 treatment protocol practiced in icddr,b. His medication included oral Paracetamol, Ivermectin 12 mg once, Doxycycline, Famotidine, Zinc, Vitamin C, and D. The patient was admitted on 19 June 2020 with complaints of fever for 11 days, the highest recorded temperature was 39.4 °C (102.92°F), associated with no chills and rigors and headache for 2 days. The patient also complained of generalized body-ache for the last 2 days and vomited fresh blood for an episode, at home, on the morning of hospital admission. On admission, the patient's weight was 85 kg (187.39 lbs.) and BMI was 31.2 kg/m2. The patient is a non-smoker, non-alcoholic, and had no co-morbidities.
On admission his temperature was 38.6 °C (101.48°F), pulse was 76 beats/minute and blood pressures were 110/79 mm of Hg. Though breathing effort (respiratory rate 24/minute) was mildly increased, the patient was well-maintaining oxygen saturation in room air (SpO2 was 99% in room air) (). The patient presented with no sign of dehydration. Systematic examinations did not show any abnormal findings.
Differential Diagnosis: We set out our differential diagnosis based on the presentation of the case, including COVID-19 with stress ulcer or either Disseminated Intravascular Coagulation (DIC) or Dengue. We conducted relevant laboratory investigations later to reach the final diagnosis, however, the unavailability of upper gastrointestinal (GI) endoscopy remained one of our limitations in excluding any possibility of GI ulcer. Furthermore, we were unable to rule out COVID-19-related frailty, which could have increased the patient's morbidity, as discussed by Van Schaik Sharon and DeWitte, who compared it to the historical context of the Black Death pandemic in the 14th century [].
[Informed written consent from the patient has been obtained for reviewing the case report and publication. The patient's identity was removed from all data. icddr,b research administration approval was sought and granted for publication in a peer-reviewed journal.]",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [79.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",89.33333,84.86666,93.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 79.0 mm Hg = 89.33333 mm Hg.
Hence, the patient's mean arterial pressure is 89.33333 mm Hg."
1439,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5379765-1,Extracted,"A 75-year-old Japanese male was transferred from another hospital after presenting with hemorrhagic shock due to hematochezia. He had been transported by ambulance to the previous hospital after complaining of discomfort and bloody stool on the previous day. He had undergone distal pancreatectomy and right lower lobectomy for pancreatic cancer and lung cancer, respectively, 5 years prior and total pancreatectomy due to residual pancreatic cancer eight months prior. The reconstruction procedure consisted of hepaticojejunostomy, Braun’s anastomosis, and gastrojejunostomy. In addition, a stent had been inserted for stenosis of the hepaticojejunostomy 1 month prior. The patient’s medical history also included atrial fibrillation, and he was taking insulin and apixaban. On arrival, he appeared to be pale and his extremities were cold. His vital signs were as follows: respiratory rate, 20 breaths/min; pulse rate, 105 beats/min (bpm); blood pressure, 77/54 mmHg; temperature, 34.9 °C. Arterial blood gas analysis detected severe lactic acidosis (lactate concentration: 9.9 mmol/L) and anemia (hemoglobin level: 3.1 g/dL). The laboratory data showed a white blood cell count of 5850/μL, C-reactive protein level of 0.08 mg/dL, procalcitonin level of 0.097 ng/mL, and serum glucose level of 389 mg/dL. Contrast-enhanced computed tomography of the abdomen did not detect any active bleeding. His melena had already ceased. Fluid resuscitation and massive transfusions resolved his hemorrhagic shock. Crystalloids were administered 800 mL over an hour. Blood products were initiated 30 min after the patient’s arrival. The patient required 16 units of red blood cell concentrate, 14 units of fresh frozen plasma and 20 units of platelets within 12 h of his arrival for hemostatic resuscitation. A classification of hemorrhage of the patient was considered as class IV based on the American College of Surgeons. Urgent upper gastrointestinal endoscopy was a poor study because of food residue and failed to identify the source of the patient’s bleeding. Thus, he was admitted to the emergency intensive care unit for careful observation. The patient’s acute physiology and chronic health evaluation (APACHE II) score on the day of admission was 24, and the Charlson comorbidity index was three.
Since fresh bleeding was detected in the terminal ileum during capsule endoscopy the next day, colonoscopy was performed without bowel cleaning. But the exam produced poor findings due to blood clot. Therefore, transanal double balloon enteroscopy was scheduled for further investigation 4 days after the patient’s admission. The patient took 5 h to ingest 2 L of PEG plus an additional liter of PEG for bowel preparation. This was the first time he had consumed PEG. 1 h after consuming the 3 L of PEG, he complained of a feverish chill and his heart rate and temperature increased to over 130 bpm and 39 °C, respectively. The transanal double balloon enteroscopy exam was performed uneventfully and did not reveal the source of the patient’s bleeding.
After the examination, he appeared to be agitated and distressed and exhibited hypotension, high fever, and an elevated lactate level, which indicated septic shock. He did not have any other complaints. His abdomen was soft, flat, and non-tender. Empirical antibiotic therapy with meropenem was administered, and two sets of blood cultures were obtained at the same time. Fluid resuscitation and a noradrenaline infusion were initiated due to septic shock, followed by intubation and mechanical ventilation. Table shows the patient’s laboratory data at the time that he suffered septic shock. Repeated lab tests revealed a significantly elevated procalcitonin level. Liver function tests produced normal results during the course, so we excluded biliary stent infection. Figure shows the patient’s clinical course during the first 15 h after he ingested PEG, the hypotensive phase of his condition, and the resuscitation period. Ongoing intensive care led to a gradual improvement in the patient’s condition and he was successfully extubated on day 4 (the day when the PEG preparation was administered was defined as day 0, at which APACHE II score was 34). An examination of his blood cultures detected C. braakii and we replaced the meropenem with ceftazidime based on the results of sensitivity tests. Later, the identity of the pathogen was confirmed by biochemical analysis and partial sequencing of 16S rRNA. Urinalysis produced normal results. Cultures of the patient’s urine and sputum at the onset of septic shock were negative. The tip cultures of central venous catheter which had been placed in a femoral vein on admission were found to be negative. Stool culture was obtained 1 week after presenting septic shock, which was also negative. Antibiotics were administered for a total of 10 days. The patient was discharged from the emergency intensive care unit on day 8. Figure shows the patient’s clinical course over the 8 days after he first suffered septic shock.
Melena occurred intermittently. Upper gastrointestinal endoscopy subsequently identified marginal ulceration of the gastrojejunal anastomosis, which was successfully treated with coagulation hemostasis. The patient was discharged on day 33.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [77.0, 'mm hg'], 'Diastolic Blood Pressure': [54.0, 'mm hg']}",61.66667,58.58334,64.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 77.0 mm Hg + 2/3 * 54.0 mm Hg = 61.66667 mm Hg.
Hence, the patient's mean arterial pressure is 61.66667 mm Hg."
1440,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8189531-1,Extracted,"A 71-year-old Caucasian male with myelodysplastic syndrome presented with dull aching pain on his right medial thigh for the past two months, after finishing a course of chemotherapy. It was associated with difficulty in walking and intermittent high temperatures. He denied any trauma to the area. The patient did not indulge in alcohol, tobacco, or recreational drug use, and had no recent travel history. He was not on any medication at the time of presentation. On examination, his vital signs were blood pressure (BP) of 110/66 mmHg, respiratory rate (RR) of 12/minute, temperature of 102.2°F, and weight of 80 kilograms. Regional evaluation displayed an area of erythema and induration on the right medial proximal thigh that was warm, edematous, and tender to touch (Figure ).
Physical examination was otherwise unremarkable. Significant laboratory findings included a white blood cell count (WBC) of 0.76 k/ul, absolute neutrophil count (ANC) of 0.26 k/ul, hemoglobin of 6 g/dl, and platelet count of 6 k/ul. The ANC had remained less than 0.5 k/ul for several months. Other laboratory findings were within the normal range. Soft tissue imaging of the area showed extensive subcutaneous and intramuscular edema but the absence of purulent inflammation (Figure ).
A provisional diagnosis of cellulitis with deep tissue myositis was made and empiric treatment with cefepime and vancomycin was initiated. Extensive microbiological evaluation including blood, urine, superficial, and deep wound cultures was negative. Workup for viral, fungal, or acid-fast organisms was negative. Gross pathological examination of a small punch biopsy from the area was consistent with chronic inflammatory skin changes with an underlying fluid collection. The lesion evolved despite escalation to broad-spectrum antibiotics including clindamycin, meropenem, daptomycin, metronidazole, and tobramycin along with micafungin and liposomal amphotericin B for fungal coverage. It gradually developed into a friable, necrotic nodule with overlying eschar and vesicles (Figure ).
A repeat scan of the pelvis showed a subcutaneous mass-like density with peripheral enhancement, measuring 5.5 cm x 5.4 cm indicating a growing phlegmon (Figure ).
The patient appeared symptomatically better after treatment with granulocyte colony-stimulating factor (GCSF) and was discharged on ciprofloxacin and doxycycline pending histopathological diagnosis. On follow-up admission, a serial scan depicted a localized open defect with previous fluid collection on the right thigh. A deeper wound biopsy reported fragments of necrotic tissue with reactive neutrophilic to infiltrate (Figures , ).
A trial of systemic and intralesional steroids based on the pathology report demonstrated drastic improvement confirming the diagnosis of pyoderma gangrenosum. The patient was discharged on doxycycline, ciprofloxacin, and oral prednisolone which was gradually tapered, with no recurrence of symptoms.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [66.0, 'mm hg']}",80.66667,76.63334,84.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 66.0 mm Hg = 80.66667 mm Hg.
Hence, the patient's mean arterial pressure is 80.66667 mm Hg."
1441,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5493,Extracted,"A 70-year-old man presents to the emergency department after a witnessed fall outside of a grocery store. He complains only of left hip pain which has been progressively worsening for the past six months. He denies hitting his head during the fall, but does complains of worsening headaches. His temperature is 98.6°F (37°C), blood pressure is 110/60 mmHg, pulse is 80/min, and respirations are 18/min. Examination of the right lower extremity reveals mild crepitus at the hip, appropriate range of motion, adequate distal sensation, and palpable posterior tibial and dorsalis pedis pulses. Laboratory workup shows the following:

Serum:
Ca2+: 9.0 mg/dL (normal: 8.9-10.1 mg/dL)
Alkaline phosphatase: 876 U/L (normal: 40-120 U/L)
25 hydroxyvitamin D: 89 ng/mL (normal: 20-100 ng/mL)
Parathyroid hormone: 30 pg/mL (normal: 10-65 pg/mL)

A CT scan of the hips is ordered and shown in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",76.66667,72.83334,80.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 60.0 mm Hg = 76.66667 mm Hg.
Hence, the patient's mean arterial pressure is 76.66667 mm Hg."
1442,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5052,Extracted,"A 57-year-old woman presents to her primary care physician with a concern for joint pain. She states that she often feels minor joint pain and morning stiffness in both of her hands every day, in particular in the joints of her fingers. Her symptoms tend to improve as the day goes on and she states they are not impacting the quality of her life. She lives alone as her partner recently died. She smokes 1 pack of cigarettes per day and drinks 2-3 alcoholic drinks per day. Her last menses was at the age of 45 and she works at a library. The patient has a history of diabetes and chronic kidney disease and her last GFR was 25 mL/min. Her temperature is 97.5°F (36.4°C), blood pressure is 117/58 mmHg, pulse is 90/min, respirations are 14/min, and oxygen saturation is 98% on room air. Physical exam is within normal limits.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [117.0, 'mm hg'], 'Diastolic Blood Pressure': [58.0, 'mm hg']}",77.66667,73.78334,81.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 117.0 mm Hg + 2/3 * 58.0 mm Hg = 77.66667 mm Hg.
Hence, the patient's mean arterial pressure is 77.66667 mm Hg."
1443,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7255565-1,Extracted,"A 57-year-old African American gentleman with sickle-cell disease, hemoglobin-SS, avascular necrosis of the bilateral hip and right shoulder, with remote right shoulder replacement, presented to the emergency department complaining of pain in multiple large joints. He complained of pain in the hips, knees, shoulders, and right elbow ongoing for three days. It was progressively worsening with no precipitating factors. He denied any fever, chills, nausea, vomiting, chest pain, palpitation, cough but did have mild shortness of breath.
On presentation, he was afebrile with a heart rate of 104 beats/min, respiratory rate of 24 breaths/min, and blood pressure of 147/90 mmHg. A cardiovascular exam revealed normal heart sounds. A respiratory exam revealed expiratory wheeze but otherwise, no decreased breath sounds or rhonchi were noted. A joint exam showed no tenderness to palpation, warmth, or swelling of any of the joints; however, there was resistance to movement at the hip joints bilaterally due to pain.
Labwork showed white cell count of 24.9 x109/L, hemoglobin 5.5 mg/dL, platelet 390 x109/L, sodium 134, potassium 3.9, blood
urea nitrogen (BUN) 31, creatinine 1.7, lactate dehydrogenase (LDH) 344, procalcitonin <0.05, and normal urinalysis. Blood and urine cultures were sent - reticulocyte count >3%, haptoglobin<30 md/dL. Sickle solubility test returned positive indicating active sickling. He was admitted with the diagnosis of vaso-occlusive crisis and a workup for sepsis and the precipitating cause was sought. He received intravenous fluid resuscitation, packed red blood cell (RBC) transfusion, and medication for pain control. However, despite the escalation of the pain control regimen, he was unable to ambulate and had persistent pain in his hips bilaterally. Despite lack of fever and absence of clinical signs of infection (swelling, warmth, tenderness), the persistently elevated white blood cell (WBC) count with worsening right hip pain and weakness, was concerning. Blood, urine, and stool cultures were negative for any growth.
Autoimmune workup showed erythrocyte sedimentation rate (ESR) was mildly elevated to 24 mm/hr, C-reactive protein (CRP) was borderline elevated, creatine kinase (CK) and myoglobin were within normal limits. Autoimmune antibodies returned negative. Chest X-ray revealed pulmonary vascular congestion (Figure ). MRI of the right hip revealed lateral hip having peripherally enhancing soft tissue fluid collection extending into the right acetabular fossa and into the proximal femur, measuring approximately 5.3 x 14 x 20 cm enlarging soft tissue fluid collection (Figures -). These areas had low signal intensity on T1-weighted imaging and high signal intensity on fluid-sensitive sequences. These signals extended along the lateral aspect of the right hip with intraosseous femoral extension, alongside evidence of femoral and acetabular subacute osteomyelitis. These radiological findings were consistent with Brodie’s abscess.
Orthopedic surgery was consulted for abscess drainage. During the operation, a large amount of pus was found within the thigh muscles, which was traced back and was seen extending from the bone. The abscess was debrided and irrigated, followed by antibiotic bead placement. Clindamycin was added to the antibiotic regimen. After the procedure, his leukocytosis improved drastically.
Wound samples from the abscess were sent for culture. The post-operative course was complicated by the re-accumulation of fluid. Repeat imaging revealed hematoma formation. It was managed conservatively with serial imaging, showing a receding size of the hematoma. Intra-operative culture report revealed the growth of Enterobacter cloacae and Citrobacter koseri. Antibiotics were changed according to the cultures. The patient made a slow recovery thereafter and was discharged to a rehabilitation facility for recuperation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [90.0, 'mm hg'], 'Systolic Blood Pressure': [147.0, 'mm hg']}",109,103.55,114.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 147.0 mm Hg + 2/3 * 90.0 mm Hg = 109.0 mm Hg.
Hence, the patient's mean arterial pressure is 109.0 mm Hg."
1444,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6243315-1,Extracted,"A 73-year-old male with a past medical history of chronic right pleural effusion, restrictive ventilatory impairment and hypertension presented for evaluation of severe right chest pain of few days’ duration and severe dyspnoea.
Upon arrival, he was haemodynamically stable with a rhythmic heart rate of 98 beats per min, blood pressure of 155/70 mmHg and respiratory rate of 38 per min. His oxygen saturation was 94% on room air.
Physical examination showed that the patient was awake and orientated but cyanotic and dyspnoeic. Upon auscultation, it was noted that breath sounds were completely absent in the right hemithorax and there was diffuse inspiratory/expiratory whooping in the contralateral hemithorax. All these physical findings were predictive of pneumothorax and the patient was admitted to the department of radiology for evaluation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [155.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",98.33333,93.41666,103.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 155.0 mm Hg + 2/3 * 70.0 mm Hg = 98.33333 mm Hg.
Hence, the patient's mean arterial pressure is 98.33333 mm Hg."
1445,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5769,Extracted,"A 42-year-old man presents to the gastroenterologist for chronic diarrhea and weight loss. He reports that the diarrhea began 3 months ago. He denies seeing blood in his stool but states that his stool is foul-smelling and often “floats in the bowl.” He reports that since his symptoms began he “can’t wear pants without belts.” He has not weighed himself recently. His normal diet consists of mainly red meats, cheese, fast food, and sugary, carbonated drinks. The patient recently immigrated from Barbados 1 year ago but has not been back since. His medical history includes arthritis and hypothyroidism. He takes aspirin and levothyroxine. The patient’s temperature is 100.9°F (38.3°C), blood pressure is 130/78 mmHg, pulse is 82/min, and respirations are 14/min. Physical examination reveals skin hyperpigmentation and swollen, painful elbows and knees. A fecal occult blood is positive. A colonoscopy is done with a biopsy and Periodic acid-Schiff staining, as shown in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",95.33333,90.56666,100.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 78.0 mm Hg = 95.33333 mm Hg.
Hence, the patient's mean arterial pressure is 95.33333 mm Hg."
1446,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6663048-1,Extracted,"A 75-year-old Caucasian woman presented to a large teaching hospital with a 1-month history of progressive dyspnoea. She had a history of pericardial effusion since 2011, which had been drained twice. A definitive diagnosis had not been established despite extensive evaluation.
On admission the patient had a blood pressure (BP) of 122/60 mmHg with a heart rate (HR) of 65 bpm. A transthoracic echocardiogram was performed, showing a severe pericardial effusion measuring 38 mm posterior and 23 mm anterior, with a mild diastolic collapse of the right ventricle.
The next day a fluoroscopy-guided pericardiocentesis was performed and 1,000 ml of lightly blood-stained pericardial fluid was removed. However, the procedure was complicated by aspiration of a large volume (1,500 ml) of haematic fluid from an unknown site.
After the procedure, the patient became hypotensive but responded to a fluid bolus and a low dose of norepinephrine (0.1 μg/kg/min). Serial haemograms were performed showing a nadir of 7.5 g/dl of haemoglobin, so the patient was transfused with 2 units of packed red blood cells. The echocardiogram after the pericardiocentesis showed normal bi-ventricular function with a small pericardial effusion.
On the second day after the procedure, the patient was haemodynamically stable without norepinephrine so was allowed out of bed but then collapsed. Immediate examination showed BP of 84/40 mmHg and HR of 110 bpm. The patient was brought to the ICU, where she was agitated, restless and diaphoretic with a stabbing chest pain and cold extremities. Importantly, there was progressive worsening of her haemodynamic status and increasing chest pain. A fluid bolus was given and norepinephrine was reinitiated with no response. An echocardiogram was performed and excluded cardiac tamponade but showed a moderately to severely enlarged right ventricle () with impaired systolic function and McConnell’s sign. Acute pulmonary hypertension was suggested by a mildly increased tricuspid regurgitation velocity and mid-systolic notching of the pulse wave Doppler profile in the right ventricular outflow tract (–).
An emergency CT chest angiogram (CTA) was ordered, but the patient’s clinical situation deteriorated, so life-saving fibrinolysis was administered with a bolus of 10 mg of alteplase. Minutes after fibrinolysis, BP started to increase and the patient became less agitated. The CTA was eventually performed and showed signs of bilateral PE, involving the segmental branches of the right lung, left superior lobar branch and segmental branches of the lower left lobe (). After less than an hour the patient was haemodynamically stable and the chest pain had resolved.
Due to the very high bleeding risk and in light of the favourable initial response, the medical team did not follow the usual thrombolysis protocol (10 mg bolus followed by infusion of 90 mg of alteplase over 2 hours) but switched to unfractionated heparin (UFH) in the first hour. UFH was given for 24 hours, before being replaced with low molecular weight heparin. The patient was transferred to the general ward after 48 hours and discharged 5 days later. She was anticoagulated with apixaban 10 mg twice a day.
The aetiological study was repeated but no abnormalities were identified. Venous ultrasound of both limbs was negative for deep vein thrombosis. The patient was reviewed in the outpatient clinic for 1 year but was asymptomatic and echocardiograms were normal.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [122.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",80.66667,76.63334,84.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 122.0 mm Hg + 2/3 * 60.0 mm Hg = 80.66667 mm Hg.
Hence, the patient's mean arterial pressure is 80.66667 mm Hg."
1447,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7556888-1,Extracted,"A Caucasian man in his 70s was admitted to his local hospital because of fever, diarrhea, and abdominal pain for the previous 10 days. His past medical history was significant for diverticulosis, and he was also being treated for locally advanced prostate cancer with goserelin and for chronic back pain with prednisolone 2.5 mg once daily.
On admission, his blood pressure was 134/85 mmHg, body temperature was 38.7 °C, heart rate was 87 beats/minute, respiratory rate was 18 breaths/minute, and oxygen saturation was 92% without oxygen support. He was slightly overweight with a body mass index (BMI) of 27 kg/m2, but the findings of his physical examination were otherwise normal. His laboratory test values, presented in Table , showed elevated C-reactive protein (CRP), thrombocytopenia, and moderately elevated ferritin. Arterial blood gas analysis revealed respiratory alkalosis with hypoxemia and normal lactate. A radiographic examination showed scattered consolidations in the right lung.
The patient had a positive test result for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) based on real-time reverse transcriptase polymerase chain reaction of a nasopharyngeal specimen. Empirical treatment with cefotaxime and ciprofloxacin was prescribed for suspected bacterial superinfection as well as an antiviral regime of lopinavir-ritonavir and hydroxychloroquine according to local guidelines at the time.
Twelve hours later, the patient’s condition deteriorated, with rapidly progressing respiratory failure, oxygen saturation at 86% on 12-L oxygen, and a respiratory frequency of 40 breaths/minute. This prompted transfer to the intensive care unit (ICU) and intubation. A new chest x-ray revealed extensive bilateral coalescent opacities qualifying as severe ARDS (ratio of arterial oxygen partial pressure to fractional inspired oxygen [FiO2], ≤ 100 mmHg).
During the first 36 hours in the ICU, the patient was in unstable cardiopulmonary condition. He required high FiO2 and norepinephrine in moderate doses, and he developed supraventricular tachyarrhythmia that was treated with repeated electrical and pharmacological cardioversion. By day 7, he had accumulated significant amounts of fluid (positive fluid balance of 8 L). His creatinine levels were rising, and he responded poorly to diuretics. Continuous venovenous hemodiafiltration was initiated to ensure a negative fluid balance.
The antiviral drug regimen was discontinued after 3 days due to a national agreement that all SARS-CoV-2 viral drug treatments should be administered through randomized controlled studies. Due to rising CRP and leukocyte counts, the antibiotics were changed to meropenem.
One week after admission, the patient achieved circulatory stability and exhibited a slowly decreasing oxygen demand, but his ferritin had risen markedly to 36,023 μg/L. This was accompanied by occasional fever and marked increases in CRP (334 mg/L), lactate dehydrogenase (LDH) (1074 U/L), neutrophil count (20.3 × 109/L), and triglycerides (5.27 mmol/L). His triglycerides were analyzed during parenteral nutrition and must be interpreted with caution.
This raised concern that the patient had developed HLH secondary to SARS-CoV-2. His soluble IL-2 receptor level was considerably elevated at 6809 U/ml (> 623 U/ml indicates immune activation and T-cell activation in particular), and a bone marrow smear demonstrated hemophagocytosis. Flow cytometry of peripheral blood showed a significant decrease in circulating CD4+ and CD8+ T cells (161/μl and 32/μl, respectively) but an expanded population of clonal B cells that expressed kappa, CD5, CD19, CD20 (weakly), CD43, CD45, and CD200. Due to the absence of lymphocytosis, and after a review of laboratory records, this was classified as monoclonal B-cell lymphocytosis (MBL) and not as chronic lymphocytic leukemia (CLL), which requires > 5000 cells/μl. A trephine biopsy confirmed MBL but no other lymphoproliferative disorders.
The patient fulfilled five of eight HLH-2004 diagnostic criteria, and his H-score estimated the probability of HLH to be 96–98% [, ]. A decision was made to give the patient tocilizumab 800 mg intravenously, a monoclonal antibody against the IL-6 receptor that is used when cytokine release syndrome (CRS) is seen following the infusion of chimeric antigen receptor T cells.
The following day, the patient’s CRP declined rapidly, followed by a significant but slow decline in ferritin and LDH levels (Table , Fig. ). After the administration of tocilizumab, no fever was observed. Three days later, the patient also received one dose of intravenous immunoglobulins pending the result of protein electrophoresis, which was normal. His clinical state improved 5–7 days later, and he was successfully extubated.
After the patient’s improvement, we analyzed serum levels of selected cytokines on the same day as tocilizumab was given (samples taken before administration) by enzyme-linked immunosorbent assay. Interestingly, his IL-6 levels were markedly elevated at 84 pg/ml (< 5 pg/ml), whereas TNF and IL-10 were moderately elevated at 55 pg/ml (< 20 pg/ml) and 38 pg/ml (< 5 pg/ml), respectively. His IL-8 (66 pg/ml) and IL-1β (< 5 pg/ml) were within the normal range of the laboratory that did the tests (Sahlgrenska University Hospital, Gothenburg, Sweden).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [85.0, 'mm hg'], 'Systolic Blood Pressure': [134.0, 'mm hg']}",101.33333,96.26666,106.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 134.0 mm Hg + 2/3 * 85.0 mm Hg = 101.33333 mm Hg.
Hence, the patient's mean arterial pressure is 101.33333 mm Hg."
1448,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3997736-1,Extracted,"An eight-year-old male presented with a mass in the right anterior neck that had been apparent for one week. Upon physical examination, blood pressure was recorded as 100/65 mmHg, heart rate was 80 beats per min, respiratory rate was 20 breaths per min and temperature was 36.1°C. A mass measuring ~4.0 cm in size, which caused difficulty in swallowing, was identified in the right anterior neck. The laboratory test results demonstrated a normal blood count and serum biochemistry, as well as normal levels of electrolytes and carcinoembryonic antigen. In addition, the test results for Epstein-Barr virus (EBV) viral capsid antigens immunoglobulin (Ig)M and IgG, human immunodeficiency virus (HIV) and hepatitis C virus antibodies, hepatitis B antigen and syphilis were negative. Furthermore, the thyroid hormone test results were as follows: Free thyroxine (FT) 4 levels of 11.8 pmol/l (normal range, 9–25 pmol/l); FT3 levels of 4.2 pmol/l (normal range, 3–9 pmol/l); thyroid-stimulating hormone levels of 0.720 μIU/ml (normal range, 0.34–5.60 μIU/ml); anti-thyroglobulin levels of 20 IU/ml (normal range, <115 IU/ml); and anti-thyroid peroxidase levels of 25 IU/ml (normal range, <34 IU/ml). The patient had no significant past medical or family history of disease. A B-mode ultrasound examination revealed a mass measuring 4.0×3.0×2.5 cm in the right lobe of the thyroid (), however, the lymph nodes surrounding the mass were normal (). The patient underwent a right lobe and isthmus thyroidectomy whereby two lymph nodes were excised simultaneously. Following the surgery, positron emission tomography-computed tomography scans showed normal metabolism in the left lobe of the thyroid and other parts of the body (). The patient’s bone marrow cytology was also normal, however, histological examination revealed diffuse infiltration of atypical lymphocytes and the observation of residual thyroid follicles and necrosis (). In addition, under low magnification, the ‘starry sky’ histology was observed in certain areas (). The atypical lymphocytes were medium-sized and consistent, with centrally located nuclei of irregular shape, displaying dispersed and deep basophilic chromatin and scanty cytoplasm. Additionally, certain neoplastic cells were visible, while varying numbers of nucleoli and apoptosis and mitosis were observed. Benign tissue cells engulfing apoptotic bodies were also observed under high magnification (), however, the isthmus of the thyroid was not infiltrated by the neoplastic cells. No reactive lymphocyte infiltration or fibrosis was identified in the stroma of the thyroid, and no oxyphilic change or squamous metaplasia was observed in the epithelial cells of the background thyroid tissues (). The only change in the two lymph nodes that were simultaneously excised, was the presence of reactive hyperplasia of the lymphoid follicles (). Immunohistochemical staining was then performed with the primary antibodies shown in (Zymed Corporation, Inc., San Francisco, CA, USA; Santa Cruz Biotechnology, Inc., Santa Cruz, CA, USA). The results showed that the neoplastic cells were diffusely positive for cluster of differentiation (CD)20 () and CD10 (), marginally positive for CD38, CD43 and B-cell lymphoma (Bcl)-6, but negative for Bcl-2 and terminal deoxynucleotidyl transferase (TDT). In addition, CD3 and CD5 stained the background T cells, and the Ki-67 proliferation index was >95% (). Analysis using an EBV-encoded small RNA (EBER) digoxin-labeled probe (PanPath B.V., Budel, Netherlands) was performed and revealed a negative result (), however, positive nuclei were observed in the nasopharyngeal carcinoma tissue, which was used as the positive control (). Analysis using the C-MYC break-apart detection probe (Guangzhou LBP Medical Science Technology Co., Ltd., Guangzhou, China) was also performed and the results revealed that ~90% of the neoplastic cells exhibited red and green signal separation, which indicated that chromosome breakage and translocation of the MYC gene had occurred in the neoplastic cells (). Immunoglobulin gene rearrangement assays were performed according to instructions of the Biomed-2 Polymerase Chain Reaction kit (Invivoscribe technologies, Inc., San Diego, CA, USA), followed by capillary electrophoresis, which was analyzed using Genemarker® v1.5. software (SoftGenetics, LLC, State College, PA, USA). Positive gene arrangements of IgH and IgK were observed in the tumor tissues, however, no positive gene rearrangements were observed for IgL (). Consequently, the patient was diagnosed with primary BL of the thyroid and underwent alternate R-B-NHL-BFM-90-A and R-B-NHL-BFM-90-B treatment, for four cycles each. The two regimens, including the dose and duration of chemotherapy, are described in . After almost four years of follow-up, the patient appears well and remains free of disease.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [65.0, 'mm hg'], 'Systolic Blood Pressure': [100.0, 'mm hg']}",76.66667,72.83334,80.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 65.0 mm Hg = 76.66667 mm Hg.
Hence, the patient's mean arterial pressure is 76.66667 mm Hg."
1449,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2964038-1,Extracted,"A 20-year-old woman presented to the emergency department complaining for a 6-day history of right groin swelling which gradually became tender to palpation during last 48 hours. Twenty-four hours before her admission to our department, the patient was examined by her gynaecologist, who did not find any obvious gynaecological disorder.
On examination to our department, her temperature was 37°C, pulse rate 76 beats/min, blood pressure 110/85 mmHg, and respiratory rate 16/min. Physical examination revealed a right groin mass in the femoral region, which was nonreducible and exquisitely tender to palpation. Abdominal examination also disclosed mild tenderness in the right lower quadrant. A gentle attempt to reduce the hard mass, under mild analgesia, was unsuccessful.
The leukocyte count was 9.700/mm3 (Ne: 79.5%), while C-reactive protein was 0.1 mg/dl. Plain abdominal radiograph was unremarkable. Ultrasonographic examination of the right groin demonstrated a hernia sac, above the femoral vessels, measuring approximately 3.4 cm on diameter and containing suspected aperistaltic bowel segment with oedematous wall (). Based on these findings, the diagnosis of an incarcerated femoral hernia was set and the patient underwent emergent operation. During exploration of the right groin region through femoral approach, a strangulated femoral hernia sac containing right fallopian tube was detected (). The uterine tube was totally in the hernia sac with its mesosalpinx, while the right ovary was palpated within the abdominal cavity ().
No signs of ischemic damage were detected and the fallopian tube was returned to the abdominal cavity. The sac was closed at its base, the redundant portion was amputated, and the femoral hernia was repaired with polypropylene plug implantation.
The patient had an uneventful recovery and was discharged on the second postoperative day.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [85.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 85.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1450,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-11309,Extracted,"A 3-year-old boy is brought to the emergency room by his mother after she found him somnolent at home next to multiple open pill bottles. The boy had seemingly opened several different pill bottles that were in a cabinet in his parent’s bathroom. The mother has brought the empty bottles to the emergency room, and they include aspirin, metoprolol, acetaminophen, levothyroxine, and lorazepam. The boy has no past medical history and takes no medications. His temperature is 98.6°F (37°C), blood pressure is 110/65 mmHg, pulse is 85/min, and respirations are 28/min. On exam, the boy is lethargic but responsive. He appears to be grasping at his ears and swaying from side-to-side when attempting to ambulate. He vomited once in the emergency room.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 65.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1451,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5453898-1,Extracted,"A 56-year-old man (height 162.3 cm, body weight 58.8 kg) presented for emergency surgery of transurethral resection for bladder tumor due to bleeding associated with bladder cancer. His medical history included hypertension, stage IV chronic kidney disease and benign prostatic hypertrophy. There was no family history of MH, and he had not been anesthetized previously.
Preoperatively, the patient had recurrent hematuria and a laboratory test revealed a hemoglobin (Hb) concentration of 4.2 g/dl. The patient received transfusion of 2 pints packed red blood cells, and the Hb concentration increased to 6.8 g/dl. Glycopyrrolate 0.2 mg was injected intramuscularly as a premedication. In the operating room, an electrocardiogram, non-invasive blood pressure measurement, and pulse oximetry were performed, and the bispectral index (BIS VISTA®, Aspect Medical Systems, Inc., Norwood, MA, USA) sensor was attached onto his forehead. The patient was preoxygenated for 2 minutes, and anesthesia was induced using 120 mg of 1% propofol and 12 mg cisatracurium. After intubation, anesthesia was maintained using desflurane in a total fresh gas flow of 3 L/min of an air/oxygen mixture via an active humidified circuit with a heated wire in the inspiratory limb. In addition, effect-site target-controlled infusion of remifentanil was adjusted between 2.5 and 4.0 ng/ml. After consultation with the surgeon for considering the possibility of a radical cystectomy, catheters were placed in the right radial artery and right internal jugular vein as a precaution.
Baseline measurements at onset of surgery were oxygen saturation (SpO2) 99%, arterial blood pressure (ABP) 115/50 mmHg, heart rate (HR) 90 bpm, end-tidal CO2 (ETCO2) 37 mmHg, and esophageal temperature 36.5℃. Approximately 120 minutes after anesthesia induction, ABP was not checked. On inspection, right arm rigidity and lower extremity rigidity were detected. Then cannulation of the right brachial artery was performed. At that time, his ABP dropped to 95/45 mmHg and ETCO2 rose to 54 mmHg. Repeated bolus injections of phenylephrine had a short duration, and hence a continuous infusion of norepinephrine was administered (0.05 µg/kg/min). The esophageal temperature was maintained at 36.2℃. We proceeded with manual hyperventilation to increase minute ventilation (MV) from 6.2 to 8.4 L/min; however, ETCO2 remained above 60 mmHg. Bilateral breath sounds were clear without wheezing and the peak airway pressure remained unchanged. At this point, arterial blood gas analysis (ABGA) showed pH 7.032, PaO2 108.1 mmHg, PaCO2 73.1 mmHg and base excess (BE) −10.8 mmol/L. (). Therefore, we administered sodium bicarbonate 60 mEq. The esophageal temperature increased gradually to 38.6℃. The clinical condition of the patient was suspected to be due to MH, and hence the operation was stopped and dantrolene sodium was prepared. One hundred and fifty minutes after induction of anesthesia, hypotension still persisted and the HR gradually rose to 120 bpm. Next, a continuous vasopressin infusion was initiated and both the breathing circuit and soda lime canister were changed. In spite of increasing MV to 14.5 L/min, the retention of CO2 intensified, and so the ventilator was replaced. In addition, desflurane was discontinued and it was washed out with 100% O2 in 18 L/min fresh gas over a period of 10 minutes. At the same time, anesthesia was switched to 2% propofol (Fresofol 2%™, Fresenius Kabi, Granz, Austria) and the ventilator was replaced with continuous manual hyperventilation. To cool off the patient, ice packs were placed on the head and chest areas and cold saline irrigation was administered through the Foley catheter and the Levin tube. The ETCO2 rose to more than 80 mmHg and the SpO2 gradually decreased to 94%. At this point, the esophageal temperature was 41.7℃ and ABGA showed pH 7.039, PaO2 150.8 mmHg, PaCO2 90.9 mmHg and BE −6.2 mmol/L. Also, serum potassium and lactic acid levels were 7.37 mmol/L and 11.7 mmol/L, respectively. We administered 10 mg furosemide and a regular insulin infusion (10 IU/h). Despite administration of norepinephrine and vasopressin, his ABP dropped rapidly to 42/23 mmHg. Epinephrine 100 and 300 µg was then injected intravenously in a sequence. Dantrolene sodium arrived in the operating room and it was reconstituted with sterile water as quickly as possible and administered through the central venous line. The esophageal temperature at this point was 40.5℃, but within the first 1–2 minutes following 60 mg dantrolene sodium, a rapid decrease in the esophageal temperature to 38.5℃ and a drop in ETCO2 to 32 mmHg were noted. However, at this time, the patient suffered a cardiac arrest with asystole. Then, the infusion of dantrolene sodium was stopped and CPR was initiated immediately following chest compression and epinephrine injection. After 15 seconds of CPR, ventricular fibrillation occurred and the patient's cardiac rhythm converted back to sinus rhythm after a single defibrillation at 200 J. Boluses of epinephrine 1 mg were injected 3 times. Despite infusion of epinephrine and vasopressin, the patient's ABP did not improve. We made a decision to initiate ECMO for providing hemodynamic support and activated an ECMO team. Peripheral venoarterial ECMO was applied by using a size of 15 French (F) arterial cannula (Biomedicus®, Medtronic, Anaheim, CA, USA) and a size of 21 F venous cannula (Biomedicus®, Medtronic, Anaheim, CA, USA) into the right femoral artery and vein, respectively. The initial blood flow rate was 3.5 L/min and the sweep gas-flow rate was 3.0 L/min. The total down time for the first cardiac arrest was 80 minutes until ECMO was ready. After applying ECMO, the patient's ABP improved. The patient was then transferred to the surgical intensive care unit (SICU) running an ECMO. No more dantrolene sodium was administered, because the rigidity of the right arm and the lower extremity had resolved, and ETCO2, body temperature and ABGA had improved before the patient was transferred to the SICU. The serum creatine kinase (CK) levels were elevated upon admission (CK 2,413 IU/L) and they continued to be elevated till the following morning (CK 17,779 IU/L). MH clinical grading scale score was 73 (MH rank was 6, ‘Almost certain’). Sixty hours later, the patient was successfully weaned off ECMO. A week later, he was inevitably scheduled for a radical cystectomy with an ileal-conduit due to the remnant bladder tumor, persistent hematuria in spite of arterial embolization and bladder necrosis. For general anesthesia, we performed total intravenous anesthesia using 2% propofol. The patient's vital signs were stable during the operation and the operation was completed uneventfully. After one week, the patient displayed a hemodynamically stable state, was extubated, and then transferred to the general ward.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [115.0, 'mm hg'], 'Diastolic Blood Pressure': [50.0, 'mm hg']}",71.66667,68.08334,75.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 50.0 mm Hg = 71.66667 mm Hg.
Hence, the patient's mean arterial pressure is 71.66667 mm Hg."
1452,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8442220-1,Extracted,"A 44-year-old female with no relevant medical history presented to the emergency department with a 1-week history of abdominal pain, nausea, shortness of breath, and fever. She had a history of recurrent urinary tract infections and denied history of biliary colic. On examination, she was febrile, agitated, and confused. Vital signs upon arrival were heart rate of 110/min, blood pressure of 80/60 mmHg, respiratory rate of 26/min, oxygen saturation of 93%, and temperature of 101.3 °F. She reported significant bloating and diffuse abdominal pain. Laboratory tests showed hemoglobin of 11.3 g/dL (reference range, 12.2-18.1 g/dL), leukocyte count of 5.3 K/uL (reference range, 4.0-11.0 K/uL), glucose of 400 mg/dL (reference range, 60-100 mg/dL), and serum creatinine of 3.7 mg/dL (reference range, 0.6-1.4 mg/dL). Arterial blood gas analysis was consistent with metabolic acidosis (pH 7.15, HCO3 18 mEq/L, PaO2 89 mmHg). Urinalysis showed positive leukocyte esterase and nitrites. Urine microscopy revealed leukocyturia, hematuria, and moderate bacteriuria. The patient denied a history of diabetes mellitus.
Abdominal x-ray revealed gas over the right renal topography (). Contrast-enhanced computed tomography scan of the abdomen revealed destruction of the right renal parenchyma, gas extending from the retroperitoneum to the retropubic space, and gas within the gallbladder wall (Figure ). Gas was also seen in the mediastinum. The diagnosis of EPN, EC, and pneumomediastinum was confirmed.
Empirical intravenous (IV) broad-spectrum antibiotics were administered. Imipenem and cilastatin with a renal dosage adjustment (250 mg IV every 12 hours) were initiated, along with fluid resuscitation with a crystalloid solution of sodium chloride at 0.9% every 8 hours. Percutaneous drainage of the kidney and gallbladder was performed 24 hours after arrival. A total of 140 mL of purulent material from the perinephric puncture was drained, as well as cloudy bile fluid from the percutaneous gallbladder puncture. Forty-eight hours later, the patient showed no clinical improvement, with persistent altered state of consciousness, high fever despite the medical management, and an increase in leukocyte count to 18.2 K/uL.
The patient was taken to the operating room for cholecystectomy and nephrectomy. A midline incision was made. The patient's gallbladder was enlarged, had a necrotic appearance, was extremely friable, and was attached to the liver. The kidney was completely destroyed and had a dark brown and necrotic appearance. At the time of renal dissection, friable perinephric tissue was found, as well as a fibrotic renal hilum, which made removal and hemostasis technically difficult. Total blood loss was 3.5 L, and the patient required 3 units of blood and 2 platelet units. A closed drain was placed in the perinephric space. Microscopy reported extensive proliferation of gram-negative bacilli in the renal parenchyma with extensive perinephric involvement and acute and chronic inflammatory changes. The gallbladder had embolic microabscesses and chronic inflammatory changes. Microbiologic analysis reported the same strain of Escherichia coli from urine, right kidney, perinephric exudate, blood, and gallbladder, suggesting hematogenous spread of the infection.
The patient required a 15-day hospital stay, with 10 days in the intensive care unit. She was discharged when her leukocyte count normalized. The drain was removed before discharge. Acute kidney injury was managed with a proper fluid replacement, and glycemic levels were within normal ranges achieved by IV insulin infusion administration. The patient currently has adequate glycemic control managed with intermediate and rapid insulin, as well as a diet managed by the nutrition team of our hospital.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [80.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",66.66667,63.33334,70,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 80.0 mm Hg + 2/3 * 60.0 mm Hg = 66.66667 mm Hg.
Hence, the patient's mean arterial pressure is 66.66667 mm Hg."
1453,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7434271-1,Extracted,"A 41-year-old male presented to the ED for worsening abdominal pain over the prior three days. The patient described the pain as intermittent, sharp, and crampy in the upper quadrants. He reported constipation but denied fevers, nausea, vomiting, or diarrhea. He reported a past medical history of hypertension and neurofibromatosis. He denied prior surgeries, smoking, alcohol abuse, or illicit drug use.
The vital signs were heart rate 94 beats per minute (bpm); respiratory rate 18 breaths per minute; blood pressure 159/90 millimeters of mercury (mmHg); temperature 36.5 degrees Celsius; and oxygen saturation 98% on room air. The patient appeared comfortable, but his physical exam was remarkable for tenderness in the upper abdomen without rebound or guarding. Murphy’s sign was negative, and no masses were palpated The remainder of his physical exam was unremarkable. The emergency physician ordered a complete blood count (CBC), comprehensive metabolic panel (CMP), lipase, urinalysis (UA), and computed tomography (CT) of the abdomen and pelvis with intravenous (IV) contrast. CBC, CMP, lipase and UA were within normal limits.
The CT revealed no acute intra-abdominal process but revealed a stable, round focus of low attenuation adjacent to the celiac artery. This was thought to be a neurofibroma given the patient’s history and stable appearance from a CT performed nine years prior. The diameter of the opacified celiac artery was also similar to the prior study at 1.2 centimeters (cm). The patient was treated with one liter normal saline bolus and famotidine. On re-evaluation he was symptom free and informed of the results of the work-up that was performed. He was diagnosed with undifferentiated abdominal pain and counseled to return to the ED for worsening pain, the development of fever, uncontrollable vomiting, or any new concerns.
The patient returned to the ED the next day for acute worsening of his pain that became diffuse and constant. He reported several episodes of non-bloody vomiting and several episodes of non-bloody diarrhea after taking milk of magnesia and a Fleet enema for his constipation. The vital signs were heart rate 75 bpm; respiratory rate 18 breaths per minute; blood pressure 170/95 mmHg; temperature 36.2 degrees Celsius; and oxygen saturation 100% on room air. The patient appeared very uncomfortable and was writhing in pain. He had diffuse tenderness on abdominal exam, but no palpable pulsatile masses or auscultated abdominal bruits. He had good distal perfusion to his extremities with distal pulses equal. Otherwise, his physical exam was unremarkable.
CBC, CMP, lipase, lactic acid, and a CT angiogram of the abdomen and pelvis were ordered, along with IV opioid and fluids. The patient received multiple doses of opiate analgesia, including hydromorphone, without relief. CBC was remarkable for leukocytosis of 17.3 x 109 per liter (L) (normal range: 4.5 to 11.0 x 109/L), and lactic acid was 2.0 millimoles per liter (mmol/L) (normal range: 0.5 to 2.0 mmol/L). CMP and lipase were unremarkable. The CT angiogram of the abdomen and pelvis ( and ) revealed a 3.2 x 2.4 cm proximal CAA with surrounding inflammatory change and trace hemorrhage. The remaining vasculature was unremarkable.
Upon return from CT, the patient’s status deteriorated. He became diaphoretic, tachycardic, and hypotensive. Point-of-care ultrasound revealed fluid in Morrison’s pouch. Central venous access was obtained and the patient was stabilized with four units of blood. He was transferred to a tertiary care facility for emergent surgical repair. The patient was brought to the operating room emergently at the tertiary care facility and underwent exploratory laparotomy. He was found to have a large retroperitoneal hematoma from a bleeding CAA. Both proximal and distal control was obtained, and the CAA was ligated.
Intraoperatively he had an estimated blood loss of eight liters and received 20 units of blood by massive transfusion protocol. He developed a coagulopathy, and the bleeding could not be controlled. The area of bleeding was packed and the patient transferred to the post-anesthesia care unit with an open abdomen, vacuum-assisted wound closure for continued resuscitation. The patient had a do-not-resuscitate order placed by family and expired a few hours after surgery.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [170.0, 'mm hg'], 'Diastolic Blood Pressure': [95.0, 'mm hg']}",120,114,126,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 170.0 mm Hg + 2/3 * 95.0 mm Hg = 120.0 mm Hg.
Hence, the patient's mean arterial pressure is 120.0 mm Hg."
1454,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4752973-1,Extracted,"An 89-year-old lady presented with a one-day history of acute shortness of breath, as well as a cough productive of brown sputum. Her past medical history was significant for chronic obstructive pulmonary disease, ischaemic heart disease, hypertension, hypothyroidism, and previous breast cancer in 2012, for which she remained on hormonal treatment. She lived with her daughter in a house with a full package of care. However her exercise tolerance was limited to only ten yards with a walking frame, which meant she was confined to downstairs living. She denied ever smoking and drank alcohol within the recommended limits. There was no history within the family of any particular illnesses.
On arrival to accident and emergency she was clearly in respiratory distress. Her observations were as follows: respiratory rate 40, oxygen saturation of 80% on room air, heart rate 130, blood pressure 200/90, and temperature 39.1 degrees Celsius.
On examination there was bronchial breathing with widespread crepitations and wheeze with nil else of significance noted on the initial examination.
An arterial blood gas revealed severe type one respiratory failure and blood tests were indicative of an acute inflammatory response with associated acute kidney injury. This lady was initially treated with intravenous benzylpenicillin and clarithromycin as per trust policy for an exacerbation of chronic obstructive pulmonary disease, as well as being supported with oxygen, intravenous fluids, steroids, and nebulisers. She was acutely unwell and had shown little response after 24 hours. As a result, it was felt that she was unlikely to survive this episode—both the patient and family were informed and the patient was placed on the supportive care pathway with a decision being made not to attempt cardiopulmonary resuscitation and for ward based management only. In the meantime her antibiotics were continued but switched to piperacillin/tazobactam (Tazocin).
She slowly began to respond to treatment and her oxygen requirements were reducing. During the second day of admission the ward received a call from the microbiology consultant stating that the blood cultures grew Pasteurella multocida within 24 hours, a common commensal organism in the oropharynx of domesticated animals. This triggered the medical team to enquire about any recent animal contact or injuries. The patient then revealed that she had one dog and two cats at home and had been bitten on her hand by her dog the day previous to admission. This information was new and had not been known previously and it was then noted on examination that there was a healing wound on the dorsum of the left hand. Interestingly the family reported that the dog had been increasingly unwell and aggressive for the previous week, with the vet explaining to the family that the dog had a “brain infection” and needed to be “put down.” Cats are more common carriers of Pasteurella multocida than dogs; however she did not provide any history of being recently scratched or licked by her cats [, ].
The patient remarkably improved on piperacillin/tazobactam antibiotics, leading to the supportive care pathway being revoked. She was discharged from hospital after receiving ten days of intravenous antibiotics and was sent home with a five-day course of oral coamoxiclav. This lady unfortunately died six months later after a readmission with pleuritic chest pain and acute type one respiratory failure. This was on a background of a recent fall and subsequent fibula fracture. She was too unwell to be investigated extensively but it was felt that the cause of death was likely to be secondary to a pulmonary embolism.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [200.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",126.66667,120.33334,133,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 200.0 mm Hg + 2/3 * 90.0 mm Hg = 126.66667 mm Hg.
Hence, the patient's mean arterial pressure is 126.66667 mm Hg."
1455,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6477471-2,Extracted,"A 19-year-old Thai man, the elder twin brother, came to the dermatology outpatient clinic with rashes on his right knee, both upper extremities, and both feet for 1 day. He had been in previous good health until 1 day earlier when he developed high-grade fever and skin rashes. Eight days earlier, he visited an emergency department due to cat scratches on his right knee. According to an abrasion wound with contact bleeding, anti-rabies vaccine (VERORAB®, Sanofi Pasteur, France) was injected at his left deltoid. After the skin sensitivity test on his right volar arm showed negative results, equine rabies immunoglobulin (TRCS ERIG®, Queen Saovabha Memorial Institute, Thailand) was infiltrated around the wound and intramuscularly into the left gluteal region. A 3-day course of oral clindamycin was also given for infection prophylaxis due to his previous history of penicillin allergy. Seven days later, a brownish itchy rash first appeared on the right knee where ERIG was infiltrated; by the following day, pruritic urticarial rashes were also observed on both dorsal hands, elbows, and dorsal feet together with low-grade fever.
On examination, his body temperature was 38°C, pulse rate 60 beats per minute, blood pressure 138/85 mm Hg, and the respiratory rate was 18 breaths per minute. A solitary, large demarcated brownish painless patch above the right knee (Fig. ) and multiple urticaria-like eruptions on extensor surfaces of both arms (Fig. ), and dorsal areas of both hands and feet were noticed. The remainder of the general examination was normal. Laboratory results were unremarkable.
In this case, prednisolone (30 mg/day) and cetirizine (10 mg/day) were given orally for 7 days. His fever resolved and skin lesions became light brown on day 7 of oral medication administration as shown in Figure . Neither recurrent skin lesion nor other systemic involvement was detected at a follow-up visit on day 10.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [138.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",102.66667,97.53334,107.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 138.0 mm Hg + 2/3 * 85.0 mm Hg = 102.66667 mm Hg.
Hence, the patient's mean arterial pressure is 102.66667 mm Hg."
1456,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8168,Extracted,"A 60-year-old man, who was a coal miner for more than 15 years presents with complaints of a cough and shortness of breath. His cough started 6 years ago and is dry and persistent. The shortness of breath started 4 months ago and is exacerbated by physical activity. When interviewed, his physician discovers that he doesn’t take any safety measures when working in the mines. Vital signs include: heart rate 85/min, respiratory rate 32/min, and blood pressure 125/90 mm Hg. On physical examination, there are diminished respiratory sounds on both sides. In his chest X-ray, interstitial fibrosis with reticulonodular infiltrate with honeycombing is found on both sides.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",101.66667,96.58334,106.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 90.0 mm Hg = 101.66667 mm Hg.
Hence, the patient's mean arterial pressure is 101.66667 mm Hg."
1457,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5687971-1,Extracted,"A 33-year-old Hispanic male of average build was admitted to our facility, complaining of dyspnea, fever, night sweats, and rapid weight loss (18 kg over a four-month period). A pertinent positive finding on the initial history taking was his having traveled to a country where tuberculosis is endemic. Physical examination revealed no acute distress and no stigmata of intravenous drug abuse. He was febrile (≤ 38.5°C), with a blood pressure of 124/72 mmHg, a heart rate of 76 bpm, a respiratory rate of 18 breaths/min, and a constant SpO2 at rest of 98%. The initial total leukocyte count was 8,200 cells/µL, with a predominant neutrophilic reaction. Blood culture was negative for aerobic and anaerobic microorganisms. Urine toxicology and HIV tests were negative. Chest X-ray and HRCT showed micronodules (1-3 mm in size) bilaterally in centrilobular distribution (). An IFN-γ assay and sputum smear microscopy for acid-fast bacilli were carried out in order to rule out mycobacterial infection. Although the results were negative for tuberculosis, the high clinical suspicion of the disease prompted empirical initiation of the four-drug antituberculous therapy. Four weeks later, the patient returned to the emergency room with worsening of the shortness of breath. A repeat HRCT revealed similar centrilobular nodules with no radiological improvement (). At that time, bronchoscopy with transbronchial lung biopsy was performed for further evaluation of the pulmonary micronodules. Examination of the BAL fluid, with Ziehl-Neelsen staining, revealed no acid-fast bacilli. Histopathological analysis of the transbronchial lung biopsy specimen showed multiple granulomas with birefringent material in the center (), confirming the diagnosis of PFBG. The patient strongly denied intravenous drug use. Unfortunately, he experienced a progressive course with a further decline in his lung function. After progressive fibrosis over the following one-year period, the patient died of chronic respiratory failure.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [72.0, 'mm hg'], 'Systolic Blood Pressure': [124.0, 'mm hg']}",89.33333,84.86666,93.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 124.0 mm Hg + 2/3 * 72.0 mm Hg = 89.33333 mm Hg.
Hence, the patient's mean arterial pressure is 89.33333 mm Hg."
1458,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7725493-1,Extracted,"Our patient is a 78-year-old female with a medical history significant for Charcot-Marie-Tooth disease, vertigo, hypertension, hyperlipidemia, depression, and Hashimoto's thyroiditis, who presented to the hospital for abdominal pain, constipation, shortness of breath, and 10 lbs weight loss for the last few weeks. In the emergency room, the vitals were temperature of 98.3 F, heart rate 100 beats per minute, respiratory rate 18 breaths/minute, Blood pressure 120/70 mm of Hg, and oxygen saturation of 98% on room air. The physical examination was unremarkable at admission. Her hemoglobin was 10.9 g/dl, white blood cell 5.8 k/ul, platelet count of 270 k/ul, alkaline phosphatase 214 u/l, aspartate aminotransferase 347 u/L, alanine aminotransferase 409 u/L, troponin 31 ng/L, 34 ng/L, and pro-B-type natriuretic peptide (pro-BNP) 265 pg/ml. The patient underwent computed tomography (CT) of the abdomen and pelvis, which showed moderate bilateral pleural effusions, a large pericardial effusion, and the liver's periportal edema. There is a gallbladder wall edema correlating to elevated right heart pressures. The patient also underwent CT of the chest, which was suspicious for the left upper lobe's lung malignancy, pleural effusions, atelectasis, a large pericardial effusion, and pathological adenopathy of the mediastinum. The echocardiographic study was significant for massive pericardial effusion with right ventricular diastolic collapse indicating cardiac tamponade (Figure ).
Pulmonary medicine was consulted for the left upper lobe lung mass and bilateral pleural effusion. The patient was evaluated by cardiology, and examination was significant for pulsus paradoxus of 12-14 mm of Hg, Becks triad, electrical alternans, low voltage QRS, and Ewart sign (Figure ).
The patient went to the critical care unit and underwent pericardiocentesis with drain placement. 1600 ml fluid was drained over two days, which was hemorrhagic with atypical cells suggestive of malignancy. The pericardial fluid was bloody, cloudy, white blood cell (WBC) 4700 cells/mm3 with 92% segmental count, and 29440000 red blood cell (RBC) cells/mm3. The patient developed paroxysmal atrial fibrillation; however, she was not a candidate for anticoagulation due to hemorrhagic pericardial tamponade. The repeat echocardiography showed resolved pericardial tamponade. The patient underwent bronchoscopy, and transbronchial biopsy showed invasive adenocarcinoma, which was moderately differentiated (Figure ).
After 15 days, the patient underwent a positron emission tomography (PET) scan, which showed a left upper lobe primary tumor with evidence of metastatic spread to the mediastinum and right hilum with possible pleural metastatic disease seen posteriorly in the left hemithorax. The patient was diagnosed with stage IV adenocarcinoma of the lung and was discharged to follow up outpatient with oncology for chemotherapy. The patient did follow up and tolerated the chemotherapy without complication at the fourth month follow up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1459,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7213832-2,Extracted,"A 71-year-old female patient with a medical history of multiple myeloma treated with bortezomib, was admitted with a 1-day history of fever, cough and dyspnoea. She tested positive for SARS-CoV-2. Her initial ECG at presentation is shown in .
On day 2 of admission, the patient became acutely hypotensive and hypoxic with a blood pressure of 70/41 mmHg, a heart rate of 125 beats per minute, a respiratory rate of 33 breaths per minute and oxygen saturation of 70% on 4 l/min of oxygen by nasal cannula. Her chest x-ray showed bilateral alveolar and interstitial opacities (). She was intubated, initiated on mechanical ventilation and transferred to the MICU for further treatment including vasopressor support. A repeat ECG showed new 1 mm ST elevation in leads V2–V6 with associated Q waves in leads V4–V6 ().
Again, due to the patient’s life-threatening respiratory failure, it was decided not to pursue reperfusion therapy. After completing loading doses, she was started on aspirin 81 mg, clopidogrel 75 mg and a heparin drip. Her other medications included azithromycin, cefepime, vancomycin, tocilizumab, norepinephrine, phenylephrine, midazolam and fentanyl. A TTE showed an ejection fraction of 65–70% with no regional wall motion abnormalities ().
The patient’s baseline troponin of 1.6 ng/ml declined to 1.5 ng/ml after 6 hours and then to 1.1 ng/ml after another 6 hours. A repeat ECG after 12 hours showed complete resolution of the ischaemic changes (). Patient was still on mechanical ventilation at the time of writing.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [70.0, 'mm hg'], 'Diastolic Blood Pressure': [41.0, 'mm hg']}",50.66667,48.13334,53.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 70.0 mm Hg + 2/3 * 41.0 mm Hg = 50.66667 mm Hg.
Hence, the patient's mean arterial pressure is 50.66667 mm Hg."
1460,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6318108-2,Extracted,"A 66-year-old Caucasian male with past medical history significant for hypertension and hyperlipidemia presented with altered mental status. Symptoms at presentation included slurred speech. He was found walking around his yard and his neighbor noted his slurred speech. His last know well state was the day before in the evening hours. Upon arrival, the blood pressure was found to be at 150/70 and his laboratory workup including complete blood count, complete metabolic profile and urinalysis were normal. Urine drug screen was positive for cannabinoids and serum alcohol level was not detectable. CT of the head showed age-related atrophy and mild small vessel ischemic changes without acute intracranial bleeding (Figure ). Questionable loss of gray-white junction and edema was found in the left frontoparietal region. On physical exam, the patient was confused but had normal movements and strength. He denied use of any tobacco products. TTE showed a normal left ventricle size, thickness, and function. The ejection fraction was estimated at 60% with normal right ventricular structure and function. There was a small PFO with predominant left-to-right shunting visualized. MRI showed an acute left middle cerebral artery territory infarction without midline shift or hemorrhagic conversion (Figure ). CTA showed the right internal carotid artery with estimated stenosis of 30-50% and the left internal carotid artery with stenosis estimated at 30-50%. TEE showed the PFO previously demonstrated and an ejection fraction of approximately 60%. Ultrasound of lower extremities failed to show deep vein thrombosis. The patient continued receiving neuro checks during the length of the stay and was started on antiplatelet therapy and atorvastatin with an outpatient follow-up and discharged with an event recorder and possible percutaneous closure of PFO after conduction abnormalities were ruled out.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 70.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1461,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8255049-1,Extracted,"A 64-year-old male with a history of hypertension and obesity was brought to the hospital following an episode of syncope at home. He had experienced chest tightness over the past few days prior to the admission. On physical exam, he was afebrile, with a heart rate of 72 beats per minute and blood pressure of 73/52 mmHg. Cardiac examination revealed a rhythmic S1 and S2, with a III/VI holosystolic murmur at the left lower sternal border. His laboratory examination revealed troponin levels of 17.92 ng/ml. His electrocardiogram revealed ST-segment elevations in leads II, III, and aVF (Figure ).
The patient was diagnosed with ST-elevation MI involving the inferior wall. Dopamine and norepinephrine were initiated. Emergent coronary angiography revealed 100% occlusion of the right coronary artery (RCA) with no collateral supply and 95% stenosis of the left anterior descending (LAD) artery (Figures , ). Aspiration thrombectomy and balloon angioplasty and subsequent stenting of the RCA were performed (Figure ).
Subsequent left ventriculography demonstrated evidence of a large ventricular septal defect (VSD) with extravasation of dye crossing from the left ventricle (LV) to the right ventricle (RV) near the apex (Video ).
A shunt run was performed to further confirm the presence of a VSD with the following results: right atrium (RA) saturation of 53.7%, RV: 90.4%, PA: 74.7%, and pulmonary capillary wedge pressure (PCWP): 95.8%. A notable step-up in the oxygen saturation between the RA and the RV was observed, consistent with a VSD.
Transthoracic echocardiogram with color Doppler was performed, which confirmed the presence of a defect in the septum. Color Doppler demonstrated a clear jet entering the ventricular septum from the LV, with the jet traversing the entire length of the septum through dissection and entering into the RV, consistent with complete IVSD (Video ).
The patient was maintained on cardiac pressors and was transferred to an outside hospital where he underwent successful bovine pericardial patch repair of the ventricular septum. The patient was ultimately discharged to a rehabilitation center in stable condition.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [52.0, 'mm hg'], 'Systolic Blood Pressure': [73.0, 'mm hg']}",59,56.05,61.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 73.0 mm Hg + 2/3 * 52.0 mm Hg = 59.0 mm Hg.
Hence, the patient's mean arterial pressure is 59.0 mm Hg."
1462,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-11638,Extracted,"A 42-year-old male presents to his primary care physician complaining of abdominal pain. He reports a 5-month history of epigastric pain that improves with meals. He has lost 15 pounds since the pain started. His past medical history is significant for a prolactinoma for which he underwent transphenoidal resection. He drinks alcohol socially and has a 10 pack-year smoking history. His family history is notable for a maternal uncle with a parathyroid adenoma. His temperature is 98.8°F (37.1°C), blood pressure is 125/80 mmHg, pulse is 85/min, and respirations are 18/min. After further workup, the patient is started on octreotide, an analogue of an endogenously produced hormone.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",95,90.25,99.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 80.0 mm Hg = 95.0 mm Hg.
Hence, the patient's mean arterial pressure is 95.0 mm Hg."
1463,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3708062-2,Extracted,"A 68-year-old male presented to the hospital with complaints of exertional substernal chest pain for three months duration. His symptoms were worsened on laboring for five days. He has a history of tobacco abuse and hypertension, but denied a prior medical history of diabetes. On admission, he was mildly hypertensive (150/70 mmHg) with a regular rhythm of 70 beats per minute. Cardiac auscultation was unremarkable. The electrocardiogram at admission revealed mild depression of the ST segment in leads II, III, aVF and marked by an exercising test. His echocardiography showed no obvious abnormal motion of ventricular wall. The report of lab analyses, such as troponin and the remaining cardiac enzymes, blood lipoids and FBG were negative. According to the results of the above examinations, he was diagnosed as having an unstable angina pectoris. The patient received conventional medicine preconditioning before the invasive angiography such as dual antiplatelet therapy (aspirin 100 mg/d and clopidogrel 300 mg once and thereafter at a dose of 75 mg/d); and the remaining therapy which included statin, nitrate and perindopril. A selective coronary angiography (CAG) with access through the right femoral artery was performed. The image of CAG revealed insignificant stenoses of the left coronary, but the wandering position of the RCA ostium. Selective cannulation of the RCA could not be achieved with either a Judkins right 3.5, or a 4.0 cm curve diagnostic catheter. Nonselective imaging of the ascending aorta revealed an aberrant origin of the RCA from antetheca of the aortic wall. Therefore, an Amplatzer left 0.75 cm curve catheter was selectively manipulated into the aberrant RCA and revealed an 85% lesion in the proximal RCA (). Subsequently, PCI was performed with a 6 Fr Amplatzer left 0.75 cm guiding catheter (Medtronic, USA), which provided terrible coaxialilty and support as a result of the anomalous anatomic originate of RCA ostium. We stepped a 0.014 inch BMW guide wire (Guidant, USA) “gone with the flow” and manipulated it to the distal-RCA predilated with a 2.5–15 mm Ryujin balloon catheter (TERUMO, Japan). Stent placement was accomplished with a 3.0–13 mm Partner drug eluting stent (Lepu, China) and delivered at 20 atm. The final result indicated insignificant remaining stenosis (). The patient was discharged on the second day of the procedures with continued dual antiplatelet therapy which included the daily regimen of aspirin 100 mg and clopidogrel 75 mg lasting for one year. There was also no dissection, thrombus, perioperative myocardial infarction, heart failure, stroke or death during the stent implanting procedure and he did not suffer from MACE during the follow-up period.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 70.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1464,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-913,Extracted,"A 64-year-old woman has progressively worsening abdominal pain 5 hours after an open valve replacement with cardiopulmonary bypass. The pain is crampy and associated with an urge to defecate. The patient reports having had 2 bloody bowel movements in the last hour. Her operation was complicated by significant intraoperative blood loss, which prolonged the operation and necessitated 2 transfusions of red blood cells. She has hypercholesterolemia and type 2 diabetes mellitus. The patient received prophylactic perioperative antibiotics and opioid pain management during recovery. Her temperature is 37.9°C (98.9°F), pulse is 95/min, and blood pressure is 115/69 mm Hg. Examination shows a soft abdomen with mild tenderness to palpation in the left quadrants but no rebound tenderness or guarding. Bowel sounds are decreased. Rectal examination shows blood on the examining finger.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [69.0, 'mm hg'], 'Systolic Blood Pressure': [115.0, 'mm hg']}",84.33333,80.11666,88.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 69.0 mm Hg = 84.33333 mm Hg.
Hence, the patient's mean arterial pressure is 84.33333 mm Hg."
1465,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5325031-1,Extracted,"A 54-year-old woman presented to us with progressive breathlessness and gradually
progressive, persistent bluish discoloration of the feet and fingers for the
preceding 4 days. She had a history of inferior wall myocardial infarction (MI)
three months back. Initial examination revealed bluish discoloration and marked
coldness of both hands and feet.
Subsequently, frank gangrene associated with mummification of the toes was observed.
( and ). The patient presented with areas of skin necrosis, purpura,
and erosions on the dorsum of the feet and hands. Her blood pressure was low
(80/60mm Hg); pulse rate was 110/minute and regular. All peripheral pulses were
normally palpable. Jugular venous pulse was not raised. The first heart sound was
soft, the second heart sound was normal, and the third heart sound presented a
gallop rhythm. We also heard bibasilar fine rales on her chest. Examination of the
other systems was noncontributory. Laboratory investigations revealed anemia
(hemoglobin: 8.2gram %), mild leukocytosis (12,000/cmm; neutrophil 72%), and low
platelet count (70,000/cmm).
C-reactive protein was elevated. Blood urea and serum creatinine levels were normal.
Blood lactate level was elevated (3.1 mmol/L). Liver function test showed slightly
raised bilirubin (1.5mg/dl) with normal transaminase levels. Lipid profile and serum
electrolytes were normal. Bacterial culture of urine, blood, and sputum revealed no
organism growth. Screening for hepatitis A, B, C, and HIV was negative. Antinuclear
antibody (Hep-2 cell line method) and ANCA were negative. D-dimer assay was positive
(400ng/dl). Abdominal ultrasonography was normal. Chest X-ray showed cardiomegaly
with pulmonary edema. ECG revealed old inferior wall infarction.
Transthoracic echocardiography showed large submitral pseudoaneurysm with large
layered thrombi within it and left ventricular systolic dysfunction (). The neck of the aneurysm was narrow
and the ejection fraction was 25%. Cardiac angiography revealed significant lesion
in the ramus intermedius and obtuse marginal arteries.
Peripheral doppler showed no significant blockage in the major lower or upper limb
arteries. Although peripheral angiography showed complete patency of the lower limb
arteries, slow flow to the distal part was reported. Lesional skin biopsy showed
non-specific inflammatory changes. Based on these features, we diagnosed symmetrical
peripheral gangrene complicating ventricular pseudoaneurysm. The patient was treated
conservatively with supportive treatment, but died on the 5th day after admission to
the hospital.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [80.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",66.66667,63.33334,70,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 80.0 mm Hg + 2/3 * 60.0 mm Hg = 66.66667 mm Hg.
Hence, the patient's mean arterial pressure is 66.66667 mm Hg."
1466,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7605055-1,Extracted,"We describe a case of 50-year-old South Asian male with past medical history of diabetes mellitus type II, hypertension, and coronary artery disease who was admitted for elective ureteroscopy under general anesthesia for ureteric stone. His home medications were aspirin 100 mg once daily, clopidogrel 75 mg once daily, metformin 500 mg twice daily, rosuvastatin 10 mg once daily, and pantoprazole 40 mg once daily. Additionally, he was prescribed levofloxacin 500 mg once daily for 7 days which were completed on the day of admission. His medication refill history from the outpatient pharmacy was regular and implies compliance to his home medications. After cardiology consultation, his urologist held aspirin and clopidogrel 6 days prior to the procedure to minimize the risk of bleeding.
On admission, his blood pressure was 100/62 mm Hg, heart rate was 64 bpm, respiratory rate was 20 bpm, and oxygen saturation was 99% on room air. Before anesthesia induction, he received 2 g of ceftriaxone intravenously, then he developed facial swelling, hypotension, and bradycardia, which progressed to pulseless electrical activity so cardiopulmonary resuscitation was performed and the patient was intubated. Although the cause of cardiac arrest was not clearly identified, it was thought to be an anaphylactic reaction to ceftriaxone.
After return of spontaneous circulation, he was shifted to the intensive care unit (ICU) for further care. Aspirin and clopidogrel were resumed while rosuvastatin and metformin were held due to elevated liver enzymes and critical illness, respectively. Additionally, lansoprazole 30 mg once daily by nasogastric route and heparin 5000 units subcutaneously twice daily were started for stress ulcer prophylaxis and for venous thromboembolism prophylaxis, respectively. Blood counts on the day of admission were as follows: white blood cells 18.2 ×103/µL, hemoglobin 15.1 g/dL, platelets 289×103/µL. Other laboratory investigations were normal except INR 1.3, creatinine 1.36 mg/dL, potassium 3 mEq/L, bicarbonate 19 mEq/L, and albumin 3 g/dL. He was extubated at the evening of the second day of admission to the ICU. He developed acute kidney injury and required 3 sessions of hemodialysis over the first 5 days of hospitalization then his kidney function started to improve gradually over his ICU stay. On day 2 of hospitalization, he started to have severe abdominal pain and diarrhea. Computed tomography of chest and abdomen showed multiple rib fractures and diffuse bowel edema.
On day 5 of hospitalization, his platelets dropped gradually to 57×103/µL from 315×103/µL on admission (). Heparin was held and heparin-induced thrombocytopenia (HIT) antibodies and fibrinogen level were requested to screen for HIT and disseminated intravascular coagulation (DIC), respectively. His medical record was reviewed, but no previous episodes of thrombocytopenia were identified. HIT antibody test was negative and fibrinogen level came to be 5.34 g/L (normal). Abdominal ultrasound was done which excluded splenomegaly.
On the next day (day 6 of admission), lansoprazole was suspected to be the cause of thrombocytopenia as it was the only newly introduced medication during admission and it was changed to ranitidine 150 mg once daily while heparin was reinitiated. His platelet count started to recover to normal gradually over the next 3 days. A full list of medications received during the first week of hospitalization is provided in . On the same day, the patient developed a urinary tract infection for which aztreonam 1 g every 8 hours was started. Two days later, his urine and blood cultures revealed extended spectrum beta-lactamase Escherichia coli, so aztreonam was changed to ertapenem 1 g once daily for 14 days according to microbiological sensitivity results. On day 14 of admission, patient developed thrombocytosis (560 ×103/µL) which was thought to be reactive secondary to infection, and his platelet count continued to increase gradually over the next few days. His peripheral smear on that day showed mild anisopoikilocytosis, anisochromia, and toxic neutrophils.
On day 18 of admission, lansoprazole 30 mg daily was prescribed due to suspicion of upper GI bleeding suggested by drop in hemoglobin (rechallenge was not intended). Packed red blood cells were transfused and colonoscopy was done that showed severe colitis with no evidence of bleeding and several biopsies were taken. After lansoprazole reinitiation, his platelets dropped from 669×103/µL to 319×103/µL on day 5 of reinitiation. On day 20 of admission, he started to pass fresh blood with stools and received 2 units of packed red blood cells. After stopping lansoprazole, there was rebound increase in his platelets to 567×103/µL. On day 25, the histopathology result of colonic biopsies was released and was suggestive of inflammatory bowel disease so mesalamine 1 g 3 times daily was started, and the patient was transferred to the medical ward after 28 days in the ICU. Diarrhea and abdominal pain improved slightly after starting mesalamine, but they didn’t resolve completely. Repeat colonoscopy was planned after few days, but the patient requested discharge to travel back to his home country so he was discharged after 30 days of hospital stay. A thorough review of his medical record showed that the patient had received lansoprazole for 7 days 30 months before this admission, but platelets were not checked at that time.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [62.0, 'mm hg']}",74.66667,70.93334,78.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 62.0 mm Hg = 74.66667 mm Hg.
Hence, the patient's mean arterial pressure is 74.66667 mm Hg."
1467,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4572425-1,Extracted,"A 59-year-old Caucasian female with history of recurrent bilateral pleural effusions was admitted with worsening dyspnea and a nonproductive cough present over the course of one week. She had undergone outpatient right-sided thoracentesis on the day prior to admission, with drainage of 1500 mL of pleural fluid.
The recurrent pleural effusions had been occurring for three months prior to this presentation, and she had undergone thoracentesis twice for the right-sided pleural effusion and six times for the left-sided pleural effusion without any conclusive diagnosis. Results from all of thoracentesis procedures were suggestive of transudative effusions and cultures were negative.
On physical exam, this patient was mildly dyspneic but without retractions or accessory muscle use. There were decreased breath sounds at both lung bases. Temperature was 98.5°F, heart rate was 94/min, respiratory rate was 18/min, blood pressure was 97/55 mm Hg, and oxygen saturations were 99% on room air. Complete blood count and basic metabolic panel showed WBC 8.6 thou/μL, Hb 14.1 g/dL, Hct 44.2 g/dL, Plt 356 thou/μL, sodium of 140 mmol/L, potassium of 4 mmol/L, chloride of 101 mmol/L, bicarbonate 32 mmol/L, BUN 13 mg/dL, Creatinine 0.8 mg/dL, and glucose 112 mg/dL. Serum immunofixation electrophoresis showed small lambda monoclonal protein and no Bence-Jones proteinuria. Chest X-ray taken at the time of admission demonstrated a moderate to large left-sided pleural effusion as well as a right lower lobe consolidation. CT scan of chest showed bilateral pleural effusions, greater on the left side (). During her hospitalization, the patient underwent thoracentesis which showed WBC 484 mm3, RBC 38 mm3, lymphocyte count of 99%, monocyte count of 1%, glucose of 106 mg/dL, total bilirubin of 2.4 gm/dL, lactate dehydrogenase (LDH) of 80 U/L, amylase 19 U/L, cholesterol of 45 mg/dL, triglyceride 17 mg/dL, and adenosine deaminase of 2.3 U/L, and the cultures for routine, acid fast bacilli, and fungus were negative. Cytology demonstrated benign findings with numerous lymphocytes present. The patient underwent biopsy of the left upper lobe of the lung as well as chemical pleurodesis for her recurrent left-sided pleural effusion. Lung biopsy showed diffuse pulmonary amyloidosis, and Congo Red staining was positive confirming the diagnosis (Figures 
–). Biopsy of the pleura was negative for any pathologic findings.
The patient underwent hematology/oncology evaluation. Echocardiogram showed left concentric ventricular hypertrophy. Rheumatoid factor and thyroid stimulating hormone levels were normal. Follow-up immunoglobulin and electron microscopy as well as bone marrow biopsy were performed and favored plasma cell myeloma over primary amyloidosis. There were 6% plasma cells on aspirate smears and 15–20% on CD138 immunohistochemical staining of biopsy and clot sections. Flow cytometry showed 1.4% of monoclonal plasma cells typical of a plasma cell dyscrasia.
The patient was started on Cyclophosphamide, Dexamethasone, and Bortezomib (Velcade) therapy and was discharged in stable condition with outpatient follow-up. She had no recurrent pleural effusions at four-month follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [97.0, 'mm hg'], 'Diastolic Blood Pressure': [55.0, 'mm hg']}",69,65.55,72.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 97.0 mm Hg + 2/3 * 55.0 mm Hg = 69.0 mm Hg.
Hence, the patient's mean arterial pressure is 69.0 mm Hg."
1468,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2186347-1,Extracted,"A 70 year old hypertensive Caucasian female patient presented to the Emergency Unit with left sided epistaxis. She had a past medical history of left-sided epistaxis 4 years ago for which she initially underwent left sphenopalatine (SPA) endoscopic ligation. During this episode epistaxis recurred so she underwent left external carotid artery and left anterior ethmoid artery ligation. She was subsequently completely free of epistaxis for 4 years. Two months prior to the episode we present she suffered a further bleed, which was successfully treated with anterior nasal packing.
During this presentation she was haemodynamically stable, with a blood pressure of 160/80 mmHg, and had normal coagulation screen, biochemistry and full blood count. During endoscopy, a bleeding point in the left SPA region was identified and bismuth iodoform paraffin paste (BIPP) nasal packing applied. She continued to bleed intermittently. Angiography was planned prior to further surgical intervention due to her past history of left SPA ligation. This confirmed complete occlusion of left ECA (figure ). The right ECA demonstrated a few small nasal branches of the right SPA crossing to the left, with no evidence of a bleeding point initially (Figure ). A literature search revealed that sphenopalatine-sphenopalatine anastomosis has not previously been reported.
A microcatheter was advanced distally in the right SPA and angiography showed pooling of a small amount of contrast in the upper part of the left nostril. Embospheres in the 80–120 μ size range and PVA particles in the 355–500 μ range were injected into the right SPA. Subsequent angiography revealed a reduction in the number of the nasal branches and no further pooling (Figure ). The nose was packed anteriorly at the end of the procedure. Packing was removed 24 hours later and the patient has had no further bleeding, and was hemorrhage free at follow up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [160.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 80.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1469,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7459753-1,Extracted,"A 49-year-old Hispanic woman was admitted to the emergency room of the Modena University Hospital in March 2020 for fever, chest pain and cough lasting 3 days. Her medical history was not significant. She reported intermittent fever, with a peak at 38.5°, without shivering. Cough was dry, without sputum, associated with constrictive chest pain. She reported dyspnea to daily home living activities. In the emergency room, blood pressure was 120/70 mmHg, heart rate 140 beats per minute, respiratory rate 16 acts per minute, temperature 39°, oxygen saturation 98%. Arterial blood gas analysis showed PO2 69.7 mmHg, PCO2 24.1mmHg, pH 7.40, SO2 96%. PaO2/FiO2 ratio was 331 with no evidence of respiratory failure. The chest radiograph showed diffuse interstitial thickening with consolidation in the right paracardiac site. Blood tests showed leukocytosis with neutrophilia (white blood cells count 19600/mmc, neutrophil 90%), alteration of C reactive protein (44 mg/dl) and procalcitonin (5 ng/ml). Nose-pharyngeal swab was performed and resulted positive infor SARS-CoV2 (polymerase chain reaction, PCR). According to Regional Guidelines for COVID-19 treatment, she received hydroxychloroquine 400 mg x 2 on day 1 and 2 and then 200 mg x 2 from day 4 to day 6, and antithrombotic prophylaxis with low-molecular-weight heparin (4000 U once a day as a standard prophylactic dose for weight under 100 kg), and antibiotic therapy with ceftriaxone 2 g/day and azithromycin 500 mg/day due to the increase in neutrophils and procalcitonin under the suspicion of bacterial infection.
Chest pain suggested an electrocardiogram, which documented right bundle branch block detection and widespread alterations of repolarization. The troponin curve, performed at 6 hour interval after admission showed the following values 820, 699, 593, 326 ng/L with further decrease in the following days, until negative at day 5. The type B natriuretic peptide (BNP) was 950 pg/mL and normalized at day 4. The echocardiogram showed a slight reduction in the ejection fraction (45%), slight pericardial effusion without signs of cardiac tamponade, moderate mitral insufficiency, a pattern compatible with myocarditis. Cardiac MRI performed on day 5, showed slight depression of the ejection fraction (54%), without significant alterations in the contractility of both ventricles (), widespread increase in myocardial T2 signal intensity (ratio with skeletal muscle 2.2-2.5), moderate pericardial effusion at the posterior lateral wall of the left ventricle (). In accordance with the position statement of the European Society of Cardiology of 2013 and the subsequent focus on the diagnostic value of Cardiac MRI of 2017, the patient had two clinical presentation criteria (acute chest pain, newonset of dyspnoea at rest or exercise, and/or fatigue) and three diagnostic criteria (ECG alterations such as previously unknown bundle branch block, myocardiocytolysis markers, functional and structural abnormalities on cardiac imaging at echo and MRI) of myocarditis.
The consultant cardiologist suggested therapy with sotalol 50 mg x 2, acylsalicylic acid 100 mg/day and ramipril 2.5 mg per day. The patient presented a progressive general improvement, with reduction up to disappearance of chest pain on day 7 after admission. During the second week of hospitalization echocardiogram showed a clear reduction in pericardial effusion and normal ejection fraction (55%). Holter ECG showed no significant changes in the records. ECG discharge showed only nonspecific abnormalities of repolarization. On day 12, the patient was discharged at home.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1470,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8651372-1,Extracted,"The patient is a 64-year-old male with a medical history of hypertension, chronic kidney disease, atrial fibrillation, heart failure with reduced ejection fraction (nonischemic cardiomyopathy) with left ventricular ejection fraction of 35%, and ventricular tachycardia with ICD in place on amiodarone and mexiletine, who presented after experiencing a shock by his ICD twice on the day of admission. The patient complained of palpitations on the day of admission and denied having chest pain, shortness of breath, cough, or loss of consciousness. On physical exam, his blood pressure was 109/71 mmHg, heart rate was 100 beats per minute, respiratory rate was 18 breaths per minute, oxygen saturation was 96% on room air, and temperature was 97.8 F. He was alert and oriented, had clear breathing sounds, bilateral, no heart murmurs, and no leg swelling. EKG showed ventricular paced rhythm with underlying atrial fibrillation. Significant laboratory showed an increase in his creatinine to 1.7 mg/dl from a baseline of 1.2 mg/dl and a TSH of 16 uIU/mL and normal free thyroid hormone levels. The ICD interrogation showed multiple sustained monomorphic ventricular tachycardia episodes. During his hospital stay, his workup revealed positive UDS for amphetamine on 2 separate occasions (urine toxicology screen), but the patient adamantly denied using amphetamine or any other illicit drugs. He ultimately underwent confirmatory drug testing for amphetamine (quantitative urine amphetamines), which was negative. Ultimately, the patient underwent successful VT ablation and was discharged home.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [109.0, 'mm hg'], 'Diastolic Blood Pressure': [71.0, 'mm hg']}",83.66667,79.48334,87.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 109.0 mm Hg + 2/3 * 71.0 mm Hg = 83.66667 mm Hg.
Hence, the patient's mean arterial pressure is 83.66667 mm Hg."
1471,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8043568-2,Extracted,"A 15-year-old male patient was referred to the ED, due to high fever (39°C) lasting 72 hours, cervical stiffness and frontal headache. No other symptoms were reported.
On physical examination, pulse rate was 100 beats/min, respiratory rate was 12 breaths/min, and blood pressure was 120/80 mmHg. Lung auscultation was normal. Cardiac sounds were normal with no murmurs. He did not have clubbing. His oxygen saturation was lower when supine (platypnea). Rest of physical examination was unremarkable. ABGs analysis revealed hypoxemia (pH: 7.45, pCO2: 36 mmHg, pO2: 68 mmHg, HCO3: 25 mmol/L, FiO2: 21%). Routine laboratory investigations were normal. Hemoglobin was 11.1 g/dL. Liver and renal panels as well as inflammatory markers were within normal limits. The patient was suspected to have meningitis and was admitted to the Special Infections Unit. A brain CT revealed an enlargement of the left temporal horn. Lumbar puncture was performed and results from the cerebrospinal fluid analysis were 300 red blood cells/mm3, 5,800 nuclear cells/mm3, 30% lymphocytes, and 70% polymorphonuclear cells. Glucose was 41 mg/dL, lactate dehydrogenase (LDH) 34 U/L, and cerebrospinal fluid albumin 108 g/dL. Cerebrospinal fluid analysis revealed normal cell count and low protein levels. In addition, glucose was 101 mg/dL (serum concentration was 115 mg/dL) and polymerase chain reaction (PCR), Gram stain and culture were negative for bacteria or bacterial and/or viral DNA and/or RNA. Chest radiograph was noticeable for three nodules in the right lung.
A subsequently post-IV contrast CT revealed numerous (>15) PAVMs in both lungs with the largest located in the right middle lobe and the superior segmental of the right lower lobe. They were perfused by branches of the pulmonary artery and had large draining veins (diameter~20 mm) (Figure ).
A brain MRI was consistent with the diagnosis of a brain abscess with peripheral edema and hemorrhage in the right temporal lobe (Figure ).
The largest one (12 mm) was located beside the interhemispheric fissure and was radiologically similar to those of a cavernous hemangioma. In addition, a more detailed history confirmed episodes of spontaneous nose bleeding and a first-degree relative with HHT (two out of three criteria for the diagnosis of HHT).
A contrast-enhanced pulmonary and abdominal aorta angiography was performed which confirmed the imaging findings of chest CT. Due to the presence of multiple arteriovenous malformations in multiple systems, this patient was referred to a specialized center for embolization.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1472,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7044523-1,Extracted,"A 61-year-old female presented to a regional hospital with a 3-week history of intermittent diarrhoea, vomiting and generalized abdominal pain. She had a diffusely tender abdomen but was not peritonitic, and was shocked with a heart rate of 110 beats per minute, blood pressure of 89/45 mmHg and was peripherally cool. Her blood tests revealed a lactate of 7.2 mmol/L, which worsened to 7.8 mmol/L during resuscitation with intravenous fluids, and white cell count was 30.9 × 109/L, with an international normalized ratio (INR) of 1.4. She had an acute kidney injury with a creatinine of 119μmol/L and estimated glomerular filtration rate (eGFR) of 43 mL/min/1.73m2. Computed tomography (CT) revealed extensive thickened loops of non-enhancing small bowel with pneumatosis, moderate free fluid and a large splenic infarction. There was extensive thrombosis of the splenic vein and superior mesenteric vein extending into the portal vein to the level of the porta hepatis. Her background history included factor V Leiden and protein S deficiency, for which she had been non-compliant with warfarin during this illness. She had no surgical history (–).
After initial assessment and fluid resuscitation, she was given broad-spectrum intravenous antibiotics and proceeded to emergent laparotomy. Intraoperative findings included an 80-cm segment of ischaemic jejunum, which was resected, with a laparostomy performed and transferred to the ICU. During laparotomy, a small 1.5-cm mass was observed arising from the antimesenteric border of the ischaemic segment, presumed to be a jejunal diverticulum and was included within the specimen. Peritoneal survey revealed splenic infarction but otherwise no other observed organ injury. She was noted to have a dusky-appearing right foot with no palpable peripheral pulse; however, arterial Doppler revealed midperoneal, posterior tibial and anterior tibial arterial stenoses, suggesting ischaemia due to a low-flow state. She was commenced on intravenous heparin. She returned to theatre 36 h later, at which time no further ischaemia was encountered, and anastomosis was performed and the abdomen subsequently closed. She recovered over a period of 1 week and was discharged home on warfarin.
Subsequent pathology revealed an incidental 45-mm, ulcerated spindle cell tumour, with immunohistochemistry in keeping with a smooth muscle tumour. A subsequent second-opinion pathology report supports the diagnosis of leiomyosarcoma of the small bowel, with the tumour being strongly positive for desmin and h-caldesmon and negative for c-kit, DOG-1, S100, MelanA, SOX10, HMB45, CD34, AE1/AE3 and CK8/18. The mitotic index was 9 mitoses/mm2. Staging CT of the chest revealed an 11-mm pretracheal lymph node, which did not show fluorodeoxyglucose (FDG) avidity on PET scan. Multidisciplinary team discussion recommended only surgical follow-up, with no adjuvant therapy.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [45.0, 'mm hg'], 'Systolic Blood Pressure': [89.0, 'mm hg']}",59.66667,56.68334,62.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 89.0 mm Hg + 2/3 * 45.0 mm Hg = 59.66667 mm Hg.
Hence, the patient's mean arterial pressure is 59.66667 mm Hg."
1473,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3843907-1,Extracted,"A 39-year-old man was admitted to our hospital because of a sudden onset of hemiparesis on his left side with dysarthria. He had a history of a SVA rupture that was surgically treated at the age of 24 (fig. ). During the surgery, there were no specific findings of cystic medial necrosis or crystalline lens subluxation due to the Marfan syndrome. In his infancy, there were no developmental abnormalities. In his school records, the subject had poor grades during childhood and adolescence. His family history over 3 generations was unremarkable in terms of neurological, psychological, and cardiac diseases. During the patient's examination, his body temperature was 37.0°C, blood pressure was 184/104 mm Hg, pulse was 83 beats per minute, respiratory rate was 20 breaths per minute, and oxygen saturation was 97% (while he was breathing ambient air). At the time of hospitalization, the patient presented with an acute stroke and the symptoms included left-sided weakness and dysarthria; these neurological symptoms lasted for a week after admission. We assessed the risk of juvenile ischemic stroke in a laboratory study, but high-risk factors that are linked to juvenile cerebral ischemia, such as collagen diseases and vasculitides, were not found. An electrocardiogram revealed a sinus rhythm within the normal range. Although we performed magnetic resonance imaging (MRI) with a 1.5-tesla unit on the first day and with a 3-tesla unit 2 weeks later, acute cerebral infarction was not detected (fig. ). Routine sonographic evaluation of the carotid arteries demonstrated a diffuse narrowing of the left ICA and a low-lying carotid bifurcation. Thereby, cerebral angiography was conducted, and it showed hypoplasty of the left ICA and a low-lying carotid bifurcation at the level of the C6 vertebra (fig. ). The A1 segment of the bilateral anterior cerebral arteries (ACAs) was united and formed an azygos type (fig. ). The common ACA duct and left posterior cerebral artery were mainly supplied by the right ICA. Aortography and 4 vessel studies (bilateral common carotid arteries and vertebral arteries) were conducted, and there was no embolic source, such as ulceration of the arterial surface or arterial dissection, or significant partial arterial stenosis. No right-to-left shunt was found in transesophageal echocardiography.123 I iofetamine single-photon emission computed tomography brain imaging was performed, and no regional reductions or abnormal accumulations of tracer uptake into the brain were observed. The patient's intelligence quotient was evaluated with the Wechsler Adult Intelligence Scale-III []; his mental faculties were found to be at a significantly low level of functioning (table ). Facial manifestations were unremarkable, but he showed symptoms of nasal speech and nasal air emission while talking. In the otorhinolaryngological examinations, velopharyngeal insufficiency was revealed by laryngoscopy. The patient was discharged after 3 weeks; MRI could not detect any significant abnormal findings such as infarction, hemorrhage, or malformation. We decided that the patient should continue with an antithrombotic therapy after assessing normal treatment for cerebral ischemia. The patient is now taking warfarin; the target range for the prothrombin time/international normalized ratio is 2.0–3.0.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [184.0, 'mm hg'], 'Diastolic Blood Pressure': [104.0, 'mm hg']}",130.66667,124.13334,137.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 184.0 mm Hg + 2/3 * 104.0 mm Hg = 130.66667 mm Hg.
Hence, the patient's mean arterial pressure is 130.66667 mm Hg."
1474,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8380076-1,Extracted,"A 40-year-old lady was presented to the hospital with 1-week history of generalized abdominal pain, moderate to severe in intensity, associated with nausea and four episodes of vomiting, with no aggravating or relieving factors. There was no history of fever, hematemesis, bleeding per rectum, chest pain, or palpitations. The patient was a known case of hypothyroidism, vitiligo, and type 1 diabetes mellitus. She was a non-smoker. The patient had no personal or family history of thrombophilia and there was no history of recurrent abortions. Physical examination revealed an afebrile patient, with a heart rate of 92 beats per minute, blood pressure 124/76 and respiratory rate 17 breaths per minute. Abdominal examination showed diffuse tenderness, no organomegaly, normal percussion note with normal bowel sounds. Cardiac, respiratory, and nervous system examination were normal.
Labs investigations showed mild neutrophilic leukocytosis, high C-reactive proteins, microcytic anemia, normal urea, creatinine, electrolytes, and liver function tests (Table ). Coagulation testing showed normal PT, aPTT, and INR (Table ).
A computed tomography (CT) scan of the abdomen with contrast showed diffuse thickening of the splenic flexure, descending colon, and sigmoid colon with surrounding mesenteric edema and fat stranding as well as a thrombus in the abdominal aorta at the level of L3 vertebra (Figures and ). However, all the thrombophilia screen and autoimmune work up were negative (Table ).
The patient was managed as a case of ischemic colitis due to spontaneous abdominal aorta thrombosis. She was started on anticoagulation with warfarin bridged by therapeutic dose enoxaparin with a target INR of 2–3. A follow-up CT scan of the abdomen that was done 2 months afterward showed resolution of thrombus and improvement of the inflammatory changes in the bowel (Figure ). Three months afterward, she presented with left-sided abdominal pain, nausea, and vomiting. CT scan of the abdomen was done, and it showed focal segmental circumferential mural thickening of the distal descending colon as a complication of the ischemic colitis the patient was admitted and underwent left hemicolectomy. She was then discharged home after improvement.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [124.0, 'mm hg'], 'Diastolic Blood Pressure': [76.0, 'mm hg']}",92,87.4,96.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 124.0 mm Hg + 2/3 * 76.0 mm Hg = 92.0 mm Hg.
Hence, the patient's mean arterial pressure is 92.0 mm Hg."
1475,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6651983-1,Extracted,"A 63-year-old male was admitted to the emergency department with a complaint of left shoulder pain for one month and chest tightness for 3 days. The patient had a history of diabetes mellitus and his glucose was well regulated. Six years prior the patient had been treated with esophagectomy and radiotherapy for esophageal cancer. After the surgery, he had 3 times of following-up gastroscopy examinations, which indicated no evidence of recurrence, while the white blood cell count (WBC) kept in relatively lower level around 3.5 × 109 /L. At admission he had no cough, vomiting and abdominal pain.
The patient had a temperature of 37.6 °C, a blood pressure of 123/87 mmHg, a pulse of 103 bpm, a respiratory rate of 20 per minute and an oxygen saturation of 97% at admission. There was no paradoxical pulse. His jugular veins were slightly distended. Lung auscultation revealed crackles at both lung bases, while the heart sounds were not distant. There was mild edema in both legs.
The laboratory examination indicated WBC of 12 × 109/L and serum procalcitonin level of 1.8 ng/ml, while the liver function tests and serum myocardial markers level (troponin T and pro-b-type natriuretic peptide) were slightly above normal. Chest computed tomography revealed a massive pyopneumopericardium, a bilateral pleural effusion, and a collapse of the lower lobe of left lung (Fig. ). Ultrasound-guided pericardiocentesis was performed and 300 ml of pus was drained. Analysis of specimens of pericardium pus indicated WBC of 20 × 109/L (100% neut), lactic dehydrogenase (LDH) > 17,000 IU/L and glucose of 0.05 mmol/L.
Parenteral treatment with ceftriaxone 2000 mg IV every 24 h was given at admission, but no clinical improvement was achieved. On the day after his admission the pericardial fluid culture indentified E. corrodens and Streptococcus anginosus, and repeated blood test indicated increased WBC of 28 × 109/L and extremely abnormal blood biochemical indexes including alanine aminotransferase (ALT) of 5,000 IU/L, aspartate aminotransferase (AST) > 10,000 IU/L, LDH of 10,000 IU/L, amylase of 366 IU/L, and hypoalbuminemia of 25 g/L. Serum myocardial markers levels increased dramatically (Troponin T of 198 ng/L and pro-b-type natriuretic peptide of 3,000 pg/ml). Arterial blood gas analysis revealed apparent acidosis and type I respiratory failure (oxygen partial pressure of 55 mmHg, lactate of 9.8 mmol/L). The patient’s vital signs worsened on day 2 after admission with blood pressure of 84/45 mmHg, pulse of 154 bpm, respiratory rate of 42 per minute and oxygen saturation of 78%. The antibiotic therapy was changed to imipenem 500 mg IV every 8 h, and mechanical ventilation was provided. But the patient’s condition still had no improvement. The antimicrobial susceptibility test showed that the isolated strain was sensitive to imipenem and ceftriaxone, while resistant to clindamycin and amykacin. The patient died three days after admission.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [123.0, 'mm hg'], 'Diastolic Blood Pressure': [87.0, 'mm hg']}",99,94.05,103.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 123.0 mm Hg + 2/3 * 87.0 mm Hg = 99.0 mm Hg.
Hence, the patient's mean arterial pressure is 99.0 mm Hg."
1476,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5664874-1,Extracted,"A 35-year-old woman presented to the emergency department with acute pulmonary edema. She had an episode of acute gastroenteritis 2 weeks beforepresentation, which was treated by a general practitioner. Subsequently, the patient developed fatigability, syncope, and breathlessness on exertion. At presentation, the patient was pale, cold, and clammy; her pulse rate was 110 beats/min, regular, low volume, and her blood pressure was 92/66 mmHg. On chest auscultation, bibasilar fine crepitations were present; cardiac examination revealed left third heart sound/S3 gallop, but no murmurs. She was kept propped up, given high flow oxygen, and intravenous (IV) furosemide, digoxin, and low dose of dopamine infusion. Her electrocardiogram showed sinus tachycardia and generalized nonspecific ST-T changes, and chest radiograph showed cardiomegaly with features of pulmonary edema. Her routine investigations revealed anemia (hemoglobin of 9.5 g/dl). The rest of the biochemical investigations including liver and renal function tests were within normal limits. The echocardiogram revealed mitral regurgitation with normal cusps, and severe left-ventricular (LV) systolic dysfunction, with an LV ejection fraction of 25%. A diagnosis of dilated cardiomyopathy with LV failure was made, and the patient was treated for the same. Despite the resolution of pulmonary edema, she continued to have systolic blood pressure recordings of 90 mmHg with associated fatigue and light-headedness. Her general condition including apathy, anorexia, and nausea, did not improve. She was also noted to have psychomotor slowing, and hoarseness of voice.
Her history revealed that she had bled profusely at the time of delivery in her first pregnancy 11 years ago. She also recalled having multiple episodes of vomiting, and headache during the episode, and being given large quantities of IV fluids and two-three units of whole blood. The patient had recovered completely following the PPH. Her neuro-imaging during the episode was found to be normal. Since then, the patient developed episodes of syncope, craving for salt and water, and cold intolerance. She continued to have a normal reproductive function, and had two pregnancies over the next 5 years, with uncomplicated delivery in hospital. She, however, had lactation failure in both the pregnancies. She continues to have normal menstrual cycles till date, 9 years after her last pregnancy. She had normal axillary and pubic hair. A clinical diagnosis of SS with partial hypopituitarism was considered. On investigation, she was found to have central hypothyroidism, hypoadrenalism, and hypoprolactinemia []. Magnetic resonance imaging of the brain showed partially empty sella with normal posterior pituitary. A diagnosis of SS with dilated cardiomyopathy was confirmed, and she was started on glucocorticoids and thyroxine. Within a week her blood pressure and postural symptoms improved remarkably, and patient felt a sense of well-being. Symptoms of heart failure regressed completely on follow-up. Repeat echocardiogram, after 6 months of treatment, revealed normal cardiac chambers and valves, with LV ejection fraction of 60%.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [66.0, 'mm hg'], 'Systolic Blood Pressure': [92.0, 'mm hg']}",74.66667,70.93334,78.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 92.0 mm Hg + 2/3 * 66.0 mm Hg = 74.66667 mm Hg.
Hence, the patient's mean arterial pressure is 74.66667 mm Hg."
1477,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8509160-1,Extracted,"A 31-year-old male presented to the emergency with acute-onset shortness of breath and palpitations for 5 days. He had had two episodes of hemoptysis in the last 2 days. There was no history of fever or cough. The patient gave a history of congenital heart disease but no history of past surgery or long-term medications for the same. On examination, blood pressure was 120/92 mm Hg, heart rate was 110 bpm, and SpO2 was 88% on room air and 95% on O2. He had central cyanosis and bilateral upper and lower limb clubbing. Blood workup revealed polycythemia with hemoglobin of 19.3 g/dL, hematocrit of 57.4%, mean corpuscular volume of 92.9 fL, mean corpuscular hemoglobin (MCH) of 31.2 pg, and MCH concentration of 33.6 g/dL. Platelet count was reduced (84,000 mcL). Chest radiograph [] was reported as normal. Electrocardiography revealed sinus tachycardia and right-axis deviation. Computed tomography (CT) pulmonary angiography (CTPA) ruled out pulmonary thromboembolism []. CT lung window (not shown) showed a wedge-shaped peripheral area of ground glassing with some consolidation in the right lower lobe of lung, suggestive of possible viral (?COVID-19) pneumonia. However, the patient tested negative for COVID-19 by reverse transcription polymerase chain reaction.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [92.0, 'mm hg']}",101.33333,96.26666,106.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 92.0 mm Hg = 101.33333 mm Hg.
Hence, the patient's mean arterial pressure is 101.33333 mm Hg."
1478,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2894490-1,Extracted,"A 4-year-old male child weighing 13 kg, presented with history of dyspnoea on exertion for 3 month duration. On examination, all peripheral pulses were palpable except on the right upper limb. His blood pressure was 140/100 mm Hg in the left upper limb and was not recordable on the right upper limb. He was evaluated for secondary hypertension and found to have Type III Takayasu's arteritis with aortography revealing 99% stenosis of left main renal artery and 60% stenosis of the right main renal artery as well as occlusion of the right subclavian artery (). He had clinical and echocardiographic evidence of left ventricular dysfunction with normal renal functions. He was stabilized on tab.nifedepine 5mg Q4H, prazosin 1mg Q6H, aldomet 250mg Q8H, minoxidil 5mg Q12H, frusemide 10 mg, digoxin 0.25 mg and aspirin once a day. He underwent balloon angioplasty and stenting of left renal artery. He presented subsequently with a history of recurrent episodes of seizures and persistently elevated blood pressure. MRI brain revealed vasculitis induced multiple infarcts. Right auto renal transplantation was considered due to refractory hypertension and ongoing complication. Preoperative vitals revealed GCS of 14/15, heart rate of 96/min, absent right radial pulse with blood pressure in left upper limb of 170/110mmHg. His blood investigations were normal with serum creatinine of 0.9mg%. Chest roentgenogram revealed cardiomegaly and electrocardiogram left ventricular hypertrophy.
The patient was fasted and premedicated with Syp.Triclofos 75mg.kg−1. Under standard monitoring (SpO2, non-invasive blood pressure, ECG, end-tidal CO2 monitor, temperature), anaesthesia was induced with air, oxygen and sevoflurane. The trachea was intubated following atracurium administration and the patient mechanically ventilated. Under ultrasound guidance, a 5F triple lumen catheter was sited in the right internal jugular vein. The left femoral artery was selected for direct arterial pressure monitoring. Anaesthesia was maintained with 50% mixture of air and oxygen, end-tidal isoflurane concentration of 1% with morphine, fentanyl and atracurium boluses as needed. Normocarbia was maintained to preserve cerebral perfusion. Surgery was done in supine position. A good perfusion pressure of the transplanted kidney was ensured by maintaining a systolic blood pressure of 130 mm Hg, CVP of 13-15 mmHg. Mannito 10.5g.kg−1 was infused 20 minutes before clamp release. Blood loss was replaced with fresh whole blood. Urine output was more than 0.5 ml.kg−1.hr−1 after the anastamosis. The intraoperative period was uneventful. Arterialblood gas analysis was within normallimits and trachea extubated at the end of the procedure. Post operatively, the child was monitored in the high dependency unit and had an unremarkable stay. Outpatient visit at 8 weeks revealed improved sensorium and blood pressure of 130/85mmHg in left upperlimb. Diethylene Tetramine Penta Acetate(DTPA) scan done at 8 weeks showed functioning of auto transplanted kidney () and antihypertensives were tapered. Colour doppler revealed good perfusion of transplanted kidney as characterized by the reduction in the peaksystolic velocity from 244.1 cm/sec to 120.5 cm/sec. ()",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",113.33333,107.66666,119,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 100.0 mm Hg = 113.33333 mm Hg.
Hence, the patient's mean arterial pressure is 113.33333 mm Hg."
1479,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7441251-1,Extracted,"A 51-year-old man presented to our hospital with bilateral testicular pain.
He had eaten raw chicken (sashimi, in Japanese) a few days before the onset of his symptoms. The testicular pain onset was gradual, beginning in the morning prior to his visiting the hospital. Throughout the day, his testicular pain had spread to his entire back and abdomen and had increased in intensity, leading him to visit our hospital that evening. He also experienced fever, headache, and general joint pain, but no nausea or diarrhea.
The patient did not have a history of significant past illnesses.
Physical examination revealed a body temperature of 38.1 °C, a heart rate of 109 beats/min, a blood pressure of 138/76 mmHg, and a respiratory rate of 20 breaths/min. He exhibited mild tenderness over a wide area, which centered in his right lower abdomen. However, his scrotum did not exhibit any abnormal findings, such as redness, swelling, warmth, or tenderness.
Blood tests showed slight increases in his white blood cell count [12360 cells/µL, (neutrophils: 81.9%)] and C-reactive protein level (1.26 mg/L); no abnormalities were detected in the patient’s urinalysis.
Abdominal computed tomography imaging revealed thickening of the ileocecal walls (Figure ), but his scrotal area appeared normal (Figure ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [138.0, 'mm hg'], 'Diastolic Blood Pressure': [76.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 138.0 mm Hg + 2/3 * 76.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1480,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-10066,Extracted,"A 67-year-old man presents to the physician with profuse watery diarrhea along with fever and crampy abdominal pain. He has been taking an antibiotic course of cefixime for about a week to treat a respiratory tract infection. At the doctor’s office, his pulse is 112/min, the blood pressure is 100/66 mm Hg, the respirations are 22/min, and the temperature is 38.9°C (102.0°F). His oral mucosa appears dry and his abdomen is soft with vague diffuse tenderness. A digital rectal examination is normal.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [66.0, 'mm hg']}",77.33333,73.46666,81.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 66.0 mm Hg = 77.33333 mm Hg.
Hence, the patient's mean arterial pressure is 77.33333 mm Hg."
1481,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9590,Extracted,"A 48-year-old man presents to the clinic with nausea, vomiting, fever, and pain in the right upper quadrant of his abdomen for the past 18 hours. He mentions that he has been experiencing intermittent episodes of pain at the same location over the last 3 months and that these episodes usually occur after a heavy meal and subside within 1 or 2 hours. On physical examination, his temperature is 38.5°C (101.3°F), pulse is 130/min, respirations are 24/min, and blood pressure is 130/84 mm Hg. On examination of the abdomen, tenderness is present over the right upper quadrant; palpation over the area produces an inspiratory pause. An urgent bedside ultrasonogram shows a dilated common bile duct stone, but no stone in the common bile duct or in the gallbladder.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [84.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",99.33333,94.36666,104.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 84.0 mm Hg = 99.33333 mm Hg.
Hence, the patient's mean arterial pressure is 99.33333 mm Hg."
1482,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2740065-1,Extracted,"A 26-year-old Caucasian man of British ethnicity was brought to the emergency department having been found unconscious at home in bed. There was a history of cocaine and alcohol ingestion the previous evening. The exact timing of his collapsed state in relation to the cocaine ingestion was unclear. His Glasgow Coma Score on arrival was 4. He was hypoxic (oxygen saturation 80%), with a respiratory rate of 50 breaths/min, heart rate of 120 and blood pressure of 90/43. Initial management consisted of oxygen and rapid fluid infusion. He required a rapid sequence induction, endotracheal intubation and mechanical ventilation. The ECG was interpreted as showing a broad complex tachycardia (). Initial blood gas showed a PaO2 8.8 KPa, PaCO2 7.52 KPa, pH 7.0 and base excess was -12 with a serum lactate of 7.2. Biochemistry revealed a serum potassium 8.9 of mmol/l, Alanine Transaminase of ~6500, Creatinine of 395, Troponin of 0.7 and creatinine kinase was unrecordably high. He was given insulin and dextrose (10 units in 50 ml 50% glucose) to treat the hyperkalemia followed by synchronized cardioversion (50 J, 100 J × 2) in an attempt to restore sinus rhythm. He remained hypotensive and was therefore commenced on a dobutamine infusion in the emergency department. Initial echocardiogram revealed severe systolic dysfunction with an ejection fraction of 20%. Because of the high risk of coronary vasospasm from cocaine and a strong family history of ischaemic heart disease he was taken for urgent coronary angiography. However the coronary vasculature was normal. Computed tomography of the brain was also normal. His cardiac rhythm normalised over the next 2 hours with a sinus tachycardia once the serum potassium levels were corrected to 5.1 mmol/l (). He remained intubated and ventilated and was transferred to intensive care. His oxygenation rapidly deteriorated and a chest X-ray showed a bat’s-wing appearance of pulmonary oedema. The metabolic acidosis persisted and he was noted to be anuric. The working diagnosis was rhabdomyolysis leading to renal failure and hyperkalemia. He required prone ventilation and continuous haemofiltration. Over the next 8 days his condition slowly improved and following a tracheostomy he was successfully weaned from ventilatory support but continued to require intermittent haemodialysis. He was discharged to the ward but 2 weeks later he suffered a grand mal convulsion and was found to have bilateral basal ganglia and internal capsule infarcts possibly secondary to the cocaine ingestion.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [43.0, 'mm hg']}",58.66667,55.73334,61.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 43.0 mm Hg = 58.66667 mm Hg.
Hence, the patient's mean arterial pressure is 58.66667 mm Hg."
1483,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4274831-1,Extracted,"A 35-year-old parturient (G2A1P0) at 37 weeks of gestation presented at emergency department with severe preeclampsia. An urgent lower segment caesarean section (LSCS) was planned by the obstetric team and anaesthesia consultation was sought for it. Her antenatal history revealed that she was a patient of chronic ITP which was diagnosed 1 year back when she developed menorrhagia after diagnostic hysterolaparoscopy. She had thrombocytopenia and her bone marrow biopsy revealed normocellular marrow with megakaryocytes. She received methylprednisolone (20 mg/day) for 6 months which was later tapered down. She was on regular antenatal care (ANC) and did not receive any treatment during pregnancy as she had mild thrombocytopenia and her platelets remained around 100–150 × 109/L. In her last ANC which was 5 days prior to admission her platelets were normal and BP was 130/80 mm of Hg. On admission she had c/o headache and blurring of vision with severe epigastric pain and vomiting. Her BP was 210/110 mm Hg and was treated with sublingual depin 10 mg and loading dose of Inj. MgSO4 followed by 5 gm IM in each buttock alternately. Inj. dexona 2 mg IV was given. Since her liver enzymes were elevated (SGPT 422 IU/L, SGOT 765 IU/L, S. Bilirubin total 3.6, direct 2.4, and indirect 1.2) HELLP syndrome was suspected. CBC showed normal S. creatinine (0.7) and electrolytes (Na, K, Ca, and Mg). Her Hb was 9 gms%. Platelet count was 60 × 109/L, LDH was 958 IU/L, and INR was normal. Blood products including platelet concentrates were kept available. She was transported to the OT with a wedge under right hip. Premedication included IV ranitidine (150 mg) and metoclopramide (10 mg). Following adequate preoxygenation with 100% O2, induction of anesthesia was achieved with thiopentone sodium 300 mg (5 mg/kg). Aided with Sellicks manoeuvre, tracheal intubation was done with Portex Cuffed Endotracheal Tube number 7.0 after adequate relaxation with succinylcholine (2 mg/kg). Anesthesia was maintained with sevoflurane before and nitrous oxide after the delivery of baby and bolus doses of atracurium were given as muscle relaxant. IV fentanyl 100 μg was given after the baby was delivered. Intraoperative monitoring included temperature, pulse, BP, SpO2, ECG, and etCO2. A healthy female child was delivered 16 minutes after incision and APGAR scores were 7 and 9 at 1 and 5 minutes, respectively. Five minutes after baby delivery BP went up to 180/100 mm of Hg and NTG infusion was started. Inj. oxytocin 20 U in IV infusion was started and Inj. prostodin 250 mg IM was given immediately after the baby's delivery. Surprisingly there were no problems of haemostasis and the patient received 1.5 litres of crystalloids. She was reversed with neostigmine (2.5 mg) and glycopyrrolate (0.2) and shifted to ICU for postoperative care. IV tramadol (2 mg/kg) was given for postoperative analgesia. In the first two postoperative days platelets went down to 25 × 109/L and LDH increased to 1592 IU/L. From the 3rd postoperative day platelet counts started improving with a decreasing trend of liver enzymes and LDH. The patient was discharged on 9th postoperative day with normal liver enzymes and platelets and LDH was down to 493 IU/L. There was no evidence of neonatal thrombocytopenia.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [210.0, 'mm hg'], 'Diastolic Blood Pressure': [110.0, 'mm hg']}",143.33333,136.16666,150.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 210.0 mm Hg + 2/3 * 110.0 mm Hg = 143.33333 mm Hg.
Hence, the patient's mean arterial pressure is 143.33333 mm Hg."
1484,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7434231-1,Extracted,"A 36-year-old male who was currently incarcerated presented to the emergency department (ED) with a chief complaint of syncope. The patient reported that the event occurred after he stood up from dinner. There were no witnesses, but the patient believes that he hit his head. He said he had a headache since the fall, and it had not responded to the acetaminophen that he received from the prison infirmary. He denied any tongue biting or loss of bowel or bladder control. The patient stated that he had felt dizzy and lightheaded over the prior few days, and that sensation continued in the ED. He also felt numb across his shoulders and had been nauseous since the fall.
He had a past medical history of seizures and bipolar disorder. His last seizure was several years prior and was described as “whole body shaking.” The patient reported compliance with his medications, which were fluoxetine, phenytoin, ranitidine, and valproic acid. He had no prior surgical history. His family history included diabetes in his grandmother. The patient drank alcohol socially and had used marijuana and abused prescription drugs in the past but had not used any substances recently.
On physical examination, he was awake, alert, and in no acute distress. He was afebrile (36.9° Celsius) with a heart rate of 84 beats per minute, a blood pressure of 116/72 millimeters of mercury, respiration 16 breaths per minutes, and oxygen saturation of 99% while breathing room air. He was 167.6 centimeters (cm) tall and weighed 63.5 kilograms (body mass index of 22.6 kg/m2), and was well nourished and well developed. There was a 2 cm × 2 cm hematoma and an overlying abrasion on his left forehead. Another abrasion on his upper lip was not actively bleeding. His external ears were normal without evidence of trauma. His nose was normal. His oropharynx was clear and moist. His pupils were 3 millimeters (mm) equal, round, and reactive to light and accommodation, and eyes were without scleral icterus. His neck was supple without tracheal deviation. He had normal range of motion of his neck and he had no cervical spinous process or paraspinal muscular tenderness. His heart was regular rate and rhythm without murmurs, rubs, or gallops. He had capillary refill of less than two seconds in all extremities. His lungs were clear to auscultation bilaterally without wheezes, rhonchi, or rales. He had regular respiratory effort without accessory muscle use. His abdomen was soft with normal bowel sounds without tenderness, rebound, or guarding. There was no costovertebral tenderness. His extremities exhibited no edema, tenderness, or deformity, and had 2+ pulses throughout. He had no spinous process or paraspinal process tenderness in his thoracic or lumbar spine.
His cranial nerves (II–XII) were intact. He was found to have bilateral and direction-changing horizontal nystagmus that was provoked on lateral gaze. No vertical or torsional nystagmus was seen. He had 5/5 strength with normal muscle tone throughout his upper and lower extremities bilaterally. He had decreased sensation across his shoulders bilaterally, but the remainder of his sensation was intact. He had slow finger to nose with overshoot bilaterally. His ambulation was limited secondary to feeling unsteady. He was oriented to person, place and time, answered questions appropriately, and followed commands without difficulty.
Initial laboratory results are shown in . His electrocardiogram (ECG) is shown in . He had a chest radiograph (). Computed tomography (CT) of his head and neck were performed (Image 3; full study is found in Supplemental Material 1). A diagnostic test was then performed, which confirmed the diagnosis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [116.0, 'mm hg'], 'Diastolic Blood Pressure': [72.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 116.0 mm Hg + 2/3 * 72.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1485,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6606923-1,Extracted,"Sixty years old male, farmer from Gadarif city, Eastern Sudan, who had a 4 years past history of intestinal obstruction due to sigmoid volvulus for which he underwent laparotomy and detwesting sigmoidopexy followed 6 weeks later by elective sigmoidectomy. He had no significant history till 2 months ago when he presented to the surgical outpatient of Gadarif Teaching Hospital, which is the main community hospital in the state, with a history of abdominal distension, constipation and vomiting for the last 3 days and severe abdominal pain for one day. He also complained of recurrent constipation which he didn’t bother to seek medical advice and used to have over the counter or traditional medications. He was previously healthy with no significant family, drug or social history. On examination he looks ill not pale, jaundiced or febrile. His pulse rate was 104 beat per minute, blood pressure was 110/70, respiratory rate was 22 cycle per minute and his temperature was 38.8 CO. His abdomen was grossly distended with full flanks, midline scar, visible dilated bowl loop and peristalsis. There was tenderness all over the abdomen and no bowl sounds were detected. Digital rectal examination revealed a 3rd degree pile and empty rectum. His investigations showed an Hb of 13 g/dl, WBCs of 14 × 109 per liter and PLTs count of 305 × 109 per liter. His renal profile and serum electrolytes were within normal range. Blood glucose was 193 mg/dl. Urine examination was unremarkable. Abdominal X-ray () showed a typically dilated omega shape colon. The diagnosis of a strangulated bowel obstruction was considered, adhesive type was the top differential. However recurrent or other site volvulus was a remote possibility despite the X-ray findings.
After optimization of his general condition with an NG tube suction and intravenous fluids resuscitation, he went for a laparotomy at the emergency department OR. This was performed by the specialist and residents on duty supervised by the consultant in our team. Under general anesthesia with muscle relaxation a generous midline incision revealed an intact, grossly dilated and apparently gangrenous large bowel that turned out to be the transverse colon (). There was a small amount of inflammatory exudate. The twisted gangrenous colon was carefully delivered (). Because of the high risk situation the decision was to do a Hartmann’s resection of transverse colon. A clearly viable segment was left from hepatic flexure and the healthy upper rectum which was anchored as stump to anterior abdominal wall with a nylon stitches. Abdomen closed in layers and the patient recovered smoothly. The resected colonic segment was 109 cm in length and 22 cm in its maximum diameter (). The patient did well postoperatively with close follow up by the nursing staff and doctors. He stayed for couple of days in the HDU and was discharged home on day 12 after healing of a minor surgical site infection. Six weeks later a colorectal anastomosis was done by our colorectal surgeon and he was discharged on the 7th post-operative day in a good condition. He presented to the refer clinic one month later completely satisfied complaining only of an unusual soft stool and regained his full normal activity. He is planned for regular clinical follow-up which can be augmented with CT or colonoscopy.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1486,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7370690-1,Extracted,"A 50-year-old male who had a past medical history of HIV with unknown cluster of differentiation 4 (CD4) lymphocyte count and not compliant with his medications was brought in by emergency medical services (EMS) after he was found in his room covered in feces and looking disheveled. They brought him to Brookdale University Hospital and Medical Center emergency room. His initial vital signs showed a temperature of 100 ºF, blood pressure of 143/91 mmHg, heart rate of 105 beats per minute, respiratory rate of 20 per minute. He was noticed to have disseminated, vesicular-pustular rash all over his body at different stages of healing and crusted skin eruption on his anterior neck and submandibular area (Figures -).
Patient’s neurological exam revealed that he was alert and oriented to self only, had a right-sided upper and lower facial droop. The patient also had impaired hearing on the right side. The muscle strength was 5/5 throughout. The patient had normal reflexes and the sensation was intact. The remainder of his physical exam did not show any other abnormal findings. Computerized tomography of the head without contrast showed no acute intracranial pathology. Subsequently, the patient had a lumbar puncture done in the emergency room which revealed a cloudy cerebrospinal fluid (CSF) with a white blood cell count of 849 cells/uL with lymphocyte predominance (72%), glucose of 39 mg/dl and protein of 364 mg/dl. Serum electrolytes, liver enzymes, and coagulation profile were all within normal limits. CSF sample was sent for a varicella-zoster polymerase chain reaction (PCR) test as well. His chest X-ray was clear without any infiltrates. His initial laboratory investigations are summarized in Table .
A presumptive diagnosis of disseminated VZV with encephalitis was made according to the patient's skin lesions and CSF analysis. Therefore, he was started on intravenous acyclovir at 10 mg/kg every eight hours and admitted to the general medical floor under contact and airborne precautions. Patient’s varicella zoster PCR from the CSF sample came back positive. Patient mental status improved rapidly within 48 hours of treatment and he became alert and fully oriented. On eye exam, the patient had diplopia with right gaze, and it was determined that he had a right sixth cranial nerve palsy. He had deficits in right sided cranial nerves VI, VII, and VIII evident by impaired right eye abduction, right sided facial weakness, as well as impaired hearing. This constellation of findings is likely secondary to Ramsay Hunt syndrome with multiple cranial nerve involvement. Intravenous acyclovir was continued, and the patient started taking prednisone 50 mg orally for five days for the treatment of Ramsay Hunt syndrome. He was also found to have otitis externa and was prescribed ciprofloxacin with dexamethasone otic drops. Magnetic resonance imaging of the brain without contrast found nonspecific white matter lesions in the high left frontal lobe measuring approximately 8 mm but otherwise no mass, hemorrhage, or acute infarct (Figure ).
The patient’s mental status came back to his baseline on day three. The patient’s rash had crusted on day six hence the isolation precautions were discontinued. He started ambulating without any difficulty and facial paralysis resolved by day eight. He was safely discharged home after nine days of hospital stay with oral acyclovir 400 mg tablets three times daily for 21 days and prednisone 50 mg tablets daily for three days.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [143.0, 'mm hg'], 'Diastolic Blood Pressure': [91.0, 'mm hg']}",108.33333,102.91666,113.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 143.0 mm Hg + 2/3 * 91.0 mm Hg = 108.33333 mm Hg.
Hence, the patient's mean arterial pressure is 108.33333 mm Hg."
1487,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4286908-1,Extracted,"A 38-year-old pregnant Hispanic woman, gravida 4, para 4, with a gestational age of 22 weeks was referred to a tertiary center with complaints of intermittent abdominal pain for the past 3 months, and worsening symptoms over the past 3 to 4 weeks. The nonradiating pain originated in the epigastric region, was of moderate to severe intensity, and worsened upon food ingestion, with no obvious relieving factor. The patient also had nausea with a few intermittent episodes of bilious vomiting; however, she denied any hematemesis, melena, or hematochezia. During routine prenatal care at another hospital, her symptoms were attributed to the underlying pregnancy. She was prescribed ranitidine, which failed to alleviate her symptoms. She denied any past medical problems and was not taking any medications prior to her pregnancy. Her prior pregnancies were full term, normal vaginal deliveries and were uneventful. She denied the use of alcohol, smoking, or illicit drugs.
On examination she was afebrile, with a heart rate of 87 bpm, blood pressure of 123/87 mmHg, and was saturating well on room air. The physical exam was remarkable, indicating a gravid uterus at around 28 weeks' of gestation. She had mild epigastric tenderness and was found to have a tender mass from midline to the left flank. The patient had no pedal edema, and (I think the physical exam should be in a separate sentence from the labs.) laboratory findings revealed normal electrolytes and creatinine; hemoglobin was 11.5 g/dl, and platelets were 277 K/µl. While carcinoembryonic antigen (CEA) and cancer antigen 19-9 (CA 19-9) levels were normal, the cancer antigen 125 (CA 125) was found to be elevated to 846 U/ml. An ultrasound revealed a normal intrauterine pregnancy (), and a left adnexal mass of heterogeneous echodensity of ~13.4 cm in the diameter at its largest side, which was distinct from the uterine mass, displaying characteristics of an ovarian neoplasm (). Magnetic resonance imaging (MRI) was recommended for further evaluation, and confirmed a large pelvic mass arising from the left adnexa, with ascites and demonstrated edema of the mesentery and omentum ().
Physicians from the Maternal Fetal Medicine (high-risk obstetrics) and gynecology oncology departments discussed the findings with the patient and decided to continue the pregnancy while proceeding with surgical staging. However, a few days after admission and prior to the scheduled date for surgery, she had worsening abdominal pain and was found to be in active labor. The patient subsequently delivered a viable infant via vaginal delivery. Gestational age at birth was 23 weeks, with the female infant weighing 510 g and having Apgar scores of 2, 6, 7. There were no fetal anomalies and the infant was admitted to the neonatal intensive care unit for further care. Postpartum, the patient underwent an exploratory laparotomy, which revealed straw colored ascites upon entry and a large mass originating from the left ovary. The neoplasm had ruptured intraoperatively, and only the solid tumor was visible. The left ovary was processed for frozen section investigation, which revealed the presence of a Krukenberg tumor (). Subsequently, an abdominal examination noted that the omentum harbored marked reactive tissue, which indicated metastases, and a tumor was palpated along the lesser curvature of the stomach, which suggested a primary gastric cancer. Palliative gastrectomy was not performed.
Based on the intraoperative exams, an esophagogastroduodenoscopy was performed, which revealed patchy areas of erythema on the non-peristaltic stomach wall, with superficial ulceration along the lesser curvature (). Multiple biopsies were obtained that showed the presence of a poorly differentiated adenocarcinoma. The patient was diagnosed as having stage IV gastric cancer and was scheduled for palliative chemotherapy. She underwent multiple hospital admissions after the advanced-cancer diagnosis for reasons including development of submassive pulmonary embolism, seizures secondary to acute ischemic stroke, and hospital-associated pneumonia. She received 2 cycles of FOLFOX before succumbing to cancer.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [87.0, 'mm hg'], 'Systolic Blood Pressure': [123.0, 'mm hg']}",99,94.05,103.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 123.0 mm Hg + 2/3 * 87.0 mm Hg = 99.0 mm Hg.
Hence, the patient's mean arterial pressure is 99.0 mm Hg."
1488,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3728598-1,Extracted,"An otherwise healthy 46-year-old male engineer, with juvenile myoclonic epilepsy, was admitted to our department following convulsive seizures 1 month after discontinuation of lamotrigine. He was diagnosed with juvenile myoclonic epilepsy at the age of 39 after having 3 generalized convulsive seizures over 3 months. An EEG and brain CT were both normal. He was started on valproic acid 900 mg and was shifted to lamotrigine 200 mg daily 3 years later. After a 5-year period without seizures, lamotrigine was slowly tapered off and the patient completely stopped the intake 1 month before the present admission. He was admitted to hospital with a right-sided hemiparesis with Babinski sign, a right-sided central facial palsy and an ataxic finger-nose test on the left side, which developed following a generalized convulsive seizure 1 day prior to admission. He had no neurological or other complaints up to the seizure. Brain CT was normal, but an MRI scan showed an infarct in the left cerebellar hemisphere (fig. ) and a left-sided pontine infarction (fig. ). Subsequent MR angiography showed a right VAD (fig. ).
In addition, the blood samples for kidney and liver function, haemoglobin and coagulation factors were all in the normal range of reference. However, there was a high leucocyte count with an overabundance of neutrophils. Moreover, the patient's blood pressure at the time of admission was normal (127/87 mm Hg), and he was afebrile. The patient was started on heparin and the oral anticoagulant warfarin, which he continued for 6 months (from January 10 until June 21). The treatment with lamotrigine was also resumed. Recovery of neurologic function was excellent, and he was discharged after 14 days. A control MR angiography 6 months later showed a normal vertebral artery (fig. ). The patient still continued treatment with aspirin and dipyridamole.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [127.0, 'mm hg'], 'Diastolic Blood Pressure': [87.0, 'mm hg']}",100.33333,95.31666,105.35,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 127.0 mm Hg + 2/3 * 87.0 mm Hg = 100.33333 mm Hg.
Hence, the patient's mean arterial pressure is 100.33333 mm Hg."
1489,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6637642-1,Extracted,"This case report describes the case of a 10-year-old boy of Algeria origin living in Ile-de-France. Due to extremely painful thoracic swelling, the boy’s parents brought him in September 2012 to our hospital. This small nodular swelling was apparent from birth and progressively increased in volume. The chest pain appeared when the boy was 10-years old and his parents consulted for a treatment request at the pediatric hospital Robert Debré. The boy failed to receive treatment prior to this. He had never experienced thoracic trauma and he did not possess any known prior medical pathology. He had no risk of exposure to toxins in his environment. Moreover, no similar case was noted in his family and there is no hereditary disease and no consanguinity between parents.
An initial clinical examination showed a well-developed child with no other physical abnormalities. His weight was 41.7 kg, blood pressure 85/140 mmHg, pulse rate 60 pulses/minute, respiratory rate 15 cycles/minute, and temperature 37 °C. His Glasgow Coma Score was 15/15. His cognitive functions were preserved. Sensitivity, motor skills, and osteotendinous reflexes were preserved in his limbs. There was no motor coordination disorder. There was no sphincter deficit. However, a clinical examination revealed a swelling of the right hemithorax (5 cm × 2.5 cm) on the midclavicular line and the fifth intercostal space. His respiratory movements caused the swelling to vary and enlarge with Valsalva maneuvers. Pulmonary and cardiovascular auscultation was normal. We diagnosed a congenital intercostal lung hernia based on the clinical information. A standard X-ray of his chest showed no anomaly for his lungs and thoracic wall (Fig. ). Laboratory findings showed hemogram, blood serum ionogram, serum creatinine, and liver function within normal range. Given the symptoms, we determined a surgical treatment was most appropriate. Two thoracic and vascular specialty pediatric surgeons performed this with a right-sided chest thoracoscopy. Under general anesthesia, our patient was placed in a left lateral position (Fig. ) and a 5 mm camera port was inserted in the sixth intercostal space on the posterior axillary line. Two working ports were also inserted: one in the sixth intercostal space behind the posterior axillary line and the second in the ninth intercostal space on the posterior axillary line.
The camera revealed an intercostal defect consisting of a muscular and aponeurotic aplasia of 4 cm × 2 cm, covered by the parietal pleura (Fig. ). A polytetrafluoroethylene (PTFE) mesh was inserted to close the defect without incising the hernial sac (Fig. ). Two semi-continuous sutures were performed with Mersuture 2/0 (Additional files , , , , , , and ). No complications occurred and a thoracic drain was placed for 48 hours. The repeated clinical and radiographic controls were normal after 1, 3, 6, and 12 months.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 85.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
1490,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-12828,Extracted,"A 55-year-old female is hospitalized following a burn on 60% of her body. She is being treated in the ICU, and her condition remains poor. On rounds one morning, her vitals are as follows: T 38.5 C, HR 100, BP 115/75 mmHg, RR 25. In addition, physical exam shows the findings in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [75.0, 'mm hg'], 'Systolic Blood Pressure': [115.0, 'mm hg']}",88.33333,83.91666,92.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 75.0 mm Hg = 88.33333 mm Hg.
Hence, the patient's mean arterial pressure is 88.33333 mm Hg."
1491,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7080,Extracted,"A 62-year-old man presents to the emergency department for evaluation of a 2-year history of increasing shortness of breath. He also has an occasional nonproductive cough. The symptoms get worse with exertion. The medical history is significant for hypertension and he takes chlorthalidone. He is a smoker with a 40-pack-year smoking history. On physical examination, the patient is afebrile; the vital signs include: blood pressure 125/78 mm Hg, pulse 90/min, and respiratory rate 18/min. The body mass index (BMI) is 31 kg/m2. The oxygen saturation is 94% at rest on room air. A pulmonary examination reveals decreased breath sounds bilaterally, but is otherwise normal with no wheezes or crackles. The remainder of the examination is unremarkable. A chest radiograph shows hyperinflation of both lungs with mildly increased lung markings, but no focal findings.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",93.66667,88.98334,98.35,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 78.0 mm Hg = 93.66667 mm Hg.
Hence, the patient's mean arterial pressure is 93.66667 mm Hg."
1492,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4256,Extracted,"A 37-year-old female with a history of type II diabetes mellitus presents to the emergency department complaining of blood in her urine, left-sided flank pain, nausea, and fever. She also states that she has pain with urination. Vital signs include: temperature is 102 deg F (39.4 deg C), blood pressure is 114/82 mmHg, pulse is 96/min, respirations are 18, and oxygen saturation of 97% on room air. On physical examination, the patient appears uncomfortable and has tenderness on the left flank and left costovertebral angle.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [82.0, 'mm hg'], 'Systolic Blood Pressure': [114.0, 'mm hg']}",92.66667,88.03334,97.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 114.0 mm Hg + 2/3 * 82.0 mm Hg = 92.66667 mm Hg.
Hence, the patient's mean arterial pressure is 92.66667 mm Hg."
1493,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5065333-2,Extracted,"The patient was a 62-year-old man and the husband of case 1. He did not have gastrointestinal or cardiovascular symptoms, alopecia, or desquamation. However, he admitted to having drunk mushroom tea with case 1. On admission, his blood pressure was 133/66 mmHg, heart rate was 66 beats/min, and body temperature was 37.5°C. He was alert with no abnormalities upon physical examination. Initial laboratory results showed a WBC count of 1.75×103/μL, ANC of 820, Hb level of 14.3 g/dL, platelet count of 12×103/μL, CRP level of 2.05 mg/dL, blood urea nitrogen level of 15.0 mg/dL, creatinine level of 0.99 mg/dL, aspartate aminotransferase level of 18 U/L, alanine aminotransferase level of 19 IU/L, and procalcitonin level of 0.07 ng/dL. He was admitted and treated with prophylactic antibiotics and G-CSF. On the fourth day of his admission, his neutropenia was aggravated, without fever. His ANC fell to <10, and his CRP level was 13.33 mg/dL. Under suspicion of concealed infection, prophylactic vancomycin was administered. This treatment was discontinued after cultures showed no growth. His antibody tests and cultures all yielded negative results (similar to case 1). On the twelfth day of his admission, his bicytopenia started to improve. On the eighteenth day of his admission, his complete blood cell count normalized, with a WBC count of 7,380/µL, Hb level of 11.0 g/dL, and platelet count of 30,000. He was subsequently discharged.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [133.0, 'mm hg'], 'Diastolic Blood Pressure': [66.0, 'mm hg']}",88.33333,83.91666,92.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 133.0 mm Hg + 2/3 * 66.0 mm Hg = 88.33333 mm Hg.
Hence, the patient's mean arterial pressure is 88.33333 mm Hg."
1494,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-829,Extracted,"A 6-year-old boy is brought to the physician because of a 2-week history of fever and pain in his right thigh that is causing him to limp. The mother thinks he may have hurt himself during soccer practice. He has no history of rash or joint pain. His older sister has systemic lupus erythematosus. His immunizations are up-to-date. The patient is at the 40th percentile for height and 45th percentile for weight. His temperature is 39°C (102.2°F), pulse is 100/min, respirations are 18/min, and blood pressure is 110/70 mm Hg. Examination shows swelling, tenderness, warmth, and mild erythema over the right upper thigh; range of motion is limited by pain. He has a right-sided antalgic gait. His leukocyte count is 12,300/mm3 and erythrocyte sedimentation rate is 40 mm/h. X-rays of the hips and lower extremities are unremarkable. An MRI of the right lower extremity shows increased T2 and decreased T1 signals over the right femur with periosteal elevation, multiple osteolytic areas in the femoral metaphysis, and bone marrow edema.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1495,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3092083-1,Extracted,"A 30-year-old female was admitted to our hospital with right lower abdominal pain for one day. Her history was unremarkable. On admission, her body temperature was 37℃, her blood pressure was 120/80 mm Hg, and her heart rate was 78 beats/min. A physical examination revealed right lower quadrant pain and tenderness, but no rebound tenderness was detected. Laboratory tests, including a peripheral blood test, a biochemical test and a urinalysis, were all normal, except for the white blood cell count (12,700/mm3). The plain abdomen exhibited no remarkable abnormal findings. Ultrasonography showed a multiseptated cystic mass associated with an intussusception at the cecum. The color Doppler image showed that flow signals at the bowel wall were preserved (). Computed tomography (CT) revealed the same cystic lesion in the cecum and showed a ""bowel within bowel"" configuration, as well as vessels and mesenteric fat within the bowel's lumen ().
An emergency laparotomy was performed, with a diagnosis of intussusception due to cecal lymphangioma. During the operation, we found an ileocolic intussusceptions, and an ilececectomy was performed after manual reduction. Macroscopically, a 9-cm submucosal tumor with fluctuations and with a round, smooth, and broad base was seen in the cecum (). The cystic lesion was filled with focal hemorrhage. Histological examination found that the cyst was located below the normal mucosal membrane and was surrounded by flat endothelial cells (). Immunohistochemstry showed negative for carcinoembrionic antigen (CEA) and positive for factor VIII. The histological diagnosis confirmed a cecal lymphangioma. The patient's postoperative course was uneventful, and she was discharged five days after the operation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1496,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7860969-1,Extracted,"A 14-year-old boy presented to our emergency department with abdominal pain in the epigastric region associated with anorexia, nausea, and vomiting for 24 hours. The patient had no fever or respiratory symptoms. There was no underlying disease. He mentioned a history of contact with his aunt who was suspected of COVID-19. On physical examination, the patient was not ill or toxic and vital signs were normal: RR: 20, PR: 98, BP: 100/65, and T: 36.9°C. The abdomen was soft, nondistended with right lower quadrant and epigastric tenderness.
Laboratory tests revealed elevated amylase (1914, normal <100 μ/l) and lymphopenia, and other blood test results were within normal limits (). Later, a nasopharyngeal swab specimen was collected which tested positive for SARS-CoV-2 on reverse transcriptase-polymerase chain reaction (RT-PCR). Due to the positive SARS-CoV-2 RT-PCR, a chest X-ray () and computed tomography (CT) () were obtained. Abdomen CT was suggestive of pancreatitis ().
The patient was treated with bowel rest, intravenous crystalloid fluid resuscitation, and ondansetron, pantoprazole, and empiric antibiotics including ceftriaxone and metronidazole. The symptoms were resolved gradually within 3 days, and the patient was discharged with decreasing amylase level.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [65.0, 'mm hg'], 'Systolic Blood Pressure': [100.0, 'mm hg']}",76.66667,72.83334,80.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 65.0 mm Hg = 76.66667 mm Hg.
Hence, the patient's mean arterial pressure is 76.66667 mm Hg."
1497,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8055,Extracted,"A 57-year-old woman with a long-standing history of liver cirrhosis presents to her primary care provider with a complaint of unintended weight loss of 8.2 kg (18.0 lb) within the last month. She has a history of intermittent right upper quadrant pain in her abdomen with decreased appetite for a few years and occasional shortness of breath. The past medical history is significant for hepatitis E infection during her first pregnancy when she was 28 years old, and a history of blood transfusion after an accident 25 years ago. She drinks about 2–3 pints of beer every week on average and does not use tobacco. The vital signs include: blood pressure 110/68 mm Hg, pulse rate 82/min, respiratory rate 11/min, and temperature 37.7 °C (99.9°F). The physical exam is normal except for moderate icterus and tender hepatomegaly. The blood tests show mild anemia with decreased iron stores. Serum electrolytes, blood sugar, and renal function are normal. The chest X-ray is normal. An ultrasound of the abdomen revealed a mass in the liver, which was confirmed with a biopsy to be hepatocellular carcinoma.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [68.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",82,77.9,86.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 68.0 mm Hg = 82.0 mm Hg.
Hence, the patient's mean arterial pressure is 82.0 mm Hg."
1498,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9866,Extracted,"A 55-year-old man comes to the emergency department with the complaint of pain in his right toe for the past hour. The pain is so severe that it woke him up. The patient has smoked a pack of cigarettes daily for the last 40 years and binge drinks alcohol after work and on the weekends. He underwent an appendectomy when he was 14 years old. He is a long-distance truck driver. Neither of his parents had any significant medical history. His temperature is 37.7°C (100°F), blood pressure is 135/75 mm Hg, pulse is 102/min, respiratory rate is 20/min, and BMI is 25 kg/m2. On examination, his right first metatarsophalangeal joint is very tender, swollen, warm, and red in color. Range of motion cannot be assessed due to extreme tenderness.
Laboratory test
Complete blood count:
Hemoglobin 11.5 g/dL
Leukocytes 16,000/mm3
Platelets 150,000/mm3
ESR 50 mm/hr
Synovial fluid is aspirated from the joint. The findings are:
Appearance Cloudy, dense yellow
WBC 30,000 cells/µL
Culture Negative
Needle-shaped birefringent crystals are observed in the joint aspirate.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [135.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",95,90.25,99.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 75.0 mm Hg = 95.0 mm Hg.
Hence, the patient's mean arterial pressure is 95.0 mm Hg."
1499,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7021241-1,Extracted,"A 23-year-old female presented to the emergency department (ED) with two days of acutely worsening bilateral blurry vision in the setting of a constant low-grade bitemporal and occipital headache different from her usual headache. She reported nausea and vomiting for the past month and seeing ""bright spots"" for two weeks. She also reported decreased appetite, night sweats, dyspnea on exertion, palpitations, and anxiety over the past month and a half. Review of system was negative for fever, chills, neck pain, head trauma, diplopia, or sudden onset of headache. Her past medical history included tension headache and anxiety. Her surgical history included appendectomy, tonsillectomy, and wisdom tooth extraction. Medications included citalopram, aspirin-acetaminophen-caffeine, ibuprofen, and levonorgestrel-ethinyl estradiol.
On arrival to the ED, the patient’s vital signs were blood pressure 161/86 mm Hg, pulse rate 114 beats/min, respiratory rate 20 breaths/min, temperature 36.8oC (98.3oF), and SaO2 95% on room air. On exam, the patient was anxious but alert and oriented with an otherwise unremarkable neurological exam. Her head and neck exam were notable for a supple neck without adenopathy and moist mucous membranes. Her cardiovascular exam was notable for tachycardia and a systolic 2/6 murmur. The patient’s ocular examination was notable for visual acuity of 20/90 in the right eye and 20/50 in the left eye, with intraocular pressures 13 and 12 mmHg, respectively. Pupils were equal and reactive without an afferent pupillary defect, and extraocular movement, confrontational visual fields, and anterior slit-lamp examination were normal. Her fundus examination, performed by an ophthalmologist, demonstrated bilateral diffuse intraretinal hemorrhages in all quadrants, white-centered retinal hemorrhage and dilated and tortuous retinal vessels without disc edema, concerning for bilateral CRVO. The reminder of her exam was unremarkable.
Laboratory testing disclosed numerous chemical and serologic abnormalities with concerning findings for hyperviscosity syndrome secondary to leukocytosis (see Table for details). Infectious workup for human immunodeficiency virus, hepatitis B, and hepatitis C was negative. Urine pregnancy test was negative. Chest radiograph (Figure ) demonstrated a widening of the mediastinal silhouette with a non-contrast computed tomography (CT) of the chest demonstrating a lobulated anterior mediastinal soft tissue mass concerning for lymphoma and splenomegaly (Figure ). Her brain CT was negative for intracranial hemorrhage or mass effect.
The patient was diagnosed with bilateral CRVO and leukemic retinopathy with serologic and radiographic testing consistent with ALL with blast crisis, characterized by an increased number of blast cells (immature blood cells). She was admitted to the oncology service where her hospitalization stay was complicated by tumor lysis syndrome, peripherally inserted central catheter line related deep vein thrombosis, hyperglycemia secondary to aggressive steroid therapy, and transient hypotension of unclear etiology with a negative infectious workup. Her bone marrow biopsy showed T-cell acute lymphoblastic leukemia (T-ALL) with >90% marrow involved with three signals for the ABL1 gene. She was initially managed with intravenous fluids, hydroxyurea, and dexamethasone, and started treatment for T-ALL with induction chemotherapy. She was discharged after 18 days of hospitalization with prophylactic acyclovir, sulfamethoxazole/trimethoprim, and prednisone as part of her chemotherapy regimen and outpatient retina clinic follow -up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [161.0, 'mm hg'], 'Diastolic Blood Pressure': [86.0, 'mm hg']}",111,105.45,116.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 161.0 mm Hg + 2/3 * 86.0 mm Hg = 111.0 mm Hg.
Hence, the patient's mean arterial pressure is 111.0 mm Hg."
1500,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5857481-1,Extracted,"A 58-year old homeless male was found unresponsive in a parking lot and was taken by ambulance to our emergency department (ED). The patient was minimally responsive and able to state only his name; no additional history could be obtained. Initial vital signs in the ED demonstrated a temperature of 37.1 °C, heart rate of 157 beats per minute, respiratory rate of 35 per minute, oxygen saturation of 78% while breathing 15 l of oxygen per minute via face mask, and blood pressure of 80/49 mmHg. On examination, he was ill appearing, icteric, and in respiratory distress. The patient had tachycardia, but no cardiac murmurs. Rales were heard at both lung bases. The entire right lower extremity was erythematous and there was extensive necrosis of the soft tissues extending from the hindfoot to the proximal thigh.
Pertinent laboratory studies on initial presentation revealed a white blood cell count of 19.2 × 103 cells/µm3, platelets of 19 × 103 cells/µm3, bicarbonate of 21 mEq/L, blood urea nitrogen of 67 mg/dL, creatinine of 1.23 g/dL, random glucose of 120 mg/dL, total bilirubin of 10.3 mg/dL, direct bilirubin of 6.1 mg/dL, alanine transaminase of 66 U/L, aspartate transaminase of 116 U/L, albumin of 1.4 g/dL, prothrombin time of 34, international normalized ratio of 3.3, partial thromboplastin time of 47 U/L, creatine phosphokinase of 851 U/L, and lactate of 3.3 mg/dL. A portable chest radiograph (CXR) showed patchy bibasilar infiltrates. Computed tomography (CT) of the chest revealed bilateral ground-glass opacities and infiltrates that were more extensive in the right lung (A).
The patient was treated with aggressive intravenous (IV) fluid hydration and vasopressors (norepinephrine, vasopressin, and epinephrine) for septic shock. He underwent tracheal intubation for acute hypoxic respiratory failure. The patient received empiric antibiotic treatment with IV vancomycin, piperacillin-tazobactam, and clindamycin. The patient was taken to the operating room where a right above-the-knee amputation was performed for his necrotizing soft tissue infection on day 0.
The patient's postoperative course was complicated by refractory septic shock requiring multiple vasopressors, acute anuric renal failure necessitating hemodialysis, bilateral chest tube drainage of pleural effusions, worsening liver failure, and progressive hypoxia requiring mechanical ventilation. On day+ 2, the patient underwent surgical disarticulation of his right hip to remove residual necrotic infected tissue. The intraoperative wound cultures grew methicillin-sensitive Staphylococcus aureus and Proteus penneri. On day+ 4, 1/4 bottles of the blood cultures grew Aerococcus species and Staphylococcus epidermidis. All four organisms were sensitive to vancomycin and/or piperacillin-tazobactam. No fungal organisms were seen on histopathological analysis of infected tissue and none were isolated from the cultured material.
The patient continued to deteriorate after surgery. On day+ 10, given the continued refractory septic shock and bibasilar patchy infiltrates seen on CXR, a bronchoalveolar lavage (BAL) was performed, and thick frothy respiratory secretions with pus were seen. Gram stain and bacterial culture of the BAL specimen were negative, and Xpert® MTB/RIF (Cepheid, Sunnyvale, CA) PCR of the sputum was negative for tuberculosis. Cytopathology was not performed.
On day+ 12, an infectious diseases consultation was obtained. On initial evaluation, it was noted that the patient had a positive serum 1,3 β-D glucan (> 500, normal < 60). Empiric antifungal treatment with IV micafungin was initiated. Serum galactomannan, cryptococcal antigen, and coccidiomycosis complement fixation tests were negative, as was the urine histoplasma antigen test. On day+ 16, a repeat CT scan of the chest revealed worsening of right lung patchy infiltrates (B). A repeat BAL was performed on day+ 18, and thick frothy respiratory secretions were again seen. A bronchoscopic biopsy was not performed because of the patient's coagulopathy and thrombocytopenia. Nonseptate hyphae were seen on cytologic analysis of the repeat BAL specimen (). The Aspergillus galactomannan assay of the BAL fluid was also positive (6.78, normal < 0.5), and IV voriconazole was initiated on day+ 19. A rapidly growing mold grew in cultures of both the BAL sample and a swab from the right chest tube site; the specimens were sent to an outside reference laboratory for identification.
The patient continued to deteriorate. On day+ 21, when the total bilirubin increased to 23.5 mg/dL, the micafungin and voriconazole were discontinued and IV L-AmB (5 mg/kg daily) was initiated. On day+ 23, a CT scan of the chest showed worsening of the infiltrates in the right lung (C). In addition, a second mold grew in BAL fungal culture. This mold had septate hyphae and conidia, but was not sent for identification. The patient expired on day+ 25. Four days later, the rapidly growing mold from the BAL and right chest tube insertion site was identified as R. arrhizus, indicating the presence of invasive pulmonary mucormycosis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [80.0, 'mm hg'], 'Diastolic Blood Pressure': [49.0, 'mm hg']}",59.33333,56.36666,62.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 80.0 mm Hg + 2/3 * 49.0 mm Hg = 59.33333 mm Hg.
Hence, the patient's mean arterial pressure is 59.33333 mm Hg."
1501,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7729390-3,Extracted,"A 21-year-old male with a past medical history of type 1 diabetes mellitus presented to the ED with weakness, fevers, cough, and pleuritic chest pain as well as elevated blood glucose readings noted at home. On admission, his temperature was 100.2 degrees Fahrenheit, blood pressure of 135/97 mm Hg, heart rate of 131 bpm, respiratory rate of 30 bpm, and oxygen saturation of 95% breathing room air. Complete blood count on admission showed elevated white blood cells of 27,900/mcL. The basic metabolic panel showed a blood glucose of 408 mg/dL, an elevated anion gap, and serum bicarbonate of 10 mmol/L. He was diagnosed with diabetic ketoacidosis and treated with insulin drip and intravenous fluids. Chest X-ray () showed bilateral perihilar infiltrates; antibiotic therapy with ceftriaxone was started. For concerns of SARS-CoV-2 pneumonia, he was started on hydroxychloroquine. He improved within 24 hours and was discharged home 2 days later. After discharge, diagnostics revealed SARS-CoV-2 positivity and blood cultures growing Streptococcus pneumoniae. Our patient was called back to return to the hospital for the treatment of bacteremia and COVID-19 pneumonia. Ceftriaxone was resumed, and vancomycin was added while awaiting sensitivities. Hydroxychloroquine was continued to complete a 5-day course. He remained afebrile and hemodynamically stable throughout the hospital course of 4 days. He did not require supplemental oxygen therapy. After confirming, repeated blood cultures were negative; he was discharged home on oral penicillin treatment.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [135.0, 'mm hg'], 'Diastolic Blood Pressure': [97.0, 'mm hg']}",109.66667,104.18334,115.15,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 97.0 mm Hg = 109.66667 mm Hg.
Hence, the patient's mean arterial pressure is 109.66667 mm Hg."
1502,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-2042,Extracted,"A 48-year-old man comes to the physician because of a 2-day history of an itchy rash. He has no history of skin problems. He had an upper respiratory infection 4 days ago that resolved with acetaminophen and over-the-counter cold medication. He has type I diabetes mellitus well-controlled with insulin. He was also diagnosed with hypertension 3 weeks ago and treatment with captopril was initiated. His temperature is 36.8°C (98.2°F), pulse is 68/min, respirations are 18/min, and blood pressure is 120/85 mm Hg. Examination shows rashes at the waistline, trunk, and over the forearms. A photograph of the right forearm is shown. The rashes are nontender and blanch on pressure. There is no lymphadenopathy or hepatosplenomegaly.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [85.0, 'mm hg'], 'Systolic Blood Pressure': [120.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 85.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1503,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3772271-1,Extracted,"A 13-year-old girl was presented with flushing and swelling on her hands and feet, sweating and critical headache for one year. On her medical history; she had previously been admitted for similar complaints and underwent surgery. Right adrenalectomy was made seven years ago and pathology result was pheochromocytoma. She had been discharged with a cure and a recommendation of interval follow-ups. But, the patient did not attend any follow-up visits nor receive any treatments over the last seven years. She started to complain of similar symptoms again since last year. On physical examination; she had cyanosis and edema on both hands and feet. The patient's blood pressure was 215/165 mm Hg, and her pulse rate was 137 beats per minute. Biochemical and radiological examinations were performed to determine recurrent pheochromocytoma. Urinary and plasma catecholamine levels were high. Urinary normetanephrine level was 30084 µg/24 h (reference values are 63-402 µg/24 h), urinary metanephrine level was 1452 µg/24 h (reference values are 32-167 µg/24 h), plasma noradrenalin level was 17540 pg/mL (reference values are 0-400 pg/mL). Contrast enhanced abdominal MRI was performed with a large mass within the left adrenal gland, measuring 65 × 50 mm in size. It was hypointense on T1-weighted and heterogeneous hyperintense on T2-weighted image with intense enhancement on post-contrast images (), suggesting residue or recurrence of the adrenal pheochromocytoma. Cranial MRI was performed because of serious headaches. T2-weighted and fluid attenuated inversion recovery (FLAIR) images showed abnormal hyperintense signals on bilateral caudate, lentiform nuclei, dentate nuclei and periventricular and deep white matter (). Furthermore, there were two hematomas; a chronic hematoma with peripheral hemosiderin rim on the right external capsule measuring 3 × 1 cm in size and a subacute hematoma on the right globus pallidus measuring 1 cm in diameter (). There was increased diffusion in the lesions consistent with the vasogenic edema. These findings were consistent with severe PRES for the involvement of periventricular and deep white matter and deep gray matter as well as parenchymal hematomas.
On the tenth day of anti-hypertensive therapy, we obtained follow-up cranial MRI with additional SWI sequence. There was remarkable regression of vasogenic edema with near completed resolution of T2 high signal intensities on periventricular and deep white matter, and complete loss of edema on caudate, lentiform, and dentate nuclei (). On SWI, many millimetric foci of hypointensity suggesting micro hemorrhages were observed on bilateral basal ganglia, periventricular white matter and brain stem (). These microhemorrhagic foci were not detectable on conventional MRI. Reversible high signal intensities supported that this condition was PRES secondary to hypertension. SWI sequence revealed many micro and macro hemorrhagic foci of hypertensive encephalopathy as a complication of untreated chronic hypertension.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [215.0, 'mm hg'], 'Diastolic Blood Pressure': [165.0, 'mm hg']}",181.66667,172.58334,190.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 215.0 mm Hg + 2/3 * 165.0 mm Hg = 181.66667 mm Hg.
Hence, the patient's mean arterial pressure is 181.66667 mm Hg."
1504,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7005,Extracted,"A 23-year-old woman visits her general practitioner with left ear pain and fever. She complains of multiple episodes of respiratory infection including bronchitis, laryngitis, and sinusitis. She was diagnosed with systemic lupus erythematosus with nephritis 8 months ago and was placed on oral prednisone. Currently, she takes prednisone daily. Her vital signs are as follows: blood pressure 130/85 mm Hg, heart rate 79/min, respiratory rate 16/min, and temperature 37.5°C (99.5°F). Her weight is 78 kg (172 lb) and height is 169 cm (5 ft 6 in). Physical examination reveals a swollen erythematous left eardrum, erythematous macular rash over sun-exposed skin, and slight calf edema.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [85.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 85.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1505,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5583761-1,Extracted,"A 21-year-old Sri Lankan male developed urticaria and difficulty in breathing one hour after ingestion of prawns, for which he was known to be allergic. He got admitted to the local hospital 2 h after the onset of symptoms. On admission to the local hospital he was dyspnoeic with a respiratory rate of 28/min and widespread rhonchi. His pulse rate was 94 beats per minute and the blood pressure was 100/70 mmHg. He was treated with intravenous hydrocortisone 200 mg, intravenous chlorpheniramine 10 mg and 0.5 ml of adrenaline (1:1000 solution) intramuscularly to the upper lateral side of the thigh (vastus lateralis). Ten minutes after the administration of adrenalin, he developed palpitations and tightening type central chest pain with autonomic symptoms. The pain lasted for about 30 min and resolved spontaneously. The first electrocardiogram (ECG), which was taken at the local hospital showed a sinus tachycardia and ST segment depressions in leads III, aVF and V1 to V5(Fig. ). He was not given any treatment for the chest pain in the local hospital and was transferred to our hospital about 2 h from the onset of the pain.
On admission to our hospital, he was not dyspnoeic and his pulse rate was 100 beats per minute and the blood pressure was 100/60 mmHg. His respiratory rate was 18/min and had a few rhonchi on auscultation. Rest of the examination was normal. The second ECG which was done in our hospital, 2 h after the 1st one, showed resolution of ST segment depressions but new T inversions in leads I and aVL (Fig. ). These T in versions persisted in subsequent ECGs (Fig. ). Troponin I done 6 h after the event was positive with a titer 2.15 ng/ml (<0.5). The test was repeated on the second day and it was still positive with a tire of 0.69 ng/ml. He was given sublingual glyceryl trinitrate 0.4 mg single dose after admission to our hospital. However antiplatelets and statins were not given and anticoagulation was not started as the most likely cause was assumed to be coronary vasospasm rather than plaque rupture.
He was previously healthy and did not have any risk factors for premature coronary vascular disease such as smoking. He has had a history urticaria to prawns but there was no previous history of anaphylaxis. He did not have asthma. There was no family history of diabetes, ischemic heart disease or premature deaths due to cardiovascular diseases. He worked as a computer operator trainee and was unmarried.
Further investigations which were done at our unit included transthoracic 2D echocardiogram which revealed an ejection fraction of 60% with no wall motion abnormalities. We did not proceed with a coronary angiogram as the patient was a young healthy adult and the cardiology team concluded that coronary artery vasospasm to be the likely cause for the myocardial ischaemia rather than atherosclerotic coronary artery disease. Subsequent stress ECG with treadmill was normal and CT coronary angiogram revealed normal coronary arteries (Fig. ). Complete blood count and renal functions were normal. Chest x ray was also normal. Fasting blood sugar was 98 mg/dl and the lipid profile was normal.
Patient was asymptomatic during the hospital stay and was discharged after 2 days. At subsequent reviews he remained asymptomatic.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [100.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 70.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1506,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3427827-1,Extracted,"A 76-yr-old man was admitted for the chief complaint of general weakness, cough, and sputum. He had a 7-yr history of middle cerebral artery infarct, which was first diagnosed in 2003. Initial vital signs were as follows: blood pressure, 111/69 mmHg; pulse rate, 87/min; respiratory rate, 21/min; and body temperature, 37.2℃. Initial laboratory test results were as follows: Hb, 15.0 g/dL; white blood cell count, 9.9×109/L (neutrophils, 79.1%; lymphocytes, 13.2%; monocytes, 4.5%; eosinophils, 2.9%; and basophils, 0.3%); and platelets, 180×109/L. Liver function test results and creatinine and glucose levels were within reference interval. His C-reactive protein level was elevated to 17.0 mg/dL; the culture of respiratory specimen indicated Klebsiella pneumoniae. No aerobic or anaerobic bacteria were isolated at initial blood culture. It was suspected the patient had aspiration pneumonia. Treatment with tazocin and levofloxacin was empirically initiated.
Two weeks later, bronchoscopic examination was performed and methicillin-resistant Staphylococcus aureus was isolated. The patient developed a fever and the previously administered antibiotics were replaced with vancomycin, meropenem, and sulfamethoxazole/trimethoprim. Three weeks after admission, blood culture yielded growth of Gram-positive and rod-shaped bacteria, without obvious spore formation, grown in an anaerobic bottle. The isolate was subcultured on a blood plate anaerobically and aerobically. Two days later, gray-white, smooth, and non-hemolytic colonies of unequal sizes were observed only on the anaerobic blood plate (). Gram staining of a purified colony indicated the presence of Gram-positive and rod-shaped bacteria with ovoid-shaped spores located sub-terminally (). Using API 20 A (bioMérieux, Marcy l'Etoile, France), the isolate was found to be positive for catalase and for acid production from glucose, lactose, saccharose, maltose, xylose, arabinose, and mannitol. It was negative for urease and indole formation, and for acid production from sorbitol. The isolate was identified as Clostridium beijerinckii/butyricum (91.6%). An antimicrobial susceptibility test of the isolate was not performed. Although the patient was treated with several antibiotics and no organisms were grown from follow-up blood culture, fever and respiratory failure developed. The patient died 2 months after admission.
We performed 16S rRNA sequencing. Bacterial suspension was centrifuged at 13,000 rpm for 5 min and added to 200 µL of InstaGene Matrix (Bio-Rad laboratories, Hercules, CA, USA), followed by incubation at 100℃ for 15 min. After centrifugation, the supernatant was utilized for PCR. The amplification reaction mixture consisted of 2.5 µL of 10× buffer, 2 µL of 2.5 mM dNTP, 0.6 units of Taq polymerase (Takara Bio, Shiga, Japan), 10 pmol of each primer, and 2.5 µL of template. Cycling parameters were as follows: 10 min of initial denaturation at 95℃; 35 cycles of 30 sec at 95℃ (denaturation), 30 sec at 60℃ (annealing), 45 sec at 72℃ (extension); and a final 10 min extension at 72℃. The PCR product was treated with ExoSAP-IT reagent (USB Corporation, Cleveland, OH, USA) according to the manufacturer's instructions. Sequencing reaction was performed using BigDye Terminator v3.1 Cycle Sequencing kit (Applied Biosystems, Foster City, CA, USA). The sequence was analyzed using MicroSeq ID 16S rRNA Library v2.0 (Applied Biosystems), GenBank Basic Local Alignment Search Tool (BLAST) (), and EzTaxon database v2.1 () [-].
We obtained a consensus sequence of 475 bp. Using MicroSeq ID 16S rRNA Library v2.0 (Applied Biosystems) the isolate was assigned to Clostridium coccoides (95.38%), Ruminococcusproductus (95.27%), Eubacteriumcontortum (94.89%), Clostridium saccharolyticum (93.15%), and Clostridium symbiosum (92.50%). The 16S rRNA sequence of R. peoriensis was not included in the MicroSeq ID 16S rRNA Library v2.0 (Applied Biosystems). With GenBank BLAST, the isolate showed 99.79% similarity with R. peoriensis strain 0910-06083 and 99.58% similarity with R. peoriensis strain HGUE-09/9434. Blautia producta, Eubacterium contortum, and Eubacterium fissicatena were the next closest matches with similarities of 95.20%, 94.78%, and 94.78%, respectively. When the sequence was submitted to EzTaxon database v2.1, we found the highest similarity with R. peoriensis (99.16%). Clostridium nexile, Eubacterium contortum, Blautia luti, and Clostridium oroticum were the next closest matches, with similarities of 95.72%, 95.48%, 95.39%, and 95.15%, respectively.
A phylogenetic tree based on the 16S rRNA sequences of the isolate and 31 organisms with similarity to the isolate was constructed using the neighbor-joining method (). Phylogenetic and molecular evolutionary analyses were conducted using Molecular Evolutionary Genetics Analysis (MEGA) software version 4.0 () []. It showed a subline closely related to Clostridium and Eubacterium spp.
We further amplified the nearly full 16S rRNA sequence with 3 different primer sets and obtained a consensus sequence of 1,415 bp. The 3 different primer sets used for full 16S rRNA gene sequencing were as follows: MSQ-1 (F: 5'-GAAGAGTTTGATCATGGCTCAG-3'; R: 5'-ACCGCGGCTGCTGGCAC-3'); MSQ-2 (F: 5'-GGGGAATATTGCACAATGG-3'; R: 5'-TCGCGTTGCATCGAATTAAA-3'); and MSQ-3 (F: 5'-GTAGTCCACGCCGTAAA-3'; R: 5'-TGTGTGAGCACTGCAAAGTA-3'). Using MicroSeq ID 16S rRNA Library v2.0 (Applied Biosystems) the isolate was assigned to Ruminococcus productus (94.17%) and Clostridium saccharolyticum (94.06%). The 16S rRNA sequence of R. peoriensis was not included in the MicroSeq ID 16S rRNA Library v2.0 (Applied Biosystems). With GenBank BLAST, the isolate showed 99.50% similarity with R. peoriensis and Clostridium oroticum (94.38%) was the next closest match. When the sequence was submitted to EzTaxon database v2.1, we found the highest similarity with R.peoriensis (98.87%), whilst Clostridium nexile was the next closest match with a similarity of 94.70%.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [111.0, 'mm hg'], 'Diastolic Blood Pressure': [69.0, 'mm hg']}",83,78.85,87.15,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 111.0 mm Hg + 2/3 * 69.0 mm Hg = 83.0 mm Hg.
Hence, the patient's mean arterial pressure is 83.0 mm Hg."
1507,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6586111-1,Extracted,"A 62-year-old male presented with nausea, vomiting, and hiccups for two days. He mentioned that he first started feeling nauseous and has since vomited three times. Vomitus was nonbilious, non-bloody, and was followed by continuous hiccups. On further questioning, he said that he has episodic hiccups for the last two years, but it has recently got worse and has started interfering with his sleep and daily activities. He denied abdominal pain, fever, chest pain, cough, dysphagia, reflux, shortness of breath, headache, dizziness, problem with hearing or vision, swelling of legs, or weight change. He endorses being pre-hypertensive 20 years ago but has not followed his primary care physician regularly and did not know his baseline blood pressure. The patient denied having any other medical conditions in the past and has not been using any medications on a regular basis.
On presentation, His blood pressure was 191/101. On initial examination, the patient looked distressed due to ongoing hiccups. Physical examination including chest, abdomen, head, neck, ear, throat and complete neurological examinations were normal.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [191.0, 'mm hg'], 'Diastolic Blood Pressure': [101.0, 'mm hg']}",131,124.45,137.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 191.0 mm Hg + 2/3 * 101.0 mm Hg = 131.0 mm Hg.
Hence, the patient's mean arterial pressure is 131.0 mm Hg."
1508,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8242277-1,Extracted,"A 17-year-old male student has presented to our emergency with complaints of bilateral loin pain and fever for 10 days. There was no urine output for the last 2 days. There was no significant past, personal, family or genetic history. There was no history of COVID-19 infection or any related symptoms. On examination, patient was sick-looking, pulse was feeble and tachycardic. Blood pressure was 90/60 mm of Hg. On abdominal examination bilateral renal angle tenderness was observed. Patient was resuscitated and investigated further. A Doppler ultrasound of the abdomen revealed bilateral enlarged kidneys with absent blood flow in the renal vasculature. His hemoglobin was 9.1gm/dl, and leukocyte count was 36,000cells/mm3. The serum creatinine was 6.5 gm/dl, and serum potassium was 5.8 mEq/L. Arterial blood gas analysis showed metabolic acidosis, for which sodium bicarbonate correction was given. After resuscitation and inotropic support a provisional diagnosis of bilateral acute pyelonephritis with acute kidney injury and renal artery thrombosis was made. Blood cultures were sent. Due to anuria, urine specimen was not available. Dialysis was done, and patient was started on intravenous ceftriaxone and clindamycin antibiotics. Patient was investigated for thrombophilia, and the results of which were normal. Sickle cell test was negative. Immunodeficiency screening was negative. Blood culture was sterile after 72 h of incubation. Chest X-ray was normal.
The patient did not improve clinically, so it was decided to further investigate the etiology on the third day of admission. Under high-risk consent and peri-procedural dialysis support, contrast-enhanced computed tomography (CECT) was performed. CECT revealed bilateral enlarged kidneys with bilateral renal artery thrombosis with global renal infarcts and mild ascitis (Figs. and ). CT-guided renal biopsy was performed in the same sitting which revealed fungal hyphae in the background of necrotic glomeruli (Fig. ). Bronchoalveolar lavage specimen did not reveal any fungal hyphae. Patient was started on liposomal amphotericin B with renal replacement therapy. However, patient deteriorated and succumbed to sepsis on the 4th day of admission.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [60.0, 'mm hg'], 'Systolic Blood Pressure': [90.0, 'mm hg']}",70,66.5,73.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 60.0 mm Hg = 70.0 mm Hg.
Hence, the patient's mean arterial pressure is 70.0 mm Hg."
1509,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7479646-1,Extracted,"A 36-year-old male presented to the emergency room (ER) for not having a bowel movement, abdominal distension, decreased appetite and increased lethargy for 3 days. Patient is nonverbal, so majority of the history was obtained from his caretaker. He reported a past medical history of severe autism. Vitals were temperature 98.8 F, blood pressure 127/88 mmHg, heart rate 125 beats per minute, respiratory rate 24 breaths per minute and oxygen saturation 94%. On physical examination patient appeared somnolent with a distended abdomen, decreased bowel sounds and mild diffuse tenderness on palpation. Laboratory results were significant for white blood count (WBC) 25.8 U/L, hemoglobin (Hg) 12.3 g/dL, platelet 370 × 103 U/L, blood urea nitrogen (BUN)/creatinine 14/0.5 mg/dL, aspartate aminotransferase (AST) 13 U/L, alanine aminotransferase (ALT) 12 U/L, alkaline phosphatase 121 U/L, lipase 25 U/L and lactic acid 4.64 mmol/L. Computed tomography (CT) scan demonstrated marked distension of the cecum and a colonic loop in the right upper abdomen due to a volvulus possibly in the ascending colon and is unable to visualize the transverse and proximal descending colon and a foreign body within the stomach (A–C). Patient was taken for an emergent exploratory laparotomy; however prior to the procedure, he underwent an esophagogastroduodenoscopy (EGD). A foreign body was found in the stomach, but it was too large to be extracted on EGD. Examination of the abdominal cavity intraoperatively revealed a dilated colon (15 cm), a large section of volvulized colon in the right upper quadrant and a segment of volvulus in the distal transverse colon. Patient underwent an extended right hemicolectomy with anastomosis of the terminal ileum to the transverse colon at the level of the splenic flexure. He also underwent a gastrotomy to remove the foreign body, which appeared to be rolled up tar paper. He was started on empiric antibiotic regimen of vancomycin, ciprofloxacin and metronidazole for 2 days. His antibiotics were de-escalated to ceftriaxone and metronidazole and continued for an additional 5 days. Patient had a nasogastric tube placed following the procedure which continued to drain bilious material for 3 days before it was removed. His diet was advanced as tolerated. He was safely discharged to his group home, and no complications were noted at patient’s 2-week follow-up with general surgery.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [127.0, 'mm hg'], 'Diastolic Blood Pressure': [88.0, 'mm hg']}",101,95.95,106.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 127.0 mm Hg + 2/3 * 88.0 mm Hg = 101.0 mm Hg.
Hence, the patient's mean arterial pressure is 101.0 mm Hg."
1510,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3542890-1,Extracted,"A 58-year-old male presents to the Emergency Department via EMS as a possible stroke. Per spouse, he woke up from sleep with left-sided facial droop, slurred speech, and left arm weakness. He had gone to sleep at approximately 10 pm and awoke with the left-sided complaints at approximately 4 am the morning of arrival. He had a past medical history of adrenal adenoma, chronic gastritis, and a vasectomy in 1993. The patient's medications prior to admission were alprazolam, esomeprazole, probiotics, and a daily multivitamin. The patient is aware of his left-sided weakness and complains of heaviness on his left side. He reports no history of alcohol, tobacco, or illicit drug use. The patient's spouse reported that he had been unwell for three months with unexplained weight loss, fever, chills, and loss of appetite. At the time of presentation, various specialists including gastroenterology failed to determine an underlying cause for the patient's complaints besides “anemia of chronic disease.” Furthermore, he was scheduled for an upper and lower endoscopy the day of presentation and was in the process of preparation (cathartics) for that. He has been on a gluten-free diet for elevated tissue transglutaminase and gliadin antibody titers by his endocrinologist. Upon arrival at patient's residence, EMS reported a positive stroke screen with a Cincinnati score of 2, positive for left arm weakness, and left-sided facial droop. Vital signs upon arrival to the Emergency Department were temperature 36.4 degrees Celsius by tympanic reading, pulse 105 beats per minute, blood pressure 116/56 mmHg, respirations 18 breaths per minute, and pulse oximetry 98% on room air. His weight was recorded as 68 kilograms. He was not in any distress but appeared pale and cachectic. His neurologic exam was positive for a left facial droop with weakness of cranial nerves 3, 5, and 7. There was no uvular deviation, and pupils were equal and reactive bilaterally with intact extraocular movements. The upper extremities had symmetric sensation to fine touch with a left pronator drift and 3/5 strength in the proximal and distal muscle groups in comparison to the right. There was no dysmetria. The lower extremities had 5/5 strength bilaterally and absent Babinski reflexes. His NIH stroke scale score was 6. The rest of his physical exam was unremarkable.
Initial labs included a metabolic panel with measured sodium of 131 mmol/L and blood glucose of 125 mg/dL but were otherwise normal. The complete blood count showed a hemoglobin of 9.6 g/dL and a hematocrit of 29.9%. The white blood cell count was 12.5 thou/cu mm with 78.8% neutrophils and no bands. Cardiac enzymes and urinalysis were both normal. The point-of-care INR was 1.5. Stroke alert protocol imaging included a CT angiogram of the head and neck with and without contrast and postprocedure multiplanar reconstructions. These revealed acute/subacute CVA in the right insula cortex and right basal ganglia () as well as significant narrowing of the proximal M1 branch of the right middle cerebral artery (MCA) secondary to either embolus or atherosclerotic disease (). Perfusion images demonstrate elevated time to peak in the posterior right MCA distribution with normal capillary transit time and normal cerebral blood volume consistent with compensated collateral blood flow ().
The patient received 300 mg aspirin per rectum and IV fluids prior to admission to the neuro-ICU. The patient was deemed an unsuitable candidate for thrombolysis as onset was estimated approximately 6 hours prior to ED arrival. Neurosurgery was consulted and decided that the risks of endovascular therapy did not outweigh the benefits for the patient.
Followup the next day revealed that the patient had an echocardiogram that showed a mass on the posterior leaflet of the mitral valve with mitral regurgitation. Following echocardiogram, the patient had an acute sudden deterioration in his mental status and displayed respiratory compromise. On examination, his pupils were “blown” (enlarged) bilaterally and he was emergently intubated for airway protection. His emergent noncontrast CT of the head () showed a subcortical hemorrhage with intraventricular extension and subfalcine herniation. Neurosurgery emergently brought the patient to the operating room with a postoperative diagnosis of right intracranial hemorrhage secondary to ruptured mycotic MCA aneurysm. On postoperative day one, the family decided to withdraw care and the patient expired.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [116.0, 'mm hg'], 'Diastolic Blood Pressure': [56.0, 'mm hg']}",76,72.2,79.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 116.0 mm Hg + 2/3 * 56.0 mm Hg = 76.0 mm Hg.
Hence, the patient's mean arterial pressure is 76.0 mm Hg."
1511,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3977941-1,Extracted,"A 64-year-old man presented to our emergency department complaining of right chest pain after a traffic accident. He denied having any other systemic diseases. On physical examination, he was afebrile (temperature 36.9°C) with normal vital signs (blood pressure 131/91mmHg, heart rate 77bpm). Pulse oximetry revealed 98% saturation on room air. His chest was clear bilaterally with a midline trachea and no crepitus, but with substantial right-sided posterolateral chest wall tenderness with decreased breathing sounds. The abdomen was soft, non-tender and non-distended, with no palpable intra-abdominal masses or organomegaly. Rectal examination was negative for gross blood or masses. His extremity examination was unremarkable. Chest radiography showed right fifth to eighth rib fractures and was suspicious for free air under his bilateral hemi-diaphragm (Figure 
). CT of the abdomen revealed interposition of bowel loops between the liver and diaphragm (Figure 
). He was treated with oral analgesics and discharged to his home five days later. During a six-month follow-up period, his recovery was uneventful.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [131.0, 'mm hg'], 'Diastolic Blood Pressure': [91.0, 'mm hg']}",104.33333,99.11666,109.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 131.0 mm Hg + 2/3 * 91.0 mm Hg = 104.33333 mm Hg.
Hence, the patient's mean arterial pressure is 104.33333 mm Hg."
1512,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7515789-1,Extracted,"A 19-year-old man, previously healthy and not on any regular medications, presented to the ED at Sultan Qaboos University Hospital (SQUH) in July 2019 with a one-day history of generalized fatigue, bilateral leg pain, and dark discoloration of the urine. There was no history of fever, chills, nausea, vomiting, or diarrhea. Moreover, there was no history of consuming alcohol, anabolic steroid, or drug abuse. His symptoms started a few hours after jogging for around 26 km to improve his fitness before military recruitment. However, he was barely practicing exercise before this attempt.
On presentation to the ED, he was alert and oriented but appeared to be in pain. He was clinically dehydrated, and his vitals were as follows: temperature 37.0°C, blood pressure 130/70 mmHg, heart rate 100 bpm and regular, and oxygen saturation 100% on room air. He had generalized bilateral lower limb swelling and tenderness, but the neurovascular examination was intact. Chest, cardiovascular, and abdominal examinations were unremarkable.
Laboratory findings are presented in Table . As summarized, the patient presented with high CK, AKI (using RIFLE criteria), DIC, and deranged liver enzymes. His initial venous blood gas showed uncompensated high anion gap metabolic acidosis, which could be explained by severe dehydration, AKI, and exhaustion. His initial electrocardiogram (ECG) and chest X-ray were normal. Immediately, using a combination of normal saline and sodium bicarbonate, IV fluid resuscitation was initiated, targeting urine output between 200 and 300 ml/h. Within the first day of admission, he experienced worsening of the bilateral, lower limb swelling and increased pain requiring opioids. Because of the high probability of acute compartment syndrome, the patient underwent double-incision, bilateral fasciotomy with debridement to relieve the bilateral, lower limb, compartment syndrome.
Despite adequate rehydration, renal function continued to deteriorate, evidenced by worsening creatinine levels (Figure ), persistent hyperkalemia (Figure ), and oliguria ( Figure ). The patient underwent the first dialysis session within two days after admission. On the ninth day, the patient became unwell, febrile, and tachycardia. After a sepsis workup, the patient was started empirically on meropenem and vancomycin. The blood cultures sampled from the dialysis line and peripheral vein grew for multidrug-resistant (MDR) Acinetobacter baumannii. Besides replacing the dialysis line, the patient received a 10-day course of meropenem and a high dose of tigecycline as recommended by the infectious disease team. Overall, the patient showed a clinical and biochemical response to the administered antibiotics.
In summary, the patient completed four sessions of tissue debridement, followed by the closure of fasciotomy wounds and six sessions of hemodialysis. The patient's kidney function (Figures -), coagulopathy measured by INR (Figure ), and CK (Figure ) gradually improved. He was discharged as soon as kidney function returned to normal. He also had bilateral foot drop, which improved remarkably with physiotherapy. Otherwise, he remained well upon follow up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 70.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1513,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6904777-1,Extracted,"A 57-year-old African American female with a history of alcohol abuse and diabetes
mellitus presented to the emergency department with a 2-day history of severe
diffuse abdominal pain with radiation to the back. Associated symptoms included
nausea and vomiting. She consumed 5 bottles of beer daily with the most recent
alcohol intake 2 days prior to presentation. Vital signs on presentation were blood
pressure 123/90 mm Hg, pulse 125 beats/minute, respiratory rate 17 breaths/minute,
and temperature 36.8°C. Physical examination was significant for a mildly tender
abdomen. Laboratory findings revealed leukocytosis of 14 600/mm3 and
lipase of 882 U/L (normal = 16-62 U/L). Computed tomographic imaging of the abdomen
with and without contrast revealed peripancreatic fat stranding suggestive of acute
interstitial pancreatitis. The patient was admitted for intravenous fluid
resuscitation and pain management.
On day 2 of admission, the patient became dyspneic and hypoxemic (digital pulse
oximetry 82%) on room air. Chest radiography showed pulmonary edema, and abdominal
ultrasound revealed a dilated inferior vena cava. Troponin I 0.97 ng/mL (normal
<0.03 ng/mL) and brain natriuretic peptide 1627 pg/mL (normal <100 pg/mL)
levels were elevated. A 12-lead electrocardiogram (ECG; ) obtained revealed diffuse ischemic
T-wave inversion. The patient was aggressively diuresed with significant improvement
in respiratory status. Transthoracic echocardiography revealed a left ventricular
ejection fraction of 40% with basal segment hyperkinesis but apical akinesis
consistent with stress-induced cardiomyopathy (). Coronary angiography revealed
normal coronary vessels.
The patient’s abdominal pain resolved, and there were no further complications from
her pancreatitis. She was started on an angiotensin converting enzyme (ACE)
inhibitor and a β-blocker and discharged to home in stable condition. A repeat
transthoracic echocardiography obtained 4 months later revealed unchanged left
ventricular ejection fraction and persistent apical akinesis in the setting of
persistent alcohol use. The ACE inhibitor and β-blocker were continued, and she was
counselled on alcohol cessation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [123.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",101,95.95,106.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 123.0 mm Hg + 2/3 * 90.0 mm Hg = 101.0 mm Hg.
Hence, the patient's mean arterial pressure is 101.0 mm Hg."
1514,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7263131-1,Extracted,"A 74-year-old man with a medical history of hypertension presented with dyspnea that had worsened during the past 3 weeks. He had been experiencing mild dyspnea on exertion for the past 6 months. On admission, he had a cough but denied other symptoms. His vital signs were as follows: respiratory rate, 20 bpm; temperature, 36.7°C; pulse, 77 bpm; and blood pressure, 130/70 mmHg. Arterial blood gas analysis revealed a partial oxygen pressure of 65 mmHg, partial carbon dioxide pressure of 39 mmHg, pH of 7.44, and oxygen saturation of 93% while resting in room air. Laboratory data included a D-dimer level of 0.44 µg/mL (reference range, 0.00–0.50 µg/mL) and an N-terminal B-type natriuretic peptide level of 15 pg/mL (reference range, 0–500 pg/mL). A chest radiograph indicated no active lesions in the lung (). Contrast-enhanced chest CT was performed to exclude pulmonary thromboembolism or other lung disease and revealed no evidence of filling defects in vessels, thus suggesting pulmonary thromboembolism. Transthoracic echocardiography indicated a mean pulmonary arterial pressure of 47 mmHg (reference range, 10–22 mmHg). On further evaluating the chest CT through the bone setting, however, we identified several hyperdense linear lesions in both peripheral pulmonary arteries that could not be identified using the lung or soft tissue windows, and this raised suspicion for PCE (). We confirmed that the patient had undergone PVP with a diagnosis of vertebral compression fracture at another hospital 14 months previously. During hospitalization, his symptoms resolved slightly after starting treatment with diuretics.
This study was a case report involving only one patient and only involved observation of the clinical effects. Therefore, approval by an ethics committee was not required. We obtained verbal consent from the patient for publication of this case report and images.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 70.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1515,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8034,Extracted,"A 50-year-old man is brought to the emergency department by his wife with acute onset confusion, disorientation, and agitation. The patient's wife reports that he has diabetic gastroparesis for which he takes domperidone in 3 divided doses every day. He also takes insulin glargine and insulin lispro for management of type 1 diabetes mellitus and telmisartan for control of hypertension. Today, she says the patient forgot to take his morning dose of domperidone to work and instead took 4 tablets of scopolamine provided to him by a coworker. Upon returning home after 4 hours, he complained of dizziness and became increasingly drowsy and confused. His temperature is 38.9°C (102.0°F), pulse rate is 112 /min, blood pressure is 140/96 mm Hg, and respiratory rate is 20/min. On physical examination, the skin is dry. Pupils are dilated. There are myoclonic jerks of the jaw present.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [96.0, 'mm hg'], 'Systolic Blood Pressure': [140.0, 'mm hg']}",110.66667,105.13334,116.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 96.0 mm Hg = 110.66667 mm Hg.
Hence, the patient's mean arterial pressure is 110.66667 mm Hg."
1516,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3560274-1,Extracted,"A 32-year-old Japanese woman with recurrent hyperthyroidism was introduced to the out-patient department of Kohnan Hospital. She had a family history of Graves’ disease. She began to feel thirst, frequent palpitations, and body weight loss from around June 2006, and hyperthyroidism was detected. Her serum free triiodothyronine (T3) was more than 20pg/mL, free thyroxine (T4) was 7.7ng/dL, TSH was less than the detectable level and anti-TSH receptor antibody (TRAb) was 77.5% (normal range, less than 10%). The 24-hour uptake of iodine-123 to the thyroid gland was 38.47% in the right lobe and 44.16% in the left lobe (total 82.63%). A head magnetic resonance imaging (MRI) with contrast medium revealed thickening of the bilateral ocular muscles, but no evident tumor in the sella turcica (Figure a). The diagnosis was established as Graves’ disease, and propylthiouracil (PTU) was administered. TRAb had fallen to the normal range, and a euthyroid state was achieved in June 2008. However, occasional elevation of free T3 was detected, so PTU administration was continued. Re-elevation of TSH was seen in December 2010 (Figure ). A head MRI revealed abnormal findings in the sella turcica, and she was introduced to the neurosurgical department of Kohnan Hospital in May 2011.
On admission her blood pressure was 152/112mmHg. Electrocardiography recorded her heart rate as 70 beats/minute but she complained of frequent palpitations. Her consciousness was clear, and no abnormal neurological signs were detected. Endocrinological examinations in the morning with oral intake of 100mg of PTU revealed free T3 of 2.77pg/mL, free T4 of 1.09ng/dL and TSH of 2.433μIU/mL. Because of her frequent palpitations the thyroid-releasing hormone (TRH) loading test without discontinuing PTU was performed, which revealed no abnormal response. All other pituitary hormones were within the normal ranges, and head MR imaging with contrast medium showed an area of less enhancement in the left lateral wing of the sella turcica with a diameter of 5mm (Figure b), and transsphenoidal surgery was planned under a diagnosis of TSH-secreting pituitary adenoma.
The milky-white soft tumor was enclosed within a thin cellulose-like membrane. Total removal was achieved in addition to medical fixation of the cleavage with pure ethanol. Postoperative histological examination showed diffuse cell arrangement with mild variation in size but without atypism or mitosis of the nucleus (Figure a,b). Immunohistochemical examination disclosed plurihormonal expression of pituitary hormones including TSH-β, and the diagnosis was established as TSH-secreting plurihormonal adenoma (Figure c,d).
Administration of PTU was discontinued from the day of surgery. Diastolic blood pressure did not exceed 100mmHg for six days after the operation. Pituitary and thyroid hormones were re-evaluated at 11 days after the operation, showing free T3 was 3.31pg/mL, free T4 was 1.00ng/dL and TSH was 1.567μIU/mL. Additional TRH loading test found no abnormal responses, and she was discharged at 12 days after the operation. Her blood pressure was 133/86mmHg, and palpitations had disappeared without medication.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [100.0, 'mm hg'], 'Systolic Blood Pressure': [152.0, 'mm hg']}",117.33333,111.46666,123.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 152.0 mm Hg + 2/3 * 100.0 mm Hg = 117.33333 mm Hg.
Hence, the patient's mean arterial pressure is 117.33333 mm Hg."
1517,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5087259-1,Extracted,"A 49-year-old Caucasian woman presented to emergency department with sudden onset of right fronto-temporal throbbing headache for 1 day. It started as 3/10 in severity and then progressed to 10/10 in about half hour. The headache was associated with right eye pain, nausea, multiple episodes of vomiting, photophobia, and phonophobia as well as chills but no fever. She denied any vision changes, dizziness, speech difficulty, focal weakness, rash, joint pains, neck pain, or rigidity. The patient was previously healthy with no history of chronic medical problems except recurrent sinus infections as well as environmental allergies. Her medications included fexofenadine and oral combined contraceptive pills (OCPs), which she has been taking regularly for 10 years for menorrhagia. She had neither personal nor family history of blood clots, bleeding disorders, or any malignancy. She never smoked but used to drink alcohol socially. The patient had no history of abortion or difficulty getting pregnant. She had three pregnancies; last one was at the age of 35 with no complications. Her mother had three miscarriages while being on phenobarbital for epilepsy. Physical examination showed normal vital signs with blood pressure of 127/70 mm Hg, pulse 88 beats/min, temperature 98.2°F (36.8°C), respiratory rate 14 per min, and oxygen saturation 99% on room air. She was alert, oriented to time, place, and person, and in no distress; cardiopulmonary examination revealed clear breath sounds bilaterally without wheezes or rhonchi, and normal heart sounds with no murmurs, gallops, or rubs. Abdominal exam showed no tenderness, masses, or organomegaly, and she had no edema of the lower extremities. Detailed neurological examination showed intact cranial nerves 2–12 and round, reactive pupils to light and accommodation with normal fundi. She had normal and symmetric motor power in both upper and lower extremities, intact sensation, and no focal neurologic deficit.
Complete blood count was abnormal for leukocytosis of 18.6 K/µL with higher lymphocyte differential count of 21% and no bands. Complete metabolic panel and coagulation studies were within normal limits. Infectious workup including blood cultures was negative. The patient was given ketorolac and hydromorphone, but failed to relieve her headache; so computed tomography (CT) of the head without contrast was done that showed venous sinus thrombosis involving the posterior sagittal sinus and extending into the dominant right transverse sinus (). CT head with contrast was done for confirmation (); it showed occlusive thrombus within the posterior superior sagittal sinus, extending inferiorly into the dominant right transverse sinus, sigmoid sinus, and superior right internal jugular vein. The diagnosis of cerebral venous sinus thrombosis was made based on the patient's presentation and CT findings. Her OCPs were stopped. Anticoagulation was started with low-molecular-weight heparin (LMWH) that was switched to warfarin with an international normalized ratio (INR) target range of 2.0 to 3.0. She received warfarin for 3 months and then switched to low-dose aspirin. Further workup during her hospital stay including carotid artery Doppler and transthoracic echocardiogram was negative. Follow-up CT head 3 months after the initial diagnosis showed complete recanalization of the occluded cerebral sinuses and veins.
Three weeks after completion of anticoagulation, the patient underwent testing for prothrombotic conditions, including protein S, protein C, and antithrombin deficiency; antiphospholipid syndrome; prothrombin G20210A mutation; and factor V Leiden; all were negative.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [127.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",89,84.55,93.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 127.0 mm Hg + 2/3 * 70.0 mm Hg = 89.0 mm Hg.
Hence, the patient's mean arterial pressure is 89.0 mm Hg."
1518,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5112829-1,Extracted,"A 30-year-old woman presented with a history of progressive shortness of breath for 7 months. Dyspnea was insidious in onset and progressed rapidly over the last month, incapacitating the patient in her daily activities. It was associated with cough with expectoration of scant mucoid sputum, noisy breathing, and wheezing for last 1 month. Patient had also noticed hoarseness of voice for the last 6 weeks. There was no history of hemoptysis, facial puffiness, distended neck veins, chest pain, or difficulty in swallowing. There were no constitutional symptoms and her past and personal history was unremarkable. She was a lifetime nonsmoker, a homemaker, and had no occupational exposure.
On general physical examination, heart rate was 116/min and blood pressure was 126/78 mm Hg. Stridor was audible which was predominantly expiratory. Patient was tachypneic (respiratory rate – 28/min) and use of accessory muscles of respiration was visible. Oxygen saturation while breathing room air was 92%. On respiratory system examination, expiratory stridor was audible. Rest of the systemic examination was unremarkable. Blood investigations revealed normal hemogram, liver and kidney function tests. Two-dimensional (2D) echocardiography was normal. Arterial blood gas analysis showed respiratory alkalosis and hypoxemia. Chest X-ray showed normal lung fields; however, there was a doubtful luminal narrowing of the lower trachea []. Contrast-enhanced computed tomography thorax showed the presence of endoluminal soft tissue growth arising from the lower tracheal wall (approximately 2 cm above the carina) causing near complete occlusion of the lower trachea []. Diagnostic flexible bronchoscopy (using pediatric bronchoscope, 2.8 mm) demonstrated multiple whitish glistening nodules over both vocal cords and lower tracheal occlusion by whitish nodular growth.
In view of critical CAO and impending respiratory failure, urgent rigid bronchoscopy and excision of the lower tracheal growth were performed. Under general anesthesia, mechanical coring of the tracheal growth was performed using rigid bronchoscope tubes of increasing sizes and tumor fragments were removed []. There were no procedural complications, and airway patency was successfully achieved. Histopathological examination of the excised specimen demonstrated numerous finger-like projection of stratified squamous epithelium supported by connective tissue stroma []. P-16 immunohistochemical (IHC) staining was positive []. Diagnosis of respiratory papillomatosis (HPV related) was established.
Following rigid bronchoscopic excision, follow-up surveillance flexible bronchoscopy at 3, 6, and 12 months postprocedure showed gradual spontaneous resolution of the residual tracheal and vocal cord papillomas and patient remains currently asymptomatic.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [126.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",94,89.3,98.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 126.0 mm Hg + 2/3 * 78.0 mm Hg = 94.0 mm Hg.
Hence, the patient's mean arterial pressure is 94.0 mm Hg."
1519,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2771959-1,Extracted,"A 60-year-old male who was suffering from CLL for the last 8 years developed anemia and thrombocytopenia 1.5 years back for which he received two courses of fludarabine. Following the therapy, his symptoms improved and he remained well for 6 months. Six months after the last course of fluderabine, he gradually became drowsy, and on the third day, he developed right partial seizures for 5–7 min, which was followed by right hemiplegia. Twelve hours later he had another partial seizure with secondary generalization that continued for 12 h. The patient did not have any past history of epilepsy, diabetes, hypertension or HIV.
On examination, he appeared to be a pale elderly male. Pulse was 80/min, BP was 120/80 mm of Hg and he had hepatosplenomegaly. The patient was comatose and responded to painful stimuli by limb extension. He had right-sided hemiplegia with hyperreflexia and right plantar response was extensor. The patient received IV fluids, intravenous ceftriaxone 2 g 12 hourly and IV phenytoin followed by sodium valproate for the control of status epilepticus. After 12 h, his seizures were controlled and consciousness started improving.
His hemoglobin was 9.5 g/dl, ESR was 13 mm for the first hour, total white cell count was 4000/mm3 with 90% polymorphs, 28% lymphocytes and 2% eosinophil and there were no immature cells. His blood sugar was 77 mg/dl, blood urea – 24 mg/dl, serum creatinine – 1.2 mg/dl, bilirubin – 1.2 mg/dl, SGOT – 471 U/L, SGPT – 41 U/L and the serum electrolyte, lipid profile, bleeding and coagulation parameters were normal. ANA, CRP, urinalysis and radiograph of chest were also normal. Electroencephalography showed diffuse theta slowing. His MRI in T1 sequence revealed subcortical left parieto-occipital and right frontal hypointensity without contrast enhancement or midline shift. The lesions were hyperintense on T2 sequence []. CSF was acellular with 45 mg% protein, 55 mg% sugar and was negative for bacteria and fungal culture. His HIV serology was negative and CSF PCR for JC virus was also negative. He was discharged after 35 days in a bed-ridden and confused state. At a three-month followup, there was no recurrence of seizures and he was able to talk, although bedridden.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [120.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1520,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4557141-1,Extracted,"The patient is a 35-year-old male, with a past medical history of nephrolithiasis and idiopathic vertigo. He had no prior influenza virus vaccination. He was discharged from another hospital the day prior with a diagnosis of CAP and was given doxycycline.
One day following discharge, the patient reported to the emergency room (ER) with syncope after waking up with shortness of breath. He also reported having fever, chills, nausea, vomiting, and palpitation. He has no family history of sudden cardiac death with syncope.
Physical examination revealed that the patient had a temperature of 101.6 F, heart rate of 98 beats/min in sinus rhythm, blood pressure of 102/66 mmHg, with respirations of 24 breaths/min. Patient was alert and oriented times three, and pupils equal, round, and reactive to light. No signs of dehydration present in mucous membranes. Jugular venous distention was 12 cmH2O and no carotid bruits present. Cardiovascular examination was performed which was evaluated to be in regular rate and rhythm with normal S1 and S2 sounds, with a S3 and S4 auscultated. Electrocardiograph was done and showed a sinus rhythm of 119 with multifocal preventricular contractions, and nonspecific ST and T wave changes followed by ventricular tachycardia (VT). Chest radiograph revealed left atrial enlargement, with no acute infiltrates. Bilateral crackles were auscultated on lung fields, all else was noncontributory. Chest computed tomography (CT scan) showed small left lower lobe consolidation. While in the ER he developed VT patient was defibrillated twice and went back into sinus rhythm.
The patients had creatine kinase-MB 11.5 ng/mL and a troponin of 0.12 ng/mL. Comprehensive metabolic panel revealed elevated serum glucose at 142 mg/dL and transaminasemia with an aspartate aminotransferase (AST) of 255 IU/L and alanine transaminase (ALT) of 105 IU/L. B-type natriuretic peptide was 185 ng/L. Patient was transferred to the coronary care unit and a cardiac catheterization demonstrated non-obstructive coronary artery disease with a low ejection fraction of approximately 30%. Cardiac magnetic resonance imaging was done and showed four-chamber enlargement with diffuse generalized dysfunction. No focal areas of enhancement were seen to suggest sites of inflammation, infection, or scarring. Legionella and Streptococcus pneumoniae testing was found to be negative. Mycoplasma IgM was <770. Blood cultures were all negative. Cytomegalovirus was also negative. Serology for influenza virus was found to be positive for influenza A.
Patient was started on furosemide 80mg intravenously (IV) and then 12 h later was changed to 40 mg IV every 12 h for acute biventricular systolic heart failure. Amiodarone was started at 900/500 mg in D5W 1mL/min IV for 6 h, then 0.5 mL/minute for the VT. Vancomycin and cefepime per IV were also started for the CAP and fever.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [102.0, 'mm hg'], 'Diastolic Blood Pressure': [66.0, 'mm hg']}",78,74.1,81.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 102.0 mm Hg + 2/3 * 66.0 mm Hg = 78.0 mm Hg.
Hence, the patient's mean arterial pressure is 78.0 mm Hg."
1521,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8437087-1,Extracted,"A 65-year-old man with the past medical history of hypertension, type 2 diabetes mellitus, and prior stroke without residual deficits presented to the emergency department (ED) with left-sided facial numbness, left-sided weakness, dysarthria, and dysphagia for one hour. On arrival to the ED, the patient had a temperature of 98.6 F, blood pressure of 212/102 mmHg, respiratory rate of 14 breaths per minute, and a pulse rate of 66 beats per minute, regular rate and rhythm. A complete blood count (CBC) and basal metabolic panel (BMP) were essentially normal except for high blood glucose levels of 420 mg/dl. Neurological examination revealed equal, round pupils reactive to light, midline tongue, left-sided facial droop, dysphagia and dysarthria. Initial motor power in all four extremities was 5/5. The patient was not given tissue plasminogen activator (TPA) because of accelerated hypertension.
Initial head computed tomography (CT) and computed tomography angiogram (CTA) of the head and neck showed no acute intracranial abnormalities. Chest X-ray (CXR) showed no acute abnormalities. Aspirin 325 mg and atorvastatin 80 mg were given immediately and aspirin 81 mg daily together with atorvastatin 80 mg bedtime was started. While in the ED, the patient fell while attempting to urinate, sustaining a laceration to the left orbit. Repeat head CT at that time was unchanged. Shortly after, the patient became cyanotic, bradycardic, and unresponsive, requiring intubation with arterial blood gas (ABG) showing pH of 7.21, partial pressure of carbon dioxide (pCO2) of 70 mmHg, partial pressure of oxygen (pO2) of 193 mmHg and bicarbonate (HCO3) of 28 mmHg. Carbon dioxide retention in this patient with no medical history of lung disease indicated possible central respiratory dysfunction. Glasgow coma scale (GCS) at the time of evaluation was 9. Neurological examination, on the next day after intubation, revealed spontaneous movement of right extremities but no spontaneous or pain induced movement of left extremities. The third head CT obtained in light of suspicion of stroke came back negative as well.
On day 3, the patient met the weaning parameters on a spontaneous breathing trial and was extubated. But subsequently after extubating, the patient became apneic and required reintubation. Considering that the patient became apneic despite of meeting weaning parameters, suspicion of posterior circulation stroke leading to central alveolar hypoventilation was high. Magnetic resonance imaging (MRI) of the head (Figure ) was obtained which demonstrated a left medullary infarction. Subsequent attempts to wean off mechanical ventilation failed due to apnea. Patient underwent tracheostomy and remained on mechanical ventilation at discharge.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [212.0, 'mm hg'], 'Diastolic Blood Pressure': [102.0, 'mm hg']}",138.66667,131.73334,145.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 212.0 mm Hg + 2/3 * 102.0 mm Hg = 138.66667 mm Hg.
Hence, the patient's mean arterial pressure is 138.66667 mm Hg."
1522,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4438411-1,Extracted,"A 78-year-old Japanese woman was admitted because of systemic oedema. Approximately 11 months earlier, her serum creatinine level was within the normal range (Cre 38.1 µmol/L), and her urinalysis was also normal at a medical check-up. Eight months earlier, non-steroidal anti-imflammatory drugs (NSAIDs) were prescribed for arthralgia. Six weeks before hospitalization, she visited us for the first time. Her serum creatinine was 101 µmol/L. Urinalysis showed proteinuria of 0.65 g/day and haematuria of 30–49 red blood cells/high-power field. The NSAIDs were discontinued, and after 2 weeks, the serum creatinine decreased to 68.6 µmol/L, although the urinalysis findings did not improve.
One month later, she came to the outpatient clinic again because of systemic oedema. Urinalysis revealed proteinuria of 10.2 g/gCre (protein-creatinine ratio), and laboratory tests showed a serum total protein of 48 g/L, a serum albumin of 26 g/L and a serum creatinine of 101 µmol/L. She was diagnosed with nephrotic syndrome and was admitted. On admission, she had a blood pressure of 148/93 mmHg and her weight had increased 11 kg in a month. A percutaneous renal biopsy was performed for accurate diagnosis of her nephrotic syndrome.
Light microscopy contained 40 glomeruli. Haematoxylin and eosin-stained sections showed massive, homogeneous, eosinophilic deposits in the mesangial space with formation of a lobular shape (A). No crescent formation was seen. Capillary walls had double contours, and almost all glomeruli had numerous periodic acid-Schiff (PAS)-positive deposits in the mesangial space and between the double-contour capillary walls (B and C). Amyloid staining and Congo-red staining were both negative. Immunofluorescence studies showed slight intensity of IgG in a peripheral pattern. However, other immunofluorescence microscopy tests were all negative. Electron microscopy revealed granular deposits in the mesangial space (D). The granular deposits showed focal fibril formation with higher magnifications (E). The fibrils were randomly arranged, with no central core, and their diameter was 12–14 nm. Fibronectin glomerulopathy was suspected because of this fibril formation and size. Therefore, plasma fibronectin immunostaining was performed. Immunohistochemistry of the fibronectin clearly showed intense staining in the mesangial space and a peripheral pattern (F). Thus, the case was diagnosed as having fibronectin glomerulopathy based on these histological findings.
She had progressive pre-renal acute kidney injury due to nephrotic syndrome. Two months after kidney biopsy, haemodialysis was started, and she became dialysis-dependent thereafter.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [148.0, 'mm hg'], 'Diastolic Blood Pressure': [93.0, 'mm hg']}",111.33333,105.76666,116.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 148.0 mm Hg + 2/3 * 93.0 mm Hg = 111.33333 mm Hg.
Hence, the patient's mean arterial pressure is 111.33333 mm Hg."
1523,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-3628,Extracted,"A 58-year-old man with chronic obstructive pulmonary disease and hypertension comes to the physician because of shortness of breath 3 days after starting propranolol. His temperature is 36.7°C (98.1°F), pulse is 64/min, respirations are 20/min, and blood pressure is 138/88 mm Hg. Auscultation of the lungs shows diffuse expiratory wheezes.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [138.0, 'mm hg'], 'Diastolic Blood Pressure': [88.0, 'mm hg']}",104.66667,99.43334,109.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 138.0 mm Hg + 2/3 * 88.0 mm Hg = 104.66667 mm Hg.
Hence, the patient's mean arterial pressure is 104.66667 mm Hg."
1524,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6637392-1,Extracted,"A 51-year-old South Asian man on maintenance HD presented with an acutely painful left thigh and breathlessness. He had a 20-year history of poorly controlled type two diabetes with associated nephropathy and retinopathy. His temperature was 38.6 °C, pulse 90 bpm, and blood pressure was 150/78 mmHg. He had bibasal chest crepitations and bilateral pedal edema. His left thigh was swollen and tender. His C-reactive protein (CRP) was 147 mg/L (< 5), and white cell count (WCC) was 8.7×109/L (4 – 11×109/L). He received 5 days of meropenem for sepsis, presumed to be due to cellulitis or an infective collection, and underwent ultrafiltration with HD. A Doppler ultrasound scan (DUSS) excluded a deep vein thrombosis (DVT) and a collection, but demonstrated edema of the superficial tissues. Blood cultures taken prior to antibiotics were negative.
The patient’s continued discomfort prompted magnetic resonance imaging (MRI). This revealed an abnormal signal from the anterior and medial left thigh muscle compartments on T1-weighted imaging (). This, in conjunction with fat suppression through short tau inversion recovery (STIR), was reflective of an inflammatory or infective process. Orthopedic and rheumatology specialist opinions were sought; prompting an autoimmune screen (anti-neutrophil cytoplasmic antibody (ANCA), anti-nuclear antibodies (ANA), anti cyclic citrullinated peptide (anti-CCP), extractable nuclear antibodies (ENA); all of which returned negative) and the suggestion of a muscle biopsy. However, a subsequent review by the diabetes multidisciplinary team concluded that the findings were consistent with DMN, and the biopsy was avoided. He was managed with gentle physiotherapy and oxycontin 5 mg twice a day, with another 5 mg as needed for break-through pain. His symptoms resolved over another 4 weeks.
Of note, this patient had presented elsewhere with similar symptoms several times in the past, prompting 7 DUSS’ and a previous MRI. He received antibiotics and was considered for muscle biopsy on each occasion, avoided only due to symptom resolution. DMN had never previously been considered.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",102,96.9,107.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 78.0 mm Hg = 102.0 mm Hg.
Hence, the patient's mean arterial pressure is 102.0 mm Hg."
1525,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5869576-1,Extracted,"A 31-year-old Filipino female presented to the emergency department with a high-grade fever over a 2-week period. This was accompanied by tender swellings in the groin bilaterally that resulted in difficulty walking. She was seen by her family practitioner twice during this episode and was prescribed a 1-week course of oral augmentin, followed by another 5-day course of oral moxifloxacin. Despite the antibiotics, her condition continued to worsen. Ten days from fever onset, she developed a rash over her hands and legs, associated with circumoral numbness. However, no swallowing problems or breathing difficulty were reported. Over the next 4 days, the rash spread to her face and ears associated with markedly tender swellings in her armpits.
She has no significant medical history and has been working in Singapore as a domestic helper in the same household for the past 8 years. She is single, with no sexual activity nor gynecologic issues. She has not returned to her native country in the past 3 years.
On systemic enquiry, there was no loss of weight or night sweats, no joint swellings or arthralgia, no alopecia, and no dry eyes or mouth. There was also no personal or family history of autoimmune disease (Fig. ).
On examination, her temperature was 39.2°C, pulse rate 120 beats per minute, and blood pressure 130/80 mm Hg. The significant findings concerned the skin, which revealed an erythematous papulonodular eruption scattered over the extensor surfaces of both upper and lower limbs. There were multiple indurated plaques on the face over the nasal bridge, the brow, the outer maxillary area and both earlobes and pinna. This was associated with ankle edema, tender, enlarged and matted cervical, axillary, and inguinal lymph nodes. The rest of the physical examination was unremarkable. The differential diagnoses considered included tumid lupus erythematosus, sarcoidosis, cutaneous amyloidosis, lymphoproliferative disease, Sweet syndrome, and Hansen disease.
Routine investigations revealed leukocytosis of 36.18 × 109/L, an erythrocyte sedimentation rate of 80 mm/h and a C-reactive protein level of 159 mg/L. HIV testing, antinuclear antibody, C3, C4, and double-stranded DNA levels were normal. Serum alkaline phosphatase was elevated at 316 IU/L with otherwise normal liver transaminases. Her albumin level was 34 g/L.
In view of the persistent high fever and multiple enlarged lymph nodes with elevated serum alkaline phosphatase, she underwent a computed tomography scan of the neck, thorax, abdomen and pelvis, which showed no intra-abdominal or hepatobiliary source of infection, or abscesses, but revealed multiple enlarged and necrotic lymph nodes in the axilla and inguinal regions consistent with the initial examination findings.
Closer examination revealed bilaterally thickened greater auricular nerves and lateral peroneal nerves, which further raised the suspicion of leprosy. Complete examination of the central nervous system did not reveal any sensorimotor loss (Fig. ).
Skin biopsy was performed and histological examination showed a diffuse inflammatory infiltrate within the dermis and subcutaneous tissue, sparing the epidermis. The inflammatory infiltrate was composed of lymphocytes, histiocytes, foamy macrophages, and neutrophils. Some of the inflammation involved the nerves and adnexal structures. Large numbers of acid-fast bacilli were identified on Fite and Ziehl-Neelsen stains. These features are consistent with the diagnosis of lepromatous leprosy with erythema nodosum leprosum.
She was started on multidrug therapy comprising of rifampicin, dapsone, and doxycycline. Due to the lack of availability of clofazimine, doxycycline was used as an interim third agent before clofazimine was obtained 2 days later. Prednisolone at 1 mg/kg was also started empirically. Of note, there was no evidence of Lucio phenomenon as she did not have skin erosions or ulcers.
She has recovered well on follow-up in the outpatient setting. The skin lesions, peripheral edema, and tender lymphadenopathy have improved.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1526,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7771253-2,Extracted,"A 20-year-old previously healthy G1P0 female at 22 weeks' gestation presented to the ED with 2 days of severe lower abdominal pain, vomiting, reduced appetite, and diarrhea, with blood in stools for 1 day. She was admitted to the intensive care unit (ICU) for monitoring. At admission, she had a temperature of 36.8°C, heart rate of 110 beats per minute, respiratory rate of 22 breaths per minute, oxygen saturation of 100% on room air, and blood pressure of 130/84 mmHg. The patient was noted to have diffuse lower abdominal tenderness below the umbilicus with no rebound and had red blood mixed with loose stools. On laboratory evaluation, her inflammatory markers, liver function tests, blood cell counts, coagulation profile, D-dimers, ferritin, and albumin levels were normal. The patient had a negative respiratory viral panel (RVP) and a positive nasopharyngeal SARS-CoV-2 RT-PCR. Abdominal ultrasound was consistent with stated gestational age and was otherwise unremarkable. Stool cultures and 2-step stool testing for PCR and antigen for Clostridium difficile were negative. The patient was diagnosed with acute hemorrhagic colitis associated with SARS-CoV-2 infection and received intravenous fluids and intravenous dexamethasone (at 6 mg/day). Broad-spectrum antibiotics (vancomycin and piperacillin/tazobactam) were discontinued after 48 hours when cultures returned negative. Gradually, the abdominal pain and diarrhea improved with no recurrence of bleeding after day 2 of hospitalization. In view of the clinical improvement, it was decided to defer endoscopy. The patient was discharged and gradually weaned off steroids, with no recurrence of symptoms noted upon outpatient follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [84.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",99.33333,94.36666,104.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 84.0 mm Hg = 99.33333 mm Hg.
Hence, the patient's mean arterial pressure is 99.33333 mm Hg."
1527,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3743519-1,Extracted,"An eighteen year old African American male presented to the emergency room with a 1-week history of sore throat, muscle aches, fever, headache, and photophobia. He also complained of nausea, one episode of vomiting, and abdominal pain. He was a college student and lived in a dormitory. He denied any recent travel or contact with ill people. Past medical history was significant for sickle cell trait and Osgood Schlatter’s disease. He was up to date on vaccinations.
Physical examination revealed a tall, thinly built young man, in mild pain with an oral temperature of 97.5°F, blood pressure of 114/69 mmHg, heart rate of 89 beats per minute (BPM) and respirations of 18/minute. He had injected conjunctiva of the right eye, and pharyngeal and tonsillar exudates. The examination of the central nervous system revealed neck stiffness; Kernig’s and Brudzinski’s signs were not elicited. Cranial nerves were intact. The power and deep tendon reflexes were essentially normal. The rest of the systemic examinations were unremarkable.
Hemoglobin was 17.5 g/dL, hematocrit 50.8 g/dL, and white count 20.3 × 109/L with 89% granulocytosis, and platelet count of 35 × 109/L. Basic metabolic profile was within normal limits, except for a potassium level of 3.2 meq/L, blood urea nitrogen of 44.9 mg/dL, and creatinine of 2.3 mg/dL. Chest X-ray revealed bilateral infiltrates in the middle and lower lung fields. Computed tomography (CT) of the head was unremarkable. The patient declined lumbar puncture. The blood culture grew penicillin sensitive Group C Streptococcus (GCS) within 24 hours of incubation. A few hours into the admission, he developed third and sixth nerve palsy. Further work-up revealed right cavernous and ophthalmic vein thrombosis on magnetic resonance imaging ( and ). Multiple patchy cavitary lesions on both lungs were seen in the chest CT. There was no vegetation on transesophageal echocardiogram. The oculomotor and abducens palsies resolved after medical management for 16 days.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [69.0, 'mm hg'], 'Systolic Blood Pressure': [114.0, 'mm hg']}",84,79.8,88.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 114.0 mm Hg + 2/3 * 69.0 mm Hg = 84.0 mm Hg.
Hence, the patient's mean arterial pressure is 84.0 mm Hg."
1528,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8403714-1,Extracted,"A 28-year-old man without previous medical history was brought to the emergency department of the hospital with worsening dyspnea, chest pain, and coughing developed following penetrating chest trauma by a nail gun which happened 5 hours earlier. He was repairing a sofa at his home using this gun when a nail was misfired to his chest accidentally. Upon primary survey, the patient's airway was intact, he was tachypneic, and had reduced lung sound at left hemithorax. He had a blood pressure of 110/70 mm Hg and heart rate of 94 beats per minute and his heart sounds were muffled but regular S1-S2 were barely heard. He had a GCS score of 15/15. Upon chest inspection, a clean circular puncture wound was noted in the third intercostal space of the left hemithorax at the midclavicular line (). According to the hemodynamic stability, he underwent chest CT scan and it revealed a nail as a sharp hyperdense foreign body that penetrated the chest wall and passed through the lower lobe of the left lung and then entered the pericardium, and finally the anterior aspect of the left ventricle (LV) reaching LV cavity. Also, patchy ground glass opacities at left lower lobe was noted which pertained to hemorrhage (, , , , ). Transthoracic echocardiography was performed and chest CT scan observation was confirmed and revealed pericardial effusion. Considering clinical and imaging findings, the patient underwent midline sternotomy. After opening the pericardium, the gush of blood was completely evacuated and controlled by Teflon felt-supported suture and to impede the left anterior descending artery involvement, Teflon-felt wrapping repair was performed in horizontal mattress manner (Video-2). After cardiac suturing, the nail was extracted from the left lung, and the chest wall (). Regarding surgery assessment, transesophageal echocardiography was done and confirmed no evidence of further intraventricular dissection, ventricular septal rupture or any residual defect. There was no postoperative complication and he was extubated on postoperative day 2 and the drain output progressively diminished and was removed serially. The patient was discharged 4 day's after admission. His outpatient follow-up, 2 weeks after surgery was uncomplicated.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1529,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8237432-1,Extracted,"A 19-year-old Sinhalese girl had neck lumps since the age of 5 years, which were not evaluated before. They have now increased in size and become tender since 1 year. She had a rash on both her lower limbs for 6 years, but no other photosensitive rashes. She had alopecia for 4 years, and pain and morning stiffness of small and large joints for 6 months. She had no gritty eyes or visual impairment. She had loss of appetite but no loss of weight. She attained menarche at the age of 13 years, and had regular menstruation since then. She had no family history of rheumatological disease or malignancy. Her mother had a history of one miscarriage. She had no history of thrombotic phenomena. She presented with a 5-day history of worsening joint pain, fever, and painful, enlarging cervical nodules.
Her blood pressure was 110/70 mmHg and pulse rate was 80 beats per minute. She had bilateral soft tender cervical lymphadenopathy involving the anterior cervical region, and tender and swollen interphalangeal and carpometacarpal joints. She had an erythematous non-blanching macular rash suggestive of a vasculitic rash on both lower limbs, but no oral ulcers. She had no malar or photosensitive rashes and no digital ulcers or calcinosis cutis. She had no hepatosplenomegaly, with normal examination of the cardiovascular and respiratory systems. She had no focal neurological signs or proximal myopathy, and fundoscopy was normal.
She had pancytopenia (white blood cell count 2.3 × 106, hemoglobin 10 g/dl, platelet count 118 × 106). She had a high erythrocyte sedimentation rate (ESR) of 92, positive anti nuclear antibodies (ANA) titer of 1:640 on Hep-2 cells, and a high anti-double-stranded deoxyribonucleic acid (dsDNA) antibody level of 15 IU/ml (positive if > 10 IU/ml), with low C3 and C4 complements of 0.5 g/l (low < 0.785 g/l) and 0.08 g/l (low < 0.145 g/l), respectively, compatible with findings of systemic lupus erythematosus (SLE). Blood picture showed moderate mixed deficiency anemia with moderate rouleaux formation. She had mild iron deficiency anemia with hemoglobin of 9.5 g/dl, low serum ferritin of 8 μg/l, and low transferrin saturation of 15% with no bleeding manifestations. She had a high reticulocyte count of 5% (0.5–1.5%), with LDH of 182 U/l (140–280 U/l). Her direct and indirect antiglobulin tests were positive, and C3d specificity was positive with negative immunoglobulin (IgG) specificity indicating autoimmune hemolytic anemia. She was seen by a hematologist and was started on iron and folic acid supplements. Ultrasound scan of the neck showed reactive lymphadenopathy in the anterior cervical region. Lymph node biopsy showed moderate reactive follicular hyperplasia, with scattered plasma cells and immunoblasts, with varying degree of coagulative necrosis, suggestive of lupus lymphadenopathy. She did not have distorted nodular architecture with cortical and paracortical nodules with proliferation of histiocytes, and karyorrhexis, and crescentic histiocytic nuclei to suggest Kikuchi–Fujimoto disease. On immunohistochemistry of the lymph node biopsy, CD20 was positive in follicles, CD5 was positive in interfollicular areas, and Bcl2 was negative, excluding lymphoma histologically.
Ultrasound abdomen and contrast-enhanced computed tomography of abdomen and chest was normal with no hepatosplenomegaly or intraabdominal lymphadenopathy. Antibodies for cytomegalovirus, Epstein–Barr virus, human immunodeficiency virus (HIV), and Mantoux were negative. Skin biopsy showed fibrinoid necrosis of the vessels with fibrin extravasation suggestive of leukocytoclastic vasculitis. Her cytoplasmic anti-neutrophil cytoplasmic antibody (cANCA), perinuclear anti-neutrophil cytoplasmic antibody (pANCA), anti-Ro, anti-La, and antiphospholipid antibodies were negative, but anticardiolipin antibody was positive. However, she did not fit the criteria for antiphospholipid syndrome as she had no history of thrombotic phenomena or pregnancy-related complications of placental insufficiency. She was advised on using compression stockings during long distance travel, adequate hydration, and thromboprophylaxis during major surgery or during future pregnancies. Her serum creatinine was normal (77 μmol/l), urine protein-to-creatinine ratio was 343 mg/g, and she had no dysmorphic red cells in urine. She was seen by a nephrologist, and it was decided that a renal biopsy was not indicated at present. She was planned to be closely monitored, and to consider renal biopsy only if urine protein was more than 500 g/dl, or red cells in urine > 5–10/high power field (HPF) with > 10% dysmorphic red cells on follow-up. Ophthalmological evaluation showed no eye involvement of SLE.
Her SLE disease activity index (SLEDAI) at diagnosis was 22. She was seen by a rheumatologist, dermatologist, nephrologist, and hematologist for specialist opinion and was started on hydroxychloroquine 200 mg daily and prednisolone 30 mg daily along with gastric protection, and vitamin D and calcium supplements for bone protection. Her symptoms improved and lymphadenopathy regressed, and prednisolone was gradually tailed off over 3 months.
Six months after the initial presentation, she developed loss of appetite, generalized edema and was found to have a blood pressure of 135/100 mmHg, which later increased to 160/110 mmHg during the course. She was found to have an increased serum creatinine of 128 μmol/l, proteinuria with a urine-to-protein creatinine ratio (UPCR) of 3854 g/dl, and 20–25 red blood cells in urine on high-power field that were dysmorphic, with red cell urinary casts. Renal biopsy confirmed mixed grade III and grade V lupus nephritis, evidenced by less than 50% of the glomeruli showing proliferation without sclerosis, and diffuse thickening of the glomerular basement membrane on light microscopy, and subepithelial immune deposits on immunofluorescence. The SLEDAI during this flare was 26. She was treated with intravenous methylprednisolone 1 g daily for 3 days and intravenous cyclophosphamide pulse therapy with the first dose being 0.75 g/m2 followed by five doses of 0.5 g/m2 for induction. She was started on cilnidipine 10 mg twice per day and telmisartan 80 mg daily for blood pressure control and reduction of proteinuria, and mycophenolate mofetil 1.5 g twice per day for maintenance, and oral methylprednisolone 8 mg daily for lupus nephritis. Methylprednisolone was continued for 5 months and gradually tailed off, after which she was normotensive with UPCR less than 500 g/dl on several occasions, the latest being 125 g/dl 7 months after induction, with no hematuria on follow-up. The SLEDAI 7 months after induction for lupus nephritis was 2.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [160.0, 'mm hg'], 'Diastolic Blood Pressure': [110.0, 'mm hg']}",126.66667,120.33334,133,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 110.0 mm Hg = 126.66667 mm Hg.
Hence, the patient's mean arterial pressure is 126.66667 mm Hg."
1530,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-12203,Extracted,"A 58-year-old man presents to the emergency department with worsening shortness of breath, cough, and fatigue. He reports that his shortness of breath was worst at night, requiring him to sit on a chair in order to get some sleep. Medical history is significant for hypertension, hypercholesterolemia, and coronary heart disease. His temperature is 98.8°F (37.1°C), blood pressure is 146/94 mmHg, pulse is 102/min, respirations are 20/min with an oxygen saturation of 89%. On physical examination, the patient's breathing is labored. Pulmonary auscultation reveals crackles and wheezes, and cardiac auscultation reveals an S3 heart sound. After appropriate imaging and labs, the patient receives a non-rebreather facemask, and two intravenous catheters. Drug therapy is initiated.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [146.0, 'mm hg'], 'Diastolic Blood Pressure': [94.0, 'mm hg']}",111.33333,105.76666,116.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 146.0 mm Hg + 2/3 * 94.0 mm Hg = 111.33333 mm Hg.
Hence, the patient's mean arterial pressure is 111.33333 mm Hg."
1531,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3816164-1,Extracted,"A 63-year-old Korean woman with a past medical history of hypertension and a 25-year history of SLE presented with a 3-week history of shortness of breath. She had been treated with hydroxychloroquine 400 mg/day and varying doses of prednisone between 5 and 15 mg/day for the SLE. Additionally, the hypertension was under control with carvedilol 25 mg/day. On examination, her blood pressure was 110/70 mmHg, pulse rate was 112 beats/min, respiratory rate was 24 breaths/min, and body temperature was 36.5℃. Jugular venous distention was noted on inspection. On cardiac auscultation, her rhythm was noted to be tachycardic but regular, weak summation gallops were heard at the cardiac apex, and no pericardial friction rubs were appreciated. Blood tests showed a white blood cell count of 4000/mm3 (normal, 4300-9400/mm3), hemoglobin of 11.5 g/dL (normal, 12-14.3 g/dL) and platelet count of 67000/mm3 (normal, 169-365/mm3). The C-reactive protein level was found to be 0.29 mg/L (normal, 0-0.75 mg/L). A blood chemistry panel revealed a blood urea nitrogen level of 25.0 mg/dL (normal, 7-20 mg/dL), creatinine of 1.3 mg/dL (normal, 0.5-1.5 mg/dL), total protein of 6.7 g/dL (normal, 6.0-8.3 gm/dL), and albumin of 3.2 g/dL (normal, 3.5-4.5 mg/dL). Analysis of the urinary sediment revealed 1-4 white blood cells/high power field (hpf), many red blood cells/hpf, and trace levels of proteinuria. Cardiac enzymelabs were drawn and found to be elevated: CK-MB of 8.7 U/L (normal, 0.6-6.3 U/L), troponin-I of 0.35 ng/mL (normal, 0.0-0.2 ng/mL), and pro-brain natriuretic peptide of 8110 pg/mL (normal, 0-125 pg/mL). Chest X-ray revealed an enlarged cardiac silhouette and an electrocardiogram revealed ST elevation in leads V1-6 (). Immunofluorescence tests were negative for double-stranded DNA antibodies and anti-extractable nuclear antigen antibodies (anti-Ro and anti-La). Complement levels were found to be low (C3 0.39 g/L, normal 0.8-1.7 g/L; C4 0.04 g/L, normal 0.12-0.36 g/L). Viral markers for cytomegalovirus, Coxsackie virus B type 2, herpes simplex virus, and Epstein-Barr virus were all negative. Echocardiography demonstrated moderate left ventricular systolic dysfunction [left ventricular ejection fraction (LVEF) was 42%] with apical akinesia but no evidence of pericardial effusion (). Echocardiography performed 2 years earlier showed mild concentric left ventricular hypertrophy with a LVEF of 70%. A coronary angiography showed normal coronary arteries.
We suspected takotsubo cardiomyopathy. However there was no trigger event as physical and emotional stress. The patient was treated with angiotensin converting enzyme inhibitor, furosemide, and intravenous nitrates. The dose of glucocorticoids was between 0.5 to 1 mg/kg for the control of SLE activity. Her dyspnea gradually improved, however, a three-week follow-up echocardiography test revealed persistent apical ballooning and a newly developed apical thrombus (size, 1.10 × 2.12 cm) () with no significant improvement in LVEF. Heparin was then administered followed by oral anticoagulation therapy with warfarin. There were no embolic events during the patient's hospital stay. On the 35th day of hospital admission, follow-up echocardiography showed slightly improved wall motion of the left ventricular apex with a partially resolved thrombus and a LVEF of 50%. Although cardiac enzymes remained elevated (CK-MB 12.80 U/L and troponin-I 0.64 ng/mL), the patient was discharged on oral anticoagulation therapy.
Three months later, she was readmitted to the hospital due to a severe herpes zoster outbreak on her left shoulder. Cardiac enzymes were again found to be elevated (CK-MB 8.8 U/L and troponin-I 0.98 ng/mL). Electrocardiography revealed persistent ST segment elevation () and echocardiography revealed mild apical hypokinesia with a LVEF 50%, but no apical thrombus (). During her hospital stay she developed a mild fever and candidemia which was treated with an intravenous antifungal agent. Unfortunately, she developed septic shock and expired on day 54 of hospital re-admission.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1532,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7361480-1,Extracted,"A 39-year-old female presented to the emergency department with 4 days of fever and stabbing, nonradiating right flank pain. The patient self-treated a reported 101.7 °F temperature at home with acetaminophen. Her history was significant for a bicuspid aortic valve corrected with aortic balloon valvuloplasty followed by Ross procedure at age 17. She denied intravenous drug use, recent dental treatment, or other invasive procedures.
On physical examination, the patient was febrile (102.9 °F), tachycardic (101 beats per minute), and hypertensive (174/103 mm Hg). A grade 4/6 holosystolic ejection murmur was heard in all cardiac windows on auscultation. Electrocardiogram was negative for abnormalities or acute ischemic changes. Mild cardiomegaly and evidence of previous sternotomy were seen on chest radiography (). A bedside transthoracic echocardiogram (TTE) was completed revealing an ejection fraction of 65% and elevated right ventricular systolic pressure of 71 mm Hg. No definitive lesions were identified. Two sets of blood cultures were collected in addition to a urine specimen before the patient was discharged home. The following day, blood cultures were found to be positive for Streptococcus anginosus, while urinalysis was negative. The patient was immediately informed of the results and returned for admission and initiation of empiric intravenous therapy with vancomycin pending sensitivity results. Fever, positive blood cultures, and a predisposing cardiac condition met the clinical diagnostic threshold for possible IE.
Cardiology was consulted to complete a transesophageal echocardiogram (TEE) given her history of a bioprosthetic valve. TEE indicated severe pulmonic stenosis with an elevated right ventricular systolic pressure of 90 mm Hg, pulmonary artery maximum velocity of 4.7 m/s, and peak gradient of 88 mm Hg. Left ventricular ejection fraction was similar to the previous TTE at 60%. Moderate aortic and tricuspid regurgitation was appreciated along with a dilated right ventricle. No vegetations were noted; however, the pulmonary valve was not well visualized. A cardiac computed tomography scan identified severe pulmonic stenosis; 5 mm right-outflow tract narrowing of the proximal main pulmonary artery and 25 × 12 mm pulmonary annulus narrowing. Orthopantomography was negative for acute disease or significant periodontal disease.
Sensitivity results to ceftriaxone, cefotaxime, and benzylpenicillin had minimum inhibitory concentrations of 0.5, <0.12, and <0.06 mg/L, respectively. Her antibiotic regimen was modified accordingly for optimal treatment. She began a 6-week course of intravenous ceftriaxone and gentamicin.
The patient continued medical management and was transferred to a tertiary care center with cardiac surgery expertise. Ultimately, she underwent successful Melody transcatheter pulmonary valve replacement after completing her course of antibiotics without complication. As of June 2020, the patient remains in good health.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [174.0, 'mm hg'], 'Diastolic Blood Pressure': [103.0, 'mm hg']}",126.66667,120.33334,133,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 174.0 mm Hg + 2/3 * 103.0 mm Hg = 126.66667 mm Hg.
Hence, the patient's mean arterial pressure is 126.66667 mm Hg."
1533,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3669048-1,Extracted,"A 63-year-old male presented with a five week history of double vision, rotational vertigo with tinnitus, progressive gait imbalance and apathy. One month earlier he had undergone tibia osteotomy surgery because of varus deformity. He used no medication. He had a history of alcohol abuse and did not smoke. He had no history of international traveling. There was no family history of neurological disease.
Except from postsurgical findings at his right knee general physical examination was normal. The blood pressure was 130/70 mmHg, pulse rate 78/minute, and he was afebrile. On initial neurological examination he was alert and cognitive functions were normal. His speech was dysarthric, chantering. Examination of the cranial nerves revealed a right abducens nerve paresis and an upbeat nystagmus. The pinprick sensation in the V3 distribution of the trigeminal nerve was symmetrically decreased. Other cranial nerve functions were normal. Strength was normal in muscles of the arms and legs and sensation was preserved. Vibration sense on both legs was diminished. The arms and legs on both sides showed atactic, dysmetric movements. Tendon reflexes were normal and the plantar reflexes were normal. He had an impressive gait ataxia and he was unable to walk without aid. His gait was further impaired due to the recent surgery.
As he was known with alcohol abuse, Wernicke’s syndrome was firstly assumed and he was promptly treated with intravenous thiamine.
However, the neurological condition of the patient further deteriorated. He developed difficulties swallowing and became incontinent for urine. His gait ataxia worsened and a slight spastic paraparesis developed.
In this patient with progressive cranial nerve dysfunction with ocular signs, ataxia and pyramidal tract signs, brain stem dysfunction with a variety of causes should be considered. The broad differential diagnosis included CNS lymphoma, primary CNS vasculitis, demyelinating diseases, paraneoplastic syndromes, sarcoidosis, tuberculosis and neurolues. The diagnosis of Wernicke’s syndrome was rejected as the clinical picture deteriorated and the pre-treatment thiamine level showed to be 118 nmol/L (normal range: 60–200 nmol/L).
MRI T2-weighted and fluid-attenuated inversion recovery (FLAIR) images of the brain demonstrated distinct hyperintensity abnormalities consisting of punctuate lesions in the pons, brachium pontis and cerebellum (Figure 
A). The lesions were gadolinium enhancing but had no significant mass effect.
Blood levels of C-reactive protein, ESR, Vit B12 and Angiotensine Converting Enzyme levels were normal. Liver parameters were normal except for a slightly elevated gamma-GT of 65 U/L (reference <55 U/L). Thyroid functions were normal.
Antinuclear antibodies, double-stranded DNA antibodies, extractable nuclear antigens, antineutrophil cytoplasmic antibodies and antineuronal antibodies (anti-Hu, anti-Yo, anti-Ri, anti-Tr, anti-amphiphysine, anti-CV2 and anti-Ma2) were not detected.
Serologic tests on Syphilis, HIV, Borrelia Burgdorferi, anti-DNase B and anti-streptolysine titer were negative. Auramine staining and PCR for M.tuberculosis complex DNA were negative.
Analysis of the cerebrospinal fluid showed a raised protein level (protein 1.3 g/L, reference range 0.2–0.5) and a slight pleiocytosis (6,0 E06, reference <5 E06). Red cell count and glucose levels were normal. The IgG index was marginally increased (0.62, reference range 0.3–0.6), no oligoclonal bands were found. Cytology study reports showed normal amounts of lymphocytes, granulocytes monocytes and erythrocytes. Malignant cells were not detected.
Cultures of urine, blood and cerebral spine fluid were all negative.
MRI of the spinal cord and CT scanning of the chest, abdomen and pelvis showed no abnormalities. Total body PET CT scanning was negative for malignancies.
On the base of the typical MRI findings and exclusion of other possible diagnoses the diagnosis of CLIPPERS was presumed. The patient was treated with 1000 mg intravenous methylprednisolone daily for a period of three days, followed by oral prednisolone 80 mg per day. Within a week from starting treatment the symptoms gradually improved and on MRI two weeks from starting treatment the pontine lesions decreased in number and intensity (Figure 
B).
Maintenance immunosupressive therapy by oral prednisolone 80 mg per day was continued, adding methotrexate 2.5 mg weekly to the regimen as long-lasting immunosuppressive therapy was probably needed.
However, the therapy was complicated in several ways. Firstly, by the end of the first month of therapy our patient developed diabetes mellitus and deep venous thrombosis. Subsequently, severe liver function abnormalities developed after methotrexate was started (Table 
). Therefore, this drug was substituted by azathioprine in a step up dosage regimen up to 100 mg daily. Hereafter, a severe and long-lasting pancytopenia developed (Table 
). Bone marrow analysis showed hyperplastic erythropoiesis and hypoplastic granulopoiesis compatible with a side effect of the immunosuppressive therapy. The azathioprine was therefore stopped and prednisone 20 mg per day was continued.
After recovering from the pancytopenia, mycofenolaatmofetil was added starting at 500 mg daily and in increased dosage to 1000 mg bid. During this whole episode prednisone treatment was maintained at a dosage of 20 mg daily. A severe intercurrent herpes infection was treated with intravenous valcyclovir.
After a course of 18 months, our patient has not had any relapse of his neurological deficits. There were no cranial nerve deficits, no pareses and his gait was normal.
We made the diagnosis of CLIPPERS combining the clinical and typical MRI findings only after exclusion of other possible diagnoses. We choose not to perform a biopsy because of the localization of the abnormalities and because the imaging results and clinical presentation were very similar to the patients described by Pittock et al.
[].
In most of previously published studies it was mentioned that discontinuation of steroid treatment led to a clinical relapse (Table 
). Mean follow up time of all published reports so far was 28 months (3–144 months), and no successful steroid discontinuation was reported.
It is known that induction of remission by using glucocorticosteroids followed by maintenance glucocorticosteroid combining other immunosuppressive therapy in autoimmune diseases such as vasculitides should be continued for at least 2–5 years
[,]. Since CLIPPERS has comparable pathologic features as in vasculitides consisting of perivascular lymphocytic infiltrate, it seems likely that tapering of maintenance therapy should be proposed only after 2–5 years of treatment guided by clinical monitoring and follow up MRI.
Finally we emphasize that in clinical practice one must pay attention to the adverse events, as described in our case. We recommend tapering immunosuppressive therapy in conjunction with frequent clinical monitoring and imaging, thus enabling us to treat any further relapse on time. Our findings support the need for further follow up studies to determine the duration of treatment.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 70.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1534,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8091996-1,Extracted,"A 62-year-old female with diabetes mellitus, hypertension, and dyslipidemia presented to the emergency department with multiple episodes of syncopal attack. Further history revealed that she had the multiple episodes of vomiting and diarrhea prior to that. She denied chest pain, shortness of breath, or any other symptoms. She was on oral telmisartan 40 mg OD, atenolol 50 mg OD, diltiazem 60 mg TDS, frusemide 60 mg OD, metformin 1 g BD, aspirin 75 mg OD, and atorvastatin 20 mg QHS. She was compliant to her medications and there was no history of drug overdose. Upon presentation, the patient was drowsy with cold peripheries and poor pulse volume. Blood pressure was 105/41 mmHg, and heart rate was 40 beats/min (bpm). Other examination findings were unremarkable. Electrocardiogram (ECG) showed junctional bradycardia with a heart rate of 40 bpm []. Renal profile showed potassium: 6.3 mmol/l (normal value: 3.3–5.1 mmol/l), urea : 10.9 mmol/l (normal value: 1.7–8.3 mmol/l), and creatinine : 175 μmol/l (normal value: 60–120 μmol/l). Intravenous (IV) bolus of 20 ml/kg of normal saline was started, and two doses of IV atropine 0.5 mg were given but there was no improvement. We proceeded with giving 10 ml of IV calcium gluconate 10%, 50 ml of dextrose 50% and 10 unit of IV insulin infusion. She required catecholamine infusion with dopamine up to a dose of 20 μg/kg per minute and adrenaline of 5 μg/minute. After completing the first dextrose/insulin infusion, potassium from blood gas returned as 5.6 mmol/l. We proceeded with second round of dextrose/insulin infusion, and she showed marked improvements with a return to sinus rhythm and heart rate of 75 [] subsequently. Catecholamine infusion was weaned off gradually. Repeated serum potassium returned to 3.5 mmol/l.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [105.0, 'mm hg'], 'Diastolic Blood Pressure': [41.0, 'mm hg']}",62.33333,59.21666,65.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 105.0 mm Hg + 2/3 * 41.0 mm Hg = 62.33333 mm Hg.
Hence, the patient's mean arterial pressure is 62.33333 mm Hg."
1535,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8665670-1,Extracted,"A 61-year-old male was admitted for acute alcohol intoxication and concern for impending withdrawal. At presentation, he was alert and oriented but tremulous and tachycardic to 110 beats per minute with normal blood pressure. Abdominal examination was normal. Clinical Institute Withdrawal Assessment Score (CIWA) of 6, indicating mild withdrawal requiring no medications. He had no nausea, vomiting, abdominal pain, or distension. Past medical history included hypertension, hyperlipidemia, alcohol abuse, and an episode of alcoholic pancreatitis. No cirrhosis, portal hypertension, or esophageal varices.
Laboratory findings were significant for an elevated alcohol level of 497 mg/dL, a microcytic anemia with a hemoglobin of 10.7 g/dL (13-15 g/dL), and mean corpuscular volume of 103 fL (80-100 fL), platelets of 111 x 10^3/μL (150-400 x 10^3/μL), aspartate aminotransferase 396 U/L (5-30 U/L), alanine aminotransferase 162 U/L (5-30 U/L), total bilirubin of 1.3 mg/dL (0.3-1 mg/dL) potassium of 3.4 mmol/L (3.5-5 mmol/L), and magnesium 1.7 mg/dL (1.7-2.2 mg/dL), lipase 149 U/L (10-150 U/L).
Initial supportive treatment included fluids with electrolyte repletion, thiamine, and folate infusion. The patient received a total of 6 mg of lorazepam (2 mg each) in the first 24 hours for CIWA scores of more than 8.
On day 3 of admission, the patient was agitated with visual and tactile hallucinations, tremulousness, and tachycardia ranging in 120s with a CIWA score of 12. The patient's lorazepam requirement went up to 16 mg over two hours. Chlordiazepoxide 50 mg every six hours was added to the regimen to control the withdrawal and was up-titrated to 100 mg every six hours. Due to concern for impending delirium tremens, the patient was admitted to the medical intensive care unit. On day 4 of his admission, the patient had become more agitated with uncontrollable shaking, raising blood pressure to 180/100 mmHg, suggestive of delirium tremens. Continuous infusion of dexmedetomidine was initiated at a rate of 0.2 μg/kg/hr and up-titrated to 1.5 μg/kg/hr with a dramatic resolution of withdrawal symptoms, and the patient became hemodynamically stable.
On the evening of his fifth day of admission, the patient was had voluminous, bilious, non-bloody vomiting with abdominal distension and diarrhea. A nasogastric (NG) tube was inserted with an estimated 1800 mL of output was noted over half an hour. Imaging was performed via bedside ultrasound (Figure ) while waiting for an x-ray (Figure ) confirmation of NG tube placement. Large, dilated bowel loops were noted on the ultrasound, confirmed by abdominal x-ray showing dilated small bowel loops (>3 cm) and dilated cecum of about 8.6 cm with no free air. Stool studies for Clostridioides difficile were negative. The patient developed hypoxic respiratory failure secondary to aspiration pneumonia and was intubated and treated with empiric piperacillin/tazobactam. He was switched from dexmedetomidine to fentanyl and midazolam for sedation. Computed tomography with oral contrast of the abdomen and pelvis showed oral contrast throughout the small bowel without evidence of mechanical bowel obstruction yet with bowel loops dilatation. Colonic dilatation was most pronounced within the transverse colon, measuring up to 6.7 cm. Laboratory data showed normal electrolytes, liver enzymes, and lipase.
The patient continued to have large volume output from the NG tube on day 7, significantly reduced by day 8 (Table ). Extubation was planned, and the patient was transitioned back to dexmedetomidine 0.2 μg/hr/kg for sedation. A correlation between days-on-dexmedetomidine and NG tube output was noticed, and we suspected a pseudo-obstruction related to dexmedetomidine; thus, on day 10 of admission, dexmedetomidine was stopped, and the patient was successfully extubated, followed by reduction of NG tube output, resumption of intestinal motility, and reduction of abdominal distension.
On day 11, NG tube was significantly reduced and was subsequently removed. The patient had an uneventful remainder of his hospital course and was discharged afterward.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [180.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",126.66667,120.33334,133,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 180.0 mm Hg + 2/3 * 100.0 mm Hg = 126.66667 mm Hg.
Hence, the patient's mean arterial pressure is 126.66667 mm Hg."
1536,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8526074-1,Extracted,"A 44-year-old female presented to the emergency department complaining of fatigue. She had an episode of chest pain approximately 15 hours before the presentation that lasted several minutes and subsided. She also had a right-sided flank and upper torso discomfort. She exercised regularly and reported that although it could have been a muscle pull, it felt different. The day prior she had experienced one episode of feeling slightly short of breath. Both the pain and shortness of breath had resolved, and she had been asymptomatic for the last 15 hours. The symptom that concerned her the most was extreme tiredness. She explained that for the last three days, she had been feeling incredibly tired despite being very active with a full-time job during the day and raising a family. She was concerned because she was wondering if her tiredness was caused by her thyroid. The patient had a thyroidectomy at age 18 for a nodule and had been on thyroid supplementation ever since. She requested to get her thyroid level checked. The patient had no risk factors for coronary artery disease, nor did she have a family history of coronary artery disease or stroke. In addition to the thyroid medication, she did not take any other medications. The patient had a normal body mass index and was a nonsmoker.
Her vital signs were temperature of 97.8°F, blood pressure 140/63 mmHg, pulse rate 54 beats per minute, respiration rate 15 breaths per minute, and oxygen saturation of 100%. The patient’s laboratory results were unremarkable (Table ).
Urinalysis revealed moderate hematuria. A chest radiograph demonstrated a contour abnormality at the right hemidiaphragm suggesting lateral eventration of the diaphragm and a pulmonary mass on the right (Figure ).
Chest CT revealed a large mass in the right lateral costophrenic recess. The imaging features were consistent with a benign pulmonary tumor such as hamartoma, given the suggestion of internal fatty features and lack of erosion or compromise of the adjacent chest wall (Figure ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [63.0, 'mm hg']}",88.66667,84.23334,93.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 63.0 mm Hg = 88.66667 mm Hg.
Hence, the patient's mean arterial pressure is 88.66667 mm Hg."
1537,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8154378-1,Extracted,"A 70-year-old man was admitted to hospital for a 2-month history of repeated cough, low grade fever, hemoptysis, and left back shoulder pain, which was not relieved by nonsteroid anti-inflammatory drugs. Meanwhile, he complained of intermittent diffuse abdominal discomfort and chronic persistent constipation. He had a history of a traffic accident 2 years ago, and his chest wall was wounded, although the thoracic computed tomography (CT) scanning at that moment did not present any significant bone fracture. Incidentally, a 2.4 × 2.5-cm solid nodule was detected in the left upper lung. He was an active smoker with a 200-pack-year smoking history. His body temperature was 36.6 °C, and blood pressure was 130/90 mm Hg. Physical examination showed slightly decreased breath sounds in left apical area on auscultation, with left back pain when pressing the scapular area; other physical examination parameters were unremarkable. Laboratory tests showed that his blood count, serum electrolytes, and renal and liver functions were within normal limits. SAA protein was 34 mg/L (normal 0–10 mg/L). Laboratory test showed elevated tumor markers, with CEA of 5.9 ng/ml (normal 0–5 ng/ml) and cytokeratin fragment of 6.9 ng/ml (normal 0.1–3.3 ng/ml). Serum immunoelectrophoresis revealed 2 minor M-peaks in the gamma region, without significant monoclonal gammopathy, and the concentration of 2 M-peaks was 1.4 g/dl. Urine protein electrophoresis were negative for Bence-Jones, whereas the rest of the hematological and biochemical parameters were all normal.
The 18F-2-fluoro-2-deoxy-D-glucose (18F-FDG) positron emission tomography/computed tomography (PET/CT) MIP revealed a large mass with intense FDG uptake in the left upper lung lobe (the maximum of standard uptake value =19.9, Fig. ) and diffuse amorphous calcifications located in the greater omentum, mesentery of small bowel and colon (Fig. ).
A percutaneous CT-guided thoracoscopic biopsy of the lung mass was subsequently performed, showing poorly differentiated squamous cell carcinoma. Meanwhile, pathological findings showed that the specimens of resected peritoneum contained amorphous, homogeneous material with some polyclonal plasma cells, lymphocytes and giant cells, while additional stain with Congo red revealed characteristic amyloid depositions (Fig. ).
The patient underwent surgery to remove the lung cancer, followed by chemotherapy. He did not receive any treatment against amyloidosis. Unfortunately, his condition rapidly deteriorated at the beginning of the fourth cycle of chemotherapy, and he died of a severe respiratory infection.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 90.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
1538,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8177025-1,Extracted,"A 53-year-old male without known significant past medical history presented to the emergency department for a gunshot wound to the left foot. He reported leaving a bar when a shot was fired, hitting him in the foot. He noted pain and bleeding but was able to walk. His pain was worsened with palpation to the affected site. The patient denied any significant family history. His social history was significant for tobacco use of two packs per day and alcohol use of six to 12 beers a day.
Upon arrival, blood pressure was 152/85 mmHg, pulse was 76 bpm, respiratory rate was 18 bpm, the temperature was 97.6°F, and O2 saturation was 100% on room air. On examination, there was a wound with associated tenderness and edema to the medial aspect of the left foot with no other findings noted. A left foot x-ray was ordered and tetanus, diphtheria, and pertussis (Tdap) vaccine were administered intramuscularly. X-ray imaging revealed a large bullet fragment in the plantar soft tissue beneath the medial cuneiform as well as punctate fragments in the medial soft tissue near the large fragment. There were no fractures noted on imaging (Figure ).
Lidocaine 1% with epinephrine was administered locally and removal of the bullet was attempted. The bullet path was tracked by following pieces of thread detached from the patient’s shoe, which was found to be wrapped around the bullet (Figure ).
Bullet extraction was performed by pulling the shoe fibers along the bullet path. The severed tendon was visible upon extraction following bullet removal. Plantar and dorsiflexion of all toes of the left foot were intact. Orthopedic surgery was consulted and recommended a repeat x-ray which showed removal of the large bullet fragment in the plantar soft tissues (Figure ).
The patient was discharged with topical bacitracin and ciprofloxacin 500 mg tablet two times daily for seven days. He was provided with crutches and instruction for outpatient management with orthopedic surgery. The patient did not follow up for further management.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [152.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",107.33333,101.96666,112.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 152.0 mm Hg + 2/3 * 85.0 mm Hg = 107.33333 mm Hg.
Hence, the patient's mean arterial pressure is 107.33333 mm Hg."
1539,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5340034-1,Extracted,"The patient was a 69-year-old Japanese man with a history of type 2 diabetes since 7 years ago. He had been taking oral medication for it but had stopped treatment on his own accord 3 years earlier. He had no co-morbids of diabetes.
He visited the emergency department for fever and general malaise that had been ongoing for 2 weeks. His vital signs were a body temperature of 38.2 °C, blood pressure of 144/60 mmHg, heart rate of 131 bpm, and saturation of peripheral oxygen (SpO2) of 95% (room air). While tenderness was observed in the right hypochondrium, no signs of peritoneal irritation were observed. Blood tests revealed markedly elevated inflammatory response with a white blood cell count of 16,400/μL and C-reactive protein level of 26.5 mg/dL. His aspartate transaminase (AST) level was 371 U/L, alanine aminotransferase (ALT) level was 331 U/L, alkaline phosphatase (ALP) level was 675 U/L, and gamma-glutamyl transpeptidase (γ-GTP) level was 197 mg/dL, indicating liver dysfunction. Procalcitonin (PCT) was high at 26.23 ng/mL, suggesting sepsis. In addition, markedly impaired glucose tolerance was noted with a blood sugar level of 571 mg/dL and glycated hemoglobin (HbA1c) level of 14.6%. The patient tested negative for urine ketones and had an arterial blood pH of 7.36, indicating no acidosis.
Simple abdominal radiography revealed gas in the right subphrenic space (Fig. ). A hypoechoic lesion with indistinct boundaries was also noted in the right hepatic lobe on abdominal ultrasound, and a number of hyperechoic findings suggestive of air were observed within this lesion (Fig. ). Abdominal computed tomography (CT) revealed an abscess 5 cm in diameter in the right hepatic lobe, within which gas-related fluid formation was observed (Fig. ). The patient underwent emergency percutaneous abscess drainage and placement of an 8-Fr tube. The aspirate was reddish-brown and purulent, and Klebsiella pneumoniae was detected in cultures (Fig. ). The same bacterium was also detected in two blood cultures. The sensitivity is presented in Table . A pathological examination of the drained effluent was also conducted, revealing no malignant findings.
The patient was admitted to the intensive care unit and started on antibiotics (meropenem at 3 g/day) and glucose control by continuous intravenous infusion of insulin. Four days later, the patient was transferred to the general ward. Based on culture sensitivity, the antibiotic was changed to ceftriaxone at 4 g/day, which was continued for 2 weeks. Upper and lower endoscopy revealed no evident abnormalities, and magnetic resonance cholangiopancreatography (MRCP) revealed no gallstones or biliary tract tumors. The patient tested negative for human immunodeficiency virus (HIV) antibodies, and, 3 weeks later, the drainage tube was removed and the patient was discharged without sequela.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [144.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",88,83.6,92.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 144.0 mm Hg + 2/3 * 60.0 mm Hg = 88.0 mm Hg.
Hence, the patient's mean arterial pressure is 88.0 mm Hg."
1540,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5351162-1,Extracted,"A 24-year-old African woman, gravida 4 para 3, presented with a 2-week history of right upper quadrant pain and an 8 weeks and 5 days amenorrhea with spotting. She first consulted in a secondary health facility where her clinical evaluation revealed a hepatomegaly on abdominopelvic ultrasound and positive urinary pregnancy test without intrauterine or tubal gestational sac. These findings motivated the medical team to refer her to our tertiary center.
This was her first episode of such pain. She had no history of sexually transmitted diseases and no history of contraception. She had never had an operation. Her hepatitis B and C status were unknown. There was no dizziness, asthenia, or jaundice.
Her vital signs were stable: blood pressure of 120/60 mm Hg, pulse rate of 70 beats per minute, respiratory rate of 16 cycles per minute, and temperature at 36.5 °C. She weighed 59 kg. She was not pale. Her right upper quadrant was tender on deep palpation but not after deep breath. There was no guarding or rebound tenderness. Her uterus was of normal size and there were no adnexal masses noted. Her rectovaginal pouch was free and non-tender. We suspected acute cholecystitis or acute viral hepatitis in pregnancy.
On another abdominopelvic ultrasound, a heterogeneous poorly vascularized mass was visible under the right lobe of her liver, of size 42 × 38 mm. There was no hemoperitoneum and her uterus was empty without adnexal masses. On full blood count, there was mild microcytic and hypochromic anemia at 10.2 g per dL, with normal leukocyte and platelet counts. Her liver transaminases and renal function were normal. Her serum β-human chorionic gonadotropin (βhCG) titers rose from 200 mUI/mL to 3000 mUI/mL in 48 hours. No gestational sac was visible on concomitant pelvic ultrasound.
Our final diagnosis was hepatic pregnancy. We chose to administer 1 mg/kg of methotrexate intramuscularly since she was hemodynamically stable and the Fernandez score [] was in favor of medical treatment. Evolution was favorable and she was discharged at day 5. Two weeks later, her serum βhCG titer was 15 mUI/mL. She did not show up at 1-month appointment.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 60.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1541,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3460157-1,Extracted,"A seventeen-year-old pregnant woman with a mesencephalic tumor and VP drainage was admitted to the Obstetric Department to be prepared for elective C-section. Anamnestically, and from the available medical data, we discovered that the patient had the mesencephalon tumor since her 9th year. During her childhood, VP drainage was implanted, because of the brain tumor, and an attempt of a stereotactic biopsy was performed. The stereotactic biopsy was unsuccessful and was not repeated due to the improvement of the patient's medical condition and the lack of evidence that the illness was progressing. Since then, the patient has been under regular annual neurosurgical control. On the most recent Magnet Resonance imaging (MR), performed one month before her pregnancy, the dimensions of the tumor were: axial 27.7 × 27.2 mm, coronal 28.9 × 19.8, sagittal 27.1 × 23. 2 mm (). Eight obstetric examinations were performed during pregnancy, but no neurosurgical control was performed. We assume that VP drainage worked well because the patient had no symptoms of increased intracranial pressure. There were some complications during the pregnancy. In the 27th week there was a urinary-infection that was treated with antibiotics, and the patient also developed gestational diabetes.
The patient was scheduled for elective C-section because of her prime disease (mesencephalic tumor), breech position of the baby, gestational diabetes and expected weight of the baby of more than 4 kg. Under the assumption that the VP drainage worked well, we decided to perform the operation under spinal anesthesia because of expected difficult airway management. The patient had a Mallampati score IV, edematous soft tissue of the face and mouth and a high Body mass index (BMI) 38.
Coagulation parameters were good: prothrombin time 10 s, platelets count 386 × 109/L, and blood pressure was 150/100 mmHg. The patient signed the informed consent and was prepared for a regional anesthesia with intravenous prehydration. Spinal block was performed with a pencil point spinal needle 27 G, at the L3-L4 intervertebral space, with hyperbaric bupivacaine 8 mg plus fentanyl 15 µg.
The patient's height was 157 cm and her weight was 95 kg. We used the manufacturer's dose recommendation (from 10-20 mg), though with a reduction because of the substitution of fentanyl. Sensory block Th 5 was reached within 5 minutes. The patient was hemodynamically stabile during the anesthesia, systolic blood pressure was between 120 and 150 mmHg, pulse was 80-120/min, and oxygen saturation was 100%. The operative procedure was uneventful; a female child was born, weighing 4,050 g, and 50 cm in length. The Apgar score in the first and fifth minute was 10/10. The postoperative period was also uneventful, so the mother and child were discharged from the hospital on the 8th day after birth.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [100.0, 'mm hg'], 'Systolic Blood Pressure': [150.0, 'mm hg']}",116.66667,110.83334,122.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 100.0 mm Hg = 116.66667 mm Hg.
Hence, the patient's mean arterial pressure is 116.66667 mm Hg."
1542,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5635456-1,Extracted,"A 70-year-old Asian man with diabetes mellitus treated with oral hypoglycemic agents and a history of myocardial infarction managed with percutaneous coronary intervention and antiplatelet drugs visited the emergency department (ED) of our hospital complaining of 7 days of progressive chest discomfort, fever, and chills. Ten days prior, he visited a local clinic with left upper back and shoulder pain. He was diagnosed with myofascial pain syndrome and received a TPI with lidocaine using a 21-gauge, 2.0-inch needle in the left upper trapezius. Three days after the injection, he complained of substernal chest pain of a squeezing nature and chills, and visited the ED of another hospital. Coronary angiography at that hospital was normal. His symptoms progressively worsened despite administration of analgesics, and he was transferred to our hospital.
He was an active smoker, with a cumulative exposure of 35 pack-years, and a heavy drinker, consuming 1 bottle of alcohol daily. He did not have clinical evidence of a recent head and neck infection or trauma. He was 163 cm tall and weighed 60.3 kg (body mass index, 22.7 kg/m2). In the ED, his blood pressure was 120/78 mmHg, heart rate was 110 beats/min, oxygen saturation was 97%, and axillary temperature was 38.2°C. A physical examination revealed tenderness and redness from the left side of the upper sternum to the same side of the shoulder. The other examination results were normal.
Laboratory data were significant for a white blood cell count of 19.9×109/L, with 86.7% neutrophils. Both C-reactive protein and erythrocyte sedimentation rate were elevated, at 26.5 mg/L (reference, <0.5 mg/dL) and 80 mm/hr (0–10 mm/hr), respectively. Arterial blood gas analysis showed pH 7.48, PCO2 28 mmHg, PO2 115.3 mmHg, and HCO3 20.9 mmol/L. Serum glucose was 249 mg/dL and a urine test strip was 4+ for glucose. Other laboratory test results were normal, including plasma levels of electrolytes, troponin, and creatinine kinase-MB. Aerobic and anaerobic blood cultures were drawn before empirical antibiotic treatment.
Chest radiography showed upper mediastinal widening, protrusion of the aortic arch, and consolidation in the left upper lobe (). Contrast-enhanced chest computed tomography (CT) revealed a 3.8×3-cm outpouching low-density lesion with an infiltrative margin arising from the aortic arch, diffuse mild wall-thickening in the aorta, and an incidental 6.8-cm heterogeneous enhancing mass in the right hepatic lobe (). Magnetic resonance imaging of the liver suggested hepatocellular carcinoma in the S7 segment.
He was treated immediately with intravenous ceftriaxone and metronidazole, and the initial blood culture revealed Staphylococcus aureus. Based on clinical and radiological features, he was diagnosed with DNM after TPI.
Fever persisted following the ED visit, and both C-reactive protein and erythrocyte sedimentation rate remained elevated, at 23.6 mg/L and 37 mm/hr, respectively. Antibiotics were changed on hospital day 3 to piperacillin/tazobactam. However, intermittent fever persisted until hospital day 5, and finally subsided when the antibiotics were changed to meropenem and vancomycin.
On hospital day 9, he had hemoptysis. Follow-up CT showed increased mediastinal infiltration and a low-density lesion with an air bubble and a penetrating atherosclerotic ulcer at the aortic arch (). Based on the CT, we explained the process of surgical drainage. However, he and his family refused aggressive management such as surgery, because of the risk of sudden death during the operation, poor prognosis of underlying hepatocellular carcinoma, and his age. Despite antibiotic therapy, his general condition worsened, and he authorized a do-not-resuscitate order. On hospital day 30, he died because of septic shock.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [78.0, 'mm hg'], 'Systolic Blood Pressure': [120.0, 'mm hg']}",92,87.4,96.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 78.0 mm Hg = 92.0 mm Hg.
Hence, the patient's mean arterial pressure is 92.0 mm Hg."
1543,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8446545-1,Extracted,"A male patient in his 50s had dizziness for 12 days that was not relieved after administration of medications. He had a history of smoking for 20 years with an average of six cigarettes per day and alcohol abuse for 30 years. Physical examination demonstrated blood pressure 123/78 mmHg, clear consciousness, slightly bad spirits, and no abnormality in the cranial nerve. Muscle strength and tension of limbs were normal. Auxiliary examination showed nothing abnormal in the electrocardiogram or laboratory tests (blood and urine routine, biochemical series, and coagulation items). MRI, MR angiography (MRA), and CT angiography (CTA) revealed occlusion of the right vertebral artery at the V4 segment (), which was confirmed by diagnostic digital subtraction angiography (DSA). The patient did not have a family history or genetic information of cerebral infarction or any previous endovascular treatment. Because medication did not perform well, the ischemic symptoms might be further aggravated, resulting in cerebral infarction and even death. To prevent aggravation of this condition, endovascular treatment was performed with written informed consent from the patient. The procedure was conducted under general anesthesia after administration of dual antiplatelet therapy with aspirin (100 mg/d) and clopidogrel (75 mg/d) for 3 days. The Seldinger technique was applied to gain percutaneous access to the femoral artery before insertion of a 6F introducer sheath, and heparin (70 U/kg) was administered intravenously to achieve an activated coagulation time of 150–200 s. DSA was performed to show the anatomy of the occluded artery, and a 300-cm Traxcess micro-guidewire (0.014 inch, Medtronic Inc., Minneapolis, MI, USA) was used to explore and navigate through the occluded segment before being put at the distal P1 segment of one posterior cerebral artery (PCA). Then, an Echelon 10 microcatheter (Medtronic) was sent along the micro-guidewire across the occluded segment to the same distal P1 segment of PCA, and gentle angiography through the microcatheter was performed to demonstrate the vascular structures. An angioplasty balloon catheter (Gateway, Boston Scientific, Natick, Massachusetts, USA) was advanced over the microwire, centered across the lesion, and inflated slowly for angioplasty (2.0 × 13 mm balloon) before an Enterprise stent (4.5 × 28 mm) was deployed at the occluded segment after accurate positioning (). At the time of stent deployment, the vertebral artery was straightened and smooth (), and the proximal end of the stent was wide open with the proximal markers of the stent being spread out (). Once the micro-guidewire and the conveying microcatheter were withdrawn, the stent proximal end was collapsed because of compression of the wall of the curved artery, which was exhibited by the closed proximal markers in close contact (). We tried to navigate a microcatheter (Excelsior SL-10, Stryker Neurovascular, Fremont, California, USA) into the proximal end of the stent, but this was unsuccessful. Then, the 300-cm micro-guidewire was navigated to the stent proximal end and passed through the proximal lateral mesh of the stent (). Once the micro-guidewire was sent to the distal segment of the basilar artery, the vertebral artery was straightened, and the stent proximal end was opened with the proximal markers being spread out again (). Then, a second 200-cm Synchro micro-guidewire was navigated right through the stent proximal end into the real lumen of the stent and sent to the distal segment of basilar artery (, ). After the 300-cm micro-guidewire was withdrawn, an Apollo 2.5 × 10 mm balloon-expanded stent (MicroPort Medical, Shanghai, China) was navigated along the Synchro micro-guidewire to overlap partially with the proximal segment of the Enterprise stent and was expanded with 4 atm pressure to support the proximal end of the first stent (). Angiography revealed good apposition of the two stents against the arterial wall with unobstructed blood flow through the stents and improved blood flow in the distal segment. Then, the micro-guidewire and microcatheter were withdrawn. Postoperative vertebral angiography showed complete recanalization of the occluded arterial segment (), and the Thrombolysis in Cerebral Infarction blood flow was grade 3. DynaCT scan revealed partially overlapped stents (). After stenting, both stents were well-patent with favorable forward flow (). At follow-up 6 months later, head CT showed no obvious abnormality, and physical examination revealed nothing abnormal in the cranial nerve. DSA demonstrated patent stents and unobstructed blood flow through the stents ().",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [123.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",93,88.35,97.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 123.0 mm Hg + 2/3 * 78.0 mm Hg = 93.0 mm Hg.
Hence, the patient's mean arterial pressure is 93.0 mm Hg."
1544,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7445108-1,Extracted,"A 40-year-old, previously healthy Sri Lankan woman was presented with a history of fever of 12 days duration, which was associated with myalgia, polyarthralgia involving large and small joints, malaise, and other constitutional symptoms. She also did admit to a history of headaches mainly confined to frontal areas without photophobia or symptoms of rhinosinusitis. She experienced nausea and vomiting for proceeding few days but denied diarrhea and abdominal pain. She had no symptoms that can localize the site of infection to either the respiratory or genito-urinary tract.
On arrival, she was alert (Glasgow Coma Scale (GCS) 15) and recorded a high-grade fever (40.0°C). A general examination revealed pale conjunctivae and an eschar noted in the right inguinal area (Figure ), with tender right inguinal lymphadenopathy. She had no neck stiffness or maculopapular rash. The initial cardiovascular assessment showed a blood pressure of 110/70 mmHg with a pulse rate of 120 regular beats per minute. The rest of the clinical examination was unremarkable. Based on the above clinical findings, she was diagnosed with scrub typhus.
Her initial investigations revealed pancytopenia, with a white blood cell (WBC) count of 1940/mm3, hemoglobin of 7.6 g/dL, and platelet count of 35,000/mm3. Inflammatory markers and hepatic transaminases were raised (C-reactive protein (CRP) 43.1 mg/L, erythrocyte sedimentation rate (ESR) 106 mm at the first hour, aspartate aminotransferase (AST) 537 U/L, alanine transaminase (ALT) 279 U/L). The rest of the basic biochemical profile, including renal function, showed no abnormalities (Table ).
Mild splenomegaly was detected on an ultrasound scan of the abdomen with no other abnormalities. The indirect fluorescent antibody test for scrub typhus was performed, and it showed positive. Laboratory evaluation for dengue fever (nonstructural protein 1 (NS1) antigen, immunoglobulin M (IgM), and IgG antibody for dengue) came negative. The blood picture showed severe neutropenia, thrombocytopenia with severe anemia, with no evidence of disseminated intravascular coagulation or abnormal cells.
On observation of progressively worsening pancytopenia, the rare association of hemophagocytic lymphohistiocytosis was considered. Further investigations revealed serum ferritin of 725 ng/mL and isolated hypertriglyceridemia of 3.72 mmol/L. Subsequently, she underwent bone marrow aspiration, which showed an increased number of histocytes and hemophagocytosis and these findings were compatible with a diagnosis of hemophagocytic lymphohistiocytosis likely to be secondary to underlying infection (Figure ). As she was fulfilling six out of eight criteria for the diagnosis of hemophagocytic lymphohistiocytosis, the rare association of hemophagocytic syndrome triggered by scrub typhus was made. Further, other common precipitating causes for hemophagocytic syndrome such as Epstein-Barr virus (EBV) and cytomegalovirus (CMV) infections were excluded by negative antibody tests.
The patient was commenced on doxycycline along with other supportive care, including packed cell transfusion. After three days of antibiotic treatment, progressive pancytopenia started to show signs of improvement in all three cell lines. On Day 6 following admission, she was sent home with hemoglobin of 8.6 g/dL, platelet of 124,000/mm3, and white blood cells of 3,600/mm3. On review in two weeks, she was asymptomatic and her biochemical and hematological profiles were back to normal as a marker of uneventful recovery.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1545,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9299,Extracted,"An otherwise healthy 27-year-old man presents to the Emergency Department with dark urine and left flank pain. He has had a fever, sore throat, and malaise for the last 2 days. Vital signs reveal a temperature of 38.1°C (100.5°F), blood pressure of 120/82 mm Hg, and a pulse of 95/min. His family history is noncontributory. Physical examination reveals enlarged tonsils with tender anterior cervical lymphadenopathy. Urinalysis shows pink urine with 20–25 red cells/high power field and 2+ protein.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [82.0, 'mm hg']}",94.66667,89.93334,99.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 82.0 mm Hg = 94.66667 mm Hg.
Hence, the patient's mean arterial pressure is 94.66667 mm Hg."
1546,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5676363-1,Extracted,"A 50-year-old male sushi chef who had never traveled outside Japan presented with a 2-day history of fever and muscle pain. Laboratory investigation yielded the following results: white blood cells (WBC): 7780/µL; platelets: 89000/µL; C-reactive protein (CRP): 36.4 mg/dL; blood urea nitrogen (BUN): 47 mg/dL; creatinine: 2.41 mg/dL; and total bilirubin (T-Bil): 2.0 mg/dL. The day after he was admitted to the hospital, the patient's condition worsened, as indicated by the laboratory data: WBC: 6700/μL; platelets: 50000/µL; CRP: 32.49 mg/dL; BUN: 66 mg/dL; creatinine: 2.81 mg/dL; and T-Bil: 5.6 mg/dL. He was presumptively diagnosed with bacterial pneumonia, atypical pneumonia, and miliary tuberculosis. He was also diagnosed with leptospirosis on the basis of jaundice, renal failure, and thrombocytopenia. He was administered the broad-spectrum antibiotics ceftriaxone, levofloxacin, and minocycline on the first day of admission to the referral hospital. Vancomycin and meropenem were administered on the second day. He was also given the antitubercular agents—isoniazid, rifampicin, pyrazinamide, and ethambutol—even though the results of a tuberculosis screening test were negative. Despite these treatments, his systolic blood pressure dropped to 70 mmHg, and his respiratory condition deteriorated; he was intubated 5 days after the onset of symptoms, which is three days after admission to the previous hospital. An X-ray showed bilateral alveolar infiltrates, and blood gas analysis revealed the following: pH: 7.390; partial pressure of arterial carbon dioxide (PaCO2): 28.3 mmHg; and partial pressure of arterial oxygen (PaO2): 70.4 mmHg HCO3− 16.8 mmol/L with fraction of inspired oxygen (FIO2) of 1.0 as well as positive end-expiratory pressure (PEEP) of 10 cm H2O. The patient developed a life-threatening condition with septic shock and severe acute respiratory failure, despite optimal medical treatment. He was referred to our center for ECMO. Our ECMO team decided to initiate V-V ECMO at the previous hospital and transport the patient on V-V ECMO because the patient was severely hypoxic and needed maximal doses of norepinephrine, epinephrine, and vasopressin to stabilize his cardiac condition. Cannulation was performed via the right femoral vein with 25-French drainage cannulae (HLS Cannulae Maquet Cardiopulmonary, Hirrlingen, Germany) for access and via the right internal jugular vein with 23-French cannulae for return. The ECMO circuit was an adult ECMO bypass custom tubing pack consisting of a Rotaflow® centrifugal pump (Maquet Cardiopulmonary GmbH, Hirrlingen, Germany) and gas exchanger (MERA NHP Excelung NSH-R HPO-23WH-C®, Senko Medical Inc., Tokyo, Japan). V-V ECMO was initiated at a blood flow rate of 4.0 L/min, with sweep gas flow through the oxygenator at 4.0 L/min of 100% oxygen. After the procedure, the patient's SpO2 was 94%, heart rate was 131 beats/min, and blood pressure was 142/74 mmHg on 0.1 μg/kg/min of epinephrine and 0.3 μg/kg/min of norepinephrine. He was transported to our center via ground ambulance.
After he was transported to our ICU, we maintained the ECMO blood flow at >3.0 L/min during the first 3 days of ECMO because his activated partial thromboplastin time was maintained at around 40–50 s, which was lower than normal because of bleeding (). After bleeding was controlled, we decreased the ECMO blood flow gradually to 1.5 L/min when peripheral capillary oxygen saturation (SpO2) was over 90%. During V-V ECMO the mechanical ventilation was set at the lung rest setting, which consisted of a driving pressure of 5 cm of water, PEEP of 12 cm of water, and FIO2 of 0.4. Fiber-optic bronchoscopy showed diffuse endobronchial bleeding. The patient was systemically heparinized to maintain an activated partial thromboplastin time of 40–50 seconds, which was lower than the normal value for V-V ECMO. Dobutamine was initiated at 3 µg/kg/min because transthoracic echocardiography showed that the ejection fraction was 30%, mitral regurgitation was moderate, and tricuspid regurgitation was severe. After initiation of dobutamine, his cardiac function improved, epinephrine was stopped the next day, and norepinephrine was stopped the day after that. He remained oliguric and needed renal replacement therapy for 7 days. At the time of presentation to our center, his WBC count was 18,000/µL, CRP level was 24.52 mg/dL, and procalcitonin level was > 100 ng/mL. Although we thought of a wide variety of infections as differential diagnoses, we strongly suspected leptospirosis on the basis of severe acute respiratory failure, myocardial pericarditis, renal failure, jaundice, and thrombocytopenia, which made us continue the broad-spectrum antibiotics, levofloxacin, vancomycin, meropenem, antitubercular agents, and add benzylpenicillin. Because of pulmonary hemorrhage, he was given a platelet transfusion (20 units) for the first 3 days of V-V ECMO therapy. Even though his pulmonary hemorrhage improved on day 8 of V-V ECMO, computed tomography scans showed bilateral ground-glass opacities, bilateral pleural effusion, and atelectasis. Rehabilitation, including sitting on the edge of the bed and standing, was initiated. On day 6 of ECMO therapy, polymerase chain reaction analysis of urine samples collected at the previous hospital confirmed the presence of leptospiral DNA. The tests for tuberculosis, Legionella urinary antigen, pneumococcal antigen, serum Mycoplasma antibody, and Chlamydia pneumoniae antibody all yielded negative results. We switched the intravenous antibiotics from broad-spectrum antibiotics to benzylpenicillin (12 million units/day).
On day 11 of ECMO therapy, blood tests showed improvements in platelet count and serum CRP, creatinine, and T-Bil levels (). In addition, the amount of sputum decreased, and improvements were observed in his chest X-ray (), compliance, and oxygenation (); therefore, we performed a 2-hour trial off-test. The patient tolerated the trial without O2 flow to the oxygenator; therefore, we decided to wean him off ECMO. He was extubated 2 days after being taken off ECMO and transferred back to the previous hospital 2 days after extubation. His last blood gas analysis revealed the following results: pH: 7.468; PaCO2: 36.6 mmHg; PaO2: 67.2 mmHg; and HCO3−: 26.2 mmol/L on room air. Laboratory investigation revealed the following results: WBC: 7400/µL; platelets: 256000/µL; CRP: 1.13 mg/dL; BUN: 29.1 mg/dL; creatinine: 1.36 mg/dL; and T-Bil: 7.9 mg/dL. Finally, paired serum antibody titer testing (on days 5 and 19 after the onset of symptoms) showed a fourfold or higher increase in antibody titers for Leptospira interrogans serovar Copenhageni and Leptospira interrogans serovar Icterohaemorrhagiae, confirming the diagnosis of leptospirosis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [70.0, 'mm hg'], 'Diastolic Blood Pressure': [74.0, 'mm hg']}",72.66667,69.03334,76.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 70.0 mm Hg + 2/3 * 74.0 mm Hg = 72.66667 mm Hg.
Hence, the patient's mean arterial pressure is 72.66667 mm Hg."
1547,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4130896-1,Extracted,"A 64-year-old man visited our emergency room complaining of epigastric pain and vomiting. He had a history of subtotal gastrectomy, involving a Billroth II reconstruction to treat a peptic ulcer perforation, 25 years previously. He had also undergone endoscopic retrograde cholangiography and cholecystectomy to treat a common bile duct stone and cholecystitis 7 years ago. His vital signs at admission included a blood pressure of 110/70 mm Hg, pulse rate of 88 beats per minute, respiratory rate of 20 breaths per minute, and body temperature of 36.3℃. Physical examination revealed icteric sclera, abdominal distension, and tenderness in the epigastric area. On admission, his complete blood analysis included a hemoglobin concentration of 15.9 g/dL, leukocyte count of 37,470/mm3 (neutrophils 73%), and platelet count of 165,000/mm3. Blood chemistry was analyzed as a total serum bilirubin concentration of 3.2 mg/dL, creatinine of 1.1 mg/dL, aspartate aminotransferase/alanine aminotransferase of 664/240 IU/L, alkaline phosphatase of 190 IU/L, γ-glutamyltransferase of 552 IU/L, amylase of 2,528 µg/dL, and lipase of 3,032 IU/L. A plain radiograph of the abdomen revealed no abnormality and the gas pattern was also normal. Computed tomography (CT) revealed a 2.7×2.5×2.1 cm sized, oval heterogeneous high density lesion in a dilated afferent loop and a diffusely enlarged pancreas with peripancreatic hazy reticular infiltration into fatty tissue ().
An emergency transparent cap-fitted endoscopy procedure was performed on the day of admission to obtain an accurate diagnosis. The site of anastomosis was intact and no stricture was evident. However, a very large yellowish enterolithic impaction was apparent in the distal afferent loop. Injected contrast material could not be passed through the afferent loop because of complete obstruction by the enterolith (). We attempted to remove the enterolith via EHL, employing direct cap-fitted endoscopy. A 3 Fr EHL probe was passed through the biopsy channel of the gastroscope. Next, we performed EHL using an electrohydraulic shock wave generator (Litho-tron EL-27; Olympus Optical, Hamburg, Germany) delivering shocks of increasing power (up to 500 mJ) at 2,000 V with continuous instillation of normal saline under direct endoscopic visualization. Endolith fragmentation was successful and a large fragment was removed by a retrieval net. Thereafter, a large active ulcerative lesion located on a blind pouch of the afferent loop, and an acute circular ulcerative lesion located at the site of stone removal was evident (). No immediate complications developed. Four days later, the patient underwent a second-look endoscopy procedure. There was no residual enterolith, although small ulcers on the proximal afferent loop caused by local pressure were apparent. The patient recovered from pancreatitis without any complications, and was discharged 16 days after the procedure.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1548,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-6079,Extracted,"A 31-year old man presents to the emergency department for blood in his stool. The patient states that he saw a small amount of bright red blood on his stool and on the toilet paper this morning, which prompted his presentation to the emergency department. The patient denies any changes in his bowel habits or in his weight. The patient has a past medical history of asthma managed with albuterol and fluticasone. The patient has a family history of alcoholism in his father and suicide in his mother. His temperature is 97°F (36.1°C), blood pressure is 120/77 mmHg, pulse is 60/min, respirations are 12/min, and oxygen saturation is 98% on room air. On physical exam, the patient has a cardiac and pulmonary exam that are within normal limits. On abdominal exam, there is no tenderness or guarding and normal bowel sounds.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [77.0, 'mm hg']}",91.33333,86.76666,95.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 77.0 mm Hg = 91.33333 mm Hg.
Hence, the patient's mean arterial pressure is 91.33333 mm Hg."
1549,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3902574-1,Extracted,"A 28-years-old woman, with no significant past history, presented with giddiness, abdominal pain, vomiting, breathlessness, and reduced urine output 12 hours after consuming 50 tablets of amlodipine [of 5 mg strength]. She was rushed to a hospital near her home, found to have hypotension with hypoxemia; was intubated, given gastric lavage, inotropic support and 24 hours later, shifted to our hospital At presentation she was found to have blood pressure (BP): 60/40 mmHg, heart rate: 128/min, respiratory rate: 32/min with spO2 on room air: 85%, raised central venous pressure [22 cm of saline], anasarca and crepititions in both interscapular area. She was admitted to the intensive care unit (ICU). Investigations revealed: Total leukocyte count: 18500/uL; neutrophils: 86%, serum creatinine: 1.8 mg/dl (normal range: 0.6-1.3 mg/dl), blood urea nitrogen 42 mg/dl (normal range: 10-20 mg/dl), and features of type -1 respiratory failure (pO2-48 mmHg, pCO2-26 mmHg, pH - 7.52, HCO3-22 mmHg). Ionized serum calcium (4.8 mg/dl; normal range: 4.6-5.6 mg/dl, serum albumin (3.9 mg/dl; range 3.5-5.5 mg/dl), and serum amylase (32 IU/L; range 18-108 IU/L) level at presentation were normal. X-ray of chest revealed bilateral reticulonodular opacities, upper lobar zone venous prominence, bilateral pleural effusion, and no cardiomegaly []. Her electrocardiogram was normal. Echocardiography revealed normal-sized chambers, valves, right and left atrial pressures, and left ventricular ejection fraction. Cultures of blood, urine, and tracheal aspirate were sterile. Intravenous inotropes were continued (dopamine: 10-15 μg/kg/min; noradrenaline: 10-12 μg/kg/min), systolic BP increased to 90-110 mmHg when iv frusemide was added. Two boluses of calcium gluconate were given (10 ml of 10% solution) 15 minutes apart, thereafter, low-dose infusion (at the rate 1 mg/kg of calcium) was started; ionized serum calcium level was maintained between 4.8-5.3 mg/dl. Thoracentesis was performed, 300 ml of exudative effusion (total count: 2800/cmm, leukocytes: 2400/cmm; predominantly lymphocytes; lactate dehydrogenase – 698 U/L; protein – 3 g/dL) was drained from either side. She was ventilated initially invasively, later non-invasively; and empiric broad-spectrum antibiotics covering Gram-positive, Gram-negative organisms and Pseudomonas aeruginosa were started in view of prior hospitalization. Monitored parameters included clinical status, central venous pressure, urine output, fluid, and electrolytes including calcium levels and ECG every 4-6 hrs for first 48, thereafter every 12 hours. Her urine output improved after 24 hours. She was successfully weaned off ventilator after 48 hours; inotropes (noradrenaline after 18 hours, dopamine after 48 hours) and calcium infusion (after 48 hours) were gradually tapered off. She was shifted to a step-down ward from ICU after 72 hours and discharged after 5 days.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [60.0, 'mm hg'], 'Diastolic Blood Pressure': [40.0, 'mm hg']}",46.66667,44.33334,49,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 60.0 mm Hg + 2/3 * 40.0 mm Hg = 46.66667 mm Hg.
Hence, the patient's mean arterial pressure is 46.66667 mm Hg."
1550,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5113,Extracted,"A 45-year-old man presents to the emergency department with concern for a rash. The patient states he has an odd rash on his legs that have not been improving. The patient has a past medical history of a recent myocardial infarction which was appropriately treated, diabetes, hypertension, and dyslipidemia. He has a family history of prostate cancer, Parkinson disease, and depression. His temperature is 98.5°F (36.9°C), blood pressure is 177/108 mmHg, pulse is 90/min, respirations are 14/min, and oxygen saturation is 98% on room air. Physical exam is notable for the finding in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [108.0, 'mm hg'], 'Systolic Blood Pressure': [177.0, 'mm hg']}",131,124.45,137.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 177.0 mm Hg + 2/3 * 108.0 mm Hg = 131.0 mm Hg.
Hence, the patient's mean arterial pressure is 131.0 mm Hg."
1551,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4438664-1,Extracted,"An 11 months 22 days old partially-breastfed female baby was admitted with the complaints of the passage of loose stool since birth, occasional vomiting, and failure to thrive. The stool was watery in nature; frequency was 8-10 times per day, and was not associated with blood or mucous. The parents were healthy but their marriage was consanguineous. Antenatal and birth history included polyhydramniosis and premature delivery at 35 weeks of gestation. The baby's birthweight was 2.1 kg. During her neonatal period, she was admitted to another hospital due to sepsis and hyperbillirubinaemia. Moreover, she had several episodes of hospitalization for the management of persistent diarrhoea before coming to our hospital. There was no history of cyanosis or congenital heart disease. On admission, the patient appeared toxic, had reduced activity, and signs of some dehydration [assessed by Dhaka Method () recommended by WHO]. Her weight on admission was 3.8 kg, and length was 61 cm. Pulse rate was 118/minute with BP 90/50 mm of Hg, temperature 36.8 oC, respiration rate 48/minute, oxygen saturation (SpO2) 99% without applied oxygen on admission. On examination, no chest indrawing was observed, lungs were clear on auscultation, abdomen was soft, mildly distended but bowel sounds were present. She also showed signs of motor delay (neck control was not yet established).
Initially, the patient was managed as a case of chronic diarrhoea with some dehydration and severe acute malnutrition. We also suspected that her reduced activity might be due to electrolyte imbalance or sepsis. Hence, the following investigations were done: complete blood count (CBC), serum electrolyte and creatinine, blood and stool for culture and sensitivity (C/S), routine microscopic examination (RME) of stool and urine, and chest x-ray. The test report for electrolytes showed hypochloraemic hypokalaemia with alkalosis ( and ) which, thereafter, became persistent. Based on these findings, our differential diagnosis now included gastric outlet obstruction, cystic fibrosis, Bartter Syndrome, and congenital chloride diarrhoea (CCD). Subsequent investigations showed normal chloride level in sweat, normal routine microscopy of stool, urinary Na+ was 16 mmol/L (reference value 54-150), K+ 24.52 mmol/L (reference value 20-80), and Cl- 12 mmol/L (reference value 110-250). Tissue transglutaminase immunoglobulin (TtG-IgA) and IgG antibodies were negative, with plasma total protein 86.47 g/L (reference value 64.0-82.0), albumin 48.97 g/L (reference value 34.0-50.0), globulin 37.5 g/L (reference value 23.0-35.0), albumin and globulin ratio 1.31 (reference value 1.10-1.80). Chloride level in stool was 126.6 mmol/L (normal range 6-17 mmol/L), potassium 30.9 mmol/L, and sodium 82.9 mmol/L (normal range 50-60 mmol/L). The diagnosis of CCD was made on the basis of the results of faecal chloride content of >90 mmol/L and faecal chloride more than the sum of faecal Na and K contents and exclusion of other suspected diseases. Genetic testing could not be done due to its unavailability in Bangladesh. Urine and stool culture showed no growth of pathogens. We started oral NaCl and KCl supplementation and commercially-available oral formulation of Omeprazole. Other recommended treatment (with oral butyrate) was not applied as it was not available in Bangladesh. After 15 days of hospitalization, the patient developed fever and respiratory distress. The respiration rate was 64/minute, she was tachycardic (175 beats per minute), and the chest x-ray was suggestive of pulmonary infiltrates. So, we suspected that this was most likely due to a hospital-acquired infection and, initially, the patient was treated with injection Ceftazidime and injection Amikacin. However, no improvement was seen even after 5 days of treatment and, subsequently, the antibiotic was changed to injection Imipenem instead of ongoing medication. In the meantime, the blood C/S report was available, and it showed Acinetobacter species sensitive to Polymyxin B. Therefore, we started injection Polymyxin B. At that time, the patient also developed a changing murmur in addition to fever and anaemia, which raised the possibility of infective endocarditis. We, therefore, arranged an echocardiogram that showed mild coarctation of aorta, mild mitral regurgitation Grade 1, and mild pulmonary hypertension with normal ejection fraction (EF) of 70%. We added Captopril to protect heart failure. After adding Captopril, we found, to our surprise, that the stool output significantly reduced, and serum potassium increased. In response to this observation, we reduced the dose of supplemental KCL and NaCL and continued the treatment with Captopril. This decision was expedited by the fact that the overall condition of the patient was improving. The stool output and consistency was also improving. The patient attended regular follow-up with us, and the electrolyte profile had been normal in the next 6 months. In the first and second follow-up visit, we used Captopril with KCl (), and it showed that the diarrhoea was resolved and serum chloride and total carbon dioxide were also normal. The mother of the patient did not provide Captopril in the preceding one week prior to the third visit according to the advice of the local cardiologist, and the patient again developed alkalosis and hypokalaemia (). The most recent echocardiogram showed trivial MR, good biventricular function: left ventricular ejection fraction (LVEF) 69%, FS 34% left ventricular internal dimension in systole (LVIDs) 15 mm, left ventricular internal dimension in diastole (LVIDd) 24 mm trivial TR were noticed, along with peak pressure gradient (PPG) 10 mmHg, intact interatrial septum (IAS), and interventricular septum (IVS). No PDA or coarctation was seen. No intra-cardiac mass or vegetation was seen. Chamber dimensions and wall motion were normal. All valves were normal. No pericardial effusion was seen; biventricular function was good and, finally, the cardiac anatomy showed normal findings. The patient was gradually gaining weight from 3.8 kg to 7.1 kg in 7 months, and control over her neck was then completely normal. Her blood pressure was normal throughout the follow-up period.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [50.0, 'mm hg']}",63.33333,60.16666,66.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 50.0 mm Hg = 63.33333 mm Hg.
Hence, the patient's mean arterial pressure is 63.33333 mm Hg."
1552,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8608246-1,Extracted,"A previously healthy 49-year-old male who had been a butcher for 10 years, often injured and wounded his hands at work. He was admitted at a local hospital with a 10-hour acute chest pain that was accompanied by sweating, bilateral lower extremity muscle soreness and limited movements. Upon examination, electrocardiogram (ECG) analysis revealed AMI, as well as hypotension with a blood pressure of 75/36 mmHg. Then, he was administered with thrombolysis therapy. Due to unsatisfactory therapeutic effect, he was referred to our hospital.
Physical examination upon admission: body temperature 37.4 °C; a heart rate of 108 beats/min, a respiratory rate of 32 breaths/min while his blood pressure was 96/67 mmHg. Red rash that was fadable by pressing was seen on the shin over the neck and on the upper chest. Heart murmurs were not detected on auscultation and muscle strength testing revealed extremity muscles strength grade 3. The left little finger of the patient exhibited a cutting wound that was attributed to slaughtering pigs 5 days ago. ECG analysis revealed mild ST-segment elevation and abnormal Q waves in III and aVF; sinus tachycardia and complete right bundle branch block (). Transthoracic echocardiography (TTE) analyses revealed suppressed motion amplitude in the basal segments of inferior wall and apical segments without any obvious sign of valve vegetation. Pulmonary computed tomographic angiography (CTA) showed bilateral pleural effusion and inflammation (). Laboratory analysis showed an increased white blood cell (WBC) count (44.84 × 10^9 cells/L) with 95.8% neutrophils, procalcitonin (PCT) at 32 ng/mL, C-reactive protein (CRP) at 170 mg/L, serum creatinine levels of 176.7 umol/L, lactic acid at 3.4 mmol/L, cardiac troponin I (cTnI) level of 24.05 ng/mL, creatine kinase MB (CK-MB) level of 40.3 ng/mL and myoglobin (MYO) at 118.9 ng/mL, while peripheral blood morphology examination revealed that the abundance of middle and late granulocytes were 3%. On this study, the primary diagnosis was AMI and sepsis. Changes in hemodynamic parameters, temperature, inflammatory and myocardial injury markers during hospitalization are shown in –, respectively.
The patient was quickly admitted to the department of cardiac intensive medicine. Aspirin and ticagrelor were administered in combination with antiplatelet aggregation, nadroparin calcium anticoagulant, rehydration, and papaverine hydrochloride, which improved coronary blood flow. In consideration of unidentified infections, he was instantly empirically intravenously administered with piperacillin/tazobactam (4.5 g, every 8 h). A day later, his blood pressure had returned to 104/64 mmHg, but his body temperature fluctuated between 37 and 38 °C. Forty-eight hours later, blood cultures in aerobic and anaerobic bottles were positive for S. suis. Unfortunately, S. suis was not identified at the serotype level due to limited assay conditions. Antimicrobial susceptibility testing revealed sensitivity to ceftriaxone, ampicillin, penicillin, linezolid and levofloxacin, as well as resistance to erythromycin and clindamycin. Based on these findings, we continued with the anti-infection regimen. On day 3 after admission, cTnI, CK-MB and MYO levels decreased to 4.760 ng/mL, 8.80 ng/mL and 45.40 ng/mL, respectively, his body temperature decreased to 36.8 °C and his haemodynamics stabilized. After communicating with family members, he was transferred to a special infectious disease hospital for further treatment on day 4. His WBC count had decreased to 11.79 × 10^9 cells/L with 71.6% neutrophils when he was transferred to the special infectious disease hospital.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [96.0, 'mm hg'], 'Diastolic Blood Pressure': [67.0, 'mm hg']}",76.66667,72.83334,80.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 96.0 mm Hg + 2/3 * 67.0 mm Hg = 76.66667 mm Hg.
Hence, the patient's mean arterial pressure is 76.66667 mm Hg."
1553,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7826,Extracted,"A 5-year-old girl is brought to her pediatrician by her mother. The mother is concerned about a fine, red rash on her daughter’s limbs and easy bruising. The rash started about 1 week ago and has progressed. Past medical history is significant for a minor cold two weeks ago. The girl was born at 39 weeks gestation via spontaneous vaginal delivery. She is up to date on all vaccines and is meeting all developmental milestones. Today, she has a heart rate of 90/min, respiratory rate of 22/min, blood pressure of 110/65 mm Hg, and temperature of 37.0°C (98.6°F). On physical exam, the girl has a petechial rash on her arms and legs. Additionally, there are several bruises on her shins and thighs. A CBC shows thrombocytopenia (20,000/mm3). Other parameters of the CBC are within expected range for her age. Prothrombin time (PT), partial thromboplastin time (PTT), and metabolic panels are all within reference range.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 65.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1554,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7434254-1,Extracted,"A 27-year-old female presented to the emergency department (ED) for swelling and redness of the left neck. She noted having a “pimple on her chin” two weeks prior, which she popped. A few days later, she developed swelling to her left neck and jaw. The swelling progressed and required emergent intubation and an intensive care unit admission at a nearby hospital for one week. Her treatment included IV antibiotics and steroids without surgical drainage. After extubation, she exhibited concern for proper treatment and left against medical advice (AMA). The next day she presented to our ED. The patient stated that she was also treated for a “lung infection,” but was unclear of the diagnosis. She noted that over the prior few days her “neck infection,” which initially improved, had increased swelling and redness. She denied any difficulty swallowing or speaking, fever, nausea, or vomiting. She was unsure of her diagnosis or specific antibiotic treatment and could not recall whether any cultures were obtained.
Upon arrival to the ED, the patient’s blood pressure was 107/68 milligrams of mercury with a pulse of 99 beats per minute and temperature of 98.2° Fahrenheit (36.8°Celsius). Her respiratory rate was 20 breaths per minute, and oxygen saturation on room air was 98%. Her height was 1.575 meters (5′2″) and weight was 83 kilogram (kg) (183 pounds) with a body mass index of 33.47 kg per meters squared (m2) (reference range 18.5–24.9 kg/m2).
On physical exam, the patient was oriented to person, place, and time; however, she appeared visibly dyspneic ambulating from the waiting area to exam room. She had a pressure ulcer on the lower lip (likely from endotracheal tube), and fluctuance, erythema, and tenderness to teeth numbered 18 and 19. There was a large area of erythema, induration, and warmth on the left mandible, approximately 10 × 6 centimeters (cm), with no central fluctuance. Exam was negative for elevation of the tongue, uvular deviation, pharyngeal edema or erythema, and brawny edema of the anterior neck. Patient’s pupils were equal, round, and reactive to light with extraocular motions intact.
Pulmonary/chest exam was notable for mild tachypnea with cough, as well as bilateral rales (right > left). She had no stridor, drooling, voice changes, or other concerning symptoms requiring emergent airway stabilization. The patient had normal rate and regular rhythm on cardiac exam, with no murmurs heard. She had a soft, non-tender abdomen with normal bowel sounds. There were no abnormal findings on neurological exam, and the patient’s skin was warm, dry, and non-diaphoretic.
Overall, suspicion for a serious medical illness upon initial presentation was high: the patient had recently been intubated for respiratory distress and follow-up management was challenged by the lack of a proper transition of care. Medical records were not available for review during her ED presentation, and she had left another hospital AMA the day prior. In addition to the patient’s obvious discomfort and fatigue, a detailed head, eyes, ears, nose, and throat exam revealed many abnormalities, most notably an intraoral abscess and significant redness and swelling to the neck concerning for large abscess vs cellulitis.
The diagnostic evaluation included laboratory testing with blood cultures (). The patient was started on broad spectrum IV antibiotics: ampicillin/sulbactam and vancomycin, as methicillin-resistant Staphylococcus aureus was also considered given her recent hospital admission. A dental consultation was obtained and an incision and drainage of an abscess at tooth 19 was performed prior to computed tomography (CT) imaging. A CT soft tissue neck with IV contrast was ordered. A CT chest was also ordered to further evaluate her recent history of “lung infection,” fatigue with ambulation, and rales on pulmonary exam. Care coordination occurred with the radiologist to consider both pneumonia and pulmonary septic emboli. The radiologist recommended a traditional pulmonary embolus protocol study.
CT findings were consistent with a diagnosis of Lemierre syndrome. CT neck images revealed a 3.2 cm area of ill-defined low density and gas in the left buccal perimandibular soft tissues, concerning for site of reported abscess status-post incision and drainage. There were numerous small areas of low attenuation overlying thickening in the left submandibular soft tissues, raising concern for possible cellulitis or thrombophlebitis sequelae (). Finally, thrombus of the left anterior jugular vein was visualized, as well as suspected thrombus of the superficial facial vein branches and left perimandibular regions. CT chest study revealed numerous cavitating nodular consolidations concerning for septic emboli given the patient’s history, in addition to a small right pleural effusion (). Pulmonology, vascular surgery, and infectious disease were consulted by the ED, and care was transitioned to the admitting hospitalist.
The patient was continued on IV antibiotics as an inpatient. Blood cultures remained negative throughout inpatient stay. Given a concern for endocarditis, a transthoracic echocardiogram was performed followed by a transesophageal echocardiogram. Both were negative for any signs of endocarditis or structural heart abnormalities. Vascular surgery did not recommend anticoagulation. The patient remained stable, transitioned to oral antibiotics, and was discharged home on a two-week course of sulfamethoxazole/trimethoprim and amoxicillin/clavulanic acid. During a follow-up appointment in primary care clinic one week after discharge, she remained afebrile without any new complaints. The plan was made to finish her oral antibiotic course and follow up with pulmonology in the clinic for a repeat CT chest study and re-evaluation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [107.0, 'mm hg'], 'Diastolic Blood Pressure': [68.0, 'mm hg']}",81,76.95,85.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 107.0 mm Hg + 2/3 * 68.0 mm Hg = 81.0 mm Hg.
Hence, the patient's mean arterial pressure is 81.0 mm Hg."
1555,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5859724-1,Extracted,"A 21-year old female presented on the gastroenterology outpatient clinic with high-grade fever for 3 days and epigastric pain for 3 weeks. She was of Somalian origin and was living in Belgium since 2 years.
Her medical history consisted of malaria in her childhood and one month prior she gave birth to her first child. The labor was induced with secondary cesarean section because of general discomfort, raised inflammatory laboratory markers and raised liver function tests of unknown cause.
Clinical examination revealed abdominal distention and tenderness in the epigastric region without muscular defense. She denied having vaginal purulent discharge and lower abdominal pain. Her vital signs demonstrated a blood pressure of 100/73 mmHg, a heart rate of 124 bpm and a body temperature of 38 °C.
Laboratory studies revealed raised inflammatory markers (total WBC count of 11,700/mm3, CRP level of 170 mg/l), mild microcytic anemia (Hb 10.2 g/dl, MCV 76 fL), significant thrombocytosis (953,000 /mm3) and mildly raised liver function tests (AST 23 U/L, ALT 51 U/L, alkaline phosphatase 279 U/l, gamma-glutamyl transferase 74 U/l). Bilirubin, albumin and prothrombin time were normal.
Viral hepatitis, human immunodeficiency virus (HIV) and Malaria were excluded.
Abdominal ultrasound confirmed the presence of ascites in the small pelvis and around the liver, with normal liver size and parenchyma. Subsequent abdominal computed tomography (CT) revealed peritoneal thickening and hypervascular adnexes with a small para-uterine abcedation on the right side, suggestive for pelvic inflammatory disease (PID) (Fig. ). There were no enlarged lymph nodes and the liver veins were patent.
Diagnostic abdominal paracentesis with evacuation of purulent fluid was performed. Ascitic fluid analysis showed a serum-ascites albumin gradient less than 1.1 g/dL with cytology showing a predominance of lymphocytic cells.
Acid fast stained smear (Ziehl-Neelsen staining) and polymerase chain reaction (PCR) for M. tuberculosis on ascitic fluid were negative.
Tuberculin skin test was negative and there were no signs suggestive of (previous) tuberculosis on chest radiography.
Gynecological evaluation revealed purulent cervical discharge, cervical motion tenderness and adnexal tenderness. Endocervical culture was negative for Neisseria gonorrhoeae, Chlamydia trachomatis and Trichomonas vaginalis. Acid fast stained smear was also negative.
Subsequently a diagnostic laparoscopy was performed, showing multiple peritoneal white nodules and perihepatic “violin string” fibrinous strands (Fig. ). These findings were very suggestive for peritoneal tuberculosis with Fitz-Hugh Curtis syndrome.
Acid fast stained smear and PCR for M. Tuberculosis on peritoneal biopsies were both negative.
Since the perioperative findings were very suggestive, the patient was started on quadruple anti-tuberculous therapy, consisting of isoniazid, rifampin, pyrazinamide and ethambutol. Rapid clinical improvement and regression of the inflammatory markers and ascites was observed.
The pathology report of the peritoneal biopsies eventually confirmed peritonitis with granulomas.
Four weeks after starting anti-tuberculous therapy direct cultures for M. Tuberculosis on peritoneal biopsies and endocervical swab were reported as positive. Ascites cultures remained negative.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [73.0, 'mm hg']}",82,77.9,86.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 73.0 mm Hg = 82.0 mm Hg.
Hence, the patient's mean arterial pressure is 82.0 mm Hg."
1556,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8474693-1,Extracted,"A 71-year old male presented in the outpatient department in August 2019 with the chief complaint of epigastric pain of 3 mo duration.
The epigastric pain was mild to moderate, localized, continuous, with no relation to meals. There was no relief with proton pump inhibitors. There was no history of jaundice, pruritus, clay-colored stools, anorexia, weight loss, dysphagia, gastrointestinal bleeding or vomiting.
The patient had undergone coronary angioplasty for coronary artery disease in 2010 and was on dual antiplatelet drugs.
He had no addictions, and his family history was non-contributory.
The patient was conscious and oriented. His pulse rate was 80 bpm and regular, and blood pressure was 110/70 mmHg. There was no pallor, icterus, or lymphadenopathy. Abdominal examination and other systemic examinations did not reveal any abnormalities.
His blood investigations were as follows: Hb 13.9 g/ dL, white blood cell count 4600/µL, platelet count 166000/µL, prothrombin time 16.5 s, serum bilirubin 0.42 mg/ dL, ALT 18 U/L, AST 17 U/L, ALP 83 U/L (< 129 U/L), gamma glutamyl transferase - 33 U/L (< 71 U/L), and serum creatinine 1.22 mg/dL (< 1.4 mg/dL).
At the local medical center, he had undergone ultrasonography of the abdomen that revealed dilatation of the CBD (15 mm) and pancreatic duct (PD) (5 mm). He was referred to our center for further management. Abdominal magnetic resonance imaging and magnetic resonance cholangiopancreatography (MRCP) showed dilated CBD (15 mm) and PD (6 mm) with abrupt cut-off at the level of the ampulla. No other abnormalities were noted (Figure ). Endoscopic ultrasonography (EUS) revealed a subepithelial, hypoechoic mass lesion at the ampulla 7 mm in size, causing upstream dilation of the CBD and PD. The lesion was free from duodenal muscularis propria. There was no regional lymphadenopathy.
The age and comorbidity of the patient, the limitations and diagnostic accuracy of endoscopy, biopsies and imaging for ampullary lesions, and suspicion of malignancy made us acquire the histological diagnosis of ampullary lesion before a highly morbid surgical intervention. EUS-guided biopsy was not possible due to technical difficulties of the tiny mobile lesion. Hence, ESP was considered a diagnostic and therapeutic intervention for the subepithelial ampullary lesion. ESP aids in achieving en bloc resection of the ampulla for histopathological diagnosis and staging. Thus, en bloc ESP was performed with a balloon-catheter-assisted technique as described by Aiura et al[]. ESP was carried out with a therapeutic duodenoscope (TJF Q 180V, Olympus Medical Systems Corp., Tokyo, Japan) with a 4.2 mm diameter accessory channel. Selective CBD cannulation was achieved with a 0.035” guidewire using a sphincterotome. The linked stone extraction balloon catheter (Fusion Quattro Extraction Balloon, Wilson Cook Medical Inc., Winston-Salem NC, USA) and a 5 Fr snare were inserted over the guidewire through the accessory channel side by side. The balloon catheter alone was advanced into the bile duct, and then the balloon was expanded with distilled water mixed with contrast. The balloon was pulled back gently towards the duodenal lumen, at which point the snare was opened so that it grasped the base of the papilla next to the inflated balloon. Pulling the balloon catheter toward the duodenal lumen made it easier to snare the papillary lesion entirely by lifting the papilla from the duodenal wall and towards the lumen[]. En bloc papillectomy was performed with a monopolar electrosurgical current (ERBE Vio3, Endocut Q mode). A 5 Fr X 7 cm single pigtail pancreatic plastic stent was placed prophylactically, and a 10 Fr X 10 cm biliary plastic stent was placed after biliary sphincterotomy (Figure ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1557,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6570968-1,Extracted,"An 11-year-old Asian girl presented with headache and skin rash on the left side of her chest that had begun 3 days earlier. She had been diagnosed with varicella when she was 2 years old and therefore had no history of receiving the VZV vaccine. She did not have any episode associated with primary immunodeficiency.
Before the onset of illness, she had been feeling fatigue due to exhaustive preparation for a school gymnastics event over the course of several weeks. She visited the local clinic due to repeated afebrile vomiting and severe headache. On the same day, she was admitted to our hospital with a concern of meningitis.
Upon her admission, physical examination revealed a body temperature of 37.2 °C, respiratory rate of 20 breaths/min, heart rate of 85 beats/min, and normal hemodynamic parameters with blood pressure of 117/68 mmHg. She was noted to have a maculopapular rash evolving into vesicles with erythematous regions on the left side of her chest (Fig. ). Her consciousness was clear, and her deep tendon reflexes were normal; Kernig’s sign was negative, although she had neck stiffness.
A cerebrospinal fluid (CSF) examination revealed normal protein concentration (36 mg/dl), normal glucose level (47 mg/dl; blood glucose level, 92 mg/dl), and lymphocytic pleocytosis (429 lymphocytes/μl). Bacterial culture of CSF yielded no growth. Varicella zoster virus (VZV) deoxyribonucleic acid (DNA) was detected in CSF by polymerase chain reaction (PCR) on day 5. Results of blood examination were within normal ranges, including white blood cells (7180/μl), leukocytes (5220/μl), lymphocytes (1507/μl), monocytes (287/μl), eosinophils (43/μl), and basophils (28/μl). Results of VZV anticomplement immunofluorescence studies revealed values of 19 mg/dl for immunoglobulin G (IgG) and below 1 mg/dl for IgM, which indicates the previous infection and acquisition of humoral immunity against VZV. Moreover, there was no increase in the inflammatory biomarker levels. She had normal levels of quantitative immunoglobulins and lymphocyte markers: IgG 1106 mg/dl (normal range, 870–1700 mg/dl), IgA 71 mg/dl (normal range, 110–410 mg/dl), IgM 132 mg/dl (normal range, 46–260 mg/dl), CD3 71.6% (normal range, 59–88%), CD4 32.1% (normal range, 29–65%), CD8 38.8% (normal range, 13–40%), CD4/CD8 ratio 0.83 (normal range, 0.9–3.2), CD19 12.8% (normal range, 4–26%), and CD56 15.5% (normal range, 2–26%).
She was diagnosed with aseptic meningitis and cutaneous manifestation of herpes zoster despite immunocompetence. Acyclovir (45 mg/kg/day) was administered intravenously for 3 days from admission. Because the symptoms of headache, neck stiffness, and skin rash eventually resolved, treatment was switched to oral valacyclovir (75 mg/kg/day) for another 10 days. Given the favorable evolution of the illness, she was discharged from the hospital on day 8. She had no apparent sequelae or comorbidities at the time of the 6-week follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [117.0, 'mm hg'], 'Diastolic Blood Pressure': [68.0, 'mm hg']}",84.33333,80.11666,88.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 117.0 mm Hg + 2/3 * 68.0 mm Hg = 84.33333 mm Hg.
Hence, the patient's mean arterial pressure is 84.33333 mm Hg."
1558,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4475514-1,Extracted,"An 83-year-old woman with the chief complaint of reduced consciousness and slight chest pain was transferred to our hospital by ambulance.
Upon arrival, her face and eyelid conjunctiva were pale and her distal limbs were cold. Her clinical values were as follows: level of consciousness, Japan Coma Scale (JCS)-1; blood pressure, 99/36 mmHg; heart rate, 128/min; body temperature, 35.8°C; and oxygen saturation (SpO2), 98% in room air. Her blood laboratory data revealed inflammation, with a C-reactive protein (CRP) level of 12.84 mg/dL and white blood cell count of 16,100/µL (neutrophils, 89.9%), and anemia, with a hemoglobin concentration of 5.8 g/dL and hematocrit of 19.6%. Her hepatic, biliary, pancreatic, and renal functions were almost normal. However, the titers of creatine phosphokinase (CPK; 403 IU/L) and brain natriuretic peptide (BNP; 738.3 pg/ml) were elevated. The patient had a previous history of hypothyroidism, but her thyroid function had normalized with medication.
Non-contrast CT performed soon after arrival revealed no abnormality (Figure ).
Approximately 4 h after the initial non-contrast CT, contrast-enhanced CT was performed without non-contrast CT. This examination revealed areas of low density surrounding the portal veins in the liver (periportal collar sign), subserosal edema of the gallbladder wall, and areas of water density in the hepatoduodenal ligament, anterior pararenal space, and bare area of the liver with minimal ascites in the right subphrenic space (Figure ).
Echocardiography was performed for suspected acute congestive heart failure. This evaluation revealed diffuse hypokinesis of the left ventricular wall motion, decreased ejection fraction (by Simpson method) of 45.34%, moderate aortic regurgitation, mitral regurgitation and tricuspid regurgitation. The right ventricular systolic pressure was estimated at approximately 40 mmHg. Acute exacerbation in chronic heart failure was diagnosed in accordance with the above-mentioned cardiac function findings.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [99.0, 'mm hg'], 'Diastolic Blood Pressure': [36.0, 'mm hg']}",57,54.15,59.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 99.0 mm Hg + 2/3 * 36.0 mm Hg = 57.0 mm Hg.
Hence, the patient's mean arterial pressure is 57.0 mm Hg."
1559,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1299,Extracted,"A 25-year-old male graduate student is brought to the emergency department for respiratory distress after he was found by his roommate coughing and severely short of breath. He was diagnosed with HIV infection 3 months ago but is not compliant with his antiretroviral therapy. He is from Chile and moved here 5 years ago. He appears unwell and is unable to speak in full sentences. His temperature is 38.2°C (100.7°F), pulse is 127/min, respirations are 32/min, and blood pressure is 95/65 mm Hg. Pulse oximetry shows an oxygen saturation of 86% on room air. No oral thrush is seen. The patient is placed on supplemental oxygen. Serum studies show:
Lactate dehydrogenase 364 IU/L
CD4 cell count 98/mm3
Beta-D-glucan elevated
Arterial blood gas analysis shows:
pH 7.50
PaCO2 22 mm Hg
PaO2 60 mm Hg
HCO3 20 mEq/L
An x-ray of the chest is shown. Standard antibiotic therapy is begun immediately.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [95.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",75,71.25,78.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 95.0 mm Hg + 2/3 * 65.0 mm Hg = 75.0 mm Hg.
Hence, the patient's mean arterial pressure is 75.0 mm Hg."
1560,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3491129-2,Extracted,"A 54-year-old man with no significant medical history and no intravenous drug use presented to our emergency department with complaints of peripheral oedema, dyspnoea, sweating and fever. On clinical examination the patient had tachypnoea. Blood pressure was 135/85 mmHg. On cardiac auscultation heart sounds were normal and he had no murmur. Pulmonary crackles were heard on both sides. Peripheral oedema was present. A splinter haemorrhage was seen under his left index fingernail. Janeway lesions were seen on the left index and middle fingers. Electrocardiography showed a sinus tachycardia of 138 beats/min, and no further abnormalities. Laboratory testing showed leucocytosis (13 × 109/L), and an increased CRP level (262 mg/L). On chest X-ray, pulmonary oedema was seen. Blood cultures proved positive for Staphylococcus aureus. At transoesophageal echocardiography, vegetations were seen on the anterosuperior leaflet of the tricuspid valve and on the anterior leaflet of the mitral valve (Fig. ). The patient was admitted to the intensive care unit for artificial respiration and treated with a 6-week course of intravenous flucloxacillin (12 g/day). During the hospital stay, the patient also developed an arthritis of the sterno-clavicular joint, which was confirmed by a positron emission tomography-computed tomography scan. Because of development of this arthritis during antibiotic treatment, the antibiotic course was extended by 2 weeks of 6 g/day flucloxacillin i.v. The vegetations decreased in size and no significant valve regurgitation or intracardiac abscess developed. Antibiotic treatment was stopped and there was no relapse.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [135.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",101.66667,96.58334,106.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 85.0 mm Hg = 101.66667 mm Hg.
Hence, the patient's mean arterial pressure is 101.66667 mm Hg."
1561,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8636855-1,Extracted,"In this article, a case involving a 27-year-old woman with gravida 2, para 1, and gestational weeks of 26 was reported. This patient suffered from a fever shortly after she became soaked in the rain 6 days previously, with the highest temperature of 40°C. Then, she had cough 3 days previously, with white phlegm and occasional bloody sputum, combined with chest tightness and asthma. These symptoms were not improved after the administration of mezlocillin sodium and sulbactam sodium as anti-infectives in the outpatient department. Subsequently, she visited the emergency department of the First Affiliated Hospital of Anhui Medical University (Anhui, China) on October 22, 2020, where she was admitted to the hospital with “fever and pregnancy status (26 weeks pregnant).” This patient developed intermittent diarrhea in the previous 3 days, with the clinical manifestations of yellow watery stool and dark urine. The patient was previously in good condition and had no other diseases. Through auscultation, breathing sounds in both lungs were thick, with obvious moist rales. On the admission day, the temperature of the patient was 38.5°C, with a heart rate of 150 beats/min, a blood pressure of 105/69 mmHg, and a respiratory rate of 35 breaths/min. The findings of laboratory examinations were as follows: hemoglobin, 88 g/L; C-reactive protein (CRP), 145.46 mg/L; white blood cell count (WBC), 14.73 × 109/L; platelet count, 189 × 109/L; procalcitonin (PCT), 19.36 ng/mL; D-dimer, 12.85 μg/mL; glutamic-oxaloacetic transaminase, 125 U/L; and creatinine, 39.3 μmol/L. Chest X-ray () revealed bilateral lung inflammation, lung abscess in the superior lobe of the left lung, and right pleural effusion. The preliminary differential diagnosis included severe pneumonia, acute respiratory distress syndrome, septic shock, and pregnancy. Although meropenem and oseltamivir were administered to resist infection, the patient's dyspnea symptoms persisted, and her high-flow oxygenation index was < 100 mmHg. After endotracheal intubation, the patient was transferred to the intensive care unit (ICU). On October 23, 2020, the patient was examined through fiberoptic bronchoscopy, sputum and alveolar lavage fluid in the left and right bronchi were aspirated, and meropenem, vancomycin, azithromycin, and oseltamivir were administered with mechanical-assisted ventilation. On October 25, 2020, the patient received metagenomic next-generation sequencing (mNGS) () of alveolar lavage fluid and blood, with both results indicating C. psittaci. Therefore, the diagnosis of C. psittaci pneumonia was confirmed, and the antibiotic regimen was adjusted to include doxycycline, cefoperazone sodium and sulbactam sodium, and moxifloxacin. Symptomatic treatment, including mechanical ventilation, anti-shock, protection of important organs, nutritional support, sedation, and analgesia, was actively administered. On October 29, 2020, bronchoscopy was performed again, with the results of metagenomic next-generation sequencing (mNGS) of alveolar lavage fluid and blood continuing to show C. psittaci. However, the level of C. psittaci () in the alveolar lavage fluid decreased compared to the earlier analysis, although the level of C. psittaci in the blood increased. On October 31, 2020, the oxygenation index of the patient reached 280 mmHg, which was significantly improved, the temperature of the patient was 40°C, with a heart rate of 105 beats/min and a blood pressure of 120/60 mmHg. The findings of laboratory examinations were as follows: hemoglobin, 93 g/L; CRP, 80.19 mg/L;WBC, 14.36 × 109/L; platelet count, 140 × 109/L; PCT, 4.87 ng/mL; D-dimer, 8.35 μg/mL; glutamic-oxaloacetic transaminase, 54 U/L; and creatinine, 26.7 μmol/L. Chest X-ray revealed improved bilateral lung inflammation and lung lesions compared with the condition at admission. However, the peak temperature of this patient was higher than before. As for those patients suffering from long-term high fever, if the temperature is not effectively controlled after extensive coverage with broad-spectrum and powerful antibiotics, non-infectious fever should be taken into account at the same time. In other cases, non-infectious fever is common in the rheumatic blood system and tumor diseases. Bone marrow puncture and smear examination were performed on November 2, 2020, and the tumor index of the patient was elevated, which was considered to be related to pregnancy and hypoproteinemia. Sputum and blood cultures showed Acinetobacter baumannii, and sputum and urine cultures showed Candida albicans and Candida tropicalis. Therefore, the antibiotic regimen was adjusted to include polymyxin + cefoperazone sodium and sulbactam sodium + doxycycline + teicoplanin + voriconazole on November 9, 2020. On November 15, 2020, ultrasound indicated that the umbilical cord was wound around the neck of the fetus for 2 weeks, the volume of amniotic fluid was decreased, and fetal kidney parenchyma echo was enhanced. After communicating with the family members of the patient and obstetrics physicians, rivanol was injected into the amniotic cavity to induce labor. On November 19, 2020, the patient became conscious, and her breathing and circulation were stable; however, she developed a cough reaction, and tried to break away from the ventilator and remove tracheal intubation. Pulmonary imaging revealed mitigated fever (temperature > 38.5°C), reduced red blood cell (RBC) count (1.99 × 1012/L) and platelet count (111 × 109/L), hypertriglyceridemia (triglycerides, 6.21 mmol/L), and hyperferritinemia (ferritin, 2,284 μg/L). Phagocytic cells were apparent on bone marrow smear and HPS could not be excluded. Besides, natural killer (NK) cell activity and soluble CD25 levels were examined, and the CD107a excitation test was improved. These results indicated that the level of sCD25 increased, and NK cell activity decreased. Therefore, the diagnosis of HPS caused by infection was confirmed. The HLH-2004 regimen, recommended by the International Histocyte Association, was applied in the treatment of HPS. Etoposide combined with hormone therapy can significantly mitigate—if not eliminate—symptoms, and immunosuppressants, such as cyclosporine A (CSA) and anti-thymocyte globulin (ATG), could be added according to the condition (). On November 20, 2020, VP-16 (150 mg) and dexamethasone (10 mg) were administered to eliminate symptoms. On November 22, 2020, the temperature of the patient returned to 36.8°C.On November 27, 2020, the temperature of the patient was basically maintained within the normal range. The finding of laboratory examinations were as follows: hemoglobin, 92 g/L; CRP, 7.48 mg/L;WBC, 11.43 × 109/L; platelet count, 103 × 109/L; PCT, 0.11 ng/mL; D-dimer, 0.93 μg/mL; glutamic-oxaloacetic transaminase, 62 U/L; creatinine, 13.3 μmol/L; RBC count, 2.83 × 1012/L; hypertriglyceridemia (triglycerides, 5.68 mmol/L); and hyperferritinemia (ferritin, 2,212 μg/L). The indices of ferritin and triglycerides for the patient did not decrease significantly compared with the previous time, and HPS had not been completely controlled. On November 27, 2020, etoposide (100 mg) was administered on the basis of dexamethasone to control the primary disease. The findings of laboratory examinations on December 3, 2020, were as follows: WBC, 6.55 × 109/L; platelet count, 155 × 109/L; triglycerides, 2.34 mmol/L; ferritin, 1,807 μg/L; and glutamic-oxaloacetic transaminase, 14 U/L. Etoposide (100 mg) was administered for the third time on December 6, 2020. On December 10, 2020, NK cell activity and sCD25 levels were re-examined, with the results showing that NK cell activity did not decrease and the level of sCD25 returned to the normal range. Therefore, it was not necessary to continue the treatment with etoposide, and dexamethasone was gradually decreased. On December 23, 2020, the fever, cough, and expectoration were obviously mitigated and breath sounds in both lungs became clear. Chest CT () revealed that the lung lesions were absorbed, and the level of sCD25 and NK cell activity suggested that the condition of the patient was basically stable; therefore, the patient was discharged from the hospital. The telephone follow-up 1 week later revealed that the patient had no complaints of discomfort, fever, cough, or expectoration, and she was advised to conduct outpatient reviews regularly ().",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 60.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1562,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7386058-1,Extracted,"A 41-year-old man visited a local doctor with a chief complaint of dyspnea and hemoptysis for 2 days. The patient was initially diagnosed with severe hypertension and renal failure and was then referred to our medical facility. He was diagnosed with hypertension 5 years prior but had not received any treatment. There was no recent history of infectious gastroenteritis or diarrhea.
On admission, a physical examination showed his blood pressure was 233/159 mmHg, heart rate was 135 bpm, and body temperature was 37.7 °C. His percutaneous oxygen saturation level was 88% on room air, and coarse crackles were heard in both lower lung fields. The patient was alert and oriented. Jugular venous distention was observed. Swelling and tenderness of the joints, rash, lower extremity edema, and neurological abnormalities were not observed. There was no skin tightening. Fundoscopy indicated bilateral hemorrhages and cotton wool spots without papilledema, which corresponded to hypertensive retinopathy according to Keith-Wagener-Barker classification III. Clinical laboratory findings from day 1 are presented in . A chest radiograph represented extensive bilateral alveolar shadowing and cardiomegaly (cardiothoracic ratio: 60%). There were no pleural effusions (A). High-resolution chest computed tomography (CT) showed diffuse perihilar ground-glass attenuation with some areas of consolidation along the bronchial vascular bundle (B). Using a bronchoalveolar lavage fluid test, macroscopic alveolar hemorrhage was observed and a large number of hemosiderin-laden macrophages were histologically confirmed (). Abdominal CT revealed no apparent atrophy in either kidney, a small amount of ascites and dilation of the inferior vena cava. An echocardiogram indicated eccentric left ventricular (LV) hypertrophy with systolic and diastolic dysfunctions; LV wall motion showed diffuse severe hypokinesis, and the ejection fraction value was 25.4%. Coronary angiography revealed no significant stenosis that would require therapeutic intervention. The patient was diagnosed with hypertensive heart failure.
According to the clinical findings, the patient was diagnosed with HE with pulmonary alveolar hemorrhage and TMA. Diagnosis of HE and TMA was made based on previous reports [, ]. The clinical course is shown in . Since thrombotic thrombocytopenic purpura (TTP), vasculitis, and connective tissue disease could not be excluded at the time of admission, steroid administration and plasma exchange were started in addition to antihypertensive therapy with calcium antagonist (nicardipine) on day 1. Hemodialysis (HD) was also initiated on day 1 due to fluid overload. On day 3, various test results, including ADAMTS13 and autoantibodies, were identified and HE was considered to be the main pathophysiology. Therefore, steroid therapy and plasma exchange were discontinued. Although a β-blocker (carvedilol) was added to the calcium antagonist therapy on day 6, the patient’s blood pressure was 150 – 160/80 – 90 mmHg and the hypotensive effect was not enough. Consequently, an angiotensin II receptor blocker (olmesartan) was initiated in addition to these agents on day 14. As a result, hypertension improved promptly, and blood pressure management stabilized with losartan (12.5 mg/day) and carvedilol (10 mg/day). Alveolar hemorrhaging gradually improved, and the diffuse ground-glass shadows disappeared on chest CT images on day 35 (). The platelet count increased to more than 100×103/µL after day 5 and maintained at 150 to 200×103/µL thereafter. Red blood cell fragments disappeared after day 2, and lactate dehydrogenase was normalized on day 23. However, renal function did not improve, and HD was continued. The first three HD sessions were performed for 3 hours and the fourth and subsequent sessions were performed for 4 hours with 1 – 3 L fluid removal per session because anuria was prolonged. A total of 14 HD sessions were performed at a frequency of 3 times per week during hospitalization. The patient’s peak body weight was 60.0 kg, which decreased to 54.0 kg after the final dialysis treatment prior to discharge.
Percutaneous renal biopsy was performed on day 27 to determine the cause of the kidney injury. Renal pathological images are presented in . The sample contained 16 glomeruli, 4 of which showed global sclerosis. On light microscopy, the main glomerular lesions were ischemic changes, and the capillary walls were thickened and wrinkled. There was no significant mesangial proliferation, endocapillary hypercellularity, or extracapillary proliferation. Interstitial architecture showed advanced interstitial fibrosis and tubular atrophy. In the interlobular artery, multiple layers of elastic lamina were observed and some showed onion skin lesions. In addition, hyperplasia of medial smooth muscle cells, including the arcuate artery, was remarkable. Severe vascular endothelial damage, including endothelial cell swelling and edematous change, led to a narrowing and occlusion of the vascular lumen. Hyalinization was observed in the arterioles. Endothelial injury was evident in vessels of a size larger than the arteriole but was not observed in the glomerular capillaries. There were no findings of vasculitis or fibroid necrosis in the tissue. Immunofluorescent staining only revealed nonspecific immunoglobulin (Ig) G deposition on glomerular capillary walls, and IgA, IgM, complement component (C) 1q, C3, C4, and C4d were negative. Based on these pathological features, the patient was finally diagnosed with malignant nephrosclerosis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [233.0, 'mm hg'], 'Diastolic Blood Pressure': [159.0, 'mm hg']}",183.66667,174.48334,192.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 233.0 mm Hg + 2/3 * 159.0 mm Hg = 183.66667 mm Hg.
Hence, the patient's mean arterial pressure is 183.66667 mm Hg."
1563,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6814919-1,Extracted,"History: a 44 year old male cattle farm help and an alcohol abuser but a non-smoker with no significant past medical or surgical, chest or abdominal trauma history, was referred to the Accident and Emergency Centre of the Komfo Anokye Teaching Hospital from a peripheral hospital, two days after having been attacked by a bull in the chest. Patient was swang about in air three times while still attached to the bull, dropped onto the floor and stomped on in the right hemithorax and right upper abdomen before the bull was chased off by fellow workers. He presented to a peripheral hospital soon after the incident with a complaint of chest pain and was given analgesics, antibiotics and tetanus prophylaxis after evaluation and had his chest wounds dressed. Imaging could not be done at the facility. He is said to have momentarily improved, but continued to have right chest and abdominal pains and was thus referred to the Komfo Anokye Teaching Hospital on the third day of injury. On arrival he was conscious and alert and well oriented with SPO2 of 96% on room air, respiratory rate of 26 breaths/minute, heart rate of 124 beats/minute with a blood pressure of 137/57mmHg. His random blood sugar (RBS) was 8.6mmol/l, haemoglobin level of 10.9g/dl and had a temperature of 360°C. Systemic review was significant for shortness of breath, chest pain, cough (non-productive) and abdominal pain. He was talking clearly and there were no concerns for the airway and cervical spine. Chest expansion was limited on the right hemithorax with extensive subcutaneous emphysema from the jugular notch to the umbilicus and reduced breaths sound. There was a 2x2cm deep wound on the right anterolateral chest wall which was not communicating with the right pleural space. He had right upper abdominal guarding and tenderness. There were no significant pelvic and musculoskeletal findings except a clean 5x2cm laceration on the posterolateral aspect of the left thigh. He had warm peripheries with normal capillary refill time. Focused assessment with sonography for trauma (FAST) was negative for haemopericardium and haemoperitoneum. The patient was started on intranasal cannula oxygen therapy at 4L/min making SPO2 of 99%. Based on the clinical signs of right pleural collection as noted above, a size 32FG right chest tube was passed into the fourth intercostal space, midpoint between the anterior axillary line and the midaxillary line draining gush of air. The wounds were debrided cleaned and sutured under local infiltration. After twelve hours on admission, his haemoglobin had dropped to 7.9g/dl from the admission haemoglobin level of 10.9g/dl requiring two (2) units of packed red blood cell transfusion. His renal function was normal. Abdominopelvic ultrasound scan did not show much. Chest radiography and chest CT scan confirmed a right diaphragmatic injury with herniated liver as shown in and . Patient was prepared for exploratory right thoracotomy.
Operation: under general anaesthesia with a size 37FG double-lumen endotracheal tube, the patient was placed in a left lateral decubitus position and a standard right posterolateral thoracotomy was done entering the 7th intercostal space or pleural bed. There was a 15cm transverse laceration of the right hemidiaphragm with herniation of the liver into the thoracic cavity, 280mls of hemothorax, fracture of the right 7th and 8th ribs and a collapsed and contused right lower lobe lung with intact pericardium, shown in . The diaphgramatic rupture was repaired in a simple interrupted fashion, in a single layer using nylon 1 after reducing the liver into the abdomen. The chest was then irrigated copiously with warm normal saline. A size 32 FG chest tube was passed and the chest closed up in layers. He was extubated on table and had an uneventful postoperative recovery. The chest tube was removed on postoperative day 3 and he was discharged on postoperative day 10.
Postoperative course: he had a regular outpatient reviews and has had no complications or sequelae so far after one year.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [137.0, 'mm hg'], 'Diastolic Blood Pressure': [57.0, 'mm hg']}",83.66667,79.48334,87.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 137.0 mm Hg + 2/3 * 57.0 mm Hg = 83.66667 mm Hg.
Hence, the patient's mean arterial pressure is 83.66667 mm Hg."
1564,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7575320-1,Extracted,"A 30-year-old African American male with no reported past medical history initially presented to the emergency department for evaluation of approximately one week of shortness of breath, non-productive cough, along with subjective transient fevers. He initially tested positive for COVID-19 via polymerase chain reaction (PCR) testing from nasopharyngeal swab. He was hemodynamically stable and discharged from the emergency department with instructions to self-quarantine for two weeks.
Eleven days following discharge, the patient developed mild right hemiparesis, sensory loss, and dysarthria. Upon presentation to the hospital, he experienced rapid resolution of his symptoms with National Institutes of Health Stroke Scale (NIHSS) improving from 4 to 1 in two hours. On arrival, the patient was afebrile, with a blood pressure of 143/77 mmHg, pulse of 107 beats per minute, and 18 respirations per minute while saturating 100% on room air. After his symptoms abated, his only complaint was mild left-sided neck swelling he noticed following a burst of coughing spells while self-isolating.
On physical exam, the patient was alert and oriented with equal strength and range of motion bilaterally. Cranial nerves were intact with 2+ deep tendon reflexes throughout. No gait abnormalities, focal neurological deficits, ataxia, or motor/sensory disturbances were observed. Physical exam was remarkable only for minimal left neck swelling with no appreciable cervical lymphadenopathy.
CT head showed chronic appearing hypodensities in the left subinsular cortex, suggesting small chronic infarcts. A nonocclusive thrombus was noted within the proximal left internal carotid artery by CT angiography (CTA) (Figure -panel A). Neither CTA nor carotid ultrasonography identified evidence of microdissection. However, multifocal ground glass opacities were visualized within the upper lungs. Chest X-ray however did not identify any acute pulmonary process. MRI brain demonstrated multiple small acute embolic strokes in the left internal carotid artery (ICA) vascular territory (Figure ). Labs demonstrated a microcytic anemia with a hemoglobin of 8.4 (12.3-15.3 g/dL) and a mean corpuscular volume of 78.4 (80-100 fL), mildly elevated C-reactive protein of 0.4 (<0.3 mg/dL), elevated erythrocyte sedimentation rate at 71 (0-15 mm/hr), and positive COVID-19 via repeated nasopharyngeal swab. D-dimer was elevated at 1.7 (0.0-0.49 mg/L) as was his interleukin-6 at 3.8 (<1.8 pg/mL). Ferritin was abnormally low at 7 (26-388 ng/mL) and iron studies suggested iron deficiency anemia with total iron of 21 (65-175 ug/dL) and percent saturation of 6% (10-55%).
In light of an intraluminal thrombus, the patient was initially treated with aspirin, statin, and heparin infusion without boluses. However, the patient’s hemoglobin continued to slowly decline over the next three days to 6.9 g/dL, prompting transfusion with two units of packed red blood cells as well as intravenous iron. Upon further questioning, the patient admitted he had noted bright red blood when defecating with intermittent passage of clots confirmed by our healthcare team. He also revealed history of bleeding internal hemorrhoids since age 15 years, not previously reported, and occurring as recently as two to three weeks prior to his stroke. Heparin was discontinued and hemorrhoids were visualized on rectal exam. He was continued on 81 mg of aspirin daily.
Hypercoagulable workup including antinuclear antibodies, factor V Leiden, anticardiolipin, antithrombin III, lupus anticoagulant, protein C and S activity, prothrombin G20210A mutation, and homocysteine were all within normal limits. Transthoracic echocardiography did not identify any intracardiac defects. To clarify his risk of recurrent thrombosis against his bleeding risk, colonoscopy, transesophageal echocardiography, and cerebral catheter angiography were sought. However, despite any respiratory symptoms, our patient repeatedly tested positive for SARS-CoV-2 via PCR on day one, three, and six, deeming the risk of aerosolization too high for such invasive procedures. Antibody testing was pursued to further stratify infectivity which showed the patient had developed immunoglobulin (Ig)G antibodies. Nevertheless, our patient did not have these procedures done inpatient as utility surrounding antibody testing did not comment on infectivity.
Our patient was ultimately discharged in stable condition after multiple studies excluded all other causes of thromboembolic large vessel stroke. Repeat CTA done three days after admission continued to show an intraluminal filling defect (Figure -Panel B). Another CTA was obtained twelve days after admission which demonstrated complete resolution of the left carotid thrombus, and without any evidence of new strokes or intracranial hemorrhage (Figure -Panel C). At the time of discharge, his hemoglobin had significantly improved following intravenous iron administration and his dimer value had decreased since admission, although remained slightly elevated. He was discharged with daily aspirin and statin for secondary stroke prevention, as well as counseling regarding diet and exercise. At one month after discharge, he had completely recovered without recurrent transient ischemic attack (TIA)/stroke.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [143.0, 'mm hg'], 'Diastolic Blood Pressure': [77.0, 'mm hg']}",99,94.05,103.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 143.0 mm Hg + 2/3 * 77.0 mm Hg = 99.0 mm Hg.
Hence, the patient's mean arterial pressure is 99.0 mm Hg."
1565,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6567735-1,Extracted,"A 64-year-old woman was admitted to hospital with a 1-month history of dyspnoea and abdominal distension. She had exertional dyspnoea that restricted her ability to perform daily activities. She also complained of abdominal distension, which was aggravated by food intake. She had a history of chronic bronchitis and smoking for the past 30 years. Physical examination showed a heart rate of 103 beats/minute, blood pressure 110/70 mmHg, respiratory rate 29 breaths/minute, mildly cyanosed lips, mildly distended jugular veins, and decreased respiratory sounds, but no wheezes or crackles. Cardiac examination showed increased bilateral cardiac borders, a normal rhythm, no murmurs and pericardial friction sounds. Her abdomen was soft and the liver and spleen were not palpable. There was moderate pitting oedema of the bilateral lower limbs.
Laboratory reports showed a white blood cell count of 12.58 × 109/L (reference range 3.5–9.5 × 109/L), neutrophils 84% (reference range, 40%–75%), N-terminal pro-brain natriuretic peptide 2550 pg/mL (reference range 0–125 pg/mL), and troponin 0.23 ng/mL (reference range 0–0.034 ng/mL). Tumour markers were neuron-specific enolase 21.4 ng/mL (reference range <25 ng/mL) and carbohydrate antigen 125 11.29 U/mL (reference range <35 U/mL). Echocardiography revealed an ejection fraction of 57%, moderate pericardial effusion, and a 79 × 37 mm hyperechoic mass in the pericardial sac, located in the visceral pericardium of the lateral wall of the right atrium. Enhanced computed tomography (CT) also revealed a 75 × 34 mm intrapericardial mass. The tumour invaded the right atrial myocardium with inhomogeneous enhancement (). The patient underwent pericardiocentesis and 300 mL of bloody pericardial effusion was sent to the laboratory for testing. The results showed exudative pericardial effusion, adenosine deaminase 28.10 U/L (reference range 4–18 U/L), lactate dehydrogenase 767 U/L (reference range 120–250 U/L), and carcinoembryonic antigen 2.13 ng/mL (reference range <3.4 ng/mL). Tuberculosis-related tests on the pericardial effusion were negative. Ultrasound-guided cardiac biopsy was performed and histopathological examination revealed a patternless distribution of oval- and spindle-shaped cells in a collagen stroma, with mitosis >40 in 10 high-power fields. Immunohistochemistry was positive for vimentin, CD34, and Bcl-2 (). Based on the above findings, the final diagnosis was pericardial malignant solitary fibrous tumour with right atrial invasion. Complete resection of the tumour was impossible because of its invasion into the myocardium. The patient refused chemotherapy and was discharged after pericardial drainage.
Written informed consent was obtained from the patient for publication of this case report.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1566,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8880,Extracted,"A 60-year-old man comes to the clinic with the complaint of knee pain for the past few weeks. The pain is located in the left knee, associated with morning stiffness for about an hour, and improves with activities throughout the day. He also has a history of diabetes mellitus, hypertension, peptic ulcer disease, and ischemic heart disease. He underwent angioplasty last year for a STEMI. The patient takes metformin, aspirin, clopidogrel, atorvastatin, ramipril, omeprazole, and bisoprolol. He used to smoke one pack of cigarettes a day for the last 45 years but stopped smoking for the past one year following his heart attack. He drinks alcohol socially. His father has Alzheimer’s disease and is in adult home care, and his mother died of breast cancer when she was 55. His temperature is 37.6°C (99.8°F), blood pressure is 132/65 mm Hg, pulse is 90/min, respirations are 14/min, and BMI is 22 kg/m2. On examination, his left knee is swollen, warm, tender to touch, and has decreased range of movement due to pain. Cardiopulmonary and abdominal examinations are negative.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [132.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",87.33333,82.96666,91.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 132.0 mm Hg + 2/3 * 65.0 mm Hg = 87.33333 mm Hg.
Hence, the patient's mean arterial pressure is 87.33333 mm Hg."
1567,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7012551-1,Extracted,"A 27-year-old female was found unconscious in the front seat of her car. On the car floor was a five-gallon (18.9 liter [L]) plastic drum containing a funnel and hose. The drum contained a green oily fluid assumed to be a mixture of sulfuric acid and formic acid because empty containers of the same were found in the vicinity of the scene. First responders measured CO levels of 400 parts per million (ppm) inside the car, which was measured after adequate ventilation. On-scene assessment documented that the patient was minimally responsive to pain with occasional tonic-clonic movements of her extremities. Initial vitals were a blood pressure of 192/125 millimeters mercury, heart rate of 135 beats per minute, respiratory rate of 24 breaths per minute and a Glasgow Coma Scale of 8/15 (best eye response 2, best verbal response 2, best motor response 4). She was started on 100% oxygen via a non-rebreather mask and transferred to the emergency department (ED).
In the ED, she was noted to be minimally responsive with tonic clonic movements of her distal extremities. This was followed by decerebrate rigidity. Her pupils were symmetric and reactive to light bilaterally. The remainder of her neurological exam was unremarkable. She remained tachycardic. The patient was eventually intubated for airway protection because of her depressed mental status. Her initial labs revealed an elevated carboxyhemoglobin (COHB) level of 15% (0–3%), lactate of 2 millimoles (mmol)/L (0.5–2.2 mmol/L) and a troponin level of 3.066 nanograms per milliliters (ng/ml) (0–0.03 ng/ml). The electrocardiogram was normal.
The patient was transferred to a hyperbaric center around four hours after being found on the scene and almost immediately underwent three sessions of hyperbaric oxygen therapy over 24 hours. The first session was at 2.8 ATA (atmospheres absolute) for 45 minutes, 2.0 ATA for 60 minutes, and a five-minute air break. The second two cycles were at 2.0 ATA for 90 minutes. She was extubated the next day with normal mentation and neurological exam. Around four weeks after discharge, her neurologic evaluation demonstrated an anterograde amnesia beginning with the suicide event. In addition, she demonstrated other neurocognitive abnormalities suggestive of delayed neurological sequelae (DNS). Brain magnetic resonance imaging (MRI) showed abnormal restricted diffusion with associated fluid-attenuated inversion recovery (FLAIR) signal abnormalities in the white matter of the right temporal lobe, bilateral globus pallidi, bilateral mesial temporal lobes, hippocampus and scattered foci within the bilateral cerebellar hemispheres suggestive of anoxic-ischemic brain injury.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [125.0, 'mm hg'], 'Systolic Blood Pressure': [192.0, 'mm hg']}",147.33333,139.96666,154.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 192.0 mm Hg + 2/3 * 125.0 mm Hg = 147.33333 mm Hg.
Hence, the patient's mean arterial pressure is 147.33333 mm Hg."
1568,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6682238-1,Extracted,"A 76-year-old Caucasian female with a past medical history significant for hyperlipidemia and poorly controlled hypertension was sent to the emergency department (ED) by her outpatient cardiologist due to abnormal labs. Her labs were most significant for a severe leukocytosis and hypokalemia. On her arrival to the ED, she was grossly asymptomatic but reported a two-week history of generalized fatigue and intermittent lightheadedness. On review of systems, she also endorsed a 10-pound weight loss over the prior six months and episodic generalized abdominal pain associated with nausea and vomiting over the prior year.
On exam, she was hypotensive to 83/42 millimeters of mercury with otherwise normal vital signs. She was awake, alert, in no acute distress, and in general was very comfortable and well appearing. She did not demonstrate any evidence of hypoperfusion on exam such as altered mental status, dizziness, or cold extremities. Her abdomen was soft and non-distended with only mild tenderness to palpation in the suprapubic region but no guarding or rebound. Her exam was otherwise notable for a diminished left radial pulse and bilaterally diminished dorsalis pedis pulses.
Routine investigations revealed a white cell count of 49.1/liters (L) (4.4–11.3×109/L) with a left shift and neutrophil predominance, potassium of 2.5 millimoles (mmol)/L (3.5–5.3mmol/L), sodium of 127 mmol/L (136–145mmol/L), blood urea nitrogen of 31 milligrams per deciliter (mg/dL) (6–23 mg/dL), creatinine of 1.53 mg/dL (0.50–1.05 mg/dL), C reactive protein of 31.44 mg/dL (<1.00) and lactate of 3.7 mmol/L (0.4–2.0 mmol/L). Her liver function tests were within normal limits. Urinalysis and chest radiograph were obtained for an infectious workup and were both unremarkable.
After a period of observation, an abdominal computed tomography (CT) was obtained given her history of chronic abdominal pain and persistent concern for infectious process with no clear source. The CT showed gallbladder wall thickening and edema with pericholecystic edema and a contained perforation of the gallbladder wall near the fundus ().
Interval CT angiogram showed severe atherosclerotic changes of the abdominal aorta and its branches with complete occlusion of the celiac artery origin and diminutive flow in its distal branches from collateral vessels, severe stenosis of the superior mesenteric artery, and mild stenosis of the inferior mesenteric artery. There was mild wall thickening of the ascending colon and transverse colon.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [83.0, 'mm hg'], 'Diastolic Blood Pressure': [42.0, 'mm hg']}",55.66667,52.88334,58.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 83.0 mm Hg + 2/3 * 42.0 mm Hg = 55.66667 mm Hg.
Hence, the patient's mean arterial pressure is 55.66667 mm Hg."
1569,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-2033,Extracted,"A 22-year-old woman comes to the physician because of a 1-month history of a light greenish, milky discharge from both breasts. There is no mastalgia. She has hypothyroidism and migraine headaches. Her mother has breast cancer and is currently undergoing chemotherapy. Menses occur at regular 28-day intervals with moderate flow; her last menstrual period was 1 week ago. Current medications include levothyroxine and propranolol. She appears anxious. Her temperature is 37.1°C (98.78F), pulse is 82/min, and blood pressure is 116/72 mm Hg. The lungs are clear to auscultation. Breast examination is unremarkable. Pelvic examination shows a normal vagina and cervix. Serum studies show:
Thyroid-stimulating hormone 3.5 μU/mL
Progesterone 0.7 ng/mL (Follicular phase: N < 3)
Prolactin 18 ng/mL
Follicle-stimulating hormone 20 mIU/mL
A urine pregnancy test is negative.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [116.0, 'mm hg'], 'Diastolic Blood Pressure': [72.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 116.0 mm Hg + 2/3 * 72.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1570,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5943845-1,Extracted,"A 71-year-old man was admitted with a complaint of episodic fever for 1 week, accompanied by general malaise, nausea, and vomiting. His past medical history was negative, except for uncontrolled diabetes mellitus. On initial admission, his body temperature was 39.5 °C. Physical examination was unremarkable. Laboratory tests showed white blood cell counts 16 × 109/L, neutrophil 91.6%, hemoglobin 116 g/L, C-reactive protein 134.4 mg/L, fasting blood glucose 17 mmol/L, and normal liver function tests (LFTs). Blood culture, tumor, and viral markers were all negative. Abdominal computed tomography (CT) scans revealed a 5 cm abscess located in liver segment IV (Fig. A). Insulin was administered subcutaneously to control his hyperglycemia. The initial broad-spectrum antibiotic therapy we had employed (cefoperazone sodium and ornidazole, intravenously) was ineffective; therefore, ultrasound guided PCD was attempted. After topical anesthesia with 2% solution of lidocaine hydrochloride, an 8-French pigtail catheter was introduced into the abscess cavity using the Seldinger technique, under ultrasound guidance. Pus was successfully drained; Burkholderia vietnamiensis was found in the pus culture. Within 24 hours following PCD, the patient complained of severe right upper quadrant pain. Three hundred milliliter hematic fluid was drained from the catheter. His hemoglobin and hematocrit levels continuously decreased (from 104 to 65 g/L and from 29.1% to 18.7%, respectively). LFTs revealed elevated liver enzymes: alanine aminotransferase 654U/L and aspartate aminotransferase 1210 U/L; while his hemodynamic status remained stable: blood pressure 112/83 mmHg, pulses 75 beats/min, Spo2 96% to 100% (room air). Creatinine, bilirubin, urinalysis, coagulation function tests, and plate counts were all within normal limits. Ultrasound indicated a 10 × 4 cm subcapsular hematoma in the right lobes. Abdominal enhanced CT further revealed intrahepatic and subcapsular hematoma extending from the right diaphragmatic face to the hilum, intra-abdominal fluid accumulation, and catheter shedding (Fig. B and C). Subsequently, emergent angiogram was performed, and revealed an absence of intrahepatic artery-venous fistula or active bleeding signs. According to these findings, a diagnosis of liver rupture without further progression was made. Under close monitoring, the patient accepted transfusions of 2 units of packed red blood cells, with hemostatic drug usage (aminomethylbenzoic acid and etamsylate, intravenously). The patient's antibiotic regimen was adjusted (imipenem and cilastatin, intravenously) according to pus culture sensitivity. After these conservative treatments continued for 5 days, the patient's fever subsided, and discomfort resolved gradually. Laboratory workup revealed that his hemoglobin had stabilized and LFTs normalized. The drainage fluid became yellow and clear. Thirty-four days after PCD, repeated abdominal enhanced CT disclosed that the previous hematoma had been absorbed significantly, with ascites resolution and abscess cavity closure (Fig. D). The local daily drainage showed a decreased volume, and the catheter was removed. The patient recovered uneventfully during following-ups.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [112.0, 'mm hg'], 'Diastolic Blood Pressure': [83.0, 'mm hg']}",92.66667,88.03334,97.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 112.0 mm Hg + 2/3 * 83.0 mm Hg = 92.66667 mm Hg.
Hence, the patient's mean arterial pressure is 92.66667 mm Hg."
1571,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1541,Extracted,"A 68-year-old man comes to the physician for a routine health maintenance examination. Over the past six months, he has had an increase in the frequency of his bowel movements and occasional bloody stools. He has hypertension, coronary artery disease, and chronic obstructive pulmonary disease. He has smoked one pack of cigarettes daily for 40 years. His current medications include aspirin, lisinopril, and salmeterol. His temperature is 37°C (98.6°F), pulse is 75/min, and blood pressure is 128/75 mm Hg. The lungs are clear to auscultation. Cardiac examination shows no murmurs, rubs, or gallops. The abdomen is soft with no organomegaly. Digital rectal examination shows a large internal hemorrhoid. Test of the stool for occult blood is positive.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [128.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",92.66667,88.03334,97.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 128.0 mm Hg + 2/3 * 75.0 mm Hg = 92.66667 mm Hg.
Hence, the patient's mean arterial pressure is 92.66667 mm Hg."
1572,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7381,Extracted,"A 26-year-old gravida 2 para 1 at 24 weeks gestation is admitted to the labor and delivery suite with mild abdominal cramps, uterine contractions, and a watery vaginal discharge. She has a history of preterm birth. The vital signs are as follows: blood pressure 125/80 mm Hg; heart rate 100/min; respiratory rate 13/min; and temperature 36.6℃ (97.9℉). The pelvic examination reveals cervical softening and shortening. Transvaginal ultrasound shows a cervical length of 12 mm, which is consistent with preterm labor. A tocolytic and a single dose of betamethasone are administered.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",95,90.25,99.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 80.0 mm Hg = 95.0 mm Hg.
Hence, the patient's mean arterial pressure is 95.0 mm Hg."
1573,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4667,Extracted,"A 17-year-old female presents to her primary care physician with right foot pain for the last 3 days. She states that the pain began gradually and is worse with weight bearing and activity. The patient states that she recently began to train for a marathon and is running much more than she did several months ago. She is healthy but has a 2-year history of irregular menstruation, with up to 3 months between periods. At this visit, her temperature is 98.5°F (36.9°C), blood pressure is 116/67 mmHg, pulse is 75/min, and respirations are 14/min. Her BMI is 17.1 kg/m^2, and she appears tired with a flat affect. Palpation of the dorsal surface of the right foot reveals point tenderness on the second metatarsal, though there is no redness, warmth, or swelling. The remainder of the exam is unremarkable. Plain radiograph of the right foot is performed and shown in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [67.0, 'mm hg'], 'Systolic Blood Pressure': [116.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 116.0 mm Hg + 2/3 * 67.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1574,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4518,Extracted,"A 32-year-old woman presents to clinic complaining of pelvic pain and heavy menstrual bleeding for the past 2 years. The patient reports that her last menstrual period was 1 week ago and she soaked through 1 tampon every 1-2 hours during that time. She does not take any medications and denies alcohol and cigarette use. She is currently trying to have a child with her husband. She works as a school teacher and exercises regularly. Her temperature is 97.0°F (36.1°C), blood pressure is 122/80 mmHg, pulse is 93/min, respirations are 16/min, and oxygen saturation is 99% on room air. Physical examination reveals an enlarged, irregularly-shaped uterus palpable at the level of the umbilicus.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [122.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",94,89.3,98.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 122.0 mm Hg + 2/3 * 80.0 mm Hg = 94.0 mm Hg.
Hence, the patient's mean arterial pressure is 94.0 mm Hg."
1575,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6290498-1,Extracted,"A 26-year-old primigravid woman, at 35 weeks gestation attended our obstetric department complaining of abdominal pain along with nausea and vomiting for 3 h. The woman’s antenatal care was uneventful. She had no significant medical, surgical or family history and no history suggestive of thromboembolism. She had never used oral contraceptives or any other hormonal therapy.
Upon arrival, she had a temperature of 36.8 °C, pulse rate of 80 beats per minute, respiratory rate of 20 breaths per minute and blood pressure of 119/71 mmHg. A physical examination on admission showed a gravid uterus just below the xiphoid process. No abdominal tenderness or rebound tenderness were appreciated. The bowel sounds were normal and there were no signs suggestive of peritonitis. A hematologic examination revealed a leukocyte count of 13.1 × 109/L (normal range 4.0 × 109/L - 10.0 × 109/L) with neutrophils accounting for 73.9% (normal range 50–70%), hemoglobin level of 98.6 g/L (normal range 100 g/L - 150 g/L), hematocrit of 0.317 (normal range 0.37–0.43), and platelet count of 187 × 109/L (normal range 100 × 109/L - 300 × 109/L). Coagulation profile and biological tests were within normal limits. Obstetric ultrasound revealed a normal fetus compatible with expected gestational age. The fetal monitor showed that fetal heart rate fluctuated between 150 and 160 beats per min and the uterus contracted occasionally. Threatened preterm labor was initially suspected and magnesium sulfate was given to inhibit uterine contractions. Acute gastritis was also considered.
The second day after admission, the patient complained of more intense abdominal pain that was centered in the right lower quadrant, and she experienced increased vomiting and abdominal distention. Physical examination demonstrated right lower quadrant tenderness without rebound tenderness and a distended abdomen and weak bowel sounds. Hematologic testing revealed leukocytosis with a left shift (leucocyte count of 26.9 × 109/L and neutrophils accounting for 91%) and hemoconcentration (hematocrit of 0.439). Serum amylase was normal. An abdominal ultrasound scan revealed dilation and effusion of the right intestinal canals, thickening of the intestinal wall and a small amount of ascites. Abdominal plain radiography was performed and showed no dilated bowel loops and no features of obstruction or pneumoperitoneum. Obstetric ultrasound revealed demise of the fetus.
Acute appendicitis with perforation was suspected and an emergency exploratory laparotomy was performed immediately. On exploration, approximately 1500 mL of serosanguineous peritoneal fluid was found in the abdomen. The entire ileum, part of the jejunum and part of the ascending colon were gangrenous, and thromboembolism in the corresponding mesenteric veins was noted. The necrotic intestine, measuring approximately 180 cm, was resected and an end-to-end jejunum-colon anastomosis was performed. Since there was no evidence of pending spontaneous labor and delivery and to avoid the release of fetally-derived necrotic materials that could complicate the clinical scenario via pro-coagulant and pro-inflammatory effects, a cesarean section was performed and the fetus and placenta were removed. The patient’s hematological values during the operation showed a white cell count of 14.58 × 109/L, neutrophils accounting for 91%, hemoglobin of 73 g/L, a hematocrit of 0.236 and a platelet count of 135 × 109/L. The pathologic examination revealed extensive mucosal denudation, edema, hemorrhage and neutrophil infiltration in the submucosa and muscularis propria of the bowel (Fig. a), and widespread thrombosis in mesenteric venous lumens (Fig. b).
The patient was transferred to the intensive care unit after surgery. Total parenteral nutrition, intravenous antibiotics and full anticoagulation with low molecular weight heparin were initiated postoperatively and continued until discharge. Thrombolytic therapy was withheld due to bleeding risk. The patient had a reasonably uneventful recovery and was discharged on postoperative day 36. Four years later, the patient was again pregnant and underwent thrombophilia testing (antithrombin, protein C, protein S, and coagulation parameters) at 30 weeks of gestation. At that time, antithrombin III activity was 64% (normal range 80–120%). Her antithrombin III activity returned to normal (96%) 4 weeks later. She delivered a healthy baby through a cesarean section at 38 weeks of gestation without thromboembolic event and without thromboprophylaxis. She has been recurrence-free for 10 years without anticoagulant therapy.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [119.0, 'mm hg'], 'Diastolic Blood Pressure': [71.0, 'mm hg']}",87,82.65,91.35,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 119.0 mm Hg + 2/3 * 71.0 mm Hg = 87.0 mm Hg.
Hence, the patient's mean arterial pressure is 87.0 mm Hg."
1576,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7720338-2,Extracted,"A 67-year-old man who had a history of hypertension and diabetes for 6 years, without a family history of coronary heart disease, presented with complaints of chest pain and shortness of breath for 2 hours. A physical examination showed a body temperature of 36.0°C, pulse rate of 72 beats/minute, respiratory rate of 19 breaths/minute, blood pressure of 162/98 mmHg, and moist rales was heard in both lungs. An ECG showed sinus rhythm and ST elevation in leads V1 to V4 (). Laboratory tests showed a CK-MB level of 25.70 ng/mL and a cTNI level of 7.16 ng/mL. The diagnosis of acute extensive anterior STEMI was made. CAG showed total occlusion of the proximal LAD artery with thrombus burden, no major stenosis of the left circumflex artery, and an invisible RCA. The distal LAD artery gave rise to the right ventricular branch and posterior descending branch ().
After obtaining consent from the family, we proceeded to primary PCI, thrombus aspiration was performed, and a 4.0 × 32-mm drug-eluting stent was implanted in the proximal LAD artery. The procedure was successful. The patient’s vital signs were stable during the operation, without any complications. This patient was also managed with antiplatelets, anticoagulants, coronary artery dilators, lipid-lowering agents, and symptomatically. Six days later, the patient was discharged from the hospital.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [162.0, 'mm hg'], 'Diastolic Blood Pressure': [98.0, 'mm hg']}",119.33333,113.36666,125.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 162.0 mm Hg + 2/3 * 98.0 mm Hg = 119.33333 mm Hg.
Hence, the patient's mean arterial pressure is 119.33333 mm Hg."
1577,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5823,Extracted,"A 77-year-old man presents to the emergency department for shortness of breath. The patient states that over the past month he has felt short of breath when doing everyday tasks, and today he even felt short of breath while taking a nap. The patient has a past medical history of obesity, diabetes, hypertension, and asthma. His current medications include lisinopril, insulin, metformin, and an albuterol inhaler. His temperature is 99.5°F (37.5°C), blood pressure is 130/90 mmHg, pulse is 85/min, respirations are 11/min, and oxygen saturation is 96% on room air. An EKG is ordered as seen in Figure A. A chest radiograph is ordered as seen in Figure B. Laboratory studies are ordered as seen below:

Serum:
Na+: 137 mEq/L
K+: 3.9 mEq/L
Cl-: 100 mEq/L
HCO3-: 24 mEq/L
Urea nitrogen: 9 mg/dL
Glucose: 122 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 10.2 mg/dL
Mg2+: 1.5 mEq/L
AST: 15 U/L
ALT: 9 U/L
Alkaline phosphatase: 32 U/L
Glutamyltransferase (GGT): 12 U/L
Albumin: 3.9 g/dL
Total protein: 6.9 g/dL
Total bilirubin: 0.9 mg/dL
Direct bilirubin: 0.2 mg/dL

On physical exam the patient appears obese and in distress. He has bilateral lower extremity pitting edema and yellowing of his toenails. Pulmonary exam is notable for bilateral crackles. Cardiac exam demonstrates a normal rate and rhythm with a displaced cardiac apex. There is JVD to the angle of the mandible.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 90.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
1578,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2845798-1,Extracted,"A 48-year-old woman was admitted to the Rheumatology clinic on 30 October 2008 with a 7-month history of pain and swelling in the right knee. The patient underwent arthroscopic arthroplasty 9 months before for relief of osteoarthritis pain. Because the pain and swelling in the right knee developed 7 months earlier, she underwent repeat arthroplasty 4 months before admission for removal of semilunar cartilage remnants. Despite the two arthroplasties, she continued to complain of pain and swelling.
Her medical history was negative for any rheumatoid diseases, cancer, renal diseases, and AIDS. She was a non-smoker, and did not take any steroids, antibiotics, or illegal drugs. On physical examination, the patient had no rashes, lymph node enlargement, or hepatosplenomegaly. The patient’s vital signs were as follows: blood pressure, 130/80 mmHg; heart rate, 88/min; respiratory rate, 20/min; and body temperature, 36.8°C (98.2°F). The patient was alert and oriented, and there were no oral ulcers or erythema. The conjunctivae were not anemic and the sclerae were not icteric. A chest X-Ray showed a normal cardiac silhouette with no signs of pulmonary edema, and an EKG showed a normal sinus rhythm.
The laboratory results were as follows: WBC, 3100/mm3 (4-10 x 103/mm3); hemoglobin, 15g/dL (12-16g/dL); PLT, 16.3 x 104/mm3 (15-45 x 104/mm3); ESR, 41 mm/hr (0-15 mm/hr); CRP, 28.9mg/dL (0-5mg/dL); total bilirubin, 0.6 mg/dL (0.2-1.4mg/dL); AST/ALT, 23/11 IU/L (5-35/5-40 IU/L); ALP, 130 IU/L (32-122 IU/L); r-GTP, 16 IU/L (7-50 IU/L); LDH, 553 IU/L (100-450 IU/L); BUN/Cr, 11.2/0.8 mg/dL (8-20/0.5-1.3 mg/dL); and uric acid, 2.2 mg/dL (2.5-8 mg/dL). Tests for anti-nuclear antibody (ANA), rheumatoid factor (RF), anti-dsDNA antibody, anti-Smith antibody, anti-Ro/La antibody, anti-RNP antibody, and HLA B27 were all negative. The C3 was 158 mg/dL (70-176 mg/dL) and the C4 was 21 mg/dL (16-45 mg/dL). The synovial fluid cytology findings were as follows: appearance, cloudy and reddish; WBC, 12,800/mm3 (0-200/mm3) with 85% neutrophils and 10% lymphocytes; RBC, 8,320/mm3 (0-400/mm3); protein, 3g/dL (1-3 g/dL); and glucose, 2 mg/dL (0-10 mg/dL). No crystals were detected in the joint aspirate. The Gram stain and acid-fast bacteria (AFB) stain showed no bacteria or tuberculosis. Candida parapsilosis was cultured in the synovial fluid on hospital day 7, which was confirmed on hospital day 8.
On hospital day 2, the radiographs of both knees showed a mottled appearance of the distal femur and proximal tibia and asymmetric joint space narrowing (Fig. ). A magnetic resonance imaging (MRI) of the right knee demonstrated a large joint effusion and enhanced synovium, indicating severe inflammation of the knee joint (Fig. ). Amphotericin B (0.7 mg/kg/day) was given intravenously for 3 weeks. As the pain and swelling of the knee subsided, the amphotericin B was discontinued and oral fluconazole (400 mg/day) was prescribed for 6 months. The last culture of synovial fluid was negative for C. parapsilosis and the patient had no complaints of pain or swelling.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1579,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7780870-1,Extracted,"Case 1: A 52-year-old male was admitted for community-acquired pneumonia with fever, cough and dyspnea to Shahid Yahyanejad Hospital, Babol, Iran. He had neither a recent travel history of China nor close contact with a COVID-19 patient. He was an otherwise healthy and non-smoker individual with no drug history.
Clinical examination revealed vital signs including temperature of 38 °C, a pulse rate of 110 beats per minute, a blood pressure of 130/80 mm Hg, a respiratory rate of 20 breaths per minute, and Oxygen saturation (SpO2) of 89% while breathing ambient air. Lung CT scan revealed bilateral multilobar peripheral ground-glass opacities (GGOs) along with interlobular septal thickening indicative of COVID-19 (). In the other words, axial non-contrast CT image showed widespread bilateral GGOs and some areas of consolidative pulmonary opacities with thickened interlobular and interlobular lines called crazy paving pattern. Also in this patient, RT-PCR assay of nasal and pharyngeal samples were positive for COVID-19. According to his laboratory data and imaging findings, he received inpatient medical and supportive treatment including supplemental oxygen for COVID-19 and his status improved thus his SpO2 reached 99% in room air, but soon after with the patient's personal consent; he was discharged.
A few hours later, the patient returned to the emergency department with worsening dyspnea and two episodes of generalized tonic–clonic seizures. His vital signs at admission included a temperature of 38.5 °C, pulse rate of 120 beats per minute, blood pressure of 140/80 mm Hg, respiratory rate of 22 breaths per minute, and SpO2 of 98% while breathing ambient air. On neurological examination, the patient was conscious and oriented.
The cranial nerves examination was normal and his pupils were midsize and reactive to light and accommodation. His serum glucose level at the time of unconsciousness was 110 mg/dL. Other laboratory data were as follows: white blood cell (WBC), 13.00×109/L with 10% lymphocytes; hemoglobin (Hb), 12.2 g/dL; platelet, 268,000/µL; C-reactive protein (CRP), 63 mg/L; interleukin-6 (IL-6), 2 pg/mL; pro-B-type natriuretic peptide (proBNP) <20 pg/mL; procalcitonin (PCT), 0.05 ng/mL; blood urea nitrogen (BUN), 11 mg/dL; creatinine (Serum), 0.6 mg/dL; sodium, 139 mEq/L; potassium, 3.8 mEq/L; magnesium, 2.2 mg/dL; phosphors, 4 mg/dL; calcium, 7.5 mg/dL; alkaline phosphatase (ALP), 170 U/L; aspartate aminotransferase (AST), 56 U/L; alanine aminotransferase (ALT), 87 U/L, and negative troponin. A brain CT scan was normal. Patients received anticonvulsant medications. A single 500 mg oral dose of chloroquine phosphate, Kaletra (lopinavir/ ritonavir) two 200 mg tablets twice daily, and azithromycin 500 mg PO daily were administered. With his condition improved and his inflammatory markers decreased, the patient was discharged.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 80.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1580,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5835582-1,Extracted,"A 27-year-old male was admitted to the emergency room (ER) with return of spontaneous circulation (ROSC) after cardiac arrest on 27 December 2015. He bought 10 bottles of EC liquid 3 hours before arrival to the ER. He was found showing seizure-like movements. At the scene, a disposable cup with brownish liquid and a suicide note were found. At the arrival of paramedics, he was found pulseless with the first-monitored rhythm as asystole. Cardiopulmonary resuscitation (CPR) was provided for 13 minutes until ROSC. The brand names of the EC liquid were DIY Flavor Shack® with a nicotine concentration of 16 mg/mL and Halo® with a nicotine concentration of 18 mg/mL. The actual amount of consumption was not detected.
At the time of arrival to ER, the vital signs were as follows: blood pressure (BP) 105/57 mmHg, pulse rate (PR) 111 beats per minute (bpm), respiratory rate (RR) 19 bpm, and body temperature (BT) 34.5°C. He was comatose with fixed pupil size of 3 mm. For post-cardiac arrest care, targeted temperature management (TTM) with 33°C was started. Activated charcoal was given via levin tube and continuous venovenous hemodiafiltration (CVVHDF) was started. Initial laboratory tests were not notable. The results included the following: pH 7.154, PCO2 47.3 mmHg, PO2 497.6 mmHg, FiO2 100%, base deficit 12.4 mmol/L, HCO3 316.3 mmol/L, SaO2 99.8%, lactic acid 9.30 mmol/L, creatine kinase (CK) 140 U/L, creatine kinase-myocardial band (CK-MB) 1.0 µg/L, high-sensitivity troponin I 0.031 ng/mL (at 3rd day of admission, high-sensitivity troponin I 4.097 ng/mL), S100 0.218 µg/L (at 2nd day of admission, 0.060 µg/L), and serum ethanol 164.56 mg/dL. The level of plasma nicotine was not measured due to the limitation of the facility's capacity.
Electrocardiography (ECG) showed sinus tachycardia with a rate of 110 bpm and ST segment depression in leads V4 to V6. Echocardiography showed decreased left ventricular (LV) systolic function with an ejection fraction (EF) of 35% and regional wall motion abnormalities (RWMAs) at the mid and proximal left ventricle. On the 5th day of admission, echocardiography showed the systolic function with EF 58% and the full recovery of RWMAs.
After 24-hour TTM, he was alert and aware. He did not remember events during the previous two months. Brain magnetic resonance imaging (MRI) showed bilateral hippocampal disruption. Amnesia was recovered on the 9th day of admission. On the 6th day of admission, he had involuntary myoclonic movement of all the extremities without any changes in brain MRI. On the 13th day of admission, he was discharged to home with a cerebral performance category (CPC) of 2.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [57.0, 'mm hg'], 'Systolic Blood Pressure': [105.0, 'mm hg']}",73,69.35,76.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 105.0 mm Hg + 2/3 * 57.0 mm Hg = 73.0 mm Hg.
Hence, the patient's mean arterial pressure is 73.0 mm Hg."
1581,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7394142-1,Extracted,"A 35-years-old female, 9 months post-endoscopic gastroplasty presented to the emergency department complaining of epigastric abdominal pain for 5 days, the pain is radiating to the umbilicus associated with nausea and vomiting. On general examination, she is vitally stable with HR 88 B/min, BP 116/66 and temperature 36.9°C, the abdominal examination showed epigastric and tenderness. On abdomen CAT scan, she had partial small bowel obstruction with adhesive band originating from the stomach (). Barium meal showed dilatation of the second part of duodenum due to band like structure (). The patient admitted to the hospital with a diagnosis of small bowel obstruction and kept NPO; Nil Per Os, on IV fluids and nasogastric tube drainage.
The patient taken to the operating room for diagnostic laparoscopy and proceed, after insufflating the abdomen the whole abdomen examined and showed proximal dilatation of small intestine with collapse of distal part of jejunum, the ileocecal junction identified and the small bowel examined proximally till the obstruction identified, which is fibrous band originating from the stomach to the proximal part of jejunum (), examination of this band showed that this band is caused by suture penetrating the stomach wall, which is going with the previous history of the endoscopic gastroplasty, reduction of the internal hernia done by releasing of the fibrous band, the herniated segment was healthy ().",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [66.0, 'mm hg'], 'Systolic Blood Pressure': [116.0, 'mm hg']}",82.66667,78.53334,86.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 116.0 mm Hg + 2/3 * 66.0 mm Hg = 82.66667 mm Hg.
Hence, the patient's mean arterial pressure is 82.66667 mm Hg."
1582,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6820899-1,Extracted,"A 33-year-old Gravida (G) one patient at 41 weeks gestation presented for a scheduled induction of labor using misoprostol to avoid post-term pregnancy complications. Her history was positive for asthma, which was stable throughout the pregnancy. The patient did not report any prior history of neurological issues or allergies. Her medications were prenatal vitamins and Metamucil. On physical examination, she exhibited the normal physical changes of pregnancy. Her prenatal laboratory values were unremarkable. Her vital signs were within normal limits, with a blood pressure of 130/98, heart rate (HR) of 22 and a temperature of 98.6° Fahrenheit. She was 5 feet 4 inches tall and weighed 88.4 kg.
The patient requested an epidural for labor pain and was assessed by the anesthesia team before placement of the epidural catheter. Standard monitors were placed. Subsequently, an epidural catheter was placed without any complications. There was no cerebrospinal fluid or heme aspiration with the utilization of a 3 mL syringe. There was also a negative test dose. The patient was given 0.1% ropivacaine with 2 mcg/mL fentanyl at 10 mL/hour basal infusion with a demand bolus dose of 10 mL every 20 minutes. She was comfortable with the epidural analgesia, and the obstetrician reported no neurological symptoms.
An hour into labor, the patient had an episode of seizures. The labor nurse reported that seizure activity started while she was supine in bed and the seizure appeared to be a generalized motor seizure. The patient had not had any changes in vital signs just before the seizure, while maintaining spontaneous ventilation throughout the seizure previously, with oxygen saturation (SpO2) of 95-100%. She was placed in the right lateral decubitus position on the bed, and supplemental oxygen was given by face mask. The patient-controlled epidural analgesia (PCEA) was turned off. Midazolam 2 mg IV was given, which caused her seizure to end. Thereafter, the patient was minimally responsive, in a postictal like state. The patient did not respond to questions but was awake with pupils responsive for approximately five minutes. After this, the patient was alert and oriented to person, place, and time, and did not recall the seizure. The patient was afebrile with blood pressure at 160/100 mmHg, tachycardia to the 140s and oxygen saturation above 95%, and with Glasgow Coma Scale at 15 without any neurological deficit. The patient did not experience any signs of fever at this time. Otherwise, the physical exam was normal.
Before the seizure, fetal heart tones were noted to be in the 80s to 90s. During the seizure, the fetal heart tones increased to 130, then further increasing to 170s and 180s after the seizure. Due to the fetal heart tones, the surgeon proceeded with the cesarean section.
The patient was taken to the operating room for an emergency cesarean section under general anesthesia. The maternal vital signs remained relatively stable throughout the operation, as per her baseline before the seizure. Cesarean section proceeded without event. Induction of anesthesia was done with Propofol and succinylcholine intravenous and the patient was intubated. Anesthesia was maintained with FiO2 100% and sevoflurane 2%. A viable female infant was delivered weighing 3,710 g; Appearance, Pulse, Grimace, Activity, Respiration (APGAR) scores of one and seven and cord pH of 6.98. The patient received a total of 1,000 mL of intravenous fluids and had an estimated blood loss of 700 mL and urine output of 250 mL.
There was a grossly normal appearance of the uterus, ovaries, and tubes. There was no evidence of abruption of the placenta. There was no evidence of intra-amniotic infection.
The patient met criteria for extubation, she was extubated in the operating room and was transferred to the intensive care unit (ICU) because of new-onset seizure activity of unknown etiology and continued tachycardia in the 120s after delivery.
In the ICU, the patient denied any chest pain, palpitations, shortness of breath, vomiting or diarrhea, however she complained of 3/10 headache that began after delivery. Glasgow Coma Scale was 15. No acute neurologic deficits found on physical exam. The patient was started on seizure prophylaxis with Keppra and Ativan as needed. Her laboratory results were within normal limits except D-dimer. Her hemoglobin (Hgb) was 12.9 g/dL and hematocrit (Hct), 38.6%. Multidisciplinary teams were consulted including the radiologist, neurologist, and neurosurgery for the next three days. CT head showed a small amount of subarachnoid hemorrhage. No definite parenchymal hemorrhage was shown.
MRI of the brain was then obtained (Figure ). It displayed extensive abnormal signal in the cortical grey matter, pons, and bilateral cerebral hemispheres. There was associated enhancement along the bilateral frontal lobes, at least some of which was cortically based. Differential considerations include an atypical presentation of posterior reversible encephalopathy syndrome or meningitis. There was no diffusion restriction to suggest infarct or hypoxic-ischemic injury. Bilateral findings would make status epilepticus unlikely. There was a small amount of extra-axial susceptibility artifact which is compatible with subarachnoid hemorrhage.
Magnetic resonance venography (MRV) of the head without contrast and magnetic resonance angiography (MRA) of the head with contrast were ordered to further establish the diagnosis. The MRI MRV was found to be normal with no evidence of vascular occlusion or thrombosis. The MRA head with contrast was normal, with no evidence of intracranial aneurysm or major vessel occlusion.
She had no further seizures during her stay.
Quantitative troponin levels were elevated at 0.06 ng/ml and further testing including echocardiogram and electrocardiogram were ordered. The echocardiogram displayed normal left ventricular size, thickness, systolic function, and wall motion. The visually estimated ejection fraction was between 60-64%. The electrocardiogram (EKG) showed normal sinus rhythm and was unremarkable.
The following day an electroencephalogram (EEG) was performed that was slightly abnormal due to a mild slowing of posterior dominant rhythm, diffuse theta slowing of the background mainly during drowsiness. The study did not capture any interictal epileptiform discharges or any electrographic ictal discharges.
The patient was discharged home after three days as her condition was stable with a normal neurological exam. Recommendations were to follow-up with neurology outpatient with the diagnosis of posterior reversible encephalopathy syndrome and repeat MRI in two months. The patient was continued on Keppra 500 mg twice a day.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [98.0, 'mm hg']}",108.66667,103.23334,114.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 98.0 mm Hg = 108.66667 mm Hg.
Hence, the patient's mean arterial pressure is 108.66667 mm Hg."
1583,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6533925-1,Extracted,"A 62-year-old female was brought to the Emergency Department with a history of altered sensorium for 1 day following an episode of syncope. The patient had a history of occipitofrontal headache and vomiting of 2-day duration. Her blood pressure was 180/100 mmHg, and heart rate was 66/min at admission. In the electrocardiogram (ECG) recorded at admission, right bundle branch block was noted []. Computed tomography angiogram of the brain showed ruptured saccular aneurysm at the right internal carotid artery–middle cerebral artery junction, as well as hemorrhage in bilateral Sylvian and interhemispheric fissures. She was admitted under the neurosurgery department and was diagnosed to have ruptured berry aneurysm with subarachnoid hemorrhage.
Six hours after admission, the patient developed generalized tonic–clonic seizures and was given slow injection of phenytoin sodium 1 g IV. About a minute after administration of the drug, she developed sudden-onset bradycardia, with a heart rate of 40 beats/min. Her blood pressure also dropped simultaneously to 90/60 mmHg. ECG recording showed sinus bradycardia with right bundle branch block []. She was managed with a fast infusion of injection normal saline 1000 mL and cardiopulmonary cerebral resuscitation. Serum electrolytes and prothrombin time- international normalised ratio (PT-INR) were within the normal range. The patient recovered within half an hour after the onset of reaction.
The following day, the patient underwent right pterional craniotomy and clipping of aneurysm, and postoperatively she was prescribed injection phenytoin 100 mg IV 8 hourly as the prophylactic anticonvulsant. She did not develop bradycardia or hypotension at this maintenance dose of phenytoin.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [180.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",126.66667,120.33334,133,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 180.0 mm Hg + 2/3 * 100.0 mm Hg = 126.66667 mm Hg.
Hence, the patient's mean arterial pressure is 126.66667 mm Hg."
1584,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7603882-1,Extracted,"We present the case of a 77-year-old right-handed man who developed a shingles rash over the ulnar half of his left hand and forearm, posterior aspect of his left upper arm, all the way proximally to behind the left shoulder. He developed a stabbing and burning pain in this distribution, with a rash that blistered and then desiccated over the course of two weeks. One week after the breakout of the rash, he noted weakness of grip of the left hand with an inability to pinch with his left hand. The weakness was restricted to the left hand and reached a nadir in two weeks. The pain required a high dose of gabapentin for relief. He also received a standard regimen of the anti-viral, famciclovir, for shingles.
His past medical history was significant for hypertension, hyperlipidemia, and chronic obstructive airway disease. His medications included lisinopril, atorvastatin, and gabapentin. He formerly smoked one pack a day and quit smoking in 1974.
On examination, his blood pressure (BP) was 120/84, pulse 76 beats per minute, height six feet, weight 202 pounds, and body-mass index (BMI) 27.4. Precordial auscultation revealed no murmurs, and carotid auscultation was negative for a bruit. His gait cadence and stability were normal. He was able to stand on his heels and toes. His speech was fluent. His cranial nerve examination was normal. Of note, there was no evidence of Horner's syndrome.
The power of the right upper extremity and lower extremities was graded at 5/5 by using Medical Research Council (MRC) grading. The left upper extremity grading of power revealed deltoids, biceps, coracobrachialis, brachialis, triceps, and wrist extensors and flexors at 5/5. Pronator teres was also graded at 5/5. Left flexor pollicis longus was graded at 2/5 and finger flexion at the metacarpophalangeal joints and proximal and distal interphalangeal joints at 3/5. Abductor pollicis brevis was graded at 3/5. Finger spreaders (interossei) were graded at 2/5. Mild atrophy of the left first dorsal interosseus, abductor pollicis brevis, and ulnar half of the left forearm was noted. The sensory exam revealed hyperesthesia to touch over the left C8 distribution, as outlined in Figure .
Weakness of the left flexor pollicis longus and flexor digitorum superficialis explains the pinch "" O "" sign, which is the inability to form the letter "" O "" by flexion of the thumb and flexion of the distal interphalangeal joints of the index finger during apposition of the thumb and index finger. This is demonstrated below and compared to the right hand (Figure ).
Atrophy of the ulnar half of the left forearm and left hypothenars reflect the pattern of weakness (Figure ).
The next step was to confirm these findings with a nerve conduction study/electromyogram (NCS/EMG). This demonstrated a reduced left median motor amplitude, markedly reduced left ulnar motor amplitude, normal left median sensory, and diminished left ulnar sensory amplitude. The left lateral antebrachial cutaneous sensory was preserved with an absent left medial antebrachial cutaneous sensory amplitude. Left radial motor and sensory amplitudes were normal. This combination of findings of abnormal left median and ulnar nerves, with absent left medial antebrachial cutaneous sensory amplitude and preserved median sensory amplitude, is highly suggestive of a left medial cord plexopathy. The lack of radial nerve involvement precludes the lower trunk of the brachial plexus; note normal left radial motor and sensory amplitudes, also noting that the median sensory nerve emerges from the lateral and not from the medial cord of the brachial plexus (Table ).
It should be noted that the sensory and motor velocities and distal motor latencies of the left median and ulnar nerves were normal or slightly reduced and are not listed in the table. There was also no evidence of ulnar nerve entrapment at the left elbow. The reduced ulnar sensory amplitude with absent left medial antebrachial cutaneous sensory amplitude with preserved left lateral cutaneous antebrachial cutaneous and median sensory amplitudes are demonstrated graphically below (Figure ).
The electromyography (EMG) study reveals acute and florid denervation of the left median and ulnar innervated muscles of the hand and forearm, with the preservation of radial, axillary, and musculocutaneous nerves (Table ).
Selected EMG of the involved muscles of the left hand and forearm reflecting the clinical pattern of weakness on examination; noting acute and florid denervation with fibrillation potentials and positive waves of involved muscles (Figure ).
One should also emphasize the absence of left lower paraspinal muscle denervation precluding cervical C8 motor nerve root involvement. However, cervical C8 sensory nerve root involvement is not excluded, as the rash extends beyond the territory of the ulnar sensory and medial antebrachial cutaneous sensory nerves, to behind the left upper arm and left shoulder. It is more than likely that we are dealing with a C8 radiculo-medial cord brachial plexopathy. The patient was referred to physical and occupational therapy and will be monitored closely.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [84.0, 'mm hg']}",96,91.2,100.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 84.0 mm Hg = 96.0 mm Hg.
Hence, the patient's mean arterial pressure is 96.0 mm Hg."
1585,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3994266-1,Extracted,"A 17-year-old girl visited Chungbuk National University Hospital, presenting with fever and abdominal pain that had developed 7 days previously. She had undergone an operation for gastroschisis repair at birth. At the time of admission, her vital signs were as follows: blood pressure, 120/80 mm Hg; pulse rate, 70 beats per minute; respiration rate, 18 breaths per minute; and body temperature, 37.5℃. She appeared emaciated and acutely ill. Her body mass index was 18.1 (height, 151 cm; and weight, 41.3 kg). A physical examination revealed icteric sclera, a very thin abdominal cavity, and a longitudinal surgical scar at the midline. Tenderness was noted in the upper abdominal area, and normal bowel sounds were heard. There was no particular finding in the limb or neurological examinations. Laboratory analysis revealed a white blood cell count of 27,000 cells/mm3; hemoglobin level, 12.3 g/dL; platelet count, 277,000 cells/mm3; aspartate aminotransferase level, 108 IU/L; alanine aminotransferase level, 144 IU/L; alkaline phosphatase level, 476 IU/L; total protein level, 6.5 g/dL; albumin level, 3.7 g/dL; total bilirubin level, 14.1 mg/dL; direct bilirubin level, 9.2 mg/dL; amylase level, 592 U/L; lipase level, 825 U/L; blood urea nitrogen level, 5.0 mg/dL; and creatinine level, 0.5 mg/dL. These data were compatible with diagnoses of acute cholangitis and acute biliary pancreatitis. An abdominal computed tomography scan revealed a round calcifying lesion near the pancreas (), and the absence of the retroperitoneal duodenum and the anterior position of the spleen with respect to the left kidney. The anterior and left-sided position of the superior mesenteric vein compared with that of the superior mesenteric artery was observed in the abdominal computed tomography scan (). The coronal view revealed the distorted architecture of the liver and a high-attenuation lesion at the extrahepatic bile duct (). Results of a barium examination revealed a right-sided duodenojejunal flexure and malpositioning of the bowel, with the small bowel on the right side and the colon on the left side (). Intestinal malrotation could be diagnosed based on these findings. ERCP was performed by using a lateral-view endoscope in the usual way. After approaching the ampulla, the endoscope was pushed against the duodenal wall to maintain the papilla in the correct position, and a selective bile duct cannulation confirmed the presence of a 12-mm round stone in the common bile duct. With a guidewire-assisted technique, the single dark brown stone was removed by using a Dormia basket after the endoscopic sphincterotomy (). The procedure lasted for 15 minutes. A cholangiogram obtained through an endoscopic nasobiliary drainage tube revealed a distorted biliary system, which was characterized with diffuse dilatation of the intrahepatic and extrahepatic biliary trees, downward-positioned gallbladder and a right intrahepatic biliary tree, and a horizontally located common bile duct. The abnormal orientation of the duodenum suggested intestinal malrotation (). Clinical symptoms and liver function tests normalized after the ERCP procedure. The patient has been monitored for 3 years and is in a normal state.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1586,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8052168-1,Extracted,"An 8-year-old girl diagnosed with AML (standard risk) was transferred to our hospital. According to the AML12 protocol of the Japanese Pediatric Leukemia/Lymphoma Study Group (JPLSG), she received combination chemotherapy (cytarabine, methotrexate, mitoxantrone, idarubicin, and etoposide) as induction therapy and achieved complete remission. Neutropenia became apparent 6 days after maintenance therapy, with neutrophil counts of <500/μL, and the patient developed febrile episodes with shaking chills 9 days after maintenance therapy. She appeared toxic, and her temperature, blood pressure, pulse rate, and respiratory rate were 38.7°C, 88/48 mmHg, 108/min, and 24/min, respectively.
Laboratory examination revealed a decreased leukocyte count of <100/μL and elevated C-reactive protein level of 3.58 mg/dL (reference range, <0.5 mg/dL). After two consecutive blood cultures taken from the peripheral vein and peripherally inserted central catheter (PICC) line, meropenem (40 mg/kg/dose, 3 times/day) was administered as empiric therapy. The standard blood culture exhibited only coryneform Gram-positive, club-shaped, slightly curved rods from the aerobic bottle 1 day after culture. Her temperature, blood pressure, pulse rate, and respiratory rate were 36.7°C, 76/40 mmHg, 96/min, and 18/min, respectively. We then added vancomycin (15 mg/kg/dose, 4 times/day) to the treatment protocol and removed the PICC line on the second day of the febrile episode. The duration of PICC placement was 69 days.
Using a MALDI Biotyper (Bruker Daltonik GmbH, Bremen, Germany) with laser desorption ionization time-of-flight mass spectrometry, we identified B. casei in the positive blood cultures containing samples taken from the peripheral vein and PICC line []. B. casei also grew in the sample collected from the PICC tip, based on which we made a diagnosis of CRBSI caused due to B. casei.
After a 24 h incubation at 37°C in a CO2 atmosphere, the Gram-positive rods formed colonies on sheep blood agar that were whitish to gray-white in color, non-hemolytic, smooth, and round and had a distinctive cheese odor (). The isolate was positive for catalase, α-glucosidase, and gelatin hydrolysis, while negative for urease, oxidase, and nitrate reduction. These biochemical features were typical of B. casei. Drug sensitivity tests were analyzed using the broth microdilution method. The minimum inhibitory concentration for the isolate was >4 μg/mL for ampicillin, sulbactam/ampicillin, and tazobactam/piperacillin; >2 μg/mL for cefazolin and cefmetazole; ≤2 μg/mL for cefepime; 0.25 μg/mL for meropenem; 2 μg/mL for clarithromycin; 4 μg/mL for ciprofloxacin; and 0.5 μg/mL for vancomycin.
There is no standardized treatment for B. casei bacteremia, and the Clinical and Laboratory Standards Institute 2011 criteria for interpreting susceptibility results are based on the recommendations that apply to Corynebacterium spp. []. In our case, antimicrobial therapy with meropenem and vancomycin and PICC line removal consequently led to a significant clinical improvement of the symptoms. We performed antimicrobial treatment for 19 days until the patient's neutropenia was ameliorated, and she recovered without sequelae. After the chemotherapy as treatment of AML, the patient remained in remission. At present, she is undergoing close follow-up as an outpatient.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [88.0, 'mmhg'], 'Diastolic Blood Pressure': [48.0, 'mmhg']}",61.33333,58.26666,64.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 88.0 mm Hg + 2/3 * 48.0 mm Hg = 61.33333 mm Hg.
Hence, the patient's mean arterial pressure is 61.33333 mm Hg."
1587,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3350210-1,Extracted,"45-year-old man with a 20-year history of methamphetamine abuse presented to emergency room with acute sudden onset of abdominal pain and hematochezia. He denied abusing any other substance. He had been seen 3 days earlier for rectal bleeding and local rectal care was advised. He was known to have pulmonary artery hypertension and cardiomyopathy attributed to methamphetamine abuse. A contrast enhanced CT of the abdomen revealed stenotic lesions at the origin of the superior mesenteric and celiac axis of approximately 70%, no bleeding sites or pseudoaneurysms were seen. The visceral stenotic lesions were demonstrated on duplex as well, SMA (pSV at origin 538 cm/sec). Physical exam: tachycardia and orthostatic hypotension. His blood pressure (HR) on admission was 133/66 (74) becoming 82/52 (81) with continued bright red blood, Hct/Hb drop from 49.8% (15 gm/dL) to 35.2% (11.7 gmm/dL despite replacement blood therapy). Endoscopy revealed the stomach and esophagus as normal; with colonoscopy extensive bleeding was encountered obscuring the required detail to identify a specific bleeding source. The bleeding site was identified arteriographically, in the rectum as the branches of the inferior rectal artery (), arteriograms of the visceral arteries (), the superior mesenteric artery (), and celiac axis () revealed diffuse narrowing the visceral vessels with focal areas of occlusion. The inferior mesenteric artery was narrowed with occlusion of the superior rectal artery. “Corkscrew collateral"" vessels were seen on the mesentery. In , the internal pudental artery was catheterized with 4 French angiographic catheter and the inferior rectal arteries selected with a 1.8 F OD microcather (Balt Extrusion, Montmorency, France, Magic Catheter), and a 0.008′′ hydrophilic wire guide (Mirage, EV3Plymouth, MN, USA). The lesion was treated with 0.5 mL of a 3 : 1 emulsion of n-Butyl Cyanoacrylate (Trufill, Cordis Neurovascular, Miami Lakes Florida) and Ethiodol (Nycomed, Inc., USA) (). Following the procedure thier immediate relief from the rectal bleeding and the patient continued to improve over the next several days with no further bleeding or signs of intestinal ischemia.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [66.0, 'mm hg'], 'Systolic Blood Pressure': [133.0, 'mm hg']}",88.33333,83.91666,92.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 133.0 mm Hg + 2/3 * 66.0 mm Hg = 88.33333 mm Hg.
Hence, the patient's mean arterial pressure is 88.33333 mm Hg."
1588,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6636589-1,Extracted,"A 39-year-old African American woman was brought to our emergency room (ER) with lethargy, progressive confusion, and generalized rash involving both lower extremities of 1-week duration. Two months ago, the patient had presented to our hospital with left lower quadrant pain and nonbloody diarrhea and dizziness. A Computed Tomography (CT) of the abdomen and pelvis had revealed pancolitis and she was treated with antibiotics. At that time she was also found to have proteinuria, pedal edema and photosensitive rash on her face. The proteinuria was attributed to glomerular disease of unclear etiology. Autoimmune work-up revealed positive ANA, anti-Smith Ab, and anti-RNP. Parvovirus IgG was also positive. She was found to have pancytopenia and the diagnosis of aplastic anemia was considered and she was transferred to another tertiary care hospital. There, she underwent a renal biopsy that revealed focal proliferative and membranous lupus nephritis classes 3 and 5. She was discharged on prednisone, mycophenolate, and hydroxychloroquine. Now she had presented with the current complains.
In the ER she was found to be lethargic. On physical examination, her temperature was 97.5°F, pulse was 102 beats per minute, the initial blood pressure was 136/79 mm of Hg, and respiratory rate was 22 breaths per minute. There was no scleral icterus. Oral mucosa was dry without visible lesions. The neck was supple. Skin was warm and had desquamating rash on both lower extremities from hip down (). The rash was nonblanching and erythematous, and Nicolsky sign was positive. The abdomen was soft but mild tenderness was noted in the epigastric region without any guarding or rebound tenderness. There was no organomegaly and the bowel sounds were sluggish. There was bilateral pitting pedal edema. The patient was arousable with verbal and tactile stimulation and was moving all extremities spontaneously. Rest of the physical examination was unremarkable.
Later she developed hypotension and was given on intravenous fluids. Sepsis was suspected and broad spectrum antibiotics were initiated. The early differential diagnosis included Steven Johnson syndrome vs. necrotizing fasciitis causing sepsis. Her labs revealed severe pancytopenia and severe metabolic acidosis. Detailed results of the laboratory parameters are given in .
She was transfused 2 units of packed red blood cells and 6 units of platelets. Within an hour of arrival to the ER she developed acute respiratory failure and was intubated and placed on mechanical ventilation. She developed septic shock requiring vasopressors. She was deemed too unstable for imaging studies but a portable chest X-ray revealed right basilar atelectasis and portable X-ray of the lower extremities showed soft tissue edema. Four hours after the initial presentation she developed asystole and expired after failed resuscitative measures. An autopsy was done that revealed CHP (), Libman Sacks endocarditis, bilateral pleural effusion, proliferative and membranous lupus glomerular nephropathy, and bilateral adrenal hemorrhage. Blood culture postmortem grew serratia marcescens.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [136.0, 'mm hg'], 'Diastolic Blood Pressure': [79.0, 'mm hg']}",98,93.1,102.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 136.0 mm Hg + 2/3 * 79.0 mm Hg = 98.0 mm Hg.
Hence, the patient's mean arterial pressure is 98.0 mm Hg."
1589,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1236,Extracted,"Eighteen hours after undergoing surgery for a splenic rupture and liver laceration following a high-speed motor vehicle collision, a 23-year-old man's pulse is 140/min, blood pressure is 80/50 mm Hg, and central venous pressure is 19 cm H2O. He was transfused with 6 units of packed red blood cells during surgery. Examination shows jugular venous distention. There is a midline surgical incision with no erythema or discharge. The abdomen is tense and distended. The total urine output over the past 6 hours is 90 mL.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [80.0, 'mm hg'], 'Diastolic Blood Pressure': [50.0, 'mm hg']}",60,57,63,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 80.0 mm Hg + 2/3 * 50.0 mm Hg = 60.0 mm Hg.
Hence, the patient's mean arterial pressure is 60.0 mm Hg."
1590,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8669203-1,Extracted,"A 60-year-old African American female with a past medical history of hypertension, chronic obstructive pulmonary disease (COPD), hyperlipidemia, sickle cell trait, class III obesity, presented to the hospital with shortness of breath two days ago, associated with a progressively worsening tongue and neck swelling that developed for five days. She was referred to the emergency room from her Primary Care Physician (PCP) office for high clinical suspicion of angioedema. Earlier that day the patient had presented to her PCP office with a progressively worsening, asymmetric (right greater than left) tongue swelling for five days. The tongue swelling had disrupted the patient's sleep and made it difficult for her to swallow solid food. She also endorsed associated painful neck swelling and shortness of breath. She did not notice any rash on her body and denied itching. She also reported having a dry cough for two months, which was persistent despite trying all cough remedies. Her home lisinopril was discontinued four weeks ago with some improvement of cough. She had previously tolerated ACE inhibitor for months without any issue. Upon arrival at the hospital, on physical examination, her vital signs included a temperature of 37.1ºC, blood pressure of 164/89 mmHg, heart rate of 102 beats per minute, respiratory rate of 22 breaths per minute, and oxygen saturation of 93% on room air. She was alert and oriented, speech and voice with wet quality, without stridor, head and neck exam was significant for lower lip swelling, diffuse neck swelling with tenderness, palpable cervical, and retro auricular lymph nodes. A heart exam revealed regular rate and rhythm. Lung examination was notable for decreased air entry bilaterally without any added sounds. Skin exam was without evidence of any erythema, swelling, or rash. The remainder of the examination was unremarkable. Her initial lab work including a comprehensive metabolic panel and complete blood count were within normal limits. Her erythrocyte sedimentation rate was elevated at 59 mm/hr. An initial chest x-ray and x-ray of the soft tissues of the neck were unremarkable. A clinical diagnosis of angioedema related to either ACE inhibitor use or other etiology was made. The patient immediately received steroids, histamine 2 (H2) receptor blockers, Icatibant, and fresh frozen plasma. The patient was evaluated by an otolaryngologist with transnasal flexible fiberoptic laryngoscopy (FFL), which revealed symmetric bilateral watery edema on the lateral edges of the lingual surface of epiglottis without evidence of laryngeal involvement. She was transferred to the Intensive care unit for closer monitoring and anticipated intubation. Further lab testing revealed normal C-1 esterase levels, complement C3 levels, complement C4 levels, and C-reactive protein. The patient’s symptoms persisted on the next day and a repeat FFL evaluation remained unchanged from prior. A computed tomography scan with intravenous contrast of the soft tissues of the neck was obtained which revealed an unremarkable exam of pharyngeal mucosal spaces, larynx, and neck spaces. She was started on antihistamines, H2 receptor blockers, and steroids. The patient received a total five-day course of steroids and had resolution of swelling without requiring intubation. In the absence of associated itching, hives, and normal C-1esterase levels; bradykinin mediated angioedema in the setting of prior ACE inhibitor use was deemed the cause of her angioedema. ACE inhibitor-induced angioedema was permanently added to the list of her allergies. She was transferred to a regular medicine floor within three days and discharged home after a seven-day hospital course with an outpatient follow-up with PCP.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [164.0, 'mm hg'], 'Diastolic Blood Pressure': [89.0, 'mm hg']}",114,108.3,119.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 164.0 mm Hg + 2/3 * 89.0 mm Hg = 114.0 mm Hg.
Hence, the patient's mean arterial pressure is 114.0 mm Hg."
1591,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5466870-1,Extracted,"A 56-year-old African man presented to our emergency department 6 hours after severe chest pain onset. He was a tobacco smoker, diabetes status unknown, neither hypertensive nor dyslipidemic, and had no history of stroke. He had no personal or family medical history, including heart disease or heart rhythm disorder, and was not under any treatment prior to diagnosis. He was from a low socio-economic level. An electrocardiogram (EKG) showed a sinus rhythm with ST-segment elevation in inferior and posterior leads (Fig. ).
At admission he was conscious, Glasgow Coma Scale (GCS) of 15/15, without motor deficit or sensory disorder; his chest pain was constrictive irradiating to his two upper limbs without syncope. Blood pressure (BP) on admission was 140/85 mmHg symmetrical, regular rhythm at 60 beats per minute (bpm), heart sounds clearly auscultated with no heart or carotid murmur, there was no murmur of mitral insufficiency or ventricular septal defect, no signs of heart failure including no crackles, and he was without edema of his lower limbs or turgor of his jugular veins leading to a right ventricular infarction. His peripheral pulses were perceived symmetrically. The rest of the examination was strictly normal. Acute inferior and posterior STEMI was diagnosed and intravenously administered TT using tenecteplase (intravenous bolus of 30 mg considering a weight of 54 kg) was performed with adjuvant antithrombotic medication (aspirin, clopidogrel, and enoxaparin).
A few minutes later, he developed motor aphasia and right hemiplegia with altered level of consciousness: GCS of 12/15. The first cerebral computed tomography (CT) performed 1 hour later was normal and the second one performed 12 hours later showed a frontal, temporal, and parietal left ischemic stroke with a hemorrhagic infarct (Fig. ). On an EKG, the ST-segment elevation regressed more than 50% at 60 minutes after TT. An echocardiographic examination (Vivid 6S) was performed following the therapy. It revealed a left ventricle ejection fraction (LVEF) at 50%, no mitral insufficiency, pulmonary artery pressure at 36 mmHg, no thrombus was detected in any cavity, no ventricular septal defect, and no pericardial effusion. An echo-Doppler of the supra-aortic trunks was not performed. The laboratory findings were as follows: troponin Ic, 18 ng/ml; normal liver function tests; glomerular filtration rate (GFR) by Modification of Diet in Renal Disease (MDRD) method at 85 ml/1.73 m2 body surface area (BSA) per minute; hemoglobin, 13.5 g/dl; platelets count, 500,000/mm3; plasmatic fibrinogen level, 2.49 g/l before TT and 5.89 g/l 12 hours after; white blood cells count (WBC), 15,000 mm3; and C-reactive protein (CRP), 72 mg/l. Antithrombotic medication was discontinued. His neurological condition worsened progressively and, after 1 week, he died.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 85.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
1592,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8702218-1,Extracted,"A 68-year-old woman was transferred to our hospital with worsening respiratory failure related to COVID-19. She was 9 days from diagnosis of COVID-19 and had been treated with favipiravir and dexamethasone at the previous hospital. She had a history of hypertension and hyperlipidemia.
The patient was obese with a height of 140 cm and a body mass index of 36.5. In the emergency department, she had clear consciousness and her vital signs and were as follows: blood pressure, 127/86 mm Hg; heart rate, 77 beats/min; respiratory rate, 28/min; saturation on pulse oximetry, 98% in O2 mask 10 L. Because she had dyspnea, she was intubated, placed on a ventilator, and admitted to the emergency intensive care unit (EICU). Favipiravir was terminated and dexamethasone was administered for 10 days. Chest computed tomography (CT) scans at the time of admission are shown in Figure A. After intubation, the ventilator settings were: assist control pressure control ventilation; fraction of inspired oxygen, 0.4; positive end-expiratory pressure, 10 cmH2O, pressure above positive end-expiratory pressure, 15 cmH2O, and partial pressure of arterial oxygen/fraction of inspiratory oxygen ratio (P/F ratio), 174—indicating moderate acute respiratory distress syndrome. It was assumed that the transpulmonary pressure was not large, based on occlusion pressure and physical findings; the patient was maintained under spontaneous breathing. A tracheostomy was performed on day 5 after EICU admission. However, on day 6, there was a sudden increase in respiratory effort and the P/F ratio worsened to 100. Chest CT scans at this time are shown in Figure B. The patient was treated in the prone position with muscle relaxants and efforts were made to achieve lung protective ventilation; but, progressive hypoxemia was observed, with a P/F ratio of 72. Since the patient was not old, and Activity of Daily Living was Independent, the indications for VV-ECMO were considered through discussion among a multidisciplinary team that included respiratory physicians, infectious disease specialists, intensivists, and nurses. Pulmonary injuries were thought to be reversible due to the short duration of ventilator management. On day 7 after admission, VV-ECMO was initiated, as follows: right femoral vein drainage, 23Fr HLS cannula (MAQUET Cardiopulmonary, Rastatt, Germany); right internal jugular vein return, 19Fr HLS cannula (MAQUET); centrifugal pump, CAPIOX SP-200 (TERUMO, Tokyo, Japan) (extracorporeal membrane oxygenation [ECMO] flow, 3.4 L; 1430 rpm; delivered fractional oxygen percentage, 1.0; sweep gas, 3 L).
After initiation of VV-ECMO, fluid balance was regulated using diuretics and the extracorporeal ultrafiltration method. To maintain safe and stable ECMO for a long period, anticoagulation was established using unfractionated heparin to achieve an activated partial thromboplastin time ratio of 1.5. A platelet transfusion was performed to achieve a platelet count of 8 × 103/μL. However, a subcutaneous hematoma appeared in an area unrelated to external factors, such as restraint and repositioning (Fig. A, 2B). On day 13 after admission, ECMO flow decreased abruptly to 1.2 L, with a simultaneous decrease in blood pressure to 79/48 mm Hg. With bleeding complications suspected, a contrast-enhanced CT scan of the trunk was performed. Active bleeding with extravasation of the left retroperitoneal space was confirmed. TAE was immediately performed and ECMO flow and blood pressure were stabilized. (Fig. C) Six hours after achieving hemostasis, anticoagulation with unfractionated heparin was restarted. However, on the following day (day 14 after EICU admission), ECMO flow again decreased and hypotension was observed; a bleeding complication was suspected. Contrast-enhanced CT scanning was performed again, and re-bleeding from the same site as previously was confirmed and immediately hemostated using TAE. Similar bleeding complications were observed on days 28, 32, and 37, all of which showed bleeding with extravasation on contrast-enhanced CT scan (Fig. D). The bleeding vessels were the lumbar artery (L1–3) and deep femoral artery. Each of these episodes required hemostasis through TAE and massive blood transfusion. Table shows the results of blood collection. No excessive anticoagulation was given. Increasing the platelet level did not stop the bleeding. The slight increase in thrombin-antithrombin complex, elevated fibrinogen degradation products, and platelet decrease in the presence of bleeding complications also suggested a bleeding tendency due to disseminated intravascular coagulation, but the rise in plasmin-α2 plasmin inhibitor complex (PIC) was slight, so it was not considered. The patient was anticoagulated with nafamostat mesilate from day 34, but bleeding complications recurred and anticoagulation was discontinued from day 37, while management continued. After anticoagulation was stopped, no bleeding complications were observed. The clinical course is shown in Figure .
The patient presented with multiple café-au-lait lesions and neurofibromas over her skin (Fig. C). NF1 was suspected; and confirmed by skin biopsy (Fig. D). On day 21, bacteremia caused by Serratia was found and antimicrobial therapy was required. On day 54, methicillin-resistant Staphylococcus aureus bacteremia persisted. On day 57 after admission, the patient was discharged dead from multiple organ failure.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [127.0, 'mm hg'], 'Diastolic Blood Pressure': [86.0, 'mm hg']}",99.66667,94.68334,104.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 127.0 mm Hg + 2/3 * 86.0 mm Hg = 99.66667 mm Hg.
Hence, the patient's mean arterial pressure is 99.66667 mm Hg."
1593,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8610,Extracted,"A 71-year-old African American man is brought to the emergency department with sudden onset lower limb paralysis and back pain. He has had generalized bone pain for 2 months. He has no history of severe illnesses. He takes ibuprofen for pain. On examination, he is pale. The vital signs include: temperature 37.1°C (98.8°F), pulse 68/min, respiratory rate 16/min, and blood pressure 155/90 mm Hg. The neurologic examination shows paraparesis. The 8th thoracic vertebra is tender to palpation. X-ray of the thoracic vertebrae confirms a compression fracture at the same level.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [155.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",111.66667,106.08334,117.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 155.0 mm Hg + 2/3 * 90.0 mm Hg = 111.66667 mm Hg.
Hence, the patient's mean arterial pressure is 111.66667 mm Hg."
1594,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6199716-1,Extracted,"A 31-month-old infant black girl was presented to our imaging department with a recurrent history of difficulty in breathing, bluish skin discoloration, easy fatigability, failure to thrive, and on-and-off swelling of the lower limbs and face. The patient’s past medical history revealed a recurrent history of cough and fevers. She was delivered at term weighing 3.5 kg, her parents’ first-born and only child. There were no perinatal complications. The patient had an Apgar score of 9/10 and breastfed immediately. Immediately after birth, her mother started noticing that the patient was frequently inactive and weak despite breastfeeding well. The patient also started developing bluish skin discoloration a few weeks after birth, which was accompanied by easy fatigability. Milestones were delayed. She started sitting unsupported at 12 months and began crawling at 20 months. Currently, she can walk for short distances owing to the easy fatigability previously mentioned. She had several episodes of upper respiratory infections that were treated on an outpatient basis because they were not serious enough to necessitate hospital admission The patient had no family history of congenital heart disease or asthma. Her mother had no history of diabetes during the index pregnancy.
The patient’s physical examination revealed she was a girl who was small for her age, alert, and afebrile; had swollen lower limbs and puffy face; and was cyanotic with finger clubbing. Her pulse rate was 168 beats/min. Her blood pressure was 102/64 mmHg. Her respiratory examination revealed her respiratory rate was 28 breaths/min, oxygen saturation was 50%, and that she had fine bibasal crepitations. Her cardiac examination revealed S1 and S2 sounds. She demonstrated systolic murmur grade 3 at the right upper sternal border. No thrill was present. A provisional diagnosis of dextrocardia with congenital cardiac disease was made.
Hematological tests revealed normal ranges of hemoglobin, leukocytes, and platelets. The results of the sickling test, rapid plasma reagin test for syphilis, and enzyme-linked immunosorbent assay for human immunodeficiency virus were negative. A chest x-ray revealed dextroposition of the cardiac silhouette and trilobed lungs (Fig. ).
Echocardiography revealed dextroposition of the heart, complete atrioventricular canal, pulmonary atresia, and reverse patent ductus arteriosus (PDA). The child was further investigated with cardiac computed tomography (CT), which revealed multiple complex congenital anomalies. Cardiac CT confirmed dextroposition of the heart with a huge ostium primum atrial septal defect and membranous ventricular septal defect (Fig. ). Right atrial isomerism, bilateral trilobed lungs, and asplenia were seen. Both lower-lobe bronchi were severely hypoplastic (Fig. ). The liver was centrally located.
Ventricular switch was seen with a morphological right ventricle on the left side giving rise to the ascending aorta. Severely hypoplastic main pulmonary artery (MPA) was seen with no direct connection to the morphologic left ventricular outlet, consistent with pulmonary atresia (Fig. ). A left-sided PDA and multiple major aortopulmonary collateral arteries supplying the right lung were noted (Fig. ).
Abnormal venous drainage was seen, as shown by a double-sided superior vena cava (SVC) and right upper lobe anomalous venous return. The right-sided SVC emptied into the right-sided atrium, and the left-sided SVC emptied into left-sided atrium. Liver drainage was split with the intrahepatic inferior vena cava, which received tributaries from right and middle hepatic veins, draining into right-sided atrium. The left hepatic vein drained into left sided atrium (Fig. ).
A final imaging diagnosis of situs ambiguus with right isomerism, l-transposition of great vessels with atrioventricular discordance, ventriculoarterial discordance, dextrocardia, and multiple complex anomalies. The patient is currently on antifailure medications and prophylactic antibiotics. Owing to the complexity of the patient’s cardiac anomalies and unavailability of corrective pediatric cardiac surgical services in Tanzania, the patient was referred abroad for further management.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [102.0, 'mm hg'], 'Diastolic Blood Pressure': [64.0, 'mm hg']}",76.66667,72.83334,80.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 102.0 mm Hg + 2/3 * 64.0 mm Hg = 76.66667 mm Hg.
Hence, the patient's mean arterial pressure is 76.66667 mm Hg."
1595,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7416,Extracted,"A 55-year-old man presents with worsening weakness of the left hand and progressive difficulty in walking for the last 2 months. He says he was previously healthy and active, hiking every weekend, but because of his increasing weakness and incoordination while walking, he stopped his weekly hiking excursion. His past medical history is unremarkable. Current medications are a daily multivitamin and occasional acetaminophen for headaches. He has no significant family history. The patient denies smoking, recreational drug use, or drinking. His vitals include: pulse 70/min, respirations 14/min, temperature 37.0°C (98.6°F), and blood pressure 130/80 mm Hg. Physical examination reveals fasciculations in the tongue and distal extremities. The left forearm shows significant atrophy, and mild lower limb muscle atrophy is also seen bilaterally. Hyporeflexia (1+) is present in the left arm, while hyperreflexia (3+) is seen in the legs bilaterally. Babinski’s sign is positive bilaterally. The patient's speech is notably slow but no evidence of productive or expressive aphasia is present. The cranial nerves are intact.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1596,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-2513,Extracted,"A 12-year-old boy is brought to the emergency department by his mother because of progressive shortness of breath, difficulty speaking, and diffuse, colicky abdominal pain for the past 3 hours. Yesterday he underwent a tooth extraction. His father and a paternal uncle have a history of repeated hospitalizations for upper airway and orofacial swelling. The patient takes no medications. His blood pressure is 112/62 mm Hg. Examination shows edematous swelling of the lips, tongue, arms, and legs; there is no rash.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [112.0, 'mm hg'], 'Diastolic Blood Pressure': [62.0, 'mm hg']}",78.66667,74.73334,82.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 112.0 mm Hg + 2/3 * 62.0 mm Hg = 78.66667 mm Hg.
Hence, the patient's mean arterial pressure is 78.66667 mm Hg."
1597,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7808832-1,Extracted,"A previously healthy 12-month-old girl presented to the emergency department with non-bilious vomiting that had started nine hours before the visit. She was presumed to have gastroenteritis and was prescribed oral rehydration solution at a pediatrician’s office. Subsequently, she vomited six more times, and in two episodes the vomitus contained spherical, green, gelatinous toys that were about 3 mm in size. No choking or swallowing of the toys was witnessed. However, the girl’s mother believed that they were water beads and that some likely remained in the girl’s body given the disappearance of several beads at home.
The initial vital signs at the emergency department included blood pressure 90/70 mmHg, heart rate 140 beats/min, respiratory rate 32 breaths/min, and temperature 37.0°C. Her weight and height were 11.0 kg (90th to 95th percentile) and 75.3 cm (50th to 75th percentile), respectively. She had a stable and mildly anxious appearance without respiratory distress or dehydration. The abdomen was soft, non-distended, and non-tender without a palpable mass.
No intestinal obstruction or radiopaque foreign bodies were found on a plain abdominal radiograph (). However, considering the mother’s concern for residual foreign bodies, abdominal POCUS was performed using an HM70A ultrasound system (Samsung Medison, Seongnam, South Korea) to detect water beads. A 7-MHz curvilinear transducer was placed midline on the epigastrium with the patient supine and the indicator on her right side.
POCUS showed the stomach as a fluid-filled sac, indicating gastric distention due to distal intestinal obstruction or retention of rehydration solution. Moreover, seven well-demarcated, round hypoechoic items approximately 10 to 15 mm in diameter were observed in the stomach and a similar, 20 mm item in the first portion of the duodenum (, ). No other foreign bodies, masses, dilated loops of bowel, or other signs of obstruction, such as intussusception, were observed on the examination. The POCUS findings indicated duodenal obstruction by ingested water beads. Of note, this examination was completed within several minutes without sedation, use of a linear transducer, or application of extra pressure on the abdomen.
Subsequently, a pediatric gastroenterologist was able to retrieve the water beads endoscopically (). A total of 11 water beads were removed from the stomach using a retrieval net. The bead in the duodenum was first broken down by endoscopic crushing. The patient’s recovery was uneventful, and she was discharged on day 3.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",76.66667,72.83334,80.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 70.0 mm Hg = 76.66667 mm Hg.
Hence, the patient's mean arterial pressure is 76.66667 mm Hg."
1598,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-12661,Extracted,"A 64-year-old woman presents to the emergency room with rapidly worsening chest pain and shortness of breath. She developed dull substernal chest pain 3 hours ago while watching a movie with her grandchildren. Her past medical history is notable for hyperlipidemia, hypertension, and knee osteoarthritis. She takes atorvastatin and lisinopril. She has a 15-pack-year smoking history and drinks 2-3 glasses of wine with dinner each night. She recently returned to the United States from a month-long trip to China. Her temperature is 98.6°F (37°C), blood pressure is 154/90 mmHg, pulse is 118/min, and respirations are 25/min. On exam, she appears uncomfortable but is able to respond to questions in complete sentences. A normal S1 and S2 are heard on cardiac auscultation. Her symptoms do not improve with sublingual nitroglycerin. Multiple troponin levels are taken and are normal. An electrocardiogram is shown in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [154.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",111.33333,105.76666,116.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 154.0 mm Hg + 2/3 * 90.0 mm Hg = 111.33333 mm Hg.
Hence, the patient's mean arterial pressure is 111.33333 mm Hg."
1599,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5998,Extracted,"A 77-year-old Caucasian woman presents to her primary care provider for a general checkup. The patient is with her daughter who brought her to this appointment. The patient states that she is doing well and has some minor joint pain in both hips. She states that sometimes she is sad because her husband recently died. She lives alone and follows a vegan diet. The patient's daughter states that she has noticed her mother struggling with day to day life. It started 2 years ago with her forgetting simple instructions or having difficulty running errands. Now the patient has gotten to the point where she can no longer pay her bills. Sometimes the patient forgets how to get home. The patient has a past medical history of obesity, hypertension, gastroesophageal reflux disease (GERD) controlled with pantoprazole, and diabetes mellitus. Her temperature is 99.5°F (37.5°C), blood pressure is 158/108 mmHg, pulse is 90/min, respirations are 17/min, and oxygen saturation is 98% on room air.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [108.0, 'mm hg'], 'Systolic Blood Pressure': [158.0, 'mm hg']}",124.66667,118.43334,130.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 158.0 mm Hg + 2/3 * 108.0 mm Hg = 124.66667 mm Hg.
Hence, the patient's mean arterial pressure is 124.66667 mm Hg."
1600,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5528,Extracted,"A 36-year-old G3P2002 presents to her obstetrician’s office for her first prenatal visit at ten weeks and two days gestation. She notes that she has felt nauseous the last several mornings and has been especially tired for a few weeks. Otherwise, she feels well. The patient has had two uncomplicated spontaneous vaginal deliveries at full term with her last child born six years ago. She is concerned about the risk of Down syndrome in this fetus, as her sister gave birth to an affected child at age 43. The patient has a history of generalized anxiety disorder, atopic dermatitis, and she is currently on escitalopram. At this visit, this patient’s temperature is 98.6°F (37.0°C), pulse is 70/min, blood pressure is 121/67 mmHg, and respirations are 13/min. The patient appears anxious, but overall comfortable, and cardiopulmonary and abdominal exams are unremarkable. Pelvic exam reveals normal female external genitalia, a closed and slightly soft cervix, a ten-week-sized uterus, and no adnexal masses.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [67.0, 'mm hg'], 'Systolic Blood Pressure': [121.0, 'mm hg']}",85,80.75,89.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 121.0 mm Hg + 2/3 * 67.0 mm Hg = 85.0 mm Hg.
Hence, the patient's mean arterial pressure is 85.0 mm Hg."
1601,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5544981-1,Extracted,"A 67-year-old Japanese woman underwent OWHTO to treat SPONK that had occurred in the left medial femoral condyle (Fig. ). The patient reported the following history of the present illness. Pain in the left knee joint initially occurred at 1 year and 4 months before admission, without any particular trigger. Her former treating physician had provided conservative treatments such as oral administration of anti-inflammatory analgesics, rehabilitation including quadriceps muscle training, and guidance on the use of a cane to relieve weight bearing. However, this treatment was not successful in relieving her symptoms, and she was referred to our department for surgery. The patient had a history of hypertension and hyperlipidemia, and she had been taking oral candesartan and atorvastatin. The patient was a housewife with no noteworthy aspects related to social, family, or environmental history. On physical examination, the patient had a height of 157 cm, a body weight of 62 kg, and a body mass index of 25.2 kg/m2. She reported feeling pain in the medial joint space of the knee during walking, as well as during climbing or descending stairs. At the time of the first admission, her systolic/diastolic blood pressure was 165/97 mmHg. Table provides an overview of the patient’s pain scores in the knee joint, ROM of the knee joint, and knee joint function. Neurological examination revealed no abnormal findings. Similarly, laboratory findings at the time of the first admission did not indicate any abnormality: total protein 7.3 g/dl, albumin 4.6 g/dl, aspartate aminotransferase 22 U/L, alanine aminotransferase 18 U/L, lactate dehydrogenase 213 U/L, alkaline phosphatase 297 U/L, γ-glutamyl transferase 18 U/L, total bilirubin 0.6 mg/dl, Na 142 mEq/L, Cl 104 mEq/L, K 4.5 mEq/L, blood urea nitrogen 21.4 mg/dl, creatinine 0.56 mg/dl, Ca 9.7 mg/dl, inorganic phosphorus 3.7 mg/dl, leukocytes 5100/μl, erythrocytes 5.00 × 106/μl, hemoglobin 14.4 g/dl, hematocrit 43.6%, and platelets 263 × 103/μl.
The HAL-SJ treatment program was divided into five phases []. Phase 1 consisted of preoperative observation from the day of hospital admission until the day of surgery. The patient’s thigh circumference and lower leg length were measured preoperatively to adjust the HAL-SJ to the patient’s physical size, which would ensure appropriate training. We palpated the patient’s quadriceps muscles (vastus medialis, rectus femoris, and vastus lateralis) and attached electrodes to each muscle to detect the bioelectric potentials of the long axis along the belly of each muscle. We instructed the patient to perform knee extension and to contract her quadriceps. On the basis of these data, we instructed the patient to simulate the knee extension training, which would be performed postoperatively. Specifically, the patient sat with her lower leg hanging down naturally, and the height of the chair was adjusted so that the patient’s feet were not in contact with the floor. The patient performed ten knee extensions with HAL-SJ assistance, using the muscle that exhibited the largest bioelectric potential amplitude.
Phase 2 involved surgery (day of surgery). The patient underwent OWHTO (Figs. and ) using TomoFix (DePuy Synthes, Bettlach, Switzerland), artificial bone (OSferion60, β-tricalcium phosphate; Olympus Terumo Biomaterials, Tokyo, Japan), and biplanar osteotomy, as described by Takeuchi et al. []. The preoperative weight-bearing line (WBL) percentage [], calculated on the basis of an anteroposterior weight-bearing radiograph of the affected leg in full knee extension, was 29.6%. The surgery was planned with a target postoperative WBL percentage of 62.5%. The actual enlarged angle and distance of osteotomy were 5.5 degrees and 7 mm, respectively.
Phase 3 consisted of postoperative observation from day 1 to day 7 postoperatively. For postoperative rehabilitation, partial weight bearing was allowed after a non-weight-bearing period of 2 weeks, and full weight bearing began at 4 weeks postoperatively. The patient received rehabilitation training under the guidance of a physical therapist (ROM exercises and muscle-strengthening training) for 20–40 minutes each day, 5 days per week, from the first postoperative day until discharge. For ROM exercises, continuous passive motion training began on the first postoperative day for 1 hour per day and continued every day until discharge. On postoperative day 7, we attached electrodes to the quadriceps muscle to detect the bioelectric potential along the long axis of the rectus femoris muscle belly (Fig. ). Then, the patient was instructed to perform active knee extension exercises that involved contracting her quadriceps, thus simulating training with HAL-SJ (Fig. ).
Phase 4 consisted of HAL-SJ therapy from postoperative day 8 to discharge. The CVC mode of HAL-SJ serves to support the patient’s voluntary motion on the basis of voluntary muscle activity and the assistive torque provided to the knee joint []. In this study, we used the CVC mode, which allowed the operator to adjust the degree of physical support to maintain the patient’s comfort while gradually reducing support as training progressed. In addition to the regular rehabilitation program (Fig. ), the patient performed HAL-JS-assisted knee extension exercises while sitting, which consisted of five sets of ten repetitions per set, twice per week (Fig. ). The training was performed six times before the patient was discharged (postoperative days 8, 10, 15, 17, 22, and 24). The mean training duration, including the time required to put on the HAL-SJ, was 15.5 ± 1.4 minutes (15 minutes, 16 minutes, 17 minutes, 16 minutes, 13 minutes, and 16 minutes during training sessions 1, 2, 3, 4, 5, and 6, respectively). There were no adverse events related to the use of HAL-SJ, and the patient was discharged 30 days after the surgery.
Phase 5 consisted of post-HAL-SJ therapy observation from discharge until 3 months after the end of HAL-SJ therapy, during which the following indicators were assessed: EL, assessed as the difference between the maximum knee joint extension angle during passive exercise and that during active exercise; knee pain rated on the visual analogue scale (VAS); isometric knee extension muscle strength (IKEMS); active ROM before surgery, before and after HAL-SJ training, and at 1 and 3 months after the end of training; and the Japanese Orthopaedic Association (JOA) score [] before surgery, at discharge, and at 1 and 3 months after the end of training. Furthermore, we used lateral radiographs to measure the tibial slope angle (TSA) and Insall-Salvati ratio (ISR) as indicators of patellar tendon shortening before surgery and after implant removal at 1 year after the operation [] (Fig. ). Measurement of knee ROM was performed using goniometry, and the landmarks used in the measurements were the greater trochanter of the femur, proximal head of the fibula, and lateral malleolus. Goniometry was used because it has been reported that goniometric measurements of ROM are more reliable than visual observation, with an accuracy of up to 1.0 degree []. The maximal IKEMS of the operated leg was assessed with the patient in a sitting position, with the hips and knees flexed at 90 degrees. A μTas F-1 handheld dynamometer (Anima Corp., Tokyo, Japan) was fixed to the chair, and two measurements were recorded. Each trial lasted 3–5 seconds, with 30 seconds of rest between trials. The higher score of two valid trials was recorded. All measurements were performed by a single trained physical therapist to eliminate interobserver variability. The EL, VAS, IKEMS, and ROM results are shown in Table . The EL improved from 3 degrees preoperatively to 0 degrees at the end of the sixth HAL-SJ training session, but it returned to 3 degrees at 1 and 3 months after the end of the training. When we compared results obtained before training against those obtained after each of the six training sessions, we observed that three sessions produced improved EL and three sessions produced improved or relatively constant VAS scores immediately after training. However, for the other three sessions, the patient reported increased pain immediately after training, with the greatest increase in pain reported immediately after the first HAL-SJ training session, when the VAS score was 1.7 times higher immediately after training than before training. The EL improved after training sessions 1 and 3, when the patient reported increased knee pain (expressed as the VAS score). However, the EL did not change after training sessions 2 and 4, when the patient reported less knee pain (improved VAS score immediately after training). The patient did not refuse to undergo training because of increased pain. The IKEMS value was the largest preoperatively (17.6 kgf) and decreased to its lowest value (30% of the preoperative strength) before the first HAL-SJ intervention at 8 days after the operation. The IKEMS remained relatively constant throughout HAL-SJ training but recovered to the preoperative value during follow-up (18.7 and 16.6 kgf at 1 and 3 months, respectively, after completion of HAL-SJ training). The active ROM also recovered to the preoperative value by the end of the sixth HAL-SJ training session. Thereafter, the extension ROM did not change, but the flexion ROM was maintained or improved. The JOA score decreased from 60 points preoperatively to 55 points at discharge, but it improved with time, reaching 65 and 85 points at 1 and 3 months, respectively, after the end of HAL-SJ training. Whereas the TSA was maintained at 13.1 degrees before and after the surgery, the ISR decreased from 1.13 preoperatively to 0.97 postoperatively. At 6 months after surgery, the passive ROM was 0–135 degrees, and the JOA score was 90 points. There were no complications throughout the preparation, surgery, or rehabilitation process.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [165.0, 'mm hg'], 'Diastolic Blood Pressure': [97.0, 'mm hg']}",119.66667,113.68334,125.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 165.0 mm Hg + 2/3 * 97.0 mm Hg = 119.66667 mm Hg.
Hence, the patient's mean arterial pressure is 119.66667 mm Hg."
1602,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2876862-1,Extracted,"A 34-year-old, 162 cm, 55 kg female patient with varicose veins was scheduled to undergo endovenous laser therapy and a varicosectomy. She had no other underlying disorders or medical history of surgery. With the exception of an allergy to dust, she had no other allergic reactions to medications and food, and there was no family history of allergies. There were no abnormalities in the preoperative physical examination, hematological test, simple X-ray test and ECG.
Thirty minutes before arriving in the operation room, 2.0 mg of midazolam and 0.2 mg of glycopyrrolate were injected into the muscle as preanesthetic medication. After arriving in the operation room, the ECG, heart rate, non invasive blood pressure manometer, pulse oximeter, and end tidal CO2 were monitored. The preanesthetic vital signs indicated a blood pressure (BP), pulse rate and oxygen saturation of 110/70 mmHg, 75 bpm and 99%, respectively. To induce general anesthesia, 110 mg of propofol mixed with 40 mg of 2% lidocaine was injected intravenously. After confirming the patient's loss of consciousness, manual ventilation was performed using a mask with oxygen 3 L/min, nitro oxide 3 L/min and, sevoflurane 3 vol%. Endotracheal intubation was performed one or two minutes after administering 40 mg of rocuronium.
Her heart rate (HR) increased immediately after the endotracheal intubation. Three minutes later, her HR and BP was 135/min and 75/35 mmHg, respectively. Suspecting the influence of inhalation anesthetics, the anesthetic medication was discontinued, but the HR continued to increase. At the same time, her systolic and diastolic blood pressure was 60-70 mmHg and 30-35 mmHg, respectively. In addition, there was slight flaring observed in the face and chest as well as angioedema around the eyes. Subsequently, the end tidal CO2 showed an obstructive pattern, and urticaria broke out with anaphylaxis. 100% oxygen was provided promptly at 6 L/min, with crystalloid and colloid solution. After administering ephedrine 4 mg twice, her vital signs recovered within 10 minutes to indicate a HR and BP of 100/min and 110/65 mmHg, respectively.
With time, the whole body flare and urticaria worsened and angioedema was observed around her eyes (). Therefore, 250 mg of hydrocortisone (Solucortef®, Pfizer, USA) and 3 mg of an antihistamine, piprinhydrinate (Plokon®, Yungjin Pharm. Co., Korea), were injected intravenously followed by 3 mg of midazolam to prevent emergence. Subsequently, her vital signs stabilized about 20 minutes after the induction of anesthesia, the urticaria, flare, and angioedema relived. It was decided that she should be under further observation to determine whether to proceed with surgery. Forty minutes after inducing anesthesia, her vital signs continued to stabilize and the urticaria and angioedema around the swollen eyes were relieved. Therefore, after a discussion with her attending surgeon and parents, a decision was made to proceed with the operation.
Anesthesia was maintained with sevoflurane 2-3%, oxygen and nitro oxide at 2 L/min. During the two hour operation, no additional muscle relaxant was administered, and the operation was completed without complications. As the operation proceeded, the obstructive pattern of the CO2 curve disappeared and the end tidal CO2 returned to normal. Extubation was performed after postoperative manual ventilation ensured the suitability of the patient's tidal volume and rate, and her vital signs were also within the normal range.
She was transferred to the recovery room after extubation with spontaneous respiration, consciousness, BP, oxygen saturation all normal. The anaphylactic reaction that developed during anesthesia was explained to both the patient and her parents. The risk of side effects during anesthesia due to the pathogenic potential of anaphylaxis to the medication employed was also explained. An intradermal skin test was advised for a differential diagnosis.
The patient wanted to take the test during her hospitalization, and on post operative day 2, an intradermal skin test was performed at the department of dermatology at our hospital to check the medications administered at the induction of anesthesia as well as the drugs used in subsequent anesthesia. Histamine was taken as a positive control while a saline solution was used as the negative control; 0.03 ml of each test substance was injected on the back of the patient with a hypodermic needle in the form of a clinically used solution diluted at ratio of 1 : 10, 1 : 100, and 1 : 1,000 from a stock solution. Twenty minutes after the injection, the size of any wheal was measured. The criterion of positivity to an intradermal skin test is the mean diameter of the measured injection papule being larger than the diameter of the wheal induced by the positive control solution or twice than that of the bleb produced by the first injection. The test was stopped every time a positive reaction occurred at a lowest density level. Among the medications used to induce anesthesia on the operation day, rocuronium elicited a positive reaction in a 1/100 dilution, and was identified as the causing agent for the anaphylaxis. In addition, another muscle relaxant, vecuronium, showed a positive reaction in an undiluted solution. The tests with the other drugs showed negative reaction ().
The patient and her parents were informed that she also had a positive reaction to vecuronium, which is commonly used as a nondepolarizing muscle relaxant for inducting operation. The patient was asked to explain her medical history to medical staff at any future procedure, and she was discharged the next day.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1603,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6124468-1,Extracted,"After a car accident without traumatic consequences, elevated arterial pressure of 190/130 mmHg (95th percentile for his age, sex, and height = 136/87 mmHg) were discovered in a 17-year-old male. Initially, arterial hypertension was attributed to his emotional state after the car accident, but during hospitalization the patient continued to be anxious and tachycardic, and arterial pressure remained high. Physical examination revealed normal somatic and pubertal development, numerous café au lait spots (13 spots with diameter >1.5 cm), axillary freckling and one plexi-form neurofibroma. He had a 2-year history of headache, and brain magnetic resonance imaging (MRI) revealed an unprogressive arachnoid cyst. The adolescent’s mother presented numerous café au lait spots and neurofibromas, and these modifications, which were also present in the patient’s grandfather and great-grandfather, were considered a family trait. Abdominal ultrasound showed a parenchymal, well-defined, inhomogeneous mass lesion of 126×110×118 mm3 at the area superior to the left upper kidney pole, and adrenal gland origin could not be ruled out (). The left kidney had pelvicalyceal dilatation, and the splenic vein was compressed by the tumor mass. The right adrenal gland and right kidney were normal. Contrast abdominal MRI confirmed the adrenal origin of the tumor (). Hormonal assays revealed elevated plasma-free metanephrines and urinary catecholamines (). Pheochromocytoma was diagnosed, and 123I-metaiodobenzylguanidine (123I-MIBG) scintigraphy ruled out extra-adrenal uptake and metastatic localization (). Echocardiography revealed left-ventricle hypertrophy. Ophthalmological findings were unremarkable. Endocrinological consultation was consistent with NF1 and pheochromocytoma, and surgical treatment was recommended. Prior to surgery, therapy with daily prazosin 2 mg was started, and after 7 days daily propranolol 60 mg was added. After 6 weeks of treatment, arterial pressure was 120/60 mmHg and heart rate had decreased to 60 bpm. Surgical removal of the tumor mass of the adrenal gland was performed, and microscopy of the adrenal mass showed histological features of Pheochromocytoma of the Adrenal gland Scaled Score of 2. After surgery, blood pressure was within normal range, and 1 week later antihypertensive therapy was stopped. Postoperative plasma free metanephrines had normalized.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [190.0, 'mm hg'], 'Diastolic Blood Pressure': [130.0, 'mm hg']}",150,142.5,157.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 190.0 mm Hg + 2/3 * 130.0 mm Hg = 150.0 mm Hg.
Hence, the patient's mean arterial pressure is 150.0 mm Hg."
1604,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6323657-1,Extracted,"A 58-year-old Japanese man with an 8-year history of T2DM had a symptom of pain in his right lower leg and visited the emergency room in Kawasaki Medical School. Previously, he had felt the same pain in the same region when his blood glucose was very high and thereby he was diagnosed as having T2DM 8 years before.
He had acute osteomyelitis in his right lower leg when he was a baby. Except for this, he had no past history. He had no remarkable family history. He was a barber; he smoked tobacco (pack-years = 0.75 pack/day × 40 years) and he drank alcohol every day. After the episode of acute osteomyelitis when he was a baby, there was no problem in his legs until he had general fatigue and felt pain in his right lower leg at the age of 50. He visited the emergency room. His vital signs were as follows: heart rate 76 beats/minute, blood pressure 116/70 mmHg, and body temperature 36.4 °C. He had a symptom of slight local swelling and heat sensation in the same area with pain in his right lower leg, but there were no findings in physical and neurological examinations. In addition, there was no ulcer or injury on his skin surface. Laboratory data (Table ) were as follows: white blood cell count, 7400/μL (neutrophil 64.7%); C-reactive protein (CRP), 2.50 mg/dl; plasma glucose, 382 mg/dL; hemoglobin A1c (HbA1c), 11.7%. He was diagnosed as having T2DM, but he had no diabetic complications. Magnetic resonance imaging (MRI) of his lower limbs showed an abscess and inflammatory change in his right lower leg (Fig. ). An axial T1-weighted (T1W) image of his right lower leg showed a slightly lower intensity, and an axial T2-weighted (T2W) image showed a markedly higher intensity (Fig. , upper panels). Based on these findings, we made a diagnosis of acute exacerbation of chronic osteomyelitis and T2DM. We thought that it would be better to hospitalize him and start administering antibiotics via a drip, but he did not agree to the hospitalization. Therefore, as an alternative, we started 300 mg/day of cefcapene pivoxil hydrochloride hydrate and insulin therapy (18 units of aspart) on an out-patient basis. After starting insulin therapy, his blood glucose level gradually decreased, and his leg pain was also gradually mitigated. Finally, his leg pain disappeared 2 weeks later. His CRP became within normal range, and 3 months later the focus in his right lower leg was markedly reduced on MRI. In addition, the focus was not detected in ultrasonography of the right tibia site. Just in case, however, we continued antibiotics therapy for 4 months. Since his glycemic control was improved 2 months later, we stopped insulin therapy and started orally administered anti-diabetic drugs.
He was then followed up as an out-patient with T2DM for approximately 8 years. The medication at that time was 1000 mg/day of metformin, 25 mg/day of alogliptin, 15 mg/day of pioglitazone, and 50 mg/day of ipragliflozin. However, he did not take the medicine for approximately 8 months on his own judgement at the age of 58. After his interruption of therapy for 8 months, he felt the same pain in the same right lower leg again. He immediately visited our hospital. He had symptoms of slight local swelling and heat sensation together with pain in the same area in his right lower leg, but again there were no findings in physical and neurological examinations at this time. His vital signs were as follows: heart rate 99 beats/minute, blood pressure 130/70 mmHg, and body temperature 37.0 °C. He had a symptom of slight local swelling and heat sensation in the same area with pain in his right lower leg, but there was no ulcer or injury on his skin surface. Laboratory data were as follows: white blood cell count, 6680/μL (neutrophil 63.4%); CRP, 0.32 mg/dl; erythrocyte sedimentation rate (ESR), 31 mm/hour; plasma glucose, 652 mg/dL; HbA1c, 6.9%; glycoalbumin 46.1%. Other laboratory data were as follows: red blood cell, 476 × 104/μL; hemoglobin (Hb), 15.9 g/dL; platelet, 25.1/μL; total protein (TP), 7.6 g/dL; albumin (Alb), 4.4 g/dL. Liver and renal function were within normal range as follows: aspartate aminotransferase (AST), 39 U/L; alanine aminotransferase (ALT), 50 U/L; γ-glutamyl transpeptidase (γ-GTP), 51 U/L; lactate dehydrogenase (LDH), 172 U/L; creatinine (Cre), 0.54 mg/dL; blood urea nitrogen (BUN), 13 mg/dL; Na, 131 mEq/L; K, 4.4 mEq/L; Cl, 96 mEq/L. Pathogenic bacteria were not detected. He had no diabetic complications, probably because his glycemic control was relatively good before the interruption of therapy. His leg MRI showed a spreading of the abscess and inflammatory change in his right lower leg (Fig. , lower panels). We hospitalized him in our institution but he did not agree to undergo surgery for remission. Therefore, we started 3.0 g/day of sulbactam sodium/ampicillin sodium and insulin therapy (24 units of aspart and 20 units of glargine). After starting insulin therapy, his blood glucose level gradually decreased, and his leg pain was also gradually mitigated. Local swelling and heat sensation disappeared approximately 5 days later. Finally, his leg pain disappeared approximately 2 weeks later, and he was discharged from our hospital. Just in case, however, we continued antibiotics therapy (450 mg/day of rifampicin and 4 g/day of trimethoprim) for approximately 2 months. After a total of 3-month antibiotics therapy during hospitalization and after discharge, we stopped antibiotics therapy. He was then followed up for approximately 6 months, and his leg MRI showed a reduction of the abscess and inflammatory change in his right lower leg. He had no symptoms and/or problems, and his inflammation markers remained within normal levels for at least 6 months.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 70.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1605,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8301578-1,Extracted,"A 27 year old previously healthy male was referred to a hospital with a two-week history of vomiting, high-grade fever, and abdominal pain, which was diagnosed as appendicitis. On admission to the referral facility, he was diagnosed with a new presentation of type 1 diabetes mellitus. Postappendectomy, he was referred to our facility for further management. On arrival, he was semi-conscious, barely responsive to pain, and had labored breathing. He also had electrolyte imbalance with severe hypokalemia of 1.6 mmol/L and an elevated random blood glucose level.
Physical examination revealed a well-nourished albeit severely dehydrated male weighing about 53kg. He was febrile and had Kussmaul breathing. His vitals were as follows: BP = 151/69 mm Hg, HR = 132 beats per minute, RR = 32 breaths per minute, SPO2 = 96% on room air, temperature =38.9℃, and random blood glucose =16.6 mmol/L. A bedside ultrasound revealed a collapsed inferior vena cava (IVC). His initial point-of-care venous blood gas showed metabolic acidosis (pH =7.20, PCO2 = 21.5 mmHg, HCO3 = 10.1 mmol/L) with severe hypokalemia of 2.2 mmol/L (3.5–5.0 mmol/L), hypernatremia of 167 mmol/L (135–145 mmol/L), and hyperchloremia of 125 mmol/L (98–109 mmol/L). Serial venous blood gases and electrolytes were performed every 3 to 6 hours (Table ). Urine analysis was unremarkable including the absence of urinary ketones.
Central venous access was obtained in the right subclavian vein, and a 4-L bolus of Ringers lactate was administered followed by a free water deficit maintenance using 5% dextrose water admixed with potassium chloride (KCl) 40 – 80 mmol which ran at 125 ml/h (KCl rate of 10 – 20 mmol/h). Simultaneously, a fast-acting insulin infusion at 0.05 U/kg/h (2.5 U/h) was also administered. Post-operative broad-spectrum parenteral antibiotics were initiated, and the patient was admitted to the ICU.
After 24 hours of admission, we noted the patient had a urinary output of 9 L of dilute urine with a negative fluid balance of 3 L. His serum potassium was persistently low despite receiving a continuous KCl infusion for over 24 hours. At this point, his serum potassium level was 1.94 mmol/L. Serum magnesium levels were ordered to rule out probable cause of refractory hypokalemia, which revealed hypomagnesemia of 0.50 mmol/L (0.66 −1.25 mmol/L). All other blood investigations including brain and abdominal CT scan were unremarkable except for the ECG which showed diffuse U-wave morphology (Figure ) correlating with hypokalemia and/or hypomagnesemia. Urinary specific gravity was found to be low with a value of 1.005. Plasma levels of antidiuretic hormone (ADH) and urine osmolality were not available at our center.
Based on these findings, a diagnosis of nephrogenic diabetes insipidus (NDI) was made secondary to hypomagnesemia induced severe hypokalemia. The treatment was modified by the addition of 4g of magnesium sulfate along with 40 mmol of KCl in 5% dextrose water (500 ml bottle) which ran at a rate of 125 ml/h, along with the same insulin rate of 0.05 U/kg/h (2.5 U/h). This treatment plan continued for 48 hours until his electrolytes normalized. In addition, oral bendroflumethiazide 5 mg twice a day, indomethacin 50 mg thrice a day, eplerenone 25 mg twice a day, and magnesium trisilicate 250 mg thrice a day were added to his treatment.
Improvement in potassium and magnesium levels were seen on the 3rd day postadmission with significant ECG improvement with the disappearance of U waves (Figure ). A decrease in the exaggerated amount of urine output was also observed with an improvement in the patient's hydration status. On the 8th day in the ICU, the patient had significant clinical improvement with normal serum electrolytes and an adequate positive fluid balance (input of 3.5 L and output of 2.9 L in 24 h). Thereafter, he was transferred from the ICU to the general ward to continue with the management and follow-up. Further follow-up as an outpatient postdischarge has yielded normal electrolyte results.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [151.0, 'mm hg'], 'Diastolic Blood Pressure': [69.0, 'mm hg']}",96.33333,91.51666,101.15,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 151.0 mm Hg + 2/3 * 69.0 mm Hg = 96.33333 mm Hg.
Hence, the patient's mean arterial pressure is 96.33333 mm Hg."
1606,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-1174869-1,Extracted,"A 58-year-old male was brought to the emergency room with confusion and an inability to speak for 1 day. He had a past history of hypertension and hypomania. He was single and he lived alone. On physical examination, his blood pressure was 80/63 mm of Hg, heart rate 126/minute, and temperature 102°F. He was awake but unable to speak due to a mixed receptive and expressive aphasia. He had right homonymous hemianopsia and hemiplegia. Cardiac examination was positive for a pansystolic murmur in the apical area. The abdominal examination was unremarkable. On rectal examination there was perianal erythema and diminished sphincter tone. Complete blood count showed WBC 15,400/mm3 with a left shift, hematocrit 49%, and normal platelets. Serum chemistries showed glucose 84 mg/dl, albumin 2.9 mg/dl, and calcium 8.5 mg/dl. Magnetic Resonance Imaging of the brain, including diffusion weighted imaging, revealed acute hemorrhagic infarction of the left occipital lobe and acute embolic infarctions of the left frontal and right occipital lobes (Fig and ). Transesophageal Echocardiogram demonstrated mitral regurgitation and large vegetations on the posterior leaf of the mitral valve. Splenic and renal infarcts were visible on Computerized Tomography of the abdomen. All of the blood culture bottles and the urine culture grew methicillin sensitive Staphylococcus aureus. Treatment of the bacterial endocarditis was started with intravenous nafcillin and gentamicin. The patient had a significant recovery of speech and motor function within a few days. When asked about recent dental work, he gave a history of a tooth extraction 2–3 days before the hospitalization but was unable to provide information about his dentist. A dentist from the hospital examined the patient and found no clinical evidence of the extraction. The patient underwent a complete neuropsychiatric evaluation. He displayed confabulation and perseverance (marriage, retirement, hospitalization were reported using the same date which was his birthday). He also had significant executive dysfunction including concrete thinking and poor insight regarding his health and cognitive problems. On hospital day 12 the patient had mitral valve replacement surgery using a bioprosthetic valve. He completed a six-week course of intravenous antibiotic treatment. He also underwent extensive rehabilitation therapy and was sent home after 8 weeks of hospitalization. On subsequent follow-up visits the patient showed complete recovery from the stroke and was back to his baseline. In response to questions about his sexual history the patient indicated having heterosexual relations with multiple partners. However, his answers were inconsistent and seemed unreliable.
A closer examination of his medical records revealed that two years prior to this hospitalization, the patient was admitted with a plastic soda bottle retained in the rectosigmoid for 3 days. The bottle had been filled with warm water and inserted into his anal canal for sexual stimulation. It slipped all the way into the rectum and could not be retrieved. His attempts to extract it at home were unsuccessful. In the emergency room his physical examination was normal except for a palpable mass in the suprapubic area, decreased anal sphincter tone and a dilated rectal vault. On X-ray of the abdomen, the outline of a plastic bottle was visible in the rectosigmoid (Fig ). The patient was taken to the operating room and under spinal anesthesia the bottle was extracted. He had multiple lacerations of the rectal mucosa but there was no perforation. He went home the next day. On follow-up visits to primary care he was noted to be overall healthy except having mild hypertension. His behavior was indicative of hypomania, but he did not get a formal psychiatric evaluation.
Foreign bodies in the rectum and methods of their extraction have been amply chronicled in the surgical literature []. Sexual stimulation is the reason in a majority of these cases []. Local trauma, perforation, and resultant peritonitis are well known complications []. An unlimited PUBMED search for articles on bacteremia or endocarditis related to rectal foreign body insertion was unfruitful (We tried MeSH terms anal/rectal/colorectal/foreign bodies/anorectal /sexual deviation for the purpose). Bacteremia and septicemia from barium enema [], and therapeutic anal dilatation [] have been published. Procedures like fiberoptic sigmoidoscopy are known to cause endocarditis [], but septic stroke resulting from endocarditis related to lower gastrointestinal instrumentation has also not been reported.
The patient's history of anorectal insertion of a plastic soda bottle for sexual gratification is consistent with published reports of use of large objects for this purpose []. The resultant rectal trauma can easily lead to bacteremia. Rectal carriage of Staphylococcus aureus is well documented and is a potential source of infection []. This organism tends to be more abundant on the rectal mucosa than within the feces []. In a study of gastrointestinal colonization, Staphylococcus aureus grew from the culture of rectal swabs in 60% cases versus 53% positive culture of nasal swabs taken from the same subjects []. This organism is known to cause endocarditis of normal heart valves [,]. Neurologic complications of infective endocarditis, particularly embolic events, tend to be higher in cases of endocarditis caused by Staphylococcus aureus [].
It is known that few patients with rectal foreign bodies will freely admit to transanal introduction []. This explains to some extent the paucity of literature linking this practice with bacteremia or endocarditis. We believe our patient was habituated to rectal insertion of foreign bodies and that is evident from his previous history along with the clinical findings of perianal erythema and diminished sphincter tone []. In the absence of a reliable history from the patient, the link between endocarditis and rectal trauma in this case is based on circumstantial evidence. A further study of patients with well-documented evidence of rectal foreign body insertion could be the next step to explore this important observation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [80.0, 'mm hg'], 'Diastolic Blood Pressure': [63.0, 'mm hg']}",68.66667,65.23334,72.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 80.0 mm Hg + 2/3 * 63.0 mm Hg = 68.66667 mm Hg.
Hence, the patient's mean arterial pressure is 68.66667 mm Hg."
1607,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8170454-1,Extracted,"A 12-year-old girl has been hospitalized with fever, headache, vomiting, and abdominal pain. She had a history of contact with COVID-19 patients and her test for SARS-CoV-2 by Reverse Transcription Polymerase Chain Reaction (RT-PCR) was positive 15 days prior to her admission. Physical examination showed fever, irritability, and bilateral submandibular adenopathy. On abdominal palpation, she had a diffuse tenderness, most pronounced over the right lower quadrant mimicking an acute surgical abdomen. Sonography and Computed Tomography Scan revealed pelvic ectopy of her right kidney. Laboratory tests showed lymphopenia (total leukocyte count = 16 × 109/l; lymphocyte count = 0.9 × 109/l) with elevated inflammatory markers (C-reactive protein = 127 mg/l). Renal and liver functions were correct. Urinary cytobacteriological investigation showed the presence of leucocyte in urine (988/mm3). Therefore, urinary tract infection was initially suspected and the child was put on intravenous antibiotics (cefotaxime and gentamycin) for 3 days without any improvement. Urine culture and hemocultures come back later negatives. The girl had persistent fever, diarrhea, and severe abdominal pain. She also developed hypotension (76/31 mmHg) and tachycardia (150/min). She was transferred to our Pediatric Intensive Care Unit after fluid resuscitation and norepinephrine infusion. Broad-spectrum antibiotics were introduced including imipenem, vancomycin and amikacin. Laboratory exams revealed elevated C-reactive protein (359 mg/l), high level of transaminases (SGOT = 491 UI/l / SGPT = 184 UI/l), renal dysfunction (urea = 15 mmol/l; creatinine = 360 μmol/l), hyponatremia (129 mmol/l), and hypokalemia (2.6 mmol/l). Complete blood count showed lymphopenia (total leukocyte counts = 15.95 × 109/l; lymphocyte count = 0.6 × 109/l) and thrombocytopenia (platelet count = 110 × 109/l). Blood gas analysis revealed metabolic acidosis with pH = 7.06; PaO2 = 40 mmHg; PaCO2 = 17 mmHg; HCO3- = 4.8 mmol/l and hyperlactatemia at 6.4 mmol/l. Computed Tomography Scan showed a few posterior pulmonary consolidation lesions associated with a small pleural and pericardial effusion, hepatomegaly, recto-sigmoiditis (Fig. a), mesenteric lymphadenopathy (Fig. b), pelvic ectopic right kidney, and a small pelvic peritoneal effusion, without any signs of appendicitis or peritonitis. Echocardiography demonstrated the existence of a small pericardial effusion with a normal ejection fraction (Ejection Fraction = 60%) and no valvular or coronary lesions. A second test for SARS-CoV-2 by RT-PCR was negative as well as hemocultures and urine culture. Dobutamine and hydrocortisone were added because of persistent hypotension despite multiple fluid resuscitation and increasing norepinephrine infusion. Clinically, multiple mucocutaneous lesions appeared including maculopapular rash (Fig. a, b, c), and subconjunctival hemorrhage. A worsened hypoxemia was noted along with neurological troubles, leading to respiratory failure and requiring intubation and assisted-ventilation. Blood test showed decreased count of platelets at 56 × 109/l and prothrombin time at 33% (Table ). Platelet and Frozen Fresh Plasma transfusion were indicated. It was a refractory shock with multiple organ failure. The diagnosis of MIS-C with features of TSS was suspected. Therefore, the child was treated with intravenous immunoglobulin (IVIG) (1 g/kg/day for two days). Despite of cardio-pulmonary resuscitation, the patient had a fatal outcome.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [76.0, 'mm hg'], 'Diastolic Blood Pressure': [31.0, 'mm hg']}",46,43.7,48.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 76.0 mm Hg + 2/3 * 31.0 mm Hg = 46.0 mm Hg.
Hence, the patient's mean arterial pressure is 46.0 mm Hg."
1608,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8243755-1,Extracted,"A 77-year-old man was transferred to our emergency department by ambulance due to shock; he had a mild disorder of consciousness (Glasgow Coma Scale, E3V4M6) and restlessness on arrival. He presented with comorbid hyperglycemia and hypertension; however, he had not been medicated for approximately 10 years. He had experienced a low-grade fever and malaise for 5 days before admission, and his oral intake had decreased. He had a blood pressure of 82/60 mmHg, a pulse rate of 116 b.p.m., a respiratory rate of 32 breaths/min, and a body temperature of 36.0°C. The abdominal findings were obscure due to the disorder of consciousness; although he complained of mild pain in the left lower quadrant, no peritoneal sign was evident. The laboratory data on admission showed a plasma glucose concentration of 1,407 mg/dL (normal range, 70–109 mg/dL) and a hemoglobin A1c level of 13.4% (normal range, <6.0%). His sodium concentration was 123 mmol/L (normal range, 138–145 mmol/L), blood urea nitrogen level was 88.2 mg/dL (normal range, 8.0–20.0 mg/dL), creatine level was 3.44 mg/dL (normal range, 0.46–0.79 mg/dL), and white blood cell count was 14,400 cells/μL (normal range, 3,300–8,600 cells/μL). The C-reactive protein concentration was 8.39 mg/dL (normal range, <0.14 mg/dL), and the concentration of procalcitonin was 23.0 ng/mL (normal range, <0.05 ng/mL). The serum osmolality was 356 mOsm/L (normal range, 270–295 mOsm/L). Arterial blood gas data (O2 10 L/min) showed a pH of 7.38, partial pressure of oxygen (PaO2) of 188, partial pressure of carbon dioxide (PaCO2) of 28.5 mmHg, an HCO3− concentration of 16.6 mmol/L, a base excess of −6.4 mmol/L, and a lactate concentration of 41 mg/dL. The analysis was negative for urinary ketones.
Computed tomography without contrast was carried out due to renal insufficiency; it revealed a small amount of HPVG in the left lobe (Fig. ). No remarkable acute mesenteric ischemia finding, such as bowel dilatation or pneumatosis intestinalis, was observed (Fig. ). Hepatic portal venous gas was classified using the classification from a retrospective analysis. In addition, we suspected intestinal ischemia/necrosis due to the high lactate concentration and small amount of HPVG on the CT. We initiated a continuous intravenous infusion of regular human insulin and Ringer’s acetate solution to treat the HHS; however, the pulse increased to 128 b.p.m. The noradrenaline dose was increased from 0 to 0.33 μg/kg/min to maintain the mean blood pressure of 60 mmHg, and the elevated lactate concentration persisted (46 mg/dL) for 5 h postadmission. We administered extracellular fluid at a rate of 2,500 mL/4 h before noradrenaline was started. The pain in the left lower quadrant had worsened and peritoneal signs became evident. Thus, we carried out contrast-enhanced abdominal CT, as intestinal necrosis was suspected. The HPVG had spread within the left lobe compared with the initial CT scan (Fig. ). The CT also revealed remarkable bowel dilatation and pneumatosis intestinalis in the absence of contrast‑induced bowel wall enhancement (Fig. ). No occlusion of the superior mesenteric artery or superior mesenteric vein due to thrombus or embolism was observed. Based on the physical examination, laboratory data, and CT findings, we suspected NOMI, requiring emergency laparotomy. At the initial operation, necrosis was observed within the small bowel, with segmental and skip lesions (Fig. ). The necrotic portion of the small bowel, 170 cm in length, was resected using an automatic suture instrument; the remaining small bowel was 20 cm from the ligament of Treitz and 210 cm from the terminal ileum. No anastomosis was carried out. The initial surgery ended with open abdominal management to allow for a second-look operation on the third hospitalization day, at which time no bowel necrosis was observed; an anastomosis was performed, followed by abdominal closure. We initiated treatment with a vasodilator with continuous intravenous prostaglandin E1 infusion after terminating vasopressor treatment from the third to the seventh hospitalization day, after which the patient was extubated. On the 10th hospitalization day, the patient initiated oral intake. Insulin therapy was substituted by an oral diabetes medication (a dipeptidyl peptidase IV inhibitor), as his plasma glucose concentration was reduced. He was discharged on the 21st day of hospitalization.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [82.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",67.33333,63.96666,70.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 82.0 mm Hg + 2/3 * 60.0 mm Hg = 67.33333 mm Hg.
Hence, the patient's mean arterial pressure is 67.33333 mm Hg."
1609,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-6098,Extracted,"A 33-year-old man presents to the emergency department with a fever and fatigue. He states that he has not felt well since he returned from a hiking trip in Alabama. He is generally healthy and has no other medical conditions. His temperature is 101°F (38.3°C), blood pressure is 127/85 mmHg, pulse is 108/min, respirations are 14/min, and oxygen saturation is 99% on room air. Physical exam including a full dermatologic inspection is unremarkable.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [85.0, 'mm hg'], 'Systolic Blood Pressure': [127.0, 'mm hg']}",99,94.05,103.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 127.0 mm Hg + 2/3 * 85.0 mm Hg = 99.0 mm Hg.
Hence, the patient's mean arterial pressure is 99.0 mm Hg."
1610,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8610460-1,Extracted,"A 26-year-old female presented to the ED in 2017 with a chief complaint of several days of nausea, abdominal pain, and a newly painful right knee associated with a migratory erythematous rash. The patient stated that one day prior, the same rash and pain were present on her contralateral knee but resolved with no treatment. Her past medical history (PMH) was significant for bipolar disorder and a chlamydia infection, successfully treated the prior year. Her social history was significant for tobacco and alcohol use, and no reported drug use. Her triage vital signs were temperature 36.7o Celsius, heart rate 87 beats per minute, blood pressure of 137/87 millimeters mercury (mm Hg), respiratory rate of 26 breaths per minute, and pulse oximetry of 99% on room air. Her physical exam (PE) was notable only for a large circular erythematous rash over the proximal aspect of her right knee and leg with full range of motion with minimal to no pain and no murmur on cardiac auscultation ().
She refused a vaginal exam. Significant laboratory results were as follows: white blood cell count 12.2 thousand per cubic millimeter (k/mm3) (reference range 4.5–11.5 K/ mm3; C-reactive protein 3.5 milligrams per liter (mg/L) (reference less than 3.0mg/L); erythrocyte sedimentation rate 16 mm per hour (hr) (0–20 mm/hr); procalcitonin less than 0.05 nanograms per milliliter (ng/mL) (less than 0.1 ng/mL); rapid plasmin reagent was negative; urinalysis showed greater than 182 white blood cells per high-power field (HPF); greater than 182 red blood cells per HPF, and 5 squamous epithelial cells per HPF; urine pregnancy test was negative; and urine gonorrhea polymerase chain reaction was positive. A computed tomography (CT) of the abdomen and pelvis with intravenous (IV) contrast showed cholelithiasis without acute cholecystitis. Given her prior history of chlamydia infection, the migratory rash and joint pain, DGI was presumed, and blood cultures were obtained with initiation of IV ceftriaxone. Arthrocentesis was deferred. Several additional labs were ordered to evaluate for autoimmune disorders upon admission. Throughout her admission, the patient manifested several fevers across numerous nursing shifts with several sets of blood cultures (four total sets including the set obtained upon admission) obtained. All eventually showed no growth. A transthoracic echocardiogram (TTE) was performed on hospital day four, which showed an abnormally thickened aortic valve. Transesophageal echocardiogram confirmed a mobile vegetation presumed to be gonococcal endocarditis, which was successfully treated with four weeks of IV ceftriaxone.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [137.0, 'mm hg'], 'Diastolic Blood Pressure': [87.0, 'mm hg']}",103.66667,98.48334,108.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 137.0 mm Hg + 2/3 * 87.0 mm Hg = 103.66667 mm Hg.
Hence, the patient's mean arterial pressure is 103.66667 mm Hg."
1611,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8362527-1,Extracted,"A 29-year-old woman presented to our department complaining of worsening pain in the lower left abdominal quadrant. Her last menstrual cycle was 7 wk and 1 d previous.
The pain had started a day before her admission and had been worsened in the last 4 h. An IVF cycle was performed with two frozen embryos transferred 5 wk ago. There were no additional symptoms.
The patient had an obstetric history of gravida 4, para 0-0-3-0. Two years after her first spontaneous abortion, she twice underwent diagnostic hysteroscopy combined with laparoscopy for secondary infertility. Then, she had a history of HP with failing intrauterine pregnancy after ovulation induction treatment. Laparoscopic bilateral salpingectomy and dilation and curettage were performed. After sterilization, she experienced two unsuccessful IVF cycles.
There is no personal and family history.
The patient’s temperature was 36.5 °C, heart rate was 95 bpm, respiratory rate was 20 breaths per min, blood pressure was 102/67 mmHg, and oxygen saturation was 98%. The general appearance was acute distress. The gynecologic examination revealed bulky uterus and tenderness in the left adnexal area, which showed signs of peritoneal bleeding and irritation but with stable vital signs.
Blood analysis revealed an erythropenia (2.58 × 1012/L) and a hemoglobin concentration of 8.0 g/dL with normal leukocyte count and platelet count. Prothrombin and partial thromboplastin times were normal. Serum human chorionic gonadotropin value was 171116.9 mIU/mL. The blood biochemistries and urine analysis were normal.
Transvaginal ultrasound showed a live intrauterine pregnancy and another live embryo with cardiac activity in the left cornu extending beyond the lateral edge of the uterus. In addition, free fluid was noted in the cul-de-sac as well as in the abdomen.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [67.0, 'mm hg'], 'Systolic Blood Pressure': [102.0, 'mm hg']}",78.66667,74.73334,82.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 102.0 mm Hg + 2/3 * 67.0 mm Hg = 78.66667 mm Hg.
Hence, the patient's mean arterial pressure is 78.66667 mm Hg."
1612,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4981,Extracted,"A 42-year-old male with a history of ulcerative colitis presents to the emergency room with four-day history of nausea, bloody diarrhea, and abdominal pain. He is on medical management with 5-aminosalicylic acid (5 ASA). Examination shows an ill appearing man with a tense, tympanitic abdominal exam. He is unable to be fully examined due to the abdominal pain. Vitals are T 38.2 C, HR 102 bpm BP 133/92 mmHg,2 RR 20 bpm, and O2 Sat 100% on room air. In the ED an abdominal radiograph is shown in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [133.0, 'mm hg'], 'Diastolic Blood Pressure': [92.0, 'mm hg']}",105.66667,100.38334,110.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 133.0 mm Hg + 2/3 * 92.0 mm Hg = 105.66667 mm Hg.
Hence, the patient's mean arterial pressure is 105.66667 mm Hg."
1613,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8082980-1,Extracted,"A 47-year-old male presented with worsening shortness of breath for the prior 2 months. The past medical history was significant for hypertension, non-ischemic cardiomyopathy with a left ventricular ejection fraction of 15% to 20%, and paroxysmal Afib. Notably, he reported noncompliance with outpatient guideline-directed medical therapy for heart failure and anticoagulation with apixaban due to financial constraints.
On presentation, he was noted to be in Afib with a ventricular rate of 160 beats per minute, blood pressure of 121/80 mm Hg, and oxygen saturation of 97% on room air. There was bipedal edema and mild pulmonary edema without respiratory distress suggestive of decompensated acute on chronic heart failure with reduced ejection fraction. He was admitted for diuresis and pharmacologic rate control strategies. Initial transthoracic echocardiography showed a left ventricular ejection fraction of 15% to 20% with an enlarged left ventricle and a mild to moderately impaired right ventricle function. There was moderate to severe mitral regurgitation with a severely dilated left atrium.
Over the ensuing few days, euvolemia was achieved but the ventricular rate persisted at around 140 beats per minute despite optimal AV nodal blocking therapies. Thus, a rhythm control strategy was planned with transesophageal echocardiogram (TEE) and subsequent electrical cardioversion. The TEE revealed an estimated ejection fraction of 10% to 15%, severe mitral regurgitation, no evidence of PFO, and no LAA clot despite very low velocities in the LAA. However, on examination of the RAA, a 2.7 × 1.7 cm clot was noted ( and ). Given these findings, cardioversion was delayed and he was placed on subcutaneous low-molecular-weight heparin injections until a therapeutic international normalized ratio (INR) of 2 to 3 could be achieved with oral warfarin. He was eventually discharged to follow-up as an outpatient for planned cardioversion.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [121.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.66667,88.98334,98.35,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 121.0 mm Hg + 2/3 * 80.0 mm Hg = 93.66667 mm Hg.
Hence, the patient's mean arterial pressure is 93.66667 mm Hg."
1614,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7768541-1,Extracted,"A 64-year-old female patient was referred to our unit for a cardiorespiratory evaluation because of dyspnea and orthopnea. She was treated with enzyme replacement therapy for 10 years because of LOPD. She had limb girdle weakness with waddling gait. The Walton score was 3. The other clinical parameters were as follows: body mass index at 26 kg/m2, systolic blood pressure at 109 mmHg, diastolic blood pressure at 65 mmHg, and diurnal oxygen transcutaneous saturation at 100%. Doppler Echocardiography showed a normal left ventricular ejection fraction (61%) with normal cardiac loading and subnormal systolic arterial pulmonary pressure (41 mmHg). We performed a diaphragm exploration using ultrasound in the same exam. From the subcostal view, we assessed the diaphragm motion using TM mode in rest and during a sniff maneuver, as previously described []. We found a paradoxical diaphragm motion during a sniff maneuver of both the right (−11 mm) and the left hemi diaphragm (−18 mm), with M mode (). Using tissue Doppler imaging, we also found a negative and reduced peak velocity of diaphragm during the sniff maneuver, measured on the right hemi diaphragm (−6 cm/s) and on the left hemi diaphragm (−4 cm/s) (). Diaphragm weakness was confirmed by the decrease in maximal inspiratory pressure (22 cm H2O), the decrease in sniff inspiratory pressure (29 cm H2O) and the drop in the predicted value of respiratory forced vital capacity (VC) from upright to supine position (from 43% to 27%). In the meantime, with transcutaneous capnometry, the patient disclosed nocturnal hypoventilation attested by an increase in the transcutaneous PCO2 (82% of the registration time with PCO2 > 50 mmHg) and a decrease in transcutaneous PO2 (39% of time with PO2 < 90%). Non-invasive nocturnal ventilation was introduced to manage the respiratory failure.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [109.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",79.66667,75.68334,83.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 109.0 mm Hg + 2/3 * 65.0 mm Hg = 79.66667 mm Hg.
Hence, the patient's mean arterial pressure is 79.66667 mm Hg."
1615,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7256,Extracted,"A 72-year-old woman presents to her primary care provider complaining of fatigue for the last 6 months. She can barely complete her morning chores before having to take a long break in her chair. She rarely climbs the stairs to the second floor of her house anymore because it is too tiring. Past medical history is significant for Hashimoto's thyroiditis, hypertension, and hyperlipidemia. She takes levothyroxine, chlorthalidone, and atorvastatin. Her daughter developed systemic lupus erythematosus. She is retired and lives by herself in an old house build in 1945 and does not smoke and only occasionally drinks alcohol. She eats a well-balanced diet with oatmeal in the morning and some protein such as a hardboiled egg in the afternoon and at dinner. Today, her blood pressure is 135/92 mm Hg, heart rate is 110/min, respiratory rate is 22/min, and temperature is 37.0°C (98.6°F). On physical exam, she appears frail and her conjunctiva are pale. Her heart is tachycardic with a regular rhythm and her lungs are clear to auscultation bilaterally. A complete blood count (CBC) shows that she has macrocytic anemia. Peripheral blood smear shows a decreased red blood cell count, anisocytosis, and poikilocytosis with occasional hypersegmented neutrophils. An endoscopy and colonoscopy are performed to rule out an occult GI bleed. Her colonoscopy was normal. Endoscopy shows thin and smooth gastric mucosa without rugae.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [135.0, 'mm hg'], 'Diastolic Blood Pressure': [92.0, 'mm hg']}",106.33333,101.01666,111.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 92.0 mm Hg = 106.33333 mm Hg.
Hence, the patient's mean arterial pressure is 106.33333 mm Hg."
1616,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3219783-1,Extracted,"A 68-year-old man (height 166 cm, weight 72 kg, BMI 26.1) underwent nephroureterectomy with cuff excision due to a left ureter carcinoma. The patient had a history of surgery for colon cancer and was on antihypertensive medication. Preoperative physical examination and laboratory investigations showed normal findings.
On arrival in the operating room, his baseline blood pressure was 150/88 mmHg and his heart rate was 68 beats/minute. After preoxygenation, anesthesia was induced with midazolam, thiopental, and fentanyl. Tracheal intubation was facilitated with rocuronium. Anesthesia was maintained with N2O, fentanyl and sevoflurane. Surgery was performed for 9 hours in the right lateral decubitus position without repositioning. The patient's blood pressure and heart rate were maintained within a range of 20 percent of baseline during the procedure. Findings from intraoperative arterial blood gas analyses performed every 2 hours were within the normal ranges. The estimated blood loss was 500 ml, with no need for a blood transfusion.
After completion of the surgery, the patient was awake and alert. He was then transferred to the postanaesthetic care unit (PACU). In the PACU, intravenous ketolorac was administered for pain relief, and the patient was transferred to the general ward. He complained of mild back pain. Blood chemistry tests that were performed 90 minutes after completion of the surgery revealed AST, 90 IU/L, and ALT, 54 IU/L. The urine volume was maintained at 1.5-3.0 ml/kg/h with no darkening of color. Serum levels of AST and ALT increased markedly to 386 IU/L and 158 IU/L, respectively, on the first postoperative day (day 1) and to 544 IU/L and 221 IU/L respectively, on day 2. Hence, the patient was referred to a gastroenterologist. Since the viral markers were all negative, ischemic liver injury or toxic hepatitis was presumed to have occurred during surgery. However, no hypotensive or hypoxic episodes occurred during surgery. The back pain did not respond to non-steroidal anti-inflammatory drugs, despite the fact that no tenderness or erythema was present in the thigh or back. Rhabdomyolysis was suspected because the patient had intraoperative risk factors, such as being overweight, having a prolonged operation, and unusual positioning without repositioning. At that time, blood chemistry tests revealed creatine kinase (CK), 26,276 IU/L; serum myoglobin, ≥3,000 ng/ml (normal, 5-60 ng/ml); lactate dehydrogenase (LD), 1,002 IU/L and albumin, 3.0 g/dl . No abnormalities were noted on alkaline phosphatase, prothrombin time, or γ-GT. Under a diagnosis of rhabdomyolysis, the patient was sufficiently hydrated to maintain high urine output, but alkalinization was not performed because his urine pH was 7.0. Renal function remained within normal limits during the entire postoperative period. Two weeks later, blood chemistry tests showed CK, 261 IU/L; LD, 239 IU/L; AST, 30 IU/L; and ALT, 42 IU/L. details the time course of AST, ALT and CK. On day 16, the patient was discharged from the hospital.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [88.0, 'mm hg']}",108.66667,103.23334,114.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 88.0 mm Hg = 108.66667 mm Hg.
Hence, the patient's mean arterial pressure is 108.66667 mm Hg."
1617,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-10712,Extracted,"A 65-year-old woman comes to clinic complaining of pain with chewing solid foods. She reports that she has been feeling unwell lately, with pains in her shoulders and hips, and she has lost five pounds in the past few months. Her vital signs are T 39C, RR 18 breaths/min, HR 95 bpm, BP 120/65 mmHg. When you ask her to stand from her chair to get on the exam table she moves stiffly but displays preserved proximal muscle strength.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [65.0, 'mm hg'], 'Systolic Blood Pressure': [120.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 65.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1618,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3014857-1,Extracted,"A 59-year-old man was admitted to our hospital complaining of anterior chest pain on exertion. He had a history of hypertension and diabetes. His blood pressure was 130/80 mmHg, and the pulse rate was 72 beats/minute. There was no audible murmur on the chest wall, and his electrocardiography (ECG) was normal. His exercise treadmill test (ETT) revealed ischemic changes accompanied by chest pain. Therefore, selective coronary angiography was performed via the right femoral approach (Seldinger technique). Coronary angiography showed critical lesion in LAD, Cx, and the contrast agent entered the left ventricle from the left anterior descending artery (LAD) during diastole (see Figures and ). We performed successful percutaneous coronary intervention and stenting to lesion in LAD and Cx. To our knowledge, this is the first case reported in the literature.
The patient's post-PTCA course was uneventful with the disappearance of angina and symptoms. One month after discharge, ETT was performed to the patient and demonstrated no ischemic ECG changes.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1619,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4531734-1,Extracted,"A 76-year-old female patient presented with a three month history of anterior neck swelling that was rapidly progressing during the last two weeks. There was no history of thyroid disease or previous malignancy. Her physician detected hypertension several years ago, but the patient took no specific medication. The patient’s family history was noncontributory. She had a 20 pack-year smoking history and drank alcohol occasionally. The patient denied fever or night sweats but had lost 6 Kg of weight during the past three months.
Physical examination showed a chronically ill-appearing woman. On examination of the neck, both lobes of the thyroid gland were diffusely enlarged with hard consistency and were relatively fixed. Multiple bean-sized, movable lymph nodes were palpable along the anterior margins of the mid-portion of both sternocleidomastoid muscles. The abdomen was nontender and nondistended, and no mass or organomegaly was found.
Her blood pressure was 130/80 mmHg: pulse rate was 78 beats per minute, and her body temperature was 36.0 °C. Laboratory blood tests showed a white blood cell count of 5800/mm3 with normal differential count: hemoglobin 11.5g/dL, hematocrit 33.6% and platelet 152,000/mm3. Data of blood chemistry were as follows: total protein 5.9g/dL, albumin 3.2g/dL, lactic dehydrogenase 373U/L (normal range 120–240 U/L), ESR 40mm/hr normal range 0–30mm/hr), aspartate amino-transferase 18U/L normal range 0–35 U/L), uric acid 107 μmol/L (normal range 90–360 μmol/L), alkaline phosphatase 78U/L (normal range 30–120U/L). There was no specific abnormality of other laboratory tests. Anti-microsomal and antithyroglobulin antibodies were negative. Thyroid function tests were as follows: free T4 21.8 pmol/L (normal range 9.0–43.76 pmol/L), TSH 0.51 mU/L (normal range 0.4–5 mU/L), and thyroglobulin 630 ng/mL (normal range 2–60 ng/mL).
Thyroid US demonstrated a diffusely enlarged thyroid gland, diffuse irregular hypoechoic lesions on the left lobe and multiple irregularly scattered hypoechoic lesions on the upper part of the right lobe. There were also multiple hypoechoic enlarged lymph nodes of 1–1.2 cm size on both sides of the neck. 99mTc pertechnetate scan demonstrated markedly decreased and heterogeneous uptake on the ultrasonographically abnormal area and showed normal uptake on the right lower pole (). 99mTc-hexakis-2-methoxy isobutyl isonitrile (MIBI) scan showed significant uptake in the abnormal area on the 10-minute image with normal washout on the right lower pole (), and significant retention of isotope on 4-hour-delayed image (). Fine-needle aspiration of the thyroid mass was indeterminate, but a cytologist suggested the probability of undifferentiated malignancy. Computerized tomographic (CT) scan of the neck showed diffuse enlargement of both thyroid lobes with more marked enlargement in the left lobe. Focal areas of normal enhancement were present in both lobes. However, other abnormal areas showed decreased density with lobulated margins. There were also multiple lymphadenopathies in both internal jugular chains ().
Chest radiology was normal, but abdominal US demonstrated large bilateral adrenal masses of homogeneous hypoechoic texture. Abdominal CT scan showed large bilateral masses in the region of the adrenal glands. The mass on the right measured 6×4×6.5 cm, and the mass on the left measured 10×6×10.5 cm. The masses were of homogeneous low attenuation. There was no evidence of abdominal or pelvic lymphadenopathy ().
Ultrasound-guided core needle biopsies of the left thyroid lobe and of the adrenal mass on the left side were done and incisional biopsy of the palpable lymph node on the left jugular chain was performed. All of them showed diffuse lesions consisting of large, oval to round monomorphic cells with scant cytoplasm. Most cells had a single nucleolus with finely stippled chromatin. Marker study of tumor cells revealed B cell origin with a final diagnosis of diffuse large B cell lymphoma (). Peripheral blood smear and bone marrow biopsy were normal. Brain MRI revealed a multifocal lacunar infarction of left basal ganglia. Echocardiography was nonspecific.
Other endocrine tests were done: plasma ACTH 15.3 pmol/L (normal range 2–11 pmol/L), cortisol 416.6 nmol/L (normal range 140–690 nmol/L), and her serum calcitonin, plasma renin activity, aldosterone, urinary vanillylmandelic acid and metanephrine were all within normal ranges.
She received CHOP regimen (cyclophosphamide 750 mg/m2, doxorubicin 50 mg/m2, and vincristine 1.4 mg/m2 intravenously on the first day, and prednisone 100 mg/m2 orally for five days). On the fifth day of first chemotherapy, her goiter was found to be markedly reduced. Gallium scintigraphy done one day after the first cycle of chemotherapy revealed no uptake of radiotracer in the region of the tumors (). Before receiving a second cycle of chemotherapy, thyroid function test and one-hour standard ACTH stimulation test were normal: free T4 12.6 pmol/L (normal range 9.0–43.76 pmol/L), TSH 0.4 mU/L (normal range 0.4–5 mU/L), basal plasma ACTH 8.76 pmol/L (normal range 2–11 pmol/L), basal serum cortisol 532.5 nmol/L (normal range 140–690 nmol/L), and serum cortisol 684.2 pmol/L 60 min after intravenous injection of 250 ug (85 nmol) of Cosyntropin. Abdominal US revealed no mass in the regions of both adrenal glands.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1620,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5943133-1,Extracted,"A 36-year-old man was admitted to West China Hospital because of low libido, decreased morning erections, and loss of axillary and pubic hair that lasted 8 years. He had a history of binocular diplopia, increased stool frequency 7 years prior to admission, and weight loss of 10 kg. He also had thyroid nodules, and thyroid functional tests showed normal FT3 (7.41, normal 3.6–7.5 pmol/L), FT4 (21.56, normal 12–22 pmol/L), and increased TSH (24.79, normal 0.27–4.2 μIU/mL). He ignored the test result, because of the normal concentration of FT3 and FT4. Four years ago the patient got married and was referred to our hospital because of sterility. At this time, the hormonal examination implied central hypogonadism with serum levels of 1.6 mIU/mL FSH (RR, 1.5–12.4), LH 1.0 mIU/mL (RR, 1.7–8.6), E2 <5 pg/mL (RR, 7.63–42.8), and T <0.03 ng/mL (RR 2.49–8.3). Magnetic resonance imaging (MRI) of the sella region was therefore performed, revealing a pituitary tumor measuring 4.3 × 4.1 × 3.0 cm in the sella, involving cavernous sinuses and extending inferior to the sphenoid sinus and third ventricle (Fig. ). He was referred to our multidisciplinary team of pituitary disease and transferred to department of neurosurgery. On physical examination at admission, the patient was 168.0 cm tall and weighed 59.0 kg with a body mass index (BMI) of 20.9 kg/m2. The patient's char-acteristics were as follows: temperature, 36.2 °C; pulse, 56 beat/min; blood pressure, 94/64 mmHg; respiratory rate, 20 breath/min. The patient presented with blurred vision. The TgAb and TPOAb were positive. The thyroid gland was diffusely enlarged and ultrasonography of the thyroid revealed a multinodular gland with a moderate parenchymal heterogeneity suggesting Hashimoto thyroiditis. The laboratory hormone examination showed hypopituitarism (Table ). The computer perimetry suggested a defective visual field. Based on these data, we diagnosed the patient with TSH-producing pituitary macroadenoma, hypopituitary, and Hashimoto thyroiditis. Two weeks after diagnosis, total resection of the pituitary macroadenoma was performed through trans-sphenoidal neurosurgery in September 2014. Upon immunohistochemical examination, the resected pituitary adenoma cells exhibited positive staining with the TSH and PRL antibody, and the percentage of positive Ki-67 was <2%, suggesting that the tumor was benign (Fig. ). After the operation, TSH and thyroid hormone rapidly decreased to a normal range. However, the concentration of ACTH, cortisol, LH, FSH, and testosterone were still extremely low. One year after the operation, this patient was attended to by our pituitary disease MDT team for reproductive reconstruction. We treated him with human chorionic gonadotropin (HCG) 2000 IU, qod and human menopausal gonadotropin (HMG) 75 IU, qod. Over the next 2 months, his sperm concentration increased, and finally his wife became pregnant naturally. The patient was administered hydrocortisone 20 mg/d, testosterone 80 mg/d, and followed up by our pituitary MDT team.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [94.0, 'mm hg'], 'Diastolic Blood Pressure': [64.0, 'mm hg']}",74,70.3,77.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 94.0 mm Hg + 2/3 * 64.0 mm Hg = 74.0 mm Hg.
Hence, the patient's mean arterial pressure is 74.0 mm Hg."
1621,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-539,Extracted,"A 68-year-old man comes to the physician because of fatigue and muscle cramps for the past 4 weeks. He has also noticed several episodes of tingling in both hands. He has not had fever or nausea. He has had a chronic cough for 10 years. He has chronic bronchitis, hypertension, and osteoarthritis of both knees. His father died from lung cancer. Current medications include salbutamol, ibuprofen, and ramipril. He has smoked 1 pack of cigarettes daily for 45 years. He is 175 cm (5 ft 9 in) tall and weighs 68 kg (163 lb); BMI is 22 kg/m2. His temperature is 36.7°C (98°F), pulse is 60/min, and blood pressure is 115/76 mm Hg. While measuring the patient's blood pressure, the physician observes carpopedal spasm. Cardiopulmonary examination shows no abnormalities. His hematocrit is 41%, leukocyte count is 5,800/mm3, and platelet count is 195,000/mm3. Serum alkaline phosphatase activity is 55 U/L. An ECG shows sinus rhythm with a prolonged QT interval.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [76.0, 'mm hg'], 'Systolic Blood Pressure': [115.0, 'mm hg']}",89,84.55,93.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 76.0 mm Hg = 89.0 mm Hg.
Hence, the patient's mean arterial pressure is 89.0 mm Hg."
1622,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2740003-1,Extracted,"A 23-year-old gravida 0, para 0, Caucasian female graduate student weighing 55 kg and 160 cm in height presented to her primary care physician with discolored digits (1 through 3) on both of her feet. She also complained that her toes were painful, blistered, and intermittently pruritic. She stated her symptoms had begun the day after receiving a pedicure before going out to a university event that same evening. The patient's vital signs were blood pressure 120/62 mm Hg, heart rate of 70 beats per minute, and respirations 14 per minute. Physical examination of her heart and lungs was unremarkable. Her medical and surgical histories were negative. She was a non-smoker and consumed less than 6 ounces of alcohol per week. She had no allergies. The primary care physician prescribed cephalexin 500 mg by mouth daily for 10 days for a presumed bacterial infection.
Ten days later she still complained of discoloration, blisters and pain, and decided to visit an Emergency Department (ED) for a second opinion. The ED physician diagnosed CA-MRSA based on the physical presentations of the lesions and the increased incidence of MRSA in the community. Trimethoprim-sulfamethoxazole double strength (160 mg/800 mg) orally every 12 hours for 10 days was prescribed. The symptoms and signs persisted and the patient arranged to see a dermatologist, who performed a biopsy of the third digit (left foot). The dermatologist declined to prescribe further treatment until the biopsy returned. The biopsy revealed a histological diagnosis of perniosis (see ,). On further inquiry by the dermatologist, the patient stated that the evening after her pedicure she had spent several hours walking outdoors before the aforementioned university event. She had worn open-toed shoes and the wind chill factor that evening had gone as low as 0° F.
The patient was counseled to keep her feet warm and avoid damp conditions. No other medications were administered and the symptoms resolved three weeks later (mid-April) with conservative care and the return of warmer ambient temperatures.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [62.0, 'mm hg']}",81.33333,77.26666,85.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 62.0 mm Hg = 81.33333 mm Hg.
Hence, the patient's mean arterial pressure is 81.33333 mm Hg."
1623,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8122131-1,Extracted,"A 52-year-old white female with past medical history of hypertension, heart failure with preserved ejection fraction, generalized anxiety disorder, and alcohol dependence/abuse presented to the emergency department with retrosternal chest pain associated with nausea. She has family history significant for hypertension, diabetes mellitus type II, and coronary artery disease. Her home medications include the following: venlafaxine 75 mg, metoprolol tartrate 12.5 mg, and zolpidem 10 mg. Patient reports long history of 10 years or more of alcohol abuse reported as half a bottle of vodka or whiskey on daily basis. Vitals upon admission were blood pressure 155/100 mm Hg and a heart rate of 110 beats per minute. Her electrocardiogram showed sinus tachycardia with no acute ST-T wave changes. Initial troponin level was negative <0.012 (ng/mL). She was admitted for observation in the progressive care unit. Further laboratory data showed triglyceride 122 mg/dL (0-149), total cholesterol 265 mg/dL (107-200), LDL 41 mg/dL (0-99), HDL 218 mg/dL (39-61) with repeated level of 200 mg/dL. Her hemoglobin A1C was 5.3% (0-5.99), TSH 1.67 uIU/mL (0.465-4.68), folic acid >20.0 ng/mL (2.76-19), and vitamin B12 of 197.0 pg/mL (239-931). Other laboratory data including complete blood count and comprehensive metabolic panel were within normal limits. The trend of cardiac markers was negative. She had myocardial perfusion scan done showing no reversible ischemia. However, due to persistent chest pain, the decision was made to send the patient for left heart catheterization which showed nonobstructive coronary artery disease with 50% stenosis in the right coronary artery. She was discharged home on omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) 1000 mg folic acid 1 mg, atorvastatin 40 mg, aspirin 81 mg, and thiamine 100 mg with recommendations for further lipidology and genetic testing.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [155.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",118.33333,112.41666,124.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 155.0 mm Hg + 2/3 * 100.0 mm Hg = 118.33333 mm Hg.
Hence, the patient's mean arterial pressure is 118.33333 mm Hg."
1624,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7149419-1,Extracted,"A 54-year-old Caucasian man presented to our hospital with a 7-day history of right otalgia and purulent otorrhea without any systemic symptoms or fever. In order to control pain, the patient was previously treated with acetaminophen alone for 3 days.
There was no significant family, social, or medical history except for a myringoplasty for tympanic membrane perforation of the right ear performed 7 years earlier and a septoplasty performed 5 years earlier.
On physical examination, the patient's blood pressure was found to be 125/70 mmHg, pulse was 80 beats per minute, temperature was 36°C, and respiratory rate was 16 breaths per minute.
We observed pain on tragus pressure, whereas no paralysis of cranial nerves was observed. The right outer ear canal contained purulence with significant hyperemia and edema of skin. Tympanic membrane was impossible to visualize due to the narrowing of the outer ear canal. The rest of the head and neck examination, including the left ear, was normal.
Laboratory data at admission revealed a hemoglobin level of 14 g/dl and white blood cell count of 14.700 per microliter with 70% neutrophils. Inflammation markers were high: erythrocyte sedimentation rate (ESR) was 25 mm/h (normal range 0–22 mm/h) in the first hour, and the level of C-reactive protein (CRP) was 15 mg/L (normal range < 3.0 mg/L).
The computed tomography scan did not show soft alterations nor mastoid, skull base, and bony changes suggestive of malignant external otitis (). We performed right ear swab for culture examination; meanwhile, we started empirical therapy with topic administration of neomycin for 7 days, without any clinical improvement.
The cultural examination showed the presence of a R. ornithinolytica infection. R. ornithinolytica isolates were identified with MALDI-TOF MS [].
On the seventh day, as soon as the susceptibility profile of R. ornithinolytica was available (), we started a systemic therapy with ciprofloxacin 500 mg twice a day for 10 days, and topic therapy using 5 ear drops composed by 3% boric acid in 70% alcohol and 5 drops of levofloxacin twice a day for 10 days, after that we observed a complete resolution of symptoms. In addition, the right ear otomicroscopy showed a dry cavity with only a small granulation on the upper anterior quadrant of the tympanic membrane that disappeared after ten more days of boric acid drops. The six months follow-up did not show recurrence.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [125.0, 'mm hg']}",88.33333,83.91666,92.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 70.0 mm Hg = 88.33333 mm Hg.
Hence, the patient's mean arterial pressure is 88.33333 mm Hg."
1625,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7445494-1,Extracted,"A 20-year-old Nepalese male was admitted to our hospital after a 3-day history of a high fever and cough. He had been previously seen at another local clinic where he was diagnosed with influenza and treated with oral oseltamivir for the first 3 days. On the fourth day, he developed dyspnea and was admitted to our hospital on the same day. He did not have any relevant past history and had not been prescribed any medications. He came to Japan for employment almost five years ago with his parents and took his residence in Saitama Prefecture.
His vital signs on the day of admission were as follows: level of consciousness, E3V4M6/Glasgow Coma Scale; blood pressure, 100/72 mmHg; heart rate, 133 beats per minute; body temperature, 38.4 °C; respiratory rate, 24 breaths per minute; and peripheral capillary oxygen saturation level at an O2 flow rate of 2 liters per minute, 94%. Physical examination revealed lower respiratory sounds, and a few moist rales were heard in both lungs on chest auscultation. Laboratory data revealed a white blood cell (WBC) count of 700/mm3, a blood platelet count of 82,000/mm3, a C-reactive protein (CRP) level of 23.2 mg/dl, a blood urea nitrogen (BUN) level of 26.3 mg/dl, and a serum creatinine level of 2.2 mg/dl. The results of liver function tests were normal except for a lactate dehydrogenase (LDH) level of 618 IU/l. A chest computed tomography (CT) scan showed infiltrative and nodular shadows with pneumatocele formation in the right upper lobe ().
At first, we diagnosed severe bacterial pneumonia after influenza and septic shock and initiated the administration of lactate Ringer’s solution, noradrenalin infusion, and intravenous tazobactam/piperacillin (TAZ/PIPC) (4.5 g, 4 times daily) and azithromycin (AZM) (500 mg, once a day). However, his vital signs did not improve, and he developed respiratory failure requiring mechanical ventilation support. After rapid deterioration of his arterial oxygenation level, we introduced veno-veno extracorporeal membrane oxygenation support. Because gram-positive staphylococci were detected from sputum and blood samples collected on admission, we added linezolid (600 mg, 2 times daily, intravenously) on day 2. On the same day, we performed a bronchoscopy, which showed diffuse inflammatory changes and easy bleeding (). Therefore, we suspected necrotizing pneumonia caused by CA-MRSA. He underwent multidisciplinary treatment; however, his respiratory condition gradually worsened. Despite resuscitation efforts, he died of multiple organ failure on day 7. The isolates from the culture of blood and sputum samples on the day of hospital admission were MRSA strains TUM18988 and TUM18989. Additionally, his father, who lived with him in Japan, had a negative nasal swab test for MRSA.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [72.0, 'mm hg'], 'Systolic Blood Pressure': [100.0, 'mm hg']}",81.33333,77.26666,85.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 72.0 mm Hg = 81.33333 mm Hg.
Hence, the patient's mean arterial pressure is 81.33333 mm Hg."
1626,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4646996-1,Extracted,"A 61-year-old Hispanic man with past medical history of benign prostatic hyperplasia (BPH) treated with transurethral resection of the prostate the preceding year presented to our emergency room with a nonhealing wound on his right thigh. He reported that he sustained a laceration to his right thigh during work with machinery one week prior to presentation and had visited the nearest urgent care. Despite suture placement at the urgent care, he continued to bleed. In addition, he reported multiple ecchymoses on his lower abdomen and extremities and severe pain in his left hip and leg. The patient had a temperature of 36.5°C, a heart rate of 101 beats per minute, a blood pressure of 138/87 mm Hg, a respiratory rate of 18 breaths per minute, and an oxygen saturation of 98% on room air. Physical exam revealed skin pallor along with diffuse ecchymoses of the abdomen, thighs, and extremities. No lymphadenopathy was noted. Labs revealed a WBC of 7.9 (normal 3.4–10.4 1000/μL), hemoglobin 8.2 (normal 13.5–17.5 g/dL), hematocrit 24.8 (normal 40.0–51.0%), platelet counts of 76 (normal 150–425 1000/μL), INR 1.8 (normal 0.8–1.1), PT 20.9 (normal 11.9–15.0 seconds), PTT 46.9 (normal 22.6–35.5 seconds), fibrinogen 40 (normal 200–430 mg/dL), alkaline phosphatase 1193 (normal 40–150 IU/L), and D-dimer >20.0 (normal <0.5 μg/mL). The patient was started on 4 units of fresh frozen plasma and 1 unit of cryoprecipitate, and a DIC panel was obtained every 6 hours.
An X-ray of the left hip and femur demonstrated extensive metastatic lesions of the left ilium, ischium, and pubic bones including involvement of the acetabulum. A contrast-enhanced chest CT revealed focal periosteal reaction in the left posteromedial 6th, 7th, and 8th ribs along with nonhomogenous mixed sclerotic and lytic appearance in the spine. An abdominal MRI with and without contrast demonstrated diffuse osseous metastatic disease but no evidence of primary malignancy in the abdomen. Nuclear medicine whole body bone scan revealed diffuse osseous metastatic disease involving the axial and proximal appendicular skeleton along with bilateral involvement of the femurs. Spinal MRI with and without contrast demonstrated diffuse osseous metastatic disease involving the cervical, thoracic, lumbar spine, and sacrum. The MRI also demonstrated an unusual finding of extensive metastatic epidural tumor deposits along the thoracic and lumbosacral spine resulting in spinal canal stenosis (). The patient required transfusions of cryoprecipitate (CP), fresh frozen plasma (FFP), platelets (PLTs), and red blood cells (PRBCs) pending workup (Figures and ). Prostate serum antigen (PSA) and α2-antiplasmin (AAP) levels were ordered and revealed PSA and AAP levels of 673.17 (normal 0.0–4.0 ng/mL) and 42 (normal 88–120%), respectively. The significantly decreased fibrinogen and AAP levels in conjunction with high PSA indicated PC with DIC XFL as the diagnosis. A prostate biopsy was not attempted given the high risk of bleeding. The patient received two subcutaneous injections of degarelix 120 mg on each side of his abdomen (total 240 mg), followed immediately by cold compresses to both areas to prevent bleeding. Over the next 7 days, he was transfused with CP, PRBCs, PLTs, and FFP. He also received Vitamin K 5 mg daily. Coagulopathy marker goals were fibrinogen level > 100 mg/dL, hemoglobin > 8 g/dL, and platelet count > 50,000/μL. Ten days after admission, his coagulopathy improved obviating the need for transfusions (Figures and ).
The patient was observed an additional two days and did not require supportive transfusions and was discharged on day 13 after admission. Over the course of his encounter, he received a total of 70 units of CP, 8 units of FFP, 4 units of PRBCs, and 3 units of PLTs. His lab values upon discharge were platelets 139,000/μL, INR 1.1, PT 14.4 sec, PTT 22.4 sec, fibrinogen 141 mg/dL, alkaline phosphatase 600 IU/L, and PSA 125.70 ng/mL.
During an outpatient followup, the patient was stable and his labs revealed no coagulopathy and his D-dimer remained persistently elevated. He decided against pursuing a prostate biopsy given his concerns of bleeding and low likelihood that results will change management. MRI of the spine one month after starting testicular suppression revealed complete resolution of the epidural deposits (). After 3 months of treatment with degarelix his PSA decreased to 26 and he achieved a very good partial response by imaging. Six months after starting hormonal therapy he developed urinary retention requiring hospitalization and urinary catheter placement. His PSA increased to 555 and a bone scan and an MRI of the spine, abdomen, and pelvis revealed extensive bone metastasis in thoracic and lumbar spine, femur, ribs, and pelvis. Bicalutamide was added; however, his disease progressed with a PSA level of 1361 and an alkaline phosphatase level of 1247 (normal 40–150 IU/L). He was started on docetaxel and received 3 cycles of therapy. His PSA remained elevated at 1200 and his performance status worsened significantly (Karnofsky performance status of 60%) necessitating admission to a rehab center. The patient shortly after decided on comfort care.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [138.0, 'mm hg'], 'Diastolic Blood Pressure': [87.0, 'mm hg']}",104,98.8,109.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 138.0 mm Hg + 2/3 * 87.0 mm Hg = 104.0 mm Hg.
Hence, the patient's mean arterial pressure is 104.0 mm Hg."
1627,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4402179-1,Extracted,"A 49-year-old retired male was admitted to the physical therapy outpatient clinic with severe back pain. From the history, it was learned that he had an acute back pain in the morning with no trauma. On the day before presentation, he had suffered a witnessed nocturnal attack, of which he had no recollection. The patient was oriented normally on arrival and reported that he had not experienced any previous nocturnal attacks like this, which was confirmed by his wife. The attack was described by his wife as follows: he started to lock his jaw, stiffened, was sweating, convulsed, and became unconscious. The duration of the seizure was about 3 minutes. Following the seizure he was briefly postictal, during which time his wife noted decreased movement of his arms and lower extremities. She reported that after the seizure he slept again and, in the morning, he had a back pain. There was no history of trauma, previous falls, prior seizures, stroke, syncope, or steroid medication. In the absence of a history of trauma, an epileptic seizure was suspected. It was learned that he had a 23-year history of Type I diabetes mellitus. For the last 20 years, he had required Humulin R three times daily (11 IU/at morning, noon, and evening), and Lantus once a day (22 IU/at midnight). Further medical history was not relevant and the patient had no history of epilepsy. The patient was not using antiepileptic drugs (AED) or corticosteroids at that time. The cardiovascular and neurological examination results were normal. There were signs of a bitten tongue. The patient had complaints of dorsal vertebrae pain, which was determined by palpation on the dorsal vertebrae during physical examination.
Vital signs were noted as follows: blood pressure: 125/80 mm/Hg, heart rate: 75/min., temperature: 36.5°C, respiratory rate: 18/min., weight; 70 kg., and height: 1.78 cm. Basic blood examination was normal except for severely raised fasting blood glucose: 216 mg/dL (65–107 mg/dL), slightly raised urea: 54 mg/dL (15–44 mg/dL), ALP: 146 U/L (30–120 U/L), and hemoglobin A1c: 6.7% (4.0–6.5%). Thoracic magnetic resonance imaging (MRI) was applied to evaluate the severity of the injury. Acute phase compression fractures on T5 (loss of 50% of vertebral height) and on T6, T7, and T8 vertebrae were determined and an additional slightly increased risk of thoracic kyphosis was reported ().
For further evaluation, the patient was referred to the Neurology Department. In addition to basic studies, detailed investigations showed normal levels of parathyroid hormone, 25-hydroxy-vitamin D3, thyroid-stimulating hormone, free T3, free T4, cortisol, vitamin B12, and folate levels. Serum levels of calcium and phosphate were also within normal limits. Investigations for epilepsy were performed. An electroencephalogram (EEG) and a cerebral MRI showed no abnormalities. The patient was referred to the Orthopaedic Department, where he was treated conservatively. At the first follow-up examination, Dual Energy X-ray Absorptiometry (DEXA) was applied to rule out major osteoporosis due to diabetes. The T scores were as follows: femoral neck: −1.5, trochanter: −1.1, total: −1.2, lumbar (L) 1: −3.1, L2: −3.3, L3: −3.5, L4: −3.7, and total: −3.4. The DEXA reported osteopenia and osteoporosis on the right hip and in the lumbar spine, respectively. The osteopenia in the femoral region and osteoporosis in the lumbar region were treated with a single dose zoledronic acid 4 mg/5 mL intravenous infusion (for 1-year treatment), calcitonin 200 IU 1 × 1, and active vitamin D 0.25 mcg 1 × 1. Bed rest was applied for 3 weeks after the initial diagnosis, and then a thoracolumbar orthosis was used for 4 months (). The patient started taking bisphosphonate at the time of diagnosis, and still continues to date. After 2 months, the patient was able to walk confidently with assistance. He made a rapid recovery and minimal deformity and little disability remained. At the most recent follow-up (17 months from the initial diagnosis), he had no complaints of back pain. Written informed consent was obtained from the patient for publication of this case report and the accompanying images.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",95,90.25,99.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 80.0 mm Hg = 95.0 mm Hg.
Hence, the patient's mean arterial pressure is 95.0 mm Hg."
1628,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5652506-1,Extracted,"This 54-year-old woman presented to a large teaching hospital with a 2-week history of fevers, difficulty in breathing and a non-productive cough. This was preceded by a 3-week history of malaise, nausea, and sharp chest and back pains. There was no history of palpitations or radiation of chest pain. She described a 9-month history of unintentional weight loss of 3–4 kg, with an accompanying loss in appetite and odynophagia.
Two weeks prior to presentation, she had seen her general practitioner who had empirically diagnosed a lower urinary tract infection and prescribed a week-long course of trimethoprim, followed by another week’s course of amoxicillin/clavulanic acid. She did not improve following these treatments, and called ambulance services when she developed clinical anorexia, vomiting, fevers and difficulty in breathing. Her significant prior medical history included a depressive disorder, hypertension, hypercholesterolaemia, gastric acid-reflux disease and eczema. She owned a private business, but was not able to work for several months due to poor health. She lived with her adolescent son, and was independent in all activities of daily living. She was an ex-smoker with a 7 pack-year history. She described a recent alcohol intake history of an estimated 60 units per week for at least a few months. She did not take any illicit substances, injected or otherwise, and did not report any recent sexual contacts in the last 5 years. She described having been sexually assaulted 20 years ago, but penetrative intercourse did not occur. She did not report a history of having been investigated for sexually transmitted infections, but her last HIV test was 5 years prior and was negative. Her long-term medication included fluoxetine and lisinopril. She was not known to be allergic to any medications.
On general inspection, she appeared fatigued. She had a temperature of 36.4°C. She had a respiratory rate of 20 breaths per minute, with a capillary oxygen saturation reading of 95% on room air. Her heart rate was 78 beats per minute, with a non-invasive blood pressure of 155/85 mm Hg. Her Glasgow Comma Scale score was 15/15. Examination of her chest was completely unremarkable, and examination of the other major systems did not yield any contributory information.
A working diagnosis of a community-acquired pneumonia was established, and the patient was admitted for further investigations and management. Her initial investigations are given below. Her initial CURB-65 severity score was calculated as zero. Further investigations were conducted to look for atypical infecting organisms, including HIV testing. She was managed with appropriate fluid resuscitation and intravenous amoxicillin and clarithromycin for broad spectrum and appropriate atypical organism coverage.
On day 1 of the pre-ECMO admission period, the patient became markedly hypoxic. An arterial blood gas performed with 2 L of O2 being delivered through nasal cannulae yielded a pH 7.49, pO2 7.1 kPa, pCO2 4.0 kPa, BE 0 mmol/L and an HCO3 22.9 mmol/L. A CT pulmonary angiogram performed on the same day ruled out a pulmonary embolus as a cause of hypoxia, but confirmed a diffuse pneumonitis.
On day 2 pre-ECMO, the patient’s HIV test was reported as positive using two separate fourth-generation test kits. The clinical picture of hypoxia, cough and consolidative changes in the lung in the context of a new HIV diagnosis with a history of weight loss signifying chronicity of disease suggested a unifying diagnosis of P. jirovecii pneumonia. Oral hair leukoplakia and oral candidiasis were clinically identified on further inspection. Previous antibiotics were stopped and intravenous piperacillin/tazobactam was commenced due to evidence of clinical deterioration. Cotrimoxazole, prednisolone and fluconazole were started as treatment for presumed pneumocystis and oral candidiasis.
On day 3 pre-ECMO, CD4 quantification revealed 12 cells/mm3 consistent with an advanced, late presentation of HIV. She developed a normocytic anaemia with a serum lactate dehydrogenase (LDH) of 1431 units/L. The patient was transferred to an intensive care setting due to deteriorating ventilation resulting in type 1 respiratory failure requiring non-invasive ventilation oxygen delivery strategies. Despite being managed on non-invasive continuous positive airway pressure ventilation (set at positive end-expiratory pressure (PEEP) 10 and FiO2 65%), her capillary oxygen saturations remained between 88% and 90%.
On day 5 pre-ECMO, deteriorating oxygen requirements necessitated elective endotracheal intubation and mechanical ventilation. In accordance with evidence-based recommendations, a lung-protective ventilation strategy was employed; with tidal volumes aimed at 6 mL/kg and peak inspiratory pressures <30 mm Hg. Bronchoalveolar washout was performed, and an immunofluorescence test confirmed the presence of P. jirovecii.
By day 10 pre-ECMO, she had progressively worsening hypercapnia and borderline metabolic acidosis. Her serum lactate LDH continued to be raised (1349 units/L). It is recognised that P. jirovecii infection causes an increase in LDH, but on the basis of possible ineffective treatment and a worsening anaemia signalling potential haemolysis after 5 days of cotrimoxazole, second-line P. jirovecii treatment was initiated with clindamycin and primaquine. A referral to the national ECMO service was made. The patient was placed in the prone position in an attempt to improve gas exchange. Her ECG showed a new left bundle branch block, but a bedside transthoracic echocardiogram (TTE) showed good biventricular function. Due to the clinical deterioration, rescue therapy using caspofungin for P. jirovecii infection was initiated. Despite these measures, the patient became increasingly haemodynamically unstable and required increasing therapeutic oxygen requirements. A decision was made to place her on respiratory ECMO via bifemoral venous cannulation (23 and 25 FR), and she was retrieved to one of the five UK national commissioned ECMO centres for further management.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [155.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",108.33333,102.91666,113.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 155.0 mm Hg + 2/3 * 85.0 mm Hg = 108.33333 mm Hg.
Hence, the patient's mean arterial pressure is 108.33333 mm Hg."
1629,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7682977-1,Extracted,"On January 28, 2020, a 69-year-old man suffering for eight months from chronic kidney disease and liver cirrhosis caused by Hepatitis C was admitted for liver transplantation. Upon admission, his medical history was examined and a physical examination was performed, revealing a temperature of 37.1 ℃, respiratory rate of 17, pulse rate of 84, and blood pressure of 130/90 millimeter Hg. The patient was diagnosed with ascites. No other significant gastrointestinal or hepatic findings such as abdominal pain, vomiting, nausea, diarrhea, or jaundice were reported. The patient received cadaveric liver transplantation according to the transplantation protocols in our hospital. Next, he was transferred to the ICU for further care before the temporary shutdown of surgical wards due to the COVID-19 outbreak in Iran.
On day 2 following transplantation, the patient showed a mild fever followed by mild dyspnea, which improved after non-invasive ventilation. Chest radiographic findings revealed a bilateral diffuse infiltration. The laboratory results indicated a white cell count of 5.1 × 109 /L, aspartate transaminase of 122 U/L, hemoglobin of 6.6 gram/deciliter, platelet of 94,000, creatinine of 2.3 milligram/deciliter, alanine transaminase of 110 U/L, overall bilirubin of 4.2 milligram/deciliter, and direct bilirubin of 2.5 milligram/deciliter. Blood gas analysis showed a PaO2 of 47.4 mmHg, a PaO2/FiO2 of 225.7, and an O2 saturation of 85.5%.
On day 4, the patient became febrile, and bilateral opacities along with left lung pleural effusion were observed in chest radiography. Thus, he was diagnosed with nosocomial pneumonia. Imipenem, meropenem, cotrimoxazole, and colistin were initiated and pleural TAP was performed. The patient received Tacrolimus and methylprednisolone according to the liver transplantation protocols. The respiratory status of the patient worsened and respiratory failure developed. The patient received invasive ventilation treatment. On day 9, the patient experienced loss of consciousness and had a GCS of 8. On day 12, oxygen saturation dropped to 50%, and the patient was intubated accordingly. Blood cultures were taken, and septicemia with pseudomonas species sensitive to ciprofloxacin and levofloxacin was detected. As a result, on day 15, a radiologic study of the patient revealed bilateral multilobar diffused ground glass opacities, which expanded to more than 70% of lungs interstitium (). A CT scan of the patient’s brain was performed due to his lack of consciousness. The results showed a hypodensity in the right parietal lobe with gray and white matter involvement, suggesting an infarction of the middle cerebral artery, which could be due to acute or sub-acute brain infarction ().
Sixteen days after transplantation, upon the announcement by the Ministry of Health and Medical Education (MOHME) regarding the outbreak of COVID-19, the disease was considered as a source of pneumonia as well. On day 19, the patient experienced another episode of LOC followed by a drop in O2 saturation to 70% and tracheostomy. The patient received continuous renal replacement therapy (CRRT) due to BUN/Cr rise during the disease. The radiographic X-ray findings of the white lung also appeared on the nineteenth day along with sepsis and anuria, indicating the side effects of CRRT (; ). There was a decline in blood hemoglobin levels through the course of the disease, and the patient received pack cell transfusions accordingly.
His platelet levels also dropped from 93,000 on day 1 to 20,000 on day 23. The patient’s health condition deteriorated on day 22. On day 23 after transplantation, a central pulse could not be detected, the patient’s O2 saturation level fell, and he became asystolic. After 45 minutes of several resuscitation attempts, the patient’s condition did not improve and he expired. A day after our patient died, his COVID-19 PCR was reported positive.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 90.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
1630,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1416,Extracted,"A 42-year-old woman comes to the physician because of progressive weakness. She has noticed increasing difficulty performing household chores and walking her dog over the past month. Sometimes she feels too fatigued to cook dinner. She has noticed that she feels better after sleeping. She does not have chest pain, shortness of breath, or a history of recent illness. She has no personal history of serious illness and takes no medications. She has smoked two packs of cigarettes daily for 25 years. She appears fatigued. Her temperature is 37°C (98.8°F), pulse is 88/min, and blood pressure is 148/80 mm Hg. Pulse oximetry shows an oxygen saturation of 98% in room air. Bilateral expiratory wheezes are heard at both lung bases. Examination shows drooping of the upper eyelids. There is diminished motor strength in her upper extremities. Her sensation and reflexes are intact.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [148.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",102.66667,97.53334,107.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 148.0 mm Hg + 2/3 * 80.0 mm Hg = 102.66667 mm Hg.
Hence, the patient's mean arterial pressure is 102.66667 mm Hg."
1631,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7336650-1,Extracted,"On April 2, 2020, a 79-year-old female with a history of hypertension and IPF presented with cough, worsening dyspnea, increased oxygen requirements, fever and diarrhea. Her vital signs include a temperature of 100.4°F, a heart rate of 98 bpm, an oxygen saturation of 85% on room air and a blood pressure of 102/56 mmHg. She is usually on oxygen two liters per minute at home for chronic hypoxic respiratory failure from IPF. She was on nintedanib 100 mg twice daily for her IPF and metoprolol 12.5 mg daily for her hypertension. Her pulmonary function test done two years ago showed moderate restrictive lung disease with a forced vital capacity of two liters (77% predicted), total lung capacity of three liters (63% predicted) and diffusion capacity of 58% predicted. Her physical exam was unremarkable. She was placed on isolation precautions because of her clinical presentation and her test for SARS-CoV-2 came back positive (Roche’s Cobas nucleic acid amplification test). She was exposed to her husband who was recently diagnosed with COVID-19. She required three liters of supplemental oxygen for her hypoxemia. Chest radiology showed multifocal consolidations in both lungs (Figure ).
She received azithromycin and hydroxychloroquine as per the protocol. However, her condition deteriorated requiring 10 liters of supplemental oxygen and on day 3 she was transferred to intensive care unit and intubated for worsening hypoxic respiratory failure. She required 100% fractional concentration of oxygen in inspired gas (FiO2) and 10 cm H2O positive end-expiratory pressure (PEEP) on the ventilator. A limited bedside echocardiogram revealed normal left and right ventricular function. Her inflammatory markers continued to worsen. Ferritin which was 600 ng/mL at the time of her presentation, worsened to 50,480 ng/mL. Her white blood cell (WBC) count was 15,000/mm3 with an absolute lymphocyte count of 800/mm3, procalcitonin was 0.14 ng/mL, D-dimer was 3.3 µg/mL and lactate dehydrogenase (LDH) was 628 IU/L. She received a single intravenous dose of tocilizumab 600 mg. On day 4, she developed severe septic shock and multiorgan dysfunction (worsening renal function, liver function, circulatory collapse and respiratory failure) requiring norepinephrine, vasopressin, phenylephrine and angiotensin II. She was started on intravenous hydrocortisone 100 mg three times daily, but despite all the aggressive measures she died on day 5. We would like to mention that at the time of this patient's presentation, other treatments like convalescent plasma and remdesivir were not readily available.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [102.0, 'mm hg'], 'Diastolic Blood Pressure': [56.0, 'mm hg']}",71.33333,67.76666,74.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 102.0 mm Hg + 2/3 * 56.0 mm Hg = 71.33333 mm Hg.
Hence, the patient's mean arterial pressure is 71.33333 mm Hg."
1632,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4673761-4,Extracted,"A 55-year-old Chinese man was send to our hospital for lasting chest pain for 6 h and sudden cardiac arrest. His past medical history were remarkable for hypertension and diabetes for 3 years. He had a 30-years history of smoking. On admission, his blood pressure was 108/52 mmHg, respiratory rate was 30 breaths/min and his heart rate was 88 beats/min. The pupil diameter was 7 mm on both sides and the light pupillary reflex was disappeared. ECG showed that ST segment depression about 0.01 mV–0.02 mV in leads V4–V6 (Figure S4 showed in the Additional file ). The levels of cTnI, CK-MB and myohemoglobin on admission were 0.1 ng/ml, 1.8 ng/ml and 125 ng/ml respectively. He suffered recurred cardiac arrest in hospital. CAG showed that a MB in the middle segment of the LAD (Fig. ). He is doing well at 4 months of follow-up after cardiac arrest.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [108.0, 'mm hg'], 'Diastolic Blood Pressure': [52.0, 'mm hg']}",70.66667,67.13334,74.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 108.0 mm Hg + 2/3 * 52.0 mm Hg = 70.66667 mm Hg.
Hence, the patient's mean arterial pressure is 70.66667 mm Hg."
1633,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2872898-1,Extracted,"A 41-year-old man, 174 cm in height, weighing 72 kg, with American Society of Anesthesiologists (ASA) physical status I, was scheduled to under go right shoulder arthroscopy for rotator cuff repair under ISB. His prior medical history was unremarkable. He took no medication. A preoperative examination revealed there was equal air entry on both sides of his chest with no evidence of wheezing. All laboratory evaluations were within the normal limits, including electrocardiogram and chest roentgenogram (). He agreed to undergo regional anesthesia.
In the operating room, after applying routine monitors, his blood pressure, heart rate, respiratory rate and oxygen saturation was 130/80 mmHg, 70 beats/min, 16-18 breaths/min, and 99%, respectively. A right ISB was performed using the Borgeat's lateral modified approach. A nerve stimulator (Stimuplex®-DIG, B/Braun, Germany) connected to a 50 mm insulated Contiplex A needle and cannula (Contiplex® A, B/Braun, Germany) was used. After obtaining pectoralis major muscle twitching at a threshold of 0.5 mA, a 22-gauge catheter was inserted 5 cm through the cannula into the brachial sheath. Subsequently, 30 ml of 0.5% ropivacaine was injected slowly throgh the catheter. After continuous ISB, his vital signs were stable.
The patient was placed in a sitting ""beach chair"" position for surgery. Intraoperatively, he was sedated with sufentanil 10 µg and a propofol infusion at 50 µg/kg/min. Throughout the procedure, supplemental oxygen was given at 6 L/min through a mask. The operation and recovery room stay were uneventful and without complications.
After surgery, the patient was transported to the recovery room. The patient was pain free and comfortable. His blood pressure, heart rate, respiratory rate and oxygen saturation was 115/70 mmHg, 60 beats/min, 14 breaths/min, and 97%, respectively. 0.2% ropivacaine (Naropin®, AstraZeneca, Sweden) infusion was started in the recovery room through the interscalene catheter using a portable battery-powered pump (Accumate® 1,000, Wooyoung Medical, Korea) at a basal rate of 6 ml/h. The patient had the option of self administering a 3 ml bolus of 0.2% ropivacaine (with a 20-minute lock out time). The infusion was continued over the subsequent 2.5 days.
On the first postoperative day, the continuous ISB produced adequate analgesia (visual analogue scale, from 0-100 mm, was 40 mm), which avoided the need for additional analgesics. However, he reported mild chest discomfort. The chest x-ray revealed an elevation of the right hemidiaphragm, which was associated with basal atelectasis of the right lower lobe without pleural effusion (). The anesthetic team was not contacted.
On the second postoperative day, he reported moderate chest discomfort that was on right side that was increased by deep inspiration. He was afebrile, and his blood pressure, heart rate and respiratory rate was 110/80 mmHg, 70 beats/min, and 20 breaths/min, respecively. The physical cardiopulmonary examination was normal. The chest x-ray revealed an elevation of the right hemidiaphragm associated with basal atelectasis of the right lower lobe, and pleural effusion without pneumothorax (). The chest CT revealed the same findings. No signs of infection or other disorders were shown on the film. This pattern was suggestive of acquired phrenic nerve palsy. Arterial blood gas analysis was within the normal limits. The local anesthetic infusion was discontinued. Before discontinuing the local anesthetic, his pain was well controlled (visual analogue scale, from 0-100 mm, was 20 mm). There were no change in the vital signs after discontinuing the continuous ISB. Patients received oral lornoxicam 4 mg three times a day on a regular basis. Rescue analgesia with 60 mg of IM diclofenac was available on demand.
On the fourth postoperative day, his symptoms appeared to have improved but the chest x-ray showed no improvement. Although the right hemidiaphragm had returned to normal, the chest x-ray on the sixth postoperative day showed residual pleural effusion and atelectasis. He was discharged on the eighth postoperative day.
On the fifteenth postoperative day, the chest x-ray showed complete expansion of the collapsed right lower lobe ().",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1634,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-225,Extracted,"A 79-year-old woman comes to the physician for the evaluation of a 2-month history of a non-productive cough and fatigue. During this period, she also has had a 4.5-kg (10-lb) weight loss and has become increasingly short of breath with mild exertion. She has congestive heart failure and hypertension. Three months ago, she was in India for 3 weeks to attend a family wedding. She worked as a seamstress in a textile factory for 50 years. She has smoked one pack of cigarettes daily for 47 years. Her current medications include enalapril, digoxin, isosorbide, spironolactone, and metoprolol. She appears thin. Her temperature is 37.0°C (98.6°F), pulse is 90/min, respirations are 25/min, and blood pressure is 110/70 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 94%. There is dullness to percussion and decreased breath sounds over the right lung base. The remainder of the examination shows no abnormalities. Laboratory studies show a glucose level of 90 mg/dL, serum lactate dehydrogenase of 227 U/L, and serum protein of 6.3 g/dL. An x-ray of the chest shows nodular pleural lesions on the right side and a moderate-sized pleural effusion. Thoracentesis shows 250 ml of turbid fluid.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1635,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8404589-1,Extracted,"A 50-year-old male known smoker, smoking 7-8 cigarettes/day for the last 10 years presented with complaints of intermittent hemoptysis for last 2 years. He denied any history of low-grade fever, loss of appetite, night sweats, weight loss, chest pain, trauma, or breathlessness. There was no history of exposure to any drugs (antiplatelets, anticoagulants) or bleeding disorder. His sputum for acid-fast bacilli (AFB) was negative. Diagnostic evaluation for his symptom on the previous occasions at other hospitals was inconclusive with a normal reported chest X-ray and computed tomography (CT) scan exam. Fiberoptic bronchoscopy findings reported blood in right and left main bronchial system. Presently, his physical examination revealed a temperature of 37°C, pulse rate of 82/min, blood pressure of 142/84 mmHg, respiratory rate of 12/min, oxygen saturation of 98%, normal respiratory sounds, and a normal chest X-ray. Laboratory investigations revealed a normal blood value including normal platelet count and coagulation parameters. His transthoracic echocardiography revealed normal right and left ventricular functions without any evidence of mitral stenosis/right-sided infective endocarditis or pulmonary hypertension. High-resolution CT scan showed localized pocket of air density medial to bronchus intermedius on axial [] and coronal sections [] suggesting accessory cardiac bronchus. No lung tissue was associated with accessory cardiac bronchus. Subsequent fiberoptic bronchoscopy confirmed accessory cardiac bronchus originating medially from bronchus intermedius opposite to the right upper lobe bronchus, whose lumen was partially obscured by small a clot. Bronchial and pulmonary angiography revealed no abnormality in tracheobronchial tree or pulmonary drainage.
A right thoracotomy was performed and accessory cardiac bronchus was identified. ACB extended 3 cm toward pericardium without any associated lobule. It was resected with preservation of vagus nerve. Bronchus intermedius was closed in two layers. Subsequent pathological examination revealed a tubular structure ending blindly with cartilage rings, inflamed and ulcerated mucosa with the collection of neutrophils and fibrous tissue. Hemoptysis was attributed to this inflamed vascularized accessory cardiac bronchus. The patient is asymptomatic currently with no recurrent hemoptysis at 6-month follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [142.0, 'mm hg'], 'Diastolic Blood Pressure': [84.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 142.0 mm Hg + 2/3 * 84.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
1636,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6700539-1,Extracted,"A 78-year-old woman visited the emergency department with complaints of progressively worsening abdominal pain for a week. She began to feel nausea and to vomit at the visit. Her medical history included hypertension, dyslipidaemia and type 2 diabetes mellitus. At the time of presentation to the emergency department, her vital signs were as follows: blood pressure, 145/71 mm Hg; pulse rate, 90/min; respiratory rate, 24/min; oxygen saturation, 95% on room air and body temperature, 35.8°C. Her height was 142.0 cm; weight was 64.4 kg and her body mass index was 31.9 kg/m2. On physical examination, her abdomen was distended and bowel sounds were hypoactive. In addition, she had generalised abdominal tenderness with guarding.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [71.0, 'mm hg'], 'Systolic Blood Pressure': [145.0, 'mm hg']}",95.66667,90.88334,100.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 145.0 mm Hg + 2/3 * 71.0 mm Hg = 95.66667 mm Hg.
Hence, the patient's mean arterial pressure is 95.66667 mm Hg."
1637,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7955,Extracted,"A 33-year-old man is being evaluated for malaise and fatigability. He says that he hasn’t been able to perform at work, can’t exercise like before, and is constantly tired. He also says that his clothes have ‘become larger’ in the past few months. Past medical history is significant for gastroesophageal reflux disease, which is under control with lifestyle changes. His blood pressure is 110/70 mm Hg, the temperature is 37.0°C (98.6°F), the respiratory rate is 17/min, and the pulse is 82/min. On physical examination, an enlarged, painless, mobile, cervical lymph node is palpable. A complete blood count is performed.
Hemoglobin 9.0 g/dL
Hematocrit 37.7%
Leukocyte count 5,500/mm3
 Neutrophils 65%
 Lymphocytes 30%
 Monocytes 5%
Mean corpuscular volume 82.2 μm3
Platelet count 190,000 mm3
Erythrocyte sedimentation rate 35 mm/h
C-reactive protein 8 mg/dL
A biopsy of the lymph node is performed which reveals both multinucleated and bilobed cells. The patient is started on a regimen of drugs for his condition. Echocardiography is performed before treatment is started and shows normal ejection fraction, ventricle function, and wall motion. After 2 rounds of chemotherapy, another echocardiography is performed by protocol, but this time all heart chambers are enlarged, and the patient is suffering from severe exertion dyspnea.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1638,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7285,Extracted,"An 85-year-old man presents with the reappearance of his Parkinson’s disease (PD) symptoms over the last few months. He says he has been treated with various drugs over the last 20 years, but that currently his symptoms worsen as he nears the time for his next dose of medication. His movements have been slower lately and it’s difficult to initiate voluntary movements. His past medical history is significant for hypertension. He was diagnosed 10 years ago and was well-managed on medication. His current medications are levodopa/carbidopa, rasagiline, aspirin, and captopril. The vital signs include: pulse 70/min, respiratory rate 15/min, blood pressure 130/76 mm Hg, and temperature 36.7°C (98.1°F). Physical examination reveals the expected ‘pill-rolling’ resting tremor, which is alleviated by movement. Increased tone of arm muscles and resistance to passive movement at the joints is noted. When asked to walk across the room, he has difficulty taking the 1st step and has a stooped posture and takes short, shuffling, rapid steps. Laboratory studies show:
Serum glucose (fasting) 97 mg/dL
Sodium 141 mEq/L
Potassium 4.0 mEq/L
Chloride 100 mEq/L
Cholesterol (total) 190 mg/dL
HDL-cholesterol 42 mg/dL
LDL-cholesterol 70 mg/dL
Triglycerides 184 mg/dL
The patient is started on a drug that increases the efficacy of his current anti-PD medication.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [76.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",94,89.3,98.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 76.0 mm Hg = 94.0 mm Hg.
Hence, the patient's mean arterial pressure is 94.0 mm Hg."
1639,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2875706-1,Extracted,"A 35-year-old Nigerian female who is a petty trader and a primary school teacher, presented to us in the renal unit of the hospital in November 2003 with a-ten day history of inability to pass urine, and an eight day history of vomiting and hiccupping.
The patient, who is not a known hypertensive or diabetic, had been in apparently good health until fifteen days before presentation when she inserted herbal vaginal pessary on the advice of a herbalist, in an attempt to have a female child, as all her children so far had been males. Five days after the herbal vaginal pessary insertion, she became anuric and two days after, she started vomiting and hiccupping. She had remained anuric until the eight day on admission when she progressively started making urine. There was no history of ingestion of oral herbal preparation, no diarrhea, facial or leg swelling nor hematuria. She had no symptoms of renal disease in the past. Her husband is a commercial taxi driver. She neither drinks alcohol nor smoke cigarette; and no family history of renal disease.
Examination revealed a young lady who was actually ill looking in mild respiratory distress. She was pale, anicteric, and afebrile to touch. There was no peripheral edema. Her pulse rate was 78 beats per minute, blood pressure was 120/70 mmHg. Her apex beat was not displaced. Fundoscopy was unremarkable. There were also no remarkable findings in the chest and abdomen. She was conscious and alert and there was no asterexis.
Laboratory investigation revealed 2+ proteinuria, many red blood cells (she was menstruating at that time) on urine microscopy, and culture yielded no growth after 48 h of incubation. Packed cell volume was 19%, total white cell count 7900/mm3.
Retroviral screening test, hepatitis B surface antigen and hepatitis C viral antigen were all negative.
Renal ultrasonographic scan revealed normal renal sizes of 11.5 × 4.5 cm and 12.0 × 5.6 cm for the right and left kidneys respectively. There was increased echogenicity with marked reduction of the corticormedullary differentiation. The serial serum electrolyte, urea and creatinine values are as indicated in .
Her creatinine clearance was 20 ml/min; and her packed cell volume at last visit remained at 27%.
She was treated with an average dose of intravenous frusemide of 100 mg every 12 h until she started diuresing. Strict input and output fluid chart was observed. She had transfusion of 2 units of packed cells (post transfusion PCV = 27%) and was subsequently placed on hematenics. She required three sessions of hemodialysis until she started diuresing, and blood urea and creatinine levels dropped to an acceptable level as shown in . She was discharged home after thirty-three days on admission. When she was last seen in outpatient clinic on the 19th March 2004, she was clinically stable but her renal function test results, as shown in , still revealed elevated serum creatinine, and low creatinine clearance. Subsequently, she was lost to follow up. All attempts made to contact her using her residential address failed as she was said to have relocated elsewhere.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1640,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7822652-1,Extracted,"A 44-year-old gravida 6 para 4 postpartum woman presented to the emergency department (ED) complaining of substernal chest pain. That afternoon, she experienced sudden-onset severe left-sided chest pain radiating to her back and shoulder. She had been discharged four days prior after induction of labor for chronic hypertension with an uncomplicated vaginal birth. Her medical history was notable only for hypertension, for which she took metoprolol. She was maintained on metoprolol with good blood pressure control for the duration of her pregnancy and after induction. The day prior to admission she was under significant emotional distress after her infant was hospitalized with hyperbilirubinemia.
In the ED, the patient was afebrile, her blood pressure was 164/101 mm Hg, her heart rate was 60 beats per minute, and she was breathing 16 breaths per minute. Her cardiovascular examination was unremarkable with normal heart sounds with no murmurs, rubs, or gallops and no jugular venous distension. Her lungs were clear, her abdomen was soft, and she had no extremity edema. Her complete blood count and comprehensive metabolic panel results were within normal limits. Her initial troponin I was 0.41 ng/mL (reference range, <0.04 ng/mL), and her electrocardiogram (ECG) () was significant for ST elevation in leads V2-V5 consistent with an anterior ST-segment elevation myocardial infarction (STEMI). Her chest X-ray showed normal mediastinum, no signs of cardiomegaly, and clear lungs.
Given the concern for acute coronary syndrome (ACS), the patient was emergently taken to the cardiac catheterization lab. Her coronary angiogram showed haziness of the midleft anterior descending (LAD) artery followed by an abrupt change in arterial caliber extending to the distal LAD and diagonal branches (). There was no clear visualization of a dissection flap, but there was a visible long segment of diffuse vessel narrowing in the mid to distal LAD highly suspicious for coronary dissection. Contrast flow in the distal vessel was normal (TIMI 3), and there were no luminal changes with the administration of intracoronary nitroglycerin. There was no angiographic evidence of atherosclerotic disease in any of her coronary arteries, and no evidence of narrowing in the coronary arteries outside of the LAD. Her chest pain was resolved during the procedure, and her ECG showed normalization of her ST elevation. Given the patient's hemodynamic stability, normal blood flow in the distal LAD, resolution of chest pain, and suspicion for dissection, she was managed conservatively.
She was started on IV nitroglycerin for hypertension, metoprolol, and dual antiplatelet therapy with aspirin and clopidogrel and then transferred to the coronary care unit for close observation. Her transthoracic echocardiogram showed normal left ventricular function with an ejection fraction of 68% and hypokinetic septal and apical walls in the distribution of the LAD. Her repeat ECG () showed the expected evolution of her STEMI with QS waves and T-wave inversions seen in leads V2-V5. She was weaned off the nitroglycerin and transitioned to captopril and nifedipine for strict blood pressure control and safety with breastfeeding.
She remained chest-pain free during the course of the hospitalization and underwent a repeat angiogram to evaluate for the progression of disease given the diagnostic uncertainty. Her repeat angiogram on day 6 of hospitalization showed complete resolution of the LAD lesion () consistent with dissection. Compared to the initial angiogram, the area of haziness was no longer present, and the vessel tapered appropriately towards the apical LAD. However, a new tubular narrowing with abrupt vessel caliber change () was noted in the midposterior descending artery (PDA), compared to her initial angiogram () with normal flow and no clear dissection flap. This event was concerning for a new dissection event. The patient was asymptomatic throughout her hospitalization and was discharged home with close obstetric, primary care, and cardiology outpatient follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [164.0, 'mm hg'], 'Diastolic Blood Pressure': [101.0, 'mm hg']}",122,115.9,128.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 164.0 mm Hg + 2/3 * 101.0 mm Hg = 122.0 mm Hg.
Hence, the patient's mean arterial pressure is 122.0 mm Hg."
1641,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6797008-1,Extracted,"Our patient was a 33-year-old male who presented with a five-day history of fever, generalized body aches, sore throat, odynophagia, nausea, vomiting, dizziness, and diffuse abdominal pain. Past medical history was significant for gastroesophageal reflux and recurrent episodes of tonsillitis, for which the patient was scheduled for a tonsillectomy.
Upon arrival to the emergency center, he was found to have a blood pressure of 144/102 mm/Hg, heart rate of 110 BPM, fever of 39 C, and a WBC count of 5,400/mm3. On physical exam, tonsils were significantly enlarged (graded 4+ on a scale of zero to four) and erythematous, and he was noted to have enlargement of his left peritonsillar area concerning for an abscess, while the remainder of the physical exam was unremarkable. A Monospot test obtained in the emergency department was positive, indicating a primary infection with infectious mononucleosis. Due to the patient’s history of recurrent tonsillitis, fever, and asymmetric tonsillar hypertrophy, a CT scan of the neck with IV contrast was also ordered. This resulted in an incidental finding of a large avidly enhancing mass within the left carotid sheath that extended from the level of the hyoid to the jugular foramen at the skull base, in addition to prominent pharyngeal and adenoidal tonsils, with bilaterally enlarged cervical chain and submental lymph nodes (Figures , ). Based on its location and characterization, this mass was deemed likely to be a carotid body paraganglioma, but required further investigation with a neck MRI and magnetic resonance angiography (MRA) per radiology recommendations. Plasma and urine catecholamines and metanephrines were also ordered, which were within normal limits.
An MRI of the neck with and without IV gadolinium re-demonstrated the enhancing left neck mass measuring 5 x 5 x 2 cm most consistent with a paraganglioma. A magnetic resonance angiography of the carotid arteries and neck vascularity re-demonstrated this left neck mass, and the mass was shown to displace the left internal and external carotid arteries without any luminal narrowing. There was extensive vascularity of the mass, being fed by multiple branches of the external carotid artery (Figure ).
After admission and treatment, the patient was discharged home and instructed to follow up outpatient with both ENT and neurosurgery to discuss medical and surgical options for removal of the paraganglioma.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [144.0, 'mm hg'], 'Diastolic Blood Pressure': [102.0, 'mm hg']}",116,110.2,121.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 144.0 mm Hg + 2/3 * 102.0 mm Hg = 116.0 mm Hg.
Hence, the patient's mean arterial pressure is 116.0 mm Hg."
1642,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6023843-1,Extracted,"A 96-year-old woman was admitted to our hospital due to a 7-day history of fever over 39°C and 2 episodes of vomiting. By the time of admission, she had had abdominal pain, nausea, and lack of appetite for over a month. The family called an emergency ambulance but twice did not allow the patient to be taken to hospital. Because of her deteriorating condition, which was showing no improvement with oral amoxicillin with clavulanic acid 3 times a day (0.625 g), she was referred to our department to improve her poor condition. She had undergone appendectomy in her forties and hip bone fracture in 2013. She had not been administered any drugs so far.
Clinical examination revealed full mental conscious, dehydration, pulse rate of 90 beats/min, blood pressure 120/70 mm Hg, a body temperature of 39.5°C, left-side alignment of the alveolar murmur at the base of the left lung, local tenderness in the right upper abdomen without muscular defense. Her initial laboratory measurements showed a white blood cell (WBC) count of 17.77 × 109/L (norm: 4 × 109–10 × 109/L), with 86.8% neutrophils, hemoglobin at 6.80 mmol/L (norm: 7.45–10.00 mmol/L), erythrocyte sedimentation rate (ESR) was 86 mm (norm: 3–15 mm), and C-reactive protein level was 177.00 mg/L (norm: 0.00–5.00 mg/L). AUS showed gallbladder enlargement with stones and widening of the common bile duct (CBD) to 16 mm. The patient was consulted by the surgeon who, due to the high risk of mortality, decided to carry out intravenous antimicrobial therapy with ciprofloxacin 2 times a day with a dose of 0.4 g, metronidazole 2 times a day with a dose of 0.5 g, intravenous rehydration and alimentation, and spasmolytic drugs. We observed a mild improvement in the patient's condition with a decrease of body temperature to 36.8°C. Unexpectedly, 10 days after admission, we observed aggravation of the abdominal pain and fever recurrence up to 39.9°C, with an increase in serum and urine amylase to 257 U/L (norm: 25–115 U/L) and 418 U/L (norm: 30–200 U/L), respectively. CT of the abdomen revealed gallbladder stones with a widening of the CBD to 13 mm and widening of the Virsung duct to 8 mm, as well as some small pancreatic cysts with a pancreas tumor of 38 mm in diameter. CT also revealed aneurysm of the abdominal aorta, left suprarenal tumor, and esophagus hernia that had not been previously diagnosed. Abdominal MRI confirmed calculous cholecystitis and pancreatitis, probably with inflammatory tumor of the pancreas. After multidisciplinary consultation, we decided to treat the patient with meropenem intravenously three times a day at a dose of 1.0 g. The patient did not consent to undergo surgery. Over the next few days, the patient's health significantly improved, and after three weeks of hospitalization she was discharged home, with neither fever nor abdominal pain. She received restricted dietary recommendations. After discharge, the patient further gradually regained her physical health and returned to the condition she had presented before the disease. Four months after hospitalization, her laboratory tests showed a WBC count of 6.09 × 109/L, with 72.5% neutrophils, hemoglobin at 7.70 mmol/L, ESR of 38 mm, and C-reactive protein level at 1.03 mg/L. The patient was administrated pancreatic enzymes twice a day at a dose of 10,000 units before meals. Her blood pressure was well-controlled and she has had no recurrence of the fever or abdominal pain.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1643,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6671876-1,Extracted,"A 73-year-old female patient, previously diagnosed with hypertension, dyslipidemia, and pulmonary emphysema, sought medical assistance complaining of weight loss of 5 kg during the last 2 months. She referred back and abdominal pain, mainly in the hypogastrium and left iliac fossa, which worsened until the day of hospital arrival. She referred episodes of melena during the last 2 weeks and one episode of enterorrhagia. More recently, she noted chills and fever of 38 °C. Nausea, vomiting, and loss of appetite were added to this clinical picture. She was taking regularly enalapril, hydrochlorothiazide, and simvastatin. She was a heavy smoker. She underwent a gastrectomy with Bilroth II reconstruction 10 years ago as she had been diagnosed with a peptic ulcer. Six years ago she was submitted to an infra renal aortic aneurysm angioplasty with a Dacron aorto bifemoral graft for correction of an abdominal aortic aneurysm.
Physical examination showed an ill-looking patient, pale, and emaciated. Her blood pressure was 110/70 mmHg; pulse rate was irregular = 90 beats per minute; respiratory rate = 20 respiratory movements per minute; and she was afebrile. The heart examination showed arrhythmic cardiac sounds with a systolic murmur; the abdomen was flat, flaccid, but painful on hypogastrium and left iliac fossa palpation. Tenderness was evident on percussion of the left dorsal region. Abdominal sounds were normal, and no signs of peritonitis were detected. Digital rectal examination and anuscopy were normal, and upper gastrointestinal endoscopy ruled out any source of bleeding until the second duodenal portion. The initial laboratory workup is shown in .
The abdominal ultrasound revealed the presence of patent aortoiliac bifemoral prosthesis, but no abnormalities were detected on the remaining accessible regions. The computed tomography scan of the abdomen revealed a tortuous and atheromatous aorta, slightly dilated in the thoracoabdominal transition.
An infrarenal endoprosthesis in aorto-bifemoral position was patent, without evidence of contrast leakage, but some tiny images associated with gas and enhancement of surround soft tissue and diffuse blurring of adipose plans around the infrarenal aortic portion were observed, suggesting graft infection ( and ).
Splanchnic arteries were patent and the inferior vena cava showed normal caliber and contours. Lymphadenomegaly was evident in the great vessels chain ().
With the hypothesis of infection of the aortic graft, vancomycin and piperacillin/tazobactan (Tazocin) were prescribed. Surgical treatment consisted in right axillobifemoral bypass with Dacron graft, followed by explant of the infected aortobifemoral graft and ligature of the infrarenal aorta. Surgery was long, eventful, required blood transfusion and the use of vasoactive drugs for hemodynamic stabilization after the infection site manipulation. No aortic or graft enteric fistulas was evidenced during surgery. Culture of the purulent secretion collected from the infection site resulted negative for aerobic bacteria.
The patient died after 4 hours of post operatory due to septic shock.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1644,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8920,Extracted,"A 4-year-old boy is brought to the emergency department with difficulty breathing. His mother reports that he developed a fever last night and began to have trouble breathing this morning. The boy was born at 39 weeks gestation via spontaneous vaginal delivery. He is unvaccinated (conscientious objection by the family) and is meeting all developmental milestones. At the hospital, his vitals are temperature 39.8°C (103.6°F), pulse 122/min, respiration rate 33/min, blood pressure 110/66 mm Hg, and SpO2 93% on room air. On physical examination, he appears ill with his neck hyperextended and chin protruding. His voice is muffled and is drooling. The pediatrician explains that there is one particular bacteria that commonly causes these symptoms.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [66.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",80.66667,76.63334,84.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 66.0 mm Hg = 80.66667 mm Hg.
Hence, the patient's mean arterial pressure is 80.66667 mm Hg."
1645,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6432830-1,Extracted,"A 22-year-old man presented to our Emergency Department with cough, haemoptysis and fever of 3 days’ duration. A teratoma had been diagnosed 2 years previously after a routine chest x-ray and chest CT. At admission, the patient’s tympanic temperature was 37.8ºC, he was tachycardic (116 beats per minute, rhythmic), eupnoeic and his blood pressure was 95/55 mm Hg. Chest examination including pulmonary auscultation, was unremarkable. Laboratory tests showed normocytic normochromic anaemia (haemoglobin 12 g/dl, mean cell volume 82 fl, mean corpuscular haemoglobin 2.05 fmol/cell), neutrophilic leucocytosis (WBC 12.4 109/l, neutrophils 81.6%) and an increased C-reactive protein (8.93 mg/dl). Renal function, liver transaminases, lactate dehydrogenase and coagulation were within the normal reference ranges. The chest x-ray revealed homogeneous hypotransparency in the left lung field () and a chest CT scan () performed afterwards documented a marked increase in the lesion compared with evaluation in the previous year, measuring 8.7×8.7×12.1 cm.
The mass was heterogeneous with extensive lipomatous content and foci of calcium density surrounded by a cystic component. The lesion was compatible with a teratoma of the anterior mediastinum.
An adjacent post-obstructive pneumonitis and signs compatible with bilateral alveolar haemorrhage were also evident, suggesting that the tumour had ruptured. The patient was started on antibiotic treatment with amoxicillin plus clavulanic acid and azithromycin. The blood cultures and pneumococcal and legionella urinary antigen tests were all negative. A good clinical and laboratory response to antibiotic therapy was observed.
After a multidisciplinary discussion, it was decided to submit the patient to an exploratory thoracotomy. A median sternotomy showed almost completely upper left lobe invasion (). Therefore, a left upper lobectomy was performed. The pathological examination revealed a mature, partially cystic teratoma () with bronchial erosion and aspects of organizing pneumonia in the non-tumour lung parenchyma. The post-operative phase was uneventful and the patient was discharged from hospital 8 days after surgery. The patient remains asymptomatic at 1 year of follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [95.0, 'mm hg'], 'Diastolic Blood Pressure': [55.0, 'mm hg']}",68.33333,64.91666,71.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 95.0 mm Hg + 2/3 * 55.0 mm Hg = 68.33333 mm Hg.
Hence, the patient's mean arterial pressure is 68.33333 mm Hg."
1646,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4502316-1,Extracted,"A 65-year-old female with type 2 diabetes mellitus, coronary artery disease, peripheral arterial disease, and a prior episode of pancreatitis presented with abdominal pain, nausea, and vomiting for 8 hours prior to admission. The abdominal pain was diffuse, cramping, and unrelenting 10 out of 10 severity. She stated that the pain was similar to pain of her prior pancreatitis of unknown etiology 18 months earlier. She had one episode of mild diarrhea with no fever, shakes, or chills prior to admission. Initial exam demonstrated normal vital signs, diffuse abdominal pain to palpation without rebounding our guarding, and negative Murphy's sign. Laboratory evaluation demonstrated lipase 754 U/L (normal level 0–160 U/L), AST 128 IU/L (normal level 0–56 IU/L), ALT 72 IU/L (normal level 7–56 IU/L), and normal complete blood count (CBC) and basic metabolic panel (BMP). Abdominal ultrasound demonstrated no cholecystitis or cholelithiasis and a normal diameter of intrahepatic and extrahepatic bile ducts. Computed tomography (CT) of the abdomen with contrast demonstrated a mild fatty infiltrate of the liver and no gallstone, splenomegaly, or pancreatitis. Pancreatitis was diagnosed, based upon the lipase and abdominal pain, accordant with practice guidelines by the American College of Gastroenterology []. Initial treatment consisted of bowel rest, intravenous fluids, and analgesics.
Over the next 36 hours she showed little improvement, developed red tinged urine, and became anemic, and evaluation revealed hemolysis. Hemoglobin declined from 13 to 8.1 g/dL, lactate dehydrogenase was found to be 5290 IU/L (normal level 140 to 280 IU/L), haptoglobin was less than 10 mg/dL (normal level 45 to 165 mg/dL), and fibrinogen and INR were normal. Peripheral smear demonstrated microspherocytes and vacuolated neutrophils with no evidence of schistocytes. Coombs test was negative. White blood cell count increased to 24 K/μL (normal level 4.5 to 10 K/μL) and creatinine increased from 1.0 mg/dL to 2.0 mg/dL. She became hemodynamically unstable with pulse 130 beats per minute, blood pressure 105/50 mmHg, and temperature 103.5 F. Additional testing demonstrated venous lactate 46 mEq/L (normal level 0.5–2.2 mEq/L), ALT 407 IU/L (normal level 7–56 IU/L), AST 1200 IU/L (normal level 0–56 IU/L), ALP 300 IU/L (normal level 44 to 147 IU/L), and total bilirubin 9.6 mg/dL (normal level 0.3 to 1.9 mg/dL). Urine analysis demonstrated 4+ blood on the dipstick with few red blood cells on microscopy. The constellation of hemolysis with sepsis raised the clinical suspicion for C. perfringens infection and she was started on high dose Penicillin G 12 million units daily and Clindamycin 900 mg every 8 hours. Hyperbaric oxygen therapy was unavailable. Repeat CT abdomen/pelvis without contrast demonstrated hepatic abscesses ().
Percutaneous drains were placed in her hepatic abscesses and gallbladder. Blood cultures drawn prior to antibiotic therapy grew Clostridium perfringens. She received 21 days of antibiotics in the hospital and was discharged home and completed 39 more days of high dose Penicillin G. She required a prolonged antibiotic course because repeat CT imaging demonstrated continued hepatic abscesses.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [50.0, 'mm hg'], 'Systolic Blood Pressure': [105.0, 'mm hg']}",68.33333,64.91666,71.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 105.0 mm Hg + 2/3 * 50.0 mm Hg = 68.33333 mm Hg.
Hence, the patient's mean arterial pressure is 68.33333 mm Hg."
1647,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5952952-1,Extracted,"A 54-year-old man, with no significant past medical or surgical history and no recent travel, presented to the emergency room with a 24-h history of nausea, vomiting, diarrhea and abdominal pain. The patient denied any ingestion of fish, contaminated food or water. He had generalized skin flushing and his vital signs were as follow: blood pressure 60/39 mmHg, heart rate 131/min and temperature 37,8°C. Aggressive fluid resuscitation and intravenous ciprofloxacin and metronidazole were initiated.
Blood tests’ results were as follow: white blood count 18.9 × 109/L, neutrophils 17,63 × 109/L, hemoglobin 162 g/L, platelets 120 × 109/L, creatinine 445μmol/L and an estimated glomerular filtration rate (GFR) of 12 mL/min. The venous blood gas (VBG) displayed metabolic acidosis with a pH of 7,29.
A non-injected computed tomography (CT) scan of the abdomen and pelvis showed a thickened terminal ileum and a distended appendix reaching 13 mm, with mild stranding of the surrounding fat.
Hemodynamic instability and a suspected intra-abdominal source warranted surgical exploration. Turbid fluid retrieved from the right lower quadrant (RLQ) was sent for Gram stain and culture. A 1 cm necrotic zone was noted at the base of the appendix, without any other significant signs of appendicular or ileal inflammation. Appendectomy and peritoneal lavage were performed.
As these findings were deemed insufficient to explain the severity of the patient’s presentation, intraoperative short colonoscopy and transesophageal echocardiography were performed. Both were normal. The patient was then admitted to the intensive care unit (ICU) where support with vasopressors continued for 2 days. He developed disseminated intravascular coagulation (DIC). After 7 days of empirical intravenous treatment with ciprofloxacin and metronidazole, the patient received an additional 7 days course of oral amoxicillin/clavulanic acid. The flushing syndrome persisted for 6 days. The patient left the ICU after 6 days, and recovered uneventfully before being discharged on postoperative Day 10.
Blood drawn at arrival and liquid from intraoperative RLQ fluid were analyzed using the MALDI-TOF MS technique (Matrix-Assisted Laser Desorption/Ionization Time-of-Flight Mass Spectroscopy). Results indicated the presence of R. ornithinolytica, which was multisensitive, notably to ciprofloxacin and amoxicillin/clavulanic.
Pathological analysis of the appendectomy specimen showed acute inflammation of the appendicular muscularis, with no inflammation of the mucosa. No perforation was objectified. Periappendicular inflammation of the fatty tissue was also noted.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [60.0, 'mm hg'], 'Diastolic Blood Pressure': [39.0, 'mm hg']}",46,43.7,48.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 60.0 mm Hg + 2/3 * 39.0 mm Hg = 46.0 mm Hg.
Hence, the patient's mean arterial pressure is 46.0 mm Hg."
1648,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3274659-1,Extracted,"A 11-year-old Korean male was admitted to the outpatient department with sudden onset dysarthria, tongue fasciculations, and right-sided tongue weakness upon awakening ().
His medical history included a normal spontaneous vaginal delivery at 39 weeks with a birth weight of 3,200 g. He had normal developmental milestones, his medical history was unremarkable, and his family history was non-specific. His vaccination history was complete. He had no recent history of upper respiratory track infection and had no snoring at night. There was no history of surgery or trauma.
Upon initial physical examination, his body temperature was 36.2℃, heart rate 72 beats/min and blood pressure 120/70 mm Hg. The neurological examination revealed right-sided deviation of his tongue upon protrusion, but cranial nerve function, cerebellar function and upper motor neuron function were non-specific; otherwise, physical exam findings were non-specific. A laboratory investigation, neck computed tomography (CT), brain magnetic resonance imaging (MRI) and otorhinolaryngology consultation were done. Laboratory evaluations revealed: hemoglobin 13.1 g/dL, hematocrit 37.5%, white blood cell 9,300/mm3, platelets 382,000/mm3, peripheral blood smear non-specific, sodium 139.1 mmol/L, potassium 3.9 mmol/L, GOT/GPT 27/23 IU/L and blood urea nitrogen/creatinine 10.1/0.6. Epstein-Bare virus (EBV) viral capsid antigen (VCA) immunoglobulin (Ig) M negative, Epstein-Barr virus nuclear antigen positive, EBV VCA IgG positive, Cytomegalovirus (CMV) IgM negative, CMV IgG negative.
Neck MRI () and brain MRI () findings were normal. The otorhinolaryngology consultation disclosed non-specific anatomical problems and no evidence of inflammation.
The working diagnosis was that of idiopathic isolated HNP. The patient was treated with Solumedrol (60 mg/day #3) for 12 days. Fifteen days after symptom onset, the patient completely recovered ().",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [120.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1649,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7561,Extracted,"A 74-year-old man presents to the emergency department by paramedics for slurred speech and weakness in the left arm and leg for 1 hour. The patient was playing with his grandson when the symptoms started and his wife immediately called an ambulance. There is no history of head trauma or recent surgery. The patient takes captopril for hypertension. The vital signs include: pulse 110/min, respiratory rate 22/min, and blood pressure 200/105 mm Hg. The physical examination shows that the patient is alert and conscious, but speech is impaired. Muscle strength is 0/5 in the left arm and leg and 5/5 in the right arm and leg. A non-contrast CT of the head shows no evidence of intracranial bleeding.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [200.0, 'mm hg'], 'Diastolic Blood Pressure': [105.0, 'mm hg']}",136.66667,129.83334,143.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 200.0 mm Hg + 2/3 * 105.0 mm Hg = 136.66667 mm Hg.
Hence, the patient's mean arterial pressure is 136.66667 mm Hg."
1650,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-2907,Extracted,"Two hours after undergoing open cholecystectomy for complicated cholecystitis, a 48-year-old woman develops dizziness, lethargy, abdominal pain, and nausea. She has systemic lupus erythematosus and hypertension. Prior to hospitalization, her medications included nifedipine and prednisolone. Her pulse is 112/min and blood pressure is 90/64 mm Hg. Examination shows central obesity. The abdomen is soft and non-tender, and the laparoscopic incisions have no discharge. Her serum cortisol and serum ACTH are decreased.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [64.0, 'mm hg'], 'Systolic Blood Pressure': [90.0, 'mm hg']}",72.66667,69.03334,76.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 64.0 mm Hg = 72.66667 mm Hg.
Hence, the patient's mean arterial pressure is 72.66667 mm Hg."
1651,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6035394-2,Extracted,"A 32-year-old woman of Fulani origin in the Northern region of Cameroon presented to our surgical ward with a 5-day history of a painful right submandibular swelling with involvement of the right side of her neck and upper anterior chest wall. There was associated right upper quadrant abdominal pain. These symptoms were preceded by 1-week history of right second and third mandibular teeth infection which was left untreated. She was newly diagnosed with retroviral infection but yet to commence highly active antiretroviral treatment (HAART) before admission. She had right submandibular fluctuant and tender swelling, which was warm to palpation. Further physical and neurological examinations were unremarkable. She had tachypnea 32 breaths/minute, tachycardia 140 beats/minute, fever 38.5 °C, and blood pressure 120/70 mmHg. An ultrasound scan of the submandibular and neck swelling showed right submandibular turbid collection with inflamed muscles. A chest radiograph revealed blunting of the right costophrenic angle. Thoracocentesis revealed a pleural fluid analysis of marked leukocytosis 57,000 cells/ul, predominantly Gram-positive cocci.
She was urgently transferred to our OR where she underwent surgical drainage of the right submandibular abscess and right CTTD connected to pleurovac and suction; she was then admitted to our ICU while sedated, ventilated on oxygen by facemask, hemodynamically stable, and febrile (38.7 °C). A laboratory test was notable for extensive leukocytosis (17,000 cells/ul). Immediately on ICU admission broad-spectrum parenteral antibiotic therapy (intravenously administered ceftriaxone 1 gm 12 hourly and intravenously administered metronidazole 500 mg 8 hourly) was initiated. On the following day, she underwent extensive washout of abscess spaces of the submandibular region and neck. The culture of the submandibular abscess isolated viridans streptococci after 72 hours and the bacteria of the isolated growth were susceptible to Augmentin and doxycycline. Figure is a pre-incision and drainage photograph of this patient showing right submandibular abscess. Figure is a plain chest radiograph and computed tomography (CT) slides showing the left thoracic empyema. Her postoperative period was essentially unremarkable with our patient showing significant relief of symptoms. On the fifth day of admission she developed sudden onset of cardiac arrest from which she could not be resuscitated and was certified dead approximately 1 hour later.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [120.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1652,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5735602-1,Extracted,"The case is a 59-year-old Hispanic female born in Mexico with a medical history of insulin-dependent type 2 diabetes and rheumatoid arthritis on methotrexate, abatacept, and prednisone. Her prednisone dose was increased because of corneal transplant two days prior to admission. The patient was seen in the emergency department multiple times over the preceding month for abdominal pain, diarrhea, and vomiting and was treated with ciprofloxacin and metronidazole a week prior. She presented with lethargy, temperature 102°F, heart rate 121 bpm, and blood pressure 102/80 mmHg. Her Glasgow Coma Scale (GCS) score was 15/15, and meningeal signs were absent. The blood leukocyte count was 16,600 cells/mcL, serum sodium was 121 mmol/L, potassium was 3.4 mmol/L, chloride was 89 mmol/L, CO2 was 10 mmol/L, and blood sugar was 222 mg/dl. Arterial blood gas analysis showed triple acid-base disturbance with high anion gap metabolic acidosis, metabolic alkalosis, and respiratory alkalosis (pH 7.35, pCO2 13, and HCO3 7.1). Urine showed large ketones. CT scan of the abdomen showed possible colitis with thickening of the colon. She was started on insulin protocol after supplementing potassium. She was started on vancomycin 1.25 g every 12 hours (q12 hr) and piperacillin-tazobactam (PTZ) 3.37 g every 6 hours (q6 hr). Immunosuppressive agents were put on hold. She became more acidotic and tachypneic requiring intubation to prevent respiratory fatigue. On day 2 (D2), blood cultures grew Gram-negative bacilli (GNB). Suspicion of strongyloidiasis was high in the setting of Gram-negative bacteremia and a recent history of persistent GI symptoms in a patient from an endemic region. Single dose of ivermectin 200 micrograms/kg was given empirically. On D3, stool and sputum microscopy reported larvae of Strongyloides spp. GNB from blood culture was identified as E. coli, which was sensitive to cefazolin and piperacillin-tazobactam (PTZ) (). Hence, PTZ was continued.
She improved clinically, remained afebrile, and got extubated on D4, was started on oral diet on D5, and was moved out of ICU to regular floor on D6. Serology for Strongyloides was reported to be positive for immunoglobulin (Ig) A. On day 7, PTZ was switched with cephalexin 500 mg q6 hr. Early the next morning, she was found to have rapidly worsening mental status and was reintubated. Cephalexin was switched with cefepime 2 g q8 hr and ampicillin 2 g q4 hr. Lumbar puncture (LP) was done, and CSF showed GNB, WBC 330 cells/mcL with 98% granulocytes and 2% monocytes, RBC 250 cells/mcL, glucose less than 10 mg/dl, and protein 458 mg/dl. Ampicillin was stopped. Repeat stool microscopy remained positive for Strongyloides spp. Ivermectin dose was increased to 400 mcg/kg daily in 40% ethanol to increase absorption, and albendazole 400 mg q12 hr was also added. On D10, CSF culture reported E. coli resistant to PTZ and cefazolin but sensitive to ceftriaxone (CTX) (). Identification and sensitivity were done by using the MicroScan WalkAway 40 SI system with Negative combo 44 panels. Cefepime was continued. Her mental status did not improve, and the electroencephalogram was reported to be consistent with vegetative state with cerebral dysfunction. Repeat LP after 2 weeks showed WBC 82 cells/mcL with granulocytes 53%, lymphocytes, 46%, and monocytes 1%, RBC 9 cells/mcL, glucose 51 mg/dl, total protein 81 mg/dl, and LDH 192, and Gram staining and culture were negative. Repeated stool exams were negative for larvae. The patient received 14 days of ivermectin and 7 days of albendazole. She did not improve and underwent palliative extubation on D19 and died 10 days later.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [102.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",87.33333,82.96666,91.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 102.0 mm Hg + 2/3 * 80.0 mm Hg = 87.33333 mm Hg.
Hence, the patient's mean arterial pressure is 87.33333 mm Hg."
1653,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4946959-1,Extracted,"A 58-year-old normotensive, non-diabetic, nonsmoker male farmer was brought to the Emergency Department of SMHS hospital, Srinagar, by his wife with a three-day history dysmasesis (difficulty in chewing) followed by severe stiffness of jaw. It was gradual in onset and progressive. This was followed by stiffness in the upper and lower limbs. The patient could not flex his limbs due to stiffness. The patient was not able to walk due to stiffness in the lower limbs and gradually felt stiffness in the whole body over a period of three days. There was a two-day history of occasional painful spasms in the upper and lower limbs. Also, there was a history of several episodes of profuse sweating.
There was a history of trauma to the right hand (palm), which the patient sustained while working in fields about 20 days earlier; unfortunately, he neglected the wound and did not apply any dressing over the wound. No history of any visual impairment, doubling of vision, any inward or outward deviation of the eyes, any facial asymmetry, deviation of the angle of the mouth, drooling of saliva, or hearing impairment was present. The patient’s history was also negative for any difficulty in swallowing, nasal twang of voice, nasal regurgitation, difficulty in breathing, muscle twitching, paresthesias, numbness of any part of the body, inability to feel hot or cold, bladder and bowel involvement, any rash, oral ulcers, joint pains, any swelling/redness/tenderness of the joints, or photosensitivity.
On examination, the patient was conscious and oriented to time, place, and person. Pulse rate was 88 beats per minute and it was regular. The patient’s blood pressure was recorded as 120/80 mmHg, the temperature was 98˚F (axillary), and respiratory rate was 16 breaths per min. There was no pallor, icterus, cyanosis, or edema. The jugular venous pressure was not raised, and there was no thyromegaly. Risus sardonicus was present as shown in Figure . Informed patient consent was obtained for treatment.
Cardiorespiratory findings were insignificant for any abnormality. However, on abdominal examination, board-like rigidity was felt and the recti abdominis were palpable, but no organomegaly or ascites was found.
On central nervous system examination, higher mental functions were normal, speech was normal, MMSE score was 26/26, and muscle bulk was normal (equal bilaterally). Both the upper and lower limb spasticity was Grade 4. Opisthotonus was present as seen in Figure . Strength could not be assessed due to generalized spasticity. Deep tendon reflexes were exaggerated (3+). Babiniski’s sign was positive. There were no cerebellar signs. Spine examination was normal. Sensory examination was also normal.
All the biochemical parameters, including complete blood count, renal function tests, and liver function tests, were normal at the time of presentation. Arterial blood gas analysis was also normal. Serum Ca2+ and PO4+ levels were normal. Routine urine examination was normal. Creatine phosphokinase levels were within normal limits. Blood and wound culture specimens were sent at the time of admission, but results were not received until a week after starting the treatment; the results were positive for the growth of rod-shaped, gram-positive Clostridium tetani. Chest x-ray and ECG were normal. Magnetic resonance imaging (MRI) of the brain was normal. Serum anti-tetanus immunoglobulin (IgG antibodies) were low at 0.04 IU/L, and the immunization history was not remembered by the patient or his attendant.
The patient was managed as a case of tetanus on high clinical suspicion. Our management modalities included nasogastric tube feeding, antiseptic dressing, and injection of human anti-tetanus globulin (3,000 units) intramuscular stat and injection tetanus toxoid intramuscular stat. The patient was then put on all of the following medications for seven days: injections of Metrogel (metronidazole), 500 mg intravenous q.i.d., diazepam tablets, 10 mg q.i.d., injections of heparin, 5,000 units subcutaneous b.i.d., and Liofen xl (Baclofen) tablets, 5 mg t.i.d. for two days, 10 mg t.i.d. for two days, 15 mg t.i.d. for 2 days, and 20 mg t.i.d. on the last day of hospitalization.
Within a week, the patient showed marked improvement, the dysmasesis, trismus, and stiffness improved significantly, and he was able to continue his daily activities without any help. The patient was discharged to follow-up in the Neurology OPD at our hospital. On discharge, diazepam, 10 mg tablets t.i.d., and Liofen xl (Baclofen), 20 mg tablets b.i.d. were prescribed for one week.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1654,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3504246-1,Extracted,"A 61-year-old African American female was found unconscious on the road after a suspected pedestrian versus motor vehicle accident. The patient was supposedly walking alongside a busy 4 lane road in the early evening time, when she was struck by a driver. EMS was notified by pedestrians, and she was found in the street unconscious at the time they arrived. There were no witnesses to the accident which came forward to aid police or medical professionals at the scene, and the vehicle involved in the incident fled. Specific details regarding the injury itself are unknown. The patient was intubated by EMS in the field and was brought to the local trauma center.
At the time of presentation to the ED, the blood pressure was 64/50 (posttransfusion and placement of pelvic binder; BP reached 150/110), heart rate of 119, and respiratory rate of 22. The abdomen was soft, nontender and nondistended. No signs of rigidity or acute abdominal trauma were seen at this time. There was an open left lower leg fracture medially with an approximately 15 × 8 cm open wound with “venous oozing.” GCS of 7 quickly deteriorated to GCS of 3. Rectal exam revealed “no” tone. There was no gross blood noted per rectum, but the patient is guaiac positive. There was no vaginal blood or blood in the urethral meatus; however, later the patient was found to have gross bright red blood draining from the catheter.
Hemodynamic instability upon arrival was apparent, and resuscitation through advanced life support (ATLS) protocol was quickly initiated shortly after arrival to the ED. IV fluids and trauma blood were given; 18 units of packed red blood cells, 11 units of FFP, and 1 unit of trauma platelets were been given to this point.
The patient was transported to angiogram for angiography of the vertebral artery and embolization due to pelvic bleeding. Images showed large amounts of extravasation of contrast in the right lower quadrant corresponding to areas identified on a recent CT. The right internal iliac artery was then selectively catheterized via interventional radiology procedures. Spot images were obtained after embolization, demonstrating a stop to the bleeding branch. An injection of contrast showed complete resolution of the bleed in the pelvis. The bleed probably represented hemorrhage from the inferior gluteal artery. A very tiny blush of contrast was demonstrated in the midpelvic region. It was elected not to embolize this area, as it would have required proximal embolization of the entire right internal iliac system. This action would have diminished the patient's opportunity for healing after pelvic reconstructive surgery. Narrowing of the right distal external iliac artery and common femoral artery was seen on fluoroscopy, thought to be due to extrinsic compression from a hematoma. The patient tolerated the procedures and remained hemodynamically stable throughout the process. She was transferred to the intensive care unit in what was considered hemodynamically stable condition. In summary, the patient had a hemorrhage in the right lower quadrant secondary to pelvic trauma which was successfully embolized.
Multiple images were taken of the patient in order to direct appropriate surgical and medical management (Figures and ). A CT brain without IV contrast revealed a subdural hematoma, fracture of the left zygomatic arch and left lateral orbit, but no depressed skull fracture. A single frontal view chest X-ray revealed no acute disease/process. Shoulder X-rays revealed no evidence of fracture or dislocation. Knee X-rays revealed no evidence of fracture or dislocation. Tibia/fibula X-rays demonstrated comminuted fractures seen to involve the distal shaft of the left tibia. At least 3 fracture sites were noted in the fibular shaft which were also comminuted, involving the mid- and distal portions. Normal alignment remained at the ankle joint and knee joint as noted by imaging. Soft tissue edema was present at the left lower extremity. The open fracture of the distal lower leg had a large opening medially, which was approximately 15 × 8 cm in length. Bony fragments were present. All compartments were soft upon physical exam. A nonenhanced CT of the cervical spine and pelvis with additional 3D-volume rendered reformatted images was obtained. This displayed a minimally displaced fracture of the right C7 transverse process, traversing the right vertebral artery foramen. No traumatic subluxation was seen in the spine. A CT thorax with IV contrast via trauma protocol was performed, revealing no evidence of pneumothorax, pleural effusion, or pulmonary contusion, normal-appearing mediastinum and great vessels with bovine type arch, and no evidence of osseous trauma.
A pelvic X-ray showed multiple pelvic fractures. CT abdomen and pelvis with IV contrast via dedicated trauma protocol was also performed. This revealed bilateral transverse process fractures of L5 and left transverse process fractures of L3-4. Comminuted pelvic fractures were evident. Bilateral comminuted acetabular fractures with protrusion of the left femoral head into the pelvis were seen. Bilateral pubic rami fractures were noted. Disruption of the left sacroiliac joint, anteriorly and posteriorly, was seen. A complex-free fluid was seen adjacent to the urinary bladder just below the pelvic brim on the right, likely representing blood and a pelvic hematoma. Via the Letournel classification of acetabular fractures, there was a right-sided T-type acetabular fracture, with communication at the anterior acetabular wall, as well as a left-sided T-type fracture with communication at the anterior and posterior acetabular walls. The left femoral head and floor of the acetabulum were medially displaced into the true pelvis. It was also apparent that there was a fracture at the junction of the left inferior pubic rami and left ischial tuberosity. Via the Young and Burgess Classification of Pelvic Ring Fractures, it could be noted that there was a pelvic lateral compression type II injury on the left, pelvic lateral compression type I injury on the right, as well as a pelvic lateral compression type III injury. A broad term to explain the pelvic trauma could be the classification designation as a “combined mechanical” injury to the pelvis.
Despite the numerous life saving measures enacted in the treatment of this patient, she subsequently passed away from her injuries. She went into a hypotensive crisis and cardiac arrest. The supposed location of hemorrhage leading to hypotension was thought to be secondary to a spinal injury to the transverse process of C7, causing dissection of the vertebral artery.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [110.0, 'mm hg']}",123.33333,117.16666,129.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 110.0 mm Hg = 123.33333 mm Hg.
Hence, the patient's mean arterial pressure is 123.33333 mm Hg."
1655,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7305628-1,Extracted,"A 64-year-old white man presented to our emergency department (ED) for persistent weakness and autonomic dysfunction the day after a 27-day stay at an outside hospital where he was treated in the intensive care unit for septic shock due to Escherichia coli urinary tract infection. He was admitted to our internal medicine teaching service for further workup of his worsening dysautonomia.
His past medical history included 3 years of progressive failure to thrive, dysautonomia characterized by frequent syncopal episodes and neurogenic bladder, occasional volume overload, and chronic non-bloody diarrhea. The syncopal episodes began occurring 1 year prior to admission and were in the setting of bowel movements or standing. He was bed-bound at the time of admission and was pre-syncopal with sitting upright. He was taking 0.2 mg fludrocortisone twice a day (we held this on admission for heart failure symptoms) and 15 mg midodrine three times a day for syncope. He was noted to have pleural effusions and ascites at the outside hospital, and he was discharged with 40 mg orally administered furosemide daily. He was not on any beta-blocker. The diarrhea was roughly three times a day, watery, and yellow to brown in color. He was taking loperamide and pancrelipase for the diarrhea with minimal improvement.
His family history was relevant for heart disease starting at old age in his sister, brother, and father. His social history included a 20 pack-year smoking history but was negative for alcohol or illicit drug use. Before his previous hospitalization, he lived at home with his wife in a rural town, and he was able to complete his ADL with minimal assistance.
On arrival to our emergency department (ED), his vital signs were: 37 °C, blood pressure (BP) 62/42 mmHg, heart rate (HR) 75, respiratory rate 10 breaths per minute, and oxygen saturation of 85% on room air. Orthostatic BPs were not able to be obtained due to his weakness and lightheadedness with sitting upright even. His body mass index (BMI) was 21.6. On physical examination he was generally frail appearing, but in no distress. An examination of his head revealed temporal wasting and macroglossia. His heart had a regular rate and rhythm without murmurs or extra heart sounds, and he did not have jugular venous distention (JVD) or peripheral edema. Crackles were auscultated up to the mid-lung fields on the right and at the base on the left with moderate volume ascites. His abdomen was slightly distended with mild lateral bulging. Bowel sounds were present, and there was no rigidity or tenderness of his abdomen. On his neurologic examination, he was alert and oriented, without cranial nerve deficits, his strength was 4/5 in all extremities, deep tendon reflexes were slightly hypoactive in the patellar and Achilles tendons, sensation was decreased in all modalities in length-dependent distribution, and coordination was intact without dysmetria. He did not have clonus or an upgoing plantar reflex. We were not able to test gait due to debilitating weakness and orthostatic hypotension.
Initial laboratory results were significant for white blood cell (WBC) count of 13.1 × 109 cells/L with neutrophil predominance, 25 WBC and slight leukocyte esterase with 100 mg/dL protein on urine analysis (UA), glomerular filtration rate was calculated to be 51 mL/minute/1.73m2, calcium was normal, and a brain natriuretic peptide (BNP) of 1037 pg/mL. Plasma cortisol on admission was 30.1 mcg/dL (repeat on day 2 10.5) and adrenocorticotropic hormone (ACTH) levels (13.4 pg/mL) were within normal limits. A chest X-ray on admission showed a moderate right pleural effusion (Fig. ). A computed tomography (CT) scan of his chest revealed large right and small left pleural effusions (Fig. a) and large abdominal ascites (Fig. b).
An electrocardiogram (EKG) was low voltage with left axis deviation and a right bundle branch block. An echocardiogram revealed severe eccentric left ventricular hypertrophy, mild dilation of the left atrium, with reduced ejection fraction of 35–40%, and a bright, speckled appearance of myocardium. Serum free lambda light chain was elevated at 1256.4 mg/L with a kappa to lambda ratio of 0.02. Initially, a fat pad biopsy was nondiagnostic. A subsequent bone marrow biopsy on hospital day 12 showed 10% plasma cells with lambda monotypic population on flow cytometry, marked extracellular eosinophilic deposits, and a focus of congophilic deposit, suggestive of amyloidosis and myeloma. Hematology came to the final diagnosis of AL amyloidosis and myeloma with nerve, cardiac, and gastrointestinal involvement.
The initial hypotension corrected to 128/87 mmHg 12 minutes after the initial reading without intervention. His pulse remained stable at 87 beats per minute. He was then given 1 L of intravenous Lactated Ringer’s solution and 10 mg intravenously administered dexamethasone and his BP remained stable until hospital day 2 when he had a BP of 84/44 mmHg with a pulse of 71 beats per minute that was not announced to the primary team as a medical emergency.
The main goal for the first few days of admission, before we knew he had amyloidosis, was to treat his heart failure and malnutrition. Because he was clinically volume overloaded with pleural effusions, hypoxia, and an elevated BNP, we gave 40 mg orally administered furosemide on the first 3 days followed by 20 mg torsemide for the next 2 days. We were balancing fluid loss from diuretics and diarrhea with 2 L of peripheral parenteral nutrition (PPN) per day because he had malnutrition estimated as severe based on the Academy of Nutrition and Dietetics (Academy)/American Society for Parenteral and Enteral Nutrition (ASPEN) clinical characteristics. He was net negative approximately 1 liter per day for the first 4 days of his hospitalization. One dose of cefepime was given in our ED, but our team did not elect to continue antibiotics as his UA was not concerning and his blood and urine cultures remained negative while his WBC count normalized.
On hospital day 2, he had two episodes of hypotension (84/44 mmHg and 71/51 mmHg later in the day) with normal pulses (71 beats per minute and 63 beats per minute, respectively). No alert for a medical emergency was called for either of these readings, and the resident on call responded by giving 1 L of intravenously administered fluids. We later increased his midodrine dose to 20 mg three times a day and his BP improved. He was not tachycardic and his creatinine was improving with diuresis (1.26 on admission to 1.04). He did not display contraction alkalosis to suggest that he was volume depleted. His WBC count had normalized by day 4 without antibiotics since the ED dose of cefepime.
Two days went by where he was stable and no changes were made, but on day 5 he started to have frequent episodes of severely symptomatic nOH with unmeasurably low BP using the electronic cuff (as low as 44/25 mmHg on manual checks) and bradycardia in the range 40s to 50s beats per minute. Each episode was associated with a bowel movement or taking medications, leading to five medical emergency events being called on the hospital overhead speaker over a 4-day period.
We considered the diuretics and diarrhea as potential exacerbators of these hypotensive episodes, so we stopped torsemide and increased his 4 mg loperamide from daily to three times a day. He was roughly net negative approximately 4 liters at the time the hypotensive and bradycardic episodes began occurring. However, without tachycardia, contraction alkalosis, or acute kidney injury we felt it unlikely that these episodes were due to volume depletion. After the fifth call for medical emergency for hypotension, on hospital day 8, we started 200 mg droxidopa three times a day.
We felt that this was not volume depletion because our patient was still volume overloaded at this point. Serum creatinine had improved with gentle diuresis, and there was no contraction alkalosis noted on laboratory results. Also, our patient was not persistently hypotensive, as one would expect if volume depleted. Further, he was bradycardic during episodes, and the episodes were clearly exacerbated by vagal maneuvers (bowel movements and one time when taking medications). He often took 10 to 20 minutes to recover to a normal HR from his bradycardia, and the drops in his BP were severe and sudden. We had previously ruled out adrenal insufficiency with normal ACTH and cortisol levels, and the events seemed too episodic to be consistent with the diagnosis. Therefore, we concluded that this was nOH secondary to amyloidosis.
His BP remained improved during the first day after starting droxidopa, and his dose was increased to 300 mg three times a day because some of his SBP readings were still in the low 90s. Droxidopa was the only medication that was changed during this time, and all other medications and fluids were continued at the same doses and rates. By the third day of treatment, he felt much more energetic and was able to sit upright in a chair, which he had been unable to do for over a month. A plot of his SBPs shows how he improved after starting droxidopa (Fig. ) (Unfortunately, several of the unmeasurably low BP readings from the automated BP cuff were not recorded in the electronic medical record, thus are not reflected in the plot). Also, his HR improved, without subsequent bradycardic episodes (Fig. ).
He was transferred to the oncology service on hospital day 14, and he was started on bortezomib, cyclophosphamide, and dexamethasone on day 19. He was noted to develop an elevated WBC count at the time of his transfer, and on day 19 he tested positive for Clostridium difficile. Treatment with orally administered vancomycin was completed, however, he still had significant diarrhea after 10 days. However, his pressures remained stable.
At discharge, 30 days after initiation of droxidopa, he was still greatly improved in his subjective well-being, stamina in a seated position, and objectively in terms of his baseline SBP, orthostatic measurements (Fig. a and b) (no orthostatics were recorded before 27 October 2019 due to profound pre-syncope with attempts), and HR. Impressively, whereas he had seven episodes of bradycardia below 50 during the first 8 days that were recorded on telemetry, after droxidopa was increased to 300 mg three times a day on day 9 there were no more recorded episodes of bradycardia recorded for the following 12 days until telemetry was discontinued. Overall, however, his prognosis at the time of discharge was very poor, and he elected to go home instead of rehabilitation. He did not attend any of his scheduled post-discharge appointments for chemotherapy or oncology. After loss to follow-up, we learned that he died 10 weeks after discharge.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [128.0, 'mm hg'], 'Diastolic Blood Pressure': [87.0, 'mm hg']}",100.66667,95.63334,105.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 128.0 mm Hg + 2/3 * 87.0 mm Hg = 100.66667 mm Hg.
Hence, the patient's mean arterial pressure is 100.66667 mm Hg."
1656,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8288,Extracted,"A 42-year-old man comes to his physician with a history of fever, non-bloody diarrhea, and headache for 10 days. He also complains of anorexia and abdominal pain. He returned from a trip to India 3 weeks ago. His temperature is 40.0°C (104.0°F), pulse is 65/min, respirations are 15/min, and blood pressure is 135/80 mm Hg. He has developed a blanchable rash on his chest and trunk. A photograph of the rash is shown. Examination of the heart, lungs, and abdomen show no abnormalities.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [135.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",98.33333,93.41666,103.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 80.0 mm Hg = 98.33333 mm Hg.
Hence, the patient's mean arterial pressure is 98.33333 mm Hg."
1657,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-11912,Extracted,"A 68-year-old man presents to his primary care provider after noticing that his urine has been pink for the last week. He does not have any pain with urination, nor has he had any associated fevers or infections. On his review of systems, the patient notes that he thinks he has lost some weight since his belt is looser, and he has also had occasional dull pressure in his back for the past two months. His temperature is 98.8°F (37.1°C), blood pressure is 132/90 mmHg, pulse is 64/min, and respirations are 12/min. The patient weighs 210 lbs (95.3 kg, BMI 31.9 kg/m^2), compared to his weight of 228 lbs (103.4 kg, BMI 34.7 kg/m^2) at his last visit 2 years prior. On exam, the patient does not have any back or costovertebral angle tenderness. On abdominal palpation, a firm mass can be appreciated deep in the left abdomen.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [132.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",104,98.8,109.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 132.0 mm Hg + 2/3 * 90.0 mm Hg = 104.0 mm Hg.
Hence, the patient's mean arterial pressure is 104.0 mm Hg."
1658,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4000300-1,Extracted,"A 35-year-old Japanese male presented to the Emergency Department of Okinawa Chubu Hospital with right hemiparesis. He had awakened from sleep with severe, sharp chest pain that was not accompanied by dyspnea. The chest pain subsided within 1 min without treatment, but medical evaluation was sought due to obvious dysarthria and weakness of the right upper and lower limbs. The patient was previously healthy, with no prior hospital admissions, surgeries, medications, or allergies, but bilateral pedal edema had developed 3 months prior to presentation. He had no dyspnea or ambulatory dysfunction and did not seek medical intervention. He worked as a house painter and lived with his wife and children. He had 15 pack-years of exposure to tobacco, and consumed 400 ml of Okinawan spirits nightly. There was no family history of cardiovascular disease, thromboembolism, or chronic kidney disease.
Physical examination revealed that the patient was alert with no distress. He was not obese (BMI 21.4 on admission, when he was edematous), and he was afebrile with a blood pressure of 140/90 mm Hg, a regular pulse of 85 beats/min, and a respiration rate of 25 breaths/min. Oxygen saturation in the room air was 100%. An examination of the head revealed a marked, right-sided facial droop, but was otherwise normal. Carotid upstrokes were symmetric without bruits. The heartbeat was regular without gallops or murmurs, and the lungs were clear; the abdominal examination was also normal. Bilateral pitting edema was present to the knees. There were no rashes or petechiae. Neurological examination revealed intense dysarthria, which made it difficult for him to communicate with others, and right-sided central facial nerve palsy. Both the right arm and leg were at Brunnstrom stage 1, with complete flaccidity and no voluntary movement. Pain and light touch sensation were absent on the right side of his body.
Table contains initial laboratory data. Blood counts revealed leukocytosis and hemoconcentration. Serum albumin was markedly low at 1.8 g/dl. Serum cholesterol, triglyceride, and low-density lipoprotein cholesterol were elevated. The urine protein to creatinine ratio was 7.5 g/g Cr, indicative of high-grade proteinuria. The examination of the urine sediment revealed oval fat bodies, and testing for anti-nuclear antibodies, anti-neutrophil cytoplasmic antibodies, and anti-phospholipid antibodies were all negative. Hepatitis B and C serologies were negative.
Diffusion-weighted magnetic resonance imaging showed high-intensity areas consistent with acute infarction in the left basal ganglia, left corona radiata, and left cerebral cortex (fig. ). Contrast-enhanced computed tomography of the neck revealed collateral blood flow around a large embolus in the left carotid artery (fig. ). Ultrasound of the left carotid revealed the embolus without any plaques or ulcers at the vessel wall (fig. ). There were no aortic dissections, pulmonary emboli, renal vein thromboses, or deep vein thromboses on the computed tomography. A transthoracic echocardiogram showed normal contractility without dilated chambers, valvular disease, vegetations, intraluminal thrombi, or any findings suggesting pulmonary embolism, such as pulmonary hypertension or right ventricular stress.
A presumptive diagnosis of ischemic cerebrovascular accident caused by a left carotid thromboembolism was attributed to a hypercoagulable state due to NS. Because of the lack of any findings of atherosclerosis or plaques at the left carotid, we believed that embolism was more likely than thrombosis. The origin of the embolus was not detected despite a thorough cardiovascular evaluation. Immediate anticoagulation with unfractionated heparin was employed, and the renal biopsy was deferred. Intravenous methylprednisolone was administered empirically at 1,000 mg/day for 3 days, followed by oral prednisone at 60 mg/day. Cyclosporine was added 30 days later in response to persistent nephrotic-range proteinuria (5.5 g/day on the 28th day). The patient was transferred to a rehabilitation hospital 47 days after first admission.
However, the blood examination performed after transfer revealed abnormal liver function on the 74th day from the first admission, the results of which are detailed in table . Serological studies and abdominal ultrasound excluded viral hepatitis or biliary obstruction. He was immediately readmitted under suspicion of drug-induced hepatotoxicity. Medications on admission included prednisolone (50 mg/day), warfarin (2.75 mg/day), cyclosporine (70 mg b.i.d.), sulfamethoxazole/trimethoprim (400/80 mg daily), eicosapentaenoic acid (900 mg b.i.d.), atorvastatin (10 mg/day), lansoprazole (30 mg/day), alfacalcidol (0.25 μg/day), andronate (35 mg/week), and calcium lactate (1 g b.i.d.). All medications except for prednisone were subsequently withheld, and warfarin was replaced by intravenous heparin. The liver test results normalized, but they deteriorated upon rechallenge with warfarin.
At this time, heparin therapy was briefly interrupted to permit a renal biopsy to evaluate refractory NS, with hypoalbuminemia (2.1 g/dl) and proteinuria (5.7 g/day). The biopsy showed MN at stage III of the Ehrenreich and Churg classification. Continued anticoagulation was deemed necessary due to severe persistent hypoalbuminemia and the severe cerebrovascular accident. Warfarin appeared to be clinically intolerable due to idiopathic hepatotoxicity despite a negative lymphocyte stimulation test. Intravenous heparin therapy was incompatible with outpatient rehabilitation.
We discussed the indication of dabigatran, the only available novel oral anticoagulant in Japan at that time, with the patient and also with cardiologists, a neurologist, and the vice-principal of our hospital, all of whom were responsible for the prescription of dabigatran, and we decided to initiate treatment. We also explained and discussed the risks and benefits of dabigatran with the patient and obtained his written and informed consent in advance. Oral dabigatran was administered at a dose of 110 mg b.i.d., and MN was treated with oral prednisone and cyclophosphamide according to Jindal's regimen []. Proteinuria decreased from a ratio of 5.1 to 1.6 g/g Cr, and serum albumin rose from 2.3 to 3.7 g/dl over 7 months. He was transferred to the rehabilitation hospital 137 days after stroke onset. At the outpatient clinic, his renal function remained stable, and he did not experience any episodes of edema, bleeding, or thromboembolism. We monitored the activated partial thromboplastin time (aPTT) to predict the risk of bleeding due to excessive anticoagulation. The aPTT values taken 4 h following administration of dabigatran in the morning were stable at around 40 s (standard aPTT was 30 s). A carotid echogram performed 2 years after the initiation of dabigatran revealed a reduced embolus, although it did still occlude the internal carotid.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1659,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7654563-1,Extracted,"A previously healthy 16-month-old male presented with febrile seizure, rash, and diarrhea. Initial workup in the emergency room, including a CT scan of the head, was not conclusive. He was sent home and returned 12 hours later with 40.4 C fever, worsening upper body rash, and diarrhea. Vital signs were significant for heart rate 120, hypotensive with blood pressure 72/40, tachypneic with respiratory rate 36, and oxygen saturation of 99% while breathing ambient air. Physical exam was prominent for periorbital edema, hepatomegaly 4cm below the right costal margin, bilateral inguinal lymphadenopathy, and slightly raised non-pruritic erythematous rash concentrated on the trunk and proximal arms.
Shortly after admission, he developed distributive shock with worsening hypotension and tachycardia. The patient was intubated with concern for acute hypoxic respiratory failure and shock state. Vasopressors and inotropes were initiated for hypotension. Blood and urine cultures were obtained, and broad-spectrum antibiotics with cefepime and vancomycin were started. Patient met Centers for Disease Control and Prevention (CDC) criteria for MIS-C with fever, anemia hemoglobin 8.8 g/dL, hypoalbuminemia 2.7 g/dL, thrombocytopenia 69 x10^9/L, elevated C-reactive protein 134 mg/L, erythrocyte sedimentation rate 10mm/hr, elevated procalcitonin 33.9 ng/mL, elevated ferritin 2763 ng/mL, elevated lactic acid dehydrogenase 987 u/L, IL6 318pg/mL, IL2 4705pg/mL, IL10 38pg/mL, coagulopathy with significantly elevated D-dimer 18 mcg/mL, prolonged prothrombin time (PT) 17.9 sec, prolonged partial thromboplastin time (PTT) 39.3 sec, elevated brain natriuretic peptide (BNP) 498 pg/mL and low anti-thrombin III 39, positive COVID-19 immunoglobulin G (IgG) antibody and negative polymerase chain reaction (PCR). The rapid viral panel was negative. Serial echocardiograms showed hyperdynamic left ventricle systolic function and mild tricuspid regurgitation with no clinical significance and ultimately resolved (Figures -). EKG showed nonspecific t-wave changes. Troponin was within a normal range. The patient received methylprednisolone 20mg/kg, anakinra 2mg/kg, intravenous immunoglobulin (IVIG) 2g/kg, and prophylactic Lovenox® dosing with 0.5mg/kg twice daily. The patient remained intubated on mechanical ventilation and remained on vasopressors/inotropes for three days with a maximum epinephrine dose of 0.08 mcg/kg/min and norepinephrine 0.15 mcg/kg/min. Anakinra dosage was gradually increased over time due to persistent fevers. The patient completed 12 days of anakinra with a maximum dosing of 12mg/kg/day, two doses of IVIG, and was maintained on a high dose of methylprednisone 30 mg/kg/day on the second and third days and then 8mg/kg/day with tapering for the rest of stay, which switched to oral prednisone once oral tolerance improved. The patient stayed at the hospital for a total of 15 days and was discharged on steroid taper. Laboratory data for the initial 10 days of admission are presented in Table .",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [40.0, 'mm hg'], 'Systolic Blood Pressure': [72.0, 'mm hg']}",50.66667,48.13334,53.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 72.0 mm Hg + 2/3 * 40.0 mm Hg = 50.66667 mm Hg.
Hence, the patient's mean arterial pressure is 50.66667 mm Hg."
1660,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4743232-1,Extracted,"A 35-year-old male farmworker arrived at the General Surgery Service of the Hospital
Universitário Oswaldo Cruz, Recife, Pernambuco, Brazil. He reported the
appearance of a mass in the right inguinoscrotal region for around one month without
pain. Two days previously he had begun to experience epigastric pain with nausea and
vomiting. He visited his local health service and received treatment for gastritis. As
the pain continued and was located in the right iliac fossa, he was admitted to
hospital. A physical examination revealed a heart rate of 100 bpm, a respiratory rate of
21 ipm, PA=130x80 mmHg and an inguinoscrotal hernia on the right side with slight
irritation of the peritoneum. He was referred for surgery and the procedure revealed an
inflamed appendix with purulent secretion at its apex within the hernial sac. As
surgical access was by transverse incision of the inguinal hernia, it was decided to
perform the appendectomy and the Bassini repair of the hernia simultaneously (). Antibiotic prophylaxis with metronidazole
and ceftriaxone was carried out for 24 hours. After two days, the patient was discharged
from hospital with no complications. The result of a biopsy confirmed the
appendicitis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1661,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4561098-1,Extracted,"A 78-year-old female with a past medical history of diabetes mellitus type II, hypertension, osteoporosis, and asthma was brought into the emergency department by ambulance with severe shortness of breath. She was afebrile, tachypneic (respiratory rate of 28 rpm), with an elevated blood pressure of 185/105 mmHg and heart rate of 111 beats per minute. Her chest X-ray revealed a large left-sided tension pneumothorax. Because of impending respiratory failure, she was intubated and placed on mechanical ventilation. A chest tube was inserted with subsequent reexpansion of the left lung. The patient was admitted to the intensive care unit for monitoring. Cardiac biomarker, troponin I, was found to be elevated at 16.529 ng/mL (reference range: ≤0.1 ng/mL). Serial Electrocardiograms (ECGs) done over the course of 12 hours demonstrated sinus bradycardia, alternating with sinus tachycardia and normal sinus rhythm. Anterior Q waves were seen, along with dynamic T-wave changes and transient ST-segment elevation was also noted in the lateral leads. Transthoracic echocardiogram revealed global left ventricular hypokinesis sparing the basal segments, apical ballooning, and severe systolic dysfunction with an estimated left ventricular ejection fraction (LVEF) of 13% ().
The patient was treated with aspirin, clopidogrel, a statin, and Ramipril and was subsequently transferred to another facility for cardiac catheterization. Coronary angiography revealed normal left and right coronary artery systems and no evidence of coronary artery disease (). She was treated supportively and her condition improved over the next few weeks. A transthoracic echocardiogram performed 12 days later revealed no left ventricular dilation, resolved wall motion abnormality, and a significantly improved LVEF of 60%.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [185.0, 'mm hg'], 'Diastolic Blood Pressure': [105.0, 'mm hg']}",131.66667,125.08334,138.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 185.0 mm Hg + 2/3 * 105.0 mm Hg = 131.66667 mm Hg.
Hence, the patient's mean arterial pressure is 131.66667 mm Hg."
1662,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7447863-1,Extracted,"The patient was a 67-year-old man from Wuhan, China. The patient’s chief complaint was
“cough and shortness of breath that had lasted for more than 1 month.” The patient
complained that on 22 January 2020, for no apparent reason, he started to have dry cough
with no sputum, which was accompanied by chest tightness, shortness of breath, fatigue,
and poor appetite. He did not have chills, fever, nausea, vomiting, or other discomforts.
The patient was admitted to Wuhan Hanyang Hospital on 3 February 2020 because of
intensified chest tightness. Physical examination upon admission showed that his body
temperature was 36.5°C, pulse was 106 beats/minute, respiratory rate was 22
breaths/minute, blood pressure was 120/70 mmHg, and oxygen saturation (SpO2)
measured using pulse oximeter was 88%. The white blood cell count was
10.44 × 109/L, platelet count was 97 × 109/L, and the percentage
of neutrophils was 91.01%. The absolute lymphocyte count was 750 cells/µL, the total
percentage of T cells was 31.4%, and the absolute T cell count was 235/µL. The patient
tested negative for influenza A and B, respiratory syncytial virus, human parainfluenza
virus, adenovirus, echovirus, group B coxsackievirus, Mycoplasma
pneumoniae, Chlamydia pneumoniae, and tuberculosis (using
anti-tuberculosis IgM antibodies). The concentration of interleukin-6, interferon gamma,
tumor necrosis factor alpha, and interleukin-10 were 167.44 pg/mL, 24.08 pg/mL, 36.36
pg/mL, and 12.06 pg/mL, respectively. The blood gas analysis showed that pH was 7.57 and
partial pressure of oxygen was 45.7 mmHg. On 4 February 2020, chest CT scan imaging showed
diffuse infections in both lungs and the results of nucleic acid test by nasopharyngeal
swab was presumptively positive. The patient was treated with moxifloxacin, tienam
combined with linezolid, and piperacillin/tazobactam for anti-infection,
methylprednisolone for anti-inflammation, ambroxol for expectoration, and thymalfasin for
immune response enhancement. However, his condition did not improve, so he was transferred
to our hospital on 26 February 2020.
Upon admission to our hospital, the patient had a body temperature of 36.5°C, a pulse of
106 beats/minute, a respiratory rate of 22 breaths/minute, a blood pressure of 120/70
mmHg, and the SpO2 was 89%. Chest physical examinations including inspection,
palpation, and percussion indicated no obvious abnormalities, while the auscultation was
not performed because of the limitations of the doctor’s protective clothing. The chest CT
scan that was performed on 2 March 2020 showed an abnormal opacity in both lungs, which
suggested viral pneumonia (). The patient’s nasopharyngeal swabs were collected and sent for nucleic acid
testing on 27 February and 4 March 2020, and both results were negative. On 5 March 2020,
the result of SARS-CoV-2-specific IgM tests was positive. The next day, three different
types of specimens (sputum from deep cough, nasopharyngeal swab, and feces) were collected
for the nucleic acid test, and the results were positive, negative, and negative,
respectively. The timeline of nucleic acid tests, IgM antibody tests, and the
corresponding results was presented in . The patient was treated with piperacillin/tazobactam for
anti-infection, ambroxol for expectoration, and thymalfasin for immune response
enhancement. His respiratory symptoms gradually improved afterward, and SpO2
increased to 95% without the assistance of a ventilator. The nasopharyngeal swabs were
collected and sent for nucleic acid testing on 14 March and 17 March 2020, respectively,
and the results were both negative. The patient was discharged on 18 March 2020 and was
isolated for 2 more weeks in a community quarantine center. Additionally, the patient
received thymalfasin treatment to enhance the immune response during hospitalization, and
follow-up data within 1 month after discharge showed that no complications had
occurred.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1663,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3285709-1,Extracted,"A 75-year-old woman was admitted to the emergency department with acute right abdominal pain of 2-hour duration. Her medical history included a hysterectomy 30 years ago. From several decades ago, she had almost always voided with abdominal strain. Also, she suffered from tenesmus and weak stream. On examination, she was oriented and cooperative. Her vital signs were as follows: blood pressure, 150/75 mmHg; pulse, 84 beats per minute and regular; respirations, 20 per minute; and body temperature, 36.0℃. Clinical examination revealed diffuse pain in the right abdomen with tenderness. However, costovertebral angle (CVA) tenderness was not prominent. Bowel sounds were increased.
Urinalysis showed 2 to 4 red cells and 0 to 1 white cells per field under high-power magnification. Complete blood cell count results were as follows: 8,500/mm3, with 44.5% neutrophils. Serum chemical analysis showed a urea level of 26 mg/dl, a creatinine level of 1.5 mg/dl, and a C-reactive protein (CRP) level of 0.99 mg/dl. Other values were within the normal limits.
After analgesic injection, her pain subsided. With a presumptive diagnosis of acute gastroenteritis, she was discharged with medication.
The following day, the patient was admitted to the gastrointestinal department with persistent right abdominal pain. An abdominal computed tomographic (CT) scan was performed, which showed a dilated urinary bladder, hydronephroureterosis, and perinephric fluid collection. The patient was referred to our urologists, who recommended insertion of an indwelling Foley catheter. About 2 L of urine was drained shortly after catheter indwelling. Because there was no delayed phase on CT, we performed a non-enhanced CT scan immediately. It showed extravasation of radiocontrast from the right upper ureter at the L3 to 4 transverse process level and improved hydronephroureterosis ().
A 8.5 F pigtail percutaneous nephrostomy catheter was inserted into the renal pelvis. After 7 days, antegrade pyelography (AGP) performed through the nephrostomy catheter showed no extravasation of radiocontrast from the ureter (). A double-J catheter (6 F, 24 cm) was placed in the right ureter. The percutaneous nephrostomy catheter and Foley catheter were removed. The next day, she was discharged without complications.
After 2 weeks, the Double-J catheter was removed and we subsequently performed a video-urodynamic study. A total of 500 ml of normal saline was filled in the bladder. The patient then tried to void with abdominal straining, but could not. Maximal detrusor pressure did not exceed 10 cmH2O. In other words, the patient showed detrusor underactivity and no vesicoureteric reflux (VUR). A follow-up CT scan was performed 2 months later. It showed resorption of urinoma in the right peri-renal space and there was neither malignancy nor obstructing lesions. She was managed with alpha-blockers and clean intermittent catheterization.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 75.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1664,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7584291-1,Extracted,"A 13-year-old previously healthy African American male presented to the ED for eight-day duration of right lower quadrant pain and new onset intractable nausea and vomiting. He was previously evaluated at another facility four days prior and discharged home with symptomatic therapy. On review of systems, the patient denied recent travel, fever, abdominal trauma, previous abdominal surgeries, blood dyscrasias, or diarrhea. The patient’s initial vital signs were blood pressure of 93/61 mm Hg, heart rate of 123 beats per minute, respiratory rate of 20 breaths per minute, and oxygen saturation of 98% in room air with a temperature of 98.7 degrees Fahrenheit. Physical exam was notable for mild right lower quadrant tenderness with rebound, but negative for costovertebral angle tenderness or testicular tenderness. Laboratory analysis reviewed a white blood cell count of 15,200 cells/µL with an 85% neutrophilic predominance, though comprehensive metabolic panel and lipase were unremarkable. Specifically, the patient's blood urea nitrogen (BUN) and creatinine were 17.9 mg/dL and 0.93 mg/dL, respectively, and the urinalysis was without blood, nitrite, or leukocyte esterase, but did contain 1+ ketones and a mildly elevated specific gravity of 1.031 (normal range 1.005-1.025). The patient underwent evaluation for acute appendicitis, and while the abdominal ultrasound (US) was non-diagnostic, MRI demonstrated a normal appendix, right perinephric fat stranding, mild hydronephrosis, and a 3 millimeter (mm) ureterolith at the right ureterovesicular junction (Figure ). The patient received 1,000 mL of Ringer’s lactate solution, 650 mg of intravenous acetaminophen, and 4 mg of intravenous ondansetron, with resolution of tachycardia and improvement of symptoms. Urology was consulted for further management, and the patient was admitted to the hospital for trial of medical therapy including medical expulsive therapy. However, due to refractory pain and emesis without stone passage, coupled with possible ureteral obstruction, the patient subsequently underwent successful cystoscopy, ureteroscopy, laser lithotripsy, and ureteral stent placement. The patient was discharged after an uneventful postoperative course, and noted resolution of symptoms at postoperative follow-up appointment.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [93.0, 'mm hg'], 'Diastolic Blood Pressure': [61.0, 'mm hg']}",71.66667,68.08334,75.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 93.0 mm Hg + 2/3 * 61.0 mm Hg = 71.66667 mm Hg.
Hence, the patient's mean arterial pressure is 71.66667 mm Hg."
1665,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4575440-1,Extracted,"A 66 year old Sinhalese Sri Lankan lady, who had been a strict vegetarian for the past 20 years, presented to our teaching hospital with 1 month’s history of numbness and tingling of both lower limbs with unsteadiness of gait, without complaints of urinary or fecal incontinence. She had no fever, night sweats, gastrointestinal symptoms or any uremic symptoms. She did not have a history of pre-existing diabetes mellitus, hypertension or ischemic heart diseases or alcohol consumption. She did not show clinical or biochemical features of pernicious anemia.
On examination, she was a thinly built lady with no hypo or hyperthyroid features. She had no pallor, icterus, peripheral edema or lymphadenopathy. Her pulse rate was 82 beats per minute with a blood pressure of 130/78 mmHg. She did not have hepato-splenomegaly.
On neurological examination, she had stocking type sensory impairment up to mid shin level and absence of joint position and vibration sensation in both lower limbs. Her ankle jerks were absent bilaterally. Romberg’s sign and Babinski sign were positive, but had no impairment of muscle power or tone. Her upper limbs, cranial nerves and higher functions were neurologically normal and had no cerebellar impairment.
Her laboratory investigations were unremarkable, with a hemoglobin concentration of 12.1 g/dl, red blood cell count of 4.39/mm3, mean corpuscular volume (MCV) of 83.3 fl, mean corpuscular hemoglobin concentration of 27.6 g/dl, platelet count of 334,000/mm3, serum creatinine of 82 mg/dl, and normal fasting plasma glucose level sand thyroid stimulating hormone levels. Her blood picture revealed no features of vitamin B12 deficiency and showed normochromic normocytes. Demyelinating polyneuropathy was confirmed with nerve conduction studies.
Even though she did not have features of anemia, the clinical picture was suspicious of vitamin B12 deficiency and associated SACD. Hence we proceeded with the serum vitamin B12 levels, which was found to be very low; 84.90 pg/ml (208–963). Thus, the clinical diagnosis of sub-acute combined cord degeneration due to deficiency of vitamin B12 without anemia was made.
She was treated with intramuscular hydroxycobalamine 1000 μg for 7 days, weekly for 6 weeks and thereafter three monthly. After 3 months of replacement therapy, the patient showed clinical improvement, with repeated B12 levels being elevated up to 308.6 pg/ml. Follow up nerve conduction study done at 1 and 3 years showed previously absent Sural sensory nerve action potentials reappearing, and common peroneal and posterior tibial nerve conduction velocities being improved. This case demonstrates early clinical improvement, with slow recovery of polyneuropathy on nerve conduction studies, despite rapid correction of vitamin B12 levels following therapy with hydroxycobalamine.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",95.33333,90.56666,100.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 78.0 mm Hg = 95.33333 mm Hg.
Hence, the patient's mean arterial pressure is 95.33333 mm Hg."
1666,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8212687-1,Extracted,"An 88-year-old male presented to our emergency department (ED) with an acute onset of a painless loss of vision to his right eye. His past medical history was significant for hypertension, coronary artery disease and atrial fibrillation (on apixaban). He stated he was lying in bed reading when he had a sudden painless loss of vision to his right eye, described as a curtain closing, for which he presented to our ED ~24 h later. He denied any other symptoms including headache, scalp pain, jaw claudication, focal weakness, numbness, angina or shortness of breath.
Vitals on arrival to the ED were as follows: 36.9°C, heart rate of 62 beats/min, respiratory rate of 16 breaths/min, blood pressure of 123/53 mmHg and pulse oximetry of 99% on room air. His cardiopulmonary exam was unremarkable. His neurologic exam was notable for a National Institute of Health Stroke Scale score of +2 for complete unilateral vision loss to the right eye. Intraocular pressures were 14 mmHg bilaterally. His remaining physical exam was notable for a right afferent pupillary defect (APD). To further assess the eye and its structures, a point-of-care ultrasound (POCUS) was then performed. Utilizing the high-frequency linear probe to the right eye, a transverse view demonstrated a retrobulbar spot sign (RBSS) in the distal portion of the central retinal artery within the optic nerve sheath (, red arrow). He had normal blood flow in his left eye (), and no blood flow was seen to the central retinal artery of the right eye, with the yellow arrow pointing to the RBSS (). The patient was then transferred to our tertiary referral center (TRC) for specialist consultation.
Ophthalmology visualized a plaque on the dilated fundoscopic exam with associated retinal ischemia. Given the onset of ~24 h prior to arrival, the risks of tissue plasminogen activator (tPA) outweighed the benefits, as such, the patient was medically managed. His head computed tomography (CT) was unremarkable for acute changes. A magnetic resonance imaging MRI could not be done, secondary to his pacemaker not being compatible. His carotid duplex was without severe stenosis or thrombus. His echocardiography showed left ventricular diastolic dysfunction with an ejection fraction of 40%, which was similar to previous studies.
Overall, his workup was without evidence of carotid artery disease or vasculitis and it was suspected to be cardioembolic in origin related to his atrial fibrillation. On further questioning, it was found that the patient’s family member had passed away 2 weeks prior, leading to depression and multiple missed doses of his anticoagulation. Compliance of his anticoagulation was stressed on discharge. At his 1-month follow-up after his hospital admission, he has regained light perception and 15% of his vision.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [123.0, 'mm hg'], 'Diastolic Blood Pressure': [53.0, 'mm hg']}",76.33333,72.51666,80.15,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 123.0 mm Hg + 2/3 * 53.0 mm Hg = 76.33333 mm Hg.
Hence, the patient's mean arterial pressure is 76.33333 mm Hg."
1667,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8111402-1,Extracted,"A 48-year-old woman with cystinuria presented to the kidney stone prevention clinic to ask whether she could undergo bariatric surgery. The patient read this case report and gave us permission to submit it for publication. Her relevant medical history began with a first episode of renal colic with a stone at the age of 42 years; the stone passed without complication and was not recovered. Three years later, she underwent extracorporeal shockwave lithotripsy directed at a large stone in the left kidney, which was found to be composed of cystine. Because some residual non-obstructing stones were noted after the lithotripsy, she underwent ureteroscopy as well. She was treated with tiopronin and potassium citrate. She saw a nephrologist who continued her treatment with potassium citrate but switched her thiol therapy to D-penicillamine, thinking that, despite the short course, the tiopronin had not been effective. He advised her to have a water intake of 4 L per day and to reduce salt and animal protein intake.
The family history was significant for calcium stones in her younger sister, who had had a parathyroidectomy. No other family members had a history of cystinuria, related genitourinary, or metabolic problems. Her medication doses included D-penicillamine 500 mg 3 times a day and potassium citrate 30 meq twice a day. She also took lamotrigine for depression, zolpidem, clonazepam, cranberry extract, levothyroxine, vitamin B6, vitamin B12, and vitamin D.
On physical exam, the patient was 104.3 kg and 155.4 cm tall with a body mass index (BMI) of 43.2 kg/m2, meeting the definition of obesity. Blood pressure was 148/84 mmHg and there was no edema at the time of the examination. Physical examination was otherwise unremarkable.
Serum chemistry test results were unremarkable, with creatinine concentration of 0.7 mg/dL, potassium 3.9 meq/L, bicarbonate 20 meq/dL, uric acid 6.9 mg/dL, and calcium 9.0 mg/dL. Liver function tests were normal and the glycosylated hemoglobin was 5.8%. demonstrates the results of 24-hour urine collections. Two collections had been done at the time of her visit; the table demonstrates the mean result of the two collections. Cystine excretion was 990 mg per day after the ureteroscopy; on subsequent collections, she had 470 mg and then 746 mg 2 months prior to initial consultation. On the initial readings, the protein catabolic rate (PCR) was at the high end of the normal range at 1.1 gm/kg/d, but went down to 0.8.
She reported a long history of attempted weight loss, depression, and significant unhappiness with her body image. She had been told that any type of bariatric surgery was not advised given her stone disease, particularly the requirement to maintain high urine volume. She was adherent to an appropriate diet but asked to increase her dosage of potassium citrate in order to reduce her fluid intake, which she found to be “exhausting”.
We were impressed with her resolve regarding the option of bariatric surgery and apparent adherence with the medical regimen prescribed. We suggested that the patient consider gastric banding as a possible alternative to the Roux-en-Y gastric bypass procedure, as it would be more easily reversed if stone formation were to become overwhelming.
After review of our consult note, the bariatric surgery team agreed to install a non-adjustable gastric sleeve, and performed the procedure 7 months later without complication. At follow-up 6 months after the procedure, the patient reported a weight loss of 45 kg and a significant improvement in her mood, affect, and performance. She continued to maintain a low sodium, near-vegetarian diet. She had stopped the vitamin D and the clonazepam.
On physical examination, blood pressure was 118/79 mmHg, pulse was 70 beats per minute, and she had no pedal edema. Ultrasound revealed a 3 mm echo-density located in the right kidney with no definite shadow. A non-contrast computed tomography scan (CT) of the abdomen done 11 months later, 17 months after the surgery, showed no stones.
It was concluded that the bariatric surgery was a success with no definite evidence of active stone disease. At the time of this report, nearly 6 years after the bariatric surgery, she was maintaining her weight at 68 kg, more than 50 kg below her peak, with BMI of 28.3 kg/m2. She has not had a recurrent symptomatic stone. The result of the post-operative 24-hour urine collection, performed 17 months after the procedure, is given in . She had a high urine volume, less sodium and cystine excretion with a relatively alkaline urine. Five years after the procedure, she had normal serum electrolytes: creatinine concentration of 0.6 mg/dL, sodium 138 meq/L, potassium 4.0 meq/L, chloride 99 meq/L, bicarbonate 26 meq/dl, uric acid 5.8 mg/dl, and calcium 9.4 mg/dL.
The patient’s history was of a relatively mild nature, given the range of stone burden experienced by patients with cystinuria. We therefore determined the patient’s genotype. A previously described nonsense mutation was detected, in heterozygosity, in SLC3A1: c.1400T>C (p.M467T). Further analysis of her DNA was performed by testing with a specific Cystinuria Multiplex Ligation-dependent Probe Amplification (MLPA) panel (MRC-Holland, Amsterdam, The Netherlands) looking specifically for large deletions or duplications within the two cystinuria genes, SLC3A1 and SLC7A9. The result was demonstrative of a previously described large duplication in SLC3A1 consisting of exon 5 through exon 9. In summary, her cystinuria was not atypical, in that she had biallelic mutations affecting SLC3A1.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [148.0, 'mm hg'], 'Diastolic Blood Pressure': [84.0, 'mm hg']}",105.33333,100.06666,110.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 148.0 mm Hg + 2/3 * 84.0 mm Hg = 105.33333 mm Hg.
Hence, the patient's mean arterial pressure is 105.33333 mm Hg."
1668,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4265531-1,Extracted,"An 87-year-old Caucasian man was transferred from another hospital after an episode of altered mental status secondary to hypercapnea requiring intubation. His past medical history included type 2 diabetes, stage 3 chronic kidney disease, and heart failure with preserved ejection fraction. He was a lifelong non-cigarette smoker. Per the family he was complaining of shortness of breath, weight gain and worsening leg swelling for 3 weeks, and was progressively more somnolent over the last week. On admission to the outside hospital the results of his laboratory tests were significant for a normal blood glucose of 176mg/dL, normal white blood cell count at 7000 cells/mm3, creatinine of 1.6mg/dL (at his baseline), elevated brain natriuretic peptide at 778pg/mL and negative toxicology screen. He had no history of opioid or benzodiazepine usage. His ABG showed acute on chronic hypercapnea with a pH of 7.22, partial pressure of carbon dioxide (pCO2) of 83mmHg and bicarbonate (HCO3) of 36mmol/L requiring intubation explaining his altered mental status. He was noted to be in congestive cardiac failure and was given diuretics and eventually he was extubated. He was transferred to our institution on nightly bilevel positive airway pressure (bipap) for his unexplained hypercapnic failure. His only complaint on transfer was his chronic two-pillow orthopnea.
On arrival he was in no acute distress with a heart rate of 74, respiratory rate of 20, blood pressure of 107/65mmHg, and oxygen saturation of 98% on 2L nasal cannula. A cardiovascular and respiratory system examination was unrevealing with normal jugular venous pressure and normal cardiac examination. There was paradoxical abdominal motion with the abdominal wall moving inwards on inspiration. A neurologic examination revealed 3/5 strength in his left deltoid and decreased biceps reflexes bilaterally. Power, tone and reflexes were normal in both his lower limbs. He also had severe osteoarthrosis of distal and proximal interphalangeal joints bilaterally with Heberden’s nodes.
His ABG on room air showed a partial pressure of oxygen of 64mmHg, pCO2 of 53mmHg, HCO3 of 28mmol/L and a pH of 7.33 with a normal A-a gradient of 18. This was consistent with chronic respiratory acidosis secondary to hypoventilation, given the normal A-a gradient. A chest X-ray showed elevated hemidiaphragms bilaterally (Figure ). Pulmonary function testing showed a restrictive pattern with a normal ratio of forced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC) of 0.79 (114% predicted), with FEV1 and FVC 49 and 42% of predicted respectively. There were also significantly decreased maximum inspiratory and maximum expiratory pressures of 27.2 and 31.4% predicted; and a decrease in FVC of 22% from the sitting to supine position suggestive of neuromuscular weakness (>20%). The diffusing capacity was normal suggesting a chest wall or neuromuscular cause of restrictive lung mechanics.
Given his abnormal neurologic examination with left deltoid weakness and decreased biceps reflexes, our differential included respiratory neuromuscular weakness from cervical spondylosis and phrenic nerve root compression (given the C5 neurological deficits); or possible cervical myelopathy at C5/C6. The absent biceps reflex (C5 and C6) raised suspicion for myelopathy at the C5 to C6 level although this is typically associated with a brisk triceps reflex (C7). The lack of neurological findings in his lower extremities also argued against myelopathy, but given the potential variable manifestations of cervical myelopathy, an electromyogram (EMG) and nerve conduction study (NCS) were performed. The EMG and NCS revealed decreased amplitude in the phrenic nerves bilaterally and radiculopathy in his upper limbs, suggestive of nerve root compression at the cervical foraminal level. There was no evidence of amyotrophic lateral sclerosis or myopathy on EMG/NCS and serum creatine phosphokinase was normal. A cervical MRI was performed and showed severe bilateral foraminal narrowing at C3, C4 and C5 with no evidence of myelopathy, confirming the diagnosis of phrenic nerve root compression from cervical spondylosis as the cause of hypoventilation. When he developed pulmonary edema, the resultant decreased lung compliance placed an increased respiratory load on his weakened neuromuscular apparatus leading to worsening hypercapnea and resultant metabolic encephalopathy with altered mental status. Carbon dioxide, being readily diffusible across the blood–brain barrier is a well-known cause of encephalopathy in the setting of hypercapnea.
He was offered surgical decompression of cervical motor roots or possible diaphragmatic pacing. Given his age, he opted for conservative management with nightly bipap to rest his respiratory muscles at night. He showed significant improvement with night-time bipap and felt less fatigued during the day, probably from the rest provided to his respiratory neuromuscular apparatus. Following discharge he remained stable but gradually became less compliant with bipap. He had four admissions in 2 years with hypercapnic respiratory failure in the setting of pulmonary edema from heart failure. Pulmonary edema and the resultant decreased lung compliance placed an increased respiratory load on his weakened neuromuscular apparatus. As expected he fatigued more easily with his weakened neuromusculature leading to hypoventilation and worsening hypercapnea. He required continuous bipap while hospitalized until diuresis improved chest wall compliance and respiratory mechanics. He continued to refuse invasive therapies and was managed conservatively with nightly bipap. He developed evidence of right ventricular failure and pulmonary hypertension on echo from a combination of pulmonary venous hypertension from heart failure and chronic hypoxia from hypoventilation secondary to his neuromuscular weakness. Given his recurrent episodes of respiratory failure and worsening heart failure he was eventually transitioned to hospice care.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [107.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",79,75.05,82.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 107.0 mm Hg + 2/3 * 65.0 mm Hg = 79.0 mm Hg.
Hence, the patient's mean arterial pressure is 79.0 mm Hg."
1669,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-12464,Extracted,"A 65-year-old man with a history of hypertension, obesity, and alcoholic cirrhosis is seen in clinic for follow-up. He feels well and currently drinks 5 glasses of wine each night. Medications include atenolol and lisinopril. On physical exam, temperature is 98.1 deg F (36.7 deg C), blood pressure is 151/82 mmHg, pulse is 71/min, and respirations are 14/min. He has spider angiomata on his chest; no asterixis, jaundice, ascites, or peripheral edema is noted. Screening ultrasound reveals a new liver nodule, and follow up CT demonstrates a 2 cm right hepatic lobe lesion with enhancement in the arterial phase. No hypodense attenuation is seen on the venous or delayed phase.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [82.0, 'mm hg'], 'Systolic Blood Pressure': [151.0, 'mm hg']}",105,99.75,110.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 151.0 mm Hg + 2/3 * 82.0 mm Hg = 105.0 mm Hg.
Hence, the patient's mean arterial pressure is 105.0 mm Hg."
1670,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5704827-1,Extracted,"A 48-year-old man with a history of polycystic kidney disease was admitted to Third Affiliated Hospital of Second Military Medical University on May 24, 2017. At the beginning of 2017, he sought for medical advice because of abdominal pain, and was diagnosed with intestinal obstruction. Computed tomography (CT) had scanned multiple cysts in both kidneys, and serum creatinine increased to 115 μmol/L. In April, though he had no sign of smoky urine, periorbital and extremities edema, ascites, or dyspnea, laboratory investigations showed increased serum creatinine (141 μmol/L), proteinuria (6929 mg/day), decreased serum albumin (19 g/L), and increased serum cholesterol (6.02 mmol/L). Abdominal ultrasound revealed multiple small cysts in both kidneys, with the right kidney measuring 11.6 cm in length, and the left kidney measuring 11.5 cm in length, no cyst in liver and spleen. Echocardiography showed left ventricular (LV) posterior wall thickness measuring 15.2 mm, interventricular septum measuring 17.2 mm, left atrial size 31.9 mm, ejection fraction measuring 69%.
Based on the typical CT and ultrasound findings, we diagnosed him as ADPKD, and prescribed tripterygium wilfordii (20 mg per day) and valsartan (80 mg per day). In addition, he has a history of HCM, and used to be treated by cardiac interventional therapy for recurrent arrhythmia even sudden cardiac arrest. The patient had no family history in either polycystic kidney or HCM.
Nevertheless, tripterygium wilfordii treatment proved to be failed 2 weeks later for anasarca, hypourocrinia, gross hematuria, and weight gain by 10 kg. On May 18, the patient was started on daily prednisone (60 mg/day) instead. But what's worse was that he was attacked by streptococcus pneumonia on May 29, which led to septic shock, type I respiratory failure, even acute renal injury. At that moment, his pulse oxygen was 95% (oxygen flow rate = 10 L/minute), pulse rate was 125 beats per minute and blood pressure was 90/61 mm Hg. A chest radiograph showed consolidation of right upper lung lobe. Serum biochemistry revealed a creatinine of 300 μmol/L, albumin16.4 g/L, brain natriuretic peptides 1070 pg/mL, C-reactive protein > 200 mg/L, procalcitonin 100 ng/mL, endotoxin 72.58 pg/mL, arterial partial pressure of oxygen 78.0 mm Hg (oxygenation index = 128). Then he turned to respiratory distress, cyanosis, oliguria, gross edema, and renal deterioration.
In consideration of severe state, ceftazidime combined with moxifloxacin was prescribed, oral prednisone was replaced by intravenous methylprednisolone, and low molecular heparin was injected subcutaneously for anticoagulation. On May 30, though vital signs were stable, urine volume was still 310 mL in day, creatinine zoomed up to 579 μmol/L, far worse than expectation. Continuous renal replacement therapy was started immediately through right femoral vein catheter. Two hundred fifty milliliters of water was removed every hour, and total ultrafiltration volume reached to 3913 mL in 3 days. In the following days, the patient was on the mend with increasing urine, releasing abdominal distension, relieved dyspnea, just ankle edema left. On June 12, he was found to have lowering creatinine (372 μmol/L), with serum albumin of 22.7 g/L, brain natriuretic peptides of 570 pg/mL, procalcitonin of 0.63 ng/mL.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [61.0, 'mm hg']}",70.66667,67.13334,74.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 61.0 mm Hg = 70.66667 mm Hg.
Hence, the patient's mean arterial pressure is 70.66667 mm Hg."
1671,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9020,Extracted,"A 38-year-old man presents to his physician for difficulty swallowing for 2 months. He describes food getting stuck down his windpipe and has been feeling very anxious around meal time because he is thinking that he may have esophageal cancer. He has had an influenza-like infection that lasted about 6 weeks in the past 3 months which exacerbated his asthma attacks. He used his puffers to relieve his symptoms and did not seek medical treatment. He is otherwise healthy. On examination, his blood pressure is 118/75 mm Hg, respirations are 17/min, pulse is 78/min, and temperature is 36.7°C (98.1°F). There is no evidence of enlarged lymph nodes or a sore throat. On palpation, the thyroid gland is enlarged and tender. He is a non-smoker with a BMI of 25 kg/m2. He has not used any medications recently.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [118.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",89.33333,84.86666,93.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 118.0 mm Hg + 2/3 * 75.0 mm Hg = 89.33333 mm Hg.
Hence, the patient's mean arterial pressure is 89.33333 mm Hg."
1672,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7860983-1,Extracted,"A 55-year-old male with a known case of hypertension under regular treatment presented to the casualty department with complaints of swelling of the penis for the preceding two weeks, burning micturition for the preceding 10 days, and inability to pass urine for the preceding two days. He also had lower abdominal pain for two days which was the colicky type with no history of genital trauma. He had a history of inability to retract prepuce for 10 years with multiple episodes of burning micturition for the last one year. He had no fever spikes, reduced urine output, high colored urine, haematuria, and pyuria. He had complaints of obstructive lower urinary tract symptoms including straining, hesitancy, and post-void dribbling for the past one week. He had no significant history of any previous surgeries in the past. He denied a history of any sexual promiscuity in the past. On examination, he was conscious, oriented, and febrile with no signs of dehydration. His pulse rate was 104 per minute with a blood pressure of 140/90 mm Hg. He had lower abdominal tenderness without a palpable bladder. Local examination revealed phimosis with a stony hard swelling over the glans penis under the prepuce with no visualization of the urethral meatus. Penile and scrotal edema were present with bilateral testes palpable and non-tender. He had enlarged tender bilateral inguinal lymphadenopathy.
The initial clinical impression was balanoposthitis with underlying carcinoma of the penis considering his age of presentation. Preputial calculus was also considered as a differential diagnosis in view of the hard consistency of the swelling. X-Ray of the pelvic region showed a radiopaque shadow in the glans region (Figure ). Ultrasound of the abdomen was done to rule out urolithiasis. Its findings included mucosal irregularity of bladder suggestive of cystitis with no associated renal calculi or hydroureteronephrosis. His creatinine and total white blood cell count were within normal limits and his urine culture was sterile. On the day of admission, cannulation with an infant feeding tube through the meatus was attempted. Finally, a dorsal slit was performed followed by catheterization with a Foley’s 12 Fr catheter. A single stone of size 4.5 cm x 3 cm (Figure ) was removed from the preputial space. He was started on intravenous ciprofloxacin and metronidazole empirically in view of the clinical diagnosis of balanoposthitis. His wound was debrided and dressed regularly with Eusol. Penile and scrotal swelling gradually subsided with the local application of magnesium sulfate. Foley’s catheter was removed and the patient started passing urine freely from the urethral meatus. The patient was better symptomatically and was discharged on the seventh day.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1673,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7249933-1,Extracted,"The patient was a 76-year-old woman who presented to our emergency room with a 3-day history of general weakness, fever, and oliguria and a 7-day history of nausea, and vomiting. The patient was bedridden due to a compression fracture of the 1st lumbar vertebra sustained 5 days prior to presentation. The patient had been taking appropriate oral medications for DM and hypertension for the past 40 years and had not developed any specific renal disease. Her prescribed oral hypoglycemic agents at the time of presentation were metformin (500 mg twice per day) and dapagliflozin (10 mg/day). Other daily medications included ezetimibe/rosuvastatin calcium (10 mg/5.2 mg), clopidogrel (75 mg), nicorandil (5 mg), imipramine (25 mg), tolterodine (4 mg), and tamsulosin (0.2 mg). Blood pressure, pulse rate, respiration rate, and body temperature at presentation were 160/80 mmHg, 120/min, 20/min, and 37.5°C, respectively. The patient was alert but experiencing malaise. Her oral mucosa was dry and skin turgor had decreased. Chest auscultation results were normal, but her abdomen was distended with decreased bowel sounds. A peripheral blood test at admission showed a white blood cell (WBC) count of 11,800/μL (neutrophils 85.3%), hemoglobin of 13 g/dL, a platelet count of 173,000/μL, and an erythrocyte sedimentation rate of 12 mm/hour. Serum biochemical examination showed the following: glucose, 410 mg/dL; blood urea nitrogen, 41.7 mg/dL; creatinine (Cr), 3.2 mg/dL; albumin, 3.8 g/dL; total cholesterol, 93 mg/dL; calcium, 8.1 mg/dL; phosphorus, 4.7 mg/dL; uric acid, 6.1 mg/dL; C-reactive protein, 54 mg/L; glycated hemoglobin (HbA1C), 8.1%; insulin, 3.3 μIU/mL (reference range, 2.6–24.9 μIU/mL); and C-peptide, 1 ng/mL (reference range, 1.1–4.4 ng/mL). Urinalysis with microscopic examination showed albumin 3+, occult blood 2+, a WBC count of 20–30/high power field, and a red blood cell count of 10–30/high power field (dysmorphic 90%). Spot urine protein to Cr ratio was 1.14 g/g. After urinary catheterization, her urine output was 1950 mL suggesting azotemia due to postrenal acute kidney injury. Abdominal computed tomography scan showed diffuse paralytic ileus and bilateral pyeloureteritis (Fig. A, B). Treatment with empirical broad-spectrum antibiotics (ceftriaxone) was initiated along with fluid therapy and total parenteral nutrition after insertion of a nasogastric tube. Fasting was prescribed. The oral hypoglycemic agents were discontinued. On day 3 of hospitalization, the patient was transitioned to a full-liquid diet through a nasogastric tube because she showed improvement in renal function (serum Cr, 0.7 mg/dL); paralytic ileus was also less severe. Treatment with metformin (1000 mg/day) and dapagliflozin (10 mg/day) was reinstituted. Previous outpatient medications were also retained and no new medications were added. Extended spectrum beta-lactamase negative, ceftriaxone–sensitive Escherichia coli was isolated from urine cultures. However, on day 6 of hospitalization, she developed consciousness alterations, including confusion, lethargy, and stupor, along with nausea, vomiting, and abdominal pain. Arterial blood gas analysis showed a pH of 6.904, partial pressure of carbon dioxide of 12.0 mmHg, and HCO3− of 3.1 mmol/L, suggestive of high anion gap metabolic acidosis with respiratory compensation. Based on the results of serum biochemical examination (Table ), we suspected eu-DKA accompanied by hypovolemia, hypernatremia, and hypokalemia. For the first 6 hours after discontinuation of dapagliflozin, we performed intravenous fluid therapy with 0.9% saline at a rate of 250 mL/hour (h) for 2 hours followed by 100 mL/h, 5% dextrose in water (5% D/W) (100 mL/h), and KCl (40 mEq/L). Regular insulin (RI) and sodium bicarbonate were not administered considering the blood glucose levels (range, 150–250 mg/dL) and arterial blood pH (>6.9). Because disturbances in serum electrolyte levels continued for 6 hours after intravenous fluid resuscitation (Table ), administration of 0.45% saline (100 mL/h) with KCl (20 mEq/L), 5% D/W (50 mL/h), and RI (2.5 U/h, 0.05 U/kg/h) was maintained. Brain magnetic resonance imaging of the patient showed no specific abnormalities, including the absence of acute ischemic brain lesions. Eventually, the patient started enteral feeding of free water through a nasogastric tube while being administered a mixed solution of 0.45% saline and 5% D/W with RI. Additional biochemical results are described in Table . After the 8th day of hospitalization, consciousness and laboratory findings improved; however, dapagliflozin was not resumed. The patient was discharged on the 14th hospital day because of resolution of consciousness impairment and laboratory abnormalities, and the patient is currently receiving insulin (glargine/insulin lispro) and metformin for management of DM.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [160.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 80.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1674,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7571780-1,Extracted,"A 10-year-old boy with no past medical history was brought by his parents in the outpatient clinic, with complaints of nausea and vomiting for two days. He also had a headache for the last month. The pain was dull, localized to the scalp, and the occipital region occurring usually in the morning and lasted for a few hours. The pain was relieved by taking an analgesic. He was in the normal state of health before one month. On initial evaluation, the temperature was 37°C, blood pressure was 120/70 mmHg, heart rate was 91 beats per minute, respiratory rate was 20/minute, and oxygen saturation was 99% on room air. On physical examination, the patient was healthy and appeared oriented and alert with intact cognition. His skin, extremities, and pulses were normal. However, the patient was anxious with frequent blinking of eyes. On neurological examination, his power, and coordination, and gait were intact, and his toes were down going. The sensation was intact bilaterally, and the reflexes were intact on both sides of the body. His cranial nerve examination was also unremarkable except ophthalmic nerve and eye examination. The patient was noted to have strabismus and diplopia. There was no evident deformity on his face or eye, and he did not have any muscle weakness. He had no history of previous trauma or fall.
Imaging studies were performed, and the magnetic resonance imaging (MRI) of the brain revealed a homogenous hyperdense and enhancing mass in the pineal region (Figure ).
The patient underwent endoscopic biopsy of the pineal region, which demonstrated cells with highly pleomorphic and hyperchromatic nuclei. A significant increase in mitotic activity was detected. There were many vessels but no area of vascular proliferation and necrosis. Granular bodies with eosinophilia were identified. Immunohistochemistry was positive for class III b-tubulin with epidermal growth factor receptor staining (EGFR) and glial fibrillary acidic protein (GFAP). Immunostaining was positive for p53, Phosphatase and Tensin homolog (PTEN), and oligodendrocyte transcription factor (OLIG2), while staining for cluster of differentiation (CD)34, cytokeratin (CK), human melanoma black (HMB)45, and isocitrate dehydrogenase (IDH)-R132H mutation was negative. That was consistent with the atypical pleomorphic neoplasm of the pineal region.
The patient underwent tumor resection via a sub-occipital trans-tentorial approach, followed by one dose of chemotherapy. The patient experienced a resolution of the symptom and was doing well on his bi-monthly follow up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1675,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3872022-1,Extracted,"A 61-year-old female was brought to the emergency department with an altered mental status. The neighbors notified emergency services (EMS) when they did not see her for 2 days. She was found in a confused state, lying on the kitchen floor. She was hemodynamically stable at the time of initial evaluation. Past medical history included osteoarthritis of the knees and alcohol dependence for the last 2 years. Her family history was noncontributory. She was admitted for alcohol detoxification 10 months prior to this event. On exam, her temperature was 98.3 F, blood pressure was 108/58 mm Hg, heart rate was 98 beats per minute, and respiratory rate was 18 per minute. She was awake but lethargic and disoriented to time, place, and person. Her gait was unsteady and she was not able to walk without assistance. Detailed neurological exam was notable only for bilaterally positive finger-to-nose test and intentional tremor of the upper extremities. Romberg test was not assessed due to her unsteadiness.
Her initial blood work revealed a serum sodium of 115 mEq/L, potassium of 3 mEq/L, serum, serum magnesium magnesium of 1 mEq/L, and an anion gap of 20 other lab parameters, including complete blood count, urine drug screen, blood ethanol level and liver function testes were essentially normal. A brain CT showed age-appropriate atrophic changes. A lumbar puncture was not performed due to unclear reasons, most likely being code status precluding invasive procedures.
She was admitted to the hospital and adequately hydrated. On the second day of admission, her speech became garbled and she became more somnolent. Her temperature dropped to 94.8 F and was immediately transferred to the intensive care unit. The hypothermia was gradually reversed by forced warm air therapy using a Bair Hugger blanket. Over time, the patient became more somnolent and lethargic. She remained disoriented and became completely aphasic. She was also noted to have developed difficulty in swallowing her food. MR images of the brain showed diffusely abnormal signal within the cerebellum. The cerebellar cortex showed low signal on T1 and symmetrically increased signal intensity on T2-weighted images (). There was increased signal on diffusion sequence throughout the cerebellar cortex (Figures and ). The radiologist interpreted this as “acute cerebellitis.” Further investigations to exclude alcohol related vitamin deficiencies were normal. Vitamin B12 levels of 749 pg/ml (211–911 pg/ml), folate of 4.76 ng/ml (<3.38 ng/ml considered deficient), thiamine of 129 nmol/L (80–150 nmol/L), copper of 1.03 mcg/mL (0.75–1.45 mcg/ml), and zinc 0.54 mcg/ml (0.66–1.10 mcg/ml). Peripheral blood herpes simplex virus (HSV) PCR was negative. Other viral panels were not obtained. Blood cultures during the admission were negative for any growth.: Although her hypothermia was successfully reversed, her altered mental status remained unchanged. She continued to be aphasic and dysphagic. After about a week of little or no improvement in her mental status, she finally began to verbalize—though confabulatory—while remaining oriented only to self.
She had a protracted hospital stay, spanning 12 weeks, albeit mostly over placement concerns. She gradually became more alert and coherent and was able to recognize the staff members who visited her frequently. She continued to require support during ambulation due to persistent gait instability. She failed multiple swallow evaluations despite aggressive speech therapy and ultimately a percutaneous gastrostomy tube was placed to facilitate enteral nutrition. She was eventually transferred to an extended care nursing home facility.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [108.0, 'mm hg'], 'Diastolic Blood Pressure': [58.0, 'mm hg']}",74.66667,70.93334,78.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 108.0 mm Hg + 2/3 * 58.0 mm Hg = 74.66667 mm Hg.
Hence, the patient's mean arterial pressure is 74.66667 mm Hg."
1676,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-12115,Extracted,"A 72-year-old man is being transported by emergency medical services to the emergency department for a stroke code. He was found on the ground by his daughter earlier today, and he was last known to be without neurological deficits two hours prior to presentation. His temperature is 99°F (37.2°C), blood pressure is 185/105 mmHg, pulse is 102/min, and respirations are 18/min. A non-contrast head CT is performed, which demonstrates a hypodense lesion affecting the left medial frontal and parietal lobe.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [185.0, 'mm hg'], 'Diastolic Blood Pressure': [105.0, 'mm hg']}",131.66667,125.08334,138.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 185.0 mm Hg + 2/3 * 105.0 mm Hg = 131.66667 mm Hg.
Hence, the patient's mean arterial pressure is 131.66667 mm Hg."
1677,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7911869-1,Extracted,"A 59-year-old man with a history significant for polycythemia vera, recurrent acute pancreatitis, status post-cholecystectomy, and recurrent pancreatic pseudocyst requiring prior stent placement presented to our hospital for large-volume hematemesis and melena after undergoing transgastric drainage of his pancreatic pseudocyst with stent placement earlier in the day. On arrival, he was hemodynamically stable with a blood pressure of 122/67 mmHg and a heart rate of 82 bpm. Admission labs were significant for a hemoglobin of 15.5 gm/dL from a baseline of 17.0 gm/dL and a troponin T of 0.01 ng/mL. He was repleted with two units of packed red blood cells in the emergency department. A computed tomography (CT) of the abdomen with angiography revealed a mixture of blood and clot within the pancreatic pseudocyst cavity with extravasation into the stomach, consistent with a pancreatic pseudocyst hemorrhage (Figure ).
He was admitted to the ICU for elective intubation for urgent esophagogastroduodenoscopy; however, prior to this, he developed ventricular bigeminy on cardiac telemetry. An electrocardiogram was obtained and showed ST-segment elevations in leads II, III, and aVF (Figure ), which were not present on electrocardiogram obtained earlier in the day (Figure ). Shortly later, he developed acute substernal chest pain, and repeat troponin T increased from 0.01 ng/mL to 0.12 ng/mL. Findings were consistent with an inferior STEMI. Aspirin load and heparin were deferred due to his GI bleed. The patient’s chest pain subsided spontaneously; however, repeat electrocardiogram revealed persistent ST-segment elevations (Figure ).
A collective discussion was held with the ICU, cardiology service, and gastroenterology service on how to manage his acute inferior STEMI in the context of active GI hemorrhage. The cardiology service did not recommend emergent percutaneous coronary intervention (PCI) due to the patient being free from chest pain and the increased risk of bleeding should he require stenting and dual anti-platelet therapy. The gastroenterology service recommended interventional radiology (IR) be involved in the control of pseudocyst bleeding; however, given that the patient was hemodynamically and clinically stable, it was not felt to be an emergency by the IR team.
The patient was managed conservatively with intravenous proton pump inhibitor therapy and close monitoring for recurrent bleeding or cardiac instability. Heparin infusion and dual anti-platelets were held. Over the course of three days, he remained clinically and hemodynamically stable and did not require further blood transfusions. Gastroenterology suspected his intracavitary bleed self-tamponaded and recommended outpatient follow-up with his gastroenterologist to determine removal timing of the transgastric stent. Echocardiogram showed right wall motion abnormalities in the basal inferior wall. The cardiologist started him on aspirin, atorvastatin, and metoprolol prior to discharge and scheduled an outpatient coronary CT angiogram.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [122.0, 'mm hg'], 'Diastolic Blood Pressure': [67.0, 'mm hg']}",85.33333,81.06666,89.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 122.0 mm Hg + 2/3 * 67.0 mm Hg = 85.33333 mm Hg.
Hence, the patient's mean arterial pressure is 85.33333 mm Hg."
1678,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5089,Extracted,"An 11-year-old boy presents to the emergency department with heavy drooling. The patient was being watched by his babysitter when she found him in this manner. His temperature is 99.1°F (37.3°C), blood pressure is 107/58 mmHg, pulse is 119/min, respirations are 14/min, and oxygen saturation is 98% on room air. Physical exam is notable for a young boy in acute distress who is drooling. The boy states he is in pain and can’t swallow. The patient’s tongue seems abnormally enlarged and erythematous.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [107.0, 'mm hg'], 'Diastolic Blood Pressure': [58.0, 'mm hg']}",74.33333,70.61666,78.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 107.0 mm Hg + 2/3 * 58.0 mm Hg = 74.33333 mm Hg.
Hence, the patient's mean arterial pressure is 74.33333 mm Hg."
1679,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6197009-1,Extracted,"A 51-year-old lady presented to our emergency department because of generalized body ache and marked weakness in both lower extremities for two days duration. She had no history of vomiting, diarrhea, frequent urination, recent use of laxatives or diuretics, current or previous use of lithium, licorice ingestion, or activities leading to profuse sweating. Past medical history was significant for type 2 diabetes mellitus, hypertension, seizure disorder and schizoaffective disorder. She also had a long-term history of alcoholism, consuming two to three pints of vodka every day for about 20 years. Her last drink of alcohol was about 48 hours prior to presentation. On examination, her weight was 79 kg, height 65 inches, body mass index 29.3 kg/m2. Vital signs were stable, temp 98.6°F, heart rate 68 bpm, respiratory rate 18, blood pressure 113/71 mmHg and oxygen saturation 98% on room air. She was alert and oriented, there was no thyromegaly or lymphadenopathy. Cardiac examination revealed a regular sinus rhythm with no murmurs. There were no deformities or edema of the extremities and distal pulses were present. There was no cushingoid facies, buffalo hump or abdominal striae noted. Neurological examination revealed bilateral lower limb weakness of 4/5, with intact sensory system and reflexes. Cranial nerve examination was unremarkable.
Biochemical analysis of the serum showed severe electrolyte disturbances, a potassium level of 2.3 mmol/L (reference 3.6−5.1 mmol/L), magnesium level of 0.9 mg/dL (reference 1.8−3.0 mg/dL), phosphorus level of 2.0 mg/dL (reference 2.4−4.6 mg/dL), corrected calcium level of 7.8 mg/dL (reference 8.9−10.3 mg/dL). Renal function was mildly deranged with Creatinine of 1.35 mg/dL (reference 0.4−1.3 mg/dL) and BUN of 12 mg/dL (reference 8−20mg/dL). The results of hepatic enzymes, AST 113 IU/l (reference 15−41 IU/l), ALT 42 IU/l (reference 17−63 IU/l) was suggestive of alcohol induced hepatic damage. Electrocardiogram (ECG) () showed no arrhythmias, but changes characteristic of hypokalemia with increased amplitude of the U-wave and marked corrected QT segment prolongation (QTc 551 ms). Patient was admitted to intensive care unit for severe hypokalemia management and cardiac monitoring. Aggressive supplementation of electrolytes was initiated (), however despite supplementation with enteral and parenteral potassium as well as magnesium and phosphate, potassium level failed to increase () and subsequently she had a sinus bradycardia followed by asystole. Cardiopulmonary resuscitation was initiated when asystole was noted, return of spontaneous circulation was obtained after 8 minutes of resuscitation. Patient was mechanically ventilated for two days and her own efficient respiration was reestablished, then she was successfully extubated. During the following days, the patient was conscious, alert and oriented to time, place and person. Further laboratory testing revealed thyroid- stimulating hormone level was 1.100 mIU/L (reference 0.45−4.50 mIU/L). Active renin level was 0.653ng/ml/hr (reference 0.167−5.38 ng/ml/hr), aldosterone levels was <0.01 ng/dL (reference 0.00− 30 ng/dL). Creatine kinase (CK) level was 6922 U/L (reference 38–297 IU/L), indicating rhabdomyolysis. The arterial blood gas analysis revealed pH of 7.430, partial pressure of carbon dioxide was 29 mmHg; partial pressure of oxygen was 74 mmHg; HCO3 was 25 mmol/L and base excess of -4.7 mmol/L. Urinalysis showed dilute urine of 1.010 g/mL specific gravity (reference 1.005 to 1.030), Urine pH of 6.5, and no proteinuria. Urine electrolytes were measured on spot urine analysis and twenty-four-hour urine collection, result depicted in . Serial electrocardiogram monitoring showed resolution of ECG changes (). Follow up laboratory tests revealed normalization of electrolytes level (). Post cardiac arrest serial ECGs didn’t reveal any ischemic changes, cardiac enzymes were not elevated and echocardiogram revealed normal left ventricular systolic function, Ejection Fraction of 60–65%. Cardiac arrest was presumed to be secondary to severe hypokalemia and there was no necessity for further cardiac evaluation. She was then discharged from the hospital with recommendations for abstinence from alcohol. Follow up outpatient appointment with primary care physician was provided.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [113.0, 'mm hg'], 'Diastolic Blood Pressure': [71.0, 'mm hg']}",85,80.75,89.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 113.0 mm Hg + 2/3 * 71.0 mm Hg = 85.0 mm Hg.
Hence, the patient's mean arterial pressure is 85.0 mm Hg."
1680,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7992525-1,Extracted,"A 60-year-old female, known to have AML, with no clinical evidence of tuberous sclerosis (TS), presented in the emergency medicine department, with complaints of acute right flank pain, visible gross hematuria, dizziness, and vomiting, for 1 day duration. She was a known diabetic on insulin therapy. On examination, she was pale, her blood pressure (BP) was 111/70 mmHg, and heart rate (HR) was 111/min with a palpable tender mass in the right upper quadrant abdomen. Labs revealed hemoglobin (Hb) of 7 g/dl and her other labs including coagulation screen were normal. On admission in ward, her BP fell to 70/30 mmHg with HR 130/min. She was shifted to intensive care unit where her Hb had decreased to 3 g/dl. She was resuscitated with intravenous fluids and packed red blood cells. Once stabilized, emergency contrast-enhanced CT was done, which revealed 11 cm renal AML with bleeder fistulating into pelvicalyceal system. Emergency angiogram and transarterial selective embolization was done [Figures -]. Postprocedure, the patient's recovery was uneventful and she was discharged home after 1 week with Hb of 8 g/dl and normal renal functions. On follow-up after 1 month, she is doing well, and on ultrasound, AML size had decreased to 10.2 cm. She will be followed up in clinic for further embolization of AML, if required.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [30.0, 'mm hg'], 'Systolic Blood Pressure': [70.0, 'mm hg']}",43.33333,41.16666,45.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 70.0 mm Hg + 2/3 * 30.0 mm Hg = 43.33333 mm Hg.
Hence, the patient's mean arterial pressure is 43.33333 mm Hg."
1681,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7725577-1,Extracted,"A 36-year-old male with past medical history most significant for morbid obesity, obstructive sleep apnea, and marijuana use disorder presented to the hospital with complaints of pounding chest pain and shortness of breath. He was sitting on his couch and smoking marijuana, after which he developed a pounding sensation in his chest, dyspnea, and diaphoresis that lasted approximately 30 seconds after which emergency medical service was called. His symptoms had resolved by the time he reached the hospital. After reaching the emergency room, his symptoms returned, and he was found to be in a monomorphic wide-complex tachycardia at a ventricular rate of 240 beats per minute () and was saturating at 89% at room air. His blood pressure was 133/84 mmHg and had a respiratory rate of 16. He was started on IV amiodarone 150 mg over 10 minutes and was continued on a drip with a rate on 1 mg/min, which resolved the arrhythmia after the initial bolus (). He smokes 3 g marijuana daily. He denied the use of any drugs other than marijuana. He also denied any history of arrhythmia in the family.
An extensive workup was performed to find the cause of ventricular tachycardia. A urine toxicology report was significant only for cannabinoids in urine. Urine metanephrines and normetanephrines were within normal range. Serum magnesium was 1.7 mg/dL; potassium was 4.6 mmol/L at the time of admission. Troponin T levels were trended which remained negative for three occurrences. TSH was 0.903 IU/ml. Morning cortisol was 9.4 microgram/dL. Cardiac catheterization was performed to rule out ischemic causes of ventricular tachycardia, which showed normal coronaries. Echocardiogram obtained showed a left ventricular ejection fraction of 55-60% with normal valvular function, and no structural disease noted on echocardiogram. He was monitored on cardiac telemetry throughout his hospital course, and he was not found to have any further episodes of ventricular arrhythmias or ectopy.
With the consideration of ventricular tachycardia in a structurally normal heart and no coronary artery disease, he was started on metoprolol succinate 25 mg daily and was discharged with outpatient follow-up. He was provided education regarding marijuana cessation and was discussed.
He did undergo an electrophysiology study after discharge, which did not reveal any inducible ventricular or supraventricular tachycardia. A cardiac magnetic resonance imaging (MRI) was offered to the patient for further workup of arrhythmia; however, patient declined further workup. He has been continued on metoprolol succinate 25 mg and has remained asymptomatic since then.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [84.0, 'mm hg'], 'Systolic Blood Pressure': [133.0, 'mm hg']}",100.33333,95.31666,105.35,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 133.0 mm Hg + 2/3 * 84.0 mm Hg = 100.33333 mm Hg.
Hence, the patient's mean arterial pressure is 100.33333 mm Hg."
1682,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5703586-1,Extracted,"A 73-year-old right-handed African-American female with a past medical history of paroxysmal atrial fibrillation, Graves’ disease, and essential hypertension presented to the emergency room after the sudden onset of dysarthria and dysphagia six hours prior to the admission. Her dysarthria was marked such that she could not speak one word without significant difficulty. Her dysphagia was noted to solids and liquids when she attempted to drink water and eat chicken at a social function. The patient denied lateralizing weakness, vision loss, confusion, bladder/bowel incontinence, dystonia, or previous episodes of weakness. She did not have a previous history of cerebrovascular accident (CVA) or transient ischemic attack (TIA). She denied a history of recent head trauma, major surgery, gastrointestinal bleeding, bleeding diathesis, or known neurologic disease. The patient was taking methimazole for Graves’s disease, but four weeks prior to admission, it was held for a radioactive iodine and uptake scan. However, the patient was restarted on a reduced methimazole dose due to increased tremulousness, anxiety, and diarrhea two weeks prior to her presentation in our emergency room. The patient’s initial vital signs were significant for tachycardia up to 116 beats per minute and tachypnea up to 24 breaths per minute, with a presenting blood pressure of 142/84. The physical examination, including a full neurologic exam, revealed only moderate dysarthria with stuttering. The patient’s sensorium, cranial nerve examination, strength, and sensation were intact with no focal weakness, sensory deficits, or cerebellar signs. The National Institutes of Health Stroke Scale (NIHSS) score for the patient was three due to her speech difficulties; the airway, breathing, circulation, disability (ABCD) scores were five, and her premorbid Modified Rankin Score was zero. The laboratory findings on admission were significant for a thyroid stimulating hormone (TSH) level of 0.01 µIU/mL, free T4 of 4.43 ng/dL, and thyroid stimulating immunoglobulins of 537. Electrocardiogram showed sinus tachycardia with a rate of 116 beats per minute, normal axis, normal PR and QT intervals, and no ST segment or T wave changes. Computed tomography of the head (CTH) without contrast was negative for hemorrhage. She was admitted to the hospital for concern of CVA versus TIA. The patient did not receive intravenous tissue plasminogen activator (tPA) due to the duration of her symptoms as well as her low NIHSS score. Magnetic resonance imaging of the brain was negative for acute ischemic change or space-occupying lesion. Computed tomography angiography (CTA) of the head and neck demonstrated no significant intracranial arterial disease. Stroke laboratory evaluation including vitamin B12, homocysteine, human immunodeficiency virus and rapid plasma reagin were all unremarkable. Serial neurologic exams failed to show new or evolving neurological deficits. Despite her negative evaluation, her dysarthria persisted for more than 24 hours after initial hospitalization. Additionally, oropharyngeal dysphagia was appreciated on bedside swallow evaluation by speech therapy. Given the findings on initial laboratory studies, endocrinology was consulted for further recommendations. They increased her methimazole dose and started Propranolol. Within 48 hours of adjusting her anti-hyperthyroid medications, the patient’s dysarthria and dysphagia rapidly improved. Videofluoroscopy on day three of hospitalization showed no evidence of oropharyngeal dysphagia. The patient was discharged on 81 mg aspirin and 40 mg Atorvastatin with the follow-up to endocrinology and neurology as an outpatient. During the outpatient neurology evaluation, the patient continued to be free of dysarthria, dysphagia, and the stigmata of TIA or CVA.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [142.0, 'mm hg'], 'Diastolic Blood Pressure': [84.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 142.0 mm Hg + 2/3 * 84.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
1683,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6507808-1,Extracted,"The patient is a 6-year-old African male who presented at our tertiary surgical referral center in Central Africa after motor vehicle accident. His past medical, social, and family history were not obtained given that the patient spoke a Northern African dialect, whereas the staff at the local hospital spoke English and a Southern dialect. Furthermore, he presented without any family member or guardians, and one sheet of poorly documented medical history.
According to this record, he was struck by a motorcycle the preceding evening, approximately 12 hours prior to presentation. He was struck by a passing motorcyclist at an unknown speed, then launched and landed head-on into a large rock. This occurred at the border of Tanzania and Malawi which is approximately 150 miles from the tertiary hospital (Fig. ). He initially presented to the closest medical facility, where he was evaluated by an orthopedic clinical technician (the only available in-house staff). His presumptive diagnosis from the technician was a depressed skull fracture with exposed brain parenchyma. No other physical examination findings or vital signs were documented. Head and lateral cervical spine X-rays were performed prior to transfer. As the tertiary hospital was the closest hospital with surgical capabilities, he was transferred for further management by police car. The patient suffered a witnessed seizure during transfer. He arrived on the morning of 26 May 2018 to the intensive care unit (ICU) at tertiary hospital.
On primary trauma survey, he was noted to have an intact airway, breathing spontaneously, and had normal vital signs. His heart rate was 126 beats per minute, blood pressure was 128 mmHg systolic over 85 mmHg diastolic, temperature was 36.0 degrees Celsius, and he was breathing 33 times per minute. His initial Glasgow coma scale score was 11. He was given one point for eye opening as his eyelids were swollen shut; five points for best verbal response since he was able to converse appropriately; and five points for best motor response with localization of pain.
His secondary survey was notable for a small, 1 cm laceration in his right frontal cranium with blood and possible brain matter leaking from the defect (Fig. ). A makeshift cervical spine collar was applied loosely, with the patient’s head rotated ninety-degrees to the left. He had no cervical spine tenderness and his collar was reapplied. Pupillary exam was impaired by severe bilateral eyelid edema, and the patient had no lateralizing neurologic deficits otherwise. There were no physical examination findings suggestive of basilar skull fracture. The remainder of his examination revealed superficial abrasions to his bilateral lower extremities but no other traumatic injuries.
The patient’s initial work-up included a full blood count, type and cross-match for transfusion, and X-ray imaging of his head and lateral cervical spine. The X-rays were both performed at the primary medical facility. Head X-ray was of poor quality, but did not reveal any obvious injuries (Fig. ). Cervical spine X-ray imaging was lost on transfer, and repeating the cervical spine X-ray at the tertiary hospital would have delayed operative treatment. Cross-sectional imaging was not performed, as CT scanning is not available at the tertiary hospital. His full blood count was notable for a hemoglobin of 11.3 g/dl and platelet count of 202 (x106 u/ml).
He was placed on supplemental oxygen per nasal cannula. Due to his open and contaminated head laceration, intravenous ceftriaxone was administered for prophylaxis. He was also given phenytoin for seizure prophylaxis []. Again, phenytoin was the only available antiepileptic available. One pint of cross-matched whole blood was ordered on call to operating theater. Blood product fractionation is not practiced at the tertiary hospital due to logistical blood-banking constraints.
The patient arrived in the operating theater at 8 am on 26 May 2018. He was orotracheally intubated and general anesthesia was induced. The patient was prepped and draped in sterile fashion. Due to unforeseen circumstances, only the minor set of instruments were available for operation. Our suture options were limited to polyglactin (Vicryl), silk, and chromic gut.
Our operative course began with an evaluation of the patient’s open skull fracture. We noted a 2 cm laceration with obvious brain matter extravasating from the wound. A 10 cm curvilinear incision was made around the defect. A scalp flap was created around the defect and hemostasis was achieved. On closer inspection, there was a stellate compound skull fracture with visible contamination and exposed, devitalized brain matter. The bone and brain matter were debrided leaving a skull defect measuring approximately 7 cm by 8 cm overlying the right frontal lobe. No bipolar electrocautery device was available, so monopolar electrocautery was used to achieve hemostasis. The galea aponeurosis layer was then reapproximated over the cranial defect using 2–0 polyglactin suture. The scalp layer was closed with skin staples, thus concluding the operation (Fig. ).
Postoperatively, the patient was transferred back to the ICU. He was continued on ceftriaxone for seven days for meningitis prophylaxis. Sinus precautions were instituted with presumed sinus injury, as further imaging studies were unavailable. Given the severity of his traumatic brain injury (TBI), phenytoin was ordered to be continued for seven days, however the hospital supply of phenytoin was depleted after only two days. He did not suffer any post-traumatic seizures after surgery. He was able to follow commands on the fifth postoperative date after which his diet was advanced appropriately. He was transferred out of the ICU to the general pediatrics ward on the seventh postoperative date where he continued to improve.
The patient remained in the hospital into postoperative Day 14 for skin staple removal. He was then discharged home in good condition, tolerating a diet, following commands appropriately, and without any neurologic deficits. Most recently, he was seen in surgical clinic on 13 June 2018 and has continued to recover well.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [128.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",99.33333,94.36666,104.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 128.0 mm Hg + 2/3 * 85.0 mm Hg = 99.33333 mm Hg.
Hence, the patient's mean arterial pressure is 99.33333 mm Hg."
1684,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7263159-1,Extracted,"A 54-year-old Indonesian man with right quadrant abdominal pain persisting for more than 1 year visited Malaysia for transnational medical advice. He was diagnosed with inflammatory bowel disease in Indonesia after a colonoscopic examination in Indonesia. However, the patient did not know whether his disease was Crohn’s disease or ulcerative colitis, and he received the medication mesalazine accordingly. No diarrhea, body weight loss, bloody stool, vomiting, or fever was noted. He appeared comfortable throughout an examination. His blood pressure was 125/60 mmHg and he did not show tachycardia. He showed mild tenderness in the right lower quadrant area without rebound tenderness. An abdominal ultrasound scan showed fatty liver, gallbladder polyps, and a small left renal stone. No other laboratory testing was performed. Colonoscopy showed multiple ulcers in the cecum and a normal terminal ileum (). Biopsy was performed, and a histopathological examination showed fragments of cecal mucosa with foci of tissue degeneration and ulceration. The degenerated tissue areas were infiltrated and mixed with inflammatory exudates, and some areas showed neutrophilic infiltration, which caused microabscesses. Residual colonic mucosa showed mainly regularly spaced glands. A few clusters of microorganisms were observed using periodic acid–Schiff staining. Special stains for fungi and acid-fast bacilli were negative. The histopathological results were consistent with amebic colitis. (). The abdominal pain resolved after taking metronidazole 750 mg three times a day for 10 days and paromomycin 500 mg three times a day for 10 days. Repeated colonoscopy 1 year later showed total healing of the ulcers.
The CARE guidelines were followed. Ethics committee approval was not required because we presented only one case of a rare condition. The patient provided informed consent for publication of the case and we have also de-identified the details.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",81.66667,77.58334,85.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 60.0 mm Hg = 81.66667 mm Hg.
Hence, the patient's mean arterial pressure is 81.66667 mm Hg."
1685,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8569503-1,Extracted,"A 93-year-old female patient (weight, 32 kg; height, 130 cm) was scheduled for general anesthesia for the reconstruction of a soft tissue defect on her left cheek. She had no remarkable medical history, except for well-controlled hypertension. Preoperative chest radiography was normal and pulmonary function tests revealed normal respiratory function.
Glycopyrrolate (0.2 mg) was administered intramuscularly for premedication 30 min preoperatively. In the OR a standard monitoring, including pulse oximetry, electrocardiography, and non-invasive blood pressure measurement, was applied. Baseline vital signs included a heart rate (HR) of 64 bpm; blood pressure (BP), 188/85 mmHg; and blood oxygen saturation (SpO2), 92% on room air. General anesthesia was induced intravenously, using 40 mg of propofol, followed by continuous administration of remifentanil (0.26 mcg/kg/min), and 30 mg of rocuronium. Oral endotracheal intubation was performed with a direct laryngoscope and a 6.0-mm reinforced ETT. An anesthesia machine supplied a gas mixture with a fraction of inspired oxygen (FiO2) of 50% at a total flow rate of 2 L/min. Anesthesia was maintained using 5.0 vol% desflurane and 0.1 mcg/kg/min of remifentanil. The tidal volume and respiratory rate were set to 200 ml and 14 per min, respectively. After induction of anesthesia was completed, the patient’s posture and position of the anesthesia machine were adjusted. In facial surgery, we routinely place the anesthesia machine on the side of the patient’s right lower limb; therefore, the breathing circuit is naturally placed on the neck, chest, and abdomen.
Given that the scheduled operation time was 6 h, a BCW was applied routinely to prevent hypothermia during anesthesia. Once surgical site preparation was almost complete, the BCW was turned on. Immediately, there was a spark with a popping sound, and smoke and flames could be seen at the patient’s end of the breathing circuit (Fig. ). An anesthesiologist and an anesthesiology resident doctor were participating in induction of anesthesia. The anesthesiologist disconnected the ETT and the breathing circuit and turned off the anesthesia machine and gas supply, within 10 s of the fire starting. Anesthesiology resident doctor extinguished the flames on the patient’s clothing by pouring water. After the fire had been completely extinguished, ventilation was restarted with an Ambu bag with 100% oxygen. The vital signs at that moment were as follows: HR, 72 bpm; BP, 159/63 mmHg; body temperature, 36.5 °C; and SpO2, 100%. As there was a significant amount of soot inside the ETT (Fig. ), we observed the upper airway using fiber-optic bronchoscopy (FOB). Soot was observed in the trachea and carina. The ETT was replaced with a new same-sized reinforced ETT using a video laryngoscope. After the fire, general anesthesia was switched from inhalation to total intravenous anesthesia and the surgery was suspended. At that time, the results of her arterial blood gas analysis were as follows: PH 7.401; PCO2, 49.5 mmHg; PO2 202.9 mmHg; and SaO2, 99.7%. The patient was transferred to an intensive care unit (ICU) with stable vital signs.
Upon arrival in the ICU, the patient underwent bronchoscopy by a pulmonologist. On FOB, no airway mucosal swelling or narrowing was observed; however, much soot were found in the carina, right main bronchus, left main bronchus, and right upper lobal bronchus (Fig. ). During bronchoscopy, the pulmonologist tried using normal saline irrigation to remove the soot to no avail. Salbutamol, N-acetylcysteine nebulizer, budesonide nebulizer, and hydrocortisone 50 mg intravenously were administered twice daily to prevent airway complications []. Prophylactic antibiotic treatment was initiated with piperacillin and tazobactam. The patient was positioned with head elevated during mechanical ventilation. There were no respiratory infection source in the culture tests performed during hospitalization. Medical treatments for inhalation burn was continued until day 26, at the time of complete weaning of mechanical ventilation.
On the third day after the inhalation burn event, mucosal erythematous edema was observed on FOB (Fig. ). Tracheostomy was necessary for the treatment of the patient, and plastic surgery could not be postponed any longer, so we decided to proceed the two surgeries together. On the fourth day, the patient underwent the originally planned plastic surgery and tracheostomy under general anesthesia without any complications. On the sixth day, the first ventilator-weaning trial failed and she was placed on a portable ventilator. Deep breathing and expectorant training were initiated at the bedside. Afterward, daytime ventilator weaning was gradually performed. On the fourteenth day, significant granulation tissue and secretion were observed in the distal trachea and carina (Fig. a). On the seventeenth day, the mucus was dried in the trachea, and granulation tissue was reduced compared to prior observations (Fig. b). By the twenty-first day, the upper respiratory tract epithelium and mucosa had normalized (Fig. c). The ventilator was completely weaned on the twenty-fourth day. On the twenty-sixth day, she was transferred to the Department of Rehabilitation Medicine for swallowing rehabilitation and rehabilitation for delirium that occurred during hospitalization. On the thirty-fourth day, granulation tissue was no longer observed, and upper respiratory tract epithelium and mucosa recovery were almost complete (Fig. d). On the thirty-eighth day, the patient underwent tracheostomy closure surgery under local anesthesia. She was discharged from the hospital 40 days after the burn event.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [188.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",119.33333,113.36666,125.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 188.0 mm Hg + 2/3 * 85.0 mm Hg = 119.33333 mm Hg.
Hence, the patient's mean arterial pressure is 119.33333 mm Hg."
1686,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7482335-1,Extracted,"A 39-year-old man was brought to our ED, 3 hours after ingesting a raw tuber plant with suicidal intent. He had swollen lips and tongue, drooling of saliva, and also minimal breathing discomfort (). He developed these symptoms within 30 minutes of ingestion. His vital signs were heart rate 120/minute, blood pressure 130/80 mm Hg, SpO2 98% at room air, and respiratory rate 28/minute. In view of angioedema secondary to unknown tuber poisoning, he was placed in a propped-up position with oxygen by simple face mask, and also was given chlorpheniramine maleate 10 mg and hydrocortisone 100 mg intravenously. Meanwhile, endotracheal intubation was planned with rescue option being surgical airway (cricothyroidotomy), if needed. With adrenaline 5 mL (1:1,000) nebulization, he remained stable and hence intubation was deferred. With repeated adrenaline nebulization over the next 2 hours, angioedema reduced significantly and further he did not develop any new symptoms. He received maintenance doses of chlorpheniramine maleate and hydrocortisone during hospitalization. His routine laboratory investigations were normal except for asymptomatic mild hypokalemia (2.9 mEq/L) and was discharged after 4 days.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1687,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6876902-1,Extracted,"An 86-year-old man was referred to our ED by his general practitioner. He complained of fatigue, lower back pain, mild abdominal discomfort, and pre-syncope. He was an ex-smoker, a long-standing, well-controlled hypertensive patient on an angiotensin-converting enzyme inhibitor who had otherwise been “well.”
Besides relative hypotension (blood pressure measured 106/58 mmHg in both arms) in the ED, the rest of the patient’s vital signs were within normal limits (heart rate 86 beats per minute, respiratory rate 20 breaths per minute, oxygen saturation 94% on room air). There was mild abdominal tenderness, but no pulsatile mass was detected. The rest of the examination was non-contributory.
A urine dipstick showed a trace of blood. Venous blood gas showed signs of mild hypoperfusion (base excess -6 mmol/L) and a slightly elevated lactate level (3 mmol/L). His hemoglobin was normal.
A bedside ultrasound was performed by the on-duty emergency physician with the portable Mindray M7 C5-2s adult convex probe (Mindray Medical International Limited, Shenzhen, China). It revealed a large 8 x 9cm infrarenal AAA (Figure ). There were heterogeneous areas of fresh hemorrhage and/or dissection within the aneurysmal thrombus structure: a very unstable condition, as bleeding or dissection into the intraluminal thrombus in abdominal aortic aneurysms is associated with rupture [-].
CT showed a large AAA with a homogenous thrombus surrounding a central lumen: a precarious but “stable” condition (Figure ). The size was the same as determined with the point-of-care ultrasound.
The patient was referred to the vascular service for urgent surgical intervention.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [58.0, 'mm hg'], 'Systolic Blood Pressure': [106.0, 'mm hg']}",74,70.3,77.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 106.0 mm Hg + 2/3 * 58.0 mm Hg = 74.0 mm Hg.
Hence, the patient's mean arterial pressure is 74.0 mm Hg."
1688,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7249895-1,Extracted,"A 72-year old male patient was admitted with a 1-year history of intermittent dyspnea, which was exacerbated for 1 day. The patient was diagnosed with pulmonary heart disease at the local hospital 1 year prior to this incident. Since then, long-term oxygen therapy has been performed. Six months prior to this incident, the patient was treated in our department for dyspnea and unconsciousness. A tracheotomy was performed and the patient had been carrying a tracheotomy cannula for 6 months. One day prior to admission to our hospital, the patient presented with cyanosis due to an exacerbation of dyspnea. The patient's caretakers noticed increasing difficulty in sputum aspiration. In addition, the patient had a prior history of chronic obstructive pulmonary emphysema for more than 30 years, bilateral pulmonary bullae for more than 20 years, cerebral infarction 1 year earlier, and an old myocardial infarction without stent implantation and drug application for 2 years.
The patient was examined in the emergency department. Vital signs: temperature 36.5°C, heart rate 130 beats per minute, respiratory rate 30 times per minute, blood pressure 145/97 mmHg, and blood oxygen saturation 60%. The physical examination showed that the patient was obese and looked sick with signs of cyanosis, wet rales in the bilateral lungs, pitting edema of the lower extremities, and sluggish pupillary light reflex. Arterial blood gas results: PO2 69.1 mmHg, Hct 60.2, Na+ 133.7 mmol/L, K+ 4.98 mmol/L, Ca2+ 1.008 mmol/L, Glu 7.1 mmol/L, Lac 1.4 mmol/L, tHb 166.3 g/L, HCO3− 31.4 mmol/L, and PCT <0.10 μg/L.
Chest computed tomography (CT) imaging revealed narrowing of the trachea, bilateral exudative lesions, and bilateral pulmonary bullae (Fig. ). The patient was diagnosed of pneumonia. The complete medical diagnosis was an acute exacerbation of chronic obstructive pulmonary disease (COPD), double lung pneumonia, pulmonary bullae, and type II respiratory failure, post-tracheotomy.
After hospital admission, the patient was immediately provided with invasive ventilator-assisted ventilation. However, his difficulty in breathing was not relieved. The blood oxygen saturation remained between 60% and 80%. The ventilator alarm indicated high airway resistance and the nurses were unable to insert the suction pipes into the airway. Immediate fiberoptic bronchoscopy showed diffuse edema and stenosis of the inferior tracheal airways (Fig. ).
Given that stent implementation and other treatment strategies were not supplied in this critical situation, we first selected a particular cannula size specific for obese patients. However, the cannula was not long enough to completely expand the narrowed airway. For this reason, tracheal intubation was used to temporarily replace the tracheotomy cannula, which successfully expanded the narrowed airways. The blood oxygen saturation returned to normal, and the symptoms were quickly relieved. After 2 days of treatment and observation in our department, the patient was stable and transferred to the pulmonary and critical care department for further treatment of airway stenosis. Supporting ventilation was withdrawn prior to the transfer.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [145.0, 'mm hg'], 'Diastolic Blood Pressure': [97.0, 'mm hg']}",113,107.35,118.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 145.0 mm Hg + 2/3 * 97.0 mm Hg = 113.0 mm Hg.
Hence, the patient's mean arterial pressure is 113.0 mm Hg."
1689,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3841542-1,Extracted,"A 47-year-old diabetic man had a stab wound to his right buttock inflicted by his roommate using a kitchen knife. On examination, his pulse was 75 beats/min and his blood pressure (BP) was 100/50 mmHg. The abdomen was soft and not tender. A single wound was seen on the medial side of the right gluteal area superior to the intertrochanteric plane []. No neurological deficits were detected. Arterial pulses of the lower limbs were well-felt. The wound was sutured in the Emergency Department and patient was scheduled for discharge. Patient felt dizzy, complained of fresh bleeding per rectum and fainted before being sent home. At this stage, his pulse rate was 105 beats/min and his BP had dropped to 65/40 mmHg. Patient was resuscitated with crystalloids and he became hemodynamically stable. Rigid sigmoidoscopic examination was performed under general anesthesia and showed blood clots in the rectum with no active bleeding. No obvious injury to the rectal wall was seen despite the injection of methylene blue through the gluteal wound. Patient was admitted to the surgical ward for close observation. He was kept fasting, had intravenous fluids and antibiotics were administered. Two days later, patient complained of lower abdominal pain. Fecal matter passed through the gluteal wound. Patient had a temperature of 38°C. There was tenderness and guarding in the lower abdomen. Abdominal computed tomography (CT) scan with oral, rectal and intravenous contrast was performed. It showed contrast leakage from the posterior wall of the rectum, intraperitoneal free air and air in the mesentery around the rectum [Figures and ]. Exploratory laparotomy was performed. No intraperitoneal fecal soiling was seen. Nevertheless, there was a significant amount of air in the retroperitoneal space and in the bowel mesentery []. The rectum was mobilized, but the extraperitoneal perforation could not be seen. Hartmann's procedure was performed. Gluteal wound exploration revealed a deep laceration lateral to the edge of the sacrum. Debridement of the necrotic tissue was performed. Post-operatively, patient had slow recovery because of intestinal ileus. The colostomy started to function on the fourth post-operative day. Patient recovered completely at day 10 and was scheduled for reversal of the Hartmann's procedure 12 weeks after surgery. He decided to travel overseas to his home country to continue his treatment.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [50.0, 'mm hg']}",66.66667,63.33334,70,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 50.0 mm Hg = 66.66667 mm Hg.
Hence, the patient's mean arterial pressure is 66.66667 mm Hg."
1690,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6825431-1,Extracted,"A 27-year-old female with a past medical history of chronic pain syndrome presented to the emergency department (ED) with complaints of generalized body fatigue and pain, with severe retrosternal chest pain over four hours duration, which initially worsened on lying down and improved with sitting up. On her presentation in the ED, the heart rate was 89 beats per minute, blood pressure was 128/80 mm Hg, and oxygen saturation was 100% on room air. Initial electrocardiogram (EKG) showed diffuse ST-segment elevations in anterior (V4 through V6) and inferior leads (II, III, aVF) (Figure ). She presented in the past with similar symptoms and was under management by the pain clinic for chronic pain syndrome.
Routine investigations were sent and serial troponin levels were measured. The first troponin was 0.023 (normal high 0.040 ng/ml). An emergent echocardiogram (ECHO) was done, which showed a preserved ejection fraction with no regional wall motion abnormalities. A repeat EKG after 15 minutes showed persistent ST elevation without any evolutionary changes typical of ST-elevation myocardial infarction (STEMI). This presentation with atypical chest pain, negative cardiac biomarkers, and normal ECHO was more compatible with acute pericarditis rather than acute coronary syndrome (ACS). The patient was admitted for close monitoring and further workup. Empiric treatment for possible pericarditis was started and the patient was followed by serial EKGs and cardiac biomarkers while awaiting the lab work.
A repeat EKG was done four hours post-presentation, which showed a resolution of ST changes that were seen initially (Figure ). Troponin was repeated, and this time, it was found to be elevated at 2.3 ng/ml. Despite the atypical nature of chest pain and normal ECHO findings, the dynamic EKG changes and new elevation in troponin prompted a diagnostic coronary angiogram to look for ischemic etiology. Coronary angiogram showed fresh in-situ thrombus in the proximal left anterior descending artery (LAD) with thrombolysis in myocardial infarction (TIMI) 3 flow across the lesion (Figure ). An aspiration thrombectomy was done, following which there was no residual thrombus burden with TIMI 3 flow (Figure ). The patient reported relief in her chest pain post-intervention. However, percutaneous intervention with stent placement was not considered appropriate, as there was no evidence of underlying atherosclerotic heart disease.
After stabilizing the patient, further detailed history revealed a previously documented APS with recurrent peripheral arterial thrombosis and multiple peripheral thrombectomies in the past. Prior to her presentation, she was kept on triple anticoagulation maintenance therapy with warfarin, aspirin 81 mg daily, and clopidogrel 75 mg daily for recurrent arterial thrombosis. However, on presentation, her international normalized ratio was in the sub-therapeutic range at 1.1, due to a lack of compliance with her medications, including warfarin.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [128.0, 'mm hg']}",96,91.2,100.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 128.0 mm Hg + 2/3 * 80.0 mm Hg = 96.0 mm Hg.
Hence, the patient's mean arterial pressure is 96.0 mm Hg."
1691,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3989827-1,Extracted,"A 12-year-old girl presented to our hospital with a history of abnormal menstruation and progressive hirsutism. She had a normal childhood until 2 years back when she started noticing appearance of hair on her face, body, extremities and pubic region. Her height, weight and body mass index were within the normal limits. Blood pressure was 104/64 mm Hg and pulse rate was 92 beats/min. There was thick black hair on the face, arms, chest, back, legs and over the pubic region. Her breasts were pre-pubertal. Pelvic examination showed enlargement of the clitoris. Results of routine lab studies including serum electrolytes were normal.
Abdominal and pelvic ultrasonography showed the presence of 10 cm × 8 cm sized well- defined, primarily hyperechoic mass lesion seen in the right adrenal region with indentation of the adjacent surface of liver and kidney. The uterus appeared small in size. Multi-detector computed tomography (MDCT) of abdomen, plain and contrast, showed a large well-defined heterogeneously enhancing predominantly fat attenuating lesion measuring 9.5 cm × 8.7 cm × 8.0 cm involving the right adrenal gland. The lesion demonstrated multifocal area of nodular calcification with enhancing solid component and was seen compressing the superolateral aspect of the right kidney with the minimal inferomedial displacement [Figure and ]. Blood tests were carried out for functional assessment of the right adrenal tumor. Serum testosterone level was raised to 2.24 ng/ml. Serum adrenocorticotrophic hormone, 17 hydroxyprogesterone, progesterone and cortisol levels as well as urinary 17 keto steroids, 17 hydroxy corticosteriods and vanilylmandelic acid levels were normal. A clinical diagnosis of adrenal myelolipoma was made and right adrenalectomy was performed. The specimen showed an encapsulated tumor measuring 10 cm × 8 cm × 7 cm []. Microscopic examination showed compressed adrenal tissue with foci of hemorrhage within the well- encapsulated tumor. The tumor nodules were primarily composed of eosinophilic lipid poor cells resembling zona reticularis. Mitotic rate was <5/50 hpf. No atypical mitosis was seen. The tumor nodules were separated by bands of hyalinized fibrous tissue containing proliferating thick walled vessels, hemorrhagic foci and sparse lymphocytic infiltrate. Islands of abundant mature adipose tissue were also seen. Scattered foci containing lipofuscin pigment were seen and no vascular/capsular invasion or necrosis was seen [].
Based on the size, weight of tumor, microscopic features and Weiss criteria a final diagnosis of lipoadenoma, a morphological variant of adenoma was made.
Post-operatively serum testosterone level returned to 0.158 ng/ml, which was within the normal limits. Patient's menstrual cycles regularized and features of hirsutism decreased [].",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [104.0, 'mm hg'], 'Diastolic Blood Pressure': [64.0, 'mm hg']}",77.33333,73.46666,81.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 104.0 mm Hg + 2/3 * 64.0 mm Hg = 77.33333 mm Hg.
Hence, the patient's mean arterial pressure is 77.33333 mm Hg."
1692,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5095,Extracted,"A 60-year-old man with known history of chronic obstructive pulmonary disease is brought by ambulance to the emergency department due to shortness of breath. He is out of breath and cannot string a sentence together. The emergency technician suggests that the man tried his tiotropium inhaler multiple times without success. The patient's vitals are as follows: afebrile, BP 90/60, HR 120, RR 24. Oxygen saturation is 90%. An EKG is obtained that shows narrow-complex tachycardia with irregular P waves preceding each QRS complex and irregular PR intervals.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",70,66.5,73.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 60.0 mm Hg = 70.0 mm Hg.
Hence, the patient's mean arterial pressure is 70.0 mm Hg."
1693,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4359532-1,Extracted,"A 62 year old Caucasian female patient (height - 1.60 m, weight 72 kg, BMI 28.1) was admitted to hospital with AKI (patient’s baseline serum creatinine was 85 μmol/L and eGFR was 63 ml/min/1.73 m2 by MDRD equation) whilst on treatment for mastoiditis. Her background medical history included hypertension, and type 2 diabetes for which she was on regular sitagliptin-metformin 50/1000 mg half tablet twice a day, metoprolol 25 mg twice daily, lisinopril 10 mg daily and simvastatin 40 mg daily. She had a long medical history of recurrent otitis media for which she required grommet insertion. She was managed as outpatient with topical and oral ciprofloxacin by her otolaryngologist. Trial of oral trimethoprim-sulphamethaxazole (Bactrim DS) was prescribed without much clinical improvement. Eight weeks prior to this admission, she had symptoms of earache, localised post auricular swelling and fever. A CT scan showed mastoiditis and a contiguous subperiosteal abscess. A brain Magnetic Resonance Imaging (MRI) scan and Technetium 99 m labelled bone scan which revealed osteomyelitis (OM) of the petrous temporal bone (Figure ). She underwent an emergency cortical mastoidectomy with drainage of the abscess and insertion of a new right ear grommet. Empirical therapy with ticarcillin-clavulanate (12.4 grams/day) was commenced.
A surface swab from the ear isolated Escherichia coli (which was sensitive to ticarcillin-clavulanate, piperacillin-tazobactam, cefepime and gentamicin, but resistant to ceftriaxone and ciprofloxacin). Susceptibilities were done using Vitek2 (Biomerieux, Marcy l’Etolie, France) using standard Gram negative card. Based on the antibiogram the isolate most likely had underlying extended spectrum beta lactamase, although confirmatory testing was not done as per current testing policy (non-sterile site isolate). The operative specimens of pus and tissue taken at the time of surgery remained sterile. Her antibiotic was changed to cefepime (6 grams/day).
She made good progress and was discharged with a plan of continuing cefepime for 6 weeks as treatment of OM on ambulatory care basis. After 2 weeks of therapy, she developed malaise and dysgeusia. At 4 weeks, she developed renal impairment (serum creatinine-140 μmol/L) and the cefepime dose was reduced to 4 grams/day. Her blood pressure at time was 130/82 mmHg. There was no fever, rash or peripheral oedema. Urine analysis done by automated iQ200 (Iris Diagnostics, Chatsworth, CA) machine and manual phase contrast microscopy showed WBC of <10 × 106 /L, no RBC and no presence of either WBC/RBC casts. 24 hour urine collection (of 2.47 L) had proteinuria of 0.77 g/day (normal range-0.08-0.15 g/day). C reactive protein was 3 mg/L (normal < 5 mg/L). At week 5 into therapy, she was noted to have worsening AKI (serum creatinine 225 μmol/L) and was admitted for further investigation (Figure ). She suffered the ‘injury stage’ of AKI according to Risk Injury Failure Loss of kidney function and End stage renal failure (RIFLE) criteria and stage 3 of Acute Kidney Injury Network (AKIN) classification at admission []. At this stage she was also noted to have serum potassium of 6.1 mmol/L (range 3.5-5 mmol/L) ,serum sodium of 148 mmol/L (range 135-145 mmol/L), serum chloride was 90 mmol/L (range 97-107 mmol/L) and blood urea of 15 mmol/L (range 2.5-7.5 mmol/L). There were no new medications including non-steroidal anti-inflammatory drugs (NSAIDs), chinese herbal supplements or any other form of naturotherapy that were taken by her.
During her inpatient stay all medications except metoprolol were ceased. Though she was clinically euvolaemic and suffered from non-oliguric renal failure, 36 hours trial of intravenous hydration with normal saline (0.9% w/v) at 80 ml/hour was administered with minimal effect on serum creatinine, blood urea and serum electrolytes. Marginal increase of urine output was noted which was commensurate with the intravenous fluid administered. Laboratory investigations of aetiology of AKI were negative or not detected. This included: Double stranded DNAs, ANCA, extractable nuclear antigens, rheumatoid factor, serum and urine protein electrophoresis, complement levels, immunoglobulin subclasses, streptococcal serology and hepatitis B and C serology. An ANA titre of 1:1280 (homogenous pattern) was noted and was thought to be related as a reaction due to cefepime therapy. Renal ultrasound revealed normal renal size, parenchyma and no obstructive uropathy. A renal biopsy showed moderate tubular atrophy with many intra-tubular casts in the medullary area. A few tubules were distended with cellular debris and acute inflammatory exudate (acute tubulitis). Moderate interstitial fibrosis was present with patchy areas of inflammatory infiltrates comprising predominantly lymphocytes, plasma cells and neutrophils. Eosinophils were not detected in the renal biopsy. Periodic acid Schiff stain and Gomori -silver stain were negative on the biopsy. Immunofluorescence staining was negative for IgA, IgG, IgM, kappa and lambda light chains, C1q, C3, amyloid and fibrinogen. Electron microscopy did not reveal any glomerular abnormality. (Figure )
It was concluded that this patient had drug-induced AIN, most likely related to cefepime. Cessation of the antibiotic led to a rapid improvement in her renal function over a week and therefore it was decided to treat her conservatively. The serum creatinine dropped from 295 μmol/L to 170 μmol/L within a week and then continued to trend downwards reaching up to 150 μmol/L on her 2 weekly follow-up post discharge. Her symptoms of malaise and dysgeusia had also abated at this visit. All the electrolytes (sodium, potassium and chloride) including blood urea were within normal ranges at this stage. Corticosteroid was not administered due to partially treated infection, diabetes and rapid improvement in renal function after cessation of antibiotics.
For completion of therapy (another 2 weeks) oral ciprofloxacin 500 mg twice daily was commenced, mindful of the fact that the isolate was resistant to ciprofloxacin with a minimal inhibitory concentration of 4 mg/L. Following discharge from hospital, she remained asymptomatic and continued to improve from her infection perspective. Sitagliptin-metformin, lisinopril and simvastatin were slowly reintroduced over the next 3 months after discharge while her renal function continued to improve.
Table shows the temporal trend in the biochemical parameters including serum creatinine and eGFR. Although serum creatinine has plateaued, mild renal impairment still exists at 8 months of follow-up (serum creatinine of 130 μmol/L and eGFR of 56 ml/min/1.73 m2).
This adverse drug reaction has been recorded permanently in her electronic medical records and also has been reported to Australian Therapeutic goods administration (TGA).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [82.0, 'mm hg']}",98,93.1,102.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 82.0 mm Hg = 98.0 mm Hg.
Hence, the patient's mean arterial pressure is 98.0 mm Hg."
1694,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8443101-1,Extracted,"A 15-year-old male presented to the clinic with complaints of fever for 3 weeks, swelling of the body for 2 weeks and reduced urine output for 1 week. Fever was intermittent up to 102°F. Swelling was noted around the eyes initially with gradual progression to involve the whole body with associated oliguria. He denied history of hematuria. There was no history of joint pain, oral ulcer, photosensitivity, malar rash, or alopecia. On examination, patient's general condition was fair. His blood pressure was 138/90 mm Hg, pulse rate 88 per minute, respiratory rate 16 per minute and temperature was 100.2°F. General examination revealed pallor, right cervical and axillary lymphadenopathy and pedal edema. Lymph nodes were small (2 × 2 cm), firm, mobile, and non-tender. Per abdomen examination was noteworthy for hepatosplenomegaly (liver span of 16 cm and palpable spleen 2 cm below the costal margin) in addition to free fluid. Chest, cardiovascular and neurological systems were within normal limits. Laboratory parameters were as following: hemoglobin 7.3 g/dl, total leucocyte count 2800 per mm3, platelet count 64000 per μL, serum creatinine 1.7 mg/dl (150.28 μmol/L), serum albumin 1.2 g/dl (normal range: 3.4–4.6 g/dl) and 24-hour urine protein 6.5 g/day. Serum complement 3 (C3) and C4 were both low; while ANA, performed by indirect immunofluorescence assay (IFA) and enzyme-linked immunoassay (ELISA), was negative. Hemolytic work up was negative except positive anti-IgG direct Coombs' test. Tropical fever work-up, which included malaria, scrub typhus, leptospirosis, and Leishmaniasis, was negative. Blood and urine culture were sterile. Epstein Barr Virus serology and cytomegalovirus polymerase chain reaction were negative. Fever had resolved after 2 days of admission, however, pancytopenia persisted. Bone marrow aspiration and biopsy, done in view of persistent pancytopenia, revealed hemophagocytosis with no evidence of atypical cells. Cervical lymph node biopsy was suggestive of reactive lymphoid hyperplasia. In view of persistent nephrotic state with renal dysfunction and pancytopenia, possibilities of post-infectious glomerulonephritis and autoimmune disease (like SLE) were considered. After stabilization with packed cells and platelet transfusion, a renal biopsy was performed. The biopsy was suggestive of proliferative glomerulonephritis, with 5 out of 18 glomeruli showing cellular crescents, 12 glomeruli showing endocapillary proliferation, 14 glomeruli showing wire loop lesions and hyaline thrombi and interstitial fibrosis/tubular atrophy involving 10–15% of cortical area []. Direct immunofluorescence showed coarse granular deposits of IgG (3+), IgA (2+), kappa (3+), lambda (3+), C3 (2+) and C1q (2+) along the capillary wall and mesangium []. Electron microscopy showed subendothelial and mesangial deposits []. Renal pathology was consistent with class IV LN. However, both ANA as well as anti-double stranded deoxyribonucleic acid (anti-dsDNA) were negative. In view of severe nephrotic state, oral prednisolone at a dose of 1 mg/kg/day was started. After 4 weeks of starting therapy, hematological abnormalities improved, serum albumin was 1.8 g/dl, serum creatinine was 1.4 mg/dl and 24-hour proteinuria declined to 4.5 g/day. Repeat serology and complements at this time revealed positive ANA (+2 homogenous, 1:80 dilution by IFA) and anti-dsDNA (42 IU/ml by ELISA) along with persistent low C3 and normal C4 levels. Low fixed dose cyclophosphamide as per Euro Lupus Regimen[] was started as an adjunctive immunosuppressive therapy as a diagnosis of SLE with LN (class IV) was now made. At the end of 3 months of therapy, patient was in partial remission with proteinuria of 1.8 g/day, serum albumin of 3.7 g/dl and serum creatinine of 0.8 mg/dl. His complete blood count showed hemoglobin of 11.8 g/dl, total leucocyte count of 5600 per mm3 and platelet count of 2,18,000 per μL. Mycophenolate mofetil (1 g/day) along with oral steroids (5 mg/day) was started as maintenance therapy. At the last visit (5 months into illness), his serum albumin was 3.8 g/dl, serum creatinine 0.9 mg/dl and proteinuria was 0.89 g/day.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [138.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106,100.7,111.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 138.0 mm Hg + 2/3 * 90.0 mm Hg = 106.0 mm Hg.
Hence, the patient's mean arterial pressure is 106.0 mm Hg."
1695,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4630261-1,Extracted,"A 38-year-old female was admitted to the University of Malaya Medical Centre (UMMC), Kuala Lumpur after 5 days of fever with right hypochondriac region abdominal pain, persistent vomiting, myalgia, headache and an episode of epistaxis. She also complained of passing tea-colored urine for 3 days duration and 2 days history of dry cough with right-sided pleuritic chest pain. There was no recent travel history and other household members were well. She denied any substance abuse, had blood transfusion or consumed any herbal or traditional medicines. There was no past medical and family history of connective tissue diseases (CTD) or hepatitis. She was not on any immunosuppressant or other regular medications and CTD screening was not performed. On admission, she was alert and deeply jaundiced. She was found to be febrile (38.6 °C), normotensive (110/70 mmHg) but tachycardic (100 bpm). There was no flapping tremor to suggest hepatic encephalopathy. The abdomen was generally soft with tender hepatomegaly. Cardiovascular, respiratory and neurological examinations were unremarkable.
Her full blood count showed leukopenia and thrombocytopenia (Fig. a). Her liver function tests showed marked elevation of transaminases as well as hyperbilirubinemia and hypoalbuminemia (Fig. b). Her coagulation profile showed deranged international normalized ratio (INR) values and prolonged activated partial thromboplastin time (aPTT) accompanied with hypofibrinogenemia (Fig. c). Abdominal ultrasound revealed non-specific increased in peri-portal echogenicity with ‘starry sky’ appearance, consistent with acute hepatitis. There was neither biliary obstruction nor ascites noted. She was hydrated with maintenance normal saline drip of 1 cc/kg/h. She was empirically started on intravenous infusion (IVI) Ceftriaxone and given intravenous vitamin K 10 mg once daily. She was tested negative for malaria, hepatitis B and C. Paracetamol and salicylate levels were undetectable. Blood cultures were negative for any bacterial or fungal growth.
At day 2 of admission (day 7 of illness), she remained alert but tachycardic. IgM serology test for dengue was positive. Clinical examination revealed minimal right-sided pleural effusion. In view of the worsening coagulation profile, she was transfused with 4 units of fresh frozen plasma and four units of cryoprecipitate. There was no bleeding tendency. Throughout her stay, her urine output and blood pressure were satisfactory. Thrombotic thrombocytopenic purpura (TTP) was ruled out as the peripheral blood film (PBF) was not suggestive and her renal function was normal. However, she was found to have splenomegaly.
By day 4 of hospitalization (day 9 of illness), she became confused and drowsy. Her Glasgow Coma Scale (GCS) was 9/15 (E3V1M5). Kernig’s sign was negative. Pupils were 5 mm equal and reactive bilaterally. She remained afebrile. Her blood pressure (BP) was 105/75 mmHg with heart rate 144 beats per minute. There was no focal neurological deficit with bilateral down-going plantar. Plain computed tomography (CT) of the brain showed no evidence of intracranial bleed or focal lesion. In view of the profound thrombocytopenia as well as marked coagulopathy, a lumbar puncture was not performed. She was electively intubated due to deteriorating conscious level and for airway protection. Broad-spectrum antibiotics were introduced which included IVI meropenem and IVI azithromycin. Blood products were transfused in an attempt to correct her coagulopathy. The gastroenterology team was consulted for her worsening liver function and she was started on IVI N-acetyl cysteine. Her serum ferritin on day 6 of illness was 6307.33 µg/L, suggesting possible macrophage activation syndrome (MAS) or HPS secondary to dengue virus infection. Intravenous dexamethasone of 8.00 mg TID was started. A bone marrow trephine and aspiration (BMAT) was performed to confirm this diagnosis.
On day 5 of hospitalization (day 10 of illness), she became polyuric. A repeated CT brain imaging showed gross generalized cerebral oedema. Further investigations confirmed a diagnosis of cranial diabetes insipidus (DI). The hematologist reviewed the BMAT, which showed minimal histiocytes that was less likely to be diagnostic for HLH. However, a diagnosis of dengue virus infection associated with subsequent HPS was established due to elevated serum level of HPS biomarkers and other clinical diagnostic criteria (Pal et al. ). Serum HPS biomarkers including ferritin, haptoglobin, soluble CD163 (sCD163) and soluble CD25 (sCD25) were measured. Her ferritin level peaked on day 2 of hospitalization (day 7 of illness) at 13,670.00 µg/mL and decreased thereafter (Fig. d). Soluble haptoglobin, CD163 and CD25 determined using commercially available enzyme-linked immunosorbent assay kits (Genway, San Diego; R&D System, Minneapolis) showed a very low level of haptoglobin (0.05 g/L) compared to healthy donor group with mean value of 228.49 g/L (data not shown). Highly elevated levels of sCD163 and sCD25 with values of 4750.00 ng/mL and 4191.00 pg/mL, respectively, in comparison to mean values of 261.65 ng/mL (sCD163) and 483.69 pg/mL (sCD25) of a group of healthy donors (n = 39) (data not shown) were observed. Despite our best effort and aggressive medical intervention, the patient succumbed to her ordeal by day 10 of hospitalization.
Tissue specimens of bone marrow, peritoneal fluid and throat swab obtained during post-mortem were used for nucleic acid amplification assays using general Flavivirus amplification primers (Teoh et al. ). Only the bone marrow tissue sample was positive for partial sequences of non-structural proteins NS1, NS2A, NS4b and NS5. Bidirectional DNA sequencing results confirmed the presence of nucleotide sequences matching that of DENV-2 with 99 % sequence similarity (data not shown).
Dengue viruses can cause a spectrum of disease ranging from mild flu-like fever to hemorrhagic fever with severe intravascular leakages and hypovolemic shock (Martina et al. ). The 2009 revised World Health Organization (WHO) dengue classification characterized severe dengue as dengue with severe plasma leakage, severe organ impairment or severe hemorrhage (World Health Organization and the Special Programme for Research and Training in Tropical Diseases (TDR) ). Although a clear molecular mechanism leading to severe dengue is still not well understood, it is thought that macrophage activation syndrome may have a role in some cases of severe dengue (Ramanathan and Duraisamy ; Rueda et al. ; Lu et al. ; Nakamura et al. ; Soler et al. ; Tan et al. ; Sharp et al. ; Riberio et al. ; De Koninck et al. ; Mitra and Bhattacharya ; Pal et al. ; Phuakpet et al. ). The increasing reports of hemophagocytosis associated with dengue infection in both endemic and non-endemic areas have raised concern of the potential threat of this emerging syndrome in causing severe and fatal complications of dengue (Ramanathan and Duraisamy ; Rueda et al. ; Lu et al. ; Nakamura et al. ; Soler et al. ; Tan et al. ; Sharp et al. ; Riberio et al. ; De Koninck et al. ; Mitra and Bhattacharya ; Pal et al. ; Phuakpet et al. ).
Clinically, according to the 2009 revised World Health Organization (WHO) dengue classification, the patient in our study met the criteria of severe dengue with presentations of severe hemorrhage and liver failure. Her low haptoglobin level provided evidence of bleeding and liver impairment, resulting in poor coagulation profile and markedly elevated liver enzymes. Furthermore, our initial suspicion that the patient was having HPS as a possible complication was supported by laboratory findings of elevated levels of serum ferritin, sCD163 and sCD25 typical of HPS (Ravelli et al. ; Bleesing et al. ). Although observation of hemophagocytosis is the gold standard for identifying macrophage activation syndrome, specific biomarkers are needed for its early detection. In this case, serum ferritin, sCD163 and sCD25 levels were charted during the course of her hospitalization. Elevated transaminases levels were also observed; and this was similar to an earlier observation which supports the possibility of HPS contributing to hepatic dysfunction (Lu et al. ). We also detected dengue viral RNA in the bone marrow tissue samples, providing direct evidence of the presence of dengue virus in the tissue. This was consistent with previous reports highlighting the involvement of bone marrow in dengue virus infection (Nelson et al. ; Nisalak et al. ). It is also worth noting that the dengue virus persisted in the bone marrow even at 15 days post onset of fever and long after viremia was over. Currently, it is not known how long dengue virus would persist in the marrow following an infection.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [105.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",85,80.75,89.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 105.0 mm Hg + 2/3 * 75.0 mm Hg = 85.0 mm Hg.
Hence, the patient's mean arterial pressure is 85.0 mm Hg."
1696,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6603324-1,Extracted,"In winter, a 70-year-old woman had taken a bath alone. When her family checked on her after 1 h, she was lying unconscious in a bathtub filled with hot water. The patient was initially transferred to another hospital. Given her comatose state (Glasgow Coma Scale [GCS] 3), severe hypotension, and multiple organ failure, she was immediately intubated and referred to our hospital for further treatment. On arrival to our hospital, her vital signs were as follows: blood pressure, 135/71 mmHg; heart rate, 105 b.p.m.; respiratory rate, 30 breaths/min; SpO2 100% using 10 L/min O2; and body temperature, 40°C. She had no stiffness in the neck and a normal Babinski reflex. Laboratory data revealed a normal white blood cell count (8,500/μL), hemoglobin, platelet, and electrolyte levels. By contrast, laboratory data showed mild elevation of C-reactive protein (5.37 mg/dL), hepatic dysfunction (aspartate transaminase, 1,305 U/L; alanine transaminase, 894 U/L), acute kidney injury (blood urea nitrogen, 24.6 mg/dL; creatinine, 1.62 mg/dL), and coagulopathy (prothrombin time – international normalized ratio, 1.14; D-dimer, 36.2 μg/dL). A computed tomography (CT) scan of the head was normal (Fig. A). A whole-body CT scan showed no abnormalities in the lungs, kidneys, or liver; therefore, infectious disease was not suspected. A rapid influenza antigen test was not carried out. The patient had no history of endocrine disease, and she used no medications internally. Based on all these factors, we suspected this deep coma and multiple organ failure with high fever indicated severe HS by exclusion. We carried out fluid resuscitation with iced saline and cooling until her body temperature reached 39°C, and her consciousness gradually improved to GCS 7T (E2VTM5). The patient was admitted to the intensive care unit and received mechanical ventilation therapy under sedation with propofol (40 mg/h). We kept her body temperature at 36°C using adhesive surface cooling pads (Arctic Sun 5000; Bard Medical, Covington, GA, USA).
On day 2, the patient remained in a deep comatose state despite withdrawal of sedative drugs. A repeat head CT revealed bilateral and symmetrical low-density areas and diffuse bilateral swelling of the thalamus. In addition, in another detailed discussion of the patient's medical history with her family, we learned she had suffered from a severe cough with high fever 2 days before hospital admission. A rapid influenza antigen test, undertaken after culturing scrapings taken from her nose, was positive. As the patient was hemodynamically unstable, we did not take a cerebrospinal fluid sample at admission. Additionally, as the head CT on day 2 also revealed diffuse brain swelling, we did not carry out a lumbar puncture. Based on the characteristic CT findings and medical history of influenza, we made a differential diagnosis of influenza A-associated ANE. Intravenous peramivir (300 mg/day), steroid pulse therapy (1,000 mg/day), and D-mannitol infusion (135 g/day) were added to her treatment protocol. Continuous renal replacement therapy and plasma exchange were also initiated. Surface cooling with Arctic Sun 5000 (Bard Medical) and mechanical ventilation therapy with a target PaCO2 of 30–40 mmHg were continued. Although acute kidney injury, acute hepatic failure, and coagulopathy improved, brain edema gradually affected the whole brain (Fig. B–D). The patient remained in a deep coma state, and spontaneous breathing ceased on day 4. Pupils were dilated and fixed bilaterally, and the pupillary light reflex had disappeared. An electroencephalogram taken at bedside on day 6 revealed electrocerebral inactivity. Treatment was withdrawn on day 7, and the patient died of ANE on day 21.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [135.0, 'mm hg'], 'Diastolic Blood Pressure': [71.0, 'mm hg']}",92.33333,87.71666,96.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 71.0 mm Hg = 92.33333 mm Hg.
Hence, the patient's mean arterial pressure is 92.33333 mm Hg."
1697,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-3841,Extracted,"A 16-year-old girl is brought to the emergency department by her parents because of fever, vomiting, rash, and worsening confusion since this morning. On questioning, her mother reports that her last menstrual period was 1 week ago and that she recently started using tampons. She appears lethargic and is only oriented to person. Her temperature is 40.4°C (104.7°F), pulse 174/minute, and blood pressure is 62/44 mm Hg. Examination shows oropharyngeal hyperemia and diffuse macular erythroderma.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [62.0, 'mm hg'], 'Diastolic Blood Pressure': [44.0, 'mm hg']}",50,47.5,52.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 62.0 mm Hg + 2/3 * 44.0 mm Hg = 50.0 mm Hg.
Hence, the patient's mean arterial pressure is 50.0 mm Hg."
1698,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-10081,Extracted,"A 42-year-old man presents to the emergency department with a 3-day history of fever and severe back pain. The fever is high-grade, continuous, without chills and rigors. The back pain is severe, localized to the thoracic region, and aggravated by deep breathing. The patient tried taking ibuprofen with little improvement. Past medical history is significant for essential hypertension, dyslipidemia, hyperuricemia, and bronchial asthma. Current medicines include allopurinol, amlodipine, atorvastatin, clopidogrel, montelukast, and a corticosteroid inhaler. The patient reports a 25-pack-year smoking history and drinks alcohol only socially. His vital signs include: blood pressure 152/94 mm Hg, pulse 101/min, temperature 39.5°C (103.1°F). BMI 36.8 kg/m2. On physical examination, the patient is alert and oriented. Multiple injection marks are visible around the left-sided cubital fossa and hand veins. The neck is supple on head flexion. Point tenderness is present in the thoracic region at the midline. Motor and sensory examinations are unremarkable with normal deep tendon reflexes. Laboratory findings are significant for the following:
Hemoglobin 14.5 mg/dL
White blood cell 24,500/mm3
Platelets 480,000/mm3
BUN 28 mg/dL
Creatinine 1.1 mg/dL
ESR 45 mm/hr
C-reactive protein 84 mg/dL
Sodium 144 mEq/L
Potassium 4.1 mEq/L
Calcium 9.7 mEq/L
A contrast MRI of the spine reveals a peripherally enhancing dorsal epidural process compressing the thecal sac and causing a mild leftwards displacement.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [94.0, 'mm hg'], 'Systolic Blood Pressure': [152.0, 'mm hg']}",113.33333,107.66666,119,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 152.0 mm Hg + 2/3 * 94.0 mm Hg = 113.33333 mm Hg.
Hence, the patient's mean arterial pressure is 113.33333 mm Hg."
1699,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4008396-1,Extracted,"The patient is a 52-year-old man who gradually suffered since about 5 years from exertional dyspnea, weakness and lack of energy, fatigue feeling, pleuritic chest pain, distension of abdomen, and peripheral edema. Patient has a past history of hospitalization one year ago due to chest pain and received coronary angiography, and it was normal. The patient also received diagnostic thoracentesis 6 months before due to dyspnea and the presence of right-side pleural effusion, and he had exudative pleural effusion with lymphocyte-dominant and nondiagnostic cytology, and for this reason, he received thoracoscopy and pleural biopsy which were nondiagnostic. The patient referred to our hospital due to pain and progressive abdominal distention in the past 10 days was hospitalized. On physical examination, the patient was hemodynamically stable (blood pressure was 110/80 mmHg and pulse was 78 beats per minute). JVP was very elevated. Heart sounds were muffle, and reduction of sound was found at the base of the right lung. In the examination, mild hepatomegaly with ascites and peripheral edema was seen. Primary laboratory evaluations were normal. Analysis of the ascitic fluid revealed a high protein content (4.1 g/dL) and an elevated serum-ascites gradient (1.6 g/dL). In abdominal sonography, congestive hepatomegaly, mild splenomegaly, ascites, and evidence of portal hypertension were seen. In upper endoscopy, esophageal varices were not seen and viral hepatitis serology was negative. In chest and abdominal CT, right pleural effusion, pericardial thickness and calcification, ascites, and inferior vena cava dilation were seen (). To study abdominal vascular thrombosis, MRV (Magnetic Resonance Venography) was performed, and the results were normal. In the conducted echocardiography, enlargement of right atrium (44 mm), right ventricle (46 mm), and left atrium (42 mm) along with mild pericardial effusion, pericardial calcification, inferior vena cava dilation (28 mm) and septal bouncing was found ().
Right and left cardiac catheterization were performed for the patient in which elevation and equalization of right atrial pressure (29 mmHg), pulmonary capillary wedge pressure (30 mmHg), mean pulmonary arterial pressure (33 mmHg), right ventricular diastolic pressure (30 mmHg), and left ventricular diastolic pressure (30 mmHg) were found. Curves recorded in right heart catheterization indicate increase of superior vena cava pressure at time of breath and descending, and then horizontal curve of right ventricular pressure (square root sign) was evident (). Coronary angiography was normal. All of the findings were consistent with CP.
The patient underwent cardiac surgery during which pericardium was fully thick and calcified (), and received pericardiectomy. Pathological study of pericardial sample indicated fibrous pericarditis without granuloma (). Gram's staining, staining for acid-fast bacilii, and culture of the pericardium for bacteria, fungus and acid-fast bacilli were negative.
One year after the operation, the patient reported a dramatic improvement in his exertion tolerance, along with decrease of dyspnea and distension of abdomen.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 80.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1700,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5728,Extracted,"A 27-year-old woman presents to her primary care physician for a concern about her pregnancy. This is her first pregnancy, and she is currently at 33 weeks gestation. She states that she has experienced diffuse swelling of her ankles and legs and is concerned that it is abnormal. Otherwise, she has no concerns. The patient has a past medical history of obesity and diabetes. Her temperature is 98.5°F (36.9°C), blood pressure is 147/92 mmHg, pulse is 80/min, respirations are 15/min, and oxygen saturation is 97% on room air. Physical exam reveals bilateral edema of the lower extremities.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [92.0, 'mm hg'], 'Systolic Blood Pressure': [147.0, 'mm hg']}",110.33333,104.81666,115.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 147.0 mm Hg + 2/3 * 92.0 mm Hg = 110.33333 mm Hg.
Hence, the patient's mean arterial pressure is 110.33333 mm Hg."
1701,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-877,Extracted,"A previously healthy 57-year-old man comes to the emergency department because of acute retrosternal chest pain that radiates to his back. The pain started suddenly while he was having dinner. A few moments prior to the onset of the pain, he experienced discomfort when trying to eat or drink anything. On the way to the hospital he took a sublingual nitrate tablet that he had at home, which helped relieve the pain. His pulse is 80/min, respirations are 14/min, and blood pressure is 144/88 mm Hg. Examination shows no other abnormalities. An ECG shows a normal sinus rhythm with no ST-segment abnormalities. An esophagogram is done and shows areas of diffuse, uncoordinated spasms in several segments along the length of the esophagus.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [144.0, 'mm hg'], 'Diastolic Blood Pressure': [88.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 144.0 mm Hg + 2/3 * 88.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1702,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3132700-1,Extracted,"A 53 year-old woman was transferred to the emergency department due to chest pain via a district hospital. Her risk factor for coronary artery disease was hypertension on medication. She denied any prior history of pregnancy, cocaine or amphetamine medication, chest trauma, connective tissue disease and family history of premature coronary artery disease.
On arrival, her vital signs were stable except for blood pressure reading of 140/84 mmHg. The physical examination revealed no evidence of tenderness on the anterior chest and no sign of joint swelling or tenderness. Initial electrocardiogram revealed anterior and inferior ST-segment elevations. Initial chest X-ray showed no sign of pulmonary edema. The levels of total cholesterol, low density lipoprotein-cholesterol (LDL-C) and cardiac enzymes were elevated. The patient's total cholesterol, triglyceride, high density lipoprotein-cholesterol, and LDL results were 236 mg/dL (0-200 mg/dL), 98 mg/dL (0-150 mg/dL), 41 mg/dL (35-55 mg/dL), 169 mg/dL (55-155 mg/dL), respectively. Creatine kinase-MB, and troponine-I levels were 113 ng/mL (0-2.8 ng/mL), and 26 ng/mL (0-0.045 ng/mL). Glucose was 95 mg/dL (70-110 mg/dL), and creatinine was 0.81 mg/dL (0.7-1.4 mg/dL). Antinuclear antibody and antinuclear and antineutrophil cytoplasmic autoantibodies were all negative. Echocardiography showed antero-apical wall hypokinesia.
Suspecting myocardial infarction, we performed emergent CAG. In the examination, a long and smooth lesion from the mid to distal left anterior descending artery (LAD) was detected, which showed an abrupt transition from the proximal LAD (). IVUS confirmed the dissecting flap with intramural hematoma compressing the true lumen at the distal LAD (), and ectatic dilatation of the proximal LAD (internal diameter: approximately 6 mm). The intimal tear site was not detected on the IVUS examination. During the procedure, the patient did not complain of chest pain and all vital signs were stable. Because the intramural hematoma was located at distal LAD and the Thrombolysis in Myocardial Infarction flow grade was three, we did not conduct any additional interventional treatments for the patient. Multi-detector computed tomography (MDCT) of coronary artery was undertaken three days later using a Siemens 64-slice scanner. We observed a luminal narrowing of the distal LAD with a perivascular low attenuation corresponding to hematoma and ectatic change of the left coronary artery ().
The patient was treated with aspirin, clopidogrel, bisoprolol, valsartan, and diltiazem, and did not suffer from any discomfort after discharge. Follow-up examinations were performed 6 months later. There was no further discrepancy of vessel size on CAG (). On the follow-up IVUS, the intramural hematoma in distal LAD was not seen (), and ectatic dilatation of the proximal LAD persisted. Follow-up MDCT of the coronary artery demonstrated dilatation of lumen size at the distal LAD with resolution of perivascular hematoma ().",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [84.0, 'mm hg']}",102.66667,97.53334,107.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 84.0 mm Hg = 102.66667 mm Hg.
Hence, the patient's mean arterial pressure is 102.66667 mm Hg."
1703,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9057,Extracted,"A 70-year-old man is brought to the emergency department with complaints of chest pain for the last 2 hours. He had been discharged from the hospital 10 days ago when he was admitted for acute myocardial infarction. It was successfully treated with percutaneous coronary intervention. During the physical exam, the patient prefers to hunch forwards as this decreases his chest pain. He says the pain is in the middle of the chest and radiates to his back. Despite feeling unwell, the patient denies any palpitations or shortness of breath. Vitals signs include: pulse 90/min, respiratory rate 20/min, blood pressure 134/82 mm Hg, and temperature 36.8°C (98.2°F). The patient is visibly distressed and is taking shallow breaths because deeper breaths worsen his chest pain. An ECG shows diffuse ST elevations.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [134.0, 'mm hg'], 'Diastolic Blood Pressure': [82.0, 'mm hg']}",99.33333,94.36666,104.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 134.0 mm Hg + 2/3 * 82.0 mm Hg = 99.33333 mm Hg.
Hence, the patient's mean arterial pressure is 99.33333 mm Hg."
1704,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4602,Extracted,"A 27-year-old man presents to the emergency department with back pain. The patient states that he has back pain that has been steadily worsening over the past month. He states that his pain is worse in the morning but feels better after he finishes at work for the day. He rates his current pain as a 7/10 and says that he feels short of breath. His temperature is 99.5°F (37.5°C), blood pressure is 130/85 mmHg, pulse is 80/min, respirations are 14/min, and oxygen saturation is 99% on room air. On physical exam, you note a young man who does not appear to be in any distress. Cardiac exam is within normal limits. Pulmonary exam is notable only for a minor decrease in air movement bilaterally at the lung bases. Musculoskeletal exam reveals a decrease in mobility of the back in all four directions.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 85.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1705,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6034342-1,Extracted,"A 16-year-old white girl presented to our academic children’s hospital on postoperative day six with a chief complaint of shortness of breath and pleuritic chest pain. She had recently undergone an uncomplicated elective ACL reconstruction with a bone-patellar tendon-bone autograft and lateral meniscus repair with a single FAST-FIX suture (Smith & Nephew, Inc., Andover, MA, USA). The surgery was performed under a general anesthetic as well as a femoral canal block as per our usual protocol. There were no intraoperative complications. Total tourniquet time was 127 minutes at 250 mmHg. Her postoperative course was uncomplicated. She was discharged later that day as her pain was well controlled and she was cleared by physiotherapy. She was encouraged to be weight-bearing as tolerated while limiting her range-of-motion to 0° to 90° of knee flexion for 6 weeks, given her meniscal repair.
On the day of surgery, she weighed 65.3 kg and her height was 165.7 cm. Her past medical history was significant for acne which was controlled with tetracycline. She was on no other regular medication nor did she take a birth control pill. She was a non-tobacco smoker. She had no family history of anesthetic or hematological issues.
She presented to our Emergency Department on postoperative day six with progressively worsening pleuritic chest pain and shortness of breath. Her vital signs upon presentation were: temperature, 36.8 °C; pulse, 104 beats per minute (bpm); respiration rate, 20/minute; blood pressure, 135/76 mmHg; and O2 saturation of 96% on room air. Baseline laboratory work was drawn (Table ) and a computed tomography (CT)-PE study was performed. This revealed bilateral lower lobe emboli with moderate clot burden and an associated opacity in the left lung base in keeping with pulmonary hemorrhage/infarction (Fig. ). She was subsequently admitted and managed medically with a weight-based dose of Lovenox (enoxaparin) twice daily in consultation with Hematology. She was discharged home 3 days later and would successfully complete 3 months of anticoagulation therapy without any further complications. Anticoagulation treatment was stopped after 3 months as per Hematology.
At her 12-month follow-up, she was asymptomatic and found to have no concerning cardiorespiratory issues. Both an echocardiogram and a pulmonary function test were performed, and found to be within normal limits. Hematology decided not to rescan her in order to assess resolution of the PE given her clinical profile. They have investigated for some treatable causes of spontaneous or acquired thromboembolism (Table ). Results for lupus anticoagulant and anti-phospholipid syndrome as well as for paroxysmal nocturnal hemoglobinuria all returned negative. Admittedly, no further testing was performed to identify causes of inherited thrombophilia (that is, factor V Leiden, prothrombin G20210A, protein C, protein S, and/or antithrombin levels), following a thorough conversation with the family, as this would not have changed treatment pathway irrespective of results.
The hematological team did recommend to our patient that she did not use an estrogen-containing oral contraceptive pill, favoring a progesterone-only oral contraction or a progesterone-containing intrauterine device. From an orthopedic standpoint, she is ambulating independently and cleared for return to sport without any restrictions.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [76.0, 'mmhg'], 'Systolic Blood Pressure': [135.0, 'mmhg']}",95.66667,90.88334,100.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 76.0 mm Hg = 95.66667 mm Hg.
Hence, the patient's mean arterial pressure is 95.66667 mm Hg."
1706,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7752387-1,Extracted,"A 30-year-old, unbooked primigravida at 39 weeks 6 days of period of gestation (POG) presented to obstetric emergency of BPKIHS, Nepal, referred from private hospital with diagnosis of intrauterine fetal death (IUFD) with obstetric cholestasis.
She had stopped perceiving fetal movements for 2 days. She gave a history of itching of the whole body, which had started at 35 weeks of gestation. Her liver function showed an increase in liver enzymes (SGPT/SGOT-224/204IU/L, respectively), and the diagnosis of obstetric cholestasis was made clinically as bile acid concentration measurement was not available. She was started with tablet ursodeoxycholic acid 300 mg BD for 1 week, and then, she stopped the medication on her own.
Her 1st and 2nd trimesters were uneventful, and no other significant past and family history was present.
She is a nonsmoker and nonalcoholic.
She was well-oriented to time, place, and person. Her vitals were within normal limits, with systolic blood pressure of 110 mm Hg and diastolic blood pressure of 70 mm Hg. Abdominal examination showed term size fetus in cephalic presentation without cardiac activity, and the patient was not in labor (Bishop score—3).
Her investigation reports at admission were all normal except increased liver enzyme values.
She was induced with 50 mcg of misoprostol, which was kept per vaginam 4 hourly on 2nd day of admission. She had progressed after 3rd dose of misoprostol and delivered a macerated female weighing 2.9 kg after 12 hours of induction. Labor and delivery were uneventful.
Around half an hour of the delivery, she had started having symptoms of hypoxia such as irritability, sweating, and anxiety. On examination, she was tachycardic and tachypneic with pulse rate of 170 beats per minute and respiratory rate of 24 breaths per minute, respectively. Oxygen saturation was up to 92% on room air. There was a drop in the blood pressure and became not recordable within a few minutes. The patient was conscious throughout with GCS of 15/15. The abdominal and local examination was normal, and there was no evidence of postpartum hemorrhage or ongoing blood loss. Resuscitation was started immediately with intravenous fluid and oxygen supplementation. Repeat blood investigations were sent, blood products were arranged, and the patient was shifted to ICU. After 1500 mL of fluid resuscitation, blood pressure was recorded up to 80/40 mm Hg, but there was no urine output. Arterial blood gas analysis showed lactic acidosis with metabolic alkalosis. The patient was started with noradrenaline as she was not maintaining blood pressure, which was continued for 36 hours and stopped gradually. The patient had started bleeding and soakage from the episiotomy site; hence, adrenaline packing was also done. Investigation reports were collected, which was suggestive of DIC. She was transfused with IV unit of fresh-frozen plasma, IV units of fresh blood, and I unit of whole blood over 48 hours. Her renal function was deranged and creatinine values worsened in the first 3 days. However, as she had started passing urine after 8 hours of resuscitative measure, she did not require hemodialysis. She was also started with broad-spectrum antibiotics and low molecular heparin, which was continued for 10 days.
The patient was improving after resuscitative measure but developed tachypnea on 4th postpartum day. A chest X-ray was done and was suggestive of pleural effusion. Diagnostic pleural fluid tapping was performed, which was suggestive of transudative effusion. Echocardiography, D-dimer, and APTT were normal, whereas electrocardiogram showed sinus tachycardia.
Multidisciplinary management of the patient was done in the maternal ICU for 8 days. She was then transferred to ward on 8th day as she was improving clinically and was discharged from hospital on 14th day. The patient was doing fine at 3rd week of follow-up after discharge.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1707,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6192067-1,Extracted,"A 38 year old newly diagnosed HIV-infected, ART naive Malawian male presented to Queen Elizabeth Central Hospital, a large teaching hospital in Blantyre, Malawi. He reported a 2 week history of headache and vomiting. He had no past medical history of smoking, hypertension or diabetes. On examination, his blood pressure was 122/80 mmHg, pulse 124 beats/min and temperature 36.7 °C. He had a Glasgow Coma Score (GCS) of 15/15, there was evidence of meningism but no focal neurological deficit. A lumbar puncture (Additional file : Table S1) showed a WCC (white cell count) 6.0 × 106/μL, glucose < 2.22 mmol/L (normal range 2.22–4.44 mmol/L), protein 1.68 g/L (normal range 0.15–0.45 g/L) and a positive lateral flow assay for cryptococcal antigen (crAg; IMMY, Norman, OK) (Additional file : Table S1). Cerebrospinal fluid (CSF) opening pressure was 28 cm H20 (normal range 5–20 cm H20). Quantitative cryptococcal culture (QCC) demonstrated 740,000 colony forming units (cfu) /ml (normal < 0 cfu/ml). CD4 count at admission was 29 cells/μl, Hb 11.6 g/dL, WCC 7.5 103/μL, lymphocytes 0.9 103/μL. A diagnosis of CM was made and the patient started on 1200 mg fluconazole once daily and flucytosine 25 mg/kg four times daily as part of the Advancing Cryptococcal Treatment for Africa (ACTA) clinical trial (Open label, multicentre randomised trial; trial no. ISRCTN45035509). The patient received 14 days of treatment as an inpatient as per protocol. He required twice daily lumbar punctures until day 7 to manage his persistently raised intra-cranial pressure (ICP). His day 7 QCC was 22,300 cfu/ml and his QCC prior to discharge on day 14 was 30 cfu/ml.
The patient re-presented 5 days post discharge with recurrence of severe headaches, neck pain, drowsiness and vomiting. On examination, he had a GCS (Glasgow coma scale) of 15/15 and had no neurological deficit. CSF opening pressure was 28 cm H20 and his CSF was crAg positive, WCC 0 106/μL, glucose 2.88 mmol/L and protein 1.22 g/L (Additional file : Table S1). The patient was commenced on amphotericin to treat suspected CM relapse whilst awaiting cryptococcal culture. The culture was subsequently negative and amphotericin was discontinued. He continued on 800 mg fluconazole once daily and was discharged 19 days later with no ongoing symptoms of meningitis. ART was started according to national guidelines (TDF/3TC/EFV) at day 39.
The patient re-presented to hospital at day 54 (16 days post ART commencement) with recurrence of headache and fever, and a sudden onset of left sided weakness. He reported adherence to his fluconazole and ART. On examination, temperature was 38.2 °C, blood pressure 135/92 mmHg, pulse 89 beats/min, respiratory rate 22 breaths/min. He had a new left sided hemiparesis involving both the upper limb and lower limb (power 4/5 using the Medical Research Council (MRC) scale), and there was no sensory deficit. The CSF opening pressure was 21 cm H20. The CSF crAg remained positive, CSF WCC 0 106/μL, CSF protein was high, 3.26 g/L. Culture remained negative (Additional file : Table S1).
His peripheral CD4 count had increased from a baseline of 29 cells/μl to 198 cells/μl. Magnetic Resonance Imaging (MRI) of the brain (performed on day 5 of symptom onset) demonstrated multi-focal DWI positive lesions in the right corona radiata (Fig. ), right posterior limb of the internal capsule, right cerebral peduncle and 1 month later, the right caudate nucleus; these changes were consistent with an acute ischemic stroke. There was high T2 signal without DWI restricted diffusion in the right brainstem and left deep white matter, suggesting previous ischemia. The MRI findings and raised CSF protein in the context of rapid immune reconstitution, following an earlier favorable clinical and microbiological response to anti-fungal treatment and a sterile CSF is consistent with paradoxical C-IRIS as opposed to acute CM infection. Because of the involvement of both anterior and posterior circulation, this met the criteria for probable cerebral vasculitis12. The 0.35 T GE MRI scanner used, does not support an ADC sequence. However, given the sudden onset of the symptoms, these focal DWI changes, in the corresponding anatomical location, occurring within a vascular territory, the etiology is unlikely to be anything other than vascular.
The development of an ischemic stroke was considered to be either a late manifestation of the CM infection or due to intensification of HIV- or CM- associated inflammation with immune reconstitution8. Fluconazole at a dose of 400 mg was continued with ART and the patient achieved good functional improvement. Corticosteroids were not given.
An MRI scan performed one month later demonstrated maturation of the ischemic stroke (Fig. ), and a new DWI lesion in the right caudate, consistent with C-IRIS. The patient however reported complete resolution of the left sided weakness and remained well at day 185.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [135.0, 'mm hg']}",98.33333,93.41666,103.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 80.0 mm Hg = 98.33333 mm Hg.
Hence, the patient's mean arterial pressure is 98.33333 mm Hg."
1708,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7310,Extracted,"A 56-year-old woman with a history of stage IIA cervical cancer presents to your office after her 5th episode of a complicated urinary tract infection. She complains of easy fatigability, weakness, and has noted that her shoes no longer fit. The physical examination is unremarkable, except for a blood pressure of 165/90 mm Hg and mild pitting lower extremity edema. The rectovaginal exam revealed no masses. Given the patient’s medical history, the specialist makes a stage IIIB diagnosis; however, to confirm this, he orders abdominal and transvaginal ultrasounds and renal function tests.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [90.0, 'mm hg'], 'Systolic Blood Pressure': [165.0, 'mm hg']}",115,109.25,120.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 165.0 mm Hg + 2/3 * 90.0 mm Hg = 115.0 mm Hg.
Hence, the patient's mean arterial pressure is 115.0 mm Hg."
1709,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4531755-1,Extracted,"A 70-year-old female was admitted to the hospital because of right flank pain. She had been relatively well until 15 days earlier when she began to have discomfort during urination. One week later, she had fever, chills and right flank pain.
There was a long history of non-insulin dependent diabetes mellitus and essential hypertension. She was treated with oral hypoglycemic and antihypertensive agents.
On admission, blood pressure was 120/80 mmHg, pulse rate 72/min, respiration rate 26/min and temperature 37.2 °C.
The results of physical examination were normal except for tenderness over the right costovertebral-angle.
The laboratory findings on admission were as follows: hemoglobin, 12.0 g/dL; hematocrit, 36.1%; WBC count, 14500/mm3 with 91.6% neutrophils and 6.0% lymphocytes; platelet, 188000/mm3; Na, 139 mEq/L; K, 3.2 mEq/L; Cl, 104 mEq/L; BUN, 9.9 mg/dL, creatinine, 0.6 mg/dL, total serum bilirubin, 0.7 mg/dL; ALP, 132 IU/L, ALT, 34 IU/L, AST, 16 IU/L; total protein, 6.2 g/dL; albumin, 2.8 g/dL; blood sugar, 145 mg/dL; PT, 84%; APTT, 30 sec. Urinalysis revealed glucosuria (300mg/dL) and the sediment contained more than 100 white cells per high-Power field. Stool examination revealed no abnormal findings.
Radiographs of the abdomen showed slightly distended loops of the small bowel and mottled density of feces in the large bowel. Radiographs of the chest were normal. An ultrasonographic examination of the abdomen showed slightly enlarged right kidney.
On admission day, the temperature rose to 38.6°C. Specimens of blood and urine were obtained for routine culture. We believed that she had urinary tract infection. So, ciprofloxacin was empirically administered intravenously.
On the third hospital day, urine culture yielded E. coli (>105 CFU) and blood culture yielded salmonella group B. We were perplexed by that result. At that time, there were not any noticeable alterations in bowel habits. Widal test, stool microscopic examination and culture were performed. Widal test showed O agglutinin titer positive at 1:160, H agglutinin titer positive at 1:320, para A agglutinin titer positive at 1:40 and para B agglutinin titer positive at 1:80. Stool culture yielded no pathogens and microscopic examination also showed no abnormal findings. So, we were not concerned about the possibility of salmonella bacteremia. However, ciprofloxacin was active in both organisms. Antimicrobial treatment with ciprofloxacin was continued. On the fifth hospital day, the fever went down some and the patient’s condition began to improve.
On the 15th hospital day, she complanied of right pleuritic chest pain and low-grade fever. Physical examination at that time revealed decreased breath sounds and fine crackles over the lateral aspect of right lower chest. The white blood cell count was 19900/mm3 with 88.6% neutrophils and 7.1% lymphocytes. The sputum cultures did not reveal an identifiable pathogen. Radiographs of the chest revealed fibrostreaky and hazy density at right lower lung field and blunting of right costophrenic angle ().
Diagnostic thoracentesis was performed. Thoracentesis revealed turbid yellowish fluid (). Laboratory data of pleural fluid revealed the following: pH, 7.168; RBC, 10000/mm3; WBC, 8300/mm3 with 70% neutrophils and 30% lymphocytes; LDH, 4470 IU/L; Protein, 3.9 g/dL; Glucose, 76 mg/dL; ADA, 81 U/L. Pleural fluid culture yielded salmonella group B.
An indwelling catheter was inserted, which drained turbid yellowish pleural fluid. Ciprofloxacin was given for 9 weeks. After antibiotic therapy and repeated therapeutic thoracentesis, the patient was improved.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1710,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8010524-1,Extracted,"A 26-year-old female P1L1 (para 1, living 1) with no previous comorbidities had full-term normal vaginal delivery. Her antenatal period was thoroughly supervised and uneventful. She was completely asymptomatic till day 5 of postpartum period, when she presented with shortness of breath with dry cough for 2 days. She was referred to our tertiary care hospital for further management in view of clinically deteriorating symptoms. At the time of presentation in emergency room (ER), she had fair general condition: pulse—120/min, BP (blood pressure)—104/70 mmHg, RR (respiratory rate)—36/min, SPO2 (oxygen saturation)—64% on room air, cardiovascular system—normal, chest ex—B/L (bilateral) crepitations present, B/L decreased breath sounds, P/A (per-abdomen)—uterus 16 weeks, well contracted, nontender, P/V (per vaginum)—episiotomy healthy, lochia healthy. On reviewing her records, chest X-ray (done 24 hrs back) showed patchy peripheral extensive consolidation along with ground-glass opacities in B/L lung fields predominantly in mid and lower zones suggestive of atypical pneumonia. ECG (echocardiograph) showed sinus tachycardia. After initial management and evaluation, she was admitted in SARI (severe acute respiratory distress isolation) ward in collaboration with Medicine Department. All routine investigations, cultures, and ABG (arterial blood gas analysis) were sent. COVID-19 testing was done using nasopharyngeal swab. She was tested positive for SARS-CoV-2 and was shifted to designated COVID-19 ICU (intensive care unit). Patient was put on NRBM (nonrebreathing mask) at 15 lt/min followed by NIV (noninvasive ventilation). Because of inability to maintain oxygen saturation, patient required intubation and was put on mechanical ventilation for a day. She was provided with supportive care guided by Government of India (GOI) guidelines, including the antiviral drug (remdesivir) and higher intravenous antibiotics with steroid therapy for 10 days. She was extubated on the very next day and was put on NIV again. Her blood reports were within normal range except indicative of infection: haemoglobin—12.2 gm/dl, TLC (total leucocyte count)—16,300, platelets—1,13,000, INR (international normalized ratio)—1.18, LFT/KFT (liver function tests/kidney function tests)—normal. Ultrasound chest was done on day 10 suggestive of B/L consolidation in left to right and no evidence of any effusion. During her hospital stay, she complained of pain left-sided abdomen. She was evaluated in conjunction with gastroenterologist. An ultrasound of the whole abdomen was done and she was diagnosed to have portal cavernoma, which did not require any active intervention. In view of persistent tachycardia, cardiology consultation was done. Her 2D echo (2-dimensional echocardiogram) revealed ejection fraction—55%, no clots, no RWMA (regional wall motion abnormalities). She was subjected to serial chest radiographs, as advised by pulmonologist, which showed a gradual resolution in sizes of patches and opacity as shown in Figures –.
There was no history of any contact with the COVID-19-positive patient; her newborn baby was also tested positive for SARS-CoV-2 and required admission in nursery but was discharged after 7 days. Her remaining contact tracing was negative. After almost 7 weeks of hospital stay, she was tested negative for COVID-19 disease in 2 consecutive reports. Due to the massive spread of infection to lower respiratory tract, the patient was required with NRBM for maintaining saturation for almost 2 months but severity of symptoms decreased significantly. She gradually started maintaining oxygen saturation on room air. At the time of writing this paper, the patient has been discharged back home in good health to join her family.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [104.0, 'mmhg'], 'Diastolic Blood Pressure': [70.0, 'mmhg']}",81.33333,77.26666,85.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 104.0 mm Hg + 2/3 * 70.0 mm Hg = 81.33333 mm Hg.
Hence, the patient's mean arterial pressure is 81.33333 mm Hg."
1711,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7910651-1,Extracted,"A 61-year-old African American male with a history of hypertension, seizure disorder due to traumatic brain injury since age 30, and alcohol disorder was admitted from the detox unit (day 2 in detox unit) of our institution for nausea, vomiting, and dizziness. Blood pressure was elevated (160/100 on the right arm and 155/98 on the left arm) on admission. The heart rate, temperature, and respiratory rate were normal. Oxygen saturation on room air was more than 95%. Routine blood work CBC (complete blood count), CMP (comprehensive metabolic panel), PT/PTT/INR (prothrombin time/partial thromboplastin time/international normalized ratio) were normal. EKG (electrocardiogram) showed normal sinus rhythm, normal PR interval, and no ST-segment changes. Troponin was negative. The chest X-ray was normal. Urine toxicology was positive for cocaine. Symptomatic management was done for nausea, vomiting, and Procardia® (nifedipine) was given for blood pressure.
On the medical floor, the patient complained of new left shoulder pain on the same day. EKG and a CT scan of the shoulder were done. CT shoulder showed dislocation of the acromioclavicular joint and sub-solid nodular densities in the left lung. EKG showed no new changes. CT chest was done for sub-solid nodular density seen in the left lung. CT chest showed aortic dissection and CTA was done for confirmation as per the radiologist's recommendation. CTA showed aortic dissection beyond the subclavian artery extending to the level of aortic bifurcation with decreased perfusion to left kidney and bilateral iliac artery aneurysm and multiple bilateral pulmonary embolisms (Figures -).
The patient did not have any history of coagulation disorders or any history of previous pulmonary embolism or deep vein thrombosis. Wells score was 1.5 (low probability for pulmonary embolism). BMI was 24.3 kg/m2. The patient transferred to the coronary care unit (CCU) and the labetalol drip started. The patient did not have any respiratory symptoms and arterial blood gas (ABG) was normal.
On the next day, blood pressure was normal and saturation remained more than 95%. EKG showed no new changes. For pulmonary embolism, the patient was closely monitored. Saturation and ABG remained normal. Anticoagulation was not used due to an increased risk of bleeding. As the dissection was Stanford type B, no surgical intervention was done. Vascular surgery was consulted for a second opinion. Medical management and close monitoring were continued. A venous duplex of lower extremities was done to rule out deep vein thrombosis as the cause of pulmonary embolism; no deep vein thrombosis was seen. An inferior vena cava filter was placed as prophylaxis to prevent further pulmonary embolism. Blood counts and the metabolic panel did not change over the days and vitals remained stable. Blood pressure was controlled with labetalol. Shoulder pain, nausea, and vomiting resolved. No further complications were seen while in the hospital. The patient was discharged with vascular surgery follow up and to complete coagulation workup as an outpatient.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [160.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",120,114,126,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 100.0 mm Hg = 120.0 mm Hg.
Hence, the patient's mean arterial pressure is 120.0 mm Hg."
1712,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-10982,Extracted,"A 55-year-old male presents to the emergency department with dyspnea and palpitations. He does not smoke cigarettes or consume alcohol, and past medical history is insignificant. Blood pressure is 115/75 mmHG and heart rate is 125/min. Heart rhythm is irregularly irregular. After initial treatment with IV digoxin the patient's heart rate drops to 85/min and remains irregular.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [115.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",88.33333,83.91666,92.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 75.0 mm Hg = 88.33333 mm Hg.
Hence, the patient's mean arterial pressure is 88.33333 mm Hg."
1713,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4794,Extracted,"A 45-year-old man with a history of biliary colic presents with one-day of intractable nausea, vomiting, and abdominal pain radiating to the back. Temperature is 99.7 deg F (37.6 deg C), blood pressure is 102/78 mmHg, pulse is 112/min, and respirations are 22/min. On abdominal exam, he has involuntary guarding and tenderness to palpation in the right upper quadrant and epigastric regions. Laboratory studies show white blood cell count 18,200/uL, alkaline phosphatase 650 U/L, total bilirubin 2.5 mg/dL, amylase 500 U/L, and lipase 1160 U/L.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [102.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",86,81.7,90.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 102.0 mm Hg + 2/3 * 78.0 mm Hg = 86.0 mm Hg.
Hence, the patient's mean arterial pressure is 86.0 mm Hg."
1714,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8987,Extracted,"A healthy 20-year-old African American man presents to the clinic for pre-participation sports physical for college football. He has no health complaints at this time. He has no recent history of illness or injury. He denies chest pain and palpitations. He reports no prior syncopal episodes. He had surgery 2 years ago for appendicitis. His mother is healthy and has an insignificant family history. His father had a myocardial infarction at the age of 53, and his paternal uncle died suddenly at the age of 35 for unknown reasons. His temperature is 37.1°C (98.8°F), the heart rate is 78/min, the blood pressure is 110/66 mm Hg, and the respiratory rate is 16/min. He has a tall, proportional body. There are no chest wall abnormalities. Lungs are clear to auscultation. His pulse is 2+ and regular in bilateral upper and lower extremities. His PMI is nondisplaced. Auscultation of his heart in the 5th intercostal space at the left midclavicular line reveals the following sound.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [66.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",80.66667,76.63334,84.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 66.0 mm Hg = 80.66667 mm Hg.
Hence, the patient's mean arterial pressure is 80.66667 mm Hg."
1715,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8270057-2,Extracted,"An 18-year-old male student with no significant past medical history was transferred to our hospital for management of worsening LV function following the second dose of the Moderna vaccine.
He initially presented to another hospital, where he reported fevers, myalgias, and acute substernal chest pain one day after receiving the second dose. On presentation, his temperature was 101°F, heart rate was 120 bpm, and blood pressure was 110/59 mmHg. Physical examination was unremarkable. ECGs demonstrated diffuse ST elevations (Figure ), and laboratory studies were notable for an elevated high-sensitivity troponin. LV systolic function on the initial echocardiogram was normal, but a subsequent echocardiogram demonstrated a mild reduction in LVEF to 50%. At our hospital, coronary computed tomography angiography revealed normal coronaries.
CMR revealed mild hypokinesis of the mid lateral wall, with corresponding elevated native T1 values (1089-1097 ms; reference range: 950-1050 ms) and T2 values (64-72 ms; reference range: 40-50 ms), and subepicardial delayed enhancement (Figure -) in the lateral wall. Viral serologies for HIV, influenza, RSV, and SARS-CoV-2 were negative. The patient’s hospital course was complicated by brief episodes of non-sustained ventricular tachycardia, and he was discharged on metoprolol succinate and a course of colchicine and ibuprofen.
Stress cardiomyopathy
A 60-year-old woman with a history of a stent placed in the left anterior descending artery (LAD) three years ago, and normal LV function and wall motion on echocardiography five months ago, presented to clinic four days after receiving her second dose of the Pfizer-BioNTech vaccine, with exertional chest pain and new inferolateral T wave inversions (Figure ). She was admitted to the hospital for further evaluation, and echocardiography revealed mildly reduced LV function with apical akinesis (Figure -). Coronary angiography demonstrated a patent LAD stent and no obstructive disease. Based on these findings, the patient was diagnosed with a stress cardiomyopathy, and she was discharged on metoprolol succinate and lisinopril.
Pericarditis
The first patient was a 21-year-old woman with a history of idiopathic thrombocytopenic purpura, who presented three weeks after her first dose of the Pfizer-BioNTech vaccine with chest pain that worsened during inspiration and while supine. She was found to have sinus tachycardia, a small pericardial effusion on echocardiogram, and elevated inflammatory markers without evidence of myocardial injury. Based on the clinical presentation, the patient was diagnosed with pericarditis []. Her symptoms improved significantly with initiation of colchicine.
The second patient was a 61-year-old woman with a history of hypertension who developed low-grade fevers, night sweats, chest discomfort and palpitations four weeks after her second dose of the Pfizer-BioNTech vaccine. She noted that her symptoms improved when leaning forward. On exam, she was found to have a friction rub. ECG revealed new-onset atrial fibrillation (Figure ) and echocardiography demonstrated a small to moderate circumferential pericardial effusion (Figure -). Inflammatory markers were significantly elevated and viral serologies were negative. Based on these clinical features, the patient was diagnosed with pericarditis []. The patient was started on colchicine with improvement in her symptoms. Both patients tested negative for SARS-CoV-2.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [59.0, 'mm hg']}",76,72.2,79.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 59.0 mm Hg = 76.0 mm Hg.
Hence, the patient's mean arterial pressure is 76.0 mm Hg."
1716,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3914169-1,Extracted,"A 63-year-old female on maintenance hemodialysis was admitted to our hospital for an initial generalized tonic seizure suffered at home. Just after admission, a second generalized tonic seizure was observed. During the seizure, conjugate eye deviation toward the upper left was noted. On admission, her pulse rate was 92 beats/min, blood pressure 134/92 mm Hg, and body temperature 36.5°C. Neither abnormal heart sounds nor rales were noted on auscultation. Brain computed tomography (CT) and magnetic resonance imaging (MRI) showed no mass lesion, hemorrhage, or infarction (Figures and ). Electroencephalography showed repetition of intermittent high-amplitude irregular slow waves in the right frontal lobe (). Based on these findings, the patient was diagnosed with generalized partial seizures. After administration of phenytoin sodium, the seizures resolved, and neurological findings normalized. According to her medical record, she had no history of diabetes mellitus or coronary artery disease, nor any family history of coronary artery disease. She had been stable on maintenance hemodialysis for 32 years, and the appropriate dry weight was maintained. Kt/V (urea) was 1.48. Her administration had included fentanyl patch, etizolam, rabeprazole sodium, celecoxib, lactomin, camostat mesilate, tocopherol nicotinate, acetaminophen, and mecobalamin. On admission, electrocardiogram (ECG) was normal.
On the second hospital day, ECG showed inverted T waves and QT prolongation in all leads without chest pain, dyspnea, or any other cardiac symptoms. Neurological findings were normal. Blood test findings were as follows: creatinine, 6.46 mg/dL; blood urea nitrogen, 55 mg/dL; sodium, 141 mEq/L; potassium, 5.3 mEq/L; calcium, 8.9 g/dL; phosphorus, 7.0 mg/dL; hemoglobin, 12.3 g/dL; aspartate aminotransferase, 19 IU/L; alanine aminotransferase, 8 IU/L; creatine kinase, 312 IU/L; and cardiac troponin t-test, negative (Troponin T kit; TROP T sensitive, Roche Diagnostics, Mannheim, Germany: cutoff value is 0.1 ng/mL). Thoracoabdominal computed tomography (CT) did not show any abnormal findings. Echocardiography demonstrated left apical akinesis. On the third hospital day, the patient underwent cardiac catheterization. While coronary angiography showed normal coronary arteries, left ventriculography showed extensive severe hypokinesis in the anteroseptal and apical segments with hyperkinesis in the basal segments (). Based on these findings, the patient was diagnosed with takotsubo cardiomyopathy.
We followed with serial ECG monitoring for several weeks. Her clinical course of takotsubo cardiomyopathy was uneventful and seizure had not been seen. After two months, left ventricular apical wall motion abnormalities on echocardiography had reversed, and the inverted T waves and QT prolongation on ECG had also resolved ().",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [134.0, 'mm hg'], 'Diastolic Blood Pressure': [92.0, 'mm hg']}",106,100.7,111.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 134.0 mm Hg + 2/3 * 92.0 mm Hg = 106.0 mm Hg.
Hence, the patient's mean arterial pressure is 106.0 mm Hg."
1717,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8325872-1,Extracted,"A 29-year-old female with a past medical history of SLE was brought to the emergency department with fluctuated mentation, fatigue, anorexia, and psychomotor retardation for the last week. She also complained of incoherent speech and intermittent choreiform movement in the upper part of the body. She was diagnosed with SLE four years back, having urticaria and erythematosus rash with itching, scaling of the palm of hands, and hyperkeratosis of the sole, for which she was taking hydroxychloroquine and prednisone. She was admitted to the hospital three weeks back due to worsening dyspnea, fever, and cough. She had tachypnea, wheezing, and a chest X-ray revealed diffuse infiltrates in both lungs. Her COVID-19 polymerase chain reaction (PCR) test was positive, and she was commenced on azithromycin and 6mg dexamethasone for five days. Her condition improved gradually, and she was discharged six days later.
On clinical examination, she looked anxious with poor speech. She had a temperature of 99oF, respiratory rate of 23/minute, heart rate of 87/minute, blood pressure of 110/70 mmHg, and oxygen saturation of 96%. Her cardiovascular and respiratory examination was unremarkable, with normal vesicular breathing and heart sounds. Neurological examination revealed psychomotor agitation, intermittent choreiform movements of upper limbs, and poor speech. She had no signs of meningeal irritation, muscle strength loss, seizure episodes, and any history of trauma and illicit drug use. Her repeat COVID-19 PCR test was negative; however, serum immunoglobulin G (IgG) antibodies were positive against COVID-19.
Her initial blood investigations revealed thrombocytopenia and mild elevation of creatinine (Table ). Infectious workup was negative for any organism. The urine screen was negative for any illicit drug use, and the result of her repeat autoimmune screening is shown in Table . Her brain magnetic resonance imaging (MRI) revealed hyperintense signals in the bilateral parietal and temporal lobes, suggestive of lupus cerebritis (Figure ). She was diagnosed with lupus cerebritis, an exacerbation of SLE due to COVID-19 infection. CSF analysis was not performed because she refused lumbar puncture.
Her initial management included 1g methylprednisolone for three consecutive days, 30mg of prednisone daily, and 5mg of olanzapine daily for two weeks. The patient was also placed on monthly 1g intravenous cyclophosphamide. Her condition started improving gradually, and she was stable on day six of hospitalization. She was discharged on maintenance oral steroid therapy with follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1718,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-11146,Extracted,"A 47-year-old man presents to his primary care provider with difficulty swallowing. He reports a 5-month history of food getting stuck in his throat due to an inability to swallow. He has also felt more fatigued than usual. He has had to quit his swimming club due to tiredness. His past medical history is notable for hypertension, obesity, and a prior myocardial infarction. He takes enalapril, spironolactone, metoprolol, and hydrochlorothiazide. He has a 35-pack-year smoking history and occasionally drinks a glass of wine with dinner. His temperature is 99.1°F (37.3°C), blood pressure is 145/80 mmHg, pulse is 102/min, and respirations are 16/min. On exam, he is a tired-appearing man in no acute distress. No lymphadenopathy is noted. The patient is pale with concave nail beds on his fingers. An endoscopy is performed with results shown in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [145.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",101.66667,96.58334,106.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 145.0 mm Hg + 2/3 * 80.0 mm Hg = 101.66667 mm Hg.
Hence, the patient's mean arterial pressure is 101.66667 mm Hg."
1719,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5712197-1,Extracted,"A 78-year-old hypertensive and diabetic man had a history of coronary artery disease with percutaneous coronary intervention in 1997. Chest X-ray (Fig. ) was normal 11 months ago. He denied major chest trauma recently. He suffered from intermittent low grade fever, dull and tingled pain over left flank region and progressive dyspnea for 1 week. He was brought to our emergency department. On arrival, vital signs were a respiratory rate of 22 breaths per min, a heart rate of 125 beats per min, a blood pressure of 158/79 mmHg and a body temperature of 36.6 °C. Physical examination revealed a pale conjunctiva, no heart murmur, absent breathing sound of left lower lung, and knocking pain over left costovertebral angle. Significant laboratory evaluation revealed white blood cell counts (WBCs) of 13,700/mm3 with 76.3% of segmented neutrophils, hemoglobin of 7.8 g/dl, red blood cell counts (RBCs) of 4.26 × 106/mm3, platelet counts of 634 × 103/mm3, creatinine 1.5 mg/dl, albumin 2.6 g/dl, protein 7.8 g/dl, lactate dehydrogenase (LDH) 384 U/l, glucose of 257 mg/dl, and high-sensitivity C-reactive protein (hs-CRP) of 18.6 mg/dl. Chest X-ray showed left pleural effusion and mild widening of upper descending aorta (Fig. ). Blood-tinged pleural effusion was confirmed via a fine-needle aspiration under sono-guide after informed consent of patient. Analysis of pleural effusion were exudative and infection of pleural effusion should be considered, including WBCs of 1625/mm3, with neutrophils of 62% and lymphocytes of 31%, RBCs of 12,500/mm3, protein of 4.5 g/dl, LDH of 266 U/l, glucose of 201 mg/dl and specific gravity of 1.030. Fever, flank pain, leukocytosis, elevated hs-CRP and hemothorax were clinical clues for high suspicion of ruptured infectious aorta. Computed tomography (CT) with intravenous contrast media depicted ruptured multiple thoracic aortic aneurysms at the level of between 8th and 11th thoracic spines with atelectasis of left lung and massive hemothorax (Fig. ), so emergency surgical intervention with resection of fragile aorta, debridement of involved periaortic soft tissue, and reconstruction for descending aorta with Dacron graft of 20 mm was performed. Although the cultures of blood, pleural fluid, and resected aortic tissue showed no growth of bacteria or mycobacterium tuberculosis, the pathological findings demonstrated injury of vascular wall with acute and chronic inflammatory cells infiltration, fibrinous material coated on the internal luminal surface, focal abscess formation in vascular wall (Fig. ) and no malignancy cells or granulation tissue. The serological screen for syphilis was non-reactive. The patient recovered gradually after surgical aortic repair, intensive care and adequate intravenous antibiotics for cover Gram-positive and Gram-negative bacteria with prostaphlin 2 g per 6 h and ceftriaxone 2 g per day for 4 weeks despite of negative-culture result. He was discharged under an uneventful condition with a regular follow-up of cardiovascular out-patient department for 2 years.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [158.0, 'mm hg'], 'Diastolic Blood Pressure': [79.0, 'mm hg']}",105.33333,100.06666,110.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 158.0 mm Hg + 2/3 * 79.0 mm Hg = 105.33333 mm Hg.
Hence, the patient's mean arterial pressure is 105.33333 mm Hg."
1720,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6410487-1,Extracted,"An 84-year-old Japanese man was diagnosed with type 2 diabetes at 58 years of age in 1987. He received human insulin treatment for 20 years, but in 2011, biphasic human insulin 30 was changed to biphasic insulin aspart 30 (BIAsp 30). He had stage 4 chronic kidney disease due to nephrosclerosis, renal anemia, hypertension, dyslipidemia, hyperuricemia, and sleep apnea syndrome. He had been taking the following medications: amlodipine 10 mg/day, rosuvastatin 2.5 mg/day, and febuxostat 20 mg/day. He drank alcohol occasionally and had smoked one to two packs of cigarettes daily for 50 years when he quit 15 years ago. He did not have any food or drug allergies. His family and social histories were not remarkable. His environmental history revealed no abnormalities. He was a retired company director. From January 2015, he experienced persistent early morning hypoglycemia (< 50 mg/dl) with daytime hyperglycemia. Despite reduction of BIAsp 30 dosage, early morning hypoglycemia concomitant with disturbance of consciousness continued to occur. Therefore, he was admitted to our hospital in February 2015.
On examination, the patient’s temperature was 36.3 °C, pulse 64 beats/min, blood pressure 126/72 mmHg, respiratory rate 20 breaths/min, and oxygen saturation 96% while breathing ambient air. He was alert and oriented to time and place on admission. Neurological examination revealed intact cranial nerves, normal limb power and sensation, and absence of cerebellar signs. No changes in sensorium or psychotic features were noted. Other physical examinations revealed no abnormalities. Laboratory findings on admission were as follows: fasting plasma glucose, 82 mg/dl; hemoglobin A1c (HbA1c), 7.0%; and glycoalbumin, 21.4%. More laboratory test results are shown in Table . Imaging studies, including computed tomography and magnetic resonance imaging, showed no significant change.
Although BIAsp 30 was discontinued after admission, early morning hypoglycemia with daytime hyperglycemia continued even after eating small frequent meals (a four or six meals per day eating pattern). Fasting blood samples revealed a plasma glucose level of 28 mg/dl, immunoreactive insulin > 2000 μIU/ml, C-peptide 3.03 ng/ml, and high titers of insulin antibody (IA) (> 50 U/ml). IA binding rate was at a high level (86.3%). Scatchard analysis showed an affinity contact (K1) of 0.00256 × 108 M− 1 and a binding capacity (B1) of 99.7 × 10− 8 M against human insulin for the high-affinity sites, indicating that the patient’s IA bound to insulin with low affinity and high binding capacity. He had no history of medication involving SH residues or supplements containing α-lipoic acid. Moreover, workup for endocrinological abnormality and autoimmune disease did not reveal any significant findings (Table ). HLA-DRB1*04:06 was undetectable, and imaging studies of the head and abdomen showed no evidence of abnormalities.
The patient’s serum creatinine level was 2.17 mg/dl, and his estimated glomerular filtration rate (eGFR) was 23.3 ml/min/1.73 m2. His arterial pH at 5:00 a.m. was 7.277, bicarbonate was 15.1 mEq/L, and base excess was − 10.7. After he was given a gradually increasing dose up to 3 g/day of sodium bicarbonate (split four times per day) for the purpose of correcting metabolic acidosis, his early morning glucose level was improved, concurrently bringing pH up to 7.4 (Fig. ). Early morning hypoglycemia disappeared after he took 3 g/day of sodium bicarbonate and three meals plus snacks at night daily (1400 kcal/day) without any oral hypoglycemic agent or insulin. The patient was discharged in late March 2015 and continued on the same treatment.
After 9 months of follow-up with these treatments, the patient’s plasma glucose level at 5:00 a.m. was 96 mg/dl, and his arterial pH was 7.376. His immunoreactive insulin level had significantly decreased to 11.4 μIU/ml, even though the titer of IA remained high (> 50 U/ml). IA binding rate decreased to 42.1%. According to the Scatchard analysis, his IA shifted to higher affinity (K1 = 0.142 × 108 M− 1) and lower capacity (B1 = 0.969 × 10− 8 M) than his previous IA. During this follow-up period, he had no symptoms of hypoglycemia, his HbA1c levels were around 6.5%, and his eGFR did not change significantly. His daily plasma glucose levels ranged from 96 to 168 mg/dl.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [126.0, 'mm hg'], 'Diastolic Blood Pressure': [72.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 126.0 mm Hg + 2/3 * 72.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1721,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8667368-1,Extracted,"A previously healthy 77-year-old Sri Lankan Tamil male from Galaha, a laborer at a vegetable farm, presented to the Teaching Hospital Peradeniya with a history of fever of 1-week duration. He was apparently well 1 week previously, and presented with high-grade fever along with arthralgia and myalgia. Apart from that, he had generalized headache with the onset of the illness. There were no associated respiratory symptoms, abdominal pain, vomiting, change in bowel habits, or urinary symptoms. He did not have significant past medical, surgical, or family history. He was unmarried and was an occasional alcohol consumer and a nonsmoker.
On examination, he was averagely built, conscious, ill looking, and severely dehydrated. He had cold peripheries. He was icteric, but there was no pallor or conjunctival suffusion. His pulse rate was 112 beats per minute, and his blood pressure was 77/48 mmHg. The abdominal, respiratory, and nervous system examination was unremarkable on admission.
The patients’ complete blood count showed white blood cells (WBCs) of 4.46 × 109/L (neutrophils 82%, lymphocytes 16%), platelet count 42 × 109/L, hemoglobin (Hb) 13 g/dL, and hematocrit (HCT) of 37%. His C-reactive protein was 345 mg/L, and creatinine was 359 µmol/L. Serum bilirubin was 62.9 mmol/L with direct fraction of 42 mmol/L and indirect fraction of 21 mmol/L. Arterial blood gases showed pH 7.37, lactate 1.1 mmol/L, HCO3 13 mEq/L, pCO2 23 mmHg, pO2 95 mmHg (Table ).
A clinical diagnosis of leptospirosis was made, and the patient was started on intravenous C penicillin, intravenous ceftriaxone, and oral doxycycline. After adequate fluid resuscitation, the patient was started on intravenous noradrenaline infusion 0.6 mcg/kg/minute. On the following day, patient became anuric for 10 hours with rising creatinine of 414 µmol/L. Ultrasound scan of the kidneys showed acute renal parenchymal disease. The patient was started on peritoneal dialysis. On the third day of admission, the patient became dyspneic, and auscultation of the lungs revealed coarse and fine crepitations in the bilateral lung fields. The oxygen saturation dropped even with a continuous positive airway pressure (CPAP) mask, and was 81%. The chest X-ray showed bilateral patchy radio-opaque shadows. The patient was electively intubated, and intensive care was given. The patient was started on intravenous methylprednisolone 1 g daily for 3 days. The electrocardiogram (ECG) showed widespread T inversions, and the 2D echocardiogram showed ejection fraction (EF) of 30% with left ventricular global hypokinesia. His procalcitonin level was 37.94 ng/mL, and the platelet count was 54 × 109/L. The patient was started on plasma exchange on the fourth day of admission, and 1840 mL plasma was removed along with transfusion of 1100 mL fresh frozen plasma and 1000 mL normal saline. Six units of platelets, intravenous tranexamic acid, and intravenous vitamin K were also started. The second plasma exchange was done on the fifth day, with removal of 1810 mL total plasma volume along with transfusion of 1500 mL fresh frozen plasma and 250 mL normal saline. His urine output markedly improved, and the peritoneal dialysis was withheld on the following day. Repeat 2D echocardiography showed improved left ventricular function, with ejection fraction of 50%. By the sixth day of admission, the patient’s inotrope requirement came down and we planned to wean off from the ventilator. Repeat chest x-ray showed clearing of opacifications in the lungs. The patient was extubated on the seventh day of admission. His serum creatinine came down to 243 µmol/L, and C-reactive protein (CRP) was 19 mg/L. Meanwhile, the diagnosis was confirmed as his serology showed positive enzyme-linked immunosorbent assay (ELISA) immunoglobulin M (IgM) for leptospirosis. By the tenth day of admission, the patient was discharged with complete recovery. In follow-up, the patient was reviewed after 2 weeks and found to be in good health.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [77.0, 'mm hg'], 'Diastolic Blood Pressure': [48.0, 'mm hg']}",57.66667,54.78334,60.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 77.0 mm Hg + 2/3 * 48.0 mm Hg = 57.66667 mm Hg.
Hence, the patient's mean arterial pressure is 57.66667 mm Hg."
1722,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5358303-1,Extracted,"A 77-year-old man is a victim of hypertension and diabetes under insulin control at our outpatient clinic. He complained of chest tightness and dyspnea on exertion for a period. He had a history of tobacco used but quit for decades. Echocardiography was performed on 2011 September and the result showed normal left ventricular function without regional wall motion abnormality. Due to frequent chest tightness complained on exertion and the symptom exacerbated. He visited our emergency department for help. At emergency department, CXR showed cardiomegaly. Cardiac enzyme was checked and it was within normal limit. Under the impression of coronary artery disease with angina, he was treated with dual antiplatelet therapy (aspirin 100 mg/day, clopidogrel loading 300 mg, then 75 mg/day) at emergency department and catheterization was suggested after admission. Three days later, catheterization was done and coronary angiography demonstrated left anterior descending artery (LAD) with critical lesion and left circumflex (LCX) atherosclerotic lesion. Angioplasty was performed and two drug-eluting stents (BIOMATRIX 3.0 × 18 and 2.5 × 18) were deployed on LAD and LCX, respectively, with clopidogrel loading 300 mg (). The hospital course was uneventful and he was discharged on aspirin and clopidogrel on the following day.
He was transferred to emergency room again at the noon on the next day after discharge, and he complained of severe acute onset chest pain with diaphoresis. On admission, his blood pressure was 150/96 mmHg, and pulse beats 110/min. His electrocardiography (ECG) showed ST elevation in leads V1-V5. Over the next 10 minutes, his blood pressure dropped to 65/48 mmHg with complete atrioventricular block by ECG monitor, and he was transferred immediately for emergency coronary angiography. After implantation of a temporal pacemaker, coronary angiography revealed totally occluded mid LAD and mid LCX at the same time, the site over the prior stents (). Balloon angioplasty restored Thrombolysis in Myocardial Infarction (TIMI) 2 flow in both sites. Because of low left ventricular ejection fraction and a large thrombus burden by SETMI secondary to stents thrombosis, re-occlusion developed later resulted in failure from primary PCI.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [96.0, 'mm hg']}",114,108.3,119.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 96.0 mm Hg = 114.0 mm Hg.
Hence, the patient's mean arterial pressure is 114.0 mm Hg."
1723,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-11966,Extracted,"A 45-year-old obese man presents to his primary care provider for an annual physical. The patient states that he has noticed increased sleepiness during the day at work over the past 6 months in addition to difficulty concentrating and worsening memory. He denies recent weight loss, and is not sure if he snores because he sleeps by himself. His past medical history is significant for hypertension and type II diabetes. Vital signs are T 98.6 F, HR 75 bpm, BP 140/90 mm Hg, RR 18/min. Physical exam reveals a 350 pound man. Jugular venous distension is difficult to evaluate due to excess tissue in the neck. There is no peripheral edema. Lung exam is normal. Routine CBC shows WBC count of 5000 cells/ml, platelet count of 350,000/mcL, hemoglobin of 18 gm/dL, and hematocrit of 54%.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1724,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7872473-1,Extracted,"An 84-year-old married male presented to the outpatient clinic for a routine annual check-up. The patient had hypertension and hypothyroidism. He had no change in his bowel habits, no melena or bleeding from any site, no weight loss, no loss of appetite, no fever, no shortness of breath, no headache or other neurologic symptoms, no chest pain, palpitation, or other cardiovascular complaints, and no urinary symptoms. He underwent bowel resection due to intestinal obstruction. Accordingly, he was taking amlodipine 5 mg, thyroxine 75 mcg, and aspirin 81 mg daily. He had no history of smoking, alcohol, or drug use, nor a family history of hematological disease. On physical examination, the patient was fully conscious oriented; his body temperature was 36.8°C, blood pressure was 131/59 mmHg, pulse was 78 beats per minute, respiratory rate was 18 breaths per minute, and oxygen saturation was 98% on room air. He was conscious, oriented, and slightly pale, and had no jaundice or nail changes. His head and neck examination showed no oral ulcers, a normal tongue, no lymphadenopathy, and no peripheral stigmata of chronic liver disease; his jugular venous pressure was not raised, and cardiovascular and respiratory examinations were normal. There were midline abdominal longitudinal and right sub-costal scares; no organomegaly was present. There was a bilateral petechial rash on the anterior aspect of both legs, extending from the knee joint to the ankle joint. His neurologic and musculoskeletal examinations were normal.
His initial laboratory finding (Table ) revealed pancytopenia with a hemoglobin of 8.2 g/dL (normal: 11.0-14.5 g/dL), platelets of 64 x 109/L (normal: 150-450 x 109/L), WBCs of 1.6 x 109/L (normal: 4-12 x 109/L), absolute neutrophilic count of 0.35 x 109/L (normal: 2-7.5 x 109/L), and absolute lymphocytic count of 0.98 x 109/L (normal: 1.0-4.4 x 109/L).
The peripheral blood smear showed macrocytosis, with frequent schistocytes of 5%, and hyper-segmented neutrophils (Figure ). The lactate dehydrogenase (LDH) was 486 U/L (high; normal: 125-220 U/L), total bilirubin was 45 umol/L (high; normal: 0-18 umol/L), haptoglobin was <0.058 g/L (low; normal: 0.36-1.95 g/L), reticulocytes count was 2.2% (normal: 0.5-1.5%); B12, folate levels, viral serology, and autoimmune workup was also conducted. The patient underwent bone marrow aspiration and trephine biopsy, and there was no evidence of acute myeloid leukemia or infiltrative bone marrow.
As per the available laboratory results, the patient was initially diagnosed with MAHA. Though the full pentad of TTP was not fully matched and rest of the laboratory workup results were awaited, he was started empirically on fresh frozen plasma (FFP) transfusion every six hours while ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) was sent for workup. However, after 72 hours of FFP, his blood count did not improve and hemolytic markers were rising. Pan CT was performed showing no hidden malignancy that could trigger MAHA. On the third day of admission, the vitamin B12 level result came back with 61 pmol/L (normal: 138-652 pmol/L); his folate level was normal. He has a normal level of ADAMTS13, normal homocysteine level, and negative anti-intrinsic and anti-parietal cell antibodies.
Finally, we deduced that the patient has severe vitamin B12 deficiency; therefore he was started on intramuscular cyanocobalamin 1,000 mcg once daily for seven days and then changed to once weekly for five weeks and then monthly lifelong.
The patient showed clinical improvement at day 3 of parenteral replacement of vitamin B12; his white blood cells increased to 3.5 x 109/L, hemoglobin to 10 g/dL, and platelet to 100 x 109/L. The schistocytes started to disappear gradually. The complete blood count and vitamin B12 levels were normalized after one month of treatment (Table ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [59.0, 'mmhg'], 'Systolic Blood Pressure': [131.0, 'mmhg']}",83,78.85,87.15,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 131.0 mm Hg + 2/3 * 59.0 mm Hg = 83.0 mm Hg.
Hence, the patient's mean arterial pressure is 83.0 mm Hg."
1725,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4144077-1,Extracted,"The patient was a 34-year-old Japanese woman (gravida 1, para 1) whose previous personal and family medical histories were unremarkable. During this pregnancy, the patient's physical findings, cervical length, laboratory data, urinalyses, and fetal growth determinations were all within normal ranges; glucosuria or ketonuria was not detected.
At 23 weeks and 6 days of gestation, physical findings, fetal growth, cervical length, laboratory data, and urinalysis were all within normal range. Two days later, the patient thought she had caught a cold because of the onset of malaise and thirst. At 24 weeks and 3 days of gestation, she presented with complaints of nausea and lumbago. Upon examination, the fetal heartbeat and movement were positive. The physician on duty at the time of admission initially diagnosed the condition as poor physical condition due to the common cold. However, 5 h later, the patient went into labor, and the gestational sac and fetal head appeared, resulting in emergent hospitalization and a subsequent premature delivery.
Upon admission, the patient was 166 cm tall, weighing 72.7 kg (before pregnancy, 63 kg), and had a body temperature of 36.9°C and a blood pressure of 156/74 mmHg. A physical examination revealed labored breathing and cold extremities. A stillborn infant (592 g, female) was soon delivered. The associated blood loss was minimal, and uterine contraction was good; the placenta and umbilical cord (130 g) appeared normal. Soon after delivery, the patient's vitals were normal, apart from a blood pressure of 129/69 mmHg and a slight tachycardia, with a pulse of 113 beats/min. The patient had no lower abdominal pain but complained of epigastric pain.
The results of laboratory tests on blood collected during labor were examined () and confirmed an extreme hyperglycemia, with a blood glucose level of 950 mg/dL. Her urinary sugar and ketones were markedly elevated. The labored breathing observed during delivery became more severe, and the patient developed clouded consciousness, leading to management in the intensive care unit (ICU).
After admission, the patient's white blood cell count, serum amylase levels, blood urea nitrogen levels (BUN), and blood creatinine levels were elevated, leading to a diagnosis of sepsis, acute renal failure, and acute pancreatitis associated with diabetic acidosis. Following a diagnosis of coma due to diabetic ketoacidosis (DKA), acute renal failure, acute pancreatitis, and sepsis, insulin therapy (regular insulin, 7 U/h) and antimicrobial therapy (meropenem trihydrate) were initiated in conjunction with adequate hydration. The patient's laboratory findings and blood gas data improved with this treatment (), and she regained consciousness 24 h after admission to the ICU. Abdominal computed tomography (CT) was performed, revealing a CT severity index of 2 ().
Despite elevated postadmission blood glucose levels, the patient's glycated hemoglobin (HbA1c) levels remained normal. However, C-peptide blood levels of 0.1 ng/mL indicated depleted insulin levels; antibodies against insulin, glutamic acid decarboxylase (GAD), and islet antigen-2 were not detected. Despite marked elevations of C-reactive protein and white blood cell levels, the patient's blood cultures were negative and she was afebrile. A search for factors contributing to DKA involved two investigations of possible viral infection (). The findings revealed elevated Coxsackie A9, B1, and B3 antibody titers. With the patient's consent, human leukocyte antigen (HLA) typing was performed; the findings showed HLA-DRB1∗0405-DQB1∗0401. The condition met all the diagnostic criteria of fulminant type 1 diabetes [] and was diagnosed as such.
The patient was discharged 13 days postpartum and her insulin levels remain depleted, 1 year later. The patient has required regular insulin (42 U/day) administration, with her blood glucose levels varying within the range of 150–250 mg/dL; occasional hypoglycemic episodes preclude higher insulin doses. The patient's HbA1c levels have recently been maintained at approximately 8%.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [156.0, 'mm hg'], 'Diastolic Blood Pressure': [74.0, 'mm hg']}",101.33333,96.26666,106.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 156.0 mm Hg + 2/3 * 74.0 mm Hg = 101.33333 mm Hg.
Hence, the patient's mean arterial pressure is 101.33333 mm Hg."
1726,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2966577-1,Extracted,"A 26-year-old female with a history of anxiety and depression presented to our Emergency Department with sudden onset of diffuse abdominal pain, nausea, and an inability to vomit of 2 hours duration. Her pain was sharp, severe, and worst in the epigastrium. She reported drinking four beers and eating a Cobb salad several hours prior to presentation. She denied diarrhea, constipation, fever, and chills. She reported no similar episodes in the past and denied the consumption of non-food items.
Physical examination revealed a thin, uncomfortable appearing young woman. Her weight was 99 pounds and height was 61 inches. Her temperature was 98.6°F, pulse was 100 beats per minute, and blood pressure was 114/77 mm Hg. The abdomen was distended, firm, and diffusely tender to palpation without peritonitis. All other examination findings were non-contributory.
Laboratory abnormalities included potassium 3.1 mEq/L, amylase 210 U/L, and lipase 114 U/L. Remaining chemistries and a complete blood count were normal. Abdominal plain film showed a grossly distended stomach filled with extensive food matter []. There was no abdominal free air. Abdominal computed tomography (CT) demonstrated an enlarged stomach, measuring 32 cm × 17.9 cm, displacing the small bowel into the right lower quadrant and the transverse colon into the pelvis [].
The patient underwent a laparotomy (through a small epigastric midline incision) which revealed a massively distended stomach. Anterior gastrotomy showed that the stomach was filled with nearly 2 gallons of partially and minimally digested food including whole pasta shells and vegetable matter. Due to the large size and thick consistency of the stomach contents, they were removed via a 40-Fr. chest tube secured in the gastrotomy site, with gentle massage of stomach contents through the tube into a basin. Following adequate decompression, the tube was removed, the stomach mobilized out of the wound, the remaining contents emptied, and the gastrotomy closed. No discrete bezoar or mechanical gastric outlet obstruction was identified. Of note, the gastric wall was poorly perfused due to the massive distention, and the site of gastrotomy showed patchy necrosis even after decompression. Thus, a portion of the anterior wall was resected to viable appearing tissues to allow for safe closure of the gastrotomy. Pathology of the excised gastric wall showed gastric mucosal necrosis.
The following day, the patient admitted to a massive 1-hour binge prior to presentation, and revealed a history of anorexia nervosa and binge eating. At age 14, she had been diagnosed with anorexia nervosa binge/purge subtype. Although she had not engaged in binge eating for 4 years, she attributed this episode to alcohol intoxication and stress.
Postoperatively, a nasogastric tube was left in place for gastric decompression, and a post-pyloric feeding tube in case of gastric ileus after the extreme distension. The nasogastric tube was removed on day 3 and a clear liquid diet started. She advanced to a full liquid diet and was discharged on day 5. She has since resumed a full diet and has reported no problems.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [77.0, 'mm hg'], 'Systolic Blood Pressure': [114.0, 'mm hg']}",89.33333,84.86666,93.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 114.0 mm Hg + 2/3 * 77.0 mm Hg = 89.33333 mm Hg.
Hence, the patient's mean arterial pressure is 89.33333 mm Hg."
1727,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7585214-2,Extracted,"A 13-year-old Maasai boy from rural Arusha, northern Tanzania, presented with a 2-month history of gradual and progressive dyspnea and cough that was dry initially but had started to produce blood-stained sputum in the past 2 weeks before admission. His past medical history was unremarkable, though his father reported that the child had lost significant weight through the course of the illness and had experienced intermittent low-grade fevers. The boy had no history of tuberculosis contact. The informant reported that before this admission, the boy had received treatment for his current illness from a local dispensary, which included antibiotics that he could not specify; however, the boy had no significant improvement. He is from a farming family and keeps livestock. Upon examination, the child was moderately pale, not cyanotic, and saturating at 98% on room air. His pulse rate was 85 beats per minute; his resting blood pressure was 108/60 mmHg; and he was afebrile with a temperature of 36.7 °C.
Chest expansion was more unilateral toward the right with reduced air entry and dull percussion note. No peripheral lymphadenopathy was appreciated. The findings of his abdominal and neurological examinations were unremarkable. A plain chest x-ray was obtained and showed a well-circumscribed cystic mass on the right hemithorax pushing the mediastinum toward the left (Fig. ). A computed tomographic (CT) scan revealed a cystic lesion on the right upper and middle thorax measuring 15 × 11 × 14 cm, displacing the mediastinum to the left side of the chest and compressing the right middle and lower lung lobes. The lesion had a thick wall with clear fluid (Fig. ). The finding of ultrasonography of the abdominopelvic region was unremarkable. His hemoglobin concentration was 12.4 g/dl, platelet count was 492 × 109, leukocyte count was 7.39 × 109/L, serum creatinine was 42 μmol/L, serum urea was 3.77 mmol/L, and ESR was elevated at 95 mm/hour. The finding of GeneXpert testing (Cepheid, Sunnyvale, CA, USA) for Mycobacterium tuberculosis was negative, and the boy’s serum electrolytes and bilirubin levels were within normal range. His urine test result was negative for leukocytes, nitrates, glucose, and proteins. We made a differential diagnosis of hydatid cyst of the right lung.
The child underwent right-sided thoracotomy through the eighth interspace. The large cyst was attached to the lung parenchyma and hence could not be removed; therefore, we performed a standard right pneumonectomy and sent a specimen for histopathological analysis (Fig. ). The child was kept on intravenous paracetamol 500 mg 6-hourly, ceftriaxone 500 mg 8-hourly, and metronidazole 250 mg 8-hourly for 10 days. He was monitored in the ICU for 8 days, during which time he developed acute urine retention on day 6, and the urology team inserted a suprapubic catheter (SPC). The chest tube was removed on day 11 postoperatively. The child was then discharged on day 12 with the SPC and an instruction to attend the urology outpatient clinic after 1 month with oral albendazole 400 mg daily for 6 months. Two weeks after discharge, the child was reviewed at the surgical outpatient clinic, where he was found to be clinically stable with a healed chest wound, and the SPC was patent. The histological reports confirmed the diagnosis of hydatid cyst of the lung (Fig. ). The child was then reviewed at the outpatient clinic 2 months later jointly with the urology team, and he was found to have no chest symptoms and a healed chest wound. His SPC was blocked, and he was voiding normally per urethra with no lower urinary symptoms.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [108.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",76,72.2,79.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 108.0 mm Hg + 2/3 * 60.0 mm Hg = 76.0 mm Hg.
Hence, the patient's mean arterial pressure is 76.0 mm Hg."
1728,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8484258-1,Extracted,"An otherwise healthy 20-year-old male basic military trainee presented to the emergency department (ED) via emergency medical services (EMS) with a one-day history of nausea, vomiting, and abdominal pain. The patient reported needing to provide a urine sample for a training program earlier in the day. Unable to provide a sample, he reportedly drank 5 to 6 liters of water until he could provide a sample. Within one hour of consumption, he became nauseated until he started vomiting and developed periumbilical/right lower quadrant abdominal pain. Additionally, he began to feel lightheaded and fatigued just prior to transportation to the ED.
EMS was called to transport the patient to the emergency department. EMS reported initial systolic blood pressure of 70 with a diastolic of 40 without compensatory tachycardia.
The patient was given two liters of intravenous lactated ringers by EMS without improvement in his blood pressure. Additionally, he was found to be hypoglycemic, with serum glucose of 58 mg/dL, and given one amp of dextrose-50 by EMS. On arrival to the ED, his vital signs were notable for systolic blood pressure or 82 with a diastolic of 54 and oxygen saturation of 89% on room air improved to 95% on two liters nasal cannula. The initial point of care glucose demonstrated persistent hypoglycemia with a glucose of 71 mg/dL. An additional amp of dextrose-50 was given. Physical examination was remarkable for pale appearing lethargic young adult male with moderate diffuse abdominal tenderness without rebound or guarding. Additionally, bibasilar crackles were appreciated on pulmonary auscultation. He was alert and oriented to person, place, and time. There were no focal neurologic deficits on examination.
Venous blood gas was obtained upon patient arrival and was remarkable for sodium of 122 mmol/L, potassium of 3.5 mmol/L, and magnesium of 1.5 mmol/L. In the setting of persistent hypotension unresponsive to fluids, he was given 100 mg hydrocortisone without improvement in his blood pressure. He was given one liter of normal saline over one hour after identifying his low serum sodium as a possible contributing factor to his presenting symptoms. Hypertonic saline was not given in the setting of a normal neurologic examination and concern for alternative diagnoses at the time of the identification of his low serum sodium.
Computerized tomography (CT) scan of the abdomen and pelvis, and a CT chest pulmonary angiogram were obtained and notable for generalized intra-abdominal edema (Figure ), and lung imaging consistent with non-cardiogenic pulmonary edema (Figure ). This constellation of findings is consistent with non-specific third spacing pathology.
The patient was in the ED for a total of four hours. The initial differential diagnosis was broad and included: sepsis, pulmonary embolism, adrenal insufficiency, and symptomatic hyponatremia. After completion of the evaluation in the ED, it was determined that the etiology of his presenting symptoms was acute water intoxication complicated by moderate symptomatic hyponatremia with diffuse fluid third spacing and resultant hypotension and hypoxic respiratory failure. A repeat serum sodium of 124 mmol/L was obtained four hours after the initial venous blood gas. In consultation with the intensive care unit and internal medicine service, the patient was started on a five percent dextrose (D5) normal saline drip at 1.5 times maintenance and was admitted to an intermediate care unit.
While inpatient, a urine osmolality of 111 mOsm/kg was obtained, which in conjunction with urine sodium less than 20 mmol/L is consistent with the patient's hypovolemia. Additionally, a serum osmolality of 264 mOsm/kg was obtained. These lab values are consistent with the diagnosis of hypo-osmolar hyponatremia complicated by diffuse third-spacing of intravascular fluid and resultant hypovolemia.
The patient's electrolytes and renal function were checked every four hours during his admission. Of note, his serum sodium rose to 133 mmol/L twenty hours into his admission, and D5-water was administered to prevent further over-correction of his serum sodium. Over a twenty-four-hour period, the total increase in his serum sodium was 11 mmol/L, slightly higher than the goal increase of 6-8 mmol/L. No complications of this over-correction were observed. He was admitted for a total of three days, and after the first twenty-four hours, his serum sodium gradually normalized. His symptoms of abdominal pain, nausea, vomiting, and lightheadedness resolved with the correction of his serum sodium. He was discharged on day three of hospitalization without complication.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [70.0, 'mm hg'], 'Diastolic Blood Pressure': [40.0, 'mm hg']}",50,47.5,52.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 70.0 mm Hg + 2/3 * 40.0 mm Hg = 50.0 mm Hg.
Hence, the patient's mean arterial pressure is 50.0 mm Hg."
1729,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7358866-1,Extracted,"A 16-year-old girl presented to emergency with complaints of pain in abdomen, vomiting, yellowish discoloration of eyes, and fever since 7 days. There was no history of taking aspirin and other known hepatotoxic drug/herbal medication. Her developmental history was appropriate for her age. There was no history of jaundice or anemia in past. On examination, her weight was 47.5 kg (between 25th and 50th percentile), height was 153 cm (between 25th and 50th percentile), temperature was 98°F, heart rate 98/minute, respiratory rate 24/minute, and blood pressure was 100/70. She was lethargic with the Glasgow coma scale (GCS) of 10 (E4V2M4), and pupils were normal size and normally reacting to light. Bilateral deep tendon reflexes were present and the Babinski sign was absent. Liver was 2.5 cm, tender. The patient was shifted to PICU in view of hepatic encephalopathy. On arrival in PICU, the patient was in shock and had signs of increased intracranial tension (hyperventilation with irregular respiration and paradoxical breathing). The GCS had deteriorated to E1V1M4, pupils were normal size and normally reacting, tone was normal, deep tendon reflexes were absent, and the plantar reflex was flexor bilaterally. The patient was having altered blood aspirates from the nasogastric tube. Laboratory findings on admission were as follows: hemoglobin—9 g/dL, total leukocyte count—6,000/mm3 (25% polymorphs and 65% lymphocytes), platelet count—1.2 lac, total bilirubin—5.5 mg/dL, direct bilirubin—3.5 mg/dL. Aspartate transaminase (AST)/alanine transaminase (ALT) (U/L)—4949/3248, alkaline phosphatase—150 U/L. Prothrombin time—35.5, international normalized ratio (INR)—3.5, blood ammonia—173 μmol/L, blood lactate—4.9 mmol/L, serum albumin—2.5 g/dL. The child was mechanically ventilated, shock was fluid responsive, and blood products were given as and when required. Other appropriate supportive care for ALF and hepatic encephalopathy was also initiated. Relevant investigations to find etiology of hepatitis including viral panel, Wilson’s disease, and autoimmune hepatitis workup were sent.
On day 3 of admission, even after appropriate supportive care patient’s encephalopathy did not improve; serum ammonia levels were persistently above >150 μmol/L with deranged INR. Hence, we planned for high-volume plasma exchange. A total of three cycles of plasma exchange were done on alternate days with fresh frozen plasma and 1.5 times of total blood volume with the centrifugation technique on the optia spectra machine. Each plasma exchange session lasted for 4 hours except for first session in which the child became hypotensive, which required 20 mL/kg normal saline bolus; other two sessions were uneventful. After two sessions of TPE, the child’s clinical condition started improving, liver function tests improved with INR -1.31, and the blood ammonia level decreased to 63 μmol/L. The child was successfully extubated after third session of TPE. At discharge, the child was completely asymptomatic with normal sensorium. Her serum sample came out to be positive for parvovirus B19 IgM and all other workup done to find out etiology of ALF was negative.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 70.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1730,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8332,Extracted,"A 67-year-old man presents to his physician with increased thirst and polyuria for the past 4 months. Patient also notes a decrease in his vision for the past 6 months and tingling in his feet. The medical history is significant for a chronic pyelonephritis and stage 2 chronic kidney disease. The current medications include losartan and atorvastatin. He reports a daily alcohol intake of 3 glasses of whiskey. The blood pressure is 140/90 mm Hg and the heart rate is 63/min. The BMI is 35.4 kg/m2. On physical examination, there is 2+ pitting edema of the lower legs and face. The pulmonary, cardiac, and abdominal examinations are within normal limits. There is no costovertebral angle tenderness noted. Ophthalmoscopy shows numerous microaneurysms and retinal hemorrhages concentrated in the fundus. The neurological examination reveals a symmetric decrease in vibration and 2 point discrimination in the patient’s feet and legs extending up to the lower third of the calves. The ankle-deep tendon reflexes are decreased bilaterally. The laboratory test results are as follows:
Serum glucose (fasting) 140 mg/dL
HbA1c 8.5%
BUN 27 mg/dL
Serum creatinine 1.3 mg/dL
eGFR 55 mL/min
The patient is prescribed the first-line drug recommended for his condition.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1731,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1578,Extracted,"A 63-year-old man comes to the physician because of a 2-day history of redness, swelling, and pain of the right leg. He also has fever, chills, and nausea. He has noticed liquid oozing from the affected area on his right leg. He has a history of hypertension and gastroesophageal reflux disease. Three months ago, he was hospitalized for treatment of a hip fracture. His current medications include metoprolol, enalapril, and omeprazole. His temperature is 38.7°C (101.7°F), pulse is 106/min, and blood pressure is 142/94 mm Hg. Examination of the right lower leg shows a large area of erythema with poorly-demarcated borders and purulent drainage. The area is nonfluctuant, warm, and tender to touch. Examination of the right groin shows several enlarged, tender lymph nodes. There is mild edema of the ankles bilaterally. Blood and wound cultures are collected.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [94.0, 'mm hg'], 'Systolic Blood Pressure': [142.0, 'mm hg']}",110,104.5,115.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 142.0 mm Hg + 2/3 * 94.0 mm Hg = 110.0 mm Hg.
Hence, the patient's mean arterial pressure is 110.0 mm Hg."
1732,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6682378-1,Extracted,"A 59-year-old male presented with a three-week history of weakness and fatigue associated with black tarry stools. Past medical history was significant for smoking, essential hypertension, diabetes mellitus, coronary artery disease, and chronic obstructive pulmonary disease. Two years earlier, CT scan of the chest showed left hilar mass (Figure ).
The patient was diagnosed with high-grade squamous cell carcinoma of the left upper lobe. At that time imaging studies showed metastatic disease to the brain. He was treated with palliative chemo-radiation therapy.
At this presentation, the patient was hypotensive with a blood pressure of 90/50 mm Hg, tachycardia at 110 beats per minute, and respiratory rate of 18 breaths per minute. He was afebrile. Physical examination revealed mild distress, moderate to severe dehydration, along with marked pallor of the skin and conjunctivae. His cardiopulmonary, abdominal, and neurological examination was unremarkable.
The laboratory workup revealed marked anemia with hemoglobin of 3.9 g/dl. All other laboratory tests were within reference ranges, including white blood cell count, platelet count, liver function panel, a metabolic panel, and PT/INR. CT scan of the pelvis and abdomen was negative for acute abnormalities or masses. He was admitted to the medical intensive care unit (ICU), started on intravenous (IV) fluid resuscitation, and transfused with four units of packed red blood cells.
After the patient was stabilized, colonoscopy was carried out revealing multiple colonic polyps which were removed and sent to the laboratory for diagnostic evaluation. One polyp showed sheets of poorly differentiated malignant cells subjacent to the overlying mucosa. These were positive for pan-keratin and negative for S100, HMB 45, CD20, CD45RO, chromogranin and synaptophysin (Figures -).
The histologic morphology matched the tumor identified two years earlier in the left upper lobe of the lung. Of note, the patient had upper and lower endoscopy two years prior this presentation. At that time, the upper GI tract appeared normal while two benign hyperplastic polyps were removed from the lower GI tract.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [50.0, 'mm hg']}",63.33333,60.16666,66.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 50.0 mm Hg = 63.33333 mm Hg.
Hence, the patient's mean arterial pressure is 63.33333 mm Hg."
1733,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1868,Extracted,"A 33-year-old man is brought to the emergency department 20 minutes after losing control over his bicycle and colliding with a parked car. The handlebar of the bicycle hit his lower abdomen. On arrival, he is alert and oriented. His pulse is 90/min, respirations are 17/min and blood pressure is 110/70 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 97%. The pupils are equal and reactive to light. There are multiple bruises over his chest and lower extremities. The lungs are clear to auscultation. Cardiac examination shows no abnormalities. The abdomen is soft and nontender. There is no pelvic instability. Rectal examination is unremarkable. A complete blood count, prothrombin time, and serum concentrations of glucose, creatinine, and electrolytes are within the reference range. Urine dipstick is mildly positive for blood. Microscopic examination of the urine shows 20 RBCs/hpf.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1734,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1114,Extracted,"A 25-year-old man is admitted to the emergency department because of an episode of acute psychosis with suicidal ideation. He has no history of serious illness and currently takes no medications. Despite appropriate safety precautions, he manages to leave the examination room unattended. Shortly afterward, he is found lying outside the emergency department. A visitor reports that she saw the patient climbing up the facade of the hospital building. He does not respond to questions but points to his head when asked about pain. His pulse is 131/min, respirations are 22/min, and blood pressure is 95/61 mm Hg. Physical examination shows a 1-cm head laceration and an open fracture of the right tibia. He opens his eyes spontaneously. Pupils are equal, round, and reactive to light. Breath sounds are decreased over the right lung field, and the upper right hemithorax is hyperresonant to percussion.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [95.0, 'mm hg'], 'Diastolic Blood Pressure': [61.0, 'mm hg']}",72.33333,68.71666,75.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 95.0 mm Hg + 2/3 * 61.0 mm Hg = 72.33333 mm Hg.
Hence, the patient's mean arterial pressure is 72.33333 mm Hg."
1735,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6195939-1,Extracted,"A 14-year-old male presented to the emergency department with two episodes of seizure preceded by a history of headache for 1 month and diminution of vision in both eyes for 5 days. His past history was significant for appendicectomy 3 years ago and severe abdominal pain 2 months ago. On examination, the patient was conscious, oriented and comprehending, with no neurological deficits. His blood pressure was 170/110 mmHg and other vitals were normal. A fundoscopic examination later revealed Grade 4 hypertensive retinopathy.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [170.0, 'mm hg'], 'Diastolic Blood Pressure': [110.0, 'mm hg']}",130,123.5,136.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 170.0 mm Hg + 2/3 * 110.0 mm Hg = 130.0 mm Hg.
Hence, the patient's mean arterial pressure is 130.0 mm Hg."
1736,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8530986-1,Extracted,"We present a 20-year-old woman (body weight, 55 kg; height, 1.60 m) with a history of IPAH diagnosed at the age of 16 after developing episodes of syncope. She initiated combination therapy with sildenafil and bosentan, which was switched to macitentan due to hepatotoxicity. Along the clinical course of the disease, the treatment was escalated to subcutaneous treprostinil due to a suboptimal response to dual therapy. Chronic adjuvant therapy included spironolactone and anticoagulation with acenocoumarol.
High-risk categorization was based on clinical variables (WHO functional class 3/4); biochemical markers [Pro-B-type natriuretic peptide (BNP): 3000 ng/mL, age-related reference value <450 pg/mL]; echocardiographic parameters (right atrium area: 43.2 cm2, right atrial volume: 113 mL/m2, and a moderate pericardial effusion measuring 15 mm); and pulmonary catheterization (right atrial pressure: 17 mmHg). As a result, switching to intravenous infusion of epoprostenol was decided in accordance with local and European guidelines.
The patient was admitted to the cardiac intensive care unit for placement of a tunnelled central line (Hickman®) and epoprostenol dose titration.
Vital signs recording on admission showed sinus tachycardia at 110 b.p.m., blood pressure 102/70 mmHg, and 97% SpO2 on room air. Cardiovascular physical examination revealed a loud and fixed S2 splitting, palpable parasternal lift at second left intercostal space with dullness on percussion, and mild peripheral oedema.
For target dose calculation, we used an approximate equivalent dose ratio of treprostinil to epoprostenol of 2:1 based on the equimolar potency of epoprostenol and the experience of other longer protocols in which the final dose reached this proportion. Thus, the target dose of epoprostenol was estimated at 32 ng/kg/min.
Drug titration began after central line placement. The infusion rate of each drug was based on its half-life and adjusted every 180 min. Treprostinil dosage decreased 4 ng/kg/min every 3 h while epoprostenol increased 2 ng/kg/min. Epoprostenol was titrated up under close monitoring of respiratory rate, heart rate, blood pressure, and blood oxygen saturation. Dosage was reduced to the previous titration step if side effects developed. The transition from SC treprostinil to IV epoprostenol lasted 48 h. There were no adverse events. Pro-BNP level at the end of titration was 2928 pg/mL.
The patient was transferred from the cardiac intensive care unit to the cardiology ward 4 days after titration. On the fifth day, she developed a non-pruritic macular rash of the limbs that faded spontaneously within hours without any dosage change and was discharged from hospital 2 days later. There were no significant changes in cardiac ultrasound parameters during hospital stay.
Despite the well-tolerated infusion of epoprostenol, absence of serious adverse events, and short length of stay, persistence in WHO functional class 3/4 and signs of right-sided heart failure on a 7-day follow-up appointment prompted referral to pre-transplant assessment. At this stage, a new echocardiogram showed a pulmonary artery systolic pressure (PASP) of 95 mmHg, impaired right ventricular systolic function, and persistent moderate pericardial effusion.
Orthotopic double lung transplantation was performed 47 days after discharge, with marked echocardiographic improvement 1 month later (PASP = 31, preserved right ventricular function, and absence of pericardial effusion).
Examination of the explanted lungs revealed medial wall thickening and muscularization, obliteration of small arteries, intimal fibrosis, and plexiform lesions consistent with IPAH.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [102.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",80.66667,76.63334,84.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 102.0 mm Hg + 2/3 * 70.0 mm Hg = 80.66667 mm Hg.
Hence, the patient's mean arterial pressure is 80.66667 mm Hg."
1737,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5987290-1,Extracted,"The patient is a 75-year-old female with a history of rheumatoid arthritis originally diagnosed at age 31 and treated with various DMARDs. She had been well managed on etanercept but was transitioned to a regimen of leflunomide and inflixamab six years prior to presentation. Approximately seven months prior to presentation, the patient was transitioned back to etanercept due to worsening disease activity. In addition, the patient had a history of spinal stenosis, treated with two L4-L5 epidural steroid injections two years prior to presentation.
The patient was initially admitted to the medical floor for management of severe back and right leg pain. Her remaining review of systems was negative with the exception of nausea and an episode of emesis en route to the hospital, and initial presenting vital signs were all within normal limits. On the evening of her admission, the patient was found somnolent with expressive aphasia. Blood pressure at that time was elevated to 188/90 mmHg. Stroke evaluation was initiated. Head CT was negative for intracranial hemorrhage, and tPA was administered within 3 hours of symptom onset. The patient remained neurologically unchanged over the next 36 hours, complaining only of a mild headache. She remained hypertensive and required a nicardipine infusion to maintain a blood pressure less than 180/105 mmHg.
On day 3 of admission, she developed an acute change in mental status. She then experienced rigors and a fever of 103°F (39.4°C). Exam at that time was notable for nuchal rigidity. A set of two blood cultures were drawn at this time, and she was then started on vancomycin, cefepime, ampicillin, and acyclovir as there was concern for a central nervous system infection. Lumbar puncture revealed 493 white blood cells/µL (90% neutrophils), 377 red blood cells/µL, glucose <5 mg/dL, and protein 410 mg/dL, and Gram staining demonstrated rare Gram-negative rods. Cultures from the lumbar puncture ultimately grew Salmonella species, and on day 4 of hospitalization, the patient was transitioned to ceftriaxone 2 grams twice daily. Stool cultures were sent to the laboratory at this time, 24 hours after initiating antibiotics. The patient also underwent HIV testing, which was negative for HIV1 and HIV2 antibodies.
Due to worsening mental status and inability to protect her airway, she was intubated. She developed hypothermia to 95.2°F (35.1°C), progressive elevation in white blood cell count to 14.0 cells/µL, and a new right lower lobe consolidation on chest X-ray. She was transitioned from ceftriaxone to vancomycin and cefepime. She completed treatment for aspiration pneumonia, was extubated, and was transitioned back to ceftriaxone. Exam was notable for ongoing aphasia and encephalopathy. She was also found to be in new-onset atrial fibrillation.
Multiple imaging studies were performed in order to identify the source of infection. MRI of the sacral, lumbar, and thoracic spine on hospital day 4 demonstrated diffuse leptomeningeal and pial enhancement, as well as a 5 mm subdural fluid collection; there was no evidence of discitis or osteomyelitis. Repeat MRI on hospital day 11 demonstrated similar enhancement with a decrease in the subdural fluid collection.
The patient's lumbar puncture was also repeated during her hospitalization. Repeat lumbar puncture on day 8 of hospital stay (and day 6 of antibiotics) no longer showed organisms but did show ongoing inflammation with 924 white blood cell/µL, glucose <5 mg/dL, and protein 370 mg/dL. A third lumbar puncture on day 15 of hospital stay, completed due to developing communicating hydrocephalus, also demonstrated persistent inflammation, but no organisms on Gram stain or culture. As the patient's mental status improved and the opening pressure downtrended from 21 cmH2O on the second lumbar puncture to 15 cmH2O on the third, no additional lumbar punctures were performed and no intervention was taken for the patient's communicating hydrocephalus. Other than the Salmonella species found on her initial lumbar puncture, no additional organisms were isolated from subsequent CSF cultures.
The patient's blood cultures drawn at the time of her initial fever had no growth at 5 days. The patient's stool cultures also did not show any pathogenic organisms. The CSF sample which grew Salmonella species was sent to the state laboratory for organism identification. At the time of this publication, the specific species isolated from the sample remain pending. The patient did not have urine cultures analyzed during this hospitalization.
Ultimately, the patient was treated with a regimen of IV ceftriaxone 2 g every 12 hours for a total of 23 days. The patient's mental status improved though she required PEG tube placement due to persistent encephalopathy and poor oral intake. Her hospitalization was complicated by a Clostridium difficile infection and development of a stage IV decubitus ulcer which limited her physical improvement. Though the patient was discharged, 4 months following initial diagnosis of Salmonella meningitis, she was readmitted to the hospital for management of septic shock, was transitioned to comfort care due to refractory shock and her prior poor quality of life, and passed away during this subsequent hospitalization. The patient's etanercept, which is a weekly administered medication, was held upon initial presentation to the hospital and never restarted.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [188.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",122.66667,116.53334,128.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 188.0 mm Hg + 2/3 * 90.0 mm Hg = 122.66667 mm Hg.
Hence, the patient's mean arterial pressure is 122.66667 mm Hg."
1738,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5467927-1,Extracted,"A 46-year-old Caucasian man with a history of repaired D-TGA presented to our clinic with complaints of exertional dyspnea and fatigue. He underwent a Mustard atrial baffle procedure when he was 18 months old. He had an intact ventricular septum, normal pulmonary artery pressure (PAP), and no pulmonic stenosis at the time of the Mustard procedure. The postoperative period was complicated by a stroke with right upper extremity weakness. He had regular follow-ups in a pediatric cardiology clinic until the middle of his second decade, but then was not seen for more than 20 years. Six months prior to this presentation, he noticed increased shortness of breath on moderate exertion and was found to be in NYHA functional class II. Echocardiogram revealed systolic dysfunction of the systemic right ventricle. PAH was not suspected based on sub-pulmonary velocities on echo. He was started on a low dose beta-blocker and angiotensinogen-converting enzyme (ACE) inhibitors, in addition to his aspirin. However, he continued to have progressive increasing exertional shortness of breath. He had no orthopnea or paroxysmal nocturnal dyspnea, chest pain, syncope, or peripheral edema. His family history was significant for D-TGA in his maternal cousin.
On examination, his blood pressure was 110/72 mmHg, heart rate was 68 beats per minute, respiratory rate was 20 per min, and oxygen saturation was 93% on room air. He had no cyanosis, clubbing, jugular venous distension, or lower extremity edema. He had no palpable second heart sound or thrill. Cardiac auscultation revealed normal first heart sound and a loud pulmonic second heart sound with a 3/6-holosystolic murmur on the lower right sternal border. He had normal breath sounds bilaterally. He had residual right upper extremity weakness with no other focal neurological findings. Electrocardiogram showed sinus bradycardia with right axis deviation, incomplete right bundle branch block, and right ventricular hypertrophy with strain pattern. Echocardiogram revealed a hypertrophied systemic right ventricle with moderately diminished systolic function, moderately dilated and hypertrophied pulmonary left ventricle with moderately reduced systolic function, and moderate pulmonic insufficiency. Cardiac magnetic resonance imaging (MRI) confirmed the presence of D-TGA corrected with Mustard atrial baffle procedure (). His systemic right ventricular function was low normal with an ejection fraction (EF) of 52% and his pulmonary left ventricle was moderately dilated with moderately reduced function, with an EF of 42% (). There was no evidence of obstruction in both the systemic venous and the pulmonary venous baffles.
On invasive hemodynamic assessment, his right atrial pressure was 8 mmHg, PAP was 134/49 with a mean of 79 mmHg, and pulmonary capillary wedge pressure (PCWP) was 14 mmHg. Cardiac output as measured by thermodilution was 3.8 L/min with a cardiac index of 1.9 L/min/m2. The pulmonary vascular resistance (PVR) was 17 Wood units. With inhaled nitric oxide, there was no acute vasodilatory response. His O2 saturations were as follows: superior vena cava 72%, right atrium 73%, pulmonary left ventricle 70%, pulmonary artery 67%, and systemic saturation 95%. There was no significant demonstrable left-to-right shunt, right-to-left shunt, or baffle leak (Qp/Qs was 1). His baffle pressure was 12 mmHg. There was moderate superior vena cava baffle stenosis with a 4-mm gradient across the superior vena cava with decompression via azygous veins. He had no inferior vena cava baffle obstruction. There was a mild 6 mmHg gradient across the pulmonary venous baffle to the systemic right ventricle. Invasive angiography confirmed the moderate superior vena cava baffle stenosis but the pulmonary venous baffle could not be well visualized during the levophase. Coronary angiogram revealed normal coronary arteries.
Ventilation perfusion scan excluded chronic thromboembolic pulmonary hypertension. His lung function test showed no evidence of restrictive or obstructive disease. His serology for antinuclear antibody, rheumatoid factor, human immunodeficiency virus, and hepatitis were negative. He had no history of obstructive sleep apnea, but did not have a formal sleep study. Electrolytes, renal function, and liver function were within normal limits. Serum brain natriuretic peptide level was elevated at 548 pg/mL. Normal PCWP excluded pulmonary venous baffle obstruction. He was diagnosed with late-onset PAH associated with repaired D-TGA. He was initiated on upfront combination therapy with Ambrisentan and Tadalafil. Three months after the onset of therapy, his six-minute walk distance improved from 437 m to 458 m but there was no significant improvement in his pulmonic left ventricular ejection fraction by cardiac MRI. On invasive hemodynamic assessment, his PAP decreased to 86/36 with a mean of 53 mmHg, PVR decreased to 9.7 Wood units, and cardiac output increased to 4.8 L/min.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mmhg'], 'Diastolic Blood Pressure': [72.0, 'mmhg']}",84.66667,80.43334,88.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 72.0 mm Hg = 84.66667 mm Hg.
Hence, the patient's mean arterial pressure is 84.66667 mm Hg."
1739,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-759,Extracted,"A 59-year-old woman comes to the emergency department because of a 2-day history of worsening fever, chills, malaise, productive cough, and difficulty breathing. Three days ago, she returned from a trip to South Africa. She has type 2 diabetes mellitus, hypertension, and varicose veins. Her current medications include metformin, lisinopril, and atorvastatin. Her temperature is 39.4°C (102.9°F), pulse is 102/minute, blood pressure is 94/68 mm Hg, and respirations are 31/minute. Pulse oximetry on 2 L of oxygen via nasal cannula shows an oxygen saturation of 91%. Examination reveals decreased breath sounds and dull percussion over the left lung base. The skin is very warm and well-perfused. The remainder of the examination shows no abnormalities. Laboratory studies show:
Hemoglobin 11.6 g/dL
Leukocyte count 15,400/mm3
platelet count 282,000/mm3
Serum
Na+ 144 mEq/L
Cl- 104 mEq/L
K+ 4.9 mEq/L
Creatinine 1.5 mg/dL
Blood and urine for cultures are obtained. Intravenous fluid resuscitation is begun.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [68.0, 'mm hg'], 'Systolic Blood Pressure': [94.0, 'mm hg']}",76.66667,72.83334,80.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 94.0 mm Hg + 2/3 * 68.0 mm Hg = 76.66667 mm Hg.
Hence, the patient's mean arterial pressure is 76.66667 mm Hg."
1740,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3492084-1,Extracted,"A 10-year-old Kurdish boy presented with bone pain and fever associated with night sweats, shortness of breath, weight loss (5kg/month), purple purpuric spots over the skin and bleeding from the nose. The patient’s history dated back to 1 month before admission. On examination, we observed pallor, cachexia, dyspnea, fever, tachycardia, tachypnea, multiple petechiae and ecchymoses all over the skin, dilated tortuous veins over the chest, pulse rate 120bpm, respiratory rate 23cycles/minute, temperature 39°C and blood pressure 90/45mmHg. Moreover, we found multiple small cervical lymphadenopathies and mild splenomegaly 3cm below the left costal margin. The boy’s liver was tender 7cm below the right costal margin, and he had gross abdominal distention. The initial blood counts were hemoglobin 64g/L, white blood cell count 34 × 109/L, platelets 25 × 109/L and blasts 38% (Figure
A). The blasts were homogeneous with a high nuclear to cytoplasmic ratio, inconspicuous nucleoli and open chromatin, and some of the blasts were vacuolated. Platelets were markedly reduced (Figure
B). There was mediastinal widening visualized on a chest X-ray (Figure
). MRI showed lumbosacral vertebrae with diffuse infiltration of the axial bone marrow of the lower dorsal and lumbar vertebrae, suggestive of bony metastases predominantly osteolytic in nature (Figure
A–
C). Bone marrow aspiration (BMA) showed no fragments but few areas of necrosis. Bone marrow biopsy showed marked BMN (Figure
A and
B). The first immunophenotyping was not conclusive, but the second was positive for CD3 and terminal deoxynucleotidyl transferase and negative for CD20, CD79a and CD10.
After admission, the patient’s condition deteriorated and features of frank superior vena cava syndrome developed. The patient was treated with chemotherapy according to the ALL protocol, and complete remission was achieved on day 28. At the 24th week of chemotherapy, his condition relapsed on treatment. He returned to our hospital with fever, chest infection and 60% blasts observed on peripheral blood film, and the complete blood count revealed severe pancytopenia. The BMA was a dry tap, but the biopsy showed hypercellular marrow with extensive infiltration by mononuclear cells and disappearance of necrosis (Figure
C and
D). Treatment was reinitiated according to the ALL protocol (bone marrow relapsed protocol), after which he developed severe mucositis, uncontrolled septicemia and electrolyte imbalance. Eventually, that led to death.
The BMA at the time of diagnosis was diluted, and the slides appeared to show artefact with a few necrotic cells. The biopsy was a 1.6cm piece of tissue that consisted of a fragment of trabecular bone showing marked BMN, as shown in the image in Figure
A (before treatment). The result of immunohistochemistry was not interpretable for the first specimen, but for the second the diagnosis was definitive as precursor T-cell ALL.
During admission, we gave the patient intravenous fluid 3000ml/m2/day, allopurinol tablets 100mg/m2/dose and antibiotics. The patient’s condition subsequently deteriorated, and he developed progressive dyspnea, chest tightness, abdominal distention and fever. The patient was near to developing frank features of superior vena cava syndrome, but later he developed bilateral lower-limb weakness. The straight leg raising test was observed to be positive bilaterally. MRI of the dorsolumbosacral spine showed diffuse focal infiltration of the axial bone marrow of the lower dorsal and lumbar vertebrae causing altered hypointense T1-weighted signal intensity (Figure
A and
B). The image was suggestive of bony metastasis that was predominantly osteolytic in nature (Figure
A and
B). Incidental hepatosplenomegaly and bilateral renal enlargement were also observed (Figure
C), but there was no pressure on the spinal cord.
We started dexamethasone intravenous infusion at 6mg/m2. Seven days after the patient’s admission, we started induction therapy with vincristine 1.5mg/m2 intravenous bolus on days 7, 14, 21 and 28. Dexamethasone 6mg/m2 was administered daily, and daunorubicin 25mg/m2 was given on the days 1 and 7.
Upon starting induction, the patient developed attacks of tonic-clonic contractions. We found computed tomography of the brain without contrast to be negative. Electrolyte measurements showed severe hypocalcemia, and we induced correction, which stabilized the convulsions. On day 28, BMA indicated a few fragments and megakaryocytes were seen. Erythroid and myeloid series were present with all stages of maturation. The data also indicated predominant neutrophils and histiocytes, but the cellular elements could not confirm an excess of blast cells. The bone marrow biopsy report showed 95% cellularity, which was composed predominantly of early-stage granulocytes and normal maturation stages of hematopoietic cells. The blasts constituted about 2% of total marrow nucleated cells. The myeloid to erythroid cell ratio was 8:1.
After a 4-week induction period, complete remission was observed and we continued giving the early consolidation chemotherapy. Unfortunately, at the 24th week of treatment, the patient returned with fever, chest infection, neutropenia and thrombocytopenia, and we found the presence of a few blasts in the peripheral blood film. The patient was not responding to supportive treatment that included antibiotics and antipyretics. The follow-up analysis of BMA showed excessive bone marrow infiltration by mononuclear cells with multiple inconspicuous nucleoli. Both erythroid and megakaryocytic precursors were suppressed in BMA, whereas in relapsed biopsy no necrosis was observed (Figure
C and
D).
On the reinduction therapy date, we followed a bone marrow relapsed protocol. On the 14th day of treatment reinduction, the patient developed severe anemia, thrombocytopenia and neutropenia. In addition, he developed grade IV mucositis with hypokalemia. The patient could not tolerate the complications, and he developed septicemia followed by sepsis. The patient’s death was an inevitable outcome. The overall survival period was 26 weeks after first diagnosis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [45.0, 'mm hg']}",60,57,63,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 45.0 mm Hg = 60.0 mm Hg.
Hence, the patient's mean arterial pressure is 60.0 mm Hg."
1741,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7296884-1,Extracted,"A previously healthy 36-year-old man presented to the emergency department with an altered mental status. Two days prior to his hospitalization, the patient experienced intermittent vomiting, with two to three episodes that were reported to a local physician. As the patient progressed to unconsciousness, he was immediately transported to the emergency department. There was no history of fever, cough, shortness of breath, or sensitivity to light. Furthermore, there was no recent or remote history of travel, medication or herbal use, previous surgery, or sick contact with individuals with COVID-19. He did not have a history of consuming alcohol, drug abuse, or unprotected sexual intercourse. On admission, the patient was isolated and tested for COVID-19.
At the initial presentation, physical examination revealed hypothermia of 35.5°C, a pulse of 88/min, blood pressure of 136/78 mmHg, and respiratory rate of 20/min with a room air oxygen saturation of 98%. His skin was jaundiced with the icteric sclera. The liver edge was not palpable and did not reveal hepatomegaly. Chest and cardiovascular examinations were normal. His Glasgow Coma Scale (GCS) score was 7/15.
Pertinent laboratory findings are presented in Table . Briefly, the findings were: AST 4,933 U/L (reference: <50 U/L), ALT 4,758 U/L (reference: <40 U/L), total bilirubin 183.9 mmol/L (reference: <21 mmol/L) with direct bilirubin 145 mmol/L (reference: <5 mmol/L), alkaline phosphatase (ALP) 212 U/L (reference: 40-129 U/L), and albumin 33 g/L (reference: 35-52 g/L) (see Table ). In addition, his international normalized ratio (INR) was >10 (reference: 0.82-1.20). Except for ammonia 74 mmol/L (reference: 16-60 mmol/L), results for all other laboratory assessments such as complete blood count, total protein, and serum chemistry were unremarkable. Computerized tomography (CT) scan of the brain, chest X-ray, and Doppler ultrasound of the liver were normal.
The differential diagnoses for active viral hepatitis (A, C, and E), HIV, autoimmune hepatitis, Wilson’s disease, cytomegalovirus, and Epstein-Barr virus antibodies were negative. The patient tested negative for HIV, hepatitis A, hepatitis C, hepatitis E, cytomegalovirus, and Epstein-Barr virus antibodies. Additional liver workup revealed hepatitis B (HB) surface Ag-positivity, HB core Ab-positivity (IgM), HB envelop (HBe) Ag-negativity, and HBe Ab positivity, suggestive of reactivation of an HBV infection. His hepatitis B DNA viral load was 2,490 IU/mL (reference: <1000 IU/mL), confirming the diagnosis of an acute HBV infection. His COVID-19 polymerase chain reaction (PCR) test results were also positive.
Due to the altered mental status and elevated enzymatic activities in the liver, admission into the ICU was initiated. The patient was started on lactulose via a nasogastric tube (NGT) and was administered cryoprecipitate on day 1. On day 2, entecavir (1 mg daily), vitamin K (10 mg daily), and intravenous thiamin (100 mg daily) administration were initiated. On day 3, his GCS improved to 11/15, with a gradual improvement in liver function parameters. Subsequently, he was shifted to the COVID-19 ward. On day 7, the patient regained complete consciousness (GCS: 15/15); his liver function parameters showed improvements with respect to transaminase and bilirubin levels (Table ). Multiple nasopharyngeal samples (3/4) for the SARS-CoV-2 PCR tested positive, but his chest X-ray remained normal. On day 16, his liver function parameters were in the cholestatic phase with decreasing transaminase levels. He tested negative for COVID-19 PCR twice, and the patient was eventually shifted to the general ward.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [136.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",97.33333,92.46666,102.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 136.0 mm Hg + 2/3 * 78.0 mm Hg = 97.33333 mm Hg.
Hence, the patient's mean arterial pressure is 97.33333 mm Hg."
1742,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4320801-1,Extracted,"A 51-year-old male presented to Jamaica Hospital Medical Center for severe abdominal pain and nausea that began abruptly during a five-hour transcontinental flight. His past medical history included only asthma. Upon arrival at the hospital, he developed recurrent nonbloody, nonbilious emesis. His initial vital signs included a blood pressure of 133/75 mmHg, pulse of 83 BPM, and temperature of 36.3°C. A physical exam revealed rebound tenderness and guarding. His initial labs were as follows: white blood cell count of 15.3 K/μL, hemoglobin of 15.7 g/dL, hematocrit of 47.8%, platelet count of 376 K/μL, and a normal coagulation profile. The patient stated that the day prior to the flight, he had a solid bowel movement with no blood or melena noted and was not vomiting at that time; he also denied any sick contacts.
After several hours in the Emergency Department, the patient attempted to stand and lost consciousness. An immediate blood pressure was noted to be 53 systolic. Repeat blood work was sent which revealed a decreasing hematocrit (48% to 30%) and hemoglobin (15.7 g/dL to 9.6 g/dL). Fluids were started and an emergent abdominal CT was performed. The CT scan revealed hyper-dense fluid present throughout the abdomen and pelvis, with heterogeneity of the fluid and an active contrast blush (). A surgical consult was called and the patient was taken to the operating room emergently for exploration.
In the operating room, Meckel's diverticulum was encountered with a mesodiverticular band that appeared to have torn, resulting in massive intraperitoneal hemorrhage. A small bowel resection was performed to include Meckel's diverticulum, and continuity was reestablished with a side-side stapled enteric anastomosis. Total blood loss for the case was 2000 mL; 3 units of packed red blood cells and 3 units of fresh frozen plasma were administered. The patient was transferred to the SICU postoperatively and subsequently discharged on postoperative day 8.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [75.0, 'mm hg'], 'Systolic Blood Pressure': [133.0, 'mm hg']}",94.33333,89.61666,99.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 133.0 mm Hg + 2/3 * 75.0 mm Hg = 94.33333 mm Hg.
Hence, the patient's mean arterial pressure is 94.33333 mm Hg."
1743,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-6262,Extracted,"A 45-year-old man presents to the emergency department after being found down in a public park. The patient is homeless and is a known IV drug abuser. He smells of alcohol, vomit, and urine. His temperature is 99.8°F (37.7°C), blood pressure is 90/38 mmHg, and pulse is 160/min. Physical exam reveals an unkempt man with a Glasgow Coma Scale of 11. There are track marks on the patient's arm and an open wound on his right forearm. The patient's oral cavity demonstrates very poor oral hygiene and bleeding gums. The patient's urine is positive for multiple illicit substances. A FAST exam and a head CT are both performed and negative for any abnormal findings. The patient is given 2L of IV fluids but his vitals remain unchanged. The patient is protecting his airway and an initial chest radiograph is unremarkable. While in the department, the patient's mental status improves and he is complaining of pain and requesting morphine.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [38.0, 'mm hg']}",55.33333,52.56666,58.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 38.0 mm Hg = 55.33333 mm Hg.
Hence, the patient's mean arterial pressure is 55.33333 mm Hg."
1744,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8760,Extracted,"A 35-year-old woman presents to her primary care physician for recurrent deep venous thrombosis (DVT) of her left lower extremity. She is a vegetarian and often struggles to maintain an adequate intake of non-animal based protein. She currently smokes 1 pack of cigarettes per day, drinks a glass of wine per day, and currently denies any illicit drug use, although she endorses a history of heroin use (injection). Her past medical history is significant for 4 prior admissions for lower extremity swelling and pain that resulted in diagnoses of deep venous thrombosis. Her vital signs include: temperature, 36.7°C (98.0°F); blood pressure, 126/74 mm Hg; heart rate, 87/min; and respiratory rate, 16/min. On physical examination, her pulses are bounding, the patent’s complexion is pale, breath sounds are clear, and heart sounds are normal. The spleen is mildly enlarged. She is admitted for DVT treatment and a full hypercoagulability workup.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [74.0, 'mm hg'], 'Systolic Blood Pressure': [126.0, 'mm hg']}",91.33333,86.76666,95.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 126.0 mm Hg + 2/3 * 74.0 mm Hg = 91.33333 mm Hg.
Hence, the patient's mean arterial pressure is 91.33333 mm Hg."
1745,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3543893-1,Extracted,"A 32-year-old man presented to us following a fall from height. He suffered from left posterior 4th to 12th rib fracture with subcutaneous emphysema, lung contusion and bilateral hemopneumothorax, intraabdominal injury with pneumoperitoneum, left renal injury (grade 3) with perinephric hematoma, and a T11 bony Chance fracture without neurological deficit. At the casualty department, bilateral chest tubes were inserted. At presentation, the patient was tachypneic with a respiratory rate of 26/min, blood pressure was 124/88 mmHg with a heart rate between 125 and 136 beats/min. He was resuscitated with fluids. An initial hemoglobin level of 9.5 g/dL was documented.
The patient underwent an emergency laparotomy with small bowel resection and end-to-end anastomosis at 13 hours posttrauma. Following this, minimally invasive percutaneous instrumentation from T10 to T12 was done. Four percutaneous screws were inserted simultaneously through four stab incisions []. The instrumentation was performed using size 5.5 mm screws for both T10 as well as T12 vertebrae. The duration of the operation was 45 min, with a blood loss of 75 mls (measured by soaked gauze). The screws were inserted simultaneously to reduce the amount of image intensifier exposures required for the procedure. The total exposure (Siemens Siremobil 2000) was 25 exposures at 75–90 kV peak and 1.5–2.0 mA. Intraoperatively, 2 units of packed red blood cells were transfused. Intraoperative hemoglobin was maintained at 10.0 g/dL. No hemodynamic instability or hypoxic episodes were documented intraoperatively.
Postoperatively, the patient was allowed to turn to his side every two hourly and was also allowed to be propped up on day 1. On postoperative day 3, once the abdominal and chest drains were removed, the patient was allowed to sit up and stand independently. Subsequently, a thoracolumbar support orthosis was applied and the patient was discharged on day 15 post injury.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [124.0, 'mmhg'], 'Diastolic Blood Pressure': [88.0, 'mmhg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 124.0 mm Hg + 2/3 * 88.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1746,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7298960-1,Extracted,"A 7-year-old boy with a negative history for any particular diseases presented with malaise and abdominal pain to the emergency room. These symptoms had appeared since 1 month before admission and were gradually worsen in the last 2 weeks. The patient had also developed polydipsia and myalgia. On admission, the patient was afebrile (body temperature [BT], 36.7), with a pulse rate (PR) of 200/min [150/min after hydration], a respiratory rate of 25/min, blood pressure (BP) of 105/65 mmHg, and blood sugar (BS) of 256 mg/ml. Oral mucosa was dehydrated but other examinations revealed no significant findings. Laboratory test results are reported in Table . The patient was admitted to endocrinology service with the diagnosis of new-onset diabetes mellitus type 1 (DM1). BS was controlled (fasting BS = 100–110 mg/dl, postprandial BS = 115–140 mg/dl) by administration of insulin. Electrocardiogram showed normal sinus tachycardia. On the transthoracic echocardiography, there was a mild pericardial effusion, left ventricular (LV) ejection fraction (EF) of 30–35%, mild LV hypertrophy and LV diameter of 33 mm. Considering sinus tachycardia, echocardiography findings, white blood cell count (WBC) of 17,200/μl, and erythrocyte sedimentation rate (ESR) of 60, the cardiologist suggested a diagnosis of cardiomyopathy due to viral myocarditis. Treatment with dopamine (1 μg/kg), milrinone (50 μg/kg stat and 5 μg/h infusion), furosemide (1 mg/kg two times daily), captopril (6.25 mg two times daily), and carvedilol (6.25 mg two times daily) was initiated and insulin therapy was continued with the same dose. BP monitoring was conducted but the patient was normotensive. PR was gradually reduced from 140 to 150/min to 105–100/min in a few days.. WBC was decreased from 17,200 to 10,940/μl (Table ). The patient was discharged and the following medications were prescribed to be taken at home: captopril (12.5 mg every 12 h), carvedilol (6.25 mg every 12 h), insulin glargine (4 units each night) and insulin aspart (2 units before each meal). In the outpatient visits, the patient had adequate BS control, normal BP, and was asymptomatic except for a mild malaise and inadequate weight gain.
After 21 months the patient was admitted again due to HT (BP, 189/140 mmHg), nausea, sudoresis, and malaise. No headache, tremor, pallor, dyspnea, and generalized weakness were seen in the patient before admission. The BP was reduced to 140/80 mmHg and transferred to ICU. The patient developed a headache during his stay in ICU.
Doppler ultrasonography of renal veins and arteries was performed but no significant pathologies were detected. Considering the positive familial history of pheochromocytoma in his uncle and clinical suspicion for pheochromocytoma, the urinary levels of metanephrine, epinephrine, norepinephrine, and vanillylmandelic acid were assessed. Hormonal assays revealed elevated serum and urinary normetanephrine, norepinephrine, and metanephrines (Table ). Furthermore, a metaiodobenzylguanidine (MIBG) scan and abdominal MRI were performed. Abdominal MRI confirmed the presence of a 35 × 25 × 16 mm mass at the left adrenal gland, which was hyper-signal on T2WI and hypo-signal on T1WI. The right adrenal gland was unremarkable (Fig. ). MIBG scintigraphy identified bilateral uptake increase in the regions of adrenal glands. Normal uptake was seen in other parts of the body. Bilateral MIBG avid areas in both adrenal glands were suggestive for pheochromocytoma (Fig. ). In transthoracic echocardiography, a mild LVH and a mild tricuspid regurgitating were reported. LVEF was 55% (Fig. ).
Treatment with oral Ca channel blocker, beta-blockers was initiated (amlodipine 5 mg and metoprolol 50 mg) and followed by losartan (25 mg daily) to adequately normalize BP.
The left side adrenal tumor was removed by surgery and the right side was examined but remained intact. Histopathological evaluations confirmed the diagnosis of pheochromocytoma. After surgery, the patient’s medications were tapered and discontinued. He remained normotensive and BS was in a normal range. The symptoms faded away and the patient was discharged with no further medications but was advised to return regularly for outpatient visits.
During 1 year follow-up after discharge, the patient remained asymptomatic. He was not receiving any medications. The BS was in the normal range and the patient was normotensive.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [140.0, 'mmhg'], 'Systolic Blood Pressure': [189.0, 'mmhg']}",156.33333,148.51666,164.15,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 189.0 mm Hg + 2/3 * 140.0 mm Hg = 156.33333 mm Hg.
Hence, the patient's mean arterial pressure is 156.33333 mm Hg."
1747,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4129160-1,Extracted,"We are reporting a case of a 43-year-old male with a past medical history of DVT of the left subclavian vein as a result of thoracic outlet syndrome, diagnosed in 2004. He was treated with warfarin for 6 months and later underwent left first rib resection in 2006. He remained asymptomatic until May 2013 when he started complaining of right upper extremity discomfort and reddish discoloration that started after minimal muscle strain of his right arm while walking his dog. The patient had no neurological deficit in the right arm and did not complain of any weakness. He visited an urgent care center and had a US Doppler of the right upper extremity that confirmed the diagnosis of right subclavian vein thrombosis. Enoxaparin was given and he was transferred to our hospital.
The patient's past medical history was unremarkable except for the above. He was not taking any medication regularly. He was not a smoker, never used any illicit drugs, and only occasionally drank alcohol. He was a brick layer and was left handed.
His family history was significant for DM in both parents. No family history of clotting disorders was present.
His vitals were stable: BP 118/80, pulse 73/minute, temperature 97.7 F, and an oxygen saturation of 96% on room air. No signs of distress were noted.
Physical exam revealed edema and mild erythema of the right forearm as compared to the left forearm. No right arm weakness was appreciated and sensations were intact. The rest of the physical exam was normal.
Laboratory tests showed HB 14.2 g/dl (12–15.3 g/dl), platelet 271 k/mm (150–450 k/mm), and WBC 6.1 k/mm (4–11 k/mm). Coagulation profile was done and showed INR 1.1 (0.9–1.1), APTT 35 seconds (23–33 seconds), homocysteine level of 8.7, anticardiolipin IgG 0.8% (<20%), anticardiolipin IgM 2.7% (<20%), anticardiolipin IgA 1.8% (<12%), protein C 92% (>69%), and protein S 77% (>59%); prothrombin mutation was positive (heterozygous genotype) for G20210A mutation in factor II gene. Factor V Leiden mutation was negative.
Patient had a chest XR that showed a small right first rib (). US Doppler of both lower extremities was done and was negative for deep vein thrombosis.
He was started on heparin infusion. After a day of anticoagulation, he had venogram that confirmed right subclavian vein thrombosis (Figures and ). Percutaneous transluminal balloon angioplasty of subclavian vein showed a narrowing at the level of the thoracic inlet that had an appearance of chronic scarring due to compression (). Finally, a pharmacomechanical thrombolysis and thrombectomy were performed.
After the procedure, the patient was put on therapeutic dose of Enoxaparin and he was discharged home on that. A week later he returned to the hospital and had right first rib removal, complete anterior and middle scalenectomy, mobilization and protection of the brachial plexus with external neurolysis of C5-T1 roots, and external venolysis of the left subclavian vein (Figures and ). Patient was discharged from the hospital on Warfarin after he was seen by a hematologist. He remained asymptomatic and is following up as an outpatient. The procedure and anticoagulation were successful in treating his condition and no recurrence of his condition has been observed in a one-year follow-up ().",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [118.0, 'mm hg']}",92.66667,88.03334,97.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 118.0 mm Hg + 2/3 * 80.0 mm Hg = 92.66667 mm Hg.
Hence, the patient's mean arterial pressure is 92.66667 mm Hg."
1748,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7836,Extracted,"A 73-year-old woman arrives at the emergency department due to intense central chest pain for 30 minutes this morning. She says the pain was cramping in nature and radiated down her left arm. She has a history of atrial fibrillation and type 2 diabetes mellitus. Her pulse is 98/min, respiratory rate is 19/min, temperature is 36.8°C (98.2°F), and blood pressure is 160/91 mm Hg. Cardiovascular examination shows no abnormalities. ECG is shown below.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [160.0, 'mm hg'], 'Diastolic Blood Pressure': [91.0, 'mm hg']}",114,108.3,119.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 91.0 mm Hg = 114.0 mm Hg.
Hence, the patient's mean arterial pressure is 114.0 mm Hg."
1749,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8456375-1,Extracted,"A 33-year-old Saudi female, Eastern region resident was admitted to the ‘Infectious Diseases’ ward of our teaching hospital King Fahad Hospital of the University, Imam AbdulRahman bin Faisal University with ‘fever of other and unknown origin’. The patient presented with a seven-day fever with chills and complained of decreased appetite and generalized body pain associated with dark urine, pale stool and diarrhea, with history of fever with chills and generalized body pains for one week. On taking detailed history, the patient stated that she had recently returned from a 20-day trip to the Ivory Coast. The patient didn’t have any form of comorbidities and denied any history of animal contact, immunocompromised status, or intake of any kind of prescribed or illicit drugs or raw milk ingestion during this period. Family history of the patient revealed absence of hereditary blood diseases and was of insignificant relation to the patient’s clinical presentation. The patient did not seek any medical facility prior her admission to our hospital and has only self-administrated paracetamol tablets in response to the fever and body aches.
On recording the vital signs (measurement of body temperature, weight, blood pressure and pulse rate), the patient was febrile with an oral temperature of 39.9°C, tachycardic with a pulse rate of 118 beats/minute, blood pressure of 135/85 mmHg, and respiratory rate of 20 breaths/minute.
Upon physical examination, the patient appeared ill and had pale conjunctivae. Lymphadenopathy was noted in the left axillary (1×1 cm and 0.5 × 1.5cm) and left inguinal region (0.5 × 2cm). Skin appeared normal and there were no petechiae. The results of hematological testing revealed the patient had normocytic normochromic anemia, pancytopenia (
), and liver function test (LFT) were borderline with significantly high levels of lactate dehydrogenase indicating an active haemolysis (
). The peripheral blood smear (PBS) depicted
P. falciparum gametocytes (crescent) and
P. vivax gametocytes (of ameboid shape with Schüffner's dots). PBS was then repeated on three, seven, 14, and 28 days. C-reactive protein (CRP) plasma level and erythrocyte sedimentation rate (ESR), which are both inflammatory blood markers that indicate an ongoing infection, were higher than the normal levels (
). Serological testing included measuring the antibody levels (both their Immunoglobulin (Ig) IgG and IgM forms) for Epstein–Barr virus (EBV), and Cytomegalovirus (CMV). The patient’s results were positive for both EBV IgG and CMV IgG (
). It is worth mentioning that there were no challenges encountered either in clinically examining the patient or getting access to the laboratory diagnostic tests.
The patient was treated as follows: oral doxycycline 100 mg once a day, artesunate 200mg orally once a day for three days, and sulfadoxine and pyrimethamine 1500mg + 75mg single dose orally on day one. On the third day, after excluding glucose-6-phophate dehydrogenase (G6PD) deficiency by measuring the G6PD enzyme level, oral primaquine 30 mg/day for three days was added to the treatment regimen. After seven days of the treatment, the patient's symptoms had resolved; the PBS was repeated and revealed the absence of morphological forms of both parasites along with normal CBC and LFT results. Treatment and care provided to the patient was free of any financial charges. During the treatment course the patient did not develop any adverse effects due to the administrated medications.
 summarizes the timeline of the case management course.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [135.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",101.66667,96.58334,106.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 85.0 mm Hg = 101.66667 mm Hg.
Hence, the patient's mean arterial pressure is 101.66667 mm Hg."
1750,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7756166-1,Extracted,"A 60-year-old, non-smoker, female, known case of hypertension, presented to the Ear, Nose & Throat (ENT) clinic with a history of hoarseness of voice, significant weight loss, and chronic cough for the past six weeks. The cough was dry initially, although at the time of presentation it turned productive of mucoid sputum. The coughing episodes were significantly more prevalent during night, and there was associated shortness of breath on exertion. She also reported a persistent globus sensation and difficulty in swallowing. There was no history of fever, night sweats, rheumatological symptoms, and chronic gastroesophageal reflux or post nasal drip symptoms. Furthermore, she reported positive exposure to biomass fuel during her childhood; however, exposure to pets was unremarkable. She was treated with montelukast and levofloxacin for suspected upper respiratory tract infection; however, this regimen did not improve her symptoms.
The patient's blood pressure measured 139/70 mmHg, pulse 76/min, temperature 37.1°C, respiratory rate of 17 breaths/min, and arterial oxygen saturation (SpO2) of 97%. Chest examination revealed bilateral vesicular breath sounds with no added sounds. The rest of the systemic and general examination was unremarkable.
A bronchoscopy performed outside our institution was unremarkable and a bronchoalveolar lavage (BAL) was negative for Acid-Fast Bacilli (AFB) smear, Gene Xpert, and fungal cultures. The serum angiotensin-converting enzyme (ACE) was 48 IU/L (reference range: 0–52/IU/L). Pulmonary functional test (PFT) demonstrated the presence of a significant restrictive pathology, with forced vital capacity (FVC) being 52% of the predicted value, forced expiratory volume in 1 sec (FEV1) 55% of predicted, and FEV1/FVC ratio being 77%.
The patient underwent flexible fibre-optic laryngoscopy which showed a fixed left vocal cord, with no lesion identified. A computed tomography (CT) scan with contrast of the thorax revealed bilateral perihilar ill-defined opacification with multifocal scattered alveolar and nodular infiltrates. Enlarged mediastinal lymph nodes (prevascular, pretracheal, paracardiac, and subcarinal) with calcifications were also noted, with the largest lymph node in the subcarinal location, measuring approximately 12 mm in the short-axis diameter (Fig. ). There was no evidence of any extra-thoracic lesions. A CT-guided core lung biopsy revealed peri-bronchial non-necrotizing granulomatous lesions. A diagnosis of pulmonary sarcoidosis with left vocal cord paralysis (VCP) was made. Due to financial constraints, and reasonable clinical confidence in diagnosis, a fluorodeoxyglucose–positron emission tomography (FDG–PET) was not performed. The patient was started on oral prednisolone at 0.5 mg/kg/day.
She responded well to corticosteroid therapy with complete resolution of symptoms. A follow-up PFT, two months post-initiation of therapy, showed markedly improved pulmonary function with FVC being 71% of predicted, FEV1 71% of predicted, and FEV1/FVC ratio being 81%. The corticosteroid therapy was tapered to a maintenance dose of 5 mg/day and the patient was started on azathioprine (100 mg/day).
The patient presented with relapse of symptoms of cough within few weeks of maintenance therapy. The patient denied any presence of dysphonia or hoarseness of voice. Repeat PFTs revealed marked deterioration, with FVC being 63% of predicted, FEV1 57% of predicted, and FEV1/FVC ratio being 91% predicted. A high-resolution CT (HRCT) chest revealed an ill-defined bilateral, perihilar patchy opacification with multifocal scattered alveolar/nodular infiltrates demonstrating mild interval progression in the right perihilar region, along with enlarged calcified mediastinal lymph nodes (including the paracardiac lymph nodes). The patient was again started on 30 mg/day prednisolone and this resulted in significant improvement of symptoms. To prevent further relapse, another immunosuppressant (mycophenolate: 1000 mg/day) was added to the treatment regimen. Once the patient started showing clinical improvement, the corticosteroid therapy was gradually tapered to a maintenance dosage 2.5 mg/day.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [139.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",93,88.35,97.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 139.0 mm Hg + 2/3 * 70.0 mm Hg = 93.0 mm Hg.
Hence, the patient's mean arterial pressure is 93.0 mm Hg."
1751,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1861,Extracted,"A previously healthy 33-year-old woman comes to the emergency department 1 hour after falling from a ladder. She is conscious. She does not smoke, drink alcohol, or use illicit drugs. There is no family history of serious illness. Her pulse is 72/min, respirations are 17/min, and blood pressure is 110/72 mm Hg. Physical examination shows ecchymosis and point tenderness over the right clavicle. An x-ray of the chest shows a nondisplaced fracture of the midshaft of the right clavicle and a 3.5-mm pulmonary nodule in the central portion of the left upper lung field. No previous x-rays of the patient are available. The fracture is treated with pain management and immobilization with a sling. A CT scan of the chest shows that the pulmonary nodule is solid and has well-defined, smooth borders.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [72.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",84.66667,80.43334,88.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 72.0 mm Hg = 84.66667 mm Hg.
Hence, the patient's mean arterial pressure is 84.66667 mm Hg."
1752,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6984167-1,Extracted,"A two years and four months old boy with no significant medical history, presented with an intermittent fever that started one month earlier, measured tympanic at 39 degrees Celsius and responding to antipyretics given at home. There was no diurnal variation. The fever was associated with a runny nose, a dry cough, and night sweats. The patient also complained of mild post-prandial generalized abdominal pain, for which he did not require any analgesia. There was no change in bowel habits nor was there any vomiting. Three days prior to the development of the fever, the patient had a painful swelling in the left ankle and knee, which lead to the patient limping throughout that period. The systemic review was otherwise unremarkable. Past history is unremarkable. The patient has no risk factors for acquiring an infectious disease. He initially sought medical attention at a nearby local private hospital, where he received three types of antibiotics (IV flucloxacillin, IV cefotaxime, and oral azithromycin), with no improvement.
Upon presentation to our hospital, the patient’s blood pressure was 116/54 mmHg, the heart rate was 148 beats per minute, respiratory rate was 28 breaths per minute, and he was afebrile at 36.4 degrees Celsius. Examination showed an irritable dehydrated child with cracked lips and no lymphadenopathy. There was bilateral lower limb pitting edema up to the tibia with no skin changes or discoloration.
Initial investigations were taken, and it revealed that the patient had anemia (hemoglobin of 9.9 g/dl), leukocytosis (19.5 x 109 cells per liter), thrombocytosis (1,036 × 109/l), high erythrocyte sedimentation rate (ESR) of 79 mm/hr and high C-reactive protein (CRP) of 65.5 mg/l. Liver function tests and renal parameters were within normal limits. No electrolyte abnormalities were seen. Infectious workup (including tuberculosis, Epstein-Barr virus, cytomegalovirus, mycoplasma, human immunodeficiency virus, hepatitis, brucella) was negative. Immunology testing was done: antineutrophil cytoplasmic antibodies (ANCA) and antinuclear antibody (ANA) were both negative. Complements (C3, C4) were within normal limits, and anti-double-stranded DNA was normal. Immunoglobulins (immunoglobulin M, immunoglobulin A and immunoglobulin E) were all normal except for a high immunoglobulin G (15.2 µg/ml). Lymphocyte markers and oxidative burst tests were all normal. Bone marrow aspirate revealed no evidence of leukemia, granuloma, or infiltration. The left foot X-ray was normal. Skeletal survey showed no lytic bone lesions. MRI of the left ankle showed a mild reactive inflammatory process. High-resolution computed tomography (HRCT) of the abdomen and the chest revealed two wedge-shaped hypodensities on the spleen, which were interpreted as splenic infarcts. Both kidneys were normal in shape and size. The patient was then discharged on oral ibuprofen with the plan to be seen in six weeks’ time for reassessment and further evaluation.
Six weeks later, the patient is readmitted. His condition was stable. He was afebrile (36.6 degrees Celsius), had no joint pain, but he had bilateral lower limb edema. Blood pressure upon this admission was 117/68 mmHg. Repeated HRCT of the chest and abdomen showed a decrease in the kidney size, post-contrast enhancement, a minimal decrease in perfusion of the right kidney, a hypodense lesion in the lower pole in addition to past findings. This was interpreted as an underlying infiltration, vasculitis, and possible granulomatous disease. Doppler ultrasound showed poor right kidney blood flow. CT angiography (Figure ) showed that the splenic artery is completely occluded 2 cm from its origin, right renal artery occlusion 2 cm from its origin, tight stenosis of the short segment is seen at the origin of the left iliac artery, left anterior tibial artery occlusion with retrograde filling at its origin, and the distal one-third of the right posterior tibial artery showed no flow. Dimercaptosuccinic acid (DMSA) scan revealed a small hypo-functioning right kidney, normal functioning left kidney with compensatory hypertrophy. Echocardiography was done and is normal.
On the second day of admission, his blood pressure was found to be 150/98 mmHg. He was shifted to the Pediatric Intensive Care Unit (PICU), and his blood pressure was controlled initially on amlodipine (3 mg), prazosin (2 mg), clonidine (90 mcg), and hydralazine when needed. He was discharged from the PICU after stabilization. Even though the patient was kept on the three aforementioned antihypertensives, he had a relapse of high blood pressure above the 99th percentile for his height. He started to develop a gradually increasing edema, manifesting as ascites, sacral edema, scrotal edema, with upper and lower limb edema. He also gained a total of three kilograms in his weight and developed proteinuria (+4 on urinalysis, 600 mg), hypoalbuminemia (22 g/dL), and hyponatremia (126 mg). He was shifted back to the PICU, his antihypertensive medications were increased to the maximum dose, minoxidil was added and he was started on labetalol infusion 50 mL. He was given three doses of intravenous albumin (0.5 g) along with furosemide. His blood pressure was reduced to 117/71 mmHg. Repeated urinalysis showed +1 sugar, +3 protein, granular cast, with a negative culture.
He was given pulse therapy consisting of methylprednisolone 30 mg per kg per day for five days, cyclophosphamide 250 mg, infliximab 5 mg per kg infusion once, methotrexate 7.5 mg subcutaneously given weekly along with folic acid 5 mg orally. The patient was kept on oral prednisolone 2 mg per kg per day as maintenance. He underwent right renal balloon angioplasty and was successful with recanalization of the right renal artery. At this point, his edema greatly improved, blood pressure was in the range of 120/70 mmHg. The right renal doppler was performed and showed a gradual but significant improvement of the blood flow in the right renal artery.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [98.0, 'mm hg']}",115.33333,109.56666,121.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 98.0 mm Hg = 115.33333 mm Hg.
Hence, the patient's mean arterial pressure is 115.33333 mm Hg."
1753,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5943118-1,Extracted,"A 42-year-old woman, presented with a history of hemoptysis for 1 month. She attended the First Affiliated Hospital of Wenzhou Medical University with a 10-day history of chest pain. There was no history of malignant thromboembolic, hematologic, or inflammatory disease. Physical examination showed her blood pressure was 126/79 mmHg, her pulse was regular with a rate of 72/min, and her breathing rate was 20/min. A systolic rumble at the apex area was noted. Arterial blood gas analysis showed pH of 7.39, PO2 of 176.7 mmHg, PCO2 of 39.1 mmHg, and oxygen saturation of 99.5% under a reserved O2 mask. Transthoracic echocardiography demonstrated a large, immobile, ovoid mass attached to the wall of the left atrium (LA); the mitral valve was involved. Echocardiography revealed moderate, mitral insufficiency, and an abnormal echoic mass in the left atrium. A diagnosis of primary cardiac tumor without metastases was considered in the clinic. Intraoperatively, a mass was found originating from the ostium of the left inferior pulmonary vein in the left atrium, extending to the mitral orifice. Wide surgical excision of the mass was performed. Macroscopically, the specimen measured 5.5 cm × 5 cm × 4 cm. The tumor was grey, solid, and firm.
Histologically, the tumor contained variable amounts of spindle cells and osseous differentiation in different areas. Primary, cardiac fibroblastic osteosarcoma had the typical appearance of interlacing hyperchromatic spindle-shaped stromal cells associated with osseous matrix (Fig. A). Osteoclastic-like, giant cells were scattered throughout without foci of hemorrhage and necrosis (Fig. B). Tumor cells were pleomorphic with spindle-shaped nuclei and hyperchromatin (Fig. C). Immunohistochemical examination showed that tumor cells were positive for vimentin, S-100 protein, and Bcl-2, but negative for cytokeratin, epithelial membrane antigen (EMA), smooth muscle actin, CD99, and CD34. The proliferative index (Ki-67) was approximately 60%. The genetic profile of this tumor by fluorescence in situ hybridization (FISH) showed the amplification of mdm-2 genes. These findings were compatible with a histological diagnosis of fibroblastic osteosarcoma. She was asymptomatic in the immediate postoperative phase. However, 3 months after the operation, her condition worsened and transthoracic echocardiography demonstrated a 3.2 cm × 2 cm recurrent mass in the wall of the left atrium (LA). She died shortly afterwards as a result of the local disease recurrence.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [126.0, 'mm hg'], 'Diastolic Blood Pressure': [79.0, 'mm hg']}",94.66667,89.93334,99.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 126.0 mm Hg + 2/3 * 79.0 mm Hg = 94.66667 mm Hg.
Hence, the patient's mean arterial pressure is 94.66667 mm Hg."
1754,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3424782-1,Extracted,"A 43-year-old obese, hypertensive man, presented in emergency department with acute onset of chest pain at rest that radiated to his jaw and left arm associated with profuse sweating. On examination his pulse was 96/minute, blood pressure 190/100 mmHg, respiratory rate-28/minute and temperature -98.4 F. Jugular venous pressure was normal. There was no cyanosis, clubbing, icterus, pallor, or lymphadenopathy. Routine biochemical, renal, and liver function tests were within normal limits. CPK-MB was raised with maximum values of 60U/L. Electrocardiogram showed ST segment depression of 2 mm in anterior precordial leads. Chest skiagram revealed cardiomegaly. Left ventricular apex and upper 1/3rd of inter ventricular septum were hypokinetic on echocardiogram with left ventricular ejection fraction of 48%. Coronary angiography revealed a fusiform LMCA aneurysm originating at the distal segment 45.7 × 30.6 mm in size [Figures and ]. The patient was advised surgery but he refused and was conservatively managed with dual antiplatelets including aspirin 150 mg and clopidogrel 75 mg and anticoagulants.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [190.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",130,123.5,136.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 190.0 mm Hg + 2/3 * 100.0 mm Hg = 130.0 mm Hg.
Hence, the patient's mean arterial pressure is 130.0 mm Hg."
1755,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3192354-1,Extracted,"A 29-yr-old man was admitted to our hospital after several weeks of lumbar pain and fever up to 38℃ on January 19, 2007. He had no significant past medical history. His vital signs were: blood pressure 130/80 mmHg, heart rate 121/min, and body temperature 38.2℃. Upon physical examination, there was no lymphadenopathy or hepatosplenomegaly. Laboratory tests revealed anemia (hematocrit (Hct) 31.8%, hemoglobin (Hb) 11.8 g/dL), white blood cell (WBC) 3.92 × 103/µL, elevated aspartate aminotransferase (AST) 78 IU/L and alanine aminotransferase (ALT) 71 IU/L, and markedly elevated lactate dehydrogenase (LDH) 1,591 IU/L. A computed tomography (CT) scan taken prior to admission revealed low attenuation of both adrenal glands, an indication of adrenal hemorrhage or acute adrenalitis (). At that time, serum cortisol level was 17.47 µg/dL at 8 AM and ACTH level was 12.1 pg/mL (normal range: 10-90). Chest radiography taken at our emergency department showed left sided pleural effusion (). Pleural fluid was aspirated and pleural needle biopsy showed that the fluid was exudate with lymphocyte predominance and the level of adenosine deaminase (ADA) was 93 IU/L (normal range: 4.3-20.3). Stain for acid-fast bacilli and polymerase chain reaction (PCR) assay on the pleural fluid was negative and pleural biopsy specimen was inadequate. Magnetic resonance imaging (MRI) of the abdomen suggested of adrenal hemorrhage or adrenalitis necessary for differential diagnosis of adrenal tuberculosis (). Therefore, the initial concern was for tuberculous pleurisy and tuberculous adrenalitis, or autoimmune adrenalitis combined with adrenal hemorrhage. The patient was started on empirical anti-tuberculous treatment, although there was no direct evidence of Mycobacterium tuberculosis due to the fever and his worsening condition. However, his fever and abdominal pain continued and there was no improvement in his conditin. Ten days after admission, pancytopenia (WBC 2.88 × 103/µL, Hb 10.7 g/dL, platelets 129 × 103/µL) developed. Bone marrow biopsy was negative for specific hematologic or malignant disorder. Another CT scan of the abdomen revealed an enlargement of the previous adrenal lesion which extended to the retroperitoneal space (). Twenty-two days after admission, explorative laparotomy targeting the adrenal lesion was performed and some tissue was obtained, which contained only necrotic debris. Despite conservative management, his condition deteriorated progressively. At that time, with a strong suspicion that he had a malignant disorder, positron emission tomography/CT (PET/CT) scan was taken and it revealed both adrenal gland and multiple cervical, mediastinal and abdominal lymph nodes with intense FDG uptake (). Therefore, a cervical lymph node was excised surgically after thirty eight days from admission. The pathologic finding was a monotonous arrangement of small tumor cells with positive nuclear staining with Ki-76 (MIB-1), and immunohistochemical staining was positive for CD45, CD30, and CD56 activity, but negative for CD20 activity (). These findings confirmed the diagnosis of non-Hodgkin T-cell lymphoma, natural killer (NK)/T-cell, nasal type. At last, he was referred to the hemato-oncology department and received combination chemotherapy of ifosfamide, mesothrexate, etoposide (IMVP-16) and prednisolone forty seven days after admission. Unfortunately, he could not receive further cycles of chemotherapy after first cycle of treatment because of postoperative wound infection and continuous fever. His disease was aggravated despite of the chemotherapy with conservative management, and finally he died on March 20, 2007, 59 days after his first admission.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1756,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6641743-1,Extracted,"A 34-year-old woman in previous good health was admitted to hospital complaining of muscle weakness and tetany/seizures for 1 year. On admission, the patient was 162.8 cm tall and weighed 53.7 kg, with a body mass index of 20.3 kg/m2. Her blood pressure was 112/78 mm Hg. She showed Chvostek's sign, but no physical signs or digestive symptoms, including anorexia nervosa, vomiting, or diarrhea. She had not taken any medications, such as laxatives, diuretics, street drugs. She had also not attempted to lose weight. She was a nonsmoker nor alcohol drinker, and she had no allergies. The family history was negative for electrolyte imbalance or other forms of endocrinopathy. Her parents were not consanguineous.
Severe hypomagnesemia, hypocalcemia, and hyperphosphatemia in addition to hypokalemia without metabolic alkalosis were observed (Table ). Urinary calcium excretion was decreased, whereas urinary magnesium was elevated compared with low serum values. Her plasma renin and aldosterone levels remained within the normal range. The serum creatinine level and glomerular filtration rate were normal. Her intact PTH level was relatively low in consideration of severe hypocalcemia. The serum alkaline phosphatase level was normal. The laboratory findings were indicative of GS, except for hypocalcemia, hyperphosphatemia, and hypokalemia without metabolic alkalosis. A renal function test using furosemide or thiazide is desirable when GS is suspected.[ Therefore, we performed a renal function test in our case for assessment of the renal reabsorption rate of chloride in the distal tubule in morning fasting according to the described protocol.[ Her renal reabsorption rate of chloride in the distal tubule was markedly decreased using furosemide (from 68.4% to 10.4%), but not by thiazide administration (70.4% to 63.5%), which led to the final diagnosis of GS. To alleviate the symptoms of muscle weakness and tetany/seizure, she had adequate electrolyte supplementation therapy of 8.5% calcium gluconate (20 ml/d) and magnesium sulfate (40 mEq/d) infusion. These supplementations were tapered within 2 days of admission. She has taken no supplementation since day 7 after admission. The clinical course was uneventful. She had a regular diet. Her serum potassium level returned to the normal range, and muscle weakness and tetany disappeared, although her serum calcium and magnesium levels persisted at 2.2 mmol/l and 0.7 mmol/l, respectively, which slightly exceed the lower limit of the normal range. Without any additional potassium gluconate and calcium replacement therapy, her serum potassium, calcium, magnesium, and phosphorus levels during oral administration of a low dose of magnesium oxide (0.6 g/d) were all within the normal range after discharge from our hospital (Fig. ). Additionally, intact PTH levels were normalized (from 6.1 to 8.2 pmol/l) after hypomagnesemia was corrected.
Genetic analysis was performed using the patient's peripheral blood lymphocytes. It was first screened by targeted sequence including all salt-losing tubulopathy causative genes followed by Sanger sequence. As a result, she had 2 heterozygous mutations in the SLC12A3 gene, one of which has been reported previously as a GS disease-causing mutation (c.1732G>A, p.Val578Met).[ The other heterozygous mutation (c.2537_38delTT, p.846fs) has not been previously reported (Fig. ).
Our case report was waived from the ethical approval or institutional review board of Hokkaido University Hospital, based upon their policy to review all intervention and observational study except for a case report. Written informed consent was obtained from the patient for the publication of this case report. The presented data are anonymized and risk of identification is minimal.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [112.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",89.33333,84.86666,93.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 112.0 mm Hg + 2/3 * 78.0 mm Hg = 89.33333 mm Hg.
Hence, the patient's mean arterial pressure is 89.33333 mm Hg."
1757,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7708967-1,Extracted,"A 69-year-old female with a history of alcohol abuse and chronic pancreatitis presented to the emergency room with diaphoresis and pallor. On initial evaluation, blood pressure was 81/47 mmHg, heart rate 140 beats/min, and hemoglobin 7.3 g/deciliter.
Shortly following admission to the intensive care unit, she suffered a bout of hematemesis. Enteric tube aspiration revealed coffee ground emesis and emergent upper endoscopy showed multiple clean-based duodenal ulcers with no source of active bleeding. Two days later, the patient developed large amounts of melanotic stool and had another episode of hematemesis.
A CTA scan of the abdomen and pelvis (pre-contrast and arterial phase) was performed to identify the source of bleeding. Pre-contrast CT [-] identified pancreatic calcifications consistent with chronic pancreatitis and a well-circumscribed hypodensity focus occupying the expected location of the pancreatic tail. Arterial phase CT angiographic images [] revealed hyperattenuating material within the hypodense focus. Close inspection on the arterial phase images demonstrated a linear extravasation of contrast material [ and ], and diagnosis of pseudoaneurysm arising from the splenic artery was made. Transabdominal ultrasound showed a 5.3 x 5.7 cm mass in the region of the pancreas []. The mass was found with strong internal Doppler flow signals as demonstrated by the yinyang sign [] consistent with pseudoaneurysm. Color doppler flow image depicts the pseudoaneurysm and its neck to the splenic artery when chasing caudally []. Follow up spectral analysis was performed that shows a bidirectional turbulent blood flow of a “to-and-fro” pattern of the pseudoaneurysm [ and ].
In the interventional radiology suite, a conventional diagnostic angiogram of the celiac axis and splenic artery shows a pseudoaneurysm at the junction of the proximal and mid third of the splenic artery []. At the delayed catheter angiography depicts contrast blush within the pseudoaneurysm without contrast extravasation into the pancreatic duct, which suggest intermittent bleeding []. The splenic artery distal to the aneurysm was cannulated with a 2.4 French microcatheter. Two detachable coils (4 mm × 13 cm and 3 mm × 8 cm) were deployed within it. Following this, the pseudoaneurysm was accessed into which eight additional coils were deployed (four 20 mm × 40 cm, three 16 mm × 39 cm, and one 18 mm × 36 cm). Further detachable coil placement was attempted to achieve maximal packing density; however, efforts were abandoned given significant tension within the coaxial catheter system. The microcatheter was then retracted to the neck of the pseudoaneurysm, and a coil was deployed from the aneurysm sac across the neck into the narrowed/irregular pre-aneurysmal splenic artery. Three additional microcoils (4 mm × 13 cm) were deployed into the inflow proximal splenic artery []. Post embolization angiographic images of the splenic artery confirmed the successful exclusion of pseudoaneurysm by coil embolization [].
The “sandwich” technique was elected by the interventional radiology team to embolized the distal and proximal flow to the pseudoaneurysm to avoid anterograde and retrograde perfusion []. Post procedure, the patient remained hemodynamically stable with no evidence of recurrent gastrointestinal bleeding over the rest of the admission.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [81.0, 'mm hg'], 'Diastolic Blood Pressure': [47.0, 'mm hg']}",58.33333,55.41666,61.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 81.0 mm Hg + 2/3 * 47.0 mm Hg = 58.33333 mm Hg.
Hence, the patient's mean arterial pressure is 58.33333 mm Hg."
1758,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8139541-1,Extracted,"A 59-year-old male presented to the emergency unit of dr. Wahidin Sudirohusodo General Hospital with complaints of recurrent near-syncope, which occurred a couple of hours ago. He described the episode as light-headedness followed by a brief blackout without loss of consciousness. He also had complaints of weakness and fatigue. He had no previous history of similar episodes. He denied any respiratory problems, fever, or close contact with COVID-19 confirmed patients. To his knowledge, he has no underlying cardiovascular conditions and was otherwise healthy. During the examination, he was afebrile, with a blood pressure of 144/88 mmHg, a heart rate of 44 beats per minute, and a respiratory rate of 20 breaths per minute with oxygen saturation of 94% on room air. Physical examination was nothing out of the ordinary, with no signs of volume overload or dehydration. Electrocardiogram (ECG) on admission (Fig. ) showed sinus bradycardia with 44 beats per minute. High sensitivity Troponin I assay showed 3.8 ng/L. A 2-h repeated assay was performed with a result of 4.9 ng/L.
Laboratory findings were significant for serum sodium of 117 mmol/L (reference range 136–145 mmol/L), serum potassium of 3.4 mmol/L (reference range 3.5–5.0 mmol/L) and increased neutrophil/lymphocyte ratio 8,36 (78.6/9.4). Blood urea nitrogen was 11.7 mg/dL (reference range: 7–20 mg/dL) and random blood glucose was 122 mg/dL, resulting in calculated plasma osmolality of 245 mOsm/kg (reference range: 275–299 mOsm/kg). Further workup revealed urine osmolality of 142 mOsm/kg (reference range: 500–850 mOsm/kg) and urinary sodium 34 mmol/L with low plasma osmolality. Thyroid-stimulating hormone and Free T4 were normal (1.77 mIU/mL and 1.41 ng/dL consecutively). The patient was planned to be admitted to the Cardiology Care Unit. However, during the routine COVID-19 screening examination, chest CT scan revealed multiple ground-glass opacities typical for COVID-19 pneumonia. Following the chest CT result, a naso- and oropharyngeal swab for SARS-CoV-2 PCR was obtained from the patient, which came back positive with an IL-6 result of 13.2 pg/ml. Further workup fulfilled the criteria for SIADH, and other potential causes of hyponatremia were excluded. No other potential etiology of SIADH was found, and the patient was assessed to have a COVID-19-associated SIADH.
The patient was treated with a slow infusion of hypertonic saline and oral potassium supplementation. After the serum sodium concentration normalized, his symptoms and heart rate improved (Table ), and further ECG monitoring showed no bradycardic events. The patient was given azithromycin and oseltamivir from the pulmonology department. Despite his asymptomatic state, the nasopharyngeal swab test remains positive until the 30th day of hospitalization. This case is the first case report concerning symptomatic sinus bradycardia related to COVID-19 associated SIADH to the author’s concern.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [144.0, 'mm hg'], 'Diastolic Blood Pressure': [88.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 144.0 mm Hg + 2/3 * 88.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1759,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8610744-1,Extracted,"An 80-year-old male patient with a history of diabetes mellitus presented to the emergency department complaining of shortness of breath and cough. His vital signs on presentation were as follows: temperature, 37°C; heart rate, 112 beats/min; blood pressure, 120/75 mmHg; respiratory rate, 28 breaths/min; and oxygen saturation, 90% on supplemental oxygen. There were no significant points in the general examination. His bilateral lower extremities were normal, and his bilateral popliteal, posterior tibial, and dorsalis pedis arterial pulses were palpable. On laboratory testing, the following values were noted: white blood cells, 7×109/L (reference, 4.5×109-11.5×109); hemoglobin, 13.6 g/dL (12-16); hematocrit, 37.3% (35%-45%); platelets, 210×109/L (140×109-440×109); glucose, 378 mg/dL (70-105); creatinine, 1.4 mg/dL (0.6-1.40); blood urea nitrogen, 11.3 mg/dL (7-23); D-dimer, 248 ng/mL (<0.5); prothrombin time, 20 sec (12.2-14.9); international normalized ratio, 1.1 (<1); partial thromboplastin time, 40 sec (21.3-35.1); C-reactive protein, 151 mg/L (<10 mg/L); and erythrocyte sedimentation rate, 88 mm/h (0-32); lupus anticoagulant, negative; interleukine-6, 76 pg/mL (5-15). His nasopharyngeal swab was positive for the severe acute respiratory syndrome coronavirus-2, and high-resolution computed tomography showed bilateral extensive interstitial lung infiltrates. As such, the patient was admitted to the intensive care unit (ICU) and was treated with Ziferon (Interferon-1b, 250 mg/mL; Zist Daru Danesh, Tehran, Iran) every two days via subcutaneous administration, dexamethasone 8 mg/day via intravenous administration, Remdesivir (100 mg/20 mL; Actoverco, Tehran, Iran) 200 mg on the first day followed by 100 mg/day, and heparin 5,000 units subcutaneously every 6 hours. On the ninth day after admission, with the patient still complaining of shortness of breath (O2 saturation: 89%), he experienced sudden pain in the right lower extremity with coldness, ischemic discoloration, paralysis, and lack of femoral pulses of the limb (). Computed tomography angiography revealed the total occlusion of the right common iliac artery with no distal run-off (). Electrocardiography did not show any arrhythmia, and the platelet count was normal on the day of the event and after. The patient underwent an emergency thromboembolectomy with spinal anesthesia via a femoral incision. A long thrombus with a cohesive, tubular consistency emerged from the iliac, femoral, and tibial arteries (, Supplementary Video 1). After the successful thrombectomy, the ischemia resolved, and the patient was transferred to the ICU. In the ICU, the patient experienced respiratory acidosis (pH, 7.27; PCO2, 55; PO2, 90; HCO3, 14.4; base excess, –2.1) but had adequate urine flow. He also received intravenous heparin at a dose of 1,000 units per hour. The right lower extremity was warm, and the symptoms of ischemia resolved. In addition, necessary measures were taken to prevent reperfusion syndrome. Ten hours after the operation, the patient’s respiratory distress worsened despite receiving 100% oxygen. He eventually suffered from cardiopulmonary arrest and died.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [75.0, 'mm hg'], 'Systolic Blood Pressure': [120.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 75.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1760,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-343,Extracted,"A 50-year-old man is brought to the emergency department because of severe headache over the past hour. He also reports nausea and one episode of non-bloody vomiting. He has a history of hypertension and type 2 diabetes mellitus. He does not smoke or drink alcohol. Medications include enalapril and metformin, but he states that he does not take his medications on a regular basis. His temperature is 37°C (98.6°F), pulse is 80/min, and blood pressure is 190/110 mm Hg. He is oriented to person but not place or time. Physical examination shows decreased muscle strength in the right leg and arm. Deep tendon reflexes are 3+ in the right upper and lower extremities. A noncontrast CT scan of the head shows a solitary hyperdense lesion surrounded by hypodense edema in the left cerebral hemisphere.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [190.0, 'mm hg'], 'Diastolic Blood Pressure': [110.0, 'mm hg']}",136.66667,129.83334,143.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 190.0 mm Hg + 2/3 * 110.0 mm Hg = 136.66667 mm Hg.
Hence, the patient's mean arterial pressure is 136.66667 mm Hg."
1761,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7812888-1,Extracted,"A 31-year-old woman was referred to our clinic from a district hospital after two episodes of haematemesis and melena requiring transfusions.
There was no history of trauma, iatrogenic causes or tumour. A month prior, the patient had experienced the first episode of gastrointestinal bleeding during the 38th wk of her second pregnancy. After 7 d of conservative therapy (i/v fluids and observation), a caesarean section was performed without any complications.
Of interest, the patient reported a history of periodical abdominal distention since she was 10 years old and nausea since she was 20 years old. An abdominal ultrasound two years prior had revealed hepatomegaly and splenomegaly.
Personal and family history was unremarkable.
The physical examination on admission revealed abdominal distension. The patient’s pulse rate was 110 beats/min, and the blood pressure was 90/60 mmHg.
Laboratory results are shown in Table . There was no encephalopathy detected. Viral and autoimmune hepatitis markers were negative.
As seen on Doppler ultrasound, arterial inflow to the fistula occurred via a hypertrophied right hepatic artery draining into a dilated venous varix of the right branch of the portal vein. The portal vein showed arterialization with reversal of flow. There was associated splenomegaly detected. Approximately 4000 mL of free fluid was detected in the abdomen.
Computed tomography (CT) angiography confirmed the ultrasound findings, showing a round irregular vascular malformation with a size of 28.0 mm × 27.1 mm × 22.4 mm in segment 5 of the liver above the gallbladder with a shunt between the right hepatic artery and right portal vein (Figure ). The right hepatic artery near the vascular malformation was 11.8 mm (normal 3-5 mm), the right portal vein was 23.6 mm (normal 4-6 mm) and the fistula was 12 mm in diameter. Upper gastrointestinal endoscopy showed multiple large oesophageal varices as the cause of bleeding.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",70,66.5,73.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 60.0 mm Hg = 70.0 mm Hg.
Hence, the patient's mean arterial pressure is 70.0 mm Hg."
1762,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8143828-1,Extracted,"A 15-year-old male presented to the emergency department for evaluation of neck and chest pain. He was running at a brisk pace when he felt a sudden sharp pain in his neck followed by sustained pain in the center of his chest and neck. He reported the sensation of shortness of breath and nausea, but no dysphagia or dysphonia. There was no history of trauma to the head, neck, or chest. He was previously healthy with no prior medical problems or prior surgeries and had no history of familial or congenital medical conditions. Most notably, the patient had no family history of sudden cardiac death, aortic disease, or connective tissue disease. The patient endorsed having no known allergies and did not take any medications on a daily basis.
On arrival, he displayed mild tachypnea with a respiratory rate of 22 breaths per minute, but otherwise had normal vital signs with a blood pressure of 128/80 millimeters of mercury, heart rate 66 beats per minute, temperature 37 degrees Celsius, with 98% oxygen saturation on room air. His airway showed no evidence of impending compromise. He appeared to be in moderate distress secondary to pain. He demonstrated respiratory splinting and held his neck and shoulders still to prevent worsening of pain. He had mild nasal flaring, but his lungs were clear to auscultation bilaterally. He had no evidence of stridor. Palpation of the chest revealed tenderness near the right sternoclavicular region of his chest. Pulses were palpable and equal in all extremities.
A chest radiograph showed lung markings to the periphery bilaterally, no consolidations, and no opacities (). The mediastinum appeared widened, which prompted a computed tomography (CT) angiogram of the chest and neck to better evaluate vascular anatomy. This revealed a pseudoaneurysm of the proximal innominate artery (). There was also high attenuation blood tracking from the superior mediastinum to the descending aorta suggesting rupture of the pseudoaneurysm and formation of a mediastinal hematoma ().
The patient was taken to the operating room where he was found to have an extensive tear of the proximal innominate artery about one centimeter from its origin. The rupture was contained by the adventitia and surrounding soft tissue. The patient received an ascending aortic to innominate artery extra-anatomic bypass graft, and drains were placed to reduce the mediastinal hematoma. He was evaluated by geneticists postoperatively who suspected a connective tissue disorder. High on the differential was vEDS given his exam exhibiting flexible digits, easy bruising, and normal aortic root dimension. The patient was discharged home on postoperative day five, and nearly three weeks later, genetic testing confirmed a pathogenic COL3A1 mutation diagnostic of vEDS.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [128.0, 'mm hg']}",96,91.2,100.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 128.0 mm Hg + 2/3 * 80.0 mm Hg = 96.0 mm Hg.
Hence, the patient's mean arterial pressure is 96.0 mm Hg."
1763,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4198564-2,Extracted,"A 30-year-old female patient was referred to our hospital emergency center with hematemesis that started several hours before her presentation. The hematemesis had a total amount of 500 mL, had the color of fresh blood, and was combined with sloughed tissue material. PV had been diagnosed in this patient 11 months previously. Two weeks previously, her dermatologist had decided to increase the quantity of her medication because of new formation of vesicles on her skin. After switching from oral methylprednisolone 2 mg daily, cyclosporine 50 mg twice daily, and MMF 1,000 mg twice daily to oral methylprednisolone 4 mg daily, cyclosporine 150 mg twice daily, and MMF 1,000 mg twice daily, the skin lesions had shown improvement at the time of admission.
On physical examination, her initial blood pressure was 140/90 mm Hg, pulse rate was 118 beats per minute, respiratory rate was 20 breaths per minute, and body temperature was 36.5℃. She did not show any newly or recently developed skin lesions but had chronic scars due to PV on the trunk, inguinal, and perioral skin areas. The baseline laboratory results were as follows: hemoglobin level, 10.0 g/dL; white blood cell count, 16,940/µL; and platelet count, 262,000/µL. The serum levels of routine chemistry markers were within the reference limits.
Initial esophagogastroduodenoscopy results revealed multiple mucosal abrasions in the oral cavity (), with combined laryngeal edema (). In the upper esophagus, there was a longitudinal ulceration covered with exudate, and diffuse mucosal friability and erythema that was consistent with the findings of exfoliative esophagitis (). There was no abnormality in the lower esophagus, stomach, and duodenum. After the administration of intravenous hydrocortisone 100 mg twice daily for 2 days, the patient did not show any other symptoms, and we were able to rapidly taper off the corticosteroids. On the third day of hospitalization, she underwent a follow-up esophagogastroduodenoscopy, which showed markedly improved mucosal exfoliative lesions in the oral cavity () and upper esophagus (), for which biopsy was done. The final pathology report indicated detached squamous epithelium, with acute and chronic inflammation and necroinflammatory exudates. She was discharged on the sixth day of hospitalization with MMF 1,000 mg twice daily. Thereafter, she was referred back to a local clinic, and has not returned to our center.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1764,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9495,Extracted,"A 46-year-old woman comes to the clinic complaining of right eye irritation. The eye is itchy and red. Discomfort has been relatively constant for the last 6 months, and nothing makes it better or worse. Past medical history is significant for hypertension, hyperlipidemia, and aggressive tooth decay, requiring several root canals and the removal and replacement of several teeth. She takes chlorthalidone, fluvastatin, and daily ibuprofen for tooth pain. She has smoked a pack of cigarettes daily since the age of 20 and drinks alcohol on the weekends. She does not use illicit drugs. She cannot provide any family history as she was adopted. Her temperature is 36.7°C (98°F), blood pressure is 135/65 mm Hg, pulse is 82/min, respiratory rate is 15/min, and BMI is 27 kg/m2. A thorough eye exam is performed and shows no foreign objects. Both eyes appear erythematous and infected.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [135.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",88.33333,83.91666,92.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 65.0 mm Hg = 88.33333 mm Hg.
Hence, the patient's mean arterial pressure is 88.33333 mm Hg."
1765,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3914239-1,Extracted,"This patient is a 38-year-old housewife who was referred from the general out-patient clinic on account of a one-month history of recurrent difficulty in breathing, associated with chest pain, recurrent headaches, blurring of vision, and dizziness with blood pressure of 260/150 mmHg. There was a history of orthopnoea and paroxysmal nocturnal dyspnoea. She had no associated cough but had a mild centrally located chest pain. There was a history of bilateral leg swelling which has been progressively worsening and associated with diminution in urine volume. She was diagnosed as hypertensive five years before presentation but had not been compliant with antihypertensive medications. There was no known family history of hypertension.
Examination showed a young woman in respiratory distress, pale, afebrile (temperature 36.8°C), bilateral pitting leg oedema up to the knee with no sacral oedema. Waist circumference was 78 cm, hip circumference 80 cm, and a body mass index (BMI) 23.8 kg/m2.
Her respiratory rate was 50 cycles/minute with reduced breath sounds in the left lower lung zones and bibasal fine crepitations. The pulse rate was 118 beats/minute, normal volume and regular. There was clinical evidence of arterial wall thickening. Blood pressure was 220/120 mmHg with a fourth heart sound and loud aortic component of the second heart sound. She also had grade 3 hypertensive retinopathy on fundoscopy and asterixis but no lateralizing signs.
An initial diagnosis of acute-on-chronic renal failure secondary to hypertensive nephrosclerosis, precipitated by malignant hypertension, was made.
Results of investigations are shown as follows.Results of investigations done: E/U/C (predialysis). Creatinine: 900 μmol/L (53–115). Urea: 30 mmol/L (2.1–7.1). Na: 136 mmol/L (135–145). K: 4.0 mmol/L (3.2–5.0). Cl: 98 mmol/L (96–108). HCO3: 28 mmol/L (22–28). HBsAg, anti-HCV, and HIV: negative. Urinalysis showed ++ proteinuria, no haematuria. Renal ultrasound scan and renal artery Doppler: renal USS/Doppler-right kidney measured 8.63 × 4.59 × 5.07 cm. There was loss of corticomedullary differentiation. Doppler insonation of the renal artery showed a velocity of 73.9 cm/second and a resistive index of 0.9 suggesting renal intraparenchymal disease. The upper margin of the left kidney appeared to be intrathoracic and could not be well deciphered. The echotexture was hypoechoic with complete loss of corticomedullary differentiation. Doppler insonation of the left renal artery showed a velocity of 195 cm/min consistent with a stenotic artery. On the basis of the finding suggestive of left renal artery stenosis, the plan was to do a renal artery angiogram, but the risk of contrast-induced nephropathy precluded this investigation. Abdominal CT scan report: the scanogram showed a left intrathoracic well-marginated upper border mass obscuring the left hemidiaphragm medially and obscuring the cardiac apex. Contiguous slices showed the left kidney to be in an abnormal location in the left hemithorax sitting between the cardiac silhouette and spleen. The right kidney was in its normal location with major blood vessels appearing normal. The left kidney was slightly bigger than the right one, (see Figures , , and ). Captopril renogram. Right kidney: intact perfusion followed by almost uniform uptake of radiotracer. Left kidney: intact perfusion followed by nonuniform uptake of radiotracer. Its upper moiety is truncated out of field of view of the camera, therefore, making computation of differential renal function impossible. High background activity indicating reduced renal function in the patient. This background activity increased after administration of captopril. Tc-99 m DMSA radionuclide scan was suggested but patient declined.
A possible diagnosis of left intrathoracic ectopic kidney with chronic kidney disease secondary to possible renovascular hypertension was made.
She is now on maintenance haemodialysis, with resolution of uraemic symptoms. Leg swelling, orthopnoea, and paroxysmal nocturnal dyspnoea had completely resolved; her blood pressure has been between 120/88 and 150/104 mmHg with serum creatinine of 248–380 μmol/L. Her medications included alpha methyldopa at 1 g bd; Amlodipine 10 mg daily; Brinerdin 1 tab bd; Atenolol 40 mg daily; and oral furosemide 80 mg twice daily.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [260.0, 'mm hg'], 'Diastolic Blood Pressure': [150.0, 'mm hg']}",186.66667,177.33334,196,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 260.0 mm Hg + 2/3 * 150.0 mm Hg = 186.66667 mm Hg.
Hence, the patient's mean arterial pressure is 186.66667 mm Hg."
1766,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-10030,Extracted,"A 24-year-old primigravida presents to her physician at 20 weeks gestation. She was diagnosed with asymptomatic bacteriuria at her last appointment 2 weeks ago, and was treated with amoxicillin. She has no concurrent diseases and no complaints. Her vital signs are as follows: blood pressure 110/80 mm Hg, heart rate 82/min, respiratory rate 11/min, and temperature 36.6℃ (97.7℉). The physical examination reveals no abnormalities. On gynecologic examination, the cervix is soft and non-tender with no discharge from the external os. The uterus is enlarged to the umbilicus and the fetal heart rate is normal.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 80.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1767,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4760027-1,Extracted,"A 48-year-old male, weighing 64 kg, with 18 years history of AS admitted for right-sided ureteroscopic stone removal.
On preoperative evaluation, patients revealed history of difficult in lying supine position without high pillow due to AS involving the cervical spine. On physical examination, suggested severe AS involving the entire vertebral column. No significant abnormality in respiratory and cardiovascular system.
Airway examination showed restricted neck movement, adequate mouth opening, Mallampati grade II. Radiograph of spine showed a fusion of vertebral bodies and calcification and ossification of posterior ligaments and soft tissue.
His baseline pulse rate was 95 beats/min and blood pressure was 140/80 mm of Hg. X-ray of spine showed cervical spondylitis, kyphosis of the thoracolumbar spine, and total ankylosis of spine. His pulmonary function tests showed normal results. Patient's hemogram, blood sugars, and electrocardiogram (ECG) were within normal limits.
Written informed consent was taken from the patient for both general anesthesia and regional anesthesia; the patient was fasted adequately. On the day of the surgery, the patient was premedicated with oral ranitidine 150 mg 2 h before surgery, with a sip of water. Emergency airway cart with a fiberoptic bronchoscope and I-gel was kept ready. In the operation room, all standard monitors, such as, the ECG, pulse oximeter, noninvasive blood pressure, and capnograph were placed, 18-gauge intravenous cannula was inserted and dextrose normal saline started.
Classical spinal anesthesia was attempted in sitting position with 23 g quinkeys spinal needle both midline and paramedian approach. Even after three attempts lumbar puncture was unsuccessful. We decided to try neuroaxial block under fluoroscopy. Patient was made to lie down in prone position with adequate cushioning, anteroposterior image with 20° ipsilateral tilt was used to identify left sided first sacral (S1) neuroforamina [], 23 gauge quinkeys spinal needle was inserted under aseptic condition along c-arm axis, transforaminal placement was confirmed by seeing the urografin dye spread along the epidural space in lateral image and nerve sheath spread in AP image []. After injecting the epidural test dose with 3 ml of 2% lignocaine adrenalin 3 ml, bolus dose 0.5% 15 ml ropivacaine was injected.
Epidural anesthesia was adequate with sensory block up to T8 level; hemodynamic parameters were stable during the intraoperative period. Postoperatively, patient was stable, and he was discharged on the second postoperative day.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 80.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1768,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6548144-1,Extracted,"A 25-year-old young male came to our emergency department (ED) in a conscious, anxious state from a nearby town with a history of roadside trauma, a head-on collision while driving a car without wearing the seatbelt, one hour back. The patient complained of a headache, chest pain, and had a bleeding wound on the forehead. On general examination, the patient was conscious, oriented, cooperative, and slight restless, with a pale look. His blood pressure (BP) was 90/60 mmHg, pulse rate (PR) 120/min, blood oxygen saturation 92%, respiratory rate (RR) 20/min, and capillary refill time was 2 seconds. There was no history of loss of consciousness, seizure, vomiting, or ear bleed.
A- Airway: It was patent and cervical spine protected; B- Breathing: There is not any distress and oxygen delivered via face mask; C- Circulation: Patient had hypotension and tachycardia, so one-liter bolus of normal saline administered intravenously; D- Disability: He was alert, moving all limbs; E- Exposure: reddish-blue discoloration over the epigastrium was seen, tenderness, and guarding present were also present.
Head: There was a lacerated bleeding wound (2cm × 1cm × scalp deep) on the forehead with pain and tenderness; Neck: There was not any tenderness and his power was 5/5 in all the four limbs; Chest: It was clear to auscultation bilaterally. there was tenderness in the lower chest. Heart sounds of S1S2 were audible, and there were no additional sounds; Abdomen: There were multiple small round reddish-blue bruises in the epigastrium of diameter 2 cm, with underlying tenderness, guarding, and rigidity; Back: log roll examination was performed. No abnormalities detected; Limbs: there was an abrasion 2cm ×1cm on right hand.
Following differential diagnosis of the state of shock in the ED were considered: neurogenic shock, head injury due to rapid deceleration impact during a head-on collision; spinal shock, cervical spine injury due to rapid deceleration impact during a head-on collision; hemorrhagic shock, due to blunt chest trauma due to steering wheel impact injury.
Blood Glucose = 136 mg/dl; arterial blood gases: pH = 7.35, pO2 = 110, pCO2 = 35, HCO3 = 18; Hb = 11 gm%; Electrocardiogram (ECG) showed sinus tachycardia; bedside echocardiography showed no regional wall motion abnormalities, no tamponade, ejection fraction (EF) = 60%. Portable chest X-ray and pelvis X-ray showed no abnormalities. The whole body computed tomography (CT) trauma protocol was followed in view of the trauma with hypotension, that consists of a non-contrast head CT followed by a multi-detector CT that includes an intravenous, contrast-enhanced scan of the chest, abdomen, up to the pelvis. The findings of the whole body CT scan were as follows: no significant abnormality detected on noncontrast CT of the head and face, and whole-spine and contrast-enhanced chest CT; Whereas contrast-enhanced CT of abdomen showed hypodense linear area within the head and body of the pancreas with free fluid in the peri-pancreatic region and also in adjacent retroperitoneum space suggestive of pancreatic transection with retroperitoneal hematoma ().
Given the above findings, the patient was admitted to the intensive care unit (ICU) by the gastrointestinal (GI) surgery team for close observation and monitoring. He was managed conservatively on intravenous fluids, antibiotics, analgesics, and vasopressors. The forehead wound was sutured, and it healed well. He showed gradual improvement and was shifted to the ward after two days. He was discharged after five days in a hemodynamically stable and afebrile condition, on a normal diet.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [60.0, 'mm hg'], 'Systolic Blood Pressure': [90.0, 'mm hg']}",70,66.5,73.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 60.0 mm Hg = 70.0 mm Hg.
Hence, the patient's mean arterial pressure is 70.0 mm Hg."
1769,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4421581-1,Extracted,"A 75-year-old woman presented with a 9-day history of general malaise, anorexia and vomiting. She had consumed only lemonade and occasional soft diet for several weeks and became drowsy 24 h prior to admission. Her background medical history included schizophrenia and depression.
She had been admitted to hospital 2 years previously with similar symptoms but had seizure activity as well as extreme metabolic acidosis requiring dialysis. Toxicology screening did not suggest common overdoses as a likely cause. At that time, she was extremely cachectic and a diagnosis of starvation ketoacidosis was made on the basis of exclusion and high serum levels of acetone.
On her current admission, she was drowsy with a Glasgow Coma Scale of 9/15. Other observations included a heart rate of 120 beats/min and blood pressure of 140/70 mmHg. Her respiratory rate was 26/min. Systemic examination was otherwise unremarkable.
Finger prick testing showed capillary blood glucose of 1.8 mmol/L (3.5–5.5 mmol/L) and urine dip was positive for ketones. Her blood gas analysis on admission revealed that she had severe metabolic acidosis with a high anion gap. She had a pH of 7.01 (7.35–7.45), pCO2 1.9 kPa (4.5–6) or 14.2 mmHg (35–45), bicarbonate 5 mmol/L (22–28), lactate 0.5 mmol/L (0.5–1.6), base excess −25.5 (−2 to +2) and pO2 13.8 kPa (10.5–13.5) or 103.5 mmHg (80–100). Her anion gap (AG) was 33.9. The low level of pCO2 reflects respiratory compensation, which is appropriate in this patient (∼1.2 mmHg decrease in pCO2 for every 1 mmol/L decrease in HCO3).
Her blood tests showed sodium of 137 mmol/L, potassium 5.9 mmol/L, urea 11.5 mmol/L (2.5–7.5) and creatinine 126 μmol/L (60–110). Her measured serum osmolality was 331 mOsm/kg (278–305) as compared to a calculated osmolality of 287 mOsm/kg (osmolar gap 44 mOsm/kg). There was no improvement in her biochemistry or acidosis with initial fluid resuscitation, and her urine output was poor and on repeated testing, her serum potassium had risen to 7 mmol/L. In the presence of an elevated osmolar gap and anion gap, the differential diagnosis included salicylate, methanol and ethylene glycol poisoning. Relevant toxicology screens were sent and she was commenced on intravenous ethanol in view of the possibility of ethylene glycol poisoning, which was later converted to Fomepizole []. She was referred to the renal team and emergency haemodialysis was initiated. Following dialysis, her repeat arterial blood gases were much improved with a pH of 7.43, HCO3 21.2 mmol/L, base excess −4.8 and AG 16.
Serum toxicology screen was negative for paracetamol, salicylates, ethanol and methanol. However, ethylene glycol (antifreeze) was initially reported to be detectable at 238 mg/L. Despite extensive questioning, the patient and her close family members denied that the patient had ingested any substance that could potentially contain ethylene glycol. Subsequent retesting of the initial sample revealed that ethylene glycol in fact was not present; the false-positive result was due to interference with the assay by the gel in SST blood sampling tubes []. Her initial urine sample did not demonstrate oxalate crystals.
In view of the unexplained elevated anion gap acidosis, further investigations on patient's admission blood and urine samples were performed. Urine analysis demonstrated high levels of beta-hydroxybutyrate and glutarate with no glycolyate or oxylate. Therefore, the patient displayed significant ketoacidosis with hypoglycaemia in the absence of alcohol excess. On this admission, the patient was no longer cachectic and had gained 3 kg in weight as compared to previously. A plasma acylcarnitine profile showed that the levels of glutarate, parahydroxylactate, hydroxydicarboxilic acid and acetone levels were elevated. These results were consistent with a lipolytic and ketogenic response to metabolic stress; other features of the plasma and urinary profile were consistent with mild riboflavin-responsive multiple acyl-CoA dehydrogenase deficiency (rr-MADD), see .
The patient was commenced on riboflavin 150 mg once daily (on Day 10) and was later prescribed carnitine supplementation. She was subsequently discharged home having made a full recovery.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 70.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1770,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6581388-1,Extracted,"A 56-year-old woman underwent an uncomplicated left shoulder bone spur removal under general anesthesia with 2 mg of versed, 100 mcg of fentanyl, 150 mg of propofol, and sevoflurane in an outpatient surgery center. After completion of the procedure, the anesthesiologist performed an interscalene nerve block for post-operative pain control utilizing 30 mL of bupivacaine (0.25%). Approximately 5 min after completion of the block, the patient developed bilateral mydriasis, paralysis of all extremities, and respiratory arrest. The patient was immediately intubated, administered IV fluids, ephedrine 15 mg IV, and transferred to an emergency department (ED).
On ED arrival the patient was being ventilated through an oral endotracheal tube and was completely paralyzed. Her vital signs were: blood pressure (BP) 108/56 mmHg; pulse 86 per minute; respiratory rate 24 breaths per minute on a ventilator. Her pupils were 6 mm and unresponsive to light bilaterally. She had no response to painful stimulation and had no spontaneous respirations on a ventilator. Her initial blood tests included a complete blood count, electrolytes, liver function tests, cardiac enzymes, and coagulation tests. The lab results were all unremarkable except for a phosphorus of 1.7 mg/dL and lactate of 4 mmol/L. In the ED she was administered a 1-L normal saline bolus and 20% intravenous lipid emulsion 85 mg. Over the next 4 h, the patient progressively regained motor and sensory functions followed by successful extubation in the ED. She was admitted to the hospital for observation and discharged home the next day without any neurologic sequelae.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [108.0, 'mm hg'], 'Diastolic Blood Pressure': [56.0, 'mm hg']}",73.33333,69.66666,77,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 108.0 mm Hg + 2/3 * 56.0 mm Hg = 73.33333 mm Hg.
Hence, the patient's mean arterial pressure is 73.33333 mm Hg."
1771,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-917,Extracted,"A 58-year-old man comes to the physician for the evaluation of intermittent dysphagia for 6 months. He states that he drinks a lot of water during meals to help reduce discomfort he has while swallowing food. He has hypertension and gastroesophageal reflux disease. He has smoked one half-pack of cigarettes daily for 32 years. He does not drink alcohol. Current medications include hydrochlorothiazide and ranitidine. He is 173 cm (5 ft 8 in) tall and weighs 101 kg (222 lb); BMI is 33.7 kg/m2. His temperature is 37°C (98.6°F), pulse is 75/min, and blood pressure is 125/75 mm Hg. The lungs are clear to auscultation. Cardiac examination shows no murmurs, rubs, or gallops. The abdomen is soft and nontender. A barium esophagogram shows complete obstruction at the lower end of the esophagus with an irregular filling defect. An upper endoscopy shows a sliding hiatal hernia and a constricting ring at the gastroesophageal junction. Biopsies from the lesion show squamocolumnar epithelium with no metaplasia.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [75.0, 'mm hg'], 'Systolic Blood Pressure': [125.0, 'mm hg']}",91.66667,87.08334,96.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 75.0 mm Hg = 91.66667 mm Hg.
Hence, the patient's mean arterial pressure is 91.66667 mm Hg."
1772,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3977111-1,Extracted,"A 30-year-old, gravida 4, para 3, woman presented in antenatal outpatient department (OPD) at 26 weeks pregnancy with complaints of facial weakness, blurring of vision, altered taste sensation, and increased noise sensitivity for 1 month. She had headache since 18 days and vomiting since 2-3 days. All her previous deliveries were at home. In her last delivery at term, she had a stillborn baby.
The present case was diagnosed with hypertension when she was three months pregnant and took prescribed antihypertensive drugs for about two months. About twenty days after stopping medication she developed facial weakness which progressed over the following 2 to 3 days. There was no history of fever, rash, trauma, or symptoms of dental/ear infection. Before visiting our institution she visited two private practitioners. Both advised admission in view of intrauterine growth restriction and oligohydramnios though her blood pressure records were normal. Finally, she visited a primary health centre from where she was referred to our tertiary care centre.
On examination the patient was conscious but kept her eye and ears covered. Her pulse was 90/min, BP was 170/120, RR was 18/min, and chest and cardiovascular examination was normal. Uterus was 18 weeks size, fetal heart rate was 100/min, and ++proteinuria was present. Opinion was taken from the neurologist regarding Bell's palsy. She was advised physiotherapy and prescribed with multivitamins.
The patient was prognosticated about the high risk condition and poor fetal outcome. She consented to admission and treatment. Antihypertensive (labetalol) and anticonvulsant (magnesium sulphate) were started. Ultrasonography revealed a single live fetus consistent with 26 weeks gestational age, with absent liquor and severe bradycardia. Baseline investigations revealed SGOT 248, SGPT 235, platelet count 77,000/μL, INR 1.5, and aPTT ratio 1.5. Diagnosis of HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome was made.
An informed decision was made to terminate the pregnancy. Six units of fresh frozen plasma (FFP) were transfused. Once the coagulation profile became normal, cervical ripening and labor induction were commenced. After 6 hours, she delivered a 450 gram stillborn. The third stage was complicated with postpartum hemorrhage with a blood loss of about 1500 to 2000 mL. The hemorrhage was successfully managed and four more units of FFP and 2 units of packed cell volume were transfused. The postnatal period was uneventful. She was evaluated for hypertension. On ultrasonography, the left kidney was found to be atrophied. Urinary protein over 24 hours was 546 mg. Fundoscopy showed pale discs.
On follow-up visit after 47 days, her palsy was noted to improve partially though her blood pressure remained elevated (220/120). ECG showed a left axis deviation. Thereafter she was advised regular followup in departments of general medicine and neurology.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [170.0, 'mm hg'], 'Diastolic Blood Pressure': [120.0, 'mm hg']}",136.66667,129.83334,143.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 170.0 mm Hg + 2/3 * 120.0 mm Hg = 136.66667 mm Hg.
Hence, the patient's mean arterial pressure is 136.66667 mm Hg."
1773,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4175894-1,Extracted,"A 74-year-old man presented with the history of breathlessness, cough with expectoration, and fever for two days. His past medical history was significant for coronary artery disease and chronic angina. His other active medical comorbidities include obstructive airway disease (OAD), hypertension, and benign prostate hypertrophy.
His drug therapy at home included carvedilol 3.125 mg twice a day, aspirin 75 mg, clopidogrel 75 mg, atorvastatin 20 mg, torsemide 5 mg, ivabradine 5mg, isosorbide mononitrate 30 mg, all once day. Digoxin 0.25 mg was prescribed once a day (5 days a week).
On arrival, he was febrile, pulse rate was 48/min (irregular), blood pressure 144/90 mm Hg with postural fall of 30 mm Hg, and respiratory rate 26/min. There were bilateral rhonchi and coarse crepitations in right interscapular region on chest auscultation. On neurological examination: Glasgow Coma Scale (GCS) 15/15, mini–mental state examination (MMSE) 26/30, frontal assessment battery (FAB) score 13/18 with no focal neurological deficit. Examination of the abdomen and cardiovascular system were unremarkable.
His initial investigations showed white blood cells 10,900/mm3, hemoglobin 13.7 mg/dL, platelets 169000/mm3, random blood sugar 182 mg/dL, and serum creatinine 1.16 mg/dL. An arterial blood gas analysis (ABG) showed mixed disorder metabolic and respiratory alkalosis with hypoxia: pH 7.5, PaCO2 31, PaO2 67, HCO3 26, and Po2/Fio2 2.4 on 28% Fio2 (Normal ABG values: pH 7.35–7.45, PaCO2 35-45 mm Hg, PaO2 80-100 mm Hg, HCO3 21-28 mEq/L). He had normal urine analysis, serum transaminases, serum electrolytes, troponin T, and thyroid function test. Electrocardiogram (ECG) showed 1st degree atrioventricular block with multiple ventricular premature contractions. 2D transthoracic echocardiography showed 20% ejection fraction with regional wall motion abnormalities. Chest X-ray revealed cardiomegaly with right lower zone consolidation.
A diagnosis of acute exacerbation of OAD due to lobar pneumonia was made by chest physician and he was treated with antibiotics (piperacillin-tazobactum, clarithromycin), and bronchodilators. Cardiologist was consulted for postural fall in blood pressure and ECG changes. On cardiologist advice, digoxin was omitted due to possibility of digoxin toxicity. Beta-blocker, ivabradine, diuretic, and nitrate were put on hold due to bradycardia and orthostatic hypotension. Ranolazine 500 mg twice/day was started as an antianginal agent.
During 48 hours after admission, his chest condition improved. The white blood cell count dropped to 7,300/mm3 and arterial blood gas analysis showed metabolic alkalosis: pH 7.45, PaCO2 40, PaO2 94, HCO3 28, Po2/Fio2 3.3 on 28% Fio2. On day 3, the patient started developing mild confusion and visual hallucinations and by the day 7 of hospitalization, he developed dysarthria, dysmetria, and difficulty in ambulation due to ataxia. Neurological examination revealed GCS 15/15, MMSE 26/30, FAB 8/18 with no focal neurological deficit. Neurologist was consulted and magnetic resonance imaging with angiography was performed to rule out acute stroke. The imaging showed chronic small vessel ischemic changes with normal angiography. Cerebrospinal fluid examination and antithyroid antibodies test performed thereafter were within normal limits.
Keeping the possibility of drug-induced toxicity, recently added drug ranolazine was stopped. Within 2 days, his neurological signs and symptoms improved markedly and returned to baseline. The presumed correlation between the adverse reaction and the administration of ranolazine was not reinforced by rechallenge. The patient was discharged on clopidogrel 75mg once/day, atorvastatin 20mg once/day, and isosorbide mononitrate 30 mg once/day. On discharge and follow-up visits, there was no recurrence of symptoms.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [144.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",108,102.6,113.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 144.0 mm Hg + 2/3 * 90.0 mm Hg = 108.0 mm Hg.
Hence, the patient's mean arterial pressure is 108.0 mm Hg."
1774,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6188032-1,Extracted,"A 43-year-old male with a past medical history of achalasia presented to the emergency department (ED) with sudden onset severe epigastric abdominal pain. The pain was constant, sharp, well localized, and lasted for several hours prior to admission without improvement. He had no nausea or vomiting and no change in bowel habits or stool. On arrival to the ED, he was afebrile, blood pressure (BP) was 142/82 mm Hg, and heart rate (HR) 60 beats per minute. Physical examination showed a soft non-distended abdomen without tenderness. He had positive bowel sounds. Labs showed a normal complete blood count (CBC), basal metabolic panel (BMP) and normal coagulation studies. Computed tomography (CT) scan of the abdomen and pelvis revealed a focal dissection and irregular enhancement of the celiac trunk with associated splenic artery embolus and large splenic infarct (, ). The radiological findings were consistent with celiac artery dissection. Transthoracic echocardiogram (TTE) showed normal ejection fraction, normal valves and no evidence of thrombus or vegetations. The patient’s condition was managed medically. He received intravenous heparin, hydration, and analgesia. Blood pressure was controlled by the addition of carvedilol 3.25 mg twice daily targeting a systolic blood pressure reading less than 110 mm Hg (). The patient was discharged on warfarin for a total duration of 6 months with a target INR of 2 - 3. On outpatient follow-up, patient blood pressure was controlled and remained below 120/80 mm Hg and accordingly carvedilol was discontinued. Vascular aorta DPLEX performed 6 months following discharge showed patent superior mesenteric artery and celiac artery, with normal flow resistance waveforms and velocities within normal limits. Further hypercoagulability workup was not performed since the patient was lost to follow up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [142.0, 'mm hg'], 'Diastolic Blood Pressure': [82.0, 'mm hg']}",102,96.9,107.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 142.0 mm Hg + 2/3 * 82.0 mm Hg = 102.0 mm Hg.
Hence, the patient's mean arterial pressure is 102.0 mm Hg."
1775,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2844590-1,Extracted,"A 72-yr-old man had been taking medication for chronic stable angina pectoris since 1 yr before, and for hypertension since 4 months before. He was referred to the department of thoracic and cardiovascular surgery due to increasing intensity of chest pain as time goes by. The patient was a current smoker, who had undergone pulmonary tuberculosis with administration of beta blocking agent, calcium channel blocker (CCB), and acetyl salicylic acid (ASA) on admission. Preoperative coronary angiogram (CAG) showed a 90% stenosis on the distal left main coronary artery, which bifurcating to left anterior descending branch and left circumflex branch (). Operation was conducted under general endotracheal anesthesia, and the left internal thoracic artery (ITA) was harvested (in situ) through median sternotomy. The left ITA was anastomosed with the radial artery to form a composite Y-graft and then cardiopulmonary bypass (CPB) was started. Bypass grafting to the left anterior descending artery and to the obtuse marginal branch was done by using composite Y-graft. The patient was transferred to intensive care unit after uneventful weaning from the CPB following a satisfactory operation. Blood pressure and pulse rate were stable as 100/60 mmHg and 90 beats/min for initial 2 hr after the operation. After for a while, the electrocardiogram (EKG) showed depression of ST-segment on all over the leads, the blood pressure fell to 80/30 mmHg, and the pulse rate reached to 100 beat/min. The persistent ischemic signs, including ST-segment depression, hypotension, LVEF of 30% and severe global hypokinesia on echocardiogram, despite of intravenous dopamine infusion of 10 µg/kg/min, made us to get an emergent CAG to confirm the patency of anastomosis. This CAG revealed severe spastic narrowing at the grafted coronary arteries (). Repetitive intracoronary infusion of nitroglycerin resolved the coronary artery spasm, but ongoing depression of ST-segment was observed on EKG. So, CAG about non-grafted, innocent right coronary artery (RCA) had to be done. CAG demonstrated severe vasospasm of RCA (), and also it was resolved with intracoronary infusion of nitroglycerin resulting in normalized ST-segment. Thereafter, he took oral medication of nicorandil as a vasodilator and CCB. He was discharged on the 15th postoperative day without reattack of coronary spasm.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [30.0, 'mmhg'], 'Systolic Blood Pressure': [80.0, 'mmhg']}",46.66667,44.33334,49,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 80.0 mm Hg + 2/3 * 30.0 mm Hg = 46.66667 mm Hg.
Hence, the patient's mean arterial pressure is 46.66667 mm Hg."
1776,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2827084-1,Extracted,"A 21-year-old white Turkish woman referred to our department for the investigation of new onset hypertension developed one week after a miscarriage. Past medical history was insignificant except for miscarriage and there was no history of hypertension before and during pregnancy period. Physical examination revealed weak femoral pulses and brachiofemoral delay. Right and left arm, and leg blood pressures were 190/110 mmHg, 140/90 mmHg, and 80/50 mmHg, respectively. A grade 3/6 systolic murmur was heard over the precordial and interscapular areas.
The electrocardiogram was normal. Rib notching was evident on chest radiography. Standard and Doppler echocardiographic findings were normally functioning bicuspid aortic valve, abnormal mitral valve with congenital elongation, coarctation of descending aorta with a measured maximum gradient of 93 mmHg across the coarctation and mild sized PDA (Figure ). Thorax CT angiography showed a strict aortic coarctation in proximal part of descending aorta, a small sized PDA, and widening and tortuosity in intercostal arteries (Figure ). The measured coarctation length was 12 mm, isthmus was 19 mm, smallest diameter of aortic coarctation was 5 mm, and postcoarctation aortic diameter was 21 mm.
Cardiac catheterization was performed under general anesthesia and right femoral artery and left femoral vein cannulated. The coarctation segment could not be crossed with 0.035 diagnostic guide wire. Therefore, we used the 0.014 hydrophilic guide wire for crossing the coarctation segment. Diagnostic multiple pores and pigtail catheter were passed across the coarctation over the hydrophilic guide wire. Measurements of aorta and coarctation segment were similar with the CT angiography. The maximal gradient across the coarctation was 102 mmHg and Qp/Qs: 1.2/1. Arcus aorta, ascending aorta and aortic branches were normal in anatomy but ascending aorta was minimally dilated (39 mm; Figure ).
Pigtail catheter was changed to a 14F, 75 cm long Mullins sheath over the 0.035 exchange guide wire. A custom-made eight-zig, 45 mm long CP covered stent (NuMed, Hopkinton, NY) loaded on a BIB balloon (inner balloon 12 mm × 9 mm, outer balloon 22 mm × 4 cm) was used. After attachment, the excess covering material is folded around the stent. The graft stent and balloon assembly was passed through the sheath, after checking for correct positioning. Firstly, the inner balloon was inflated and the position was rechecked by angiography and then the outer balloon was inflated fully (Figure ). Both balloons were then deflated, with the inner one being deflated first before being withdrawn through the sheath. Control aortography showed that stent-graft in position covering the coarctation segment and complete occlusion of the patent ductus arteriosus was achieved without any complication. Maximum gradient across the coarctation was measured as 30 mmHg. Therefore, stent-graft was over dilated using high-pressure balloon (22 mm × 4 cm, NuMed, Hopkinton, NY). The gradient across the coarctation was decreased and measured as 0 mmHg (Figure ). The coarctation segment of aorta was increased from 6 mm to 19 mm. The procedure was completed without complication.
After the procedure, patient was monitored for 48 hours for possible complications and blood pressure control. Blood pressure was returned to normal limits as were the discrepancy between arm and legs. No anti-hypertensive medication was needed after the procedure and the patient was discharged with 300 mg acetyl salicylate. The patient was followed for eight months without any problem and on her last visit repeat catheterization showed no gradient across the grafted segment or evidence of PDA.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [190.0, 'mm hg'], 'Diastolic Blood Pressure': [110.0, 'mm hg']}",136.66667,129.83334,143.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 190.0 mm Hg + 2/3 * 110.0 mm Hg = 136.66667 mm Hg.
Hence, the patient's mean arterial pressure is 136.66667 mm Hg."
1777,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8510663-1,Extracted,"We present a case of an 80-year-old Caucasian woman with history of arterial hypertension, dyslipidemia, type 2 diabetes mellitus and ischemic cardiomyopathy with preserved ejection fraction. She presented to the emergency department with a 3-month history of progressive fatigue, malaise and anorexia, and 5 weeks of cough with blood-streaked sputum and progressive peripheral edema. She denied having fever, weight loss, arthralgia, and skin rash. Multifocal pneumonia and acute kidney injury (serum creatinine 5.69 mg/dL from a baseline of 0.99 mg/dL, reference range (RR): 0.6 - 1.2) associated with iron deficiency anemia (hemoglobin 7.6 g/dL, RR: 11.9 - 15.6) was diagnosed and she was admitted to intensive care unit (level 2). Intravenous (IV) fluid administration was started, as well as empiric amoxicillin-clavulanate and azithromycin, for 2 days, switched to piperacillin-tazobactam due to clinical worsening. Additional laboratory test showed elevated erythrocyte sedimentation rate (ESR), negative ANCA, anti-GBM and antistreptolysin O (ASO) antibodies titers, normal C3 and C4 levels, chronic HBV infection, negative anti-hepatitis C virus (HCV) and human immunodeficiency virus (HIV), and microscopic hematuria with subnephrotic proteinuria. Computed tomography (CT) of the chest and the abdomen revealed bilateral nodular infiltrates predominantly perihilar () and normal sized kidneys without hydronephrosis. During hospitalization, she had hemoptysis and bronchoscopy (FOB) with bronchoalveolar lavage (BAL) was performed; bronchial secretions were seen, and bacterial, mycobacterial and fungal infection was excluded. Cytologic analysis showed alveolar macrophages and predominance of polymorphonuclear cells. The hemosiderin-laden macrophages were not identified.
Despite optimal medical management, renal function was worsening, and she was transferred to our hospital to initiate renal replacement therapy.
On admission, she was pale and afebrile, her blood pressure was 130/70 mm Hg and pulse rate was 87 beasts/min. She was tachypneic and oxygen saturation was 94% on 2 L/min nasal cannula. On chest auscultation, there were fine crackles in the lower two-thirds of bilateral hemithorax. She had peripheral edema and skin examination did not reveal any rash.
On arrival in our hospital, new tests were performed: hemoglobin 8 g/dL (RR: 11.9 - 15.6), white blood cell count 13.2 × 109/L (RR: 4 - 11 × 109/L), C-reactive protein 79.8 mg/L (RR: < 3.0), ERS 66 mm/h (RR: < 20), serum creatinine 7.3 mg/dL (RR: 0.6 - 1.2) and blood urea nitrogen 197 mg/dL (RR: 15 - 39). HBV viral load was 337,600 IU/mL. Platelet count, coagulation tests, serum bilirubin (total and conjugated), aspartate and alanine aminotransferases were within normal range. Albumin and total serum protein were normal and immunoelectrophoresis revealed no monoclonal peak. Urinalysis showed 25 - 50 red blood cells/high-power field (RR: 0 - 2) and urinary protein 1.46 g/24 h (RR: < 0.05 - 0.08). Chest X-ray showed diffuse nodular infiltrate parenchymal disease involving both lungs ().
Given the bilateral nodular pulmonary infiltrates, along with cough with blood-streaked sputum, hemoptysis and iron deficiency anemia, DAH seemed highly probable. Therefore, we suspected that the patient had a PRS and the autoimmune tests were repeated, on second day of hospitalization: MPO-ANCA 121.1 U/mL (RR: < 10), PR3-ANCA 312.6 U/mL (RR: < 20), anti-GBM antibody 202 U (RR: < 40) and rheumatoid factor 26 IU/mL (RR: < 15), normal C3 and C4 levels, and negative antinuclear antibody, cryoglobulins and anti-dsDNA ().
On second day, IV high-dose methylprednisolone therapy was started (500 mg/day for 3 days), followed by oral prednisolone at 60 mg/day, without renal biopsy. Pulses of IV cyclophosphamide (7.5 mg/kg) given at intervals of 2 weeks as part of induction therapy and nine sessions of plasma exchange (PE) over 2 weeks were also started, until anti-GBM antibody and ANCA titers were undetectable. Entecavir 0.5 mg weekly was started too.
On sixth day, renal biopsy was performed, and cellular crescents were found in 57% glomeruli with focal fibrinoid necrosis and mildly interstitial fibrosis accompanied by moderate inflammatory infiltrate, without vasculitis (). Immunofluorescence showed linear deposition of immunoglobulin G along the GBM (). After these results, the patient maintained the ongoing therapy.
Progressive improvement occurred during 3 weeks of therapy, with resolution of hypoxemia, no recurrence of cough and blood-streaked sputum; however, renal function did not improve. On day 20, chest CT scan showed resolution of pulmonary infiltrates.
She was discharged after 34 days of hospitalization and despite this aggressive treatment, renal function did not recover. Oral glucocorticoid therapy was gradually reduced.
After 6 months of therapy with entecavir 0.5 mg weekly, HBV viral load became undetectable. Abdominal ultrasound showed normal liver morphology with a liver stiffness value compatible with F0-F1 (no or minimal fibrosis).
After 2 years, the patient is still dialysis-dependent, but did not have relapse of DAH and ANCA and anti-GBM antibody titers remain negatives.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 70.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1778,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2738322-1,Extracted,"A 65-year-old male was admitted to our ICU with a history of restlessness following accidental ingestion of 50 mg of Amlodipine along with his usual dose of 50 mg Atenolol, six hours earlier. He was a known case of hypertension for 15 years, on regular medications. He was diagnosed to have mild renal insufficiency 6 years prior to present admission, with a stable serum creatinine level. On examination he was conscious, oriented with normal sinus rate of 62/ min, blood pressure of 112/76 mmHg and bilateral pedal edema. Respiratory, cardiovascular and neurological examinations were normal. Electrocardiograph showed normal sinus rhythm. Initial hemogram, random blood sugar, serum electrolytes, arterial blood gas and electrocardiogram were unremarkable. Blood urea and serum creatinine values were 79 mg/dl and 4.3 mg/dl respectively. Echocardiography revealed left ventricular hypertrophy with normal LV systolic and diastolic function.
The patient was given 30 ml of 10 % calcium gluconate - over 5 mins, followed by an infusion of calcium gluconate at a rate of 10 ml/hr and after a bolus dose of Glucagon of 10 mgm, an infusion of Glucagon at a rate of 3 mg/hr was commenced. Over the next six hours the patient became hypotensive not responding to volume resuscitation and requiring inotropic support with adrenaline and dopamine infusion. His sensorium gradually deteriorated. Twelve hours following the overdose he was unresponsive to painful stimuli. Arterial blood gas analysis revealed mixed respiratory and metabolic acidosis with a pH of 6.8, pCO2 of 115 mmHg, pO2 of 76 mmHg and a HCO3 of 16 mmol/L. He was on high dose inotropic support with normal central venous pressure and there was a drop in the hourly urine output. Gastric aspirate was coffee ground. He was electively intubated and ventilated. Ultrasonography of the abdomen showed normal kidney size with increased echogenicity. UGI endoscopy revealed erythematous gastric mucosa without any ulcer crater.
The next day the patient started showing signs of improvement. His sensorium improved but he remained oliguric. Arterial blood gas analysis showed pH of 7.2 pCO2 of 34. mm Hg, pO2 of 115 mmHg and a bicarbonate of 13.7 mmol/L. Repeat potassium was 7.8 mEq/L. In view of oliguria, persistent acidosis and hyperkalemia hemodialysis was started. Over the next 24h, his condition stabilised and inotropic support, glucagon, calcium infusions were tapered off. He was successfully weaned off from the ventilator on the following day. On day 10 of admission he was discharged from the hospital.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [112.0, 'mm hg'], 'Diastolic Blood Pressure': [76.0, 'mm hg']}",88,83.6,92.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 112.0 mm Hg + 2/3 * 76.0 mm Hg = 88.0 mm Hg.
Hence, the patient's mean arterial pressure is 88.0 mm Hg."
1779,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9570,Extracted,"A 33-year-old African American woman presents to the office complaining of blurry vision and headache for the past 2 weeks. She states that she has not been feeling herself lately and also fell down once after a dizzy episode. Her medical history is remarkable for hypertension and pulmonary sarcoidosis treated with hydralazine and prednisone respectively. She had a recent bout of acute optic neuritis, requiring high-dose IV methylprednisolone. Her temperature is 37°C (98.6°F), the blood pressure is 112/76 mm Hg, the pulse is 78/min, and the respirations are 14/min. On examination, the patient is mildly disoriented. Head and neck examination reveals a soft, supple neck and a right-sided facial droop. There is 5/5 muscle strength in all extremities. VDRL test is negative. A head MRI is pending.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [76.0, 'mm hg'], 'Systolic Blood Pressure': [112.0, 'mm hg']}",88,83.6,92.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 112.0 mm Hg + 2/3 * 76.0 mm Hg = 88.0 mm Hg.
Hence, the patient's mean arterial pressure is 88.0 mm Hg."
1780,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4593,Extracted,"A 57-year-old woman presents with a cough, hemoptysis, fever, chills, and weight loss that has persisted since she returned from her trip to Thailand. She admits to having sexual contact with several prostitutes. The patient is generally healthy and is not taking any medications. She has a family history of glaucoma, diabetes mellitus, factor V Leiden, and an ischemic stroke. Her temperature is 101°F (38.3°C), blood pressure is 125/84 mmHg, pulse is 99/min, respirations are 19/min, and oxygen saturation is 95% on room air. Physical exam is notable only for some coarse breath sounds. A chest radiograph is performed as seen in Figure A. Treatment for this patient's condition is started. The patient returns to clinic with decreased visual acuity mainly in her right eye. She also reports pain in both eyes with movement. On physical examination, when a penlight is shined into the right eye, there is no pupillary constriction in either eye. The rest of her neurological exam is unremarkable.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [84.0, 'mm hg'], 'Systolic Blood Pressure': [125.0, 'mm hg']}",97.66667,92.78334,102.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 84.0 mm Hg = 97.66667 mm Hg.
Hence, the patient's mean arterial pressure is 97.66667 mm Hg."
1781,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8482717-3,Extracted,"A 33-year-old male with a history of salvage treatment for relapsed acute myeloid leukemia who recently was admitted with influenza pneumonia and complicated UTI presented with a fever. He was undergoing chemotherapy with high-dose cytarabine for AML with last dose received one month prior to infection. A SARS-CoV-2 RT-PCR test was administered which returned a positive result. The patient was subsequently admitted. Upon admission, blood pressure was 129/81 mmHg, heart rate 94 beats per minute, respiratory rate 17 breaths per minute, body temperature 37.2°C, pulse 94 beats per minute. Labs included an elevated ferritin of 6753 ng/mL and D dimer of 53 420 ng/mL. After three days of hospitalization, clinical symptoms improved and he was discharged home with instructions on oxygen saturation monitoring.
One week later, the patient returned with persistent fatigue, fever, and intermittent shortness of breath since he was discharged. He has had a productive cough of clear sputum and central chest discomfort. He denies any abdominal pain, diarrhea, blood in the stool or urine, and experiences no burning during urination. During this time, body temperature was 38.1°C, blood pressure 110/69 mmHg, heart rate 103 beats per minute, pulse 103 beats per minute, and oxygen saturation at 94%. Imaging revealed worsening left basilar consolidation suspicious for pneumonia ( and ). He was administered 10 mg of intravenous dexamethasone, 2000 mg of intravenous cefepime, 250 mg of oral azithromycin every 24 hours, and 800 mg–160 mg oral sulfamethoxazole/trimethoprim. The following day, the patient reported feeling better with resolving symptoms of fatigue and shortness of breath. He still however had intermittent episodes of dyspnea. After a 10 day hospital course, his symptoms gradually improved and he was asymptomatic for >72 hours. He was then discharged with instructions on self-isolation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [129.0, 'mm hg'], 'Diastolic Blood Pressure': [81.0, 'mm hg']}",97,92.15,101.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 129.0 mm Hg + 2/3 * 81.0 mm Hg = 97.0 mm Hg.
Hence, the patient's mean arterial pressure is 97.0 mm Hg."
1782,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8284758-1,Extracted,"A 15-year-old boy was admitted to our hospital complaining of gross hematuria with fatigue, anorexia, nausea, and recurrent abdominal distension for 1 week without any obvious evidence of preceding infection. He had been diagnosed with IgAN at 8 years of age after presenting with gross hematuria with a baseline serum creatinine of 60 μmol/L. His renal biopsy at the time showed diffuse mild mesangial and endothelial proliferation with mesangial IgA deposits, and he received corticosteroids and cyclophosphamide for 1 year.
On examination, his weight and height were 50 kg and 170 cm respectively, with a body mass index of 17.3 kg/m2. Blood pressure was 120/93 mmHg. Other physical examination was unremarkable, tonsils were normal in appearance, the abdomen was soft and non-tender with normal bowel sounds, and he had no dependent edema. His initial laboratory workup was the following: creatinine, 96 μmol/L (40–135); estimated glomerular filtration rate, 101 ml/min/1.73 m2 (CKD-EPI formulae); albumin, 38.6 g/L (40–55); blood leucocytes, 5.56 × 109/L (3.5–9.5); hemoglobin, 148 g/L (130–175); Other blood examinations were normal, including tests for antinuclear antibody, antineutrophil cytoplasmic antibodies, and complement C3 and C4. Urine microscopy showed 1765 RBC/high-power field with no casts, and 24-hour urine protein was 4.71 g.
Considering the persistent gross hematuria for more than 1 week with relatively normal renal function, Doppler ultrasonography was done, which revealed that LRV that runs between the aorta and the SMA is very narrow, and the anteroposterior diameter at the hilar portion divided by that at the aortomesenteric portion was 8.8 (1.06 cm/0.12 cm), and the ratio of LRV peak velocity (aortomesenteric portion to the hilar = 159 cm/sec/15 cm/sec) was 10.6 and the aortomesenteric angle was 10°. These findings were consistent with nutcracker syndrome (Fig. ). After his admission, anorexia and abdominal distension with normal flatus and defecation were the most obvious discomforts, especially after eating, which needed parenteral nutrition supplementation. An upper gastrointestinal gastrografin study demonstrated compression of the third portion of the duodenum by the overlying superior mesenteric artery (Fig. ). This suggests SMA syndrome.
At this point, his serum creatinine increased to 186 μmol/L, and repeated percutaneous kidney biopsy was done at the right kidney, which showed IgAN with segmental glomerular necrotizing lesions in 24.3% of glomeruli, cellular crescents in 16.3% of glomeruli, interstitial fibrosis in 20% of the cortical area, and mild diffuse mesangial proliferation and matrix expansion (Fig. ).
The decision was taken to initiate a pulse dose of methylprednisolone 500 mg daily for 3 days, followed by 1 mg/kg orally and mycophenolate mofetil 0.75 g twice a day. The patient's position was suggested to be maintained in the left lateral deviation position, prone position, or knee-chest posture. One month later, his abdomen symptoms such as anorexia and abdominal distension eased a lot with body weight increase of about 3 kg, serum creatinine decreased to 93 μmol/L, and urine microscopy showed 611 RBC/high-power field with 2.04 g urine protein per day. After 6 months of follow-up, his body weight increased to 57 kg, serum creatinine decreased to 63 μmol/L, and urine microscopy showed 75.5 RBC/high-power field with 0.3 g urine protein per day.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [93.0, 'mm hg']}",102,96.9,107.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 93.0 mm Hg = 102.0 mm Hg.
Hence, the patient's mean arterial pressure is 102.0 mm Hg."
1783,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6372251-1,Extracted,"A 55-year-old intoxicated homeless man presented to the hospital with a cough and chest pain. His past medical history was notable for chronic alcoholism and untreated latent tuberculosis, based on a positive interferon-gamma release assay three years prior to presentation. He had worked as a car mechanic. He smoked half a pack of cigarettes daily and drank a few beers every day. He denied illicit drug use. He reported concern of a cough productive of a moderate amount of yellow sputum that is occasionally streaked with blood. He had the cough for about four weeks with no improvement. His cough was associated with dyspnea on exertion, pleuritic chest pain, chills, night sweats, and a 10-pound weight loss over the past few months.
The patient’s vital signs revealed a temperature of 98.2°F, a heart rate of 92 beats per minute, a respiratory rate of 18 breaths per minute, and a blood pressure level of 96/55 mmHg. His oxygen saturation was 98% breathing ambient air. The patient’s lung examination revealed normal work of breathing and decreased breath sounds on the left lung fields without wheezing, crackles, or rhonchi. The results of his cardiac, abdominal, and neurological exams were all within the reference range. No lymph nodes were palpated. Results from the laboratory workup included a complete blood count and comprehensive metabolic panel, both of which were within the reference ranges. The findings of his chest radiography were unremarkable. Figure represents the initial presentation of the patient three months ago and Figure represents the computed tomography scan of his chest that revealed bilateral ground-glass opacities involving all lung lobes; the largest measured 5.7 cm in diameter.
The patient was placed in respiratory isolation, and an empiric antibiotic therapy was started to cover community-acquired and aspiration pneumonia. Sputum stain tests for acid-fast bacilli were negative on three consecutive days, and respiratory isolation was discontinued. A Gram stain showed normal respiratory flora. Urine legionella and histoplasma antigen test results remained negative. The results of Streptococcal antigen, Aspergillus antigen, and Fungitell® assays were negative. Human immunodeficiency virus (HIV) serology, anti-nuclear antibody, rheumatoid factor, and antineutrophilic cytoplasmic antibody workup results were negative. The erythrocyte sedimentation rate and complement levels were within reference range. His immunoglobulin panel showed an elevated immunoglobulin E (IgE) level at 3309 IU/mL, a low immunoglobulin G (IgG) level at 601 mg/dL, and a low immunoglobulin M (IgM) level at 25 mg/dL. Immunoglobulin A (IgA) levels were within reference range, and the levels were checked again during follow-up and they were completely normal. Initial decrement in levels might be due to the patient's ongoing illness. The patient underwent a surgical lung biopsy. Pathology testing revealed pulmonary fibrosis, reactive alveolar changes, granulomatous inflammation with focal calcifications, positive fungal stains, a mucicarmine rich capsule, and morphology consistent with cryptococcal infection. There was no evidence of malignancy or vasculitis. On the sixth hospital day, empiric antibiotic therapy with ceftriaxone, azithromycin, and metronidazole was discontinued in favor of treatment specific for cryptococcal pneumonia—14 days of intravenous amphotericin B and oral flucytosine. Following induction, the patient was discharged on oral fluconazole, to continue for six to 12 months. Outpatient follow-up was scheduled with the infectious diseases and immunology clinics. The patient was lost to follow-up after a one-time show-up in the medical clinic.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [96.0, 'mm hg'], 'Diastolic Blood Pressure': [55.0, 'mm hg']}",68.66667,65.23334,72.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 96.0 mm Hg + 2/3 * 55.0 mm Hg = 68.66667 mm Hg.
Hence, the patient's mean arterial pressure is 68.66667 mm Hg."
1784,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3662630-1,Extracted,"A 26-year-old Portuguese woman presented to the emergence department with a 48 hour history of progressive dispnea, generalized edema and left lower chest pain with non-productive cough. The patient had a 6 months history of inflammatory polyarthralgias involving initially interphalangeal joints, evolving, at some time later, the knees and elbows bilaterally. After ongoing rheumatologist evaluation, she started prednisolone 10 mg qd and hydroxychloroquine 400 mg qd, while waiting laboratory results. 12 days before admission, she had had symptoms of a urethritis episode, associated with unexplained anorexia and asthenia, which led her to suspend the therapeutic, even against medical advice. On examination, patient was feeling very ill, afebrile, with tachycardia (144 bpm), tachypnea (34/min), blood pressure 143/82 mmHg, peripheral oxygen saturation of 94% on 40% oxygen and raised jugular venous pressure. Intermittently she presented an obtunded state of consciousness. Aside a diffuse moderate edema and a livedoid skin discoloration, an erythematous rash over the cheeks and nasal bridge was noted. On auscultation heart sounds were found to be diminished and diffuse coarse crackles were noted on both lungs, with depressed vocal transmission in right basal thorax. Abdominal examination revealed moderate hepatomegaly and ascites. The electrocardiogram showed atrial fibrillation and low voltage QRS complexes. On chest roentgenogram (Figure ) cardiomegaly and right pleural effusion were evident. Initial arterial blood gas showed metabolic acidosis (pH-7.134, PCO2-18 mm Hg, PO2-85 mm Hg, and HCO3-6 mEq/L). Intravenous fluid replacement was started, blood and urine were sent for culture and treatment was started with empiric antibiotics (ceftriaxone 2 g iv id plus ciprofloxacin 400 mg iv bid) and methylprednisolone 1 g iv bolus for 3 days. Patient was admitted to a high-dependency unit (HDU) for further evaluation, monitoring and support. An ultrasound of the heart showed a large circumferential pericardial effusion without signs of tamponade, which to the consulted assistant cardiologist merit only monitoring. Complementary CT scan (Figures and ) excluded pulmonary embolism or other thrombotic events, revealed an enlarged and homogeneous liver and confirmed pleuropericardial effusion and ascites. The laboratory survey revealed a white blood cell count (WBC) of 5.300 cells/mm3, with 70% polymorphonucleated cells (PMNs), a platelet count of 417.000 per mm3 and hemoglobin 7,8 g/dL. Her INR was 2.4. An extended metabolic and liver panel demonstrated: sodium 131 mmol/L, BUN 38.4 mg/dL, creatinine 1.4 mg/dL, total bilirubin 0.62 mg/dL, AST 401 U/L, ALT 85 U/L, and alkaline phosphatase 128 U/L. Ammonia was 38 μmol/L. C reactive protein 160 mg/l and ESR 87 mm/h. Urine evaluation demonstrates > 50 leucocytes and erythrocytes per high-power field, associated with proteinuria > 75 mg/dL Meanwhile, an immunologic panel, done 1 month earlier, was sent to us, showing: polyclonal hypergammaglobulinemia; positive ANA (1:160), anti-dsDNA antibodies (75 UI/mL) with positivity to anti SSA, SSB and Histone. Pleural fluid analysis showed an exsudate with no bacteria on a Gram stain. By the 2nd HDU day patient was feeling much better with remarkable edema regression. Blood gas normalized. The microbiologic results of the blood, pleural fluid and urine cultures became negative and antibiotherapy was suspended. Immunological panel revealed frank hypocomplementemia (C3 <1 UI; C4 – 9 UI; CH50 <10 UI); ANA (1:320), anti-dsDNA antibodies (175 UI/mL) with persisting positivity to anti SSA, SSB and Histone, as well as hypergammaglobulinemia and a direct positive Coombs test. A 24 hour urine collection demonstrates 2,1 g proteins. The patient was discharge by the 10th hospital day, on a therapeutic regimen of 60 mg/day of prednisolone plus hydroxychloroquine 400 mg/day, after an arrangement with the nephrologic clinic to eventually proceed to a renal biopsy.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [143.0, 'mm hg'], 'Diastolic Blood Pressure': [82.0, 'mm hg']}",102.33333,97.21666,107.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 143.0 mm Hg + 2/3 * 82.0 mm Hg = 102.33333 mm Hg.
Hence, the patient's mean arterial pressure is 102.33333 mm Hg."
1785,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4667049-1,Extracted,"C. K., a 53-year-old Caucasian female, was referred by her primary care physician for abnormal liver function tests. She was first diagnosed with HCV exposure in 2005 with genotype 3a and had undergone pegylated interferon monotherapy weekly for six months. She achieved end of treatment response. Subsequently, she continued to use intravenous drugs. On presentation to our clinic on 05/04/2011, patient was found to have reinfection with genotype 1a with an HCV viral load of 29,000 IU/mL. She had no nausea, vomiting, heartburn, abdominal pain, or dysphagia. She had lost some weight but she was dieting. She denied any intravenous drug and alcohol use in last 3 years.
Her past medical history was notable for methicillin resistant staphylococcus aureus (MRSA) endocarditis, vertebral osteomyelitis, hyperlipidemia, diverticulosis, and Helicobacter pylori gastritis. There was no family history of celiac disease, type 1 diabetes or any other autoimmune diseases. She is a former smoker. Her medications included butalbital/acetaminophen/caffeine, simvastatin, and esomeprazole.
Initial physical examination showed temperature of 98.2°F, pulse of 72 beats/minute, BP of 116/70 mm/Hg, and weight of 146 pounds. Physical examination was normal “without stigmata of liver disease or malnutrition and so forth.”
Laboratory data on initial visit showed normal complete blood count (CBC), complete metabolic profile (CMP), and iron studies. Pt was found to have HCV viral load of 4,515,392 IU/ml and genotype 1a. Other causes of liver disease including hepatitis B, autoimmune hepatitis, Wilson disease, and HIV were ruled out. The patient underwent a liver biopsy which showed Metavir grade 2 inflammatory activity and stage 1 fibrosis ().
Colonoscopy was also done on 6/25/2008 at different facility, which did not show any polyps but showed diverticular disease of descending colon and sigmoid colon. The patient underwent upper gastrointestinal endoscopy (EGD) done on 10/7/2009 which was unremarkable.
Treatment was initiated on dual therapy with pegylated interferon alfa-2a at 180 μg subcutaneous weekly plus ribavirin 600 mg orally twice per day for a 4-week lead-in phase, followed by triple therapy using boceprevir (BOC) 800 mg orally three times per day for total of 28 weeks. HCV viral loads which were collected at weeks 4, 8, 12, 21, and 24 were undetectable by polymerase chain reaction. During treatment, the patient developed neutropenia and anemia, which were treated with pegfilgrastim and darbepoetin alfa.
Approximately 4 weeks after initiation of triple therapy the patient developed loose nonbloody bowel movements, which was not reported at the time. She experienced nausea and decreased appetite but no vomiting or abdominal pain. Occasionally she felt bloated. There was no fever, chills, or skin rash.
Three months following cessation of treatment the patient complained of ongoing weakness and dyspnea on exertion which had begun after the initiation of therapy but which had not resolved completely. She had ten-pound weight loss during treatment which persisted, but she also now admitted to having 5-6 watery loose bowel movements for the preceding five months. Repeat CBC showed low hemoglobin of 10.7 g/dL (baseline 14 g/dL). The patient failed to give stool samples for analysis. She underwent an EGD and colonoscopy. During EGD, mucosa in the stomach and second and third part of duodenum appeared normal but biopsies from second portion of the duodenum revealed mild villous blunting, mild crypt hyperplasia, and minimal intraepithelial lymphocytes consistent with CD (). The tissue transglutaminase IgA was 85 U/mL. The patient was started on gluten-free diet. Her intestinal symptoms improved and the hemoglobin returned to normal.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [116.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",85.33333,81.06666,89.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 116.0 mm Hg + 2/3 * 70.0 mm Hg = 85.33333 mm Hg.
Hence, the patient's mean arterial pressure is 85.33333 mm Hg."
1786,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4002007-1,Extracted,"Herein, we report a case of a 71-year-old female patient hospitalized for anemia, motor incoordination, gait disturbance, weakness, and decline of her functional state. She was asymptomatic eight months prior to the day she was hospitalized, when she had asthenia, adynamia, hyporexia, symptoms of dizziness, and vertigo. Six months prior to admission, the symptoms increased, with onset of loss of balance, and postural instability. The patient also developed deterioration for walking, with repeated falls, which led her to stop walking for fear of falling, and limited her physical daily living activities to simply transferring from the chair to the bed. Likewise, it was noted that upon flexing her neck, she reported feeling an electrical discharge irradiating from her back to her legs. Two months before hospital admission, she noted lesions on the tongue, which produced a burning sensation and pain when swallowing foods - leading her to decreased intake of food and a loss of 5 kg coupled with increased feeling of weakness in her general state. She consulted with her local hospital, where she was diagnosed with paraparesis and anemia to continue studies.
As personal antecedents, she revealed hypertension managed with captopril 50 mg every 12 h. She did not report alcohol consumption, vegetarian nutritional habits, or other personal or family antecedents of importance.
Upon physical exam for admission, she was in poor general state, pale, and marked loss of muscle mass. Blood pressure was 130/80 mm/Hg, without orthostasis, respiratory rate 17 per min and heart rate 85 per min. Her weight before developing the diseasewas 70 kg; her current weight is 60 kg, height 1.65 m. The oral cavity showed smooth, shiny, reddish depapillated tongue with ulceration at lateral level ).
Neurological exam revealed that she was alert and oriented in all three spheres, no cranial nerve involvement, or abnormal movements. She had muscle weakness grade 3/5 and spasticity in all four limbs, tone and tropism diminished. The superficial sensitivity, touch, pain, and temperature systems were normal. Deep sensitivity was altered, with lack of vibratory sensation of the sense of position in upper and lower limbs, numbness in hands and feet, and positive Lhermitte's sign. Gait was characteristic of sensory ataxia with postural instability, broad support polygon, positive Romberg's sign, diminished osteotendinous reflexes especially in lower limbs and bilateral flexor plantar reflex present. Different para clinical studies were carried out (). Urinalysis, serology, and direct Coombs test were also performed under normality parameters. Additionally, extended blood test was conducted, revealing red cell anisocytosis, macrocytosis, and poikilocytosis. White series with hypersegmented neutrophils and platelet series without alterations were found. Upper gastrointestinal endoscopy was performed with the biopsy showing chronic atrophic gastritis positive for Helicobacter pylori.
Geriatric assessment scales were applied, showing: mini-mental exam (28/30), geriatric depression scale (4/15), physical aspect of Barthel's scale of activities of daily living (60/100), JH Downton's scale of risk of falling in the elderly (3 points), and assessment of nutritional state through the mini nutritional assessment (16/30 points).
Vitamin B12 deficit diagnosis was performed with hematological manifestations given by macrocytic anemia, neurological manifestations by ataxic gait, and in skin and mucosa by Hunter's glossitis. Because of the neurological alterations in association with ataxic gait and low levels of vitamin B12, nuclear magnetic resonance of the cervical and thoracic spine was requested, which documented images compatible with sub-acute combined degeneration of the spine (.
Replacement with Cbl was begun, showing after three weeks increased Hemoglobin values with decreased levels of lactate dehydrogenase indicating improvement in ineffective erythropoiesis. Glossitis was resolved after a month of establishing Cbl reposition (C and D). After three months of treatment, gait improved with the patient walking independently; sensitive symptomatology also improved.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1787,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3601985-1,Extracted,"A 31-year-old Japanese man who worked as a janitor was admitted to Tokyo Metropolitan Bokutoh General Hospital for coma and convulsion in September 2010. During this summer, an exceptional heat wave was experienced in Japan, during which 1718 individuals died from heatstroke [].
Until admission, he had conducted a non-strenuous work in a hot environment for one or two hours. A work colleague found him staggering in the corridor and moved him to a cool room, where he developed convulsions lasting for 15 seconds.
A diagnosis of essential hypertension had been established at the age of 26, when a combination treatment of 50mg losartan and 12.5mg hydrochlorothiazide, and doxazosin mesilate at 1mg were initiated. Since control of his blood pressure became poor, eplerenone at 50mg was initiated five days before admission.
Prior to his admission, no abnormal findings other than hypertension and obesity, with a body mass index of 27kg/m2, had been detected on routine physical examinations and laboratory testing. Repeated blood tests failed to show any abnormal findings in serum electrolyte levels.
His initial evaluation showed consciousness disturbance and a Glasgow Coma Scale level of 10 (E4V2M4). The temperature in his urinary bladder was 40.6°C. His blood pressure was 116/52torr, and his heart rate was 157 beats/minute. His respiratory rate was 34 breaths/minute.
The initial laboratory test findings are shown in Table . Abnormal findings comprised serum levels of creatinine 1.4mg/dL, sodium 114mEq/L and creatine kinase 756IU/L. He met the criteria for systemic inflammatory response syndrome [].
Except for severe hyponatremia of 114mEq/L, there were no abnormal findings leading to the development of consciousness disturbance. Serum levels of thyroid hormones and cortisols were normal. The results of blood culture tests were negative. No signs suggesting the presence of sepsis were documented. A computed tomography scan of our patient’s head failed to show any abnormal findings.
Based on these findings, the initial diagnosis was heatstroke complicated by dehydration, rhabdomyolysis, hyponatremia, renal failure and a hyper-coagulable state.
The initial treatment comprised cooling, intravenous fluid administration, tracheal intubation, and mechanical ventilation. The anti-hypertensive drugs and diuretics were withdrawn. We administered 5700mL of normal saline intravenously during the first nine hours. His urine output was 2000mL during the same periods. He was additionally given 1920mL of normal saline during the next 24 hours, when 3000mL of urine was excreted.
Our patient’s levels of consciousness rapidly recovered to 12 (E4V3M5) with his core body temperature returning from 40.6°C to 38.2°C within three hours of the initiation of cooling and intravenous fluid.
On the next day, he became fully conscious without development of central pontine myelinolyis. His serum sodium concentration improved from 114mEq/L to 124mEq/L within 18 hours. His core body temperature returned to normal (36.9°C). His general condition improved rapidly, and he was discharged on the fourth day.
Eplerenone was resumed and the hyponatremia did not recur. Because hyponatremia is a common complication of thiazides, we withheld the losartan/hydrochlorothiazide. Challenge tests were omitted because our patient did not agree to undertake them.
After he recovered, we took another careful review of our patient’s medical history. Surprisingly, he did not recognize feeling hot while working in a hot environment. Considering his clinical course, a diagnosis of heatstroke preceded by consciousness loss due to severe hyponatremia was made.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [116.0, 'mm hg'], 'Diastolic Blood Pressure': [52.0, 'mm hg']}",73.33333,69.66666,77,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 116.0 mm Hg + 2/3 * 52.0 mm Hg = 73.33333 mm Hg.
Hence, the patient's mean arterial pressure is 73.33333 mm Hg."
1788,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7331778-1,Extracted,"A 75-year-old male with a past medical history of hypertension and diabetes presented to the hospital with worsening shortness of breath, dry cough, fatigue, and fever for three weeks. On presentation, the patient was awake, alert, in moderate respiratory distress, and had left-sided wheezes. He was afebrile with a respiratory rate of 30, oxygen saturation of 95% on nonrebreather mask, blood pressure of 156/81, and heart rate of 86. Chest X-ray (CXR) showed airspace disease involving the left lung (Figure ). Electrocardiogram showed sinus rhythm with premature atrial complexes. Influenza antigen was negative. Laboratory testing was unremarkable. COVID-19 test was sent and the patient was started on azithromycin and cefepime. The patient had worsening of symptoms and the next day laboratory testing revealed: elevated D-Dimer, ferritin, troponin, lactic acid dehydrogenase, C-reactive protein, white blood cells, and a positive COVID-19 test. The patient was started on HCQ but shortly thereafter, he developed multiple episodes of nonsustained ventricular tachycardia, and HCQ was stopped which led to the resolution of the aforementioned rhythm (Figure ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [81.0, 'mm hg'], 'Systolic Blood Pressure': [156.0, 'mm hg']}",106,100.7,111.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 156.0 mm Hg + 2/3 * 81.0 mm Hg = 106.0 mm Hg.
Hence, the patient's mean arterial pressure is 106.0 mm Hg."
1789,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8029552-1,Extracted,"An 85-year-old man with a history of hypertension treated with candesartan was admitted to our hospital at midnight due to chest discomfort. His blood pressure was 93/47 mmHg, and his pulse rate was 61 bpm without heart murmurs or leg pitting edema. Electrocardiography revealed a complete atrioventricular block and ST elevations in Ⅱ, Ⅲ, aVF, and V3R–V5R lead with reciprocal changes. Transthoracic echocardiography detected akinesis of the inferior wall with an ejection fraction of 40%. Blood tests showed an elevated white blood cell count and creatinine level, but no elevation of creatine phosphokinase or the troponin T level. Under the diagnosis of acute inferior myocardial infarction, an emergency coronary angiography revealed 99% stenosis in the proximal right coronary artery, and an ad hoc percutaneous coronary intervention (PCI) was successfully performed.
On the day following the PCI, we discontinued the patient's candesartan 4 mg and introduced enalapril 2.5 mg. His blood pressure was 149/60 mmHg at the time of the introduction of enalapril. About 6 h later, slight swelling was noted on the patient's tongue and neck (Figure ). The amount of sputum increased, and his tongue turned a dark-red color. Twenty hr after the patient took the first dose of enalapril, the tongue and neck swelling worsened, and the patient began to experience dyspnea. Tracheal intubation failed due to the edematous tongue and neck, necessitating an emergent tracheostomy (Figure ).
Computed tomography showed marked edema of the tongue and soft tissue of the neck compressing the trachea (Figure ). We suspected the presence of angiotensin-converting enzyme inhibitor-induced angioedema (ACEI-AE) based on the clinical presentation and sequence of events. We discontinued the enalapril, and the edema improved in about 72 h (Figure ). The patient's laboratory data showed no decrease in the levels of C4 or C1 esterase inhibitors (C1-INH); therefore, hereditary angioedema and acquired C1-INH deficiency could be ruled out with a presumptive diagnosis of ACEI-AE. We carefully re-introduced candesartan, which the patient had taken before, and there was no recurrence of angioedema. Fiberoptic laryngoscopy revealed improvement in the pharyngeal and laryngeal edema, and the tracheotomy was surgically closed on the 26th hospital day. The patient was discharged on the 36th day of illness.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [149.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",89.66667,85.18334,94.15,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 149.0 mm Hg + 2/3 * 60.0 mm Hg = 89.66667 mm Hg.
Hence, the patient's mean arterial pressure is 89.66667 mm Hg."
1790,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7042143-1,Extracted,"Patient 1 is a 65-year-old man with persistent atrial fibrillation, and a history of hypertension, hyperlipidaemia, hyperuricaemia, and kidney stones; of transient ischaemic attack, coronary artery disease status post-percutaneous coronary angioplasty of the left anterior descending artery; of catheter ablation of atrial fibrillation; and of two electrical cardioversions after catheter ablation, normal left ventricular function and no valvular abnormality as per his last echocardiogram. He was presented to our outpatient clinic with palpitations and dizziness. Electrocardiogram on admission revealed atrial fibrillation. His height and weight were 160 cm and 79 kg, respectively. His blood pressure was 122/84 mmHg. His electrolytes were as follows: sodium 138 mmol/L, potassium 4.4 mmol/L, and calcium 2.32 mmol/L. His current list of medications included rivaroxaban 20 mg o.d., and rosuvastatin 10 mg o.d.; he was off of antiarrhythmic drugs and/or beta-blockers. He received 300 mg of amiodarone intravenously before cardioversion. shows his ECG prior to cardioversion. He received one DC shock at 200 J and was reverted back to sinus rhythm. shows his ECG during cardioversion. shows his ECG after electrical cardioversion. The patient’s clinical status has been unremarkable since electrical cardioversion. He has not experienced any recurrence of atrial fibrillation and is currently on rivaroxaban 20 mg o.d., rosuvastatin 10 mg o.d., and sotalol 80 mg b.i.d.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [122.0, 'mm hg'], 'Diastolic Blood Pressure': [84.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 122.0 mm Hg + 2/3 * 84.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1791,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3519780-1,Extracted,"A 43 year-old male was referred to the Emergency Department (ED) of our hospital after his workplace colleagues noted increasingly strange behavior for three days. The patient arrived complaining of generalized fatigue, lethargy, fevers, severe band-like headache, slurred speech, and increasing confusion. Though it was felt that the patient’s history was not completely reliable secondary to confusion, he was able to deny throat pain, chest pain, diarrhea, abdominal pain, recent sick contacts, or recent travel. Review of systems was limited secondary to altered mental status, but he did admit to mild dry cough.
Though initially denying immune compromise in the ED, the patient later disclosed he was HIV+. He could not recall his CD4 count but stated that his last viral load was undetectable. Past medical history was significant for hypertension and hypercholesterolemia. Outpatient medications included Atripla, spironolactone, and gemfibrozil. He had a history of unprotected anal sex with men but denied new partners. He had no recent contact with animals. He smoked a pack of cigarettes per day but did not drink or use drugs.
In the ED, the patient’s temperature was 103.9°F (39.9°C). Heart rate was 121 beats per minute, and respiratory rate was 30 breaths per minute. Oxygen saturation was 94% on room air. Blood pressure was 142/90. The patient appeared unwell. He was somnolent but easily aroused. Pertinent findings on general physical exam included a supple neck and decreased breath sounds diffusely. On neurologic exam, he was noted to be dysarthric. He had general slowness of thought and processing. He was slightly confused, though he was oriented and able to name the days of the week forwards and backwards if given sufficient time.
Initial laboratory evaluation was notable for a white blood cell (WBC) count of 10.1 × 103 cells/mm3, [lab reference range 4.0–10.8], hemoglobin of 15.7 g/dL [lab range 14.0–18.0], platelet count of 135 × 103/mm3 [lab range 150–350]. Automated differential showed 87.5% segmented cells (lab range 30-85%), 9.3% lymphocytes (lab range 15-55%), 2.4% monocytes (lab range 0-10%), 0.8% eosinophils (lab range 0-5%), and 0% basophils. No manual differential was performed. A basic metabolic panel showed serum sodium of 134 mmol/L [lab range 137–145], serum potassium of 4.2 mmol/L (lab range 3.5-5.1), serum chloride of 100 mmol/L (lab range 98–107), and CO2 of 19 mmol/L [lab range 22.0–30.0]. Blood urea nitrogen, serum creatinine, and serum glucose were elevated at 33 mg/dL [lab range 9–20], 1.8 mg/dL [lab range 0.7–1.3] and 159 mg/dL [lab range 70–99], respectively. C-reactive protein (CRP) was high at 581 mg/dL [lab range 0–10]. Liver function studies showed an albumin level of 4.4 g/dL (lab range 3.5-5.0), total protein of 7.6 g/dL (lab range 6.3-8.2), total bilirubin of 0.7 mg/dL (lab range 0.2-1.3), direct bilirubin of 0.5 mg/dL (lab range 0–0.3), alkaline phosphatase of 62 U/L (lab range 38–126), alanine aminotransferase (ALT) of 49 U/L (lab range 13–69), and aspartate aminotransferase (AST) of 89 U/L (lab range 15–46). Urinalysis showed 2+ albumin, 3+ blood, trace WBC esterase, negative nitrite, 5–10 WBC, 0–5 red blood cells (RBC), 5–10 epithelial cells, 5–10 hyaline casts, 3+ amorphous cells, and 1+ mucous. A non-contrast computed tomography (CT) scan of the head did not reveal any abnormalities. Nasopharyngeal influenza assay was negative.
Due to the combination of altered mental status, headache, and fever, a lumbar puncture was performed. The results demonstrated an elevated cerebrospinal fluid (CSF) glucose of 97 mg/dL [normal 40–70], CSF protein of 37 mg/dL [normal 12–60], and normal cell count and gram stain. Blood cultures were sent.
A chest x-ray was done and was read as a left hilar mass extending down towards the left lower lobe (see Figure 
). A chest CT was obtained to better characterize the hilar mass (see Figure 
). This chest CT demonstrated a left lower lobe consolidation with air bronchograms suggesting a diagnosis of pneumonia. Based upon the aforementioned findings, the patient was started on azithromycin and ceftriaxone for community-acquired pneumonia, as well as empiric acyclovir for herpes encephalitis.
Given the findings of dysarthria and altered mental status in an HIV + individual with unknown CD4+ count, a brain MRI was obtained. No contrast was administered secondary to acute renal injury. The diffusion-weighted coronal cut can be seen in Figure 
, demonstrating abnormal restricted diffusion and swelling of the splenium of the corpus callosum without other significant abnormalities. Abnormal T2-weighted signal in the SCC can be seen in Figure 
. These MRI findings in an HIV + individual raised concern for CNS opportunistic infection. However, since the patient was hemodynamically stable, was on antiretroviral therapy, and had a negative lumbar puncture, it was decided to treat the pneumonia initially and closely monitor the patient’s mental status.
Over the first two to three days of hospitalization, the patient continued to have high fevers, confusion, and dysarthria. His laboratory markers improved on antibiotics. His serum CRP trended down from 581 mg/L at admission to 200 mg/L on day three. After day three the patient began to demonstrate significant clinical improvement. The patient’s admission CD4+ count returned on day three at 156 cells/mm3, and an HIV viral load came back on day four at <20 copies/mL. On day four, urine antigens for Streptococcus pneumoniae and Legionella pneumophila serogroup 1 were sent. By day five the patient’s neurologic symptoms had resolved, as had his acute renal insufficiency. This same day his Legionella pneumophila urinary antigen returned positive.
On hospital day six a repeat MRI was obtained to monitor radiologic progression of the SCC lesion. This repeat study showed partial interval clearing of the previously noted abnormalities: restricted diffusion, abnormal increased flair, and abnormal T2 signally in the SCC. On hospital day seven the patient was discharged home on oral azithromycin. He had no residual deficits. Initial CSF viral studies including herpes simplex virus 1 and 2, varicella, cytomegalovirus, enterovirus, and JC virus all returned negative, as did the syphilis, hepatitis B, and hepatitis C serologies. Sputum for acid fast bacilli and routine culture were negative. Legionella antibody IgG titers sent on day four later came back at 1:64.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [142.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",107.33333,101.96666,112.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 142.0 mm Hg + 2/3 * 90.0 mm Hg = 107.33333 mm Hg.
Hence, the patient's mean arterial pressure is 107.33333 mm Hg."
1792,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4377789-1,Extracted,"A 25-year-old woman with a history of chronic hypokalemic metabolic alkalosis and hypomagnesemia following chemotherapy and radiation at the age of 2 for a yolk sac tumor was referred to our clinic. She had recently moved to our area and had a peripherally inserted central catheter line in place for the IV infusion therapy of potassium and magnesium that had been prescribed by her previous physicians. She wanted to establish care with us to continue these IV infusions.
In the 23 years since her chemotherapy, multiple physicians had treated this patient. Starting at the age of 9, she had episodes of muscle weakness and fatigue secondary to her electrolyte abnormalities and was started on IV replacement therapy. Her serum potassium (K) and magnesium (Mg) levels ranged between 2.2–3.1 and 0.35–0.60 mmol/L, respectively, throughout her management with IV potassium chloride (60 mEq) and magnesium sulfate (3 g) replacement administered three times a week. Initially, gastrointestinal causes for her diarrhea were excluded; ongoing diarrhea was attributed to the use of oral magnesium oxide prescribed to supplement the IV magnesium.
During her first visit with us, she was noted to have a normal blood pressure of 124/80 mmHg and a heart rate of 72 beats per minute. She was 167 cm in height and 50 kg in weight. Her exam was otherwise with in normal limits.
After our first encounter with the patient, she underwent an extensive workup that included serum and urine studies. Her results suggested renal losses of K and Mg as the cause of her electrolyte abnormalities (see Table ). Urinalysis was normal without any evidence of hematuria or proteinuria. A renal ultrasound performed at that time revealed a kidney size of 9.1 by 4.5 by 3.3 cm on the right and 10.2 by 5.2 by 6.2 cm on the left; otherwise, the results were normal and no other normal abnormalities were noted.
In order to decrease the urine electrolyte wasting, and with the objective of keeping the patient only on an oral K–Mg replacement regimen, we recommended a high-potassium diet and started the following pharmacological approaches that were introduced one at a time in intermittent visits: oral benazepril up to 5 mg daily, amiloride 5 mg daily, magnesium chloride 192 mg daily and, eventually, potassium chloride 60 mEq daily. The sitting blood pressure remained at normal levels (122/80 mmHg), and the orthostatic measurement was 140/98 mmHg supine and 138/96 mmHg standing. The diarrhea improved on this regimen, and the levels of K and Mg were maintained at 3.1 and 0.6 mmol/L, respectively, for >1 year without the need for IV replacement (Table ).
During one of her clinic visits in the second year of follow-up, the patient reported that she had switched back to magnesium oxide on her own accord due to the high cost of the magnesium chloride, but this seemed to worsen her diarrhea, and her magnesium levels were low again at 0.45 mmol/L. Following our recommendation, she restarted the magnesium chloride, with subsequent improvement in her diarrhea and an increase in her magnesium level to 0.55 mmol/L.
More than 2 years after presenting to us, she had a repeat endoscopy due to her ongoing diarrhea, which, although improved, was still present to a mild effect. The biopsy showed very slight villous atrophy in the small intestine, consistent with mild gluten enteropathy. After the patient was placed on a gluten-free diet, her diarrhea resolved. At this point, she had been on an oral replacement regimen for >36 months and no longer required IV replacement therapy.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [124.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",94.66667,89.93334,99.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 124.0 mm Hg + 2/3 * 80.0 mm Hg = 94.66667 mm Hg.
Hence, the patient's mean arterial pressure is 94.66667 mm Hg."
1793,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4254080-2,Extracted,"A 26-year-old nulliparous Caucasian woman at 38 weeks of gestation came to the obstetric emergency room complaining of complete blindness and headache. She had gained 30 kilograms since the beginning of her pregnancy and weighted 120 kilograms (BMI = 44). Until then, her pregnancy had been free of complications. Her blood pressure was 205/105 mmHg and she had severe peripheral edema. Laboratory exams showed high LDH (271 mu/mL) without any other anomalies. Arterial hypertension was only partially controlled by oral nifedipine with intravenous infusion of labetalol and magnesium sulphate. Cesarean section was performed. Because of the predicted difficult management of airways (full stomach, obesity, and El Ganzouri score 6) and since she had a normal state of consciousness, single shot subarachnoid anesthesia was chosen (12 mg of hyperbaric 0,5% bupivacaine at L4-L5 level). The anesthetic sympathetic blockade, combined with the ongoing antihypertensive treatment, was associated with good control of blood pressure and no hypotension. No anesthetic or surgical complications occurred. The neonate weighed 3.8 kg and presented Apgar scores of 9 at 1 minute, and 10 at 5 minutes, with arterial pH 7.2 and base excess −6 millimoles/L. Brain CT showed hypodense occipital lesions (). The patient was transferred to the ICU, where intravenous nitroprusside was started because of recrudescence of hypertension. Four hours after the Cesarean section, the blindness had resolved, but right facial droop and mild paresis of the right leg were observed. Pheochromocytoma and kidney dysfunction were excluded by abdominal CT and hormonal assays. Three days later she was discharged from the ICU with normal blood pressure controlled by oral antihypertensive therapy and normal neurological findings. MRI including T2 FLAIR and DWI performed 7 days later was normal (). Diagnosis of PRES was made on the basis of the reversibility of symptoms and of the radiological lesions. On the sixteenth day she was discharged from the hospital in good health with antihypertensive therapy. Placental examination showed chronic hypoxia, intimal hyperplasia of stromal vessels, and intervillous thrombus.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [205.0, 'mm hg'], 'Diastolic Blood Pressure': [105.0, 'mm hg']}",138.33333,131.41666,145.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 205.0 mm Hg + 2/3 * 105.0 mm Hg = 138.33333 mm Hg.
Hence, the patient's mean arterial pressure is 138.33333 mm Hg."
1794,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-433,Extracted,"A 69-year-old man is scheduled to undergo radical retropubic prostatectomy for prostate cancer in 2 weeks. He had a myocardial infarction at the age of 54 years. He has a history of GERD, unstable angina, hyperlipidemia, and severe osteoarthritis in the left hip. He is unable to climb up stairs or walk fast because of pain in his left hip. He had smoked one pack of cigarettes daily for 30 years but quit 25 years ago. He drinks one glass of wine daily. Current medications include aspirin, metoprolol, lisinopril, rosuvastatin, omeprazole, and ibuprofen as needed. His temperature is 36.4°C (97.5°F), pulse is 90/min, and blood pressure is 136/88 mm Hg. Physical examination shows no abnormalities. A 12-lead ECG shows Q waves and inverted T waves in leads II, III, and aVF. His B-type natriuretic protein is 84 pg/mL (N < 125).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [88.0, 'mm hg'], 'Systolic Blood Pressure': [136.0, 'mm hg']}",104,98.8,109.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 136.0 mm Hg + 2/3 * 88.0 mm Hg = 104.0 mm Hg.
Hence, the patient's mean arterial pressure is 104.0 mm Hg."
1795,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3510922-1,Extracted,"A 25-year-old gentleman reported to the Department of Oral and Maxillofacial Surgery with a chief complaint of inability to open the mouth, pain, and swelling in relation to the lower jaw and neck since a day. On physical examination, he had respiratory distress and was toxic in appearance and his vital signs were monitored immediately. His temperature was 101.8°F with a pulse rate of 106 beats per minute, blood pressure of 140/90 mmHg, and a respiratory rate of 25 breaths per minute. Mouth opening was limited to 1.5 cm (interincisal distance) and revealed grossly decayed lower right second molar tooth with drainage of pus. Extra-oral swelling was indurated, nonfluctuant with bilateral involvement of the submandibular and sublingual glands []. An immediate diagnosis of Ludwig's angina was made, and the patient was posted for surgical decompression under general anesthesia. However, elective tracheostomy was planned for airway maintenance with the help of an otolaryngologist. The blood report was normal except for raise in ESR, eosinophilia. Elective tracheostomy was done under local anesthesia, airway secured and general anesthesia was provided. Separate stab incisions was made in relation to the submandibular space bilaterally and submental space. A sinus forceps was introduced to open up the tissue spaces and pus was drained. The wound was irrigated with normal saline, and a separate tube drain was placed and secured to the skin with silk sutures []. Intravenous administration of cefotaxime 1 g Bd, gentamycin 80 mg Bd, metrogyl 500 mg, Tid were given for 5 days with a tapering dose of decadran 8–4 mg Bd for first two postoperative days. Postoperative irrigation was done through the drain which was removed after 36 h along with the infected tooth. Tracheostomy tube care was taken in the postoperative period, and the skin was strapped on the fifth postoperative day after the removal of the tracheostomy tube. Patient recovery was satisfactory.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1796,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8683106-1,Extracted,"A 60-year-old man with the past medical history of hypertension and diabetes presented to the hospital with diffuse cramping abdominal pain that started 3 weeks before his presentation and worsened on the day of admission. The pain was non-radiating without any worsening or relieving factors.
The pain was not related to food or bowel movements. He did endorse 30 lbs weight loss over the last 3 months as well as loss of appetite. He denied any night sweats, fever, chills, dysuria, diarrhea, constipation, nausea or vomiting. In the emergency room (ER), temperature was 36.8 °C, heart rate was 86/min, blood pressure was 164/78 mm Hg, respiratory rate was 18/min, and oxygen saturation was 100%. Laboratory studies were unremarkable except white blood cell count of 14,000 cells/µL.
Computed tomography (CT) scan of the abdomen showed a 7.2 × 6.4 × 3.3 cm hypodense amorphous collection versus mass within mesentery, with the possibility of the necrotic tumor (). General surgery, gastroenterology and interventional radiology teams were consulted for a multidisciplinary approach. Owing to the proximity of the transverse colon and stomach to the mass, it was decided to proceed with endoscopy (EGD) with endoscopic ultrasound (EUS)-guided biopsy and colonoscopy. EGD was suggestive of an irregular hypoechoic mass measuring 3.7 cm in its longest axis outside the gastric echo layer from a distal body position (). Ultrasound-guided fine-needle biopsy (FNB) was performed with four passes from the distal body of the stomach. The EUS view of the pancreas, left kidney, adrenal, spleen, liver lobes and portal vein was unremarkable. The common bile duct and pancreatic duct were not dilated. Colonoscopy showed external and internal hemorrhoids. At descending colon, there was an irregular 8 mm, polypoid, granular appearing lesion with surrounding edema likely due to diverticulitis or the mesenteric mass eroding the colon. Cold forceps biopsies were taken from that area. Also, the area around it was marked by India Ink preparation for the surgical references during laparotomy if needed. The terminal ileum showed no abnormalities. Biopsy results of the EUS and colonoscopy were non-specific.
Due to the non-specific nature of biopsies and continued pain, diagnostic and therapeutic laparoscopy was performed which showed a large abscess cavity in the base of transverse colon, mesentery, and the loop of small bowel. Abscess cavity was drained with removal of inflammatory mass and necrotic tissue, and small bowel was separated. Culture results were negative for any infection. Histopathology analysis of the surgical specimen confirmed the mass as extensive fat necrosis and nodules in the mesentery suggestive of sclerosing mesenteritis ().
His abdominal pain resolved postoperatively, and he was discharged with the outpatient follow-up with our surgical team and primary care provider.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [78.0, 'mm hg'], 'Systolic Blood Pressure': [164.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 164.0 mm Hg + 2/3 * 78.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1797,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3354461-1,Extracted,"A 22 year old male presented with progressive breathlessness on exertion, increasing jaundice, easy bruising and petechial rash over a period of 15 days. There was no history of epistaxis, gingival bleeding, hematuria, hemoptysis, fever, weight loss, neurological sign or thromboembolism. Neither there was family history of coagulation disorders, nor recent past exposure to heparin or heparinoids. On examination, his blood pressure was 110/70 mmHg, and heart rate 90/min and regular. He was afebrile. His jugular venous pressure was elevated 9 cm above the angle of Louis, and he had ecchymosis. He had facial puffiness and soft tender hepatomegaly as a sign of right ventricular inflow obstruction. On cardiac auscultation, we found a long mid diastolic murmur in the tricuspid area and harsh phasic ejection systolic murmur grade III/VI without ejection click in the pulmonary area. His direct bilirubin level, total leukocyte count and neutrophil count were elevated with severe thrombocytopenia in the peripheral smear.
Bone marrow study showed normal cellularity and erythroid prominence (myeloid:erythroid ratio 1:1, normoblastic erythropoesis, normal orderly myelopoesis, no blast prominence, increase in megakaryocytes number with few hypoblastic forms and prominence of histiocytes). Chest radiograph and electrocardiography were normal. Abdominal ultrasound showed uniform congestive hepatomegaly with normal size spleen. Color Doppler ruled out deep vein thrombus in abdomen or lower limbs. Trans-thoracic echocardiography [] showed dilated right atrium, and hypertrophied and dilated right ventricle. There was a solitary, giant pedunculated, lobulated, homogenous mobile mass obstructing right ventricular inlet and outlet, exactly similar to a large right atrial myxoma originating from fossa ovalis.
Contrast enhanced computerized tomography (CT) of chest and abdomen showed a single large non enhancing soft tissue density occupying the right atrium, right ventricle and right ventricular outflow tract, measuring 10 × 7.5 mm, and extending into inferior venacava with dilated of right atrium and right ventricle []. Mediastinum and lung parenchyma were normal. There was a mild bilateral pleural effusion, homogenous hepatomegaly and mild ascites, with other viscera as normal. Hence, the possible radiological diagnosis was of an intra cardiac thrombus. Anti phospholipids antibody, anti systemic lupus erythematosus (SLE) antibodies and anti platelet factor 4 (PF4) antibodies were negative. He was treated with empirical intravenous antibiotics, intravenous methyl prednisolone and 20 units of single donor platelet transfusion. Neither anticoagulants nor thrombolytic agents were used during the treatment. Excisional biopsy was not possible because of continuous decline in platelet counts, and none of the serial follow up platelet count levels were above 15, 000/mm3. On the 15th day of hospitalization, he died of cardiac arrest just one day after an episode of melena. We could not manage pathological autopsy because of the lack of consent.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1798,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3878525-1,Extracted,"On 22nd March 2012, a 46-year-old right-handed Chinese male, who had been misdiagnosed with multiple sclerosis three years earlier in another hospital because of the white matter lesions in MRI, came into the hospital due to sudden dysarthria and left hemiparesis. His blood pressure was 130/80 mmHg and his temperature was 36.6˚C. A neurological examination revealed left hemiparesis, dysarthria, spasticity in his extremities and diffuse brisk deep tendon reflexes, corresponding to a diagnosis of pure motor stroke []. Mini-mental status examination was normal (a score of 28 out of 30).
An acute subcortical infarction was found in the right basal ganglia and periventricular areas on the 2nd day of hospitalization (Figure A, B). There was no significant stenosis or malformation of major cerebral arteries on MR angiography (Figure C). MRI confirmed the severe white matter lesions concentrated around the periventricular, pons, external capsule and the anterior temporal pole and multiple subcortical lacunar infarcts (Figure D-F). Some cerebral microbleeds (CMBs) were also present in the bilateral basal ganglia and subcortical areas (Figure G). There was no evidence for head trauma, cavernous hemangioma, arteriovenous malformations, aneurysms or neoplasia. In the past, he did not have any episodes of migraine and any vascular risk factors other than smoking. His family history disclosed that his brother had a similar episode of dysarthria. Blood tests, including a complete blood cell count, glucose, cholesterol, creatinine, erythrocyte sedimentation rate, homocysteine, and C-reactive protein were normal. Hemocoagulation tests were within normal values. Coagulation factors such as factor II, V, VII, VIII, IX and von Willebrand factor were normal. Serological tests for collagen disease were unremarkable, as was the cerebrospinal fluid testing. Lactate and pyruvate levels were normal in blood. Urine analysis was normal with no proteinuria. Cocaine urine test was negative. An echocardiogram was normal, and electrocardiographic monitoring did not show arrhythmias.
Since CADASIL was suspected based on the characteristic MRI findings and his family history, a skin biopsy and NOTCH3 gene analysis was performed on hospital day 13 after the informed consent. Ultrastructural examination showed the accumulation of GOM in small arterial walls (Figure A). NOTCH3 gene testing revealed a heterozygote Arg90Cys mutation in exon 3 (Figure B). The patient remained normotensive throughout his hospital stay. He was not given any antithrombotics because of gastric hemorrhage 1 year ago. The modified Rankin scale (mRS) score at 30 days after this ictus was 1 point.
Two months after discharge, he was admitted again to our hospital with a sudden unresponsiveness. Initial blood pressure was 138/98 mmHg and neurological examination showed mild coma and right spastic hemiplegia. The admission Glasgow Coma Scale score and NIH Stroke scale (NIHSS) score was 11 and 20 respectively. An immediate computed tomography (CT) scan demonstrated an acute ICH in the left basal ganglia extending into the ventricular system (Figure A). There was no evidence of trauma on head CT. Follow-up CT three days later showed no significant change of hematoma size (Figure B). The patient showed gradual recovery from his right hemiplegia without hematoma evacuation. The 30-day Barthel index and NIHSS score after ICH was 45 and 14 respectively. Then, the patient had an mRS of 2 at 12 months after ICH onset, supporting a favorable outcome. In addition, the patient developed migraine at about 10 months after the second hospital admission.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1799,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2769310-1,Extracted,"A 25-year-old Caucasian male with a history of tobacco use, alcohol abuse, and gastroesophageal reflux disorder (GERD) was admitted to our hospital with a chief complaint of upper airway obstruction. He was initially seen one week prior to admission by his primary care physician for a complaint of back pain. At this visit, the patient reported recent contact with a co-worker who was recovering from mononucleosis and thus a blood smear was performed which revealed atypical lymphocytes. A subsequent Monospot test was positive for heterophile antibodies. Further blood tests for viral hepatitis were negative. He first began developing symptoms four days after diagnosis, which included fevers, nightsweats, diffuse body aches, and a sore throat. These continued to worsen in the following two days, so the patient sought attention at the urgent care clinic. Workup at this time for superimposed streptococcus infection was negative. The patient returned home without treatment. Symptoms worsened overnight including difficulty swallowing and handling oral secretions as well as fevers to 104°F. Two days later, the patient was short of breath with continued fevers, throat pain, and difficulty swallowing leading to one episode of blood-tinged emesis.
Medical history included GERD, anxiety, and moderate tobacco and alcohol use. He was on no medications. His family history was significant for epilepsy and hyperthyroidism. He was a student and worked as a manager of a restaurant. He drank five beers 3-4 times per week, smoked a ½ pack per day, and denied illicit drug use. The patient had no known drug allergies.
On physical exam, he was alert and awake with a flushed face and spoke with a hyponasal or raspy voice. This muffled vocal characterization is referred to as “hot potato voice” by some physicians []. He was in no apparent respiratory distress. Height was 72 inches and weight was 191 pounds. His vitals were T 99.3°F, P 106, R 24, BP 133/88, 96% on room air. Head and neck exam revealed tender cervical lymphadenopathy with erythematous, swollen tonsils that were in apposition with minimal white exudates. There was no evidence of inflammation in the internal auditory canal, sclera were non-injected, no stridor, no trismus, and the trachea was midline. Lung exam was clear to auscultation bilaterally. Heart sounds were regular without murmurs or clicks. The abdomen was soft, non-tender, and without hepatosplenomegaly. Extremities were without edema, clubbing, or cyanosis. Neurological exam revealed no focal deficits. Laboratory values were remarkable for a white blood cell count of 20 K/cmm with an absolute monocytosis of 2.97 K/cmm. Liver enzymes were elevated with an alkaline phosphatase of 270 U/L, AST 136 U/L, ALT 275 U/L.
In the emergency department, CT scan of the head and neck showed tonsillar swelling with lymphadenopathy ( & ). Laryngoscopy confirmed these findings and revealed no other causes of obstruction. He was treated with 10 mg intravenous dexamethasone and 3 g ampicillin/sulbactam with rapid improvement. The patient was then admitted to the medical service where steroid treatments were continued overnight and he was discharged the following day on no medications.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [133.0, 'mm hg'], 'Diastolic Blood Pressure': [88.0, 'mm hg']}",103,97.85,108.15,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 133.0 mm Hg + 2/3 * 88.0 mm Hg = 103.0 mm Hg.
Hence, the patient's mean arterial pressure is 103.0 mm Hg."
1800,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5935,Extracted,"A 60-year-old man visits his primary care doctor after being discharged from the hospital 3 weeks ago. He presented to the hospital with chest pain and was found to have ST elevations in leads I, aVL, and V6. He underwent cardiac catheterization with balloon angioplasty and was discharged on appropriate medications. At this visit, he complains of feeling deconditioned over the past week. He states that he is not able to jog his usual 3 miles and feels exhausted after walking up stairs. He denies chest pain. His temperature is 98.6°F (37°C), blood pressure is 101/62 mmHg, pulse is 59/min, and respirations are 18/min. His cardiac exam is notable for a 2/6 early systolic murmur at the left upper sternal border. He describes mild discomfort with palpation of his epigastrium. The remainder of his exam is unremarkable.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [101.0, 'mm hg'], 'Diastolic Blood Pressure': [62.0, 'mm hg']}",75,71.25,78.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 101.0 mm Hg + 2/3 * 62.0 mm Hg = 75.0 mm Hg.
Hence, the patient's mean arterial pressure is 75.0 mm Hg."
1801,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5977495-1,Extracted,"A 75-year-old Japanese (Asian) woman underwent a right nephrectomy for RCC approximately 15 years ago. Our patient did not present symptoms at admission, and her past medical, social, family, and environmental history was not appreciable. Her occupation was home manager, and she was on no medication prior to diagnosis. She did not smoke and consume alcohol, and her temperature was 36.3 °C, her blood pressure was 122/82 mmHg, and her pulse was 68 per minute. Laboratory findings at admission are shown below. Her white blood cell count was 3800 × 103/μL, red blood cell count 414 × 104/μL, hemoglobin 13.0 g/dL, hematocrit 39.1%, platelets 19.6 × 104/μL, total bilirubin 0.7 mg/dL, direct bilirubin 0.2 mg/dL, aspartate transaminase 23 IU/L, alanine transaminase 9 IU/L, total protein 7.3 g/dL, albumin 4.5 g/dL, lactate dehydrogenase 188 IU/L, γ-glutamyltransferase 11 IU/L, alkaline phosphatase 201 IU/L, amylase 129 IU/L, blood urea nitrogen 13.6 mg/dL, creatinine 0.64 mg/dL, sodium 137 mEq/L, potassium 3.9 mEq/L, chlorine mEq/L, C-reactive protein 0.03 mg/dL, carcinoembryonic antigen 1.5 ng/mL, carbohydrate antigen 19–94 U/mL, urinalysis pH 7.0, no uric protein, no urinary sugar, no ketone body, no uric blood, no bilirubin, and no white blood cell. No microbial examination was performed.
The tumor was 9.1 × 7.8 cm in diameter and confined to the capsule of the kidney. Pulmonary lobectomy was performed for left lung metastasis 11 years after the primary resection and an additional lung partial resection was performed for the metachronous left lung metastasis 14 years after the primary resection.
Examinations including whole body computed tomography (CT) before each surgery demonstrated no evidence of distant metastasis. A surveillance follow-up CT scan revealed a gallbladder lesion. No symptoms suggested cholecystitis, and the only biochemical abnormality was a slight elevation in levels of aspartate transaminase and alanine transaminase. Ultrasonography (US) showed a mass at the gallbladder fundus. Its surface was smooth, and the inner echo was slightly high and homogenous (Fig. ).
A contrast-enhanced CT scan showed a 12-mm polypoid mass with high attenuation, enlarged from 4 mm 2 years ago (Fig. ). It had significantly high intensity in the arterial phase. On the coronal reconstruction image, attenuation was inhomogeneous in the mass and relatively higher on the wall side (Fig. ). There was no significant accumulation of contrast agent in any organ other than the gallbladder.
Based on these image findings and the patient’s medical history, we initially thought the gallbladder mass was a malignant tumor such as a gallbladder carcinoma. The possibility that the tumor was metastatic cancer remained, and we therefore performed open approach cholecystectomy to confirm the diagnosis and perform adequate treatment.
The isolated specimen showed a pedunculated tumor in the fundus of the gallbladder, and the surface of the tumor appeared black as a result of bleeding (Fig. ). Microscopically, we observed prominent vascular proliferation in the stalk and basal part of the tumor (Fig. ). The tumor was hypercellular and composed of clear cells arranged in funicular or alveolar growth with vascular interstitial tissue (Fig. ). The surface of the tumor was covered by epithelium, and extensive hemorrhage was observed under the surface (Fig. ). These histopathologic characteristics coincided with those of the renal tumor resected 15 years earlier (Fig. ).
We performed immunohistochemical staining for vimentin and cytokeratin 7 (CK7). The tumor stained strongly for vimentin, but staining for CK7 was almost negative (Fig. ), although for CK7, we observed a partially nonspecific immune reaction due to use of an automated immunostainer. These pathological features were similar to those of the renal primary tumor. Therefore, we diagnosed the gallbladder tumor as a metastasis from renal cell carcinoma. Our patient’s postoperative course was uneventful and she was discharged at postoperative day 5. She is alive and recurrence free 3 years after cholecystectomy.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [122.0, 'mm hg'], 'Diastolic Blood Pressure': [82.0, 'mm hg']}",95.33333,90.56666,100.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 122.0 mm Hg + 2/3 * 82.0 mm Hg = 95.33333 mm Hg.
Hence, the patient's mean arterial pressure is 95.33333 mm Hg."
1802,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-171,Extracted,"A 46-year-old woman comes to the physician because of a 2-week history of diplopia and ocular pain when reading the newspaper. She also has a 3-month history of amenorrhea, hot flashes, and increased sweating. She reports that she has been overweight all her adult life and is happy to have lost 6.8-kg (15-lb) of weight in the past 2 months. Her pulse is 110/min, and blood pressure is 148/98 mm Hg. Physical examination shows moist palms and a nontender thyroid gland that is enlarged to two times its normal size. Ophthalmologic examination shows prominence of the globes of the eyes, bilateral lid retraction, conjunctival injection, and an inability to converge the eyes. There is no pain on movement of the extraocular muscles. Visual acuity is 20/20 bilaterally. Neurologic examination shows a fine resting tremor of the hands. Deep tendon reflexes are 3+ with a shortened relaxation phase.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [98.0, 'mm hg'], 'Systolic Blood Pressure': [148.0, 'mm hg']}",114.66667,108.93334,120.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 148.0 mm Hg + 2/3 * 98.0 mm Hg = 114.66667 mm Hg.
Hence, the patient's mean arterial pressure is 114.66667 mm Hg."
1803,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5155085-1,Extracted,"A patient aged 27 years was admitted to Department of Obstetrics and Gynecology, Tanta University Hospitals, in a shock state with a pulse rate of 120 b/m and blood pressure of 80/50.
The patient had history of primary infertility for 6 years and history of ovulation induction in the cycle preceding this pregnancy, history of uterine anomaly, and history of amenorrhea for 7 weeks. This means that this pregnancy was induced by ovulation induction.
Immediate routine investigations included complete blood count and renal and liver functions with bleeding and coagulation times. All investigations were within normal except for hemoglobin which was 9.7 g/dl and hematocrit value of 30.21. Specific investigations requested were pregnancy test and b-HCG level which revealed pregnancy with b-HCG level of 2140 IU. Immediate resuscitation was done by insertion of 2 wide pore cannulas and intravenous fluids with immediate ultrasound which revealed bicornuate uterus and moderate free fluid in the abdomen; pelvic hematoma about 10 × 3 cm was also detected in the pelvis. The uterus was empty and pregnancy sac was found between the two horns of bicornuate uterus with high peripheral vascularity surrounding the sac “Ring of Fire,” .
Taping of free fluid which revealed altered dark blood confirmed the diagnosis of ectopic pregnancy. The patient did not receive preoperative blood and was immediately transferred to operation room with 2 units of crossmatched blood ready to be used intraoperatively or postoperatively. Laparotomy revealed moderate to severe internal hemorrhage with blood clots in pelvis. Pelvic hematoma was anterior to the bicornuate uterus between uterus and bladder covering pregnancy sac. Both fallopian tubes and ovaries were inspected and were healthy with no lesions denoting that the ectopic pregnancy was primary.
Suction of blood and clearing retrovesical hematoma revealed pregnancy sac in between the 2 horns of bicornuate uterus which was enucleated and debridement of its site and repair of its bed to control bleeding as shown in .
Closure of ectopic pregnancy site by Vicryl 2/0 and the end picture were shown in .
The abdomen was irrigated by 2 liters of warm saline and closure of abdominal wall was then commenced in anatomical layers. Postoperative follow-up consisted of monitoring vital signs and urine output. The patient was given the 2 units of blood one inside operation room and one after 12 hours. Complete blood count was requested before discharge with hemoglobin 10.8 g/dl. The case was discharged 24 hours after operation in a good condition.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [50.0, 'mm hg'], 'Systolic Blood Pressure': [80.0, 'mm hg']}",60,57,63,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 80.0 mm Hg + 2/3 * 50.0 mm Hg = 60.0 mm Hg.
Hence, the patient's mean arterial pressure is 60.0 mm Hg."
1804,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8519212-2,Extracted,"The second case was a 38-year-old male, who did not smoke and had no related medical history, social history, or family history. He was sent to the hospital because of persistent cough and dyspnea for 6 years and progressive dyspnea for 1 week. His job was a cooker. On admission, the physical examination showed a body temperature was 36.6°C, heart rate was 96 beats/minute, respiratory rate was 30 breaths/minute, and blood pressure was 101/78 mmHg. He had an accentuated second pulmonic heart sound. The 6-minutes walking distance was 350 m. The arterial blood gases test indicated that PaO2 was 47 mmHg and PaCO2 was 29 mmHg in breathing room air. The results of the hematologic and biochemical tests were within the normal range. Laboratory workup was negative for HIV, antinuclear antibody, thyroid stimulating hormone, rheumatic factor, antineutrophil cytoplasmic antibody, and erythrocyte sedimentation rate et al. The concentration of N-terminal pro-brain natriuretic peptide was 4480ng/mL. The transthoracic echocardiogram revealed a dilated right ventricle with a normal left ventricular function and an estimated right ventricular systolic peak pressure of 95 mmHg. The chest CT scan images showed ground-glass opacities (Fig. ). Lower extremities duplex was negative for acute or chronic deep venous thrombosis. Considering the possibility of PH, right heart catheterization was done. The results showed severe pulmonary arterial hypertension with mean pulmonary artery pressure at 68 mmHg, pulmonary artery wedge pressure at 11mmHg, and cardiac output 2.8 L/min/m2. The patient was diagnosesd as IPAH initially and PAH-targeted drugs (Ambrisentan 10 mg once a day and tadalafil 20 mg once a day) were used also. After treatment, dyspnea improved. NGS for whole exome was also tested in blood samples of the patient. A biallelic mutation was found in the coding sequence region in exon 9 of EIF2AK4 (c.989-990 delAA [p. Lys330fs]) (Fig. ). So the diagnosis of PVOD was confirmed. Because he had a good response to the drugs, the treatment was unchanged. Over a period of >20 months, he has a good response to PAH-targeted drugs. No signs of pulmonary edema were found. Lung CT scan was repeated and pulmonary edema was not detected (Table ).
Standard care is performed for these 2 patients, so ethical approval is not applicable in this study. Written informed consent was obtained from the patients.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [78.0, 'mm hg'], 'Systolic Blood Pressure': [101.0, 'mm hg']}",85.66667,81.38334,89.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 101.0 mm Hg + 2/3 * 78.0 mm Hg = 85.66667 mm Hg.
Hence, the patient's mean arterial pressure is 85.66667 mm Hg."
1805,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7642559-1,Extracted,"An 83-year-old male patient came to our hospital for emergency treatment due to 26 h of middle and upper abdominal pain.
The patient had mid-upper abdominal pain 26 h ago, a persistent pain, severe with nausea but no vomiting. There was no waist and back pain, no chest tightness, shortness of breath, but the patient felt palpitations and fatigue. The patient has had chills since abdominal pain occurred, and the degree of abdominal pain has been increasing since the onset. We observed that the patient had a catheter inserted, and there was about 50 mL of yellow urine in the urine bag.
After a careful medical history inquiry, the patient was found to have been bedridden for a long period of time and suffered from many diseases, including hypertension, cardiac pacemaker implantation, history of atrial fibrillation, chronic obstructive pulmonary disease, prostatic hyperplasia and catheter indwelling status. The patient was diagnosed with benign prostatic hyperplasia 8 years ago due to symptoms of impaired urination, but he refused surgery. Three years ago, the patient could not rule out urination because of prostate hyperplasia, so he chose catheterization. For so many years, patients have been living with urinary catheters, so urinary tract infections often occur.
When the patient came to the hospital, his temperature was 37.2°C, heart rate was 56 bpm, respiratory rate was 19 breaths per minute, blood pressure was 197/70 mmHg and oxygen saturation was 97%. Physical examination revealed slightly swollen abdomen and no obvious prominent lumps. Abdominal palpation showed tense abdominal muscles, a platy abdomen and obvious tenderness in the whole abdomen accompanied by rebound pain. Percussion of the abdomen indicated the presence of fluid in the abdominal cavity. Auscultation of the abdomen indicated that the sound of bowel movement in the abdominal cavity was slightly weakened.
Routine blood tests showed that the patient’s leukocyte count did not increase significantly (7.38 × 109/L), and the percentage of neutrophils was 91.2% with an increased hypersensitive C-reactive protein (132.81 mg/L). The patient’s red blood cell count was normal (4.92 × 109/L), but the platelet count was low (80 × 109/L). The significant increase in troponin (50 ng/L) and brain natriuretic peptide (630.53 pg/mL) indicated that the function of the patient’s heart was poor. Prothrombin, d-dimers and partial thromboplastin times were normal.
Computed tomography of the abdomen revealed a small amount of free gas under the diaphragm and edema in part of the small intestine and intestinal wall with surrounding exudation. There was gas accumulation in the middle and upper abdomen and intestinal cavity, a small amount of effusion around the right liver, multiple cystic foci in the liver and cirrhosis. The distal end of the common bile duct showed calculi with multiple gallbladder calculi. The bladder wall was thickened with multiple bladder diverticulum and gas accumulation (Figure ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [197.0, 'mm hg']}",112.33333,106.71666,117.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 197.0 mm Hg + 2/3 * 70.0 mm Hg = 112.33333 mm Hg.
Hence, the patient's mean arterial pressure is 112.33333 mm Hg."
1806,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8046447-1,Extracted,"A 46-year-old male was referred for surgery from the peripheral center with diagnosis of spine tumor. The patient presented with complaint of sudden onset of asymmetrical weakness on both lower extremities over a period of 3 days. He has associated mild back pain around dorsolumbar region for more than 3 months duration. There was no history of trauma or any injury over the back. Treatment in the previous facility was mainly in the form of diagnostic in the form of MRI and symptomatic in the form of oral gabapentin and nonsteroidal anti-inflammatory medications. He had history of hypertension for 2 years and was on antihypertensive medications in the form of combination of losartan and hydrochlorothiazide. There was no family history with similar weakness. There was no significant history with similar illness. Physical examination revealed heart rate of 102 beats/min, blood pressure of 150/102 mmHg, oxygen saturation (SpO2) of 96%, temperature of 98 degree F, and respiratory rate of 26/min. There were no pallor, icterus, lymphadenopathy, cyanosis, clubbing, edema, and dehydration noted. No jugular venous distension or swelling around neck (goiter) was appreciated. Cardiac examination revealed regular rhythm with normal heart sounds. Respiratory examination revealed tachypnea with decreased breath sounds in bilateral basal areas. Abdominal examination was normal. On neurological examination, cranial nerve functions were grossly intact, however, power in all muscle groups in the right lower extremity was 2/5 and in left lower extremity was 3/5. The sensations of all four limbs were normal; however, the deep tendon reflexes were absent with bilateral flexor plantar response. There was no tenderness or swelling over back noticed. The patient did not have any problem with bowel and bladder movement.
MRI of dorsolumbar spine showed evidence of intradural extramedullary lesion at L1 level (right-sided prominent) measuring 9.9 × 9.4 × 11 mm in size (). MRI of brain with cervical screening was normal. Primary blood investigations including complete blood count and random blood sugar were within normal range. Considering his neurological deterioration and MRI imaging, he was primarily admitted in ward for further work-up with possibility of surgical option. In intensive care unit (ICU), further hematological work-up suggested normal renal, liver, and thyroid functions. However, his serum potassium level (K+) was significantly low with the value of 1.6 mmol/L (normal: 3.5–4.5). His serum sodium, ionized calcium, and magnesium level were 146 mmol/L (normal: 135–145), 3.79 mg/dl (normal: 4.49–5.29), and 2.86 mg/dl (normal: 1.6–2.3), respectively. Twelve standard leads electrocardiogram revealed changes of severe hypokalemia such as flattening of T wave, ST segment depression, prolongation of PR interval (228 ms), prolonged QT corrected interval (593 ms), and presence of U waves (). ABG (arterial blood gas) analysis showed mixed respiratory alkalosis with K+ of <1.5 mmol/L. The patient also started developing mild weakness in his both upper extremities within next 8 h, and power in his both upper extremities was around 4/5 while power in both lower extremities was further deteriorated to 1/5. Reflexes in all extremities were sluggish with preserved sensations.
Endocrinologist and cardiologist were consulted immediately. The patient was shifted to ICU and simultaneously treated with intravenous potassium, calcium, and other supportive measurements. Consecutively, appropriate tests were requested. Since the patient had hypokalemia, metabolic alkalosis with hypertension, primary hyperaldosteronism was primarily suspected. The plasma aldosterone-renin ratio was ordered after correction of the potassium levels and keeping all the pre-test conditions in mind. The plasma aldosterone-renin ratio was significantly elevated. A saline loading test was performed which showed failure of adequate suppression of aldosterone, confirming the diagnosis of primary hyperaldosteronism (Conn’s syndrome). Other laboratory investigations such as transtubular potassium gradient (TTKG), Vitamin D3, and parathyroid hormone serum cortisol were 5.55 (normal <3), 44.05 (normal: 13.1–35), 14 ng/ml (normal: 30–100), 74.5 pg/ml (normal: 7.5–53.5), and 3.77 mcg/dl (afternoon level: 3–10), respectively. The thyroid function test was normal. Creatine phosphokinase (CPK) was 5391 U/L (normal: 55–170) increasing up to 21,000 U/L, which returned to normal level with adequate hydration. Nerve conduction velocity was normal. Ultrasound of whole abdomen was not significant. Contrast-enhanced computed tomography (CECT) of whole abdomen showed a well-defined peripherally enhancing nodular lesion suggestive of a right adrenal adenoma. There was also hyperplasia of the left adrenal gland ().
Therefore, the diagnosis was kept as primary hyperaldosteronism primarily in a case of spinal intradural tumor. The patient was treated conservatively in spite of intradural tumor, which was decided to observe closely for further decision later on. On the 2nd day of admission, potassium level was increased up to 1.9–3.2 mmol/L, which again increased to 2.4–3 mmol/L and 4.3 mmol/L on the 3rd and 4th day, respectively. Meanwhile, the patient’s power in both upper extremities became 5/5 and in both lower extremities became 4/5. Therefore, potassium infusion was stopped and oral spironolactone was added []. The patient was able walk after 72 h with assistance and after 96 h independently. He was discharged after 5 days along with antihypertensive and potassium sparing diuretic (spironolactone).
The patient is maintained on regular visit with endocrinology and spine department till his last follow-up at 6 months. Since the patient had a right adenoma and a hyperplasia of the left adrenal gland, the patient would require adrenal venous sampling if surgical management for primary hyperaldosteronism is to be considered. However, the patient had normal blood pressure and normal potassium levels with adequate dose of spironolactone and adrenal venous sampling followed by surgical resection was deferred. There is no recurrence of such symptoms and intradural tumor remains of same size without further sequel.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [102.0, 'mm hg'], 'Systolic Blood Pressure': [150.0, 'mm hg']}",118,112.1,123.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 102.0 mm Hg = 118.0 mm Hg.
Hence, the patient's mean arterial pressure is 118.0 mm Hg."
1807,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5599436-3,Extracted,"Patient 3: a 71-year-old man (BMI 30.0 kg/m2) on metformin, canagliflozin, liraglutide, enalapril, allopurinol, pantoprazole and torasemid presented to the ED because of acute gastroenteritis lasting for 6 days. The laboratory analyses revealed acute renal failure (creatinine 1203 µmol/l, blood urea nitrogen 36.9 mmol/l) and metabolic acidosis with hyperventilation (pH = 7.16, HCO3 = 10 mmol/l, pCO2 = 20 mm Hg or 2.7 kPa). On admission, the BP was 111/38 mm Hg, HR 73/min, oxygen saturation 98%, body temperature 35.8 °C, arterial pO2 88 mm Hg (11.7 kPa), base excess −20 mmol/l, and the anion gap was 21.6 mmol/l. The initial lactic acid level was 5.9 mmol/l, serum ketoacids were ≥8 mmol/l at a blood glucose level of 150 mg/dl. Abdominal sonography and chest X‑ray revealed no pathologies. Continuous venovenous hemofiltration was started and parenteral glucose infusion initiated. Metabolic acidosis receded (Fig. c) and renal function slowly recovered. The patient was discharged after 9 days.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [111.0, 'mm hg'], 'Diastolic Blood Pressure': [38.0, 'mm hg']}",62.33333,59.21666,65.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 111.0 mm Hg + 2/3 * 38.0 mm Hg = 62.33333 mm Hg.
Hence, the patient's mean arterial pressure is 62.33333 mm Hg."
1808,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6437957-1,Extracted,"A 32-year-old man was admitted to our hospital on June 5, 2018, with a 2-month history of recurrent fever and the loss of 5 kg of weight. Two months prior, he suffered chills after eating kebabs, followed by a fever (up to 39 °C), accompanied by a headache and dizziness. He received anti-infective and anti-inflammatory therapy for a pulmonary infection at the local hospital. However, he still had a high fever with fatigue. On April 23, the serum agglutination test for Brucella was positive, with a titer of 1:400. Both the blood and bone marrow cultures were negative, and after he was diagnosed with brucellosis, therapy with doxycycline, moxifloxacin, and streptomycin was initiated. After 1 month of regular anti-brucellosis therapy, although the peak temperature had dropped to 38 °C, he still had the fever and aggravated anaemia. Due to the negative repeat test for Brucella, the regimen was adjusted to isoniazid, levofloxacin, streptomycin, rifampicin and dexamethasone anti-tuberculosis therapy. He continued to experience the recurrent fever until admission to our hospital on June 5.
In March 2009, he had undergone a Bentall procedure and ventricular septal repair due to congenital heart disease and was found to be positive for the hepatitis B surface antigen but did not receive antiviral therapy. The patient was immunocompetent, serologically negative for human immunodeficiency virus (HIV) and denied any history of contact with cattle and sheep.
At admission, his body temperature was 37.5 °C, his heart rate was 78 beats/min, his respiratory rate was 18 breaths/min, and his blood pressure was 120/66 mmHg. On physical examination, he was found to be anaemic. His abnormal laboratory findings were as follows: aggravated normochromic anaemia (haemoglobin: 71 g/mL), elevated levels of inflammatory markers (C-reactive protein: 43.1 mg/L; procalcitonin: 0.38 ng/mL), acute renal insufficiency (blood urea nitrogen: 23.1 mmol/L; creatinine: 343 μmol/L) and hypoproteinemia (albumin: 30 g/L) with normal levels of aminotransferase (Table ). An interferon-gamma release assay (IGRA) for tuberculosis was positive. Furthermore, next-generation sequencing (NGS) detected M. tuberculosis complex from two blood samples. However, the Xpert MTB assay and acid-fast bacilli smear for sputum samples were both negative. The blood cultures remained negative. A computed tomography (CT) scan of the chest suggested bilateral pneumonia (Fig. ). Abdominal ultrasound revealed enlargement of his liver, spleen (169 × 65 mm) and kidney (left: 145 × 67 mm; right: 146 × 52 mm). Echocardiography showed mechanical prosthetic aortic valve paravalvular abscess without vegetation formation (Fig. ). Then, the patient was empirically administered fosfomycin and daptomycin as a treatment for gram-positive bacterial infection, but his body temperature remained high (up to 38.4 °C). Thus, the regimen was switched to anti-tuberculosis drugs (isoniazid 0.3 g once daily, ethambutol 0.75 g once daily, moxifloxacin 0.4 g once daily and linezolid 0.6 g once daily); however, his temperature remained between 37 and 38.5 °C.
Then, he was transferred to the Department of Cardiac Surgery, Shanghai Sixth People’s hospital for a second surgery on June 25. Surprisingly, NGS detected a large number of M. tuberculosis complex sequences in intraoperative samples of the aortic root abscesses. The patient had postoperatively intermittent fever, mostly peaking in the afternoon. After 2 weeks of combined anti-tuberculosis treatment with linezolid (0.6 g once daily), rifampicin (0.3 g twice daily), pyrazinamide (0.5 g three times daily), ethambutol (0.75 g once daily), isoniazid (0.3 g once daily) and moxifloxacin (0.6 g once daily), his body temperature returned to normal, and his laboratory parameters improved (Table ); finally, he was discharged. On July 31, the culture of the aortic valve intraoperative scrapings was found to be positive for M. tuberculosis, which further confirmed the diagnosis of tuberculous PVE. To date, he continues to receive oral anti-tuberculosis treatment.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [66.0, 'mm hg']}",84,79.8,88.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 66.0 mm Hg = 84.0 mm Hg.
Hence, the patient's mean arterial pressure is 84.0 mm Hg."
1809,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8019539-1,Extracted,"A 47-year-old white female with MDD, OUD, and chronic pain by history presented to the emergency department with recurrent suicidal ideation. Her medication history included numerous psychotropic medication trials; she had previously been stable for 5 years on the combination of fluoxetine, doxepin, methadone, cyclobenzaprine, gabapentin, and naproxen (see for complete dosing regimens). The patient had multiple medical conditions, including COPD, scoliosis, endometriosis, hypertension, and persistent pedal edema.
On admission, the patient's vitals were as follows: blood pressure (BP) 104/78 mm Hg, heart rate 86 beats/min, respiratory rate (RR) 25 breaths/min, temperature 36.4°C, oxygen saturation (SpO2) 94%, and QTc 448 ms. BMI was 27.2 kg/m2. A urine toxicology test (fluorescence immunoassay) reacted positive to methadone and tricyclic antidepressants as expected. Serum creatinine was elevated at 1.23 mg/dL, and hepatic function, complete blood count, and electrolytes were all unremarkable. Psychiatric evaluation was positive for restlessness, tangential speech, and anxiety. She described her mood as “sad,” and her affect was labile. There were no perceptual disturbances. Based on her current presentation and collateral information, which revealed a history of mania, a diagnosis of mood disorder unspecified, current episode mixed was made. Treatment with risperidone 1 mg PO once daily and lorazepam 1 to 2 mg PO 4 times daily as needed was initiated.
The patient's psychiatric conditions deteriorated quickly upon admission. She became increasingly disorganized, confused, and intrusive and her mood was extremely labile. To target mood lability, the following changes were made between days 1 and 5: risperidone was changed to divalproex enteric-coated tablets 250 mg PO in the morning and 500 mg PO at bedtime and quetiapine 100 mg extended-release PO at bedtime and 25 to 50 mg immediate-release 4 times daily as needed were added (see ). A tapering regimen was initiated for fluoxetine and doxepin discontinuation as these unopposed antidepressants were thought to be contributing to worsening of manic symptoms.
On day 6, the patient was found unresponsive 3 to 4 hours after the administration of her morning medications. On examination, it was found BP 80/50 mm Hg, RR 8 breaths/min, SpO2 95% to 100%, and QTc 456 ms. Three doses of naloxone 0.4 mg IM injection were administered with 2 minutes in between doses. The patient responded immediately and became agitated, combative, and reported feeling cold. She scored 8 (mild withdrawal) on the Clinical Opiate Withdrawal Scale and was given 1 dose of clonidine 0.1 mg and 3 doses of lorazepam 2 mg for withdrawal symptoms. Her liver function tests and electrolytes were unremarkable. She had a small increase in serum creatinine to 1.37 mg/dL. Creatinine kinase (CK) was elevated to 907 U/L, which was attributed to the use of physical restraints. The patient denied intake of nonprescribed medications, and no substances or substance-related paraphernalia were found in her room or belongings. Results of the urine toxicology test were not clinically meaningful due to a delay in acquiring the sample.
Methadone, quetiapine, divalproex, cyclobenzaprine, fluoxetine, doxepin, and gabapentin were held following this incident due to concerns of repeat CNS depression. When the patient's clinical presentation improved later the same day, gabapentin was restarted for pain management, and the tapering regimens of fluoxetine and doxepin were reinitiated. Methadone was restarted 2 days later (day 8) at 30 mg PO once daily to be titrated by 10 mg each day until at 60 mg daily. Divalproex 250 mg PO in the morning and 750 mg PO at night was restarted on day 8 for mania (valproic acid blood levels recorded 4.8 mcg/mL on day 9), and cyclobenzaprine 10 mg PO twice a day was restarted on day 10. Lorazepam remained available for as-needed use for opioid withdrawal symptoms and anxiety during this time.
On day 11, the patient was found unresponsive 4 hours after administration of her morning medications, which included cyclobenzaprine, divalproex, gabapentin, and methadone. She was having 2 to 3 seconds of apnea, RR 4 to 6 breaths/min, SpO2 of 86%, and BP of 88/51 mm Hg. One dose of naloxone 0.4 mg IM was administered with good response; an increase in RR, BP, and SpO2 were noted, and the patient reported feeling cold, nauseated, and restless. The patient's RR decreased again 90 minutes later to 6 breaths/min with periods of apnea from 11 to 15 seconds long, and another dose of naloxone 0.4 mg IM was given with good response. She received clonidine in tapering doses, 1 IM dose of lorazepam 1 mg and 1 PO dose of lorazepam 1 mg for opioid withdrawal symptoms. Urine toxicology tested positive to methadone, tricyclic antidepressants, and benzodiazepines. Her creatinine levels (0.81 mg/dL) and liver function tests were normal. CK was elevated (1305 U/L) as it had been from days 7 to 10 and normalized on day 16 (150 U/L).
Following this incident, cyclobenzaprine and methadone were discontinued, and a trial of buprenorphine/naloxone was initiated using a microdosing protocol from days 12 to 23. However, due to patient dissatisfaction of suboptimal pain control, cyclobenzaprine was reinitiated on day 23, and buprenorphine/naloxone was changed back to methadone on day 24. Of note, lorazepam was used as needed for anxiety at doses between 1 and 7 mg/d until day 23. The patient was discharged on day 26 with marked improvement in her psychiatric condition. At time of discharge, the patient was being managed on divalproex 750 mg/d (at a therapeutic level of 75.7 mcg/mL), methadone 30 mg/d, and cyclobenzaprine 10 mg 3 times daily as needed. Informed consent was provided by the patient for the preparation of this case report.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [78.0, 'mm hg'], 'Systolic Blood Pressure': [104.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 104.0 mm Hg + 2/3 * 78.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1810,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8143821-2,Extracted,"A 39-year-old woman with chronic back pain was brought to the ED for altered mental status. According to family, she became depressed over the prior few months as a result of unemployment and the pandemic. Over the preceding two days, she had stopped eating and began to have episodes of non-bilious, non-bloody emesis. On the morning of presentation, she was found unresponsive at home and emergency medical services were called.
On physical examination, her vital signs included a blood pressure of 107/80 mm Hg, a pulse of 100 beats per minute, a respiratory rate of 16 breaths per minute, a temperature of 98.3oF, an oxygen saturation of 100% (bag valve mask on 10 L of oxygen), and a point-of care glucose of 93 mg/dL. On general inspection, the patient appeared to be an incoherent, mumbling woman with poor hygiene and dried vomitus around her mouth. She was tachycardic, with normal heart sounds and clear lungs. Abdominal examination was notable for diffuse tenderness. She was subsequently intubated for airway protection. The initial laboratory data is shown in the .
Other than leukocytosis the rest of her laboratory evaluation was not contributory. Blood and urine cultures were drawn. The electrocardiogram was significant for a prolonged absolute QT interval of 557 milliseconds (reference range in women: < 460 milliseconds). Computed tomography of the head, chest, abdomen, and pelvis was negative for acute pathology. In the ED, the patient received broad spectrum antibiotics, thiamine, two liters of 0.9% sodium chloride, and a total of 80 milliequivalents of potassium supplementation.
Thereafter, she was admitted to the medical intensive care unit (MICU). While in the MICU, blood cultures grew Staphylococcus aureus and urine cultures grew Proteus mirabilis. The patient was continued on antibiotics, fluids, and potassium supplementation. She was extubated on hospital day two and transferred to the medical floor. Prior to leaving against medical advice on day four, her venous blood gas demonstrated a pH of 7.50, a pCO2 of 38 mm Hg, and a lactate of 1.0 mmol/L.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [107.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",89,84.55,93.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 107.0 mm Hg + 2/3 * 80.0 mm Hg = 89.0 mm Hg.
Hence, the patient's mean arterial pressure is 89.0 mm Hg."
1811,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6046359-1,Extracted,"A 32-year-old Korean woman, gravida 2, para 1, was referred for uncontrolled high blood pressure (systolic blood pressure >200 mmHg) at 37 weeks' gestation. She complained of severe headache and posterior neck pain. She was otherwise asymptomatic and there was no remarkable past medical history or family history. Upon physical examination, she had no fever, but was soaked in sweat. On admission, her blood pressure was 220/137 mmHg and her heart rate was over 140 beats/minute. Her systolic blood pressure remained higher than 200 mmHg even though she was treated with hydralazine, labetalol, and magnesium sulfate. Routine laboratory findings revealed that hepatic enzyme levels were mildly elevated at 60 IU/L for aspartate aminotransferase, 50 IU/L for alanine aminotransferase, and a 4+ dipstick urine protein reaction was noted. A presumptive diagnosis of severe preeclampsia was made. At that time, regular uterine contractions were detected on cardiotocography and prolonged fetal heart rate deceleration was observed. An emergent cesarean section was immediately performed under general anesthesia. A male infant weighing 3,670 g was delivered and the Apgar score was 8/9 at 1/5 minutes. Focal placenta abruptio was found upon gross examination and histology later confirmed focal infarction and hemorrhage. During the induction of anesthesia and the operation, blood pressure fluctuated between 210/130 mmHg and 180/90 mmHg. Nicardipine and nitroglycerin were administered continuously. During recovery, her blood pressure ranged from 160/100 mmHg to 140/90 mmHg and she complained of intermittent headache, palpitation, dizziness, and excessive sweating. Tachycardia of 140–160 beats/minute failed to respond to medications. We suspected a thromboembolic lesion in the chest or possibly a pheochromocytoma. There was no evidence of pulmonary thrombosis on chest computed tomography imaging, but the patient had a 4-cm sized mass in the para-aortic space near the left renal hilum (). Paraganglioma was strongly suspected. Measurement of 24-hour urine catecholamines demonstrated elevated norepinephrine and metanephrine levels of 91.7 μg/day (reference range [RR], 15–80) and 5.5 mg/day (RR, 0–1.3), respectively. Her plasma normetanephrine level was elevated at 5,710 pmol/L (RR, 0–900). Echocardiography revealed normal cardiac function. Treatment with doxazosin and nifedipine was started. She remained mildly hypertensive (140/90 mmHg) to normotensive with no hyperadrenergic complicated symptoms during recovery. Additional positron emission tomography scanning was done to detect hypermetabolic tumors and their metastasis. There was one hypermetabolic mass in the left para-aortic space but no metastatic masses were found. On subsequent laparotomy, a 4-cm sized round, firm, encapsulated tumor was surgically removed. During tumor removal, the patient's blood pressure rose to 190/110 mmHg by just gentle manipulation. The patient's postoperative course was uneventful and her blood pressure and heart rate stayed within normal range without the use of antihypertensive drugs. Pathologic findings revealed classical features of paraganglioma (). The resection margins were clear and focal necrosis was observed. The diagnosis was firmly established from positive immunohistochemistry staining for chromogranin A (). The patient was discharged in good condition without any medication. Blood tests and urinary assays of catecholamine, performed at post-operative 4 weeks, revealed that the values had normalized.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [220.0, 'mm hg'], 'Diastolic Blood Pressure': [137.0, 'mm hg']}",164.66667,156.43334,172.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 220.0 mm Hg + 2/3 * 137.0 mm Hg = 164.66667 mm Hg.
Hence, the patient's mean arterial pressure is 164.66667 mm Hg."
1812,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7584326-1,Extracted,"A 45-year-old woman, farmer by occupation, presented to our center with fever, swollen lymph nodes in the neck, and painful rash in the lower extremities. She was apparently well until before 15 days when she developed a fever and sore throat followed by a painful rash on her legs three days later. She visited a primary care center where she was prescribed a seven-day course of intramuscular ceftriaxone with a provisional diagnosis of streptococcal pharyngitis, which resolved the sore throat and fever but not the rash. When her fever relapsed several days later, this time accompanied by swelling of cervical nodes, the patient was referred to Nork Infectious Clinical Hospital in Yerevan for further evaluation and management. At presentation, her blood pressure was measured 115/70 mmHg, the temperature was 102˚F, pulse rate was 102 beats per minute, and the respiratory rate was 18 per minute. General examination revealed few enlarged tender cervical nodes on the left side of her neck and multiple red, firm, and tender lump-like rash (erythema nodosum) on both her legs (Figure ).
Systemic examination was unremarkable. Blood workup revealed leukocytosis with relative lymphocytosis, raised erythrocyte sedimentation rate of 55 mm per hour, and C-reactive protein of 35 mg/L. We admitted her for a thorough evaluation. Serology for Streptococcus, Epstein-Barr virus, HIV, hepatitis B and C virus, Cytomegalovirus, Brucella, and leptospirosis were all negative. With unremarkable chest X ray and negative tuberculin test, we also eliminated sarcoidosis and tuberculosis as possible infectious causes of the erythema nodosum. She was diagnosed with tularemia based on latex agglutination testing, which came positive. A 14-day course of intramuscular streptomycin two grams daily divided into two doses was prescribed. Five days into treatment, the patient’s fever subsided, the buboes shrank, and the erythema nodosum resolved. The patient was discharged on the eighth day of admission with subsequent follow-up. Potentially exposed persons, particularly the family members, were advised to be vigilant about the symptoms, especially the development of fever for two weeks. They were informed about the water and food hygiene, which might have been the possible source of infection. The incidence was reported to the local health authority as a part of the standard protocol. The patient was doing better on the follow-up visit at three weeks with complete resolution of symptoms and return to a normal routine.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [115.0, 'mm hg']}",85,80.75,89.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 70.0 mm Hg = 85.0 mm Hg.
Hence, the patient's mean arterial pressure is 85.0 mm Hg."
1813,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6075500-1,Extracted,"A 65-year-old female was transported to the emergency department (ED) at approximately 2:00 AM following a witnessed cardiac arrest. According to the patient’s husband, she had been asleep in bed when she awoke suddenly, sat upright, and reached for her albuterol inhaler before “collapsing.” He found her to be pulseless and initiated cardiopulmonary resuscitation (CPR) while placing a call to emergency medical services (EMS). On EMS arrival, the patient was unresponsive and continued to receive CPR. She was intubated in the field using a size 7.0 endotracheal tube. Her initial rhythm was pulseless electrical activity (PEA), but she converted to normal sinus rhythm after receiving 1mg of epinephrine intravenously and 15 total minutes of CPR. No further history was available.
Per her husband, her past medical history was notable for “thyroid problems.” Her only medications were an albuterol inhaler, recently prescribed by her primary physician, and a multivitamin. She had no known drug allergies. On social history, the patient was not known to drink alcohol, smoke cigarettes, or use other substances. A family medical history and review of systems could not be obtained due to the acuity of her condition.
On examination, the patient was an obese female, intubated, and unresponsive. Her temperature was 37.1 degrees Celsius, blood pressure was 97/65 millimeters Hg, heart rate was 75 beats per minute (bpm). Her body mass index was estimated at 32. She was initially receiving assisted ventilation by EMS, but on examination in the ED she was found to have a spontaneous respiratory rate of 12 breaths per minute with an oxygen saturation of 98% on 40% fraction of inspired oxygen. Her head was atraumatic and normocephalic. Her pupillary exam showed mid-dilated symmetric pupils with sluggish reactivity to light. There was no hemotympanium or Battle’s sign. She had no apparent facial droop. An oral endotracheal tube was in place, confirmed with radiography and audible bilateral breath sounds. She had a full, supple neck without palpable masses, but additional exam was limited by body habitus. On cardiopulmonary exam, her lungs were clear to auscultation bilaterally and her heart had a regular rate and rhythm with no murmurs, gallops, or rubs. The patient’s abdomen was soft and nondistended with normal bowel sounds. On neurologic exam, her Glascow Coma Scale was 3T. She had diffusely decreased muscle tone, and 1+ patellar and brachioradialis deep tendon reflexes. Her musculoskeletal exam was unremarkable for deformity, erythema, or edema. Skin exam did not show any rashes, wounds or other lesions.
Initial electrocardiogram (ECG) () showed normal sinus rhythm at a rate of 70 bpm, normal axis, normal intervals and no pathologic t-wave inversions or ST-segment changes. A complete blood count and complete metabolic panel were done (). Additional laboratory tests, including thyroid studies, were unremarkable except for an elevated lactic acid of 6.9 millimoles/liter (L) (). A point-of-care echocardiogram was performed, which demonstrated grossly normal heart chamber sizes and systolic function with no pericardial effusion (). A point-of-care ultrasound of the abdomen and thorax was negative for any intra-abdominal free fluid. There was bilateral lung sliding present and no B lines. An anterior to posterior chest radiograph (CXR) is shown in .
The etiology of the patient’s cardiac arrest was unknown until a further diagnostic test was performed that revealed the diagnosis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [97.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",75.66667,71.88334,79.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 97.0 mm Hg + 2/3 * 65.0 mm Hg = 75.66667 mm Hg.
Hence, the patient's mean arterial pressure is 75.66667 mm Hg."
1814,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-6216,Extracted,"A 17-year-old boy is brought to the emergency room by his mother for altered mental status. His mother reports that over the past month, the patient has been failing his high school exams. She has noticed reduced attention and poor memory. She has had to repeat conversations that they had only hours ago. Then this morning, the patient woke up at home confused, asking where he was. His mother states that he is normally a “bright student” and is in all honors classes. The patient was on a “delayed vaccine schedule"" as a child and developed measles at age 6. Since then, he has been healthy. He has no chronic medical conditions and takes only a daily multivitamin. His maternal grandfather has Huntington disease. His temperature is 99°F (37.2°C), blood pressure is 110/82 mmHg and pulse is 86/min. On physical examination, there is no nuchal rigidity. The patient is disoriented to time and place. His mini mental status exam score is 16/30. The mother adds that 2 months ago her son told her that he was attracted to men. She is not sure if he is sexually active. She denies recent travel. She is unsure about recent sick contacts but says he started volunteering at a local hospital 3 weeks ago and received a flu vaccination. Labs are drawn and a drug screen is pending. Magnetic resonance imaging (MRI) of the brain is obtained, as shown in Figure A. Within 3 days of hospital admission, the patient develops unilateral, slow-myoclonic jerks.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [82.0, 'mm hg']}",91.33333,86.76666,95.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 82.0 mm Hg = 91.33333 mm Hg.
Hence, the patient's mean arterial pressure is 91.33333 mm Hg."
1815,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-6371,Extracted,"A 68-year-old man presents to the emergency department with leg pain. He states that the pain started suddenly while he was walking outside. The patient has a past medical history of diabetes, hypertension, obesity, and atrial fibrillation. His temperature is 99.3°F (37.4°C), blood pressure is 152/98 mmHg, pulse is 97/min, respirations are 15/min, and oxygen saturation is 99% on room air. Physical exam is notable for a cold and pale left leg. The patient’s sensation is markedly diminished in the left leg when compared to the right, and his muscle strength is 1/5 in his left leg.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [152.0, 'mm hg'], 'Diastolic Blood Pressure': [98.0, 'mm hg']}",116,110.2,121.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 152.0 mm Hg + 2/3 * 98.0 mm Hg = 116.0 mm Hg.
Hence, the patient's mean arterial pressure is 116.0 mm Hg."
1816,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5413,Extracted,"A 52-year-old man presents to the clinic with a headache and dizziness for the past month. The patient reports that about 4 weeks ago he developed a “nagging” headache. He thought he had a cold, so he tried over the counter ibuprofen that provided only mild and temporary relief. Recently, he also started feeling dizzy and nauseous, which only resolves when he steps outside to shovel the snow. The patient’s medical history is significant for hypertension, type II diabetes mellitus, and asthma. His medications include amlodipine, metformin, glimepiride, and a fluticasone/salmeterol inhaler. The patient has been living at his upstate cabin for the past 5 weeks but denies other recent travel. He denies smoking tobacco or illicit drug use. The patient’s temperature is 99°F (37.2°C), blood pressure is 130/78 mmHg, pulse is 72/min, and respirations are 16/min with an oxygen saturation of 98% on room air. The patient is currently asymptomatic while sitting in the office, and physical examination is unremarkable.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",95.33333,90.56666,100.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 78.0 mm Hg = 95.33333 mm Hg.
Hence, the patient's mean arterial pressure is 95.33333 mm Hg."
1817,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7546790-1,Extracted,"A 27-year-old man was admitted to the cardiology department with symptoms of biventricular heart failure (NYHA class III), excessive sweating, and pain in the postoperative wound area at the site of thrombectomy 6 months prior to hospitalization.
His family history was unremarkable. Parents were not consanguineous. The father died at the age of 35, in a traumatic accident, and to the best of the patient’s knowledge, had no cardiac complaints. At the time of the first hospitalization, the mother was 56 years old and had no complaints. The proband had a sister who died at 15 days of age due to a congenital heart disease (transposition of the great arteries). No other relative was diagnosed with cardiomyopathy of other cardiac disease before 50 years of age. External risk factors: smoking average of three cigarettes/day for 7 years. No alcohol abuse or other toxic factors were mentioned.
Personal medical history with main milestones and medications taken (when possible) was reconstructed from the available medical records ().
The patient had an average height (174 cm) and weight of 79 kg for his age, BMI 26.1 kg/m2, and normal arterial blood pressure (120/80 mmHg). Edema of the leg and slight serous discharge from the wound in the right groin area were found on the initial physical examination.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1818,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1212,Extracted,"A 60-year-old man comes to the physician because of a 2-day history of blood in his urine, lower abdominal pain, and a burning sensation while micturating. Five months ago, he was diagnosed with high-grade non-Hodgkin lymphoma and a deep vein thrombosis of his right popliteal vein. His medications include polychemotherapy every 3 weeks and a daily subcutaneous dose of low molecular weight heparin. The last cycle of chemotherapy was 2 weeks ago. His temperature is 37°C (98.6°F), pulse is 94/min, and blood pressure is 110/76 mm Hg. Examination shows bilateral axillary and inguinal lymphadenopathy, hepatosplenomegaly, and mild suprapubic tenderness.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [76.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",87.33333,82.96666,91.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 76.0 mm Hg = 87.33333 mm Hg.
Hence, the patient's mean arterial pressure is 87.33333 mm Hg."
1819,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8054788-1,Extracted,"A 62-year-old male from Tamil Nadu presented with a 2-week history of fever and acute onset of abdominal pain for 4 days. He was a chronic diabetic and hypertensive and not on proper medications. Physical examination showed a pulse rate of 105 beats/min and blood pressure of 148/90 mmHg. Abdominal examination revealed tenderness in the left hypochondrium and epigastrium. Examination of other systems was unremarkable. His blood investigations showed normal hemogram, serum amylase, and lipase levels. His liver and renal function tests were within normal limits. His HbA1c was 9.2%, suggesting poor glycemic control. CECT abdomen revealed mildly bulky distal body and tail regions of pancreas with peripancreatic fat streakiness []. The retro-pancreatic portion of the splenic vein was distended with non-enhancing intraluminal thrombus and vessel wall enhancement, suggestive of acute thrombosis []. Prominent venous collaterals were noted in the periportal, peripancreatic, omental, and retroperitoneal locations. The head, neck, and proximal body of the pancreas were normal. The main pancreatic and common bile ducts were not dilated. Mild splenomegaly was also noted. MRI abdomen showed a mildly bulky pancreas. The retro-pancreatic portion of the splenic vein showed T2 hyperintense thrombus with restricted diffusion []. In view of the history of fever with normal amylase and lipase levels, the possibility of infective cause of pancreatic inflammation with splenic vein thrombosis was postulated.
Blood culture from this patient revealed a safety pin appearance of Gram-negative bacilli in the routine Gram staining [], and colonies showed a metallic sheen on MacConkey's agar plate []. After an incubation period of 72 h, using the VITEK2 (Biomerieux) automated system, the causative agent was revealed to be B. pseudomallei. The patient was managed with parenteral meropenem (1 g every 8 h t.i.d) and oral co-trimoxazole (960 mg every 12 h b.i.d) with subcutaneous enoxaparin (1 mg/kg b.i.d) for splenic vein thrombosis. He received subcutaneous antidiabetic medication human Actrapid® for 2 weeks. He improved symptomatically during the intensive phase of treatment and achieved glycemic control, subsequently discharged after switching to oral anticoagulation and oral hypoglycemic drugs, and suggested for regular follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [148.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",109.33333,103.86666,114.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 148.0 mm Hg + 2/3 * 90.0 mm Hg = 109.33333 mm Hg.
Hence, the patient's mean arterial pressure is 109.33333 mm Hg."
1820,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7556,Extracted,"A 34-year-old woman is recovering in the post-operative unit following a laparoscopic procedure for chronic endometriosis. She had initially presented with complaints of painful menstrual cramps that kept her bedridden most of the day. She also mentioned to her gynecologist that she had been diagnosed with endometriosis 4 years ago, and she could not find a medication or alternative therapeutic measure that helped. Her medical history was significant for surgery she had 6 years ago to remove tumors she had above her kidneys, after which she was prescribed hydrocortisone. An hour after the laparoscopic procedure, she calls the nurse because she is having difficulty breathing. The nurse records her vital signs include: blood pressure 85/55 mm Hg, respirations 20/min, and pulse 115/min. The patient suddenly loses consciousness. Intravenous fluids are started immediately. She gains consciousness, but her blood pressure is unchanged.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [85.0, 'mm hg'], 'Diastolic Blood Pressure': [55.0, 'mm hg']}",65,61.75,68.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 85.0 mm Hg + 2/3 * 55.0 mm Hg = 65.0 mm Hg.
Hence, the patient's mean arterial pressure is 65.0 mm Hg."
1821,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8223842-1,Extracted,"A 26-year-old man was referred to our hospital with chest discomfort.
The chest discomfort located substernal area started suddenly 30 min ago and was accompanied by palpitation.
About two years prior, he had a history of taking some medicines for three months at another clinic because of arrhythmia but did not know the details of the previous event and did not follow up with the clinic since then. Alcohol consumption was approximate 30 g per week. A family history related to cardiovascular disease could not be confirmed because the parents no longer have been out of touch with him after the divorce.
A family history related to cardiovascular disease could not be confirmed because the parents no longer have been out of touch with him after the divorce.
Upon arrival, vital signs were as follows: blood pressure of 150/90 mmHg, pulse rate of 94 bpm, respiratory rate of 20 per minute, and body temperature of 36.6 °C. His blood pressure during the hospitalization period did not exceed over 130/84 mmHg. He had no history of hypertension. There was no symptom and sign suggesting volume overload.
A chest X-ray revealed cardiomegaly, but there was no evidence of pulmonary congestion and pleural effusion. The ECG showed AF with the controlled ventricular response and left ventricular hypertrophy (LVH) in voltage criteria by the Sololow-Lyon index (R in V5 > 35 mm) upon visit at the emergency department (Figure ).
The results of blood chemistry were as follows: BUN, 11.0 mg/dL, creatinine, 0.73 mg/dL; troponin-I, 0.1 ng/mL (ref. 0.0-0.16); and N terminal pro-B type natriuretic peptide, 136.0 pg/mL. The amount of albuminuria for 24 h was 17.6 mg (the category A1 as normal to mildly increased range < 30 mg).
Transthoracic echocardiography (TTE) showed interventricular septum/Left ventricular posterior wall thickness, measured as 14/14 mm, respectively; left ventricular mass index, 200 g/m2; the left ventricular ejection fraction, 65%; left atrial volume index, 45 mL/m2; thickened mitral valve leaflets without functional abnormality and no wall motion abnormality (Figure ).
Transesophageal echocardiography (TEE) was performed to control the symptom before electric cardioversion. Spontaneous restoration of sinus rhythm during the TEE was noticed. The 12 Leads-ECG followed by the TEE revealed the link between P and R waves that was abnormally shortened. The follow-up ECG showed a short PR interval of less than 120 ms but no delta waves (Figure ). The relationship between P and R waves on the following ECG, severely symmetric LVH without a history of hypertension, and unusual presenting with AF in the young age group suggested congenital myocardial disease. The patient was needed to re-evaluate the other missing clinical symptoms and signs related to multi-organ involvement. Additionally, there were bilateral mild hearing loss, neuropathic pain, anhidrosis, and angiokeratoma on the trunk and hands. (Figure ). Corneal verticillata on the ophthalmic examination was observed. Genetic tests and GLA enzyme activity were performed to confirm AFD. The enzyme activity of GLA was 1.7 nmol/hr/mg (< 0.1% of normal range), and mutation of the GLA gene was detected in exon-7 with c.1024C>T variant.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",110,104.5,115.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 90.0 mm Hg = 110.0 mm Hg.
Hence, the patient's mean arterial pressure is 110.0 mm Hg."
1822,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7733146-1,Extracted,"A 75-year-old Japanese man presented to the emergency department of our hospital with edema of the legs and dyspnea on exertion for 3 weeks. The patient had been in his usual state of health until 3 weeks prior to admission. His medical history included mitral and aortic valve replacement, tricuspid valvuloplasty, chronic heart failure, nonsustained ventricular tachycardia, and bradycardia atrial fibrillation treated with a pacemaker at the age of 72. Since diagnosis, he had been taking medications including amiodarone with the dosage adjustments. From the day of admission, he was treated with amiodarone (200 mg), carvedilol (10 mg), and furosemide (10 mg) daily. He had taken the same medication and same dosage for at least 6 months without laboratory test.
On the day of admission, the patient had a temperature of 37.6°C, respiratory rate of 28 breaths per minute, heart rate of 71 beats per minute (irregularly irregular), blood pressure of 134/40 mmHg, and an oxygen saturation of 88% while breathing ambient air. His general appearance seemed agitated in acute distress. General physical examinations revealed sclerae icteric, no thyroid enlargement (without tenderness or bruit). Respiratory sounds were inspiratory coarse crackles bilaterally. His legs revealed slow pitting edema bilaterally. Laboratory analysis revealed normal complete blood count. Aspartate transaminase and alanine aminotransferase levels were 178 and 202 IU/L, respectively. Total-bilirubin (T-Bil), direct-bilirubin (D-Bil) an indirect-bilirubin (ID-Bil) were 5.0, 3.4, and 1.6 mg/dL, respectively. Alkaline phosphatase (ALP) and γ-glutamyl transpeptidase (GTP) levels were normal. Free T3 and free T4 levels were higher than 11.40 pg/mL (reference value 2.30–4.00 pg/mL) and 6.99 ng/dL (reference value 0.90–1.70 ng/dL), respectively. Thyroid-stimulating hormone (TSH) level was less than 0.015 μIU/mL (reference value 0.500–5.00 μIU/mL), and anti-TSH receptor antibodies were negative. His electrocardiogram showed atrial fibrillation. Thyroid ultrasonography revealed normal size and hypovascularity without nodules. Chest radiograph showed bilateral lung congestion, 60% of cardiothoracic ratio, and implantation of pacemaker (Fig. ). Computed tomography of the abdomen demonstrated high density throughout the liver and dilation of the hepatic veins and inferior vena cava (Fig. ).
His physical examination and laboratory data revealed acute congestive heart failure, thyrotoxicosis, and hepatic dysfunction with hyperbilirubinemia. We suspected thyroid storm likely caused by AIT because of no pre-existing thyroid disease and long-term use of amiodarone. High-density area throughout the liver on computed tomography suggested amiodarone administration (Fig. ). His hepatic dysfunction was caused by hyperthyroidism in addition to toxicity from amiodarone accumulation. Hepatic dysfunction related to hyperthyroidism encompasses abnormalities associated with the effects of thyroid hormone excess, drug-related hepatic injury, and the presence of concomitant liver disease. His Burch and Wartofsky’s score was 55 (a score of 45 or more is highly suggestive of thyroid storm, a score of 25-44 supports the diagnosis, and a score below 25 makes thyroid storm unlikely; Table ). On the basis of these clinical features, he was diagnosed with thyroid storm associated with type 2 AIT. As a result, amiodarone was discontinued and he was treated with methimazole (60 mg), potassium iodine (200 mg), carvedilol (10 mg), and hydrocortisone (300 mg) daily. In addition, he was treated with furosemide for acute congestive heart failure and warfarin for atrial fibrillation. Following these treatment routines, his symptoms and laboratory findings improved gradually. The dosage of these medications for thyroid storm was gradually decreased once the euthyroid state had been achieved. He required no additional therapy for his arrhythmia, irrespective of whether or not amiodarone was stopped. He was discharged on day 28, and advised regular check-ups with his family doctor.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [40.0, 'mm hg'], 'Systolic Blood Pressure': [134.0, 'mm hg']}",71.33333,67.76666,74.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 134.0 mm Hg + 2/3 * 40.0 mm Hg = 71.33333 mm Hg.
Hence, the patient's mean arterial pressure is 71.33333 mm Hg."
1823,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3713676-1,Extracted,"A 25-year-old man sustained fracture dislocation at T7-T8 vertebrae following a road traffic accident. He was scheduled for pedicle screw fixation of T7-T8 vertebrae two weeks after injury. On pre-anesthetic evaluation, patient presented with complaints of inability to move his lower limbs and numbness in lower half of body. Clinical examination revealed a conscious, well oriented, afebrile patient with pulse rate of 76 beats per minute and blood pressure of 110/70 mmHg. Central nervous examination revealed complete bilateral flaccid paralysis (paraplegia) and loss of all sensations below T9 dermatome with areflexia. There was no voluntary contraction of the anal sphincter with absence of sensation around the anus. Magnetic resonance imaging showed complete transaction of spinal cord at T10 level. All routine investigations were within normal limits.
While applying standard monitoring in the operating room, it was found that patient’s urinary bladder was distended up to the umbilicus though a bladder was in situ. It was decided to induce anesthesia and thereafter change of blocked urinary catheter and place central venous pressure and intra-arterial pressure monitoring lines. After adequate preloading, general anesthesia was induced with fentanyl 100 mcg and thiopentone 250 mg intravenous (IV). Tracheal intubation was done after adequate relaxation with 6 mg vecuronium. Anesthesia was maintained with isoflurane in mixture of oxygen and nitrous oxide. Post-induction vitals were stable with 100% saturation and end-tidal carbon dioxide of 36 mmHg. Blocked urinary catheter was removed and re-catheterization done. 1500 ml of urine was drained. Subsequent to bladder catheterization and decompression, patient developed polymorphic premature ventricular contractions with hypertension. Isoflurane concentration was increased, but it was followed by severe bradycardia (38 beats per minute) with malignant hypertension (220 mmHg/100 mmHg). Sodium nitroprusside was started at a rate of 1 mcg/kg/min. As bradycardia was refractory, atropine 1 mg IV was administered. Despite this, patient developed asystole. Cardiopulmonary resuscitation (CPR) was started with 100% oxygen. Sodium nitroprusside was stopped immediately and repeat dose of atropine 1 mg IV was given. Advanced cardiac life support was continued for 30 min with no return of spontaneous circulation. Autopsy revealed mildly dilated heart with a weight of 350 g. All three major coronary arteries were normal and histological examination showed no infarction.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1824,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8508477-1,Extracted,"A 60-year-old woman without known comorbidities was transferred to our hospital due to fever and abnormal laboratory test findings. She had not taken any medications prior to the emergence of symptoms. She had climbed a mountain about two weeks prior to our hospital admission and had no memory of insect or tick bite. The patient was admitted to another hospital due to fever after 7 days of climbing. She had a fever with a maximum temperature of 39 °C, aggravating nausea, and vomiting. Abdominal CT revealed hepatosplenomegaly. Therefore, she was referred to our hospital seven days after the onset of symptoms. The patient was alert with a blood pressure of 90/60 mmHg, pulse of 84 beats/min, and body temperature of 37.6 °C on admission. Physical examination revealed no palpable lymph nodes, and there were mild macular rashes on the trunk and both thighs but no eschar. The patient stated that the skin lesions tended to improve 1–2 days before admission. Mild tenderness of the right upper quadrant of the abdomen was noted. She complained of febrile sensation, vomiting, and nausea. The initial complete blood count revealed leukopenia and thrombocytopenia. She had increased aspartate aminotransferase (AST), alanine transaminase, and lactate dehydrogenase (LDH) levels. The blood test findings are shown in .
Based on the patient’s outdoor activity history and laboratory findings, an SFTSV infection or other tick-borne diseases were suspected. Since SFTSV infection and other tick-borne diseases cannot be differentiated based on clinical characteristics alone, and the relevant serological test results take time, ciprofloxacin (400 mg intravenously twice a day) and doxycycline (100 mg twice a day) were administered empirically while waiting for the test results (). The patient’s fever and vomiting gradually improved, and the white blood cell and platelet counts approached normal levels. Since the patient’s LDH remained elevated, she underwent 18F-FDG PET/CT on the eighth hospitalization day to exclude other malignant lymphomas. She had increased FDG uptake by the lymph nodes, including the neck, left axilla, and left supraclavicular lymph nodes (a,b). The 18F-FDG PET/CT results of maximum standardized uptake values (SUVmax) of the lymph nodes were as follows: left level III lymph node (SUVmax; 4.4), left level IV (SUVmax; 8.2), left level V (SUVmax; 5.2), left supraclavicular area (SUVmax; 10.0), and left axillary lymph node (SUVmax; 25.3). Additional evaluation was conducted to exclude lymphoma secondary to enlarged axillary lymph nodes due to a high SUVmax value on 18F-FDG PET/CT. A core needle biopsy of lymph nodes was also performed to exclude lymphoma. The real-time RT-PCR targeting the M and S segments of SFTSV in the blood was positive on the same day. On pathologic examination, the left axillary and supraclavicular lymph nodes exhibited extensive necrosis with atypical lymphoid hyperplasia (). These findings were similar to those of Kikuchi disease. There were no immunohistochemical staining findings suggestive of lymphoma.
As the prevalence of tick-borne infectious diseases such as Q fever, brucellosis, anaplasmosis and Lyme disease is low in South Korea [], these were not considered during initial evaluation. Additional tests for Q fever and brucellosis were planned in cases where the patient’s clinical symptoms did not improve or the initial tests could not demonstrate any significant results. However, the results of SFTSV real-time RT-PCR on blood samples were confirmed to be positive in this case, and the patient’s condition gradually improved without steroids or antiviral agents. She was therefore discharged without further evaluation on hospital day 14.
The axillary and supraclavicular lymph nodes were of a normal size on CT one month later (a,b). She was clinically diagnosed with necrotizing lymphadenitis caused by SFTSV. SFTSV-PCR was performed on the remaining lymphoid tissue and the test was negative. However, the tissue sample was expectedly insufficient. In this case, the patient’s 18F-FDG PET/CT findings and necrotizing lymphadenitis mimicked malignant lymphoma. The present study was approved by the institutional review board of Pusan National University Yangsan Hospital (IRB No. 05-2021-077).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",70,66.5,73.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 60.0 mm Hg = 70.0 mm Hg.
Hence, the patient's mean arterial pressure is 70.0 mm Hg."
1825,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8384532-1,Extracted,"A 65-year-old female with no past medical history presented to the emergency department on 5/12/2021 with a complaint of periumbilical abdominal pain that radiated to the back. The pain was described to be tearing and sharp in nature, measuring 10/10 on the pain scale. The pain started suddenly after waking up earlier that morning. The patient presented six hours from the onset of symptoms. Upon presentation, the patient was evaluated by the emergency room staff vitals were obtained, and appeared to be within normal limits except for blood pressure in 150's systolic and over 90's diastolic. A full set of labs were obtained, which indicated a white blood cell count of 8.1 K/uL, hemoglobin of 15.5 g/dl, hematocrit of 45.4%, and platelets of 198 K/uL. Basic metabolic panel and coagulation studies were within the normal range.
Computed tomography chest, abdomen, and a pelvis with intravenous contrast were obtained and indicated infrarenal abdominal aortic tortuosity as well as 68 mm abdominal aortic aneurysm with dissection. The infrarenal abdominal aorta was proximally tortuous leading into the fusiform infrarenal abdominal aorta aneurysm and short segment dissection with a wide intimal defect with equal opacification of the true and false lumen. The aneurysm extended to the level of the bifurcation. There were two left and one right renal arteries that were patent. Vessels were coursing along the left lateral aspect of the aneurysm (Figure -). There were concerns for impending rupture.
Given the concerns for impending rupture, the patient required immediate surgical intervention. Unfortunately, the patient was not a candidate for endovascular therapy due to the juxta-renal nature of the aneurysm and the lack of adequate proximal neck. Therefore, the patient underwent an open retroperitoneal repair, where she was found to have a large dissection with a prominent intimal flap as indicated in Figure . A 16 mm Dacron graft was placed and the aneurysm sac was closed over the graft using interrupted 3-0 vicryl sutures. The patient tolerated the procedure well, was successfully extubated, and was transferred to the ICU for hemodynamic monitoring. The patient did very well and was successfully discharged on post-operative day three.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",110,104.5,115.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 90.0 mm Hg = 110.0 mm Hg.
Hence, the patient's mean arterial pressure is 110.0 mm Hg."
1826,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6288932-1,Extracted,"A 19-year-old Hispanic female with a past medical history of acne, asthma, and extensive psychosocial distress but no psychiatric diagnoses, presented to the ED with complaints of an episode of lightheadedness, generalized weakness, diaphoresis, diarrhea, and vomiting. Previously, she presented to the hospital with similar complaints two other times; however, she was not seen by our team until the third visit. On this first visit she stated that she used the blood glucose monitor of her girlfriend/roommate, who is a type 1 diabetic, and that her blood sugar reading was 53 mg/dL and later rose to 80 mg/dL after she ate two sandwiches and some chocolate. Upon arriving to the ED, the patient’s symptoms had improved. Vital signs obtained at the time of triage were: blood pressure (BP) 98/65 mmHg, heart rate 81 beats per minute (bpm), respiratory rate 18 breaths per min, oxygen saturation (SpO2) of 100% on room air, and an oral temperature of 37 °C (98.6 °F). The patient reported no pertinent past surgical history. She stated that she was allergic to pineapples and that she does not take any medications. In addition, she did not report any tobacco or alcohol use. Initial examination revealed a well-developed, asymptomatic, obese young female in no acute distress. Her blood glucose according to the glucose monitor was 60 mg/dL, which was confirmed with lab draw. Physical exam and labs were unremarkable, and the patient was discharged after being given intravenous (IV) 0.9% sodium chloride (NaCl) for volume restoration, ondansetron for her nausea and vomiting, further directions on diet for hypoglycemia (i.e. adding protein to each meal and eating small frequent meals), and instructions on follow-up with her primary care provider (PCP) for recommendation on further testing for the cause of her hypoglycemic episode and GI symptoms.
The next day, the patient arrived via emergency medical services (EMS) to the ED after she was found unresponsive. She stated that she was not feeling too well due to a virus and became very lightheaded and passed out. Her blood sugar was 46 mg/dL at home prior to administration of half an ampule of dextrose (D50W). Her family mentioned the patient has a history of her blood sugar dropping rather frequently and that they are unsure what to do for this problem. Vital signs obtained at the time of triage were: BP 122/75 mmHg, heart rate 100 bpm, respiratory rate 18 breaths per minute, SpO2 of 100% on room air, and an oral temperature of 36.7 °C (98 °F). Physical exam and other labs were unremarkable, and the patient was discharged after being given instructions once again on following-up with a PCP.
Three weeks after her initial presentation, she was rushed to the ED via EMS after being found unresponsive at work with a blood glucose level of 23 mg/dL. She was given 1 ampule of IV D50W by EMS at the scene and her blood sugar rose to 172 mg/dL. Upon arrival to the ED, her blood sugar had dropped back down to 61 mg/dL; and she was noted to again have symptoms of dizziness and decreased alertness with her hypoglycemia. Vital signs obtained at the time of triage were: BP 135/78 mmHg, heart rate 108 bpm, respiratory rate 18 breaths per minute, SpO2 of 100% on room air, and an oral temperature of 36.4 °C (97.6 °F). She was given one half of an ampule of D50W IV because of her symptoms of dizziness and evidence of decreased alertness with a decreased blood glucose level, which was suspected to still be dropping. She responded to this treatment with improvement of dizziness and alertness but later had a second hypoglycemic episode in the ED. At this time she was treated with a full ampule of D50W IV and was started on dextrose 5% with 0.45% NaCl (D5 half-normal). Despite a brief improvement a few minutes after starting D5 half-normal, she had a third episode of hypoglycemia in the ED and was treated with another ampule of D50W IV and her IV changed to dextrose 10% in water (D10W) at 100 cm3 (cc’s) an hour. Despite this change, her blood glucose further dropped to 105 mg/dL from 140 mg/dL, so her D10W was increased to 150 cc’s an hour. Detailed glucose readings throughout this time are reported in Table . Her girlfriend/roommate was asked to leave the patient to rest, in order to help determine whether the patient, her roommate, or both might be involved in giving insulin to cause the abrupt hypoglycemic episodes. The patient was weak, confused, profusely sweating with chills, short of breath, nauseated, had heart palpitations, and an altered mental status during all of her hypoglycemic episodes. Of note, once alert, the patient told the charge nurse that her PCP had found a mass in her pancreas that was responsible for her hypoglycemic episodes. Due to the critical nature of her recurrent hypoglycemic episodes in the ED, the patient was admitted to the ICU, where she became more responsive. An electrocardiogram demonstrated normal sinus rhythm, normal axis and intervals, and no acute changes in ST-segment or T wave morphology. The laboratory findings from all three ED visits are reported in Table .
Standard drug screen was done to rule out any symptoms from toxicity; however the results were negative. To determine if factitious use of insulin was the cause for the patient’s presentation, further tests were performed: hemoglobin A1C of 5.1%, C-peptide level of 9.9 ng/mL, free insulin level of 370 mIU/L and a total insulin level of 377 mIU/L.
To rule out any neurological causes, a computed tomography (CT) scan of the head without IV contrast was performed and revealed no evidence of intracranial findings or suspicious intracranial mass. To rule out any pancreatic masses, CT of the abdomen was obtained and showed a 1.8 cm collapsing cyst in the right ovary and trace fluid in the pelvis, which is likely physiological (Fig. ). Otherwise, no acute intra-abdominal or intra-pelvic process was seen.
The patient was interviewed at length by the ED hospital team in the ICU the following day, and the diagnosis of factitious disorder was suggested. The encounter revealed that the patient is an undocumented immigrant from Honduras, who has been in the US since she was 14 years old. She used to reside with foster parents. However, she recently graduated from being a minor and is currently living at a halfway house with four other women. She works full-time at a thrift store. She is unaware of her family history. She states that she was heavily involved with illicit drug use in the past but does not smoke or drink alcohol anymore. When confronted with evidence about no mass found on imaging, the patient did not deny injecting insulin. She had significant knowledge about insulin administration as well as the amount of units her girlfriend/roommate currently injects for her type 1 diabetes management. She mentioned that she frequently checks her blood sugar at home, where her readings range from 30s – 100 s mg/dL. The patient reported missing several meals throughout the day due to time restraints and work. Her caregiver called the hospital to let the hospital staff know that the patient had been taking her girlfriend/roommate’s insulin resulting in her previous ED visits. She has also asked for insulin needles and may have taken insulin to gain attention.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [135.0, 'mmhg'], 'Diastolic Blood Pressure': [78.0, 'mmhg']}",97,92.15,101.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 78.0 mm Hg = 97.0 mm Hg.
Hence, the patient's mean arterial pressure is 97.0 mm Hg."
1827,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7069,Extracted,"A 12-year-old boy admitted to the intensive care unit 1 day ago for severe pneumonia suddenly develops hypotension. He was started on empiric antibiotics and his blood culture reports are pending. According to the nurse, the patient was doing fine until his blood pressure suddenly dropped. Vital signs include: blood pressure is 88/58 mm Hg, temperature is 39.4°C (103.0°F), pulse is 120/min, and respiratory rate is 24/min. His limbs feel warm. The resident physician decides to start him on intravenous vasopressors, as the blood pressure is not responding to intravenous fluids. The on-call intensivist suspects shock due to a bacterial toxin.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [58.0, 'mm hg'], 'Systolic Blood Pressure': [88.0, 'mm hg']}",68,64.6,71.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 88.0 mm Hg + 2/3 * 58.0 mm Hg = 68.0 mm Hg.
Hence, the patient's mean arterial pressure is 68.0 mm Hg."
1828,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8262744-1,Extracted,"A 49-year-old Caucasian female with a past medical history of hypertension, psoriasis, morbid obesity, and tobacco abuse presented to our hospital for evaluation of chest pain. The patient had intermittent chest pain of one-week duration, substernal, pressure-like, non-radiating, and 10/10 in severity. There were no aggravating or alleviating factors. The pain was associated with diaphoresis, vomiting, exertional dyspnea, and swelling of the lower extremities. She did not have any recent cold-like symptoms, fever, or cough suggesting viral myocarditis.
On examination, her vital signs were as follows: temperature of 36.7 degrees Celsius, blood pressure of 182/112 mmHg, heart rate of 92 beats/min, respiratory rate of 18 breaths/min, SpO2 of 99% on room air, and body mass index (BMI) of 42.5 kg/m2. The cardiopulmonary examination was otherwise unremarkable.
Electrocardiogram (EKG) showed left ventricular hypertrophy by voltage criteria along with T-wave inversion in leads I and aVL (Figure ).
Laboratory studies revealed elevated serum troponin I level of 1.91 ng/mL (reference range: ≤0.03 ng/mL) and brain natriuretic peptide level of 399 pg/mL (reference range: ≤100 pg/mL). The other blood investigations were within normal limits. A transthoracic echocardiogram showed reduced ejection fraction (45-50%) with severe hypokinesis of the mid-distal left ventricle. Other imaging, including a plain chest X-ray and a contrast CT pulmonary angiogram, did not reveal pulmonary infiltrates or pulmonary arterial embolism.
The patient was deemed to have NSTEMI based on the clinical presentation and elevated troponin level. She received aspirin and clopidogrel and was subsequently started on unfractionated heparin infusion as per the acute coronary syndrome (ACS) treatment protocol.
The patient’s symptoms improved after the initiation of medical therapy. Given the regional wall motion abnormalities detected on echocardiography, the patient underwent elective coronary angiography, which showed no significant epicardial coronary artery stenoses. A gadolinium-enhanced cardiac MRI (CMR) was obtained for the diagnosis of MIOCA (myocardial infarct with open coronary arteries). CMR demonstrated interval normalization of regional and global left ventricular systolic function compared to echocardiography. However, a well-demarcated cardiac mass involving the epicardial, mid-lateral left ventricular wall, and the anterolateral papillary muscle base was detected. The mass signal characteristics on various CMR sequences and post-contrast were consistent with a cardiac lipoma (Figure ).
Retrospective review of the initial contrast chest CT images correlated with the findings on CMR and showed regions of low-fat range attenuation in the same location (Figure ).
The patient’s condition improved, and she was discharged home in a stable condition with a recommendation of an outpatient follow-up CMR in three months for surveillance. The patient continues to do well to date.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [112.0, 'mm hg'], 'Systolic Blood Pressure': [182.0, 'mm hg']}",135.33333,128.56666,142.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 182.0 mm Hg + 2/3 * 112.0 mm Hg = 135.33333 mm Hg.
Hence, the patient's mean arterial pressure is 135.33333 mm Hg."
1829,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7978146-1,Extracted,"A 65-year-old female with a history of chronic obstructive pulmonary disease, and hypothyroidism presented to the emergency department (ED) with shortness of breath which was progressively worsening two days prior to presentation. She also reported having a fever with a temperature of 38 degrees Celsius ( ͦC), chills, and nonproductive cough in the last two days. The patient denied exposure to sick contacts, recent travel outside the state, or recent immobilization. Her temperature on admission was 39 ͦC, blood pressure 132/80 mmHg, heart rate 110 beats per minute, respiratory rate of 18 per minute. Physical examination was significant for lethargy, bilateral rales on auscultation of lung fields. Her oxygen saturation was 88% while on 5 liters per minute delivered through nasal cannula so she was placed on noninvasive positive pressure ventilation. Chest X-ray showed bilateral interstitial opacities consistent with viral pneumonia. The patient tested positive for SARS-CoV-2. Laboratory results at the time of admission are presented in Table .
She was started on remdesevir and dexamethasone as per institutional guidelines for the treatment of COVID-19 viral pneumonia. A 12-lead electrocardiogram revealed atrial fibrillation with a ventricular rate of 120 per minute, so anticoagulation was started with low molecular weight heparin (LMWH) 1mg/kg dosing twice daily and rate-controlling medications were administered. 12 hours after admission to the hospital, right arm motor drift, facial droop, and dysarthria were noted. National Institute of Health Stroke Scale (NIHSS) was 3. Emergent CT of the head revealed age indeterminate lacunar infarct in the left basal ganglia, with no intracranial hemorrhage. CT perfusion study of head and neck showed occlusion of the supraclinoid segment of the left internal carotid artery (ICA) with occlusive thrombus extending into the proximal left anterior cerebral artery (ACA) and middle cerebral artery (MCA) (Figure ).
Left ACA opacified via an anterior communicating artery. Corresponding large 126 ccs of ischemic penumbra involving the left frontal, temporal and parietal lobes, basal ganglia were also seen. Anticoagulation was switched from LMWH to unfractionated heparin (UFH) in anticipation of the revascularization procedure. The case was discussed with an Interventional neurologist and the decision was made not to proceed with revascularization due to low NIHSS. While the patient was being monitored in the stroke unit, on day 3 of admission, she developed new right-sided hemiplegia, aphasia with altered mentation. The emergent CT of the head showed an increasing size of the infarct within the left basal ganglia and corona radiata. CT perfusion showed stable left ICA/MCA occlusion, however, due to progressive symptoms she underwent emergent left ICA/MCA thrombectomy. The weakness improved after revascularization with an increase in muscle strength from 1/5 to 3/5 in both right upper and lower extremities. UFH was discontinued due to an elevated risk of bleeding post revascularization.
On day 7 after the procedure, anticoagulation was restarted with LMWH due to coexisting atrial fibrillation and COVID-19 infection. At this point, the patient completed a 10-day course of remdesevir and dexamethasone and was saturating well with 3 liters per minute supplemental oxygen through the nasal cannula. two days after restarting anticoagulation, a stroke code was called due to sudden onset, left lower extremity weakness. CT perfusion of head and neck demonstrated new distal left M2 branch occlusion within the Sylvian fissure. Mural thrombi were noted in the distal aortic arch and descending aorta. A complete angiogram of the chest and abdomen was done to determine the extent of clot burden. CT angiogram of the chest confirmed the presence of mural thrombus (Figure ).
Along with that, a large filling defect was noted within the right interlobar pulmonary artery with extension into the right middle and lower lobe pulmonary artery as well as segmental and subsegmental branches of the right lower lobe compatible with pulmonary embolism (Figure ). CT angiogram of the abdomen showed thrombus in left common femoral artery extending into proximal internal iliac as well as left external iliac arteries (Figures , ). There is a reconstitution of flow within both arteries distally. Platelets dropped from 174 to 63 within few days after restarting anticoagulation (Figure ). 4T score for screening of HIT was 6 (2 each for greater than 50% drop and nadir >30, timing within 5-10 days of exposure and new thrombosis). LMWH was switched to argatroban infusion. Platelet factor 4 antibody test and serotonin release assay test (SRA) were positive (Table ).
The patient underwent a left lower extremity angiogram by vascular surgery and treated with tissue plasminogen activator catheter-directed thrombolysis (tPA-CDT). Revascularization was successful with three-vessel runoff and dopplerable pulses in the left lower extremity. Anticoagulation was subsequently switched to apixaban. The patient recovered from COVID-19 and was discharged to the nursing home for rehabilitation for stroke.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [132.0, 'mm hg']}",97.33333,92.46666,102.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 132.0 mm Hg + 2/3 * 80.0 mm Hg = 97.33333 mm Hg.
Hence, the patient's mean arterial pressure is 97.33333 mm Hg."
1830,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5004014-1,Extracted,"A 57-year-old male with a known past medical history of squamous cell carcinoma of the oropharynx T2N0 on radiation therapy, chronic alcohol abuse, ulcerative colitis, and chronic obstructive pulmonary disease presented to the emergency department with 3 episodes of syncope and decreased oral intake over the week prior to presentation. He also reported difficulty swallowing solid foods over the past month. His last alcohol intake was 2 days prior to admission. On initial evaluation, vitals were significant for heart rate of 122 beats/min, blood pressure of 100/70 mmHg, respiratory rate of 20/min, and temperature of 37°C. Physical examination revealed a dry oral mucosa and decreased skin turgor. Laboratory studies were remarkable for sodium level of 126 mEq/L, potassium of 4.3 mEq/L, chloride of 86 mEq/L, bicarbonate of 28 mEq/L, BUN of 33 mg/dL, and creatinine of 4.2 mEq/L with a baseline of 0.6 mEq/L, platelets of 124,000/mm3, AST of 83 IU/L, ALT of 62 IU/L, ALP of 129 IU/L, and bilirubin of 1.9 mg/dL. Ammonia and albumin levels were noted to be within the normal range. Initial computerized tomography (CT) of the head was negative for acute intracranial process. The patient was started on IV fluids and admitted for further management.
Over the next few days, the patient's hydration status improved and his appetite increased. His creatinine trended down and his sodium level increased to 130 mEq/L. On fourth day of admission, the patient was noted to be combative towards the medical staff. He also started showing signs of alcohol withdrawal with tachycardia, diaphoresis, tremors, anxiety, and confusion. Examination revealed progressively worsening abdominal distention. Sodium levels rose steadily to 140 mEq/L over the next four days. On the eighth day of admission, intravenous (IV) fluids were changed to D5W in light of the increasing sodium level. A CT scan of the abdomen was obtained for the increasing abdominal distention, which revealed dilatation of the small bowel (see ) extending from the proximal jejunum to the distal ileum as well as marked dilatation of the cecum extending to the proximal descending colon, suggestive of adynamic ileus. Cirrhosis of the liver and recto sigmoid diverticula were also noted. A nasogastric (NG) tube was placed and put to wall suction. Flexible sigmoidoscopy was performed but the scope had to be withdrawn prematurely due to the risk of perforation of diverticuli. He continued to be agitated and confused, requiring frequent doses of lorazepam to control his symptoms. On days 9 and 10, patient's sodium level increased steeply from 142 mEq/L to 151 and 159 mEq/L, respectively. On day 12, the patient had decreased response to verbal and physical stimuli. It was noted at this time that the patient was no longer on lorazepam. Ongoing free water losses from diarrhea, NG suction, and extensive third spacing into the bowel delayed the rapid reversal of hypernatremia despite aggressive IV fluid hydration. He became increasingly lethargic and developed worsening dysarthria and dysphagia. Neurological exam revealed disconjugate gaze with exotropia, flaccid quadriparesis, and absent deep tendon reflexes. Magnetic resonance imaging (MRI) of the brain (see Figures and ) demonstrated increased T2 and flair signals in the central basis pontis consistent with central pontine myelinolysis.
On the 13th day of the hospital course, the patient started developing respiratory distress with tachypnea into the 30 s; examination revealed rapid shallow breathing and use of accessory muscles. CT scan of the chest showed significant debris in the right main stem bronchus along with collapse of the right lower lobe consistent with aspiration pneumonitis (see ). Per patient's family's wishes, comfort measures were initiated and patient passed away later that day.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [100.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 70.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1831,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8387066-2,Extracted,"This 43-year-old woman had a spontaneous vaginal delivery at term, 4 years prior, and an abortion at 6 weeks gestation, 14 years prior. She also had a history of gestational diabetes mellitus, a cholecystectomy (8 years prior) and mitral valve prolapse with mitral regurgitation. She had asthma, first diagnosed at age 5, but had not required medication since 10 months prior (when she had pneumonia). The patient conceived by in vitro fertilization. Transabdominal ultrasound 13.1 weeks after conception showed a 15.1week intrauterine gestation, with an echogenic intracardiac focus in the fetal left ventricle, and an anterior, low-lying placenta; amniocentesis revealed a normal male karyotype and an alpha fetoprotein level of 17.63 mcg/mL (0.98 MoM). The patient had gestational diabetes mellitus diagnosed at 33 weeks gestation.
At 36-4/7 weeks gestation, the patient presented at 23:10 to an urban hospital emergency department in the Midwest USA with an exacerbation of asthma. She had worsening dyspnea for approximately one week, associated with sharp back pain, a cough with deep breathing, and an episode of syncope with a fall. She had taken no medication for this until the day before, when she started using her inhalers. On examination, her temperature was 35.7o C, heart rate 100/minute, blood pressure 134/83 mm Hg, respirations 20/minute and saturation 93% on room air. She had shallow respirations, but no wheezing. Her saturation was 96% on supplemental oxygen at 1 L/minute and 98% on 5 L/minute by nasal cannula. She was given a combination albuterol and ipratropium treatment. She was discharged at 02:45 with combination fluticasone and salmeterol inhaler and albuterol inhaler. Over the course of the day, her dyspnea worsened.
At 36-6/7 weeks gestation, she returned to the emergency department at 00:40, about 22 hours after her discharge. Her temperature was 35.4o C, pulse 115/minute, blood pressure 112/84 mm Hg, respiratory rate 24/minute and oxygen saturation 94% on room air. She had diffuse pulmonary crackles and mild extremity edema. Her oxygen saturation increased to 96% on supplemental oxygen at 5 L/minute by nasal cannula. At 01:25 she received nebulizer treatment with no improvement. The respiratory therapist heard pulmonary rales over the right middle and lower lobes, and little air movement. A fetal heart monitor was applied. At 02:00 her white blood cell count was 9,600/mm3 (neutrophils 75%, lymphocytes 19%, monocytes 5%), hemoglobin 13.9 g/dL, and platelets 160,000/mm3. Chest x-ray revealed a right lower lobe infiltrate. Fetal heart tracings showed a reactive pattern at a rate of 120-160/minute. At 02:50 the patient was comfortable and able to speak in complete sentences without dyspnea. At 04:00 she was transferred to an inpatient hospital unit.
At 04:30 the patient's temperature was 35.8o C, heart rate 105/minute, blood pressure 104/65 mm Hg, respirations 24/minute and saturation 97% on oxygen at 4 L/minute. She reported dyspnea and back pain she rated 10/10. She had decreased urine output. At 04:45 the patient complained of nausea. Her saturation was 98% on oxygen at 4 L/minute. A bladder catheter was placed. At 05:25 she received another nebulizer treatment with no improvement. She complained of dizziness. At 05:30 she complained of not feeling well, light-headedness and sweatiness. Her blood pressure was 79/62 mm Hg, with unchanged heart rate and respiratory rate. Her glucose was 137 mg/dl. She was given intravenous normal saline for her hypotension, a 500 ml bolus followed by 125 ml/hour. At 06:00 the patient was given azithromycin (500 mg intravenously) for suspected community-acquired pneumonia and she had dyspnea, nausea and a 50 ml emesis. Her temperature was 35o C, pulse 95/minute, blood pressure 90/50 mm Hg, respiratory rate 18/minute and saturation 98% on oxygen at 4 L/minute. She was anxious and diaphoretic. She had pulmonary crackles. She was given ondansetron. At 06:30 her pulse was 110/minute, blood pressure 87/62 mm Hg and respirations 30/minute. At 07:30 the patient was upset, complaining of back pain and discomfort from having a bladder catheter. She said the antibiotic ""made me feel terrible; get me out of here."" She was refusing further antibiotic therapy. At 08:00 she had back and lower abdominal pain. Her heart rate was 106/minute, blood pressure 86/72 mm Hg and saturation 92% on oxygen at 4 L/minute. Her lips were ""dusky"". Her abdomen was non-tender. Her supplemental oxygen was increased. Shortly after 08:00 the nurse was unable to locate fetal heart tones. At 08:30 intrauterine fetal death was confirmed by ultrasound examination. When informed of this, the patient was upset. Her abdomen was non-tender. She requested removal of her bladder catheter so she could go to the bathroom ""normally"". She ambulated to the bathroom, off supplemental oxygen without difficulty, but shortly following this, a nurse was unable to draw blood for blood counts, type and cross-match, and the patient's blood pressure was found to be in the 70s systolic. She was given another 500 ml bolus of normal saline. Over the next 30-45 minutes, the patient had progressive back and lower abdominal pain. She thought she was having uterine contractions. Her abdomen was moderately firm. At 09:00 she was given ceftriaxone (1 gram intravenously). The patient was alert, oriented and talkative, but her skin was becoming cool, and repeated attempts to draw blood and obtain blood pressure by Doppler were unsuccessful.
At 09:25 the patient was transferred to an ICU, where she had dyspnea. She was pale and lethargic, with cold extremities, mottled skin, and fundal tenderness. Bilateral femoral catheters were placed, and aggressive fluid resuscitation started. At 09:30 her temperature was 34.6o C, pulse 106/minute, blood pressure 76 mm Hg systolic and respirations 34/minute. At 10:00, her hemoglobin was 13.4 g/dL, platelets 154,000/mm3, INR 0.97, PTT 25.6 seconds and fibrinogen 433 mg/dL. At 10:10 her temperature was 34.5o C, pulse 102/minute, blood pressure 85/46 mm Hg, respiratory rate 36/minute and oxygen saturation 95% on 100% oxygen by non-rebreather mask. She had decreased air entry bilaterally, shallow breathing and pulmonary crackles over the right lower lobe. She developed respiratory distress and her saturation began to drop. The patient was intubated and, shortly following intubation, at 10:25, she became pulseless and cardiopulmonary resuscitation was started. At 10:45 an infusion of dopamine was started, and arterial blood showed pH 7.17, PCO2 59 mm Hg, PO2 25 mm Hg and bicarbonate 20.7 mEq/L. At 10:55 the patient's white blood cell count was 9,600/mm3 (neutrophils 80%, lymphocytes 15%, monocytes 3%, bands 2%), hemoglobin 13.6 g/dL, platelets 61,000/mm3, INR 1.58, PTT 32.9 seconds and fibrinogen 216 mg/dL. After thirty minutes of resuscitation, the patient's abdomen was tense and fluids would not flow through the femoral lines. The membranes were ruptured, releasing a large amount of bloody fluid.
Cesarean section was performed at 11:00, revealing approximately one liter of clotted blood behind the placenta, and placental abruption was diagnosed. The stillborn fetus was delivered with placenta immediately following. Epinephrine infusion was started at 11:10. The patient continued to have heavy vaginal bleeding, with estimated blood loss of 2 liters. She received 10 units of red blood cells and 4 units of fresh frozen plasma in addition to 5 liters of normal saline. Attempted resuscitation was halted and death pronounced at 11:25.
Autopsy demonstrated numerous small pulmonary blood vessels containing aggregates of platelets, lipid vacuoles, aggregates of neutrophils, occasional cytokeratin-positive cells, rare condensed fibrin emboli, three probable syncytiotrophoblasts (one cytokeratin positive on immunohistochemical stain), and a fragment of calcified material. Both lungs had red, congested and edematous parenchyma. The left lung weighed 515 grams and the right lung 600 grams. Microscopic examination demonstrated moderate acute pneumonia in right middle and lower lobes with abundant fibrin exudate, and foci of very early acute pneumonia in left upper and lower lobes and right upper lobe with abundant fibrin exudate. There were serous pleural effusions, 300 ml left, 500 ml right.
The heart showed acute cor pulmonale with moderate right ventricular dilatation. There was also moderate dilatation of the left atrium and mitral valve prolapse with moderate redundant tissue, particularly of the posterior leaflet. Microscopic examination of mitral valve showed moderate fibrous and myxoid expansion. The liver showed severe passive congestion in the periphery. There were numerous sites of hemorrhage in lungs, heart, thoracic aorta, liver, hypopharynx, duodenum, stomach, left ovary, left renal pelvis and bladder.
Approximately 20% of the placenta was detached from the uterus, supporting the diagnosis of placental abruption. The uterine placental site had an attached fragment of placenta including villi and calcified material. The placenta was thin and small, <10th percentile for gestational age.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [70.0, 's mm hg'], 'Diastolic Blood Pressure': [62.0, 'mm hg']}",64.66667,61.43334,67.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 70.0 mm Hg + 2/3 * 62.0 mm Hg = 64.66667 mm Hg.
Hence, the patient's mean arterial pressure is 64.66667 mm Hg."
1832,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7557616-1,Extracted,"A 65-year-old male patient was admitted to our hospital with chest pain in the coronary intensive care unit. Upon the detection of instable angina pectoris, 60 mg low-molecular-weight heparin (LMWH) and 300 mg clopidogrel were initiated. The patient was on antihypertensive treatment for 15 years due to essential hypertension and he also used acetylsalicylic acid 100 mg/day. The patient did not have any a recent head or spinal trauma and surgical treatment, and he did not smoke.
He experienced sudden-onset severe neck pain and occipital headache on the third day of ACS treatment and felt muscle weakness and numbness in bilateral upper and lower extremities about 24 h after the onset of pain. On his physical examination, the patient was alert, orientated, and afebrile with a blood pressure of 140/90 mmHg. The muscle strength of upper extremities was 2/5 proximally and 1/5 distally, while that of the lower extremities was 0/5 proximally and distally. There was anesthesia below the C4 dermatome. Also, no deep tendon reflex could be elicited. The rectal examination revealed reduced anal sphincter tone and anesthesia in the perineal region. Routine laboratory and coagulation parameters (prothrombin time and activated partial thromboplastin time, and the international normalized ratio) were within normal limits. Neurology and neurosurgery consultations were requested, and urgent spinal magnetic resonance imaging (MRI) was performed. The MRI showed a space occupying formation extending from the level of C4 to T1 in the cervical spine which did not cause abnormal signal changes in the spinal cord and which was isointense in the T1-weighted images and heterogeneous signal intensity in the T2-weighted images. Spinal cord injury was assessed as Grade A complete injury according to the American Spinal Injury Association (ASIA) Impairment Scale. The patient underwent emergency decompressive laminectomy and hematoma evacuation with the diagnosis of SSEH approximately 40 h after the onset of symptoms. On the postoperative Day 1, no neurological recovery was noted, while the muscle strength of the lower extremities was 1/5 after two weeks. The range of motion exercises for upper and lower extremities, muscle strength enhance training, seat balancing training, transfer training (from the bed to a wheelchair), and respiratory function training were given to the patient as the early rehabilitation program. Also, clean intermittent self-catheterization was initiated for him in whom urinary retention persisted. After 60 sessions of rehabilitation program, neurological recovery was achieved in the upper (proximal 3/5, distal 1/5) and lower (proximal 2/5, distal 1/5) extremities. A written informed consent was obtained from the patient.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1833,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-55,Extracted,"A 40-year-old woman presents to her primary care physician with a 5-month history of worsening bladder discomfort. Her discomfort is relieved by voiding. She voids 10–15 times per day and wakes up 2–3 times per night to void. She has not had any involuntary loss of urine. She has tried cutting down on fluids and taking NSAIDs to reduce the discomfort with minimal relief. Her past medical history is significant for bipolar disorder. She is sexually active with her husband but reports that intercourse has recently become painful. Current medications include lithium. Her temperature is 37°C (98.6°F), pulse is 65/min, and blood pressure is 110/80 mm Hg. Examination shows tenderness to palpation of her suprapubic region. Urinalysis shows:
Color clear
pH 6.7
Specific gravity 1.010
Protein 1+
Glucose negative
Ketones negative
Blood negative
Nitrite negative
Leukocyte esterase negative
WBC 0/hpf
Squamous epithelial cells 2/hpf
Bacteria None
A pelvic ultrasound shows a postvoid residual urine is 25 mL. A cystoscopy shows a normal urethra and normal bladder mucosa.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 80.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1834,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6218792-1,Extracted,"An 85-year-old man visited our hospital for treatment of sustained ventricular tachycardia (VT), which caused an unstable hemodynamic state. His medical history was significant for acute myocardial infarction (AMI) 2 weeks prior, and a drug-eluting stent was implanted in the left main trunk. On admission, the patient was asymptomatic. His vital signs were as follows: blood pressure, 144/78 mm Hg; pulse rate, 80 beats/min; respiratory rate, 16 breaths/min. His oxygen saturation was 99% in room air, whereas his laboratory test showed the following results: sodium, 140 mmol/L; potassium, 4.5 mmol/L; creatine kinase, 28 U/L; creatine kinase-muscle/brain, 9 U/L. Electrocardiography showed sinus rhythm with T-wave inversions in the I, aVL, and V1-V6 leads. Chest radiography revealed mild widening of the cardiac silhouette and right pleural effusion (). After the admission, he presented with sustained VT. Intravenous amiodarone was administered and CPR was performed, but amiodarone was ineffective in terminating VT. Hence, emergency coronary angiography (CAG) was performed for suspected myocardial ischemia. Intra-aortic balloon pumping and percutaneous cardiopulmonary support were established before emergency CAG because of his unstable hemodynamic state. CAG revealed 90% stenosis at the middle segment of the left descending artery, thus, ad hoc percutaneous coronary intervention (PCI) was performed. During the PCI, his serum hemoglobin level decreased from 11.1 to 3.0 g/dL. Chest radiography revealed pleural effusion in the right lung, which was not present on admission. Noncontrast CT was performed after emergency PCI, which revealed right hemothorax without any chest wall fractures. A right chest tube was placed, and 1.8 L of pleural effusion was drained over 6 hours. Despite blood transfusion of 12 units of red blood cells and 12 units of fresh frozen plasma, his serum hemoglobin level decreased, suggesting persistent blood loss. To identify the source of the bleeding, contrast CT was performed, which revealed small anterior mediastinal hematoma and bloody pleural effusion (). Three-dimensional contrast CT demonstrated an extravasation at the branch of the right IMA (Figures and ). The patient's deteriorating hemodynamic condition precluded thoracotomy or embolization to stop the bleeding. He subsequently died on the next day of hospitalization.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [144.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 144.0 mm Hg + 2/3 * 78.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1835,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2783112-1,Extracted,"The patient was a 57-year-old Caucasian male. He was an ex-smoker and reported normal alcohol consumption. His medical history included coronary artery disease, hypertension and gastrointestinal reflux. He had been diagnosed with type 2 diabetes mellitus back in 1996. At the time he got the diabetes diagnosis, he reported that his stools for many years had tended to be a little loose. However, he described it as a minor problem, the main annoyance being the passing of loose stools once every morning. Initially he was treated with glipizide (a SU drug). Metformin was added in 1999. The dose had been gradually increased, and since 2004 he had been taking 1 g with breakfast and 0.5-1 g with supper. He had no known complications to his diabetes.
He was admitted to the Medical Ambulatory in March 2008 because of carpal and calf spasms, pain (especially in the legs), paresthesias of the lips, hands and feet, and malaise. His GP had diagnosed hypomagnesemia, hypocalcemia and hypokalemia. When seen in the Medical Ambulatory, he reported a substantial diarrhoea problem which had lasted a long time. He did not recall exactly when the diarrhoea had become a problem, but at least he remembered that it was after the introduction of metformin in 1999. When asked about any relation between the diarrhoea and the introduction of metformin or increase of metformin dose, he had not noticed any such relation. The last months before his admission in March 2008 his diarrhoea had worsened even more. These months he had been passing loose stools on average four times a day. Sometimes he had observed some mucilage in the stools. His additional medication included glimepirid (a SU drug), metoprolol, isosorbide mononitrate, ramipril, atorvastatin, clopidogrel, aspirin, and lansoprazol.
On examination his blood pressure was 192/100 mmHg. Sodium was 143 mmol/l (reference range 137-145), potassium 3.4 mmol/l (3.6-4.6), calcium 1.97 mmol/l (2.15-2.51), magnesium 0.33 mmol/l (0.71-0.94), albumin 45 g/l (36-45), creatinine 80 μmol/l (62-133), glucose 9.9 mmol/l (4.0-6.0), HbA1c 7.1% (4.0-6.0), Vitamin B12 272 pmol/l (113-603), free thyroxin 17.2 nmol/l (9.0- 19.0), TSH 2.32 mU/l (0.20- 4.5), PTH 2.3 pmol/l (1.3-7.6), 25-OH-Vitamin D 67 nmol/l (20-100), 1.25-(OH)2-Vitamin D 113 pmol/l (48-160), and anti-tissue transglutaminase antibodies IgA was negative. Thus, the blood tests showed hypomagnesemia, hypocalcaemia and hypokalemia.
It was concluded that he suffered from severe hypomagnesemia, most likely due to diarrhoea caused by metformin. Therefore, metformin was discontinued and daily intake of magnesium and potassium was instituted. He reported that the consistency of his stools improved markedly in the course of a few days after the discontinuation of metformin.
At a follow-up consultation three weeks later, magnesium was 0.80 mmol/l, calcium 2.49 mmol/l, albumin 43 g/l and potassium 4.4 mmol/l. However, his blood glucose was found to be unacceptably high. The glimepiride dose was increased, and he also started to take sitagliptin. In addition, he was suggested to try a reduced metformin dose, 0.5-1.0 g daily. When seen again in August 2008, he was still not feeling well. Because of diarrhoea he had stopped taking metformin a few days after the reinstitution of the drug, and again the stools' consistency had improved rapidly. His plasma glucose was 10-20 mmol/l. Therefore, the oral antidiabetic drugs were discontinued and a two-dose NPH insulin regime was instituted. At a follow-up consultation in December 2008 his diabetes was well regulated, serum electrolyte levels were within the normal range and loose stools now was a minor problem. About two months before this consultation the patient, without consulting any physician, had discontinued the magnesium and potassium tablets.
When seen last time in September 2009, he still was in good shape and with only minor bowel problems. His blood tests were all within the normal range: magnesium 0.99 mmol/l, sodium 142 mmol/l, potassium 4.1 mmol/l, calcium 2.40 mmol/l, creatinine 102 mmol/l, and albumin 45 g/l.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [100.0, 'mm hg'], 'Systolic Blood Pressure': [192.0, 'mm hg']}",130.66667,124.13334,137.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 192.0 mm Hg + 2/3 * 100.0 mm Hg = 130.66667 mm Hg.
Hence, the patient's mean arterial pressure is 130.66667 mm Hg."
1836,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6898921-1,Extracted,"A 39-year-old West African man who was a teacher was referred for weight loss and recent abdominal pain. He presented the following symptoms: generalized episodic abdominal pain of progressive onset that was relieved by diarrheal stools occasionally associated with rectal bleeding over the past 2 months. The patient had recurrent skin lesions of different ages on the lower limbs that had started to appear 6 months before the onset of abdominal pain. These lesions began with an inflammatory nodule that resolved within a few days with a pustule that ruptured quickly and spontaneously gave way to an ulceration whose diameter quickly reached several centimeters. The healing was spontaneous and left hypertrophic stigmata.
The patient was not a drinker or smoker and was of middle socioeconomic status. He had no personal or family medical history, especially cancer or blood or inflammatory disease. Upon admission, he had a body temperature of 37.4 °C, a pulse rate of 81 beats per minute, and a blood pressure of 110/85 mmHg. His physical examination revealed a moderate general condition, moderately colored conjunctiva, pain in the left iliac fossa, and hypogastrium without a palpated mass. The result of his rectal examination was normal. His dermatological examination demostrated objectified large, circumferential scarring lesions on both lower limbs and progressive ulceration on the posterior side of the left thigh (Fig. ). His Glasgow Coma Scale score was 15; he had no sensory or motor deficit, and the result of examination of his cranial nerves was normal. Biopsy of the progressive lesion showed a suppurative and inflammatory central zone with ulceration and neutrophil infiltration. The results of cytobacteriological (aerobic and anaerobic culture) and fungal studies were negative.
We concluded that these skin lesions were PG. Colonoscopy for the exploration of abdominal symptomatology revealed a necrotic and hemorrhagic budding lesion 20 cm from the anal margin, confirmed by contrast enema, which showed a narrowing of the lumen of the rectosigmoid junction. Biopsies taken during colonoscopy revealed an adenocarcinoma. An abdominopelvic computed tomographic scan revealed thickening of the rectosigmoid without associated metastases (Fig. ). The results of preoperative checkup (rhesus grouping; complete blood count; prothrombin time; activated cephalin time; tests for uremia, creatinemia, and glycemia; chest x-ray; and electrocardiogram) and liver checkup (serum glutamic-oxaloacetic transaminase (SGOT), serum glutamate-pyruvate transaminase (SGPT), alkaline phosphatase, gamma glutamyltransferase (GGT), total and direct bilirubin) were normal. A median subumbilical laparotomy confirmed a stenosing tumor of the rectosigmoid junction. A rectosigmoid carcinologic excision was performed with immediate colorectal anastomosis. Regular bandages were placed on the PG lesions. Postoperative treatment was initiated with ciprofloxacin 500 mg and metronidazole 500 mg twice daily for 10 days and tramadol 50 mg three times daily for 5 days. The anatomopathological examination of the surgical specimen (using hematoxylin and eosin-stained sections) confirmed the diagnosis of adenocarcinoma of the rectosigmoid junction (Fig. ). The tumor was classified as pT2N0M0 with negative excision margins. There were no postoperative complications, and the patient was discharged on postoperative day 7. No adjuvant treatment was performed. Thirteen months after the operation, all the skin lesions had healed without reemergence of new lesions, and the patient did not have metastases or tumor recurrence.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [85.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 85.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1837,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4744615-1,Extracted,"A 52-year-old woman was presented to the emergency department with complaint of unspecific abdominal pain and a 2-week hypermenorrhea. The patient did not have nausea, vomiting, fever, or any other symptoms. She had a history of diabetes mellitus for which she was under medical treatment, and a surgical history of a cesarean section 20 years ago. On arrival, she was vitally stable. Her blood pressure was 120/68 mmHg, with a heart rate of 82 beats/minute and a respiratory rate of 20 breaths/minute. She was afebrile. Her abdominal examination revealed a lower segment cesarean section scar, lower abdominal fullness and a round mobile palpable mass in right lower quadrant. Bowel sounds were normal. Physical examination of all other parts did not show any positive findings. Complete blood cell count and biochemistry profiles were requested and all were reported in normal range. Carcinoembryonic antigen (CEA) as well as alpha-fetoprotein were also normal. The patient underwent abdominopelvic computed tomography (CT), the results of which are shown in and .
What is your diagnosis?
Diagnosis:
Abdominopelvic CT revealed an 8×7×6 cm round well-defined soft tissue mass containing cystic and solid components in the lower right abdominal area, suggesting a gynecologic tumor. A surgical resection of the tumor was performed, and the macroscopic pathological study revealed a gossypiboma inside the mass with a foreign body reaction.
Case fate:
With concern of right ovarian carcinoma, she underwent an exploratory laparotomy. An encapsulated sponge surrounded by omentum was removed. The patient had an uneventful postoperative recovery and was discharged two days later.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [68.0, 'mm hg']}",85.33333,81.06666,89.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 68.0 mm Hg = 85.33333 mm Hg.
Hence, the patient's mean arterial pressure is 85.33333 mm Hg."
1838,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5052756-1,Extracted,"A 57-year-old gentleman presented to hospital with a widespread itchy, rash. He had a three-day history of watery diarrhoea up to six times a day, intermittent, crampy abdominal pain and fever. This illness developed a day after he had eaten crab cakes, which were out of date. On examination, he was dehydrated with dry mucous membranes. Abdomen was mostly tender in the umbilical and epigastric region but there were no signs of peritonism. The rash was well defined with circular target lesions on his upper and lower limbs. The remainder of physical examination was unremarkable. Vital observations on admission were as follows: temperature of 38.2℃, pulse rate of 110, blood pressure 102/68, respiratory rate of 22 and oxygen saturations of 96% on room air.
Initial blood tests revealed normal full blood count (Hb 147 gd/L, WBC 5.3 × 109/L, platelets 142 × 109/L), lipase (10 U/L) and electrolytes (sodium 136 mmol/L, potassium 3.8 mmol/L, magnesium 0.81 mmol/L, phosphate 1.07 mmol/L, adjusted calcium 2.22 mmol/L). However C-reactive protein was raised (83 mg/L), there was acute kidney injury (urea 13.4 mmol/L, creatinine 120 µmol/L, eGFR 34 mls/min/1.73 m2) and liver function tests showed a mixed hepatitic and cholestatic picture (Bilirubin 20 mmol/L, AST 64 U/L, ALT 111 U/L, ALP 155 U/L, GGT 103 U/L and albumin 25). Urinalysis and chest X-ray were unremarkable. He received IV fluids and empirical IV Piperacillin/Tazobactam for sepsis. Stool samples were sent as work up of acute diarrhoea and campylobacter species was isolated. The stool samples were negative for Giardia, Cryptosporidium, Salmonella, Shigella and E. coli. Clostridium difficile toxin was not found in any of the stool samples. Blood cultures were negative. IV antibiotics were stopped upon discussion with microbiology.
His diarrhoea, abdominal pain and fever resolved over the four days following admission. Renal function and liver function also improved. However, the rash had spread to his chest, neck, back and hands ( and ()). Dermatology opinion was sought and erythema multiforme major was diagnosed. Histology of a skin biopsy demonstrated a superficial perivascular chronic inflammatory infiltrate in the dermis with features of an interface dermatitis, i.e. basal vacuolation of the epidermis with lymphocytes involving the basal layer. This is consistent with erythema multiforme (). He was treated with Chlorphenamine and topical emollient cream. Over the following five days, the rash slowly resolved.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [102.0, 'mm hg'], 'Diastolic Blood Pressure': [68.0, 'mm hg']}",79.33333,75.36666,83.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 102.0 mm Hg + 2/3 * 68.0 mm Hg = 79.33333 mm Hg.
Hence, the patient's mean arterial pressure is 79.33333 mm Hg."
1839,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5385225-1,Extracted,"A 24-year-old man with a protein-losing gastroenteropathy due to an intestinal lymphangiectasia was treated with glucocorticoids (prednisolone, 7.5 mg/day) and developed low-grade fevers 7 months before admission. He did not have any remarkable life histories. Five months before admission, the man complained of headaches, fatigue, and a hearing abnormality. Then, he experienced nausea, diarrhea, and drowsiness for 6 days and subsequently sought evaluation at our hospital. The physical examination at the time of admission revealed that he was slow to respond (Japan Coma Scale 1-1). The following measurements were obtained: height, 161.2 cm; weight, 51.0 kg; BMI, 19.6 kg/m2; blood pressure, 119/78 mmHg; heart rate, 62 bpm; and body temperature, 37.4°C. The remainder of the examination findings were normal, without any signs of meningitis.
The initial laboratory data showed a white blood cell count of 11700/μL, with 87.0% neutrophils (86% segmented and 1% band neutrophils), 2.0% lymphocytes, 10%monocytes, 0% eosinophils, 1% metamyelocytes, hemoglobin = 15.7 g/dL, and a platelet count of 157,000/μL. The serum C-reactive protein level was slightly elevated (0.80 mg/dL). Although the serum sodium level was slightly decreased (130 mEq/L), the potassium (4.6 mEq/L), chloride (97 mEq/L), creatinine (0.59 mg/dL), fasting glucose (85 mEq/L), and HbA1c (5.1%) concentrations were normal.
An abdominal computed tomography (CT) showed bilateral adrenal enlargement (right, 10.0 × 20.0 mm; left, 29.0 × 29.0 mm). A retrospective analysis of the CT images revealed that the enlargement in the left adrenal gland developed 5 months before admission (), which coincided with the onset of fevers and headaches. Subsequently, the bilateral adrenal enlargement progressed (). The differential diagnosis of adrenal enlargement includes metastatic carcinoma, bilateral adrenal hyperplasia, tuberculosis, and fungal infections. A whole-body examination failed to find a primary malignant lesion. The QuantiFERON-TB test and HIV antibody titer were negative.Although there were no signs of meningeal irritation, a diagnostic lumbar puncture was performed. The cerebrospinal fluid revealed an increased white blood cell count (240/μL), a normal protein level, a decreased glucose level (0.10 g/l), and a positive cryptococcal antigen titer. The pathologic specimen showed the presence of yeast-like organisms, such as Cryptococcus spp. on Alcian blue staining, which was subsequently determined to be Cryptococcus neoformans.
Although the level of serum adrenocorticotropic hormone (ACTH) was elevated (131.3 pg/mL; normal range, 7.2–63.3 pg/mL) at the time of the diagnosis of cryptococcosis (), cortisol release in response to ACTH (Cortrosyn), which was evaluated 1 day after prednisolone cessation, was increased (). Oral prednisolone (7.5 mg/day) was then resumed as treatment for the protein-losing gastroenteropathy. The other endocrinological data of adrenal gland ruled out the possibility of pheochromocytoma and aldosterone-secreting tumors in this patient ().
Amphotericin B (250 mg/day) was initiated, followed by the addition of fluconazole (400 mg/day). The symptoms improved gradually after beginning antifungal treatment. Fluconazole alone was continued after discharge. After the initiation of antifungal treatment, the elevated ACTH levels were decreased and varied during the treatment (), suggesting a stressed condition with infection at the diagnosis and unstable absorption of prednisolone due to the protein-losing gastroenteropathy. Mild hyponatremia probably due to relative adrenal insufficiency was improved to the normal range (138 mEq/L) one month after the initiation of the antifungal treatment.
An abdominal CT, which was routinely obtained during follow-up, showed that the size of the adrenal glands decreased following antifungal therapy and became normal without any abnormal findings, including calcifications, 6 months after starting treatment ().",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [119.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",91.66667,87.08334,96.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 119.0 mm Hg + 2/3 * 78.0 mm Hg = 91.66667 mm Hg.
Hence, the patient's mean arterial pressure is 91.66667 mm Hg."
1840,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5292830-1,Extracted,"A 25-year-old male patient (63 kg, 180 cm) visited our hospital for an anal condyloma. Excisional biopsy under spinal anesthesia was scheduled. On preoperative examination, the blood test showed positive for HIV antibodies. Thus, a lymphocyte subset test was performed, and the patient was diagnosed with HIV based on the following results: CD4(+) T-cells 324/μl, CD4 14.2% (28.4–56.4), and CD4/CD8 0.2 (0.9 − 3.6). There was no record of particular significance in the patient's past medical history. His blood test showed following: Hemoglobin 15.8 g/dl, hematocrit 45.7%, and platelet 217,000 cell/mm3. The patient's blood coagulation was also in the normal range with a prothrombin time (PT) of 13.5 s (INR 1.3) and an activated partial thromboplastin time of 35.7 s. His chest X-ray and electrocardiograph findings were also normal.
Without premedication, on arriving at the operating room, the patient's vital signs read as follows: Blood pressure (BP) 147/66 mmHg, pulse 70 beats/min, and O2 saturation 100%.
Spinal anesthesia was performed in sitting position with midline approach at L3–4 space, using a 25-gauge, Quincke (Hakko Co. Ltd, Chikuma, Japan) needle. The drug used 8 mg of 0.5% bupivacaine (Marcaine®, AstraZeneca) was administered successfully in the first attempt. His vital signs were stable. The operation was concluded in 35 min without any abnormal findings. After 4 h, the patient started to experience a headache without nausea and vomiting in the general ward.
The symptom was not related to the position. A headache improved partially following bed rest and taking 650 mg of acetaminophen (Tylenol ER®). The patient was discharged 1 day after the surgery with no abnormal symptoms.
One day after the discharge, the patient experienced a headache with accompanying nausea and vomiting. The patient visited the emergency room after a headache had aggravated further. BP was 150/81 mmHg, and pulse was 95 beats/min at the time. There were no neurologic anomalies found during the physical exam. He was hospitalized at the neurology department for further evaluation and conservative management.
On the 1st day, the patient's headache did not improve despite fluid management, nonsteroidal anti-inflammatory drugs (NSAIDs), and bed rest. We performed an enhanced brain magnetic resonance imaging to identify the cause of a headache and found a small amount of SDH in the left occipital region and interhemispheric fissure [].
On the 2nd day, an epidural blood patch (EBP) was performed because the patient's symptoms still did not improve. A 20-gauge Tuohy needle (Portex®, Smiths Medical) was used to administer 10 ml of autologous blood through an L3–4 epidural space. After EBP, a headache (numeric rating scale, level 6) regardless of the patient's posture was continued. After that, a headache improved gradually following bed rest and hydration.
On the 7th day, a computed tomography scan was performed; the amount of SDH decreased, and there were no other abnormal organic findings that may have induced headache []. The patient was discharged because his headache was mitigated with no other neurologic symptoms.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [66.0, 'mm hg'], 'Systolic Blood Pressure': [150.0, 'mm hg']}",94,89.3,98.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 66.0 mm Hg = 94.0 mm Hg.
Hence, the patient's mean arterial pressure is 94.0 mm Hg."
1841,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5708079-1,Extracted,"A 20-year-old man with a developmental disorder collided with a steel tower while downhill skiing. The patient sustained a whole-body contusion and was airlifted to our hospital. Upon arrival, his blood pressure was 99/65 mmHg and heart rate was 87 bpm. His consciousness was lucid, and he complained of pain in the left upper arm and right thigh. Physical examination revealed subcutaneous emphysema and tenderness in the left anterior chest, although he did not complain of dyspnea. A chest X-ray showed a wide mediastinum, enlarged aortic knob, rightward deviation of the nasogastric tube, and a smudgy aortopulmonary window, which led us to suspect thoracic aorta injury (Fig. ). Contrast-enhanced computed tomography confirmed dissection in zone 3 to 4 of the thoracic aorta, a hematoma in the left supraclavicular fossa and mediastinum, and the presence of hemothorax (Fig. , ) without active bleeding. X-ray examination of the limbs and pelvis revealed fractures of left humeral head and femoral neck. Blood examination showed a slightly elevated white blood cell count and slightly elevated aspartate aminotransferase, lactate dehydrogenase, and creatine phosphokinase concentrations. The D-dimer concentration was 15.3 μg/mL. We chose conservative therapy for the acute aortic dissection because the patient was hemodynamically stable and the multiple fractures might have caused uncontrollable bleeding during heparinization for cardiopulmonary bypass. His blood pressure was strictly controlled at <120 mmHg by continuous intravenous administration of nicardipine and nitroglycerin. Eight days after admission, the fractures of the left humeral head and femoral neck were surgically repaired. We then surgically repaired the aortic dissection 42 days after admission. An upper-half sternotomy was performed until the fourth intercostal space was reached, and cardiopulmonary bypass was initiated with a 29-Fr right atrial cannula, a 10-Fr common carotid arterial cannula, and a 12-Fr axillary arterial cannula. After induction of moderate hypothermia at a rectal temperature of 28 °C, selective antegrade cerebral perfusion was begun. An open stent graft (J-Graft; Japan Lifeline, Tokyo, Japan) with a 21-mm diameter and 6-cm length was inserted via an aortotomy on the aortic arch just distal to the left subclavian artery during circulatory arrest. The proximal end of the stent was sutured to the aortic wall with 4–0 polypropylene by continuous suture (Fig. ). Then, the aortotomy was closed by continuous suture. The total operation time was 345 min, the cardiopulmonary bypass time was 192 min, and the arrest time was 53 min. The patient made steady progress postoperatively; he was weaned from the ventilator 3 h after the surgery. He began orthopedic rehabilitation on postoperative day 19. Computed tomography revealed no endovascular stenosis or endoleaks (Fig. ). He was discharged from the hospital on postoperative day 43 (Fig. ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [99.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",76.33333,72.51666,80.15,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 99.0 mm Hg + 2/3 * 65.0 mm Hg = 76.33333 mm Hg.
Hence, the patient's mean arterial pressure is 76.33333 mm Hg."
1842,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6984147-1,Extracted,"A 51-year-old man was admitted to our hospital in mid-April with a history of edema in the lower extremities since the beginning of April. Medical history included FRNS at 15 years of age that had been treated using PSL at an initial dosage of 1.0 mg/kg/day at the time of relapse. Steroid therapy had finished by 42 years of age, after which time complete remission was maintained. Since he had developed depression as a part of SIPS at 16 years of age, he had been regularly seeing a psychiatrist and had maintained control of psychiatric symptoms under a stable condition using fluvoxamine maleate acid at 300 mg/day.
On admission, body weight was 68.1 kg, representing a gain of about 10 kg to a higher than usual weight over the preceding 2 weeks. Blood pressure was also high, at 159/103 mm Hg. Major laboratory examinations on admission showed: white blood cells, 7,340/μL; blood hemoglobin, 13.7 g/dL; platelet count, 36.1 ×104/μL; partial thromboplastin time, 10.3 s; activated partial thromboplastin time, 23.0 s; D-dimer, 3.4 µg/mL; total protein, 4.3 g/dL; serum albumin, 1.5 g/dL; lactate dehydrogenase, 240 U/L; aspartate aminotransferase, 17 U/L; alanine aminotransferase, 7 U/L; low-density lipoprotein cholesterol, 326 mg/dL; triglyceride, 278 mg/dL; blood urea nitrogen, 12.9 mg/dL; serum creatinine, 0.85 mg/dL; sodium, 142 mEq/L; potassium, 4.2 mEq/L; chloride, 104 mEq/L; C-reactive protein, 0.03 mg/dL; glycated hemoglobin (HbA1c), 5.6%; C3, 167 mg/dL; C4, 40.3 mg/dL; hemolytic complement activity (CH50), 58 mg/dL; immunoglobulin (Ig)G, 949 mg/dL; IgA, 398 mg/dL; IgM, 52 mg/dL; antinuclear antibody, (–); and antineutrophil cytoplasmic antibodies, (–). Urinalysis revealed: proteinuria, 7.8 g/day; glycosuria, (–); occult blood, (–); and urinary protein selectivity, 0.20. Immunoelectrophoretic study showed no myeloma protein. Chest X-ray disclosed mild bilateral pleural effusion.
These findings suggested relapse of MCNS because of the high selective glomerular proteinuria, hypoalbuminemia, hyperlipidemia, and peripheral edema. We therefore performed percutaneous renal biopsy and obtained the following findings. Light microscopy revealed 29 glomeruli, none of which were globally or segmentally sclerotic. Glomeruli were nearly normal but showed up to mild mesangial proliferation (Fig. ). Immunofluorescent staining showed normal findings. However, electron microscopy showed diffuse effacement of the foot processes (Fig. ). Finally, we reached a definitive diagnosis of recurrent FRNS.
We started immunosuppressive therapy with PSL at an initial dosage of 0.3 mg/kg/day (20 mg/day) in combination with CsA at an initial dosage of 1.5 mg/kg/day (Fig. ). Standard immunosuppressive therapy for recurrent FRNS is PSL alone at an initial dosage of 1.0 mg/kg/day for a minimum of 4 weeks, but the history of depression as a part of SIPS necessitated a reduction in the dosage and duration of steroid therapy. On the other hand, CsA requires cautious use to avoid CsA-induced nephrotoxicity. To prevent CsA-induced nephropathy, maintaining the appropriate blood CsA concentration within a narrow therapeutic window appears essential. Monitoring of CsA was thus performed using concentrations at 2-h post-dose, with a target window of 600–900 ng/mL []. Complete remission of FRNS was achieved by 2 weeks after starting treatment, but SIPS recurred the day after remission. We thus promptly reduced the dosage of PSL (weekly reduction by 2.5–5 mg/day), and SIPS quickly showed improvements. The dosage of PSL was 5 mg/day as a maintenance dose at 5 weeks after the start of treatment, and complete remission was further maintained without relapse.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [159.0, 'mm hg'], 'Diastolic Blood Pressure': [103.0, 'mm hg']}",121.66667,115.58334,127.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 159.0 mm Hg + 2/3 * 103.0 mm Hg = 121.66667 mm Hg.
Hence, the patient's mean arterial pressure is 121.66667 mm Hg."
1843,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1853,Extracted,"A 29-year-old man comes to the physician for a routine health maintenance examination. He has no history of serious illness. His mother has hypertension and his father died of testicular cancer at the age of 51 years. He does not smoke or drink. He is sexually active and uses condoms consistently. He takes no medications. His immunization records are unavailable. He works as a financial consultant and will go on a business trip to Mexico City in 2 weeks. His temperature is 36.7°C (98.7° F), pulse is 78/min, and blood pressure is 122/78 mm Hg. Cardiopulmonary examination shows no abnormalities.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [122.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",92.66667,88.03334,97.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 122.0 mm Hg + 2/3 * 78.0 mm Hg = 92.66667 mm Hg.
Hence, the patient's mean arterial pressure is 92.66667 mm Hg."
1844,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-3390,Extracted,"A 70-year-old man comes to the physician because of a 6-month-history of worsening shortness of breath on exertion and bouts of coughing while sleeping. He has hypertension, hyperlipidemia, and type 2 diabetes mellitus. Current medications include lisinopril, simvastatin, and insulin. The patient appears tired but in no acute distress. His pulse is 70/min, blood pressure is 140/85 mm Hg, and respirations are 25/min. He has crackles over both lower lung fields and 2+ pitting edema of the lower extremities. An ECG shows T wave inversions in leads V1 to V4.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 85.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
1845,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6309395-1,Extracted,"A female patient aged 65 years with Type 2 diabetes mellitus, hypothyroidism, and hypertension came to our center with edema and was detected to have 4+ albumin on urine dipstick and proteinuria of 3.8 g/day. Her serum creatinine was 1.1 mg/dl and serum albumin was 2.5 g/dl. One year ago, she was diagnosed elsewhere as minimal change disease (MCD) following a kidney biopsy, for which she was given oral prednisone, which had resulted in partial remission. At our center, she was reinitiated on 1 mg/kg/day of prednisone and had partial remission at 12 weeks to 1.2 g/day. However, when we started tapering her steroids, her proteinuria increased to nephrotic range. She continued to take thyroid replacement therapy. She also complained of anorexia, weight loss, and fever. Secondary workup was redone, and her viral markers, antinuclear antibody serology, serum protein electrophoresis, and stool occult blood were all negative. She had pallor, blood pressure was 120/80 mmHg, heart rate was 97 bpm, and body mass index was 17 kg/m2. The systemic examination was otherwise unremarkable. She had no costovertebral angle tenderness. Urine analysis showed dipstick albuminuria of 3+ with many white blood cells, granular casts, and no hematuria. Other investigations showed hemoglobin of 9 g/dl, erythrocyte sedimentation rate of 126 mm at 1 h, serum creatinine of 0.7 mg/dl, and serum albumin of 3 g/dl. Urine culture showed no growth. We tapered her steroids to 5 mg/day and stopped it gradually.
We decided to rebiopsy her as she was steroid dependent and had some secondary characteristics. Incidentally, we found a 1.5 cm × 1.5 cm mass on the left kidney which was not reported previously. The renal biopsy revealed FSGS, tip variant [] with an area showing sheets of large polygonal cells with eosinophilic granular cytoplasm and small round-to-oval nucleus with distinct nucleolus, suggestive of RCC []. A positron emission tomography (PET) - computed tomography scan was performed which revealed a metabolically active mass in the left kidney [], left para-aortic nodal enlargement at the same level, and two small cavitary lesions in the right lower lobe of the lung []. The sputum examination was negative for malignancy and infection. A formal diagnosis of RCC was made, and laparoscopic left radical nephrectomy was done. The cut-section of the kidney revealed a circumscribed, tan-colored lesion with purulent necrotic material at the mid pole. The necrotic material involved the capsule of the kidney. Microscopic examination showed sheets of similar cells as described in the biopsy. At foci, loose clusters of macrophages with Michaelis–Gutmann bodies were seen []. Immunohistochemistry markers vimentin, CD-10, epithelial membrane antigen, and CD-68 were strongly positive. A diagnosis of eosinophilic variant of conventional RCC with incident malakoplakia was made. Repeat urinalysis 4 weeks post surgery was negative for dipstick protein and a protein creatinine ratio of 0.6 mg/g [].",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1846,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8412216-1,Extracted,"A 12-year-old female presented to our emergency with history of neck pain for seven days associated with gradual left side upper and lower limb weakness and numbness that affected her ability to walk. She denied any history of trauma, fever, loss of weight, urinary and bowel symptoms.
At the start of her symptoms, she was managed in a small community hospital as a case of meningitis. Brain and cervical CT scans were unremarkable. An empirical antibiotic was commenced with no improvement. As weakness progressed, patient was referred to the emergency department in our institute.
On presentation, the child was alert. She had an oral temperature of 37.3°C, 22/minute respiratory rate, 85/minute pulse rate, and 114/56 mmHg blood pressure and 97% oxygen saturation on room air. Her motor examination revealed intact motor power for right upper extremity (5/5), weakness of right lower extremity (3/5), and weakness of upper and lower left extremities (1/5). No sensory deficits were present. The patient’s deep tendon reflexes were only appreciated in the right lower limb. Her rectal tone and peri-anal sensation were intact. No other upper motor neuron lesion signs were detected.
Lab tests revealed white blood cell (WBC) = 8900/μl, platelet count = 457000/μl, hemoglobin = 12.8 mg/dl, sodium = 136 mEq/L, potassium = 4.4 mEq/L, erythrocyte sedimentation rate (ESR) = 11 millimeter/hour, prothrombin time (PT) = 14 seconds, partial thromboplastin time (PTT) = 33.2 seconds, and international normalized ratio (INR) = 1.01. An urgent MRI showed posterolateral space-occupying epidural lesion which appears isointense on T1-weighted and hyper-intense on T2-weighted images without enhancement of contrast in the post gadolinium T1 study causing a spinal cord compression (Figures , ).
The patient was hospitalized in our institute, an emergent posterior cervical decompression and evacuation of hematoma from C4-6 along with instrumented fusion from C3-6 with bone grafting. Our aim was to start with partial laminectomy but unfortunately it was not feasible to evacuate the hematoma due to blood clots and this finding lead to do full laminectomy from C4-C6. There was no obvious pus or vascular malformation identified. A tissue sample was taken for laboratory analysis and was sent for cultures and histopathology. Lateral mass screws were inserted from C3-6 bilaterally excluding C4 due to difficult entry. Homeostasis was maintained, bone graft applied over lateral mass and wound was closed over a drain. Intraoperative cultures did not grow any bacteria. The surgical pathology report revealed a histological feature consistent with an organizing hematoma.
The patient’s initial post-operative recovery was slow, and neurological status remained the same until day five, then the patient started to improve. The patient was kept in our hospital for rehabilitation for two weeks, upon discharge motor examination of left shoulder abduction and elbow flexion was 2/5 and for wrist/hand power was 4/5, motor examination of left lower extremity was 4/5, right upper and lower extremity motor examination was 5/5. The patient’s latest follow-up three months after surgery showed full neurological recovery.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [56.0, 'mm hg'], 'Systolic Blood Pressure': [114.0, 'mm hg']}",75.33333,71.56666,79.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 114.0 mm Hg + 2/3 * 56.0 mm Hg = 75.33333 mm Hg.
Hence, the patient's mean arterial pressure is 75.33333 mm Hg."
1847,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2754079-1,Extracted,"A 28-year-old Gravida 1 Caucasian female without significant medical history presented to her obstetrician for a routine office visit at 37 weeks gestation. Her examination revealed a blood pressure of 150/98 mmHg, 1+ pedal edema, and 1+ proteinuria. Further laboratories demonstrated a hemoglobin of 10.1 g/dL, platelet count 106 K/mm3, aspartate aminotransferase (AST) 290 IU/L, and lactate dehydrogenase (LDH) of 371 IU/L. She was presumptively diagnosed with HELLP syndrome and admitted for urgent Caesarean section.
While the surgery was uneventful, several hours later she developed acute lower back pain and hypotension. Repeat laboratory studies showed hemoglobin of 6.0 g/dL, platelet count 10 K/mm3, AST 1696 IU/L, alanine aminotransferase (ALT) 1253 IU/L, LDH 1262 IU/L. Abdominal ultrasound and CT demonstrated subcapsular and perihepatic hemorrhage with free intraabdominal blood. She was transfused red blood cells and platelets and treated with high doses of intravenous corticosteroids. Vasopressor agents were required to maintain adequate blood pressure and continuous renal replacement therapy (CRRT) was instituted for anuric renal failure.
Four days after delivery, her mental status deteriorated. She was endotracheally intubated and transferred to our institution for further management. Upon arrival, laboratory studies showed hemoglobin 8.4 g/dL, platelets 39 K/mm3, international normalized ratio 1.49, factor V 32%, blood type O, AST 1319 IU/L, ALT 763 IU/L, bilirubin 7.6 mg/dL, LDH 2215 IU/L, creatinine 4.1 mg/dL, and lactic acid 5.1 mmol/L. Serologic evaluation for other causes of liver disease and human immunodeficiency virus was negative. CMV IgM was negative and IgG was positive. There was no evidence of abdominal compartment syndrome. Head CT showed no apparent cerebral edema.
As there were no signs of improvement despite intensive therapy for fulminant hepatic failure, six days postpartum she was listed for liver transplantation as a United Network of Organ Sharing (UNOS) status 1. Over the next five days, her clinical course deteriorated further, necessitating 100% forced inspiratory oxygen and high dose vasopressors. Since no suitable ABO compatible livers had been offered, on the fifth day after listing (11 days postpartum), the decision was made to accept a blood type A1 liver.
Orthotopic liver transplantation was performed using the piggyback technique. The donor was 31 years old with a body mass index of 24 kg/m2. No gross fatty change was appreciated; liver biopsy was not performed. Cold ischemic time was six hours and 40 minutes and warm ischemic time was 23 minutes. Gross inspection of the native liver revealed obvious hepatic rupture, with the organ surrounded by hematoma (). Histology demonstrated massive hepatic necrosis, marked steatosis, widespread bile ductular proliferation, profound cholestasis, and necrotic vessels with intravascular thrombi (Figures and ).
She was treated with a renal-sparing immunosuppressive regimen including high dose intravenous immune globulin, thymoglobulin, methylprednisolone, mycophenolate Mofetil, and, beginning on day 7, tacrolimus. Daily plasma exchange was performed with blood group A antigen specific immunoadsorbent columns. Over the first seven days, serum transaminases and coagulation studies steadily improved, although she continued to require full ventilatory support and CRRT. Although somnolent, she became arousable to stimulation. Over the next 48 hours, however, the transaminases and bilirubin worsened. Liver biopsy demonstrated mild reperfusion injury, mild cholangitis, spotty apoptosis, but no cytopathic effect or endothelialitis. A C4d stain was negative. Direct antiglobulin and Coomb's tests were negative on three separate occasions. Biliary obstruction, vascular thromboses and infections, including cytomegalovirus, were excluded (). On postoperative day 11, she was comatose and laboratory studies showed bilirubin 14.5 mg/dL, AST 1747 IU/L, ALT 939 IU/L, INR 1.75. As a result of continued deterioration, she was relisted for transplantation with a MELD score of 35 on postoperative day 15.
An ABO compatible liver became available within 24 hours. Histology of the failed allograft demonstrated numerous areas of hemorrhagic necrosis; 30% of the left lobe was completely necrotic (Figures , , and ). On post-operative day 1, the patient became alert and oriented. Over the next several weeks she was extubated and CRRT was discontinued. She was discharged on post-operative day 32 (17 days after re-transplantation) with baseline mental status and normal serum liver tests and creatinine. She and her baby are alive and well thirty months after transplant.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [98.0, 'mm hg']}",115.33333,109.56666,121.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 98.0 mm Hg = 115.33333 mm Hg.
Hence, the patient's mean arterial pressure is 115.33333 mm Hg."
1848,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5439,Extracted,"A 55-year-old man presents to the emergency department for abdominal pain. The patient states that he has had abdominal pain for a while, but it became unbearable today and he is concerned. He also endorses a weight loss of 20 pounds this past month and complains of bulky and foul-smelling stools. The patient is homeless and is currently living by a local wash where he obtains his drinking water and cleans his clothes. He admits to recently eating raw meat that he found. The patient has a past medical history of alcohol abuse, malnutrition, Wernicke-Korsakoff psychosis, IV drug use, and a recent hospitalization for intoxication of unknown etiology. The patient is not taking any medications currently. His temperature is 99.1°F (37.3°C), blood pressure is 100/67 mmHg, pulse is 120/min, respirations are 11/min, and oxygen saturation is 98% on room air. On physical exam, the patient complains of epigastric tenderness. Cardiopulmonary exam is within normal limits. The patient is started on IV fluids, thiamine, folate, magnesium, and dextrose. Laboratory values are ordered as seen below:

Hemoglobin: 9.0 g/dL
Hematocrit: 25%
Leukocyte count: 5,500 cells/mm^3 with normal differential
Platelet count: 222,000/mm^3

Serum:
Na+: 137 mEq/L
Cl-: 102 mEq/L
K+: 4.1 mEq/L
HCO3-: 24 mEq/L
BUN: 24 mg/dL
Glucose: 68 mg/dL
Creatinine: 1.4 mg/dL
Ca2+: 9.8 mg/dL
Amylase: 22 U/L
Lipase: 22 U/L
Aspartate aminotransferase (AST): 58 U/L
Alanine aminotransferase (ALT): 18 U/L

A computed tomography (CT) scan is obtained as seen in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [67.0, 'mm hg'], 'Systolic Blood Pressure': [100.0, 'mm hg']}",78,74.1,81.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 67.0 mm Hg = 78.0 mm Hg.
Hence, the patient's mean arterial pressure is 78.0 mm Hg."
1849,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8522164-1,Extracted,"This professional female soccer player (32 years old, Northern European ethnicity, white) reported episodes of sharp pain in the Achilles tendon for about 2 years. During sudden change of direction and sprinting, she described sudden sharp pain in the midportion of the Achilles tendon; a symptom that initially rapidly settled within minutes, and she could continue to train and play. However, over time, her pain episodes increased in frequency and intensity. After a couple of days of rest, her pain would settle and she was able to return to full training. Eventually, she had to cease training and match play. Clinical examination showed a minimal thickening of the Achilles tendon midportion, with some tenderness localized to the medial and superficial side of the Achilles tendon, suggesting a diagnosis of midportion tendinopathy. Although treatment with eccentric training was trialed, these exercises caused more irritation in the affected region. As the condition failed to settle and the athlete could not properly train and play at desired level, she presented for an assessment at our clinic.
She was a non-smoker, did not abuse alcohol, was on no medication, and had no allergies. During initial clinical examination, blood pressure was 120/70 mmHg and resting pulse 60 bpm. Clinical findings were similar as found previously, with minor thickening in the Achilles midportion and tenderness localized to the medial and superficial side. Ultrasound examination showed a normal Achilles tendon measuring 5 mm in the midportion and with normal blood flow. Dynamic ultrasound scanning identified the plantaris tendon proximally. Following the plantaris distally to the region with localized tenderness, a wide and thick plantaris tendon was located on the superficial side of the Achilles midportion (Fig. ).
The suspected diagnosis was plantaris tendon-related pain, and the patient was surgically treated with local removal of the plantaris tendon performed under local anesthesia (5 ml Xylocaine + adrenaline) (Fig. ). The procedure took about 30 minutes. During surgery, the thick and wide plantaris tendon was found to be located on the superficial side of the Achilles tendon midportion (Fig. ). Between the tendons, there was a richly vascularized fatty layer that was scraped loose and removed [].
After surgery, there was rest with elevated foot overnight, and pain cure using paracetamol 500 mg, 2 tablets every 6 hours during the first 24 hours, if needed. There was a relatively quick (4–6 weeks) rehabilitation, with immediate weight bearing and range of motion (ROM) exercises, gradual increase in loading according to a specific program, and a return to running activities after 4 weeks. At follow-up at 8 weeks, the patient was in full training, and had not experienced any further episodes of sharp pain during change of direction and sprinting.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1850,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7505622-1,Extracted,"A 79-year-old African American male with a past medical history of hypertension presented with a static slurred speech that manifested with sudden onset two days prior to his hospital visit in late January of 2020. Following the slurred speech the next day he had chills, however, did not record his body temperature at home. He initially considered his symptoms as a minor flu, however, later decided to seek medical care due to nonresolving speech impairment. On presentation, he was febrile with an oral temperature of 100oF. His blood pressure was 124/74 mmHg. He endorsed compliance of his antihypertensive medication. He did not give a history of tobacco abuse, shortness of breath, cough, or intermittent palpitation. Physical examination showed an irregular pulse at the rate of 96 beats/min, respiratory rate at 18 breaths/min, and fine crackles in bilateral lower lungs on auscultation. His blood oxygen saturation level was 95%. Neurological examination was unremarkable except mild dysarthria. From his dysarthria assessment it was inferred that he had a low pitched phonation, impaired prosody for the sentence “ I am hungry”, lack of hypo- or hyper-nasality, decreased rate of repetitions (repeated the word “buttercup” only four times in five seconds), impaired articulation of the word “PresbyEpiscopal” and letters “P, B, F”, but with normal articulation of the words “la-la-la”. The initial National Institute of Health Stroke Scale (NIHSS) was one.
The real-time reverse transcription polymerase chain reaction (RT-PCR) analysis of SARS-CoV-2 infection tested positive from the nasopharyngeal swab. Pertinent initial laboratory findings showed a white blood cell count of 9.3 (4.5-11 K/μL), lymphocyte count of 0.6 (1.2-3.4 K/μL), and giant platelet morphology with normal count. He had mild elevated creatinine 2.4 (0.7-1.5 mg/dL) and procalcitonin levels 0.19 (0.02-0.10 ng/mL). His interleukin-6 92 (0-6.3 pg/mL), ferritin 505 (15-150 ng/L), and D-dimer 1201 (0-230 ng/mL) levels were abnormal. His cardiac troponin levels were normal, but the transaminase levels were elevated. The electrocardiogram showed an AF with a rapid ventricular response (Figure ).
The CHA2DS2-VASc score was four (calculated from his risk factors: age, hypertension, and stroke). A pulmonary CT scan showed bilateral peripheral ground glass opacities without pulmonary embolism (Figure ), and a brain MRI showed a punctate left frontal lobe infarction (Figure ).
A magnetic resonance angiogram of the head and neck showed no significant stenosis and transthoracic echocardiogram showed normal systolic function, moderate left atrial enlargement without thrombus or atrial septal defect (Figure ).
The patient was treated with IV unfractionized heparin infusion at the rate of 15 units/kg/hour and metoprolol tartrate 25 mg two times a day. The COVID-19-associated pneumonia was treated with oral azithromycin and hydroxychloroquine and was closely monitored in the ICU setting. Still, after a week, the patient got an increased respiratory distress as a consequence of a cytokine storm and required mechanical ventilation. The laboratory findings during this time showed highly abnormal interleukin-6 330 (0-6.3 pg/mL) level. The patient was treated with IV steroids and tocilizumab, but his condition further deteriorated, complicated by a multi-system organ failure, including septic shock, acute respiratory distress syndrome, acute myocardial injury (NT-proBNP 936 pg/mL), acute kidney injury, and dyselectrolemia. Despite aggressive supportive measures that included hemodialysis, the patient died two and half weeks after his admission.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [74.0, 'mm hg'], 'Systolic Blood Pressure': [124.0, 'mm hg']}",90.66667,86.13334,95.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 124.0 mm Hg + 2/3 * 74.0 mm Hg = 90.66667 mm Hg.
Hence, the patient's mean arterial pressure is 90.66667 mm Hg."
1851,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4762,Extracted,"A 17-year-old male presents to the clinic with complaints of a new-onset rash. He describes initially seeing a circular lesion on his abdomen three days prior and then many smaller new lesions occurring in the following days. The skin lesions are generally asymptomatic, although some are intermittently itchy. His past medical history is significant for sickle cell trait and seasonal allergies. His medications include folic acid and fexofenadine as needed. In addition, he had a recent episode of sore throat associated with congestion and rhinorrhea for which he took azithromycin. He does well in school and is on the wrestling team. His temperature is 99.1°F (37.3°C), pulse is 60/min, blood pressure is 110/64 mmHg, respirations are 13/min, oxygen saturation is 99% on room air. Physical exam is notable for a diffuse rash on the trunk (Figure A).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [64.0, 'mm hg']}",79.33333,75.36666,83.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 64.0 mm Hg = 79.33333 mm Hg.
Hence, the patient's mean arterial pressure is 79.33333 mm Hg."
1852,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3425291-1,Extracted,"A 40-year-old male Trackman by occupation in the Railways was posted for fasciotomy and drainage of right thigh and leg in emergency. His presenting complaint on admission was pain in the right knee since 10 days and swelling in the right lower limb and difficulty in walking since 4 days. He had a history of blunt trauma on right knee by metal trolley at workshop 10 days back. At the same time, he had developed diarrhoea as well, for which he took medicines and was relieved within 2–3 days. He had no history of any chronic medical illness, but was a chronic alcoholic.
On the pre-anaesthetic check-up, the patient had a toxic look, pallor, icterus and pitting oedema. His pulse was 110/min, blood pressure was 110/62 mmHg and respiratory rate was 16/min. Systemic examination was normal. Investigations were: haemoglobin (Hb), 13.2 gm%; white blood cell count (WBC), 11500/mm3; differential counts, within normal limits; fasting blood sugar (FBS), 245 mg%; post-prandial blood sugar (PPBS), 245 mg%; prothrombin time (PT), 13.8 s; international normalised ratio (INR), 1.27; blood urea nitrogen (BUN), 112.7 mg/dL; creatinine 3.49 mg/dL; total bilirubin, 1.7 mg/dL (direct, 0.9 mg/dL and indirect, 0.8 mg/dL); and SGPT, 69.4 U/L. X-ray hip and knee joint came out to be normal. Doppler study of the lower limb was done to rule out deep vein thrombosis (DVT), which showed a normal vascular study but large abscess on deep fascia from mid thigh to knee, then below knee toward the medial aspect in between the fascia. Ultrasonography (USG) abdomen showed fatty liver, while the remainder was normal. Physician referred the case for deranged renal functions. Intravenous (IV) fluid given to rehydrate the patient and Injection (inj) insulin was started as per the sliding scale. Repeat BUN and creatinine had come down to 105 mg/dL and 2.35 mg/dL, respectively.
The patient was taken to the operation theatre with American Society Anesthesiologist (ASA) Grade III (E) physical status, with informed consent. The patient was given a left lateral position with partial flexion of the right limb for spinal anaesthesia after adequate pre-loading. He was unable to flex the hip joint due to pain. Then, after aseptic preparation, SAB was attempted at the L3-L4 space with a 25G Quincke spinal needle. The subarachnoid space was located easily with give-way feeling, but cerebrospinal fluid (CSF) flow did not come. The stylet was reinserted and removed to clear the lumen of the needle and the needle was then withdrawn gradually. It was further advanced gradually but CSF could not be aspirated. Space was again located and a second attempt was made in the same space. Then, the space changed to L4-L5 and then L2-L3 with a 23G spinal needle, but CSF flow was absent in spite of a good give-way feeling. Finally, in the subarachnoid space at L2-L3 through a 23G spinal needle after confirming with give-way feeling, aspiration of CSF was tried but failed. Then, the needle was angled towards the right lateral recess of the subarachnoid space by mild manipulation and again aspirated, but this attempt was also futile. Then, while considering giving drug in this space even in the absence of CSF to take chance, to great surprise, straw-coloured thick material at the hub of the spinal needle was noticed []. The spinal needle removed and sent for culture and sensitivity of the pus. Surgery was deferred temporarily to evaluate further and the patient was advised urgent magnetic resonance imaging (MRI) of the dorsolumbar spine.
MRI scan on the second day reported that there was a large abscess in the right iliac fossa and gluteal region on either side with epidural extension of the abscess in the lumbar spine from L2 to the sacral segments compressing the thecal sac and traversing nerve roots []. Diffuse reduction in the marrow signal intensity of the spinal vertebrae suggested hypercellularity. The screening whole spine also revealed a large localised abscess in the right supraclavicular region and around the right sternoclavicular joint.
USG abdomen and thigh done on the second subsequent day showed no evidence of psoas abscess bilaterally. Pus for acid fast bacillus stain was negative and HIV I and II- tests were also negative.
On the third day, BUN and Sr creatinine came down to 45.4 mg/dL and 1.22 mg/dL, respectively. FBS was 119 mg/dL, SGOT was 52 U/L, SGPT was 37 U/L and alkaline phosphatase was 128 U/L. Culture and sensitivity (CandS) of pus from the spinal needle and aspiration from the thigh showed growth of gram positive Staphylococcus with coagulase test positive. On the third day, fasciotomy of the right thigh and leg were done under general anaesthesia. Inj Ticarcillin disodium and clavulanate potassium 3.1 gm iv 8-hourly and inj Metronidazole 100 mg iv 8-hourly was started with inj insulin. On the fifth day, pus CandS after 48 h showed growth of gram positive Staphylococcus with coagulase test positive. Blood C and S was negative.
On the sixth day, MRI of the pelvis showed a multiloculated abscess in the soft tissue musculature of the right iliac fossa, gluteal region bilaterally and the right thigh with diffuse alteration in the marrow signal intensity of the L5 vertebrae and along the right sacro-Iliac joint. The finding is suggestive of an infective etiology. The screening of T2W images of the lumbar spine reveals an epidural extension of the abscess with compression of the thecal sac at the L2-L5 level.
He was continued with antibiotics. Gradually, wound at the drainage site healed, pain subsided, he was able to walk and there was no neurological deficit. During this stay, his Hb had gone down to 7.7 gm/dL and he received two units of blood transfusions. The patient remained hospitalised for a total of 40 days. He was discharged with all biochemistry investigations normal.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [62.0, 'mm hg']}",78,74.1,81.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 62.0 mm Hg = 78.0 mm Hg.
Hence, the patient's mean arterial pressure is 78.0 mm Hg."
1853,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5965116-1,Extracted,"A 74-year-old man on rivaroxaban for paroxysmal atrial fibrillation presented with the gradual onset of neck pain. The pain started while he was walking in the woods and was associated with progressive weakness and numbness from the clavicles downward. He was able to walk back to his cabin, but upon arrival he was unable to maintain his balance and fell forward striking his head. He denied any loss of consciousness. He was unable to move for about 45 minutes. Emergency medical services was called and they noted the patient to be completely paralyzed with fecal incontinence. He also had shortness of breath. During his transport to the emergency department (ED) he started to regain strength and feeling in his arms and legs and improvement of his shortness of breath. He denied any recent fevers, upper respiratory infection, rash or tick bites. All other review of systems was negative. Past medical history was significant for hypertension, atrial fibrillation, and coronary artery disease.
On initial examination, the patient was alert and oriented to person, place, and time. Temperature was 92.0 degrees Fahrenheit tympanic, pulse 56 beats per minute, respiratory rate 20 breaths per minute, blood pressure 122/56 mmHg, oxygen saturation 100% on four liters nasal cannula. Lungs were clear to auscultation bilaterally without wheezes, rhonchi, or rales. Heart was regular rate and rhythm, without any murmurs. Abdomen was soft, non-tender, non-distended with normal bowel sounds. Back had no evidence of trauma or deformity, non-tender to palpation. On extremity exam he had 4/5 strength in all extremities. After 20 minutes in the ED, he developed flaccid paralysis of all extremities with 0/5 strength. His voice also became softer and he developed shortness of breath. After five minutes he was able to wiggle his left toes. Over the next hour he slowly regained strength in his right lower extremity and his voice returned to normal. After another 40 minutes the patient was able to move his right upper and lower extremity and wiggle his toes on his left lower extremity. He was still unable to move his left upper extremity.
A computed tomography angiography (CTA) of the chest, abdomen, and pelvis was performed and did not show any evidence of aortic dissection. MRI of the cervical spine showed a prominent epidural hematoma, primarily dorsal, that extended from the foramen magnum down to cervical vertebra C7 and contributed to severe mass effect on the thecal sac (). Findings were the worst at C2–C3, where the hematoma measured 7–8 mm in width with compression of the cervical spinal cord and associated cord signal abnormality. In retrospect, findings were also visible on the preceding CTA. Patient was taken emergently to surgery for evacuation of the hematoma.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [122.0, 'mm hg'], 'Diastolic Blood Pressure': [56.0, 'mm hg']}",78,74.1,81.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 122.0 mm Hg + 2/3 * 56.0 mm Hg = 78.0 mm Hg.
Hence, the patient's mean arterial pressure is 78.0 mm Hg."
1854,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6586102-1,Extracted,"A 29-year-old man with past medical history of Addison’s disease and hypothyroidism who recently relocated to the USA from Puerto Rico presented to the emergency department (ED) with chief complaints of fatigue, palpitations, and light headedness.
He was previously maintained on twice daily hydrocortisone and daily levothyroxine supplementation but had been off his medications for 5 days. He denied chest pain or shortness of breath. He also denied tremors, easy fatigability, weight gain, hoarseness of voice, or changes in bowel habit. Of note, he reported a childhood history of recurrent seizures due to hypocalcemia and had since been on calcium and vitamin D supplementation. He had no family history of autoimmune disease and review of systems was otherwise unremarkable. His knowledge about his medical condition was limited.
On physical examination, he was in no acute distress. He was hypotensive with BP 89/67 and tachycardic with pulse rate of 115 bpm. Other vital signs were normal. Chvostek sign was negative and there was no thyromegaly on neck palpation. Oral examination showed multiple hyperpigmented lesions on the dorsum of his tongue () and multiple deformed and pitting finger nails in both hands (). The remainder of the physical examination was unremarkable.
Basic metabolic panel revealed hyponatremia with Na 129 meq/L (136–145) and potassium of 4.8 meq/L (3.5–5.1). He was also severely hypocalcemia with ionized calcium of 0.96 mmol/L (1.15–1.33). Fasting blood glucose was normal. Thyroid function test showed elevated thyrotropin level at 5.807 uIU/mL (0.450–5.330) with normal free thyroxine level at 0.94 ng/dL (0.58–1.64). AM cortisol was markedly reduced at <1 mcg/dL (6.7–22.6). ACTH was markedly elevated at 785 pg/mL (7–69) and direct renin was also very elevated at 390 pg/mL (2.5–45.7). Parathyroid hormone was markedly reduced at <6 pg/mL (12–88). Complete blood count was normal, as was coagulation profile.
ECG also showed sinus tachycardia with no ischemic changes.
The patient was given intravenous saline and double his normal dose of his steroids. His levothyroxine dose was continued at 75 mcg daily while intravenous and oral calcium were given to correct hypocalcemia. His symptoms gradually improved, and he was discharged home on hydrocortisone 20 mg in the morning and 10 mg at night with fludrocortisone 0.1 mg daily and levothyroxine 75 mcg daily.
On follow-up in clinic 2 weeks later, patient was noted to be doing well. Patient education regarding medication adherence and stress dosing to avoid potentially life-threatening adrenal crisis and the importance of medic alert bracelets was reinforced. The patient was classified as having APS type 1 because of the presence of hypoparathyroidism, Addison’s disease, and chronic muco-cutaneous candidiasis, and promptly referred to the endocrinologist for continuity of care ().",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [67.0, 'mm hg'], 'Systolic Blood Pressure': [89.0, 'mm hg']}",74.33333,70.61666,78.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 89.0 mm Hg + 2/3 * 67.0 mm Hg = 74.33333 mm Hg.
Hence, the patient's mean arterial pressure is 74.33333 mm Hg."
1855,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7210,Extracted,A 30-year-old woman presents to her new doctor at 27 weeks' gestation with her second pregnancy. Her blood type is B- and the father of the child is B+. Her first child had an Apgar score of 7 at 1 minute and 9 at 5 minutes and has a B+ blood type. The fetus has a heart rate of 130/min and blood pressure of 100/58 mm Hg. There is a concern that the fetus may develop erythroblastosis fetalis (EF).,What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [58.0, 'mm hg']}",72,68.4,75.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 58.0 mm Hg = 72.0 mm Hg.
Hence, the patient's mean arterial pressure is 72.0 mm Hg."
1856,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8476338-1,Extracted,"A 33-year-old male with no significant medical history presented to the emergency room with progressive weakness, easy fatigability and headache. He had no evidence of lower or upper gastrointestinal bleeding and he reported no abdominal pain, nausea, vomiting, anorexia, fever or weight loss.
The patient’s symptoms started 3 wk prior and had worsened over the last 4 d.
There was no significant medical history.
There was no significant medical history.
In the emergency room, the patient was clinically stable, with a normal temperature (36.7 °C). The patient exhibited an oxygen saturation level of 97% while he was breathing ambient air. His blood pressure was 102/61 mmHg and his heart rate was 91 beats per minute. The patient was awake, alert, and fully oriented. Physical examination revealed signs of pallor and an absence of lymphadenopathy, hepatosplenomegaly, bone tenderness or jaundice. Examination of the rectum revealed a few external hemorrhoids, but there was no blood or melena in the rectal vault; there were no skin tags, fissures or palpable masses.
The initial laboratory findings showed low hemoglobin levels (7 g/dL), a white blood cell count of 11250 per mm3, a platelet count of 221000 per mm3 and a C-reactive protein of 1.31 mg/dL. Two pints of packed red blood cells were therefore transfused and the patient was admitted to the gastroenterology department. Electrocardiography (ECG) showed sinus rhythm at 93 beats per minute and the results of the patient’s chest radiography were normal.
The patient’s next blood test, showed a mean corpuscular volume of 72.5 fl, a mean corpuscular hemoglobin of 25.6 pg, and a reticulocyte count of 1%. The patient’s iron level was 38 μg/dL, his ferritin level was 17 ng/mL, and his transferrin saturation was 9%. The hemolysis study was negative. Hence, the patient’s anemia was classified as iron deficiency anemia.
During this period, an upper gastrointestinal endoscopy and a colonoscopy were performed to study the patient’s anemia. The colonoscopy revealed internal hemorrhoids without any other relevant findings while the upper gastrointestinal endoscopy showed no abnormalities. The patient remained stable and was discharged and the study was completed on an outpatient basis with oral iron treatment.
During his visit to the outpatient clinic 3 wk later, the patient remained anemic, with a hemoglobin level of 8.8 g/dL. The anemia study was completed with a capsule endoscopy, which revealed a lifted erosion and mild bulge in the ileum of approximately 8-9 mm in size (Figure ). These findings of appearance of a subepithelial bulge in the ileum suggested an inverted Meckel diverticulum. Normal intestinal mucosa was seen on the surface of the tumor with a longer small intestine transit time suggestive of Meckel’s diverticulum. A technetium-99m pertechnetate radioisotope scintigraphy (Meckel’s scan) was performed and was negative. The patient subsequently underwent an ultrasound examination, which revealed no pathological findings. Finally, an abdominal computed tomography (CT) was performed and showed a central area of fat attenuation surrounded by a thick collar of soft tissue attenuation (Figure ) suggestive of inverted Meckel’s diverticulum.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [102.0, 'mm hg'], 'Diastolic Blood Pressure': [61.0, 'mm hg']}",74.66667,70.93334,78.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 102.0 mm Hg + 2/3 * 61.0 mm Hg = 74.66667 mm Hg.
Hence, the patient's mean arterial pressure is 74.66667 mm Hg."
1857,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8350353-1,Extracted,"An 80-year-old woman was admitted to a long-stay hospital for Alzheimer’s dementia with previous history of chronic subdural haematoma, old cerebral infarction, dysphagia, and glaucoma on 24 October 2016. With an anxious expression on her face, physical examination revealed that she was 150 cm tall and body weight 30.1 kg with vital signs of body temperature 37.1°C, blood pressure 94/65 mmHg, heart rate 70 b.p.m. with ECG features of normal sinus rhythm, respiratory rate 20 breaths/minute, and transcutaneous arterial oxygen saturation 94%. White blood cell count (WBC) was 12 490 count/μL on admission and increased to 17 580 count/μL on 29 November. C-reactive protein also drastically increased from 1.31 mg/dL on admission to 2.20 mg/dL on 29 November. On admission, brimonidine tartrate drop was administered. After admission, she developed myelodysplastic syndrome (MDS) with anaemia and thrombocytopenia. MDS is a heterogeneous disorder related to haematopoietic abnormalities that are frequently found in elderly people. As ingestion intake was difficult, nutritional support via a central venous hyperalimentation route was adopted. She developed suspected sepsis and was treated with ampicillin sodium (3000 mg/day) on 22 November, with meropenem hydrate (500 mg/day) from 29 November, with ceftazidime hydrate (1000 mg/day) and gentamicin sulphate (80 mg/day) from 7 December, with ampicillin sodium (1500 mg/day) from 30 December, and with meropenem hydrate (250 mg/day) from 11 January 2017.
From 5 January to 7 January, ANMS monitoring showed a marked linear decrease in the LF and HF of HRV components. Furthermore, from 7 January to 12 January, both the LF and HF showed low and linear values (). On 7 January, at 2:00 p.m., the ANMS automatically registered the CSR pathogenesis () around the intersection of two lines, that is, the decreasing LF line (from 5 January to 7 January) and the constant LF line (from 7 January to 12 January). The intersection of the LF lines overlapped with the intersection of the decreasing HF line (from 5 January to 7 January) and the constant HF line (from 7 January to 12 January). Our patient died from multiple organ dysfunction syndrome 20 days after the registration of daytime CSR pathogenesis.
The attenuation rate of HF (1340 ms2/day) was higher than that of LF (956 ms2/day). The heart rate increased by ∼10 b.p.m. during these 3 days.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [94.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",74.66667,70.93334,78.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 94.0 mm Hg + 2/3 * 65.0 mm Hg = 74.66667 mm Hg.
Hence, the patient's mean arterial pressure is 74.66667 mm Hg."
1858,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8654109-1,Extracted,"A 34-year-old man with no previous history of chronic illness and a non-smoker presented with a history of headache, fatigue, diarrhea, vomiting, and insomnia for three days. During the initial examination, he was conscious and alert. His blood pressure (BP) was 111/71, pulse rate (PR) 40, respiration rate (RR) 14/min, body temperature 36.7, and oxygen saturation (SpO2) 96% under ambient oxygen conditions. The patient had a clear chest, without any crepitating sounds in the cardiovascular system (CVS; S1+S2+0). An abdominal exam showed a soft and lax abdomen, and both lower limbs were normal. The status of the central nervous system (CNS) was normal, all cranial nerves were intact, and chest X-ray and chest CT scans were performed (Figures -). EKG showed sinus rhythm, first-degree heart block with prolonged QT interval, and bigeminy (Figure ). Echo revealed a normal echo study (Figure ). General clinical and blood parameters of the patients are shown in Table . Due to the COVID-19 pandemic, all patients reporting to the hospital with fever were routinely tested with the PCR test for COVID-19. Also, a nasopharyngeal swab was tested by RT-PCR and proved to be positive for SARS-CoV-2.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [111.0, 'mm hg'], 'Diastolic Blood Pressure': [71.0, 'mm hg']}",84.33333,80.11666,88.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 111.0 mm Hg + 2/3 * 71.0 mm Hg = 84.33333 mm Hg.
Hence, the patient's mean arterial pressure is 84.33333 mm Hg."
1859,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4998494-1,Extracted,"A 60-year-old man with past history of allergic rhinitis noticed the swelling of bilateral submandibular glands (SMGs) in June 2014. Serum creatinine elevation (1.37 mg/dL) was pointed out at routine health checkup around the time and was admitted to our hospital for work-up.
Physical examination revealed normal blood pressure 127/83 mm Hg and body temperature 36.6°C. The findings of ocular, lung, cardiovascular, abdominal, neurological, and skin examination were normal. Although his bilateral SMGs were swelling with no tenderness, his labial salivary gland (LSG) appeared normal.
Laboratory tests revealed elevated serum creatinine (1.78 mg/dL, normal range: 0.61–1.10 mg/dL), IgG (1856 mg/dL, normal range: 870–1700 mg/dL), IgG4 (314 mg/dL, normal range: 4.8–105 mg/dL), and slightly elevated C-reactive protein (0.74 mg/dL, normal range: <0.30 mg/dL). Other blood tests, including blood count, serum electrolyte levels, liver enzyme levels, and blood glucose were within normal ranges. Antinuclear antibody, anti-SS-A, and SS-B antibodies were all negative. Urinalysis showed neither proteinuria, occult blood, white blood cells nor casts.
Computed tomography (CT) revealed enlarged bilateral SMGs and the left kidney, the left hydronephrosis, and high-density area at the periaorta soft tissue (Fig. A). Positron-emission tomography-CT demonstrated abnormal accumulation of fluoro-2-deoxyglucose-positron at the identical area (bilateral SMGs, left kidney, and periaorta) (Fig. ).
IgG4-RD was suspected; however, biopsy of the periaorta had risk of the injury of abdominal aorta, and kidney biopsy was contraindicated owing to hydronephrosis. He did not agree on submandibulectomy for fear surgical risk. A fine needle biopsy of SMG would be inadequate for sampling in IgG4-RD patients.[ Thus, we performed less invasive lip biopsy in an attempt to obtain pathological specimen with patient agreement. Histological examination of his LSG revealed heavy infiltration of lymphocytes and hyperplastic germinal center formation (Fig. A), adding massive plasma cells infiltration revealed by CD138 staining (Fig. B). Forty-seven percent of those plasma cells with IgG immunoreactivity (Fig. C) were positively immunolabeled with antibody for IgG4 (Fig. D).
We diagnosed him as IgG4-RD based on the 2011 comprehensive diagnostic criteria,[ and treatment with 60 mg/d (0.8 mg/kg) of prednisolone was initiated. Three months later, although the reevaluation of LSG tissue after glucocorticoid treatment was not conducted, the swelling of SMGs and left kidney and periaortitis in CT remarkably improved (Fig. B). During follow-up of 14 months, serum levels of creatinine normalized to 1.10 mg/dL and IgG4 to 74 mg/dL. The dose of prednisolone was gradually tapered, and he has been treated with 5 mg daily without recurrence.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [127.0, 'mm hg'], 'Diastolic Blood Pressure': [83.0, 'mm hg']}",97.66667,92.78334,102.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 127.0 mm Hg + 2/3 * 83.0 mm Hg = 97.66667 mm Hg.
Hence, the patient's mean arterial pressure is 97.66667 mm Hg."
1860,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4810,Extracted,"A 36-year-old female with a history of end stage renal disease secondary to poorly controlled type I diabetes on peritoneal dialysis presents to her nephrologist's office with chest pain, shortness of breath, and extreme fatigue. She has a history of inadequate dialysis due to poor compliance. In the office, the patient's vitals are BP: 94/58; HR: 90; RR: 20; T: 98.0 F. EKG is shown below (Figure A). The patient is immediately taken to the emergency department.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [94.0, 'mm hg'], 'Diastolic Blood Pressure': [58.0, 'mm hg']}",70,66.5,73.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 94.0 mm Hg + 2/3 * 58.0 mm Hg = 70.0 mm Hg.
Hence, the patient's mean arterial pressure is 70.0 mm Hg."
1861,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6580836-1,Extracted,"A 26-year-old male was admitted at our center with a short history of febrile illness of 1-week duration. He had gradually progressive symptoms of involuntary, hyperkinetic movements and weakness of both upper and lower limbs. Autonomic dysfunction had manifested in the form of excessive sweating and insomnia. Behavioral abnormalities along with auditory hallucinations were also present.
General examination findings revealed signs of autonomic dysfunction as his resting pulse rate remained consistently above 110 beats/min, whereas his blood pressure was found to be frequently elevated above 160/100 mm of Hg. Wasting of muscles of all four limbs was also evident.
Laboratory investigations initially unveiled hypokalemia (serum potassium: 3.2 mEq), with hypoproteinemia(total protein: 5.8 g/dl, albumin: 3.8 g/dl, and globulin: 2.0 g/dl).
He was further evaluated for possible causes of neuromyotonia. The patient had a positive serum anti-CASPR2 antibody, a subtype of VGKC complex detected by using immunofluorescence method and considered to be the hallmark of Morvan syndrome.[]
Initial treatment with high-dose steroids and intravenous immune globulin (IVIG) for 2 weeks offered no improvement in his condition. Given progression of the disease, decision to carry out therapeutic plasma exchange (TPE) was considered. As per the latest ASFA guidelines (2016), <100 cases have been reported in the literature,[] where TPE has been used as a treatment option for reducing antibodies against VGKC. Morvan syndrome also falls under this broad category of neurological disorders and a Category II indication for carrying out TPE. A thorough review of literature was carried out and considered in context of McLeod's criteria, which states if the disorder's pathophysiology is understood and the apheresis procedure could modify it, the risk–benefit ratio of carrying out TPE should be evaluated. The same was done for this patient and as the potential benefits outweighed the risks, the decision to carry out the procedure was considered appropriate.[]
A double-lumen femoral line was placed under strict aseptic precautions for carrying out TPE, using MCS plus 9000 (Hemonetics, Unites States) apheresis platform. Another peripheral venous access was established for infusion of calcium. Patient's potassium levels were corrected before the start of the procedure. FFP and saline were chosen as the replacement fluid (in the ratio of 70:30). Although albumin is considered the ideal replacement fluid, it could not be used in this case due to financial constraints of the patient. The procedure was carried out in an Intensive Care Unit in view of abnormal vital parameters. Patient's total plasma volume was calculated as per his body weight, and 100% of this total plasma volume was exchanged (1 plasma exchange) on alternate days for five sessions of TPE.
The process of carrying out TPE proved to be very challenging from the 1st cycle. Persistent hyperkinetic movements of all the limbs caused recurrent hindrance to the flow through femoral line and tubing. The process had to be paused intermittently to manually rectify the obstruction and restore normal flow. Constant vigil on tubing was required to avoid kinks and maintain a normal flow rate. Later, the patient had to be restrained by cuffing the limbs, after obtaining consent from his relatives. Tablet methyl prednisolone was also given to the patient as part of the management along with tablet clonazepam for its antiepileptic as well as sedative effect.
The patient developed an allergic reaction to FFP during the first sitting itself in the form of rashes over entire body which subsided on treatment with antihistamines. Rest of the TPE sessions were carried out after premedicating the patient with antihistamines, and allergic reaction to FFP was not observed again.
Due to persistently elevated blood pressure (>160/100 mm of Hg) and tachycardia (>110 bpm), any further rise in his vital parameters during the procedure could have been detrimental. To ensure optimum safety of the patient, the entire procedure was carried out in an Intensive Care Unit, and an intensivist was on standby in case of any eventuality.
His serum protein was on lower side (5.2 g/dL) before the start of TPE. The patient was also transfused with four units of FFP postprocedure, after each TPE session. This enhanced FFP support rectified his total serum proteins (7.2 g/dL) before the fourth TPE commenced. Flow rate and amount of fluid exchanged were kept at lower levels during each exchange cycle, using apheresis bowl of a lower volume (125 ml) to ensure that the patient remained hemodynamically stable.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [100.0, 'mm hg'], 'Systolic Blood Pressure': [160.0, 'mm hg']}",120,114,126,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 100.0 mm Hg = 120.0 mm Hg.
Hence, the patient's mean arterial pressure is 120.0 mm Hg."
1862,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-707,Extracted,"A 32-year-old woman, gravida 2, para 2, comes to the physician for the evaluation of a palpable mass in her right breast that she first noticed 1 week ago. She has no associated pain. She has never had a mammogram previously. She has type II diabetes mellitus treated with metformin. She has no family history of breast cancer. She has smoked half a pack of cigarettes daily for 15 years. Her temperature is 37°C (98.6°F), pulse is 78/min, respirations are 14/min, and blood pressure is 125/75 mm Hg. Examination shows a firm, nonpainful, nonmobile mass in the right upper quadrant of the breast. There is no nipple discharge. Examination of the skin and lymph nodes shows no abnormalities. No masses are palpated in the left breast.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [75.0, 'mm hg'], 'Systolic Blood Pressure': [125.0, 'mm hg']}",91.66667,87.08334,96.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 75.0 mm Hg = 91.66667 mm Hg.
Hence, the patient's mean arterial pressure is 91.66667 mm Hg."
1863,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-3513,Extracted,"A 25-year-old woman comes to the physician because of a 2-week history of episodic bleeding from the nose and gums and one episode of blood in her urine. She was treated with chloramphenicol 1 month ago for Rickettsia rickettsii infection. Her pulse is 130/min, respirations are 22/min, and blood pressure is 105/70 mm Hg. Examination shows mucosal pallor, scattered petechiae, and ecchymoses on the extremities. Laboratory studies show:
Hemoglobin 6.3 g/dL
Hematocrit 26%
Leukocyte count 900/mm3 (30% neutrophils)
Platelet count 50,000/mm3
The physician recommends a blood transfusion and informs her of the risks and benefits.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [105.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",81.66667,77.58334,85.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 105.0 mm Hg + 2/3 * 70.0 mm Hg = 81.66667 mm Hg.
Hence, the patient's mean arterial pressure is 81.66667 mm Hg."
1864,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5405667-1,Extracted,"A 29-year old gentleman had acute episodes of breathlessness, vomiting, headache, and decreased urine output 18 months before presentation. He denied a history of photophobia, fever, fatigue, joint pain, weakness or skin rashes on the face, neck, and upper body. There were no symptoms suggestive of Raynaud's phenomenon. He did not have palpitation, sweating, syncope, muscle weakness, mood changes, or weight gain. On evaluation, elsewhere, he was found to have bilateral chest crepitation, raised blood pressure (BP), and serum creatinine– 11 mg%. Rest of the physical examination were normal. He underwent four sessions of hemodialysis. He required five antihypertensives (torsemide/clonidine/metoprolol/prazosin /nifedipine) for control of BP. His hemoglobin (Hb)-10.9 g%, urea-45 mg%, serum creatinine – 1.92 mg%, 24 h urine protein-745 mg. Additional screening for vasculitis, systemic lupus erythematosus, cushing, and pheochromocytoma were negative.
His BP on five antihypertensives was 200/100 mmHg. Computed tomography angiography showed bilateral renal artery stenosis (RAS) with multiple collateral vessels on both sides. Stenting of the renal vessels was not possible as the ostial lumen was narrowed and guide wire could not be passed on angiography [].
He initially underwent left renal revascularization with a splenorenal end to end anastomosis.
Subsequently, he had a right iliac fossa renal autotransplantation 1 month later.
Postoperative renogram showed a good perfusion of both the kidneys [].
His serum creatinine was 1.01 mg%, urea: 36 mg%, 24 h protein: 146 mg%, hemoglobin: 16 g%, serum electrolytes: normal, and BP: 140/90 mmHg on two antihypertensives (metoprolol and prazosin) on follow-up.
An 18-year old gentleman was diagnosed to have bilateral RAS while being evaluated for progressive vision dimness and hypertension. He had no skin infection, rash, arthritis, hemoptysis, lower urinary tract symptoms, or symptoms suggestive of Raynaud's syndrome. He underwent right renal artery stenting followed by left renal artery angioplasty and stenting within a gap of 6 months. His serum creatinine was 1.48 mg%, serum urea – 24 mg%, Hb – 10.3 g%, 24 h urine protein – 3.7 g%, and BP – 140/90 mmHg on five antihypertensives. His BP continued rise for which right renal artery stenting was reattempted after a year. This was followed by right laparoscopic nephrectomy for nonfunctioning right kidney. Histopathology showed right hilar renal artery with medial fibroplasia.
His BP progressively rose and had several episodes of generalized tonic–clonic seizures. Imaging revealed worsening of left RAS []. He underwent end to end left lienorenal arterial revascularization under general anesthesia.
Postoperative blood findings serum creatinine – 0.89 mg%, urea – 15 mg%, 24 h urine protein – 271 mg%, Hb – 11.9 g%, S. electrolytes – normal. He was on three antihypertensives (prazosin/cilnidipine/bisoprolol) at time of discharge and his BP was 130/80 mmHg.
Operative procedure: the patient was placed in right lateral with the operation table flexed. A lumbar incision was made and 11th rib excised. Gerota fascia opened, the renal hilum exposed anteriorly, and the renal vein was identified. The renal artery was spotted posteriorly. The splenic artery discerned and isolated, the distal splenic artery was left untouched. The splenic artery was divided after applying vascular bulldog clamps and spatulated. The renal artery was divided till there was adequate lumen. Splenorenal anastomosis was done with interrupted 7-0 prolene. Hemostasis achieved and abdomen closed in layers.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [200.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",133.33333,126.66666,140,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 200.0 mm Hg + 2/3 * 100.0 mm Hg = 133.33333 mm Hg.
Hence, the patient's mean arterial pressure is 133.33333 mm Hg."
1865,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4173236-1,Extracted,"A 26-year-old lady presented with chief complaint of headache of 4 months duration. It was off and on initially and then became continuous with increase in severity. One week, prior to presentation, the headache worsened in severity associated with transient blurring of vision. She had no other focal neurological or systemic symptoms. Past history revealed consuming dexamethasone (0.5 mg/day) and cyproheptadine (4 mg/day) tablets for intentional weight gain, obtained over the counter without any prescription. She used the tablets for a period of 1 year and stopped abruptly 6 months back. However, she has not developed any acute symptoms of steroid withdrawal. The headache had started around 2 months after she stopped the medications.
At the time of evaluation, she weighed 53 kg. Her height was 143 cm, body mass index (BMI) was 25.9 (18.5-25: Normal; 25-29.9: Overweight; >30: Obese). Her ideal body weight (Devine formula) was 45.9 kg.[] Her blood pressure was 110/80 mmHg. Rest of the systemic examination was unremarkable. Examination revealed visual acuity of 6/6 in both eyes with normal intraocular pressure. Fundus showed bilateral optic disc edema with splinter hemorrhage in the left eye []. There were no cotton wool spots/macular edema. Visual field charting by Humphrey perimeter showed enlarged blind spot bilaterally with superior and inferior areas of depression in the right eye. Rest of the neurological examination was normal. In view of the gradually progressive headache and bilateral optic disc edema, raised intracranial pressure was considered and evaluated for the same.
Complete blood counts, erythrocyte sedimentation rate, blood sugar, renal and liver function tests, serum electrolytes, HIV, Venereal disease research laboratory test (VDRL), thyroid function tests were within normal limits. Brain magnetic resonance imaging (MRI) showed tortuosity of the bilateral optic nerves with prominence of the subarachnoid space around the optic nerves, flattening of the posterior sclera, partial empty sella []. There was no intracranial mass lesion. The lateral ventricles were small and symmetrical. MR venography did not show any occlusion/thrombosis. After brain MRI, diagnosis of idiopathic intracranial hypertension was considered. Lumbar puncture revealed a high opening pressure of 280 mm H2O and normal cerebrospinal fluid (CSF) (clear, colorless, white blood cell count 2, red blood cell 0, protein 14.5 mg/dL, glucose 76 mg/dL, chloride 114 meq/dL, India ink-negative). Following drainage of 20 mL of CSF, there was a significant reduction in the severity of headache lasting 2-3 days. A diagnosis of intracranial hypertension was made based on modified Dandy criteria.[] She was started on acetazolamide 250 mg TID and advised 5%-10% weight loss. She has attained a weight loss of 8 kg (15%) over 6 months by dietary control and is completely asymptomatic now. Patient's prior approval was obtained for academic publication.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 80.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1866,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-10109,Extracted,"A 29-year-old African American woman presents with incidentally noted bilateral hilar lymphadenopathy on a recent chest radiograph for the evaluation of pneumonia 1 month earlier. Upon questioning, she reports a cough, dyspnea, and angina. The report provided by a previous ophthalmologic consultation did not demonstrate any eye abnormalities. Clinical laboratory pathologic analysis reveals an elevated level of angiotensin-converting enzyme. Her physical examination reveals no obvious abnormalities. Her vital signs show a heart rate of 76/min, respiratory rate of 16/min, and blood pressure of 123/73 mm Hg.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [73.0, 'mm hg'], 'Systolic Blood Pressure': [123.0, 'mm hg']}",89.66667,85.18334,94.15,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 123.0 mm Hg + 2/3 * 73.0 mm Hg = 89.66667 mm Hg.
Hence, the patient's mean arterial pressure is 89.66667 mm Hg."
1867,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4881657-1,Extracted,"A 58-year-old male with no known medical history developed sudden onset chest pain, dyspnea, and a sensation of fullness in his throat. He was transported to the emergency room where he was found to be hypotensive (82/54 mmHg), bradycardic (40 beats/min), and tachypneic (26 breaths/min). His oxygen saturation was normal, and he was awake and alert and exhibited no neurologic deficits. His electrocardiogram showed normal sinus rhythm without acute ST-T wave changes, and his troponin T was normal. Given the concern for pulmonary embolism, a computed tomography (CT) scan with contrast was obtained. The CT scan revealed acute type A dissection arising from the aortic root and extending to the left iliac system. The left coronary ostium, all three great vessels, the celiac trunk, superior mesenteric artery, and left renal artery appeared to be involved. He was scheduled for emergent aortic reconstruction with deep hypothermic circulatory arrest.
The patient underwent induction of general anesthesia with tracheal intubation. Transesophageal echocardiography (TOE) was subsequently performed, which confirmed the presence of a dissection flap in the ascending aorta []. The flap was observed to prolapse across the aortic valve into the LV outflow tract during diastole [ and Online ]. Remarkably, there was no aortic valve insufficiency [], the LV wall motion was normal, and there was no hemopericardium. Following sternotomy and opening of the pericardium, heavy bleeding through the aortic wall was encountered. Cardiopulmonary bypass (CPB) via femoral cannulation was initiated, and the patient was cooled to 18°C. During 37 min of circulatory arrest, the ascending aorta and inside curve of the aortic arch were excised and replaced with vascular graft (hemiarch). The aortic valve and root were replaced with a valved conduit, and the coronary buttons were implanted into the conduit. After the anastomosis of the valved conduit to the hemiarch graft, the patient was separated from CPB, coagulopathy was corrected, the chest was closed, and the patient transported to the intensive care unit intubated and sedated. The patient had a prolonged recovery that was complicated by cognitive impairment and critical illness neuromyopathy.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [54.0, 'mm hg'], 'Systolic Blood Pressure': [82.0, 'mm hg']}",63.33333,60.16666,66.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 82.0 mm Hg + 2/3 * 54.0 mm Hg = 63.33333 mm Hg.
Hence, the patient's mean arterial pressure is 63.33333 mm Hg."
1868,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5910,Extracted,"A 63-year-old man presents to the emergency department with periorbital swelling. He states that he was gardening, came inside, looked in the mirror, and then noticed his eyelids were swollen. He denies pain, pruritus, or visual disturbances. He states that he was drinking “a lot of water"" to prevent dehydration, because it was hot outside this morning. His medical history is significant for rheumatoid arthritis. He takes methotrexate and acetaminophen as needed. The patient’s temperature is 98°F (36.7°C), blood pressure is 168/108 mmHg, and pulse is 75/min. Physical examination is notable for periorbital edema, hepatomegaly, and bilateral 1+ pitting lower extremity edema. Labs and a urinalysis are obtained, as shown below:

Leukocyte count: 11,000/mm^3
Hemoglobin: 14 g/dL

Serum:
Na: 138 mEq/L
K+: 4.3 mEq/L
Cl-: 104 mEq/L
HCO3-: 25 mEq/L
Urea nitrogen: 26 mg/dL
Creatinine: 1.4 mg/dL
Glucose: 85 mg/dL
Aspartate aminotransferase (AST, GOT): 15 U/L
Alanine aminotransferase (ALT, GPT): 19 U/L
Albumin: 2.0 g/dL

Urine:
Protein: 150 mg/dL
Creatinine: 35 mg/dL

An abdominal ultrasound reveals an enlarged liver with heterogeneous echogenicity and enlarged kidneys with increased echogenicity in the renal parenchyma. A biopsy of the kidney is obtained.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [168.0, 'mm hg'], 'Diastolic Blood Pressure': [108.0, 'mm hg']}",128,121.6,134.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 168.0 mm Hg + 2/3 * 108.0 mm Hg = 128.0 mm Hg.
Hence, the patient's mean arterial pressure is 128.0 mm Hg."
1869,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-11303,Extracted,"A 10-year-old boy is referred to a pediatric neurologist by his pediatrician for lower extremity weakness. The boy is healthy with no past medical history, but his parents began to notice that he was having difficulty at football practice the previous day. Over the course of the past 24 hours, the boy has become increasingly clumsy and has been “tripping over himself.” On further questioning, the boy had a viral illness the previous week and was out of school for 2 days. Today, the patient’s temperature is 99.3°F (37.4°C), blood pressure is 108/72 mmHg, pulse is 88/min, respirations are 12/min. On motor exam, the patient has 5/5 strength in hip flexion, 5/5 strength in knee extension and flexion, 3/5 strength in foot dorsiflexion, and 5/5 strength in foot plantarflexion. The findings are the same bilaterally. On gait exam, the patient exhibits foot drop in both feet.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [108.0, 'mmhg'], 'Diastolic Blood Pressure': [72.0, 'mmhg']}",84,79.8,88.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 108.0 mm Hg + 2/3 * 72.0 mm Hg = 84.0 mm Hg.
Hence, the patient's mean arterial pressure is 84.0 mm Hg."
1870,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6450235-1,Extracted,"A 61-year-old woman arrived at our emergency department because of the appearance of intense palpitations for 3 days. She denied cardiovascular risk factors or a previous cardiac disease, did not assume pharmacological therapy, and reported only a recent domestic accidental fall without apparent complications. The heart rhythm appeared tachycardic and irregular, and the remaining vital parameters were normal with a good hemodynamic compensation (systemic blood pressure 135/75 mmHg, SaO2 98%). Electrocardiogram reported atrial fibrillation with high ventricular response (136 bpm). The blood tests were all normal, except for a mild and nonspecific increase in the high-sensitivity troponin T.
The patient underwent a cardiology consult in order to plan the following therapy procedure. Subsequent transthoracic echocardiogram revealed a dilated LA with an interior septum which extended across the longitudinal length of the atrial chamber, by causing the obstruction to the left ventricular (LV) filling, in the absence of additional pathologic findings. By considering that the atrial fibrillation had begun more than 48 h before and the need of investigating the above findings, we have decided to perform a transesophageal echocardiogram (TEE) the following day.
The TEE documented the presence of atrial thrombosis in the appendage, a spherical image with clear margins and fibrin branches inside, and a seamless cleavage with the posterolateral wall of the LA, which determined an obstacle to the ventricular filling [].
We decided to perform an urgent contrast-enhanced cardiac computed tomography (CT) which confirmed a capsulated lesion within the posterolateral left atrial wall with sharp margins and a basal density of + 30 HU, without any significant contrast enhancement in the arterial and late phases, features resembling those of a chronic hematoma [].
After a consultation with our cardiac surgeon, and suspecting an atrial dissection, we planned to perform a cardiac magnetic resonance (CMR). CMR was performed with a 1.5T scanner with cine B-TFE, black-blood turbo spin echo, phase-sensitive inversion recovery, and THRIVE sequences before and after a standard 0.2 mmol/kg gadolinium contrast agent dose. CMR confirmed the intramural formation, within the inferolateral wall of the LA, with diameters of 4.3 cm × 6.2 cm × 4.4 cm, characterized by marked hyperintensity in T2-weighted sequences and high signal in both unsuppressed and fat-suppressed T1-weighted images, as well as the absence of signs of local invasiveness; a thin hypointense rim demarcated the lesion in the steady-state cine sequences. In contrast-enhanced images, a thin rim of peripheral enhancement is appreciated, mostly evident on the posterior side. These findings were deemed compatible with the original hypothesis of an intramural hematoma of the wall of the atrium, probably subacute/chronic [].
In consideration of the extension of the intramural hematoma and the LV inflow tract obstruction, the patient underwent a surgery to empty the hematoma and reattach the atrial wall.
Histological examination confirmed the presence of histiocytes, crenated red blood cells, and crystals, hence a chronic hematoma [].",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [135.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",95,90.25,99.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 75.0 mm Hg = 95.0 mm Hg.
Hence, the patient's mean arterial pressure is 95.0 mm Hg."
1871,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-2343,Extracted,"An 84-year-old woman is brought by her caretaker to the physician because of a 2-day history of fever, severe headache, neck pain, and aversion to bright light. She appears uncomfortable. Her temperature is 38.5°C (101.3°F), pulse is 110/min, and blood pressure is 145/75 mm Hg. Physical examination shows involuntary flexion of the bilateral hips and knees with passive flexion of the neck. Cerebrospinal fluid analysis shows a leukocyte count of 1200/mm3 (76% segmented neutrophils, 24% lymphocytes), a protein concentration of 113 mg/dL, and a glucose concentration of 21 mg/dL. A CT scan of the brain shows leptomeningeal enhancement.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [145.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",98.33333,93.41666,103.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 145.0 mm Hg + 2/3 * 75.0 mm Hg = 98.33333 mm Hg.
Hence, the patient's mean arterial pressure is 98.33333 mm Hg."
1872,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2876706-1,Extracted,"A 24-year-old man was referred to the emergency department with a complaint of dyspnea of four months' duration, which was worse for the last one week. This was associated with productive cough for the same duration. There was no history of fever, chest pain, wheeze, anorexia, and weight loss. There was history of cigarette smoking of one pack per day for the last 10 years. He was a spinner in a cotton spinning and weaving mill for eight years and was exposed to heavy cotton dust without using respiratory protection. There was no history of exposure to any other dust.
On examination, his pulse rate was 98 beats per minute, respiratory rate was 32 breaths per minute, blood pressure was 125/75 mmHg, and temperature was 39.5°C. The patient was also noted to be cyanosed with gross clubbing. Respiratory examination revealed bilateral diffuse crepitations and rhonchi. Chest radiograph showed diffuse bilateral alveolar opacification, more marked in the middle and lower zones []. The possibilities considered were COPD with super-added infections, pulmonary tuberculosis, alveolar cell carcinoma, diffuse fibrosing alveolitis, and PAP with secondary infections due to bacteria or fungi. The results of liver and renal function tests, complete blood count, and urine analysis were normal. Sputum tested negative for acid-fast bacilli (AFB) by Ziehl Neelson stain (done daily) and for malignant cells and fungi, and grew no organism on culture. Spirometry could not be done. The patient was managed with antibiotics, bronchodilators, and oxygen therapy, following which he became afebrile but his general condition and dyspnea got worse; and he died 16 days after admission. Parts of lung were procured from postmortem for histopathological examination.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",91.66667,87.08334,96.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 75.0 mm Hg = 91.66667 mm Hg.
Hence, the patient's mean arterial pressure is 91.66667 mm Hg."
1873,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8543317-4,Extracted,"An 82-year-old man presented to our hospital's emergency room with severe upper abdominal pain. He had a history of acute thoracic aortic dissection surgery and cholecystectomy. His vital signs in the emergency room were BT 37.7°C, BP 152/86 mm Hg, HR 112 beats/min, and RR 30 breaths/min. Laboratory tests showed serum amylase 3,592 U/L, lipase 5,256 IU/L, CRP 2.80 mg/dL, WBC 7,100/μL, T-Bil 2.86 mg/dL, AST 382 U/L, ALT 263 U/L, ALP 588 U/L, γ-GTP 929 U/L, and LDH 452 U/L. We decided to perform urgent ERCP because CT and MRI findings suggested a biliary stone impacting the ampulla of Vater. As expected, we found an impacted biliary stone. We removed the stone and performed EBS and NPD. The patient's severe pain resolved after the procedure (Fig. ). The clinical course was good despite the high risk of mortality from AP.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [152.0, 'mm hg'], 'Diastolic Blood Pressure': [86.0, 'mm hg']}",108,102.6,113.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 152.0 mm Hg + 2/3 * 86.0 mm Hg = 108.0 mm Hg.
Hence, the patient's mean arterial pressure is 108.0 mm Hg."
1874,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7811567-2,Extracted,"Presentation: A 45-year-old male presented with high BP (208/131 mmHg), acrocyanosis, vasculitic skin rashes (), and nonhealing ulcers ().
Investigations: Fundoscopy showed optic disc blurring in the left eye and full blood count (FBC) revealed thrombocytosis (PLT -953 × 109/L). Bone marrow biopsy confirmed JAK2-mutation-positive essential thrombocytosis.
Outcomes and follow-up—unlike our Case 1 patient, no renal artery stenosis was found. BP was well-controlled (reaching 130/70 mmHg) with nifedipine.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [131.0, 'mm hg'], 'Systolic Blood Pressure': [208.0, 'mm hg']}",156.66667,148.83334,164.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 208.0 mm Hg + 2/3 * 131.0 mm Hg = 156.66667 mm Hg.
Hence, the patient's mean arterial pressure is 156.66667 mm Hg."
1875,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5488048-1,Extracted,"A 33-year-old man was examined because of hypertension and easy fatigability of the lower extremities. The femoral pulses were poorly present. His blood pressure, measured indirectly at admission, was 180/120 mmHg at the brachial artery and 90/70 mmHg in the thigh. His medical history included isolated, poorly controlled arterial hypertension despite aggressive pharmacotherapy (amlodipine, ramipril, nebivolol and methyldopum). The resuts of routine laboratory examinations were normal, including C-reactive protein and procalcytonin.
On admission, transthoracic echocardiography showed a left ventricle with preserved systolic performance (left ventricular ejection fraction 56%) and aortic valve with correct morphology and function. Due to a slight dilatation of the ascending aorta on routine examination (chest X-ray, echocardiography), he was referred for magnetic resonance (MRI) imaging of the aorta.
On MRI, the ascending aorta and aortic arch were normal. Approximately 25 mm distal to the left subclavian artery orifice, a severely stenotic segment of the descending aorta was visualised. Critical (3–4 mm) aortic coarctation was diagnosed. It confined not only the thoracic aorta, but also the abdominal aorta up to the coeliac trunk (total lesion length 180 mm) (). Moreover, the supradiaphragmatic descending aorta was completely occluded. The aortic arch branches and coeliac and renal arteries were normal without any changes compromising flow. The collateral circulation was excessively developed, predominantly through the intercostal branches and markedly dilated left and right thoracic arteries (). In the narrowed aortic wall, signal enhancement was noted in the short time inversion recovery (STIR) MRI window, which suggested an underlying chronic inflammatory process, or aortitis.
Surgery was performed through a left thoracotomy and abdominal retroperitoneal approach by cardiac and vascular surgeons. First, the descending aorta was side-clamped distal to the left subclavian artery and a 22-mm-diameter prosthetic vascular graft was anastomosed in an end-to-side fashion. Then it was passed through a small incision in the left lateral portion of the diaphragm. Eventually, distal anastomosis was performed 15 mm below the renal arteries to a macroscopically normal aortic wall. During surgery, specimens from the anastomosis sites were taken for histological examination.
The patient’s postoperative course was complicated by transient paresis of the brachial plexus. Aggressive postoperative rehabilitation at both the cardiac surgery department and rehabilitation centre enabled complete functional recovery. After surgery, there was no need for hypertensive agents and his arterial pressure was well controlled (brachial blood pressure of 110/70 mmHg and femoral pressure of 100/65 mmHg). Prednisone was added as oral therapy. Histopatological examination of the aortic specimens showed a chronic inflammatory process and eventually the final diagnosis of chronic aortitis was established.
Two-year follow-up MRI angiography and computed tomographic (CT) examinations showed the new graft was patent, with no abnormalities at the anastomosis sites (). At the last follow up, he was asymptomatic with no neurological dysfunction.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [180.0, 'mm hg'], 'Diastolic Blood Pressure': [120.0, 'mm hg']}",140,133,147,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 180.0 mm Hg + 2/3 * 120.0 mm Hg = 140.0 mm Hg.
Hence, the patient's mean arterial pressure is 140.0 mm Hg."
1876,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6940374-1,Extracted,"A 56-year-old man was diagnosed as pancreatic cancer with multiple liver metastases at a tertiary care teaching hospital in Seoul, the capital city of Korea, 8 months before visit to us. The patient had received chemotherapy, but it was not effective. Two and half weeks before visit to us, stent insertion was performed on the common bile duct to resolve the biliary tract obstruction at the same hospital in Seoul. From 4 days after stent insertion, he had felt tolerable febrile sense and chills controlled with antipyretics and analgesics at home in Daegu, a regional city of Korea. Two weeks after the stent insertion, he had been admitted to nursing care hospital in Daegu for 2 days and then visited the emergency room (ER) of a secondary care teaching hospital in Daegu, complaining of unresolved fever, chill and abdominal pain. He had diabetes mellitus on vidagliptin/metformin 50 mg/1,000 mg once a day. When he visited our ER, he was acutely ill, his blood pressure was 100/60 mmHg, decreased to 90/60 mmHg 1 hour after visit, respiratory rate 20 breaths per minute, pulse rate 90 beats per minute, and body temperature 38.8°C.
The laboratory results were as follows: white blood cell (WBC) count 1,250/mm3 (92.5% neutrophils, 4.0% lymphocytes), hemoglobin 5.9 g/dL, platelet count 14,000/mm3, C-reactive protein 19.75 mg/dL, aspartate aminotransferase 274 UI/L, alanine aminotransferase 143 IU/L, total/direct bilirubin 4.11/2.71 mg/dL, total protein 4.4 g/dL, albumin 2.0 g/dL, prothrombin time (international normalized ratio) 25.3 second (2.21), active partial thromboplastin time 60.7 second, blood urea nitrogen 34.5 mg/dL and creatinine 1.9 mg/dL. The arterial blood gas analysis breathing room air was pH 7.515, pCO2 31.6 mmHg, pO2 78.8.0 mmHg, HCO3 25.5 mmol/L, and O2 saturation 96.9%. Abdomen computed tomography (CT) showed pancreatic cancer with multiple liver metastases and metallic stent inserted in common bile duct.
There was no evidence of any bleeding. The primary impression for him was the acute cholangitis with septic shock. Intravenous piperacillin/tazobactam, teicoplanin, and norepinephrine were administered. The packed red cells and platelets were transfused. He was admitted to the intensive care unit (ICU) 8 hours later. On admission, the Acute Physiology and Chronic Health Evaluation (APACHE) II score was 19 and predicted death rate was 32.2%. Two days after admission, WBC and platelet counts deteriorated to 250/mm3 and 8,000/mm3, respectively. He died of refractory septic shock 5 days after admission. On the day of his death, carbapenem-resistant K. pneumoniae grew on the blood cultures taken on the day of hospitalization. Antimicrobial susceptibility testing demonstrated resistance to all beta-lactams, including carbapenems, as well as tigecycline (). Species identification and antimicrobial susceptibility tests were performed on VITEK II system (bioMérieux, Durham, NC, USA). Two days after his death, K. pneumoniae with same antimicrobial resistance pattern grew again on the blood cultures taken on the 3 day after hospitalization. The Rapidec Carba NP test (bioMerieux, Marcy I'Etoile, France) revealed that the isolates were carbapenemase producers.
The isolates were transferred to Korea Centers for Disease Control and Prevention (KCDC), which revealed that the isolates were MCR1 possessing ST307/Tn4401a[blaKPC2] K. pneumonia. The multilocus sequence typing (MLST) and isotyping the Tn4401 were performed in accordance with the previous research method []. The sequences of the primers were MCR1 IF (5′-CAGTGCGCCAAAAGATACCA-3′) and MCR1 IR (5′-ACCGTTCTCACCCAGACTTT-3′). Each reaction was carried out by using a final volume of 20 µℓ mixture containing 2 µℓ of 10x buffer, 10 pmol of each primer, 2 uM of each dNTP, 1U of amfisure Taq polymerase (P3016, GeneDEPOT, Texas, USA), and 20 ng of genomic DNA. The PCR was performed with a eppendorf vapo-protect mastercycler (eppendorf, Hamburg, Germany) under the following conditions: initial denaturation step (5 min at 94°C), follwed by 30 cycles (30 sec at 94°C, 1 min at 52°C, 45 sec at 72°C) and a final extension step (10 min at 72°C). The expected size of the amplicon was 784 bp. E. coli (NCCP 16284, the clonal isolate of USU-ECO-12704) was used as a positive control, while sterile distilled water used as negative control []. The DNA amplicon from our KPC-KP showed a fragment of 784 bp, consistent with positive control in agarose gel electrophoresis. Antimicrobial susceptibility testing for carbapenems, tigecycline and colistin was performed by using sensititre broth microdilution plates (KORGNGC, Thermofisher scientific, Massachusetts, USA) and interpreted according to the European Committee on Antimicrobial Susceptibility Testing (EUCAST) for tigecycline and The Clinical and Laboratory Standards Institute (CLSI) for others () []. E. coli (ATCC 25922) was used as a positive control. No outbreak by this strain in the hospital occurred. The study was approved by the Institutional Review Board of Kyungpook National University Hospital (KNUCH 2018-09-010).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [60.0, 'mm hg'], 'Systolic Blood Pressure': [90.0, 'mm hg']}",70,66.5,73.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 60.0 mm Hg = 70.0 mm Hg.
Hence, the patient's mean arterial pressure is 70.0 mm Hg."
1877,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6579323-1,Extracted,"A three-year-old male child was admitted to the pediatric ward of Dr. Ruth KM Pfau, Civil Hospital Karachi (CHK) with a one-year history of generalized weakness, loose motions, decreased appetite and intermittent fever not associated with rigors, chills or night sweats, an eight-month history of inability to walk and sit, polydipsia, polyurea, abdominal distention and loss of neck holding for 14 days. He had a previous history of hospitalization six months ago due to the same complaints. The patient was accompanied by his mother. He weighed 6 kg, is the 7th born child to his parents and was delivered at term to a 37-year-old G7P7 mother via normal vaginal delivery. The mother did not report any complications or illnesses during pregnancy. He cried immediately after birth, and there were no complications during or after birth. There is no consanguinity between mother and father. The child was vaccinated but was malnourished, with an unremarkable family history.
The patient also developed diarrhea which was bulky in consistency, green in color with seven episodes per day after every meal intake. Diarrhea was associated with abdominal distention and vomiting. The mother then started giving him a combination of trimethoprim-sulfamethoxazole, after which diarrhea subsided. The child developed neck holding at four years of age, he started sitting at eight months and started walking with support at 12 months of age. The child was first breastfed within three hours of delivery and was exclusively breastfed up to six months. Complimentary feeding was started after six months with pulses, mashed potatoes, porridge and chicken. Breastfeeding was continued up to two years. Currently, the child takes 1-2 feeds per day. The personal history revealed that the patient was sleeping normally, but the appetite was decreased. The mother also noticed a weight loss, altered bowel habits, and micturition was normal.
On examination (O/E), the patient was lying on the bed irritated, severely wasted and emaciated with visible bony deformities. Initial vitals included blood pressure (BP) 110/70 mmHg, a regular pulse of 90 beats/min, a respiratory rate of 20 breaths/min, and a low-grade fever of 100° F. The patient was anemic and dehydrated, while, there was no presence of edema, clubbing, cyanosis, and lymphadenopathy. On further examination, parietal and frontal bossing, rachitic rosary (Figure ), widening of wrists and knock knees (it's a valgus deformity in which legs curve inwards so that the feet are apart when the knees are touching) were found as well. On abdominal examination, it was soft, non-tender, distended with mild tenderness on both flank regions, with a centrally placed umbilicus. The liver was palpable three fingers below the right costal margin. Gut sounds were audible 3-4 sounds/min. All other systems were unremarkable.
The anthropometric measures of the child are as follows: weight = 6.5 kg, occipitofrontal circumference = 49.5 cm, height = 72.5 cm, mid-upper arm circumference = 8 cm, upper segment = 45 cm, lower segment = 27.5 cm, weight for height = 6.5/9 *100 = 72.2 (moderately low) and height for age = 72.5/94.6*100 = 76.6 (severely low).
On investigations performed, complete blood count (CBC) showed a hemoglobin (Hb) of 5.4 gm/dl, mean corpuscular volume (MCV) of 82 fl and a platelet count of 187,000/mL. The total leukocyte count (TLC) was 10.6 x 109/L, including 39% neutrophils and 48% lymphocytes. His inflammatory markers were raised with a C-reactive protein (CRP) of 23 mg/L [Normal (N) = 3] and an elevated erythrocyte sedimentation rate (ESR) of 115 mm/hr (N = 0-22) for men and (N = 0-29) for women. The clotting profile showed an international normalized ratio (INR) of 1.01, while prothrombin time (PT) was 10.6 seconds.
The urea creatinine electrolytes (UCE) were within normal range except decreased potassium levels of 2.8 mEq/L. The levels of calcium, magnesium and phosphate in blood were 15.1, 1.9 and 4 mg/dL, respectively. The blood culture showed a growth of Burkholderia species. The urinalysis showed a pH of 5.0, specific gravity of 1.025, with the presence of protein and blood. Additionally, numerous red cells were seen along with yeast and 4-6 pus cells per high power field (HPF). The urine culture showed growth of Candida species. The stool analysis showed that the stool was hard, acidic, brown in color with 1-2 pus cells per HPF. His vitamin D levels came out to be 54.29 ng/mL, and parathyroid levels were 8.36 pg/ml. Liver function tests showed a total bilirubin of 0.28 mg/dL, direct bilirubin of 0.21 mg/dL and levels of alkaline phosphate alanine aminotransferase were 368 and 3 units per liter, respectively.
The X-rays of the chest (Figure ), skull (Figure ) and femur (Figure ) are attached below. Additionally, ultrasound of kidney ureters and bladder (KUB) showed an incidental finding of bilateral renal calculi (right kidney at lower pole measuring 0.7 cm, in the left kidney at mid pole measuring 0.7 cm), along with bilateral grade 2 renal parenchymal changes. The urinary bladder was normal in thickness with no presence of focal mass, calculus or diverticulum.
Considering the diagnosis of OI, an ophthalmology review was done to look for lens dislocation and blue sclera, but neither was present in both eyes. However, the left eye showed a corneal thinning nasally, temporally and inferiorly.
During the hospital stay, the patient was intravenously given cefotaxime 220 mg, piperacillin-tazobactam 700 mg, and meropenem three times a day. Additionally, linezolid 70 mg was injected every eight hours, along with injections of bisphosphonate 7 mg for three days, amikacin 55 mg twice a day for 14 days and fluconazole 85 mg loading dose, 45 mg once a day for 10 days. The patient was also given a teaspoon of the combination (artemether and lumefantrine) once a day. Three pints of red blood cells were transfused as well, after which his Hb became 10.6 mg/dL. During the stay, the child had a prolonged course of fever with pancytopenia, which improved on injections of meropenem, amikacin, and fluconazole.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1878,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9503,Extracted,"An otherwise healthy 39-year-old woman presents to her primary care provider because of right-leg swelling, which started 4 months ago following travel to Kenya. The swelling has been slowly progressive and interferes with daily tasks. She denies smoking or alcohol use. Family history is irrelevant. Vital signs include: temperature 38.1°C (100.5°F), blood pressure 115/72 mm Hg, and pulse 99/min. Physical examination reveals non-pitting edema of the entire right leg. The overlying skin is rough, thick and indurated. The left leg is normal in size and shape.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [115.0, 'mm hg'], 'Diastolic Blood Pressure': [72.0, 'mm hg']}",86.33333,82.01666,90.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 72.0 mm Hg = 86.33333 mm Hg.
Hence, the patient's mean arterial pressure is 86.33333 mm Hg."
1879,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7299603-1,Extracted,"Patient 1: a 52-year-old woman, non-diabetic, non-hypertensive, was referred to the emergency with a history of large-volume, frank hematemesis (four episodes in 3 days). Positive history included recurrent cough for the past 1 year and low-grade fever for 3 months. No history of dysphagia, jaundice, abdominal distension, pain abdomen or altered sensorium. No history of chronic medications (oral anticoagulants or anti-platelets), analgesic intake or any substance abuse. She had received four units of packed red cells at an outside facility prior to admission. She was conscious, oriented, hemodynamically labile (heart rate: 110/min; BP: 86/60 mm Hg) with mild fever (99°F). General survey revealed obvious pallor. All other system examinations were within acceptable limits. Her hemoglobin (Hb) was 7.3 gram%, total leukocyte count (TLC) was 6400 cells/mm3, total bilirubin was 1.31 mg/dl and total protein was 4.75 gram%. An urgent UGI endoscopy revealed an opening in the posterior wall of the lower third of the esophagus, with a diverticulum. Inflammatory changes were noted in the diverticulum (). Contrast-enhanced computed tomogram (CECT) revealed erosion of the pouch into the thoracic aorta (), and a diagnosis of AEF with acute UGI hemorrhage was made.
The patient was resuscitated with packed red cells and definitive surgical management was emergently undertaken. A left posterolateral thoracotomy was performed, and pus was found in the pleural cavity and posterior mediastinum. After debridement of the chest cavity, partial bypass was instituted by cannulating the aortic arch in between the left common carotid artery and the left subclavian artery, and connecting this via the cardiopulmonary bypass machine to another cannula in the descending thoracic aorta just above the diaphragm (). The aorta was cross-clamped above and below the suspected fistulous region and opened longitudinally. A 2 × 2 cm opening was seen in the wall of the aorta, adjoining the esophagus (), and this was internally repaired with a Dacron patch (), and the aorta was primarily closed. The esophageal opening was debrided and then repaired with interrupted polypropylene sutures, superimposed with a vascularized intercostal muscle pedicle (). Bypass was successfully discontinued and a gastrostomy and jejunostomy were created. She remained on broad-spectrum antibiotics and the rest of her postoperative course was uneventful.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [86.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",68.66667,65.23334,72.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 86.0 mm Hg + 2/3 * 60.0 mm Hg = 68.66667 mm Hg.
Hence, the patient's mean arterial pressure is 68.66667 mm Hg."
1880,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8104944-1,Extracted,"A 79-year-old woman presented to the emergency department with 2 hours of sudden-onset, severe epigastric pain. The pain was constant and severe. She reported feeling bloated but had been passing hard bowel motions in the days prior and had passed flatus that morning. There was no history of weight loss or rectal bleeding. Past medical history included coronary artery disease, hypertension, hypercholesterolaemia and blastocystis. She had no history of abdominal surgery and was an independent, non-smoker.
On examination she was mildly tachypnoeic, with normal oxygen saturations, heart rate was 74/min, with a blood pressure of 151/80 mmHg. On palpation, she was grossly distended, guarding and peritonitic throughout with no palpable hernias. Blood tests revealed an elevated white cell count of 13.4 × 109/l and a lactate of 2.3 mmol/l. An urgent computerized tomography (CT) scan of the abdomen and pelvis was performed. The CT demonstrated a large volume of free intraperitoneal fluid, with multiple loops of distended small bowel ( and ) without pneumoperitoneum. Although not noted in the report, there was concern about a ‘swirl’ in the mesentery, raising the possibility of a small bowel volvulus (SBV).
The patient was taken urgently to theatre for an exploratory laparotomy. Upon entering the peritoneal cavity, a large volume of white liquid was drained. Biochemical analysis of this fluid confirmed triglycerides of 770 mg/dl. Cytology was negative for malignant cells and no organisms cultured. The small bowel was distended, its mesentery congested and white (), with a volvulus at the root of the small bowel mesentery. The volvulus was detorted, congenital adhesions near the base of the mesentery divided after which the mesentery and bowel returned to normal colour. The small bowel walked from terminal ileum to duodenal–jejunal flexure with no further obstruction point evident. Inspection of the rest of the abdomen was unremarkable. The abdomen was washed, and the fascia was closed with 0-nylon and the skin closed with staples. On Day 4 a repeat CT scan demonstrated an ileus. Her ileus settled with conservative management and on Day 7 after surgery was discharged tolerating a full diet. Four weeks later she was reviewed in the clinic and was recovering well.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [151.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",103.66667,98.48334,108.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 151.0 mm Hg + 2/3 * 80.0 mm Hg = 103.66667 mm Hg.
Hence, the patient's mean arterial pressure is 103.66667 mm Hg."
1881,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5963,Extracted,"A 23-year-old woman presents to the emergency department with pain and frequent urination. She states she has felt uncomfortable with frequent small-volume urinary voids for the past 3 days, which have progressively worsened. The patient has no past medical history. She currently smokes 1 pack of cigarettes per day and engages in unprotected sex with 2 male partners. Her temperature is 103°F (39.4°C), blood pressure is 127/68 mmHg, pulse is 97/min, respirations are 17/min, and oxygen saturation is 98% on room air. Cardiac, pulmonary, and abdominal exams are within normal limits. There is tenderness upon palpation of the left costovertebral angle and the left flank. Urine is collected and a pregnancy test is negative.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [127.0, 'mm hg'], 'Diastolic Blood Pressure': [68.0, 'mm hg']}",87.66667,83.28334,92.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 127.0 mm Hg + 2/3 * 68.0 mm Hg = 87.66667 mm Hg.
Hence, the patient's mean arterial pressure is 87.66667 mm Hg."
1882,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8148626-1,Extracted,"A 57-year-old male with an unknown past medical history presented to our emergency department by law enforcement and emergency medical services (EMS) after being found wandering in the woods. Reportedly the patient has been neglecting to eat or drink with the intent of starving himself to death. It was estimated that he had been depriving himself of food for eight to 10 days. On arrival and admission, the patient was acutely agitated, non-cooperative, and psychotic. There was unclear history of prior alcohol or drug abuse. During admission, the patient had the following vitals: a heart rate of 78 beats per minute, respiratory rate of 16 breaths per minute, blood pressure 127/40 mmHg, pulse oximetry 98 on room air, an axillary temperature of 96.2°F. Initial cardiac telemetry showed normal sinus rhythm. Initial electrolytes values were as seen in Table , column ‘Admission’.
The patient refused intravenous (IV) and per oral (PO) medications including IV fluids. The patient had an unknown history of alcohol abuse and was started on IV fluids with supplementation of IV thiamine/multivitamin “Banana Bag” in the emergency department but the infusion was not able to be completed as the patient removed his own IV access. Following admission, the patient was allowed to eat an unrestricted diet.
On hospital day 2, the patient continued to be delirious, uncooperative, and agitated. His blood pressure was gradually declining from an early morning reading of 105/70 to 65/40 by noon; his heart rate on cardiac telemetry demonstrated a high degree of variance with a range of 50 to 140 beats per minute.
A transthoracic echocardiogram was ordered showing ejection fraction 50-54%, no significant diastolic dysfunction or wall motion abnormality, and trivial valvulopathy. A review of cardiac telemetry readings showed a pattern suggestive of sick sinus syndrome with tachycardia and sinus arrest (Figure ), followed by progression into persistent bradycardia with a mean heart rate of 40-45 (Figure ). Troponin-I levels were normal.
The patient was lethargic but otherwise not in acute distress. Crystalloid and colloid fluids included isotonic solutions of Plasmalyte and Lactated Ringers and 50 grams of 5% albumin solution; with a total volume of 3 liters. Despite volume resuscitation, the patient remained hypotensive. Systolic blood pressure continued to trend down to 55 mmHg. A repeat of electrolyte labs before IV fluid resuscitation revealed values as stated in Table , column “Hospital day 2”.
The patient was admitted to ICU and placed on a dopamine drip to mitigate the progression of cardiogenic shock. He was monitored with serial electrolyte labs and free feeds discontinued to prevent worsening of the electrolyte abnormalities. Upon normalization of the patient’s electrolytes, he was taken off the dopamine drip once his severe bradycardia had resolved. The patient’s sick sinus syndrome resolved and he was able to be downgraded from the ICU after two more days.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [127.0, 'mm hg'], 'Diastolic Blood Pressure': [40.0, 'mm hg']}",69,65.55,72.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 127.0 mm Hg + 2/3 * 40.0 mm Hg = 69.0 mm Hg.
Hence, the patient's mean arterial pressure is 69.0 mm Hg."
1883,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1780,Extracted,"A previously healthy 46-year-old woman comes to the physician because of a 3-month history of fatigue and progressive shortness of breath. She does not take any medications. Her pulse is 93/min and blood pressure is 112/80 mm Hg. Examination shows no abnormalities. Her hemoglobin concentration is 8 g/dL, leukocyte count is 22,000/mm3, and platelet count is 80,000/mm3. A peripheral blood smear shows increased numbers of circulating myeloblasts. Bone marrow biopsy confirms the diagnosis of acute myeloid leukemia. ECG, x-ray of the chest, and echocardiogram show no abnormalities. The patient is scheduled to start induction chemotherapy with cytarabine and daunorubicin.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [112.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",90.66667,86.13334,95.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 112.0 mm Hg + 2/3 * 80.0 mm Hg = 90.66667 mm Hg.
Hence, the patient's mean arterial pressure is 90.66667 mm Hg."
1884,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9109,Extracted,"A 43-year-old woman presents to the neurology clinic in significant pain. She reports a sharp, stabbing electric-like pain on the right side of her face. The pain started suddenly 2 weeks ago. The pain is so excruciating that she can no longer laugh, speak, or eat her meals as these activities cause episodes of pain. She had to miss work last week as a result. Her attacks last about 3 minutes and go away when she goes to sleep. She typically has 2–3 attacks per day now. The vital signs include: blood pressure 132/84 mm Hg, heart rate 79/min, and respiratory rate 14/min. A neurological examination shows no loss of crude touch, tactile touch, or pain sensations on the left side of the face. The pupillary light and accommodation reflexes are normal. There is no drooping of her mouth, ptosis, or anhidrosis noted.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [132.0, 'mm hg'], 'Diastolic Blood Pressure': [84.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 132.0 mm Hg + 2/3 * 84.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1885,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7872594-1,Extracted,"A 52-year-old male with a past medical history of hypertension, diabetes mellitus type 2, end-stage renal disease (ESRD) on hemodialysis (HD), coronary artery disease status post coronary artery bypass grafting, and past cerebrovascular accident presented to the emergency department (ED) with altered mental status. The patient had been well, per family, including an uncomplicated HD session earlier that day, until the evening of presentation when family noted that he had increasing confusion and agitation, progressive for three to four hours, prompting them to call 911. On arrival to the patient’s home, paramedics noted that he was severely agitated, moaning loudly, and “jerking about,” particularly the bilateral upper extremities. To facilitate safe transfer to the hospital and due to paramedic concern for possible seizure-like activity, they administered midazolam five milligrams (mg) intramuscularly.
Upon presentation to the ED, the patient was noted to be febrile (38.94°C), tachycardic (115 beats per minute), and hypertensive (blood pressure 224/104 millimeters mercury (mmHg). He was moaning loudly with no coherent speech and unable to follow specific commands; however, he was responding to painful stimuli and appeared to respond to his name. Additionally, the patient was moving all extremities spontaneously and had no appreciable cranial nerve defects. The remainder of his physical exam revealed clear breath sounds bilaterally, no abdominal distension or perceived tenderness, and warm, dry, intact skin with no signs of breakdown or ulcers. Further evaluation and treatment were initiated, and the patient was started on vancomycin, ceftriaxone, azithromycin, and acyclovir for empiric meningitis coverage. A clevidipine infusion at one mg per hour was also started in the ED.
One hour after arrival and treatment initiation, the patient’s blood pressure was 143/90 mm Hg, and the infusion was discontinued. Additionally, chest radiograph did not show any acute abnormality, and computed tomography (CT) of the head without contrast showed chronic changes in the left putamen in the setting of known remote cerebrovascular accident. Laboratory evaluation was significant for an elevated blood urea nitrogen of 60 mg per deciliter (mg/dL) (reference range: 7–20 mg/dL) and creatinine of 8.3 mg/dL (0.8–1.2 mg/dL) in the setting of known ESRD. Otherwise, urinalysis did not show evidence of infection, urinary drug screen was negative, white blood cell count was 7.05 × 103/microliter (mL) (4.5–11 × 103/mL), and salicylate and acetaminophen levels were within normal limits. However, nasopharyngeal polymerase chain reaction (PCR) swab returned positive for SARS-CoV-2. A lumbar puncture was also performed, which evidenced clear cerebrospinal fluid (CSF), white blood cell count of zero per cubic millimeter (mm3) (0–5/mm3), protein of 46 mg/dL (10–60 mg/dL), and mildly elevated glucose of 121 mg/100 mL (50–80 mg/100 mL). The patient was admitted to the intensive care unit (ICU) for further management.
During ICU admission, the patient remained encephalopathic despite administration of antipyretics in the ED. His blood pressure remained stable with systolic less than 180 mm Hg with lisinopril 20 mg and amlodipine 10 mg daily. Antibiotic coverage was discontinued after approximately 48 hours as no signs of infection were present clinically or by laboratory evidence, and CSF culture returned negative (including varicella, herpes simplex, and cytomegalovirus). Magnetic resonance imaging (MRI) of the brain was performed on the morning of ICU day two, which did not show any acute pathologic changes. Continuous electroencephalogram for 24 hours was begun approximately six hours after initial presentation and showed evidence of mild, diffuse cerebral dysfunction. On ICU day three, the patient’s mentation began to improve, and he was noted to be increasingly alert, able to follow basic commands and speak simple phrases. On hospital day four, the patient was downgraded to a floor bed setting where he remained for an additional five days until his mentation was considered “back to baseline” with subsequent hospital discharge.
Repeat SARS-CoV-2 testing during outpatient follow-up 20 days after his initial ED presentation was negative. To date, the patient appears to have fully recovered from this episode of encephalopathy without neurologic sequelae.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [224.0, 'mm hg'], 'Diastolic Blood Pressure': [104.0, 'mm hg']}",144,136.8,151.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 224.0 mm Hg + 2/3 * 104.0 mm Hg = 144.0 mm Hg.
Hence, the patient's mean arterial pressure is 144.0 mm Hg."
1886,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8221133-1,Extracted,"A 50-year-old Caucasian male with a medical history of gastroesophageal reflux disease (GERD), hypertension, and chronic smoking presented to the emergency department with chest discomfort. His vitals on presentation were a temperature of 98.4 F, blood pressure (BP) of 159/89 mmHg, pulse rate of 72/minute, respiratory rate of 22/minute, and oxygen saturation of 95% on room air. He did not report any significant family history of coronary artery disease or cardiomyopathies. His blood troponin levels were within normal limits and he did not have any new changes on his ECG. He was admitted to the hospital and an echocardiogram was done which showed normal left ventricular function with trace valvular insufficiencies and mildly dilated aortic root (). Acute coronary syndrome (ACS) was ruled out and the patient was referred for an outpatient exercise stress echocardiogram, which showed no evidence of ischemia. There were no changes to his medication regimen during this encounter.
Six months later, he called emergency medical services (EMS) with episodes of stabbing chest pain associated with shortness of breath, lightheadedness, and dizziness. The patient was found to be in VF arrest en-route and was defibrillated by the EMS. On arrival, his mental status returned to baseline and the patient was conversant. His vital signs were within normal limits, and an ECG showed normal sinus rhythm but his blood work revealed elevated troponin levels that peaked at 11.74 ng/ml. An emergency cardiac catheterization was done which did not show any evidence of obstructive lesions, or focal or diffuse vascular spasms except for mild right coronary artery plaque. A computerized tomography (CT) angiogram of his chest did not show aortic aneurysm or dissection. He had frequent episodes of non–sustained ventricular tachycardia on telemetry as an inpatient (). A single chamber implantable cardiac defibrillator (ICD) was placed with settings at ventricular tachycardia (VT) monitor zone 160 and VFib zone 200 for secondary prevention of VF. He was discharged on diltiazem 180 mg daily and isosorbide mononitrate 60 mg daily.
About one month later, he again presented to the hospital with spontaneous ICD shock following an episode of transient chest pain at rest, with no notable precipitating factors. An interrogation of his ICD was done which revealed VF episodes that led to ICD firing. Subsequently, he was started on sotalol and his diltiazem was switched to amlodipine 5 mg. His ICD was reprogrammed after evaluation by an electrophysiologist.
Seven months after discharge, the patient came to the emergency department complaining of sudden substernal chest discomfort, which he rated at 10 out of 10 in intensity. His vital signs on presentation were temperature of 98.6 F, BP 166/93 mmHg, pulse rate of 69/min, respiratory rate of 48/min, and an oxygen saturation of 93% on room air. His chest discomfort improved with sublingual nitroglycerine and morphine. An ECG revealed ST elevations in lead I and aVL with reciprocal ST–T wave changes in inferior leads (). He underwent emergency cardiac catheterization with concerns for ACS, which revealed no focal coronary spasms, and non–occlusive disease with a left ventricular ejection fraction (EF) of 50–55% and mild hypokinesia in the anterolateral wall. His labs showed an elevated troponin level of 2.58 ng/ml (normal <0.03). A complete blood count, basic metabolic panel, serum electrolytes, and lipid panel were all within normal limits. A repeat ECG showed resolution of prior ECG changes (). The patient was discharged on aspirin 81 mg once a day, atorvastatin 40 mg once a day, increased amlodipine to 10 mg, sotalol 120 mg twice a day, and nitroglycerin 0.4 mg as needed for chest pain. Of note is his Imdur had been stopped a few days prior to his presentation as he had not had any recurrent` chest pain and had started using sildenafil citrate as needed for erectile dysfunction.
On follow up, the patient has not had any more hospitalization or further episodes of chest pain or ICD shocks on the current medication regimen.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [159.0, 'mm hg'], 'Diastolic Blood Pressure': [89.0, 'mm hg']}",112.33333,106.71666,117.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 159.0 mm Hg + 2/3 * 89.0 mm Hg = 112.33333 mm Hg.
Hence, the patient's mean arterial pressure is 112.33333 mm Hg."
1887,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5872667-1,Extracted,"A 60-year-old female with a past medical history significant for chronic myeloid leukemia, end stage renal disease on hemodialysis, hypertension, chronic right foot osteomyelitis, and chronic pain syndrome/neuropathy presented for evaluation of altered mental status and acute visual loss. History was provided by Emergency Medical Services and the Dialysis Center and minimally from the patient secondary to altered mental status. The patient went to dialysis as per the patient's scheduled sessions, initially awake, alert, and oriented to person, place, and time. During dialysis, the patient reportedly became acutely “sleepy” and difficult to arouse. The patient when aroused complained of blindness in both eyes and exhibited repetitive speech. No other history was obtainable and no prior history of visual loss. The patient was disconnected from the dialysis unit and sent directly to the emergency department. Patient's vital signs in the emergency department were blood pressure 143/38 mmHg, heart rate 80 bpm, respirations 18/min, oxygen saturation 96% on room air, and afebrile (35.9°C). The exam was performed by the emergency medicine physician: patient exhibited normal ocular motions, sclera, and periorbital structures but exhibited bilateral homonymous hemianopia. No signs of acute trauma were noted. The patient was oriented only to herself and was moving all her extremities. Bilateral arms had AV fistulas with palpable thrills. The patient was given an NIH stroke scale of 8 (1 point for LOC questions, 1 point each for motor drift in each extremity, and 3 points for bilateral hemianopia). The rest of her exam was noncontributory.
Given the nature of altered mental status and neurologic findings, an emergent noncontrast head CT was performed (). CT was read as multiple punctate curvilinear foci of hypoattenuation regional to the vein of Galen and deep cerebral veins medial to the left thalamus and left occipital sulcus. Given recent hemodialysis, findings were consistent with air in vascular structures. The patient was placed on 100% oxygen via nonrebreather and placed in Trendelenburg position. Discussion with interventional neurosurgery was undertaken regarding potential for aspiration of air, but it was considered too diffuse and widespread to be efficacious. She was then transferred to a nearby hyperbaric center for definitive management. The patient was taken immediately by the hyperbaric team to the dive chamber, where she underwent a five hour session at 3 atm. MRI performed immediately after hyperbaric therapy demonstrated multiple subacute supra and infratentorial embolic infarctions in the bilateral occipital lobes, left thalamus, parietal lobe, and cerebellar tonsil, with minimal midline shift. Multiple areas showed sequela of small vessel and perfusional ischemic disease. The plan was to monitor for 4–6 hours followed by consideration of a second session if hemodynamic and neurologic assessment allowed/necessitated further care. The patient's inpatient stay was complicated by Klebsiella bacteremia and septic shock requiring intubation, multiple vasopressors, AV fistula malfunction, and runs of supraventricular tachycardia. No further hyperbaric therapy was performed for these reasons. The patient's mental status was further affected by hypoactive ICU delirium. A transthoracic echocardiogram with agitated saline did not demonstrate an intra-atrial communication. After a prolonged hospital course the patient's mental status improved. Evaluation by neurocritical care documented that patient was conversive, oriented to person and place, but was inattentive and needed constant redirection. The patient continued to have bilateral hemianopia. Extremities were full against gravity and sensation was intact. Of note, the patient was seen subsequently in the ED 3 months later for an unrelated visit by an author, her mental status had improved but she remained with severe visual deficits consistent with her bilateral homonymous hemianopia and had persistent difficulty with maintaining attention.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [143.0, 'mm hg'], 'Diastolic Blood Pressure': [38.0, 'mm hg']}",73,69.35,76.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 143.0 mm Hg + 2/3 * 38.0 mm Hg = 73.0 mm Hg.
Hence, the patient's mean arterial pressure is 73.0 mm Hg."
1888,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8409202-1,Extracted,"A 47-year-old woman complained that the physical examination found a hemangioma for more than 10 years.
The patient was diagnosed with a right hepatic hemangioma for more than 10 years and had failed interventional hepatic artery embolization at a local hospital 1 year ago. The hemangioma showed an increase in size during 10 years (from 3 cm to near 10 cm in diameter).
The patient had a history of caesarean section and unilateral salpingectomy and had failed interventional hepatic artery embolization at a local hospital.
The patient’s temperature was 36.5 °C, heart rate was 75 bpm, respiratory rate was 19 breaths per minute, blood pressure was 120/72 mmHg, and oxygen saturation in room-temperature air was 99%. She had no tenderness or rebound pain in the abdomen. The frequency of bowel sounds was four per minute, and there were no other pathological signs.
Blood, biochemistry, and urine analyses were normal. Electrocardiogram, chest X-ray, and arterial blood gas results were also normal.
Abdominal contrast-enhanced computed tomography (CT) showed the following: The right lobe of the liver had a low-density mass with a size of approximately 95 mm × 97 mm × 117 mm, the boundary was clear, and the density was uniform, which suggested a right hepatic hemangioma (Figure ). Ultrasound angiography showed that the right posterior hepatic lobe displayed a strong echogenic area with a size of 95 mm × 97 mm × 117 mm, and the boundary was clear. After a total of 2.4 mL of sulfur hexafluoride microbubble solution was injected through the anterior elbow vein, a small amount of enhancement was observed around the arterial phase in the strong echo zone. During this period, the contrast agent was significantly filled. Contrast-enhanced ultrasound showed a right hepatic posterior hemangioma (Figure ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [72.0, 'mm hg']}",88,83.6,92.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 72.0 mm Hg = 88.0 mm Hg.
Hence, the patient's mean arterial pressure is 88.0 mm Hg."
1889,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4753743-1,Extracted,"A 51-year-old female was diagnosed to have essential hypertension since 12 years and CKD since last 4 years. She progressed to end-stage renal disease 2 years back and was initiated on maintenance hemodialysis. For initial 1-year, she was on twice-weekly hemodialysis, which was subsequently increased to thrice weekly. She presented to us with complaints of progressive painless abdominal distension of 8-month duration along with anorexia and weight loss. There was no history of abdominal pain, altered bowel habits, pedal edema, fever, jaundice and no history to suggest hypothyroidism or connective tissue disease. There was no history of diabetes mellitus, jaundice, abdominal surgery and anti-tubercular treatment in past. Her medication included prazosin 10 mg/day, amlodipine 10 mg/day, calcium carbonate 1500 mg/day, twice weekly subcutaneous erythropoietin, oral iron and multivitamin. On examination, she had normal sensorium with blood pressure of 180/120 mm of Hg, pulse rate - 110/min, respiratory rate - 20/min, was afebrile and pale. Her abdomen was symmetrically distended with fluid thrill. There were no visible veins; hernial sites were normal with no cutaneous stigmata of chronic liver disease. Patient had hemoglobin of 7.7 g/dl, total leukocyte count (TLC) of 10400/mm3, with normal differential, platelet count 2.50 lakh/mm3, mean corpuscular volume 90.8 fl, mean corpuscular hemoglobin 30.1 pg/cell, mean corpuscular hemoglobin concentration 33.2 g/dl, normal coagulogram, urea 197 mg/dl, creatinine 9.4 mg/dl, sodium 144 mEq/L, potassium 6.1 mEq/L, chloride 110 mEq/L, aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase were 27, 15 and 254 IU/L respectively, bilirubin 0.8 mg/dl, total protein and albumin 6.5 and 2.7 g/dl, calcium 9.7 mg/dl, phosphorous 9.3 mg/dl, and intact parathyroid hormone 346.8 pg/mL. The serology was negative for hepatitis B, hepatitis C and human immunodeficiency virus. On tapping, the ascitic fluid was hemorrhagic and showed TLC of 70/mm3 with 70% polymorphonuclear cells, protein was 3.8 g/dl, sugar 83 mg/dl, with adenosine deaminase of 32 IU/L, and serum ascites albumin gradient of 0.8. The Ziehl–Neelsen stain and Gram-stain were negative, as was the culture for Mycobacterium tuberculosis, and pyogenic organisms. The TB polymerase chain reaction and ascitic fluid for malignant cytology were also negative. Other cancer markers such as cancer antigen (CA) 125, CA 19–9, and carcinoembryonic antigen were also normal. Her electrocardiogram revealed left ventricular hypertrophy with strain pattern, while echocardiography revealed mild mitral regurgitation, left ventricular ejection fraction of 45–50% with no evidence of systolic or diastolic dysfunction. An ultrasound abdomen performed showed gross ascites, bilateral contracted kidneys and cholelithiasis while other abdominal organs were normal. Subsequently, a contrast-enhanced computed tomography (CECT) abdomen was performed which revealed gross ascites with peritoneal enhancement and hyper-densities within fluid, in addition to the finding of contracted kidneys and cholelithiasis []. Suspecting inadequate dialysis, the patient was subjected to daily dialysis. However, there was no improvement in her ascites, and it required repeated therapeutic aspiration. To ascertain the cause of refractory ascites, the patient was subjected to exploratory laparotomy, which showed hemorrhagic ascitic fluid, thickened peritoneum and dense adhesions in-between the bowel loops and bowel loops with the abdominal wall. Keeping the possibility of cocoon abdomen, an intra-operative peritoneal biopsy was taken, which showed hyalinized fibrocollagenous tissue devoid of any lining epithelium with fibrin deposition and inflammatory cell infiltrate. There was no evidence of granulomatous inflammation or malignancy in biopsy specimen []. A diagnosis of cocoon abdomen secondary to uremia was made, and the patient was managed with daily intensive hemodialysis. Over next 1-month, there was gradual improvement in her symptoms along with decrease in ascites.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [120.0, 'mm hg'], 'Systolic Blood Pressure': [180.0, 'mm hg']}",140,133,147,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 180.0 mm Hg + 2/3 * 120.0 mm Hg = 140.0 mm Hg.
Hence, the patient's mean arterial pressure is 140.0 mm Hg."
1890,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-252,Extracted,"A 51-year-old man comes to the physician because of a 1-day history of progressive pain, excessive tearing, and blurry vision of his right eye. He first noticed his symptoms last evening while he was watching a movie at a theater. His left eye is asymptomatic. He wears contact lenses. He has atopic dermatitis treated with topical hydrocortisone. His temperature is 37°C (98.6°F), pulse is 85/min, and blood pressure is 135/75 mm Hg. Examination shows a visual acuity in the left eye of 20/25 and 20/40 in the right eye. The right eye shows conjunctival injection and an edematous cornea with a whitish exudate at the bottom of the anterior chamber. Fluorescein staining shows a round corneal infiltrate.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [135.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",95,90.25,99.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 75.0 mm Hg = 95.0 mm Hg.
Hence, the patient's mean arterial pressure is 95.0 mm Hg."
1891,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8659991-1,Extracted,"An African American gentleman in his early 40s with a history of hypertension, heart failure with reduced ejection fraction, and tobacco use disorder, as well as a family history significant for unspecified heart disease in his mother, presented to the emergency department with recurrent chest pain, shortness of breath, and two syncopal episodes spaced two days apart. The chest pain was sharp, retrosternal, mild, non-radiating, non-exertional, with frequent recurrence, and associated with palpitations. His shortness of breath was exertional but improved following a recent admission for decompensated heart failure. Following his recent discharge, he noted an episode of dizziness associated with palpitations and transient loss of consciousness. He had a similar episode while on a train ride two days later. He could not determine the duration for which he was passed out but denied confusion, tongue biting, and bowel or bladder incontinence.
He was diagnosed with heart failure with reduced ejection fraction (left ventricular ejection fraction of 20%-25%) eight months prior and was placed on guideline-directed medical therapy with carvedilol and losartan. The patient had multiple prior emergency visits for chest pain, which had been deemed non-anginal with recent left heart catheterization demonstrating no evidence of coronary artery disease. He however had poor outpatient follow up and poor medication adherence.
Vital signs on presentation included a mildly elevated blood pressure of 138/108 mmHg, heart rate of 86 beats per minute, respiratory rate of 18 cycles per minute, temperature of 36.4 degrees Celsius, and oxygen saturation of 100% in room air. Physical examination was significant for absent jugular venous distention, clear lungs to auscultation, and trace pedal edema. Electrocardiography (ECG) on presentation showed normal sinus rhythm with occasional ectopic premature complexes, normal axis, left and right atrial enlargement, left ventricular hypertrophy, and T wave inversions in leads aVL and V4-6 representing left ventricular strain pattern, unchanged compared to prior ECGs (Figure ). Laboratory investigations including serum electrolytes, blood urea nitrogen, serum creatinine, complete blood count, and cardiac enzyme panel were without gross derangements. Specifically, troponin-I on presentation was 0.02 ng/mL (normal range <0.028 ng/mL) and B-type natriuretic peptide (BNP) was 73 pg/mL (normal range <100 pg/mL).
He was admitted for further workup and placed on telemetric monitoring. Overnight telemetry revealed multiple runs of non-sustained ventricular tachycardia. Transthoracic echocardiography showed an estimated ejection fraction of 20%-25% (similar to his baseline from eight months prior), severe diffuse hypokinesis with regional variations as well as prominent trabeculations of the left ventricular wall suggestive of LVNC (Figure ). Cardiac magnetic resonance imaging (MRI) was ordered which revealed a severely dilated left ventricle with increased trabeculations within the mid to apical inferior, mid to apical lateral, and true apex. There was myocardial thinning along the left ventricular apex. Maximal ratio of trabeculated non-compacted myocardium to compacted myocardium wall measured approximately 2.6 in the lateral/inferolateral wall in end-diastole. Right ventricular size, shape, function, and diastolic wall thickness were within normal limits. On the delayed post-contrast sequences, there was a thin stripe of mid-myocardial enhancement in the basal to mid anterior wall and basal to mid septum. In addition, there was focal hyperenhancement of the posteromedial papillary muscle (Figures -).
He was counseled extensively on the importance of compliance with his medications and was recommenced on guideline-directed medical therapy (same regimen as above) before being discharged to follow up with a cardiac electrophysiologist. He was also counseled for and subsequently had an automatic implantable cardioverter-defibrillator (ICD) placed. A recent device interrogation revealed an episode of sustained ventricular tachycardia lasting over 40 seconds which was not associated with symptoms.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [108.0, 'mm hg'], 'Systolic Blood Pressure': [138.0, 'mm hg']}",118,112.1,123.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 138.0 mm Hg + 2/3 * 108.0 mm Hg = 118.0 mm Hg.
Hence, the patient's mean arterial pressure is 118.0 mm Hg."
1892,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7313138-1,Extracted,"A 70-year-old Chinese man was admitted to our hospital complaining of a 12-h history of paroxysmal chest distress and chest pain. He had a past medical history of midbrain hemorrhage 6 years ago. He denied a history of hypertension, diabetes, paroxysmal headache, palpitations, or profuse sweating. He denied a history of drug abuse or recent intense emotional stress. His family history was unremarkable. The patient, without obvious inducement, suddenly experienced chest tightness and pain while in bed at 1 a.m. The paroxysmal chest pain lasted about 1 h each time and was accompanied by a feeling of crushing in the precordial region, sweating, shortness of breath, orthopnea, and nausea. Upon admission, a physical examination revealed a blood pressure of 185/122 mmHg, a heart rate of 100 beats/min, and a respiratory rate of 32 breaths/min. A pulmonary examination showed diffuse moist rales in the lungs. The initial results of laboratory findings (Table ) showed elevated white blood cell count, myocardial enzyme, and troponin I levels. The extremely high levels of brain natriuretic peptide and arterial blood gases suggested that the patient might have heart and respiratory failure. Electrocardiography findings suggested sinus tachycardia and mild ST-segment depression in leads V4-V6. A pulmonary computed tomography (CT) scan showed bilateral pulmonary edema and a massive lesion in the left adrenal area. Transthoracic echocardiography showed left ventricular regional wall (apical wall and mid septal wall) motion abnormalities with an ejection fraction of 34%. The clinical diagnosis was ACS, heart failure, and respiratory failure. The patient was given a venturi mask for oxygen inhalation, morphine for pain relief and vasodilation, furosemide for diuresis, isosorbide nitrate for coronary artery dilation, aspirin combined with clopidogrel for antiplatelets, low molecular weight heparin for anticoagulation, and atorvastatin for lipid- lowering.
The next morning, the patient experienced severe chest distress and shortness of breath. His blood pressure fluctuated from 200/100 mmHg to 55/30 mmHg. An electrocardiogram showed ST- segment elevation in leads II, III, aVF, and V4–V6 and paroxysmal ventricular tachycardia. The levels of myocardial enzyme and troponin I increased progressively. Coronary angiography was performed to investigate possible acute myocardial infarction; however, the coronary arteries appeared normal. Based on the coronary angiography results, we stopped the antiplatelet and anticoagulation treatments.
At this time, we noticed that the patient had a left adrenal area mass that was accidentally discovered on a CT scan of the lung. An abdominal and pelvic CT scan revealed a left adrenal mass with an inhomogeneous density measuring 9.6 × 8.3 cm, and a contrast-enhanced CT scan demonstrated heterogeneous enhancement and multiple internal septum changes (Fig. (a)). The apparent ACS and labile blood pressure associated with the enormous left adrenal mass raised the suspicion of pheochromocytoma, which was further supported by markedly elevated levels of catecholamine metabolites, plasma normetanephrine> 10,000 pg/mL (reference value, 19–121 pg/mL), and plasma metanephrine levels of 6356.17 pg/mL (reference value, 14–90 pg/mL). Subsequent laboratory tests were performed, and the following results were obtained: 24-h urinary epinephrine, 139 μg (reference value, 0–20 μg); 24-h urinary norepinephrine, 377 μg (reference value, 15–80 μg); serum calcitonin< 2.0 pg/mL (reference value, 0–8.4 pg/mL); and parathyroid hormone 27.8 pg/mL (reference value, 12–65 pg/mL). Intravenous urapidil hydrochloride was administered for hypertension, while endotracheal intubation and mechanical ventilation were initiated for respiratory support. His blood pressure and levels of myocardial enzyme and troponin I gradually recovered to normal. On day 5 of admission, a repeat echocardiogram showed no obvious segmental abnormalities in the left and right ventricular wall, with recovery of the ejection fraction to 63% and normal systolic function.
After the patient’s condition improved, some examinations were carried out. Plasma aldosterone/renin activity ratio, sex hormones, and 17-hydroxyprogesterone tests were in the normal range; No abnormalities were found in 24-h urinary free cortisol excretion and 1 mg overnight dexamethasone suppression test. Thyroid ultrasound and cranial magnetic resonance imaging (MRI) results were unremarkable. Considering that contrast-enhanced CT of the chest and abdomen and cranial MRI scans did not indicate suspicious metastases or extra-adrenal lesions, we decided to perform a left adrenalectomy. Terazosin was administered and titrated over approximately 3 weeks to provide an adequate alpha blockade before the surgical procedure. A histological examination of the adrenal gland mass confirmed that it was a pheochromocytoma (Fig. ). Postoperatively, the patient’s condition drastically improved. His blood pressure normalized, and he experienced no chest distress or pain. During the 9 months of regular follow-up, he had no symptoms and was in good condition. His levels of metanephrine, normetanephrine, parathyroid hormone, serum calcium, and calcitonin were in the normal range. His electrocardiogram and echocardiogram findings were normal. No suspicious lesions were found on the abdominal and pelvic CT enhanced scans.
At this point, we reviewed his past medical history of a midbrain hemorrhage 6 years prior. The patient was referred to the hospital with a 7-day history of suddenonset diplopia and dizziness. A cranial CT revealed a high-density lesion in the midbrain. An abnormal patch signal was found in the midbrain on cranial MRI, high signal intensity on T2-weighted imaging, a higher signal intensity on T1-weighted imaging, a slightly higher signal intensity on a diffuse weighted imaging sequence, and a heterogeneous intensity on a fluid-attenuated inversion recovery sequence. The results of the cranial MRI suggested a small midbrain hemorrhage (Fig. ). No abnormalities were found on CT angiography (CTA) of the vertebrobasilar artery. After medical treatment, the symptoms of diplopia and dizziness gradually improved. At that time, a lung CT revealed a mass (4.4 × 4.0 cm) in the left adrenal area [Fig. ]. We believed that the left adrenal mass that existed six years prior was the pheochromocytoma currently confirmed by histological examination.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [185.0, 'mm hg'], 'Diastolic Blood Pressure': [122.0, 'mm hg']}",143,135.85,150.15,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 185.0 mm Hg + 2/3 * 122.0 mm Hg = 143.0 mm Hg.
Hence, the patient's mean arterial pressure is 143.0 mm Hg."
1893,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9582,Extracted,"A 63-year-old man with a history of stage 4 chronic kidney disease (CKD) has started to develop refractory anemia. He denies any personal history of blood clots in his past, but he says that his mother has also had to be treated for deep venous thromboembolism in the past. His past medical history is significant for diabetes mellitus type 2, hypertension, non-seminomatous testicular cancer, and hypercholesterolemia. He currently smokes 1 pack of cigarettes per day, drinks a glass of wine per day, and he currently denies any illicit drug use. The vital signs include: temperature 36.7°C (98.0°F), blood pressure 126/74 mm Hg, heart rate 87/min, and respiratory rate 17/min. On physical examination, the pulses are bounding, the complexion is pale, but breath sounds remain clear. Oxygen saturation was initially 91% on room air, with a new oxygen requirement of 2 L by nasal cannula. His primary care physician refers him to a hematologist, who is considering initiating the erythropoietin-stimulating agent (ESA), darbepoetin.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [74.0, 'mm hg'], 'Systolic Blood Pressure': [126.0, 'mm hg']}",91.33333,86.76666,95.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 126.0 mm Hg + 2/3 * 74.0 mm Hg = 91.33333 mm Hg.
Hence, the patient's mean arterial pressure is 91.33333 mm Hg."
1894,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3465865-1,Extracted,"A 68-year-old woman presented to the emergency department with fever, chills, nausea, and vomiting. She was diagnosed with a urinary tract infection by urinalysis and discharged home on ciprofloxacin 500 mg twice daily. She returned the following day with persistent fevers, chills, nausea, vomiting, and new onset confusion, diaphoresis, abdominal and left-sided flank pain. Her significant past medical history included uncontrolled type 2 diabetes mellitus, hypothyroidism, chronic obstructive pulmonary disease (COPD), and tobacco use.
On examination, the patient was febrile (39.4°C), hypotensive (75/20 mmHg), tachycardic (pulse 104 beats/minute), tachypneic (respiratory rate 24/minute), and hypoxic (oxygen saturation of 78% on room air). She was confused and appeared fatigued. Left-sided costovertebral angle tenderness and suprapubic tenderness were noted. Laboratory data showed a normal white cell count (of 5.0 × 109/L). Blood glucose was elevated at 362 mg/dL (normal 70–110 mg/dL). Blood urea nitrogen and creatinine were elevated at 28 mg/dL (normal 10–20 mg/dL) and 1.7 mg/dL (normal 0.6–1.1 mg/dL), respectively. Urinalysis showed a pH of 5 (normal 5–8), negative nitrites, 3 plus leukocyte esterase/high powered field (hpf), 20–30 white blood cell (WBC)/hpf and glucose of 1000 mg/dL.
The patient was admitted to the intensive care unit with suspected sepsis from a renal source. Intravenous antibiotics were initiated including vancomycin 1 gram every 24 hours and cefepime 2 grams every 24 hours. Imaging with retroperitoneal ultrasound and abdominopelvic computerized tomography showed a partially obstructing 6 mm left ureteral calculus with mild left hydronephrosis. Cystoscopy was performed with placement of a double J stent with stone manipulation into the kidney. Urine cultures from her original emergency department visit and subsequent hospitalization of both clean catch and straight catheterized specimens demonstrated Lactobacillus species of >100,000 colony forming units (CFU)/mL.
Blood cultures grew gram positive rods in both aerobic and anaerobic bottles in four out of four sets. Recovered blood-culture isolate revealed Lactobacillus delbrueckii. Susceptibility testing was performed and minimum inhibitory concentration (MIC) in mcg/mL was interpreted and reported for ampicillin (≤0.120, susceptible), clindamycin (≤0.500, susceptible), erythromycin (≤0.250, susceptible), gentamicin (≤2, susceptible), penicillin (≤0.060, susceptible), and vancomycin (≤0.250, susceptible) according to Clinical and Laboratory Standards Institute (CLSI) guidelines.
Following identification of Lactobacillus species, vancomycin and cefepime were discontinued and the patient was started on ampicillin 2 grams IV every 6 hours. All subsequent blood and urine cultures were negative. The patient continued to improve throughout hospitalization and was discharged to a skilled nursing facility one week following admission with close out-patient follow up. She completed a 2-week course of ampicillin then underwent ureteroscopy and holmium laser lithotripsy of the caculi. She has been stable to date, 9 months following presentation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [75.0, 'mm hg'], 'Diastolic Blood Pressure': [20.0, 'mm hg']}",38.33333,36.41666,40.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 75.0 mm Hg + 2/3 * 20.0 mm Hg = 38.33333 mm Hg.
Hence, the patient's mean arterial pressure is 38.33333 mm Hg."
1895,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4527811-1,Extracted,"A 78-year-old man admitted to emergency department with abdominal pain, distension, nausea, vomiting, and dyspnea for nearly 1 week and oliguria for 2 days. There was no history of nephrotoxic drug use or intravenous contrast exposure. Ultrasonographic and tomographic imagings did not reveal urinary tract obstruction. Bilateral renal parenchymal echo increased consistent with the acute kidney failure and the bladder was empty. Also there was no electrolyte disturbances that could contribute to kidney injury such as hypercalcemia, hypokalemia, hyperphosphatemia, or hyperuricemia. He had a history of prostate adenocarcinoma diagnosed 6 months ago but he did not accept the antineoplastic therapy performed for him. On physical examination, blood pressure was 115/80 mmHg, oral mucosa was wet and there was severe abdominal distension and tenderness. At admission laboratory values were as follows; urea: 116 mg/dL, creatinine: 4.7 mg/dL, C-reactive protein (CRP): 77 mg/dL, chloride: 90 mmol/L, lactate dehydrogenase (LDH): 556 μ/L, pH: 7.49, pCO2: 35.9 mmHg, HCO3: 28 mmol/L. On urinalysis; urine pH was <5 and density was 1017. On CT there were multiple lymph nodes in the abdominal cavity, also gastric and duodenal distension due to lymph node compression on distal duodenal segment (Fig.). Intravesical pressure of the patient was 36 mmHg (normal levels of intra-abdominal pressure: 0–5 mmHg). Endoscopy revealed gastric dilatation and duodeno-gastric reflux. After nasogastric (NG) tube insertion, 8 L of gastric fluid discharged suddenly. After medical decompression intervention, urine output increased gradually and creatinine levels started to regress. But after the removal of NG tube, clinical status deteriorated again. Therefore, surgical decompression (gastrojejunostomy) was performed. After decompression operation beside the clinical and radiological status (Fig.), laboratory values improved, but intravesical pressure was not measured again. After operation laboratory values were as follows; creatinine: 2.4 mg/dL, CRP: 27 mg/dL, LDH: 399 μ/L. During follow- up period creatinine levels fell to 2 mg/dL, gradually.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [115.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",91.66667,87.08334,96.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 80.0 mm Hg = 91.66667 mm Hg.
Hence, the patient's mean arterial pressure is 91.66667 mm Hg."
1896,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7899040-1,Extracted,"A woman aged 77 years was referred to our hospital due to respiratory distress. She had no medical history until then like hypertension, dyslipidemia or diabetes. And she also did not have any risk factors like thrombophilia, history of trauma, hospitalization steroids use, hormonal contraceptives, current smoking, chronic respiratory disease, infection, recent surgery, cancer and chemotherapy. Her blood pressure was 132/74 mmHg, she had a regular heart rate of 108 bpm and a respiratory rate of 18 breaths/min, and her oxygen saturation was 85% on room air. Electrocardiography showed inverted T waves in leads V1–3. Chest X-ray showed dilatation of the pulmonary artery and a cardiothoracic ratio of 60% ().
Echocardiography showed right ventricular dilatation and a tricuspid regurgitation pressure gradient of 70 mmHg (). Computed tomography (CT) revealed thrombotic occlusions of both pulmonary arteries and, coincidentally, a thrombus in an aneurysm in the popliteal vein of the left leg ( and ). Right to left ventricle (RV:LV) diameter ratio, measured on the four-chamber view, was high (2.11). Based on these findings, acute PE was diagnosed and the patient was started on rivaroxaban (15 mg orally twice daily for the first 21 days, followed by a maintenance dose of 20 mg orally once daily).
After 12 weeks of anticoagulant therapy, the thrombus in the popliteal vein aneurysm was disappeared (). The D-dimer value had normalized (from 14.6 μg/mL to 0.5 μg/mL). CT angiography showed dissipation of the pulmonary thrombus, but RV:LV diameter ratio remained high (1.25). Perfusion scintigraphy showed that multiple perfusion defects remained ( and ). Swan–Ganz catheterization was also performed. Mean pulmonary artery pressure was 26 mmHg, and pulmonary vascular resistance, 6.65 Wood units. Pulmonary angiography revealed organized distal thrombi. Based on these findings, we diagnosed CTEPH due to recurrent formation of thrombi in the PVA.
The patient is now due to undergo balloon pulmonary angioplasty (BPA) and surgery to treat the CTEPH and PVA, respectively.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [132.0, 'mm hg'], 'Diastolic Blood Pressure': [74.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 132.0 mm Hg + 2/3 * 74.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1897,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8586,Extracted,"A 28-year-old man is admitted to the emergency department with a gunshot wound to the abdomen. He complains of weakness and diffuse abdominal pain. Morphine is administered and IV fluids are started by paramedics at the scene. On admission, the patient’s blood pressure is 90/60 mm Hg, heart rate is 103/min, respiratory rate is 17/min, the temperature is 36.2℃ (97.1℉), and oxygen saturation is 94% on room air. The patient is responsive but lethargic. The patient is diaphoretic and extremities are pale and cool. Lungs are clear to auscultation. Cardiac sounds are diminished. Abdominal examination shows a visible bullet entry wound in the left upper quadrant (LUQ) with no corresponding exit wound on the flanks or back. The abdomen is distended and diffusely tender with a rebound. Aspiration of the nasogastric tube reveals bloody contents. Rectal examination shows no blood. Stool guaiac is negative.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",70,66.5,73.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 60.0 mm Hg = 70.0 mm Hg.
Hence, the patient's mean arterial pressure is 70.0 mm Hg."
1898,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4983335-1,Extracted,"A 30-year-old right hand (RH) dominant Hispanic male with no past medical history presented to the ED after injuring his finger during a recreational football game. The patient attempted to catch the ball but jammed and dislocated the fourth digit of his RH at the middle phalangeal joint (MPJ). The patient presented with the following vital signs: blood pressure (BP) 126/83 mmHg, heart rate (HR) 90 beats/min, respiratory rate (RR) 18 breaths/min, SpO2 100% on room air (RA), and temperature 36.3°C. The patient underwent a hand radiograph that demonstrated a fracture dislocation of the proximal phalanx. The patient received an ultrasound-guided ulnar nerve block using a total of 5 mL of 1% lidocaine without epinephrine for pain control. After five minutes, adequate anesthesia was obtained as noted by the patient, and the reduction and splinting were successfully performed. The ED physician noted the reduction was easy to perform; the patient noted only minimal pain while performing the nerve block and was pain-free during the reduction and splinting of the digit. The patient had complete return of sensation to his hand prior to discharge. Vital signs at the time of discharge were blood pressure (BP) 120/80 mmHg, heart rate (HR) 80 beats/min, respiratory rate (RR) 20 breaths/min, and SpO2 100% on room air (RA). The patient was discharged with a prescription for Vicodin for pain control.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [126.0, 'mm hg'], 'Diastolic Blood Pressure': [83.0, 'mm hg']}",97.33333,92.46666,102.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 126.0 mm Hg + 2/3 * 83.0 mm Hg = 97.33333 mm Hg.
Hence, the patient's mean arterial pressure is 97.33333 mm Hg."
1899,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-973,Extracted,"A 54-year-old man comes to the emergency department because of a 2-day history of increasingly severe abdominal pain, nausea, and bilious vomiting. His last bowel movement was yesterday and he has not passed flatus since then. He underwent appendectomy at the age of 39. He has psoriasis, hypertension, type 2 diabetes mellitus, and chronic back pain. He drinks two beers daily. He takes a topical corticosteroid, ramipril, metformin, and ibuprofen daily. He is 176 cm (5 ft 9 in) tall and weighs 108 kg (240 lb); BMI is 35.4 kg/m2. His temperature is 36.8°C (98.4°F), respirations are 15/min, pulse is 90/min, and blood pressure is 112/67 mm Hg. Examination shows thick, scaly, plaques over both elbows and knees. Abdominal examination shows three well-healed laparoscopic scars. The abdomen is distended and there are frequent, high-pitched bowel sounds on auscultation. Digital rectal examination shows an empty rectum. Laboratory studies show:
Hematocrit 44%
Leukocyte count 9,000/mm3
Platelet count 225,000/mm3
Serum
Na+ 139 mEq/L
K+ 4.1 mEq/L
Cl− 101 mEq/L
HCO3− 26 mEq/L
Glucose 95 mg/dL
Creatinine 1.1 mg/dL
Alkaline phosphatase 78 U/L
Aspartate aminotransferase (AST, GOT) 19 U/L
Alanine aminotransferase (ALT, GPT) 14 U/L
γ-Glutamyltransferase (GGT) 52 U/L (N=5–50 U/L)
Hemoglobin A1C 6.4%
Abdominal ultrasound shows nonpropulsive peristalsis of the small bowel.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [112.0, 'mm hg'], 'Diastolic Blood Pressure': [67.0, 'mm hg']}",82,77.9,86.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 112.0 mm Hg + 2/3 * 67.0 mm Hg = 82.0 mm Hg.
Hence, the patient's mean arterial pressure is 82.0 mm Hg."
1900,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2944860-1,Extracted,"A 45-year-old woman weighing 122 kg with a height of 161 cm (BMI = 47 kg/m2 ) was scheduled to undergo decompression and fixation of lumbar spine. Preoperative evaluation revealed that she was breathless in supine position and was used to sleeping in a recumbent position. She had hypertension, diabetes mellitus, as well as limited effort capacity because of her obesity. Her blood pressure and blood glucose levels were within normal limits with antihypertensive agents (.amlodepine) and oral hypoglycemic drugs (glimipride). She gave history of snoring and symptoms of obstructive sleep apnea. Her heart rate was 88 beats/min and blood pressure in recumbent position was 140/90 mmHg. On auscultation, heart sounds were normal. Air entry was bilaterally decreased at the bases with a respiratory rate of 24–26/min at rest with saturation of peripheral oxygen (SpO2 ) of 93% on air. Her Mallampati score was class 3, mouth opening was adequate, and she had a short neck (thyromental distance was 6 cm) and a thick pad of fat all around her neck with a neck circumference of 42 cm. Routine biochemical results were within normal limits. The electrocardiogram showed a sinus rhythm. Increased bronchovascular markings were seen in the preoperative chest radiograph. Preoperative echocardiogram showed a concentric hypertrophy of the left ventricle and a borderline-sized left atrium. Left ventricular ejection fraction was 50% with no regional wall motion abnormality. Pulmonary artery systolic pressure was 72 mmHg and tricuspid regurgitation was GrI/III. Analysis of blood gases on room air (fraction of inspired oxygen 0.21) revealed partial pressure of oxygen (PaO2 ) of 65 mmHg, partial pressure of carbon dioxide (PaCO2 ) of 47 mmHg, pH of 7.5, and oxygen saturation of 95%.
Two days before surgery, the patient was transferred to the intensive care unit (ICU) for optimization and she was ventilated with bi-level positive airway pressure (BiPAP) intermittently. She was given chest physiotherapy, nebulization with asthalin, steam inhalation, incentive spirometry, and was taught deep breathing exercises. Bilateral venous Doppler was done to rule out deep vein thrombosis, and a sequential compression device was used for prophylaxis of the same. A 7-Fr triple lumen catheter was secured in the right internal jugular vein under local anesthesia in the ICU.
On the morning of the surgery, the patient's blood sugar level was 178 mg/dL. After premedication with pantoprazole 40 mg and mosapride 10 mg, the patient was transferred to the operating room on her large-sized ICU bed. All equipments required in the case of difficult intubation were kept ready. After attaching monitors, such as, pulse oximeter, cardioscope, and noninvasive blood pressure (large size cuff) monitor, the patient was premedicated with fentanyl 1 µg/kg i.v., midazolam 0.03 mg/kg i.v., and glycopyrrolate 0.2 mg i.v. The patient was induced with propofol 2 mg/kg i.v. We were able to mask ventilate the patient adequately, so intermediate acting muscle relaxant atracurium 0.5 mg/kg i.v. was given. On direct laryngoscopy with stubby handle and Macintosh blade, Cormack Lehane view II was found and we were able to intubate the patient with a 7.5-mm cuffed flexometallic endotracheal tube. Proper tube placement was confirmed with end-tidal carbon dioxide (ETCO 2) and bilateral auscultation of chest being equal and clear. A radial artery catheter of 20 G was placed in the left hand and invasive blood pressure monitoring was done. The eyes were taped shut and padded. The patient was made to lie in a prone position; taking care that the bolsters were placed far enough to prevent abdominal compression. All pressure points were padded with cotton rolls. Her head was placed on a gel head support avoiding eye compression.
Anesthesia was maintained with O 2 :N 2O::50:50, sevoflurane 1%–1.5%, fentanyl 1 µg/kg/h i.v., and atracurium 0.2 mg/kg/h i.v. The patient was ventilated with volume control mode with a tidal volume of 550 mL at 16 breaths per min with peak airway pressure of 34 cm H 2 O with a positive end-expiratory pressure (PEEP) of 6–8 cm of H 2 O. Initial reading of ETCO 2 was 36–38 mmHg, which was constantly monitored to diagnose any embolism. She maintained SpO 2 of 95%–98% and central venous pressure (CVP) around 10–12 cm H 2 O. Her arterial blood gas analysis, CVP, urine outflow, blood glucose, and temperature were continuously monitored during the surgery. Intraoperative arterial blood gas revealed PaO 2 of 85 mmHg, PaCO 2 of 47mmHg, pH of 7.35, HCO 3 24, and oxygen saturation of 96%. PaO 2 /FiO 2 was 170, PAO 2 of 297, and the alveolar arterial (A-a) gradient of 212.7. There was an unexplained drop in the blood pressure an hour after incision, which responded to dopamine infusion of 5µg/kg/h. Operative procedure lasted for 3.5 h. Intraoperative course was uneventful. She received diclofenac 75 mg i.v. for postoperative pain relief. At the end of the surgery, neuromuscular blockade was not reversed and she was transferred to the ICU for a gradual weaning. In the ICU, we ventilated her with a 10 cm H 2 O PEEP and continued respiratory physiotherapy. She was extubated on the second postoperative day and was given BiPAP ventilation till the third postop day. She was transferred back to the ward on the postop day 4 after she had recovered spontaneous breathing and sufficient muscle strength. Further postop period was uneventful and she went home on postop day 7.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1901,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3125363-1,Extracted,"A 71-year-old Japanese woman was referred to our institution for further evaluation of chest discomfort, heavy dizziness and nausea after the use of nitroglycerin prescribed by a general practitioner.
On physical examination, cardiac auscultation revealed a systolic ejection murmur at her left sternal border. Her blood pressure was 130/60 mmHg, heart rate 68 beats/min, and her peripheral oxygen saturation was 98% in the room air. The 12-lead electrocardiogram revealed small negative T waves in leads III and a VF. A chest X-ray showed no pulmonary congestion, and the cardiothoracic ratio was 51%. Mild hypercholesterolemia was shown on her blood chemistry. Her B-type natriuretic peptide level was 81 pg/ml.
Transthoracic echocardiography revealed right ventricular hypertrophy, and a calcified lesion around her tricuspid valve (Figure ). A Doppler study showed a high velocity flow signal in her right ventricular outflow tract (RVOT), and a mild tricuspid regurgitation (Figure ). Her tricuspid valve area was calculated to be 2.2 cm2.
Multislice cardiac enhanced computerized tomography (CT) scanning showed an anomalous muscular bundle, dividing her right ventricle into two different compartments, which led to the RVOT stenosis. The stenosis was not obvious in the diastole, but especially severe in the systole. A calcification around her tricuspid valve, which seemed to be involved in the stenosis, was also observed (Figure ). No calcification was observed around the other three valves. On the cardiac enhanced magnetic resonance imaging (MRI), the calcified lesion contained very little parenchymatous tissue and revealed no enhancement (Figure ).
A cardiac catheterization was performed. Her coronary angiography showed no abnormalities. Right to left flow through her patent foramen ovale, but no left to right shunt flow, was observed (Figure ). Her pulmonary artery pressure was 24/13 mmHg; the pullback pressure recordings demonstrated a pressure gradient of 74 mmHg across the RVOT stenosis, and her right ventricular pressure was 97/5 mmHg (Figure ). The diagnosis of double chambered right ventricle was confirmed based on the stated findings. Our patient refused surgical correction, and so beta-blockade (calvedilol) was prescribed. This was effective in reducing her symptoms after discharge.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 60.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1902,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5282411-1,Extracted,"A 30-year-old woman was admitted to our hospital with a 10-day history of fever, nausea, and malaise. She had a recent upper respiratory tract infection with sore throat and nonproductive cough and took a beta-lactam antibiotic and paracetamol. She noted that 3 days prior to admission she had realised the jaundice of her sclera. Her past medical history was unremarkable. She had no drug allergies and she had no history of alcohol consumption, blood transfusion, injection drug use, and recent travel. She had no family history of liver disease. On admission she had a body temperature of 39.2°C, pulse rate of 112/min, and respiratory rate of 16/min. Blood pressure was 110/70 mmHg and jaundice of sclera and skin was observed. Tonsil and pharynx were normal. On examination of the abdomen, the right upper quadrant was tender and painful, hepatomegaly was not present, and the spleen was enlarged two fingers below the costal margin. Initial laboratory tests revealed aspartate aminotransferase (AST): 233 (8–37) U/L, alanine aminotransferase (ALT): 220 (15–65) U/L, gamma glutamyl transferase (GGT): 471 (5–55) U/L, alkaline phosphatase (ALP): 376 (50–136) U/L, lactate dehydrogenase (LDH): 909 (81–234) U/L, C-reactive protein (CRP): 13.6 (0–0.5) mg/dL, erythrocyte sedimentation rate (ESR): 34 (0–15) mm/h, total bilirubin: 15.4 (0.0–1.0) mg/dL and direct bilirubin: 14.5 (0.0–0.3) mg/dL, white blood cell (WBC) count: 8.7 × 103 (4.5–11 × 103)/mm3 with 66.4% neutrophils, 27.1% lymphocytes, and 5.6% monocytes, hemoglobin (Hb): 10.4 (11.7–15.5) g/dL, hematocrit: 30.6 (35–45)%, and platelets: 121 × 103 (150–450 × 103)/mm3. Bacterial cultures of urine and blood were negative. Chest X-ray did not show any pathologic changes. Serological markers for hepatitis A, B, and C viruses, anti-HIV, CMV IgM, toxoplasma IgM, anti-nuclear antibody, anti-mitochondrial antibody, smooth muscle antibody, anti-dsDNA, and ANCA tests were negative. Brucella agglutination and Gruber Widal tests were negative. Serology performed for EBV revealed the acute EBV infection: IgM and IgG antibodies against viral capsid antigen (VCA) were positive whereas IgG antibodies against Epstein-Barr nuclear antigen (EBNA) were negative. An ultrasound scan of the upper abdomen showed a thickened and oedematous gallbladder wall (7.4 mm) with pericholecystic and perihepatic fluid and absence of cholelithiasis or dilatation of the biliary tract, suggesting an acute acalculous cholecystitis. On the 4th day of hospital stay, AST, ALT, total bilirubin, and direct bilirubin increased to 469 U/L, 361 U/L, 19.1 mg/dL, and 17.7 mg/dL, respectively, and ALP and GGT decreased to 289 U/L and 308 U/L, respectively. During admission hemolysis developed with a drop in Hb from 10.4 to 8.6 g/dL. After the 5th day of hospital stay, aminotransferase and bilirubin levels began to decrease; ALP and GGT levels continued to fall which were already decreasing since the first day of admission. Platelets were low on the day of admission (121 × 103/mm3) and rose to normal level on the 4th day. We did not use antibiotic and because symptoms and clinical course gradually improved with the conservative therapy, percutaneous drainage was thought to be unnecessary. Abdominal pain and fever resolved, and the patient was discharged on the 7th day of admission. At the 1-month follow-up, the patient was asymptomatic, jaundice had resolved, and laboratory findings were normal.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1903,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6329273-1,Extracted,"A 48-year-old female presented in our outpatient department with on-and-off colicky pain in the left hypochondrium along with loose stools, emaciation, and on-and-off fever with chills for the last 1½ years. On clinical examination, there was pallor, pulse rate was 120/min, oral temperature was 100.2°F, and blood pressure was 110/70 mmHg. On palpation, abdomen was soft with mild tenderness in the left hypochondrium, with no definitive palpable mass. Blood investigations revealed hemoglobin: 5.4 g/dl, platelet count: 1.76 million/mm3, total leukocyte count: 17600/mm3, and differential leukocyte count was predominantly neutrophilic (85%). The patient's renal function tests, fasting blood sugar levels, and liver function tests were normal. The hydatid serology (immunoglobulin G antibodies, ELISA) of the patient was positive.
A computed tomography scan done 2 months back at some other infirmary revealed a large air-filled cystic lesion with a rim of peripheral calcification in the left upper quadrant []. Since it had no thoracic communication, thus the most likely source of air was its communication with the bowel.
At our institution, an X-ray abdomen (erect, anteroposterior [AP] view) was done. It showed a radiolucent area in the left upper quadrant with membrane-like densities []. Subsequently, the patient underwent a contrast-enhanced computed tomography abdomen. It showed a large, well-defined, rounded cystic lesion measuring 11.4 cm × 9.2 cm × 10.8 cm approximately (AP × TRA × CC) in the inferior aspect of spleen with no appreciable enhancement but with air-fluid level, wall calcifications, and calcified intraluminal membranes []. There was also a large exophytic component with loss of fat planes with splenic flexure of transverse colon and lateral abdominal wall []. The involved splenic flexure had thickened walls (wall thickness: 6.8 mm). On administration of diluted nonionic contrast per rectum, the contrast was found to accumulate within the cyst []. A nonenhancing, wedge-shaped, hypodense area was also noted in the upper pole of the spleen (7.2 cm × 3.4 cm) suggestive of an infarct []. The left kidney was shrunken and pushed posteriorly by the cyst []. The patient had mild hepatomegaly and no other abnormality was found in the liver and lungs.
About 4 units of packed red blood cells were given preoperatively to build up the hemoglobin of the patient. Vaccines for Streptococcus pneumonia, Haemophilus influenzae, and meningococcus were administered 2 weeks before surgery.
Intraoperatively, a large cystic lesion was seen over the convex surface of the spleen which was densely adherent to the lateral abdominal wall. At lower end, cyst was seen communicating with splenic flexure of colon. 10% povidone-iodine-soaked sponges were used to pack whole of abdominal cavity except small area over cyst. On aspiration of cyst, initially, free gas having foul fecal smell came out followed by faecal matter. Cavity was opened and its contents (faecal matter with peel of vegetables) were sucked out. No active daughter cyst and germinal layer were found due to calcification. Whole of the spleen along with calcified cyst and part of transverse colon were excised []. Colocolic primary anastomosis was made along with covering loop ileostomy.
The patient was kept nil per oral till stoma became functional. Thereafter, the patient was started orally and subsequently discharged with oral albendazole 10 mg/kg to be taken twice a day for 2 weeks. The patient is on regular follow-up and doing well. We plan to close the ileostomy after distal cologram to ensure that there is absolutely no leakage from colocolic anastomosis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1904,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-1852901-1,Extracted,"A 38-year-old multigravida with an intrauterine pregnancy at 35
weeks was found unconscious at her home and airlifted to the
nearest tertiary care center. Throughout transport and upon
arrival at the ED, her mental status alternated between combative
and lethargic and was unable to provide any coherent information
regarding her present condition or past medical history. Her
family later reported that the patient had presented to her
primary care physician five days earlier with complaints of left
otalgia and low grade fever. Treatment was initiated with
azithromycin for otitis media, but her pain continued to worsen
precipitating an emergency room visit the day before her admission
to the hospital. She received prescriptions for
amoxicillin-clavulanate and opioids at this visit but had not yet
started these medications. Her husband reported several bouts of
emesis that same evening before her changes in mental status the
following morning. Her primary obstetrician was also contacted and
she verified an uncomplicated prenatal care with a term vaginal
delivery in her first pregnancy, followed by a caesarian delivery
for breech presentation in her second pregnancy. The patient had
been counseled during this pregnancy regarding mode of delivery
and opted for repeat caesarean section at 39 weeks.
On arrival in the ED, she was febrile to 38.7 C, with a pulse rate
of 152 bpm, respiratory rate of 40, blood pressure of 147/80,
and Glasgow coma score of 11 (4 for eye opening, 1 verbal, 6
movement). Fetal heart tones were noted to be 170 bpm with
reassuring variability. Uterine contractions were noted every 2-3
minutes and initial sterile vaginal exam indicated cervical
dilation of 4 cm with 50% effacement. The fetus was
vertex in presentation with a size consistent for stated
gestational age and a normal amniotic fluid index. The remainder
of the physical examination was significant for purulent drainage
from her left ear with marked erythema of both tympanic
membranes. She was also noted to have decreased breath sounds at
the base of the right lung. Complete blood count revealed a
leukocytosis of 55 000 with 70% granulocytes and
22% bands. Chest X-ray indicated a possible infiltrate in
the right middle and lower lobes. The patient was then intubated
for airway protection, sedated, and given cetriaxone (2 g q 12
hours, IV) for empiric treatment of meningitis before being sent
to the radiology suite. CT scan of the head revealed fluid
collection in the middle ear and mastoid on the left. She was
transferred to the intensive care unit and lumbar puncture
obtained with 12 750 leukoctyes (80% PMN), glucose <5,
and protein of 965. Preliminary blood and cerebrospinal fluid
cultures indicated gram positive cocci in chains, consistent with
S. pneumoniae. Vancomycin (1 g q 24 hours,
IV) was then added for broader coverage, and dexamethasone (10
mg q 6 hours, IV) started as adjuvant therapy. Myringotomy at
bedside revealed frank purulence in the middle ear which was
evacuated and sent for culture. Continuous fetal and uterine
monitoring was initiated with an experienced labor and delivery
nurse posted at bedside for signs of fetal distress or continued
preterm labor. This comprehensive level of care was continued
until the level of sedation was decreased and the patient was
extubated. Uterine contractions ceased in regularity after the
first 24 hours with no further cervical change noted. Patient
remained intubated until hospital day eight when her mental
status had returned to baseline. At this time, she was
transferred to the antepartum floor for two additional days of
surveillance before discharge home. Final cultures from blood,
CSF, and ear were consistent with S. pneumoniae
with sensitivity to vancomycin. Patient completed the final four
days of a 14-day course of vancomycin and ceftriaxone at home.
Her obstetrical care was then returned to her primary
obstetrician.
At 38 weeks gestation, the patient presented to her primary
obstetrician with uterine contractions and was noted to be 9 cm
dilated. She had a successful VBAC delivery of a male infant
weighing eight pounds with APGAR scores of 8 and 9, at 1 and 5
minutes, respectively. Mother and child are doing well at the
time of this writing, with no sequelae since delivery.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [147.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",102.33333,97.21666,107.45,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 147.0 mm Hg + 2/3 * 80.0 mm Hg = 102.33333 mm Hg.
Hence, the patient's mean arterial pressure is 102.33333 mm Hg."
1905,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7495951-1,Extracted,"A 59-year-old female with a history of smoking presented with complaints of gradually worsening shortness of breath over five months. She denied chest pain, cough, and hemoptysis. She had a decreased appetite but no weight loss. She also reported dull right shoulder pain for three months. She had smoked one pack of cigarettes per day for 40 years but had quit 17 months ago. She had worked in the printing business for 23 years. She had no known history of exposure to tuberculosis or asbestosis. Family history was significant for squamous cell lung cancer in her sister at the age of 32 years.
On examination, blood pressure was 137/62 mmHg, heart rate was 81 beats/min, and the temperature was 36.7 °C. She did not have any palpable cervical, supraclavicular, or axillary adenopathy. Heart sounds were regular. Lung sounds were clear bilaterally. The abdomen was non-distended with no hepatosplenomegaly. No rashes, pedal edema, or soft tissue nodules were appreciated. Initial lab work revealed a white blood cell count of 8.3 x 103/μL, hemoglobin of 9.5 g/dL, and platelet count of 509 x 103/μL. Basic metabolic panel revealed serum sodium of 137 mEq/L, serum potassium of 4.2 mEq/L, blood urea nitrogen of 8 mg/dL, and creatinine of 0.5 mg/dL.
A CT scan of the chest was done, which showed right upper lobe mass and ipsilateral mediastinal adenopathy (Figure ). Biopsy of the lung mass showed necrotic tissue, which was non-diagnostic (Figure ). Subsequently, an endo-bronchial ultrasound-guided fine-needle aspiration (EBUS-FNA) biopsy was performed, which revealed enlarged, hyperchromatic cells with coarse chromatin and prominent nucleoli in the right subcarinal and paratracheal lymph nodes (Figure ). Tumor markers were positive for cytokeratin-7 (CK7), thyroid transcription factor 1 (TTF-1), and napsin A, consistent with lung adenocarcinoma. Mutation analysis was negative for BRAF V600E, epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK) 2p23, and ROS1 6q22 gene arrangement. The programmed death ligand-1 (PD-L1) tumor proportion score was 100%. At this point, given that she had at least stage IIIA disease and a fairly bulky tumor, she was deemed to not be a candidate for surgery and neoadjuvant chemotherapy. MRI of the brain was negative for metastases; however, a positron emission tomography (PET) scan showed significant fluorodeoxyglucose (FDG) avidity in the right upper lobe lung mass with direct extension through the chest wall along with the involvement of the ipsilateral mediastinal, neck, and axillary lymph nodes. It was thought that this could be due to lymphatic spread secondary to chest wall invasion, which would classify this malignancy as stage III disease. Notably, the PET scan also showed FDG-avid nodules in the soft tissues of the bilateral buttocks (Figure ). Thereafter, these lesions were biopsied and revealed metastatic lung adenocarcinoma (Figure ). Palliative treatment with pembrolizumab, cisplatin, and pemetrexed was initiated. Unfortunately, her disease continued to progress and ultimately she died from complications five months after diagnosis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [137.0, 'mm hg'], 'Diastolic Blood Pressure': [62.0, 'mm hg']}",87,82.65,91.35,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 137.0 mm Hg + 2/3 * 62.0 mm Hg = 87.0 mm Hg.
Hence, the patient's mean arterial pressure is 87.0 mm Hg."
1906,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2771838-1,Extracted,"An 86-year-old woman presented with worsening nausea and vomiting. Because of her progressive dysphagia to solids for the last 6 months, she had ingested only semisolids and liquids. Three days before seeking evaluation at our hospital, she had difficulty in swallowing liquids, along with nausea and vomiting. She had lost about 5 kg of weight. The medical history revealed that she had been diagnosed with primary hypertension, an ascending aortic aneurysm, congestive heart failure, moderate aortic regurgitation, and moderate mitral regurgitation 6 years previously. Because of old age, she did not undergo an operation and she was on symptomatic treatment. She had undergone vertebroplasty due to multiple compression fractures of the thoracic and lumbar vertebrae 5 years ago. On admission to the hospital, she had a chronically ill appearance. The blood pressure was 130/90 mmHg, the pulse rate was 64 beats/min, the respiratory rate was 28 breath/min, the body temperature was 36.0℃, the height was 1.43 m, and the body weight was 37 kg. The physical examination showed a diastolic murmur at the right upper sternal border and a pansystolic ejection murmur at the left lower sternal border. The laboratory findings were as follows: the white blood cell (WBC) count was 5,100/mm3, the hemoglobin was 11.8 g/dL, the platelet count was 151,000/mm3, the blood urea nitrogen (BUN) was 39.8 mg/dL, the creatinine was 1.5 mg/dL, the total protein was 5.8 g/dL, the albumin was 3.2 g/dL, the lactate dehydrogenase (LDH) was 546 IU/L, and the creatinine phosphokinase (CPK) was 380 IU/L. An electrocardiogram (ECG) demonstrated a left axis deviation and left ventricular hypertrophy. Her chest radiograph revealed blunting signs at both costophrenic angles, cardiomegaly with a cardio-thoracic ratio of 0.8, and an enlarged, tortuous aorta (). Computed tomography (CT) of the chest demonstrated an enlarged, tortuous aorta (). The diameters of the ascending thoracic aorta, the descending thoracic aorta, and the proximal abdominal aorta were 7 cm, 6 cm, and 5.3 cm, respectively. There was an intramural thrombus at the level of the descending aorta. The upper gastrointestinal barium study revealed marked extrinsic compression of the distal esophagus just above the esophagogastric junction (). We concluded that the symptoms and the results of the imaging studies were consistent with dysphagia aortica. Although we recommended surgical correction of the aortic aneurysm or percutaneous endoscopic gastrostomy, the patient declined any invasive procedures and she was transferred to a nursing home on the 12th hospital day.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 90.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
1907,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8088014-1,Extracted,"A 36-year-old Caucasian man with a past medical history significant for hypertension, depression, substance abuse, and dyslipidemia presented to the hospital after an intentional overdose with tizanidine. He was found by a friend in a state of reduced consciousness and severe weakness. He had consumed alcohol the night prior to presentation and had been vomiting profusely per report. In line with his presention, there were several abnormalities on his chemistry panel, including severe hypokalemia, hypomagnesemia, and acute kidney injury. Initial potassium concentration was 2.7 mmol/L; sodium concentration, 140 mmol/L magnesium, 1.4 mg/dL; and creatinine, 1.4 mg/dL (with a previously noted baseline of 0.8 mg/dL). Initial blood pressure was 105/68 mm/Hg, pulse was 82 bpm, and temperature was 98.5 degrees Fahrenheit. On physical exam he appeared to be comfortable and was cooperative. His head was atraumatic, and pupils were equal, round, and reactive to light. He had flat neck veins, and the lungs were clear to auscultation anteriorly and laterally. His abdomen was soft with normal active bowel sounds. He had no dependent edema. He had reduced muscle strength in both upper and lower extremities in a symmetrical fashion and had reduced patellar reflexes bilaterally. Results from an electrocardiogram were abnormal. He was found to have mild prolongation of the QT interval (corrected QT [QTc] 497 ms) with the presence of U waves having the appearance of T-U fusion waves (Fig. ). Home medications included atorvastatin, levothyroxine, cetirizine, lisinopril, and tizanidine 4 mg every 6 h as needed.
He was admitted to the medical intensive care unit with continuous monitoring of his cardiac telemetry. The inpatient nephrology service was promptly consulted. He was provided with aggressive intravenous fluid resuscitation with isotonic crystalloid (lactated Ringers + 40 meq KCl/L at 125 ml/h); additional potassium replacement began in earnest both orally and parenterally. He was also administered magnesium sulfate 4 gm intravenously. Serial chemistries were ordered every 4 h. Further laboratory testing revealed an ethanol level of 219 mg/dL; acetaminophen, salicylates, and tricyclics were undectable. The urine drug screen was positive for cocaine. With further hydration and electrolyte replacement, his sensorium improved and he revealed that he had ingested 80 mg of tizanidine with 24 ounces of beer approximately 20 h before his initial presentation to the Emergency Department. The cocaine use was nearly a week prior to his presentation.
Twenty-four hours after admission, after having received 100 mEq of potassium chloride his potassium remained extremely low at 2.8 mmol/L. At this point, the serum magnesium level had improved to 1.9 mg/dL. Repeat ECG confirmed ongoing mild QT prolongation with QTc of 497 ms. The patient’s urine potassium level was abnormally elevated at 38 mEq/L (should be < 20 mEq/L in the setting of severe hypokalemia), alluding to a defect in renal potassium handling, and not losses of gastrointestinal secretions which would have led to renal potassium conservation. Since he had achieved resolution of his acute kidney injury (creatinine was now down to 0.81 mg/dL), oral spironolactone 25 mg twice daily was started. The patient was transferred out of the intensive care unit to the cardiac step-down unit for ongoing monitoring of his telemetry and rhythm. Despite further improvement in his magnesium levels (> 2.0 mg/dL), his hypokalemia persisted for approximately 72 h more, during which time he required > 100 mEq daily, totaling nearly 500 meq. The potassium levels finally stabilized at 4.5 mmol/L, and the final ECG confirmed normalization of the QT interval with QTc of 471 ms (Fig. ). On hospital day 5 he was transferred to the inpatient psychiatry service, at which time his electrolyte levels and renal function were normal. He was maintained on spironolactone 25 mg twice daily with no supplemental potassium requirements. Shortly after discharge, the patient’s aldosterone level returned to 3 ng/dL. The aldosterone to plasma renin activity ratio was reported as 7.7, which is not suggestive of primary hyperaldosteronism.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [68.0, 'mm hg'], 'Systolic Blood Pressure': [105.0, 'mm hg']}",80.33333,76.31666,84.35,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 105.0 mm Hg + 2/3 * 68.0 mm Hg = 80.33333 mm Hg.
Hence, the patient's mean arterial pressure is 80.33333 mm Hg."
1908,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3975747-1,Extracted,"A 46-year-old male patient with scrotal and pedal edema was admitted to our department in August 2012. He had been burned in a gas leakage accident 2 weeks ago. Laboratory examination showed proteinuria (4+) and more than 775 red blood cells in the urine without casts. This patient had been treated for his 2nd- to 3rd-degree burn injuries in a local burn center. He had no inhalation injury or sepsis during the whole treatment process. At the admission time, he had a body temperature of 36.6°C, a pulse rate of 75 beats/min, a respiratory rate of 16/min, and a blood pressure of 118/80 mm Hg. Physical examination revealed cutaneous convalescence after full-thickness burns of both hands, the coronal plane of the body and both legs. The skin showed fuscous, slight exudation, bleeding cracks, mild scaling and itch during the treatment process (fig. ). Severe edema in the bilateral lower extremities and scrotums were also observed.
No lymphadenopathy, hepatosplenomegaly, or neurological abnormalities were shown. Electrocardiogram and chest X-ray were normal. Abdominal ultrasonography showed bilateral normal-sized kidneys. No antineutrophil cytoplasmic antibodies, antiglomerular basement membrane antibodies and antinuclear antibodies were detected. The laboratory test results of the urine and blood for this patient are listed in table . He was diagnosed as having nephrotic syndrome on the basis of a diminished serum albumin level of 23 g/l and an increased proteinuria excretion of 10.0 g/24 h. During the treatment course, microbiological examination of wound secretion was performed twice a week and no infection was observed.
A percutaneous renal biopsy was performed on September 11, 2012 (day 57 after burn injury) to explore the cause of proteinuria. The examination under light microscopy revealed a diffuse and moderate proliferation of mesangial cells and endothelial cells without observable crescents in 20 glomeruli. Hyaline droplets containing proteins and lipids in tubules were observed. Meanwhile, red blood cells in some tubules were also observed. The interstitium showed diffuse edema and scattered infiltration of mononuclear cells. Arterioles presented as normal status. Neither tubular atrophy nor interstitial fibrosis was found, as shown in figure .
IgA and C3 are predominant immunoreactants for the diagnosis of IgAN. Immunofluorescence revealed IgA (3+), trace IgM, C3 (3+), IgG (–), C4 (–) and C1q (–) in a coarse granular pattern with mesangial and capillary distribution (fig. ), and inconspicuous staining for IgM along the glomerular capillary walls in a granular pattern. In addition, this patient showed negative staining of HBsAg and HBcAg.
Ultrastructural studies showed high-density deposits of mesangial and subendothelial cells. The mesangial hypercellularity and increased mesangial matrix were present between the glomerular basement membrane and glomerular endothelium. The thickened capillary wall was composed of basement membrane-like materials, interposed mesangial cells, and electron-dense immune-type deposits (fig. ).
Based on the proliferative properties of glomerular lesions, the patient was started on therapy with oral prednisone at a dose of 1 mg/kg/day. After treatment, the excretion of urinary protein revealed a significant decrease from 10.0 to 5.20 g/24 h in 2 weeks. Then, the patient was discharged and treatment was continued at the outpatient section. The patient had been followed up to date and showed normal renal function and mild proteinuria.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [118.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",92.66667,88.03334,97.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 118.0 mm Hg + 2/3 * 80.0 mm Hg = 92.66667 mm Hg.
Hence, the patient's mean arterial pressure is 92.66667 mm Hg."
1909,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3212605-1,Extracted,"A 37-year-old woman visited our hospital complaining of weakness in both hands. Five years prior to admission, she had noticed mild weakness of insidious onset in her left hand. However, she did not undergo medical treatment or visit clinics. Weakness developed in her right hand 2 years later. The weakness in both hands progressed gradually and the severity increased. She began to experience difficulty in writing, handling chopsticks, and making a fist. The patient visited local clinics, but was not sufficiently evaluated. On admission the patient had severe weakness and muscle atrophy in both hands, without sensory change. Her past medical history and the antenatal and postnatal periods had been uneventful. She had attended school and had led an apparently normal life until she noticed neurological manifestations. Relevant diseases, a familial history of neurological disease, smoking, and alcohol were not noted. She had taken an antihypertension drug and oral thyroid hormone at a local clinic. On examination, her vitals sign were stable, with a blood pressure of 140/90 mmHg and a heart rate of 72 beats/min. A neurological examination revealed that she was alert and her orientation was intact. Cognitive impairment was not detected. There were no abnormal findings on cranial nerve examination.
Motor system examinations using the Medical Research Council (MRC) grade revealed severe motor weakness in both hands (flexor pollicis longus, MRC grades 3/5 and 2/5 on the right and left, respectively; flexor digitorum profundus and sublimis, MRC grades 3/5 and 3/5; flexor carpi ulnaris and radialis, MRC grades 3/5 and 3/5; extensor pollicis brevis and longus, MRC grades 3/5 and 2/5; extensor carpi radialis, MRC grade 3/5 and 2/5; extensor carpi ulnaris, MRC grades 3/5 and 3/5; extensor digitorum communis, MRC grades 2/5 and 2/5; abductor pollicis brevis, MRC grades 3/5 and 3/5; and abductor digiti minimi, MRC grades 2/5 and 2/5). Prominent muscle atrophy and deformities were observed distally in both hands (). The motor power of both lower extremities was normal. The deep tendon reflex was decreased in the upper extremities.
The patient exhibited symmetric and intact responses to all sensory stimuli, and her cortical senses were intact. Her neck was supple, no carotid bruit was audible, and the results of a cerebellar function test were normal.
Laboratory investigations revealed a normal hemogram, serum electrolytes, and renal function. Cerebrospinal fluid findings were normal. Evaluations for vasculitis involving rheumatoid factor, anti-dsDNA antibody, lupus anticoagulant, anticardiolipin antibody, antithrombin III, antineutrophil cytoplasmic antibody, anti-SSA and SSB (Sjogren syndrome A and B) antibody, complement 3/4, anti-jo-1 antibody, cryoglobulin, immunofixation electrophoresis/protein electrophoresis, anti-GM1 antibody, and anti-GD1b antibody were within the normal range or negative, with the exception of a mildly elevated fluorescent antinuclear antibody titer (1 : 40). The results of tumor screening tests involving alpha-fetoprotein, carcinoembryonic antigen, cancer antigen (CA)-19-9, and CA-125 were normal. Hexosaminidases A and B, and creatine kinase were also within the normal ranges. However, a thyroid function test revealed an abnormally elevated antithyroglobulin antibody titer (794 U/mL, normal range: 0-100 U/mL) and antimicrosomal antibody (26,030 U/mL, normal range: 0-100 U/mL), but the thyroid hormone levels, including T3, free T4, and thyroid stimulating hormone, were normal.
Cervical magnetic resonance imaging revealed no prominent abnormalities except mild disc protrusion at the C5-6 and C6-7 levels. NCSs and electromyography were performed using standard techniques of percutaneous supramaximal stimulation and recordings. These examinations revealed motor neuropathies in the median motor nerve, ulnar motor nerve, and radial motor nerve, with definite motor conduction block manifesting as the compound muscle action potential amplitude being more than 50% lower for proximal than for distal stimulation across a standard peripheral nerve segment (). However, the findings of sensory NCSs in the upper extremities, and motor and sensory NCSs in the lower extremities were normal. Thus, even though the patient was negative for antiganglioside antibodies, the electrophysiological study and clinical manifestations resulted in a diagnosis of MMN.
A biopsy of the patient's thyroid tissue by ultrasound-guided aspiration revealed diffuse lymphocyte infiltration, a finding that is consistent with Hashimoto's thyroiditis (). She was treated with high-dose intravenous immunoglobulin (0.4 g/kg/day) for 5 consecutive days and then discharged. When she visited our Outpatient Department 1 month later, the weakness and deformity in her right hand was considerably improved () and the conduction block of the motor nerves were mildly improved, as evaluated by follow-up NCSs (). This patient will be continuously followed up at the Outpatient Department.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1910,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4307704-1,Extracted,"A 17-year-old Caucasian female presented to the emergency department with the complaint of left forearm pain. She initially noted paresthesia of the left hand and then left forearm pain. The pain had been progressive over the previous 10 hours and was exacerbated with flexion or extension of the wrist. She could not recall any injury or inciting event. She was otherwise healthy and without any significant past medical history. Her family history was unremarkable with the exception of her mother’s brother who died of Duchenne muscular dystrophy. Her mother had been tested for Duchenne carrier status and was negative. Her only medication was an oral contraceptive. She denied the use of tobacco, alcohol, and illicit drugs. Her initial vital signs were an oral temperature of 36.8°C, pulse of 76 beats per minute, blood pressure of 144/96 mm Hg, respiratory rate of 16 breaths per minute, and room air pulse oximetry of 100%. The physical examination of the left forearm revealed it to be firm and tender to palpation, and it measured 2cm larger in circumference than the right. Her radial pulse was palpable and her fingertip capillary refill was less than two seconds. The skin appeared normal without overlying erythema or calor. The patient experienced pain with flexion or extension of the digits and wrist. No sensory deficits of the hand or forearm were noted. Her initial laboratory evaluation showed the following: leukocytosis of 15,300 10(3)/mcL, blood glucose of 93mg/dl, elevated creatine phosphokinase of 15, 750U/L, normal erythrocyte sedimentation rate, and slightly elevated c-reactive protein at 1.27mg/L. No coagulation studies were obtained. A radiograph of the forearm was obtained and demonstrated only soft tissue swelling. Venous and arterial duplex studies of the extremity were performed. The arterial duplex demonstrated no evidence of arterial thrombosis, stenosis, or occlusion. The venous studied showed normal flow and compressibility, but the waveforms were continuous. Compartment pressures were measured in the volar and dorsal compartments of the forearm with a Stryker Needle™ (Stryker Intra-Compartmental Pressure Monitor, Stryker Corporation, USA) and found to be 86mmHg and 62mmHg, respectively. The patient was taken to the operating suite and underwent an emergent 10cm long fasciotomy of both the volar and dorsal compartments of her left upper extremity. Intraoperative cultures were obtained and showed no growth. Fortunately, the patient required minimal debridement. Total hospital course was four days. A precipitating cause could not be identified. The patient’s fasciotomy sites were surgically closed and she was discharged home with a diagnosis of idiopathic compartment syndrome. At 18-month follow up, the etiology of the compartment syndrome has not been identified, although she has been found to have a chronically elevated creatine phosphokinase (1,500U/L).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [144.0, 'mm hg'], 'Diastolic Blood Pressure': [96.0, 'mm hg']}",112,106.4,117.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 144.0 mm Hg + 2/3 * 96.0 mm Hg = 112.0 mm Hg.
Hence, the patient's mean arterial pressure is 112.0 mm Hg."
1911,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3366319-1,Extracted,"A 72-year-old woman (72 kg, 158 cm) was admitted to hospital with dyspnea and hoarseness. She had been experiencing these symptoms for a year since she had undergone a thymectomy to remove a thymoma. In the hospital, she was diagnosed with bilateral vocal cord paralysis and was scheduled to undergo a percutaneous dilatational tracheostomy with a right laser cordectomy using a suspension laryngoscope under general anesthesia. Her vital signs were stable, she had no current medical problems, and her laboratory test values were within the normal limits. The preoperative chest radiograph was unremarkable except for evidence of previous surgery. She was a non-smoker with was no history of asthma, chronic obstructive lung disease or pneumothoraces.
Before the induction of anesthesia, the patient's blood pressure, heart rate and SpO2 was 130/80 mmHg, 80 beats/min and 98%, respectively. The patient was induced with pentothal sodium 5 mg/kg and succinylcholine 1 mg/kg in preparation for a potentially difficult intubation. A 6.5-mm reinforced endotracheal tube was inserted successfully with a stylet on the first attempt. Anesthesia was maintained with air 1 L/min, O2 1 L/min, sevoflurane 1.5-3 vol%, and rocuronium. During the procedure, the end tidal CO2 was maintained at approximately 30-35 mmHg, peak airway pressure was < 20 cm H2O, and SpO2 approximately 97-99%. Her vital signs, airway pressures, and end-tidal CO2 remained stable during surgery. The total time under anesthesia was two hours; the operative time was 90 minutes. There was minimal blood loss during the surgery, and the patient received a total of 800 ml Lactated Ringer's solution. The procedure was performed as planned. The patient was extubated after confirming full recovery of motor function as tested by the hand grip strength and head control. At the time of extubation, a T-cannula was inserted through the stoma site, and the patient was encouraged to breathe through the cannula. After confirming that the patient was stable, she was transferred to the recovery room.
Her vital signs first recorded in the recovery room were a blood pressure, heart rate and SpO2 of 130/80 mmHg, 85 beats/min and 99%, respectively. Approximately two minutes after arrival, her blood pressure decreased to 70/50 mmHg, heart rate increased to 140 beats/min and SpO2 dropped to approximately 65%. The patient experienced severe dyspnea and appeared cyanotic. Blood oozing from the tracheostomy site had saturated the gauze dressing. A physical examination revealed decreased bilateral breath sounds and diffuse crepitus around the neck and shoulder, suggesting subcutaneous emphysema. 10 mg ephedrine was injected to increase her blood pressure, and an arterial line was inserted through the right radial artery for continuous blood pressure monitoring. Initially, a perforated endotracheal connector () was attempted because a T-piece was not available at that time. But the connector was not perforated (). As the connector was changed with perforated piece immediately after the patient's vital signs and SpO2 became poor, the oxygen supply through this closed connector would be maintained for approximately one minute at 5 L/min. The results of the first arterial blood gas analysis approximately three minutes after changing the connector were as follows: pH 7.342, PaCO2 49.0 mmHg, PaO2 87.7 mmHg, HCO3- 26.0 mmol/L, SaO2 94.3%, and bicarbonate -0.2 mmol/L. To identify the potential focus of bleeding that might have been the cause of the airway obstruction, the T-cannula was removed temporarily and suction was applied after confirming the stabilization of her vital signs and SpO2 but only a small amount of blood-tinged secretions was removed. The otolaryngologist examined the stoma site with a portable bronchoscope and found no complications related directly to the tracheostomy. At this point, the cause of deterioration of patient's condition was attributed to the closed endotracheal connector. A portable chest radiograph was requested to check for a potential pneumothroax. The portable chest radiograph revealed mild to moderate bilateral pneumothoraces as well as extensive subcutaneous emphysema over both shoulders, supraclavicular area, and left chest wall (). The radiograph also showed both pneumomediastinum and pneumoperitoneum. A thoracic surgeon was called to the bedside, where he inserted a chest tube into the left chest wall to treat the more extensive pneumothorax. After chest tube insertion, the patient's vital signs became more stable, her mental status was alert, and she could follow verbal commands. The follow-up chest radiograph revealed improvement in the left-sided pneumothorax (). The results of the arterial blood gas analysis performed 30 minutes after the chest tube insertion were as follows: pH 7.353, PaCO2 45.1 mmHg, PaO2 170.0 mmHg, HCO3- 24.7 mmol/L, SaO2 98.9%, and bicarbonate 1.0 mmol/L.
CT scans of the chest, abdomen and pelvis were performed for a further evaluation, revealing extensive subcutaneous emphysema over the chest and abdominal walls, bilateral pneumothoraces, pneumomediastinum, massive pneumoperitoneum, and pneumoretroperitoneum (). An MRI of the brain was performed to evaluate the damage caused by the air embolism but no specific abnormalities were found. Despite the extensive air distributed throughout the patient's trunk, the general and thoracic surgeons jointly decided to treat her conservatively.
The patient was transferred to the ICU for careful monitoring and supportive care where she remained for a week; the chest tube was left in place for ten days. Follow-up radiographs of the chest and abdomen revealed near-complete resolution of the pneumothorax, pneumomediastinum, and pneumoperitoneum. Given these findings and the cessation of symptoms, the patient was discharged two weeks after her tracheostomy. The follow-up chest radiograph three months after discharge showed no further evidence of pneumothorax or pneumoperitoneum.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1912,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-6729,Extracted,"A 16-year-old boy is brought to the emergency department by his parents after collapsing at home. He was resting at home after an uneventful dental procedure that involved the extraction of several teeth. He became drowsy and then unconscious and was unrousable. At the hospital, his temperature is 37.0° C (98.6° F), respiratory rate is 15/min, pulse rate is 67/min, and blood pressure is 122/98 mm Hg. Oxygen saturation is 85% on room air. The patient is deeply cyanosed despite a good respiratory effort and a clear airway. His lungs are clear to auscultation, bilaterally. Even though an endotracheal tube is introduced and assisted ventilation is induced, his condition does not improve. A review of dental records reveals the details of the procedure where the local anesthetic pilocarpine was administered.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [122.0, 'mm hg'], 'Diastolic Blood Pressure': [98.0, 'mm hg']}",106,100.7,111.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 122.0 mm Hg + 2/3 * 98.0 mm Hg = 106.0 mm Hg.
Hence, the patient's mean arterial pressure is 106.0 mm Hg."
1913,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4942625-1,Extracted,"A 42-year-old Iranian woman was brought to the emergency department with a sharp, persistent pleuritic chest pain beginning after an emotional stress. She had neither remarkable past medical history for coronary risk factors nor any relevant past interventions. Physical examination revealed a heart rate of 85 beats per minute, blood pressure of 120/80 mmHg, and normal S1 and S2 with S3 gallop as well as a triphasic friction rub (one systolic and two diastolic sounds) at cardiac auscultation. An initial electrocardiogram (ECG) demonstrated 1-2 mm ST elevation in leads I, II, III, aVF, and V4–V6, as well as ST depression and PR elevation at aVR (). A transthoracic echocardiography (TTE) on admission showed an apical akinesia with a preserved basal function, a mild pericardial effusion, an ejection fraction of 40%, and a moderate mitral regurgitation ().
After finding wall motion abnormality on TTE and because of persistent chest pain, despite the initial clinical diagnosis of acute pericarditis, the patient was immediately transferred to the cardiac catheter laboratory in order to look for any coronary artery disease requiring intervention. CAG demonstrated a severe muscle bridge at mid portion of the left anterior descending artery (LAD) and otherwise normal coronary arteries (); left ventriculography showed characteristic systolic ballooning of the apex in favor of TCM (). Result of the laboratory tests revealed mildly elevated serum levels of cardiac enzymes: creatine kinase MB = 30 ng/mL (normal range < 25 ng/mL) and troponin I = 0.89 ng/mL (normal range < 0.01).
The patient was treated with an angiotensin-converting enzyme inhibitor (captopril 6.25 mg three times per day), a diuretic (furosemide 20 mg three times per day), and a beta-blocker (carvedilol 3.125 two times per day). She also received aspirin for 4 days at high enough doses for treating pericarditis (650 mg three times per day). On serial ECG mild T-wave inversion was found in leads I, II, III, aVL, aVF, and V4–V6 at 2nd day of admission which then became deeper at 3rd day (Figures and ).
The patient's general condition considerably improved over the next few days and her chest pain was completely resolved. One week later, a subsequent TTE at discharge day revealed an improved left ventricular ejection fraction of 50–55% with no apical ballooning, no significant mitral regurgitation, and no pericardial effusion.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1914,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2769379-1,Extracted,"A 28-year-old previously healthy Moroccan woman presented to the emergency department 15 days after open subtotal cholecystectomy for acute cholecystitis with a 5 days history of rightsided chest pain, dyspnea and cough. She had no abdominal pain, no fever, no vomit and no jaundice. The patient was not using any specific medication and her medical history did not suggest any major disease. She had no prior history of abdominal surgery or trauma. She had a difficult partial cholecystectomy due to severe inflammation in the Calot’s triangle, large empyema in the gall bladder and, excessive bleeding during difficult dissection between gall bladder and liver bed. Subtotal cholecystectomy was done as the cystic duct could not be isolated. The physical examination revealed a conscious woman who’s had a temperature 37 degree C, a pulse rate 90 beats per minute (bpm), a blood pressure 120/70 mm Hg. The abdominal examination revealed a right upper scar without abdominal tenderness. There were no palpable masses or liver enlargement. Laboratory data revealed an hematocrit of 41%, an hemoglobin of 12,6 g/dl, white blood cells of 11,100/mm³ (83% neutrophils), a blood urea of 0,25 g/L, and a creatinine level of 10 mg/L. Liver enzymes showed a total bilirubin of 13 mg/L with a direct component of 6 mg/L; SGOT and SGPT were 87 U/L and 166 U/L, respectively (normal range for SGOT is 17–59 U/L and for SGPT is 21–72 U/L). The chest X-ray showed right-sided chest opacity that simulates pleural effusion (). Ultrasonography (US) of the abdomen revealed a large unilocular subcapsular fluid-filled collection in the right lobe of the liver with no free intra-abdominal fluid. Thoraco-abdominal computed tomography (CT) confirmed results of US and concluded a large hepatic sub capsular biloma measuring (21 cm × 16 cm × 14 cm) ( and ). Based on the imaging findings, we made a decision to perform a percutaneous US-guided puncture which removed 2000 ml of bile.
After draining the abscess a drainage catheter was positioned and left in place. The catheter drained more than 500 ml of bile over 5 days and it was removed 2 days later when the output was ceased and, a follow up US showed a near-complete resolution (). No complication occurred. We noted that the liver enzymes were normal en days following drainage. The patient was free of any symptoms at the 3 month follow up. A further US, performed after six month later was normal and, did not show any abnormalities.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1915,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-10149,Extracted,"A 72-year-old man presents to the outpatient clinic today. He has New York Heart Association class III heart failure. His current medications include captopril 20 mg, furosemide 40 mg, potassium chloride 10 mg twice daily, rosuvastatin 20 mg, and aspirin 81 mg. He reports that he generally feels well and has not had any recent worsening of his symptoms. His blood pressure is 132/85 mm Hg and heart rate is 84/min. Physical examination is unremarkable except for trace pitting edema of the bilateral lower extremities.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [132.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",100.66667,95.63334,105.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 132.0 mm Hg + 2/3 * 85.0 mm Hg = 100.66667 mm Hg.
Hence, the patient's mean arterial pressure is 100.66667 mm Hg."
1916,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-2402,Extracted,"A 13-year-old African-American boy is brought to the physician because of a 4-week history of left groin and buttock pain. The pain is worse with activity but also present at rest. He has had many episodes of abdominal, back, and chest pain that required hospitalization in the past. He is at the 20th percentile for height and 25th percentile for weight. His temperature is 36.7°C (98°F), blood pressure is 115/82 mm Hg, and pulse is 84/min. Examination shows tenderness over the lateral aspect of the left hip with no swelling, warmth, or erythema. There is pain with passive abduction and internal rotation of the left hip. Leukocyte count is 8,600/mm3.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [115.0, 'mm hg'], 'Diastolic Blood Pressure': [82.0, 'mm hg']}",93,88.35,97.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 82.0 mm Hg = 93.0 mm Hg.
Hence, the patient's mean arterial pressure is 93.0 mm Hg."
1917,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-1618845-1,Extracted,"The patient was a 19 year old male who was 204.2 cm in height and weighted 145.15 kg. He was afebrile and had a blood pressure of 128/80, left arm, seated. Otherwise healthy, he experienced gradual right wrist pain over the hamate and did not report a traumatic golf injury, although he does play golf. He had a previous fracture to the left hamulus over one year prior [Fig ] that apparently occurred on an attempt at ball strike with a sand wedge while playing golf, in which he struck a rock just behind the ball. In that case, immediate pain was noted and the condition was misdiagnosed by a sports medicine clinic prior to evaluation by the chiropractic clinician in his chiropractic office []. The left hook had to be excised due to failure of fragment fusion after plaster splinting, which was applied for six weeks for the treatment of a suspected scaphoid fracture. The patient's wrist injury healed post-surgically with some complications involving a subsequent navicular-lunate ligament tear and the patient was eventually able to return to golf.
Since there was a previous misdiagnosed fracture to the left wrist in this case, the patient called the chiropractic office first. Due to his history, computed tomography [CT] was ordered immediately following an examination which demonstrated mild to moderate pain on all right wrist movements, point tenderness over the hamate and previous difficulty in obtaining a carpal tunnel view on plain film x-ray.
The CT scan revealed a complete, slightly displaced fracture of the hook of the right hamate with associated soft tissue edema [Fig ]. A referral to an orthopedic surgeon was made to assess the need for excision of the hook of the hamate. Because of prior history, the patient elected to have the hook excised without conservative therapy.
Bilateral fracture of the hamate is uncommon. In a case-report by Bray, Swafford and Brown in 1985 [], their search of the literature found only 19 cases prior to 1977. In this case, the left wrist had an apparent mechanism of injury classic for fracture at this site, as it is the left hamate that contacts the butt of the club in a right-handed golfer []. However, the right wrist did not have this mechanism of injury. This may suggest some preexisting condition of the hamate in this patient. A condition known as hamate bipartite affects the hamate in some patients [,]. This condition, which is thought to be the result of fibrocartilagenous union between the body and hook of the hamate, typically causes symptoms in this part of the wrist and is characterized by a weak or ununited appearance of the hook that can be detected on CT or plain film radiographs [].
Hamate bipartite tends to be suspected in cases where there is no history of trauma or surgery to the wrist []. In our case, there was a denial of traumatic golf injury to the right wrist but was apparent in the left.
Features of hamate bipartite according to Pierre-Jerome & Roug [] include;
• Bilaterally similar bipartite hamulus
• No sign or history of traumatic wrist injury or edema or soft tissue changes suggestive of un-united fracture
• Equal size and uniform signal intensity on MRI evaluation of each part
• Absence of progressive degenerative changes between the two components of the hamate or elsewhere in the wrist
• Smooth, well corticated and rounded margins of the hamate and un-united hook.
Symptoms were noted in the case of the left fracture immediately upon the patient's dubbed ball strike and only surgical excision relieved the pain []. Additionally, the original radiological report accompanying the images of the right wrist was indicative of fracture and not otherwise. The attending radiologist noted degenerative changes within the right wrist, separation of the naviculolunate interspace and 1–2 mm of separation of the hook from the body of the hamate. There was also some indication of a possible previous fracture of the capitate noted by the radiologist, which would further indicate possible previous trauma to the right wrist. However, the patient denied previous trauma.
Hamate fractures represent approximately 2–4% of all fractures involving the carpal bones []. Fractures involving the hamulus, or hook, represent one of the two groups of fractures of the hamate []. Norman and others documented three radiographic signs suggestive of fracture of the hamulus []. According to their criteria, the most frequently encountered and most important feature is the lack of visualization of the hook. On the dorsovolar view the hamulus is seen en face super-imposed over the hamate and demonstrates a cortical ring shadow known as the ""eye sign"" []. A blurry or indistinguishable appearance of the ""eye"", as well as sclerosis of the hamulus, seen associated with nonunion, represents the other two radiographic features that suggest fracture of the hook [,].
Various radiographic positioning techniques can prove useful in the evaluation of potential hamate fractures. These may not always be of diagnostic quality due to limited range of motion experienced by the patient as a result of pain, especially in acute or subacute fractures []. Moreover, these fractures are commonly overlooked on standard radiographic studies of the wrist due to the lack of specific physical exam findings and a low index of suspicion []. Conventional radiographic examination of the wrist usually consists of the dorsovolar view, which demonstrates the radiographic signs first described by Norman and colleagues as discussed previously, as well as the lateral and medial oblique projections [].
The use of the carpal tunnel view [Fig ] has increased in an attempt to better elucidate the presence of a hamulus fracture []. Originally described by Gaynor and Hart [,], it is set with the patient positioned such that the flexor surface of their forearm lies against the film with slight radial rotation and the long axis of their hand is made as vertical as possible. The central ray is directed toward the palmar surface distal to the base of the third metacarpal with 25–30° of tube angulation. The patient may use their other hand or some other appropriate device to hold their wrist in this extended position [].
The ""radial-deviated, thumb-abducted lateral view"" [Fig ] is considered by some authors, an underused technique that adequately demonstrates the hamate between the thumb and index finger and clearly displays fractures of the hamulus []. This radiograph is performed by positioning the patient with their forearm in neutral and the medial aspect of their wrist against the film cassette. Their thumb is fully extended and abducted and their wrist deviated radially. This position results in maximum widening of the index finger-thumb web space []. The central ray is directed at the center portion of the index finger and thumb web. Alternately, the radial deviation can be excluded and a 15° tube angulation, oriented toward the wrist, can be used []. Bhalla and colleagues consider this view a cost-effective and time-saving adjunct to traditional wrist series when fracture of the hook of the hamate is suspected.
The hamulus, which develops from its own ossification center, may fail to fuse with the body of the hamate []. This normal variant is referred to as the os hamuli proprium and may be difficult to differentiate from avulsion fractures of the hamate hook []. In equivocal cases, computed tomography [CT] of the wrist is an effective advanced imaging technique to confirm the diagnosis of hamulus fractures due to its ability to provide an image that is orthogonal to the plane of the hamulus base fracture, while avoiding the possibility of superimposed anatomical structures [,]. In fact, it has been suggested that it is pointless to obtain plain films when hamulus fracture is suspected clinically and that CT should be the initial imaging modality chosen [].
Moreover, with the newer generation spiral CT multiple imaging planes can be obtained after a single scan []. With complete fractures, CT clearly reveals an osseous fragment demonstrating indistinct and irregular apposing cortical margins separated from the parent bone []. Incomplete fractures exhibit partial cortical disruption without osseous fragment separation. Additionally, internal joint derangements, such as injuries to the triangular fibrocartilage complex, may be found in association with fracture of the hamulus depending on the mechanism of injury such as a fall on the outstretched, pronated arm. Physical examination of these patients reveals tenderness between the pisiform and ulnar styloid on the ulnar border of the wrist []. Typically, however, there would be no indication of fracture in these patients and imaging would make the differential diagnosis []. Further, magnetic resonance imaging [MRI] is, in the opinion of the authors, most effective in determining the presence and extent of these injuries.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [128.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",96,91.2,100.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 128.0 mm Hg + 2/3 * 80.0 mm Hg = 96.0 mm Hg.
Hence, the patient's mean arterial pressure is 96.0 mm Hg."
1918,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8055361-1,Extracted,"Case 1: The patient (the brother of case 2) was a 17-year-old male admitted to the hospital with a lifelong absence of bilateral breasts and nipples.
Physical examination: temperature (T): 36.5°C; pulse (P): 68 beats/minute; respiration (R): 20 breaths/minute; blood pressure (BP): 108/67 mmHg. The shape of the head was normal, the distance between the eyes was increased, single eyelid epicanthus ( and ). No abnormality was found in the heart and lungs, the aperture of the thorax had no malformation, and bilateral nipple areolas were absent (). No gland tissue was palpated. Bilateral axillary hair was sparse, and no axillary web was found (). The fingers of both hands were short, the distal phalanx of the little fingers presented with slight flexion and deformity, and both hands were webbed (). Chest magnetic resonance imaging (MRI): bilateral greater and lesser pectoral muscles were normal, and no malformation was found in the ribs. Breast color Doppler ultrasound: no glandular echo was found in the subcutaneous space of the bilateral chest walls. Color Doppler ultrasound of the liver, gallbladder, spleen, and urinary system: no abnormalities were found.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [108.0, 'mm hg'], 'Diastolic Blood Pressure': [67.0, 'mm hg']}",80.66667,76.63334,84.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 108.0 mm Hg + 2/3 * 67.0 mm Hg = 80.66667 mm Hg.
Hence, the patient's mean arterial pressure is 80.66667 mm Hg."
1919,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5457557-1,Extracted,"A 50-year-old woman was presented to our department with a thyroid nodule. She reported no dysphagia, respiratory compromise, hoarseness, chronic coughing, or loss of voice in high pitch ranges. Her medical history included breast cancer, and she had undergone a modified radical left mastectomy. She had no history of surgery or radiation to the head or neck. The patient was a farmer. She lived in the South-Central China and had not traveled outside. She was a nonsmoker and didn’t drink alcohol.
On physical examination, the patient was afebrile. The pulse was 76 beats per minute, the blood pressure 126/75 mmHg, and the respiratory rate 20 breaths per minute. The neck was supple, and a nodule was palpable in the thyroid on the right side. There was no palpable lymphadenopathy in the cervical region. The rest of the examination was normal.
The blood level of thyrotropin was 2.56 μIU per milliliter (reference range, 0.35 to 4.94). Ultrasonography of the thyroid gland revealed a solid and hypoechoic nodule measuring 18 × 16 mm, including cystic necrotic areas in the mid pole of the right thyroid lobe. The nodule had lobulated margins, scattered central calcification, and rich central blood flow. There was no enlarged lymph node in the cervical region. The result of fine-needle aspiration cytology showed papillary carcinoma. The preoperative laryngoscopy revealed left vocal cord paralysis (Fig. ). Right thyroid lobectomy was scheduled for the patient.
Thyroid lobectomy with Wu Gaosong’s procedure was performed and the nerve monitoring (NIM-Response 3.0 System, Medtronic) was applied during the operation [, ]. We resected the thyroid gland from the inferior pole to the superior pole to allow for a good visualization of the RLN, sternothyroid–laryngeal triangle and the external branch of the superior laryngeal nerve (EBSLN). The right RLN and EBSLN were identified and found to follow the usual course of the nerve. An electromyography activity with amplitude of 724 uV was recorded when the right RLN was stimulated by the nerve stimulator. After freeing and medially mobilizing the left thyroid gland, an exploration was made for the left RLN. The left RLN was identified below the inferior thyroid artery. When the left RLN was dissected superiorly toward the cricothyroid muscle and larynx, it was seen to ascend along the medial edge of the superior thyroid pole and finally disappear beneath the superior cornu of the thyroid cartilage without any tracheal, esophageal, or laryngeal branches (Fig. , Additional file 1). On electromyography monitorization, no electromyography activity was recorded when the left RLN and vagus nerve were stimulated. All the nerves were carefully preserved.
Postoperatively, the patient’s voice and serum calcium were normal. Left vocal cord paralysis was reported on the postoperative laryngoscopy of the patient. The final pathology was papillary thyroid carcinoma. The patient was discharged on the third postoperative day with the diagnoses of papillary thyroid carcinoma and congenital left vocal cord paralysis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [126.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",92,87.4,96.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 126.0 mm Hg + 2/3 * 75.0 mm Hg = 92.0 mm Hg.
Hence, the patient's mean arterial pressure is 92.0 mm Hg."
1920,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7584298-1,Extracted,"An 82-year-old woman presented to our hospital’s emergency department with new onset confusion. Her past medical history includes type 2 diabetes mellitus, hypertension, hyperlipidemia, and age-related osteoporosis on intravenous (IV) bisphosphonate yearly.
Six weeks prior to this admission, she was treated for pyelonephritis at a different hospital. At that time, laboratories were notable for a total calcium of 12.8 mg/dl (ref range, 8.4-10.5 mg/dl), albumin 3.6 g/dl (ref range, 3.5-5.3 g/dl), creatinine 1.6 mg/dl (ref range, 0.50-0.90 mg/dl), phosphorus of 2.7 mg/dl (ref range, 2.5-4.5 mg/dl), alkaline phosphatase (ALP) of 150 U/L (ref range, 35-105 U/L), parathyroid hormone (PTH) intact of 7 pg/ml (ref range, 15-65 pg/ml), and 25-hydroxy vitamin D level of 28.1 ng/ml (ref range 30-80 ng/ml). A 1,25-dihydroxy vitamin D level was not checked. CT of the abdomen without contrast revealed fatty infiltration predominantly of the right lobe of the liver and two hypodense lesions, one at hepatic segment V (largest diameter of 8 cm) and another at hepatic segment VI (largest diameter of 3.4 cm). On the day of discharge, she had a calcium level of 10.6 mg/dl and a creatinine of 0.89 mg/dl. She was discharged with oral ciprofloxacin and 800 units of cholecalciferol daily in addition to her regular outpatient medications.
On presentation to our hospital, her initial vitals were temperature 98.3˚F, heart rate of 81 beats/minute, respiratory rate of 18 cycles/minute, blood pressure of 142/65 mmHg, and oxygen saturation of 100% on ambient air. Physical examination was notable for a cachectic, non-toxic appearing woman with altered mentation. Otherwise, physical examination was unremarkable. Initial laboratory data were notable for a blood urea nitrogen (BUN) of 19 mg/dl, creatinine of 1.5 mg/dl, calcium level of 16.7 mg/dl, albumin of 3.4 g/dl ref (3.9-4.9 g/dl), hemoglobin of 9 g/dl, mean corpuscular volume (MCV) of 79 fl, and ALP of 175 U/L. Bilirubin, aspartate transaminase (AST), and alanine aminotransferase (ALT) were normal. CT head was negative for any acute pathology.
A work-up for hypercalcemia showed a low serum intact PTH of 8 pg/ml (ref range 15-65 pg/dl) and a low parathyroid hormone related peptide (PTHrP) of <2 pmol/L. 1,25 dihydroxy vitamin D was elevated at 81 pg/ml (ref range 19.9-79.3 pg/dl). The patient was admitted and treated for vitamin D dependent hypercalcemia with IV 0.9% sodium chloride infusion, subcutaneous calcitonin, and zoledronate infusion. Calcium levels were closely monitored and gradually trended down. Serum immunofixation did not identify a monoclonal band, and both serum and urine protein electrophoresis were normal.
CT of the abdomen was performed and showed two adjacent hypoenhancing large masses in the right hepatic lobe with central areas of hypodensity/necrosis: one at segment V measuring approximately 8.8 × 7.1 × 5.7 cm, while the other at segment VI measuring 6 × 5.8 × 5.3 cm (Figure ). Alpha-fetoprotein (AFP) and carcinoembryonic antigen (CEA) levels were normal. Because the initial impression was concerning for hepatocellular carcinoma, a triphasic CT scan of the liver was done but provided no definitive diagnosis. Viral hepatitis serologies were also negative. A CT of the chest was unremarkable.
Percutaneous liver biopsy under ultrasound guidance was then pursued. Histology, immunohistochemistry (Figure ), and fluorescent in situ hybridization (FISH) report (Figure ) showed diffuse proliferation of atypical cells positive for CD10, BCL-2, and BCL-6 with low C-myc positivity, consistent with large B cell lymphoma. The patient was evaluated by the inpatient oncology team for chemotherapy. She was discharged five days later and is currently receiving rituxan-cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone (R-CHOP regimen).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [142.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",90.66667,86.13334,95.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 142.0 mm Hg + 2/3 * 65.0 mm Hg = 90.66667 mm Hg.
Hence, the patient's mean arterial pressure is 90.66667 mm Hg."
1921,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2890927-1,Extracted,"A 25-year-old man presented to the emergency department with multiple injuries sustained in a road traffic accident. On primary survey, he was hemodynamically unstable and had reduced bilateral air entry on chest auscultation and increasing respiratory distress. He was intubated and connected to a ventilator. Bilateral intercostal tube drainage was also performed. He was hypotensive (blood pressure 90/50 mm Hg). Resuscitation attempts were carried out using large amounts of intravenous (IV) fluids and, under continuous monitoring of the blood pressure and the respiratory rate, a contrast-enhanced CT (CECT) scan of the thorax and abdomen was performed on a 40-channel multislice CT scanner (SOMATOM Sensation, Siemens, Erlangen, Germany) after intravenous injection of 100 ml of non-ionic iodinated contrast material.
The patient had a cardiac arrest during the CT scan. The CT scan showed contrast pooling in the dependent portions of the superior vena cava (SVC) and the inferior vena cava (IVC), the hepatic veins, and the right renal vein [Figure –], with the formation of a blood-contrast level. The right chambers of the heart were opacified and there was also opacification of the pulmonary veins []. There was no contrast in the left heart chambers.
The patient had a left iliac wing fracture and multiple rib fractures, with extensive subcutaneous emphysema involving the thoracic wall.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [50.0, 'mm hg']}",63.33333,60.16666,66.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 50.0 mm Hg = 63.33333 mm Hg.
Hence, the patient's mean arterial pressure is 63.33333 mm Hg."
1922,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7353709-1,Extracted,"A 34-year-old male patient with an unremarkable medical history consulted his local emergency department for intractable emesis for the past 48 h. The day before, he had been given a diagnosis of hand, mouth and feet syndrome with a possible cross-transmission from his 4-year-old daughter. He had a single bout of non-bloody diarrhea. Notable clinical signs consisted in elevated blood pressure (167/98 mmHg), purpura of the lower limbs and papulovesicular acrodermatitis of both hands and wrists. Prominent biological abnormalities consisted of KDIGO stage 3 AKI (Blood urea: 30 mmol/L plasma creatinine: 497 μmol/L) and hematological thrombotic microangiopathy (TMA) (hemoglobin levels: 13.1 g/dL, platelets: 47000 / mm3, haptoglobin levels < 0.20 g/dl, greatly elevated LDH levels: 1843 UI/L and schistocytes were detected). Proteinuria was in the nephrotic range (6 g/24 h), consisted primarily of albumin (66%) and was associated with microscopic hematuria upon urine culture. The patient was referred to an intensive care department and was started immediately on plasma exchange (PE). Neurological examination was normal. After two rounds, PE were discontinued owing to normal ADAMTS13 activity (113%). Additional etiological workup included negative HIV, HBV, HCV testing, unremarkable lymphocyte immunophenotyping and normal levels of C3, C4 and CH50. He was next referred to our renal intensive care unit. Quantitative explorations of the alternate complement pathway (ACP) disclosed normal levels of MCP, Factor H and Factor I and negative testing for anti-FH antibodies. Accordingly, renal biopsy identified double contours and several foci of mesangiolysis as well as focal segmental glomerulosclerosis of the tip variant affecting one glomerulus (Fig. ). Following supportive care with rehydration and blood pressure control, signs of peripheral TMA resolved while plasma creatinine levels declined to 350 μmol/L. The presence of shigatoxin (stx2b) and hemolysin (ehxa) were detected via PCR assessment in the stool samples and stool culture confirmed the presence of the enterohemorrhagic O128 Escherichia coli clone. Together these results ruled in favor of STEC-HUS. One month later the patient was readmitted in our unit owing to the recurrence of peripheral thrombotic microangiopathy (platelets: 130000/mm3, Hemoglobin: haptoglobin < 0.01 g/dl, schistocytes: 1%, LDH: 740 UI/L) and AKI with a creatinine level of 470 μmol/L. Repeated stool culture did not find evidence for the persistence of the predetermined E. coli clone or shigatoxin. Due to gradual worsening of the kidney function and platelet levels the patient was empirically started on eculizumab pending genetic findings. In the course of 15 days, creatinine levels gradually decreased from 630 μmol/L to 193 μmol/L and signs of TMA resolved. Genetic testing revealed that the patient was a heterozygous carrier of a CFHR1/CFH hybrid gene demonstrated to be associated with aHUS []. An attempt to discontinue eculizumab therapy 9 months after its initiation resulted in a second recurrence with an increase of creatinine levels to 430 μmol/L along with overt signs of peripheral TMA. After resuming eculizumab therapy, TMA resolved once again and creatinine levels fell back to baseline levels.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [167.0, 'mm hg'], 'Diastolic Blood Pressure': [98.0, 'mm hg']}",121,114.95,127.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 167.0 mm Hg + 2/3 * 98.0 mm Hg = 121.0 mm Hg.
Hence, the patient's mean arterial pressure is 121.0 mm Hg."
1923,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4421254-1,Extracted,"A 47-year-old female was diagnosed with end-stage renal disease of unknown aetiology and on chronic haemodialysis twice weekly since 1994. She received a living-related kidney transplant in December 2003. Unfortunately, her transplant was complicated by graft rejection in December 2004 and haemodialysis became necessary in July 2005. In November 2007, she developed anaemia despite receiving 80 U/kg/week of erythropoietin. She was diagnosed with pure red cell aplasia from hypocellular bone marrow and positive anti-EPO in January 2008 and she needed chronic blood transfusions, of about 1–2 units of packed red blood cells per month. She developed iron overload in May 2008 with a serum ferritin level of 2650 ng/mL. She was treated with deferoxamine 1500 mg twice weekly.
In August 2008, the patient was struck by a fish bone in the right hand while she was boning fresh water fish. Subsequently, she developed a high-grade fever and generalized muscle pain the next day. Due to the progressive pain and redness of the wound, she presented to our hospital on the third day of fever.
On admission, the patient's body temperature was 39.2 °C, with a pulse rate of 100/min, a respiratory rate of 24/min and a blood pressure of 140/90 mmHg. The wound at the ridge of her right hand was swollen but there was no fluctuation (Figure ). Her right hand and right arm were also swollen and tender. Marked generalized muscle tenderness was noted which caused the patient to avoid moving her arms or legs. Initial laboratory investigation revealed that her white blood cell count (WBC) was 9700 cells/ mm3 with a neutrophil predominance. The haematocrit was 22.5% and platelet count was 101 000/mm3. Blood biochemistries showed sodium 129 mEq/L, potassium 6.23 mEq/L, chloride 93 mEq/L, bicarbonate 22.8 mEq/L, blood urea nitrogen 84 mg/dL, creatinine 15.9 mg/dL, aspartate transaminase 31 U/L, alanine transaminase 35 U/ L and creatinine phosphokinase (CPK) 1218 U/L. Urinalysis was marked positive for blood with marked proteinuria without red blood cell or white blood cell sediment.
Because of the severe sepsis, the patient received meropenem and vancomycin as empirical antibiotics. Blood cultures revealed Aeromonas hydrophila that was susceptible to the second and third generation of cepha- losporins, gentamicin, trimethoprim–sulfamethoxazole and fluoroquinolones. The antibiotics were switched to ceftriaxone after the results of the blood culture. Although fever rapidly subsided within 3 days, the WBC and CPK continued to rise. Meanwhile, she developed pustular skin lesions compatible with septic embolism over all extremities (Figure ). On the sixth day of admission, ciprofloxacin was added. Cultures from the skin lesion also recovered A. hydrophila. WBC peaked at 43 300 cells/mm3 on the 7th day of admission and returned to a normal value on the 15th day. CPK peaked at 13 317 U/L on the fourth day of admission and returned to a normal value on the ninth day (Figure ). She needed more frequent haemodialysis than her previous schedule during the first few days because of severe hyperkalaemia caused by rhabdomyolysis. No further skin lesion developed after the 11th day of admission. She was discharged on the 19th day of admission. The clinical course is shown in Figure .",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1924,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4047696-1,Extracted,"The case we present here is about a 65-year-old female patient who was admitted in intensive care unit (ICU) with a history of fever since 5 days, pain abdomen and decreased urine output. She had no previous history of any comorbidity.
On admission, her blood pressure was 110/70 mmHg, heart rate 98 beats/min, and respiratory rate 28 breaths/min. Physical examination revealed dry skin and oral mucosa, and tender right hypochondrium. On laboratory analysis, her serum glucose was 124 mg/dL, creatinine 1.3 mg/dL, hematocrit 39%, platelets 50,000/mm3, and leukocytes 11,000/mm3(70% neutrophils), serum amylase 677 U/L and serum lipase 580 U/L, and dengue serology (IgM and IgG) was positive. The electrocardiogram showed sinus tachycardia, chest radiography was normal.
The provisional diagnosis of severe dengue fever with acute pancreatitis and acute kidney injury (AKI) was made and she was resuscitated as per World Health Organization guidelines.[] She was not started on any antibiotics in the absence of any associated bacterial infection and her chest X-ray was within normal limits. On day 2, her renal functions deteriorated with decrease urine output, arterial blood gas showed metabolic acidosis and hyperkalemia, for which she was hemodialyzed. In view of persistent anuria, she required alternate day hemodialysis. On day 6, she developed cough with mucoid expectoration, tachypnea and hemoptysis. Her chest X-ray showed new left lingular lobe and upper lobe nonhomogenous infiltrates []. Tomography of the chest showed air space consolidation with multiple nodules in the left upper and middle lobe []. Sputum examination revealed branched septate hyphae on gram's stain and sputum cultures grew Aspergillus flavus (A. flavus). Fiber-optic bronchoscopy and bronchoalveolar lavage (BAL) done on day 8, also was positive for A. flavus []. She was started on intravenous voriconazole 800 mg/1st day, 400 mg/day for 2 days more and then switched to oral voriconazole 400 mg/day in two divided doses with suspicion of IPA. She started showing clinical improvement with resolution of AKI and was discharged from ICU on day 9 and from hospital on day 11. She was continued on oral voriconazole for 6 weeks and her chest X-ray showed clearance of consolidation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mmhg'], 'Diastolic Blood Pressure': [70.0, 'mmhg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1925,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7705765-1,Extracted,"Our 14-year-old female with no significant past medical history presented to
the pediatric intensive care unit with headache and hypertensive urgency in
the setting of 4 to 6 weeks of nonbloody diarrhea, abdominal pain, anemia,
weight loss, and high blood pressures noted by per primary care physician.
She also noted associated abdominal fullness, pain with eating, and early
satiety. Social history included lack of sexual activity, smoking, or
alcohol use. She was active in volleyball. There was no recent travel.
Family history included Crohn’s disease in her father and her sister. Per
the pediatrician’s workup prior to presentation, she had normal basic
laboratory work, thyroid studies and electrocardiogram.
She was emaciated, alert, afebrile, and hypertensive (blood pressure
180/100 mm Hg) on presentation. She had unremarkable HEENT (head,
ears, nose and throat), lung, and skin examinations. Her abdominal
examination was notable for a mid-line bruit. Her cardiovascular
examination revealed no murmurs, rubs, or gallops, normoactive
precordium, normal, and symmetric pulses throughout. There were no
neurologic deficits. Musculoskeletal examination was unremarkable.
Given her hypertensive urgency on presentation, she had screening
laboratory tests, a urinalysis, and a head computed tomography. Though
slightly hyponatremic, basic metabolic panel was otherwise
unremarkable. She had no leukocytosis. Urinalysis and head computed
tomography were normal. Erythrocyte sedimentation rate and C-reactive
protein were elevated at 78 mm/h and 9 mg/dL, respectively.
Retroperitoneal ultrasound showed a small right kidney with diffuse
cortical thinning. Echocardiogram had a mildly dilated ascending
aorta. A renal ultrasound with Doppler was obtained and demonstrated
blunted arterial waveforms consistent with stenosis of the main right
renal artery.
Given her multiorgan presentation, cardiology, nephrology, and
gastroenterology were consulted. At that time, differential diagnoses
included Crohn’s disease with extraintestinal manifestations, systemic
lupus erythematosus, or systemic vasculitis. Her hypertension was
thought to be secondary, not primary renal disease. Her aortic
dilatation could have been caused by her anemia and acute weight loss.
After initial stabilization of her hypertension during the pediatric
intensive care unit stay, she was discharged. Her antinuclear antibody
was negative and complements were normal. The following week, an
angiogram was obtained to more fully investigate the right renal
artery stenosis. This revealed multifocal areas of large vessel
occlusion and stenoses ( and ); angiogram
findings were strongly suggestive of a systemic vasculitis. The
patient had an esophagogastroduodenoscopy and colonoscopy, which
showed chronic inflammatory changes on the esophagus and right colon
with ulcerations, sparing the terminal ileum. The biopsies were
consistent with Crohn’s disease. Her full body positron emission
tomography scan showed localized areas of aortic wall thickening with
increased fluorodeoxyglucose uptake in multiple areas () and
cardiac magnetic resonance imaging (), concerning for
TA. She was started on pulse dose steroids, infliximab, and
methotrexate as induction therapy for her disease process. Her
clinical symptoms have markedly improved and inflammatory markers have
normalized on follow-up. Prednisone continues to be tapered and she
remains on outpatient infliximab infusions as well as antihypertensive
medications with improved blood pressure control.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [180.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",126.66667,120.33334,133,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 180.0 mm Hg + 2/3 * 100.0 mm Hg = 126.66667 mm Hg.
Hence, the patient's mean arterial pressure is 126.66667 mm Hg."
1926,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6109974-1,Extracted,"A 52-year-old Caucasian man who had no medical history presented with sacral region pain that had continued for 3 months in April 2012. There was no significant family or psychosocial history. He did not take any medications. He was a computer engineer and his job scope was mainly office work. He lived with his wife and one child in a small flat in Istanbul. He was an active tobacco smoker with a 10 pack year smoking history. Currently, he smoked five cigarettes a day. He did not consume alcohol. His physical examination revealed tenderness and swelling in the sacral region. His vital signs were stable with blood pressure 125/65, pulse rate 70/minute, and temperature 36.2 °C. A systemic examination was normal and no neurological abnormality was detected. Vertebral magnetic resonance imaging (MRI) showed a pathological fracture in L5. After a Tru-Cut biopsy, he was diagnosed as having chondroid chordoma. He was treated with preoperative stereotactic radiotherapy to L5 vertebra at a total dose of 15 Gray in two fractions with CyberKnife followed by surgery in May 2012. We aimed to reduce surgical complications by preoperative stereotactic radiotherapy. Two years later, in May 2014, he presented with lumbosacral region pain and MRI suggested recurrent tumor involving L4, L5, and S1 vertebrae. He was not eligible for surgery and was treated with definitive radiotherapy with intensity-modulated radiotherapy (IMRT) mainly for palliative intent. Between 7 July 2014 and 8 August 2014, he received 40 Gray to L4, L5, and S1 vertebrae in 20 fractions 5 days a week for 4 weeks. In January 2016, he presented with paraplegia. Control imaging showed local recurrence, multiple lung nodules, and sternal metastasis. Imatinib 400 mg was started in February 2016 and continued until July 2017 when control imaging showed the progression of his disease. He received a total of 16 months of treatment. During this period, he received 400 mg/day of imatinib and no dose reduction was done. The laboratory results are given in Table . Overall, he tolerated treatment well and did not report any side effects. The best supportive care was offered. He was treated with best supportive care until May 2018. He died on 25 May 2018.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",85,80.75,89.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 65.0 mm Hg = 85.0 mm Hg.
Hence, the patient's mean arterial pressure is 85.0 mm Hg."
1927,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6824101-1,Extracted,"A 49-year-old Asian woman was admitted to our intensive care unit (ICU) after undergoing esophagectomy for esophageal cancer with whole-stomach reconstruction. She had a past medical history of asthma and cervical/lumbar disk herniation and a surgical history of two cesarean sections and vocal polyp resection under general anesthesia. She had no significant allergies, family history, or environmental or employment history. She was well maintained on 120 mg of fexofenadine hydrochloride and had an inhaler of procaterol hydrochloride and fluticasone furoate/vilanterol trifenatate for her asthma. She has smoked one pack of cigarettes each day for the past 24 years and does not consume alcohol. During the surgery, the surgeons decided not to place a nasogastric tube, because placement of the nasogastric tube was difficult, and they instead tried to avoid leakage at the anastomosis site. After admission to the ICU and sedation, the patient was orally intubated with an endotracheal tube, allowing suction above the cuff (internal diameter 7.0-mm Mallinckrodt™ TaperGuard Evac oral tracheal tube; Covidien, Minneapolis, MN, USA), because we routinely perform extubation and examine the function of the vocal cords on postoperative day 1. The patient’s vital signs were initially stable. Upon physical examination, she was not in acute distress, and she had a heart rate of 82 beats/minute, blood pressure of 110/42 mmHg, respiratory rate of 17 breaths/minute, body temperature of 37.4 °C, and oxygen saturation of 100% with mechanical ventilation (fraction of inspired oxygen [FiO2], 0.3) with spontaneous breathing in the pressure support mode. The rest of her physical examination was unremarkable, including the neurological examination. Laboratory studies revealed a white blood cell count of 7300/μl, hemoglobin level of 12.4 g/dl, platelet count of 186 × 103/μl, and hematocrit of 35.1%. The patient’s level of aspartate aminotransferase was 142 U/L, and her alanine aminotransferase level was 153 U/L. Her creatinine level was 0.51 mg/dl. The result of her initial chest x-ray examination in the supine position was unremarkable.
However, 12 hours after admission to the ICU, the patient rapidly developed tachypnea. On physical examination, she was in acute distress; her heart rate was 78 beats/minute, blood pressure was 92/58 mmHg, respiratory rate was 28 breaths/minute, and oxygen saturation was 96% with mechanical ventilation (FiO2, 1.0). Furthermore, chest examination revealed decreased respiratory sounds on the right side. Arterial blood gas analysis revealed that her carbon dioxide pressure was 44 mmHg and oxygen pressure was 109 mmHg, meaning the ratio of oxygen pressure to fraction of inspired oxygen (P/F) was 109 mmHg, together indicating failure of oxygenation. Chest radiography performed with the patient in the supine position revealed a mediastinal shift without lung parenchymal markings in the upper and middle lung fields (Fig. ). Chest ultrasonography revealed absence of the sliding sign. Hence, an aspiration catheter was inserted into the right pleural space under a presumptive diagnosis of tension pneumothorax 2 hours after the development of respiratory distress. Dark red blood (300 ml) and a small amount of air were released from the catheter, and the P/F ratio improved slightly to 236 mmHg. Subsequently, chest computed tomography was performed, which revealed a significantly distended reconstructed stomach that was compressing the nearby lung parenchyma (Figs. and ). The patient’s respiration improved markedly immediately after portable X-ray fluoroscopy-guided nasogastric tube placement in the ICU 5 hours after the aspiration catheter insertion. Chest radiography performed after nasogastric tube placement revealed return of the mediastinum to the right, indicating right lung inflation. The patient’s respiratory rate decreased to 15 breaths/minute, and her P/F ratio improved to 516 mmHg. After the procedure, we were able to successfully extubate the patient 30 minutes after nasogastric tube placement. On the 3rd day after admission to the ICU, the patient was moved to the medical ward, and on the 18th day after admission to the ICU, she was discharged to home without any problems. At a hospital visit 1 year after discharge, the patient claimed that she was doing well, and though she occasionally experienced chest discomfort after eating, she had not experienced severe dyspnea or respiratory problems since her stay in the ICU.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [42.0, 'mm hg'], 'Systolic Blood Pressure': [110.0, 'mm hg']}",64.66667,61.43334,67.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 42.0 mm Hg = 64.66667 mm Hg.
Hence, the patient's mean arterial pressure is 64.66667 mm Hg."
1928,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5798186-1,Extracted,"A 33-year-old white man presented to our hospital with sudden onset pleuritic chest pain and dyspnea of 1 day’s duration. The chest pain started when he was lifting a heavy trash bag and described the pain as sharp, constant, and radiating to his back. He also complained of diffuse body aches and chills but denied any fever, cough, hemoptysis, or weight loss. He denied any history of dental caries, recent travel, or exposure to sick contacts. He had no significant past medical history and was not taking any routine medications. He smoked half a pack of cigarettes a day for the past 10 years and denied any alcohol or illicit drug use. He worked as a waste collector in a garbage disposal firm.
At the time of presentation, he was: alert; oriented in time, place, and person; afebrile with a temperature of 37.06 °C (98.7 °F); tachycardic (heart rate of 110 beats/minute); and tachypneic (respiratory rate of 18/minute) with a blood pressure of 126/78 mmHg. An oral examination revealed normal dentition. A cardiopulmonary examination showed normal S1 and S2 with no murmurs and clear lung fields to auscultation bilaterally. An abdominal examination revealed a soft, non-tender abdomen with no organomegaly. A neurological examination showed intact cranial nerves and sensory system, and his muscle strength was 5/5 in all limbs with normal tone. Deep tendon reflexes were normal. An initial laboratory workup showed mild leukocytosis with white blood cell (WBC) count of 13,700 cells/mm3, elevated inflammatory markers of erythrocyte sedimentation rate (ESR) 48 mm/hour and C-reactive protein (CRP) 84 mg/dl, and moderately elevated serum transaminases of aspartate aminotransferase (AST) 634 U/L and alanine aminotransferase (ALT) 326 U/L. A basic metabolic panel was within normal limits. Three sets of cardiac enzymes done 8 hours apart were normal. An electrocardiogram was obtained which showed sinus tachycardia and diffuse ST segment elevations. A chest radiograph showed normal bilateral lung fields and normal cardiac silhouette. Computed tomography (CT) of his chest (Fig. ) ruled out aortic dissection but showed pericardial effusion. A transthoracic echocardiogram showed normal left ventricular systolic function with ejection fraction of 55% and a small pericardial effusion with no signs of tamponade physiology.
He was diagnosed as a case of acute pericarditis with minimal pericardial effusion. He was discharged home on indomethacin and was asked to follow up in the out-patient clinic. Two weeks later, when he was seen in our out-patient clinic, he complained of worsening dyspnea and chest pain. He was readmitted to hospital and an urgent transthoracic echocardiogram was obtained, which showed moderate to large pericardial effusion and tamponade physiology with right ventricular diastolic collapse and dilated inferior vena cava (Fig. ). An emergency pericardiocentesis was done and approximately 550 ml of purulent pericardial fluid was drained. The pericardial fluid was sent for culture, cell analysis, and cytology. Pericardial fluid WBC count was 15,376 cells/mm3 with 98% segmented neutrophils. A Gram stain of the pericardial fluid showed Gram-positive cocci in chains. He was started on broad-spectrum antibiotics with intravenously administered vancomycin (dosed on trough concentration) and piperacillin-tazobactam (3.375 g every 8 hours). Pericardial fluid cultures grew alpha hemolytic streptococci which were characterized as S. intermedius by matrix-assisted laser desorption/ionization time-of-flight mass spectroscopy (MALDI-TOF MS). S. intermedius was susceptible to penicillin and ceftriaxone. Anaerobic, fungal, and acid-fast bacilli cultures were negative. Pericardial fluid cytology was also negative for any malignant cells. Extensive workup with CT abdomen, CT chest, urine analysis, urine culture, and blood culture to look for source of infection failed to identify any other focus of infection. Human immunodeficiency virus (HIV) and tuberculosis QuantiFERON testing were negative. Antibiotics were deescalated to intravenously administered ceftriaxone (2 g every 24 hours) as per culture sensitivity.
His hospital course was complicated with the development of a pulmonary embolism for which he was started on an intravenously administered heparin infusion. However, within a few days of starting heparin, there was a steady decline in his platelets count. Heparin-induced thrombocytopenia (HIT) was suspected and heparin infusion was stopped. Our patient was started on argatroban infusion at a rate of 140 mcg/minute. HIT antibodies and serotonin release assay were sent which came back positive. He was subsequently transitioned to orally administered warfarin with target international normalized ratio (INR) range of 2 to 3. However, with the course of time, he did not have complete resolution of symptoms with persistence of chest pain and dyspnea. Hemodynamic and echocardiographic features were consistent with development of constrictive pericarditis. Surgical pericardiectomy with median sternotomy approach was performed which revealed thickened pericardium (Fig. ). He reported improvement in his symptoms after pericardiectomy. He was discharged home in a stable condition and received a total of 7 weeks of intravenously administered ceftriaxone. Six months post-discharge he reported complete resolution of his symptoms. A repeat echocardiography was normal and showed resolution of pericardial effusion.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [126.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",94,89.3,98.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 126.0 mm Hg + 2/3 * 78.0 mm Hg = 94.0 mm Hg.
Hence, the patient's mean arterial pressure is 94.0 mm Hg."
1929,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3198189-1,Extracted,"A 16-month old, baby girl, weighing 9.5 kg and measuring 74 cm, visited the hospital because of a cough. In a chest radiograph done under the suspicion of an upper respiratory infection, a round foreign object with a diameter of 21 mm was detected in the upper esophagus (). In a sleep endoscopy, it was confirmed to be a circular battery (), and ingestion was estimated to occur three days prior to the hospital visit, and it was determined that endoscopic removal would not be easy. Therefore, it was decided to immediately remove the battery under general anesthesia.
The infant had no underlying disease, and glycopyrrolate 0.05 mg was IM injected 30 minutes before arriving at the operating room as premedication for the anesthesia. The infant was monitored by ECG, non-invasive blood pressure (NIBP), and a pulse oximetry, and before anesthesia, her blood pressure was 85/61 mmHg; her heart rate was 160 beats/min with 100% oxygen saturation. 10 mg of Ketamine was IV injected and after loss of consciousness, 5 mg of Rocunium was IV injected. When the muscles were sufficiently relaxed, an uncuffed endotracheal tube with a 4 mm inside diameter was intubated. After intubation, both lungs were checked through a stethoscope and found to be normal, and the endotracheal tube was set to 11 cm in accordance with the top front teeth. Anesthesia was maintained by 2 L/min of air, 2 L/min of O2, and 2.0-3.5 vol% of sevoflurane. The tidal volume was 90 ml; respiratory rate was 18/min through volume-controlled mechanical ventilation to maintain an end-tidal CO2 (EtCO2) pressure of 35-40 mmHg and the peak inspiratory pressure (PIP) at this point was 19 cmH2O.
An adult endoscope with a 9 mm outer diameter was used for the removal procedure because the hospital did not have a pediatric endoscope with forceps. 2 minutes after inserting the endoscope, severe abdominal inflation was observed, and PIP increased up to 28-30 cmH2O with the tidal volume decreasing to less than 50 ml. The battery had caused an inflammatory change and conglutinated onto surrounding tissue in the esophagus, and 3 minutes after inserting the endoscope, oxygen saturation decreased to 80%, and EtCO2 pressure rose to 70 mmHg therefore the surgery was stopped and the endoscope was removed. By manual ventilation using 100% oxygen, oxygen saturation was recovered to 100% and EtCO2 pressure to 40 mmHg, and thereafter, the endoscope was reinserted.
In the second attempt of the procedure, manual ventilation was done instead of mechanical ventilation. However, 1 minute after the insertion of the endoscope, a sudden strong resistance was felt in the reservoir bag, and the tidal volume was less than 20 ml despite applying more than 35 cmH2O for the PIP. Oxygen saturation dropped below 60% so the procedure could not be continued; therefore, the endoscope was removed again. Here, a PIP of 25-30 cmH2O and a tidal volume of 50 ml were maintained. The endoscope was reinserted after recovering oxygen saturation to 100%, but due to the increased airway pressure, ventilation was not possible, and oxygen saturation dropped back down to less than 40%. The authors suspected the possibility of TEF considering the period of intake and the excessive air volume seen in the stomach in the chest radiograph taken before the surgery. Hence, the endotracheal tube was inserted until one lung ventilation was possible and then retreated while auscultating to secure onto the location where the pulmonary sound from both lungs became equal. The adjusted position of the endotracheal tube was 15 cm based on the top front teeth. A PIP of 25-30 cmH2O and a tidal volume of 80-100 ml were maintained. In the next insertion of the endoscope, A PIP of 30 cmH2O and a tidal volume of 50 ml were maintained but abdominal inflation was excessive so air in the stomach was partially removed with the endoscope, and the operating doctor was required to use the minimal amount of air for the surgery to proceed. A PIP of 25-30 cmH2O, a tidal volume of 50-80 ml, and oxygen saturation of 100% were maintained during the procedure, and the battery was removed.
After the removal of the battery, the vital signs were blood pressure 96/69 mmHg, heart rate 152 beats/min, and 100% oxygen saturation. The patient was not extubated but moved to postoperative intensive care, and after pediatrics observed vital signs for about 3 hours to verify that there were no abnormalities, extubation was done. Subsequent vital sign checks and physical exam were normal, and there were no abnormalities found in the blood test. Moreover, the right main bronchus appeared on the screen in the postoperative esophagography (), and the chest CT scan found TEF at 1.4 cm in the upper carina (). The guardian wanted to have surgery for TEF at another hospital; therefore, 3 days after the surgery, she was transferred.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [96.0, 'mm hg'], 'Diastolic Blood Pressure': [69.0, 'mm hg']}",78,74.1,81.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 96.0 mm Hg + 2/3 * 69.0 mm Hg = 78.0 mm Hg.
Hence, the patient's mean arterial pressure is 78.0 mm Hg."
1930,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6415464-1,Extracted,"A 71-year-old female with comorbidities such as hypertension and end-stage renal disease (on hemodialysis) presented to our emergency department with complain of back pain of 1 day duration. Only significant finding noted on physical examination was decreased range of motion in lumbar spine associated with moderate to severe pain. Review of systems was otherwise reported negative. The patient had low-grade fever 100.4°F, tachycardia 115 beats per minute, respiratory rate 22 breaths per minute, and blood pressure 160/78 mm Hg on admission. Complete blood count on admission was significant for macrocytic anemia with hemoglobin 10.1 mg/dL and mean corpuscular volume 101.3. Significant left shift was noted on differential white blood cell (WBC) count with 96.2% neutrophils (total WBC count on admission was 9500/dL). Comprehensive metabolic panel showed deranged renal function blood urea nitrogen 40 mg/dL (8-20 mg/dL) and creatinine 9.79 mg/dL (0.4-1.3 mg/dL). The patient met systemic inflammatory response syndrome criteria; therefore, 2 sets of blood cultures were sent for further sepsis workup and patient was started on broad-spectrum antibiotics (vancomycin and meropenem) empirically. Computed tomography chest/abdomen/pelvis was done, which was negative for any pulmonary or intra-abdominal focus of infection. However, computed tomography abdomen/pelvis showed presence of spinal canal stenosis in the lumbar area. Blood cultures sent on day 1 and day 3 (total 3 sets) grew C septicum. Repeat blood culture sent on day 5 was reported negative. Based on sensitivity report, antibiotics were switched to piperacillin/tazobactam.
Due to patient’s new-onset symptoms of worsening back pain, magnetic resonance imaging lumbar spine was done, which ruled out acute process/any mass lesion in the lumbar spine. Presence of multilevel degenerative disease and spinal canal stenosis was confirmed and any other pathology was ruled out.
The patient improved symptomatically and WBC count also improved over the next few days. However, due to known but rare association of C septicum with GI malignancy, upper GI endoscopy and colonoscopy () was performed on day 6, which showed nonobstructive mass in ascending colon suspicious for malignancy. Biopsy was taken and sent for histopathology examination, which was reported positive for well-differentiated adenocarcinoma ().
As there was no metastasis, the patient underwent hemicolectomy for the aforementioned lesion in the ascending colon. She was followed-up in 3 months and underwent surveillance colonoscopy, which showed no local recurrence of the malignancy.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [160.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",105.33333,100.06666,110.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 78.0 mm Hg = 105.33333 mm Hg.
Hence, the patient's mean arterial pressure is 105.33333 mm Hg."
1931,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9936,Extracted,"A 49-year-old woman is brought to the emergency department with progressive dyspnea and cough which she developed approx. 8 hours ago. 2 weeks ago she had a prophylactic ovariectomy because of a family history of ovarian cancer. She is known to have type 2 diabetes mellitus and stage 1 hypertension, but she does not take her antihypertensives because she is not concerned about her blood pressure. Also, she has a history of opioid abuse. She takes metformin 1000 mg and aspirin 81 mg. She has been smoking 1 pack of cigarettes per day for 22 years. Her vital signs are as follows: blood pressure 155/80 mm Hg, heart rate 101/min, respiratory rate 31/min, and temperature 37.9℃ (100.2℉). Blood saturation on room air is 89%. On examination, the patient is dyspneic and acrocyanotic. Lung auscultation reveals bilateral rales over the lower lobes. A cardiac examination is significant for S2 accentuation best heard in the second intercostal space at the left sternal border and S3 presence. There is no leg edema. Neurological examination is within normal limits.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [155.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",105,99.75,110.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 155.0 mm Hg + 2/3 * 80.0 mm Hg = 105.0 mm Hg.
Hence, the patient's mean arterial pressure is 105.0 mm Hg."
1932,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-12583,Extracted,"A 5-year-old boy is brought to the pediatrician for anal pain. He and his mother immigrated to the United States from Trinidad and Tobago 3 months ago. The boy reports severe pain with defecation. He is frequently constipated and has approximately 1-2 bowel movements per week. He has seen blood on the toilet paper after wiping multiple times and sometimes feels a need to ""push"" his anus back inside. More recently, he has been unable to hold his bowel movements and has had 2 episodes of fecal incontinence. His temperature is 99°F (37.2°C), blood pressure is 110/70 mmHg, pulse is 82/min, and respirations are 18/min. On exam, his anus appears normal. However, when asked to strain slightly, a notable finding is shown in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 70.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1933,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4186487-1,Extracted,"A 59-year-old male was admitted to the Department of Poisoning and Occupational Disease at the Qilu Hospital of Shandong University three days following an attempted suicide by PQ poisoning via oral admission. The patient became intoxicated, and ingested ~50 ml PQ at 13:20 on August 17, 2013. Minutes later, the patient was found by his family and was found to have vomited. On the third day the patient was transferred to our hospital for further treatment. The patient was lethargic on the way to the hospital, following administration of an emetic.
The patient was treated at the local hospital for alcohol consumption, without gastolavage and hemoperfusion. On the second day, the patient admitted to ingesting PQ; thus, was subsequently treated with steroid pulse therapy. The patient had no previous history of disease. During physical examination on admission to our local hospital, the patient was conscious with a blood pressure of 138/82 mmHg, a pulse rate of 61 bpm, a respiratory rate of 18 breaths/min, a blood oxygen saturation level of 98% and pharyngeal swelling was observed. The concentration of PQ in the urea was ~30 μg/ml. Analysis of the blood revealed a white blood cell count of 16.98×109/l, a serum creatine level of 141 μmol/l and a blood sugar level of 19.8 mmol/l. In addition, effusion shadows and an unclear boundary in the double lower lobe were observed in the lungs following a computed tomography scan ().
The patient was administered 1,000 mg methylprednisolone, which was gradually reduced according to the health condition. Furthermore, whole gastrointestinal lavage, protection of the gastrointestinal mucosa, free radical scavenging, protection of the liver and kidneys, myocardial nutrition and maintenance of the water and electrolyte balance were applied via the administration of the ‘Qilu scheme’ (Department of Poisoning and Occupational Diseases) (). However, on August 23, bradycardia occurred, and the patient had a pulse of 35 bpm. The heart rate of the patient gradually increased to 53 bpm following an intramuscular injection of atropine, but decreased to 40 bpm after 3 h. The following day, isoprenaline was administered continuously via an intravenous drip, while 0.6 mg atropine was administered orally three times a day. However, the heart rate remained low at 35–45 bpm. An ultrasonic cardiogram revealed enlargement of the right atrium, widening of the ascending aorta, moderate mitral valve regurgitation, light-medium tricuspid regurgitation and mild pulmonary valve regurgitation (). Furthermore, the ultrasound revealed that the thyroid gland was normal in size; however, a cyst (0.15 × 0.13 cm) was observed in the left lower pole (). Additional biochemical analyses revealed that the creatine kinase (CK) level was 50 IU/l, the CK-MB level was 0.9 ng/ml, the cardiac troponin I level was 0 ng/ml, the triglyceride (TG) level was 2.59 mmol/l, the free triiodothyronine (T3) level was 1.18 pg/ml, the free thyroxine (T4) level was 10.90 pmol/l and the thyroid stimulating hormone (TSH) level was 2.550 μIU/ml. Atropine and isopropyl adrenaline treatments were stopped and thyroid tablets were administered (80 mg per day). The heart rate increased to 50–55 bpm and was steady. Changes in the electrocardiograms are shown in . Following the treatment, the main examination index returned to normal with mild obstructive ventilation dysfunction observed in lung function. The patient was discharged from hospital, but received a follow-up examination one month later. The heart rate of the patient was 63 bpm and the level of N-terminal pro-brain natriuretic peptide was 22.17 pg/ml, the cortisol level was 15.75 μg/dl, the thyroglobulin antibody level was 18.26 IU/ml and the antithyroid peroxidase antibodies level was 14.08 IU/ml. With the exception of a degree of pulmonary fibrosis, the other examinations, including blood routine examinations and blood biochemical tests, were found to be normal. A written informed patient consent was obtained for this study.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [138.0, 'mm hg'], 'Diastolic Blood Pressure': [82.0, 'mm hg']}",100.66667,95.63334,105.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 138.0 mm Hg + 2/3 * 82.0 mm Hg = 100.66667 mm Hg.
Hence, the patient's mean arterial pressure is 100.66667 mm Hg."
1934,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4475,Extracted,"A 17-year-old African American female presents to the emergency room complaining of severe chest pain, cough, and shortness of breath. She has had many of painful crises before but has never sought medical attention. Her vital signs are T 102 deg F, HR 105 bpm, BP 130/95 mmHg, RR 16, SpO2% 85%. Physical exam is notable for pallor and hepatomegaly. EKG and troponins are within normal limits. CXR shows an infiltrate in the right middle lobe.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [95.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 95.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1935,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4556711-2,Extracted,"Patient 2 (the younger brother of Patient 1) was a 16-year-old boy who had polydactyly, mental retardation, central obesity (height 165 cm, body weight 93 kg, body-mass index 34.2), and hypogonadism. The waist circumference was 107 cm. The blood pressure was 128/61 mmHg, and the heart rate was 77 beats/min. He had normal heart sounds with clear breath sounds. The serum creatinine level was normal. Ultrasonography showed no anomalies in the kidneys. He did not have hepatic fibrosis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [128.0, 'mm hg'], 'Diastolic Blood Pressure': [61.0, 'mm hg']}",83.33333,79.16666,87.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 128.0 mm Hg + 2/3 * 61.0 mm Hg = 83.33333 mm Hg.
Hence, the patient's mean arterial pressure is 83.33333 mm Hg."
1936,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6306916-1,Extracted,"A 42-year-old Hispanic man with diabetes mellitus (DM) type 2 diagnosed five years ago and regularly treated with glybenclamide 5 mg once daily. Otherwise, the patient’s personal and familiar past medical history was unremarkable. He also denied consumption of alcohol, cigarettes, and illegal drugs. He presented to emergency department (ED) on 1 September 2017 with a history of malaise, headache, fever, and generalized body pain during the last 6 days. Three days before admission, he developed watery diarrhea (3 to 4 times a day), tachypnea, and confusion. During the following days, malaise and bowel movement frequency increased (up to 6 times a day). On the day of admission, the patient became drowsy, dyspneic, and looked very ill.
Physical examination: Body weight 50 kg, Body Mass Index 16.8 kg/m2, blood pressure: 60/30 mmHg, respiratory rate: 32 bpm, heart rate: 78 bpm, axillar temperature: 36 °C, SatO2: 99% (FiO2: 0.21); the patient was severely dehydrated, thyroid gland was not palpable; respiratory system: tachypnea, Kussmaul’s breathing; cardiovascular system: Sweaty mottled skin, and cold extremities with prolonged capillary refill time; neurologic system: Tremor in both hands, patellar and ankle hyperreflexia.
Lab: Hemoglobin 12.9 g/dL, hematocrit 40, platelets 198,000/mm3, white blood cells 10,100/mm3, segmented neutrophils 70%, bands 1%; serum glucose 460 mg/dL, urea 115 mg/dL, creatinine 1.3 mg/dL. Arterial blood gas analyses (ABG) are shown in . Liver function tests were normal, except for hypoalbuminemia and hypoproteinemia (3.0 g/dL and 5.18 g/dL, respectively). Urinalysis: pH 5, urine density 1030, leukocytes 2–4/field, granular casts 3+, glucose 3+, ketones 2+, and leucocyte esterase was negative.
Treatment with intravenous normal saline, potassium chloride, insulin infusion, sodium bicarbonate, norepinephrine, and empiric antibiotics (ceftriaxone + metronidazole) was administered. After 10 h of intensive treatment, ABG did not change significantly. So, differential diagnosis was extended and complementary exams were ordered: plasmatic amylase 96 U/L (reference range: 28–100 U/L), lipase 17 U/L (13–60 U/L), TSH 0.024 μIU/L (adult reference range: 0.27–4.2 μIU/L), free-T4 2.16 ng/dL (reference range: 0.82–1.63 ng/dL), total-T3 0.18 ng/mL (reference range: 0.5–2.0 ng/mL), free-T3 0.42 pg/mL (reference range: 2.1–3.8 pg/mL); CPK-MB 101.3 U/L (reference range: 0–25 U/L), total CPK 505.7 U/L (normal: 39–308 U/L); troponin T 25.0 ng/mL (reference range: 0.12–0.6 ng/mL). Based on these results, hydrocortisone 100 mg every 8 h, methimazole 20 mg every 8 h, and Lugol’s solution 10 drops every 8 h, were added on the second day of treatment. Because of shock, beta-blocker was not administered. On the third day of treatment a good evolution was observed, norepinephrine and insulin infusion were discontinued, and NPH insulin was initiated. Based on physical examination, chest x-ray (CXR) ( and ), and progressive decrease in partial oxygen pressure () compatible with acute lung edema, intravenous furosemide 20 mg every 12 h was administered for 2 days.
Although ECG was normal, troponin determinations were repeated over the next days and persisted elevated. Echocardiography (5 September 2017) showed borderline pulmonary artery systolic pressure (35 mm Hg), severe LV systolic dysfunction (LV ejection fraction 35%), diastolic dysfunction of restrictive type and global hypokinesia ().
On the 6th day of treatment, hydrocortisone and Lugol’s solution were stopped, and methimazole was reduced by half. The patient was discharged on 7 September 2017, with almost complete recovery.
We also performed other complementary exams: Twenty-four hour-urine sodium, chloride, and potassium levels were also normal. Direct stool examination showed 0–1 leucocytes/HPF, no parasites, no blood, no erythrocytes. Urine culture and HIV serology was negative. Anti-TPO and anti-thyroglobulin antibodies were negative. Cardiac catheterization and endomyocardial biopsy were not performed. Follow-up echocardiography at 6 months was completely normal. After the patient was discharged, no additional (blood or imaging) study was performed, other than echocardiography.
Written informed consent was obtained from the patients for publication of this article and accompanying images.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [60.0, 'mm hg'], 'Diastolic Blood Pressure': [30.0, 'mm hg']}",40,38,42,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 60.0 mm Hg + 2/3 * 30.0 mm Hg = 40.0 mm Hg.
Hence, the patient's mean arterial pressure is 40.0 mm Hg."
1937,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7002898-1,Extracted,"A 42-year-old woman presented with progressive shortness of breath for two months, accompanied by palpitation, pitting oedema, and fatigue. On the day of admission, she had an episode of presyncope. On physical examination, her vital signs showed a body temperature of 37°C, blood pressure of 157/103 mmHg, tachycardia with a heart rate of 126 bpm, and tachypnoea with a respiratory rate of 28 bmp. Her oxygen saturation (SpO2) was only 86% in room air. There was a visibly engorged jugular vein, palpable right ventricular heave, pansystolic murmur at the tricuspid area, fine crackles bilaterally over the lungs, and pitting oedema of the lower limbs bilaterally. The D-dimer value was 1094.6 ng/mL (normal range < 500 ng/dL). Arterial blood gas values revealed respiratory alkalosis (pH: 7.46, partial pressure of carbon dioxide (pCO2): 30 mmHg). Complete blood count, liver function tests, and renal function tests were normal. Chest X-ray showed cardiomegaly and bilateral pleural effusion. Electrocardiogram (EKG) revealed sinus tachycardia and right axial deviation. Echocardiography showed severe right ventricular systolic dysfunction, pulmonary artery hypertension, dilated right atrium, and dilated right ventricle. Considering the diagnosis of pulmonary thromboembolism, computed tomography (CT) was performed, which revealed nodular soft tissue-like filling defects in the pulmonary trunk and right pulmonary arteries with heterogeneous contrast enhancement (Fig. ). Pulmonary artery tumour was thus suspected; however, pulmonary embolism was not ruled out. Subsequent investigations revealed no risk of pulmonary embolism and no thrombus in the lower extremities on sonography, which favoured the diagnosis of pulmonary tumour.
The patient subsequently underwent surgical intervention with resection of the pulmonary artery mass for therapeutic management.
At surgery, frozen biopsy specimens obtained from the right main pulmonary artery revealed a pulmonary artery intimal sarcoma, and the patient then underwent resection of the tumour, resection of involved pulmonary artery, and reconstruction of the involved pulmonary artery with graft subsequently.
On macroscopic view, the specimen was a grey-whitish, solid, soft tissue mass measuring 10 × 5.3 × 3.1 cm. Histopathologically, it revealed a picture of abundant hyperchromatic spindle cells and pleomorphic cells with myxoid background. Immunohistochemical study of the neoplastic cells was positive for vimentin, actin, and MDM2. The morphology and immunohistochemistry (IHC) stain were compatible with the diagnosis of pulmonary artery intimal sarcoma (Fig. ). However, the surgical margin could not be evaluated because of intraoperative tumour fragmentation.
After surgery, the patient received adjuvant chemotherapy with 6 cycles of combination chemotherapy regimen of epirubicin, ifosfamide, and mesna (MAI) regimen Q3W (epirubicin 60 MG/M2, ifosfamide 1.8 GM/M2, and mesna 0.36 GM/M2) as the chest CT showed residual tumour with direct compression over the graft. A series of subsequent chest CTs showed regression of the residual tumour and releasing of the compression.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [157.0, 'mm hg'], 'Diastolic Blood Pressure': [103.0, 'mm hg']}",121,114.95,127.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 157.0 mm Hg + 2/3 * 103.0 mm Hg = 121.0 mm Hg.
Hence, the patient's mean arterial pressure is 121.0 mm Hg."
1938,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6451794-1,Extracted,"A 53-year-old woman was referenced from primary care physician to her local hospital due to fever at evening and a weight loss of 5% in one month. The patient had a previous history of total hysterectomy and atrophic gastritis and was under proton pump inhibitors. No relevant familial history was known.
At admission, she was pale, with 37.9°C of temperature, normal blood pressure (119/69mmHg) and heart rate (91/min), and 61 Kg of weight (BMI 25.5Kg/m2), without Cushing syndrome signs or other relevant clinical findings.
Patient's laboratory tests at admission () revealed marked thrombocytosis (platelets 743x109/L), normocytic anemia (Hb 10.1 g/dL), and slight leukocytosis (WBC 10.2x109/L) with elevated ferritin, C-reactive protein levels [(22.74 mg/dL (<0.5)], and normal procalcitonin. No pathogenic agents were found on blood, urine, and cerebrospinal fluid cultures nor alcohol-acid resistant bacilli. Viral serological markers were also negative. She also presented elevated fasting blood glucose (130mg/dL) and A1C of 6.4% as well as slight elevation of liver enzymes and decreased albumin. Brain tomography showed no alterations and echocardiogram showed slightly enlarged left atrium and normal left ventricular ejection fraction.
The patient was initially medicated with levofloxacin during 7 days but without any improvement. Then, a thoracic and abdominal tomography (CT) was performed and revealed a nodular lesion of 4.2 cm length, with heterogeneous contrast enhancement, not clear if the origin was the gastric fundus or the left adrenal (). Upper digestive endoscopy showed a hiatus hernia and erosive antral gastritis, without any suspicious features. The abdominal magnetic resonance imaging revealed a left adrenal tumor with 4.3cm length, hyperintense in T2-weighted images and hypointense in T1, with peripheral contrast enhancement and increased washout, possibly indicating a pheochromocytoma. The patient was then referred to our department and when asked, she also referred 3 to 4 episodes per day of palpitations, sweating, headache, and limbs paresthesia, mainly related with efforts, which were not initially considered. At biochemical evaluation, she presented elevation of plasma and urinary normetanephrine [3503 pg/mL (<120) and 5505 ug/24h (50-650) resp.] with plasma and urinary metanephrine and 3-methoxythyramine within reference range (). Adrenal androgens were also normal. However, ACTH was suppressed [<5pg/mL (9-52)] with asleep plasma midnight cortisol [7.1ug/dL (<1.8)], urinary free cortisol [96ug/24h (10-80)], and cortisol after 1 mg overnight dexamethasone suppression test (3.7ug/dL) slightly elevated, consistent with autonomous cortisol production. 125I-metaiodobenzyl guanidine (MIBG) scintigraphy showed an accumulation of the isotope in the left adrenal tumor. After integration of these clinical, laboratory, and imaging data, the diagnosis of pheochromocytoma was made. In the presence of a SIRS in a patient with a newly diagnosed pheochromocytoma, the measurement of plasma IL-6 was requested and it was elevated [26.7 ng/L (<7.0)], consistent with IL-6-producing pheochromocytoma. Biochemical screening of MEN2 syndrome was negative.
Patient started preoperative alpha-blockade treatment with phenoxybenzamine 10 mg id that was increased to 10 mg 2id after one week and beta-blockade treatment was added with propranolol 10 mg id. During treatment, her minimum BP was 86/53mmHg and maximum was 116/57mmHg and minimum heart rate was 73/min and maximum was 115/min. She remained without fever during this period. After 23 days of alpha-blockade single-port laparoscopy, left adrenalectomy was performed without complications. Histological examination showed a well-delimitated pheochromocytoma with 3.0x2.5x1.8cm and potential malignant biological behavior with PASS score = 11 () (potential malignant biological behavior if PASS score ≥ 6 []). Immunohistochemistry revealed strong positivity to chromogranin A, synaptophysin, and neuron-specific enolase and negativity to cytokeratin AE1/AE3, calretinin, and inhibin A. Ki67 proliferation index was 1-2%. After surgery, the alpha- and beta-blockade was stopped and due to autonomous cortisol production with suppressed ACTH, hydrocortisone was initially prescribed at stress dose and then tapered to 20 mg per day.
In reevaluation two months after surgery she had no complaints. Plasma and urinary normetanephrine were within reference range and IL-6 was undetectable (). Total blood count and inflammatory parameters have all normalized. Hydrocortisone was tapered to suspension just before revaluation and a short Synacthen® test was performed, which excluded adrenal insufficiency (plasma cortisol 60 minutes after 250 μg of tetracosactide: 19 mg/dL). Abdominal CT and MIBG scintigraphy had no evidence of persistent disease. A genetic test was requested and no germline mutations were detected in the following genes: RET, VHL, SDHAF2, SDHB, SDHC, SDHD, MAX, and TMEM127.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [119.0, 'mm hg'], 'Diastolic Blood Pressure': [69.0, 'mm hg']}",85.66667,81.38334,89.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 119.0 mm Hg + 2/3 * 69.0 mm Hg = 85.66667 mm Hg.
Hence, the patient's mean arterial pressure is 85.66667 mm Hg."
1939,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7127,Extracted,"A 30-year-old woman is brought to the urgent care clinic by her husband. She complains of numbness around her lips and a tingling sensation in her hands and feet. She underwent near-total thyroidectomy for an enlarged thyroid gland a month ago. Vital signs include: blood pressure is 130/70 mm Hg, pulse is 72/min, respiratory rate is 16/min, and temperature is 37.0°C (98.6°F). A surgical incision scar is present in the anterior aspect of the neck. The attending physician inflates the blood pressure cuff above 150 mm Hg and observes the patient a couple of minutes while measuring her blood pressure. The patient develops sudden stiffness and tingling in her hand. Blood test results are as follows:
Hemoglobin (Hb%) 10.2 g/dL
White blood cell count 7000/mm3
Platelet count 160,000/mm3
Calcium, serum (Ca2+) 6.0 mg/dL
Albumin 4 g/dL
Alanine aminotransferase (ALT), serum 15 U/L
Aspartate aminotransferase (AST), serum 8 U/L
Serum creatinine 0.5 mg/dL
Urea 27 mg/dL
Sodium 137 mEq/L
Potassium 4.5 mEq/L
Magnesium 2.5 mEq/L
Urinalysis shows no white or red blood cells and leukocyte esterase is negative.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 70.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1940,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7586564-1,Extracted,"Mrs. S is a 56-year-old lady who was brought to our hospital with history of alleged snake bite. Patient had been working in the fields when she was bitten by a snake. Patient was not able to identify the snake. She had informed her daughter-in-law who took her to a traditional medical practitioner. The practitioner had taken some leaves from a plant in his garden; he then crushed it and applied the crushed leaves to the bite site. The milky fluid which was obtained from crushing the leaves was given to the patient to drink by the healer. The patient on questioning later remembered that the fluid caused severe burning and irritation in the throat. After taking the medication the patient was taken home. At home the patient progressively worsened and became drowsy, so the relatives decided to take her to the District hospital a few kilometers away.
At the district hospital the doctors on arrival noticed that she was hypotensive and her blood pressure was not recordable. She was immediately intubated ventilated with ambu bag with oxygen initiated on ionotropes and referred to a tertiary care center for further management.
Patient was brought to our accident and emergency department, at this time her blood pressure was 90/60 mmHg, heart rate: 112/min, cardiovascular system there were normal heart sounds and no murmurs or gallop, respiratory system there were bibasal crackles up to the angle of scapula. Central nervous system the Glasgow coma scale was 2T/15, pupils were equal and reacting to light, dolls eye movement was present, deep tendon reflexes were present the plantars were mute. The patient was admitted to the intensive care unit, mechanical ventilation, and ionotropes were continued. Local examination revealed fang marks over the dorsum of the right hand.
The patient was admitted and investigations revealed that her sugars were high at admission [] and potassium was slightly low otherwise all investigations were normal. But her echocardiogram done after admission into the medical intensive care unit showed global hypokinesia with a low ejection fraction 30%.
At this point the diagnosis we considered was that of cardiogenic shock due to plant toxin with cardiotoxicity, secondary ton antidote for the snake bite given by the traditional practitioner. We requested the patient's relatives to bring the plant, this was identified as calotropis. We sent the patients serum and urine for toxicological analysis.
The toxidrome of our patient did not fit into the clinical presentation of any of the big four snakes associated with snake envenomation in our country. There was no neurological weakness, bleeding diathesis, or renal failure [] ruling out snake envenomation related illness.
The patient was diagnosed to have severe calotropis poisoning with cardiovascular collapse. The patient was managed with ionotropes and she improved rapidly she was weaned off the ventilator and shifted to the ward, but she developed severe irritant cellulitis [] at the site of the application of the calotropis it improved with debridement and regular dressings. At discharge the repeat echocardiogram showed left ventricular hypertrophy with normal ejection fraction 56.7%",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [60.0, 'mm hg'], 'Systolic Blood Pressure': [90.0, 'mm hg']}",70,66.5,73.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 60.0 mm Hg = 70.0 mm Hg.
Hence, the patient's mean arterial pressure is 70.0 mm Hg."
1941,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-605,Extracted,"A 43-year-old man is brought to the emergency department 45 minutes after his wife found him on the floor sweating profusely. On arrival, he is lethargic and unable to provide a history. He vomited multiple times on the way to the hospital. His temperature is 37.3°C (99.1°F), pulse is 55/min, respirations are 22/min, and blood pressure is 98/65 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 80%. Examination shows profuse diaphoresis and excessive salivation. He withdraws his extremities sluggishly to pain. The pupils are constricted and reactive. Scattered expiratory wheezing and rhonchi are heard throughout both lung fields. Cardiac examination shows no abnormalities. There are fine fasciculations in the lower extremities bilaterally. Muscle strength is reduced and deep tendon reflexes are 1+ bilaterally. His clothes are soaked with urine and feces.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [65.0, 'mm hg'], 'Systolic Blood Pressure': [98.0, 'mm hg']}",76,72.2,79.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 98.0 mm Hg + 2/3 * 65.0 mm Hg = 76.0 mm Hg.
Hence, the patient's mean arterial pressure is 76.0 mm Hg."
1942,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6223080-1,Extracted,"A 54-year-old man was admitted to our hospital for a mass in RA on an echocardiography examination occasionally. There was no symptom or sign of fever, chest pain, dizziness, palpitations and no history of a heart disease and tumor. He was a teacher, running and training on a weekly basis. He also was a non-smoker and drank 50 ml Chinese liquor each day for 30 years. There was no other medical history of note and no family history of sudden death. Clinically, the patient has stable vital signs with no fever, a heart rate of 68 beats per minute and blood pressure of 128/79 mmHg. The serum tumor markers and D-dimer were normal. An electrocardiogram (ECG) showed normal sinus rhythm. The chest X-ray showed normal cardiac size and clear lungs.
The echocardiography (Siemens, ACUSON SC2000) showed normal left ventricular systolic function (ejection fraction 66%), normal left and right ventricular cavities and normal cardiac valves. Only mild tricuspid and aortic valve regurgitate. Incidentally, an apparently smooth mass-like echogenic structure (9*11 mm) attached to tricuspid valve was noted in the right atrium and suggestive of a thrombus or a tumor in four-chamber apical view (Fig. ).
Due to the limitation of acoustic window of echocardiography, the patient was arranged to our center of nuclear medicine for PET/MRI for diagnostic work up of the mass to be determined. Cardiac PET/MRI was performed with Siemens Biograph mMR (Software version B20P, Siemens Healthcare, Erlangen, Germany). The MRI showed the findings: Cine gradient-echo image in four-chamber view confirmed the presence of a banded structure (arrowhead) attached to the posterior wall of RA and the mass moved during systole and diastole period (Fig. ) (See Additional file : Video S1). On T2-weighted short tau inversion recovery (T2-STIR) of the four chamber and short axis view (Figs. and ), the mass (arrowhead) had similar signal intensity to myocardium revealing a myocardial structure. On T2-STIR with fat suppression of the four chamber and short axis view (Figs. and ), the results were consistent with T2-STIR images. There was no abnormal enhancement about the mass (arrowhead) on late gadolinium enhancement (LGE)-MRI (Figs. and ). Furthermore, PET/MRI indicated no obvious 18F-fluorodeoxyglucose (18F-FDG) uptake on the mass (Fig. , arrowhead), which exclude malignant tumor. These typical findings detected by PET/MRI lead to the diagnosis of a prominent crista terminalis. The case follow-up hitherto had no special symptom.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [128.0, 'mm hg'], 'Diastolic Blood Pressure': [79.0, 'mm hg']}",95.33333,90.56666,100.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 128.0 mm Hg + 2/3 * 79.0 mm Hg = 95.33333 mm Hg.
Hence, the patient's mean arterial pressure is 95.33333 mm Hg."
1943,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7526969-1,Extracted,"A 73-year-old previously healthy female who was a heavy smoker (60 pack-years) presented to our center with chief complaints of insidious onset and gradually progressive abdominal distension, acid reflux, bloating, and loss of appetite for the last six months. She tried over-the-counter antacids with minimal relief. On examination, the patient had a temperature of 37°C, heart rate of 70 beats per minute, blood pressure was 120/75 mm Hg, respiratory rate of 20 breaths per minute, and oxygen saturation of 96% on room air. Examination of the abdomen revealed gross ascites. On chest examination, there was decreased breath sounds bilateral. The remainder of the physical examination was unremarkable. She underwent paracentesis with the removal of 3.5 liters of ascitic fluid. The analysis of ascitic fluid was consistent with adenocarcinoma (Figure ).
CT scan of the abdomen and pelvis revealed abdominopelvic collections and features suggestive of PC.
A CT scan of the chest further showed a 50.3-mm mass in the lower lobe of the left lung along with an enlarged left-sided mediastinal lymph node (Figure ).
Bronchoscopy with endobronchial ultrasound-guided biopsy of the lung mass consistent with poorly differentiated non-small cell carcinoma of the lung (Figure ).
The immunohistochemistry was positive for CK7 and CK5/6 and negative for P40 (Figure ) and TTF1 (Figure ).
Napsin, CK20, PAX8, calretinin, WT1, CDX2, GATA3, and GCDFP15 were suggestive of a poorly differentiated squamous cell carcinoma. MRI of the brain was negative for any metastasis. Positron emission tomography (PET) scan showed increased uptake in the left lower lobe of the lung and hilar and subcarinal lymph nodes (Figure ).
Pelvic ultrasound showed a large bulky uterus secondary to multiple intramural fibroids with thickening of the endometrium. The patient had no vaginal bleeding. Further workup showed carcinoembryonic antigen (CEA) 1.2 (normal <3 ng/ml) and alpha-fetoprotein (AFP) 1.6 (normal <10 ng/dl). She was offered an endometrial biopsy, but she refused.
Given her squamous cell carcinoma of the lung, she was planned to be started on platinum-based doublet chemotherapy (carboplatin and paclitaxel) along with an immune checkpoint inhibitor (pembrolizumab) every three weeks for four cycles, followed by maintenance therapy with pembrolizumab every three weeks. She reported improvement in abdominal distension and bloating with weekly therapeutic paracentesis, but dyspnea continued. She was started on for three liters of oxygen via the nasal cannula.
After her initial diagnosis, the patient began to have progressive weakness and was unable to walk without support. The goals of care were discussed, and the patient elected to not continue with aggressive cytotoxic chemotherapy. She was started on hospice care after a detailed discussion of treatment and prognosis. Unfortunately, she passed away a few months later.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 75.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1944,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5713656-1,Extracted,"A 12-year-old Amhara boy from the Northwest Gondar Amhara regional state complained of left flank swelling for the last 3 months. Three days before admission he started to experience pain in his left flank, which was associated with high grade fever, chills, rigor, and vomiting. At the time he had no urinary or respiratory symptoms. Maternal pregnancy course and medical history were noncontributory, and he had an attended birth at a health center; his past medical history was unremarkable. He has seven siblings, none of whom had similar symptoms. His mother had no history of radiation exposure, use of traditional medicine, or chemotherapy during pregnancy.
No dysmorphisms were noted in his general appearance. His vital signs were: pulse rate (PR) 142 beats/min, respiratory rate (RR) 33 breaths/min, temperature (T) 38.5 °C, and blood pressure (BP) 105/65 mmHg. Anthropometric measurements showed severe stunting. An abdominal examination revealed distended abdomen, asymmetric with bulging left flank, visible horizontal line, upward umbilical slit, and absent rectus abdominis muscles. His abdomen was soft with a tender cystic, bimanually palpable mass on the left flank measuring 13 × 11 cm. Both testes were undescended (Fig. ). He also had scoliosis and developmental dysplasia of the hips with waddling gate.
Urinary analysis demonstrated many red blood cells (RBCs) and positive leukocyte esterase. He had a normal renal function test with creatinine of 0.72 mg/dl and blood urea nitrogen (BUN) of 44 mg/dl, normal hemoglobin of 12.7 gm/dl, and normal electrolyte. Ultrasound showed a large cystic mass in his left kidney area with echo debris. His right kidney had normal echo texture and size. An X-ray of his hips showed bilateral developmental dysplasia of the hip (DDH; Fig. ). Our facility does not have the capacity to perform a genetic study to support the diagnosis of PBS.
His left kidney is cystic and enlarged; there is no parenchyma tissue, both testes are intraperitoneal just below the kidneys, tortuous left renal vein, enlarged bladder reaching above umbilicus, and left megaureter (Fig. ). A bilateral orchidectomy and left nephrectomy were done.
After surgical removal of cystic mass and testes, he was given intravenously administered antibiotics for treatment of pyelonephritis for 14 days. Subsequently he showed significant improvement and was discharged home with an appointment for follow up to consider hormonal replacement therapy and possible abdominoplasty. His parents were also counseled about the PBS and the care they can give him at home.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [65.0, 'mm hg'], 'Systolic Blood Pressure': [105.0, 'mm hg']}",78.33333,74.41666,82.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 105.0 mm Hg + 2/3 * 65.0 mm Hg = 78.33333 mm Hg.
Hence, the patient's mean arterial pressure is 78.33333 mm Hg."
1945,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5630964-1,Extracted,"An 83-year-old gentleman with a history of bioprosthetic aortic valve placement and aortic arch repair for aortic aneurysm two years prior to presentation was admitted with 3–4 weeks history of malaise, chills and left lower leg pain. The patient also had an acute embolic cerebrovascular accident which left him with left sided hemiparesis, left facial droop, dysarthria and mild cognitive impairment six month prior to presentation. On examination, he was afebrile with a blood pressure of 111/70 mm Hg and heart rate of 100 beats per minute. He had a grade II/VI systolic ejection murmur. The left lower extremity was cool to the touch and tender to palpation with diminished pulses. His white blood cell count was 8.7 K µl−
1 (reference range 3.8–10.8 K µl−1). A lower extremity angiogram showed a thrombosed popliteal artery aneurysm. He underwent arterial bypass and ligation of the aneurysm on hospital day 3. Both of two blood culture sets from the day of admission were positive for Gram-positive rods which were initially identified by multiplexed PCR (FilmArray BC-ID, bioMerieux) as Listeria monocytogenes. Subsequent growth on solid media recovered both L. monocytogenes, later confirmed by the public health laboratory, and Listeria innocua. No recent history of antibiotics use was reported prior to admission and the patient did not receive any antibiotics upon admission. On hospital day 1, two out of two blood culture sets again were positive for Listeria monocytogenes and Listeria innocua. From one of the two blood culture sets Escherichia coli was also simultaneously isolated. The patient was started on ampicillin and gentamicin, targeting all recovered organisms. Subsequent blood cultures on days 3 and 4 of hospitalization were negative. A transesophageal echocardiogram revealed a vegetation measuring 14×8 mm on the aortic aspect of the bioprosthetic valve. Magnetic resonance imaging of the brain showed a preexisting infarct and multiple new punctate, subacute, locunar infarcts involving the left thalamus and left precentral gyrus. Results of imaging of chest, abdomen and pelvis were remarkable for evidence of splenic infarcts but otherwise no other infectious sources were identified. The patient subsequently underwent a redo of the aortic valve and aortic graft replacement two weeks into admission. Gross pathology of the bioprosthetic valve showed a markedly disrupted trileaflet valve. Histopathology was remarkable for acute inflammation () and tissue Gram staining detected Gram-positive coccobacilli in intracellular spaces (). No Gram-negative bacilli indicative of E. coli were observed. The unfixed valve tissue which was sent to a reference laboratory (University of Washington) for broad-range bacterial 16S rRNA PCR and DNA sequence analysis by Sanger sequencing detected Listeria monocytogenes.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [111.0, 'mm hg']}",83.66667,79.48334,87.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 111.0 mm Hg + 2/3 * 70.0 mm Hg = 83.66667 mm Hg.
Hence, the patient's mean arterial pressure is 83.66667 mm Hg."
1946,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8088721-1,Extracted,"A 37-year-old Chinese man was referred to the West China Hospital of Sichuan University for treatment of acromegaly, having presented with a 6-year history of increasing ring and shoe sizes. Approximately 2 years earlier, he began to experience loss of libido. Other medical history included tuberculous pleurisy that had been successfully treated with anti-tuberculosis drugs 13 years previously and a laparoscopic cholecystectomy for gallstones 5 years previously. No family history of particular disease was present. Over the past 10 years, his body weight had gradually increased by 15 kg. In addition, the patients did not receive vitamin D or vitamin A supplement, and never used any other drugs, including lithium and thiazide. When he first attended our hospital, he was found to be 165 cm tall and weighed 86 kg (BMI 31.59 kg/m2). Physical examination revealed a high blood pressure (153/105 mmHg). He exhibited classical features of acromegaly, including enlarged nose, lips, hands, and feet, large pores, and prognathism; his visual field was normal. A review of previous photographs suggested that his appearance had begun to change at least 6 years earlier. Examinations of cardiac, pulmonary, abdominal, and nervous systems were unremarkable.
Pituitary magnetic resonance imaging (MRI) with contrast showed a 2.0 × 1.7 × 1.9-cm sellar tumor that was compressing the pituitary and invading the right cavernous sinus. Laboratory examinations revealed significantly increased serum concentrations of GH (10.97 ng/mL, minimum value after 75 g glucose oral test) and PRL (585 ng/mL, normal range 4.6–21.4 ng/mL), mild hypercalcemia (10.7 mg/dL, normal range 8.5–10.1 mg/dL), hyperphosphatemia (5.48 mg/dL, normal range 2.6–4.6 mg/dL), slightly low PTH concentration (24 pg/mL, normal range 14.5–62.7 pg/mL), and increased bone turnover markers (c-terminal telopeptide [CTX] 1.99 ng/mL, normal range 0.299–0.573 ng/mL; bone alkaline phosphatase [B-ALP] 23.9 ug/L, normal range 11.4–24.6 ug/L). Serum concentrations of testosterone (0.51 ng/mL, normal range 2.5–9.08 ng/mL) were markedly decreased; however, luteinizing hormone (2.5 IU/L, normal range 1.7–8.6 IU/L) and follicle-stimulating hormone (2.2 IU/L, normal range 1.5–12.4 IU/L) were within the normal range, as was thyroid function (Table ). As to adrenocortical function, on admission his plasma total cortisol (PTC) concentration was 374.1 nmol/L at 08:00. Synchronous adrenocorticotrophic hormone (ACTH) was 43.09 ng/L, whereas post-stress concentrations of PTC and ACTH were 657.3 nmol/L and 45.69 ng/L, respectively. After a 1 mg dexamethasone overnight inhibition test, the serum cortisol concentration at 08:00 was 32.43 nmol/L, indicating that his hypothalamic–pituitary–adrenal axis was functioning normally. Additionally, his liver and renal function, blood lipids, blood glucose, and glycated hemoglobin were all normal. Tumor markers, including alpha-fetoprotein, carcinoembryonic antigen, serum carbohydrate antigen 19 − 9, serum carbohydrate antigen 125, non-small cell lung cancer antigen, neuron specific enolase and total and free prostate specific antigen, were all in the normal range. Chest and abdominal plain and enhanced CT (computerized tomography) showed bilateral pleural thickening and adhesion, no visible gallbladder, and left renal cyst. Ultrasound examination of the genitourinary system showed calcification in the left kidney. Gastroscopy showed mild esophagitis and colonoscopy revealed multiple polyps in rectum and colon, and pathological examination was hyperplastic polyps.
Finally, the patient was diagnosed with a GH and PRL co-secreting pituitary macroadenoma. Surgery was suggested to him, but he refused. So cabergoline together with somatostatin was prescribed (cabergoline 0.5 mg orally twice weekly, octreotide acetate 20 mg intramuscularly every 4 weeks). Thereafter, his GH, PRL, and serum and urinary calcium concentrations decreased sharply, and had reduced further 5 months later. Meanwhile, his PTH and bone turnover markers gradually returned to within the normal range (Table ). Although the size of the pituitary tumor did not change much after 5 months of follow-up, the patient still refused surgery.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [153.0, 'mm hg'], 'Diastolic Blood Pressure': [105.0, 'mm hg']}",121,114.95,127.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 153.0 mm Hg + 2/3 * 105.0 mm Hg = 121.0 mm Hg.
Hence, the patient's mean arterial pressure is 121.0 mm Hg."
1947,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8506958-1,Extracted,"The present case report is of a 32-week- and 4-day-old female fetus through cesarean section at Mahzad Obstetrics and Gynecology Hospital, Urmia, Iran. The mother had a history of miscarriage and a normal delivery at the age of 32. She was also from a family with a good socioeconomic status resided in Urmia city. During this pregnancy, she had regularly visited a gynecologist for receiving health examinations, in which the fetus was shown to be completely healthy on a color Doppler ultrasound. The mother did not mention any particular drug history and also denied a history of substance or alcohol use. However, she mentioned a history of smoking (one cigarette a day for 10 years).
After the onset of labor signs and contractions, the mother went to the hospital and gave birth to a 32-week-and 4-day-old female fetus with a birth weight of 1800 g, height of 42 cm, and head circumference of 32 cm. Vital signs of the infant at birth were as follows: Temperature: 36.7, Heart Rate: 163 bpm, Respiration Rate: 66 bpm, Blood Pressure: 63/24 mmHg, Oxygen Saturation: 98%. The infant's Apgar score was 7 and 8 at birth and 5 min after birth, respectively. Concerning the preterm birth and respiratory distress, the infant was transferred to the NICU and placed in an incubator at an appropriate temperature. On the first day after birth, the infant underwent a chest radiograph, the results of which showed no health problem (). After sterile pre-procedural prepping and draping, a trained nurse first inserted the PICC into the basilic vein using a special angiocatheter and directed it into the vein using an angiocatheter guide (). Then the catheter (the Arrowg+ard Blue Advance™ PICC made in United States country), was pushed from the catheter insertion site to the middle of the clavicle bone and then to the mid-sternal region. Finally, the catheter was fixed with an IV fixing bandage (sterile disposable cannula catheter fixing IV Non-woven dressing made in China). After the PICC placement, the infant underwent an anterior-posterior chest X-ray again and a neonatologist confirmed the correct placement of the PICC tip in the SVC. In addition, the catheter insertion site was dressed with a sterile transparent dressing based on the medical protocol to make the catheter insertion site visible and timely diagnose local complications. Two hours after the PICC placement, the infant's oxygen saturation decreased and her vital signs changed as follows: Temperature: 36.9, Heart Rate: 199 bpm, Respiration Rate: 76 bpm, Blood Pressure: 60/25 mmHg, Oxygen Saturation: 45%. Despite 8-liter-per-minute oxygen therapy using an oxygen tent, oxygen saturation did not increase so that the patient received Continuous Positive Airway Pressure (CPAP) ventilation with the Fraction of Inspired Oxygen (FiO2) = 80% and the Positive End-Expiratory Pressure = 5 cm H2O. The infant underwent a chest radiograph again, in which the presence of a complete white-out of the right hemithorax indicated pneumothorax and right lung collapse (). Moreover, the reduction of right lung sounds indicated a collapse of the right lung, because of which a chest tube (disposable medical closed chest drainage bottle made in china) was immediately placed in this region.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [24.0, 'mm hg'], 'Systolic Blood Pressure': [63.0, 'mm hg']}",37,35.15,38.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 63.0 mm Hg + 2/3 * 24.0 mm Hg = 37.0 mm Hg.
Hence, the patient's mean arterial pressure is 37.0 mm Hg."
1948,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2650990-1,Extracted,"A 19-yr-old man was admitted to Chonbuk National University Hospital, South Korea with fever, dyspnea, palpitation, sweating, and drowsiness. On admission his vital signs were blood pressure 140/90 mmHg, heart rate 136/min, body temperature 38.1℃, and respiratory rate 45/min. On physical examination, the patient appeared acutely ill and presented with petechiae in the throat, erythematous rash on the body, conjunctival suffusion without eyeball protrusion, mild non-tender swelling of the neck area with thrill, and abdominal tenderness with hepatosplenomegaly. Before admission, he had no medical problems and had no family history of medical disease. Recently, his parents observed the patient's trend of weight loss and irritability, but he had no complaint of his health status. Laboratory findings are shown in . The patient was treated with fluid therapy in balance with urine output, empirical antibiotics, methimazole, and non-selective beta blocker. On day 4, hypothermia and hypotension occurred, and on day 6, oliguria developed. However, the patient was tolerable and so supportive fluid therapy was continued with the monitoring of urine amount. Thyroid ultrasonography and scan were also performed (), which showed findings compatible with hyperthyroidism. On day 14, the patient was stabilized in terms of physical and laboratory findings (, ) and was discharged with complete recovery on day 21. Before discharge, the titer of hantaan virus and thyroid function test including thyrotropin binding inhibitory immunoglobulin (TBII) were re-checked () and the results strongly showed that the diagnosis of GD and hantaan virus infection and treatment targeting to these diseases had been reasonable.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1949,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2769404-1,Extracted,"12-year-old Kashmiri boy of Indian ethnicity had right lower abdominal pain, fever and nausea of 23 hours’ duration. General physical examination revealed pulse of 98/min, blood pressure of 100/70 mm Hg and fever. Per abdominal examination findings were presence of tenderness in right lower quadrant, rebound tenderness, Rovsing’s sign and L-sign. In this case, L-point was adjacent to highest point of iliac crest on lateral abdominal wall. X-ray abdomen was unremarkable. On ultrasonography of abdomen, probe tenderness was recorded. There was presence of leucocytosis of 9, 5000/mm3. Patient had appendectomy and 12.6 centimeter inflamed appendix preileal in position with fecaliths inside was seen. Histopathology of specimen revealed appendicitis. Patient regularly attended our follow up clinics and was uneventful.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 70.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1950,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2575206-1,Extracted,"A 30 year old woman presented to the Emergency Ward after mid-night, complaining of severe, squeezing chest pain, radiating to the left arm. This discomfort started approximately 5 hours prior to admission. Associated symptoms included nausea and fatigue. Patient also noted that for a few months has had productive cough and night sweats. Patient suffered from mild arterial hypertension for six years, since her first pregnancy and was not under antihypertensive medication. She underwent cholecystectomy 4 years ago. Patient did not have a history of diabetes mellitus, hyperlipidemia, tobacco use, alcohol, drug abuse or oral contraceptive usage. She also denied having family history of premature coronary artery disease.
Her vital signs were as following: blood pressure 140/90 mmHg; pulse rate 110 beats/min.; respiration rate 17/min.; body temperature 37.5°C. Heart auscultation revealed regular heart rhythm, clear sounds and diastolic murmur 2/6 on the second right intercostal space. On lung auscultation there was normal breathing. Other systems had no remarks on physical examination.
ECG showed normal sinus rhythm, heart rate of 110/min., and ST segment elevation of 1–3 mm in inferior and antero-lateral wall leads (figure and ). Initial enzyme profile that could be obtained in our Emergency Centre Laboratory displayed following results: ALT: 32 IU/l, AST: 72 IU/l, CK: 493 IU/l and CK-MB: 21 IU/l, with upper limit reference values for CK and CK-MB being 110 IU/l and 12 IU/l, respectively. Troponin data could not be attained in our hospital. Subsequent enzyme results showed lower values. CRP level was 20 mg/l, whereas lipid profile revealed the following results: total cholesterol = 4.81 mmol/l; HDL cholesterol = 2.02 mmol/l; LDL cholesterol = 2.41 mmol/l; VLDL = 0.24 mmol/l; and triglycerides = 1.2 mmol/l. All other laboratory findings were within normal reference range.
Based on these findings patient was admitted in the Coronary Unit and was treated as acute myocardial infarction, with analgesics, Oxygen, Aspirin, thrombolytic therapy (Streptokinase), a beta blocker and low dose of ACE inhibitor. Chest X-ray and echocardiography were done that morning.
Chest X-ray discovered homogenous shades, well defined, of solid tissue intensity, located mainly in the para-tracheal part of the left lung (figure ).
Echocardiography findings demonstrated: very mild thickening of the septal wall (11,5 mm), thickening of aortic cusps, grade 2 aortic regurgitation, grade 1 mitral regurgitation, diastolic dysfunction of the left ventricle, and hypokinesis of the inferior, anterior and lateral myocardial walls. There was no evidence of echo-free space amid epicardium and pericardium and separation between them was not detected. Pericardium was not thickened. Echocardiography measurements were as follows: Aortic root = 34 mm; Left Atrium = 35 mm; Mid right ventricular diameter = 27 mm; Right atrium diameter = 30 mm; Interventricular septum = 11.5 mm; Posterior wall = 11 mm; Left ventricular end diastolic diameter = 55 mm; Left ventricular end systolic diameter = 38 mm; Fractional shortening (FS) = 31%; Ejection Fraction (EF) = 58%; E/A = 0.8; E wave deceleration time = 240 ms.
Patient's chest pain went away the next day and did not recur during the 12 day hospitalization period, while weakness, intermittent coughs and night sweats persisted. ECG of the second day showed decrease of ST elevation and terminal T wave inversion in leads V3–V6 and T wave inversion in D2, D3 and aVF. ECG of the third day demonstrated changes consistent with non-Q-wave myocardial infarction of the inferior and lateral wall, and Q-wave infarction of the anterior wall. This ECG pattern remained the same throughout the hospitalization time (figure ).
Due to chest X-ray abnormalities of unknown nature, a pulmologist was consulted. Hexagon TB test and PPD resulted positive. Patient was diagnosed by pulmologist as Active Pulmonary Tuberculosis and was put under tuberculostatic therapy. Eight weeks later Mycobacterium tuberculosis was isolated from the Löwenstein sputum specimen.
Patient was asked to undergo coronary angiography and endocardial biopsy, but due to her socioeconomic status and in the absence of medical insurance system in our country, she was not able to complete it.
At follow-up visit, two weeks after hospital discharge, patient did not experience any chest pain, ECG changes were indistinguishable from the discharge ECG and echocardiography findings did not differ from the ones obtained during hospitalization.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
1951,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-488,Extracted,"A 66-year-old man comes to the physician because of yellowish discoloration of his eyes and skin, abdominal discomfort, and generalized fatigue for the past 2 weeks. He has had dark urine and pale stools during this period. He has had a 10-kg (22-lb) weight loss since his last visit 6 months ago. He has hypertension. He has smoked one pack of cigarettes daily for 34 years. He drinks three to four beers over the weekends. His only medication is amlodipine. His temperature is 37.3°C (99.1°F), pulse is 89/min, respirations are 14/min, and blood pressure is 114/74 mm Hg. Examination shows jaundice of the sclera and skin and excoriation marks on his trunk and extremities. The lungs are clear to auscultation. The abdomen is soft and nontender. The remainder of the examination shows no abnormalities. Laboratory studies show:
Hemoglobin 12 g/dL
Leukocyte count 5,000/mm3
Platelet count 400,000/mm3
Serum
Urea nitrogen 28 mg/dL
Creatinine 1.2 mg/dL
Bilirubin
Total 7.0 mg/dL
Direct 5.5 mg/dL
Alkaline phosphatase 615 U/L
Aspartate aminotransferase (AST, GOT) 170 U/L
Alanine aminotransferase (ALT, GPT) 310 U/L
γ-Glutamyltransferase (GGT) 592 U/L (N = 5–50 U/L)
An ultrasound shows extrahepatic biliary dilation. A CT scan of the abdomen shows a 2.5-cm (1-in) mass in the head of the pancreas with no abdominal lymphadenopathy. The patient undergoes biliary stenting.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [114.0, 'mm hg'], 'Diastolic Blood Pressure': [74.0, 'mm hg']}",87.33333,82.96666,91.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 114.0 mm Hg + 2/3 * 74.0 mm Hg = 87.33333 mm Hg.
Hence, the patient's mean arterial pressure is 87.33333 mm Hg."
1952,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3236149-1,Extracted,"A 23-year-old previously healthy Caucasian woman, G2P0A1, presented at 36 weeks gestation to the emergency department (ED) after sudden onset of dyspnea, nausea, and vomiting for 5 minutes, then collapse and unresponsiveness. Her pregnancy had been complicated by pregnancy-induced hypertension treated with labetalol 400 mg 3 times daily. She had no other medical, surgical, or drug-use history. On arrival, she was agitated, altered, uncooperative, and moving all extremities. Her heart rate was 151 beats per minute, blood pressure 118/78 mmHg, respiratory rate 32 breaths per minute, with SpO2 86% on a nonrebreather mask. The patient did not appear Marfanoid or dysmorphic, with a height of 5′7″ and weight 147 lbs. On physical exam, the patient had perioral cyanosis, tachycardia with distant heart sounds, no edema, and gravid abdomen.
The patient immediately underwent rapid sequence orotracheal intubation and was mechanically ventilated. Her initial hemoglobin (HemoCue) was 12.5 g/dL. The patient quickly became pulseless with pulseless electrical activity (PEA). Chest compressions were initiated. A bedside ultrasound examination showed a large clot inside the pericardium, pericardial fluid, and empty, poorly contracting ventricles. A pericardiocentesis was performed with 5 mL of blood aspirated. A thoracotomy was immediately performed by the ED physicians. The obstetrical team concurrently performed an emergent perimortem cesarean delivery. A baby boy was delivered, intubated, and transferred to the Neonatal Intensive Care Unit.
The thoracotomy had findings of blood in the pericardial sac and a boggy, fibrillating heart with no evidence of active bleeding or cardiac injury. Cardiac massage was initiated resulting in palpable carotid pulses. This was followed by intracardiac epinephrine injection, internal defibrillation, and intravenous bicarbonate infusion.
At this time, the cardiothoracic surgical team arrived. On further exploration of the chest cavity, the source of bleeding could not be isolated. The cardiothoracic surgeons then inserted a thoracostomy tube into the right chest, which drained 100 mL of serous fluid. The patient continued to decompensate and was pronounced dead 1 hour after her initial presentation to the ED.
On autopsy, the patient was found to have a 0.5-cm tear in the aortic adventitial tissue and a 3-cm ragged tear in the posterolateral aorta superior to the aortic valve and extending 3 cm vertically. The tear was not consistent with chest compressions performed during cardiopulmonary resuscitation. The heart had severe left ventricle hypertrophy and weighed 450 gm, which was much larger than the expected 250 gm.
The baby boy was discharged a month later to the care of his father.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [118.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",91.33333,86.76666,95.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 118.0 mm Hg + 2/3 * 78.0 mm Hg = 91.33333 mm Hg.
Hence, the patient's mean arterial pressure is 91.33333 mm Hg."
1953,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8768,Extracted,"A 58-year-old man presents to his physician with breathlessness on exertion for the last 2 years. He mentions that initially, he used to become breathless upon climbing 2 flights of stairs, but now he becomes breathless after walking a couple of blocks. He has no known medical condition except obesity (most recent BMI of 36 kg/m2); he has been obese for the last 10 years. There is no history of substance abuse. His temperature is 36.9°C (98.4°F), the pulse is 90/min, the blood pressure is 130/88 mm Hg, and the respirations are 20/min. Auscultation of the chest reveals a loud pulmonic component of the second heart sound. Auscultation over the lung fields does not reveal any specific abnormality. His chest radiogram shows enlargement of the central pulmonary arteries, attenuation of the peripheral pulmonary vessels, and oligemic lung fields.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [88.0, 'mm hg']}",102,96.9,107.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 88.0 mm Hg = 102.0 mm Hg.
Hence, the patient's mean arterial pressure is 102.0 mm Hg."
1954,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7755679-1,Extracted,"A 23-year-old female with a family history of SLE, presented with nausea and vomiting for two weeks and “not acting like herself” for three days. The patient had been admitted two weeks prior for calculus cholecystitis and underwent cholecystectomy. She was accompanied by a nurse caretaker, who said the patient had been acting like a child for the last three days. She had also been experiencing joint pain before hospitalization. On exam, she was normotensive with a blood pressure of 138/85, tachycardic with a heart rate of 106, and a temperature of 98.6°F. She was awake and alert with a Glasgow Coma Scale of 12. She was unable to recall recent events. The general examination was otherwise unremarkable.
At the time of admission, complete blood count (CBC) revealed a hemoglobin of 7.8 g/dL (reference range: 12.0-15.8 g/dL), hematocrit of 24.1% (reference range: 36.0-47.0%), mean corpuscular volume (MCV) of 92.3 fL (reference range: 80-94 fL), mean corpuscular hemoglobin concentration (MCHC) of 32.7 g/dL (reference range: 33-37 g/dL). Complete metabolic panel (CMP) revealed hypokalemia of 2.9 mmol/L (reference range: 3.5-5.1 mmol/L), and total bilirubin of 1.2 mg/dL (reference range: 0.2-0.8 mg/dL). A computed tomography (CT) scan of the abdomen and pelvis was done. This revealed a fluid collection that was present in the gallbladder fossa suggesting a post-operative seroma (Figure ). CT of the head (Figure ) was done without contrast as the patient had a change in mental status, which did not show any acute intracranial abnormality. The patient continued to have confusion, meanwhile, a biliary drain was placed. During the admission, the patient also had some shortness of breath. A CT scan of the chest (Figure ) was done and revealed a moderate-sized pleural effusion on the left, with compression atelectasis of the lower lung. There were also small calcified right hilar lymph nodes and subcarinal lymph nodes related to the old granulomatous disease. Small calcified right hilar lymph nodes and subcarinal lymph nodes related to old granulomatous disease were also appreciated.
Neurological workup including lumbar puncture, brain MRI, and EEG was done. Brain MRI (Figure ) showed small vessel ischemic changes and abnormal T2 flair/periventricular signal. EEG findings were consistent with diffuse cerebral dysfunction. Lumbar puncture findings were not significant for any pathology. Based on the MRI and EEG findings, the patient was suspected to have a multisystemic disorder and a rheumatologic workup was done. C-reactive protein (CRP) was 1.40 mg/dL (reference range <1.00 mg/dL), erythrocyte sedimentation rate (ESR) 47 mm/h (reference range: 0-20 mm/h), ANA titer >=1:2560, anti-double-stranded DNA Ab >300 IU/mL (reference range: <5 IU/mL), anti-Smith antibody 5.1 AI (reference range: <1.0 AI), anti-Smith/U1-RNP antibody 4.2 AI (reference range: <1.0 AI), positive perinuclear antineutrophil cytoplasmic antibody (pANCA).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [138.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",102.66667,97.53334,107.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 138.0 mm Hg + 2/3 * 85.0 mm Hg = 102.66667 mm Hg.
Hence, the patient's mean arterial pressure is 102.66667 mm Hg."
1955,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8572029-1,Extracted,"A 73-year-old African American male presented to the hospital for lower back pain and symptoms of urinary tract infection and a chronic great toe wound with discharge. His history was significant for type 2 diabetes mellitus, hypertension, and coronary artery disease, post-stenting five years ago.
His blood culture collected at the time of hospital admission was positive for Streptococcus dysgalactiae. Other significant laboratory findings at the time of admission were a complete blood count of 17000/mm, hemoglobin of 13 gm/dL, the random blood sugar of 212 mg/dL, blood urea/creatinine of 13/1.37 mg/dL, and raised inflammatory markers (erythrocyte sedimentation rate [ESR]: 140 mm/hr, c-reactive protein [CRP]: 299 mg/L). The patient was started on vancomycin and cefepime based on his blood culture report. Right hallux wound incision and drainage had Streptococcus dysgalactiae, Staphylococcus capre, and methicillin-resistant Staphylococcus aureus, then MRI confirmed right hallux osteomyelitis. He underwent right hallux amputation. Further workup showed that patient had a spinal abscess, which developed due to the seeding of bacteria from his toe infection. He underwent bilateral laminectomy and decompression with drainage of the abscess.
A transthoracic echocardiogram done to rule out infective endocarditis showed no vegetations. Due to high suspicion of infective endocarditis, transesophageal echocardiography was also performed using benzocaine 20% spray to the back of the throat before procedure initiation. In addition, the patient was given 1 mg of midazolam and 25 mcg of fentanyl for pre-procedure sedation. Within minutes after the procedure, the patient was cyanotic, diaphoretic, confused, and developed a facial droop on the operating table. Code Stroke was called. Vitals were blood pressure 99/56, heart rate 106, respiratory rate 30, saturating 76% on room air. He was started on supplemental O2 with a non-rebreather mask. He was intermittently bagged with saturation improving to 85% on 100% O2 with on and off improvement in mental status and facial droop resolved. The decision was made not to intubate the patient, and an arterial blood gas analysis (ABG) was done, which showed chocolate-brown colored blood and a partial pressure of oxygen (PaO2) of 185 mmHg with 70% methemoglobin (ABG-pH/PaO2/PaCO2/HCO3: 7.48/185/37/27.6). The patient was immediately given 1 mg/kg of methylene blue and transferred to the intensive care unit (ICU). Within 15 minutes, the patient was improving, with improved cyanosis, mental status, and improving diaphoresis. One hour repeat ABG showed methemoglobin levels of 31. Poison control was called, and they recommended methemoglobin levels less than 30, with a goal of less than 20, and resolution of symptoms. In the following hour, the attending toxicologist recommended re-dosing with another 1 mg/kg for a total of 2 mg/kg (100 mg) methylene blue for persistently elevated methemoglobin levels greater than the goal level. The repeat ABG after the second dosing of methylene blue showed methemoglobin levels less than 10. The toxicologist recommended following the methemoglobin levels on Arco oximetry ABG. His final ABG showed a methemoglobin level of 2.6 and saturation maintained with oxygen supplementation via nasal cannula. The patient was discharged the next day to a rehabilitation center with antibiotics.
We report this case to draw attention to rare circumstances of methemoglobinemia following the use of local anesthetics. This may not be considered and missed during code scenarios due to uncommon encounters, a general lack of awareness, and limited availability of standard co-oximetry for an accurate diagnosis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [56.0, 'mm hg'], 'Systolic Blood Pressure': [99.0, 'mm hg']}",70.33333,66.81666,73.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 99.0 mm Hg + 2/3 * 56.0 mm Hg = 70.33333 mm Hg.
Hence, the patient's mean arterial pressure is 70.33333 mm Hg."
1956,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3025968-1,Extracted,"A 26-year-old Caucasian woman presented to our emergency department complaining of a persistent fever (ranging between 38.5°C and 40°C) over the previous three days. She had been in her usual state of health until this time. She also complained of palpitations, chills and diaphoresis. She denied any other symptoms. She described no known contact with sick individuals, no trauma, insect bites or any history of travel.
She was born full term to a 24-year-old mother via vaginal delivery, weighing 7 lbs 3oz. At three-weeks of age, she developed diffuse petechiae which persisted and, after multiple studies, she was diagnosed as having a long-standing refractory pancytopenia with multi-lineage dysplasia. Her average blood count values were a white blood cell (WBC) count of 1.5×103 cells per mm3 with severe neutropenia, with an approximate absolute neutrophil count (ANC) in the 400 range. Her hemoglobin level was 8 g/dL and her platelet count was approximately 45×103/mm3. Despite her condition, she had an infrequent history of infections. These included otitis media and adenitis at eight months of age, Staphylococcal cellulitis at 15 months and two instances of uncomplicated pyelonephritis at ages 15 and 21 which were treated successfully with amoxicillin and gatifloxacin. She had two uneventful pregnancies and a third which was complicated by severe pre-eclampsia. She noted occasional petechiae and some bruising, but had not had any serious hemorrhages. Please refer to Figure for a graphic description outlining the 10-year span blood count numbers for this patient.
She has had a bone marrow biopsy performed every two years as a follow-up procedure for her refractory pancytopenia, and no clear etiology has been defined. This lack of diagnostic certainty and her ongoing concerns regarding her future health and that of her children has caused her major distress. She has also been told by some physicians that she and her family may carry an increased risk for hematological malignancies.
On physical examination, she was febrile with a temperature of 38.3°C. Her heart rate was 105 beats per minute, her blood pressure was 115/82 mmHg and her respiratory rate was 17 breaths per minute with an oxygen saturation of 99 percent at room air. Her physical examination was unremarkable except for sinus tachycardia. On her admission to our hospital, our laboratory studies showed a WBC count of 1.53×103 cells per mm3 with 20 percent neutrophils and 66 percent lymphocytes. Her ANC was 400, her hemoglobin level was 6.8 g/dL, her Mean Corpuscular Volume was 82 fL and her platelet count was 47×103/mm3. Her electrolytes were within normal range. Her prothrombin time was 19.1 seconds, and the International Normalized Ratio -INR- was 1.1.
She was diagnosed with febrile neutropenia and she was started on empiric IV piperacillin/tazobactam after we obtained blood and urine cultures. A computed tomography (CT) scan of her chest, paranasal sinuses, abdomen and pelvis were ordered to evaluate the source of the fever. All the imaging studies showed no abnormalities.
On day two, her blood count values still remained low. After the ingestion of an oral contrast, she developed soft stools which prompted us to undertake stool studies. These were negative for lactoferrin, Clostridium difficile and fecal leukocytes. Assessment for ova and parasites as well as a stool culture were also negative. A direct Coombs test was negative, her reticulocyte count was 0.2 percent, and an iron study panel revealed serum iron levels of 7 mmol/L, ferritin 72 ug/L, and iron saturation levels of four percent. Her lactate dehydrogenase and bilirubin levels were unremarkable.
She continued to spike fevers overnight with no evident source of infection. A bone marrow biopsy was completed, suggesting once again the diagnosis of refractory pancytopenia with multi-lineage dysplasia. No increased blasts were noted. Fluorescent in situ hybridization (FISH), flow cytometry and cytogenetics did not reveal any major abnormalities. While investigating possible causes of the refractory, long-standing pancytopenia, the possibility of a polyagglutinable state was suggested. Blood samples were sent to the laboratory for an analysis of mixed-field seed lectin agglutination assay. A serum lectin panel confirmed the final diagnosis of Tn-activation (Dolichos biflorus +, Glycine soja +, Salvia sclerea +) and TnP was diagnosed. She responded to treatment very well and after 48 hours of being afebrile, she was discharged with a five day course of cefpodoxime. Her samples were sent for Tn monoclonal antibody immunochemistry which reconfirmed her diagnosis.
TnP is a rare disorder that has been reported on only six occasions in the medical literature and never before in the setting of febrile neutropenia. TnP is an acquired disorder, characterized by the defective biosynthesis of red blood cell (RBC) membrane glycoproteins that results in the exposure of normally cryptic N-acetylgalctosamine residues (GalNAc) [,].
Polyagglutination is the term applied to RBC that are agglutinated by almost all samples of human sera from adults, but not by autologous serum or sera of newborns [-] (Figure ). Previously, all cases of TnP, and many other polyagglutinable phenomenons, were diagnosed during infancy or at the moment when a blood group classification for a transfusion was made, as former techniques of hemoclassification were performed using human adult serum containing multiple antibodies. However, current blood grouping practice uses murine diluted monoclonal antibody re-agents that do not include any other potentially pro-agglutinating immunoglobulins (Ig), thus denying the opportunity to recognize polyagglutinable cells and their implications [,]. This has been reflected in a lack of reports about this condition over the last 30 years.
Tn RBC are polyagglutinable because most adult sera contain naturally occurring anti-Tn. T and Tn antigens (from Hiibener-Thomsen-Friedenreich) are normally inaccessible to the immune system. These antibodies occur primarily due to the exposure to the intestinal flora, where highly immunogenic T and Tn-specific structures are present in most Enterobacteriaceae [-]. The Tn defect can also be found on the membranes of platelets, granulocytes and lymphocytes []. The first example of TnP was encountered in a patient with hemolytic anemia, and many of the other cases observed since then have revealed a common association with leukopenia and thrombocytopenia [].
Tn antigen is caused by a hemizygous pleiotropic somatic mutation or gene suppression in adults at the pluripotent stem cell level, creating an abnormal clone in expansion through an autoimmune process, in which it is hypothesized that the patient's Natural Killer cells (NK) target the O-glycans of the normal blood cells and selectively destroy the normal blood cell population. This leads to the loss of anti-Tn and possibly the multi-lineage dysplasia and subsequent cytopenias [].
Further studies have shown that TnP results from the inactivation of C1GALT1C1, a gene located at Xq24, which encodes a chaperone required for the correct functioning of T-synthase (syn.Gal-b-1-3transferase), a key enzyme in the synthesis of O-glycans. This results in the exposure of GalNAc-linked to serine or threonine on polypeptide backbones, exposing the otherwise cryptic Tn antigen to the erythrocyte surface [].
A diagnosis of TnP is made using mixed-field seed lectin agglutination. Lectin typing reagents contain proteins that recognize specific carbohydrates on RBC membranes, causing their direct agglutination. Positive agglutination reactions following exposure of the patient's red blood cells to specific lectins derived from seeds of Dolichos biflorus, Glycine soja and Salvia sclerea plant species are considered as pathognomonic for diagnosis (Table ). The only exception occurs in patients with blood group A, due to its chemical similarity with the Tn antigen [-,]; monoclonal anti-Tn reagents are available for these cases []. Many other types of agglutination have been described in the literature. Most of them are transient and related to episodes of acute infection where bacterial enzymes (for example, neuraminidase and endoβ-galactosidase) expose such antigens (T, Th, Tk, TX, VA). There are some other inherited types of agglutination whose frequency has not been established (Cad [Sda], HEMPAS, NOR, Hyde Park, Tr) [-].
TnP is not directly linked to malignancy or an increased risk of invasive infections, with many reports of elderly Tn individuals in apparently good health. However, the Tn antigen itself has been widely studied as a marker of tumor cells: O-glycans are common constituents of membranes and secreted mucins and an exposure of Tn and sialyl-Tn has been demonstrated in many carcinomas [].",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [115.0, 'mm hg'], 'Diastolic Blood Pressure': [82.0, 'mm hg']}",93,88.35,97.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 115.0 mm Hg + 2/3 * 82.0 mm Hg = 93.0 mm Hg.
Hence, the patient's mean arterial pressure is 93.0 mm Hg."
1957,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3173668-1,Extracted,"A 71-year-old male patient with diabetes mellitus and hypertension visited the emergency room of our hospital because of hemoptysis. He was diagnosed with a 7 cm sized aortic arch aneurysm 2 years earlier. He was recommended to undergo an operation for the aneurysm, but refused to do so. He also did not take his medicine and was without a follow up examination over that period.
At the time of admission, his blood pressure was 150/100 mmHg, pulse rate was 86 beats/min, respiratory rate was 20 breaths/min and body temperature was 36.5℃. The patient was alert, but looked quite ill in appearance. His heart sounds were regular without murmurs, and the lung sounds were decreased at the left lung field. All other aspects of the physical examination were normal.
The initial laboratory findings showed that his hemoglobin level was 8.1 g/dL, white blood cell count was 9.7×103/µL and platelet count was 170×103/µL. Additional laboratory studies were normal. An electrocardiogram showed normal sinus rhythm without specific abnormal findings and a chest X-ray showed a mass-like lesion in the left hilar zone (). The chest CT showed a 9 cm sized saccular aneurysm 0.5 cm distal to the left subclavian artery with thrombus in the aortic arch, which was oozing to the anterior wall owing to rupture of the aneurysm, and there was a hemothorax in the left lung (). Labetalol was infused intravenously for controlling blood pressure.
We recommended an operation for treating the ruptured aortic arch aneurysm, but the patient and his family refused an operation because of the risk of surgery. Therefore, we decided to perform a hybrid procedure that consisted of a carotid to carotid bypass operation and the placement of stent grafts in the aortic arch aneurysm to save the left carotid artery. We planned to sacrifice the left subclavian artery intentionally and later performed a second stage left carotid to left subclavian artery bypass operation if the patient displayed subclavian steal syndrome, severe dizziness and/or left arm pain. Before endovascular stent graft placement, we checked the whole aortogram and excluded the presence of stenosis that would interfere with collateralization in the carotid or vertebral arteries. We referred him to a thoracic surgery to perform the carotid to carotid bypass operation connecting from the right carotid artery to the left carotid artery in advance for revascularization of the post-stent grafting. Insertion of the aortic stent grafts was performed following the successful by-pass operation. The aortography showed the presence of a huge aortic arch aneurysm 0.2 cm distal to the left subclavian artery (). We deployed two pieces of aortic stent grafts (40 mm×10 cm, 36 mm×10 cm, S&G biotech, Korea) across the left carotid artery and left subclavian artery through the left femoral artery (). The second aortic stent graft (36 mm×10 cm, S&G biotech) was deployed in the first aortic stent graft with a 7 cm overlapped segment to protect against disconnection of the aortic stent grafts. The post-procedure aortography showed no endoleak or other complications.
Directly after the procedure, the patient was transferred to the intensive care unit, where he complained of aggravated dyspnea and massive hemoptysis. Chest X-ray showed total haziness in the left lung field and a chest CT showed successful stenting in the aortic arch aneurysm and total ateletasis of the left lung due to external compression of the left main bronchus by hematoma (). Therapeutic bronchoscopy was performed to remove a large amount of blood clots in the left bronchus. The left atelectasis improved on the chest X-ray taken 5 days after a bronchoscopy procedure (). Follow up CT angiography of the aorta after 7 days showed successful stenting, no endoleak and no thrombus in the aortic arch ().
The patient was discharged from our hospital without any further adverse clinical events. No cardiovascular events were observed during 1 year of follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",116.66667,110.83334,122.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 100.0 mm Hg = 116.66667 mm Hg.
Hence, the patient's mean arterial pressure is 116.66667 mm Hg."
1958,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2311322-1,Extracted,"A seventeen year old girl presented as an emergency with a two-day history of lower abdominal and back pain. She experienced rigors and appetite loss but no nausea, vomiting, dysuria, cystitis or vaginal discharge. Three months previously, she had undergone immediate appendicectomy for a gangrenous retrocaecal appendix. Other intraoperative findings at the time were a macroscopically normal right ovary and fallopian tube.
There was no history of recent sexual activity or pelvic inflammatory disease. Menstrual cycles were regular and every 28 days and the patient was mid-cycle at the time of presentation.
On examination, she had a temperature of 38.5°C, pulse of 100 beats per minute and blood pressure of 114/59. Lower abdominal rebound tenderness, guarding and absent bowel sounds were present. The patient had a leucocytosis of 16.4 × 109.l-1 and C-reactive protein concentration of 322 mg.l-1. A pregnancy test was negative and an emergency computerized tomographic scan showed a complex pelvic mass associated with or near to the right ovary and overriding, but not connected to the uterus (Figure ). She subsequently underwent an emergency laparotomy. The right fallopian tube was found in the midline above the uterus. It was grossly enlarged, measuring 10 × 5 cm, with multiple necrotic areas oozing pus. The fimbrial end was oedematous with a radius of 2 cm. The left fallopian tube was slightly enlarged and was found postrolateral to the uterus, adherent to the sigmoid colon by fibrinous adhesions. There was no visible enterosalpinx fistula and no appendicular stump leak. The left salpinx was released by blunt dissection and pus drained from both fallopian tubes by retrograde ""milking"". Both tubes were irrigated generously with a 0.9% saline and Betadine mixture. Microbiological analysis of the pus revealed Escherichia coli and anaerobes but not Chlamydia or Candida spp. A postoperative Gastrografin enema did not reveal an occult fistula (Figure ).
The patient was treated postoperatively with intravenous Co-Amoxiclav and Metronidazole for a week and made an uneventful recovery. However, she now faces the long-term sequelae of potential infertility, ectopic pregnancy and chronic pelvic pain.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [114.0, 'mm hg'], 'Diastolic Blood Pressure': [59.0, 'mm hg']}",77.33333,73.46666,81.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 114.0 mm Hg + 2/3 * 59.0 mm Hg = 77.33333 mm Hg.
Hence, the patient's mean arterial pressure is 77.33333 mm Hg."
1959,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7943396-1,Extracted,"A 65-year-old female with a past medical history of achalasia presented to the emergency department (ED) with complaints of worsening shortness of breath, nausea, non-bilious hematemesis with some regurgitated food and water, and chest pain over the past day. Her symptoms were accompanied by sweating, fatigue, and intermittent dysphagia for both solid foods and liquids. Although she declined any treatment, she continued to live a relatively normal life through lifestyle interventions consisting of a pureed diet, carbonated beverages to aid in digestion, eating smaller and more frequent meals, and indulging in specific maneuvers such as lifting her neck and shoulders back to further enhance esophageal emptying. The patient denied the regular use of tannins, NSAIDs or aspirin, immunosuppressants, and any unintentional weight loss, melena, and hoarseness of her voice.
Her vitals in the ED were significant for a temperature of 36.1°C, hypotension of 106/60 mmHg with a tachycardia of 110 beats/minute, respiratory rate of 14 breaths/min, and oxygen saturation of 96% on room air. Her physical exam was pertinent for pale conjunctiva and nail beds with a decreased capillary refill time. Her complete blood count (CBC) showed normocytic anemia with a hemoglobin of 9.5 g/dL, which was significantly lower than her baseline of 12 g/dL, a hematocrit of 23.6%, and leukopenia of 4.59x103/mL. The patient’s basic metabolic profile was unremarkable except for a slight acute kidney impairment with a creatinine of 0.88 and blood urea nitrogen (BUN) of 28.0, likely due to her hypotension. She was then given three liters of intravenous fluids, 40mg of Protonix®, and 10mg of Reglan® with mild symptomatic relief.
While she was being escorted for radiological testing, she experienced a second large episode of bright red hematemesis accompanied by severe dizziness and fatigue. A repeat CBC showed her hemoglobin dropping to 7.2 g/dL, and a blood transfusion was then given. A chest X-ray showed mediastinal widening with a dilated megaesophagus occupying most of the right hemithorax. In addition, CT angiography (CTA) was done to rule out aortic dissection, and it illustrated significant distention of the esophagus with non-specific intraluminal fluid with a small amount of gas (Figures -). Luminal narrowing at the level of the esophagogastric junction was also evident. In addition, moderate ground glass opacifications were seen in the inferior right upper lobe, right middle lobe, right lower lobe, and left lower lobe suggesting possible atelectasis or aspiration with a dilated right main bronchus suggesting obstruction.
An emergent esophagogastroduodenoscopy (EGD) revealed areas of the esophageal mucosa containing fibrosis and necrosis with some food debris and diffuse dark red blood throughout, preventing adequate visualization of the bleeding source (Figure ). These findings suggested that the bleeding was likely coming from an underlying ulcer caused by pressure necrosis from retained food. The endoscope was unable to pass through the gastroesophageal junction due to a severely dilated and aperistaltic esophagus. The patient was hemodynamically unstable after the procedure and was transferred to another facility the next day for an esophagectomy.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [106.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",75.33333,71.56666,79.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 106.0 mm Hg + 2/3 * 60.0 mm Hg = 75.33333 mm Hg.
Hence, the patient's mean arterial pressure is 75.33333 mm Hg."
1960,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-7041,Extracted,"A 32-year-old woman presents for a follow-up visit. She was diagnosed with type 2 diabetes mellitus a month ago but refused to start medications despite counseling due to her fear of gaining weight. She tried exercising and eating healthy in an attempt to ''cure'' her diabetes. She managed to lose 1.8 kg (4 lb) in a month. Today she still complains of increased urinary frequency, the same symptom that leads to her initial suspicion of diabetes. No other significant past medical history. She is happily married and plans on having kids in the next few years. The patient is a non-smoker, denies illicit drug use, and drinks socially. Her vital signs show a pulse of 80/min, a respiratory rate of 16/min, a blood pressure of 120/80 mm Hg, and a temperature of 36.9°C (98.4°F). Her BMI is 33.0 kg/m2. Physical exam findings are unremarkable. Her fingerstick glucose today is 214 mg/dL.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [80.0, 'mm hg'], 'Systolic Blood Pressure': [120.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1961,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5254,Extracted,"A 37-year-old G1P1 woman gives birth to a male infant at 36 weeks gestation. The patient had an uncomplicated Caesarean delivery and gave birth to a 6-pound infant. The patient has a past medical history of cocaine and heroine use but states she quit 8 years ago. She also suffers from obesity and type II diabetes mellitus. Her blood sugar is well-controlled with diet and exercise alone during the pregnancy. Her temperature is 98.4°F (36.9°C), blood pressure is 167/102 mmHg, pulse is 90/min, respirations are 13/min, and oxygen saturation is 98% on room air.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [167.0, 'mm hg'], 'Diastolic Blood Pressure': [102.0, 'mm hg']}",123.66667,117.48334,129.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 167.0 mm Hg + 2/3 * 102.0 mm Hg = 123.66667 mm Hg.
Hence, the patient's mean arterial pressure is 123.66667 mm Hg."
1962,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8052988-1,Extracted,"A 40-year-old non-alcoholic male with a past medical history of hypertension and type 2 diabetes mellitus was admitted with abdominal pain, diarrhea, shortness of breath, and confusion. His temperature was 98.7°F, heart rate was 78 bpm, oxygen saturation was 90% in room air, and blood pressure was 96/54 mmHg. On examination, abdominal tenderness was present, with reduced bilateral air entry and altered mental status. Laboratory studies showed elevated white blood cells (13.3 K/UL), and a CO2 level of 11 mmol/L, blood urea nitrogen (BUN) of 131 mg/dL, creatinine of 6.90 mg/dL, total bilirubin of 1.2 mg/dL, alanine aminotransferase (ALT) of 34 U/L, aspartate aminotransferase (AST) of 29 U/L, glucose of 131 mg/dL, lactic acid of 3.6 mmol/L, and creatine kinase level of 2,282 U/L. His oxygen requirement increased on day 2, requiring 3 L of oxygen. Chest X-ray showed increased bilateral interstitial marking (Figure ). He continued to have increased abdominal pain and underwent a computed tomography (CT) scan of the abdomen without contrast, which showed fluid distension in the small bowel and colon consistent with enterocolitis (Figure ). Polymerase chain reaction (PCR) for COVID-19 and PCR and enzyme immunoassay (EIA) C. difficile was positive, as he had persistent diarrhea. Remdesivir and steroids were not administered due to acute kidney injury and CDI; instead, intravenous fluids and oral vancomycin were administered. His kidney functions improved with intravenous fluids as recommended by the nephrology team. His renal functions improved on the fourth day of admission: creatinine was 2.10 mg/dL and BUN 69 was mg/dL. He remained confused; a CT scan of the head did not show any acute intracranial abnormalities, and he had an ammonia level of 102 umol/L. Lactulose was not started due to ongoing diarrhea secondary to CDI. His mentation improved, and his ammonia levels were reduced to 37 umol/L, and he was discharged on day 12.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [54.0, 'mm hg'], 'Systolic Blood Pressure': [96.0, 'mm hg']}",68,64.6,71.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 96.0 mm Hg + 2/3 * 54.0 mm Hg = 68.0 mm Hg.
Hence, the patient's mean arterial pressure is 68.0 mm Hg."
1963,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1199,Extracted,"A 12-year-old girl is brought to the physician because of fatigue, dyspnea, and mild chest pain on exertion for 1 week. She does not have a fever or a rash. She had an upper respiratory infection 3 weeks ago. She returned from summer camp in Colorado 3 days ago. She says they went hiking and camping as part of their activities. Her temperature is 36.9°C (98.4°F), heart rate is 96/min, and blood pressure is 106/74 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 96%. Physical examination reveals jugular venous distention and 1+ pitting edema on both ankles. A few scattered inspiratory crackles are heard in the thorax and an S3 is heard at the apex. Abdominal examination is unremarkable. Her hemoglobin concentration is 11.6 g/dL, leukocyte count is 8900/mm3, and ESR is 10 mm/hr. An x-ray of the chest shows mild cardiac enlargement.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [106.0, 'mm hg'], 'Diastolic Blood Pressure': [74.0, 'mm hg']}",84.66667,80.43334,88.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 106.0 mm Hg + 2/3 * 74.0 mm Hg = 84.66667 mm Hg.
Hence, the patient's mean arterial pressure is 84.66667 mm Hg."
1964,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5944102-1,Extracted,"An 86-year-old New Zealand European white man was diagnosed as having smoldering myeloma of IgA lambda subtype in June 2008. His diagnostic bone marrow aspirate showed 38% plasma cells. His paraprotein at diagnosis was 9 g/L and gradually increased to 46 g/L by mid-2016 without any evidence of end organ damage (Fig. ).
His other medical history includes L2–3, L5–S1 spondylosis and early stage prostate adenocarcinoma, T2A Nx M0, Gleason grade 6, which was successfully eradicated with radical radiotherapy in 2000. He takes cholecalciferol 1.25 mg once monthly, cilazapril 2.5 mg daily, amitriptyline 10 mg daily, and paracetamol 1 g twice daily and is intolerant of Augmentin (amoxicillin-potassium clavulanate; diarrhea). He lives with his wife and is fully independent with all his activities of daily living. He does not smoke tobacco and he consumes two units of alcohol per day.
In June 2016, he developed mild normochromic anemia of 104 g/L and 6 weeks later he was hospitalized with melena in the context of recent non-steroidal anti-inflammatory drug (NSAID) use for low back pain. No bleeding source was identified on upper and lower endoscopies. The ibuprofen was stopped and he was started on omeprazole. He was also found to be mildly vitamin B12 deficient with a raised methylmalonic acid, and was commenced on vitamin B12 treatment. His hemoglobin fell to a nadir of 72 g/L during the NSAID-induced gastrointestinal bleed, but quickly recovered to its new baseline of 92–97 g/L and remained unchanged for the next 12 months. With regards to his back pain, a computed tomography (CT) skeletal survey and subsequent magnetic resonance imaging (MRI) of his lumbar spine showed mild osteoporotic compression fractures of L1–4 without any evidence of lytic disease. A follow-up bone density scan confirmed osteoporosis with a T-score of −2.7 in the left neck of his femur. He was treated with a single dose of zoledronic acid in August 2016 and a weaning course of analgesia. Concordant with his hemoglobin, his paraprotein remained stable at 45–50 g/L over the subsequent 12 months. Given the absence of other myeloma-defining events and unclear etiology of the anemia, he continued with watchful observation.
In August 2017, he was prescribed a 10-day course of roxithromycin 150 mg twice daily for a clinically diagnosed community-acquired pneumonia. He had presented to his general practitioner with a 10-day history of productive cough, malaise, and anorexia. His temperature was 37.4 °C, blood pressure 140/70 mmHg, heart rate 70 beats per minute, and O2 saturations 98% on room air. Focal crepitations were heard at his left base and the rest of his physical examination was unremarkable. On review 4 days later, he had clinically deteriorated with a temperature of 39.0 °C, blood pressure 140/70 mmHg, heart rate 100 beats per minute, and O2 saturations 97% on room air but his physical examination findings were otherwise unchanged. Cephalexin 500 mg twice daily for 1 week was added to his treatment regime. He completed full courses of both antibiotics with eventual complete recovery. No blood test or sputum sample was submitted to the laboratory, and a chest X-ray was not performed. He did not receive any corticosteroids or herbal remedies with his chest infection.
At his next routine hematology follow-up a week later, his paraprotein level (quantified by capillary electrophoresis) had decreased by 57% from 46 to 20 g/L. Over the next 4 months, while off all treatment, it slowly increased to 23, 26 then 28 g/L. Quantitative IgA levels demonstrated a similar pattern, falling from 54 to 22 g/L, before increasing to 27, 31 then 33 g/L. His hemoglobin increased from a pre-treatment average of 97 to 123, 126 then 132 g/L over the next 4 months. The rest of his laboratory parameters remained stable; his creatinine was 102 mmol/L, adjusted calcium 2.3 mmol/L, and albumin 32 g/L. Serum free light chains were not measured. When reviewed 4 months after the course of roxithromycin, he was asymptomatic apart from his chronic intermittent low back pain, which was improving.
His International Staging System was calculated as II in August 2016. Clearly, his myeloma had a favorable slow progressive phenotype, as evidenced by the prolonged latent phase (8 years) from diagnosis and the stability of symptoms and paraprotein despite being untreated.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 70.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
1965,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4677009-1,Extracted,"A 21-year-old female, previously healthy, was admitted to the ear-nose-throat (ENT) ward with severe left submandibular nonfluctuant swelling, being erythematous and warm to palpation. Furthermore, mild trismus and sublingual edema were noted. Otherwise, physical and neurological examination was unremarkable. She had a sinus tachycardia of 130 b/min, fever 39°C, and blood pressure 150/90. The chest X-ray on admission was normal. She had a one-week history of a left mandibular second and third molar teeth untreated infection (periodontitis). The patient was urgently transferred to the operating room (OR) where she underwent surgical drainage of the abscess and thereafter admitted to our GICU while sedated, mechanically ventilated, hemodynamically stable, and febrile (38.7°C). Laboratory tests were noted for extensive leukocytosis (30000 cells∖ul). Immediately on ICU admission broad-spectrum antibiotic therapy (ciprofloxacin 400 mg bid and clindamycin 900 mg tid) was initiated. On the following day, extensive bilateral abscesses in parapharyngeal, retropharyngeal, and paratracheal spaces were shown on an urgently performed CT () and the patient was transferred to the OR again for exploration of deep neck infection.
A large amount of purulent fluid was drained; three days later cultures were positive for Propionibacterium acnes. The patient remained febrile (39.3°C, WBC of 24.5) though hemodynamically stable. An additional CT scan of the head, neck, and chest with contrast iodine two days later () showed a new abscess in the anterior superior mediastinal space. An urgent right thoracotomy was performed.
A large amount (about 30 cc) of purulent fluid, pH 7.18, was drained from anterior mediastinum and subcarinal space; the patient was transferred back to the GICU. Bacterial culture samples of serous fluid were positive again for Propionibacterium acnes. The patient continued antibacterial therapy by clindamycin only due to bacterial susceptibility and isolated growth of Propionibacterium. During the next four days she went to OR two additional times for surgical debridement, drainage, and washout of neck wounds. The patient continued the neck wound washout and antibiotic therapy over the next three weeks. She was discharged from the unit four weeks after admission.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",110,104.5,115.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 90.0 mm Hg = 110.0 mm Hg.
Hence, the patient's mean arterial pressure is 110.0 mm Hg."
1966,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-12488,Extracted,"A 37-year-old male presents to his primary care physician complaining of abdominal pain and diarrhea. He reports a two-week history of progressively worsening right upper quadrant pain accompanied by multiple bloody loose stools. He recently returned from a trip to rural Bangladesh. His temperature is 101.4°F (38.6°C), blood pressure is 120/70 mmHg, pulse is 110/min, and respirations are 20/min. Laboratory analysis reveals a white blood cell count of 14,000/mm^3. Findings from a stool sample with trichrome stain are shown in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1967,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7103031-1,Extracted,"We report a 29-year-old Ethiopian male patient who presented to the emergency room of Tikur Anbessa specialized hospital with 4 days history of persistent interscapular back pain, which is of stabbing nature and radiating to the anterior chest bilaterally. He also had persistent high-grade fever, vomiting for ingested matter, easy fatigability, and difficulty in swallowing.
He also complained of painful recurrent oral ulcers in the past 5 years (three recurrences of mouth ulcer in the past 1 year), scrotal ulcer of 2 years, and right side eye blindness of 1 year duration. It started gradually from the buccal cavity of the mouth and inner side of the lower lip. It completely healed and recurred three times in the past one year. The scrotal and penile shaft ulcers were pus discharging.
The past history was significant for chronic superior sagittal and sigmoid sinus thrombosis 9 years back. For this, he was on warfarin and discontinued the medication 4 months prior to current presentation for unspecified reasons. He had also repeated history of treatment for sexually transmitted infections.
Otherwise, he did not have previous history of abdominal pain, yellowish discoloration of eyes, body swelling, and reddish discoloration of urine, dysuria, or change in urine amount. He has no previous history of sexual transmitted diseases. He was admitted to hospital several times for the above compliant. He had been treated with muconazol gel and several courses of antibiotics, but there was no improvement.
On arrival to the emergency room, physical examination revealed an acutely sick looking young man in pain. His vital signs were as follows: blood pressure was 100/70 mm Hg; heart rate was 104 beats per minute regular and full in volume; respiratory rate was 36 breaths per minute and oxygen saturation was 95% at atmospheric air. Pertinent findings were on HEENT and musculoskeletal and nervous systems. He had scattered whitish superficial ulcers on the ventral side of the tongue and buccal surface of the lower lip. He had healed old scar on the penile shaft and active pus discharging ulcer at the base of the penile shaft and under the surface of the scrotum with scattered pustules. The nervous system evaluation revealed bilaterally pale and mildly atrophic tongue with right side corneal opacity. Other physical examinations were unremarkable.
Complete blood count showed leukocytosis of 15,540 cells (72.3% neutrophils and 19.2% lymphocytes), and the other cell lines were normal. Serology test of VDRL for syphilis and HIV rapid test were negative. Gram staining and AFB from scrotal ulcer swab were negative. Random blood glucose level was 124 mg/dl, and ESR was 80 mm/HR. Blood chemistry, cardiac biomarkers, serum electrolytes, and ECG were normal. Pathergy test was positive.
A chest CT scan with contrast showed right lateral proximal descending aorta secular outpouching with narrow neck measuring 4.8 cm with surrounding intramural hematoma with mass effect on the esophagus. There was no evidence of aortic dissection.
The patient was directly taken from the triage to the resuscitation area. He was put on the monitor. Intravenous line was secured, and he received morphine syrup (4 mg IV every 4 hours and subsequently escalated to continuous infusion 4 mg/HR.), metoprolol (5 mg IV stat with maintenance 25 mg PO BID, which was subsequently escalated to 50 mg PO QID), vancomycin (1 g IV BID), cefepime (2 g IV TID), and cimetidine (200 mg IV BID).
After 2 days of emergency department stay, he developed worsening of dysphagia and bloody vomiting with an estimated loss of 500 ml of blood. He was treated with omeprazole (80 mg IV stat) and resuscitated with 1 unit of whole blood and 3 liter of normal saline. Subsequently, he was taken to the operating room with the impression of aortoesophageal fistula. He received ketamine (25 mg IV) for pain control. Left posteriolateral thoracotomy was performed. Intraoperatively, there was a 5 × 4 cm proximal descending aortic aneurysm just distal to the origin of the left subclavian artery with adhesion and fistulization to mid-esophagus posteriorly. Aortic aneurysmorhaphy (primary repair) was performed, and there was a mid-esophageal 3 cm necrosis and fistula formation which was repaired over a nasogastric tube. A chest tube was inserted on the left side. The patient was transferred to intensive care unit, and his immediate postoperative course was smooth. He was transferred to regular ward on the 3rd day.
On his 8th postoperative day, the patient developed severe retrosternal chest pain and chest X- ray was taken, and it reveled significant mediastinal widening. Unfortunately, the patient passed away on the 9th postoperative day after he developed massive upper gastrointestinal bleeding in the surgical ward.
The diagnosis of Bechet's disease in our patient was made retrospectively according to the International Criteria for Bechet's Disease (ICBD) [] based on genital ulcer (two points), ocular lesions (two points), oral ulcer (one point), skin manifestations (one point), vascular lesions (one point), and pathergy test (one point, done postoperatively). For diagnosis of Bechet's disease, the ICBD recommends at least three points, and the patient fulfilled all criteria (eight points), as shown in .",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",80,76,84,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 70.0 mm Hg = 80.0 mm Hg.
Hence, the patient's mean arterial pressure is 80.0 mm Hg."
1968,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4071718-1,Extracted,"The present case report is about a 25-year-old Hispanic female with a history of depression since age of 12 years, bipolar disorder, borderline personality disorder, purging type bulimia and history of suicide attempts at age 12 was admitted to the intensive care unit after attempted suicide by consuming an unknown number of VPA pills. This patient had recently started taking VPA (Depakote®) as a mood stabilizer at a dose of 250 mg at bed time about 3 days earlier, after a failed therapy. VPA was started 4 days after she discontinued topiramate. Patient was taking paroxetine 20 mg for depression; this was incremented to 40 mg at the time VPA was started. She reported that the change to VPA made her listless, “lowered” her mood, decreased her motivation, worsened her depression and caused suicidal thoughts. She overdoses herself on VPA which she took with alcohol. After ingesting the pills she notified her family who then brought her to the emergency room. On admission, her vitals were stable (blood pressure: 118/72 mm Hg; temperature: 98.7°F; pulse: 82 beats/min; oxygen saturation: 99% on room air). On initial examination she looked disheveled, although drowsy, was oriented to person, place and time. No focal neurological deficits, abnormal cardiologic or respiratory signs were found. Her abdomen was soft, non-distended and non-tender. Her electrocardiogram showed normal sinus rhythm. The complete blood count and comprehensive metabolic panel that was recorded initially and subsequently were unremarkable []. The initial VPA and ammonia levels were elevated []. Patient was administered activated charcoal and one dose of haloperidol 5 mg intramuscularly. Subsequently, she was administered oral lactulose once and then 1400 mg of levocarnitine orally every 6 h for the next 2 days. Her VPA levels which peaked after admission continued to trend down over the next 4 days, the ammonia levels also peaked subsequent to admission then showed an initial dip followed by a very slow down-trend []. The normalized log-linear plot of VPA serum concentration over time showed a down-trending linear first-order kinetics with a calculated t½ =15.08 h [] (expected t½ for Depakote®: 9-16 h following oral dosing regimens of 250-1000 mg.[] The serum ammonia normalized log-linear plot in contrast showed two different decay kinetics: initial sharp down-trend for VPA levels greater than 90.9 μg/mL but much slower downtrend for VPA levels less than 90.9 μg/mL down into the subtherapeutic range of 8.5 μg/mL. Patient continued to complain of lethargy for the next 4 days which subsequently alleviated. At 14 days the patient was asymptomatic and her ammonia levels found to be normal (<35 μmol/L).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [118.0, 'mm hg'], 'Diastolic Blood Pressure': [72.0, 'mm hg']}",87.33333,82.96666,91.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 118.0 mm Hg + 2/3 * 72.0 mm Hg = 87.33333 mm Hg.
Hence, the patient's mean arterial pressure is 87.33333 mm Hg."
1969,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3542920-1,Extracted,"A 47-year-old man with a history of hypertension presented with fever, dyspnea, and chest discomfort for one day. He denied any other medical history, including HIV infection. On arrival in the emergency department, his body temperature was 38°C, and blood pressure was 207/125 mm Hg. Physical examination was unremarkable. The laboratory findings were as follows: white blood cell 14300/mm3 with predominance of neutrophils (89.8%) and C-reactive protein 213 mg/L (normal reference < 6 mg/L). Cardiac enzyme, arterial blood gas analysis, renal function, and electrolytes were within normal range. Chest X-ray did not show pneumonia patch, and urinalysis did not reveal pyuria. Computed tomography (CT) of chest and abdomen showed an aortic intramural hematoma from the arch to suprarenal level (). Intravenous ceftriaxone (2 g every 12 hours) was administered under the impression of infected aortic aneurysm after collection of two sets of blood culture. Two days later, cultures of blood grew K. pneumoniae which is only resistant to ampicillin. Because he continued having intermittent pyrexia, antibiotic was switched to ceftazidime (2 g every 8 hours) and gentamicin (80 mg every 8 hours). Thereafter, the patient's fever gradually subsided, and repeat blood cultures were negative. On the 20th day, sudden onset of fever (39°C) recurred, and hypotension developed. Repeat CT showed progressive dilated aorta and enlarged intramural hematoma (). Emergency operation with aortic grafting was performed, but the patient's condition gradually deteriorated, and the patient died eight days after surgery. The repeated blood culture on hospital day 20 and the specimen of excised aorta all grew K. pneumoniae. All of the K. pneumoniae isolates have the same antibioticgram, which is only resistant to ampicillin. The pathology report disclosed atherosclerosis, necrotizing inflammation, organized hematoma, and bacterial clumps in the aortic wall, which are compatible with mycotic aneurysm. Finally, the diagnosis of K. pneumonia-related mycotic aneurysm was confirmed.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [207.0, 'mm hg'], 'Diastolic Blood Pressure': [125.0, 'mm hg']}",152.33333,144.71666,159.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 207.0 mm Hg + 2/3 * 125.0 mm Hg = 152.33333 mm Hg.
Hence, the patient's mean arterial pressure is 152.33333 mm Hg."
1970,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4190867-1,Extracted,"History of present illness: a female patient aged 75 years old, suffering from unstable walking and inaccurate hand holding for 8 months. Eight months before admission, the patient experienced unstable walking without obvious inducement and sometimes fell down, similar to being drunk. During the last 6 months before admission, she exhibited inaccurate hand holding. During the last three months before admission, she experienced limb numbness. During the last half month before admission, she felt dizziness, without nausea, vomiting, head distention, disturbance of consciousness, urinary and fecal incontinence, and tinnitus or deafness. She was diagnosed as having an aging brain using cranial CT in the outpatient clinic of Fengxian Central Hospital. She was hospitalized for further treatment. Since onset, the patient had normal appetite, normal sleep, and normal urine and stool, and did not display signs of influenza or fever.
History of past illness: hypertension, maximum 160/90 mmHg (1 mmHg = 0.133 kPa); taking Zhenjujiangya tablets.
Family history: four sisters; two had similar diseases and died from cardiovascular disease.
On admission observations were as follows: body temperature, 36.7°C; heart rate, 69 beats/minute; blood pressure, 135/85 mmHg; respiration, 20 times/minute; showing normal heart and lung function; normal abdomen examination.
Nervous system examination revealed: clear mind, equivocal language, dialogue relevant to the subject, normal orientation and possessiveness, mask-like face, two pupils of the same size with a diameter of 0.3 cm, light reflex, horizontal nystagmus, normal visual acuity, without hemianopia; symmetrical nasolabial fold, normal lifting of the soft palate, positive pharyngeal reflex; limb muscle force of grade IV, gear wheel-like increase of limb muscle tension, radial periosteal hyperreflexia, patellar tendon hyperreflexia, with physical reflex, bilateral positive Babinski sign; inaccurate nose touch, inaccurate heel-knee-tibia test, sensory disturbance of limb extremities; positive Romberg's sign; tuning fork hypopallesthesia of both limbs.
Auxiliary examination showed normal blood examination, electrolyte, cardiac troponin I, myoglobin and creatine kinase-MB isoenzyme, clotting mechanism, hepatic function, renal function, blood glucose, glycosylated hemoglobin, myocardial enzyme, blood lipid, homocysteine, stool, thyroid function and tumor index. Transcranial Doppler sonography revealed an increased blood flow resistance index. Brainstem auditory evoked potential was normal. Nerve conduction velocity: the motor conduction velocity of the right median nerve was slightly low. The sensory conduction velocities of the median and ulnar nerves were normal. The amplitude of the motor conduction velocity of the right common peroneal nerve was low. The wave form of the sensory conduction velocity of the left superficial peroneal nerve was dispersing. The frequency of the F wave of the median nerve was low. The latency of the F wave of the ulnar nerve was normal. Hoffmann's reflex of the bilateral tibial nerve was within the normal range.
Using 1.5 T permanent magnet magnetic resonance equipment (Phillips, Amsterdam, the Netherlands), the parameters of the spin-echo sequence were as follows: axial, sagittal T1 weighting (repetition time = 500 ms, echo time = 30 ms) and axial T2 weighting (repetition time = 5 000 ms, echo time = 102 ms), 5–8 mm gap, matrix 256 × 256. The plane through the midbrain aqueduct and the fourth ventricle at the cerebellomedullary cistern was designated the measurement plane. On the workstation, the following parameters were measured using computer function keys[]: (A) the distance between the midpoint of the anterior border of the cerebral peduncle and the midpoint of the midbrain aqueduct; (B) shortest distance between the midpoint of the anterior border of the pons and the floor of the fourth ventricle; (C) the distance between the midpoint of the anterior and posterior borders of the medulla oblongata; (D) shortest distance between the floor and top of the fourth ventricle; (E) shortest anteroposterior diameter of the pontine cistern; (F) anteroposterior diameter of the medullar cistern (shortest distance between the midpoint of the anterior border of the medulla oblongata and the clivus). Accuracy of the above-described indices was 0.1 mm. Each parameter was measured twice, and an average value was obtained ().
MRI displayed cerebellar and brainstem atrophy ().
A total of 3 mL of ulnar vein blood was separately obtained from the MJD patient and her son, treated with ethylenediamine tetraacetic acid anticoagulant, and stored at 4°C in the Molecule Room of Huashan Hospital. Total DNA was extracted, and the SCA3/MJD gene was amplified by PCR. Primer sequences were in accordance with reference 11 as follows: upstream: SCA3-F, 5º-CCAgTgACTACTTTg ATTCg-3º; downstream: SCA3-R, 5º-TggCCTTTCACA TggATgTg-3º. Primers were synthesized by Sangon Biotech Co., Ltd. (Shanghai, China). Total reaction volume was 25 μL: DNA extract 2 μL, 20 mM forward and reverse primers each 0.5 μL, 5 U/L TaqDNA polymerase 0.2 μL, 25 mM dNTP 10 μL, 10 × buffer solution (MgCl2 15 mM) 4 μL, R110 and R6G fluorescein-labeled dUTP 0.25 μL. These reagents were purchased from Perkin-Elmer, Fremont, CA, USA. Double distilled water was used as required. Using a PCR thermocycler (9600 DNA thermal cycler, Perkin-Elmer, USA), cycling conditions were 3 minutes at 95°C, 40 seconds at 94°C, 50 seconds at 56°C, 40 seconds at 72°C for 30 cycles, followed by 7 minutes at 72°C. An Abiprism™ 310 genetic analyzer was utilized for capillary electrophoresis and fragment length analysis using the following parameters: electrophoretic medium, POP-4 gel; electrophoresis condition, 15 kV for 24 minutes; capillary, 47 cm (length) × 50 μm (inner diameter). Using the capillary tube method for Stp-PCR, the reaction was run on a low melting point agarose gel, followed by column purification. PCR products were concentrated using a cryogenic vacuum apparatus. Results revealed an abnormal number of CAG repeats and mutation of the SCA3/MJD gene. Agarose gel electrophoresis showed an abnormal amplified band ().
By Stp-PCR sequencing, the CAG repeat number was found to be 77 in the mutated allele, which exceeded the normal range ()",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [135.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",101.66667,96.58334,106.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 85.0 mm Hg = 101.66667 mm Hg.
Hence, the patient's mean arterial pressure is 101.66667 mm Hg."
1971,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-12645,Extracted,"A 50-year-old woman returns from a family trip to the Caribbean with three days of fever, watery diarrhea, and vomiting. She states that she tried to avoid uncooked food and unpeeled fruits on her vacation. Of note, her grandson had caught a cold from daycare prior to the trip, and she had been in close contact with the infant throughout the trip. She denies rhinorrhea or coughing. On exam, her temperature is 99.1°F (37.3°C), blood pressure is 110/68 mmHg, pulse is 113/min, and respirations are 12/min. Her stool culture is negative for bacteria.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [68.0, 'mm hg']}",82,77.9,86.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 68.0 mm Hg = 82.0 mm Hg.
Hence, the patient's mean arterial pressure is 82.0 mm Hg."
1972,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8607664-1,Extracted,"A 53-year-old female patient was admitted to our hospital due to chest pain radiating to the throat. This symptom had developed 1 month previously, and episodes lasted approximately 30 min before temporarily relief was achieved by oral nitroglycerin administration. The patient had been diagnosed with SLE at the age of 33 years and treated with oral corticosteroids (12.5 mg/day prednisone), leflunomide, and hydroxychloroquine thereafter. However, no records of periodic interviews or comprehensive documents were available. She denied a history of smoking or drinking Thirteen years after the diagnosis of SLE, she was diagnosed with hypertension with a blood pressure of 180/90 mmHg and began treatment with oral nitrendipine at a dose of 10 mg/day. Physical examination on the current admission revealed a heart rate of 88 beats per minute, a respiration rate of 18 breaths per minute, and a blood pressure of 118/62 mmHg with regular heart rhythm and no positive signs, suggesting the hypertension was well controlled by the medication. An electrocardiogram showed normal sinus rhythm, right axis deviation, and no ST-T abnormality, but did reveal fractional shortening by 29%, an ejection fraction of 56%, a small amount of pericardial effusion, and a decreased amplitude of the ventricular septum and left ventricular inferior wall, indicating heart dysfunction. Coronary angiography then revealed a giant aneurysm in the middle segment of the left anterior descending artery (LAD; Fig. a and b). In the left circumflex artery (LCX), proximal cystic-like dilatation and distal subtotal occlusion with TIMI grade I flow were observed (Fig. b). In addition, varying degrees of dilatation were detected in the middle segment of the right coronary artery (RCA; Fig. c).
Laboratory examination results for creatine kinase-muscle/brain (2.00 ng/ml, normal range 0–4.3 ng/ml) showed that oral nitroglycerin was effective in the early stage. However, elevated serum levels of myoglobin (155.00 ng/ml, normal range 0–107 ng/ml), cardiac troponin I (0.62 ng/ml, normal range 0–0.05 ng/ml), and aspartate aminotransferase (75.4 U/L, normal range 13–35 U/L) indicated irreversible myocardial infraction. In the meantime, the presence of active SLE was verified by the autoimmune profile results, including normal complement C3 (0.82 g/L, normal range 0.7–1.4 g/L) and complement C4 (0.27 g/L, normal range 0.1–0.4 g/L) levels as well as positive detection of anti-dsDNA (IIF) at 1:10, homozygous antinuclear antibodies (ANA) at 1:100, and nuclear membrane type ANA at 1:320 along with a high C-reactive protein concentration (16.20 mg/L, normal range 0–3.5 mg/L) and high erythrocyte sedimentation rate (44 mm/1 h, normal range 0–20 mm/1 h). Two risk factors for both SLE and cardiovascular disease also were identified in this case. First, renal parameters were abnormal with a 1 + positive urine protein, positive urinary nitrite, and elevated levels of urea nitrogen (20.59 mmol/L, normal range 2.6–7.5 mmol/L) and creatinine (167.8 µmol/L, normal range 41–73 µmol/L). Additionally, elevated lipid levels including a cholesterol level of 7.17 mmol/L (normal range 2.6–6.0 mmol/L) and triglyceride level of 2.86 mmol/L (normal range 0.28–1.8 mmol/L) implied dyslipidemia. Finally, The patient had been diagnosed with SLE, CAA,hypertension and acute coronary syndrome.
Surgical treatment of giant aneurysms is considered to be a major trauma, so patients choose interventional therapy.At the same time, surgical treatment is our second option. To prevent thromboembolic complications and further myocardial infarction, anticoagulation (low-molecular-weight calcium heparins, 5,000 U subcutaneously every 12 h) and antiplatelet therapy (oral aspirin 100 mg/day and oral clopidogrel hydrogen sulfate 75 mg/day) were administered. At the same time, one stent was implanted at the distal end of the LCX to effectively limit further expansion of the affected coronary segments (Fig. a). Repeated coronary angiography revealed that the occlusion was recanalized and TIMI grade III flow was restored (Fig. b). Finally, the patient was discharged with resolved chest pain. New oral anticoagulant (rivaroxaban) and dual antiplatelet therapy recommended at discharge. Furthermore patient has ectasia and a significant stenosis in proximal RCA.Coronary angiography was recommended after 1 month, but the patient refused..After 1 month, they were treated with rivaroxaban and aspirin. During 6 months of follow-up, the patient is in good health.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [118.0, 'mm hg'], 'Diastolic Blood Pressure': [62.0, 'mm hg']}",80.66667,76.63334,84.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 118.0 mm Hg + 2/3 * 62.0 mm Hg = 80.66667 mm Hg.
Hence, the patient's mean arterial pressure is 80.66667 mm Hg."
1973,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6298258-1,Extracted,"A 38-year-old, elderly Indian primigravida was referred and underwent ultrasonography (USG) where she was found to have a severe oligohydramnios. The patient had a history of amenorrhea of 6 months and married life of 5 years. Her menstrual history was irregular, and her last menstrual period was not known. Her history indicated dyspnea on moderate exertion and chest pain off and on. There was no significant medical history otherwise. The patient had undergone laparoscopic ovarian cystectomy and infertility treatment about 1-year previously, but detail records were not available. There was no family history of diabetes mellitus, hypertension, and any genetic illness. The patient did not have any side effect with any drug.
There were no symptoms of Marfan-like syndrome or any other dysmorphology. Her gait was normal; pallor was present; clubbing, icterus and cyanosis were absent. Oral hygiene was well-maintained. Neck glands were not palpable, and jugular venous pressure was normal. Pulse rate was 82/minute, irregular, with no radio-femoral delay. Blood pressure (BP) was 150/100 mmHg in right arm supine position. Respiratory rate was 16/min. On cardiovascular examination, we observed apex beat in 4th intercostal space, grade 3 pansystolic murmur over mitral area radiating to aortic area. Chest examination was clear, and no added sounds were observed. No organomegaly except gravid uterus was present during abdominal examination. The size of uterus was 20-22 weeks and fetal heart sounds were present.
The patient was Rhesus negative and Hb was 12 gm%. Complete blood count, thyroid, and coagulation profile were within normal limits. Electrocardiogram (ECG) showed multiple ectopic beats pre-mature ventricular contractions. On two-dimensional echocardiography, dilated cardiomyopathy with concentric left ventricular hypertrophy, mitral regurgitation, tricuspid regurgitation, and aortic regurgitation were observed. Aortic root diameter was 4 cm and left ventricular ejection fraction was 40-45%. The repeat USG showed 25 weeks 4 days fetus with severe oligohydramnios and intrauterine growth restriction with amniotic fluid index 1-2 cm. Fetal targeted scan found no anomaly.
Cardiologist opinion was taken and the patient was put on antihypertensive therapy. Two days later, the patient had a sudden onset of inter-scapular back pain and chest pain. Vitals were stable and ECG was done immediately and was same. The patient was kept under close observation. On the same day evening, patient suddenly had dyspnoea with chest discomfort. On examination, there was pallor +++, no cyanosis, SpO2- was 70%, BP - 90/60 mm Hg, Pulse - 104/m irregular. Respiratory Rate (RR) - 22/m, decreased B/L lung air entry, cardiovascular system-pansystolic murmur was present. Hemoglobin level had fallen to 6 gm%. ECG showed ST depression and sinus tachycardia. Chest X-ray showed a huge collection of fluid in the pleural cavity. USG of chest showed B/L moderate pleural effusion.
X-ray of the chest showed an obliteration of costophrenic angle with a moderate bilateral collection of fluid in pleural cavity, with tracheal shift to right. Repeat obstetric USG showed 26-week single intrauterine fetus in the transverse lie with no cardiac activity. Immediately USG-guided intercostal drain was inserted on the left side of the chest and around 2 liters of frank hemorrhagic fluid were drained from thorax. Cytology of the pleural fluid was found to be exudative.
The chest computed tomography showed a large amount of left hemothorax and mediastinal hematoma with aortic dissection involving the descending thoracic and abdominal aorta (Stanford Type B) with focal tubular outpouching of contrast in mediastinum at the origin of aortic dissection. This was suggestive of aortic contrast extravasation that is Ruptured Aortic Dissection []. An underlying collapsed consolidation of the entire left lung was seen. There were cardiomegaly and a small fusiform aneurysm, 2.5 cm long segment with a diameter of 1.6 cm of the left subclavian artery was present. In the Intensive Care Unit, the patient received 4 units of blood transfusion. On stabilization of vitals, obstetric hysterotomy was done under epidural and local anesthesia. A dead fetus of around 800 g was delivered. Placental weight was 150 g. Intraoperative and postoperative period was uneventful except for fever. On the 8th postoperative day, there was complete stitch removal. The patient was followed up 15 days later and was found to be normal.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg']}",116.66667,110.83334,122.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 150.0 mm Hg + 2/3 * 100.0 mm Hg = 116.66667 mm Hg.
Hence, the patient's mean arterial pressure is 116.66667 mm Hg."
1974,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7402743-1,Extracted,"A 11-year-old boy was admitted to our outpatient department on October 15, 2018, with chest tightness after exercise for 5 years, aggravated in half a month, and repeated hemorrhinia for 2 years. The patient had a history of syncope 1 year ago. His grandmother had a history of pulmonary hypertension. On admission examination, his heart rate was 78 beats/min, his blood pressure was 102/65 mm Hg, and his SpO2 was 96%. The heart sounds were regular, and no murmur was detected. No obvious abnormalities were observed in the rest of the physical examinations. Blood tests noted normal hemoglobin (146 g/L, normal 130–175), increased N-terminal pro-brain natriuretic peptide (NT-ProBNP, 643pg/ml, normal <125), increased total bilirubin (30 μmol/L, normal 3.4–21.1), increased direct bilirubin (10.1 μmol/L, normal < 6.8), increased indirect bilirubin (20.6 μmol/L, normal < 3.1–17.0), and increased alkaline phosphatase (324U/L, normal 45–125). Electrocardiograph (ECG) revealed a sinus rhythm, and right axis deviation reached + 132° (Fig. ). Transthoracic echocardiography revealed a right atrial dimension of 40 mm, a right ventricular dimension of 30 mm, a left atrial dimension of 28 mm, a left ventricular end-diastolic dimension of 43 mm, a left ventricular end-systolic dimension of 30 mm, a left ventricular ejection fraction of 73%, a tricuspid annular plane systolic excursion of 15 mm, a maximum tricuspid regurgitation velocity, and a pulmonary artery systolic pressure of 91 mm. Cardiac magnetic resonance revealed a enlargement of right atrium and right ventricle (Fig. ). Cardiopulmonary exercise test showed that the overall functional status of cardiopulmonary motor function, the effectiveness of oxygen uptake ventilation and nitrogen dioxide ventilation were significantly limited. Computed tomographic pulmonary angiography (CTPA) showed enlargement of right ventricle, dilatation of main pulmonary artery, changes of pulmonary hypertension, and diffuse small patches of light ground glass opacity in both lungs.
The patient underwent right cardiac catheterization, acute pulmonary vasodilator testing (AVT) and pulmonary angiography on October 29, 2018. Details are as follows: (1) Baseline blood pressure was 115/54/74 mm Hg, pulmonary arterial pressure (PAP) was 95/40/59 mm Hg, pulmonary artery wedge pressure was 8/7/6 mm Hg, cardiac output was 4.23L/min, cardiac index was 2.9L/min/m2, and pulmonary vascular resistance was 12.53 Wood U, (2) PAP was 109/32/60 mm Hg after inhalation of vantamivir (AVT negative), (3) Pulmonary angiography showed dilatation of left and right pulmonary arteries, no obvious stenosis, filling defect or occlusive lesions, no decrease or absence of distal segmental perfusion, and the perfusion velocity was acceptable.
Later, we used high-throughput gene sequencing technology to detect all exon genes for the patient. Genetic tests revealed that the patient carried a non-sense mutation of BMPR2, c. 1452G > A, which resulted in the termination of BMPR2 protein at 484 position and significantly affected the function of the protein (Table ). Mutation analysis of ACVRL1, ENG, and SMAD4 was normal.
According to the symptoms, signs and examination results, we diagnosed familial pulmonary arterial hypertension and suspected hereditary hemorrhagic telangiectasia. The patient was discharged from hospital on October 28, 2018, and was treated with ambrisentan 2.5 mg qd.
On November 26, 2018, the patient had a large amount of black stool. The stool was hard and normal in shape, and there was little blood on the surface. The patient had abdominal discomfort and no bleeding and ecchymosis on the skin. At 4 am on November 28, 2018, the patient woke up in sleep, followed by convulsion, characterized by sudden loss of consciousness, eyeball upturn, sudden generalized and ankylosing facial and extremity muscle convulsions, cyanosis of lips, incontinence of urine and feces, and self-remission after 30 seconds. The patient was immediately admitted to the emergency department. Blood tests noted decreased hemoglobin (62 g/L, normal 130–175), increased NT-ProBNP (1010pg/ml, normal < 125), increased creatine kinase (721U/L, normal 55–170), increased lactate dehydrogenase (247U/L, normal 135–225). Faecal occult blood test was positive. There were no significant changes in echocardiographic data. Short-range video electroencephalogram was normal. No obvious abnormalities were found in cranial magnetic resonance imaging and magnetic resonance angiography. We planned to have further gastrointestinal endoscopy, but the patient's family refused. Acute gastrointestinal bleeding and convulsions caused by acute ischemic-hypoxic encephalopathy were considered in the diagnosis. Therapeutically, omeprazole was given to inhibit gastric acid secretion, tranexamic acid and etamsylate were used to stop bleeding, and suspended red blood cells were infused. On December 2, 2018, hemoglobin was 104 g/L, and fecal occult blood test was negative. During the follow-up for the next month, the patient had no black stool, no hemorrhinia, and no significant changes in chest tightness.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [102.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg']}",77.33333,73.46666,81.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 102.0 mm Hg + 2/3 * 65.0 mm Hg = 77.33333 mm Hg.
Hence, the patient's mean arterial pressure is 77.33333 mm Hg."
1975,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-710,Extracted,"A 33-year-old woman comes to the emergency department because of a 3-day history of lower abdominal pain and severe burning with urination. Two years ago, she was diagnosed with cervical cancer and was successfully treated with a combination of radiation and chemotherapy. She has systemic lupus erythematosus and finished a course of cyclophosphamide 3 weeks ago. She is sexually active with multiple male and female partners and uses a diaphragm for contraception. She has smoked two packs of cigarettes daily for 12 years. Current medication includes hydroxychloroquine. Her temperature is 36.6°C (97.9°F), pulse is 84/min, and blood pressure is 136/84 mm Hg. The abdomen is soft and there is tenderness to palpation over the pelvic region.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [136.0, 'mm hg'], 'Diastolic Blood Pressure': [84.0, 'mm hg']}",101.33333,96.26666,106.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 136.0 mm Hg + 2/3 * 84.0 mm Hg = 101.33333 mm Hg.
Hence, the patient's mean arterial pressure is 101.33333 mm Hg."
1976,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3464728-1,Extracted,"A 40-year-old Asian male patient presented with fever and more aggravated generalized weakness for 1 week. A month ago, he complained of hematuria, fever and generalized weakness. He was diagnosed with PNH associated with another bone marrow disorder (aplastic anemia). For control of acute hemolysis, red cells transfusion and immunosuppressive drugs (corticosteroid and danazol) were prescribed and he was discharged after stabilized. At that time, his chest X-ray showed old pulmonary calcified nodules in both lung field (Figure ). He was diagnosed with pulmonary TB about 21 years ago and he was completely cured after anti-TB medication (Isoniazid, Ethambutol, Rifampicin, Pyrazinamide) for 6 months. On readmission, vital signs were followed; BP 140/80 mmHg, pulse rate 76 beats/min, respiration rate 20 times/min, and body temperature 39.1°C. Jaundice was observed in both sclera, and breath sounds were decreased in both lung field. The laboratory findings revealed white blood cells, 720/uL (segment neutrophil 75.6%; lymphocytes 15.7%); hemoglobin, 9.6 g/dL; and platelets, 55,000/uL. AST/ALT, total bilirubin and LDH were 167/312 IU/L, 3.9 mg/dL and 2,543 IU/L respectively. Blood urea nitrogen and serum creatinine were 20.3 mg/dL and 1.4 mg/dL. In chest radiographs, the miliary nodules were observed in both lung field (Figure A). Chest CT scan showed miliary nodulation and patch underlying perinodular ground glass appearance in both lung field, suggestive of miliary TB (Figure B). TB PCR was positive. After 3 weeks of immunosuppressive drugs, he was diagnosed to miliary TB. Due to elevated liver enzyme, Ethambutol/Moxifloxacin/Cycloserine were selected. To expect the rise of drug effects, supportive care such as G-CSF administration, blood transfusion and nutritional support were done. After 5 days of the anti-TB medications, patch density in chest X-ray was progressed and he complained of severe dyspnea, nausea, vomiting and aggravated weakness (Figure ). We considered ventilator care, but the patient was tolerable at the 10L of oxygen mask apply. We added 1st line anti-TB drugs (Isoniazid, Rifampicin) stage by stage. After continuous intensive care for 3 weeks, dyspnea was getting better and he needed only 2L of oxygen apply. The chest X-ray has got better. He was improved and the resistance strain was not seen in 8 weeks after culture. He had taken 1st line anti-TB drugs (Isoniazid, Ethambutol, Rifampicin) and warfarin in outpatient of hospital, and nowadays he finished anti-TB drugs except warfarin (Figure ).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 80.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
1977,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-481,Extracted,"Five days after undergoing an emergency appendectomy under general inhalational anesthesia while on a trip to Haiti, a 43-year-old woman develops low-grade fever, vomiting, and abdominal pain. During the surgery, she received a transfusion of 1 unit of packed red blood cells. Three days after the surgery, she was stable enough to be transported back to the United States. She has no history of serious illness and takes no medications. Her temperature is 38.3°C (100.9°F), pulse is 80/min, and blood pressure is 138/76 mm Hg. Examination shows jaundice of the skin and conjunctivae. Abdominal examination shows moderate tenderness over the liver. The liver is palpated 2 to 3 cm below the right costal margin. Laboratory studies show:
Hemoglobin count 12.0 g/dL
Leukocyte count 10,400 mm3
Segmented neutrophils 55%
Bands 1%
Eosinophils 13%
Lymphocytes 28%
Monocytes 3%
Platelet count 160,000 mm3
Serum
Alkaline phosphatase 102 U/L
Aspartate aminotransferase 760 U/L
Bilirubin
Total 3.8 mg/dL
Direct 3.1 mg/dL
Anti-HAV IgG positive
Anti-HAV IgM negative
Anti-HBs positive
HBsAg negative
Anti-HCV antibodies negative
Abdominal ultrasonography shows an enlarged liver. A biopsy of the liver shows massive centrilobular necrosis.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [138.0, 'mm hg'], 'Diastolic Blood Pressure': [76.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 138.0 mm Hg + 2/3 * 76.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
1978,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5620389-1,Extracted,"A 40-year-old woman was admitted to the orthopedic surgery department of a tertiary-care hospital in Seoul, Korea. This patient had injured her left thumb with a kitchen knife right before visiting the hospital. She had a history of hypertension, but did not have any other diseases. There was no redness, swelling, pus or serous discharge from her wound upon physical examination. Radiological evaluation showed no evidence of left thumb fracture. The size of the wound was 1 cm in width and 1 cm in depth. Her vital signs were as follows: body temperature, 36.5°C; blood pressure, 120/82 mmHg; pulse, 96/min; and respiratory rate, 20/min. The laboratory results were as follows: white blood cell count, 9.69 ⨯ 103/mm3 (reference value, 4.0 ⨯ 103 to 10.8 ⨯ 103/mm3) with 74.4% neutrophils (reference value, 40 to 73% of total leukocytes); and erythrocyte sedimentation rate, 16 mm/h (reference value, 0 to 20 mm/h). Routine blood chemistry and electrolytes showed values within reference ranges. She was diagnosed with a rupture of the extensor pollicis longus tendon of the left thumb, and she underwent tenorrhaphy on the second hospital day. A deep wound culture was taken before the operation. She was discharged home the day after surgery without any complications.
The deep wound sample was inoculated onto 5% sheep blood agar (Asan Pharmaceutical, Seoul, Korea) and MacConkey agar (Asan Pharmaceutical) plates. The cultures were incubated in 6% CO2 at 35°C for 2 days. Grayish mucoid colonies were grown on the 5% sheep blood agar, and colorless colonies were grown on the MacConkey agar after 48 h incubation. Both cultures were positive for oxidase and catalase reactions. Gram-negative short rods were seen in stained preparations, which were confirmed using Scanning Electron Microscopy (SEM) (FE SEM S-800, Hitachi, Tokyo, Japan) at the acceleration voltage of 20 Kv. The organism was 1.5-2.0 μm in length and 0.5-1.0 μm in width with a single flagella (). Motility was confirmed using motility-indole-ornithine (MIO) semi-solid agar (Asan Pharmaceutical).
Biochemical features were investigated using VITEK® 2 Gram-negative (GN) Identification cards with the Vitek 2 system (bioMérieux, Marcy l'Etoile, France) and API 20NE cards (bioMérieux). The GN card identified the isolate as Sphingomonas paucimobilis, but with low probability (91%). The API 20NE card identified the isolate as within the Shewanella putrefaciens group, with low probability (90%). Data on the assimilation of carbon-sources, hydrolysis of chromogenic substrates, and enzyme activities of the isolate are described in . Matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF MS) (MicroflexTM MALDI Biotyper, Version 3.1, Bruker Daltonics, Bremen, Germany) identified the organism as Massilia sp. with a score of 1.621. The analysis of 16S rDNA sequence was also performed with the universal bacterial primers 27F (5’-AGA GTT TGA TCC TGG CTC AG -3’) and 1541R (5’-AAG GAG GTG ATC CAG CCG CA-3’), amplifying a 1,362-bp segment. Sequences of the partial 16S rDNA fragment were 100% identical to those of strain CCUG 35299T (GenBank accession number NR_042652.1), the type strain of M. varians, when compared using BLAST ().
Antimicrobial susceptibility tests were performed by disk diffusion method, according to Clinical and Laboratory Standards Institute (CLSI) guideline []. And minimal inhibitory concentrations (MICs) were determined by Etest® (bioMérieux) (). The antimicrobial susceptibility patterns of the isolate were similar with those of the CCUG 35299T type strain.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [82.0, 'mm hg']}",94.66667,89.93334,99.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 82.0 mm Hg = 94.66667 mm Hg.
Hence, the patient's mean arterial pressure is 94.66667 mm Hg."
1979,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-4974,Extracted,"A 25-year-old man is brought to the emergency department by police. He was found at a local celebration acting very strangely and was reported by other patrons of the event. The patient is very anxious and initially is hesitant to answer questions. He denies any substance use and states that he was just trying to have a good time. The patient's responses are slightly delayed and he seems to have difficulty processing his thoughts. The patient tells you he feels very anxious and asks for some medication to calm him down. The patient has a past medical history of psoriasis which is treated with topical steroids. His temperature is 99.5°F (37.5°C), blood pressure is 120/75 mmHg, pulse is 110/min, respirations are 15/min, and oxygen saturation is 99% on room air. On physical exam, you note an anxious young man. HEENT exam reveals a dry mouth and conjunctival injection. Neurological exam reveals cranial nerves II-XII as grossly intact with normal strength and sensation in his upper and lower extremities. Cardiac exam reveals tachycardia, and pulmonary exam is within normal limits.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg']}",90,85.5,94.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 75.0 mm Hg = 90.0 mm Hg.
Hence, the patient's mean arterial pressure is 90.0 mm Hg."
1980,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-10931,Extracted,"An 84-year-old female presents to the emergency department from her nursing home with complaints of fever and a productive cough with rust-colored sputum that has developed over the last 2 days. She also endorses shortness of breath and severe fatigue. Her vital signs are as follows: T 38.5 C, HR 98, BP 110/66, RR 18, SpO2 94% on room air. Physical examination is significant for decreased breath sounds and crackles over the the right middle and lower lobes on auscultation. A chest radiograph is obtained and is shown in Figure A. A sputum sample is also collected for gram stain and culture, with the results of the gram stain shown in Figure B.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [66.0, 'mm hg']}",80.66667,76.63334,84.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 66.0 mm Hg = 80.66667 mm Hg.
Hence, the patient's mean arterial pressure is 80.66667 mm Hg."
1981,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-6029,Extracted,"A 27-year-old woman presents to the emergency department with pain in her ankle and leg. The patient states the pain has slowly been worsening and is exacerbated by running. The patient is currently training for a marathon, and she has been training more vigorously lately. She is on oral contraceptive pills and does not smoke or drink alcohol. Her temperature is 98°F (36.7°C), blood pressure is 120/64 mmHg, pulse is 70/min, respirations are 12/min, and oxygen saturation is 99% on room air. Physical exam is notable for tenderness in the anterior midline of the tibia just superior to the ankle. A radiograph is performed as seen in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [64.0, 'mm hg'], 'Systolic Blood Pressure': [120.0, 'mm hg']}",82.66667,78.53334,86.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 64.0 mm Hg = 82.66667 mm Hg.
Hence, the patient's mean arterial pressure is 82.66667 mm Hg."
1982,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7580470-1,Extracted,"We report a case of 50 years old female who visited the emergency department with a chief complaint of acute chest pain. She is a known case of hypothyroidism under thyroxine. However, she had no history of diabetes and hypertension. She is a non-smoker and non-alcoholic. On general physical examination, her vitals were stable with pulse rate 82 beats/ minute, blood pressure 100/80mmHg and systemic examination and laboratory investigations were within normal limit. Her ECG finding was normal; echo finding was normal left ventricular systolic and diastolic function with a normal left ventricular ejection fraction of 60%. Then, she was planned for CT coronary angiography in our center. It revealed anomalous coronary anatomy with both right and left coronary artery arising from large common trunk-off the right coronary cusp, left main coronary artery has a trans-septal course, there was no flow-limiting coronary artery disease (, and ).
She was medically managed and discharged with single antiplatelet therapy, beta-blockers, and statin per-oral medications.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 100.0 mm Hg + 2/3 * 80.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1983,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5728071-1,Extracted,"A 64-year-old woman who complained of worsening nocturnal dyspnea was admitted to our hospital. Two and half years previously, the patient had felt exertional chest pain and lower extremity edema and had been admitted to our hospital. She did not have a history of hypertension, diabetes, or smoking. On her previous admission, chest X-ray showed an enlarged cardiac silhouette with a cardiothoracic ratio of 68.7% and right side pleural effusion. Electrocardiogram showed T-wave inversion in leads II, III, aVF, and precordial leads (Fig. ). Echocardiography showed that left ventricular wall motion was diffusely reduced with the left ventricular ejection fraction of 24% (Fig. ). The end-diastolic left ventricular dimension was 53 mm. Coronary artery angiography showed no physiologically significant stenosis and left ventriculography showed diffuse hypokinesis of the left ventricle (Fig. ). Histological examination of endomyocardial biopsy samples showed interstitial fibrosis, but neither amyloid deposition nor granulomatous degeneration was observed. Echocardiography 1.5 years later also showed the reduced global left ventricular contractility (Fig. ).
The chief complaint of the patient on the current admission was exertional dyspnea and edema of lower extremities. On admission, her body temperature was 35.8°C, blood pressure was 104/79 mmHg, and pulse rate was 100 bpm. Electrocardiography showed T wave inversion on leads I, II, aVF, and precordial leads, which was more prominent than that observed previously (Fig. ). Echocardiography showed dyskinesis of the apical (Fig. , arrows) and hypercontraction of the basal walls (Fig. ). Emergency coronary angiography showed, again, no significant stenosis in the coronary arteries (Fig. ) and apical ballooning and basal hypercontraction were demonstrated by left ventriculography (Fig. ). Laboratory examinations showed elevated levels of serum creatine kinase, its MB fraction, and plasma B-type natriuretic peptide (Table ). In addition to the treatment with diuretic drugs, the patient was treated with anticoagulant drugs because of the thrombus formation in the left ventricular apex – intravenous administration of heparin for 12 days followed by the oral administration of warfarin. Administration of beta blocker, bisoprolol, was also started. On day 15, follow-up electrocardiogram showed no apparent changes in the giant T-wave inversion (Fig. ); however, echocardiography showed the disappearance of hypercontraction of the left ventricular basal wall (Fig. , arrowheads) in addition to recovery of the contraction of the thickened apical wall (arrows). The patient was diagnosed with Takotsubo cardiomyopathy []. Finding of electrocardiogram, T-wave inversion, normalized at 3 months after the discharge and it remained normal at 8 months after the discharge.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [104.0, 'mm hg'], 'Diastolic Blood Pressure': [79.0, 'mm hg']}",87.33333,82.96666,91.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 104.0 mm Hg + 2/3 * 79.0 mm Hg = 87.33333 mm Hg.
Hence, the patient's mean arterial pressure is 87.33333 mm Hg."
1984,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5314264-1,Extracted,"A 43-year-old male with a 3-mo history of asthma was admitted to the Rheumatoid Immune Department of Shengjing Hospital in July 2013. The patient complained of a cough of one-month duration, blood-stained sputum, 14-d peripheral purpura, 3-d diarrhea, and an oral ulcer. His height was 176 cm and weight was 72 kg when admission. His temperature was 37.2 °C, his pulse was 78 per minute, and his blood pressure was 128/78 mmHg. Multiple skin purpura was found in the physical examination. Heart sounds were clear and regular with no murmur. A few moist rales were heard with lung auscultation. Abdominal examination was unremarkable. Laboratory studies revealed leukocytosis (15600/mm3) with eosinophilia (20.3%), a marked increase in inflammatory indices (ESR: 69 mm at the first hour; CRP: 176 mg/L), rheumatoid factor (656 UI/mL), and positive pANCA antibody. A pulmonary computed tomography (CT) scan revealed multiple low-density oval shadows, with the largest one measuring about 3.2 cm × 2.6 cm (Figure ). A diagnosis of vasculitis was made. A biopsy of the nasal mucosa revealed an eosinophilic infiltration. We diagnosed EGPA according to the revised international Chapel Hill nomenclature. The patient received methylprednisolone (120 mg intravenously daily) and ifosfamide for the treatment of the pulmonary lesions. The patient’s condition exacerbated during the first three days following admission; the methylprednisolone dose was increased to 500 mg (intravenously daily × 2) and then was gradually tapered. On the 13th day after admission (160 mg methylprednisolone intravenously daily), he experienced a sudden onset of fever and abdominal pain. The physical examination revealed generalized abdominal tenderness without apparent rebound tenderness, and muscle tension. No specific treatment was given. After 11 h, the abdominal pain exacerbated and peritonitis developed. An abdominal CT scan showed an amount of free gas in the abdominal cavity (Figure ). A laparotomy was performed immediately, which revealed scattered eleven perforations in the intestine. The proximal one was located approximately 150 cm distal from the ligament of Treitz ligament, and the distal one located approximately 50 cm from the ileocecal valve, with the largest measuring about 3 cm × 3 cm (Figure ). Considering the high risk of short bowel syndrome, we made a simple repair of the intestinal perforations. Histopathological examination did not reveal either eosinophilic infiltration or granuloma formation of the vessels (Figure ).
Continued intravenous therapy with intermittent ifosfamide as well as somatostatin and esomeprazole was administered postoperatively. The hormone dosage was tapered from 160 mg downward. On postoperative day 6, when the steroid was reduced to 80 mg, the patient’s vasculitis exacerbated and he developed fever and new purpura on the entire body. Eight days postoperatively, an intestinal fistula developed, which was confirmed by fistulography (Figure ). With continuous saline washing through a double-lumen cannula connected to a negative pressure suction apparatus, the drainage was about 300 mL intestinal fluid daily; the fistula slowly healed. The patient began eating on postoperative day 45. Gastric retention occurred after eating; it was treated with decompression via a nasogastric tube, total parenteral nutrition, and a gastric motility stimulating agent. The patient resumed eating about two months postoperatively, and the drainage was minimal. When the steroid dosage was reduced to 60 mg intravenously, the fistula healed and the patient was discharged.
Unfortunately, four months later, an intestinal fistula and vasculitis recurred. Although the amount was 5 mL daily, he was readmitted and underwent continuous washing and negative pressure suction. The fistula healed slowly during one month. When last seen in the outpatient clinic in March 2014, he was in good health without any symptoms or eosinophilia. Laboratory analysis revealed 0.1% eosinophils and negative pANCA antibodies.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [128.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",94.66667,89.93334,99.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 128.0 mm Hg + 2/3 * 78.0 mm Hg = 94.66667 mm Hg.
Hence, the patient's mean arterial pressure is 94.66667 mm Hg."
1985,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-843,Extracted,"A 22-year-old man comes to the emergency department because of sudden onset of facial swelling, abdominal pain, and nausea 1 hour after eating some trail mix. He does not have shortness of breath or hoarseness. He has never had a similar episode before. He has asthma treated with an albuterol inhaler, which he uses less than once a month. His pulse is 90/min, respirations are 25/min, and blood pressure is 125/80 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 99%. Physical examination shows perioral swelling and scattered urticaria over the face and the fingers of his right hand. There is no swelling of the oropharynx and no audible stridor. The lungs are clear to auscultation bilaterally. Treatment with intravenous diphenhydramine is begun. Shortly after, the abdominal pain and nausea have resolved, the swelling has improved, and the rash has started to fade.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",95,90.25,99.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 80.0 mm Hg = 95.0 mm Hg.
Hence, the patient's mean arterial pressure is 95.0 mm Hg."
1986,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7916987-2,Extracted,"A seven-year-old boy arrived in our emergency department with a five-day history of fever, complicated the day of his admission by acute abdominal pain, tenderness, nausea, vomiting, and low urine output. His previous medical history was unremarkable. On admission, a physical examination revealed fever of 38,5°C, irritability, disorientation, bilateral conjunctivitis, cheilitis, edema of the hands, and feet, tachycardia, heart rate was 140 beats/min, low blood pressure at 72/38 mmHg, while the respiratory rate was normal. Besides, an increased abdominal wall rigidity, distension, and generalized ileus were noted.
Blood tests revealed anemia, lymphocytopenia, deep thrombocytopenia, hypertriglyceridemia, significantly increased ferritinemia levels and other inflammatory markers, and increased serum creatinine levels (Table ). A chest CT scan revealed a double focus of bilateral pneumonia. An abdominal CT scan revealed splenomegaly, ileitis, and multiple deep abdominal adenopathies but without peritoneal fluid (Figure ). The blood cultures and the urinalysis were steril. A nasopharyngeal swab specimen was negative, while serology was positive for SARS-CoV-2. The echocardiography found dilation of a left coronary artery at 5 mm and dilation of the right coronary artery at 4 mm with minor aortic valvular regurgitation and minimal pericardial effusion. The patient was diagnosed with multisystem inflammatory syndrome associated with SARS-CoV-2 infection. Intravenous immunoglobulin (IVIG), a high dose of aspirin, and methylprednisolone at 2 mg/kg/day were applied besides a supportive treatment. The outcome was favorable with defervescence as the third day, prompt general improvement, and normalization of blood tests as the fourth day. A follow-up echocardiogram performed 15 days later showed the same finding.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [72.0, 'mm hg'], 'Diastolic Blood Pressure': [38.0, 'mm hg']}",49.33333,46.86666,51.8,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 72.0 mm Hg + 2/3 * 38.0 mm Hg = 49.33333 mm Hg.
Hence, the patient's mean arterial pressure is 49.33333 mm Hg."
1987,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-532,Extracted,"A 58-year-old man comes to the emergency department because of increasing shortness of breath and a nonproductive cough for the last week. Three weeks ago, he had a fever and a cough for 6 days after he returned from a trip to Southeast Asia. He has had a 4-kg (9-lb) weight loss over the past 3 months. He has bronchial asthma and hypertension. He has smoked one pack of cigarettes daily for 41 years. Current medications include an albuterol inhaler and enalapril. His temperature is 37.6°C (99.7°F), pulse is 88/min, respirations are 20/min, and blood pressure is 136/89 mm Hg. There is dullness to percussion, decreased breath sounds, and decreased tactile fremitus over the left lung base. Cardiac examination shows no abnormalities.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [89.0, 'mm hg'], 'Systolic Blood Pressure': [136.0, 'mm hg']}",104.66667,99.43334,109.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 136.0 mm Hg + 2/3 * 89.0 mm Hg = 104.66667 mm Hg.
Hence, the patient's mean arterial pressure is 104.66667 mm Hg."
1988,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3926295-1,Extracted,"A 33-year-old multigravida at the 38th week of gestation was admitted to our clinic with complaints of headache. She had no visual abnormalities and her blood pressure was 210/120 mmHg with pulse rate of 108/minute. Urinalysis revealed 2+ proteinuria and she had bilateral pedal oedema. There was no past history of hypertension, vision abnormalities, seizures, or any other pathologies. Complete blood count revealed a hemoglobin level of 9.1 g/dL and a platelet count of 162.000/mm3. Renal and hepatic function tests as well as electrocardiogram were within normal limits. Magnesium sulphate 4 g loading dose was administered intravenously, followed by continuous intravenous infusion at 2 g per hour. After labour induction, a 3100 g baby was born with normal vaginal delivery. She complained of blindness 13 hours after delivery. MRI brain images obtained after neurology consultation revealed hyperintense and FLAIR signal lesions extending beyond the occipital lobes and involved both cerebellar hemispheres (Figures , , and ). Clinical and radiological findings were assumed to be consistent with PRES. Three days after delivery, her blood pressure was controlled and her visual symptoms nearly disappeared. Meanwhile, the patient had no episodes of seizures and on the 6th postpartum day, there was a complete recovery from blindness and she was discharged without any recurrent symptoms afterwards.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [120.0, 'mm hg'], 'Systolic Blood Pressure': [210.0, 'mm hg']}",150,142.5,157.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 210.0 mm Hg + 2/3 * 120.0 mm Hg = 150.0 mm Hg.
Hence, the patient's mean arterial pressure is 150.0 mm Hg."
1989,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3370328-1,Extracted,"A 9-year-old, 96-cm-tall, and 18-kg female patient whose sister died at the age of 14 years due to MPS type VI was also diagnosed as having Maroteaux-Lamy syndrome at the age of 2.5 years. She had undergone an inguinal hernia operation in the same year that she was diagnosed, and there were no complications in airway control or the anesthetic course. Follow-up echocardiography when she was three years old revealed mitral valve prolapse, moderate mitral valve insufficiency, and a bicuspid aorta. Although she had no limitation in exercise capacity at earlier ages, she developed exercise dyspnea at age 7. The patient had been treated with recombinant N-acetylgalactosamine-4-sulfatase enzyme (Naglazyme®, Biomarin, USA) 15 mg/kg–1/week–1 and digoxin drops 2.5 mg/d–1 for the last three years. Her preoperative echocardiography showed an ejection fraction of 83%, along with mitral valve prolapse, severe mitral insufficiency, mild aortic valve stenosis, and mild aortic incompetence. Based on these findings, mitral valve replacement surgery was scheduled.
The pre-anesthetic examination showed failure to thrive, microcephaly, macroglossia, coarse face, corneal opacity, gum hypertrophy, short neck, and kyphoscoliosis (Figures 1 and 2). The patient's ASA score was class III, and her Mallampati score was class II. The physical examination revealed no hepatosplenomegaly. Findings in other systems and biochemical analyses were within the normal limits, except for exercise dyspnea. The platelet count and coagulation tests were also in the normal ranges (platelets: 312×109/L; prothrombin time: 12.4 seconds; international normalized ratio: 1.06; activated partial thromboplastin time: 39.7 seconds).
The patient was premedicated with midazolam 1 mg i.v. in the operating room, and five-derivation ECG, SpO2, non-invasive arterial pressure and invasive arterial pressure were monitored. Her heart rate was 112 bpm, her arterial blood pressure (ABP) was 105/66 mm Hg, her SpO2 was 95%, and her ECG showed a sinus rhythm. During the induction of anesthesia, the necessary devices and materials for adequate airway control were available, and the surgical team was prepared to perform a tracheostomy.
Following pre-oxygenation, induction of anesthesia was achieved with sevoflurane and midazolam 3 mg i.v. Once ventilation was determined to be non-problematic, the patient received propofol 50 mg i.v., fentanyl 25 µg, and vecuronium 2 mg i.v. During direct laryngoscopy, the Cormack-Lehane classification was determined to be class IV. Intubation via direct laryngoscopy was unsuccessfully attempted four times. Patient ventilation using a mask was satisfactory between intubation attempts. The patient was successfully intubated with a TrueView laryngoscope (Truphatek, USA) and a No. 5 tube on the fifth attempt.
A 5-F internal jugular vein catheter with three lumens was inserted. Following intubation, the patient's heart rate was 140 bpm, her ABP was 92/40 mm Hg, her central venous pressure (CVP) was 26 mm Hg, and her SpO2 was 99%. The arterial blood gas parameters were as follows: pH: 7.39, PaCO2: 41.1 mm Hg, PaO2: 200 mm Hg, SpO2: 99.1%, Hb: 12 g/dL–1, Hct: 36.8%, glucose: 164 mg/dL–1, lactate: 0.6 mmol/L–1, Na: 139 mmol/L–1, K: 3.5 mmol/L–1, Cl: 106 mmol/L–1, Ca: 0.92 mmol/L–1, BE: 0.1 mmol/L–1, and HCO3: 24.4 mmol L–1. Volume-controlled mechanical ventilation was maintained as follows: VT: 180 mL, frequency: 20 min–1, I/E: ½, FiO2: 0.5, and PEEP: 4 cmH2O. The peak airway pressure was 22 cm H2O, and EtCO2 was 31 mm Hg.
The cardiopulmonary bypass circuit (Dideco EOS Pediatric Oxygenator, Biodevices Inc., Italy) was primed with 650 mL of crystalloid and mannitol solution. After a median sternotomy, anticoagulation was provided with a single dose of 6,000 U heparin. The activated clotting time was measured at 525 seconds. Cardiopulmonary bypass (CPB) was conducted under moderate hypothermia. Myocardial protection during aortic cross-clamping was achieved with cold crystalloid cardioplegia (Plegisol, Hospira Inc., USA). Following standard mitral valve implantation (St. Jude Medical No. 25 mechanical valve, St. Jude Medical, USA), the patient was weaned off CPB with 10 µg/kg/min of dobutamine. Conventional ultrafiltration was also used, and a volume of 600 mL was removed.
The duration of anesthesia was 245 min, including 165 min for surgery, 50 min for cross-clamping, and 78 min for CPB. In total, 400 mL of isotonic NaCl and 340 mL of erythrocyte suspension were administered intraoperatively. The urine output was 300 mL, and the bleeding volume was 150 mL. The patient was taken to the intensive care unit under dobutamine support with a normal sinus rhythm and the following parameters: heart rate: 123 bpm; SpO2: 100%, ABP: 90/48 mm Hg, and CVP: +28 mm Hg. Dobutamine infusion was administered for 3 h postoperatively. After considering and preparing for re-intubation, the patient was intubated when she was fully awake and met the standard extubation criteria at the 18th hour. She was transferred to the general patient ward at the postoperative 48th hour. The patient was discharged from hospital on the 5th postoperative day under Coumadin treatment.
Histopathological examination of the resected mitral valve revealed a macroscopic nodular appearance, microscopic hyalinization, fibrotic thickening, and single or clustered histiocytes with large, granular cytoplasms.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [105.0, 'mm hg'], 'Diastolic Blood Pressure': [66.0, 'mm hg']}",79,75.05,82.95,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 105.0 mm Hg + 2/3 * 66.0 mm Hg = 79.0 mm Hg.
Hence, the patient's mean arterial pressure is 79.0 mm Hg."
1990,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1941,Extracted,"A 23-year-old female college senior comes to the physician with a 1-year history of recurrent palpitations accompanied by sweating, facial blushing, and sometimes nausea. The symptoms are worse during class when she is occasionally called out to speak, which causes her to feel embarrassed. She has been skipping class on discussion days because she is concerned that her classmates may notice her symptoms. The patient does not enjoy jogging in the park anymore and has gained 2 kg (4 lbs 7 oz) over the past 2 months. Her appetite is unchanged. She has no history of serious illness. She does not smoke or drink alcohol. She has experimented with marijuana but does not use it currently. She appears nervous and does not make eye contact with the physician. Her vitals show a pulse of 85/min, her blood pressure is 125/70 mmHg, and her temperature is 36.8°C. Mental status examination reveals full range of affect. Neurological exam shows no abnormalities.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",88.33333,83.91666,92.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 125.0 mm Hg + 2/3 * 70.0 mm Hg = 88.33333 mm Hg.
Hence, the patient's mean arterial pressure is 88.33333 mm Hg."
1991,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5942209-2,Extracted,"A 66-year-old Caucasian woman with no significant past medical history presented to the emergency department with a 2-month history of progressively worsening dyspnea. The dyspnea was worse with exertion or laying down flat. She also complained of a productive cough, fatigue, and weight loss. She denied any sick contacts or recent travel. The patient has not been seen by a primary care physician for many years. She had 25 pack-years smoking history. She also endorsed occasional marijuana and cocaine use. Family history was notable for lung cancer in her mother.
Physical examination in the emergency room revealed a cachectic female in moderate respiratory distress who was alert and oriented. She was afebrile with a pulse of 106 beats per min, blood pressure of 119/76 mm Hg, respiratory rate of 24 breaths per min, and oxygen saturation of 99% on 2 L oxygen via nasal cannula. No jugular venous distension was noted. S1 and S2 heart sounds were distant with no audible murmurs, rubs, or gallops. Lung sounds were severely decreased in the right mid and lower fields but otherwise normal in the other fields. No edema, clubbing, or cyanosis was observed in the extremities.
Laboratory work up revealed leukocytosis (WBC 15.8 K/uL), hyponatremia 128 mmol/L, hypochloremia 92 mmol/L, and lactic acidosis 2.94 mEq/L. B-type natriuretic peptide and troponin were within normal limits. Arterial blood gas on 2 L oxygen revealed a pH of 7.45, a partial carbon dioxide pressure of 30 mm Hg, a partial oxygen pressure of 92 mm Hg, and bicarbonate of 23.1 mEq/L. A 12-lead electrocardiogram showed sinus tachycardia (). Chest radiograph revealed a cavitary lesion with an air-fluid level in the right upper lobe and an enlarged cardiac silhouette (). CT of chest, abdomen, and pelvis with contrast was performed, and it revealed a right upper lobe necrotic mass, pericardial effusion, and right pleural effusion along with right middle lobe medial segment collapse (). Extensive mediastinal adenopathy and bilateral adrenal masses were also noted. Echocardiogram revealed left ventricular ejection fraction of > 70% with right ventricular and right atrial diastolic collapse ( a-b).
The patient underwent emergent pericardiocentesis and placement of pigtail catheter to evacuate pericardial and pleural fluid, respectively, for therapeutic relief and fluid analysis. Approximately 850 mL of serosanguineous fluid was removed from the pericardial cavity. Later on, a pericardial window was placed by cardiothoracic surgery. Cytology studies indicated primary lung adenocarcinoma with positivity for Napsin-A and TTF-1. Further analysis revealed high expression of PD-L1 and positive BRAF c.1780G>A (p.D594N) mutation. Blood cultures and acid-fast bacilli smear performed on admission were negative for any acute infection. The patient’s shortness of breath improved during the hospital stay, and her electrolyte abnormalities were corrected. She was discharged to a skilled nursing facility once she was hemodynamically stable. She was given outpatient follow-up with an oncologist for treatment of stage IV non-small cell lung cancer.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [119.0, 'mm hg'], 'Diastolic Blood Pressure': [76.0, 'mm hg']}",90.33333,85.81666,94.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 119.0 mm Hg + 2/3 * 76.0 mm Hg = 90.33333 mm Hg.
Hence, the patient's mean arterial pressure is 90.33333 mm Hg."
1992,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6075504-1,Extracted,"A 71-year-old, 86 kilogram male with a history of alcohol abuse, dementia, chronic kidney disease, and hypertension presented to the emergency department (ED) after the ingestion of approximately half of a retail lava lamp’s contents. On-scene vitals by emergency medical services (EMS) were notable for 90% oxygen saturation on room air. The patient was placed on two liters of oxygen by nasal cannula (NC), and the North Carolina Poison Control Center was called; they recommended supportive care, laboratory studies, and an electrocardiogram (ECG) with continuous cardiac monitoring. The risk of toxic ingestion was thought to be low because of the recent manufacture date, which theoretically minimized toxic contents previously found in similar products because of regulatory changes.
In the ED, EMS reported that the patient had consumed the lava lamp because he believed it to contain alcohol. The patient was unsure of the time of ingestion, though all history was limited by his chronic dementia. Initially, he remembered having nausea and vomiting at home, but was asymptomatic on evaluation. On physical exam, vital signs were notable for a blood pressure of 129/68mmHg, heart rate of 74 beats per minute (bpm), and oxygen saturation of 97% on two liters NC. Patient was tearful but in no distress. He had equal and reactive pupils, his heart rate was regular, breath sounds were clear, abdomen was soft, and he had a normal cranial nerve exam. Family in the room reported he was at his baseline mental status: delayed speech and baseline dementia. They seemed unconcerned about any new or significant mental status changes.
Routine laboratory results were normal except for the following: white blood cell count 14.4×109/liter, hemoglobin 10.0 g/dL, potassium 6.3 mmol/L, bicarbonate 14mmol/L, blood urea nitrogen 37 mg/dL, calcium 12.1 mg/dL, creatinine 2.3 mg/dL, and anion gap 23 mmol/L. Serum drug screen was negative for ethanol, acetaminophen, and salicylate. A 12-lead ECG showed normal sinus rate, with concern for peaked T-waves in the apical leads. A chest radiograph was read as persistent low lung volumes with bronchovascular crowding and bibasilar opacities, likely reflective of atelectasis.
The patient was treated for hyperkalemia with calcium gluconate, insulin, dextrose, and sodium bicarbonate; the Poison Control Center was updated on the findings and initial treatments. Within three hours, the potassium had corrected to 5.5 mg/dL and creatinine increased to 2.8 mg/dL. His mental status was unchanged. He continued to saturate in the low 90s, originally managed with two liters NC, but later requiring slight increases in his NC needs. Initially, it was thought that his lower saturations were attributed to a possible aspiration event, especially with reports of vomiting earlier in the morning.
About six hours into his ED visit, while pending admission, the nursing staff called providers to the room for an acute change in mental status with concomitant aspiration event. The patient’s oxygen saturation acutely dropped to 85% on NC, and high-flow NC was initiated. The patient’s saturation remained 85% on the Masimo SET™ pulse oximeter despite oxygen supplementation, and he was responsive to only painful stimulation. On auscultation, his lungs were clear bilaterally without wheezes or rales; his skin, especially distal, appeared gray and mottled. His blood pressure was 101/52 mmHg, and he became tachycardic to 101 bpm. A non-rebreather oxygen mask was applied at 15 liters and albuterol was administered with no change in respiratory status. Repeat radiograph was unchanged and it was thought this could be due to aspiration pneumonitis or acute respiratory distress syndrome. However, with the acute change, a venous blood gas was then also sent with the following notable results: pH of 7.22, methemoglobin of 45.6% and a lactate of 2.7 mmol/L.
Given this finding and the fact that his oxygen saturation remained the same on supplementation, the patient was diagnosed with methemoglobinemia. Subsequently, he was administered two doses of methylene blue (50 mg intravenously) 20 minutes apart. Over the next half-hour, his color and oxygen saturation improved, followed by a return of his mental status to baseline at initial presentation. A follow-up arterial blood gas at 45 minutes showed pH of 7.28 and methemoglobin of 9%. The patient was admitted to the intensive care unit.
The Poison Control Center was later updated. After research and testing, it was discovered that the components of the lava lamp ingested included 76% calcium nitrate, 23% water, and 1% potassium enol.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [129.0, 'mm hg'], 'Diastolic Blood Pressure': [68.0, 'mm hg']}",88.33333,83.91666,92.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 129.0 mm Hg + 2/3 * 68.0 mm Hg = 88.33333 mm Hg.
Hence, the patient's mean arterial pressure is 88.33333 mm Hg."
1993,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7481472-3,Extracted,"Patient 3: 40-year-old female, with dyslipemia, chronic venous insufficiency, obesity, attending the emergency department for bilateral pneumonia with respiratory failure. Her blood pressure was 107/73, heart rate 79 beats per minute, SpO2 92%, and she had elevated D-Dimer levels. Home treatment: Lorazepam (1 mg), olanzapine (10 mg), risperidone (3 mg), lactitol monohydrate and lactulose. Chest X-ray: Interstitial pattern of right and left basal predominance, with patchy opacities in the middle and upper third of the right hemithorax, suggestive of a viral infectious process. Confirmation of COVID-19 was made by RT-PCR using a throat swab. She was treated with hydroxychloroquine (for 5 days), lopinavir-ritonavir and lithium carbonate (starting on day 2, 400 mg/12 h). The patient was discharged after 11 days.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [107.0, 'mm hg'], 'Diastolic Blood Pressure': [73.0, 'mm hg']}",84.33333,80.11666,88.55,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 107.0 mm Hg + 2/3 * 73.0 mm Hg = 84.33333 mm Hg.
Hence, the patient's mean arterial pressure is 84.33333 mm Hg."
1994,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8715837-1,Extracted,"A 28-year-old male was brought to the emergency department in a state of irritability following the history of ingestion of alcohol with snake venom, as narrated by his relative, one hour back. The patient was a snake charmer by occupation. The patient had a history of alcohol addiction for 15 years and had a history of repeated failed attempts to quit alcohol addiction in the past. On examination, pulse was 88 beats per minute, regular in rhythm and volume, having no special character, blood pressure was 120/70 mm of Hg and there were no signs of any bleeding tendencies. The patient was conscious and irritable, deep tendon reflexes were normal, bilateral plantar were flexor and there was no neuro deficit.
The abdomen was soft and non-tender, heart sounds were normal, the chest was bilaterally clear.
The patient’s whole blood clotting time was normal, random blood sugar was 80 mg/dl and the rest of the laboratory investigations including complete blood count, renal function test and liver function test were within normal limits. Upon providing injectable thiamine and 25% dextrose 100 ml, the patient improved clinically and became conscious and oriented. The patient then provided a history of snake venom addiction which began four months back, when he got divorced from his wife. It started as an addiction to snake bites which provided him the high sensation that he was using as an alternative to alcohol to reduce his alcohol consumption. Following a single snake bite, the patient used to get a high sensation for a period of 6-7 days, as a result of which his alcohol consumption reduced significantly. For the last one month, the patient was mixing his alcohol drinks with the venom of snakes in order to increase the duration of high effect with less amount alcohol. Cut-down, Annoyed, Guilt, Eye-opener (CAGE) score of the patient was calculated to be 3 out of 4 and the alcohol use disorder identifying test score was 26. The patient was started with cognitive behavioral therapy, chlordiazepoxide 10 mg hs (hora somni), along with a short serotonin reuptake inhibitor (escitalopram 10 mg once in a day). He improved clinically and was discharged after one week of admission in stable condition. He is currently doing well on follow-up with the de-addiction team of our hospital, participating actively in group therapies and motivational enhancement therapy.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Systolic Blood Pressure': [120.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
1995,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4744067-2,Extracted,"A 54-year-old non-hypertensive man presented with a history of the sudden onset of weakness of the right-sided extremities, complicated by headache and nausea. On examination, his BP was 180/110 mm of Hg. GCS was E4, V4, and M6 with right-sided hemiparesis of power grade 1/5. A plain CT scan detected a 2.8 x 2.4 cm acute bleed in the right thalamus and posterior limb of the internal capsule (Figure ). On digital subtraction angiogram (DSA), VA fenestration was demonstrated in the selective left vertebral angiography (Figure -).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [180.0, 'mm hg'], 'Diastolic Blood Pressure': [110.0, 'mm hg']}",133.33333,126.66666,140,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 180.0 mm Hg + 2/3 * 110.0 mm Hg = 133.33333 mm Hg.
Hence, the patient's mean arterial pressure is 133.33333 mm Hg."
1996,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6051126-1,Extracted,"A 64-year-old Caucasian female presented to our emergency department (ED) with a two-day history of bleeding from her left breast. She has had a slowly enlarging growth on her left breast for the past two years, which initially started as a small papular lesion in the nipple areolar complex. Most recently, the mass became ulcerated with active serous discharge; however, due to the lack of health insurance, the patient did not seek any medical attention. For the past two days prior to presentation, she developed significant bleeding and oozing from the ulcerated mass, forcing her to report to the ED. There was associated localized breast pain, but no weight loss, fever, nausea, vomiting, abdominal pain, back pain, abdominal pain, shortness of breath, cough, blurry vision, nor headaches.
She had no prior personal or family history of skin and breast cancers. She had no history of excessive exposure to sunlight, radiation exposure, arsenic ingestion, or a history of immunosuppression.
Physical examination reveals an elderly female in no apparent distress. Vital signs were stable apart from an elevated blood pressure of 164/85 mmHg. Examination of the left breast revealed a large fungating mass of >10 cm in size, occupying most of the mid and outer breast with a distortion of the nipple areolar complex (). There were several open wounds with active bleeding and a foul smell. The area of erythema was noted. There were palpable left axillary lymph nodes. The rest of the physical examination was unremarkable.
The provisional diagnosis was breast cancer with possible metastasis. Subsequently, the patient underwent workup to further characterize the mass and assess for metastasis. Computer tomography (CT) scan of the chest, abdomen, and pelvis was positive for a large, partially enhancing heterogeneous mass in the left breast and a calcified granuloma in the right lung field, in addition to mildly enlarged left axillary lymph nodes. No evidence of metastasis was identified in the abdomen and pelvis. Magnetic resonance imaging (MRI) of the brain with and without contrast was negative for brain lesions. There was no evidence of osseous metastatic disease as evident by the negative nuclear medicine bone scintigraphy.
Trucut excisional biopsy of the mass was performed. The initial histopathological exam was suggestive of an epidermal origin of the cancerous cells, raising the possibility of an adnexal primary such as basal cell carcinoma (Figures and ). Immunohistochemical (IHC) profile also favored a primary skin disorder over a breast primary (Figures and ). Utilizing NeoGenomics®, the cells were consistent with cutaneous basal cell carcinoma.
Post diagnosis, the patient underwent left modified radical mastectomy with axillary lymph node dissection. After histopathological exam for the dissected tissue and lymph nodes, a final diagnosis of invasive cutaneous basal cell carcinoma was made. The margins were tested negative for carcinoma. All the dissected 16 lymph nodes were negative for cancer. Subsequent treatment and oncological follow-up were scheduled with oncology.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [164.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",111.33333,105.76666,116.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 164.0 mm Hg + 2/3 * 85.0 mm Hg = 111.33333 mm Hg.
Hence, the patient's mean arterial pressure is 111.33333 mm Hg."
1997,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-50,Extracted,"A 57-year-old man is brought to the emergency department for worsening pain and swelling of his left ankle for the past 2 hours. The pain is severe and awakened him from sleep. He has hypertension and hyperlipidemia. Current medications include hydrochlorothiazide and pravastatin. His temperature is 37.8°C (100.1°F), pulse is 105/min, and blood pressure is 148/96 mm Hg. Examination shows exquisite tenderness, erythema, and edema of the left ankle; active and passive range of motion is limited by pain. Arthrocentesis of the ankle joint yields cloudy fluid with a leukocyte count of 19,500/mm3 (80% segmented neutrophils). Gram stain is negative. A photomicrograph of the joint fluid aspirate under polarized light is shown.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [148.0, 'mm hg'], 'Diastolic Blood Pressure': [96.0, 'mm hg']}",113.33333,107.66666,119,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 148.0 mm Hg + 2/3 * 96.0 mm Hg = 113.33333 mm Hg.
Hence, the patient's mean arterial pressure is 113.33333 mm Hg."
1998,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8346777-1,Extracted,"A 29-year-old Asian lady with no previous significant past medical history presented in May 2020 to the maternity unit of our facility with a 5-day history of fever, cough, breathlessness, and diarrhea.
She was 24 weeks pregnant (gravida 4, para 3 with three previous caesarean sections). She was a nonsmoker and did not consume any alcohol. She was not taking any regular medications. On admission, she had a fever of 37.7 °C, blood pressure of 90/54 mmHg, and pulse of 115 beats per minute. She was found to be in mild respiratory distress with a respiratory rate of 20 breaths per minute, and oxygen saturation was 94% on room air.
Her initial chest X-ray (CXR) (Fig. A) showed extensive and bilateral patchy opacification suggestive of COVID-19 illness. She tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on Real-time polymerase chain reaction (RT-PCR) on nasopharyngeal swab. Blood tests revealed normal renal and liver function tests, normal Hemoglobin (Hb) of 128 mg/dl, and normal platelets and white cell count including differentials. Her C-reactive protein (CRP) and interleukin-6 (IL6) levels were raised at 51 mg/L and 96 pg/ml, respectively. Her d-dimer level was 0.86 μg/ml and fibrinogen 4.2 g/L (Table).
She was started on supplemental oxygen, hydroxychloroquine 400 mg twice daily, intravenous ceftriaxone 1000 mg twice daily, subcutaneous enoxaparin 40 mg once daily, lopinavir–ritonavir 80 mg–20 mg, two tablets twice daily, hydroxychloroquine 400 mg twice daily, and acetylcysteine 600 mg orally twice daily as per the local guidelines for COVID-19 management. Her oxygen saturation continued to drop, and after 24 hours of admission, she was on 8 L/minute of oxygen via face mask and managed in high-dependency unit.
By day 5 of admission, there was no clinical improvement. She still required respiratory support in the form of high-flow oxygen 40 L/minute and was showing signs of respiratory failure on arterial blood gases (ABGs), which revealed a pH of 7.45, pO2 of 55 mmHg, and pCO2 of 23 mmHg. Her chest X-ray (Fig. B) showed marked progression. In addition, she had become restless. Proning was proving difficult, and she was started on Bilevel positive airway pressure (BIPAP). Her inflammatory markers continued to deteriorate. Her IL6 was 96 pg/ml on admission and rose to 193 pg/ml. Her clinical picture was in keeping with a cytokine storm syndrome, which was not responding to her current treatment regime. A multidisciplinary meeting was called, and it was decided to administer tocilizumab 400 mg intravenously once.
Subsequently, she was intubated and ventilated because of acute respiratory failure. Her intensive care unit (ICU) admission was complicated by candidemia, treated successfully. She improved gradually and was extubated on day 16 of admission. She had an uneventful recovery with improvement in respiratory symptoms, oxygen requirements, and CXR appearances (Fig. C). She was discharged from the hospital after 35 days of hospitalization. Repeated fetal ultrasound scans during admission demonstrated no evidence of fetal distress. Emergency caesarean section was not indicated during hospitalization.
She later had an elective caesarean section at 38 weeks of gestation under spinal anesthesia owing to history of previous three caesarean sections and delivered a normal male child. The initial neonatal assessment was unremarkable. No further follow-up information is available.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [54.0, 'mm hg']}",66,62.7,69.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 54.0 mm Hg = 66.0 mm Hg.
Hence, the patient's mean arterial pressure is 66.0 mm Hg."
1999,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7752447-1,Extracted,"A 75-year-old female patient presented to tertiary referral academic hospital, Harare Central Hospital, from a provincial hospital with a 2 week history of pain and darkening of all her fingers and toes. A month prior to visiting hospital she developed a constant rest pain in her hands and feet. The pain was exacerbated by manual work and was not relieved by analgesia. She highlighted intermittent episodes of severe pain in her hands and feet occurring over the last 1 year. Her fingers and toes became dusky in appearance, and this was associated with blistering of the fingers and toes. The patient highlighted sensory loss in her fingers and toes. There was no history of intermittent claudication. The patient did not drink alcohol or smoke, and she had no known chronic illnesses. There was no family history of diabetes mellitus, hypertension, heart disease, dyslipidemias, and connective tissue disorders. The patient did not admit to a history of eating mouldy grain or bread. In the review of systems, she did not have any history of chest pain or palpitations. The patient did not have any history of headaches, seizures, or hallucinations. The past medical history was insignificant. She was negative for human immunodeficiency virus (HIV) and was not on any medications.
Examination of the patient at the referral center revealed she was fully conscious, and not in any apparent distress. She had a normal pulse rate of 90 beats per minute, with a normal blood pressure (systolic reading of 128 mm Hg and diastolic of 59 mm Hg). She had a pyrexia of 37.8°C with no lymphadenopathy. There were no Janeway lesions or Xanthoma on examination. The cardiac, respiratory, and abdominal examinations were normal. On examination of the hands, the patient had dry gangrene of all the fingers of the hands which had demarcated. She had very good peripheral pulses in the upper limbs. In the lower limbs, she had dusky hyperpigmented toes. All the peripheral pulses in the lower limb were present and full volume. See Figure
The complete blood count on admission showed a raised white cell count of 16.1 × 109/L, with a low hemoglobin of 11.6 g/dL. Her renal function and lipid profile were normal. A random blood sugar done on admission was within normal limits. A chest x-ray and electrocardiogram (ECG) were done and were normal. An echocardiogram (Echo) was done as part of her workup, and she had a structurally normal heart with no thrombi and a good ejection fraction of 67%.
Fluid resuscitation was commenced with intravenous crystalloid solution and empiric antibiotics therapy with her pyrexia settling on the third day after admission. Her toes demarcated as dry gangrene by day 3 postadmission. The patient was consented for amputation of the gangrenous parts of her hands and feet. Amputation of the digits of her fingers was done with transmetartasal amputation of her feet done bilaterally. The surgery was uneventful. Two weeks after the initial surgery, the patient had split skin grafting to cover the bare amputation sites with excellent uptake of the grafts. See Figure . Pathological evaluation of amputated tissue did not report any vasculitis. There were microthrombi in the small vessels with sparing of the large caliber vessels.
She was discharged home 5 days after split skin grafting. The patient underwent physiotherapy and occupational therapy sessions at her local hospital to assist with rehabilitation and mobilization. On review 1 month later, all her wounds had healed and the patient was well with no complaints.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [128.0, 'mm hg'], 'Diastolic Blood Pressure': [59.0, 'mm hg']}",82,77.9,86.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 128.0 mm Hg + 2/3 * 59.0 mm Hg = 82.0 mm Hg.
Hence, the patient's mean arterial pressure is 82.0 mm Hg."
2000,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3369993-1,Extracted,"A Thai 37-year-old man presented at Burapha University with a sudden bilateral progressive hearing loss. He had a known case of hypertension, well-controlled with amlodipine. He suddenly lost his left hearing and experienced tinnitus and aural fullness. A high dose of steroids (prednisolone, 60 mg/day) was administered by the first physician. He subsequently developed a right hearing loss without left ear improvement and was referred to the first author. He had no history of either otitis media or any ototoxic medication. His blood pressure was 145/85 mmHg. Ear examination was unremarkable. Weber testing with a 512 Hz tuning fork showed no hearing response by the patient in both ears. He was diagnosed as bilateral progressive ISSNHL. Magnetic resonance imaging of the brain and the cerebropontine angle was unremarkable. Venereal disease research laboratory (VDRL), treponema pallidium hemagglutination (TPHA), and anti-human immunodeficiency virus (HIV) were non-reactive. Complete blood count found no leukocytosis and no anemia. Fasting blood sugar was 95 mg/dL.
A high dose of oral steroid treatment (prednisolone, 60 mg/day) was administered by the first physician 3 days after the onset of the hearing loss. Audiogram was repeated after a week of standard treatment. The audiogram revealed right profound sensorineural hearing loss with a threshold of 78 dB and left deafness with a threshold of 90 dB. Administration of systemic steroids was then discontinued.
Intratympanic membrane steroids (methylprednisolone, 40 mg/mL) were administered in the left ear 3 times within a week (at day 9, 10, 16 after the onset). The hearing level after the third dose showed minimal improvement for both ears. The air conductive thresholds were 60 dB and 53 dB for the right and left ears, respectively. The bone conductive threshold was 43 dB for both ears.
As HBOT is not yet standard for sudden sensorineural hearing loss, it was introduced to this patient as an alternative therapy. With no further improvement after the last audiogram (day 16), the patient decided to undergo HBOT (day 36) for a salvage treatment after a discussion with the authors.
The HBOT program was scheduled for 10 sessions according to the US Navy treatment table (2 ATA 90 minutes) (). We used a 6-seat multi place chamber for the HBOT ( and ), which was started at day 36 after the hearing loss onset. After the third session of HBOT (day 38), normal hearing returned, with no tinnitus in both ears. The following audiogram revealed normal hearing with a right threshold of 20 dB and a left threshold of 30 dB. Tinnitus was evaluated to be resolved by the visual analog scale. The patient was sent for the 4th (day 41) and the 5th sessions (day 42) as scheduled. The following audiogram 3 months after the entire treatment showed normal hearing level with a right threshold of 22 dB and a left threshold of 20 dB.
Audiograms and the time course are displayed in and , respectively. No adverse events during or following HBOT and the intratympanic membrane injection were reported.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [145.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",105,99.75,110.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 145.0 mm Hg + 2/3 * 85.0 mm Hg = 105.0 mm Hg.
Hence, the patient's mean arterial pressure is 105.0 mm Hg."
2001,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2769365-1,Extracted,"A 68-year-old Caucasian lady presented with left sided upper abdominal pain and left renal angle pain to her GP. The GP ordered lumbar X-rays of the spine, which had shown a possible 7 cm renal stone (). The pain had been occurring for several months and there were no exacerbating or relieving factors. The pain did not radiate and was not severe. She had no lower urinary tract symptoms importantly no haematuria or dysuria. Other medical problems included rheumatoid arthritis, SLE and controlled hypertension. She had no previous urological or surgical history. She was referred to a urologist for an opinion.
Laboratory investigations showed a serum creatinine of 119 mg/dl and a urea of 8.1 mg/dl. Urinalysis was normal and her blood pressure was 140/80 mmHg. Her symptoms of back pain had subsided and on examination she had no loin pain. She was subsequently sent for a CT scan, which revealed that the substance of her left kidney had almost totally been replaced by a dense calcification. There was also calcification of the distal ureteric wall on the same side. Both of these findings are evident from the reconstructed CT image (). When she was subsequently reviewed again in clinic, it came to light that she had had TB in her chest at the age of 16. A diagnosis of TB “auto nephrectomy” was made. From the time of her original referral she had no further episodes of pain and it was felt that her symptoms had been due to musculoskeletal problems and not due to the TB kidney. A review of the present literature suggested that nephrectomy may be considered for patients that are hypertensive. Our patient had well controlled hypertension and after discussion with the patient it was not felt that nephrectomy was warranted. She was discharged back to her GP, with advice to monitor her blood pressure and renal function.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 80.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
2002,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6683594-1,Extracted,"A 65-year-old man, hypertensive, smoker and without a history of cardiovascular diseases presented to ED due to intermittent chest pain, radiating to both arms, of 6-hour duration. The patient was asymptomatic at admission with vital signs of BP 152/83 mmHg, O2-saturation 97% on room air, oral temperature 36.4 °C, heart rate 73 bpm. Physical examination and chest x-ray were unremarkable. ECG showed biphasic T-wave in precordial leads V1–V4 ().
Two-dimensional (2D) echocardiography revealed hypokinetic mid-distal anterior wall and apex with mildly depressed left ventricular ejection fraction (LVEF). As WS was suspected, the patient was pre-treated with aspirin, ticagrelor and enoxaparin. First, cardiac serum biomarkers were slightly elevated: high-sensitive cardiac troponin T (hs-cTnT) (161 ng/mL, n.r. 0-40 ng/mL) and CK-MB (6.6 mg/dl n.r. 0-6.5 mg/dl). Blood assessment every 3 hours did not show any increases while ECG recorded during a pain period revealed T-wave pseudo-normalization. Patient history, positive hs-cTn, wax and wane symptoms nitrate responder, push the patient to underwent coronary angiography that revealed a proximal LAD critical lesion () that was stented with one Drug Eluting Stent 3.5/18 mm ().
The patient was discharged in good condition two days later, with the recommendation to maintain double antiplatelet therapy for 12 months. The patient was still pain free at one-month follow-up.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [152.0, 'mm hg'], 'Diastolic Blood Pressure': [83.0, 'mm hg']}",106,100.7,111.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 152.0 mm Hg + 2/3 * 83.0 mm Hg = 106.0 mm Hg.
Hence, the patient's mean arterial pressure is 106.0 mm Hg."
2003,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5840811-1,Extracted,"A 60-year-old Japanese woman was brought to the emergency department of our hospital, complaining of left flank pain. The pain had started the previous day and had gradually increased in severity. On examination, she was found to be alert, with a blood pressure of 173/101 mmHg, heart rate of 110 beats/minute, oxygen saturation of 95% (on room air), and respiratory rate of 20/minute. Her past medical history included myelodysplastic syndrome (MDS), hypertension, and cerebral infarction, leading to left hemiplegia. She had no history of pancreatitis and abdominal surgery. She was taking antihypertensive and acid-reducing medications, but no antiplatelet or anticoagulant medication. Her abdomen was flat, but there was moderate tenderness in her left flank. Her laboratory findings included hemoglobin level of 7 g/dL, hematocrit level of 20.8%, platelet count of 118,000/microL, prothrombin time of 13.3 seconds, activated prothrombin time of 31.9 seconds, and fibrinogen level of 209.4 mg/dL. Her normal hemoglobin level was approximately 8 g/dL. Blood chemistry findings were almost within normal limits. A computed tomography (CT) scan of her abdomen with intravenously administered contrast agent showed a solid mass of 5 × 5 × 8 cm in the left middle abdominal quadrant (Fig. ). The mass was found to be fed by a branch of the superior mesenteric artery (SMA). The contrast agent leaked in the mass. An orally administered contrast agent was not used because she had nausea. On completion of CT, the working diagnosis was an impending rupture of an aneurysm located in a branch of SMA. We decided to perform a transcatheter arterial embolization (TAE); however, angiography of SMA and inferior mesenteric artery (IMA) did not indicate extravasation of the contrast agent. Her blood pressure remained stable, but her pulse rate was still fast. We decided to perform surgery in line with the diagnosis of an impending rupture of the visceral artery aneurysm. Her peritoneal cavity was entered with a midline incision, and there were no ascites. The mass was attached to the antrum of her stomach. There was a smooth surfaced mass at the greater curvature of the antrum. We suspected intra-tumor bleeding of the gastric submucosal tumor. We performed a wedge resection of her stomach including the mass with a 1 cm margin. The surgical specimen was opened and it revealed a large amount of clots (Fig. ). There were no tumoral lesions.
Subsequently, pathological findings indicated that the mass had not included tumor cells and was simply filled with a large amount of clots. The etiology of the hematoma was not proven by pathological findings. She was admitted to the general surgical ward after surgery, and she was transfused with six units of packed red blood cells postoperatively. She was discharged from our hospital to a nursing home on day 63 after rehabilitation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [101.0, 'mm hg'], 'Systolic Blood Pressure': [173.0, 'mm hg']}",125,118.75,131.25,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 173.0 mm Hg + 2/3 * 101.0 mm Hg = 125.0 mm Hg.
Hence, the patient's mean arterial pressure is 125.0 mm Hg."
2004,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7680121-1,Extracted,"An 85-year-old woman presented with epigastric pain for four days and associated nausea and vomiting. A nonadherence to hypertension treatment was recorded. On the admission day, the patient experienced, epigastric pain but there was no fever and no tenderness in abdominal physical examination. Heart rate was 94 bpm while blood pressure was 190/70 mmHg. One litre of gastric contents was drained by a nasogastric tube. Blood count demonstrated slight increase of white blood cell (12.77 K/µL). The serum potassium concentration was 2.68 mmol/L, a significantly decreasing. Other blood results such as level of serum bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), amylase and renal function were normal.
Hypertension and electrolyte disturbance were adjusted by giving amlodipine 5 mg, captopril 25 mg and potassium chloride infusion. Abdominal CT scan was then performed. Rigler’s triad was detected on abdominal CT scan including duodenal obstruction with dilated stomach, ectopic gallstone within duodenum indicating cholecystoduodenal fistula, pneumobilia (). Additionally, gastroduodenoscopy illustrated signs of duodenal obstruction such as gastroduodenal dilatation and filled fluid in duodenum. However, no stone was visible. She underwent an elective open surgery. She was classified into ASA III (American Society of Anesthesiologists III).
During the surgery, we found that there was chronic cholecystitis and tightly adhered to duodenum and hepatic hilum there was cholecystoduodenal fistula. A huge gallstone which was 9×6 cm in size had migrated to the lower second part of the duodenum (D2). This stone caused duodenal obstruction. With this site of impaction, we had a long distance to the stomach and jejunum. Another important issue was that the anterior duodenal wall had been widely impaired by the fistula and the healthy wall of D2 was much narrowed as a consequence. Therefore, we firstly performed fistulotomy to remove the gallstone. describes stone after being extracted. Then cholecystectomy, fistulectomy were done. After that duodenal defect was addressed. With the size defect of 7 cm in diameter, we performed a side-to-side Roux-en-Y duodenojejunostomy. A nasogastric tube was passed through the anastomosis and a surgical drain was placed into the right infrahepatic space.
On the first postoperative day, the patient had bowel motility, nasogastric tube drained 50–100 mL gastric content per day. Right infrahepatic drain had little fluid. She was supplied with total parenteral nutrition for seven days. Then oral intake was increasingly applied from clean water, soup, milk, and finally solid foods. There was no enteric obstruction and intra-abdominal infection. Hypertension with systolic pressure ranged from 160–200 mmHg on the first postoperative day. This was controlled during a seven-day period with a therapy of Adalat LA 30 mg tid.
However, on the seventh postoperative day, she developed nosocomial pneumonia with purulent cough, inspiratory crackles, right upper lobe atelectasis on chest radiography, CRP of 82 ng/mL, WBC of 16 K/µL and %Neu of 86%. She was treated with meropenem, levofloxacine for a period of 10 days. The patient was discharged on the sixteenth postoperative day. After six months of follow-up, no complication was found.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [190.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",110,104.5,115.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 190.0 mm Hg + 2/3 * 70.0 mm Hg = 110.0 mm Hg.
Hence, the patient's mean arterial pressure is 110.0 mm Hg."
2005,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6363593-1,Extracted,"A 70-year-old Caucasian male presented to emergency with 10 days of dry cough, dyspnoea, and fatigue. His respiratory rate was 18 per minute with saturations of 93% on 2 L of nasal prong oxygen, heart rate 75 beats per minute and in sinus rhythm, blood pressure 104/60 and was afebrile. Examination demonstrated globally reduced air entry with bibasal crackles with no other pertinent findings.
His medical history included HIV diagnosed in 1997 and well controlled with combination anti-retroviral therapy (sequential viral loads undetectable and CD4 >500/mm3) and Barrett's oesophagus. His surgical history included a trans-urethral prostate resection for hypertrophy as well as a left total knee replacement and a decompression for spinal stenosis. Medications were allopurinol, rosuvastatin, atazanavir, ritonavir, lamivudine, zidovudine, and pantoprazole. He had a 40 pack-year smoking history (quit 15 years ago), minimal alcohol, and no illicit substance history. He worked in an office, was an active swimmer, and not in a relationship. Vaccines were up to date.
Initial investigations revealed a haemoglobin of 115 g/L, neutrophils 8.19 × 109/L, lymphocyte 0.49 × 109/L, eosinophils 0.17 × 109/L, and platelets 390 × 109/L. Creatinine was 441 micromol/L (86 six months prior), urea 25.4 mg/dL, and C-reactive protein 148 mg/L. Chest film demonstrated diffuse bilateral infiltrates predominantly in the lower zones. Urinalysis demonstrated >500 erythrocytes, 10 leucocytes, and no bacteria.
With a provisional diagnosis of pneumonia he was commenced on ceftriaxone, azithromycin, and oxygen. Intravenous fluids continued.
The following day his creatinine increased to 512 despite 3 L of intravenous fluid. An arterial blood gas showed type 1 respiratory failure with a haemoglobin 98 g/L. A broad screen for infectious and non-infectious aetiologies was performed, and a routine HIV viral load taken 4 days prior to presentation was 146 copies/mL. Anti-retrovirals were changed to dolutegravir, efavirenz, and lamivudine due to renal failure.
By day 3 his fatigue and dyspnoea had worsened without new symptoms. Repeat chest film demonstrated worsening infiltrates (Fig. ). His oxygen requirement had increased to 50 L/min, 50% FiO2 via hi-flow nasal cannulae. Dialysis was commenced with red cell transfusions as his haemoglobin was now 82 g/L. A repeat urine had >500 erythrocytes, protein 1100 mg/L, creatinine 188 g/mol, myoglobin 14 μg/L, and normal haemosiderin.
Day 4 returned a Perinuclear-ANCA (P-ANCA) titre >1:640 with all other diagnostic investigations unremarkable, and a provisional diagnosis of MPA was made. Treatment with intravenous cyclophosphamide (800 mg second weekly, three doses), plasma exchange (second daily, seven sessions) and methylprednisolone (500 mg daily for 3 days, then long-course prednisolone) was started. He also received prophylactic trimethoprim/sulphamethoxazole, intravenous iron, and darbepoetin alfa.
With a substantial clinical and radiological improvement (Fig. ) he was discharged after a 29-day stay with ongoing thrice weekly haemodialysis. Renal biopsy five days after discharge demonstrated crescentic-class pauci-immune necrotizing glomerulonephritis without granulomata, consistent with MPA.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [104.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",74.66667,70.93334,78.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 104.0 mm Hg + 2/3 * 60.0 mm Hg = 74.66667 mm Hg.
Hence, the patient's mean arterial pressure is 74.66667 mm Hg."
2006,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-2737788-1,Extracted,"An 87-year-old man presented with a 1-week history of episodic, sharp and non-radiating epigastric pain. He also had abdominal bloating, anorexia, vomiting and loose stools. Three years previously, he had a laparotomy for perforated jejunal diverticula that required segmental jejunal resection and primary end-to-end anastomosis. The resection was of a 45 cm length of jejunum that contained two inflamed and perforated diverticula but the adjacent and distal 45 cm segment of jejunum containing non-inflamed diverticula was left alone. The man's other background history was of colonic diverticula disease, right inguinal hernia repair and transurethral resection of the prostate. On examination, his abdomen was distended with tenderness and guarding in the right upper quadrant but without overt peritonism as he had a soft abdomen without rebound tenderness. His pulse was regular at 117 beats per minute, blood pressure was 130/90 mmHg, and he was apyrexial. His C-reactive protein level was raised at 46 mg/L whilst his white blood cell count was within the normal limits at 7.7 × 109/L. His renal and liver function tests were normal. Erect chest X-ray did not reveal free air under the diaphragm. A computed tomography (CT) scan of the abdomen showed evidence of a localised perforation of the small bowel with multiple dilated loops of small bowel surrounding an area of marked soft tissue stranding with multiple small locules of gas, which appeared to connect to a loop of small bowel (Figure ). The CT finding, together with the presence of jejunal diverticula, was most consistent with the diagnosis of a second perforation of the jejunal diverticula.
It was felt most appropriate to treat the man conservatively as he remained stable and without features of peritonism, and so a nasogastric (NG) tube was inserted to decompress the small bowel together with administration of intravenous fluids, ciprofloxacin and metronidazole. He made a good symptomatic recovery and was discharged on the fourth day after admission on a course of oral antibiotics and has remained well since.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 90.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
2007,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-12175,Extracted,"A 24-year-old healthy male presents to the emergency room complaining of severe abdominal pain. He reports that he was playing rugby for his college team when he was tackled on his left side by a member of the opposing team. He is currently experiencing severe left upper abdominal pain and left shoulder pain. A review of his medical record reveals that he was seen by his primary care physician two weeks ago for mononucleosis. His temperature is 99°F (37.2°C), blood pressure is 90/50 mmHg, pulse is 130/min, and respirations are 26/min. He becomes increasingly lethargic over the course of the examination. He demonstrates exquisite tenderness to palpation over the left 8th, 9th, and 10th ribs as well as rebound tenderness in the abdomen. He is eventually stabilized and undergoes definitive operative management.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [50.0, 'mm hg'], 'Systolic Blood Pressure': [90.0, 'mm hg']}",63.33333,60.16666,66.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 50.0 mm Hg = 63.33333 mm Hg.
Hence, the patient's mean arterial pressure is 63.33333 mm Hg."
2008,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4531584-1,Extracted,"An 84-year-old man with end stage renal disease secondary to diabetic nephropathy for 1 year was admitted to hospital because of dyspnea and poor oral intake of 1 weeks duration. He had been diagnosed with gout 13 years previously, and had been managed at another clinic for glaucoma, diabetes mellitus and hypertension 10 years previously. He had a history of admission to our hospital due to chronic renal failure 1 year previously, after which he had not been followed up at our OPD unit. He did not have any allergic or family medical history. Physical examination at admission revealed blood pressure of 140/80 mmHg, heart rate of 107/min, body temperature of 36.8°C, and respiratory rate of 20/min; other findings were unremarkable. At that time, complete blood count revealed a hemoglobin level of 11.1 g/dL, WBC count was 24,500/mm3 (neutrophil, 93%; lymphocyte, 5%; monocyte, 2%), platelet count was 216,000/mm3, serum BUN was 143 mg/dL, Cr was 5.7 mg/dL, uric acid was 13.3 mg/dL, calcium was 9.3 mg/dL, phosphorus was 7.4 g/dL, albumin was 3.5 g/dL, alkaline phosphatase was 94 IU/L, total bilirubin was 1.1 mgf/dL, AST/ALT was 29/28 IU/L, and parathyroid hormone was 92.26 pg/mL. Urine analysis was albumin (++), blood (+), RBC count 3-5/HPF, and WBC count 20–30/HPF. Twenty-four hour urine protein level was 467 mg/day. Twenty-four hour urine creatinine clearance level was 5.4 mL/min. He was started on hemodialysis with temporary internal jugular catheter. On the twenty-fifth day after admission, a peritoneal catheter was inserted. Three weeks after peritoneal catheter insertion, he was started on peritoneal dialysis with a 6-hour exchange of 2L 1.5% peritoneal dialysate. On the ninth day after the start of peritoneal dialysis, he developed turbid peritoneal effluents with fever (38.4°C), abdominal pain and tenderness. Dialysate WBC count was 180/mm3 (neutrophil, 20%; lymphocyte, 4%; eosinophil, 76% [eosinophil count: 136/mm3]).
Complete blood count was WBC of 7,650/mm3 (eosinophil, 5.5%), hemoglobin level of 8.9 g/dL, and platelet count level of 337,000/mm3. Peripheral blood eosinophilia was not observed. Cultures of peritoneal fluid showed no growth of aerobic or anaerobic bacteria, or of fungus. AFB stain was negative. CAPD was commenced, and he was started on intraperitoneal ceftazidime (1.0 g/day) and cefazolin (1.0 g/day) with heparin at 8000 unit. After two weeks, dialysate had cleared up and clinical symptoms were improved. Dialysate WBC count decreased to 8/mm3 and eosinophils were not detected in peritoneal fluid ().
There was no recurrence of eosinophilic peritonitis on follow-up evaluation and he continued with CAPD. However, he died of sepsis and pneumonia fifteen weeks after admission.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 80.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
2009,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-8897,Extracted,"A 63-year-old woman presents to her physician with hip pain. She has had pain in both hips for almost 5 years, and it has progressed over time. She notes that it gets worse as the day goes on, making it difficult for her to walk her small dog in the evening. She has a little morning stiffness which subsides quickly after she starts to walk. In the last week, her pain became worse. The past medical history includes hypertension, hyperlipidemia, and mild hypothyroidism. She takes captopril, atorvastatin, and levothyroxine. She has also been taking acetaminophen almost every day with a dose increase up to 4,000 mg, but there is no significant decrease in pain. Both of her parents died in their 80's. The blood pressure is 135/85 mm Hg, heart rate is 74/min, respiratory rate is 12/min, and the temperature is 37.0°C (98.6°F). The BMI is 35 kg/m2. On physical examination, the leg strength is normal bilaterally. The neurological exam of both upper and lower extremities is normal. Her gait is difficult to assess due to pain. A radiograph of her left hip joint is shown in the image below.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [135.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",101.66667,96.58334,106.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 135.0 mm Hg + 2/3 * 85.0 mm Hg = 101.66667 mm Hg.
Hence, the patient's mean arterial pressure is 101.66667 mm Hg."
2010,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5758171-1,Extracted,"A 26-year-old Chinese female patient was referred to our hospital for recurrent spontaneous hypoglycemia on January 14, 2016. Complaining of palpitations, sweating, tremors, and anxiety, she was diagnosed with Graves disease at the local hospital on August 24, 2015, and prescribed methimazole 10 mg 3 times daily. She became pregnant on October 31, 2015. On November 31, 2015, she frequently developed episodes of dizziness, fatigue, cold sweat, palpitations, tremor, and symptoms of drowsiness during the night and morning. In the evening of January 14, 2016, she suddenly lost consciousness and was immediately sent to a local hospital and diagnosed with hypoglycemia based on a plasma glucose concentration of 1.9 mmol/L (normal range, 3.90–6.10 mmol/L). Her symptoms were relieved following intravenous glucose infusion. Later, she repeatedly experienced hypoglycemia (blood glucose 2.1–2.8 mmol/L) at night and early morning. Laboratory measurements were fasting C-peptide 10.56 ng/mL, 2-h postprandial C peptide 12 ng/mL, and 2-h postprandial insulin 276.53 ng/L.
To identify the reasons for hypoglycemia and to exclude islet beta cell tumor disease, the patient was referred to our hospital for further evaluation and treatment. She had no history of diabetes mellitus, hypertension, or previous exposure to insulin or oral antidiabetic agents. There was no family history of diabetes mellitus. She had a 6-month history of Graves disease and pregnancy for 10 weeks.
On physical examination at admission, her weight was 52 kg, height 1.55 m, body mass index (BMI) 21.64 kg/m2, blood pressure 104/76 mm Hg, and pulse rate 106 beats per min. The swollen thyroid was II degrees and bump texture soft, no obvious palpable nodules or tenderness, and no extra vascular murmur.
Routine laboratory blood tests of hemoglobin concentration, erythrocyte sedimentation rate, renal function, adrenocorticotropic hormone (ACTH), growth hormone (GH), liver function, and adrenal function were found to be normal (Table ). C-reactive protein, rheumatoid factor, antinuclear antibodies, and anti-dsDNA antibodies were negative. Human chorionic gonadotropin level was positive for pregnancy. The thyroid function test indicated hyperthyroidism (Table ).
At 03:00 h on January 17, 2016, blood glucose was 2.26 mmol/L and glycosylated hemoglobin was 5.4% (normal range 4.5∼6.3%). She had no history of prolonged fasting. Spontaneous symptomatic hypoglycemic occurred again soon after admission and serum insulin, blood glucose, and serum C-peptide release were measured (Fig. ). The serum levels of insulin and C-peptide were both inappropriately elevated in the presence of hypoglycemia, confirming the diagnosis of hyperinsulinemic hypoglycemia. Blood glucose monitor using the Dextrostix/Eyetone system (LifeScan Company, Johnson & Johnson, New Jersey, New Brunswick) results indicated hypoglycemia at 02:00 to 04:00 h, the lowest result was 1.65 mmol/L, but during the day glucose results were generally normal. In addition, unusually high levels of insulin autoantibodies (up to 33.69%; normal < 5%) were measured in the serum, and we assumed that these insulin-binding autoantibodies belonged to the IgG class. Anti-islet β-cell autoantibodies tests indicated that ICA, tyrosine phosphatase antibody (IAA-2), and glutamic acid decarboxylase antibody (GADA-65) were negative, but the insulin autoantibody (insulin resistance IgG antibody) level was positive (Table ).
To further identity the relationship between the serum concentrations of insulin, glucose, and C-peptide, the patient had an oral glucose tolerance test (OGTT), insulin release test, and C-peptide release test (Table ). The levels of insulin and C-peptide were markedly increased, and there was no history of exogenous insulin administration as the cause of hypoglycemia. Magnetic resonance of the abdomen and ultrasound results showed no space-occupying lesions in the pancreas. The outcomes indicated that IAS might have induced the hypoglycemia.
After inspection of the symptoms and laboratory, endocrinological, and imaging results together with no history of diabetes mellitus and hypertension, and no previous exposure to insulin or oral antidiabetic agents, we excluded insulinoma and adrenal hypofunction. Consequently, we made a diagnosis of IAS with possible methimazole association. However, pregnancy is another factor that can induce IAS.
The patient had an abortion, discontinued methimazole and switched to oral prednisone (30 mg once daily) and propylthiouracil (100 mg 3 times daily) for 3 months. During the follow-up visit after 3 months, the patient had not experienced any further hypoglycemic episodes, and prednisone was maintained at 5 mg once daily. The insulin and C-peptide levels had decreased to normal levels, and insulin autoantibodies levels were negative. The symptoms caused by Graves disease had also improved with drug treatment. The serum thyroid-stimulating hormone (sTSH) level was <0.005 mU/L, free triiodothyronine (FT3) level was 16.10 pg/mL, and free (unbound) thyroxine (FT4) was 5.58 ng/dL.
Ethical approval was not necessary because our study is a case report.
This patient signed an informed consent before publication.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [104.0, 'mm hg'], 'Diastolic Blood Pressure': [76.0, 'mm hg']}",85.33333,81.06666,89.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 104.0 mm Hg + 2/3 * 76.0 mm Hg = 85.33333 mm Hg.
Hence, the patient's mean arterial pressure is 85.33333 mm Hg."
2011,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6062715-1,Extracted,"A 52-year-old African American woman, with a past medical history of SSc diagnosed 5 years earlier and progressively worsening constipation refractory to treatment with multiple bowel regimens, presented to the Emergency Department with abdominal pain and distention, regurgitation, and intermittent vomiting for the last few weeks. She reported weight loss of roughly 10 pounds, from 115 to 105 pounds, over the last 1–2 months. She denied any recent symptoms of fevers, chills, diarrhea, blood in the stool, or black stools. She denied any recent change in her diet or any recent history of travel outside the United States. She reported that none of her family members had experienced similar symptoms. Her social history was remarkable for a former cigarette smoking history of 10 pack-years. She denied any alcohol use or illicit drug use. And, she denied any drug allergies. Two months ago, the patient had undergone esophagogastroduodenoscopy (afterward reported as normal) and colonoscopy (afterward reported a dilated lumen with no mucosal lesions).
On physical examination, the patient appeared emaciated and exhausted. She was afebrile (temperature 97.6°F) and hemodynamically stable (pulse rate 68 BPM, blood pressure 142/85 mm Hg). The abdomen was moderately distended with no tenderness. There was no guarding nor rigidity. Bowel sounds were decreased. Laboratory testing was performed and the comprehensive metabolic panel was remarkable for hypokalemia with potassium of 3.4 mEq/L (3.5–5.0 mEq/L) and hypochloremia with chloride of 94 mEq/L (96–110 mEq/L). The complete blood count was remarkable for hemoglobin of 9.6 g/dL (12.0–15.5 g/dL) with an unknown baseline, hematocrit of 29.4% (34–48%), and mean corpuscular volume of 102 fL (80–96 fL) – findings consistent with a macrocytic anemia. Thyroid function tests were within normal limits. She was later found to have several vitamin deficiencies.
Plain abdominal X-rays were performed and showed dilatation of the small and large bowel (Fig. ). Computed tomography scan of the abdomen was performed and showed marked dilatation of the small and large bowel with air-fluid levels (Fig. ). The gastric emptying study could not be performed due to intolerance and vomiting of the preparation.
The patient improved with medical treatment consisting of intravenous hydration, correction of electrolyte imbalances, and, later, total parenteral nutrition for a short time. Since then, with conservative treatment with prokinetic agents, laxatives, and occasional enemas, she has been able to tolerate small quantities of oral feeds several times each day but continues to have periods of severe constipation.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [142.0, 'mm hg'], 'Diastolic Blood Pressure': [85.0, 'mm hg']}",104,98.8,109.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 142.0 mm Hg + 2/3 * 85.0 mm Hg = 104.0 mm Hg.
Hence, the patient's mean arterial pressure is 104.0 mm Hg."
2012,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-9657,Extracted,"A 34-year-old gravida-1 at 8 weeks gestation seeks evaluation for a fever and sore throat for 3 days. She also reports generalized body pain and fatigue over this period. She was diagnosed with Graves’ disease 6 months ago. Before conception, methimazole was switched to propylthiouracil. She appears ill. The vital signs include: axillary temperature 38.0℃ (100.4℉), pulse 88/min, respiratory rate 12/min, and blood pressure 120/80 mm Hg. A 1 × 1 cm ulcer is seen on the side of the tongue. The ulcer is tender with surrounding erythema. Examination of the neck, lungs, heart, and abdomen shows no abnormalities.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",93.33333,88.66666,98,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 80.0 mm Hg = 93.33333 mm Hg.
Hence, the patient's mean arterial pressure is 93.33333 mm Hg."
2013,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3424900-1,Extracted,"A female aged 32 years presented with uncontrolled hypertension on four drugs for 5 years. She also had a history of recurrent spontaneous abortions. She had been treated for TD with steroids. Her blood pressure in both arms was 180/116 mm Hg. Abdominal examination revealed a bruit in the umbilical region. Her serum creatinine was 1.6 mg/dl, erythrocyte sedimentation rate (ESR) 18 mm/h (Wintrobe's), C-reactive protein (CRP) 4.2 mg/dl, normal hepatic functions, and a negative lupus anticoagulant. Computerized tomography (CT) scan of the abdomen showed a left kidney of 7.5 cm with poor contrast uptake, while the right kidney was 10 cm with good contrast uptake. An isotope renal diethylene triamine penta acetic acid (DTPA) scan showed global glomerular filtration rate to be 40 ml/min and differential function right: left::80%: 20%. Angiogram showed bilateral RAS (right 50% and left 90%), fusiform dilatation of abdominal aorta in infrarenal region, and early branching of the right RA []. Because of unfavorable morphology of aortoiliac region, endovascular therapy was not attempted and surgical revascularization of the right kidney was planned. The patient was not put on any steroids as her inflammatory markers were normal. On exploration, right RA was normal distally. Hepatic artery and gastroduodenal artery were exposed. A free IIA graft was taken along with origins of both anterior and posterior divisions (Y-graft) as conduit. The hepatic artery was occluded and the gastroduodenal artery was ligated and divided at its origin. The ostium was enlarged and the Y-graft was sutured end to side with the hepatic artery and end to end with both the RA branches []. The anastomosis time was 9 min and no perioperative cooling was used. The right kidney was well-vascularized on a postoperative angiogram []. Her serum creatinine was 1.4 mg/dl. She is being followed up now for last 2 years and on a single antihypertensive with normal blood pressure.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [180.0, 'mm hg'], 'Diastolic Blood Pressure': [116.0, 'mm hg']}",137.33333,130.46666,144.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 180.0 mm Hg + 2/3 * 116.0 mm Hg = 137.33333 mm Hg.
Hence, the patient's mean arterial pressure is 137.33333 mm Hg."
2014,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6942917-1,Extracted,"A 33-year-old female who was 23 weeks pregnant was transferred to our emergency department complaining of nausea and vomiting. Her past medical history included hypothyroidism from 24- to 32 years-old, which was treated with thyroid hormone intake. No depression, psychological disorders, or previous overdoses were reported. The patient had become depressed around her 20th week of pregnancy. She stated that she ingested 200 caffeine tablets containing approximately 4000 mg of caffeine obtained over-the-counter in a drugstore in a suicide attempt. Two hours after the self-poisoning, her mother found her vomiting and coughing and called emergency medical service.
On arrival at the emergency department, the patient was oriented with a Glasgow Coma Scale score of 14 (E3V5M6). She complained of a severe headache and nausea. Vital signs included respiration rate of 16 breaths per minute, blood pressure of 111/60 mmHg, heart rate of 111 beats per minute, and fever of 36.5ºC. Her pupil size was bilaterally 4 mm with prompt light reflex. No abnormalities were noted during her systemic physical examination, and neurological tests for conditions like anisocoria, paralysis, or seizures were unremarkable. Her electrocardiogram presented supraventricular tachycardia without QT prolongation. Her blood gas analysis results were: pH: 7.431; PCO2: 36.2 mmHg; HCO3: 23.5 mmol/L; and lactate: 1.29 mmol/L.
Her laboratory data was as follows: white blood cells, 10920/μL; hemoglobin, 11.6 g/dL; serum creatine kinase, 73 IU/L; sodium 136 mmol/L; potassium, 2.6 mmol/L; blood glucose 96 mg/dL; blood urea nitrogen 5.7 mg/dL; creatinine 0.66 mg/dL; total bilirubin 0.3 mg/dL; aspartate aminotransferase 19 IU/L; alanine aminotransferase 13 IU/L; and lactate dehydrogenase 170 IU/L. Although urine drug screening tests (Triage®, Biosite, San Diego, CA, USA) were negative, blood samples taken for toxicological examination on admission and revealed a high caffeine concentration (90.4 µg/mL). Fetal wellbeing was confirmed: heart rate 160 bpm, biparietal diameter 56.3 mm, abdominal circumference 17.1 cm, femur length 40.1 mm, and estimated fetal weight 564 grams.
As we diagnosed the patient with caffeine intoxication based on her interview, physical examination, and high blood caffeine concentration, gastric lavage and fluid resuscitation were performed. Since her blood pressure remained steadfastly low (systolic reading in the 80s) and she responded inadequately to catecholamine injection, after admission to the intensive care unit four hours after overdosing, CHDF with dialyzer of UT-1100 was initiated to remove caffeine from the circulation rapidly. The conditions of CHDF were as follows: blood flow rate of 80 mL/minute, filtration flow rate of 1200 mL/hr, dialysate flow rate of 800 mL/hr, and replacement flow rate of 400 mL/hr.
After 12 hours of CHDF treatment, the patient’s clinical symptoms wholly recovered, with caffeine concentration decreasing to 54.3 µg/mL. The following day, her blood caffeine concentration was 32.5 µg/mL and returned to normal undetectable levels within three days. The patient recovered without sequelae and was sent to the local hospital’s obstetrics and gynecology ward on the seventh day after her overdose, with psychological follow-up, as she was taking paroxetine, etizolam, and flunitrazepam medications. At 38 weeks, she delivered a healthy infant weighing 2796 g, who had one- and five-minute Apgar scores of 8 and 9, respectively. Currently, both the infant and mother are doing well.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [111.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",77,73.15,80.85,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 111.0 mm Hg + 2/3 * 60.0 mm Hg = 77.0 mm Hg.
Hence, the patient's mean arterial pressure is 77.0 mm Hg."
2015,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5556997-1,Extracted,"The presented case involves a 74-year-old male, Caucasian patient suffering from progressing swelling and gradually oncoming pain of the upper right extremity. No trauma was recollected. The symptoms had initially occurred the previous night. The patient denied any sore throat or congestion, dyspnea, chest pain or palpitations, abdominal pain, nausea, vomiting, diarrhea, dysuria, or rash.
The previous medical history included an excised soft tissue sarcoma of the left thigh with postoperative irradiation 5 years ago and regular follow-ups without pathological findings, as well as a benign prostatic hyperplasia and hyperuricemia. Regular medication included an uricostatic agent and an alpha receptor antagonist.
Physical examination indicated an edematous swelling of the right hand and forearm with superficial skin lesions of unknown cause, no reddening, a body temperature of 36.3 °C, a heart rate of 60 beats/min, an oxygen saturation of 94% with a respiratory rate of 19/min, and an arterial blood pressure of 156/69 mm/Hg with palpable pulses of the radial and ulnar artery, generalized tenderness upon palpation, and painfully restricted flection of all fingers. Laboratory tests showed a leukocytosis of 16,510/μl, and elevated levels for the C-reactive protein (CRP, 17.5 mg/dl) and creatine-kinase (CK, 669 U/l).
Computed tomographic imaging with application of a contrast agent (Ultravist® 300, Bayer Vital, Leverkusen, Germany) showed a generalized subcutaneous edema as well as a subfascial fluid accumulation around the musculature of the fore- and upper arm, moreover a reduction of density along the brachialis muscle. The supplying arterial blood vessels (Aa. brachialis, radialis and ulnaris) presented regularly.
Within 6 h a severe deterioration of the clinical findings occurred with progressive swelling and development of a compartment syndrome of the arm: a palm sized livid discoloration located at the medial elbow occurred, multiple blisters, a hypoesthesia of all fingers and heavy pain resistant to analgesics treatment. The radial and ulnar artery were not palpable anymore and no arterial flow was detectable using doppler sonography.
With the clinical symptoms of a compartment syndrome of the upper extremity, the patient was consequently admitted to the theater for emergency surgical exploration, debridement as well as medial and lateral fasciotomy of the fore- and upper arm. An extensive excision of the necrotic tissue was performed. Blood cultures were taken as well as multiple tissue samples for histopathologic and microbiological analyses. Predominately, the forearm flexors appeared at risk (pronator teres, flexor carpi radialis and ulnaris, flexor digitorum superficialis and profundus, palmaris longus, pronator quadratus, flexor pollicis longus). The skin and underlying fascia were affected to a lower extend and excised to healthy tissue. The resulting soft tissue defect was temporarily covered with Epigard®.
After sample collection intravenous antibiotic therapy was started with Clindamycin and Penicillin G.
Postoperatively, the patient was transferred to the ICU. Microbiological analysis revealed group A β-hemolytic streptococcus, susceptible to Clindamycin and Penicillin G, histology a bacterial interstitial myositis with necrotic muscular fibers. Consecutively, the initially elevated blood infection parameters such as leukocyte count, and C-reactive protein levels were continuously decreasing.
However, the biochemical profile showed rising CK levels (5560 U/l) which were treated by fluid resuscitation and high-ceiling diuretics in the following to prevent an imminent crush syndrome. The morning after surgery CK levels had already decreased to 3537 U/l to further drop to 514 U/l the following day and 337 U/l another day later.
Three days after primary surgery, the patient was discharged from ICU and transferred to the general surgical ward for further observation and treatment.
The patient needed ten further visits to the theater for dressing changes but minimal further debridement prior to application of dermatotraction techniques to initiate wound closure as described previously []. Dermatotraction involved vessel loops anchored to alternate edges of the wound using skin staples. Remaining soft tissue defects of the upper arm were reconstructed with a pedicled, fasciocutaneous parascapular flap, the defects of the forearm with a free, ipsilateral anterolateral thigh flap (lateral circumflexing femoral artery perforator flap) (Fig. ). On day 43 antibiotic therapy was consecutively switched to oral Ciprofloxacin and continued for 10 more days.
After a total of five sessions of plastic reconstructive surgery, the wounds healed uneventfully, and after physiotherapy the patient was discharged from hospital 63 days after admission. Follow-up appointments were scheduled on a monthly basis at first, with continuing physio- and ergotherapy.
At the final follow-up 14 months after discharge, the flaps presented vital without any signs of inflammation or infection (Fig. ). The range of motion of the affected joints was as follows: elbow: extension/flexion 0°/0°/95°, supination/pronation 60°/0°/60°. Wrist joint: extension/flexion 50°/0°/30°, abduction/adduction 20°/0°/10°. Metacarpophalangeal joints 2–4: extension/flexion 0°/20°/80°.
An active flexion of the proximal and distal interaphalangeal joints 2–4 was not possible, as the superficial and deep flexor muscles of the forearm were significantly weakened as a result of the extensive necrosectomy. The opposition of the thumb was also partially restricted, gripping and writing was however possible even though in a limited fashion.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [156.0, 'mm hg'], 'Diastolic Blood Pressure': [69.0, 'mm hg']}",98,93.1,102.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 156.0 mm Hg + 2/3 * 69.0 mm Hg = 98.0 mm Hg.
Hence, the patient's mean arterial pressure is 98.0 mm Hg."
2016,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8529302-1,Extracted,"A previously healthy 11-year-old male presented with fever, abdominal pain, and vomiting of
7 days duration. He had no significant medical history. His growth and development were
appropriate for his age. His immunizations were complete for his age. There was no travel
history. His vital signs were as follows: temperature of 36.8°C, respiratory rate of 32
breaths per minute, blood pressure of 108/70 mm Hg, and oxygen saturation of 100% on room
air. The patient was drowsy and looked sick. His physical exam showed diffuse abdominal
tenderness, distention, and rigidity. He has white blood cell count of 30,400/mm3
with 32% bands. Computed tomography (CT) of the abdomen demonstrated perihepatic large
collection consistent with abscess. He was diagnosed with complicated appendicitis.
Subsequently, he was admitted to the intensive care unit (ICU) and was started on empiric
broad-spectrum antibiotics. He underwent open laparotomy with appendectomy and drain
placement. His intrabdominal wound culture grew polymicrobial growth of Escherichia
coli, Pseudomonas Aeruginosa, Streptococcus
constellatus, and Bacteroides.
The patient improved gradually, became afebrile, and was weaned off blood pressure support
medications. His wound was closed by delayed primary closure. On post-operative day (POD) 7,
blood pressure readings were trending up gradually. The highest reported reading on POD 9
was: 164/117 mm Hg (95th percentile for age, height, and gender is 118/78 mm Hg). On POD 10,
he became drowsy and developed two episodes of tonic-clonic seizures. Seizures were treated
with intravenous lorazepam. CT of the head was done and showed hypodensities in the
bilateral subcortical parietal regions (). Subsequently, MRI, magnetic resonance arteriography (MRA), and magnetic
resonance venography (MRV) were done. These early studies showed abnormal FLAIR hyperintense
signal more prominently in the bilateral parietal regions, but also extended to the frontal
and occipital regions, mainly in the subcortical regions, with associated gyral and
leptomeningeal enhancement. There was no diffusion restriction, venous sinus thrombosis, and
no evidence of intracranial hemorrhage (). In addition, there were no ring enhancing lesions or evidence of septic
emboli.
The patient’s clinical condition improved quickly, and he returned to his normal mental
status in 24 h. Hypertension was treated with oral isradipine. Repeat MRI 48 h later showed
worsening of the subcortical FLAIR signal changes in the parietal, occipital, and frontal
regions, but a significant improvement in the appearance enhancement pattern seen on the
previous exam, still with no diffusion restriction or evidence of bleed (). The imaging findings with the
pattern of evolution of the abnormalities were more consistent with PRES. Four months later,
he was seen by pediatric nephrology where he had no reported elevated blood pressure or
neurological deficits. He had no further work up at that point since he remained
normotensive. No further follow-up imaging was obtained because patient was doing well
clinically.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [164.0, 'mm hg'], 'Diastolic Blood Pressure': [117.0, 'mm hg']}",132.66667,126.03334,139.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 164.0 mm Hg + 2/3 * 117.0 mm Hg = 132.66667 mm Hg.
Hence, the patient's mean arterial pressure is 132.66667 mm Hg."
2017,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-11710,Extracted,"A 22-year-old male presents to the emergency room complaining of neck stiffness. He reports that his neck started “locking” three hours ago. He is now unable to move it. His past medical history is notable for schizophrenia and asthma and he currently takes albuterol as well as another medication whose name he does not remember. His temperature is 99.0°F (37.2°C), blood pressure is 130/90 mmHg, pulse is 105/min, and respirations are 18/min. On physical examination, the patient appears anxious and diaphoretic. He speaks in full sentences and is oriented to person, place, and time. The patient’s neck is flexed and rotated to the right approximately 40 degrees. The right sternocleidomastoid and trapezius are firm and contracted. Extraocular movements are full and intact. Upon further questioning, he reports that he took more medication four hours ago because he was hearing voices.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [90.0, 'mm hg'], 'Systolic Blood Pressure': [130.0, 'mm hg']}",103.33333,98.16666,108.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 90.0 mm Hg = 103.33333 mm Hg.
Hence, the patient's mean arterial pressure is 103.33333 mm Hg."
2018,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5364771-1,Extracted,"A 25-year-old male weighing around 50 kg, with background history of schizophrenia, under treatment with olanzapine for 6 months presented to emergency department with somnolence and vomiting after 12 h of self-ingestion of 400 mg of olanzapine.
At presentation, his Glasgow Coma Scale (GCS) was 12/15. His pulse rate was 90 beats/per min, blood pressure 110/60 mmHg, respiratory rate 16 breaths/min, oxygen saturation 92% on room air, and temperature of 98.5°F. Respiratory, cardiovascular and per abdominal examinations were normal. All the routine laboratory parameters including complete blood count, chest X-ray, 12 lead electrocardiogram (ECG), renal function, urine routine and microscopic examination, and random blood sugar were within normal limits. Arterial blood gas showed respiratory alkalosis. CPK levels were 5780 U/L, serum alanine aminotransferase (ALT) was 146 U/L, and serum aspirate aminotransferase (AST) was 100 U/L.
He was started on normal saline 175 ml/h and vitals were monitored continuously. Urine output of over 3 ml/kg/h was aimed. He had gradual improvement in GCS over 2 days. CPK levels were 4000 U/L; ALT was 100 U/L, AST was 60 U/L on the 2nd day. CPK level was ordered daily thereafter which revealed CPK of 3000 U/L on day 3, 1500 U/L on day four and it progressively decreased to 100 U/L on day 7 []. The patient was admitted to Intensive Care Unit and then transferred to ward.
He did not receive any intramuscular injection, nor developed fever, seizure, electrolyte abnormalities during hospital stay and was discharged home after 8 days of hospital stay. He did not develop any complications during the follow-up period of 2 weeks.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",76.66667,72.83334,80.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 110.0 mm Hg + 2/3 * 60.0 mm Hg = 76.66667 mm Hg.
Hence, the patient's mean arterial pressure is 76.66667 mm Hg."
2019,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7297492-1,Extracted,"A 77-year-old man with right renal calculi measuring 1.0 × 0.8 cm underwent primary ESWL with satisfactory efficacy. Follow-up renal ultrasound showed no remaining calculi. Although he felt pain in the abdomen at the time of ESWL, he paid little attention to it. Five days later, his abdominal pain had worsened and he was admitted to the emergency department. Physical examination showed significant tenderness of the abdomen and high blood pressure of 176/105 mmHg. Enhanced computed tomography (CT) revealed a contained rupture of the abdominal aorta with a retroperitoneal hematoma (33 × 25 mm) around the periaortic area. More remarkably, a disruptive calcified plaque was found at the level between the third and fourth lumbar vertebrae (). The patient reported that his medical history included smoking, hypertension, and diabetes. Liver function, renal function, lipid and blood parameters, and other routine laboratory examination findings were within the reference range.
Preoperative CT angiography demonstrated normal morphology of the abdominal aorta, renal artery, and superior mesenteric artery. Based on the patient’s history and CT results, we suspected rupture of the abdominal aorta after ESWL. We identified the contained rupture, which was essentially a pseudoaneurysm of the abdominal aorta. The size of the hematoma was 33 × 25 mm (). Considering the risk of mortality associated with a ruptured abdominal aorta, we performed endovascular aortic repair. Preoperative preparation included strict bed rest and control of the blood pressure to less than 130/80 mmHg. The surgery was performed in the digital subtraction angiography room under general anesthesia. Open femoral exposure was performed, and a pigtail catheter was inserted to the aorta. Aortic angiography showed the location of the aortic lesions. However, no extravasation of contrast agent was found in the abdominal aorta, possibly because of a minor intimal tear.
Through the right common femoral artery, a 26-26-80-mm Ankura stent graft (Lifetech Scientific Ltd., Shenzhen, China) was placed with its proximal end immediately below the renal arteries. The stent graft was deployed successfully, and the abdominal aortic area between the third and fourth lumbar vertebrae was completely covered (). The patient had an uneventful recovery with effective blood pressure control and infection prevention measures during postoperative follow-up. One week after the operation, enhanced CT revealed that the size of the hematoma around the periaortic area had remained constant, and repeat enhanced CT 1 month later showed that the hematoma had been significantly absorbed ().
The patient was treated at our hospital from March 2012 to May 2016. During follow-up, he remained asymptomatic until he died of myocardial infarction at the age of 81 years.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [176.0, 'mm hg'], 'Diastolic Blood Pressure': [105.0, 'mm hg']}",128.66667,122.23334,135.1,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 176.0 mm Hg + 2/3 * 105.0 mm Hg = 128.66667 mm Hg.
Hence, the patient's mean arterial pressure is 128.66667 mm Hg."
2020,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-365,Extracted,"A 23-year-old woman comes to the physician because of increasing pain and swelling of her hands and wrists for 3 days. She has been unable to continue her daily activities like writing or driving. She has had a nonpruritic generalized rash for 4 days. She had fever and a runny nose one week ago which resolved with over-the-counter medication. She is sexually active with a male partner and uses condoms inconsistently. She works as an attendant at an amusement park. Her temperature is 37.1°C (98.8°F), pulse is 90/min, and blood pressure is 118/72 mm Hg. Examination shows swelling and tenderness of the wrists as well as the metacarpophalangeal and proximal interphalangeal joints. Range of motion at the wrists is limited. A lacy macular rash is noted over the trunk and extremities. The remainder of the examination shows no abnormalities. Laboratory studies, including erythrocyte sedimentation rate and anti-nuclear antibody and anti-dsDNA serology, show no abnormalities.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [118.0, 'mm hg'], 'Diastolic Blood Pressure': [72.0, 'mm hg']}",87.33333,82.96666,91.7,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 118.0 mm Hg + 2/3 * 72.0 mm Hg = 87.33333 mm Hg.
Hence, the patient's mean arterial pressure is 87.33333 mm Hg."
2021,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1764,Extracted,"A 45-year-old man with a history of epilepsy comes to the physician for a follow-up examination. He has had trouble moving the right side of his body for 2 weeks. Three weeks ago he was admitted to the hospital for a generalized convulsive seizure. He was treated with intravenous lorazepam and phenytoin; the seizure activity resolved after 50 minutes on EEG monitoring. He was discharged 2 days later after no further epileptic activity occurred. Physical examination at discharge showed no abnormalities. He has had multiple hospitalizations for similar episodes over the past year. His only medication is lamotrigine, though he says that he sometimes forgets to take it. His temperature is 37°C (98.6°F), pulse is 70/min, and blood pressure is 130/80 mm Hg. Physical examination shows right-sided hemiparesis, right homonymous hemianopsia, and receptive aphasia.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",96.66667,91.83334,101.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 130.0 mm Hg + 2/3 * 80.0 mm Hg = 96.66667 mm Hg.
Hence, the patient's mean arterial pressure is 96.66667 mm Hg."
2022,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1292,Extracted,"Two days after admission to the hospital, a 74-year-old man develops confusion and headache. He has also been vomiting over the past hour. His temperature is 36.7°C (98°F), pulse is 98/min, respirations are 22/min, and blood pressure is 140/80 mm Hg. He is lethargic and oriented only to person. Examination shows flushed skin. Fundoscopic examination shows bright red retinal veins. Serum studies show:
Na+ 138 mEq/L
K+ 3.5 mEq/L
Cl- 100 mEq/L
HCO3- 17 mEq/L
Creatinine 1.2 mg/dL
Urea nitrogen 19 mg/dL
Lactate 8.0 mEq/L (N = 0.5 - 2.2 mEq/L)
Glucose 75 mg/dL
Arterial blood gas analysis on room air shows a pH of 7.13.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg']}",100,95,105,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 80.0 mm Hg = 100.0 mm Hg.
Hence, the patient's mean arterial pressure is 100.0 mm Hg."
2023,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6503651-4,Extracted,"A 15-year-old boy was an unrestrained passenger in the rear seat of a vehicle which struck a tree at high speed. He was found outside of the vehicle and was transported to the ED by EMS. On arrival to the ED, he was moaning and had a Glasgow Coma Scale of 8, facial abrasions, bleeding from both ears, diminished breath sounds on the left, cool extremities, and palpable pulses. Initial vital signs were HR, 141 BPM; RR, 35 breaths per minute; BP 140/69 mmHg; and O2 saturation, 81%. He was immediately intubated. Chest x-ray and focused assessment with ultrasound for trauma exam revealed hemothorax with tension pneumothorax on the left. Needle decompression was performed and a thoracostomy tube was placed with the return of fresh blood. He became hypotensive with a BP of 71/51 mmHg. Two liters of normal saline were infused by LifeFlow through a left antecubital 18-gauge IV catheter, each over approximately 5 mins, with an increase in BP to 110/56 mmHg. He was transported to the pediatric intensive care unit and did not require blood transfusion until hospital day 3. Additional injuries included traumatic brain injury with temporal bone fracture, rib fractures, and pulmonary contusion. He made a complete recovery and was discharged within two weeks.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [69.0, 'mm hg']}",92.66667,88.03334,97.3,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 69.0 mm Hg = 92.66667 mm Hg.
Hence, the patient's mean arterial pressure is 92.66667 mm Hg."
2024,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8380438-1,Extracted,"A 36-year-old man was admitted to Shonan Kamakura General Hospital because of heart failure, lung edema, and a severely elevated blood pressure (BP) of 224/116 mmHg. Although he had a multiyear history of hypertension, sufficient BP control was not achieved until admission. His serum creatinine level was 1.5 mg/dL 10 months before admission.
Laboratory tests showed serum creatinine of 7.56 mg/dL, lactate dehydrogenase of 1366 U/L, and hemoglobin of 8.2 g/dL. Peripheral blood smear showed schistocytes. An abnormal signal in the cerebrum in T2-weighted magnetic resonance imaging and Keith-Wagener stage IV retinopathy were also noted. Kidney biopsy revealed severe narrowing or occlusion of small arteries with severe endothelial damage as well as shrunken glomeruli and interstitial cell infiltration (Figure ). Compared with normotensive normal kidney tissue that showed isometric nuclei of vascular endothelial cells (ECs) forming an orderly line (Figure ), varying sized EC nuclei were prominent, and there were fewer nuclei within the arterioles in the patient (Figure ), indicating severe vascular EC damage due to severely elevated blood pressure. Based on the above findings, we diagnosed this patient's AKI as acute with chronic ischemic renal damage due to refractory hypertension with microangiopathic hemolysis. He was intensively treated by intermittent hemodialysis, and his heart failure and accompanying pulmonary congestion gradually improved.
Although BP control by nicaldipine and olmesartan allowed hemodialysis withdrawal after six treatment sessions, the serum creatinine level remained high. After written informed patient consent, we performed autologous CD34-positive cell transplantation for AKI. This was the first case in a phase I/II clinical trial of autologous G-CSF-mobilized peripheral blood CD34-positive cell transplantation for severe AKI with a CD34-positive cell dose-escalating protocol (trial number jRCTb030190231) to evaluate the safety and efficacy as primary and secondary endpoints, respectively. In this trial, three doses (into one renal artery) were set: low dose (5 × 105/kg body weight), middle dose (1 × 106/kg body weight), and high dose (2 × 106/kg body weight) for three patients in each group. After safety was confirmed, the dose of CD34-positive cells was increased to the next higher dose. The low starting dose (5 × 105/kg body weight, ie, 1 × 106/kg body weight, bilateral renal arteries) was based on a consideration of safety in previous reports that used CD34-positive cells for other diseases, including critical limb ischemia and liver cirrhosis. This dose-escalating protocol was approved by the special committee for class 2 regenerative medicine certified by the Ministry of Health, Labor, and Welfare in Japan (SKRM-2-003). After 800 μg/d (400 μg/m2 body surface area) of G-CSF treatment for 5 consecutive days, leukapheresis (COMTEC, Fresenius Kabi Japan Co., Tokyo, Japan) was performed to harvest peripheral blood mononuclear cells on day 5. Magnetic separation of CD34-positive cells using a CliniMACS instrument was performed on day 6 using anti-CD34 antibody-labeled magnetic nanobeads (Miltenyi Biotec, Bergisch Gladbach, Germany). Immediately after CD34-positive cells were separated and the viability (98.1%) and purity (95.6%) of collected cells were confirmed, 90 million CD34-positive cells were dissolved in 100 mL saline. A guiding catheter was placed in either renal artery through right femoral artery by an interventional radiologist. Cells were directly administered into each renal artery (45 million CD34-positive cells in 50 mL saline) at a rate of 150 mL/h (90 million CD34-positive cells in total) using a syringe driver.
The patient's general condition was unremarkable except for a transient elevation in body temperature to 38.1°C 5 days after transplantation. Platelet count and serum levels of interleukin (IL)-6 and IL-8 transiently increased during the early post-treatment course (Table ). The patient was discharged to home 10 days after cell transplantation.
Twenty-three weeks after cell therapy, his serum creatinine level was 2.96 mg/dL. Blood pressure was well controlled with 60 mg of nifedipine and 20 mg of olmesartan.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [224.0, 'mm hg'], 'Diastolic Blood Pressure': [116.0, 'mm hg']}",152,144.4,159.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 224.0 mm Hg + 2/3 * 116.0 mm Hg = 152.0 mm Hg.
Hence, the patient's mean arterial pressure is 152.0 mm Hg."
2025,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5287175-1,Extracted,"A 65-year-old woman with dyspnea was admitted to our hospital. Two years prior, she was diagnosed with a rheumatic valvular heart disease with moderate mitral stenosis and mild mitral regurgitation (MR). Over the years, her HF symptoms progressed and left ventricular ejection fraction (LVEF) worsened, despite guideline-directed optimal medical treatment, including angiotensin-converting enzyme inhibitors, diuretics and beta blockers. One year prior to admission, coronary computed tomography angiography was performed to rule out myocardial ischemia; significant stenosis was not noted. Echocardiography showed severe LV dysfunction with an LVEF of 25%, and her LV end-diastolic diameter was 72 mm ( and in the online-only Data Supplement). Severe MR was noted, which was mainly due to dilation of the LV. The effective regurgitant orifice of the mitral valve was 45 mm2, and the regurgitation volume was 43.6 mL. Dyssynchronous cardiac motion was also observed on echocardiography. Twelve-lead electrocardiogram (ECG) revealed atrial fibrillation, left bundle branch block, and prolonged QRS duration of 141 ms (). After admission, HF was aggravated and pulmonary edema () developed, along with acute kidney injury. Although high doses of dopamin, and norepinephrine were continuously infused, the blood pressure plummeted to 63/41 mmHg and heart rate (HR) was 105 bpm. Ischemic colitis developed with prolonged low cardiac output status. Mechanical circulatory support was started using venoarterial (VA) ECMO via cannulation of the femoral artery and vein. The patient's hemodynamic status stabilized with ECMO support having a flow rate of 2.5-3.0 L/min.
Volume overload, dyssynchrony, and increased MR are known to aggravate HF; ultrafiltration and continuous renal replacement therapy were therefore performed. However, there was no improvement in hemodynamic status even after 8 L of body fluid was removed. Echocardiography revealed persistent severe MR and a dilated inferior vena cava with low collapsibility, which are consistent with increased central venous pressure. Despite mechanical circulatory support with ECMO for 6 days, tachycardia (maximum HR rate 150 bpm) persisted, and ECMO flow was increased to 3.3 L/min. Amiodarone was started to control rapid ventricular response. Although the ventricular rate reduced to 70-80 bpm after amiodarone infusion, the ECMO flow could not be reduced below 2.9 L/min.
Biventricular pacing with atrioventricular (AV) node ablation was simultaneously performed while the patient was still under ECMO support, using a Quadra Assura™ CRT-D device (St. Jude Medical, St. Paul, MN, USA). Using a 0.14 inch guide wire, a quadripolar LV lead (Quartet™ lead; St. Jude Medical, St. Paul, MN, USA) was placed in the lateral branch of the coronary sinus after superselecting the cardiac vein. The selection of coronary vein was performed to enable the longest electrical delay. Under fluoroscopic guidance, a single-coil implantable cardioverter defibrillator lead was positioned in the apical septum. A right atrial lead was not implanted due to atrial fibrillation. We ablated the bundle at the His region, using a 3.5 mm tip deflectable ablation catheter. Radiofrequency energy at 25-30 watts was applied to the bundle. AV block was noted after AV node ablation, and complete biventricular capture was achieved. The first LV lead threshold was 2.25 V/0.5 ms and the impedance was 290 ohm; the right ventricular lead threshold was 0.75 V/0.5 ms and the impedance was 380 ohm. Each pacing output was 3.0 V, 2.5 V. Biventricular pacing was done over 80 bpm. The lower boundary ventricular tachycardia zone was programmed to 330 ms (181 bpm), while the ventricular fibrillation zone was set to 270 ms (222 bpm).
LV systolic function recovered, and chamber size decreased, immediately after implantation of the CRT device. The inferior vena cava decreased in size with high collapsibility; however, the amount of MR did not change compared to the previous examination. After five days, pulmonary edema and cardiomegaly improved (). ECMO weaning was successful, and LV function and chamber size were further improved on predischarge evaluation: QRS duration was 132 msec (), LVEF 42%, and LV end-systolic dimension 60 mm ( and in the online-only Data Supplement). The patient was discharged under treatment, after prescribing angiotensin II receptor blocker, diuretics, and beta blockers; there were no further recurrences of cardiogenic shock or symptoms of HF ( in the online-only Data Supplement).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [63.0, 'mm hg'], 'Diastolic Blood Pressure': [41.0, 'mm hg']}",48.33333,45.91666,50.75,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 63.0 mm Hg + 2/3 * 41.0 mm Hg = 48.33333 mm Hg.
Hence, the patient's mean arterial pressure is 48.33333 mm Hg."
2026,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-5943,Extracted,"A 33-year-old man with a history of IV drug and alcohol abuse presents to the emergency department with back pain. He states that his symptoms started 3 days ago and have been gradually worsening. His temperature is 102°F (38.9°C), blood pressure is 127/68 mmHg, pulse is 120/min, respirations are 17/min, and oxygen saturation is 98% on room air. Physical exam is notable for tenderness over the mid thoracic spine. Laboratory values are only notable for a leukocytosis and an elevated ESR and CRP.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [127.0, 'mm hg'], 'Diastolic Blood Pressure': [68.0, 'mm hg']}",87.66667,83.28334,92.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 127.0 mm Hg + 2/3 * 68.0 mm Hg = 87.66667 mm Hg.
Hence, the patient's mean arterial pressure is 87.66667 mm Hg."
2027,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-1689,Extracted,"A 40-year-old woman comes to the physician for the evaluation of fatigue, poor appetite, and an unintentional 10-kg (22-lb) weight loss over the past 6 months. The patient also reports several episodes of nausea and two episodes of non-bloody vomiting. There is no personal or family history of serious illness. Menses occur at regular 27-day intervals and last 6 days. Her last menstrual period was 3 weeks ago. She is sexually active with her husband, but states that she has lost desire in sexual intercourse lately. Her temperature is 37°C (98.6°F), pulse is 100/min, and blood pressure is 96/70 mm Hg. Physical examination shows no abnormalities.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [96.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",78.66667,74.73334,82.6,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 96.0 mm Hg + 2/3 * 70.0 mm Hg = 78.66667 mm Hg.
Hence, the patient's mean arterial pressure is 78.66667 mm Hg."
2028,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8053007-1,Extracted,"A 66-year-old male with a past medical history of hypertension presented to the emergency room with acute-onset chest pain and shortness of breath. He had been diagnosed with COVID-19 nine days prior after developing fever and cough, but those symptoms had since resolved. The patient complained of fatigue and reduced oral intake following his diagnosis of COVID-19. He had no family history of VTE, no recent travel, no recent surgery or immobilization, and was up to date with his cancer screening. On examination, the patient was in no distress. Vital signs on admission were as follows - temperature: 98 ℉; heart rate: 97 beats/minute; blood pressure: 92/64 mmHg; respiratory rate: 20 breaths/minute; and oxygen (O2) saturation: 87% on room air. The physical examination was normal except for elevated jugular venous pressure. Investigations including complete blood count, basic metabolic panel, lactate dehydrogenase, ferritin, and lactic acid levels were normal. D-dimer was elevated at 8,583 ng/mL, C-reactive protein was 62.4 mg/L, and troponin was 0.44 ng/mL. Chest CT angiogram (CTA) revealed large filling defects in the right and left main pulmonary arteries with right heart strain (Figure ). No lung infiltrates were present (Figure ). Ultrasound of lower extremities revealed DVT of the left proximal femoral vein (Figure ).
The patient was administered 500 ml of normal saline with improvement in blood pressure to 126/74 mmHg. O2 saturation improved to 96% on O2 at 3 L/minute via nasal cannula. Anticoagulation with intravenous heparin was started. Due to concern for additional PE burden from his extensive DVT, an inferior vena cava filter was placed. Over the next 24 hours, his symptoms and hypoxia improved, and he was subsequently discharged on apixaban.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [126.0, 'mm hg'], 'Diastolic Blood Pressure': [74.0, 'mm hg']}",91.33333,86.76666,95.9,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 126.0 mm Hg + 2/3 * 74.0 mm Hg = 91.33333 mm Hg.
Hence, the patient's mean arterial pressure is 91.33333 mm Hg."
2029,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-8383615-1,Extracted,"A 20-year-old man with no significant past medical history presented with palpitations after ingesting 2 g of methamphetamine. He soon after became obtunded and was intubated for airway protection. He was later found to be hypertensive with a pressure of 160/86 mm Hg, hyperthermic with a temperature of 42 °C and tachycardic with a heart rate of 112 beats per minute. A few hours later, the patient was found to be hypotensive with a pressure of 82/59 mm Hg with minimal response to fluids, central line was placed and patient was started on norepinephrine. Physical exam showed an obtunded individual, with normal breath sounds in bilateral lung fields and an increased heart rate, with normal rhythm without murmurs.
On admission, the patient’s urine toxicology was positive for amphetamines, and laboratory findings (labs) showed an aspartate transaminase (AST) of 121 IU/L with an alanine transaminase (ALT) of 32 U/L and a protime/prothrombin time (PT) of 19.4 s with a partial thromboplastin time (PTT) of 36.5 s with an international normalized ratio (INR) of 1.61, and a normal bilirubin.
Poison control was contacted and recommended supportive care with the initiation of NAC. Intravenous (IV) NAC loading dose followed by a maintenance dose was started around 6 h after admission.
Within 24 h of admission, the patient started to develop multi-organ failure including ALF with an AST of 1,324 IU/L, an ALT of 217 U/L, a PT of 25.8 s, a PTT of 43 s, an INR of 2.32 and a bilirubin of 0.6 mg/dL. On day 3 of hospital admission, the patient’s labs showed a bilirubin of 1.6 mg/dL, an AST of 2,350 IU/L, an ALT of 2,145 U/L, an INR of 3.19, a PTT of 44.8 s and a PT of 33.1 s. Conversely, his serum total protein and serum albumin reached a nadir around the same time period.
After 3 - 4 days of NAC therapy, there was a significant recovery in liver enzymes. The starting of normalization of AST, ALT and PT/INR/PTT was observed by day 5.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Diastolic Blood Pressure': [86.0, 'mm hg'], 'Systolic Blood Pressure': [160.0, 'mm hg']}",110.66667,105.13334,116.2,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 160.0 mm Hg + 2/3 * 86.0 mm Hg = 110.66667 mm Hg.
Hence, the patient's mean arterial pressure is 110.66667 mm Hg."
2030,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3520695-1,Extracted,"A comatose 56-year-old Japanese man with no significant familial medical history was admitted to the emergency room. He delivered newspapers and usually consumed alcohol two hours before delivery. According to colleagues, during his usual morning routine, he suddenly fell on his back. On admission, his temperature was 36.0°C, pulse rate 77 beats/min, blood pressure 153/94mmHg and Glasgow Coma Scale score was E2V2M1. On examination, splenohepatomegaly was detected, but heart murmur, chest rales, tongue biting, incontinence, diaphoresis, seizure, and xanthoma were not evident. He maintained a balanced diet and was not obese (height 164cm, weight 58.8kg and body mass index 21.9kg/m2).
Arrhythmia was not detected on admission. Laboratory test results revealed high blood glucose (28.2mmol/L), high glycated hemoglobin (11.4 percent), considerably high serum lipid levels (triglycerides 171.5mmol/L, total cholesterol (T-Chol) 17.7mmol/L, high-density lipoprotein (HDL) 0.5mmol/L, low-density lipoprotein (LDL) 1.9mmol/L and type V hyperlipoproteinemia (Figure 
), and slightly elevated liver enzyme levels. Serum osmotic pressure was 356mOsm/L, and alcohol concentration was 15.1mmol/L. His white blood cell count, electrolyte levels (Mg, inorganic phosphorous, and Ca), C-reactive protein level, renal function, NH3 level, coagulation (prothrombin time/international normalized ratio, activated partial thromboplastin time, fibrinogen, fibrin/fibrinogen degradation products), thyroid function, urine drug levels, vitamin levels, pyruvic acid level, and β-hydroxybutyric acid level were normal. Venous blood gas was almost normal (pH 7.389, pCO2 38.7mmHg, pO2 102.6mmHg, HCO3 22.8mmol/L, anion gap 14.3 and base excess −1.8mmol/L). Plasma viscosity was 1.90mPa/s (normal range 1.10 to 1.30mPa/s at 37°C; Lovis 2000 M/ME, Anton Paar, Graz, Austria), as observed later. Results of electrocardiography, chest radiography, brain computed tomography (CT), chest and abdominal contrast-enhanced CT, diffusion-weighted magnetic resonance imaging, magnetic resonance angiography including examination of the cervical internal carotid arteries, electroencephalography, and auditory brainstem response testing were normal. Cultures of blood, urine, and cerebrospinal fluid were negative. Fundus examination was not performed. Hyperglycemia immediately decreased following isotonic saline infusion with no insulin therapy. By contrast, triglyceride levels gradually decreased after administration of intravenous fluids. Our patient’s consciousness level improved gradually over three days (Figure 
). All serum lipid levels decreased seven days after admission (triglycerides 12.8mmol/L, T-Chol 9.5mmol/L, HDL 0.7mmol/L, and LDL 6.3mmol/L).",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [153.0, 'mm hg'], 'Diastolic Blood Pressure': [94.0, 'mm hg']}",113.66667,107.98334,119.35,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 153.0 mm Hg + 2/3 * 94.0 mm Hg = 113.66667 mm Hg.
Hence, the patient's mean arterial pressure is 113.66667 mm Hg."
2031,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7941952-1,Extracted,"A 43-year-old female was referred to our department for evaluation of recurrent febrile attack for 3–4 days, leg pain, and urticarial eruption. No family history of recurrent febrile attack was reported. Three years before the visit, a weekly febrile attack of > 39 °C occurred that lasted 3–4 days. Her symptoms started with urticarial rash in the trunk and legs associated with high fever and progressing leg pains. The urticarial rash initially occurred once every 2 weeks but gradually increased in frequencies. Febrile attacks were accompanied with coxalgia and urticarial eruption not resolved after the fever declined. On physical examination, her blood pressure was 120/72 mmHg, pulse rate was 92 beats/min and respiratory rate 24/min. Chest and abdominal examinations revealed no findings; however, a tenderness was observed in the left hip joint. The temperature at the first visit was 37.1 °C; however, she presented with febrile attack (> 39 °C) 10 days before the first visit. The urticarial rash appeared over the entire body, including the trunk and both upper and lower extremities (Fig. ). It had aggravated by coldness and accompanied by arthralgia and bone pain of both femurs. The febrile attack lasted for 3–4 days, whereas urticarial rash did not resolve completely. Laboratory findings showed leukocytosis (11,900/μl) and elevated C-reactive protein levels (6.18 mg/dl) and serum amyloid A (SAA, 32.5 μg/ml). Markers for autoimmune diseases, including an anti-nuclear antibody and anti-neutrophil cytoplasmic antibody were negative. There was no M protein in immunoelectrophoresis. Liver and renal functions were negative. Serological testing was negative for HBV, HCV, and Syphilis. Neither cytomegalovirus antigenemia nor EBV or Parbovirus B19 DNA were detected. Interferon γ release assay for Mycobacterium tuberculosis infection (T-SPOT) and B-D-glucan tests were both negative. Although one of the diagnostic criteria for SchS requires findings of monoclonal gammopathy, serum immunoelectrophoresis showed no evidence of monoclonal gammopathy. In addition, bone marrow aspirates showed no abnormality.
PET/CT showed the diffuse fluorodeoxyglucose (FDG) uptake in the bone marrow of both femoral and pelvic bones (Fig. a). MRI of both femurs (Fig. c-d) show diffusely abnormal signal in the medullar bone of both femoral bones. Histological findings of the biopsied urticarial lesions showed a neutrophilic urticarial dermatosis demonstrating perivascular and interstitial neutrophilic infiltrations without leukocytoclastic vasculitis (Fig. ). Based on the urticarial rash, recurrent fever, abnormal bone remodeling with bone pain, and elevated acute phase reactants, SchS was suspected, despite the absence of monoclonal gammopathy. The patient had been treated with high-dose prednisolon, antihistamines, omarizumab, and cyclosporine A; however, she was unresponsive to these various treatments. The observation that she did not respond to any conventional medications indicated the possibility of autoinflammatory diseases. Therefore, written informed consent for gene analysis for autoinflamatory genes was obtained from the patient, and the ethical approval for the study was obtained from the Fukushima Medical University Ethics Committee for this retrospective study (No 2019–188) and in accordance with the Declaration of Helsinki. In order to exclude the mutations in the genes of autoinflammatory diseases, the genetic screening was performed in genomic DNA samples from the patient whole blood under analysis by next-generation sequencing. A panel was created to identify possibly disease-causing mutations in 14 autoinflammation/immune-related genes (MEFV, TNFRSF1A,NLRP3,NLRP12,VK,PLCG2,NOD2,TMEM173,PSMB8,PSMA3,PSMB4,PSMB9,POMP,NLRC4). However, neither mutation nor rare variant was found in these genes (data not shown). Despite the lack of diagnostic criteria for the typical SchS (absence of monoclonal gammopathy) and CAPS (absence of NLRP3 mutation or somatic mosaicism), we did not exclude the possibility of antoinflammatory diseases including SchS. Neutrophilic urticarial with systemic inflammation (NUSI) characterized by urticarial skin lesions with neutrophilic infiltration likely mediate by IL-1 []. The differential diagnosis of NUSI should be considered in this case with antihistamine or immunosuppressant-resistant urticaria with systemic inflammation []. Exclusion of known inflammatory diseases is necessary for the diagnosis of NUSI []. Although inflammatory arthritis could be associated with NUSI [], bone pain with bone remodeling, one of the clinical findings of SchS, may not be present with NUSI. The lack of monoclonal gammopathy does not necessarily deny SchS because monoclonal gammopathy may not be present at disease onset []. She fulfilled the diagnostic criteria for SchS except monoclonal gammopathy.
After these extensive diagnostic workouts, the SchS diagnosis was suspected by bone pain with compatible imaging findings.
Recent guideline suggests a diagnosis of IL-1-neduated autoinflammtory disease such a situation []. She suffered from sustained recurrent fever, urticarial rash, and bone pain with the elevated levels of acute phase reactants for more than 3 years. The association of AA amyloidosis was reported in untreated patients with SchS [] sustaining elevations of acute phase reactant, SAA, contribute to the AA amyloidosis development as a precursor protein for AA amyloid [].
Therefore, Il-1β monoclonal antibody, canakinumab (Iralis<, Novartis) 150 mg was subcutaneously injected with a 4-week interval. Skin rash and bone pain were resolved within 2 days of the first injection. Inflammatory markers, such as CRP and SAA, were normalized after 7 days from the first injection. The patient noticed significant improvement and recurrent febrile attack was completely disappeared.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [72.0, 'mm hg']}",88,83.6,92.4,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 72.0 mm Hg = 88.0 mm Hg.
Hence, the patient's mean arterial pressure is 88.0 mm Hg."
2032,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-5770871-1,Extracted,"A 38-year-old woman with significant MS, history of ischemic stroke, and hypertension was admitted for PMBV.
In echocardiography LA enlargement to 30.0 cm2, thickening of mitral leaflets and subvalvular apparatus, fusion of posterior commissure were observed. Mitral valve area (MVA) was 0.8 cm2 by the pressure half-time (PHT) formula. Trans-mitral gradient was 21.7/10.5 mm Hg maximum and mean, respectively. The standard PMBV with the Inoue balloon was initiated via the right femoral vein. Atrial septum puncture was performed under transesophageal echocardiography (TEE) guidance. In the case of LA enlargement the right atrium is pushed to the front. So, as in the typical place of puncture the ascending aorta might be present, we usually puncture the atrial septum slightly posteriorly. Then hemodynamic measurements were made. After having placed the balloon in the LA, all of the maneuvers aiming to cross the mitral valve orifice with the balloon failed. During the second approach, a modified PMBV technique was used with a transseptal veno-arterial loop serving as a rail for the balloon’s entry into the LV (). The TEE-guided atrial septum puncture was performed again. The dedicated 6 Fr Swan-Ganz catheter, with 0.035 mm lumen, was introduced to the LA and next to the left ventricle (LV), through which a 300 mm long, 0.035 inch wire was advanced from the LA into the LV. Using the arterial access, a Multi-snare loop (PFM Medical, Germany) was advanced in a retrograde fashion through a 6 Fr-JR guide catheter into the ascending aorta and directed into the LV. Then the wire tip was caught with it and pulled out through the guide catheter and arterial sheath, completing the veno-arterial loop. The next steps of PMBV were done using the standard approach. The Inoue balloon was advanced over a 0.035 inch wire across the mitral valve and dilated to 28 mm. The procedure was successful. Pulmonary artery pressure decreased from 105/32/65 mm Hg to 58/25/37 mm Hg, systolic/diastolic/mean, respectively. The fluoroscopy time was 39 min.
Trans-mitral gradient decreased to 13/5.3 mm Hg (maximum/mean) and MVA increased to 1.25 cm2 by the PHT formula and 1.6 cm2 by planimetry.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [105.0, 'mm hg'], 'Diastolic Blood Pressure': [32.0, 'mm hg']}",56.33333,53.51666,59.15,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 105.0 mm Hg + 2/3 * 32.0 mm Hg = 56.33333 mm Hg.
Hence, the patient's mean arterial pressure is 56.33333 mm Hg."
2033,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6981339-1,Extracted,"A 66-year-old woman with a history of controlled hypertension presented with IED 1 month after PCI and the stenting of the left anterior descending artery and the right coronary artery while taking ASA (80 mg daily) and clopidogrel (75 mg daily). The patient presented to the emergency department with severe sudden-onset retrosternal chest pains with radiation to the interscapular region associated with odynophagia and dysphagia. She had 1 episode of hematemesis shortly after presentation. She had neither a history of hard food or foreign body ingestion nor trauma before presentation.
Electrocardiography (ECG) and laboratory studies were obtained. The ECG showed a normal sinus rhythm with no significant abnormality. She was hemodynamically stable at presentation with a heart rate of 80 beats per minute, blood pressure of 140/90 mmHg, and a respiratory rate of 18 breaths per minute. No fever was detected. In the physical examination, the patient was conscious and complained of retrosternal chest pains. The cardiac examination was unremarkable, and the lung examination revealed reduced respiratory sounds in the base of the right lung with dullness on percussion in that region. The abdominal examination demonstrated no tenderness or organomegaly. The examination of the peripheral and carotid pulses indicated no abnormality. The laboratory data showed a hemoglobin level of 11.6 g/dL.
Given the possibility of acute aortic syndromes, computed tomography angiography (CTA) was performed. The CTA demonstrated no significant abnormalities in the aortic or peripheral arteries, but it illustrated a large mass-like area along the posterior aspect of the thoracic esophagus and mild bilateral pleural effusion (more at the right side) ( and ).
The patient was transferred to the intensive care unit (ICU), where an urgent gastroenterology consult was requested and, consequently, an upper gastrointestinal endoscopic examination was performed. It depicted a long segment of esophageal denudation with no active bleeding. No bleeding site was reported in the stomach or the duodenum.
ASA and clopidogrel were discontinued, and the patient underwent conservative management in light of the cessation of active bleeding.
Laboratory tests were repeated while the patient was in the ICU 8 hours after presentation; they were within the normal limits except for hemoglobin (8.9 g/dL). A chest roentgenogram revealed mild right-sided pleural effusion. Other laboratory tests including coagulation tests, troponin, platelet, and white blood cell counts were within the normal limits. Serial hemoglobin levels were checked, and the patient was observed for recurrent bleeding during hospitalization. She had melena on the first day of hospitalization. She was retained in the ICU for 2 days and then transferred to the ward. There were no signs of recurrent bleeding and no further reductions in the hemoglobin level. Accordingly, ASA (80 mg daily) and clopidogrel (75 mg daily) were initiated.
The patient was discharged home after 4 days of uncomplicated hospitalization on the mentioned antiplatelet regimen. CTA was done 2 months after discharge and showed the complete resolution of the intramural esophageal hematoma.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
2034,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3838205-1,Extracted,"A 21-year-old female with a known history of aHUS presented to our emergency department in September 2012. She complained of general aches and pains consistent with her previous episodes of aHUS. She had three relapses before when she was aged 8, 10, and 20. They all occurred in September. She presented with 3 days of fever and sore throat followed by dark urine. On examination, she was found to be afebrile, alert, oriented, and she was talking in full sentences. Her sitting blood pressure was 140/90 mmHg and her heart rate was 70 beats per minute with an oxygen saturation of 99% on room air.
Hematological investigations revealed a hemoglobin (Hb) count of 96 g/L, platelet count 16 × 109/L, red cell count 3.01 × 1012/L, and a hematocrit of 0.27 L/L. These results were consistent with normochromic normocytic anemia with mild polychromasia. There was also marked thrombocytopenia and microangiopathic anemia on the film, features suggestive of relapse of known HUS. Biochemistry results showed a lactate dehydrogenase (LDH) level of 1,201 U/L, haptoglobin <0.06 g/L, potassium 3.7 mmol/L, urea 20.7 mmol/L, creatinine 202 umol/L, estimated glomerular filtration rate 27 mL/minute, and C-reactive protein (CRP) of 27 mg/L. High levels of LDH and low haptoglobin levels pointed to severe hemolysis while the renal markers, such as creatinine, urea, and estimated glomerular filtration rate showed a deteriorating renal function. Earlier attempts to perform the biochemical tests had been futile due to severe hemolysis.
After a multidisciplinary team collaboration that involved the Intensive Care Unit, Hematology, Nephrology, and the Emergency Department, a left femoral vascath was inserted with the view of commencing TPE using 3 L of fresh frozen plasma (FFP). The procedure was scheduled to be done in the emergency department using a membrane based TPE machine (mTPE). Plasma FLUX PSu 2S plasma exchange filters manufactured by Fresenius SE & Co (Bad Homberg, Germany) were used. These filters have a surface area of 0.6 m2, blood priming volume of 70 mL, and a plasma sulphone membrane. Filtration is primarily based on pressure gradients allowing filtration of molecules of up to 1,000 kDa including immunoglobulins, complement factors, and albumin. Soon after commencing TPE, the machine showed a blood leak alarm and it was evident that the membrane had ruptured gauging by the color of the effluent (). The filter was replaced with another one which also did not last long before the machine showed a blood leak alarm. The procedure was aborted after exchanging only three bags of FFP. An attempt was made to resume treatment with a centrifuge based TPE machine (cTPE). The centrifugal device we used was a Spectra Optia Apheresis System, a product of Terumo BCT (Lakewood, CO, USA). This machine operates by separating blood products according to their specific gravity using centrifugal force. The spill over alarm persisted on cTPE and “red blood cell detected” was shown on the machine. At this point, it was agreed to stop TPE due to the nature of the technical problems which were attributed to severe hemolysis.
On day 2, it was agreed that the patient could be treated with eculizumab (complement C5 blocker), but the drug was not available for compassionate access. We then revisited cTPE and the consultant overseeing our cTPE machine was contacted. We were advised to “disable” the red blood cell detector and cTPE was initiated successfully using a very low inlet flow rate ranging from 20–70 mL/minute with an anticoagulant infusion rate of 1.0 mL/minute. Heavily hemolyzed effluent was noted (). The patient continued to receive daily cTPE until day 16 when a decision was made that she had reached clinical remission, and she was discharged home. Her hematological () and biochemical () results continued to improve. A follow up of this patient after 6 weeks revealed that she was clinically well and had resumed her normal daily routines. However, plans had been made for her to have a permanent vascular access in the form of an arterio-venous fistula (AVF) in the setting of these recurrent aHUS episodes which seem to resolve after aggressive TPE treatment.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
2035,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-7568822-1,Extracted,"A 27-year-old man (75 kg) presented to our emergency department and was monitored by a cardiologist. Dissection occurred following weightlifting across his chest and shoulders. He described multiple episodes of faintness over the preceding hours. These were associated with sweating, dyspnea, and temporal right eye vision deficit. The first episode began during heavy weight lifting (180 kg) and lasted 10 minutes before resolving with rest and drinking fluids. The second episode began while lifting weights again, which was more intense in severity and lasted for 20 minutes. The third fainting episode occurred when he left the gym, whereby he fell over the floor outside the club. The patient was a coach and a professional bodybuilder. During the first lifting, he remembered weight training heavier than his normal regimen involving squatting with weights of around 140 kg in the supine position across the anterior chest wall. He initially denied taking illicit drugs but, upon insistence, he confessed that he took intramuscular 250 mg testosterone twice per week and human growth hormone 20 mg/day for two years. In the emergency room, the patient’s vital signs were a blood pressure of 90/60 mmHg, heart rate of 120 beats/min, respiratory rate of 26 breaths/min, and temperature of 36 oC. Blood chemistry revealed increased levels of cardiac troponin (up to 7.6 ng/mL) and creatine kinase (CK) (up to 597 IU/L). Transthoracic echocardiography (TTE) revealed ascending aorta dissection with severe aortic regurgitation. The patient underwent emergency cardiac surgery.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg']}",70,66.5,73.5,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 90.0 mm Hg + 2/3 * 60.0 mm Hg = 70.0 mm Hg.
Hence, the patient's mean arterial pressure is 70.0 mm Hg."
2036,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-3603612-1,Extracted,"A 4-year-old girl was referred to our hospital with hypertension and suspected aortic coarctation. She was a full-term normal delivery without any antenatal or postnatal complications and a birth weight of 2.5 kg. At 5 months of age, heart murmur due to a small ventricular septal defect was diagnosed at a referred hospital. At the age of four, a regular medical examination revealed elevated arterial blood pressure of 140/90 mmHg at the upper arm and weak femoral arterial pulse. She had no complaint of headache and no history of any type of seizure. In addition, her family history was not suggestive of neurofibromatosis. On physical examination at our hospital, she weighed 22 kg and her height was 106 cm. She had a strong pulse in the upper extremities and a weak pulse in the lower extremities, and posterior cardiac auscultation revealed systolic murmur of grade 4 (Levine scale) in the interscapular area. She also had more than 6 cafe-au-lait spots larger than 5 mm, and ophthalmological examination revealed multiple Lisch nodules of the iris. Brain magnetic resonance imaging uncovered multiple focal areas of signal intensity in the globus pallidus, thalamus, hippocampus, and dental nucleus on T2-weighted images. Chest radiography showed normal pulmonary vascularity and no cardiomegaly (cardiothoracic ratio, 50%), and the results of electrocardiography did not fulfill the criteria for left ventricular hypertrophy. Two-dimensional echocardiography showed increased left ventricular posterior wall thickness (6.8 mm; 120% of normal) with normal left ventricular systolic function. Pulsed Doppler echocardiography findings of the suprasternal notch and descending aorta indicated characteristic flow patterns of significant aortic coarctation (Figures and ). No abnormal intracardiac shunts were detected. Cardiac catheterization revealed ascending aorta pressure of 140/90 mmHg (mean, 120 mmHg) and distal thoracic aorta pressure of 100/80 mmHg (mean, 90 mmHg). Aortography of the descending aorta (left anterior oblique view) showed a 5 cm long hourglass-shaped thoracic coarctation at the Th5-to-Th6 level with the narrowest section having a diameter of 4 mm, as well as a large internal thoracic artery (). Cardiac surgery was performed, and the coarctation was excised and replaced with a 14 mm ePTFE graft without complications. Pathologic examination of the specimen showed the accumulation of smooth muscle cells and collagen tissue in the intimal layer of the thoracic aorta, resulting in hyperplasia that narrowed the lumen (). The patient was discharged in good hemodynamic condition without a difference in blood pressure between the arms and lower extremities. During the postoperative period, angiotensin converting enzyme inhibitor therapy was initiated because of persistent postoperative hypertension.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg']}",106.66667,101.33334,112,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 140.0 mm Hg + 2/3 * 90.0 mm Hg = 106.66667 mm Hg.
Hence, the patient's mean arterial pressure is 106.66667 mm Hg."
2037,5,Mean Arterial Pressure (MAP),physical,decimal,usmle-10928,Extracted,"A 26-year-old male presents to his primary care physician complaining of diarrhea. He recently returned from a two-week hike in the Peruvian Andes mountains, during which time he ate undercooked chicken and beef. Since returning, he has experienced frequent bloating, flatulence, and several foul-smelling watery stools per day. He has recently noticed blood on the toilet paper after wiping. His past medical history is notable for asthma. He takes albuterol and low-dose budesonide. His temperature is 100°F (37.8°C), blood pressure is 120/70 mmHg, pulse is 90/min, and respirations are 20/min. A stool sample is shown in Figure A.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg']}",86.66667,82.33334,91,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 120.0 mm Hg + 2/3 * 70.0 mm Hg = 86.66667 mm Hg.
Hence, the patient's mean arterial pressure is 86.66667 mm Hg."
2038,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-6033235-1,Extracted,"A 52-year-old man with a history of hypertension, coronary artery disease and end-stage renal disease under continuous ambulatory PD treatment for 3 years presented to the PD clinic with cloudy dialysate effluent and diffuse abdominal pain lasting 2 h. Two weeks before this presentation, he was diagnosed with community-acquired pneumonia, which was treated with 400-mg oral moxifloxacin daily for 10 days. However, persistent intractable cough did not seem to improve. Two days before this presentation, he visited the emergent department due to epigastric pain and an intractable cough. He had no nausea, vomiting or fever. Physical examination showed epigastric tenderness without guarding and rebound pain. Laboratory studies indicated a white blood cell (WBC) count 12,000 cells/mm3 with 87% neutrophils and 8% lymphocytes, hemoglobin 8.0 g/dL, alanine transaminase 35 U/L, amylase 19 U/L, total bilirubin 0.56 mg/dL, creatinine 16.7 mg/dL, sodium concentration 133 mEq/L and potassium concentration 4.2 mEq/L. Chest radiography indicated no signs of pneumonia. PD dialysate effluent analysis revealed WBC 2/μL without polymorphonuclear leukocyte (PMN). Abdominal ultrasonography only showed a distended gallbladder with sludge. Severe strains of abdominal muscles from persistent and intense cough were impressed. He was discharged with antitussives and analgesics.
At the PD clinic, his vital signs were body temperature 36 °C, heart rate 104 per minute, respiratory rate 19 per minute and blood pressure 121/91 mmHg. Physical examination confirmed diffuse abdominal tenderness with peritoneal irritation and clean exit site of PD catheter. PD dialysate effluent analysis revealed WBC 1783/μL including 50% PMN. He was diagnosed with PD peritonitis and admitted to ward. Cefuroxime and amikacin were administered intraperitoneally empirically. He had diffuse abdominal pain, nausea and vomiting. Daily analysis of PD dialysate effluent showed WBC counts of 1565/μL(PMN 71%) on day 2 and 3755/μL (PMN: 66%) on day 3 and 4805/μL (PMN:86%) on day 4. PD effluent culture was positive for Klebsiella pneumoniae on day 3. Cefuroxime and amikacin were replaced by Cefepime intraperitoneally. Owing to persistent symptoms, we repeated dialysate culture on Day 3 and it grew yeast-like organism on day 6. Amphotericin was administered immediately and surgery to remove the PD catheter was scheduled. On the same day, dark yellow dialysate was obtained (Fig. ). The color became green after a 24-h fast (Fig. ). An enhanced computed tomography (CT) scan of abdomen only revealed a distended gallbladder with modest wall thickening and distended bowel (Fig. ).
Exploratory laparotomy was performed on day 8. Despite a thorough examination of the intestine and stomach, no perforation was identified. The gallbladder was neither reddish nor edematous. A 0.3-cm rupture was found on the fundus of gallbladder. Primary closure of gallbladder was done with external drainage. The PD catheter was removed uneventfully. After antibiotic treatment and intensive care, he recovered without sequelae. He was discharged after 37 days hospitalization and received maintenance hemodialysis three times a week.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [121.0, 'mmhg'], 'Diastolic Blood Pressure': [91.0, 'mmhg']}",101,95.95,106.05,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 121.0 mm Hg + 2/3 * 91.0 mm Hg = 101.0 mm Hg.
Hence, the patient's mean arterial pressure is 101.0 mm Hg."
2039,5,Mean Arterial Pressure (MAP),physical,decimal,pmc-4499603-1,Extracted,"A 66-year-old man visited our hospital, Asan Medical Center, due to a cough persisting for 5 months. Seven years earlier, he had been treated for pan-susceptible pulmonary tuberculosis (TB), which lasted for 9 months. This treatment was successful but a chest X-ray (CXR) at the time of treatment completion showed parenchymal destructive lesions, with fibrotic changes in the right upper lung field (). He also suffered from a mild chronic cough. He remained relatively well thereafter. A CXR taken about 1 year earlier showed no significant changes in the TB-destroyed lung. However, his cough became aggravated 6 months prior to presentation at our clinic.
Physical examination revealed that the patient was alert and not in distress. His vital signs were as follows: temperature, 35.6℃; blood pressure, 123/78 mm Hg; pulse, 63 beats per minute (with a regular rhythm); and respiratory rate, 20 breaths per minute. Auscultation revealed decreased breath sounds in the right upper anterior chest. Blood tests showed a white blood cell count of 7,500/mm3 (67% neutrophils); hemoglobin, 12.6 g/dL; and a platelet count of 268,000/mm3. Routine chemical laboratory data were all within the normal ranges. The patient was negative for antibodies to human immunodeficiency virus.
Compared with the CXR taken 6 years earlier, his CXR showed increased infiltration of the right middle lung field, with small nodular densities (). A chest computed tomography (CT) scan revealed a newly developed segmental centrilobular nodular lesion in the right lung (). Smears and cultures of multiple sputum specimens were positive for acid-fast bacilli, which a GenoType Mycobacterium Assay (Hain Diagnostika, Nehren, Germany) identified as M. malmoense ().
Based on these clinical and laboratory data, the patient was given a diagnosis of lung disease caused by M. malmoense, according to the American Thoracic Society (ATS) criteria. M. malmoense was subjected to several rounds of drug susceptibility testing; however, all failed due to contamination. The patient was treated with oral isoniazid, rifampicin, ethambutol, moxifloxacin, and clarithromycin, and his symptoms improved rapidly. Sputum culture conversion was observed after 2 months. Due to the improved clinical course, moxifloxacin was stopped 8 months after initiation. Also, we had to discontinue ethambutol after 10 months due to the onset of optic neuropathy. Treatment was completed 12 months after achieving sputum culture conversion (i.e., treatment lasted 14 months in total). A CXR and CT scan taken 12 months after the start of treatment showed an improvement in the lung lesions (). The patient received regular follow-up for 3 months after treatment completion with no relapse of M. malmoense infection.",What is patient's mean arterial pressure in mm Hg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [123.0, 'mm hg'], 'Diastolic Blood Pressure': [78.0, 'mm hg']}",93,88.35,97.65,"The mean average pressure is computed by the formula 1/3 * (systolic blood pressure) + 2/3 * (diastolic blood pressure). Plugging in the values, we get 1/3 * 123.0 mm Hg + 2/3 * 78.0 mm Hg = 93.0 mm Hg.
Hence, the patient's mean arterial pressure is 93.0 mm Hg."
2040,6,Body Mass Index (BMI),physical,decimal,pmc-5067398-1,Extracted,"A 19-year-old man presented to the orthopedic surgery department with pain in the left buttock after military training which including running with hyper-flexion of hip for 3 hours, twice a day for 5 days. When he hyper-flexed his left hip joint, he felt and heard a crack. Initially about one week later, he referred to the local hospital because of persisting hip pain. On radiographic evaluation, he diagnosed as pelvic bone fracture and recommended for further evaluation. However, he refused to get more examination due to the alleviation of the hip pain. Although he got rest without any military training for the next six weeks, there was no improvement and tingling sense developed over the posterior aspect of left thigh. During the first consultation with the patient, he complained difficulty on sustained standing and sitting on a locked position.
His body weight, height, hip and lumbar T-score for dual-energy x-ray absorptiometry (DXA) scan were 76 kg, 183 cm, –0.7 and –0.1 respectively. On physical examinations, there was no limitation on range of motion of the left hip joint. Also he could walk without any pain except mild tenderness on the area distal from the ischial tuberosity. On the radiographs of the pelvis anteroposterior and frog leg view (), there was a 35×40×20 mm sized bony fragment, 15 mm distance from the left ischial tuberosity. After the patient admitted to our hospital, he had an examination of computed tomography () and magnetic resonance imaging for rule out pathologic conditions. There was a bony fragment at left ischial tuberosity, which was mainly from conjoined origin of biceps femoris and semitendinosus tendons without any bone marrow edema (). Overall, he diagnosed as old avulsion fracture at ischial tuberosity. He determined to get conservative treatment on condition of a gradual alleviation of the symptom. During the admitted 2 months, he just got rest and high intensity laser therapy. Thanks to the improvement except discomfort on running, he discharged and returned to his military unit.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [76.0, 'kg'], 'height': [183.0, 'cm']}",22.69402,21.55932,23.82872,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 183.0 cm, which is 183.0 cm * 1 m / 100 cm = 1.83 m. The patient's weight is 76.0 kg. The patient's bmi is therefore 76.0 kg / (1.83 m * 1.83 m) = 22.69402 kg/m^2."
2041,6,Body Mass Index (BMI),physical,decimal,pmc-5490092-1,Extracted,"A 54-year-old female (weight 55 kg, 160 cm) was referred by an orthopedic surgeon to our pain clinic for persistent low back pain radiating down to right leg. She had a history of low back pain associated with radiculopathy, which was more on the right side and radiated till the big toe for more than 6 weeks. The impression on the magnetic resonance imaging (MRI) revealed a right paracentral disc protrusion at levels L4-L5, L5-S1 causing thecal sac indentation, effacement of the right lateral recess and right exiting nerve root impingement. There was no associated lumbar canal stenosis and no evidence of facet arthropathy. She had been taking analgesics tablet diclofenac 650 mg, tablet pregabalin 75 mg, tablet nortriptyline 10 mg, and regular physiotherapy for the last 6 weeks. She even underwent an epidural steroid injection (ESI) through the caudal route with 4 ml of 0.5% bupivacaine, 1 ml of methylprednisolone, and 5 ml of normal saline at a tertiary care center 4 weeks back after which her symptoms improved marginally for a period of 1 week and then she again started with debilitating pain, not getting relieved with analgesics and other modes of conservative management. The complete motor and sensory examination of the patient revealed motor power of Grade V, i.e. the muscle can move the joint; it crosses through a full range of motion against gravity and resistance. The sensations were intact as elicited by pain, temperature, vibration, position sense, stereognosis, and two-point discrimination. All the superficial and deep tendon reflexes were intact with an SLR of 10° on the right side and 70° on the left side. The patient had full control over the bladder and bowel.
We hence planned, fluoroscopic-guided transforaminal ESI (TFESI) using clonidine as an adjuvant at levels L4-L5 and L5-S1 on the right side, after discussing both with the patient and the orthopedic surgeon.
After taking an informed written consent, an 18-gauge intravenous cannula was secured. All routine monitors (electrocardiography, noninvasive blood pressure, and oxygen saturation) were attached. The patient was positioned on the operating room table with a pillow underneath the abdomen in the prone position. Under fluoroscopic guidance, the standard safe triangle was identified with pedicle of the vertebrae forming one arm of the triangle, lateral border of vertebral body forming the second arm, and the hypotenuse being formed by the exiting nerve root. Under all aseptic precautions, the skin overlying the target area was anesthetized with 2 ml of 1% lidocaine. The level of the epidural injection was chosen depending on the MRI findings and physical examination as L4- L5 and L5-S1.
A 22-gauge spinal needle was then advanced under fluoroscopy aiming the needle at the superior and anterior part of the intervertebral foramen through the safe triangle. The needle placement was confirmed after injecting 1–2 ml of omnipaque, nonionic water-soluble contrast medium iohexol dye, demonstrating the contrast going through the foramen. Furthermore, the confirmation of the needle position with contrast dye reduced the possibility of misplacement or intravascular placement of the needle, which is always a risk in ESIs performed without fluoroscopy. The needle was advanced into the safe triangle, and its placement was then confirmed both by anteroposterior and lateral view. One milliliter methylprednisolone (40 mg) mixed with 0.5 ml clonidine (50 μg) and 1 ml bupivacaine 0.5% were given at each level (volume 2.5 ml).
After the completion of the procedure, the patient was transferred to the recovery area. The patient's hemodynamic parameters were monitored during and after the procedure. Assessment of pain relief and any motor or sensory deficit was checked immediately and then hourly after the procedure till discharge from the recovery area.
The patient was discharged after having met the following discharge criteria after 2 h:
The patient was able to walk unaided The patient was able to void her bladder without any difficulty.
She was assessed for any numb or weak feeling in her back or legs for a few hours after the injection.
After 24 h, the patient was discharged from the hospital, and there was a significant improvement in the pain with an improvement in the SLR to 60°.
Following instructions were given at the time of discharge:
To report any untoward incident To continue taking analgesics as advised To start back muscle strengthening exercises after 3 days if there was considerable pain relief.
Patient was then reassessed at 2 weeks, 1 month, and 3 months interval after the procedure. There was a significant improvement in the pain after single injection of TFESI using clonidine as depicted by the visual analog scale (VAS) score; there was a much reduced drug dose intake and an improvement in the daily life activities as stated by the patient.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.0, 'kg'], 'height': [160.0, 'cm']}",21.48437,20.41015,22.55859,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.6 m * 1.6 m) = 21.48437 kg/m^2."
2042,6,Body Mass Index (BMI),physical,decimal,pmc-5804640-1,Extracted,"A 35-year old primigravida (height 150 cm; weight 60 kg) presented with exertional dyspnea at 23 weeks of gestation. A contrast-enhanced computed tomography (CT) scan showed bilateral pulmonary artery thrombi and deep venous thrombus in the lower limb (Fig. ). A transthoracic echocardiography revealed a right ventricular thrombus (Fig. ). She was referred to our hospital at 28 weeks of gestation after insertion of IVC filter and heparin administration. Fetal development was normal. Due to the mobility of right ventricular thrombus and the risk of cardiac arrest, an emergency thrombectomy was planned. An intracardiac echography probe (AcuNav™; Siemens AG, Munich, Germany) was inserted via the right femoral vein to monitor the umbilical artery pulse wave via Doppler, in addition to transabdominal fetal monitoring. After induction of anesthesia, the patient’s blood pressure was undetectable; hence, emergency cardiopulmonary bypass (CPB) was performed via median sternotomy, followed by cardiac resuscitation. While switching to extracorporeal circulation approximately 10 min after the hemodynamic collapse, the fetal heart rate decreased to approximately 80 beats per minute. Immediately after establishing extracorporeal circulation, the fetal heart rate recovered rapidly and remained stable throughout the procedure, while the CPB average perfusion pressure was maintained above 70 mmHg. Thrombectomy and tricuspid valve plication were performed under cardiac arrest (Fig. ). Catecholamines and nitric oxide were administered at a concentration of 20 ppm to treat hypotension and pulmonary hypertension, respectively, during withdrawal from CPB. The patient was admitted to the intensive care unit without chest closure. Total time for surgery, anesthesia, cardiopulmonary, and aortic cross clamp was 345, 483, 208, and 147 min, respectively. The total volume of hemorrhage, transfusion, infusion, urine, and water balance was 1470, 3600, 2150, 1520, and +657 ml, respectively. Chest closure was performed on postoperative day 3 and extubation on postoperative day 6. Heparin administration was resumed after confirming postoperative hemostasis. At 32 weeks of gestation, magnetic resonance imaging (MRI) was performed to assess the fetal brain function; no remarkable changes were observed. The patient was discharged with subcutaneous injection of heparin calcium, due to persistent lower limb thrombus.
She was readmitted at 38 weeks of gestation. Labor was induced at 40 weeks using oxytocin, after discontinuation of heparin. Epidural anesthesia was administered to protect the thoracic wound site and reduce the cardiac load. An epidural catheter was placed between the L3-L4 vertebrae, after confirming the recovery of hemostatic function by measuring activated partial thromboplastin time. Continuous epidural ropivacaine 0.1% with 2 mcg/ml fentanyl was administered through patient controlled epidural analgesia. Analgesia was adequate throughout labor, with no hemodynamic changes. A healthy male infant weighing 3446 g (+1.07 SD) was delivered by vacuum extraction with an Apgar score of 8/8. Total delivery time was 3 h and 37 min, with total blood loss of 928 ml. No remarkable changes were observed in the neonate’s brain on CT and MRI just after delivery. The patient was prescribed oral warfarin for anticoagulation, and both mother and child were discharged without complications.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.0, 'kg'], 'height': [150.0, 'cm']}",26.66667,25.33334,28,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 150.0 cm, which is 150.0 cm * 1 m / 100 cm = 1.5 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.5 m * 1.5 m) = 26.66667 kg/m^2."
2043,6,Body Mass Index (BMI),physical,decimal,pmc-4069803-1,Extracted,"A 54-year-old woman presented to her personal physician and complained the pain on her right breast. She underwent a breast surgery in our hospital. The patient and her family’s medical histories were unremarkable.
The patient was 157 cm tall and weighed 53 kg. Physical examination of the right breast (area C) revealed an elastic hard mass measuring 2.5 cm × 2.5 cm. Margins were distinct, with relatively good mobility and a tumor-nipple distance of 3.2 cm. No axillary or cervical lymph nodes were palpable. Hematological and biochemical blood test results were normal. The levels of tumor markers, such as carcinoembryonic antigen, carbohydrate antigen 15-3, and National Cancer Center-Stomach-439, were within normal limits.
Mammography revealed an indistinct margined hyper dense mass in the right outer portion, which was assessed as Breast Imaging-Reporting and Data System category 4C (: MLO view, : CC view). Breast ultrasonography (US) revealed complex cystic lesion, and the tumor was large with 2.5 cm diameter (). Complex cystic lesion on US with blood content on fine-needle aspiration (FNA) cytology revealed malignant cells. Preoperative magnetic resonance imaging (MRI) findings and a T2 weight image revealed an early enhancement image with no intraductal spread (). No distant metastases was identified on computed tomography or bone scan. The tumor stage was T2N0M0. Breast-conserving surgery and sentinel lymph node biopsy were performed.
The results exposed two sentinel lymph nodes and no malignant cell. The tumor measured 2.0 cm in diameter and contained a central cystic area (,). Histopathological examination showed low papillary growth in the cystic cavity surface, which was covered by adenocarcinomatous components associated with some squamous metaplasia. Most of the lesions comprising the cyst wall were a mixture of irregular bundles of spindle-shaped tumor cells and fibrous connective tissue proliferation. The tumor was diagnosed as spindle cell ().
Immunostaining of spindle-shaped tumor cells showed positive results for cytokeratin (AE1/AE3) and vimentin (,), partially positive results for s-100, and negative results for desmin and α-actin. The final histopathological diagnosis was spindle cell carcinoma. Histological grade from malignancy was grade III. Lymphatic invasion was negative, whereas blood vessel invasion was positive. Lymph node metastasis was negative, and p-stage I was diagnosed. Estrogen receptor, progesterone receptor, and human epidermal growth factor receptor type 2 (HER2), which showed negative results by biochemical tests, were called triple negative type in subtype classification. The postoperative course was uneventful. The patient received six courses of FEC-100 chemotherapy. Radiotherapy included simultaneous integrated boost enforced 60 Gy (2 Gy/day) to the residual breast tissue. After 24 months of postoperation, no recurrence has been detected.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.0, 'kg'], 'height': [157.0, 'cm']}",21.50189,20.4268,22.57698,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 157.0 cm, which is 157.0 cm * 1 m / 100 cm = 1.57 m. The patient's weight is 53.0 kg. The patient's bmi is therefore 53.0 kg / (1.57 m * 1.57 m) = 21.50189 kg/m^2."
2044,6,Body Mass Index (BMI),physical,decimal,pmc-6124823-1,Extracted,"A 29-year-old Caucasian man from East province of Saudi Arabia who’s known for homozygous sickle cell anemia admitted to the hospital with acute left scrotal pain and swelling for 1 week that did not respond to antibiotic. The patient had been in his usual health until 1 week before this admission when pain in the left testis developed. The pain started suddenly, progressive and was associated with intermittent fever (38.2) and progressive enlargement of the left scrotum. There was no history of trauma or lower urinary tract infections symptoms or hematuria or urethral discharge. 1 week before this admission, he presented to another health center for evaluation where he was diagnosed with urinary tract infection and managed as outpatient with a prescription for 7-day course of amoxicillin/clavulanate potassium. The SCA course of this patient was remarkable for recurrent vaso-occlusive crisis and splenectomy at the age of 13 years, but there were no complications such as acute chest syndrome, cerebrovascular accidents, or genitourinary complications. He is not known to have any other medical problems, and he is not on any medications currently apart from intermittent use of analgesics. His vaccinations are up to date. There is additional history for discontinuation of hydroxyurea 4 months ago for improving fertility. He was married and worked as a pharmacist. He did not smoke, drink alcohol, use illicit drugs, or any kind of herbs. He had a family history of diabetes mellitus and hypertension. On examination, the temperature was 37.1°C and pulse 100 beats/min; the other vital signs were normal. The height of the patient was 163 cm and his weight was 55 kg. Swollen, red, and tender left scrotum was present. The examination was otherwise normal. Ultrasound scrotum showed heterogeneous hypoechoic left testicle with no blood flow [].
Laboratory investigations showed white blood cells 40 (3.5–10.5 billion cells/L), hemoglobin 80 (135–170 g/L), mean corpuscular volume 80 (80–96 fl), platelets 1140 (150–450 billion/L), and reticulocytes 10.7%. Hemoglobin electrophoresis came out with hemoglobin S 79% and hemoglobin F 4.6%. Urine analysis was unremarkable. Conservative strategy has been followed with this patient. He received antibiotics (piperacillin/tazobactam 4.5 g IV q6 h), parenteral hydration, morphine, high-dose hydroxyurea (1000 mg oral daily), and aspirin (81 mg oral daily). There was no significant improvement of patient’s symptoms for 7 days. Repeated ultrasound confirmed aforementioned findings. The urologist decided to proceed with the left orchiectomy. Pathology resulted in extensive infarcted testicular tissue with marked acute inflammatory changes and focal hemorrhage of the testis.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.0, 'kg'], 'height': [163.0, 'cm']}",20.70082,19.66578,21.73586,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.63 m * 1.63 m) = 20.70082 kg/m^2."
2045,6,Body Mass Index (BMI),physical,decimal,pmc-4776617-1,Extracted,"A 7-year-old HIV infected girl presented with chronic diarrhea and hypocalcemic tetany (serum calcium = 5.6 mg/dl [normal = 8.5 to 11 mg/dl]). She was on trimethoprim-sulfamethoxazole (TMP-SMX) prophylaxis. She had herpes zoster 2 years back. Both the parents were also HIV infected but not on ART. On examination, her weight was 12 kg, height was 103 cm, had generalized as nonsignificant lymphadenopathy with edema feet and pallor. On systemic examination, she had hepatosplenomegaly. Other systems were normal. Her mantoux test was negative; barium meal follow through was normal, and stool showed 20–25 pus cells/hpf. She was treated with intravenous (IV) ceftriaxone, metronidazole, nitazoxanide, and fluconazole to which she responded along with calcium supplements. Her CD4 count was 158 cells/cumm with CD4:CD8 of 0.22. She was started on ART consisting of stavudine, lamivudine, and nevirapine. After 1 month of ART, she was admitted with diarrhea. Stool showed the presence of giardiasis and budding yeast. She was treated with IV cefotaxime, amikacin, TMP-SMX, and required inotropes in the form of dopamine and dobutamine, and also prednisolone to which she responded. She was subsequently tapered off the steroids and were doing well.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [12.0, 'kg'], 'height': [103.0, 'cm']}",11.31115,10.74559,11.87671,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 103.0 cm, which is 103.0 cm * 1 m / 100 cm = 1.03 m. The patient's weight is 12.0 kg. The patient's bmi is therefore 12.0 kg / (1.03 m * 1.03 m) = 11.31115 kg/m^2."
2046,6,Body Mass Index (BMI),physical,decimal,pmc-5423887-1,Extracted,"A 9-year-old boy (height:131.3 cm, weight: 22.7 kg) with the diagnosis of cholelithiasis was booked for laparoscopic cholecystectomy. After preoperative optimization, a small abdominal incision for insertion of the camera port (5-mm) was made in umbilicus. The pressure of pneumoperitoneum was kept at 6 mmHg, which is lower than that for an adult (8-10 mmHg). To use ultrasonically activated device (USAD), a 5-mm port was inserted below the xiphoid process, but to reduce the interference of the forceps within the restricted working space and for aesthetic considerations, two 2-mm diameter grasper forceps (BJ needle; NITI-ON, Chiba, Japan) were inserted in the right hypochondrium for the surgeon’s left hand and the assistant. Cystic artery was coagulated with USAD. Cystic duct was double ligated using 4-0 absorbable sutures. Duration of surgery was 45 min, and there was minimal blood loss.
A 9-mm black stone was found within the gallbladder. Calculus analysis indicated that its composition was 36% calcium carbonate, 33% calcium phosphate, and 31% calcium bilirubinate. The patient was discharged on the fourth day after surgery without any complication.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [22.7, 'kg'], 'height': [131.3, 'cm']}",13.16729,12.50893,13.82565,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 131.3 cm, which is 131.3 cm * 1 m / 100 cm = 1.313 m. The patient's weight is 22.7 kg. The patient's bmi is therefore 22.7 kg / (1.313 m * 1.313 m) = 13.16729 kg/m^2."
2047,6,Body Mass Index (BMI),physical,decimal,pmc-6854976-2,Extracted,"The patient was a 22-year-old, male, third-ranked sumo wrestler (height, 173 cm; weight, 136 kg). He was injured during sumo training. Two days after the injury, he visited our hospital. Radiography revealed fractures of the proximal epiphysis of the fifth metatarsal bone and thickening of the periosteum (). We diagnosed Jones fracture and performed conservative treatment with cast fixation for three weeks. Subsequently, we removed the cast and put on a brace. Radiography showed gradual bone union; thus, his amount of training gradually increased (Figures –). Six months after the injury, his foot was refractured (). We started treatment with Low-Intensity Pulsed Ultrasound (LIPUS) in combination with the brace [], but he discontinued treatment at his own discretion. However, he continued to sumo wrestle.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [136.0, 'kg'], 'height': [173.0, 'cm']}",45.44088,43.16884,47.71292,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 173.0 cm, which is 173.0 cm * 1 m / 100 cm = 1.73 m. The patient's weight is 136.0 kg. The patient's bmi is therefore 136.0 kg / (1.73 m * 1.73 m) = 45.44088 kg/m^2."
2048,6,Body Mass Index (BMI),physical,decimal,pmc-5175055-1,Extracted,"A 68-year-old female patient presented to our emergency service with inability to pass gas and feces for 2 days, abdominal distension, and vomiting. Her personal medical history was unremarkable, without any previous disease or operation. This multipara patient was 155 cm tall, and weighed 40 kg. Her vital signs were as follows: ABP: 120/70 mmHg, pulse rate: 78/min, respiratory rate: 23/min, body temperature: 36.7°C. Physical examination revealed abdominal distension without abdominal guarding, and rebound tenderness. The rectal ampulla was empty on digital rectal examination. Other system examinations were unremarkable. Results of laboratory tests were as follows: Htc: 43.1%; WBC: 11700/mm3, glucose: 125 mg/dL, BUN: 61mg/dL, creatinine: 1.21 mg/dL, sodium: 135 mEq/L, potassium: 4.3 mEq/L. Standing KUB revealed air-fluid level of intestines (). On whole abdominal ultrasound, dilated intestinal loops, and free fluid between intestinal loops were detected. Computed tomography (CT) demonstrated obstructive obturator hernia on the left side (Figures , ). The patient was operated urgently with the diagnosis of intestinal obstruction caused by strangulated obturator hernia. On exploration, a strangulated intestinal loop was detected within the left obturator channel, and reduced. Intestinal ischemia, necrosis or perforation were not detected, so additional intervention was not performed. The defect was repaired using a polypropylene mesh placed in the preperitoneal region. The patient was lost on postoperative 3rd day because of acute respiratory failure.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [40.0, 'kg'], 'height': [155.0, 'cm']}",16.64932,15.81685,17.48179,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 40.0 kg. The patient's bmi is therefore 40.0 kg / (1.55 m * 1.55 m) = 16.64932 kg/m^2."
2049,6,Body Mass Index (BMI),physical,decimal,pmc-2630299-1,Extracted,"A 51-year-old Caucasian left-handed housewife lady (weight 61 kg, height 159 cm) was admitted to our institution because of severe sudden onset headache followed by transient loss of consciousness and vomiting. On examination she was fully conscious and oriented and complained of severe headache. Nuchal rigidity was evident. No focal neurological deficit was found. Temperature was 38°C and other vital signs were stable. Past medical history was negative and she did not consume any medication.
CT scan of the head revealed acute subarachnoid hemorrhage prominently occupying the right sylvian fissure. CT angiography was performed (figure ). The cerebral vasculature was found to harbor three saccular aneurysms at: (1) right MCA trifurcation, (2) left ICA bifurcation, and (3) distal basilar artery. The right MCA aneurysm was presumed to be the ruptured aneurysm due to location of subarachnoid clot and irregular shape of the aneurysm.
A right pterional craniotomy was performed with the patient in the supine position and head rotated 30 degrees to left. After elevation of the craniotomy flap, the sphenoid ridge was drilled flush with the orbital roof to facilitate exposure of the basilar tip aneurysm. After duratomy, gentle frontal lobe retraction allowed CSF drainage from the optic and carotid cisterns. Right optic nerve and right ICA were identified and the Sylvian fissure was opened from medial to lateral, following the bifurcation of right ICA to MCA trifurcation. A saccular aneurysm was found in the MCA trifurcation projecting inferolaterally. After dissection of the neck it was clipped. Next, opening the membrane of Liliequist, let to the distal basilar aneurysm from the corridor between the right optic nerve and right ICA. The aneurysm was located between the right PCA and right SCA with a wide neck, and its dome projected laterally to right. Successful clipping was achieved. The left ICA bifurcation aneurysm was identified after following the right A1, anterior communicating and left A1 arteries with minimal brain retraction, and gaining benefit from favorable neuroanesthesia. The aneurysm projected superiorly and was also clipped (figure ).
The patient experienced an uneventful post-operative period and was discharge within 5 days of surgery. A follow-up CT angiography confirmed successful obliteration of all lesions and preservation of normal cerebral vasculature (figure ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.0, 'kg'], 'height': [159.0, 'cm']}",24.12879,22.92235,25.33523,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 159.0 cm, which is 159.0 cm * 1 m / 100 cm = 1.59 m. The patient's weight is 61.0 kg. The patient's bmi is therefore 61.0 kg / (1.59 m * 1.59 m) = 24.12879 kg/m^2."
2050,6,Body Mass Index (BMI),physical,decimal,pmc-2803985-1,Extracted,"We are presenting a case with acute abdomen, i.e. ileoileal intusussception, caused by Burkitt lymphoma. A sixteen-year-old Caucasian Kosovar boy, presented in the surgical emergency clinic as acute abdomen, with abdominal pain, nausea, vomiting, and problems with defecation and flatulence. The symptoms started three days ago, worsening on admission day.
The patient's height was 178 cm, and his weight was 70 kg. His vital signs were: blood pressure 120/80 mmHg; pulse rate: 76 beats/min; respiratory rate 20/min; body temperature 37.1°C.
During physical examination, a distended, diffusely tender and painful abdomen with lower abdomen rebound was revealed. The patient's skin was pale with sweats.
Plane abdominal radiography showed mechanical obstruction. (Fig. )
The emergency laboratory tests presented as follows: Red blood cells (RBC): 4.61 × 109/L; white blood cells (WBC): 7.3 × 109/L; Hemoglobin (Hgb): 128 g/L; Hematocrit (Htc): 0.42; blood sugar: 5.42 mmol/L; blood urea nitrogen (BUN): 2.6 mmol/L; serum creatinine: 88 μmol/L; BUN/Creat ratio: 8.5; total protein: 72 g/L; albumin: 36 g/l; ALP: 60 IU/L; ALT: 26 IU/L; AST:40 IU/L; direct bilirubin: 5.8 μmol/L; total bilirubin: 20.5 μmol/L; indirect bilirubin: 14.7 μmol/L; Gama GT: 26 IU/L; C-reactive protein: 15.6 mg/L; serum amylase: 30 U/L: electrolytes: Na: 138 mmol/L; K: 3.75 mmol/L; Cl: 102 mmol/L; urinalysis: 2-4 Leucocytes, some bacteria and some uric acid crystals. Blood group: O Rh(D) poz.
Three weeks prior he had been surgically treated as acute abdomen caused by acute appendicitis and Mckelly Diverticulitis. Appendectomy and short resection of the ileum with diverticulum, and end-to-end anastomosis was performed. The immediate post operative period went well. After his discharge, his second hospital admission was two weeks after operation with abdominal pain and constipation problems which released spontaneously after two days.
At his third admission as acute abdomen, urgent laparotomy was performed in general endo tracheal anesthesia on the day after admission. Intra operative findings revealed small bowel dilatation, with intussusceptions of the terminal ileum, 2 cm from ileocecac valve. There were multiple enlarged mesenteric lymph nodes at the meso of the terminal ileum, ascending and the transverse colon, without palpable liver metastases.
We have done des intussusceptions caused by tumor from the wall of the ileum. (Fig. , , )
Adhesions at the anastomosis, and 60 cm above that, were released. The right extended haemicolectomy with end to end ileum-transverse anastomosis was performed. Post operative period went well; blood pressure was 120/80 mmHg, pulse rate beats: 65/min; temp.: 36.7°C. The wound healed per primam. He was treated with frozen fresh plasma (several doses-seven), red blood cells (one dose); antibiotic, analgesics, H2 blockers, vitamins, amino acids, human albumins. He was discharged on the 10th postoperative days, with good bowel movements. He was oriented to the Hematology Department for further treatment, for Burkitt Lymphoma with chemotherapy.
HP opinion: Giemsa staining demonstrated neoplastic lymphocytes infiltration. Immunochemical testing was positive for Burkitt lymphoma (CD10, CD20, CD34, Bcl-2, Ki67, IgM, MIB-1 with a proliferation index of over 90% of neoplastic cells) and c-myc translocation determined by FISH analysis (fusion and split). (Fig. , , , , )",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [178.0, 'cm']}",22.09317,20.98851,23.19783,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 178.0 cm, which is 178.0 cm * 1 m / 100 cm = 1.78 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.78 m * 1.78 m) = 22.09317 kg/m^2."
2051,6,Body Mass Index (BMI),physical,decimal,pmc-3060392-1,Extracted,"A 9-year-old girl with developmental delay was born at 37 weeks gestation and had a birth weight of 2.84 kg. Her presenting height, weight and head circumference were 135.3 cm (10th percentile), 38 kg (50th percentile) and 53 cm (50th percentile), respectively. Past medical history, perinatal history and family history were unremarkable. The patient's intelligence quotient was measured to be 60. Her language was at the level of a 6 year old. Chromosome analysis showed a 46, XX karyotype with a breakage at 3p14.
Ophthalmologic examination revealed an esotropia of 8 prism diopters (PD) at distance and near in the primary position. Ductions and versions showed a mild limitation of abduction in both eyes (). The pupils were isocoric and reactive to light, and the fundoscopic examination was normal. Cycloplegic refraction revealed a hyperopic astigmatism of +1.75 Dsph -0.50 Dcyl × 180A in both eyes. The corrected visual acuity was 20/30 in both eyes. With correction, there were 4 PD of intermittent exotropia at distance and 2 PD of intermittent exotropia for near vision. The patient recognized nothing with the Randot stereotest. She fused 4 dots at a distance and near with the Worth four-dot test.
The patient had sparse arched eyebrows, long palpebral f issures and eversion of the lateral third of the lower eyelids (), a broad and depressed nasal tip, cleft palate, gynecomastia, short, incurved fifth fingers, epicanthal folds, retrognathia, a small mouth, a tented upper lip, a short nasal septum, and prominent ears. A single flexion crease was observed on each of the fourth and fifth fingers. These features are characteristic of Kabuki syndrome.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [38.0, 'kg'], 'height': [135.3, 'cm']}",20.75812,19.72021,21.79603,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 135.3 cm, which is 135.3 cm * 1 m / 100 cm = 1.353 m. The patient's weight is 38.0 kg. The patient's bmi is therefore 38.0 kg / (1.353 m * 1.353 m) = 20.75812 kg/m^2."
2052,6,Body Mass Index (BMI),physical,decimal,pmc-3888855-1,Extracted,"A 40-year-old woman, 169 cm, 57 kg, underwent laparoscopic right adrenalectomy due to an adrenal pheochromocytoma. Preoperative evaluation of the patient was unremarkable. General anesthesia was induced using thiopental sodium, fentanyl, vecuronium and sevoflurane. A 7.5 Fr 3-lumen catheter was inserted under ultrasonographic guidance (linear probe: UST-5546, 5-10 MHz, machine: Prosound SSD-4400®, Aloka Medical, Co., Ltd., Tokyo, Japan) into the right internal jugular vein, and lung sliding was confirmed in both thoraces. Next, the patient was placed into the left lateral decubitus position. Before incision, ETCO2, Pmax, and peripheral oxygen saturation (SpO2) were determined to be 33 mmHg, 17 cmH2O, and 100%, respectively. Pneumoperitoneum was established using CO2, intraabdominal pressure was maintained < 15 mmHg, and Pmax was 23 cmH2O at the time. Thirty minutes after inducing pneumoperitoneum, the ETCO2 and Pmax levels gradually increased to 43 mmHg and 30 cmH2O, respectively. Thereafter, SpO2 decreased acutely to 92%. On auscultation, the breath sounds from the left lung field were normal. However, the right side of the chest demonstrated no sounds. Immediately, the fraction of inspired oxygen (FiO2) increased from 0.5 to 0.8, and the endotracheal tube was withdrawn back to 2 cm in order to rule out endobronchial intubation. Because the depth of the endotracheal tube was 18 cm at the incisor teeth and confirmed the depth of endotracheal tube by cuff palpation at the sternal notch, we supposed that it was enough to rule out one-lung intubation without using bronchoscope. SpO2 was maintained at between 98-100%, though the right thorax was still silent. Pneumothorax was strongly suspected, and the chest was examined using ultrasonography. Lung sliding and seashore sign were demonstrated in the left lung (), however there was no sliding with barcode sign in the right lung (). Although the surgeon simultaneously inspected the diaphragm in detail, no apparent injuries or defects were found. Because the vital signs were stable and SpO2 and ETCO2 were normal, as indicated by an increased FiO2 and respiratory rate, the operation was laparoscopically completed.
When the operation was concluded, a positive end-expiratory pressure (PEEP) of 5 cmH2O was applied to inflate the collapsed lung. The patient was examined using ultrasonography whilst in the supine position, and at the same time, portable chest radiography was called to assess a pneumothroax. The ultrasonographic probe was placed on the right lower lateral chest wall between anterior and mid axillary line (), and we identified the ""lung point"" sign, which can be used to diagnose pneumothorax []. Also, chest radiography indicated a < 30% collapse of the right lung (). As the right hemithorax was continuously examined using ultrasonography, auscultation of the right lung improved, as well as the appearance of lung sliding sign and the disappearance of the lung point sign in whole right hemithorax within about 30 minutes after the end of the operation. No hemodynamic instability was noted, and SpO2 was maintained at 100% using only medical air. Hence, pneumthorax was considered to be capnothorax, and the patient was extubated without the insertion of a chest tube. The patient was transferred to the postanesthetic care unit (PACU) and did not complain about any respiratory disturbance.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [57.0, 'kg'], 'height': [169.0, 'cm']}",19.95728,18.95942,20.95514,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 169.0 cm, which is 169.0 cm * 1 m / 100 cm = 1.69 m. The patient's weight is 57.0 kg. The patient's bmi is therefore 57.0 kg / (1.69 m * 1.69 m) = 19.95728 kg/m^2."
2053,6,Body Mass Index (BMI),physical,decimal,pmc-6531112-1,Extracted,"A 77-year-old, Asian male patient (weight: 60 kg, height: 165 cm) with end-stage renal disease (ESRD) undergoing periodic hemodialysis, was hospitalized due to acute exacerbation of chronic obstructive pulmonary disease. He had no known history of psychosis prior to admission to the hospital. His social history was positive for alcohol consumption (25 mL a day for 10 years) and smoking (40 cigarettes a day for 30 years).
On admission, the patient was conscious and oriented to person, time, and place. Complete neurological examination including mental state was normal. The patient was in shortness of breath with the following vital signs: temperature 36.2 °C, blood pressure 156/91 mmHg, pulse 98 beats/min, and respiratory rate 20 per minute. He reported progressively worsening cough productive of yellow purulent sputum. Bilateral moist crackles were heard in both lungs on auscultation but with no wheezing. Markers of systemic inflammation were elevated (white blood cell count [WBC] 10.25 × 103/μL, C-reactive protein [CRP] 57.50 mg/L, procalcitonin [PCT] 0.49 ng/mL). Laboratory analysis revealed increased baseline serum creatinine (10.63 mg/dL, estimated creatinine clearance 4.94 mL/min). His liver function was moderately impaired and classified into Child-Pugh class B. Chest computed tomography (CT) scan showed diffuse inflammation and interstitial change and a small amount of pleural effusion in bilateral lungs.
Intravenous moxifloxacin was initiated 400 mg daily as empiric treatment for pulmonary infection on hospital day 1. A sputum sample was collected for microbiological culture before initiation of antibiotics and the result came back negative. On day 12, the patient was feeling tired and weak with hyperthemia (38.1 °C), hypertension (184/91 mm Hg), and worsened shortness of breath (26 beats/min). Plasma indicators for infection were elevated (WBC 11.50 × 109/L, neutrophils 97.1%, PCT 22.10 ng/mL). On the 13th day, moxifloxacin was switched to meropenem 500 mg intravenous every 8 hours. On 16th day, sputum culture revealed multidrug-resistant (MDR) A baumannii (resistant to carbapenem but sensitive to tetracycline). Then intraveous tigecycline was added to the regimen at a loading dose of 100 mg followed by 50 mg every 12 hours.
Fourteen hours after tigecycline initiation, the patient became confused, disoriented to location, and the time. He had difficulty understanding instructions and was clearly disturbed in attention during the conversation. He was agitated, fearing that people around him were trying to harm him. Then he became verbally aggressive toward his family members and medical staff. His mental disorder worsened in the next 2 to 3 hours then he began having hallucinations, seeing a huge ball in the ceiling and asking the nurse to take it down so he could eat it. He asked other people to gather together and said he had important things to announce. His Confusion Assessment Method, which is a valid tool for the detection of delirium, was negative prior to the initiation of tigecycline, but became positive after it was started. His clinical manifestations also met the key features listed by the Diagnostic and Statistical Manual of Mental Disorders fifth edition (DSM-V) criteria from the American Psychiatric Association that characterizes delirium.[
No focal neurological disease was noted after neurological examination. A computerized tomographic scan of the head was then performed, and no abnormalities were identified. Oxygen supplementation (4 L/min via nasal cannulae) was initiated after the arterial blood gas analysis showed hypoxemia (pH 7.41; PaCO2 25 mmHg; PaO2 68 mmHg; Na+ 132 mEq/L; K+ 5.5 mEq/L). The patient did not have any prior history of mental illness. Drug-induced delirium was suspected and tigecycline was speculated to be the most likely offending agent after medication review (Table ). Since his delirium was treated with little success with olanzapine, tigecycline therapy was discontinued the next morning after the patient stayed awake the whole night. During the following day after discontinuation of tigecyline, the patient's mental state improved and delirium cleared slowly. He restored the ability of focus and orientation. Perceptual disturbances disappeared, and no visual illusions or vague delusions of harm were noted again.
Meanwhile, markers of systemic inflammation were elevated (WBC 43.91 × 109/L, neutrophils 98.2%, PCT 34.04 ng/mL, CRP 89.09 mg/L). On Day 19, antibiotic therapy was switched to meropenem (i.v., 500 mg q8 h) combined with minocycline (p.o., 400 mg q12 h), and amikacin (i.v., 200 mg qd). The regimen continued for 5 days but the patient did not respond well, showing even higher systemic inflammation markers and exacerbated dyspnea. Antibiotic therapy was switched to meropenem 500 mg every 8 hours, and he started again on tigecycline 50 mg every 12 hours on 24th day with no loading dose.
In the morning of Day 25, the patient showed reduced psychomotor activity, decreased speech, but no obvious hallucinations. He had no idea of the time of day, nor where he was, although the day before he was fully orientated. The patient experienced a hypoactive state of delirium. CT examination of the chest showed increased inflammatory pulmonary lesions in bilateral lungs. Blood gas analysis revealed hypoxemia without carbon dioxide retention, and the electrolytes were found to be within range. Also, no significant changes in blood profile like levels of liver enzymes or serum creatinine was observed compared with the last test taken before the delirium appeared again. Tigecycline was discontinued and delirium resolved in the afternoon. Antibiotic treatment was then switched to levofloxacin (i.v., 600 mg qd) and minocycline (p.o., 100 mg q12 h). But the patient did not respond well to the present antibiotic therapy and his dyspnea exacerbated. He was transferred to the intensive care unit 6 days later as mechanical ventilation was required. Unfortunately, the patient died of recurrent attacks of left heart failure probably caused by uncontrolled serious infections on 33th day.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.0, 'kg'], 'height': [165.0, 'cm']}",22.03857,20.93664,23.1405,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.65 m * 1.65 m) = 22.03857 kg/m^2."
2054,6,Body Mass Index (BMI),physical,decimal,pmc-7725136-1,Extracted,"A 57-year-old male with a 7-day history of fever and dyspnea was admitted to a local hospital and intubated for respiratory failure. COVID-19 was confirmed by a positive polymerase chain reaction (PCR) test result obtained via a nasopharyngeal swab. Thus, he was transferred as a severe COVID-19 pneumonia case in need of intensive care. He had a medical history of hypertension, dyslipidemia, and asthma. His height was 173 cm and his weight was 71.6 kg.
On arrival, the physical examination revealed body temperature of 38°C, blood pressure of 112/47 mmHg, pulse of 106 beats/min, and respiratory rate of 14 breaths/min. He was deeply sedated (Glasgow Coma Scale score: E1VtM4) and suffered severe respiratory failure; arterial blood gas analysis showed pH 7.283, partial pressure of carbon dioxide (PaCO2) 45 mmHg, partial pressure of oxygen (PaO2) 64 mmHg with invasive mechanical ventilation [pressure control ventilation with positive end-expiratory pressure (PEEP) of 12 cmH2O, peak inspiratory pressure (PIP) of 24 cmH2O, the fraction of inspired O2 (FiO2) of 0.75, inspiratory time of 1.6 s, frequency of 14/min, and the delivered tidal volume was about 470 mL]. The computed tomography scan revealed a bilateral consolidation with lower lung predominance; bulla or emphysema was not observed (Fig. ). Favipiravir, hydroxychloroquine, and tocilizumab were administered for the COVID-19 treatment. As mechanical ventilation, in accordance with the acute respiratory distress syndrome (ARDS) strategy, did not show sufficient improvement, prone position ventilation was also initiated. His oxygenation improved slightly but not enough; PaO2 was 78.4 mmHg with FiO2 of 0.6.
On the 15th day after admission, the chest X-ray suggested a giant bulla in the right lung (Fig. ). One day later, his respiratory condition deteriorated and the chest X-ray revealed the presence of severe right-sided pneumothorax (Fig. ). A 24-Fr chest drain was immediately inserted, covering the patient’s right chest with a plastic sheet and attaching an in-line filter to the suction tubing to minimize aerosolization. However, a significant air leak continued, and severe ventilator settings were still required (pressure control ventilation with PEEP of 12 cmH2O, PIP of 28 cmH2O, FiO2 of 0.6, inspiratory time of 0.9 s, frequency of 20/min, and the delivered tidal volume was about 320 mL) to compensate for the respiratory acidosis (pH 7.266, PaCO2 62.2 mmHg, PaO2 73.3 mmHg). The Murray score was 3. In addition, the pneumothorax was considered to be intractable and the continuous air leak increased the risk of medical staffs’ exposure. Thus, VV-ECMO treatment (MERA centrifugal blood pump system HCS-CFP; Senko Medical Instrument, Tokyo, Japan) was promptly initiated for lung protection at 5 h after performing the tube thoracotomy. The right internal jugular vein was cannulated with a 19-Fr heparin-coated cannula for blood return, and the right femoral vein was cannulated with a 24-Fr heparin-coated cannula for blood access. The blood flow was 4.5 L/min and sweep gas was 5.0 L/min. Heparin was given to maintain an activated partial thromboplastin time of about 50 s.
The PEEP was initially set to 0 cmH2O and the PIP was set to 5 cmH2O. After the air leak diminished, we gradually increased the pressure. On the 3rd day after starting ECMO, the PEEP was set to 5 cmH2O and the PIP was set to 10 cmH2O. On the 7th day, the PEEP was set to 8 cmH2O and the PIP was set to 12 cmH2O. On the 10th day, during the sweep gas off test, the arterial blood gas analysis showed pH 7.383, PaCO2 49.4 mmHg, PaO2 81.7 mmHg with PEEP of 10 cmH2O, PIP of 22 cmH2O, FiO2 of 0.4, inspiratory time of 1.1 s, frequency of 18/min, and the delivered tidal volume was about 480 mL. Thus, the patient was weaned from the ECMO and the chest drain was removed on the following day with no major comorbidities.
We performed the PCR test every other week. The PCR test result was negative on the 31st day after admission. The patient underwent tracheostomy on the 34th day. The ventilator management was completed on the 52nd day and he was transferred for rehabilitation on the 61st day.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [71.6, 'kg'], 'height': [173.0, 'cm']}",23.92329,22.72713,25.11945,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 173.0 cm, which is 173.0 cm * 1 m / 100 cm = 1.73 m. The patient's weight is 71.6 kg. The patient's bmi is therefore 71.6 kg / (1.73 m * 1.73 m) = 23.92329 kg/m^2."
2055,6,Body Mass Index (BMI),physical,decimal,pmc-5134105-1,Extracted,"A 76-year-old, 166-cm, 71.3-kg Asian man with chest pain of 2 months’ duration due to coronary artery disease was admitted for coronary artery bypass graft (CABG) revascularization surgery. He had a history of hypertension and diabetes mellitus. He had a dilated left atrium, minimal tricuspid regurgitation, and normal left ventricular systolic function. He had no history of dysphagia or esophageal regurgitation. Preoperative magnetic resonance angiography revealed that his right internal carotid artery was severely occluded. The neurologist recommended a right carotid endarterectomy before CABG. The right carotid endarterectomy was performed uneventfully 2 days before CABG, and the total anesthesia time was 3 h 30 minutes.
A peripheral intravenous catheter was inserted into the left forearm, and an arterial catheter was inserted at the right radial artery. Anesthesia was induced with remifentanil 32 μg, propofol 120 mg, and rocuronium 70 mg. We inserted an OmniPlane TEE probe (Philips Medical Systems, Andover, MA, USA) into the esophagus without any difficulty or resistance. TEE examination was done with the CABG procedure. For patient safety, the comprehensive intraoperative TEE guidelines of the American Society of Echocardiography Council for Intraoperative Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force were followed.
The CABG was successful. The cardiopulmonary bypass time was 105 minutes. During cardiopulmonary bypass, the patient’s temperature was lowered to 33.0 °C at the rectum (33.0 °C at the nasal membrane). The TEE probe was in a neutral position in the upper esophagus and frozen to prevent injury. The average pump flow rate was 2.4 L/minute/m2. At the end of the procedure, the patient was rewarmed to 36.3 °C at the rectum (36.8 °C at the nasal membrane) for 60 minutes. During rewarming, TEE examination was performed, and the temperature of the TEE probe was increased to 39 °C. The TEE examination was discontinued intermittently and automatically to reduce the probe temperature. During the TEE examination, any movement or manipulation was gentle. Dopamine and nitroglycerin were given during weaning from bypass. The TEE probe was removed at the end of anesthesia. It was clean with no signs of blood. Extubation was done 11 h postoperatively.
The patient developed intermittent fever on the first postoperative day. Leukocytosis (19,440 white blood cells/μl) and a high level of C-reactive protein (30.0 mg/dl) were detected in the postoperative laboratory examination. The patient’s fever ranged from 37.0 °C to 38.3 °C and did not subside until postoperative day 3, despite empirical treatment with tazobactam and ciprofloxacin. Computed tomography done to evaluate the coronary arteries incidentally found signs of abscess formation or air-containing tissue in the retrosternal, pericardial, and paraesophageal areas (Fig. ). Esophagography revealed contrast leakage in the right wall of the middle esophagus (Fig. ). The patient’s hemodynamic variables, including blood pressure and heart rate, remained stable and were monitored closely. The patient was managed conservatively with fasting, parenteral nutrition, and intravenous antibiotics. We were prepared for surgical intervention, such as open esophageal repair or endoscopic primary repair, if there was any indication of unstable vital signs. The patient’s postoperative fever abated on postoperative day 4. Follow-up esophagography disclosed no change in the esophageal lesion. The patient was allowed to drink sips of water 35 days postoperatively. On postoperative day 39, he began a normal diet. He was discharged without complications on postoperative day 42.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [71.3, 'kg'], 'height': [166.0, 'cm']}",25.87458,24.58085,27.16831,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 71.3 kg. The patient's bmi is therefore 71.3 kg / (1.66 m * 1.66 m) = 25.87458 kg/m^2."
2056,6,Body Mass Index (BMI),physical,decimal,pmc-3420415-1,Extracted,"A 53-year-old white man, suffered from type 2 diabetes diagnosed 20 years ago, was referred to our department for evaluation of recent discovery of incipient nephropathy and retinopathy. He was previously visiting another endocrinologist in the town but because of a change of job, he moved into the city. He brought a letter specifying that his glucose control had been acceptable since the diagnosis of diabetes (HbA1c lower than 7%). Recently, he was diagnosed of incipient nephropathy (microalbuminuria 200 mg/24 hours), high systolic blood pressure (140 mmHg), high LDL cholesterol (134 mg/dL), and retinal hard exudates close to the macula treated with laser photocoagulation. His current medication included metformin (2.550 mg/day), Detemir insulin (50 U/day), premeals Aspart insulin, simvastatin (20 mg/day), Candesartan (16 mg/day), and AAS (100 mg/d). Physical examination revealed the following: weight of 120 Kg, height of 174 cm, body index mass of 30,27 Kg/m2, blood pressure of 150/75 mmHg, and normal auscultation. The skin of the upper back and posterior neck was erythematous, indurated, and painless () with moderate restriction of range of motion of the shoulders and neck.
Blood analysis revealed the following: leukocytes of 7500 μL, haemoglobin of 16,3 g/dL, platelets of 281000 μL, sedimentation glomerular rate of 10 mm, glucose of 135 mg/dL, creatinine of 0,3 mg/dL, cholesterol of 157 mg/dL, HDL-c of 58 mg/dL, LDL-c of 81 mg/dL, triglycerydes of 90 mg/dL, C peptide of 3,8 ng/mL, TSH of 1,78 μUI/mL, negative antithyroid antibodies, microalbuminuria of 240 mg/24 h, and HbA1c of 6,7%. The serum protein electrophoresis was normal, excluding monoclonal gammopathy.
When we noticed the lesion on the skin and asked about it, the patient explained that for the last 10 years he had noticed a progressive hardening of the skin of this area, that became less sensitive, and he also noticed a decrease in motility of his neck and shoulders. He did not remember if he was febrile 10 years ago when the lesion appeared on his back. He had never been studied for the skin disorder that he related with his obesity. The patient was sent to the dermatologist who suspected the diagnosis of scleredema and performed a skin biopsy. Histopathologic study demonstrated thick collagen bundles separated by spaces filled with mucin in the deep reticular dermis, consistent with scleredema adultorum of Buschke (). He recommended physiotherapy and UV-A1 therapy. The latter treatment was not made because of a lack of this modality of phototherapy in his town, then he started PUVA therapy.
After two months of PUVA therapy (total cumulative UVA dose 120 J/cm2) and physical exercises, the patient has noticed amelioration of the mobility of the back and shoulders, and on exploration, the redness of the upper back has disappeared, and the skin was softer.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [120.0, 'kg'], 'height': [174.0, 'cm']}",39.63535,37.65358,41.61712,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 174.0 cm, which is 174.0 cm * 1 m / 100 cm = 1.74 m. The patient's weight is 120.0 kg. The patient's bmi is therefore 120.0 kg / (1.74 m * 1.74 m) = 39.63535 kg/m^2."
2057,6,Body Mass Index (BMI),physical,decimal,pmc-6054848-1,Extracted,"A 65-year-old male, 155 cm tall and weighing 53 kg, was scheduled to undergo mesh cage insertion and posterior spinal fusion from T6 to L5 for severe kyphosis due to spinal tuberculosis. Preoperative chest radiography revealed severe kyphosis of the thoracolumbar spine; however, there was no active lesion in the lungs. Thoracolumbar magnetic resonance imaging and computed tomography revealed spinal fusion at the level of T9–L3, with volume decrease and deformity associated with severe kyphosis. The kyphotic angle was approximately 115 degrees (Fig. ). Preoperative pulmonary function tests revealed a mild restrictive pattern with a forced vital capacity (FVC) of 1.81 L (63% of normal), a forced expiratory volume in 1 s (FEV1) of 1.53 L (73% of normal), and an FEV1/FVC ratio of 85%. Preoperative electrocardiography revealed normal sinus rhythm. In the preoperative visit, the patient exhibited limited neck motion because of severe kyphosis; he was Mallampati class III.
In the operating room, the patient was monitored using three-lead electrocardiography, pulse oximetry, non-invasive blood pressure monitoring, and bispectral index. Due to inability to lie on his back without any supportive devices, the head of the operating bed was raised approximately 30–40 degrees, and anesthesia was induced in the semi-recumbent position. Anesthesia was induced using a target-controlled infusion of propofol (Schnider model) and remifentanil (Minto model); rocuronium bromide 0.6 mg/kg was administered to facilitate tracheal intubation. Before tracheal intubation, preoxygenation was performed for 5 to 10 min with 100% oxygen in a face-to-face approach, with bimanual mask holding and mechanical ventilation. Although the awake intubation technique may be considered in cases of anticipated difficult intubation, the cause of difficult intubation in the present case was attributed to a kyphotic change, and not the airway itself, such as an anteriorly deviated glottis or soft tissue swelling; therefore, the authors believed that the patient’s airway could be adequately maintained using bimanual mask-holding in a face-to-face position. Initially, direct laryngoscopy and video laryngoscopy were attempted; however, it was exceedingly difficult to visualize the vocal cords because of the patient’s semi-recumbent position, his short stature, and the relatively large bed size. Moreover, a conventional lightwand technique from the head end of the patient was also difficult to perform. Although fiberoptic bronchoscopy can be considered as a first choice, it was temporarily unavailable because of an insufficient number of devices and well-trained staff. As the conventional overhead approach using laryngoscopy or lightwand was difficult, an alternative face-to-face approach using a lightwand was attempted. After all lights in the operating room were turned off, the anesthetist opened the patient’s mouth while facing him, and slowly inserted the tracheal tube-launched lightwand, of which the tip was bent at an angle of 90 degrees along the base of the tongue in the midline. The bright red light at the tip of the stylet was transilluminated and positioned at the center of the neck; subsequently, the tracheal tube was gently inserted at the location of light on the neck. (Fig. ). Face-to-face lightwand intubation was successful on the first attempt, and no specific complications, such as hemodynamic instabilities, intraoral traumas, or others, were encountered. After tracheal intubation, invasive arterial blood pressure was monitored through a cannula placed in the left radial artery using a hemodynamic monitoring device (EV1000 clinical platform, Edward Lifesciences Corp., Irwin, CA, USA). The surgery lasted approximately 7 h, during which vital signs were adequately maintained. After completion of surgery, neuromuscular blockade was reversed using sugammadex 200 mg followed by extubation in the operation room. Adequacy of respiration was confirmed, and the patient was transferred to the intensive care unit with continued monitoring. Although there was no postoperative sore throat or hoarseness of voice, there was suspicion of pulmonary congestion on chest radiography. On arterial blood gas analysis, the partial pressure of oxygen (PaO2) while breathing room air was 64 mmHg. However, the patient was not dyspneic, and pulmonary congestion and PaO2 improved over time. On postoperative day 2, the patient was transferred to the general ward without any significant problems.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.0, 'kg'], 'height': [155.0, 'cm']}",22.06035,20.95733,23.16337,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 53.0 kg. The patient's bmi is therefore 53.0 kg / (1.55 m * 1.55 m) = 22.06035 kg/m^2."
2058,6,Body Mass Index (BMI),physical,decimal,pmc-7337418-1,Extracted,"A 58-year-old Chinese female was admitted to our department of neurology with weakness of both arms and legs. Two months prior to admission, she had developed weakness in her bilateral limbs as well as pain in both shoulders. So, she went to a local hospital and reported that she felt the pain ease after receiving traditional Chinese medicine therapy. However, the weakness of her limbs gradually increased. So, she came to our hospital for further diagnosis and treatment. Her past medical history included well-controlled hypertension and diabetes mellitus. Furthermore, she had experienced pyrexia at times in recent years but without the detection of a raised temperature, and she did not seek diagnosis and treatment. She had no history of smoking, alcohol consumption, or recreational drug use. Her family history was unremarkable.
On admission, her height was 158 cm, body weight was 42 kg, body temperature was 38.9°C, pulse was regular at 122 beats/min, respiratory rate was 28 breaths/min, and blood pressure was 170/98 mm Hg. The physical examination revealed that multiple lymphadenopathies were present in the bilateral axillary and the right side of the middle neck triangle, hyperpigmentation in the abdomen, and bilateral pitting pedal edema. The neurological examination showed bilateral upper and lower limb muscle weakness. The upper and lower extremity strength scores, as determined by manual muscle testing, were 3/5 and 4/5, respectively. Tendon reflexes were absent in all extremities, and pathological reflexes were negative. The patient was lucid, and the neurological examination revealed no cranial nerve abnormalities.
Laboratory data on admission (Table ) revealed an elevated platelet count, but the coagulation profile was normal. The erythrocyte sedimentation rate was 41 mm/h (normal range 0 to 20 mm/h). The concentration of C-reactive protein was increased. The testing showed strongly raised creatine kinase (CK) activity (7845 U/L, normal range 40–200 U/L) and elevated liver enzymes in the serum. Blood tests showed a glucose level of 5.88 mmol/L and a glycosylated hemoglobin level of 7.1%. The renal function testing revealed that her creatinine level was normal, but Cystatin C was elevated, and her glomerular filtration rate was decreased. Meanwhile, her urine protein content was 133.35 mg/L (normal range 0 to 10 mg/L). Furthermore, her creatine kinase-MB, MB, and hs-TnT concentrations were significantly increased. Thyroid function tests revealed hypothyroidism. The thyroxin stimulating hormone level was 12.069 uIU/mL (normal range 0.35–4.94 uIU/mL), but the free-T3 and T4 concentrations were normal. The adrenocorticotropic hormone concentration was 3.24 pg/mL (normal range 4.7 to 48.8 pg/mL). The cortisol concentration was 1.1 ug/dL in 4pm (normal range 2.9 to 17.3 ug/dL). Human immunodeficiency virus, serology for hepatitis B and C, and tumor markers (cancer antigen 125, alphafetoprotein, careinoembryonic, carbohydrate antigen 199, cancer antigen 153, cancer antigen 242, prostate specific antigen and neuron specific enolase) were negative. Electrodiagnostic study showed that the motor conduction velocities, sensory nerve action potential, compound muscle action potential, and F wave latency were in the normal range in the bilateral median, ulnar, sural, and tibial nerves. Electromyography analysis showed there were mass abnormal spontaneous activities (fibrillation and positive sharp wave) in the left first dorsal interossei, biceps brachii, tibialis anterior, and the medial head of quadriceps femoris muscle, and myotonic potential in the left iliopsoas and tibialis anterior muscles. The neck triangle lymph node biopsy showed lymphadenosis, but the patient refused an immunohistochemical examination. On the thorax computed tomography (CT) scan, multiple enlarged axillary lymph nodes were observed (Fig. A). The flexor carpi radialis muscle biopsy showed many infiltrated lymphocytes, and the congo red staining test was negative. Combined with the symptoms, physical examination, and laboratory tests, we made a diagnosis of myositis. Hence, we treated the patient with methylprednisolone. However, she did not show a significant improvement, despite receiving standard therapy. Thus, immunoelectrophoresis was performed. Immunoelectrophoresis showed monoclonal IgA lambda serum. A bone marrow biopsy examination revealed that the plasma cell content was slightly elevated (0.84%). Furthermore, the concentrations of serum IgA and lambda free light chains were elevated. Serum IgG, IgM, and IgE levels and complements of C3, C4, and kappa free light chains were within the normal range. Furthermore, the VEGF concentration was slightly elevated. In addition, a X-ray of the skull revealed a small bone defect in the frontal lobe (Fig. B). Ultrasonography showed no cardiomegaly, hepatosplenomegaly, or pleuroperitoneal fluids. Based on the observed skin manifestations, lymphadenopathies, pedal edema, IgA-λ restricted paraproteinemia, plasma cell dyscrasia in bone marrow, elevation of VEGF, and other features, we made a diagnosis of atypical POEMS syndrome without polyneuropathy.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [42.0, 'kg'], 'height': [158.0, 'cm']}",16.82423,15.98302,17.66544,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 158.0 cm, which is 158.0 cm * 1 m / 100 cm = 1.58 m. The patient's weight is 42.0 kg. The patient's bmi is therefore 42.0 kg / (1.58 m * 1.58 m) = 16.82423 kg/m^2."
2059,6,Body Mass Index (BMI),physical,decimal,pmc-8383548-1,Extracted,"A 33-year-old Japanese woman visited our hospital due to 1 week of continuous low-grade fever, low back pain, and numbness of the entire left lower limb. These symptoms occurred when she lifted a heavy suitcase. She had visited an orthopedic doctor and received a caudal block 4 days prior, followed by a high-grade fever and deteriorating low back pain starting 1 day prior. Her medical history included surgery to enlarge both breasts when she was 14 years old. She was not taking any medicines on a regular basis. She had a smoking history of five cigarettes a day starting at the age of 20, and no history of drinking alcohol. She underwent periodic medical exams, and the latest one, which had been 2 months before, appeared normal. The patient was employed at a film factory, as a product inspector, and had no food or drug allergies. She had no history of casual sex, intramuscular injections, or IV drug use.
She was 153 cm tall, and weighed 42 kg. Her vital signs were abnormal, with blood pressure of 104/85 mm Hg, a heart rate of 123 regular beats/min, a body temperature of 38.1 °C, oxygen saturation of 98% in ambient air, and a respiratory rate of 16/min; her Glasgow Coma Scale score was 15 (E4V5M6) points. She complained of percussion tenderness to the lower thoracic vertebra and the upper sacral bone. Her manual muscle testing score for the left lower limb was 4; on the other hand, nothing else abnormal, including skin or neurologic findings, was detected upon physical examination.
A routine laboratory examination of the patient revealed increased values of white blood cells, creatinine, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR), and decreased values of blood urea nitrogen and creatine kinase. On the other hand, other values were normal, including complete blood count (CBC), biochemistry, urine tests, and cerebrospinal fluid examination (). She also tested negative for rheumatoid factor, autoantibodies such as anti-nuclear antibodies, anti-neutrophil cytoplasmic antibodies, serologic test for hepatitis B and C, syphilis, HIV, thyroid hormone, soluble interleukin-2 receptor, flu test, and 2/2 sets of blood culture. Head and chest-abdomen computed tomography (CT) scans and transesophageal echocardiography revealed normal results. On the other hand, a complete spine magnetic resonance imaging (MRI) scan revealed a 0.5- mm-thick layer of spinal epidural fluid in the posterior epidural space in the whole thoracic and anterior epidural space from the L5 to S2 vertebral body level region, which compressed the epidural space (, and , respectively). These findings were revealed as low intensity in a T1-weighted image, and high intensity in a T2-weighted image. Other findings, such as discitis, were not confirmed.
At this point, we suspected a diagnosis of disseminated SEA, but the origin was still unknown. However, an orthopedic surgeon recommended against performing CT-guided percutaneous needle aspiration of the abscess, based on the locations of the lesions. The patient was hospitalized, and we started 13.5 mg/day of piperacillin-tazobactam, following which she gradually became symptom-free. However, on the 14th hospital day, she strongly requested that she be discharged from the hospital, so we changed her antibiotics to 500 mg/day of levofloxacin tablets, and continued treatment. During her return visit, 16 days after her discharge, she was well. We confirmed normal values of inflammation biomarkers, including WBC, CRP, and ESR, and in addition we also confirmed abscess improvements in both the thoracic and sacral regions through an MRI scan (, and , respectively). Based on these findings, we ended her treatment that day without treatment complications.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [42.0, 'kg'], 'height': [153.0, 'cm']}",17.94182,17.04473,18.83891,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 153.0 cm, which is 153.0 cm * 1 m / 100 cm = 1.53 m. The patient's weight is 42.0 kg. The patient's bmi is therefore 42.0 kg / (1.53 m * 1.53 m) = 17.94182 kg/m^2."
2060,6,Body Mass Index (BMI),physical,decimal,pmc-8059042-1,Extracted,"A 53-year-old man (height, 170 cm; weight, 89 kg) was admitted to the hospital because of a 1-year history of shortness of breath after exercise. The patient was a smoker, had a history of hypertension, and was taking captopril and nimodipine. Breathing was reduced in the left lung. However, neither rhonchus nor moist rales were heard during auscultation. Chest computed tomography revealed a GEB, and the left lung was compressed by about 95% with a right mediastinal shift (). An electrocardiogram showed normal findings, and echocardiography revealed that the heart was located in the right thoracic cavity. The left ventricular diastolic function was decreased, and the left ventricular ejection fraction was 64%. Laboratory tests showed no obvious abnormalities. Arterial blood gas analysis showed the following: pH: 7.43, PaCO2: 41 mmHg, PaO2: 94 mmHg, lactate: 1.4 mmol/L, potassium: 3.6 mmol/L, sodium: 138 mmol/L, calcium: 1.10 mmol/L, FiO2: 21%, and SpO2: 98%.
On the day of surgery, the patient’s electrocardiogram, blood pressure, SpO2, and bispectral index were monitored upon entry into the operating room. A radial artery catheter and right internal jugular venous catheter were placed. The patient’s arterial blood pressure was 175/109 mmHg, heart rate was 90 beats/minute, and SpO2 was 94%. Before anesthesia, 40 µg of dexmedetomidine was infused within 10 minutes. The thoracic surgeon then created a small incision at the intersection of the sixth intercostal space and the left mid-axillary line to puncture the lung bulla and insert an indwelling catheter (14 Ga, 16 cm in length; Arrow International/Teleflex, Wayne, PA, USA) into the GEB to drain it for 15 minutes. The patient was preoxygenated with 100% oxygen at 6 L/minute for 5 minutes. Anesthesia was administered using 100 mg of propofol, 30 µg of sufentanil, and 50 mg of rocuronium. A 37-Fr right double-lumen endotracheal tube was inserted with the help of a visual laryngoscope, and single-lung ventilation was performed after proper alignment had been confirmed by fiberoptic bronchoscopy. The tidal volume was set at 5 to 6 mL/kg, the respiratory rate was 15 to 17 breaths/minute, the positive end-expiratory pressure was set at 5 cmH2O, and the inhalation:expiration ratio was 1:2. Propofol, remifentanil, and sevoflurane were used to maintain anesthesia. The intraoperative bispectral index was maintained at 40 to 50. After resecting the GEB (), one-lung ventilation was switched to two-lung ventilation and the lungs slowly expanded with a low tidal volume until complete lung re-expansion was observed. During the 3-hour surgery, the patient experienced 50 mL of blood loss, was administered 1300 mL of lactated Ringer’s solution, and excreted 500 mL of urine. After the operation, the double-lumen endotracheal tube was replaced with a single-lumen endotracheal tube and the patient was sent to the intensive care unit for monitoring and further treatment. Two hours after entering the intensive care unit, the patient was fully awake and the tracheal tube was smoothly removed. The following day, the patient was transferred to the thoracic surgery ward, where he recovered; he was discharged 12 days later. Postoperative chest computed tomography showed that the lungs were well inflated with no abnormalities ().",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [89.0, 'kg'], 'height': [170.0, 'cm']}",30.79585,29.25606,32.33564,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 89.0 kg. The patient's bmi is therefore 89.0 kg / (1.7 m * 1.7 m) = 30.79585 kg/m^2."
2061,6,Body Mass Index (BMI),physical,decimal,pmc-3189105-1,Extracted,"A 41-year-old Chinese woman was referred to the Department of Neurology, Nanfang Hospital of Southern Medical University, Guangzhou, China, with the chief complaint of high spiking fever for approximately a month with bilateral lower limb fatigue and difficulty in defecation for more than five months. She had been residing in Yingde City of Guangdong Province for 10 years with no known prior exposure to any infectious or occupational diseases. In July 2010, she was diagnosed with 'whole body multiple metastases of lymphoma'. Due to economic reasons, the patient was transferred at the end of July 2010 to Donghua Hospital of Yingde City for treatment of her symptoms of infection, constipation, low potassium and leukopenia. By August 2010, the patient was unable to walk with bilateral lower limb fatigue and was subsequently admitted to the Department of Radiation Oncology at Nanfang Hospital.
On admission, the patient was 152 cm tall and weighed 52 kg. Her blood pressure was 112/82 mm Hg, temperature 38.5°C with a respiratory rate of 16 times per minute. No superficial enlarged lymph nodes were palpable. Inspiratory and expiratory sounds were normal to auscultation. There was no percussion tenderness over the liver or kidney. Muscle strength of upper limbs was normal and that of lower limbs was 3/5. Bilateral Babinski sign was positive. Sensation of pain and touch below the knees were slightly reduced. Physiological reflexes were slightly active. There was no pedal edema. All other physical tests were normal.
Laboratory findings were as follows: total urinary protein, 5.61 g/dL (56.1 g/L); serum albumin, 2.89 g/dL (28.9 g/L); blood urea nitrogen, 2.24 mg/dL (1.6 mmol/L); and creatinine, 0.54 mg/dL (48 μmol/L). The urine protein and occult blood values were negative. Urinary leukocyte count was 48/μL (4.8 × 107/L); erythrocyte count, 3.78 × 106/μL (3.78T/L); hemoglobin, 9.9 g/dL (99 g/L); lymphocyte count, 1.12 × 103/μL (1.12 g/l) and platelet count, 1.73 × 105/μL (173 g/l).
Bone marrow aspiration was performed and the slide smear revealed 41.5% immature cells of unknown origin. Positron Emission Tomography-Computed Tomography (PET-CT) showed the following changes (Figure ). The bilateral renal parenchyma was markedly swollen with obvious diffuse increase in signal intensity. Increased signal intensity was observed in multiple thoracic vertebral bodies, multiple lumbar vertebral bodies, bilateral sacrum, ilium, proximal humerus and femur medullary cavities. Mildly increased signal intensity was observed in both lungs. The possibility of interstitial pneumonia was not excluded. Multiple bilateral neck and mediastinum lymph nodes were mildly enlarged with inflammatory proliferation. The spleen was markedly enlarged with mild diffuse increase in signal intensity. A large volume of pelvic effusion was detected.
The day after admission, a percutaneous renal biopsy was performed. Eleven glomeruli were present with no evidence of mesangial cell proliferation or capillary wall thickening. Island-like accumulations of medium to large lymphoid cells were observed in many areas of the interstitium, with round vesicular nuclei containing distinct basophilic nucleoli (Figure ). Immunohistochemical analysis showed the atypical lymphoid cells to be positive for B-cell markers CD20 (Figure ) and negative for CK, CD3, CD45RO and CD10. They were positive for large B-cell lymphoma marker mum-1 (Figure ). Immunohistochemical staining using anti-CD34 confirmed the accumulation of lymphoid cells to be localized within the peritubular capillary lumina (Figure ). Immunofluorescence revealed negative staining of IgG, IgA, IgM, C3 and C1q with no glomerular immune deposits. Electron microscopy did not detect any electron dense deposits, but did show a cluster of atypical lymphocytes encircled by a peritubular capillary wall.
Pathologic examinations of percutaneous renal biopsies confirmed the diagnosis of intravascular large B-cell lymphoma of Stage IVE. The patient returned to the local hospital for symptomatic treatment after diagnosis. Ten days later she was readmitted into Nanfang hospital due to sudden bilateral lower limb fatigue and inability to walk. She was treated with chemotherapy consisting of CHOP (cyclophosphamide 1.0 g D1+Doxorubicin 60 mg D1+leurocristime 2 mg D1+Prednisone 100 mg D1-5) for a week. Palliative radiotherapy DT 40Gy/20F and other supportive treatment were provided for metastatic foci in the medullary cavity of sternum, T1-7. The patient regained muscle strength in both lower limbs and was able to walk again. She was discharged after hepatic and renal function values had returned to normal. Follow-up data shows the patient to be alive, nine months after discharge.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [52.0, 'kg'], 'height': [152.0, 'cm']}",22.50693,21.38158,23.63228,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 152.0 cm, which is 152.0 cm * 1 m / 100 cm = 1.52 m. The patient's weight is 52.0 kg. The patient's bmi is therefore 52.0 kg / (1.52 m * 1.52 m) = 22.50693 kg/m^2."
2062,6,Body Mass Index (BMI),physical,decimal,pmc-7329962-3,Extracted,"Case 3: a 65-year-old male (182 cm, 67 kg) diagnosed with femoral metastasis of gastric cancer was planned for elective intramedullary nailing. He was receiving oral oxycodone 20 mg/day for more than 50 days. His bone cancer pain was under control. Regional anesthesia was chosen as the surgery was a simple procedure. He took the regular morning dose of oxycodone before surgery and lumbar anesthesia was performed with 2.6 ml hyperbaric 0.5% bupivacaine, and he was free from pain (no record of anesthesia level). Continuous RR and end-tidal CO2 monitoring with the standard monitoring during the surgery showed no apnea nor bradypnea during the surgery (surgery time, 1 h 33 min) (Fig. ) with average RR of 18 ± 5/min while he was observed to be sleeping without any sedatives during the operation.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [67.0, 'kg'], 'height': [182.0, 'cm']}",20.22703,19.21568,21.23838,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 182.0 cm, which is 182.0 cm * 1 m / 100 cm = 1.82 m. The patient's weight is 67.0 kg. The patient's bmi is therefore 67.0 kg / (1.82 m * 1.82 m) = 20.22703 kg/m^2."
2063,6,Body Mass Index (BMI),physical,decimal,pmc-5778632-1,Extracted,"A 6-year-old male from the West Region of Cameroon diagnosed with HIV 3 years back and on pediatric first line highly active antiretroviral therapy (HAART) regimen—Abacavir, Lamivudine and Efavirenz (ABC/3TC/EFZ),—was referred from a health center to our institution for suspicion of pulmonary TB based on a 10 days history of productive cough, intermittent nocturnal fever and generalized abdominal pain, which persisted despite administration of undocumented broad spectrum intravenous antibiotics for 8 days. His mother was on the first month of hospitalization at our institution for management of MDR-TB, a referral hospital for MDR-TB.
On examination, the child had respiratory distress with a pulse rate of 137 beats/min, respiratory rate of 22 cycles/min and temperature of 40.1 °C. His weight and height were 20 kg and 80 cm, respectively. There was pallor of the conjunctivae, palms and soles. The BCG scar was present on the left forearm. The heart was tachycardic with audible functional systolic murmurs. A bilateral consolidation syndrome was also noted on examination of the lungs. An initial diagnosis of pediatric pulmonary TB/HIV coinfection, associated with a clinical anaemia was made. MDR-TB was the principal differential diagnosis.
A sputum analysis done was positive for acid-fast bacilli. Since he was a household contact of the mother and given that he became very ill, and unable to produce one more sputum, we chose to collect the gastric aspirate and sent for gene Xpert MTB/RIF and culture/DST in other to make a good diagnosis early enough. The gastric aspirate was positive for a Mycobacterium tuberculosis Rifampicin resistant strain using Xpert MTB/RIF assay. After performing the proportional method -drug susceptibility testing (PM-DST) on Lowenstein Jensen slopes, the child was found to have the same resistance pattern like the mother (Isoniazid-susceptible, Rifampicin-resistant, Ethambutol-susceptible, Kanamycine-susceptible, Ofloxacine-susceptible and streptomycine-not done). Due to the severe anaemia at 6.1 g/dl, he received 20 ml/kg (400 ml) of whole blood in emergency. The results of his pre-therapeutic work-up for MDR-TB regimen were as follows: slightly raised Aspartate Aminotransferase but normal Alanine Aminotransferase at 68 and 28.5 U/l, respectively; Serum Creatinine was normal at 0.45 mg/dl. An antero-posterior view chest X-ray revealed a bilateral micro-nodular interstitial opacity associated with bilateral hilar adenopathy (Fig. ). Also an audiogram and electrocardiogram (ECG) done were not contributive.
After discussing the case with the MDR-TB consultant of the National Tuberculosis Program (NTP), with regards to the results of his pre-therapeutic work-up, the short 9 month—regimen was initiated according to his weight: 4 months of Amikacin/Moxifloxacin/Prothionamide/Isoniazid/Clofazimin/Ethambutol/Pyrazinamid for the initiation phase, followed with 5 months of Moxifloxacin/Clofazimin/Ethambutol/Pyrazinamid for the continuation phase [4(AmMfxPtoHCfzEZ)/5(MfxCfzEZ)]. His viral load was 23,144 copies/µl and the CD4 cell count 149cells/mm.
Day 36 of hospitalization was marked by another episode of decompensated severe anaemia at 3.9 g/dl and non-infectious enteritis (with abdominal pains and watery stool). This prompted another transfusion of whole blood cells at 20 ml/kg (400 ml), and iron and folic acid syrup at a dose of 6 mg/kg/day (120 mg) were continued twice daily for a month. In addition, the patient presented with mild bilateral knee pain which was immediately controlled with 2 mg/kg (40 mg) dose of diclofenac divided twice a day. He also presented with a progressive brownish discoloration of the eyes with no visual impairment for which he is been followed-up. During the course of the treatment, the child was doing well and was able to produce a good sputum sample; he was discharged 4 months after the initiation phase with consecutively negative monthly sputum controls (Table ). The child is presently on the ninth month of treatment with no further complaints.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [20.0, 'kg'], 'height': [80.0, 'cm']}",31.25,29.6875,32.8125,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 80.0 cm, which is 80.0 cm * 1 m / 100 cm = 0.8 m. The patient's weight is 20.0 kg. The patient's bmi is therefore 20.0 kg / (0.8 m * 0.8 m) = 31.25 kg/m^2."
2064,6,Body Mass Index (BMI),physical,decimal,pmc-6856503-1,Extracted,"A 38-month-old boy was brought to the Seoul National University Children's Hospital due to a sudden onset of respiratory difficulty. The patient had no perinatal problems but began to develop intermittent alcoholic stool at 1 year of age. Beginning at 2 years of age, the patient suffered from frequent abdominal cramps. The patient presented with dyspnea and tachypnea but did not show signs of fever, cough, cyanosis, chest pain, vomiting, or abdominal pain.
The patient's height and weight were 95.6 cm (25–50th percentile) and 13.3 kg (10–25th percentile), respectively. His vital signs were as follows: blood pressure, 123/72 mmHg; pulse rate, 152 beats/min; respiratory rate, 36 breaths/min; and body temperature, 36.9°C. The chest wall expanded symmetrically with chest retraction. Decreased breathing sound was heard in the left lung field.
Chest radiography and computed tomography (CT) showed massive left pleural effusion (). Percutaneous catheter drainage (PCD) was conducted and pleural effusion was drained. Pleural fluid revealed elevated amylase levels of 25,460 U/L and lipase levels of >6,000 U/L. Serum results also revealed elevated amylase levels of 888 U/L and lipase levels of 1,067 U/L, which was suggestive of acute pancreatitis.
Abdomen CT showed retroperitoneal fluid collection, diffuse pancreatic ductal dilatation, and atrophy in the pancreatic body and tail parenchyma, which was suggestive of CP. Although the abdomen CT did not reveal a definite PPF tract, the elevated amylase and lipase levels from the pleural fluid were suggestive of a fistula tract between the pancreas and pleura. Magnetic resonance cholangiopancreatography (MRCP) revealed suspicious luminal narrowing of the pancreatic duct, with probable pancreatic duct stone and sludge. A tract near the left diaphragm is thought to be the fistula that connects to the pleural cavity ().
The patient was kept under fasting conditions with massive intravenous hydration, and octreotide continuous infusion and total parenteral nutrition were initiated. Endoscopic retrograde cholangiopancreatography (ERCP) was performed to further clarify the possible duct anomaly and subsequent treatment. The pancreatic duct was tortuous and dilated, and there was a filling defect due to the pancreaticolith (). A single pigtail plastic stent was inserted at the pancreatic duct and some white stones and protein plugs were removed. After symptoms improved, the PCD was removed and octreotide was tapered.
The pancreatic stent was removed spontaneously via defecation 8 days after stent insertion. After 3 days, a fever of up to 39.4°C developed and left pleural effusion increased. Serum amylase and lipase levels were elevated to 285 U/L and 527 U/L, respectively. Medical treatment, including fasting and octreotide continuous infusion, was restarted, and PCD insertion was conducted again. A second ERCP was done, and the stent was placed at the minor papilla through the major papilla. The pleural drain was removed after a week of post-stent insertion with no recurrence or effusion. The patient was discharged at hospital day 32. The stent was removed after 3 months. The patient is being followed-up regularly for exocrine dysfunction and recurrence of pancreatitis by monitoring fecal elastase, and serum amylase and lipase levels, respectively.
This patient had a family history of pancreatic diseases (). The patient's uncle underwent 80% distal pancreatectomy due to CP with multiple stones, and the grandfather had pancreatic cancer. The great-aunt and first cousin also had pancreatic diseases. The patient and his family underwent genetic tests, which revealed that the patient, mother, uncle, and grandfather were R122H heterozygotes for PRSS1 gene which encodes cationic trypsinogen. His father and brother had negative results.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [13.3, 'kg'], 'height': [95.6, 'cm']}",14.55244,13.82482,15.28006,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 95.6 cm, which is 95.6 cm * 1 m / 100 cm = 0.956 m. The patient's weight is 13.3 kg. The patient's bmi is therefore 13.3 kg / (0.956 m * 0.956 m) = 14.55244 kg/m^2."
2065,6,Body Mass Index (BMI),physical,decimal,pmc-8494847-1,Extracted,"Male, 41 years old, with a 7-year history of DM, was admitted for evaluation of acute renal dysfunction (from 1.65 mg/dL to 3.0 mg/dL serum creatinine, from 36.7 mL/min/1.73 m2 to 19.9 mL/min/1.73 m2 eGFR for 56 day intervals). Treatment with dapagliflozin 5 mg daily was started from 19 months before this admission. The patient’s height was 162 cm and weight increased from 84 to 93 kg, following treatment with dapagliflozin. Urinary protein was 0.28 g/day and negative for ketones. The patient’s blood pressure was 128/76 mmHg; HbA1c, 6.1%; blood sugar level, 74 mg/dL; and plasma renin activity was 8.9 ng/ml/hr (normal 0.3–2.9). Renal biopsy was performed to evaluate renal dysfunction.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [93.0, 'kg'], 'height': [162.0, 'cm']}",35.43667,33.66484,37.2085,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.0 cm, which is 162.0 cm * 1 m / 100 cm = 1.62 m. The patient's weight is 93.0 kg. The patient's bmi is therefore 93.0 kg / (1.62 m * 1.62 m) = 35.43667 kg/m^2."
2066,6,Body Mass Index (BMI),physical,decimal,pmc-7590902-1,Extracted,"Our patient is a 4-year-old African-American boy born full-term via vaginal delivery, following an uneventful pregnancy, with a birth weight of 2722 grams (9th percentile). He required two weeks in the Neonatal Intensive Care Unit for neonatal abstinence syndrome and poor feeding. He was only breastfed a handful of times, and various formulas were tried without success. His difficulties with feeding persisted following discharge, and soon after birth, he developed chronic diarrhea. Throughout his first year of life, he also suffered from multiple respiratory tract infections. His motor development was appropriate while both social and language development were advanced; he was very talkative and interactive. He first presented at two years of age with rectal prolapse. Given his history and presentation, cystic fibrosis was considered (frequency of 1:15,000 in the African American population) [], but sweat chloride testing was negative. He went on to develop recurrent rectal prolapse, requiring a surgical reduction at three years old. The cause of the rectal prolapse was likely diarrhea and malnutrition, secondary to his underlying diagnosis [].
At three years of age, he was again admitted for emesis and weight loss in the setting of chronic diarrhea and worsening abdominal distention. It was reported that despite his persistent weight loss, he typically had a good appetite. His family denied both generalized protein aversion and episodes of severe illness following protein-rich meals. At the time of presentation, he weighed 13.2 kg (3.2 percentile) and was 93 cm (1.6 percentile) tall. His hair had gradually become straighter and lighter than was typical for him over the preceding year. He had significant hepatomegaly, with a liver span of 18 cm on ultrasound. Laboratory examinations demonstrated mild anemia, hypokalemia and hypoalbuminemia in the setting of transaminitis with a normal ammonia. Radiographs of his femurs and hands bilaterally, in addition to lumbosacral spine and pelvis, all demonstrated osteopenia. An echocardiogram showed mild left atrial enlargement, a small pericardial effusion and respiratory mitral inflow variability, all consistent with constrictive pathophysiology, thought to be secondary to his systemic processes. Congenital disorders of glycosylation were considered, however carbohydrate deficient transferrin levels were only slightly elevated, inconsistent with congenital disorders of glycosylation, though possible in cases of hereditary fructose intolerance. Urine amino acids were significant for elevated lysine and ornithine, though not to the extent expected in lysinuric protein intolerance. He was discharged with a working diagnosis of hereditary fructose intolerance, instructed to follow a fructose-free diet.
Though he had initially improved on the fructose-free diet, after three days, his condition worsened. He developed food aversion and began spiking intermittent fevers. He was readmitted two weeks later with fever, decreased oral intake, weight loss, worsening abdominal distension and pain following an additional episode of rectal prolapse. The 60 most common CFTR mutations were tested at this time and were all negative. Plasma and urine amino acids were collected and the patient was started on empiric citrulline while awaiting results (, ).
Targeted DNA Sequencing looking for SLC7A7 gene variants was ordered, and was negative for any pathogenic mutations. However, deletions, duplications and intronic variants will not be detected by this testing. LPI can be caused by deletion or duplication of SLC7A7 in approximately 15–20% of patients; however, a deletion/duplication assay could not be obtained []. Biopsies of the middle and distal esophagus, stomach, duodenum, terminal ileum and ascending and transverse colon were significant only for a focal increase in lamina propria eosinophils in the duodenum. Liver biopsy was significant for moderate to severe steatosis of the parenchyma, focal mild cholestasis, mild inflammatory infiltrate with scattered eosinophils and fibrosis. Both an upper GI series and contrast enema were completed but unrevealing.
Following protein restriction and initiation of citrulline to correct for the intracellular defects of arginine and ornithine, carnitine was also started as levels were found to be low. On this regimen, our patient’s condition improved. His family reports he has had significantly more energy and his hair has begun to darken. Follow-up after 5 months showed a significant improvement regarding his nutritional status. His weight is 17.1 (45th percentile) but his height is still at 1st percentile.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [17.1, 'kg'], 'height': [93.0, 'cm']}",19.77107,18.78252,20.75962,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 93.0 cm, which is 93.0 cm * 1 m / 100 cm = 0.93 m. The patient's weight is 17.1 kg. The patient's bmi is therefore 17.1 kg / (0.93 m * 0.93 m) = 19.77107 kg/m^2."
2067,6,Body Mass Index (BMI),physical,decimal,pmc-7939150-1,Extracted,"A 15-year-old female was admitted to our hospital complaining of edema in the lower extremities, which had been occurring for the previous 2 months. She had no symptoms of fever, gross hematuria, foamy urine, photosensitivity, alopecia, oral ulcers, skin rash, joint pain, or urgency or pain in urination.
Her physical examination on admission showed no remarkable findings other than the mild edema of the lower extremities. Her body weight was 50 kg, height was 159 cm, and blood pressure was 114/82 mm Hg. There were no palpable lymph nodes, and the chest and abdominal exams were normal.
Laboratory tests showed hemoglobin, 129 g/L; white blood cells, 8.17 × 109/L; and platelets, 151 × 109/L. Urinalysis was positive for 4+ protein; RBC, 3/HP protein/creatinine ratio, 4.88 g/g Cr; and urine protein, 4.74 g/24 hour. Blood biochemistry analysis revealed albumin, 23.8 g/L; blood nitrogen urea, 5.60 mmol/L; serum creatinine, 50.0 μmol/L; uric acid, 208.0 μmol/L; and cholesterol, 6.24 mmol/L.
ANA was positive (1:1000); anti-dsDNA antibody was positive; anti-Sm antibody was negative; serum C3 was 0.6720 g/L (normal range 0.785–1.520 g/L); and C4 was 0.0806 g/L (normal range 0.145–0.360 g/L). There were negative findings for C-reactive protein, rheumatoid factor, anti-streptolysin O, anti-neutrophil cytoplasmic antibodies, and anti-glomerular antibodies. Immunofixation electrophoresis did not reveal monoclonal immunoglobulin. Renal ultrasonography showed that the size of the right kidney was 10.5 × 4.5 × 4.2 cm3, while the left measured 11.5 × 5.0 × 4.9 cm3.
A renal biopsy was performed, and light microscopy revealed that 35 glomeruli had thickening of the GBM (Fig. A) and subepithelial fuchsinophilic protein deposition (Fig. B). Immunofluorescence microscopy revealed granular deposition of IgG and C3 along the glomerular capillary wall. The glomerular capillary was negative for PLA2R and THSD7A staining. An electron micrograph revealed subepithelial electron-dense deposits, thickening of the GBM, and foot process fusion (Fig. D).
We diagnosed the patient with membranous lupus nephritis (LN) (pure class V LN). We stained EXT1 by immunohistochemistry after the association of exostosin 1/exostosin 2 (EXT1/EXT2) and secondary MN was reported.[ The results showed positive staining for EXT1 along the glomerular capillary wall (Fig. C).
The patient was given prednisone at a dose of 40 mg per day, which was tapered down after 1 month, hydroxychloroquine, and aspirin. Four 200 mg doses of RTX were given with the frequency of doses dependent on CD19+ B-cells counts; the average interval between doses was 2 months (Fig. ).
The patient achieved complete remission 8 months after her hospital admittance. The serum albumin increased from 23.8 g/L to 38.7 g/L. The urinary protein creatinine ratio level dropped from 4.88 g/g Cr to 0.27 g/g Cr. The ANA and anti-dsDNA antibody were negative. The serum C3 increased to 0.7840 g/L. She remained in remission during a 16-month period of follow-up, with a maintenance dose of 7.5 mg of prednisone per day.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [50.0, 'kg'], 'height': [159.0, 'cm']}",19.7777,18.78881,20.76658,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 159.0 cm, which is 159.0 cm * 1 m / 100 cm = 1.59 m. The patient's weight is 50.0 kg. The patient's bmi is therefore 50.0 kg / (1.59 m * 1.59 m) = 19.7777 kg/m^2."
2068,6,Body Mass Index (BMI),physical,decimal,pmc-6967248-1,Extracted,"A 53-year old man (height, 175 cm; weight, 87 kg) was scheduled to undergo subtotal stomach-preserving pancreatoduodenectomy with portal vein reconstruction for pancreatic cancer after receiving neoadjuvant chemotherapy with gemcitabine and nab-paclitaxel. Laparoscopic left nephrectomy for renal cell carcinoma was performed 1 year prior; therefore, harvesting the left internal jugular vein for portal vein reconstruction was planned because the left renal vein was too short. Preoperative serum creatinine level and potassium level were 1.39 mg/dL and 4.1 mEq/L, respectively.
General anesthesia was induced rapidly with propofol, rocuronium, fentanyl, and remifentanil and maintained with desflurane. The patient’s vital signs remained stable while resection of the distal stomach, gallbladder, distal common bile duct, and pancreatic head was performed. Bleeding from the first jejunal vein (J1V) occurred during adhesion detachment around the superior mesenteric vein (SMV), and clamping of the J1V was required to control the bleeding. Immediately after J1V clamping, bowel congestion progressed because the patient’s intestinal blood flow had been bypassed from the SMV to the inferior pancreaticoduodenal vein through J1V due to complete obstruction of the portal vein by the tumor. Therefore, a heparin-coated bypass tube (ANTHRON™ bypass tube, TORAY MEDICAL Co., Tokyo, Japan) was inserted from the SMV to the right great saphenous vein to relieve the bowel congestion. Several minutes after insertion of the ANTHRON™ bypass tube, blood potassium level rose from 4.7 mEq/L to 6.0 mEq/L, and pulseless ventricular tachycardia occurred. Chest compression was promptly performed by surgeons, and anesthesiologists attempted direct current defibrillation several times; epinephrine, magnesium sulphate, bicarbonate, lidocaine, and amiodarone were also administered. In addition to resuscitation, anesthesiologists inserted a blood-access catheter to the right internal jugular vein and started continuous renal replacement therapy to prevent elevation of blood potassium level. Spontaneous circulation was recovered after 30 min. The surgical team decided to discontinue the surgery, and the patient was transferred to the intensive care unit (ICU) after packing gauze into the abdomen and with the ANTHRON™ bypass tube left inserted. Total blood loss was 5620 mL, and total fluid balance was + 6115 mL. The operation time was 10 h 30 min.
Two days after the first operation, the patient was scheduled to undergo tumor resection and portal vein reconstruction with REIV. The surgical team abandoned using the left internal jugular vein for portal vein reconstruction because of concerns that brain congestion after harvesting the jugular vein could affect brain function recovery. Anesthesia was maintained with dexmedetomidine, fentanyl, rocuronium, and remifentanil. Continuous hemodiafiltration had been performed in the ICU due to persistent anuria and continued during the operation to prevent hyperkalemia. Both legs were compressed with a pneumatic compression device throughout the operation to prevent deep venous thrombosis formation. A section of the REIV 5 cm in length was harvested intraperitoneally with a surgical stapler, and the REIV distal end was closed with a 4-0 polypropylene running suture. The inferior epigastric vein, pubic branch of the obturator vein, and the deep circumflex iliac vein were preserved. A surgical nurse noticed swelling of the patient’s right leg 2 h after harvesting; the surgical team ensured careful observation throughout the surgery because a transient change by congestion of the right leg was suspected. Blood potassium level was slightly elevated after REIV resection, but ventricular arrhythmia was absent. Surgery was completed as scheduled (operation time, 7 h 3 min), and the patient was transferred to the ICU again. Total blood loss and total fluid balance were 2485 mL and + 2587 mL, respectively.
On ICU admission, distention and fullness of the right leg worsened. An orthopedist diagnosed the patient with acute compartment syndrome, and right leg elevation to lower the intracompartmental pressure was initiated. Blood potassium level was rapidly elevated immediately after leg elevation (Fig. ), which caused sustained ventricular tachycardia despite efforts to lower blood potassium level such as the administration of bicarbonate, glucose-insulin, and continuous hemodialysis with potassium-free dialysate. Chest compressions were initiated immediately. Ventricular tachycardia was prolonged; therefore, veno-arterial extracorporeal membrane oxygenation (V-A ECMO) was induced, and spontaneous circulation was recovered after resolution of hyperkalemia (Fig. , Table ). Emergent fasciotomy was performed by orthopedists 1 h after induction of V-A ECMO because the intracompartmental tissue pressure of the anterior compartment was 70 mmHg.
V-A ECMO was withdrawn 2 days later, and the patient was extubated 10 days after portal vein reconstruction. He had no apparent neural deficits; however, paralysis and paresthesia of the right leg persisted after discharge from the ICU 17 days post-operatively.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [87.0, 'kg'], 'height': [175.0, 'cm']}",28.40816,26.98775,29.82857,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 175.0 cm, which is 175.0 cm * 1 m / 100 cm = 1.75 m. The patient's weight is 87.0 kg. The patient's bmi is therefore 87.0 kg / (1.75 m * 1.75 m) = 28.40816 kg/m^2."
2069,6,Body Mass Index (BMI),physical,decimal,pmc-4422421-1,Extracted,"We described a male patient, born to a 38 years old mother at 30 weeks’ gestation by emergency Cesarean section, performed because of pre-eclampsia and IUGR associated with poly-hydramnios, detected by 26 weeks. The pregnancy was complicated by maternal type 2 DM, requiring subcutaneous insulin, Antenatal serologies (TORCH, HIV, Treponema and Hepatitis) were protective. Cytogenetic investigation of the fetus by villocentesis confirmed a normal 46,XY karyotype. Paternal medical history was unremarkable. Parents were non-consanguineous Caucasians.
Apgar scores were 6 at 1 minute and 7 at 5 minutes of life. Physical parameters were as follows: weight 1190 g (<10° centile), length 36 cm (<3° centile) and head circumference 26 cm (<10° centile). Physical examination was normal except for a moderate respiratory distress, During the first hours of life, the respiratory status worsened, evolving towards a third-degree hyaline-membrane disease that required surfactant administration, mechanical ventilation for a 24 hour period and non-invasive ventilation for 10 days.
Throughout the first 3 days of life, the patient experienced a significant weight loss (as high as 19% of the birth weight), associated with polyuria (4.7-5.5 ml/kg/h) and hypernatremia (serum sodium 152–159 mEq/l), despite adequate fluid intake. At first, hypernatremia was interpreted as a consequence of the excessive weight loss and treated with large amounts of daily intravenous fluids (180–200 ml/kg/d). The clinical course was complicated by one episode of Serratia Marcescens septic shock during the second week of life and disseminated intravascular coagulation requiring plasma administration, platelet transfusion and aggressive antibiotic therapy.
CDI was subsequently suspected as a result of persistent hypernatremia (serum sodium 150 mEq/L), high plasma osmolarity (322 mOsm/L) and low urine osmolarity (190 mOsm/l) with a Uosm/Posm ratio < 1 associated with failure to thrive during the first four weeks of life. The diagnosis of CDI was confirmed by the desmopressin test, showing a normal urine concentrating capability after nasal desmopressin (DDAVP) administration with rapid raise in urine osmolarity and reduced plasma osmolarity and the brain MRI at 34 weeks postmestrual age demonstrating the lack of posterior pituitary hyperintense signal. Bilateral asymmetrical optic nerve hypoplasia associated with right orbital bone hypoplasia was also observed, suggesting the diagnosis of WF []. No other abnormalities of the CNS were found.
Ophthalmologic examination revealed eyeball and right optic disc hypoplasia, associated with exotropia. Visual evoked potential confirmed the pathological findings of the right optic pathway, while the electroretinogram resulted normal. Audiological examinations were normal. Borderline TSH values with normal thyroid function were recorded during hospitalization, but no treatment was required until the end of the first year of life, when levo-thyroxine substitutive therapy was started because of primary non-autoimmune central hypothyroidism with a small thyroid gland. During the five years follow-up mild psychomotor and mental retardation were diagnosed. No glucose intolerance or diabetes mellitus have been detected so far.
After the catch-up growth, length and head circumference has stabilized around the 50° centile and, after the first year of life, body weight was above the 97° centile.
Water and electrolyte balance is maintained with standard doses of nasal desmopressin.
No progression of the bilateral asymmetrical OA was noted at the 1-year follow-up MRI. However, new pathological signs (reduced corpus callosus, moderate ventricular dilatation, asymmetric hippocampus and altered occipital peri-ventricular white matter signal intensity) [] were noticed.
Genetic investigation of the patient and his relatives revealed a segmental paternal heterodisomy of the chromosome 4 (segmental pat-hUPD4), involving at least part of the promoter and the first exon of WFS1 that we hypothesized could remove splicing regulatory motifs located in intron 1. Direct sequencing analysis of WFS1 cDNA showed a mixed sequencing pattern including the wild-type transcript sequence and two splice variants. The first splice variant was a previously described 4-bp deletion in exon 2, while the second one exhibited the complete skipping of exon 2 and, probably, the loss of the transcription start site. RT-PCR confirmed a normal mRNA expression compared to young controls, while Western blot analysis showed a significantly decreased Wolframin expression []. Informed consent for genetic studies was obtained from all subjects involved in the study.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [1190.0, 'g'], 'height': [36.0, 'cm']}",9.1821,8.72299,9.64121,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 36.0 cm, which is 36.0 cm * 1 m / 100 cm = 0.36 m. The patient's weight is 1190.0 g so this converts to 1190.0 lbs * kg/1000 g = 1.19 kg. The patient's bmi is therefore 1.19 kg / (0.36 m * 0.36 m) = 9.1821 kg/m^2."
2070,6,Body Mass Index (BMI),physical,decimal,pmc-2930169-1,Extracted,"In March 2007, a 65-year-old man with ADPKD, and consequently underwent hemodialysis since June 2001, was admitted to our hospital with symptoms of poor oral intake due to abdominal distention. His daily urine volume was approximately 300 mL and his abdomen was distended, with a maximum circumference of 105 cm. His weight and height were 63.8 kg and 170 cm, respectively. The laboratory findings were as follows: hemoglobin, 11.7 g/dL; albumin, 3.2 g/dL; BUN, 38 mg/dL; creatinine, 6.5 mg/dL; and total cholesterol, 206 mg/dL. A computed tomography (CT) of the abdomen revealed markedly enlarged polycystic kidneys bilaterally and multiple liver cysts. The renal volumes, appearing as an ellipsoid on CT images, were 3,309 mL and 3,173 mL on the right and left sides, respectively, according to the following formula: (π/6) × (length × width × depth).
Written informed consent was obtained from the patient. A TAE was performed in March 2007. This procedure was performed through the right femoral artery using the Seldinger technique, which involved the insertion of a Terumo guide wire (Radiofocus M; Terumo, Tokyo, Japan) and a 5-Fr Cobra catheter (Cook, Bloomington, IN) under local anesthesia. The arteriogram before the renal TAE showed bilateral narrowing (left > right), and stretched the renal arteries. Absolute ethanol was injected via the coaxial catheter (Progreat microcatheter system; Terumo, Tokyo, Japan) into the right renal artery. Seven mL of ethanol with 2 mL of Lipiodol was used to detect reflux of the radiolucent ethanol. After 5 minutes, the right renal artery was completely embolized. At this time, a renal TAE was performed on one side of the kidney only because the patient will only want to repeat the procedure on the contralateral kidney if the results of the first TAE are good. A second TAE of left renal artery was performed in March 2008. The procedure was the same as the previous TAE. At this time, we used a balloon catheter to prevent the reflux of the ethanol. After performing a selective renal arteriography, a 5-mm-diameter, 2-cm-long, 3-Fr balloon catheter (Savvy; Cordis Europe, Roden, The Netherlands) was positioned in the main renal artery. With the balloon inflated, 3 mL of ethanol was slowly injected for complete embolization ().
After the TAE, the patient experienced abdominal and lower back pain, which were ameliorated with opioids (pethidine - 25 mg three times a day for 2 days). The patient developed a fever the next day, which was controlled by a non-steroidal anti-inflammatory agent. He recovered and was discharged three days after the TAE. The poor oral intake due to abdominal distention was relieved one month after the TAE. Over the course of an 18 month follow-up period, the patient's general condition improved. His kidney size decreased bilaterally after the TAE (). The abdominal maximum circumference was reduced from 105 to 80 cm. The patient's dry weight decreased from 63 to 58 kg and hypertension did not develop. The daily 300 mL urine output did not change. The patient's serum hemoglobin and cholesterol levels did not change, but the albumin level increased slightly (). In summary, the patient experienced no recurrent symptoms or complications at 18 months after treatment.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [58.0, 'kg'], 'height': [170.0, 'cm']}",20.0692,19.06574,21.07266,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 58.0 kg. The patient's bmi is therefore 58.0 kg / (1.7 m * 1.7 m) = 20.0692 kg/m^2."
2071,6,Body Mass Index (BMI),physical,decimal,pmc-8105093-1,Extracted,"A 14-month-old boy presented to our department with a 2-day history of high fever and appetite loss, without any signs of upper respiratory infection such as cough or nasal discharge. He had been diagnosed with bilateral CC at 35 weeks' gestation by prenatal pleurocentesis. He was delivered by emergency caesarean section due to progressive hydrops fetalis at 36 weeks and 1 day gestation with a birthweight of 3,426 g. Immediately after birth, he was intubated in the operating room () because of a lack of spontaneous respiration, and bilateral chest tubes were inserted. The left-sided chest tube was removed on the 13th day of life owing to gradual reduction of the left chylous fluid. He was also diagnosed with supravalvular pulmonary stenosis (PS) with a pressure gradient of 40–45 mmHg (Figures and ) between the right ventricle and pulmonary artery. In addition to hydrops fetalis, lymphatic maldevelopment, and PS, he showed the unique facial features such as tall-forehead and low posterior hairline, hypertelorism, and down-slanting palpebral fissures, which led us to diagnose Noonan syndrome []. Furthermore, he showed pectus carinatum diagnosed using CT-based pectus index of 1.90 () (diagnostic range: 1.42–1.98 []). Thus, according to the scoring system of clinical features [], he had 3 major symptoms and 2 minor symptoms of Noonan syndrome (). Hydrops fetalis is also reported to be associated with Noonan syndrome []. Balloon angioplasty was performed on day 54 of life, which proved to be ineffective. Right-sided chylous fluid was constantly drained until around 30–40 days, and then the draining was gradually decreased and stopped at 71 days of life after various treatments, including intravenous administration of prednisolone and octreotide complemented with serum albumin and immunoglobulin and feeding with a medium-chain triglyceride (MCT) formula. Although he temporarily tolerated an increased ratio of breast and ordinary milk to the MCT formula, reincreasing the right chylous fluid led him to be fed by pure MCT formula with essential unsaturated fatty acids and fat-soluble vitamins. He was discharged on the 141st day of life from the neonatal care unit with some residual pleural effusion on the right ().
On physical examination, he weighed 8.9 kg (1.0 standard deviation), and his height was 75 cm (0.8 standard deviation). His temperature was 39.8 C, blood pressure was 95/45 mmHg, heart rate was 180 bpm, and oxygen saturation was 98% with 1.5 L/min of oxygen inhalation through a face mask. He showed no otolaryngologic findings. On lung auscultation, right-sided breath sounds were decreased with chest retractions and tachypnoea. His heart examination revealed a grade-3 systolic murmur in the left second intercostal space. Laboratory findings indicated an increased inflammatory response with a white blood cell count of 38,200 μL, 83.4% neutrophils, and C-reactive protein level of 27.49 mg/dL. Immunological studies revealed that his immunoglobulin ratio (G/M) was 975/96 mg/dL, complement component ratio (3/4) was 99/22.3 mg/dL, complement activity (CH50) was 42.3 U/mL, and the percentages of CD4+ T cells, CD8+ T cells, CD19+ B cells, and CD56+ NK cells were 21.8%, 9.0%, 41.8%, and 15.7%, respectively. Urinalysis showed no signs of urinary tract infection.
Chest radiography revealed pleural effusions within the entire circumference of the right lung with prominent intestinal dilatation (). We percutaneously drained purulent pleural effusions and started empirical antibiotic therapy with ceftriaxone. The triglyceride concentration of pleural effusions was 299 mg/dL, and lactate dehydrogenase (LDH) level was 1214 U/mL, which confirmed the diagnosis of chylothorax [, ]. Two days later, E. coli was detected in the effusions and blood culture which were obtained on admission. In view of the sensitivity to aminobenzyl penicillin (ABPC), we decided to deescalate ceftriaxone to ABPC. Although respiratory symptoms resolved with decreased levels of inflammatory biomarkers, intermittent fever continued. On the 18th day of hospitalization, the boy developed high fever, and contrast medium-enhanced computed tomography (CT) revealed a low-density lesion (3 cm in diameter) with a high-density capsule in the right inferior lobe (). The lesion was diagnosed as a lung abscess that resulted from thoracic empyema. Medication was changed from ABPC back to ceftriaxone for another three weeks. After confirming abscess improvement on CT and chest radiograph (Figures and ), the patient was discharged from our department on the 59th day of hospitalisation. Cardiac catheterization to evaluate PS before discharge showed 7 mmHg of right atrial pressure (RAP), systolic right ventricular pressure (RVP)/end-diastolic pressure (EDP) of 90/10 mmHg, and main pulmonary arterial pressure (PAP) of 24/10 (mean 16). Thus, RV-main PA pressure gradient was 66 mmHg. He underwent surgical repair of the supravalvular PS. Postoperative echocardiography revealed trivial tricuspid valve regurgitation (TR) with estimated RVP of 24 mmHg and PS of 1.6 m/s with estimated RV-PA pressure gradient of 10 mmHg. After the surgery, there was no recurrence of empyema or chylothorax.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [8.9, 'kg'], 'height': [75.0, 'cm']}",15.82222,15.03111,16.61333,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 75.0 cm, which is 75.0 cm * 1 m / 100 cm = 0.75 m. The patient's weight is 8.9 kg. The patient's bmi is therefore 8.9 kg / (0.75 m * 0.75 m) = 15.82222 kg/m^2."
2072,6,Body Mass Index (BMI),physical,decimal,pmc-5428599-2,Extracted,"A 22-year-old woman (G2P0, weight 57 kg, height 163 cm) with a 36-week gestation was admitted for a 1-day history of bloating in the lower abdomen on August 2010. She was diagnosed with VSD in the childhood but remained asymptomatic without treatment. There was no other significant past medical history. On physical examination, the patient showed no acute distress. Vital signs were temperature 36.5°C, heart rate 105 beats/min, respiratory rate 20 breathes/min, blood pressure 145/57 mm Hg, and oxygen saturation by pulse oximetry 98% on room air. Auscultation revealed a grade 5/6 continuous murmur along the lower left sternal border with thrill. Breath sounds were normal in both lungs. Her functional capacity was NYHA II.
Laboratory tests were normal. Transthoracic color Doppler echocardiography showed a 9 mm × 10 mm aneurysm in the right coronary sinus of Valsalva, with a 7 mm rupture into the RVOT; a 4 mm supracristal VSD with left-to-right flow at rest, mild aortic, mitral, and tricuspid regurgitation, a 4 mm pericardial effusion, enlarged left atrium (42 mm) and left ventricle (58 mm) and an estimated left ventricular ejection fraction of 63% at rest.
Because ultrasonography revealed a complete placenta previa, an elective cesarean delivery under epidural anesthesia was planned.
Both patients were managed by a multidisciplinary team of obstetricians, cardiologists, and anesthesiologists, and the cesarean deliveries were planned in a cardiac operating room with cardiopulmonary bypass capabilities on standby. Intravenous infusion of metoclopramide 10 mg and ranitidine 40 mg was used as for aspiration prophylaxis 30 minutes before the operations. Antibiotic prophylaxis of surgical infection with intravenous penicillin was started 30 minutes prior to skin incision.
Upon arrival in the operating room, both patients were monitored with a 2-channel 5-lead electrocardiography, pulse oximetry, and noninvasive blood pressure. Uterine displacement was applied by a 15° left-tilt of the operation table, and a radial arterial line and a central venous catheter via the right internal jugular vein were placed under the guidance of ultrasonography. Epidural catheter was inserted via the L1–L2 intervertebral space on the left lateral decubitus position. After a 3 mL epidural test dose (2% lidocaine without epinephrine), incremental doses of 3 to 5 mL of 2% plain lidocaine were administered every 5 minutes, to avoid systemic hypotension. A total of 19 mL and 18 mL of 2% lidocaine was used for the 2 patients, respectively, including the test dose. An upper sensory level of T6 was achieved, tested by sharp pinprick. A prophylactic low-dose phenylephrine infusion was part of a standard protocol for preventing hemodynamic instability during epidural anesthesia.[ The surgeries proceeded uneventfully without pain or discomfort, with delivery of newborns with satisfactory Apgar scores (Table ).
For case 1, the invasive blood pressure (IBP) abruptly decreased to 90/55 mm Hg following slow intravenous bolus injection of 5-unit oxytocin for prophylaxis against uterine atony, and marked bradycardia developed after a higher dose of phenylephrine infusion. So norepinephrine infusion was started instead immediately, at a rate of 0.05 to 0.08 μg kg−1 min−1. Intraoperative fluid therapy was guided by IBP, HR, and central venous pressure (CVP). Patient-controlled epidural analgesia of 0.2% ropivacaine was started with a background dose of 6 mL/h and 4 mL as a bolus with a 20-minute lockout interval, which was removed 48 hours later, achieving a 0 to 30 visual analog scale of pain for both patients.
After the operation, both patients were doing well without any complications, and surgical closure of VSD and correction of ruptured SVA under general anesthesia with cardiopulmonary bypass was planned. The procedures proceeded uneventfully 13 days and 7 days postpartum, respectively, for the 2 cases. Postoperatively, no residual shunt or aortic regurgitation was noted by transthoracic echocardiography at regular follow-ups. Both mothers and babies were doing well 12 months later, without any complications.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [57.0, 'kg'], 'height': [163.0, 'cm']}",21.45357,20.38089,22.52625,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 57.0 kg. The patient's bmi is therefore 57.0 kg / (1.63 m * 1.63 m) = 21.45357 kg/m^2."
2073,6,Body Mass Index (BMI),physical,decimal,pmc-7724120-2,Extracted,"An 88-years-old woman (height 146 cm, weight 50 kg) presented with complaints of low back and bilateral buttock pain as well as numbness in both lower extremities. The patient was suffering from a gait disorder which severely restricted her mobility without a wheelchair. A history of congestive heart failure and cerebral infarction was reported. The patient also had a 5-year history of lumbar nerve root and epidural blocks to manage her symptoms. MRI revealed multiple old compression fractures (T10–12, L2–4), vertebroplasty at T7, 10, 11, and L4 and spinal canal stenosis (severe central stenosis L1/2, bilateral mild foraminal stenosis T10–L1) (). On presentation, a fluoroscopy-guided epidural steroid injection was scheduled. In the prone position, the injection site was disinfected and 1% lidocaine was injected. The L5/S1 interspace was identified by fluoroscopy, and an 18-gauge Tuohy needle was advanced into the interlaminar space under an AP fluoroscopic view. The needle was advanced into the epidural space using the LOR technique with a 1-ml air-filled syringe though the LF and a location where the syringe would not rebound. However, CSF aspirated, and on injecting 0.5 ml of the contrast, a dural puncture was confirmed through the fluoroscopic AP and lateral images (). The procedure was aborted immediately. After explaining the occurrence of the dural puncture to the patient, she was sent to the recovery room. Her blood pressure was 103/61 mmHg, HR was 87 beats/min and oxygen saturation was 96%. Normal saline was infused intravenously and oxygen (5 L/min) was administered using a facial mask with a reservoir. One hour later, she complained of severe (NRS score 5–6) bilateral temporal headache and pain on the top of her head that persisted regardless of posture changes. Tramadol administration did not reduce her headache. A case of pneumocephalus was suspected. Brain CT examination showed the presence of air at the ventricular frontal horn, anterior interhemispheric fissure, right ambient cistern, and around bilateral cavernous sinuses (). The patient was admitted to the hospital after an explanation was provided to her and her guardian. After the admission, oxygen (5 L/min) was administered. Twenty-two hours later, the headache was reduced by 70%. Follow-up brain CT confirmed the reduction of the pneumocephalus. Therefore, she was discharged the next day. Follow-up 2 weeks after discharge, indicated complete resolution with no complaint of headache. Her physical examination was negative for pneumocephalus.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [50.0, 'kg'], 'height': [146.0, 'cm']}",23.45656,22.28373,24.62939,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 146.0 cm, which is 146.0 cm * 1 m / 100 cm = 1.46 m. The patient's weight is 50.0 kg. The patient's bmi is therefore 50.0 kg / (1.46 m * 1.46 m) = 23.45656 kg/m^2."
2074,6,Body Mass Index (BMI),physical,decimal,pmc-8026339-2,Extracted,"A 4-year-old phenotypic female patient who presented with a bulging right inguinal area underwent right hernioplasty. As the hernia sac displayed prepubertal testis without ovarian stroma, she was referred to our endocrinology clinic for further evaluation of disorders of sexual development. She was born at full-term through caesarean section, and her birth weight was 3.41 kg. She did not have a specific medical or family history. Physical examination revealed normal female external genitalia with a normal clitoris, urethra, and vaginal opening. Her growth status was normal, with a height and weight of 115 cm and 23.9 kg (90th–95th percentile in age-matched girl), respectively. Her blood pressure was 145/100 mm Hg (>97th percentile). Initial endocrinological investigations were as follows: LH, 28.6 mIU/mL; FSH, 70.8 mIU/mL; testosterone, <2.5 ng/dL; estradiol, <8 pg/mL; cortisol, 0.7 µg/dL (reference range, 2.8–16.4 µg/dL); ACTH, 112.0 pg/mL (reference range, 7.2–63.3 pg/mL); serum aldosterone, 140 pg/mL (reference range, 10–160 pg/mL); and PRA, 0.10 ng/mL/hr (reference range, 1.31–3.95 ng/mL/hr). The findings indicated mild hypocortisolism and elevated gonadotropin (). Meanwhile, she presented a normal 17-OH-progesterone (1.09 ng/mL) and elevated progesterone (5.97 ng/mL; reference range, 0.2–0.5 ng/mL) and 11-deoxycorticosterone level (0.46 ng/mL; reference range, 0.02–0.19 ng/mL). The aldosterone-to-renin ratio was 140, indicating hyperaldosteronism, although an electrolyte imbalance was not observed. A high-dose synthetic ACTH stimulation test revealed no response of cortisol, 17-OH-progesterone, 17-OH-pregnenolone, and DHEA, but rather revealed an elevated progesterone response (from 5.97 to 9.97 ng/mL) (). Chromosomal analysis and fluorescence in situ hybridization revealed a normal male karyotype, 46,XY, with SRY. Pelvic ultrasonography revealed no visible uterus or ovaries in the pelvic cavity, and genitography revealed a normal urethral and vaginal opening. With the suspicion of 17α-hydroxylase/17,20-lyase deficiency, we performed next-generation sequencing-based targeted gene panel for hypogonadism that encompassed 36 related genes (AKAP6, AMH, CDKL5, CGA, CRK, CYP17A1, CYP19A1, CYP1A1, DLK1, ESR1, FSHR, GH1, GHRH, GNAS, HRAS, IGF1, IGFALS, INS, KISS1, KISS1R, LEP, LEPQTL1, LEPR, LHB, LHCGR, LIN28B, MKRN3, NF1, NFIX, NNT, NOTCH1, NR0B1, OGDHL, PROKR2, PTPN11, and STK11) using Miseq (Illumina, Inc.). A homozygous p.His373Leu (c.1118A>T) mutation of the CYP17A1 gene was identified, confirming 17α-hydroxylase/17,20-lyase deficiency ().
Oral hydrocortisone (12 mg/m2/day) treatment was initiated. Given her clinical features, sex of rearing, and parents’ opinion, the patient was raised as a girl, and she underwent orchiectomy on the opposite side. Pathological assessment revealed a prepubertal testis with no evidence of residual germ cells and slightly increased Leydig cells. After treatment with hydrocortisone, the patient's blood pressure and serum levels of cortisol and ACTH remained within normal ranges. Low-dose oral estradiol treatment was initiated at 12 years of age to promote the development of secondary sexual characteristics.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [23.9, 'kg'], 'height': [115.0, 'cm']}",18.07183,17.16824,18.97542,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 115.0 cm, which is 115.0 cm * 1 m / 100 cm = 1.15 m. The patient's weight is 23.9 kg. The patient's bmi is therefore 23.9 kg / (1.15 m * 1.15 m) = 18.07183 kg/m^2."
2075,6,Body Mass Index (BMI),physical,decimal,pmc-4578058-1,Extracted,"A 21-year-old male patient was referred for evaluation of thrombocytopenia and blurred vision in his left eye for one month. He did not have any ocular or systemic diseases before. He was neither a smoker nor an alcoholic, nor did he have a history of drug abuse. Family history was also unremarkable. His height was 175 centimeters and his body weight was 68 kilograms. His blood pressure was 130/80 mmHg. The corrected visual acuity on his first visit was 20/20 in his right eye and 20/20 in his left eye.
On ophthalmic examination, the left eye disclosed branch retinal vein occlusion and superficial flame-shaped retinal hemorrhages on superotemporal arcade (). The right eye showed normal sizes of the retinal vessels and retina.
On laboratory studies, platelets were 37,700/mm3, 7,520/mm3 leukocytes (67% neutrophils, 21.6% lymphocytes), 15.6 g/dL hemoglobulin. Erythrocyte sedimenstration rate (ESR) was 2 mm/hr, 0.2 mg/dL CRP. Prothrombin (PT) and partial thromboplastin time (aPTT) were in normal range. Serum creatinine, aspartate aminotransferase, alanine aminotrasferase, alkaline phosphatase and urine analysis were all normal range. An immunologic study revealed high titer (>120 U/mL) IgG aCL antibody (normal, <10 U/mL) but the antinuclear antibody, anti-dsDNA antibody, lupus anticoagulant, IgM antiphospholipid antibody and antiplatelet antibody were negative. The serologic test for syphilis was negative; protein C and S antigen were also normal range.
He was started on warfarin to maintain an international normalization unit (INR) of 2.0 to 3.0 and high dose prednisolone (1 mg/kg/day) for a month at first. One month later, the patient’s visual acuity deteriorated to 20/400 in his left eye during anticoagulant therapy. Warfarin was switched to a low dose of aspirn (100 mg/day) after developing viterus hemorrhage. On the second month, prednisolone was tapered to 10 mg daily because platelet kept above 50,000/mm3. His visual acuity did not change during follow-up a year’s.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [68.0, 'kg'], 'height': [175.0, 'cm']}",22.20408,21.09388,23.31428,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 175.0 cm, which is 175.0 cm * 1 m / 100 cm = 1.75 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.75 m * 1.75 m) = 22.20408 kg/m^2."
2076,6,Body Mass Index (BMI),physical,decimal,pmc-7171631-1,Extracted,"A 44-year-old Japanese woman presented with postprandial abdominal pain since 2 months. She had been diagnosed with SLE at the age of 37 years. The patient also had lupus nephritis, Basedow's disease, steroid diabetes, idiopathic thrombocytopenic purpura, and hypertension, for which she had been taking tacrolimus, azathioprine, hydroxychloroquine, prednisolone (10 mg/day), nifedipine, eplerenone, hydralazine, lansoprazole, propylthiouracil, alfacalcidol, and sodium ferrous citrate. She was a social drinker and an ex-smoker who smoked 30 cigarettes/day for 10 years. On examination, her body temperature was 36.7°C, blood pressure was 123/80 mmHg, and pulse rate was 103 bpm. Her height was 148.5 cm and weight was 42.4 kg. Physical examination revealed conjunctival anemia, exophthalmos, enlarged thyroid, and distended abdomen with hyperactive bowel sounds, but there was no palpable mass or tenderness in her abdomen. Laboratory tests showed decreased values for hemoglobin concentration (9.0 g/dL) and hematocrit (28.3%). The C-reactive protein (4.11 mg/dL), erythrocyte sedimentation rate (104 mm/h), and soluble interleukin-2 receptor (779 U/mL) levels were elevated. The white blood cells, platelets, lactate dehydrogenase, creatine phosphokinase, anti-double stranded DNA IgG antibody, complements, carcinoembryonic antigen, and carbohydrate antigen 19–9 were within the normal range. Urinalysis revealed proteinuria, leukocytes (20–29 cells/high power field), and tubular epithelium. Hematuria was absent.
Computed tomography scanning showed whole circumferential thickening of the jejunum with aneurysmal dilatation, which is a typical feature of malignant lymphomas of the intestine (). On positron emission tomography scanning, tracer uptake was observed in the thickened intestinal wall (). Double balloon enteroscopy revealed circumferential ulcer and necrotic debris in the jejunum (). A contrast study during enteroscopy showed dilated jejunal lumen (). Based on the morphology of the jejunal lesion, we suspected small intestinal lymphoma rather than cancer. Thus, we performed flow cytometry analysis with 2 endoscopically biopsied fragments, as described previously () []. The κ/λ ratio of CD19 + CD20+ cells was 3.3 (53.36/16.39), indicating monoclonal proliferation of the B cells producing the κ light chain. The isolated cells were negative for CD5 and CD10 on flow cytometry analysis. Bone marrow biopsy and cytology revealed no lymphoma cell invasion. Biopsy of the jejunal lesion showed infiltration of atypical, large lymphoid cells that were positive for CD20 and BCL2 and negative for CD3, CD5, CD10, and cMYC (). The cells were diffusely positive for Ki-67. The results of in situ hybridization for Epstein–Barr virus-encoded small RNA-1 were also positive. The jejunal tumor, which had invaded the transverse colon, was surgically resected. Lymphadenopathies of the mesentery were observed intraoperatively. Consequently, a diagnosis of diffuse large B-cell lymphoma in the jejunum at stage II1E (large intestine) was made. Chemotherapy with cyclophosphamide, adriamycin, vincristine, and prednisone plus rituximab was administered postoperatively.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [42.4, 'kg'], 'height': [148.5, 'cm']}",19.22706,18.26571,20.18841,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 148.5 cm, which is 148.5 cm * 1 m / 100 cm = 1.485 m. The patient's weight is 42.4 kg. The patient's bmi is therefore 42.4 kg / (1.485 m * 1.485 m) = 19.22706 kg/m^2."
2077,6,Body Mass Index (BMI),physical,decimal,pmc-8045545-1,Extracted,"A 42-year-old male presented to us with complaints of diffuse abdominal pain and abdomen distension for 2 days. He had a history of constipation for 2 days, but no vomiting. The patient was brought after an episode of seizure for 3 min, followed by a brief period of altered sensorium. He was diagnosed with a seizure disorder 9 years ago for which he was on irregular medications. He is a chronic alcoholic for the past 25 years and had an episode of alcohol binge drink 2 days ago. On examination (height – 168 cm; weight – 45 kg), the patient was drowsy with a Glasgow Coma Score (GCS) of E3V4M6-13/15. His blood pressure was 80/48 mm of Hg. His heart rate was 102/min; the respiratory rate was 22 per minute and the temperature was 99°F. Abdomen examination revealed mild abdomen distension, diffuse tenderness with neither guarding nor rigidity, and absent bowel sounds. Digital rectal examination showed altered dark-colored stools. Respiratory system examination showed the presence of equal air entry bilaterally with basal crepitations.
The capillary blood glucose (CBG) at admission was 32 mg/dl. After initial stabilization with intravenous fluids, 25% dextrose, and supportive measures, further investigations were done. A complete blood count showed an elevated total count of 15.4 × 109/L with a neutrophil predominance. X-ray abdomen showed multiple air–fluid levels. CT of the abdomen showed diffuse dilatation of the jejunal and ileal loops and the collapse of the large bowel with a transition point probably at the terminal ileum or ileocecal junction. All these features suggested a small bowel obstruction and the patient was planned for an emergency laparotomy as per the hospital protocol in emergencies. The patient responded well to the initial resuscitation with intravenous fluids, 25% dextrose, and inotropes, and his GCS improved to 15/15 and CBG increased to 180 mg/dl. The patient did not develop any further seizures.
During the emergency laparotomy, the following were found: (1) dilated jejunal and ileal loops, (2) collapsed large bowel, and (3) at 20 cm from the ileocecal junction, there was an ileoileal intussusception []. The involved ileal segment was resected and stomas were fashioned. On examining the specimen, it was found that 7 cm of proximal ileum had telescoped into the distal part and that the telescoped part was gangrenous.
Postoperatively, the patient had a cough with expectoration and he revealed that he had similar episodes for the past 1 month. A chest X-ray which was done preoperatively showed opacity in the left middle zone. Subsequently, the CT chest which was performed showed evidence of consolidation with air bronchogram in the left lower lobe and evidence of cavity with surrounding consolidation in the anterior aspect of the left upper lobe, suggesting an active infection in the lung []. Sputum smears examined with Ziehl–Neelsen stain did not reveal any acid-fast bacilli, but molecular testing by nucleic acid amplification (GeneXpert) was positive for Mycobacterium tuberculosis with moderate sensitivity to rifampicin. The histopathological examination of the resected bowel segment confirmed the presence of numerous epithelial granulomas with aggregations of epithelioid histiocytes and scattered Langhans type of giant cells, suggesting a tuberculous origin of the lesions [Figures and ]. Subsequently, the patient was started on antitubercular treatment with isoniazid, rifampin, pyrazinamide, and ethambutol according to the local national guidelines. This leads to the conclusion that the small bowel obstruction was due to intussusception and the lead point for the intussusception would have been the tuberculous lesion. The patient recovered well postoperatively and is awaiting reversal of his stoma.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.0, 'kg'], 'height': [168.0, 'cm']}",15.94388,15.14669,16.74107,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 45.0 kg. The patient's bmi is therefore 45.0 kg / (1.68 m * 1.68 m) = 15.94388 kg/m^2."
2078,6,Body Mass Index (BMI),physical,decimal,pmc-3623538-1,Extracted,"A 26-year-old man who appeared healthy was transferred to our facility for persistent intermittent low abdominal and perineal pain for the previous 2 months. The patient had also experienced urinary symptoms including frequency, urgency, gross hematuria, and dysuria for a month and had no history of any medical or surgical procedures prior to the visit. He was treated with antibiotics for 2 months under a diagnosis of cystitis and Meckel's diverticulum or Crohn's disease at local clinics; however, there were no pathologic findings on colonoscopy and no complaint about bowel symptoms. His family history was not notable for Crohn's disease.
He was 177 cm in height and 72 kg in weight with no acute distress. On physical examination, there were no abnormal findings. There was pyuria and microscopic hematuria on urine analysis; however, the other laboratory findings were within normal range. Cystoscopy showed diffuse erythematous mucosal thickening on the right side wall of the bladder dome (). However, there was no stool debridement no any fistulous opening in the bladder. A computed tomography (CT) scan showed that there was a tubular structure connected with the right side wall of the bladder, suggesting Meckel's diverticulum with fistula formation to the bladder as well as a mass-like bladder wall thickening ().
With an impression of Meckel's diverticulum with fistula with the bladder, a laparoscopic operation was performed through 3 abdominal ports (one 10 mm port placed at 10 mm above the umbilicus [camera] (KARL STORZ GmbH & Co. KG, Mittelstr, Tuttlingen, Germany), one 12 mm port for the right pararectal trocar, and one 5 mm port placed between the left anterior iliac spine and the umbilicus). The distal tip of the long appendix, which had a normal shape on its body and base was found to be densely adhered to the right side wall of the bladder (). Laparoscopic appendiceal ligation was performed with 10 mm Hem-O-Lok clips (Teleflex Medical, Research Triangle Park, NC, USA) and 2-0 Vicryl (Ethicon Inc., Somerville, NJ, USA). After removing the proximal appendix, dissection of the bladder around the tip of the appendix was performed. There was a dense fibrotic change around the tip of the appendix. Partial cystectomy was performed and laparoscopic two-layered bladder repair was done with 3-0 Vicryl (Ethicon). The total surgical time was 75 minutes and the estimated intraoperative blood loss was minimal.
On the 7th postoperative day, cystography was performed and no urinary leakage around the bladder was demonstrated. The urinary symptoms including gross hematuria, dysuria, and frequency improved and abdominal discomfort symptoms also subsided. The other laboratory findings were within normal range. The surgical specimen showed a 9.2×1.2 cm appendix attached to a 4.3×3.2 cm bladder with dense fibrotic change without any malignancy.
At 1 month postoperatively, he had no symptoms including frequency, urgency, sense of residual urine, or intermittent gross hematuria. Nor were there any abnormal findings by CT which was performed 1 year postoperatively.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [72.0, 'kg'], 'height': [177.0, 'cm']}",22.9819,21.8328,24.131,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 177.0 cm, which is 177.0 cm * 1 m / 100 cm = 1.77 m. The patient's weight is 72.0 kg. The patient's bmi is therefore 72.0 kg / (1.77 m * 1.77 m) = 22.9819 kg/m^2."
2079,6,Body Mass Index (BMI),physical,decimal,pmc-4600996-1,Extracted,"A 56-year-old woman with a height of 157 cm and weight of 55.1 kg presented to the outpatient clinic having the history of abdominal distention since September 2005 and was referred to our hospital on November 2005. She worked at an iron factory for 4 years without known exposure to asbestos. She had no history of pain, abdominal mass, significant weight loss, dyspnea, cough, chest pain, or constitutional symptoms. In addition, she had no other relevant past medical and surgical history or no significant drug history. Her travel, family and social histories were unremarkable.
On presentation, she was non-anemic, non-icteric, her blood pressure was 139/84 mmHg, heart rate 87 beats/min and temperature 36.8°C. Peripheral lymph nodes were not palpable. The physical examination revealed that her abdomen was soft and non-tender but much distended. No masses were palpable, but massive ascites was pointed out. Laboratory analysis revealed thrombocytosis, hypoalbuminaemia and elevated C-reactive protein. The white blood cell count, erythrocyte count, renal function tests and level of serum electrolytes were normal. Liver function test yielded elevated level of ALP (292 IU/L) and LDH (159 IU/L). However, AST, ALT, γ-GTP, AMY levels were normal. Serum total cholesterol and triglycerides were also normal. The level of carcinoembryonic antigen (CEA), alpha-fetoprotein (AFP), carbohydrate antigen19-9 (CA19-9), carbohydrate antigen125 (CA125), and CYFRA in serum were found to be within normal limit. Serum KL-6 was examined for early detection of interstitial pneumonia which might be a potential adverse effect of chemotherapy. It was unexpectedly elevated at 9000 IU/mL (normal up to 500 IU/mL). CT scans revealed thickened greater omentum with massive ascites () but no lung tumor or interstitial pneumonia. FDG-PET scan demonstrated positivity in the peritoneum () and negativity in the ovary. Diagnostic paracentasis yielded yellow exudative fluid (Protein 5.2 g/dL), 1.036 specific gravity (normal up to 1.016) and showed 3610 total cells with predominance of mononuclear cells. CA125 and KL-6in ascites fluid was 86 U/L and 7500 U/mL, respectively. The level of hyaluronic acid in serum and peritoneal fluid was at 60 ng/mL and 11,900 ng/mL, respectively. Cytological examination suggested the possibility of peritoneal mesothelioma, but it was insufficient for the diagnosis. Diagnostic laparoscopy along with peritoneal biopsy was performed to obtain histopathological and immunohistochemical analysis for establishing the definitive diagnosis. Laparoscopy showed multiple yellowish small nodular lesions of the peritoneal surface and the thickened greater omentum. Hematoxylin and Eosin (H&E) stain at low magnification revealed sheet like epithelioid tumor cells with monotonous and bland in appearance () and higher magnification showed oval shaped mesothelioma cells, with indistinct border, moderate cytoplasm, and prominent nuclei with inconspicuous nucleoli (). Microscopic features were consistent with peritoneal mesothelioma with epithelioid type. In addition, immunohistochemical stains were performed with the avidin-biotin peroxidase complex (ABC) method (LSAB kit; Dako, Carpinteria, CA) using antibodies against AE1/AE3, cytokeratin 5/6 (CK5/6), epithelial membrane antigen (EMA), calretinine, WT-1, D2-40, CEA, MOC-31, Ber-EP4, and thyroid transcription factor (TTF)-1. Staining procedures were conducted according to the manufactures’ instructions. The neoplastic cells showed strong positivity for AE1/AE3 (), moderate surface positivity for calretinine (), and surface and cytoplasmic positivity for CK 5/6, strong surface positivity for EMA, nucleonic positivity for WT-1, and weak surface positivity for D2-40 (data not shown). The tumor cells are completely negative for CEA, MOC-31, Ber-EP4, and TTF-1 (data not shown). All of these pathological results were compatible with peritoneal malignant mesothelioma with epithelioid type. Based on the serum elevation of KL-6, we examined KL-6 by immunohistochemistry using the anti KL-6 antibody (kindly provided by Eisai Co.) as described elsewhere, revealing distinct surface positivity for the mesothelioma cells (). Fuzzy and fluffy pattern was evident for ascitic tumor cells (). Sequential four regimens of palliative chemotherapy including gemcitabine plus cisplatin, paclitaxel plus carboplatin, irinotecan plus cisplatin, and pemetrexed plus cisplatin were administered and serum KL-6 level was monitored. After the chemotherapy with gemcitabine plus cisplatin, serum and ascitic KL-6 once dropped, but these levels increased in association with worsening of the disease. Despite chemotherapy, the patient died 32 months after the initial diagnosis.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.1, 'kg'], 'height': [157.0, 'cm']}",22.35385,21.23616,23.47154,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 157.0 cm, which is 157.0 cm * 1 m / 100 cm = 1.57 m. The patient's weight is 55.1 kg. The patient's bmi is therefore 55.1 kg / (1.57 m * 1.57 m) = 22.35385 kg/m^2."
2080,6,Body Mass Index (BMI),physical,decimal,pmc-7674729-1,Extracted,"A boy aged 15 years and 4 mo was referred for an evaluation of orthodontic treatment at the Orthodontic Department, Peking University School of Stomatology, with the chief complaint of tooth crowding.
His medical history was unremarkable, but his dental care was irregular and he had a bad habit of thumb sucking. The patient had passed his growth peak period, his height was 183 cm and weight was 77 kg at his first visit.
His immediate family members have no similar malocclusions.
The extra-oral examination (Figure , Photographic machine: EOS 60D, Canon, Oita Prefecture, Japan) showed that the patient had a lower anterior facial height and a convex profile with a retruded mandible. His lip looked competent with a slightly acute nasolabial angle and a deep labiomental sulcus. There was no significant facial asymmetry.
Intraoral clinical examination (Figure ) revealed cusp to cusp class II molar relationships on both sides, and a full class II relationship on the right canine as well as cusp to cusp class II relationships on the left canine. His maxillary anterior teeth were in protrusion with an 11-mm overjet and an 80% overbite, which led to a traumatic bite on his left incisors. The upper and lower arch form was both V shaped and symmetric. He had moderate crowding in both arches and a deep curve of Spee in his mandibular arch. He also had cross-bite on his right second molars. His maxillary dental midline was coincident with his facial midline, and the mandibular dental midline deviated 0.5 mm to the left.
The lateral cephalometric analysis (Figure , Software used for cephalometric measurements: Huazheng software, developed by the Craniofacial Growth and Development Center, School of Stomatology, Peking University, and School of Computer Science, Peking University, Beijing, China) indicated a skeletal class I pattern based on the subspinale-nasion-supramental (ANB) angle (4.27°), but skeletal class II pattern according to the Wits value (6.40). It also showed protruding upper incisors [upper first incisor (U1): Sella-nasion (SN) = 123.72], well-positioned lower incisors [U1: Mandibular plane (MP) = 97.82], and a low mandibular plane angle (MP:SN = 19.52).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [77.0, 'kg'], 'height': [183.0, 'cm']}",22.99262,21.84299,24.14225,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 183.0 cm, which is 183.0 cm * 1 m / 100 cm = 1.83 m. The patient's weight is 77.0 kg. The patient's bmi is therefore 77.0 kg / (1.83 m * 1.83 m) = 22.99262 kg/m^2."
2081,6,Body Mass Index (BMI),physical,decimal,pmc-2586011-1,Extracted,"A 44-year-old male, manual worker, non – smoker, presented to our outpatient orthopaedic department for chronic pain in the volar side of the right wrist. He was of Greek origin. His weight was 82 kg and height 1, 78 m. He had no past medical history and was social alcohol drinker. He did not reported any major family history. There was no history of trauma and no previous operation in the upper limb. Physical examination revealed tenderness on palpation of the area over the triquetrum. There was no sensory deficit involving the median nerve and no other pathological signs. Antero – posterior and lateral x-rays were performed and the co-existence of ulnar and radial exostoses together with 4th and 5th short metacarpal bones and two sesamoid ossicles in the wrist area were found (Fig. ). X-ray examination of the left hand was normal. Hence, the symptoms were attributed to the presence of the one sesamoid ossicle over the triquetral bone at the volar aspect of the wrist. Pain alleviate medications were prescribed and the patient was advised to avoid heavy manual work.
The exostoses arose from the distal metaphysis of the radius and ulna (Fig. ). The radial one emerged from the ulnar side of the distal metaphysis and had a sideway and proximal direction. The length was measured to be around 2.3 cm. The ulnar exostosis emerged from the radial side, had a triangular contour and a size of about 0.5 cm.
The sesamoids were 2, both in the volar aspect of the wrist (Fig. and ). The first one was located anterior to the triquetral bone; its diameter was measured to be 0.55 cm and considered to be the cause of pain. The second one was located anterior to the hamate bone and the base of the 4th metacarpal bone and its diameter was measured to be 0.48 cm. There was no pain on palpation in this area.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [82.0, 'kg'], 'height': [1.78, 'm']}",25.88057,24.58654,27.1746,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.78 m. The patient's weight is 82.0 kg. The patient's bmi is therefore 82.0 kg / (1.78 m * 1.78 m) = 25.88057 kg/m^2."
2082,6,Body Mass Index (BMI),physical,decimal,pmc-4967637-1,Extracted,"A 51-year-old man who had been diagnosed with sigmoid colon cancer four years earlier had undergone treatment with a subtotal colectomy, chemotherapy, and radiotherapy. He had received a craniotomy to excise a brain tumor one month previously. His height was 177 cm and his weight was 73 kg. His current chief complaint was a two-month history of severe back pain, accompanied by a tingling sensation, with radiation of the pain into both inguinal regions, especially the right. The patient's knee jerk reflexes were normal without neurologic deficits. Magnetic resonance imaging (MRI) revealed multiple metastatic lesions in the patient's lumbar spine, at L1, L2, L4, and L5. The main cause of the patient's symptoms was a lesion in L1, which had metastasized to the posterior vertebral body wall and right pedicle, resulting in spinal cord compression (). The patient had received radiation therapy before visiting the pain clinic, and he was taking oxycodone 40 mg and gabapentin 300 mg three times a day with no complications. Despite these interventions, he continued to experience significant pain. The pain was aggravated by changes in position from lying to sitting and relieved when he was lying. He rated his pain as 6–10 on the numeric 0–10 rating scale (NRS).The patient's average pain score with respect to the NRS was 8/10. However, he did not wish to undergo open surgery because of his poor general condition and short life expectancy. We initially planned to reduce the patient's pain using an epidural block prior to secondary interventional management, but he was not able to tolerate the prone position required to receive the epidural block due to the severe radiating pain he experienced in that position. Therefore, it was necessary to treat the patient's pain maximally in a single therapeutic session. Thus, we proposed to perform BRFD with PVP and the patient agreed to undergo the procedure.
We proceeded under conscious sedation administered by an experienced anesthesiologist, because of the patient's poor general condition and in order to prevent neurological complications during the procedure. For analgesia, a 12 µg fentanyl patch was applied to the patient's right upper thorax twelve hours before the procedure, and an intramuscular injection of pethidine 25 mg was also administered ten minutes before the procedure. One hour before the procedure, the patient received an intramuscular injection of midazolam 3 mg for sedation. During the procedure, the patient's heart rate, blood pressure, oxygen saturation, and electrocardiogram were monitored. The patient was placed on an operating table in the prone position with a flexed hip. His skin was prepared and draped in a sterile fashion. The entry point of the needle through the skin was determined using an axial MRI (). The needle was inserted 9 cm lateral to the midline. After a subcutaneous 1% lidocaine injection, a small incision was made with a blade, and under continuous fluoroscopic monitoring, an 18 gauge needle and guidewire were inserted sequentially through the incision site until the tip of the needle reached the middle portion of the L1 pedicle. Then, a dilator was used to insert a 2.7 mm diameter cannula (Disc-FX® System, Elliquence, LLC, Baldwin, NY, USA) to the middle portion of the pedicle in the lateral view and the medial pedicular margin in the anteroposterior (AP) view. A trephine was inserted through the working channel to the posterior body line in the lateral view and the median vertebral line in the AP view. After removing the guidewire and trephine, a 2.5 mm diameter bipolar probe (Trigger-Flex® Bipolar System, Elliquence) was inserted through the working channel (). An energy generator (Surgi-Max®, Elliquence) that emits high radiofrequency and low temperature radiowaves was connected to the Trigger-Flex® Bipolar probe and we shrank the tumor mass by ablation using the turbo-modulation mode. We also used the bipolar hemo-modulation mode for thermocoagulation to prevent bleeding. We conducted five cycles of the procedure while subtracting from the midline of the vertebral body to the lateral border of the right pedicle at the L1 level. The procedure was repeated using the turbo-modulation mode and the hemo-modulation mode in shifts per five second. Once the radiofrequency ablation procedure was completed, we performed PVP at the L1 and L2 bodies. The bone puncture needles were inserted into the posterior 1/3 aspect of the L1 body and the medial part of the L2 body in the lateral view and the median vertebral line in the AP view through the right pedicle. Two ml of sterile polymethyl methacrylate (PMMA) powder (Exolent Spine, Elmdown, Ltd., London, UK) and the liquid components were injected to the L1 and L2 bodies under frequent fluoroscopic lateral and AP views to avoid PMMA leakage into the venous system and the epidural space (). We completed the procedure after confirming via fluoroscope that there was no leakage of cement. The patient's radiating pain disappeared after the procedure, and there were no complications. Following the procedure, the patient's vital signs were monitored and he was observed for any neurological complications for 30 min in the outpatient recovery room, after which he was transferred to the general ward.
The patient was discharged the day after the procedure because he reported relief of his pain to a level of 1/10 on the NRS without any complications, and he was able to sit without pain. He was then able to undergo continuous chemotherapy and radiotherapy for treatment of the multiple bone metastases. At a 6-month follow-up, the patient's average pain score with respect to the NRS was 1/10. He could sit and walk in his daily life without the recurrence of radicular pain.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [73.0, 'kg'], 'height': [177.0, 'cm']}",23.30109,22.13604,24.46614,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 177.0 cm, which is 177.0 cm * 1 m / 100 cm = 1.77 m. The patient's weight is 73.0 kg. The patient's bmi is therefore 73.0 kg / (1.77 m * 1.77 m) = 23.30109 kg/m^2."
2083,6,Body Mass Index (BMI),physical,decimal,pmc-5903216-1,Extracted,"A 12-year-old male with CMTD (weight 23 kg and height 130 cm) was scheduled for thoracolumbar kyphoscoliosis surgical correction. He had a history of childhood asthma, which resolved at about 3 years of age. He also had beta-thalassemia minor and hypoplastic kidneys. He had a history of GA for umbilical hernia repair surgery 5 years ago, where he experienced a delayed awakening from anesthesia and respiratory function impairment, in which his ventilation was supported mechanically for 5 hours in the post anesthesia unit while he was intubated due to insufficient respiratory force. On his preoperative evaluation, chest and lower limbs deformities were obvious ( - ). Spirometry showed a moderate restrictive pattern with FVC about 65% of the predicted value. All laboratory tests were within normal range. In the physical examination, neck extension was reduced, however, airway assessment was near normal otherwise. Heart sounds were normal and the lungs were clear and equal bilaterally. Continuous EA as the main part of intraoperative analgesia combined with GA to secure airway and maintain ventilation was planned for this surgery.
After getting informed consent, standard monitoring and oxygenation with Hudson mask began in the operating room followed by intravenous light sedation provided with fentanyl and propofol. Epidural catheter (B. Braun Perifix ONE epidural set 18G) was introduced into his L4-L5 intervertebral space in the lateral decubitus position without difficulty after skin preparation and draping. We chose this intervertebral level for catheter insertion due to the fact that it was away from the surgical field. Then, the catheter was threaded about 15 centimetres beyond the needle tip guided by ultrasound following a test dose of 0.1 mL/kg lidocaine 1.5%. No paraesthesia was elicited during this stage. A compound ultrasound system (Medison Samsung, SonoAace X8) and a 5 MHz curved array transducer were used for guidance. The ultrasound revealed the catheter tip at about the lower margin of the 9th thoracic vertebra. A total volume of 18 mL lidocaine 1% with 1:200.000 epinephrine was injected incrementally into the epidural catheter. Almost 15 minutes later, analgesia was confirmed within the surgical field by the pinprick test.
Then, following administration of premedication in supine position, anesthesia was induced by propofol (2.5 mg/kg) and atracurium (0.45 mg/kg). After inserting and fixation of a cuffed endotracheal tube sized 6 and placement, pressure control mode ventilation was started and light anesthesia was maintained with isoflurane 0.8% and oxygen 75%. An arterial cannula was fixed in his radial artery for invasive blood pressure monitoring.
Longitudinal incision was made from T2 to L4 by the surgeon following changing the position into prone. Long thoracolumbar deformity was corrected by posterior instrumentation and fusion from T3-L3 by pedicular screws and titanium 5.5 rods (). Intraoperative blood loss was within the expected range and the operation proceeded uneventfully. Neuromuscular blockers were not repeated during the surgery. Finally the paralysis was reversed by neostigmine (1.5 mg) and atropine (0.75 mg). The whole operation lasted for 4.15 hours, during which the epidural catheter was charged 3 times with 6 mL bupivacaine 0.25% for each time. The patient was extubated and observed in the recovery area for 30 minutes, during which he fully regained his consciousness. His verbal analog pain score (VAS) was 3 out of 10 and Ramsay sedation score (RASS) was 2 out of 6 before being transferred to the general ward. The patient received 0.125% bupivacaine (4 mL/hour) as “patient controlled epidural analgesia” for the next 2 days and was discharged on the 4th postoperative day. One month later, in his follow-up session, he had no new neurological problems.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [23.0, 'kg'], 'height': [130.0, 'cm']}",13.60947,12.929,14.28994,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 130.0 cm, which is 130.0 cm * 1 m / 100 cm = 1.3 m. The patient's weight is 23.0 kg. The patient's bmi is therefore 23.0 kg / (1.3 m * 1.3 m) = 13.60947 kg/m^2."
2084,6,Body Mass Index (BMI),physical,decimal,pmc-3350097-1,Extracted,"A 41-year-old woman (height 1.66 m; weight 62 kg) with SMA type IV was scheduled for mammectomy. The diagnosis of SMA type IV was based on clinical progressive symptoms of limb muscular weakness that began eight years ago. She has been on wheelchair since five years ago. At present, she even could not lift her arms up but had no difficulty in swallowing or breathing. She had a family history of SMA, her mother (died at 50 years old) and uncle both had the same disease. She had resection of right breast fibroadenoma under local anesthesia 6 years ago and right oophorocystectomy under epidural anesthesia 12 years ago. Physical examination revealed that she had a hoarse throat, normal gape degree, proximal muscular atrophy of the limb, muscular strength 2–4 degrees (with 4 degrees in the upper limb and 2 degrees in the lower limb), decreases of tendon reflex in extremities, no pyramidal tract signs, and paraesthesia. Chest X-ray showed increases in lung markings. ECG was normal. The laboratory examinations were normal except serum creatinine 31.00 μmol/L (normal value is 44–133 μmol/L). Bronchofiberscopy showed limitation of vocal fold abduction. A size 6 cm × 6 cm lump (benign fiber-epithelial tumor confirmed by a biopsy pathological examination) was found in her right breast, and at her request, her admission was scheduled to remove her right breast in fear of malignancy in the future.
On the operating day, no premedication was given to the patient. Electrocardiogram, cuffed blood pressure, and SpO2 were monitored. External jugular vein was inserted with an 18 ga catheter due to collapse of extremity veins. Anesthesia was induced with remifentanil (target-controlled infusion at plasma concentration of 3 ng/mL) and propofol (target-controlled infusion at plasma concentration of 3 μg/mL) and a size 4 laryngeal mask airway (LMA) was tried to but failed. Then rocuronium 30 mg was given to facilitate the endotracheal intubation. The patient was intubated with an insertion of a size 7 endotracheal tube. Anesthesia was maintained with intravenous remifentanil (target-controlled infusion at plasma level of 2-3 ng/mL), propofol (target-controlled infusion at plasma level of 3-4 μg/mL), and 50% nitrous oxide balanced with oxygen. The hemodynamic parameters were stable during the one-hour surgery. Morphine 3 mg was given intravenously 30 minutes before the end of operation. The patient woke up quickly after cessation of anesthesia and could raise her head. Antagonists of muscle relaxant (neostigmine 2 mg plus atropine 1 mg) were given. She was extubated and transferred to the surgical intensive care unit (SICU), where she recovered uneventfully. She returned to the general ward on the following day and was discharged from hospital 5 days after operation.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [62.0, 'kg'], 'height': [1.66, 'm']}",22.49964,21.37466,23.62462,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.66 m. The patient's weight is 62.0 kg. The patient's bmi is therefore 62.0 kg / (1.66 m * 1.66 m) = 22.49964 kg/m^2."
2085,6,Body Mass Index (BMI),physical,decimal,pmc-3030023-1,Extracted,"A 27-year-old primipara at the 38th week of pregnancy visited the neurosurgery department with the complaint of a headache that continued from 2 years ago. She was diagnosed with Moyamoya disease and followed-up in the neurosurgery department. No other neurologic symptom was found except the hemorrhage in the left lateral cerebral ventricle by the brain MRI.
Cesarean section was carried out in the 38th week of pregnancy. The patient's consciousness was lucid and the preoperative physical examination results were weight 77.5 kg, height 167 cm, blood pressure 120-140/60-80 mmHg, and heart rate 62-80/min. The blood test results were hemoglobin 12.0 g/dl, platelet 159,000/µl, and PT/aPTT 9.8 (INR 0.89)/23.4. The findings from all the other tests, including electrocardiography and chest X-ray imaging, were in the normal range.
For the preanesthetic treatment, an intravenous injection of famotidine 20 mg and an intramuscular injection of glycopyrrolate 0.2 mg were carried out 30 minutes beforethe operation. The heated, lactated Ringer's solution 700 ml was intravenously injected after the patient's arrival in the operating room. The patient's blood pressure was 120/80 mmHg and heart rate was 65/min after arriving in the operating room. Before the peridural anesthesia, a radial artery catheter was inserted to start the continued blood pressure monitoring.
After letting the patient be in the left lateral recumbent position, the epidural space was verified with the loss of resistance method usingan 18 G Tuohy paracentesis needle by the median lumbar puncture in between L4-5 lumbar spines, and the catheter was installed and fixed. After an injection of 1.5% lidocaine 3 ml, the tested amount, containing 1 : 200,000 epinephrine, no increase in the heart rate or spinal anesthesia symptom was found. To make the total volume of phenylephrine and ephedrine 20 ml, phenylephrine 0.5 mg and ephedrine 30 mg were mixed with physiological saline and infused at the flow rate of 40 ml/hr.
Thereafter, dural tapping was carried out using a 25 G paracentesis needle by the median lumbar puncture method in between the L5-S1 lumbar spines. After checking the cerebrospinal fluid, the intraspinal injection of 0.5% bupivacaine 7 mg and fentanyl 20 µg followed. After changing the patient's position into the supine position, the right hip was supported with a pillow so that the uterus could be tilted toward the left. The operation started after checking that the sensory deprivation reached T4-5 by the pinprick test.
The intraoperative vital signs were relatively stable with the blood pressure of 120-150/60-80 mmHg and the heart rate of 65-85/min. A Venti®ask, from which the oxygen fraction of inspired air was 35%, was applied, and a capnometer was installed below the patient's nose to monitor the capnogram. The oxygen saturation measured with a pulse oximeter was 100%. The continued infusion of phenylephrine and ephedrine was stopped 15 minutes after the spinal anesthesia because the blood pressure was kept stable.
A 2,900 g healthy female infant was given birth and the Apgar score of the newborn child was 9 at 1 minute and 10 at 5 minutes. The patient did not complain of any discomfort and the total duration of the operation was 1 hour. The total amount of the fluid infused during the operation was 2,000 ml and the amount of urine was 1,100 ml. For the postoperative desensibilization, the patient-controlled epidural analgesia was performed by mixing morphine 8 mg and fentanyl 500 mcg with 0.125% ropivacaine 100 ml, totally 118 ml, and infusing the mixture at the flow rate of 1.5 ml/hr. The vital signs in the recovery room were stable. The Visual Analogue Scale (VAS) was maintained at 0 to 1 during the hospitalization. The patient was discharged on the fifth day after the operation without any specific finding and is now followed up as an outpatient in the neurosurgery department.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [77.5, 'kg'], 'height': [167.0, 'cm']}",27.78873,26.39929,29.17817,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 167.0 cm, which is 167.0 cm * 1 m / 100 cm = 1.67 m. The patient's weight is 77.5 kg. The patient's bmi is therefore 77.5 kg / (1.67 m * 1.67 m) = 27.78873 kg/m^2."
2086,6,Body Mass Index (BMI),physical,decimal,pmc-5605360-3,Extracted,"A 16-year-old male with type III OI presented with left subtrochanteric peri-implant fracture after falling on the ground (September, 2014). His height and weight were 130 cm and 27 kg. He was diagnosed as type III (Silence classification)/Congenita A (Shapiro classification) during antenatal care period, and treated with intravenous bisphosphate therapy since the age of 19 mo. He had previous bilateral leg deformity and had been treated with bilateral femoral and tibial corrective osteotomy. The radiographs showed displaced left subtrochanteric fracture below osteotomy plate with varus angulation, and bilateral distal femur extension deformity (Figures , 4A, and 5A). The left and right medullary canal diameters were 8.6 and 9.0 mm respectively.
Surgical technique: After preoperative planning was discussed, bilateral staged femoral reconstructions were planned as: (1) osteotomy plate removal and humeral nail insertion (August, 2014) (Figure ); (2) corrective hinged osteotomy left distal femur with humeral nail (June 2015) (Figure ); and (3) corrective osteotomy right distal femur with humeral nail (March, 2016) (Figure ). All operations were performed using the same technique as mentioned above with Expert humeral nail (Synthes®, Inc.). The operative times were 2.5, 3.5, and 3 h respectively. The lengths of hospital stay were 4, 4, and 3 d. Estimated blood loss were 200, 500, and 350 mL, respectively.
Postoperative care and rehabilitation: After the first and second operation on left femur, due to bilateral deformity, the patient was allowed for 8-wk wheel chair mobilization, and followed by weight bearing as tolerated with full weight bearing after 3 mo postoperatively. The subtrochanteric fracture and osteotomy site both showed clinical union and radiographic union at 3-mo and 8-mo postoperatively (Figures and ). After the third operation on his right femur, the postoperative protocol was the same as case no.1 and no.2 due to complete fracture healing with good alignment on left femur. The clinical and radiographic union were shown at 3-mo and 5-mo postoperatively, respectively (Figure ). At the most recent follow-up (postoperative 10 mo after the third operation), the patient showed normal hip range of motion with pain-free weight bearing. No avascular necrosis of femoral head was found.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [27.0, 'kg'], 'height': [130.0, 'cm']}",15.97633,15.17751,16.77515,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 130.0 cm, which is 130.0 cm * 1 m / 100 cm = 1.3 m. The patient's weight is 27.0 kg. The patient's bmi is therefore 27.0 kg / (1.3 m * 1.3 m) = 15.97633 kg/m^2."
2087,6,Body Mass Index (BMI),physical,decimal,pmc-5892612-1,Extracted,"In April 2014, a 31-year-old woman presented to our hospital with preexisting diagnosis of hepatic hemangioma (made 6 years earlier). Her medical history provided the following clinical course: ultrasound detection of a lesion (1.7×1.3 cm) in the posterior right lobe of the liver in 2008 and consistent detection of increasing amounts and growth of lesions yearly, with the largest mass measured by ultrasound being 4.3×3.0 cm. In 2012, the patient developed sporadic episodes of confusion, blurred vision, trembling hands, palpitations, and sweating, which resolved spontaneously and usually within 10–15 min. Sequential consultations with a neurologist and psychiatrist led to psychological diagnosis of hysteria or conversion disorder. The symptoms continued to occur and with increased frequency, appearing to correspond with physical activity and to be relieved following food intake. The patient developed a preference for sweet taste and her weight increased by 20 kg. In March 2014, the patient underwent a blood glucose test (fingertip prick) and was found to be hypoglycemic (2.52 mmol/L; normal range: 3.6–6.1 mmol/L), prompting her presentation to our hospital. She did not have any family history of endocrine tumors or diseases.
We performed a complete physical examination upon her admission, and general findings included height of 165 cm, weight of 93 kg, and no palpable lymph nodes in the neck, axilla, or inguinal region. Abdominal examination produced no remarkable findings. Serology testing showed fasting serum glucose 3.4 mmol/L (normal range: 3.6–6.1 mmol/mL), meanwhile serum insulin of 193.3 µIU/mL (normal range: 2.6–24.9 µIU/mL) and serum C-peptide of 9.6 ng/mL (normal range: 1.1–4.4 ng/mL), chromogranin A (CgA) of 19.71 ng/mL (normal: <100 ng/mL), and gastrin of 51.6 pg/mL (normal: <100 ng/mL); the lowest postprandial blood glucose level was 1.8 mmol/L. Abdomen contrast-enhanced CT imaging showed multiple lesions in the liver (largest being 4.3×3.5 cm) and one enhanced lesion (3.5 cm) located at the proximal jejunum; all lesions were intensified by contrast, and the pancreas appeared normal ( images).
The patient then underwent liver biopsy. Histological analysis indicated the lesions to be well differentiated and of neuroendocrine tumor (NET) type, grade G1. Immuno-histochemical analysis showed the lesions to be CgA(+), Syn(+), CD56(+), CK8/18(+), Ki-67(+2%), and insulin focal positive (–). Octreoscan showed high expression of somatostatin receptor (SSTR) in the jejunum area, liver tumors, and mesenteric lymph nodes, but no expression of SSTR was detected in any portion of the pancreas (). 68Ga-exendin-4 PET/CT confirmed the lesion located at the jejunum section, below the pancreas body, where glucagon-like peptide-1 receptor (GLP-1R) expression was detected and the most hypercaptant area was located (standard uptake value [SUV], 21.7); these findings supported the lesion to be of NET origin, located outside of the pancreas ().
The diagnosis of malignant insulinoma derived from ectopic pancreas was made. This patient was highly suspected of having multiple endocrine neoplasia type 1 (MEN-1). Magnetic resonance imaging (MRI) of the patient’s head showed Rathke’s cyst within the pituitary gland (8.6×5.6 mm, as shown in ). Ultrasound of the parathyroid showed mild hyperplasia, which was accompanied by a slightly elevated serum level of parathyroid hormone (PTH; 104.2 pg/mL, normal range: 12–88 pg/mL). Serum and urine levels of growth hormone and calcium were normal, and no symptoms related to the Rathke’s cyst were observed.
The patient’s multiple metastases precluded surgical therapy to resect all of the insulin-secreting tumors. Thus, in order to control the patient’s symptoms and suppress tumor growth, we prescribed everolimus (10 mg po qd) plus long-acting SSA octreotide (20 mg i.m. Q21d; Sandostatin LAR, Novartis) starting from June 2014. One week after the treatment initiation, hypoglycemia did not recur. Over the next 4 months of treatment, the largest lesion shrank to 2.2×2.1 cm, the amount of lesions reduced, and the jejunum lesion shrank to 1.8 cm, showing an overall partial tumor response according to Response Evaluation Criteria In Solid Tumors 1.1 criteria.
During the treatment course, the patient developed oral mucositis (grade 2), rashes, and recurrent respiratory infection (grade 2) related to the everolimus administration; these issues lessened upon gradual decrease of the everolimus dose (from 10 to 5 mg qd, and then to 5 mg orally every other day). Since the tumor remained stable during the dosage modification and the patient had experienced so many adverse events related to the drug, the everolimus was stopped in March 2015, from which time that patient was continued on the SSA alone as maintenance treatment. Till the date of this report, the SSA treatment has continued uninterrupted (for 3 years now), and no decision has been made on its cessation.
The patient provided written informed consent to authorize use and disclosure of her protected health information for publication.
The patient attended regular follow-up clinic visits every 2–3 months for the past 3 years; at the time of the writing of this report, the latest follow-up visit had occurred in June 2017. The patient has remained euglycemic and free of symptoms. Her serum level of PTH remained normal, being 86.3 pg/mL (normal range: 12–88 pg/mL) at the latest follow-up visit. Ultimately, the patient tolerated the treatment with SSA alone well, without incidence of side effects and with partial tumor response. The latest images taken by enhanced MRI in June 2017 () shows the partial response of the tumor located in liver and jejunum compared to base line status.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [93.0, 'kg'], 'height': [165.0, 'cm']}",34.15978,32.45179,35.86777,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 93.0 kg. The patient's bmi is therefore 93.0 kg / (1.65 m * 1.65 m) = 34.15978 kg/m^2."
2088,6,Body Mass Index (BMI),physical,decimal,pmc-4131164-1,Extracted,"An 80-year-old woman developed unsteadiness of gait and required assistance to walk one week after she noted lower back pain. One week later, the patient presented with headache, nausea, and low-grade fever and was admitted to a local hospital. Acute multiple cerebral infarctions were diagnosed via brain magnetic resonance imaging (MRI), and anti-coagulant therapy was initiated. However, despite continuing medical treatment for 7 days, consciousness disturbance developed and she was transferred to our hospital. At the time of admission, the patient was 155 cm tall and weighed 61 kg. Her body temperature was 37.4°C, her blood pressure was 145/85 mmHg, and her pulse rate was 66/min. There was no blood pressure differential between the right and left arms. The physical examination, including palpations of the lymph nodes, chest and abdomen, was unremarkable. There was mild edema in the lower legs. Neurological examination revealed mild consciousness disturbance with a Glasgow Coma Scale (GCS) of 12 (E3V4M5), mild left facial paralysis, and bilateral positive Babinski’s sign. The patient displayed no motor weakness or sensory disturbances. Marked nuchal stiffness and a positive Kernig’s sign were observed.
The patient’s laboratory data showed a white blood cell count of 12,100/μL with 87.3% neutrophils, C-reactive protein levels of 11.69 mg/dL, and D-dimer levels of 18.1 μg/mL. Cerebrospinal fluid (CSF) analysis disclosed 5 mononuclear cells/μL, a glucose level of 42 mg/dL (CSF-blood glucose ratio: 0.35), and a protein value of 46 mg/dL (Table ). An electroencephalogram revealed frequent bilaterally asynchronous sharp wave activities. Brain MRI revealed hydrocephalus, and high signal intensities in the right cerebellar hemisphere, corona radiata, caudate nucleus, and the left parietal lobe on diffusion-weighted imaging (Figure A, B), with corresponding reduced apparent diffusion coefficient maps. No enhancement was observed in these lesions or the meninges on post-contrast T1-weighted images (Figure C, D). MR angiography showed intracranial vessel irregularities and stenoses of the right middle cerebral artery and vertebral artery. Electrocardiography displayed a sinus rhythm. Neither a potential cardiac source of embolism nor a source of the right-to-left shunt, including patent foramen ovale, was demonstrated via transthoracic and transesophageal echocardiography. A computed tomography scan of the chest detected calcification of the aortic arch. The patient was treated with intravenous heparin.
The subacute clinical course, marked nuchal stiffness, and mild mononuclear pleocytosis with a decreased CSF-blood glucose ratio (Table ) led us to consider meningoencephalitis due to tuberculosis or fungi; subsequently, antitubercular and antifungal drugs were administered. However, the CSF exams resulted in a negative cryptococcus antigen test and a low adenosine deaminase level (<2.0 IU/L). Additionally, CSF culture for bacteria, acid-fast bacilli and fungi was negative. The CSF cytology on admission revealed adenocarcinoma (Figure ). Tumor markers were within normal ranges. The chest, abdominal, and pelvic computed tomography and gallium scintigraphy findings showed no evidence of malignancy. However, upper gastrointestinal endoscopy disclosed scirrhous gastric cancer, which was pathologically diagnosed as adenocarcinoma (signet-ring cell). The final diagnosis was meningeal carcinomatosis and excessive coagulation related to occult gastric cancer. Following discussion with the patient’s family, and based on the patient’s age, worsening consciousness levels (GCS of 6 on week 3), and poor performance status, she was transferred to the other hospital 22 days after admission, and supportive care rather than active management was administered.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.0, 'kg'], 'height': [155.0, 'cm']}",25.39022,24.12071,26.65973,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 61.0 kg. The patient's bmi is therefore 61.0 kg / (1.55 m * 1.55 m) = 25.39022 kg/m^2."
2089,6,Body Mass Index (BMI),physical,decimal,usmle-5313,Extracted,"A 13-year-old girl presents to her primary care physician due to concerns of not having her first menstrual period. She reports a mild headache but otherwise has no concerns. She does not take any medications. She states that she is sexually active and uses condoms inconsistently. Medical history is unremarkable. Menarche in the mother and sister began at age 11. The patient is 62 inches tall and weighs 110 pounds. Her temperature is 99°F (37.2 °C), blood pressure is 105/70, pulse is 71/min, and respirations are 14/min. On physical exam, she is Tanner stage 1 with a present uterus and normal vagina on pelvic exam. Urine human chorionic gonadotropin (hCG) is negative. Follicle-stimulating hormone (FSH) serum level is 0.5 mIU/mL (normal is 4-25 mIU/mL) and luteinizing hormone (LH) serum level is 1 mIU/mL (normal is 5-20 mIU/mL).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [110.0, 'lbs'], 'height': [62.0, 'in']}",20.11904,19.11309,21.12499,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 62.0 in, which is 62.0 in * 0.0254 m / in = 1.5748 m. The patient's weight is 110.0 lbs so this converts to 110.0 lbs * 0.453592 kg/lbs = 49.89512 kg. The patient's bmi is therefore 49.89512 kg / (1.5748 m * 1.5748 m) = 20.11904 kg/m^2."
2090,6,Body Mass Index (BMI),physical,decimal,pmc-4712542-1,Extracted,"A 7-year-old girl visited the emergency room for abdominal pain with 10 times of vomiting within 24 hours. It was the first time she had. She felt a dull ache intermittently. She was healthy without any prior illness. Her height was 130.1 cm (97 percentile) and the weight was 29 kg (90-95 percentile). She was slightly dehydrated but not severely ill looking. On physical examination, her belly was very soft and there was no abdominal tenderness. The hemoglobin was 12.9 g/dL and other laboratory findings including amylase, lipase, and liver profile were within normal range. Simple abdomen revealed a 3 cm sized soft tissue density near the pylorus without small bowel obstruction (). We checked computed tomography and noticed a well demarcated mass near the ampulla of Vater in the 2nd portion of duodenum (). Ultrasonography and upper gastrointestinal series revealed a polypoid mass with short stalk in the 2nd portion of duodenum ( and ). We attempted endoscopic examination and removal. However, the lumen was nearly obstructed by the mass and the stalk was too broad and hard to excise. We therefore decided on surgical resection. On laparotomy, we could palpate the mass after Kocher's maneuver. It was an approximately 3 cm well-demarcated mass broadly attached to duodenal wall. We opened the anti-mesenteric side of duodenum. The base of mass was attached to mesenteric side of duodenum just above the ampulla of Vater (). We completely removed the mass without injury of ampulla of Vater and pancreas parenchyma. The duodenotomy was closed transversely with a single-layer absorbable suture. The patient could take sips of water after 3 days of operation and recovered uneventfully. Pathologically, there were multifocal scattered nodular lesions, up to 0.3×0.2 cm in diameter in the submucosa and muscularis propria (hematoxylin and eosin [H&E] stain, ×40 or ×100). Microscopically nodular lesions were composed of variably dilated ductular mucinous and pancreatic exocrine acinar tissue (H&E, ×200). Immunohistochemistry of acini tissue showed positive reaction to CK19 (CK19, ×200). It was confirmed as HP, ductal and acini component (type 2 by Heinrich classification []) (). Postoperatively, the patient has been well without any discomfort and there was no abnormal finding in computed tomography during the 1 year follow-up period.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [29.0, 'kg'], 'height': [130.1, 'cm']}",17.13339,16.27672,17.99006,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 130.1 cm, which is 130.1 cm * 1 m / 100 cm = 1.301 m. The patient's weight is 29.0 kg. The patient's bmi is therefore 29.0 kg / (1.301 m * 1.301 m) = 17.13339 kg/m^2."
2091,6,Body Mass Index (BMI),physical,decimal,pmc-6942505-1,Extracted,"This is a seven-year-old boy who was born by spontaneous vaginal delivery at full term with a birth weight of 2.5 kg with no neonatal ICU admission. He first presented to the dermatology clinic at the National Guard Hospital, Makkah, Saudi Arabia when he was five years old complaining of dry scaly patches on the skin. The patient’s medical history revealed that it started at the age of four months in the form of desquamation and erythema on the hand and feet, sparing the trunk, back, and face. The father noticed that he is mouth breathing and has nasal discharge for three months with congested nasal turbinates. He is developmentally up to age and has taken all his vaccines. He has allergies to fish. On examination, he was active, alert with no dysmorphic features, and vitally stable. His height was 106 cm and his weight was 16 kg. Upon inspection, he was found to have erythematous hyperkeratotic skin plaques and papules with scales over the planter and palmar aspect of both hands with similar lesions observed on both feet, legs, scalp, and ears with nail pitting (Figures -). All routine labs were within normal limits. He was diagnosed as having psoriasis and was treated by calcipotriol cream and moisturizing cream. During the follow ups he was not improving so he was given acitretin capsules and a skin punch biopsy was ordered. He started to show improvement after that. The results showed he had mild psoriasiform spongiotic dermatitis with no evidence of psoriasis. Accordingly, the patient was referred to pediatric genetics for further investigations. He was also referred to dental services for dental caries and delayed teething (Figure ), and to an otolaryngologist to rule out nasal polyps. He was found to have positive family history, where his one-year-old brother and maternal aunt had similar conditions. A WES was done and it identified pathognomic variants in CTSC that cause autosomal recessive PLS (PALS; OMIM: 245000) (variant: c.899G>A p.(Gly300Asp) chr11:88027667). The patient did not follow up on his appointments with the dental care and otolaryngologist",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [16.0, 'kg'], 'height': [106.0, 'cm']}",14.23994,13.52794,14.95194,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 106.0 cm, which is 106.0 cm * 1 m / 100 cm = 1.06 m. The patient's weight is 16.0 kg. The patient's bmi is therefore 16.0 kg / (1.06 m * 1.06 m) = 14.23994 kg/m^2."
2092,6,Body Mass Index (BMI),physical,decimal,pmc-5070190-1,Extracted,"A 2-year-old Japanese boy was admitted to a regional hospital with massive hematemesis just after consuming milk. Prior to admission, he had lunch as usual and then drank milk in the evening. He was well until he experienced an episode of hematemesis. Of note, he had no significant past medical illness. On physical examination, he was pale, with a temperature of 35.9 °C, a pulse rate of 108 beats per minute, and a blood pressure of 108/52 mmHg. His height and body weight were 90 cm and 14 kg, respectively. An abdominal examination was unremarkable, and no neurological abnormalities were noted. His laboratory results showed normal hemoglobin (Hb; 12.6 g/dl), leukocyte, and platelet counts. A blood coagulation test result was also normal. However, his blood urea nitrogen (28.8 mg/dl)/creatinine (0.3 mg/dl) ratio was increased. The results of other laboratory tests (including liver enzymes) were unremarkable. He was managed conservatively with H2 blockers, intravenous fluids, and kept nil by mouth. However, on the day of admission, he developed another massive hematemesis; he was subsequently transferred to our department the following day.
On admission in our department, his Hb had decreased to 8.0 g/dl. Blood biochemistry showed raised urea (34.1 mg/dl) with normal creatinine level (0.3 mg/dl). His rapidly progressive anemia associated with massive hematemesis indicated the presence of an active bleeding in his upper GI tract. We performed emergency gastroscopy under general anesthesia using small diameter upper endoscopes with a transparent hood over the head. During gastroscopy, fresh blood and clotting were observed within his stomach. A careful observation revealed the presence of an abnormal visible vessel with an adherent clot on the lower body of his stomach (Fig. ). No mucosal abnormality surrounding the lesion was noted; the lesion was thus diagnosed as DL. One hemostatic clip was placed on the DL and excellent hemostasis was obtained (Fig. ). The hemoclip (HX-610-135, Olympus) was applied with a rotatable clip-fixing device (HX-110-LR) using an endoscope (XQ240, Olympus Optical Co., Japan) with a 2.8 mm diameter accessory channel. The clip was fixed onto the lesion for a week or more (Fig. ). Following endoscopic hemostasis, he was initiated on an intravenous proton pump inhibitor (0.7 mg/kg) daily for 2 days. He recovered without blood transfusion and was discharged 4 days post-endoscopy with a 1-month prescription of oral proton pump inhibitor. He was well at 6-months follow-up, with no recurrence of hematemesis.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [14.0, 'kg'], 'height': [90.0, 'cm']}",17.28395,16.41975,18.14815,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 90.0 cm, which is 90.0 cm * 1 m / 100 cm = 0.9 m. The patient's weight is 14.0 kg. The patient's bmi is therefore 14.0 kg / (0.9 m * 0.9 m) = 17.28395 kg/m^2."
2093,6,Body Mass Index (BMI),physical,decimal,pmc-3822029-1,Extracted,"A 73-year-old male, height 172 cm and weight 75 kg, was referred to our institution after having been seen 3 months previously due to worsening lower back pain which radiated to the left buttock and thigh as well as claudication that had lasted three months. His lower back pain had been treated with caudal blocks for the last 3 years. A lumbar spine radiograph revealed degenerative scoliosis and narrowing of multiple intervertebral disc spaces. A magnetic resonance imaging (MRI) scan demonstrated marked lumbar 3-4 (L3-4) intervertebral disc extrusion, lumbar spinal stenosis, and an L3 compression fracture. He was treated with one L3-4 epidural block, medial branch blocks, and received nonsteroidal anti-inflammatory drugs. His radicular pain and claudication improved, but he complained of low back pain consistently. Therefore, a transforaminal epidural block and percutaneous epidural neuroplasty were performed. After the treatments, all symptoms improved, and only mild lower back pain which increased with walking remained. However, 2 weeks later, he was hospitalized for left leg paralysis and excruciating lower back pain that did not diminish when laying down. MRI was repeated, which identified aggravated L3-4 disc extrusion and a dilatated abdominal aortic aneurysm of nearly 6.0 cm (). Careful review of the previous MR images identified a curvilinear atherosclerotic (calcified) lateral wall of an abdominal aortic aneurysm and fusiform aneurysmal dilation of the abdominal aorta anterior to the vertebral body (). The patient was referred to the neurosurgery department of our hospital for further examination and treatment for the disc extrusion and abdominal aortic aneurysm.
He presented to our hospital with intractable lower back pain and pitting edema of both lower extremities. His blood pressure was 110-130/79-90 mmHg and his pulse rate was 70-80 min. Abdominal contrast enhanced computed tomography (CT) confirmed a focal lower abdominal aortic aneurysm with crescent-form mural thrombus formation, without evidence of rupture (). A sensory conduction study and motor conduction study revealed left lumbar radiculopathy mainly of the L4, L5 nerve roots, as well as hypoesthesia on the right L4 to L5 dermatomes. Muscle strength was fair plus in left L5 innervations on manual muscle testing. The range of motion and reflexes were normal. In all extremities, the arteries were readily palpable and no pulsating mass was detected on abdominal palpation. There were no other abnormal findings on the physical examination. Bloodwork showed total cholesterol 191 mg/dl, triglycerides 137 mg/dl, LDL cholesterol 137 mg/dl, HDL cholesterol 30 mg/Dl and HDL ratio 6.3. The surgeons elected to perform decompressive hemi-laminectomy and microdiscectomy on L3-L4 and transforaminal lumbar interbody fusion on L3-L4. After neurosurgery, the patient's neurologic symptoms improved except for the lower back pain. He was transferred to the thoracic surgery department and underwent endovascular aneurysm repair and aortic stent graft interposition. After surgery, his lower back pain diminished. He underwent physiotherapy for 1 month and was then discharged.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [75.0, 'kg'], 'height': [172.0, 'cm']}",25.35154,24.08396,26.61912,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 172.0 cm, which is 172.0 cm * 1 m / 100 cm = 1.72 m. The patient's weight is 75.0 kg. The patient's bmi is therefore 75.0 kg / (1.72 m * 1.72 m) = 25.35154 kg/m^2."
2094,6,Body Mass Index (BMI),physical,decimal,pmc-8020339-1,Extracted,"A 27-year-old woman had persistent headache and amenorrhea. In addition, the size of her foot was increased by 0.5 cm for 6 months and lower jaw protrusion was observed. Thereby, she was referred to our institution. The data at that time were as follows: growth hormone (GH), 82.44 ng/ml; insulin-like growth factor-1 (IGF-1), 1,390 ng/ml; prolactin (PRL), 28.2 ng/ml. In addition, enlargement of pituitary fossa was observed in head X-ray, and thickening of heel pad was observed in foot X-ray. Based on these findings, she was diagnosed as acromegaly and hospitalized in our institution for further examination and treatment.
On admission, her height and body weight were 163.0 cm and 48.0 kg. Blood pressure and heart rate were 110/60 mmHg and 68 bpm. Body temperature was 37°C. Swelling of superciliary arch, hypertrophy of nose and lip, macroglossia, lower jaw protrusion, thickening of the plantar, enlargement of the palm and bitemporal hemianopsia were observed all of which were compatible with acromegaly. There were no abnormalities in heart and lung sound and in abdomen. The data on admission were as follows: GH, 51.12 ng/ml; IGF-1, 1,538.9 ng/ml; free triiodothyronine (FT3), 5.56 pg/ml (reference range: 2.3–4.3 pg/ml); free thyroxine (FT4), 2.52 ng/dl (0.9–1.7 ng/ml); TSH, 2.26 μU/ml. Other endocrine hormone levels were within normal range: adrenocorticotropic hormone (ACTH), 44.0 pg/ml; cortisol 8.5 μg/dl; dehydroepiandrosterone sulfate (DHEA-S), 375 μg/dl; plasma renin activity (PRA), 1.1 ng/ml/h; plasma aldosterone concentration (PAC), 29.7 pg/ml; luteinizing hormone (LH), 1.2 mU/ml; follicle stimulating hormone (FSH), 3.3 mU/ml; PRL, 26.2 ng/ml; estradiol, 26 pg/ml; testosterone 1.02 ng/ml. Thyroid-related antibodies including anti-Tg antibody, anti-TPO antibody and thyroid receptor antibody were all negative. Liver and renal function was within normal range. Inflammatory and tumor markers such as C-reactive protein (CRP), carcinoembryonic antigen (CEA) and colorectal carcinoma 19-9 (CA19-9) were also within normal range. In thyroid echography, both lobes of the thyroid gland were swelling although increase of blood flow was not observed (
). In brain magnetic resonance imaging (MRI), there was a giant tumor (51 × 34 × 22 mm) around pituitary fossa, pressuring on optic chiasm from the middle (
). Bilateral internal carotid arteries were surrounded by the tumor, and infiltration into the cavernous sinus was observed. Based on these findings, we finally diagnosed her as pituitary adenoma producing GH and TSH at the same time. After such diagnosis of GHoma and TSHoma, pituitary tumor resection was performed. Most of the tumor was resected during the pituitary surgery, although we fail to show what percentage of the tumor was resected.
In hematoxylin and eosin (HE) staining of the resected pituitary adenoma, solid proliferation of chromophobe cells was observed (). In CAM5.2 staining, many cytokeratin-producing cells were observed (). In MIB1 staining, percentage of MIB1-positive cells was about 3%, indicating that the proliferative activity was relatively low (). Based on these findings, she was pathologically diagnosed as sparsely granulated somatotroph adenoma. In GH staining, many GH-producing cells were observed () and in TSH staining, many TSH-producing cells were observed (), whereas in prolactin staining, prolactin-producing cells were not detected at all (). These findings further confirmed our diagnosis that this subject had pituitary adenoma producing GH and TSH simultaneously.
After the surgery GH level was markedly decreased although it was still higher compared to its normal range (reference range in our institution: ≤2.47 ng/ml). After the surgery, IGF-1 level was also markedly decreased and became within normal range (reference range in our institution: 141–328 ng/ml) (). About 1 year later, IGF-1 level was increased again. After then, cyber knife therapy and treatment with somatostatin analog octreotide were performed. After the cyber knife therapy together with octreotide, IGF-1 was marked decreased and became within normal range (). However, since digestive symptoms were observed after the octreotide treatment, we started a combination therapy with GH receptor antagonist and octreotide based on the previous reports (, ). After then, GH and IGF-1 levels did not increase at least for 6 years (). After the operation, since thyroid function was not sufficiently suppressed, we started anti-thyroid drug thiamazole. After then, thyroid function was normalized and we stopped thiamazole. But TSH, FT3 and FT4 levels did not increase at least for 6 years (). In addition, there were no particular abnormalities in brain MRI taken 1 month after operation (), 1 year after operation (half year after cyber knife therapy) () and 4 years after operation ().",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [48.0, 'kg'], 'height': [163.0, 'cm']}",18.06617,17.16286,18.96948,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 48.0 kg. The patient's bmi is therefore 48.0 kg / (1.63 m * 1.63 m) = 18.06617 kg/m^2."
2095,6,Body Mass Index (BMI),physical,decimal,pmc-3110300-2,Extracted,"A 74-year-old male patient (168 cm, 53 kg) visited our institution complaining of difficulty in swallowing for the past 8 years and the frequent occurrence of aspiration pneumonia for the past 1year. Lateral radiography of the cervical spine demonstrated extensive osteophyte formation from C2 to C4 () and decompression of the osteophyte was planned. His medical history was significant for diabetes. He had been diagnosed with stable angina but rejected PCI. Preoperative electrocardiogram and echocardiogram revealed tolerable status. Blood chemistry revealed hyperglycemia, but hepatic and renal function and coagulation were normal. On physical examination, the patient was alert and afebrile; and his vital signs were stable. Oral examination was unremarkable and neck extension was normal. He had minimal dyspnea in the supine position. Indirect laryngoscopy revealed a large hard mass protruding from the posterior wall of the hypopharynx that concealed the arytenoids cartilage (). A preoperative neck CT showed slight narrowing of the airway at the level of the epiglottis. Vocal fold mobility was preserved. No narrowing of the subglottic region was observed when flexible endoscopy was performed. Preoperative tracheostomy was done under local anesthesia and general anesthesia was induced with thiopental sodium 250 mg and rocuronium 50 mg and maintained with sevoflurane. Complete decompression of the osteophyte was performed for 210 minutes using an anterolateral transcervical approach, which proceeded without any complications. The postoperative course was uneventful. On the second postoperative day, indirect laryngoscopy was performed by an otolaryngologist to decide if removal of the tracheostomy cannulawas appropriate. However, this examination revealed significant laryngeal edema including the epiglottis and posterior laryngeal wall (). On 29th postoperative day, flexible endoscopic examination was performed again and copious secretion, decreased vocal cord mobility and narrowing of the upper airway were observed () and the patient was discharged on the 33rd postoperative day with a double cannula having a speech valve. On the 59th postoperative day, the tracheostomy cannula was removed () at the outpatient clinic without any complication.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.0, 'kg'], 'height': [168.0, 'cm']}",18.77834,17.83942,19.71726,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 53.0 kg. The patient's bmi is therefore 53.0 kg / (1.68 m * 1.68 m) = 18.77834 kg/m^2."
2096,6,Body Mass Index (BMI),physical,decimal,pmc-3674643-1,Extracted,"A 99-year-old female (height 1.60 m; weight 45 kg, ASA III) was admitted to our hospital and underwent major abdominal surgery (sigmoid colon carcinoma resection with colorectal anastomosis) under general anesthesia, and the surgery duration was about 220 minutes. Her medical history revealed mild degree heart failure, chronic normocytic anemia, gastritis, and allergy for NSAIDs and penicillin antibiotics.
Her preoperative laboratory tests: hemoglobin 8.8 mg·dL−1, hematocrit 30.9%, leukocytes 11,500 mm−3 without deviation, platelets 453,000 mm−3, sodium 131 mg·dL−1, potassium 4 mg·dL−1, magnesium 0.58 mg·dL−1, creatinine 0.5 mg·dL−1, and total calcium 8.24 mg·dL−1.
In the preoperative room we prepared our patient by antibiotics prophylaxis: ciprofloxacin 2 gm; metronidazole 500 mg and an antiemetic agent; ondansetron 4 mg.
Our patient was monitored by pulse oximetry, expiratory capnography, invasive and noninvasive blood pressure, electrocardiogram, bispectral index (BIS), neuromuscular transmission (TOF Guard), and diuresis.
A peripheral venous access (20 G) was established in upper right limb, and also a central venous access was done immediately after the induction phase as it was needed for postoperative chemotherapy afterwards.
We induced our anesthesia by oxygen, propofol 50 mg, fentanil 100 mcg, and rocuronium bromide 30 mg, and then we proceeded to a rapid sequence endotracheal intubation (tube diameter was 6.5 mm),
The maintenance of the anesthesia was achieved by continuous infusion of remifentanil in a dose of 0.2 mcg/kg/min, rocuronium bromide 10 mg, xenon 60–65%, and O2 35–40%, the fluid replacement was calculated depending on her diuresis, plasma fluid, intraoperative blood loss, and anemia, and she was refunded by ringer lactate 1500 mL, Nacl 0.9% 1000 mL, fresh plasma fluids 1000 mL, and packed red cells 500 mL.
A closed-circuit anesthesia machine (Felix Dual, Taema) was used for xenon gas delivery. The ventilation parameters were the following: “pressure-cycled mechanical ventilation with inhalation pressure indexes of 19 cm H2O, respiratory frequency 12 incursions per minute, PEEP 5 cm H2O, FiO2 35–40%, and inspiratory/expiratory time ratio 1 : 2, and the exhaled tidal volume was around 380 mL.”
Blood gas analysis was performed twice: 30 minutes after the start and 30 minutes before the end of surgery.
We registered electrolyte disorders, and they were resolved by administration of KCL 40 mEq and Ca++ gluconate in dose of 1 g·10 m−1 (Tables and ).
After 5 minutes from the end of the surgery we noticed our patient starting a voluntary respiratory activity with a high BIS level, so we decided to proceed for the emergence phase and extubation reversing the neuromuscular blocking by sugammadex in a dose of 100 mg [] with careful monitoring for her cardiovascular and respiratory functions. Both modified Aldrete score and BIS values were recorded ().
After 13 minutes we got the complete recovery of our patient, she was awake without any confusion state, delirium, or cognitive dysfunction, also she had excellent and stabile both hemodynamic and respiratory functions, postoperative pain control was achieved by continuous intravenous infusion of morphine (5 mg over 24 h), and she was transferred to ICU for close monitoring.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.0, 'kg'], 'height': [1.6, 'm']}",17.57812,16.69921,18.45703,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.6 m. The patient's weight is 45.0 kg. The patient's bmi is therefore 45.0 kg / (1.6 m * 1.6 m) = 17.57812 kg/m^2."
2097,6,Body Mass Index (BMI),physical,decimal,pmc-6334399-1,Extracted,"A 67-year-old Japanese man with advanced colon cancer with liver metastasis presented with bowel obstruction in May 2007 and underwent emergency surgery (left hemicolectomy with D3). A pathological examination revealed a well-to-moderately differentiated, type 2, intermediate-type tubular adenocarcinoma (70 × 40 mm) arising in the descending colon. The lesion was associated with pathological evidence of serosal invasion (pSE), an infiltrative growth pattern (INFβ), moderate lymphatic invasion (ly2), and moderate venous invasion (v2). There was no involvement of the proximal margin (pPM0, 150 mm), no distant metastasis (pDM0, 120 mm), and no lymph node metastasis (0/27). A liver biopsy revealed metastatic adenocarcinoma.
His medical history indicated a gastric ulcer in 2003. We did not note any personal or family history of kidney disease, autoimmune disease, or asthma. He worked in an office. He had smoked five cigarettes per day for 50 years and drank alcohol socially.
One month after the operation, he initially received hepatic arterial infusion therapy with 5-fluorouracil (5-FU) from June through to October 2007. After receiving five courses of simplified l-leucovorin plus 5-FU (sLVFU), he had strangulating intestinal obstruction and underwent emergency surgery in January 2008. Second-line treatment with fluorouracil, leucovorin, and irinotecan (FOLFIRI) was started in October 2008 and terminated in May 2009 as a result of renewed progression. From June 2009 he received third-line treatment with modified leucovorin, fluorouracil, and oxaliplatin regimen (mFOLFOX-6) plus bevacizumab. However, in June 2010 a computed tomography (CT) scan revealed progression of liver metastasis again. Considering that our patient had already been treated with the combination chemotherapies FOLFIRI and mFOLFOX-6 and the wild-type RAS status of his primary tumor, treatment with bi-weekly panitumumab monotherapy (500 mg/m2) was initiated on July 20, 2010. He had no adverse events after the initial course of panitumumab. A second course of panitumumab was administered on August 2, 2010. General malaise, leg swelling, and skin rash developed 2 days after the second cycle of panitumumab (2 weeks after the initial dose), and around August 18 the symptoms intensified. However, he had neither joint pain nor abdominal pain during the period. When he visited the out-patient department on August 23, bilateral edema of his legs and bilateral purpura of his forearms had progressed (Figs. and ). Blood tests showed grade III acute renal failure with blood urea nitrogen (BUN) level of 33.8 mg/dL and a creatinine level of 3.10 mg/dL, as well as nephrotic syndrome with a total protein (TP) level of 4.5 g/dL and an albumin level of 1.4 g/dL. Urine analysis showed blood (3+) and urinary protein (4+). Several acanthocytes and 5–9 white blood cell casts were observed in the urinary sediment. He was therefore immediately admitted to our hospital. His height was 164.cm and body weight was 50 kg (6 kg increase in 3 weeks). His blood pressure was 110/60 mmHg and pulse rate was 84 beats per minute. His body temperature was 36.4 °C. The results of his physical examination were relatively unremarkable, except pretibial pitting edema and diffuse purpura on his whole body. There was no neurologic abnormality including mononeuropathy multiplex.
He underwent examinations for differential diagnosis from other kidney diseases: immunoglobulin G (IgG), immunoglobulin A (IgA), immunoglobulin M (IgM), C3, C4, cryoglobulin, proteinase 3-antineutrophil cytoplasmic antibody (PR3-ANCA), and myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA). However, no clinically significant findings were obtained (Table ). Because oliguria (urine volume, 400 mL/day) was present after admission, an albumin preparation (12.5 g twice daily) and furosemide were administered for 3 days. Treatment with prednisolone 40 mg/day was begun immediately. After this treatment, his urine volume increased to 1100 mL, and the generalized edema improved slightly. A skin biopsy was performed to evaluate the purpuric lesions on the lateral lower region of his left leg on August 25, and LCV was diagnosed (Fig. ). A drug lymphocyte stimulation test (DLST) was performed as a supplementary test to differentiate the cause of the drug-induced allergic symptoms. However, the results of all tests were negative for both cetuximab and panitumumab (Table ). As local therapy, betamethasone ointment and moisturizer were applied topically. The skin lesions gradually improved, and only crust remained on August 31. Around August 27, his urine volume decreased to 600–900 mL/day, and edema and his body weight increased. Thus, treatment with indapamide was started on August 31. After this treatment, his urine volume increased to 1500–1700 mL/day. The urinary protein excretion decreased from 7.14 g/day to 6.83 g/day during hospitalization, indicating that he had nephrosis. His kidney function gradually improved after his BUN and creatinine reached peak levels of 60.5 mg/dL and 3.36 mg/dL, respectively, on August 30. His levels of BUN and creatinine on September 9 were respectively 40.1 mg/dL and 2.01 mg/dL, indicating a tendency to decrease, and he was discharged from our hospital on September 13 (Fig. ).
Because the nephrotic syndrome continued, he was hospitalized for kidney biopsy on November 1, but it was cancelled due to emerging hydronephrosis. His serum magnesium level was 1.5 mg/dl (1.9–2.5 mg/dl). This case was discussed at a multidisciplinary conference of the Cancer Institute Hospital. Rechallenge of panitumumab was denied considering the increasing nephrotoxicity. The best supportive care was eventually provided. On November 11, our patient agreed with our decision to provide supportive care. He died of colon cancer progression in May 2011, 48 months after the onset of initial symptoms and after having received 9 months of best supportive care. A needle necropsy of the kidney was performed approximately 40 minutes after death. Global sclerosis was found in 6 of approximately 50 glomeruli, and fibrous crescent formation was recognized in 3 glomeruli, while the components of other glomeruli had collapsed (Figs. and ). On immunohistochemical staining, no deposition of IgA or IgG was found in the glomeruli.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [50.0, 'kg'], 'height': [164.0, 'cm']}",18.59012,17.66061,19.51963,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 164.0 cm, which is 164.0 cm * 1 m / 100 cm = 1.64 m. The patient's weight is 50.0 kg. The patient's bmi is therefore 50.0 kg / (1.64 m * 1.64 m) = 18.59012 kg/m^2."
2098,6,Body Mass Index (BMI),physical,decimal,pmc-5253166-1,Extracted,"An 8-year-and-1-month old Caucasian female presented to her pediatrician with complaints of nocturnal enuresis and hyperactivity. Child was adopted at 2 years of age along with her younger sibling due to history of parental neglect by biological parents. Adoptive parents reported hyperactivity as a major concern. Physical examination revealed her weight to be 24.8 Kg (25th percentile for age) and height to be 128.7 cm (35th percentile for age). Vitals were stable and blood pressure at presentation was 113/75 mmHg. A comprehensive neurologic exam by her pediatrician revealed fine tremors in the upper extremity. Laboratory workup was initiated and a comprehensive metabolic panel revealed sodium (Na) of 124 mEq/L. She was referred to our medical center for comprehensive evaluation. Initial exam revealed an otherwise healthy child who was alert and oriented in time, space, and person. Vitals including blood pressure were normal for age. Admission chemistry and other laboratory values are shown in .
While the causes of hyponatremia can be extensive [, ], her presentation was consistent with euvolemic hyponatremia suggestive of Syndrome of Inappropriate Antidiuretic Hormone (SIADH). Evaluation by us confirmed our impression of SIADH with serum Na of 123 mEq/L, serum osmolality of 264 mOsm/Kg (ref range 280–300), and urine osmolality of 614 mOsm/Kg (300–900). Adrenal function as assessed by early morning cortisol of 8.6 mcg/dL and thyroid function tests were normal. Magnetic resonance imaging of the brain demonstrated asymmetric T2/FLAIR hyperintense, nonenhancing enlargement of the right hypothalamus, concerning for a hypothalamic glioma (). Other workups including ultrasound of abdomen, pelvis, chest X-ray, and a PPD (purified protein derivative) skin test to rule out tuberculosis were essentially negative.
Initial management consisted of fluid restriction, furosemide (at a dose of 2 mg/Kg/day divided into three doses), and salt and potassium chloride supplementation. Though this resulted in her Na levels gradually improving to a maximum value of 130 mEq/L, the fluid restriction regimen was very difficult to follow and family expressed ongoing frustration. Given limitations for treatment options in treating children with SIADH and with Na levels trending down (range: 121–124 mEq/L), we initiated Arginine Vasopressin (AVP) V2 receptor antagonist therapy with oral tolvaptan. Current literature is lacking data on use of these agents in children. So tolvaptan therapy was started at a dose of 7.5 mg under close supervision in the inpatient setting. The dose initiated was half of the lowest approved dose in adults which is 15 mg []. Initial response to therapy was dramatic in terms of correction of hyponatremia, with Na improving to low 130 mEq/L range.
With initiation of tolvaptan therapy, her Na levels improved allowing us to loosen our recommendation on water intake to a maximum of 2.5 L/day. Liberalization of fluid intake with this regimen seemed to help the family initially. Gradually though, Na levels trended down because her water intake was much more than her urine output with the therapy (). Child psychology and later child psychiatry were involved to help family and child be compliant with the fluid restriction. Dose of tolvaptan had to be increased gradually to a maximum of 30 mg daily. In an effort to keep the Na levels up, water restriction to 2.5 L/day was encouraged. But even this degree of fluid restriction proved to be difficult as she developed compulsive drinking behaviors. She would sneak water from bottles in trash cans, bathtub, faucet, and even toilets.
With ongoing management issues due to behavior problems and recent black box warning issued by the Food and Drug Administration (FDA) for liver failure in patients on long-term therapy [], decision was made to wean tolvaptan. She was weaned off V2 antagonist therapy over a period of 6 months. While her persistent hyponatremia was concerning, the limited benefits we were observing with treatment and the potential side effects led us to make this decision. Following this, patient was briefly on oral furosemide, which was eventually discontinued as long-term furosemide is known to exacerbate chronic hyponatremia [].
She was also noted to develop hypertension with blood pressures ranging around 140/106 mmHg requiring input from pediatric nephrology during the course of her treatment. She was initially started on amlodipine 2.5 mg twice a day but needed the addition of enalapril maleate in 4 months due to poor control of her blood pressure. She is currently on amlodipine 2.5 mg twice a day and enalapril 10 mg twice a day. Secondary causes of hypertension were ruled out by pediatric nephrology team. While hypertension was noticed after initiation of therapy, this is not a reported side effect of V2 receptor antagonist therapy. Her hypertension continued after she was weaned of tolvaptan therapy. It is unlikely that the hypertension was caused by volume overload as her weight continued to be stable. Etiology of hypertension is unclear as preliminary workups including renal ultrasound and renal Doppler were all within normal limits.
A complete neuropsychological assessment revealed IQ to be low normal. Patient had reading, attention, and auditory processing problems making school more challenging for her. She had no difficulties in doing grade level mathematics and spelling. These contributed to ongoing difficulties at school. Due to the well-known determinant effect of hyponatremia on bone health [], DXA scan was done which revealed Z-score of −1.8 at AP spine and −1.1 at total body less head region. Since she never suffered from any pathological fracture, education was provided to optimize calcium and vitamin D intake. 25-Hydroxyvitamin D levels checked periodically were always in the sufficient range (>30 ng/mL).
Currently, she is off all pharmacological therapy for her hyponatremia and her sodium levels range within 113–118 mEq/L. Fluid restriction is encouraged but not very strictly enforced due to fear of her developing unhealthy drinking habits. She is performing at age appropriate level in school. Regular monitoring for endocrinopathies by stimulation testing has so far been normal.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [24.8, 'kg'], 'height': [128.7, 'cm']}",14.97251,14.22388,15.72114,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 128.7 cm, which is 128.7 cm * 1 m / 100 cm = 1.287 m. The patient's weight is 24.8 kg. The patient's bmi is therefore 24.8 kg / (1.287 m * 1.287 m) = 14.97251 kg/m^2."
2099,6,Body Mass Index (BMI),physical,decimal,pmc-4002007-1,Extracted,"Herein, we report a case of a 71-year-old female patient hospitalized for anemia, motor incoordination, gait disturbance, weakness, and decline of her functional state. She was asymptomatic eight months prior to the day she was hospitalized, when she had asthenia, adynamia, hyporexia, symptoms of dizziness, and vertigo. Six months prior to admission, the symptoms increased, with onset of loss of balance, and postural instability. The patient also developed deterioration for walking, with repeated falls, which led her to stop walking for fear of falling, and limited her physical daily living activities to simply transferring from the chair to the bed. Likewise, it was noted that upon flexing her neck, she reported feeling an electrical discharge irradiating from her back to her legs. Two months before hospital admission, she noted lesions on the tongue, which produced a burning sensation and pain when swallowing foods - leading her to decreased intake of food and a loss of 5 kg coupled with increased feeling of weakness in her general state. She consulted with her local hospital, where she was diagnosed with paraparesis and anemia to continue studies.
As personal antecedents, she revealed hypertension managed with captopril 50 mg every 12 h. She did not report alcohol consumption, vegetarian nutritional habits, or other personal or family antecedents of importance.
Upon physical exam for admission, she was in poor general state, pale, and marked loss of muscle mass. Blood pressure was 130/80 mm/Hg, without orthostasis, respiratory rate 17 per min and heart rate 85 per min. Her weight before developing the diseasewas 70 kg; her current weight is 60 kg, height 1.65 m. The oral cavity showed smooth, shiny, reddish depapillated tongue with ulceration at lateral level ).
Neurological exam revealed that she was alert and oriented in all three spheres, no cranial nerve involvement, or abnormal movements. She had muscle weakness grade 3/5 and spasticity in all four limbs, tone and tropism diminished. The superficial sensitivity, touch, pain, and temperature systems were normal. Deep sensitivity was altered, with lack of vibratory sensation of the sense of position in upper and lower limbs, numbness in hands and feet, and positive Lhermitte's sign. Gait was characteristic of sensory ataxia with postural instability, broad support polygon, positive Romberg's sign, diminished osteotendinous reflexes especially in lower limbs and bilateral flexor plantar reflex present. Different para clinical studies were carried out (). Urinalysis, serology, and direct Coombs test were also performed under normality parameters. Additionally, extended blood test was conducted, revealing red cell anisocytosis, macrocytosis, and poikilocytosis. White series with hypersegmented neutrophils and platelet series without alterations were found. Upper gastrointestinal endoscopy was performed with the biopsy showing chronic atrophic gastritis positive for Helicobacter pylori.
Geriatric assessment scales were applied, showing: mini-mental exam (28/30), geriatric depression scale (4/15), physical aspect of Barthel's scale of activities of daily living (60/100), JH Downton's scale of risk of falling in the elderly (3 points), and assessment of nutritional state through the mini nutritional assessment (16/30 points).
Vitamin B12 deficit diagnosis was performed with hematological manifestations given by macrocytic anemia, neurological manifestations by ataxic gait, and in skin and mucosa by Hunter's glossitis. Because of the neurological alterations in association with ataxic gait and low levels of vitamin B12, nuclear magnetic resonance of the cervical and thoracic spine was requested, which documented images compatible with sub-acute combined degeneration of the spine (.
Replacement with Cbl was begun, showing after three weeks increased Hemoglobin values with decreased levels of lactate dehydrogenase indicating improvement in ineffective erythropoiesis. Glossitis was resolved after a month of establishing Cbl reposition (C and D). After three months of treatment, gait improved with the patient walking independently; sensitive symptomatology also improved.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.0, 'kg'], 'height': [1.65, 'm']}",22.03857,20.93664,23.1405,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.65 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.65 m * 1.65 m) = 22.03857 kg/m^2."
2100,6,Body Mass Index (BMI),physical,decimal,pmc-6579323-1,Extracted,"A three-year-old male child was admitted to the pediatric ward of Dr. Ruth KM Pfau, Civil Hospital Karachi (CHK) with a one-year history of generalized weakness, loose motions, decreased appetite and intermittent fever not associated with rigors, chills or night sweats, an eight-month history of inability to walk and sit, polydipsia, polyurea, abdominal distention and loss of neck holding for 14 days. He had a previous history of hospitalization six months ago due to the same complaints. The patient was accompanied by his mother. He weighed 6 kg, is the 7th born child to his parents and was delivered at term to a 37-year-old G7P7 mother via normal vaginal delivery. The mother did not report any complications or illnesses during pregnancy. He cried immediately after birth, and there were no complications during or after birth. There is no consanguinity between mother and father. The child was vaccinated but was malnourished, with an unremarkable family history.
The patient also developed diarrhea which was bulky in consistency, green in color with seven episodes per day after every meal intake. Diarrhea was associated with abdominal distention and vomiting. The mother then started giving him a combination of trimethoprim-sulfamethoxazole, after which diarrhea subsided. The child developed neck holding at four years of age, he started sitting at eight months and started walking with support at 12 months of age. The child was first breastfed within three hours of delivery and was exclusively breastfed up to six months. Complimentary feeding was started after six months with pulses, mashed potatoes, porridge and chicken. Breastfeeding was continued up to two years. Currently, the child takes 1-2 feeds per day. The personal history revealed that the patient was sleeping normally, but the appetite was decreased. The mother also noticed a weight loss, altered bowel habits, and micturition was normal.
On examination (O/E), the patient was lying on the bed irritated, severely wasted and emaciated with visible bony deformities. Initial vitals included blood pressure (BP) 110/70 mmHg, a regular pulse of 90 beats/min, a respiratory rate of 20 breaths/min, and a low-grade fever of 100° F. The patient was anemic and dehydrated, while, there was no presence of edema, clubbing, cyanosis, and lymphadenopathy. On further examination, parietal and frontal bossing, rachitic rosary (Figure ), widening of wrists and knock knees (it's a valgus deformity in which legs curve inwards so that the feet are apart when the knees are touching) were found as well. On abdominal examination, it was soft, non-tender, distended with mild tenderness on both flank regions, with a centrally placed umbilicus. The liver was palpable three fingers below the right costal margin. Gut sounds were audible 3-4 sounds/min. All other systems were unremarkable.
The anthropometric measures of the child are as follows: weight = 6.5 kg, occipitofrontal circumference = 49.5 cm, height = 72.5 cm, mid-upper arm circumference = 8 cm, upper segment = 45 cm, lower segment = 27.5 cm, weight for height = 6.5/9 *100 = 72.2 (moderately low) and height for age = 72.5/94.6*100 = 76.6 (severely low).
On investigations performed, complete blood count (CBC) showed a hemoglobin (Hb) of 5.4 gm/dl, mean corpuscular volume (MCV) of 82 fl and a platelet count of 187,000/mL. The total leukocyte count (TLC) was 10.6 x 109/L, including 39% neutrophils and 48% lymphocytes. His inflammatory markers were raised with a C-reactive protein (CRP) of 23 mg/L [Normal (N) = 3] and an elevated erythrocyte sedimentation rate (ESR) of 115 mm/hr (N = 0-22) for men and (N = 0-29) for women. The clotting profile showed an international normalized ratio (INR) of 1.01, while prothrombin time (PT) was 10.6 seconds.
The urea creatinine electrolytes (UCE) were within normal range except decreased potassium levels of 2.8 mEq/L. The levels of calcium, magnesium and phosphate in blood were 15.1, 1.9 and 4 mg/dL, respectively. The blood culture showed a growth of Burkholderia species. The urinalysis showed a pH of 5.0, specific gravity of 1.025, with the presence of protein and blood. Additionally, numerous red cells were seen along with yeast and 4-6 pus cells per high power field (HPF). The urine culture showed growth of Candida species. The stool analysis showed that the stool was hard, acidic, brown in color with 1-2 pus cells per HPF. His vitamin D levels came out to be 54.29 ng/mL, and parathyroid levels were 8.36 pg/ml. Liver function tests showed a total bilirubin of 0.28 mg/dL, direct bilirubin of 0.21 mg/dL and levels of alkaline phosphate alanine aminotransferase were 368 and 3 units per liter, respectively.
The X-rays of the chest (Figure ), skull (Figure ) and femur (Figure ) are attached below. Additionally, ultrasound of kidney ureters and bladder (KUB) showed an incidental finding of bilateral renal calculi (right kidney at lower pole measuring 0.7 cm, in the left kidney at mid pole measuring 0.7 cm), along with bilateral grade 2 renal parenchymal changes. The urinary bladder was normal in thickness with no presence of focal mass, calculus or diverticulum.
Considering the diagnosis of OI, an ophthalmology review was done to look for lens dislocation and blue sclera, but neither was present in both eyes. However, the left eye showed a corneal thinning nasally, temporally and inferiorly.
During the hospital stay, the patient was intravenously given cefotaxime 220 mg, piperacillin-tazobactam 700 mg, and meropenem three times a day. Additionally, linezolid 70 mg was injected every eight hours, along with injections of bisphosphonate 7 mg for three days, amikacin 55 mg twice a day for 14 days and fluconazole 85 mg loading dose, 45 mg once a day for 10 days. The patient was also given a teaspoon of the combination (artemether and lumefantrine) once a day. Three pints of red blood cells were transfused as well, after which his Hb became 10.6 mg/dL. During the stay, the child had a prolonged course of fever with pancytopenia, which improved on injections of meropenem, amikacin, and fluconazole.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [6.5, 'kg'], 'height': [72.5, 'cm']}",12.36623,11.74792,12.98454,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 72.5 cm, which is 72.5 cm * 1 m / 100 cm = 0.725 m. The patient's weight is 6.5 kg. The patient's bmi is therefore 6.5 kg / (0.725 m * 0.725 m) = 12.36623 kg/m^2."
2101,6,Body Mass Index (BMI),physical,decimal,pmc-3695252-1,Extracted,"A 76-year-old male with 160 cm in height and 58 kg in weight, respectively, was admitted for surgery with known aortic stenosis. He has a previous history of diabetes, hypertension and asthma. He had taken glimepiride, telmisartan, furosemide and bisoprolol. Preoperative echocardiography exams revealed the followings: aortic valve calcification and severe stenosis, a decreased left ventricular systolic function, trivial tricuspid regurgitation and ejection fraction of 40-45%. In a coronary artery angiography, right coronary artery was originated from the left coronary sinus (). However, compression of the coronary arteries by major vessels was not revealed. Coronary computed tomography (CT) was not checked. The patient was scheduled for aortic valve replacement.
At the operating theatre, routine noninvasive and invasive blood pressure monitoring, electrocardiography (EKG), pulse oximetry and bispectral index monitoring was established. Anesthetic induction was done under target-controlled infusion (TCI) of propofol and remifentanil. Then pulmonary artery catheter and transesophageal echocardiography (TEE) probe were inserted. TEE revealed severe calcified and stenotic aortic valve, trivial tricuspid regurgitation and a good regional wall motion. Until the CPB initiation, vital signs were maintained well.
At the time of the operation, aortic valve and annulus were severely calcified and both coronary arteries were originated from the left coronary sinus, but have different ostia. Aortic valve was replaced with 19 mm St. Jude Medical xenoartic bioprosthesis Epic (St. Jude Medical, Minnesota, USA) and the surgery were done without specific event. During cardiopulmonary bypass weaning, blood pressure and cardiac output were unstable. The changes of ST segment in EKG were detected. These situations were repeated for about 30 minutes, and dopamine and norepinephrine infusion were started. TEE showed intermittent hypokinesia of inferoposterior wall motion. Air was not detected, and nitroglycerin infusion was not effective. Epinephrine was infused and intraaortic balloon pump (IABP) was inserted. Cardiac wall motion was progressively normalized and vital signs were stabilized. The total surgery and CPB time was 360 minutes and 161 minutes, respectively. The patient was transferred to coronary care unit after surgery, and vital signs were also stable. Anomalous origin of the right coronary was considered as the culprit for the difficult weaning process. IABP was removed the next day, and the patient was discharged without any special events.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [58.0, 'kg'], 'height': [160.0, 'cm']}",22.65625,21.52344,23.78906,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 58.0 kg. The patient's bmi is therefore 58.0 kg / (1.6 m * 1.6 m) = 22.65625 kg/m^2."
2102,6,Body Mass Index (BMI),physical,decimal,pmc-7190964-1,Extracted,"A 25-year-old Asian woman presented with a constant left lateral lower abdominal pain of increasing severity for 3 d, associated with nausea and vomiting for the previous 3 d at our emergency department.
She had left lower abdominal pain initially and then became diffuse abdominal pain with quality of cramping. She visited other hospital at first and painkillers were prescribed. However, the symptoms did not relieve.
She had been diagnosed with ARS and congenital glaucoma since her infancy and she underwent trabeculotomy at the age of 1-year-old.
Her family history was unremarkable.
Upon her admission, significant observations were telecanthus, microdontia, and an underweight build (height 149 cm, weight 39 kg, body–mass index 17.6 kg/m2). Further physical examination revealed pallor, a soft nondistended abdomen, and a nontender palpable mass in the left lower quadrant.
Laboratory findings were all within the normal range.
Computed tomography (CT) with intravenous contrast material showed a non-homogeneously enhanced splenic parenchyma with a twisted vascular pedicle (Figure ). Moreover, the spleen was seen below the pancreatic tail in the left iliac fossa instead of its standard anatomical position.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [39.0, 'kg'], 'height': [149.0, 'cm']}",17.56678,16.68844,18.44512,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 149.0 cm, which is 149.0 cm * 1 m / 100 cm = 1.49 m. The patient's weight is 39.0 kg. The patient's bmi is therefore 39.0 kg / (1.49 m * 1.49 m) = 17.56678 kg/m^2."
2103,6,Body Mass Index (BMI),physical,decimal,pmc-7671568-1,Extracted,"A two-year-old male patient presented to the emergency room with a two-day history of melena and hematemesis. His prenatal, birth history and neonatal period were unremarkable. At one year of age, he was diagnosed with polycystic kidneys. However, the parents did not follow up with scheduled appointments. He had no history of previous episodes of abdominal pain or jaundice. The physical examination showed an acutely ill-looking boy, with a protuberant abdomen, non-icteric, asthenic, and with evident paleness. His weight and height were 11 kg and 82 cm, at 10th and 9th percentile for age respectively. His abdomen was distended with an abdominal circumference of 56 cm with hepatomegaly of 7 cm below the costal margin and splenomegaly of 4 cm below the costal margin.
Laboratory studies revealed a hemoglobin level of 9.9 g/dL, hematocrit of 26.8%, leukocyte count of 9460 /µL, creatinine of 1.1 mg/dL, blood urea nitrogen (BUN) of 74 mg/dL, alanine aminotransferase (ALT) of 32 UI/L, alkaline phosphatase of 196 UI/L.
An upper gastrointestinal endoscopy showed esophageal varices secondary to portal hypertension (Japanese classification FIII) which were subsequently ligated. Serology for hepatitis B, hepatitis C, Epstein-Barr virus, and cytomegalovirus were negative. Other negative test results included thick blood smear, latex agglutination test, anti-Smith antibodies, hemoglobin electrophoresis, and liver and kidney type 1 anti-microsomal antibody (anti-LKM-1). His serum ferritin levels, transferrin saturation index, and ceruloplasmin were within normal limits.
Abdominal ultrasound revealed an enlarged liver (size 11.1 cm) with alteration in its echogenicity, defined borders, no masses or cysts, and a patent portal vein measuring 6.2 mm. The spleen was enlarged, measuring 9.4 x 3.7 cm, which appeared homogenous with no focal or diffuse lesions. The bile duct was not dilated. Both kidneys were increased in size, hyperechoic, and with loss of corticomedullary differentiation. There were no stones or dilation of the collecting system. A normal abdominal Doppler ultrasound and transthoracic echocardiography ruled out Budd Chiari syndrome.
Due to the inconclusive results of the abdominal ultrasound and Doppler, a computed tomography (CT) angiography and liver biopsy were requested. The CT angiography found significant hepatomegaly with a craniocaudal diameter at the level of the right hepatic lobe that reached 11.4 cm (normal 6-10 cm) and splenomegaly with a longitudinal diameter of 13.1 cm (normal 5-8 cm). Multiple intrahepatic images were found which corresponded to the dilated saccular bile ducts. Both liver lobes were affected, and there was no apparent obstruction. Dilatation of the portal vein was also observed, with a transverse diameter of up to 10 mm, and large esophageal varices. The common bile duct was dilated with a transverse diameter of 7 mm. Finally, important vascularization at the level of the hemorrhoidal plexus was observed. The concluding findings were highly suggestive of CD with evident signs of portal hypertension, vesicular hydrops, multiple mesenteric and retroperitoneal lymphadenopathy, and polycystic kidney disease (Figures , ).
A liver biopsy revealed nodular liver tissue with marked fibrosis between nodules, which confirmed the presence of CHF (Figures , ). The discharge treatment was symptomatic, including antihypertensive drugs, beta-blockers for portal hypertension, and a proton pump inhibitor.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [11.0, 'kg'], 'height': [82.0, 'cm']}",16.35931,15.54134,17.17728,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 82.0 cm, which is 82.0 cm * 1 m / 100 cm = 0.82 m. The patient's weight is 11.0 kg. The patient's bmi is therefore 11.0 kg / (0.82 m * 0.82 m) = 16.35931 kg/m^2."
2104,6,Body Mass Index (BMI),physical,decimal,pmc-3970275-1,Extracted,"A 48-year-old male was referred to the endocrinology clinic complaining of generalized edema, increased blood pressure and blood glucose levels. The patient was on medication due to hypertension that was diagnosed 1 year ago. Recently, the blood pressure was not well-controlled, the blood glucose level was high and generalized edema developed.
The patient was diagnosed with MTC 14 years ago; total thyroidectomy with right cervical lymph node dissection was performed and I-131 metaiodobenzylguanidine (MIBG) 200 mCi was administered. He was treated with tumor resection for recurred MTC on a mediastinal lymph node 13 years ago. Nine years ago, MTC recurred on the left cervical and left parahilar lymph nodes and was treated with I-131 MIBG 200 mCi after surgery. Two years ago, MTC recurred thirdly on the cervical and mediastinal lymph nodes and lung and was treated with cervical and mediastinal lymph node dissection and the left upper lobe wedge resection of the lung. Since then, the patient has not shown any signs or symptoms of recurrence.
The patient's height was 172 cm and weight was 84 kg, 2 kg over his usual weight. His blood pressure was 185/110 mm Hg with a pulse rate of 90 beats per minute and a breathing rate of 18 breaths per minute. The patient's body temperature was 37℃. Moon face and facial flushing were observed. Buffalo hump and purple striae were absent. Mild pitting edema was observed on the anterior tibia and slight skin pigmentation was present.
Peripheral blood examination showed a white blood cell count of 14,450 cells/µL, hemoglobin of 15.3 g/dL, and platelet count of 358,000 cells/µL. On serum biochemical examination, total cholesterol was 252 mg/dL with total protein of 6.5 g/dL, albumin of 4.1 g/dL, total bilirubin of 1.1 mg/dL, alkaline phosphatase of 101 U/L, aspartate aminotransferase of 17 U/L, alanine aminotransferase of 62 U/L, blood urea nitrogen of 10.3 mg/dL, and creatinine of 0.6 mg/dL. On serum electrolyte examination, sodium was 145 mmol/L with potassium of 2.8 mmol/L, chloride of 94 mmol/L, and bicarbonate of 40.4 mmol/L. Fasting plasma glucose level was 168 mg/dL with glycated hemoglobin of 8.6%. Hormone examination showed total T4 of 12.75 µg/dL (range, 5 to 13) and thyroid stimulating hormone of 0.07 µIU/mL (range, 0.15 to 5.0). Serum calcitonin was 127.86 pg/mL (<10.0) and carcinoembryonic antigen was 29.46 ng/mL (<5). Plasma ACTH concentration was measured with immunoradiometric assay (ELSA-ACTH kit, CisBio, Belford, MA, USA), and was 203.9 pg/mL (range, 6.0 to 60.0). Serum cortisol concentration was 36.0 µg/dL (range, 5 to 25.0) with a 24-hour urine cortisol of 2,237.1 µg/day (range, 20 to 90). On the low dose dexamethasone suppression test, inhibited serum cortisol was 32.50 µg/dL. The 24-hour urine examination results were as follows: metanephrine 14.46 µg/day (range, 52 to 341), normetanephrine 28.21 µg/day (range, 88 to 444), epinephrine 6.57 µg/day (<40), norepinephrine 26.43 µg/day (<80), and vanillylmandelic acid 3.51 mg/day (<8). To validate the RET gene mutation, peripheral blood was collected from the patient and white blood cells were separated by centrifugation to extract genomic DNA. For polymerase chain reaction, BIGDYE version 3.1 cycles sequencing kit (Applied Biosystems, Foster, CA, USA) reagent was utilized and 3,730 automated sequencer (Applied Biosystems) was used to analyze DNA sequence. The DNA sequencing showed no RET gene mutation.
Chest and abdomen computed tomography revealed recurred lesions on the mediastinal lymph nodes, lungs, and liver (), but no abnormal findings in adrenal glands (). Sellar magnetic resonance imaging showed no abnormality in the pituitary gland (). Gastroscopy, colonoscopy, and positron emission tomography did not identify suspicious primary lesions in other regions.
Calcitonin and chromogranin A staining was positive on resected tissues on the third recurrence 2 years ago, which is indicative of MTC. ACTH immunohistochemistry staining was negative ().
Because curative resection of the MTC lesions was difficult on the fourth recurrence, close follow-up with further chemotherapy was considered. To control the ectopic ACTH syndrome, the patient was administered ketoconazole. The dosage was gradually increased over 3 months up to the maximum dosage (1,200 mg/day), but the serum cortisol concentration level did not decrease. Therefore, bilateral adrenalectomy was performed. After surgery, ACTH remained above 200 pg/mL, but plasma glucose and blood pressure levels were improved sufficiently and the oral antidiabetic agent and antihypertensive medication were discontinued. The patient has been living in good condition until 6 months after the surgery without any medication other than glucocorticoid and mineralocorticoid agents.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [84.0, 'kg'], 'height': [172.0, 'cm']}",28.39373,26.97404,29.81342,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 172.0 cm, which is 172.0 cm * 1 m / 100 cm = 1.72 m. The patient's weight is 84.0 kg. The patient's bmi is therefore 84.0 kg / (1.72 m * 1.72 m) = 28.39373 kg/m^2."
2105,6,Body Mass Index (BMI),physical,decimal,pmc-8072617-2,Extracted,"Case C-II-1 (upper panel in ), a 3-year-old male with DD and congenital agenesis of the radius noted at birth, was referred for genetic diagnosis. The pregnancy was uneventful, and his parents are both healthy and non-consanguineous. During pregnancy, there was no exposure to drugs, alcohol, or tobacco. He was born at 39 + 5 weeks via normal spontaneous delivery, and his birth weight was 2590 g. After the birth, he revealed congenital agenesis radius and hypoplastic carpal bones of both forearms. He exhibited torticollis, and a neck sonogram identified sternocleidomastoid muscle thickening. An echocardiogram showed a known cause of cardiac murmur and showed an atrial septal defect (type: ostium secundum). The atrial septal defect was closed 4 weeks after the birth. Special evaluation for skeletal dysplasia including laboratory tests and imaging was within the normal range. We examined him using the Bayley-III scale at the age of 39 months and found global DD (cognitive, motor, and language developmental ages: 19–22 months, 23–26 months, and 15–19 months, respectively). He had fine motor impairment in throwing a small ball, stacking small blocks, and making a mark on paper with a crayon at 42 months. His body weight was 13.5 kg (3rd percentile), height was 100 cm (10 to 25th percentile), and head circumference was 48.5 cm (10th percentile) at age 4. He attended additional education programs, including speech therapy, fine motor exercise, and social skill training. The boy inherited the 15q11.2 BP1–BP2 deletion from his unaffected mother. His sister (age of 32 months) also has this deletion, but is phenotypically unaffected ().",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [13.5, 'kg'], 'height': [100.0, 'cm']}",13.5,12.825,14.175,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 100.0 cm, which is 100.0 cm * 1 m / 100 cm = 1.0 m. The patient's weight is 13.5 kg. The patient's bmi is therefore 13.5 kg / (1.0 m * 1.0 m) = 13.5 kg/m^2."
2106,6,Body Mass Index (BMI),physical,decimal,pmc-8223890-1,Extracted,"A 56-year-old man weighing 102 kg and 188 cm tall (Figure ) was referred to our hospital because of an evident thickening around the neck. He had had the enlargement for the last 10 years and lately, the condition worsened. He was also a heavy alcohol drinker for the last 30 years and had 50 pack-years of smoking upon presentation. He was employed as a farmer and construction worker and had never demanded health care for his condition in the past.
More specifically, during the last 3 years, the enlargement became a collar-like mass around the neck and dyspnea crises with cough and upper airway excretions appeared, especially when bending the neck. He was relieved after some minutes of neck extension. The patient reported progressive difficulty sleeping due to extensive bulk of the mass, while he never had a problem of snoring, sleep deprivation, or other sleep apnea-associated symptoms. Additionally, he complained of weakness and chronic fatigue during these last years. The mass presented with cervical pain upon weight lifting, while he did not have any signs of neuropathy.
He referred a known history of hypertension with frequent hypertensive crises with systolic blood pressures of 220-230 mm Hg after heavy drinking, for which he used an angiotensin II receptor blocker (ARB) and hydrochlorothiazide and was usually referred to the local hospital. The cardiac assessment was normal. He had suffered from hypothyroidism for the last 15 years.
Upon examination, he had a circular mass of the neck, semi-hard on the anterior and hard on the posterior in a double oval-shaped configuration. The mass was not fixed to the overlying skin. His articulation was disturbed, and he had stridor while bending the head. Interestingly enough, we noticed that his legs and arms had lipohypertrophic along with lipoatrophic areas and that his supraclavicular regions were hypertrophic. The identification of the “pseudoathletic” type of Madelung's disease (type I), and hence, the diagnosis was delayed because the patient's physique was attributed to his occupation as a construction worker. Neurological examination was normal.
High values of uric acid, cholesterol, triglycerides, CPK, and LDH were reported. A slight elevation of SGOT along with a double γ-GT price was compatible with alcohol abuse.
A facial, cervical, and thoracic computed tomography (CT) showed a bilateral and symmetrical fat mass of the posterior and anterior region of the neck and of the upper trunk, without displacement or infiltration of the trachea (Figure ). Based on these findings, the diagnosis of Madelung's disease was made and we decided to treat the patient surgically.
Two different operations took place. In the first one, orotracheal intubation was impossible, so nasotracheal intubation was performed. A Gluck-Sorenson incision was performed, and fat tissue was excised in a similar fashion as in bilateral functional lymph node neck dissection with preservation of the accessory and marginal and cervical branches of the facial nerves. More specifically, we dissected levels I-V on the right side and levels I-VI on the left side. The dissection of the tissue in the carotid triangles was laborious (the fat tissue had septa that extended between the structures). The excised specimen's size was 27 × 12 × 18 cm, and its weight was 627 g (Figure ). A tracheostomy was performed before completion.
In the second operation, which took place 3 weeks later, the patient was placed in a prone position. The fat masses of the cervical, occipital, suboccipital, retro-auricular, and upper dorsal regions were removed surgically and with liposuction. The weight of the fat tissue was 114gram. We continued with removing the fat mass from the upper anterior cervical region. Part of the skin was removed because of its excess. The tracheostomy from the first operation remained and was finally removed 6 days after the second operation.
Histological examination after both the operations confirmed the initial diagnosis.
During the next 6 months, we suggested the use of a soft collar because we desired extra tension of the musculocutaneous tissue over the neck triangles for better healing. The patient did not follow our orders for alcohol abstinence.
In Figure , we can see the final result three months later.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [102.0, 'kg'], 'height': [188.0, 'cm']}",28.85921,27.41625,30.30217,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 188.0 cm, which is 188.0 cm * 1 m / 100 cm = 1.88 m. The patient's weight is 102.0 kg. The patient's bmi is therefore 102.0 kg / (1.88 m * 1.88 m) = 28.85921 kg/m^2."
2107,6,Body Mass Index (BMI),physical,decimal,pmc-6426513-1,Extracted,"A 38-year-old pregnant woman [28+1 weeks of twin pregnancy, gravida 3, para 2 (G3P2)] was transferred from a local hospital to our emergency room on March 28, 2018 due to complaints of persistent productive cough, with increased expectoration, dyspnea, dizziness, fatigue, and irregular abdominal pain. The admission diagnoses were as follows:
suspected pulmonary infection and heart failure;
single chorionic twin pregnancy;
moderate anemia;
pregnancy with severe rachiterata accompanied by a huge dorsal mass; and
G3P2 28 + 1 weeks of intrauterine pregnancy of twin live fetus.
The patient has been suffering from severe congenital scoliosis and kyphosis deformity with a huge dorsal mass, with ulcers repeatedly appearing in the surface of the dorsal mass for more than 10 years. She had a history of 2 deliveries. The first induction in 2008 was an 8-month-old stillbirth. In 2011, she delivered a premature infant who fortunately survived. As she and her husband wanted a male child, they risked another pregnancy.
The last menstrual period before the third pregnancy was unknown by the patient, but it was assumed that the patient was approximately 3-months pregnant during the admission. The patient had not had prenatal care since the beginning of pregnancy. She did not have any discomforts during the earlier weeks of pregnancy. However, she started having persistent cough without sputum production on the 24+ weeks of pregnancy, which continued to worsen. She had 2-week treatment in a local hospital prior to her admission in our institution.
Upon admission, the patient's vital signs were as follows: temperature of 36.5°C, heart rate of 107 beats per minute (bpm), respiratory rate of 35 breaths per minute, blood pressure of 107/67 mmHg, and blood oxygen saturation of 92%. Her weight and height were 46 kg and 133 cm, respectively. She was conscious and half-lying on her left side in a decubitus position owing to a huge dorsal mass (Fig. ). Her head was slightly advanced forward. She had a barrel-shaped chest, showing obvious shortening in length. The right shoulder was slightly higher than the left one. The outline of the right chest was larger than that of the left, and the tri-retraction sign was visible upon inhalation. Auscultation of both lungs revealed coarse rales, especially obvious at the lower portion of the right lung. A huge brown soft mass was found covering almost the whole back of the patient, with a size of approximately 26 × 22 × 8 cm and an ulcerative area (10 × 4 cm) at the center. No obvious abnormalities were found in other systems as well as the abdomen and pelvis.
At admission, the laboratory examination results were as follows: white blood cell (WBC), 15.9 × 109/L; neutrophil percentage (N%), 86.3%; hemoglobin concentration (HGB), 76 g/l; C-reactive protein (CRP), 67.0 mg/l; and PCT (calcitonin), 11.96 ng/ml. Mixed bacterium (Streptococcus, a small amount of yeast-like fungus, and Neisseria) were found in the sputum culture.
The initial diagnosis of heart failure was excluded because the electrocardiogram (ECG) showed sinus tachycardia, and the left ventricular ejection fraction was 0.69%, measured by color Doppler echocardiography, which indicated that the diastolic and systolic pressures of the left ventricle were normal. The myocardial marker, B-type natriuretic peptide (BNP), was normal as well.
Chest radiographs showed bilateral thoracic asymmetry (Fig. ), spinal protrusion with lateral bending deformity, kyphosis with “S”-type distortion, partial fusion of the left rib, consolidation of the lower portions of both lungs, and bilateral pleural effusion, which may have been caused by the pulmonary infection.
The pathogeny of the large dorsal mass could not be identified; however, the possibility of it being either a hemangioma or a neurofibroma cannot be excluded. Nevertheless, Staphylococcus aureus was cultured from the exudate of the local skin rupture.
B ultrasound showed the following: fetal 1 (left): heart rate: 154 bpm, left occipitoanterior (LOA), biparietal diameter of 6.44 cm, and femur length of 4.76 cm; and fetal 2 (right): heart rate of 148 bpm, right sacrum anterior (RSA), biparietal diameter of 6.41 cm, and femur length of 4.66 cm. Fibrous membrane echoes were found between the twins.
Before delivery, we had carried out a series of active symptomatic treatments and intensive monitoring for both the patient and her fetuses. For the mother, we tried to control the lung infection by administering third-generation cephalosporin and transfusing erythrocyte suspension to address her anemia. Daily nursing and treatment of surface ulcers of the dorsal mass were implemented as well. For the fetuses, in addition to fetal electronic monitoring every day, the patient had intramuscular injections of corticosteroid to promote fetal lung maturation.
Two weeks later, the patient's condition worsened. She was weak, anorexic, and in a low mood. She was also dyspneic and had persistent cough with thick sputum, which is difficult to expectorate. After multidisciplinary consultation, we decided to induce labor as soon as possible, in consideration of the critical situation of the patient, to ensure safety of the mother and fetuses.
The Cook Cervical Ripening Balloon (Fig. A) was used for mechanical dilation of the cervical canal prior to labor induction at term because the cervix was unfavorable for induction. On April 11, 2018 at 14:28 pm, owing to the complete dilation of the cervical, the patient was transferred to the delivery room. Given that she was dyspneic and had spinal deformity accompanied with a huge dorsal mass, she was placed on a right side-lying position while the upper body was elevated 45° to help facilitate the delivery process (Fig. B). At 15:00 pm, transvaginal examination and palpation revealed that fetal 1 had a head presentation, while fetus 2 had breech presentation. Moreover, the foot of fetus 2 was found on the right side of fetus 1's head. Considering that they come from 2 different chorionic cavities, our experienced midwife immediately prepared the patient for delivery. As soon as the rupture of membrane of fetus 1 occurred, the midwife pushed the foot of fetus 2 to the upper right until the foot could not be palpable using her right index and middle fingers, while simultaneously assisting the head of fetus 1 to descend using her ring and little fingers (Fig. C). Fetus 1 was successfully delivered at 16:15 pm, and fetus 2, who had breech presentation, was born at 16:19 pm via transvaginal-assisted delivery (Fig. D and E). The Apgar scores were 6-9-9 for both 2 premature infants. After tracheal intubation, the newborns were transferred to the neonatal intensive care unit immediately (Fig. F and G)
The mother's vital signs postpartum were stable. Interestingly, at 24 hours after delivery, the mother's dyspnea and coughing episodes gradually improved. One week later, the patient's temperature was normal, and the uterus contracted well with less vaginal bleeding. Then, she gradually recovered and was discharged soon enough.
The 2 neonates survived after treatment and were discharged from the hospital 1 month later.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [46.0, 'kg'], 'height': [133.0, 'cm']}",26.00486,24.70462,27.3051,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 133.0 cm, which is 133.0 cm * 1 m / 100 cm = 1.33 m. The patient's weight is 46.0 kg. The patient's bmi is therefore 46.0 kg / (1.33 m * 1.33 m) = 26.00486 kg/m^2."
2108,6,Body Mass Index (BMI),physical,decimal,pmc-6787834-1,Extracted,"A 53-year-old man was referred to our hospital for evaluation and management of hypertension and hypokalemia. He was diagnosed with hypertension at the age of 40 years, and his blood pressure was poorly controlled with a calcium channel blocker (nifedipine at 40 mg/d). He also had a past medical history of vasospastic angina and was a nonsmoker and social drinker. In addition, he had no family history of cardiovascular diseases. On admission, the patient was 168 cm tall and weighed 59 kg. He was afebrile, with a blood pressure of 161/96 mm Hg and a regular pulse of 61 beats per minute. There was no evidence of lung rales, cardiac murmurs, or an abdominal bruit. His neurological examination was unremarkable. Laboratory tests revealed that his serum creatinine level was 1.1 mg/dL, urea nitrogen level was 19 mg/dL, and serum sodium level was 140 mEq/L. He also exhibited hypokalemia with a serum potassium concentration of 2.9 mEq/L; however, he had no subjective symptoms, including muscle weakness. Plasma renin activity (PRA), plasma aldosterone concentration (PAC), and aldosterone-to-renin ratio (ARR) were <0.1 ng/mL/h, 292 pg/mL, and >2920, respectively. Other adrenal hormone levels were within normal limits. A chest radiograph and transthoracic echocardiogram showed no significant findings. An electrocardiogram suggested nonspecific ST-T wave changes with premature atrial contractions.
Primary hyperaldosteronism was suspected, and therefore, a captopril challenge test and a saline infusion test were performed. All these investigations revealed positive test results (Table ), which confirmed a diagnosis of PA. A low-dose dexamethasone suppression test to exclude the diagnosis of subclinical Cushing's syndrome was negative. An abdominal computed tomography (CT) scan was performed, which showed a left adrenal mass (13 mm) (Figure ). In adrenocorticotropic hormone (ACTH)-stimulated AVS, although aldosterone hypersecretion was observed in the left adrenal gland, the lateralization of the disease was not determined due to incomplete cannulation of the right adrenal vein (Table ). The criteria of successful cannulation were based on the current Expert Consensus Statement.
131I-adosterol scintigraphy under dexamethasone suppression showed an equivalently increased uptake in both adrenal glands (Figure ). Because we could not exclude the bilateral PA, including aldosterone-producing adenoma (APA) with microadenoma in the right adrenal gland, we performed the medical therapy with mineralocorticoid receptor antagonists (MRA). Although we administrated multiple antihypertensive agents including an MRA (eplerenone at 100 mg/d), an angiotensin II receptor blocker (azilsartan at 40 mg/d), a dual action beta blocker/alpha-1 blocker (carvedilol at 20 mg/d), a calcium channel blocker with an increased dose (nifedipine at 80 mg/d), an alpha-1 blocker (doxazosin at 2 mg/d), and an alpha-2 agonist (guanabenz at 4 mg/d), a home reading of the patient's blood pressure was above 140/90 mm Hg. Moreover, he needed a large quantity of potassium chloride to compensate for his hypokalemia.
Despite intensive medical therapy, he underwent percutaneous coronary intervention due to stable angina. Following this, we performed AVS again, but the right adrenal vein was not successfully cannulated (Table ). We discussed further the indication for surgery and decided to remove the left adrenal gland. After laparoscopic left adrenalectomy, his blood pressure and serum potassium remained normal after the withdrawal of eplerenone, doxazosin, guanabenz, and potassium chloride and a dose reduction of azilsartan (at 20 mg/d), carvedilol (at 10 mg/d), and nifedipine (at 10 mg/d). The PRA and PAC were 0.8 ng/mL/h and 57.1 pg/mL, 3 months after the adrenalectomy, respectively. Macroscopic findings of the resected specimen showed a yellowish colored nodule (13 mm in diameter) in the adrenal gland. We confirmed a diagnosis of an adrenocortical adenoma based on a histopathologic examination (Figure ); we also confirmed that the tumor cells were rich in the cytoplasm and were eosinophilic without malignant cells.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [59.0, 'kg'], 'height': [168.0, 'cm']}",20.9042,19.85899,21.94941,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 59.0 kg. The patient's bmi is therefore 59.0 kg / (1.68 m * 1.68 m) = 20.9042 kg/m^2."
2109,6,Body Mass Index (BMI),physical,decimal,pmc-3425296-1,Extracted,"A 21-year-old male, a known case of SWS, was posted for open reduction and internal fixation of fracture left ankle. He was 165 cm tall and weighed 78 kg. He had port wine stain on the left side of the face, left eyelid and left half of the palate. He had left hemiparesis. His mental status was normal. On examination, he was found to have grade 5/5 power on the right side and 3/5 on the left side. His mouth opening was adequate and the modified Mallampati classification was 2. All routine tests were unremarkable. He had undergone surgical correction for glaucoma of the left eye, and his intraocular tension was normal. Computed tomography (CT) scan brain showed atrophy and calcification of the left cerebral hemisphere. General anaesthesia was planned. Written informed consent was obtained and adequate duration of fasting was confirmed. The patient was premedicated with midazolam 1 mg intravenously (IV) to allay anxiety. Fentanyl 100 μg IV was given for pain relief. The patient was induced with Propofol 2 mg/kg. The trachea was intubated with an 8 mm internal diameter portex tube facilitated by 0.1 mg/kg vecuronium bromide. Patient's modified Cormack Lehane score was 3 and no vascular malformations were noted in the airway. Anaesthesia was maintained with N2O:O2 ratio of 60:40 and 1–2% sevoflurane, with intermittent doses of vecuronium. Intraoperative course was uneventful. After the surgery, once spontaneous breathing returned, anaesthesia was reversed with neostigmine 0.05 mg/kg and glycopyrrolate 5 mcg/kg. Extubation was performed after confirming return of adequate motor power. He was observed in the post anaesthesia care unit for 2 h before being transferred to the ward. The post-operative course was uneventful.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [78.0, 'kg'], 'height': [165.0, 'cm']}",28.65014,27.21763,30.08265,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 78.0 kg. The patient's bmi is therefore 78.0 kg / (1.65 m * 1.65 m) = 28.65014 kg/m^2."
2110,6,Body Mass Index (BMI),physical,decimal,pmc-7727885-1,Extracted,"A 34 year old male presented to the emergency department with a history of hemoptysis since 5 days. He had a history of loss of weight and appetite. He had no history of tuberculosis (TB) or TB contact, smoking, fever, or drugs. He also had a history of the inability to father a child and have never sought medical treatment for the same. There was no history of loss of libido, hypothyroidism, radiation to head or neck, surgery to head or abdomen, or symptoms of raised intracranial tension. On examination, his height was 156 cm and weight was 45 kg. His vitals were stable. He had pallor and digital clubbing. External genital examination showed genital ambiguity in the form of bifid scrotum, which was rugose and pigmented with a phallus of length 9 cm with well-formed glands []. The right gonads were not palpable in labioscrotal fold or elsewhere and the left gonads were palpable in the left inguinal region. There was no vaginal opening. Sexual maturity rate (SMR) P2 B1 with no axillary hair. He had poor facial and body hair. A natal history was later reviewed with him and there was no history of salt-wasting crisis, maternal virilization, or history of sex reversal. We considered the possibility of 46XY disorder of sex development (DSD), MGD, or ovotesticular DSD.
Laboratory investigations included hemoglobin of 8 g/dl, total leukocyte count of 8000/mm3, platelet count of 4.5 lakhs, and erythrocyte sedimentation rate of 60. Liver function test (LFT), renal function test (RFT), blood glucose, serum electrolytes, cortisol (8 am cortisol 16.08 mcg/dl), and 17-OH-progesterone were normal (1.1 ng/ml). Pooled follicle-stimulating hormone and luteinizing hormone levels were 14 mIU/mL and 9 mIU/mL, respectively; thyroid-stimulating hormone: 3.8 mIU/L, T4: 130 nmol/L (60–140), basal total testosterone: 240 ng/dL, estradiol 20 pg/ml (normal male: 10–50 pg/ml), prolactin 12 ng/ml (5–20 ng/ml), and inhibin B 156 ng/ml (80–300 ng/ml). Work up for tuberculosis (TB) which includes sputum acid fast bacilli and TB polymerase chain reaction study with sputum and blood specimens were negative. Chest-X ray was normal.
High-resolution computed tomography chest showed irregular solid lesions in the right upper lobe suggestive of a lung metastasis. Search for primary malignancy was done and investigations included upper endoscopy, colonoscopy, USG abdomen and pelvis, and tumor markers study (alpha fetoprotein, lactate dehydrogenase, carcinoembryonic antigen, and prostate-specific antigen levels). Ultrasound of the pelvis showed hypoplastic uterus with no gonads visualized. Tumor markers and gastrointestinal study were normal. Karyotyping (30 cells and 100 cells) revealed 45, X genotype. In view of the possibility of malignancy arising from a dysgenetic gonad and the inability to localize primary malignancy from the initial evaluation, we proceeded with a laparoscopy. Laparoscopic examination was done and visualized the right gonads and ducts. Laparoscopy showed enlarged right gonads in the ovarian fossa with bilateral fallopian tubes and hypoplastic uterus []. The right gonad was adhering to the adjacent peritoneum. The left gonad was visualized in the left inguinal region and biopsy was taken to confirm the type of gonad. The right gonad with fallopian tubes and rudimentary uterus was removed. A thorough histopathological examination of the right gonad showed dysgerminoma, and the left gonad showed testicular tissue (seminiferous tubules and Leydig cells). Dysgerminoma arising from the right gonad showed sheets or nests of large, uniform polygonal cells with clear or eosinophilic cytoplasm with distinct squared off cell membranes and with loose stroma []. No ovarian tissue was noted in these sections. Fluorescence in situ hybridization (FISH) for the identification of Y chromosome was done in gonadal tissue. FISH showed mosaic pattern with 90% cells of 45, X and 10% showing X and Y chromosomes 45, X/46, XY.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.0, 'kg'], 'height': [156.0, 'cm']}",18.49112,17.56656,19.41568,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 156.0 cm, which is 156.0 cm * 1 m / 100 cm = 1.56 m. The patient's weight is 45.0 kg. The patient's bmi is therefore 45.0 kg / (1.56 m * 1.56 m) = 18.49112 kg/m^2."
2111,6,Body Mass Index (BMI),physical,decimal,pmc-6196019-1,Extracted,"Our patient was a 15-year-old Han Chinese boy who presented with fever, weakness, pallor, edema, dyspnea, and gradually increasing abdominal girth for 2 weeks. His parents denied consanguineous marriage. His medical history was not significant. His one older sister and two younger sisters were all healthy. He was delivered after full-term normal pregnancy. His growth and development were markedly slow after birth, but his school records were excellent. His spleen was resected due to unexplained enlargement at the age of 9. He had a history of multiple prolonged hospital admissions for pyrexia of unknown origin, without reaching a clear diagnosis.
The results of an initial assessment on admission were: he looked unwell, height 135 cm, weight 30 kg, and no sign of secondary sex characters. He had fever with a temperature fluctuating between 37.2 and 39.7 °C, pallor, wakefulness, distress, and clarity of mind. There was no jaundice, petechiae, or fresh rash on skin. Superficial lymph nodes were palpable in inguinal region. His eyelids were swollen, no cyanosis, pharynx without congestion, and bilateral tonsils III° large. There was no thyroid enlargement. Trachea in midline. There were audible harsh breath sounds and crackles bilaterally. His heart beat was 114/minute with normal rhythm, no murmur was heard. He had a distended abdomen with hepatomegaly; liver palpable 10 cm below costal margin with firm consistency and free from tenderness. He had a huge scar located in the left upper quadrant (Fig. ). Murphy sign (−); shifting dullness sign (+). There was marked pitting edema in his lower extremities. A neurological assessment was normal. The results of other systemic examinations were essentially normal.
Initial and subsequent laboratory tests and imaging revealed the following results:On routine blood tests conducted over several days, white blood cell (WBC) count was more than 20 × 109/L with normal classification, whereas hemoglobin (Hb) and platelets (PLT) decreased continuously (Fig. ). Liver enzymes and bilirubin were increased slightly to moderately with hypoproteinemia: lactate dehydrogenase (LDH) 301 U/L, aspartate transaminase (AST) 45 U/L, alkaline phosphatase (ALP) 218 U/L, total bilirubin (TBIL) 72.9umol/L, albumin (ALB) 29 g/L, but a kidney function test and urine analysis were unremarkable. Prothrombin time (PT) and activated partial thromboplastin time (APTT) were prolonged slightly; D-Dimer increased moderately. Other positive indicators were: procalcitonin (PCT) fluctuated around 0.2 ng/ml; antistreptolysin (ASO) was 259 IU/mL; Widal’s test TH 1:160, TO 1:320; tumor marker CA-25 was 384.0 U/mL, CA724 was 38.78 U/mL; ferritin was 550.58 ng/mL; hepatitis E virus antibody IgG(+); and Legionella pneumophila serum antibody IgM(±). The tests of thyroid function, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), CD64 index, T-lymphocyte subsets, and glucose-6-phosphate dehydrogenase (G6PD) were normal. Coombs test, interferon-γ release assay, antinuclear antibodies (ANAs), hepatitis A virus (HAV)\hepatitis B virus (HBV)\hepatitis C virus (HCV)\human immunodeficiency virus (HIV) antibody test, and herpes simplex virus (HSV)\cytomegalovirus (CMV)\Epstein–Barr virus (EBV)-deoxyribonucleic acid (DNA) test were negative. Blood and fungal cultures were negative. Bone marrow smear showed infectious bone marrow image and occasional atypical lymphocytes. Ultrasound revealed grossly enlarged liver (right oblique diameter 164 mm) with normal echotexture, gallbladder wall swelling, left renal calculi, massive peritoneal effusion, but portal vein and common bile duct had normal diameters. There was slight pericardial effusion with normal pulmonary arterial pressure. Enhanced computed tomography (CT) scans showed severe pulmonary interstitial fibrosis with infection, multiple lymph node display, liver shape irregularity, and no obvious abnormality in abdominal angiography (Fig. ).
After receiving therapies including anti-infection, anti-virus, atomization inhalation, diuresis to eliminate swelling, liver-preserving and gallbladder protection, human serum ALB, immunoglobulin and blood transfusion, the symptoms of our patient improved, and his peak body temperature decreased (Fig. ). However, it was difficult to explain the illness with “one etiology”; it was assumed that it was probably a kind of rare genetic metabolic disease associated with infection. To confirm the diagnosis, pathological sections of the spleen were borrowed from another hospital, where the boy underwent splenectomy 6 years previously.
Hematoxylin-eosin (HE) staining of the spleen sections showed that red pulp was occupied by a large number of Gaucher cells, splenic trabecula disappeared, and some splenic nodules remained. The results of specific stains were: Rf (+) and periodic acid–Schiff (PAS) (−). The results of immunohistochemical stains were: CD68 (+), Lyso (+), Vim (+), KI-67 (+<5%), Pan-CK (−), EMA (−), HHF35 (−), CD31 (−), CD34 (−), LCA (−), and S-100 (−) (Fig. ). Final diagnosis was GD (type 1). However, our patient’s family declined to test beta-glucosidase levels, gene mutation site, or purchase imiglucerase (enzyme replacement therapy). Finally, he was discharged from hospital after his temperature had declined to normal.
During a subsequent 6-month telephone follow-up, he said that he was able to continue with his school life, and do some mild physical activities; he no longer had a fever. A routine blood examination at a local hospital showed mild anemia, and a CT scan showed no significant progress of pulmonary infection. After raising enough money, his family would consider using imiglucerase.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [30.0, 'kg'], 'height': [135.0, 'cm']}",16.46091,15.63786,17.28396,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 135.0 cm, which is 135.0 cm * 1 m / 100 cm = 1.35 m. The patient's weight is 30.0 kg. The patient's bmi is therefore 30.0 kg / (1.35 m * 1.35 m) = 16.46091 kg/m^2."
2112,6,Body Mass Index (BMI),physical,decimal,pmc-6054085-2,Extracted,"The second patient was a woman 74 years old, weight 75 kg, height 160 cm with a diagnosis of cutaneous fistulization resulting from a previous local radiotherapy to the left breast.
The pathological anamnesis found non-controlled arterial hypertension, insulin-dependent diabetes mellitus (Type 1) with low control, and a dysmetabolic/exotoxic hepatic cirrhosis. In 1990, she underwent a left quadrantectomy with ipsilateral axillary lymphadenectomy followed by local radiotherapy and chemotherapy for ductal breast cancer.
As in the previous case, we made a hepatic evaluation before the surgery. This revealed hepatic cirrhosis with multifactorial aetiology: dysmetabolism (diabetes poorly controlled for years, overweight) and toxic alcohol-induced (previous abuse, now notably reduced) and a possible minor iatrogenic component (post quadrantectomy chemotherapy in 1990). The patient had a minimal hepatic cytolysis in progress with moderate increase in indicators of cholestasis. To further complicate the situation, we observed signs of compromised hepatic function (Child Pugh class A6), portal hypertension with thrombocytopenia and diffused esophageal varices.
We did not find any contraindication to surgery, but underlined a risk of clinical decompensation and a hepatic functional risk in the post-surgical setting (surgical stress, anesthesiological toxicity...). The chosen surgical procedure for this patient was a complete left simple mastectomy and surgical debridement of the fistulised mammary area. The evening before surgery the patient received Arnica montana 15CH pills once and Apis mellifica 15CH pills once. On the day of surgery, the patient underwent to two sessions of electro-acupuncture with frequencies of 23–70 Hz for 20 minutes, repeated after 30 minutes. The chosen points for this intervention were the following: 1LU - 22 KI - 27 KI - 24 GB - 14 ST - 18 ST - 4 LI - 36 ST. At the same time, the patient took a homeopathic treatment consisting of Arnica montana 15CH 5 pills and Apis mellifica 15CH 5 pills.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [75.0, 'kg'], 'height': [160.0, 'cm']}",29.29687,27.83203,30.76171,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 75.0 kg. The patient's bmi is therefore 75.0 kg / (1.6 m * 1.6 m) = 29.29687 kg/m^2."
2113,6,Body Mass Index (BMI),physical,decimal,pmc-8057902-1,Extracted,"A 62-year-old male was referred to our centre after sustaining injury to his left leg in a landslide. On arrival in the emergency department (ED), his Glasgow Coma Scale (GCS) was 15 with a pulse rate of 88 beats per minute and blood pressure of 120/80 millimetre (mm) of mercury (Hg). The oxygen saturation in room air was 85% with respiratory rate of 20 per minute. He was subjected to trauma imaging, and an X-ray of his left pelvis revealed intertrochanteric fracture of femur (). A workup for the patients low oxygen saturation was performed, as there was no history of acute or chronic respiratory illness. On auscultation, there were diminished breath sounds on the right chest. Chest radiography was performed which showed heterogeneous infiltrations in his right lung, with crowding of the ribs and scoliotic spine with narrow intervertebral space (). A nasopharyngeal swab for Reverse Transcriptase Polymerase Chain Reaction (RT PCR) for Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) was collected. He was managed in the ED with oxygen via a nasal prong at 3 litres per minute, antibiotics, analgesics, and incentive spirometry and skin traction on the affected limb. The patient was planned for operative intervention and stabilisation of the fracture by proximal femoral nailing.
During the preoperative assessment of the patient, it was revealed that the patient was a known case of skeletal dysplasia. No further inquiry to ascertain the type of dysplasia was conducted previously. Both his son and daughter also suffered from skeletal dysplasia. The patient was a farmer by profession and had good functional status with a metabolic equivalent of more than four. He had a short stature with a body length of 127 centimetres (cm) () and weight of 45 kilograms (kg). On airway evaluation, the patient had adequate mouth opening with an interincisor distance of 4 cm, Mallampati class III, and missing multiple teeth. He had a short neck with a sternomental distance of 10 cm and thryomental distance of 4.5 cm. On systemic examination, a chest deformity, pectus carinatum, () was visible with a small rib cage. His spine was also examined and had dorsolumbar scoliosis with narrow intervertebral space. Rest systemic examination findings were within normal limits. The lab reports were also within normal limits. A pulmonary function test (PFT) was sought with restrictive lung disease in mind, and an echocardiography was ordered to assess the effect of restrictive lung disease on the heart. Echocardiography showed mild tricuspid regurgitation and mild pulmonary arterial hypertension with a pulmonary artery systolic pressure of 44 mm of Hg with an ejection fraction of 60%. Due to technical issues, the PFT could not be performed.
The patient was planned for regional anaesthesia considering the difficult airway and pulmonary issues. CSA was opted following counselling of the patient and after acquisition of informed written consent. On the day of surgery, the patient was shifted to the operating theatre, and standard American Society of Anaesthesiologists (ASA) monitoring was performed. Injection (Inj.) cefuroxime 750 grams was infused as a part of the infection prevention protocol. A paediatric Tuohy epidural needle 19 gauge was used in an attempt to access subarachnoid space. The procedure, however, was technically very challenging due to positional pain and spine anatomy. During the needling, a whitish discharge was noted from the skin puncture site, which was sent for microbiological examination, and the procedure was abandoned. A spine MRI was performed for further evaluation. It, however, did not reveal any infective pathology, but there was diffuse disc bulge along with disc desiccation of all visible intervertebral discs. A dorsolumbar scoliosis with cervico-dorsal-lumbar spondylosis was also noted.
After observation for 48 hours, the patient was scheduled once again for the contemplated procedure, as microbiological examination was negative for any infective pathology.
In the theatre, the patient was the given Inj. midazolam 1 mg and Inj. fentanyl 50 mcg. Ultrasound guided lumbar plexus block and trans-gluteal sciatic nerve block were performed in the lateral position to provide analgesia for positioning of the patient for CSA and also as a backup in case the planned spinal anaesthesia failed. After twenty minutes of the block, the patient was positioned for spinal anaesthesia in the sitting position. This time, the numeric rating scale for positional pain was 3 out of 10. With the help of a paediatric Tuohy needle, the dura was punctured at 3 cm depth and free flow of the cerebrospinal fluid (CSF) was observed. Then, a paediatric epidural catheter 22 gauge was inserted and fixed at 6 cm. Backflow of CSF was checked, and 0.4 millilitres (ml) (2 mg) of hyperbaric 0.5% Bupivacaine was administered over a minute. The effect of spinal anaesthesia was confirmed on the patient's normal leg. Approximately after eight minutes, the level of sensory block reached T8. Surgery was then allowed to commence as the motor blockade measured by the modified Bromage score reached 2. During the two hours of surgical duration, a single episode of hypotension was noted which resolved with fluid bolus. Based on the assessment of block height regression, the patient received further three aliquots of 0.4 ml of hyperbaric bupivacaine. So, the entire procedure was completed with 8 mg of 0.5% hyperbaric bupivacaine. We removed the catheter in the postoperative unit after infusing another 0.4 ml of hyperbaric bupivacaine. The catheter was removed as the expertise to handle CSA in the postoperative ward was inadequate. The patient was discharged from postoperative care after 24 hours of uneventful stay.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.0, 'kg'], 'height': [127.0, 'cm']}",27.90006,26.50506,29.29506,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 127.0 cm, which is 127.0 cm * 1 m / 100 cm = 1.27 m. The patient's weight is 45.0 kg. The patient's bmi is therefore 45.0 kg / (1.27 m * 1.27 m) = 27.90006 kg/m^2."
2114,6,Body Mass Index (BMI),physical,decimal,pmc-3469360-1,Extracted,"A 52-year-old Japanese man with no significant prior medical history and unknown smoking habits was referred to a urologist for investigation of hematuria, and was diagnosed as having urinary bladder cancer after further examination. He underwent three sessions of transurethral resection of the bladder tumor and intra-vesical instillation therapy (doxorubicin and cacillus Calmette-Guerin) and was then placed under observation. During the follow-up period no abdominal symptoms were observed, and an abdominal computed tomography (CT) scan revealed the incidental finding of dissection of the superior mesenteric artery (SMA). Our patient was then referred to our hospital.
His physical examination findings on admission were height of 176cm, weight of 64.5kg, blood pressure of 111/69mmHg, and pulse rate of 70bpm. Our patient had no fever and no other abnormal physical findings such as abdominal symptoms. His blood biochemistry test results were also normal. A contrast-enhanced abdominal CT scan revealed an arterial aneurysm and a dissection located approximately 1.5 and 5cm distal to the ostium of the SMA (Figure ). A false lumen of the artery was partially occluded by a thrombus. Distal to this occlusion, the arterial wall was irregularly shaped with both narrow and wide sections. The inferior mesenteric artery was also observed to have an irregular arterial wall. The renal artery also showed dissection, with an occluded false lumen; an ipsilateral renal infarction was observed as well.
On the basis of good CT contrast enhancement of the artery distal to the dissected portion and the absence of increased inflammatory parameters or clinical symptoms, our patient was prescribed oral aspirin and placed under observation. After two months, a follow-up CT scan revealed an enlargement of the pancreatic tail adjacent to the splenic artery (Figure ). In view of the absence of clinical symptoms or elevated levels of pancreatic enzymes, our patient was again placed under observation. Follow-up was carried out using three-dimensional CT scans, which showed re-expansion of the true lumen, gradual improvement of the arterial wall irregularities, and reduction of the renal infarction and pancreatic enlargement (Figure ). These changes continued to improve to almost normal over the following 15 months (Figures , and ). No findings suggestive of a recurrence of the disorder have been observed in our patient in the three years after his initial presentation.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [64.5, 'kg'], 'height': [176.0, 'cm']}",20.82257,19.78144,21.8637,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 176.0 cm, which is 176.0 cm * 1 m / 100 cm = 1.76 m. The patient's weight is 64.5 kg. The patient's bmi is therefore 64.5 kg / (1.76 m * 1.76 m) = 20.82257 kg/m^2."
2115,6,Body Mass Index (BMI),physical,decimal,pmc-5463293-1,Extracted,"A 13-month-old male presented to the pediatric surgery department with a complaint of bilateral undescended testis. A long, tubular structure (testis?) was palpated within the canal. Ultrasonography revealed absence of a testicular structure in the left inguinal canal or scrotum. On the right side, two structures measuring 12x8 mm and 11x7 mm and thought to be testes were observed in the proximal and middle parts of the inguinal canal. These findings were interpreted as transverse testicular ectopia on the right. During laparoscopic examination of the ectopic testis, tissues suggestive of a uterus, fallopian structures, and ovaries were observed inside the abdomen. Gonad biopsy was performed and the patient was referred to the pediatric endocrinology department with a preliminary diagnosis of sexual development disorder. At physical examination, weight was 10.2 kg [standard deviation score (SDS): -1.06] and height was 81 cm (SDS: -0.39). Blood pressure was 98/60 mm/Hg, Quickly score 2. The testes were not palpable and the phallus was 3.5 cm in length. The mother and father were first-degree relatives. Karyotype analysis revealed a XY, SRY (+) karyotype. Serum follicle-stimulating hormone level was 0.44 mIU/L (0.26-3 mIU/L), luteinizing hormone was 0.27 mIU/L (0.02-0.3 mIU/L), free testosterone 0.3 pg/mL (0.15-0.6 pg/mL), total testosterone 0.1 ng/dL (0.2-1.3 ng/dL), E2 <20 ng/mL (<15 ng/mL), and AMH >22 ng/mL (4.9-264.5 ng/mL). Immature seminiferous tubular structures were observed in gonad biopsy specimens sent from the pediatric surgery department. AMHR2 gene sequence analysis performed with a preliminary diagnosis of AMH receptor resistance revealed a previously undescribed homozygous c.24G>A (p.W8X) mutation. The parents had the same mutation in heterozygous form. The patient was evaluated as a case of AMH receptor resistance and presented to our “Sex Development Disorders Council”. Upon their decision, orchiopexy was performed.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [10.2, 'kg'], 'height': [81.0, 'cm']}",15.54641,14.76909,16.32373,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 81.0 cm, which is 81.0 cm * 1 m / 100 cm = 0.81 m. The patient's weight is 10.2 kg. The patient's bmi is therefore 10.2 kg / (0.81 m * 0.81 m) = 15.54641 kg/m^2."
2116,6,Body Mass Index (BMI),physical,decimal,pmc-8580087-1,Extracted,"The first patient was a 10-year-old girl with a history of short stature, growth retardation, intellectual disability, hirsutism, and ocular anomaly. She was born to non-consanguineous Chinese parents via vaginal delivery at 38 weeks, with a birth weight of 3.1 kg. No obvious intra-uterine growth restriction was observed by antenatal ultrasound scanning. She was noticed to have growth retardation at 1 year of age. At 4 years old, she was referred to our endocrinology department for comprehensive evaluations. Physical exam suggested that she had no obvious facial dysmorphism (Figure left), while her height was 84.8 cm (<−3 SD) and weight was 23 kg (>2 SD). Basal hormonal evaluation revealed normal levels of T3, T4, TSH (thyroid stimulating hormone), CORT (8 am and 8 pm), ACTH (adrenocorticotropic hormone), and IGFBP3 (insulin-like growth factor binding protein), but decreased level of IGF-1 (insulin-like growth factor-1; 33.2 ng/ml, reference range >55 ng/ml), which suggested IGF-1 deficiency. Glucagon stimulation testing showed peak growth hormone (GH) level was 10.5 ng/ml (reference range >10 ng/ml), indicating no obvious GH deficiency. A hand x-ray showed that her bone age was only 2.5 years. Brain MRI (Magnetic Resonance Imaging) identified increased pituitarium. At the age of 10 years, she came to our rehabilitation department for re-evaluation, since she exhibited symptoms of poor learning ability in mathematics, severe sensory integration dysfunction, as well as defective communication and socialization skills. She presented mild facial asymmetry, epicanthus tarsalis accompanied with severe ptosis of the upper eyelid and small palpebral fissures, as well as serious ocular abnormality of astigmatism (Johnson, ). In particular, her height (118 cm) and weight (23 kg) were more than 3 SD below the mean values for her age.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [23.0, 'kg'], 'height': [118.0, 'cm']}",16.51824,15.69233,17.34415,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 118.0 cm, which is 118.0 cm * 1 m / 100 cm = 1.18 m. The patient's weight is 23.0 kg. The patient's bmi is therefore 23.0 kg / (1.18 m * 1.18 m) = 16.51824 kg/m^2."
2117,6,Body Mass Index (BMI),physical,decimal,pmc-5842090-1,Extracted,"The patient's information released was permitted after discussion by the hospital ethics committee.
A 66-year-old woman with recurrent intermittent upper quadrant abdominal pain visited our hospital for further evaluation and treatment. Physical examination and initial vital signs were as follows: body temperature, 37.0℃; pulse rate, 66 beats/min; respiratory rate, 18 breaths/min; and blood pressure, 140/90 mmHg. Her height and body weight were 158 cm and 66 kg. She had a 10-year history of hypertension with good blood pressure control from oral Valsartan (40 mg/day). Her familial history was unremarkable. Laboratory examinations showed a low white blood cell count of 3,920/µL, a hemoglobin level of 11.8 g/L, and a platelet count of 124,000/µL. The liver function test results were as follows: serum aspartate transaminase: 14 U/L; alanine transaminase: 19 U/L; alkaline phosphatase: 88 IU/L; gamma-glutamyl transferase: 16 U/L; total bilirubin: 4.05 µmol/L; albumin, 35.7 g/L; and international normalized ratio: 0.93. CA 19-9 and α-FP were assayed for a malignancy workup, with results of 16.35 U/mL and 2.61 ng/mL, respectively. The results for viral markers including HBV surface antigen and anti-HCV were negative. Abdominal CT revealed an atrophic left lobar and dilated bile duct with the middle hepatic vein close to the cystic lesion (). Abdominal MRCP revealed irregular intrahepatic bile duct dilatation (IHBDD) of the left lobe with the left hepatic duct obstructed, while the common bile duct and right intrahepatic bile duct were normal (). However, we found that the irregular cystic dilatation of the bile duct was limited to the left liver and contained stones inside the cysts. No obvious abnormal dilated bile duct was found in the right liver. The common bile duct and the hepatic duct were normal, and no obvious dilatation was found. This patient was diagnosed with Caroli disease (type V). The surgical indication for the patient was explicit. However, the treatment prescription required consideration of the cystic wall being adjacent to the middle hepatic vein, the left hepatic atrophy and structure disorder, and the observation that the left hepatic vein was not visible. Although complete resection of the cysts may be a curative treatment for unilobar Caroli disease, this treatment was impossible for this patient due to the close adherence of the middle hepatic vein to the cystic wall. Therefore, we decided to perform laparoscopic left LR for the patient, while preserving a partial cystic wall close to the middle hepatic vein.
The standard laparoscopic equipment used to perform laparoscopic hepatectomy included a 30° 5-mm laparoscope, a hook dissector, 5-mm laparoscopic forceps, a 5-mm atraumatic grasper, a 10-mm GIA (Johnson & Johnson Medical, Shanghai, China), 5-mm harmonic (Johnson & Johnson Medical) and 10-mm locking pliers.
The conventional fully laparoscopic multiport approach was adopted. The patient was placed in a supine position, and the surgeon stood on the right side. Under general anesthesia, five 5- to 10-mm incisions were made in a “U” configuration. Division of the liver parenchyma was performed with Harmonic or Endo-GIA. Large pedicles were stapled or clipped.
Upon surgical exploration, the left lobe of the liver was found to be atrophied, and the right liver had developed compensatory hyperplasia with a red-brown and smooth surface. However, the left liver lobe was severely adherent. We gradually dissected the adhesion using harmonic pliers and exposed the atrophic left lobe (5 cm × 6 cm × 2 cm). The gallbladder was approximately 7 cm × 4 cm × 2 cm in size and was filled with bile and gallstones. Through intraoperative exploration, we confirmed the diagnosis of Caroli disease, limited to the left lobe of the liver. We obtained a biopsy from the edge of the lesion and performed a rapid intraoperative pathological examination to exclude malignant tumor. We then decided to perform a laparoscopic left liver and gallbladder resection. The difficulty was that the lesion was close to the middle hepatic vein. We opened the cysts and resected most of the lesion while retaining part of cystic wall close to the middle hepatic vein. After laparoscopic left half-liver and gallbladder resection, the liver lesion tissue and gallbladder were removed completely from the abdominal cavity. Histopathologic findings showed congenital dilatation of the intrahepatic bile ducts, confirming the preoperative diagnosis of Caroli disease (). Histopathology of the resected specimen revealed large, cystic dilations of the large intrahepatic bile ducts. This patient was seen regularly every 3 months at the outpatient department. There was no recurrence of abdominal pain, and no complications were discovered after 18 months of follow-up.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [66.0, 'kg'], 'height': [158.0, 'cm']}",26.43807,25.11617,27.75997,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 158.0 cm, which is 158.0 cm * 1 m / 100 cm = 1.58 m. The patient's weight is 66.0 kg. The patient's bmi is therefore 66.0 kg / (1.58 m * 1.58 m) = 26.43807 kg/m^2."
2118,6,Body Mass Index (BMI),physical,decimal,pmc-5023828-1,Extracted,"In the past year, a 57-year-old Caucasian female (61 kg, 166 cm) felt gradually empty, exhausted, tired, and lethargic. In addition, she perceived constipation and cold intolerance, which was accompanied by a decline of appetite, concentration, and productivity. She attributed her complaints to the growing level of distress at her work as a teacher and preferred to watch and wait without consulting a physician. Apart from that, her medical, addiction, and familial history were unremarkable. In the last four weeks, she developed a state of apathy and mutism combined with fluctuating confusion, amnesia, disorganization, and incontinence, which led to hospital treatment that was initiated by her husband. Upon emergency admission, a hypoactive delirium and severe hypothyroidism were diagnosed (). Physical and neurologic examination showed signs of hypothyroidism (shortness of breath, bradycardia, hypothermia, swollen limbs, dry skin, delayed relaxation of tendon reflexes, and myalgia) []. Transabdominal echocardiography found pericardial effusion []. Routine lab checks revealed further signs of hypothyroidism, such AST- and CK-elevations and hypercholesterinemia () []. Alcohol intoxication and hyperammonemia were excluded. Moreover, macrocytic anemia was found together with slight hyperhomocysteinemia (12.4 μmol/L, reference level <9 μmol/L), but without laboratory vitamin B deficiency (normal serum levels of vitamins B1, B6, B9, and B12, methylmalonic acid, and holotranscobalamin). Vitamin D was found to be slightly reduced and substituted then. The EEG was slightly slowed (). The brain MR imaging showed a few unspecific T2-hyperintense areas in the white matter (WMH) of both temporal lobes, which could be compatible with severe hypothyroidism, vasculitis, or autoimmune encephalopathy. In the serum, elevated TPO-Abs () were found which pointed to Hashimoto thyroiditis [, , ] being responsible for the hypothyroidism. This was underlined by an atrophic thyroid gland in ultrasound. Regarding the remaining serum antithyroid autoantibodies, TSH-receptor autoantibodies (TR-Abs, ) were also elevated and thyroglobulin autoantibodies were normal. Later on, elevated autoantibodies against parietal cells (PC-Abs, ) and intrinsic factor (11.43 U/mL, normal <1.5 U/mL) were found, which most likely corresponded to a helicobacter pylorus-negative lymphocytic gastroduodenitis in histopathology (up to 80 intraepithelial lymphocytes per 100 epithelial nuclei, T-lymphocytes) and macrocytic anemia. The lymphocyte typing of the blood found increased T-helper-lymphocytes (1350/μL, normal 645–1289/μL), cytotoxic T-lymphocytes within its normal range, and no evidence of a cellular immune deficiency as being measured in the last asymptomatic month (). Helicobacter pylori antibodies were negative. There were no clinical or immunologic signs of Addison's disease, diabetes mellitus, vitiligo, alopecia, or celiac disease. Thus, outside the CNS, the autoimmune disease appeared to be limited to a gastroduodenal-thyroidal syndrome, classified as autoimmune polyendocrine syndrome type 3B []. Other forms of limbic encephalopathies that could have been associated with antibodies against intracellular, synaptic, or other cell surface antigenic targets [], neoplasm, connective tissue, or vasculitis diseases [, ] were excluded.
In the CSF, TPO-Abs (33.8 IU/mL, normal: 0–8 IU/mL) [] were detected, while TR-Abs and thyroglobulin antibodies were not investigated. Moreover, CSF protein (43.7 mg/dL, normal 15–35 mg/dL), S-100 protein (3200 pg/mL, normal <2700 pg/mL), and neuronal specific α-enolase (NSE, 16.9 μg/L, normal <13 μg/L) were elevated. Pleocytosis or oligoclonal bands were missing. Also, neurodegeneration markers (beta-amyloid, tau-, and phospho-tau protein), angiotensin converting enzyme (ACE), lysozyme, titers of immunoglobulins (IgM, IgA, and IgG), IgM-, IgA-, and IgG-indices, antibody index for either herpes simplex virus, varicella zoster virus, cytomegalovirus, measles virus, rubella virus, or Borrelia burgdorferi, and 14-3-3 protein were unremarkable in the CSF.
Ophthalmological, angiological, and nephrological examinations were unremarkable, too. Subsequent electrocardiograms, abdominal ultrasound, chest X-ray, and the remaining serum routine lab including ferritin and transferrin were normal as well as immunoglobulins including subclasses, carbohydrate deficient transferrin, parathyroid hormone, lysozyme, ACE, carbohydrate deficient transferrin, gastrin, and serum autoantibodies against thyroglobulin and the amino terminal of α-enolase (NAE). Virus hepatitis, HIV, herpes, syphilis, Lyme disease, and M. Whipple were excluded. Drug urine screen was negative.
Regarding the increasing somnolence and falling heart rate (down to 40 bpm) and body temperature (down to 33.8°C) the critical care management included an accelerated thyroid hormone replacement therapy (THRT) with L-thyroxine (IV, 250 μg/day in the first 5 days) and IV glucocorticoids (125 mg/day IV methylprednisolone) to prevent the progression of the hypoactive delirium to myxedema coma []. In the next few days, the critical condition improved. Hypothermia and bradycardia resolved within 36 hours and thyroid-stimulating hormone (TSH) started to fall. Simultaneously, the delirium turned into a mixed state (), requiring low doses of haloperidol (up to 10 mg/day) and clonazepam (up to 1 mg/day) to cope with arising visual or auditory hallucinations and agitation.
When the results of elevated serum TPO-Abs came in, the IV glucocorticoid treatment was enhanced to 250 mg/day IV methylprednisolone assuming that the delirium was based on HE [, ]. Thereafter, the mixed delirium (fluctuating vigilance, disorientation, disorganization, starring, memory impairment, irritability, hallucinations, and delusion of reference) turned to a hyperactive state with striking manic features (euphoria, grandiosity, racing thoughts, sleeplessness, and risky and reckless behavior). Meanwhile, the patient's physical condition had been stabilized and she was voluntarily transferred from the critical care unit to the psychiatric ward. Assuming that the glucocorticoids had evoked the mania, the prednisolone dose was reduced to 25 mg/day which was followed by a worsening of both delirium and mania (). A subsequent pulse therapy of 1000 mg/day IV methylprednisolone over 3 days was associated with a prompt resolution of the delirium and improvement of the mania (). As the mania did not completely resolve along with oral prednisolone (100 mg/day), the treatment was augmented with quetiapine (up to 300 mg/day). The patient became euthymic within the next 3 weeks and could be transferred to an outpatient treatment (). Quetiapine and prednisolone were tapered within the subsequent 4 and 24 weeks, respectively, without changing the normal mental and physical health condition under THRT alone, which is still continuing up until now, 3 years later (). No further medications were required. Vitamin D supplementation was stopped after 6 months and the 25-OH-vitamin D-levels were normal in the controls carried out every six months.
Serum antithyroid autoantibody titers respond to the glucocorticoid treatment without a timely correlation with the patient's mental status (). TR-Abs sustainably normalized while TPO-Abs gradually increased after glucocorticoid taper, however, without a worsening of her normal mental status (). Simultaneously, the THRT could be reduced (). Macrocytic anemia resolved although the PC-Ab titers increased progressively () and antibodies against the intrinsic factor were found. Vitamin B levels, holotranscobalamin, and homocysteine were controlled every six months and remained normal. Brain MR imaging and EEG normalized under the combined glucocorticoid and thyroid hormone treatment, which corresponded to the resolution of delirious mania (). Furthermore, brain MR imaging and EEG were normal in the controls carried out 12 and 30 months after termination of the glucocorticoid treatment.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.0, 'kg'], 'height': [166.0, 'cm']}",22.13674,21.0299,23.24358,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 61.0 kg. The patient's bmi is therefore 61.0 kg / (1.66 m * 1.66 m) = 22.13674 kg/m^2."
2119,6,Body Mass Index (BMI),physical,decimal,pmc-4548756-1,Extracted,"A 40-year-old woman with undifferentiated connective tissue disease had been taking hydroxychloroquine for 7.7 years. She was originally on 400 mg/day but more recently was taking 300 mg/day. Her height was 162.6 cm, her ideal body weight was 63.5 kg, her actual body weight was 65.8 kg, and her cumulative dose was 1,124 g. Her adjusted daily dose was 6.29 mg/kg/d based on her ideal body weight, which is in a range recognized as nontoxic. She had no renal or liver disease and no preexisting maculopathy. shows four consecutive 10–2 VFs performed with a red target. The first VF (January 25, 2007) had a single scotoma point on the defect depth display (circled in red) that resolved on the second field (February 12, 2008), which in turn had four new scotoma points (circled in green). Three of the four green-circled scotoma points occurred in the low-risk zone outside the 2°–8° annulus encircling the fixation point. In the third field (February 17, 2009), all four scotoma points circled in green had resolved, and remained so in the fourth field (March 22, 2010). As the patient had a low pretest probability of retinopathy (nontoxic daily dosing, no renal disease, and no liver disease), no intensified testing was done. shows that in 2014, she had normal mfERG ancillary testing, corroborating the lack of evidence of retinopathy seen in all of the VFs.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [65.8, 'kg'], 'height': [162.6, 'cm']}",24.8877,23.64331,26.13209,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.6 cm, which is 162.6 cm * 1 m / 100 cm = 1.626 m. The patient's weight is 65.8 kg. The patient's bmi is therefore 65.8 kg / (1.626 m * 1.626 m) = 24.8877 kg/m^2."
2120,6,Body Mass Index (BMI),physical,decimal,pmc-2642859-1,Extracted,"The patient was a 26-year-old female with a 10-year history of vomiting. She had been hospitalized and had required intravenous hydration more than 30 times for that condition. Vomiting usually started with mild left abdominal pain, and did not subside even when the stomach contents had been emptied resulting in ""dry heaves"". Episodes usually persisted for several days. Throughout the vomiting episodes, her consciousness was clear. Antiemetic, antianxiety, and anticonvulsant drugs were not effective. When she was 25 years old, she first came to our psychosomatic medicine department where she received medical and behavioral treatments for what was diagnosed as cyclic vomiting syndrome (CVS) []; however, her symptoms were poorly controlled. When the patient was 26 years old, she was hospitalized and underwent a thorough medical examination.
The patient's height was 165 cm and body weight was 55 kg. Her past and family medical history was noncontributory. The results of physical and neurological examinations, esophageal-gastrointestinal endoscopy, and routine biochemical examinations were all normal. She had not experienced external injuries, convulsion, loss of awareness, or migraine headaches. Electroencephalograms (EEGs) were recorded from 19 electrodes (International 10/20 System) with A1+A2 as the recording reference. The patient kept both eyes closed during the recording. The recording was done approximately 500 times. On EEGs performed at high amplitude, 5~6 Hz waves and slow waves (Figure ) were evident but there were no sudden abnormal waves. In the background, 9–10 Hz alpha waves were recorded around the occipital lobes. Results of brain emission computed tomography (CT) and single photon emission CT (SPECT) of the brain were normal and no atrophy or tumors were evident.
During one hospital stay, the patient complained that she could not speak smoothly, had cramping of the tongue, and clenched her teeth against her will. These symptoms subsided naturally within a few hours. After this episode, we learned that she had experienced such cramping twice previously. We considered this to be a symptom of automatism. Although consciousness was not impaired and haloperidol was not effective in stopping the vomiting, epilepsy was cited as a possible diagnosis. After recording EEGs several times, a high amplitude slow wave was obtained while the patient was awake, which correlated with the vomiting (Figure ). When she was drowsy, spike and wave complexes appeared in the left temporal lobe (Figure ) and repeated irregular slow wave bursts (Figure ) were recorded. Through the administration of from 1 to 2 mg clonazepam, background wave activity improved substantially (Figure ) and vomiting episodes decreased, although the spike and wave complex was noted with drowsiness.
On first consulting with this patient, we suspected that her illness had a complex etiology and that both psychological and medical approaches to treatment would be required. We reasoned that a psychological problem might be a trigger for her episodes of epilepsy. The patient's family and previous doctors had told her that her illness was caused by mental weakness. She had not attended college nor had she ever been employed, and as a result she had no hope for her future. She was in despair over her health, gave up being understood by others, and would not confide in others. She unconsciously needed the symptoms to escape from reality. We used both physical and psychological approaches in her treatment, involving relaxation techniques, breathing exercises, drawing pictures and counseling. She slowly started to discuss the family situation that had begun in childhood and had continued to the present. She said that her mother often disagreed with what she wanted to do and she began to think that it was no use thinking for herself. Her life at that time was filled with a sense of ""abandonment"". After she made a friend in the hospital and opened her heart to others, she began to speak tearfully in the therapeutic sessions. She said that she was aware that her symptoms had not been due to a physical problem but rather a mental one, and she expressed the feeling that she would be better off living away from her family. As a child she had been well behaved, and her mother paid little attention to her because she was busy caring for her elder sister, who easily got colds and became tired. When her elder sister entered college and was seldom at home, the mother began nagging the patient to do certain things and was overprotective of her. After several therapeutic sessions, her attitude was more positive. To support her ""to do things on her own"", we intervened with the family, who were of the opinion that ""the patient with the illness was wrong"". We tried to encourage the patient to become independent and to separate from the family, and we asked the father and sister to assist in that effort. We complimented the patient's mother for her efforts in caring for her daughter. When she left the hospital, she no longer felt ""abandonment"" but instead was committed to ""live her own life by herself"".
After she left the hospital, she had some ictal vomiting when excessively stressed. We listened to her with empathy and acceptance, supported her both mentally and physically, and assisted her in establishing independence. Her symptoms markedly improved when she obtained job training as a home-helper and subsequently found employment. When she began to live alone and support herself, all of her symptoms disappeared (Figure ). Within several months she was able to decrease and finally discontinue medication and no longer required medical care. An EEG while the patient was awake and unmedicated showed irregular waves in the background and there were no high amplitude slow waves (Figure ). She has been in good health without requiring medication for more than seven years.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.0, 'kg'], 'height': [165.0, 'cm']}",20.20202,19.19192,21.21212,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.65 m * 1.65 m) = 20.20202 kg/m^2."
2121,6,Body Mass Index (BMI),physical,decimal,pmc-3420388-1,Extracted,"A 6-year-old boy presented to our emergency room because of vomiting and abdominal pain. His parents reported that he had a 3-day history of low-grade fever together with abdominal pain, emesis, and constipation. There was no history of altered mental status, coryzal symptoms, or headaches. He was reported to have “autism”, and four weeks earlier he had been placed on a “specific carbohydrate diet” including “egg protein shakes.” Two days later, he developed “hives”, and the egg protein shakes were discontinued. However, pruritus continued and he developed excoriated and dry lips over the next few days. These latter symptoms continued until his presentation to our emergency room.
His past medical history was significant for premature birth at 30 weeks gestation, nocturnal enuresis for the past 8 months with some recent improvement using a bed alarm, and an inguinal hernia repair at the age of 3 years. He had been diagnosed with pervasive behavioral/developmental disorder attributed to autism. In an attempt to manage his behavior, he was started on a casein- and gluten-free “specific carbohydrate diet” (eggs, fruits, vegetables without complex carbohydrates) together with protein shakes. These had been discontinued two weeks prior to admission because of the development of a skin rash and pruritis. He had also been placed on multiple dietary and vitamin supplements as part of the management of his autism. These included 6 drops/day of vitamin A (equivalent to 30,000 IU per day) added to his diet for the past 4 months, Vitamin B12 shots twice per week, a custom-made multivitamin, Vitamin E Drops, Coenzyme Q and Omega-3 fatty acids.
Family history revealed that his father had a history of kidney stones as a young adult, which had not been further evaluated and have not recurred. Maternal grandmother had thyroid surgery for an “overactive thyroid.” There was no family history of hyperparathyroidism, thyroid neoplasms, pheochromocytomas, pituitary tumors, or islet cell tumors.
On examination when he was initially seen in the emergency unit, his weight was 21.6 kg (50th percentile) and height 123.5 cm (80th percentile). He was sleepy and in discomfort complaining of abdominal pain. He was mildly dehydrated. He was noted to have cheilitis and a blanching erythematous rash on his face. He had symmetric hyperreflexia in all four limbs with normal muscle tone. Funduscopic examination was within normal limits. HEENT, abdominal, cardiovascular, and respiratory exam were all within normal limits. There was no evidence of thyromegaly, and thyroid gland was nontender. Sexual maturation was Tanner Stage 1.
On initial presentation, he had a normal basic metabolic profile except that the total calcium was 13.7 mg/dL (normal range: 8.6–10.3). Serum creatinine was 0.6 mg/dL and BUN 26 mg/dL indicative of his mild dehydration. Intravenous hydration was initiated, and he was hospitalized for evaluation and treatment of hypercalcemia. He was initially treated with intravenous hydration using 0.9% saline at 3 L/m2/day. He also received a single dose of intravenous furosemide 1 mg/kg. His calcium stabilized with hydration and furosemide therapy within 48 hours and remained stable (though still near or slightly above the upper limits of normal) off IV fluids for 24 hours (see ).
Supplemental vitamin A was discontinued on admission. During his initial hospitalization, serum phosphorus was 4.0 mg/dL (normal: 3.0–6.0 mg/dL), intact PTH <3 pg/mL (normal: 14–72), 25-hydroxy-vitamin D 22.3 ng/mL (normal: 10–55), and 1,25 dihydroxy-vitamin D 16 pg/mL (normal: 22–67). TSH 2.29 mcIU/mL (normal: 0.35–5.5), Free T4 0.95 ng/dL (normal: 0.9–1.8 ng/dL), alkaline phosphatase 209 IU/L (normal: 140–420), AST 76 IU/L (normal: 10–60), and ALT 34 IU/L (normal: 10–35). EKG showed normal sinus rhythm. A urinary calcium/creatinine fractional excretion ratio was 0.03, and calcium/creatinine ratio was 0.9 at the time when serum calcium was 13.1 mg/dl. Both parents had normal serum calcium and phosphorous levels. Serum vitamin A level was 1738 mcg/L (normal: 360–1200 mcg/L).
He was discharged home on the fifth hospital day with instructions for oral fluid intake of at least 1.5 L/m2/day. His total serum calcium on the day of discharge was 10.9 mg/dL. Serum calcium was to be checked by his primary physician daily and was stable for two days. Three days after discharge, he presented again to the emergency unit with recurrence of abdominal pain, vomiting, and generally not feeling well. He had not been able to keep up with the recommended oral hydration plan of at least 1.5 L/m2/day. At this point in time, mother also gave a history of hair loss since discharge. He had lost 2 kg in weight. He had marked blanching erythema on the cheeks and rest of the body together with cheilosis. Total calcium at this time was 12.6 mg/dL. He had not received any vitamin A since the initial admission seven days earlier. He was hospitalized once again and started on 3.0 L/m2/day normal saline hydration, 2 mg/kg/day of prednisone, and furosemide 1 mg/kg BID. Despite these measures, his calcium rose to 14.7 mg/dL during the next 24 hours () at which point he was given a single dose of pamidronate 0.5 mg/kg IV.
Calcium came down to 9.8 mg/dL over the next two days and to 8.4 mg/dL five days after pamidronate. He was changed to oral hydration, and serum calcium remained normal over the next few days. He was discharged home after six days to continue oral hydration and close followup. During this second admission, he had a skeletal survey that was remarkable only for a bilateral coxa valga deformity and mild generalized osteopenia. His serum vitamin A level was 2668 mcg/L. Tuberculin test was negative, and a chest X-ray and renal ultrasound were normal. Parathyroid hormone-related peptide (PTHrP) was 0.3 pmol/L (normal: <2 pmol/L). He also had a normal bone scan. After discharged home, he remained stable without additional hypercalcemia. His serum Vitamin A level 30 days after discontinuation of vitamin A was at 1201 mcg/L and serum calcium of 8.9 mg/dL.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [21.6, 'kg'], 'height': [123.5, 'cm']}",14.16184,13.45375,14.86993,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 123.5 cm, which is 123.5 cm * 1 m / 100 cm = 1.235 m. The patient's weight is 21.6 kg. The patient's bmi is therefore 21.6 kg / (1.235 m * 1.235 m) = 14.16184 kg/m^2."
2122,6,Body Mass Index (BMI),physical,decimal,pmc-8679167-1,Extracted,"A 7-year-old female was referred to the Paediatric Liver Clinic for
hepatosplenomegaly found incidentally on assessment following a minor motor vehicle
accident. The patient was asymptomatic aside from endorsing a history of easy
bruising, pain to her upper and lower limbs, and occasional epistaxis.
Developmentally, she was age appropriate with no neurological symptoms, fevers,
weight loss, night sweats, or manifestations of chronic liver disease. Her past
medical history was significant only for asthma and recurrent tonsillitis. The
patient’s parents were nonconsanguineous. Her mother was of Scottish, Irish, and
possibly Turkish descent, and her father was Ethiopian. Family history was
significant for amyotrophic lateral sclerosis in the biological father.
On physical examination, the patient’s vital signs were stable. Her weight was 23.7
kg (50th percentile) and height was 118.3 cm (15th percentile). She did not have any
dysmorphic features. Her abdomen was soft and nontender with a liver palpable 4 cm
below the right costal margin. Her splenic edge was palpable at the umbilicus. There
was no evidence of anemia, jaundice, finger clubbing, or lymphadenopathy.
Neurological examination was unremarkable.
An ultrasound of her abdomen demonstrated an elongated spleen of 16 cm and liver of
14 cm. Parenchymal echogenicity of the liver and spleen were satisfactory. Color
Doppler studies did not detect any hemodynamic lesions. As seen in , the differential
diagnosis for hepatosplenomegaly is broad.
As such, initial laboratory investigations were performed in the Paediatric Liver
Clinic (). An
infectious screen revealed a negative heterophile antibody test and nonreactive
hepatitis A, B, and C serology. An immunological liver workup revealed normal
immunoglobulins, C3 and C4, antinuclear antibody, anti-double stranded DNA,
anti-MPO, anti-PR3, α-1-antitrypsin, and ceruloplasmin. Hematological investigations
including hemoglobin electrophoresis, Coomb’s test, and G6PD deficiency screen were
also negative. An α-fetoprotein level was also unremarkable. Metabolic storage
disease was suspected, and testing revealed low leukocyte β-glucocerebrosidase
activity and high plasma chitotriosidase activity (). In the context of
hepatosplenomegaly, bony pain, easy bruising, and occasional epistaxis, we made a
diagnosis of GD Type 1.
The patient was referred to the Paediatric Metabolic Genetics team for further
assessment. DNA sequencing of GBA identified 2 pathogenic variants,
c.1226A>G and c.116_1505 deletion, confirming a diagnosis of GD Type 1. The
c.1226A>G p.(N 409S; also known as N370S) is a common pathogenic variant. The
c.116_1505 deletion is a novel deletion that spans exons 3 to 11 of
GBA. A whole-body magnetic resonance imaging was performed to
assess for bony abnormalities and identified mild femoral Erlenmeyer flask
deformities bilaterally.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [23.7, 'kg'], 'height': [118.3, 'cm']}",16.93475,16.08801,17.78149,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 118.3 cm, which is 118.3 cm * 1 m / 100 cm = 1.183 m. The patient's weight is 23.7 kg. The patient's bmi is therefore 23.7 kg / (1.183 m * 1.183 m) = 16.93475 kg/m^2."
2123,6,Body Mass Index (BMI),physical,decimal,pmc-4897161-1,Extracted,"A 33-month-old girl presented with edema and proteinuria. Following clinical diagnosis of NS, she was treated with prednisolone (60 mg/m2/day) for 4 weeks, but NS has been persistent. When the patient was transferred to our hospital, physical examination revealed generalized edema, but no evidence of thromboembolism. Her vital signs were stable, with a blood pressure of 103/66 mmHg. Her weight was 12 kg (25th–50th percentile) and her height was 91 cm (25th–50th percentile). Laboratory studies revealed a white blood cell count of 8.38×109/L, hemoglobin level of 15.9 g/dL, hematocrit level of 46.1%, and platelet count of 284×109/L. Biochemistry showed the following: total protein, 5 g/dL; albumin 2.5 g/dL; total cholesterol, 235 g/dL; blood urea nitrogen, 11 mg/dL; creatinine, 0.3 mg/dL; calcium, 8.7 mg/dL; phosphorus, 5.7 mg/dL, and normal electrolyte level. Prothrombin time and activated partial thromboplastin time were both within normal range. Urinalysis revealed proteinuria of 4+ and the spot urine protein-to-creatinine ratio was 31.23 g/g Cr. Test results for antinuclear antibody and antineutrophil cytoplasmic antibody were negative, and the IgG, IgA, and IgM levels were 391.0 mg/dL, 82.0 mg/dL, and 142.0 mg/dL, respectively. Ultrasonography revealed normal-sized kidneys with diffuse increased renal parenchymal echogenicity. Renal biopsy revealed a collapsing variant of focal segmental glomerulosclerosis (FSGS) ().
To manage the patient's steroid-resistant NS, high-dose intravenous methylprednisolone (MP) pulse therapy at a dose of 30 mg/kg was administered every 2 days. Angiotensin-converting enzyme inhibitor and intermittent albumin replacement followed by diuretics were also prescribed. After the first dose of MP, she complained of intermittent left lower leg pain, which was assumed to be a side effect of MP. After the third round of MP, her lower leg pain became continuous, progressed to both legs, and caused her to stop walking. The skin on the dorsum of her feet was pale and cold and capillary refill was slow. The dorsalis pedis pulse, posterior tibialis pulse, and popliteal pulse were palpable but not strong. Emergency Doppler ultrasonography of her lower extremities revealed turbulent flow in both her femoral and popliteal arteries. Magnetic resonance angiography showed multifocal segmental luminal occlusion of the common iliac arteries, external iliac arteries, and popliteal arteries (). The lumen of the common femoral arteries and superficial femoral arteries were relatively patent with distal flow reconstitution. The hemostasis study was as follows: thrombin time, 19.9 seconds (control, 17.0 seconds); fibrinogen, 362 mg/dL (reference, 180–380 mg/dL); D-dimer, 0.48 µg/mL (reference, 0–0.4 µg/mL); plasminogen activator, 86% (reference, 70%–140%); factor VIII, 214% (reference, 52%–190%); antithrombin (AT)-III activity, 91% (reference, 80%–120%); protein C, 243% (reference, 70%–140%); and protein S, 97% (reference, 65%–116%). Test results for anticardiolipin and anti-β2-glycoprotein-I antibodies were all negative. The factor V Leiden (1691G>A) mutation was absent.
TEC was suspected, and MP pulse therapy was discontinued and heparinization started, followed by mechanical thrombectomy of both iliac arteries and popliteal arteries using Forgarty balloon catheters. Thrombus cultures were obtained during mechanical thrombectomy despite the absence of clinical infection. Staphylococcus hominis subspecies hominis (S. hominis subsp. hominis) was isolated, which was found to be ampicillin-resistant and vancomycin-susceptible. Since peripheral blood culture results were negative, systemic antibiotics were not administered. Anticoagulant treatment was continued for 8 months with warfarin. Two months later, a follow-up Doppler ultrasonography of her lower extremities showed patent lumen and intact flow patterns in the common femoral arteries, superficial femoral arteries, and popliteal arteries. The severity of proteinuria, which was consistent with NS, persisted despite various combinations of oral steroids, cyclosporine A, tacrolimus, and rituximab. The patient's renal function deteriorated and progressed to end-stage renal failure, and renal replacement therapy of peritoneal dialysis was started 22 months after TEC onset.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [12.0, 'kg'], 'height': [91.0, 'cm']}",14.491,13.76645,15.21555,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 91.0 cm, which is 91.0 cm * 1 m / 100 cm = 0.91 m. The patient's weight is 12.0 kg. The patient's bmi is therefore 12.0 kg / (0.91 m * 0.91 m) = 14.491 kg/m^2."
2124,6,Body Mass Index (BMI),physical,decimal,pmc-2813625-1,Extracted,"A 10-year-old girl was referred to our institution, King Abdulaziz University Hospital, Riyadh, Saudi Arabia, for the management of stridor. According to the referral history, the patient was known to have bronchial asthma and used medication as needed and presented initially with difficulty in breathing at the age of 9 years. She apparently had no other medical history and was healthy prior to the first presentation. On endoscopy a growth had been seen in the larynx similar to polyposis of the larynx, and she was diagnosed as a case of RRP. That mass was excised. She again developed the same symptoms within 7 months and was operated on for another mass. She was referred for further management because of the recurrence of her symptoms.
At the time of presentation to our institute 2 months after the last surgery she had biphasic stridor, with minimal signs of respiratory distress and so was admitted for a work-up. A general examination showed that her weight was 23 kg and stature was 120cm, both below the fifth percentile, and systemic examination was unremarkable. A near-nose-throat examination was unremarkable except that on fiberoptic endoscopy, the larynx showed a papillomatous growth involving both the true vocal cords and interarytenoid area. She had a narrow airway. Her vocal cords were mobile. Her blood work showed WBC count of 12.9×109/L, with an eosinophil count of 60%. The erythrocyte sedimentation rate was 54 mm/hr. Due to her recurrent attacks of bronchial asthma associated with chest infections, poor weight gain and non-resolving chest symptoms and a possible history of exposure to tuberculosis in the family, a purified protein derivative test was done and the result was negative. Serology for human papilloma virus 6 and 11 was negative. c-ANCA tested positive with a titer of 28 c-ANCA tested positive with a titer of 32 AU (more than 15 AU is considered positive, normal up to 20 AU), levels were measured using a commercially available direct PR3-ANCA ELISA kit (Euro-diagnostica, Malmo, Sweden).
Direct laryngoscopy confirmed involvement of the glottic region with a papillomatous lesion bilaterally with extension into the subglottic region mainly on the left side (). Excision of the lesion was done using CO2 laser and the growth was sent for histopathology, which showed multiple vessels with evidence of vasculitis and fibrin deposits in the walls (). A number of eosinophils, plasma cells and macrophages were seen in the perivascular area. The diagnosis of CSS was made based on both histopathological and serological findings along with suggestive clinical presentation.
Within the next two months the patient had recurrence of symptoms and was again admitted with stridor. Along with stridor, she had developed a mass in the right vestibule of the nose. Flexible fiberoptic examination showed papillomatous growth involving the true vocal cord on the left side, the anterior commissure, the interarytenoid region, the subglottic region and the dorsum of the posterior third of tongue. Her vocal cords were mobile. Another surgical intervention was made to clear the airway. Excisional biopsies of the nasal mass and tongue base mass were done during the same intervention. A CT scan of the chest done postoperatively showed chronic inflammatory airway disease with a small rounded lesion in the upper lobe of the right lung. A repeat lung biopsy, which was a firm piece of tissue measuring 1×0.7×0.2 cm whose sections revealed lung tissue with parenchymal fibrosis, lymphocytic, plasma cells and eosinophilic infiltration along with fibrinoid thickening of medium-sized blood vessels and pulmonary tissue with multiple vessels showing evidence of vasculitis () The vessel wall showed fibrin deposits. Perivascular area showed a number of eosinophils with plasma cells and macrophages. The lung biopsy was consistent with the same pathology (CSS), as were tongue and nasal biopsies. The specimens also underwent Gomori methenamine silver and Steiner stains and was negative. Immunostains were not suggestive and culture showed no growth of micro-organisms.
At the time of the latest presentation the child was started on prednisone at a dose of 1 mg/kg/day for 6 months and this dose was tapered down over 4 month. The child was under regular follow up both by the pediatrician and our team with no further airway compromise. Her last follow-up visit was 4 years after the last intervention, when flexible fiberoptic examination of her larynx showed a clear airway. She had, however, before the last follow-up been to the emergency department from time to time for acute exacerbation of bronchial asthma. During the course of follow-up there was no sign suggesting neurological or cardiac involvement.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [23.0, 'kg'], 'height': [120.0, 'cm']}",15.97222,15.17361,16.77083,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 120.0 cm, which is 120.0 cm * 1 m / 100 cm = 1.2 m. The patient's weight is 23.0 kg. The patient's bmi is therefore 23.0 kg / (1.2 m * 1.2 m) = 15.97222 kg/m^2."
2125,6,Body Mass Index (BMI),physical,decimal,pmc-2783133-1,Extracted,"One month after an acute ST-elevation myocardial infarction (CK 7230 U/L [<174], CK-MB 557 U/L [<6.7]) with stent placement in the left anterior descending coronary artery, an 84-year-old Caucasian man (180 cm, 75 kg) was admitted to the emergency department with atypical chest pain. Laboratory testing revealed a mild elevation of CK (CK 188 U/L [<174]) and CK-MB (CK-MB 6.9 U/L [<6.7]), while Troponin (T < 0.03 μgL [<0.03]) was negative. His current medication included clopidogrel (75 mg), acetylicsaliciylic acid (100 mg) and (metoprolol 100 mg). The patient's clinical history comprised appendectomy at the age of 16 and a myocardial infarction one month before admission. His cardiovascular risk factors were a history of smoking (45 pack/years) as well as arterial hypertension. The physical examination was unremarkable. There were no new ECG changes comparing to the previous hospital stays. As these findings were considered neither unequivocally indicative for a new occlusive CAD, nor in-stent restenosis, cardiac CT was performed. ECG-gated MSCT coronary angiography (64 × 0.6 mm, 120 kV, 750 mAseff., 80 ml Iopromide 370 injected at 4 ml/s) revealed an in-stent restenosis (Figure ). An early perfusion deficit was detected during the arterial phase imaging. Late phase images were obtained 10 minutes after contrast injection showing a transmural late-enhancement in the apical-anterior, the apical-septal segments of the left ventricle as well as the right ventricular apex. Moreover, cardiac MSCT depicted left and right ventricular thrombi (Figure ). Extensive aortic valve calcifications raised the suspicion for aortic valve stenosis (Figure ).
Based on the CT examination the patient underwent coronary angiography confirming an in-stent restenosis, which was treated with balloon angioplasty. Aortic valve stenosis was echocardiographically confirmed with a mean transvalvular gradient of 24 mm/Hg and MR imaging confirmed the extent of the myocardial late-enhancement and ventricular thrombus. For treating ventricular thrombi the patient was put on warfarin. Enzyme levels returned to normal within 48 hours after angioplasty. Three days later he was discharged in good condition. On follow-up echocardiography 6 months after discharge from hospital the thrombus had completely resolved.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [75.0, 'kg'], 'height': [180.0, 'cm']}",23.14815,21.99074,24.30556,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 180.0 cm, which is 180.0 cm * 1 m / 100 cm = 1.8 m. The patient's weight is 75.0 kg. The patient's bmi is therefore 75.0 kg / (1.8 m * 1.8 m) = 23.14815 kg/m^2."
2126,6,Body Mass Index (BMI),physical,decimal,pmc-5855273-1,Extracted,"A 12-year-old female child patient reported to the Department of Periodontology and Implantology with the chief complaint of gum swelling in the upper right quadrant of oral cavity. The patient also complained of gum bleeding on provocation and difficulty in mastication owing to multiple oral ulcers in the vestibular region. The swelling had been present for approximately 6 months and was gradually increasing in size to attain the present dimension [].
On enquiry, medical history reports revealed the patient to be a case of KS. Treatment procedures carried out to treat it included vaginoplasty, urethroplasty, esophageal dilatation, and transfusion for immune thrombocytopenic purpura. Family history revealed a consanguineous descent.
General physical examination revealed the patient to be small stature and underweight for her age. Therefore, height and weight were recorded which showed 100 cm and 25 kg, respectively. The patient presented with multiple hyper- and hypo-pigmented macules distributed all over the body including face with prominent poikilodermatous changes, xerosis, atrophy of the skin, sparse, and thin hair []. Sclera appeared icteric []. The dorsum of the hands and feet revealed cigarette paper-like wrinkling []. The patient appeared mentally sound.
Dental history revealed excision of a similar type of overgrowth in mandibular posterior region 2 years back. Details were not presented.
Extraoral examination revealed facial asymmetry with diffuse swelling extending superoinferiorly from zygomatic arch to lower border of mandible and anteroposteriorly from right commissure of the lip to tragus of the right ear. Bilateral angular cheilitis was discernible.
Intraoral hard tissue examination revealed the presence of all permanent teeth except third molars in maxillary arch; mandibular arch revealed retained deciduous first and second molars bilaterally. Slight mobility was noted on all teeth in maxillary right quadrant. Proclination of anterior teeth were noted. Oral hygiene status appeared poor. A 2 × 2” ovoid pedunculated, lobulated, tender reddish pink gingival overgrowth was noted in the buccal and palatal aspect of maxillary right quadrant. The surface appeared smooth with ulceration. Its extension beyond the occlusal plane gave an appearance of open mouth. The gingiva appeared erythematous with an increased tendency to bleed. The differential diagnosis included was pyogenic granuloma, peripheral giant cell granuloma, and ulcerative fibroma.
Radiographic surveillance with orthopantomogram and intraoral periapical of maxillary posterior area revealed normal anatomic structures and presence of mixed dentition. Maxillary arch revealed developing tooth buds of 18 and 28. Mandibular arch showed erupting tooth bud of 34, 35, 44, and 45. An erupting 34 was appreciated at the level of the alveolar ridge. Periapical aspect of 75 revealed presence of tooth bud of 35 and the mesial root resorption of 85 [ and ].
Hematological screening reports revealed no abnormality. A medical consent was obtained from physician to perform minor surgical procedure under local anesthesia. Two weeks after phase I therapy, the overgrowth was excised by electrosurgical unit after scaling. Antibiotics, analgesics, and nutritional supplements were prescribed for 5 days. Oral hygiene instructions included the use of a soft toothbrush, nonfoaming toothpaste, chlorhexidine mouthwash, and 20% benzocaine ointment for application on mucosal ulcers []. She was advised to consume bland food with lots of fluid intake and refrain from eating hot and spicy food, acidic beverage which could lead to soreness.
Histopathological examination of the excised specimen at ×50, ×200, and ×400 revealed epidermis layer with ulcerated stratified squamous epithelium and mild hyperkeratosis in stratum corneum. Epithelial zone showed polymorphonuclear leukocytes and lymphocytes with focal areas showing mild reactive atypia and dysplasia in the lower one third involving stratum basale and spinosum. Aggregates of plasma cells and proliferation of the vascular channels in the superficial region of dermis layer were seen. Collagenized stroma with deeper areas showed predominantly plasma cells aggregates around the dilated blood vessels; thus, overall features suggested a diagnosis of “granulomatous lesion with plasma cell infiltrate” [–].
On follow-up visit, after 10 days, uneventful healing was appreciated. The patient was relieved as she could occlude and masticate properly. The patient was followed up for 1, 2, and 3 months []. Although periodontal therapy proved to be beneficial to have food and proper nutrition, owing to restored masticatory activity, persistent, and recurrent oral ulcers were seen in buccal mucosa which compromised her oral hygiene activity. The patient underwent oral prophylaxis once again with reinforcement for proper oral hygiene maintenance. She is put on recall therapy with shorter periodic intervals of 4 weeks.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [25.0, 'kg'], 'height': [100.0, 'cm']}",25,23.75,26.25,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 100.0 cm, which is 100.0 cm * 1 m / 100 cm = 1.0 m. The patient's weight is 25.0 kg. The patient's bmi is therefore 25.0 kg / (1.0 m * 1.0 m) = 25.0 kg/m^2."
2127,6,Body Mass Index (BMI),physical,decimal,pmc-7044392-1,Extracted,"The patient was a 3-year-old girl with a height of 107 cm and a weight of 14 kg. She developed ventricular fibrillation while she was running and received cardiopulmonary resuscitation (CPR). She received three times of electrical defibrillation during CPR, but did not receive epinephrine. Return of spontaneous circulation was achieved with 10 min of CPR. Afterward, premature ventricular contraction occurred frequently, and an oral β-blocker (Nadolol) was started. Long QT syndrome and Brugada syndrome were negated in the resting electrocardiogram. Additionally, there was no structural heart disease on the echocardiogram. Hence, insertion of an ICD using epicardial pacing under sternotomy was scheduled due to suspicion of CPVT. Her preoperative neurological condition was intact but nervous, and so premedication of rectal midazolam (0.5 mg/kg) was given. An intravenous catheter was placed preoperatively before the patient entered the operating room. Electrocardiography, percutaneous oxygen saturation, and noninvasive arterial blood pressure were used for monitoring, and electrode pads of a defibrillator were attached to the patient in the operating room. After preoxygenation with 6 L/min oxygen for 3 min, general anesthesia of 3 mg of midazolam, 50 μg of fentanyl, 14 mg of rocuronium intravenously was induced rapidly. She was intubated with a cuffed endotracheal tube (4.0 mm internal diameter). Anesthesia was maintained with a gas mixture of oxygen, air (fraction of inspired oxygen (FIO2), 0.3–0.6), and midazolam (0.2 mg/kg/h); additionally, remifentanil (0.15–0.5 μg/kg/min), rocuronium (7 μg/kg/min), and fentanyl (intermittent injection of total 250 μg) were administered. The operation was performed without any complications. The operation time was 3 h. The amount of bleeding was 72 ml. She remained intubated and was transferred to the intensive care unit (ICU). Dexmedetomidine (0.6 μg/kg/h) and fentanyl (approximately 1 μg/kg/h) were administered in the ICU. Tracheal extubation was performed in the morning of postoperative day (POD) 1. Postoperative pain was controlled by suppositories of acetaminophen. Fatal arrhythmia due to CPVT did not occur in the perioperative period. She was discharged from the hospital on POD 21 with oral Nadolol. No fatal arrhythmia has occurred since discharge.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [14.0, 'kg'], 'height': [107.0, 'cm']}",12.22814,11.61673,12.83955,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 107.0 cm, which is 107.0 cm * 1 m / 100 cm = 1.07 m. The patient's weight is 14.0 kg. The patient's bmi is therefore 14.0 kg / (1.07 m * 1.07 m) = 12.22814 kg/m^2."
2128,6,Body Mass Index (BMI),physical,decimal,pmc-3570312-1,Extracted,"A 58-year-old man was found to have intrahepatic and extrahepatic bile duct dilatation on B ultrasound on 12 June 2009, and was hospitalized for further examination and treatment on 20 June 2009. Our patient was 171 cm tall and weighed 86 kg. There was no anemia or jaundice in the palpebral or bulbar conjunctivas. The superficial lymph nodes were not palpable. The abdomen was flat without any palpable mass. He had had diabetes and hypertension that had been under regular medical control for the past 20 years. Abdominal ultrasonography was carried out and a 4.3 × 5.2 cm protruding tumor was found in the lower pole of the right kidney. The laboratory test results showed total bilirubin was 20.6 μmol/l and direct bilirubin was 10.3 μmol/l, the results of a magnetic resonance imaging (MRI) scan showed (1) a lesion in the lower pole of the right kidney, (2) cysts in the left renal area and (3) abnormal signals in the ampulla of Vater. Intrahepatic bile duct dilatation could be seen on the MRI scan, but the head of the pancreas and distal bile duct showed no tumor signals leading to a diagnosis of periampullary carcinoma and right renal carcinoma. Considering the trauma of pancreaticoduodenectomy combined with renal resection operation is greater, and laparoscopic resection of renal tumors is feasible with fast recovery, after weighing the risks of endoscopic retrograde cholangiopancreatography (ERCP) we carried out the laparoscopic right renal radical resection first without carrying out ERCP. After general anesthesia, our patient was operated on via a 2 cm skin incision under the costal margin on the right posterior axillary line; a retroperitoneal CO2 artificial pneumoperitoneum was established, the anatomical landmarks were observed under endoscope, the right renal artery was dissected, clipped with a blood vessel clip and cut. Then, the renal vein was dissected and cut, the adrenal gland was retained and the ureter was cut; the right kidney was then resected. Pathological examination results were as shown in Figure
a. The clinical stage and TNM staging of the renal tumor was T1N0M0 and Robson stage I. Our patient recovered well and was discharged on the ninth postoperative day. Then, our patient presented with abdominal pain, fever, and body weight loss of about 10 kg the following month. He was hospitalized for further examination and treatment on 31 July 2009.
ERCP showed that an infiltrative ulcerative mass was visible in the duodenal descending part and papilla involving the lumen half cycle; the mucosa was ulcerative and the intestinal wall was stiff. No nipple and wrinkled wall structure could be seen. We tried to carry out nipple angiography but were not successful. Papillary carcinoma of the duodenum was diagnosed (Figure
b). Our patient presented fever and other symptoms of cholangitis at this time. Percutaneous transhepatic cholangiography drainage was carried out under the guidance of computed tomography (CT) (Figure
a,b). Endoscopic views of the duodenum are shown in Figure
. Postoperative anti-infection treatment (perazone sodium and sulbactam sodium) was applied. Our patient recovered well, then 30 days later the pylorus-preserving pancreaticoduodenectomy was carried out; the type was determined to be pancreatic duct jejunum anastomosis. However, postoperative intra-abdominal infections occurred on the sixth day and bleeding occurred in the peripheral arteriolar branch around the anastomosis on the eighth day; our patient improved after vascular interventional microcoil embolization for the treatment of hemostasis. The second operation was performed 14 days latter. A large number of dark red blood clots were seen on abdominal cavity exploration, mainly concentrated in the liver, gastric and pancreatic body and tail. Celiac necrotic tissues and blood clots were eliminated. At the same time, the gastrointestinal anastomosis had an approximately 1 cm split and bile was leaking from the biliary intestinal anastomosis, so jejunal fistulization was performed and peritoneal lavage and drainage was carried out repeatedly. The clinical stage and TNM staging of the pancreatic tumor was stage 1B and T2N0M0. Our patient improved gradually without undergoing chemotherapy and was discharged on the 58th postoperative day. There has been no tumor recurrence after a follow-up of 26 months.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [86.0, 'kg'], 'height': [171.0, 'cm']}",29.41076,27.94022,30.8813,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 171.0 cm, which is 171.0 cm * 1 m / 100 cm = 1.71 m. The patient's weight is 86.0 kg. The patient's bmi is therefore 86.0 kg / (1.71 m * 1.71 m) = 29.41076 kg/m^2."
2129,6,Body Mass Index (BMI),physical,decimal,pmc-8705005-1,Extracted,"A 91-year-old woman with a history of transcatheter aortic valve replacement two years ago was admitted to our institute complaining of bilateral leg edema and dyspnea on exertion (New York Heart Association functional class III). She had received bisoprolol 0.625 mg/day, olmesartan 10 mg/day, tolvaptan 3.75 mg/day, and azosemide 60 mg/day as well as rivaroxaban 10 mg/day. She did not have any history of malignancy.
Body height was 143 cm and body weight was 54 kg. Blood pressure was 113/47 mmHg and pulse rate was 71 bpm. Chest X-ray showed mild cardiomegaly, dilatation of pulmonary artery, and mild pleural effusion (A). An electrocardiogram showed heart rate 99 bpm, atrial fibrillation, and complete left bundle branch block (B). Hemoglobin was 8.5 g/dL, erythropoietin was 41.1 mIU/mL, ferritin was 303 ng/mL, transferrin saturation was 30.3%, and reticulocyte was 0.3%. Fecal occult blood test was negative. Serum lactate dehydrogenase level was 143 IU/L. Estimated glomerular filtration ratio was 18 mL/min/1.73 m2 and Plasma B-type natriuretic peptide was 414 pg/mL.
Following the admission, intravenous furosemide and potassium canrenoate were administered. The dose of tolvaptan was increased to 7.5 mg/day and that of azosemide was decreased to 30 mg/day to prevent hypovolemia and preserve renal function. Daprodustat 2 mg/day was initiated to treat renal anemia before the index discharge.
At index discharge, body weight was 48 kg, hemoglobin was 8.8 g/dL, estimated glomerular filtration ratio was 15.6 mL/min/1.73 m2, and plasma B-type natriuretic peptide was 276 pg/mL. Transthoracic echocardiography showed left ventricular end-diastolic diameter of 42 mm, left ventricular ejection fraction of 72%, E/e’ ratio of 14.0, and left ventricular mass index of 107 g/m2 (A). Cardiac output was 2.30 L/min.
Following the index discharge, daprodustat was continued for six months without any adverse events, including thromboembolism. Systolic blood pressure remained around 110 mmHg. Medications remained unchanged except for daprodustat, which was up-titrated to 4 mg/day at 70 days following the index discharge ().
During the 6-month follow-up period, the hemoglobin level increased gradually from around 9.0 g/dL up to 10.0 g/dL. Plasma B-type natriuretic peptide decreased from around 250 pg/mL down to 150 pg/mL. Renal function remained unchanged. At 6-month follow-up, left ventricular mass index decreased to 88 g/m2 and cardiac output increased to 2.66 L/min (B). Ferritin was 216 ng/mL. The degree of tricuspid regurgitation remained trace. New York Heart Association functional class improved to II.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [54.0, 'kg'], 'height': [143.0, 'cm']}",26.40716,25.0868,27.72752,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 143.0 cm, which is 143.0 cm * 1 m / 100 cm = 1.43 m. The patient's weight is 54.0 kg. The patient's bmi is therefore 54.0 kg / (1.43 m * 1.43 m) = 26.40716 kg/m^2."
2130,6,Body Mass Index (BMI),physical,decimal,pmc-7042143-3,Extracted,"Patient 3 is a 66-year-old man with a history of catheter ablation of atrial fibrillation in January 2016, status post two electrical cardioversions in 2014 and 2015; coronary artery disease with percutaneous coronary angioplasty of the left anterior descendent artery in 2008; and hypertension and dyslipidaemia, but normal left ventricular function and no valvular abnormality as per the most recent echocardiogram. He was presented to the emergency room with palpitations. His height and weight were 185 cm and 77 kg, respectively. His blood pressure was 125/77 mmHg. His electrolytes were as follows: sodium 139 mmol/L, potassium 3.6 mmol/L, and calcium 2.06 mmol/l. His list of medications included bisoprolol 2.5 mg o.d., amlodipine 5 mg o.d., pantoprazole 20 mg o.d., ramipril 5 mg o.d., rivaroxaban 20 mg o.d., and atorvastatin 10 mg o.d. Electrocardiogram on admission revealed atrial fibrillation. He received 300 mg of amiodarone intravenously before cardioversion. shows his ECG prior to cardioversion. He received one DC shock at 200 J and was reverted back to sinus rhythm. shows his ECG during cardioversion. shows his ECG after electrical cardioversion. The patient had a recurrence of atrial fibrillation 5 months after cardioversion and a redo catheter ablation for atrial fibrillation afterwards. Since then, no documented recurrence of atrial fibrillation but at least one episode of palpitation lasting 1 h was noted. He is currently on long acting flecainide 200 mg o.d., bisoprolol 2.5 mg o.d., and rivaroxaban 20 mg o.d.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [77.0, 'kg'], 'height': [185.0, 'cm']}",22.49817,21.37326,23.62308,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 185.0 cm, which is 185.0 cm * 1 m / 100 cm = 1.85 m. The patient's weight is 77.0 kg. The patient's bmi is therefore 77.0 kg / (1.85 m * 1.85 m) = 22.49817 kg/m^2."
2131,6,Body Mass Index (BMI),physical,decimal,pmc-6966963-1,Extracted,"A 51-year-old man (165 cm, 81 kg) underwent internal fixation of a left proximal humeral fracture under general anesthesia. After inducing anesthesia with propofol, remifentanil, and rocuronium, an 8.0-mm tracheal tube was placed using a Macintosh blade uneventfully. The depth and intracuff pressure of the tracheal tube were 23 cm and ≤ 12 cmH2O, respectively. The 105-min long procedure was performed in the beach-chair position. Anesthesia was uneventful, except for the displacement of the patient’s head and neck, which required repositioning—the head and neck were often deflected to the right while traction was applied to the left forearm during fracture reduction. After emergence from anesthesia, the patient was hoarse. On postoperative day 1, he complained of dysarthria, dysphagia, and leftward deviation of the tongue. On postoperative day 2, magnetic resonance imaging of the head did not show any abnormalities. Subsequent swallowing videofluoroscopy and laryngeal endoscopy revealed pharyngeal retention without aspiration and left vocal cord paralysis. He was diagnosed with combined left hypoglossal and recurrent laryngeal nerve palsy. All symptoms subsided within 8 months, without systemic administration of corticosteroids.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [81.0, 'kg'], 'height': [165.0, 'cm']}",29.75207,28.26447,31.23967,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 81.0 kg. The patient's bmi is therefore 81.0 kg / (1.65 m * 1.65 m) = 29.75207 kg/m^2."
2132,6,Body Mass Index (BMI),physical,decimal,pmc-7429016-1,Extracted,"A 17-year-old boy who was 174-cm tall and weighed 65 kg admitted to the hospital due to abdominal pain since one day before admission. The pain was in the periumbilical area and right lower quadrant of the abdomen and started after an excessive exercise (boxing). The patient had no nausea, vomiting, but anorexia.
The patient was also a known case of G6PD deficiency since birth time. The G6PD deficiency test was conducted, and the result was deficient and confirmed the diagnosis. He had no hemolytic crisis, jaundice, and blood transfusion up-to-date. At first, in the hospital, before and after the operation, the patient and his family members did not give an appropriate history of growth hormone abuse, but gave a history of using growth hormone for growth problems and short stature under an endocrinologist follow-up from childhood; but after a precise history taking, we found that the patient had started illegally to use recombinant human growth hormone (a five mg injection under the skin) for bodybuilding and strength advantage from two month prior to surgery once a day at bed time (Norditropin FlexPro (somatropine) subcutaneous solution (5 mg/1.5 mL)). The patient had no delayed bone age, but had normal velocity growth. The patient had visited an endocrinologist 15 days prior to his admission to the hospital and was sent for a health check-up and also checking for insulin-like growth factor 1 (IGF 1) and a thyroid function test (TFT). TFT showed normal range T3, T4, and TSH as 1.51 nmol/ml, 9.1 g/dl, and 1.82 mIU/ml, retrospectively, and IGF 1 was 180.6 ng/ml (reference interval 75–850).
The patient had left wrist fracture 3 years before the current hospital admission, but no prior surgeries were found. Moreover, his grandparents and father received general anesthesia without recognized complications.
The patient's physical exam was normal except for right lower quadrant (RLQ) abdominal tenderness, rebound tenderness, and positive Rovsing's sign without any evidence of fever. Laboratory studies were unremarkable, and there was no evidence of active hemolysis. His hemoglobin (Hb) level was 14.1 g/dl; however, other hemolytic laboratory parameters were not evaluated because there was no history of G6PD deficiency-related sequelae such as hemolysis, jaundice, or blood transfusion. The patient was sent to the operation room with the impression of acute appendicitis for open appendectomy.
In the operation room, the patient's vital signs immediately before induction of anesthesia were as follows: pulse rate = 86 beat/minutes, blood pressure = 120/80 mm Hg, respiratory rate = 12 breaths/minutes, and axillary temperature = 36.7 degrees Celsius. In the supine position, under continuous electrocardiography, pulse oximetry, capnography, monitoring ETCO2, blood pressure monitoring, and temperature measurement (axillary), the patient underwent 3 min of denitrogenation with 100% oxygen through a facemask. Anesthesia was induced using midazolam (2 mg), thiopental sodium (200 mg), and isoflurane in oxygen using the Bain circuit. After confirming the loss of consciousness, atracurium (30 mg) and fentanyl (25 mcg) were administered, and then, endotracheal intubation was performed using a 7.5 mm tube (internal diameter) with an inflatable cuff. After applying the ventilator, ETCO2 was 34 mmHg. The patient received cefazoline 1 gr IV for one dose for antibiotic prophylaxis, and the operation started. Anesthesia was maintained with isoflurane in oxygen during operation.
At the end of the operation, about 45 minutes after starting the induction of anesthesia and starting surgery, while the patient was still intubated and going to be awake and having his own spontaneous respiration, he developed with (in order of occurrence) an increased heart rate to 124 beat/minutes (sinus tachycardia), increased body (axillary) temperature to about 41.7 degrees Celsius, gasping like respiration, increased ETCO2 to 153 mmHg, MMR, and then generalized body rigidity, so the malignant hyperthermia susceptibility was considered. Blood pressure was mildly elevated and was 140/80 mmHg. The color and volume of the perioperative urine was normal. Immediately, inhalational anesthetics were discontinued, and the Bain circuit and machine were exchanged to be replaced with an uncontaminated one; next, dantrolene rapid intravenous (IV) bolus (2.5 mg/kg) was given, and one vial of sodium bicarbonate was infused. An internal Foley catheter and nasogastric tube were inserted, and the bladder and the stomach were irrigated with cold saline, and the patient was hydrated with 1000 cc cold crystalloids for two times to reach the urine output of at least 2 cc/kg/hour. The patient was further cooled with a wet sponge applied to the surface of the body. About 30 minutes after administration of dantrolene and cooling measures, the heart rate was dramatically decreased to 80 beats/minutes, ETCO2 decreased from 153 to 35 mm Hg, and temperature decreased to 38.5°C (axillary), and cooling measures were stopped. The patient could not be extubated due to a low level of consciousness at the end of the operation, and was sent intubated to the surgical intensive care unit (ICU). In the ICU, dantrolene was continued at 1.0 mg/kg every 6 hours for 24 hours.
The patient had been in the hospital for twelve days; the first three nights were in the ICU for stabilization and, then, till the discharge day in the surgical ward. The patient was under close observation, and continuous monitoring of heart, blood pressure, temperature, and urine output was performed while checking for arterial blood gases (PH, partial pressure of carbon dioxide (PCO2), HCO3− and base excess in the extracellular fluid compartment (BEecf)), white blood cell count (WBC), Hb, platelet count, liver enzymes as aspartate aminotransferase (AST), alanine aminotransferase (ALT), total and direct bilirubin, alkaline phosphatase (AlK–P), albumin (Alb), blood urea nitrogen (BUN), creatinine (Cr), blood sugar (BS), electrolytes (Na+ and K+), calcium (Ca2+), CPK, creatine kinase-muscle/brain (CKMB), and lactate dehydrogenase (LDH) (Tables and ).
In this case, the urine output did not decrease, the urine color did not change, and urine analysis was considered to be normal. Reticulocyte and corrected reticulocyte count were 1.5% and 1%, respectively. A peripheral blood smear was taken and showed no fragmented red blood cells (RBCs), but mild leukocytosis (neutrophilia). Direct Combs and indirect Combs tests were both negative. Viral markers as hepatitis B surface (HBS) antigen-antibody, hepatitis C virus (HCV) antibody, and human immune-deficiency virus (HIV) antibody were negative by the enzyme-linked immunosorbent assay (ELISA) technique. C-reactive protein (CRP) and uric acid were checked and were in the normal range (0.7 and 3.3 mg/dl retrospectively). Troponin I was checked and was positive, so it was titrated and was 41.5 ng/l, and echocardiography was performed which revealed a normal ventricular function without residual pulmonary valve stenosis or pulmonary regurgitation. The antinuclear antibody (ANA) titer was 0.289 and was negative. Ceruloplasmin was 0.398 g/l and was in the normal range. Serum sodium, magnesium (Mg), prothrombin time (PT), partial thromboplastin time (PTT), the international normalized ratio (INR), hemoglobin (Hb), platelet (Plt), blood urea nitrogen (BUN), and creatinine (Cr) were all in the normal range.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [65.0, 'kg'], 'height': [174.0, 'cm']}",21.46915,20.39569,22.54261,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 174.0 cm, which is 174.0 cm * 1 m / 100 cm = 1.74 m. The patient's weight is 65.0 kg. The patient's bmi is therefore 65.0 kg / (1.74 m * 1.74 m) = 21.46915 kg/m^2."
2133,6,Body Mass Index (BMI),physical,decimal,pmc-5176076-2,Extracted,"Male patient, aged 4 years and 8 months, born and residing in the municipality of
Diadema, was referred to our service from HMD, where he was hospitalized.
The mother reported that the BHU pediatrician started to realize that the patient did
not gain weight after 3 years of age. She denied abdominal distension and diarrhea.
She reported that the patient ate adequately and, according to the nutrition team
assessment, it was not possible to identify any protein-calorie restriction in
relation to age.
On physical examination, the child showed regular general status, was very emaciated,
weight=7.585kg (weight/age Z-score=−5.73) and height=80cm
(height/age Z-score=−6.35).
At the first consultation, the diagnosis of severe protein-calorie malnutrition was
made and the patient started to be investigated for the same causes of malabsorptive
diseases that his brother was undergoing, with negative test results. The duodenal
biopsy disclosed fingerlike villi and celiac disease was ruled out ().
The patient remained hospitalized for two months at HMD with his brother, receiving a
high calorie and high-protein diet, showing excellent nutritional recovery ( and ), which reinforced the diagnostic suspicion of abuse.
During one of the visits to our clinic, when the children were already living in the
shelter, we asked the social worker about the fact that her mother sometimes said her
name was Maria das Graças and, sometimes, Ana Paula. The social worker informed us
that up until the older brother was aged 2 and a half years, the children and their
parents lived near the rest of the relatives; however, they moved to an unknown
destination and lost contact with the family. In this new home, the patient's mother
told the neighbors her name was Ana Paula.
Regarding the children's father, he said that he worked all day and did not realize
that the mother did not feed children adequately. He was considered an accomplice and
the children were kept away from him.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [7.585, 'kg'], 'height': [80.0, 'cm']}",11.85156,11.25898,12.44414,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 80.0 cm, which is 80.0 cm * 1 m / 100 cm = 0.8 m. The patient's weight is 7.585 kg. The patient's bmi is therefore 7.585 kg / (0.8 m * 0.8 m) = 11.85156 kg/m^2."
2134,6,Body Mass Index (BMI),physical,decimal,pmc-7005623-1,Extracted,"This male proband was born at 39 1/7 weeks to a 35-year-old Caucasian woman and her 38-year-old Asian partner, weighing 3,635 g (71.73rd centile), with length 50.8 cm (65.79th centile), and occipital frontal circumference (OFC) 34.5 cm (51.23rd centile) via repeat cesarean section following in vitro fertilization (IVF. An older son is healthy, family history was noncontributory, and consanguinity was denied. Prenatal ultrasound demonstrated left hydronephrosis, left foot postaxial polydactyly, and polyhydramnios, and after birth, a patent foramen ovale and pelviectasis with a duplicated left ureter were noted. Prenatal chromosome microarray and karyotype were normal. Newborn screening, including cystic fibrosis, was normal. He was admitted to the neonatal intensive care unit (NICU) at day 1 of life due to presumed bowel obstruction. At 1 week of age, he had an intestinal resection due to severe bowel obstruction with meconium ileus. Hirschsprung's disease was ruled out by biopsy. Two weeks after the initial resection, he continued to have absent bowel function and a second resection was performed. Thick, sticky meconium was noted at the anastomotic site, and normal bowel function returned thereafter, allowing him to be discharged home at age 24 days.
Rapid trio exome sequencing and testing for cystic fibrosis sequencing (including deletion/duplication analysis of CFTR) were received at the lab for testing concurrently at day 17. At day 22 of age, the genetic counselor was called and given the verbal report of two biparentally inherited alterations of uncertain significance in GUCY2C (c.2575A > G [p.I859V] and c.2864_2865delCCinsTA [p.S955L]), and CFTR was 100% covered at 10x on exome. CFTR sequencing and deletion/duplication analysis was reported as normal at day 23.
GUCY2C interacts with CFTR and encodes the guanylate cyclase C (GC-C) receptor, an epithelial transmembrane receptor expressed throughout the intestine (OMIM_601330). GC-C plays a role in the regulation of electrolyte and fluid release to the intestinal lumen, as well as epithelial differentiation, proliferation, and tumorigenesis (von Volkmann et al., ). Autosomal recessive alterations in this gene have been associated with meconium ileus (OMIM_614665).
The c.2575A > G (p.I859V) alteration was observed in 92 of 269,026 total alleles studied (0.03%), having been seen in 0.5% (91/18,174) East Asian alleles and <0.001% (1/124,596) European non-Finnish alleles and conserved throughout vertebrates (Lek et al., ). The p.I859V alteration is also predicted to be probably damaging by Polyphen and deleterious by SIFT in silico analyses (Adzhubei et al., ; Kumar, Henikoff, & Ng, ).
Identification of the GUCY2C alterations led to a definitive diagnosis and accurate genetic counseling that alleviated possible concerns regarding cystic fibrosis. Further evaluations and possible treatment for CF (sweat chloride test, referral to CF clinic, pancreatic enzymes) were deemed unnecessary and discharge planning was altered accordingly. As results were available prior to the patient's discharge, the family received in-person genetic counseling the same day the results were provided by the lab instead of waiting weeks or months for an outpatient appointment.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [3635.0, 'g'], 'height': [50.8, 'cm']}",14.08565,13.38137,14.78993,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 50.8 cm, which is 50.8 cm * 1 m / 100 cm = 0.508 m. The patient's weight is 3635.0 g so this converts to 3635.0 lbs * kg/1000 g = 3.635 kg. The patient's bmi is therefore 3.635 kg / (0.508 m * 0.508 m) = 14.08565 kg/m^2."
2135,6,Body Mass Index (BMI),physical,decimal,pmc-8367080-1,Extracted,"A 78-year-old male patient (168 cm, 70 kg) was scheduled for video-assisted thoracoscopic wedge resection due to recurrent secondary right-sided pneumothorax despite the insertion of a chest tube. In the preoperative chest computed tomography (CT) scan, the take-off of a TrB could be identified in the tracheal wall on the right side, approximately 1.9 cm above the carina (). This originating level was based on the lower margin used in previous reports,, and it has been reported that OLV could be successfully performed with a DLT in most cases of the TrB originating within 2 cm from the carina. Therefore, the left-sided Broncho-Cath (Covidien, Mansfield, MA, USA), and a 37-Fr tube was chosen based on the left main bronchus (LMB) diameter on chest CT. Standard monitoring (including electrocardiography, pulse oximetry, and non-invasive blood pressure) was performed. Total intravenous anesthesia was performed using propofol and remifentanil, and 70 mg of rocuronium was administered intravenously for muscle relaxation. Tracheal intubation was performed using a video-laryngoscope (UEscope®, Zhejiang UE Medical Co., Zhejiang, China), and then a flexible bronchoscope (aScope™ 4 Broncho Large 5.8/2.8, Ambu® A/S, Ballerup, Denmark) was used to confirm the DLT position. When the bronchoscope was inserted into the tracheal lumen of the DLT, to the right of the tracheal carina a ridge and a partially obstructed orifice could be seen in the bottom right of the monitor of the bronchoscopy system (). The DLT was located to the left of tracheal carina; however, there was a slight herniation of the bronchial cuff of the DLT out of the LMB, which is not shown clearly in . The problems in this case can be summarized as follows. 1) Because the tube depth at contact with the patient’s teeth had already been indicated as 31 cm, the DLT could not be advanced any further to optimally reposition the herniated bronchial cuff—the Broncho-Cath was short to be used in this patient. 2) Moreover, the TrB orifice was already partially obstructed when viewed through the tracheal lumen, indicating that it could become completely obstructed if the tube was advanced further. An air leakage occurred while clamping the connector for the non-dependent lung, and satisfactory OLV required for surgery could not be achieved. Therefore, we decided to replace the existing DLT with a 37-Fr left-sided Human Broncho (Insung Medical Co., Wonju, Korea) that differs from a Broncho-Cath in terms its structure. Under bronchoscopic view after replacing, the bronchial cuff of the DLT showed no herniation and was located to the left just below the tracheal carina, and the TrB orifice was not obstructed by the tracheal lumen (). The patient’s vital signs and respiratory parameters were unremarkable without any air leakage during clamping of the connector for the non-dependent lung. In the thoracoscopic view after starting surgery, the operative lung collapse was accomplished, and right upper lobe apex and right lower lobe superior segment bullectomies were performed successfully without any other events. There were no findings of postoperative air leakage; the patient was discharged after chest tube removal and is currently healthy. The patient has provided informed consent for the publication of this case report.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [168.0, 'cm']}",24.80159,23.56151,26.04167,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.68 m * 1.68 m) = 24.80159 kg/m^2."
2136,6,Body Mass Index (BMI),physical,decimal,pmc-6966725-1,Extracted,"A 42-year-old man (175 cm in height, 61.8 kg in weight), with no medical and family history, experienced a temporal headache and nausea. He began to experience excessive sweating after meals and subsequently developed high blood pressure with the systolic pressure reaching 180 mmHg. Further examination revealed an elevated level of urinary noradrenaline excretion of 6460 μg/day (approximately 40 times above the upper limit of normal) and an increased serum concentration of interleukin-6 (IL-6) (74 ng/L, normally < 4.0 ng/L). Computed tomography (CT) images showed a 4.6-cm round mass on his right adrenal gland. Increased uptake of iodine-123-metaiodobenzylguanidine (MIBG) in both adrenal glands observed during iodine-123-MIBG scintigraphy and positron emission tomography (Fig. ) led to the diagnosis of bilateral pheochromocytomas.
The patient was scheduled for surgical resection and was treated with a combination of bunazosin hydrochloride, phentolamine mesylate, and carvedilol to achieve prophylactic cardiovascular stabilization. Approximately 3 weeks later, he suddenly experienced dyspnea with a persistent fever peaking at 38.9 °C, and systemic administration of broad spectrum antibiotics was immediately initiated for a suspected bacterial pneumonia. However, the antibiotics were ineffective, and his respiratory condition deteriorated with PaO2 at 69 mmHg while receiving 5 L/min of oxygen via a face mask. Chest radiographs and CT images showed bilateral infiltration and air bronchograms, indicating pulmonary edema (Fig. ). We found increased serum concentration of liver transaminases, suggesting hepatic insufficiency. Transthoracic echocardiography showed no signs of cardiac failure. The patient was suspected of developing pheochromocytoma multisystem crisis, a life-threatening condition that could cause permanent organ damage in a short span of time, and we thus decided to perform an emergency bilateral total adrenalectomy.
On arrival in the operating room, the vital signs were as follows: ABP 144/78 mmHg, heart rate 109 beats/min (sinus rhythm), SpO2 95% (under 5 L/min of oxygen via a face mask), and body temperature 38.7 °C. General anesthesia was induced with target-controlled infusion (target-controlled infusion pump: TE-371 Telfusion ® TERUMO Co.Tokyo, Japan) of an effect site concentration of 2.5 μg/mL propofol, 200 μg of fentanyl, and 40 mg of rocuronium bromide to facilitate endotracheal intubation. Epidural anesthesia was waived because of his respiratory discomfort. General anesthesia was maintained with continuous infusion of propofol (constantly set at 2.6 μg/mL during the surgery with the bispectral index 45–63) and remifentanil (constantly set at 0.25 μg/kg/min) and intermittent supplementation of rocuronium bromide. The PaO2/FiO2 ratio was 72 at the beginning of the surgery.
The radial artery catheter was connected to the FloTrac™ sensor (third generation: version 3.06, Edwards Life Science, Irvine, CA, USA) to measure APCO along with arterial waveform and stroke volume variation (SVV). The pulmonary artery catheter, which was placed in the right jugular vein, was connected to the Vigilance™ monitor (Edwards Life Science, Irvine, CA, USA) to measure PACO using the thermodilution method. Phentolamine mesylate, landiolol hydrochloride, and prostaglandin E1 were continuously infused to stabilize blood pressure and heart rate. When the surgeons started to operate the right adrenal gland, ABP surged to 218/113 mmHg, which required an immediate bolus injection of phentolamine mesylate. Once the right adrenal gland vessels were ligated, ABP dropped to 70/30 mmHg and SVV jumped from 8 to 9% to 17%, probably as a result of systemic vasodilation and hypovolemia. Administration of a continuous infusion of norepinephrine (0.05–0.2 μg/kg/min) in combination with a rapid infusion of 1000 mL of albumin solution stabilized hemodynamics with ABP raising to 91/50 mmHg and SVV returning to less than 10%.
While the right adrenal gland was being operated, APCO fluctuated markedly in more or less inverse proportion to the change in ABP, whereas PACO shifted rather smoothly (Fig. ). However, there was no appreciable difference between APCO and PACO while the left adrenal gland was being resected, the histological examination of which revealed no abnormal findings. After bilateral resection of the adrenal glands, ABP remained around 80/40 mmHg with a continuous infusion of norepinephrine (0.1 μg/kg/min). The total time required for surgery and general anesthesia were 214 and 308 min, respectively. The intraoperative fluid balance was + 1575 mL (5.1 mL/kg/h) with an estimated blood loss of 610 mL and urine output of 415 mL. The patient did not receive blood transfusions.
After surgery, he remained ventilated for 3 days in the intensive care unit (ICU). The PaO2/FiO2 ratio, which was initially 214, improved gradually over the next few days. Norepinephrine was tapered off, and the circulatory hemodynamics was stable thereafter. After being extubated on postoperative day (POD) 4, he was transferred to the ward on POD 5 and was uneventfully discharged on POD 14.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.8, 'kg'], 'height': [175.0, 'cm']}",20.17959,19.17061,21.18857,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 175.0 cm, which is 175.0 cm * 1 m / 100 cm = 1.75 m. The patient's weight is 61.8 kg. The patient's bmi is therefore 61.8 kg / (1.75 m * 1.75 m) = 20.17959 kg/m^2."
2137,6,Body Mass Index (BMI),physical,decimal,pmc-8311308-1,Extracted,"A 79-year-old man with a 3-month history of chest discomfort unrelated to exercise was admitted to our hospital. The patient reported a medical history of asthma and chronic obstructive pulmonary disease, which were well-controlled by medication. On initial examination, his blood pressure was 115/82 mm Hg, heart rate was 78 beats/min, respiratory rate was 12 breaths/min, pulse oximetric oxygen saturation was 98% in room air and his temperature was 36.2°C. The patient’s height and weight were 170 cm and 66 kg, respectively. Clinical examination of the cardiovascular system revealed no murmurs, and the lungs were clear. His jugular venous pressure was not elevated, and he did not exhibit heart failure symptoms, such as shortness of breath and leg oedema.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [66.0, 'kg'], 'height': [170.0, 'cm']}",22.83737,21.6955,23.97924,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 66.0 kg. The patient's bmi is therefore 66.0 kg / (1.7 m * 1.7 m) = 22.83737 kg/m^2."
2138,6,Body Mass Index (BMI),physical,decimal,pmc-8008611-1,Extracted,"The patient was a 65-year-old Caucasian woman, with a history of cutaneous mastocytosis. She was divorced, with two children, and was a retired teacher. The patient did not smoke or drink alcohol. She had no major medical history except the presence of lumbar and femoral osteopenia. A detailed medical examination was performed on admission and revealed very good general condition, weight 54 kg, height 163 cm, blood pressure 120/85 mmHg, pulse 52 beats per minute, body temperature 37.3°C, supple abdomen, without hepatosplenomegaly, and normal cardiovascular, pulmonary, and neurological examinations. She had exhibited symptoms of mastocytosis for 36 years with pruritus and was diagnosed by skin biopsy. Dermatological examination revealed small brown-red maculopapules on the thorax, back, and arms (Fig. ). A positive Darier’s sign was elicited 5 minutes after skin scratching (the skin becomes swollen, itchy, and red). Additional laboratory analyses were performed. Complete blood count, blood ionogram, and glycemia were normal. No abnormal liver or renal functions were detected. Moderate proteinuria (0,18 g/24 hours) was diagnosed and had to be monitored,. The serum tryptase level was slightly higher than normal (23.3 ng/ml) during crisis. Magnetic resonance imaging showed no evidence of skeletal involvement, and paraclinical examination had concluded the absence of extracutaneous manifestations. The systemic form of the disease had thus been excluded, and the diagnosis of cutaneous mastocytosis had been confirmed. A dermatological treatment was prescribed to the patient: application of a dermocorticoid cream once or twice a day with a maximum of two tubes of creams per month (clobetasol propionate at 0.05%, at the time of skin lesions with prurit). It was supplemented by oral administration of an antiallergic antihistamine drug (levocetirizine dihydrochloride 5 mg, two tablets per day). These local and oral treatments have been ineffective in the long term. Finally, photochemotherapy was also proposed to the patient. Photochemotherapy combines treatment with psoralen and exposure of the skin to long-wave ultraviolet radiation (PUVA). At the time of the assessment, PUVA therapy (30 sessions, 1500 J) had been given each year for 4 years. The sessions had achieved reduction of pruritus with persistence of a moderate Darier’s sign, but very unaesthetic skin lesions had persisted with profuse thrusts. These cutaneous symptoms significantly decreased the quality of life of the patient.
During the medical consultation, the patient was informed of the objectives and procedures of the psychobehavioral assessment of the Millon Behavioral Medicine Diagnostic (MBMD) tool [–]. MBMD is a self-report inventory containing 165 true–false items. It provides scales to assess psychobehavioral factors, such as negative health habits, psychiatric indications, coping styles, stress moderators, treatment prognostics, and management guides. The scale aimed to identify attitudes that may affect health of the patient.
At the next visit, after giving consent, the patient told her life history during a structured interview. The Holmes and Rahe Social Readjustment Rating Scale [] was used to score each stressful life event in “Life Change Units” (LCU). The life events and LCU were collected in an Excel file and classified chronologically. LCU applied to life events for 1 year were summed to assess the annual stress score. In parallel, the medical data of the electronic health records were chronologically integrated in the Excel file to establish a comprehensive dermatological history of the mastocytosis. An automatized graph integrating annual stress scores and cutaneous symptoms was generated.
Analysis of life history and cutaneous symptoms indicated that stressful events could have exacerbated the symptoms of cutaneous mastocytosis (Fig. for details). We observed that, if annual stress score of life events exceeded 50 LCU on the Holmes and Rahe scale, skin manifestations in relation to mastocytosis were induced subsequently. An annual score of 50 LCU could thus be considered as the threshold for stress tolerance of this patient.
The MBMD results detailed the psychobehavioral profile of the patient (Fig. ). This scale identifies attitudes and relationships that may affect health (with significant prevalence score >75) []. The psychiatric indicators (anxiety–tension, depression, cognitive dysfunction, emotional lability, guardedness) did not evidence significant psychiatric comorbidities at the time of assessment (Fig. a). The MBMD results detailed the stress moderators of the patient (Fig b). For the patient, social isolation and the absence of spiritual support reinforced the stressful effect of life events, which could exacerbate the dermatologic symptoms of mastocytosis. Coping styles are shown in Fig c. They reflect ways of dealing with life stress and illness. The significant prevalence scores revealed denigrated coping style. This personality trait would predispose the patient to somatic manifestations. In Fig d, the significant prevalence score of treatment prognostics indicates the patient’s characteristics that should be considered by the clinicians because they influence treatment outcome. We noticed a low compliance with treatment as well as periods of medication abuse, which did not help care. Regarding everyday behavior, the MBMD test did not reveal negative health habits at that time (alcohol, drugs, eating, caffeine, inactivity, smoking, data not shown.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [54.0, 'kg'], 'height': [163.0, 'cm']}",20.32444,19.30822,21.34066,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 54.0 kg. The patient's bmi is therefore 54.0 kg / (1.63 m * 1.63 m) = 20.32444 kg/m^2."
2139,6,Body Mass Index (BMI),physical,decimal,pmc-6764550-1,Extracted,"A 78-year-old woman was admitted to the internal medicine department because of a recent onset of palpitations, fatigue, epigastric pain, and vomiting. She was on antihypertensive treatment, and she had a diagnosis of hypothyroidism secondary to a previous thyroiditis. An urticarial vasculitis had been diagnosed when she was 75.
At admission, blood pressure (BP) was 140/70 mmHg, heart rate 90 b.p.m., with a regular pulse, temperature 36.2°C, oxygen saturation 96% in room air, and she was not in pain; body weight was 47 kg and height was 152 cm. Thoracic, abdominal, and neurological examinations were normal, heart sounds were normal without murmurs and peripheral pulses were normal, without arterial bruits appreciable. Electrocardiogram (ECG) confirmed sinus rhythm. Laboratory exams displayed increased C-reactive protein and erythrocyte sedimentation rate without clinical evidence of infection or inflammatory disease. Other laboratory test results are shown in Table.
In consideration of the weight loss (4 kg), fatigue and the presence of anaemia, an ultrasound of the abdomen was performed, showing few hypo-echogenic pancreatic lesions. At a subsequent abdomen contrast-enhanced CT the pancreatic lesions were described as uncomplicated cysts, and a thrombus in the superior mesenteric artery with collateral reperfusion was observed (Figure).
Thromboembolism (for instance embolization in a visceral vessel from a thrombus in aorta or cardio-embolic origin), thrombophilia, or vasculitis may be the cause of a thrombosis of the superior mesenteric artery.
The patient had no previous finding of atherosclerotic diseases and only one cardiovascular risk factor (hypertension), with documented good control of BP values by antihypertensive treatment. An ECG-Holter monitoring showed sinus rhythm throughout the 24 h of recording, in the absence of arrhythmic episodes or ‘silent’ atrial fibrillation. A transthoracic echocardiogram showed normal cardiac chambers dimensions, normal wall thicknesses, and regional contractility, with a 50% ejection fraction, and normal aortic, mitral, and tricuspid valves structure.
Lupus anti-coagulant, anti-phospholipid antibodies (including anti-β2GPI and anti-cardiolipin), and homocysteinaemia normal values excluded thrombophilia. Other autoimmunity tests, including antinuclear antibodies, complement fractions consumption, anti-neutrophil cytoplasmic antibodies, anti-extractable nuclear antigen, and cryoglobulins were all negative.
The patient underwent a fludeoxyglucose (18-F) PET in order to investigate the presence of vasculitis, in particular Takayasu’s arteritis, giant cell arteritis, Behcet disease, IgG4 related-disease, or Cogan syndrome. An intense tracer signal was observed in the lumen of the thoracic aorta, suggesting the presence of endovascular thrombus, due to an inflammatory process or a neoplastic disease; in addition, intense metabolic activity was described at the level of the VIII posterior right rib, suggesting a neoplastic process (Figure).
Subsequently, a thorax and abdomen contrast-enhanced CT was performed to evaluate the entire thoracic and abdominal aorta. The CT showed the presence of a large aortic thrombus (7 cm in length) in the descending thoracic tract, causing a focal sub-occlusion (6 mm in diameter), with thickening of the aortic wall, but not atherosclerotic plaques. The rib osteolytic lesion was also confirmed on CT imaging (Figures and ).
Therefore, two apparently different clinical conditions were to be considered: a large vessel vasculitis and a skeletal neoplastic lesion of unknown origin.
At serum protein electrophoresis a monoclonal gammopathy was shown with a double monoclonal component IgGk and IgGλ at immunofixation, possibly suggesting multiple myeloma. Therefore, a bone marrow biopsy was performed, showing a low percentage of plasma cells and excluding the diagnostic hypothesis of multiple myeloma.
At magnetic resonance, performed in order to more precisely assess the thrombus and the aortic wall structure, the presence of a large size thrombus, with irregular and sub-occluding profile was confirmed, with a clear thickening of the aortic wall and oedema at the site of the thrombus (Figure). In addition, the patient underwent a CT-guided biopsy of the VIII right rib to evaluate the origin of the metastatic bone lesion; at histology the features of a vascular neoplasm, mostly compatible with an angiosarcoma were described: high cell density including inflammatory cells and atypical cells, with larger size, epithelioid and fusate morphology, pleomorphic and irregular nucleus, hypodense chromatin, and eosinophilic nucleolus. The immunohistochemical analysis showed positivity for endothelial markers (CD-31, WT-1, FLI-1) (Figure).
After a multidisciplinary discussion, including the vascular surgeon, the oncologist, and the internist, the surgical removal of the neoplastic thrombus was ruled out because of the presence of metastasis and chemotherapy, based on the oral administration of propranolol and paclitaxel, was started. The patient underwent irradiation of the rib and completed five cycles of treatment with paclitaxel.
Despite treatment, the patient died due to the progression of the disease, 7 months after the diagnosis.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [47.0, 'kg'], 'height': [152.0, 'cm']}",20.3428,19.32566,21.35994,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 152.0 cm, which is 152.0 cm * 1 m / 100 cm = 1.52 m. The patient's weight is 47.0 kg. The patient's bmi is therefore 47.0 kg / (1.52 m * 1.52 m) = 20.3428 kg/m^2."
2140,6,Body Mass Index (BMI),physical,decimal,pmc-5096502-1,Extracted,"A 15-year-old female patient presented with absence of pubertal development, primary amenorrhoea and parental concern regarding severe growth retardation. She was the first child of non-consanguineous parents. The medical history of the family was noncontributory. The patient was born at term with a length of 50 cm and a weight of 3450 g; the neonatal period and infancy were uneventful. At physical examination, she was prepubertal with Tanner stage I breast development and stage III pubic hair development. Her height was 149 cm [-2.1 standard deviation (SD)] which is below the third percentile (mid-parental height; between the 10th and 25th percentiles), and her weight was 48 kg (-0.72 SD), i.e. between the 10th and 25th percentiles. Physical examination revealed a normal female external genitalia phenotype. Further physical examination was unremarkable although her bone age was delayed by 3.5 years (Greulich and Pyle method). A baseline blood screen (urea, electrolytes, calcium, phosphate, liver enzymes, and full blood count), screening for thyroid function, and screening for coeliac disease antibodies revealed normal values. Hormone assays revealed low oestradiol (<10 pg/mL; normal 21-85 pg/mL), high FSH (73.7 mIU/mL; normal 1.8-11.2 mIU/mL), and high LH (33 mIU/mL; normal 1.5-9.0 mIU/mL) levels, indicating hypergonadotropic hypogonadism. Pelvic US revealed a small uterus 4.7 cmx1.3 mm in diameter and hypoplastic gonads (left pelvic gonad: 15 x 12 mm; right pelvic streak gonad: 7x6 mm). Due to the presence of a hypoplastic Müllerian structure, streak gonad, short stature, and primary amenorrhoea in this patient with a female phenotype and hypergonadotropic hypogonadism, a tentative diagnosis of Turner syndrome was made. However, the characteristic physical stigmata of Turner syndrome were not present. Chromosomal analysis and FISH of SRY showed an SRY-positive 46,XY karyotype. These findings indicate that gonadal dysgenesis should be considered in this differential diagnosis. Due to the fact that an SRY-positive 46,XY genotype and rudimentary gonads are associated with a high risk of malignancy, the parents and patient were informed of the malignancy risk of dysgenetic gonads. A bilateral gonadectomy was carried out by the laparoscopic method. Histopathological examination of the excised left gonad revealed features of an ovotestis with both ovarian and testicular tissues present in addition to a gonadoblastoma on the base of dysgerminomas (). Histopathological examination of the right rudimentary gonad revealed streak gonad parenchyma with epididymis and papillary tuba hyperplasia (PTH; ). Laparoscopic examination revealed a left tubular structure arising from the rudimentary uterus that ended with the left gonad (), and a streak right gonad.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [48.0, 'kg'], 'height': [149.0, 'cm']}",21.62065,20.53962,22.70168,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 149.0 cm, which is 149.0 cm * 1 m / 100 cm = 1.49 m. The patient's weight is 48.0 kg. The patient's bmi is therefore 48.0 kg / (1.49 m * 1.49 m) = 21.62065 kg/m^2."
2141,6,Body Mass Index (BMI),physical,decimal,pmc-8107892-1,Extracted,"An 80-year-old man was hospitalized due to pain in the right hip joint with restricted mobility.
The patient’s symptoms started after trauma 3 d ago.
The patient had a history of pemphigus for 3 years, for which he was taking oral prednisone acetate (one 5 mg tablet daily). He also had a history of Parkinson’s disease for over 10 years, for which he had not received any specific treatment.
Physical examination findings were: height 170 cm and weight 42 kg; severe tremoring of both hands; extensive erosion and purulent scabs on the chest, abdomen, and all four limbs, but with a better integrity of the skin on the back; and scattered moist rales in both lungs. The degree of mouth opening was two fingers wide, with erosion and bloody scabs in the mouth and oral mucosa, and a Mallampati grade of III. There was neither pain or stiffness nor swelling or redness below the knees.
Auxiliary examination showed that the coagulation function was normal. Biochemical liver test showed that aspartate aminotransferase was 77.73 IU/L, alanine aminotransferase was 66.21 IU/L, and albumin was 26.88 g/L. Arterial blood gas analysis findings were: pH 7.52, partial pressure of oxygen 51 mmHg, and partial pressure of carbon dioxide 42 mmHg.
Cerebral computed tomography revealed bilateral multiple lacunar infarcts, leukoaraiosis, and encephalatrophy. Chest computed tomography showed scattered inflammatory lesions in both lungs, with mild bilateral pleural effusion, and mild pericardial effusion. Echocardiography showed widening of the ascending aorta, reduced diastolic left ventricular function, mild mitral and aortic regurgitation, and an ejection fraction of 57%. Vascular color Doppler ultrasound revealed acute-stage intramuscular venous thrombosis in the right calf.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [42.0, 'kg'], 'height': [170.0, 'cm']}",14.53287,13.80623,15.25951,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 42.0 kg. The patient's bmi is therefore 42.0 kg / (1.7 m * 1.7 m) = 14.53287 kg/m^2."
2142,6,Body Mass Index (BMI),physical,decimal,pmc-8140543-1,Extracted,"The patient, a 65-year-old woman, 149 cm in height, 47 kg weight, gravida 4, and para 2, was urgently referred to our hospital for invasive treatment of endometrial cancer following LSC treatment for POP. Full informed consent was obtained from the patient. This study was conducted in accordance with the Declaration of Helsinki (as revised in Fortaleza 2013) and approved by the IRB of Kagoshima University (approval no. 190230).
The patient had visited a gynecological clinic complaining of abdominal discomfort 3 months before being admitted to our hospital. A vaginal pessary for uterine prolapse had been inserted 7 years earlier, which was severely adhered to the vaginal wall and could not be removed. At the time, endometrial cytology was negative, and she was introduced to a urologic clinic for POP surgery. A supracervical hysterectomy, LSC, and perineoplasty were performed. During the operation, the mesh was sutured to the bladder neck with five stitches, and the cervical stump was sutured with three stitches. The other side of the mesh was fixed to the front of the sacrum with two needles and covered with the peritoneum. Pathological findings of a resected uterine specimen revealed endometrioid carcinoma, Grade 1, and negative vessel permeation. However, the POP relapsed within 2 months following surgery; the vaginal wall was relaxed, and the cervix had re-prolapsed exceeding vaginal introitus, which was complicated with cystocele Stage III []. At this stage, the patient was referred to our hospital.
Neither distant metastasis nor lymph node swelling was seen using computed tomography. The patient underwent invasive surgery with a simple trachelectomy, bilateral adnexectomy, anterior-posterior colporrhaphy, and vaginal apex suspension and uterosacral ligament suspension and round ligament fixation in laparotomy. Mesh was sutured to the upper cervix and the suture was not frayed; the resected cervix was complicated by cervical elongation up to 9 cm []. The pathology of a resected specimen did not indicate carcinoma, and washing cytology was negative. Finally, Stage 1A was confirmed, and there was no adjuvant therapy. There were no complications, and no evidence of disease relapse has been reported for 6 months.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [47.0, 'kg'], 'height': [149.0, 'cm']}",21.17022,20.11171,22.22873,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 149.0 cm, which is 149.0 cm * 1 m / 100 cm = 1.49 m. The patient's weight is 47.0 kg. The patient's bmi is therefore 47.0 kg / (1.49 m * 1.49 m) = 21.17022 kg/m^2."
2143,6,Body Mass Index (BMI),physical,decimal,usmle-9854,Extracted,A 22-year-old Caucasian G1 presents to her physician at 29 weeks gestation for a checkup. The  medical history is unremarkable and the current pregnancy has been uncomplicated. Her weight is 81 kg (178.6 lb) and the height is 169 cm (5 ft 6 in). She has gained 13 kg (28.6 lb) during the pregnancy. She has no abnormalities on physical examination.,What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [81.0, 'kg'], 'height': [169.0, 'cm']}",28.36035,26.94233,29.77837,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 169.0 cm, which is 169.0 cm * 1 m / 100 cm = 1.69 m. The patient's weight is 81.0 kg. The patient's bmi is therefore 81.0 kg / (1.69 m * 1.69 m) = 28.36035 kg/m^2."
2144,6,Body Mass Index (BMI),physical,decimal,pmc-7273683-1,Extracted,"The proband was a 19-year-old pregnant woman who was referred to the department of medical genetics at the hospital for prenatal diagnosis due to a family history of intellectual disability. She was delivered vaginally at full-term. During the neonatal period, she was hypotonic and very passive. Her growth milestones were recalled. She walked at 1 year and 8 months of age, and learned to say “mama” at 2 years. She talked at nearly 3 years and showed severe ID. She began the first period of menstrual at the age of 13 years, and got married at 18 years. She was in pregnancy at 18 weeks’ gestation when referred for genetic counseling and prenatal diagnosis. She had facial dysmorphism including a prominent forehead; flat face; flat nasal bridge and a short upturned nose; thin lips; and small ears (Fig. ). Examinations in psychological clinic showed that her height was 154 cm [0 SD]; weight was 61 kg [− 0.2 SD]; and head circumference was 54 cm [− 1.12 SD] [, ]. Her IQ score was 32 as accessed by the Wechsler Adult Intelligence Scale-Revised China (WAIS-RC). In terms of the scale, a score ≤ 75 is considered as low intelligence, and a score of 32 suggests severe ID. Reportedly, she was able to care for herself in daily life. Clinical observation showed that she was introverted; seldom talked; had dementia and social dysfunction without depression and anxiety. Both her electroencephalogram (EEG) and brain MRI result were normal. No history of heart diseases was noted. Her father was reported to have low intelligence, but an on-site examination for her father was not achieved. Her mother was of normal intelligence but had scoliosis. Her paternal grandparents and uncles and the fetus’ father had no noticeable congenital anomalies.
Written informed consent was obtained from the family (The proband was under the guardianship of her mother). Peripheral blood for each participant and the amniotic fluid of the proband were drawn for genetic testing. Heart rate, blood pressure and electrocardiogram of the proband were monitored before amniocentesis. Conventional G-banded karyotype analysis showed a normal female karyotype (46,XX) in the proband. However, CMA using the CytoScan 750 K Array from Affymetrix (Thermo Fisher Scientific, USA) revealed a 936.3 kb heterozygous deletion of chromosome 1q22 (arr[GRCh37] 1q22 (155016052_155952375)×1) in the proband (Fig. ). The microdeletion was also detected in the proband’s father (II-2) and the fetus (IV-1), but absent in her mother (II-1), grandparents (I-1, I-2) and paternal uncles (II-3, II-4). Other members within the pedigree were not tested. For all tested individuals, no other CNVs were detected except known polymorphisms (frequency > 1%).
In search of public databases (Decipher, DGV and ClinVar) and literature, a few cases reported copy number losses of the 1q22 region including ASH1L and the associated phenotypes including ID with MCA (Table ). Furthermore, haploinsufficiency of ASH1L is strongly associated with DD/ID and MCA in multiple individual cases [, ]. On the basis of these observations, plus the co-segregation of genotype and phenotype in the current case, the detected CNV is considered to be pathogenic, being in line with the guidelines from the American College of Medical Genetics (ACMG) []. After full consideration, the family chose to terminate the pregnancy.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.0, 'kg'], 'height': [154.0, 'cm']}",25.72103,24.43498,27.00708,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 154.0 cm, which is 154.0 cm * 1 m / 100 cm = 1.54 m. The patient's weight is 61.0 kg. The patient's bmi is therefore 61.0 kg / (1.54 m * 1.54 m) = 25.72103 kg/m^2."
2145,6,Body Mass Index (BMI),physical,decimal,pmc-3866345-1,Extracted,"72-year-old man (height 163 cm, weight 72 kg) with a 10-year history of diabetes mellitus presented with intermittent intolerable sharp and lancinating pain over the left anterior chest wall and the back for 1 month. He received 300 mg/day of carbamazepine, 300 mg/day of gabapentin, and 1500 mg/day of valacyclovir orally for 7 days following diagnosis with acute herpes zoster at a local private clinic. He reported severe pain in the affected area (a score of 8 or 9 on a visual analog scale where 0 indicated ""no pain"" and 10 indicated ""the strongest pain imaginable"") despite a healed skin rash. A physical examination revealed allodynia and hyperalgesia over the left T2 and T3 dermatomes. The pain relief was maintained for only 3 days through the use of a thoracic epidural block with 10 ml of 0.1% bupivacaine and 10 mg of triamcinolone at the intervertebral space between the T1 and T2 (a visual analog scale pain score of 2 or 3). Simultaneously, the gabapentin and carbamazepine dosages were increased to 900 mg/day and 400 mg/day, respectively, and the antiviral therapy was completed. The patient received 6 subsequent blocks, but each block relieved the pain for only 3 days. He complained about the short-lasting effect of the blocks and the frequent follow up. After reviewing the benefit-risk ratio of the various available forms of therapy, the decision was made to implant a subcutaneous port connected to an epidural catheter for the continuous infusion of opioids and local anesthetics.
On arrival in the operating room, the arterial pressure, electrocardiogram, and peripheral oxygen saturation (SpO2) of the patient were monitored, and venous access was secured. The patient was positioned on an operating table in the lateral decubitus position with the patient's side for the port pocket nondependent. His arms were extended at the shoulders and secured in position away from the surgical field. The skin was prepared, and sterile drapes were applied. The radiographic C-arm was then positioned across the thoracic region to provide a cross-table anteroposterior view of the thoracic spine. Using fluoroscopy, the T7-8 interspace, which was thought to be the most appropriate interspace, was identified for the subcutaneous tunneling of an epidural catheter connected to an injection port placed in the right upper quadrant of the abdomen. An epidural catheter was then inserted through an 18-gauge Tuohy needle using a loss of resistance technique until the tip was at the intervertebral space between the T1 and T2 (). The needle was then withdrawn. An 8 cm transverse incision was made in the right upper quadrant of the abdomen, and a subcutaneous pocket was created caudad to the incision using a blunt dissection. A tunneling device was then extended within the subcutaneous tissue between the needle insertion site and the pocket. The catheter was then advanced through the tunnel and trimmed to a length that allowed a small loop of catheter to remain deep to the port (Celsite®, B. Braun, Boulogne-Billancourt, France). The port was connected to the epidural catheter and sutured to the abdominal fascia. Finally, the skin incision was closed. A port needle (Hubsite®, B. Braun, Ecouen, Germany) with a length appropriate for the thickness of the subcutaneous needle was used to deliver epidural medications: 25 mg of morphine, 200 mg of bupivacaine, and 185 ml of normal saline (a total volume of 250 ml) (). The background infusion rate was 2 ml/hr (no bolus).
After the completion of the procedure, the patient was delivered to the general ward and was observed closely for morphine-induced respiratory depression using pulse oximetry. The other side effects related to the use of epidural morphine and bupivacaine (pruritus, nausea, vomiting, urinary retention, constipation, systemic toxicity, motor weakness, etc.) were also monitored. Oral bisacodyl (5 mg) and docusate (16.75 mg) were administered daily for constipation prophylaxis. Because no side effects or complications associated with the epidural catheterization, implanted injection port and epidural medications were reported during the 11 days of admission, the patient was discharged and followed up every 10 days to exchange the port needle and epidural infusion pump (Accufuser®, WooYoung Medical, Seoul, Korea). The epidural infusion and concurrent administration of 900 mg/day gabapentin and 10 mg/day amitriptyline were maintained for 66 days. During treatment, the patient's pain intensity was successfully reduced from 10 (using the visual analog scale) and maintained between 2 and 3. The patient was very satisfied with the treatment. He reported slight hypoesthesia over the left anterior chest and back in the early treatment period. There were no complications associated with the epidural catheters or the medications used. Sixty-six days after the procedure, the subcutaneous port and epidural catheter were removed due to the obstruction of the catheter. He did not complain of pain thereafter but reported a slight numb sensation that remained over the lesion site for 3 months, during which oral gabapentin and amitriptyline were tapered off uneventfully. The patient was thereafter lost to follow up.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [72.0, 'kg'], 'height': [163.0, 'cm']}",27.09925,25.74429,28.45421,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 72.0 kg. The patient's bmi is therefore 72.0 kg / (1.63 m * 1.63 m) = 27.09925 kg/m^2."
2146,6,Body Mass Index (BMI),physical,decimal,pmc-5177698-1,Extracted,"The 7-year- and 6-month-old boy was born from a 29-year-old mother. The family had no consanguinity and no specific remarkable family history of seizure, delayed development, hypotonia, or language delay. His 24-month-old younger brother was healthy.
The patient was transferred from a local clinic for the evaluation of heart murmur at 9 days of life. At that time, a large patent ductus arteriosus (PDA) 4.2 mm in size, a small secundum atrial septal defect, and a small apical muscular ventricular septal defect were detected by Doppler echocardiography. The patient weighed 3.3 kg (less than 3rd percentile) and had a length of 53.1 cm (10th–25th percentile). During the follow-up, he still showed poor weight gain and a short stature, with microcephaly. At the age of 14 months, he weighed 7.4 kg (less than 3rd percentile) and had a length of 75.9 cm (10th–25th percentile) and a 43.8 cm head circumference (less than 3rd percentile). PDA ligation was done at the age of 4 months. According to the parents, the patient had a delayed gross motor milestone from head control. The Bayley study performed at the age of 6 and 24 months showed a significant delay in both the motor and mental aspects, respectively. The brain magnetic resonance imaging (MRI) that was done at the age of 5 months showed mild ventriculomegaly in the left lateral ventricle, and an arachnoid cyst ().
When the patient was 5 years and 3 months old, he was admitted to the hospital due to afebrile generalized seizure. Before the admission, he had had recurrent febrile seizures since he was 12 months of age, with a frequency of 2 to 4 times per year, with a semiology of ocular deviation to the upward and generalized tonic-clonic type lasting for 30–60 seconds. During the patient's hospital stay, brain imaging and electroencephalography (EEG) were done (, ). The interictal EEG showed moderate abnormality with intermittent bifrontal sharp waves, which were sometimes generalized (). As the baby's mother refused antiepileptic drugs medication, the natural course was observed without medication. At that time, the patient still showed severe global developmental delay, remarkable hypotonia, a short stature, and dysmorphic features such as microcephaly; small, low-set ears; dark, straight eyebrows; deep-set eyes; flat nasal bridge; midface hypoplasia; and a small, pointed chin (). The previous diagnostic work-up done at other hospitals, including the conventional chromosomal analysis, revealed no definite causes. As such, array-CGH analysis was done. The patient was rebrought to the hospital for the recurrence of seizure. An antiepileptic drug (valproic acid) was started at age 5 years and 11 months. The array-CGH analysis showed 1p36 deletion syndrome with a 9.15-Mb copy loss of the 1p36.33-1p36.22 region (). The FISH analysis confirmed the diagnosis (). At age 6 years and 10 months, the patient's developmental milestone showed 12 months of gross motor development, a 15-month fine motor status, an 18-month personal-social age, 18 months of language development, and a 16-month cognitive-adaptive status. He is now on a 120 mg valproic-acid twice a day (15 mg/kg/day) and has been seizure-free for 17 months.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [7.4, 'kg'], 'height': [75.9, 'cm']}",12.84542,12.20315,13.48769,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 75.9 cm, which is 75.9 cm * 1 m / 100 cm = 0.759 m. The patient's weight is 7.4 kg. The patient's bmi is therefore 7.4 kg / (0.759 m * 0.759 m) = 12.84542 kg/m^2."
2147,6,Body Mass Index (BMI),physical,decimal,pmc-3306553-2,Extracted,"Patient 2 (#726) () is a 12-year-7 month-old boy, first child of nonconsanguineous and healthy parents. He was born at term by caesarian after a pregnancy of normal course. His birth weight was 3,500 g (50th centile). He showed speech delay and three episodes of myoclonic seizures. Psychometric evaluation at 11 years recorded an IQ of 50. Array-CGH analysis (105 K) was normal. Physical examination at 11 years and 6 months showed: height 138 cm (25th centile), weight 35 kg (50th centile), OFC 54 cm (75th centile), triangular face, and long ears. His language was simple and he showed hyperactivity and abnormal behavior.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [35.0, 'kg'], 'height': [138.0, 'cm']}",18.37849,17.45957,19.29741,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 138.0 cm, which is 138.0 cm * 1 m / 100 cm = 1.38 m. The patient's weight is 35.0 kg. The patient's bmi is therefore 35.0 kg / (1.38 m * 1.38 m) = 18.37849 kg/m^2."
2148,6,Body Mass Index (BMI),physical,decimal,pmc-4396542-2,Extracted,"A 55-year-old male (height 170 cm and body weight 65.4 kg) was diagnosed with CAD in 2012 when he did not show anemia, apart from a slight increase in total bilirubin levels (2.2–3.0 mg/dL). One year later, after exposure to cold, he again visited a clinic and was found to be mildly anemic (Hb 8.0 g/dL); however, he was not systematically tested or treated. In his history he had inappropriate dietary intake but no drug use. In February 2014, he was hospitalized via emergency medical transport due to the fact that he was severely anemic (Hb 4.3 g/dL) as well as icteric, with a peripheral blood smear showing significant red blood cell agglutination (data not shown). A CT scan revealed no lymphadenopathy, but pulmonary edema, bilateral pleural fluid, and mild splenomegaly were noted. The laboratory data are summarized in . His cold agglutinin level was extremely high (1 : 16,834) and he had monoclonal M-proteins (IgM-kappa) in association with hypogammaglobulinemia (IgG, 584 mg/dL) and hypocomplementemia. In addition, he had megaloblastic anemia associated with low serum levels of vitamin B12 and folate. A bone marrow smear showed an increase in megaloblasts associated with dyserythropoietic features of polychromatic erythroblasts (), with an M/E ratio of 0.92; these data were compatible with a diagnosis of both hemolytic and megaloblastic anemia. No increase in the number of myeloma cells or lymphoma cells was noted. Bone marrow cells showed a normal karyotype (46 XY; 20/20). He was treated with a heated RBC transfusion (a total of 10 U) and received oral folate (5 mg/day × 3/day) and vitamin 12 (mecobalamin 500 μg × 3/day) but declined intravenous rituximab therapy. Unfortunately, this patient was discharged not for medical recovery but for his personal reasons and became lost to follow-up.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [65.4, 'kg'], 'height': [170.0, 'cm']}",22.62976,21.49827,23.76125,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 65.4 kg. The patient's bmi is therefore 65.4 kg / (1.7 m * 1.7 m) = 22.62976 kg/m^2."
2149,6,Body Mass Index (BMI),physical,decimal,pmc-6708912-3,Extracted,"Patient 3 was a 43-year-old man, height 173 cm, weight 80 kg, who was a nonsmoker with spondyloarthropathy secondary to ulcerative colitis and sclerosing cholangitis presenting with very severe neck pain that worsened on rotation and head tilt that required opioid medication. He was working full-time with a desk job and was not on sick leave. The duration of neck pain was 1–2 years but had recently increased over the past few months (VAS 6). He had no arm pain and his fine motor skills were good/normal. He could walk more than 1 km and his EMS was 18 points (normal). At physical examination, there were no signs of neuropathy or myelopathy. Images revealed osteoarthritis and destruction of the right AA joint (Fig. A, B). We performed C1–C2 fusion to relieve his neck pain and used a joint spacer to balance the head. Traction was applied during surgery but no preoperative skull traction was performed. At 4-months follow-up, the patient had no ongoing neck pain and bony fusion was confirmed with CT. At 1-year of follow-up, the patient was working full-time at the same job, and walking more than 1 km with an EMS of 17 points (normal), VAS for neck pain of 0, with fine motor skills that were good/normal and a global assessment of “symptoms improved after surgery”.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [80.0, 'kg'], 'height': [173.0, 'cm']}",26.72993,25.39343,28.06643,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 173.0 cm, which is 173.0 cm * 1 m / 100 cm = 1.73 m. The patient's weight is 80.0 kg. The patient's bmi is therefore 80.0 kg / (1.73 m * 1.73 m) = 26.72993 kg/m^2."
2150,6,Body Mass Index (BMI),physical,decimal,pmc-7482009-1,Extracted,"An 11-year-old boy admitted with vomiting, generalized edema, and hyperglycemia, which was preceded by 5 days of coryzal symptoms, lethargy, and oral aft without fever. He was admitted to another hospital with hypotensive syncope and severe vomiting (20 times/day), and intravenous hydration was initiated. His blood glucose was 13.8 mmol/L and urine glucose was +++ at admission. Initially, he was diagnosed with stress hyperglycemia and acute gastroenteritis. After one day, he was referred to our hospital because of his persisting symptoms and hyperglycemia. There was no specific indicative feature in his personal or family history. His weight was 30 kg (−1.02 SDS), height was 147 cm (+0.75 SDS), heart rate was 118/minute, and blood pressure was 90/40 mm/Hg, and generalized nonitching systemic edema was present on his physical examination.
The laboratory tests showed that severe hemoconcentration was present. His biochemical findings were as follows: white blood cell count: 1.8 × 109 L; hemoglobin: 184 g/L; hematocrit: 51.3%; sodium: 130 mmol/L; potassium: 4.8 mmol/L; chloride: 105 mmol/L; urea: 20 mmol/L; creatinine: 45 µmol/L; and blood glucose: 11.1 mmol/L. On arterial blood gas analysis, pH was 7.33 and HCO3 was 13.6 mmol/L (). On sepsis work-up, CRP was 3 mg/L, and urine, stool, and blood culture were negative. Respiratory virus panel PCR was positive for respiratory syncytial virus (RSV) and enterovirus.
Aggressive fluid replacement was initiated at admission due to hypotension. Although urine output was normal during the first two days of hospitalization, his diuresis was inadequate on the third day (0.3 cc/kg/hr), and so 3000 cc/m2 5% dextrose and 0.45% NaCl were administered as maintenance fluid therapy. The patient's serum albumin levels, as well as his globulin levels, were highly reduced because of capillary leak (). There was severe hypogammaglobulinemia at admission. Additional laboratory examinations were performed in order to make the differential diagnoses of generalized edema, hyperglycemia, hyponatremia, prerenal acute renal failure, hypoalbuminemia, and hemoconcentration. The urine analysis showed that the urine density was 1033, and the 24-hour urine protein test, blood lipids, and renal tubular tests were within normal limits excluding renal diseases. To eliminate congestive heart failure, chest radiography, electrocardiography, cardiac enzymes test, and echocardiography were performed and were all proven to be within normal limits. The patient's feces alpha-1 antitrypsin level was negative, and protein-losing enteropathies were excluded. Complement studies and lymphocyte subset analysis by flow cytometry were within normal ranges when compared to his age references.
After initial stabilization with intravenous fluid boluses and insulin infusion the first two days, the patient's generalized edema increased, albumin values dropped to 1.9 g/dL, he had diarrhea, and he gained 3 kg of weight. Subcutaneous insulin treatment started with a dose of 0.3 IU/kg/day at the end of the second day. Intravenous human albumin treatment was given on the 2nd, 4th, and 7th day of admission. On the fourth day, the patient was given the ISCLS diagnosis by ruling out other causes. Following the diagnosis, intravenous immunoglobulin (IVIG) treatment was given on two consecutive days (). His edema decreased on the fifth day, and he was deemed clinically well on the 7th day, weighing 29 kg. As for the systemic effects of ISCLS, there was seldom amount of free fluid in the abdomen, the diameter of the appendix was increased, and minimal pleural effusion was found bilaterally. There was no compartment syndrome, rhabdomyolysis, or pulmonary edema during the recovery period.
For the differential diagnosis of DM, his fasting serum glucose was 13.8 mmol/L, simultaneous C-peptide was 0.44 nmol/L, HbA1c was 64 mmol/mol, and urine ketone was positive. Antiglutamic acid decarboxylase, anti-insulin antibody, and islet cell antibody were negative. The patient harbors type 1 DM predisposing HLA II haplotypes as follows: DRB1∗0301, DRB1∗0302, and DRB1∗0201. Although there was no family history for DM, since his autoantibodies were negative, next-generation gene sequencing for 14 MODY genes including GCK, HNF1A, HNF4A, HNF1B, PDX1, CEL, KLF11, NEUROD1, PAX4, INS, and BLK was analyzed, and they were all negative. Whole exome sequencing of the patient for candidate genes is ongoing. At the 6th and 12th month marks, as well as at the last outpatient visit, his insulin dose was still 0.4 IU/kg/day and HbA1c was 40 mmol/mol.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [30.0, 'kg'], 'height': [147.0, 'cm']}",13.8831,13.18895,14.57726,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 147.0 cm, which is 147.0 cm * 1 m / 100 cm = 1.47 m. The patient's weight is 30.0 kg. The patient's bmi is therefore 30.0 kg / (1.47 m * 1.47 m) = 13.8831 kg/m^2."
2151,6,Body Mass Index (BMI),physical,decimal,pmc-5709897-1,Extracted,"A 15-year-old boy was referred to the neurodevelopmental clinic of our child and adolescent mental health services for a diagnostic assessment. He was assessed in the presence of his parents.
The primary concerns included difficulty in sustaining his concentration, organizing sequential tasks, completing tasks on schedule, being forgetful often, and easily distractible shifting to different tasks in quick succession. He was reported to be restless and fidgety in multiple settings including at school and home, with his difficulty being seated at his desk in classroom. He also encountered difficulties in waiting for his turn or in a queue and engaging in group activities. His symptoms were associated with significant impairment in his functioning at home and school. The rating scales from his parents as well as teachers (Conner's questionnaires) in addition to the school observation and occupational therapy group assessment reports supported the above findings. There were no pointers toward autistic traits or intellectual difficulties. Furthermore, there was no history suggestive of anxiety or mood symptoms.
He lives with his parents and two biological siblings. There is a family history of ADHD in one of his paternal cousin brothers (who has not been genetically tested). His antenatal history was uneventful. However, there were reported difficulties with sucking, feeding, and a low-pitched crying. He also appeared floppy though these difficulties eventually self-resolved. There were also delays in gross motor and language milestones, which he was eventually caught up with. There are no active physical health concerns currently. There is no history of seizure episodes.
During the assessment, he came across as a lively and boisterous boy who was warm and friendly. He made appropriate eye contact and expressed a range of facial emotions. However, he was constantly distracted by different environmental stimuli. He could not be engaged in a conversation on any specific topic beyond a few minutes since he kept losing thread of the conversation. There were no autistic traits elicited in history or during the interview.
On review of previous investigations, it was noted that genetic analysis fluorescent in situ hybridization technique was carried out, and it revealed chromosome 15 duplication (tested for the following constellation of clinical features: hypotonia, weak cry, and difficulties with sucking and feeding). No formal IQ testing has been carried out since he has been above average with his school lessons despite his attentional and behavioral difficulties, and there are no other pointers suggestive of intellectual or learning difficulties. Downslanting palpebral fissures were noted during the general examination. His height was measured to be 162.5 cm (14th centile) and he weighed 45.3 kg (8th centile) on the day of diagnostic assessment. His cardiovascular parameters (blood pressure and pulse rate) were within normal limits.
A diagnosis of ADHD and combined subtype was made based on the history, mental state examination, and other reports. His carers were psychoeducated regarding the disorder and different management options (pharmacological and nonpharmacological). Conners’ rating scale (parental version) was administered at baseline (t-score >70).[] The side effects of stimulant medication were discussed along with the potential benefits emphasizing that individuals with chromosomal mutations may tolerate stimulant medication differently. Taking this into account, it was decided to initiate him on 5 mg of methylphenidate, to be titrated upward gradually. It was also explained that we would be monitoring his growth at every visit (height and weight) along with his cardiovascular parameters (blood pressure and pulse rate). They were also provided self-help material on ADHD, and the parents were referred for parenting classes after their consent.
He was reviewed subsequently on multiple occasions. There was some initial increase in restlessness and agitation over the initial week. Fortunately, he later tolerated the medication reasonably well and no significant side effects were reported. The dose of methylphenidate was very gradually increased to 30 mg daily, and thereafter, he was shifted to longer acting preparation of methylphenidate, concerta-extended release 27 mg once daily to simplify the drug regimen. At a subsequent review 4 months from the index visit, Conners’ rating scale (parental version) was readministered (t-score <60) demonstrating a significant reduction in symptomatology.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.3, 'kg'], 'height': [162.5, 'cm']}",17.15503,16.29728,18.01278,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.5 cm, which is 162.5 cm * 1 m / 100 cm = 1.625 m. The patient's weight is 45.3 kg. The patient's bmi is therefore 45.3 kg / (1.625 m * 1.625 m) = 17.15503 kg/m^2."
2152,6,Body Mass Index (BMI),physical,decimal,pmc-4823429-2,Extracted,"A 54-year-old 175 cm tall man weighing 84 kg underwent right craniotomy for clipping of an unruptured middle cerebral artery aneurysm. A Spetzler catheter inserted at L4-5 interspace drained 100 mL of CSF, and was removed post-craniotomy. The patient did well initially, however, on POD 3, he developed a partial right third nerve palsy and lethargy. A Head CT revealed midline shift with an epidural air collection (). Re-exploration was performed to address the mass effect attributed to the epidural collection. At craniotomy, however, the dura and brain were depressed and not under pressure. Postoperatively, upright intracranial pressure (ICP) was -14 mmHg, and increased to 0 with supine positioning. Arteriography demonstrated no vasospasm; although the basilar artery was kinked (). A head CT revealed an oval shape midbrain (), consistent with brain sag. Two days after re-exploration, he was awake but confused, oriented to self, following only simple commands. His right pupil was dilated and nonreactive to light. He remained too lethargic to complain of positional headache but became more alert while supine.
Brain sag was confirmed by the constellation of persistent lethargy, third nerve palsy, radiographic findings and low ICP (0-3 mmHg). Seven days after aneurysm clipping, a L4-5 EBP was performed with 25 mL of blood. Within the hour, he became more awake and appropriate. Within four hours, he engaged in a telephone conversation and fully recovered to baseline neurological state. One day after EBP, he was ready for transfer to rehabilitation medicine and remained neurologically intact thereafter.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [84.0, 'kg'], 'height': [175.0, 'cm']}",27.42857,26.05714,28.8,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 175.0 cm, which is 175.0 cm * 1 m / 100 cm = 1.75 m. The patient's weight is 84.0 kg. The patient's bmi is therefore 84.0 kg / (1.75 m * 1.75 m) = 27.42857 kg/m^2."
2153,6,Body Mass Index (BMI),physical,decimal,pmc-8191267-1,Extracted,"A 68-year-old woman (165 cm; 64 kg) with no known allergies to medication and a past history significant for arterial hypertension, chronic bronchitis, ischemic heart disease (stent in the circumflex artery in 2017) and obstructive HOCM was scheduled to undergo an elective extended transaortic septal myectomy. Her usual treatment consisted of bisoprolol, torasemide, disopyramide, pantoprazol, acetylsalicylic acid and bronchodilators. She was referred to our hospital from another center following a diagnosis of HOCM manifesting clinically as intense dyspnea on exertion, occasional dizziness and episodes of chest pain extending to the left arm.
Preoperative ECG showed sinus rhythm (56 bpm), left ventricular hypertrophy (LVH) and repolarization abnormalities, while a cardiac MRI scan revealed a maximum left ventricular thickness of 19 mm. TTE showed findings suggestive of HOCM involving the anterior ventricular septum, with a maximal wall thickness of 20 mm, peak LVOT gradient of 144 mmHg, grade-2 diastolic dysfunction, normal systolic function, systolic anterior motion (SAM) with moderate mitral insufficiency (MI), biatrial enlargement and mild pulmonary hypertension.
Upon entry to the operating room, the patient was monitored for the following: arterial blood pressure by invasive monitoring through the left radial artery, ECG with ST-segment analysis, oxygen saturation through pulse oximetry, capnography, Bispectral Index (BIS™) monitoring to measure the hypnotic effects of anesthesia, Near-infrared spectroscopy (INVOS™ 5100C Cerebral/Somatic Oximeter, Covidien®), body temperature using an esophageal thermometer, central venous pressure and hourly urine output. When the patient arrived in the operating room, her arterial pressure was 145/69 mmHg and she had a heart rate of 72 bpm and oxygen saturation of 96%.
She was then given intravenous midazolam (2 mg), propofol (60 mg), fentanyl (150 μg) and rocuronium (50 mg). The trachea was intubated with 7.5 cuffed tube. Intraoperative TEE revealed severe hypertrophy (20 mm) of the intermuscular septum and LVOT obstruction with SAM associated with the mitral valve [] as well as a peak gradient between the left ventricle (LV) and the aorta (Ao) of 100 mmHg. Following the sternotomy, another measurement was taken from the surgical field using two catheters placed directly in the LV and the Ao respectively, revealing a gradient of 116 mmHg. Anesthesia was maintained with sevoflurane, fentanyl and rocuronium. As the patient displayed a tendency toward hypotension, she required single-dose boluses of phenylephrine and continuous perfusion of noradrenaline at a rate of 0.04 mcg/kg/min to achieve an average arterial pressure of >60 mmHg until cardiopulmonary bypass was performed. An extended transaortic septal myectomy was conducted without incident. When CPB was discontinued, the patient presented ventricular fibrillation, which resolved with amiodarone (300 mg) and 3 automated internal defibrillator shocks of 10 J. At this time, the patient entered sinus rhythm at 40 bpm and atrial and ventricular pacemaker electrodes were placed at a rate of 80 bpm. Postoperative TEE evidenced resolution of hypertrophy in the LVOT [], an LV-Ao gradient of 8 mmHg, mild MI, absence of iatrogenic ventricular septal defects and normal biventricular function. LV-Ao gradient measurement from the surgical field was 7 mmHg [], which closely resembled the value obtained using TEE and thereby confirmed that the intervention had been done successfully. Given the absence of complications associated with the surgical procedure CPB was terminated and the patient was shifted to the intensive care unit with stable hemodynamics. The traquea was extubated after 6 h and shifted to hospitalization ward after 24 h.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [64.0, 'kg'], 'height': [165.0, 'cm']}",23.50781,22.33242,24.6832,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 64.0 kg. The patient's bmi is therefore 64.0 kg / (1.65 m * 1.65 m) = 23.50781 kg/m^2."
2154,6,Body Mass Index (BMI),physical,decimal,pmc-5903093-1,Extracted,"A 59-year-old Japanese woman was admitted to our hospital for evaluation of muscle weakness. Hypertension had been detected at the age of 30 years. When she was 47, ADPKD was diagnosed because computed tomography showed polycystic kidneys and her father had this disease. At 53 years, primary aldosteronism was diagnosed after detection of hypokalemia and a left adrenal tumor. Spironolactone was administered. An angiotensin II receptor blocker (ARB; olmesartan at 40 mg/day) was added to treat hypertension, after which her blood pressure and serum potassium level were normalized despite discontinuation of spironolactone (Table ). At 58 years, tolvaptan therapy was started at 60 mg/day (morning and afternoon doses of 45 and 15 mg) to treat her renal disease (Table ; Fig. ). Hypertension became more severe after the initiation of tolvaptan. Although the dual action beta blocker/alpha-1 blocker carvedilol (15 mg/day), calcium channel blocker cilnidipine (20 mg/day), and ARB telmisartan (40 mg/day) were added, her hypertension was not controlled. Eight months after starting tolvaptan, muscle weakness and numbness of the lower limbs became problematic. At 12 months, she was admitted to our hospital.
On admission, the patient was 152 cm tall, weighed 61 kg, and had a blood pressure of 182/84 mm Hg. Laboratory tests revealed that serum creatinine was 1.1 mg/dL (eGFR: 39.7 mL/min/1.73 m2), urea nitrogen was 24 mg/dL, Na was 144 mmol/L, K was 2.5 mmol/L, and Cl was 99 mmol/L. Renin activity was < 0.2 ng/mL/h (normal: 0.3–2.3), and the aldosterone concentration was 130 ng/dL (normal: 3.0–15.0). Urinary K excretion was 65 mmol/day, Na excretion was 130 mmol/day, and Cl excretion was 120 mmol/day (Table ).
Before admission, hypokalemia was exacerbated after starting tolvaptan therapy, and her hypertension became refractory (Fig. ). The patient hoped to continue tolvaptan use. Therefore, a potassium supplement was administered, but her serum potassium only increased to 3.5 mmol/L. Tolvaptan was discontinued temporarily, and serum potassium increased to 4.0 mmol/L. Next, tolvaptan (60 mg/day) and spironolactone (50 mg/day) were administered concomitantly, but the serum potassium level dropped to 3.0 mmol/L. Subsequently, tolvaptan was tapered to a daily dose of 30 mg, and spironolactone was increased to a daily dose of 100 mg. Thereafter, serum potassium remained above 4.0 mmol/L, and control of the blood pressure improved.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.0, 'kg'], 'height': [152.0, 'cm']}",26.40235,25.08223,27.72247,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 152.0 cm, which is 152.0 cm * 1 m / 100 cm = 1.52 m. The patient's weight is 61.0 kg. The patient's bmi is therefore 61.0 kg / (1.52 m * 1.52 m) = 26.40235 kg/m^2."
2155,6,Body Mass Index (BMI),physical,decimal,pmc-3249579-2,Extracted,"A 16-year old male patient who was 172 cm in height and 73 kg in weight, and whose mother was diagnosed with Carney complex, had removal surgery of myxoma in the left atrium three years ago. He was diagnosed with Carney complex after presenting with a thyroid nodule, adrenal gland tumor, and sertoli cell tumor in the testicular gland. He also underwent left orchiectomy and left adrenalectomy two years ago. Afterwards, he had been under ambulatory follow-up monitoring for the thyroid nodule, pituitary adenoma, and Cushing's syndrome.
Pre-operative echocardiography confirmed a 34 × 24 mm sized myxoma in the posterior mitral valve leaflet of the left atrial posterior side, which is a rare location for myxomas to occur ( and ). It also showed mild eccentric aortic regurgitation with an ejection fraction of 66.2%. Sellar magnetic resonance imaging showed a 1 cm sized pituitary adenoma on the fossa floor. Before the operation, the department of endocrinology and neurology were consulted. Because results of a quadruple test showed no abnormality in the pituitary functions, it was discussed that there would be no problem to continue on with myxoma removal surgery.
The electrocardiography showed sinus bradycardia with sinus arrhythmia, and the chest radiography showed no active lung lesions. Upon arrival on to the operating room, the blood pressure was 130/80 mmHg, and the heart rated was 78 bpm. The electrocardiography, pulse oxymeter, and arterial blood pressure were monitored as fentanyl 200 µg, etomidate 20 mg, and rocuronium 50 mg were administered for anesthetic induction. The patient was a Cormack-Lehane grade I, allowing easy endotracheal intubation. Intra-operative blood pressure was maintained at 140-160/60-80 mmHg and heart rate was 80 bpm. The surgery was performed as a median sternotomy, and with a cardiopulmonary bypass a 3 cm friable mass with a broad stalk in the posterior wall of the left atrium was removed through the right atrium. After surgery, the patient was transferred under sedation to the intensive care unit for observation. The patient stabilized, and two days later he was transferred to the general ward.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [73.0, 'kg'], 'height': [172.0, 'cm']}",24.6755,23.44172,25.90928,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 172.0 cm, which is 172.0 cm * 1 m / 100 cm = 1.72 m. The patient's weight is 73.0 kg. The patient's bmi is therefore 73.0 kg / (1.72 m * 1.72 m) = 24.6755 kg/m^2."
2156,6,Body Mass Index (BMI),physical,decimal,pmc-4973067-1,Extracted,"The 6 year old female was born at term to consanguineous parents after uneventful pregnancy. Birth weight was 2800 g (−1.2 SD), length and occipitofrontal circumference at birth were not recorded. Other 3 male siblings are healthy with no symptoms suggestive of FBS and no other family member with diabetes mellitus. First hospitalization was at age 17 month for evaluation of inadequate weight gain and abdominal distension. Her weight was 6600 g (−5.3 SD), length 69 cm (−3.3 SD) and occipitofrontal circumference 43 cm (−2.6 SD). Physical examination showed hepatomegaly and doll-like face. Laboratory findings included high serum triglycerides, mildly elevated serum aspartate aminotransferase, alanine aminotransferase, low phosphorous and elevated alkaline phosphatase. She had polyuria >6 ml/kg/h, massive generalized aminoaciduria, phosphaturia and glucosuria. Serum ammonia, lactic acid, calcium, parathyroid hormone and 25-hydroxyvitamin D were normal (Table ). Abdominal ultrasound revealed hepatomegaly and minimal calcification of both renal calyces. Radiological findings included generalized osteopenia and rachitic changes. Genetic analysis showed that the patient is homozygous for the mutation R301X (C>T) in exon 7 of the GLUT2 gene. Treatment included anhydrous phosphate (Joulie’s) solution 5 ml given every 4 h, 5 times daily (0.75 g/24 h), alpha D3 drops (alphacalcidol) 1 µg/day, galactose-restricted diet and uncooked cornstarch 1.6 g/kg given every 6 h during night time to prevent hypoglycemia. Metabolic acidosis was mild and did not require treatment.
The clinical phenotype was characterized by improvement of growth parameters with age. Rickets resolved with normalization of serum phosphate, alkaline phosphatase and triglyceride. She still shows laboratory findings of renal tubular dysfunction including polyuria, massive aminoaciduria, glucosuria and phosphaturia.
At age 6 years, her weight was 18 kg (−0.8 SD) and height 107 cm (−1.6 SD) (Fig. ). Physical exam showed mild hepatomegaly and renal ultrasound showed resolution of calyceal calcifications.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [18.0, 'kg'], 'height': [107.0, 'cm']}",15.7219,14.9358,16.508,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 107.0 cm, which is 107.0 cm * 1 m / 100 cm = 1.07 m. The patient's weight is 18.0 kg. The patient's bmi is therefore 18.0 kg / (1.07 m * 1.07 m) = 15.7219 kg/m^2."
2157,6,Body Mass Index (BMI),physical,decimal,pmc-3036813-1,Extracted,"A previously healthy girl of Filipino descent, 2 years and 8 months old, had a 4-week history of rounding of her face, acne on her forehead, an increased appetite, and weight gain of 3.2 kg. Two weeks later, signs of virilization were noted. The maternal grandfather and his brother, both reported to be heavy smokers, died from lung cancer in their 50s. On admission, the patient weighed 16.7 kg (percentile, 95.7) and was 95 cm tall (percentile, 58). Her blood pressure was 142/92 on admission. She had a Cushingoid build with round moon facies and truncal obesity. No abdominal masses were palpable. She had acne on the forehead and increased oiliness of the facial skin. There was no axillary hair and no breast development. The genitalia showed signs of virilization. Laboratory tests revealed 5-dehydroepiandrosterone at 4546 ng/dL (normal, 19–42), testosterone at 84 ng/dL (normal, < 10), and cortisol at 35.1 μg/dL at 8:00 am and 32.3 μg/dL at midnight (normal, < 5). Abdominal computed tomography confirmed the finding of a 4.5 × 4.0 × 4.0 cm right adrenal mass. The mass, involving the right adrenal gland, displaced the kidney inferiorly. The mass was smoothly marginated and appeared fairly vascular with heterogeneous enhancement.
The patient underwent exploratory surgery through a right subcostal incision. The mass was removed intact without violation of its capsule. Postoperatively, her Cushingoid features resolved, and she lost 1.4 kg in 3 months despite adequate oral hydrocortisone therapy. All of her laboratory markers normalized. To date, there has been no evidence of a recurrence clinically, biochemically, or sonographically.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [16.7, 'kg'], 'height': [95.0, 'cm']}",18.50416,17.57895,19.42937,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 95.0 cm, which is 95.0 cm * 1 m / 100 cm = 0.95 m. The patient's weight is 16.7 kg. The patient's bmi is therefore 16.7 kg / (0.95 m * 0.95 m) = 18.50416 kg/m^2."
2158,6,Body Mass Index (BMI),physical,decimal,pmc-6971472-1,Extracted,"A 56-year-old woman was admitted to our emergency department (ED) with disturbance of consciousness and respiratory failure. She had influenza-like symptoms including cough and fatigue without fever 2 days prior to presentation. She did not have a medical history but took an over-the-counter drug that contains ibuprofen for headache.
The patient's height was 139 cm and weight was 29.0 kg. Her vital signs were: blood pressure, 131/78 mm Hg; heart rate, 78 b.p.m. and regular; axillary temperature, 35.1°C; respiratory rate, 30 breaths/min; SpO2, 85% with oxygen delivered through a face mask (3 L/min); and a Glasgow Coma Scale score of E3V3M5 on admission.
Rapid viral testing was positive for influenza A virus. Significant laboratory results included hypoglycemia (serum glucose, 48 mg/dL), transaminitis (aspartate aminotransferase [AST] 12,548 IU/L and alanine aminotransferase [ALT] 5,725 IU/L), hyperbilirubinemia (total bilirubin 3.5 mg/dL and direct bilirubin 1.6 mg/dL), elevated international normalized ratio (INR; 3.16), hyperammonemia (ammonia 102 μg/dL), lactic acidosis (7.0 mmol/L), azotemia (blood urea nitrogen 55 mg/dL), hypercreatinemia (serum creatinine 2.32 mg/dL), hyponatremia (134 mmol/L), hyperkalemia (6.7 mmol/L), hypolipidemia (total cholesterol 114 mg/dL and triglyceride 29 mg/dL). Carnitine was normal (223 μmol/L). Her liver function was normal 5 days before presentation.
The head computed tomography (CT) revealed no specific findings, although the head magnetic resonance imaging showed hyperintense signals at the bilateral globus pallidus in diffusion-weighted images and fluid attenuation inversion recovery (FLAIR)-weighted images and a hyperintense signal at the left front parietal lobe in FLAIR-weighted images (Fig. ). Abdominal CT revealed fatty and enlarged liver. Chest CT showed diffuse alveolar type infiltrates in the patient's right middle lobe with air bronchograms and respiratory muscle loss. Based on these findings, we diagnosed the patient with RS induced by influenza A virus and pneumonia. The clinical course of the patient is shown in Figure . She was intubated and placed on mechanical ventilation in the ED then transferred to the intensive care unit for supportive care. She was treated with prednisolone (500 mg/day for 3 days) and peramivir (100 mg/day for 5 days) for influenza encephalopathy. The patient's liver function gradually improved with supportive care, fresh frozen plasma, and vitamin K. Her transaminase trended down from AST 7,546 IU/L and ALT 4,127 IU/L on day 2, to AST 85 IU/L and ALT 704 IU/L on day 7, and to AST 23 IU/L and ALT 169 IU/L on day 14 of hospitalization. Her INR trended down from 3.16 on day 1, to 1.28 on day 7, and to 1.07 on day 14. A tracheostomy was carried out on day 12 because of respiratory insufficiency type II due to muscle atrophy with chronic malnutrition.
On 14 day, the patient's condition had dramatically improved, with no abnormal neurological findings. Her appetite returned to normal and anorexia resolved. Her total duration of hospital stay was 71 days, and she was transferred to a rehabilitation hospital without neurological deficits.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [29.0, 'kg'], 'height': [139.0, 'cm']}",15.00958,14.2591,15.76006,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 139.0 cm, which is 139.0 cm * 1 m / 100 cm = 1.39 m. The patient's weight is 29.0 kg. The patient's bmi is therefore 29.0 kg / (1.39 m * 1.39 m) = 15.00958 kg/m^2."
2159,6,Body Mass Index (BMI),physical,decimal,pmc-6036688-1,Extracted,"A 52-year-old Chinese woman presented to our hospital in September 2012 with a complaint of recurrent renal stones for 6 years. The renal stones were first discovered at a local hospital 6 years ago and then she underwent bilateral ureteroscopic lithotomy and ultrasonic lithotripsy several times, but the calculus still relapsed and her serum creatinine gradually increased to 240 to 300 umol/L. She was a teacher living with her husband and two children, all healthy, in a small city. She did not smoke tobacco or consume alcohol. She had no significant past medical history, she had not suffered from any infectious disease, and she did not suffer from any chronic illness. There was no family history of similar disease or any other chronic illness. There was no history of allergy to any food or drugs. On physical examination: temperature (T) 37.5 °C, pulse (P) 82/minute, respiratory rate (R) 20/minute, blood pressure (BP) 130/80 mmHg, weight (W) 51 kg, and height (H) 154 cm. Respiratory movement and cardiac examination were normal. On abdominal examination no masses or tenderness were noted on both light and deep palpation. Her liver and spleen were not palpable. A sensory and motor system examination did not reveal any abnormality. Her neurological reflexes were normal. A routine urine examination showed: white blood cell 87/hpf (WBC2+), red blood cell 34/hpf (RBC2+), and pH 7. 0. A routine blood test showed: hemoglobin (Hb) 95 g/L. Her serum potassium was 3.2 mmol/L, calcium 2.92 mmol/L, phosphate 1.3 mmol/L, carbon dioxide combining power (CO2CP) 17.8 mmol/L, creatinine 249 μmol/L, serum parathyroid hormone (PTH) 1147 pg/ml (Table ), 25-hydroxyvitamin D3 level 42.98 nmol/L with reference range (RR) of 47.7–144 nmol/L, 24-hour urinary calcium 8.98 mmol/day (RR, 2.5–7.5 mmol/day), and 24-hour urine potassium 26.8 mmol/day. Liver and thyroid functions were all normal. Urine culture showed the presence of Escherichia coli. Renal ultrasound showed multiple stones, cysts, and calcified lesions. Computed tomography (CT) of her kidney showed MSK and polycystic kidney disease (Fig. ). Ultrasonography of her thyroid and parathyroid showed two hypoechoic nodules in the right lobe of her thyroid with the larger one of 26 × 18 mm. She was diagnosed as having MSK complicated with tertiary hyperparathyroidism and underwent right parathyroidectomy on September 18, 2012. Histopathologic examination revealed adenomatous hyperplasia of parathyroid glands (Fig. ). After surgery, her serum potassium was 3.3 mmol/L, calcium 2.81 mmol/L, phosphate 1.01 mmol/L, CO2CP 16.1 mmol/L, PTH 742.5 pg/ml, and serum creatinine 231 μmol/L (Table ). The oral form of iron and calcitriol was administered.
In March 2013, 6 months after resection of her right parathyroid glands she was re-hospitalized because of generalized bone pain of 1 month’s duration. A routine urine examination showed: white blood cell 45/hpf (WBC1+), red blood cell 27/hpf (RBC1+), and pH 7. 5. A routine blood test showed: Hb 88 g/L. Her serum potassium was 3.1 mmol/L, calcium 2.83 mmol/L, phosphorus 1.21 mmol/L, CO2CP 19.7 mmol/L, creatinine 265 μmol/L, and PTH 1378 pg/ml (Table ). Her 24-hour urinary calcium was 8.5 mmol/L and 24-hour urinary potassium 29.6 mmol/L. A bone scintigraphy for whole body with 99mTc revealed increased activity in skull, rib, and sternum (Fig. ). Parathyroid and thyroid ultrasound showed multiple hypoechoic masses in left lobe, with largest ones being 25 × 23 mm and 22 × 20 mm. She was diagnosed as having MSK and tertiary hyperparathyroidism and underwent left lobe parathyroidectomy on March 27, 2013. A pathological examination of the resected parathyroid tissue showed parathyroid nodular hyperplasia (Fig. ). After surgery, her serum calcium was 2.25 mmol/L, phosphorus 1.07 mmol/L, potassium 3.7 mmol/L, CO2CP 16.8 mmol/L, PTH 47.81 pg/ml, and creatinine 257 μmol/L (Table ). Subsequently she was prescribed with oral form of iron and calcitriol at the time of discharge; later, she did not return for the scheduled follow-up visits.
On July 7, 2016, 4 years after parathyroidectomy she was readmitted to our hospital with the complaint of dizziness. A physical examination showed pale appearance, visible thyroid surgery scar, and mild swelling of both lower extremities. A routine urine analysis showed: white blood cell 41/hpf (WBC +) and pH 7.0. A routine blood test showed: Hb 76 g/L, potassium 4.0 mmol/L, calcium 2.09 mmol/L, phosphorus 2.37 mmol/L, CO2CP 15.6 mmol/L, serum creatinine 766 μmol/L, and PTH 766.4 pg/ml (Table ). Renal ultrasound showed MSK, multiple stones in both kidneys, and polycystic kidney disease. She was diagnosed as having MSK and tertiary hyperparathyroidism and underwent renal replacement therapy (hemodialysis). She was started on replacement therapy. At 1-year follow-up, she was undergoing hemodialysis twice a week. A routine blood test showed: Hb 80 g/L. A routine urine analysis showed: PH 7.5 and protein positive (Pro2+). Her serum potassium level was 4.2 mmol/L, calcium 2.22 mmol/L, phosphorus 1.53 mmol/L, CO2CP 26.1 mmol/L, creatinine 619 μmol/L, and PTH 546 pg/ml.
Given the key role of the GDNF–RET interaction in kidney and urinary tract development, anomalies in these molecules are reasonable candidates for explaining a disorder such as MSK. However, mutations in RET proto-oncogene are also present in 97% of individuals with multiple endocrine neoplasia (MEN) 2A (MEN2A). In order to explore the possible genetic mechanisms, we analyzed the GDNF and RET genes in this patient. After obtaining informed consent from our patient, genomic DNA was extracted from peripheral blood leukocytes by standard phenol–chloroform procedures. All 20 exons and flanking splice sites of the GDNF and RET genes were amplified by polymerase chain reaction (PCR) with the primers listed in Table . Mutations were identified by direct sequencing of PCR products on an ABI 3730xl automated sequencer (Applied Biosystems, USA). Two RET polymorphisms were found in this patient, one was nonsynonymous c.2071G>A (G691S; rs1799939) located in exon 11 (Fig. ); the other was synonymous c.2712C>G (p.S904S; rs1800863) located in exon 15 (Fig. ). No mutation was found in the GDNF gene. Both parents of our patient are deceased. Further genetic testing of her husband, daughter, and sister were all negative for this polymorphism.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [51.0, 'kg'], 'height': [154.0, 'cm']}",21.50447,20.42925,22.57969,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 154.0 cm, which is 154.0 cm * 1 m / 100 cm = 1.54 m. The patient's weight is 51.0 kg. The patient's bmi is therefore 51.0 kg / (1.54 m * 1.54 m) = 21.50447 kg/m^2."
2160,6,Body Mass Index (BMI),physical,decimal,pmc-5814789-1,Extracted,"Written informed consent was obtained from the patient for this case report.
A 67-year-old man (170 cm, 71 kg) was admitted to our hospital to undergo laparoscopic colectomy for rectal cancer. He had no significant past medical history including bleeding disorder, and his family history was also unremarkable. Preoperative laboratory tests showed an abnormal coagulation profile. Although his aPTT and platelet count were normal (29.6 s and 23.1 × 104 μl, respectively), his PT was prolonged. PT was 43.4 s and PT-INR was 3.58 (normal range, 0.8–1.2). He did not suffer from liver disease, and laboratory data for liver function were normal. Given his high PT-INR with normal aPTT, FVII deficiency was suspected. A following laboratory test of coagulation factors showed that only FVII activity was significantly decreased to 1.4 % of normal. Since he was not taking any drugs that inhibit FVII activity and had no FVII inhibitor, he was diagnosed with congenital FVII deficiency.
We planned anesthetic management by general anesthesia without epidural anesthesia for his surgery to avoid bleeding associated with an epidural block procedure. Fresh frozen plasma (FFP) or rFVIIa was not transfused preoperatively. In the operating room, an electrocardiogram, noninvasive blood pressure, percutaneous oxygen saturation, and nasopharyngeal temperature were monitored. Radial artery pressure was also monitored. General anesthesia was induced with propofol (3.0 μg ml−1 via target-controlled infusion (TCI)) and remifentanil (0.3 μg kg−1 min−1), and then, the trachea was intubated following administration of rocuronium. Anesthesia was maintained with propofol (2.0–3.0 μg ml−1 via TCI), remifentanil (0.1–0.3 μg kg−1 min−1), rocuronium (5.0–7.0 μg kg−1 min−1), and oxygen-in-air gas mixture.
During the perioperative period, FVII activity and PT-INR were monitored. PT-INR and FVII activity during the clinical course are summarized in Table . Since FVII activity and PT-INR were 1.5 % of normal and 3.66, respectively, before starting surgery, 1 mg of rFVIIa (15 μg kg−1), which is recommended by the manufacturer for patients with congenital FVII deficiency, was intravenously administered immediately prior to surgery. Then, surgery was started. It has been suggested that FVII activity of less than 10 % is associated with bleeding complications [], and since the half-life of rFVII is 2–4 h, we checked FVII activity during surgery every 2 h to maintain FVII activity above 10 %. Two hours after administration of rFVIIa, FVII activity was 205.7 % of normal, and PT-INR was normalized to 0.9. The surgery was uneventfully completed in 3 h and 46 min. Since FVII activity and PT-INR were 86.8 % and 0.89, respectively, after completion of surgery (4 h after administration of rFVIIa), additional rFVIIa or FFP was not transfused. Blood loss was 15 ml, and bleeding/oozing was not observed. Since hemoglobin at the end of the surgery was 12.1 g/dL, blood was also not transfused. After the surgery, fentanyl-based intravenous patient-controlled analgesia (iv-PCA) was started for postoperative pain management. The iv-PCA regimen was as follows: a solution of 1400 μg fentanyl and 2.5 mg droperidol mixed with physiological saline to a total volume of 100 ml, 1 ml of bolus dose, 2 ml h−1 of basal infusion, and 15 min of a lockout time. The patient was transferred to the general ward in a stable condition without any sign of hemorrhage.
The amount of drainage from the pelvic tube was 50 ml on postoperative day (POD) 1, but it increased to 125 ml and became bloody on POD 2. Therefore, 1 mg of rFVIIa was administered intravenously on POD 2. However, FVII activity and PT-INR were 1.7 % of normal and 2.93, respectively, and the fluid from the pelvic tube was still bloody on POD 3. Therefore, rFVIIa was repeatedly administered every 8 h until POD 4. Since the amount of drainage from the pelvic tube was decreased to 55 ml and the drainage had become serous fluid on POD 4, the pelvic drainage tube was removed on POD 4. His postoperative pain was controlled well by iv-PCA, and the pain intensity score at rest was 0–2 of 10 in numeric rating scale through the postoperative period. The patient was discharged without any episode of bleeding or thrombosis on POD 10.
Although congenital deficiency of FVII increases the risk of posttraumatic and postoperative bleeding [], it is difficult to predict the perioperative risk of bleeding due to a poor correlation between FVII activity and severity of bleeding in patients with congenital FVII deficiency []. A recent retrospective study has suggested that FVII activity of less than 10 % is a risk factor for bleeding complications associated with a surgical procedure []. In our case, since preoperative FVII activity and PT-INR were 1.4 % and 3.58, respectively, we planned to substitute FVII.
Prothrombin complex concentrates, FFP, and rFVIIa have been used to increase plasma FVII level. Administration of rFVIIa has become the most widely accepted therapeutic option for congenital FVII deficiency in surgical settings because no human serum or proteins are used in the production of rFVIIa []. National guidelines regarding the use of blood products in Japan recommend administration of each coagulation factor concentrate rather than FFP if it is available. There are several reports showing the effectiveness of administration of rFVIIa for perioperative coagulation management of a patient with congenital FVII deficiency [, ].
While the optimal regimen for perioperative administration of rFVIIa has still not been established, the recommended dose range of rFVIIa for general surgery is 15–30 μg kg−1 every 4–6 h until hemostasis is achieved []. At least 10 % of FVII activity would be needed for hemostasis []. In our case, the decision to administer rFVIIa was made on the basis of assessment of FVII activity and PT-INR. Accordingly, bolus administration of 15 μg kg−1 of rFVIIa was sufficient to maintain FVII activity above 10 %, and additional administration of rFVIIa was not needed during surgery. Since the time course of FVII activity after rFVIIa administration is different in each patient [], the measurement of FVII activity would be useful for the determination of the dose and timing of rFVIIa administration for each patient.
Possible complications of replacement therapy with rFVIIa are thrombosis and production of antibodies against FVII [, ]. A previous systematic review showed that rFVIIa dose-dependently increased the risk of arterial thromboembolic events in patients who received a placebo or rFVIIa at doses of less than 80 μg kg−1, 80 to 120 μg kg−1, or more than 120 μg kg−1 []. Since the dose we administered (15 μg kg−1), which is recommended for congenital FVII deficiency, is lower than the doses used in that study, the risk for thromboembolic events in our case might have been relatively low. However, since surgical stress is a well-known risk factor for thrombosis, administration of rFVIIa during surgery may increase the incidence of thromboembolic events. The measurement of the FVII activity and PT-INR may be helpful for preventing overdose administration. Recently, continuous infusion of rFVIIa has been used to maintain the appropriate plasma concentration of FVII during surgery []. It has been shown that continuous infusion is safe, effective, well-tolerated, and cost-effective compared to bolus administration. However, bolus administration rather than continuous infusion is recommended in Japan.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [71.0, 'kg'], 'height': [170.0, 'cm']}",24.56747,23.3391,25.79584,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 71.0 kg. The patient's bmi is therefore 71.0 kg / (1.7 m * 1.7 m) = 24.56747 kg/m^2."
2161,6,Body Mass Index (BMI),physical,decimal,pmc-6937415-1,Extracted,"We report a 15-year-old girl who presented with recurrent headaches, arterial hypertension, and a systolic murmur.
Echocardiographic examination in a medical practice had revealed a potential coarctation of the aorta.
The patient had no history of serious illness.
There were no medically relevant aspects from the patient’s personal history. Other than arterial hypertension and coronary artery disease in the patient’s grandfather, there was no known cardiac disease within the family.
The patient presented in good general condition. Body weight was 61 kg and height were 172 cm. Her blood pressure in the right arm with 144/86 [MAP (mean arterial pressure) 110 mmHg] was significantly higher than that in the left arm [118/82 (MAP 96) mmHg] and of the right leg [118/72 (MAP 91) mmHg]. We consistently felt an unequal pulse between the right and left radial arteries (right stronger than left). A 2/6 systolic murmur was identified ventrally in the second and third left intercostal space, and, less prominently, dorsally between the shoulder blades. All other aspects of the physical examination were normal.
No laboratory examinations were done in the diagnostic work-up.
Echocardiography and cardiac MRI revealed a hypoplastic native aortic arch with a bi-carotid trunk and a segment just proximal of the left subclavian artery which was stenosed by 75% ().",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.0, 'kg'], 'height': [172.0, 'cm']}",20.61925,19.58829,21.65021,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 172.0 cm, which is 172.0 cm * 1 m / 100 cm = 1.72 m. The patient's weight is 61.0 kg. The patient's bmi is therefore 61.0 kg / (1.72 m * 1.72 m) = 20.61925 kg/m^2."
2162,6,Body Mass Index (BMI),physical,decimal,pmc-7937578-1,Extracted,"The patient was a 71-year-old woman (body weight, 49 kg; height, 148 cm) with a history of hypertension. THA was performed due to osteoarthritis of the hip using a posterolateral approach. General anesthesia was maintained by propofol (TCI, 2.3–3.3 μg/mL) and remifentanil (0.15 μg/kg/h) with stable hemodynamics. A total of 200 μg of fentanyl was used during surgery. Postoperatively, the patient developed mild pain upon movement in the outer side of the thighs but did not require additional pain management. The patient was able to start using a walker and increase loading on the affected side from POD1, with a Bromage score of 0 (Table ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [49.0, 'kg'], 'height': [148.0, 'cm']}",22.37034,21.25182,23.48886,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 148.0 cm, which is 148.0 cm * 1 m / 100 cm = 1.48 m. The patient's weight is 49.0 kg. The patient's bmi is therefore 49.0 kg / (1.48 m * 1.48 m) = 22.37034 kg/m^2."
2163,6,Body Mass Index (BMI),physical,decimal,usmle-8904,Extracted,"A 62-year-old Caucasian man visits his primary care provider with recurrent episodes of moderate to severe abdominal pain, nausea, and anorexia for the past 2 years. Additional complaints include constipation, steatorrhea, weight loss, polyphagia, and polyuria. His personal history is relevant for a 2-year period of homelessness when the patient was 55 years old, cigarette smoking since the age of 20, alcohol abuse, and cocaine abuse for which is currently under the supervision of a psychiatry team. He has a pulse of 70/min, a respiratory rate of 16/min, a blood pressure of 130/70 mm Hg, and a body temperature of 36.4°C (97.5°F). His height is 178 cm (5 ft 10 in) and weight is 90 kg (198 lb). On physical examination, he is found to have telangiectasias over the anterior chest, mild epigastric tenderness, and a small nodular liver.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [90.0, 'kg'], 'height': [178.0, 'cm']}",28.4055,26.98522,29.82578,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 178.0 cm, which is 178.0 cm * 1 m / 100 cm = 1.78 m. The patient's weight is 90.0 kg. The patient's bmi is therefore 90.0 kg / (1.78 m * 1.78 m) = 28.4055 kg/m^2."
2164,6,Body Mass Index (BMI),physical,decimal,pmc-5564175-1,Extracted,"The first patient was a 57-year-old man (weight: 89 kg, height: 174 cm), with a traumatic cervical herniation of the nucleus pulposus, scheduled for an anterior cervical discectomy and interbody fusion due to weakness in both hands and neck pain. He was an alcoholic and smoker, but did not have any other underlying disease. His neck extension was slightly limited because of the brace and instability, and his Mallampati score was Class III. Therefore, we prepared alternative approaches to intubation such as a FOB. However, we did not perform awake intubation because the patient was very nervous, compliance was poor, and the limitation of neck movement was not severe. Total intravenous anesthesia was administered using remifentanil and propofol for using evoked potential monitoring. We injected 80 mg of 2% lidocaine for reducing propofol injection pain and to control vital sign reactions to intubation. After setting the target effect site concentration of remifentanil at 3.0 ng/ml and that of propofol at 3.0 µg/ml, we initiated anesthetic infusion and administered 10 mg of vecuronium for muscle relaxation.
After the patient lost consciousness and paralyzed, we attempted conventional endotracheal intubation with a direct laryngoscope. However, no part of the uvula was visible and the patient exhibited a traumatic cervical lesion. Since we could not hyperextend the neck drastically, we attempted FOB-guided intubation. However, it was not easy to approach to trachea through both the mouth and nose, and two trials of endotracheal intubation failed, even after the introduction of a FOB into the trachea. There was uncertainty regarding depth sufficiency of the introduced FOB owing to large amounts of secretion and blood, and because it was difficult to distinguish the vocal cords from the carina. The tube was then advanced into the esophagus, instead of the trachea, and we decided to apply an ILMA that was successfully placed after four attempts. Ventilation via ILMA was effective. Following this, a silicone wire-reinforced tracheal tube was inserted via the blind technique; however, it could only be positioned in the esophagus despite several attempts. Finally, we attempted an ILMA and a FOB combination approach. The tip of the FOB was placed into the wire-reinforced ILMA tracheal tube and inserted through the ILMA. It approached the vocal cords with ease, and after arrival at 3 cm above the carina, the tube was railroaded into the trachea. In the process of railroading, we utilized a conventional guide wire stick (e.g. a stylet) instead of an ILMA stabilizer rod. The distance from the external opening of the ILMA to the vocal cord was barely 3-4 cm shorter than the endotracheal tube (ETT). Since, it was unclear if the ETT was in the trachea after removal of the FOB, we had to push the external tip of the ETT deeper using other methods prior to removing the FOB. Furthermore, our stabilizer rod was too short to push the ETT, and immobilization of the ETT when removing the FOB or ILMA was compromised. Therefore, we used a stylet when railroading the ETT (when the FOB was in place) deeper and for maintaining the position of the ETT when removing the FOB.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [89.0, 'kg'], 'height': [174.0, 'cm']}",29.39622,27.92641,30.86603,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 174.0 cm, which is 174.0 cm * 1 m / 100 cm = 1.74 m. The patient's weight is 89.0 kg. The patient's bmi is therefore 89.0 kg / (1.74 m * 1.74 m) = 29.39622 kg/m^2."
2165,6,Body Mass Index (BMI),physical,decimal,pmc-2803961-1,Extracted,"Mrs. S., a 46-year-old woman from Azerbaijan who had lived in Germany for the past eight years, had always been healthy and had never been under the care of a general practitioner. In November she visited a general practitioner complaining of right upper abdominal pain with no radiation. The pain, which was described as pressing in character, had been present for about three months and was intermittent. There was no nausea, vomiting, weight loss, melaena, change in bowel habit, urinary symptoms, or fever. The patient denied alcohol abuse and said that she was a nonsmoker and took no regular medication.
Blood pressure 140/80 mmHg, weight 75 kg, height 170 cm. Heart and lungs normal to percussion and auscultation. No lymph node enlargement. Abdomen slightly obese and soft. Tenderness present in the right upper abdomen. Bowel sounds normal. Renal angles clear. The clinical findings did not indicate a need for immediate hospital admission. On the basis of the history and the findings at the initial consultation, a series of laboratory tests and an ultrasound scan of the abdomen were ordered.
Relevant abnormal laboratory test results: C-reactive protein 108 mg/l (normal range < 5 mg/l), erythrocyte sedimentation rate 91 mm after two hours (normal range < 20 mm). The following values were within normal limits: blood count, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltransferase, alkaline phosphatase, creatinine, bilirubin, serum electrolytes. Sonography showed an irregularly echogenic, partially calcified septate cystic structure in segment VIII of the liver (Fig. ). No other abnormalities were apparent. In view of the sonographic findings, the radiologist arranged for the immediate performance of a contrast-enhanced computed tomographic scan of the abdomen. This showed a circumscribed rounded lesion measuring 5.8 × 4.7 × 5 cm in hepatic segment VIII (Fig. ). The lesion showed a thick rim of calcification and a suggestion of fine septa with no affinity for contrast medium. The liver was otherwise homogeneous and of normal appearance. The other parenchymal abdominal organs appeared normal and there were no enlarged lymph nodes.
Additional laboratory tests showed an antibody titre of 1:512 for E. granulosus and the presence of anti-E. multilocularis IgG. A western blot analysis was positive for Echinococcus granulosus and negative for Echinococcus multilocularis. After being informed about possible treatment options, the patient was referred to the university hospital. There she underwent hepatic segmental resection and cholecystectomy. Histological preparation of the material removed at operation showed caseating necrosis with a moderately severe, partly giant-cell, inflammatory reaction at the margin of an echinococcal cyst. There was no evidence of malignancy. The histological appearance was consistent with Echinococcus granulosus infection. Moderately severe chronic cholecystitis with moderate fibrosis of the gallbladder wall and cholecystolithiasis were also present. The skin sutures were removed on the tenth postoperative day. As a result of wound dehiscence, the wound healed partly by second intention. The patient was free of symptoms. Follow-up treatment with Eskazole® 400 mg (active ingredient: albendazole) b.i.d. was given. The patient's subsequent progress was without complication.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [75.0, 'kg'], 'height': [170.0, 'cm']}",25.95156,24.65398,27.24914,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 75.0 kg. The patient's bmi is therefore 75.0 kg / (1.7 m * 1.7 m) = 25.95156 kg/m^2."
2166,6,Body Mass Index (BMI),physical,decimal,pmc-4124700-1,Extracted,"An 8-year-old Japanese boy developed a generalized convulsion that lasted for 5 min and occurred while he was playing on November 10, 2012. When he was admitted to our hospital by an ambulance, he was conscious and afebrile (temp. 36.3°C). His body height was 120 cm, body weight 21.3 kg, blood pressure 96/42 mmHg, heart rate 92/min, and SpO2 100% at room air. He was neither anemic nor icteric and did not exhibit hepatosplenomegaly, without ataxia, deafness, or mental retardation. No signs showing intracranial hypertension were noted. His past history was unremarkable, except for complaining of muscle weakness after playing football. His family history revealed that his older brother was treated with an anticonvulsant because of attention-deficit hyperactivity disorder. The patient's laboratory findings were white blood cell counts 11,000/μL, Hb 14.1 g/dL, platelet counts 485,000/μL, and serum C-reactive protein 0.04 mg/dL. As summarized in , his renal function was normal, but the electrolyte assay revealed hypokalemia and blood gas analysis showed the presence of metabolic alkalosis. Endocrine function analyses were within normal with the following values: TSH 3.48 (normal 0.35–4.94) μU/mL, free T3 4.65 (normal 1.73–3.71) pg/mL, free T4 1.41 (normal 0.70–1.48) ng/dL, ACTH 9.5 (normal 7.2–63.3) pg/mL, cortisol 8.2 (normal 4.5–21.1) μg/dL, and aldosterone 14.6 (normal 3.6–24) ng/dL; however, high renin activity was noted (). The patient was diagnosed with seizure of unknown cause, probably epilepsy, on the basis of the electroencephalogram findings, which showed abnormal spike and waves at the right parietotemporal region (). The patient was prescribed potassium L-aspartate (300 mg, two tab/day) for the hypokalemia and carbamazepine (220 mg/day, in two divided doses) to control the seizures. Over the following year, the patient was asymptomatic. However, a year after the hospital admission, the patient was found to still have similar metabolic alkalosis, hypokalemia, hypomagnesemia, high renin activity, and slightly high aldosterone levels (32.0 ng/dL), as well as marked hypocalciuria (the urinary Ca/creatinine ratio was 0.006; normal > 0.2). The hypomagnesemia was associated with extremely high urinary excretion of Mg (7.2 g/L; normal 0.1-0.2 g/L) (). As summarized in , FEMg and FECa [] were dramatically altered to the opposite direction while FEK and TTKG [] were not significantly changed.
These findings indicated that the patient might have had GS at his initial presentation, which prompted us to examine his SLC12A3 gene for mutations. For the genetic studies, a written informed consent was obtained from the patient's family in accordance with the Declaration of Helsinki. The institutional review boards of Uji-Tokushukai Medical Center and Hokkaido Graduate School of Medicine approved the genetic diagnosis of the SLC12A3 gene. Direct sequencing of the SLC12A3 gene was done as reported previously []. Sequencing analysis revealed the presence of compound heterozygous mutations of the codon 642-encoded arginine amino acid in the cytoplasmic tail of the TSC protein: in one gene, the arginine had become a histidine and was inherited from the father; in the other gene, it had become a tryptophan and was inherited from the mother; thus the patient had the R642H/R642W mutation (). His older brother had only one of these heterozygous mutations (R642H).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [21.3, 'kg'], 'height': [120.0, 'cm']}",14.79167,14.05209,15.53125,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 120.0 cm, which is 120.0 cm * 1 m / 100 cm = 1.2 m. The patient's weight is 21.3 kg. The patient's bmi is therefore 21.3 kg / (1.2 m * 1.2 m) = 14.79167 kg/m^2."
2167,6,Body Mass Index (BMI),physical,decimal,pmc-4131310-1,Extracted,"A 56-year-old Saudi male was admitted to King Khalid University Hospital (KKUH) with the chief complaint of epigastric pain for 3 months associated with feeling of fullness, heartburn, and constipation. He had a past medical history of a surgical operation for renal stones and tympanoplasty, but with no significant family history. The vital signs recorded upon admission were as follows: Temperature 36.8°C, blood pressure 147/76 mmHg, pulse rate 72 beats/min, respiratory rate 20 breaths/min, and oxygen saturation 97%. His weight was 64 kg and height was 162 cm. Upon examination, the patient's abdomen was soft and lax with no tenderness, rigidity, or guarding noted.
Laboratory tests revealed an increase in white blood cells (WBC) and bilirubin with decreased red blood cells (RBC), hematocrit (HCT), and sodium level. Upper and lower endoscopic procedures were done, and colonoscopic findings were non-significant up to terminal ileum while gastroesophageal endoscopy showed a moderate hiatus hernia with peptic esophagitis Grade A and thickening of the mucosal folds at the pylorus. Ultrasound of the upper abdomen showed small cysts in both kidneys. Abdominal computerized tomography (CT) showed a small polypoidal lesion at the ileocecal valve []. The patient was later on discharged with home medication of Pantoprazole.
Laparoscopic right hemicolectomy was later performed. Histopathology of the resected specimen showed dilated lymphatic vessels consistent with a lymphangioma. Excess fat and congested blood vessels were also seen near the described lymphangioma. There was no evidence of malignancy and the excision appeared complete [Figures and ]. This finding confirms the lymphatic nature of the vessels shown in .
Patient was discharged without complications and he has been keeping well until this date.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [64.0, 'kg'], 'height': [162.0, 'cm']}",24.38653,23.1672,25.60586,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.0 cm, which is 162.0 cm * 1 m / 100 cm = 1.62 m. The patient's weight is 64.0 kg. The patient's bmi is therefore 64.0 kg / (1.62 m * 1.62 m) = 24.38653 kg/m^2."
2168,6,Body Mass Index (BMI),physical,decimal,pmc-6735169-1,Extracted,"The first case is a 51-year-old male with HCV+genotype 3a chronic liver disease. OLT is indicated because of the presence of a hepatocellular carcinoma (HCC) complying with the Milan criteria. The physical measures of the patient were as follows: height, 176 cm; weight, 90 kg; abdominal perimeter, 109 cm; and thoracic perimeter, 111 cm. A first OLT was performed with a graft from an 81-year-old donor. In the first 48 hours, the patient developed severe primary malfunction, for which a second OLT was indicated. He received a graft from a second donor with the following measures: height, 160 cm; weight, 68 kg; abdominal perimeter, 93 cm; and thoracic perimeter, 95 cm. The recipient/donor weight ratio was 1.3. The surgery was performed following our habitual technique with vena cava preservation (piggyback) with an anastomosis between a common stump from the recipient suprahepatic veins and the donor's cava after completely resecting the cuff of the previous graft's vena cava.
In the course of the intervention, a rotation of the liver was observed due to a discrepancy between the graft's size and the space in the hepatic fossa that impaired the venous drainage causing hepatic congestion. To solve this problem, a Sengstaken-Blakemore tube was placed under the liver in the right hypochondrium with the gastric and esophageal balloons filled, thus correcting its rotation and achieving an immediate improvement in the venous drainage ().
In the 7th postoperative day, a liver hemodynamic study was performed through the jugular vein. The THCG was measured with the balloons full and empty, observing that it did not increase after deflating them, so subsequent removal of the catheter was deemed safe. The patient was discharged 4 weeks after the surgery with optimal liver function, without ascites or other associated complications.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [90.0, 'kg'], 'height': [176.0, 'cm']}",29.05475,27.60201,30.50749,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 176.0 cm, which is 176.0 cm * 1 m / 100 cm = 1.76 m. The patient's weight is 90.0 kg. The patient's bmi is therefore 90.0 kg / (1.76 m * 1.76 m) = 29.05475 kg/m^2."
2169,6,Body Mass Index (BMI),physical,decimal,pmc-8528648-1,Extracted,"A 78-year-old man (163 cm, 70 kg) was referred to the emergency department of our hospital due to severe abdominal pain, which had worsened over the last 2 days. He had abdominal pain due to chronic alcoholic pancreatitis and underwent side-to-side pancreaticojejunostomy (PR procedure) 14 years previously. After the operation, he had suspended alcohol intake and had lived without pain related to pancreatitis.
On general examination, his blood pressure was 127/81 mmHg, heart rate was 120 bpm, body temperature was 37.7 ℃, and peripheral oxygen saturation on room air was 95%. Abdominal examination showed severe upper abdominal pain and a rigid abdominal wall. Contrast-enhanced computed tomography revealed necrosis of the Roux-en-Y (R-Y) limb tip at the anastomotic site, causing perforation peritonitis (Figure , ). Laboratory results showed inflammation and multiorgan failure: White Blood Cell count 7800/µl (stab 21%, segment 48%, metamyelocyte 17%, myelocyte 6%), C-reactive protein 20.3 mg/dL (reference range 0-0.3), Amylase 617 IU/L (reference range 39-134), Blood urea nitrogen 32.3 mg/dL (reference range 8-20), Creatinine 1.14 mg/dL (reference range 0.6-1.1), and Prothrombin Time Test international normalized ratio 1.33 (reference range 0.9-1.1). Arterial blood gas analysis showed metabolic acidosis with respiratory compensation; pH 7.422, partial pressure of oxygen and carbon dioxide 73.4 Torr and 26.1 Torr, respectively, lactate 3.6 mmol/L, bicarbonate 16.7 mmol/L, and base excess -6.0 mmol/L.
Emergency laparotomy was performed after examination. In the upper abdominal cavity, severe adhesions were observed in the thick greater omentum, stomach, and transverse colon. After careful adhesiolysis, complete necrosis and perforation of the R-Y limb tip in the pancreaticojejunostomy site was observed. This could not be repaired by suturing (Figure , ). We removed the necrotic jejunum, confirmed the main pancreatic duct opened for anastomosis, and then used the remaining R-Y limb to re-construct the anastomosis between the jejunum and pancreatic duct using 4-0 PDS II (Johnson & Johnson, New Jersey, USA) interrupted suture (Figure ). The operative time was 260 minutes, while blood loss was 1498 ml. Pathological findings included ischemic changes in the intestinal wall with mucosal cell effacement, intestinal crypt atrophy, and general tissue edema. Although luminal stricture was found near the anastomotic site, there were no malignant findings (Figure , ). Microscopic investigations did not reveal the cause of the R-Y limb stricture.
After the operation, the patient developed a grade C postoperative pancreatic fistula (POPF) (Revised 2016 ISGPS classification and grading of POPF []), which was treated with continuous drainage in the intensive care unit (ICU). His general condition slowly improved, and the pancreatic fistula gradually decreased. He was discharged from the ICU on postoperative day (POD) 18 and left the hospital without abdominal symptoms on POD 251.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [163.0, 'cm']}",26.34649,25.02917,27.66381,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.63 m * 1.63 m) = 26.34649 kg/m^2."
2170,6,Body Mass Index (BMI),physical,decimal,pmc-7315259-1,Extracted,"A 30-year-old Japanese woman (height, 153 cm; weight, 45 kg), gravida 5, para 2, delivered a healthy infant by vaginal delivery at an obstetric clinic. She had no significant past medical history, and there was no problem during the course of her pregnancy. After the delivery of the infant and placenta, the bleeding could not be controlled, and the bleeding volume reached 2,000 mL. The patient diagnosed with PPH due to atonic bleeding with cervical laceration was admitted to our hospital after suturing of the cervical laceration and administration of crystalloid. At the clinic, blood transfusion was not performed.
On arrival at our hospital, although anemia was existing (hemoglobin concentration, 6.3 g/dL; hematocrit, 18.4%), the results of the blood coagulation test were almost within normal limits except for D-dimer (platelet count, 135 × 109/L; prothrombin time-international normalized ratio (PT-INR), 0.92; activated partial thromboplastin time (APTT), 30.5 sec; fibrinogen, 258 mg/dL; D-dimer, 7.5 µg/mL). The bleeding could not be controlled by uterotonics, intrauterine balloon tamponade, or blood transfusion as replenishment of coagulation factors. She developed hemorrhagic shock, which leads to an emergency hysterectomy under general anesthesia.
At the beginning of the surgery, she was acidotic (arterial blood pH, 6.97) and hypothermic (body temperature, 33.8°C). Intraoperatively, uterine rupture due to cervical laceration followed by DIC (fibrinogen, 65 mg/dL; platelet count, 6.0 × 109/L at an intraoperative blood test) was diagnosed based on the obstetrical DIC score, which is commonly used in Japan [, ]. After the hysterectomy, oozing related to DIC persisted; therefore, gauze packing was inserted into the pouch of Douglas as DCS by the obstetricians, and temporary abdominal closure was performed. During the surgery, her mean arterial pressure was maintained within 60–75 mmHg and urine output was maintained at >1 mL/kg/hr. After the surgery, the patient was transferred to the intensive care unit (ICU) with mechanical ventilation.
On the day of surgery, blood transfusion was continued and the patient recovered from hemorrhagic shock. In addition, 4.5 g tazobactam/piperacillin was administered intravenously every 8 hours while packing was in place. On the first postoperative day (POD 1), the coagulation status gradually improved. A surgery to remove the intraperitoneal gauze was done on POD 2 because the bleeding from the drains had been decreased. Although there was a subcutaneous hematoma, bleeding in the peritoneal cavity had stopped. The total cumulative bleeding volume at POD 2 was 23,929 mL.
After the second surgery, the patient's general condition was gradually improved. The artificial respiration was ended on POD 5, and she was discharged from the hospital without complications on POD 16. Her clinical course and blood test results are shown in .",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.0, 'kg'], 'height': [153.0, 'cm']}",19.22338,18.26221,20.18455,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 153.0 cm, which is 153.0 cm * 1 m / 100 cm = 1.53 m. The patient's weight is 45.0 kg. The patient's bmi is therefore 45.0 kg / (1.53 m * 1.53 m) = 19.22338 kg/m^2."
2171,6,Body Mass Index (BMI),physical,decimal,pmc-5664252-1,Extracted,"A 3-year-old girl of Greek descent was referred to our hospital due to gait disturbance and undiagnosed skin lesions.
The patient presented bilateral spasticity of the legs. Acquisition of motor skills was delayed, as she achieved standing without support and walking at the age of 13 and 16 months, respectively. At the age of 16 months, she spoke 8–10 words. There was no history of epileptic seizures. Upon examination, she presented with extensive hyperkeratosis and scaling of the skin especially on palms and soles and hyperpigmented skin flexures (Figures –). Her hair and fingernails were normal. There was a history of recurrent chalazia. Her birth was at full-term (39 weeks), following an uneventful pregnancy. She is the fourth living child of a consanguineous couple who reported being third cousins, all other siblings having no significant medical history.
Height (104 cm), weight (16.5 kg), and head circumference (53.5 cm) were within normal age limits at presentation. Neurological evaluation revealed spastic diplegia of lower extremities, mild generalized increase in muscle tone, deep tendon reflexes of the lower extremities, and positive Babinski reflexes bilaterally. Intelligence was normal (IQ 95). Electroencephalopathy, otoacoustic emission test (OAE), abdominal and renal ultrasound, and X-ray of the chest and hips appeared to be normal.
Conventional magnetic resonance imaging (MRI) of the brain disclosed diffuse symmetrical high-intensity lesions in the deep white matter of the centrum semiovale and the frontal lobes and milder-intensity diffuse lesions in the posterior parietal lobes and the corpus callosum, while magnetic resonance spectroscopy (MRS) showed moderate increase of lipid and myoinositol levels. Other metabolites like N-acetyl aspartate (NAA), choline (Cho), and creatine (Cr) were within normal limits (Figures –).
Fundoscopy was performed to search for signs of metabolic retinopathy, and no abnormal features were detected in either eye. Absence of retinal deposits or other pathology was confirmed with optical coherence tomography of the macula. The patient had a history of recurrent chalazia. Cycloplegic retinoscopy revealed high refractive error (right eye C −4.50 D × 20°, left eye C −4.00 D × 170°). Visual acuity, measured with the ETDRS chart at 4 meters, was LogMAR 0.5 in the right eye and LogMAR 0.3 in the left eye with her glasses, which was presumed to be the result of refractive amblyopia and not of retinal pathology.
Histopathology of skin biopsy from the right axillary region and right thigh showed orthokeratotic hyperkeratosis, acanthosis, and papillomatosis of the stratum spinosum.
Clinical findings led to a differential diagnosis of Sjögren-Larsson syndrome, Refsum disease, Rud syndrome, and Chanarin-Dorfman syndrome, and so genetic testing was performed. Sequencing of the polymerase chain reaction product using the exon-specific primers revealed a c.551C>T mutation of the ALDH3A2 gene on chromosome 17p11.2 in homozygous state and confirmed the diagnosis of Sjögren-Larsson syndrome. Parents were tested and both were found to be heterozygous for this mutation. The patient was prescribed emollient baths and moisturizing creams, while physiotherapy was advised to improve spasticity.
No other clinical signs developed during three years of follow-up.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [16.5, 'kg'], 'height': [104.0, 'cm']}",15.25518,14.49242,16.01794,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 104.0 cm, which is 104.0 cm * 1 m / 100 cm = 1.04 m. The patient's weight is 16.5 kg. The patient's bmi is therefore 16.5 kg / (1.04 m * 1.04 m) = 15.25518 kg/m^2."
2172,6,Body Mass Index (BMI),physical,decimal,pmc-6076043-1,Extracted,"Case 1 was that of a 62-year-old man (163 cm, 70.7 kg) who works with machinery and other heavy equipment. He was mainly concerned about his appearance as his abdominal fat steadily increased without there being any change to his body weight. His family history was normal. His minor complaints included chronic rhinitis, severe snore, and low back pain with spinal stenosis (L4–5). He has an aversion to any type of modern Western medicine, and has difficulties with his eating habits and exercise style. Therefore, we suggested pharmacopuncture treatment with WGC, which he agreed to.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.7, 'kg'], 'height': [163.0, 'cm']}",26.60996,25.27946,27.94046,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 70.7 kg. The patient's bmi is therefore 70.7 kg / (1.63 m * 1.63 m) = 26.60996 kg/m^2."
2173,6,Body Mass Index (BMI),physical,decimal,pmc-4478361-1,Extracted,"A 5-year-old Caucasian boy presented with worsening, episodic leg, and ankle pains since two years of age. Painful episodes lasted several days and were typically intermittent, about every four to six weeks. Increasing frequency and new symptoms in feet and hands prompted referral to our facility. Past medical history was notable for difficulty to gain weight, complex partial seizure disorder, and long-term constipation. The constipation was managed with 5 mL oral mineral oil administered bidaily by syringe since postnewborn age. At age of 5 years, he weighed 19.7 kg (49th percentile) and was 113.2 cm tall (69th percentile). Examination was normal, including lung exam, except for swelling of the dorsum of wrists with decreased dorsiflexion, extension, and pain with motion. Hemoglobin, white blood count, and morphology were all identified within normal ranges. He had elevated rheumatoid factor (RF) at >802 IU/mL, anti-cyclic citrullinated peptide antibody 121 U (strongly positive > 60), positive anti-histone antibody 1.3 U (nl < 1.0 U), erythrocyte sedimentation rate at 27 mm/h, and C-reactive protein (CRP) < 3 mg/L. There were no known cardiac, pulmonary, or renal abnormalities, but outside chest radiography “opacifications” during an evaluation for “pneumonia” were noted.
Magnetic resonance imaging of the right wrist showed diffuse mottled edema and hazy enhancement of carpal bones. There was moderate thickening and enhancement of the synovium and soft tissue surrounding the carpus. Soft tissue wrist biopsy of the extensor sheath showed fibrovascular and synovial tissue with moderate lymphoplasmacytic inflammation. A routine chest radiogram showed a left lower lobe infiltrate. Subsequently, a chest computed tomography scan () revealed a mixed alveolar interstitial infiltrate in left and right lower lobe, lingula, and right middle lobe with a crazy-paving pattern. Fiber optic bronchoscopy demonstrated a normal larynx and tracheobronchial tree. An oil red O cytochemical stain was performed on the bronchoalveolar lavage specimen, which was strongly positive for exogenous lipoid aspiration. Lipid-laden macrophage index was 84%.
The diagnoses were consistent with chronic lipoid pneumonia, a silent complication of chronic occult mineral oil aspiration and inflammatory arthritis consistent with RF positive JIA. Discontinuance of mineral oil and initiation of hydroxychloroquine (100 mg/day) and methotrexate (12.5 mg/week) lead to a moderate improvement in frequency and severity of symptoms. At age of 7 years he has not achieved clinical remission and he continues to have episodic flairs of joint pain leading to school absence and restricted activity.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [19.7, 'kg'], 'height': [113.2, 'cm']}",15.37352,14.60484,16.1422,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 113.2 cm, which is 113.2 cm * 1 m / 100 cm = 1.132 m. The patient's weight is 19.7 kg. The patient's bmi is therefore 19.7 kg / (1.132 m * 1.132 m) = 15.37352 kg/m^2."
2174,6,Body Mass Index (BMI),physical,decimal,pmc-3668109-2,Extracted,"A 40-yr old man (body weight: 73 kg, height: 172 cm) was scheduled for living donor liver transplantation surgery due to acute liver failure. One week ago, he developed grade 1 hepatic encephalopathy. In the preoperative evaluation, electrocardiography and echocardiography were within normal range. Chest X-ray showed mild pleural effusion on both lungs. His laboratory examination showed Hb 9.9 g/dl, platelet count 107 × 109/L, prothrombin time 2.2 international normalized ratio, fibrinogen 82 mg/dl, antithrombin III 12%, sodium 135 mmol/L, potassium 3.0 mmol/L, creatinine 1.1 mg/dl, glucose 144 mg/dl, albumin 3.0 g/dl, total bilirubin 23.1 mg/dl, and ammonia 82 µmol/L. Her Child-Pugh and Model for End-Stage Liver Disease scores were 12 and 28, respectively.
Upon arrival at the operating room, his mental state was alert. His systolic/diastolic arterial blood pressure and heart rate were 132/68 mmHg and 98 beats/min, respectively. After establishing institutional standard monitoring, an ultrasound ONSD measurement was done by a physician well-trained in ocular ultrasonography. His ONSD just before anesthesia induction was 4.8 mm (). The bispectral index and suppression ratio were 98 and 0, respectively, and right and left regional cerebral oxygen saturations were 43 and 44%, respectively.
General anesthesia was induced and maintained by the standard protocol at our institute. His lungs were ventilated with a tidal volume of 8-10 ml/kg at a respiratory rate of 10 breaths/min (PaCO2, 35-40 mmHg). Intraoperative hemodynamics and laboratory data were shown . He experienced severe hypotension (systolic/diastolic arterial blood pressure: 62/48 mmHg) and bradycardia (56 beats/min) after graft reperfusion, and was treated with epinephrine (20 µg), after which systolic/diastolic arterial blood pressure (122/72 mmHg) and heart rate (92 beats/min) rapidly recovered to within the normal limit. His ONSD was dilated at 5.7 mm to 5 min after reperfusion (), and hyperventilation was performed with a tidal volume of 12 ml/kg at a respiratory rate of 13 breaths/min (PaCO2, 28 mmHg). His ONSD decreased to 5.1 mm at 30 min after reperfusion (), and ventilation was adjusted to maintain normocarbia until the end of surgery. He was moved to the surgical intensive care unit after surgery, and then transferred to a general ward without any complications on the seventh postoperative day.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [73.0, 'kg'], 'height': [172.0, 'cm']}",24.6755,23.44172,25.90928,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 172.0 cm, which is 172.0 cm * 1 m / 100 cm = 1.72 m. The patient's weight is 73.0 kg. The patient's bmi is therefore 73.0 kg / (1.72 m * 1.72 m) = 24.6755 kg/m^2."
2175,6,Body Mass Index (BMI),physical,decimal,pmc-6966997-1,Extracted,"A 72-year-old woman (140 cm, 56.9 kg) complained of low back pain and numbness and was admitted to our institution for posterior lumbar interbody fusion (PLIF) at L5-S1 and partial laminectomy at L2-L4. She had a prior history of PLIF at L4-5 at 68 years of age. She had no significant medical history except hypertension but no history of epilepsy. Her preoperative laboratory tests were within normal limits. Anesthesia was induced with propofol 70 mg and remifentanil 0.3 μg/kg/min. The trachea was intubated with an aid of rocuronium 50 mg. Anesthesia was maintained with desflurane 3–4% and remifentanil 0.1–0.2 μg/kg/min. Fentanyl 300 μg and rocuronium 20 mg were added during surgery. Bispectral index (BIS) was not monitored. Cerebrospinal fluid (CSF) leakage was not detected, even when inflation of the lungs by employing sustained positive end-expiratory pressure of 20 cm H2O for 5 s. The intraoperative course was uneventful and her hemodynamics remained stable during the 4 h and 55 min surgery. A 5-mm-diameter subfascial drainage tube was placed on the dorsal side of the lamina and opened about 10 min before the surgery was completed. After she was moved to the supine position, all anesthetics were stopped and the muscular relaxant was reversed with sugammadex 100 mg. Immediately thereafter, she developed symmetric, generalized, tonic seizure beginning in the upper extremities and advancing to the lower extremities. The seizure was immediately suppressed with propofol 80 mg; however, the cause of the seizure remained unclear. In order to rule out intracranial hemorrhage, brain computed tomography (CT) was performed under sedation with midazolam 10 mg. Brain CT showed no hemorrhage (Fig. ). Arterial blood gas analysis showed normal acid-base balance, serum electrolytes, and glucose. Propofol was continued because of subsequent repeated seizure.
Although there was minimal output from the drainage tube, our surgical team suspected cauda equina incarceration or the other unknown cause of seizure in the surgical field, because they knew that any neurologic manifestation could appear by intracranial hypotension after spinal surgeries [, ]. Six hours after the initial surgery, the patient was taken back to the surgical suite to confirm and repair a suspected spinal dural laceration. The re-opened surgical field was wet with diluted blood. We suspected that the blood was diluted with the leaked CSF, because the fluid over there might not have the others of the CSF. However, an evident point of dural laceration was not found. There was no cauda equina incarceration. The dura was covered with fibrin glue.
On the first postoperative day, generalized seizure reappeared when sedation was held. Valproic acid 800 mg and levetiracetam 500 mg were added for anticonvulsive therapy. Brain magnetic resonance imaging (MRI) revealed a subarachnoid hemorrhage (SAH) at the right cerebellopontine angle (Fig. ). At that time, we retrospectively noticed that a CSF cavity on the post-surgical brain CT had not been present (Fig. ), suggesting intracranial hypotension. Ultimately, the cause of the seizure was thought to be SAH due to intracranial hypotension. The seizure resolved on postoperative day 2, and her trachea was extubated. She suffered severe headache with typical signs of a classic post-dual puncture headache. Therefore, she was maintained in the Trendelenburg position until postoperative day 3. She was discharged on postoperative day 27 without any neurologic sequelae, and valproic acid and levetiracetam were continued for an additional 3 weeks.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [56.9, 'kg'], 'height': [140.0, 'cm']}",29.03061,27.57908,30.48214,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 140.0 cm, which is 140.0 cm * 1 m / 100 cm = 1.4 m. The patient's weight is 56.9 kg. The patient's bmi is therefore 56.9 kg / (1.4 m * 1.4 m) = 29.03061 kg/m^2."
2176,6,Body Mass Index (BMI),physical,decimal,pmc-8326001-1,Extracted,"A 12-year-old girl presented to our clinic with a chief complaint of trismus. A few months ago, she noticed a bulge in the left maxillary gingiva and trismus. There was no spontaneous pain, but pressure pain was felt. She was afebrile, had no history of trauma or medications. During her first medical examination at our clinic, she was 164 cm tall, weighed 54 kg. Extraoral examination revealed a slight bulge in the left cheek with countenance, right and left asymmetry and trismus. The range of mouth opening was 18 mm, and there were no swollen lymph nodes that I could feel in the neck. Intraoral findings revealed a neoplastic lesion extending from the left maxillary first molar to the maxillary tuberosity (). It interfered with the occlusion on that side.
Panoramic radiography showed impaction of the left maxillary second molar and resorption of alveolar bone between the left maxillary molar area and the maxillary tuberosity ().
Computed tomography (CT) images showed a mass that extended from the left masticator space to the buccal space and the alveolar regions of the maxilla and mandible and pressure resorption of the anterior border of ramus, rear wall of the maxillary sinus and lateral plate of the pterygoid process. Involvement of the maxillary sinus was also suspected. Contrast-enhanced T1-weighted magnetic resonance imaging (MRI) showed a high signal in a range similar to CT (). Contrast-enhanced effects in the left cervical and retropharyngeal (Rouviere) lymph nodes were also detected. 18F-fluorodeoxyglucose (18FDG)-positron emission tomography/CT showed a mass measuring 63 × 38 × 45 mm (long axis × minor axis × height) located in the left maxillary gingiva, accompanied by abnormal accumulation of 18FDG (standardized uptake value [SUV] max, 8.3), and left cervical lymphadenopathy, accompanied by abnormal accumulation of 18FDG (SUVmax, 41.72), which was suspected as metastasis. Abnormal accumulation was not observed in the other organs.
The differential diagnosis for a malignant tumor of oral soft tissue includes squamous cell carcinoma, sarcoma and salivary gland malignant tumor. Ameloblastoma is considered in the differential diagnosis for a maxillary tumor with trismus. Ameloblastoma is a benign tumor that presents as a bulge on the jawbone and causes bone resorption. It has included extraosseous/peripheral ameloblastoma [].
Three days after the first medical examination, a biopsy of the lesion was performed in the left maxillary gingiva with the consent of the patient and parents to obtain a definitive diagnosis. The sectioned surface was milky-white with enhancing characteristics (). Histopathological examination showed proliferation of oval to spindle-shaped cells, with hyperchromatic nuclei and a high nuclear-cytoplasmic ratio, arranged in a fascicular pattern (). Mitotic figures were frequently observed. Focally, the tumor cells were arranged in small nests and in a pseudo-capillary pattern in the sclerotic collagenous stroma (). Immunohistochemical examination revealed that the tumor cells were positive for desmin, myoD1, myogenin, mammary serum antigen and glial fibrillary acidic protein (). The Ki67 proliferation index was ~30% per HPF (). The details of immunostaining are shown in . The patient was diagnosed with RMS classified as Group III according to the Intergroup Rhabdomyosarcoma Study (IRS) grouping system []. The left maxillary gingiva RMS was treated via proton beam irradiation at 59.4 Gy and with vacuum-assisted wound closure therapy with 14 cycles of vincristine, actinomycin D and cyclophosphamide. After chemoradiotherapy, a complete response was documented via image evaluation.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [54.0, 'kg'], 'height': [164.0, 'cm']}",20.07733,19.07346,21.0812,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 164.0 cm, which is 164.0 cm * 1 m / 100 cm = 1.64 m. The patient's weight is 54.0 kg. The patient's bmi is therefore 54.0 kg / (1.64 m * 1.64 m) = 20.07733 kg/m^2."
2177,6,Body Mass Index (BMI),physical,decimal,pmc-4851541-1,Extracted,"A 6-year-old boy was admitted to our department due to vomiting, weakness, polyuria, polydipsia, irritability and weight loss in the last few weeks. The patient is the third child of the fourth pregnancy, one of which ended up with abortion. He was born at term, through Cesarean section, weighting 3400 g. Down syndrome was suspected clinically at birth and confirmed by karyotyping (47XX, t21).
The body weight on admission was 14.5 kg and the body height was 93 cm (20th and 5th percentile for sex and age in Down syndrome, respectively) ().
Typical features of Down syndrome were present, including typical facies and generalized hypotonia. A 3/6 heart murmur was heard on auscultation, and transthoracic echocardiography revealed a low grade aortic regurgitation. The rest of his physical examination was unremarkable.
Laboratory studies revealed red blood cell count 2.14 × 1012/l, Hb 6.1 gr/dL, Htc 17.5%, platelet count 272000/mm3, white blood cell count 7800/mm3, ESR 60 mm/h, CRP 26 mg/l, urea 12.7 mmol/1, creatinine 160 umol/1, Na 136 mEq/L, K 2.7 mEq/L, Cl 108 mEq/L, Ca 9.8 mg/dL, ionised Ca 1.28 mmol/1, Mg 1.0 mmol/1, total serum proteins 59.6 g/l, albumins 32.3 g/l, fasting blood glucose 5.6 mmol/l, cholesterol 6,1 mmol/l, triglycerides 2.3 mmol/l and alkaline phosphatase 49 U/l. Results of the capillary blood gas analysis were as follows: pH 7.25, PCO2 26 mmHg, HCO3 14 mEq/L.
Routine urine analysis showed mild proteinuria (+) and negative glucose. Urine microscopy showed 15 erythrocytes/hpf, 20 leucocytes/hpf and 20-30 bacteria/hpf; specific gravity was 1.005, and urinary pH was 7.0. Urine culture resulted positive for E. Coli.
Urinary uric acid was low at 774.0 umol/24h (normal values 1480-4430 umol/24h) as was citrate 21 mg/24h (normal value >115mg/24h). The urine calcium to creatinine ratio was 1.2 mmol/mmol (normal value < 1.1 mmol/mmol). In the view of normal anion gap hyperchloremic metabolic acidosis, alkaline urine and hypokalemia the diagnosis of dTRA was made.
Additional analysis searching for etiology of dTRA revealed serum 1,25-dihydroxyvitamin D 1.2 ng/ml (normal values 10.8-54 ng/ml), parathyroid hormone 27.2 pg/ml (normal values 6.5-36.8 pg/ml), free serum T4 2.20 pmol/l (normal values 10.3-25.8 pmol/l) and thyroid-stimulating hormone >1000.0 mU/l (normal values 0.54-4.21 mU/l). Prolactin was 163.9 ng/mL (normal values 3.2-20 ng/mL), while other hormonal profiles such as adrenocorticotropic hormone, luteinizing hormone, follicle-stimulating hormone and growth hormone were normal. Anti-thyroid peroxidase (TPO) antibody was >1000.0 IU/ml (normal value <50 IU/ml) and Thyroglobulin (hTg) was 3.41 ng/ml (normal values 0.2-70.0 ng/ml). Hence, Hashimoto thyroiditis as a possible cause was postulated. Moreover, antinuclear antibodies (ANA) test resulted negative.
The renal ultrasound showed hyper-echoic regions in the renal medulla consistent with bilateral nephrocalcinosis grade I (), also confirmed by abdominal CT (). Brain magnetic resonance imaging revealed pituitary enlargement ().
Treatment and follow up
Intravenous rehydration was started. The bicarbonate deficit was calculated, and KCl was added after the patient had his first urinary void. Blood gas analysis after 12 hours revealed increasing pH, HCO3 and K values. Packed red blood cells were then administered. The patient was put on potassium citrate and thyroid hormone substitution therapy. Also, intravenous antibiotherapy and oral ferrous supplements were started to treat urinary tract infection and anemia, respectively. On follow-up after six months, no evidence of metabolic acidosis and a nearly normal serum potassium level (3.4 mEq/L) were found. Urinary random analysis was normal. Patient’s weight was 16 kg and his height 98 cm (25th and 10th percetile, respectively). His thyroid hormone profile was within normal range. Also, prolactin, cholesterol, triglycerides and complete blood count analysis were normalizing. The patient is on regular follow-up.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [16.0, 'kg'], 'height': [98.0, 'cm']}",16.65973,15.82674,17.49272,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 98.0 cm, which is 98.0 cm * 1 m / 100 cm = 0.98 m. The patient's weight is 16.0 kg. The patient's bmi is therefore 16.0 kg / (0.98 m * 0.98 m) = 16.65973 kg/m^2."
2178,6,Body Mass Index (BMI),physical,decimal,pmc-5551223-1,Extracted,"A 23-month-old, male, Bulgarian child was admitted to our hospital, owing to worsening of general conditions, unsteady walking, and the association of neurological symptoms. His birth weight was in the normal range, and no neonatal problems had been reported. His physical, cognitive, communicative, and socio-emotional development milestones were regularly reached. There was no history of neuromuscular congenital or autoimmune disease in his family except for in a 50-year-old aunt with autoimmune thyroiditis.
A personal history evaluation revealed that the child had been hospitalized in Bulgaria twice. The first time, six months before our admission, was due to a sudden refusal to walk associated with acute weakness of both legs and loss of deep tendon reflexes. Electromyography showed an axonal demyelinating injury of the distal nerves of the lower limbs, and lumbar puncture showed protein-cytological dissociation in the cerebrospinal fluid (white blood cells, 16 cells/µL; proteins, 910 mg/dL). On the basis of these clinical and laboratory findings, GBS was diagnosed, and intravenous immunoglobulins (500 mg/kg/day i.v.) were given for five days. This treatment resulted in a mild improvement in walking, although the deep tendon reflexes were still depressed. Reflexes of the upper limbs were preserved during the entire treatment.
Two months later, he experienced a new episode characterized by a new sudden walking refusal associated with a 1.5-kg weight loss during this period. He was hospitalized again in Bulgaria, and no diagnostic examination was performed. An anti-inflammatory therapy with ibuprofen and a cow’s milk protein-free diet was prescribed. After discharge, he still did not walk, was irritable and showed gastrointestinal symptoms such as vomiting, loss of appetence, and the presence of stools containing undigested food.
The child was brought to our attention six months after the onset of GBS. Examination revealed an irritable, pale, and mildly dehydrated child with scarce adiposity and muscle hypotrophy. He was unable to walk. His weight was 11.3 kg (30th percentile), his height was 86.5 cm (45th percentile), and his head circumference was 46 cm (10th percentile). Growth curves showed a stunting from the beginning of his disorders. Neurological examination documented a normal mental status, decreased muscle tone, and the absence of deep tendon reflexes in both legs. Strength and sensorial evaluation of the upper limbs was normal. There were no cranial nerve deficits, nor cerebellar or meningeal signs. The Babinski sign was bilaterally absent. He had cold, swollen ankles. His abdomen was severely distended, with lively peristalsis ().
The initial work-up showed low levels of pre-albumin (13.4 mg/dL) and albumin (2 g/dL) as well as increased liver enzymes (SGOT 120 UI/L, SGPT 76 UI/L) and an altered coagulation framework (PT 26.2 s, INR 2.23, ratio 2.17). He was not anemic and had normal levels of ferritin and serum iron, and a normal transferrin saturation index. Blood fat-soluble vitamins (i.e., vitamin D, vitamin E, and vitamin K) were extremely low. Vitamin B12 and folic acid levels were normal. Intramuscular vitamin K supplementation was performed with rapid normalization of liver function and coagulation function. Vitamin D oral replacement therapy and physiotherapy were also started. Electromyography was not repeated because of the lack of parental consent. Considering the clinical features, peripheral neuropathy, gastrointestinal symptoms, and laboratory findings, the child was finally assessed for CD. The deamidated gliadin protein antibody (AGA) levels were 164 U/mL (normal values, <10 U/mL), transglutaminase levels were 46 U/mL (normal values, <10 U/mL), and he was positive for anti-endomysium antibodies (EMAs). Human leukocyte antigens (HLA) II typing confirmed a genetic predisposition to CD (DQ2 positive and DQ8 negative). According to the latest European Society for Paediatric Gastroenterology Hepatology and Nutrition (ESPGHAN) Guidelines [], a duodenal biopsy was not performed because he was highly symptomatic with anti-EMA IgA- and HLA DQ2-positive with IgG anti-AGA and IgA anti-transglutaminase levels largely higher than the cut-off values. Fecal exams resulted negative for viruses and bacteria, including Campylobacter jejuni.
CD was diagnosed, and the child began a gluten-free diet and subsequently experienced a progressive recovery of walking, general clinical status improvement, and significant decrease in abdominal distention. Deep tendon reflexes were weak bilaterally. He went back to Bulgaria after one month of hospitalization and the administration of a gluten-free diet. HLA typing was suggested for first-degree relatives.
summarizes the main clinical and laboratory findings in the study child according to his age.
At the follow-up, after three months of the gluten-free diet, at 27 months of age, the child was found to be able to walk independently, was no longer irritable, and had no gastrointestinal symptoms. Deep tendon reflexes were normally evoked in both legs. There was a complete recovery in his weight and length. His weight was in the 90th percentile, his length was in the 75th percentile, and his cranial circumference was in the 50th percentile. After general examination, his skin appeared normally hydrated, with well represented adipose tissue and a plain abdomen (). The ankle edema had resolved. The nutritional panel was normal: pre-albumin was 20.4 md/dL and albumin 4.5 g/dL. Liver function and vitamin values were in a normal range.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [11.3, 'kg'], 'height': [86.5, 'cm']}",15.10241,14.34729,15.85753,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 86.5 cm, which is 86.5 cm * 1 m / 100 cm = 0.865 m. The patient's weight is 11.3 kg. The patient's bmi is therefore 11.3 kg / (0.865 m * 0.865 m) = 15.10241 kg/m^2."
2179,6,Body Mass Index (BMI),physical,decimal,pmc-6008769-1,Extracted,"A 14-year-old male with DMD has been on daily oral steroid since 9 years of age. He weighed 53 kg (47th percentile) and was 147 cm tall (less than 3rd percentile). He became nonambulatory at 12 years of age. Forced vital capacity (FVC) was 2.37 L or 80% predicted. A polysomnogram was completed and revealed moderate obstructive sleep apnea. His echocardiogram (ECHO) was normal with cardiac magnetic resonance imaging (MRI) demonstrating normal left ventricular ejection fraction (LVEF). He participated in many school activities including wheelchair soccer.
He presented to the emergency department with confusion, tachycardia, tachypnea, and fever up to 39.2 degrees Celsius a few hours following soccer practice. During practice, he had been transferred from his wheelchair and his right leg had brushed the ground causing him to have to be placed on the ground until more help was obtained to put him back in his wheelchair. Brain computed tomography (CT) was negative for any acute intracranial process contributing to his current state. Chest computed tomography (CT) scan was negative for pulmonary embolism but showed patchy diffuse nodular airspace opacities seen scattered throughout both lung fields (). He had progressive acute hypoxic respiratory failure requiring mechanical ventilation. Shortly after intubation, he suffered cardiac arrest requiring 3 minutes of cardiopulmonary resuscitation (CPR) before return of spontaneous circulation. ECHOs were consistent with increased pulmonary vascular resistance including moderate right ventricle dysfunction and elevated pulmonary arterial pressure. Duplex ultrasound evaluation of lower extremities was without evidence of deep venous thrombosis bilaterally. X-rays of lower extremities revealed cortical step off at the proximal left femoral neck and nondisplaced fracture at the distal right tibial metaphysis and fibular metaphysis (). Ophthalmologic exam revealed Purtscher-like retinopathy. The patient was treated with 48 hours of antibiotics that were discontinued with negative blood, urine, and mini bronchoalveolar lavage (BAL) culture. The patient was treated with mechanical ventilation and right ventricular afterload reduction with milrinone and inhaled nitric oxide for pulmonary hypertension. These therapies were able to be weaned off, and the patient was able to be extubated on day five of admission. He was later transferred to the pediatric floor and later discharged home without any residual effects from the entire event.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.0, 'kg'], 'height': [147.0, 'cm']}",24.52682,23.30048,25.75316,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 147.0 cm, which is 147.0 cm * 1 m / 100 cm = 1.47 m. The patient's weight is 53.0 kg. The patient's bmi is therefore 53.0 kg / (1.47 m * 1.47 m) = 24.52682 kg/m^2."
2180,6,Body Mass Index (BMI),physical,decimal,pmc-8615442-1,Extracted,"A 62-year-old male (height, 168 cm; weight, 90 kg) who complained of bilateral knee pain and limited mobility for 10 years was scheduled to undergo right knee arthroplasty. He had a history of hypertension, and was taking irbesartan hydrochlorothiazide 12.5 mg and levamlodipine besylate (5 mg daily). He had undergone a right femur fracture surgery 30 years previously. Systemic examination revealed no significant abnormalities. Other than a high platelet count (498 × 109/L) laboratory investigations were within normal limits, with a prothrombin time of 10.9 s, activated partial thromboplastin time 24.4 seconds, and fibrinogen level of 3.38 g/L. Ultrasonic examination showed that left ventricular posterior wall thickness (diastolic) was 10 mm, left ventricular diameter (systolic) was 27 mm, and ejection fraction was 73%. No thrombosis or other abnormalities were seen in the blood vessels of either lower limb. Electrocardiogram and lung computed tomography also showed no abnormalities. The Caprini score was 3.
After electrocardiography, non-invasive blood pressure, and oxygen saturation monitoring, general anesthesia was induced with intravenous etomidate (18 mg), fentanyl (0.3 mg), and rocuronium (50 mg). After tracheal intubation, propofol (6 mg/kg/h) and remifentanil (0.2 μg/kg/min) were infused for maintenance of anesthesia.
Upon sterilizing the surgical area, TXA (1.6 g) was intravenously administered. Several minutes later, the patient's end-tidal carbon dioxide decreased from 35 to 7 mm Hg. Concomitantly, his blood pressure was 45/19 mm Hg, and oxygen saturation could not be analyzed. The patient developed ventricular fibrillation and severe acute pulmonary embolism was suspected. Epinephrine (100 μg followed by 1 mg) was administered immediately, and cardiopulmonary resuscitation was initiated. After electro-defibrillation, the patient recovered spontaneous circulation.
The patient was catheterized in the radial artery and internal jugular vein for intensive monitoring. Hemodynamics was maintained with epinephrine (0.3 μg/kg/min). Blood gas analysis revealed a partial pressure of oxygen of 63.2 mmHg and partial pressure of carbon dioxide of 46.6 mmHg. Transesophageal echocardiography revealed a floating hypoechoic mass (5.9 × 1.8 cm) in the right atrium, which could be traced to the superior vena cava and right ventricle (3.9 × 2.0 cm), fluttering with heartbeat (Fig. A, B), while transthoracic echocardiography revealed no thrombosis in the jugular and femoral veins. After urgent multidisciplinary consultation, thrombolytic therapy was recommended. Thus, urokinase at 200,000 U for 10 minutes, followed by 300,000 U for 30 minutes was intravenously administered.
Fifty minutes after thrombolysis, the mass in the ventricle disappeared. Only a shrunken mass of 2.0 × 2.3 cm was observed in the right atrium (Fig. C). After another half an hour, no abnormal echoes were seen in the right heart chambers (Fig. D).
The operation was cancelled. After stable hemodynamics was preliminarily attained, the patient was transferred to the intensive care unit. Intraperitoneal hemorrhage and acute kidney failure were detected. After seven days of respiratory support and 11 days of renal replacement therapy, he returned to the general ward. He was discharged after 43 days without any organ dysfunction.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [90.0, 'kg'], 'height': [168.0, 'cm']}",31.88776,30.29337,33.48215,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 90.0 kg. The patient's bmi is therefore 90.0 kg / (1.68 m * 1.68 m) = 31.88776 kg/m^2."
2181,6,Body Mass Index (BMI),physical,decimal,pmc-4439899-1,Extracted,"An 11-year-old boy was admitted to our clinic with complaints of fatigue, anorexia and weight loss which developed in the past eight months. He also had a history of severe psychological stress prior to the symptoms. Three months before the beginning of symptoms he had driven his father’s car without permission and crashed the car. There was not any physical injury in that accident, but the patient experienced serious psychological distress with the feeling of guilt. His parents also describe him as a sensitive, overly cautious and anxious child. His thyroid stimulating hormone level was found as 12.4 mIU/mL with positive thyroid antibodies and he was diagnosed as a case of subclinical hypothyroidism due to “Hashimoto thyroiditis”. He was prescribed 50 µg/day L-thyroxine (L-T4) therapy. However, despite this treatment, clinical deterioration occurred. He lost 8 kg in body weight within three months.
Physical examination at presentation revealed a blood pressure level of 90/40 mmHg and presence of grade 1 goitre. Height was 141 cm and weight was 32 kg (standard deviation score values were 0.54 and -0.74, respectively). Pubertal findings were consistent with Tanner stage 1. The patient had a suntanned appearance, but there was no marked hyperpigmentation in the skin or mucosa. A low cortisol level accompanied by a high adrenocorticotropic hormone (ACTH) level confirmed presence of primary adrenal insufficiency. Laboratory findings at referral and follow-up visit are presented in . Thyroid ultrasonography revealed a heterogeneous pattern of the parenchyma with no nodular lesion. The electrolyte imbalance was treated with saline infusion. A diagnosis of adrenal insufficiency was considered and treatment with glucocorticoids (10 mg/m2/day hydrocortisone) and mineralocorticoids (0.1 mg/m2/day fludrocortisone) was started. L-T4 treatment was ceased and started again as soon as the clinical findings improved. A very long-chain fatty acid profile was normal and adrenoleucodystrophia was excluded. Investigation for other associating autoimmune endocrine diseases revealed positive findings for anti-glutamate dehydrogenase, anti-islet cell, anti-gliadin and anti-endomysium antibodies. The oral glucose tolerance test revealed a normal fasting blood glucose level and normal glucose tolerance values (). Endoscopic biopsy revealed villous atrophy, proliferation of the crypts and increased lymphocytic infiltration, confirming the presence of gluten-sensitive enteropathy (celiac disease).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [32.0, 'kg'], 'height': [141.0, 'cm']}",16.09577,15.29098,16.90056,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 141.0 cm, which is 141.0 cm * 1 m / 100 cm = 1.41 m. The patient's weight is 32.0 kg. The patient's bmi is therefore 32.0 kg / (1.41 m * 1.41 m) = 16.09577 kg/m^2."
2182,6,Body Mass Index (BMI),physical,decimal,pmc-4437790-1,Extracted,"A 28-year-old African woman (72kg, 166cm) with anti-Cromer Tc(a) and anti-Jka antibodies was admitted to the obstetric emergency department at our University Hospital at 31+4 weeks’ gestation for heavy vaginal bleeding. She had a history of two prior at-term cesarean deliveries (in 2006 and 2010) and two voluntary abortions. She had a positive indirect Coombs test near the beginning of pregnancy. Low-titer anti-Tc(a) antibodies had been identified and closely monitored.
A month before admission to our department (at 27+3 weeks’ gestation), she had been hospitalized for cervical shortening (23mm). Ultrasonography at that time had revealed full placenta previa and a high risk for placenta accreta. In accordance with the guidelines of the Royal College of Obstetricians and Gynaecologists [], the ultrasound report was as follows: “… in grey-scale, a thinning of the hyperechoic serosa–bladder interface and abnormal placental lacunae were found. Moreover, the placental tissue on the left side of the uterus appeared to reach the serosa.” During the initial hospitalization, two injections of betamethasone (12mg) were administered to prevent fetal respiratory distress, and a consulting hematologist requested further immunohematological testing.
Because of the rarity of antibodies of the Cromer blood group system and the high risk of heavy bleeding associated with placenta accreta, it was necessary to establish specific policies for the planned delivery by cesarean section. In preparation, parenteral iron supplementation was administered twice weekly beginning in the 28th week to raise hemoglobin (Hb) values above 12g/dL from an initial Hb of 10.5g/dL. Meanwhile, the Transfusion Medicine Department consultant planned two autologous blood donations because no compatible blood was found in a search of the United States Blood Bank network or the network of European blood banks (World Health Organization International Rare Donor Panel). Unfortunately, the autologous blood could not be collected because of sudden worsening of the patient’s clinical condition.
At her readmission to our Obstetrical Emergency Department, serial ultrasound examinations and fetal monitoring with cardiotocography were performed. Because vaginal bleeding stopped within a few hours in response to tocolytic therapy, the attending physicians decided to maintain a conservative strategy. Elective cesarean delivery was scheduled with multidisciplinary team cooperation because of the extreme complexity of the case. The cesarean section was performed 3 days later, after a long and detailed discussion among anesthesiologists, obstetricians, radiologists, hematologists and intensivists. Her preoperative Hb was 10.2g/dL.
Before cesarean section, the patient provided written informed consent and was brought to the angiography suite (Philips Medical Systems, Best, Netherlands). We placed two 14-gauge and one 16-gauge peripheral venous catheters and performed radial artery cannulation to monitor intra-arterial pressure throughout the procedures. After local anesthesia of her groin bilaterally, her femoral arteries were punctured with Seldinger technique and 4-Fr sheaths (Terumo, Leuven, Belgium) were placed to allow bilateral cross catheterization of her hypogastric arteries with a C1 “Cobra” catheter (Terumo Leuven, Belgium). Using a 0.035 inch 150cm Amplatz guidewire (Cordis, Fremont, CA, USA), the 4-Fr sheaths were exchanged with two 45cm 5-Fr Brite Tip® sheaths (Cordis, Fremont, CA, USA), with the distal tips in the anterior branches of both hypogastric arteries. This allowed placement of two Fogarty 80cm 4-Fr balloons over the distal tips of the 5-Fr sheaths, within her uterine arteries. Proper positioning of the Fogarty balloons and the effectiveness of vascular occlusion were confirmed with fluoroscopy (Figure ). Maternal and fetal monitoring were conducted throughout the procedure, without complications.
She was transferred from the angiography suite to the obstetric operating room. A single fluoroscopic image was made with a moveable C-arm to confirm that the Fogarty balloons remained in the proper position. While she underwent the angiographic procedure, the operating room was set up with an intraoperative blood salvage system (Cell Saver®; Haemonetics Corp., Braintree, MA, USA), a rapid infusion system (Haemonetics Corp., Braintree, MA, USA), fluid warmers (Level 1 H-1200; Smiths Medical, Kent, UK) and forced air warming systems (Bair-Hugger™, 3M, St. Paul, MN, USA). Before anesthetic induction, she received premedication with hydrocortisone (200mg) as recommended by the hematologist in case of emergent need to transfuse incompatible blood. She also received antibiotic prophylaxis and intravenous tranexamic acid (750mg) to prevent peripartum hemorrhage []. Anesthesia was induced with 200mg propofol, 200mcg fentanyl and 40mg rocuronium and was maintained with sevoflurane gas. A low transverse skin incision through her previous cesarean scars and a lower uterine segment incision were performed, avoiding the upper margin of the anterior placenta. Immediately after delivery of the fetus and umbilical cord clamping, the uterine artery balloons were inflated. As per the obstetrician’s request, the uterine arteries were embolized with Gelfoam® sponge (Jinling Pharmaceutical Company, Nanjing, China) to stop bleeding. Because the placenta could not be completely removed as a result of its strong adhesion to the posterior wall of the uterus, and because of the risk of postoperative hemorrhage, the surgeons decided to perform a total hysterectomy, as recommended by Royal College of Obstetricians and Gynaecologists guidelines []. When adequate hemostatic control was achieved, the balloons were deflated. After the uterine lumen and abdominal cavity were closed and no vaginal bleeding was confirmed, the Fogarty balloons were removed. The 5-Fr sheaths were maintained for 24 hours in case further embolization was necessary. The total intraoperative blood loss was 1000mL and the surgery lasted approximately 150 minutes. During the cesarean section, 150mL of blood was reinfused through the cell salvage technology and limited crystalloid fluid therapy was administered (1L of lactated Ringer’s solution). Her temperature was maintained at approximately 37°C throughout the procedure and serial blood gas analyses were performed to monitor for metabolic acidosis and electrolyte abnormalities. Further details of our hemorrhage management protocol have been reported previously [].
After surgery, she was admitted to our Intensive Care Unit (ICU) for close monitoring of bleeding and coagulation profiles. Immediately after ICU admission, ventilation was optimized, adequate analgesia was provided and she was awakened and extubated. Because no further bleeding was recorded from the abdominal drain, the angiographic 5-Fr sheaths were removed the day after surgery and she was transferred to the obstetric ward with a Hb of 8.9g/dL.
Four days after cesarean section, she was discharged from our hospital with a prescription for oral iron therapy for at least 30 days and plans for blood count recheck 15 days after discharge.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [72.0, 'kg'], 'height': [166.0, 'cm']}",26.12861,24.82218,27.43504,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 72.0 kg. The patient's bmi is therefore 72.0 kg / (1.66 m * 1.66 m) = 26.12861 kg/m^2."
2183,6,Body Mass Index (BMI),physical,decimal,pmc-7437126-1,Extracted,"An 11-year-old Japanese male (weight, 38.0 kg; height, 149.6 cm) was admitted to the hospital after having lost 3 kg of body weight in one month. He complained of neither subjective symptoms nor abdominal pain. He had undergone surgery for a perianal abscess at the age of nine years, but there were no signs of disease during treatment. He showed elevated serum amylase (AMY) and lipase levels of 524 U/L and 1,114 U/L, respectively. Contrast-enhanced abdominal CT scanning revealed slight pancreatic enlargement. He had a fever once during the course of the disease, but the levels of the pancreatic enzymes spontaneously decreased with fasting. On the 22nd day of hospitalization, he had a fever of 40℃, rigors, and low systolic blood pressure of 70 mmHg. He was, therefore, transported to our hospital for intensive care.
During our examination, he was restless, and his blood pressure, pulse rate, respiratory rate, oxygen saturation, and body temperature were 75/35 mmHg (mean arterial pressure [MAP] 48 mmHg), 150 beats/min, 30 breaths/min, 98% and 38.2°C, respectively. There were no specific physical findings in the chest, abdomen, skin, or anus.
Arterial blood gas analysis showed a lactate level of 40 mg/dL, suggestive of lactic acidosis. The leukocyte count was 7,800/μL, the hemoglobin level was 9.2 g/dL, and the platelet count was 98,000/μL. The blood urea nitrogen level was 40.8 mg/dL, the creatinine level was 1.67 mg/dL, and the AMY level was 349 U/L. The lipase, C-reactive protein (CRP), procalcitonin, and blood sugar levels were all abnormal at 372 U/L, 12.99 mg/dL, over 100 ng/dL, and 49 mg/dL, respectively. Coagulation abnormalities were also present, with an activated partial thromboplastin time of 44.4 seconds, a prothrombin time of only 28.2% of the normal range, 44.2 μg/mL of fibrin/fibrinogen degradation products, a D-dimer level of 22.87 μg/mL, a fibrinogen level of 345 mg/dL, and an antithrombin III level of only 61.8% of the normal range. The Sequential Organ Failure Assessment (SOFA) score was 10 points, and the Japanese Association for Acute Medicine disseminated intravascular coagulation (DIC) diagnostic criteria score was 6 points [,]. Abdominal CT revealed mild swelling in the liver, kidneys, and pancreas and multiple lymph node enlargements, but no obvious infectious findings such as abscesses or intestinal perforations (Figure ).
Microbiological testing detected Enterobacter cloacae in two sets of blood culture samples and Enterobacter cloacae, Enterococcus faecalis, and Proteus mirabilis in the urine culture sample. Since the urine had a small amount of bacteria and no pyuria was observed, we judged it to be only bacterial carriage.
The patient was admitted to the intensive care unit (ICU) with a diagnosis of septic shock and DIC due to an intra-abdominal infection. Crystalloid fluid infusion, meropenem (MEPM), thrombomodulin alfa (TM), noradrenaline (NA), and antithrombin (AT) were administered (Figure ). As the patient continued to be anuric despite massive infusions, continuous hemodialysis (CHD) and polymyxin B-immobilized fiber column direct hemoperfusion (PMX-DHP) were introduced. On the second day in the ICU, endotracheal intubation was performed, and he was placed on a ventilator owing to signs of worsening respiratory condition, including tachypnea and nasal alar breathing.
After overnight administration of 4,000 mL of crystalloid fluid and a maximum dose of 0.2 μg/kg/min of NA, a MAP of 65 mmHg was achieved, and serum lactate levels were decreased to 18 mg/dL by day 2 of being in the ICU.
Colonoscopy was performed to detect the source of the intra-abdominal infection on day 4 of being in the ICU. The erosions and ulcers had a tendency to run longitudinally, and skip lesions were observed (Figure ). As a result, CD was diagnosed. Since there were no other obvious findings, we assumed that the intestinal tract was the entry point for the infection in the bloodstream.
On day 7 of being in the ICU, the patient was extubated, and the blood purification therapy was terminated after CHD was exchanged for granulocytapheresis (G-CAP).
On the eighth day in the ICU, the patient was transferred to the general pediatric ward for the treatment of CD. On the 117th day of hospitalization, he was discharged in good general condition.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [38.0, 'kg'], 'height': [149.6, 'cm']}",16.97932,16.13035,17.82829,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 149.6 cm, which is 149.6 cm * 1 m / 100 cm = 1.496 m. The patient's weight is 38.0 kg. The patient's bmi is therefore 38.0 kg / (1.496 m * 1.496 m) = 16.97932 kg/m^2."
2184,6,Body Mass Index (BMI),physical,decimal,pmc-8101107-1,Extracted,"The patient, a 3 years old boy (Fig. ), is the third child of healthy unrelated French parents. The mother, 45 years old at the time of conception, had two healthy children from a previous union.
The patient was born at a gestational age of 37 weeks with a birth weight of 2750 g (32nd percentile), a birth length of 46 cm (13th percentile) and a birth head circumference of 34 cm (55th percentile). As usually, he had vitamin D prescription (1200 UI of cholecalciferol/day) that he received irregularly during the first 2 months of life. At the age of 9 months, he was referred to the Department of Paediatrics due to growth retardation. Biological tests and clinical examination were normal.
At the age of 12 months, he was evaluated for persistent short stature and developmental delay with feeding difficulties and vomiting. A parental abuse was suspected but feeding difficulties and vomiting persisted during hospitalisation. His weight was 6270 g (− 2.5 SD) and his length was 70.5 cm (− 2.5 SD). On evaluation, there was no evidence for a secondary growth disorder. Except a mild developmental delay, neurological examination was normal. Cardiac ultrasonography and cerebral MRI did not reveal any abnormality. Thyroid function tests and concentrations of IGF-1, calcium, inorganic phosphate and alkaline phosphatase were all within normal limits. There was no evidence of a metabolic disease (Table ).
Clinical examination suggested a mild facial dysmorphism with a frontal bossing, a high anterior hairline, deep-set eyes, small low-set backward-rotated ears, and a thin upper lip corresponding at 3 out 6 on the Netchine-Harbison clinical scoring system for SRS criteria [] (Fig. ). The clinical features of our patient are compared to a cohort of UPD(20)mat reviewed by Hjortshøj et al. [] (Supplementary Table 1).
After this evaluation, calcium/vitamin D supplementation was resumed.
At the age of 18 months, a renal ultrasonography showed a bilateral nephrocalcinosis grade II, associated to hypercalciuria, hypophosphatemia, increased 1,25 OH vitamin D with abnormally low parathyroid hormone level (PTH) (Table ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [6270.0, 'g'], 'height': [70.5, 'cm']}",12.61506,11.98431,13.24581,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 70.5 cm, which is 70.5 cm * 1 m / 100 cm = 0.705 m. The patient's weight is 6270.0 g so this converts to 6270.0 lbs * kg/1000 g = 6.27 kg. The patient's bmi is therefore 6.27 kg / (0.705 m * 0.705 m) = 12.61506 kg/m^2."
2185,6,Body Mass Index (BMI),physical,decimal,pmc-5084582-1,Extracted,"A 26-year-old female was referred to the medicine OPD for follow-up of her thyroid status. She was previously diagnosed to have hyperthyroidism from an outside hospital and was on carbimazole for the last 5 years.
On review of her complaints, she recollected that she was always the shortest in her class in the school years. There was also a history of subnormal intelligence, poor scholastic performance, hearing loss, and attention deficit hyperactivity disorder (ADHD). There was a history of short stature in the family in the maternal side, and they were being treated for hyperthyroidism. She developed goiter 10 years back, but she did not have any clinical symptoms of hyperthyroidism (palpitations, tremors, and moist skin) nor had any ocular signs or symptoms. During the evaluation for goiter, her thyroid hormone levels showed increased T4, T3, free T4 and free T3, with a normal thyroid stimulating hormone (TSH), for which she was started on antithyroid drugs.
On clinical examination, she was conscious and alert, short statured (height 142 cm, weight 47 kg). She had tachycardia with a pulse rate of 102/min. She was normotensive and afebrile at presentation. Examination of the thyroid gland showed diffuse enlargement of the thyroid, World Health Organization Grade 2 without palpable nodules []. There was no bruit on auscultation, and the eye examination was normal. The systemic examination was within normal limits.
Laboratory investigations showed elevated T3 and T4 with T3 - 3.15 (0.95–2.5 nmol/L), free T3 - 5.12 (2.3–4.2 pg/mL), T4: 233 (60–120 nmol/L), and free T4 - 3.1 (0.8–1.8 ng/L). The TSH was inappropriately normal - 4.39 (0.2–5 µIU/L).
Ultrasonography thyroid was done which showed multiple hyperechoic well-defined subcentimetric nodules with peripheral halo and no internal vascularity in both lobes of the thyroid-features suggestive of multinodular goiter.
The possibilities of thyroid hormone resistance and TSH-secreting adenoma were considered, and a magnetic resonance imaging (MRI) pituitary was done to look for a pituitary mass, which turned out to be normal. A sex hormone binding globulin levels were done to look for peripheral action of thyroid hormone, which was normal - 48.3 ng/L (normal - 11.7–137.2 ng/L), indicating the resistance of thyroid hormone action at the level of liver.
A pure tone audiometry done showed a moderate hearing loss with mixed component at mid frequency [].
Thyroxin suppression testing was done which showed poor suppression of TSH (3.29 µIU/L), confirming the diagnosis of thyroid hormone resistance.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [47.0, 'kg'], 'height': [142.0, 'cm']}",23.30887,22.14343,24.47431,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 142.0 cm, which is 142.0 cm * 1 m / 100 cm = 1.42 m. The patient's weight is 47.0 kg. The patient's bmi is therefore 47.0 kg / (1.42 m * 1.42 m) = 23.30887 kg/m^2."
2186,6,Body Mass Index (BMI),physical,decimal,pmc-6043957-1,Extracted,"A 15-year-old Japanese girl with a diagnosis of adolescent idiopathic scoliosis was admitted to our hospital to undergo posterior spinal fusion at T4–L3. She was a high school student and did not present any symptoms at admission. She did not take any medications prior to the surgery. Her past medical, social, environmental, and family history was not appreciable. She was 147 cm tall, and her weight was 40 kg. She had a Cobb angle of 60 degrees. She had no neurological symptoms. Her temperature was 36.8 °C, her blood pressure was 118/64 mmHg, and her pulse was 92 beats per minute. Laboratory findings at admission were as follows. Her white blood cell count was 6860/μl, red blood cell count 472 × 104/μl, hemoglobin 14.3 g/dl, hematocrit 42.1%, platelets 30.8 × 104/μl, aspartate transaminase 19 IU/L, alanine transaminase 15 IU/L, total bilirubin 0.5 mg/dl, γ-glutamyl transferase 16 IU/L, alkaline phosphatase 371 IU/L, total protein 8.2 g/dl, albumin 5.2 g/dl, blood urea nitrogen 11 mg/dl, creatinine 0.39 mg/dl, sodium 141 mEq/L, potassium 4.5 mEq/L, chloride 102 mEq/L, C-reactive protein 0.01 mg/dl, urinalysis pH 6.0, no uric protein, no urinary sugar, no ketone body, and no uric blood. No microbial examination was performed.
We planned general anesthesia using a target-controlled infusion of propofol and a continuous infusion of remifentanil to record MEPs and somatosensory evoked potentials (SSEPs). In addition, we planned to use both bolus and continuous infusions of ketamine, followed by intravenous patient-controlled fentanyl as postoperative analgesia because we believed that ketamine did not affect MEP monitoring.
After securing an intravenous line in the patient’s forearm, general anesthesia was induced using a target-controlled infusion of propofol 4 μg/ml and remifentanil 0.3 μg/kg/minute. After administration of rocuronium 20 mg, the trachea was intubated using a reinforced endotracheal tube. Thereafter, 1 g of cefazolin sodium was administered intravenously every 3 hours during the surgery and every 12 hours until postoperative day 1.
We started preparation for recording the MEPs and SSEPs. MEPs were evoked by transcranial electrical stimulation (a train of five pulses with an interstimulus interval of 2 milliseconds; supramaximal stimulus, 400 V) with screw electrodes fixed at 2 cm anterior to C3 and C4 (cathode and anode, respectively, following the international 10–20 system). MEPs and SSEPs were recorded using an intraoperative neurophysiologic monitoring system (Neuromaster MEE-1216; Nihon Kohden, Tokyo, Japan). MEPs were recorded bilaterally from the abductor pollicis, quadriceps femoris, tibialis anterior, and flexor hallucis brevis muscles. SSEPs were evoked by stimulation (30 mA) of the sciatic nerve and recorded from 2 cm posterior to Cz (averaging the signals generated by 200 stimulations).
After the patient was turned to a prone position, we confirmed that we could record MEPs from all targeted muscles without difficulty. We maintained general anesthesia using a target-controlled infusion of propofol 3.3 μg/ml and remifentanil 0.2 μg/kg/minute. The patient’s bispectral index values were below 60, and her vital signs were stable. Several minutes before the skin incision was made, the attending anesthesiologist evaluating the MEPs discovered that they were markedly attenuated (Fig. ). The attending anesthesiologist had not changed the propofol infusion rate and had not administered any other drugs except for intravenous bolus administration of ketamine 50 mg (1.25 mg/kg). Ketamine was administered about 3 minutes before the change in MEP waveforms. The patient’s blood pressure, heart rate, peripheral oxygen saturation, end-tidal CO2, and body temperature remained stable. The surgery had not started at that time. About 6 minutes after administration of ketamine, the MEP amplitudes were recovered.
The surgery was performed uneventfully, and the patient had no neurologic deficit when she emerged from general anesthesia. Intravenous patient-controlled analgesia (a combination of fentanyl 25 μg/ml and ketamine 2.5 mg/ml, background infusion 1 ml/hour, bolus 1 ml, and lockout time 10 minutes) was used for postoperative pain management. The patient was discharged on postoperative day 11 without any complications. She was well without complications at 2 years after the surgery.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [40.0, 'kg'], 'height': [147.0, 'cm']}",18.51081,17.58527,19.43635,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 147.0 cm, which is 147.0 cm * 1 m / 100 cm = 1.47 m. The patient's weight is 40.0 kg. The patient's bmi is therefore 40.0 kg / (1.47 m * 1.47 m) = 18.51081 kg/m^2."
2187,6,Body Mass Index (BMI),physical,decimal,pmc-5374574-1,Extracted,"An 8-year-old Cameroonian boy with no significant past history was brought to our emergency service following a road traffic accident. On crossing a road, he was knocked down by an oncoming motorbike weighing approximately 125 kg, medium sized, and traveling at moderate speed. The motorbike fell on the boy with the handlebar catching him in the abdomen as its rider lost control. He sustained a lesion to the head with no initial loss of consciousness. On arrival, he complained of pain in his head and a swelling in the left upper quadrant of his abdomen.
On examination, he was conscious, with a Glasgow coma score of 15/15, blood pressure of 119/83 mmHg, pulse of 90 beats per minute, respiratory rate of 18 breaths per minute, temperature of 37.3 °C; he was 96 cm tall and weighed 26 kg. There was a 2 cm laceration in the occipital region of his head, and a swelling in his left lumbar region with mild bruising of the overlying skin (Fig. ). The swelling was reducible and disappeared in the supine position. There was no guarding and no rebound tenderness. He had normal bowel sounds on auscultation and the rest of the examination was unremarkable.
A diagnosis of mild head injury and a handlebar hernia was made. After resuscitation, his scalp laceration was closed with a one point suture and he was programmed for surgery for the handlebar hernia the next day. A surgical exploration of the area showed a 7 cm laceration of his lateral abdominal wall (Fig. ), running from the external oblique aponeurosis through all the muscle layers to his peritoneum with loops of small bowel present in the opening. There was no blood or feces in the area immediately surrounding the lesion. Exploration of the bowel loops closest to the opening did not reveal signs of intra-abdominal injury. The abdominal wall defect was repaired in layers. The abdominal incision was closed in a standard manner. His postoperative period was uneventful. He was discharged on postoperative day 9 and scheduled 2 weeks later for a follow-up visit, but unfortunately was lost to follow-up.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [26.0, 'kg'], 'height': [96.0, 'cm']}",28.21181,26.80122,29.6224,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 96.0 cm, which is 96.0 cm * 1 m / 100 cm = 0.96 m. The patient's weight is 26.0 kg. The patient's bmi is therefore 26.0 kg / (0.96 m * 0.96 m) = 28.21181 kg/m^2."
2188,6,Body Mass Index (BMI),physical,decimal,pmc-5728880-1,Extracted,"A 46-year-old man who served as a government official first visited our hospital with complaints of 8-month history of involuntary movements during sleep time, and 3- month history of slow response and walking unsteady. He had begun feeling depressed without a known cause 8 months ago. At almost the same time, he had started to engage in involuntary movement such as kicks and grasps during nighttime sleep, with snoring and sleep apnea. He took diazepam tablets, but it did not work. Afterwards, he noticed excessive sweating and felt hot and cold waves. His maximum body temperature was 37.2°C; after he used nimesulide, the temperature dropped to 35.0°C and was subsequently increased, with difficulty. Moreover, he got terrible constipation at that point. He visited mental health centers and was diagnosed with “mild depression” without auxiliary examinations or treatment 4 months ago. About 3 months ago, his family noticed that he had lost approximately 20 kg in weight, choked when drinking, and exhibited slow response, visual hallucinations, and walking unsteady. He got frequent drops from bed during sleeping due to his substantial actions; meanwhile, gasping breath and sleep apnea fragmented his sleep. Eventually, he spoke seldom and seemed to be blunt with shuffling gait.
The patient did not have any relevant medical history. He denied having history of trauma, prior blood transfusions, intravenous drug use, and alcohol abuse (Table ).
The patient was the fourth individual in his large family to exhibit the same clinical manifestations. The other 3 members all died within a year after onset (Fig. , pedigree chart).
Eight months after the onset, he was taken to our hospital by his families. We did series of tests at that time.
The middle-aged man appeared dull. During check-up, he fell into “sleep” easily and soon was awakened in horror by his involuntary sleep movements or snoring. The skin and general examination were normal. Temperature: 36.5°C, respiratory rate 20/min, Blood pressure (lying): 165/109, Pulse: 115. Blood pressure (standing): 150/100 mm Hg, Pulse: 110. Weight: 77 kg. Height: 178 cm.
He exhibited severe cognitive impairments, particularly with respect to orientation, attention, calculation power, delayed memory, and visuospatial dysfunction (his Mini-Mental State Examination and Montreal Cognitive Assessment scores were 15/30 and 9/30, respectively).
He had slurred speech and dysarthria
Cranial nerves (CNs) I-VIII and XI-XII revealed no deficits. CN IX and X showed slowness of bilateral gag reflex, and limited symmetrical elevation of soft palate to phonation.
Muscle tone was normal. Muscle strength was 5/5 for all groups tested. Spontaneous and evoked myoclonus was evident.
Bilateral biceps reflex and bilateral triceps reflex were 3/4, and bilateral patellar reflex and bilateral Achilles reflex were 4/4. Hoffman sign and Babinski sign were absent. Frontal lobe signs palmomental and grasp were not elicited.
Touch, pin, vibratory, and proprioception sensations were normal. Romberg test was negative.
Coordination was inaccurate for finger/nose testing and heel/knee/shin testing; rapid alternating movements were clumsy.
Arm swing was absent. There was bradykinesia and postural instability. Rapidly progressive dementia, ataxia (dysarthria and gait instability), and myoclonus were typical signs in prion diseases.
Temperature monitoring revealed that the patient's body temperature fluctuated from 36.0°C to 37.8°C, and the loss of circadian rhythm was observed. Blood pressure monitoring indicated a steady high blood pressure of approximately 150/100 mm Hg and the loss of dipper-type blood pressure rhythm, with a heart rate that fluctuated approximately 100 beats per minute. A dynamic electrocardiogram revealed sinus rhythm with the incidental discovery of multifocal ventricular premature beat.
Blood examinations such as blood routine, coagulation function, liver and kidney function, electrolytes, myocardial enzyme, blood ammonia, homocysteine, folic acid, VitB12, microelement (calcium, cadmium, cobalt, chromium, copper, iron, lithium, magnesium, manganese, nickel, lead, thallium, zinc), thyroid function and antibodies, rheumatism biomarker, infection-related antibodies (hepatitis B virus, hepatitis C virus, syphilis, HIV), and tumor marker showed normal. Cerebrospinal fluid (CSF) examination (intracranial pressure was 200 mmH2O, cell number 1, glucose, chloride, protein, acetic acid, IgA, IgM, IgG, Oligoclonal bands, PCR for JC virus, EB virus, HSV-I virus, Mycobacterium tuberculosis) appeared normal and 14–3–3 protein was negative. Autoimmune encephalopathy related antibodies (N-methyl-D-aspartic acid receptor, contactin-associated protein 2, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid 1 receptor, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid 2 receptor, leucine-rich glioma inactivated protein 1, gamma-aminobutyric acid B), and paraneoplastic syndrome related antibodies (CV2/CRMP5, PNMA2, RI, Yo, Hu, Amphiphysin) in blood and CSF were all detected, but none of them indicates abnormity. Routine urinalysis and fecal analysis were normal. Hormone secretion detection demonstrated the abnormal secrete rhythmicity of prolactin and growth hormone.
Extensive θ activity and scattered slow waves are recorded in an electroencephalogram (EEG). Brain magnetic resonance imaging (MRI) revealed atrophy of the frontal and temporal. Polysomnogram (PSG) demonstrated the patient's obvious deprivation of total sleep time; neither spindle nor slow wave sleep was detected during his “fragmented sleep,” even when he showed snoring, mentalis relaxation, sleep apnea, and hyoxemia (Fig. ).
The nucleotides from 12742 to 13318 (GenBank accessionnumber U2918) of exon I in PRNP were amplified; then, polymerase chain reaction products were directly sequenced on an ABI 377 automatic sequencer. The results were analyzed using DNA Sequencing Analysis Software version 3.4.1 (Gene Codes Corp, Ann Arbor, Michigan). Genetic analysis found that the patient harbored a D178N/129M haplotype mutation in PRNP (a GAC→AAC homozygous mutation at codon 178 and a methionine polymorphism at codon 129).
The patient had been diagnosed with FFI and received treatment with drugs to improve brain metabolism, such as idebenone, ganglioside, and coenzyme Q10. During the follow-up by telephone, his wife told us that he got once improvement in his responsiveness soon after discharge; however, sudden death occurred 3 months later. The total disease course was 11 months.
The patient information involved in our manuscript has been obtained and informed consent was obtained from his legal representatives. All human studies have been approved by the appropriate ethics committee and have therefore been performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki and its later amendments.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [77.0, 'kg'], 'height': [178.0, 'cm']}",24.30249,23.08737,25.51761,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 178.0 cm, which is 178.0 cm * 1 m / 100 cm = 1.78 m. The patient's weight is 77.0 kg. The patient's bmi is therefore 77.0 kg / (1.78 m * 1.78 m) = 24.30249 kg/m^2."
2189,6,Body Mass Index (BMI),physical,decimal,pmc-8072617-1,Extracted,"Case B-II-1 (upper panel in ), a 6-year-old female with DD, was referred for genetic diagnosis. She is a first child of non-consanguineous parents, and there is no family history of neurodevelopmental disorders. The pregnancy was uneventful, with normal fetal movements. She was born via normal vaginal delivery at 40 weeks, and her birth weight was 3.5 kg. During infancy, early signs of developmental delay were noticed by the parents. She could roll over at 6 months and crawled at 14 months. She experienced unprovoked generalized tonic-clonic seizures at 6 months, and treatment with valproic acid was administrated for 1 year. She spoke a single word, “Mama”, at 22 months, and ten or more words at 30 months. She ran fairly well, stooped without bumping into things or falling at 30 months, and walked downstairs alone at 36 months. We examined her using the Bayley scale of infant and toddler development, third edition (Bayley-III), at the age of 48 months and found global DD (cognitive, motor, and language developmental ages: 13–18 months, 23–32 months, and 16–20 months, respectively). She formed sentences that were two words long at age 6. Formal psychometric tests at 6 years of age revealed an IQ of 45, and she attends a specialized primary school. She had no facial dysmorphism and showed a normal growth pattern. Her body weight was 20 kg (50th percentile), height was 112 cm (25th percentile), and head circumference was 52 cm (75th percentile). The girl inherited the 15q11.2 BP1–BP2 deletion from her unaffected father. Her sister does not have this deletion.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [20.0, 'kg'], 'height': [112.0, 'cm']}",15.94388,15.14669,16.74107,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 112.0 cm, which is 112.0 cm * 1 m / 100 cm = 1.12 m. The patient's weight is 20.0 kg. The patient's bmi is therefore 20.0 kg / (1.12 m * 1.12 m) = 15.94388 kg/m^2."
2190,6,Body Mass Index (BMI),physical,decimal,pmc-4409735-1,Extracted,"A 47-year-old woman was transported to our hospital because of the sudden onset of severe pain in her left lower back. She was alert and conscious, with a blood pressure of 165/95 mmHg, pulse of 77 beats/minute, and oxygen saturation of 95%. She appeared to be in distress and complained of sharp spontaneous pain in her left lower back. She was 162.0 cm tall and weighed 84.5 kg. There were no physical features suggestive of Cushing’s syndrome. The patient had been healthy with no particular past medical history or familial disease. Her white blood cell count was 11,800/μL and her hemoglobin level was 8.8 g/dL. Other than these findings, biochemical tests and urinalysis on admission demonstrated no particular abnormalities (Table ). Emergency contrast-enhanced computed tomography (CT) of the abdomen revealed a tumor-like soft mass accompanied by massive bleeding in the retroperitoneum on the upper pole of the left kidney, in addition to vascular leakage from the middle suprarenal artery (Figure a, b). Immediately after obtaining the results of the CT scan, transcatheter embolization therapy of the left middle adrenal artery was performed based on a diagnosis of acute adrenal hemorrhage, possibly from a ruptured adrenal tumor (Figure a, b). The patient’s condition subsequently stabilized and a detailed investigation of the cause of the adrenal hemorrhage was initiated. Magnetic resonance imaging (MRI) revealed a hematoma expanded within the Gerota’s fascia, and a round tumor was detected in addition to the hematoma, with a rich vasculature and possible necrotic area (Figure a, b). No liver nodules or swelling of the retroperitoneal lymph nodes suggestive of metastasis were observed. Endocrine function of the adrenal gland appeared normal. The above findings indicated a ruptured non-functional adrenocortical tumor. Imaging confirmed the absence of metastatic lesions, and the tumor was removed by elective laparotomy surgery 2 months later. Regarding the surgical findings, no hemorrhage or abnormal adhesion was observed in the abdominal cavity. A soft elastic tumor measuring 10 cm was palpable in the retroperitoneum at the inferior border of the pancreatic body. Although it adhered closely to the surrounding retroperitoneal fatty tissue, the tumor was removed en bloc by partially excising Gerota’s fascia, without leaving any remnants. No invasion into the surrounding organs, lymph node metastasis, or liver metastasis was observed. The operative time was 229 min, and the surgical blood loss was approximately 500 mL. The patient recovered uneventfully. The tumor measured 13.5 × 8.6 × 4.2 cm and weighed 380 g. The cut surface indicated a yellowish solid tumor, with areas of bleeding accompanied by necrosis in a branched pattern (Figure a, b). The normal adrenal gland could not be identified visually. Histopathological examination revealed proliferated tumor cells with an atypical morphology, with an eosinophilic or clear cytoplasm and large nucleus containing a distinct nucleolus (Figure a, b). Nuclear atypia and abundant nuclear mitotic images were observed (≥11 per 50 high-power fields (HPF)). A wide focus of necrosis was also noted, although there was no apparent invasion outside the capsule. The final diagnosis was a ruptured, non-functioning left adrenocortical carcinoma, pT2N0M0, stage II. Mitotane administration for 2 years was planned as adjuvant therapy. The patient was alive at 6 months after surgery, with no serious adverse events or relapse.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [84.5, 'kg'], 'height': [162.0, 'cm']}",32.19784,30.58795,33.80773,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.0 cm, which is 162.0 cm * 1 m / 100 cm = 1.62 m. The patient's weight is 84.5 kg. The patient's bmi is therefore 84.5 kg / (1.62 m * 1.62 m) = 32.19784 kg/m^2."
2191,6,Body Mass Index (BMI),physical,decimal,pmc-2946041-1,Extracted,"A 45-year-old woman was scheduled for arthroscopic left knee meniscectomy. Her preoperative medical history, hematological, and biochemical findings were within normal limits. Her weight, height, and body temperature were 80 kg, 158 cm, 36.5℃, respectively. Upon arrival to the operating room she appeared stable, but expressed fear and worry. Her blood pressure was 160/80 mmHg, heart rate 80 beats/min, and pulse oximetry saturation 100%. Prior to propofol injection, 1% lidocaine 50 mg was intravenously injected for pain control. Subsequently, she suddenly expressed hyperventilation, seizure like activity, then tonic-rigid muscle tone, dyspnea with periodic breathing (not involving cyanosis), profound sweating, and clouding of consciousness. She was ventilated with 100% oxygen 7 L/min by mask. Her pupillary light reflex was normal, blood pressure was 170/110 mmHg, heart rate was 100-110 beats/min, and electrocardiogram revealed a normal sinus rhythm. We prepared midazolam; however, this event stopped spontaneously after 2-3 minutes. Her mental status returned to alert with the following vital signs, blood pressure 140/70 mmHg, heart rate 70 beats/min, body temperature 36.4℃, and a normal respiration rate. Sweating disappeared and she was able to obey commands. The operation was canceled, and she was sent to the recovery room. Except for a mild headache, her level of consciousness was alert, and she exhibited no neurological deficits on physical examination. In the recovery room, we carefully checked her medical history. It indicated that over the previous three years, several instances of sudden dyspnea, severe sweating attacks with mental change, had occurred during stressful events in her life.
She consulted with a neurosurgeon and psychiatrist. The magnetic resonance imaging (MRI) was normal however, upon psychiatric evaluation, she was diagnosed with anxiety, depressive disorder, and additionally, the cognitive function evaluation revealed lowered cognitive, attentive, and discriminative ability, and her IQ, as measured by the Korean-Wechsler Adult Intelligence Scale, was 85. Historically, she had experienced economic and familial problems. Together with clinical findings, we evaluated her as having conversion disorder.
After accurate reassurance coupled with reasonable rehabilitation to suit her symptoms, and with the suggestion of full recovery, further education, and drug treatment with milnacipran, buspirone, and lorazepam, her mood improved. Forty days later, she was subsequently readmitted for arthroscopic left knee meniscectomy. Upon arriving in the operating room, she indicated more comfort as compared to her previous experience. We injected midazolam 3.0 mg immediately after arriving to the operating room, and she underwent the procedure on her left knee without incident under general anesthesia. Following up with appropriate oral medication through our psychiatric outpatient center resulted in symptomatic improvement.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [80.0, 'kg'], 'height': [158.0, 'cm']}",32.04615,30.44384,33.64846,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 158.0 cm, which is 158.0 cm * 1 m / 100 cm = 1.58 m. The patient's weight is 80.0 kg. The patient's bmi is therefore 80.0 kg / (1.58 m * 1.58 m) = 32.04615 kg/m^2."
2192,6,Body Mass Index (BMI),physical,decimal,usmle-6447,Extracted,"A 1-year-old boy is brought to his pediatrician for a follow-up appointment. He was recently diagnosed with failure to thrive and developmental delay. His weight is 7 kg (15.4 lb), height is 61 cm (24 in), and head circumference is 42 cm (16.5 in). The patient’s father had a younger sister who suffered from mental and physical delay and died at a very young age. The patient was able to raise his head at the age of 7 months and began to sit alone only recently. He babbles, coos, and smiles to other people. On presentation, his blood pressure is 75/40 mm Hg, heart rate is 147/min, respiratory rate is 28/min, and temperature is 36.4°C (97.5°F). He has a coarse face with small deep orbits, proptotic eyes, big lips, and gingival hyperplasia. His skin is pale with decreased elasticity. His lung and heart sounds are normal. Abdominal examination reveals diminished anterior abdominal wall muscle tone and hepatomegaly. Muscle tone is increased in all groups of muscles on both upper and lower extremities. The physician becomes concerned and performs testing for the suspected hereditary disease. A blood test shows increased lysosomal enzyme concentration in the serum and decreased N-acetylglucosamine-1-phosphotransferase (GlcNAc phosphotransferase) activity within the leukocytes.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [7.0, 'kg'], 'height': [61.0, 'cm']}",18.81215,17.87154,19.75276,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 61.0 cm, which is 61.0 cm * 1 m / 100 cm = 0.61 m. The patient's weight is 7.0 kg. The patient's bmi is therefore 7.0 kg / (0.61 m * 0.61 m) = 18.81215 kg/m^2."
2193,6,Body Mass Index (BMI),physical,decimal,pmc-5665743-1,Extracted,"A 19-year-old male patient reported to the department of oral medicine and radiology with a chief complaint of pain on the left side of his face for the previous 7 months and a reduction in size of the left side of his face over the past 5 years ().
It started with a taut feeling on the left side that was followed by increased pigmentation in that area, and after few months the patient noticed that the left side of his face looked smaller than the right. The reduction in size was first noticed on the forehead. The patient also complained of a reduction in the hair present on the involved area. Over the previous 2 years, the patient was concerned about periodic and intense sharp painful spasms on the left side of the face, which interfered with mastication and speech. The spasm (3–4 episodes per day) lasted for 7–8 minutes each. Past medical history suggested maternal anemia during pregnancy. No history of trauma or infections was given.
The patient's vital signs were within normal limits, he was 6 feet tall and weighed 105 kg. Extra-oral inspection revealed gross facial asymmetry with marked atrophy on the left side of the face. A linear depression extending 2 cm from the hairline on the scalp involving the forehead (coup de sabre) till the glabella was noted. The left zygomatic arch, malar process, supra and infra-orbital rim were noticeably smaller when compared to the right side. Obliteration of the naso-labial fold with slight deviation of mouth and chin were also present on the left side. Skin on the left side of the face was hyper-pigmented. On palpation, the masseter and temporalis muscles were taut and had multiple tender points. The VAS score was 8. The temporo-mandibular joint also was tender, showed asynchronous movements of the condyles, with aggravated movements on the left side. Mouth opening was 4.5 cm. When the trigeminal and facial nerves were examined clinically, there was no detectable abnormality present.
Intraoral examination showed a retained left deciduous molar. The patient had Angles class 1 malocclusion, which means “The mesio-buccal cusp of the maxillary first permanent molar articulates in the mesio-buccal groove of the mandibular first permanent molar.” []. He also had a posterior open bite on the left side and cross bite, i.e. the left mandibular central incisor overlapped the left maxillary central incisor. Electrocardiogram and cone beam computed tomography (CBCT) were advised. The ECG was normal. The CBCT scan showed that the dimensions of the entire maxilla on the left side was smaller when compared to the right side along with a hypoplastic malar process (). A provisional diagnosis of left hemi-facial atrophy with spasm of the masseter muscle was made which was also confirmed by a neuro physician.
The patient was advised to take ultrasound therapy and TENS therapy on alternate days for 2 weeks. Ultrasound therapy was given with a frequency of .8 watt/cm2 on pulsed mode for 7 minutes, followed by TENS which was given on high TENS mode with a frequency of 80 Hz for 12 minutes. The electrodes were kept on the left masseter and temporalis.
At the end of 2 weeks of combination therapy, the patient reported a drastic reduction in the number of episodes of muscle spasm from 3-4 episodes per day to 1 per day. The VAS score for tenderness in the masseter and temporalis was also markedly reduced to 5 from 8 on the VAS. The pain which was initially intense and sharp now became dull and did not interfere much in his daily activities like speech or mastication.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [105.0, 'kg'], 'height': [6.0, 'ft']}",31.39474,29.825,32.96448,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 6.0 ft, which is 6.0 ft * 0.3048 m / ft = 1.8288 m. The patient's weight is 105.0 kg. The patient's bmi is therefore 105.0 kg / (1.8288 m * 1.8288 m) = 31.39474 kg/m^2."
2194,6,Body Mass Index (BMI),physical,decimal,pmc-7713807-1,Extracted,"An 83-year-old man (weight: 65 kg, height: 167 cm) was scheduled to undergo open reduction and internal fixation of a pertrochanteric fracture of the right femur. His past medical history was nonspecific. He had no history of allergy to drugs or food. Preoperative assessment including blood biochemistry, chest X-ray, and electrocardiography showed results within the normal range. Two hours before arriving at the operating room, the patient was administered 1 g of cefotetan sodium (Yamatetan®, Jeilpharm, Korea) intravenously (IV). Preoperative skin test to the Yamatetan® was negative.
Upon arriving at the operating room, the patient was monitored using noninvasive blood pressure (BP) measurement, electrocardiography, and pulse oximetry (SpO2) equipment. The pre-anesthetic BP, heart rate (HR), and SpO2 values were 172/108 mmHg, 94 beats/min, and 95%, respectively.
Spinal anesthesia was administered in the left lateral decubitus position using hyperbaric bupivacaine (13 mg) and fentanyl (10 μg) while oxygen was supplied at 6 L/min via a facial mask. After 5 min, sensory blockade of T10 was checked. For sedation, 1 mg of IV midazolam was administered. During the 50 min of the spinal anesthesia, that is 25 min after the start of surgery, the systolic blood pressure was between 110 and 120 and pulse rate was maintained in the early 100 s, and these were stable. By then, the patient had received 0.4–0.5 L of crystalloid (plasma solution), the estimated blood loss was about 50 ml, and the urine output was about 1.5 ml/kg/h.
After 25 min from the start of surgery, BP, HR, SpO2 values were 116/72 mmHg, 94 beats/min and 100%, respectively. The HES 130/0.4 (6% Volulyte®, Fresenius Kabi Korea, Korea) infusion was started through a peripheral IV route to replace the expected post-operative bone bleeding and an additional 2 mg of IV midazolam was administered. Five minutes after the administration of 50 ml of HES, the BP suddenly dropped to 84/52 mmHg, and the HR increased to 111 beats/min. SpO2 was reduced to 95%. To restore the BP, 100 μg of IV phenylephrine was administered immediately. Subsequently, the patient exhibited confusion and agitation. For further sedation, 1 mg of midazolam was administered, but the patient did not calm down and tried to move his fixed arms. Skin rash was observed on the face and neck first, which then spread to the entire body. The rechecked BP, HR, and SpO2 after phenylephrine administration, were 84/45 mmHg, 117 beats/min, and 97%, respectively. Additional 100 μg of IV phenylephrine bolus was administered. Immediately, the test for skin sensitivity to Yamatetan® was re-performed, and the result was negative. The patient’s agitation was reduced and the vital signs were maintained after multiple phenylephrine bolus were administered. The surgery was nearing completion; hence, general anesthesia was not considered.
Clinical signs including hypotension, tachycardia, and mild hypoxemia, as well as the appearance of a skin rash were consistent with the clinical criteria for an anaphylactic reaction. Other antibiotics or blood components were not administered during the surgery, and the anaphylactic reaction occurred within 5 min of HES exposure. The infusion of HES was terminated within 10 min, as it was considered the cause of the anaphylactic reaction. Subsequently, 5 mg of IV dexamethasone was administered. The total amount of IV injected phenylephrine was 400 μg. The patient received 1 L of the crystalloid (plasma solution) and 50 ml of the colloid (HES). Estimated blood loss and urine output were 100 ml and 200 ml, respectively. The total anesthesia time was 2 hours and the operation time was 46 min.
In the recovery room, laboratory tests including immunoglobulin E (IgE) levels and tryptase assessment were performed. The patient was taken chest X-ray due to observation of mild hypoxemia; however, the radiologist interpreted no unusual findings compared with the preoperative examination. The skin rash on the entire body persisted while the patient stayed in the recovery room; hence, IV dexamethasone 7.5 mg and chlorpheniramine 6 mg were administered along with 800 ml of crystalloid fluid for symptom relief.
The patient was transferred to the general ward with stable vital signs (BP: 111/78 mmHg, HR: 96 beats/min, SpO2: 100%) after close observation in the recovery room for 75 min. The patient’s urine output was sufficient (1–2 ml/kg/h) for 24 h after operation.
The result of the skin test to detect a reaction against HES performed on the next day was negative. Testing of a blood sample drawn in the operating room revealed the presence of 13.9 ng/ml of tryptase (normal range: < 11.4 ng/ml) and 211 IU/ml of total IgE, as determined using paper radioimmunosorbent test (PRIST) (normal range: 0–100 IU/ml). On the twenty-first day after the surgery, the patient was discharged without any complications.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [65.0, 'kg'], 'height': [167.0, 'cm']}",23.30668,22.14135,24.47201,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 167.0 cm, which is 167.0 cm * 1 m / 100 cm = 1.67 m. The patient's weight is 65.0 kg. The patient's bmi is therefore 65.0 kg / (1.67 m * 1.67 m) = 23.30668 kg/m^2."
2195,6,Body Mass Index (BMI),physical,decimal,pmc-8136308-1,Extracted,"This study involved 3-year-old boy who was born at full term and had previously undergone examination at a local eye clinic at around the age of 2.5 years after his parents noticed exotropia of his right eye. At around 6 months after that first examination, he was subsequently referred to our hospital for a more detailed examination. At the first examination, his visual acuity measured on the decimal acuity chart was unmeasurable in the right eye and 0.6 in the left eye. The eye position was mild exotropia for both near and distant vision, with no limitation of eye movement. Hirschberg-method testing revealed that the strabismus angle was approximately 30 prisms. In the patient's right eye, the fundus was not visible and there was no reflex due to the vitreous hemorrhage, and B-mode ultrasound examination revealed total retinal detachment (Fig. ). In the patient's left eye, a retinal hemorrhage and hard exudates were observed in the temporal retina, as well as a small retinal hemorrhage inferior to the optic disc (Fig. ). Since the patient was scheduled to undergo vitreous surgery in the right eye and a detailed ophthalmologic examination of the left eye under general anesthesia, a systemic examination was performed. There was nothing of note in the parents' family history.
The systemic examination findings revealed that the patient's blood test results were as follows: RBC 317 × 104/μL, Hb 10.0 g/dL, Ht 31.1%, MCV 97.9 fL, MCH 31.5 pg, MCHC 32.2%, WBC 5,910/μL, Plt 4.5 × 104/μL, Fe 74 μg/dL, TIBC 379 μg/dL, and UIBC 305 μg/dL. Since the patient had anemia and thrombocytopenia, a detailed pediatric examination was performed. His height was 89.0 cm, indicating a short stature (2.0 standard deviation below the mean), weight was 12.5 kg, vital signs were normal, skin was slightly anemic, and there was a deformity in the nail of the first toe. He was also found to have a mild developmental disability. MRI findings showed cerebellar atrophy (Fig. ). The findings of a bone marrow examination performed at the Department of Pediatrics of our University Hospital were as follows: nucleated cell count: 2.9 × 104/μL, megakaryocyte percentage: 0%, and myeloid/erythroid ratio (i.e., the ration of maturing myeloid cells to erythroid cells in the bone marrow): 6.15.
Those findings revealed mild bone marrow hypoplasia with almost no megakaryocytes, and there were mild megaloblastic changes and pseudo-Pelger-Huët anomaly cells. Refractory cytopenia of childhood, among other possibilities, was suspected, and a bone marrow biopsy was performed. The cellularity of the bone marrow was 60%, showing almost normocellular bone marrow; the myeloid/erythroid ratio was 2, and no mature megakaryocytes were present in the sample. Immunohistologically, there were no p53-positive cells. The possibility of congenital hematopoietic failure was suspected and genetic testing (i.e., DKC1 and TERC) was performed, yet no clinically significant mutations were observed. However, a telomere length test showed a shorter telomere length compared to that of healthy controls (i.e., −4.45 standard deviation below the mean). Thus, the presence of the shortened telomere length, as well as the other clinical symptoms, was suggestive of DKC. In regard to the familial history, it should be noted that the patient's great-grandmother on the father's side had been diagnosed with myelodysplastic syndrome that progressed into acute myeloid leukemia.
For treatment, the patient underwent vitreous surgery in the right eye and detailed ophthalmologic examination of the left eye under general anesthesia. His right eye had vitreous hemorrhage and severe proliferative membrane formation, and the condition was considered to be proliferative vitreoretinopathy (grade D-3) (Fig. ). The retinal detachment was longstanding and the retina was no longer extensible. The pre- and subretinal membranes were removed as much as possible, and liquid perfluorocarbon was injected. However, the extension was insufficient. Considering that the prognosis was poor, no further treatment was performed. For the patient's left eye, fluorescein fundus angiography was performed under general anesthesia. A wide retinal avascular area was observed in the temporal retina, and retinal neovascularization, exudative changes, such as hard exudates, and preretinal hemorrhage were observed in the marginal region (Fig. ). Transpupillary photocoagulation was performed in the retinal avascular area using a binocular indirect ophthalmoscopic photocoagulator (Fig. ). Following surgery, there were no remarkable complications, and the patient was discharged at 1 week postoperatively. However, it should be noted that after surgery, phthisis bulbi occurred in the patient's right eye, while the retinal neovascularization in the patient's left eye had regressed and the preretinal hemorrhage had diminished by laser treatment (Fig. ). Optical coherence tomography imaging of the left eye revealed residual hard exudates at the temporal area to the macula (Fig. ), and the corrected visual acuity in that eye at 6 months and 1 year postoperatively was 0.8 and 1.0, respectively, thus illustrating a favorable course.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [12.5, 'kg'], 'height': [89.0, 'cm']}",15.78084,14.9918,16.56988,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 89.0 cm, which is 89.0 cm * 1 m / 100 cm = 0.89 m. The patient's weight is 12.5 kg. The patient's bmi is therefore 12.5 kg / (0.89 m * 0.89 m) = 15.78084 kg/m^2."
2196,6,Body Mass Index (BMI),physical,decimal,pmc-5564160-1,Extracted,"The patient was a 24-year-old man (178 cm/67 kg) who had no specific underlying medical problems. He was scheduled for two-jaw surgery as a result of malocclusion. With the use of facial computer tomography, it was determined that the patient had an upper airway obstruction that extended from the pharynx to the larynx. After arriving in the operating room, the patient was monitored with a bispectral index, an electrocardiogram, an automated noninvasive blood pressure device, and pulse oximetry. For the induction of anesthesia, an intravenous injection of propofol (120 mg) and rocuronium (50 mg) was used. Nasotracheal intubation was performed with no specific difficulties. Arterial cannulation was performed via the dorsalis pedis artery for monitoring arterial blood pressure and performing a blood test. Additionally, a 16-gauge cannula was placed in the great saphenous vein for venous cannulation. Total intravenous anesthesia was maintained using propofol and remifentanil. During surgery, no special events occurred and the vital signs and oxygen saturation of the patient were normal.
The total operation time was 5 hours and 50 minutes. The total anesthetic time was 6 hours and 40 minutes. The total fluid input was 2000 mL (crystalloid) and 1000 mL (colloid). The estimated blood loss was approximately 800 mL and the total urine output was 1700 mL.
After the operation was finished, pyridostigmine bromide (15 mg) and glycopyrrolate (0.4 mg) were administered for the reversal of muscle relaxation. Intraoral blood and secretions were sufficiently suctioned. Following the return of regular spontaneous breathing and a fair recovery of the patient's level of consciousness, he was transferred to the post-anesthesia care unit—(PACU) in the Semi-Fowler's position—with a nasotracheal tube in-situ.
While in the PACU, the patient maintained a regular respiration rate with a T-piece while still in the Semi-Fowler's position. Oxygen saturation was maintained at 100% with the administration of oxygen at a rate of 5 L/min. Thirty minutes later, the surgeons requested extubation. The patient was in a bimaxillary fixation state with a wafer. The anesthesiologist ensured that the patient was conscious and observed as the patient performed a head lift for more than 5 seconds and fully grasped with hands. A hematoma secondary to bleeding from both jaws was confirmed by a hand examination.
After deep breathing, extubation was conducted and an oxygen mask was applied immediately with oxygen administered at a rate of 5 L/min. At that moment, the patient complained of respiratory difficulty, even though the anesthesiologist lifted the patient's chin. Despite untying the bimaxillary fixation and ambubagging, the oxygen saturation fell below 90%; thus, the patient called a team member for help. As a result of a narrow mouth opening (about 1 cm), an emergency airway was obtained by inserting a Combitube (37 Fr, Mallinckrodt). Oxygen saturation rose to 100% and the patient regained regular respiration (). An emergency operation was deemed necessary on the suspicion of a bleeding problem; thus, the Combitube was exchanged for a nasotracheal tube with a fiberoptic endoscope. It was confirmed that the breathing difficulty was not due to bleeding. The operation to verify a bleeding problem lasted 2 hours and 30 minutes. The patient was transferred to the intensive care unit in the oral surgery unit with a nasotracheal tube in-situ. The following day, a facial computer tomography was taken to verify airway space (). We observed that the airway space narrowing was severe compared to its pre-operational state. The patient's state was examined in the PACU for extubation. Tongue thrust and head lift were normal after the bimaxillary fixation was untied. After the swelling subsided, the patient was successfully extubated without complications.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [67.0, 'kg'], 'height': [178.0, 'cm']}",21.14632,20.089,22.20364,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 178.0 cm, which is 178.0 cm * 1 m / 100 cm = 1.78 m. The patient's weight is 67.0 kg. The patient's bmi is therefore 67.0 kg / (1.78 m * 1.78 m) = 21.14632 kg/m^2."
2197,6,Body Mass Index (BMI),physical,decimal,pmc-3408519-1,Extracted,"A 69-year-old man (height, 170 cm; weight, 85 kg) with prostate cancer underwent a retropubic radical prostatectomy. Preoperatively, he had a history of taking medications for bronchial asthma, and laboratory findings were within normal limits.
Anesthesia was induced and maintained with propofol, rocuronium, fentanyl, and sevoflurane. The patient was placed in the lithotomy position with his arms abducted to 90° on soft-pad-covered arm boards, and they were fixed loosely with cloth bands. Soft-pad-covered shoulder braces were placed over the coraco-clavicular joints. Cannulations were done uneventfully in the upper limbs, right internal jugular vein, and right radial artery. We used fluid warmer (Automer®, Ace Medical, Seoul, Korea) and warm respiration circuit (Heated circuit®, Ace Medical, Seoul, Korea) to prevent hypothermia during the surgery.
Because of the patient's obesity and massive adhesion, the operation time was 14 h and 40 min, and anesthesia time was 16 h and 30 min. The patient's position was lithotomy with Trendelenburg position (about 20-30°) during the surgery. Patient position was returned to level position every 4 hours for 10 to 15 minutes. The patient was hemodynamically stable during the anesthesia. There was no significant hypoxemia, hypothermia, hypovolemia and metabolic acidosis (). Blood loss was estimated around 800 ml, and urine output was not monitored due to the type of surgery. The total infused volume was 6% hydroxyethyl starch 2,000 ml, normal saline 3,000 ml, and lactated Ringer's solution 2,900 ml. Two units of packed red blood cells and four units of fresh frozen plasma were also infused.
After surgery, the patient recovered uneventfully and transferred to the intensive care unit. The patient had moderate facial edema but there was no respiratory difficulty after extubation. The patient had a 3 × 4 cm sized, elevated skin lesion on his right shoulder and a 1 × 2 cm sized, lesion on his left side. After 6 h in the intensive care unit, the patient complained of numbness with motor weakness in his right hand and forearm. He had flaccid paralysis in his forearm and hand, elbow and wrist flexion/extension were grade 2, shoulder abduction/adduction were grade 2, and hypoesthesia was observed in the whole radial and median nerve site. On the sixth postoperative day (POD 6), his brachial plexus injury showed no improvement, and the pain with tingling sensation was increased. Physical treatments included arm elevation, transcutaneous electrical nerve stimulation, and hot packs that were continued for two weeks. On POD 20, the motor function of his right arm mildly improved, right shoulder abduction/flexion was grade 3/2, right elbow flexion/extension was grade 1/3, first and second finger abduction/flexion was grade 1/2, and right fingertip dysthesia was positive.
A neurological examination was performed on POD22. The sensory nerve conduction study showed no response in the right median nerve, the superficial radial nerve, and the medial/lateral antebrachial cutaneous nerve stimulation. The motor nerve conduction study showed decreased amplitude in the right median (wrist, elbow level), the ulnar (wrist, below elbow, above elbow), the radial, and the axillary nerves. In the musculocutaneous nerve, the amplitude was only 0 to 0.1 mV. Needle electromyography showed no activity in the right biceps brachi, the triceps brachi, and the flexor carpi radialis muscles. The result was right brachial plexus injury with whole arm type-neuropraxic state or early partial axonotmesis. The patient was transferred to the rehabilitation department, and physical therapy was continued. However, the motor function of his right forearm did not recover, and his arm showed localized hyperthermia on the right, dorsal aspect of his hand with thermography, which estimates complex regional pain syndrome. On POD 38, the patient was discharged, and physical therapy was continued at the outpatient department. A follow-up neurological examination was performed on the fifth visit to the rehabilitation outpatient department after discharge (20 weeks after surgery), and his right shoulder abduction was grade 3, his elbow flexion/extension grade was 0/3, his wrist ventral flexion/dorsiflexion was grade 3/2, and it was otherwise unremarkable. A sensory and motor nerve conduction study and electromyography were also performed, and the result was an incompletely recovered state in the axillary branch while other nerves were in a stationary state.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [85.0, 'kg'], 'height': [170.0, 'cm']}",29.41176,27.94117,30.88235,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 85.0 kg. The patient's bmi is therefore 85.0 kg / (1.7 m * 1.7 m) = 29.41176 kg/m^2."
2198,6,Body Mass Index (BMI),physical,decimal,pmc-3250004-1,Extracted,"A 3-year-old male child was referred to casualty department with a thread protruding from mouth. On examination, he was 14 kg in weight and 88 cm in height. No sign of malnutrition was apparent and there was no alopecia. Abdominal examination revealed a non-tender smooth abdominal mass in the left upper quadrant emerging from beneath the left costal margin and extending over the midline. Rigid esophagoscopy was done and a bunch of hair about 50 g was found in esophagus which was extended into stomach. Laparotomy was planned and was carried out through an upper midline incision. A large 10×4 cm J-shaped foul-smelling black bunch of hairs, about 200 g, was retrieved through a longitudinal anterior gastrotomy [Figures and ]. There was also a daughter bezoar of 6×4 cm in size and about 100 g in jejunum about 30 cm away from duodenojejunal junction which was retrieved through enterotomy. Tail of the daughter bezoar was seen to have gone through the duodenum to jejunum. Abdomen was closed and patient was shifted to post-anesthesia care unit and then to surgical ward. His postoperative recovery was good and uneventful. He was discharged on 10th postoperative day. Psychiatric consultation was advised and child was followed up for a period of 1 year. No recurrence occurred.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [14.0, 'kg'], 'height': [88.0, 'cm']}",18.07851,17.17458,18.98244,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 88.0 cm, which is 88.0 cm * 1 m / 100 cm = 0.88 m. The patient's weight is 14.0 kg. The patient's bmi is therefore 14.0 kg / (0.88 m * 0.88 m) = 18.07851 kg/m^2."
2199,6,Body Mass Index (BMI),physical,decimal,pmc-3675438-4,Extracted,"Patient 4 was a 6.5-year-old boy, the second of four children to non-consanguineous Lebanese parents. The mother and maternal uncle had epilepsy. Pregnancy and delivery were uneventful, with the following birth measures: weight 3756 g, length 51 cm and OFC 35 cm (all measures at the 50th centile). He walked at age 16 months. When tested at age 4 years and 3 months with Reynell Developmental Language Scales, his language development was delayed by 1.5 years. Testing with WPPSI-III at age 6.5 years gave a borderline IQ of 74 (borderline intellectual functioning: IQ 70–84). He performed best on verbal tests, despite being bilingual. Cerebral MRI and EEG examinations at age 6 years were normal. At the last examination, at age 6.5 years, his weight was 23.9 kg (50th centile), height 126 cm (75th centile) and OFC 52 cm (25th centile). He had balance and coordination problems (Additional file
: Video Patient 4). Finger opposition was inadequate and he performed poorly when asked to stand on one leg at a time, jump, or walk on his toes or heals. Muscle tone was normal. Hearing and vision were normal. Due to early-onset muscular hypotonia he had been extensively examined for the possibility of neuromuscular disease, however, with normal results. Testing for metabolic abnormalities was also normal. Dysmorphic facial features (Figure
) and minor congenital anomalies in this patient are listed in Table
.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [23.9, 'kg'], 'height': [126.0, 'cm']}",15.05417,14.30146,15.80688,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 126.0 cm, which is 126.0 cm * 1 m / 100 cm = 1.26 m. The patient's weight is 23.9 kg. The patient's bmi is therefore 23.9 kg / (1.26 m * 1.26 m) = 15.05417 kg/m^2."
2200,6,Body Mass Index (BMI),physical,decimal,pmc-5560641-1,Extracted,"A 74-year-old male with the height of 162 cm and weight of 68 kg was scheduled for mitral valve plasty for cardiac failure caused by mitral valve regurgitation. An atrial septal defect had been surgically closed when the patient was 56 years old. Preoperative oral medications were digoxin, furosemide, aspirin, and warfarin. The patient also had chronic atrial fibrillation. The cardiothoracic ratio on a preoperative chest radiograph was 72%. Preoperative transthoracic echocardiography showed severe mitral regurgitation with an annulus enlargement and decreased posterior leaflet mobility, ejection fraction of 70%, estimated PA pressure of 65 mmHg, moderate pulmonary hypertension, and tricuspid regurgitation with a peak pressure gradient of 46 mmHg. There was no residual shunt at the atrial septum. Renal function was mildly reduced without electrolyte disturbance. Preoperative percutaneous oxygen saturation was 98%.
Anesthesia was induced via intravenous administration of propofol, remifentanil, rocuronium, and sevoflurane inhalation. Volume-controlled ventilation was started with a fraction of inspired oxygen (FiO2) of 0.6, tidal volume of 0.8 mL/kg, and a positive end-expiratory pressure of 0 cmH2O. A transesophageal echocardiography probe was inserted. General anesthesia was maintained with inhalation of sevoflurane, and intravenous administration of remifentanil and rocuronium.
After endotracheal intubation, a central venous catheter was inserted from the right internal jugular vein at the level of the thyroid cartilage; the inserted length was 10 cm from the site where the catheter was inserted transcutaneously. A PA catheter sheath introducer® (Edwards Lifesciences, CA, USA) was then inserted into the right internal jugular vein at the level of the cricoid cartilage. The PA was catheterized with a Swan Ganz thermodilution catheter® (Edwards Lifesciences) of size 8 Fr and length 110 cm. After a 15-cm PA catheter inserted through the sheath, the balloon was inflated with 1.5 mL of air. We slowly advanced the tip of the PA catheter forwards, while monitoring the pressure and detecting its waveform from the catheter tip. When the tip of the PA catheter showed the PA pressure waveforms, systolic pressure of 32 mmHg and diastolic of 21 mmHg following right ventricular pressure, the PAWP was 21 mmHg at the end-expiration. We then deflated the balloon and pulled the tip of the PA catheter back 3 cm so that the inserted length was 58 cm from the sheath inlet. We confirmed that the tip of the PA catheter showed a waveform typical of the PA and appropriate a and v waves, and also transesophageal echocardiography showed that the tip of the PA catheter was located in the right PA.
We collected 0.5 mL of blood through the tip of the PA catheter without inflating the catheter balloon. The blood sample had an oxygen partial pressure (PaO2) of 358.8 mmHg, carbon dioxide partial pressure (PaCO2) of 20.1 mmHg, and oxygen saturation of 99% ().
Alveolar PaO2 is calculated as follows:
PaO2 = (PB - 47 mmHg) × FiO2 - PaCO2 / 0.8
Where PB: atmospheric pressure, FiO2: fraction of inspired oxygen, and PaCO2: partial pressure of carbon dioxide in arterial blood. In the present case, PaO2 was calculated as 374.5 mmHg after PB of 760 mmHg, FiO2 of 0.6, and PaCO2 of 32.0 mmHg applied to the equation. The blood sample collected from the tip of the PA catheter showed a PaO2 of 358.8 mmHg; therefore, the sample must have either been from the pulmonary vein or alveolar blood. We have never performed blood sampling from the pulmonary veins, because sampling from pulmonary veins requires obstruction of the PA branch. We thought that the tip of the PA catheter had been over-inserted into a branch of the PA and pulled the tip of the PA catheter back 5 cm, but the second blood sample showed the same results (). We then pulled the PA catheter back until the inserted length of the PA catheter was 47 cm, while watching the location of the catheter tip on X-ray fluoroscopy ( and ). The blood gas testing on a sample collected through the catheter tip showed an oxygen saturation of 84.4 % and PaO2 of 41.6 mmHg (). The surgical procedure was performed without problems.
Postoperative chest radiography showed proper placement of the PA catheter, but a chest radiograph taken the next day showed over-insertion, although the insertion length was unchanged ( and ). The PA catheter was removed from the patient. The postoperative course was uneventful, but long-term rehabilitation was required. The patient was discharged from the hospital 2 months after the surgery.
Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [68.0, 'kg'], 'height': [162.0, 'cm']}",25.91068,24.61515,27.20621,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.0 cm, which is 162.0 cm * 1 m / 100 cm = 1.62 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.62 m * 1.62 m) = 25.91068 kg/m^2."
2201,6,Body Mass Index (BMI),physical,decimal,pmc-2908227-1,Extracted,"A 72-year-old man, 169 cm tall and weighing 56 kg, complained of general weakness and the diagnostic workup suggested lung cancer with mediastinal lymphadenopathy and syndrome of inappropriate secretion of anti-diuretic hormone (SIADH). To obtain a tissue diagnosis, the patient was scheduled for a mediastinoscopic biopsy.
He had smoked two packs of cigarettes a day for 55 years and had drunk one-and-a-half bottles of soju a day for 50 years. There was no history of neuromuscular disorders and no family history of neuromuscular disease. Four years earlier, he had complained of vertigo and gait disturbance for 1 month and a neurologist had suspected of encephalitis.
Preoperatively, the routine laboratory values were within normal limits, except for hyponatremia (125 mEq/L). He had no symptoms or signs of hyponatremia, such as nausea, vomiting, visual disturbances, depressed level of consciousness, agitation, confusion, muscle cramps, weakness, etc. After a nephrology consultation, we decided to perform the scheduled biopsy based on the absence of symptoms and signs associated with hyponatremia and the need to obtain a tissue biopsy to decide on treatment. Pulmonary function tests showed small airway disease.
In the operating room, routine monitoring was used, although neuromuscular transmissions were not monitored. General anesthesia was induced with propofol and succinylcholine. After tracheal intubation, anesthesia was maintained with inhaled sevoflurane 1.5-3 vol% and 50% nitrous oxide in oxygen. Intravenous vecuronium 4 mg was administered for muscle relaxation. Perioperative fluid administration was restricted due to the SIADH. The biopsy was obtained and the pathology showed small cell carcinoma of the lung. It took about 1 hour to incision closure from the time vecuronium was given.
At the end of the procedure, intravenous glycopyrrolate 0.4 mg and pyridostigmine 15 mg were administered to reverse the blockade, but the patient remained motionless and could not breathe spontaneously 40 minutes after reversal. Therefore, we administered atropine 0.5 mg and neostigmine 1.0 mg intravenously in case the dose of the reversal agent had been inadequate. However, there was no improvement in neuromuscular function. His pupils were equal and reactive. The oral body temperature was 36.2℃ and no antibiotics known to cause neuromuscular blockade had been administered.
We monitored neuromuscular function by attaching a nerve stimulator (TOF-Watch®, Organon Ireland Ltd., Dublin, Ireland). There was no twitch response to TOF stimulation, although there was a very weak response to tetanic stimulation at 50 Hz for 5 seconds with no post-tetanic potentiation. A blood sample was drawn to check the serum electrolytes. There were no abnormal values, other than a serum sodium that was lower than the preoperative level. We thought that sympathetic activation due to the operation might have led to significantly increased levels of ADH in the absence of volume constriction. We began to correct the hyponatremia with 3% hypertonic saline, slowly, to prevent cerebral edema or central pontine myelinolysis.
About 2 hours after the end of the procedure, he began to move his fingers slightly and there were four twitch responses to TOF stimulation. However, there was no voluntary respiratory movement or eye opening. We believed that he was alert because he could move his fingers in response to verbal commands.
He was taken to the postanesthesia care unit and placed on a mechanical ventilator. With time, his hyponatremia improved slowly to within the normal range and his neuromuscular function improved. He could move his forearm and hands, but lacked sufficient muscle strength to breathe spontaneously and be extubated. We began to suspect a neuromuscular transmission disorder and a consultation with a neurologist established the diagnosis of LEMS by electromyography (). He was given anticholinesterase via a nasogastric tube, but there was no improvement in neuromuscular function. Two weeks postoperatively, all the laboratory values were within normal limits. He could sit up and write letters. However, weaning from the mechanical ventilator was impossible. He was discharged with a portable ventilator.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [56.0, 'kg'], 'height': [169.0, 'cm']}",19.60716,18.6268,20.58752,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 169.0 cm, which is 169.0 cm * 1 m / 100 cm = 1.69 m. The patient's weight is 56.0 kg. The patient's bmi is therefore 56.0 kg / (1.69 m * 1.69 m) = 19.60716 kg/m^2."
2202,6,Body Mass Index (BMI),physical,decimal,pmc-6606978-1,Extracted,"A 4-year-old boy was referred to our hospital because of recurrent KH. He was born at full term and had a birth weight of 2940 g. At the age of 2 years and 7 months, the patient developed KH for the first time. When he was 4 years old, he suffered from recurrent hypoglycemia approximately every 2 months. The patient's hypoglycemic episodes mostly occurred in the morning within 12 hours from his last meal, even though he ate dinner as usual. In particular, the patient became hypoglycemic during infections. At the age of 4 years and 11 months, the patient was started on a bedtime uncooked cornstarch supplement to prevent nocturnal hypoglycemia. Since then, he has experienced no hypoglycemic episodes.
At the age of 5 years and 4 months, the patient's height was 113.0 cm (+0.9 SD) and his weight was 20.4 kg (+0.7 SD). Fasting for 14.5 hours induced hypoglycemia (Table ). Endocrinologic data, including thyroid-stimulating hormone, growth hormone, adrenocorticotropic hormone, free triiodothyronine, free thyroxine, insulin, cortisol, epinephrine, norepinephrine, and dopamine, showed no abnormality. Urinary organic acid analysis and blood acylcarnitine analysis showed nonspecific profiles. During our investigations, the patient exhibited no signs of hepatomegaly, and the concentrations of transaminases in his serum were normal. The patient is currently 9 years old, and his physical and mental development is normal. Bedtime supplementation with uncooked cornstarch was stopped when the patient was aged 9 years and 1 month. The patient's elder sister has experienced no hypoglycemic episodes, and his 6-year-old brother has experienced KH only once. As far as we examined, there are no relatives who had experienced recurrent hypoglycemia.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [20.4, 'kg'], 'height': [113.0, 'cm']}",15.97619,15.17738,16.775,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 113.0 cm, which is 113.0 cm * 1 m / 100 cm = 1.13 m. The patient's weight is 20.4 kg. The patient's bmi is therefore 20.4 kg / (1.13 m * 1.13 m) = 15.97619 kg/m^2."
2203,6,Body Mass Index (BMI),physical,decimal,pmc-3376881-2,Extracted,"A 46-year-old male patient (185 cm, 80 kg) with a history of myocardial infarction and limited cardiac function (LVEF 20%) underwent resection of a massive left ventricular anterior wall aneurysm combined with mitral valve annuloplasty. Despite adequate filling pressures, use of multiple inotropic agents including levosimendan and insertion of an intraaortic balloon pump, cardiogenic shock occured postoperatively. He was transferred to the operating room for venoarterial extracorporal membrane oxygenation (ECMO, Medtronic, Biomedicus, MI, USA) rescue therapy. Since weaning from ECMO remained unsuccessful for four days, a permanent left ventricular assist device (Jarvik 2000) was inserted. Postoperatively, the patient suffered from right heart failure resistant to inhalation of iloprost and milrinone, so that venoarterial ECMO had to be re-implanted. Despite good function of both cardiac assist devices the patient suffered from severe vasodilatory shock resistant to high dosages of norepinephrine (3.0 mg/h) and vasopressin (8.0 I.U./h). Administration of methylene blue resulted in a reduction of norepinephrine and vasopressin to acceptable dosages within four hours (). However, no therapeutic option was suitable for this patient: switching to a synchronized biventricular assist device was technically not possible any more. The patient died 18 hours after methylene blue administration.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [80.0, 'kg'], 'height': [185.0, 'cm']}",23.37473,22.20599,24.54347,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 185.0 cm, which is 185.0 cm * 1 m / 100 cm = 1.85 m. The patient's weight is 80.0 kg. The patient's bmi is therefore 80.0 kg / (1.85 m * 1.85 m) = 23.37473 kg/m^2."
2204,6,Body Mass Index (BMI),physical,decimal,pmc-2803941-1,Extracted,"A 57-year-old man was admitted on March 2006 to our hospital referring acute pain when accidentally injured by a plastic object at head. He mentioned a palpable, soft, immovable and tender mass at the left temporal bone. His left orbit was also painful. He had already used analgesic and anti-inflammatory drugs. No fever, elevated regional temperature nor lymphadenopathy was recorded. The physical and neurological examination had no pathological signs. He did not present numbness, weakness or remarkable tendon reflexes and muscular tone. The mobility of the head was normal. The vision and hearing was not affected.
The patient had a height of 1.78 m and weighted 80 kgrs. He belongs to Arabic nation (born in Lebanon) but he has the Greek ethnicity living in Greece the last 40 years. 31 years ago psoriasic arthritis was diagnosed with the joint of the left elbow mainly affected. He received no therapy for the disease. 10 years ago he presented acute myocardial infarction and undertook bypass. Since then he received drug therapy for hypertension. The patient smoked 2 packs of cigarettes since the age of 25 and consumed 1-2 glasses of alcohol per day. No family history of tumors is known.
Blood examination revealed no pathological findings, neither elevation of leukocytes nor of erythrocyte sedimentation rate. Heart ultrasound revealed no present pathology.
A first attempt to excise the lesion failed as there was an erosion of the temporal bone. Material for histological examination was extracted and we found a domination of histiocytes. No malignancy was suspected. We continued with radiological depiction of the skull.
Plain radiographs demonstrated a large oval-shaped osteolytic area in the left temporal bone [figure ]. Its borders were regular and no bone formation was noted. Its size was about 2 cm. CT verified a lytic lesion at the left temporal bone of the skull [figure ]. The estimated size was 1.8 × 1.6 cm. The borders were sharp and periosteal reaction was obvious. The meninges were almost exposed to environment and that is the reason why a moderate injury led to intense pain. No fluid was present. Scintigraphy with Tc-99m demonstrated a non absorbent focus in the left temporal bone [figure ]. Left elbow was also depicted as highly absorbent because of the psoriatic arthritis. No secondary or multiple foci were enhanced.
A radical excision of the lesion on health borders of 2 cm was performed. The tumor was gelatinous and brownish without hematomas. It was perforating the whole diploe and part of the external meninga. We excised a piece of a diameter of 5 cm including the lesion and used a periosteal transplant to bridge the gap. No cranioplasty was done at first time. The patient received vancomycin and cefoxitime for two days. Material was sent for histological examination which showed many Langerhans cells, eosinophils, neutrophils and lymphocytes. No fibroblasts or giant cells were found. The S-100, CD1a and Langering proteins were positive. There were necrotic elements too. Diagnosis of eosinophilic granuloma of the skull was set. The patient was administered five cycles of low-dose post-surgical radiotherapy were administered.
Carnioplasty with a heterologous transplant (Porex) was performed eight months later. The aesthetic result was excellent and there were no complications. On March 2008, a new CT of the brain depicted no further lesion and the aesthetical result was excellent.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [80.0, 'kg'], 'height': [1.78, 'm']}",25.24934,23.98687,26.51181,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.78 m. The patient's weight is 80.0 kg. The patient's bmi is therefore 80.0 kg / (1.78 m * 1.78 m) = 25.24934 kg/m^2."
2205,6,Body Mass Index (BMI),physical,decimal,pmc-6188736-1,Extracted,"The patient was a 60-year-old man who was diagnosed with alcoholic liver cirrhosis and type 2 diabetes when he was 50 years old. His drinking history was 540–720 mL Japanese sake per day for 35 years, and his smoking history was 30 cigarettes per day for 30 years. His ascites increased in 2008 when he was 57 years old, and he repeatedly exhibited symptoms of hepatic encephalopathy. Due to the liver cirrhosis symptoms, the patient was treated with several medications including furosemide, spironolactone, lactulose, and total amino acid preparation. To prevent the complications of liver cirrhosis, coil embolization to a portal venous shunt was performed twice. The patient was admitted to our hospital in June 2012 because of slowly progressive renal impairment and nephrotic syndrome.
Upon admission, the patient's height and weight were 166 cm and 64 kg, respectively. His body temperature was 36.7°C and his blood pressure was 150/60 mmHg. His consciousness was clear. His abdomen was slightly expanded but exhibited no tenderness. The liver and spleen were not palpable. No rash or purpura was noted on the skin. Diabetic and/or hypertensive changes were not observed in the ocular fundus.
The laboratory findings on admission were hemoglobin level of 9.4 g/dL (normal range 13.5–17.6 g/dL), platelet count of 11x104/μL (normal range, 13.1–36.2x104/μL), prothrombin time measurement of 68% (normal range, 70–130%), total bilirubin level of 0.9 mg/dL (normal range, 0.3–1.2 mg/dL), NH3 level of 85 mg/dL (normal range, 30–80 mg/dL), blood urea nitrogen level of 41 mg/dL (normal range, 8–20 mg/dL), serum creatinine concentration of 1.77 mg/dL (normal range, 0.5–1.1 mg/dL), serum total protein level of 5.7 g/dL (normal range, 6.7–8.3 g/dL), serum albumin level of 2.1 g/dL (normal range, 3.5–5.2 g/dL), total cholesterol of 188 mg/dL (normal range, 120–219 mg/dL), and HbA1c of 5.8% (normal range, 4.3–5.8%). The serum levels of IgG were 1558 mg/dL (normal range, 870–1700 mg/dL), of IgA were 481 mg/dL (normal range, 110–410 mg/dL), of IgA1 were 398 mg/dL (normal range, 50–314 mg/dL), of IgA2 were 83 mg/dL (normal range, 10–156 mg/dL), and of IgM were 219 mg/dL (normal range, 35–220 mg/dL). The serum levels of free κ and λ light chains were 149.0 mg/L (normal range, 3.3–19.4 mg/L) and 106.0 mg/L (normal range, 5.7–26.3 mg/L). The serum free light chain ratio was within normal range. The serum level of complement factor C3 was 79 mg/dL (normal range, 65–135 mg/dL), of C4 was 17 mg/dL (normal range, 13–35 mg/dL), and of CH50 was 41.1 U/mL (normal range, 30–50 U/mL). All of the other serology findings including anti-nuclear antibody, hepatitis B virus surface antigen, hepatitis C virus antibody, anti-neutrophil cytoplasmic antibody, and anti-glomerular basement membrane antibody were negative. There was no M-spike on serum and urine protein electrophoresis. A serum test for a cryoglobulin precipitation was negative.
The urinary sediments showed many red blood cells in high power fields together with granular casts and dysmorphic red blood cells. The urinary protein excretion was 4.7 g/day. The 24-hour creatinine clearance was 45 mL/min. Computed tomography revealed liver deformity with moderate accumulation of ascites. The kidneys were normal in size and there were no signs of urinary tract obstruction.
The renal biopsy specimens contained a total 28 glomeruli, 12 of which were globally sclerotic. The degree of interstitial fibrosis/tubular atrophy was 50–60% of the total biopsy specimen identified. Moderate fibrous intimal hyperplasia was observed in the arcuate artery. Diffuse segmental double-contours of the glomerular basement membrane and mesangial cell hypercellularity were identified in nonsclerotic glomeruli, exhibiting a membranoproliferative glomerulonephritis-like pattern (). Some glomeruli showed moderate-to-severe endocapillary hypercellularity, accompanied by fibrocellular crescents (). Fluorescent immunostaining showed granular staining of IgA and C3, but not of IgG, IgM, or C1q, on glomerular capillaries and some mesangial areas (Figures –). Among the IgA subtypes, staining of IgA1 (GenWay Biotech, San Diego, CA, USA) was observed, but staining of IgA2 (GenWay Biotech) was not identified (Figures and ). With light chain immunostaining, only κ (SouthernBiotech, Birmingham, AL, USA) was identified and no λ staining (SouthernBiotech) was seen (Figures and ). On electron microscopy, the glomerular capillary walls showed double contours. Electron-dense deposits were found in the paramesangium and around the subendothelial space of the glomeruli (). No organized structure deposits were identified (). Based on these findings, this case was histologically diagnosed as diffuse membranoproliferative glomerulonephritis with monoclonal IgA1-κ deposits.
Because this case was accompanied by moderately advanced decompensated liver cirrhosis, there was a concern that the patient may have serious side effects due to aggressive treatment such as the administration of corticosteroids. Thus, supportive treatment based on medications such as RAS inhibitors/diuretics, in addition to dietary therapy including salt restriction/branched-chain amino acid administration, was selected. Although these treatments led to a modest decrease in the urinary protein excretion, the patient's renal dysfunction slowly progressed and finally resulted in end-stage renal failure and initiation of dialysis therapy.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [64.0, 'kg'], 'height': [166.0, 'cm']}",23.22543,22.06416,24.3867,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 64.0 kg. The patient's bmi is therefore 64.0 kg / (1.66 m * 1.66 m) = 23.22543 kg/m^2."
2206,6,Body Mass Index (BMI),physical,decimal,pmc-5588509-1,Extracted,"The proband was a 12-year-old male child, the youngest child of first-cousin healthy parents, who presented with developmental delay, speech delay, ataxia and bilateral cataracts. He was born at term through normal vaginal delivery following an uncomplicated pregnancy with a birth weight of 3.5 kg. There were no postnatal problems. At 12 years his weight was 33 kg (10th to 25th centile), height was 147 cm (25th centile), and head circumference was 53 cm (50th to 75th centile). The parents reported that he was an active and cooperative boy. He had subtle dysmorphic features, including bushy eyebrows and a flat mid face with a high arched palate. He had an ataxic gait, with dysmetria, intention tremor and dysdiadochokinesia. A convergent squint was present in the left eye. His muscle tone was normal and deep tone reflex was elicited. Pectus carinatum was observed, and the patient was noted to have bilateral clinodactyly of the fifth fingers as well as flat feet. A skeletal survey was normal, except for a mild kyphosis seen at the lower thoracic spine. He was able to stand with support, and walked with support with an ataxic gait. A developmental assessment at 8 years of age showed that he was able to say full sentences, but with poor articulation, and needed help with dressing and feeding. At 6 years of age a pelvic ultrasound had detected a left undescended testis, for which he had undergone orchidopexy. He had also been diagnosed with infantile bilateral cataract, which had been surgically corrected.
X-ray computer tomography and magnetic resonance imaging of the brain revealed cerebellar atrophy with a dilated 4th ventricle (fig. ). All other investigations were normal and the family history was unremarkable. The patient's four living siblings were all healthy. The mother had had one spontaneous abortion. Based on the clinical features, a tentative diagnosis of MSS was made.
Informed written consent was obtained and genomic DNA was extracted from the patient and both of his parents. Ten milliliters of venous blood was drawn from each of the individuals and sampled in EDTA tubes. The coding region of exons 2–10 and the exon-intron boundaries of the SIL1 gene were amplified by polymerase chain reaction (PCR) and sequenced directly by Bioscientia (Ingleheim, Germany). The resulting sequence data was compared with the reference sequence NM_022464. For confirmation of the results, an independent PCR product was sequenced, also by Bioscientia.
The sequencing of SIL1 revealed a homozygous deletion from the 5′ untranslated region (UTR; c.-197) to exon 1 (c.90). Instead of the deleted bases, there was a homozygous insertion of one base (C) of unclear origin and 20 bases from intron 1. Both parents turned out to be heterozygous carriers of the same c.-197_90delinsCTGTACTTTCTCAGTTCACT mutation (fig. ). This mutation was not found in the EXAC Browser or in the GalaxC™ Allele Frequency Database, which contains >2.5 million unique Middle Eastern pathogenic mutations and variants.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [33.0, 'kg'], 'height': [147.0, 'cm']}",15.27141,14.50784,16.03498,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 147.0 cm, which is 147.0 cm * 1 m / 100 cm = 1.47 m. The patient's weight is 33.0 kg. The patient's bmi is therefore 33.0 kg / (1.47 m * 1.47 m) = 15.27141 kg/m^2."
2207,6,Body Mass Index (BMI),physical,decimal,pmc-6786676-1,Extracted,"A 55-year-old man was brought to emergency room after accidental ingestion of insecticide, methidathion (also known as methion in Korea) while he was drunken. According to his family member, he ingested a paper cup full of 40% original solution. He had history of non-insulin dependent diabetes mellitus. His body weight was 75 kg and height was 173 cm.
In the emergency room, he was semi-comatose, but had intermittent myoclonus-like movements. Blood pressure was 67/50 mmHg and heart rate was 48 beats per minute. His trachea was intubated and he was placed on mechanical ventilation. Initial resuscitation efforts included intravenous infusion of atropine (50 mcg/minute) after a bolus of 1 mg, norepinephrine (0.25 mcg/Kg of body weight/minute), vasopressin (0.3 units/minute), dobut-amine (30 mcg/Kg/min), epinephrine (0.25 mcg/Kg/min), and PAM-A (Pralidoxime chloride, cholinesterase reactivator, 2.5 mg/min), in addition to intravascular volume expansion with crystalloids, in efforts to keep the mean arterial pressure higher than 65 mmHg. Also given were midazolam, remifentanyl, and vecuronium. Gastric lavage was done. The initial arterial blood gas analysis while he was being mechanically ventilated with 100% of oxygen showed that pH was 6.96, PCO2 98 mmHg, PO2 85 mmHg, HCO-3 19 mEq/L, and BE -14.8. His ethanol level in blood was 144 mg/dl. Albumin was 4.4 g/dl, glucose 359 mg/dl, Hemoglobin A1c 11.4%, and total CO2 content 16.9 mEq/L. The levels of total bilirubin, aminotransferases, sodium, chloride, potassium and troponin I were normal, so were prothrombin time, international normalized ratio, and activated thromboplastin time. Leukocyte count was 17,400 cells/mm3, hemoglobin 15.4 g, hematocrit 46% and platelets 266,000/mm3 . The repeated analysis of arterial blood gases showed that pH was 7.09, PCO2 29 mmHg, PO2 66 mmHg, HCO-3 20 mEq/L, BE –11.3 and lactate 7.8 mEq/L. Urine output had been in the range of 200 to 600 mL/hour. Serum cholinesterase level was 12 (normal, 620-1,370) units/L.
The patient was transferred to intensive care unit. Tests for hepatitis A, B, and C were negative, so was human immunodeficiency virus test. Free T4 level was 3.84 mcg/L. Arterial blood gases showed that pH was 7.23, PCO2 59 mmHg, PO2 78 mmHg, HCO-3 24 mEq/L and lactate 1.7 mEq/L. Blood cultures, of which blood samples were taken from the central venous line, arterial line and percutaneous punctures, were all negative. Intravenous infusion of vecuronium was discontinued. On the 2nd hospital day, intravenous infusion of epinephrine was tapered off. The infusion of norepinephrine was reduced to 0.15 mcg/kg/min, vasopressin to 0.15 units/min and dobutamine to 20 mcg/kg/min. There was no longer metabolic acidosis. Urine output decreased to 300 ml/h. On the 4th hospital day, intravenous infusion of atropine was discontinued. Glycopyrrolate was given intermittently whenever heart rate became less than 60 beats per min. Urine output was running about 100 ml/h. Daily chest radiography had been unremarkable. Sputum culture revealed the growth of Klebsiella pneumoniae, which was sensitive to all antibiotics except ampicillin. Piperacillin/tazobactam was started. On the 5th hospital day, doses of vasopressors and inotropic were not able to be reduced. Interleukin-6 was 335 pg/ml and procalcitonin 92 ng/ml. Intravenous infusion of remifentanil and midazolam had been maintained for sedation. Despite the use of high doses of vasopressors and inotropic, the patient’s hands and feet were warm and pink, and there was no metabolic acidosis, thus indicating that there was no peripheral vasoconstriction or poor peripheral perfusion. On the 6th hospital day, lactate level was 1.3 mEq/L. Fibrinogen was 966 mg/dl and d-dimer 6.53 mg/L. The absence of deep vein thrombosis was confirmed with ultrasonography and transthoracic echocardiography ruled out an acute pulmonary embolism (no right ventricular dysfunction). Total parenteral nutrition was started. Enteral feeding was not considered appropriate at this time. On the 9th hospital day, intravenous midazolam infusion was discontinued. Over the following several days, vasopressors and inotropic were able to be reduced gradually. On the 11th day, all vasoactive medications were completely tapered off. The patient opened eyes on command. Intravenous infusion of ketamine was added. On the 14th hospital day, ulnar nerve stimulation test using train-of-four technique to assess neuromuscular junction activity revealed the presence of depolarizing block, indicating the persistent muscle paralysis by cholinergic crisis. Sputum culture showed the growth of methicillin-resistant Staphylococcus aureus. Vancomycin was started. On the 17th hospital day, pH of arterial blood decreased 7.29 from 7.41 and PCO2 increased to 56 mmHg from 42 mmHg in the afternoon, compared with those of morning values. Leukocyte count increased to 17,750 cells/mm3 from 12,000. Platelet count also increased to 765,000/mm3 from 576,000/mm3. Ultrasonography of abdomen showed a large amount of ascites. CT scan of abdomen revealed multiple perforations of small bowel. While the exploratory laparotomy was being arranged, pulmonary artery catheter was inserted via right subclavian vein under ultrasonographic guidance. Pulmonary artery pressure was 36/18 mmHg with pulmonary capillary wedge pressure of 12 mmHg. On laparotomy, almost the whole small bowel was found gangrenous and there were multiple perforations of small bowel. The portion of bowel from the distal duodenum to the ascending colon was resected. Since there was no gross evidence of peritonitis, the peritoneum was closed. Postoperatively, vasopressors and inotropic were required overnight, but quickly tapered off by the following morning. Urine output was running in the range of 100 to 300 ml/h. Analysis of arterial blood gases showed that pH was 7.44, PCO2 44 mmHg, PO2 83 mmHg and HCO-3 29.2 mEq/L, while the patient was on mechanical ventilator with 10 cmH2O and 0.6 of FiO2. Lactate was 1.8 mEq/L. Creatinine was 1.15 mg/dl. Leukocyte count was 17,690 cells/mm3 and platelet 352. Fibrinogen level was 305 mg/dl. On the 20th hospital day, glycopyrrolate was given for the last time. Cultures from the peritoneal drain and blood were all negative. Procalcitonin was 5.03 ng/dl, interleukin-6 92.2 pg/dl, C-reactive protein 16.32, fibrinogen 432 mg/dl and platelet count 230,000/mm3. Repeated ulnar nerve stimulation test using train-of-four technique revealed the presence of depolarizing block, indicating the persistent muscle paralysis by cholinergic crisis. Pathologic report of surgical specimen revealed the aspergillosis infection causing gangrene and abscess formation with multiple bowel perforations. Serum Aaspergillus antigen (galactomannan) was negative. Voriconazole was started. On the 27th hospital day (10th postoperative day), culture of peritoneal drain fluid showed the growth of methicillin-resistant S. aureus. Blood culture was negative. On the 31th hospital day, the second laparotomy revealed a diffuse peritonitis, gangrenous colon and abscess formation with perforations. Total colectomy was done. Postoperatively, the patient developed a severe septic shock, requiring vasopressors and inotropic in escalating doses. Intravascular volume expansion was done with guidance of pulmonary artery catheter. Thermodilution cardiac output was running in the range of 10 to 12 L/min. The patient developed a severe metabolic acidosis with rising level of lactate. On the 38th hospital day, lactate level rose to 10.7 mEq/L. Repeated test for Aspergillus antigen (galactomannan) became positive (5.42 index). The patient developed a sudden cardiac arrest. A prolonged effort of cardiopulmonary resuscitation became futile.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [75.0, 'kg'], 'height': [173.0, 'cm']}",25.05931,23.80634,26.31228,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 173.0 cm, which is 173.0 cm * 1 m / 100 cm = 1.73 m. The patient's weight is 75.0 kg. The patient's bmi is therefore 75.0 kg / (1.73 m * 1.73 m) = 25.05931 kg/m^2."
2208,6,Body Mass Index (BMI),physical,decimal,pmc-3543891-1,Extracted,"An 8-year-old female presented to the emergency department with a 4 day history of right hip pain and limping. The pain was of spontaneous onset without any history of trauma. She achieved normal milestones till the age of 6 years. Her past medical history was significant for psoriasis, controlled by topical medications. Dietary history revealed a normal intake of a balanced nonvegetarian diet.
On examination, she was noted to have skin lesions due to mild psoriasis. There were no phenotypic features of Albright's hereditary osteodystrophy (AHO) which is PHP type 1a. Her weight was 25.8 kg (50th percentile for age and sex), height 131 cm (75th percentile for age and sex), with a height velocity of 4.25 cm/year. Examination of her lower limbs showed a painful right hip with minimal shortening and restricted external rotation. Biochemical investigations revealed low serum calcium and high alkaline phosphatase []. The liver enzymes, coagulation screen, renal function tests, serum phosphorus, serum albumin, and serum magnesium were all within normal limits. Radiological investigations showed grade 2 SCFE on the right side and grade 1 on the left side according to Southwick's classification [Figures and ]. Clinically, she had stable slips according to Loder's classification.
The operative treatment planned was in situ pinning of both hips using cannulated screws. The right hip was operated on within 24 h of presentation and the asymptomatic left hip was operated 2 weeks later. Due to her small bony anatomy, 5 mm cannulated screws were used for fixation on both sides. The procedure was otherwise similar to the technique described by Loder. The early postoperative recovery was uneventful and postoperative radiographs were satisfactory. The patient was discharged with advice to eat a calcium rich diet and to take calcium supplements and vitamin D3 (cholecalciferol). As the patient was feeling better, she did not come for the followup appointments. At the 4th postoperative month, she presented with the complaint of pain in her left knee. Clinically her left knee had 5° more valgus than her asymptomatic right knee. Radiographs of both knees showed widening of the lateral distal femoral physis with abnormal ossification within the metaphysis []. Radiographs of the hips revealed a similar appearance to the postoperative radiographs.
At this stage, the bone profile showed persistent low calcium levels with elevated alkaline phosphatase, in spite of treatment with calcium and vitamin D3[]. This persistent hypocalcemia prompted us to carry out further endocrinologic evaluation. Her parathyroid hormone (PTH) level was 172 pg/mL (normal range is 10–60 pg/mL). Further investigations revealed normal thyroid function.
The combination of high PTH and low calcium with no possible explanation led us to suspect end organ resistance to PTH, which is known as PHP. The absence of AHO phenotype favoured the diagnosis of PHP type 1b. The patient was referred to a geneticist and an endocrinologist for further evaluation. Genetic testing revealed GNAS1 methylation defects, confirming the diagnosis of PHP type 1b. She was started on calcium carbonate supplements and alfacalcidol (1-alpha-hydroxyvitamin D3) 0.5 μg once daily. In a week, her sense of general well being improved and there was a marked reduction in the left lower limb pain. Her serum calcium and vitamin D level increased, and at the same time, serum alkaline phosphatase and PTH levels decreased []. The alfacalcidol dose was slowly increased at weekly increments of 0.5 μg to a final dose of 1.5 μg once daily. She was allowed to bear weight in 1 month.
At her last follow up, 2 years after the in situ fixation, the patient remained without symptoms. Radiographs of the hips showed good remodeling of the proximal femur with no evidence of avascular necrosis [Figure , and ,]. Radiographs of her distal femur showed improved ossification and narrowing of the distal femoral physis []. The valgus deformity in her left knee had also improved, but correction with hemiepiphysiodesis may be required in the future. The patient was advised to continue calcium carbonate and alfacalcidol lifelong. Followup till skeletal maturity was planned, but unfortunately the family was lost to followup.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [25.8, 'kg'], 'height': [131.0, 'cm']}",15.03409,14.28239,15.78579,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 131.0 cm, which is 131.0 cm * 1 m / 100 cm = 1.31 m. The patient's weight is 25.8 kg. The patient's bmi is therefore 25.8 kg / (1.31 m * 1.31 m) = 15.03409 kg/m^2."
2209,6,Body Mass Index (BMI),physical,decimal,pmc-6396477-1,Extracted,"A 15-month-old female Filipino infant with congenital type I biliary atresia and without any other anomalies or malformations, who had not undergone Kasai’s surgical procedure for biliary atresia, was referred by a liver center in the Philippines. She weighed 8.1 kg and had a height of 67.3 cm. She had jaundice (total serum bilirubin, 22.2 mg/dL), hypoalbuminemia (serum albumin level, 2.58 g/dL), coagulopathy (prothrombin time > 20 s compared to that of a normal control), ascites, splenomegaly, portal hypertension (portal vein velocity, 3.9–5.6 cm/sec with hepatopetal flow measured by Doppler ultrasound), and repeated bleeding of the varices after three doses of intravascularly administered Histoacryl 1 ampoule mixed with Lipiodol UF 8 mL (Auckland, New Zealand) in the EV (Fig. ). A Doppler ultrasound was used to investigate the portal hemodynamics before EIS. The diameter of the portal vein was 6.1 mm with reversal hepatofugal flow in portal vein velocity. After the first EIS, the portal vein diameter was 4.4 mm without thrombosis. After the third EIS, the end point of EIS was further investigated, and computed tomography angiogram revealed that the intrahepatic portion of the portal vein was not clearly demonstrated. Prominent GV and EV were occluded by EIS (Fig. ). The sclerosing agent was not only present in the EV and GV but also retrogradely occluded the main portal vein, splenic mesenteric junction, and splenic vein, causing an engorged inferior mesenteric vein (Fig. ). The patient underwent total hepatectomy and living donor liver transplantation (LDLT) via a left lateral segment graft (segments 2, 3, and 4 of the middle hepatic vein trunk) and left portal vein graft for the recipient inferior mesenteric vein anastomosis. Portal vein stent placement via segment 4 of the portal vein stump was performed from the inferior mesenteric vein to the umbilical portion of the left portal vein (Fig. ). The patient is still alive and doing well after the LDLT.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [8.1, 'kg'], 'height': [67.3, 'cm']}",17.8836,16.98942,18.77778,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 67.3 cm, which is 67.3 cm * 1 m / 100 cm = 0.673 m. The patient's weight is 8.1 kg. The patient's bmi is therefore 8.1 kg / (0.673 m * 0.673 m) = 17.8836 kg/m^2."
2210,6,Body Mass Index (BMI),physical,decimal,pmc-8019405-1,Extracted,"A 67-year-old man in good health reported numbness and weakness of his lower legs in June 2010. He presented to the clinic due to the spread of the symptoms to his upper limbs. Magnetic resonance imaging revealed multiple lacuna infarctions. Laboratory analysis revealed anemia (hemoglobin [Hb], 9.8 g/dL) and renal dysfunction (creatine, 2.7 mg/dL). He was admitted to a nearby hospital for further examination and was diagnosed with hypertension and multiple mononeuropathy. In addition, laboratory findings revealed increased levels of C-reactive protein (CRP, 16.82 mg/dL). After 8 days in the hospital, severe right-flank pain suddenly occurred, and anemia worsened (Hb, 6.8 g/dL). Abdominal computed tomography (CT) without enhancement revealed a right perirenal hematoma. He was then transferred to our hospital for investigation and treatment.
On admission, his height was 156.0 cm, and his weight was 54.5 kg (approximately 2-kg loss over months). His blood pressure was 192/114 mm Hg; pulse, 98 bpm; and body temperature, 37.1 ℃. On physical examination, palpebral conjunctiva was pallid, and he had severe right-flank pain with muscular defense. No skin rush was evident in the extremities, although hypesthesia was detected by neurologic examination. Laboratory findings on admission are presented in Table . The results of the urine tests were as follows: protein levels, 2.4 g/g⋅Cr; occult blood 3+ by dipstick test; red blood cells ≧ 100/high-power field; and sediment contained granular cast 2+ . The results of serum examinations were as follows: white blood count, 13,610/µL (with 74.0% neutrophils and 16.0% eosinophils); hemoglobin, 6.2 g/dL; platelet count, 32.1 × 104/µL; alkaline phosphatase, 1,867 IU/L; γ-glutamyl transpeptidase (γ-GTP), 360 IU/L; blood urea nitrogen, 39 mg/dL; Cr, 1.3 mg/dL; erythrocyte sedimentation rate, 156 mm; C-reactive protein, 11.5 mg/dL; immunoglobulin (Ig) G, 2533 mg/dL; IgA, 306 mg/dL; IgM, 106 mg/dL; C3, 83 mg/dL; C4, 15 mg/dL; and CH50, 48 U/mL. ANA, PR3-ANCA, MPO-ANCA, anti-GBM antibody, and HBs-antigenemia were not detected. Contrast-enhanced CT revealed bilateral pleural effusion, right small renal infarction, and right perirenal hematoma. CT angiography revealed multiple small aneurysmal dilatations in the intrarenal branches of the bilateral renal arteries and the intrasplenic branches of the splenic artery (Fig. a–c). Emergency selective coil embolization was conducted to the right renal artery aneurysm, which was responsible for the bleeding (Fig. ). To obtain a definitive diagnosis, we performed a left sural nerve biopsy (Fig. ). We confirmed a small arterial occlusion with inflammatory cell infiltration in the sural nerve tissue, although a histological examination did not reveal fibrinoid necrosis or granuloma. Collectively, and based on his clinical and radiographic findings, we diagnosed polyarteritis nodosa.
On the fifth hospital day, we started oral prednisolone therapy at 40 mg/day. On the 8th and 15th hospital days, intravenous methylprednisolone pulse (500 mg/day) therapy was started for 3 consecutive days. Although these therapies suppressed the disease activity, including inflammatory response, urine protein, and pleural effusion, the patient failed to achieve remission. Intravenous pulse cyclophosphamide therapy was, therefore, given on the 30th day. Clinical symptoms such as numbness and weakness of limbs gradually diminished, and laboratory findings dramatically improved. Moreover, contrast-enhanced CT revealed the disappearance of pleural effusion and the decreased size of perirenal hematoma concomitant with aneurysms. The patient was then transferred to another hospital for rehabilitation training (Fig. ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [54.5, 'kg'], 'height': [156.0, 'cm']}",22.39481,21.27507,23.51455,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 156.0 cm, which is 156.0 cm * 1 m / 100 cm = 1.56 m. The patient's weight is 54.5 kg. The patient's bmi is therefore 54.5 kg / (1.56 m * 1.56 m) = 22.39481 kg/m^2."
2211,6,Body Mass Index (BMI),physical,decimal,pmc-7325546-1,Extracted,"A 4-year-old boy had started with the limited movement of his fingers since he was 2 years old. His mother found that he could not lift his arms to his head. He frequently asked for help when he wore clothes. The symptoms worsened, so he was hospitalized. The clinical features included coarse face, joint stiffness, short stature, and mental retardation (). He was healthy at birth.
He was 92 cm tall and weighted 13 kg. His hands and feet were large and rather short. Skeletal examination showed short stature with relatively short limbs. The chest X-ray result showed paddle-shaped widened ribs (). The respiratory and cardiovascular examination was normal. He had mental retardation. Auditory manifestations and ocular functions were normal.
A blood test MS/MS assay indicated an α-iduronidase deficiency. This result determined the diagnosis with MPS type I.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [13.0, 'kg'], 'height': [92.0, 'cm']}",15.35917,14.59121,16.12713,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 92.0 cm, which is 92.0 cm * 1 m / 100 cm = 0.92 m. The patient's weight is 13.0 kg. The patient's bmi is therefore 13.0 kg / (0.92 m * 0.92 m) = 15.35917 kg/m^2."
2212,6,Body Mass Index (BMI),physical,decimal,pmc-4176648-1,Extracted,"A 62-year-old man (weight, 68 kg; height, 170 cm; waist, 86.36 cm) with controlled diabetes mellitus, hypertension, dyslipidemia, diabetic retinopathy, diabetic foot (foot ulcer), and early diabetic nephropathy presented at Kyunghee-saeng Korean Medicine Clinic. He was previously diagnosed with type 2 diabetes at another hospital and had been receiving oral hypoglycemic agents to control blood glucose levels from 1984 until 2000 when he suffered a stroke. His blood glucose levels were subsequently found to be poorly controlled and therefore insulin injection therapy was recommended. At the same time, diabetic retinopathy was also detected, which was treated by a combination of laser photocoagulation and an adjusted calcium dobesilate dose of 250 mg/day. The patient subsequently modified his lifestyle and continued his medication. In 2011, amputation of the right second and third toes was performed due to the presence of diabetic foot ulcers. Insulin therapy was discontinued in January 2012 because of several hypoglycemic events and oral hypoglycemic therapy was resumed (sitagliptin 100 mg/day, metformin 500 mg/day). However, in November 2013, diabetic nephropathy corresponding to stage 3 chronic kidney disease (CKD) was detected by routine medical checkups and treatment with Perindopril commenced. This failed to improve kidney function and he presented at our clinic on April 7, 2014, seeking to recover his renal function level with herbal medicine.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [68.0, 'kg'], 'height': [170.0, 'cm']}",23.52941,22.35294,24.70588,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.7 m * 1.7 m) = 23.52941 kg/m^2."
2213,6,Body Mass Index (BMI),physical,decimal,pmc-3790041-1,Extracted,"A hospitalized 56-year-old male patient diagnosed with hepatocellular carcinoma was under the care of the Digestive Internal Medical Department. In order to control the patient's pain level, the Digestive Internal Medical Department requested joint treatment from our pain clinic. The patient was 160.5 cm tall and weighed 54.5 kg. At the time of arrival at our pain clinic, the patient's blood pressure was 145/90 mmHg and the heart rate was 68 beats per min (bpm). The patient complained of general weakness and right flank pain. Results of the laboratory examination showed an AST and ALT of 106 and 83, respectively, and no evidence of bleeding. Liver computed tomography (CT) and positron emission tomography (PET) CT taken one week prior revealed a 1-9 cm sized multiple mass and a right portal vein thrombosis in the liver parenchyma. On a simple chest X-ray, no active lesion was seen. Pulmonary function test (PFT) was not performed as a part of this procedure. The patient's main symptoms were back pain and flank pain limited to the T7 and T8 dermatome level. In order to determine the pain level, epidural block was performed one time at the T7 and T8 level. A consent form was signed by the patient after a detailed explanation of the medical procedure and its possible complications. The epidural block was not performed with the aid of a C-arm guide. In the left decubitus position, 6 ml of 1% lidocaine was administered as a local anesthesia after betadine was used to cleanse the expansive back region. The paramedian approach was executed using a 22-gauge Tuohy needle at the T7-8 level. Using a Tuohy needle connected to a syringe filled with 5 ml of air, intermittent pressure was applied in order to locate the epidural space using the LOR technique. On the first attempt, approximately at a 5 cm depth, the lamina of the vertebra was contacted. After the needle was slightly retracted, the needle was advanced towards the cephalad slightly, and at about at 5.5 cm depth, the LOR was not definitive. Thus, we applied pressure approximately 4 times into the syringe which was fixed at the same depth. After that, one more attempt was made. At the same depth, a slight LOR was continuous, and therefore, we came to the conclusion that it was the epidural space. Following the injection of 8 ml of 0.8% mepivacaine and 20 mg of triamcinolone, the patient stabilized after being in the supine position for one hour. After one hour, the patient was moved to the ward. His visual analog scale decreased to 3/10 from 7/10. The patient's blood pressure was 130/93 mmHg and his heart rate was 90 bpm. Chest discomfort and dyspnea were not observed and there were no other unusual impressions. Three hours after the patient was transferred to the ward, a PET-CT was performed in order to prepare the patient for Transarterial Chemoembolization (TACE). The results of the PET-CT revealed a new occurrence of pneumomediastinum in addition to the liver mass and portal vein thrombosis observed one week before (). The position of the pneumomediastinum was extended from T10 (the site where the epidural block was performed) to the C2 epidural space. In addition, air was observed in the paraspinal muscle and epidural space (). After the patient was informed of the pneumomediastinum, the patient was supplied with oxygen at 2 L/min by a nasal cannula and observed closely in the ward. The patient did not have any unusual complaints and was stabilized in bed and a chest CT taken 7 days later showed no signs of pneumomediastinum and pneumothorax.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [54.5, 'kg'], 'height': [160.5, 'cm']}",21.15663,20.0988,22.21446,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.5 cm, which is 160.5 cm * 1 m / 100 cm = 1.605 m. The patient's weight is 54.5 kg. The patient's bmi is therefore 54.5 kg / (1.605 m * 1.605 m) = 21.15663 kg/m^2."
2214,6,Body Mass Index (BMI),physical,decimal,pmc-3350073-1,Extracted,"An 85-year-old gentleman (73 kg, 180.3 cm) with severe, symptomatic achalasia felt to be a poor surgical risk and therefore a poor candidate for surgical myotomy or pneumatic dilatation presented to the outpatient ambulatory endoscopy center for EGD with esophageal BOTOX injection under anesthesia after previously undergoing an uncomplicated similar procedure some months before. Prior to the procedure, he was kept nil per os (NPO) for 18 hours to promote esophageal drainage. Standard monitors (SpO2, ECG, and noninvasive BP) and nasal cannula oxygen (4 L) with capnometry were applied. Intravenous midazolam (1 mg) and glycopyrrolate (0.2 mg) were administered, the patient was placed in the left-lateral decubitus position, and an oral bite block was inserted. A bolus of 6 mL of ketofol (propofol 10 mg/mL with ketamine 1 mg/mL) was given and the procedure started. Spontaneous ventilation, as assessed by observation and capnometry, was maintained. The endoscope passed smoothly into the proximal esophagus without a patient response, but upon esophageal insufflation a bolus of solid food matter was propelled into the oropharynx accompanied by active patient coughing. Prompt and thorough oropharyngeal suctioning was performed along with a jaw thrust and chin lift. The patient continued to make respiratory efforts, but no air exchange was detected by capnometry, and paradoxical chest wall movement was observed. Passage of a lubricated nasal trumpet and placement of a Guedel airway did not alleviate the obstruction, and significant oxygen desaturation occurred. The procedure was abandoned. Face mask oxygen and gentle positive pressure via bag-mask ventilation promptly restored gas exchange and oxygen saturation to >95%, and the patient began to emerge from anesthesia. Brief flexible fiberoptic examination of the glottic opening via the right naris revealed no particulate matter or other obstruction in the glottic inlet. Under light sedation and topicalization of the oropharynx, a pulmonologist performed a complete flexible bronchoscopic exam that revealed extensive tracheomalacia from the vocal cords to the carina, including portions of the right mainstem bronchus (). Dynamic tracheal collapse was evident during spontaneous ventilation involving the anterolateral but not posterior wall. The patient emerged from anesthesia and was transported to the recovery room on nasal cannula oxygen. He was awake and alert with stable vital signs and SpO2 94–99%. Chest CT performed shortly after the aborted procedure revealed mild inflammation and an enlarged sigmoid-shaped esophagus consistent with long-standing achalasia. Dynamic airway maneuvers to assess tracheal diameters were not performed.
The patient was rescheduled for EGD and BOTOX injection after 48 hours of NPO. He was brought to the procedure room at which time standard monitors and nasal cannula oxygen with capnometry were applied. The patient was placed in the left recumbent position and glycopyrrolate 0.2 mg IV was administered followed by dexmedetomidine 1.5 mcg/kg over fifteen minutes then infusion at 0.7 mcg/kg/h. Topical anesthesia of the right naris was accomplished with lidocaine. An intravenous bolus of 0.5 mg/kg ketamine was given followed by infusion at 1 mcg/kg/min. A flexible pediatric fiberoptic bronchoscope was passed via the right naris to obtain a clear view of the vocal cords, and smooth passage of the endoscope into the esophagus was also visualized. The patient demonstrated minimal response to either procedure, while spontaneous ventilation and oxygenation were maintained. The residual liquid contents of the dilated esophagus were briskly evacuated, and 100 units of BOTOX were injected into the gastroesophageal junction in divided doses. There was no evidence of proximal airway obstruction from the limited view via the fiberscope. The patient coughed several times in response to secretions reaching the arytenoid cartilages suggesting preservation of protective airway reflexes under the sedation regimen. The procedure was completed smoothly, and the patient was awake and conversant within ten minutes of the cessation of infusions. During the procedure, there was no evidence of dynamic airway collapse: continuous capnographic evidence of CO2 was present and the patient demonstrated no hemodynamic instability, respiratory depression, or decrease in oxygen saturation. The patient was discharged to outpatient followup with a plan for repeat EGD in due course and evaluation for possible nighttime CPAP delivery.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [73.0, 'kg'], 'height': [180.3, 'cm']}",22.45595,21.33315,23.57875,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 180.3 cm, which is 180.3 cm * 1 m / 100 cm = 1.803 m. The patient's weight is 73.0 kg. The patient's bmi is therefore 73.0 kg / (1.803 m * 1.803 m) = 22.45595 kg/m^2."
2215,6,Body Mass Index (BMI),physical,decimal,pmc-6158874-1,Extracted,"The patient was a 79-year-old man with chief complaints of exertional dyspnea, leg edema, and weight loss. On transthoracic echocardiography (TTE), a 25 × 40 mm mobile pedunculated mass continuous with the right ventricular heart muscle was detected in the right atrium and the patient was admitted to our department for close examination and treatment. At admission, his height was 162.0 cm, body weight was 61.1 kg, body temperature was 36.3 °C, pulse was 62 beats/min, blood pressure was 112/59 mmHg, and SpO2 was 100% (room air). Pulmonary sounds were clear with no crackles, and heart sounds were regular with no murmur. Leg edema was present.
Plain chest radiography revealed a cardiothoracic ratio of 49% with no cardiac dilation. Electrocardiography revealed a sinus rhythm with a heart rate of 71 beats/min with nonspecific ST-T segment changes. Blood chemistry revealed the following: white blood cell (WBC) count of 51.9 × 104/μL, hemoglobin (Hb) of 14.9 g/dL, platelet (Plt) count of 16.3 × 104/μL, creatine kinase (CK) of 81 U/L, creatine kinase-MB (CKMB) of 8 ng/mL, lactate dehydrogenase (LDH) of 161 U/L, C-reactive protein (CRP) of 0.10 mg/dL, carcinoembryonic antigen (CEA) of 0.7 ng/mL, prostate-specific antigen (PSA) of 1.2 ng/mL, squamous cell carcinoma (SCC) antigen of 1.2 ng/mL, and soluble IL-2 receptor: 633 U/mL. Inflammatory parameters were within the normal range and the soluble IL-2 receptor level was slightly elevated, but the levels of other tumor markers were within their normal ranges. A coronary computed tomography (CT) scan showed no significant stenosis. It was deemed very difficult to completely excise, so we decided on partial tumor resection with MICS to reduce the risk of tumor embolism and to obtain an accurate pathology diagnosis. Therefore, we did not perform CAG. If we had performed a CAG, we may have seen arteries feeding the tumor.
TTE showed a 40 × 30-mm mobile pedunculated tumor in the right atrium that was continuous with the right ventricular heart muscle (Fig. ). Transesophageal echocardiography (TEE) showed a solid septated tumor with an irregular surface invading the free wall of the right atrium and surrounding the annulus of the anterior cusp and right and left coronary cusps of the aortic valve (Fig. ). Contrast-enhanced CT showed invasion based on soft tissue intensity near the tricuspid valve above the anterior right ventricle in the region between the aorta and pulmonary artery and around the pulmonary artery (Fig. , ). Cardiac magnetic resonance imaging (MRI) showed a thickened anterior wall near the tricuspid valve and a mass protruding into the lumen and expanding into the region between the aorta and the pulmonary artery (Fig. , ); in addition to the patient’s advanced age, these features made it difficult to perform extended cardiac surgery. On fluorodeoxyglucose positron emission tomography (F-18 FDG-PET), there was abnormal accumulation in the right atrium surrounding the aortic root (Fig. ).
Surgery was performed to prevent tumor embolism-induced sudden death and to obtain a pathological diagnosis. Anticoagulation was not performed preoperatively because it was unlikely that the tumor was a thrombus. A double-lumen tube was inserted during surgery and a Swan-Ganz catheter and 14-Fr cannula were inserted through the right internal jugular vein after draping. In a supine position with 30° elevation of the right side, a 4-cm skin incision was made in the fourth intercostal region at the medial aspect of the nipple. Meanwhile, the femoral artery (FA) and femoral vein (FV) were exposed. A pericardiotomy was performed 2 cm anterior to the phrenic nerve and the pericardium was elevated. After systemic heparinization, an 18-Fr blood supply tube was inserted through the right FA, and a 25-Fr cannula was inserted through the right FV to establish a cardiopulmonary bypass (CPB). The superior vena cava was blocked with a bulldog clamp and the heart rate was controlled at 40–50 bpm with a β-blocker. An oblique incision was made in the right atrium with the heart beating, and the lumen was observed. The tumor adhered to the anterior surface of the right atrium but not to the annular region and had marked mobility. The tumor was grasped with an Endocatch and the pedicle of 1-cm width was transected using electric cautery (Fig. ). The lack of any residual right atrial tumor or shunt was confirmed and the right atrium was closed in a double suture pattern; the patient was then weaned from CPB. The pericardium was closed as far as possible, the wound was closed by the standard method, and surgery was completed. The operative time was 1 h 56 min, and the duration of CPB was 38 min (Additional file ).
Intraoperative macroscopic findings revealed a tumor with a smooth, greyish-white surface (Fig. ). A blackish-brown region suggestive of hemorrhage was present inside and on pathological examination (Fig. ), a diffuse proliferation of round cells with a high nuclear-to-cytoplasmic (N/C) ratio were observed on hematoxylin and eosin staining. The tumor cells were mainly medium- and small-sized cells that contained nuclei with a shallow cut that were the same size or slightly smaller than the nuclei of vascular endothelial cells; large cells were also present. Broken nuclear products and histiocytes phagocytosing these products were also observed. Upon immunohistological staining, the tumor cells were CD79α-positive and CD3-negative. B-cell-derived cells were overwhelmingly predominant, which suggested that the lesion was a B-cell-derived tumor. Epithelial membrane antigen (EMA) immunostaining was negative. Based on these findings, the patient was diagnosed with diffuse large B-cell lymphoma (DLBCL).
Extubation was performed 6 h after surgery and the patient was transferred to a general ward 2 days after surgery. The disappearance of the tumor from the annular region was confirmed on TTE 5 days after surgery and the patient was discharged when he was able to independently walk 6 days after surgery. After observation at an outpatient clinic, rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) therapy was initiated 37 days after surgery. After 8 cycles were administered in total, an FDG-PET scan performed 456 days after surgery showed no abnormal accumulation (Fig. ), indicating CR.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.1, 'kg'], 'height': [162.0, 'cm']}",23.28151,22.11743,24.44559,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.0 cm, which is 162.0 cm * 1 m / 100 cm = 1.62 m. The patient's weight is 61.1 kg. The patient's bmi is therefore 61.1 kg / (1.62 m * 1.62 m) = 23.28151 kg/m^2."
2216,6,Body Mass Index (BMI),physical,decimal,pmc-5773430-1,Extracted,"We treated a 62-year-old man with a several-year history of neuropathic pain. In 2002, he developed dizziness and diplopia. Intracranial chondrosarcoma diagnosed after a biopsy of a tumor at the right cerebellopontine angle (medial clivus and petrous part of the temporal bone). He underwent CyberKnife radiosurgery in 2002, and a right suboccipital craniectomy and tumor removal due to regrowth of the tumor in 2004 at another hospital. Since then, he had experienced left hemiplegia with a hemisensory deficit, right facial palsy, right cranial nerve VI palsy, and dysphagia. He suffered from neuropathic pain manifest as an uncomfortable cold squeezing and tightness, with allodynia to light touch in the left hemibody, especially the posterior thigh.
He was referred to the Department of Neurosurgery at St. Vincent's Hospital for a neuromodulation technique to treat the pain. In 2008, deep brain stimulation (DBS) was performed using the right ventral posterolateral nucleus and periventricular grey matter as targets. After the DBS and medication, the pain disappeared. However, the DBS was discontinued in 2013 because he developed a headache, and he took only medication to treat the pain. There was no evidence suggesting tumor regrowth on follow-up magnetic resonance imaging (). Although the pain in the left posterior thigh gradually worsened, he could not take opioids (oxycodone, hydromorphone, or a fentanyl patch) or more than 1,200 mg of gabapentin because of side effects. He had been taking the maximum daily tolerable dosage of medication, a combination of gabapentin 1,200 mg, amitriptyline 10 mg, diazepam 4 mg, tramadol 100 mg, and duloxetine 60 mg. The regimen was not sufficient to reduce his pain.
In August 2016, his neurological symptoms worsened and he developed hoarseness of voice due to a right vocal cord palsy caused by recurrence of the sarcoma (). In addition, his neuropathic pain worsened. He could not sit on a wheelchair because of severe pain. Together with his family and a physiatrist, the patient decided to see if the neuropathic pain could be managed with an injection of BTX-A, so that he could sit. BTX-A 100 units (Botox; Allergan, Irvine, CA, USA) was diluted in 2.4 mL normal saline. The preparation was injected subcutaneously in the most painful area of the posterior left thigh at 16 locations based on height and weight of 168 cm and 52 kg, respectively (). No immediate side effects were seen after the injection. The day after the injection, his pain had decreased from 6/10 before the injection to 2/10 on a visual analogue scale (VAS). The pain was well-controlled (2–3/10 on the VAS) 12 weeks after the injection and he was satisfied with the BTX-A injection.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [52.0, 'kg'], 'height': [168.0, 'cm']}",18.42404,17.50284,19.34524,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 52.0 kg. The patient's bmi is therefore 52.0 kg / (1.68 m * 1.68 m) = 18.42404 kg/m^2."
2217,6,Body Mass Index (BMI),physical,decimal,pmc-3922247-1,Extracted,"A 79-year-old man with angina pectoris, hypertension, giant-cell tumor of the tendon sheath, and cataracts was admitted to our hospital in late 2008. He had also undergone surgery for prostate and gallbladder cancers, which were cured. He had smoked approximately ten cigarettes per day during his twenties. From 2005 onwards, he occasionally felt tension in his lower abdomen. Upper and lower gastrointestinal endoscopy showed only multiple colonic diverticula. Due to worsening of his lower abdominal pain, he was treated with nonsteroidal anti-inflammatory drugs (NSAIDs) since the beginning of 2008. In October 2008, he was diagnosed with diabetes mellitus, and medication therapy was started. In December 2008, he had an unsteady gait and general fatigue and his lower abdominal pain worsened. Therefore, he was admitted to our hospital.
Upon admission, the patient was 160 cm tall and weighed 62.7 kg. He had a body temperature of 37.1 °C, a pulse rate of 64 bpm, and a blood pressure of 140/68 mmHg. He had a white tongue, moon face, mildly thinning skin, pitting edema in the extremities, extravasated blood spots on the dorsal surface of his hands, central obesity, and crural and gluteal muscle atrophy. His abdomen was flat and soft, and there were no signs of guarding or peritonitis. He had been taking aspirin, amlodipine besylate, rosuvastatin calcium, famotidine, teprenone, mosapride citrate hydrate, and glimepiride.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [62.7, 'kg'], 'height': [160.0, 'cm']}",24.49219,23.26758,25.7168,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 62.7 kg. The patient's bmi is therefore 62.7 kg / (1.6 m * 1.6 m) = 24.49219 kg/m^2."
2218,6,Body Mass Index (BMI),physical,decimal,pmc-5836285-1,Extracted,"A 37-year-old male was seen in the outpatient clinic because of weight loss, fatigue, and abdominal discomfort. Current height was 175 cm, weight 67 kg, with an unintended weight loss of 6 kg over the last few months. There had been symptoms of fatigue, which the patient attributed to increased workload. The abdominal discomfort included distention without pain or nausea. There were normal and unchanged stools and no icterus.
The patient had no other symptoms at presentation and showed a good performance status. At age 8, he had been diagnosed with right-sided WT with metastases to lymph nodes and lungs, and with thrombosis of the inferior vena cava and right renal vein. He was treated with intended curative right-sided nephrectomy and thrombosis evacuation, in combination with adjuvant radiation and chemotherapy. He received chemotherapy pre- and postoperatively with dactinomycin, actinomycin D, and vincristine, and 20 cycles with 30 Gy of radiation treatment to the right side of the abdomen for lymph node metastases. There was a cover over a large portion of the right lobe of the liver.
The patient had mildly elevated liver enzymes during the pre- and postoperative chemotherapy, with a maximum ASAT at 224 U/L (10–40), an elevated alkaline phosphatase level between 350 and 650 U/L (80–250), with persistent normal γ-glutamyltransferase.
The liver enzymes normalized after the end of treatment. There was no evidence of hepatomegaly, jaundice, ascites or liver pain during the 10 years of follow-up after radiation and chemotherapy. Follow-up included periodically clinical evaluation, blood tests, whole-body CT scan, ultrasound of the abdomen, and a plain thoracic X-ray. Blood tests were normal apart from a moderate thrombocytopenia at 90–125 × 109/L (150–450). Radiographically, there were venous collaterals at the level of the previous inferior vena cava thrombosis. In addition, ultrasound showed slowly progressive splenomegaly to 16 cm developing over the years, which was not further investigated. Five years after treatment, an abnormal ultrasound pattern was observed in the liver parenchyma without signs of cirrhosis and normal flow in the portal and liver veins; no further action was taken. At the age of 18, after 10 years of follow-up, the patient was discharged in a clinically stable condition. Hereafter, the patient had had no contact with the health care system until the current admission.
On admission, aged 37, the patient's physical presentation was normal, apart from the findings of cutaneous abdominal varices and an enlarged spleen. Laboratory examinations showed elevated ALAT at 115 U/L (10–70), alkaline phosphatase at 199 U/L (35–105), low albumin at 35 g/L (36–48), normal bilirubin at 22 μmol/L (5–25), and thrombocytopenia at 75 × 109/L (145–350). Other results, including a full blood count and screening for metabolic, viral, and autoimmune liver disease, were all normal. A CT scan of the thorax/abdomen showed no sign of malignancy, but hypoplasia of liver segments 2 and 3 was seen, a reduced perfusion in the liver segments 6 and 8 as well as splenomegaly at 18 cm. In addition, several enlarged lymph nodes (1–3 cm) were observed in the retroperitoneum and around the celiac trunk and radiation sequelae in the right colon (Fig. ). A lymph node biopsy showed reactive changes without evidence of malignancy and bone marrow biopsy was normal. A colonoscopy revealed minor inflammation, histologically compatible with radiation sequelae.
Two months after initial presentation, the patient developed ascites and new imaging with CT and ultrasound showed otherwise unchanged conditions. A gastroscopy revealed grade 2 esophageal varices.
A needle biopsy of the liver was performed. This revealed an enlargement of most portal tracts, with varying mild to moderate fibrosis. There was some degree of periportal fibrosis, but only occasional short septa with no evidence of bridging fibrosis or of cirrhosis. Several of the fibrotic portal tracts showed evidence of obliterative portal venopathy, normal portal veins being either lost (with evidence of replacement by many smaller vascular structures), or showing sclerosis with fibrous thickening of the portal vein wall (Fig. ). In other portal areas, portal veins were dilated with herniation into the surrounding liver parenchyma (so-called periportal shunt vessels; Fig. ).
A combined liver vein and spleen pulp pressure measurement was performed as previously described [] and showed a normal pressure gradient across the liver (5 mm Hg), but a high gradient from the spleen to the free hepatic vein (29 mm Hg). This confirmed the expected presinusoidal hepatic origin of the patient's NCPH.
The patient was treated with loop diuretic medicine and an aldosterone antagonist for ascites and propranolol was administered to reduce the portal pressure gradient. As a result, the patient became asymptomatic without ascites and is able to work full time.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [67.0, 'kg'], 'height': [175.0, 'cm']}",21.87755,20.78367,22.97143,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 175.0 cm, which is 175.0 cm * 1 m / 100 cm = 1.75 m. The patient's weight is 67.0 kg. The patient's bmi is therefore 67.0 kg / (1.75 m * 1.75 m) = 21.87755 kg/m^2."
2219,6,Body Mass Index (BMI),physical,decimal,pmc-3530764-1,Extracted,"A 45-year-old, ASA physical status IV woman (78 kg, 172 cm) with ovarian cancer was scheduled for abdominal hysterectomy and bilateral salpingoophorectomy with epidural anesthesia, after her refusal for general anesthesia. The patient had been successfully subjected to cesarean section under epidural anesthesia four years ago.
Her clinical history revealed an ischemic infarct of the left frontal lobe since the age of 19, multiple sclerosis since the age of 20, antiphospholipid syndrome (heterozygote for the methylenetetrahydrofolate reductase (MHTFR) gene), and heterozygous β-thalassemia. On her admission, normotensive sinus tachycardia (115 bpm), fever and intense lower abdominal pain along with ascites and nausea were noted. The patient presented with 26.5% hematocrit, a platelet count of 465.000/L, and normal bleeding tests. Neurological examination revealed right hemiparesis, dropping of the left corner of the mouth, impaired oropharyngeal function with dysphagia to both solids and liquids, and altered walking gait. The patient had been receiving cinnarizine 10 mg daily, bromazepam 3 mg three times per day, and paracetamol occasionally.
In the operating room, with the patient positioned in the left lateral decubitus position, a 18-gauge Tuohy needle was inserted at L1-L2 intervertebral space; the epidural space was found using the loss-of-resistance technique. A polyamide catheter was easily introduced and placed at the 12 cm catheter mark. A test dose of 3 mL of 2% lidocaine was injected. After catheter placement the patient turned supine and was given 15 mL of ropivacaine 0.75% and 100 μg fentanyl. A sensory block to T3 was established 15 minutes later. During the 2-hour surgery, another 5 mL of ropivacaine 0.75% and 10 mL of lidocaine 2% were given as the patient complained of discomfort during peritoneal traction. Entonox inhalation was used to alleviate patients' discomfort during peritoneal traction and abdominal wall closure. At the recovery room, 1/2 an hour after the last epidural dose, the patient experienced severe pain and was administered 8 mL of ropivacaine 0.2% and 2 mg of preservative free morphine followed by 6 mL of ropivacaine 0.375% fifteen minutes later. A sensory block to T12 was present 11/2 hours later with no motor block at recovery.
Postoperative analgesia with 8 mL ropivacaine 0.2% four times daily, 2 mg morphine twice a day, and rescue dose of 6 mL ropivacaine 0.375% failed and the regimen was replaced by a continuous epidural pump, set to infuse 2 mL of ropivacaine 0.2% and 8 μg fentanyl hourly. The patient also received 3 g of paracetamol daily and triple antiemetic drug combination (metoclopramide 30 mg, 5HT3 antagonist 12 mg, and dexamethasone 8 mg). On the second postoperative day, pain was effectively managed with the continuous pump infusion but nausea persisted. Neurological examination revealed no signs of deterioration of the preexisting disease. The epidural catheter was removed on the fifth postoperative day. Nausea was not alleviated despite rigorous treatment. The patient developed paralytic ileus on the sixth postoperative day that resolved spontaneously two days later.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [78.0, 'kg'], 'height': [172.0, 'cm']}",26.3656,25.04732,27.68388,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 172.0 cm, which is 172.0 cm * 1 m / 100 cm = 1.72 m. The patient's weight is 78.0 kg. The patient's bmi is therefore 78.0 kg / (1.72 m * 1.72 m) = 26.3656 kg/m^2."
2220,6,Body Mass Index (BMI),physical,decimal,pmc-6966748-1,Extracted,"A 24-year-old woman (height, 169.2 cm; body weight, 79.2 kg) with WD was scheduled for emergency cesarean delivery at 30 weeks of gestation.
The patient was diagnosed with WD at 3 years of age. Her liver function had deteriorated severely enough to require liver transplantation at 20 years of age. However, anti-copper therapy improved her liver function and was continued during pregnancy. She was hospitalized at 25 weeks of gestation for thrombocytopenia and fetal growth restriction (FGR) caused by placental insufficiency. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) serum levels were normalized during pregnancy, while antithrombin III (AT-III) levels were significantly lower (Table ). On hematological evaluation, performing anticoagulation therapy with AT-III concentrate was suggested to prevent thrombophilia-induced placental dysfunction.
The patient’s body weight had rapidly increased by 1 kg/day with marked ascites and severe edema. She experienced dyspnea and could not ambulate due to dramatic weight gain. She was also diagnosed with obstetric DIC presenting with oliguria, thrombocytopenia, respiratory distress, liver dysfunction, and severe coagulopathy []. At 30 weeks of gestation, emergency cesarean delivery was performed under general anesthesia to improve her liver function. We performed supplementation with 10 units of platelet transfusion, 3 packs of cryoprecipitate, and 3 g fibrinogen concentrate.
In the operating room, a 16G venous catheter was inserted. We used rotational thromboelastometry (ROTEM® sigma, Tem Innovations GmbH, Munich, Germany), which showed normal coagulation function (Table ). Under standard monitoring and bispectral index, we performed rapid sequence induction using 130 mg propofol, 0.05 mg remifentanil, and 70 mg rocuronium. Because her face and tongue were edematous and the Mallampati classification was III, intubation difficulties were expected. Therefore, we used a video laryngoscope (McGRATH MAC#3) for tracheal intubation. We maintained with oxygen in nitrous oxide (2:3) and 0.7% sevoflurane until delivery.
After delivery, the baby (1173 g) showed respiratory distress. Tracheal intubation and administration of intratracheal lung surfactant were performed. One- and 5-min Apgar scores were 2 and 5, respectively. The neonatologists performed mechanical ventilation management for 2 days after delivery. The infant was discharged without further complications.
After delivery, continuous intravenous administration of propofol and remifentanil was started. Intraoperatively, 0.5 mg intravenous fentanyl was administered, and continuous fentanyl injection was started at 0.04 mg/h for postoperative analgesia. Intraoperative hemorrhage was 1813 mL (including amniotic fluid), and ascites was 1000 mL. The operation time was 61 min, and anesthesia time was 179 min. Urine volume was 80 mL, and infusion volume was 1954 mL (654 mL of crystalloids and 1300 mL of colloids). The patient also received 3 units of red blood cells and 6 units of fresh frozen plasma (FFP). The operation was completed without massive bleeding. However, a postoperative chest X-ray indicated pulmonary edema. We decided to continue mechanical ventilation in the intensive care unit (ICU). Albumin and diuretic administration improved the patient’s oxygenation and allowed for extubation the next day. She was transferred to the obstetrics ward 3 days postoperatively.
On the 15th postpartum day, her body weight showed a decrease of 20 kg, and she was discharged from the hospital. Subsequently, coagulation status was improved to pre-pregnancy levels 40 days after delivery.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [79.2, 'kg'], 'height': [169.2, 'cm']}",27.6646,26.28137,29.04783,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 169.2 cm, which is 169.2 cm * 1 m / 100 cm = 1.692 m. The patient's weight is 79.2 kg. The patient's bmi is therefore 79.2 kg / (1.692 m * 1.692 m) = 27.6646 kg/m^2."
2221,6,Body Mass Index (BMI),physical,decimal,pmc-4027095-1,Extracted,"A 23-year-old woman with Turner syndrome was hospitalized because of incidentally identified hypercalcemia during routine blood tests at out-patient clinic. She was diagnosed with Turner syndrome (45,X) due to short stature at age 11 years and had received recombinant human growth hormone (rhGH) for about 4 years. Since she was 13 years, she has been on estrogen priming and estrogen-progesterone cyclic therapy.
Her vital signs were normal with blood pressure of 112/74 mmHg, heart rate of 80 bpm, respiratory rate of 20/min, and body temperature of 36℃. She was short in stature despite long-term therapy and overweight, measuring 151.2 cm (standard deviation score [SDS], -2.093) and weighing 55.4 kg (SDS, -0.367). She showed typical signs of Turner syndrome, such as high arched palate, webbed neck, shield chest deformity, and cubitus valgus on both sides. Mild scoliosis was noted in simple T-L spine radiographs. Tanner stage was breast III and pubic hair II.
The laboratory profiles demonstrated normal complete blood count and electrolytes. Serum calcium and ionized calcium levels were elevated to 11.2 mg/dL (8.4 to 10.2 mg/dL) and 5.07 mg/dL (3.9 to 4.5 mg/dL), respectively, while phosphorous and alkaline phosphatase were normal (2.6 mg/dL and 107 IU/L, respectively). Thyroid stimulating hormone and free T4 were both within normal range (3.3 µU/mL and 1.4 ng/dL, respectively). Serum parathyroid hormone level increased up to 159 pg/mL (9 to 65 pg/mL), whereas 25-hydroxyvitamin D3 decreased to 15.1 ng/mL (20 to 100 ng/mL). Hypergonadotropic hypogonadism was present in spite of estrogen/progesterone replacement therapy (follicle stimulating hormone of 32.4 mIU/mL, luteinizing hormone of 10.5 mIU/mL, and estradiol of 21.2 pg/mL). Urinalysis indicated mild occult hematuria. Increase in both calcium/creatinine (Cr) ratio (0.211 mg/mg; Cr, <0.14 mg/mg) and phosphorus/Cr ratio (0.985 mg/mg; Cr, 0.21 to 0.75 mg/mg) were observed.
Additional tests were carried out to exclude multiple endocrine neoplasia, however, all of the tests were normal: serum and urine catecholamine level and calcitonin were within normal range and abdomen ultrasonography did not show any specific findings in the pancreas and adrenal glands, nor any stone-related abnormalities in both kidneys. Dual-energy X-ray absorptiometry (DEXA) scan revealed osteoporosis with bone mineral density (BMD) of the spine (L1-L4) (0.736 g/cm2; z score, -3.5) and femur (0.651 g/cm2; z score, -2.7). In parathyroid scintigraphy, a locally increased activity in the lower right lobe of a parathyroid was not washed out even after 2 hours (). An oval-shaped, low attenuated, hypervascular mass in the lower pole of the right parathyroid was observed in neck ultrasonography measuring 1.2 cm×0.8 cm×0.6 cm, suggesting parathyroid adenoma.
The lower right parathyroid gland was completely resected, and pathologic findings confirmed the diagnosis of parathyroid gland adenoma measuring 1.3 cm×0.9 cm×0.8 cm (). Two days after operation, serum calcium level, ionized calcium and parathyroid hormone levels were normalized (). After discharge, the subject has been monitored by laboratory tests such as serum chemistry and urine calcium/Cr ratio until now and follow up image is under considered.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.4, 'kg'], 'height': [151.2, 'cm']}",24.23294,23.02129,25.44459,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 151.2 cm, which is 151.2 cm * 1 m / 100 cm = 1.512 m. The patient's weight is 55.4 kg. The patient's bmi is therefore 55.4 kg / (1.512 m * 1.512 m) = 24.23294 kg/m^2."
2222,6,Body Mass Index (BMI),physical,decimal,pmc-3876680-1,Extracted,"The patient was a 27-year-old man (weight: 66 kg; height; 166 cm) with no underlying disease. This patient became aware of coxalgia 1 year earlier. The coxalgia was associated with continuous pain that became more severe, and at the time of presentation he could not walk without an axillary crutch. X-ray images showed joint narrowing and multiple bone erosions of the left hip joint (). Computed tomography (CT) clearly showed femoral neck and acetabular bone erosions as well as ONFH (Figures and ). In contrast, magnetic resonance (MR) imaging showed ONFH and mass lesions around the femoral neck. T2-weighted fat-suppressed MR imaging also revealed an irregular tumoral lesion (). The patient had type C ONFH according to the Nishii et al. classification [] and stage 4 ONFH according to the Association Research Circulation Osseous classification [].
We performed an arthroscopic biopsy before radical treatment. Histological analysis of the synovial tissue showed diffuse PVNS. The patient subsequently underwent total hip arthroplasty (THA) (KYOCERA Medical Corporation, Osaka, Japan) with complete synovectomy and tumor resection using an argon laser (). Severe invasive PVNS was seen in the inferior space of the hip joint, particularly around the femoral neck.
Pathological findings from an analysis of permanent preparations of the synovium and femoral head were consistent with PVNS and avascular bone necrosis, respectively. Proliferative histiocyte-like mononuclear cells were observed with multinucleated giant cells in the fibrotic stroma. Hemosiderin-laden macrophages and foamy cells were also occasionally observed. The subchondral zone of the femoral head showed avascular bone necrosis. Both empty lacunae and fat necrosis were found in the resected femoral head. Fibrosis and proliferation of vessels were observed around the necrotic trabeculae, and new bone apposition was present.
After the procedure, the Harris hip score improved from 79 to 97. No operative complications occurred, and no recurrence of PVNS was detected for 3 years after the procedure.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [66.0, 'kg'], 'height': [166.0, 'cm']}",23.95123,22.75367,25.14879,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 66.0 kg. The patient's bmi is therefore 66.0 kg / (1.66 m * 1.66 m) = 23.95123 kg/m^2."
2223,6,Body Mass Index (BMI),physical,decimal,pmc-4166389-1,Extracted,"A 77-year-old man (height, 168 cm; weight, 70 kg) presented at our hospital with black tarry stool. An esophagogastroduodenoscopy was performed and a gastric intestinal stromal tumor 4 cm in size was detected. Thereafter, endoscopic full-thickness gastric resection (EFTGR) was planned. EFTGR can be regarded as a hybrid form of NOTES or as an intermediate form step since a full-thickness incision in the gastric wall is made endoscopically and closure is achieved laparoscopically. We planned the surgery in such a way that endoscopic resection of the tumor would be performed by an endoscopic operator experienced in internal medicine and the laparoscopic dissection and closure of the stomach would be performed by a general surgeon.
The patient had a history of diabetes mellitus and hypertension, and he been taking medicines for these disorders. His preoperative routine laboratory values were within the normal range and a preoperative electrocardiogram (ECG) showed sinus bradycardia of 58 beats/min. The patient was premedicated with 1 mg of butorphanol and 0.2 mg of glycopyrrolate intramuscularly before surgery. His vital signs were stable upon arrival at the operating room and were monitored thereafter using ECG (lead II), pulse oximetry, end-tidal carbon dioxide concentration (ETCO2), and noninvasive blood pressure (BP) determination Because the endoscopes were placed in his mouth, the patient's temperature was measured using a skin temperature probe.
Anesthesia was induced using 120 mg of propofol, 50 mg of rocuronium, and 100 µg of fentanyl and nasotracheal intubation was performed using a nasal RAETM tracheal tube with a 7.5 mm inner diameter (ID), because nasotracheal intubation is convenient for endoscopic procedures. General anesthesia was maintained using O2 at 2 L/min, N2O at 2 L/min, and 1.5-2.5 vol% of sevoflurane, and the concentration of sevoflurane was controlled using the bispectral index. Mechanical ventilation with a tidal volume of 600 ml and a respiratory rate of 10 breaths/min was maintained. After induction, the peak inspiratory pressure (PIP) and ETCO2 were 16-17 cmH2O and 35-37 mmHg, respectively.
The patient was placed in the supine position while the laparoscopic operator remained on the right side of the patient to insert the port and perform the stomach dissection. A pneumoperitoneum was created using carbon dioxide (CO2) gas at a pressure of 14 mmHg throughout the surgery. After CO2 injection, the ETCO2 increased up to 40 mmHg, and hence, the respiratory rate was controlled; however, no change was made to the tidal volume as the PIP was maintained at 23-25 mmHg. After laparoscopic dissection, the endoscopic operator moved into position near the patient's head to perform an endoscopic full-thickness resection of the tumor with sufficient surgical margins (). During endoscopic resection, visibility was ensured through air insufflations, and the PIP pressure was approximately 5-7 mmHg lower than that measured during the laparoscopic procedure using CO2. After confirming no active bleeding, the endoscope was removed, and the laparoscopic operator performed closure of the stomach and sutured the skin wound.
During the entire procedure, hemodynamic stability was maintained and ETCO2 was maintained at 32-37 mmHg. The time required for the laparoscopy was 70 min and that for the endoscopy was 60 min; the anesthesia time was 160 min. Upon completion of the surgery, the patient was transferred to the general ward. No specific complications were observed during the postoperative period, and the patient was discharged on postoperative day 4.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [168.0, 'cm']}",24.80159,23.56151,26.04167,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.68 m * 1.68 m) = 24.80159 kg/m^2."
2224,6,Body Mass Index (BMI),physical,decimal,pmc-7132803-1,Extracted,"A 62-year-old Chinese man was scheduled for combined dissection of the tongue, mandible, and neck, right forearm free flap transplantation, mandibular titanium plate implantation, and tracheotomy. He was a smoker, 170 cm in height, and 51 kg in weight. Except for hypertension, which was treated with losartan potassium, the patient had no other medical history and denied any allergies. Two sessions of chemotherapy (docetaxel injection 120 mg, nedaplatin injection 120 mg) were completed before admission. The patient provided consent for publication of this case report, and the Institutional Review Board of the University of the Chinese Academy Of Sciences (Ningbo No. 2 Hospital) granted approval for the study protocol (YJ-KYSB-NBEY-2019-120-01).
On the day of surgery, the patient received 2 mg of intravenous midazolam as preoperative medication. Standard American Society of Anesthesiologists monitors were applied and a loading dose of dexmedetomidine was intravenously infused at 0.6 µg/kg over 10 minutes before induction. Induction was performed by propofol (80 mg), sufentanil (20 µg), and rocuronium (50 mg) followed by tracheal intubation. An invasive arterial catheter and an internal jugular vein catheter were placed. Anesthesia was maintained with sevoflurane (1% to 2%), propofol (150–200 mg/hour), and intermittent sufentanil 10 µg and rocuronium 10 mg, which were titrated to hemodynamic status and surgical requirements.
Urine output increased 30 minutes after the dexmedetomidine infusion was completed, reaching approximately 1900 mL within 2 hours. Pituitrin 2 U/hour was infused intravenously and changed to 3 U/hour 30 minutes later until the operation was over. Urine output showed a downward trend since the pituitrin treatment, and decreased to 500 ml/hour 2 hours later. Serial urine output is shown in .
The surgery lasted for 14 hours, during which time the patient received 5500 mL of lactated Ringer’s solution, 2000 mL of hydroxyethyl starch (130/0.4), and 375 mL of packed red blood cells. The estimated blood loss was 600 mL and the total urine output was 7150 mL.
The patient’s serum sodium level was 135 mmol/L 5 days before surgery and rose to 143 mmol/L intraoperatively. The patient’s serum osmolality was within normal limits at 2 hours after surgery (). The patient was hemodynamically stable throughout the procedure without major episodes of hypotension or tachycardia.
The patient was transferred to the intensive care unit after the operation with no diuresis or abnormal electrolyte and plasma osmotic pressure. He was discharged on postoperative day 18 without further related complications.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [51.0, 'kg'], 'height': [170.0, 'cm']}",17.64706,16.76471,18.52941,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 51.0 kg. The patient's bmi is therefore 51.0 kg / (1.7 m * 1.7 m) = 17.64706 kg/m^2."
2225,6,Body Mass Index (BMI),physical,decimal,pmc-7892247-1,Extracted,"A 14-year-old girl presented with chronic recurrent pelvic pain since her menarche. Her pain aggravated monthly during her menstruation; however, she had a regular and normal menstrual flow. Her personal history and family history were not significant, and she had no previous sexual history. Different kinds of anti-inflammatory medications had been prescribed for her during the past two years. The patient had also received oral contraceptive pills (OCPs) for two months, but none of the medications had been significantly effective. On physical examination, she was a well-developed girl with normal vital signs. She showed normal pubertal development with a height of 160 centimeters (percentile: 47%) and weight of 48 kilograms (percentile: 43%), and normal adrenarche and thelarche (stage 4). Pelvic examination of the external genitalia was normal with no evidence of imperforated hymen. No definite palpable mass was detected during abdominal examination. Ultrasonography was requested, which showed normal size and myometrial echogenicity of the uterus with normal endometrial thickness. There was evidence of a left-sided heterogeneous and mostly hyperechoic 35 × 30 mm adnexal mass with close contact to the left ovary (). Color Doppler showed some internal vascularity. A small right-sided simple ovarian cyst was also seen on ultrasound. The cervix and vaginal canal were unremarkable on imaging. For further characterization of the mentioned lesion, pelvic MRI was performed, which revealed a well-defined heterogeneous mass with high signal intensity on T2-weighted images and low-to-intermediate signal intensity on T1-weighted images with significant enhancement after administration of gadolinium. The mass was located on the left side of the pelvic cavity, close to the left ovary and uterus; however, no connection to the uterus or ovary was detected. There was no pelvic lymphadenopathy or ascites. Based on the imaging findings, a paraovarian mass or a myoma was suspected. Subsequently, the patient underwent laparotomy, and a well-defined fleshy mass was seen on the left side of the pelvic cavity. The mass was located just under the round ligament, close to but separated from the left ovary with no adhesion to the surrounding structures. Both ovaries and uterus were normal except for a simple right-sided ovarian cyst with no endometrial implants. The uterus had two normally developed fallopian tubes with no fundal impression or contour abnormality and two normal cornua. On close observation, the uterus was completely separated from the mentioned mass. Several collateral vessels arising from the left uterine artery, which provided arterial supply to the mass, were ligated during surgery to obtain hemostasis. Frozen section revealed normal myometrial muscle with reactive endometrium. Finally, the mass was successfully resected by enucleation and incision through the serosa. While performing complete excision, a chocolate-colored fluid flowed out from the mass. The patient had an uneventful postoperative recovery and was discharged one day after surgery. She continued to be asymptomatic with complete resolution of the cyclic pelvic pain after one year of follow-up. Gross evaluation of the pelvic mass revealed a cavitated mass with a thick muscular wall, and pathological examination showed normal irregular myometrium lined by functional endometrium (). Thus, a final diagnosis of accessory and cavitated uterine mass was made. Retrospective re-evaluation of pelvic MRI demonstrated a well-defined mass with signal intensity similar to the uterus on both T1-weighted and T2-weighted sequences with central hypersignal endometrium and normal endometrial-myometrial interface (Figures and ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [48.0, 'kg'], 'height': [160.0, 'cm']}",18.75,17.8125,19.6875,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 48.0 kg. The patient's bmi is therefore 48.0 kg / (1.6 m * 1.6 m) = 18.75 kg/m^2."
2226,6,Body Mass Index (BMI),physical,decimal,pmc-8130080-1,Extracted,"A 68-year-old Japanese man (height: 160 cm, weight: 75 kg) was admitted to our hospital with chest pain and acute dyspnea. He worked as a truck driver and had never traveled abroad.
The chest pain and dyspnea had started a few days previously and had worsened over time. The patient had not received treatment prior to admission.
The patient’s medical history included type 2 diabetes mellitus and hypertension that were treated with oral metformin hydrochloride (750 mg daily) and valsartan (80 mg daily), respectively. His diabetes was poorly controlled, with a hemoglobin A1c of 7.7%.
He denied a history of similar diseases in close relatives.
On auscultation, his heart sounds were normal with no murmur. Coarse crackles were heard in both lungs. No other abnormalities were detected.
Laboratory data at the time of admission are shown in Table . In summary, his white blood cell count and C-reactive protein levels were high. Myocardial enzymes lactate dehydrogenase and aspartate aminotransferase were elevated, and troponin-T was positive. An anti-human immunodeficiency virus (HIV) antibody test result was negative.
His chest radiography on admission showed consolidation in the right upper lobe and bilateral congestion (Figure ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [75.0, 'kg'], 'height': [160.0, 'cm']}",29.29687,27.83203,30.76171,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 75.0 kg. The patient's bmi is therefore 75.0 kg / (1.6 m * 1.6 m) = 29.29687 kg/m^2."
2227,6,Body Mass Index (BMI),physical,decimal,pmc-5644139-1,Extracted,"A 57-year-old Japanese man presented to the emergency department with sudden onset of severe epigastric pain. His medical history included untreated hypertension and hyperuricemia for 3 years; Family history was unremarkable. He was a nonsmoker and did not consume alcohol. He was admitted to the hospital for further treatment.
On admission, his height was 165 cm and weight, which had been unchanged over the past 10 years, was 49 kg. His body temperature was 36.5 °C, and blood pressure was 168/94 mmHg. His heart rate was 90 beats/min and regular. With the exception of tenderness on palpation over the epigastrium, his physical examination was unremarkable. Blood tests showed elevated white blood cell count (WBC, 16,200/mm3 [normal range, 3300–8600/mm3]) as well as elevated levels of lactate dehydrogenase (246 U/L [normal range, 124–222 U/L]), uric acid (529 μmol/L [normal range, 230–420 μmol/L), and C-reactive protein (CRP, 39.8 mg/L [normal, <1.5 mg/L]). Hemoglobin concentration was normal (141 g/L; normal, 137–168 g/L). Serum concentrations of lactic acid, electrolytes, and bicarbonate were normal, as was his anion gap. An abdominal X-ray was unremarkable.
Contrast-enhanced abdominal CT demonstrated an intimal flap inside the SMA at the proximal portion of the aneurysm (Fig. ), suggesting that aneurysm formation might have ensued from spontaneous SMA dissection. Luminal stenosis of the SMA, with concentric intramural hematoma without extravasation, and aneurysm formation at the distal portion of the SMA were also observed (Fig. ). Notably, CT angiography demonstrated two lesions showing segmental dilatation proximal to the SMA aneurysm (Fig. ). Because of the risk of SMA aneurysm rupture, antihypertensive therapy was started; specifically, continuous intravenous infusion of nicardipine (2 μg/kg/min) was begun soon after obtaining the CT, and the patient’s blood pressure decreased to about 110/60 mmHg. Although there was narrowing of the SMA, especially in the proximal portion of the aneurysm, anticoagulation therapy was not instituted.
On hospital day 2, the patient’s epigastric pain persisted. Contrast-enhanced abdominal CT was again performed, but no obvious changes were seen compared with the CT findings on admission. Thereafter, his epigastric pain gradually resolved. By hospital day 4, the patient’s WBC count had normalized to 5400/mm3 and serum CRP had decreased to 15.4 mg/L. The patient’s epigastric pain had completely resolved by hospital day 5 but recurred on day 6. Contrast-enhanced abdominal CT on the same day revealed a notable increase in the size of the SMA aneurysm to 31 × 29 mm, from 23 × 24 mm on admission, and a decrease in the aneurysm’s wall thickness in some areas (Fig. ). CT angiography strongly suggested occlusion of the distal SMA because SMA blood flow distal to the aneurysm, which had been detected on CT angiograph on admission, disappeared (Fig. ). WBC count and serum CRP level were also elevated to 8700/mm3 and 37.6 mg/L, respectively. Because of the risk of aneurysm rupture and ischemic bowel necrosis, the decision was made to perform surgical resection of the SMA aneurysm and partial distal ileum; the length of the resected ileum was 43 cm. This was performed on day 6. During the bowel resection procedure, the SMA was divided at a point showing segmental vasodilation, just proximal to the lesion (Fig. ). Gross inspection revealed no obvious bowel necrosis, but there was evidence of the formation of a pseudoaneurysm inside the mesentery (Fig. ). The SMA distal to the pseudoaneurysm was occluded by thrombus.
Histopathologic examination of specimens of the resected SMA focused on the four regions shown in Fig. . On microscopic examination, there was latent dissection inside the lesion, with vasodilatation adjacent to the proximal resection stump, and the pseudolumen of the dissection was filled with fibrin (Fig. ). In addition, the internal and external elastic membranes of the SMA had partially disappeared, and the lesion was seen to have medial vacuolization and lysis without infiltration of inflammatory cells (Fig. ). In an area slightly distal to this lesion, the internal elastic membrane was preserved (Fig. ), but partial vacuolization and lysis in the arterial media and eccentric intimal proliferation remained (Fig. ). At the neck of the SMA aneurysm, dissection of the arterial media was evident, and both medial vacuolization and partial disappearance of internal elastic membrane were again observed. Notably, remarkable stenosis of the true lumen due to intimal proliferation was evident (Fig. ). The arterial wall at the distal aspect of the SMA aneurysm showed a normal structure of internal elastic membrane and notably less vacuolization in the arterial media (Fig. ).
Postoperatively, the patient was in good condition. Intravenous administration of nicardipine was discontinued on hospital day 12 (postoperative day 6), and oral amlodipine (5 mg/day), valsartan (80 mg/day) and allopurinol (100 mg/day) were started on hospital day 13 (postoperative day 7). He was discharged from our hospital on hospital day 14 (postoperative day 8). The patient has now been followed for 6 months and has had no recurrence of SMA dissection or associated aneurysm formation.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [49.0, 'kg'], 'height': [165.0, 'cm']}",17.99816,17.09825,18.89807,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 49.0 kg. The patient's bmi is therefore 49.0 kg / (1.65 m * 1.65 m) = 17.99816 kg/m^2."
2228,6,Body Mass Index (BMI),physical,decimal,pmc-6806546-1,Extracted,"Twin A and B were idenitical monoamniotic twins born to a 24-year-old G3 P2 mother and a 31-year-old father. The pregnancy was complicated by twin gestation diagnosed at 7 weeks, and gestational diabetes in the last month of pregnancy, which was controlled by diet. Delivery by repeat Caesarean section at 35 ½ weeks of secondary to prior uterine surgery for an ectopic pregnancy.
The neonatal period was unremarkable. At two and a half months he had an incarcerated left inguinal hernia that was repaired surgically. He has had a history of clinical seizures since the age of 15 months controlled by medication including topiramate, clonazepam, and sodium valproate.
On examination at 8.4 years his height was 127.3 cm (50%), weight 25.9 kg (50%), and head circumference 52.5 cm (50%). Physical findings included brachycephaly, mid-facial retrusion, prognathism, macrostomia, wide-spaced teeth, tongue thrusting and strabismus. General examination of heart, lungs, and abdomen was unremarkable. On neurological exam, cranial nerves were grossly intact. His motor examination was notable for truncal hypotonia and increased tone in all extremities. He had jerky movements and a wide-based gait with his arms held in flexion when walking. His EEG at age 8 years was abnormal with widespread delta slowing maximal posteriorly at the fully alert state but dominant frontally in addition to delta, notched delta blunted spike waves or frank spike waves were seen of which one was associated with a clinical event (grunting).
Twin B had mild respiratory distress at birth and was admitted to the Neonatal Intensive Care Unit for 10 days for antibiotic therapy for pneumonia. He began to have seizures at 15 months of age, during which he would tighten his jaw, make growling noises, and have rhythmic tremors. His seizures were controlled by medication EEG obtained at 8 years was suggestive of an active seizure disorder, very characteristic of Angelman syndrome with widespread posterior discharges consisting of delta, notched delta and spike waves. On examination at 8 y. and 5 mo., his height was 128.2 cm (50%), weight 26 kg (50%) and head circumference 53 cm (50-75%). Craniofacial features were identical to his twin. Unlike his twin, he aexhibited mild scoliosis. Both twins were diagnosed with Angelman syndrome at 16 months of age through FISH testing with probes from D15S11 and GABRB3 that showed a typical Angelman syndrome Class I deletion at chromosome 15. DNA methylation studies were conducted and concluded to be diagnostic of AS.
Twins C and D were born to a 29 year old G2 P0 mother and 34 year old father. The pregnancy was naturally conceived and a routine ultrasound at 16 weeks gestation revealed monoamniotic monochorionic twins. There were no exposures during the pregnancy. An ultrasound disclosed no problems. The pregnancy was complicated by preterm contractions beginning at 29 weeks, treated with bedrest and terbutaline, and HELLP syndrome, treated with MgSO4. At 34 weeks gestation, rupture of membranes occurred, and induction of labor was undertaken. Twin D was born vaginally, but twin C was delivered by emergency caesarean section due to cord prolapse.
Both twins had severe muscle hypotonia that persisted beyond a year of age and were diagnosed with Prader-Willi syndrome based on FISH at 13 months. Breast feeding was not successful due to a weak suck and they were fed breast milk in a bottle with a preemie nipple for 1 month and then transitioned to formula. Their coloring was lighter than expected for the family. At 2 years of age, the diagnosis was changed to Angelman syndrome based on DNA methylation results. Twin C was examined at 5 years and 8 months and twin D was examined at 7 years of age. Their chromosome 15q11-q13 deletion associated with Angelman syndrome was characterized as a Class I deletion.
Twin C weighed 2.15 kg, measured 47 cm, and had Apgar scores of 4 and 7. He stayed for 9 days in the Neonatal Intensive Care Unit for temperature regulation and feeding issues. He had febrile seizures in association with a respiratory infection at age 4 months, and non-febrile convulsions began at age 28 months. He had several episodes of status epilepticus and failed management with 6 anti-epileptic medications. Severe failure to thrive necessitated percutaneous gastrostomy tube placement at 3 years of age. When evaluated at age 5 years 8 months, he weighed 16 kg (12%), measured 112 cm (70%), and had a head circumference of 49 cm (75%). He had microbrachycephaly with an occipital ridge, exotropia, midface retrusion, prognathism, and macrostomia with widely spaced teeth. He had a moderate rightward thoracic and leftward lumbar scoliosis and pronated ankles. He had generalized muscle hypotonia.
Twin D weighed 2.13 kg, measured 47 cm, and had Apgar scores of 4 and 7. He was gavage fed for 3 days and discharged home at 9 days. Exotropia and sleep disturbance were noted from infancy. Food refusal and severe failure to thrive necessitated percutaneous gastrostomy tube placement at 3 years of age. There were multiple episodes of otitis media and pneumonia, the latter presumed due to aspiration. Gagging and gastroesophageal reflux disease resulted in many episodes of emesis per day.
Seizures with fever began at 4 months, and afebrile seizures started at 28 months of age. Nearly all developmental skills were lost until seizure control was achieved approximately several months later, following which skills were regained slowly. On examination at 7 years of age, he weighed 19.5 kg (10%), measured 119.3 cm (30%) and had a head circumference of 49.4 cm (50%). He had alternating exotropia, midface retrusion, prognathism, widely spaced teeth, and mild rightward thoracic and leftward lumbar scoliosis. His truncal tone was low, and there was high extensor tone in all extremities.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [25.9, 'kg'], 'height': [127.3, 'cm']}",15.98244,15.18332,16.78156,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 127.3 cm, which is 127.3 cm * 1 m / 100 cm = 1.273 m. The patient's weight is 25.9 kg. The patient's bmi is therefore 25.9 kg / (1.273 m * 1.273 m) = 15.98244 kg/m^2."
2229,6,Body Mass Index (BMI),physical,decimal,pmc-7720419-1,Extracted,"A 8-year-old girl presented in pediatric clinic with upper respiratory infection symptoms: fever, cough, rhinorrhea and pharyngodynia, no other accompanying signs or symptoms, a medical history of hospital admission of dehydration and fatigue, family history: older 14-year-old female sibling with uninvestigated primary amenorrhea and absence of secondary sexual characteristics. On physical examination: weight: 28 kg (69.497th percentile), height: 130 cm (62.225th percentile), BP 150/90 mmHg (99th percentile plus 5 mm Hg), Tanner stage: breast papilla elevation only (Stage1), pubic Hair: no pubic hair (Stage1), normal female external genitalia. Laboratory investigations: sodium = 142.78 mmol/L, potassium = 2.6 mmol/L, arterial blood gas (ph = 7.49, PaCO2 = 22, PaO2 = 96), Cortisol A.M = 3.09 ug/dl (normal = 6.2–19.4), ACTH = 198.3 pg/ml (normal = 5–60), aldosterone (standing) = 335.9 pg/ml (normal: supine = 10–160, standing = 35–300), plasma renin activity (PRA) (erect) = 0.61 ng/ml/h (normal: erect 0.98–4.18, supine: 0.51–2.64), follicle-stimulating hormone (FSH) = 31.65 mlU/ml (normal = 0.3–11), normal thyroid functions, metanephrine in 24 h urine sample = 0.79 (normal: up to 1), DHEA-S (dehydroepiandrosterone sulfate) = 2.47 ug/dl (normal: males 6–9 years: 10–85 ug/dl, females 6–9 years: 13–114), 17-OH progesterone (17-OHP) =0.411 ng/ml (normal prepubertal: 0.07–153). Abdominal and pelvic ultrasound revealed no evidence of ureteral or ovarian tissues. Renal artery echo Doppler was within normal in both sides. Normal male karyotype (46,XY). Combination of hypokalemic hypertension, high aldosterone, low cortisol, high ACTH, high FSH and normal male karyotype (46XY) in a normal female phenotype at childhood led to the diagnosis of 17OHD. The patient was prescribed low dose hydrocortisone (10 mg/m2/day). After 3 months of treatment, a remarkable regression of high blood pressure value to normal range measuring 100/60 mm HG, biochemical laboratory tests showed: PRA (standing) = 4.12 ng/ml/h, aldosterone 256.9 pg/ml (normal: supine = 10–160, standing = 35–300) compared to 0.61 ng/ml/h, 335.9 pg/ml, respectively before treatment.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [28.0, 'kg'], 'height': [130.0, 'cm']}",16.56805,15.73965,17.39645,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 130.0 cm, which is 130.0 cm * 1 m / 100 cm = 1.3 m. The patient's weight is 28.0 kg. The patient's bmi is therefore 28.0 kg / (1.3 m * 1.3 m) = 16.56805 kg/m^2."
2230,6,Body Mass Index (BMI),physical,decimal,pmc-3640171-1,Extracted,"An 80-year-old woman (weight, 53 kg; height, 154 cm) was scheduled for TKRA of the left knee due to degenerative joint disease. She was diagnosed with hypertension 1 year ago but did not receive any medication. Preoperative blood and coagulation tests were normal. She had not undergone any previous operations. At admission, her vital signs were stable. Preoperative electrocardiography (ECG) showed normal sinus rhythm and a complete right bundle branch block (). A chest X-ray showed a hypertensive heart contour. We did not perform an echocardiogram, because it was obtained at another hospital, and cardiac function was normal except for the hypertension.
The patient was premedicated with glycopyrrolate 0.2 mg intramuscularly 30 min before anesthesia. Upon arrival in the operating room, standard ECG, pulse oximeter, noninvasive blood pressure, and bispectral index monitoring (Model A-2000; Aspect Medical Systems, Newton, MA, USA) were applied. Her vital signs were pulse rate, 76 beats/min (bpm); oxygen saturation, 97%; and blood pressure, 177/83 mmHg. Anesthesia was induced with 40 mg lidocaine and 60 mg propofol. Rocuronium was given at a dose of 0.6 mg/kg to facilitate endotracheal intubation after loss of consciousness. After a few minutes, the ECG showed a complete AV block and ventricular rhythm of about 40 bpm (). Despite the administration of 0.5 mg atropine, the arrhythmia persisted (blood pressure, 90/40 mmHg; pulse rate, 30-49 bpm). At that time, her trachea was intubated with a 7.0-sized endotracheal tube under direct laryngoscopy, and a radial arterial line was placed for continuous arterial pressure monitoring and blood gas analysis. A central venous catheter was also inserted via the right internal jugular vein catheter. About 10 minutes after the propofol injection, her blood pressure was 145/55 mmHg, and her pulse rate was 66 bpm. The ECG showed a sinus rhythm. The operation was delayed, and she was transferred to the intensive care unit until fully awake for close observation and further evaluation.
We assessed the patient's creatine kinase-MB, troponin T, and myoglobin, and all values were normal. An echocardiography taken the next day exhibited a left ventricular ejection fraction of 63%, which was suggestive of an indeterminate left ventricular filling pattern due to complete AV block. In addition, a 24-h ECG Holter monitor showed AV dissociation. Three-dimensional (3D) computed tomography of the heart revealed that the proximal and middle parts of the left anterior descending artery were narrowed by 50%. She also had a focal aortic valve and mitral annular calcification.
We had planned to perform the surgery again. She received a temporary pace maker (VDD mode) with the minimum rate was set to 60 bpm. She was taken to the operating room, where her blood pressure was 180/95 mmHg and pulse rate was 72 bpm. A 22-gauge catheter was placed in the left radial artery for blood pressure monitoring. A central venous catheter was already inserted via the right internal jugular vein. The patient was placed in the right lateral decubitus position, and spinal anesthesia was performed at the L4/L5 interspinous space with 0.5% hyperbaric bupivacaine 8 mg. The sensory level reached the 10th thoracic segment. The surgeon then began the operation with an initial blood pressure of 170/80 mmHg and a heart rate of 90 bpm. The operation lasted about 2 h. She asked for sedation and we administered midazolam 3 mg intravenously. However, because adequate sedation was not achieved, she received a continuous infusion (50 µg/kg/min). A few minutes after the propofol infusion, the ECG showed a complete AV block with a ventricular rhythm of about 40 bpm. The complete AV block disappeared soon after the propofol infusion was stopped. During the remainder of the surgery, her vital signs were stable. At the end of the operation, she had a blood pressure of 150/55 mmHg, a pulse rate of 55 bpm, and oxygen saturation of 96%.
A permanent pacemaker (DDDR mode) on postoperative day 2 was inserted (). On postoperative day 27, she remained hemodynamically stable and was discharged from the hospital uneventfully.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.0, 'kg'], 'height': [154.0, 'cm']}",22.34778,21.23039,23.46517,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 154.0 cm, which is 154.0 cm * 1 m / 100 cm = 1.54 m. The patient's weight is 53.0 kg. The patient's bmi is therefore 53.0 kg / (1.54 m * 1.54 m) = 22.34778 kg/m^2."
2231,6,Body Mass Index (BMI),physical,decimal,pmc-7530739-2,Extracted,"The patient was a 7 year-old boy (107 cm, 16.4 kg). Disease onset occurred at the age of 2 months. Although IVIG was administered three times after IVIG and methylprednisolone pulse therapy, the inflammatory responses persisted, and bilateral coronary artery aneurysms were found 1 week after admission. The patient was transferred to our hospital on disease day 17. After admission to the intensive care unit, the patient was intubated to maintain sedation, and the heart rate and blood pressure were suppressed using nicardipine and sedatives. Despite those therapies, large aneurysms were detected at all three coronary arteries. At 3 months of age, 1 month from disease onset, there were no symptoms, but deepQ wave in lead III on ECG suggested ischemic changes and the troponin and CK-MB levels were elevated on blood test. We diagnosed the patient with AMI, and CAG was performed. On CAG, a huge long segmental aneurysm on RCA was observed with a maximum diameter of 12 mm, the blood flow was almost arrested, and the presence of a thrombus was confirmed (). On the left side, the aneurysmal size on LAD was 9.2 mm and that on LCX was 3.3 mm.
Emergency ICT using t-PA was performed for the RCA thrombus. The thrombus disappeared on the echocardiogram; however, the fever persisted, and infliximab was administered on day 18. The body temperature began to decline on the next day, and the heart rate stabilized. One week later, the patient was extubated, and sedation was discontinued. Therapy was continued with aspirin, ARB, and warfarin. Thereafter, the patient underwent regular follow-up evaluations with ECG, chest radiography, echocardiography, and coronary angiography.
At 1 year of age, 10 months after the acute phase, CAG revealed that the main RCA was completely occluded. However, peripheral blood flow was maintained from the LCX. The LAD vessel diameter still had aneurysmal change, but the diameter improved to 5 mm, no stenotic lesion was detected, and LCX also returned to its normal size. Subsequently, CAG exhibited similar findings as those observed at 1 year after the acute phase. At 2 years of age, 2 years from disease onset, CAG was performed and similar findings were observed. At that time, his body weight was <15 kg, and we speculated that performing CABG using RITA would be difficult at this age. Thus, CABG was postponed. After CAG, he went to the hospital for a regular check-up and underwent exercise ECG. He did not complain of any discomforts or chest pains, even while performing exercises at school. However, at 7 years of age (weight, 16.4 kg), 7 years from onset, he lost consciousness while exercising and underwent another CAG. The LAD was completely occluded and stenosis of the LCX of 0.9 mm was observed. Drug-loaded myocardial scintigraphy showed extensive ischemia of the sidewall; however, the left ventricular EF was maintained at 70%. He had symptoms and sufficient weight and ischemic findings on examination to warrant surgery. Then, CABG was performed. Anastomosis was performed at the following two places: LITA-LAD and RCA-GEA. However, the LITA was too small to be skeletonized; thus, anastomosis was performed using only milrinone injection. The RITA was also preserved for future stenotic episodes. Angiography performed at ~1 year after surgery showed a good blood flow in both vessels ().
Both patients provided written informed consent.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [16.4, 'kg'], 'height': [107.0, 'cm']}",14.3244,13.60818,15.04062,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 107.0 cm, which is 107.0 cm * 1 m / 100 cm = 1.07 m. The patient's weight is 16.4 kg. The patient's bmi is therefore 16.4 kg / (1.07 m * 1.07 m) = 14.3244 kg/m^2."
2232,6,Body Mass Index (BMI),physical,decimal,pmc-3927006-1,Extracted,"A 70-year-old male patient underwent a Bentall operation due to annulo-aortic ectasia, which was combined with severe aortic valvular insufficiency. The patient's height and weight were 165 cm and 50.9 kg, respectively and he had no co-morbid diseases except for hypertension, which was treated with a calcium channel blocker and an angiotensin converting enzyme inhibitor. The patient had a normal sinus rhythm, and the preoperative transthoracic echocardiography (TTE) revealed a left ventricular ejection fraction of 58% with no other intracardiac pathologies. Coronary angiography also revealed normal coronary arteries. After anesthetic induction, the patient's hemodynamic variables were as follows; systemic blood pressure 113/38 mmHg, heart rate 83 beats/min, central venous pressure 9 mmHg, and pulmonary arterial pressure 33/15 mmHg. A Bentall procedure was uneventfully performed and the patient was weaned off from cardiopulmonary bypass (CPB) without difficulty. The total aorta cross clamp time was 95 minutes and the total CPB time was 115 minutes. Before leaving the operating room, there was no evidence of fluid collection in the pericardial and pleural space in the transesophageal echocardiography (TEE), with the estimated left ventricular ejection fraction being 50%. Receiving norepinephrine 0.08 µg/kg/min, milrinone 0.25 µg/kg/min, and vasopressin 0.8 IU/hr, the hemodynamic parameters were as follows: heart rate of 80 beats/min, blood pressure of 87/48 mmHg, CVP of 10 mmHg, pulmonary arterial pressure of 24/15 mmHg, cardiac index of 3.4 L/min/m2, mixed venous oxygen saturation of 90%, right ventricular ejection fraction of 39%, and right ventricular end diastolic volume index of 141 mm/m2. The patient was transported to the intensive care unit (ICU) without any further events. In the ICU, as in the operating room, the patient's lungs were ventilated with a tidal volume of 500 ml at a rate of 12 breaths/min, with a fraction of inspired oxygen of 40% medical air, along with 5 cmH2O of positive end-expiratory pressure. The corresponding peak airway pressure and plateau airway pressure were 19 cmH2O and 17 cmH2O, respectively. The arterial blood gas analysis revealed pH 7.419, PaO2 123.8 mmHg, and PaCO2 34.7 mmHg. Over a period of 30 minutes in the ICU, the CVP increased from 10 to 23 mmHg, and the pulmonary artery diastolic pressure increased from 14 to 17 mmHg. The blood pressure was 90/49 mmHg, and the cardiac index was maintained at 2.7 L/m/m2 without increasing doses of norepinephrine, milrinone, and vasopressin. The electrocardiogram (ECG) revealed nonspecific ST wave changes without any changes in the height of the QRS waves, and the chest X-ray showed partial atelectasis of the right lung and moderate cardiomegaly. The patient's respiratory mechanics and follow-up arterial blood gas analysis showed no significant changes. His hemoglobin was 8.7 g/dl which is near the former value measured in the operating room of 9.0 g/dl. The platelet count was 82 × 109/L and the International Normalized Ratio of the prothrombin time was slightly elevated at 1.54. During the first 15 minutes after the surgery, 100 ml of blood were drained from his mediastinal and chest drains. Because, there was no further chest tube drainage, 100 ml of 6% hydroxyethyl starch 130/0.4 solution was infused without any transfusions.
A TEE examination was immediately performed to confirm the cause of the CVP elevation, which revealed minimal pericardial fluid collection and preserved biventricular function in the midesophageal four-chamber view and the transgastric short axis view. The midesophageal bicaval view showed the right atrium (RA) being pushed anteriorly and laterally by a large mass measuring 6.06 cm × 8.78 cm (). The mass contained echogenic materials with some echo-free areas, which is consistent with hematoma, and as a result the SVC was almost completely obliterated by it. In the midesophageal aortic valve long axis view, the hematoma occupied the transverse sinus as well (). The patient was immediately transferred to the operating room for re-exploration. A loculated hematoma around the valved graft was found to compress the entire SVC and extended to the RA. After evacuation of the hematoma, the CVP decreased immediately from 23 to 11 mmHg. The cardiac index and the blood pressure remained stable despite the discontinuation of the vasopressor and inotropic agents. However, the patient's postoperative course deteriorated, with the development of acute renal failure and adult respiratory distress syndrome, which resulted in the prolongation of ICU stay. The patient was then transferred to the general ward at postoperative day (POD) 52 for rehabilitation, and discharged at POD 109.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [50.9, 'kg'], 'height': [165.0, 'cm']}",18.69605,17.76125,19.63085,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 50.9 kg. The patient's bmi is therefore 50.9 kg / (1.65 m * 1.65 m) = 18.69605 kg/m^2."
2233,6,Body Mass Index (BMI),physical,decimal,pmc-2633322-1,Extracted,"We are presenting a case with acute abdomen, i.e. ileum perforation, caused by accidentally ingesting a chicken wishbone.
A fifty-year-old male was presented in the surgical emergency clinic with abdominal pain, nausea, and vomiting. The symptoms had started two days earlier. He used tobacco, but denied having consumed alcohol. The patient's height was 170 cm and his weight was 120 kg. His vital signs were: blood pressure 120/80 mmHg; pulse rate 90 beats/min.; respiration rate 19/min.; body temperature 38.5°C. His past medical history consisted of surgery for a thrombophlebitis in his right arm one year earlier.
Upon physical examination, a distended and diffusely tender abdomen with right lower abdomen rebound was revealed. The patient's skin and mucosa were pale.
The emergent laboratory tests revealed as follow: white blood cells (WBC): 12.6 × 109/liter; serum creatinine: 126 mol/L; blood urea nitrogen: 8.6 mmol/L; blood sugar: 11.6 mmol/L; Na: 141 mmol/L; K: 4.0 mmol/L; Ca++: 1.08 mmol/L; urinalysis: a lot of mucus, 4–6 Leucocytes; some epithelial cells. Plain abdominal radiography showed mechanical obstruction. Urgent abdominal ultrasound revealed mechanical obstruction, dilated small bowels and free liquid in the peritoneal cavity.
Laparotomy was performed in general anesthesia on the day the patient was admitted. Intra operative findings revealed diffuse fibro purulent peritonitis with adhesions between small bowels; and about 40 cm from Bauchini valve the presence of a sharp chicken wishbone perforated the ileum at the ante mesenteric site (Figure ). The wall of that part of the ileum was thick and succulent. The patient was treated after the adhesiolisis with resection of the perforated distal ileum and ileum stoma. The postoperative treatment went well; the wound healed per secundum. Clebsiela spp. was isolated in the stained abdominal liquid and treated with the proper antibiotics. Four months after the first operation and losing 25 kg, the patient underwent reconstruction of bowel continuity, and discharged on the tenth postoperative day with normal bowel movements.
Retrospectively, after the first operation the patient admitted that four days earlier he had rapidly eaten and swallowed several mouthfuls of chicken meat without chewing and accidentally ingested a chicken bone.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [120.0, 'kg'], 'height': [170.0, 'cm']}",41.52249,39.44637,43.59861,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 120.0 kg. The patient's bmi is therefore 120.0 kg / (1.7 m * 1.7 m) = 41.52249 kg/m^2."
2234,6,Body Mass Index (BMI),physical,decimal,pmc-8442815-1,Extracted,"A 95-year-old woman (135 cm and 40 kg) presented with right intertrochanteric femoral fracture requiring surgery. She had a history of hypertension, dyslipidemia, and dementia, which were controlled by amlodipine and olmesartan, pravastatin, and donepezil, respectively. Physical examination findings were normal, and laboratory examination revealed mild anemia with hemoglobin (Hb) level of 11.8 g/dL and coagulopathy of prothrombin time [PT] of 58% (PT-international normalized ratio, 1.3) probably owing to advanced age. Transthoracic echocardiography, electrocardiography, and respiratory function test revealed no abnormalities.
Anesthetic chart is shown in Fig. . In the operating room, the patient’s vital signs were as follows: blood pressure (BP), 136/70 mmHg; heart rate, 88 bpm; and oxygen saturation on room air, 92%. BIS value was > 90 before inducing anesthesia. General anesthesia was induced by intravenous administration of fentanyl (50 μg), remifentanil (0.15 μg/kg/min), and remimazolam (1.2 mg/kg/h). She lost consciousness 4 min after initiation, and subsequently tracheal intubation was performed after administration of rocuronium (40 mg). After the operation was started, the remimazolam dose was adjusted so that the BIS value became 40–60 0.125 μg/kg/min of remifentanil infusion. Eventually, remimazolam dose was decreased to 0.2 mg/kg/h although BIS value remained < 40. The operation was uneventfully completed with a small amount of blood loss in approximately 90 min. During the operation, she remained hemodynamically stable with administration of ephedrine 4 mg bolus and phenylephrine 50 μg bolus only twice to maintain systolic BP at > 90 mmHg, without the need of continuous administration of vasopressor agents. At the time of suture, 50 μg of fentanyl was administered, the remifentanil dose was decreased to 0.075 μg/kg/min, and remimazolam was maintained at 0.2 mg/kg/h. After completion of the operation, administration of these agents was discontinued and 200 mg of sugammadex was administered. Although 2.0 mg of remimazolam was administered as a bolus owing to the BIS value of > 70 during postural change for radiographic examination, 10 min after the bolus administration, she recovered consciousness without flumazenil and received extubation. Any consciousness problem, including resedation or postoperative cognitive function disorder, was not observed during the postoperative course. After rehabilitation, she was discharged on postoperative day 15.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [40.0, 'kg'], 'height': [135.0, 'cm']}",21.94787,20.85048,23.04526,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 135.0 cm, which is 135.0 cm * 1 m / 100 cm = 1.35 m. The patient's weight is 40.0 kg. The patient's bmi is therefore 40.0 kg / (1.35 m * 1.35 m) = 21.94787 kg/m^2."
2235,6,Body Mass Index (BMI),physical,decimal,pmc-4166086-1,Extracted,"The patient was a 29-year-old man admitted to the hospital four years ago (June 2009) due to hematemesis. The problem was diagnosed as esophageal variceal bleeding and the proper treatment was provided. He had no history of alcohol consumption or diabetes mellitus. Moreover, the tests were negative for all types of viral hepatitis (B, C), EBV (Epstein–Barr virus), herpes, CMV (Cytomegalovirus), autoimmune hepatitis, HIV, celiac and Wilson’s disease. The colonoscopy result was normal. On April 2010, liver biopsy showed cirrhotic changes and the patient was diagnosed with cryptogenic cirrhosis. His name went to the list of liver transplantation candidates and the academic management for cirrhotic patients was started for him.
The patient first visited Behesht Clinic of Tehran University of Medical Sciences in Tehran for Iranian traditional medicine on September 2011, about 17 months after being diagnosed. At the time, his medicinal prescription included spironolactone, propranolol, prednisolone and doxepin. The patient stopped taking all the medications after one month.
His height was 173 cm and his weight was 57 kg. In his first visit, he had flatulence, dyspepsia, and heartburn. He was generally thirsty and drank up to eight glasses of cold water a day. He also had severe itching sensation of skin and would not sweat even during intense physical activities. His sclera was icteric.
From his first visit to Behesht Clinic on September 2011 till February 2013, the patient was visited 16 times and each time, considering his general state and by performing physical examinations, the necessary traditional medication was prescribed for him. After three weeks of treatment, his itching sensation was significantly reduced, he felt energetic, and his flatulence and heartburn decreased. During four months of treatment, the patient gained 6 kg without any sign of ascites in abdominal ultrasonography. From the first admission (June 2009) until the end of study (February 2013), the alpha-fetoprotein (AFP) level was always in the normal range. The traditional medicine preparations used for this patient were based on the book “Al-Qanoon fi al-Tibb” by Avicenna. What follows is a list of different medicines used at different stages of the treatment:
Monzeje soda, kabed capsuls, sekanjebine-bozoori, sekanjebine-sadri, samgh capsuls, eksir syrup, khabasolhadid, goleghand, habolroman, javareshe amole, aftimoon syrup, araghe-kasni shahtare, araghe-zenyan. and show the changes in the patient’s test results before and after the traditional medication. At the moment, the patient is in a good general condition and there is no need for liver transplantation.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [57.0, 'kg'], 'height': [173.0, 'cm']}",19.04507,18.09282,19.99732,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 173.0 cm, which is 173.0 cm * 1 m / 100 cm = 1.73 m. The patient's weight is 57.0 kg. The patient's bmi is therefore 57.0 kg / (1.73 m * 1.73 m) = 19.04507 kg/m^2."
2236,6,Body Mass Index (BMI),physical,decimal,pmc-4815057-1,Extracted,"A 12-year-old boy was admitted to our hospital for further evaluation of proteinuria, and renal insufficiency. He had megacystis microcolon intestinal hypoperistalsis syndrome (MMIHS), a form of pseudo-Hirschsprung’s disease. He had been on HPN by CVC for 8 years. Two months before admission, he presented with macroscopic hematuria. He developed proteinuria and renal insufficiency 1 month before admission. On admission, his height was 137.8 cm (−1.49 SD) and body weight was 34.2 kg (−0.83 SD). His blood pressure was 100/54 mmHg, and the chest and abdomen exhibited no abnormal findings. Blood examination revealed hypoalbuminemia (serum albumin of 3.1 g/dL), renal insufficiency (serum creatinine of 0.68 mg/dL), estimated glomerular filtration rate (e-GFR), 70.8 mL/min/1.73 m2, hypocomplementemia (C3, 4 mg/dL, C4, 3.4 mg/dL, and CH50, 10 U/mL) and positive PR3-anti-neutrophil cytoplasmic antibodies (ANCA) (33 U/mL; normal range 0–9 U/mL). Urinalysis revealed proteinuria (urinary protein 137.0 mg/dL, urinary creatinine, 63.5 mg/dL), and hematuria (>100 erythrocytes per high power field). Renal biopsy was performed after admission. Light microscopy (LM) revealed mesangial proliferation with one crescent formation in 23–30 glomeruli. Immunofluorescence microscopy revealed C3, C1q and immunoglobulin (Ig) M deposits along the capillary, and in mesangial region. Electron microscopy (EM) revealed paramesangial deposits. The pathological findings were consistent with membranoproliferative glomerulonephritis. We treated him with 60 mg of oral prednisolone and 150 mg of mizoribine for 10 days, but his urinary findings and renal function did not improve. He suddenly developed fever on the 12th day after admission, and blood culture did not reveal S. epidermidis (MSSE) colonization in the peripheral blood but in the CVC instead. We immediately stopped both prednisolone and mizoribine, removed the CVC, and administered cefazolin for 10 days.
After the removal of CVC, his renal function gradually improved, and proteinuria and hematuria spontaneously disappeared in 6 months (Fig. a). Recurrence of proteinuria and hematuria has not been occurred.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [34.2, 'kg'], 'height': [137.8, 'cm']}",18.01058,17.11005,18.91111,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 137.8 cm, which is 137.8 cm * 1 m / 100 cm = 1.378 m. The patient's weight is 34.2 kg. The patient's bmi is therefore 34.2 kg / (1.378 m * 1.378 m) = 18.01058 kg/m^2."
2237,6,Body Mass Index (BMI),physical,decimal,pmc-3794967-1,Extracted,"A 33-year-old woman was admitted to our general medicine department with FUO which had persisted for longer than 2 months and was resistant to treatment with nonsteroidal anti-inflammatory drugs and prednisolone 20 mg/day. Her fever was remittent, and body temperature ranged from 37.5°C to 38.5°C. She reported sweating and headache, but did not complain of body weight change, pain, nausea, abnormal vaginal bleeding, or diarrhea.
To treat dysmenorrhea and premenstrual syndrome, she had been prescribed oral contraceptives (levonorgestrel, ethinylestradiol) for 7 years, and the dose had remained unchanged during that period. She had no history of pregnancy, and a gynecologic examination revealed no infectious or malignant findings.
She had been receiving regular follow-up care for mild depression for 3 years at our department of psychiatry and had been prescribed the antidepressants, aripiprazole and duloxetine hydrochloride, until 2 months before admission. Her depressive symptoms were stable upon presentation to our department. She had asthma, which was well controlled with the inhaled steroid budesonide (200 μg, once daily).
She was a housewife and only had sexual contact with her husband who had no sexually transmitted diseases. She had no pets and no animal or insect bites. She had not traveled for one year and had no history of drug abuse. A family history revealed no hereditary cause of fever.
Her height was 152 cm and body weight was 56 kg. Her mental status was alert, and blood pressure was 92/60 mmHg in a sitting position. Although the rise in body temperature was accompanied by an increase in pulse rate, her pulse was normal, ranging from 58 to 82 beats per minute. Her pulse rate was regular in rhythm, and its size, and tension were within the normal ranges. Her body temperature was 38.5°C and her respiratory rate was 15 per minute. Physical examination revealed no abnormalities, such as focal inflammation, lymph node swelling, skin rash, or abnormal heart sounds.
Laboratory analysis showed no biological inflammation C-reactive protein 0.0 mg/L, and interleukin-6 (2.1 pg/mL, normal range <4.0 pg/mL) and tumor necrosis factor-α (0.6 pg/mL, normal range 0.6–2.8 pg/mL) were normal. A chest X-ray showed no abnormal findings, and sputum culture for acid-fast bacteria was negative. In addition, an interferon-γ release assay (QFT-2G, Oxford Immunotec Co, Ltd Oxford UK) was not positive (0.30 IU/L, normal range <0.80 IU/L). The results for the remaining biological tests were all in the normal ranges, as shown in . Contrast thoracic and abdominal computed tomography, brain magnetic resonance imaging, and gallium scintigraphy excluded infection, including tuberculosis, and rheumatic/inflammatory, neoplastic, or other focal abnormalities.
Fever decreased 2 days after adding Yokukan-san to 7.5 g of powdered OGT, which is the standard dose for adults (). OGT was then prescribed for an additional 10 days, and fever has not relapsed after a follow-up period of 2 months.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [56.0, 'kg'], 'height': [152.0, 'cm']}",24.23823,23.02632,25.45014,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 152.0 cm, which is 152.0 cm * 1 m / 100 cm = 1.52 m. The patient's weight is 56.0 kg. The patient's bmi is therefore 56.0 kg / (1.52 m * 1.52 m) = 24.23823 kg/m^2."
2238,6,Body Mass Index (BMI),physical,decimal,pmc-7784184-1,Extracted,"A 16-year-old Indian girl presented to the endocrinology out-patient department with short stature and delayed pubertal development with absence of menarche. She also complained of gradually progressive difficulty in chewing food since last 2 years. There was no history suggestive of dental malocclusion, trauma or any abnormalities in jaw opening or closing. There was no family history of growth retardation or pubertal delay, neither any surgical intervention nor radiation exposure during childhood. She was born of an uneventful pregnancy at 36 weeks gestation age by normal spontaneous vaginal delivery with normal birth length and weight. There was no history of any chronic illness during childhood. She studied in 8th grade and her academic performance was average.
On examination, facial puffiness was prominent along with a dry and scaly skin. There was crowding of her incisors (). She had a large sized tongue, more evident on protrusion (). Her hair seemed brittle with mild alopecia noted in the frontal region. There was no madarosis of eyebrows. There were no signs of goitre while the higher mental functions and neurological examination were within normal limits with slightly sluggish deep tendon reflexes in the lower limbs (grade 1+). Anthropometric measurements revealed a standing height of 134 cm (<3rd percentile for age and sex) and an arm span of 132 cm. She weighed 28 kg (<3rd percentile for age and sex). The mid-parental height as calculated from her parents was 164 cm. Tanner scoring was B1, P1 and A1.
Her investigations revealed the following (): Hemoglobin=10.2 g/dl, and general blood picture suggestive of normocytic normochromic anemia, normal serum electrolytes, CPK and LDH. Liver functions and kidney functions were within normal limits. Thyroid function tests revealed TSH level >150 μIU/L (normal: 0.4-5) with low T4 and T3 levels, suggestive of overt hypothyroidism. Anti-thyroid peroxidase antibody (Anti TPO Ab) was >1000 IU/ml (normal: 0-50 IU/ml). Ultrasound study of the thyroid gland was mostly normal with a few hypoechoic lesions noted. Her bone age from x-ray of the left hand as calculated by Tanner-Whitehouse 2 was 8.9 years. Her gonadotropin levels (both FSH and LH) were low, implying pre-pubertal status. Thus, her short stature, delayed bone age and delayed pubertal development were attributed to hypothyroidism due to Hashimoto’s thyroiditis.
She was started on levothyroxine replacement and counselled appropriately. After 6 months of therapy, she noted improvement in her chewing abilities. She is being monitored regularly for catch up growth and subsequent pubertal development.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [28.0, 'kg'], 'height': [134.0, 'cm']}",15.59367,14.81399,16.37335,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 134.0 cm, which is 134.0 cm * 1 m / 100 cm = 1.34 m. The patient's weight is 28.0 kg. The patient's bmi is therefore 28.0 kg / (1.34 m * 1.34 m) = 15.59367 kg/m^2."
2239,6,Body Mass Index (BMI),physical,decimal,pmc-7873350-1,Extracted,"The patient was an 84-year-old female; 145.1 cm in height and 54.0 kg in weight at the time of her initial examination; a housewife; and described as sincere and calm in personality. Her chief complaints were loss of appetite and weight loss, and she had a medical history of angina with onset at the age of 75. With regard to the history of her present illness, she came to our hospital in January X−3 due to noticeable amnesia such as not being able to recognize the faces and names of relatives and grandchildren. She was diagnosed with Alzheimer's disease based on a 16-point score on the Mini-Mental State Examination (MMSE) and on functional imaging findings such as cerebral blood flow single-photon emission computed tomography (SPECT). She was treated with galantamine and outpatient care for lifestyle diseases such as hypertension, and her instrumental ADLs (IADLs) improved to the point where she was able to prepare meals, go shopping, and take the bus.
She was treated with galantamine. However, her functional ability to perform ADLs gradually declined; and in the summer of X−1, her functional impairment in ADLs progressed to the point where she required emergency treatment, including intravenous fluids, due to heat stroke. In December X−1, she fell on the stairs at a train station, fractured her right femur, and underwent an artificial femoral head replacement. Although she was discharged from the hospital in April X, she was unable to take her medication or do household tasks on her own that she was previously able to do. She was unable to prepare meals and often did not eat when her eldest daughter prepared meals for her. In October X, she had frequent hallucinations at home when someone was in the room; she started to eat much less food; and she weighed 50.4 kg, showing a decrease of 4 kg in 6 months. Although she was able to walk on her own, her IADLs declined as indicated by scores of 48 on the Dementia Assessment Sheet for Community-based Integrated Care System 21-items (DASC-21), 4 on the Lawton IADL scale, 3 on the level of long-term care required, 21 on the MMSE, and 14 on the Frontal Assessment Battery (FAB). Her muscle mass was 30.2 kg as measured by a body composition analyzer (InBody 270) using bioelectrical impedance analysis. The calculated weight after removing the body fluid weight (19.1 kg) from the total body weight (50.4 kg) was 31.3 kg. Since October X, she had been instructed to take 3.75 g of Ninjin'yoeito once before bedtime for her loss of appetite and weight loss.
In April X+1, improvement in her appetite was observed. Her weight was 52.2 kg, showing an increase of 1.8 kg. Her muscle mass was 31.1 kg, showing an increase of 0.9 kg. The weight after subtracting the body fluid weight was 52.2–19.7 kg = 32.5 kg, showing an increase of 1.2 kg. In July X+1, her weight dropped slightly by 0.8 to 51.4 kg, and her muscle mass also dropped by 0.3 to 30.8 kg. Eventually, there was an increase of 1.0 kg in body weight and 0.6 kg in muscle mass, and the weight after removing the body fluid weight was 51.4–19.5 kg = 31.9 kg, showing an increase of 0.6 kg. With regard to ADLs, a decrease in basic ADLs (BADLs) in addition to IADLs was observed, such as leaving a pot on the fire, requiring assistance to take medication, being unable to flush the toilet, and being unable to bathe and wash her hair, but her hallucinations and insomnia improved and she was no longer required to take sleeping medication and/or antipsychotic medication.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [54.0, 'kg'], 'height': [145.1, 'cm']}",25.64832,24.3659,26.93074,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 145.1 cm, which is 145.1 cm * 1 m / 100 cm = 1.451 m. The patient's weight is 54.0 kg. The patient's bmi is therefore 54.0 kg / (1.451 m * 1.451 m) = 25.64832 kg/m^2."
2240,6,Body Mass Index (BMI),physical,decimal,pmc-2639571-1,Extracted,"A 55-year-old Iranian woman (height: 168 cm weight: 78 Kg), a known case of ADPKD, was admitted to our hospital with 3-week history of malaise, severe bilateral flank pain, dysuria, frequency, chills, and fever. She had also pertinent past medical history of diabetes mellitus and hypertension for 8 years and was receiving atenolol 50 mg and glibenclamide 25 mg daily. She had neither history of cigarette smoking nor alcohol consumption. Her family history was unremarkable. She had three normal full term pregnancy without any complications. On physical examination, she was febrile and ill. Mild pretibial edema and tenderness over the costovertebral angles were also noted. Laboratory studies showed anemia, elevated level of blood urea nitrogen (BUN), serum creatinine, and serum glucose. Urinalysis showed pyuria, and urine culture yielded growth of Escherichia coli and Pseudomonas aeroginosa (more than 105 colonies per high power field). Hence, antibiotic therapy was begun with the administration of ciprofloxacin intravenously. Abdominal Ultrasonography (US) demonstrated both enlarged kidneys measuring 18 cm on the right side and 23.6 cm on the left contained multiple cysts. The largest cysts in the right and left kidney were 8 cm and 10 cm respectively, with most of the remaining cysts measuring 4 to 5 cm. A renal calculus was also seen in the left pelvicalyceal system. No hepatic cyst was noted. Due to the lack of clinical improvement, intravenous piperacillin/tazobactam was added to ciprofloxacin on the 5th day of her admission. Further US investigation on the 12th day, showed numerous cystic space-occupying lesions with low level internal echoes, septations, and increased wall thickness of the cysts that representing infected cysts (Fig. ). So, intravenous trimethoprim-sulfamethoxazole (TMP-SMX) was added to the former antibiotic therapy. This 2-week intensive antibiotic therapy had no beneficial effect. After informing the patient and her family about her condition and obtaining a signed consent, the antibiotics were discontinued and then we decided to perform puncture and irrigation of the cysts for confirming the diagnosis of pyocyst, determining the causative organisms, and treating the refractory infected cysts. After sterile preparation, US-guided percutaneous puncture was carried out by using a 20-gauge Chiba needle (TSK, Japan) in the supine position and 40 ml of purulent fluid was evacuated and sent for microbiological and serological studies. The culture was positive to E. coli and Pseudomonas aeroginosa. On the second stage, the largest cysts in the left side were punctured by an identical method. Cystic fluid was aspirated as completely as possible. To achieve this, the needle tip was monitored with US so that it remained in the center of the cyst during aspiration. Immediately after that, an 8 Fr. Catheter was inserted into the cystic cavity with US guidance and irrigation and drainage with 20 ml of 0.9% sodium chloride solution, and 20 ml of 10% povidone iodine was carried out. Forty-eight hours later, the same procedure was repeated for the largest cyst (8 cm in diameter) of the right kidney (Fig. ); however, the patient showed no improvement. Despite the repeated irrigation and drainage via the inserted catheters, no response to the procedures was seen. Therefore we decided to schedule her for bilateral nephrectomy on the 23rd day, but she didn't consent to the operation. We continued irrigation of catheters with 10 ml of 0.9% saline solution every 8 hours for removing the infected debris and draining the purulent discharge. Ultimately, a catheter was inserted into another large cyst of the left kidney for irrigation and drainage. After 3 days, fever disappeared and clinical state and laboratory tests showed improvement. Repeated US showed decreasing amount of internal echoes and thick septa of the drained cysts (Fig. ). Two catheter in the left and one in the right side were removed once the amount of drainage became less than 10 ml and sterile. Then, antibiotic therapy was appropriately changed to oral TMP-SMX. After 2 months of hospitalization, she completely recovered and was discharged to home. One year after discharge, she remained asymptomatic.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [78.0, 'kg'], 'height': [168.0, 'cm']}",27.63605,26.25425,29.01785,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 78.0 kg. The patient's bmi is therefore 78.0 kg / (1.68 m * 1.68 m) = 27.63605 kg/m^2."
2241,6,Body Mass Index (BMI),physical,decimal,pmc-3167139-1,Extracted,"A 12-year-old (150 cm, 48 kg) female was scheduled for microtia reconstructive surgery. Preoperative laboratory findings and her chest radiograph were all normal. She was premedicated with midazolam 2 mg and atropine 0.5 mg IM, and general anesthesia was induced with propofol 100 mg and rocuronium 50 mg and maintained with oxygen (2 L/min), N2O (2 L/min), and sevoflurane (2.0-3.0 vol%).
Costal cartilage was harvested from the left 6, 7, 8, and 9th ribs and modeled to form an auricle, which was then implanted at the reconstruction site. The cartilage donor site was soaked with saline and then the Valsalva maneuver was performed to detect air bubbles to exclude pneumothorax. No air bubbles were detected. After surgery, intravenous patient-controlled analgesia with fentanyl and ketorolac was administered for postoperative pain management until the 3rd postoperative day. In addition, analgesics were administered as needed from the 4th postoperative day because she complained about ongoing pain in the surgical area that interfered with sleep. However, the pain management was less than effective and anxiety and pain levels were relatively high (her VAS score at the time was 6).
On the 5th postoperative day, the patient complained of a cough and mild chest discomfort, which was increased by deep inspiration on the left side. However, she was afebrile and her vital signs were normal. Chest radiography performed at the time revealed a small left-sided pleural effusion (). Thoracentesis was not indicated emergently, and she was managed conservatively.
On the 9th postoperative day, her symptoms were relieved and chest radiography showed complete resolution of the effusion with minimal pleural thickening on the left side (). She was discharged on the 14th post-operative day in a stable condition.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [48.0, 'kg'], 'height': [150.0, 'cm']}",21.33333,20.26666,22.4,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 150.0 cm, which is 150.0 cm * 1 m / 100 cm = 1.5 m. The patient's weight is 48.0 kg. The patient's bmi is therefore 48.0 kg / (1.5 m * 1.5 m) = 21.33333 kg/m^2."
2242,6,Body Mass Index (BMI),physical,decimal,pmc-6454623-1,Extracted,"A 6-year-old boy was born of the second pregnancy and first childbirth to healthy nonconsanguineous parents. The first pregnancy ended in an early miscarriage. Family history is not burdened.
Pregnancy was with threatened spontaneous interruption. He was delivered by scheduled Cesarean section due to high myopia. His birth weight was 3650 g and height was 52 cm. Apgar scores were 8 and 9 at 1 and 5 min respectively. He was noted to have hypotonia at birth.
His motor milestones were delayed: held head by 7 months, rolled from back to side at 8 months, put into sitting position by 24 months, walked with support at 2,5 years and walked independently at 4 years. His speech development was delayed: at the age of 6 years he had no words.
At 8 month he was hospitalized to Scientific and Practical Centre of Pediatric psychoneurology. Brain computed tomography revealed signs of leukodystrophy and cortical atrophy of frontal, parietal and temporal areas. Radiological studies (neuroimaging) have never been performed until the age of 8 months.
At 13 months he was admitted to the National Medical Research Centre for Children’s Health and was monitored for the next 5 years.
At admission in 13 months brain MRI revealed signs of leukodystrophy, lissencephaly of left occipital lobe, polymicrogyria of both frontal lobes, secondary ventriculomegaly, brain atrophic changes with enlargement of sub-arachnoid spaces. Biochemical analysis showed creatine kinase (CK) level to be elevated to 2024 U/L (normal range 25–140 U/L), alanine aminotransferase (ALT) to 59 U/L (upper limit of normal 40 U/L), aspartate aminotransferase (AST) to 82 U/L (upper limit of normal 42 U/L) and lactate dehydrogenase (LDH) level to 318 U/L (upper limit of normal 225 U/L). On electromyographic examination, signs of primary muscle lesion have been identified.
At admission in 6 years weight was 21 kg, height was 113 cm, head circumference was 53 cm. Convergent strabismus, insufficiency of convergence and accommodation were noted. He had hypotonia, distal more than proximal. Trunk ataxia, walking on his toes with an atactic component, flat valgus foot were noted. Patient reacted favorably to examination. He can maintain short-term eye contact; speech is misunderstood. The face is hypomimic. In active speech there are long vocalized sounds, rarely - simple babbling syllables, no words. Behavioral features are manifested by periodic fading with subsequent rapidity of breathing and stereotyped swings of hands (Fig. ).
Orthopedic examination revealed thoracic hypokyphosis, lumbar hyperlordosis, double-sided coxa valga, pathological antetorsion on the right, equinox flat valgus feet. Limb movements were not restricted except for restriction of back flexion in the ankles.
Ophthalmological examination revealed congenital high myopia, partial atrophy of an optic nerve and retinal atrophy in both eyes.
MRI revealed hypoplasia of temporal lobes and opercular areas from two sides, hypoplasia of caudal parts of the cerebellum worm with the expansion of external subarachnoid spaces of the cerebral hemispheres (more in the temporal areas), expansion of retrocerebellar cistern, symmetrical expansion of the ventricular system, pachygyria-polymicrogyria of cerebral hemispheres with preservation of the occipital lobe. Increased intensity of MR signal was observed in T2 and T2 FLAIR images. Decreased intensity of MR signal was observed in T1 image. In the cerebellum multiple small cysts, hypoplasia of the corpus callosum and pons with the extension of the anterior and covering cisterns are revealed (Fig. ).
Biochemical analysis showed CK level to be elevated to 2253 U/L (normal range 25–194 U/L), ALT to 70,4 U/L (upper limit of normal 40 U/L), AST to 62 U/L (upper limit of normal 42 U/L) and LDH level to 503 U/L (upper limit of normal 314 U/L). Other blood and urine indicators were within normal limits. Patient level of CK was increased 10–15 times and for two years decreased from 3126 (3 years 4 months) to 1986 (at 5 years 2 months). The level of CK-MB was also increased - 61.1 (upper limit of normal 25 U/L).
On electroneuromyographic examination (ENMG), signs of primary muscle lesion have been identified. Motor unit potentials (MUP) were short in duration and low in amplitude. The number of polyphasic MUP has increased. Spontaneous activity in each test muscle was determined.
Electroencephalography (EEG) did not reveal epileptiform activity.
The electrocardiogram (ECG) showed a vertical position of the electrical heart axis, mild bradycardia and arrhythmia, nonspecific intraventricular block, early repolarization syndrome of the ventricles.
A standard karyotype was normal 46, XY. Tandem mass spectrometry did not reveal any changes in the plasma level of amino acids and acylcarnitines.
Genotek Ltd. did clinical exome sequencing. Genomic DNA from peripheral blood sample was extracted using QIAamp DNA Mini Kit (Qiagen) according to manufacturerʼs protocol. DNA libraries were prepared using NEBNext Ultra DNA Library Prep Kit for Illumina (New England Biolabs) with adapters for sequencing on Illumina platform according to manufacturer’s protocol. We used SureSelect XT2 (Agilent Technologies) for target enrichment. Enriched samples were sequenced on Illumina HiSeq 2500 using pair-end 100 base pairs reads. After sequencing, we trimmed 3′-nucleotides with read quality below 10 using Cutadapt []. Raw reads were aligned to reference genome hg19 (GRCh37.p13) using BWA MEM []. Deduplication of reads was done using SAMtools rmdup []. FastQS was used for data quality control []. We called short variants using GATK HaplotypeCaller [] according to GATK Best Practices DNA-seq [, ]. The effect of each mutation was assessed using snpEff []. To assess pathogenicity and conservatism, the data was extracted from the dbNSFP [], Clinvar [, ], OMIM database [] and HGMD [], as well as using the SIFT [] and PolyPhen-2 [, ] utilities to predict pathogenicity of the mutation. Information on frequency of mutations was taken from 1000Genomes project [, ], ExAC [, ] and Genotek frequency data. Pathogenicity was predicted according to the Standards and Guidelines developed by ACMG (American College of Medical Genetics and Genomics), AMP (Association for Molecular Pathology) and CAP (College of American Pathologists) []. Copy number alterations were determined using CNVkit [].
Sanger sequencing confirmed POMGNT1 pathogenic variants identified by exome sequencing. For labeling amplicons with fluorescent labels, BigDye Terminator Cycle Sequencing Kit v3.1 (Thermo Fisher Scientific) was used. Sanger sequencing was performed on ABI PRISM 3500 Genetic Analyzer (Applied Biosystems) according to manufacturerʼs protocol.
After exome sequencing, patient was commenced on muscle relaxants and anticonvulsants. His condition is stable.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [21.0, 'kg'], 'height': [113.0, 'cm']}",16.44608,15.62378,17.26838,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 113.0 cm, which is 113.0 cm * 1 m / 100 cm = 1.13 m. The patient's weight is 21.0 kg. The patient's bmi is therefore 21.0 kg / (1.13 m * 1.13 m) = 16.44608 kg/m^2."
2243,6,Body Mass Index (BMI),physical,decimal,pmc-8107250-1,Extracted,"The patient provided written informed consent for the publication of his information.
A 60-year-old man diagnosed with esophageal adenoma (high-grade dysplasia) was scheduled for ESD under general anesthesia. He was 169.9 cm tall and weighed 69.2 kg. He had underlying hypertension, with normal preoperative laboratory and chest radiography findings. He had no history of pulmonary disease.
As premedication, 0.2 mg mobinul and 2 mg midazolam were administered intramuscularly. His initial vital signs before anesthesia were as follows: blood pressure (BP), 170/100 mmHg; heart rate, 100 beats/min; and peripheral oxygen saturation (SpO2), 99%. As induction agents, 150 mg propofol, 50 mg rocuronium bromide, and 50 µg fentanyl were administered. Mask ventilation was provided for 3 min with 8 L/min oxygen for preoxygenation, and intubation was performed with an 8.0-mm endotracheal tube. Anesthesia was maintained with 6 vol% desflurane, 1.5 L/min N2O, and 1.5 L/min O2. Mechanical ventilation was set at pressure control and volume guarantee mode with a tidal volume of 600 ml and a respiratory rate of 12 beats per min. During the procedure, the patient was placed in the left lateral decubitus position, and his peak inspiratory airway pressure (PIP) was maintained at 25 cmH2O.
The patient’s PIP suddenly increased to 35 cmH2O 30 min after the operation. His vital signs were as follows: BP, 160/110 mmHg; heart rate, 80 beats/min; SpO2, 100%; and end-tidal carbon dioxide, 27 mmHg. To decrease the PIP, the tidal volume setting was reduced to 500 ml from 600 ml; however, the PIP increased to 40 cmH2O within seconds. The endotracheal tube was confirmed to be intact but extensive subcutaneous emphysema was observed around the neck and chest areas. N2O was stopped and 8 L/min O2 was supplied using a fraction of inspired oxygen (FiO2) of 1.0. The operator suspected a mid-esophageal perforation. Within a few minutes, the patient’s actual tidal volume had decreased to < 100 ml.
The surgeon stopped the procedure and repositioned the patient in the supine position from the lateral decubitus position. Breathing sounds were barely heard in both lungs during manual ventilation. Portable chest X-ray (CXR) and arterial blood gas analysis showed the following: pH, 7.22; PaCO2, 61 mmHg; PaO2, 86 mmHg; HCO3-, 25.0 mmol/L; and SaO2, 94% for a FiO2 of 1.0. While waiting for the CXR to be uploaded (approximately 10–20 min in our center), the patient’s lung was scanned using ultrasound (Sonosite Edge, FUJIFILM Sonosite Inc., USA) with a multi-frequency linear array transducer probe (HFL38x, 13–6 MHz, 6 cm, FUJIFILM Sonosite Inc.). The lung sliding sign (to-and-fro movement of the pleural line) was not observed in the B-mode and parallel lines, termed barcode or stratosphere sign, were identified in the M-mode at the right third intercostal space and mid-clavicular line, indicating a suspected pneumothorax (). Additionally, lung pulse and B-lines were absent and real images, such as consolidation or effusion, were not present in the sonographic evaluation. Despite the presence of broad subcutaneous emphysema, the emphysema depth did not significantly hinder identification on the sonographic image. However, the lung point was not clearly identified with the probe sliding laterally and inferiorly.
Even with a FiO2 of 1.0 before ultrasound scanning, the patient’s SpO2 decreased and facial cyanosis was apparent. Within minutes, his SpO2 decreased to 52%, and his systolic BP decreased to 70 mmHg. Immediately after this vital sign instability, an 18-gauge needle was inserted into the right second intercostal space at the mid-clavicular line for needle thoracostomy, and an emergency doctor was called for chest tube insertion. Immediately after needle thoracostomy, the patient’s SpO2 and systolic BP increased to 96% and 100 mmHg, respectively. The CXR was uploaded after needle thoracostomy and the diagnosis of bilateral (right-dominant) tension pneumothorax was confirmed (). After chest tube insertion on the right side by the emergency doctor, the patient’s vital signs stabilized within minutes. As the patient was stabilized, the medical providers decided to transfer the patient promptly to the intensive care unit for further evaluation and management. Using the endotracheal tube, the patient was ventilated with an Ambu bag with oxygen supply during transfer. However, while being transported to the intensive care unit, his SpO2 and systolic BP decreased to 89% and 80 mmHg, respectively. A left chest tube was inserted while the patient was in the intensive care unit, and his vital signs recovered soon after. Three days later, video-assisted thoracoscopic esophagectomy and esophagogastrostomy were performed. After a successful operation, the patient was discharged without further complications.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [69.2, 'kg'], 'height': [169.9, 'cm']}",23.97283,22.77419,25.17147,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 169.9 cm, which is 169.9 cm * 1 m / 100 cm = 1.699 m. The patient's weight is 69.2 kg. The patient's bmi is therefore 69.2 kg / (1.699 m * 1.699 m) = 23.97283 kg/m^2."
2244,6,Body Mass Index (BMI),physical,decimal,pmc-3995150-1,Extracted,"The patient was a 75-year-old man. He had undergone surgery for a left inguinal hernia 23 years earlier, but the details were unknown.
Four years earlier, the left inguinal hernia recurred and underwent repeated prolapse, spontaneous rectification, and self-reduction. Since last year, the hernia occasionally became incarcerated. On each occasion, the patient was treated by manual reduction as an outpatient, but he did not wish to undergo surgery, and the situation continued as it was. Over the previous month, the hernia frequently became incarcerated, and the patient visited our hospital as usual for manual reduction of the incarceration. This time the patient agreed to surgery and was admitted and treated surgically on the same day. Physical findings were as follows: height 170 cm, weight 70 kg, and temperature 36.6°C. The left lower abdomen was slightly tender, but there were no symptoms of peritoneal irritation such as rebound tenderness or guarding. After hernial reduction, neither inguinal region had any palpable swelling, and chest findings were normal.
Blood test findings were WBC 8600/μL, Hb 10.4 g/dL, and CRP 0.19 mg/dL, indicating mild anemia and no inflammatory response. Abdominal X-ray on admission showed a dilated small bowel and niveau formation, indicating bowel obstruction. Pelvic CT revealed that the hernia had prolapsed into the left scrotum and the small bowel was dilated. There was no ascites.
The first operation used the anterior approach. When the tissue that adhered around the spermatic cord was peeled back, a direct hernia was seen protruding from directly above the pubic bone into the scrotum (). The sac was partially released and investigated as far as possible into the abdominal cavity, but the operation was completed by radical surgery using a Mesh Plug (DAVOL Inc., Warwick, RI) without it being possible to confirm necrosis of the small bowel.
Although the patient's postoperative clinical course included bowel movements and expulsion of flatus, abdominal CT was done because of fluid drainage from the nasogastric tube and persistence of gas in the small bowel on X-ray. The small bowel was less dilated than at admission, but a portion of it appeared to be tumor-like inside the pelvic cavity (). This was thought to be the result of repeated hernial incarcerations over many years that had led the small bowel to adhere globosely. An ileus tube was inserted on the 8th day of admission. Subsequent drainage was <300 mL/day, and there were bowel movements and expulsion of flatus. The ileus tube was removed on the 13th day of admission because ileus tube imaging showed transfer of contrast agent to the colon after 1 hour (). From the 14th day of admission, the patient resumed eating and was able to consume an entire meal, and his clinical course was problem-free, but when the diet was increased to 7 : 1 rice gruel on the 20th day of admission, he developed sudden abdominal pain, fever, and symptoms of peritoneal irritation over the whole abdomen. Abdominal CT detected free air, and emergency abdominal surgery was performed (2nd operation) based on a diagnosis of peritonitis due to gastrointestinal perforation.
The lower abdomen was opened by midline incision, revealing the abdominal cavity to be contaminated with intestinal fluids. Tracing the dilated small bowel, thickened peritoneum in the vicinity of the left internal inguinal ring was found to be protruding into the abdominal cavity, and the small bowel was pinched at the same site and perforated on the dilated oral side directly before entering the hernial sac (Figures and ). It was thought that reduction en masse of the incarcerated hernia had taken place during reduction, causing perforation of the small bowel. There was no necrosis of the incarcerated small bowel. The perforated portion of the small bowel was resected, and the internal inguinal ring was closed by suture from the abdominal cavity. There were no notable postoperative complications, and on the 6th day of admission after the 2nd operation, the patient resumed eating and was discharged.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [170.0, 'cm']}",24.22145,23.01038,25.43252,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.7 m * 1.7 m) = 24.22145 kg/m^2."
2245,6,Body Mass Index (BMI),physical,decimal,pmc-5635189-1,Extracted,"A 30-year-old female presented to our hospital with trivial injury to her right thigh, following which she had pain over right thigh and unable to weight bear on the involved lower limb. Other associated injuries were ruled out at the time of admission in the emergency room. Physical examination revealed swelling, tenderness, and deformity over the middle-third of her right thigh region without neurovascular deficit. Patient was stabilized initially in our emergency department, and radiograph of right femur showed displaced transverse fracture in the femoral shaft (). The other radiographic findings were diffuse osteosclerosis and narrow medullary canal. The patient gave a history of earlier episodes of fracture for which conservative treatment in form of native splinting had been done. Thus, a diagnosis of pathological fracture was made. On general examination, the patient had short stature and dysmorphic facies with radiological signs of generalized osteosclerosis and narrow medullary canal. A detailed history, clinical, and radiological examination was carried out. She was second child of four siblings. The first child died days after delivery, of unknown cause, and other two younger siblings had similar clinical features ().
Parents had a first-degree consanguinity. The antenatal history was not significant. Milestone and intelligence attainted appropriate for age. There was a history of frequent episodes of upper respiratory tract infection, snoring during sleep since childhood. The patient also gave a history of hard of hearing on the right side. The patient went through regular general medical checkups, and there was no significant treatment history.
On general physical examination, weight of patient was 63 kg; her standing height was 126 cm; her upper segment and lower segment length were 64 and 62 cm, chest expansion of 3 cm, respectively, with a head circumference of 49 cm. Other clinical features include dysmorphic facies, frontal and parietal bossing, beaked nose, midfacial hypoplasia, short hands and feet with dysplastic nail (), grooved palate (), dental caries, impacted and malposed tooth, and sandal gap deformity of the foot (). Radiograph of the skull was found to be widely open anterior and posterior fontanelle, with obtuse mandibular angle and separated cranial sutures (). Radiograph of the hand showed aplastic terminal phalanges with acroosteolysis. Abovementioned clinical and radiographic findings suggested pyknodysostosis as the most likely diagnosis. The patient was taken up for surgery within a week from injury. An intramedullary interlocking nailing was contemplated initially for fracture fixation.
However, for this case, we preferred plate osteosynthesis because of the altered anatomy of the bone with a narrow medullary canal and severe osteosclerosis. Under Spinal anaesthesia, through lateral approach to the middle third of femur, a 12 cm incision was made. After deep dissection, fracture site was identified and exposed. After reducing fractures fragments an “8 holed broad dynamic compression plate with 3 proximal and 3 distal screws in compression mode was used for fracture fixation ().”
The difficulty encountered in the intra-operative period include, a difficulty in drilling the cortices and excess blood loss. The wound was closed in layers after adequate hemostasis. The immediate post-operative period was uneventful, and the patient discharged on the 14th post-operative day. The patient was discharged with advice of non-weight bearing walking with the help of walker support for minimum of 2 months and advised to review in the out-patient department for follow up every fortnight. At 10-week post-operative, after patient has been started on partial weight bearing walking, the patient reported with the complaints of pain over surgical site. On radiological examination, patient was found to have no signs of union at the fracture. Patient was immobilized for one month, but even after that, there were no signs of union. Hence, an additional stabilization procedure was done in the form of plating with autogenous cancellous bone grafting. Bone graft harvested from ipsilateral iliac crest was inadequate, and there was heavy bleeding from donor site so that an additional synthetic bone graft substitute was used. In the immediate post-operative period, patient developed deep seated infection which showed organism grown was staphylococcus aureus for which wound debridement was done. Patient was started on Intravenous antibiotics of Linezolid 600 mg twice a day after obtaining culture and sentivity report for period of 2 weeks, followed by oral antibiotics for 4 weeks. Patient was discharged 4 weeks later after complete subsidence of infection. Patient was advised physiotherapy in form of static and dynamic Quadriceps strengthening exercises, followed by hip and knee mobilization exercises and strict non weight bearing for 2 months.. At 3-month post-operative follow-up, there were signs of union clinically and radiologically ( and ). The patient at present in the 6-month post-operative period with fracture united and on full weight bearing carrying out her daily activities without difficulty ().",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [63.0, 'kg'], 'height': [126.0, 'cm']}",39.68254,37.69841,41.66667,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 126.0 cm, which is 126.0 cm * 1 m / 100 cm = 1.26 m. The patient's weight is 63.0 kg. The patient's bmi is therefore 63.0 kg / (1.26 m * 1.26 m) = 39.68254 kg/m^2."
2246,6,Body Mass Index (BMI),physical,decimal,pmc-7542499-1,Extracted,"The patient is a 32-year-old Caucasian female, of height 166 cm and weight 50 kg, with uneventful early development who became noteworthy at age 7 y because of poor school performance due to impaired memory and concentration. She had nocturnal enuresis until age 14 y and menarche at age 13 y with normal periods thereafter. At age 17 y, recurrent, spontaneous myocloni of all four limbs began. A first generalised tonic-clonic seizure occurred at age 19 y. The postictal period was characterised by severe muscle weakness and muscle aching during 24 h. Electroencephalography (EEG) recording revealed epileptiform discharges in the frontocentral regions under hyperventilation and a decreased photoparoxysmal threshold. Valproic acid (VPA) was begun.
Despite VPA, seizures recurred with a frequency of 1-2 seizures/month. In addition to generalised seizures, she rarely experienced focal seizures (). Seizures could be triggered by flickering light or by looking at small stones, leaves, or dirty snow on the ground. Walking safely for 1 km with one stop was possible only after sunset. Nerve conduction studies revealed a mixed axonal/demyelinating neuropathy. Electromyography was myogenic. MRI of the brain at ages 19 y, 21 y, and 28 y revealed cerebellar atrophy exclusively. At age 20 y, VPA was replaced by levetiracetam (LEV) 3000 mg/d. Genetic work-up at age 21 y revealed the variant m.8344A > G with a heteroplasmy rate of 50% in blood lymphocytes. EEG at age 24 y revealed bilaterally synchronous spike-wave complexes in the occipital area. Flickering light triggered generalised, bilaterally synchronous spike-wave and polyspike-wave complexes (). The patient had been married between ages 19 y and 25 y but never became pregnant. Work-up for infertility at age 20 y revealed a PCOS for which she received desogestrel (150 μg/d) + estradiol (20 μg/d) twice a year for three months since age 26 y. Since age 27 y, ataxic gait worsened such that she required support from another person for walking. Elevated serum lactate levels up to double the upper reference limits were noted for the first time. At age 27 y, topiramate (TPM) was added. Seizures had not recurred during 42 months prior to the last follow-up at age 32 y ().
The family history was positive for easy fatigability (mother (48 yo), brother (26 yo), great aunt from mother's side), photosensitivity (mother, grandmother from mother's side, 2 great aunts from mother's side, 2 aunts and 1 uncle from mother's side), hand tremor (brother), myocloni (grandmother from mother's side, 2 aunts, 1 uncle, 2 cousins from the mother's side), seizures (1 great aunt from the mother's side, 1 cousin), Parkinsonism (1 great aunt from the mother's side, 1 uncle), ataxia (2 great aunts from the mother's side), and hypothyroidism (mother) (). The mother felt unpleasant with flickering light and when looking at many stones, leaves, or dirty snow on the ground. Both mother and brother of the index patient carried the m.8344A > G variant, the mother had a heteroplasmy rate of 40% and the brother was homoplasmic. Clinical neurologic exam of the index patient at age 32 y revealed cognitive impairment, ataxia, photosensitivity, dysarthria, uncoordinated speech, myocloni of upper limbs, generalised wasting, absent tendon reflexes, and gait disturbance. The current medication included LEV (4000 mg/d), clonazepam (CLZ) (1.5 mg/d), TPM (25 mg/d), coenzyme-Q (200 mg/d), L-carnitine (2 g/d), and vitamin-E (400 mg/d).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [50.0, 'kg'], 'height': [166.0, 'cm']}",18.14487,17.23763,19.05211,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 50.0 kg. The patient's bmi is therefore 50.0 kg / (1.66 m * 1.66 m) = 18.14487 kg/m^2."
2247,6,Body Mass Index (BMI),physical,decimal,pmc-7756316-1,Extracted,"Patient IV-1 is a 14-year-old male Saudi patient. He was born to consanguineous healthy parents after an unremarkable pregnancy course at full term by cesarean section due to fetal distress. His birth weight was 5 kg (>95th percentile) and the APGAR score was 9 and 9 at 1 and 5 min, respectively. After delivery, the patient was discharged immediately from the hospital.
The patient performed well with normal development until the age of 3, when he started to show speech delay and poor concentration. The patient (IV-1) developed a febrile seizure at the age of 3.5 during febrile illness, with a body temperature reaching 40°C. The duration of the seizure was short and did not require antiepileptic medication. He started to speak for the first time at the age of 4. Later, at the age of 5, he developed anxiety in the form of separation anxiety and poor sleeping at night. At the age of 10, he started to develop repetitive tics, in the form of repeated blinking, head nodding, eye-rolling (nystagmus), and jaw tics. His intelligence quotient (IQ) assessment revealed a borderline score of 69.
He was referred to the genetic service at the age of 10 for genetic evaluation. At the age of 10, he started to write his name and was enrolled in a special needs school, with an average academic performance. Currently, the patient has normal gross motor development, with speech delay, since he can speak in sentences but incomprehensively. The patient (IV-1) has a major deficiency in memory and mathematical abilities.
On examination, he was vitally stable with the following growth parameters: height, 163 cm (50th percentile); weight, 41.2 kg (10th percentile); and head circumference, 56 cm (50th percentile). The patient had subtle dysmorphic features, including a triangular face, broad forehead, plagiocephaly, mild synophrys, and tooth crowding (Figure ). Other systemic examinations were unremarkable, except for mild hirsutism.
All the basic metabolic investigations were unremarkable. The karyotype, comparative genomic hybridization (CGH) array, and screening for fragile X were unremarkable. Radiological investigations, including brain MRI and skeletal surveys, were also unremarkable.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [41.2, 'kg'], 'height': [163.0, 'cm']}",15.50679,14.73145,16.28213,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 41.2 kg. The patient's bmi is therefore 41.2 kg / (1.63 m * 1.63 m) = 15.50679 kg/m^2."
2248,6,Body Mass Index (BMI),physical,decimal,pmc-4041959-1,Extracted,"A 31-year-old female patient with a height of 164 cm and weight of 60 kg was admitted to undergo ethanol sclerotherapy for a large painful vascular malformation in her left leg. Magnetic resonance imaging revealed an AVM measuring 28 × 7 × 4 cm in her left calf (). All preoperative examinations, including laboratory tests, electrocardiography, and chest X-ray, were normal. Vital signs before general anesthesia were stable: her blood pressure was 130/80 mmHg and her heart rate was 82 beats/min. Following the application of routine hemodynamic monitoring (3-lead electrocardiogram, noninvasive blood pressure, and pulse oximetry), anesthesia was induced using a bolus intravenous injection of 120 mg propofol and 40 mg rocuronium. A 20-gauge catheter was inserted into the radial artery to monitor her arterial blood pressure continuously. The target controlled infusion of 2% propofol and remifentanil (2-3 µg/ml and 2-5 ng/ml of the effect-site concentrations, respectively) was applied to maintain anesthesia. Immediately following the injection of ethanol, the patient's blood pressure and heart rate rose slightly to 160/100 mmHg and 100 beats/min, respectively. Thereafter, the patient's blood pressure and heart rate were stable throughout the procedure while she was in the prone position. A total dose of 50 ml of 99% ethanol was injected into the lesion over a period of 30 minutes without the use of a tourniquet. As soon as the patient was turned from prone to supine after finishing the procedure, an abrupt drop in her arterial blood pressure occurred, 40-50 mmHg systolic and 10-15 mmHg diastolic blood pressure with a simultaneous increase in her heart rate to 100-110 beats/min. To restore blood pressure, 20 mg of ephedrine was immediately injected, but the patient's heart rate rather decreased abruptly to < 30 beats/min. Chest compressions were performed along with the simultaneous injection of 50 µg of epinephrine. A few minutes later, the patient's blood pressure and heart rate recovered to 180/100 mmHg and 100-110 beats/min. At that moment, the arterial blood gas analysis showed metabolic acidosis with otherwise normal findings (pH 7.29, PaCO2 28 mmHg, PaO2 466 mmHg, SaO2 100%, base excess -11.6, Hematocrit 38%, Na+ 137 mEq/l, K+ 3.7 mEq/l, and Ca2+ 1.11 mmol/l). The patient was transferred to the intensive care unit with the endotracheal tube in place. Transthoracic echocardiograph (TTE) and embolism computed tomography (CT) were performed to confirm pulmonary hypertension or pulmonary embolism. There was no evidence of pulmonary embolism on CT. In addition, the peak tricuspid regurgitation jet velocity on TTE was 2.3 m/s, indicating no evidence of pulmonary hypertension at that moment (). However, TTE revealed dilated right ventricle () and severely decreased right ventricular function.
On postoperative day 1, the patient regained her consciousness and was discharged five days after the operation without any complications.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.0, 'kg'], 'height': [164.0, 'cm']}",22.30815,21.19274,23.42356,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 164.0 cm, which is 164.0 cm * 1 m / 100 cm = 1.64 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.64 m * 1.64 m) = 22.30815 kg/m^2."
2249,6,Body Mass Index (BMI),physical,decimal,pmc-4121498-1,Extracted,"A 73-year-old female patient was diagnosed with spinal stenosis on L1-L5, and it was decided to perform posterior lumbar spinal fusion. The patient had height of 154 cm and weight of 72 kg. Except for hypertension, no other specific medical history was known. Prior to surgery, there were no abnormal findings in the complete blood count, and electrolyte and blood coagulation tests.
Before anesthetic induction, the patient's blood pressure was 150/70 mmHg, heart rate was 82 beats/min, and oxygen saturation was 98%. Anesthetic induction was conducted with injection of propofol 120 mg and rocuronium 50 mg, followed by endotracheal intubation. General anesthesia was maintained through sevoflurane (1-1.5 %)-O2(2 L/min)-N2O (2 L/min). For direct measurement of the arterial pressure, right radial artery cannulation was performed. It was planned that the patient would be managed in the intensive care unit for a few days after the surgery, and at the request of the orthopedic surgeon, a subclavian venous catheter, which is comparatively convenient for long term maintenance, was to be inserted. Due to a skin lesion in the right subclavian area, central venous catheter insertion was conducted in the left subclavian vein with a two-lumen CVC set (Arrow International, Inc., Reading, PA, USA). The catheter was fixed at a depth of 15 cm while the intravenous supply after blood regurgitation was confirmed. Afterwards, the patient was turned into the prone position on the Wilson frame (OSI, Union City, CA, USA) for the surgery (). After changing the position, the upper chest area from above the nipples and including the subclavian area showed overall compression. In order to prevent pressure by compression, a surgical cotton pad was applied to the applicable area, and free flow of fluid through the CVC was checked before commencing the operation. During the whole operating time of 4 hours and 45 minutes, the mean arterial blood pressure and the heart rate were maintained at 65-75 mmHg and 60-75 beats/min, respectively, showing stable vital signs. Total fluid input during the surgery amounted to 1,200 ml of normal saline, 500 ml of colloid, 5 units of packed red blood cell and 3 units of fresh frozen plasma, and the actual blood loss amounted to 1,500 ml and the urine output was 850 ml. After the operation, the patient was transferred to the intensive care unit. The patient was mentally alert, with a blood pressure of 130/80 mmHg and heart rate of 61 beats/min. In the blood coagulation test carried out immediately after the operation, the prothrombin time (INR) was measured at 1.13 and activated partial thromboplastin time was 42.3 seconds.
On the next day, there was a sudden occurrence of severe edema in the patient's left arm, and the fingertips of her left hand felt cold. The CVC was removed from the patient immediately. A blood test conducted on the day of the symptom showed that D-dimer had increased above 20 g/ml, which led to the suspicion of deep vein thrombosis. To suppress the swelling, the patient's left arm was wrapped with a pressure bandage, and ultrasonography and computed tomography scan were performed on the patient. On ultrasonography, extensive deep vein thrombosis was observed in the left subclavian vein and caudal branch () while on computed tomography, thrombosis was found in the left brachiocephalic vein and subclavian vein (). Immediately, thrombolysis was conducted in the upper left arm through a venogram (). Over the next 3 days after the thrombolysis, anticoagulation therapy was carried out by concurrently administering heparin 500 IU/h and urokinase 100,000 IU/h, and over the next 6 days, urokinase was stopped and only heparin was administered. The patient showed no more particular complications, and was discharged from the hospital 2 weeks after the treatment.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [72.0, 'kg'], 'height': [154.0, 'cm']}",30.35925,28.84129,31.87721,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 154.0 cm, which is 154.0 cm * 1 m / 100 cm = 1.54 m. The patient's weight is 72.0 kg. The patient's bmi is therefore 72.0 kg / (1.54 m * 1.54 m) = 30.35925 kg/m^2."
2250,6,Body Mass Index (BMI),physical,decimal,pmc-6940134-1,Extracted,"A 38-year-old man, 166 cm in height and 62 kg in weight, with type I neurofibromatosis presented with pain associated with a large mass in the upper back region. He reported that the mass had been growing gradually since being excised 8 years prior. One day before the current admission, pain had begun to emanate from the mass, which had gradually increased to 7 cm in diameter. Its visible diameter on the surface reportedly kept increasing, and it was 15 cm at the time of the current admission. Preoperative enhanced chest computed tomography revealed a huge mass of 28 cm in width and 8 cm in height (Fig. ).
On physical examination, the mass was hard and exhibited heat and tenderness on palpation. Pain from the mass prevented the patient from lying supine, but neck motion was not restricted. Complete blood cell count on admission revealed hemoglobin 13.0 g/dL, platelet count 255,000/μL, and leukocyte count 11,500/μL. These parameters had abruptly changed to hemoglobin 6.6 g/dL, platelet count 135,000/μL, and leukocyte count 16,700/μL by 21 hours after admission, and his respective systole, diastole, and heart rate had changed from 120/70 mmHg and 78 beats/min to 130/80 mmHg and 160 beats/min. Due to suspected active bleeding from the mass, emergent evacuation of the hematoma was planned.
The patient was admitted to the operating theater in right LDP. A pad was placed beside the right side of his head to maintain it in a neutral position. Electrocardiography and pulse oximetry were continuously monitored. The right radial artery was catheterized under ultrasound guidance for continuous monitoring of arterial blood pressure and frequent arterial blood sampling. During catheterization, the patient was preoxygenated with 100% oxygen, and a non-inflatable LMA (size 4 i-gelTM, Intersurgical Ltd., Wokingham, Berkshire, UK) was prepared by lubricating the back, side, and front of the cuff with its orifice spared.
Anesthesia was then induced via 70 mg ketamine and 3 mg midazolam. In conjunction with the loss of consciousness 70 mg rocuronium was administered to facilitate the insertion of the prepared LMA, and the patient was manually ventilated via a mask. After the train of four count became 0, the LMA was inserted into the laryngopharynx. During its insertion an assistant placed the patient's head in the sniffing position with the head extended and the neck flexed. The anesthesiologist gently introduced the LMA downwards and backwards along the hard palate until resistance against insertion was encountered (Fig. ). After the LMA was inserted the patient was manually ventilated to confirm appropriate placement of the LMA based on detection of end-tidal carbon dioxide from the exhaled gas via capnography. The position of the LMA was secured by taping its integral bite block to the facial skin. The lungs were mechanically ventilated with 50% oxygen. The tidal volume and respiratory rate were adjusted to maintain an end-tidal carbon dioxide concentration between 35 and 40 mmHg and a peak airway pressure below 20 cm H2O. Anesthesia was maintained with sevoflurane to maintain state entropy values between 40 and 60.
At the conclusion of the LMA insertion the patient was placed in a supine position. Pads and pillows were placed behind the head and the body trunk below the mass in order that the mass not be compressed while he was in the supine position (Fig. ). After the LMA was removed from the mouth, the trachea was intubated with a 7.5-mm internal diameter cuffed reinforced endotracheal tube using a portable videolaryngoscope (UEscope, UE Medical Devices Inc., Newton, MA). The capnographic waveform confirmed the placement of the tube into the airway. Auscultation of breath sounds in both lungs ruled out endobronchial placement of the tube. Mechanical ventilation was maintained as described above. Under ultrasound guidance the right internal jugular vein was catheterized to administer blood products and fluids and to monitor central venous pressure continuously. The patient was then placed in a prone position with the head turned to the left (Fig. ).
The dependent eye was protected from external compression. Arms were not abducted greater than 90°. Every pressure point was padded. Endotracheal tube positioning, adequate ventilation, and patency of the arterial and venous lines were reassessed after instigation of the prone position. The surgery took 100 minutes. During the surgery the patient received 900 mL of packed red blood cells, 640 mL of fresh frozen plasma, 2890 mL of plasmalyte, and 50 mL of 6% hydroxyethyl starch 130/0.4 to compensate for blood loss. He was also administered 10 mg ephedrine, 20 μg norepinephrine, and 600 mg CaCl2. At the end of the surgery the patient could be placed in a supine position and the neuromuscular blockade maintained by a total of 100 mg rocuronium was reversed via 200 mg sugammadex.
After recovery of spontaneous breathing and consciousness, the endotracheal tube was withdrawn uneventfully. The patient was transferred to the surgical intensive care unit. On the first postoperative day, he was discharged to the general ward and was satisfied with the results of the surgery (Fig. ). The remnant mass was excised 1 month after the surgery, and at that time-point, the patient had experienced no complications related to the preceding above-described surgery. The patient has provided informed consent for the publication of this case report.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [62.0, 'kg'], 'height': [166.0, 'cm']}",22.49964,21.37466,23.62462,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 62.0 kg. The patient's bmi is therefore 62.0 kg / (1.66 m * 1.66 m) = 22.49964 kg/m^2."
2251,6,Body Mass Index (BMI),physical,decimal,pmc-6011332-1,Extracted,"The second patient is a 5-year old boy, born as a first child to healthy non-consanguineous parents. The mother reported two previous early spontaneous abortions. Otherwise, the family history is unremarkable. He was born after an uneventful pregnancy in the 37th week of gestation after a spontaneous start of the delivery. The boy’s birth weight was 2430 g (10-25P), birth length 46 cm (10-25P), and head circumference 34.5 cm (75-90P). He had gastroesophageal reflux in the first few months, the abdominal ultrasound was normal. Due to apnoic attacks the boy was administered to hospital at the age of 5 months. The pH-metry confirmed gastroesophageal reflux, ECG and CMCRF were normal. The neurologist described a mild hypertonus and related mild motor delay. He sat independently at 9 months of age and he started walking at 20 months of age. The parents noted shortness of breath and tiredness after simple physical tasks, therefore, he was evaluated by a paediatric cardiologist. Two haemodynamically significant ASDs were noted and a slightly dilated right ventricle; corrective surgery is planned. The tests of acylcarnitine profiles and aminoacids in blood and organic acid in urine were normal. At the age of four his height and weight were in the normal range (height 99.2 cm (17P), weight 16.1 kg (46P)), however, the head circumference showed macrocephaly - 53.8 cm (>97P).
Microarray analysis (180 K CGH array, Agilent Technologies- Fig. ) revealed a de novo microduplication of 2.06 Mb in chromosome 2p16.1p15 region (arr[GRCh37] 2p16.1p15(60308869_62368583)× 3 dn). No other pathogenic genomic imbalance was detected in the proband’s sample.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [16.1, 'kg'], 'height': [99.2, 'cm']}",16.36072,15.54268,17.17876,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 99.2 cm, which is 99.2 cm * 1 m / 100 cm = 0.992 m. The patient's weight is 16.1 kg. The patient's bmi is therefore 16.1 kg / (0.992 m * 0.992 m) = 16.36072 kg/m^2."
2252,6,Body Mass Index (BMI),physical,decimal,pmc-5424183-1,Extracted,"A 40-year-old woman (height, 160 cm; weight, 60 kg) with ocular myasthenia gravis was scheduled for robotic thymectomy. Computed tomography (CT) revealed a thymoma of 35 mm in diameter in the anterior mediastinum. Her trachea was not deviated and her left mainstem bronchus was 40 mm in length. Preoperative pulmonary function values were normal. Arterial oxygen tension (PaO2) and carbon dioxide tension (PaCO2) under room air were 70.4 mmHg and 45.1 mmHg, respectively. The rest of the preoperative examination was unremarkable.
General anesthesia was induced and the trachea was intubated with a 35-French left-sided DLT (Broncho-Cath®, COVIDIEN, Dublin, Ireland) under bronchofiberscopic guidance, confirming that the proximal bronchial cuff end was located about 5 mm distal from the carina. The DLT was fixed at a depth of 27 cm at the right angle of the mouth. Surgery was initiated in the supine position, and left one-lung ventilation (OLV) was started. CO2 insufflation to the right thorax was started at 5 mmHg and then increased to 10 mmHg. She was ventilated by pressure-controlled ventilation, volume-guaranteed mode (PCV-VG®, GE Healthcare, Little Chalfont, England) at a tidal volume (TV) of 450 mL, respiratory rate of 12 breaths/min, positive end-expiratory pressure (PEEP) of 5 cmH2O, and upper limit of peak inspiratory pressure (PIP) of 30 cmH2O, with 50% oxygen. The robot arms (da Vinci Surgical System SI®, Intuitive Surgical Inc., Sunnyvale, CA, USA) were then connected to the thoracic port, and robotic thymectomy was performed.
Three hours after starting surgery, the left mediastinal pleura was incised to divide adhesions between the tumor and the left lung, and CO2 was insufflated to the bilateral thoraxes at 10 mmHg. In the operative field, the left (dependent) lung contracted rapidly and its expansion was severely interrupted (). Although SpO2 was maintained at 98% with 50% oxygen, end-tidal CO2 (EtCO2) and PIP increased from 38 to 40 mmHg and 20 to 23 cmH2O, respectively (). Ten minutes after left pleural incision, TV decreased to 350 mL and PIP increased to 30 cmH2O of the upper limit while the surgeon was pulling the left lung and dividing the adhesion between the tumor and the left lung. We attempted to assess the DLT position by bronchofiberscopy from the tracheal lumen; however, the space between the end of the tracheal lumen and tracheal wall was so narrow that we could not find the carina and bronchial cuff. The patient's cart and robot arms of da Vinci located just above her head prevented the manipulation of bronchofiberscopy. Inspired oxygen was increased to 100% and manual ventilation was started. TV reached only 250 mL at 40 cmH2O PIP and EtCO2 increased to 60 mmHg. SpO2 simultaneously decreased to 90%. Bronchofiberscopy from the bronchial lumen was avoided because hypoxia had already occurred and interrupting ventilation was unavailable. The surgeon pointed out that only the left lower lobe was ventilated, although we could not find where the bronchial cuff was located by bronchofiberscopy. Finally, TV decreased to 150 mL at 40 cmH2O PIP, and SpO2 decreased to 80%.
At that point, CO2 insufflation was discontinued, and the robot was promptly disconnected. We immediately started double-lung ventilation. PIP decreased to 20 cmH2O and TV increased to 700 mL. The bronchofiberscopic view was improved and we found that the bronchial cuff was distally located. When we tried to readjust the position, the DLT was accidentally extubated, and then a single-lumen tube was used for intubation. We inserted a bronchial blocker (COOPDECH® endobronchial blocker, Daiken-iki, Osaka, Japan), and left OLV was resumed. The operation was restarted in thoracoscopic surgery and completed thereafter uneventfully without conversion. Operative time was 327 minutes and blood loss was less than 100 mL. She was extubated in the operating room and transferred to an intensive care unit (ICU). She was discharged from the ICU on postoperative day 1 and was discharged from the hospital on postoperative day 8 without complications.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.0, 'kg'], 'height': [160.0, 'cm']}",23.4375,22.26562,24.60938,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.6 m * 1.6 m) = 23.4375 kg/m^2."
2253,6,Body Mass Index (BMI),physical,decimal,pmc-7493228-1,Extracted,"The index case is a 10-year-old Mexican male with unrelated healthy parents. He is the first and only son. The parents came to the clinic searching for treatment of their son’s refractory epilepsy and insomnia. The patient was born by cesarean section at 38 weeks gestation. During the pregnancy, there was no intrauterine growth restriction; at birth, the patient’s weight was 3 200 g and his length was 52 cm, with an APGAR score of 9-9. Four hours after birth, the patient developed perioral cyanosis and was transferred to the intensive care unit with a probable diagnosis of neonatal sepsis. During his hospital stay, an echocardiogram reported patent ductus arteriosus that closed spontaneously. The newborn screening was reported as normal. He was discharged after 11 days.
Since the first days of life, the patient presented recurrent pulmonary infections associated with multiple hospital admissions, severe gastroesophageal reflux, and breast milk intolerance. At 6 months, he underwent a Nissen fundoplication and gastrostomy.
From the age of 7 months until now, the patient has presented atonic seizures and childhood spasms that are difficult to control. He initially responded well to valproic acid, but developed Fanconi syndrome as a secondary adverse event. He also had a good response to oxcarbazepine but developed severe hyponatremia, so both medications had to be withdrawn. Other prescribed medications included phenobarbital, phenytoin, atomoxetine, aripiprazole, quetiapine fumarate, haloperidol, sertraline, pregabalin, olanzapine, topiramate, levetiracetam, mirtazapine, and ethyl loflazepate, but these medications could not control the seizures either or led to adverse reactions such as irritability, insomnia, tremors, and hallucinations, among others. He is currently treated with lacosamide, clobazam, brivaracetam, and acetazolamide, which have decreased the number of seizures (5 events/month). He recently developed hypokalemia secondary to the use of acetazolamide but was successfully treated with potassium supplementation.
Since his first year of life, his weight, height, and head circumference have been below the third percentile. In addition, at 18 months of age, the patient was diagnosed with subclinical hypothyroidism and selective immunodeficiency of immunoglobulin (Ig)G and IgA, as well as nephrocalcinosis.
The primary dysmorphic features included microcephaly, elongated eyelid fissures with eversion of the outer third of the lower eyelid, arched and broad eyebrows, a depressed nasal tip with a short columella, small and spaced teeth, and micrognathia. He had large cup-shaped ears with low implantation, and bilateral retroauricular pits. Polydactyly of the right hand and left foot were present from birth and were treated surgically. He also had bilateral palmar aberrant folds (dermatoglyphics) and a sacral dimple. This clinical picture fulfilled the findings of a suspected diagnosis of Kabuki syndrome (OMIM 147920); however, sequencing the KMT2D gene—the most commonly associated—ruled out the diagnosis.
Since this diagnostic possibility was excluded, ES was performed. It was only carried out in the patient’s amplifying exome (>98% of the coding regions); mitochondrial DNA was sequenced with an Illumina platform. ES resulted in a homozygous variant in the OTUD6B gene, c.433C>T (p.Arg145*). This nonsense variation (rs368313959) has been described in Clinvar and Baylor Genetics as pathogenic, and other databases have reported an allelic frequency of 0.00014 (Genome Aggregation Database) and 0.00015 (Exome Sequencing Project). No other relevant findings were identified. According to the ACMG scoring guidelines, it appears to be a rare variant fulfilling PVS1, PM2, and PP5 criteria, which could be classified as pathogenic.
Currently, the patient weighs 24 kg (below p3) and measures 1.24 m (below p3). He has presented delayed overall development in terms of head support, sitting with support, and with no gait development, he only emits sounds, and obeys simple commands. He is receiving solid foods orally and liquids by gastrostomy. Furthermore, he is well controlled with levothyroxine and gamma globulin for the management of subclinical hypothyroidism and selective immunodeficiency, respectively. Recently, the patient was diagnosed with insulin resistance and allergic colitis. shows the patient’s current facial and hand features.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [24.0, 'kg'], 'height': [1.24, 'm']}",15.60874,14.8283,16.38918,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.24 m. The patient's weight is 24.0 kg. The patient's bmi is therefore 24.0 kg / (1.24 m * 1.24 m) = 15.60874 kg/m^2."
2254,6,Body Mass Index (BMI),physical,decimal,pmc-4886394-1,Extracted,"A 16-month-old female Caucasian child was admitted to our hospital for recurrent and postprandial vomiting episodes, which started at 11 months of age. A history of gastroesophageal reflux, unresponsive to drug therapy, was present until she was 1 year old, in association with recurrent respiratory infections. On physical examination, her weight was 9.97 kg (less than the fiftieth percentile) and height 82.5 cm (less than the ninety-fifth percentile). Her general condition at admission was good, with abdominal bloating in the absence of organomegaly. A routine basic metabolic panel was performed, along with general functional tests, complete blood count, and C-reactive protein test. All results were normal, in association with plasma amino acids, celiac serology, urinalysis, cytomegalovirus serology, stool test, and parasitological examination of stools. A neurological examination with electroencephalogram and fundus oculi was normal. A barium study showed stomach rotation along a horizontal plane of the stomach, with partial rotation of the greater curvature toward the diaphragmatic side; the stomach was markedly dilated with delayed gastric emptying (Fig. ). Esophagogastroduodenoscopy was negative for mucosal alterations. A diagnosis of chronic organoaxial GV was advanced with evidence of increasing difficulty in feeding. Due to the persistence of episodes of vomiting, in combination with progressive failure to thrive, gastropexy and Nissen fundoplication were performed. At the 6-month follow-up, the child demonstrated catch-up growth with regular calorie intake.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [9.97, 'kg'], 'height': [82.5, 'cm']}",14.6483,13.91588,15.38072,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 82.5 cm, which is 82.5 cm * 1 m / 100 cm = 0.825 m. The patient's weight is 9.97 kg. The patient's bmi is therefore 9.97 kg / (0.825 m * 0.825 m) = 14.6483 kg/m^2."
2255,6,Body Mass Index (BMI),physical,decimal,pmc-5347368-1,Extracted,"A 63-year-old man presented to Orthopaedics Outpatient Department (OPD), All India Institute of Medical Sciences, New Delhi with a history of pain in bilateral knees for 10 years. He had more pain on the left knee as compared to the right knee. He had developed a sudden onset foot drop in the left lower limb for the last four months.
His pain in the left knee was severe to an extent that he was not able to walk even up to one block. He had to use a walker for ambulation. His activities of daily living such as using a transport, climbing stairs, squatting and sitting cross legged were limited. He also gave a history of recurrent episodes of giving way in the left knee. He developed a localized swelling on the lateral aspect of left knee, which was insidious in onset and progressed gradually over a period of the last one year. He had no history of any trauma to the left knee. He did not have any back pain or any radiating pain in his left lower limb. He had a history of coronary artery disease in the past for which he received treatment in the form of an angioplasty with a cardiac stent.
On physical examination, the patient was 178 cm tall and weighed 74 kg. He walked with high steppage gait and had a varus thrust. The tibiofemoral angle was 10° varus (), on weight bearing. On palpation, the patient had medial joint line tenderness and there was patellofemoral crepitus. There were two swellings located on the lateral aspect of the knee. The first swelling was located 1 cm above the lateral joint line and 4 cm lateral to the lateral patellar border and measured 4 cm × 6 cm. The other swelling was located 1 cm below the lateral joint line and 2.5 cm lateral to the lateral patellar tendon measuring 2 cm × 4 cm (). The skin around both the swellings was normal. The patient had 10° of flexion contracture and the range of motion was 10–110° flexion. Examination of the ligaments in maximal extension revealed 10 mm of opening of the lateral joint line on varus stress test with a soft end point and with valgus stress the alignment of the knee improved to normal with a bony end point ( and ).
Neurological examination revealed a 0/5 motor power in the tibialis anterior and the extensor hallucis longus of the left lower limb. The sensory examination revealed decreased sensation over the dorsum of the left foot and the first dorsal web space. Examination of the hip and the spine revealed no abnormality.
Radiographs of both the knees’ anteroposterior and lateral views showed tricompartmental osteoarthritis of both the knees with opening of the lateral joint space. There was lateral subluxation of the tibia with respect to the femur ( and ). Electromyography and nerve conduction study revealed a peroneal nerve neuropathy at the level of the knee.
A total knee arthroplasty (TKA) along with exploration and decompression of peroneal nerve for the left knee was done. A primary TKA (NEXGEN; Zimmer Biomet, Warsaw, Indiana) was performed (). Ligament balancing was done by performing medial release. We used posterior stabilized insert with cemented femoral and tibial components with a tibial stem.
The peroneal nerve was explored and decompressed by making a 3–5 cm oblique incision parallel to the course of nerve at the neck of the fibula. Skin and the subcutaneous fascia were cut in the same plane. With the help of Metzenbaum scissors and blunt dissection, the retinaculum was identified. The cysts were found under the fascia. Blunt dissection showed cystic wall. An effort was made to remove the cyst without violating the cystic wall, however decompression of the cyst was necessary. Incision of the cyst extruded viscous yellow tinted liquid. The decompressed cyst was then clamped with the Alice forceps and the dissection was started from proximal to the distal directions taking care not to injure the common peroneal nerve around it. The cyst was then removed in toto and was sent for histopathology (). The peroneal nerve was found to be embedded between the two cysts and had a flattened surface. The nerve was freed of all the adhesions around it (). Furthermore, the nerve was decompressed at the level of deep peroneal muscle fascia after exposing the underlying peroneal muscles.
The patient was made to walk 24 h later with protected weight bearing with the assistance of a walker. The patient was evaluated at two weeks and three months postoperatively. At three months postoperatively, the knee pain has resolved completely and the patient is able to walk and climb stairs unassisted. The power of the left ankle and toe dorsiflexors has improved to 5/5.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [74.0, 'kg'], 'height': [178.0, 'cm']}",23.35564,22.18786,24.52342,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 178.0 cm, which is 178.0 cm * 1 m / 100 cm = 1.78 m. The patient's weight is 74.0 kg. The patient's bmi is therefore 74.0 kg / (1.78 m * 1.78 m) = 23.35564 kg/m^2."
2256,6,Body Mass Index (BMI),physical,decimal,pmc-4232616-1,Extracted,"A 12-year-old Caucasian girl with no notable medical history, except for allergic rhinitis, presented with asymptomatic gross haematuria lasting for 7 days. She had no systemic symptoms, sore throat, skin rash, or dysuria, and had no known recent infections. There was no family history of kidney disease. The initial examination showed a temperature of 37°C, blood pressure of 109/55 mmHg, pulse rate of 76 beats/min, and a respiration rate of 20 breaths/min. She had a stable body weight of 39.5 kg that was appropriate for her height of 149 cm. The cardiovascular, lung, and neurologic examinations were unremarkable. Urine output was maintained. The laboratory evaluation showed a normal blood cell count, normal serum protein and albumin concentrations, and normal renal (Cr 0.66 mg/dl) and lipid profiles. The urinalysis revealed an increased urine protein-creatinine ratio (uPCR) of 3580 mg/g and an active urinary sediment (erythrocytes >50/HCF, leukocytes 25–50/HCF, and red blood cell casts 2–5). Multiple serologic examinations, including an antistreptolysin O titer, antinuclear, glomerular basement membrane, and antineutrophil cytoplasmic antibodies, serum protein electrophoresis, cryoglobulins, hepatitis serologic tests, and human immunodeficiency virus, were normal or negative. A complement protein evaluation showed a decreased serum C3 (50.6 mg/dl [normal 81–167 mg/dl]) and normal C4 (26.4 mg/dl [normal 11–42 mg/dl]) concentrations. No infectious cause or other triggering event was detected, as blood and urine cultures were negative. An ultrasound examination revealed hyperechogenicity in the renal cortex bilaterally.
The C3 remained persistently decreased, and the patient failed to clinically improve over the subsequent 7 weeks; therefore, a renal biopsy was performed. Histopathologic examination of the tissue showed cellular crescent formations in more than 80% of 23 glomeruli that were evaluated (Figure a); the formations tended to be large but were not circumferential (Figure b). There was no interstitial inflammation, tubular atrophy, or interstitial fibrosis observed. The vessels were unremarkable. The mesangium along the capillary wall showed strong (+2) staining on immunofluorescent evaluation (Figure c). A C3 glomerulopathy was suspected and was clarified by electron microscopy. Ultrastructure examination revealed mesangial and paramesangial intermediate electron-dense deposits; sausage-shaped, large electron-dense deposits were not observed (Figure d).
Based on the characteristic pathology and the isolated dysfunction in AP activity, the patient was diagnosed with C3 glomerulonephritis (C3GN) with a CsGN histologic pattern.
Because of the crescentic pattern, the patient was initially administered intravenous methylprednisolone (1 g) three times on alternate days, followed by oral prednisolone (60 mg/day). The serum complement concentration subsequently normalised, and the gross haematuria ceased. Enalapril (at a maximally tolerated dose of 20 mg daily) and cyclophosphamide (intravenous bolus of 500 mg monthly) were administered over the next 6 months, and the corticosteroid dose was gradually tapered as the uPCR decreased. During this period, she experienced a single episode of gross haematuria, which promptly resolved with an increase in the corticosteroid dose. No additional episodes of decreased C3 or C4 was noted on serum examinations during treatment. However, immediately after discontinuing cyclophosphamide, the AP functional activity decreased to very low values (6.1%, [normal range 30%–113%]); this trend promptly reversed with the introduction of mycophenolate mofetil, and the AP functional activity increased to 85.4%. The circulating C3NeF was negative, the serum CFH concentration was 99.4 mg/dl (normal range 34.5–59 mg/dl), and the soluble membrane attack complex (sC5b9) was normal. The genetic analysis was negative.
Eight months after beginning treatment, the patient was well and asymptomatic. She remained stable as the prednisolone was tapered to 15 mg every other day along with 1.5 g of mycophenolate mofetil daily. She maintained normal renal function (Cr 0.4 mg/dl) and showed no signs of analytic AP dysfunction, though she continued to show a persistent mild haematoproteinuria (urine erythrocytes 5–10/HCF and uPCR 960 mg/g).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [39.5, 'kg'], 'height': [149.0, 'cm']}",17.79199,16.90239,18.68159,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 149.0 cm, which is 149.0 cm * 1 m / 100 cm = 1.49 m. The patient's weight is 39.5 kg. The patient's bmi is therefore 39.5 kg / (1.49 m * 1.49 m) = 17.79199 kg/m^2."
2257,6,Body Mass Index (BMI),physical,decimal,pmc-6329250-1,Extracted,"A 43-year-old female (weight, 52 kg; height, 152 cm) with no history of allergic disorders was scheduled for open reduction and internal fixation of the right humerus. At the first visit, physical examination, chest roentgenogram [], and electrocardiogram were normal. Blood analysis showed hemoglobin (Hgb) 5.6 g/dl and hematocrit (Hct) 17.4%. Because she was diagnosed as having folate-deficiency anemia, she was transfused 2 units packed red cells twice (4 units in total) 6 and 3 days prior to the surgery at the orthopedist and hematologist's discretion. Her hemoglobin increased to 8.3 and 9.4 g/dl, after transfusion. After the second transfusion, she suffered from coughs with wheezes and was diagnosed as bronchial asthma. She was treated with aminophyllin 250 mg DIV and hydrocortisone 100 mg IV, and recovered rapidly.
On admission, her blood pressure (BP) and heart rate (HR) were 148/92 mmHg and 116 beats/min (bpm), respectively. Pulsed oxygen saturation (SpO2) was 98% under room air. Her Hgb and Hct were 9.1 g/dl and 27.4%, respectively. Physical examination showed no other abnormalities.
Just before induction of anesthesia, her BP was 155/95 mmHg, and her HR was 108 bpm. General anesthesia was induced with propofol 100 mg and fentanyl 100 μg, and her trachea was intubated smoothly after inducing vecuronium 6 mg IV. Anesthesia was maintained with isoflurane 0.7–1.2% in 67% nitrous oxide in oxygen under mechanical ventilation. Forty-five min after induction of anesthesia, airway pressure increased suddenly and SpO2 decreased to 88%. Coarse crackles with obvious secretion were heard. Oxygen 100% was given, but SpO2 was not fully improved (94%). Chest roentgenogram taken immediately after surgery revealed that the lungs were congested and her heart was markedly enlarged []. Arterial blood gas analysis showed pH 7.280; PaCO2 55.8 mmHg; PaO2 74.0 mmHg; and SpO2 92.9%. She apparently showed the state of circulatory overload. Until this sudden onset of respiratory failure, estimated blood loss was 300 ml, and 500 ml of lactated Ringer's solution was administered during the procedure. She had been fasted for over 15 h before surgery, and 300 ml of lactated Ringer's solution was given during this period. Urine output was 225 ml. Methylprednisolone sodium succinate 500 mg and furosemide 30 mg was given IV. As a result of these treatments, additional 1800 ml of urine was excreted, and oxygenation improved under spontaneous respiration with insufflated oxygen 3 l/min (pH 7.430; PaCO2 37.6 mmHg; PaO2 142.2 mmHg; and SpO2 98.9%). Pulmonary congestion was alleviated on chest roentgenogram []. Hence, her trachea was extubated and oxygen 3 l/min using a face mask was given. Because desaturation was not observed for more than 10 min, she left the operating room 1.5 h after the end of operation. The patient's subsequent course was uneventful, and she was discharged 1 week after surgery.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [52.0, 'kg'], 'height': [152.0, 'cm']}",22.50693,21.38158,23.63228,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 152.0 cm, which is 152.0 cm * 1 m / 100 cm = 1.52 m. The patient's weight is 52.0 kg. The patient's bmi is therefore 52.0 kg / (1.52 m * 1.52 m) = 22.50693 kg/m^2."
2258,6,Body Mass Index (BMI),physical,decimal,pmc-8225500-1,Extracted,"A 14-year-old girl complained of severe dysmenorrhea that had developed and progressively worsened since menarche at age 12 years. She experienced lower abdominal pain for more than 10 days around her menstrual period, along with nausea and vomiting. She had taken oral analgesics during these periods; however, they did not relieve the pain. She had to visit the emergency room and miss school several times. Her body weight was 47 kg, and her height was 157 cm. Physical examination revealed diffuse tenderness of the lower abdomen and bimanual pelvic examination was not performed because she was a virgin. Laboratory tests were all within normal limits.
Transrectal ultrasound revealed a 3-cm hyperechogenic mass on the right side of the uterus that was independent of the normal endometrium and ovaries. Pelvic MRI revealed a fluid collection in the right horn of the uterus. The preoperative MRI showed a bicornuate uterus with a noncommunicating horn (). After obtaining written consent, hysteroscopy was performed under general anesthesia, demonstrating a normal uterine cavity and bilateral ostia. Under general anesthesia with a muscle relaxant was used to avoid hymenal damage. Laparoscopy revealed a mass bulging out in the right anterior wall of the uterus. The myometrial wall over the cystic lesion was opened with monopolar scissors, and chocolate-like fluid was expelled from the cyst. The endometrial and myometrial tissue surrounding the cyst were completely resected using the monopolar hook. The myometrial defect was sutured by V-loc (Covidien, Mansfield, MA, USA) in two layers and reinforced interruptedly with 0-Polysorb Vicryl (Ethicon, Norderstedt, Germany) (). The abdominal cavity was thoroughly irrigated with saline, and the uterine wound was covered with Seperafilm (Genzyme Biosurgery, Framingham, MA, USA). The total operating time was 125 minutes, and the estimated blood loss was about 50 mL. Pathological examination showed a cyst wall lined with endometrial glandular epithelium and stromal cells surrounded by myometrium (). The postoperative period was uneventful. She was discharged 4 days after the operation. Her abdominal pain was completely resolved after surgery. She has had regular menstruation without complaints for 2 years after surgery.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [47.0, 'kg'], 'height': [157.0, 'cm']}",19.06771,18.11432,20.0211,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 157.0 cm, which is 157.0 cm * 1 m / 100 cm = 1.57 m. The patient's weight is 47.0 kg. The patient's bmi is therefore 47.0 kg / (1.57 m * 1.57 m) = 19.06771 kg/m^2."
2259,6,Body Mass Index (BMI),physical,decimal,pmc-5719913-1,Extracted,"A 5-year-old girl was admitted to the emergency department owing to vomiting and abdominal pain for 2 weeks. She was born at 40 weeks (full term), weighing 2.4 kg, and received full vaccination up-to-date. Her medical and family histories were unremarkable. At admission, her height and weight were 116 cm and 20 kg, respectively. On physical examination, she had tenderness and rebound tenderness at the epigastric area. However, no mass was palpated on her abdomen. The laboratory findings revealed the following values: hemoglobin (Hb), 14.3 g/dL; hematocrit (Hct), 41.4%; white blood cells (WBC), 19,680/μL; and platelets, 464,000/mL. The C-reactive protein (CRP) level was slightly increased (0.33 mg/dL). Her stool Hb level was 201 ng/mL, although hematochezia or melena was not detected on rectal examination.
On abdominal ultrasonography (US), an intussuscepted inner segment was detected on the edematous outer bowel, at the left upper quadrant of the abdomen (). Abdominal computed tomography (CT) revealed an intussusception at the proximal jejunal loops without a lead point (). Three air reductions and one saline reduction were attempted. However, her symptoms recurred, and repeated US still detected jejunal intussusception. On laparoscopic examination for jejunal reduction and investigation of a lead point of intussusception, no lead point was detected. She still complained of intermittent abdominal pain 1 month after the laparoscopic examination. Capsule endoscopy was not performed owing to the risk of retention. Therefore, enteroscopy using a gastroscope (GIF-Q260; Olympus, Tokyo, Japan) was performed under fluoroscopic guidance and sedation. Enteroscopy revealed a few variable-sized polypoid lesions with erosions on the proximal jejunum. The largest lesion nearly obstructed the jejunal lumen (). On histopathological examination of the tissues obtained via endoscopic biopsy, chronic inflammation was found without specific findings for diagnosis. After obtaining the histopathological result, we repeated the enteroscopy to remove the jejunal lesions. In the second enteroscopy, the total procedure time was 55 minutes, and moderate sedation was achieved using midazolam and propofol. During the procedure, a total of 6 mg of midazolam and 170 mg of propofol were used. After the enteroscopy, she recovered from the sedation without any complications.
Histopathological evaluation of the resected tissues showed a foveolar epithelium with a cystic change (). On immunohistochemical staining, the polyps expressed MUC4, which is present in the normal gastric mucosa; MUC5AC, which is expressed in the foveolar cells of the body and the antrum; MUC6, which is expressed in the gastric antral and pyloric glands; and the focally expressed MUC2 marker []. However, it showed a negative expression for MUC1. Finally, the polyps were diagnosed as hyperplastic polyps arising from the HGM. Her symptoms did not recur within 1 year after the endoscopic treatment.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [20.0, 'kg'], 'height': [116.0, 'cm']}",14.86326,14.1201,15.60642,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 116.0 cm, which is 116.0 cm * 1 m / 100 cm = 1.16 m. The patient's weight is 20.0 kg. The patient's bmi is therefore 20.0 kg / (1.16 m * 1.16 m) = 14.86326 kg/m^2."
2260,6,Body Mass Index (BMI),physical,decimal,pmc-7905720-1,Extracted,"A 68-year-old Peruvian man had been suffering from lumbar pain for several days. His CT scan revealed a mass compressing his right ureter and iliac vessels. He underwent exploratory laparotomy with radical resection of a retroperitoneal tumor (10 cm × 8.3 cm × 8 cm), as well as ileocecectomy and ileocecal anastomosis. Pathological analysis () showed that the tumor was a DDL (T2 N0 M0, FNCLCC grade 2, stage IIIA, <50% necrosis, R0). This diagnosis was corroborated by immunohistochemistry markers (ie, the positivity of D33 and NSE and negativity of h-CD and S100). One month after the surgery (for details of the disease course, see ), his initial postoperative scan showed the absence of disease. However, 2 months later (3 months after the surgery), his new CT scan revealed a 1.6 cm × 2.3 cm mass anterior to the right iliac vessels (first recurrence). He received neoadjuvant chemotherapy with doxorubicin plus ifosfamide (6 cycles). Then he underwent resection of the retroperitoneal tumor (R0) and right ureterectomy. The patient further received 3 cycles of doxorubicin plus ifosfamide postoperatively. Eight months after chemotherapy (11 months after the second surgery), a control imaging revealed 2 anterior psoas masses measuring 1.5 cm × 1.5 cm and 1.3 cm × 1 cm (second recurrence). The biopsy of one of the lesions revealed a malignant spindle cell neoplasm compatible with DDL. Two months later, the CT scan showed that the masses had enlarged to 3.0 cm × 1.9 cm and 2.1 cm × 1.6 cm. However, CT scans and a chest x-ray revealed no evidence of metastatic disease. The patient underwent a third surgery wherein the 2 masses and a right pelvic mass were resected entirely (R0). At this point, the patient sought for different treatment options involving an integrative approach. Three months later, he came to the Centro Médico Antroposófico (CMA) and became our patient.
The recommended treatment was subcutaneous injections of VAE obtained from the host tree ash (AbnobaVISCUM® Fraxini); the injections were given thrice per week in increasing doses. The application of VAE Fraxini in the periumbilical area started at 0.2 mg; after 6 months, the dose was increased to 2 mg, which was then maintained for 7 months. The subcutaneous VAE injections occasionally induced self-limited local erythema and swelling of the skin around the application site, which could be tolerated by the patient. Nine months after the VAE treatment was initiated (12 months after the third surgery), a retroperitoneal mass measuring 4.1 cm × 3.0 cm was noticed (third recurrence). After 5 more months, the dose of VAE was increased to 20 mg thrice per week. Three months later, the patient underwent resection (fourth surgery) of a right iliac fossa tumor (a mass measuring 4.7 cm × 3.5 cm with a moderate amount of surrounding fibroadipose tissue) and a right juxtarenal psoas tumor (a well-encapsulated, focal fibro-fatty soft tissue measuring 8.7 cm × 6.5 cm with central areas of probable necrosis). Both tumors were DDLs (FNCLCC grade 3, pT2b). The patient had a negative margin resection (R0) for the larger sarcoma, and the other exhibited focal involvement by the tumor. A cholecystectomy (mild chronic cholecystitis and cholelithiasis) and appendectomy were also performed, and both organs were negative for tumor. Additionally, he received 12 cycles of three-dimensional conformal radiotherapy post-surgery.
As a result of the previous surgeries, which involved a partial right ureter resection with psoas bladder hitch, the patient developed obstructive renal failure as evidenced by the right ureteral obstruction and abnormal serum creatinine levels. The patient then underwent a right percutaneous nephrostomy with stent placement.
Throughout this time, the patient continued to receive VAE Fraxini. Follow-up magnetic resonance imaging was performed periodically post-surgery. Three-month breaks without VAE Fraxini application were set twice per year after obtaining the first negative follow-up magnetic resonance imaging result. The frequency of subcutaneous VAE Fraxini application was reduced to twice per week from month 54 on. The patient reached a recurrence-free interval of 69 months; however, the magnetic resonance imaging performed on month 86 of VAE Fraxini treatment showed a mass in the right iliac fossa. The tumor measuring 8.1 cm × 4.8 cm (FNCLCC grade 3, pT2b) was resected. The tumor showed areas of well-differentiated liposarcoma, which were mixed with areas of intermediate to highly dedifferentiated myxoid fibrosarcoma and high-grade undifferentiated pleomorphic sarcoma. The tumor was relatively well-circumscribed and mostly surrounded by fibroconnective and fibroadipose tissues of variable thickness. However, the resection margins were involved by the sarcoma. One month after the surgery, the VAE treatment was resumed. The patient started receiving intravenous infusion of 100 mg VAE obtained from pine as host tree (Helixor® P); the injections were administered in 500 mL of standard saline solution over 2 hours thrice a week. The dose was increased by 100 mg per application until 400 mg was reached which was maintained until 12 applications were completed. Then, the patient was subjected again to subcutaneous injection with 20 mg VAE Fraxini thrice per week. Five months after the surgery, multiple abdominal and retroperitoneal nodular tumor implants were detected, and their number and size increased within the following 9 months. For 2 weeks, the patient received intravenous infusion of VAE (Helixor® P, maximum dose: 400 mg) followed by subcutaneous infusion of 20 mg VAE Fraxini. One of the implants caused urinary tract obstruction, and the patient developed renal and abdominal pain, which was treated with buprenorphine 20 mg/25 cm2 transdermal patches and with anthroposophic remedies (Wala® Solum Inject, Wala® Plexus coeliacus D15, Wala® Bryonia/Stannum, Weleda® Formica comp injections, thrice per week). Weleda® Equisetum sulfuratum tostum D3 was applied (thrice a day) to support the urinary function. When the pain was relieved and controlled, intravenous infusions of VAE were resumed. He also received 1 cycle of eribulin (1.65 mg IV infusion). In month 103 of the VAE treatment, the patient underwent pleurodesis due to pleural effusion; however, he died 2 weeks later. Altogether, the patient received a total of 103 months (8.6 years) of VAE treatment and achieved 10.5 years of survival.
Within approximately 2 years during which the first 3 surgeries were performed, the patient’s weight decreased from 84 kg to 71 kg. Since the VAE treatment started, the patient’s quality of life progressively improved as seen in his increased appetite, resulting in weight gain (up to 77 kg) during the low-dose VAE treatment. After the fourth surgery, his weight was 70 kg to 74 kg. After the fifth surgery, his weight decreased to 66 kg and then increased again to 70 kg (). The ideal body weight based on his height (172 cm), gender, and age is 54.7 kg to 74.0 kg.
The patient was married and had 3 grown-up children. He had a history of tobacco use, but he quit after being diagnosed with DDL. He consumed alcoholic beverages occasionally. His medical history included diphtheria and hemorrhoidectomy. His father died of leukemia, and his paternal uncle had an unknown cancer of the lower extremity. Further medications included allopurinol tablets for high blood uric acid level and a combination preparation of hydrocodone 10 mg and bitartrate and acetaminophen 500 mg tablets for left lumbar region pain. The patient stopped taking these medications on month 18 of VAE treatment.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [172.0, 'cm']}",23.66144,22.47837,24.84451,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 172.0 cm, which is 172.0 cm * 1 m / 100 cm = 1.72 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.72 m * 1.72 m) = 23.66144 kg/m^2."
2261,6,Body Mass Index (BMI),physical,decimal,pmc-6026788-1,Extracted,"A 35-year-old female (body weight 60.5 kg; height 1.55 m; body fat 16%; back squat 143 kg; front squat 125 kg; clean 97 kg; snatch 63 kg) without medical history of disease presented worsening abdominal pain approximately 24 h after completing a rigorous extreme conditioning competition (), which consisted of two days of five workouts. She was healthy overall and had been active in ECP over the previous five years and trained four or five times per week. The patient gave informed written consent for the use of her clinical and personal data in this paper.
The patient visited her physician one day after the ECP competition and was found to have a serum CK of 43,322 U/L. However, after receiving initial medical attention, she was sent home with instructions to take Tenoxicam (anti-inflammatory drug), bed rest, and drink plenty of water. On the third day post-competition, the pain and muscle swelling did not diminished, and she checked into an emergency room. At this stage her CK concentration was tested again and was 77,590 U/L. However, her kidney function, as indicated by blood urea, creatinine, sodium, and potassium concentrations was normal. On the other hand, her liver enzymes were elevated (aspartate aminotransferase (AST) of 477 U/L and alanine amino transferase (ALT) of 74 U/L). Chronological values of serum biochemistry and associated biomarkers over 25 days of follow-up are presented in . The patient was diagnosed with rhabdomyolysis by the medical attending physician and was treated with aggressive intravenous fluid resuscitation.
She was discharged on the fourth day of hospitalization and she was advised to avoid intense exercise. A follow-up examination revealed that her serum level of CK was still elevated to 3034 U/L on the 10th day and 1257 U/L on the 25th day following the ECP competition (). The subject reported myalgia even 25 days after the ECP competition.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.5, 'kg'], 'height': [1.55, 'm']}",25.1821,23.92299,26.44121,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.55 m. The patient's weight is 60.5 kg. The patient's bmi is therefore 60.5 kg / (1.55 m * 1.55 m) = 25.1821 kg/m^2."
2262,6,Body Mass Index (BMI),physical,decimal,pmc-8442815-2,Extracted,"A 103-year-old woman (approximately 150 cm and 40 kg) presented with right intertrochanteric femoral fracture requiring surgery. She had a history of chronic kidney disease (CKD) due to hypertension, which was treated with amlodipine, furosemide, and valsartan. Moreover, she took ticlopidine for the prevention of cerebral infarction. Physical examination results were normal, and laboratory examination revealed stage 3b CKD with serum creatinine level of 1.18 mg/dL (estimated glomerular filtration rate, 31.6 mL/min/1.73 m2) and mild anemia with Hb level of 10.0 g/dL. Transthoracic echocardiography and electrocardiography revealed no abnormalities.
Anesthetic chart is shown in Fig. . In the operating room, she was hemodynamically stable with vital signs as follows: BP, 157/58 mmHg, heart rate, 84 bpm; and oxygen saturation on room air, 94%. BIS value was > 90 before anesthesia. General anesthesia was induced by intravenous administration of fentanyl (100 μg), remifentanil (0.3 μg/kg/min), and remimazolam (1 mg/kg/h). She lost consciousness 3 min after initiation, and subsequently tracheal intubation was performed after administration of rocuronium (40 mg). After the operation was started, the remimazolam dose was adjusted so that the BIS value became 40–60 0.1–0.3 μg/kg/min of remifentanil infusion. Eventually, the remimazolam dose was decreased to 0.1 mg/kg/h with BIS value of approximately 50–60. The operation was uneventfully completed with a small amount of blood loss in approximately 100 min. During the operation, she remained hemodynamically stable without administration of any vasopressor agents, except when general anesthesia was induced. After completion of the operation, administration of remifentanil and remimazolam was discontinued and 200 mg of sugammadex was administered; 8 min after discontinuation of these agents, she recovered consciousness without flumazenil and received extubation. Any consciousness problem, including resedation or postoperative cognitive function disorder, was not observed during the postoperative course. After rehabilitation, she was discharged on postoperative day 29.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [40.0, 'kg'], 'height': [150.0, 'cm']}",17.77778,16.88889,18.66667,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 150.0 cm, which is 150.0 cm * 1 m / 100 cm = 1.5 m. The patient's weight is 40.0 kg. The patient's bmi is therefore 40.0 kg / (1.5 m * 1.5 m) = 17.77778 kg/m^2."
2263,6,Body Mass Index (BMI),physical,decimal,pmc-6967284-1,Extracted,"This case report follows CARE (CAse REport) guidelines []. We explained the purpose of the study to the patient and obtained written informed consent to publish our findings.
A 66-year-old woman (63 kg; height, 152 cm) with VP was scheduled to undergo distal pancreatectomy for pancreatic cancer. She had been hospitalized for 3 years at the age of 28 years with abdominal pain, ileus, mental disorder, and quadriplegia. During that time, she was diagnosed with VP based on the results of several types of examination. Although she had undergone a tracheostomy due to quadriplegia during hospitalization, her neurologic symptoms disappeared after hospital discharge. Her only daughter presented with abdominal pain during her twenties, at which time she had been diagnosed with VP. She had suspected that her mother’s abdominal pain was also due to VP, although her mother had not been diagnosed with VP definitively. At the present admission, she had a history of abdominal pain that occurred every few months, which she had self-treated with sugar intake and body warming. She was also on medications for hypertension and chronic kidney disease. The creatinine level in serum was increased slightly to 2.12 mg/dL, but there were no abnormalities in other laboratory parameters, such as urinary levels of porphobilinogen and delta-aminolevulinic acid.
We selected total intravenous anesthesia (TIVA) with target-controlled infusion (TCI) as a suitable method of anesthesia []. In the operating theater, the upper body was covered by a forced air blanket to prevent hypothermia. General anesthesia was induced with TCI of propofol (3 μg/mL) with remifentanil (0.4 μg/kg/min) followed by rocuronium (40 mg) and tracheal intubation. An indwelling catheter was inserted into the radial artery for regular measurement of levels of glucose and electrolytes in the blood. Anesthesia was maintained with TCI of propofol and remifentanil with monitoring of the bispectral index. Rocuronium was administered intermittently to maintain a train-of-four count of 1. A total of 0.4 mg of fentanyl was administered intraoperatively, with 50 μg/h of fentanyl administered continuously for postoperative analgesia.
Blood-gas tests were undertaken via the arterial catheter every 60 min, and we checked for electrolyte abnormalities and measured blood glucose levels. All electrolytes were within the normal range intraoperatively. The blood glucose level before as well as 1, 2, 3, and 4 h after starting surgery was 102, 120, 121, 106, and 97 mg/dL, respectively. The glucose level decreased 3 h after starting surgery despite the administration of an extracellular fluid containing 5% glucose, so we administered glucose (10 g, i.v.). Body temperature decreased from 36.0 °C preoperatively to 35.5 °C 1 h after starting surgery, so we started the amino acid infusion to increase body temperature []. Body temperature 2, 3, and 4 h after starting the surgery was 35.4, 35.7, and 35.9 °C, respectively. The total volume of the amino acid infusion was 550 mL. Distal pancreatectomy was completed in 224 min. After confirming a train-of four count of 2, sugammadex (140 mg) was administered and the tracheal tube removed, followed by administration of oxygen (3 L/min) via a nasal cannula. She was admitted to the high dependency unit. Our patient had no neurologic abnormalities or VP symptoms. She was moved to the general ward on postoperative day 5 and was discharged from the hospital with good progress on postoperative day 15.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [63.0, 'kg'], 'height': [152.0, 'cm']}",27.26801,25.90461,28.63141,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 152.0 cm, which is 152.0 cm * 1 m / 100 cm = 1.52 m. The patient's weight is 63.0 kg. The patient's bmi is therefore 63.0 kg / (1.52 m * 1.52 m) = 27.26801 kg/m^2."
2264,6,Body Mass Index (BMI),physical,decimal,pmc-8342838-2,Extracted,"A 68-year-old Caucasian man (Patient B) from the United Kingdom (height 177 cm, weight 85 kg) was admitted with cough and a week-long increasing dyspnea, before which he was healthy. His wife and daughter probably had COVID-19 with resolving symptoms, and they were all living in the same house. The patient markedly experienced shortness of breath on the day of admission to the emergency department (ED) and, therefore, called an ambulance. His laboratory results on admission were as follows: Hb: 140 g/L, creatinine: 117 μmol/L, WBC: 8.6 × 109/L, lymphocytes: 0.2 × 109/L, platelet count: 126 × 109/L, INR: 1.4, APTT ratio: 1.3, D-dimer > 20,000 μg/L (i.e., higher than the upper limit of the measurement range), fibrinogen plasma concentration: 6.8 g/L, and CRP: 336 mg/L. His chest radiograph showed dense bilateral mid-zone and right lower zone consolidation. PCR result was positive for SARS-CoV-2 and negative for influenza/RSV. Blood cultures showed coagulase-negative staphylococci. The patient was treated with antibiotics (ceftriaxone and doxycycline, according the hospital’s COVID-19 protocol). Antiviral therapy and dexamethasone were not administered. As the patient was severely hypoxemic in the ED, he was transferred directly to the ICU. Orotracheal intubation and IPPV (positive end-expiratory pressure 15 mmHg) were performed about 3 hours after ICU admission as respiratory effort was not improved by face mask CPAP therapy. Chest radiography repeated after intubation showed bilateral interstitial lung changes similar to the imaging conducted earlier on the same day. Prone position did not improve oxygenation. Laboratory results on the next day were as follows: Hb: 133 g/L, creatinine: 265 μmol/L, WBC: 16.3 × 109/L, platelet count: 56 × 109/L, INR: 1.6, APTT ratio: 1.5, D-dimer: 4,340 μg/L, fibrinogen plasma concentration: 2.9 g/L, and CRP: 478 mg/L. By ROTEM, Patient B presented with hypocoagulability in the EXTEM assay with a prolonged CT of 99 s, clot formation time (CFT) of 253 s, and decreased clot firmness amplitudes (A5, 22 mm and MCF, 48 mm) (). Furthermore, EXTEM and FIBTEM analyses demonstrated a complete fibrinolysis shutdown []. Both hypocoagulability and fibrinolysis shutdown have been shown to be associated with increased mortality in bacterial sepsis [,]. The FIBTEM trace was within normal limits which may be owing to impaired fibrin polymerization, given that fibrinogen concentration was elevated. The patient deteriorated within a few hours of ICU admission and died the following day despite invasive ventilation, norepinephrine for hypotension, and renal replacement therapy for acute kidney failure. Patient B did not show any clinical signs of thrombosis during his hospital stay.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [85.0, 'kg'], 'height': [177.0, 'cm']}",27.13141,25.77484,28.48798,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 177.0 cm, which is 177.0 cm * 1 m / 100 cm = 1.77 m. The patient's weight is 85.0 kg. The patient's bmi is therefore 85.0 kg / (1.77 m * 1.77 m) = 27.13141 kg/m^2."
2265,6,Body Mass Index (BMI),physical,decimal,pmc-3348632-1,Extracted,"A 38-year-old woman with a childhood history of atopic dermatitis and allergic rhinitis came to our outpatient clinic because of polyarthralgia and swelling of her fingers. Five days prior to her visit, she had upper respiratory symptoms and a low grade fever (). Oral administration of 400 mg acetaminophen relieved those symptoms. Then, however, she developed a butterfly-shaped erythema on her face and swelling of her fingers. Three days later, although the facial erythema had improved, she developed joint pain in her fingers, wrists, shoulders, and knees, for which acetaminophen did not work. On physical examination, the patient looked tired. Her body temperature was 36.7°C, blood pressure was 94/50 mmHg, and pulse rate was 61 beats/min. She weighed 48 kg and was 153 cm tall. She had no rash except for a malar erythema that was faint at that time. All her fingers were swollen, but her wrist, shoulder, and knee joints were not. Both her legs had pretibial pitting edema. Laboratory data showed mild hypoproteinemia (serum protein 6.4 g/dL) and slightly decreased peripheral white blood cell count (4,100/μL). However, other hematologic parameters were relatively normal (hemoglobin 11.2 g/dL, hematocrit 35.2%, reticulocyte 1.4%, and platelet count 230,000/μL). Liver enzymes and C-reactive protein levels were not elevated. Regardless of hypocomplementemia (C3 72 mg/dL, C4 9 mg/dL, and CH50 18.6 U/mL), the tests for serum antinuclear antibodies and rheumatoid factor were negative. Althoughthe IgG antibody was not examined, a positive result for HPV-B19 IgM antibody (index 7.97) indicated a recent infection of the virus []. Since microbiological tests for other viruses, such as measles and rubella, were negative, a diagnosis of HPV-B19 infection was finally made. Because her symptoms deteriorated despite the use of acetaminophen, oral administration of loxoprofen (180 mg/day) was alternatively started immediately after the diagnosis (). The symptoms, including facial erythema, polyarthralgia, and the swelling of her fingers, rapidly disappeared within 12 hours after the initiation of the drug. No recurrence of the symptoms or signs was noted afterwards, indicating the complete remission of the disease.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [48.0, 'kg'], 'height': [153.0, 'cm']}",20.50493,19.47968,21.53018,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 153.0 cm, which is 153.0 cm * 1 m / 100 cm = 1.53 m. The patient's weight is 48.0 kg. The patient's bmi is therefore 48.0 kg / (1.53 m * 1.53 m) = 20.50493 kg/m^2."
2266,6,Body Mass Index (BMI),physical,decimal,pmc-7548041-1,Extracted,"A 15-year-old Han Chinese girl presented to our department in June 2019 with the chief complaint of amenorrhea for 2 years. She experienced menarche more than 2 years ago with a menstrual cycle of 18–21 days and menstruation lasting 6–7 days with normal menstrual flow. However, the menstruation ceased 7 months after menarche with no obvious cause. Her last menstruation was on June 26, 2017. Her past medical history revealed recurrent attacks of urticaria 6 years ago, which were attributed to allergies to abalone, milk, soy, and eggs. She was diagnosed as having Graves’ disease 4 years ago. She was treated with thiamazole, which was discontinued after more than 2 years of treatment and her thyroid function returned to normal with monitoring. Her personal history revealed that she had a full-term birth and a birth weight of 2.85 kg. The developmental milestones of raising her head, turning over, sitting up, crawling, and walking were achieved at normal times, and her academic performance was good. Her mother was 42-years old and had regular menstruation; our patient’s maternal grandmother experienced menopause at the age of 50.
A physical examination revealed: a body temperature of 36.2 °C; pulse, 63 beats/minute; respiratory rate, 20 breaths/minute; blood pressure, 93/60 mmHg; height, 161.5 cm; body weight, 47 kg; upper body height 80.5 cm; lower body height 81 cm; and arm span 161.5 cm. The appearance of her vulva was normal, with Tanner II breast development and Tanner I pubic hair development. Cardiopulmonary and abdominal examinations revealed no abnormalities, and there were no malformations such as webbed neck, cubitus valgus, or shortened metacarpals. Supplemental examination results of adrenocorticotropic hormone, cortisol, sex hormones, and thyroid hormones are shown in Tables , and . The results of blood, urine, and fecal tests were normal; the results of electrolytes test, liver function test, and kidney function test were normal. Ultrasound examinations of her breasts, thyroid, and abdomen revealed no abnormalities. Her lumbar spine bone density T-score was − 1.5. Her growth hormone level at 1 hour of deep sleep was 2.19 ng/mL (reference range, 0.123–8.05) and parathyroid hormone level was 30.5 pg/mL (reference range, 15–68.3). Her anti-Müllerian hormone level was < 0.06 ng/mL (reference range, 2.80–6.3). Serum anti-ovarian antibody, antinuclear antibody, rheumatoid factor, antineutrophil cytoplasmic antibodies, and extractable nuclear antigens polypeptide titers were negative. A transrectal color Doppler ultrasound revealed the size of her uterus to be 19 × 15 × 22 mm, with a small volume and an intimal thickness of approximately 3 mm. The sizes of her left and right ovaries were 16 × 7 × 8 mm and 18 × 7 × 9 mm, respectively, indicating that both ovaries were small. A 3.7 × 3.3 mm sized follicle was visible in her left ovary. Magnetic resonance imaging of her pituitary gland indicated no abnormalities. Her bone age was approximately 15–16 years. Her chromosomal type was 46,XX as per the karyotype analysis of 50 cells. Whole-exome genetic testing did not reveal mutations associated with amenorrhea. Gene copy number testing revealed no obvious pathological copy number variation (CNV).
After learning about the disease, our patient suffered from anxiety and insomnia. Psychologists counselled and reassured her that treatment could lead to improvement. Estazolam was prescribed as a sleep aid for a short period, together with 0.5 mg estradiol once daily, calcium, and vitamin D replacement. Follow-up and ultrasound re-examination after 6 months of treatment revealed that her uterus had increased in size to 24 × 16 × 25 mm. There was no significant change in the bilateral ovarian size, and no follicles were found. Further examination showed Tanner III breast development and Tanner I pubic hair. Her lumbar spine bone density T-score was − 1.0. The treatment had had a favorable effect and resulted in improving our patient’s psychological anxiety.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [47.0, 'kg'], 'height': [161.5, 'cm']}",18.01992,17.11892,18.92092,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 161.5 cm, which is 161.5 cm * 1 m / 100 cm = 1.615 m. The patient's weight is 47.0 kg. The patient's bmi is therefore 47.0 kg / (1.615 m * 1.615 m) = 18.01992 kg/m^2."
2267,6,Body Mass Index (BMI),physical,decimal,pmc-4649734-2,Extracted,"A 59-year-old male with a diagnosis of alcoholic liver disease was referred to our hospital with general fatigue and marked liver dysfunction (tables , ; fig. ). His height and body weight were 176 cm and 69 kg, respectively. He was positive for HEV genotype 3 RNA and IgA anti-HEV antibody (fig. ). We diagnosed him as having HEV infection. After admission to our hospital, he was given bed rest and peripheral parenteral nutrition, and his condition improved. This patient had consumed deer meat approximately 1 month before admission.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [69.0, 'kg'], 'height': [176.0, 'cm']}",22.27531,21.16154,23.38908,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 176.0 cm, which is 176.0 cm * 1 m / 100 cm = 1.76 m. The patient's weight is 69.0 kg. The patient's bmi is therefore 69.0 kg / (1.76 m * 1.76 m) = 22.27531 kg/m^2."
2268,6,Body Mass Index (BMI),physical,decimal,pmc-3229443-1,Extracted,"A 68 year-old woman (weight 74 kg, height 162 cm) with a pathological fracture of the fourth thoracic vertebrae (T4) was scheduled to undergo total removal of the vertebrae by a right transthoracic approach. Her past medical history included hypertension controlled with 20 mg enalapril once a day. Preoperative airway examination revealed a class II Mallampati with a normal mouth opening and normal dentition, a thyromental distance of 6.0 cm and limited neck extension. Paraplegia was present and no other abnormalities were detected on physical examination. All laboratory values, chest x-ray and 12-lead electrocardiogram were normal. The patient was premedicated with 10 mg diazepam on the night before surgery along with overnight fasting. After adequate preoxygenation, anesthesia was induced with 50 μg fentanyl, TIVA of propofol and remifentanil, and muscle relaxation was achieved with 50 mg rocuronium. Conventional direct laryngoscopy was performed and Cormack and Lehane grade was II (only the posterior extremity of the glottis visible). A 37F left-sided polyvinylchloride Carlens DLT (SUMI®, Portex Inc., Mexico) was placed using standard technique, although difficult to achieve because of a narrowed trachea. The patient's lung was ventilated through both lumens of the tube, with tracheal cuff inflated, but a resistance at manual ventilation was felt immediately after intubation. Chest auscultation revealed bilaterally equal and diminished breath sounds with pulse oximetry saturation decreasing from 99% to 96%. DLT was removed and before a second left endobronchial intubation attempt, examination of the DLT showed no carinal hook (Figure ). An 8.0 mm ID single-lumen endotracheal tube was placed and then fiberoptic bronchoscopy was performed. An increased in pulse oximetry saturation (from 95% to 99%) with normal chest auscultation was noted. The fiberoptic examination showed the carinal hook located in the right mainstem bronchus, which was removed with the use of forceps. No evidence of a traumatized airway was noted. Two further attempts were made with another 37F Carlens DLT, by a different physician and with the aid of fiberoptic bronchoscopy (external diameter: 4.5 mm). However, DLT rotation failed because of a narrowed trachea. Smaller DLTs were not available. Thoracotomy was performed in left position with an 8.0 mm ID single-lumen endotracheal tube. The patient's hemodynamics was stable throughout this period. Her postoperative period was uneventful.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [74.0, 'kg'], 'height': [162.0, 'cm']}",28.19692,26.78707,29.60677,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.0 cm, which is 162.0 cm * 1 m / 100 cm = 1.62 m. The patient's weight is 74.0 kg. The patient's bmi is therefore 74.0 kg / (1.62 m * 1.62 m) = 28.19692 kg/m^2."
2269,6,Body Mass Index (BMI),physical,decimal,pmc-3772693-1,Extracted,"A 17-year-old female presented to our outpatient clinic complaining of a sensation of a lump in her throat and moderate dysphagia following an episode of acute rhinopharyngitis. Her height was 158 cm and weight was 63 kg. The patient had no family history of metabolic abnormalities. The ear, nose and throat examination identified a swelling of the base of the tongue. The swelling appeared round with an approximate diameter of 3 cm; it was near the foramen cecum; it had a reddish color; and it had an irregular nonulcerated surface. Fiberoptic endoscopy identified the swelling in the glossoepiglottic area (). It was mobile during deglutition. A thyroid scintigraphy, with technetium-99 pertechnetate, showed a single contrast enhancement in the sublingual region, instead of in the normal anatomical position of the thyroid (). Determination of blood levels of the thyroid hormones showed a free triiodothyronine (FT3) of 3.0 pg/mL (normal range: 2.4–4.2 pg/mL), a free tetraiodothyronine (FT4) of 1.0 ng/dL (normal range: 0.8–1.7 ng/dL), and TSH of 5 IU/mL (normal range 0.3–5.0 IU/mL).
The patient started medical suppressive therapy with levothyroxine 25 mcg/day for the first 2 weeks and 50 mcg/day for the next 9 months, but no reduction in either swelling or symptoms was observed, so she was scheduled for surgical treatment.
A preoperative neck computed tomography (CT) identified an nonhomogeneous, hyperdense soft tissue with distinct margins and round shape at the base of the tongue, with a maximum diameter of 3 cm, and absence of the thyroid gland.
The vascularization of the mass was evaluated through carotid arteriography. The mass was vascularized by collateral branches of the lingual arteries in its anterior and posterior regions. The superior and inferior thyroid arteries were bilaterally absent ().
Surgery was then performed using a transoral approach, under general anesthesia. The mass was removed, with an electrosurgical needle, along a cleavage plane from the foramen cecum backwards to the glossoepiglottic vallecula; hemostasis was adequate. A surgical reconstruction of the base of the tongue was performed by suturing the remaining area of the tongue, and a nasogastric tube was inserted. The nasogastric tube was removed 6 days after surgery, and the patient was discharged a day later with hormone replacement therapy, without deficiency in swallowing or speaking.
The hormone replacement therapy was based on thyroxine tablets 50 μg/day.
Histologically, the mass was found to be “thyroid tissue with alternation of hyperplastic and colloid cystic areas, coated with a layer of squamous epithelium.” The surgical specimen measured 3 × 3 cm ().",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [63.0, 'kg'], 'height': [158.0, 'cm']}",25.23634,23.97452,26.49816,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 158.0 cm, which is 158.0 cm * 1 m / 100 cm = 1.58 m. The patient's weight is 63.0 kg. The patient's bmi is therefore 63.0 kg / (1.58 m * 1.58 m) = 25.23634 kg/m^2."
2270,6,Body Mass Index (BMI),physical,decimal,pmc-4823414-1,Extracted,"A 31-year-old male patient (height 173 cm, weight 70 kg) with no medical history of particular significance had been receiving treatment at a dermatology clinic for ten years for erythematous patches accompanied by non-painful itching in both nasal alar creases, both perioral areas, and both posterior auricular folds (). A topical steroid treatment was chosen, as he had tested negative on the KOH test. The steroid treatment alleviated the symptoms but could not eliminate them completely. It was notable that even on the steroid treatment, skin lesions appeared when he consumed alcohol or was dehydrated. The patient was on the topical steroid treatment when he visited our hospital, and erythematous patches were visible in the nasal alar creases and perioral areas. As a previous study had reported a case of acne vulgaris treatment with SGB [], and the mechanisms of acne vulgaris and seborrheic dermatitis are presumed to be similar, we determined to use SGBs on this patient. An anterior blind approach was selected. The patient was positioned with the anterior spine extended, so that the transverse process of the C6 vertebra (Chassaignac's tubercle) could be easily detected. A needle was vertically inserted at the anterior tubercle and was placed on the transverse process. Five ml of 1% mepivacaine were injected after fixing the needle in position and confirming that there were no abnormal sensations in the upper limb or blood aspiration []. The same procedure was performed daily, on one side each day. After administration of the injection on one side, ipsilateral ptosis and nasal obstruction occurred but faded about two hours later. The skin lesions disappeared within three days, after which the patient wished to stop the treatment for personal reasons. However, the patient revisited the hospital two months later due to a relapse. During the follow-up, the patient noted that there had been no symptoms up to one week before the revisit. We initiated the same treatment procedure and the patient's skin lesions disappeared after five trials (). Fifty more trials were performed, and the patient has not seen a relapse of the symptoms or side effects since.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [173.0, 'cm']}",23.38869,22.21926,24.55812,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 173.0 cm, which is 173.0 cm * 1 m / 100 cm = 1.73 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.73 m * 1.73 m) = 23.38869 kg/m^2."
2271,6,Body Mass Index (BMI),physical,decimal,pmc-4346931-1,Extracted,"Patient 1: A 17-month-old boy was referred to the neuropediatrician because of generalized hypotonia and reduced cranial growth perimeter. He was the full-term product of a third pregnancy (preceded by a spontaneous miscarriage) resulting from a non-consanguineous relationship. His birth weight was 4.2 kg (60th percentile) and height was 51 cm (50th percentile), he had normal immunization and had an Apgar score of 9. However, he showed global developmental delay according to the Peabody Developmental Motor Scale 2 (PDMS-2) and the Battelle developmental inventory 2 (BDI-2; see ).
Head support was achieved at seven months, with stable seating and autonomous position attained at 12 months; he started to walk autonomously at 30 months, and his first raw words appeared at 12 months. There was no family history of metabolic or neurological disease. Upon physical examination, his weight was 10 kg (50–75th percentile), height was 72 cm (90th percentile), head circumference was 41.5 cm (10th percentile, microcephaly), and his general condition was regular except for generalized hypotonia and loss of strength in the upper part of his lower-limbs but with normal deep tendon I/IV reflexes. No dysmorphic features, skin blemishes, or cardiopulmonary alterations were observed.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [10.0, 'kg'], 'height': [72.0, 'cm']}",19.29012,18.32561,20.25463,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 72.0 cm, which is 72.0 cm * 1 m / 100 cm = 0.72 m. The patient's weight is 10.0 kg. The patient's bmi is therefore 10.0 kg / (0.72 m * 0.72 m) = 19.29012 kg/m^2."
2272,6,Body Mass Index (BMI),physical,decimal,pmc-2621134-1,Extracted,"An 85-year-old unconscious Japanese woman with hypertension, dementia was admitted to the neurosurgery department of our hospital. Her height was about 140 cm and she weighed 35 kg. On admission, her head Computed Tomography (CT) illustrated the fourth ventricle hemorrhage with hydrocephalus. Admission electrocardiogram (ECG) showed the QT interval to 420 ms with a sinus rhythm at a rate of 72 beats/min. According to Bazett's formula, the QTc interval was 460 ms. Medications she was using just before admission included slow-release nifedipine 10 mg twice daily and famotidine 10 mg twice daily. After her admission, these medications were stopped because of her unconsciousness. Clinical laboratory findings at the time of admission were as follows; serum aspartate-amino transferase level was 22 IU/L, serum alanine transaminase level was 9 IU/L, serum total bilirubin level was 0.7 mg/dl, serum potassium level was 4.0 mEq/L, serum urea nitrogen level was 25.9 mg/dl and serum creatinine level was 0.6 mg/dl. Thus, renal dysfunction, hepatic dysfunction and hypokalemia were not observed on admission. Other biochemical tests were normal. On the fifth day after admission, the ventriculo-peritoneal shunt was performed for hydrocephalus. As the result, her consciousness was improved remarkably, therefore slow-release nifedipine and famotidine were restarted on the seventh day after admission. On the twenty-first day after hospitalization, the right forearm pain and swelling were developed, so oral moxifloxacin 400 mg daily was initiated for the right forearm cellulitis. In a few days, the right forearm pain and swelling were reduced. But on the sixth day of moxifloxacin administration, her pulse rate indicated 40 beats/min that was bradycardia, so monitor ECG was performed and it showed prolongation of the QT interval to 640 ms. Using Bazett's formula, the QTc interval was 523 ms (Figure ). When the severe QTc interval prolongation was developed, the serum electrolytes, renal function and hepatic function were normal. We assumed that the cause of severe QTc interval prolongation was moxifloxacin, because the severe QTc interval prolongation was observed after moxifloxacin therapy. Therefore, moxifloxacin was discontinued. Furthermore, because the cases of QT interval prolongation associated with famotidine have been reported [], famotidine was also stopped. On the sixth day after moxifloxacin discontinuance, monitor ECG showed the QT interval to 400 ms with a sinus rhythm at a rate of 70 beats/min. According to Bazett's formula, the QTc interval was 432 ms that was improved to normal range (Figure ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [35.0, 'kg'], 'height': [140.0, 'cm']}",17.85714,16.96428,18.75,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 140.0 cm, which is 140.0 cm * 1 m / 100 cm = 1.4 m. The patient's weight is 35.0 kg. The patient's bmi is therefore 35.0 kg / (1.4 m * 1.4 m) = 17.85714 kg/m^2."
2273,6,Body Mass Index (BMI),physical,decimal,pmc-7561635-1,Extracted,"A 44-year-old woman (height 155 cm, body weight 65 kg) was diagnosed with right breast carcinoma and was scheduled to undergo right MRM surgery under general anesthesia and right SAP block. The patient had ASA physical status II, and preoperative examinations were unremarkable. The procedure was performed after informed consent for the SAP block was obtained. The procedure was performed under ultrasonography (USG) guidance using a 38-mm 6 MHz linear transducer and a 22G 100-mm regional block needle. The patient was in the left lateral decubitus position. Aseptic and antiseptic techniques were done around the area of mid-axillary line. Scans were performed while moving the transducer laterally and distally until the 4th and 5th ribs were visualized. The transducer was then rotated into the coronal plane and tilted posteriorly until the serratus anterior muscle and latissimus dorsi muscle were identified. After local infiltration with 1% lidocaine 2 ml and confirming no intravascular injection by aspiration, 0.25% bupivacaine 30 ml was injected on the fascia between the serratus anterior muscle and latissimus dorsi muscle (Fig. ). For general anesthesia, patients were induced using 1% propofol 2 mg/kg with titration, isoflurane 1.5–2.0 vol%, and atracurium 0.1 mg/kg. The patient was intubated using direct laryngoscopy with endotracheal tube (ETT) no. 7. Ringer lactate was used as the maintenance liquid. The duration of the surgery was 120 min. Intravenous ketorolac 30 mg/8 h and oral paracetamol 500 mg/8 h were given as postoperative analgesia for 48 h. Intravenous tramadol 100 mg/8 h was also given for 24 h. The patient was monitored for 2 h postoperatively in recovery room, then for 24 h postoperatively in medical ward. Postoperative NRS is demonstrated on Fig. . The patient does not report any nausea/vomiting or breakthrough pain during monitoring period.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [65.0, 'kg'], 'height': [155.0, 'cm']}",27.05515,25.70239,28.40791,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 65.0 kg. The patient's bmi is therefore 65.0 kg / (1.55 m * 1.55 m) = 27.05515 kg/m^2."
2274,6,Body Mass Index (BMI),physical,decimal,pmc-4252348-1,Extracted,"A 77-year-old woman, 156 cm in height and weighing 55 kg, was diagnosed as having angina pectoris and aneurysm of the thoracic aorta, and she was scheduled to undergo coronary artery bypass grafting and aortic arch replacement. She had been a smoker for more than 50 years and had also been diagnosed as having chronic obstructive pulmonary disease (COPD) complicated by PA hypertension. The patient was receiving treatment with oral diltiazem hydrochloride (100 mg/day) and furosemide (20 mg/day), and mean preoperative PA pressure was 20-30 mmHg. Preoperative laboratory tests revealed no coagulation abnormalities or any other notable abnormalities. At surgery, anesthesia was induced with propofol (80 mg), fentanyl (200 µg) and muscle relaxation with rocuronium (40 mg), and tracheal intubation was performed using a normal endotracheal tube (7 mm in internal diameter; Parker Flex-Tip™, Parker Medical, USA). No marked circulatory variations or abnormalities were observed during the induction of the general anesthesia. Anesthesia was maintained with 40% of oxygen, propofol (target-controlled infusion: 2.0 µg/ml), and remifentanil (0.2 µg/kg/min). A central venous catheter and a PA Swan-Ganz catheter were placed via the right internal jugular vein prior to the start of the surgery. The PA Swan-Ganz catheter was advanced up to the PA while the pressure waveforms were checked under the guidance of transesophageal echocardiography, and it was fixed at 40 cm after 1 cm was pulled out confirming wedging of the catheter tip in the PA. PA pressure after Swan-Ganz catheter insertion was 22 mmHg (mean), and pulmonary capillary wedge pressure was 18 mmHg.
Maximum airway pressure suddenly increased to 26 cmH2O from 15 cmH2O 30 minutes after the beginning of surgery, when the internal carotid artery graft was being secured for the coronary artery bypass. Endotracheal hemorrhage was detected, and the tracheal tube became filled and occluded with blood. There had been no change in wedge waveform of the PA Swan-Ganz catheter before the bleeding occurred. Ventilation was disrupted for 3 minutes with a transient fall of SpO2 to 86%. However, positive pressure ventilation was maintained at airway pressures as high as 20 to 30 cmH2O with positive end-expiratory pressure (PEEP: 6 cmH2O) while suction of the blood filling the tracheal tube was performed, and the bleeding ceased 15 minutes after it had been detected. Bronchoscopic observation revealed numerous clots in the tracheal tube, with complete occlusion of the right main bronchus. A total of 300 ml of blood was aspirated from the airway. As continuation of the surgery was deemed impossible, the surgery was suspended and the patient was admitted to the intensive care unit (ICU) with the tracheal tube in place.
A postoperative chest X-ray showed decreased lucency of the right lower lung field. Chest CT revealed a contrast-enhanced false aneurysm measuring 2 cm in diameter in the right PA (). Conservative treatment by mechanical ventilation with applied PEEP (6-8 cmH2O) was selected over invasive treatment because the false aneurysm was small in size and bleeding from the aneurysm had ceased. Retrospectively, chest 3D CT images were confirmed (). The right main PA was pressed by the thoracic aortic aneurysm. A chest 3D CT after surgery revealed that the PA Swan-Ganz catheter had shifted at the thoracic artery aneurysm level (). The tip of the PA Swan-Ganz catheter was maintained at a distance from PA aneurysm (). A repeat chest X-ray and CT on the 16th postoperative day revealed improvement, and the contrast-enhanced false PA aneurysm could no longer be visualized. The patient's respiratory condition also improved, and she was extubated and discharged from the ICU on the 20th postoperative day.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.0, 'kg'], 'height': [156.0, 'cm']}",22.60026,21.47025,23.73027,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 156.0 cm, which is 156.0 cm * 1 m / 100 cm = 1.56 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.56 m * 1.56 m) = 22.60026 kg/m^2."
2275,6,Body Mass Index (BMI),physical,decimal,pmc-7844464-1,Extracted,"A 61-year-old man (height, 168 cm; weight, 70 kg) presented to our emergency room (ER) with head trauma after falling on a cement floor from a 5-meter-tall construction site. Upon arrival at the ER, the patient had a Glasgow coma scale score of 11 and the following vital signs: blood pressure (BP), 147/83 mmHg; heart rate (HR), 86 beats per minute (bpm); respiratory rate, 24 breaths per minute; body temperature from the auditory canal, 36.8°C; and percutaneous oxygen saturation (SpO2), 97%. Upon discovering signs of acute subdural hemorrhage, subarachnoid hemorrhage, and intraventricular hemorrhage from a brain computed tomography (CT) scan performed in the ER, we admitted the patient to the intensive care unit (ICU) for close monitoring. After approximately 6 hours, we performed follow-up brain CT because the patient’s mental status had deteriorated from drowsy to stupor. Upon observing a mass effect characterized by an increase in the hemorrhage volume and a left midline shift on the CT images, the patient was scheduled for immediate intubation and emergency decompressive craniectomy ().
Although the patient had a history of ischemic heart disease with percutaneous coronary intervention (PCI), it was difficult to obtain accurate information because there was no relevant data in the patient’s medical records from the authors’ hospital, and his drowsy state interfered with detailed interviews. According to the chest CT scan performed immediately after admission, coronary stents had been inserted at the bifurcation site of the left main coronary artery (). It also appeared that the inserted stents were drug-eluting stents (DES) considering that he had received dual antiplatelet therapy (DAPT) with aspirin and clopidogrel (Plavix®; Sanofi, Bridgewater, NJ, USA) a switching platelet P2Y12 inhibitor, for approximately 4 months. However, DAPT was discontinued owing to the worsening cerebral hemorrhage after hospitalization; bridging antiplatelet therapy was also not performed. Before the surgery, the patient showed a normal electrocardiogram (ECG), and cardiac biomarker testing revealed a troponin-T concentration of 0.006 µg/L, which was within normal limits (). The patient demonstrated satisfactory functional capacity to be able to work at a construction site just before the trauma. Therefore, an additional preoperative cardiac evaluation was not considered necessary.
Immediately after admission to the ICU, the patient’s bladder temperature was 38.0°C. Using a hydrogel-coated water-circulating pad (Arctic Sun®; Medivance Inc., Louisville, CO, USA), which is a surface cooling device, the patient underwent mild therapeutic hypothermia with a target temperature of 33.0°C. During therapeutic hypothermia, sedation and shivering control were performed using continuous rate infusions of midazolam at 5 mg/hour and remifentanil at 0.2 µg/kg/minute. The patient’s bladder temperature was 33.4°C just before he was transferred to the operating room. Preoperative laboratory tests showed no unusual findings except for mildly elevated aspartate aminotransferase (73 U/L) and alanine aminotransferase (51 U/L) concentrations.
The patient’s vital signs upon arrival at the operating room were a BP of 130/70 mmHg and SpO2 of 100%. Lead II of the ECG was monitored, and there were no unusual findings except sinus tachycardia with an HR of 100 bpm on the initial ECG. Arterial BP (ABP), central venous pressure (CVP), and esophageal temperature were monitored from the right radial artery, right subclavian vein, and lower third of the esophagus using a temperature sensor attached to the esophageal stethoscope, respectively. The initial ABP, CVP, and esophageal temperature were 140/85 mmHg, 6 mmHg, and 33.0°C, respectively. Arterial blood gas analysis was performed in the arterial line, with values calculated as for a body temperature of 37°C, which revealed the following: pH, 7.400; partial pressure of carbon dioxide (PCO2), 40 mmHg; partial pressure of oxygen (PO2), 174 mmHg; bicarbonate (HCO3), 24.8 mmol/L; base excess, 0.0; lactate, 0.17 mmol/L; ionized calcium, 1.04 mmol/L; and potassium, 3.3 mmol/L. Total intravenous (IV) anesthesia was performed using a target-controlled infusion of propofol and remifentanil in accordance with the Schnider and Minto models, respectively. Propofol and remifentanil were infused continuously with effect-site concentrations (Ce) of 1.5 µg/mL and 1.5 ng/mL, respectively. Concurrently, 50 mg of rocuronium was administered by IV bolus injection for neuromuscular blockade. Mechanical ventilation was adjusted to maintain the end-tidal carbon dioxide value at 30 to 33 mmHg.
As ABP decreased to 78/42 mmHg and CVP decreased to 4 mmHg within 10 minutes after anesthesia, the Ce of propofol and remifentanil were lowered to 0.8 µg/mL and 1.0 ng/mL, respectively, and approximately 1 L of balanced crystalloid fluid loading was performed. However, the patient’s BP did not recover, and a dopamine continuous infusion (5 µg/kg/minute) was initiated. When a surgical incision was made 10 minutes after beginning the dopamine infusion, the patient’s ABP and HR increased to 115/70 mmHg and 120 bpm, respectively, and marked ST-segment depression (−2.4 mm) was found, which was not observed on the preoperative or initial ECGs (). Subsequently, the depth of anesthesia was increased by increasing the Ce of propofol to 1.0 to 1.2 µg/mL, followed by a continuous infusion of isosorbide dinitrate (1 µg/kg/minute). While HR was maintained at 110 to 120 bpm, ABP gradually decreased to 70/40 mmHg after approximately 5 minutes. To treat the hypotension, isosorbide dinitrate was discontinued, and a bolus injection of 100 µg phenylephrine was administered, after which, ABP increased temporarily to 95/60 mmHg. Subsequently, HR decreased suddenly and rapidly, and ventricular fibrillation occurred. The anesthesiologists immediately discontinued the surgery and performed cardiopulmonary resuscitation (CPR). The patient’s esophageal temperature at the time was 32.0°C.
Chest compressions were performed with periodic defibrillation with 200 J, and epinephrine injections were administered every 3 minutes; these measures elicited no response. During CPR, ECG monitoring showed temporary severe bradycardia (HR, 10–30 bpm). However, this was considered pulseless electrical activity because no pulse was detected in the patient’s femoral artery. Soon afterward, there was a rapid transition to ventricular fibrillation, and CPR was repeated. At the time, the patient’s esophageal temperature dropped to 30.0°C. According to the refractory state after the defibrillation and drug injections, we considered that the cardiac arrest was caused by hypothermia. To reverse the cause, a forced-air warming device and a warming blanket (Bair Hugger®; Arizant Healthcare Inc., Eden Prairie, MN, USA) were used for surface warming, the IV fluids were warmed, and surgical wound closure and dressing were performed rapidly to prevent surface heat loss. The first arterial blood gas analysis after ventricular fibrillation, calculated as for a body temperature of 37°C, showed the following: pH, 7.690; PCO2, 15 mmHg; PO2, 260 mmHg; HCO3, 18.1 mmol/L; base excess, −1.2; lactate, 0.33 mmol/L; ionized calcium, 0.88 mmol/L; and potassium, 5.0 mmol/L. Follow-up arterial blood gas analyses were repeated periodically. As we continued to perform CPR, the patient developed severe metabolic acidosis and hypocalcemia characterized by a pH of 6.840, HCO3 of 15.4 mmol/L, and ionized calcium of 0.66 mmol/L. To correct the abnormal findings, we administered appropriate amounts of sodium bicarbonate and calcium chloride. After an hour-long CPR and rewarming, the patient’s esophageal temperature recovered to 33.0°C, which was followed by observing sinus rhythm characterized by an HR of 75 bpm on an ECG monitor and detecting a pulse in the femoral artery with a characteristic ABP waveform that eventually led to the recovery of BP to 130/55 mmHg. Upon confirming recovery of spontaneous circulation (ROSC), the patient was transported to the ICU while we administered dopamine (10 µg/kg/minute), norepinephrine (0.1 µg/kg/minute), and vasopressin (2 U/hour). ABP, HR, and esophageal temperature during anesthesia are shown in .
Cardiac biomarker testing performed after the patient’s transfer to the ICU showed an increased troponin-T level of 1.432 µg/L. Portable Doppler transthoracic echocardiography (TTE) revealed total occlusion of the left main coronary artery, which had undergone PCI previously. Because emergency coronary artery bypass grafting (CABG) was impossible at the time, repeated PCI was considered an alternative treatment option. However, even after his transfer to the ICU, the patient experienced repetitive ventricular fibrillation. Four hours after the patient’s transfer to the ICU, the patient’s guardian requested that CPR should be stopped. Without resuscitation, the patient died.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [168.0, 'cm']}",24.80159,23.56151,26.04167,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.68 m * 1.68 m) = 24.80159 kg/m^2."
2276,6,Body Mass Index (BMI),physical,decimal,pmc-7160938-1,Extracted,"The patient is a 19-year-old female, the first child of non-consanguineous Lithuanian parents (Fig. a, individual II-1; Fig. b). She was born at the 41st-42nd gestational week by cesarean delivery due to signs of fetal asphyxia. Her birth weight was 2700 g (<3rd centile), her length was 48 cm (3rd –10th centile), and Apgar scores at 1, 5 and 10 min were 8, 9 and 10. Psychomotor developmental delay was noticed from infancy. According to the medical documentation, the girl’s height was below 3rd centile (130 cm and 138 cm at age of 15 and 16 years, respectively), weight was also below 3rd centile (28 kg and 36 kg at age of 15 and 16 years, respectively). At the age of 19 years, her head circumference was 51 cm (<3rd centile), her height was 147 cm (<3rd centile), her weight was 45 kg (<3rd centile), and her weight/height dependence was 75th–90th centile. She was found to have mild intellectual disability, microcephaly, micrognathia, upslanted palpebral fissures, coarse facial features, short neck, wide chest, spine deformation, and delayed puberty (according to Tanner B2, Ph2). An echocardiogram revealed an abnormality of the aortic valve and atrial septal defect with atrial septal aneurysm. No endocrine pathology was found, and bone age corresponded to chronological age. A chest X-ray showed S-shaped scoliosis of the thoracolumbar spine and no deformation of the ribs. No abnormalities were detected in a neck X-ray. An audiogram showed a mild neurosensory hearing impairment. Abdominal and renal ultrasound and brain MRI were normal. The patient’s IQ was measured at age 19 using the Wechsler Adult Intelligence Scale-III []: total IQ 56, verbal IQ 56, and non-verbal IQ 54.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.0, 'kg'], 'height': [147.0, 'cm']}",20.82466,19.78343,21.86589,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 147.0 cm, which is 147.0 cm * 1 m / 100 cm = 1.47 m. The patient's weight is 45.0 kg. The patient's bmi is therefore 45.0 kg / (1.47 m * 1.47 m) = 20.82466 kg/m^2."
2277,6,Body Mass Index (BMI),physical,decimal,pmc-6232809-1,Extracted,"A 75-year-old woman with cough, rhinorrhea, sore throat, and appetite loss was evaluated at our hospital for anterior cervical pain and thyrotoxicosis. The patient's height was 145 cm, and her body weight was 40.0 kg. At her first visit to our hospital, her blood pressure was 137/81 mmHg, with a regular pulse rate of 116 beats/min. Her body temperature was 37.0°C. An electrocardiogram showed sinus tachycardia. She had no family history of autoimmune thyroid diseases. Nor did she take any medicines.
Her neck pain initially appeared on the left side and subsequently moved to the right side. Laboratory data showed a normal white cell count (8,290 cells /µL) and slightly elevated C-reactive protein (3.94 mg/dL) and alkaline phosphatase (460 U/L) levels (). Thyroid hormone levels were also elevated (free triiodothyronine, 20.27 pg/mL; free thyroxine, 6.53 ng/dL; thyroglobulin, 183 ng/mL), whereas thyroid-stimulating hormone (TSH) was undetectable. Ultrasonography (US) of the thyroid revealed heterogeneous and hypoechoic areas, which are features of subacute thyroiditis, in both thyroid lobes (). Biopsy was not performed.
The patient was treated with prednisolone (PSL, 20 mg/day), and her neck pain disappeared shortly thereafter. Two weeks after treatment initiation, we found strong anti-TSH receptor antibody (TRAb) and anti-thyroid-stimulating antibody positivity (). The PSL dose was gradually tapered, and thyroid hormone levels decreased, although they were still above normal 6 weeks after treatment start (). At this time, the patient received both PSL (10 mg/day) and methimazole (MMI, 10 mg/day). Four weeks later, thyroid hormone levels improved, and US showed hypervascularity and fewer hypoechoic areas in the thyroid. However liver function worsened, and MMI treatment was therefore stopped. One week after MMI withdrawal, the damaged liver had recovered, but the thyroid hormone levels were again elevated. Propylthiouracil (PTU, 100 mg/day) was administered, and levothyroxine (25 µg/day) was later added to control thyroid function.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [40.0, 'kg'], 'height': [145.0, 'cm']}",19.02497,18.07372,19.97622,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 145.0 cm, which is 145.0 cm * 1 m / 100 cm = 1.45 m. The patient's weight is 40.0 kg. The patient's bmi is therefore 40.0 kg / (1.45 m * 1.45 m) = 19.02497 kg/m^2."
2278,6,Body Mass Index (BMI),physical,decimal,usmle-7374,Extracted,"A 56-year old man is brought in by ambulance to the emergency department and presents with altered consciousness, confabulation, and widespread rash. He is recognized as a homeless man that lives in the area with a past medical history is significant for traumatic brain injury 4 years ago and chronic gastritis. He also has a long history of alcohol abuse. His vital signs are as follows: blood pressure 140/85 mm Hg, heart rate 101/min, respiratory rate 15/min, and temperature 36.1°C (97.0°F). His weight is 56 kg (123.5 lb) and height is 178 cm (5.8 ft). The patient is lethargic and his speech is incoherent. Examination reveals gingival bleeding, scattered corkscrew body hair, bruises over the forearms and abdomen, multiple petechiae, and perifollicular, hyperkeratotic papules over his extremities. His lung and heart sounds are normal. Abdominal palpation reveals tenderness over the epigastric area and hepatomegaly. Neurologic examination demonstrates symmetrically diminished reflexes in the lower extremities.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [56.0, 'kg'], 'height': [178.0, 'cm']}",17.67454,16.79081,18.55827,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 178.0 cm, which is 178.0 cm * 1 m / 100 cm = 1.78 m. The patient's weight is 56.0 kg. The patient's bmi is therefore 56.0 kg / (1.78 m * 1.78 m) = 17.67454 kg/m^2."
2279,6,Body Mass Index (BMI),physical,decimal,pmc-6966728-1,Extracted,"The patient gave written informed consent for publication of this case report and any accompanying images, and the presentation was approved by the institutional review board of Juntendo University (JHS 18-027).
A 67-year-old male, 170 cm tall, weighing 72 kg, was scheduled to undergo left lower lung lobectomy via open thoracotomy for non-small cell lung carcinoma. He had no relevant medical history, and his preoperative blood examination revealed no abnormal findings. We decided to preoperatively insert a thoracic epidural catheter for postoperative analgesia.
On the day of surgery, no premedication was administered. He was monitored by ECG, noninvasive blood pressure monitoring and pulse oximetry. Before general anesthesia induction, the patient was positioned in the right lateral position for catheter insertion. We initially attempted the epidural puncture at the thoracic (Th) 6–7 interspace, which we changed to the Th 5–6 interspace after 15 min due to difficulty in an epidural puncture at the original site. Using a right paramedian approach, an 18 G Tuohy needle (Perican® epidural needle, 18G × 80 mm, B. Braun, Hessen, Germany) was used for epidural puncture 1 cm caudal and 1 cm to the right of the spinous process. After confirming accurate placement of the needle tip in the epidural space by the loss of resistance to injection of normal saline, the epidural catheter (Perifix® epidural catheter, standard 1000 mm, B. Braun) was inserted via the Th 5–6 intervertebral space with no resistance. The final total insertion length was 13 cm: 6 cm through the skin and 7 cm placed in the epidural space. After the catheter was appropriately secured in place, the patient was turned to the supine position in preparation for general anesthesia. Before general anesthesia induction, we gave a test dose of 2 ml of 2% plain lidocaine via the epidural catheter, followed by administration of 50 μg fentanyl and 4 ml of 0.25% levobupivacaine. We were able to confirm the loss of cold sensation around the left T5 area 5 min after local anesthetic administration. After induction of general anesthesia, endotracheal intubation with a double-lumen tube was performed to enable single lung ventilation during surgery.
At the beginning of surgery, an approximately 12- cm posterolateral incision was made at the level of the fifth to sixth intercostal space. Blood pressure and heart rate remained stable, suggesting the adequacy of analgesia in the incision area. However, when the surgeon opened the thoracic cavity, he saw the epidural catheter below the fifth rib. The catheter seemed to follow the course of the intercostal nerve. The tip of the catheter could be seen 3 cm from the dorsal edge of the incision (Fig. a, b).
Fortunately, the catheter had not been severed during the surgical procedure. After discussion with the surgical team, we decided to withdraw the catheter via the skin of his back under direct observation by the surgeon in the surgical field. The catheter was successfully withdrawn and examined for intactness of the tip. Thereafter, intraoperative analgesia was achieved mainly by continuous intravenous infusion of remifentanil and intermittent administration of fentanyl. For postoperative analgesia, a continuous intravenous infusion of 1 mg (20 ml) fentanyl and 20 ml normal saline was administered as patient-controlled analgesia (PCA) at the rate of 1 ml/h, with bolus doses of 1 ml and a lockout time of 10 min, the infusion being commenced in the latter half of surgery. The scheduled surgery was completed uneventfully without any complications.
We also performed TPVB under ultrasound guidance, injecting 20 ml of 0.25% levobupivacaine in the paravertebral space, besides the Th5 transverse process, before the patient’s emergence from general anesthesia and while he was still in the lateral position.
Anesthesia emergence and his subsequent recovery from anesthesia were uneventful. During the postoperative period, his numerical rating scale score ranged from 0 to 1 and he required a single administration of supplemental analgesic (15 mg pentazocine) and six IV PCA boluses within 24 h. He did not complain of any paresthesia around the intercostal region. He was discharged from the hospital without any paresthesia or complications on the fifth day after surgery.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [72.0, 'kg'], 'height': [170.0, 'cm']}",24.91349,23.66782,26.15916,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 72.0 kg. The patient's bmi is therefore 72.0 kg / (1.7 m * 1.7 m) = 24.91349 kg/m^2."
2280,6,Body Mass Index (BMI),physical,decimal,pmc-5309409-1,Extracted,"We present the case of a 12-year-old Colombian male patient, son of first cousins, who was diagnosed with intrauterine growth restriction at 6 months prenatally and was born at term, with normal weight (3000 Kg) and height (49 cm) for gestational age (40 weeks). Since the age of 3 months he started developing multiple skin lesions, initially in the face, which then extended to the whole body, mainly in sun-exposed areas. The family history revealed similar recurrent skin cancers in 2 cousins on the maternal side of the family, who died at ages 8 and 12 years (). At the time of evaluation the patient had developed approximately 15 basal and squamous cell carcinomas in the face, ears, nose, eyes, and the extremities, which were surgically removed and no melanoma had been diagnosed. In addition to the dermatologic manifestations, the patient had been diagnosed with vitamin D deficiency due to excessive sun protection and also with detrusor hyperactivity plus detrusor-sphincter dyssynergia. Since infancy the patient also developed cognitive alterations, attention deficit/hyperactivity disorder, pes cavus, and progressive gait alterations. At 7 years he was diagnosed with bilateral cryptorchidism and hypogonadism by pediatric endocrinology. The physical exam revealed short stature (height: 133 cm) (<2 SD), microcephaly (head circumference: 47.5 cm) (<2 SD), low weight (26 Kg), intellectual disability, altered speech, ataxic gait, and hyperreflexia, accompanying the skin findings: alopecia, freckle-like skin lesions, actinic keratoses sparing unexposed areas, and marked skin atrophy in eyelids and around the mouth (). Electromyography of the extremities and auditory evoked potentials were normal. Spine MRI revealed a normal spinal cord and cerebral MRI showed parenchymal volume loss, cerebellar atrophy, and white matter gliosis (). A commercial Xeroderma Pigmentosum Next Generation Sequencing panel including the genes DDB2, ERCC2, ERCC3, ERCC4, ERCC5, POLH, XP-A, and XPC revealed a homozygous germline sequence variant designated c.547A>T in the XPC gene, which was confirmed by Sanger sequencing. This variant is predicted to result in premature protein termination (p.Lys183) and has not been previously reported in ClinVar and in The Human Gene Mutation Database, but is expected to be pathogenic. The karyotype was normal: 46XY with no structural or numerical chromosomal alterations. Genetic counseling, before and after genetic testing, was performed.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [26.0, 'kg'], 'height': [133.0, 'cm']}",14.6984,13.96348,15.43332,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 133.0 cm, which is 133.0 cm * 1 m / 100 cm = 1.33 m. The patient's weight is 26.0 kg. The patient's bmi is therefore 26.0 kg / (1.33 m * 1.33 m) = 14.6984 kg/m^2."
2281,6,Body Mass Index (BMI),physical,decimal,pmc-8560281-1,Extracted,"A 79-year-old woman was transferred to Sanjo General Hospital for maintenance hemodialysis and rehabilitation. She had no family history of renal disease. Her medical history was complex. About two years before transfer, she was diagnosed with gastric non-Hodgkin lymphoma (diffuse large B-cell type) in a medical examination at the first hospital. She was treated with six cycles of rituximab, tetrahydropyranyl adriamycin, cyclophosphamide, vincristine, and prednisolone. These drugs, excluding prednisolone, were not used since then. However, two months after her last chemotherapy for lymphoma, a residual tumor was confirmed. Definitive radiotherapy was performed with a curative intent, totaling 40 Gray in 20 fractions. A complete response was confirmed by an upper gastrointestinal endoscopy after radiotherapy, with no progression observed. After 17 months, about 13 weeks prior to her transfer to our hospital, she was noted to have proteinuria, renal dysfunction, hemolytic anemia, and thrombocytopenia for the first time on follow-up medical examinations. She was referred to the second hospital because of acute kidney injury (AKI) with hemolytic anemia and thrombocytopenia (platelet count was 99,000/µL). Her physical examination findings on to the second hospital were as follows: height, 158.0 cm; weight, 53.0 kg; blood pressure, 136/88 mmHg; and body temperature, 36.8°C. On admission, urinalysis revealed microscopic hematuria (urinary sediment, 50–99 erythrocytes/high-power field) and the urine protein/creatinine ratio was 4.7. Her hematocrit was 30.5%, hemoglobin concentration was 9.9 g/dL, platelet count was 178,000/µL, and leukocyte count was 6,690/µL. Red cell fragments were observed on peripheral blood smear. Her serum urea nitrogen level was 36 mg/dL, creatinine (Cre) level was 2.55 mg/dL, and lactate dehydrogenase level was 485 IU/L. The total complement level was 14 (reference range: 30–46) IU/L, complement 3 (C3) level was 41.8 (73–138) mg/dL, and complement 4 (C4) level was <5 (11–31) mg/dL. Additional laboratory data at the second hospital are summarized in . Abdominal ultrasound revealed mildly atrophic kidneys. Her renal function very rapidly worsened, and she had a severely high blood pressure (200/100 mmHg). Assuming malignant hypertension and a collagen vascular disease-related kidney injury such as lupus nephritis, hemodialysis was immediately initiated; simultaneously, a 3-day course of intravenous methylprednisolone (500 mg/day) followed by oral prednisolone at 45 mg/day was started; however, she became anuric in about a week. The possibility of TMA was investigated. However, she was in poor general condition and did not get the consent of her family, so no invasive searches, such as a kidney biopsy, were performed. Prednisolone was gradually tapered to a dose of 5 mg/day (). She was transferred to Sanjo General Hospital for rehabilitation and maintenance hemodialysis.
When we carefully reassessed her, we observed that her urine volume had increased to 700 mL/day. In addition, since her serum Cre level before dialysis was very low (1.59 mg/dL), steroid treatment seemed to be effective to some extent. Kidney atrophy was unnoticeable, so with the consent of her and her family, we performed kidney biopsy to investigate the cause of renal failure.
On performing light microscopy, we observed the following: the biopsied sample contained 43 glomeruli, of which 8 showed global sclerosis, 1 showed segmental sclerosis, and 1 showed a thrombus (). Diffuse global or segmental mesangial expansion was seen, which was accompanied by mesangiolysis. Segmental endocapillary hypercellularity, focal double contours without spike formation, and mesangiolysis were observed (Figures and ). Wrinkling of the glomerular basement membrane (GBM) was also observed (). A segmental thrombus was observed in one glomerulus (). Tubular atrophy and interstitial fibrosis were noticed (). Some arterioles revealed thickness of the arterial intima and narrowing or complete obstruction of the vessel lumina (Figures and ). Immunofluorescent examination revealed no significant deposits of immunoglobulins or complement components. Electron microscopy revealed wrinkling of the glomerular basement membrane (GBM), expansion of the subendothelial space, mesangial interposition, and reduplication of the GBM ().
Based on her clinical and histological findings, such as double contours and wrinkling of the GBM, mesangiolysis, and thickness of the arterial intima, she was diagnosed with TMA. The course of her disease was variable; hence, we reviewed her past medical history in detail. Gastric non-Hodgkin lymphoma had been in complete remission at the onset of TMA. She presented with severe hypertension; however, she did not meet the criteria for malignant hypertension. Although the disease was pathologically consistent with radiation nephropathy, there was no reliable evidence. Laboratory data revealed normal disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13) activity (check before the initiation of HD); hence, she was unlikely to have thrombotic thrombocytopenic purpura (TTP). Throughout the course, there was no obvious infection. Due to a complicated medical history and rapid course of AKI, it was difficult to perform a kidney biopsy and identify the definite cause of disease immediately after the onset of AKI. Imidapril, an angiotensin-converting enzyme inhibitor, 5 mg/day was initiated. Her urine volume gradually increased. She was able to withdraw from hemodialysis therapy two weeks after the initiation of imidapril.
To further examine the genetic involvement of the complement system, we performed extensive diagnostic testing to identify the cause of TMA. Samples for the extensive complement analysis were taken. Plasma-soluble C5b-9 complement levels were 526.4 (reference range: 37.0–260.6) ng/mL, complement factor Ba levels were 3,970.4 (275.6–685.2) ng/mL, CFH levels were 391.7 (229.8–714.6) µg/mL, and complement 5a levels were 15.84 (0.20–15.62) ng/mL. Enzyme-linked immunosorbent assay for anti-CFH IgG was negative (510.6 (393.9–1069.0) AU/mL). After obtaining informed consent, we collected DNA from the patient. Genomic DNA was extracted from whole blood, and targeted next-generation sequencing of candidate genes for aHUS was performed. Sequencing of the exonic regions of 9 genes (CFH, CFHR5, C3, CFI, CFB, MCP, THBD, DGKE, and PLG) conducted at the Japanese Association for Complement Research revealed a heterogeneous very rare missense variant (exon 5; NM_000186.3:c.526 T > C: p.Phe176Leu) in the CFH gene. Despite the CFH variant, serum and plasma CFH levels were normal. It was not possible to completely deny the possibility that CFH p.Phe176Leu may have some influence as a causative genetic mutation; however, we did not use eculizumab (ECZ). A diagnosis of SLE was considered on account of reduced C3 and C4 counts along with the gradual effect of steroid treatment. However, the hemolytic anemia was attributable to TMA, and there were no other findings to suspect lupus nephritis; hence, a clear diagnosis of SLE could not be made.
The subsequent clinical course was relatively better. Hemodialysis was discontinued. Two years later, her creatinine level stayed at 1.91 mg/dl.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.0, 'kg'], 'height': [158.0, 'cm']}",21.23057,20.16904,22.2921,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 158.0 cm, which is 158.0 cm * 1 m / 100 cm = 1.58 m. The patient's weight is 53.0 kg. The patient's bmi is therefore 53.0 kg / (1.58 m * 1.58 m) = 21.23057 kg/m^2."
2282,6,Body Mass Index (BMI),physical,decimal,pmc-7948355-1,Extracted,"A 5 year old Japanese girl who had previously been diagnosed with LS was referred to the orthodontic clinic in the Fukuoka Dental College Medical and Dental Hospital in Fukuoka, Japan, because she had posterior crossbite. She is the second child with healthy parents who have no family history of genetic disorders. The diagnosis of LS was based on clinical findings. At birth, she had knee joint dislocations, equinovarus foot deformities, and a cleft of the soft palate only with no extension to the hard palate, alveolus, or lip (type 1 of Veau’s classification []). Operations for dislocations and equinovarus deformities were respectively performed at the ages of 4 and 9 months. Furlow’s palatoplasty was performed for the soft palate repair when she was 1.7 years old. She had not undergone any orthodontic treatment including presurgical orthodontics. The Enjoji scale [], recorded at the age of four, revealed delays of social behavior and emotional and language development.
She underwent orthodontic examinations, including general, facial and intraoral examinations, lateral and frontal cephalometric analyses, and a study model examination for orthodontic diagnosis. On general examination, her height and weight were 112.3 cm and 15.1 kg, respectively. These were below the reference for the 75th and 10th percentile in her age and sex group, respectively. The hand–wrist radiograph was used to examine her skeletal maturity (Fig. a). The patient's skeletal age was matched at 5.3 years by the TW2 RUS method applied to the Japanese population, whereas the Greulich–Pyle Atlas method estimated the corresponding age at 5.5 years []. Based on these methods, her skeletal age almost matched her chronological age of 5.6 years. She had long cylindrically shaped fingers (Fig. b). Dysmorphic facial features were noted, including hypertelorism, a prominent forehead, depressed nasal bridge, and a flattened midface. Her facial profile was straight. Her chin point deviated toward the right side from the facial midline (Fig. ).
Intraoral examination revealed the complete primary dentition with an overjet of 2.0 mm, an overbite of 2.0 mm, and mesial step-type terminal planes on both sides. There were no spaces around the fused tooth with the left deciduous central and lateral incisors in the upper dentition, while the lower dentition exhibited anterior crowding and mesial rotation of the first deciduous molars on both sides. On the right side, posterior crossbite was observed resulting from a functional lateral shift of the mandible owing to the premature contacts between the maxillary and mandibular right primary molars. In centric relation prior to the mandibular shifting, the mandibular dental midline was nearly consistent with the facial midline. In centric occlusion, the maxillary and mandibular dental midlines deviated 1.5 mm to the left and 2.0 mm to the right relative to the facial midline, respectively. As a result, the upper and lower dental midline discrepancy was 3.5 mm (Fig. ).
On study models examination, the arch widths between the primary canines, and the first and second molars were measured to compare them with the standard values obtained from Japanese children with normal primary occlusions (Fig. and Table ) []. In the case of the primary canine, all the distances of the bilateral tips and the bilateral palatal or lingual cervical lines were measured. In the cases of the primary molars, the distances between the bilateral buccal grooves of the first and second molars were also measured. On the maxillary and mandibular dentitions, all the arch width measurements were significantly smaller than one standard deviation (SD) below the Japanese norms matched for the patient’s age.
The panoramic radiograph showed that the maxillary left lateral incisor was congenitally missing. The tooth germ of the maxillary left second molar was not present. The tooth crown of the unerupted, maxillary right central incisor was rotated and was close to that of the maxillary right lateral incisor. The fused tooth with the left deciduous central and lateral incisors showed the union of tooth crowns by the dentin and two roots with independent root canals (Fig. ).
Figure shows the lateral and frontal cephalogram of the patient. Cephalograms were taken in a standard manner with a magnification ratio of 1.1. Figure a, b shows the conventional cephalometric analyses. The results are given in Table . These indicated the posteriorly positioned maxilla and mandible (SNA, SNB, and facial angle), skeletal Class III jaw relationship (ANB), steep mandibular plane (FMA) with the large Gonial angle, and growth tendency of the mandible (Y-axis) toward the postero-inferior direction. Inclination of the maxillary primary incisors was within the normal range (U1 to SN), while the mandibular primary incisor inclined more lingually than the norm (L1 to Mandible) [].
Figure c shows the facial depth measurements used in this study. The horizontal positions of the six landmarks in relation to a line perpendicular to the S–N line that passed through sella, were measured based on the method proposed by Ono []. The results of the facial depth measurements were shown in Table . The depths measured on Or, PTM, Pog, Me, and Ar were smaller than one SD below the Japanese norms matched for the patient’s age and sex, while the depth of the nasion was within the normal range []. For the posterior part of the mandible, the facial depths measured on Go were close to one SD below the norms. These indicated that the orbitale, the maxilla, and mandible were positioned posteriorly relative to the anterior cranial base.
The frontal cephalometric analysis was performed as shown in Fig. . The facial midline was drawn through the Crista Galli and perpendicular to the line that passed through the latero-orbitale (Lo) bilaterally. For each of the 14 landmarks used, the distance to the facial midline was measured on both sides. The facial widths were obtained based on the addition of the bilateral distances measured on each landmark []. Table shows the results of the facial width measurements. Compared with the Japanese norms matched for the patient’s age and sex, the cranial width measurements taken at MCB(p), Lo, OSM, OSL, and CN yielded values that exceeded the Japanese norms by one SD. The widths measured on the Mx, cMoU, and cMoL, were smaller than those of the Japanese norms, and indicated narrow maxillary basal arch and maxillary and mandibular dental arch widths.
Based on the examinations performed, an orthodontic diagnosis of unilateral posterior crossbite due to a functional lateral shift of the mandible, a skeletal Class III jaw relationship, narrow maxillary and mandibular dental arches, mandibular anterior mild crowding, and congenital missing of the maxillary left lateral incisor and the maxillary left second molar was made. The proposed treatment plan included (1) the maxillary dental arch expansion to eliminate the premature contacts between the maxillary and mandibular right primary molars and to improve the lateral shift of the mandible, (2) observation of the jaw growth and occlusal development with potential options of the maxillary protraction and the mandibular dental arch expansion, and (3) a fixed appliance treatment for the permanent dentition. We initiated the treatment with the use of the removable expansion plate for the maxillary dental arch expansion. No obvious problems have been observed in treatment response of the patient so far.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [15.1, 'kg'], 'height': [112.3, 'cm']}",11.9734,11.37473,12.57207,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 112.3 cm, which is 112.3 cm * 1 m / 100 cm = 1.123 m. The patient's weight is 15.1 kg. The patient's bmi is therefore 15.1 kg / (1.123 m * 1.123 m) = 11.9734 kg/m^2."
2283,6,Body Mass Index (BMI),physical,decimal,pmc-6805605-1,Extracted,"The patient was a 28-year-old man who had developed NS at the age of 5 years. Renal biopsy was performed, and it showed no glomerular lesions. In addition, immunofluorescence (IF) disclosed no immunoglobulin and complement deposition. He was pathologically diagnosed with MCD, for which he received various immunosuppressive drugs including steroid pulse therapy, mizoribine, cyclosporine, cyclophosphamide, and mycophenolate mofetil for FRNS. However it had been difficult to maintain long-term remission. Twenty-one times of recurrences had occurred before having a tonsillectomy, and more than half of them were triggered by tonsillitis. He was diagnosed by an otolaryngologist with chronic tonsillitis, as he had four or more episodes of acute tonsillitis a year, and bilateral palatine tonsillectomy was performed for chronic tonsillitis to reduce the recurrence of tonsillitis. Informed consent for the operation was obtained from the patient. On admission, his height was 161.5 cm, body weight was 60.6 kg and blood pressure was 118/64 mmHg. No abnormality was observed on general physical examination. Urinalysis showed urine specific gravity of 1.021 and pH of 7.5. By urinary qualitative, urine protein and occult blood were negative. Urinary protein level was 0.02 g/day; β2-microglobulin was 139 μg/day. His blood urea nitrogen was 15.0 mg/dL, albumin was 4.0 g/dL, creatinine was 0.59 mg/dL, and cystatin C was 0.69 mg/L. Immunoglobulin and complement levels were normal.
The pathological findings of the tonsils are shown in Fig. . The lymphoid follicles and germinal centers were observed various sizes. The boundary of each follicle was unclear and the distance between follicles was expanded. T-cell nodules were enlarged due to infiltration of CD4+ cells. Abnormal reticulation of the crypt epithelium was observed by cytokeratin staining. Peripheral blood CD4 + CD25+ Treg count increased from 379/μL to 444/μL between 2 months pre and post tonsillectomy. After the tonsillectomy, the patient was followed up for 3 years, and the average number of recurrences of NS per year decreased from 1.1 times to 0.33 times.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.6, 'kg'], 'height': [161.5, 'cm']}",23.23419,22.07248,24.3959,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 161.5 cm, which is 161.5 cm * 1 m / 100 cm = 1.615 m. The patient's weight is 60.6 kg. The patient's bmi is therefore 60.6 kg / (1.615 m * 1.615 m) = 23.23419 kg/m^2."
2284,6,Body Mass Index (BMI),physical,decimal,pmc-6506424-1,Extracted,"The first patient was a 16-year-old female (height: 1.58 m, weight: 41.7 kg) with a recent diagnosis of CD, who two days prior had received her first infusion of infliximab. She was admitted to the gastroenterology service for severe abdominal pain which began that morning. The patient was unable to tolerate anything by mouth due to severe nausea. At that time, the grayscale US demonstrated a narrowing of the terminal ileum, with a thickened submucosal layer and decreased peristalsis. Contrast US showed avid contrast enhancement of the narrowed terminal ileum. Quantitative evaluation of the terminal ileum, compared to the jejunum as an internal control, demonstrated more prompt wash-in, higher peak intensity, and higher area under the curve. The kinetic perfusion parameters are reported in . Average elastography value of the terminal ileum was 0.64 m/s. MRE demonstrated wall thickening and inflammation in the terminal ileum, resulting in narrowing and proximal dilation in the distal ileal segments. Adjacent to the terminal ileum, there was mesenteric inflammation as evidenced by contrast enhancement (). Given the patient's MRE findings and her clinical improvement with a second infusion of infliximab, her flair was determined to be acute inflammation.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [41.7, 'kg'], 'height': [1.58, 'm']}",16.70405,15.86885,17.53925,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.58 m. The patient's weight is 41.7 kg. The patient's bmi is therefore 41.7 kg / (1.58 m * 1.58 m) = 16.70405 kg/m^2."
2285,6,Body Mass Index (BMI),physical,decimal,pmc-5417292-1,Extracted,"Patient 2 is a 10-year-old girl born to a 37-year-old mother and a 39-year-old father. Parents are healthy and nonconsanguineous. The mother had a healthy son 13 years before. She also had a spontaneous abortion. For his part, the father also had a healthy daughter 13 years before. A daughter of a mother’s sister has epilepsy, otherwise the family history is unremarkable. The patient was born in the 39th week of gestation with a birth weight of 2620 g (percentile 3-10) and a height of 48 cm (percentile 10-25). The cranial perimeter at birth and the Apgar scores are not known. Early neuromotor development is referred as normal or lightly slow, sitting at 6 to 7 months of age and walking at 16 to 17 months of age. However, a slower development of speech was noted, and first words appeared at 30 months of age. Otherwise her general health is good; she had only frequent upper respiratory tract infections in the first 3 years of life requiring no hospitalization. At the age of 4.5 years, she was first assessed in a neuropediatric setting because of poor attention and hyperactive behavior. A mild neurodevelopmental delay was found. At the age of 6.5 years, she showed difficulties with learning to read. In a neuropsychological assessment at the age of 7 years, she showed intellectual performances at the level of the average and low reading performances for her age, and a specific reading disability was suspected. Moreover, short attention span, increased motor activity, and oppositional and defiant behavior were observed. A specific reading rehabilitation was started. She was newly reassessed at the neuropediatric setting at the age of 9.5 years. She attended regular school with curriculum adaptation; she was not yet able to read appropriately. On examination, her weight was 26.3 kg (percentile 3-10), her height was 130.5 cm (percentile 10-25), and her cranial perimeter was 52 cm (percentile 50). Except a mild clinodactyly of the fifth fingers, she showed no dysmorphic features. She had a high-arched palate. General examination showed no more anomalies. Neurological examination only showed poor motor coordination without ataxia and speech, with poor morphosyntactic skills and some difficulties in pronunciation. Ear, nose, and throat assessment was normal. Electroencephalography and brain magnetic resonance imaging performed at the age of 9.5 years showed no abnormality. Multiplex Ligation-dependent Probe Amplification analysis for the Xq28 region (SALSA P015-E1, P049-B2, and P061-B2 probemix by MRC-Holland) showed a de novo duplication including the gene MECP2 and a part of the gene FLNA. This was confirmed by 400 k array comparative genomic hybridization analysis that showed a 350 kb duplication including 8 MIM genes: IRAK1 (until exon 13), MECP2, OPN1LW, TEX28, TKTL1, FLNA, EMD, and RPL10 (). Due to the small size of the duplication, karyotype was normal. Fluorescent in situ hybridization showed no signal on autosomal chromosomes. Likewise, microsatellite analysis did not report information on the origin of the duplicated chromosome X. A random X chromosome inactivation with a ratio of 45:55 was demonstrated.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [26.3, 'kg'], 'height': [130.5, 'cm']}",15.44311,14.67095,16.21527,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 130.5 cm, which is 130.5 cm * 1 m / 100 cm = 1.305 m. The patient's weight is 26.3 kg. The patient's bmi is therefore 26.3 kg / (1.305 m * 1.305 m) = 15.44311 kg/m^2."
2286,6,Body Mass Index (BMI),physical,decimal,pmc-8212948-1,Extracted,"A previously healthy 7-year-old female child presented with skin lesions, suggestive of impetigo, in her lower limbs and buttocks, which progressed after 2 weeks with asthenia, loss of appetite, generalized edema, macroscopic hematuria, and oliguria. At admission, her anthropometric evaluation revealed weight: 22 Kg (z-score: 1), height: 122 cm (z-score: 1) and her blood pressure was 120/90 mmHg (stage 2 hypertension). At this time, the patient was hospitalized in her home city and diagnosed with an acute post-infectious glomerulonephritis. Laboratory findings that corroborated the diagnostic were a serum creatinine 3.5 mg/dL, anti-streptolysin O 1010.4 IU/mL, anti-deoxyribonuclease B 711 U/mL, normal complement, nephrotic proteinuria (3,864 mg/24 H−138 mg/kg/24 H), urine analysis with hematuria (60 red blood cells per field) and leukocyturia (26 white blood cells per field), positive antinuclear antibody 1:160 with a fine speckled pattern and reagent nucleus, and negative hepatitis B, C, and HIV serology. At that time, there were no reports of patient contact with other persons positive for SARS-CoV-2 infection.
During her hospital stay, the patient was evaluated by a nephrologist, who conducted the case as a post-infectious glomerulonephritis. She received supportive treatment that included diuretics, anti-hypertensive drugs, low sodium diet and water restriction, even in the setting of laboratory tests showing a progressive worsening of renal function. The patient undergone clinical deterioration 20 days after hospitalization, with fever, tachycardia, and mild tachypnea (respiratory rate ranging between 36 and 40 irpm), but with no need for supplementary oxygen therapy. The renal dysfunction was maintained, however, without abnormalities in diuresis and electrolyte/acid-base balance. Chest computed tomography showed bilateral ground-glass opacities diffusely distributed with consolidated areas in the right lung (). At this point, the patient was transferred to a tertiary hospital handling suspected COVID-19 cases. Due to the favorable epidemiological context for SARS-CoV-2 infection and a compatible clinical and radiological condition, the patient received the institutional treatment protocol for SARS-CoV-2 infection (chloroquine 8.5 mg/kg/dose and azithromycin 10 mg/kg/dose, for 5 days). Reverse transcriptase polymerase chain reaction (RT-PCR) for SARS-CoV-2 was positive in two samples.
On the 24th day of hospitalization, the patient started on hemodialysis due to progressive worsening of renal function and reduced urine output, poorly responsive to diuretics. Laboratory tests showed a urea level of 248 mg/dL, creatinine level of 6.59 mg/dL, and serum potassium level of 6.5 mmol/L. The patient's general clinical condition improved, however, renal dysfunction and oligoanuria remained. After the infection was under control, pulse therapy with methylprednisolone (30 mg/kg/dose for 3 days) was started on the 34th day of hospitalization due to the clinical and laboratory suspicion of rapidly progressive glomerulonephritis.
Some laboratory tests used for the etiological clarification of acute kidney injury (AKI) were noteworthy, such as a positive anti-nuclear factor (ANA) test with a fine speckled pattern and reagent nucleus at a titration of 1:160, positive direct coombs test, serum albumin level of 3.3 g/dL, urine 1 microscopic hematuria, a urine protein/creatinine ratio > 2, normal levels of serum complement fractions, a non-reactive perinuclear anti-neutrophil cytoplasmic antibody, negative anticardiolipin IgG and IgM, negative lupus anticoagulant test, non-reactive beta-2-glycoprotein I IgG and IgM, non-reactive anti-Smith, non-reactive anti-native DNA, lactic dehydrogenase level of 497 U/L, transient thrombocytopenia (ranging between 96,000 and 116,000/mm3) between days 28 and 31 of her hospital stay. Ultrasound of the kidneys and urinary tract showed normal-sized kidneys with acute nephropathy.
Nineteen days after the diagnostic confirmation of SARS-CoV-2 infection, the patient developed fever (38.3°C), abdominal pain, nausea, vomiting, and moderate respiratory distress (respiratory rate 50 irpm, moderate respiratory effort, and oxygen saturation of 90%). She required oxygen therapy with a concentrating oxygen mask at 5 liters/min. The following findings were highlighted in the clinical decompensation investigation: increased cardiac area on chest X-ray, inflammatory marker changes (ferritin 1,819 ng/ml; D-dimer 10,000 ng/mL), increased cardiac injury markers (peptide natriuretic type B 749 pg/mL; troponin 0.87 ng/mL), and positive blood culture for Acinetobacter spp. Echocardiography showed dilation of the left coronary artery trunk (), corroborating the diagnosis of Multisystemic Inflammatory Syndrome in Children (MIS-C) with a “Kawasaki-like” disease.
The patient was immediately treated with a single dose of human immunoglobulin (2 g/kg), acetylsalicylic acid (50 mg/kg/dose for 6 weeks), and broad-spectrum antibiotic therapy due to the bloodstream infection. Five days after starting treatment, the patient had clinical improvement and cardiac injury marker normalization. A coronary artery computed tomography angiography performed 80 days after the immunoglobulin infusion excluded left coronary artery dilation, thus showing cardiac injury recovery and immunoglobulin therapy responsiveness.
However, even with resolution of the infectious context and cardiac decompensation, renal dysfunction and anuria remained, and the patient needed dialysis therapy. A renal biopsy was performed 70 days from admission and revealed 23 glomeruli, all of which were globally sclerotic or in almost global sclerosis, most with fibrous or fibro-cellular growth, and six had capillary tuft necrosis. Some arterioles had concentric wall hyperplasia, while others had endotheliosis. Immunofluorescence showed 12 glomeruli under study conditions with the following findings: IgG ++, IgA +, IgM ++, C3 ++, fibrinogen ++, kappa ++, lambda ++, and C1q ++, which was compatible with “Full-House” Nephropathy, thrombotic microangiopathy and advanced chronic kidney disease (). A possible differential diagnosis for the renal condition is class VI Lupus Nephritis, hence, Systemic Lupus Erythematosus (SLE), however this diagnosis may not be stablished since the other criteria may be related to COVID-19 infection.
After clinical improvement of Covid-19 complications and resolution of the investigation of renal disease, the patient was discharged after 125 days of hospitalization for treatment of chronic kidney disease requiring hemodialysis therapy three times a week, and no evidence of renal function recovery.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [22.0, 'kg'], 'height': [122.0, 'cm']}",14.78097,14.04192,15.52002,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 122.0 cm, which is 122.0 cm * 1 m / 100 cm = 1.22 m. The patient's weight is 22.0 kg. The patient's bmi is therefore 22.0 kg / (1.22 m * 1.22 m) = 14.78097 kg/m^2."
2287,6,Body Mass Index (BMI),physical,decimal,pmc-5818770-1,Extracted,"A 41-year-old man (height 171.5 cm, body weight 67 kg) was transferred to the regional medical center due to right hemiplegia and aphagia. Cerebral magnetic resonance imaging revealed cerebral infarction caused by occlusion of the left middle cerebral artery, while cerebral magnetic resonance angiography showed the development of a network of abnormal collateral vessels. Hence, the patient was diagnosed with MMD.
Before cerebral revascularization surgery, severe MR (III/IV) due to the prolapse of the P2 leaflet in the mitral valve was indicated by transthoracic echocardiography. Cardiac catheterization indicated elevated pulmonary arterial pressure (PAP) (systolic/diastolic/mean: 86/33/60 mmHg) and pulmonary capillary wedge pressure (32 mmHg) at the systemic arterial pressure of 120/83/102 mmHg. Hence, the patient was admitted to our university center for the surgical treatment of MR.
Preoperative single-photon emission computed tomography revealed reduced cerebral blood flow in the left cerebral hemisphere (especially in the external left frontal cortex; Fig. ). Neurosurgeons at our center judged that the patient did not have an indication for cerebral revascularization surgery, which is used to prevent ischemic complications during the perioperative period of mitral valve plasty. This was because his left frontal lobe showed extensive cerebral infarction and no cerebral infarction symptoms were observed in the right cerebral hemisphere. Therefore, mitral valve plasty without cerebral revascularization was chosen.
In the operation room, the patient’s monitoring of electrocardiogram, oxygen saturation, systemic arterial pressure via right radial artery catheter, bispectral index, and regional cerebral oxygen saturation (rSO2) at the right and left forehead (INVOS™ 5100C, Somanetics, USA) was initiated before the administration of general anesthesia. The rSO2 values for the left and right forehead were 72 and 81 %, respectively.
General anesthesia was induced by intravenous administration of 3 mg of midazolam, 0.4 mg of fentanyl, and 50 mg of rocuronium. After tracheal intubation, a transesophageal echocardiography (TEE) probe was inserted. Then, a central venous catheter and right heart catheter were inserted via the right internal jugular vein, and central venous pressure, PAP, cardiac output, and mixed venous oxygen saturation were measured. The nasopharyngeal temperature and urinary bladder temperature were also measured.
Before CPB, general anesthesia was maintained by inhalation of sevoflurane (1–1.5 % of end-tidal concentration). The patient’s PaCO2 was maintained between 38 and 42 mmHg. Intra-aortic balloon pumping (IABP) was placed at the start of surgery and the augmented pressure was maintained. The mean arterial pressure was constantly above 70 mmHg. Before CPB, rSO2 values were almost above 80 % on both sides (Fig. ).
During CPB, administration of sevoflurane via the oxygenator was also continued because of its cerebrovascular dilatation activity and potential preconditioning effect against focal cerebral ischemia. PaCO2 was maintained between 45 and 50 mmHg, and alpha-stat management of pH was performed. Hypothermia was induced; the temperature at the bottom of the nasopharyngeal temprature was 28 °C. We used pulsatile perfusion assist to maintain cerebral circulation during CPB with IABP. A decrease in rSO2 was observed 162 min after the initiation of CPB. Our perfusionist increased the CPB pump flow from 2.2 L/min/m2 to 2.8 L/min/m2 in order to increase cerebral blood flow. Moreover, the concentration of sevoflurane was increased to 2 %. Yet, rSO2 desaturation (15 % reduction from baseline) was not improved. We decided to increase the depth-of-anesthesia with another dose of midazolam. After administration of 3 mg of midazolam, the rSO2 values increased from 67 to 73 % on the right side and from 71 to 74 % on the left side. During CPB, the lowest values (and variation) of rSO2 in the left and right forehead were 71 % (−2 %) and 67 % (−17 %), respectively. Mitral valve plasty was performed as planned.
At the weaning from the CPB, the disappearance of MR was confirmed by TEE; the weaning was not difficult. Pulmonary hypertension also improved (PAP was 26/12 mmHg, while systemic arterial pressure was 105/56 mmHg). After CPB, inhalation of sevoflurane (1–1.5 % of end-tidal concentration) was also continued. The rSO2 values were almost above 75 % on both sides and not below the awake rSO2 values (Fig. ). CPB and aortic cross-clamping lasted 352 min and 289 min, respectively. On the completion of the surgery, the IABP was discontinued and sevoflurane administration was stopped. The patient was transferred to the intensive care unit with ventilator support under propofol sedation.
On the 1st postoperative day (POD), the patient was weaned from the ventilator, and the patient did not complain about any new neurological deficits. We monitored the rSO2 of his forehead until the 2nd POD and no significant decrease (−20 %) of the rSO2 values was confirmed. The postoperative course was uneventful. On the 15th POD, single-photon emission computed tomography revealed that the low cerebral blood flow lesions had not changed (Fig. ), and the patient was discharged from our hospital on the 16th POD.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [67.0, 'kg'], 'height': [171.5, 'cm']}",22.77962,21.64064,23.9186,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 171.5 cm, which is 171.5 cm * 1 m / 100 cm = 1.715 m. The patient's weight is 67.0 kg. The patient's bmi is therefore 67.0 kg / (1.715 m * 1.715 m) = 22.77962 kg/m^2."
2288,6,Body Mass Index (BMI),physical,decimal,pmc-7763634-1,Extracted,"The patient, a boy 1 year and 4 months old, was born from a second pregnancy. The first pregnancy ended in miscarriage. The patient was a single birth to nonconsanguineous, healthy parents. His pedigree was unremarkable. Written informed consent was obtained from the parents of the patient for the publication of the clinical data and pictures. The study was approved by the local Research Ethics Committee of the Research Institute of Medical Genetics, Tomsk NRMC (no. 106 from 27 June 2017).
The patient was born at the 38th week of gestation. His birth weight was 2720 g (3–10th centile), birth length was 48 cm (10th centile), head circumference was 31 cm (<3rd centile), and chest circumference was 31 cm (3rd centile). His Apgar score was 8. Preauricular tag of the left ear, curvature of the nasal septum to the left, and pectus excavatum of the right foot were observed at birth. The early development of the child showed pronounced delays.
When the boy was 1 year old, echoencephalography showed ventriculomegaly, and echocardiography revealed a small heart abnormality, patent foramen ovale. When the patient was 1 year and 4 months of age, his height was 80 cm (75th centile), his weight was 8.6 kg (3rd centile), and his head circumference was 40.5 cm (<3rd centile). His constitution was disproportionate and asthenic. There was a severe delay in neuropsychological development. The boy could not stand up or remain standing on his own and walked only with bilateral support; he did not sit on his own but remained seated when already sitting. His gait was hesitant, and he slightly tightened his left leg (extra step). The patient held his posture weakly, i.e., his back was rounded. He did not crawl or turn over while lying on his stomach, and his support when on his hands was weak. A more detailed clinical description of the patient at the time of cytogenetic analysis is shown in .
At the time of last examination, the boy was 2.5 years old (). He had dolichocephaly, narrowing of the skull in the temporal areas, an elongated face, bushy eyebrows, long eyelashes, conjunctivitis, abnormal ears with a preauricular tag of the left ear, macrotia, a high and narrow nasal bridge with a broad nasal tip, a short and broad philtrum, hypotonia of the mandible, micrognathia, an open mouth, thick lips, widely spaced teeth, and motor alalia. The child swallowed only liquid food. Gastroesophageal reflux was constantly present. The tone of the chewing and temporal muscles was reduced, as were facial movements. There were problems with fine motor skills. The patient walked with support only, and the gait was abnormal. Contact with the child was difficult, as there were periods of increased excitability, and the child was unemotional.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [8.6, 'kg'], 'height': [80.0, 'cm']}",13.4375,12.76562,14.10938,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 80.0 cm, which is 80.0 cm * 1 m / 100 cm = 0.8 m. The patient's weight is 8.6 kg. The patient's bmi is therefore 8.6 kg / (0.8 m * 0.8 m) = 13.4375 kg/m^2."
2289,6,Body Mass Index (BMI),physical,decimal,pmc-4166849-1,Extracted,"A 7-month-old male was brought with developmental delay. He was born to nonconsanguineous parents, mother aged 36 years and father aged 38 years, with three normal elder daughters. The fourth baby was a male, who died 6 h after birth. He had dysmorphism, and the parents were told that the baby had some genetic disorder. However, no documentation of dysmorphic features or karyotype was available. The fifth pregnancy, 1-year later, was a spontaneous abortion at 3 months gestation.
The proband was conceived as the sixth pregnancy. The family came to medical attention at 23 weeks 3 days of pregnancy when an ultrasound had detected bilateral club feet, thickened nuchal skin fold, cerebral ventriculomegaly, hypoplastic cerebellum, unilateral right renal pelviectasis. The findings suggested chromosomal anomaly and amniocentesis was done for fluorescent in-situ hybridization for chromosome 21 and karyotype analysis. The fluorescent in-situ hybridization for chromosome 21 showed two signals in each cell. Karyotype showed an “extra genetic material” on a long arm of chromosome 6 []. The parents were counseled about the risk of mental retardation in the baby and were advised to undergo chromosomal analysis. They, however, decided to continue the pregnancy in view of advanced gestational age.
At term, the mother went into labor. Fetal distress was detected in the form of fetal bradycardia and meconium stained liquor. The baby was delivered by a lower segment cesarian section. He cried immediately at birth. He developed fast breathing and received oxygen and intravenous fluids. He improved gradually and was discharged after 6 days. There was no history of seizures, encephalopathy, or jaundice in the neonatal period.
He developed social smile at 3 months, and was recognizing his mother and reaching out for objects at the time of presentation. He had achieved partial neck holding. Vision and hearing were normal. There was no history of seizures.
On examination, the infant had an abnormal posture with his legs in abducted and flexed position. He weighed 7.5 kg (<25th centile for age), measuring 72.5 cm in crown-heel length (>75th centile for age). The child had microcephaly (head circumference of 40 cm, <−3 standard deviation). He had facial asymmetry, strabismus involving the left eye, narrow down-slanting palpebral fissures, prominent nose, overhanging columella, long philtrum, small pointed chin, midline crease in the lower lip and high arched palate []. He also had club feet, and long tapering fingers, with middle finger being overlapped by other fingers. The neurological and systemic examination was normal.
Investigations revealed a normal hemogram, liver, and kidney function tests. Ultrasonographical evaluation of the abdomen revealed no abnormality. Magnetic resonance imaging of the brain revealed mild thinning of the corpus callosum without any other abnormalities. Echocardiography was normal.
Karyotype analyses of parents were carried out in view of previous sibling death with dysmorphism and history of spontaneous abortion in mother. Father's karyotype was normal. Karyotype of the mother revealed a balanced translocation between chromosomes 6 and 15; t (6;15)(q26;q22) [].
From the above dysmorphic features, physical findings and the patient's and his mother's karyotype, a diagnosis of partial trisomy of chromosome 15 (q22 → qter) due to balanced translocation in the mother was made. As the child inherited the derivative chromosome 6 from the mother, it was clear that, he also had terminal deletion of 6q (q26 and q27). The child was started on physical and occupational therapy.
Genetic counseling was provided to the family. The family was able to understand that the anomalies and developmental delay are due to the chromosomal imbalances in the affected child. They also were able to understand that the chromosomal anomaly in this child and probably some of the previous pregnancy losses are related to the balanced translocation in one of the parents. The recurrence risk and availability of prenatal testing early in pregnancy has been explained. Other reproductive options like use of a donor ovum have also been discussed. The importance of extended family screening for the same balanced translocation on the mother's side; and its importance for the prevention of recurrences in the extended family has been explained.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [7.5, 'kg'], 'height': [72.5, 'cm']}",14.26873,13.55529,14.98217,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 72.5 cm, which is 72.5 cm * 1 m / 100 cm = 0.725 m. The patient's weight is 7.5 kg. The patient's bmi is therefore 7.5 kg / (0.725 m * 0.725 m) = 14.26873 kg/m^2."
2290,6,Body Mass Index (BMI),physical,decimal,pmc-3136071-1,Extracted,"A 14-year-old female was referred to cytogenetic laboratory for chromosomal analysis because of primary amenorrhea and short stature. The proband is the first born to the consanguineous parents. Her height was 122 cm (<third centile) and weight 23 kg (<third centile). She had absence of secondary sexual characters. Ultrasonography revealed hypoplastic uterus and ovaries. X-ray of right wrist and hand, right forearm revealed fused carpel bone centers, which is suggestive of bone age of 10 years. Hormonal evaluation showed elevated levels of FSH (65.91 mIU/ml) and reduced levels of LH (22.31 mIU/ml). Her prolactin and thyroid profile were within normal limits. The mother's age at the time of birth was 20 years and father was 24 years. Parental reproductive history showed no family history of abortions, bad obstetrics history and children with mental retardation. The proband has three siblings including one younger sister and two younger brothers.
Cytogenetic study was carried out from proband, siblings and parents. Chromosomal preparation obtained from PHA-M stimulated peripheral blood cultures using standard procedure. Chromosomal preparations were subjected to GTG-banding and karyotyped according to ISCN 2005.[] At least 50 well spread and good-banded metaphases were scored in each case. Chromosomal analysis of the proband revealed 45,X, rob(13;14)(q10;q10),inv(9)(p13q33),i(Xq) (qter---q10::---qter) [Figure and ]. Father's karyotype was 45,XY,rob(13;14)(q10;q10),inv(9)(p13q33) 
[Figure and ]. Both the male siblings karyotype was same as father's karyotype i.e. 45,XY,rob(13;14)(q10;q10),inv(9)(p13q33). Proband's younger sister's chromosomal analysis was 46,XX,inv(9)(p13q33). Mother's chromosomal analysis revealed normal karyotype. Fluorescence in situ hybridization (FISH) was performed using centromeric probe (14/22, X) and partial chromosome paint (PCP) (Xq, 9q) [Figure ]. The FISH results confirmed iso(Xq) with PCP Xq probe and inv(9) with PCP.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [23.0, 'kg'], 'height': [122.0, 'cm']}",15.45284,14.6802,16.22548,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 122.0 cm, which is 122.0 cm * 1 m / 100 cm = 1.22 m. The patient's weight is 23.0 kg. The patient's bmi is therefore 23.0 kg / (1.22 m * 1.22 m) = 15.45284 kg/m^2."
2291,6,Body Mass Index (BMI),physical,decimal,pmc-7463145-4,Extracted,"A girl named S, 15 years old, with osteosarcoma, 3rd day of care. At the time of assessment, according to her mother, the child had complained of fever for three days. The peak fever was 38°C. Fever complaints were accompanied by nausea and vomiting twice. The mother also said that the child was having difficulty accepting the condition of her body, walking with crutches. The child did not talk much or tell stories. The child seemed introverted and did not want to communicate other than with her family; that is, her mother. The child lacked in support from peers and siblings because she was far from home. The results of the study also found that there were surgical wounds on the child’s right knee that had healed. The wounds were dry and not covered in gauze. The child had alopecia. Hb: 10 gr/dL, Ht: 30%, leukocytes 3000/mm3, platelets: 264,000/mm3, ANC: 306/mm3, Humpty Dumpty score was 9 (low risk), BP: 126/91 mmHg, HR: 95 x/minute, RR: 18 x/minute, body temperature 37.60°C, SpO2: 98%, BW: 41 kg, BH: 146 cm, LLA: 22.5 cm, malnutrition. The child’s hydration status was adequate, with a positive fluid balance and without any signs of overload. The child’s rest and sleep statuses were adequate.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [41.0, 'kg'], 'height': [146.0, 'cm']}",19.23438,18.27266,20.1961,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 146.0 cm, which is 146.0 cm * 1 m / 100 cm = 1.46 m. The patient's weight is 41.0 kg. The patient's bmi is therefore 41.0 kg / (1.46 m * 1.46 m) = 19.23438 kg/m^2."
2292,6,Body Mass Index (BMI),physical,decimal,pmc-4384410-1,Extracted,"A 35-year-old female (weight, 65 kg; height, 159 cm) was scheduled to undergo a planned repeat CS. She had undergone a CS under spinal anesthesia 2 years previously. Her medical history revealed no seizures or other neurological disorder during her current or previous pregnancies. Preoperative evaluation revealed no remarkable risk factors such as hypertension or glucose intolerance. Thus, the patient was considered to have an American Society of Anesthesiologists physical status of I during the preoperative consultation, and a combined spinalepidural anesthesia technique was planned. The patient was not premedicated. Monitoring involved electrocardiography, noninvasive blood pressure, and pulse oximetry. Body temperature was monitored by a thermistor equipped at the top of a urinary catheter.
With the patient fully awake, the epidural catheter was placed at the T12/L1 space, and a spinal tap was performed at the L2/L3 space with a 25-G Quincke needle in the left lateral decubitus position after skin sterilization with 0.5 w/v% chlorhexidine gluconate/ethanol. After backflow of clear cerebrospinal fluid, 12.5 mg of hyperbaric 0.5% bupivacaine without preservatives (AstraZeneca, Osaka, Japan) with 15 µg of fentanyl (Janssen Pharmaceuticals) were injected into the subarachnoid space. The patient was then placed in the supine position. Discernible sensory block to cold sensation was promptly observed. Finally, before the start of the surgical incision, a sensory block to cold to the T3 level with accompanying motor block was obtained. Vasopressors, including 8.0 mg of ephedrine and 0.6 mg of phenylephrine, were administrated to maintain systolic blood pressure at >100 mmHg during the operation. In total, 900 ml of a crystalloid and 500 ml of a colloid were administrated intravenously.
The surgical procedure proceeded uneventfully, and a live male infant and placenta were delivered 9 and 11 min after skin incision, respectively. All other surgical findings were unremarkable, and routine antibiotics and uterotonic oxytocin were administered. No drugs were administered into the epidural space. Because no hypnotics were used for sedation, the patient was awake during the operation.
The operation was completed 1 h 10 min after the spinal tap. At the time of completion, involuntary movements began ( and ). The movement was observed in both upper extremities, but the movement of the left side was more pronounced (). No remarkable vital sign changes were observed before or during the movement. The patient's systolic blood pressure, diastolic blood pressure, and heart rate were 105 mmHg, 74 mmHg, and 87 beats/min before the beginning of the movement and 110 mmHg, 69 mmHg, and 93 beats/min immediately after the beginning of the movement, respectively. The sensory block to cold subsided to the T8 level, and sensory and motor functions in her upper extremities were intact. The patient was fully conscious, calm, and responsive. She complained that she could not stop the movement. She did not complain that she felt cold. The body temperature at her bladder was 36.8℃, and no coldness of the upper extremities was observed. Because she was alert and in a calm mental state, she was untreated until examination by a neurologist. After the examination, 2 mg of midazolam were administered after 33 min of involuntary movement. Three minutes after administration, the involuntary movement stopped ().
The patient was subsequently transferred to the ward, and the involuntary movement did not recur. Five hours after the surgery, the spinal block had completely subsided. No abnormal sensation or spontaneous pain of the upper or lower extremities was observed. The patient was discharged on foot on postoperative day 3.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [65.0, 'kg'], 'height': [159.0, 'cm']}",25.71101,24.42546,26.99656,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 159.0 cm, which is 159.0 cm * 1 m / 100 cm = 1.59 m. The patient's weight is 65.0 kg. The patient's bmi is therefore 65.0 kg / (1.59 m * 1.59 m) = 25.71101 kg/m^2."
2293,6,Body Mass Index (BMI),physical,decimal,pmc-8036176-1,Extracted,"In the first case, a 77-year-old man was found dead in the sauna of his family home. It was suspected that the body had been lying in the sauna for about 3 days. A craftsman had been unable to meet the owner of the house several times on the agreed date and alerted the emergency services. When the man was found, the sauna door was closed, and the sauna showed a temperature of 78 °C. The upper body was lying on the right side of the first bench with the legs stretched out in the middle of the sauna. The body had already begun to decay and the skin was partially mummified. The man was a recovered alcoholic, and no other previous illnesses were known.
The autopsy was conducted promptly. The man had a body weight of 73 kg and a body length of 179 cm. The autopsy revealed an advanced decayed body with partly leather-like dried skin (Fig. ). The assessability of the internal organs was considerably limited because of the putrefaction and heat-related hardening and dehydration. Moderate general arteriosclerosis and coronary sclerosis, thickening of the left ventricular wall (approx. 2 cm) as a sign of arterial hypertension, cholecystolithiasis, and gastritis were found. The spleen was already liquefied. There were no indications for death-related violence. Histological examinations of the heart tissue showed a fatty degeneration of the myocardium and coronary sclerosis. Irregular enlargement of the myocytes and areas of myocardial fibrosis could also be detected.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [73.0, 'kg'], 'height': [179.0, 'cm']}",22.78331,21.64414,23.92248,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 179.0 cm, which is 179.0 cm * 1 m / 100 cm = 1.79 m. The patient's weight is 73.0 kg. The patient's bmi is therefore 73.0 kg / (1.79 m * 1.79 m) = 22.78331 kg/m^2."
2294,6,Body Mass Index (BMI),physical,decimal,pmc-6449622-1,Extracted,"A 13-year-old male patient presented with complaints of new-onset polydipsia, excessive urination, and weight loss. The patient stated he had lost 7 kg over a period of 2 months. His past medical history included neurosensory hearing loss from birth and patent ductus arteriosus that was discovered at three months of age in the Pediatric Cardiology Department. He had no response to voice warnings at 3 months of age, and his neurosensory hearing loss was diagnosed with an auditory brainstem evoked responses test. In addition, the patient was followed by the Child and Adolescent Psychiatry Department due to behavioral problems and learning disabilities; he had been diagnosed with autistic spectrum disorder. There was no kinship between his parents. The patient's mother had a fever and a red rash on her face during the second trimester of pregnancy, although she was not diagnosed with rubella infection at that time.
On physical examination, the patient's weight was 42.7 kg (25th–50th percentile), height was 153.2 cm (25th–50th percentile), and his head circumference was 46 cm (<3rd percentile). A 2/6 cardiac murmur and hearing aid were noted. Laboratory examinations revealed blood glucose was 619 mg/dL, urine ketone was +3, blood gas showed metabolic acidosis (pH, 6.92; HCO3, 4 mEq/L; PaCO2, 24 mmHg), insulin was 4.1 IU/mL (range, 2–18 IU/mL), and serum C-peptide level was 1.23 ng/mL (range, 1.1–4.4 ng/mL). The patient's glycosylated hemoglobin value was 15.9%, anti-insulin antibody was 0.78 U/mL (range, 0–0.5U), anti-GAD was 22.8 U/mL (<1U/mL), and the islet cell antibody was positive. Orbital magnetic resonance imaging demonstrated no optic atrophy and normal optic nerve thickness, so Wolfram syndrome was excluded. In addition, genetic analysis for Wolfram's syndrome was normal.
The patient was diagnosed with immune-mediated type I DM, and intravenous fluid and insulin therapy were started according to the degree of dehydration. After the patient's metabolic acidity was corrected and blood glucose regulation was achieved, his medication was switched to subcutaneous insulin therapy 1.2 units/kg/day. Considering the patient’s patent ductus arteriosus, microcephaly, and neurosensory hearing loss, his immune-mediated type 1 diabetes was thought to be associated with a congenital rubella infection following his mother’s febrile rash illness during pregnancy.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [42.7, 'kg'], 'height': [153.2, 'cm']}",18.19325,17.28359,19.10291,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 153.2 cm, which is 153.2 cm * 1 m / 100 cm = 1.532 m. The patient's weight is 42.7 kg. The patient's bmi is therefore 42.7 kg / (1.532 m * 1.532 m) = 18.19325 kg/m^2."
2295,6,Body Mass Index (BMI),physical,decimal,pmc-6213993-1,Extracted,"Our patient was a 4-year-old Italian boy who visited our pediatric hospital for incidental head trauma with a linear fracture of the right parietal bone and a small hematoma. He presented with a Glasgow Coma Scale of 15/15 and normal neurological testing. His weight was 21 kg (>97th percentile), height was 113 cm (>97th percentile), and head circumference was 54.5 cm (>97th percentile). The patient exhibited dysmorphic facial appearance with trigonocephaly, frontal bossing, large ears, prominent chin, and high palate with dental malposition. Physical examination of the skin found one “café-au-lait” spot on the right hemithorax (2 cm × 0.5 cm) and an irregular skin lesion with a rubbery consistency and fibrosis (3 cm × 4 cm) on the right femoral side. He also exhibited syndactyly of the second and third right toes and learning difficulties. He was born at full-term via caesarean section because of macrosomia. His birth weight was 4.050 g (>97th percentile). His parents were healthy and unrelated. His older brother was also healthy and had normal development. His grandfather died at the age of sixty to chronic lung disease ().",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [21.0, 'kg'], 'height': [113.0, 'cm']}",16.44608,15.62378,17.26838,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 113.0 cm, which is 113.0 cm * 1 m / 100 cm = 1.13 m. The patient's weight is 21.0 kg. The patient's bmi is therefore 21.0 kg / (1.13 m * 1.13 m) = 16.44608 kg/m^2."
2296,6,Body Mass Index (BMI),physical,decimal,pmc-8080403-1,Extracted,"A 45-year-old man with acute myeloid leukemia (AML-M5b) was subject to human leukocyte antigen-haploidentical relative HSCT for persistent minimal residual disease (MRD) (Fig. a). Apart from AML, the patient did not have any potentially relevant pre-existing conditions or medical treatments that may have impacted on bacterial colonization, clearance, or drug tolerance. The conditioning regimen comprised busulfan (0.8 mg/kg/q6h), cyclophosphamide (60 mg/kg/d), and semustine (250 mg/m2/d). Cyclosporin A, methotrexate, and mycophenolate mofetil were used for GVHD prophylaxis, and levofloxacin and cefotaxime/sulbactam were given for antimicrobial prophylaxis. Prior to conditioning therapy, carbapenem-resistant Klebsiella pneumoniae (CRKp) colonization, which has a high level of resistance to most routine antibiotics except for tigecycline (Additional file : Figure S1), was identified during routine rectal screening, while no decolonization strategies were performed. Six days after allo-HSCT, the patient developed neutropenic fever and the organism that grew in the blood culture was identified as CRKp which with the same resistance pattern as the previous one. CRKp bacteremia was successfully controlled by tigecycline. Hematopoietic stem cells were engrafted on day +11 and the patient discharged on day +20. During regular follow-up, the patient was in remission, but suffered chronic oral GVHD as it had not responded well to prednisone and tacrolimus. Thus, the patient remained in a very poor nutritional state, weighing approximately 45 kg (height = 168 cm).
A second fever episode was accompanied by chills, cough, and expectoration on day +421. On this occasion, lung computerized tomography (CT) suggested pulmonary infection, and sputum and stool cultures were both positive for CRKp. This confirmed previous susceptibility tests, although blood cultures were negative. Infection was controlled by administering an antibiotic therapeutic regimen, including tigecycline. However, sputum and stool cultures remained positive for CRKp, indicating persistent CRKp colonization. Based on the same resistance patterns, we speculated that they were the same strain. Moreover, a previous study indicated that most bacteremia cases originated from the gut [, ]. Thus, FMT was planned to reduce the risk of infection and improve future quality of life.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.0, 'kg'], 'height': [168.0, 'cm']}",15.94388,15.14669,16.74107,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 45.0 kg. The patient's bmi is therefore 45.0 kg / (1.68 m * 1.68 m) = 15.94388 kg/m^2."
2297,6,Body Mass Index (BMI),physical,decimal,pmc-3757812-1,Extracted,"A 24-year-old female Caucasian patient, 171 cm tall and weighing 60 kg, was to undergo bilateral breast augmentation, exchange of implants, and mammaplasty for bilateral breast ptosis and capsular contracture. Past medical history included bilateral breast augmentation in 2008 and abdominoplasty in 2007 after 90 kg weight loss, lower Cesarean section in 2004, and tonsillectomy as a child. She was otherwise well and did not take any regular medication. The pre-operative physical examination showed good neck extension and mouth opening, and a straightforward endotracheal intubation was anticipated. Two hours before the induction of anesthesia, she received chlorazepam 20 mg orally as premedication. General anesthesia was induced with fentanyl 0.1 mg and 200 mg propofol, and atracurium 25 mg was used to prevent laryngospasm during insertion of the endotracheal tube. At intubation, the Cormack and Lehane grade was described as 1, using a standard size 3 Macintosh blade. A 7.5-mm Magill tube was used. After intubation, proper placement of the endotracheal tube was confirmed by bilateral breath sounds. The endotracheal tube cuff was inflated with air until the cuff pressure was 30 cm H2O. During surgery, the patient received intermittent positive pressure ventilation with 67% nitrous oxide in oxygen, 0.8-1.2% isoflurane, supplemented with fentanyl 0.15 mg. The maximum endotracheal tube cuff pressure did not exceed 34 cm H2O. The patient was placed in a 30° elevated supine position and the head was supported in position with a donut-type pillow. Surgery was completed uneventfully within 90 min, blood loss was minimal, and fluid replacement was done with 1000 ml of full electrolyte solution Jonosteril (Fresnius, Bad Homburg, Germany) and 500 ml of conventional 6% hetastarch 130/0.4 (Tetraspan, B. Braun, Melsungen, Germany). No significant changes in cardiovascular or respiratory parameters occurred during the operation. When spontaneous respiration and muscle tone were considered to be adequate, the endotracheal tube was carefully removed and transferred to the recovery unit. After 35 min, the patient was discharged to the ward.
The next morning, she complained of slight difficulty in swallowing solid foods but was able to drink water. On clinical examination, her tongue deviated to the right on protrusion and she was unable to move it to the left; there were no further detectable cranial nerve abnormalities. Magnetic resonance imaging of her brain did not demonstrate any evidence of an ischemic event or focal abnormality. A neurologist diagnosed an isolated paralysis of the right hypoglossal nerve. The neurologist recommended supportive treatment and did not prescribe any pharmacological therapy. Two weeks post surgery, the patient attended the neurology out-patient clinic; at this time, she had complete resolution of symptoms and had made a complete recovery.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.0, 'kg'], 'height': [171.0, 'cm']}",20.51913,19.49317,21.54509,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 171.0 cm, which is 171.0 cm * 1 m / 100 cm = 1.71 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.71 m * 1.71 m) = 20.51913 kg/m^2."
2298,6,Body Mass Index (BMI),physical,decimal,pmc-8251549-2,Extracted,"Patient 2 was a 14-month-old boy who was born at 34 weeks gestation. He had been diagnosed at 34 weeks gestation with a head enlargement. His weight at birth was 2635 g (+2.1 SD), length was 47.5 cm (+1.6 SD), and head circumference was 35.3 cm (+3.0 SD). After birth, a head MRI showed polycerebral gyrus at parasylvius fissures, cortical dysplasia of bilateral cerebral hemisphere, partial myelination delay, and hypoplasia of corpus callosum (Figure ). He had mild congenital hearing impairment. An electrocardiogram and a renal echogram showed no anomalies. He showed distinctive dysmorphic features with high hairline, thick eyebrow, short nose, anteverted nares, long philtrum, thin upper-lip vermilion, and a retrognathia. His developmental milestones were delayed; he gained head control and rolling over at 8 months of age, sat without support at 11 months of age, and slithering at 1 year of age. He was able to stand with support at 1 year of age. At 1 year and 1 month of age, his weight was 10.42 kg (+0.3 SD), height was 81.0 cm (+1.9 SD), and head circumference was 52.0 cm (+3.9 SD).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [10.42, 'kg'], 'height': [81.0, 'cm']}",15.88173,15.08764,16.67582,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 81.0 cm, which is 81.0 cm * 1 m / 100 cm = 0.81 m. The patient's weight is 10.42 kg. The patient's bmi is therefore 10.42 kg / (0.81 m * 0.81 m) = 15.88173 kg/m^2."
2299,6,Body Mass Index (BMI),physical,decimal,pmc-6890279-1,Extracted,"A 20-year-old Japanese woman visited our institute for treating her scoliosis. She was a second-born child among dichorionic diamniotic twins. She had visited a pediatrics division at another hospital because she experienced restriction in the range of the motion in both elbow joints, and clubfoot. When the patient was 3 years old, she was diagnosed with focal segmental glomerulosclerosis due to proteinuria. At the age of 7 years, she was diagnosed with MCTO based on multiple osteolysis and a typical facial appearance associated with a small forehead and hypotelorism. At the age of 18 years, she underwent genetic testing; a MafB missense polymorphic mutation was identified, and a definitive diagnosis was established. Scoliosis was apparent since she was 12 years old, but she had not sought treatment until the age of 19. The patient weighed 38.6 kg and had a height of 155 cm. Medical examination showed a typical facial appearance associated with a small forehead and hypotelorism; shortening of the fingers of both hands fingers and both upper limbs were observed in addition to clubfoot. No café au lait spots or mental retardation were seen. On the other hand, the trunk showed evidence of an irregular waistline and a rib hump that obviously suggested scoliosis (Fig. ).
Due to the remarkable deformation of upper limbs beyond the elbow joint, upper limb muscular strength could not be evaluated accurately. Further, due to the remarkable deformation of lower limbs beyond the ankle joint, lower limb muscular strength could not be evaluated accurately. Other muscle weakness was not present. There were no walking problems. No hypoesthesia, numbness, or dysuria was found. Hyperreflexia was observed in the upper and lower limbs, but no neurological deficit was observed. No laterality was found in the limbs and Babinski reflex was positive. Spirometry showed a decrease in forced vital capacity (FVC) by 67.4%. Although proteinuria was observed, no renal dysfunction or hypertension was present.
X-ray images of the limbs showed remarkable osteolysis in joints of the hand, elbow, and ankle (Fig. ).
The major curve of scoliosis was 82° (MC, Th7-L2; Th11 apical vertebra), and the upper curve was 77° ay (UC, Th1-6; Th3 apical vertebra). In a recumbent-traction position, major curve was 54° and upper curve was 56°. The results of sagittal plane measurement were as follows. Sagittal vertical axis: 30 mm; pelvic tilt (PT), 17°; sacral slope (SS), 60°; lumbar lordosis (LL), 71°; and pelvic incidence (PI), 77°. In terms of sagittal plane alignment, the PI–LL angle was <10° and no mismatch was observed; thoracic kyphosis was decreased to 16° (Fig. ).
Computerized tomography revealed a partially narrowed vertebral arch, with no findings suggesting osteolysis. Magnetic resonance images showed deviation of the spinal cord, while neither Chiari malformation nor spina bifida was observed (Fig. ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [38.6, 'kg'], 'height': [155.0, 'cm']}",16.0666,15.26327,16.86993,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 38.6 kg. The patient's bmi is therefore 38.6 kg / (1.55 m * 1.55 m) = 16.0666 kg/m^2."
2300,6,Body Mass Index (BMI),physical,decimal,pmc-4805227-1,Extracted,"A 13-year-old female patient presented to our endocrinology clinic for evaluation of short stature. She had been shorter than her peers throughout her life. She was the third child of non-consanguineous parents and her two siblings were normal.
Adjunct to short stature, her examination revealed physical stigma for Turner syndrome (TS) such as a short/webbed neck, cubitus valgus, and short 4th metacarpal bones. She stood 139.3 cm [-2.57 standard deviation (SD)] and weighed 41.2 kg (+2 SD). Both breast and pubic hair development were consistent with Tanner stage 3. Her external genitalia appeared completely female. Bone age determined by Greulich and Pyle atlas was 13 years.
She had a follicle-stimulating hormone level of 121 IU/L, luteinizing hormone (LH) level of 28.8 IU/L, and an estradiol level of 28.6 pg/mL. Complete blood count, celiac markers, thyroid function tests, insulin-like growth factor-1, and insulin-like growth factor-binding protein-3 were all within normal range. She had a uterus of 9x14x33 mm in size, but her ovaries could not be visualized by ultrasonography. Further magnetic resonance imaging to evaluate internal genital organs revealed a right gonad with a size of 22x14x19 mm, an invisible left gonad, and a hypoplastic uterus. The chromosomal study of peripheral blood lymphocytes (PBL) with GTG-banding analysis of 55 metaphases showed a 45,X[30]/46,XY[25] karyotype. Y-derived sequences (SRY, AZF, Ycen, and Yqh) were analysed by polymerase chain reaction (PCR); they were all present except for microdeletions in AZF regions (SY254, SY255) on PBL DNA.
Due to an increased malignancy risk to the gonads, an explorative laparotomy and bilateral gonadectomy were performed. During explorative laparotomy, she was found to have a streak gonad on the left side and a 3-cm irregular nodule in the ovarian fossa on the right. The capsules of the gonadal tissues were intact, and the gonads were successfully removed. The frozen sample of the right nodule was consistent with dysgerminoma. On inspection, the uterus and fallopian tubes were normal, and there was no evidence of malignancy or abnormality in the pelvic organs. Histopathological examination of the left streak gonad revealed a gonadoblastoma. In the right gonad, together with a normal ovarian stroma, centrally located dysgerminoma and gonadoblastoma in neighbouring areas were identified. Twenty-three metaphases were analysed in each gonad. The karyotype of the right and left gonadal tissues were 45,X[97,3]/46,XY[2,7] and a 45,X[92,7]/46,XY[4,5]/47,XYY[2,8] mosaic, respectively. The microdeletion in the AZF region was detected by using PCR analysis.
The patient was discharged one week later, after an uneventful postoperative course. She then consulted with paediatric oncology. Based on their recommendations, computed tomography scans of the chest, abdomen and pelvis were performed for metastatic evaluation and did not reveal an abnormality. GCT markers (lactate dehydrogenase, human chorionic gonadotropin, alpha-fetoprotein) were measured, and all were within normal limits. After the first oncological evaluation, a follow-up plan was designed for every 3 months during the first year and every 6 months thereafter. At the same time, hormone replacement therapy was started to maintain secondary sexual characteristics and to prevent bone loss.
The patient and especially her parents had numerous questions regarding fertility and gender identity, and therefore, she was referred to an adolescent psychiatrist and a gynaecologist. Her gender identity was that of a woman, and she was worried about having children. Future fertility treatment options, such as adoption and oocyte-donor in-vitro fertilization (IVF), were also discussed.
Her regular follow-up has been ongoing in outpatient clinics of related departments nearly for the past postoperative 2 years and no complications have been noted.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [41.2, 'kg'], 'height': [139.3, 'cm']}",21.2322,20.17059,22.29381,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 139.3 cm, which is 139.3 cm * 1 m / 100 cm = 1.393 m. The patient's weight is 41.2 kg. The patient's bmi is therefore 41.2 kg / (1.393 m * 1.393 m) = 21.2322 kg/m^2."
2301,6,Body Mass Index (BMI),physical,decimal,pmc-5366765-1,Extracted,"A 14-year-old boy was referred by his General Practitioner with history of abdominal pain and rash on his back for 12 months. The rash was treated with multiple topical agents including antifungal, antibiotic, and steroid ointments with no improvement. There was no history of loss of appetite, loose stools, diarrhoea, or bloating. He had no significant past medical history or medical problems within the family. He was weaned to solids without any difficulties and had no known food allergies.
On examination, he had a maculopapular and urticarial rash on his back and knees. The rest of his examination was normal.
Investigations including FBC, LFT, U&E, ESR, CRP, anti-tTG, IgA, IgG, and IgM all were normal, but anti-endomysial antibody was weakly positive.
Upper GI endoscopy showed normal oesophagus, mild antral erythema (negative CLO test), and normal mucosa in the duodenum. Partial villous atrophy with crypt lengthening and increasing intraepithelial lymphocytes was seen on histology. A diagnosis of seronegative CD was made. Quick mucosal lactase test was mildly suggestive of lactose intolerance.
The patient noticed a significant improvement in his rash within 12 days of starting gluten-free diet (GFD). He continued to improve on a GFD and when seen in the follow-up clinic a year later reported complete resolution of symptoms. His weight improved from 66.5 kg to 75 kg and height improved from 179.3 cm to 183.6 cm. Repeat investigations including anti-tTG antibody were normal. As there was improvement in his clinical symptoms, height, and weight, we did repeat endoscopy or do HLA-DQ2 and HLA-DQ8 investigations.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [75.0, 'kg'], 'height': [183.6, 'cm']}",22.24928,21.13682,23.36174,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 183.6 cm, which is 183.6 cm * 1 m / 100 cm = 1.836 m. The patient's weight is 75.0 kg. The patient's bmi is therefore 75.0 kg / (1.836 m * 1.836 m) = 22.24928 kg/m^2."
2302,6,Body Mass Index (BMI),physical,decimal,pmc-8138198-1,Extracted,"A 54-year-old Japanese female (height 156.0 cm; weight 73.0 kg) with HCV-associated cirrhosis (genotype Ib) visited our clinic for the treatment of cirrhosis. She was treated with the oral administration of ursodeoxycholic acid at 600 mg/day. From May 31, 2011, injection of 80 mL of Stronger Neo-Minophagen C (usually used to lower serum transaminase, 2–3 times a week) was carried out until the end of August 2019.
Abdominal computed tomography (CT) was carried out on February 10, 2011, which showed unevenness of the surface of the liver with splenomegaly, and she was diagnosed with a cirrhotic state. For eradication of HCV, PEG-IFN/ribavirin therapy was performed from August 5 to December 5, 2012, but it was not effective. Thereafter, CT performed on February 6, 2018, showed ascites and pleural effusion (Fig. ) and she was diagnosed with decompensated liver cirrhosis. Furosemide and Aldactone A were administered, but pleural effusion and ascites remained. For the low albumin level, albumin infusion was carried out from March 22, 2016, to August 30, 2019 (every 2 weeks).
On August 3, 2019, a new DAA drug, SOF (NS5B inhibitor, 400 mg)/VEL (NS5A inhibitor, 100 mg), was administered until October 25, 2019 (about 12 weeks). HCV-RNA became negative on August 30, 2019. Abdominal CT performed on September 25 showed neither ascites nor pleural effusion (Fig. ).
Hepatic encephalopathy (grade I–II), which appeared on July 23, 2019 (the patient claimed cloudiness of sensation, serum ammonia level of 112 μg/dL), disappeared on October 7, 2019 (serum ammonia level of 85 μg/dL) (Fig. ). She stated that her consciousness was cloudy and it took many hours for the preparation of each meal just before the SOF/VEL treatment, but after the disappearance of HCV-RNA by the therapy, her consciousness became clear and she could prepare a meal in a short time. Furthermore, she also stated that the sensation of fatigue had disappeared, and it had become easier to move by the 6th week of administration of the drugs. In addition, she also showed marked improvements in the albumin level (Fig. ) and in prothrombin time (Fig. ). As a result, the Child-Pugh classification [, ] improved from Child B to Child A.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [73.0, 'kg'], 'height': [156.0, 'cm']}",29.99671,28.49687,31.49655,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 156.0 cm, which is 156.0 cm * 1 m / 100 cm = 1.56 m. The patient's weight is 73.0 kg. The patient's bmi is therefore 73.0 kg / (1.56 m * 1.56 m) = 29.99671 kg/m^2."
2303,6,Body Mass Index (BMI),physical,decimal,pmc-8654094-1,Extracted,"This is a case of 41-month-old infant girl who presented with weight loss and intractable diarrhea associated with oral feeding. She is a product of full-term pregnancy, delivered through spontaneous vaginal delivery, with a birth weight of 2 kg, and she did not require admission to the neonatal intensive care unit (NICU). The pregnancy was uneventful. Parents are first-degree cousins, and the patient has two older healthy siblings.
At the age of six months, she presented to another hospital afebrile with a loss of weight and had watery, non-bloody diarrhea, six to seven times per day. Both endoscopy and biopsy from the duodenum were normal according to the mother. The patient was initially misdiagnosed with cow milk protein allergy, so hypoallergenic formula was given but there was no improvement, then after two months, she was switched to amino acid-based infant formula 200 ml five times per day. In the beginning, there was an improvement, but with time, she stopped gaining weight again. At the age of 10 months, she came to the gastroenterology and genetics teams at our facility with chronic diarrhea, poor growth, and abnormal hair. Her weight and height were 5.30 kg (<3rd percentile) and 61 cm (<3rd percentile), respectively. The diagnosis of THES was confirmed by whole exons sequence (WES) analysis, which identified the homozygous variant (c.1201G > A) p. (Glu401Lys) in the SKIV2L gene. Upon literature review, we did not find the mentioned variant mutation in any previous literature (Table ).
At 12 months of age, she was admitted for dehydration and nasogastric tube (NGT) feeding due to poor weight gain. Her body measurements upon admission were 5.64 kg (<3rd percentile) for the weight, and her height was 63 cm (<3rd percentile). Upon examination, she had some dysmorphic features such as a depressed nasal bridge, broad forehead, low set ears, and scanty dry hair. During her admission, she was having watery diarrhea with mucus two to three times a day. She was managed with intravenous fluid and the clinical nutritionist prepared a high-calorie formula. The nutrition therapy plan was to provide 180 ml of hypoallergenic baby formula (0.67 kcal/ml) every four hours orally, as much as she can tolerate, and if she did not complete her meal, give the rest through the NGT. This plan provided her with 192 ml/kg fluids and 135 kcal/kg/day energy. Her laboratory workup results were sodium 138 mmol/l, potassium 3 mmol/l, chloride 113 mmol/l, aspartate aminotransferase (AST) 40 units/l, alanine aminotransferase (ALT) 30 units/l, and gamma-glutamyl transferase (GGT) 32 units/l. Her immunoglobulins workup showed low immunoglobulin E <25 au/ml, and normal immunoglobulin G and A levels. She was improving and gained 100 grams in two days. On the seventh day of admission, she was able to tolerate oral feeding, so the patient was discharged on the same plan and to add 1 ml of medium-chain triglycerides oil every other day.
At the age of 21 months, the mother reported in a follow-up visit that her daughter’s weight has been improved and reached 7.8 kg, but still under the third percentile. The patient was continued on hypoallergenic baby formulas and a regular diet. At the age of 41 months, the patient presented with progressive bullous itchy skin rash, and fluid-filled vesicles on erythematous background with red erosions and fissures all over the body but sparing abdomen and back. It was associated with cough, rhinorrhea, fever, and decreased urine output and oral intake, but without gastrointestinal complications. The diagnosis of bullous impetigo was made, and the patient was admitted. Amoxicillin, clavulanate, and diphenhydramine were administered intravenously with topical clindamycin and tretinoin cream. The patient showed clinical improvement in three days. The patient was discharged on oral Augmentin, Mupirocin, and Loratadine (Figure ).
On follow-up evaluation at the age of 41 months, her weight and height were 10 kg (<3rd percentile) and 85 cm (<3rd percentile), respectively. She was able to tolerate normal oral feeding. She did not show any signs of intellectual disability, and she is developmentally up to her age now. She is active and plays with her cousins. She can speak and understand both Arabic and English, and according to the mother she is starting to memorize songs.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [10.0, 'kg'], 'height': [85.0, 'cm']}",13.84083,13.14879,14.53287,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 85.0 cm, which is 85.0 cm * 1 m / 100 cm = 0.85 m. The patient's weight is 10.0 kg. The patient's bmi is therefore 10.0 kg / (0.85 m * 0.85 m) = 13.84083 kg/m^2."
2304,6,Body Mass Index (BMI),physical,decimal,pmc-7000934-1,Extracted,"A 30-year-old male patient was detected as having pancytopenia for 23 years and fever for 11 d.
Twenty-three years ago, at six years of age, a Chinese boy sought medical attention with major complaints of rapidly progressive weakness, fatigue, and pallor. This patient was detected as having pancytopenia and diagnosed with AA by BM aspirate and biopsy at several centers. He was prescribed cyclosporine (CsA) and stanozolol, showing a good hematological response. His symptoms gradually improved, but his peripheral blood cell counts had never reached the normal levels. In 2004, he experienced his first relapse 8 mo after the discontinuation of CsA, and was reinstituted on CsA, again showing a good response. In 2011, he underwent his second relapse 3 mo after the discontinuation of CsA. This time, he was referred to our center. On admission, major complaints included progressive weakness and fatigue for 1 mo and high-grade fever for 11 d. His peak body temperature had risen to 39.7 °C, with the absence of evident localized signs or symptoms.
The patient had no history of diseases of the hematopoietic system or significant infections before the diagnosis of AA.
He had a history of dimethylbenzene exposure due to his house being decorated 8 mo before being sent to the doctor.
No family history of inherited, hematological, or autoimmune diseases was recorded.
His height was 173 cm, and his body weight 63.5 kg. The body temperature was 38.7 °C; breathing rate 23 bp/min; heart rate 98 bp/min; and blood pressure (BP) 124/82 mmHg. Upon physical examination, except for the bruising pallor complexion, no physical abnormalities were recorded. Conspicuous mucocutaneous hemorrhage, jaundice, or exanthemata was not presented. No significant signs of the nervous system, respiratory system, cardiovascular system, gastrointestinal symptom, urogenital system, and skeletal musculature system were found.
On admission, routine blood test revealed the following results: white blood cells (WBCs), 1730/µL; absolute neutrophil count (ANC), 270/µL; red blood cells (RBCs), 1860000/µL; hemoglobulin level (Hb), 5.4 g/dL; platelets (Plts), 6000 /µL; absolute reticulocyte count (Ret), 7600/µL; and C-reaction protein (CRP), 145.8 mg/L. No abnormalities were detected in his urine examination, coagulation profile, liver and renal function, lactate dehydrogenase, antinuclear antibodies, or serological tests for hepatitis A, B, and C, and anti-HIV antibodies. His blood culture was sterile. Expression of CD55 and CD59 was within the normal limits. Evaluation of BM smears from the posterior superior iliac spine revealed severe hypocellularity with severe fatty replacement, predominantly lymphocytes, with few erythrocyte and myeloid precursors as well as no megalokaryocytes or dysplasia (Figure ). Peripheral blood smears confirmed the severe neutropenia without atypical blood cells. No positive cytogenetic findings were identified by culturing the BM sample. A reticulocyte reaction was not observed following a tentative treatment with folinate and mecobalamin.
No signs of pulmonary infection were noted by chest computed tomography. Lymphadenopathy and hepatosplenomegaly were not observed by ultrasonographic examination.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [63.5, 'kg'], 'height': [173.0, 'cm']}",21.21688,20.15604,22.27772,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 173.0 cm, which is 173.0 cm * 1 m / 100 cm = 1.73 m. The patient's weight is 63.5 kg. The patient's bmi is therefore 63.5 kg / (1.73 m * 1.73 m) = 21.21688 kg/m^2."
2305,6,Body Mass Index (BMI),physical,decimal,pmc-3811713-1,Extracted,"A 48-year-old woman.
Incidentally found bilateral adrenal masses.
The patient had been diagnosed with hypertension 3 years prior, and had been receiving carvedilol 25 mg as prescribed by a private clinic. However, the patient's blood pressure (BP) had not been under control for about 3 months prior to the visit at our hospital. A year prior, the patient's menstrual cycle had become irregular and her weight had increased by 5 kg in the last year. The patient had visited our hospital due to the identification of bilateral adrenal masses from abdominal CT during a routine health examination.
Nothing specific except hypertension.
Nothing specific.
At the time of the visit to our hospital, the patient's height was 150 cm, weight was 53.8 kg, BP was 145/95 mm Hg, pulse rate was 72 beats per minute, respiratory rate was 20 times per minute, and body temperature was 37.1℃. She had an alert mental state, no visible signs for acute or chronic illness and no abnormal findings for skin, sclera and conjunctiva. Examination of the head and neck revealed a moon face, while a buffalo hump deformity was observed upon thoracic examination. There was no specific finding on the abdominal examination and no edema of extremities was identified. The patient had no accompanying muscle weakness or sensory deterioration.
The peripheral blood test performed at the time of visit to the hospital showed the following; white blood cell, 6,450/mm3; hemoglobin, 12.9 g/dL; hematocrit, 41.6%; and platelet, 289,000/mm3. The serum biochemical assay showed the following; calcium, 9.4 mg/dL; phosphorus, 3.3 mg/dL; total protein, 7.0 g/dL; albumin, 4.2 g/dL; aspartate aminotransferase, 21 IU/L; alanine aminotransferase, 19 IU/L; alkaline phosphatase, 43 IU/L; blood urea nitrogen, 10 mg/dL; creatinine, 0.7 mg/dL; sodium, 144 mEq/L; potassium, 3.4 mEq/L; and chlorine, 102 mEq/L.
The hormone test indicated that the morning baseline blood cortisol was 15.7 µg/dL and ACTH was less than 5 pg/mL. The 24-hour urine free cortisol excretion increased to 198.7 µg/day (normal range, 23 to 135). In addition, the following were in the normal range; metanephrine, 63 µg/day (normal range, 52 to 341); normetanephrine, 176 µg/day (normal range, 88 to 444); epinephrine, 3.1 µg/day (normal range, 0 to 20); norepinephrine, 28.9 µg/day (normal range, 15 to 80); and vanillylmandelic acid, 5.4 mg/day (normal range, 0 to 8). The 24-hour urine creatinine was 0.5 g/day (normal range, 0.8 to 1.8) and the creatinine clearance was calculated to be 122.4 mL/min (normal range, 75 to 125), indicating that the urine sampling was done relatively well. The plasma aldosterone concentration was 7.5 ng/dL and plasma renin activity was 0.4 ng/mL/hr, indicating that the aldosterone/renin activity ratio was 18.7 and there was no finding of primary aldosteronism.
The serum cortisol after an overnight 1 mg dexamethasone suppression test was 14.5 µg/dL, which was not suppressed. The low-dose dexamethasone suppression test demonstrated that the 24-hour urine free cortisol excretion increased to 397.8 µg/day and the blood cortisol concentration increased to 21.1 µg/dL, so we diagnosed the patient's condition as Cushing Syndrome. In the high-dose dexamethasone suppression test, the urine free cortisol excretion and blood cortisol concentration were not suppressed ().
Bilateral adrenal tumors were identified on adrenal CT, with one sized 2.8×2.0 cm on the right side and the others sized 2×2.3 cm and 1.7×1.4 cm, respectively, on the left side (). There were no abnormal findings from the Sella MRI.
Adrenal vein sampling (AVS) was done in order to identify the location of a functional tumor secreting cortisol in between the bilateral adrenal tumors. AVS was conducted without an ACTH stimulus on the day after the high-dose dexamethasone suppression test. The blood cortisol concentration was measured by sampling the blood twice from catheterization to the femoral vein and bilateral adrenal veins ().
When the bone density was measured by dual energy X-ray absorptiometry, osteopenia was found based on the finding that the T score of lumber spine was -2.1, T score of femoral neck was -1.0 and T score of the total hip was -0.7.
As the adrenal vein cortisol measured from AVS was eight times higher than that of the inferior vena cava, it was determined that the AVS was done selectively. The blood cortisol concentration was measured as high from the bilateral adrenal veins with AVS. Therefore, we diagnosed the patient with Cushing Syndrome induced by bilateral cortisol-secreting adenomas. To treat the patient, we removed all of the bilateral adrenal tumors by laparoscopic bilateral adrenalectomy. Immediately after the surgery, the patient was discharged because there was no specific complication while implementing supplementary therapy with prednisolone and fludrocortisone, and we had discontinued the antihypertensive agent as the BP had improved to 120/80 mm Hg at the 2-month follow-up observation. At 5 months postoperatively, the blood cortisol concentration was 5.0 µg/dL, ACTH was 19.0 pg/mL, the plasma aldosterone concentration was 15.0 ng/dL, and the plasma renin activity was 3.0 ng/mL/hr, indicating no evidence of recurrence. The patient is currently under follow-up study as an outpatient while receiving prednisolone 5 to 2.5 mg and fludrocortisone 0.1 mg.
A single mass was found on each of the adrenal glands and their sizes were 2.6×2.3×1.7 cm for the left side mass and 2.6×2.5×1.6 cm for the right side mass. Based on the visual findings, the left mass was in the shape of a dumbbell with a narrowed mid-part, showing a light brown cross-section, and the right mass had a brown cross-section ().
From the optical microscopic findings, the bilateral adenomas were composed of large round vacuolar cells of consistent shape and size, and with good differentiation, whereas the normal tissues of the adrenal cortex around the adenoma were atrophic. As an atypical nucleus and necrosis, hemorrhage, or reverse differentiation were not found, the findings were appropriate for adrenal adenoma ().",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.8, 'kg'], 'height': [150.0, 'cm']}",23.91111,22.71555,25.10667,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 150.0 cm, which is 150.0 cm * 1 m / 100 cm = 1.5 m. The patient's weight is 53.8 kg. The patient's bmi is therefore 53.8 kg / (1.5 m * 1.5 m) = 23.91111 kg/m^2."
2306,6,Body Mass Index (BMI),physical,decimal,pmc-7106884-3,Extracted,"Patient 3 is a 59-year-old female whose primary cause of the liver disease was nonalcoholic steatohepatitis with a preoperative MELD score of 29. Her liver disease was complicated by hepatic encephalopathy and ascites requiring paracentesis. Her comorbidities included depression, anxiety, colitis, and tricuspid regurgitation, and history of roux-en-y gastric bypass. She received a deceased donor orthotopic liver transplant with a graft volume of 1977 cm3 (as estimated by donor preoperative CT volumetry). At the time of surgery, her height was 167.6 cm, and her weight was 78.1 kg. Her donor height and weight were 165.1 cm and 92 kg, respectively, giving a donor-weight-to-recipient-weight ratio of 1.18. The transplant was performed using the piggyback technique on veno-venous bypass with choledocho-choledochostomy and recipient ductoplasty. A large amount of ascites was evacuated intraoperatively. Due to large graft size, a bridging Vicryl knitted mesh was placed in the right lateral part of the chevron incision to avoid compartment syndrome. On postoperative day 4, the level of her liver enzymes was acutely elevated. Liver ultrasound showed normal resistive indices, and she was started on stress dose steroids for suspected acute cellular rejection. Her liver enzymes responded appropriately to the steroids. Her postoperative course was also complicated by hypotension requiring pressors for 48 hours, acute kidney injury, and ileus, all of which resolved by her discharge on postoperative day 10. She is currently five months postoperatively, and her liver enzymes remain within normal limits.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [78.1, 'kg'], 'height': [167.6, 'cm']}",27.80373,26.41354,29.19392,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 167.6 cm, which is 167.6 cm * 1 m / 100 cm = 1.676 m. The patient's weight is 78.1 kg. The patient's bmi is therefore 78.1 kg / (1.676 m * 1.676 m) = 27.80373 kg/m^2."
2307,6,Body Mass Index (BMI),physical,decimal,pmc-6240425-1,Extracted,"Patient 1 (III:9) was a 11 years old male, who presented with a history of multiple fractures after mild trauma since the age of 6 months. His first fracture of right clavicle occurred at the age of 6 months, followed by fracture of right tibial shaft at the age of 8 years, and fracture of right and left femora at 9 years. Pregnancy and birth were uneventful. His parents were distant cousins (IBD proportion < 6%). Presently, the index individual is wheelchair bound because of multiple fractures, deformities and weakness of lower extremities. His weight is 20 kg, height 106 cm and head circumference 52 cm. Physical examination revealed brachycephalic head, flat face, mild blueness of sclerae, right eye squint, short neck, marked thinness of upper and lower extremities, anterior angulation of both femora and right tibia, and flat feet (Fig. ). Skeletal radiographs revealed generalized osteopenia, bowing of clavicles, compression of thoracic vertebrae, narrowing of intercostal spaces, and bowing of long bones.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [20.0, 'kg'], 'height': [106.0, 'cm']}",17.79993,16.90993,18.68993,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 106.0 cm, which is 106.0 cm * 1 m / 100 cm = 1.06 m. The patient's weight is 20.0 kg. The patient's bmi is therefore 20.0 kg / (1.06 m * 1.06 m) = 17.79993 kg/m^2."
2308,6,Body Mass Index (BMI),physical,decimal,pmc-7873350-3,Extracted,"The patient was an 81-year-old male; 166.0 cm in height and 46.8 kg in weight at the time of his initial examination; running a restaurant business; and described as slovenly in his personality. His chief complaints were memory loss and weight loss, and he had a medical history of hypertension and reflux esophagitis. As to the history of the present illness, he had been suffering from memory loss since around November X−1. He had been treated at a local doctor's clinic for hypertension, but his forgetfulness worsened, as he was asking the same questions over and over again, unable to tell the date of the day, and unable to take his medication, and therefore he came to our clinic in September X. He was diagnosed with Alzheimer's disease, which was already several years advanced, with impairment in recent memory, semantic memory, executive function, and frontal lobe function shown by the scores of 11 on the Hasegawa's dementia scale, 18 on the MMSE, 10 on the FAB, and 10 on the clock-drawing test (CDT), as well as atrophy of the frontal and medial temporal lobes observed on MRI images. In September X, he complained that he was unable to stop drinking and was not eating, and he weighed 46.8 kg, with a decrease of 1.5 kg in 2 months. His muscle mass measured by a body composition analyzer (InBody 270) using bioelectrical impedance analysis was 34.3 kg. The weight after removing the body fluid weight (21.7 kg) from the total body weight (46.8 kg) was 25.1 kg. Since September X, he started taking Ninjin'yoeito 3.75 g once before bedtime.
In November X+1, improvement in his appetite was observed. His weight was 49.3 kg, showing an increase of 2.5 kg. His muscle mass was 36.7 kg, showing an increase of 2.4 kg. The weight after removing the body fluid weight was 49.3–23.2 kg = 26.1 kg, showing an increase of 1.0 kg.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [46.8, 'kg'], 'height': [166.0, 'cm']}",16.9836,16.13442,17.83278,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 46.8 kg. The patient's bmi is therefore 46.8 kg / (1.66 m * 1.66 m) = 16.9836 kg/m^2."
2309,6,Body Mass Index (BMI),physical,decimal,pmc-3841568-1,Extracted,"A 13-year-old Hindu male child 4th born to a consanguineously married couple with uneventful perinatal event, having delayed social and personal development was brought with spasms of the upper and lower limbs. He has been suffering from similar episodes of spasms frequently since the age of 5 years. He also had developmental bilateral cataract for which he was operated at the age of 6 years. At admission, he had carpopedal spasm and his vitals were normal. His weight was 29 kg (<5th centile), height 132 cm (<5th centile) and head circumference 49 cm (<3rd centile). On examination, he had facial dysmorphism features like long face, prominent forehead, bilateral dropping of eyelids, preauricular tag on the right side, bilateral pseudophakia with posterior capsular opacification (secondary), beaked nose, depressed nasal bridge, long philtrum, high arched palate, maloccluded teeth, micrognathia and microcephaly []. Latent tetany signs Trousseau sign and chvostek sign were positive. Intelligent quotient assessment revealed mild mental retardation. Other systems examinations were normal. One of his sisters also had operated for developmental cataract at the age of 4 years, having delayed social and personal development, similar facial dysmorphism [] but no tetany or latent tetany signs. Both parents and other two sibs were phenotypically normal.
His investigations revealed normal blood counts and peripheral smear. His serum calcium was 6.8 mg/dl, serum phosphorus 7.1 mg/dl, serum magnesium 2.2 mg/dl, serum albumin 3.2 g/dl, alkaline phosphatase 124 U/L and intact PTH was 5.46 pg/ml (N = 15-65 pg/ml). Blood urea, blood sugar, serum creatinine and electrolytes were normal. Urine chromatography was normal and urinary pH 8. His urine for sugar and ketones was absent. Chest X-ray, humerus X-ray and ultrasound abdomen was normal. Computerized tomographic (CT) scan of the head showed bilateral globus pallidus calcification. Audiogram showed mild hearing loss on the left side with normal hearing on the right side. He was started on intravenous calcium gluconate slow infusion for 2 days followed by calcium tablets. His facial dysmorphic sister serum calcium, phosphorus, magnesium, albumin, alkaline phosphatase, intact PTH and CT head were normal.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [29.0, 'kg'], 'height': [132.0, 'cm']}",16.64371,15.81152,17.4759,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 132.0 cm, which is 132.0 cm * 1 m / 100 cm = 1.32 m. The patient's weight is 29.0 kg. The patient's bmi is therefore 29.0 kg / (1.32 m * 1.32 m) = 16.64371 kg/m^2."
2310,6,Body Mass Index (BMI),physical,decimal,pmc-6452495-1,Extracted,"A 71-year-old male (height 157 cm, body weight 40.0 kg and performance status 1) who presented with anorexia and abnormal liver function following a blood examination was diagnosed with a type II advanced GC in the lesser curvature of the antrum after an upper gastrointestinal endoscopy (Figure ). At the same time, an enhanced computed tomography scan (eCT) revealed multiple liver metastases and enlarged lymph nodes along the branch of superior mesenteric artery region (Figure A). Biopsy results from the gastric tumor yielded a diagnosis of a moderately differentiated adenocarcinoma (Figure A) and 3 + HER2 status by immunohistochemistry (IHC) (Figure B). The clinical diagnosis was L-Less type 2 T3 N3 M1 H1 stage IVb (according to the 15th edition of Japanese classification of gastric cancer).
For this patient, we chose to treat with T-mab and XP chemotherapy; T-mab was given by intravenous infusion at a dose of 8 mg/kg on day 1 of the cycle. Cisplatin 80 mg/m2 was given on day 1 by intravenous infusion. Capecitabine 1000 mg/m2 was given twice a day, orally, for 14 days followed by a 1-week rest. Two weeks following the first treatment, impairment of renal function and anorexia were observed as adverse reaction to cisplatin; the estimated creatinine clearance was reduced to under 30 mL/min, and the severity of anorexia was categorized in grade 1 according to National Cancer Institute Common Terminology Criteria for Adverse Events version 3.0. Therefore, we terminated the administration of cisplatin and converted the regimen of systemic chemotherapy to T-mab plus capecitabine combination therapy (T-mab + capecitabine). After the start of T-mab + capecitabine therapy, serum CEA was decreased rapidly and the multiple liver metastases, metastatic lymph nodes (Figure B), and primary tumor region showed a remarkable regression at the eighth course of T-mab + capecitabine as a partial response due to RECIST ver. 1.1 (Figure B).
The patient has survived for 40 months without progression of either liver metastases or primary tumor due to continuation of T-mab + capecitabine chemotherapy.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [40.0, 'kg'], 'height': [157.0, 'cm']}",16.22784,15.41645,17.03923,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 157.0 cm, which is 157.0 cm * 1 m / 100 cm = 1.57 m. The patient's weight is 40.0 kg. The patient's bmi is therefore 40.0 kg / (1.57 m * 1.57 m) = 16.22784 kg/m^2."
2311,6,Body Mass Index (BMI),physical,decimal,pmc-5290507-1,Extracted,"A 31-year-old man visited our hospital for evaluation of dyspnea and malaise. He had been ill for 1 week prior to admission. His dyspnea gradually started to worsen 2 days prior to admission. One day before admission, he could not get out of the bathtub because of severe dyspnea. The following day, he was found in the bathtub by his family after about 10 h had passed and was transported to our hospital.
The patient had been diagnosed with mild dilated cardiomyopathy without coronary artery stenosis and valvular insufficiency 2 years previously, and diuretics were prescribed by the clinic. However, he stopped taking the diuretics and returning for regular checkups. On arrival to our hospital, his height was 163 cm, weight was 115.4 kg, and vital signs were as follows: blood pressure, 82/53 mmHg; regular heart rate, 125 beats/min; oxygen saturation, 100% (oxygen mask, 6.0 L/min); respiratory rate, 42 breaths/min, and body temperature, 38.7°C. Physical examination revealed peeling skin on his buttocks and pressure marks associated with the long bath time extending from the back over the buttocks. Wheezing and moist rales were heard in the lungs.
Laboratory examination showed the presence of inflammation (white blood cell count, 13,100 cells/μL; C-reactive protein, 16.7 mg/dL; procalcitonin, 41.95 ng/mL), renal impairment (blood urea nitrogen, 53.0 mg/dL; creatinine, 1.55 mg/dL), thrombocytopenia (platelet count, 3.9 × 104/μL), heart failure (N-terminal pro-brain natriuretic peptide, 49,804 pg/mL), and coagulation system abnormalities (D-dimers, 20.6 μg/mL; P-fibrin degradation products, 44.5 μg/mL).
Transthoracic echocardiography (TTE) at admission showed diffuse hypokinesis of wall motion and an ejection fraction of 56% without vegetation. An enlarged heart shadow and a patchy shadow were observed in the right middle lung field on a chest X-ray. Whole-body computed tomography (CT) showed nodules in the right middle lobe of the right lung, suspicious for septic emboli, along with splenomegaly.
Two sets of blood cultures were obtained. Under a preliminary diagnosis of disseminated intravascular coagulation and systemic inflammatory response associated with infection, intravenous administration of meropenem was initiated at 1 g every 8 h. The next day, both sets of blood cultures exhibited growth of Gram-positive streptococci (BD BACTEC blood culture system, Becton, Dickinson and Company, Sparks, Maryland, USA). The antimicrobial treatment was then switched from meropenem to combination therapy comprising ampicillin at 2 g every 8 h and clindamycin at 600 mg every 8 h for toxic shock. The Gram-positive culture was identified as SDSE (VITEK 2 system; BioMerieux Japan, Tokyo, Japan) on the third day. TTE on the third day revealed a reduction in the ejection fraction to 46%, emergence of severe mitral valve regurgitation, and a 5-mm vegetation on the anterior leaflet mitral valve (Fig. ). Using the modified Duke criteria, we diagnosed IE (one major criterion and three minor criteria) caused by SDSE. The ampicillin and clindamycin were continued.
A whole-body CT scan on hospital day 12 revealed a hemorrhagic infarction of the right frontal lobe (Fig. A), abscesses on the right frontal and occipital lobes, and an aneurysm of the mesenteric artery (Fig. B). A rapidly progressive new aneurysm emerged (as shown by comparison of the CT examinations on days 1 and 12) during the clinical course of SDSE bacteremia, and radiological examination was compatible with an infected aneurysm. Therefore, we diagnosed infectious aneurysms caused by SDSE. On day 18, gentamicin was added at 60 mg every 24 h with dose adjustment according to the patient's renal function. Because of the possibility of brain hemorrhage and concern about worsening infection due to embolization, we decided not to perform surgical and radiological intervention. On hospital day 41, the patient complained of sudden abdominal pain, and an abdominal CT scan revealed that the infected aneurysm of the splenic artery had ruptured and caused massive bleeding (Fig. A); there was a significant increase in the size of the aneurysm in the upper mesenteric artery (Fig. B), and new aneurysms were present in the right colic artery. Transcatheter arterial embolization (TAE) for the aneurysms of the splenic and upper mesenteric arteries was performed (Fig. ). A follow-up abdominal CT performed on day 68 demonstrated organized aneurysms of the right colic artery without intestinal ischemia or any additional bleeding.
The antimicrobial agents were adjusted according to the patient's renal function, and the ampicillin was increased to 12 g per day. The intravenous clindamycin and gentamicin were continued for 10 weeks, and the ampicillin was continued for 11 weeks. Several blood cultures were performed throughout the treatment period, but none were positive. A follow-up TTE on hospital day 70 demonstrated organization of the vegetation. The patient was discharged in good clinical condition after 3 months of treatment.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [115.4, 'kg'], 'height': [163.0, 'cm']}",43.43408,41.26238,45.60578,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 115.4 kg. The patient's bmi is therefore 115.4 kg / (1.63 m * 1.63 m) = 43.43408 kg/m^2."
2312,6,Body Mass Index (BMI),physical,decimal,pmc-3795405-2,Extracted,"A 74-year-old woman, 152.0 cm tall and weighing 57.5 kg with no history of OA visited our hospital. At her first visit, she complained of right hip joint pain (P4). Plain radiographs showed OA at KL grading IV (Fig. ). Since then, joint pain has shown repeated remission and deterioration. Recent plain radiographs also showed OA at KL grading IV. MRI was performed at the time of right hip joint pain (P4). MRI showed high signal change in the entire femoral head and acetabulum in T2-STIR (Fig. ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [57.5, 'kg'], 'height': [152.0, 'cm']}",24.88747,23.6431,26.13184,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 152.0 cm, which is 152.0 cm * 1 m / 100 cm = 1.52 m. The patient's weight is 57.5 kg. The patient's bmi is therefore 57.5 kg / (1.52 m * 1.52 m) = 24.88747 kg/m^2."
2313,6,Body Mass Index (BMI),physical,decimal,pmc-7896659-1,Extracted,"A 50-year-old female who had a history of positive hepatitis B surface antigen for more than 10 years presented to The Infectious Department of our hospital complaining of aggravating anorexia and fatigue. During her presentation in The Infectious Department, she had nausea and vomit symptoms.
The patient’s symptoms started a week ago with gradually increasing gastrointestinal symptoms including anorexia and nausea. Her liver function tests showed elevated transaminases.
She had a past medical history of being a carrier of HBV for more than 10 years without antiviral treatment. She had no cardiac function abnormalities, arterial hypertension or diabetes mellitus. She had no negative drug history, and no alcohol intake.
The patient reported that her four siblings were infected with HBV, her mother died from hepatocellular carcinoma, and her father was in good physical condition.
After admission, the patient’s temperature was 36.6 °C, heart rate was 91 bpm, respiratory rate was 20 breaths per minute, blood pressure was 145/104 mmHg and oxygen saturation in room air was 99%. The patient was 160 cm tall and weighed 53 kg. The clinical examination revealed light scleral icterus without any other pathological signs.
Laboratory values on admission and during hospitalization are shown in Table . A series of tests were performed after admission to The Infectious Disease Department. Blood analysis revealed the following: Alanine aminotransferase, 575 U/L; Aspartate aminotransferase, 593 U/L; Total bilirubin, 108.3 μmol/L; Alkaline phosphatase 116 IU/L; Positive hepatitis B surface antigen, anti-LKM-1 > 1:80; Positive anti-soluble liver antigen/liver-pancreas; Positive anti-mitochondrial antibody; and Positive anti-SSA antibody and anti-SSB antibody.
The hematoxylin and eosin staining of liver tissue: The structure of hepatic lobules is unclear. The hematoxylin and eosin staining showed varying degrees of hepatocyte edema with moderate to severe piecemeal necrosis and scattered eosinophilic bodies (Figure , arrows). Small bile duct in the portal area was accompanied by lymphocyte-predominant inflammation with a small amount of eosinophil infiltration (Figure , filled triangles).
Immunohistochemistry analysis of liver tissue: The proliferation of small bile ducts in the portal area were obvious (Figure , arrows), with more infiltration of lymphocytes and plasma cells and positive marker detection including hepatitis B surface antigen (+), HBcAg (+-), bile duct epithelium (CK19+), IgG (+), and IgG4 (-) combined hepatocellular and cholangiocarcinoma. Findings were consistent with mild chronic hepatitis compatible with HBV infection, without histological stigmata of autoimmunity (Figure ).
Mesh fiber staining of liver tissue: The reticular fiber staining showed that the hepatic lobular stent was significantly damaged (Figure , arrows). The characteristic floral ring structure of AIH was not seen (Figure ).
Masson staining of liver tissue: The portal area was enlarged with fibrosis, the formation of bridging fiber band was visible in the focal area, and collagen fiber proliferated in the portal area by Masson staining (Figure , arrows).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.0, 'kg'], 'height': [160.0, 'cm']}",20.70312,19.66796,21.73828,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 53.0 kg. The patient's bmi is therefore 53.0 kg / (1.6 m * 1.6 m) = 20.70312 kg/m^2."
2314,6,Body Mass Index (BMI),physical,decimal,pmc-3348632-2,Extracted,"A 36-year-old woman with a past history of allergic rhinitis came to our outpatient clinic because of polyarthralgia and swelling of her fingers. Ten days prior to her visit, she had a low grade fever () when her 9-year-old son was diagnosed as having erythema infectiosum because of his slapped cheek rash. Seven days later, she developed a butterfly-shaped erythema transiently on her face that disappeared the next day. Then, she developed swelling of her fingers and joint pain in her shoulders, ankles, and knees. Since oral administration of acetaminophen did not relieve her symptoms, she came to our clinic. On physical examination, the patient looked tired. Her body temperature was 37.0°C, blood pressure was 110/72 mmHg, and pulse rate was 66 beats/min. She weighed 52 kg and was 160 cm tall. At that time, she presented no malar erythema and no rash in her body. Although all her fingers were swollen, the swelling of her shoulder, ankle, and knee joints was not obvious. Laboratory data showed normal hematologic parameters (white blood cell count 6,300/μL, hemoglobin 12.6 g/dL, hematocrit 37.6%, and platelet count 264,000/μL). Liver enzymes and C-reactive protein levels were not elevated. Due to a positive result for HPV-B19 IgM antibody in the serum (index 8.20) and the preceding infection of her son, a diagnosis of HPV-B19 infection was made. Oral administration of loxoprofen (180 mg/day) was immediately started after the diagnosis (). Her deteriorating symptoms, including polyarthralgia and the swelling of her fingers, quickly disappeared within 12 hours after the initiation of the drug.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [52.0, 'kg'], 'height': [160.0, 'cm']}",20.3125,19.29688,21.32812,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 52.0 kg. The patient's bmi is therefore 52.0 kg / (1.6 m * 1.6 m) = 20.3125 kg/m^2."
2315,6,Body Mass Index (BMI),physical,decimal,pmc-5564175-2,Extracted,"The second patient was a 74-year-old man (weight: 60 kg, height: 164 cm) scheduled for an external endonasal dacryocystorhinostomy. He did not have any underlying disease, his laboratory findings were all within normal limits, and no abnormalities were found on echocardiogram and chest radiograph examination. Neck extension was sufficient and his Mallampati score was Class II. Pre-anesthetic medication was not administered. After pre-oxygenation, 250 mg pentothal sodium, 50 mg rocuronium, and 100 µg fentanyl was administered. Once the patient lost consciousness, we attempted a conventional endotracheal intubation with a Macintosh blade #3. The epiglottis was slightly visible and could not be raised sufficiently. Two blind intubation attempts were unsuccessful. Tracheal intubation using a gum elastic bougie also failed. After three failed attempts, we prepared a FOB. However, there was some bleeding in the throat that obstructed our field of vision; therefore, we selected a combination of an ILMA and a FOB. ILMA provided an effective airway and allowed sufficient ventilation and oxygenation. We approached the vocal cords with a FOB and the endotracheal tube was railroaded into the trachea with ease.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.0, 'kg'], 'height': [164.0, 'cm']}",22.30815,21.19274,23.42356,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 164.0 cm, which is 164.0 cm * 1 m / 100 cm = 1.64 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.64 m * 1.64 m) = 22.30815 kg/m^2."
2316,6,Body Mass Index (BMI),physical,decimal,pmc-3950435-1,Extracted,"A healthy 29-year-old man (weight 75 kg, height 169 cm, American Society of Anesthesiologists class 1) was scheduled for elective arthroscopic repair of a left shoulder Bankart lesion. Aside from the orthopedic injury, the patient's history, physical examination, and laboratory data were normal. He was given 2 mg of lorazepam orally 2 h before arriving in the operating room. On arrival to the operating room, an 18-gauge venous cannula was inserted and the patient was connected to standard monitoring equipment, an oxygen face mask (5l/min) and was intravenously given 2 mg of midazolam. The patient was positioned supine with his neck extended to the contra-lateral side to facilitate performance of an ultrasound (US) interscalene brachial plexus block (ISBPB). After skin preparation with povidone-iodine and infiltration with lidocaine 1%, US-ISBPB was performed. An 18-gauge, 2-inch insulated needle (B. Braun Medical Inc., Bethlehem, PA, USA) was inserted into the middle scalene muscle immediately superior to and out of the plane with the L38 × 10−5 MHz transducer linear array. A 9 cm scan depth probe was used to visualize the brachial plexus using an M-Turbo US machine (SonoSite, Bothell, WA, USA). In the middle portion of the scalene muscle, the needle was redirected anteriorly and advanced toward the interscalene space. Normal saline (1-2 ml) was injected in increments into the anterior border of the middle scalene muscle to expand the fascial plane between the brachial plexus and the middle scalene muscle. While intermittently aspirating under direct US visualization, 10 ml of 0.25% bupivacaine was injected into the interscalene space. A 20-gauge catheter was then inserted into the skin through the thin-walled needle to a depth of 10 cm. To locate the catheter position before placement of a clear adhesive dressing, 0.5 ml of air was injected after negative aspiration while imaging the interscalene space. The US image clearly demonstrated echogenic contrast entering the interscalene space, thereby confirming appropriate positioning of the catheter. The surgical procedure was performed under general anesthesia using the propofol, fentanyl, and cis-atracurium with the patient in a beach chair position. Following an uneventful two-hour surgery, the patient was extubated and moved to the recovery room. Analgesia was maintained with a top-up of 0.2% bupivacaine every 8 h through the interscalene catheter. Free from pain and resting comfortably, the patient was discharged from the recovery room. Eight hours after the initial bolus (visual analog pain scale 1-2 at rest), the patient received 10 ml 0.2% bupivacaine, which was administered through the interscalene catheter by the on call team. One hour later, the patient developed Horner's syndrome on the ipsilateral side, including meiosis, ptosis, enophthalmia, anhydrosis, and conjunctival hyperemia. No swelling around the site of catheter insertion was noted. The catheter was withdrawn immediately and symptoms of Horner's syndrome disappeared approximately 2 h later. Analgesia was then changed to paracetamol and non-steroidal anti-inflammatory drugs.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [75.0, 'kg'], 'height': [169.0, 'cm']}",26.25958,24.9466,27.57256,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 169.0 cm, which is 169.0 cm * 1 m / 100 cm = 1.69 m. The patient's weight is 75.0 kg. The patient's bmi is therefore 75.0 kg / (1.69 m * 1.69 m) = 26.25958 kg/m^2."
2317,6,Body Mass Index (BMI),physical,decimal,pmc-3102882-1,Extracted,"An 8.5-yr-old girl was referred to an endocrine clinic because of vaginal bleeding and uncontrolled hypertension on January 15, 2004. At 7.5-yr-old, the girl presented with severe headaches and nausea and was diagnosed with hypertension. She was prescribed antihypertensive drugs (Unipril 10 mg and Norvasc 10 mg). However, the hypertension remained uncontrolled. Concurrently, she showed breast development, and 3 months later, frequent vaginal spotting was observed. At 8-yr-old, pubic hair was observed. The girl had undergone surgery at 15 months of age due to bilateral grade III vesicourethral reflux but was subsequently found to be healthy. Her grandfather had been treated with hypertension.
Upon presentation to our clinic, the patient's height was 149 cm (> 95 percentile) and her weight was 42 kg (> 95 percentile). Her arterial blood pressure was 140/90 mmHg. On physical examination, the Tanner stages of breast and pubic hair were at stage III. Neurological examination was normal. Neither androgenic nor glucocorticoid excess was detected.
Laboratory investigations revealed normal renal function and low serum potassium (2.7 mEq/L). Plasma renin (133.5 ng/mL/hr; normal: < 4.4 ng/mL/hr), angiotensin II (5,230 pg/mL; normal: 9-47 pg/mL) and aldosterone levels (824.1 pg/mL; normal: < 130 pg/mL) were extremely elevated. The remaining serum electrolyte and complete blood cell count were normal, but proteinuria was detected in the urine analysis. Thyroid function was normal, and there was very mild prolactin elevation (33.69 ng/mL; normal 0-29.5 ng/mL). There was no elevation in Luteinizing hormone (0.29 mIU/mL) or Follicle-stimulating hormone (< 0.1 mIU/mL); however, estradiol was elevated (290.38 pg/mL). Prepubertal response was observed in a Gonadotropin-releasing hormone (GnRH) stimulation test, and beta HCG was in the normal range.
On radiologic tests, the patient's bone age was advanced (12 yr old by the Greulich-Pyle method). Pelvic computed tomography confirmed the well-defined right solid ovarian tumor (5.1 × 4.0 cm, ). Right oophorectomy was performed and antihypertensive treatment was tapered off over several days.
On gross examination, the right ovary measured 5.0 × 4.0 cm and the capsule was intact. The cut surface showed a bright yellow solid tumor with lobulation. There was no hemorrhage or necrosis.
Histological examination revealed that the ovarian tumor had sheets of clear or eosinophilic cells surrounded with a delicate fibrous stroma. The tumor cells showed small, dark-stained single nuclei with occasional nucleoli. Cells undergoing mitosis were counted less than 2 per 10 high power fields. Immunohistochemistry revealed a diffuse positive reaction for renin, alphainhibin in tumor cells. Ovarian stromal cells were positive for progesterone receptor ().
In conjunction with the clinical history, these findings supported a diagnosis of renin-secreting ovarian steroid cell tumor, NOS.
The patient was progressing well 16 months after surgery. Her blood pressure was normal (100/60 mmHg) without medication, and proteinuria had disappeared. Plasma renin, aldosterone and potassium levels had returned to normal, a normal pubertal response was shown in a GnRH stimulation test, and regular menstruation was present.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [42.0, 'kg'], 'height': [149.0, 'cm']}",18.91807,17.97217,19.86397,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 149.0 cm, which is 149.0 cm * 1 m / 100 cm = 1.49 m. The patient's weight is 42.0 kg. The patient's bmi is therefore 42.0 kg / (1.49 m * 1.49 m) = 18.91807 kg/m^2."
2318,6,Body Mass Index (BMI),physical,decimal,pmc-8116530-1,Extracted,"Case 1 was a 59-year-old male with a history of rhabodomyolysis. The patient was referred to our hospital because of gradually progressive dyspnea on exertion. His height was 155.5 cm, the body weight was 51.8 kg and the percentage of oxygen saturation (SpO2) was 95%. His respiratory test results are shown in . Chest computed tomography (CT) demonstrated subpleural fibrotic opacities with traction bronchiectasis in the upper and lower lung fields. He was clinically diagnosed as IPF with pleuroparenchymal fibroelastosis-like lesions based on the guidelines () (). He was treated with nintedanib ethanesulfonate and 7.5 g (divided into two doses) of ninjin'yoeito. The appetite score [Simplified Nutritional Appetite Questionnaire, SNAQ (, )] showed improvement, increasing from 15 before administration to 16 after both 4 and 12 weeks of administration (SNAQ consists of four items related to appetite. All questions are scored from 1 to 5 points, with a total score ranging from 4 to 20 points. The lower the score, the poorer the appetite). Similarly, the lassitude score [Chalder Fatigue Scale, CFS (, )] improved from six before administration to four after 4 and 12 weeks of administration (CFS consists of 11 items related to physical and mental fatigue. All questions are scored from 0 to 3 points, with a total score from 0 to 33 points. The higher the score, the stronger the fatigue). The breathlessness score [Modified Medical Research Council dyspnea scale, mMRC ()] also improved from two before administration to one after both 4 and 12 weeks of administration (mMRC scale uses a 5-grade scale, with Grade 0 representing almost no breathlessness and Grade 4 representing severely impaired activities of daily living due to breathlessness. The higher the grade, the stronger the breathlessness). Body weight increased from 51.8 kg before administration to 54.5 and 55.2 kg after 4 and 12 weeks of administration, respectively. The blood albumin level increased from 3.6 g/dL before administration to 4.5 g/dL after both 4 and 12 weeks of administration, and the Hb level showed an increasing trend, changing from 14.9 g/dL before administration to 15.6 and 15.4 g/dL after 4 and 12 weeks of administration, respectively. The CONUT scores were zero before and 12 weeks after ninjin'yoeito administration. A trend for improvement was also observed with respect to respiratory function test results. Serum KL-6 decreased from 499 to 481 U/ml. LDH increased from 162 to 181 IU/L (). There was no occurrence of transaminitis during the treatment. He had an increase in walking distance from 383 to 440 m in a 6-min walk test (6MWT) 12 weeks after administration. The value of the lowest SpO2 at 6MWT remained unchanged at ~90% for 12 weeks. The CT finding did not show significant changes before and after treatment with ninjin'yoeito.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [51.8, 'kg'], 'height': [155.5, 'cm']}",21.42244,20.35132,22.49356,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.5 cm, which is 155.5 cm * 1 m / 100 cm = 1.555 m. The patient's weight is 51.8 kg. The patient's bmi is therefore 51.8 kg / (1.555 m * 1.555 m) = 21.42244 kg/m^2."
2319,6,Body Mass Index (BMI),physical,decimal,pmc-6708912-1,Extracted,"Patient 1 was an 85-year-old woman, height 166 cm, weight 39 kg, and who smoked 10 cigarettes/day. She was retired but had worked fulltime at a desk job until the age of 65 years. She had RA with severe destruction and deformation of the joints in her hands, fingers, wrists, shoulders, hips knees, ankles, and feet. Her hands were especially affected and all the fingers on both hands were subluxated, partially preventing her from using a pen, fork, or dress. She had suffered from neck pain for more than 2 years. Over a couple of weeks, she had rapidly lost the ability to walk, was EMS 9 (grade 2), and her neck pain had increased to unbearable (VAS 10), although she had no arm pain. At physical examination, she presented with cervical myelopathy (Ranawat 3b[). Her legs were weak, and although she could move them when lying in bed she was unable to stand or walk. Hoffman's sign was positive, and her lower extremities showed hyperreflexia. Preoperative CT revealed vertical instability, VAAI 0.22 (Fig. A), with severe destruction and lateral subluxation of the AA joint (Fig. B) and odontoid fracture. Preoperative MRI revealed spinal cord compression by the atlas. Cervical traction with 4 kg for 2 days improved the patient's neurological symptoms and gross alignment. We performed C1–C2 fusion with a spacer in the right AA joint (Fig. D), a C1 claw (right side), a C1 lateral mass screw (left side), and bilateral C2 pedicle screws. The patient's myelopathy improved without C1 decompression (postoperative VAAI 0.69, Fig. C). At 4 months follow-up the patient could walk 100 m with a walker and at 7 months the patient's neck pain was reduced to VAS 2. Her EMS had improved to 13 (grade 1) and the global assessment was “symptoms improved after surgery”.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [39.0, 'kg'], 'height': [166.0, 'cm']}",14.153,13.44535,14.86065,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 39.0 kg. The patient's bmi is therefore 39.0 kg / (1.66 m * 1.66 m) = 14.153 kg/m^2."
2320,6,Body Mass Index (BMI),physical,decimal,pmc-5857148-5,Extracted,"This case is especially interesting. This is because a 63-year-old obese male (1.78 m, 119 kg) who was admitted to the hospital with hoarseness was examined by an ENT surgeon (indirect laryngoscopy). He was not sure whether the patient had a polyp or a tumor of the entry to larynx. Laryngoscopy was performed with the C-MAC videolaryngoscope using a standard size three blade after premedication and a topical anesthetic of the upper airway. Laryngoscopy confirmed the tumor of the vocal cords.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [119.0, 'kg'], 'height': [1.78, 'm']}",37.55839,35.68047,39.43631,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.78 m. The patient's weight is 119.0 kg. The patient's bmi is therefore 119.0 kg / (1.78 m * 1.78 m) = 37.55839 kg/m^2."
2321,6,Body Mass Index (BMI),physical,decimal,pmc-5981599-2,Extracted,"In 2014, a 29-year-old Japanese woman who had RAML associated with TSC was admitted to our hospital due to abdominal distention. She had a history of RAML-associated hemorrhage at 21 and 24 years of age, which had been treated by selective renal TAE. At the age of 21 years, her total renal volume had been calculated as 986 cm3, but it continued to increase thereafter.
On admission, she was 162.9 cm tall and weighed 58.1 kg, with a blood pressure of 105/68 mm Hg and a temperature of 36.7°C. Laboratory tests revealed that serum creatinine was 0.55 mg/dL, eGFR was 106.0 mL/min/1.73 m3, and proteinuria was 0.04 g/day (Table ). CT showed huge lipid-rich RAML, with the total renal volume being 4,035 mL and the maximum RAML diameter being 28.0 cm (Fig. ). Genetic testing was negative for abnormalities of TSC1 and TSC2, but TSC was diagnosed according to clinical criteria because she had more than two major features (Table ).
Everolimus was initiated at 10 mg/day. After 1 year, her total renal size was reduced to 3,043 cm3 (75%), while it was 3,246 cm3 after 3 years (80%). Solid lesions decreased in size, but lipid-rich lesions persisted (Fig. ). RAML-associated hemorrhage has not occurred since everolimus was initiated. In addition, renal function is unchanged and proteinuria has not been detected.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [58.1, 'kg'], 'height': [162.9, 'cm']}",21.89445,20.79973,22.98917,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.9 cm, which is 162.9 cm * 1 m / 100 cm = 1.629 m. The patient's weight is 58.1 kg. The patient's bmi is therefore 58.1 kg / (1.629 m * 1.629 m) = 21.89445 kg/m^2."
2322,6,Body Mass Index (BMI),physical,decimal,pmc-3814538-1,Extracted,"A fifteen-day-old male infant was admitted to our pediatric emergency department because of recurrent generalized tonic convulsions and apneic events associated with bradycardia and cyanosis. He was born at full term to a 24-year-old G2, P2 woman by caesarean section, following an uncomplicated pregnancy. Birth weight and length were 4050 g and 52 cm, respectively. The baby was mixed-fed (with breast milk and an infant formula). His weight at admission was 4025 g (50th-75th percentile), his height was 53 cm (50th -75th percentile), and his head circumference was 37.3 cm (50th-75th percentile). Physical examination revealed an active, afebrile baby with normal physical findings and facial appearance. Initial plasma glucose level was 91 mg/dL. Complete blood count (CBC) revealed a hemoglobin level of 14 g/dL, hematocrit 45%, white blood cell 18500/mm3 and a platelet count of 300000/mm3. SCa level was 1.5 µmol/L (normal range, 1.9 to 2.8), free Ca level was 0.64 µmol/L (normal range, 1 to 1.18), serum phosphate (P) 2.38 mmol/L (normal range, 1.2 to 2.2), alkaline phosphatase (ALP) 270 U/L (normal range, 48 to 406), and magnesium 0.8 mmol/L (normal range, 0.7 to 1.2). PTH and 25-hydroxy vitamin D [25(OH)D] levels were relatively low: 21.63 pg/mL (normal range, 15 to 65) and 6.45 ng/mL (normal range, 8 to 21), respectively. A combination of hypoparathyroidism and vitamin D deficiency were considered as the cause of hypocalcemic seizures. The baby’s Ca level reached 1.75 µmol/L with IV Ca gluconate, and he was started on 1α-hydroxyvitamin D3 in a dose of 0.25 μg/day, vitamin D3 2000 IU/day, and oral Ca lactate (50 mg/kg/day). Treatment with 1α-hydroxyvitamin D3 and oral Ca lactate were stopped at 2 months of age. The patient’s SCa, phosphate, ALP, and 25(OH)D levels returned to normal at age 3 months and the 2000 IU/day of vitamin D3 treatment was also discontinued. At age 6 months, the patient’s growth and development status as well as his Ca and 25(OH)D levels were all normal. His echocardiography performed at this time showed no cardiovascular defects.
The patient’s mother had no complaints, nor a history of major illness. Her physical examination was normal. Biochemical evaluation revealed a serum total Ca level of 2.65 µmol/L (normal range, 2.1 to 2.57). Serum P level was 1.32 mmol/L (normal range, 0.87 to 1.45), and ALP level was 155 U/L (normal range, 30 to 120). Urinary Ca was also elevated to 310 mg/day (normal range, 50-200). Renal sonography revealed nephrolithiasis at the lower poles of both kidneys. The PTH level was found to be 201 pg/mL (normal range, 15 to 65), while 25(OH)D level was low (8.05 ng/mL; normal range, 10 to 55). Parathyroid SPECT was performed with 99m Technetium-MIBI and two adenomas were demonstrated. Primary hyperparathyroidism along with vitamin D deficiency was diagnosed and surgery was planned for the adenomas.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [4025.0, 'g'], 'height': [53.0, 'cm']}",14.32894,13.61249,15.04539,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 53.0 cm, which is 53.0 cm * 1 m / 100 cm = 0.53 m. The patient's weight is 4025.0 g so this converts to 4025.0 lbs * kg/1000 g = 4.025 kg. The patient's bmi is therefore 4.025 kg / (0.53 m * 0.53 m) = 14.32894 kg/m^2."
2323,6,Body Mass Index (BMI),physical,decimal,pmc-3205363-1,Extracted,"Our patient was a 27-year-old man who was diagnosed with adult-onset type II citrullinemia (CTLN2) at age 24. The patient's height was 178 cm with a body weight of 60 kg. The patient had been treated with a low protein diet and oral administration of lactulose. Intermittent lactulose enemas were provided for intermittent alteration of consciousness. Recently, the patient has had more frequent alterations of his mental status with irritability and altered consciousness. Even though oral administration of L-arginine, Kanamycin and intravenous hyperalimentation with branched chain amino acids was started, his plasma levels of ammonia and citrulline were highly elevated, up to 844 µg/dL (normal range, 19 to 87 µg/dL) and 682 µmol/L (normal range, 12 to 55 µmol/L), respectively. Despite the conservative medical treatment including alternative pathway medication, intermittent continuous renal replacement therapy and hemodialysis, his condition failed to improve. Therefore, living donor liver transplantation was planned using a right lobe graft from his 25-year-old sister. However, the estimated volume of the donor's right lobe was 800 mL compared to 180 mL of the left and in addition there was a type III portal vein anomaly. We eventually decided to perform an APOLT using the extended left lobe of the liver from the donor. The patient underwent APOLT in February of 2008. The actual graft volume was 200 g and the graft-to-recipient weight ratio (GRWR) was only 0.33%. The patient's extended left lobe (including caudate lobe) was resected and the extended left lobe graft (including middle and left hepatic vein) was transplanted orthotopically. The left and middle hepatic vein trunk of the extended left lobe graft was anastomosed to the left and middle hepatic vein trunk of the recipient in end-to-end fashion with interposition venoplasty using the recipient's greater saphenous vein as a patch. The left portal vein of the graft was anastomosed to that of the recipient in end-to-end fashion. Considering that the graft was too small, the recipient's right portal vein was narrowed by surgical clipping, instead of total diversion, for prevention of the development of portal venous hypertension. The left hepatic artery of the graft was anastomosed to that of the recipients in end-to-end fashion. Intraoperative Doppler ultrasonography demonstrated that portal and arterial blood flow were well maintained in both the native liver and the graft. Biliary drainage was accomplished by a Roux-en-Y hepaticojejunostomy. On postoperative day 7, abdominal computed tomography demonstrated orthotopically transplanted small left lobe graft with well-enhanced pattern (). The post-operative course was uneventful and the patient was discharged without any problems. The plasma concentrations of ammonia were at the upper limits of normal, so only a low protein diet (50 g/day) was supplied without any specific medication. On post-operative day 33, the patient reported a sudden severe visual disturbance and the plasma levels of ammonia were noted to have increased up to 209 µg/dL. The estimated computed tomography volume of the graft was decreased to 190 mL and a left portal vein stenosis was suspected. Direct portography was performed and a severe left portal vein stenosis was confirmed. Immediate coil embolization of 8th segmental branch of right anterior portal vein and self-expandable stent placement for left portal vein was performed in order to increase the portal flow to the graft (). On post stent insertion day 7, the calculated computed tomography volume of the graft was increased to 250 mL (). The plasma level of ammonia was within normal range. By the thirtieth postoperative month, the patient had no signs of rejection or vascular problems.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.0, 'kg'], 'height': [178.0, 'cm']}",18.937,17.99015,19.88385,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 178.0 cm, which is 178.0 cm * 1 m / 100 cm = 1.78 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.78 m * 1.78 m) = 18.937 kg/m^2."
2324,6,Body Mass Index (BMI),physical,decimal,pmc-3242060-1,Extracted,"A previously healthy 74-year-old woman, 143 cm in height and 49 kg in weight, visited our hospital to undergo esophagogastroduodenoscopy (EGD) for a check-up. She experienced abdominal discomfort to soybean without skin lesion and asthma, but she had no other remarkable medical history including allergy. An EGD procedure using 15 mg propofol was performed twice in this patient prior to this admission without any side effects. Her initial blood pressure (BP) was 130/70 mmHg and heart rate was regular, ranging from 80 to 90 beats per minute. We did not use lidocaine for oropharyngeal anesthesia, and all of the medical team involved in her exam used vinyl gloves. Under standard monitoring, sedation was induced with 15 mg intravenous propofol (Propofol Inj., Jeil Pharm, Seoul, Korea). The patient was then sedated and we began the exam. Approximately 1 minute following administration of intravenous propofol, stridor was heard and oxygen saturation fell to 56% on pulse oximetry. We immediately applied inhaled oxygen (6 L/min) via nasal prong, but oxygen saturation did not increase. We decided to stop the exam, and tried to remove the endoscope. However, the endoscope became stuck in her throat. Thus, we removed the endoscope by compulsion. Ten seconds after endoscope removal, severe wheezing was heard and her oxygen saturation fell to 56%. The larynx was observed using a laryngoscope for endotracheal intubation. At that time, marked swelling and severe edema of the epiglottis extending to the arytenoids cartilage was detected. Epinephrine (1 mg) was immediately administered subcutaneously, together with 125 mg intravenous methylprednisolone infusion. Because the patient's symptoms did not improve after 1 minute, 1 mg epinephrine was administered intravenously. After a further 1 minute, her oxygen saturation recovered to 98% and the wheezing subsided. The patient's BP never went below 130/70 mmHg during the event. She recovered smoothly from anesthesia without signs of airway obstruction and was transferred to the general ward. Blood samples were drawn immediately after the event. Tryptase level (normal range, 0-13.5 µg/L) was 4.65 µg/L at 5 minutes and 6.61 µg/L at 2 hours. Arterial blood gas analysis showed pH 7.404, pCO2 42.5 mmHg, pO2 119.6 mmHg, HCO3- 26 mEq/L, and SaO2 98.3%. Total IgE was 111 kU/L. The patient underwent skin-prick testing 14 days after the event. The skin-prick tests of 55 common inhalant allergens were negative. However, propofol and 20% intralipid (SMOFlipid®, Fresenius Kabi, Bad Homburg, Germany) showed an immediate reaction (). Thus, we suspected the soybean in intralipid, a component of propofol, as the cause of the anaphylaxis, because she had a food allergy history to soybean. She was informed of the results and of the risk for anaphylaxis if re-exposed to propofol or nutritional supplements containing soybean in the future.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [49.0, 'kg'], 'height': [143.0, 'cm']}",23.96205,22.76395,25.16015,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 143.0 cm, which is 143.0 cm * 1 m / 100 cm = 1.43 m. The patient's weight is 49.0 kg. The patient's bmi is therefore 49.0 kg / (1.43 m * 1.43 m) = 23.96205 kg/m^2."
2325,6,Body Mass Index (BMI),physical,decimal,pmc-2841068-1,Extracted,"A 26 year old man with a background of Morquio syndrome, was admitted for an elective left total hip replacement. Osteoarthritis of the hips secondary to avascular necrosis of the head of femur bilaterally had been diagnosed. There was no past medical history of note; however review of systems revealed snoring and daytime somnolence, suggestive of obstructive sleep apnoea. Clinical inspection demonstrated a man of short stature, his weight was 63 Kg and height 150 cm, with a large head and short neck, the head appeared to be sitting directly on his thorax. On inspection the thorax had an increased anterior-posterior diameter and kyphosis. Clinical examination including respiratory, neurological and cardiovascular systems were normal. Pulmonary function testing and baseline laboratory tests were normal.
Preoperative airway examination demonstrated bulky soft tissue in the pharynx, grade 2 macroglossia, an enlarged uvula and tonsils, an exuberant gag reflex and a Mallampatti grade II airway. Preanaesthetic neutral and extension cervical x-rays were performed and demonstrated a hypoplastic odontoid process, and widening of the atlanto axial joint upon flexion, the joint measured 3 mm in diameter, the upper limit of normal (figure ). Magnetic Resonance Imaging (MRI) of the cervical spine revealed an intermedullary syrinx extending from the second cervical vertebra spine down to the thoracic spine (figure ), this findings ruled out regional spinal anaesthesia. Based on these findings and after discussion with the patient, an awake fibreoptic intubation for the procedure was planned.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [63.0, 'kg'], 'height': [150.0, 'cm']}",28,26.6,29.4,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 150.0 cm, which is 150.0 cm * 1 m / 100 cm = 1.5 m. The patient's weight is 63.0 kg. The patient's bmi is therefore 63.0 kg / (1.5 m * 1.5 m) = 28.0 kg/m^2."
2326,6,Body Mass Index (BMI),physical,decimal,pmc-5881327-2,Extracted,"An unanticipated airway difficulty was encountered in a 34-year-old female patient (70-kg, 152-cm, ASA physical status-I) scheduled for spine decompression surgery (L4–5 discectomy, interbody fusion). Direct laryngoscopy with Macintosh#3 blade revealed a Cormack and Lehane grade-III view with a relatively large and hypermobile epiglottis. Each time attempts to lift the epiglottis for vocal cords visualisation proved problematic. When the blade tip was positioned in vallecula, on each displacement manoeuvre, the epiglottis tended to move into glottic-opening. Further, lifting epiglottis with the blade tip positioned beyond the vallecula threatened to abrade the arytenoid mucosa. TTI-aided tracheal intubation was deemed appropriate to overcome the difficulty. This time, the effort was made to lift the epiglottis with the blade tip placed in vallecula and ELM was exercised to move the glottic-opening to the right of lateral epiglottic margin. An Eschmann™ multiple-use introducer was tried, but it failed to pass through the visible slit-like glottis opening for its soft-tip got folded on itself each time it contacted the glottic-opening. A 'modified' Eschmann multiple-use introducer (body strengthened until the base of the angled tip)[] passed the cords but could not be advanced further inside the trachea. Finally, a 'new' Portex™ introducer with a lower angled-tip front width passed the cord and moved freely inside the trachea. Tracheal tube (6.5-mm ID) railroading was uneventful.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [152.0, 'cm']}",30.29778,28.78289,31.81267,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 152.0 cm, which is 152.0 cm * 1 m / 100 cm = 1.52 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.52 m * 1.52 m) = 30.29778 kg/m^2."
2327,6,Body Mass Index (BMI),physical,decimal,pmc-2542401-1,Extracted,"A 39-year-old man was admitted in October 2006 with a 2-week history of sharp, non-radiating pain of the right shoulder blade with associated dyspnea upon exertion and 5 kg loss of weight. He denied fever, chills, night sweats or cough. His symptoms did not interfere with his occupation as a gardener. Vitals demonstrated a normotensive, afebrile 155 cm, 100 kg man with an oxygen saturation of 96% on room air.
Physical examination was normal with the exception of decreased breath sounds half way up the right lung field along with dullness to percussion and without tactile fremitus. A chest radiograph showed a moderately sized, right pleural effusion (Figure ). The right thoracentesis fluid analysis showed a slightly cloudy and yellow fluid. Cell count results were 1,164 nucleated cells, 12% polymorphonuclear leukocytes, 80% lymphocytes, 7% monocytes, 1% eosinophils, glucose 123 mg/dl, lactate dehydrogenase (LDH) 103 units/l, and protein 5.3 g/dl (pleural to serum protein ratio, 0.8; pleural to serum LDH ratio, 0.7). Bacterial Gram stain and culture, acid-fast bacilli smears, fungal culture and cytology were all negative. Histopathological evaluation of the pleural biopsy noted granulomatous inflammation and fungal elements consistent with coccidioides (Figure ). Cultures for tuberculosis remained negative even after 7 weeks. Purified protein-derivative skin test to the right forearm produced a 0 mm induration. Tests for human immunodeficiency virus were negative by both enzyme-linked immunosorbent assay and Western blot. Serum coccidioidomycosis complement fixation was normal (< 1:2). A post-thoracentesis chest radiograph did not reveal any evidence of parenchymal infiltrate. After several weeks of fluconazole therapy, the patient improved clinically, and follow-up chest radiograph showed near-complete resolution of the pleural effusion.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [100.0, 'kg'], 'height': [155.0, 'cm']}",41.62331,39.54214,43.70448,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 100.0 kg. The patient's bmi is therefore 100.0 kg / (1.55 m * 1.55 m) = 41.62331 kg/m^2."
2328,6,Body Mass Index (BMI),physical,decimal,pmc-7358866-1,Extracted,"A 16-year-old girl presented to emergency with complaints of pain in abdomen, vomiting, yellowish discoloration of eyes, and fever since 7 days. There was no history of taking aspirin and other known hepatotoxic drug/herbal medication. Her developmental history was appropriate for her age. There was no history of jaundice or anemia in past. On examination, her weight was 47.5 kg (between 25th and 50th percentile), height was 153 cm (between 25th and 50th percentile), temperature was 98°F, heart rate 98/minute, respiratory rate 24/minute, and blood pressure was 100/70. She was lethargic with the Glasgow coma scale (GCS) of 10 (E4V2M4), and pupils were normal size and normally reacting to light. Bilateral deep tendon reflexes were present and the Babinski sign was absent. Liver was 2.5 cm, tender. The patient was shifted to PICU in view of hepatic encephalopathy. On arrival in PICU, the patient was in shock and had signs of increased intracranial tension (hyperventilation with irregular respiration and paradoxical breathing). The GCS had deteriorated to E1V1M4, pupils were normal size and normally reacting, tone was normal, deep tendon reflexes were absent, and the plantar reflex was flexor bilaterally. The patient was having altered blood aspirates from the nasogastric tube. Laboratory findings on admission were as follows: hemoglobin—9 g/dL, total leukocyte count—6,000/mm3 (25% polymorphs and 65% lymphocytes), platelet count—1.2 lac, total bilirubin—5.5 mg/dL, direct bilirubin—3.5 mg/dL. Aspartate transaminase (AST)/alanine transaminase (ALT) (U/L)—4949/3248, alkaline phosphatase—150 U/L. Prothrombin time—35.5, international normalized ratio (INR)—3.5, blood ammonia—173 μmol/L, blood lactate—4.9 mmol/L, serum albumin—2.5 g/dL. The child was mechanically ventilated, shock was fluid responsive, and blood products were given as and when required. Other appropriate supportive care for ALF and hepatic encephalopathy was also initiated. Relevant investigations to find etiology of hepatitis including viral panel, Wilson’s disease, and autoimmune hepatitis workup were sent.
On day 3 of admission, even after appropriate supportive care patient’s encephalopathy did not improve; serum ammonia levels were persistently above >150 μmol/L with deranged INR. Hence, we planned for high-volume plasma exchange. A total of three cycles of plasma exchange were done on alternate days with fresh frozen plasma and 1.5 times of total blood volume with the centrifugation technique on the optia spectra machine. Each plasma exchange session lasted for 4 hours except for first session in which the child became hypotensive, which required 20 mL/kg normal saline bolus; other two sessions were uneventful. After two sessions of TPE, the child’s clinical condition started improving, liver function tests improved with INR -1.31, and the blood ammonia level decreased to 63 μmol/L. The child was successfully extubated after third session of TPE. At discharge, the child was completely asymptomatic with normal sensorium. Her serum sample came out to be positive for parvovirus B19 IgM and all other workup done to find out etiology of ALF was negative.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [47.5, 'kg'], 'height': [153.0, 'cm']}",20.29134,19.27677,21.30591,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 153.0 cm, which is 153.0 cm * 1 m / 100 cm = 1.53 m. The patient's weight is 47.5 kg. The patient's bmi is therefore 47.5 kg / (1.53 m * 1.53 m) = 20.29134 kg/m^2."
2329,6,Body Mass Index (BMI),physical,decimal,pmc-3830271-1,Extracted,"A 22-year-old unmarried female presented with a 4-year history of general fatigue, weight loss and hypotension. She was born of non-consanguineous parents after a normal full term vaginal delivery. She reported no family or personal history of autoimmune diseases. She had no history of trauma and she did not have a history of receiving glucocorticoids.
There were no abnormal findings on clinical examination, she was normally pigmented, blood pressure was 95/60 mmHg with no postural fall, and she had normal body hair. Her height was 170 cm and her weight was 53 kg. Thyroid palpation was normal. She had normal pubertal development. Her menarche started at the age of 12 years and she had regular periods. She had no galactorrhea. She had no headaches, visual disturbances, polyuria, or polydipsia.
Blood examinations showed natremia of 138 mEq/L, kaliemia of 4.1 mmol/L, calcemiaof 2.38 mmol/L, plasma glucose of 4.3 mmol/L and normal blood cell count.
Clinical findings led us to consider the possibility of adrenocortical insufficiency, and the patient underwent detailed endocrine investigations, the results of which are shown in .
Cortisol deficiency was shown clearly by both insulin-induced hypoglycemia and depot Synacthen test [intravenous injection (IV), 1μg]. Secondary hypoadrenalism was confirmed by the finding of low basal ACTH level (13.8 pg/mL, reference range: 10.3-48.3), at which the plasma cortisol was 34 ng/mL. Prolactin level was elevated at 39 ng/mL (Normal range: 5-29 ng/mL in females). She had normal growth hormone levels concomitant to hypoglycemia. In contrast, basal concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol, thyroid stimulating hormone (TSH), and free thyroxine (FT4) were normal. These results excluded panhypopituitarism and led us to diagnose the patient with IAD. Magnetic resonance imaging (MRI) of the hypothalamus and pituitary showed a normal-sized pituitary (pituitary height 6 mm), with no mass lesion. Thepituitary stalk has a normal thickness of 2 mm and was not deviated. Thehyperintense signal of the posterior pituitary was in the normal location.
The diagnosis of IAD probably secondary to LYH was made. Investigation for autoimmune diseases, including assessment of anti-thyroid peroxidase antibody (anti-TPO), anti-thyroglobulin antibody (anti-TG), anti-ovarian antibodies, anti-adrenal antibodies, anti-glutamic acid decarboxylase (anti-GAD) antibodies, and antinuclear antibodies (ANA) was negative.
A daily dose of hydrocortisone (25 mg) was administered. After 8 months of follow-up, the patient was well-controlled, and she experienced no signs or symptoms of endocrine dysfunction.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.0, 'kg'], 'height': [170.0, 'cm']}",18.3391,17.42214,19.25605,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 53.0 kg. The patient's bmi is therefore 53.0 kg / (1.7 m * 1.7 m) = 18.3391 kg/m^2."
2330,6,Body Mass Index (BMI),physical,decimal,pmc-7670349-1,Extracted,"A 26-year-old Japanese male who had presented epigastralgia for 10 months visited our hospital. He had lost about 6 kg because of his poor appetite. He did not complain of fever, cough, and chronic diarrhea. He had a proton pump inhibitor for those symptoms from a doctor nearby, but no improvement was observed. On physical examination, his height and body weight were 153 cm and 42.0 kg, respectively. He had mild epigastric tenderness, but no masses were palpable on his whole abdomen. No peripheral edema was observed. His nails were intact, and no pigmentation was found in his whole skin or mucous membranes. Alopecia was not observed. He did not have any relatives with polyposis in the gastrointestinal (GI) tracts. Blood examination showed negative Helicobacter pylori antibody, antinuclear antibody, and normal serum IgG4 levels.
Chest and abdominal X-rays were normal. The patient underwent esophago-gastro-duodenoscopy (EGDS), which revealed diffuse multiple sessile polypoid lesions in the whole stomach, but no polypoid lesions were seen in the esophagus or the duodenum (Fig. ). Colonoscopy showed similar multiple polypoid lesions in the terminal ileum, but no such polypoid lesions were observed in the whole colon (Fig. ). Pathology of the gastric polypoid lesions revealed hyperplastic mucosa, but focal dilated cystic glands were not seen (Fig. ). The tissue biopsy from the terminal ileum showed similar findings (Fig. ). He lacked chronic diarrhea and ectodermal abnormalities, which were seen in the typical CCS cases. No appropriate explanations of the diffuse gastrointestinal polyposis except for CCS were found, based on a combination of clinical, endoscopic and pathological findings. Therefore, we diagnosed him as having CCS.
The patient was treated with daily oral prednisolone, which was initially administered at a dose of 0.5 mg/kg with a proton pump inhibitor (vonoprazan fumarate: 20 mg daily), following tapered prednisolone and continued at a daily dose of 5 mg. After initiation of corticosteroids, he gradually recovered his appetite and gained weight up to 5 kg, accompanied by improved protein synthesis such as serum albumin, cholinesterase and total cholesterol levels (Table ). EGDS 1 year after initiation of corticosteroid revealed that the size and the numbers of polypoid lesions had decreased, and the reddish lesions had changed to normal color (Fig. ). During these observations, he had never experienced any chronic diarrhea or ectodermal symptoms.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [42.0, 'kg'], 'height': [153.0, 'cm']}",17.94182,17.04473,18.83891,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 153.0 cm, which is 153.0 cm * 1 m / 100 cm = 1.53 m. The patient's weight is 42.0 kg. The patient's bmi is therefore 42.0 kg / (1.53 m * 1.53 m) = 17.94182 kg/m^2."
2331,6,Body Mass Index (BMI),physical,decimal,pmc-5628183-3,Extracted,"A fetal ultrasound screening on a 35-year-old pregnant woman revealed a large (3.10 cm2), high echogenic tumor in the LV outlet septum of a 34-week-old male fetus. He was born by cesarean section at 37.5 weeks, with a weight (2.72 kg), height (48 cm), and head girth (33.5 cm) that were all within the 15–50th percentile. Echocardiography showed that the tumor not only exerted compression on the LV outflow tract, but also extended outward to the septum between the ascending aorta and the MPA, pushing them apart (Fig. a, b). The surface areas of the tumor were 2.60 cm2 in the long axis view and 4.10 cm2 in the short axis view. Electrocardiograms also detected frequent episodes of isolated ventricle premature contractions (VPC). We began everolimus therapy at 0.125 mg/day (0.658 mg/M2/day), along with a low dose of digoxin (5 μg/kg/day) on his second day of life. On the fifth day of therapy, the serum level was 16.12 ng/mL (higher than our target range); therefore, we reduced the daily dose to 0.0625 mg (0.33 mg/M2/day) (Fig. ). The following three weekly serum levels of everolimus were 4.41, 3.39, and 2.86 ng/mL, respectively. When he was discharged on his 32nd day of life, we increased the dose to 0.125 mg/day (0.51 mg/M2/day). Three months later, echocardiography revealed a remarkable shrinkage of the tumor (0.80 cm2 in long axis view, Fig. c), but his weight and height had decreased to less than 15th percentile for age; thus, we suspended the everolimus therapy. However, follow-up echocardiograms revealed a steady regrowth of the tumor. Specifically, its surface area increased to 0.99 cm2 after 2 weeks and to 2.97 cm2 after 2 months; the compression effect on the LV outflow tract also recurred. When he was 5 months old, we reinstituted everolimus therapy at 0.125 mg/day (0.379 mg/M2/day). Although all of the follow-up serum levels were less than 1.5 ng/mL, the tumor regressed smoothly. At 9-months-old, he contracted chicken pox, and the therapy was stopped again. He recovered smoothly without using antichicken pox medication. At 10 months of age, his weight (8.3 kg) and head girth (44.5 cm) had improved to the 15–25th percentile for his age, but his height (70.5 cm) remained below the 15th percentile. The specific loci for TSC-1 and TSC-2 gene abnormality were also negative.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [8.3, 'kg'], 'height': [70.5, 'cm']}",16.69936,15.86439,17.53433,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 70.5 cm, which is 70.5 cm * 1 m / 100 cm = 0.705 m. The patient's weight is 8.3 kg. The patient's bmi is therefore 8.3 kg / (0.705 m * 0.705 m) = 16.69936 kg/m^2."
2332,6,Body Mass Index (BMI),physical,decimal,pmc-6079435-1,Extracted,"A 12-year-old boy, S. R., came to an evaluation in October 2015 in the Orthodontic Department of Sapienza University of Rome. His weight was 24 kg (<3 centile) and height was 1.20 m (<3 centile), born from cesarean delivery at 39 weeks to a mother affected by CCD. He presented open fontanels and patent sutures at birth. Closure of anterior fontanel occurred at 3 years of age. In 2016, he underwent a complete clinical and auxological evaluation at the Department of Rare diseases of Sapienza University of Rome. His weight was 21.5 kg (25 centile) and height was 118.5 cm (25 centile), and the hand-wrist X-ray showed skeletal age of 6 years. Clinical examination showed narrow clavicles and accentuated joint mobility. The patient can oppose the shoulders on the midline. Orthopedic assessment showed left lumbar scoliosis and right dorsal scoliosis.
Audiological examination: normal audiometry and impedentiometry with tympanogram type A on the right and type C on the left. The cocleostapedial reflex was present bilaterally for both ipsilateral and contralateral stimulations.
(1) Laboratory findings: deficit of vitamin D 25-OH (17.5 ng/ml), Beta-Cross Laps levels of 0.81 ng/ml. DEXA z-score -2.8.
X-Ray of the spine (2 projections) and long bones (2 projections) shows pseudarthrosis of the medial third of both clavicles, that appears hypoplastic. Iliac wings appear squared and narrow. Hypoplastic pubic bones. Valgus femoral necks. Widened cephalic nuclei of the femoral bone. Proximal pseudoepiphysis of the second and fifth metacarpi in both hands. Brachy-telefalangy with hypoplastic nails. Retarded skeletal age between 6 and 7 years. TC of the head: mastoid appear thickened and ivory. Narrow antral cavities with thickened walls. Tympanic cavities with thickened walls. Cochlea surrounded by compact dense bone. Hyperemia of presphenoidal adenolymphoid tissues. Deviation of nasal septum.
The orthodontic diagnosis is summarized in (Figures –).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [21.5, 'kg'], 'height': [118.5, 'cm']}",15.31094,14.54539,16.07649,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 118.5 cm, which is 118.5 cm * 1 m / 100 cm = 1.185 m. The patient's weight is 21.5 kg. The patient's bmi is therefore 21.5 kg / (1.185 m * 1.185 m) = 15.31094 kg/m^2."
2333,6,Body Mass Index (BMI),physical,decimal,pmc-8309925-1,Extracted,"A 23-year-old woman with SCA type 7 diagnosed 6 years ago visited our clinic. Her chief complaints were postural instability and gait disturbance. She was fully conscious and reported no other underlying conditions. She was 167 cm tall and weighed 55.3 kg. The muscle strength of both lower extremities was graded as 4 (normal = grade 5). Contracture of major joints and spasticity were not checked. On the first visit, the patient could only walk short distances using a walker due to body sway. For symptom management, a rehabilitative intervention program was established.
An 8-week intervention program was prepared for the patient. The training program involved three 30-min sessions per week for 8 weeks, for a total of 24 sessions. Each session consisted of three parts: standing training (5 min), weight-bearing and weight-shifting exercises (5 min), and overground walking in a flat hallway while wearing the exoskeleton (20 min). The walking speed during training was adjusted according to the patient’s natural pace. All training sessions were conducted in our rehabilitation center under the supervision of a physical therapist ().
The ANGELLEGS device (SG Robotics, Seoul, Korea) was used as a gait-assistive exoskeletal device. This exoskeletal device weighs approximately 10 kg and consists of hip, knee, and ankle segments and a controller box located in the individual’s back. Only the hip and knee joints are motorized and actuated.
For individualized gait assistance in accordance with the patient’s gait phase, both force and kinematic sensors were employed. Pneumatic force sensors in both soles detected the pressure of toes and heels. As the patient started to walk, this ground force sensors sent the ground force data to the controller box and sensed the initial swing phase and initial contact phase of gait cycle. On the other hand, the kinematic sensors located in the actuation units detected the joint angle and enabled us to identify the appropriate timing for torque assistance.
Using the ground force and angular data as an input signal, the actuator can provide a predefined assistive torque tailored for the individual patient based on their gait phase and pattern. The magnitude and duration of assistive torque can be modulated depending on the individual’s functional status. Each motor can generate a continuous assistive torque of 24.3 Nm.
An additional noteworthy feature of ANGELLEGS is the low impedance of joint motor. Unlike many other overground exoskeletons with a large actuator friction, the ANGELLEGS reduces the resistive torque of actuation unit up to 0.5 Nm and allows it to prevent unexpected resistance while wearing the device.
ANGELLEGS can be used in various individuals with the partial impairment of gait function: elderly, stroke, spinal cord injury, neuromuscular diseases, etc. Individuals with cognitive impairment, pregnancy, or other critical medical conditions need to be excluded. In our case, we applied ANGELLEGS in an SCA patient who could walk partially with physical assistance.
Several functional assessments were performed before the program (T0), after the program (T1), and 4 weeks after the end of the program (T2). The Manual Muscle Test (MMT), Modified Ashworth Scale (MAS), Korean-Modified Barthel Index (K-MBI), Berg Balance Scale (BBS), Scale for the Assessment and Rating of Ataxia (SARA), European Quality of Life 5-dimension scale (EQ-5D), a 10-m walking test, a timed up-and-go test, and a three-dimensional gait analysis were implemented by a physical therapist and an occupational therapist. In addition, three-dimensional dynamic posturography (PRO-KIN system; TecnoBody Srl, Dalmine, BG, Italy) was used to examine static stability. The patient was asked to stand on both feet on the instrument’s tilting board for 30 s. While the patient tried to stand on the board without moving, movement of the center of pressure (COP) was recorded, and the average position of the COP was measured along the anterior–posterior (AP) and medial–lateral (ML) axes. The standard deviation (SD) of the COP was our main focus, as it indicates body sway. To assess cardiopulmonary function, we asked the patient to walk along a 10 m aisle 10 times at a comfortable pace while wearing the portable gas analyzer (model K4B2; COSMED Srl, Rome, Italy), and VO2 levels and metabolic equivalents (METs) were estimated.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.3, 'kg'], 'height': [167.0, 'cm']}",19.82861,18.83718,20.82004,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 167.0 cm, which is 167.0 cm * 1 m / 100 cm = 1.67 m. The patient's weight is 55.3 kg. The patient's bmi is therefore 55.3 kg / (1.67 m * 1.67 m) = 19.82861 kg/m^2."
2334,6,Body Mass Index (BMI),physical,decimal,pmc-5177720-1,Extracted,"A 2-month-old female presented with 2 days of fever. The fever persisted for more than 5 days after admission. Generalized erythematous macular rash was followed. She was born with 40 weeks of gestational age and 2.7 kg of body weight without significant perinatal illness. She has been completely well without irritability, dyspnea, tachypnea, or cyanosis prior to illness. The height was 57.7 cm (10th–25th percentile) and body weight was 5.4 kg (10th–25th percentile). The blood pressure and the pulse rate were 84/60 mmHg and of 148 beats per minute respectively. The cardiac examination was unremarkable except for sinus tachycardia and breathing sounds was equal bilaterally. The laboratory results were as follows: white blood cell, 9,640/µL; hemoglobin, 9.3 g/dL; platelet, 571,000/µL, erythrocyte sedimentation rate, 61 mm/hr; C-reactive protein, 12.9 mg/dL; procalcitonin, 1.96 ng/mL; prohormone of brain natriuretic peptide, 2,077 pg/mL; creatinine phosphokinase, 19 IU/L; troponin I, 0.024 ng/mL. Electrocardiography showed sinus tachycardia without ST-T changes or abnormal Q wave (). The chest X-ray showed normal heart contour and size. Because of concern of Kawasaki disease and infective endocarditis for prolonged febrile exanthema, transthoracic echocardiogram was done. The origin of the RCA was from the main pulmonary artery with RCA to pulmonary artery steal, predominantly diastolic (). It showed a dilated left coronary artery with normal origin and collaterals from left anterior descending coronary artery to RCA on short axis view (). The cardiac structure, function, and dimension were within normal range but ischemic change of posterior wall of left ventricle was noted (). The fever was subsided on 4th hospital day and the causative infectious agent was concluded as rhinovirus. Coronary angiography was arranged for further evaluation. Aortogram demonstrated prominent left main coronary artery, normal left anterior descending artery and circumflex artery. The left main coronary artery arose from the appropriate sinus without aneurysm or stenosis (). After a slight delay, the posterior descending and RCA were filled up in a retrograde fashion through collaterals of the left coronary artery (). On the 11th hospital day, the patient underwent direct reimplantation of anomalous RCA to aortic root establishing dual ostial circulation (). On the last follow-up, 5 months after the surgery, she was perfectly well on acethyl salicylic acid therapy. The echocardiographic study showed the normal biventricular function. The forward flow was well seen from aorta to RCA.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [5.4, 'kg'], 'height': [57.7, 'cm']}",16.21967,15.40869,17.03065,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 57.7 cm, which is 57.7 cm * 1 m / 100 cm = 0.577 m. The patient's weight is 5.4 kg. The patient's bmi is therefore 5.4 kg / (0.577 m * 0.577 m) = 16.21967 kg/m^2."
2335,6,Body Mass Index (BMI),physical,decimal,pmc-8272273-1,Extracted,"This was a 2-month-old male patient who was born at term with a birth weight of 3450 g. He was the second child of non-consanguineous Chinese parents. Since 2 weeks old he was admitted to local hospital due to recurrent vomiting, diarrhea, poor feeding, dehydration, hyponatremia, and hyperkalemia. Prompt therapy with sodium chloride (NaCl) and 5% dextrose as well as sodium bicarbonate infusion were initiated, then the patient was transferred to our unit for further investigation.
Physical examination (PE) on admission showed: weight of 4 kg (−1SD), length of 55 cm (0 SD), no dehydration, no hyperpigmentation, and normal external genitalia. The laboratory findings were as follows: Plasma Na 130 mmol/L (Normal Range [NR] 135 ~ 145 mmol/L), K 6.86 mmol/L (NR 3.5 ~ 5.0 mmol/L), Cl 104 mmol/L (NR 96 ~ 106 mmol/L), Adrenocorticotropic hormone (ACTH) 3.37 pmol/L (NR 1.6 ~ 13.9 pmol/L), cortisol < 5μg/dl (NR 5 ~ 20μg/dl), plasma renin activity (PRA) 1019.2 pg/ml (NR adult 4 ~ 24 pg/ml, neonatal renin 2.5–20 times higher than adult []), and plasma Ald 117.0 pg/ml (NR infants 1-12 months 50-900 pg/ml []). Further analysis showed plasma testosterone (T), progesterone (P), Androstenedione (A4), and 17-hydroxyprogesterone (17-OHP) levels were in the normal range. Urinalysis and CT scan for adrenal and renal were also normal. Patient was treated with fludrocortisone (Fc) 0.1 mg/day along with sodium supplementation 2-3 g/day. Since 6-month-old his mother had stopped sodium supplementation. FC dose had been reduced from 1.5 years old till 1.67 years old and was then fully discontinued by his parents. Currently, he is 5.17 years old with height of 104 cm (− 1.93SD). He is asymptomatic with normal serum electrolyte levels.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [4.0, 'kg'], 'height': [104.0, 'cm']}",3.69822,3.51331,3.88313,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 104.0 cm, which is 104.0 cm * 1 m / 100 cm = 1.04 m. The patient's weight is 4.0 kg. The patient's bmi is therefore 4.0 kg / (1.04 m * 1.04 m) = 3.69822 kg/m^2."
2336,6,Body Mass Index (BMI),physical,decimal,pmc-3085333-1,Extracted,"A 50-year-old Italian man was admitted to the hospital because of severe febrile illness associated with profound malaise, headache, sweating, and worsening jaundice of five-day duration. Two weeks before the onset of sickness he had returned from a business trip in Cameroon. The patient had not taken any chemoprophylaxis against malaria. He was obese (weight 98 Kg; height 176 cm), and an excessive use of alcohol was reported. He had not previously suffered from hypertension or any other known cardiovascular disease. Upon admission, he complained additionally of nausea, vomiting, and diarrhoea. He was fully conscious, normotensive with a blood pressure of 120/80 mm/Hg, but clinical examination revealed tachycardia and severe jaundice; his peripheral oxygen saturation was 95%. A neurological inspection did not show significant alterations. Full blood count revealed thrombocytopenia (17 × 109/L), haemoglobin at 14.6 g/dL, and white cell count at 10 × 109/L. Liver function tests documented hyperbilirubinaemia, moderate increase in serum transaminases, and moderate renal impairment; blood glucose levels were also raised. Coagulation screen did not show evidence of disseminated intravascular coagulation. Cardiac enzymes were normal (). A blood film revealed a heavy P. falciparum parasitaemia of 20%. A chest X-ray was normal, and the unique alteration observed in the electrocardiogram (ECG) was a low amplitude in QRS complexes. Serological testing for Cytomegalovirus, Epstein-Barr virus, seasonal influenza viruses A and B, adenoviruses, Chlamydia psittaci, Coxiella burnetii, Mycoplasma pneumoniae, respiratory syncytial virus, the Widal-Wright reaction and the slide macro-agglutination test for leptospirosis were negative. The patient was treated with 10 mg/kg b.w. (namely, 1000 mg) of I.V. quinidine gluconate t.i.d., plus ceftriaxone 2 g q24h I.V. and oral doxycycline 100 mg b.i.d., while waiting for the results of blood cultures. Within 12 hours of admission, a slow but progressive worsening of multiorgan failure was observed despite a marked reduction of parasitaemia. Given the severity of clinical setting, I.M. artemisin (300 mg loading dose, followed by 100 mg/daily) was initiated. At 40 hours after admission, the patient worsened suddenly. He became restless, confused, bradiarythmical, hypotensive (80/60 mmHg), and died in spite of prompt mechanical ventilation and cardiac resuscitation. The post-mortem evaluation revealed acute heart failure (bilateral pulmonary oedema) but no signs of myocardial ischaemia. The liver and the spleen were not enlarged. However, an histology of severe acute myocarditis with myocardiolysis was detected: diffuse lymphocytic infiltrates were surrounding the myocardial capillaries, inside which some intravascular parasitized RBCs were visible (). No sequestered parasites could be revealed in brain vessels.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [98.0, 'kg'], 'height': [176.0, 'cm']}",31.6374,30.05553,33.21927,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 176.0 cm, which is 176.0 cm * 1 m / 100 cm = 1.76 m. The patient's weight is 98.0 kg. The patient's bmi is therefore 98.0 kg / (1.76 m * 1.76 m) = 31.6374 kg/m^2."
2337,6,Body Mass Index (BMI),physical,decimal,pmc-6283716-1,Extracted,"A 34-year-old man (weight: 79 kg, height: 180 cm), who underwent removal of an oligodendroglioma in the left temporal lobe 4 years ago, was admitted for the removal of the recurrent tumor. An awake craniotomy was planned. Preoperative routine laboratory tests did not indicate any abnormal findings. The patient had no problems with cognition or communication but complained of intermittent headaches with a visual analog score of 3–5. During the preoperative assessment, he was fully cooperative and understood the surgical and anesthetic (asleepawake-asleep technique) procedures. Magnetic resonance imaging showed a hyperintense lesion in the left temporal pole and insula, suggesting the progression of a recurrent tumor. Computer tomography (CT) scans of the brain and skull radiography showed a bony cleft that was 2 mm wide in the left half of the skull (). Two hours prior to surgery, 1.5 g 5-aminolevulinic acid hydrochloride was ingested on neurosurgeon’s instructions. Upon entering the operating room, pulse oximetry, non-invasive blood pressure monitoring, and electrocardiogram monitoring were applied. An arterial catheter was inserted under local anesthesia for direct blood pressure measurements. The blood pressure and pulse rate were 124/62 mmHg and 57 beats/min, respectively. Following the intravenous administration of 50 μg fentanyl, the scalp nerve block and a ring block in the left hemisphere were performed over 30 minutes using a 25-gauge × 40 mm needle at the supraorbital, supratrochlear, zygomaticotemporal, auriculotemporal, greater occipital, and lesser occipital nerves. A local anesthetic mixture of 60 ml (20 ml 2% lidocaine, 20 ml 0.75% ropivacaine, and 20 ml normal saline with 1 : 200,000 epinephrine) was used. The patient tolerated the scalp nerve block with no evidence of intravascular injection.
Approximately 15 minutes after block completion, the seizure occurred initially with a sudden move up his trunk, followed by trembling of both extremities for 10 seconds. His mentality became stupor with dilated (7–8 mm) pupils without light reflex. The blood pressure and heart rate were 167/81 mmHg and 78 beats/min, respectively, with sinus rhythm and an oxygen saturation of 100%. Although the seizure subsided spontaneously, the patient remained in a stupor with dilated and fixed pupils (right: 7 mm; left: 8 mm) with no light reflex. The operation was postponed, as it was decided that proceeding with the awake craniotomy would not be feasible, and emergency CT was conducted in order to investigate the cause of the seizures. When the scan was completed after 15 minutes, the patient remained drowsy but could respond briskly to verbal commands. His pupils were anisocoric (right: 4 mm; left: 8 mm) with light reflex. The CT scan showed a localized fluid collection and small intracerebral hemorrhage (ICH) near the temporoparietal cortex beneath the skull defect ( and ). At 30 minutes after the seizure, he continued to remain drowsy but could respond to verbal commands. Pupils were asymmetric but responded well to light. At 55 minutes after the seizure, he fully recovered without neurological sequelae but could not recall the incident. He had a muscle power of 5/5 in his upper and lower extremities and a Glasgow coma scale score of 15. His pupils were isocoric (2 mm) with prompt light reflex. Prior to this, the patient had not complained of nausea, dizziness, or perioral numbness.
After being closely monitored for 1 hour and 20 minutes in the postanesthetic care unit, the patient was transferred to the neurosurgical care unit (NCU) for 6 hours and 40 minutes. Since no hemodynamic or neurological deterioration was observed, the patient was moved to an operating room, where he underwent the surgery for 7 hours and 30 minutes under general anesthesia. The lungs were extubated in the NCU 1.5 hours after the operation. He was transferred to the general ward on post-operative day 2 and released from the hospital on post-operative day 10.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [79.0, 'kg'], 'height': [180.0, 'cm']}",24.38272,23.16358,25.60186,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 180.0 cm, which is 180.0 cm * 1 m / 100 cm = 1.8 m. The patient's weight is 79.0 kg. The patient's bmi is therefore 79.0 kg / (1.8 m * 1.8 m) = 24.38272 kg/m^2."
2338,6,Body Mass Index (BMI),physical,decimal,pmc-4025146-1,Extracted,"A 50-year-old Japanese woman was referred to Chiba University Hospital in April 2012 because of jaundice and abnormal liver tests. She took several drugs for her depression and hypertension and drank alcohol (∼90 g daily). One year before admission, she had had a history of DILI by mianserin for her depression. Her height and body weight were 152 cm and 55 kg, respectively. She did not have hepatic encephalopathy. Laboratory findings were as follows: white blood cell count 7,100/μl (eosinophils 0.8%), platelets 155,000/μl, prothrombin time 18% (INR 2.36), total protein 5.3 g/dl, total bilirubin 21.9 mg/dl (direct bilirubin 15.0 mg/dl), alkaline phosphatase 313 IU/l, aspartate aminotransferase (AST) 314 IU/l, alanine aminotransferase (ALT) 112 IU/l, and γ-glutamyl transpeptidase 190 IU/l. Serum immunoglobulin G of 1,695 mg/dl and immunoglobulin M of 116 mg/dl were normal, but antinuclear antibody (ANA) was not positive (×80). Virus serology was negative for hepatitis A, B, C and E viruses, cytomegalovirus and Epstein-Barr virus acute infection. Computed tomography and abdominal ultrasound findings showed a non-atrophic liver with slightly ascites. We suspected a diagnosis of DILI or AIH, although her AIH score was underscored [, ], and administered corticosteroids. She was given bed rest and peripheral parenteral nutrition.
After 2 weeks, AST (73 IU/l), ALT (136 IU/l), total bilirubin (3.4 mg/dl) and prothrombin time (92%) were improved and liver biopsy was performed to diagnose her disease (fig. ). Hepatic architecture was preserved without cirrhosis, and inflammation of the periportal area was obvious with centrilobular necrosis. There were mononuclear cells in the portal area, but marked plasma cell infiltration was not observed. This observation might have been affected by the corticosteroid therapies. We diagnosed her as acute exacerbation of chronic hepatitis of unknown etiology. After ∼1 month, she was discharged (AST 22 IU/l, ALT 56 IU/l, total bilirubin 1.8 mg/dl and prothrombin time 98%). Two months later, her liver test had suddenly deteriorated (AST 76 IU/l, ALT 249 IU/l and γ-glutamyl transpeptidase 1,262 IU/l). At the same time, we became aware of her alcohol consumption and she was diagnosed with alcohol dependence by a psychiatrist.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.0, 'kg'], 'height': [152.0, 'cm']}",23.8054,22.61513,24.99567,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 152.0 cm, which is 152.0 cm * 1 m / 100 cm = 1.52 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.52 m * 1.52 m) = 23.8054 kg/m^2."
2339,6,Body Mass Index (BMI),physical,decimal,pmc-7796768-2,Extracted,"A 48-year-old male patient (weight 84 kg, height 186 cm) was scheduled for an ileostomy reversal surgery. ESP block was performed from the left side at the Th8 level with 20 mL 0.25% bupivacaine. The total amount of given fentanyl was 400 μg. After the operation, the patient complained of having pain 5/10 and 1 g metamizole was given. 2 h after operation, the pain was 6 at rest and on coughing, thus, 1 g paracetamol was given. After 6 h, the pain was 3/10 at rest and on coughing, but after 12 h he received 100 mg tramadol (the pain was 6 at rest and 8 on coughing). After 24 h, the pain was 5/10 at rest and 6/10 on coughing, thus, 1 g paracetamol was given, and after 36 h, the pain was 2/10 at rest and on coughing. Pain scores 4/10 at rest and 5/10 on coughing were reported after 48 and 72 h, respectively and 1 g paracetamol was given.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [84.0, 'kg'], 'height': [186.0, 'cm']}",24.28026,23.06625,25.49427,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 186.0 cm, which is 186.0 cm * 1 m / 100 cm = 1.86 m. The patient's weight is 84.0 kg. The patient's bmi is therefore 84.0 kg / (1.86 m * 1.86 m) = 24.28026 kg/m^2."
2340,6,Body Mass Index (BMI),physical,decimal,pmc-4331399-2,Extracted,"Case 2: A 47-year-old female diagnosed with type 2 diabetes 2 years before, and treatment started immediately thereafter. However, after a year, she stopped taking medications on her own decision. She presented to emergency department of our hospital with a fever of 38°C and bilateral lower leg pain for three days. She was hospitalized with a diagnosis of lower right leg cellulitis, and we began cefazolin administration at 3 g/day. On admission, her diabetic control was poor (HbA1c, 11.5%, postprandial blood glucose, 268 mg/dL); in addition, her body temperature was 39.2°C, pulse rate 106 beats/min, blood pressure 137/71 mmHg, height 166 cm, and body weight 61 kg. Routine laboratory testing showed an elevated leukocyte count of 13.8 × 103 cells/μL and a C-reactive protein level of 4.49 mg/dL. Serological tests for syphilis and HIV were negative. Soon after starting antibiotic treatment, her fever subsided. Five days later, redness and swelling disappeared; therefore, we changed treatment to cefdinir at 900 mg/day. She was discharged on day 8. The following day, we confirmed H. cinaedi from the blood culture taken on day 1; nevertheless, we decided to adopt a wait-and-see approach because no exacerbation of disease was observed since her initial admission.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.0, 'kg'], 'height': [166.0, 'cm']}",22.13674,21.0299,23.24358,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 61.0 kg. The patient's bmi is therefore 61.0 kg / (1.66 m * 1.66 m) = 22.13674 kg/m^2."
2341,6,Body Mass Index (BMI),physical,decimal,pmc-4623346-1,Extracted,"A 10-year-and-4-month-old boy (height 150 cm, 75-95 percentile, weight 67 kg, >97 percentile) was admitted to the intensive care unit via the emergency center with a chief complaint of mental change after one episode of generalized tonic-clonic seizure.
Prior medical history revealed that the patient had had one suspicious episode of seizure 6 years before, and had received an evaluation including blood tests, brain computed tomography (CT) scanning and electroencephalogram (EEG). All of the results were normal except for a subtle abnormality in the EEG, which was considered clinically insignificant. He had shown no more suspicious seizure events since that time without medication. He has been diagnosed with intellectual disability (intelligence quotient score of 44) and attention deficit hyperactivity disorder (ADHD) in a local psychiatric clinic. Medications included methylphenidate, atomoxetine, aripiprazole, fluvoxamine, benztropine, and topiramate on a daily basis. There was not any notable family history.
The physical examination revealed that the patient was in a comatose state, not responding to any noxious stimuli. Pupils were fixed and equal with a diameter of 5 mm each. Lung sounds were decreased on auscultation and the heart examination was normal. The abdomen was soft and not distended, and hypoactive bowel sounds were present. Rectal examination revealed hypotonic sphincter tone. Admission vital signs were as follows: pulse of 75 beats per minute, abnormally high blood pressure of 167/118 mmHg, respirations of 22 per minute, and temperature of 36.2℃.
Initial chest x-ray and chest CT scan showed findings compatible with pulmonary edema, and brain CT scan revealed severe brain swelling. Brain magnetic resonance imaging (MRI) showed severe brain swelling with tonsillar and uncal herniation ().
Although the laboratory findings 3 months prior to admission, performed when he visited our emergency center due to cervical lymphadenopathy, showed no abnormal findings, on the admission day, severe hypo-osmolar hyponatremia (serum Na, 101 mmol/L [basal reference values {BRV}, 135-145 mmol/L]; serum osmolality, 215 mOsm/kg [BRV, 289-308 mOsm/kg]) was found on the initial laboratory examination, along with low urine osmolality and low spot urinary sodium concentration (urine osmolality, 108 mOsm/kg [BRV, 50-1,200 mOsm/kg]; urine Na, 19 mmol/L). Serum glucose, total protein, albumin, blood urea nitrogen, and creatinine levels were all within normal range. The plasma adrenocorticotropin level was slightly low (5.54 pg/mL [BRV, 7.2-63.3 pg/mL]), while the serum cortisol level was in the normal range (12.5 µg/dL [BRV, 6.7-22.6 µg/dL]). Thyroid hormones were in the normal range (T3, 0.67 ng/mL [BRV, 0.58-1.59 ng/mL]; free T4, 0.97 ng/dL [BRV, 0.7-1.48 ng/dL]; thyroid-stimulating hormone, 2.97 µIU/mL [BRV, 0.35-4.94 µIU/mL]). The antidiuretic hormone (ADH) level was mildly elevated (13.34 pg/mL [BRV, 0-6.7 pg/mL]).
Shortly after admission, the patient experienced respiratory arrest. Endotracheal intubation was immediately done, and the patient was put on mechanical ventilation. After intubation, his blood pressure fell to 64/39 mmHg, and intravenous inotropics were administered. During the first 3 hours after admission, the patient showed polyuria with urination of 700 mL in 3 hours. After 3 hours, however, oliguria developed with sudden decrease in urination to 30 mL/hr even though diuretics were administered. The patient was put on continuous renal replacement therapy (CRRT) using continuous veno-venous hemodialysis.
After acute management, further past history was taken from the patient's mother, and it was revealed that for several months prior to admission, he had suffered from worsening of inattention, impulsivity, and hyperactivity, which led to him dropping out of school in the prior month. He also had difficulty controlling impulsive eating, and ate one type of food in excessive amounts for a period time. For example, he ate a lot of toothpaste for a while, and there was also a period of time when he ate a lot of soap. Since around 2 to 3 months prior to the event, his mother noticed that the patient drank excessive amounts of water, even drinking water directly from the shower tap, but she had not yet reported this change to the psychiatrist. The polydipsia had become worse in the previous few days, resulting in water regurgitation from his stomach when he lay down, as well as frequent bed-wetting.
Together with the patient's history and laboratory results, we concluded that the patient was in hypotonic hyponatremia due to psychogenic polydipsia.
For the treatment of brain edema, intravenous mannitol was administered. For hyponatremia, increment of serum sodium concentration was done by administration of hypertonic saline solution and intravenous furosemide, and fluid restriction. Using 3% sodium chloride fluid and normal saline solution together, 5.5 mEq/kg of sodium was first administered, and the sodium concentration of the fluid and fluid balance target were continuously adjusted according to the patient's serum electrolytes that were measured every 2 to 4 hours. The patient's serum sodium level had increased from 101 to 108 mmol/L by 8 hours after admission, and the subsequent serum sodium concentration were 110 mmol/L at 24 hours after admission, 117 mmol/L at 48 hours after admission, 127 mmol/L at 72 hours after admission, and reached the normal range at 96 hours after admission at 139 mmol/L ().
On the third day of his admission, a sudden increase in urine output (>350 mL/hr) occurred, with an increase in serum osmolality (291 mOsm/kg) and a decrease in urine osmolality (67 mOsm/kg). With the impression of central diabetes insipidus (DI), desmopressin acetate (Minirin, Ferring pharmaceuticals, Saint-Prex, Switzerland) was subsequently started, and CRRT was discontinued. The patient remained on desmopressin acetate after that, and his electrolytes were kept stable.
An EEG was performed on the fourth day of admission, and showed extremely low voltage and featureless background rhythms. The patient did not show self-respiration during an apnea test. On the 20th day of admission, after thorough neurological examinations together with the results of the EEG and brain MRI, the patient was declared to be in a state of brain death by a panel of neurologists.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [67.0, 'kg'], 'height': [150.0, 'cm']}",29.77778,28.28889,31.26667,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 150.0 cm, which is 150.0 cm * 1 m / 100 cm = 1.5 m. The patient's weight is 67.0 kg. The patient's bmi is therefore 67.0 kg / (1.5 m * 1.5 m) = 29.77778 kg/m^2."
2342,6,Body Mass Index (BMI),physical,decimal,pmc-5662356-1,Extracted,"A 12-year-old boy presented with recurrent fever for more than 2 years and was referred to Peking Union Medical College Hospital in 2014. The recurrent fever began without obvious predisposition and lasted 4 to 14 days per attack. The intervals between episodes range from 4 to 20 days. Temperature peak was up to 40°C. No cough, expectoration, rash, joint pain, or other discomfort appeared. He was referred to local clinics and had been diagnosed with Epstein–Barr virus (EBV) infection many times with positive EBV antibodies (EBV-Ab) and elevated plasma virus copies. Details of his physical examination, laboratory results, and therapies were unavailable.
He visited a hospital in Beijing owing to another fever in February 2014. Enlargement of lymph nodes and hepatosplenomegaly were discovered in physical examination. Assay of EBV-Ab and virus copies were performed, which indicated that IgA/early antigen (EA), IgA/viral capsid antigen (VCA), IgG/VCA, NA-IgG were positive and the virus copies were elevated to 3.45 × 10^5/mL. Diagnosis of EBV infection was made and then ganciclovir was employed, which ameliorated his symptoms and reduced the virus copies.
In May 2014, his fever relapsed and then he was referred to Peking Union Medical College Hospital for further treatment. Reviewing the history of the patient before the onset of recurrent fever, we found that he had frequent respiratory infections with twice a month. Physical examination indicated that his growth and development were within normal limits, weighing 38.5 kg and 146 cm in height (both in the range of the tenth percentile to the twenty-fifth percentile). Ichthyosis rash could be seen on his lower limbs. Several enlarged lymph nodes were palpable in the anterior region of the neck. No erythema or exudate of the throat or enlargement of tonsils was observed. There were no obvious abnormalities with cardiopulmonary examination. On the abdominal physical examination, hepatomegaly was found with 2 cm below the ribs, medial hardness, and a clear margin. Spleen could not be palpated. No deformity of joints was found as well.
On laboratory examination, peripheral blood count showed a decreased number of neutrophils and proportions of lymphocytes and neutrophils were inverse (63.2% and 25.9%, respectively). Acute phase reactants increased (erythrocyte sedimentation rate was 34 mm/h and C reactive protein was 15 mg/L). Liver function tests revealed slightly elevated glutamic oxaloacetic transaminase (AST) and normal alanine aminotransferase (ALT) (see Fig. ). Serum immunoglobulin was normal (IgG, 16.44 g/L; IgA, 5.24 g/L; IgM, 0.75 g/L) with decreased T cells in the peripheral blood (see Table ). Table summarizes the values of lymphocyte subsets changing with time and therapy. The numbers of CD3+ T cell especially the CD4+ T cell markedly decreased, while NK cell significantly increased. These abnormal results persisted despite treatment with cyclosporine A for 4 months from July 2015 to November 2015. Recombinant human interferon α-2a began to be used in November 2015 with a dose of 1 MU, 3 times a week. Four months later in February 2016, the above abnormality still existed despite the remission of his symptoms and improvement of other laboratory examinations. Dosage of recombinant human interferon α-2a was then added to 2 MU, 3 times a week. Henceforward, the values of lymphocyte subsets gradually returned to normal level. Positivity of EBV-Ab (see Table ) and elevated virus copies (1.5 × 10^6 copies/mL, see Fig. ) were observed. As we can see in Table , IgA/EA, IgA/VCA, IgG/VCA, NA-IgG were persistently positive no matter what treatment was used. Abdominal ultrasonography indicated hepatosplenomegaly (oblique diameter of right lobe of liver was 13.0 cm and spleen diameter was 14.3 cm). Cardiac ultrasound showed that he had patent ductus arteriosus.
His symptoms, abnormal signs, and laboratory indexes repeatedly occurred during the follow-up, which were improved with repeated treatment of ganciclovir. The diagnosis of CAEBV was established on the basis of diagnostics guideline proposed by Okano et al.[ The following aspects of our patient fulfilled the Okano guideline: recurrent infectious mononucleosis-like symptom include fever, swelling of lymph nodes, and hepatosplenomegaly; unusual pattern of anti-EBV antibodies with raised anti-VCA and anti-EA, and detection of increased EBV genomes in the peripheral blood; and exclusion of other chronic illness such as other infections, autoimmune diseases, and neoplastic diseases upon completion of related examinations.
The repeated use of ganciclovir could not prevent the frequent relapses of EBV infection for our patient. The combination of cyclosporine A for 4 months could not reduce the virus copies to normal level as well. With the possibility of immunodeficiency disease, next-generation sequencing (NGS) was performed to analyze all known PID genes followed by Sanger sequencing to verify results. The patient possessed 2 novel compound heterozygous mutations of JAK3 (see Fig. ). The p.H27Q mutation came from his father, while p. R222H from his mother. Thus, his diagnosis was corrected for JAK3-deficiency PID and CAEBV. Antiviral therapy was replaced with subcutaneous injection of recombinant human interferon α-2a with 1 to 2 MU, 3 times a week since November 2015. The virus copies gradually decreased to the normal level and his symptoms ameliorated significantly. Moreover, ALT decreased to normal level after 3 months. His latest follow-up was in February 2017. He has hardly had a fever for nearly 1 year and the virus copies and ALT were normal.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [38.5, 'kg'], 'height': [146.0, 'cm']}",18.06155,17.15847,18.96463,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 146.0 cm, which is 146.0 cm * 1 m / 100 cm = 1.46 m. The patient's weight is 38.5 kg. The patient's bmi is therefore 38.5 kg / (1.46 m * 1.46 m) = 18.06155 kg/m^2."
2343,6,Body Mass Index (BMI),physical,decimal,pmc-2943688-1,Extracted,"Patient: 63-year-old male
Major complaint: Fever
Pre-existing history: Mitral valve insufficiency
Family history/lifestyle history: Nothing particularly relevant
A slight fever had persisted from about June 2008 until 10 days before surgey. In July 2008, the patient underwent a TUR-P for prostatic hyperplasia using 3 days of cefotiam (CTM) i.v. 0.5g ×2/day and was discharged from the hospital on Day 10 after surgery without fever. On about Day 40 after surgery, a fever of 38–39°C was observed, so the patient was suspected of having a urinary-tract infection and was admitted to the hospital.
Body height: 166.3 cm; Body weight: 59.5 kg; Body temperature: 37.8°C; Pulse rate: stable at 84/min; Blood pressure: 116/76 mmHg. Respiratory sound: resonant; Cardiac sound: clear/no noise; Abdomen: flat/soft; Neurological findings: nothing in particular. Laboratory data at the time of admission:
Hematological values: WBC 9000/µL, RBC 4.01 × 106/µL, Hb 10.3 g/dL, Ht 30.5 %, Plt 36.6 × 104/µL , PT 78 %, PT-INR 1.14, APTT 29.4 sec, Fib 628 mg/dL
Biochemistry: TP 6.8 g/dL, Alb 3.2 g/dL, T-bil 0.5 mg/dL, D-bil 0.0 mg/dL, AST 24 IU/L, ALT 35 IU/L, ALP 631 IU/L, γ-GTP 102 IU/L, Ch.E 198 IU/L, LDH 203 IU/L, CK 18 IU/L, Amy 71 IU/L, T-chol 193 mg/dL, TG 80 mg/dL, LDL 122 mg/dL, BUN 9 mg/dL, Cre 0.7 mg/dL, UA 2.4 mg/dL, Na 139 mEq/L, K 4.2mEq/L, Cl 103 mEq/L, Ca 9.4 mg/dL, IP 3.5 mg/dL, Glu 95 mg/dL, HbA1c 5.4%, CRP 5.6 mg/dL
Urinalysis: pH 7.5, RBC many/hpf, WBC many/hpf
After admission, CTM 0.5 g × 2/day was administered for 3 days, but the CRP did not become negative, so Meropenem (MEPM) 0.5 g × 2/day was administered instead. A tendency for pyretolysis was observed, but because recovery from the urinary-tract infection was slow, echocardiography was performed for the purpose of eliminating endocarditis. In the echocardiogram findings, vegetation was observed, so Ampicillin (ABPC) 2 g × 4/day and Gentamicin (GM) 60 mg × 2/day were administered for four weeks. Pyretolysis and decreased CRP were observed, but the CRP did not become negative. Even after the 4-week administration of antibiotics, the vegetation persisted in the echocardiogram and a possibility of valve failure was suspected, so a valve replacement was performed. Furthermore, the head and chest to pelvic CT did not show any obvious abscess formation.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [59.5, 'kg'], 'height': [166.3, 'cm']}",21.51456,20.43883,22.59029,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.3 cm, which is 166.3 cm * 1 m / 100 cm = 1.663 m. The patient's weight is 59.5 kg. The patient's bmi is therefore 59.5 kg / (1.663 m * 1.663 m) = 21.51456 kg/m^2."
2344,6,Body Mass Index (BMI),physical,decimal,pmc-3219782-1,Extracted,"The patient was a 30-year-old primipara with a twin pregnancy at 36 weeks. She had an accompanying premature rupture of the membrane and had planned to have a cesarean section. She did not have a past medical history and her height and weight was 164 cm and 69 kg, respectively. The physical examination, blood test, urine analysis, chest x-ray, and EKG were all within normal limits (). Combined spinal-epidural anesthesia was planned because the patient wanted regional anesthesia for the twin pregnancy and there were with no special contraindications.
Preanesthesia medication was not used. EKG monitoring, non-invasive automatic blood pressure measuring, and pulse oximetry were set up after the patient arrived at the surgical theatre. The patient's blood pressure was 130/80 mmHg; heart rate was 90 beats per minute before induction. 3 L of oxygen was provided through nasal prong while observing the patient's vital signs. She was positioned left lateral decubitus for the regional anesthesia using an 18 G modified Tuohy (Espocan®, B. Brown, Germany) needle, and epidural access between the third and fourth lumbar vertebrae was attempted. Right after the puncture, bleeding was observed through the needle, and the puncture needle was immediately removed. Compression was attempted for bleeding control. Since there was no observed bleeding or hematoma in the puncture area, a second attempt at puncture was tried between the second and third lumbar vertebrae with a 27 G subarachnoid needle inserted in an 18 G epidural needle after examining the epidural area with the loss of resistance technique. After observing spontaneous flow of CSF fluid, 5 mg of 0.5% bupivacaine dextrose was injected, and then, the subarachnoid needle was removed. The subarachnoid needle bevel was toward the cephalic, with a 20 G epidural catheter (Perifix® soft tip, Braun, Germany) located 3 cm from the cephalic. Then, the patient was repositioned to the supine position. There were no difficulties during the procedure, and she did not complain of any dysesthesia, numbness, or pain. After no blood or CSF had been aspirated, a 3 ml test amount of epinephrine (1 : 200,000) was injected through the epidural catheter with a 3-minute observation period. The patient was stable with blood pressure at 130/80 mmHg and heart rate at 95 beats per minute. 10 minutes after intraspinal injection, the level of the sensory block was at the tenth thoracic spinal nerve segment. In order to increase the level of the sensory block, after checking again that no blood had been aspirated, 5 ml of 2% lidocaine mixed with epinephrine (1 : 200,000) was injected repeatedly with a total of 20 ml being injected. After 20 minutes, the level of the sensory block did not change remaining at the tenth thoracic spinal nerve segment. Therefore, it became necessary to switch to general anesthesia. 250 mg of Thiopental and 75 mg of succinylcholine were infused. After observed loss of consciousness and muscle relaxation, intubation was done. While the surgery was proceeding, the anesthesia was maintained using 2 L/min of O2, 2 L/min of N2O, 5 vol% of desflurane, and 4 mg of vecuronium until the babies were delivered. 4 minutes after induction, the baby boy was delivered through cesarean section, and the baby girl was delivered 1 minute after the birth of the boy. The babies weighed 2.4 kg and 2.6 kg with 5-minute-apgar scores of 7 and 8. After the placenta was expelled, 20 units of oxytocin mixed with 100 ml of normal saline were infused, but uterine contraction did not successfully proceed. Bleeding of more than 3,000 ml occurred in the 5 minutes after delivery. 0.2 mg of methylergonovine was injected to advance uterine contraction, but the bleeding continued. Her hemoglobin level dropped to 8.4 mg/dl. Since massive bleeding was not expected before operation, there was no blood prepared. One hour after the operation, 2 units of packed RBCs prepared under emergency conditions were transfused. Crystalloid solution and colloid solution was infused before the transfusion with repeated injections of ephedrine to maintain systolic blood pressure above 90 mmHg. After the operation, blood pressure was maintained above 90/40 mmHg without an inotropic or vasopressor agent. Total anesthetic time was 2 hours 10 minutes; the operation time was 1 hour 20 minutes. Total bleeding during anesthesia was approximately 4,000 ml; urine amount was approximately 200 ml, and 2 units of packed RBCs were transfused. 1,000 ml crystalloid and 2,000 ml colloid solutions were infused. In the recovery room, the patient received an extra 2 units of packed RBCs and 2 units of fresh frozen plasma were transfused.
After arriving at the recovery room, the level of the sensory block was below T12. She was transferred to the ward after 1 hour after partial recovery of sensory and motor function was observed and the epidural catheter was removed. Right after arriving at the ward, a blood test was done; hemoglobin was 10.1 mg/dl with prolonged PT and aPTT each measured at 21.1 sec and 52.3 sec, respectively. Vaginal bleeding continued after arriving at the ward. Intrauterine compression was attempted by foley catheter insertion and 2 units of fresh frozen plasma were transfused. 4 hours after the operation, PT and aPTT were 19.3 sec and 46.4 sec. Hemoglobin level decreased to 7.1 mg/dl and platelet count decreased to 82,000/mm3. 3 units of packed RBCs and 10 units of platelet concentrate were transfused. The vaginal bleeding continued but decreased.
At the ward, the patient complained of abdominal pain and back pain but was able to get some sleep by controlling pain through patient-controlled-analgesia (PCA). Next morning, 10 hours after the operation, the back pain continued, and sensory and motor paralysis on both lower extremities were observed. Emergency magnetic resonance imaging (MRI) was done and a compressive mass was found at the posterior of the lumbar vertebrae (). Acute epidural hematoma was diagnosis, and an infusion of high dose steroid therapy was carried out. The patient was transferred to the surgical theatre 4 hours after symptoms developed. An emergency decompression laminectomy was done to get rid of the epidural hematoma at the L2/L3 segment of the lumbar vertebrae. The patient's coagulation process did not work well and more than 1,000 ml of bleeding occurred with 3 units of packed RBCs being transfused. After the operation, motor and sensory function of the lower extremities did not change but the pain in the back had mildly improved. However, 1 day after the hematoma was removed, the back pain had become aggravated. Another emergency MRI was done and the hematoma was found to have occurred again, and the operation was done again. She complained of excessive numbness in her lower extremities but muscle strength gradually recovered. One month after the operation, she was discharged after she was able to walk without any working aid with some restrictions. Five months after the operation, neurological symptoms were totally improved without any sequelae.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [69.0, 'kg'], 'height': [164.0, 'cm']}",25.65437,24.37165,26.93709,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 164.0 cm, which is 164.0 cm * 1 m / 100 cm = 1.64 m. The patient's weight is 69.0 kg. The patient's bmi is therefore 69.0 kg / (1.64 m * 1.64 m) = 25.65437 kg/m^2."
2345,6,Body Mass Index (BMI),physical,decimal,pmc-8072816-1,Extracted,"The patient was born with C/S at 38 weeks of gestation with a birth weight of 3820 g; was the 3 rd alive child of a 35-year-old mother in her 4th pregnancy. His mother’s second pregnancy was a male with agenesis of corpus callosum (ACC), congenital heart disease and absence of nasal bone which were detected on ultrasound at 24th week. The pregnancy had been terminated without genetic tests or autopsy. The patient’s antenatal ultrasonographic investigation showed an IACC at 18 weeks of gestation but fetal MRI was not performed and amniocentesis revealed 46, XY karyotype. He had not defecated for the first three days of life; he defecated a large amount of stool after rectal stimulation. The patient underwent laparotomy for intestinal biopsies and diagnosed with HSCR and ileostomy was opened.
He presented to our clinic when he was one year old with fever for two days. His weight was 8.4 kg (3 rd percentile); height 74 cm (3 rd percentile); and head circumference 46 cm (25th percentile). Hypertelorism, uplifted earlobes with a central depression, frontal bossing, telecanthus, deeply set eyes, infraorbital fold, long lashes, broad eyebrows with a medial flare, a wide nasal bridge with prominent and rounded nasal tip, low-hanging columella, open-mouth expression, thin “M” shaped upper lip, prominent chin, short neck, wide-spaced nipples, overlapping toes, and pes planus were noted (
–). Abdominal examination showed no guarding or rebound tenderness; he had orange-colored liquid stool in an ileostomy bag. He had eye contact, social smile, and stereotypic hand movements, speaking indistinguishable three words. Traction response was poor, and he was hypotonic on vertical suspension. He could not sit unassisted. Deep tendon reflexes were normal; bilaterally plantar reflexes were extensor; sustained Achilles clonus was noted. At admission, urinalysis showed pyuria. Acute pyelonephritis was diagnosed. Urinary ultrasound and voiding cystourethrogram showed grade 3 hydronephrosis affecting the right ureter. Cranial magnetic resonance imaging (MRI) demonstrated enlargement of the third and lateral ventricles, the occipital and temporal horns. There was a bilateral incomplete hippocampal inversion, enlargement of thalamus, nucleus caudate, and ACC (
–). A heterozygous “class 2” c.646dupT (p.Cys216LeufsTer23) mutation on exon 6 of ZEB2 (zinc finger E-box binding homeobox 2) gene was detected by a mutation surveyor program, and the diagnosis of MWS was made. At 16 months, he presented with fever due to pneumonia and generalized seizure for 5 minutes. His EEG showed no epileptic discharge but an immature parietooccipital rhythm for his age. Valproic acid was initiated. The patient is still on follow- up for developmental delay, renal, and gastrointestinal problems.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [8.4, 'kg'], 'height': [74.0, 'cm']}",15.33966,14.57268,16.10664,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 74.0 cm, which is 74.0 cm * 1 m / 100 cm = 0.74 m. The patient's weight is 8.4 kg. The patient's bmi is therefore 8.4 kg / (0.74 m * 0.74 m) = 15.33966 kg/m^2."
2346,6,Body Mass Index (BMI),physical,decimal,pmc-2553057-1,Extracted,"A 15 year old otherwise healthy Caucasian male student (52 kilograms of weight, 170 centimeters of height, no smoker, no drinking alcohol, not assuming medications with no significative family history) presented to the Emergency Department with a 24 hours abdominal pain and increase of his abdominal girth. The pain was non-continuous, poorly localized, and was non-colicky and non-radiating in nature. There was no history of vomiting, bowel or urinary symptoms. Over the prior 2 months, he reported one other similar episode that had resolved spontaneously. He was afebrile and his vital signs were stable. Abdominal examination revealed marked diffuse abdominal tenderness and guarding. A large hypogastric abdominal mass was palpable. Urinalysis and urine culture were normal; he had a white cell count of 19.4 × 109/L, hemoglobin 11.0 g/dL and platelets 410 × 109/L). On abdominal sonography, no spleen could be demonstrated in the normal position; the left upper quadrant was filled with bowel loops. An enlarged spleen extending from lower-polar region of the left kidney to the pelvis was seen. A large hypoechoic area was seen, suggestive of infarction, with a streak of perisplenic fluid. Ultrasonography demonstrated no blood flow in the splenic vein and in the splenic artery. Subsequent contrast-enhanced CT scan also showed absence of the spleen in the left upper quadrant as well as an enlarged spleen in the left lumbar and iliac region. The splenic parenchyma showed poorly, inhomogenous enhancing areas suggestive of infarction. The splenic vein was dilatated and showed a non-enhancing filling defect near the hilum, indicating the presence of a thrombosis. The splenic vessels, pancreatic tail, and the surrounding fat formed a whorled appearance, supermedial to the splenic hilum, that was suggestive of torsion.
The patient underwent exploratory laparotomy through a midline incision. This revealed the absence of all splenic ligamentous attachments and short gastric vessels with a consequently dislocation of a bigger and congested spleen in the pelvis. This organ, wrapped in the omentum, was in a serious ischemic suffering due to a 720° clock torsion around its exceptionally long pedicle (≈ 20 cm); besides was confirmed pancreatic body and tail ectopy (Figure ). Following the derotation, the volume of the organ has decreased but became fixed in above norm dimensions (Figure ). A total splenectomy was performed in view of a symptomatic wandering spleen, with hypersplenism and portal hypertension. The patient's post-operative course was uneventful.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [52.0, 'kg'], 'height': [170.0, 'cm']}",17.99308,17.09343,18.89273,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 52.0 kg. The patient's bmi is therefore 52.0 kg / (1.7 m * 1.7 m) = 17.99308 kg/m^2."
2347,6,Body Mass Index (BMI),physical,decimal,pmc-7891243-1,Extracted,"A 79-year-old woman was referred to our hospital for recurrent paroxysmal AF with palpitation. She had a history of transient ischaemic attack and hypertension. She was on candesartan (8 mg once daily), amlodipine (2.5 mg once daily), and apixaban (2.5 mg twice daily). Her body weight was 39 kg, and height was 159 cm. All laboratory findings were within normal range. Electrocardiogram showed normal sinus rhythm and no evidence of ischaemic changes or ST elevation. Chest X-ray was unremarkable. She showed a dilated left atrium (LA diameter: 31 mm, LA volume index: 35 mL/m2) and normal left ventricular systolic function (left ventricular ejection fraction: 76%). Pre-procedural cardiac computed tomography (CT) showed four pulmonary veins, and slight dilated ascending aorta (maximum diameter: 40 mm, ) with mild calcific plaques. We decided to perform CA for AF, and recommended TOE before the CA to assess the presence or absence of left atrial appendage thrombus (LAAT) because she had a CHADS2 score of 4.
On the day before the CA, TOE was performed with an iE33 (Philips Medical System, Andover, MA, USA) with a 4-MHz OmniPlane probe. After local pharyngeal anaesthesia with lidocaine spray, the patient was placed in the left lateral position and midazolam (3 mg) was administered for mild sedation. Her physical examination showed a regular pulse rate (PR) of 62 b.p.m., a blood pressure (BP) of 117/84 mmHg, and a normal temperature. Her physical examinations at the time of TOE procedure were unremarkable. At 3 min after probe insertion, she had a BP of 117/84 mmHg, PR of 62 b.p.m., and there was no abnormal finding of the ascending aorta at that time (). We then administered additional midazolam (2 mg) due to body movement. At 5 min after the insertion, we confirmed that the absence of LAAT (BP: 95/40 mmHg, PR: 76 b.p.m.). However, TOE showed ascending aortic dissection without pericardial effusion (). The probe was removed at the end of anaesthesia after flumazenil (0.2 mg) infusion. After waking, she had severe back pain, and underwent a contrast-enhanced cardiac CT. Cardiac CT demonstrated Stanford type A aortic dissection extending from the aortic root to the bifurcation of common iliac arteries, and tight stenosis in the right coronary artery (maximum diameter; 49 mm, ). An electrocardiogram showed a normal sinus rhythm and no ST-segment abnormalities. The patient underwent a replacement of the ascending aorta, and a coronary artery bypass graft surgery for the right coronary artery. After surgery, the patient gradually stabilized, and she was transferred to a rehabilitation hospital on the 60th postoperative day. After 9 months of follow-up, the patient is doing well.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [39.0, 'kg'], 'height': [159.0, 'cm']}",15.4266,14.65527,16.19793,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 159.0 cm, which is 159.0 cm * 1 m / 100 cm = 1.59 m. The patient's weight is 39.0 kg. The patient's bmi is therefore 39.0 kg / (1.59 m * 1.59 m) = 15.4266 kg/m^2."
2348,6,Body Mass Index (BMI),physical,decimal,pmc-5646148-1,Extracted,"A 9-year-old girl (130 cm,33 kg) was scheduled for open resection of a right 5 × 4 cm extra adrenal paraganglioma encircling the abdominal aorta (Fig. )and a 2 × 1.4 cm metastatic tumor in liver(Fig. ). Her medical history included dyspnea on exertion and persistent hypertension(150–160/90-100 mmHg).Her serum adrenaline, noradrenaline and dopamine levels were 0.617 pmol/ml(normal,0.05–1.39 pmol/ml),97.417 pmol/ml(normal,0.51–3.62 pmol/ml)and0.046 pmol/ml(normal,0.07–0.68 pmol/ml). The coagulation studies and NT-proBNP level were normal, but a transthoracic echocardiogram demonstrated mild mitral regurgitation and left ventricular dilation(LVEDV,43 mm) with an estimated LVEF of 49%. The diagnosis of paraganglioma and catecholamine-induced cardiomyopathy was made.
Preoperatively, her blood pressure was 120–130/80-90 mmHg, well controlled on phenoxybenzamine(20 mg/Q12h orally).Fluid(2000 ml/d)had been given for 4 weeks to restore the blood volume. On the morning of the operation, her supine blood pressure was 120/70 mmHg with heart rate 80–100 beats/min. Midazolam 1 mg was administered intravenously as premedication. On arriving in the operating room, she acted calm and cooperative. Left radial arterial blood pressure monitoring was established under local anesthesia before anesthesia induction. Simultaneous measurements of cardiac output and stroke volume variation as determined by the FloTracTM device (Edwards Lifesciences)were also recorded. General anesthesia was induced with propofol 60 mg,sufentanyl 30 μg and rocuronium 30 mg.The trachea was intubated without an increase in blood pressure. An invasive central venous catheter was placed via the right internal jugular vein. Anesthesia was maintained with inhaled sevoflurane in oxygen, combined with sufentanyl and rocuronium injected intravenously. The operation was performed in the supine position with her systolic pressure stabilized at 100 mmHg, central venous pressure at 8 mmHg and heart rate at 90 beats/min. When the skin incision was made, her blood pressure kept stable without the infusion of vasodilators. Before the tumor manipulation, we started a continuous intravenous infusion of 0.5 mg/h of sodium nitroprusside. Just after the start of tumor manipulation, her blood pressure and heart rate exceeded 180/110 mmHg and 120 beats/min respectively, and a bolus injection of phentolamine 2 mg was followed. Blood pressure and heart rate decreased to 150–170/80-100 mmHg and 110 beats/min with the continuous infusion of sodium nitroprusside at 2 mg/h. Removal of the right-sided paraganglioma was difficult, immediately after the resection of the tumor, blood pressure and heart rate decreased to 110/60 mmHg and 100 beats/min, managed with the continuous infusion of sodium nitroprusside at 1.2 mg/h. According to the estimated blood loss (approximately 400 ml), a combination of two unit packed red blood cells and 200 ml fresh frozen plasma were transfused and CVP increased from 6 mmHg to 8 mmHg.During the dissection of the metastatic tumor in the liver, blood pressure and heart rate increased to 150/90 mmHg and 120 beats/min again. Hemodynamics could be satisfactorily controlled with a further 2 mg intravenous phentolamine. Before the resection of the metastatic tumor, continuous infusion of sodium nitroprusside was stopped, but systolic blood pressure decreased rapidly to approximately 70 mmHg after removal of the tumor. The status was corrected by continuous infusion of norepinephrine at 0.05 μg/kg/min to maintain an reasonable level in systolic blood pressure to 100 mmHg.At that time,the CVP was 7 mmHg and HR was 110 beats/min(Table ). Blood glucose remained between 9 and 11 mmol/L under anesthesia and body temperature was 36.5–37.3 °C. The patient was transferred to the ICU with trachea intubated and a continuous infusion of norepinephrine at 0.12 μg/kg/min. The total operative duration was 5 h and 29 min. The blood loss was 600 ml and the total quantity of fluid administered was 2800 ml(1700 ml crystalloid solutions, 500 ml colloidal solutions, two unit packed red blood cells and 200 ml fresh frozen plasma).
When the girl arrived at the intensive care unit,norepinephrine infusion was continued at 0.12 μg/kg/min together with esmolol infusion at 100 mg/h to maintain the hemodynamics relatively stable with about 20% deviation from the baseline. In the first 24 h after the operation, the intropic support was continued and the patient received 2520 ml of crystalloids and colloids for blood volume expansion. But the norepinephrine infusion had to increased to 0.4 μg/kg/min under the guidance of consistent monitoring of BP(range,80–90/40-50 mmHg),HR(range,90-110beats/min)and CVP(range,5-8 mmHg). The coagulation studies was normal, but NT-proBNP was 844 pg/ml while her echocardiogram showed a deteriorated LVEF of 41% and mild left ventricular hypertrophy. Considered as the factor of insufficient blood volume, in the next 24 h, acetated Ringer solution (2600 ml),concentrated red blood cells(200 ml)and albumin (100 ml)had been rapid infused. Her arterial blood pressure slowly improved to 110/60 mmHg and the estimated LVEF improved to 50% with adequate urine output. All intraoperative monitoring was continued for 5 days before cardiovascular stability was conformed without the vasoactive drugs support, and she was discharged home by postoperative day 15.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [33.0, 'kg'], 'height': [130.0, 'cm']}",19.52663,18.5503,20.50296,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 130.0 cm, which is 130.0 cm * 1 m / 100 cm = 1.3 m. The patient's weight is 33.0 kg. The patient's bmi is therefore 33.0 kg / (1.3 m * 1.3 m) = 19.52663 kg/m^2."
2349,6,Body Mass Index (BMI),physical,decimal,pmc-3782506-1,Extracted,"A 22-month-old male was admitted to our hospital due to fever and cough. The fever was subjective and intermittent for 4 days. The cough was described as dry and of 5 days duration. There was no vomiting, diarrhea, rash, or seizures. The mother denied witnessing any ingestion of acetaminophen or toxic material. Past medical history and family medical history were unremarkable. Immunization, including influenza/H1N1, was reported as up to date per parents.
Vitals on admission were as follows: temperature 39°C, respiratory rate 50 breaths per minute, blood pressure 100/70 mmHg, pulse rate 110 beats per minute, oxygen saturation 90% in room air, weight 12.3 kg (50th percentile), height 88 cm (75th percentile), and head circumference 48.2 cm (50th percentile).
On examination, the child was drowsy; oral mucosa was dry; pharynx was erythematous with no associated cervical lymphadenopathy; the respiratory exam showed bilateral diffuse coarse crepitations and no wheezing; the abdomen was soft and mildly distended, with audible bowel sounds; the liver was palpated 3 cm below the right costal margin, with possible tenderness in the right upper quadrant, but there was no rebound. The rest of the physical exam was unremarkable.
Initial laboratory investigations were as follows: complete blood count showed a white blood count of 3,500/uL, hemoglobin 12.5 g/dL, platelets of 195,000/uL; erythrocyte sedimentation rate 17 mm/hour; creatinine of 66 umol/L, albumin 25 g/L, alanine aminotransferase (ALT) 2,106 U/L, aspartate aminotransferase (AST) 850 units/L, alkaline phosphatase (ALP) 291 units/L, gamma glutamyl transferase (GGT) 107 units/L, and total bilirubin 13 umol/L; the rest of the chemistry results were unremarkable, as were the coagulation profile, ammonia, and lactate. His venous blood gas was pH 7.2, carbon dioxide partial pressure (pCO2) 44 mmHg, partial pressure of oxygen (pO2) 29 mmHg, bicarbonates (HCO3) 17 mEq/L, with a base excess of 11. Polymerase chain reaction (PCR) was conducted on the nasopharyngeal secretion and was positive for H1N1. Cerebrospinal fluid studies were normal, and urine and blood culture did not grow any organisms. Hepatitis A immunoglobin (Ig)-M was negative, hepatitis B surface antigen and core antibody were negative, hepatitis B surface antibodies were positive, and hepatitis C IgM was negative. Furthermore, and because of the fever and mildly enlarged liver, PCR was conducted on a blood sample to check for herpes simplex virus, adenovirus, Epstein–Barr virus, and cytomegalovirus; results were negative.
A chest radiograph showed bilateral streaky infiltrates with no focal consolidation. An ultrasound of the abdomen showed mild coarse hepatic echo texture with no focal lesion.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [12.3, 'kg'], 'height': [88.0, 'cm']}",15.88326,15.0891,16.67742,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 88.0 cm, which is 88.0 cm * 1 m / 100 cm = 0.88 m. The patient's weight is 12.3 kg. The patient's bmi is therefore 12.3 kg / (0.88 m * 0.88 m) = 15.88326 kg/m^2."
2350,6,Body Mass Index (BMI),physical,decimal,pmc-8107244-1,Extracted,"Written informed consent was obtained from the patient for the publication of this case.
A 73-year-old patient with a height of 162.1 cm and weight of 71.4 kg was admitted to the hospital for scheduled transurethral resection of bladder tumor and the prostate (TUR-BT and TURP) for the treatment of bladder cancer and benign prostate hyperplasia. The patient had been taking metformin and rosuvastatin for type 2 diabetes mellitus and hyperlipidemia, respectively. In preoperative testing, blood glucose levels measured at fasting and 2 h postprandial were 142 mg/dl and 257 mg/dl, respectively. HbA1c was 8.3%. The patient did not have any complications. Other preoperative screening test results were within normal limits. He underwent TUR-BT and TURP under general anesthesia.
General anesthesia was induced by intravenous administration of propofol (90 mg). The patient was ventilated with a bag and mask using oxygen and desflurane. Rocuronium 50 mg was injected intravenously to block the neuromuscular junction. Manual ventilation using a bag and mask was easy, and there was no excessive compression on the patient’s face. Four minutes after the rocuronium injection, the patient was intubated using a video laryngoscope and 7.5 mm cuffed endotracheal tube. After confirming that the breath sounds could be auscultated symmetrically in both lung fields, the endotracheal tube was fixed at a depth of 23 cm at the right corner of the patient's mouth. Anesthesia was maintained with desflurane and remifentanil. Entropy was maintained within the range of 40–60 during the surgery. The surgery lasted for 75 min uneventfully. Intraoperative blood glucose level was 110 mg/dl. At the end of the surgery, the train-of-four (TOF) count was measured as 0. Neuromuscular blockade was reversed with the intravenous administration of 200 mg of sugammadex. The patient was extubated after the anesthesia provider confirmed that the TOF ratio was 100%. The patient was transferred to the postanesthetic care unit and was shifted to the general ward after full recovery from anesthesia.
On the following day, the patient complained of numbness of the lower lip, and a consultation was requested to the anesthesia department on postoperative day 2. When we visited the patient, the sensation of touch, temperature, and pain in the left lower lip were intact, but he complained of mild hypoesthesia of touch on the right lower lip. There was no abnormality in the motor function of the lip. In the results of a neurological consultation on postoperative day 4, it was mentioned that the symptom could be related to mononeuropathy due to underlying diabetes mellitus. Since there were no other neurologic symptoms and because mental nerve injury is difficult to diagnose with general neuromuscular tests, the neurologist suggested close observation. The patient was discharged on postoperative day 7 after confirming that he had no difficulties in daily life, such as eating or speaking. The symptoms resolved spontaneously after 6 weeks.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [71.4, 'kg'], 'height': [162.1, 'cm']}",27.17266,25.81403,28.53129,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.1 cm, which is 162.1 cm * 1 m / 100 cm = 1.621 m. The patient's weight is 71.4 kg. The patient's bmi is therefore 71.4 kg / (1.621 m * 1.621 m) = 27.17266 kg/m^2."
2351,6,Body Mass Index (BMI),physical,decimal,pmc-4384408-1,Extracted,"A 55-year-old, 167 cm, 70 kg male suffering from alcoholic end-stage liver cirrhosis with a 'model for end stage liver disease' score of 15 points, and Child-Pugh class C, was scheduled for deceased-donor liver transplantation. He had a history of hepatic encephalopathy, refractory ascites, and undergoing a repetitive paracentesis over the previous 6 months. When he first arrived at our hospital 3 months earlier, he had suffered from hepatic hydrothorax, which waxed and waned. Pleural fluid analysis revealed transudative fluid. The preoperative transthoracic echocardiography revealed elevated right ventricular systolic pressure (46 mmHg) without coexisting cardiopulmonary disease. The preoperative chest computed tomography showed massive pleural effusion and related passive atelectasis in the right middle and lower lobe (). On the day of surgery, he was in mild respiratory distress and a plain chest radiograph revealed massive pleural effusion of the right lung and associated lung collapse (). An 8.5-French percutaneous pigtail catheter was placed in the right pleural space 3 h before surgery and 600 ml of transudative pleural fluid were drained naturally.
Anesthesia was induced with fentanyl (100 µg), midazolam (3 mg), thiopental sodium (250 mg), and rocuronium (40 mg). Anesthesia was maintained with a 50% oxygen/air mixture and sevoflurane. Neuromuscular block was maintained with cisatracurium. Hemodynamic monitoring included the right radial and femoral arterial, central venous, pulmonary arterial, and pulmonary capillary wedge pressures, and cardiac output measurements (Vigilance monitoring, Edwards Lifesciences, Irvine, CA, USA) using pulmonary artery catheter (CCOmbo V; 7.5 French, Edwards Lifesciences).
The prehepatic and anhepatic phase was uneventful and during that period, 500 ml of transudate were drained through the pigtail catheter. After reperfusion of a graft, he required a bolus of epinephrine (10 µg), dobutamine infusion (5-10 µg/kg/min) and norepinephrine infusion (0.05-0.1 µg/kg/min) to maintain mean arterial pressure > 65 mmHg. At this time, his ventilation was well controlled and the results of arterial blood gas analysis were unremarkable, as shown in . However, 30 min after reperfusion, we found a straw-colored fluid emanating from the ET tube. The trachea was intermittently suctioned and total volume suctioned via ET tube was over 500 ml in 30 min. The characteristics of the regurgitated fluid were similar to those of fluid drained through the pigtail catheter, which decreased visibly at that time. Hypoxemia did not occur with a FIO2 of 0.5, as indicated by the stable SpO2 during the entire intraoperative period. Thus, we suspected the presence of a connection between the airway and pleural space on the affected side and that the pleural fluid on the right side was regurgitated towards the ET tube. We changed a standard ET tube to a 37-French double-lumen tube (DLT; Covidien, Mansfield, MA, USA) to provide differential lung ventilation. A regurgitated fluid was obtained continuously from the right bronchus, but not from the left bronchus. After a discussion with the operating surgeons and a thoracic surgeon, we decided to open the diaphragm to check for the presence of APF. Air leakage via a 1.0 cm defect on the right lung surface during positive-pressure ventilation was detected through a 1.5 cm incision of the right side of the diaphragm ( and ). The APF and incised diaphragm was repaired with a suture with a minimal residual APF. The remaining surgical procedure was otherwise uneventful. At the end of surgery, the chest tube was inserted in the right pleural cavity. During the 550-min anesthesia, 7,400 ml of crystalloid, 200 ml of 20% albumin, 12 units of leukocyte depleted red blood cell, and 10 units of fresh frozen plasma were infused. Urine output was 880 ml and the estimated blood loss was about 10,000 ml.
Following the surgery, the patient was transferred to the intensive care unit with the placement of a DLT. An immediate postoperative chest radiograph suggested a decreased pleural effusion and mild bilateral pulmonary edema (). As the amount of regurgitated fluid decreased, the DLT was replaced with a standard ET tube on the day after the operation. On the second postoperative day, pneumothorax developed on the right side (), which resolved 2 days later. The ET tube was removed on the fourth postoperative day. In total, 500-1,000 ml of drainage were obtained daily via the chest tube during 2 weeks with ongoing ascites. Drainage decreased slowly thereafter, and the chest tube was removed on postoperative day 21 ().",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [167.0, 'cm']}",25.0995,23.84452,26.35448,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 167.0 cm, which is 167.0 cm * 1 m / 100 cm = 1.67 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.67 m * 1.67 m) = 25.0995 kg/m^2."
2352,6,Body Mass Index (BMI),physical,decimal,pmc-3861361-1,Extracted,"The participant we describe here was a healthy 24-year-old woman (height 174 cm, weight 56 kg) with no history of drug allergy and alcohol use. Laboratory tests conducted during screening on July 17, 2009, found that she was negative for HIV, syphilis, and hepatitis B. Her hepatic enzymes and creatinine clearance were within normal limits.
After about 8 weeks of taking TDF-FTC, this participant complained of mild paresthesiae, numbness, and a tingling sensation in her upper limbs that was associated with pain and cold. The symptoms did not affect her daily activities, physical examination was normal, and she had not taken any medications that are known to cause peripheral neuropathy upon interaction with TDF-FTC. After an additional 4 days, she developed a disabling weakness of her upper limbs and bilateral weakness of power grip of grade 3–4 and fine tremors in her hands at rest and with activity. Neurological examinations found normal orientation in time and place as was her pupillary light reaction and fundoscopy. Muscle tone, reflexes, and somatic sensations were also normal, but there was a mild deviation of the mouth and the tongue to the left, on protrusion.
After trial closure, analysis of her plasma and intracellular drug levels at week 4 and 8 were consistent with moderate adherence to TDF-FTC., At week 10, TDF-FTC was temporarily withheld due to safety concerns and as per the study protocol. The participant was given oral Neurorubine® (Vitamins B1, B6, and B12; Mepha Ltd, Aesch, Switzerland) for 2 weeks. Within 2 weeks after stopping the study drug, she was free of all symptoms. At week 12, she was restarted on the study drug according to the protocol. However, 1 month after restarting the pill, the participant complained of other neurological symptoms of posture-dependent numbness of her upper limbs. The numbness occurred while bending down and resolved after assuming an upright posture. She did not experience the earlier disabling muscle weakness or tremors. Her neurological exam was normal, and she continued taking the study drug. Her drug levels at week 24 (analyzed on stored samples after study closure) were consistent with low adherence to TDF-FTC.
At week 25, the study team decided to withdraw the study drug until neurologic exploration was completed. At week 28, the participant reported having taken a traditional herbal medicine, orally as a single dose. The nature of the herbal medication could not be determined by the study team.
At week 29, the magnetic resonance imaging (MRI) of her brain and cervical spine was found to be normal. Blood tests (performed at that time) revealed her lactate dehydrogenase was elevated at 514 U/L (normal range: 230–460), but her aldolase and creatinine phosphokinase were normal. The neurologist – with extensive experience in the treatment of HIV-infected patients – who assessed the participant observed:
The clinical manifestation in this patient was not the usual peripheral neuropathy known in patients receiving TDF-FTC. A typical TDF-FTC-related neuropathy starts with feet and only later goes to upper extremities. The fact that the paresthesiae occurs when the patient bends forward (Lhermitte’s sign) suggests a possible lesion of the cervical spine, though MRI findings were normal.
In addition to the study drug, Neurorubine®, and the unknown herbal medication, the participant reported taking the following medications: 1) medroxyprogesterone acetate, from enrolment throughout the study period; 2) ibuprofen at week five for one day; 3) amoxicillin/clavulanic acid at week seven for 10 days; and 4) diclofenac at weeks 9 and 10 for 3 and 7 days respectively.
Overall, for safety concern, the participant was managed as if she was assigned the TDF-FTC arm. The clinical team decided not to un-blind the participant’s study group allocation, because this would not influence clinical case management. The participant’s postural numbness gradually improved and was completely resolved by her week 36 visit. The participant finished study follow-up on September 28, 2010. Her symptoms did not reoccur after she discontinued the study pill.
After trial closure, levels of vitamin B12 on her stored blood samples at weeks 4, 8, 12, and 16 all showed normal values: 625, 727, 744, and 791 ng/L respectively (normal range: 239–931 ng/L).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [56.0, 'kg'], 'height': [174.0, 'cm']}",18.4965,17.57167,19.42133,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 174.0 cm, which is 174.0 cm * 1 m / 100 cm = 1.74 m. The patient's weight is 56.0 kg. The patient's bmi is therefore 56.0 kg / (1.74 m * 1.74 m) = 18.4965 kg/m^2."
2353,6,Body Mass Index (BMI),physical,decimal,pmc-6439983-1,Extracted,"The proband (designated patient V:1) is a 6.5 years old girl, born to consanguineous parents of Iraqi Jewish descent, who first presented to the pediatric rheumatology clinic with bilateral painless thickening of PIPs joints of two months duration. She denied any history of fever, trauma or rash. She was born after uneventful pregnancy and labor, at a birth weight of 3700 g. Her previous medical history was notable only for several episodes of pneumonia before the age of 3 years, and normocytic anemia. On presentation, physical examination revealed symmetric thickening of the DIPs and PIPs of both hands with no evidence of joint effusion, tenderness or stress pain. All joints showed normal range of motion. There was no evidence for tenosynovitis. All other joints showed no signs of synovitis, tenosynovitis or enthesitis. Muscle strength was normal and no evidence for muscle wasting. The skin was clear and no nail changes were noted. Her height was 110 cm (10th percentile) and weight was approximately 19 kg (~30th percentile). The initial evaluation included radiographs of the hands demonstrating short distal phalanges with bilateral swelling of soft tissue around the DIPs and PIPs (Fig. b); normal radiographs of the feet and pelvis; radiograph of the spine which showed shortening of the intervertebral spaces D 4–5-6 and D 10–11-12; and laboratory tests which included a complete blood count with absolute and relative eosinophilia (2.2 K/microL, Normal < 0.7 K/microL; 24.2%), normal C-reactive protein (CRP) and erythrocyte sedimentation rate (0.07 mg/l and 13 mm/hour, respectively), and biochemistry, CPK, complement levels, Rheumatic factor (RF) and serum lipid profile all within normal range. Testing for antinuclear antibody (ANA) was negative as well. Ophthalmological evaluation was normal and showed no evidence of uveitis, and abdominal ultrasound showed no evidence of hepatosplenomegaly. During several hospitalizations to our center an extensive evaluation ensued, and several working diagnoses were entertained, including mucopolysaccharidosis, pachydermatodactyly and Winchester syndrome.
On a follow up visit at the age of 9.5 years, she had a further progression of the joint deformation (Fig. a), including restricted range of motion of the neck (80° on extension, 60° on lateral rotation bilaterally) and wrists, limited flexion and extension of the fingers at the PIPs level, knees and ankles. Back movements were within normal range. Once again, no evidence of active synovitis, tenosynovitis or enthesitis was noted. Due to the multiple joint involvement, physical therapy, occupational therapy and hydrotherapy were initiated in order to maintain range of motion.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [19.0, 'kg'], 'height': [110.0, 'cm']}",15.70248,14.91736,16.4876,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 110.0 cm, which is 110.0 cm * 1 m / 100 cm = 1.1 m. The patient's weight is 19.0 kg. The patient's bmi is therefore 19.0 kg / (1.1 m * 1.1 m) = 15.70248 kg/m^2."
2354,6,Body Mass Index (BMI),physical,decimal,pmc-6023039-1,Extracted,"A 56-year-old man had experienced lower back pain one to two times per year since the age of 23 years. At 28 years of age, he began to experience neck pain, for which he received acupuncture and moxibustion treatment as well as massages. However, from around 34 years of age, his symptoms, including the lower back pain, gradually became exacerbated. Upon experiencing limited anteflexion and rotation of the torso and cervical spine, he presented to a local clinic. Despite a follow-up observation with nonsteroidal anti-inflammatory drugs, his symptoms progressed and he was diagnosed with AS based on the findings of plain radiography and magnetic resonance imaging (MRI) of the spine performed at 41 years of age. Treatment with sulfasalazine and etanercept was initiated; however, it was discontinued within only 2 months because of the development of systemic urticaria and acute colitis.
At 44 years of age, the patient developed respiratory distress upon exertion and chest pain attacks, and close examination by echocardiography and cardiac catheterization revealed AR. Although the AR required prosthetic blood vessel replacement, there were findings that could not be explained only by AS with concurrent AR (e.g., a difference in blood pressures in the right and left arms). Therefore, the patient presented to our hospital, where he was admitted for the purpose of undergoing close examination of AR complicated with AS and surgery for treatment of cardiovascular disease.
At the time of admission, the patient’s height was 154.5 cm and weight was 42.4 kg. A significant difference was observed in the blood pressures in his right and left arms: 150/30 mmHg in the right arm and 110/68 mmHg in the left arm. Upon chest auscultation, diastolic murmurs characteristic of AR were heard.
Blood testing revealed a leukocyte count of 7,000/µL (neutrophils: 70.2%, monocytes: 4.1%, lymphocytes: 23.4%, eosinophils: 2.0%, and basophils: 0.3%), C-reactive protein (CRP) level of 5.7 mg/dL, and erythrocyte sedimentation rate of 91 mm/h; testing for anti-nuclear antibodies by indirect immunofluorescence was negative. Furthermore, the brain natriuretic peptide level was high (417.0 pg/mL; reference range, 0.0–18.4 pg/mL). The patient tested positive for HLA-A2, B46, and B61 but negative for HLA-B27, B52, and B67. Furthermore, eye examination revealed a history of uveitis in the right eye, and bilateral funduscopy revealed dilatation and tortuosity of the retinal veins, which were thought to involve vasculitis.
shows the plain radiographs of the lumbar and cervical spine. Bone erosion and osteosclerosis were observed surrounding the sacroiliac joint, and findings suggestive of vertebral body squaring and ossification of the spinal ligament were seen on the lumbar and cervical spine radiograph; these findings were consistent with AS. Furthermore, while the electrocardiogram showed a sinus rhythm, there were findings suggestive of left ventricular hypertrophy and left atrial loading. Echocardiography revealed an ejection fraction of 0.35–0.40; severe AR and first-degree MR were observed with dilatation of the left ventricle and ascending aorta. No significant stenosis of the coronary artery was observed on coronary three-dimensional computed tomographic angiography (3D-CTA); however, magnetic resonance angiography (MRA) of the chest revealed stenosis of the left subclavian artery and left-side common carotid artery (). Furthermore, 3D-CTA of the chest and pelvis revealed no abnormal findings in the branching vessels peripheral to the thoracic aorta (e.g., renal artery); however, the common carotid and left subclavian artery findings were consistent with the MRI findings (), which led to strong suspicion for the presence of TA. Furthermore, no intracranial abnormal findings were observed on cranial MRI and MRA.
These test results and clinical findings satisfied the clinical and radiographic criteria of the Modified New York Criteria for AS proposed by van der Linden et al. in 1984 as well as the diagnostic criteria for TA recommended by the American College of Rheumatology in 1990 (i.e., difference in blood pressures of the left and right arms, difference in brachial pulses of the left and right arms, and stenosis of the left subclavian artery). Therefore, the patient was thought to have AS with concurrent TA.
The AR was severe, and dilatation of the ascending aorta with a maximum diameter of 45 mm was observed; thus, aortic valve replacement and prosthetic blood vessel replacement of the ascending artery were considered appropriate. However, based on the results of various tests, it was highly likely that the elevated CRP level and erythrocyte sedimentation rate contributed to the AS and TA; the active vasculitis in the aorta was deemed to have an unfavorable effect on the postoperative progress. Therefore, 30 mg/day of prednisolone was initiated 44 days prior to performing surgery primarily to treat the TA. On day 14 of treatment, the CRP level normalized, and when the dose was reduced to 15 mg, the Bentall procedure and hemiarch replacement were performed for annuloaortic ectasia. The intraoperative aortic biopsy sample was stained with hematoxylin–eosin and elastica van Gieson and was analyzed at high- and low-power fields for pathological examination (). Hematoxylin–eosin staining revealed hypertrophy of the aortic tunica adventitia, destruction and necrosis of the elastic fibers indicating lymphocyte invasion in the tunica media, and hypertrophy in the intima. Elastica van Gieson staining revealed giant cell invasion at the site of severe inflammation, which was consistent with the findings for TA.
The postoperative course was uneventful, and the patient was discharged on postoperative day 14. Thereafter, treatment continued with prednisolone, methotrexate, and warfarin potassium, and the patient’s condition remained stable.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [42.4, 'kg'], 'height': [154.5, 'cm']}",17.7627,16.87456,18.65084,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 154.5 cm, which is 154.5 cm * 1 m / 100 cm = 1.545 m. The patient's weight is 42.4 kg. The patient's bmi is therefore 42.4 kg / (1.545 m * 1.545 m) = 17.7627 kg/m^2."
2355,6,Body Mass Index (BMI),physical,decimal,pmc-6066631-1,Extracted,"A 16-month-old girl presented with complaints of vomiting and fast breathing for 1 day. There was no history of fever, cough, diarrhea, abdominal distension, and jaundice. She had history of recurrent admissions with similar complaints for 5 months of age. She was first born of a nonconsanguineous marriage with an uneventful neonatal period and normal developmental milestones.
On examination, she was lethargic with pulse rate 92/min, respiratory rate 56/min, and blood pressure 96/70 mmHg with no signs of dehydration. Her weight (9.3 kg) and height (77 cm) corresponded to the 25th–50th centile on the WHO charts. Per abdomen, nontender, firm hepatomegaly was present 3 cm below right costal margin. Rest of general physical and systemic examination was within normal limits.
Laboratory workup showed hemoglobin 12.5 mg%, total leukocyte count 7800 cell/mm3, blood sugar 84 mg/dl, mildly deranged liver enzymes, normal kidney function tests, and mild ketonuria (1–2+). Venous blood gas revealed high anion gap (AG) metabolic acidosis (pH = 7.1, HCO3
− = 15.1 mEq/L, AG = 20 mEq/L (range 8–16 mEq/L)) with high serum lactate levels (53.6 mg/dl, normal 7–14 mg/dl). Ultrasound showed mild hepatomegaly with normal echotexture. Both serum lactate (18.94 mmol/L, normal 0.6–3.2 mmol/L) and cerebrospinal fluid lactate (9.6 mmol/L, normal 1.1–2.8 mmol/L) were elevated with normal blood lactate-to-pyruvate ratio (12.3:1). Blood tandem mass spectrometry and urine metabolic screen was normal with no organic aciduria in urinary gas chromatography-mass spectroscopy.
She was managed with intravenous maintenance fluids and sodium bicarbonate with marked clinical improvement within 36 h. She was discharged on parental request pending further work-up. Two weeks after discharge, she presented again with generalized convulsions and rapid breathing. There was a history of prolonged fasting for 8–10 h before this episode. Mild tachypnea and hepatomegaly were the only findings in otherwise normal clinical examination. On investigation, she had hypoglycemia (21 mg/dl) with high anion gap metabolic acidosis (pH = 7.0, HCO3-=18.1 meq/L, AG = 16 meq/L) and high serum lactate (19.8 mmol/L). Laboratory workup ruled out possibility of infection or meningitis and revealed hyperuricemia (12 mg/dl), hypertriglyceridemia (196 mg/dl), and hypercholesterolemia (176 mg/dl). She improved within 24 h on 25% dextrose, anti-epileptics, intravenous fluids, sodium bicarbonate, and oral allopurinol. A differential diagnosis of FBP1 deficiency or glycogen storage disorder type 1 (GSD1) was considered.
In view of mild hepatomegaly with normal echotexture on ultrasound, a molecular analysis was planned first. The molecular analysis of all the coding exons of FBP1 gene revealed a compound heterozygous mutation IVS4-1G>A (c.426 + 1G>A) in exon 3 and mutation c.611_614delAAAA in exon 6, confirming the diagnosis of FBPase deficiency. The molecular analysis of parents revealed heterozygous mutation in one gene each, making both of them a carrier (Father - heterozygous for c.611_614delAAAA and Mother - heterozygous for IVS4-1G>A [c.426 + 1G>A]), for which they were given appropriate genetic counseling. The patient was given preventive feeding advice including frequent feeding, avoiding fasting, and foods with high fructose:glucose ratio (grapes, apples, cherries, and honey) and to use more uncooked starch such as rice powder in her diet. On follow-up, she was found to have normal growth and development with normalization of metabolic parameters and decrease in her liver size.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [9.3, 'kg'], 'height': [77.0, 'cm']}",15.68561,14.90133,16.46989,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 77.0 cm, which is 77.0 cm * 1 m / 100 cm = 0.77 m. The patient's weight is 9.3 kg. The patient's bmi is therefore 9.3 kg / (0.77 m * 0.77 m) = 15.68561 kg/m^2."
2356,6,Body Mass Index (BMI),physical,decimal,pmc-7860507-1,Extracted,"An 8-month old male infant presented with bilateral cryptorchidism since birth was referred to our hospital and hospitalized. His mother had tocolytic treatment prior to his birth. The patient’s medical and family history revealed nothing unusual. The patient had received no prior treatment for the bilateral cryptorchidism. Physical examination showed that the patient was 68.5 cm high, weighed 9.5 kg, had a head circumference of 42.4 cm and was in good general health except for the bilateral cryptorchidism. Examination of the patient’s four limbs and chest, palpation of the spine and musculoskeletal examination revealed no abnormality, and the patient had normal vision and hearing. An X-ray revealed no obvious pulmonary abnormality. The patient had bilateral flat and empty scrotum with no split and there was no obvious inguinal mass on either side (Fig. a, b). The patient had a properly developed corpus cavernosum and normal urinary meatus. B-mode ultrasound indicated bilateral cryptorchidism and visualized a left testis of 1.4 × 0.8 cm and a right testis of 1.2 × 0.6 cm in the lower abdominal cavity. In addition, the ultrasound also visualized the upper margin of the left testicle as a hypoechoic mass extending to the spleen. The ultrasound findings suggested an undescended right testis and a possible SGF on the left side (Fig. a). The ultrasound did not reveal any abnormality in the patient’s heart, liver or spleen. Magnetic resonance imaging (MRI) visualized no obvious testis on either side and no obvious abnormality in the patient’s heart, spleen or liver. In addition, MRI showed no obvious uterus, ovary or fallopian tube-like structures. As to the patient’s kidneys, both the ultrasound and MRI visualized kidneys with normal sizes and shapes at normal positions, intact renal capsule, and renal pelvis and ureter that were not dilated, In addition, per our routine practice, we assessed the patient’s External Masculinization Score (EMS) to summarize clinical features representing his genitalia and to determine the degree of masculinization of this male infant, he had an EMS score of 10 out of 12 []. Overall, our physical examination of the patient ruled out other obvious congenital disorders.
We also screened for genetic variant(s) related to disorder of sex development with panel based next generation sequencing (NGS) test using multiple ligation-dependent probe amplification (MLPA). The NGS test did not reveal any known SGF related genetic variant, although the test did indicate that the patient carries a missense mutation in the gene encoding SET binding protein 1 (SETBP1) (c.2608G>A [p.Gly870Ser]), a causative variation for Schinzel-Giedion syndrome (OMIM #269150) [], a frameshift or nonsense mutation in SETBP1 known to cause autosomal dominant mental retardation-29 (OMIM #616078) [], and a mutation in the oligophrenin-1 gene (OPHN1) known to cause X-linked mental retardation with cerebellar hypoplasia (OMIM #300486) [].
The first laparoscopic surgery was performed on January 11, 2018, single-site laparoscopy revealed closed internal rings on both sides, right testis in the in the iliac fossa, positioned approximately 2 cm above the right internal ring, at about the same height as the junction between the iliac vessel and the ureter (Fig. b, c). It also showed that the left testis was about 3.5 cm above the left internal ring and 1.5 cm above the junction between the iliac vessel and the ureter, and that the left testis was fused to the spleen with a clear demarcation (Fig. d). In addition, the left and right vas deferens were also visualized. No obvious uterus, ovary or fallopian tube-like structure was visible. The laparoscopic examination further revealed that the patient’s right spermatic vessel was poorly developed and short (Fig. b, c). A diagnosis of undescended right testis and continuous SGF on the left side was made. The patent’s Internal Masculinization Score (IMS) was also assessed during the examination as part of our routine practice to summarize clinical features of his internal sex organ and to determine the degree of masculinization of the male infant, and he had an IMS score of 9 out of 10 [].
As the European Association of Urology (EAU) guideline for paediatric urology recommends that “If a testis has not concluded its descent at the age of six months (corrected for gestational age), and since spontaneous testicular descent is unlikely to occur after that age, surgery should be performed within the subsequent year, and by age eighteen months at the latest” [], we decided to perform the orchiopexy immediately. Considering the fact that the positions of the patient’s testes were high and in the abdominal cavity, and that the right spermatic vessel was poorly developed and short, it would be very difficult and risky to complete their descent into the scrotum through the internal rings and inguina or through the straight hernia triangle with single-stage Fowler-Stephen orchiopexy. It has been reported that although the risk of postoperative testicular atrophy was comparable between single-stage and 2-stage Fowler-Stephen orchiopexy, 2-stage Fowler-Stephen orchiopexy could lead to a more favorable testicular position in the scrotum []. As the patient’s mother had history of multiple miscarriages and received tocolytic treatment prior to the patient’s birth, the patient’s parents wanted the procedure to be as safe and effective as possible. Therefore, we decided to perform separate 2-stage laparoscopic staged Fowler-Stephen orchiopexies for both the left and the right sides. In order to reduce the risk of bilateral testicular atrophy, we decided against performing Stage 1 for both the left and the right sides simultaneously. Rather, we decided that Stage 1 for the right side should be performed first, if it was successful, Stage 2 for the right side and Stage 1 for the left side should then be performed months later, and if this was also successful, Stage 2 for the left side should be performed months after that. We completed stage 1 of laparoscopic staged Fowler-Stephen orchiopexy for the right testis without treating the SGF on the left side during the same single-site laparoscopic examination. Ultrasound monitoring immediately after the surgery revealed that the right testis had normal shape and good blood supply. B-mode ultrasound taken four months later (May 2, 2018) visualized a right testis of 1.2 × 0.6 × 0.6 cm with a normal shape and good blood supply and a testis-shaped hypoechoic mass of 1.5 cm × 0.8 cm extending to the spleen with good blood supply.
7 month later, on August 20, 2018, stage 2 of laparoscopic staged Fowler-Stephen orchiopexy for the right testis (descent of the right testis into the scrotum), separation of the left testis from the spleen as well as stage 1 of laparoscopic staged Fowler-Stephen orchiopexy for the left testis were performed. Ultrasound monitoring immediately after surgery revealed that both testes had normal shapes and good blood supply. B-mode ultrasound taken 4 months later (December 12, 2018) showed a right testis of 1.0 × 0.6 × 0.6 cm and a left testis of 1.1 × 0.5 × 0.4 cm, both with adequate blood supply.
Stage 2 of laparoscopic staged Fowler-Stephen orchiopexy for the left testis was performed 7 months later (March 12, 2019), the left testis descended into the scrotum. The residual spleen tissue was cut from the left testis (Fig. e) and post-operative biopsy confirmed that it was accessory spleen tissue. Ultrasound monitoring immediately after surgery revealed that both testis had normal shapes and good blood supply, it also visualized smooth tunica vaginalis and multiple hyperechoic spots without acoustic shadows indicating possible testicular microlithiasis (Fig. a–d). B-mode ultrasound taken 1 month later (April 20, 2019) revealed that both testes were in the scrotum and that the left and right testes had a size of 1.3 × 0.7 × 0.6 cm and 1.3 × 0.8 × 0.7 cm, respectively. Both testes had healthy blood supply and the spleen had a normal shape. The patient had an uneventful recovery and suffered no adverse or unanticipated events. Follow-up ultrasound 1 year after the surgery revealed no obvious abnormalities in the shapes of the testes or their blood supply (Fig. e, f) and the patient’s penis and scrotum had normal appearance (Fig. c).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [9.5, 'kg'], 'height': [68.5, 'cm']}",20.24615,19.23384,21.25846,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 68.5 cm, which is 68.5 cm * 1 m / 100 cm = 0.685 m. The patient's weight is 9.5 kg. The patient's bmi is therefore 9.5 kg / (0.685 m * 0.685 m) = 20.24615 kg/m^2."
2357,6,Body Mass Index (BMI),physical,decimal,pmc-7064361-1,Extracted,"A 40-year-old, 166-cm-tall premenopausal woman weighing 57 kg visited outpatient clinic with gradually increasing left wrist pain for the past months without a history of trauma. Seven years prior to the visit, she had been treated with lateral impingement of the ankle secondary to a calcaneal deformity for a similar episode of worsening right heel pain. At that time, plain radiography and computed tomography of the right ankle revealed significantly reduced bone density, particularly affecting the calcaneus, suggesting osteoporosis (). A whole-body bone scan revealed persistent high tracer uptake at the right calcaneus (). Calcaneal lateral wall ostectomy and bone biopsy were performed and multifocal lesions with both osteoblastic areas and osteoclastic bone resorption were observed (). No conclusive diagnosis was established, and the patient was followed-up regularly for persistent right heel pain. Three years after surgery, she presented with a trivial ankle sprain and was diagnosed with an avulsion fracture of the posterior tuberosity of the right calcaneus (). She received conservative treatment, and a short leg cast was applied until bone union and the patient was referred to the endocrinology unit for further workup.
Initial laboratory investigations revealed all biochemical, endocrine, rheumatology, and hematology evaluations were within normal, but serum osteocalcin, C-terminal telopeptide of type I collagen (CTX), and bone alkaline phosphatase (ALP) levels were elevated (). A bone mineral density (BMD) scan showed Z-scores of −1.3, −2.2, and −2.7, in her Lumbar 1 to 4 spines, left (Lt) femur and right (Rt) femur, respectively. The patient started ibandronate injections every 3 months on an impression of secondary osteoporosis without cause. After 1-year of treatment, her laboratory test values had returned to the normal range (), and BMD scans revealed that her Z-scores had improved to −0.5, −1.9, and −2.5, in her Lumbar 1 to 4 spines, Lt femur and Rt femur, respectively. Her heel pain was also subsided.
Based on previous history and a positive response to bisphosphonate therapy, PDB was sustained so bone biopsy was performed on the radial aspect of distal radius which radiograph showed osteopenia (). Histopathological findings revealed irregular broad trabeculae with disorganized cement lines and a patchy mosaic pattern in addition to a few distinct areas of osteoclastic bone resorption and prominent osteoblastic rimming (). During the further evaluation, old 2nd lumbar wedge compression fracture was noticed so follow up whole body bone scan was taken 7 years after initial scan. There was still persistent uptake in right calcaneus () and plain X-ray presented bony deformity (). She is still being treated with bisphosphonate with regular follow-up.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [57.0, 'kg'], 'height': [166.0, 'cm']}",20.68515,19.65089,21.71941,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 57.0 kg. The patient's bmi is therefore 57.0 kg / (1.66 m * 1.66 m) = 20.68515 kg/m^2."
2358,6,Body Mass Index (BMI),physical,decimal,pmc-4339863-1,Extracted,"Mr. AD was a 25-year-old student who was an active footballer until ten days prior to presentation to Cardia Heart Clinic (CHC), Kano, Nigeria, when he started having dyspnoea on exertion, which progressed to dyspnoea at rest, associated with orthopnoea, paroxysmal nocturnal dyspnoea, easy fatigability, abdominal and leg oedema, upper right abdominal discomfort, easy satiety, and subsequently cough with frothy sputum. He denied having urinary symptoms, fever, or other symptoms. Prior to his self-referral to CHF, he had visited another clinic where a chest X-ray, complete blood count, and renal function assessment were carried out.
Physical examination revealed a young man in mild respiratory distress. There were no skeletal anomalies or digital clubbing, and he was 1.76 meters tall with body weight of 68 Kg. His axillary body temperature was 37.1°C, oxygen saturation on room air was 91%, and he had bilateral pitting pedal oedema extending to the shins. He had regular heart rate of 104 beats/minute, blood pressure of 100/80 mmHg, raised jugular venous pressure (approximately 8 cm), displaced apex, third heart sound with loud component of second heart sound, and grade IV mitral regurgitation and grade III tricuspid regurgitation murmurs. There were bilateral basal crepitations, soft and tender hepatomegaly of 12 cm below the right costal margin, and mild ascites. Other aspects of physical examination were not remarkable.
Chest X-ray revealed cardiomegaly, pulmonary venous congestion, and minimal left pleural effusion. Electrocardiogram showed sinus tachycardia with bifascicular block (complete right bundle branch block plus left posterior hemiblock). Echocardiogram (see Figures and ) revealed absent interatrial septum (common atrium) with deformed mitral and tricuspid valves (MV and TV, resp.), which were severely regurgitant. The right ventricle was dilated with a basal diameter of 50 mm, but left ventricular (LV) end diastolic diameter was normal (39 mm), and LV was hypercontractile (LV ejection fraction (LVEF) = 90%). His mean pulmonary artery systolic pressure was approximately 36.8 mmHg, consistent with moderate pulmonary hypertension. The pulmonary veins and superior vena were normally positioned. The pericardium was mildly thickened with moderate pericardial effusion (average echo free space = 15.5 mm). Fibrin strands were not seen within the effusion. The complete blood count showed total white blood cell count of 11.6 × 109/L, neutrophils = 8.3 × 109/L, lymphocytes = 2.6 × 109/L, haemoglobin = 16.3 g/dL, haematocrit = 54.9%, and platelets = 522 × 109/L. Serum creatinine was 92 μmol/L, and other renal function parameters were all normal.
The overall diagnosis was ADHF with preserved LVEF and progressive secondary pulmonary hypertension, caused by CA, associated with moderate pericardial effusion and indirect evidence suggestive of acute bacterial infection.
After the initial cardiac evaluation at CHC which is an out-patient facility, the patient was immediately referred to the emergency unit of a tertiary level hospital in the city for admission and further treatment. The patient gave a written informed consent for his case to be reported. Unfortunately, the patient died about 20 hours after admission at the tertiary level hospital, but details of the in-patient management are not available to us, and postmortem examination was not carried out.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [68.0, 'kg'], 'height': [1.76, 'm']}",21.95248,20.85486,23.0501,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.76 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.76 m * 1.76 m) = 21.95248 kg/m^2."
2359,6,Body Mass Index (BMI),physical,decimal,pmc-4847504-3,Extracted,"A 49-year-old man, standing at 170 cm tall and weighing 70 kg, was seated in the front of the airplane (). The patient reported severe back pain after the accident with erected seated position, without other pain or any numbness. A full neurological examination yielded no deficits, and his back pain improved in a few days.
X-ray of the thoracic spine raised the suspicion of a compression fracture (). Similarly, sagittal CT images also pointed to a compression fracture of the T8 vertebral body (). T1 sagittal MRI revealed a wedge compression fracture of the anterior upper portion of the T8 vertebral body ().
Patient was treated conservatively with two weeks of bed rest. The patient improved during his hospital course and was discharged wearing a spinal orthotic.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [170.0, 'cm']}",24.22145,23.01038,25.43252,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.7 m * 1.7 m) = 24.22145 kg/m^2."
2360,6,Body Mass Index (BMI),physical,decimal,pmc-7813030-1,Extracted,"A 73-year-old man was admitted to our hospital because he had repeated episodes of hypoglycemia before meals for 4 months. He suffered from chronic glomerulonephritis and had been on dialysis for 18 years.
Body height and weight were 159 cm and 65.1 kg, respectively, and physical examination was almost normal. Analysis of the daily energy intake pattern showed meals of 1800 kcal/d and snacks of 200 kcal thrice daily, although the plasma glucose level was 40-70 mg/dL throughout the day. Glycemic support was provided in the form of continuous infusion of 245 g/24 h (10 g/h) dextrose. The results of laboratory tests showed hypoglycemia, hyperinsulinemia, high C-peptide, low HbA1c, and mild hypocarnitinemia (Table ). He was treated with carnitine 1000 mg intravenously after each hemodialysis, but this did not improve hypoglycemia. Enhanced abdominal CT identified a 5 mm-hypervascular tumor in the duodenal wall. All images were negative for pancreatic lesions. The results of ASVS were interesting; injection of calcium gluconate resulted in increase in serum insulin levels in the proximal superior mesenteric artery (pSMA), proximal splenic artery (pSA), gastroduodenal artery (GDA) within 60 seconds, together with increase within 120 seconds in all other regions (Figure ). Since the case fulfilled the Whipple's triad and positive findings of ASVS were detected in pancreatic head arteries, the provisional diagnosis was a small pancreatic head insulinoma that could not be detected by images.
The gastroenterology surgery team performed tumor sampling. Although intraoperative ultrasound detected a hypoechogenic lesion in the pancreatic head, histopathological examination of the obtained biopsy material was negative for malignancy. The duodenal submucosal tumor and 13a lymph nodes were also negative for discrete lesions. No tumor could be detected during the operation, and accordingly, pancreaticoduodenectomy was performed with resection of approximately 70% of the pancreas.
Surgery did not alleviate PHH and the patient continued to require glycemic support. The histopathological findings were consistent with the diagnosis of nesidioblastosis. The patient was treated with a hormone suppressing regimen using octreotide. Octreotide was effective against hyperinsulinemia as confirmed by the results of octreotide loading test, although the dose induced severe nausea and vomiting. We started bolus subcutaneous injection (BSI) of 25 µg octreotide twice a day, but the dose failed to suppress insulin level. On the other hand, 50 µg twice a day induced side-effects. In the next step, we replaced BSI with CSI, which resulted in the disappearance of the side-effects, and we were able to increase the dose up to 100 µg/24 h. This regimen resulted in clinical meaningful insulin suppression and glucose level control (Figure ). Attempts to increase the dose to 150 µg/24 h to improve nighttime hypoglycemia failed due to the appearance of side-effects. Accordingly, prednisolone at 5 mg/d at evening was added. The combination therapy prevented hypoglycemia (Figure ). Two years after discharge, the patient showed marked improvement in quality of life while on the same combination treatment.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [65.1, 'kg'], 'height': [159.0, 'cm']}",25.75056,24.46303,27.03809,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 159.0 cm, which is 159.0 cm * 1 m / 100 cm = 1.59 m. The patient's weight is 65.1 kg. The patient's bmi is therefore 65.1 kg / (1.59 m * 1.59 m) = 25.75056 kg/m^2."
2361,6,Body Mass Index (BMI),physical,decimal,pmc-6967019-2,Extracted,"A 68-year-old man (170 cm, 70 kg) was planned for his first elective PDD TURBT under spinal anesthesia. The patient was medicated with losartan (25 mg/day) for hypertension and tamsulosin (0.2 mg/day) for dysuria. Preoperative examinations were within the normal ranges. On the day of the operation, the BP and PR were 126/81 mmHg and 71 bpm in the early morning, respectively. Daily medications were orally administered. Subsequently, crystalloid infusion was started. About 3 h before the PDD TURBT, the patient took a 5-ALA (1.5 g) solution. Thirty minutes before entering the operation room, the BP and PR were 96/57 mmHg and 80 bpm, respectively. When the patient stood up and headed to the operation room, he felt sick. The S-BP was 42 mmHg at that time. After 20 min, the vital signs were 76/44 mmHg and 68 bpm, respectively. He complained of dizziness with cold sweat and no rash. Fluid resuscitation with the Trendelenburg position was initiated. The operation was canceled due to sustained hypotension, and continuous dopamine infusion (0.3% solution; 3 mL/hr) was started. About 16 h after the 5-ALA pretreatment, the vital signs were 67/32 mmHg and 78 bpm, respectively. Continuous dopamine infusion was necessary until the next day. No reason was found for the hypotension except the 5-ALA pretreatment.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [170.0, 'cm']}",24.22145,23.01038,25.43252,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.7 m * 1.7 m) = 24.22145 kg/m^2."
2362,6,Body Mass Index (BMI),physical,decimal,pmc-4805226-1,Extracted,"A 13-year and 8-month-old boy was admitted because of spasm of the hands for approximately two weeks. Hypocalcemia was detected, and the patient was referred to pediatric endocrinology clinic. He was a full-term infant born from non-consanguineous parents with a birth weight of 2,400 gr. Neuromotor development was delayed and school performance was poor. He did not have a history of chronic disease, medication, or surgery. Family history did not reveal mental retardation, hypocalcemia, renal disease, and deafness.
He appeared well and conscious in physical examination. The heart rate was 94/min, the blood pressure was 120/75 mmHg, and Chvostek sign was present. His height was 165.9 cm (50-75 p), weight was 57.5 kg (50-75 p). He had facial dysmorphism characterized by hypertelorism (), low-set ears, and highly-arched palate. Thyroid gland was non-palpable, and pubertal stage was Tanner stage 5. Cataract was not detected in ophthalmologic examination. Laboratory findings were as follows: serum calcium (Ca) was 6.7 mg/dL, phosphorus (P): 9.5 mg/dL, parathyroid hormone (PTH): 20 pg/mL, 25 hydroxy-vitamin D (25OHD): 27 ng/mL, magnesium: 1.8 mg/dL, Ca/creatinin ratio in spot urine: 0.05. Serum albumin, glucose, electrolytes, renal functions, and complete blood count were normal. Early morning cortisol was 14.7 mcg/dL, thyroid functions were normal, and thyroid antibodies were negative.
The patient was diagnosed to have hypoparathyroidism. Oral calcitriol and Ca replacement treatment was commenced. Renal ultrasonography (USG) revealed that the right kidney was 96x57 mm in normal localization, while the left kidney was ectopic and significantly smaller than the right one. Decreased renal function in the ectopic kidney was detected by dimercaptosuccinic acid (DMSA) scan. Multiple calcifications in bilateral centrum semiovale, corona radiate, and basal ganglions were shown by cranial computed tomography (CT) (), echocardiography was normal, and audiometer revealed bilateral mild sensorineural hearing loss. Intelligence quotient (IQ) score was reported as 57 in Weschler Intelligence Scale For Children test, suggesting mild mental retardation.
Clinical and laboratory findings were supporting the diagnosis of HDR syndrome. Family members were also evaluated in terms of hypocalcemia, hearing loss, and renal dysgenesis. His mother had horse-shoe kidney, but others did not have any of the suspected findings.
The karyotype of this patient was 46, XY. Genetic analysis using a next-generation sequencer identified a missense mutation in exon 4 p.R276Q (c.827G>A) of GATA3 gene (). This mutation was confirmed by Sanger direct sequencing. The mutation was not detected in his parents, brother, or sister.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [57.5, 'kg'], 'height': [165.9, 'cm']}",20.89176,19.84717,21.93635,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.9 cm, which is 165.9 cm * 1 m / 100 cm = 1.659 m. The patient's weight is 57.5 kg. The patient's bmi is therefore 57.5 kg / (1.659 m * 1.659 m) = 20.89176 kg/m^2."
2363,6,Body Mass Index (BMI),physical,decimal,pmc-3401772-1,Extracted,"A 16-year-old girl was admitted with progressive thinning and weakness of both upper and lower limbs with severe myalgia for 1 year duration. She had become bed bound in the last 3 months. She also had poor appetite and nausea. She was unable to flex or extend the neck. She also had primary amenorrhea. She was the second born girl of second-degree consanguineous marriage and her only sibling had died due to undiagnosed illness.
On examination, her height was 131 cm (<3rd centile), weight was only 23 kg (< 3rd centile), and had webbing of neck. She also had severe restriction of neck flexion and hyperconvex nails. There were features suggestive of rachitic rosary [], anterior bowing of tibia [], and proximal myopathy. The LH was 157.3 mIU/ml and FSH was 138.9 mIU/ml. Her karyotype showed 45 XO pattern, confirming Turner's syndrome. Her biochemical features showed hypocalcemia (6.5 mg/ dl), normal phosphorus (3.6 mg/dl), and raised alkaline phosphatase level (1813 IU/l). Serum parathormone was greatly elevated (1652.5 pg/ml, normal 14–74 pg/ml) and 25-hydroxy vitamin D was decreased. (17.6 ng/ ml, normal >30 ng/ ml). She also had uremia (serum urea: 124 mg/dl and serum creatinine: 3.8 mg/dl) and her ultrasound showed bilateral shrunken kidneys.
Her arterial blood gases revealed an uncompensated metabolic acidosis with pH of 7.19, HCO3 of 11.4 mmol/l and pCO2 of 31 mmHg. The anion gap was elevated (–19.6). X-ray of spine showed non-union of the ring apophyses [] with the body of the vertebra and those of long bones and skull revealed features of osteosclerosis and metaphyseal widening []. Tc99m bone scan showed metabolic bone disease with no renal uptake, i.e. metabolic superscan []. Her parathyroid MIBI scan did not show any uptake by parathyroid glands. Echocardiography and audiometry were normal. Her thyroid function was normal.
She was diagnosed to have Turner's syndrome with renal osteodystrophy. Her chronic kidney disease was deemed to be due to chronic glomerulonephritis and was managed conservatively. She was given 3,00,000 IU bolus injection of cholecalciferol and followed with supplementation of calcium 1500 mg/day and calcitriol 0.75 mcg/day. With treatment, her calcium improved to 7.5 mg/dl. She also had significant reduction in bone pain and PTH dropped to 627 pg/ml.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [23.0, 'kg'], 'height': [131.0, 'cm']}",13.40248,12.73236,14.0726,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 131.0 cm, which is 131.0 cm * 1 m / 100 cm = 1.31 m. The patient's weight is 23.0 kg. The patient's bmi is therefore 23.0 kg / (1.31 m * 1.31 m) = 13.40248 kg/m^2."
2364,6,Body Mass Index (BMI),physical,decimal,pmc-8222750-1,Extracted,"A 9 year-old girl was admitted to this hospital for evaluation of fever and jaundice. Two days before this admission, the patient was taken to a local hospital where she was found to have severe anemia with a hemoglobin of 3.4 gm/dl. She was suspected and worked up on the line of hemolytic condition for which two units of packed RBCs were transfused, and she was referred to our center for further evaluation.
The patient had been in her usual state of health until 10 days before this admission, when she was noted to have intermittent fever with chills and rigor, maximum documented being 38.9°C, yellowish discoloration of skin, and dark-colored urine. She also had right upper abdominal pain but no nausea, vomiting, hematemesis, hemoptysis, pruritus, passage of clay-/dark-colored stool, skin rashes, or joint pain.
The patient had been delivered vaginally at full term. Subsequent growth and development were reportedly normal, and her immunizations were up to date. She had no known medical conditions, was not taking any medications, and had no known allergies to medications. She lived in a family with no history of consanguinity, and they were involved in cattle rearing.
On examination, she was ill appearing and appeared tired. The temperature was 38.3°C, the heart rate 92 per minute, the blood pressure 90/60 mmHg, the respiratory rate 22 per minute, and the oxygen saturation 98% while breathing ambient air. The weight was 26 kg (25.78th percentile), and height was 134 cm (55.5th percentile). She had conjunctival icterus and pallor but no clubbing, palmar erythema, cyanosis, lymphadenopathy, and edema. The lungs were clear on auscultation. The abdomen was soft, with mild right upper quadrant tenderness, and liver was palpable 6 cm below the coastal margin with a span of 14 cm. Abdominal guarding, rebound tenderness, and Murphy's sign were absent. The spleen tip was palpated one cm below the left coastal margin. There was no fluid thrill or shifting dullness. The skin examination revealed no lesions, rash, abnormal pigmentation, or abnormality of the nails. She was alert and oriented and followed commands. The remainder of the examination was normal.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [26.0, 'kg'], 'height': [134.0, 'cm']}",14.47984,13.75585,15.20383,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 134.0 cm, which is 134.0 cm * 1 m / 100 cm = 1.34 m. The patient's weight is 26.0 kg. The patient's bmi is therefore 26.0 kg / (1.34 m * 1.34 m) = 14.47984 kg/m^2."
2365,6,Body Mass Index (BMI),physical,decimal,pmc-3835515-1,Extracted,"A 21-yr-old Korean man was referred to the Department of Endocrinolgy and Metabolism from his primary physician for proper management of hyperglycemia and metabolic impairment on September 21 of year 2012. During the 2 yr since the patient's discharge from military service he had lost approximately 10 kg in body weight. At admission, he complained of polyuria and polydipsia. He had no known medical past history or fracture history, but his mother and elder brother had been diagnosed with HCS along with osteoporosis and multiple compression fractures of the spine (, ). On admission the patient showed stable vital signs and alert mental status. Blood pressure was 107/63 mmHg and pulse rate was 59/min. His height was 175 cm (50 percentile) and weight was 55 kg (10 percentile). The physical examination revealed dysmorphic features, such as marked eyebrow, which was similar to that of his brother in whom HCS had been diagnosed at the age of 20. Short and clubbed fingers were found (). Laboratory investigations revealed hemoglobin of 11.8 g/L, total white blood cell count of 4,800/µL (73% neutrophils). Serum biochemistry, hormones, and bone markers were tested (). No antibody to glutamic acid decarboxylase was detected. Arterial blood gas analysis revealed metabolic acidosis (pH 7.318, base excess -15.2 mM/L, bicarbonate 8.6 mM/L) with incomplete respiratory compensation (pCO2 17.2 mmHg). Urine analysis revealed that specific gravity of 1.024, strong positive in glucose and ketone bodies. A chest X-ray was normal and electrocardiography showed normal sinus rhythm. After an initial treatment for DKA, evaluations for metabolic bone disease were performed. Laboratory findings showed follicle-stimulating hormone 0.7 IU/L, luteinizing hormone 1.2 IU/L, testosterone 2.25 ng/mL (7.8075 nM/L), osteocalcin 8.9 ng/mL (1.5219 nM/L), 25-hydroxy-Vitamin D 5.7 ng/mL (14.2272 nM/L), intact parathyroid hormone <8 ng/L, and urine N-telopeptide 151 nM/mM creatinine. A hand X-ray revealed brachydactyly of the 5th finger of both hands (). Thoracolumbar spine X-ray revealed a fracture of T12 and L3 (). Skull X-ray revealed wormian bone (). Bone mineral density revealed osteoporosis (L1-L2 0.826 g/cm2, T-score -2.6, Z-score -2.5, total femur 1.203 g/cm2, T-score 2.0, Z-score 1.8) (). To confirm the diagnosis of HCS, DNA sequencing was conducted. The sequence analysis revealed that the patient and his mother had a heterogenetic mutant allele in the NOTCH2 gene (c.6443T>G) () leading to an amino acid substitution from a leucine to a stop codon (p.Leu2148*) (). The patient was diagnosed with HCS and DKA. To manage DKA, fluid resuscitation and insulin treatment was initiated. His metabolic acidosis normalized. Since then the patients has been treated with 1,250 mg of calcium carbonate and 1,000 IU of cholecalciferol per day under the diagnosis of osteoporosis and compression fracture due to HCS, and with 5 units of basal insulin and 7 units of pre-prandial insulin injection for type 1 DM. Laboratory analyses conducted during the course of treatment showed improved HbA1c (7.5%) and fasting glucose (175.8 mg/dL or 9.768 mM/L).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.0, 'kg'], 'height': [175.0, 'cm']}",17.95918,17.06122,18.85714,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 175.0 cm, which is 175.0 cm * 1 m / 100 cm = 1.75 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.75 m * 1.75 m) = 17.95918 kg/m^2."
2366,6,Body Mass Index (BMI),physical,decimal,pmc-2740319-1,Extracted,"We report a case of a 9-year-old Caucasian Italian girl, treated for growth hormone deficiency (GHD) with recombinant human growth hormone (rhGH) at a total weekly dose of 6 mg. At the diagnosis of GHD her weight was 24.6 kg, her height was 113 cm; physical examination, mental and developmental status were all normal. The diagnosis was made on laboratory criteria (two pathological GH stimulation tests) and on the MRI of the head which excluded brain tumour and anatomical abnormalities.
Three months after starting rhGH, she complained of progressive and bitemporal headaches, nausea, vomiting, diplopia and visual loss. Acute comitant esotropia was the only abnormality in the neurological examination. Ocular fundus examination revealed bilateral papilledema and a lumbar puncture showed an increased intracranial pressure (210 mm H2O) with normal cerebrospinal fluid. An MRI scan ruled out intracranial lesions (including venous sinus thrombosis), leading to a final diagnosis of idiopathic intracranial hypertension (IIH) (pseudotumor cerebri).
Since the association between IIH and rhGH treatment has already been described, we promptly discontinued rhGH and started treatment with acetazolamide at the dose of 20 mg/kg/die. Four days after starting acetazolamide, there was no clinical improvement at all, with persistence of headaches, diplopia, nausea, vomiting and weakness. After two more days, despite increasing the dose of acetazolamide up to 30 mg/kg/die, there was no recovery. Indeed, weakness worsened, arterial blood analysis showed metabolic acidosis (pH 7.29; PCO2 31.1; HCO3 15.7; BE - 7.3), likely due to acetazolamide. Therefore we stopped acetazolamide and started the treatment with intravenous dexamethasone (0.4 mg/kg/die). After only one day there was a dramatic clinical response with complete disappearance of headache, progressive improvement in the esotropia and regression of the papilloedema. We decreased intravenous steroids, switching to oral prednisone (1 mg/kg/die) after one week. Ten days after discharge, the girl no longer had headaches nor weakness, and there was no more esotropia or diplopia. Eye examination revealed further improvement of papilloedema. Therapy was tapered down in 3 weeks with no worsening. After two weeks rhGH was restarted at a dose of 1.8 mg weekly, and progressively increased up to 6 mg weekly; the treatment was well tolerated, without any side effects.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [24.6, 'kg'], 'height': [113.0, 'cm']}",19.26541,18.30214,20.22868,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 113.0 cm, which is 113.0 cm * 1 m / 100 cm = 1.13 m. The patient's weight is 24.6 kg. The patient's bmi is therefore 24.6 kg / (1.13 m * 1.13 m) = 19.26541 kg/m^2."
2367,6,Body Mass Index (BMI),physical,decimal,pmc-4719091-1,Extracted,"A 93-year old woman was suspected of ovarian mass 2 years ago under a diagnosis of huge ovarian mass at the age of 91 and was recommended for inpatient care and surgical treatment. However, the patient was discharged at the time of the first visit, since her family resisted getting any treatment due to old age. She did not undergo any treatment for 2 years, and she re-visited our emergency unit due to severe abdominal pain and vaginal bleeding and admitted to our hospital for surgical treatment after taking computed tomography (CT) and magnetic resonance imaging (MRI) scans at a primary care center nearby.
Her obstetrical history was gravida 6. The menarche age was 16 and the menopause age was 41. She had no specific family history, but had a history of hypertension. On admission, she had a blood pressure of 140/90 mmHg, a heart rate of 70 beats/min and a body temperature of 36.3℃. Her height was 150 cm and weight was 40 kg. She was associated with distended abdomen and pain to touch. Her pelvic exam revealed that bilateral adnexae and uterus were indistinguishable. A 15-cm firm and mobile mass was palpated above the symphysis pubis. Her laboratory findings revealed a low hemoglobin level of 8.3 g/dL, a hematocrit of 25.3%, and a slightly elevated white blood cell count of 15,320/mm3. The results of routine chemical test, blood coagulation test and liver function evaluation were normal. Compared to test results from 2 years ago, the test for serum tumor markers revealed an elevated level of cancer antigen (CA)-125 from 27.3 U/mL to 111.6 U/mL (normal range 0-35), and an elevated level of CA 19-9 from 146.3 U/mL to 831.3 U/mL (normal range 0-27). The levels of alpha-fetoprotein and beta-human chorionic gonadotropin were normal. The level of carcinoembryonic antigen (CEA), a tumor marker was slightly elevated at 5.24 ng/mL (normal range 0-4.7). The results of chest X-rays were normal, and the size of pelvic mass enlarged from 8 cm on the first visit 2 years ago to 15 cm on pelvic ultrasonography. Ultrasound demonstrated an inhomogeneous, hypoechoic, water-filled mucinous mass. Abdominal and pelvic CT revealed a large volume of ascites in the abdomen, and a 15-cm firm and mobile mass was palpated above the symphysis pubis. A 15-cm irregular multiloculated mass was observed in the abdominal cavity (). Like CT scans, MRI scans presented a 15-cm inhomogeneous mass with a large volume of ascites, and many septa and nodules were detected within the tumor (). Considering patient's old age, collaborative practice was carried out between cardiology and pulmonology departments before surgery. Anesthesia and operation were performed carefully to avoid extended operation time and volume overload. For open abdominal surgery, an incision was made at the center on the lower abdomen under general anesthesia. The mass originated from left ovary and its size was 16.5 × 12.0 × 9.5 cm. The mass had traces of rupture, the volume of ascites was about 2,500 cc, and hemoperitoneum was seen in the cecum. The patient had atrophic uterus and right ovary, but no specific finding of abdominal adhesion was found. There were no specific findings suspected of tumor metastasis in the peritoneum, greater omentum, intestines, mesentery and others. To minimize anesthesia and operation time considering patient's old age, frozen section biopsy was not performed with the consent of patients' family. To remove ovarian mass, only left salpingo-oophorectomy was done. After the surgery, the patient was treated in intensive care unit for 3 days (). The left ovarian mass was sized 16.5 × 12.0 × 9.5 cm and weighed 980 g. The fallopian tube was attached and the mass had the finding of rupture. The outer surface of multilocular mass was whitish gray and smooth, and the inner surface was smooth and filled with gelatinous contents. Firm portion or nodules were not identified. The wall thickness of septum was relatively thin, less than 0.1 cm, and the fallopian tube was 15.5 cm in length and 0.3 cm in diameter (). The final diagnosis was confirmed as mucinous BOT in the left ovary. For her age, there was no specific postoperative complication. She was treated with anemia because of a decreased hemoglobin level of 8.6 g/dL and a hematocrit of 25.8%. She was discharged on the 18th postoperative day. She is relatively healthy with no specific symptom and currently under outpatient follow-up.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [40.0, 'kg'], 'height': [150.0, 'cm']}",17.77778,16.88889,18.66667,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 150.0 cm, which is 150.0 cm * 1 m / 100 cm = 1.5 m. The patient's weight is 40.0 kg. The patient's bmi is therefore 40.0 kg / (1.5 m * 1.5 m) = 17.77778 kg/m^2."
2368,6,Body Mass Index (BMI),physical,decimal,pmc-7529567-1,Extracted,"A 59-year-old man was admitted to our hospital with abnormal findings on chest X-ray (Fig ). On physical examination, he weighed 63.0 kg and was 176 cm tall. The patient had diabetes for 20 years and suffered from diabetic retinopathy. He had unremarkable medical and family histories, but a smoking history of 90 packs per year. Chest CT revealed a 30 mm mass in the right upper lung lobe and mediastinal lymph nodes with advanced calcification (Fig ). Transbronchial biopsy resulted in a diagnosis of adenocarcinoma. [18F]-fluoro-2-deoxy-D-glucose (FDG) positron emission tomography (PET) showed increased tumor uptake, with a maximum standardized uptake value of 6.16, and slight FDG uptake in the mediastinal lymph nodes. No metastases were detected by brain magnetic resonance imaging or FDG-PET (Fig ). Mediastinal lymph node #4 had a short-axis diameter < 1 cm, but was considered potentially to be lymph node metastasis because of the slight accumulation of FDG-PET; therefore, preoperative adjuvant treatment was performed. HgbA1c of 10.5 indicated diabetes was poorly controlled and required treatment before surgery. Diabetic nephropathy did not coexist and blood calcium and phosphate concentrations were within the standard range. During diabetes treatment, he received neoadjuvant chemotherapy (pemetrexed (500 mg/m2) plus cisplatin (75 mg/m2). The patient achieved no significant radiological improvement with two courses of this regimen. Based on radiological findings, he was diagnosed with yc-T1cN0M stage 1A, and surgical treatment was planned. He underwent right upper lobectomy and dissection of the upper mediastinal lymph nodes (2R and 4R). The lymph nodes were firmly adherent to the surrounding tissue, the sidewall of the superior vena cava was firmly fused, and there was invasion of the vascular wall. Despite this, the lymph nodes and superior vena cava sidewall were removed. The chest drain tube was removed on postoperative day 3 and the patient was discharged on postoperative day 14. Macroscopically, the tumor was well circumscribed and most of the tumor was calcified (Fig ). There was no bronchial or pleural involvement within the tumor. Acinar adenocarcinoma tissue was mixed with calcified tissue and PBs were confirmed. Similar features were found in calcified lymph nodes. The tumor was diagnosed as p-T2aN2M0 stage 3A (Union for International Cancer Control eighth edition). Immunohistochemistry revealed tumor cells positive for parathyroid hormone-related proteins (PThrP) 1 and 2. Postoperative examination indicated PThrP levels were within the standard range.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [63.0, 'kg'], 'height': [176.0, 'cm']}",20.33833,19.32141,21.35525,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 176.0 cm, which is 176.0 cm * 1 m / 100 cm = 1.76 m. The patient's weight is 63.0 kg. The patient's bmi is therefore 63.0 kg / (1.76 m * 1.76 m) = 20.33833 kg/m^2."
2369,6,Body Mass Index (BMI),physical,decimal,pmc-4800375-1,Extracted,"A 20-year-old female underwent reconstruction of right ventricular outflow tract for PA-IVS soon after birth. Postoperative follow-up was uneventful. She was referred to our hospital with the chief complaint of insidious clubbing fingers. Her family could not remember when her clubbing fingers appeared. At the outpatient clinic, neither lip cyanosis nor oxygen desaturation was discernible. At admission, she was 54 kg in weight and 168 cm in height. Pulse rate was 82/min, and respiratory rate 20/min. Hemoglobin was 14.9 gm/L. Clubbing fingers were remarkable (). Peripheral pulse oximeter showed marked fluctuations of oxygen saturations (SpO2), ranging from 84% to 95% in the supine position and from 80% to 88% in the upright position. There was no pathological heart murmur. Liver and blood coagulation functions were normal. Initial trans-thoracic echocardiography (TTE) with bubble study in the supine position failed to detect any intracardiac shunt. However, TTE with bubble study performed in the seated position did reveal an interatrial right-to-left shunt (). Hemodynamic data are summarized in . There was a step-down of oxygen saturation from the pulmonary vein to the left atrium, indicating an interatrial right-to-left shunt. Besides, there was no trans-atrial pressure gradient, right ventricular hypertension, and pulmonary arterial hypertension. Intracardiac echocardiography (ICE) with Doppler showed a secundum ASD with a right-to-left shunt. Balloon sizing showed an indentation of 21.84 mm in diameter (). Before implantation, a bolus of 2000 units of heparin was infused into the delivery system. A 22-mm ASO was chosen to occlude this defect (). After implantation, ICE showed complete occlusion (). We wiggled the cable to test the stability and relieved the device smoothly. Interestingly, the anatomic lie of ASO was positioned more ventrally oblique in the present patient () than those in the usual patients with a secundum ASD (). SpO2 of ascending aorta and left ventricle elevated to 99–100%. In a 24-month follow-up, she was free of POS.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [54.0, 'kg'], 'height': [168.0, 'cm']}",19.13265,18.17602,20.08928,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 54.0 kg. The patient's bmi is therefore 54.0 kg / (1.68 m * 1.68 m) = 19.13265 kg/m^2."
2370,6,Body Mass Index (BMI),physical,decimal,pmc-7148413-1,Extracted,"The patient is a 41-year-old male. His chief complaint is left flank pain. He has no medical history/family history.
The subject consulted a nearby doctor with left stomachache and fever as chief complaints in 1 month prior to the surgery. Diverticulitis of the descending colon splenic flexure was doubted in CT and the subject was hospitalized. A colonoscopy revealed an irregular flat elevated lesion on the splenic flexure. The subject was transferred to our hospital for examination and medical treatment.
The height is 175 cm, body weight 54.6 kg, pulse 66 beats/m, body temperature 36.3, and blood pressure 114/76 mmHg. The abdomen was slightly distended, and mild left stomachache was recognized. The stool frequency was 1 time/day.
In blood biochemistry examination, values were as high as 22.5 ng/ml in CEA and 81.0 U/ml in CA19-9 tumor markers.
Significant hyperplasia (4 cm) of the colon mucous membrane was observed on the descending colon splenic flexure and it was accompanied by elevation of surrounding adipose tissue density. The surrounding lymph nodes swelled up to around 5 mm. Since strong hyperplasia was seen in the mucous membrane, it was thought as reactive enlargement accompanied by inflammation. The finding that indicates distant metastasis was not seen in the liver and lung (Fig. ).
A semicircular, lateral spreading tumor of granular-type (i.e., an aggregate of IIa-like tumors) was observed in the descending colon splenic flexure (Fig. a).
Notable abnormality such as irregular ulcer and scar or bamboo joint-formed appearance was not recognized.
Biopsy was performed twice for the lateral spreading tumor of granular-type of descending colon. The tumor was diagnosed pathologically as a tubular adenoma without evidence of malignancy. However, we judged that the lesion in the descending colon was a cancer based on the elevated CEA level and CT findings. We also considered the possibility of coexistence of inflammatory lesion near the tumor because of an edematous change of the mucosa (Fig. b). Therefore, it was determined to place a covering stoma 20 cm proximal from the terminal ileum at the time of surgery.
D3 left hemicolectomy and loop type stoma construction were performed. No abnormality was confirmed in the small intestine such as thickness, fistula, mass, and adhesion to abdominal wall during the operation.
Gross examination confirmed that the main tumor was a laterally spreading tumor (granular-type) in the descending colon (Fig. a, b). No gross findings were recognized that supported Crohn’s disease, e.g., longitudinal ulcers, their scars, or cobblestone appearance. Histopathologically, the surface of the main tumor was composed of uniform proliferation of atypical glands (either tubular or villous in configuration) and containing both low- and high-grade areas (Fig. a, b). This lesion stained diffusely positive for p53 by immunohistochemistry (Fig. c). Therefore, we diagnosed these atypical glands in the surface area this as dysplasia, and this lesion continuously invaded the muscularis propria (Fig. d). In deeper areas of the main tumor, deposition of extracellular mucin was observed leading the diagnosis of mucinous adenocarcinoma (Fig. a). p53 was positive in 50% of tumor cells in mucinous carcinoma (Fig. b). The final diagnosis was mucinous adenocarcinoma associated with dysplasia, in the descending colon, type 5, 50 × 48 mm in size, pT4a (SE) pN2a (4/28), Ly1, V1, cM0, pStage IIIC (UICC TNM classification, 8th ed., and Japanese classification of colorectal carcinoma, 9th ed) []. Furthermore, another dysplasia, not continuous from the main tumor, was confirmed by multiple sampling analyses in the resected specimen approximately 5.2 × 1.8 cm in size (indicated by blue line in Figs. and ). This dysplasia was not associated with adenocarcinoma (i.e., completely confined in the mucosa). We further obtained the following findings that supported pre-existing transmural chronic inflammation (e.g., Crohn’s disease) as follows: (a) irregular thickening of the muscularis mucosae, (b) fibrosis in the submucosa and muscularis propria, and (c) sporadic formation of lymphoid aggregates in the submucosa and subserosa in the resected colon specimen (Fig. ). Taken together, the histopathological features of main tumor were consistent with colitis-associated cancer.
The ileus state was prolonged for over 40 days after the surgery. On day 55 endoscopies were performed to newly find orbicular ulcers in the terminal ileum (Fig. a, b). We excluded the possibility of tuberculosis or cytomegalovirus by an interferon-gamma release assay and serum antibody assay. Re-examination of endoscopy on day 77 revealed the development of longitudinal ulcers in the ileum (Fig. c). With a clinical diagnosis of Crohn’s disease, the patient received infliximab administration, and the lesions of small intestine ameliorated significantly on day 103. Furthermore, ileus was improved and therefore the subject was discharged on day 112 (Fig. d). Seventy-three days after the discharge, CEA suddenly was elevated and intestinal edema, and ascitic fluid appeared in abdominal contrast-enhanced CT. The subject was diagnosed as ileus attributable to peritoneal dissemination. Overall status gradually worsened and he passed away on day 207. The final cause of death was judged as peritoneal dissemination.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [54.6, 'kg'], 'height': [175.0, 'cm']}",17.82857,16.93714,18.72,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 175.0 cm, which is 175.0 cm * 1 m / 100 cm = 1.75 m. The patient's weight is 54.6 kg. The patient's bmi is therefore 54.6 kg / (1.75 m * 1.75 m) = 17.82857 kg/m^2."
2371,6,Body Mass Index (BMI),physical,decimal,pmc-5803708-1,Extracted,"A 61-year-old Japanese female (height: 163.0 cm; weight: 53.0 kg) with HCV-associated chronic hepatitis (genotype 1b) visited our clinic for treatment with oral DAAs. The patient had received acupuncture 28 years ago to treat persistent epigastralgia. Three weeks thereafter, her mother noticed slight icterus of her skin. One year later, when she was 35 years old, a test in another hospital revealed that her transaminases levels were rising. The peak of alanine transaminase (ALT) reached as high as about 280 IU/L. When she was 38 years old, her home doctor began to inject 60 mL of Stronger Neo-Minophagen C (it is usually used to lower serum transaminase) twice a week. This was continued for several years. However, her transaminases were unstable. She was told that HCV antibody was positive at that time. She did not receive IFN therapy (including PEG-IFN/ribavirin therapy). This was her first IFN-free DAA treatment, which is a standard therapy available in Japan for chronic HCV infection.
Table shows the laboratory data at the beginning of the therapy and at the time of gingival bleeding (at the same time of inflammation of the genital vulva). The abnormal data at the beginning were as follows; serum alanine transaminase was 46 U/L, alkaline phosphatase was 389 U/L, total cholesterol was 114 mg/dL, and HCV-RNA was 3.6 logIU/mL of the viral load (real-time PCR). HCV was of the 1b type.
Abdominal ultrasonography and computed tomography revealed a normal-sized liver with a regular liver surface and no marked splenomegaly. Moreover, the architecture of the liver in ultrasonography was rough, suggesting chronic hepatitis.
As antiviral treatment, elbasvir (NS5A inhibitor, 50 mg/day) and grazoprevir (NS3/4A protease inhibitor, 100 mg/day) were administered from April 8, 2017 to June 30, 2017 (Fig. ). Interestingly, she experienced the sensation of being hungry from the beginning of the therapy. She became hungry 2 h after each meal, and took 5 meals every day. Severe gingivitis and gingival bleeding occurred from 3 weeks after the beginning of the therapy and it lasted for about 10 days. She felt instability of the gingiva and pain on biting foods. At the same time, she felt severe burning of the throat. Simultaneously, she developed inflammation of the genital vulva (redness and edematous swelling) and also it lasted about 10 days. However, she tolerated the many adverse events, and finally completed the full regimen and achieved SVR12.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.0, 'kg'], 'height': [163.0, 'cm']}",19.94806,18.95066,20.94546,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 53.0 kg. The patient's bmi is therefore 53.0 kg / (1.63 m * 1.63 m) = 19.94806 kg/m^2."
2372,6,Body Mass Index (BMI),physical,decimal,pmc-2988807-1,Extracted,"In mid February 2008 a 14 year old girl came under our observation. She had been suffering for about 3 months from persistent fever (38 ° C), weight loss (9 kilos), headache and asthenia and was previously treated with several courses of antibiotics and prednisone. Family history shows that her paternal grandmother suffers from scleroderma, her paternal grandfather from rheumatoid arthritis, her maternal grandmother from autoimmune thrombocytopenia, and her mother from thyroiditis. At admission, she had a body weight of 45 kg (10th -25th percentile) and a height of 154 cm (10th -25th percentile). Physical examination revealed a rash on the face, livedo reticularis, acrocyanosis at the first and second toe of the left foot, arthritis in knees and ankles. Blood tests showed: anemia (hemoglobin 10.5 gr/dl), leukocitopenia (3300/μl) with lymphopenia (30%), normal platelet count (289000/μl), increased inflammatory indexes (erythrocyte sedimentation rate 53 mm/1 hour; C-reactive protein 1,44 mg/dl); increased serum IgG (2270 mg/dl), lengthening of prothrombin time (57.5 seconds), reduced serum iron (16 μg/dl) and reduced levels of C3 (70 mg/dl) and C4 (9 mg/dl). Urinalysis excluded renal involvement, and instrumental examinations (chest x-ray, abdominal ultrasound, echocardiography) ruled out the presence of serositis or other signs of disease. An eye examination, echocolordoppler of lower limbs and capillaroscopy were also negative. A diagnosis of Systemic Lupus Erythematosus (SLE) was considered and confirmed, according to the diagnostic criteria laid down by American College of Rheumatology, for the presence of antinuclear antibodies (1:1280, homogeneous appearance), anti-dsDNA (107 IU/ml; normal < 30), anti-Sm (129 AU/ml, normal <30), anti-Sm/RNP (120 AU/ml, normal <30), lupus anticoagulant (1.48; normal 0-1.3) and anticardiolipin antibodies (25 U/ml, normal up to 20). Her lupus anticoagulant and anticardiolipin antibodies were positive on one occasion, but subsequently negative with no other evidence to suggest anti-phospholipid syndrome. The patient was discharged with the following therapy: prednisone (60 mg daily); hydroxychloroquine (200 mg); anti-aggregating platelet therapy (acetyl salicylic acid); ranitidine; vitamin D3 and calcium carbonate. After two weeks of therapy there was an improvement in the symptoms with normalization of biochemical indices of inflammation but a worsening of peripheral cyanosis, with the appearance of an intensely painful and infected ischemic ulcer on the plantar surface of the second toe of the left foot. Echocolordoppler and capillaroscopy were again performed and were both negative. A local ulcer treatment was started with medications and cleansing performed by a consultant surgeon. The ulcer, oval in shape, evolved in a pejorative sense at a distance of 3 months after onset, reaching a maximum diameter of about 1 centimeter. For this reason, and because of the deepening of the lesion and the risk of osteo-tendinous impairment, it was decided to associate with the medical therapy a course of HBOT, with a protocol of 5 weekly sessions of 90 minutes at a pressure of 2.6 atmospheres absolute (ATA). Before starting the hyperbaric therapy, the ulcer appeared painful and oval shaped with regular margins. It was covered by an infected eschar and the surrounding skin was cold, thick and ranging from deep red to bluish in color. After a week of therapy, the cyanosis disappeared (figures and ), while the ulcer healed after 16 sessions. The HBO was well tolerated by the patient and 32 sessions were carried out in total without any side effects (figure ). From the interruption of hyperbaric therapy, there were no relapses in the following months. After four weeks from the beginning of the immunosuppressive therapy, the daily dosage of prednisone was reduced by 5 mg every 15 days; and when it reached 20 mg/day, it was further reduced by 2.5 mg every four weeks until the current dose of 10 mg/day. The immunosuppressive therapy was well tolerated by the patient, blood tests were normal and there have been no new flares of the disease so far.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.0, 'kg'], 'height': [154.0, 'cm']}",18.97453,18.0258,19.92326,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 154.0 cm, which is 154.0 cm * 1 m / 100 cm = 1.54 m. The patient's weight is 45.0 kg. The patient's bmi is therefore 45.0 kg / (1.54 m * 1.54 m) = 18.97453 kg/m^2."
2373,6,Body Mass Index (BMI),physical,decimal,pmc-6329249-2,Extracted,"A 70-year-old male weighting 85 kg, with a height of 183 cm, was admitted to the Post Anesthesia Care Unit (PACU) after an explorative midline laparotomy with the findings of a diffuse tumour infiltration. His comorbidities included hypertension, insulin-dependent diabetes and severe chronic back pain. His medications included furosemide, valsartan, insulin and oxycodone. Since the clinical cause of the severe back pain was not clear, the anaesthesiologist decided not to place an epidural catheter and instead planned an elastomeric pump with 600 mg of tramadol and 400 mg of ketoprofen.
The surgery was uneventful. Pain relief could not be achieved in the first postoperative day (NRS 6–10) despite multiple boluses of morphine (27 mg total). For this reason, an analgesia with an ESP block was proposed and accepted by the patient. The ESP block technique was performed at T9 level, as described above, and it was executed by a bilateral injection of 20 ml of 2% ropivacaine. Although adequate analgesia was reported by the patient within 40 min (NRS 0), the pain relief lasted just 6 h (NRS 3); after 12 h the patient requested further opioids.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [85.0, 'kg'], 'height': [183.0, 'cm']}",25.38147,24.1124,26.65054,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 183.0 cm, which is 183.0 cm * 1 m / 100 cm = 1.83 m. The patient's weight is 85.0 kg. The patient's bmi is therefore 85.0 kg / (1.83 m * 1.83 m) = 25.38147 kg/m^2."
2374,6,Body Mass Index (BMI),physical,decimal,pmc-4345050-1,Extracted,"An eight-year-old boy with a history of a self-limited head trauma last year seemed restless and rather unable to stand still during inspection. History of the patient revealed no medical treatment related with thyroid disorders and no history of neck irradiation or thyroid surgery. There was no family history related with any of the thyroid diseases. Physical examination was normal and no congenital anomaly was demonstrated. The thyroid gland was unpalpable. The child was 120 cm in height and weighed 21.5 kg. He was euthyroid, FT4: 1.00 ng/dL (range, 0.70–1.48 ng/dL) and TSH: 3.2 μIU/mL (range, 0.35–4.94). Thyroid ultrasonography (US) was performed in supine position with a Mindray DC-7 US device (Shenzhen Mindray Bio-Medical Electronics Co., Ltd., Shenzhen, China), using 8 MHz linear-array transducer. The length, width, and depth of the right lobe were measured, and the volume was calculated by the mean of the elliptical shape volume formula (π/6 × length × width × depth) [, ]. The dimensions of the right lobe were 37.1 × 14 × 12.5 mm and its volume was 3.4 mL revealing minimal hyperplasia, as the age, gender, weight, and height of the child were of concern []. The echotexture of the right lobe was normal and homogeneous. Its margins were regular. Anterior to trachea, a thin, band-like image isoechoic to the right lobe, measuring 1.7 mm in thickness and resembling a thin isthmus, was noticed; however a left lobe could not be demonstrated. Strap muscles, left common carotid artery, jugular vein, and other regional vascular structures were displaced to fill the location of the left lobe (). On US examination of other parts of the neck, pyramidal lobe, any midline cyst such as thyroglossal cyst or any mass consistent with an ectopic thyroid tissue such as lingual thyroid could not be demonstrated. For ruling out any ectopic thyroid tissue, thyroid scintigraphy was performed by intravenously administering 2.5 mCi Tc-99m pertechnetate. Images of the head and neck were taken 20 minutes later with dual-head gamma camera (Siemens e-cam, Erlangen, Germany), using parallel-hole and pinhole collimators. Additionally, planar scintigraphic imaging of thorax, abdomen, and pelvis was performed. Scintigraphically, right lobe of the thyroid gland showed minimal hyperplasia, though uptake was homogeneous. Tc-99m uptake of the right lobe was 3.6% (normal range, 0.3–3%). No nodule was demonstrated at the right lobe. At the location of the left lobe of thyroid gland and any other parts of the neck, no accumulation of radioactivity could be obtained (Figures and ). Thoracal, abdominal, and pelvic scintigraphic imaging revealed no ectopic thyroid gland activity.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [21.5, 'kg'], 'height': [120.0, 'cm']}",14.93056,14.18403,15.67709,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 120.0 cm, which is 120.0 cm * 1 m / 100 cm = 1.2 m. The patient's weight is 21.5 kg. The patient's bmi is therefore 21.5 kg / (1.2 m * 1.2 m) = 14.93056 kg/m^2."
2375,6,Body Mass Index (BMI),physical,decimal,pmc-7419391-1,Extracted,"A 65-year-old male who complained of dyspnea was diagnosed with hypertrophy based on X-ray findings and was hospitalized emergently for an acute heart failure. His past medical history included hypertension and 8 years of hemodialysis treatment due to chronic kidney disease (stage 5GD) by unknown causes. His height and weight were 176 cm and 55 kg, respectively. His laboratory data were abnormal as follows: C-reactive protein, 1.84 mg/dl; N-terminal pro-brain natriuretic peptide, > 35,000 pg/ml; troponin T, 0.111 ng/ml; BUN, 58.2 mg/dl; and Cr, 9.2 mg/dl. Cardiothoracic ratio was 63% based on chest X-ray with butterfly shadow. Electrocardiogram indicated a sinus rhythm, a heart rate of 101 bpm, and a QS pattern in V2–3. Transthoracic echo showed the following findings: ejection fraction (EF), 59%; left ventricular internal dimension in diastole/systole (LVDd/Ds), 57/30 mm; interventricular septum thickness, 20 mm; posterior LV wall thickness, 15 mm; diameter of left atrium, 56 mm; LV mass index, 201 g/m2; aortic valve pressure gradient, 104/54 mmHg (max/mean); aortic valve area, 0.54 cm2; and aortic regurgitation mild, mitral regurgitation mild, and tricuspid regurgitation mild (pressure gradient, 27 mmHg). The patient’s coronary angiography result indicated stenosis of left anterior descending branch #6, 75%, and left circumflex coronary artery #11, 75%, and computed tomography revealed left-sided pleural effusion. Finally, he was diagnosed with aortic valve stenosis (AS) and angina pectoris, and it was decided to perform elective surgery of aortic valve replacement (AVR) and cardiac artery bypass.
After the initiation of CPB and aortic clamping, cardiac arrest was induced immediately after cardioplegia infusion and maintained with 500–700 ml infusion every 30 min. Left internal thoracic artery–left anterior descending branch (LITA–LAD) and saphenous vein–right coronary artery (SVG–RCA) anastomoses and AVR (Magna EaseTM 23 mm) were performed. When the aortic forceps were declamped at 13:57 (marked “A” in Fig. ), VF occurred immediately as shown in Fig. (anesthetic record). Several attempts of EC with lidocaine (100 and 50 mg) and landiolol (2.5–15 mg) and three times of administrations of nifekalant (5–15 mg) were temporarily effective at 14:12–25 (marked “B”), and the patient ECG suggested sinus rhythm with premature ventricular counts. However, the sinus rhythm and VT occurred alternatively, and the rhythm subsequently changed to torsades de pointes (TdP), which might have occurred because of the overdose of nifekalant at around 14:55 (marked “C”). Therefore, we administered 2 g of magnesium sulfate followed by amiodarone three times, reaching a total of 450 mg (each dose of 150 mg), and initiated continuous infusion at 50 mg/h (c.f. Fig. ). We also initiated the pacemaker (VVI setting) and IABP at 14:50 and 15:16 (marked “D” and “E”), respectively.
All these procedures appeared to be effective at terminating the VT and subsequently succeeded in weaning from CPB. Thus, the situation with the sinus rhythm was sustained until the end of surgery. During this period, we also took caution to maintain normothermia with no electrolyte imbalance. The flow of the two bypass grafts was assessed using a flowmeter, i.e., LITA–LAD, 50 ml/min, and SVG–RCA, 9 ml/min. Transesophageal echocardiography revealed only diffuse hypokinesis with approximately 20% of EF just after aortic declamping, which gradually improved toward the weaning of CPB to approximately 30% of EF. After admission to the intensive care unit (ICU), the patient showed no VF or VT under the continuous infusion of amiodarone (50 mg/h), and the IABP was withdrawn on postoperative day (POD) 1 and extubated on POD 2. The patient was discharged from the ICU on POD 3 and from the hospital on POD 12 without any complication.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.0, 'kg'], 'height': [176.0, 'cm']}",17.75568,16.8679,18.64346,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 176.0 cm, which is 176.0 cm * 1 m / 100 cm = 1.76 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.76 m * 1.76 m) = 17.75568 kg/m^2."
2376,6,Body Mass Index (BMI),physical,decimal,pmc-3639674-1,Extracted,"A 38-year-old woman (height 1.61 metres and weight 52 kg) presented with a long history of chronic deep dyspareunia and secondary dysmenorrhea. She was para 1, having had a normal vaginal delivery of a 3.5 kg baby ten years ago. She had no significant medical or surgical history. The clinical examination detected a well-distinguishable mass in the anterior wall of the uterus. The preoperative workup revealed at magnetic resonance imaging (MRI) a large thirteen-centimeter anterior interstitial fibroid (Figures and ). After careful deliberation and multidisciplinary discussions with the radiology team, a decision was taken to undertake the myomectomy via the vaginal route. Patient did not resort to GnRH analogues or preoperative embolisation.
Surgical procedure was performed under general anesthesia. The uterine mobility through the vagina was preliminary evaluated to ensure that the cervix reached the vulvar vestibulum. Arciform anterior colpotomy was initiated. The myoma was completely enucleated and exteriorized after morcellation via the anterior vaginal colpotomy (). Uterine myography was performed in multiple layers with Vicyl 0 to ensure effective hemostasis. Anterior vaginal pouch was closed with separate point Vicryl 0. A vaginal compression and bladder catheterisation were ensured for 24 hours. Operative duration was one hour and blood loss was evaluated at 350 mLs.
The patient had an uneventful immediate postoperative recovery. Her preoperative haemoglobin was 12 gm/dL and at day 1 postoperative haemoglobin was 11 g/dL. The hospital inpatient stay was 48 hours under antibiotic cover (CEFAZOLINE 2 g/24 H) and Oxytocin (SYNTOCINON) infusion at 15 units/hr for 24 hours.
Clinical examination at follow-up consultation was normal. A postoperative MRI reveals a complete uterine cicatrization ().",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [52.0, 'kg'], 'height': [1.61, 'm']}",20.06095,19.0579,21.064,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.61 m. The patient's weight is 52.0 kg. The patient's bmi is therefore 52.0 kg / (1.61 m * 1.61 m) = 20.06095 kg/m^2."
2377,6,Body Mass Index (BMI),physical,decimal,pmc-7868309-1,Extracted,"A 62-year-old man (body weight, 80 kg; height, 185 cm) with traumatic descending aorta dissection was transferred to our hospital. He was in a state of shock (blood pressure, 75/61 mmHg; heart rate, 142 beats/min) and emergency thoracic endovascular aortic repair was planned. After entering the operating room, arterial cannulation was performed in the radial artery. Anesthesia was induced with intravenous fentanyl, propofol, and rocuronium, and his trachea was intubated. Anesthesia was maintained with air, oxygen, desflurane, and remifentanil. After the induction of anesthesia, he remained in a state of shock with systolic blood pressure of 60–70 mmHg, and common carotid artery palpation was weak. Using short-axis ultrasound imaging, a 12-gage central venous catheter (CV RegaForce EX®, Terumo, Tokyo) was inserted in the right internal jugular vein by the Seldinger technique. After catheter placement, the pressure waveform from the central venous catheter showed the arterial blood pressure waveform, indicating arterial cannulation. Since administration of heparin was planned during surgery, we decided not to remove the catheter that had been inserted into the artery. The endovascular surgery was completed in 1 h and 59 min. A postoperative chest radiograph showed the catheter in his right chest. He was transferred to the intensive care unit (ICU) without extubation.
After entering the ICU, the shock state persisted despite continuous administration of noradrenaline and dopamine. Contrast-enhanced CT showed intra-abdominal bleeding from liver injury and intestinal necrosis. It also showed that the tip of the catheter was located in the right brachiocephalic artery. A laboratory examination revealed coagulopathy: low fibrinogen level (70.0 mg/dL), prolonged PT-international normalized ratio (INR) (2.60), and prolonged aPTT (≥ 200.0 s). The catheter was therefore not removed. Two hours after entering the ICU, hepatic artery embolization, small intestine resection, and right hemicolectomy were performed.
On the 6th day after entering the ICU, he remained to be intubated and received noradrenaline and dopamine to maintain his blood pressure. His blood coagulability was improved: fibrinogen level, 415.0 mg/dL; PT-INR, 1.22; and aPTT, 31.2 s. We therefore planned to remove the catheter. We considered that surgical repair would be highly invasive for the patient and decided to place a percutaneous intravascular stent after removal of the catheter. Angiography showed that the catheter was inserted into the artery near the bifurcation of the right vertebral artery and subclavian artery (Fig. a). A stent (GORE® VIABAHN® Stent graft, Japan Gore, Tokyo) was percutaneously inserted through the right axillary artery. The position of stent deployment was adjusted so that the stent covered the catheter insertion site and did not occlude the opening of the right vertebral artery (Fig. b). After the catheter was removed, the stent was immediately expanded. Post-procedural angiography revealed that there was no leak from the catheter insertion site and no occlusion of the right subclavian artery and right vertebral artery (Fig. c). There were no obvious hematoma or thrombotic complications.
Although the catheter was successfully removed, the patient’s general condition gradually deteriorated. Thirteen days after entering the ICU, he died of multiple organ failure.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [80.0, 'kg'], 'height': [185.0, 'cm']}",23.37473,22.20599,24.54347,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 185.0 cm, which is 185.0 cm * 1 m / 100 cm = 1.85 m. The patient's weight is 80.0 kg. The patient's bmi is therefore 80.0 kg / (1.85 m * 1.85 m) = 23.37473 kg/m^2."
2378,6,Body Mass Index (BMI),physical,decimal,pmc-4318869-1,Extracted,"A 70-year-old woman with a five-year history of diabetes mellitus required ureter stone removal with general anesthesia. The height and weight of the patient were 153 cm and 59.6 kg, respectively.
Four months previous she received a dual pacing, dual sensing and dual response pacemaker for the treatment of second-degree heart block. At that time, transthoracic echocardiography (TTE) showed mild left ventricular hypertrophy and normal left ventricular ejection fraction (EF = 74%) with no regional wall motion abnormalities. The pacemaker was checked by a cardiologist one month previous. She had received no anticoagulant therapy.
A follow-up electrocardiogram (ECG) showed normal sinus rhythm and laboratory studies were unremarkable. On consultation with a cardiologist, the patient was evaluated to have low Class II with 0.9% complications on Revised Cardiac Risk Index for the operation.
The patient was not premedicated. The intraoperative monitoring of the patient included non-invasive blood pressure, ECG (leadII, aVL), pulse oximetry (SpO2), Bispectral index (BIS), and end-tidal CO2 concentration (EtCO2) measurements. Initial blood pressure was 160/80 mmHg. Heart rate was 82 beats/min, and SpO2 was 99%. Anesthesia was induced using mask administration of 100% O2. Fentanyl 50 µg, 2% lidocaine 40 mg, propofol 100 mg and rocuronium 40 mg were administered intravenously, and the trachea was intubated using a 7.0 mm cuffed endotracheal tube. Anesthesia was maintained using 2 L/min O2, 2 L/min nitrous oxide, and 6 vol% desflurane.
Ureteroscopic lithotripsy was performed in the lithotomy position. Blood pressure was maintained with systole 100-90 mmHg, diastole 60-50 mmHg, heart rate 60-55 beats/min and SpO2 99%. After approximately 40 minutes, SpO2 was suddenly not detected, BIS decreased from 45 to 19, blood pressure was not checked. EtCO2 dropped from 30 to 11, and both pupils dilatated without light reflex. ECG monitored the pacemaker's rhythm. External cardiac massage was immediately initiated and 1 mg doses of epinephrine and 0.5 mg doses of atropine were administered. TTE was immediately examined and showed full of multiple thrombi in all the cardiac chambers. Urokinase and two additional doses of epinephrine (1 mg) were administered, after which most thrombi dissolved or embolized via aorta (). Defibrillation was performed using 200 J, when ECG revealed ventricular fibrillation (VF). The patient was not resuscitated and died, despite continued cardiopulmonary resuscitation for about 60 minutes.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [59.6, 'kg'], 'height': [153.0, 'cm']}",25.46029,24.18728,26.7333,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 153.0 cm, which is 153.0 cm * 1 m / 100 cm = 1.53 m. The patient's weight is 59.6 kg. The patient's bmi is therefore 59.6 kg / (1.53 m * 1.53 m) = 25.46029 kg/m^2."
2379,6,Body Mass Index (BMI),physical,decimal,pmc-4891543-1,Extracted,"A 40-year-old woman (weight, 70 kg; height, 165 cm) was scheduled for a repeat cesarean section at 38 + 1 weeks of gestation. She was a second gravida, and had been diagnosed with systemic lupus erythematosus (SLE) due to an erythematous rash on her nose and chins during the prior pregnancy. At that time, she had undergone a cesarean delivery under epidural anesthesia, and there had been a rash on the skin of neonate for several months after birth. After delivery, no residual symptoms were noted and no medication was administered. During the second pregnancy, she complained of similar rash on her nose along with mild itching and dry skin in the first trimester. An autoimmune disease such as SLE was suspected, and laboratory tests were performed to identify autoantibodies (). The results revealed that anti-Ro/SSA and anti-La/SSB antibodies were positive; hence, the patient was diagnosed with Sjogren's syndrome rather than SLE. Because of the risk of CHB, fetal echocardiograms were routinely checked from 15 weeks of gestation, and fetal heart rate was approximately 150 beats/min at each examination. The skin rash on the patient improved spontaneously after the second trimester, and there were no other symptoms such as dry eyes, dry mouth, or arthralgia. To prevent cardiac complications of fetus, the patient received hydroxychloroquine from 25 weeks of gestation until delivery.
An elective cesarean section was scheduled at 38 + 1 weeks of gestation. Preoperative laboratory tests, electrocardiogram (ECG), and chest X-ray were normal. After arriving in the operating room, noninvasive blood pressure, ECG, and pulse oximetry monitoring commenced. Her initial blood pressure was 118/71 mmHg, heart rate was 77 beats/min, respiratory rate was 16 breaths/min, and oxygen saturation was 100%. Oxygen at 5 L/min was supplied via a facial mask.
After placing the patient in the right lateral decubitus position, the median approach was performed with the 25 G Whitacre spinal needle at the L3-4 intervertebral space. After the stylet was removed and cerebrospinal fluid was confirmed to be draining well, 9 mg of 0.5% hyperbaric bupivacaine with 20 µg of fentanyl was injected. Then, she was positioned supine with a left lateral tilt of 15°, and the height of the block checked by a pin-prick test was T4.
Nine minutes after the skin incision, a female neonate (weight, 2.8 kg) was delivered and her Apgar score was 8 at 1 minute and 9 at 5 minutes. Two minutes after the delivery, the placenta was removed and intravenous infusion of 20 International Units (IU) of oxytocin mixed with 800 ml of 0.9% saline was started. The initial neonatal heart rate was 160 beats/min, and the neonate was transferred to the neonatal intensive care unit (NICU) immediately for continuous monitoring of ECG. The patient's vital signs were stable during the operation, and the estimated blood loss was about 500 ml. During the NICU stay, the neonate's ECG findings showed no abnormality, and the heart rate was approximately 140–170 beats/min. The patient and her neonate were discharged on the fifth postoperative day without any complication.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [165.0, 'cm']}",25.71166,24.42608,26.99724,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.65 m * 1.65 m) = 25.71166 kg/m^2."
2380,6,Body Mass Index (BMI),physical,decimal,pmc-2426701-1,Extracted,"We report the case of a 39-year-old man with a height of 178 cm and weight of 72 kg, working as a bellboy in a hotel. He had developed renal insufficiency 8 years previous, had undergone hemodialysis and had received a left renal transplantation after 2.5 years of hemodialysis. The patient had taken 8 mg methylprednisolone once a day for 3.5 years following the renal transplantation. The nephrologist following-up our patient decreased the methylprednisolone dose to 4 mg 1 week before admission.
The patient had complained of increasing back and neck pain for 6 months prior to admission. He had been diagnosed with paravertebral spasm at two different locations. There was no history of trauma. After admission, the patient showed no improvement, and experienced worsening pain. The pain was an acute shooting pain resembling an electrical flash at the cervicodorsal site. Weight bearing was an occupational requirement, and the patient claimed that there was more pain while bearing heavy weights. There was also a history of night pains at the cervicodorsal site and pain and paresthesia of the upper extremity and chest.
Neurological examination was normal. There was pain at the cervicodorsal site during neck movements, particularly during neck flexion. Based on the suspicious images of the spinous processes of the C7 and D1 vertebrae in the X-rays of the cervical and dorsal vertebrae (Figure ), cervicodorsal computerized tomography was performed (Figure ). The spinous process fractures of the C7, D1 and D2 vertebrae were diagnosed as Clay-shoveler's fractures. The patient was treated with a cervical collar for 1.5 months. Due to the patient's history of renal transplantation and corticosteroid use, whole body bone densitometry was performed. The mean lumbar spine T-score was -2.7, and the mean femoral neck T-score was -2.1. The patient was given 10 mg oral alendronate once a day. At the second month of follow-up, the control dual energy X-ray absorptiometry (DEXA) value of the mean lumbar spine T-score regressed to -2.6 and the mean femoral neck T-score regressed to -2.0, and at the fourth month, the scores had regressed to -2.4 and -1.9. Following the collar and alendronate treatment, the patient's pain regressed rapidly in 1.5 months. The patient was followed-up for 12 months, and he continued on oral methylprednisolone 4 mg/day during the follow-up.
Alendronate treatment was discontinued when the patient's T-scores reached -2.0 (the mean lumbar spine T-score) and -1.3 (the mean femoral neck T-score) on the 12-month DEXA scan. For evaluation of the patient's renal function, urinary creatinine clearance was measured at 1, 2, 3, 6, 9, and 12 months after the alendronate treatment. No renal malfunction was observed. He was given a rest report that prohibited him from weight-bearing activities for a total of 6 months. Control computerized tomography scanning was performed 6 months after the resolution of the pain (Figure ) and the fracture sites were evaluated for union of the fractures. There was no pain at the follow-up examination 24 months after the fracture.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [72.0, 'kg'], 'height': [178.0, 'cm']}",22.7244,21.58818,23.86062,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 178.0 cm, which is 178.0 cm * 1 m / 100 cm = 1.78 m. The patient's weight is 72.0 kg. The patient's bmi is therefore 72.0 kg / (1.78 m * 1.78 m) = 22.7244 kg/m^2."
2381,6,Body Mass Index (BMI),physical,decimal,pmc-6857201-1,Extracted,"Our patient was a 71-year-old Caucasian non-Hispanic male who presented with chronic left knee pain after undergoing a TKA 18 months prior. He had an uncomplicated past medical history of hypertension, hyperlipidemia, and reflux, which were well controlled with medical management. He was 70 inches tall and weighed 215 lbs. He had no history of any additional surgeries. He was married and lived at home with his wife. He was now retired and prior to his surgery maintained an active lifestyle including exercise and daily life activities. His social history included social alcohol consumption and was negative for tobacco use (Fig. ).
Following his TKA, the patient complained of persistent and progressively worsening post-operative pain of his knee. Orthopedic evaluation determined his implant to be normally functioning without evidence of hardware loosening or infection. On presentation, he described the pain as sharp, 7/10 (VAS) in severity though poorly defined, with radiation to the left ankle, and associated paresthesias in the same distribution. On physical exam, he experienced symptoms of hyperesthesia and allodynia along the anterior aspect of his knee. His postsurgical incision was well healed, without evidence of erythema, swelling, or gross changes in color. Strength was 5/5 with flexion and extension of the lower left leg, but was limited by guarding due to pain. His right lower extremity had 5/5 strength in all myotomes, and otherwise he had 5/5 strength in the left leg with flexion and extension of the thigh, inversion, eversion, plantar flexion, and dorsiflexion of his left foot.
Given his symptomatology of hyperesthesia, allodynia, preserved strength, and absence of orthopedic aberrancy, a diagnosis of postsurgical CRPS of the left lower extremity was made. Initial management of his pain was conservative including physical therapy, non-steroidal anti-inflammatory, muscle relaxant, neuropathic, and opioid medications, which provided little or no relief of symptoms. Following a trial of lumbar sympathetic block, he reported improvement in pain, with a reduction on VAS to 3/10, lasting approximately 1 month in duration. Given a dramatic improvement in his knee symptoms, he subsequently underwent a successful SCS trial and uneventful implantation of two 16-contact Boston Scientific leads with a Boston Scientific Spectra WaveWriter™ SCS system. His generator was programmed to provide simultaneous traditional paresthesia-based therapy at a frequency of 50 Hz along with the combination of burst therapy at a frequency of 450 Hz, with six pulses per burst, as well as sub perception stimulation therapy at a frequency of 1.2 kHz. Upon first post-procedural follow-up, the patient experienced dramatic pain relief, reporting complete resolution of his symptoms. Moreover, at 6 months post SCS implantation, he continued to experience complete resolution and had successfully completed an opioid wean to discontinuation.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [215.0, 'lbs'], 'height': [70.0, 'in']}",30.84895,29.3065,32.3914,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 70.0 in, which is 70.0 in * 0.0254 m / in = 1.778 m. The patient's weight is 215.0 lbs so this converts to 215.0 lbs * 0.453592 kg/lbs = 97.52228 kg. The patient's bmi is therefore 97.52228 kg / (1.778 m * 1.778 m) = 30.84895 kg/m^2."
2382,6,Body Mass Index (BMI),physical,decimal,pmc-8484880-1,Extracted,"A 14-year-old boy presented to the Children's Hospital, Zhejiang University School of Medicine, with main complaints of recurrent abdominal pain accompanied by fever for 14 days. He had middle and upper abdominal pain on day 1 of presentation, accompanied by vomiting and diarrhea. He was diagnosed with acute gastroenteritis at a local clinic, and the symptoms relieved after being administered with intravenous cefuroxime and anisodamine. On day 2 of presentation, his abdominal pain worsened and localized at the right lower abdomen. He also had a low-grade fever, with a temperature of 38.0 °C. Thus, he went to Shaoxing People's Hospital, and physical examination showed obvious pressing pain at McBurney's point at the right lower abdomen. B-ultrasound examination revealed appendicitis (diameter 6 mm) and several lymph node echoes in the right lower abdomen, the largest size of which was 21 × 10 mm. The surgeon considered it was acute appendicitis, and an emergency laparoscopic operation was performed. During the operation, about 10 ml of light yellow transparent liquid was sucked from the ileocecal junction. The normal appendix and swollen lymph nodes in dark red were found in the operative field (). Lymphadenectomy, as well as appendectomy, was performed for pathological examination. After the operation, intravenous cefotiam and metronidazole were prescribed empirically, and symptom of abdominal pain was relieved. Since day 3 postoperation (day 5 of presentation), his temperature decreased to near normal level. The pathological examination indicated almost normal appendix and necrotizing lymphadenitis (). The patient was discharged from Shaoxing People's Hospital on day 6 postoperation (day 8 of presentation) with body temperature at 37.7 °C.
After discharge, the boy had low-grade fever accompanied by mild abdominal pain occasionally. Since day 10 of presentation, his body temperature rose to as high as 39.4 °C. Intravenous ceftriaxone for 4 days was prescribed in a local clinic, and his symptoms did not improve at all.
As a result, the boy was moved to the Children's Hospital, Zhejiang University School of Medicine. During the course of his illness, he had poor appetite and sleep. He had no past medical history, and his parents denied familial inherited disease. Physical examination on admission finding includes the following: temperature of 38.6°C, heart rate at 100 number/minute (n/min), respiration at 24 n/min, blood pressure at 117/90 mmHg, weight of 53 kg, and height at 170 cm. Enlarged lymph nodes without tenderness were found in the cervical, axillary, and inguinal area. The size of the largest one was 15 × 10 mm. Heart and lung exams were normal. No abdominal tenderness was evoked during abdominal examination. The liver and spleen were not palpable. The diagnoses were KFD and postoperative appendectomy. After admission, the results of the PPD test, mycoplasma antibodies detection, tuberculosis T-SPOT test, and autoantibody test were all negative. The level of procalcitonin in serum was normal. On the fourth day after admission (on day 17 of presentation), the patient agreed to receive intravenous methylprednisolone, and his body temperature dropped to normal at the same day. After being treated with methylprednisolone for 5 days (intravenous for 3 days, 1 mg/(kg/d), twice a day; oral for 3 days, 0.5 mg/(kg/d), twice a day), he was discharged without any symptoms. He completed therapy with methylprednisolone according to the doctor's advice, including oral methylprednisolone 6 mg twice a day for 3 days, 6 mg once a day for 3 days, and 2 mg once a day for 7 days. He was followed up for 2 years after discharge, and no similar symptoms or abnormal laboratory findings recurred. The laboratory findings of the patient during the course of illness are shown in .",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.0, 'kg'], 'height': [170.0, 'cm']}",18.3391,17.42214,19.25605,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 53.0 kg. The patient's bmi is therefore 53.0 kg / (1.7 m * 1.7 m) = 18.3391 kg/m^2."
2383,6,Body Mass Index (BMI),physical,decimal,pmc-4782425-1,Extracted,"A 25-year-old, 167 cm, 64 kg female patient, diagnosed with a papillary thyroid carcinoma presented for a robot-assisted endoscopic total thyroidectomy. In computed tomography, the right thyroid lobe showed an 8 mm sized nodule. Her medical history was unremarkable. Her mouth opening was restricted to two fingers due to trismus owing to an erupting wisdom tooth. The pre-operative electrocardiogram (ECG), chest and neck radiographs, laboratory investigations and indirect laryngoscopic findings were normal. In the operation theatre, routine monitors (ECG, pulse oximeter, capnograph and non-invasive blood pressure) were applied. After pre-oxygenation, anaesthesia was induced with intravenous midazolam 1.5 mg, fentanyl 80 μg, propofol 70 mg and atracurium 50 mg. On direct laryngoscopy (prior to giving the neuromuscular blocking agent), Cormack and Lehane Grading was 2B and both the vocal cords were mobile. The trachea was intubated with an ID 7 mm cuffed reinforced Lo-Contour™ flexometallic endotracheal tube (ETT) (Covidien, Mallinckrodt Medical Ltd., Athlone, Ireland) using the C-Mac D-Blade™ video laryngoscope. The tracheal cuff was inflated, and a circle system with inspiratory and expiratory tubings twice the standard length (improvised in advance) was connected. After capnographic confirmation of proper placement, the tube was fixed on the left side of the mouth at the 19 cm mark. A bispectral index-guided intravenous propofol infusion along with desflurane in 66% air-oxygen mixture was utilised for the maintenance of anaesthesia. Continuous atracurium infusion was given under peripheral nerve stimulator monitoring of neuromuscular blockade. Ventilatory parameters were adjusted to maintain an end-tidal CO2 between 35 and 40 mmHg.
The patient was placed in supine position with head extended, neck flexed, right arm abducted and the left arm adducted. The robotic arms were inserted via the right axillary approach after utilising a Chung's retractor to facilitate exposure []. At the end of surgery, after reversing the neuromuscular blockade, on insertion of the video laryngoscope, we found the right true vocal cord to be immobile. Patient-controlled analgesia (PCA) pump with morphine infusion, intraoperative subcutaneous ropivacaine infiltration and 1 g intravenous paracetamol infusion were utilised for post-operative pain relief.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [64.0, 'kg'], 'height': [167.0, 'cm']}",22.94812,21.80071,24.09553,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 167.0 cm, which is 167.0 cm * 1 m / 100 cm = 1.67 m. The patient's weight is 64.0 kg. The patient's bmi is therefore 64.0 kg / (1.67 m * 1.67 m) = 22.94812 kg/m^2."
2384,6,Body Mass Index (BMI),physical,decimal,pmc-8582956-1,Extracted,"T.M.I, a 33-year-old physician, was multiparous. On February 23, 2021, at 34 weeks of gestation, she received the first 0.5 mL dose of the CoronaVac® vaccine (Instituto Butantan, São Paulo, Brazil) containing 600 SU of the inactivated virus antigen to SARS-CoV-2. A second dose of equal volume and composition was administered on March 15, 2021, when she was at 37 weeks of gestation. No complications were detected during prenatal care. She attended 10 antenatal consultations without any symptoms of SARS-CoV-2 infection. There was a weight gain of 14 kg, and she ended the pregnancy at a weight of 110 kg and height of 166 cm.
The delivery took place at 39 weeks of gestation by cesarean section on April 9, 2021. The newborn was male, weighed 3.44 kg, was 48 cm long, and had a head circumference of 33 cm. He was breastfed, and a comprehensive physical assessment revealed that he was healthy. The Apgar scores at 1 and 5 minutes were 9 and 10, respectively.
Blood specimens were collected by peripheral venipuncture 24 h after birth to detect neutralizing antibodies against SARS-CoV-2/COVID-19. The serological test, carried out by enzymatic immunoassay (cPass™ SARS-CoV-2 Neutralization Antibody Detection Kit, GenScript, Make Research Easy), showed a result of 22%, which was considered positive based on the cutoff value of 20%. The cPass™ SARS-CoV-2 Neutralization Antibody Detection Kit is a blocking enzyme-linked immunosorbent assay (ELISA) intended for the qualitative direct detection of total neutralizing antibodies to SARS-CoV-2 in human serum and K2-EDTA plasma as a detection tool. Using purified receptor binding domain, protein from the viral spike (S) protein, and the host cell receptor ACE2, this test is designed to mimic the virus-host interaction by a direct protein-protein interaction in a test tube or a well of an ELISA plate. This highly specific interaction can then be neutralized in the same manner as in a conventional virus neutralization test.
This study was approved by the Research Ethics Committee of the University of Southern Santa Catarina (opinion no. 4.728.687) on May 24, 2021. Informed consent was obtained from the mother of the child prior to the data collection.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [110.0, 'kg'], 'height': [166.0, 'cm']}",39.91871,37.92277,41.91465,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 110.0 kg. The patient's bmi is therefore 110.0 kg / (1.66 m * 1.66 m) = 39.91871 kg/m^2."
2385,6,Body Mass Index (BMI),physical,decimal,pmc-5369859-1,Extracted,"An 80-year-old Japanese woman presented to the Dermatology Department of the Showa General Hospital on day 0 with a 1-month history of spreading ulcers due to pyoderma gangrenosum. Her past medical history included pyoderma gangrenosum, diabetes mellitus, and rheumatoid arthritis. Her daily medications included alfacalcidol, salazosulfapyridine, polaprezinc, methotrexate, lansoprazole, folic acid, diclofenac, and felbinac.
On initial physical examination, she had a temperature of 37.0 °C (98.6 °F) and a blood pressure of 111/45 mmHg, with a heart rate of 51 beats per minute. Her height was 145.5 cm, and her body weight was 45.5 kg. The patient presented with several ulcers on all her extremities but had otherwise unremarkable findings. The initial laboratory workup (day 0) showed hyperglycemia of 237 mg/dL, leukocytosis (white blood cell count [WBC], 16,040/µL), and abnormal renal function (blood urea nitrogen [BUN], 39.6 mg/dL; creatinine 1.64 mg/dL). An echocardiogram showed a heart rate of 38 beats per minute and a complete atrioventricular block.
The clinical course is shown in . The patient was treated with prednisolone 40 mg/day for pyoderma gangrenosum; moreover, tazobactam/piperacillin was administered since an infection of the ulcers was suspected. On day +19, a pacemaker was implanted to treat the complete atrioventricular block. On day +23, Gram staining of the blood culture showed numerous yeast cells that were identified as C. glabrata (), on API® ID32C (API-bioMérieux France). Micafungin 250 mg/day was administered (starting on day +23) followed by 150 mg/day (starting on day +29) after exclusion of fungal endophthalmitis. The pacemaker was removed to remove a possible source of infection on day +23. On day +30, a central venous (CV) catheter was inserted; it was subsequently removed and reinserted on day +38. On days +40 and +54, skin grafting was performed for the ulcers. As guidelines state that antifungal treatment should be completed >2 weeks after a negative blood culture (on day +31), micafungin therapy was discontinued on day +77 after a total of 54 days of treatment. On day +88, the CV catheter was removed and then reinserted. On day +105, Gram staining of the blood culture showed the recurrence of numerous yeast cells that were again identified as C. glabrata (). As this was a recurrence of the C. glabrata BSI, we re-administered micafungin 150 mg/day and removed and reinserted the CV catheter. On day+109, another skin grafting procedure was performed. On day +120, Gram staining of the blood culture showed numerous yeast cells yet again; consequently, the micafungin dose was increased to 250 mg/day and the CV catheter was removed and then reinserted. On day +127, the blood culture and the CV catheter culture tested positive for C. parapsilosis (), identified by API® ID32C (API-bioMérieux France).
Micafungin was switched to liposomal amphotericin B (3 mg/kg/day), as this medication is effective for both C. glabrata and C. parapsilosis. On day+155, liposomal amphotericin B therapy was discontinued after a total treatment duration of 28 days, as the treatment had been provided >2 weeks after the negative blood culture result (day+134). On day+156, the CV catheter was removed and the patient was discharged from the hospital after successful treatment.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.5, 'kg'], 'height': [145.5, 'cm']}",21.49242,20.4178,22.56704,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 145.5 cm, which is 145.5 cm * 1 m / 100 cm = 1.455 m. The patient's weight is 45.5 kg. The patient's bmi is therefore 45.5 kg / (1.455 m * 1.455 m) = 21.49242 kg/m^2."
2386,6,Body Mass Index (BMI),physical,decimal,pmc-8016778-1,Extracted,"A 68-year-old male with a height and weight of 174.5 cm and 43.6 kg, respectively, and a primary complaint of anemia was admitted to our facility. Abdominal examination revealed that the abdominal region was leveled and soft without any pressure or pain, and no palpable masses or superficial lymph nodes were observed. Hematological tests showed a hemoglobin (Hb) level of 11.8 g/dL, indicating anemia, and no abnormalities were indicated by CEA, CA19-9, and AFP tumor markers were observed. Esophagogastroduodenoscopy revealed a submucosal tumor-like mass with delle and bridging fold in the greater curvature of the lower stomach, and the tumor was suspected as the cause of anemia (Fig. ). Ultrasound endoscopy revealed a submucosal tumor (SMT) (with the fourth layer as the main locus) and a tumor (with the third layer as the main locus), with some areas of indistinct borders (Fig. b). Tissue biopsy of this tumor indicated group 5 tubular adenocarcinoma, and thoracoabdominal computed tomography (CT) showed a tumor with a mottled contrast stain in the stomach body and no regional lymph nodes or distant metastases (Fig. ). Based on the above findings, the patient was diagnosed with collision tumor of gastric cancer and SMT (GIST was highly suspected). Gastrectomy was performed via laparotomy, and the surgical findings were a diagnosis of H0P0CY0 according to the 3rd English edition of the latest edition of the Japanese classification of gastric carcinoma issued by the Japan Gastric Cancer Society []. Distal gastrectomy was performed with D2 lymph node dissection according to the Japanese Gastric Cancer Treatment Guidelines [].
The tumor was located in the greater curvature of the antrum of the stomach and measured 50 × 45 mm in size (Fig. a). On the cut surface, a nodular tumor was mainly observed in the submucosal layer, and the mucosal surface was ulcerated (Fig. b). A large part of the tumor was observed to be mixed and some of the cancer parts and GIST alone sites were observed. (Fig. c). The nodular tumor was characterized by the intermingled proliferation of carcinoma cells and spindle cells (Fig. d). The spindle cells formed a nodular tumor in the submucosal layer and the subserosal layer. Carcinoma cells invaded the nodular tumor of the spindle cells. Pathological examination revealed Ki67 positive cells comprised 2% of the GIST. The average mitotic count was ≤ 5 mitotic figures per 50 high power fields. GIST was classified as very low risk according to the guidelines for GIST risk stratification []. Tubular adenocarcinoma had reached the subserosa, and no lymph node metastases were observed. The pathological findings were a diagnosis of pT3N0M0 pStageIIA, according to the 3rd English edition of the latest edition of the Japanese classification of gastric carcinoma issued by the Japan Gastric Cancer Society []. Immunohistochemical staining demonstrated a positive reaction for cytokeratin (AE1/AE3) in the carcinoma cells (Fig. a). Further, the nuclei of adenocarcinoma cells were positive for TP53 (Fig. b). Although the spindle cells were negative for cytokeratin (AE1/AE3) and TP53, these cells were positive for c-kit (Fig. c), weakly positive for DOG-1, and negative for desmin and S-100. As a result, the tumor was diagnosed as a collision tumor of GIST and adenocarcinoma. Lymph node metastasis of GIST or adenocarcinoma was not observed, and the resected margins were negative for neoplastic cells. Histologically, the intratumoral GIST sections contained different KIT exon 17 mutations, and KIT exon 17 mutation corresponding to amino acid substitution Asp820Lys was observed. On the other hand, the adenocarcinoma section detected no KIT mutation.
No complications were observed postoperatively, and the patient was discharged from the hospital on postoperative day 14. No adjuvant therapy was required for GIST, as per the international guidelines for GIST risk stratification []. The patient was clinically and radiographically disease-free at 2.5 years after surgery.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [43.6, 'kg'], 'height': [174.5, 'cm']}",14.31844,13.60252,15.03436,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 174.5 cm, which is 174.5 cm * 1 m / 100 cm = 1.745 m. The patient's weight is 43.6 kg. The patient's bmi is therefore 43.6 kg / (1.745 m * 1.745 m) = 14.31844 kg/m^2."
2387,6,Body Mass Index (BMI),physical,decimal,pmc-3726851-1,Extracted,"A 73-year old male patient of 173 cm height and 52 kg weight visited hospital. The chief complaint was cellulitis in right ankle. He was under medication after being diagnosed with diabetes, hypertension, congestive heart failure, and left chronic tuberculous empyema ten years ago. He was undergoing hemodialysis three times a week after diagnosis of end-stage renal disease eight years previously. There were no specific findings during the hospital stay. He maintained normal blood pressure of 130/80 mmHg and heart rate of 65-80 beats per minute. Atrial fibrillation, normal left ventricular function, moderate concentric left ventricular hypertrophy, moderate pulmonary hypertension, severe tricuspid regurgitation, moderate mitral regurgitation, aortic regurgitation, and moderate pericardial effusion were observed in echocardiography () performed during his hospital stay. Left lung empyema, right pleural effusion, pericardial effusion were confirmed by chest CT scans () and simple chest X-rays () and pulmonary function test showed a moderate restrictive pattern. Hemodialysis was performed the day before the operation and the result of the complete blood count before hemodialysis were hemoglobin level 8.8 g/dl.
On the fourth day of his in-hospital stay, sudden respiratory distress occurred after performing needle aspiration test of the right pleural effusion. Despite taking a simple chest X-ray immediately, our medical staff could not find any cause and observed him with oxygen therapy via nasal cannula. Respiratory distress got worse at a respiratory rate of 30 times per minute and an oxygen saturation level of 85% with changing mental status. Our staff inserted right chest tube 2 hours 30 minutes after performing needle aspiration biopsy. Approximately 1,500 ml of blood was drained for about 10 minutes after chest tube insertion, with blood pressure of 90/40 mmHg, heart rate of 66 beats per minute, respiratory rate of 22 times per minute, and body temperature of 36.4℃. Rapid fluid replacement with 1L of normal saline via central venous catheter placed in the right internal jugular vein was performed and an emergency operation was decided upon. The patient's electronic medical record (EMR) was unidentifiable by anesthesiologists because of computer network error at that time. Hence, the emergency operation was began only by acknowledging that the patient with diabetes and hypertension was receiving hemodialysis and massive bleeding occurred during needle aspiration test at right pleura.
He was transferred to the operating room without any preoperative medication 20 minutes after chest tube insertion. At that time, his vital signs were blood pressure of 130/50 mmHg, heart rate of 60 beats per minute, respiratory rate of 22 times per minute, and body temperature of 34.9℃. He was stuperous and his skin was cold but other physical examination could not be performed. Preoxygenation was attempted with 100% oxygen at 8 L/min via mask and warm Voluven® (6% hydroxyethyl starch, Fresenius Kabi, Germany) was rapidly administered. In addition, non-invasive blood pressure, oxygen saturation, and electrocardiogram (ECG) were monitored. An arterial catheter for continuous hemodynamic monitoring was placed via the right femoral artery and a central venous catheter via the right femoral vein and 500 ml of Voluven® was rapidly administered. After IV administration of 90 mg ketamine and 50 mg rocuronium for induction, endotracheal intubation was performed with a 35 Fr left-sided double lumen endotracheal tube (Broncho-Cath®, Mallinckrodt Medical Athlone, Ireland) and flexible fiberoptic bronchoscope (LF-GP, Olympus, Japan) was used for confirmation of proper placement. During lung ventilation, tidal volume of 100-120 ml, a peak inspiratory pressure of 40 cmH2O, blood pressure of 130/50 mmHg, a heart rate of 65 beats per minute, and a central venous pressure of 17-18 mmHg in supine position was checked. We attempted to maintain anesthesia with 1.5 L/min of oxygen, 1.5 L/min of nitrous oxide, and 2 vol% of sevoflurane. However, inspired oxygen concentration was changed to 100%, sevoflurane administration was stopped, and 1 mg of midazolam was administered intravenously every 15 minutes after oxygen saturation fell to 84%. After the patient was changed to left-sided lateral position, the location of tube was confirmed by a flexible fiberoptic bronchoscope with a central venous pressure of 21 mmHg. Left one-lung ventilation (OLV) was performed five minutes after changing the position to left-sided lateral position. Tidal volume and oxygen saturation decreased to 170-180 ml and 80% respectively. Peak inspiratory pressure increased up to 38 cmH2O.
Immediately on opening the right pleural cavity via right posterolateral thoracotomy, blood pressure decreased catastrophically and 1,500 ml of blood gushed out of the pleural cavity followed by about additional 1,200 ml of blood loss. Arterial blood gas analysis was performed 25 minutes after the beginning of surgery (). Subsequently, 3 L of Voluven® and 1 L of normal saline were administered rapidly during the half an hour after the beginning of surgery. At half an hour after the beginning of surgery, our hospital computer network was restored; packed red blood cells and fresh frozen plasma were administered. Then central venous pressure increased up to 38 mmHg with decreased active bleeding, fluid administration was minimized for concern about volume overload. Oxygen saturation level decreased continuously even though peak inspiratory pressure was above 40 cmH2O during one-lung ventilation. One-lung and two-lung ventilation were performed in turn along with manual and mechanical ventilation by maintaining tidal volume of 120 ml, respiratory rate of 60-70 times per minute, peak inspiratory pressure of 22 cmH2O, inhaled oxygen concentration of 100%, and oxygen saturation of 91-93%. Although fluid administration was minimized, central venous pressure increased up to 50 mmHg, blood pressure and heart rate were maintained at 120/60 mmHg and 67 beats per minute respectively and there were no abnormal ECG finding. Initial blood loss via chest tube before surgery was 1,500 ml, estimated blood loss during operation was 2,700 ml for 40 minutes and there was no urine output. The patient was administered 4,000 ml of Voluven®, 2,000 ml of normal saline, 5 pints of packed RBCs, and 5 pints of fresh frozen plasma. At 45 minutes after the beginning of surgery, central venous pressure suddenly increased up to 58 mmHg with falling in blood pressure of 70/40 mmHg, bradycardia of 25-30 beats per minute. 0.5 mg of atropine and 0.5 mg of epinephrine were administered immediately through a central line and the pericardium was checked by the surgeon for suspected pericardial tamponade while resuscitation was being prepared. The surgeon confirmed pericardial expansion and made a pericardial window immediately. After approximately 800 ml of yellow serous fluid with no blood was drained from the pericardial space, vital signs stabilized with recovering heart rate 60 beats per minute. Thereafter, blood pressure of 115/50 mmHg and heart rate of 65 beats per minute were maintained and central venous pressure was reduced to 45 mmHg. To maintain blood pressure, 20 mg of ephedrine and 1 g of calcium gluconate were administered divided. Arterial blood gas analysis was performed 30 minutes after pericardial window (). Although no active bleeding focus was found in the surgical field, blood leak continued under the damaged diaphragm. It was decided to observe the patient in the intensive care unit after primary closure. Flexible fiberoptic bronchoscopy was performed postoperatively and a small fresh blood clot was detected at the right bronchus. The patient was transferred to the ICU while maintaining a double lumen endotracheal tube from concern about failure of finding the bleeding focus and the risk of rebleeding. The total amount of fluid administrated during surgery was 4,100 ml of Voluven®, 3,000 ml of normal saline, 7 pints of packed RBCs, and 5 pints of fresh frozen plasma. Blood loss before surgery was 1,500 ml and intraoperative blood loss was 2,700 ml. Upon arrival on the ICU, the patient was stable with blood pressure of 97/72 mmHg, heart rate of 74 beats per minute and a tympanic membrane temperature of 35.7℃. No pulmonary edema was observed on postoperative chest X-ray (). Hemoperitoneum was confirmed on abdominal CT scan but we decided to observe carefully because there was no active bleeding focus in the abdominal cavity on the celiac artery angiogram. The patient exhibited stable vital signs after continuous renal replacement therapy during follow-up period and about 900 ml of bleeding via chest tube occurred on the first postoperative day. However, the chest tube was removed and hemoperitoneum was resolved as bleeding diminished 10 days postoperatively. Moderate pericardial effusion was detected again on echocardiography. The patient is currently admitted to the intensive care unit under mechanical ventilation due to respiratory failure.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [52.0, 'kg'], 'height': [173.0, 'cm']}",17.37445,16.50573,18.24317,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 173.0 cm, which is 173.0 cm * 1 m / 100 cm = 1.73 m. The patient's weight is 52.0 kg. The patient's bmi is therefore 52.0 kg / (1.73 m * 1.73 m) = 17.37445 kg/m^2."
2388,6,Body Mass Index (BMI),physical,decimal,pmc-8329551-1,Extracted,"The proband was a 5-year-old boy who was admitted to our hospital for recurrent seizure and growth retardation for 4 years. He was born at 35 weeks with a birth weight of 2,000 g. He had nystagmus at the first month of age. Growth and motor delays were noted at early childhood. He can sit at 1 year of age. He was unable to walk unsupported while still rapidly losing his balance after taking a few steps at around 2 years of age. At the age of four, he can walk and speak a few words.
The patient had a history of anemia. His mother was diagnosed mild anemia at 38 years old but did not receive any treatment; his mother's sister was also diagnosed with mild anemia. His grandmother's brother had intellectual problem and died at an early age with unknown cause, and his grandfather died because of respiratory disease without any neurological symptoms.
The patient's first generalized seizure occurred at 11 months of age. He initially failed treatment with a single dose of levetiracetam (40 mg/kg/day) but achieved seizure control with a combined therapy of levetiracetam (40 mg/kg/day) and topiramate (1.5 mg/kg/day). Gesell Development Scales (GDS) estimated at 5 years old indicated severe to extremely severe delay (scores of Gesell gross motor, fine motor, visual motor, language, and social were 28, 37, 31, 24, and 30, respectively). Scores of the Checklist for Autism in Toddlers-23 (CHAT-23) and the Clancy Autism Behavior Scale (CABS) were 20 and 15, respectively, both of which indicated he might have autism.
At the age of 5 years and 4 months, his height (97.5 cm), weight (15 kg), and head circumference (44 cm) were under the third percentile. The bilateral testicles were not palpable in the scrotum. Neurological examination showed decreased tendon reflexes, and plantar responses were flexor. Decreased muscle tone in the proximal upper and lower limbs and normal muscle strength were found. Sensation was intact. He had mild ataxic gait with wide-based steps. Nystagmus was noted. During his hospitalization, his hematological examinations showed mild normochromic anemia (). The examination of urinary organic acids showed significantly increased 2-hydroxyisobutyric acid, glycolic acid, oxalic acid, phosphoric acid, and glyceric acid (). Interictal electroencephalogram was found with spikes and sharp waves over the bilateral frontal region, anterior midline region, and centrotemporal region during both the waking and sleeping periods (). MRI showed lacunar infarction in the left basal ganglia with glial proliferation around and small tiny left transverse sinus, sigmoid sinus, and internal jugular vein (). Bilateral cryptorchidism was detected by ultrasonography (). Because of the subtle anemia (Hb 113 g/l) without any symptoms, the patient's parents refused to perform the further examination. His blood chemistry test (creatinine, liver enzymes, creatine kinase, lactate, electrolyte, and plasma ammonium), thyroid function (thyroid stimulating hormone and free thyroxine), chest X-ray, and heart ultrasound examination were normal.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [15.0, 'kg'], 'height': [97.5, 'cm']}",15.77909,14.99014,16.56804,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 97.5 cm, which is 97.5 cm * 1 m / 100 cm = 0.975 m. The patient's weight is 15.0 kg. The patient's bmi is therefore 15.0 kg / (0.975 m * 0.975 m) = 15.77909 kg/m^2."
2389,6,Body Mass Index (BMI),physical,decimal,pmc-7737526-1,Extracted,"In 2008, a 59-year-old Japanese woman was admitted for evaluation of renal disease. RA had been diagnosed at another hospital in 1972 when she presented with bilateral arthropathy of the hands, knees, ankles, and feet. Treatment was started with a combination of a gold preparation and nonsteroidal anti-inflammatory drugs (NSAIDs), but was not been effective. Prednisolone (PSL; 15 mg daily) and bucillamine (BUC; 200 mg daily) were started in 1987, but her disease remained active. Methotrexate (MTX; 5 mg daily) was started in 1995 but was discontinued because of nausea. In 2002, urinary protein was found to be positive by a dipstick urine test, and BUC was stopped. Then treatment was continued with PSL (5 mg/day) and loxoprofen (50 mg/day). However, urinary protein excretion increased in 2007, and serum creatinine (Cre) was elevated to 1.96 mg/dL.
On admission, the patient was 154.2 cm tall and weighed 44.0 kg, with a blood pressure of 128/60 mmHg and temperature of 36.4 °C. Physical examination did not reveal any abnormalities of the heart and lungs. The joints of her hands, knees, ankles, and feet showed bilateral swelling and deformity. In addition, the lower extremities were edematous. Her cervical spine was unstable, with flexion causing numbness in the upper limbs.
Laboratory findings were as follows: serum Cre was 4.2 mg/dL, the estimated glomerular filtration rate (eGFR) was 9.3 mL/min/1.73m3, C-reactive protein (CRP) was 0.9 mg/dL, and SAA was 43.2. In addition, rheumatoid factor (RF) was positive at 59 U/mL (normal: < 10), and cyclic citrullinated peptide (CCP) antibodies were positive at 218.5 (normal < 4.5). 24-hour urinary protein excretion was 6.5 g, and the urine sediment contained 1 – 5 red cells per high-power field (HPF). The disease activity score (DAS)-CRP was 7.1. Radiographs showed deformation of the finger and foot joints as well as atlantoaxial joint subluxation. Renal biopsy was performed for evaluation of her kidney disease.
Renal biopsy
Light microscopic examination of a biopsy specimen containing 4 glomeruli revealed global sclerosis in all 4. There was severe tubular atrophy, and tubulointerstitial fibrosis occupied ~ 95% of the entire renal cortex. All 4 glomeruli contained multinodular structures of amorphous material with a PAM-positive border. This material was positive for Congo-red and amyloid A, but was negative for κ and λ chains, β-2 microglobulin, and transthyretin (). Electron microscopy showed randomly arranged fibrils measuring 8 – 12 nm in diameter corresponding to the amyloid deposits (f). AA amyloidosis was diagnosed from these findings. In addition to the glomeruli, amyloid deposits were mainly observed in the interlobular artery walls and tubulointerstitium (e). Endoscopic biopsy of the stomach, duodenum, and colon revealed AA-positive deposits in the small arteries and tissues of the submucosal layer (a).
Clinical course
PSL was discontinued, and administration of a soluble tumor necrosis factor (TNF) receptor inhibitor (etanercept; 25 mg every 2 weeks) was started in May 2008, but it was not effective. By September 2008, Cre was increased to 6.0 mg/dL. She underwent surgery to prepare an arteriovenous fistula for hemodialysis. Etanercept was discontinued, and a humanized anti-interleukin-6 receptor antibody (tocilizumab; 8 mg/kg = 360 mg/month) was started in February 2009. After 3 months, her CRP decreased to 0.0 mg/dL, and the DAS28-CRP sore was 2.12. After 2 years of tocilizumab therapy, urinary protein excretion was decreased to 1.1 g/day, and Cre was 4.0 mg/dL. Subsequently, Cre remained in the range of 4.5 – 5.0 mg/dL until December 2017. While Cre increased to 7.1 mg/dL after initiation of treatment with denosumab (a human monoclonal antibody that binds to receptor activator of NFκB ligand) for osteoporosis in October 2018, it remained at 7.0 mg/dL in June 2019 ().
Gastroduodenal biopsy was performed in May 2013 and May 2017. On both occasions, no amyloid deposits were detected in the submucosal blood vessels (b).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [44.0, 'kg'], 'height': [154.2, 'cm']}",18.50478,17.57954,19.43002,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 154.2 cm, which is 154.2 cm * 1 m / 100 cm = 1.542 m. The patient's weight is 44.0 kg. The patient's bmi is therefore 44.0 kg / (1.542 m * 1.542 m) = 18.50478 kg/m^2."
2390,6,Body Mass Index (BMI),physical,decimal,pmc-7732407-1,Extracted,"A 32-year-old Sri Lankan female presented to the psychiatry services with fearfulness, undue suspicion, and hearing voices. She believed that somebody has implanted a camera inside her head to record her thoughts. She was irritable. In addition, she had begun to neglect her functions as a housewife and a mother. These symptoms were present for one year and had worsened over the previous two weeks.
Over the previous year, she was also experiencing lethargy, constipation, and cold intolerance. Symptom review was negative for postural dizziness, polyuria, polydipsia, headache, and visual disturbances.
She was a mother of three children; the youngest was one year and four months old. Her last pregnancy was complicated with gestational diabetes and pregnancy-induced hypertension. Childbirth by vaginal delivery was complicated with heavy bleeding. She experienced inability to lactate her child. An intrauterine contraceptive device was inserted six weeks postpartum. She did not experience any menstrual bleeding since childbirth.
She had no other comorbidities. Assessment of personality indicated that she was a well-adjusted person prior to the onset of illness without any maladaptive traits. This was her first presentation to a psychiatry service.
She was from a poor socioeconomic setting having poor family support, and her husband was alcohol dependent. This has led to a delay in seeking healthcare advice.
She was average built with a weight of 49 kg and a height of 151 cm. She was slow in response with dry skin of normal complexion and facial puffiness. There was no goitre. She had bradycardia (heart rate of 56/min) with a supine blood pressure of 80/60 mmHg and a standing blood pressure of 70/50 mmHg. The rest of the physical examination was normal.
Her mental state examination revealed an anxious mood with fleeting passive suicidal ideas. She had persecutory delusions involving an unidentified persecutor and a bizarre delusion that an external object has been implanted in her head to monitor her mental activity. She also had delusions of thought possession and elementary auditory hallucinations. Her delusions and hallucinations were observed to be transient. They were changing throughout the hospital stay. Initial persecutory delusions disappeared and the content of bizarre delusions changed in subsequent mental state examinations.
Her orientation with regard to time, day, month, place, and city was normal. Attention and concentration tested with digit span were impaired, and she could repeat only four digits forward (normal is 5 to 9 digits) and three in reverse (normal being 6 or more). Her short-term and long-term memory as well as other aspects of extended cognitive assessment was normal.
Initial laboratory investigations showed hyponatraemia, elevated creatine phosphokinase, and low free T4 with normal thyroid-stimulating hormone (TSH) (). A provisional diagnosis of organic delusional disorder (schizophrenia-like) was made and risperidone 1 mg daily was started.
She was referred to the endocrinology team for further evaluation and management. With a 9am cortisol of 221 nmol/L, she was started on levothyroxine under the cover of hydrocortisone. After normalizing free T4, she underwent an insulin tolerance test withholding hydrocortisone for 24 hours (). A diagnosis of panhypopituitarism was made. MRI of the pituitary gland showed a normal-sized sella turcica filled with cerebrospinal fluid (CSF). There was no pituitary gland, suggesting empty sella. The pituitary stalk was slightly deviated to the right extending up to the sellar floor showing normal signal and diameter ().
Levothyroxine and hydrocortisone were continued. Symptoms, including psychotic symptoms and hyponatraemia, improved remarkably within two weeks and risperidone was discontinued. Oestrogen and progesterone replacement therapy was initiated later. The patient is currently satisfied with her clinical outcome.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [49.0, 'kg'], 'height': [151.0, 'cm']}",21.49029,20.41578,22.5648,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 151.0 cm, which is 151.0 cm * 1 m / 100 cm = 1.51 m. The patient's weight is 49.0 kg. The patient's bmi is therefore 49.0 kg / (1.51 m * 1.51 m) = 21.49029 kg/m^2."
2391,6,Body Mass Index (BMI),physical,decimal,pmc-2740175-1,Extracted,"An 11-year-old Indian boy from Bijapur district of Karnataka State was referred to the paediatric unit of the Al Ameen Medical College Hospital with history of short stature, dysmorphic facies and failure to thrive for evaluation. Patient was good weight normal full term delivery at home. Maternal and Neonatal History was uneventful. Immunization was adequate with normal developmental milestones and intelligence. Parents denied any history of trauma or fractures. There was no history of frequent respiratory tract infections, snoring or tuberculosis contact. He was the youngest of three siblings born of second degree consanguineous marriage. Other siblings and parents are normal. On admission child’s weight was 28 kg. His standing height was 126 cm and upper segment was 65.5 cm and lower segment was 60.5 cm. Head circumference was 51 cm. He had mid facial hypoplasia with proptosed eyes.
He had frontal and bilateral parietal bossing .The sagittal, coronal and lambdoid sutures were separated and anterior and posterior fontanels were widely open. Examination of the mouth revealed a narrow high arched grooved palate. The teeth were hypoplastic with lateral open bite and multiple missing teeth. Bilaterally temporomandibular joints were retracted with slight deviated nasal septum to left. Scoliosis was seen. His digits were short, spoon shaped, stubby with joint laxity, metaphyseal widening and dystrophic nails. A sandal gap deformity was seen. There was no significant pallor, hepatomegaly or lymphadenopathy. Sexual maturity rating showed pre-adolescent stage. Laboratory investigations such as complete blood count, serum calcium, serum inorganic phosphate and alkaline phosphatase were normal.
The radiological findings were significant showing diffuse skeletal hyperostosis with sparing of medullary cavity. Skull X-rays showed widely separated cranial sutures and widely open anterior and posterior fontanel. The paranasal sinuses were non-pneumatised with angle of the mandible being obtuse. Acro-osteolysis was seen. The bone age was equal to his chronological age. Audiometry showed mild to moderate bilateral conductive hearing loss.
Fundus examination showed bilateral vitreous hyperplasia with lots of fibrous bands.
He was diagnosed as Pycnodysostosis based on characteristic clinical and radiological findings.
The parents of the child were offered an option for CTSK gene mutation testing for confirmation of diagnosis of pycnodysostosis, however they refused for same in view of financial constraints as the same testing is not available currently in our country (India).
We suggest for active screening of all children diagnosed with pycnodysostosis for hearing defects and ophthalmological evaluation as similar evaluation was not seen previously in published literature.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [28.0, 'kg'], 'height': [126.0, 'cm']}",17.63668,16.75485,18.51851,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 126.0 cm, which is 126.0 cm * 1 m / 100 cm = 1.26 m. The patient's weight is 28.0 kg. The patient's bmi is therefore 28.0 kg / (1.26 m * 1.26 m) = 17.63668 kg/m^2."
2392,6,Body Mass Index (BMI),physical,decimal,pmc-7370336-1,Extracted,"A 48-year-old woman, Jehovah’s Witness, presents to the outpatient of pulmonology service, with 8-year history of chronic cough and dyspnea, along with a progressive deterioration of her functional class (NYHA IV), along with permanent requirement of oxygen therapy and decline in the quality of life. Computed tomography scan of the chest revealed interstitial lung disease (see and ). Rheumatoid factor was positive and anticardiolipin antibodies were in indeterminate range; rest of autoimmune profile was negative. The patient did not present with clinical features of autoimmune disease. A diagnosis of autoimmune featured interstitial lung disease was made; cyclophosphamide cycle was administered without improvement of symptoms. Lung biopsy was taken via video-assisted pulmonary wedge resection, under general anesthesia. Pathology showed a histologic pattern consistent with usual interstitial pneumonia. Due to failure of medical therapy, the patient was accepted as a transplant candidate. However, due to religious beliefs, the patient stated that she does not accept blood products. Pulmonary function tests revealed a forced vital capacity (FCV) of 1.33 (44%), a forced expiratory volume in one second (FEV1) of 1.10 (44%), FEV1/FVC ratio of 83%, partial pressure of oxygen (PO2) of 91.3 mmHg and partial pressure of carbon dioxide (PCO2) of 55.1 mmHg, diffusing capacity for carbon monoxide (DLCO) 8.1 mL/mmHg/min (31%), 6-minute walk distance of 422 meters (73%), and a minimal oxygen saturation of 76 % without oxygen therapy.
Several months later, and after meticulous case review held by the lung transplant board (anesthesia, thoracic surgery, pulmonology), abdominal organ transplant board, and ethics committee, the patient was admitted for single-lung transplantation. She signed an informed consent declining transfusion of blood components, however agreeing to continuous cell-saver use. In the case of major perioperative bleeding, the patient also accepted the use of a prothrombin complex concentrate (which has advantages over fresh frozen plasma as it allows rapid correction of coagulation factor deficits with less volume infusion) and desmopressin. Blood loss during surgery was planned to be restored with 5% lactalbumin, in order to reduce the use of crystalloids in the event of significant bleeding.
The patient’s anthropometrics were 71 kg weight and 160 cm height. Regarding general procedure information, length of the procedure was 135 minutes. Cold Ischemia time was 230 minutes; there was no need for ECMO support. Bleeding during the procedure was estimated at 300 mL. Pulmonary artery pressure (PAP) was continuously measured, achieving a mean PAP of 18 mmHg in average during surgery.
Regarding hemostatic perioperative management for this patient, recommendations established in the current literature within the “Patient Blood Management” at the time were taken into account. Since preoperative hemoglobin was within normal values (14.6 g/dL), no additional measures were taken to optimize erythropoiesis. To minimize bleeding in the intraoperative setting, blood preservation methods were used: prophylactic use of antifibrinolytics was planned preoperatively, using an initial bolus of tranexamic acid 1 g, followed by continuous infusion during surgery. Fluids were adjusted at 2 to 4 cc/kg/h and readjusted according to intraoperative hemodynamic and metabolic variables. Insensible fluid loss was restored infusing a total of 870 cc of Ringer’s lactate. Normothermia was maintained with the use of Blanketrol heating system, and electrocautery scalpels were used to obtain a thorough surgical hemostasis with the help of topical hemostatic agents (tissue sealant/Surgicel). The patient agreed to intraoperative closed-system cell salvage, as it did not represent a conflict with her religious beliefs. Bleeding during surgery was calculated as of 300 cc, from which 120 cc were reinfused postoperatively. Finally, during the postoperative period, a drainage thoracostomy was positioned for a better quantification of postoperative bleeding and adequate blood evacuation from the lung. Erythropoietin was initiated during hospitalization.
After surgery, the patient was admitted to the intensive care unit, early extubation was successfully achieved, and there was no need of vasopressors or inotropes. PaO2/FiO2 ratio of 480 mmHg. Chest radiography revealed right perihilar infiltrates. The previous findings suggested a primary graft dysfunction grade 1 (see and ). Intensive care unit length of stay was 4 days, and total hospitalization length of stay was 13 days. Hemoglobin levels decreased at the end of hospitalization (see ). The patient was discharged without further complications with hemoglobin levels of 10.6 g/dL, which was treated in the outpatient setting with subcutaneous erythropoietin 2000 IU 3 times per week as ordered by internal medicine and pulmonology physicians. Hemoglobin levels increased to 11.4 g/dL at 1-week follow-up.
Pulmonary function tests after LT revealed FVC of 1.88 (53%), FEV1 of 1.73 (59%), FEV1/FVC of 92%, 6-minute walk distance of 353 meters (67%), and a minimal oxygen saturation of 94% without oxygen therapy. The patient final hemoglobin level was 11.4 g/dL.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [71.0, 'kg'], 'height': [160.0, 'cm']}",27.73437,26.34765,29.12109,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 71.0 kg. The patient's bmi is therefore 71.0 kg / (1.6 m * 1.6 m) = 27.73437 kg/m^2."
2393,6,Body Mass Index (BMI),physical,decimal,pmc-6413596-2,Extracted,"A 4-year-old girl presented with focal epilepsy and motor deficit of the right hemi-body. The onset of symptoms dated back to October 2014 and was marked by secondary general seizures in a febrile context, complicated by an alteration of consciousness for a month. On awakening, she developed cognitive and language disorders associated to right hemi-corporeal motor impairment. She received speech therapy and motor physiotherapy. She was put on phenobarbital at 50mg dosage. Epileptic seizures persisted with increasing frequency (approximately 12 focal seizures per day).
Regarding the antecedents, the pregnancy was completed at term and without incident. Delivery was by cesarean section for severe oligoamnios and cephalic presentation. The Apgar score was 7-8-10 and the weight was 2900g. On day 3, she was admitted to pediatric intensive care unit for neonatal infection. The evolution was favorable with discharge after 10 days under antibiotics. The vaccination status was up to date. Psychomotor development was normal until September 2014.
The physical examination of September 6, 2016, showed a fairly good general condition. The temperature was 37°C and weight was 15kg for a size of 99cm. The cranial perimeter was 49cm and brachial circumference was 16cm.
On the neurological level, her walk faltered to the right. Spastic right hemiparesis was noted with a muscular force rated at 4/5 on british medical council muscular testing. The osteotendinous reflexes were sharp on the right. The Babinski and Hoffmann signs were present on the right. Superficial hyperesthesia was observed on the right hemi-body associated to right lateral homonymous hemianopia and right hyposmia.
The neuropsychological assessment noted moderate language impairment with conservation of understanding, good oral mobility, and perfect repetition of vowels. However, a deformation of some consonants with velar | K | and | 9 |, liquids | I | and | R |, and fricative | Z | was observed. The active and passive lexicons were quite rich with some difficulty of access to the exit lexicon.
Paraclinical assessment included biology, EEG, and medical imaging. Cerebrospinal fluid reported a protein concentration of 0.50g/L. The search of specific antibodies and inflammatory cells was inaccessible. The EEG showed an asymmetric theta background rhythm, associated with spike wave discharges and generalized polyspikes predominating on the left side such as periodic lateralized epileptiform discharges (PLEDs) [Figures and ]. The brain scan showed atrophy of the left cerebral hemisphere with dilatation of the Sylvian valley and enlargement of the cortical furrows []. The patient was started on sodium valproate and carbamazepine in a progressively effective dose. She received motor physiotherapy and speech therapy. At 6 weeks control, we had noted the persistence of three to ten (3-10) focal seizures a day. Cognition and language had the same disturbances. We stopped valproic acid and associated phenobarbital to carbamazepine and levetiracetam. Three months later, a reduction to five single focal seizures per day was observed, which reduced to three daily seizures at 6 months.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [15.0, 'kg'], 'height': [99.0, 'cm']}",15.30456,14.53933,16.06979,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 99.0 cm, which is 99.0 cm * 1 m / 100 cm = 0.99 m. The patient's weight is 15.0 kg. The patient's bmi is therefore 15.0 kg / (0.99 m * 0.99 m) = 15.30456 kg/m^2."
2394,6,Body Mass Index (BMI),physical,decimal,pmc-3675438-2,Extracted,"Patient 2 was a 4-year-old boy, the third child to non-consanguineous healthy Norwegian and English parents. Pregnancy and delivery were uneventful, with the following birth measures: weight 4090 g, length 52 cm and OFC 36 cm (all measures at the 75th centile). From an early stage his eye contact and speech were delayed, and he walked independently at 2 years of age. Testing with Bayley Scales of Infant and Toddler Development, third edition (Bayley III) at age 3.5 years showed cognitive functioning corresponding to 1.5 years, suggesting moderate intellectual disability. He did not fulfill the criteria for autism spectrum disorders (ASDs) according to the Autism Diagnostic Observation Schedule (ADOS). At the same age, a cerebral MRI examination was normal. Seizure-suspected syncope episodes occurred during infancy. EEG performed at age 8 months was normal, whereas cardiologic work-up revealed an atrial septal defect that closed spontaneously. At the last examination, at age 4 years, his weight was 19 kg (90th centile), height 105 cm (75th centile) and OFC 52 cm (50th centile). His language development was severely delayed; he could only speak a few words. He had a broad-based and unsteady gait (Additional file
: Video Patient 2) and seemed unable to stand on one leg at a time. Muscle tone was normal. Hearing and vision were normal. Dysmorphic facial features (Figure
) and minor congenital anomalies in this patient are listed in Table
.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [19.0, 'kg'], 'height': [105.0, 'cm']}",17.23356,16.37188,18.09524,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 105.0 cm, which is 105.0 cm * 1 m / 100 cm = 1.05 m. The patient's weight is 19.0 kg. The patient's bmi is therefore 19.0 kg / (1.05 m * 1.05 m) = 17.23356 kg/m^2."
2395,6,Body Mass Index (BMI),physical,decimal,pmc-2900113-1,Extracted,"A 5-year-old male child, known case of bilateral Tessier 7 facial cleft syndrome, was posted for total correction of facial deformity. He was a preterm child delivered vaginally. Presence of gross macrostomia at birth precluded breastfeeding. Till the age of 3 months, he was fed through a nasogastric tube after which a feeding gastrostomy was done under general anaesthesia, details of which were not available. Feeding gastrostomy was closed at the age of 2 years under GA, the details of which are not known. The child was on liquids and semi solid food since then. Before the surgery at our Hospital, he was kept NBM for 6 hours. There were no other associated congenital deformities. Milestones were normal. A history of snoring and repeated upper respiratory tract infections was present. On general examination, height was 95cm and weight was 15kg with a low set of ears. Airway examination revealed a facial cleft extending from angle of the mouth across the cheek to the ear on both sides amounting to gross macrostomia (Fig & ). Mouth opening was 3cm ( Showing lateral view), Mallampatti classification-IV and thyromental distance-2.5cm with severe retrognathia. Teeth were severely maloccluded. Neck movements and other systems were normal. Routine investigations were normal. Preoperatively, the child was kept fasting for 6 hrs. Venous access was taken in the ward. No sedative premedication was administered in the ward due to history of snoring. In the operation theater, a difficult airway cart including fiberoptic bronchoscope and tracheostomy kit was kept ready. Monitoring included a precordial stethoscope, electrocardiogram, pulse oximeter, non invasive blood pressure cuff, capnogram and temperature probe. Plan of intubation was to secure a non surgical airway in an anaesthetised patient. Awake fiberoptic intubation was not possible since it would require a quite cooperative child for good bronchoscopic views. Our PLAN A was to attempt a direct laryngoscopy after sevoflurane induction. PLAN B was to do LMA™ guided fiberoptic intubation. For preoxygenation, we had to use a No 5 face mask due to the gross macrostomia. Gamgee pads were applied around the mask to reduce the leak and improve the seal. Injection glycopyrrolate 0.06 mg was administered and the child was anaesthetised with sevoflurane. Direct laryngoscopy revealed Cormack Lehane IV. Since it was becoming increasingly difficult to maintain the airway with mask, we decided to introduce an LMA™ size 2½. After confirming adequate ventilation with the LMA™, fentanyl 30 mcg, propofol 30 mg, atracurium 10 mg were given intravenously. Then, through the LMA™, fiberoptic bronchscope with a 5mm safety flex tube mounted on it was introduced. The tube was then passed across the cords to secure the airway.
Although the child was being ventilated adequately, the LMA™ had to be removed as it would hinder the oral surgery. Hence, we decided to remove the LMA™-tube assembly over a Cook® airway exchange catheter (). Finally, the same 5mm safety flex tube was then railroaded back over Cook® catheter and ventilation was confirmed with EtCO2. We have used two uncuffed tubes of the same size without the connectors. The distal tip of the upper tube including the Murphy eye was cut away and then the cut end was plugged into the enlarged cavity of the proximal end of the lower tube to form a stable tube of double length. The tube was then fixed in midline with surgical sutures and the throat was packed. Surgery was uneventful. Post operatively the child was shifted to Paediatric ICU on ventilator.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [15.0, 'kg'], 'height': [95.0, 'cm']}",16.6205,15.78947,17.45153,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 95.0 cm, which is 95.0 cm * 1 m / 100 cm = 0.95 m. The patient's weight is 15.0 kg. The patient's bmi is therefore 15.0 kg / (0.95 m * 0.95 m) = 16.6205 kg/m^2."
2396,6,Body Mass Index (BMI),physical,decimal,pmc-8489098-1,Extracted,"We saw a 59-year-old White female patient with a history of sarcoidosis at the outpatient department in early September 2012. On first sight, the left side of her face was significantly swollen, and she had pain in the preauricular area. The condition had started a few days earlier with swelling of the lips and progressed to left-sided facial edema and unilateral painful preauricular mass.
C-reactive protein was elevated at 54 mg/l (normal concentration up to 5mg/l). Transaminases, cholestasis and retention parameters, urinalysis, and microbiological findings were unremarkable. At this time, the patient was treated with 1 mg tacrolimus 1-0-0, 20 mg leflunomide 1-0-0, and 7.5 mg prednisolone.
For clarification, an inpatient admission to our tertiary center was arranged.
During the clinical examination, we saw a patient in moderate general condition and obese nutritional status with a body weight of 104.7 kg and a height of 168 cm. The patient did not show temperature elevation. Blood pressure was normal at 120/80 mmHg, and pulse rate was 80 beats/minute. On oral examination, the patient showed tender firm swelling of lips, erythematous and swollen gingiva of the upper and anterior teeth, and fissured tongue. In addition, there was generalized gingivitis, and the left side of the face was also markedly swollen and red. Furthermore, there was left-sided fascial paresis. There was no evidence of mouth sores, and odontogenic infections were ruled out. The eyes did not show any pathology. The heart rhythm was regular, the heart sounds S1/S2 were pure, and there were no heart murmurs. Examination of the lungs was without pathological findings. Pressure pain in the area of the abdomen could not be triggered, there was no organomegaly, and bowel sounds were unremarkable. Peripheral edema was absent on both sides, and no calf pressure pain could be induced. The joints were unremarkable. The neurological examination was regular except the facial palsy.
Magnetic resonance imaging of the neck on admission showed an enlargement of the left parotid gland with enhancement of contrast medium susceptive of abscess formation. Furthermore, on magnetic resonance imaging, there was a suspicion of a necrotic melting in the left parotid gland, which was displayed with a total extension of approximately 4–5 cm in the three spatial directions. The meltings are displayed with different signal strengths T2-hyperintense and T1-hypointense, and showed both marginal and septal internal contrast enhancement at this time. The findings further included the ramus mandibulae from the dorsal side and extended medially to the pterygoid muscles and laterally to the masseter muscle. The masseter muscle partially showed adjacent contrast enhancement with suspected inflammatory co-reaction. The angle of the jaw showed only small lymph nodes on both sides (Fig. ).
After surgical excision of the abscess formation and systemic antibiotic therapy, the patient developed soft-tissue ulceration in pre- and retroauricular area (Fig. b). A few days later, a left-sided peripheral facial palsy developed (Fig. a). The peripheral left facial palsy was due to swelling and inflammation from parotitis and developed independently of surgery.
No bacteria could be isolated from several wound swabs. Immunoglobulin M (IgM) antibody titer and polymerase chain reaction (PCR) for herpes simplex virus were negative. In addition, a PCR for atypical mycobacteria was done, and again the test was negative. IgM antibody titer and PCR for herpes simplex virus were negative.
Histopathological examinations of the parotid gland revealed necrotizing tissue but also epithelioid granulomas. Malignancy could be excluded.
At that point, a systemic corticosteroid therapy with methylprednisolone 500 mg daily for 3 days was given with no significant improvement of the soft-tissue ulcerations. Therefore, a parotidectomy was performed. Microbiological examinations on bronchoalveolar fluid were negative for pathogenic species. Serological tests such as tuberculosis were also negative. The patient did not report intestinal problems at any time that would have suggested Crohn’s disease. Hence, a colonoscopy did not seem to be justified.
This condition appeared under an immunosuppressive therapy with leflunomide 20 mg once a day in combination with 1 mg tacrolimus daily starting due to pulmonary sarcoidosis, diagnosed 2 years earlier.
The patient was known to have autoimmune thyroid disease with hypothyroidism prior to the diagnosis of sarcoidosis. In addition, the patient had a history of kidney stone disease and had undergone surgery on the menisci of both knee joints. The patient has an allergy to amoxicillin, and did not have any pregnancies. She has never smoked or had significant alcohol consumption. There was no history of tuberculosis. The patient worked as a commercial employee and was continuously working in the office and not exposed to any noxae.
In October 2009, the patient had a severe feeling of illness with a body weight loss of 15 kg, bloody sputum, and a marked tendency to sweat. Bronchoscopy initially revealed chronic florid inflammation with epitheloid-cell-containing granulomas. Despite slightly elevated antineutrophil cytoplasmic antibody (c-ANCA), there was no evidence of granulomatosis with polyangiitis. Malignancy could also be excluded. From December 2009, the patient was treated with glucocorticoids, and as there was only partial remission in January 2010, the patient was treated with azathioprine for 4 months. Since there was insufficient improvement while taking azathioprine, therapy was switched to methotrexate in May 2010. Methotrexate was then used for a total of 11 months. With disease activity not adequately controlled, methotrexate was discontinued in February 2011, and oral cyclophosphamide was started after four courses of cyclophosphamide pulse therapy. After oral cyclophosphamide therapy, the patient was switched to tacrolimus and leflunomide in September 2011. Recurrent gingivitis occurred from summer 2012 onward. Beside recurrent gingivitis, the patient had orofacial edema and lip swelling as well as a fissured tongue in the past. The final diagnosis based on clinical and histopathological findings was MRS in the context of sarcoidosis.
After treatment with systemic steroids, the labial and facial swelling improved. However, the preauricular ulcerations did not respond to this treatment. At that point of time, the medication with clofazimine 100 mg per day was initiated, which was well tolerated. After 4 weeks of therapy, the tissue ulceration resolved gradually, so that 150 mg of clofazimine three times a week was given for 15 weeks (Fig. ). After that, clofazimine treatment could be stopped. During 7 years of follow-up, there was no recurrence (Fig. a, b).
During the course of the 4-month successful therapy with 150 mg clofazimine 1-0-0, the underlying disease was treated with rituximab. Initially, induction therapy was given with 4 × 375 mg at weekly intervals followed by B-cell and immunoglobulin-controlled therapy. Starting from June 2013, rituximab has been given in combination with 15 mg methotrexate once per week.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [104.7, 'kg'], 'height': [168.0, 'cm']}",37.09609,35.24129,38.95089,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 104.7 kg. The patient's bmi is therefore 104.7 kg / (1.68 m * 1.68 m) = 37.09609 kg/m^2."
2397,6,Body Mass Index (BMI),physical,decimal,pmc-7260760-1,Extracted,"This was a case study of a 23-year-old female jumper competing on a Division I National Collegiate Athletics Association (NCAA) track and field team. Four and a half years prior to this data collection, the subject had an 8 x 345 mm Stryker T2 nail surgically implanted in her left tibia as treatment for a chronic anterior tibial stress fracture. The Stryker T2 nail is a titanium alloy that contains aluminum, vanadium, and iron (personal communication, Stryker, Inc.).
The subject was informed of the intent to use her data for a published case study. The university's Institutional Review Board approved the data collection, and the subject signed a written informed consent as well as an authorization for the use of protected health records.
Height was measured to the nearest 0.1 cm with a wall-mounted stadiometer (Seca 216, Seca Corp.), and weight was measured to the nearest 0.1 kg with a digital scale (Seca 869, Seca Corp.). The subject was wearing only a t-shirt and shorts for the data collection.
The subject laid supine on a nonconducting treatment table with arms and legs abducted to approximately 30° to 45° from the trunk for 5 min. This time frame is adequate for the total body water to stabilize (Gibson, Beam, Alencar, Zuhl, & Mermier, ). During this time, the dorsal surface of the wrists, hands, ankles, and feet were cleaned with an alcohol wipe. Electrodes were applied in a tetrapolar configuration on both sides of the body using anatomical landmarks suggested by the manufacturer: (a) the superior borders of detecting electrodes of the wrist and ankle at the level of the ulnar head and medial malleolus, respectively, and (b) signal electrodes at the metacarpal-phalangeal joint of the middle finger and at the base of the metatarsal-phalangeal joint of the second toe.
A single-frequency BIA machine operating at 50 kHz (Quantum II, RJL Systems, Clinton Township) was used to apply the current and read the resistance. Measurements were made in duplicate on both sides of the body. The multiple readings were done in quick succession, and the subject remained in the same position throughout.
In addition to the resistance and reactance values obtained directly from the analyzer, FFM was estimated using the equations of Fornetti, Pivarnik, Foley, and Fiechtner (), Lohman (), and Sun et al. () (Table ). The Fornetti et al. () formula was chosen because it is specific to female collegiate athletes. In a review of BIA for athletes, Moon () recommended the BIA formula of Lohman () specific to active females aged 18–35 years. Finally, the Sun et al. (2013) formula was selected because it is a commonly used, general-population BIA formula that has been cited over 400 times and was validated against a multicomponent model. Subsequent to calculating FFM, FM was determined by BM–FFM, and body fat percentage (%BF) was calculated as (FM/BM) × 100.
The subject had a height and weight of 173.3 cm and 70.3 kg, respectively. Although, repeated measures on the same side of the body were consistent to within ± 1 ohm, the resistance and reactance from the subject's left side (tibia containing the metal implant) were substantially less than the right side (Table ). Consequently, this led to a larger estimate of FFM when BIA was applied to the implant side, and a reduction in the %BF estimation of 0.6%BF to 2.7%BF depending on the prediction equation used.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.3, 'kg'], 'height': [173.3, 'cm']}",23.40767,22.23729,24.57805,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 173.3 cm, which is 173.3 cm * 1 m / 100 cm = 1.733 m. The patient's weight is 70.3 kg. The patient's bmi is therefore 70.3 kg / (1.733 m * 1.733 m) = 23.40767 kg/m^2."
2398,6,Body Mass Index (BMI),physical,decimal,pmc-4847504-2,Extracted,"A 33-year-old woman, measuring 170 cm tall and weighing 57 kg, was seated in the middle of the airplane (). When the plane crashed, she reported feeling her body move in all directions with chest knee position, and afterward, an inflatable evacuation slide burst into the airplane and hit her. She lost consciousness, and then woke up with severe back pain. When she came to our hospital, she reported severe back pain, with pain elicited upon direct palpation of the lower back and left flank. Full neurological examination yielded no deficits.
X-ray of the lumbar spine revealed anterior wedge compression fracture of the L2 vertebral body (), and MRI revealed a wedge compression fracture involving the middle column of the same vertebral body with posterior column signal change due to posterior ligament complex injury (). The wedge compression rate was approximately thirty percent. Whole body bone scan () showed uptake at the L2 vertebral body and left 10th, 11th, and 12th ribs.
A diagnosis of a stable L2 vertebral body fracture was made, and we recommended conservative management consisting of bed rest and spinal orthotic with regular follow up.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [57.0, 'kg'], 'height': [170.0, 'cm']}",19.72318,18.73702,20.70934,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 57.0 kg. The patient's bmi is therefore 57.0 kg / (1.7 m * 1.7 m) = 19.72318 kg/m^2."
2399,6,Body Mass Index (BMI),physical,decimal,pmc-6907138-1,Extracted,"An 8-year-old Chinese boy presented with fever, dizziness and recurrent vomiting for 3 days. The patient had been diagnosed with bacterial meningitis in another tertiary hospital and prescribed with cefatriaxone, vancomycin, intravenous immunoglobulin (IVIG) and mannitol for 2 days. He has history of one episode of acute bacterial meningitis at 4 years of age and one episode of pneumonia and sepsis with Staphylococcus epidermidis at 5 years old. There was no history of recurrent infections and blood transfusion. He was naturally conceived and born at term by Caesarean section with birth weight being 2.8 kg. He has healthy parents and a healthy 15-year-old female sibling. None of the family’s relatives were known to be subject to recurrent severe infections or were diagnosed with immunodeficiency disorders.
On physical examination, the patient was febrile, tachycardic and tachypneic. Neck rigidity, Kernig’s and Brudzinski’s signs were positive, but there was no focal neurological deficit. Other systemic examinations didn’t reveal any abnormality. His weight was 24.1 kg and height was119.3 cm. His height was at the fifth percentile for age, whereas his weight was within normal range.
The level of IgG, IgA and IgM done before IVIG treatment in another tertiary hospital was 1.9 g/L, 0.27 g/L and 0 g/L respectively. A routine blood examination: white blood cell (WBC):40.9 × 109/L,neutrophils:90%,lymphocytes:2%,platelet:322 × 109/L,hemoglobin:102 g/L.C-creative Protein (CRP):243.80 mg/L. Urine and stool analysis was normal. Liver,cardiac and renal function was within normal limits by blood biochemistry examination. Serum lactate and electrolyte were normal. Human Immunodeficiency Virus (HIV) and syphilis serology was negative. Cerebrospinal fluid (CSF) analysis: WBC:548cells/μL, neutrophils:57%, protein:1.83 g/L, glucose:0.96 mmol/L. Gram staining and india ink staining were negative. CSF and blood cultures remained negative. DNA of herpes simplex virus, cytomegalovirus, enterovirus, Epstein-Barr virus, mycoplasma pneumonia and chlamydia pneumonia was negative amplified by polymerase chain reaction (PCR). The immune parameters before treatment in our hospital were shown in Table . There was no abnormality in chest X-ray, echocardiography and ultrasound of abdominal and pelvic cavity. Magnetic resonance imaging (MRI) scan of brain suggested meningoencephalitis and nasosinusitis (Fig. ). The outcome of EEG was normal and brainstem auditory evoked potential (BAEP) showed prolonged latency of bilateral waves I and III respectively. His bone age was normal.
The clinical presentation, neuroimaging findings and results of CSF were suggestive of bacterial meningoencephalitis, despite the negative gram staining and cultures of the CSF. The patient was treated with broad-spectrum antibiotics with vancomycin and meropenem. By the following day, the patient’s fever resolved and dizziness and vomiting disappeared.
During the first episode of bacterial meningitis at 4 years of age, CSF and blood culture showed growth of pneumococci. MRI scan of brain revealed meningitis, subdural effusion, nasosinusitis and mastoiditis (Fig. ). The immune parameters before treatment were shown in Table .The patient received intravenous vancomycin and meropenem and responded well to the treatment.
After informed consent had been obtained, genomic DNA was extracted from peripheral blood samples for genetic analysis with immunodeficiencies panel (Mygenostics Inc, Beijing, China). Next generation sequencing was adopted to make genetic analysis, and results were confirmed by Sanger sequence. Sequencing of the BTK coding regions revealed a point mutation, hemizygous c.1349 + 5G > A, which is an intron mutation and has been previously reported to be responsible for X-linked agammaglobulinemia []. After the diagnosis of proband was confirmed, the BTK gene of the parents was analyzed with informed consent signed. Genetic analysis revealed mother had a heterozygous c.1349 + 5G > A, while father was free of any genetic mutations in BTK. The results of BTK gene sequence analysis with reverse sequence were shown in Fig. .
The patient had received IVIG treatments every month since diagnosed with XLA, and had been free from severe infection since then.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [24.1, 'kg'], 'height': [119.3, 'cm']}",16.93309,16.08644,17.77974,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 119.3 cm, which is 119.3 cm * 1 m / 100 cm = 1.193 m. The patient's weight is 24.1 kg. The patient's bmi is therefore 24.1 kg / (1.193 m * 1.193 m) = 16.93309 kg/m^2."
2400,6,Body Mass Index (BMI),physical,decimal,pmc-3614763-1,Extracted,"A previously healthy 7-year-old boy was brought to the emergency department by his mother with complaints such as vomiting, fatigue and colicky abdominal pain associated with diffuse, self-limiting arthralgias, and petechial rash of both legs. His medical history revealed having throat infection one month before admission. Complete blood count was within normal range for his age, as were his serum electrolytes. Blood examinations revealed an elevation of C-reactive protein and revealed both normal white blood cell and platelet counts. Serum IgA, C3 and C4 levels were all within normal limits and a urine examination also showed normal findings. Physical examination revealed mild proteinuria, hypertension and moderate anasarca (periorbital edema, ascites, and lower-extremity pitting edema). No medication and renal biopsy were performed because of the silent findings. However, two weeks later, after the admission for HSP, he complained of polydipsia and polyuria complaints and a physical examination revealed a 10-kg decrease in his baseline weight. There was no parental history of diabetes. In physical examinaTion weight: 16 kg (3rd percentile); height: 115 cm (25–50th percentile); pulse rate: 80/min; respiratory rate: 24/min; blood pressure: 100/60 mmHg; temperature: 36°C, his general state was poor and his consciousness was lethargic. Skin turgor and tonus were also diminished. There were petechial rashes on his abdomen and lower extremities that progressed to nonblanchable macules (Figure ). He also had a fruity breath smell, dry mucous membranes, and tachypnea. Other examinations were normal. Laboratory studies yielded the following values (normal ranges were given in brackets): white blood cell count; 14.200/mm3 (6000–17500) with a normal differential formula; blood urea nitrogen, 9.34 mg/dL (5.7–20.1); serum creatinine, 0.6 mg/dL (0.1–0.9); albumin, 4.2 g/dL (3.5-5); sodium, 127 mmol/L (139–146); potassium, 4.51 mmol/ L (3.5–6.0); phosphorus, 2.8 mg/dL (4.9–7.9); and glucose, 27.83 mmol/L (3.3–5.0). Arterial blood gas values showed a pH of 7.10 (7.35–7.45); and bicarbonate: 8.4 mmol/L (21–28). Urine and serum ketones were positive. Urinalysis showed glycosuria. HbA1c was 11.7% (4.2-6.4). C-peptid level was 0.7 ng/mL (1.1-3.2). Insulin level was 4.28 μIU/mL (1.9-23). Autoantibodies including insulin, islet cell, glutamic acid decarboxylase were negative. Thyroid function tests were normal. Prothrombine time and partial thromboplastin time, immunoglobulin A, complement proteins C3 and C4, anti-DNA, antinuclear antibodies, and ASO levels were normal, as were serological tests for EBV and TORCH. Serum antigliadin and anti-endomysium antibodies were negative for the diagnosis of Celiac disease. Occult blood test in stool, urine and throat cultures were negative. The diagnosis of type 1 DM which presented with diabetic ketoacidosis accompanied by HSP was clinically made. A bolus of normal saline (20 mL/kg) was given intravenously, after which intravenous fluids were continued. Regular insulin via a continuous infusion at 0.1 IU/kg/h was started, and potassium was administered at 1 mEq/kg/day. The patient subsequently recovered and was followed by the Pediatric Diabetes Unit and given continued insulin treatment.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [16.0, 'kg'], 'height': [115.0, 'cm']}",12.0983,11.49338,12.70322,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 115.0 cm, which is 115.0 cm * 1 m / 100 cm = 1.15 m. The patient's weight is 16.0 kg. The patient's bmi is therefore 16.0 kg / (1.15 m * 1.15 m) = 12.0983 kg/m^2."
2401,6,Body Mass Index (BMI),physical,decimal,pmc-8007840-1,Extracted,"A 31 month-old boy was referred to the pediatric GI department for evaluation of intractable constipation. He had difficulty defecating with a frequency of 2 bowel movements per week requiring intermittent enemas and laxatives from the time that he was 2 months of age. His mother reported that his symptom was difficult to manage, because even a small amount of laxative often caused diarrhea.
He was born to a diabetic mother at the gestational age of 37 weeks with a birth weight of 2.65 kg. The mother stated that her blood glucose had been difficult to control with insulin since the early weeks of her pregnancy. At 11 days of age, he had a history of admission for hypocalcemic tetany without any identified underlying disease. He was diagnosed with a congenital hearing impairment through the newborn hearing screening test. He had also been hospitalized several times for febrile illnesses, such as influenza infection, bronchiolitis, and viral pneumonia.
On examination, his height was 84 cm (10th–25th percentile), and his body weight was 12 kg (10th–25th percentile). He was active and had low-set ears wearing hearing aids. His abdomen was slightly distended, with hard stools noted on a digital rectal examination. In addition, we observed that he had small, flat buttocks with bilateral buttock dimples and a short intergluteal cleft (). He passed normal mental developmental milestones except for a delay in language development, and there were no motor deficits or gross deformities in his extremities. His mother reported that he showed urinary dribbling and a weak urine stream since infancy.
When we reviewed the plain radiographs, including those taken during previous hospitalizations, no abnormal findings were initially recognized, except for an excessive amount of stool from the colon to the rectum (). Under the suspicion of spinal dysraphism, however, we performed another pelvic X-ray, after disimpaction with an enema, that finally revealed the absence of the distal sacrum and the coccyx (). Magnetic resonance imaging (MRI) of the spine demonstrated an abrupt termination of the conus medullaris at the T12 to L1 level and a thickened filum terminale (). A voiding cystourethrogram with contrast showed poor filling in the bladder, suggesting a neurogenic bladder. No other remarkable findings were identified through abdominal and kidney ultrasonography, echocardiography, barium enema, and brain MRI.
After being diagnosed with CRS, he was followed up over a 5-year period in the department of Pediatric GI, Urology, Neurosurgery, Rehabilitation, and Otorhinolaryngology. He has been wearing diapers for his urinary incontinence and has continued to use laxatives or enemas whenever he has difficulty with bowel movements. He did not have other progressive neurological deficits that need other interventions, except for a mild delay in language and intellectual functioning.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [12.0, 'kg'], 'height': [84.0, 'cm']}",17.0068,16.15646,17.85714,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 84.0 cm, which is 84.0 cm * 1 m / 100 cm = 0.84 m. The patient's weight is 12.0 kg. The patient's bmi is therefore 12.0 kg / (0.84 m * 0.84 m) = 17.0068 kg/m^2."
2402,6,Body Mass Index (BMI),physical,decimal,pmc-4209027-1,Extracted,"A 13-year old, 40 kg, 159 cm boy underwent laparoscopic appendectomy. Anesthesia was induced with 80 mg propofol, 0.33 μg/kg/min remifentanil, and 30 mg rocuronium. After an uneventful intubation, anesthesia was maintained with sevoflurane and remifentanil. About 15 minutes after intubation, 50 mg flurbiprofen axetil was administered. During the surgery, oxygen saturation was maintained in the high 90% range and ETCO2 was within normal limits. Baseline blood pressure (BP) was approximately 116/78 mm Hg, remaining in the 90/40 mm Hg range for most of the case. Heart rate (HR) remained at 50 to 60 bpm. The total operation time was 118 minutes. Before extubation, sugammadex 2 mg/kg was injected to antagonize residual neuromuscular blockade. Shortly after the injection, the patient’s trachea was extubated when he was able to breathe spontaneously. After extubation, the patient demonstrated global swelling of the face and a low consciousness level. At this point, his blood pressure fell to unmeasurable values and he developed tachycardia of between 150 and 160 bpm. Suspecting a possible allergic reaction to sugammadex, he was treated with 100 mg hydrocortisone and 0.1 mg adrenaline IV. The patient needed to be re-intubated because of difficulty with bag mask ventilation. Blood gas analysis showed hypercapnea (PCO2 = 66.4 mmHg). His trachea was re-intubated after re-induction of anesthesia with 80 mg propofol and 50 mg rocuronium. Additional treatment with 200 mg aminophylline and 200 mg hydrocortisone was given after the intubation, because the occurrence of an asthmatic attack could not be excluded. The patient stayed in the ICU until his trachea was extubated 17 hours after the event. A prick test with dilutions of propofol, rocuronium, ropivacaine, flurbiprofen axetil, and sugammadex was performed 7 weeks after the operation, which showed an immediate reaction only to sugammadex (Table ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [40.0, 'kg'], 'height': [159.0, 'cm']}",15.82216,15.03105,16.61327,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 159.0 cm, which is 159.0 cm * 1 m / 100 cm = 1.59 m. The patient's weight is 40.0 kg. The patient's bmi is therefore 40.0 kg / (1.59 m * 1.59 m) = 15.82216 kg/m^2."
2403,6,Body Mass Index (BMI),physical,decimal,pmc-8221662-2,Extracted,"A 50-year-old ASA I physical status woman (60 kg, 165 cm) underwent routine colonoscopy. The colonoscope was passed through the anus under direct visualization and was advanced only to 40 cm due to technical difficulties. Biopsies were obtained from the sigmoid, but the doctor performing the colonoscopy was suspicious of perforation. The patient tolerated the procedure well and was transferred to the ward for a 3-day monitoring. The next day, she developed subcutaneous emphysema with air tracking up into the neck, excruciating pain to the chest, and radiating to the right shoulder; dyspnea; and tachycardia. Pain was not alleviated by intravenous administration of morphine 2 mg and paracetamol 1 g. An upright chest radiography revealed subdiaphragmatic air. Conservative approach was the method of choice and the subcutaneous emphysema resolved on the second postoperative day. The patient had an uncomplicated postoperative course and was discharged, in a stable condition, home shortly.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.0, 'kg'], 'height': [165.0, 'cm']}",22.03857,20.93664,23.1405,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.65 m * 1.65 m) = 22.03857 kg/m^2."
2404,6,Body Mass Index (BMI),physical,decimal,pmc-4166852-1,Extracted,"A 15-year-old boy presented for the evaluation of short stature and delayed puberty in our outpatient department (OPD). Parents noticed that the child is not growing well as compared to his peers, and also noted that the child has not developed any sign of puberty in the form of the moustache, beard growth, pubic hair and scrotal growth. He has been well with no chronic medical problems, no hospitalizations, and no surgeries. The child is a product of nonconsanguineous marriage and uneventful 8 months vaginal delivery in the hospital with breech presentation. The child had a history of birth asphyxia and cried 10 min after birth. There were no history of feeding difficulties, seizures, neonatal jaundice, lactose intolerance; developmental milestones - gross motor, fine motor, social delay. The child is average in studies at school. Social, family and peer interactions are normal and no behavioral problems. The child has two elder siblings with normal growth and development. There is no such history in family members and relatives.
Height: 126.5 cm (<3rd percentile), standard deviation: 8.0, standard deviation score: 4.75, lower segment (LS): 64 cm, upper segment (US): 64 cm, US/LS: 1.0, arm span (AS): 128 cm, weight: 30.7 kg, miles per hour (MPH): 160.0 cm, corrected MPH: 166.5 cm, Tanner's score: A1P1 TV < 4 ml (bilaterally), stretch penile length (SPL): <4 cm, fundus examination: Within normal limits (WNL).
His growth chart showed an average growth velocity of 3 cm/year. Complete blood count (CBC), erythrocyte sedimentation rate (ESR), thyroid function tests (TFT's), urinalysis (UA), and serum electrolytes are normal. Hormonal analysis shows thyroid stimulating hormone (TSH): 3.80 μIU/ml (N = 0.4–5.0 μIU/ml), T4: 2.90 μg/dl (N = 5–12 μg/dl), follicle-stimulating hormone (FSH) (basal): 0.98 mIU/ml (N = 1-10 mIU/ml), luteinizing hormone (LH) (basal): 0.12 mIU/ml (N = 2-8 mIU/ml), prolactin: 50.46 ng/dl (N = 2-15 ng/dl), fasting morning cortisol: 1.5 μg/dl (N = 5-25 μg/dl), testosterone: <0.45 nmol/L (N = 10-35 nmol/L), growth hormone (GH) stimulation test (Insulin): <0.05 ng/ml (normal > 10 ng/ml), X-ray hand (T2-weighted): 7.4 years (bone age). MRI brain: Anterior pituitary hypoplasia, EPP and absent pituitary stalk [Figures and ].",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [30.7, 'kg'], 'height': [126.5, 'cm']}",19.1848,18.22556,20.14404,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 126.5 cm, which is 126.5 cm * 1 m / 100 cm = 1.265 m. The patient's weight is 30.7 kg. The patient's bmi is therefore 30.7 kg / (1.265 m * 1.265 m) = 19.1848 kg/m^2."
2405,6,Body Mass Index (BMI),physical,decimal,pmc-4306403-1,Extracted,"The patient was a 70-year-old male with a 20-year history of sick sinus syndrome, for which he had a permanent cardiac pacemaker. He also had a 2-year history of interstitial pneumonia. While under treatment for angina pectoris 2 years before admission, he was found to have kidney dysfunction (serum creatinine, 1.4 mg/dL; blood urea nitrogen, 30 mg/dL; and 4+ protein and 2+ occult blood on urinalysis). In early December 2008, he had orthopnea, which worsened gradually. On December 24, he had a checkup in our hospital and was admitted. The medications he was taking on admission included aspirin, ticlopidine, allopurinol, carvedilol, atorvastatin, and carbocisteine. He was 171 cm tall and weighed 61 kg. His temperature was 37.0°C. His blood pressure was 145/70 mmHg. Lung auscultation revealed bilateral coarse crackles. An abdominal examination was normal. Pretibial pitting edema was evident. Laboratory findings on admission are shown in . The kidney function test had worsened, compared with 2 years earlier. There were significant hypoalbuminemia and elevation of C-reactive protein. Results of a urinalysis were 3+ positive for protein and 3+ positive for blood, with many red blood cells, 2+ for granular casts, and 1+ for red blood cell casts in the urinary sediment. The amount of proteinuria was 5.12 g/day. Urine culture results were negative on admission. An electrocardiogram showed a ventricular pacing rhythm. A chest X-ray revealed bilateral pleural effusion and pulmonary congestion. MPO and PR3-ANCA were both negative by enzyme-linked immunosorbent assay (ELISA), but P-ANCA was detected by indirect immunofluorescence (IIF; ). Bactericidal-/permeability-increasing protein (BPI), elastase, and lysozyme antibodies were also positive on ELISA (Wieslab ANCA panel kit) despite negative results for azurocidin, cathepsin G, and lactoferrin.
After admission, we stopped the allopurinol and atorvastatin because several studies have shown a relationship between these drugs and the immediate development of ANCA-associated vasculitis. His pulmonary congestion was improved using diuretics. However, his kidney function worsened gradually. We performed a kidney biopsy on February 4, 2009. The renal biopsy specimen contained 15 glomeruli for light microscopic evaluation, of which 3 were globally sclerotic. There were 5 cellular, 3 fibrocellular, and 3 fibrotic crescents in the remaining 12 nonsclerotic glomeruli (). No necrotic lesion was found. Marked thickening and spike and bubbling formations were observed in the GBM by periodic acid-Schiff methenamine silver (PAM) staining (). There was tubular atrophy, especially around the globally sclerotic glomeruli, with interstitial fibrosis and inflammation involving numerous lymphocytes. An immunofluorescence microscopic evaluation revealed granular staining along glomerular capillary walls for immunoglobulin IgG (2+) and C3 (2+) (). There was no staining for IgA, IgM, or C1q. Electron-dense deposits in the subepithelial lesions and fused podocyte foot processes were revealed by electron microscopy (). Based on these findings, the present case was diagnosed histopathologically as crescentic glomerulonephritis, concurrent with MGN (Ehrenreich-Churg classification: Stage III).
Due to extraocular myositis, an inflammatory disease that selectively affects the muscles around the eyes, which occurred on January 26, 2009, he received oral prednisolone (30 mg/day) and the symptoms improved rapidly. Despite steroid therapy, his kidney dysfunction progressed severely (serum creatinine 6.23 mg/dL, urea nitrogen 54 mg/dL on February 3). After he started hemodialysis on February 12, his laboratory findings did not show significant signs of improvement in terms of kidney function. The dose of corticosteroid was tapered without recurrence of extraocular myositis.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.0, 'kg'], 'height': [171.0, 'cm']}",20.86112,19.81806,21.90418,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 171.0 cm, which is 171.0 cm * 1 m / 100 cm = 1.71 m. The patient's weight is 61.0 kg. The patient's bmi is therefore 61.0 kg / (1.71 m * 1.71 m) = 20.86112 kg/m^2."
2406,6,Body Mass Index (BMI),physical,decimal,pmc-3161475-1,Extracted,"A 48-years-old man weighing 68 kg, and of height 170 cm, was brought to the emergency unit after sustaining an open fracture right femur in a road traffic accident. He was scheduled for external fixation. On examination, the patient was conscious and well oriented. There was no history of loss of consciousness, vomiting or bleeding from oral and nasal cavities. The patient was a smoker since last 25 years (10 cigarettes/day). He denied any other medical comorbidity or surgical treatment in the past. Non-contrast computed tomography (CT) of head was normal, blunt trauma chest and abdomen was ruled out, no cervical spine injury was observed and hemodynamic parameters were also stable. Airway examination revealed mouth opening of 3 cm, thyromental distance of 8 cm, and full range of neck movements. Airway was classified as Mallampatti class II. Preoperative chest radiograph was normal and electrocardiography (ECG) showed normal sinus rhythm. Hemogram, coagulogram and renal and liver function tests were within normal limits. Functional capacity was more than 4 metabolic equivalents (METS).
After explaining the procedure and risk involved to the patient, written informed consent was taken. In the operating room, ECG, noninvasive blood pressure (NIBP), and pulse oximetry were attached and baseline parameters noted. An 18-G intravenous cannula was secured. Preoperative heart rate (HR) was 90/min, blood pressure (BP) 130/80 mm Hg, respiratory rate 16/min, and SpO2 (on room air) was 97%. Arterial blood gases (ABG) showed pH 7.35, pO2 98, pCO2 26, HCO3 15, BE –5, and SaO2 97%.
An 18-G epidural catheter was inserted via the L3-L4 space with the patient in a sitting position, using midline approach, and fixed at 11 cm. At the same level, 15 mg of 0.5% bupivacaine heavy was administered in the subarachnoid with a 25-G Quincke's spinal needle. Supplemented oxygen was administered by a venturi facemask (FiO2 0.5). A sensory loss up to T10 level was achieved with adequate motor paralysis after 9 min and surgery was then started. ECG, NIBP, and SpO2 were monitored. About 35 minutes after the administration of the subarachnoid block, the patient complained of dyspnea and chest pain. There was a sudden fall in SpO2 to 82% from 100%. The patient became tachypneic, started coughing and his HR rose to 126/ min. However, BP was within normal limits and ECG showed no marked changes. ABG showed pH 7.36, pO2 65.6, pCO2 45, HCO3 17.2, BE –6.1, and SaO2 82%. The patient was given continuous positive airway pressure of 100% oxygen with a facemask. SpO2 increased from 82% to 96%. A sample for D-dimer test was sent with the suspicion of pulmonary embolism. The patient had another bout of cough and SpO2 fell to 79-80%, BP to 81/54 mm Hg, and HR was 125/min. Dopamine infusion was started. On chest auscultation, there was reduced breath sounds on the right side. ABG values were pH 7.32, pO2 55.5, pCO2 54.2, HCO3 17, BE –6.9, and SaO2 80%. Anesthesia was induced with intravenous fentanyl 70 μg and thiopental 300 mg. Intravenous vecuronium 7 mg was administered and trachea secured with 8.5 mm endotracheal tube. The position of the tracheal tube was confirmed by capnography. Anesthesia was maintained with isoflurane in 100% oxygen. A chest radiograph was taken immediately, which showed a right-sided pneumothorax. Cardiothoracic consultation was taken and an underwater seal intercostal drain placed. After 5 minutes, HR improved to 80/min, BP 110/69 mm Hg, and SpO2 97%. The surgery lasted for 130 minutes and was completed without any further complication. Postoperatively, SpO2 was 97%, BP 105/62 mm Hg, and HR 113/min. The patient was shifted to the intensive care unit (ICU) and mechanically ventilated on Synchronized Intermittent Mandatory Ventilation (SIMV) mode with pressure support.
In ICU, the patient was monitored closely with invasive blood pressure, central venous pressure, oxygen saturation, airway pressure, and serial ABG. The D-dimer test report showed elevated values and color Doppler of lower limbs showed deep vein thrombosis of the right lower limb. Low-molecular-weight heparin therapy (enoxaparin 1 mg/kg subcutaneously 12 hourly) was started. Bed-side two-dimensional echocardiography in the ICU showed mild tricuspid regurgitation, mild pulmonary hypertension [RV systolic pressure (RVSP) = right atrial pressure (RAP) + 31 mm Hg], and hypokinesia of the right ventricular wall.
Postoperative analgesia was achieved with epidural injection of 8 ml of 0.125% bupivacaine 6 hourly, and epidural catheter was removed after 48 hours. The patient was weaned off ventilator support after three days and the trachea was extubated. Oxygen supplementation with venturi facemask (FiO2 0.5) was given for another two days. Inotropic support was removed on the fourth day and the patient shifted to the ward on the fifth day. Chest drain was removed after 9 days, and he was discharged to home on the 15th postoperative day.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [68.0, 'kg'], 'height': [170.0, 'cm']}",23.52941,22.35294,24.70588,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.7 m * 1.7 m) = 23.52941 kg/m^2."
2407,6,Body Mass Index (BMI),physical,decimal,pmc-7253637-1,Extracted,"A 14-year-old girl presented to the Department of Gynecology of the First Affiliated Hospital of Xi'an Jiaotong University with no obvious cause of persistent and severe lower abdominal pain that began 8 h prior. After receiving 450 mL of plasma at another hospital, she was referred to our facility since her test results suggested that her fibrinogen was only 0.10 g/L. She developed spontaneous epistaxis bleeding 7 days after she was born. At 2 years of age, CFD was diagnosed. She had a history of spontaneous auditory canal bleeding at 7 years of age. Her menarche took place at the age of 13, every menstrual period she needed to use more than 40 sanitary pads, accompanied by fatigue, rapid heartbeat, and unable to attend physical education classes or daily physical exercise, showing that she may have hypermenorrhea. She even had two hospitalizations due to hemorrhagic anemia caused by menorrhagia 9 and 3 months prior. But no medical treatment was performed afterwards. Upon presentation at our hospital, she was in the middle of her menstrual cycle. Her abdominal pain was accompanied by nausea, vomiting, dizziness, and palpitation. Besides, she denied the history of smoking.
After admission to the Department of Gynecology, we had a detailed physical examination. She was 155 cm and weighed 50 kg. Her vital signs exhibited blood pressure of 107/74 mmHg, a heart rate of 105 beats/min, a respiration rate of 23 breaths/min, and the body temperature of 36.5°C. General examination revealed marked pallor, but the mind was clear and no bleeding spots on skin. Abdominal examination revealed a soft abdomen without tenderness or rebound pain, but the mobile voiceless was positive. No obvious abnormalities were found in other physical examinations. Since the girl and her parents firmly asserted a history of asexual life, we didn't perform a gynecological examination.
Then the patient underwent transabdominal ultrasound demonstrating that a visible 3.1 cm × 2.4 cm cystic mass next to her right ovary. The mass boundary was clear and the morphology was regular. No obvious blood flow signal was observed. The fluid dark area in front of her uterus was approximately 8.3 cm × 8.0 cm, and the fluid dark area of her uterus rectal lacuna was 5.5 cm × 2.8 cm, where sparse spot reflection was visible. The right iliac fossa level was 3.9 cm, and that of the left iliac fossa was 2.0 cm. There was no abnormality in the appendix.
The patient's coagulation function examination revealed signs of difficult coagulation. Her prothrombin time was 23.30 s (normal: 11–14 s), prothrombin activity was 37% (normal: 84–128%), international standard ratio was 2.07 (normal: 0.94–1.3), activated partial thromboplastin time was 43.8 s (normal: 28–43.5 s), thrombin time was 33.3 s (normal: 14.0–21.0 s), fibrinogen was 0.30 g/L (normal: 2–4 g/L). Her hemoglobin was 71 g/L.
When the girl was admitted to our hospital due to abdominal pain, we considered it may be ruptured corpus luteum, ruptured follicles, ectopic pregnancy, torsion of the ovarian cyst or appendicitis. Since the girl was too young, and deny the history of sex life resolutely, we ruled out the possibility of ectopic pregnancy. Her abdominal pain was not metastatic, and there were no signs of peritoneal irritation. Ultrasound showed the appendix was normal, so appendicitis can also be ruled out. Ultrasound images confirmed the presence of hemoperitoneum, so the possibility of torsion of ovarian cyst pedicles was also low, thus the initial judgment was ruptured corpus luteum or ruptured follicles. The complete diagnosis of the girl included: hemoperitoneum (ruptured corpus luteum? ruptured follicles?), CFD, abnormal uterine bleeding-coagulation (AUB-C), and hemorrhagic anemia (moderate).
Considering the patient's vital signs were stable, based to the advice of a Department of Hematology consultation, we utilized conservative treatment including rehydration support, aminocaproic acid hemostatic treatment, 2 units of red blood cell suspension, 200 mL of frozen plasma, and 6 g of fibrinogen. After 3 days of hospitalization, her fibrinogen reached 0.50 g/L. We then placed a LNG-IUS (52 mg/piece) under intravenous anesthesia. Diagnostic curettage was performed simultaneously. The pathological results suggested that it was the proliferative phase of the uterus (), it also clarified that this hemoperitoneum was caused by ruptured follicles rather than the corpus luteum. The patient received COC (30 μg ethinylestradiol with desogestrel, 30 DSG) on the day of surgery, and then one tablet at approximately the same time every day for 63 consecutive days. When her anemia was corrected, COC administration was changed to 21 days of continuous medication as usual.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [50.0, 'kg'], 'height': [155.0, 'cm']}",20.81165,19.77107,21.85223,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 50.0 kg. The patient's bmi is therefore 50.0 kg / (1.55 m * 1.55 m) = 20.81165 kg/m^2."
2408,6,Body Mass Index (BMI),physical,decimal,pmc-3763621-3,Extracted,"A 9-month old female infant, with weight 5.6 kg, length 65.9 cm (weight-for-length z-score −3.04, weight-for-age z-score −3.29, length-for-age z-score −1.89) presented in icddr,b's Dhaka Hospital. She had a history of soft stool and cough for five days, fever for three days, vomiting for one day, and respiratory distress for 10 hours. On admission, physical examination revealed a temperature of 36.6 ºC, heart rate 118/min, respiration rate 60/min, and blood pressure 60/40 mmHg. In addition, the patient was very lethargic, there was lower chest wall-indrawing and some dehydration. On auscultation, coarse crackles were found in the right lung, and the heart sounds were normal. The abdomen was soft, non-tender, and bowel sounds were present. Chest x-ray showed patchy shadowing in the right lung field, and plasma electrolyte tests revealed hypokalaemia (K 2.05 mmol/L) and hypophosphataemia (P 2.5 mg/dL). Based on the physical findings and laboratory results, an initial diagnosis of severe pneumonia complicated by severe malnutrition, sepsis, hypokalaemia, and hypophosphataemia was made. Initial treatment was given with intravenous antibiotics and fluid therapy, with additional management given according to the icddr,b's standardized management protocol for severely-malnourished children. On the second day, plasma electrolyte analysis revealed a rise in potassium (K 2.87 mmol/L) but a drop in phosphate (P 1.1 mg/dL) levels. By the 7th day of admission, the patient became afebrile, clinically much improved, and the plasma electrolytes were almost corrected (Na 138.3 mmol/L, K 2.93 mmol/L, Ca 2.0 mmol/L, and P 2.8 mg/dL). Unfortunately, the family members removed the patient from the hospital against medical advice at this point.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [5.6, 'kg'], 'height': [65.9, 'cm']}",12.89488,12.25014,13.53962,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 65.9 cm, which is 65.9 cm * 1 m / 100 cm = 0.659 m. The patient's weight is 5.6 kg. The patient's bmi is therefore 5.6 kg / (0.659 m * 0.659 m) = 12.89488 kg/m^2."
2409,6,Body Mass Index (BMI),physical,decimal,pmc-4661371-1,Extracted,"A 21-year-old man was referred to our hospital due to progressively worsening headache of two-month duration. He was diagnosed with hypertension 7 years ago and was treated with angiotensin II receptor blocker (ARB) and calcium channel blocker. His mother had a history of hypertension. The headache had become gradually aggravated during the prior 2 months, and was associated with dizziness. He did not complain of any coughing, hemoptysis, abdominal discomfort, nocturia, sweating, or focal neurological symptoms.
On admission, blood pressure and heart rate was 152/108 mmHg and 76 beats/min, respectively. His height was 175 cm and weight was 91 kg. Physical examination revealed normal lung and cardiac sounds. Abdominal bruits, tenderness, or masses were not observed.
Initial laboratory findings revealed normal blood urea nitrogen (17 mg/dL), serum creatinine (1.1 mg/dL), sodium (137 mmol/L), potassium (3.5 mmol/L), fasting glucose (175 mg/dL), and calcium (8.8 mg/dL). Electrocardiogram and chest x-ray showed normal sinus rhythm and unremarkable radiographic findings. Echocardiographic features were normal, without evidence of heart failure or aortic coarctation. Twenty four hour urinary catecholamine and vanillymandelic acid level (5.3 mg) was within normal range. Plasma renin and aldosterone level were 6.67 ng/mL/hr and 11.09 ng/dL in the supine position, respectively and 9.96 ng/mL/hr and 20.47 ng/dL, respectively, when upright.
Kidney ultrasonography revealed no evidence of definite renal artery stenosis and computed tomography (CT) showed a well-defined mass, 1.7×1 cm in size, in the middle pole of the right kidney (). Magnetic resonance imaging (MRI) also revealed a 1.8 cm small and solid mass in the same right kidney (), which had iso-signal intensity in the T1-weighted image and heterogenous, mild, low signal intensity in the T2-weighted image. Whole body bone scan showed no active bone lesions.
The patient underwent partial nephrectomy to remove the mass in the right kidney. Grossly, the renal parenchyme was a well-demarcated and oval mass with gray fish flesh-like cut surface and focally hemorrhage, measuring 1.5x1 cm (). The lesion was close to the surgical resection margin and low mitotic figures were identified. On microscopic examination, a relatively well-circumscribed tumor was identified. Thick-walled blood vessels were well developed, with a characteristic hemangio-pericytic pattern. Immunohistochemically, vimentin and CD34 staining were positive. On electron microscopy, the tumor cells displayed numerous secretory granules, some of which showed typical rhomboid crystalline-material that was thought to be renin protogranules (). Consequently, this mass was confirmed as a juxtaglomerular cell tumor.
On the second day after surgery, the level of plasma renin decreased to 0.01 ng/mL/h and blood pressure had normalized (120/80 mmHg). The antihypertensive regimen was decreased (amlodipine 5 mg only) on discharge. At the 2-month follow-up, blood pressure (112/80 mmHg) and serum potassium level (4.3 mmol/L) remained normal.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [91.0, 'kg'], 'height': [175.0, 'cm']}",29.71429,28.22858,31.2,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 175.0 cm, which is 175.0 cm * 1 m / 100 cm = 1.75 m. The patient's weight is 91.0 kg. The patient's bmi is therefore 91.0 kg / (1.75 m * 1.75 m) = 29.71429 kg/m^2."
2410,6,Body Mass Index (BMI),physical,decimal,pmc-2533002-2,Extracted,"A 29 year-old white woman, G2P1, presented complaining of atypical cyclic pain on the scar of a previous cesarean section, performed six months earlier. Patient history details were as follows: Occupation: Secretary; Ethnicity: Greek; Weight: 65 Kg; Height: 167 cm; Medical history: one previous cesarean section, otherwise unremarkable; Family history: unremarkable; Patient habits and medications: non-smoker, no alcohol consumption, no current medications. On clinical examination, a firm lump was found on the abdominal scar. Ultrasound scan showed a large hypoechoic mass with internal echoes, measuring approximately 10 mm, located at the lateral margin of the scar (Figure ). Power Doppler sonography showed increased vascularity within the mass (Figure ). On static MRI the mass appeared isodense to muscle (Figure and ), while T2-weighted imaging showed increased signal-intensity within the lesion. After total surgical excision, histological examination showed that the mass consisted of endometrial tissue and stroma, suggesting cutaneous endometriosis.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [65.0, 'kg'], 'height': [167.0, 'cm']}",23.30668,22.14135,24.47201,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 167.0 cm, which is 167.0 cm * 1 m / 100 cm = 1.67 m. The patient's weight is 65.0 kg. The patient's bmi is therefore 65.0 kg / (1.67 m * 1.67 m) = 23.30668 kg/m^2."
2411,6,Body Mass Index (BMI),physical,decimal,pmc-7995720-1,Extracted,"An 18-year-old Persian man (60 kg, 180 cm) with a case of Marfan syndrome (MFS) identified from family history and genetic assessment was referred to our center. He presented mainly with right thoracic scoliosis of 70° and excessive joint laxity, without any previous disease history (Fig. ). Scoliosis of 70° and the deteriorating condition of our patient led to the decision to perform surgery. In April 2016, a right thoracotomy for anterior spinal fusion (ASF) was performed from the sixth rib under general anesthesia in the left lateral decubitus position. After 3 days, posterior spinal fusion and instrumentation (PSF) was done successfully. He was discharged with a total contact body brace. On the 2 months postoperative visit, he complained of weakness of the right upper limb during overhead activities. On physical examination, the right upper limb was intact for both sensory and motor innervation, but the right scapula was winged and he was not able to flex his arm forward over 60° (Fig. ). Electromyography (EMG) and nerve conduction velocity (NCV) confirmed long thoracic nerve injury. A conservative treatment, physiotherapy, was provided for 3 months. Ultimately, the patient recovered completely in the last follow-up visit 6 months after the surgery. Electromyography and nerve conduction velocity revealed a return to normal position. However, scapula is more prominent than normal due to the hyperlaxity of MFS (Fig. ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.0, 'kg'], 'height': [180.0, 'cm']}",18.51852,17.59259,19.44445,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 180.0 cm, which is 180.0 cm * 1 m / 100 cm = 1.8 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.8 m * 1.8 m) = 18.51852 kg/m^2."
2412,6,Body Mass Index (BMI),physical,decimal,pmc-5820059-1,Extracted,"An 8-year-old girl with severe sternum depression and a history of exercise intolerance, fatigue, and shortness of breath on exertion was assessed. The patient also referred nocturnal dyspnea. Family history revealed an older sibling with asymptomatic severe PE that required surgical correction (Nuss procedure) at 7 years of age. Our patient's sternal depression was visible since birth and symptoms had started earlier in life (6–7 years of age), followed by rapid progression of symptoms which were more notable in the past 6 months. Genetic tests were performed to rule out Marfan syndrome as well as other abnormalities. The physical examination showed a prepubescent female with a height of 131 cm and weight of 22 kg. Her chest revealed a deep, asymmetric PE deformity (
).
As part of the assessment protocol, a computed tomography (CT) scan was ordered (see
). Chest CT evaluation showed that the sternum depression was posterior to the anterior vertebral column rendering the Haller and correction index, to the best of our knowledge unmeasurable. Other severity indexes were calculated: sternal rotation angle was 40° and the asymmetry index of 58%, indicating a marked left-sided asymmetry.
As part of the functional evaluation, a spirometry and echocardiogram were indicated. The preoperative spirometry indicated an obstructive ventilation pattern (forced expiratory volume in 1 second = 74.4%). The echocardiogram revealed a dilated inferior vena cava, mitral valve prolapse with normal ventricular function, all signs of ventricular compression.
After multidisciplinary committee evaluation, considering the severity of the symptoms and available resources, the indication of surgical repair was offered to the family. A MIRPE approach was designed. Right thoracoscopic visualization was achieved with a 0° and 10mm Storz endoscope placed at the fourth intercostal space. Although an angled scope offers a better view, it was not available at the time of the repair. This was followed by placement of a midsternum 7.5 mm cannulated bone screw (Laffitte). This would generate upward traction that would allow better visualization of the substernal dissection plane. After careful dissection, two 9-inch steel bars were slipped under the sternum through the fifth and seventh intercostal space following the Nuss procedure indications. Two steel bars and stabilizers on both sides of the bar were placed to fully correct the deformity and to prevent bar displacement.
Postoperative care was uneventful allowing for a painless and quick recovery. At the 2 months' spirometry evaluation, an improvement in FEV1 and other parameters was observed (see
), and cardiac compression signs disappeared on cardiac ultrasound. The patient referred that most symptoms had disappeared by the 3-month follow-up (nocturnal dyspnea and shortness of breath upon slight exertion), with great improvement in quality of life. Exercise was restricted during the initial 4 months, after which normal activity other than contact-sports were allowed. The desired sternum shape was achieved, with slight overcorrection noticed around 18 months postoperatively. The steel bars were removed after a 2-year period. At the 3-month follow-up, all of the patient's exercise intolerance had disappeared, and she was now more physically active. Postoperative bar removal imaging showed an acceptable correction of the deformity (see
and
). During follow-up, the patient is content with the aesthetic result of the procedure; also the patient can carry out normal exercise.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [22.0, 'kg'], 'height': [131.0, 'cm']}",12.81977,12.17878,13.46076,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 131.0 cm, which is 131.0 cm * 1 m / 100 cm = 1.31 m. The patient's weight is 22.0 kg. The patient's bmi is therefore 22.0 kg / (1.31 m * 1.31 m) = 12.81977 kg/m^2."
2413,6,Body Mass Index (BMI),physical,decimal,pmc-2612654-1,Extracted,"Presenting complain – A 5 yr old Indian girl presented at the hospital with the chief complain of pain and distension of the abdomen. She complained of pain for last 4 days, the pain was continuous in nature and diffusely involved the whole abdomen but was more so in the umbilical and the hypo-gastric regions, pain was non-radiating, was relieved on lying still and aggravated on movement. No predisposing cause of the pain could be found and the girl's mother said that she complained of stomach pain suddenly. The pain had gradually increased in intensity over time. Abdominal distension developed about 2 days after she complained of pain. She also complained of multiple episodes of vomiting (about 15 per day), the vomitus was greenish yellow in colour, non bloody, odourless and copious in amount. She complained of burning micturation as well and described an increase in pain during urination. She also complained of loss of appetite and mild constipation but denied any fever or cough. Past history – Her mother described that she had developed similar kind of features 4 yrs back when a ceiling fan had fallen on her stomach, she was hospitalized and was diagnosed as a case of intrauterine rupture of urinary bladder. Exploratory laparotomy was performed and bladder rupture was repaired. The post operative recovery was uneventful with no further complains.
Birth history – She was a full term normal spontaneous vaginal delivery, her development milestones and vaccination status are up to date.
The girl was conscious and alert and was in pain.
Height-103 cms, Weight-28 kgs
Vital signs as follows: temp-98.8^F, pulse-126/min, RR-28/min, BP-100/70 mm Hg.
Abdominal exam-previous operative scar, abdomen distended, diffuse tenderness over whole abdomen, no rigidity, no guarding, liver and spleen impalpable, shifting dullness and fluid thrill were found to be present, bowel sounds were absent.
Examination of rest of the systems was uneventful.
Hb-12.5 gm%, TLC-14000, Na-130 mEq/L, K-6.5, Urea-210 mg/dl, creatinine-2.4 mg/dl, bilirubin-0.6(direct-0.3)mg/dl, AST-85 iu, ALT-49 iu.
X-ray abdomen erect showed diffuse ground glass appearance in the abdomen (Fig. ). No air fluid levels no gas under diaphragm was seen.
Abdominal ultrasound showed intraperitoneal fluid collection.
Diagnostic peritoneal tapping revealed a non bloody straw colour fluid which was found to be urine. The collected urine was found to be sterile.
IVP or cystogram were not undertaken as the peritoneal tap and ultrasound confirmed the presence of urine in the abdomen, in case of doubt i definetely recommend these tests.
The patient was catherized and put on intravenous ceftriaxone and metronidazole pre-operatively and was continued on the same for a period of 5 days. Emergent exploratory laparatomy was performed; intraperitoneal rupture of the bladder as a result of scar dehiscence of the previous bladder rupture repair was found located on the dome of the bladder and was repaired in layers. About two litres of urine was drained out of the peritoneal cavity. The rest of the bladder was found to be absolutely normal. The girl's recovery was fast and uncomplicated; her blood urea and creatinine levels were in the normal range in just two days after the operation. Subsequently she was discharged on oral antibiotics and dietary supplements with advice for regular follow up.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [28.0, 'kg'], 'height': [103.0, 'cm']}",26.39269,25.07306,27.71232,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 103.0 cm, which is 103.0 cm * 1 m / 100 cm = 1.03 m. The patient's weight is 28.0 kg. The patient's bmi is therefore 28.0 kg / (1.03 m * 1.03 m) = 26.39269 kg/m^2."
2414,6,Body Mass Index (BMI),physical,decimal,pmc-5346828-1,Extracted,"A 5-year-old boy with a two year history of the lithophagia, was treated for IDA several times. He had been diagnosed with hypochromic microcytic anemia, but he showed no response to repeated therapeutic iron supplementation. His history revealed several episodes of abdominal distention and long standing constipation that aggravated with iron supplements. Also, he had temptation to lithophagia. Recently, he developed abdominal pain and distention and no defecation for at least 15 days. On arrival, he seemed chronically ill, but his weight and height were acceptable for his age (height=110Cm, weight=20 Kg); moreover, he belonged to a high socio-economic family.
Physical examination documented abdominal distention with decreased bowel sounds but no evidence of organomegaly. Due to his avoidance of rectal examination, plain abdominal X-ray was taken for evidence of fecal impaction, revealing multiple, well-defined radio-opaque foreign bodies in all parts of his colon. (, )
According to his laboratory assessments, he had heamoglobine 80g/dl, mean circular volume55fl, RBC 3300000, WBC10000, RDW18, total protein 65g/l, and albumin40g/l. With this history of IDA unresponsive to iron supplementations, we were suspicious to CD and total IgA and Anti Tissue Trans-Glutaminase Antibody (TTG-IgA) was measured; TTG-IgA was 400 (normal=20) and total IgA was in a normal range. After that, Esophagogastrointestinal endoscopy was done and multiple biopsy was obtained. Histological examination revealed normal esophagus and stomach but duodenum biopsies documented Marsh-III villus atrophy with an extensive epithelial lymphocyte infiltration in favor of CD.
The subject commenced lactolose with a dose of 3 ml /Kg/day divided into two equal doses for disimpaction and Gluten free diet. The patient passed rocks without any complication 3 weeks after initiation of lactolose () and his desire to lithophagia was diminished with Gluten free diet.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [20.0, 'kg'], 'height': [110.0, 'cm']}",16.52893,15.70248,17.35538,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 110.0 cm, which is 110.0 cm * 1 m / 100 cm = 1.1 m. The patient's weight is 20.0 kg. The patient's bmi is therefore 20.0 kg / (1.1 m * 1.1 m) = 16.52893 kg/m^2."
2415,6,Body Mass Index (BMI),physical,decimal,pmc-3485098-1,Extracted,"A 74-year-old Japanese man was being treated at home for type II respiratory failure due to COPD, but at the end of July 2011 he developed a fever of around 38°C and his dyspnea worsened. The oxygen flow rate was increased, but his hypoxemia failed to improve, and acute exacerbation of COPD was diagnosed on examination by his primary care physician. He was referred to our hospital and was hospitalized for further testing and treatment.
Our patient was 160cm tall, weighed 40kg, and had a temperature of 37.6°C. His heart rate was normal, at 110 beats/min, with an elevated respiratory rate of 28 breaths/min, blood pressure of 116/77mmHg, and oxygen saturation (SpO2) of 97% on nasal oxygen at 3L/min. Chest auscultation revealed bronchial rales in both his lower pulmonary fields. His white blood cell count was within the normal range, but his levels of C-reactive protein were highly elevated. Blood gas testing revealed pronounced hypercapnia (pH 7.292, partial pressure of oxygen (PaO2) 118.8mmHg, partial pressure of carbon dioxide (PaCO2) 81.5mmHg, bicarbonate (HCO3-) 38.2mmol/L, O2 intake 3L/min).
Radiography showed bilateral emphysematous lesions across all his pulmonary fields, with left diaphragmatic elevation and a right mediastinal shift (Figure 
).
Chest radiography and computed tomography showed no evidence of pneumonia, and he was diagnosed with acute exacerbation of COPD due to a respiratory tract infection on the basis of his clinical symptoms and sputum test results. He was placed on 24-h NPPV using a BiPap® Vision® Ventilatory Support System (IPAP, 8cmH2O; expiratory positive airway pressure (EPAP), 4cmH2O; spontaneous-timed (ST) mode), and was started on an antibiotic and a diuretic. As his respiratory status stabilized, he was taken off NPPV, which was then used only while sleeping at night, and his physical findings temporarily resolved. From around hospital day 32, however, a respiratory tract infection that may have been caused by aspiration triggered another episode of acute COPD exacerbation, with a depressed level of consciousness. This time, NPPV management was implemented using a Respironics V60 Ventilator (recently introduced at our institution) in AVAPS mode (IPAP, 8 to 10cmH2O; EPAP, 4cmH2O; target tidal volume, 350mL). Initial findings of pH 7.189, PaCO2 136mmHg, PaO2 108.1mmHg and HCO3- 50.0mmol/L were indicative of hypercapnia and acidosis, and improved markedly to pH 7.508, PaCO2 251.1mmHg, and PaO2 75.9mmHg after one day on the V60 ventilator. NPPV was conducted using two different ventilators for his two episodes of acute COPD exacerbation. During BiPAP, his tidal volume was significantly decreased during sleep compared with waking hours, but use of the AVAPS mode of the Respironics V60 Ventilator automatically corrected the IPAP and was able to improve his sleep-related alveolar hypoventilation (Figure 
 and Additional file 
: Table S1). A polysomnography (PSG) was performed to diagnose our patient’s sleep respiratory disorder after his second episode of acute exacerbation.
The results of the PSG were as follows: sleep efficiency, 75.5%; apnea-hypopnea index, 14.0/h; apnea index, 2.7/h; hypopnea index, 11.3/h; mean nocturnal SpO2, 94%; minimum SpO2, 87%; SpO2<90% time (min) 15.0% with NPPV (ST with IPAP, 8cmH2O; EPAP, 4cmH2O; respiratory rate, 14/min; O2, 1.5L/min).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [40.0, 'kg'], 'height': [160.0, 'cm']}",15.625,14.84375,16.40625,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 40.0 kg. The patient's bmi is therefore 40.0 kg / (1.6 m * 1.6 m) = 15.625 kg/m^2."
2416,6,Body Mass Index (BMI),physical,decimal,pmc-4325654-1,Extracted,"A 49-year-old female patient came to the outpatient clinic with complaint of general weakness, mild discomfort and heat sensation in the abdomen. Diagnosed with PNET with multiple liver metastases at another hospital, she was transferred to our clinic for bloodless surgery owing to the patient's religious faith. The patient's height was 152 cm and weight was 53.6 kg. She didn't have any other underlying medical diseases such as hypertension, diabetes, hepatitis, tuberculosis and so on. Physical exams revealed mildly distended abdomen and a non-tender palpable intraabdominal mass. The serum tumor markers including CEA, CA 19-9, and α-FP were within normal limits, whereas liver function test levels including total bilirubin (1.3 mg/dL), aspartate transaminase (58 U/L), and alanine transaminase (49 U/L) were slightly elevated. Radiological tools including abdominal-pelvic CT scan, biliary and pancreas dynamic MRI with contrast, PET/CT scan, and bone scan contributed to diagnosis and therapeutic plan. According to the results of radiological imaging studies, a huge well capsulated tumor (about 8-cm diameter on the longest distance) was located in the pancreatic body and tail, which was highly enhanced by the contrast material. Multiple hepatic metastases were found in both lobes ().
Sono-guided biopsies on liver and pancreas showed proliferation of uniform round cells in ribbon, consistent with metastatic well-differentiated PNET from the pancreas. Results revealed positive staining of chromogranin A and cytokeratin (CK). Ki67 labeling index was about 4%-5% that corresponded to grade 2. For treatment of PNET with multiple liver metastases, serial therapies were scheduled. First of all, transarterial chemoembolization (TACE) was performed prior to surgery. The interventional radiologist performed TACE with mitomycin and lipiolol, which were injected to the patient's metastatic hepatic tumors. After a total of 3 sessions of successful TACE for multiple liver metastases over 4 months (), the size of multiple liver metastases decreased dramatically in the following abdomen CT (). Meanwhile, the patient suffered from liver failure with total bilirubin increased up to 23 mg/dL. Careful conservative management without transfusion was carried out for treatment of liver impairment. For the systemic treatment, octreotide acetate injection was given before surgery. Initial dose was 0.1 mg via subcutaneous injection every 8 hours over 3 days for response test, and then 4 injections at 20 mg were given daily via intramuscular route per 28 days.
The attending surgeon and anesthesiologist discussed the risks of bloodless major operations. The patient signed a consent form for the operation without the use of blood products. She allowed albumin and acute normovolemic hemodilution (ANH). Considering that it was a cancer surgery, Cell Saver was not allowed due to risk of shed cancer cells. The preoperative albumin level was 3.7 g/dL, hemoglobin was 12.6 mg/dL, and hematocrit was 36.8%. The dissection of RAMPS procedure started from the left side, which is the neck of the pancreas, to the right side with splenic vessels and celiac node dissection. Afterwards, the plane of dissection proceeded posteriorly in a sagittal plane along the celiac artery and the superior mesenteric artery down to the level of the aorta, in sequence, going on laterally to the left adrenal gland (). There was severe adhesion of omentum to the hepatic tumors and pancreatic tumor, however, the celiac trunk and the superior mesenteric artery were relatively well isolated from the tumor. The pancreatic tumor was well vascularized, capsulated, and abutted to the renal arteries and veins, but not invading (). Histological diagnosis was consistent with well-differentiated pancreatic neuroendocrine carcinoma with negative resection margin but extending to the peripancreatic soft tissue and splenic venous wall. It showed angioinvasion and neural invasion containing ischemic necrosis. Immunohistochemical examination revealed that chromogranin A, CD56, CD10, and CK were positive (). Pathologic staging was T3N0M1 stage IV according to American Joint Committee on Cancer/Union for International Cancer Control TNM staging for pancreatic tumors.
Total operative time was 4 hours 30 minutes. Estimated blood loss was 800 mL and while the patient received 3 pints of ANH and intravenous dextran during the operation. The postoperative albumin was 2.8 g/dL, hemoglobin 11.5 mg/dL, hematocrit 33.8%, and fibrinogen 248 mg/dL. As an assistant therapy for a transfusion free patient, recombinant human erythropoietin 4,000 IU and 1 ample of iron hydroxide sucrose complex were given daily for five days after surgery. Postoperative abdominal CT scan didn't show any evidence of pancreatic fistula or fluid collections around the pancreatic resection margin.
The patient took a sip of water on day 2 and began a soft diet on day 4, postoperatively. She was discharged 12 days after the operation. We had future plans to give octreotide acetate injection for the systemic treatment and additional TACE for liver metastasis",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.6, 'kg'], 'height': [152.0, 'cm']}",23.19945,22.03948,24.35942,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 152.0 cm, which is 152.0 cm * 1 m / 100 cm = 1.52 m. The patient's weight is 53.6 kg. The patient's bmi is therefore 53.6 kg / (1.52 m * 1.52 m) = 23.19945 kg/m^2."
2417,6,Body Mass Index (BMI),physical,decimal,pmc-6831326-1,Extracted,"A 52-year-old woman (height 159 cm, weight 94 kg) with idiopathic pulmonary fibrosis and obesity was presented for bilateral sequential lung transplantation with right lung graft first under extracorporeal membrane oxygenation (ECMO). Preoperative pulmonary function test (%, predicted) showed forced expiratory volume in 1 second, 0.88 L (37%); forced vital capacity in 1 second, 0.92 L (30%); forced expiratory volume in 1 second/forced vital capacity, 95%; and diffusing capacity of carbon monoxide, 8.3 L/mmHg/min (28%). Veno-venous ECMO, tracheostomy, and mechanical ventilation were applied to the patient for 39 days preoperatively as a bridge for lung transplantation. Preoperative chest radiography showed severe diffuse lung consolidations (Fig. A). Preoperative cardiac echocardiography showed reduced right ventricle systolic function, mild pulmonary hypertension (right ventricular systolic pressure 47 mmHg), D-shaped left ventricle with slightly decreased left ventricle systolic function (ejection fraction 56%).
The anesthesia was induced with midazolam 3.0 mg, sufentanil 50 μg, and rocuronium 50 mg. Initially, a 35 Fr left-sided DLT (Shiley, Covidien, Mansfield, MA) was inserted via oral route for lung isolation and blindly placed at 28.5 cm depth at the level of upper incisor of the patient according to the height-based blind positioning of DLT. However, both lungs were unable to ventilate, and the confirmation for the positioning of DLT with FOB (FIVE 4.0, Karl Storz, Tuttlingen, Germany) was impossible due to massive pulmonary secretion (Fig. B). Despite the effort to suck out the pulmonary secretion with the suction catheter and FOB, any anatomic structures of tracheobronchial tree were invisible. We decided to use a new DLT (ANKOR, Insung Med, Wonju, South Korea) of left-sided 35 Fr (Fig. A). After the carinal cuff of the tube passed through the vocal cord of the patient, the tube was turned to left side, and carinal cuff was inflated with 6 mL of air (Fig. B). The tube was advanced further toward left main bronchus, and it stopped at 26.0 cm of depth at the level of upper incisor of the patient. After the deflation of the carinal cuff, the tracheal cuff and the bronchial cuff of the tube were inflated with 5 and 2 mL of air, respectively (Fig. C). After the completion of right lung graft, bronchoscopic finding showed that the tube was properly positioned at the tracheobronchial tree of the patient showing the upper margin of the bronchial cuff was slightly seen at between the carina and the left main bronchial orifice without the obstruction of the tracheal lumen (Fig. D). Surgeons indicated that the use of the new DLT provided excellent operating conditions during both lung grafts. The operation time was 10 hours and 50 minutes under veno-arterial ECMO. The patient was transferred to intensive care unit with veno-venous ECMO. ECMO was applied for postoperative day (POD) 13, and the patient was moved to the general ward at POD 37.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [94.0, 'kg'], 'height': [159.0, 'cm']}",37.18207,35.32297,39.04117,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 159.0 cm, which is 159.0 cm * 1 m / 100 cm = 1.59 m. The patient's weight is 94.0 kg. The patient's bmi is therefore 94.0 kg / (1.59 m * 1.59 m) = 37.18207 kg/m^2."
2418,6,Body Mass Index (BMI),physical,decimal,pmc-8078372-2,Extracted,"A 107-month-old Chinese girl who was the second child of this family was likely to be a GSD VI due to the abnormal gene. She had no overt clinical manifestation, such as abdominal distention, hepatomegaly, except growth retardation and occasionally presence of blood in stools what they did not value. Her academic achievement is below the average. Physical examination suggested growth retardation with a height of 125 cm (−2SD to −1SD) and a weight of 22 kg (−2SD to −1SD). The liver was swollen to 4 cm below the right costal margin without abdominal distention. Vegetations existed in the anus at 6 o’clock. Laboratory examinations revealed mildly reduced fasting blood glucose (lowest 3.66 mmol/L). Adrenaline stimulation test had no positive effect to disintegrate glycogen. Alpha-fetoprotein and liver transaminases were within reference ranges. She had hematochezia and enteroscopy was performed. The results were normal. The liver pathology was compatible with GSD (Fig. ). Hepatic lobular structures were present, with hepatocytes arranged neatly in most of the areas. Small areas of hepatocytes were arranged in a nodular pattern. The masson staining had fibrosis observed around portal areas. PAS in hepatocytes without diastase treatment was strongly positive, while PAS obviously receded following diastase treatment. It was also worth noting that masson staining showed more collagen fibroplasia in the distensible portal area. The Ishak score was 4 for inflammation and 3 for fibrosis. She was treated with uncooked cornstarch (2 g/kg, 6 hours intervals, taken between meals, before bedtime and at night). For 12 months of follow-up visit, various data of the girl had changed (Table ). By the 12th month of return visit, the girl had no obvious symptoms. The liver size changed from 4 cm to 2.5 cm below the right costal margin. The liver transaminases returned to normal. The fasting blood glucose was still mildly reduced (3.83 mmol/L). Lactate was normal (2.29 mmol/L).
The results of gene suggested that both 2 cases inherited compound heterozygous mutations on the PYGL gene, including c.2467C>T (p.Q823X) on exon 20 (chr14:51372187) from father and c.2178-2A>C on exon 18 (chr14:51375675) from mother. Based on the clinical manifestation, physical, laboratory, and pathology, they were diagnosed as GSD VI. Their eldest sister, the first child of parents, inherited c.2178-2A>C heterozygous mutation from mother, but no c.2467C>T mutation (Fig. ). The father, mother and eldest sister were disease-free with single heterozygotes. They belonged to carriers of gene mutation. In summary, the inheritance of the mutation in this family accords with the law of Mendelian inheritance and the mode of inheritance accords with the characteristics of autosomal recessive inheritance (Fig. ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [22.0, 'kg'], 'height': [125.0, 'cm']}",14.08,13.376,14.784,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 125.0 cm, which is 125.0 cm * 1 m / 100 cm = 1.25 m. The patient's weight is 22.0 kg. The patient's bmi is therefore 22.0 kg / (1.25 m * 1.25 m) = 14.08 kg/m^2."
2419,6,Body Mass Index (BMI),physical,decimal,pmc-6411325-1,Extracted,"A 13-year-old female patient presented to the Dental University Hospital at King Saud University, Riyadh, Saudi Arabia. The patient was referred by an orthodontist to restore her teeth before starting orthodontic treatment. Her weight was 125 kg and her height was 173 cm, which were abnormal for her age. The patient did not report any pain, discomfort or medical problems; however, the patient's response was late during the history taking. The patient had a history of successful repair of cleft lip and palate. Upon extra-oral examination, the frontal view showed facial asymmetry on the left side and flattening of the nasal bridge, increased intercanthal distance (35 centimeters) (orbital hypertelorism) and frontal bossing (54 centimeters), multiple skin lesions on her arms, and right foot and palmar/ plantar pits (Figures , , ).
The intra-oral examination revealed multiple carious teeth, painless hard swelling in the left side of the mandible, and mild pain on percussion in all the left mandibular posterior teeth. An orthopantomogram (OPG) showed bilateral radiolucent lesions associated with a partially erupted mandibular second molar teeth. The left mandibular lesion was extended up to the ramus of the mandible; moreover, the patient had a horizontally impacted maxillary right second molar and congenitally missing second premolars and third molars (Figure ).
Cone beam computed tomography (CBCT) was requested for detailed radiological assessment of the mandibular lesions. Accidentally, CBCT revealed another large lesion associated with the impacted right maxillary second molar, which extended up to the right maxillary sinus. In addition, the lower left lesion was severely expanded in all directions (buccolingual, anteroposterior, and superoinferior), and perforations were noticed in the buccal and lingual borders of the mandible (Figure ). A skull X-ray revealed calcification of the falx cerebra on the posteroanterior and lateral views.
In addition, the anteroposterior view of a chest X-ray showed a bifid fifth rib on the left side (Figure ).
A diagnosis of Gorlin-Goltz syndrome was made. Both maxillary and mandibular right cystic lesions of the jaws were enucleated surgically. Marsupialization was done for the mandibular left lesion and a biopsy was performed. The histopathological examination of the tissues showed KCOT of the right and left mandibular lesions and a dentigerous cyst of the maxillary right-side lesion. The patient was followed up every week after the surgery in the first month. The patient will then be followed-up once each month for six months. The tube will be removed after six months and then the patient will be followed up every six months.
After two months of follow-up, the marsupialized cyst showed improvement and bone deposition (Figure ). Informed consent (written) was obtained from the patient and her parents. (The IRB approval number is E-18-3544).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [125.0, 'kg'], 'height': [173.0, 'cm']}",41.76551,39.67723,43.85379,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 173.0 cm, which is 173.0 cm * 1 m / 100 cm = 1.73 m. The patient's weight is 125.0 kg. The patient's bmi is therefore 125.0 kg / (1.73 m * 1.73 m) = 41.76551 kg/m^2."
2420,6,Body Mass Index (BMI),physical,decimal,pmc-2946042-1,Extracted,"A 5-year-old male patient of 111 cm and 19 kg, who experienced an osteosarcoma in the left fibula was to go undergo insertion of a totally implantable central venous access device for chemotherapy. But the right totally implantable subclavian central venous catheter was infected. Hence, the patient was admitted for surgery for the removal of the infected catheter and for left totally implantable subclavian central venous catheterization. The patient underwent numerous chemotherapy treatments (CDDP, Adriamycin, Methotrexate, Ifofamide, VP-16). He had been on antibiotics for over 3 weeks due to an infection at the TICVAD site.
In the blood test before surgery, the platelet level had decreased to 64,000/mm3. Electrocardiography, echocardiography, and chest x-ray tests appeared normal. While the patient was on the OR table, a very severe infectious ulcer and abscess of 5 cm in diameter was observable to the human eye on the skin and the tissue below the skin at the right TICVAD site.
No premedication was given. On the operating table, the EKG, pulse oximeter, and a noninvasive blood pressure cuff were attached. The measured systolic/diastolic blood pressure was 100/50 mmHg, and heart rate was 90. Glycopyrrolate (0.06 mg) and thiopental (100 mg) were administered to induce loss of consciousness. Oxygen and sevoflurane were used for manual ventilation. After securing airway patency, fentanyl 20 µg and rocuronium 15 mg were administered. After adequate muscle relaxation, a noncuffed endotracheal tube (I.D. 5.0 mm) was inserted. After endotracheal intubation, N2O and oxygen were used to maintain the inspired oxygenconcentration at 0.5. Sevoflurane 1.5-3 vol% was used for anesthesia during manual ventilation. For the end-tidal CO2 concentration to be 35 mmHg, the tidal volume and the respiratory rate were controlled. The thoracic surgeon used a 21 G. introducer needle to puncture the left subclavian vein. For this procedure, we reduced the manual ventilation to prevent the occurrence of pneumothorax. When the left vessel was punctured, the beat of the arterial blood was not found in the small amount of aspired blood. So the blood was assumed to be venous. While inserting a guide wire and a 6.5 Fr. dilator, aspiration of blood that appeared to be arterial blood was observed. Therefore, all catheters were quickly removed, and pressure was applied for hemostasis. Afterwards, puncture of the left subclavian vein was attempted again, but the introducer needle was removed after repeated arterial puncture, and pressure was applied for hemostasis. Venous puncture was attempted 2 or 3 times, but it failed. Then puncture of the left internal jugular vein was attempted, but it also failed.
A slight edema was noted in the neck and the left subclavian area. So the puncture attempts on the upper body were stopped. Instead, the puncture of the left femoral vein was attempted successfully. A 6 Fr. TICVAD (X-Port® Bard Access Systems, USA) was inserted. During the venous puncture, the patient was assumed to have hemorrhaged. So a plasma expander (HES-plazma®6%, ChoongWae, Korea) 200 ml was infused. During the central venous catheterization, no serious decrease in blood pressure was found. The right central venous catheter and the port were removed.
Curettage of the tissue near the infection was performed, and then the site was closed, ending the surgery. After the surgery, the patient was completely awake, could open his eyes, and move his arms and legs. However, a sudden drop in blood pressure occurred. The arterial hematocrit was measured at 20%. A vasopressor, ephedrine 2.5 mg and packed RBC 1U were administered. Then the arterial hematocrit rose to 28%. Because of a continuous drop in blood pressure (60-90/30-40 mmHg) and acute acidemia, dopamine HCl (Dopamine free mix 80 mg®, CJ, Korea 10-20 µg/kg/min) was continuously administered, and bicarbonate was intermittently administered. Then midazolam (1 mg)and rocuronium (5 mg) were administered. In the first chest x-ray (), a very large right hemothorax was discovered. Immediately, the thoracic surgeon inserted a chest tube and 500 ml of blood was drained. Packed RBC were continuously administered, which helped maintain the arterial hematocrit level at 33-35%. Continuous low blood pressure (60-90/30-40 mmHg) and tachycardia (140-150 bpm) were observed. Hence, dopamine was continuously administered. Acidemia (pH = 7.051, Base Excess = -16 mEq/L) and hyperkalemia (K+ = 6.2 mmol/L) were found, so bicarbonate, calcium gluconate, and diuretics were intermittently administered. Midazolam and vecuronium were used for maintaining anesthesia. When 3U of Packed RBC were administered, the airway pressure started to slowly increase. When 24-26 cm H2O was measured, the tidal volume was decreased and the respiratory rate was increased. In a retaken chest x-ray (), a large amount of blood had not been drained from the right chest area, so a second tube was inserted in the chest. Afterwards, over 2,000 ml of blood was drained. Using a stethoscope, we found that the left pulmonary sound was reduced. Hence, in the next chest x-ray (), the right hemothorax was almost all gone, but a pneumothorax on the left-side was discovered. Thus, a third chest tube was inserted. However, the first and second chest tubes on the right-side continuously drained blood, and the blood pressure was not maintainable at 40-70 mmHg/20-40 mmHg. So, after discussions with the thoracic surgeon, a median sternotomy was done for hemostasis. A mid-surgery increase in hemorrhaging was predicted, so an 18 G intravenous catheter was inserted into the right external jugular vein. The hematocrit level in the arterial blood was maintained at 33-37%. The drop in blood pressure could not be corrected, so a large amount of epinephrine 0.5-1.0 µg/kg/min was continuously administered. Epinephrine (10-100 µg), bicarbonate, calcium gluconate, and diuretics were intermittently administered. In the sternotomy, damage to the main blood vessels (the subclavian vein, the subclavian artery, and the pulmonary artery and vein) was not discovered. However, a severe bulging of the parietal pleura in the upper portion of the right chest, a dissection between the parietal pleura and visceral pleura, and a hematoma between the 2 pleurae were observed (). In the posterior portion of the right upper thorax, there was an abscess pocket, which burst and leaked abscess in mid-surgery. The patient was assumed to be in a septic state, so the pediatrician administered dexamethazone 5 mg. However, the patient continued to have low blood pressure. The thoracic surgeon could not find the exact hemorrhage site on the right-side of the chest. Because of the progression of the disseminated coagulation disorder, it was deemed not viable to continue with the surgery, so the surgery was ended. While closing up the patient's chest, 900 cc of blood was drained from the chest tube. Packed RBC and fresh frozen plasma 3U were administered. A continuous high concentration of epinephrine and dopamine, intermittent epinephrine, calcium gluconate, and bicarbonate were administered. In the OR, the administered amount of fluid and blood amounted to Packed RBC 10 U, fresh frozen plasma 3 U, and fluid 3,000 ml. After surgery, the patient was moved to the ICU and connected to an EKG when bradycardia was observed. Atropine and epinephrine were administered, and blood pressure was reduced (60/30 mmHg). In the ICU, blood continued to drain from the chest tube. So Packed RBC were continuously administered, but the hematocrit level was 24%. Within 20 minutes of arriving at the ICU, the patient experienced cardiac arrest. Thus, cardiopulmonary resuscitation was immediately performed. A cardiac beat and a measurable blood pressure were found. However, 15 minutes later, cardiac arrest was again observed, so cardiopulmonary resuscitation was attempted. The patient died 1 hour after the end of surgery.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [19.0, 'kg'], 'height': [111.0, 'cm']}",15.42083,14.64979,16.19187,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 111.0 cm, which is 111.0 cm * 1 m / 100 cm = 1.11 m. The patient's weight is 19.0 kg. The patient's bmi is therefore 19.0 kg / (1.11 m * 1.11 m) = 15.42083 kg/m^2."
2421,6,Body Mass Index (BMI),physical,decimal,pmc-3259137-1,Extracted,"A 60-year-old female patient with a height of 150 cm and weight of 42 kg visited the pain clinic for continuous pelvic and coccyx pain which began simultaneously with multiple metastases 8 months earlier. The patient had been diagnosed with ovarian cancer 5 years previously and had undergone transabdominal hysterectomy and bilateral salpingo-oophorectomy. At the time of her visit, metastases to the lung, spleen, and peritoneum were observed, but there was no evidence of bone metastasis. The patient complained of splitting pain of the perianal area which continued for about 2 hours 3 times a day, on average, and of dull pelvic pain. The visual analogue scale (VAS) score was 9/10 and worsened during coughing or the Valsalva maneuver, and eased with standing or walking. Ultracet® 3 T/day and nortriptyline 10 mg/day were administered as drug treatment, and a caudal block was performed for pain control. The patient's pudendal pain had decreased, but she complained of continuous pelvic pain, so an additional SHPB was planned. During the procedure, the patient was placed in the prone position and a pillow was propped beneath her lower abdomen to decrease the lumbar lordosis. After checking the lumbar 4-5 intervertebral space with C-arm fluoroscopy, the skin was disinfected with betadine. Local anesthesia was performed using 1% lidocaine at a skin insertion point 5 cm to the right of the midline. Using a 15 cm, 22 G Chiba needle (Cook Medical Inc., Bloomington, IN, USA), we attempted to insert the needle at a 45 degree angle medioinferiorly, avoiding the transverse process of the L5 vertebra. However, the transverse process of the L5 vertebra and the iliac crest were in contact due to degenerative changes, so needle insertion failed (). Therefore, we decided to perform bilateral SHPB by inserting a catheter through the left superior hypogastric plexus. After checking the lumbar 4-5 intervertebral space through C-arm fluoroscopy, local anesthesia was performed using 1% lidocaine with at a skin insertion point 5 cm from the left of the midline. Then an 8 cm, 18 G epidural needle (Perican®, B-Braun Inc., Melsungen, Germany) was inserted and positioned. When the epidural catheter (Perifix®, B-Braun Inc., Melsungen, Germany) was inserted, a slight resistance was felt. It was similar to the resistance felt when inserting an epidural catheter through an epidural needle. Therefore, we advanced the epidural catheter approximately 3 cm farther from the epidural needle tip. Then, 2 ml of contrast media (Omnipaque300®) was injected, and after verifying the adequate spread of the contrast media, 0.38% ropivacaine 8 cc was injected (, ). After the procedure, the patient reported reduced pelvic pain, with a VAS score of 3/10, so three days later SHPB was performed by the same method. After confirming that there was no motor nerve loss, 6 ml of 99% dehydrated ethanol was injected, followed by 0.5 ml of normal saline to inject all the alcohol left in the catheter, and the catheter was removed. The patient's pain improved to 3/10 on the VAS without complications, and she was discharged.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [42.0, 'kg'], 'height': [150.0, 'cm']}",18.66667,17.73334,19.6,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 150.0 cm, which is 150.0 cm * 1 m / 100 cm = 1.5 m. The patient's weight is 42.0 kg. The patient's bmi is therefore 42.0 kg / (1.5 m * 1.5 m) = 18.66667 kg/m^2."
2422,6,Body Mass Index (BMI),physical,decimal,pmc-7796768-4,Extracted,"A 65-year-old male (weight 110 kg, height 186 cm) and 54-year-old female (weight 68 kg, height 165 cm) patients were scheduled for laparoscopic cholecystectomy. The total amount of fentanyl given in the male patient was 350 μg and 150 μg in the female patient. 2 h after surgery, the male patient-reported pain 5/10 at rest and 6/10 on coughing, and thus, 1 g paracetamol was given. After 4, 8, and 12 h, the pain was 4/10 at rest and on coughing and 1 g metamizole and 1 g paracetamol were given alternately. 24 h after surgery, the pain was 2/10 at rest and 3/10 on coughing and no analgesic was given. In the female patient, after 1 h of the surgery pain was 5/10 at rest and 6/10 on coughing, and thus, 1 g paracetamol was given. After 4, 8, and 12 h, the pain was 2/10 at rest and 5/10 on coughing and was treated alternately with paracetamol and metamizole. 24 h after surgery pain was 4/10 at rest and 5/10 on coughing, therefore, 1 g paracetamol was given.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [110.0, 'kg'], 'height': [186.0, 'cm']}",31.79558,30.2058,33.38536,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 186.0 cm, which is 186.0 cm * 1 m / 100 cm = 1.86 m. The patient's weight is 110.0 kg. The patient's bmi is therefore 110.0 kg / (1.86 m * 1.86 m) = 31.79558 kg/m^2."
2423,6,Body Mass Index (BMI),physical,decimal,pmc-4376932-1,Extracted,"Our patient was a 54-year-old male who presented with anuria, fever, and lower-leg edema. On June 3, 2012, the patient visited the urology department of a local community hospital with macroscopic hematuria and dysuria. He was diagnosed with acute prostatitis and began treatment with levofloxacin hydrate, loxoprofen sodium hydrate, and cernitin pollen extract. However, his condition did not improve, and he subsequently developed lower extremity numbness, bilateral flank pain, and diarrhea, followed by anuria. On June 11, he visited another hospital in his community and was eventually transferred to our hospital on June 13 for inpatient treatment of possible acute kidney injury.
Physical examination on admission revealed the following: height 175 cm; body weight 80 kg; systolic and diastolic blood pressure values 179 and 102 mm Hg, respectively; pulse 98 beats/min (regular), and body temperature 37.9°C. The patient had a normal mental status despite persistent headache. His palpebral conjunctivae indicated signs of anemia. Radiographic images showed no abnormal findings. Both lower limbs were edematous. The results of clinical laboratory tests obtained on admission are summarized in table . Urinalysis showed high protein levels (3 g/l), blood (+++), pyuria, and a fractional sodium excretion rate of 20.3%. Hematological analyses of peripheral blood yielded a white blood cell count of 9.61 × 109 cells/l (neutrophils 85.0%, lymphocytes 8.5%), a red blood cell count of 3.44 × 1012 cells/l, a hemoglobin level of 100 g/l, the presence of fragmented red blood cells, and a platelet count of 90 × 109 cells/l. C-reactive protein levels were as high as 160,900 μg/l. The fibrinogen degradation product level was 1.168 g/l, the prothrombin time was 45.6 s, and the fibrinogen level was 4.1 g/l. These measurements resulted in a disseminated intravascular coagulation score of 6 points. Serum biochemistry tests yielded a blood urea nitrogen level of 58.1 mmol/l and a creatinine level of 2,044 μmol/l, suggesting significant renal impairment. The lactate dehydrogenase level was 765 IU/l, and the haptoglobin level was below 1.2 μmol/l. The patient had hypoproteinemia, as evidenced by a total serum protein level of 58 g/l and an albumin level of 24 g/l. Serum samples were negative for anti-nuclear antibodies as well as myeloperoxidase- and proteinase 3-specific antineutrophil cytoplasmic autoantibodies, although anti-GBM antibody levels were high at 230 ELISA units. Stool examination was negative for occult blood, intestinal pathogens, and verotoxins. Plain chest radiographs revealed no alveolar hemorrhage or other abnormal signs. On interview, the patient reported a history of cervical disc herniation diagnosed at the age of 52 years. He had no noteworthy family history and was not taking any medications on a regular basis at the time of admission to our hospital.
Changes in platelet counts, lactate dehydrogenase levels, and mean blood pressure over time during the 119-day hospital stay are schematically represented in figure , along with major therapeutic interventions. Computed tomography (CT) imaging conducted on admission indicated renal atrophy and ascites, but no collapse of the inferior vena cava. These findings negated the possibility of prerenal and postrenal failure and suggested an acute aggravation of chronic kidney disease rather than a typical acute kidney injury. Since the patient had not undergone regular medical checkups, it was not clear whether proteinuria had existed in the past. During the early hospitalization period, we administered γ-globulin, diuretics, and hemodialysis, under the assumption that the patient had either sepsis- or drug-induced acute kidney injury. Peripheral blood smears revealed the presence of fragmented red blood cells (hospital day 2), suggesting hemolytic uremic syndrome (HUS) resulting from food poisoning caused by Escherichia coli O-157:H7 or other pathogenic strains. However, the patient had no diarrhea and was negative for intestinal pathogens and verotoxins. Epistaxis developed on hospital day 4, platelet counts and hemoglobin levels decreased to 29 × 109 cells/l and 55 g/l, respectively, and the lactate dehydrogenase level rose to 1,253 IU/l. The patient's anemia was unresponsive to erythropoiesis-stimulating therapy, and frequent blood transfusions were required (i.e., a total of 16 units of irradiated red cell concentrates). His fever remained in the range of 38-39°C despite treatment with γ-globulin. The patient was diagnosed with TMA [thrombotic thrombocytopenic purpura (TTP) or HUS] based on the following findings: thrombocytopenia, hemolytic anemia evidenced by anemic signs and elevated lactate dehydrogenase levels, signs of renal impairment, fever, bleeding episodes (i.e., epistaxis), neuropsychiatric manifestations (i.e., headache), direct and indirect Coombs test results, and haptoglobin levels below 1.2 μmol/l.
Assays conducted several days later indicated an ADAMTS13 activity of 31.6% (reference range 70-120%), and ADAMTS13 inhibitors were negative. Serum factor H measured by the ELISA method was 0.473 g/l (the standard value of factor H ranges from 0.3 to 0.6 g/l). These findings led us to administer plasma exchange therapy with a total of 30 units of fresh frozen plasma, starting on hospital day 8. On hospital day 15, steroid pulse therapy (3 methylprednisolone doses of 1,000 mg/day) was initiated to lower the elevated anti-GBM antibody level. Following the completion of this 3-day course, the patient was given oral prednisolone at a starting dose of 50 mg/day, which was gradually tapered and discontinued. After this, platelet counts rose to 197 × 109 cells/l, and kidney biopsy was conducted on hospital day 22 (fig. ). Seventeen glomeruli examined by optic microscopy all showed destructive patterns with characteristic architecture ranging from atypical proliferative changes to global sclerosis. Renal arterioles, both afferent and efferent, showed extensive endothelial cell edema and swelling, indicative of glomeruloid changes. Renal tubules showed focal atrophy with massive lymphocyte infiltration. Congo red staining of the biopsy specimen was negative. Electron microscopy showed that the loss of glomerular structure observed under optic microscopy was the result of an extensive and dense extracellular deposition of fibrillar components, which were larger in diameter than amyloid fibers and aggregated to form large bundles. Immunofluorescence analysis for immunoglobulin G and third component (C3) deposits was not carried out because of glomerular collapse. Available findings supported the diagnosis of FGN involving severe glomerular destruction. On hospital day 29, a second course of steroid pulse therapy was started due to significantly decreased platelet counts.
On hospital day 46, the mean blood pressure values started to increase gradually. Although the target body weight was lowered and arotinolol hydrochloride and methyldopa hydrate were added to nifedipine and candesartan cilexetil, these measures did not achieve successful blood pressure control.
On hospital day 56, the patient had a mild seizure. T2-weighted fluid-attenuated inversion recovery (FLAIR) magnetic resonance scans of the bilateral cerebellum, occipital lobe, and parietal lobe showed multiple high-intensity areas, suggesting a diagnosis of reversible posterior leukoencephalopathy syndrome (fig. ). Despite antihypertensive therapy with imidapril hydrochloride, carvedilol, nifedipine, and nitroglycerin infusion, hypertension persisted, and the patient's headache continued. On hospital day 61, generalized convulsions recurred, and head CT images showed multiple hemorrhagic lesions in the right temporal, right parietal, and right frontal lobes (fig. ). Doses of intravenous hemostatic medications were increased, while antihypertensive agents were administered nasogastrically. Blood pressure levels gradually decreased with the increase in platelet counts, starting around hospital day 65. On hospital day 72, the patient started rehabilitation exercises. The patient recovered enough to walk with a cane (fig. ). He was transferred to a rehabilitation hospital on hospital day 119.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [80.0, 'kg'], 'height': [175.0, 'cm']}",26.12245,24.81633,27.42857,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 175.0 cm, which is 175.0 cm * 1 m / 100 cm = 1.75 m. The patient's weight is 80.0 kg. The patient's bmi is therefore 80.0 kg / (1.75 m * 1.75 m) = 26.12245 kg/m^2."
2424,6,Body Mass Index (BMI),physical,decimal,pmc-4959676-1,Extracted,"A 70-year-old male with past medical history of hypertension only presented to the emergency department with left hand weakness and numbness for past 7 hours. He was unable to extend his wrist and fingers and had loss of sensation and paresthesia on the dorsum of the left hand. He had experienced a similar episode 3 days ago, which resolved in a few hours; the patient had initially attributed these symptoms to old age and muscle spasms. Today his symptoms did not resolve in the past few hours, hence he decided to come to the emergency room for further investigation. He denied any dizziness, lightheadedness, loss of consciousness, slurring of speech, ambulatory dysfunction, or difficulty maintaining balance. He denied any weakness or loss of sensation in any other extremity. His home medications were amlodipine, benazepril, and vitamin D3. He did have a family history significant for stroke and diabetes mellitus. He denied smoking or alcohol or drug abuse.
His vitals were temperature 36.9, heart rate 98, respiratory rate 20, blood pressure 140/65, oxygen saturation 98% on room, weight 68 kg, height 170 cm. On examination he was alert and oriented in time, place, and person. His gait and cranial nerves were intact. Motor examination demonstrated weakness of left wrist and finger extensor muscles with a muscle strength grading of −4. Strength in the left bicep, brachoradialis, tricep muscle, flexors of the fingers and wrist was normal. Sensory examination demonstrated mild decrease in sensation on the dorsal aspect of the left hand, predominantly in the anatomical snuff box. Strength and sensation in the other extremities were normal. Other systemic examinations were unremarkable.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [68.0, 'kg'], 'height': [170.0, 'cm']}",23.52941,22.35294,24.70588,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.7 m * 1.7 m) = 23.52941 kg/m^2."
2425,6,Body Mass Index (BMI),physical,decimal,usmle-7952,Extracted,"A 21-year-old woman presents with irregular menses, acne, and increased body hair growth. She says her average menstrual cycle lasts 36 days and states that she has heavy menstrual bleeding. She had her menarche at the age of 13 years. Her blood pressure is 125/80 mm Hg, heart rate is 79/min, respiratory rate is 14/min, and temperature is 36.7°C (98.1°F). Her body weight is 101.0 kg (222.7 lb) and height is 170 cm (5 ft 7 in). Physical examination shows papular acne on her forehead and cheeks. There are dark hairs present on her upper lip, periareolar region, linea alba, and hips, as well as darkening of the skin on the axilla and posterior neck.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [101.0, 'kg'], 'height': [170.0, 'cm']}",34.9481,33.20069,36.6955,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 101.0 kg. The patient's bmi is therefore 101.0 kg / (1.7 m * 1.7 m) = 34.9481 kg/m^2."
2426,6,Body Mass Index (BMI),physical,decimal,pmc-6528262-1,Extracted,"A 48-year old woman (weight 52 kg, height 152 cm, ASA II) was admitted in Sept 18th 2016 because of a ground glass opacity (GGO) which had been detected in the right lung 2 years ago. She had her left pneumonectomy through uniportal VATS owing to the left upper lobe adenocarcinoma invasive to the left main bronchus in Mar 2014. Her pre-operative diagnoses were GGO in the right upper lobe, suspect for malignancy and left postpneumonectomy (Fig. ). No abnormal findings were detected among other tests, and some of the important figures in the arterial blood gas test were showed as follows: pH 7.44, PaCO2 37 mmHg, PaO2 84 mmHg, SaO2 97.7%. Her pulmonary function test showed FEV1 46.9%, FEV1/FVC 83.3%, and her predicted postoperative FEV1% would be close to 44.7%. Although other tests of evaluating cardiopulmonary reserve function and lung parenchymal function were not performed, her regular 3-floor climbing activity was not compromised. The operation was scheduled as right anterior segmentectomy through uniportal VATS under general anesthesia. Routine monitoring was applied and the first data were recorded as follows: body temperature 36.7 °C, blood pressure 123/70 mmHg, heart rate 86/min and Sp02 98% when the patient was placed in a supine position in the operation room. After the insertion of an 18-gauge intravenous cannula and the right internal jugular vein catheter, intravenous induction was carried out with an injection of midazolam 0.03 mg/kg, sufentanil 0.6 μg/kg, propofol 1 mg/kg, and rocuronium 0.8 mg/kg. Intubation preparation: the patient was scheduled to have the right anterior segmentectomy through VATS after the left pneumonectomy, which entailed us to make a good balance between ventilation and collapse on the right lung only, to make good use of ventilation in the lower and middle lobes, and to produce an effective collapse in the upper lobar. After a prudent study of the following parameters, the diameter of the narrowest part of the tracheal is 11.9 mm, the length of right upper lobe bronchus is 6.2 mm, the angle of the right main bronchus and right upper lobe bronchus is close to 90 degree, the diameter of the bronchus intermedius is 8.8 mm, and the length of bronchus intermedius is about 15 mm, a 32 Fr left-sided DLT was chosen and adapted (Fig. ). Permission was granted by our hospital ethical committee to adapt the DLTs. The cutting edge of the tube should be smooth and clean, only in this way can we make sure that it won’t do any harm to the airways. One cut (cut just for once) would be best in adapting. Whether the cutting edge is qualified or not can be detected by our sensitive finger tips. And this technique has been proved safe from our experience in tracheal and bronchial operations. The 32Fr left-sided DLTs have been used among short women for left thoracic operations in our facility, and its external diameter is about 10.7 mm, the bronchial internal diameter is about 3.5 mm. But it’s our first time to insert the left-sided DLT to the right for the right lung surgery. As we can see from Fig. , the mediastinum has shifted to the left, the intubation should be gentle and carried out by an experienced anesthesiologist in case of any possible injury or even perforation to the former carina. After induction, we performed a FOB (3.0 mm diameter) guided endobronchial intubation with the bronchial cuff into the right bronchus intermedius, and the tracheal cuff’s orifice up against the upper bronchial port (Fig. ), in this way, the ventilation of the dependent right middle and lower lobes and the collapse of the upper lobar were guaranteed (Fig. ), thus an appropriate balance between surgical field and oxygenation was achieved, and the blood and sputum from the upper lobe bronchial port can be sucked out. An automatic infusion of propofol and sufentanil combined with manual administration of rocuronium maintained the anesthesia for the operation. And a lung protective mechanical ventilation strategy was taken, positive end-expiratory pressure (PEEP) 5 cmH2O, tidal volume (Vt) 4–6 ml/kg, frequency 15–18/min. In the meantime, end tidal CO2 and arterial blood gas analysis were recorded to adjust ventilation. The lung recruitment, air leak test and sputum suction went well throughout the operation and the surgery was completed as planned. The patient recovered well after the surgery, so she was extubated in the operation room and sent to the postanesthesia care unit (PACU) for transition, where a routine oxygen supplementation was applied. Oxygenation, ventilation, and circulation were all strictly monitored and no adverse events were recorded in the PACU. She recovered better on the next day follow-up and was discharged from the hospital 6 days later. The pathological diagnosis was invasive adenocarcinoma.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [52.0, 'kg'], 'height': [152.0, 'cm']}",22.50693,21.38158,23.63228,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 152.0 cm, which is 152.0 cm * 1 m / 100 cm = 1.52 m. The patient's weight is 52.0 kg. The patient's bmi is therefore 52.0 kg / (1.52 m * 1.52 m) = 22.50693 kg/m^2."
2427,6,Body Mass Index (BMI),physical,decimal,pmc-7841863-1,Extracted,"A 22-year-old Chinese man with a 2-year history of hypertension and left flank pain after activity was admitted to the Department of Interventional Radiology, the First Hospital Affiliated to the University of Science and Technology of China. The patient’s hypertension and left flank pain had often occurred simultaneously throughout the last 2 years, with his blood pressure fluctuating within 130–150/90–100 mmHg without treatment. Seven months previously, he had developed severe headache and worsening left flank pain, and his blood pressure reached 200/105 mmHg. Amlodipine (5 mg twice daily) and spironolactone (40 mg twice daily) were administered to reduce his blood pressure, but treatment was ineffective. His blood pressure had recently fluctuated within 150–180/95–110 mmHg, and he was hospitalized for further investigation.
On admission, the patient was 182 cm tall and weighed 68 kg. Physical examination revealed slight throbbing pain over the left kidney area with a visual analog scale score of 4. No other obvious abnormalities were found.
Laboratory data revealed a normal 24-hour urine protein level at 135 mg (reference range, 0–150 mg/24 hours), microscopic hematuria (2+), and increased plasma renin activity (renin activity, aldosterone, angiotensin I, and angiotensin II) (). Color Doppler ultrasound examination (HD9 color Doppler ultrasound system; Philips, Amsterdam, Netherlands) revealed diffuse renal lesions, a broadened inner diameter of the LRV (approximately 12.7 mm), and an inner LRV diameter of 4.1 mm at the level of the SMA–aorta angle. These findings were consistent with a diagnosis of NCS (). In addition, a computed tomography (CT) examination was performed using a GE Discovery CT750 (GE Healthcare, Chicago, IL, USA) with the following scanning parameters: tube voltage, 120 kV; tube current, 160–360 mA; scanning slice thickness, 5 mm; and reconstruction slice thickness, 1.25 mm. CT angiography (CTA) confirmed NCS (). The patient had no history of familial hypertension or special medications. His thyroid function, cortisol concentration, prolactin concentration, and adrenocorticotropic hormone concentration were normal. Thin-section enhanced CT of the adrenals showed no adrenal enlargement or occupying lesions. Pituitary magnetic resonance imaging showed no abnormalities. Renal artery CTA showed no stenosis. None of the above secondary hypertension-related examinations showed significant abnormalities. These findings indicated the possibility that the hypertension might be associated with the observed abnormal LRV anatomy.
Selective renal arteriography and venography (GE Innova 3100; GE Healthcare) were performed. The renal arteriography data were normal, but left renal venography indicated that the LRV was significantly narrowed before descending into the inferior vena cava, with clear regular compression; the anterior vein was significantly dilated (approximately 13 mm), and left-side varicoceles were seen (). The inferior vena cava pressure was 6 mmHg, and the LRV pressure was 15 mmHg. These findings confirmed a definitive diagnosis of NCS.
Considering that the patient had severe flank pain and that his hypertension might have been associated with this pain, an endovascular stent (14 × 60 mm; C. R. Bard, Murray Hill, NJ, USA) was placed into the stenosed part of the LRV. As a result, normal blood flow resumed and the collateral circulation was reduced (). Follow-up renal venography revealed a 2-mmHg pressure gradient between the LRV and inferior vena cava. Finally, the patient’s blood pressure was reduced to 130–140/80–95 mmHg 1 day later without drugs, and his 3-day postoperative visual analog scale score for the left flank pain was reduced to 1 to 2. Aspirin (0.1 once daily; Bayer, Leverkusen, Germany) and clopidogrel (75 mg once daily; Sanofi, Paris, France) were administered as a blood thinner and decongestant, respectively. The hypertension and flank pain did not recur during the following 11 months. Because the patient declined to undergo a biopsy, a pathological examination could not be performed.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [68.0, 'kg'], 'height': [182.0, 'cm']}",20.52892,19.50247,21.55537,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 182.0 cm, which is 182.0 cm * 1 m / 100 cm = 1.82 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.82 m * 1.82 m) = 20.52892 kg/m^2."
2428,6,Body Mass Index (BMI),physical,decimal,pmc-8344967-1,Extracted,"A 5-year-old boy with normal past medical history was admitted to Haiphong Children's Hospital with abdominal pain around the navel after having symptoms for 5 h. He also had a mild fever and an inability to pass stool or gas. On physical examination, the boy was conscious, able to communicate but tired, with a temperature of 37.5°C. His pulse rate was 100 beats per minute; his blood pressure was 90/60 mmHg; and the respiratory rate was 30 breaths per minute. His height was 100 cm, and he weighed 18 kg. All of these numbers were in the normal range for his age. The abdominal examination noted that he had abdominal distension and obvious abdominal muscle guarding in the right iliac and umbilical region. His complete blood count: the number of white blood cells was 14.8 × 109/L, neutrophils accounted for 75.8%, and serum C-reactive protein (CRP) was 21 mg/L. The abdominal ultrasound result showed that his intestines contained fluid and increase motility. The abdominal X-ray did not show abnormal images (See Figure ).
He was diagnosed with acute appendicitis and had had laparoscopic surgery. We saw little fluid around intestines through the laparoscopic camera, with no pseudomembrane, no Douglas fluid, and a normal appendix. While examining the ileum, we did not find Meckel's diverticulums but a sharp foreign object that punctured the intestine from the lumen of the intestine to the outside, about 35 cm from the ileum—cecum (See Figures and ). After that, we removed the foreign object, stitched the hole in the intestine, cleaned the abdomen, and closed incisions.
The boy made a full recovery and was discharged in a satisfactory condition following 7 days of treatment",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [18.0, 'kg'], 'height': [100.0, 'cm']}",18,17.1,18.9,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 100.0 cm, which is 100.0 cm * 1 m / 100 cm = 1.0 m. The patient's weight is 18.0 kg. The patient's bmi is therefore 18.0 kg / (1.0 m * 1.0 m) = 18.0 kg/m^2."
2429,6,Body Mass Index (BMI),physical,decimal,pmc-5818729-1,Extracted,"The patient was a 65-year-old man (177 cm, 78 kg). He had a history of right upper lobectomy for adenocarcinoma in the right upper lobe 3 years prior. He was admitted to our hospital for VATS (Video Assisted Thoracic Surgery) S6 segmentectomy for the recurrence cancer. He had no other past history of note, and had no medication before hospitalization. He smoked 1 pack of cigarette per day for 45 years. Preoperative laboratory test showed no abnormality. Preoperative electrocardiogram showed arterial fibrillation for the first time, and intravenous unfractionated heparin infusion started after the hospitalization. Heparin infusion was stopped 6 h before operation.
VATS S6 segmentectomy was successfully performed with the patient in the left lateral position. Anesthesia was maintained with sevoflurane (1.0–1.5 %) and remifentanil with left one-lung ventilation. After the chest closure, the patient was repositioned to the supine and we stopped sevoflurane administration. Before emergence from anesthesia, massive bleeding started suddenly from the drainage tube placed in the right thorax. The patient’s systolic blood pressure decreased to 30 mmHg and end-tidal CO2 (EtCO2) also decreased from 40 to 10 mmHg. The patient was immediately placed in the head-down position, his head cooled with the ice pack for the cerebral protection, a hemodialysis catheter inserted from his right internal jugular vein for the purpose of rapid transfusion. After the rapid transfusion of crystalloids, hetastarch, and blood products along with inotrope infusions (dopamine and norepinephrine), his systolic blood pressure increased to 60 mmHg but he was hemodynamically unstable. Right pulmonary artery rupture was suspected. Surgeon decided there was urgent need to complete hemostasis and only in the lateral position should the culprit artery be accessible. Then the patient was placed in the left lateral position again for the open chest hemostasis. Left one-lung ventilation was started again, and then his right chest was re-opened.
As soon as thoracotomy, his systolic blood pressure fell to 50 mmHg followed by the ventricular fibrillation (VF). The patient’s body temperature was 36.9 °C. Defibrillation (biphasic, 200J) was immediately delivered, but electrocardiogram (ECG) showed asystole and we started CPR. The patient was firmly fixed in the left lateral position and immediate conversion to the supine position for chest compression was impossible. Direct heart compression seemed infeasible because of firmly adhesive right lung and mediastinum. Extracorporeal CPR seemed also infeasible because of firmly fixed lateral positioning. So chest compression by two surgeons started with the patient in the lateral position (Fig. ). One surgeon stood in front of the patient and placed his both palms on patient’s sternum, another surgeon placed his both palms on the patient’s mid-thoracic spine from his back, and chest compression was performed from both sides simultaneously at approximately 100 times per minute. During chest compression, the patient’s arterial pressure waveform appeared sinusoidal in tune with chest compression with systolic value about 35–50 mmHg, and diastolic value about 25–35 mmHg. EtCO2 was 5–20 mmHg. One-lung ventilation was returned to two-lung ventilation. Pulse check was performed every 2 min during CPR and ECG showed asystole every time, and then chest compression by two practitioners was restarted after intravenous bolus infusion of 1 mg epinephrine. The culprit of bleeding was right main pulmonary artery. We also used an auto-transfusion system so as to conserve blood transfusion. After the anastomosis and hemostasis of culprit right pulmonary artery, the waveforms of ECG changed from asystole to VF, and two times of defibrillation (biphasic, 200J) were delivered, which was effective. ECG waveform converted to sinus rhythm and the patient’s pulse became palpable, so we stopped CPR. CPR time was 25 min. During the reminder of the procedure the patient was hemodynamically stable under the high dose of inotrope infusion (epinephrine, norepinephrine, and dopamine). After the final check of hemostasis the patient’s chest was closed and the operation finished. The overview of resuscitation is shown in the Fig. . The patient received 2520 ml of packed red blood cells, 1200 ml of fresh frozen plasma, 200 ml of platelet and 2600 ml of intraoperative blood salvage, in addition to 5350 ml of fluid administration. At the end of surgery, the patient’s body temperature was 35.7 °C. He showed bilateral mydriasis and loss of light reflex.
The patient was transferred to ICU intubated and ventilated. All the sedatives were stopped for the neurological evaluation. Three hours after the operation, bilateral light reflex appeared. Approximately 6 h after the operation, the patient regained conscious and responded to verbal commands. No apparent limb paralysis was observed. The patient’s body temperature was kept around 36.0 °C. On the second postoperative day he was extubated. His Glasgow Coma Scale (GCS) score was E4V5M6 at the time of extubation. He was re-intubated on the 5th day of operation due to the deterioration of oxygenation, and underwent tracheostomy on the 7th day of operation. He was enrolled in a pulmonary rehabilitation program, and was successfully weaned from artificial ventilation on the 36th day of operation. His tracheostomy hole healed itself and closed during hospitalization. He was discharged from our hospital on the 60th day of operation without any cardiac and neurological complication. No head CT or MRI scan was performed after the surgery because the patient showed no neurological abnormality.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [78.0, 'kg'], 'height': [177.0, 'cm']}",24.89706,23.65221,26.14191,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 177.0 cm, which is 177.0 cm * 1 m / 100 cm = 1.77 m. The patient's weight is 78.0 kg. The patient's bmi is therefore 78.0 kg / (1.77 m * 1.77 m) = 24.89706 kg/m^2."
2430,6,Body Mass Index (BMI),physical,decimal,pmc-8495443-1,Extracted,"A 33-year-old Egyptian female with a 4-week history of fever, abdominal pain, malaise, and progressive fatigue was referred for hospital admission after being discovered to have pancytopenia. She had a 5-year history of SLE and antiphospholipid syndrome (APS) featuring arthritis, oral ulcers, leukopenia, positive antinuclear antibodies (ANA), Anti-double stranded DNA (Anti-dsDNA), recurrent venous thromboembolism (VTE), miscarriages, and antiphospholipid antibodies, confirming the diagnosis of SLE (ACR 5/11 and SLICC 5/13) with APS [, ]. She had no previous history of skin rash, For the previous 8 months, she had been taking hydroxychloroquine (400 mg/day), prednisolone (7.5 mg/day), and warfarin (5 mg/day). Upon admission, she was febrile with a maximum temperature of 38.6 °C, pulse was 107 beats per minute, and she had otherwise normal vital signs. She had a height of 175 cm and weighed 80 kg. Physical examination revealed an enlarged liver of 3 cm and a spleen of 4 cm palpable below the costal margin, while examination of the respiratory system, nervous system, and precordium was normal. Laboratory studies showed pancytopenia, reticulocytosis, hyponatremia, liver dysfunction, and proteinuria. Further workup showed that she had marked elevated d-dimer, ferritin, lactate dehydrogenase (LDH), and triglycerides, prolonged activated partial thromboplastin time (aPTT), decreased complement levels (C3), and elevated erythrocyte sedimentation rate (ESR), with positive direct antiglobulin (Coombs) test. A 24-hour urine protein test demonstrated proteinuria in the subnephrotic range (0.54 g/24 hours). Abdominal ultrasonography confirmed hepatosplenomegaly, while chest X-ray and echocardiography were normal. The SLE Disease Activity Index (SLEDAI) score was 11, indicating a moderate flare.
Our differential diagnosis was taken into consideration: MAS, SLE flare-up, viral infection, sepsis, leukemia, and lymphoma. The diagnosis, however, was difficult in part owing to strong similarities between MAS, SLE flare, and sepsis. Repeated blood, urine cultures, and viral panels for SARS-CoV-2, hepatitis B and C viruses, Epstein–Barr virus, herpes simplex virus, coxsackievirus, cytomegalovirus, human immunodeficiency virus, and parvovirus B19 were all shown to be negative. Renal biopsy was considered. However, due to the patient’s severe thrombocytopenia, it was postponed.
Based on the laboratory and clinical findings in accordance with the HLH diagnostic criteria, a diagnosis of MAS secondary to SLE flare was made. Intravenous methylprednisolone (mPSL) 1 g/day for 3 days followed by oral prednisone 60 mg daily and IVIG 2 g/kg over 5 days was started. Subsequently, oral cyclosporine 300 mg daily was started. The fever, abdominal pain, malaise, and fatigue were partially resolved while her counts were a little improved 7 days after starting treatment. Hence, we decided to switch from oral prednisolone to intravenous DSP 9 mg/day. Within 4 days, the platelet, white blood cell (WBC) counts, hemoglobin, inflammatory indices, LDH, and ferritin levels all eventually returned to normal (Table ).
Afterward, following the late acceptance of her husband, a bone marrow biopsy was performed 7 days after starting the treatment with mPSL, which showed focal evidence of hemophagocytosis (Fig. ). The patient was discharged without symptoms, with monthly follow-up of complete blood count, LDH, ferritin, 24-hour urine protein, anti-dsDNA antibody, and complement levels. Oral prednisone was gradually tapered to 20 mg daily, and oral cyclosporine of 300 mg daily was continued. One year after treatment, the patient remains symptom-free without any potential adverse effects of the adherent medications, and the patient-reported outcome shows patient satisfaction.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [80.0, 'kg'], 'height': [175.0, 'cm']}",26.12245,24.81633,27.42857,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 175.0 cm, which is 175.0 cm * 1 m / 100 cm = 1.75 m. The patient's weight is 80.0 kg. The patient's bmi is therefore 80.0 kg / (1.75 m * 1.75 m) = 26.12245 kg/m^2."
2431,6,Body Mass Index (BMI),physical,decimal,pmc-5618396-1,Extracted,"A 51-year-old Japanese woman was admitted for evaluation of proteinuria in 2011. She had a history of appendicitis at 12 years of age, cholelithiasis at 30 years of age, myoma at 46 years of age, and at least a 5-year history of dyslipidemia. Proteinuria (1+) had been first identified during a medical checkup 3 years prior and was ignored until increasing to 3+ in 2011. Her parents and brothers suffered from dyslipidemia but had no history of renal disease.
On admission, her height and weight were 161 cm and 49 kg, respectively, and her blood pressure was 137/94 mm Hg. On physical examination, slight pitting edema was observed; however, there were no xanthomas. Urinary protein excretion was 4.12 g/g Cre, and the serum triglyceride level was high. She did not exhibit nephrotic syndrome. The other laboratory findings are shown in Table . A computed tomography scan showed neither atrophy nor enlargement of the kidneys.
A renal biopsy specimen was processed in August 2011 using standard methods, and in the sections for light microscopy, the renal cortex was found to contain 11 glomeruli, 2 of which showed sclerosis. The remaining glomeruli were enlarged by distinct dilatation of the capillary lumina, which were filled with thrombus-like substances that stained slightly with periodic acid-Schiff. Some glomeruli exhibited moderate mesangial cell proliferation and increased mesangial matrix, and double contours of the capillary wall were partially observed. No crescents or adhesion in glomeruli were found (Fig. –c). A direct immunofluorescence showed no deposition of IgG, IgA, IgM, C1q, C3, or fibrinogen in glomeruli. Staining with Oil red O showed lipid droplets in the capillary lumina, which were stained positive for apoE (Fig. , e). Electron microscopic findings showed capillary dilation and occlusion with numerous lamellated lipid granules. Thin basement membranes with swollen endothelial cells were also observed. The histological findings and the results of apoE analysis (described below) satisfied the diagnostic criteria for LPG [].
Treatment with fenofibrate and irbesartan was initiated. Two weeks later, serum triglycerides and urinary protein excretion were reduced to 200 mg/dL and 1 g/g Cre, respectively. Two months later, the former was within the normal range, and the latter was reduced to less than 0.5 g/g Cre. Eight months later, urinary protein excretion ceased and did not recur thereafter (Fig. ).
In a second biopsy in August 2013, the specimen contained 22 glomeruli, 4 of which were obsolescent. Two of the glomeruli were filled with thrombi, but thrombi were absent in the other glomeruli (Fig. ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [49.0, 'kg'], 'height': [161.0, 'cm']}",18.90359,17.95841,19.84877,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 161.0 cm, which is 161.0 cm * 1 m / 100 cm = 1.61 m. The patient's weight is 49.0 kg. The patient's bmi is therefore 49.0 kg / (1.61 m * 1.61 m) = 18.90359 kg/m^2."
2432,6,Body Mass Index (BMI),physical,decimal,pmc-2740281-1,Extracted,"A 57-year-old Caucasian female presented to our emergency department complaining of neck pain one month after having a fall from a height and an injury on her occipital bone. The patient was non-smoking, non-drinking and with a free medical history. She weighed 61 kg and had a height of 162 cm.
The patient had already visited two physicians. The first assessment was made at the day of the injury at a hospital elsewhere. This first clinical examination revealed pain at the cervical spine and deficiency in the range of the cervical spine motion but no neurologic impairment was present. No radiologic examination was ordered and the patient received analgesics and recommendation for physiotherapy sessions. Persistence of pain led to a second assessment by another physician one week later at another hospital. Analgesics were once more prescribed and radiological screening was once more not considered essential.
On examination in our department, the patient showed no neurologic deficit, whereas restriction of range of motion and pain remained. Three-view radiographs (lateral, anteroposterior and odondoid) ordered by the attending emergency physician showed bilateral C5-C6 dislocation causing instability (Figure ). CT and MRI scan showed olisthesis of C5 over C6, anterior angulation and narrowing of the spinal canal without spinal cord pressure from disc material (Figure ). The electrophysiological testing was normal.
The patient was transferred to the operating theatre at the day of the admission. Open reduction of the bilateral dislocation and spinal fusion with posterior instrumentation were performed under continuous intraoperative neurophysiological monitoring (Figure ). Duration of hospitalization was four days. Mobilization began the second postoperative day and the patient was discharged using a Philadelphia collar. After twelve months of follow up, the patient reported free of complaints and with excellent return to her every day activities.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.0, 'kg'], 'height': [162.0, 'cm']}",23.24341,22.08124,24.40558,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.0 cm, which is 162.0 cm * 1 m / 100 cm = 1.62 m. The patient's weight is 61.0 kg. The patient's bmi is therefore 61.0 kg / (1.62 m * 1.62 m) = 23.24341 kg/m^2."
2433,6,Body Mass Index (BMI),physical,decimal,pmc-2547098-1,Extracted,"A 43-years-old Caucasian male (height 198 cm, weight 115 kg, tobacco smoker – 1 packet of cigarettes/day) was admitted to the intensive care unit (ICU) of a university hospital from a municipal hospital because of multiorgan dysfunction syndrome associated with infection and necrosis of the skin, subcutaneous tissue, and fascia of the left lower leg. The signs and symptoms of the disease – edema and pain affecting the left leg-began 7 days before admission. The patient's medical history was significant for hepatitis C (HCV), treated with ribavarin and interferon, and diabetes mellitus treated with insulin. On the day of admission the HCV-RNA test was negative. A mosquito bite was the probable triggering event.
On admission to the ICU the patient was confused, with a Glasgow Coma Scale (GCS) of 9. He was afebrile, had tachycardia, with a heart rate of 120 beats per minute, hypotension, with a blood pressure of 90/50 mmHg, and relative respiratory insufficiency (oxygen saturation of 88% – 90%). He had moderately-dilated pupils with a delayed light reflex. We noted crepitus over the bilateral lung fields, a tender abdomen with absent bowel sounds, and oliguria. There were numerous hemorrhagic extravasations on the skin. Examination of the left leg revealed diffuse edema of the skin, with marked erythema and necrosis; margins of infection were sharply demarcated, spreading onto the buttock and perineum on the left side (Figure ). Laboratory tests showed a metabolic acidosis, with the following values: base excess -15 mmol/l, lactate level 7.3 mmol/l, PaO2 64 mmHg, platelet count 29,000/mm3, International Normalized Ratio (INR) 2.24, serum creatinine 691.6 μmol/l, bilirubin 62.6 μmol/l, and C-reactive Protein (CRP) 224.6 μg/dl.
The Acute Physiology and Chronic Health Evaluation (APACHE) II score on the day of admission was 31 points and the Sequential Organ Failure Assessment (SOFA) score was 18 points. The patient required fluid resuscitation, endotracheal intubation, mechanical ventilation in BiPAP (bilevel positive airway pressure) mode, continuous intravenous infusion of catecholamines (epinephrine, norepinephrine) and low doses of steroids to restore blood pressure. After obtaining cultures from the affected tissue, blood and bronchoalveolar lavage (BAL) in appropriate media, empirical, broad-spectrum antibiotics were immediately administered (meropenem 3 g/day in a 3-h infusion, vancomycin 3 g/day in continuous infusion, metronidazole 1.5/day in 3 divided doses). Because of progressive organ dysfunction, therapy was started with activated protein C, in doses of 24 μg/kg/h; continuous veno-venous hemofiltration (CVVH) was also started. After several hours, the patient developed atrial fibrillation with a ventricular rate of 140 beats per minute and his blood pressure decreased to 80/50 mmHg. Electrical cardioversion was performed three times, followed by continuous infusion of cordarone (12 mg/kg/day). During this time, intensive fluid resuscitation was administered. During the first day, the patient received 12,800 ml of fluid (colloids and crystalloids). His unstable condition did not allow for early surgical management.
The cultures from the affected areas of skin contained Streptococcus pyogenes and Staphylococcus sciuri. Based on sensitivity results, vancomycin and metronidazole were discontinued, and penicillin G was started at a dose of 60 million units a day (intravenous) in 6 divided doses. Because the patient's poor condition persisted and the microbes were sensitive to clindamycin, it was added at 2.7 g/day in 3 divided doses. In spite of the lack of information about G-pathogens, meropenem was continued. The patient also received 40 g of commercially available gamma-globulin (intravenous), 8 units of packed red blood cells, 6 units of fresh frozen plasma, and 8 units of platelets. After several days his condition improved, with urine output of 100–150 ml/h and resolution of his metabolic acidosis. On the sixth day, the patient's hemodynamic parameters deteriorated again, with tachycardia to 160 beats per minute and a decrease in blood pressure to 85/60 mmHg. CVVH was administered again for detoxification. On the seventh day, the necrotic tissue was surgically excised (Figures , ). We also noted a progressive decline in the white blood cell count to 2,200/mm3, and administered granulocyte colony stimulating factor.
Cultures of the BAL showed 104 colony-forming units/ml of methycillin resistant Staphylococcus aureus (MRSA). (The patient had been a carrier of methycillin susceptible Staphylococcus aureus [MSSA] isolated from his nose vestibule on admission.) Because MRSA also was present in blood cultures and the patient's condition remained poor, linezolid 1.2 g a day in 2 divided doses was initiated based on additional results of susceptibility tests. After 10 days of intensive treatment, the patient was hemodynamically stable, and we discontinued mechanical ventilation. 25 days after admission the patient was discharged to the trauma surgery ward for plastic reconstruction of his wounds.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [115.0, 'kg'], 'height': [198.0, 'cm']}",29.33374,27.86705,30.80043,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 198.0 cm, which is 198.0 cm * 1 m / 100 cm = 1.98 m. The patient's weight is 115.0 kg. The patient's bmi is therefore 115.0 kg / (1.98 m * 1.98 m) = 29.33374 kg/m^2."
2434,6,Body Mass Index (BMI),physical,decimal,pmc-3762013-1,Extracted,"A 5-day-old male baby presented with enlarging head size and multiple physical abnormalities. He was the first child of nonconsanguineous parents. The pregnancy had been uneventful. He was born by caesarean section with birth weight of 2600 gm (5th centile), length 50 cm (50th centile), and head circumference 38 cm (>90th centile). The baby was on breast feeds. There was no relevant family history.
On physical examination, the baby had marked right-sided hemihypertrophy involving face and cranium. The facial hemihypertrophy included enlarged palpebral fissure, cheek, ear, and lip []. There was marked wasting of subcutaneous tissue of arms and thighs on both sides. Capillary hemangioma large in size was present in both flanks. There was venous prominence over scalp and trunk. Multiple subcutaneous masses were palpable over both thighs clinically appearing to be lipomas. The second and third toes of the left foot were significantly enlarged []. The head circumference has increased to 39.2 cm (95th centile).
A cranial ultrasonogram (USG) was carried out which revealed selective dilatation of the right ventricle with partial occlusion of the right foramen of monro []. The brain parenchyma, left lateral ventricle, corpus callosum and cerebellum were normal. The cranial USG finding together with rapidly increasing head circumference in our patient indicated toward right-sided unilateral hydrocephalus. Computed tomography of the head was advised to confirm the USG finding and to detect any other associated CNS anomalies. But the baby became lethargic on day 7 of life. He developed marked respiratory distress. Examination revealed a bluish discoloration over anterior trunk and a large venous prominence visible over left side of chest and abdomen originating from mid axillae with flow from upward to downward []. The platelet count was 30×103/μl. Other parameters of hemogram and sepsis screen were normal. Duplex scan of chest and abdomen was advised but the baby died before the investigation. Parents refused to go for autopsy.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [2600.0, 'g'], 'height': [50.0, 'cm']}",10.4,9.88,10.92,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 50.0 cm, which is 50.0 cm * 1 m / 100 cm = 0.5 m. The patient's weight is 2600.0 g so this converts to 2600.0 lbs * kg/1000 g = 2.6 kg. The patient's bmi is therefore 2.6 kg / (0.5 m * 0.5 m) = 10.4 kg/m^2."
2435,6,Body Mass Index (BMI),physical,decimal,pmc-7318102-3,Extracted,"Patient IV-2 is a 5-year-old boy. He is the stepbrother of patient IV-4 and his parents are first cousins. The pregnancy course and delivery were unremarkable. The patient's growth parameters after delivery were within the normal range. Since birth, the patient was found to have bilateral club feet and were floppy. Additionally, he has a global developmental delay.
Currently, his height and weight are below the third percentile—height: 97 cm, weight: 13.7 kg, and head circumference: 50 cm at the 25th percentile. The patient exhibits dysmorphic features, that is, a triangular face, bulbous nose, everted ears, short and flat philtrum, and retrognathia. The patient displays mild axial hypotonia and he has club feet showing dorsal clonus. All other systemic examinations were normal.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [13.7, 'kg'], 'height': [97.0, 'cm']}",14.56053,13.8325,15.28856,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 97.0 cm, which is 97.0 cm * 1 m / 100 cm = 0.97 m. The patient's weight is 13.7 kg. The patient's bmi is therefore 13.7 kg / (0.97 m * 0.97 m) = 14.56053 kg/m^2."
2436,6,Body Mass Index (BMI),physical,decimal,pmc-6220483-1,Extracted,"A 7-year-old male patient who presented at the Neurology service for a headache in his right temporal region that had evolved during one week, of intermittent nature, mild to moderate intensity, each episode between 3-4 seconds; and with subsequent, complete recovery. No history of trauma; he denies presenting fever or other systemic manifestations. There was no distal coldness, crying, or pallor, no feeling of dizziness, nausea, emesis, photophobia, phonophobia, or autonomic symptoms, no relationship with valsalva, or associated with exercise. Neither the patient nor his parents identified any triggering factors.
The patient reports four episodes of PSH in the week prior to the consultation, without interfering with his sleep hours. There is no history of other neurological symptoms, epileptic seizures or changes in personality. The interrogation did not recognize alterations in neurodevelopment, he presents a good school performance and an adequate sleep pattern. No personal background of relevance. No headaches or other related pathologies are reported in the family history.
On physical examination, he presented normal vital signs, a weight of 22 kg and 1.22 m of height. In the neurological examination, neither alterations nor skin stigmas indicative of neuro-cutaneous syndromes were identified.
The intervention was started with a one-month observation period, in which the child's caregiver was asked to prepare a headache diary that would allow characterizing and quantifying the episodes (date and time, laterality, associated activity, duration and need for medication).
The following month, he was cited for a control, where 21 episodes were quantified with the clinical characteristics described above but without a predominant laterality; no triggering or attenuating factors were identified. A simple and contrasted cerebral magnetic resonance imaging was performed, which showed no alterations of any kind. Based on the characteristics of the episodes, the clinical course and the results of the MRI, he was diagnosed with PSH, so a therapeutic test was prescribed with Coenzyme Q10, in a dose of one 100-mg tablet given orally every 12 hours as a prophylactic treatment, and the diary registry of headaches continued.
After two months of administration of Coenzyme Q10, no improvement in symptoms was identified. Due to this therapeutic failure, it was decided to suspend that medication. Two weeks later, it was initiated a new treatment with half a tablet of 1.5 mg melatonin daily (0.07 mg/kg), administered at night; with this therapy, it was achieved a reduction in the frequency of headaches during the first two weeks of treatment: only two episodes occurred during this period. Along the six months of follow-up, no new episodes or adverse effects have been documented (), and both tolerability and therapeutic adherence have been optimal, as assessed by the scale of 8-item therapeutic adherence of Morisky .",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [22.0, 'kg'], 'height': [1.22, 'm']}",14.78097,14.04192,15.52002,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.22 m. The patient's weight is 22.0 kg. The patient's bmi is therefore 22.0 kg / (1.22 m * 1.22 m) = 14.78097 kg/m^2."
2437,6,Body Mass Index (BMI),physical,decimal,pmc-2740151-1,Extracted,"A 58-year-old woman, a University Lecturer of Yoruba ethnicity in Nigeria. She weighed 52 kg and 1.55 m in heght. She presented on 2nd of January 2007 with 4 days history of an insidious onset of right hypochondrial colicky abdominal pain which progressed and became generalized a day prior to admission. It was associated with anorexia, nausea and one episode of non - bilious, projectile vomiting. She had dyspepsia and early satiety a couple of days prior to the onset of abdominal pain. Although she also had low grade fever there were no chills and rigor. She was never fat intolerant and had not suffered previous jaundice. She is Para 3 + 0 3 alive woman last menstrual period was 12 years ago. She neither drink alcohol nor smoke cigerratte.
Physical examination essentially revealed an exhausted, dehydrated, tachycardic (pulse rate of 120 per minute, small volume but regular) woman in painful distress with a Blood Pressure of 140/100 mmHg. There was a firm, tender, irregularly surfaced globular abdominal mass measuring 20 cm lengthwise and extending from her right hypochondrium to the iliac fossa. Its upper limit was tucked under the rib cage and could not be reached. Although bowel sounds were hypoactive, there was no clinically demonstrable ascites.
Clinical diagnosis of infected mucocoele or empyema of the gallbladder was entertained with a differential diagnosis of infected hepatic cyst. Ultrasonography and Computerized axial tomography respectively reported mucocoele and empyema of the gallbladder with impacted stone at the neck. Her haematocrit was 39% and except for a mild azotaemia (urea level of 6.3 mmol/L), possibly due to dehydration, the electrolytes were within normal limits. Electrocardiogram showed occasional supraventricular ectopic beat.
She was adequately resuscitated with intravenous fluid and antibiotics and analgesic (intravenous ceftriaxone and intramuscular petazocine). She then had an emergency exploratory laparotomy and retrograde cholecystectomy. Operative findings included minimal serous ascites, massively distended and oedematous gallbladder measuring about 24 cm in longitudinal diameter (half as big as a full term baby)(, ). With generally glistening surface except for patches of dark discolorations of the fundus and surprisingly with no thickening of its wall. The upper third of the posterior wall of the gallbladder was completely embedded in the hepatic parenchymal. There were multiple small stones in the gallbladder and there was also an obstruction due to impacted stones at the neck and the aspirate was bilio - purulent. There were surrounding adhesions and the tissue planes were oedemtous. She had an uneventful post operative course and she had been followed up for more than a year with satisfactory outcome.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [52.0, 'kg'], 'height': [1.55, 'm']}",21.64412,20.56191,22.72633,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.55 m. The patient's weight is 52.0 kg. The patient's bmi is therefore 52.0 kg / (1.55 m * 1.55 m) = 21.64412 kg/m^2."
2438,6,Body Mass Index (BMI),physical,decimal,pmc-6314751-1,Extracted,"A-30-year-old, 50-kg, 160-cm woman, ASA I, was prepared to undergo resection of her vocal cord polyps, before which she had undergone no other surgery. During our preoperative assessment, no significant family history or personal history was found and no special laboratory or radiographic examination concerned to us. We used 10 mg propofol, 0.2 mg fentanyl for the anesthesia induction. Succinylcholine 100 mg was administered to facilitate endotracheal intubation, after which we used cisatracurium 4 mg for the intraoperative muscle relaxation. Without any complications, the whole surgery lasted for 30 minutes approximately with propofol and remifentanil for anesthesia maintenance. Unexpectedly, the patient had not been breathing spontaneously for 10 minutes since the end of the surgery. Then we used neostigmine 1 mg and atropine 0.5 mg to reverse the neuromuscular blockade. However, the patient showed no reaction for the next 30 minutes. In order to exclude the effect of residual fentanyl, we added naloxone 0.2 mg. Without knowing the reasons for the patient's spontaneous breathing failure to recover, we immediately gave her a blood biochemical test and found the plasma cholinesterase was measured and was low at 27 U/L, far below the normal level (4000 U/L to 13500 U/L). Then with stable vital signs, the patient was left intubated and transferred to the intensive care unit (ICU) for further treatment, provided with mechanical ventilatory support. Without any complications, she was extubated when she had been breathing spontaneously the next morning, when was about 10 hours after the operation. Since this patient had no diseases that would cause cholinesterase deficiency previously, we highly suspect her cholinesterase deficiency is congenital. Although after she was discharged from the hospital, we would like to conduct further examinations for her, which includes genetic test, but failed to obtain patient consent.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [50.0, 'kg'], 'height': [160.0, 'cm']}",19.53125,18.55469,20.50781,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 50.0 kg. The patient's bmi is therefore 50.0 kg / (1.6 m * 1.6 m) = 19.53125 kg/m^2."
2439,6,Body Mass Index (BMI),physical,decimal,usmle-9111,Extracted,"A 45-year-old G3P3 presents complaining of the feeling of a foreign body in her vagina that worsens on standing. She does not have urinary or fecal incontinence or any other genitourinary symptoms. She has no known gynecologic diseases. There were no complications with her pregnancies, all of which were full-term vaginal deliveries. She is sexually active with her husband and no longer uses oral contraceptives. She has an 11 pack-year history of smoking. Her weight is 79 kg (174 lb) and her height is 155 cm (5 ft). Her vital signs are within normal limits. The physical examination is unremarkable. The gynecologic examination reveals descent of the cervix halfway towards the introitus. On Valsalva and standing, the cervix descents to the plane of the hymen. The uterus is not enlarged and the ovaries are non-palpable.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [79.0, 'kg'], 'height': [155.0, 'cm']}",32.88241,31.23829,34.52653,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 79.0 kg. The patient's bmi is therefore 79.0 kg / (1.55 m * 1.55 m) = 32.88241 kg/m^2."
2440,6,Body Mass Index (BMI),physical,decimal,usmle-4329,Extracted,"A 1-year-old male presents to his pediatrician for a well-child visit. Through a history from the mother and physical examination, the pediatrician learns that the baby babbles non-specifically, takes several steps independently, and picks up his cereal using two fingers. His weight is currently 22 lbs (birth-weight 6 lbs, 9 oz), and his height is 30 inches (birth length 18 inches).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [22.0, 'lbs'], 'height': [30.0, 'in']}",17.18612,16.32681,18.04543,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 30.0 in, which is 30.0 in * 0.0254 m / in = 0.762 m. The patient's weight is 22.0 lbs so this converts to 22.0 lbs * 0.453592 kg/lbs = 9.97902 kg. The patient's bmi is therefore 9.97902 kg / (0.762 m * 0.762 m) = 17.18612 kg/m^2."
2441,6,Body Mass Index (BMI),physical,decimal,pmc-7746474-1,Extracted,"A 13-year-old, previously fit and well, male presented with pain and swelling to his right lower leg. A bone cyst was identified on imaging including plain radiographs and MRI scans (Figures and ). He underwent curettage on three occasions, including one with a bone graft, with recurrence on each occasion. An ABC was confirmed on biopsy on tissue obtained during curettage. En bloc resection of the proximal tibia was not thought to be viable due to the extent of disease and involvement of major neurovascular structures. Vascular embolization was not possible because no feeding vessels were identified on angiogram. Throughout this period, he had ongoing severe leg pain, was unable to weight-bear or attend school, and was at significant risk of pathological fracture.
Denosumab therapy was subsequently commenced following discussion of a bone tumour treatment multidisciplinary team. The weight at the start of treatment was 36 kg, with a height of 161 cm. The patient received four doses of subcutaneous denosumab (70 mg/m2) on a weekly basis for four weeks with significant improvement in pain, allowing him to return to school shortly after, although he was still immobile. There was a subtle initial radiological response with a slight reduction in size of the lesion. There was asymptomatic mild hypocalcaemia (corrected calcium 2.03 mmol/L; normal range 2.25–2.74 mmol/L) in the early stages of treatment which was treated with oral calcium supplementation (calcium carbonate 1.25 g daily). He remained on this supplementation throughout treatment. The patient went on to receive six further doses of denosumab at four-week intervals at the same dose.
On review following six months of treatment, there was ongoing radiological improvement, with bony consolidation (). The patient remained pain free, and he began partial weight-bearing over the subsequent few months. However, there was also evidence of some calcification of the lower limb growth plates, possibly as a result of denosumab therapy. Therefore, the dose interval was increased initially to two months, and then at 12 months of treatment, to three months.
After 18 months of treatment, the patient was walking without protection and fully weight-bearing without pain. The ABC was stable radiologically, and the dosing interval was further increased to four months.
On review after 27 months of treatment (following the 17th dose; cumulative dose 1554 mg), the patient remained pain free and was able to play gentle sport. Given the good response, the plan was for two further doses of denosumab every six months before stopping therapy.
On presentation for the first six-month dose, the patient was found to have a blood pressure of 170/100 mmHg. He reported he had felt generally unwell for several weeks with malaise, anorexia, polyuria, and headaches. His weight was 47 kg which was significantly lower than his last clinic review four months earlier when it was 50.7 kg, demonstrating a weight loss of 3.7 kg. Height was static in this four-month period at 172 cm. Initial blood tests demonstrated hypercalcaemia (corrected calcium 4.04 mmol/L). There were normal levels of phosphate (1.35 mmol/L; normal range 0.74–1.55 mmol/L) and alkaline phosphatase (201µ/L; normal range 55–236µ/L). 25-Hydroxyvitamin D2 was <5 nmol/L, and 25-hydroxyvitamin D3 was 84 nmol/L (normal range >50 nmol/L). In addition, there was an acute kidney injury (AKI) with a creatinine of 293 µmol/L (normal range 46–102 µmol/L) and a urea of 13.4 mmol/L (normal range 2.5–6.7 mmol/L). His parathyroid hormone level on presentation was suppressed at 1.0 pmol/L (normal range 1.1–6.9 pmol/L). Urine calcium/creatinine ratio was high at 3.62 mm/mm Cr (normal range 0–0.6 mm/mm Cr), however was not performed until 11 days after presentation and initial management. Lab values on this presentation and in subsequent management are summarised in .
Initial management was with intravenous (IV) fluids, IV furosemide (60 mg six hourly), and cessation of the supplemental calcium. There was no initial biochemical improvement, with corrected calcium peaking at 4.18 mmol/L and creatinine at 314 µmol/L. 200 units of calcitonin, initially subcutaneously, and then intravenously, was introduced once a day with limited improvement in calcium level and renal function, despite increasing to twice daily dosing over a nine-day period. Therefore, two doses of IV pamidronate (0.25 mg/kg and then 0.5 mg/kg, 24 hours apart) were given. Bisphosphonate therapy led to the normalisation of calcium levels (corrected calcium 2.74 mmol/L) within three days, with subsequent improvement to normal range of the high creatinine (97 µmol/L) a further three days later. Amlodipine (2.5 mg daily), which had been commenced to control the hypertension, could also be stopped at this stage with no adverse effect on the now normal blood pressure. He was discharged the following day.
Calcium levels were monitored closely following discharge with a further episode of rebound hypercalcaemia (corrected calcium 3.44 mmol/L), with an associated AKI (creatinine 115 µmol/L), 13 days after initial pamidronate treatment (). A further dose of IV pamidronate (0.5 mg/kg) was given, again with a positive response (corrected calcium 2.50 mmol/L four days later). A further episode occurred two weeks later (corrected calcium, 3.15 mmol/L), this time successfully treated with IV zoledronic acid (0.05 mg/kg).
A bone density scan (DEXA scan) was performed approximately two months following the third episode of hypercalcaemia and was within normal range, with a Z-score of 0.5 for the lumbar spine and 1.0 for the whole body (normal range >−2.0). Recurrence of hypercalcaemia has not subsequently occurred, and the patient remains mobile and pain free 16 months since the last denosumab dose and nine months since the third and last episode of hypercalcaemia. Now at 18 years old, his fatigue and appetite, without the need for a low calcium diet, have improved and he is gaining weight (now 53.8 kg).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.8, 'kg'], 'height': [172.0, 'cm']}",18.18551,17.27623,19.09479,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 172.0 cm, which is 172.0 cm * 1 m / 100 cm = 1.72 m. The patient's weight is 53.8 kg. The patient's bmi is therefore 53.8 kg / (1.72 m * 1.72 m) = 18.18551 kg/m^2."
2442,6,Body Mass Index (BMI),physical,decimal,pmc-3159929-1,Extracted,"According to the police report, a 19-year-old woman who majored in Security Services in college died while attending a picnic party. She had a lunch and climbed a mountain for almost two hours. She then rested for an hour. After resting, she suddenly lost consciousness while too competitively playing the stretch-the-legs game as a team member, Resuscitation was performed by her colleagues. She was then immediately taken to a hospital where she failed to recover and died. Her family reported that she had previously been in good health. However, her colleagues stated that she had one recent episode of exertional dyspnea while rafting and was absent from school for three days. Unfortunately, we have no any her medical records for further evaluation or treatment of this symptom.
She was approximately 160 cm tall and weighed 66 kg. Upon external examination, there were defibrillator related bruises on the chest and two needle punctures in the cubital fossa. Internally, the lungs weighed 904 g and 923 g, respectively. There were petechial subpleural hemorrhages on the interlobular surfaces. The heart showed slightly hypertrophic (weighed 349 g). There were petechial hemorrhages on the posterior interventricular groove. The right and left coronary arteries simultaneously opened to a single bifurcated ostium on the left sinus of Valsalva (). The left coronary artery was dominant. The left coronary artery and subsequent branches followed a normal route and distribution. However, the right coronary artery arose from the left sinus of Valsalva and proceeded between the ascending aorta and the pulmonary artery (). Both coronary arteries had neither arteriosclerotic change nor thromboemboli in the lumen, and acute myocardial lesions like infarction or myocarditis were not observed. Histologically, every organ showed congested, although there were neither pathological changes nor congenital abnormalities that could possibly be the cause of her death. In the wall of the coronary arteries, no pathological lesions such as atherosclerosis, angiitis or fibromuscular dysplasia were observed. There was no evidence of any specific disease or injury. No toxic agents or alcohol components were detected in the blood or gastric contents.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [66.0, 'kg'], 'height': [160.0, 'cm']}",25.78125,24.49219,27.07031,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 66.0 kg. The patient's bmi is therefore 66.0 kg / (1.6 m * 1.6 m) = 25.78125 kg/m^2."
2443,6,Body Mass Index (BMI),physical,decimal,pmc-8239095-2,Extracted,"An 80-year-old woman was admitted to our hospital with suspected primary lung cancer in the right upper lobe clinical T1bN0M0, stage IA2. Thoracoscopic right upper lobectomy and superior mediastinal node dissection were performed under general anesthesia with selective lung ventilation using a double-lumen tube. Nodes in # 2R and # 4R were removed en bloc. Nodes in # 2R and # 4R were dissected along the anterior surface of the trachea (Fig. ). The patient complained of hoarseness one day after the operation and consulted an otolaryngologist on the sixth day after the operation because no improvement was observed. Consequently, the patient was diagnosed with left vocal cord paralysis by laryngoscopy (Fig. ). Postoperative hoarseness has been present for more than 3 years, but no improvement has been seen. The patient was 148.4 cm tall and weighed 46.8 kg and used a 32 Fr double lumen tube for left intubation as the intubation tube. Pathological analysis revealed that it was a primary lung adenocarcinoma, pT1aN0.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [46.8, 'kg'], 'height': [148.4, 'cm']}",21.25094,20.18839,22.31349,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 148.4 cm, which is 148.4 cm * 1 m / 100 cm = 1.484 m. The patient's weight is 46.8 kg. The patient's bmi is therefore 46.8 kg / (1.484 m * 1.484 m) = 21.25094 kg/m^2."
2444,6,Body Mass Index (BMI),physical,decimal,pmc-5411553-2,Extracted,"A 62-year-old woman was admitted to our hospital because of general fatigue and chest discomfort. She had experienced acute glomerulonephritis 6 years previously, but the details of the clinical course were not known. Proteinuria had been detected while she was pregnant, and she had been treated for hypertension for 15 years. She had been diagnosed with ET at another hospital 3 years earlier. No remarkable cardiac problems were found when she was examined at the Department of Cardiology after admission. She was referred to the Department of General Medicine for a renal biopsy to investigate the persistent proteinuria.
The patient’s height, weight, and blood pressure were 148 cm, 55 kg, and 179/107 mmHg, respectively. Her consciousness level was alert and she looked well. A systolic murmur was detected at the 4 left sternal border. She did not have remarkable abnormalities in the lungs and abdomen and did not show pitting edema.
The laboratory data were as follows: hemoglobin, 11.4 g/dl; hematocrit, 39.8 %; platelets, 978,000/μl; white blood cells, 14,400/μl; C-reactive protein, <0.2 mg/dl; blood urea nitrogen, 15.8 mg/dl; serum creatinine, 0.7 mg/dl; total cholesterol, 227 mg/dl; total protein, 7.3 g/dl; albumin, 4.5 g/dl; globulin, 2.8 g/dl; lactate dehydrogenase, 811 IU/l; aspartate aminotransferase, 22 IU/l; alanine aminotransferase, 11 IU/l; total bilirubin, 0.3 mg/dl; γ-glutamyl transpeptidase, 21 IU/l; alkaline phosphatase, 470 IU/l; Na, 144 mmol/l; K, 5.0 mmol/l; and Cl, 107 mmol/l. Urinalysis showed 4+ proteinuria (1.51 g/day) and no evidence of hematuria.
Renal biopsy was performed (Fig. ), and 19 glomeruli could be evaluated, 2 of which exhibited global sclerosis. The histological findings included mild glomerular changes with arteriolosclerotic changes. Immunofluorescence staining was positive for IgM and weakly positive for IgA. Electron microscopy did not show any obvious electron-dense deposits. She was treated with felodipine, an antihypertensive, as well as antiplatelet drugs. The control of her blood pressure was slightly poor. Her renal function remained stable, but the proteinuria persisted.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.0, 'kg'], 'height': [148.0, 'cm']}",25.10957,23.85409,26.36505,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 148.0 cm, which is 148.0 cm * 1 m / 100 cm = 1.48 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.48 m * 1.48 m) = 25.10957 kg/m^2."
2445,6,Body Mass Index (BMI),physical,decimal,pmc-5642869-1,Extracted,"A 9-year-old female patient was diagnosed with FD by family screening at 5 years of age, mutation c.1244T>C (p.L415P) in heterozygous status, alpha galactosidase in dried blood spot on filter paper of 1.5 umol/l/h (reference value ≥ 4.0).
It is a patient with normal physical and neurological development according to age. On examination, the following is found: preserved vital signs with normal blood pressure, weight 52 kg, height 151 cm, rare bronchospasms, mild acroparesthesias with good response to carbamazepine 200 mg/day, and few periumbilical angiokeratomas ().
Complementary Studies. Laboratory findings are as follows: creatinine of 0.34 mg/dl (estimated glomerular filtration rate by Schwartz formula of 183 ml/min), albuminuria of 2.7 ug/min (reference value from 0 to 15), and proteinuria of 30 mg/24 hours (reference value < 150), with blood Lyso-Gb3 of 69.9 nmol/l (reference value < 1.2), normal electrocardiogram for their age, Doppler echocardiography with physiologic tricuspid and pulmonary regurgitation, normal brain magnetic resonance imaging, ophthalmological examination with slit lamp showing cornea verticillata in both eyes, and normal abdominal and renal ultrasound.
Although the patient did not present clinical data of nephropathy (albuminuria/proteinuria), due to the presence of glomerular hyperfiltration associated with peripheral neuropathy and an elevated blood Lyso-Gb3, a renal biopsy was performed. Light microscopy: after staining with hematoxylin and eosin, periodic acid-Schiff, Masson's trichrome, and silver-methenamine (Jones stain), glomeruli were observed with some degree of podocyte vacuolization that occupies on average 30% of the podocytes. Tubules: some distal tubules with clarification and microvacuolization of the cytoplasm. Interstitium and vessels were without alterations (). Electron microscopy: glomeruli showed microvacuolization in one-micron sections (Fogo classification score 2), with mild clarification in the cytoplasm of proximal and distal tubules and Interstitium and vessels without alterations. Typical myeloid or zebra bodies were observed in the cytoplasm of several podocytes, confirming the diagnosis of FD (). After a multidisciplinary evaluation, it was decided to start enzyme replacement therapy (ERT) with agalsidase beta at doses of 1 mg/kg body weight every 2 weeks by intravenous infusion.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [52.0, 'kg'], 'height': [151.0, 'cm']}",22.80602,21.66572,23.94632,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 151.0 cm, which is 151.0 cm * 1 m / 100 cm = 1.51 m. The patient's weight is 52.0 kg. The patient's bmi is therefore 52.0 kg / (1.51 m * 1.51 m) = 22.80602 kg/m^2."
2446,6,Body Mass Index (BMI),physical,decimal,pmc-3671823-1,Extracted,"A 41-year-old previously healthy female was admitted to the Department of Neurology, Taizhou People’s Hospital in March 2012, for two transitory episodes of syncope during a 5-h period. The patient had an unhealthy lifestyle of physical inactivity. No urinary and fecal incontinence, general fatigue, chest pain, breathing difficulty, hemoptysis or fever were observed during the course of disease. Following admission, physical examinations revealed a body weight of 75 kg, body height of 159 cm, body temperature of 36.0°C, pulse of 80 bpm, respiratory rate of 23 bpm and blood pressure of 120/60 mmHg. The patient had a slightly haggard expression, no cyanosis of the lips and no jugular vein distention. Bilateral respiratory movements were identical and vocal fremitus was equal. Dullness was heard in the right lower lung on percussion. Breath sounds were diminished and no moist rales were heard. The patient’s heart rhythm was regular, P2>A2 (pulmonary second sound was higher than aortic second heart sound) and there was no edema in the lower extremities.
A complete blood test revealed a white cell count of 11.21×109 cells/l and the percentage of large white blood cells was 57.2%. Biochemical tests revealed 1.4 mmol/l triglycerides, 0.75 mmol/l high-density lipoprotein and 3.61 mmol/l low-density lipoprotein. Blood gas analysis revealed a pH of 7.471, 61.1 mmHg PaO2, 23.5 mmHg PaCO2 and 18.2 mmol/l HCO3− (under the condition of a low flow rate of oxygen inhalation). Chest radiographs revealed pulmonary hilar enlargement and a broadened shadow on the right superior pulmonary artery. An electrocardiogram revealed a flat V1–V3 T wave and magnetic resonance angiography of the head revealed ∼60% luminal stenoses of the right posterior cerebral artery and the left external carotid artery.
After admission, ‘reflex syncope’ was suspected and the patient was administered oral calcium antagonists (Nimotop 30 mg qd) and intravenous Alprostadil for injection (Alprostadil 10 μg qd) to boost the cerebral circulation, without effect. A further episode of syncope occurred during the 18 h after admission and the patient was transferred to the Department of Respiratory Medicine for a D-dimer assay, which indicated a value of 1,200 μg/l. An enhanced chest computed tomography (CT) scan revealed filling defects in the right main pulmonary and left inferior pulmonary arteries, as well as bilateral pleural effusion (). Color ultrasonography of the heart revealed a dilated right ventricle and right heart overload, severe tricuspid regurgitation and severe pulmonary hypertension and the systolic pulmonary arterial pressure was 130 mmHg (). The patient was finally diagnosed with MPE.
Following confirmation, the patient underwent interventional mechanical thrombectomy combined with local and systematic thrombolytic therapy with low-dose urokinase.
Following the above therapies, digital subtraction angiography (DSA) of the deep veins of the lower limbs and the inferior vena cava demonstrated unobstructed blood flow, with no apparent thrombosis. A 4–5F double J tube was inserted through the right femoral vein to the main pulmonary artery for DSA of the pulmonary artery, to confirm the filling defect in the right main pulmonary artery (). An exchange guide wire was then inserted to coordinate with the tube for twists and drags to disintegrate the embolus. Following disintegration of the embolus, 500,000 units urokinase were injected into the tube for thrombolysis over 30 min. Subsequent DSA of the pulmonary artery indicated an improvement in the filling defect compared with before treatment (). The patient’s condition was significantly alleviated and the anoxia was reduced. A blood gas assay performed 2 h after surgery indicated a pH of 7.51, 72 mmHg PaO2, 29 mmHg PaCO2 and 23.1 mmol/l HCO3− (under the condition of a low flow rate of oxygen inhalation).
A postoperative intravenous drip of low-dose urokinase (200,000 units) was initiated and the patient was also treated with 5,000 units low-molecular-weight heparin, administered subcutaneously once every 12 h for three consecutive days. Warfarin (2.5 mg) was administered orally once every 12 h on a daily basis. The prothrombin time (PT) and international normalized ratio (INR) were monitored; when the PT and INR were twice and 2.5 times their respective normal levels, warfarin therapy was administered singly, plus anti-infective, supportive and oxygen therapies.
Three days after surgery, the patient demonstrated a distinctly improved mental condition with no further syncopal attacks. An enhanced chest CT scan 10 days after surgery revealed evident improvement of the thrombosis in the right main pulmonary artery and left inferior pulmonary artery branch, as well as disappearance of the pleural effusion, compared with the previous chest CT scan (). Color ultrasonography revealed a significant decrease of pulmonary artery pressure and right heart load; the systolic pulmonary arterial pressure was 71 mmHg. The patient was discharged from hospital 26 days after admission, with continued daily administration of 2.5 mg warfarin. Based on the monitoring of PT and INR, the doctor suggested discontinuation of warfarin 3 months after hospital discharge. The study was approved by the Ethics Committee of Taizhou People’s Hospital, Jiangsu, China and according to the Declaration of Helsinki. Written informed consent was obtained from the patient.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [75.0, 'kg'], 'height': [159.0, 'cm']}",29.66655,28.18322,31.14988,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 159.0 cm, which is 159.0 cm * 1 m / 100 cm = 1.59 m. The patient's weight is 75.0 kg. The patient's bmi is therefore 75.0 kg / (1.59 m * 1.59 m) = 29.66655 kg/m^2."
2447,6,Body Mass Index (BMI),physical,decimal,pmc-3545965-1,Extracted,"A 62-year-old man with NF-1 had mild liver dysfunction diagnosed by medical examination, and he was admitted to our hospital for further examination. In his past history, he had developed blindness in childhood because of pigmentary retinal dystrophy. There was no history of hypoglycemia or peptic ulcer. On admission, he had no clinical symptoms. His height was 141 cm and his body weight was 52 kg. Numerous café-au-lait macules and cutaneous neurofibromas were noted over his whole body (Figure
). There were no palpable lymph nodes in the surface or mass lesions in the abdomen. The patient’s blood pressure was 112/70 mmHg and heart rate was 72 beats per min without abnormality on electrocardiogram examination. Alkaline phosphatase, leucine aminopeptidase, and γ-glutamyl transpeptidase levels were slightly elevated; other biochemical data, including tumor markers, were almost within the normal ranges. Values for fasting plasma glucose, hemoglobin A1c, and serum glucagon were within the normal limits, but the serum gastrin level was slightly higher than the normal upper limit. Upper gastrointestinal endoscopy showed a reddish, chorioepithelial hyperplasia of the second part of the duodenum. A biopsy specimen of the lesion revealed hyperplasia of Brunner’s glands. There was no peptic ulcer in the stomach and duodenum. Colonoscopy showed no abnormality. An abdominal contrast-enhanced computed tomography (CT) scan demonstrated a low-attenuating tumor in the head of the pancreas, measuring 30 mm in diameter, with slow enhancement (Figure
). The upper common bile duct was extended, but the main pancreatic duct was not dilated. Some lymph nodes around the hepatic hilum were swollen, with a maximal diameter of 25 mm. No tumor was detected in the liver and lung, or in the pituitary and parathyroid glands. Endoscopic retrograde cholangiopancreatography (ERCP) showed that the lower common bile duct and main pancreatic duct were oppressed without any encroachment. Endoscopic ultrasonography (EUS) showed a low echoic tumor, measuring 35 mm in diameter, near the papilla of Vater, compressing both the common bile duct and main pancreatic duct. The lesion continued to the fourth layer of the duodenal wall. Swollen lymph nodes were detected near the common bile duct. Fine-needle aspiration biopsy under EUS revealed that the pancreatic mass was a neuroendocrine tumor, compatible with a diagnosis of PNET. A subtotal stomach-preserving pancreaticoduodenectomy was performed. At laparotomy, there was no fluid collection, peritoneal dissemination, or liver metastasis. Because we found two small nodules in the jejunum and one small nodule in the stomach, partial resection of the jejunal wall and gastric wall was performed.
Macroscopically, a white and elastic hard tumor, 30 × 35 × 40 mm in size, was identified in the head of the pancreas, and it had invaded the duodenum (Figure
). Microscopically, tumor cells were composed of ribbons, cords, and solid nests with an acinus-like structure (Figure
a). Tumor cells were considered to have islet cell origin because they had uniform nuclei with a salt-and-pepper appearance, and hyperplasia of islet cells was frequently found in the non-neoplastic pancreas (Figure
b). On the other side, in the part of acinus-like pattern mimicking normal acinar cells, cytoplasms of these cells were eosinophilic and granular, associated with zymogen granules, which were positive for α-antitrypsin and α-antichymotrypsin. These tumor cells were smaller than formerly, and sometimes vacuolar changes could be observed. A pattern of transmigration into normal acinar cells was shown; thus, the tumor suggested including an exocrine-derived component. On immunohistochemical examination (all antibodies for immunohistochemical examination were listed on Table
), neuroendocrine tumor markers, such as chromogranin A, synaptophysin, and CD56, were positive (Figure
c/d/e). Some of the tumor cells, particularly in the acinus-like structure, were also positive for α1-antichymotrypsin and α1-antitrypsin (Figure
f/g). Neurofibromin protein expression was negative in the tumor cells (Figure
h), in contrast being strongly positive in islets in the non-neoplastic pancreas (Figure
i). According to the WHO classification (2010), the tumor was diagnosed as “neuroendocrine tumor, NET G2,” because the Mib1 index (%) is 7% and proliferation rate is 4 mitoses per 10HPF
[],and the tumor was composed acinar and neuroendocrine cells. The acinar component was about 15% and neuroendocrine component about 55%; cells with both characterscomprised about 30%. According to the TNM classification
[], the tumor was classified as pT3N1M0, G2, R0, stage IIB. The tumors of the jejunum and stomach were compatible with a diagnosis of gastrointestinal stromal tumor (GIST) presenting with positive expression for c-Kit and CD34 on immunohistochemistry. The patient received adjuvant chemotherapy with TS-1 for 1 year. At follow-up 2 years after surgery, the patient remained well without any recurrent pancreatic disease.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [52.0, 'kg'], 'height': [141.0, 'cm']}",26.15563,24.84785,27.46341,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 141.0 cm, which is 141.0 cm * 1 m / 100 cm = 1.41 m. The patient's weight is 52.0 kg. The patient's bmi is therefore 52.0 kg / (1.41 m * 1.41 m) = 26.15563 kg/m^2."
2448,6,Body Mass Index (BMI),physical,decimal,usmle-7204,Extracted,"A 13-year-old girl is brought to the outpatient clinic by her parents with a complaint of episodic spasm in her fingers for the past few months. Upon further questioning, her mother notes that the girl has not been doing well at school. She also believes that the girl is shorter than the other children in her class. On examination, her pulse is 72/min, temperature 37.6°C (99.7°F), respiratory rate 16/min, and blood pressure 120/88 mm Hg. The girl has short 4th and 5th fingers on both hands, a round face, and discolored teeth. Her height is 135 cm (4 ft 5 in) and she weighs 60 kg (132 lb).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.0, 'kg'], 'height': [135.0, 'cm']}",32.92181,31.27572,34.5679,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 135.0 cm, which is 135.0 cm * 1 m / 100 cm = 1.35 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.35 m * 1.35 m) = 32.92181 kg/m^2."
2449,6,Body Mass Index (BMI),physical,decimal,pmc-6103365-1,Extracted,"In a 47-year-old Caucasian male (weight 70 kg, height 177 cm), with a known history of hypertension, beta-lactam-documented allergy, and on hemodialysis for 3 years prior to this event, a dialysis catheter was inserted 30 months prior to the incident. Peripheral blood cultures as well as blood drawn from the catheter revealed methicillin-sensitive S. aureus (MSSA) bacteremia. To avoid possible allergic manifestations, the patient was treated with vancomycin 2,000 mg i.v. (28.5 mg/kg) as a loading dose in the last 90 min of dialysis followed by 1,000 mg i.v. (14.2 mg/kg) after each subsequent dialysis (in the last 30–60 min of dialysis) plus combination vancomycin (2.5 mg/mL)/4% citrate antibiotic lock for 3 weeks. Vancomycin pre-hemodialysis concentrations were > 15 mg/L (target 15–20 mg/L) during the 2 weeks of intravenous antibiotic therapy. The treatment was initiated while the patient was an outpatient. The patient experienced complete resolution of bacteremia confirmed by negative blood cultures. The catheter was removed 5 months after transplant surgery.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [177.0, 'cm']}",22.34352,21.22634,23.4607,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 177.0 cm, which is 177.0 cm * 1 m / 100 cm = 1.77 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.77 m * 1.77 m) = 22.34352 kg/m^2."
2450,6,Body Mass Index (BMI),physical,decimal,pmc-7499275-1,Extracted,"A 5-month-old male was admitted with severe diarrhea and failure to thrive. The baby was born at term after an uneventful pregnancy and delivery with a birth weight of 2.97 kg. He was exclusively breast-fed. At 2-1/2 months of age, he developed frequent, large volume, watery stools with occasional blood streaks. There was no fever, emesis, or any infectious contacts. The family history was only significant for two paternal second-degree relatives with celiac disease and one-second degree relative with a thyroid disorder and type 1 diabetes mellitus.
On initial examination, the child appeared ill, pale, malnourished, and dehydrated. The weight was 5.19 kg (<3rd percentile), length was 59.7 cm (<3rd percentile), and head circumference was 40.5 cm (between 3rd and 10th percentile). Other than some diaper rashes, the physical examination was unremarkable with no atopic dermatitis or icthyosis.
The results of initial investigations are shown in . The absolute eosinophil count was only slightly elevated. Immunoglobulins including IgE were normal. The serum albumin was low, consistent with the protein losing enteropathy. Stool examination did not reveal any pathogens. Stool electrolytes showed secretory diarrhea. The antinuclear antibody and direct antiglobulin were negative.
Endoscopy and biopsies revealed acute and chronic inflammation, marked autoimmune enteropathy with total villous atrophy, and abundant CD3+ T- and CD20+ B-cell aggregates in the small intestine and colon.
Further immunological workup showed intact IL-10 receptor function since endotoxin-induced tumor necrosis factor (TNF) production in mononuclear cells was suppressed by IL-10. Initial T- and B-cell phenotype analysis was normal. The percentage of circulating Treg cells and FOXP3 protein expression in these cells measured by flow cytometry were also normal (Figures and ).
Analysis of all coding regions and exon/intron boundaries of the FOXP3 gene was carried out. This revealed a hemizygous missense mutation (c.1190G > A, p.Arg397Gln) which would result in a nonfunctional FOXP3 protein and Treg cells, similarly in the patient's mother, who is a healthy career. The anti-islet cell antibody was negative, insulin-like growth factor-1 level was normal, and the patient never developed type 1 diabetes mellitus. Thyroid function was also normal.
The patient required intensive resuscitation with intravenous fluids. He was then managed with parenteral nutrition and high-dose intravenous corticosteroids. He was maintained on oral prednisone and tacrolimus. The clinical condition gradually improved, and he was able to initiate oral intake with an elemental formula in a few weeks.
The patient had a matched unrelated hematopoietic stem cell transplant (HSCT) with reduced intensity conditioning including alemtuzumab, fludarabine, and melphalan at 8 months of age. Early transplant period was complicated with donor Epstein–Barr virus (EBV) reactivation treated with rituximab. He developed autoimmune hemolytic anemia. Initially, enteropathy significantly improved; however, colitis recurred 3 months after the transplant when, unfortunately, there was decreasing mixed chimerism and secondary bone marrow rejection. Donor lymphocyte infusions were unsuccessful, and the patient required a second transplant at 14 months of age from the same donor with busulfan, fludarabine, and alemtuzumab conditioning this time.
Two years after the second HSCT, the patient has mixed chimerism and 65% of donor haematopoiesis but 91% of donor Treg cells (). The gut function gradually recovered, and graft-versus-host disease was ruled out on repeated gut biopsies. Currently, he is doing well, except having eczema of typical distribution and morphology seen in toddlers and responding to high-potency topical corticosteroids. He is immunocompetent and has sustained protective antibody titres to several vaccine antigens.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [5.19, 'kg'], 'height': [59.7, 'cm']}",14.56192,13.83382,15.29002,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 59.7 cm, which is 59.7 cm * 1 m / 100 cm = 0.597 m. The patient's weight is 5.19 kg. The patient's bmi is therefore 5.19 kg / (0.597 m * 0.597 m) = 14.56192 kg/m^2."
2451,6,Body Mass Index (BMI),physical,decimal,pmc-5518768-1,Extracted,"A 66-year-old female was admitted to a nearby hospital with dyspnoea and an abnormal shadow on chest computed tomography (CT) in September 2014. Contrast-enhanced CT of the chest showed a PAVM, approximately 5 cm in size, in the left lower lung lobe. She was referred to our hospital for observation and treatment. However, because her symptoms were controlled, she was not admitted, and no follow-up for the PAVM was conducted.
In June 2016, due to worsening symptoms, she was admitted to our hospital. Her mMRC score was 2. She had no other relevant medical history. Close relatives had experienced intracranial haemorrhage and two descendants had presented with recurrent nosebleeds. However, no one was diagnosed with hereditary haemorrhagic telangiectasia (HHT). At admission, her weight was 66 kg and height was 155 cm. Her vital signs were: Glasgow coma scale, 15 (E4V5M6); blood pressure, 98/77 mmHg; pulse rate, 112 beats/min; pulse oximetry, 83% in room air; respiratory rate, 22/min; and body temperature, 38.0°C. Her quick sepsis-related organ failure assessment (qSOFA) score was 2 (respiratory rate ≥ 22/min and systolic blood pressure ≤ 100 mmHg). Chest auscultation revealed a vascular murmur in the left lung field. She had no cutaneous telangiectasia. Blood tests revealed inflammatory findings associated with infection, disseminated intravascular coagulation (DIC), and liver dysfunction. No significant findings were obtained in various culture tests. Thoracic radiographs demonstrated the presence of a PAVM in the left lower lobe (Fig. A). Enhanced CT of the chest and three-dimensional reconstructed images revealed that the PAVM had one feeding artery and one draining vein with diameters of 10 and 12 mm, respectively. The sac was 16 mm in diameter (Fig. B, C). Abdominal CT and ultrasonography revealed a low-density area and hypoechoic lesion in the spleen, which was consistent with splenic infarction and abscessation (Fig. D). Needle aspirations of the splenic abscess were not performed because she had DIC. No findings suggestive of infective endocarditis and congenital heart disease were found on performing echocardiography. Lung perfusion scintigraphy gave a shunt ratio of 13.9%. Furthermore, brain magnetic resonance imaging revealed multiple cerebral infarctions and a cerebral aneurysm, whereas upper gastrointestinal endoscopy detected gastric varices. Although HHT was suspected, her clinical features did not satisfy its diagnostic criteria .
Anticoagulant and antimicrobial therapies [doripenem 1 g intravenous (i.v.) every 8 h for 25 days, following oral amoxicillin/clavulanate 250 mg every 6 h and metronidazole 250 mg every 6 h for 3 days and then amoxicillin/clavulanate 250 mg every 6 h and clindamycin 300 mg every 8 h for 32 days] were initiated. Approximately 30 days later, the splenic abscess and the patient's general condition had improved. Embolization of the PAVM was then performed (Fig. ). No complications occurred during or after embolization.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [66.0, 'kg'], 'height': [155.0, 'cm']}",27.47138,26.09781,28.84495,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 66.0 kg. The patient's bmi is therefore 66.0 kg / (1.55 m * 1.55 m) = 27.47138 kg/m^2."
2452,6,Body Mass Index (BMI),physical,decimal,pmc-3579059-1,Extracted,"An 8-year-old boy, previously diagnosed as cerebral palsy with developmental delay, microcephaly and mental retardation, presented with sudden onset of huge swelling of the tongue for last 24 hours. Two weeks back, he developed generalized tonic clonic convulsion with status epilepticus for the first time. He was then admitted to a nursing home and managed with intravenous diazepam followed by loading dose of phenytoin as per standard protocol. He was discharged with instruction to get intravenous phenytoin (300 mg/day) once daily at home for the next 15 days. There was no history of headache or vomiting. There was no history of respiratory distress, swelling of face, itching, and loose stool. No history of atopy or similar type of episodes seen in other family members.
On examination, the child was conscious but irritable. There was swelling of whole dorsum of tongue, which was protruding outside the mouth with oozing of blood over both the edges of tongue following superadded infection []. The oral cavity was so blocked by edematous tongue that the child could not speak or swallow anything. Face, lips, and gums were normal. His body weight was 24.5 kg, height was 123 cm and head circumference was 45.5 cm. His pulse rate was 144/min, regular, normal volume, respiratory rate 32/min, blood pressure 120/70 mm of Hg, temperature 99.8°F. The child had mild pallor without any pedal edema or cyanosis. Abdomen was soft without any visceromegaly. There was mild respiratory distress due to oro-pharyngeal obstruction. Auscultation of his chest including cardiovascular system was otherwise normal. There was no ataxia, nystagmus, or altered sensorium. However, he had neurologic manifestation of spastic diplegic cerebral palsy with associated complication.
Investigation revealed hemoglobin of 12.8 g/dL. Total leukocyte count of 16900/cmm, polymorphs 86%, lymphocytes 12%, platelet counts 2.2 lakhs/cmm, ESR 22/1st hour. Biochemistry showed serum sodium 138 meq/L, potassium 5.2 meq/L, calcium 8.6 mg/dL. Renal function and liver function tests were normal. Chest X-ray and sonography of abdomen did not reveal any abnormality.
Serum C1 esterase inhibitor was 0.62 mg/L (normal: 0.21-0.39 mg/L), which excludes hereditary angioedema. Serum phenytoin level (37.20 μg/ml, toxic range > 20 μg/ml) was elevated.
The child responded to supportive management along with parenteral empirical antibiotics and with intravenous steroids (hydrocortisone), antihistamines, and epinephrine within 2 days. Macroglossia due to edema was reduced and the tongue could be repositioned within the oral cavity []. He was discharged with valproate sodium and other advice like physiatric management, etc.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [24.5, 'kg'], 'height': [123.0, 'cm']}",16.19406,15.38436,17.00376,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 123.0 cm, which is 123.0 cm * 1 m / 100 cm = 1.23 m. The patient's weight is 24.5 kg. The patient's bmi is therefore 24.5 kg / (1.23 m * 1.23 m) = 16.19406 kg/m^2."
2453,6,Body Mass Index (BMI),physical,decimal,pmc-7796768-1,Extracted,"A 56-year-old male patient (weight 100 kg, height 192 cm) was scheduled for open surgery of supraumbilical and inguinal hernia repair from the right side. Bilateral ESP block was performed before the induction to general anesthesia, at Th10 level with 20 mL 0.25% bupivacaine from both sides. Anesthesia was induced with midazolam 0.04 mg/kg, lidocaine 1 mg/kg, fentanyl 2 μg/kg, propofol 2 mg/kg, and rocuronium bromide 0.6 mg/kg and were same in all patients. It was maintained with sevoflurane (MAC 0.7–1) and additional bolus doses of fentanyl. The total amount of fentanyl was 350 μg. Visual analog scale (VAS) score 2 h after surgery was 2 at rest and 3 on coughing. After surgery, at 6, 12, and 24 h, the pain was 3 at rest and 4 on coughing, thus, 1 g paracetamol was given. 19 h after surgery pain was 10/10 and 100 mg tramadol was given. After 36 and 48 h, the pain was 3 at rest and on coughing, and after 72 h was 2 at rest and on coughing.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [100.0, 'kg'], 'height': [192.0, 'cm']}",27.12674,25.7704,28.48308,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 192.0 cm, which is 192.0 cm * 1 m / 100 cm = 1.92 m. The patient's weight is 100.0 kg. The patient's bmi is therefore 100.0 kg / (1.92 m * 1.92 m) = 27.12674 kg/m^2."
2454,6,Body Mass Index (BMI),physical,decimal,pmc-7020965-3,Extracted,"Patient R.O.H, male, 31 years old, amateur soccer athlete (2 times/week), without risk factors for early CAD, without previous use of drugs, anabolic, ergogenic, illicit or anorectic drugs. Negative family history for coronary heart disease, cardiomyopathy or thrombotic disease. Sought medical guidance due to dyspnea and tiredness which started after practicing 1h of football.
Symptoms progressively worsened, progressing to moderate-intensity retrosternal chest pain and irradiation to the left upper limb, with a 2h course, with no other associated symptoms.
He reported a similar and single episode about a month earlier, in a similar situation, with spontaneous resolution after 2h feeling bad and having dyspnea.
On admission to hospital, he was in good general conditions, hypotensive, sweating, tolerating ambient air, normal color, acyanotic, feverless and anicteric.
He weighed 74 kg; was 1.69 m tall; and had a heart rate of 48 bpm; and BP 60/30 mmHg. BP maintenance was required, which increased rapidly after an infusion of 500 mL crystalloid (119/90 mmHg).
There were no changes in cardiac and pulmonary auscultation; extremities were not infiltrated.
On admission, the ECG showed ST-segment junctional rhythm in DII, DIII, aVF, V7, and V8 leads, and the was diagnosed with inferodorsal ST-segment elevation myocardial infarction.
Measurements for ACS were performed and referred to CATE, showing right dominance with severe proximal lesion (95%) in SCAD and a large amount of thrombi.
Primary ATC performed for thrombus aspiration SCAD. Thrombi migrated to the distal portion of the ventricular and posterior descending arteries, and tirofiban was initiated ( and ).
He remained hospitalized for 4 days, with asymptomatic evolution, being discharged with a prescription of daily use of AAS 100 mg; clopidogrel 75 mg; atenolol 50 mg and rosuvastatin 10 mg.
Remains asymptomatic and has returned to football practice approximately 4 times/week.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [1.69, 'm'], 'weight': [74.0, 'kg']}",25.90946,24.61399,27.20493,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.69 m. The patient's weight is 74.0 kg. The patient's bmi is therefore 74.0 kg / (1.69 m * 1.69 m) = 25.90946 kg/m^2."
2455,6,Body Mass Index (BMI),physical,decimal,pmc-5097346-1,Extracted,"A-70-year-old man with symptomatic osteoarthritis of the right hip, weighing 79 kg, tall 177 cm was presenting for a primary THA. He was recently diagnosed with systemic indolent mastocytosis with multiple sclerotic and osteolytic laesions. History showed no allergic reactions in the past. In 1998 cannulated hip screws were used to treat a left proximal transcervical femur fracture successfully. Multiple insufficiency vertebra fractures were treated non-operative in 2015. A multimodal oral analgesic regime consisting of paracetamol 1 g, naproxen 500 mg and gabapentin 600 mg was administered 1–2 h pre-operatively. On the pre-anesthetic care unit the blood pressure was 150/95 mmHg with a saturation of 95 % and 11,85 mg Dexamethasone and Cefazoline 2000 mg soluted in 20 ml Sodiumchloride (NaCl) 0.9 % was administered intravenously. In the operating room spinal anesthesia with 7.5 mg bupivacaine 0,5 % plain via the L2/3 vertebral interspace with a standardized intraoperative regime for fluid administration, consisting of 0,9 % saline (500 ml) was given. After spinal anesthesia the patient received sedation with propofol TCI 0,8 ug/ml (0,1–2.0 ug/ml). To reduce blood loss, tranexamic acid 1000 mg was given at the beginning of surgery. To reduce nausea and vomiting ondansteron 4 mg IV is added in this multimodal regimen. To reduce chronic pain, ketamine 15 mg IV is titrated after starting the sedation. The blood pressure was 120/70 mmHg after spinal anesthesia and starting the sedation. Three liter of Oxygen was added during sedation. Thirty minutes after induction the orthopedic surgeon inserted a cemented acetabular component. Blood pressure dropped from 90/50 to 60/40 mmHg. Saturation dropped from 95 to 80 %. Oxygen 100 % with a Ventimask was administered and rapid infusion of NaCl 0.9 % 1000 ml as well as Phenylephrine 4 × 100 ug, phenypephrine 2 × 200 ug and 10 mg ephedrine was given intravenously. Phenylephrine infusion was started and replaced by Noradrenaline 5 mg/50 ml NaCl 0.9 % 2.0–9.0 ml/h. The breath sounds remained normal, and no angioedema, urticaria or rash occurred. All the time, the patient was conscious and able to respond questions. With rapid infusion and finally Noradrenaline he recovered hemodynamically within 15 min, blood pressure 100/50 mmHg with 95 % saturation. Forty-five minutes after onset of the symptoms, the surgical procedure was completed after inserting a press fitted uncemented femoral stem component. The patient was transported to the Intensive Care Unit (ICU) for optimal postoperative treatment and monitoring. Biochemistry showed stable hemoglobin levels (8.3 mmol/l on ICU arrival and 8.4 mmol/l after 4 h), elevated white blood cell count (19.3 × 109/l), normal levels of electrolytes, liver enzymes, creatine kinase and troponin, and an arterial blood sample of pH 7.36 pCO2 6.1 kPa; pO2 14.4 kPa; HCO3 26 mmol/l; Base excess 0.4 mmol/l; Fys. O2 sat 98.7 %; FiO2 30 %; lactic acid 1.0 mmol/l. Electrocardiography (on ICU arrival and after 24 h) remained normal, and echocardiography showed no left or right ventricular disfunctioning or elevation of the right atrial pressure. Within six hours after surgery the patient started to ambulate following our standard fast-track rehabilitation regime. Post-operative day one he was discharged according strict functional criteria to the specialized Orthopedic Department. After 5 hospital days the patient was discharged to his home.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [79.0, 'kg'], 'height': [177.0, 'cm']}",25.21625,23.95544,26.47706,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 177.0 cm, which is 177.0 cm * 1 m / 100 cm = 1.77 m. The patient's weight is 79.0 kg. The patient's bmi is therefore 79.0 kg / (1.77 m * 1.77 m) = 25.21625 kg/m^2."
2456,6,Body Mass Index (BMI),physical,decimal,pmc-8383513-1,Extracted,"A 23-year-old female patient (height: 150 cm, weight: 48 kg) was diagnosed as G-6-PD deficiency at the age of 7 years after a hemolytic episode, and she received a blood transfusion at that time; no other episodes were reported. She presented to the Otolaryngology-Head and Neck Surgery Clinic with symptoms of nasal obstruction, nasal tone of voice, and mouth breathing. A routine laboratory investigation was revealed: hemoglobin of 12.3 g/dL, white blood cell counts of 4.63 × 109/L, RBC counts of 4.09 × 1012/L, and platelet of 158 × 109/L; all are within normal limits. Computerized tomography (CT) of paranasal sinuses showed deviated nasal septum, minimal mucosal thickening seen in the maxillary sinuses, left upper molar radicular cyst, and asymmetrical thickening of the nasopharyngeal mucosa.
The planned surgery was for coblation adenoidectomy with septoplasty and turbinectomy. Intraoperatively, a 20-gauge intravenous cannula was established, and the patient was monitored by electrocardiogram (ECG), bispectral index sensor (BIS) and the measurement of oxygen saturation (SpO2), non-invasive blood pressure (NIBP), temperature, and followed by preoxygenation. Pre-induction vital signs revealed blood pressure of 118/81 mm Hg, heart rate of 82 beats per minute (bpm), SpO2 of 100%, and a temperature of 36.4 °C. Thereafter, general anesthesia induced with fentanyl (100 µg), propofol (150 mg), rocuronium (30 mg), and dexamethasone (16 mg). The patient was intubated by a direct laryngoscope with oral endotracheal Ring-Adair-Elwyn (RAE) tube (internal diameter (ID): 6.5 mm) with an inflatable cuff and connected to the circuit of the anesthesia machine. Anesthesia has been maintained by the inhalational anesthetic agent sevoflurane (2.0%) with O2/N2O mixture (1.0/1.0 L/min). The patient was positioned supine for the surgery. Before the incision was made, cefazolin (2 g) was given as a prophylactic antibiotic. At 40 min into the surgery, we administered paracetamol (1 g) followed by oxycodone (4 mg). Also, she received isotonic, crystalloid fluid (Ringer’s lactate) with a total infusion of 650 mL. The estimated blood loss was 50 mL. Intraoperatively, the patient was vitally stable. The duration of the surgery was approximately 90 min. At the end of the surgery, we reversed the residual neuromuscular medication with glycopyrrolate (0.4 mg) plus neostigmine (2.5 mg), and when the patient was fully awake, the trachea was extubated successfully. Postoperatively, oxycodone has been used as a postoperative analgesia. Moreover, we monitored the patient for any signs or symptoms of an acute hemolytic crisis. The patient was discharged on the second postoperative day (POD) after assuring the result of complete blood count (CBC) is normal.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [150.0, 'cm'], 'weight': [48.0, 'kg']}",21.33333,20.26666,22.4,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 150.0 cm, which is 150.0 cm * 1 m / 100 cm = 1.5 m. The patient's weight is 48.0 kg. The patient's bmi is therefore 48.0 kg / (1.5 m * 1.5 m) = 21.33333 kg/m^2."
2457,6,Body Mass Index (BMI),physical,decimal,pmc-3079136-1,Extracted,"A 32-year-old woman presented to the outpatient clinic with a cardiac murmur that had been detected at a local clinic. There were no associated cardiac symptoms and she did not complain of any other health issues. Her body weight was 64.5 kg and height was 159 cm. She appeared healthy and there were no abnormal findings on the physical examination except for a grade 3/6 continuous murmur at the left middle sternal border. There was no definite history of chest trauma. The chest X-rays were normal and the electrocardiogram was also normal. A 2-dimensional-echocardiogram was performed and there were neither intracardiac anomalies nor patent ductus arteriosus. The chest computed tomography and angiogram showed that the left internal mammary artery (LIMA) was dilated; but the reason for this finidng were not readily apparent. However, a further, selective angiogram showed dilated LIMA and a fistula from the LIMA to the internal mammary vein (). We did not evaluate the shunt amount but we decided to do the embolization. Total occlusion was completed with a 4 mm Amplatzer® vascular plug (AGA Medical Corp., Golden Valley, MN, USA); yet, a continuous murmur was still heard after the procedure. We decided that another embolization with two Gianturco coils of 3 mm and 5 loop (Cook, Inc., Bloomington, IN, USA) was needed because another fistulous tract in an anterior intercostal artery from the lateral thoracic artery to the internal mammary vein was detected ( and ). During the procedure, a grade 1 or 2 continuous murmur was detected in the same area. Consequently, we decided to stop the procedure, but continue to follow the patient in the outpatient clinic.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [159.0, 'cm'], 'weight': [64.5, 'kg']}",25.51323,24.23757,26.78889,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 159.0 cm, which is 159.0 cm * 1 m / 100 cm = 1.59 m. The patient's weight is 64.5 kg. The patient's bmi is therefore 64.5 kg / (1.59 m * 1.59 m) = 25.51323 kg/m^2."
2458,6,Body Mass Index (BMI),physical,decimal,pmc-2553054-1,Extracted,"In a healthy Greek male physician, 35-years-old, 173 cm height, 72 Kg weight, never-smoker with no more than one or two drinks weekly, with known natural infection since five years, six TSTs were applied in 12 November 1985 (Figure ). The hands belong to the first author, specialised in Pulmonology at Athens Thorax Diseases Hospital 1976–1980. During this period he had repeatedly negative Mantoux/Sokal TSTs; last negative 10 April 1980. The first positive Mantoux occurred 20 June 1980. Between 11 February 1980 and 11 April 1980 he had no contact at all; thus the most probable period of infection was between 11 and 20 April 1980, his first week in the army, when there was contact with a very probable tuberculosis patient. He received chemoprophylaxis (300 mg isoniazide and 25 mg pyridoxine every morning) from July 1980 to May 1981.
All vials of 1, 2, 5, 10, 20, 50 TU per 0.1 mL purified protein derivative (PPD) RT23 were provided by the Greek Pasteur Institute on the same day, preserved under identical conditions, and administered within a few days after production, long before their expiry date.
The tester was the domiciliary nurse of the Ioannina anti-tuberculosis campaign, with more than twenty years of experience. All six tests were injected lege-artis (one sharp bevelled disposable 25 G needle with a plastic tuberculin syringe per test; intradermal injection of exactly one tenth of a millilitre of PPD tuberculin; 4 mm white blister). Induration was read 72 hours later, using Sokal's technique (Figure ).
The results are presented in Figure . Skin reaction was not a linear function of tuberculin dose; induration was increased with a decreasing rate as tuberculin dose increases (Figure ), while an unexpected decrease occurred in the dose of 10 TUs. Erythema (redness) was not measured but it was parallel to induration (Figure ). No side-effects occurred.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [173.0, 'cm'], 'weight': [72.0, 'kg']}",24.05693,22.85408,25.25978,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 173.0 cm, which is 173.0 cm * 1 m / 100 cm = 1.73 m. The patient's weight is 72.0 kg. The patient's bmi is therefore 72.0 kg / (1.73 m * 1.73 m) = 24.05693 kg/m^2."
2459,6,Body Mass Index (BMI),physical,decimal,pmc-5457868-1,Extracted,"The patient was a 5-year-old Chinese woman. She presented to the emergency department with complaints of cough for 2 weeks and fever for 5 days. She also had headache, vomiting, and altered interactions with her parents for 1 day. She was admitted to the pediatric intensive care unit. She hailed from a large island in East China Sea (6-hours drive to the mainland city center). She had an uncomplicated birth and roughly normal growth during the first 3 years of life but retarded height growth and decreased activity in the recent 2 years (as reported by her parents) without further medical assessment. The patient had no history of medication. On physical examination, the patient's height and weight were 109 cm and 22 kg (z = 0.5 and −1, respectively). Her vital signs included temperature of 38.7 °C, heart rate of 105 beats per minute, respiratory rate of 35 breaths per minute, and blood pressure of 90/55 mmHg. Her oxyhemoglobin saturation was 90% in room air. She showed generalized puffiness and non-pitting edema of the face and extremities capillary refilled time was >3 seconds (Fig. ). Rales were found on the auscultation of both lungs. The cardiac auscultation was normal. Her abdomen was soft, mildly distended with normal bowel sounds. Neurological examination revealed that the patient was slightly confused and could not properly respond to commands.
Additional laboratory examinations were conducted immediately after admission. A complete blood count showed hemoglobin level of 97 g/L, white blood cell count of 2.5 × 109/L, with 70% neutrophils and blood platelet was 75 × 109/L. The levels of electrolytes, glucose, albumin, and creatine kinase were normal. The blood gas was also normal at admission. Chest computed tomographic (CT) scan confirmed left lobe pneumonia and mild pleural effusion (Fig. ). The echocardiogram showed mild pericardial effusion with normal cardiac ejection fraction. The magnetic resonance imaging (MRI) scan of the brain and cerebrospinal fluid exam was normal. The patient was initially diagnosed as pneumonia and sepsis. Empiric antibiotic therapy, immunoglobulin supply (IVIG 2 g/kg) as immune supportive therapy, and restricted fluid administration were given immediately after admission.
Her mental status subsequently deteriorated. She became comatose on the second day after the admission, her temperature dropped to 35 °C. She also developed hypotension, arrhythmia, and hypoxia with SaO2 decreased to 75% (Fig. ). Electrocardiogram confirmed prolonged Q–T interval (Fig. ). Thyroid studies were ordered at admission due to the retarded growth. The thyroid test results were received on the next day while the patient developed coma. Thyroxin (T4) was undetectable in the plasma (reference range, 58.1–140.6 nmol/L, Table ). The thyroid stimulating hormone (TSH) level was extremely high (>150 uIU/mL; reference range, 0.55–4.78 uIU/mL). Laboratory results revealed extremely elevated anti-thyroid peroxidase (TPO-Ab) and anti-thyroglobulin (TgAb) levels in plasma (Table ) after 2 days. Ultrasound of the thyroid revealed mild bilateral enlargement with small tubercles in the left side.
The patient was diagnosed with MC complicated with untreated hypothyroidism on the second day after her admission. The thyroid test indicated that the hypothyroidism was secondary to autoimmune thyroiditis (Hashimoto's thyroiditis). Hormone replacement was immediately started. Intravenous dexamethasone at a dosage of 0.3 mg/kg/d divided every 12 hours was administered for the stressed state early morning on the second day of admission. Later that day, once the thyroid test results were obtained, oral levothyroxine was administered at a dose of 100 μg/m2/d (4 μg/kg/d) once daily by nasogastric tube. The patient also received vasopressor, mechanical ventilation, and continuous renal replacement treatment for hypotension, hypoxemia, and anuria, respectively. Two days after starting levothyroxine, her consciousness was restored and temperature returned to normal. She was extubated on the fifth day after the initial hormone administration (Fig. ).
The dosage of oral levothyroxine was reduced to 3 μg/kg/d once daily 2 weeks after initial administration (Fig. ). She was discharged on this regimen and continues to do well (Fig. ).
Eight months after discharge, her height reached 118 cm, and had increased 9 cm since the initial hormone therapy. She was also reported to be more active than before. Her family was recommended to undergo thyroid tests. Her father and grandmother were confirmed with Hashimoto's thyroiditis as well.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [109.0, 'cm'], 'weight': [22.0, 'kg']}",18.51696,17.59111,19.44281,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 109.0 cm, which is 109.0 cm * 1 m / 100 cm = 1.09 m. The patient's weight is 22.0 kg. The patient's bmi is therefore 22.0 kg / (1.09 m * 1.09 m) = 18.51696 kg/m^2."
2460,6,Body Mass Index (BMI),physical,decimal,pmc-2740165-1,Extracted,"A 36-year-old Indian man was hospitalized 72 hours after forceful vomiting followed by the onset of chest pain, dyspnoea and fever. The patient had no previous medical history and no family history of relevance. He worked as construction worker. He was non-smoker and consumed an average of 40 unit of alcohol per week. His height was 170 cm and his weight was 64 kg. Initial chest radiography showed left-sided hydropneumothorax with mediastinal emphysema. Computed tomography of the chest with contrast showed spontaneous esophageal perforation (Boerhaave’s syndrome) in the left lower third of thoracic esophagus. Patient underwent emergency direct surgical repair with pleural flap reinforcement (first operation). Subsequently he developed an esophageal leak with mediastinitis and empyema, followed by a septic shock. Esophagectomy with cervical esophagostomy, gastrostomy and feeding jejunostomy was done (second operation) with a preparation for esophageal reconstruction at a later stage. Six weeks later, a retrosternal gastric transposition with CEGA was performed using circular stapler (third operation). Transmediastinal gastric transposition was found to be difficult because of the two previous surgeries and inflammatory process. Five days later, the patient developed discharge from the neck incision which required bedside drainage and packing. Contrast study revealed a major disruption of the cervical anastomosis ().
Patient underwent exploration which revealed a necrosis of the gastric tip, resulting in complete anastomotic disruption. Complete median sternotomy was done with extra care not to injure the retrosternal gastric conduit, followed with tedious blunt dissection of the stomach that was firmly adherent to the sternum anteriorly and mediastinum posteriorly. Finally, it was freed with maximum possible mobilization, in order to gain a sufficient length. After generous excision of the necrotic gastric tip and the edge of cervical esophagus, a new CEGA was performed, using manual anastomosis with interrupted 4-0 vicryl (forth operation). Patient made steady postoperative recovery with no signs of sterna infection or mediastinal collection. On the 10th postoperative day esophagogram with gastrograffin showed a patent and competent anastomosis (). Patient was discharged in a stable condition and remained well six months later.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [170.0, 'cm'], 'weight': [64.0, 'kg']}",22.14533,21.03806,23.2526,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 64.0 kg. The patient's bmi is therefore 64.0 kg / (1.7 m * 1.7 m) = 22.14533 kg/m^2."
2461,6,Body Mass Index (BMI),physical,decimal,pmc-3271453-1,Extracted,"A four-year-old girl presented with flank pain that had begun two months ago along with hematuria, pyuria, anemia and thrombocytopenia in her laboratory test results []. She also had low-grade fever which resolved after two days by antibiotic therapy. Her growth indices were in normal range (weight 18 kg above +1 SDS and height 98 cm (0 to +1 SDS), her sonography showed a hypo echoic mass, technetium-99m-dimercaptosuccinic acid scan (Tc99 DMSA) failed to take radiotracer in the upper and middle part of the right kidney []. Thus contrast computerized tomography (CT) has been done [].
Urine culture was positive (50000 colony count of E. coli). After a complete antibiotic therapy for E. coli infection, her voiding cystourethrography showed nothing.
She went under operation for excising mass, (sized 10 × 7 × 6 cm, weighed 350 g), and spherical creamy shaped mass removed and diagnosed as chronic pyelonephritis. In the first month after her operation her thrombocytopenia resolved.
In the second admission four months later she was febrile with pyuria, her computerized renal scan showed a new episode of pyelonephritis in her normal left side; [] which was not affected earlier, according to her previous DMSA and CT scans. She treated with antibiotics for 14 days. She left hospital with antibiotic prophylaxis with attention to her recurrent urinary tract infection.
Her cystourethrogram showed no vesicoureteral reflux. [].",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [18.0, 'kg'], 'height': [98.0, 'cm']}",18.74219,17.80508,19.6793,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 98.0 cm, which is 98.0 cm * 1 m / 100 cm = 0.98 m. The patient's weight is 18.0 kg. The patient's bmi is therefore 18.0 kg / (0.98 m * 0.98 m) = 18.74219 kg/m^2."
2462,6,Body Mass Index (BMI),physical,decimal,pmc-2631534-1,Extracted,"A 31-year-old man was admitted to the hospital because of sterility. The patient was the oldest of three normal siblings born to consanguineous healthy parents. He had normal phenotypic features with unremarkable medical history. He had tall stature (height, 193 cm; weight, 74 kg) with an arm span of 206 cm. Endocrinological testing demonstrated increase in the FSH and LH levels (26.5 and 16.9 mIU/mL, respectively), and a very low level of testosterone (1.8 ng/mL). Seminal analysis revealed azoospermia.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [193.0, 'cm'], 'weight': [74.0, 'kg']}",19.86631,18.87299,20.85963,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 193.0 cm, which is 193.0 cm * 1 m / 100 cm = 1.93 m. The patient's weight is 74.0 kg. The patient's bmi is therefore 74.0 kg / (1.93 m * 1.93 m) = 19.86631 kg/m^2."
2463,6,Body Mass Index (BMI),physical,decimal,pmc-6911283-1,Extracted,"A 24 year-old, 95 kilogram (Kg), 165 centimeter (cm) woman was scheduled for a diagnostic laparoscopy for an indeterminate pelvic mass. Historical workup more than 5 years prior for congenital hypotonia, delayed acquisition of motor skills, persistent discoordination, and chronic fatigue included a muscle biopsy with pathologic examination and oxidative phosphorylation enzymology as well as a mitochondrial deoxyribonucleic acid (DNA) and multi-gene panel for cellular energetic defects including 656 genes. Skeletal muscle oxidative phosphorylation enzymology was equivocal for a possible complex 1 defect and decreased enzymatic activity of complex 1 was observed. Although no associated mitochondrial DNA defect was identified, she acquired a diagnosis of possible MM. Gene sequencing revealed a variant of uncertain significance, reported with conflicting predictions of “possibly damaging” and “tolerated,” in the ryanodine receptor 1 (RYR1) gene (Position Chromosome 19: 38955314, Exon 23, Variant c.[2822C > T]), suggestive of possible MH susceptibility. There was no family history of MH. Additional studies included normal electromyography, brain magnetic resonance imaging, electrocardiogram, and transthoracic echo. Her past medical history was otherwise notable for fibromyalgia/chronic musculoskeletal pain, possible spondyloarthropathy, endometriosis, adnexal cyst, and ectopic pregnancy. She had undergone prior surgical procedures with neuraxial or peripheral nerve blockade. She was warned by medical providers elsewhere to avoid propofol, lactated Ringer’s solution, and succinylcholine.
Given this history, we favored regional anesthesia and the surgical service agreed to an open rather than the originally scheduled laparoscopic procedure. She was pre-medicated with 1 gram (g) oral acetaminophen and intravenous (IV) fentanyl 50 micrograms (mcg) and midazolam 3 milligrams (mg). A combined spinal epidural procedure was performed with the patient sitting upright and with midline approach at lumbar interspace 3–4 with an 18 gauge Tuohy needle, 27 gauge Whitacre needle, and 20 gauge epidural catheter. Loss of resistance with preservative-free normal saline was obtained at 6 cm. Intrathecal injection of 2 milliliters (mL) 0.75% bupivacaine with 8.25% dextrose, 15 mcg fentanyl, and 200 mcg epinephrine was performed. The epidural catheter threaded easily and a test dose of 3 mL of 1.5% lidocaine with 5 mcg/mL epinephrine was negative for intrathecal or intravascular catheter location. Approximately 30 min later, the patient had a dermatomal level around thoracic (T) spinal nerve T8, so the catheter was bolused with 10 mL of 2% lidocaine. After confirming T6 dermatomal level, incision was made. Anesthesia was maintained with divided doses of 10 mL 0.5% bupivacaine with 5 mcg/mL epinephrine and 10 mL 2% lidocaine. For sedation, in addition to previously mentioned pre-medications, she received IV divided doses of 30 mg ketamine, 9 mg midazolam, and 550 mcg fentanyl. For antiemetics she received 0.625 mg droperidol IV, 4 mg dexamethasone IV, and 4 mg ondansetron IV. She was maintained on a 5% dextrose and normal saline IV infusion at 100 mL/hour with intraoperative point-of-care glucose monitoring. Baseline and perioperative lactates were not monitored, although in retrospect we would include this laboratory evaluation. Skin temperature was monitored and normothermia was maintained with a forced air warmer. Surgical time was 4 h and included Pfannenstiel incision, lysis of adhesions, and left ovarian cystectomy. At the conclusion of the case the surgeons infiltrated the wound with a solution of 20 mL 1.3% liposomal bupivacaine in 100 mL normal saline and the epidural catheter was removed. The procedure was well tolerated without complications. The patient was discharged home on postoperative day three.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [95.0, 'kg'], 'height': [165.0, 'cm']}",34.8944,33.14968,36.63912,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 95.0 kg. The patient's bmi is therefore 95.0 kg / (1.65 m * 1.65 m) = 34.8944 kg/m^2."
2464,6,Body Mass Index (BMI),physical,decimal,pmc-3514939-1,Extracted,"A 5-year-old girl, only child, born to nonconsanguineous parents was brought to our out patient clinic with complaint of a large anterior tooth in the maxillary arch. On clinical examination the child was of normal built (weight: 20 kg, height: 112 cm, and head circumference: 49 cm). The philtrum was indistinct. Intraoral examination revealed an absent maxillary median labial frenulum with a large, symmetrical, midline tooth, and fused right mandibular incisors []. The incisive fossa was prominent along with a very prominent midpalatal ridge []. The intraoral periapical radiograph revealed only one central incisor with single root and root canal and no impacted tooth but with only one developing succedaneous tooth []. Intraoral periapical radiograph of mandibular incisors confirmed fusion of right primary central and lateral incisors []. Family history revealed that her father also had a similar anomaly with midline single maxillary incisor.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [112.0, 'cm'], 'weight': [20.0, 'kg']}",15.94388,15.14669,16.74107,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 112.0 cm, which is 112.0 cm * 1 m / 100 cm = 1.12 m. The patient's weight is 20.0 kg. The patient's bmi is therefore 20.0 kg / (1.12 m * 1.12 m) = 15.94388 kg/m^2."
2465,6,Body Mass Index (BMI),physical,decimal,pmc-8499496-2,Extracted,"Eight years ago, a 10-year-old female patient underwent a bone marrow aspiration to investigate growth retardation and splenomegaly, which indicated trilineage hypoplasia. Symptomatic blood transfusion treatment was given. However, the patient’s condition did not improve. Five years ago, she developed pain in the right hip joint with limited mobility, which was considered as a hip abscess. The joint cavity was punctured and drained, and the pus was cultured, which was negative. The joint symptoms improved following the treatment of antibiotics, component blood transfusion, and intravenous human immunoglobulin. Blood investigation showed: WBC 1.87–2.66 × 109/L; reduced neutrophil, 0.42 × 109/L; Hb 53–80 g/L; reduced RBC 2.32–2.45 × 1012/L; PLT 125–152 × 109/L; CRP 8–69 mg/L; AESR 19–140 mm/60 min; SF 520.18 ng/ml; and serum zinc 4.38 mg/L. Whole-exome genetic testing suggested a spontaneous PSTPIP1 c.748G > A (p.E250K) mutation (see Fig. for gene mutation profile), hence, the diagnosis of PAMI syndrome was made. After administration of infliximab 5 mg/kg twice, the patient developed an allergic reaction. So we discontinued inflicimab, and started oral colchicine 0.125 mg for 1 month, which was ineffective. Therefore, we changed to subcutaneous injection of etanercept (0.8 mg/kg) once a week and methylprednisolone 1 mg/kg orally once a day. At 3-year follow-up, the patient did not have arthralgia any more and splenomegaly improved than before. The WBC remained low, between 2 and 3 × 109/L. The haematocrit and platelets were normal. In addition, the CRP and AESR returned to normal. Six months before, when methylprednisolone was reduced from 4 mg to 2 mg every other day, the patient developed pyoderma gangrenosum (PG: Figs. and ), and the secretion culture showed Enterobacter cloacae. Besides, serum zinc level was 6.65 mg/L and faecal calprotectin level was 72.4 μg/L. we did local debridement and gave her antibiotic. In addition, we increased methylprednisolone to 6 mg/d. after treatment, her PG improved considerably (Figs. and ). The patient’s height was 78 cm and weight was 9 kg, which were 3% below the average of her age and gender before treatment. However, after treatment her height and weight were 128 cm and 31.5 kg, respectively, which were 50% for her age and gender.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [128.0, 'cm'], 'weight': [31.5, 'kg']}",19.22607,18.26477,20.18737,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 128.0 cm, which is 128.0 cm * 1 m / 100 cm = 1.28 m. The patient's weight is 31.5 kg. The patient's bmi is therefore 31.5 kg / (1.28 m * 1.28 m) = 19.22607 kg/m^2."
2466,6,Body Mass Index (BMI),physical,decimal,pmc-4371897-3,Extracted,"A 38-year-old female with systemic lupus erythematosus had been taking HC for 11 years. She was 168 cm tall and weighed 60 kg, so her actual body weight was less than her ideal body weight. Her daily dose based on actual body weight was 6.7 mg/kg/d and she had a cumulative dose of 1,606 g. There was no history of concomitant renal or liver disease.
HC toxicity was diagnosed based on taking a potentially toxic dose of HC in conjunction with diffuse central sensitivity loss on visual field testing (), a weak central waveform signal on multifocal ERG testing (), and a generalized loss of the ellipsoid zone through the fovea and parafoveal macula. The near infrared reflectance image did not show a bull’s eye maculopathy ().",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [168.0, 'cm'], 'weight': [60.0, 'kg']}",21.2585,20.19558,22.32143,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.68 m * 1.68 m) = 21.2585 kg/m^2."
2467,6,Body Mass Index (BMI),physical,decimal,pmc-5574512-1,Extracted,"A 63-year-old man (height: 176 cm, weight: 69 kg) presented to a nearby hospital complaining of exertional chest pain. He had experienced similar pain a month earlier, 2 h after his evening meal. Blood examination, chest radiography, electrocardiogram (ECG), and computed tomography (CT) showed no specific abnormalities, and he was referred to our hospital for further evaluation. A 12-lead ECG at our facility showed T-wave inversion in leads V1 through V3. Transthoracic echocardiography showed severe hypokinesis from the antero-septal wall to the mid-apex. He was admitted to our hospital to undergo CAG for suspected myocardial ischemia. The patient had a history of hypertension, chronic kidney disease, sudden deafness, and smoking. He had no history of dyslipidemia, diabetes mellitus, or alcohol consumption, and there was no history of ischemic heart disease in his family. Although he was diagnosed with IgG4-RD 1 year prior, he had not received any treatment for that condition. At that time, pathological examination of a submaxillary gland showed an infiltration of small lymphocytes, acidophilic leukocytes (acidocytes), and plasma cells, particularly IgG4+ plasma cells. The IgG4+/IgG+ plasma cell ratio was >40%. Four months previously, he had also been diagnosed with IgG4-related nephritis on the basis of a renal biopsy.
His physical examination showed a blood pressure of 138/74 mmHg, a pulse of 48 beats per minute, a respiratory rate of 12 breaths per minute, and an oxygen saturation of 96% on room air. No cardiac murmurs or abnormal respiratory sounds in the lungs were detected with auscultation. Blood examination revealed elevated levels of creatinine (1.12 mg/dL; normal: 0.65–1.09 mg/dL), triglycerides (163 mg/dL; normal: 35–150 mg/dL), and brain natriuretic peptide (53.4 pg/mL; normal: 0.0–18.4 pg/mL), and a normal level of β2 (1.9 mg/dL; normal: 0.8–2.0 mg/dL). Immunological examination showed elevated levels of IgG (1896 mg/dL; normal: 739–1649 mg/dL), IgG4 (527 mg/dL; normal: 4–108 mg/dL), and soluble interleukin-2 receptor (sIL-2R; 751 U/mL; normal: 220–530 U/mL) and low levels of C3 (82 mg/dL; normal: 86–160 mg/dL) and IgM (29 mg/dL; normal: 46–260 mg/dL).
CAG showed a 90% stenosis in the mid-left anterior descending (LAD) coronary artery (). The stenosis looked smoother than those seen in arteriosclerotic stenosis. No other lesions were detected. After a guide wire crossed the lesion, IVUS (View It; Terumo, Tokyo, Japan) catheter was inserted to visualize the characteristics of the LAD lesions. IVUS demonstrated a thickened black layer beneath the intima at the lesion and nearly normal vessel wall at the proximal and distal LAD (). Compared to proximal and distal arteries, stenosis of the lesion consisted of thickened intima-media, especially black layer beneath the intima. The LAD lesion was treated with percutaneous coronary intervention (PCI) using a drug-eluting stent. PCI was successful with no complications, and the patient’s exertional chest pain resolved after treatment. Two months later, the patient was started on corticosteroid therapy for the treatment of sudden deafness. Follow-up CAG at 1 and 3 years later showed no de-novo lesions and no in-stent restenosis.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [176.0, 'cm'], 'weight': [69.0, 'kg']}",22.27531,21.16154,23.38908,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 176.0 cm, which is 176.0 cm * 1 m / 100 cm = 1.76 m. The patient's weight is 69.0 kg. The patient's bmi is therefore 69.0 kg / (1.76 m * 1.76 m) = 22.27531 kg/m^2."
2468,6,Body Mass Index (BMI),physical,decimal,pmc-4173574-1,Extracted,"A 30-year-old woman presented with the chief complaints of pain and swelling in the right elbow joint. There was no history of fall, fever, or weight loss. Patient was diagnosed as having pathological fracture of right radius. Patient gave history of breathlessness and was of New York Heart Association grade II. On general physical examination, patient weight was 55 kg, 160 cm in height, Polydactyl of all four limbs [], clinodactyly and loss of thenar prominence [] are noted. The airway assessment showed Mallampatti grade I, thyromental distance of 6 cm, and mouth opening of three fingers. Systemic examination showed fixed spilt second heart sound with grade two systolic murmur, regular good volume pulse. There was no organomegally, no raised jugular venous pressure, and no signs of congestive cardiac failure noted.
Preoperative hemogram, random blood sugar, electrolytes, renal function tests, and chest radiograph were normal. Electrocardiogram revealed right bundle branch block. The echocardiography showed large ostium primum ASD with left to right shunt, with cleft in anterior mitral leaflet, mild mitral regurgitation, moderate tricuspid regurgitation, moderate pulmonary artery hypertension, dilated right atrium, and ventricle with mild left ventricular dysfunction.
The patient received premedication of Tab. Diazepam 5 mg and Tab. Ranitidine 150 mg per oral night before surgery and on the day of surgery in the morning. Tab. amoxicillin 2 g orally 1 h prior to surgery was given to prevent infective endocarditis. Patient was kept nil per oral for 6 h before surgery and received intravenous (I.V.) fluids of 1 mL/kg/h.
On arrival to operating room blood pressure was 118/70 mm hg, heart rate 76/min, respiratory rate 14/min and oxygen saturation 96%. Electrocardiography monitoring was established, together with monitoring of noninvasive arterial pressure and pulse oximeter.
There are no data in the literature to suggest preferred anesthetic technique. Since the procedure was at the elbow region, the peripheral nerve block, that is, supraclavicular brachial plexus block was selected as it is much superior compared with general anesthesia in this case. Patient received Inj. Midazolam 2 mg and Inj. Fentanyl 55 mcg intravenously for procedural sedation. We identified the supraclavicular brachial plexus by peripheral nerve stimulator technique. A combination of inj. Lignocaine (2%) 5 mg/kg body weight and Inj. Bupivacaine (0.5%) 2 mg/kg body weight was injected after negative aspiration for blood. We did avoid combination of Ing Lignocaine with Adrenaline in view of possible new onset of arrhythmias. Successful block was achieved and procedure was uneventful. Patient received the inj. Diclofenac 75 mg I.V. infusion postoperatively after 4 h as the visual analogue score was 5. Patient was shifted to high dependency unit for monitoring 24 h and followed-up to note any complications related to nerve block.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [160.0, 'cm'], 'weight': [55.0, 'kg']}",21.48437,20.41015,22.55859,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.6 m * 1.6 m) = 21.48437 kg/m^2."
2469,6,Body Mass Index (BMI),physical,decimal,pmc-5331980-1,Extracted,"A 31-year-old pregnant woman, gravida 2, para 1, in the 11th week of gestation was referred to our nephrology clinic for evaluation of hypokalemia detected incidentally during a routine health exam. She complained of chronic fatigue and recurrent numbness of both her hands. She had no relevant medical history, and denied laxative or diuretic abuse. There was no history of renal disease in her family.
On examination, she was thin (height 160 cm, weight 40 kg) with blood pressure of 90/60 mmHg without significant postural drop and no evidence of dehydration or fluid overload.
Biochemical investigation revealed hypokalemia with metabolic alkalosis, hypocalciuria, increased plasma re-nin activity and aldosterone (serum K, 2.57 mmol/L; total CO2, 32.3 mmol/L; random urine calcium/creatinine (Cr), 0.00016 mg/mg Cr; plasma renin activity, 10.83 ng/mL/hr; aldosterone, 24.9 ng/dL; respectively). The patient’s transtubular potassium gradient (TTKG) was elevated despite hypokalemia (TTKG, 8.25). Serum magnesium level was within normal range (2.11 mg/dL) (). Neither proteinuria (33 mg/gCr) nor hematuria was detected. These findings suggested Gitelman syndrome, with the exception of the normal magnesium level. The diagnosis was confirmed when a mutation c.2716C>T (p.Pro906Ser) (heterozygote) in the SLC12A3 gene was found on genetic analysis (). Oral potassium supplementation was started, and the patient underwent routine examination during her pregnancy (). Spironolactone was not given because of the possible antiandrogenic effects on the male fetus.
When the patient was at 33 weeks’ gestation, she visited the emergency department with a tingling sensation and tetany in both the upper and lower extremities. Her blood pressure was 120/80 mmHg, within normal range, but higher than her usual blood pressure (90/60 mmHg). Her Cr level was elevated (2.03 mg/dL) and renal protein excretion was slightly increased (0.2 g/gCr). Additional laboratory results were compatible with HELLP (hemolysis, elevated liver enzyme, low platelet) syndrome, including decreased haptoglobin (8 mg/dL) and increased plasma hemoglobin (12.5 g/dL) levels, increased lactic acid dehydrogenase (969 IU/L) levels, schistocytes on peripheral blood smears, elevated liver enzymes (aspartate aminotransferase, 210 IU/L; alanine transaminase, 108 IU/L), and decreased platelet counts (101,000/mm3). Fractional excretion of sodium was 0.72% and serum uric acid was 23.86 mg/dL.
The patient had abnormal uterine contractions resulting in spontaneous vaginal delivery of a male infant weighing 1,630 g (50% for his gestational age). His Apgar score was 4 in the first minute and 5 after five minutes, and he was admitted to the neonatal intensive care unit. Hyperbilirubinemia (peak total bilirubin 9.87 mg/dL, indirect bilirubin 1.03 mg/dL) was detected, but his electrolytes were normal other than mild hyponatremia (sodium, 126.7 mmol/L; potassium, 3.01 mmol/L; chloride, 88.8 mmol/L). Postpartum, the patient suffered from disseminated intravascular coagulation (platelets, 89,000/μL; prothrombin time, 9.9 sec; activated partial thromboplastin time, 32.4 sec; D-dimer, 2.60 μg/mL; fibrin degradation products 8.1 μg/mL; and antithrombin III, 22%). The patient and neonate recovered slowly during the following weeks (). The patient was discharged on daily oral potassium and spironolactone (). Outpatient follow-up after five months revealed patient blood pressure of 90/60 mmHg and serum potassium and magnesium levels of 3.03 mmol/L and 2.17 mg/dL, respectively.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [160.0, 'cm'], 'weight': [40.0, 'kg']}",15.625,14.84375,16.40625,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 40.0 kg. The patient's bmi is therefore 40.0 kg / (1.6 m * 1.6 m) = 15.625 kg/m^2."
2470,6,Body Mass Index (BMI),physical,decimal,pmc-6822454-1,Extracted,"During the pregnancy of the proband by a 23-year-old G1P0 mother, prenatal ultrasound of the fetus revealed congenital anomalies including dilated right cerebral ventricle (suspected germinal matrix hemorrhage), pyelectasis, echogenic bowel, and hypoplastic nasal bone. 36-week gestational fetal MRI revealed cystic encephalomalacia in region of left caudate nucleus and caudothalamic groove appears more conspicuous, likely reflecting sequela of germinal matrix hemorrhage, similar prominent left lateral ventricles without evidence of obstructive hydrocephalus, and mild left fetal pyelocaliectasis.
The proband was born at 37-week-6-day gestational age by cesarean due to breech presentation, and abnormal prenatal ultrasound/MRI findings. The mother was group B streptococcus positive. At birth, his weight was 2.915 kg, his length is 47 cm, and his occipital–frontal circumference (OFC) was 34.5 cm. His Apgars were 7 and 8 at 1 and 5 min, respectively. He had decreased respiratory effort after birth and requiring blow by oxygen briefly. His echo showed small patent ductus arteriosus with left to right shunting, ductal velocity indicating elevated pulmonary artery pressures, and insufficient tricuspid valve regurgitation for estimation of right ventricular systolic pressure. His ultrasound revealed resolving left germinal matrix hemorrhage. He had no acute hemorrhage, no pyelectasis, no echogenic bowel, and a normal size of the ventricles. His MRI revealed periventricular white matter cystic encephalomalacic change at the left frontal horn and caudothalamic groove, likely representing sequela of prior germinal matrix hemorrhage. He had bilateral undescended testes with right testis located within the inguinal canal, and the left testis seen coursing between the left lower pelvis and upper inguinal canal.
At the age of 4 months, his height was 55.9 cm (<1st centile; 50th centile for a 1-month old), his weight was 5.1 kg (<1st centile; 50th centile for an 1.5-month old), and his OFC was 41.4 cm (38th centile). He had failure to thrive, developmental delay, severe tracheomalacia, stridor/difficulty breathing along with decreased oral intake, bilateral inguinal, gastroesophageal reflux disease, and bilaterally undescended testes. He also had possible seizure disorder, increased tone, and abnormal rigid movements with significant jitteriness and frequent myoclonic jerks. His anterior fontanelle was open and flat. He had facial dysmorphisms including small nose and depressed nasal bridge with possible hypertelorism.
His mother had intellectual disability and lived with her mother. Paternal grandmother and paternal great grandmother had seizure. Father’s family members had attention deficit hyperactivity disorder, anxiety, and depression disorders. No cancer-related disorders were found on either side of the family.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [5.1, 'kg'], 'height': [55.9, 'cm']}",16.32099,15.50494,17.13704,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 55.9 cm, which is 55.9 cm * 1 m / 100 cm = 0.559 m. The patient's weight is 5.1 kg. The patient's bmi is therefore 5.1 kg / (0.559 m * 0.559 m) = 16.32099 kg/m^2."
2471,6,Body Mass Index (BMI),physical,decimal,pmc-7078131-2,Extracted,"A 33-year-old man with newly diagnosed diabetes was admitted to our department for glycemic control. He had been married for 6 years with no children. He had a tall stature (height 188.0 cm, bodyweight 101.6 kg) and small testes. He showed a marked decrease in serum total testosterone (0.91 ng/mL), and elevated gonadotropin (LH 30.0 mIU/mL, follicle-stimulating hormone 25.7 mIU/mL). Human chorionic gonadotropin-stimulated total testosterone level was low (2.18 ng/mL). G-band karyotyping showed 47, XXY, diagnostic of KS. Testosterone enanthate was initiated, and diabetes was treated with metformin and teneligliptin. He was also referred to an infertility clinic for assisted reproduction.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [188.0, 'cm'], 'weight': [101.6, 'kg']}",28.74604,27.30874,30.18334,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 188.0 cm, which is 188.0 cm * 1 m / 100 cm = 1.88 m. The patient's weight is 101.6 kg. The patient's bmi is therefore 101.6 kg / (1.88 m * 1.88 m) = 28.74604 kg/m^2."
2472,6,Body Mass Index (BMI),physical,decimal,pmc-7270203-1,Extracted,"This 31-year-old Hungarian female patient was born at term with 2,380 g birth weight and 47 cm length. During the time Hungary was polluted from air by the radiation originated from Chernobyl in May 1986 her mother spent a full day outdoor and developed an undiagnosed disease with fatigue, dizziness and diarrhea lasting for a week. Otherwise the pregnancy was uneventful, and the patient was born with no complication. The patient's father developed bladder cancer at age 41 which was treated successfully by surgery and chemotherapy. The umbilical cord of the patient detached 13 days after birth and local infection of the stub by Candida was diagnosed and treated successfully with local agents. She was immunized with Bacille-Calmette-Guérin vaccine at 3 days after birth and had seropurulent discharge from the site of injection at 6 and 9 months of age, respectively, for a few days. She received other childhood immunizations including diphtheria, pertussis, tetanus, poliomyelitis (Sabin vaccine), and one shot of measles-mumps-rubella vaccine without complication. Remarkably, she developed fever of 39–40 °C after each shot. At 7 months of age she developed aphthous stomatitis which recurred monthly at the beginning and more frequently later on but oral candidiasis was not visible. The second episode of aphthous stomatitis at age 3 required hospitalization and this time oral candidiasis was also diagnosed and she was treated with local nystatin and metronidazole. Pharyngeal and stool cultures yielded C. albicans. Sedimentation rate was 9 mm/h, platelet number, 122.5 Giga/L, serum iron and zinc levels were 5.5 and 7.43 μM, respectively. Tuberculin skin test evoked an 8 × 8 mm erythematous nodule, HIV serology and direct and indirect Coombs tests were negative. T cell number evaluated with rosetta test was 55% of lymphocytes (normal, 75–80%), T cell proliferation assay showed 35% blasts (normal, 40–45%), serum IgM, 1,15 g/L, IgA, 1,12 g/L, IgG, 12,3 g/L), complement hemolytic activity and granulocyte respiratory burst activation (nitroblue tetrazolium reduction and superoxide anion generation) were normal. She was discharged with the clinical diagnosis of undefined “Immunodeficiency.” At age 5 she developed chickenpox, received hyper immune globulin and oral acyclovir and developed only about 20 vesicles and a mild course of the disease. Later on, however, she developed herpes simplex each year for 4–5 years, usually in August, and from age 24 she had recurrent herpes simplex every other year for 3 times mostly in the back and once in the lower abdomen with lesions of 8–10 cm size. At age 7 she was admitted to hospital with high fever and cough. WBC was 19,3 Giga/L, sedimentation rate, 98 mm/h, platelet number, 224 Giga/L, hemoglobin, 122 g/L, serum IgM, A, and G were 0.87, 1.14, and 20.8 g/L, respectively. Chest X-ray showed signs of bacterial pneumonia and did not suggest fungal etiology. Culture of urine, stool, throat scrub, nasal scrub, sputum and stool did not yield bacterial or candida pathogen. Serology and sputum culture for Mycoplasma, Chlamydia, Legionella, and P. jiroveci gave negative results. Treatment with various combinations of vancomycin, ceftazidime, brulamycin, clindamycin, and monobactam antibiotics and diflucan, the latter given because of the prolonged antimicrobial treatment, resulted in recovery from the severe, lower respiratory tract infection. At 13 years of age she met a bicycle accident and developed multiple fractures in her left tibia and fibula. Even after normal bone healing her left lower extremity remained 2 cm shorter than the right one. Since the first hospital admission she was scheduled for yearly immunology checkup and a decrease in the ratio of CD3+ and CD4+ T lymphocytes and occasionally an increase in the B lymphocytes was detected. Autoimmune and allergy serology tests gave negative results, only ASCA IgA and IgG was somewhat elevated (26–67 U/l) over the years. During her school age she was no more susceptible to viral respiratory or gastrointestinal infections than her schoolmates. She was somewhat even more resistant to community infections including flu compared to her schoolmates. Remarkably, however, when she had infection occasionally, she always had high fever and when she received antibiotic treatment, she always developed oral stomatitis. Despite the lack or recurrent infections her weight percentile remained below 3 and she had microcytic anemia all over the time. Since her school age she has had persistent and recurrent eczema in the crook of the arm, the ham, the neck and the eyelids. At 17 years of age she was hospitalized for high fever, bilateral cervical lymphadenopathy, severe stomatitis with deep ulcers and difficulty eating and swallowing. Epstein-Barr virus serology revealed past infection with negative serum anti-VCA IgM and positive anti-EBV nuclear antigen. Adenovirus and cytomegalovirus serology gave negative results. Elevated liver enzymes were first detected at age 18 and remained slightly elevated afterwards. At age 18 she developed gastroenteritis and high fever which was attributed to Campylobacter species infection. At the age 21 chest X-ray was performed because of cough and rales on both sides and revealed patchy alveolar infiltrations around both hilus and fine interstitial infiltrations in both lower lobes. Inactive, 5–6 mm-sized, homogenic infiltrations were found in the upper lobes. Amoxicillin-clavulanic acid, clarithromycin and methylprednisolone treatment resulted in partial relief of cough, and the pneumonia finally resolved for levofloxacin and amoxiclav. Bronchoscopy and mycobacterial culture gave negative results. Calcification of the previously found upper lobar lesions was detected by X-ray. A host of autoimmune and allergy serology tests gave negative results and the etiology of the lung disease remained undefined. Campylobacter coli infection was diagnosed again at age 22. Between 19 and 25 years of age when she was a medical student, oropharyngeal and esophageal ulcers developed more and more frequently and at age 25 she did not become symptomless and had daily fever without defined infectious disease. During this period, she underwent esophago-gastro-duodenoscopy 9 times and colono-ileoscopy twice. These examinations revealed severe ulcerous lesions all over the length of the esophagus once with Candida patches, scars and narrowing at several locations. In the stomach and duodenum lymphatic stasis was detected. Colono-ileoscopy ruled out inflammatory bowel disease; however, histology of the esophagus at the peak of the symptoms complied with the manifestation of the Crohn's disease in the upper gastrointestinal tract, and no histology could detect any sign of fungal infection. At age 25 she underwent surgery for gluteal abscess and treated with amoxiclav and ciprofloxacin empirically.
We first saw the patient at age 25 during the episode what the patient defined as the most severe attack of oropharyngeal ulceration (). Her weight was 37 kg and her height was 167 cm. Several deep ulcers of 5–14 mm in the buccal mucosa were seen and the patient could only swallow liquid. The facial skin was covered with papulopustulosus lesions of rosacea mostly in the nasolabial and maxillary areas. Chest CT scan revealed miliary lesions in the left apical and posterior segments. Blood culture yielded alfa-hemolytic Streptococci and buccal swab culture was positive for S. aureus. Bronchofiberoscopy showed atrophic, fragile bronchial mucosa but mucosal swab culture gave negative result. Coccidioides serology on admission and 8 months later revealed “TP” antibodies in the serum. CMC was thought and targeted STAT1 sequencing was performed which revealed a novel sequence variant affecting the DBD. Functional analysis suggested GOF mutation (see Results). Parenteral acyclovir, clindamycin and fluconazole treatment was started, but her condition did not improve. Her treatment was switched to a combination of Caspofungin and low dose (30 mg/day) prednisone with local agents including nystatin, amphotericin B, xanthoflavin, lidocaine, and ascorbic acid was applied. Her condition improved in a week and full oral food intake and calorization could be started. The patient's general condition and appetite improved, and she started to gain weight. After she became free of ulcer, fluconazole maintenance therapy at a dose of 150 mg/week and prednisone at a 5 mg maintenance dose were continued for a few weeks. She was without therapy and remained stable for 1 year. At 27 year of age she became pregnant and in the second semester she developed upper respiratory tract disease and took amoxiclav for 7 days which precipitated stomatitis and ulcers. Prednisone at 10 mg dose was effective for the ulcers but in the third semester soor appeared on the oral mucosa and C. glabrata was detected from the vaginal scrub. At this age she experienced onychomycosis in her right thumb which proved to be recalcitrant to local therapy. She started again fluconazole at a dose of 2 × 150 mg/week Her mucositis was well controlled by treatment with local antifungals and 10 mg, and later on 5 mg per day prednisolone. Otherwise the pregnancy was uneventful, and in January 2016, she gave birth to a girl of 2,740 g and 47 cm (Patient 2, see below). She went off medications and for more than a year was well. At 29 years of age she again developed oropharyngeal and esophageal ulcers that was treated with steroids and fluconazole which resulted in rapid improvement. Over the past years she has had transient and mild oral aphtha and esophagitis responsive to short courses of prednisolone (maximal 30 mg per day) and fluconazole (maximal 2 × 150 mg weekly). She has been on 5 mg per day prednisolone and 150 mg per week fluconazole maintenance therapy.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [37.0, 'kg'], 'height': [167.0, 'cm']}",13.26688,12.60354,13.93022,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 167.0 cm, which is 167.0 cm * 1 m / 100 cm = 1.67 m. The patient's weight is 37.0 kg. The patient's bmi is therefore 37.0 kg / (1.67 m * 1.67 m) = 13.26688 kg/m^2."
2473,6,Body Mass Index (BMI),physical,decimal,pmc-3404937-1,Extracted,"The patient is a 63-year-old Caucasian man. He is 1.61 meters tall and weighs 66 kilograms. After working as a car mechanic for 36 years, he had been receiving disability benefits for 11 years. He was working part-time as a caretaker averaging 10 hours per week until two and a half years ago. At the age of 35, the patient began having bouts of severe back pain approximately twice a year. When these episodes occurred, he took non-steroidal anti-inflammatory drugs for three to four weeks for pain relief. At the age of 40, lumbar spondylolisthesis was diagnosed by radiography. At the age of 50, he suddenly developed severe right hip pain. He suffered from substantial arthrosis on the right side, which was treated with a total hip replacement one year later.
Three years ago, he began to develop neurological symptoms in both hands. Pain and loss of function of his fingers prevented him from working as a caretaker. The pain radiated from his neck bilaterally down to his fingers and was described as parasthesia-like in nature. He also complained of weakness in his hands. Left hand digit flexion was classified as J1 and right hand as J4. Digit extension was classified as J4 on the left and J2 on the right and abduction on the left was classified as J0 and on the right as J1. The patient also had difficulty walking (Nurick 4, EMS 10/18) as he had to support himself using his surroundings in order to stand upright and was unable to walk unassisted. He was referred to a neurologist by his general practitioner who in turn referred him to a neurosurgeon. Radiographs (Figure ) magnetic resonance imaging (Figure ) and computed tomography (CT) revealed a spondylolisthesis between C7 and T1. Using the Meyerding classification [], which was initially developed for grading the degree of lumbar spondylolisthesis, the patient would have been diagnosed with a cervico-thoracic spondylolisthesis of the second or third degree. The spondylolisthesis, measured using the method developed by Kawasaki et al. [], was 13 mm. In view of the special nature of the case, a collaborative treatment between neurosurgeons and orthopedic surgeons was favored and subsequently implemented.
The surgical management was performed as follows:
The patient was placed in the supine position. The intervertebral disk at C7-T1 was exposed using blunt dissection. The disk was then removed to the point of the ligamentum flavum. A subsequent resection of the lateral parts of the intervertebral discs significantly mobilized the spondylolisthesis.
The wound was closed and the patient was rotated to the prone position. First, the dislocation between vertebras C7 and T1 was reduced while positioning the head.
Subsequently, the lateral masses were prepared from a dorsal approach between C5 and T3. Then, lateral mass-screws were inserted into C5 and C6. We had noticed considerable laxity between C6 and C7. In addition, C5 and C6 were naturally fused and we decided to include them in the instrumentation. There was also a rigid displacement between C7 and T1.
Bicortical screws were then inserted into the transverse processes of T2 and T3. These were inserted into at least two segments from both sides in divergent directions. The length of these screws was 10 to 12 mm, with a diameter of 3.2 mm.
This was followed by a laminectomy. Since the roots of C7 and C8 were exposed, the lateral masses of C7 and C8 had to be resected. Longitudinal rods were placed. Proper reduction in lordosis and the preservation of a 5 mm intervertebral space between C7 and T1 were confirmed by radiograph. Set screws were used to fix the instrumentation in the desired position. Chips of cortical and cancellous bone were placed lateral to the longitudinal rods.
The dorsal wound was then closed. The patient was again rotated to the supine position to reopen the ventral wound. Now, instead of the previously seen displacement, a large gap was visible between C7 and T1. The endplates between C7 and T1 were milled and the ligamentum flavum was resected using punches. Then, the spinal canal was exposed completely, using a Caspar opener.
Subsequently, a Harms basket, filled with autograft bone chips, was inserted into the intervertebral space. Three drains were placed and the wound was closed. For prophylactic infection control, the patient was perioperatively given intravenous 1.5 g cefuroxime twice a day for the next four days. Intraoperative and postoperative radiographs (Figure and ) were taken to confirm correct placement of the instrumentation.
Following the operation, the patient was transferred to the intensive care unit. His vital signs were stable enough for him to be transferred to the general postoperative recovery ward on the fourth postoperative day. Eleven days after surgery, the patient left the hospital and entered an orthopedic and neurologic rehabilitation program.
The pain and parasthesias in his fingers resolved after the operation. Two months postoperatively, his ability to walk had noticeably improved after completing his rehabilitation program (Nurick 3).
Today, two years postoperatively, the patient is able to walk without assistance (Nurick 2). Flexion of the fingers on his left hand was graded as J3 and as J5 on the right hand. Extension of the fingers on his left hand was graded as J4 and as J2 on the right. Abduction was graded as J4 for his left hand and as J2 for his right hand (EMS 14/18).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [1.61, 'm'], 'weight': [66.0, 'kg']}",25.46198,24.18888,26.73508,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.61 m. The patient's weight is 66.0 kg. The patient's bmi is therefore 66.0 kg / (1.61 m * 1.61 m) = 25.46198 kg/m^2."
2474,6,Body Mass Index (BMI),physical,decimal,pmc-3789027-1,Extracted,"A 54-year-old female (weight, 46 kg; height, 153 cm), was transferred to Tri-Service General Hospital on account of an unexpected large pancreatic tumor. The clinical history of the patient included paroxysmal headaches, mildly elevated blood pressure (BP), diaphoresis and occasional palpitations. The patient was previously diagnosed with ventricular arrhythmia by cardiovascular departments in numerous hospitals, without any other significant findings. The patient was not administered regular treatment for the headaches or hypertension as the symptoms were considered insignificant. One month prior to surgery, the patient underwent a detailed health checkup and an abdominal mass was identified using abdominal sonography. A large, well-encapsulated pancreatic tail tumor, measuring 9 cm in length, was observed on abdominal computed tomography (). The patient was consequently transferred for surgical intervention.
On admission, mildly elevated BP (138–160/80–90 mmHg) with a heart rate (HR) of 70–90 beats per minute (bpm) was noted. The ECG revealed a normal sinus rhythm with two ventricular premature contractions (VPCs). Other laboratory tests showed no significant abnormalities. An exploratory laparotomy with a resection of the tumor was scheduled. Thoracic epidural anesthesia was initially performed without adverse events, followed by general anesthesia. When the pancreas was approached, no any abnormal lesions were identified, with the exception of a bulging mass from the retroperitoneal region. The mass originated from the adrenal gland and presented as a capsulated, vessel-rich tumor. The systolic BP surged to 260 mmHg abruptly with fluctuations and the HR increased to 150 bpm during the manipulation of the tumor. The concentration of the anesthesia was increased along with an additional administration of 100 μg intravenous (i.v.) fentanyl. The fentanyl was ineffective and 5 mg i.v. labetalol was administered twice. However, the hypertensive crisis remained. The surgeon made a temporary stay of surgery until the vital signs were under control and then the tumor was removed.
The BP dropped (75/50 mmHg) once the tumor was removed. Aggressive fluid replacement and vasopressors were administered until the patient was hemodynamically stable. The endotracheal tube was then removed. At one day post-surgery, the patient was completely asymptomatic and no sequelae were identified. The pathological report confirmed a diagnosis of pheochromocytoma () and the patient was discharged five days later.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [46.0, 'kg'], 'height': [153.0, 'cm']}",19.65056,18.66803,20.63309,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 153.0 cm, which is 153.0 cm * 1 m / 100 cm = 1.53 m. The patient's weight is 46.0 kg. The patient's bmi is therefore 46.0 kg / (1.53 m * 1.53 m) = 19.65056 kg/m^2."
2475,6,Body Mass Index (BMI),physical,decimal,pmc-4928445-1,Extracted,"A 38-year-old female patient (height: 153cm, weight: 55kg) was scheduled for kidney transplantation from cadaveric donor. She had been diagnosed with chronic kidney disease about two years ago and on hemodialysis for one year.
Anesthesia was induced with propofol 100mg and atracurium 25mg with equipment of monitoring including BIS, invasive arterial pressure, pulse oximeter and electrocardiogram. After tracheal intubation, the anesthesia was maintained by 6% desflurane, 0.1μg/kg·min remifentanil and intermittent atracurium. Triple lumen venous catheter was placed in the right internal jugular vein with fluid infusion and central venous pressure monitor. Esophageal probe was inserted to record body temperature. Warming blanket with convective air warming system covered chest, both arms and head to keep body temperature normal (). BIS value maintained from 35 to 50 and electromyography (EMG) was almost fixed at 27 during one and half hour of operation. BIS Signal Quality Index (BIS-SQI) and Suppression Ratio (SR) was 100 and 0, respectively. Blood pressure was 131 over 72 mmHg, and heart rate was 69 beats per minute. WarmTouch™ was operated for body heating because esophageal temperature dropped from 36.3 to 36.0ºC. BIS and EMG increased to 74 and 37, respectively. BIS-SQI and SR was 100 and 0, unchanged. Hemodynamics was steady state. The anesthesiologist added up desflurane to 8% concentration and inject atracurium 5mg. However, BIS was over 70 and EMG was 37. After turning off WarmTouch™, BIS and EMG returned to 45 and 27. BIS and EMG was raised again to same numerical value after switch on WarmTouch™. Heated and humidified breathing circuit (Heated Circuit Kit®, Ace Medical, South Korea) was applied for normothermia without activation of WarmTouch™. Esophageal temperature was maintained at 36.0 ºC to recovery of anesthesia. Total operation time was four hours and the patient did not recall any intraoperative event. The patient was discharged without any symptom or complication on postoperative 22 days.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [153.0, 'cm'], 'weight': [55.0, 'kg']}",23.49524,22.32048,24.67,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 153.0 cm, which is 153.0 cm * 1 m / 100 cm = 1.53 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.53 m * 1.53 m) = 23.49524 kg/m^2."
2476,6,Body Mass Index (BMI),physical,decimal,pmc-3973812-1,Extracted,"A 49-year-old Chinese rural woman was admitted to our hospital with chest tightness for 10 days, complaining of mild shortness of breath without past medical history. She was a nonsmoker, and maintained a healthy weight of 50 kg for her 163 cm height. On examination, the patient was found to have absent breath sounds accompanied by dullness on percussion in the right low lung field. Laboratory workup was normal. The results of lung function tests, which showed FEV1/FVC was 99%, furthermore FVC was 64.1% of its predicted value, were consistent with the impression of restrictive ventilatory disorder result from thoracic large tumor.
A routine chest roentgenogram (Figure A) showed a large homogenous mass in the lower half of the right lung field. A computed tomography (CT) scan of the chest revealed a large fatty density (-105 Hounsfield units) with scattered stripped soft tissue density (42 Hounsfield units) mass which compressed the right lower lobe (Figure B). A provisional diagnosis of intrathoracic lipoma was made.
Right thoracotomy revealed a round, yellowish, consistently soft tumor which had a smooth surface (Figure C), and occupied approximately 75% of the right pleural cavity. The tumor attached to the pleura of the 7th anterior intercostal space with its pedicle of 2.0 cm in diameter, compressing the right lower lobe of the lung. There was no adhesion between the tumor and the surrounding organs, and the entire mass was successfully extirpated en-bloc after ligation of its pedicle. The tumor weighed a total of 2850 grams and measured 25 × 20 × 18 centimeters.
Final histologic result was pleural lipoma. The investigation of this tumor revealed an encapsulated tumor with abundant mature adipose tissue, a few scattered strands of fibro connective tissue, no presence of sarcomatous changes (Figure D).
The patient’s postoperative course was uneventful, with no recurrence on one-year follow-up.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [50.0, 'kg'], 'height': [163.0, 'cm']}",18.81892,17.87797,19.75987,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 50.0 kg. The patient's bmi is therefore 50.0 kg / (1.63 m * 1.63 m) = 18.81892 kg/m^2."
2477,6,Body Mass Index (BMI),physical,decimal,pmc-4377251-1,Extracted,"A 16-year-old boy complained fever and persistent cough unresponsive to antibiotics. Chest X-ray was normal. After 2 weeks skin petechiae and ecchymoses appeared and the boy was admitted to an Infectious Disease Division. Peripheral blood count showed: hemoglobin 11.9 g/dL, platelet 1 × 103/μL, white blood cells 8.5 × 103/μL, neutrophils 87%, lymphocytes 5%. ITP was suspected and intermediate dose methylprednisolone (0.5 mg/kg/day) was administered for 2 days. CT scan showed multiple masses both in the chest and abdomen, enlarged liver, and hypodense areas in the spleen. On admission to our center, clinical examination revealed obesity (weight 125 kg and height 171 cm), diffuse petechiae all over the skin and ecchymoses on upper and lower limbs. No enlarged peripheral lymph nodes were found. Liver and spleen margins were 2 and 2.5 cm under the lower costal limit, respectively. Laboratory investigation confirmed thrombocytopenia (platelet count 10 × 103/μL) with hemoglobin 12.2 g/dL and white blood cells 13.6 × 103/μL. Erythrocyte sedimentation rate measured 104 mm/h, reactive C protein 17.4 mg/dL (n.v. <0.8), lactate dehydrogenase level 1051 IU/L. Liver function tests including albumin, bilirubin, alkaline phosphatase, gamma glutamyltransferase, coagulation parameters, and transaminases as well as serum immunoglobulin (Ig) levels were within the normal range. Viral serology for EBV, hepatitis A, B, and C viruses and HIV as well as autoimmune markers were negative, thus excluding secondary thrombocytopenia. FDG-PET documented high metabolic activity in all the sites evidenced as pathologic by CT scan. Leukemia/lymphoma diagnosis was suspected. Bone marrow aspirate and trephine biopsy revealed normal cellularity with no evidence of neoplastic infiltration and increased megakaryocytes, a picture compatible with ITP. A tru-cut biopsy of one of the abdominal masses was excluded due to adiposity and, consequently, it was decided to perform a laparoscopic procedure. In order to achieve a safe platelet value, a dose of 30 g of IVIG for two consecutive days was administered before surgery. Platelet rose to 30 × 103/μL and two units of platelets were transfused immediately before and during surgery.
Laparoscopy was complicated by copious bleeding and converted to open surgery. Bleeding was soon controlled with no further complications. Due to the need of respiratory and hemostasis surveillance, the patient was transferred to Intensive Care Unit for 5 days. The platelet count fell to 22 × 103/μL and intravenous methylprednisolone (1 g daily for 3 days) was administered with a prompt rise of platelet count (204 × 103/μL at day 3). Histological report revealed Hodgkin lymphoma, nodular sclerosis type (immunophenotypic profile: CD 30+, CD15+/–, CD20–, CD3–, CD43–, LCA–, EMA–, ALK–). Chemotherapy was started according to AIEOP LH 2004 protocol, which includes 6 COPP/ABV cycles (cyclophosphamide, vincristine, procarbazine, prednisone/adriamycin, bleomycin, vinblastine) followed by involved field radiotherapy. Platelet count showed an asymptomatic second fall to 75 × 103/μL during the first course and rose up to normal values without the need of additional treatments. The boy is now in complete remission, with a normal platelet count, 13 months after the end of treatment (Fig.).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [125.0, 'kg'], 'height': [171.0, 'cm']}",42.7482,40.61079,44.88561,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 171.0 cm, which is 171.0 cm * 1 m / 100 cm = 1.71 m. The patient's weight is 125.0 kg. The patient's bmi is therefore 125.0 kg / (1.71 m * 1.71 m) = 42.7482 kg/m^2."
2478,6,Body Mass Index (BMI),physical,decimal,pmc-7264904-1,Extracted,"A 66-year-old female patient (height, 155 cm; weight, 53 kg) with breast cancer (left breast; pT1N2M0, stage IIIA) underwent modified radical mastectomy and breast reconstruction using LDMCF in March 2008. Drainage was removed on the 12th day after surgery and the first round of chemotherapy was administered on the 21st day postoperatively. During hospitalization, there were no complications at the donor site or any other issues, and she was discharged on the 36th day after the operation. She received three more rounds of chemotherapy after discharge, and outpatient follow-up for the next 7 years was uneventful. In July 2015, 7 years after surgery, the patient complained of a palpable mass on her back, at the donor site, at the outpatient clinic of the Department of General Surgery. Seroma was diagnosed, aspiration and drainage were performed, and the symptoms were relieved. In March 2018, 10 years after surgery, symptoms of a palpable mass recurred at the donor site. Incision, drainage, and bacterial culture were performed at the Department of General Surgery. The drained discharge from the donor site revealed a serous fluid pattern, including blood clot–like material, and no bacteria were identified in the culture. After repeated drainage of the serous fluid, the symptoms did not improve. Therefore, the patient was referred to the Department of Plastic Surgery, where she underwent irrigation and betadine gauze dressing (). In April 2018, the patient underwent surgery for the seroma under general anesthesia since serous discharge continued and the seroma remained unchanged. A serous capsule pouch located in the subcutaneous tissue layer was identified intraoperatively. The capsule pouch was completely excised by meticulous dissection and the inside of the capsule was observed. Within the capsule, serous fluid was found containing a brown-colored material with the appearance of a blood clot (-). A permanent biopsy was performed of the completely excised serous capsule pouch. The histological findings showed that the brown-colored substance that had accumulated in the cyst was eosinophilic proteinaceous material, not a blood component. Multinucleated giant cells and epithelioid histocytes were irregularly distributed in the fibrous cystic wall that had formed around the brown-colored material. Therefore, the cyst was suggestive of chronic granulomatous inflammation (). Two weeks after the operation, the drainage volume was less than 30 mL and the drain was removed. The patient was then discharged. There was no evidence of seroma recurrence or other complications during 8 months of follow-up.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [155.0, 'cm'], 'weight': [53.0, 'kg']}",22.06035,20.95733,23.16337,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 53.0 kg. The patient's bmi is therefore 53.0 kg / (1.55 m * 1.55 m) = 22.06035 kg/m^2."
2479,6,Body Mass Index (BMI),physical,decimal,pmc-8614163-1,Extracted,"A 31-year-old G1P0 woman with six weeks of amenorrhea and a positive urine pregnancy test presented to the obstetrics emergency department due to moderate/heavy vaginal bleeding with three days of evolution, with no pain nor other associated symptoms. She had been observed in an obstetrics consultation at the onset of symptoms and was diagnosed with an early miscarriage. It was recommended to have a follow-up ultrasound within a week. Her past medical and surgical history was irrelevant, except for laser vaporization of the cervix due to persistent low-grade squamous intraepithelial lesion. In terms of biometrics, she weighed 85 kg and was 1.72 m high (body surface of 2 m2). Vital signs were normal, with blood pressure of 136/81 mm Hg and pulse rate of 87 bpm. On physical examination, she presented with clots in the vagina in moderate to abundant amounts, and the cervix was enlarged and violet in color (Figure ).
Transvaginal ultrasound revealed at the cervical level, in the thickness of the posterior lip, a gestational sac measuring 35 x 27 mm, containing an embryo measuring 8 mm with no cardiac activity (Figure ).
This cervical thickening caused an ""8"" figure of the uterus (Figure ).
In the endometrial cavity, an anechogenic image was detected, measuring 19 mm, without trophoblastic reaction and no visible embryonic structures, suggesting intracavitary blood retention. The initial hCG value was 72.194 mIU/mL. She had mild anemia with a hemoglobin of 10.5 g/dL. Other laboratory values were within normal limits: normal platelets, coagulation tests, and liver and renal functions.
According to the diagnosis and since the patient was nulliparous and wished to preserve fertility, an inpatient conservative approach was the therapeutic option. An intramuscular dose of systemic methotrexate 100 mg (50 mg/m2) was initially administrated. Since the hCG values ​​remained high and the echographic dimension of the gestational sac was similar, four days after an intra-amniotic injection of methotrexate 50 mg was performed (Video ).
On the 12th day of hospitalization, due to worsening vaginal bleeding, selective embolization of the cervical branch of the left uterine artery was undertaken (Figure ).
The next day, the surgical removal of trophoblastic tissue was carried out under general anesthesia. The curettage was performed under ultrasound guidance, with an easy detachment of the trophoblast and minimal blood loss. The surgical specimen was sent to the pathology laboratory (Figure ).
On the second postoperative day, the patient was discharged from the hospital. The clinical evolution was favorable. Follow-up included a weekly control of hCG, which became negative on the fourth week after discharge (49th day after diagnosis). Transvaginal ultrasound done on the first and second week after discharge still showed at the cervical level a nodular and cavitated image measuring 18 x 13 mm (Figure ), with mild peripheral vascularization (Figure ), suggesting residual trophoblastic tissue in resorption.
On the third week, the ultrasound was completely normal. Currently, the patient is clinically well under oral contraception.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [85.0, 'kg'], 'height': [1.72, 'm']}",28.73175,27.29516,30.16834,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.72 m. The patient's weight is 85.0 kg. The patient's bmi is therefore 85.0 kg / (1.72 m * 1.72 m) = 28.73175 kg/m^2."
2480,6,Body Mass Index (BMI),physical,decimal,pmc-2771150-1,Extracted,"A 72-year-old woman was admitted to our hospital for surgery for esophageal cancer. At admission, her blood pressure was 120/70 mmHg and pulse rate was 76 beats per minute. She was 152 cm in height and weighted 62 Kg. Physical examination was unremarkable. Preoperatively, renal function was moderately decreased (creatinine, 0.95 mg/dL, blood urea nitrogen: 16.5 mg/dL, uric acid: 5.7 mg/dL, sodium: 144 mEq/L, potassium: 4.1 mEq/L, chloride 110 mEq/L, phosphorus 3.7 mg/dL). During the thoracoscopic esophagectomy, blood loss was 460 ml, and hemodynamics were stable.
Postoperatively, approximately 2 L of hypotonic fluid (0.2% saline with 4.3% dextrose) daily were administered, urine volume was stable (1.1–1.8 L), and plasma sodium levels were unchanged (140 mEq/L). However, on the third postoperative day, she suddenly developed polyuria (3.8 L/day) together with a decrease in CVP (). Serum sodium levels dropped to 124 mEq/L on the next day. Despite volume-to-volume correction with isotonic saline, the serum sodium levels dropped to a nadir of 112 mEq/L together with hyperkalemia (5.6 mEq/L) on the fifth postoperative day, and her consciousness level deteriorated. When her urine volume was 3.8 L and 3.5 L, there was a negative water balance (without including perspiration); −0.9 L and −0.5 L, respectively. The hematocrit value increased from 27.4% to 33.7% during the 2 days without blood transfusion. The next day, our department was consulted for further evaluation. She appeared dehydrated and there was an additional decrease in her CVP to a nadir of 1 cm of H2O. Laboratory findings on consultation are shown in . Urinary sodium concentrations were markedly high and serum uric acid levels were decreased from 5.7 mg/dL to 1.4 mg/dL. Urinary N-acetyl-β-glucosamininase (NAG) and β2-microglobulin were high and the calculated maximal tubular reabsorption of phosphorus per glomerular filtration rate (TmP/GFR) was relatively low (2.4 mg/dL), suggesting proximal tubule dysfunction. Furthermore, the calculated transtubular potassium gradient (TTKG) value was low (3.6) for her serum potassium levels (4.7 mEq/L), suggesting that aldosterone action at cortical collecting duct (CCD) was impaired. These features were not consistency with the diagnosis of a SIADH. Thus, she was diagnosed as having SLN due to renal tubular dysfunction. Sodium correction was done with 3% saline and fludrocortisone was started at a dose of 0.05 mg/day. Thereafter, urinary volume decreased and there was a gradual increase in serum sodium levels to 138 mEq/L and serum uric acid levels to 3.4 mg/dL. Her consciousness level completely recovered. On the 20th postoperative day fludrocortisone was discontinued and she was discharged. She has been followed as an outpatient without recurrence of the hyponatremia.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [152.0, 'cm'], 'weight': [62.0, 'kg']}",26.83518,25.49342,28.17694,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 152.0 cm, which is 152.0 cm * 1 m / 100 cm = 1.52 m. The patient's weight is 62.0 kg. The patient's bmi is therefore 62.0 kg / (1.52 m * 1.52 m) = 26.83518 kg/m^2."
2481,6,Body Mass Index (BMI),physical,decimal,pmc-4007744-1,Extracted,"A 24-year-old male from the East of Thailand was found asymptomatic with functional class I and was found to have a heart murmur by routine checkup. He has no significant past medical history. Physical examination revealed a healthy man with height 176 cm and weight 60 kg. The Pulse rate was regular 60 bpm, blood pressure was 110/70 mmHg, and respiratory rate was 20 per min. Cardiac auscultation revealed a fixed split second sound with a grade 2/6 systolic ejection murmur at left upper parasternal border. Other systems were normal. Chest X-ray showed mild cardiomegaly with increase pulmonary blood flow. Transthoracic echocardiogram (TTE) and transesophageal echocardiogram(TEE) demonstrated right atrial and right ventricular enlargement with ASD secundum of 26 × 31 mm and cor triatriatrium with wide opening of 20 mm of fenestration as type A2 of Rodefeld classification [].
() There was no evidence of turbulent flow through fenestration and pulmonary hypertension. There were adequate rims (length of rims more than 10 mm) around ASD secundum, then closure of ASD using the transcatheter approach was decided.
Transcatheter closure was performed with the patient under general anesthesia. Heparin 5,000 IU and cefazolin 1gram were administered intravenously before the procedure. Vascular access was obtained via the right femoral vein using 7-Fr sheath and the right femoral artery using 5-Fr sheath. TEE was performed. Right and left cardiac catheterization was performed and showed a pulmonary arterial pressure of 30/13 mmHg, Qp : Qs 2 : 1, and normal pulmonary venous drainage into the left atrium.
The first attempt for transcatheter closure using CocoonR ASD device (Vascular Innovations, Nonthaburi, Thailand) size 30 mm failed because we could not pull to deploy left atrial disc of device over atrial septum since cor triatriatum membrane was slipped into left atrial disc. Then we performed the second attempt using the Occlutech FigullaR device. 6-Fr multipurpose (MP) catheter (Cook, Bloomington, USA) was placed in left upper pulmonary vein through ASD, then 0.035 Amplatz super stiff guide wire (Boston Scientific, Galway, Ireland) was inserted into MP catheter. PTS sizing balloon sizing (Numed, Cornwall, ON, Canada) 30 mm was inserted over super stiff guide wire. TEE demonstrated stretch diameter of ASD which was 31 mm by balloon sizing. 14-Fr Mullin's sheath (Cook, Bloomington, USA) was advanced through ASD over stiff guide wire. Occlutech FigullaR device size 33 was loaded into delivery sheath and advanced by pusher cable to the left atrium. Device was deployed. () TEE revealed proper site of device without obstruction, no residual shunt, and residual fenestration of cor triatriatum membrane was 12 mm. We used TEE to recheck that the device will not occlude pulmonary venous return, and TEE revealed no turbulence flow of pulmonary veins and no turbulence flow of blood flow through fenestration of cor triatriatum membrane (). Stability testing was performed. The device was released (). No complication was found. TTE was performed in the next day and revealed the same result with TEE and no turbulence flow through fenestration of membrane. The patient was discharged with aspirin 300 mg once daily to be taken for 6 months.
Follow-up echocardiogram in the next 2, 6, and 12 months revealed the same result. The patient remained asymptomatic and no audible heart murmur was detected at auscultation. No complication was found.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [176.0, 'cm'], 'weight': [60.0, 'kg']}",19.36983,18.40134,20.33832,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 176.0 cm, which is 176.0 cm * 1 m / 100 cm = 1.76 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.76 m * 1.76 m) = 19.36983 kg/m^2."
2482,6,Body Mass Index (BMI),physical,decimal,pmc-7042143-4,Extracted,"Patient 4 is a 56-year-old man with a history of initial idiopathic dilated cardiomyopathy with a stable left ventricular ejection fraction of 45–50%, pre-diabetes and previous cerebrovascular accidents presented to the emergency room with palpitations and shortness of breath. His height and weight were 168.5 cm and 92 kg, respectively. His blood pressure was 146/92 mmHg. His electrolytes were as follows: sodium 139 mmol/L, potassium 4.1 mmol/L, and calcium 2.30 mmol/l. His list of current medications included: bisoprolol 5 mg o.d., sacubitril-valsartan 100 mg b.i.d., digoxin 62.5 mcg o.d., and dabigratan 150 mg b.i.d. Electrocardiogram on admission revealed atrial fibrillation. He received 300 mg of amiodarone intravenously before cardioversion. shows his ECG prior to cardioversion. He received a total of three DC shocks and was reverted back to sinus rhythm with early recurrence of atrial fibrillation. shows his ECG during cardioversion. shows his ECG after the last electrical cardioversion. The patient was left in a state of permanent atrial fibrillation with rate control medications as listed above; no further clinical events have been reported in the follow-up.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [168.5, 'cm'], 'weight': [92.0, 'kg']}",32.40321,30.78305,34.02337,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.5 cm, which is 168.5 cm * 1 m / 100 cm = 1.685 m. The patient's weight is 92.0 kg. The patient's bmi is therefore 92.0 kg / (1.685 m * 1.685 m) = 32.40321 kg/m^2."
2483,6,Body Mass Index (BMI),physical,decimal,pmc-3384798-1,Extracted,"A 65-year-old man, 163 cm in height and 60 kg in weight, was admitted to the emergency room with a cough, blood tinged sputum and dyspnea. He underwent percutaneous mitral balloon valvuloplasty 15 years earlier due to MS. He had a history of a cerebral infarction and hypertension. Electrocardiography revealed atrial fibrillation (A-Fib). Minimal coronary artery occlusive disease was identified during coronary angiography. Transthoracic echocardiography (TTE) revealed severe MS (mitral valve area of 0.79 cm2; mean diastolic pressure gradient of 12.5 mmHg; left atrial volume index [LAVI] of 115 ml/m2), mild tricuspid regurgitation, and a right ventricle systolic pressure of 47 mmHg and ejection fraction (EF) of 72%. Despite mild swirling in the left atrium (LA), no mass or thrombi were observed. The patient was medicated with digoxin, torasemide, simvastatin, and 3 mg of warfarin. For MVR, warfarin was discontinued and heparinization was initiated four days before surgery until midnight of the day before surgery. The international normalized ratio (INR) and activated partial thromboplastin time (aPTT) one day before surgery were 1.00 and 26.3 seconds, respectively.
Before CPB, in TEE, severe spontaneous echo contrast (SEC) in the LA was noted with no evidence of thrombus at any angle (). CPB was instituted and after injecting 18000 units of heparin, the activated clotting time (ACT) was increased to 489 seconds. During CPB, the ACT was maintained at more than 500 seconds with an additional 3000 units of heparin. The body temperature was decreased to 33℃. The surgeon confirmed the absence of any removable organized thrombus in the LAA and performed MVR with a Carpentier-Edward 27 valve.
After unclamping the aortic cross clamp (ACC), a well functioning bioprosthetic mitral valve (MV) without paravalvular leakage was confirmed through TEE. The pump flow rate was lowered to wean the patient from CPB and during de-airing of the heart, TEE revealed a newly formed non-mobile mass in the LAA (). At that time, the ACT was 569 seconds. After discussion with the surgeon, a re-bypass was planned, and the mass was removed via a left atriotomy after ACC. The clot was removed as a single piece, which measured approximately 33 × 33 mm, which had the appearance of a fresh, newly formed thrombus by a visual inspection (). Weaning from the CPB was performed uneventfully. The total CPB and ACC time was 81 minutes and 53 minutes, respectively.
The patient awoke six hours after arriving at the intensive care unit with no neurological deficits and was extubated at postoperative day (POD) 1. Anticoagulation was started with warfarin at POD 2. He was transferred to the general ward at POD 3 and discharged at POD 9. His postoperative TTE revealed a well functioning bioprosthetic MV, a slightly decreased LA size with a normal LV function, and no remaining MS or mitral regurgitation.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [163.0, 'cm'], 'weight': [60.0, 'kg']}",22.58271,21.45357,23.71185,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.63 m * 1.63 m) = 22.58271 kg/m^2."
2484,6,Body Mass Index (BMI),physical,decimal,pmc-3830331-1,Extracted,"A 21-year-old female was evaluated in our clinic because of primary amenorrhea and poor breast development. She is a child of non-consanguineous parents. Her birth event, perinatal and neonatal period were uneventful. Her growth and development were normal with normal intelligence. At the time of presentation, her height was 160 cm and weight 47 kg. On examination, there was no facial dysmorphism, no features suggestive of Turner syndrome like webbing of the neck or wide carrying angle. No skeletal deformity was found. Her blood pressure was 110/70 mmHg in both arms. Her pubic hair and breast development were in tanner 3 stage and there was scanty axillary hair. Genital examination revealed blind vaginal pouch. She had history of seizure at the age of 19 years and she is on antiepileptic medications. Her hemoglobin was 11.2 g/dl with normal differentials. Her renal function tests and liver function tests were normal. Hormonal evaluation showed elevated follicle-stimulating hormone (100 IU/L) and luteinizing hormone (32 IU/L) with undetectable estradiol (<5 pg/ml) and testosterone (<0.1 ng/ml). Her serum thyroid stimulating hormone (2.3 mIU/ml) and cortisone (10 μg/dl) levels were normal. Ultrasound of pelvis did not show uterus or ovaries. Laparoscopy revealed absent of uterus, normal fallopian tubes and streak ovaries. Her computed tomography scan of the brain revealed bilateral periventricular and corona radiata hypointensity with undulation of both lateral ventricles suggestive of ischemic insult, rest of brain parenchyma and pituitary were normal. Her karyotype, obtained from peripheral blood lymphocytes by G-staining, was 46XX (20 cell lines). We obtained ovarian samples during laparoscopy and histopathology of ovarian tissues revealed streak ovaries. We confirmed coexistence of two disorder namely, gonadal dysgenesis and MRKHS in this patient. She was put on ethinyl estradiol 10 μg/day, daily for development of secondary sexual characteristics and bone health.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [160.0, 'cm'], 'weight': [47.0, 'kg']}",18.35937,17.4414,19.27734,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 47.0 kg. The patient's bmi is therefore 47.0 kg / (1.6 m * 1.6 m) = 18.35937 kg/m^2."
2485,6,Body Mass Index (BMI),physical,decimal,pmc-5313358-6,Extracted,"A 28-year-old primiparous woman visited because of back pain. She had delivered 3 months previously and back pain had started 3 weeks before the hospital visit. Her height was 161 cm and her weight was 52 kg. She had no past surgical or family histories. Lumbar spine MRI revealed recent compression fractures of T6–T9, T12, L2, and L5. She was given calcium 500 mg daily and cholecalciferol 1,000 IU for 8 months.
Pretreatment BMD Z-score determined by dual energy X-ray absorptiometry in all patients was -2.5±0.3 at L1–L4 and -1.5±0.7 at femur (). The post-treatment mean BMD Z-score was -1.7±0.6 at L1–L4 and -1.4±0.4 at femur. The mean BMD Z-score change was 0.8±0.6 at L1–L4, 0.1±0.4 at femur in all patients, 0.5±0.4 at L1–L4, 0.2±0.1 at femur in calcium/vitamin D supplementation group and 1.3±0.6 at L1–L4 and -0.2±0.81 in those treated with teriparatide.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [161.0, 'cm'], 'weight': [52.0, 'kg']}",20.06095,19.0579,21.064,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 161.0 cm, which is 161.0 cm * 1 m / 100 cm = 1.61 m. The patient's weight is 52.0 kg. The patient's bmi is therefore 52.0 kg / (1.61 m * 1.61 m) = 20.06095 kg/m^2."
2486,6,Body Mass Index (BMI),physical,decimal,pmc-4512597-1,Extracted,"Our patient is a 61-year-old 90 kg 177.8 cm male with a history of coronary artery disease and amyotrophic lateral sclerosis who was admitted to the intensive care unit for ventilator support. On arrival to the emergency department he was profoundly hypoxic and was emergently intubated. He was subsequently transferred to the intensive care unit. On initial evaluation the patient was alert and was able to follow commands and communicated via writing. His overall strength was poor, 2/5 in both his hands and feet with minimal ability to lift his proximal arms and legs. His cranial nerves were all grossly intact. His level of function prior to admission was heavily dependent on assistance for activities of daily living. He was, however, able to talk and swallow without difficulty and was receiving no respiratory support.
Subsequent to his admission to the ICU he met parameters for extubation during a trial of spontaneous breathing, and the endotracheal tube was removed. He failed spontaneous ventilation and was reintubated within 2 hours following extubation. Over the next three days, multiple attempts were made to wean the patient from the ventilator; however, he failed multiple trials of spontaneous breathing and could not be extubated. The decision was made among the ICU team, the patient, and the family to proceed with tracheostomy insertion. The Oral Maxillofacial Surgery (OMFS) service was then consulted. See for the preoperative chest X-Ray (CXR).
This patient was taken to the operating room by the OMFS service. An open tracheostomy was performed with placement of a 6.0 cuffed Shiley tracheostomy tube, under flexible fiberoptic tracheoscopy (FFT) assistance, without difficulty. It was noted in the operative report that the patient had hardening and calcification of the first, second, and third tracheal cartilages. It was also noted that he had a short neck and a posterior trachea. No tracheal abnormalities were observed during FFT after tracheostomy insertion. Within a few hours of the patient returning to the ICU a cuff leak developed. The OMFS service was consulted and he was emergently taken back to the operating room a second time with a concern that the tracheal tube might have become displaced. Intratracheal placement of the leaking tube was confirmed by FFT. Again no tracheal abnormalities were observed. A Cook Exchange Catheter (CEC) was placed through the tracheostomy tube and the damaged tube was withdrawn. A 6.0 cuffed endotracheal tube was placed over the CEC. Verification of tracheal placement was confirmed with both end tidal CO2 and FFT.
Placement of a longer 6.0 cuffed Shiley was attempted but aborted due to difficulty in placement. A reinforced 6.5 endotracheal tube was then placed over the CEC. Tracheal placement of the reinforced endotracheal tube was confirmed by ETCO2 and FFT with no noted tracheal abnormalities. The patient was returned to the ICU.
Two days later the patient was noted to have gurgling at the tracheostomy site and was taken to the operating room a third time. The 6.5 reinforced ETT was removed over a bougie and a 6.0 cuffed Shiley with proximal extension was placed and sutured to the skin. Good ventilation was confirmed. During FFT, no tracheal abnormalities were noted. Later that same day gurgling was again noted and our patient returned to the operating room a fourth time to replace the leaking tube. The tube was exchanged over a Pediatric Cook Exchange Catheter. Examination of the cuff of the removed tube revealed a leak from the left anterior aspect of the cuff. During this procedure the OMFS surgeon explored the wound further to attempt to delineate a cause for the multiple cuff leaks. In order to gain access to trachea, Army-Navy retractors were down in the surgical site. With further exposure of the surgical site with a Debakey forcep, a 10 mm by 4 mm piece of sharp calcified cartilage was discovered protruding into the tracheal lumen in a location consistent with the previously noted cuff damage. The team was not able to obtain an image of the protruding cartilage. Additionally, the ruptured cuff was tested for bubbles in an emesis basis intraoperatively, though images were not obtained. The cartilage was excised, and an 8.0 Bivona adjustable tracheostomy tube was placed without further difficulty. The patient returned to the ICU. On POD #5 a Neck Soft Tissue CT, which was obtained in order to rule out complications from the repeated tracheostomy attempts, demonstrated increased diffuse tracheal calcification (see ). He experienced no further complications with the tracheostomy tube during his hospitalization and was subsequently discharged for further rehabilitation.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [90.0, 'kg'], 'height': [177.8, 'cm']}",28.46944,27.04597,29.89291,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 177.8 cm, which is 177.8 cm * 1 m / 100 cm = 1.778 m. The patient's weight is 90.0 kg. The patient's bmi is therefore 90.0 kg / (1.778 m * 1.778 m) = 28.46944 kg/m^2."
2487,6,Body Mass Index (BMI),physical,decimal,pmc-6967110-1,Extracted,"A woman in her 30s (height 163 cm, weight 64 kg) was presented as an emergency due to acute and intense right leg pain. The patient had no significant history of emotional or physical stress events 48 h before emergency visit and also no history of past personal or family history of thrombus formation (i.e., thrombogenesis), but used oral contraceptives. Her pre-operative coagulation profile revealed normal prothrombin time of 10.8 s, prothrombin time-international normalized ratio 0.93, and activated partial thromboplastin time 27.0 s, but fibrin/fibrinogen degradation products and D-dimer level were increased to 16.9 and 4.9 μg/mL. Contrast-enhanced computed tomography revealed right femoral artery thrombus (Fig. ), and emergency thrombectomy was scheduled. Pre-operative electrocardiogram showed non-specific ST elevation and a left bundle branch block (Fig. ), but no abnormal findings were seen on chest X-ray. On arrival in the operating room, the patient was alert and her blood pressure was 115/85 mmHg. Heart rate was 98 beats per minute, and oxygen saturation was 93% on 2 L/min oxygen by nasal cannula. The patient complained of strong right leg pain, but no dyspnea or chest pain. General anesthesia was inducted using a rapid sequence method with remifentanil, propofol, and rocuronium and maintained with remifentanil and sevoflurane as per standard protocol. After tracheal intubation, poor pulmonary oxygenation was observed, with PaO287.0 mmHg and FIO2 0.44; therefore, a recruitment maneuver was performed and oxygenation improved to PaO2 174 mmHg (Table ). During the operation, her vital signs remained stable, and she was transferred to the intensive care unit (ICU) after successful surgery. In the ICU, the patient’s oxygen saturation decreased to 90% on oxygen 5 L/min with use of a facemask. As pulmonary embolism was suspected, transthoracic echocardiography (TTE) was performed. TTE showed Takotsubo cardiomyopathy-like left ventricular dysfunction with left ventricular thrombus (Fig. –). Although she showed severe left ventricular dysfunction, creatine kinase-MB (CK-MB) and troponin T elevated modestly (creatine kinase and CK-MB were 270, and 30 U/L, troponin T was 0.23 ng/mL). Continuous intravenous heparin was immediately started at 20,000 U/day for 10 days.
Noninvasive positive pressure ventilation was used for 2 days until her oxygen saturation improved. Ten days after surgery, the patient was discharged from the hospital as the left ventricular thrombus disappeared and left ventricular wall motion improved. No inherited or secondary thrombophilia was identified.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [163.0, 'cm'], 'weight': [64.0, 'kg']}",24.08822,22.88381,25.29263,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 64.0 kg. The patient's bmi is therefore 64.0 kg / (1.63 m * 1.63 m) = 24.08822 kg/m^2."
2488,6,Body Mass Index (BMI),physical,decimal,pmc-8310650-1,Extracted,"We present the case of a 49-year-old male patient (1.83m, 88 kg) with a 12-month history of left-sided knee pain with concomitant limitation of the knee flexion to 90 degree. The initial conservative treatment consisted of analgesics and physiotherapy. Persistent pain led to subsequent radiographic ( and ) and magnetic resonance imaging (-) that revealed an excessive hyperostosis of the left femur with an extraosseous lesion in the fossa intercondylaris femoris. The patient was subsequently referred to our specialized center for musculoskeletal oncology.
Based on the clinical and radiographic findings, we established the diagnosis of melorheostosis and the patient underwent surgical resection of the symptomatic extraosseous lesion in the fossa intercondylaris through a direct open approach under meticulous protection of the cruciate ligaments. Postoperatively, the histological findings were consistent with the diagnosis of melorheostosis () and the patient was allowed full weight-bearing with no limitation to the range of motion of the left knee joint.
At 6-week follow-up, the patient reported no persisting pain but a lasting limitation to his left knee flexion that was subsequently addressed with an intensive physiotherapeutic treatment. At 12-month follow-up, the patient was pain free and showed an improved knee flexion to 110 degree.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [1.83, 'm'], 'weight': [88.0, 'kg']}",26.27729,24.96343,27.59115,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.83 m. The patient's weight is 88.0 kg. The patient's bmi is therefore 88.0 kg / (1.83 m * 1.83 m) = 26.27729 kg/m^2."
2489,6,Body Mass Index (BMI),physical,decimal,pmc-5564175-3,Extracted,"The third patient was a 64-year-old man (weight: 52 kg, height: 158 cm) with a cervical disc herniation scheduled for an emergent decompressive laminoplasty C3-6 and anterior interbody fusion. Pre-operative evaluation revealed grade III motor weakness of both hands, but there was no other underlying disease or abnormal laboratory findings. Since it was not an elective surgery, the anesthesiologists did not have sufficient patient information, particularly regarding the airway. Preoxygenation, induction was performed using 250 mg pentothal sodium, 7 mg vecuronium, and sevoflurane. When we opened his mouth, the opening was barely 4 cm wide and his neck was extremely stiff. In addition, we could not verify the airway anatomy when we lifted his tongue via direct laryngoscopy. Therefore, we decided to use a combination of an ILMA and a FOB immediately. Furthermore, since the operation had to be conducted with the patient in the prone position, we required the establishment of a more definite airway than an ILMA. After placing the ILMA, a FOB was introduced through with ease and an ETT was then advanced along the FOB into the trachea. Sufficient insertion was confirmed by easy bag ventilation and a capnogram, followed by administration of dexamethasone 5 mg to prevent laryngeal edema.
It was unnecessary to prepare for invasive airway access in these three cases that included surgical or percutaneous airway, jet ventilation, and retrograde intubation because facemask ventilation was adequate and a definite airway was created through an ILMA. The three patients were fully informed of the surgery and anesthesia, and all potential complications were disclosed through written consent.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [52.0, 'kg'], 'height': [158.0, 'cm']}",20.83,19.7885,21.8715,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 158.0 cm, which is 158.0 cm * 1 m / 100 cm = 1.58 m. The patient's weight is 52.0 kg. The patient's bmi is therefore 52.0 kg / (1.58 m * 1.58 m) = 20.83 kg/m^2."
2490,6,Body Mass Index (BMI),physical,decimal,pmc-5729455-2,Extracted,"A 47-year-old Japanese man was admitted to our hospital for evaluation of renal disease in May 2013. Edema of the lower limbs was initially noted in August 2012. He consulted a local clinic in February 2013 with generalized edema and weight gain to 113 kg. Proteinuria was detected (5.2 g daily). His anasarca was treated with furosemide (100 mg daily) and restriction of salt and fluid intake (to 6 g of salt and 700 mL of water daily), achieving weight reduction to 90.0 kg. He had a history of drinking one-third of a bottle of whisky daily for 34 years starting from 13 years old. On admission, he was 174 cm tall and weighed 90.0 kg, with a blood pressure of 144/88 mmHg and bilateral lower limb edema. Laboratory findings are shown in Table . Total protein was 6.0 g/dL, albumin was 2.7 g/dL, urea nitrogen was 23 mg/dL, and Cre was 1.66 mg/dL. In addition, 24-h urinary protein excretion was 1.17 g and the urine sediment contained more than 100 erythrocytes per high-power field.
Computed tomography showed gastric varices with anastomoses to the left renal vein, as well as cirrhosis and splenomegaly.
This patient was also diagnosed as having alcoholic cirrhosis due to his 34-year history of alcohol abuse and negative tests for HBV and HCV infection. As with case 1, renal biopsy was performed to evaluate his renal disease.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [90.0, 'kg'], 'height': [174.0, 'cm']}",29.72652,28.24019,31.21285,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 174.0 cm, which is 174.0 cm * 1 m / 100 cm = 1.74 m. The patient's weight is 90.0 kg. The patient's bmi is therefore 90.0 kg / (1.74 m * 1.74 m) = 29.72652 kg/m^2."
2491,6,Body Mass Index (BMI),physical,decimal,pmc-5838199-1,Extracted,"The patient was a 32-year-old male with MPS type 2. His height and body weight were 134 cm and 47 kg, respectively. When he was an elementary school student, he underwent surgery for an inguinal hernia. Mental retardation was not indicated. He (first-born child) had two brothers. They also had the same disease and underwent aortic valve replacement when they were elementary school students. At the age of 13 years, the patient was diagnosed with aortic valve regurgitation. Since 19 years of age, he had been followed up in the Department of Cardiology of our hospital. Aortic valve replacement was performed due to an increase in the regurgitation volume. There were no heart failure-related symptoms, and the NYHA grade was evaluated as I. Preoperative electrocardiography showed a sinus rhythm, and echocardiography revealed moderate aortic valve regurgitation, an end-diastolic left ventricular diameter of 56 mm and left ventricular ejection fraction of 51%. Coronary angiography did not show any significant stenosis.
A preoperative examination showed trismus (Mallampati grade IV), brevicollis, posterior cervical flexure disturbance, and megaloglossia. Coronal sections on magnetic resonance imaging (MRI) indicated similar findings, suggesting that airway management is difficult. Preanesthetic medication was not performed. After the patient was admitted to the operating room, a percutaneous oxygen saturation monitor, electrocardiograph, non-invasive blood pressure monitor, Bispectral Index monitor, and near infrared ray brain tissue oxygen saturation monitor were attached. In addition to the intravenous administration of fentanyl at a total dosage of 200 μg and midazolam at 2.5 mg, propofol at 1.0 mg/kg/h and remifentanil at 2.0 μg /kg/h were continuously administered under oxygen administration. The Richmond Agitation Scale Score (RASS) ranged between − 1 and − 2. Under spontaneous respiration, a 22G needle was inserted into the right radial artery, and continuous arterial pressure monitoring was started. The sedation level reached the degree of mouth opening in response to a strong call, and 8% lidocaine spray was sprayed into the oral cavity for local anesthesia. A McGrath® X blade™ was inserted to spread the larynx; however, difficulties were associated with inserting it into the oral cavity due to trismus. It was exchanged for a McGrath® #3 blade, facilitating an approach to the epiglottis. However, the Cormack grade was evaluated as III. After applying lidocaine jelly to the bilateral nasal cavities, a cuffed tracheal tube measuring 7.0 mm in inner diameter was transnasally inserted from the left nasal cavity to the pharynx. The larynx was spread using a McGrath® #3 blade and examined by inserting a soft type of fiber optic bronchoscope (FOB) (Olympus) into the tube, facilitating visual recognition of the glottis. After spraying 8% lidocaine onto the glottis, the FOB was inserted from the subglottic area into the trachea, and FOB-guided intubation was attempted; however, difficulties were associated with inserting the tube into the subglottic area due to the stimulation of the site of the fissure and a reflex to it. Symptoms of airway obstruction appeared. Since percutaneous oxygen saturation decreased to 60%, sevoflurane (1%) was administered, followed by the intravenous administration of succinylcholine at 0.9 mg/kg, facilitating positive-pressure ventilation. While spreading the larynx again, FOB-guided intubation was attempted. Even in the state of muscle relaxation, it was difficult to insert the cuffed tracheal tube for adults, measuring 7.0 mm in inner diameter, into the trachea. A cuff-free tracheal tube measuring 6.0 mm in inner diameter was transnasally inserted into the trachea and exchanged for a cuffed tube measuring 6.5 mm in inner diameter using a soft tip-type catheter for endotracheal tube exchange (Cook Medical Corporation). The cuffed tube was fixed. The interval from the start of anesthesia until intubation was 35 min. The oral insertion of a gastric tube was then possible; however, it was impossible to insert a transesophageal echocardiographic probe. Since the cervical shape made internal jugular vein puncture impossible, a central venous catheter was inserted by 20 cm through the right femoral vein. A pulmonary artery catheter was not inserted, and an arterial pressure cardiac output monitor (Flo Trac Sensor®) (Edwards Lifesciences Corporation) was used. The surgery progressed without complications. The aortic valve was resected under cardiopulmonary bypass and substituted for a 19-mm mechanical valve. The operative time was 3 h and 5 min. The duration of cardiopulmonary bypass was 1 h and 31 min. The duration of aortic blockage was 1 h and 10 min. The volume of blood loss was approximately 2000 g. Two units of packed autologous red blood cells and 2 units of frozen fresh autologous plasma were used for blood transfusion. After surgery, artificial respiratory care was performed under continuous sedation with propofol at 0.4 to 3.0 mg/kg/h in the intensive care unit (ICU). On the first postoperative day, awakening was achieved, and the artificial respirator was removed. Laryngeal development was attempted before extubation; however, the strong pharyngeal reflex made the visual recognition of the larynx impossible. After confirming mouth opening and tongue motility, extubation was conducted while inserting a tube exchanger (Fig. ). After extubation, there were no symptoms of upper airway obstruction or nasal hemorrhage. Since intubation was more difficult than expected, the airway was reassessed after surgery. Cervical/thoracic computed tomography (CT) was performed. The nasopharynx and larynx were subsequently examined using a transnasal fiberscope by an otorhinolaryngologist. Transnasal fiberscopy indicated adenoid vegetation, pharyngolaryngeal narrowing, and favorable glottic mobility; however, the subglottic area was difficult to observe (Fig. a, b). On a three-dimensional (3D) cervical CT, the airway was patent (Fig. ) and the cervical vertebrae comprised a straight neck. The glottis was present at the level of the sixth cervical vertebra. Furthermore, displacement/circumflex of the airway axis involving the upper airway to the subglottic area was noted (Fig. a, b).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [134.0, 'cm'], 'weight': [47.0, 'kg']}",26.17509,24.86634,27.48384,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 134.0 cm, which is 134.0 cm * 1 m / 100 cm = 1.34 m. The patient's weight is 47.0 kg. The patient's bmi is therefore 47.0 kg / (1.34 m * 1.34 m) = 26.17509 kg/m^2."
2492,6,Body Mass Index (BMI),physical,decimal,pmc-4845710-1,Extracted,"A 24-year-old female patient complained of frequent yawning over the past month while
standing up at work. Her lips were occasionally cyanotic, as noticed by her mother.
The patient had undergone extracardiac TCPC at the age of 8 years due to a complex
of congenital cardiovascular malformations, including heterotaxy/asplenia/right
atrial isomerism, bilateral superior vena cava, common atrium, common
atrioventricular valve, double-inlet and double-outlet left ventricle,
dextro-transposition of the great arteries, supravalvular pulmonary stenosis, left
aortic arch, and total anomalous pulmonary venous connection.
During evaluation at the outpatient clinic, the patient presented orthodeoxia
detected by pulse oximetry, with an oxygen saturation (SpO2) of 96% in
the supine position and 88% in the upright position. Platypnea was not observed at
that time. With a diagnostic suspicion of secondary pulmonary arteriovenous
malformation (PAVM) following the TCPC, the patient was admitted for further
evaluation and treatment.
On admission, she weighed 63 kg and her height was 166 cm. Her blood pressure was
120/71 mmHg, pulse rate was 88 beats/min, and respiratory rate was 20 breaths/min.
Laboratory tests showed a hemoglobin level of 15.6 g/dL, and normal liver function
and blood coagulation tests. No information regarding the underlying cause of the
orthodeoxia could be obtained from plain chest radiograph and electrocardiogram
evaluations.
Cardiac catheterization, performed after the patient granted informed consent, showed
an SpO2 on the ascending aorta of 93%. Peak systolic pressure in the
inferior vena cava, TCPC conduit, left superior vena cava, and branch pulmonary
arteries were all 16 mmHg. Pulmonary capillary wedge pressure was 13 mmHg,
end-diastolic left ventricular pressure was 9 mmHg, and transpulmonary capillary
gradient was 7 mmHg. An angiography showed three anomalous systemic veins
corresponding to a VVM draining in sequence from the inferior vena cava, hepatic
vein, pulmonary veins, and pulmonary venous atrium (functional left atrium) ( and ). This VVM caused a right-to-left shunt, accounting for the oxygen
desaturation.
A percutaneous transvenous coil occlusion was performed uneventfully. After the
procedure, an angiography of the inferior vena cava showed complete occlusion of the
VVM ( and ). At a 12-month follow-up, the patient reported that the
yawning-orthodeoxia had disappeared, and a postural change test showed no oxygen
desaturation in the upright and supine positions, with SpO2 measurements
of ~92-96% (> 90%).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [63.0, 'kg'], 'height': [166.0, 'cm']}",22.86253,21.7194,24.00566,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 63.0 kg. The patient's bmi is therefore 63.0 kg / (1.66 m * 1.66 m) = 22.86253 kg/m^2."
2493,6,Body Mass Index (BMI),physical,decimal,pmc-6784619-1,Extracted,"The patient was an 80-year-old man (weight 49.7 kg, height 1.60 m), who was scheduled to undergo subtotal gastrectomy due to stomach cancer. No specific findings were noted in his medical history, and his preoperative chest x-ray and electrocardiogram were normal. Additionally, all of the patient’s laboratory test results were in the normal range. He had a history of total hip replacement under spinal anesthesia; however, he did not experience awareness during anesthesia for that procedure. This particular operation (gastrectomy) was his first time under general anesthesia.
His blood pressure (BP) was 100/60 mmHg, with a heart rate of 78 beats/min, and a body temperature of 36.5°C; all vital signs were within the normal range in the waiting room before the operation. Premedication of 0.2 mg of glycopyrrolate was administered by intramuscular injection. After arrival to the operating room, the patient’s pre-induction BP was 110/65 mmHg, heart rate 72 beats/min, and oxygen (O2) saturation 98%, which were all in the normal range; BIS (BisVISTA, Aspect Medical Systems, USA) was >95.
Anesthesia was induced by inhaling 8 L/min of 100% O2 for 2 min through a face mask, followed by an intravenous injection of propofol 100 mg. The loss of eyelid reflex was confirmed before intravenous administration of rocuronium bromide 50 mg and fentanyl 50 μg. After confirmation of muscle relaxation, an endotracheal tube was inserted, which was ventilated 10 times/min using a tidal volume of 8 mL/kg while end-tidal carbon dioxide was maintained in the range 35 to 36 mmHg. Thereafter, ETAG concentration was measured while anesthesia was maintained with desflurane 4.0–5.0% vol, O2 (1.5 L/min), and nitrous oxide (1.5 L/min). Post-induction BP was approximately 85/45 mmHg. Therefore, desflurane was maintained at 4.0% vol, and BIS at the time was maintained in the range 35 to 37, and ETAG was 0.9 MAC. From approximately 50 min after the initiation of anesthesia, the patient’s BP slowly escalated to approximately 120/80 mmHg. Subsequently, fentanyl 50 μg and rocuronium bromide 10 mg were additionally administered, and desflurane was maintained at 5.0% vol. At that time, the BIS remained in the range 37 to 43, and the ETAG was 1.2 MAC.
Multiple metastatic lesions were found on the abdominal wall, as well as on the omentum, during the operation. Hence, the patient’s family member was called in approximately 1 h after the initiation of anesthesia and was informed that due to severe cancer metastasis, it was not possible to continue the operation any further. Subsequently, the operators immediately closed the incision, and the patient exhibited stable vital signs approximately up to 120/80 mmHg until completion of the surgery. No sudden increase in BP or heart rate was observed (). The total duration of anesthesia was 2 h and, because the patient was able to sufficiently breathe on his own, the endotracheal tube was removed and the patient was transferred to the post-anesthesia care unit (PACU). After complexly recovering consciousness in the PACU, he did not exhibit any specific expression of awareness during anesthesia. However, immediately after he was moved back to his in-patient room, he complained of awareness during anesthesia by telling his guardian that he overheard the conversation between the operator and his caregiver, felt the pain, and experienced inability to move during a short period of time. The patient did not exhibit any specific sequelae, despite the episode of awareness during anesthesia, and was able to tolerate further treatment processes.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [49.7, 'kg'], 'height': [1.6, 'm']}",19.41406,18.44336,20.38476,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.6 m. The patient's weight is 49.7 kg. The patient's bmi is therefore 49.7 kg / (1.6 m * 1.6 m) = 19.41406 kg/m^2."
2494,6,Body Mass Index (BMI),physical,decimal,pmc-7945347-1,Extracted,"A 79-year-old female patient was admitted to the emergency department of Kyung Hee University Hospital at Gangdong, Seoul, Korea, complaining of abdominal pain that started one day prior. She was 150 cm tall and weighed 40 kg. She was on medication for diagnosed atrial fibrillation and had surgical history for uterine prolapse, rectal prolapse, and left femur neck fracture. Although the patient was not bedridden, she had spent most of her days in bed since undergoing left total hip replacement surgery two years prior. Her average frequency of defecation was every 3 days. Trauma or external injury was denied by the patient and her family.
At the emergency department, her body temperature was 36.7 ℃, blood pressure was 81/51 mmHg, heart rate was 106/min, and respiratory rate was 21 breaths/min. Whole abdominal distention and direct tenderness were noted. Laboratory examinations showed leukopenia (1.88 × 103/uL), and her serum C-reactive protein was 1.1 mg/dL. Blood biochemistries and urine analysis were normal.
An abdominal-pelvis computed tomography (CT) scan revealed pneumoperitoneum with diffuse mesenteric fat haziness of the left abdomen (Fig. a). However, the perforated site could not be clearly delineated. Because the patient’s abdominal pain was aggravated and her blood pressure gradually decreased, she underwent emergency surgery without further evaluation.
Intravenous fluid resuscitation was performed in the emergency department. Second-generation cephalosporin and metronidazole were administered before emergency surgery. We performed laparoscopic surgery with the patient under general endotracheal anesthesia. The camera was inserted through an infraumbilical 12-mm trocar, and two 5-mm trocars were inserted at the right upper and lower quadrants. A 3-cm-sized perforated site was found at the antimesenteric border of the sigmoid-descending junction colon, with fecal material and reactive fluid outside the colon (Fig. b). In addition, a moderately dilated descending colon was found and was filled with hard feces. We mobilized the lateral detachment to create a colostomy using the perforation site (exteriorization) and formed a loop colostomy at the left upper quadrant. The patient developed ileus at postoperative day eight and recovered with conservative treatment including Levin tube insertion. No other events were observed, and she was discharged at postoperative day 29.
Three months after the emergency surgery, the patient visited the outpatient clinic and required colostomy repair surgery. Colonoscopy was performed to identify causes of perforation, such as diverticulum or malignancy, which were negative. The patient was given a detailed explanation about the high possibility of perioperative morbidity and mortality due to advanced age, underlying diseases, and poor performance status; however, she requested colostomy removal. We performed colostomy repair under general anesthesia, with hand-sewn end-to-end anastomosis. The patient was discharged at postoperative day 10 without any adverse events.
Two years 4 months later, the patient was re-admitted to our hospital with abdominal pain. The patient had spent most of her days bedridden due to general weakness; her average frequency of defecation was every 4 or 5 days.
On admission at the emergency department, her body temperature was 36.5 ℃, blood pressure was 91/62 mmHg, heart rate was 112/min, and respiratory rate was 20 breaths/min. Whole abdominal distention and direct tenderness were noted. Leukocytosis was identified (12.10 × 103/uL), and predominant neutrophils (91%) with low hemoglobin (8.4 g/dL) were found. Serum C-reactive protein was increased at 8 mg/dL, and the erythrocyte sedimentation rate was 43 mm/h. Blood biochemistry showed hypoalbuminemia (2.7 g/dL) and hyponatremia (129 mEq/L), and the carcinoembryonic antigen (CEA) level was increased at 12.4 ng/mL.
An abdominal-pelvis CT scan revealed pneumoperitoneum and wall discontinuity in the transverse colon, with adjacent dirty fluid collection in the mid- to left side mesentery, suggesting distal transverse colon perforation with spillage of fecal material (Fig. a).
A treatment strategy similar to the previous procedure was applied. Intravenous fluid resuscitation was conducted, and second-generation cephalosporin and metronidazole were administered before emergency surgery. We performed another laparoscopic surgery under general endotracheal anesthesia. The camera and trocars were inserted through an infraumbilical approach via the right upper and lower quadrants. A 2-cm-sized perforation was found at the antimesenteric border of the distal transverse colon with fecal material, proximal to the previous perforation site (Fig. b). However, additional fecal material and dirty fluid were identified compared with the findings from 2 years prior. After the splenic flexure was completely mobilized, a loop colostomy was performed using the perforated site at the left upper quadrant (Fig. ).
The patient showed uneventful fever (38 ℃) and vomiting at postoperative day 18. A 3-cm-sized intraabdominal fluid collection was found at the left abdomen on CT scan (Fig. a), and she underwent emergency laparoscopic surgery. A small abscess was found and removed, and irrigation with saline was performed (Fig. b).
Small bowel obstruction occurred 4 days after the second surgery, and a Levin tube was inserted. She recovered without additional surgeries or adverse events and was discharged at 20 days after reoperation (38 days in total). Positron emission tomography, gastroscopy, and chest CT were performed to find the causes of elevated CEA before discharge, but no evidence of malignancy was found. She visited the outpatient clinic within one week and decided to use colostomy as a long-term approach.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [150.0, 'cm'], 'weight': [40.0, 'kg']}",17.77778,16.88889,18.66667,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 150.0 cm, which is 150.0 cm * 1 m / 100 cm = 1.5 m. The patient's weight is 40.0 kg. The patient's bmi is therefore 40.0 kg / (1.5 m * 1.5 m) = 17.77778 kg/m^2."
2495,6,Body Mass Index (BMI),physical,decimal,pmc-4190473-1,Extracted,"A 156 cm, 60 kg, 56-year-old woman complained of mild motor aphasia and right hemiparesis. MRI revealed a mass lesion with ring-like enhancement (45 × 42 × 48 mm) in the left frontal lobe with midline shift. Awake craniotomy with iMRI was scheduled because the tumour was located in the left superior and middle frontal gyri.
General anaesthesia was induced. Following left frontal craniotomy and dural incision, the first iMRI was performed (Fig. ). One hundred fifty-eight minutes from induction, the patient regained consciousness after all anaesthetics were ceased. Tumour resection was performed with free conversation. However, after 143 min of surgery under the awake condition, the patient came to complain of excessive sleepiness though she could respond to verbal commands. Electrocorticogram (ECoG) did not detect after-discharge. The tumour was successfully removed en bloc fashion. Progressive brain swelling was not observed. The second iMRI was commenced 182 min into the awake phase (Fig. ). Thirteen minutes from the beginning of the second iMRI scanning, the patient did not respond to noxious stimuli. When the patient was removed from the gantry, she was unconscious and had stopped spontaneous breathing. Her pupils were isocoria and did not dilate. Neither epileptic seizure nor anaphylactic reaction occurred. The peripheral oxygen saturation was not measurable, but cardiac instability or signs of vomiting were not observed. We decided to discontinue the operation under the awake status. No electrolyte imbalance or hypoglycaemia was observed. Subsequently performed iMRI identified a thin subdural haematoma in the contralateral side (Fig. ). The fourth iMRI confirmed that most of the haematoma was evacuated following right frontal craniotomy.
Postoperative computed tomography (CT) revealed neither intracranial haematoma nor pin-related fracture. The patient was extubated 90 min after the end of operation. Both blood pressure and coagulation parameters were kept within normal limits. She recovered without neurological deficits.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [156.0, 'cm'], 'weight': [60.0, 'kg']}",24.65483,23.42209,25.88757,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 156.0 cm, which is 156.0 cm * 1 m / 100 cm = 1.56 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.56 m * 1.56 m) = 24.65483 kg/m^2."
2496,6,Body Mass Index (BMI),physical,decimal,pmc-5096484-1,Extracted,"A 26-year-old man presented with a gradually enlarging multinodular goiter. Previously, he had been a patient in another hospital, but was lost to follow-up in the past 5 years. He had initially presented with delayed bone growth and muscular hypotonia at 4 months of age and was diagnosed to have congenital goitrous hypothyroidism. Levothyroxine (LT4) therapy was started. He was born to non-consanguineous parents. His father is Thai and had no thyroid disorder; however, his mother is German, and in her teens was diagnosed with primary hypothyroidism without goiter and began receiving LT4 replacement. She had neither a history of neck surgery nor radiation. No other family member was reported to have a thyroid disorder.
During childhood, the patient had been regularly followed up by a pediatric endocrinologist. His growth and development were normal except for moderate impairment in fine motor skills and coordination. Ultrasonography of the thyroid gland had revealed that its size was in the upper normal range and LT4 therapy could not be withdrawn. The patient was born and lived in Germany, but later the family moved to Thailand. He graduated with a bachelor’s degree and currently works in the family business. He reported that his goiter size had gradually increased over the past 5 years. He had received LT4 replacement irregularly at a dose of 125 µg/day before he came to us with a concern about the enlargement of his goiter.
At presentation, his body weight was 66 kg and his height was 180 cm. A large multinodular goiter without signs of compression was noted. Thyroid function tests revealed that serum thyroid-stimulating hormone (TSH) level was higher than 100 mIU/L (normal range 0.27-4.2 mIU/L) and serum free thyroxine (fT4) was less than 0.40 ng/dL (normal range 0.93-1.70 ng/dL). Ultrasonography of the thyroid gland showed an enlarged goiter (9.5x8 cm) with multiple solid/cystic nodules in both lobes, ranging in size from 0.8 to 3.6 cm. Microcalcification was also detected in the left lobe of the thyroid gland. At that time, surgery was advised due to a concern about possible thyroid carcinoma. No perchlorate discharge test was done to establish the cause of congenital hypothyroidism. After adequate LT4 replacement, the patient underwent a near-total thyroidectomy and had no complications. Pathology revealed a benign multinodular goiter without any evidence of cancer. Thyroid hormone replacement was given at a dose of 200 µg/day to maintain his thyroid function.
Total triiodothyronine (TT3), fT4, TSH, antibody to TPO (anti-TPO), and antibody to thyroglobulin (anti-Tg) were measured using electrochemiluminescent immunoassays (Abbott Diagnostics, Illinois, USA). Written consent was obtained from the patient and family members. The study was approved by the Ethics Committee of Theptarin Hospital and the Faculty of Medicine Ramathibodi Hospital, Mahidol University.
Genetic analysis was performed in the proband and in all available family members after obtaining informed consent. Because TPO gene mutation is the most frequent cause of thyroid dyshormonogenesis, the entire exons 1-17 and flanking regions of TPO gene were sequenced directly from genomic DNA. To identify a novel mutation, a co-segregation study and human genetic bioinformatics analysis were performed.
The pedigree is shown in . We identified a compound heterozygous mutation on the TPO gene in the index case (II-3). The paternal allele had a frameshift mutation due to an insertion of one nucleotide (c.2268_2269insT) in exon 13. This T insertion caused a stop codon after the insertion point, resulting in a truncated polypeptide of 756 amino acids. The maternal allele had a novel missense mutation (c.1727C>T) in exon 10 resulting in an amino acid substitution from alanine to valine at codon 576 (p.Ala576Val). Based on analysis using two bioinformatic software programs, this variant is likely causing protein damage (SIFT score=0 and Polyphen-2 score=1.0).
These findings were also confirmed by their absence in 100 ethnically matched normal control subjects (courtesy of Professor Joachim Pohlenz).
The patient’s father (I-1) and older brother (II-2) had a heterozygous c.2268_2269insT mutation and normal thyroid function. The father has autoimmune thyroid disease (AITD) as evidenced by high levels of anti-TPO 113 IU/mL (normal range 0-34 IU/mL) and anti-Tg 272 IU/mL (normal range 0-115 IU/mL). The mother (I-2) with primary hypothyroidism was receiving LT4 therapy and had a heterozygous c.1727C>T mutation. She had no positivity of anti-TPO and anti-Tg.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [66.0, 'kg'], 'height': [180.0, 'cm']}",20.37037,19.35185,21.38889,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 180.0 cm, which is 180.0 cm * 1 m / 100 cm = 1.8 m. The patient's weight is 66.0 kg. The patient's bmi is therefore 66.0 kg / (1.8 m * 1.8 m) = 20.37037 kg/m^2."
2497,6,Body Mass Index (BMI),physical,decimal,pmc-6014478-1,Extracted,"Patient 2, a 1-year-old boy, presented with microcephaly (OFC 43.5 cm; −2.8 SD) and attacks of abnormal arm extension. His motor and speech development were delayed. He showed truncal hypotonia on physical examination. His length was 84 cm, he weighed 10 kg. EEG results were normal. MRI showed a short and hypoplastic corpus callosum of which the splenium was affected more than the rostrum (Figure ). He had an upward slant, a small and somewhat sloping forehead, depressed nasal bridge, small and upturned nose tip and nostrils, elongated philtrum and a thin upper lip. A de novo nonsense variant was found: Chr1(GRCh37):g.244217655G>A, NM_205768.2(ZBTB18): c.579G>A (p.(Trp193*)) that leads to a premature stop codon.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [84.0, 'cm'], 'weight': [10.0, 'kg']}",14.17234,13.46372,14.88096,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 84.0 cm, which is 84.0 cm * 1 m / 100 cm = 0.84 m. The patient's weight is 10.0 kg. The patient's bmi is therefore 10.0 kg / (0.84 m * 0.84 m) = 14.17234 kg/m^2."
2498,6,Body Mass Index (BMI),physical,decimal,pmc-5075151-1,Extracted,"A 57-year-old man was referred to our hospital for severe lumbago. His symptoms appeared approximately 3 months prior to referral. After experiencing such symptoms for about a month, the patient consulted an orthopedist. A lumbar spinal radiography showed no significant findings. Despite treatment for pain relief, his lumbago persisted. At presentation, the patient reported no particular past medical history or known allergies. His medication included oxycodone hydrochloride hydrate, loxoprofen sodium hydrate, rebamipide, prochlorperazine maleate, and magnesium oxide. He did not smoke or consume alcohol, and worked as a designer. His mother had diabetes mellitus, hypertension, and hepatocellular carcinoma, and his sister had colon cancer. On physical examination, the patient weight 82 kg and was 174 cm tall. His blood pressure was 189/128 mmHg; his pulse was 92 beats per minute; body temperature was 36.9 °C; respiratory rate was 18 breaths per minute, and the oxygen saturation level was 98 % while breathing ambient air. No swelling of the lymph nodes was palpable. His physical examination was otherwise normal. Laboratory data showed a white blood cell count of 11,100/mm3, platelet count of 73,000/mm3, international normalized ratio for prothrombin time of 1.15, fibrinogen level of 102 mg/dL, fibrin degradation products of 65.7 μg/mL, d-dimer level of 18.1 μg/mL, antithrombin-III activity of 61 %, C reactive protein level of 3.63 mg/dL, creatinine level of 1.32 mg/dL, calcium level of 11.3 mg/dL, aspartate aminotransferase level of 164 U/L, alanine aminotransferase level of 119 U/L, alkaline phosphatase level of 547 U/L, and lactate dehydrogenase level of 552 U/L. Other test results are shown in Table . These laboratory data suggested that the patient had DIC.
Abdominal ultrasonography showed mild splenomegaly. Non-contrast chest computed tomography (CT), gastrointestinal endoscopy, and colonoscopy detected no abnormal findings. Non-contrast abdominal CT revealed multiple bone masses (Fig. ); however, no tumors were found in the liver, adrenal glands, kidneys, bladder, prostate, or pancreas. Therefore, a bone marrow biopsy was performed at the left iliac, revealing poorly differentiated adenocarcinoma cells (Fig. ). Immunohistochemical studies of the biopsy specimen showed positivity for keratin 7, carcinoembryonic antigen (CEA), and cancer antigen (CA) 19-9; negativity for prostatic acid phosphatase (PAP) and napsin A, while inconclusive for keratin 20 and thyroid transcription factor (TTF)-1. Positron emission tomography (PET)-CT disclosed diffuse abnormal uptake in the bones and tail of the pancreas (Fig. ), and contrast enhanced whole-body CT depicted a tumor of approximately 28 mm in diameter with poor enhancement in the pancreatic tail (Fig. ). The patient’s final diagnosis was pancreatic cancer located in the tail of the pancreas with diffuse bone metastases and DIC. His DCBM was thus believed to originate from the pancreatic cancer.
We administered nafamostat mesilate to treat DIC and opioid analgesics to relieve the patient’s lumbago and sharp osteocopic pain. However, we were unable to administer systemic chemotherapy owing to his poor condition. The patient’s general status rapidly deteriorate, and he was transferred to a palliative care unit (PCU). Laboratory data at discharge are shown in Table . He died at the PCU approximately 2 months after admission to our hospital.
A pathological condition derived from carcinoma and diffuse bone metastases with DIC was first reported by Jarcho in 1936 []. Hayashi et al. later defined such a pathological condition with DIC or microangiopathic hemolytic anemia as DCBM []. Almost all the previously published reports have shown that DCBM results from gastric cancer, colon cancer, lung cancer, and breast cancer []. To the best of our knowledge, only one prior report has described pancreatic cancer as the origin of DCBM []. In the present case, contrast whole-body CT revealed a tumor with poor enhancement in the tail of the pancreas and multiple bone masses. No other abnormal structures were identified by CT, gastrointestinal endoscopy, or colonoscopy, whereas PET-CT demonstrated diffuse abnormal skeletal uptake. Laboratory data in the above-mentioned case showed marked elevation of Span-1 and DUPAN-2 and DIC, while the left iliac bone marrow biopsy revealed adenocarcinoma cells. Such findings were probably indicative of pancreatic cancer with DCBM. The condition of our patient was very severe at admission, although his tumor size was significantly smaller than that in the previously reported case (28 mm vs. 55 mm) [], and he died within 2 months of diagnosis. A young age and poorly differentiated carcinoma have been suggested to be associated with poor prognosis in gastric cancer cases with DCBM [, ]. Our patient was diagnosed at 57 years of age and had poorly differentiated carcinoma, which might explain his extremely poor prognosis despite a small pancreatic tumor size.
A previous report indicates that the tumor detection rate with non-contrast CT was 23 % when tumor size was less than 20 mm, 59 % for tumors measuring less than 40 mm, and 100 % in cases of tumors measuring more than 40 mm []. In the present case, the tumor size was 28 mm, and it was undetectable via non-contrast CT. It was subsequently found by PET and contrast-enhanced CT imaging.
While the serum CA19-9 levels were normal in cases of gastric cancer with DCBM [–], the serum CA19-9 levels were markedly elevated in cases of pancreatic cancer with DCBM in the present study as well as those in a previous study []. Although the mechanism for this finding is unknown, the extremely high CA 19-9 levels might be helpful in the early diagnosis of pancreatic cancer with DCBM before the histopathological examination results are obtained.
Exacerbation of DCBM occurs rapidly, and the mean survival time is 4.6 months after the onset of DCBM []. A proper diagnosis and timely administration of chemotherapy and treatment of DIC are crucial to prolong survival []. Pancreatic tumors are occasionally challenging to detect with non-contrast CT. Therefore, it is important to consider the pancreas as a possible origin of DCBM and perform contrast-enhanced CT when multiple bone metastases are observed.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [82.0, 'kg'], 'height': [174.0, 'cm']}",27.08416,25.72995,28.43837,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 174.0 cm, which is 174.0 cm * 1 m / 100 cm = 1.74 m. The patient's weight is 82.0 kg. The patient's bmi is therefore 82.0 kg / (1.74 m * 1.74 m) = 27.08416 kg/m^2."
2499,6,Body Mass Index (BMI),physical,decimal,pmc-4332014-2,Extracted,"This case involved a 51-year-old female patient, with a weight of 63 kg and a height of 160 cm. The initial diagnosis was made in January 2010; the pathological diagnosis showed a bronchioalveolar carcinoma, and biopsy revealed an adenocarcinoma. The primary lesion was located in the right upper lobe (RUL) of the lung. Initially no lymph nodes tested positive, but metastasis– was found in the Rt. pleura in February 2013. The initial stage of the cancer was IA (TNM: pT1bN0), and the present stage is IV. A RUL lobectomy and a wedge resection of the right middle lobe (RML) were performed on February 16, 2010, and chemotherapy was administered from February 21, 2013, to the present (p.o. Iressa). Common complaints were dizziness, nausea, vomiting, insomnia, fatigue, diarrhea, and dyspnea.
Medications included Iressa (Gefitinib) 250 mg 1-0-0 antineoplastics. Pulmonary tuberculosis (Rt. lung) was diagnosed in 2008.
The patients was admitted from December 9, 2013, to January 7, 2014, and ANP was administered from December 23, 2013, to January 2, 2014, for a total of 5 times. No analgesics were used.
The patient was initially diagnosed with an adenocarcinoma of the lung in the right upper lobe region and received a RUL lobectomy and a RML wedge resection. After 3 years of follow-up, pleural metastases were confirmed. After taking oral anti-tumor medication for a month, the patient complained of a rash, dry skin, and diarrhea, and 5 days after admission, she also mentioned having pain in the right flank. The pain was described as an electric-shock sensation that radiated from the right flank to the inner upper right abdominal region with a VAS score as high as 7 when severe. This type of cancer pain was suspected to be caused by pleural seeding. The pain disappeared the day after her first ANP treatment. After 5 treatments of ANP, the patient was discharged from the hospital pain free (VAS score = 0). The patient was able to perform daily activities without taking any analgesics during her admission (Table ), (Fig ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [63.0, 'kg'], 'height': [160.0, 'cm']}",24.60937,23.3789,25.83984,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 63.0 kg. The patient's bmi is therefore 63.0 kg / (1.6 m * 1.6 m) = 24.60937 kg/m^2."
2500,6,Body Mass Index (BMI),physical,decimal,pmc-7568629-1,Extracted,"A male Chinese patient aged 42 years with a height of 193 cm, weight of 95 kg and a history of chronic hepatitis B infection for >20 years. The patient presented with an obstructive liver lesion, as assessed by physical examination, and was admitted to hospital for 2 weeks. Computed tomography (CT) imaging evaluation identified a single tumor with diameter approximately 3 cm located in segments V and VIII of the liver without macrovascular invasion. The tumor was staged as TNM stage T1bN0M0 Ib, corresponding to Barcelona Clinic Liver Cancer (BCLC) Stage A. The patient had an Eastern Co-operative Oncology Group Performance Score (ECOG PS) of 0, no jaundice of the skin or sclera, and negative abdominal signs. Laboratory tests revealed that the patient had normal liver function (Child-Pugh Score 5 and Grade A) and coagulation, an AFP level 4.45 ng/mL, hepatitis B surface antigen titer of 1816, HBV DNA level of 3.45×104 IU/mL and Protein Induced by Vitamin K Absence or Antagonist-II (PIVKA-II) level 34 mAU/mL. Based on the single liver lesion, early stage of disease, good liver function and discussion with the patient, a hepatectomy was performed.
After a successful hepatectomy with a surgical margin of 1 cm to the tumor, pathological examination revealed the tumor had a diameter of approximately 3 cm with a negative surgical margin consisting of moderately differentiated HCC and without tumor thrombus or satellite foci. After surgery, the patient received one cycle of TACE to identify residual lesions and confirm successful resection, and no residual tumor was observed. Post-surgery, the patient received thymosin to prevent the relapse of HCC, as well as oral entecavir (500 mg/day) for the management of hepatitis B. The patient experienced tumor recurrence 14 months after surgery with a single tumor of approximately 2 cm diameter located between the left and right hepatic pedicle of the first porta hepatis. The tumor was close to the portal vein and biliary tract without macrovascular involvement. The recurrent tumor was early stage (T1aN0M0 Ia) and based on the Milan criteria the patient was a potential candidate for liver transplantation. However, the patient refused to undergo liver transplantation and underwent a CT-guided microwave ablation procedure. Post-surgery TACE revealed complete tumor ablation without residual tumor. The patient continued to receive thymosin to prevent HCC recurrence, as well as oral entecavir for hepatitis B.
After a further 11 months, the patient experienced a second recurrence characterized by multiple disseminated metastases in the left and right lobes of the liver and possible macrovascular invasion. No distant metastasis was identified and the patient had an ECOG PS of 0 with Child Pugh Stage 5 and Grade A. However, the tumor stage of the patient was relatively advanced beyond transplantation criteria (BCLC Stage B/C) (). Based on guideline recommendations, the patient was advised to initiate systemic therapy., Genetic testing indicated a low tumor mutation burden and immunohistochemical analysis was negative for programmed cell death ligand 1 (PD-L1) expression. A microsatellite stability test found no variation for MLH1, MSH2, MSH6, and PMS2, which indicated a low probability of benefit from immune therapy and this was communicated to the patient. The patient therefore initiated treatment with lenvatinib (Lenvima®, Eisai Co., Japan) 12 mg once daily and achieved a partial remission (mRECIST criteria) by imaging evaluation after 3 months of treatment (), and a reduction in PIVKA-II levels from 254 to 142 mAU/mL. Three months after initiation of lenvatinib, the patient decided to transfer to another hospital (Peking Union Medical College Hospital) with specialized expertise in the use of anti-programmed cell death 1 (PD-1) antibody therapy, at which they could begin additional treatment with anti-PD-1 antibodies (off label, toripalimab, Shanghai Junshi Biosciences, Shanghai, China) (240 mg). The patient experienced a severe immune reaction (Stevens-Johnson syndrome) 6 days after initiating immune therapy. Subsequently, the patient immediately terminated PD-1, and after returning to our institution received intravenous glucocorticoid therapy for one month, before switching from lenvatinib to apatinib monotherapy (off-label, Aitan®, Jiangsu Hengrui Medicine, China) (850 mg daily) for 10 days. The patient was then found to have progressive disease as evaluated by imaging examination (), accompanied by an increase in PIVKA-II level from 142 to 1019 mAU/mL. After multidisciplinary consultation, the patient was switched back to lenvatinib monotherapy.
After one month of lenvatinib treatment, the patient was found to have again achieved a partial response (). In addition, the patient’s PIVKA-II level had decreased from 1019 to 324 mAU/mL and the tumor stage recovered to BCLC Stage A. Based on the Milan criteria the patient was suitable for a liver transplantation and was advised to make the most of this “window of opportunity”. However, the patient refused surgery. After being in remission for 4 months, the patient’s PIVKA-II level increased, which was defined as progressive disease. The tumor stage of the patient advanced to BCLC C and the patient missed the opportunity for radical hepatectomy. At this stage, the patient was switched from lenvatinib to regorafenib 80 mg daily. The patient was followed up for the last time on April 21, 2020, and PET-CT revealed bone and lung metastasis ().",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [193.0, 'cm'], 'weight': [95.0, 'kg']}",25.50404,24.22884,26.77924,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 193.0 cm, which is 193.0 cm * 1 m / 100 cm = 1.93 m. The patient's weight is 95.0 kg. The patient's bmi is therefore 95.0 kg / (1.93 m * 1.93 m) = 25.50404 kg/m^2."
2501,6,Body Mass Index (BMI),physical,decimal,pmc-8519668-1,Extracted,"Written informed patient consent for publication was obtained. Approval from Committee on Health Research Ethics was not required according to Danish law.
A 39-year-old woman (height 165 cm; weight 75 kg) presented for elective cesarean section. She had a 13-year history of psoriatic arthritis with severe spondylitis and involvement of the temporomandibular joint. In 2013, the patient underwent subacute cesarean section (category 3) []. Spinal anesthesia was difficult and without a sufficient effect. The decision for general anesthesia was made, and a rapid sequence induction was performed. Direct laryngoscopy revealed a Cormack and Lehane score of four, and even with a hyperangulated videolaryngoscope (McGrath–Series 5, Aircraft Medical, Edinburgh, UK), intubation was impossible. The surgical procedure was thus performed with a facemask and the patient breathing spontaneously on sevoflurane. In 2019, a minor elective gynecological procedure again necessitated anesthesia. Spinal anesthesia was attempted once again, but despite multiple attempts by two anesthesiologists, it proved to be impossible. The procedure was instead performed under surgically placed local anesthesia and propofol sedation on spontaneous breathing.
Airway examination preoperatively revealed a Simplified Airway Risk Index (SARI) score of 8. Mouth opening was 25 mm (). Neck movements were severely limited, and the head could not be extended from the neutral position (0°), but flexion could be performed (about 30–40°). The modified Mallampati score was 3, the thyromental distance was 6–6.5 cm, and the patient was unable to prognath. The cricothyroid membrane was easy to palpate. A computed tomography (CT) scan from 2020 showed block vertebrae C2/C3 and C5/C6 and fusion of facet joints C2–C6 in the cervical region and fusion of multiple facet joints and fusion of all spinous processes in the lumbar region ().
Needle-through-needle combined spinal-epidural anesthesia proved impossible, even though attempts were made by two consultants on multiple levels, using both median and paramedian techniques and with ultrasound guidance.
The patient was placed in an upright sitting position, supplementary oxygen by nasal cannula 3 L/minute was provided, and propofol and remifentanil infusions were initiated (0.4–0.6 μg/kg/minute and 0.03–0.05 μg/kg/minute, respectively). Glycopyrrolate 0.2 mg IV (Meda, Solna, Sweden) and ondansetron 4 mg IV (Accord, Solna, Sweden) were administered. At all times, the patient was alert and oriented, able to respond in short sentences, and had sufficient respiration with peripheral saturations above 99%. Topicalization was performed with lidocaine 2% with 5 μg/ml epinephrine (Amgros, Copenhagen, Denmark). A different formulation was used for spray application only, which was lidocaine 10% (Xylocaine Pump Spray 100 mg/ml, AstraZeneca, Södertälje, Sweden). Inhalation (4 ml ×2), transtracheal injection (2 ml ×1), spray application (3 puffs ×3), and for potential backup, nasal route application with a mucosal atomization device (MAD Nasal, Teleflex, Waine, PA, USA) and a local anesthetic soaked ribbon gauze (1 ml ×1, respectively, 3 ml ×1) were applied. Intubation was performed with an FB (Ambu aScopeTM Regular, Ambu A/S, Ballerup, Denmark), an LMA FastrachTM endotracheal tube with an internal diameter of 6.5 mm (Teleflex, Beaconsfield, UK), a Berman intubating airway (Vital Signs, Totwa, NJ, USA), and the Infrared Red Intubation System (IRRIS, Guide In Medical, Nazareth, Israel). The procedure was straightforward, and the intubation itself took less than 2 minutes (). Visual confirmation of tube placement, gentle cuff inflation, and immediate capnography were followed by induction with propofol 100 mg IV and sevoflurane for maintenance of anesthesia. After delivery of a baby girl (Apgar scores of 8/10), this was changed to propofol and remifentanil infusions.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [165.0, 'cm'], 'weight': [75.0, 'kg']}",27.54821,26.1708,28.92562,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 75.0 kg. The patient's bmi is therefore 75.0 kg / (1.65 m * 1.65 m) = 27.54821 kg/m^2."
2502,6,Body Mass Index (BMI),physical,decimal,pmc-5769410-1,Extracted,"A 68-year-old man was admitted to our hospital due to aortic arch anastomotic pseudoaneurysm with concomitant aortic root enlargement and coronary artery stenosis. At 56 years of age, the patient had undergone a total arch replacement at another hospital, with three-branched island reconstruction performed using the T-graft technique for a chronic aortic dissection, expanding from the ascending aorta to distal aortic arch (Figs. and ). In the aortic arch island reconstruction, the adventitia and intima of the arteries were combined and reinforced externally by a felt, and end-to-end anastomosis was performed with a 30-mm synthetic vascular graft with one branch. Thereafter, the patient was followed up by a local physician; however, a computed tomography (CT) scan was not performed, as no relevant symptoms were observed. A CT scan at another hospital, however, showed a giant pseudoaneurysm at the site of the island reconstruction 11 years later. Though endovascular repair was considered, the patient was ultimately determined to be inoperable by the other hospital, as enlargement of the aortic root was also observed. He was subsequently referred to our hospital and he opted to undergo surgery at our institution.
At the time of presentation, the patient was 168 cm in height and weighed 71 kg. His vital signs were as follows: body temperature, 36.1 °C; blood pressure, 120/60 mmHg (no difference between left and right arms); pulse rate, 70 bpm (regular); and SpO2, 100% (room air). Upon physical examination, his consciousness was clear, but expressed hoarseness in his voice. The patient had a median sternotomy scar. A diastolic murmur was detected in the third intercostal space at the left sternal border on thoracic auscultation. Breath sounds were normal, and the abdomen was soft and flat. An electrocardiogram showed normal sinus rhythm. A chest X-ray revealed enlargement of the left 1st arch and elevation of the left diaphragm. His cardio-thoracic ratio was 55.4%.
There were no abnormal laboratory findings nor did echocardiography reveal abnormal cardiac function upon admission.
Contrast-enhanced CT (Fig. ) showed that a giant arch pseudoaneurysm (81 mm wide) had formed in the island-shaped arch branch. No false lumen was observed in the aneurysm, and its enlargement was omnidirectional. The diameter of the aortic root was also enlarged to approximately 56 mm in size. In addition, coronary angiography indicated that there was 99% stenosis of the left anterior descending coronary artery at #7, collateral circulation from the right coronary artery, and 75% stenosis of the left circumflex artery at #13.
Based upon these observations, the patient underwent a repeat total arch replacement, aortic root replacement (i.e., Bentall procedure), and coronary artery bypass grafting [the left internal thoracic artery (LITA) and saphenous vein graft (SVG) were used]. Under general anesthesia, extracorporeal perfusion was initiated. We re-performed a median sternotomy and successfully opened the thorax without causing any damage to the aneurysm, while gradually decreasing the rectal temperature to 28 °C while sending blood to the right femoral artery and right axillary artery, while removing blood from the right femoral vein. We were able to switch the cannula from the femoral vein to the superior and inferior vena cava, as needed. After removing the previously used vascular graft, the coronary ostia on the right and left were confirmed and excised in the shape of a button. A 23 mm Carpentier-Edwards Perimount (CEP)® bovine pericardial bioprosthesis (Edwards Life Science, Irvine, CA) and a 28 mm Vascutek® Gelweave Valsalva Graft (Terumo Vascutek, Renfrewshire, Scotland, UK) were combined with a running suture, and the skirt portion and the aortic valve annulus were attached with a 3–0 PROLENE running suture (Ethicon, Somerville, NJ, USA), with a felt strip between them. The right and left coronary arteries were continuously sutured with 5–0 PROLENE (Ethicon, Somerville, NJ, USA) for reconstruction of the Carrel patch. When the rectal temperature reached 28 °C, circulation of the lower body was arrested and antegrade selective cerebral perfusion was initiated by the insertion of balloon-occludable catheters to each cervical branch of the aorta. Upon incision of the aneurysm, it was revealed that the inner wall was covered by atheroma, although no false lumen was observed inside the aneurysm or arch branches. After removing as much of the aneurysm as possible, three separate perfusions of cervical branches were performed. On the distal side, another vascular graft was retained and connected to a 26 mm, four-branched synthetic vascular graft (J-graft SHIELD NEO®, Japan Lifeline, Japan) with 3–0 PROLENE (Ethicon, Somerville, NJ, USA) using the open distal technique. After a restart of blood flow from the synthetic vascular graft branch, the left subclavian artery was reconstructed. In addition, the SVG and LITA were sutured to #14 and #8, respectively, and the Valsalva graft and the 26 mm J-graft were attached with running sutures of 4–0 PROLENE (Ethicon, Somerville, NJ, USA). The central side of the SVG was then anastomosed to the J-graft to allow the release of the aorta clamp. Finally, the left common carotid artery and brachiocephalic artery were reconstructed.
The operation was completed under stable hemodynamics. The operation time was 660 min, extracorporeal circulation time was 363 min, aortic clamp time was 172 min, circulatory arrest time was 38 min, the lowest rectal temperature was 27.6 °C, and intraoperative bleeding was 3240 mL.
Although the patient was re-intubated on the fourth postoperative day after extubation for ventilator failure, he was extubated again and discharged from the ICU on the eighth postoperative day. An indwelling pacemaker was inserted on the 40 s postoperative day due to sick sinus syndrome and the patient was ultimately discharged from the hospital on the fiftieth postoperative day (Fig. ). He has been visiting the hospital as an outpatient and is in favorable condition.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [168.0, 'cm'], 'weight': [71.0, 'kg']}",25.1559,23.8981,26.4137,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 71.0 kg. The patient's bmi is therefore 71.0 kg / (1.68 m * 1.68 m) = 25.1559 kg/m^2."
2503,6,Body Mass Index (BMI),physical,decimal,pmc-7716315-1,Extracted,"A 74-year-old man presented with dyspnea on exertion that started two months earlier.
The patient presented anemia and a hemoglobin level of 6.4 g/dL during an ophthalmology consultation for cataract treatment. The patient presented dyspnea on exertion, a symptom that had aggravated over the past two months. The patient visited the hematological department.
The patient had a past medical history of cataract and ossification of a posterior longitudinal ligament.
The patient had been a smoker for 50 years.
Vital signs were within normal limits at presentation, with a heart rate of 80 bpm, blood pressure of 135/60 mmHg, and a temperature of 36.1 ℃. His height and weight were 171 cm and 75 kg, respectively.
Laboratory tests indicated a WBC count of 2190 cells/µL, a hemoglobin level of 6.2 g/dL, a platelet count of 7.4 × 104/µL, a lactate dehydrogenase level of 283 IU/L, and a ferritin level of 620.41 ng/mL. The WT1 mRNA was 4800/µg RNA of peripheral WBCs, and the serum d-ROM level was 435 Carratelli units. The bone marrow aspiration was dry tap, and the bone marrow biopsy showed MDS with fibrosis.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [171.0, 'cm'], 'weight': [75.0, 'kg']}",25.64892,24.36647,26.93137,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 171.0 cm, which is 171.0 cm * 1 m / 100 cm = 1.71 m. The patient's weight is 75.0 kg. The patient's bmi is therefore 75.0 kg / (1.71 m * 1.71 m) = 25.64892 kg/m^2."
2504,6,Body Mass Index (BMI),physical,decimal,pmc-8223295-1,Extracted,"The patient was a 71-year-old Japanese woman who was diagnosed with chronic kidney disease due to ADPKD 3 years previously. She received surgical clipping for an unruptured aneurysm of the right middle cerebral artery 4 years earlier. She did not drink alcohol and was a non-smoker. She was taking amlodipine for hypertension, topiroxostat for hyperuricemia, and ferric citrate hydrate for hyperphosphatemia. Continuous erythropoietin receptor activator was administered subcutaneously for renal anemia once a month. She was followed up in an outpatient clinic and suddenly developed right abdominal pain one month previously. As abdominal computed tomography (CT) showed a ruptured liver cyst in the right lobe, which had not been observed seven months previously (Fig. a, b), she was admitted to our hospital. While her white blood cell count was within the normal range at 5900/µL, C-reactive protein was a little high at 0.4 mg/dL. She was treated with bed rest and intravenous cefmetazole administration (1 g/day) on suspicion of cyst infection. Oral acetaminophen 500 mg was occasionally used when needed, and her symptoms improved with conservative management and she was discharged from the hospital after one week. Although she was asymptomatic for a while, she noticed bilateral leg edema, abdominal distension, and general malaise at one month after hospital discharge. Since abdominal CT showed massive ascites (Fig. c), she was admitted to our hospital again.
On admission, her height was 166 cm, and her body weight was 62 kg. A physical examination revealed the following: body temperature, 37.2 °C; blood pressure, 114/73 mmHg; pulse, 94 beats/min; and oxygen rate, 97% on room air. Abdominal distention was observed without tenderness, and pitting edema was observed in the bilateral legs. The laboratory data are shown in Table . Her serum creatinine, alkaline phosphatase, γ-glutamyl transpeptidase, total bilirubin, and CA19-9 were 5.2 mg/dL, 1992 U/L, 355 U/L, 3.1 mg/dL, and 5006 U/mL, respectively.
Abdominal paracentesis revealed amber transparent ascites (Fig. d) and the bilirubin and CA19-9 concentrations were high at 13.3 mg/dL and 244,700 U/mL, respectively. Ascites culturing and cytology were negative. She was diagnosed with biliary peritonitis due to a ruptured liver cyst. Hemodialysis was initiated due to the exacerbation of chronic kidney disease. As conservative treatment did not improve her symptom, drainage of the ascites was initiated from day 11. The outflow of the ascites was 1000 mL per day and there was no tendency to decrease. Drip infusion cholangiography (DIC)-CT revealed that the ruptured cyst in the right posterior segment S6 of the liver was enhanced with contrast medium (Fig. e). Three-dimensional views of DIC-CT showed communication between the ruptured cyst and an intrahepatic bile duct (Fig. f, g). Because of her markedly high CA19-9 levels in serum and ascites, upper endoscopy and repeated ascites cytology were required to rule out cancer. On day 24, oral cefditoren pivoxil (100 mg/day) was initiated because her C-reactive protein was still high at 7.4 mg/dL. On day 31, she was transferred to a university hospital, and the ascites culture on the same day was found to be positive for Enterococcus faecalis. Abdominal surgery was performed. The surface of the liver became yellowish due to bile leakage and a ruptured necrotic cyst was observed on the right liver lobe (Fig. h). After removing the necrotic roof, the orifice that was the source of the bile leakage was identified and sutured (Fig. i). As gallbladder stones had been pointed out, cholecystectomy was performed at the same time. Cholangiography showed no stones in the common bile duct. Intravenous flomoxef sodium (0.5 g/day) was initiated for 3 consecutive days, followed by intravenous sulbactam/ampicillin (1.5 g/day) for 12 days. Abdominal CT one month after the operation showed no recurrence of ascites and she was discharged on day 49. Hemodialysis treatment was discontinued immediately after discharge because her urine volume had increased and her creatinine level had decreased to 3.8 mg/dL. There has been no recurrence of ascites since then.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [166.0, 'cm'], 'weight': [62.0, 'kg']}",22.49964,21.37466,23.62462,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 62.0 kg. The patient's bmi is therefore 62.0 kg / (1.66 m * 1.66 m) = 22.49964 kg/m^2."
2505,6,Body Mass Index (BMI),physical,decimal,pmc-8532189-1,Extracted,"A 49-year-old woman presented with diarrhea approximately once every 30 min for two days prior to her visit. On arrival, she had a fever of 39.0°C with chills. The patient had persistent diarrhea and fever and had trouble moving; hence she required emergency assistance and was brought to our hospital. She was a current smoker, who smoked 10 cigarettes/day for 29 years and consumed 1,500 mL of cocktails per day. She owned a pet cat, and the cat licked her body surface regularly. She had a history of depression; however, she had not consulted a doctor for five years. She had no other medical history and was not taking any medications, including any over-the-counter medications.
Her height and body weight were 162 cm and 60 kg, respectively. On admission, consciousness was assessed using the Glasgow Coma Scale (score, 14) (E4V4M6), her body temperature was 38.0℃, pulse was 132 beats/min, blood pressure was 88/51 mmHg, respiratory rate was 24 breaths/min, and the peripheral arterial oxygen saturation was 94% (nasal cannula, 1 L). Physical examination revealed livedo reticularis on the lower limbs. There was no site of soft tissue infection with redness, heat, or swelling throughout the body. The blood tests that were performed are shown in Table . Arterial blood gas analysis showed mixed alkalosis and hyperlactatemia (serum lactate, 8.4 mg/dL). Conventional abdominal computed tomography revealed mild enlargement and a diffuse low-density area of the liver.
The patient was admitted to the intensive care unit in a state of septic shock with alcoholic cirrhosis, hypokalemia (serum potassium, 1.9 mEq/L) with frequent diarrhea, and disseminated intravascular coagulation syndrome. The clinical course of the patients is shown in Figure . Blood, urine, and spinal fluid specimens were cultured, and piperacillin-tazobactam (4.5 g) was administered as an empiric therapy with the initiation of potassium replacement through a central vein. On the same day, the antibacterial agents were changed to meropenem (1 g every 12 h) and vancomycin (1.5 g every 24 h) due to deteriorating clinical conditions. Artificial respiration was started on the same day as the patient's respiratory condition worsened. After admission, she did not have frequent diarrhea. On the second day of admission, the patient’s renal function (serum creatinine, 2.6 mg/dL) and liver function (prothrombin time, 35.6%; total bilirubin, 6.0 mg/dL) worsened, thereby requiring continuous hemodiafiltration (CHDF), plasma exchange therapy, and coagulation factor replacement. In addition, venoglobulin and amikacin 400 mg were administered for sepsis. The dosage of meropenem was changed to a severe dose of 2 g every 12 h considering the worsening clinical condition and the dosage of vancomycin was changed to 1 g every 24 h as the renal function worsened and CHDF was initiated. However, metabolic acidosis and hyperlactatemia progressed, and the patient died in the early hours of the third sick day. On the third day of admission, blood culture yielded P. multocida, which was susceptible to piperacillin-tazobactam and meropenem.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [162.0, 'cm'], 'weight': [60.0, 'kg']}",22.86237,21.71925,24.00549,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 162.0 cm, which is 162.0 cm * 1 m / 100 cm = 1.62 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.62 m * 1.62 m) = 22.86237 kg/m^2."
2506,6,Body Mass Index (BMI),physical,decimal,usmle-8534,Extracted,"A 67-year-old woman presents to her physician for a regular checkup. She is a community-dwelling, retired teacher without any smoking history. She has arterial hypertension and takes hydrochlorothiazide 12.5 mg and valsartan 80 mg daily. She was recently discharged from the hospital after admission for an ulnar fracture she received after a fall from the second step of a ladder in her garden. A year ago, she had a clavicular fracture from tripping over some large rocks in her yard. She does not report lightheadedness or fainting. Her medical history is also significant for an appendectomy 11 years ago. She is in menopause. She mostly consumes vegetables and dairy products. Her height is 163 cm (5 ft 4 in) and weight is 55 kg (123 lb). Her blood pressure is 130/80 mm Hg without orthostatic changes, heart rate is 73/min and regular, respiratory rate is 14/min, and temperature is 36.6°C (97.9°F). Her lungs are clear to auscultation. Cardiac auscultation reveals S2 accentuation over the aorta. The abdomen is mildly distended on palpation; there are no identifiable masses. The neurological examination is unremarkable.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [163.0, 'cm'], 'weight': [55.0, 'kg']}",20.70082,19.66578,21.73586,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.63 m * 1.63 m) = 20.70082 kg/m^2."
2507,6,Body Mass Index (BMI),physical,decimal,pmc-2882553-1,Extracted,"A 72-year-old female (height: 161 cm, weight: 63 kg) was admitted to the hospital with progressive and generalized muscle spasms associated with risus sardonicus and opisthotonus. Tetanus was diagnosed, and she was transferred to the intensive care unit (ICU). She was intubated and mechanically ventilated because of respiratory distress. After the intubation, a central venous catheter (CVC) (Certofix Trio, SB 730, 30-cm in length, 7F, 3Lumen, B. Braun, Melsungen AG, Melsungen, Germany) was inserted into the left subclavian vein using the Seldinger technique. The left subclavian vein was punctured at the first attempt, and blood was freely aspirated from the vein before and after insertion of the catheter. Correct positioning of the catheter tip in the superior vena cava was confirmed by chest radiography (CXR) (). Radiography was performed with a portable bedside machine in the antero-posterior direction with the patient lying in the supine position. The patient was sedated with intravenous diazepam and dexmedetomidine infusions.
Intermittent positive pressure ventilation was started as a pressure-controlled ventilation [frequency: 14 beats/min, PEEP: 3 cmH2O, inspiration pressure (Pins): 12 mmHg] (GE Healthcare, Engström Carestation). Prior the 5th day of ICU care, no CXR was taken because the patient’s hemodynamic and arterial blood gas analyses were stable. On the 5th day, the patient developed progressive hypotension. Although the intravenous fluid infusion dose was increased, hypotension continued, and therefore, a dopamine infusion was started. In addition to hypotension, the patient began to suffer from a decrease in PaO2. Auscultation revealed that neither lung was aerated, and it was not possible to aspirate blood from the CVC ports. Therefore, a new CVC was inserted into the right internal jugular vein. CXR was then ordered, but it was not immediately performed due to technical reasons. Before a radiograph was obtained, the left subclavian CVC was removed because of a misunderstanding between experienced staff and a junior doctor. After that, CXR was performed, which detected a large left pneumothorax and a right hydrothorax (). Bilateral thoracentesis was performed, and 2000 ml of clear fluid was drained into the right thorax tube. This volume was comparable to the volume of fluid the patient received through the catheter. The patient’s condition markedly improved, and lung expansion and gas exchange normalized ( and ). A tracheotomy was performed on the 9th day, mechanical ventilation was discontinued on the 34th day, and the patient was discharged from the ICU on the 45th day without problems.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [161.0, 'cm'], 'weight': [63.0, 'kg']}",24.30462,23.08939,25.51985,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 161.0 cm, which is 161.0 cm * 1 m / 100 cm = 1.61 m. The patient's weight is 63.0 kg. The patient's bmi is therefore 63.0 kg / (1.61 m * 1.61 m) = 24.30462 kg/m^2."
2508,6,Body Mass Index (BMI),physical,decimal,pmc-4595414-1,Extracted,"A 38-year-old female patient with an incidentally found gastric submucosal tumor was referred to our hospital for the consultation of the possibility of NOTES gastrectomy. The patient herself wished to undergo NOTES as a surgical alternative, due to possible less pain and better cosmesis. Her body weight was 41 kg and height was 155 cm. The patient was asymptomatic and otherwise healthy without any gastrointestinal disorders. The lesion, 2.5 cm in size, was demonstrated on the posterior wall of the gastric fornix by preoperative abdominal computed tomography. Endoscopy revealed a SMT with intra-gastric growth, with the distance of 2.0 cm below the esophago-gastric junction (Fig. ). Biopsy was not attempted due to the size and location of the lesion. The patient experienced one childbirth with normal transvaginal delivery. After intensive discussion among the team, transvaginal NOTES partial gastrectomy was indicated as a surgical alternative. We informed the patient of its experimental nature, our previous clinical experience, the procedure’s short- and long-term outcomes, the possible risks/complications, and the details of the procedure itself. Surgery was conducted under the protocol approved by the University’s Institutional Review Board (IRB Folio No. 08063). Table demonstrates our inclusion/exclusion criteria for transvaginal NOTES gastrectomy, which was approved by the University’s Institutional Review Board.
The routine part of our transvaginal NOTES technique has been described elsewhere [, ]. Briefly, after placing two laparoscopic ports at the umbilicus (5 mm) and the left mid-abdomen (3 mm), the posterior vaginal sac was exposed and punctured under laparoscopic guidance. This entry site was secured with an extra-long endoscopic over-tube, and a standard flexible gastrointestinal endoscope was advanced into the abdomen. The peri-gastric ligaments were dissected with energy devices passed through the endoscope to mobilize the involved portion of the stomach. The endoscope was then replaced with a linear stapling device. EGD was advanced trans-orally into the stomach to calibrate the EGJ and to obtain adequate surgical margin during stapling (so-called gastric calibration). Stapled partial gastrectomy was accomplished under laparoscopic monitoring. The specimen was isolated in a plastic bag and was delivered via the vagina. The vaginal entry site was closed with sutures under direct vision.
In this particular patient, we employed new techniques and newly developed accessory devices.
The transvaginal over-tube was secured with a thin loop-retracting device (Mini Loop Retractor, Hakko, Nagano, Japan), which was introduced via the umbilical incision under retroflexed flexible endoscopic guidance. This technique enabled intentional “steering” of long and flexible over-tube in the abdominal cavity and greatly enhanced its stability while controlling the tip of the flexible endoscope (Fig. ).
Currently available over-tube has been designed to be used as a “guide” for flexible endoscope, and is not suitable to maintain pneumoperitoneum. Its distal orifice is not leak-proof; therefore, carbon dioxide, once fed through the trans-abdominal trocar, continuously leaks from the space between the over-tube and the endoscope. To solve this problem, we have developed a reinforced anti-leak adapter, and it was commercialized as an endoscopic accessory (Leak Cutter, Top Corporation, Tokyo, Japan) in 2012. With this simple device, pneumoperitoneum was successfully established and maintained all through the procedure without causing any major gas leakage (Fig. ).
This newly developed device (Endoshower, Yamashina Seiki Co., Ltd., Siga, Japan) is a flexible catheter which passes the standard biopsy channel of current flexible endoscopes. Endoshower enables “laparoscopy-like” irrigation and suction under sterile condition. With this device, the abdomen was diffusely irrigated, and the fluid in the sub-diaphragmatic space was safely drained without causing any mis-suction and injuries on the splenic capsule (Fig. ).
The procedure was successfully completed without any complications. No additional trocar was required, and no trans-abdominal energy device was used. The operative time was 260 min, and the blood loss was 20 ml. The patient showed uneventful and rapid postoperative recovery without any analgesic. She discharged from the hospital without any abdominal/gynecological complaints on the fifth postoperative day, which was determined by the IRB-approved clinical protocol. The postoperative pathology revealed leiomyoma of the stomach, 28 × 15 × 10 mm in size. Both umbilical and mid-abdominal scars are now well consolidated and virtually invisible.
One of the technical challenges in human NOTES is how to control and stabilize flexible endoscope in the abdominal cavity [, , , ]. Various commercially available/non-available over-tubes, i.e., platforms, have been attempted; however, virtually none of them have archived true clinical success [, ]. Our “over-tube steering technique” using loop-retracting device is simple, effective, and inexpensive; however, its true advantage in reducing operating time/blood loss was not shown in this single case report. This technique is applicable to any type of NOTES and practical since it is compatible with any kind of off-the-shelf endoscopic over-tubes. Further accumulation of clinical cases is definitely needed, to establish this technique as an attractive surgical option. The authors believe that future platform for pure NOTES should have at least “anchoring” mechanism that anchors the platform onto the abdominal lining.
How to maintain pneumoperitoneum is another fundamental but difficult problem in NOTES [, ]. Since commercially available endoscopic over-tubes are not designed to maintain a steady-pressure environment, they are not as leak-proof as laparoscopic trocars. Our newly developed “Leak Cutter,” now available in Japanese market as a reinforced anti-leak adapter for routine endoscopy, works perfect to prevent gas leakage during the case. The device has a Luer lock-type stopcock for emergent evacuation in case of over-insufflation. This stopcock can also be used as an insufflation inlet in future pure NOTES, where trans-abdominal insufflation via laparoscopic trocar will no longer be available.
The intra-abdominal irrigation via current flexible endoscope is feasible; however, it is technically demanding due to its one-direction spray from the tip of the endoscope. The use of sterile saline solution via built-in air/water channel requires specific and cumbersome preparation and setting. The suction from the tip of the endoscope is further challenging, since conventional technique requires “diving” of the endoscope beneath the fluid. While diving the endoscope, the visualization is temporally lost. This is acceptable in the gut lumen where no other organs exist; however, this is not acceptable in the abdominal cavity where blind mis-suction may lead to serious organ damage. Our new product, Endoshower, is one of the solutions. This device, 2.6 mm in outer diameter, has 24 side holes of 0.4 mm in size at its tip. With this device, sterile irrigation and safe suction under endoscopic visual control were feasible in the present case.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [41.0, 'kg'], 'height': [155.0, 'cm']}",17.06556,16.21228,17.91884,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 41.0 kg. The patient's bmi is therefore 41.0 kg / (1.55 m * 1.55 m) = 17.06556 kg/m^2."
2509,6,Body Mass Index (BMI),physical,decimal,pmc-5510143-1,Extracted,"A 53-year-old male patient (75kg, 172cm) received general anesthesia (GA) for retinal detachment surgery. The patient had no notable medical history other than diabetes, and his preoperative test findings were all within the normal range. GA was induced with propofol 120mg, vecuronium 8mg, and glycopyrolate 0.2mg and the patient was mask-ventilated for 3 minutes with 100% oxygen and 7.0 Vol% Sevoflurane. There were no particular difficulties in maintaining airway via a mask. After additionally administering 1 mg of alfentanyl, the endotracheal intubation was performed with a Macintosh size 3 laryngoscope blade. The Cormack-Lehane grade 1 view was obtained and patient was intubated using 7.5-mm-ID endotracheal tube at the first attempt. The tube was fixed at about 23 cm to right lower lip.
The anesthesia was maintained with 1.5 L/min of oxygen, 1.5 L/min of nitrogen, sevoflurane MAC 1.0-1.2, and there were no noticeable changes in the patient’s vital signs during the surgery. After the surgery was completed, the patient was extubated upon confirmation of recovery of spontaneous breathing (TOF ratio >0.9). However, as the airway was obstructed immediately after the extubation, we inserted an oral airway by fixing the mask with triple airway maneuver. Soon after, the obstruction disappeared naturally, and breathing was recovered.
It took less than 2 minutes for natural recovery, and the SpO2 was maintained at 100%. The patient did not show any abnormal symptoms and was moved to the recovery room. The total length of anesthesia was 120 minutes.
In the recovery room, the patient only had minor pain in the surgical area. The following morning, he showed dysarthria and complained of difficulty in moving his tongue. When he showed his tongue, a leftward deviation was clearly observed (). However, there were no signs of intrinsic muscle atrophy or fasciculation. Moreover, there were no other symptoms of cranial nerve palsy, such as ageusia, facial palsy, reduced facial sensation, loss of gag reflex, and uvular deviation. We referred the patient to the neurology department under a suspicion of left hypoglossal nerve palsy. Although we did not perform facial CT, the neurology department recommended outpatient follow-up if no additional neurological symptoms were present, and the patient was discharged two days after the surgery. At the 1 week postoperative follow-up, the patient pointed out his slurred speech has slightly improved, although the leftward deviation of the tongue was still present. At the 4 weeks follow-up, the patient showed complete recovery.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [172.0, 'cm'], 'weight': [75.0, 'kg']}",25.35154,24.08396,26.61912,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 172.0 cm, which is 172.0 cm * 1 m / 100 cm = 1.72 m. The patient's weight is 75.0 kg. The patient's bmi is therefore 75.0 kg / (1.72 m * 1.72 m) = 25.35154 kg/m^2."
2510,6,Body Mass Index (BMI),physical,decimal,pmc-8504087-1,Extracted,"A 19-month-old Syrian boy was referred to our clinic for steatorrhea, vomiting, and abdominal distension. He was born a full-term, normal pregnancy without any complications after birth. The birth weight was 4 kg. The newborn screening test was normal. Since early infancy, he suffered from feeding intolerance and diarrhea described 5 times per day; oily, bulky, and foul-smelling without vomiting or bilious emesis. He was on breast and bottle feeding. By the age of 6 months, there was an obvious failure to weight gain and the family started seeking medical advice. Investigations were performed which excluded primary cystic fibrosis, alpha 1 antitrypsin, Metabolic disease (lipid metabolism disease), thyroid diseases, adrenal insufficiency, diabetes mellitus, and celiac disease. There were fatty drops in the stool examination. A diagnosis of non-specific malabsorption was made and the patient was treated with multivitamins without any improvement in general condition. The family started feeding him PediaSure® formula milk - only by chance- from around 10 months of age with partial improvement in his symptoms and observed weight gain. His development was normal for his age. The child underwent all the compulsory immunizations for his age. There was no relationship between the parents and the family history was noncontributory.
On physical examination, his body weight was 9 kg (− 3 SD), the length was 75 cm (− 3 SD), he was vitally stable and generally well. The abdomen was distended but soft, with no masses or organomegaly. The neurological assessment was normal. The patient underwent multiple investigations. Complete blood count (CBC), C- reactive protein (CRP), blood film, blood gases, renal and liver function, electrolytes, glucose, bilirubin, ammonia, amylase, lipase, and urine were normal (Table ). Stool microscopy revealed fat globules. Abdominal ultrasound showed revealed intestinal wall thickening with normal findings (Liver steatosis was not observed). An ophthalmologic (funduscopic examination), cardiac assessment (echocardiogram) was normal. We performed an Esophagogastroduodenoscopy (EGD) that showed a milky white “snow-storm” appearance of the duodenal mucosa (Fig. ) and the histological biopsies from the duodenum showed fat-laden vacuolization of enterocytes without villous atrophy (Fig. a, b). That suggested lipid trafficking disorder. The Differential Diagnosis included abetalipoproteinemia (ABL), hypobetalipoproteinemia (HBL), or CRD. Therefore, more specialized additional investigations were performed including total cholesterol (TC), Low-Density lipoprotein cholesterol (LDL-C), and total lipid which were markedly reduced; high-Density lipoprotein cholesterol (HDL-C) was borderline low with normal very-low-density lipoprotein (VLDL) and Triglycerides (TG). Total Creatine kinase (CK) was elevated. Vitamin A, D levels were borderline low with low vitamin E levels (Table ). Lipoprotein electrophoresis of postprandial plasma did not show the presence of chylomicrons. Immunoblot testing showed a decrease in apolipoprotein A1 and apolipoprotein B.
The clinical and laboratory findings were more consistent with CRD. A blood sample for genetic analysis in directional direct DNA sequencing (AB 3730 DNA analyses equipped with seascape software) of SARB coding exons and exonic-intronic junctions from genomic DNA was obtained. Genotyping identified a homozygous SAR1B gene variant as the deletion of one of the two repeated Glutamine in position 113 or 114. It was the first description of this variant in the fourth helix of SAR1B protein (NM_0161032.: c.[del340-342]; [del340-342], p. [Glu114del]; [Glu114del]). His parents were heterozygous for the same variant (NM_0161032.: c.[del340-342]; [=], p. [Glu114del]; [=]).
The patient was started on the restriction of dietary fats, hydrolyzed formula with a higher medium-chain triglyceride content, some vegetable oils (sun-seed, olive oil, almond oil) in his daily diet in addition to fat-soluble vitamin supplementation (hydrosoluble vitamin E 50 UI/kg/d; vitamin A 15,000 IU/d; vitamin K 15 mg/wk.; vitamin D 1000 UI/kg/d).
During follow-up, the child showed catch-up growth in weight–height and a clinical examination were unremarkable with normal laboratory findings (Table ) (Fig. ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [9.0, 'kg'], 'height': [75.0, 'cm']}",16,15.2,16.8,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 75.0 cm, which is 75.0 cm * 1 m / 100 cm = 0.75 m. The patient's weight is 9.0 kg. The patient's bmi is therefore 9.0 kg / (0.75 m * 0.75 m) = 16.0 kg/m^2."
2511,6,Body Mass Index (BMI),physical,decimal,pmc-3510931-1,Extracted,"A 22-year-old female presented to the endocrinology unit with complaints of irregular periods since menarche and hyperpigmentation of face and neck for the past 5 years. There had been acneform eruptions on the face since the last 3 years, but she denied any hirsuitism. She had noticed changes in her physical appearance, with face and neck getting fuller and muscles of hands and legs getting more prominent.There was no history of diabetes mellitus, PCOS or similar physical appearances in any of the family members.
On examination,she was of average built with height – 160.8 cm and weight – 52.8 kg, and BP – 110/60 mmHg. Hypertrophy of calves, biceps, and triceps was noted. There were changes in the fat distribution pattern in her body, with loss of subcutaneous fat in the abdominal and gluteal region and accumulation of fat in the face,neck, and in the paraumbilacal region.Acanthosis nigricans was present on the face (tip of the nose was spared), neck, axilla, and pubic region. Hypertrophy of labia was noted. Asymmetry in her breast size was present, with left being bigger in size than the right one. Acneform eruptions were present on the face with minimal hair on the chin.There were no significant findings on cardiovascular/CNS and chest examination.
Lab evaluation revealed normal hemogram, liver function, and kidney function tests. Urine examination was normal.There was no cardiac abnormality evident on echocardiography. Response to glucose tolerance test was impaired (0 hr. - 97 mg/dl, 1 hr. – 197 mg/dl, 2 hr. –157 mg/dl.) and basal and post-glucose insulin levels were high (0 hr – 40.05 μIu/ml, 1 hr. – 882.67 μIu/ml and 2 hr.- 281.94 μIu/ml), respectively. High triglycerides and low HDL levels were noted (T. Cholesterol: 168 mg/ dl, HDL – 29 mg/dl, LDL – 96 mg/dl, VLDL - 43 mg/dl, and triglycerides:213 mg/dl). Hormonal profile revealed normal TFT, FSH, and LH values (T3 - 3.66 pg/ml, T4 - 1.10 ng/ dl, TSH - 4.10mIU/L, LH - 5.22 mIU/ml, FSH - 7.43 mIU/ml, respectively). Total testosterone was 0.658 nmol/L (0.198 - 2.67 nmol/L), free testosterone was 0.649 pg/ml(0.4 - 4.18 pg/ml), DHEAS - 0.72 μg/ml (0.48 - 2.75 μg/ml), and 17 OHP - 1.44 ng/ ml (0.2 - 1.3 ng/ ml) levels were normal.
Ultrasound abdomen and adnexae revealed- hepatomegaly with diffuse fatty infiltration, and both the ovaries revealed multiple small follicles in peripheral distribution with increase in stromal echogenicity suggestive of polycystic pattern of ovaries (right ovary measured – 3.2 × 1.9 × 1.7 cms with a vol of 5.5 cc. and left ovary measured- 2.7 × 1.8 × 1.5 cms with a volume of 4.1 cc) []. Non-enhanced computed tomographic scan of the neck, chest, and abdomen revealed excessive accumulation of face and neck with marked reduction of fat in the chest and abdomen [Figures and ]. There was a loss of fat from the breasts with preserved muscle bulk with fibroglandular tissue within the breasts. Peritoneal fat was preserved, and excessive deposition of fat was also noted in the perineal region and labia majora. These findings were suggestive of partial lipodystrophy associated with polycystic ovarian disease.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [160.8, 'cm'], 'weight': [52.8, 'kg']}",20.42029,19.39928,21.4413,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.8 cm, which is 160.8 cm * 1 m / 100 cm = 1.608 m. The patient's weight is 52.8 kg. The patient's bmi is therefore 52.8 kg / (1.608 m * 1.608 m) = 20.42029 kg/m^2."
2512,6,Body Mass Index (BMI),physical,decimal,pmc-8462229-1,Extracted,"A healthy 54-year-old man (height, 175 cm; weight, 73 kg) was referred to the anesthesiology department for a movement disorder similar to myoclonus following spinal anesthesia.
The patient underwent a metal implant removal surgery after surgical correction for bilateral cavovarus feet. The operation was limited to the area below the knee. The patient had received spinal anesthesia without premedication. A lumbar puncture was performed at the L3-4 level using a 25-gauge Quincke needle with the patient in the right lateral position, and 3 mL of 0.5% hyperbaric bupivacaine was administered. Loss of sensation to cold occurred below the T8 sensory dermatome. A complete inability to raise the legs straight (Bromage grade 3) was confirmed. Dexmedetomidine was administered for sedation—75 μg of dexmedetomidine was injected intravenously at the antecubital fossa for 10 min, followed by continuous infusion at a constant rate (1.0 μg/kg/h) using an infusion pump. The infusion was stopped 30 min before the end of the surgery. The operation proceeded uneventfully and lasted 225 min. The patient was then transferred to the general ward after observation in the postoperative care unit for 30 min. Approximately 7 h later, after hyperbaric bupivacaine administration, the patient involuntarily lifted the left lower leg (Figure ). Every two minutes, the patient’s left lower extremity involuntarily raised with hip flexion (Video). This symptom occurred without prior stimulation.
The patient had no significant medical history, including neurologic disorders, seizures, or spinal or brain tumors. There was no glucose intolerance in the preoperative evaluation, as verified by an HbA1c of 5.66%.
The patient had no remarkable personal and family history.
The patient was fully conscious and oriented, and his vital signs were normal. Sensations were same in both the extremities upon touching with alcohol-soaked cotton balls. When asked to lift his legs against gravity, he could lift both the legs voluntary without any problems. The dorsalis pedis and posterior tibial arterial pulses were good in both feet. The anal sphincter had normal strength, and the patient did not complain of headache or dizziness.
Postoperative serum electrolyte panel, complete blood count, and renal and hepatic function tests performed on the day of the surgery revealed normal results (Table ).
Plain radiographs of both feet were acquired before and after surgery, and no abnormalities were identified (Figure ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [175.0, 'cm'], 'weight': [73.0, 'kg']}",23.83673,22.64489,25.02857,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 175.0 cm, which is 175.0 cm * 1 m / 100 cm = 1.75 m. The patient's weight is 73.0 kg. The patient's bmi is therefore 73.0 kg / (1.75 m * 1.75 m) = 23.83673 kg/m^2."
2513,6,Body Mass Index (BMI),physical,decimal,pmc-6658382-1,Extracted,"A 77-year-old Chinese woman visited our hospital with epigastric discomfort for more than 4 years and worsened for 1 month.
Her medical history was notable for chronic atrophic gastritis.
She had a longstanding history of chronic atrophic gastritis in January 2014 with gastroscopy. According to the Kimura/Takemoto classification[], atrophy of the gastric mucosa was classified as C-2. She had received recommended dose of H. pylori eradication therapy twice, once 7 d for omeprazole + amoxicillin + clarithromycin and once 14 d for pantoprazole + bismuthate + tetracycline + metronidazole. She was followed up with annual gastroscopy and had not taken any PPIs since then. In addition, she had a history of myoma of uterus for more than 40 years, without operation.
On physical examination upon admission, she was 1.54 meters in height and 60 kilogram in weight. She had a blood pressure of 117/68 mmHg with pulse rate of 65 beats per minute. Her jugular venous pressure was not elevated. She had clear lungs and normal heart sounds with no murmurs or gallops on auscultation. There were no other pathognomonic signs during physical examination, except for slight tenderness in the upper abdomen.
After admission, the patient was thoroughly evaluated with routine blood tests, routine urine tests, routine fecal tests and occult blood test, blood biochemistry, and infection indexes. No significant abnormal laboratory results were recorded in this patient.
Gastroscopy revealed a 6 mm submucosal tumor (SMT)-like slightly elevated lesion in the anterior wall of the lower part of the gastric body, which had faint yellow discoloration (Figure ). Atrophy of the gastric mucosa was classified as C-2, yet the local background mucosa of the lesion showed no apparent atrophy, after eradication of H. pylori. No fundus gland polyp (FGP) was found in other sections of the stomach.
A biopsy of the SMT-like lesion was obtained, and histopathological findings showed numerous cells with basophilic cytoplasm and mildly atypical nuclei-like chief cells of the fundic gland, which were arranged in irregular branching and anastomosing tubules in a layer of the lamina propria mucosae (Figure ).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [1.54, 'm'], 'weight': [60.0, 'kg']}",25.29938,24.03441,26.56435,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.54 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.54 m * 1.54 m) = 25.29938 kg/m^2."
2514,6,Body Mass Index (BMI),physical,decimal,pmc-4156988-1,Extracted,"A previously healthy 12-year-old girl presented with worsening headaches of six-month duration, described as diffuse, throbbing, and intense, occurring daily and lasting up to eight hours or more. They were not associated with time of day, posture, activity, and prodromal visual, auditory, or gustatory symptoms, and there were no associated neurologic abnormalities. Headaches were occasionally accompanied by lightheadedness, nausea, palpitations, and flushing. She had lost roughly 25% of her preillness body weight, had been fatigued and “warm,” and noted polydipsia and polyuria for several days prior to admission. The patient's mother, an experienced cardiology nurse, reported that the patient's blood pressure had been as high as 200/160 mmHg. The patient had a history of prematurity, being born at 27-week gestation and requiring intubation and mechanical ventilation for prematurity-induced respiratory distress. However, aside from exercise-induced reactive airways disease, she had no other ongoing medical problems. The patient had normal growth and development and was doing well in school. Family history was noncontributory for oncologic or endocrine diseases.
At her primary care physician's office, the patient's blood pressure was 205/160 mmHg, and the heart rate was 120 beats per minute. An abdominal CT scan, ordered to investigate the possibility of a neuroendocrine tumor, revealed a large right-sided suprarenal mass, which prompted a referral to our institution for further workup and management. The patient was referred to our service with the presumptive diagnosis of malignant hypertension secondary to a catecholamine-secreting pheochromocytoma (PCC) of the right adrenal gland. On arrival, the patient was alert, well-appearing, and in no distress. She was well-developed and nondysmorphic. The height was 152 cm (25th percentile for age) and weight was 54 kg (75th percentile for age). She was afebrile, the respiratory rate was 20 breaths per minute, the heart rate was 124 beats per minute and regular, and the blood pressure was 157/107 mmHg (the 95th percentile for a girl her age and height is 123/80 mmHg). Oxygen saturation was >95% on room air. She was mildly diaphoretic but had normal skin turgor and perfusion. Capillary refill was brisk and she was slightly flushed in her cheeks. Skin examination revealed no rashes, abnormal lesions, growths, café-au-lait spots, or axillary freckling. Cardiac examination revealed a hyperdynamic precordium and a grade II/VI systolic murmur best heard at the upper left sternal border. Peripheral pulses were 2+ throughout and all extremities were warm and well-perfused. The abdomen was soft, nontender, and nondistended without palpable masses or organomegaly. The patient was alert and oriented to person, place, and time. The neurologic and musculoskeletal exams were nonfocal.
The patient's CBC, differential, peripheral blood smear, electrolytes, and liver function tests were all normal except for serum glucose of 125 mg/dL (normal 60–99 mg/dL). Serum uric acid was mildly elevated at 7.0 mg/dL (2.3–5.9 mg/dL), and serum lactate dehydrogenase (LDH) fell within the normal range (201 U/L; normal 110–293 U/L). Ionized calcium, serum cortisol, and thyroid stimulating hormone (TSH) were normal. Serum and urine catecholamines were markedly abnormal, especially plasma norepinephrine and urine normetanephrine (). Radiographic imaging confirmed a large right-sided suprarenal mass (). The patient was diagnosed with malignant hypertension secondary to PCC. She was placed on telemetry and was started on intravenous fluids and α-blockade with phenoxybenzamine; headaches, flushing, diaphoresis, and nausea resolved within 24 hours. The patient was treated with progressive α and β catecholamine blockade (); the patient's medication history and vital findings are summarized (). The tumor was completely resected on the fifteenth day of catecholamine blockade. The patient tolerated anesthesia well, and the blood pressure and heart rate remained stable. The patient's postoperative course was complicated by rebound hypotension requiring robust fluid support which led to pulmonary edema and respiratory failure requiring mechanical ventilation and pressor support. The patient recovered and was discharged 10 days after tumor resection. Histologic examination of the resected tumor confirmed that it was a PCC ().
Currently, the patient is well now nine months after diagnosis. She is symptom-free and has normal blood pressure and plasma catecholamines. Because of the strong association between PCC and inherited cancer syndromes, the patient was evaluated for known genetic mutations associated with PCC and PGL (paraganglioma). The NF1, RET, TMEM127, VHL, MAX, and succinate dehydrogenase (SDHx) genes were sequenced, revealing a p.R27∗ point mutation in SDHB (c.79C>T) resulting in the change of a cytosine to a thymine and creating a premature stop codon in exon 2. This mutation, known to predispose to PGLs and PCCs, also increases risk for renal cell carcinoma [–].
Because of the risk of relapse and/or development of a secondary malignancy, we have educated the patient and her family about signs/symptoms that might indicate disease recurrence (e.g., headache, hypertension, flushing, diaphoresis, etc.). Following National Comprehensive Cancer Network (NCCN) guidelines, our surveillance plan includes a careful history and physical, blood pressure measurement, and urine and plasma catecholamine assessment every three months through the first year and every 6–12 months thereafter through 10 years. We will incorporate abdominal ultrasonography and/or MRI at her clinic visits as well as yearly FDG-PET scans. Critically, we have referred her immediate family for formal genetic evaluation to screen for SDHB mutations and to provide genetic counseling regarding the implications of the patient's identified cancer syndrome.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [152.0, 'cm'], 'weight': [54.0, 'kg']}",23.37258,22.20395,24.54121,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 152.0 cm, which is 152.0 cm * 1 m / 100 cm = 1.52 m. The patient's weight is 54.0 kg. The patient's bmi is therefore 54.0 kg / (1.52 m * 1.52 m) = 23.37258 kg/m^2."
2515,6,Body Mass Index (BMI),physical,decimal,pmc-4472263-1,Extracted,"In March 2010 a 24 year old Caucasian man with marphanoid habitus (height: 175 cm; weight: 65 Kg) was referred to us for severe hypertension that was resistant to beta blockers, angiotensin converting enzyme (ACE) inhibitors, and diuretics. Four years earlier he had undergone total thyroidectomy with lymphadenectomy due to MTC (pT4N+; stage III UICC 2009). The preoperative diagnostic workup had excluded PHEO, and his family history was negative for MEN2B-related tumors. Genetic testing for germline mutations in RET proto-oncogene was not done. However, after his thyroid surgery a progressive increase of the urinary metanephrines and catecholamines was noted, with absence of abnormal findings at the magnetic resonance imaging (MRI) and metaiodobenzylguanidine (MIBG) scan.
At our clinical examination, a severe systo-diastolic hypertension (220/140 mmHg) was observed, and mucosal neuromas of the tongue were found. Laboratory findings included severe hypokaliemia (potassium 2.5 mEq/L), hyperreninemia and mild hyperaldosteronism. Urinary catecholamines were also increased, as well as urinary metanephrines and vanil-mandelic acid. Inappropriate cortisol secretion was ruled out on the basis of the presence of normal serum and urinary free cortisol and detectable adrenocorticotropic hormone (ACTH) levels (Table ). An ultrasound of the kidneys revealed a mass of approximately 2 cm at the right kidney with an increased artery resistance (0.88; normal value < 0.7). Furthermore, an enlargement of both adrenal glands was detected.
The genetic test for RET germline mutations showed the substitution of methionine for threonine in exon 16 at codon 918 (p.M918T) which was not present in other family members (father, mother and sister). A recurrence of MTC was excluded through assessment of serum markers, showing undetectable levels of serum calcitonin and normal carcinoembryonic antigen (CEA) levels, and an ultrasound of the neck which was negative. Replacement therapy with levothyroxine (150 mcg/day) appeared to be adequate and post-surgical hypoparathyroidism was well controlled with calcitriol (0.5 mcg/day).
An abdominal MRI confirmed the presence of adrenal bilateral hyperplasia with multiple adrenal masses (16 and 18 mm in the right gland, and 10 and 15 mm in the left gland), and the right kidney nodular lesion of 20 x 20 mm, hyperintensive in T2-weighted sequences. MIBG scintigraphy showed bilateral adrenal uptake, strongly suggestive for bilateral PHEO. Thus, the patient started anti-hypertensive therapy with phenoxybenzamine 20 mg four-times daily, nifedipine slow release 30 mg twice-daily, and atenolol 50 mg once-daily. Blood pressure control eventually improved. An ecocardiography showed dilated cardiomyopathy and moderate systolic dysfunction (ejection fraction 46 %). One month later the patient underwent bilateral adrenalectomy and right nephrectomy. No hypertensive crisis occurred during the surgery. The tumors were soft brown-red well-circumscribed masses without cystic degeneration. Histology of the adrenal glands confirmed the presence of bilateral and multifocal adrenal PHEO. No vascular or capsular invasion was noted; mitotic figures were less than 3/10 high power field and no atypical mitoses were present. The Ki 67 index was 2 % and immunoistrochemistry was positive for chromogranin A and synaptophysin. The histology of the right kidney mass revealed a capsulated neoplasm with nests and diffused sheets of tumor cells interrupted by abundant vascularity in the form of capillary channels and sinusoids, which were suggestive for reninoma.
After surgery, glucocorticoid replacement therapy with hydrocortisone was immediately started together with adequate hydration. Anti-hypertensive therapy was withdrawn and blood pressure was low to normal. Laboratory evaluation showed a sudden reduction of urinary metanephrines and catecholamines. Serum ACTH levels increased accordingly to post-surgical hypoadrenalism while serum cortisol was undetectable, but renin levels were normal-low (10 μUI/ml), in the absence of mineralocorticoid supplementation. Currently, 3 years after surgery, the patient is tumor-free. During this follow-up, the patient has been treated with replacement therapy comprised of hydrocortisone 30 mg, levothyroxine 150 mcg, and calcitriol 0.5 mcg.
Because of the persistence of normal renin values and serum electrolytes (Table ) and normal blood pressure values mineralocorticoid substitutive therapy was not proposed. Surprisingly, aldosterone serum levels were detectable in spite of bilateral adrenalectomy (Table ). MRI evaluation performed during follow-up failed to reveal adrenal remnants which could justify these clinical and biochemical findings. Moreover, undetectable serum cortisol performed about 18 h after the last hydrocortisone administration, was extremely suggestive for the absence of adrenal remnants or for the presence of ectopic functioning adrenal tissue. To further investigate this unusual feature, we hypothesized that it could be due to a dysregulation of RAA axis. After obtaining the informed consent, we searched for ACE polymorphisms. Genetic test revealed ACE I/D polymorphism.
After obtaining informed consent, genomic DNA was isolated from peripheral blood by a manual method (Roche Diagnostics, Basel, Switzerland, ), while spectral analysis was performed spectrophotometrically in order to determine DNA concentration and purity (NanoPhotometer™, Implen, München Germany, ). Mutation analysis of the RET gene was performed by sequencing of coding region and exon-intron boundaries of the exons 2, 5, 8, 10, 11, 13–16. Primers used and the respective annealing temperatures are reported in Table . PCR products were sequenced using the Big Dye Terminator v1.1 Cycle Sequencing kit (Applied Biosystems, Foster City, CA, USA, ) in an automated sequencer ABI Prism 3500 Genetic Analyzer (Applied Biosystems).
Finally, using the SeqScape® Software v2.5, sequences were aligned to the reference sequence NG_007489.1.
For detecting ACE I/D polymorphism we followed the molecular method reported in literature [].",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [175.0, 'cm'], 'weight': [65.0, 'kg']}",21.22449,20.16327,22.28571,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 175.0 cm, which is 175.0 cm * 1 m / 100 cm = 1.75 m. The patient's weight is 65.0 kg. The patient's bmi is therefore 65.0 kg / (1.75 m * 1.75 m) = 21.22449 kg/m^2."
2516,6,Body Mass Index (BMI),physical,decimal,pmc-7815663-1,Extracted,"A 30-year-old female (weight 65 kg and height 158 cm) came to our emergency department with injury to the left foot, due to fall from the stool of height approximately 2 feet. She lost her balance while arranging things in overhead cupboards when she was standing on a stool with heels elevated and landed on the floor with plantar flexion at ankle joint and abduction at midfoot. She presented to us immediately after trauma with pain and swelling over the midfoot region without any external wounds. On clinical examination, there was severe tenderness over mid-foot, and abnormal bony prominence was present over the dorsomedial aspect of the left foot, without any distal neurovascular deficit. Midfoot joint movements were severely restricted, making the patient unable to walk. The radiographs of the left foot were done in the form of anteroposterior, lateral, and obliques views. Radiographs revealed naviculocuneiform joint dislocation and fracture of anterior process of the calcaneus with calcaneocuboid joint dislocation ().
Closed reduction under anesthesia was attempted by traction and manipulation of midfoot, but it was not successful. Hence, open reduction and internal fixation with K-wire was planned. Calcaneocuboid and naviculocuneiform joints were approached with the help of two mini-open incisions 3 cm (dorsolateral) and 4 cm (dorsomedial), respectively, over midfoot. There was a disruption of interosseous ligament and medial naviculocuneiform joint capsule. The soft tissues entrapped between calcaneocuboid and naviculocuneiform joints were removed. Using axial traction in line with 1st metatarsal and adduction of midfoot, navicular was reduced. After confirming congruent reduction with the help of an image intensifier, two parallel, 2 mm K-wires were passed through medial cuneiform and navicular into the talus. A transverse Kwire was passed through medial cuneiform into middle cuneiform to give complete stability to the medial column. For the lateral column, a 2 mm K-wire was passed from cuboid to calcaneal head. Postoperatively, ankle and foot were immobilized in the below-knee slab posteriorly ().
Sutures were removed after 2 weeks and below knee cast applied with strict non-weight-bearing. K-wires and below-knee cast were removed after 8 weeks and gradual weight-bearing as per tolerance started. At the end of 5 months, there was only a mild restriction of midfoot range of movements (adduction 5° and abduction 5°) with American Orthopaedic Foot and Ankle Society (AOFAS) midfoot score of 85. At 24-month follow-up, she had a full range of midfoot movements and complained of mild pain only after fast walking and running with AOFAS midfoot score of 95 ().",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [65.0, 'kg'], 'height': [158.0, 'cm']}",26.03749,24.73562,27.33936,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 158.0 cm, which is 158.0 cm * 1 m / 100 cm = 1.58 m. The patient's weight is 65.0 kg. The patient's bmi is therefore 65.0 kg / (1.58 m * 1.58 m) = 26.03749 kg/m^2."
2517,6,Body Mass Index (BMI),physical,decimal,pmc-6389502-1,Extracted,"The patient was a 34-year-old Japanese man, whose family history included a father with hypertension, and a mother that suffered a subarachnoid hemorrhage, but which did not include either a consanguineous marriage or any incidence of renal cysts. At the age of 31, the patient presented with mild albuminuria, and a serum creatinine (Cr) level of 2.98 mg/dL. At the age of 34, the patient was admitted to hospital with a creatinine level of 8.2 mg/dL.
Upon admission, the patient's height, weight, and blood pressure were 179 cm, 58 kg, and 126/80 mm Hg, respectively. The patient exhibited anemia (Hb 8.2 g/dL), azotemia (Cr 8.38 mg/dL), hyperphosphatemia, metabolic acidosis, and secondary hyperparathyroidism; thus, he was diagnosed with ESRD. An abdominal ultrasonography revealed that, although the size of both kidneys appeared to be normal, the patient's renal parenchyma showed increased brightness. We performed a percutaneous renal biopsy; histologically, six of 16 glomeruli displayed global sclerosis, along with mild cellular infiltration, conspicuous interstitial fibrosis, renal tubular atrophy, and cystoid irregular dilation (Figure ), suggesting an NPHP diagnosis. We performed targeted sequencing using a next-generation sequencer, with the approval by the research ethics committee of Tokyo Medical and Dental University in accordance with the Declaration of Helsinki and the patient's written informed consent. A homozygous full gene deletion of NPHP1 (NM_000272.3:g110879716-110962709) was resultantly identified, as well as heterozygous substitutions in PKD1 (NM_0001009944.2:c.6395T>G(p.Phe2132Cys)) (Figure ), BBS1 (NM_024649.4:c.908T>C(p.Val303Ala)), and INPP5E (NM_019892.4:c.1652C>T(p.Thr551Met)).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [179.0, 'cm'], 'weight': [58.0, 'kg']}",18.10181,17.19672,19.0069,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 179.0 cm, which is 179.0 cm * 1 m / 100 cm = 1.79 m. The patient's weight is 58.0 kg. The patient's bmi is therefore 58.0 kg / (1.79 m * 1.79 m) = 18.10181 kg/m^2."
2518,6,Body Mass Index (BMI),physical,decimal,pmc-3405157-1,Extracted,"A 13-year-old previously healthy girl presented to the emergency department with a right supraclavicular mass incidentally found one month prior to her arrival. The aspiration biopsy showed that it consisted of degenerative squamous cells with necrosis. At that time, she had a sore throat and felt feverish. The mass at the right supraclavicular area got bigger and tender three days prior to her arrival at Samsung Medical Center. An initial white blood cell (WBC) checked in the other hospital was 199,200×103/uL, and blasts were observed on the peripheral blood smear. An initial diagnostic work up for leukemia was started. She had no significant cardiopulmonary symptoms on admission.
There was no history of medical illness. Her birth history was unremarkable. Her family consists of her father, mother, older sister, and her twin brother. There was no family history of leukemia, congenital heart disease, or cancer.
The patient's height was 160.3 cm (50 to 75th percentile) and weight was 56.9 kg (50 to 75th percentile). On physical examination, her temperature was 37.9℃, heart rate was 115 beats/min, and respirations were 20/min. Blood pressure was 110/75 mmHg. She was noted to be ambulatory without assistance and in no apparent distress. She was awake, alert, and speaking in full sentences.
There was a palpable lymph node at the right supraclavicular area; it was 1×2 cm in size with tenderness upon palpation and movable. It had no redness and was not warm to the touch. There was another small palpable lymph node. Cardiac examination revealed regular tachycardia and a nondisplaced point of maximal impulse. There were no murmurs, rubs, gallops, or jugular venous distension. Chest wall movement was symmetrical, with clear and equal breath sounds. There were no motor or sensory deficits. She exhibited good coordination. The remainder of the physical examination was unremarkable.
Bone marrow analysis showed blasts of 30%, which was compatible with acute leukemia (, ). The chest radiograph was normal, and the electrocardiogram showed normal sinus rhythm. Two-dimensional echocardiography before chemotherapy revealed a 16×18×18 mm sized cardiac mass that was highly mobile and attached to the right ventricular free wall and chordae of the tricuspid valve. Its shape was bizarre, with heterogeneous echogenecity (). The mass looked like an avascular mass on cardiac magnetic resonance imaging (). RV thrombus, vegetation, or metastasis were considered as possible etiologies. To rule out cardiac vegetation and diagnose infective endocarditis, blood cultures were done, but no organism was isolated. A blood test to rule out thromboembolism was conducted: D-dimer was 60 ug/mL, and another coagulation test, International Normalized Ratio, was 1.52 (reference range, 0.9 to 1.1). In addition, fibrinogen was 87 mg/dL (reference range, 182 to 380) and antithrombin III activity was 67% (reference range, 83 to 123). There was no bleeding tendency.
The patient received intravenous antibiotics and antifungal agents in order to treat possible infective endocarditis with vegetation. Heparinization was also started for possible thrombus. Treatment for acute leukemia including intravenous hydration and alkalization, plasmapheresis, and low dose oral prednisolone was started along with other treatments. On the following day, she developed sudden chest pain and dyspnea, which turned out to be caused by pulmonary embolism, which was discovered by chest computed tomography (). Despite heparinization and antibiotics, the RV mass size appeared to grow, as shown by a follow-up 2-dimentional echocardiogram. She was transferred to the pediatric intensive care unit because of progressive dyspnea. Sudden hemodynamic collapse developed the next morning. Extracorporeal membrane oxygenation (ECMO) support and emergency surgery was performed due to acute pulmonary embolism and for removal of the cardiac mass.
On surgical findings, the mass was fragile and easily crumbled and attached to a dysplastic tricuspid valve (). Also, irregular shaped masses were found in both pulmonary arteries. Pathology revealed that the cardiac mass and pulmonary artery mass consisted of an aggregation of small round necrotic cells that were compatible with leukemic cells (, ).
In spite of aggressive postoperative ECMO support, the patient died of disseminated intravascular coagulation and heart failure the day after surgery.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [160.3, 'cm'], 'weight': [56.9, 'kg']}",22.14345,21.03628,23.25062,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.3 cm, which is 160.3 cm * 1 m / 100 cm = 1.603 m. The patient's weight is 56.9 kg. The patient's bmi is therefore 56.9 kg / (1.603 m * 1.603 m) = 22.14345 kg/m^2."
2519,6,Body Mass Index (BMI),physical,decimal,pmc-8605939-1,Extracted,"An 83-year-old man with a past medical history of two myocardial infarctions, chronic obstructive pulmonary disease, and hyperlipidemia presented to the emergency room shortly before midnight with sharp chest pain, nausea, and dyspnea. The patient states he has had chest discomfort and food intolerance for the past week, but that his symptoms were far worse tonight. He notes no inciting event, recent trauma, or aggravating factors. On exam he appears uncomfortable, anxious, and is in a semi-tripod position. Vitals are pertinent for a heart rate of 144, systolic blood pressure in the 180 s, and oxygen saturation of 89% on 1L O2 via nasal cannula. Of note, the patient weighed 67.2 kg, and was 173 cm tall. Chart review showed that he had lost approximately 4 kg (last recorded weight in chart was 71.2 kg), since his last medical visit.
Primary survey was overall unremarkable. Airway was secure, patient’s breathing improved with 3 L oxygen, breath sounds were present and equal bilaterally, vascular access was obtained, and GCS was 15. Intravenous pain medication was given which improved the patient’s blood pressure to systolic 140 s. Given this patient’s overall clinical picture, the most pressing disease processes included myocardial infarction (given history of coronary artery disease and prior infarcts), aortic dissection (given symptoms, hypertension, and medical history), pneumothorax, pulmonary embolism (the previous two diagnoses given his chest pain and decreased O2 even on 1 L of oxygen), and cardiac wall rupture (given multiple prior MIs). Other considerations include congestive heart failure, hypertensive crisis, and an underlying infection.
Labs were drawn to include a CBC, renal panel, cardiac panel, lactate, and a type and cross. EKG was unremarkable. A chest X-ray was obtained which revealed a widened mediastinum (Fig. ).
The patient was stabilized, but the underlying cause of his symptoms had not yet been identified. His widened mediastinum is troubling, and further drives the differential. Aortic (dissection, aneurysm), cardiac (tamponade, wall rupture), and esophageal pathology (rupture versus other masses) now move to the top of the list of diagnoses. Labs continued to be pending. Given his now overall hemodynamically stable status and clinical improvement, the decision was made to obtain a CT chest/abdomen/pelvis which revealed the following (Fig. ).
Along with the CT scan; the initial set of labs resulted and were pertinent for leukocytosis (white blood cell count/WBC) of 19,000/mcL, creatinine of 1.4 mg/dL, lactate of 3.94 mmol/L, and troponin of 0.101 ng/mL. Although no official read of the images were immediately available, a preliminary read by the team was concerning for mega-esophagus versus a strangulated hiatal hernia. Treatment of the pathology to limit the degree of heart strain (increased troponin), ischemia (as evidenced by the WBC and lactate), and possibility for future perforation were now the primary goals. Night Hawk radiology was contacted for an emergent read, who stated that the images were consistent with a severely dilated esophagus. No pulmonary emboli were visualized, and no other acute abnormalities were reported.
The findings, treatment modalities, risks, and benefits were discussed in depth with the patient. Given his dilated esophagus which was severe enough to cause him chest pain, dyspnea, alter his vitals, elevate his WBC, elevate lactate levels, and cause heart strain. Esophagogastroduodenoscopy (EGD) with possible video-assisted thoracoscopic surgery (VATS), possible thoracotomy, possible laparoscopy, and possible laparotomy were recommended to the patient. The goal was for direct visualization of area, decompression, and repair of any defects. The patient was in full agreement with the plan, and was taken to the operating room shortly thereafter. In the mean time, given the location of the pathology and concern for developing septic picture, the patient was started on broad spectrum antibiotics and an antifungal.
On EGD, the patient’s esophageal distention was found to be from a large bezoar which spanned from the broncho-aortic region of the esophagus to his lower esophageal sphincter. The bezoar was a phytobezoar, with evidence of medication and food particles (meat, vegetables) incorporated into it. The esophageal tissue appeared tenuous and appeared to be the cause of the patient’s lab derangements (Fig. ).
The decompression was done carefully and meticulously by fragmenting the bezoar endoscopically using a snare device. About 2 h into the procedure, a repeat set of labs were drawn which showed significant improvement in his labs showing a WBC of now 7600/mcL (from 19,000/mcL), creatinine of 0.9 mg/dL (from 1.4 mg/dL), lactate of 0.86 mmol/L (from 3.94 mmol/L), and a troponin of 0.046 ng/mL (from 0.101 ng/mL). A discussion between the surgical team, anesthesia, and gastroenterology (via telephone) was done in the operating room for planning. Given his hemodynamic stability, improving lab values, and previous CT scan which showed no gross evidence of a leak, the decision was made to end the procedure for further resuscitation with plans to return to the OR for interval endoscopy to re-assess the esophagus. In the meantime, the patient was continued on broad spectrum antibiotics (to include antifungal coverage). He was kept Nil per os (NPO) and was admitted to the intensive care unit.
The patient remained hemodynamically normal and clinically stable throughout the night. The multi-disciplinary team determined the best course of action to be complete bezoar debridement, placement of NG tube, nutrition and medical optimization, workup for possible underlying esophageal pathology (to include completion EGD, manometry, and pH probe), and eventual endoscopic versus surgical management of determined condition. The above was again relayed to the patient and his family who fully supported the plan. The bezoar debridement was completed, and the esophagus was inspected for luminal integrity. An NG tube was able to be carefully placed under direct visualization.
The patient did well and was eventually able to be downgraded to the regular surgical floor. During his stay, a gastrostomy tube was obtained for feeding access and nutritional optimization. He would undergo several follow-up EGDs during his hospitalization to completely clear the bezoar and assess the esophageal lumen (Figs. and ). After discharge, the patient was further worked up and was found to have achalasia and esophagitis. Thorough workup includes a barium swallow study (patient’s barium swallow shown in Fig. ), EGD, manometry, pH study, and a chest CT (for, among other things, surgical planning). He was followed up in the outpatient setting for further management.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [173.0, 'cm'], 'weight': [67.2, 'kg']}",22.45314,21.33048,23.5758,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 173.0 cm, which is 173.0 cm * 1 m / 100 cm = 1.73 m. The patient's weight is 67.2 kg. The patient's bmi is therefore 67.2 kg / (1.73 m * 1.73 m) = 22.45314 kg/m^2."
2520,6,Body Mass Index (BMI),physical,decimal,pmc-4008446-1,Extracted,"A 48-year-old male finished Triple-Ironman distance in 41 hours and 18 minutes (11.4 km swimming, 540 km cycling, and 126 km running). At the time of the examinations, he had been practising his current diet of raw vegan diet for 6 years. Prior to this, the vegan athlete had been living as a vegan for 3 years and as a vegetarian for the previous 13 years.
All last competitions were performed only based on a raw diet. At the time of both examinations, the vegan athlete was 48 years of age and 1.80 metres in height. In the sporting season he was 79.7 kg in weight, with a body fat index of 12.9%; in the off-season he weighed 80.3 kg with a body fat index of 16.3%. Clinical examination showed a regular heart rhythm at 60 beats/min. Blood pressure was 115/70. The heart sounds were normal.
Prior to the spiroergometry, echocardiography was performed based on ASA criteria (1).
For comparison purposes, we refer to the values for 10 Ironman triathletes of similar age living on a mixed diet.
The results of the spiroergometry are shown in , those of echocardiography are in , and blood analysis findings are presented in . The athletes of the control group were aged 47.4 ± 5.2, weighed 76.2 ± 8.9 kg (with 13.4 ± 2.0% body fat), and were 1.816 metres ±6.6 cm in height. In the active phase the vegan athlete was training on average 18 hours per week, consisting of 2 hours of swimming, 11 hours of cycling, and 5 hours running. This involved covering distances of 5 km (swimming), 330 km (cycling) and 50 km (running). The athletes of the control group were training for a total of 15.9 ± 2.1 hours weekly, involving 2.5 ± 0.7 hours and 5.6 ± 1.5 km swimming, 8.6 ± 1.5 hours and 215.5 ± 53.0 km cycling, and 4.9 ± 0.7 hours and 55.2 ± 6.5 km running.
In terms of performance diagnostics, the vegan athlete showed comparable VO2max, VO2 at VAT, and %VO2max at VAT values as compared with the control group (statements regarding significant differences are not possible). VO2 and %VO2max at RCP were somewhat higher for the vegan athlete. The maximum ergometric performance is higher for the vegan athlete in absolute terms but not relative to the body weight. At RCP the ergometric performance of the vegan athlete is somewhat higher than that of the control group. The vegan athlete had lower pulse rates at rest, at VAT, at RCP, and at the endurance limit. In comparison with the off-season, in the active season the vegan athlete had a higher maximum ergometric performance, VO2, and %VO2max, as well as cardiac frequency at RCP.
In morphological terms, the vegan athlete showed a greater left ventricular end diastolic diameter, with consecutively higher end diastolic volume and stroke volume. The systolic and diastolic functions seem to be similar for the vegan athlete and the control group.
Besides a mild thrombopenia, slightly higher CK-NAC levels in the active season and a slight drop of free testosterone (in both examinations) all remaining values were within normal ranges.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [1.8, 'm'], 'weight': [80.3, 'kg']}",24.78395,23.54475,26.02315,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.8 m. The patient's weight is 80.3 kg. The patient's bmi is therefore 80.3 kg / (1.8 m * 1.8 m) = 24.78395 kg/m^2."
2521,6,Body Mass Index (BMI),physical,decimal,pmc-2827127-1,Extracted,"A 34-year-old Albanian, Kosovan male was sent to our centre to undergo echocardiography, in order to clarify the unexplained chest pain that had started two days earlier. Patient explained that his chest pain started after physical exertion, which consisted of carrying wood. This pain radiated to the back and was of strong intensity. He was visited by an internal medicine doctor and was then referred to the cardiologist.
Patient reported that this was the first time to experience such pain. He had been suffering from bronchial asthma since childhood. Patient was not aware of suffering from other diseases, nor was he aware of serious diseases or sudden deaths among his family members. His parents did not show features of the Marfan syndrome and the patient did not have other siblings.
He was 176 cm tall and weighed 61 kg, had elongated arms, arachnodactyly and moderate joint laxity. Patient had serious chest wall deformities, which included thoracic scoliosis of the vertebral column and pectus excavatum (Figure ). On auscultation of the heart, a diastolic murmur 1-2/6 over the aortic area was heard. Auscultation of the lungs demonstrated prolonged expiration and mild wheezing. Blood pressure was 150/90 mmHg. ECG displayed sinus rhythm, heart rate of 80/minute, without any abnormalities.
Chest X-ray revealed osseous deformities previously mentioned and a heart size that encompassed almost entire left hemi-thorax.
Transthoracic echocardiography showed enormous size of the aortic bulb, measuring 80 mm on short axis parasternal view at the level of aortic cusps (Figure ). Despite the very large size of the aortic root, aortic regurgitation was mild. Mitral valve prolaps of the anterior leaflet with mild mitral regurgitation was also noted (Figure ).
Transesophageal echocardiography confirmed the massive size of the aortic root and normal size of the aortic arch and descending thoracic aorta (Figures and ). We were unable to detect signs of aortic dissection, thus computed tomography (CT) of the chest was recommended.
Contrast CT of the chest demonstrated severe enlargement of aortic root measuring 78.7 mm, and intramural hematoma that reached the aortic arch (Figure ).
An ophthalmologic examination discovered the presence of myopia, of -3 diopters. No signs of ectopia lentis or retinal ablation were found. Ocular pressure was 12 mmHg.
In accordance with Ghent criteria, patient was diagnosed as having Marfan syndrome, complicated by severe aortic root aneurysm and type A intramural hematoma with no intraluminal tear or flap being detected. As a result, patient was put on Beta blocker therapy and was referred immediately for surgical intervention, replacement of the affected aorta with composite aortic valve- ascending aortic conduit, in a specialized cardio-surgery centre abroad. Unfortunately, patient ended up fatally during the open heart surgery.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [176.0, 'cm'], 'weight': [61.0, 'kg']}",19.69267,18.70804,20.6773,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 176.0 cm, which is 176.0 cm * 1 m / 100 cm = 1.76 m. The patient's weight is 61.0 kg. The patient's bmi is therefore 61.0 kg / (1.76 m * 1.76 m) = 19.69267 kg/m^2."
2522,6,Body Mass Index (BMI),physical,decimal,pmc-4556711-1,Extracted,"Patient 1 (p.R89X mutation and IVS7-27 T>G in the BBS5 gene), a 20-year-old man, had mental retardation (MiniMental State Examination 23; normal >24), rod-cone dystrophy, central obesity (height 158 cm, body weight 63 kg, body-mass index 25.2), and hypogonadism since the age of 5 years. He did not have polydactyly. Esophageal, gastric, and rectal varices developed at the age of 5 years, with fibrosis of the liver. The waist circumference was 83.5 cm at the age of 20 years. The blood pressure was 131/85 mmHg, and the heart rate was 61 beats/min. He had normal heart sounds with clear breath sounds. The serum creatinine level was normal. Ultrasonography showed no anomalies in the kidneys at the age of 20 years. The non-consanguineous parents of Patients 1 and 2 were apparently healthy.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [158.0, 'cm'], 'weight': [63.0, 'kg']}",25.23634,23.97452,26.49816,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 158.0 cm, which is 158.0 cm * 1 m / 100 cm = 1.58 m. The patient's weight is 63.0 kg. The patient's bmi is therefore 63.0 kg / (1.58 m * 1.58 m) = 25.23634 kg/m^2."
2523,6,Body Mass Index (BMI),physical,decimal,pmc-3948446-2,Extracted,"A 34-year-old man (160.5 cm, 48.9 kg) was presented to the authors for mitral valve (MV) replacement. The patient had been diagnosed with SLE and APS after being admitted to the hospital for treatment of palpitations and dyspnea ten years earlier, and he had taken an anticoagulant medication. During the outpatient clinic follow-up, 24-hr Holter monitoring revealed the increasing frequency of non-sustained atrial fibrillation. An operation was thus scheduled to reduce the risk of atrial thrombosis. The preoperative blood coagulation tests showed prolonged results. The aPTT was 57.8 s and dRVVT was 47.2 s (reference: 25.9-35.7 s). The result with patient plasma from the mixing test was 27.3 s, and the mixed plasma result was 37.6 s, while SCT was 52.1 s (reference: 22.3-42.7 s). In addition, the patient was positive for LA, negative for ACA IgG, and had borderline results for ACA IgM. Intravenous heparin and oral deflazacort tablets were used for preoperative management.
Invasive blood pressure monitoring was conducted via the patient's radial artery. Anesthesia induction and maintenance were performed as usual, and routine cardiac anesthesia monitoring was done. The ACT level increased from 129 s to 850 s after the injection of 150 mg of heparin. After the insertion of cannulas into the aorta, superior vena cava, and inferior vena cava, CPB was started. One hour after the administration of heparin, the ACT level was found to have decreased to 524 s. Therefore, an additional 50 mg of heparin was injected. After the mitral annuloplasty, valvuloplasty was performed, and weaning from CPB was attempted. Due to the risk of thrombosis, a half dose (75 mg) of protamine was administered. Five minutes after the injection of protamine, the ACT level was found to be 220 s. The total administered dose of heparin during the surgery was 200 mg, and the total CPB time was 52 min. The EBL during surgery was 500 ml and urine output was 455 ml. 800 ml of crystalloid and 500 ml of colloid were infused during surgery. The patient did not receive any transfusion during the surgery.
Following the surgery the patient was transferred to the ICU without significant bleeding. The immediate postoperative PT/INR was 1.39 and aPTT was over 180 s. Postoperative prophylactic anticoagulation was maintained with warfarin. Ten days after the operation, the patient was discharged without specific complications.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [160.5, 'cm'], 'weight': [48.9, 'kg']}",18.98274,18.0336,19.93188,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 160.5 cm, which is 160.5 cm * 1 m / 100 cm = 1.605 m. The patient's weight is 48.9 kg. The patient's bmi is therefore 48.9 kg / (1.605 m * 1.605 m) = 18.98274 kg/m^2."
2524,6,Body Mass Index (BMI),physical,decimal,pmc-4988297-1,Extracted,"A 43-year-old female patient was admitted to our clinic with 1-year history of weakness, swelling in leg, weight loss and recurrent upper respiratory infections. The patient had no past medical history. In this period she had lost 10% of her weight. The patient was 163 cm in height and weighed 46 kg; she appeared weak and the physical examination showed no abnormalities except 2+ pretibial edema. She had a blood pressure of 130/80-mmHg and pulse rate of 64 per minute without any cyanosis. She had symmetric thoracoabdominal breathing. Abdominal examination revealed no distension, no rebound, no ascites, no hepatosplenomegaly and normoactive bowel sounds. The complete blood cell count was in normal limits except decreased lymphocytes cells (lymphocyte = 250/mm3), and the biochemical analysis of the blood for hepatic and renal function, urine analysis and fecal occult blood test were all within normal limits only lower albumin (albumin = 2.1 g/dl) level was observed. The tumor markers for CEA and CA 19-9, celiac markers and autoimmune indicators were also normal. Upper endoscopy revealed erythematous antral gastritis. No lesions were observed on the colonoscopy and the abdominal ultrasound. No pathology was detected in echocardiography.
Ultrasonography (USG) revealed multiple anechoic cystic nodularities in the intestinal wall protruding into the fluid-filled lumen (Fig. ). Because of any diagnose could be done by ultrasound, abdominal computerized tomography (CT) has decided to withdraw.
CT showed increased wall thickness on 40 cm segment of ileum. Capsule endoscopy was performed and a polypoid infiltrating area was found ~40–50 cm segment of middle and distal jejenum (Fig. A and B). Bone marrow biopsy was performed for suspicious lymphoproliferative disease. Biopsy result showed normocellular bone marrow. Flow cytometry of bone marrow mononuclear cells with the work done by immunophenotyping detected no significant antigenic exploration. It was decided to take a PET-CT for to clarify a suspicious tumor or paraneoplastic syndrome in patient. PET-CT showed diffuse wall thickness increase in the ileum. These results are in line with the assessment of the causes of protein-losing enteropathy; lymphangiectasia, intestinal lymphoma and tuberculosis. After all, surgical decision was taken with these presumptive diagnoses.
Operation started with diagnostic laparoscopic approach but nothing specific has been detected in small intestine and its meso. Then it was decided to go laparotomy. Terminal ileum was seen normal but swollen intestinal wall and pathological lymph node in the mesentery of 35–40 cm to the proximal terminal ileum were found. Excised lymph node was sent to pathology for frozen observation. Pathology result showed as lymphorrhagia. Patient was perop consulted with gastroenterology clinic and resection of the affected part of ileum decision was taken. Segmental resection including affected bowel loops were made and functional end-to-end anastomosis performed. Specimen was sent to pathology. Bowel movements are normal, and gas outlet with defecation was observed postoperatively third day. Then oral feeding was allowed on the post-op fourth day. Patient was discharged sixth day postoperatively. No further therapy was needed because of the benign manner of the lesions.
Microscopic examination of the resected specimens revealed expanded cystic vascular lesions partly extending to the intestinal mucosa in small bowel mesentery and subserosa (Fig. ). Immunohistochemically the endothelial cells, lining the vascular structures, were reactive with D2-40, CD31 and ERG whereas negative with CD34 (Fig. ). Present findings were found to be consistent with intestinal lymphangiomatosis.
In the control physical examination after 1 month surgery, the patient's complaints improved and pretibial edema was not seen. Laboratory values of lymphocytes, total protein and albumin were found to increase in normal values. Patient was seen without complaints on 10-month follow-up.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [163.0, 'cm'], 'weight': [46.0, 'kg']}",17.31341,16.44774,18.17908,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 46.0 kg. The patient's bmi is therefore 46.0 kg / (1.63 m * 1.63 m) = 17.31341 kg/m^2."
2525,6,Body Mass Index (BMI),physical,decimal,pmc-7803851-1,Extracted,"A 53-year-old Nigerian male with hepatitis C virus (HCV) infection treated with peginterferon alfa-2a and ribavirin, to which he showed a null response, presented to our hospital. Three months after the initial visit, multiple hepatocellular carcinomas (HCCs) were detected in segments 7 and 8 of the liver according to the Brisbane 2000 Nomenclature of Liver Anatomy and Resections [], and radiofrequency ablation (RFA) was performed for each HCC. Seventeen months after RFA, a recurrence of HCC was detected in segment 4 (the medial section) by follow-up computed tomography (CT), and the patient was referred to our department.
Physical examination showed that the patient was an 87.9 kg, 168.5 cm male in good condition. The patient received medical treatment for diabetes mellitus and hypertension. He had neither a history of transfusion nor a history of SCT. The laboratory test results showed moderate liver damage, as shown in Table . Microscopic examination of peripheral blood erythrocytes did not show any morphological abnormalities.
Contrast-enhanced CT showed a 4.0 × 3.4 × 3.2 cm tumor in segment 4 adjacent to the left branch of the portal vein and the middle hepatic vein (Fig. ). An irregular liver surface; the hypertrophy of segments 1, 2 and 3; and splenomegaly all suggested the presence of cirrhosis. The normal liver parenchyma of the medial section accounted for 10% of the total liver volume according to CT volumetry.
With the diagnosis of solitary HCC in segment 4, left medial sectionectomy was conducted. Hepatic resection was performed with intraoperative ultrasonography (IOUS) guidance with Pringle’s maneuver (hepatic inflow occlusion time 15–30 min and reperfusion time 5 min; the total blood flow occlusion time was 165 min). Multiple IOUS examinations and inspections of the liver surface revealed no hepatic blood flow impairment during surgery (Fig. ). At the end of the operation, laboratory data showed no conspicuous abnormalities, with total bilirubin (T-Bil) 1.6 mg/dL, aspartate aminotransferase (AST) 316 IU/L, alanine aminotransferase (ALT) 323 IU/L, hemoglobin (Hb) 11.6 g/dL, and prothrombin time (PT)% 52.5%. A drain was inserted along the resected plane of the liver. The operation time was 305 min, and the estimated blood loss was 714 mL. No blood transfusion was performed.
However, the laboratory tests on postoperative day (POD) 1 revealed severe liver damage and acidosis: T-Bil 2.8 mg/dL, AST 9250 IU/L, ALT 6120 IU/L, PT% 20.9%, blood pH 7.29, lactate 6.6 mmol/L, and base excess − 5.4 mmol/L. Figure shows the trends of postoperative laboratory data. The bedside US did not indicate an impairment of hepatic blood perfusion. The drain output was 460 mL/15 h, with serosanguineous appearance. Because his vital signs were stable and it was difficult to identify a cause of the acute severe liver damage, we selected conservative management while performing fresh frozen plasma transfusion. The values of AST and ALT declined gradually, but the level of T-Bil continued to increase, and renal and respiratory dysfunction emerged and subsequently deteriorated; therefore, we initiated continuous hemodiafiltration and plasma exchange under mechanical ventilation. Contrast-enhanced CT showed a slightly heterogeneous enhancement of the liver parenchyma without apparent major vessel occlusion on POD 13 (Fig. a), and diffuse cerebral infarction on POD 16 (Fig. b).
Although clinico-radiological examinations could not identify the cause of acute liver damage, the pathological examination of the resected specimen revealed that the intrahepatic peripheral blood vessels were occluded by sickled erythrocytes (Fig. ). Morphological abnormalities were not found by microscopic examination of the peripheral blood erythrocytes after surgery, but we requested an analysis of the patient’s hemoglobin by high-performance liquid chromatography (HPLC) with a suspicion of hemoglobinopathy. HPLC demonstrated an abnormal sharp peak indicating the presence of abnormal hemoglobin, which accounted for 34.4% of total hemoglobin (Fig. ). These findings strongly suggested the presence of HbS. Despite intensive treatments, he died of multiple organ failure on POD 20. Autopsy was rejected by his bereaved family for religious reasons.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [168.5, 'cm'], 'weight': [87.9, 'kg']}",30.95915,29.41119,32.50711,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.5 cm, which is 168.5 cm * 1 m / 100 cm = 1.685 m. The patient's weight is 87.9 kg. The patient's bmi is therefore 87.9 kg / (1.685 m * 1.685 m) = 30.95915 kg/m^2."
2526,6,Body Mass Index (BMI),physical,decimal,pmc-4912772-1,Extracted,"The patients were siblings from a non-consanguineous Uzbekistan family. Patient 1 was a 3-yr-old 46,XX female with ambiguous genitalia. She was previously evaluated for her abnormal genital development and underwent first genital surgery in Turkey. On an initial evaluation at age 2 y 8 m, her height was 100 cm (+2.1 SD), her weight was 15.8 kg, (+1.4 SD), blood pressure (BP) was 110/70 mmHg (94th/96th percentiles). The physical examination revealed that the phallus was 5 cm long and 2 cm wide (Prader grade IV); no gonads were palpable in the inguinal region. The areola and palmar creases were pigmented bilaterally. An ACTH stimulation test (250 μg) showed grossly elevated baseline ACTH (238 pg/mL) and basal cortisol of 4.7 μg/dL with non-response to ACTH and moderately elevated progesterone and 17OHP after 60 min; 11-deoxycortisol and androstenedione concentrations were markedly high (Table ). The serum sodium was 136 mmol/L, potassium 3.1 mmol/L, plasma renin activity (PRA) was very low at 15 ng/dL/h (nl, 171–1115), and aldosterone 2 ng/dL (nl, 3–35). Her total testosterone levels were 132 ng/dL (nl, <3–10) and dehydroepiandrosterone sulfate (DHEAS) 165.2 μg/dL (nl, <5-57). She was followed up at the King Chulalongkorn Memorial Hospital (Bangkok, Thailand) due to the family relocation at age 3 yr for further management. After receiving the results of an ACTH stimulation test, she was started treatment with hydrocortisone, 5 mg thrice daily (10 mg/m2/d) which improved BP into the normal range (90/60 mmHg), suppressed testosterone, and PRA became measurable (200–496 ng/dL/h).
Patient 2 is the younger brother of Patient 1. He presented at 2 years of age with acne and masculinization (isosexual precocious puberty). Physical examination revealed an advanced maturation of external genitalia as well as a low-pitched voice. His Tanner stages were G3 and PH1, and each of his testes was 3 mL in volume. His height was 97 cm (+3.2 SD) and weight was 17 kg (+2.9 SD). Height gain was accelerated from 12-month-old on the growth chart (from +2.6 SD to +3.2 SD). Skin pigmentation appeared consistent with his ethnicity, but no evident mucosal pigmentation. His BP was 110/65 mmHg (92th/95th percentiles). Labs revealed serum Na 136 mmol/L, K 4.3 mmol/L, bicarbonate 24 mmol/L, BUN 12 and Cr 0.3 mg/dL, respectively. An ACTH stimulation test showed elevated baseline ACTH, a low basal cortisol (2.3 μg/dL) with non-response to ACTH and moderately elevated 17OHP after 60 min (Table ). 11-deoxycortisol concentrations were not measured. PRA was low at 106 ng/dL/h (nl, 171–1115), and low aldosterone 0.2 ng/dL (nl, 3–35). He was then treated with hydrocortisone 2.5 mg thrice daily (11 mg/m2/d). His blood pressure was well controlled, and PRA was increased up to 738 ng/dL/h.
Genomic DNA from peripheral blood leucocytes of the patients and their parents was extracted by using the QIAamp® DNA Blood Mini Kit (Qiagen, Valencia, CA) after taking informed consent. The coding sequence of CYP11B1 gene including exon-intron boundaries was amplified in eight fragments using specific primers (Table ). PCR products were treated with ExoSAP-IT (USP Corporation, Cleveland, OH), and sent for direct sequencing at Macrogen Inc. (Seoul, Korea). Analyses were performed by Sequencher 4.2 (Gene Codes Corporation, Ann Arbor, MI).
We performed a minigene in vitro experiment of the CYP11B1 splicing mutation. A segment of the wild-type (WT) and mutant (IVS7 + 1G > A) genomic DNA (gDNA) of CYP11B1 gene consisting of exons 6 to 9 and their in-between introns was amplified by PCR using the oligonucleotides listed in Table . We used the gDNA of a normal control and the patient with IVS7 + 1G > A CYP11B1 mutation as a template of minigene constructs. PCR reactions were carried out in a 20 μl volume containing 50 ng gDNA, 10xPCR buffer, 25 mM MgCl2, 10 μM dNTPs, 5 U/μl Taq polymerase and 10 μM of each primer, using the following parameters: 30s at 94 °C, 30s at 60 °C and 1.30 min at 72 °C. The PCR product was cleaved with BamHI-HF and XbaI enzymes and cloned into the corresponding sites of pcDNA™3.1/myc-His B mammalian expression vector (Invitrogen, Carlsbad, CA) using T4 DNA ligase (New England BioLabs, UK). The wild-type and mutant vectors were confirmed by direct sequencing using NCBI Reference Sequences (RefSeq) NG_007954.1 as the genomic reference and NM_000497.3 as the mRNA reference.
COS-7 cells were cultured in Dulbecco’s Modified Eagles Medium, High Glucose (HyClone Laboratories, Logan, UT) supplemented with 10 % fetal bovine serum (Sigma-Aldrich, Singapore) and 0.01 % penicillin/streptomycin (HyClone Laboratories) at 37 °C in a humidified 5 % CO2 incubator. Cells were grown on 6-well plates and transiently transfected with the wild-type and mutant minigene constructs (1 μg) using Effectene® Transfection Reagent (Qiagen). Cells incubated for 48 h after transfection and then were washed 3 times with PBS and kept frozen at − 20 °C. Total cellular RNA was extracted using QIAamp® RNA Blood Mini Kit (Qiagen) and treated with DNaseI (Qiagen). The RNAs were then used as template for cDNA synthesis using ImProm-II™ Reverse Transcription System (Promega Corporation, Madison, WI). Finally, both the WT and mutant cDNAs were amplified by PCR using the same primers and conditions as used for the minigene construction. The PCR products were analyzed by electrophoresis on a 1 % agarose gel followed by staining with ethidium bromide. Each PCR product was confirmed by Sanger sequencing after subcloning into pGEM®-T Easy vectors (Promega).",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [15.8, 'kg'], 'height': [100.0, 'cm']}",15.8,15.01,16.59,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 100.0 cm, which is 100.0 cm * 1 m / 100 cm = 1.0 m. The patient's weight is 15.8 kg. The patient's bmi is therefore 15.8 kg / (1.0 m * 1.0 m) = 15.8 kg/m^2."
2527,6,Body Mass Index (BMI),physical,decimal,pmc-3483495-1,Extracted,"A 75-year-old woman (height 150 cm, weight 63.5 kg) was admitted to the hospital for phased total knee replacement on the both sides under the diagnosis of bilateral degenerative arthritis. She had no other specific diseases than osteoporosis. She had a history of a right shoulder joint replacement and a lumbar discectomy. Blood test, EKG, chest x-ray, and pulmonary function test performed prior to surgery were within normal ranges, and echocardiography showed ejection fraction of 60%, and manifested diastolic dysfunction of the left atrium. The patient's blood type was O Rh-positive and the preoperative cross matching and antibody screening test turned out to be negative. Under general anesthesia, right total knee replacement arthroplasty was first performed and after surgery she received 2 units of packed red blood cells (RBCs). After transfusion, there was no episode of transfusion reaction.
Two weeks after surgery, preoperational test for left total knee replacement indicated that hemoglobin level was 10.2 g/dl and hematocrit was 29.2%, and the antibody screening test was negative. On surgery day, she received 0.2 mg of glycopyrrolate intramuscularly one hour before induction of anesthesia. In the operating room, EKG, noninvasive blood pressure monitoring and a pulse oximetry monitor were placed. Anesthesia was induced with propofol 120 mg and rocuronium 50 mg, and maintained using O22 L/min and N2O 2 L/min, and sevoflurane 2 vol% after tracheal intubation. For continuous monitoring of blood pressure and arterial blood gas analysis, 20 G catheter was placed to the left radial artery and central venous catheter was inserted to the internal jugular vein for central venous pressure (CVP).
One hour and 20 minutes after the onset of surgery when the total amount of blood loss was estimated more than 800 ml, transfusion of packed RBCs was started. A cross-matching test turned out to be negative again, suitable for transfusion. During transfusion, the patient showed stable vital signs. Five minutes after 1 unit of packed RBCs was transfused, red-colored urine, which was suspected as hemoglobinuria, was observed. For immediate treatment, fluid was administered while 10 mg furosemide was injected. Then we asked the Department of Laboratory Medicine to conduct ABO-Rh blood typing test of the patient's and the donor's blood, cross-matching, antibody screening test, direct anti-globulin test (DAT) and indirect anti-globulin test (IAT), and urinalysis. Hereafter, no big blood loss developed and the surgery was completed without further transfusion. Except for the incidence of red-colored urine sustained during surgery, patient's vital signs were stably maintained. At the completion of surgery when her spontaneous respiration and consciousness were confirmed, she was extubated and transported to the recovery room.
Red-colored urine sustained even in the recovery room, but the color was waning and the patient's vital signs were normal, so she was referred to a ward. Post-operative test results showed that the transfused blood and patient's blood were compatible and that antibody screening test result was negative. IAT was negative while DAT was positive. Cross-matching turned out to be negative again. Urinalysis findings indicated 3+ blood, 0 RBC/HPF, and 2+ protein. Examination of patient's blood tested by an independent laboratory to determine more exact cause revealed that anti-Dia antibody was identified in an unexpected antibody screening test.
Since the next day of surgery, red-colored urine was not observed, which made additional urinalysis unnecessary. Hemoglobin level measured right after surgery was 8.7 g/dl, showing a decrease, but thereafter no significant change further took place and BUN and creatinine level also sustained in the normal range, not followed by any other transfusion reaction. Then, she was discharged without any complications.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [150.0, 'cm'], 'weight': [63.5, 'kg']}",28.22222,26.81111,29.63333,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 150.0 cm, which is 150.0 cm * 1 m / 100 cm = 1.5 m. The patient's weight is 63.5 kg. The patient's bmi is therefore 63.5 kg / (1.5 m * 1.5 m) = 28.22222 kg/m^2."
2528,6,Body Mass Index (BMI),physical,decimal,pmc-8313509-1,Extracted,"A 14-year-old girl consulted from the Pediatric Department to the Dermatovenerology Department of Saiful Anwar Hospital (RSSA) with a chief complaint of painful erythematous blister all over the body. The patient experienced the complaint since 4 days before consultation. The complaint initiated with fever and lower leg pain followed by appearance of blisters on the lower leg. New blisters appeared on the right buttocks afterward, then the lesion multiplied and spread to the body, limbs, and face. Several vesicles on the lower leg fused into large and painful bullae. The blisters multiplied, accompanied by pain with VAS 9/10 and itch with VAS 2/10. When consulted, the patient did not experience fever, headache, cough, nausea, vomiting, and pain in eye. The patient had a good appetite.
The patient had chickenpox when she was 7 years old and there were no complaints afterward. Approximately 3 months before consultation, the patient was diagnosed as SLE and 2 months later the patient was diagnosed as lupus nephritis by the pediatrician at RSSA. The patient’s family experienced no similar complaints. Around 2 weeks before the blisters appeared, the patient was admitted to RSSA due to SLE and lupus nephritis. During admission, methylprednisolone pulse dose 1 g per day was given for 3 days, and continued daily doses of methylprednisolone 80 mg twice daily. Other medication consumed by the patient including captopril 1.5 mg once daily, valsartan 60 mg daily, aspirin 80 mg three times daily, nifedipine 5 mg three times daily, vitamin B tablet once daily, vitamin C 100 mg once daily, and vitamin E 100 IU once daily. Since skin lesion appeared, neither oral nor ointment medication was given to the patient. The patient is the third child of three siblings. The patient had a complete immunization.
The patient’s general condition was fully alert, and appeared moderately ill. The patient’s vital sign was 114 times per minute for heart rate, 20 times per minute for respiratory rate, and 37 °C for axillary temperature. The patient’s body weight was 45 kg and body height was 159 cm. There was no cervical, axillary, and inguinal lymph node enlargement. Dermatologic examination of the facial, anterior and posterior trunk, gluteal, right and left upper extremity, back of the hand, tibial region, femoral region, and soles region found vesicles with erythematous base, and several vesicles were confluent, well-defined, irregular edged, and of varied shape and size ( and ). At the right cruris and pedis region, vesicles fused into well-defined bullae with erythematous base with various shapes and sizes ( and ).
Tzanck smear examination at the bullae and vesicle showed polymorphonuclear cells (PMN) and multinucleated giant cells (MGC). However, there were no acantholytic cells (). Laboratory examination showed anemia (hemoglobin 9.80 g/dL), decrease of erythrocyte (3.70×106/µL), neutrophilia (89.5%), and lymphopenia (8.4%). Urinalysis examination showed proteinuria +1. Laboratory results of renal and liver function were within normal limits.
Based on anamnesis, physical examination, and additional microscopic examination, the patient was diagnosed as HZD with SLE and lupus nephritis as comorbidity. Management for this patient included multidisciplinary management from the Pediatric and Dermatovenerology Departments. Treatment from the Dermatology Department was acyclovir 800 mg five times daily per oral given for 10 days. Vesicles and bullae were treated with normal saline compress three times daily for 10 minutes every day. Sodium fusidate cream twice daily was given onto the ruptured vesicles and bullae. Analgesic acetaminophen 450 mg three times daily (10 mg/kg BW/day) if fever occurred, methylprednisolone 80 mg once daily (2 mg/kg BW/day), chloroquine 140 mg once daily (3 mg/kg BW/day), captopril 1.5 mg three times (0.1 mg/kg BW/day), valsartan 60 mg once daily, aspirin 80 mg three times daily, nifedipine 5 mg three times daily, vitamin B tablet once daily, vitamin C 100 mg once daily, vitamin E 100 IU once daily, high calories and high-protein diet, and routine formula milk 200 mL three times daily were given.
On day 10 of follow up since acyclovir was given, complaints regarding skin lesion were improved. There was no new lesion, and the pain was decreased to VAS 2/10. Vesicles at the face, trunk, and upper extremity already deflated, leaving brownish marks. Blisters at the gluteal region, lower extremity, and cruris already deflated. Some were burst into a brownish crust. Dermatologic examination at the facial, anterior and posterior trunk, left and right upper extremity region showed multiple well-defined hyperpigmented macules and patches, irregular in shape, and of varied shape and size (). Multiple hyperpigmented patches with various shape and size at the gluteal region, right femur, right cruris, dorsum, and plantar pedis region, multiple hyperpigmented patches with varied shape and size, and several sagging bullae burst into erosion covered by a brownish crust (). Management was continued with normal saline 0.9% compress 3×10 minutes on the blisters and erosion and sodium fusidate cream twice daily on the erosion. Acyclovir treatment was stopped.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.0, 'kg'], 'height': [159.0, 'cm']}",17.79993,16.90993,18.68993,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 159.0 cm, which is 159.0 cm * 1 m / 100 cm = 1.59 m. The patient's weight is 45.0 kg. The patient's bmi is therefore 45.0 kg / (1.59 m * 1.59 m) = 17.79993 kg/m^2."
2529,6,Body Mass Index (BMI),physical,decimal,pmc-3030020-1,Extracted,"A 31-year-old female patient who was diagnosed with thyroid cancer underwent robotically assisted total thyroidectomy. The patient was 157 cm tall and weighed 47 kg. Other than appendectomy 1 year earlier, she had no special past medical or surgical history. She had a history of allergy to shellfish and grogram. According to preoperative electrocardiogram, no abnormal findings were identified (normal regular sinus rhythm and heart rate 70 beats per minute). Therefore, additional tests in association with cardiac electrophysiology and carotid sinus hypersensitivity were not attempted before surgery. Results from blood chemistry tests, including serum electrolytes, were normal.
Premedication was not given preoperatively. After preoxygenation, 2% propofol solution (Fresofol, Fresenius Kabi, Bad Homburg, Germany), 50 ml in the Schinder model, and remifentanil (Ultiva, GlaxoSmithKline, Brentford, UK), which was diluted to 40 µg/ml in the Minto model, were intravenously administered for induction and maintenance using a target controlled infusion pump. During induction, target effect concentrations of propofol and remifentanil were adjusted to 5 µg/ml and 4 ng/ml, respectively. Rocuronium 50 mg, was used to induce muscle relaxation for intubation, which was intraoperatively maintained using atracurium diluted to 5 mg/ml by normal saline and continuously infused at a rate of 5 µg/kg/min.
No problematic events occurred during induction or intubation. For maintenance of anesthesia, the target effect concentrations of propofol and remifentanil were 4 µg/ml and 3 ng/ml, respectively, and were adjusted by units of 0.5, if needed. Mechanical ventilation was supported by nitrous oxide 2 L/min and oxygen 2 L/min. Radial artery cannulation was performed for tight monitoring of vital signs during surgery.
The patient's neck was hyperextended and the left arm was elevated, stretched, and fixed in supine position for passage of endoscopy and surgical devices via an axillary approach. For insertion of robotic arms, the surgeon made a 3.5 cm sized perpendicular incision at the axillary area and dissected tissues under the platysma muscle from the upper border of the pectoralis major muscle to the inner border of the sternocleidomastoid muscle using a Harmonic Scalpel. For visibility of surgery, an extractor was inserted in the incised axillary area, and connected to an elevator for elevation of the dissected flap. Another 0.5 cm sized incision was made between the midpoint of the left clavicle and the left nipple for insertion of a camera in the robot arm for visualization of the surgical field. The robot was placed at the right side of the patient, and its three arms were inserted into the incised axillary area for surgery. To aid the surgeon, one assistant inserted an endoscopic device through the incised axillary area. To expose the thyroid gland, a total of four arms of the robot and one endoscopic device were used in dissection of the sternohyoid muscle from the inner border of sternocleidomastoid muscle.
The patient's vital signs were managed stably at the beginning of surgery. Systolic and diastolic blood pressure were maintained in a range of 100-120 mmHg and 60-80 mmHg, respectively, and heart beat showed regular sinus rhythm in a range of 70-80 rates per minute. The surgeon dissected ipsilateral left thyroid tissue at the incision site, and then the contralateral side of the thyroid, except for the isthmus area. Around the time when the left thyroid area was almost dissected, the robotic arms crossed the left carotid bifurcation, and multiple manipulations in that area were broken. At that time, a sudden absence of electrical waves was detected on the electrocardiogram, arterial line, and pulse oximetry. Sinus bradycardia or hypotension in monitoring of vital signs was not preceded before the attack. As soon as we recognized cardiac arrest, we urged the surgeon to stop surgical manipulation and administered atropine 0.5 mg intravenously. The patient's cardiac rhythm was restored to normal sinus rhythm in a short time (). Total length of cardiac arrest time was 5.8 seconds. During cardiac arrest, no electrical wave was observed in the electrocardiogram, right radial arterial blood pressure, and peripheral oxygen saturation monitoring device. After recovery to normal sinus rhythm, sinus tachycardia of 100-110 rates per minute continuously was followed temporarily. However, no recurrence of cardiac arrest, sinus bradycardia, or hypotension was observed. Atracurium infusion was stopped near 30 minutes before the end of surgery and pyridostigmine and glycopyrrolate were administered for reverse neuromuscular block. After the patient's self-respiration recovery was confirmed, extubation was safely performed in the operating room.
After restoration of consciousness in the post anesthetic care unit (PACU), we inquired and investigated the patient's past medical history again. However, she had no special problems, such as syncope, headache, or dizziness. Neurologic examination showed no abnormal findings at that time. The patient stayed in the PACU for one and a half hours without any problems, and then sent to the general ward. The patient was discharged four days after surgery with no special sequelae.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [157.0, 'cm'], 'weight': [47.0, 'kg']}",19.06771,18.11432,20.0211,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 157.0 cm, which is 157.0 cm * 1 m / 100 cm = 1.57 m. The patient's weight is 47.0 kg. The patient's bmi is therefore 47.0 kg / (1.57 m * 1.57 m) = 19.06771 kg/m^2."
2530,6,Body Mass Index (BMI),physical,decimal,pmc-5577842-1,Extracted,"A 63-year-old female patient developed bronchial asthma at approximately 5 years of age. Her asthma did not spontaneously resolve and she subsequently suffered from regular asthma attacks. Specific IgE testing was positive for house dust, Dermatophagoides pteronyssinus, Chironomid midges, and negative for Aspergillus fumigatus, Candida albicans, Penicillium notatum and other common allergens. Despite the treatment with the combination of budesonide 1280 μg and formoterol 36 μg per day, a leukotriene receptor antagonist, and low-dose theophylline, she experienced exacerbations several times. The asthma control test (ACT) score was 18, and %FVC 86.7%, FEV1.0 0.88 mL, %FEV1 46.1% at 2 month before omalizumab therapy which initiated the year at in September 2013. Table presents the term-course of her clinical data. She has a height of 157 cm and a weight of 66 kg, and her serum total IgE level was 580 IU/mL. Based on the omalizumab dose table, she was started on a biweekly administration of 375 mg omalizumab. At week 16, we conducted an evaluation to assess whether the drug should be continued. We observed an improvement in the patient’s subjective symptoms and morning peak expiratory flow levels. The level of airway obstruction had improved according to the respiratory function tests, and because there were no exacerbations within 16 weeks, we decided to continue omalizumab administration. Because there were no clear aggravations, we continued treatment with omalizumab at the same dose for 36 months. We measured her serum free IgE levels at 2, 4, 8, and 26 weeks after initiating omalizumab and found that the serum free IgE levels were extremely low at 72.8, 40.50, 18.1, and 11.3 ng/dL, respectively (Fig. ). Because her symptoms had stabilized after initiating omalizumab with no exacerbations, she inquired whether it was possible to reduce the frequency of administration from once every 2 weeks to once every 4 weeks. Her ACT scores in the past 6 months were 23–25, her morning peak expiratory flow was stable, and there were no exacerbations in the past year; hence, we accepted her request and reduced the frequency of administration from biweekly to monthly without changing the dose of 375 mg omalizumab per administration beginning from August 2016. Therefore, the dosage was reduced by half. The serum free IgE trough level transiently increased to 129.3 ng/mL at 4 weeks after reducing the dosage; however, thereafter, the serum free IgE level decreased to 93.6 ng/mL within 4 weeks and gradually to 20.6 ng/mL, which is well below the desired level, 30 ng/mL (Fig. ). She experienced no exacerbations during this period, and her ACT score remained at 25. FEV1 measured via pulmonary function testing almost unchanged after reduction of omalizumab (Fig. ). Moreover, her asthma was controlled over the 9-month period since the dosage was reduced.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [157.0, 'cm'], 'weight': [66.0, 'kg']}",26.77593,25.43713,28.11473,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 157.0 cm, which is 157.0 cm * 1 m / 100 cm = 1.57 m. The patient's weight is 66.0 kg. The patient's bmi is therefore 66.0 kg / (1.57 m * 1.57 m) = 26.77593 kg/m^2."
2531,6,Body Mass Index (BMI),physical,decimal,pmc-3971547-1,Extracted,"The patient was an 85-year-old woman with a chief complaint of epigastric pain and a past history of nephrotic syndrome, hyperlipidemia, diabetes mellitus, and status postbilateral cataract surgery. In 2009, she developed nephrotic syndrome, which was treated with steroid therapy until February 2011, when complete remission was achieved and the therapy was discontinued. No kidney biopsy was performed because of her advanced age, and the cause of her nephrotic syndrome remained unknown. In February 2013, the nephrotic syndrome relapsed, and she was admitted to the Department of Nephrology of our hospital for steroid therapy. Steroid semipulse therapy (500 mg of methylprednisolone daily for 3 days) and posttherapy (prednisolone tapering from 30 mg daily) were initiated. During admission, she developed sudden epigastric pain and was referred to our department for consultation.
She was 147 cm tall and weighed 44 kg, with a physical status of ASA 3. Her heart rate was 108/min, blood pressure 158/92 mmHg, and respiratory rate 15/min, with an SpO2 of 95%. There was diffuse abdominal tenderness, rebound tenderness, and muscular defense (see and ).
Bowel gas was deviated toward the midline, suggesting ascites. No free intraperitoneal gas was noted ().
Multiple sigmoid diverticula and a large amount of ascitic fluid were observed, with no evidence of bowel perforation ().
This patient was an elderly woman who had nephrotic syndrome as an underlying condition and was taking steroids. Imaging studies failed to reveal any evidence of gastrointestinal perforation, presenting a diagnostic challenge as to whether or not to perform emergency surgery. Therefore, we performed abdominal paracentesis in the presence of a large amount of ascitic fluid.
The ascitic fluid was milky, clear, odorless, with a protein content of 0.3 g/dL, an LDH level of 488 IU/L, and a specific gravity of 1.010 ().
Since the ascitic fluid had no smell of feces or that of the digestive system and was transudative, we considered that the presence of intestinal bacteria in the ascitic fluid, which should normally be sterile, would raise the possibility of gastrointestinal perforation. In addition, since it was at night when laboratory technicians were absent, a physician performed Gram staining.
A small number of Gram-negative rods and a large number of leukocytes were seen ().
Since Gram staining showed the presence of Gram-negative rods in the ascitic fluid, we strongly suspected digestive tract perforation and performed emergency surgery.
The abdomen was opened through a long midline abdominal incision. Ascitic fluid had accumulated in the peritoneal cavity. There were multiple sigmoid diverticula, one of which was perforated, and so Hartmann's procedure was performed with a diagnosis of perforated sigmoid diverticulum.
The operative time was 2 h and 43 min. The amount of blood loss was 160 mL. Two units of MAP, 10 units of PCs, and 2 units of FFP were transfused.
The resected sigmoid colon specimen measured 10 × 8 cm and showed multiple stool-filled diverticula, one of which had a perforation, through which stool was visible ().
Multiple diverticula extending into the subserosa were present, and one of them was perforated. At this site, the diverticular wall was disrupted, and the surrounding tissue was infiltrated by neutrophils ().
At a later date, the results of microbiological examinations of ascitic fluid were reported by the laboratory technician. Gram-stained smears showed a small number of Gram-negative rods, Gram-positive cocci and rods, and +2 leukocytes. Cultures were positive for intestinal bacteria, including Bacteroides fragilis, being consistent with the results of the rapid diagnosis by Gram staining ().
The postoperative course was uneventful, and the patient was transferred to the general ward. Later, her hospital course became complicated by a urinary tract infection, but she was discharged, after rehabilitation, on the 64th postoperative day.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [147.0, 'cm'], 'weight': [44.0, 'kg']}",20.36189,19.3438,21.37998,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 147.0 cm, which is 147.0 cm * 1 m / 100 cm = 1.47 m. The patient's weight is 44.0 kg. The patient's bmi is therefore 44.0 kg / (1.47 m * 1.47 m) = 20.36189 kg/m^2."
2532,6,Body Mass Index (BMI),physical,decimal,pmc-6011100-1,Extracted,"A 12-year-old girl (height, 144 cm; weight, 40 kg) was presented to the hospital with an episode of seizure with impaired consciousness. Her BG at that time was 60 mg/dL (normal value of casual BG: 70–200 mg/dL). Glucose was administered and she recovered consciousness. She had no significant comorbidities prior to hospital admission. From her family history and further investigation, she was diagnosed as having insulinoma and hyperparathyroidism in MEN-1. Arterial phase images of computed tomography showed a vascularity-rich tumor of 20 mm in diameter located in the head of the pancreas. The feeding artery of the tumor was not clearly demonstrated by angiography and selective arterial calcium injection. We considered that extended surgical procedures such as pancreatoduodenectomy might be required depending on intraoperative findings; therefore, open abdominal surgery rather than laparoscopic surgery was scheduled. Her intact parathyroid hormone level was 66.0 pg/ml (normal value: 10–65 pg/mL) and her adjusted serum calcium level was 10.3 mg/dL (normal value: 8.7–9.9 mg/dL), although parathyroid ultrasound examination revealed no parathyroid tumor. Other tumors complicated with MEN-1 were not detected. The results of other preoperative examinations were unremarkable. On the day before surgery, an Enlite™ sensor of MiniMed™ 620G (Medtronic Diabetes, Northridge, CA, USA) SCGM system was inserted into her upper arm. Although MiniMed 620G was combined with an insulin pump, we did not use the pump. The SCGM system was calibrated as recommended by the manufacturer with capillary BG measured by OneTouch® UltraVue™ Blood Glucose Meter (Johnson & Johnson, New Brunswick, NJ, USA).
No premedication was given and she walked into the operating room. Capillary BG was 80 mg/dL and the SCGM system was calibrated. Continuous glucose infusion was started at 4.6 g/hr, and general anesthesia was induced with 80 mg of propofol, 50 mcg of fentanyl, and 0.02 mcg/kg/min of remifentanil. Muscle relaxation was obtained by administration of 30 mg of rocuronium, and the trachea was intubated. After induction of general anesthesia, an epidural catheter was inserted at the eighth and ninth thoracic interspace. Anesthesia was maintained with 1.7% sevoflurane, 0.01–0.02 mcg/kg/min of remifentanil, and intermittent thoracic epidural administration of 0.25% levobupivacaine (3 ml). An arterial catheter was inserted, and arterial BG measured by an ABL800 Flex Blood Gas Analyzer (Radiometer, Brea, CA, USA) was 71 mg/dL, which was compatible with IG of 73 mg/dL. An additional 2 g of glucose was given intravenously before the start of surgery, and IG increased from 77 mg/dL to 101 mg/dL at 20 minutes (). After that, IG mildly decreased and returned to almost the same level after 1 hour. The surgeon informed us that the tumor would be removed by enucleation shortly. Just before tumor resection, arterial BG was 76 mg/dL and IG was 80 mg/dL. At 20 minutes after tumor resection, IG showed a rapid increase. We therefore decreased the continuous glucose infusion rate to the usual dose of 1 g/hr, and IG gradually decreased and was stabilized at about 140 mg/dL. During surgery, blood pressure was between 90/50 and 120/70 mmHg, and heart rate was between 60 and 90 bpm. She was extubated in the operating room and transferred to the general surgery ward. The operation time was 2 h and 24 min, and the anesthesia time was 3 h and 53 min. Postoperative pain was controlled well by continuous epidural analgesia (12 mcg of fentanyl and 0.2% levobupivacaine at 4 ml/hr) and administration of 600 mg of acetaminophen (every 6 hr). Her postoperative course was uneventful and she was discharged on POD 10.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [144.0, 'cm'], 'weight': [40.0, 'kg']}",19.29012,18.32561,20.25463,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 144.0 cm, which is 144.0 cm * 1 m / 100 cm = 1.44 m. The patient's weight is 40.0 kg. The patient's bmi is therefore 40.0 kg / (1.44 m * 1.44 m) = 19.29012 kg/m^2."
2533,6,Body Mass Index (BMI),physical,decimal,pmc-4555212-1,Extracted,"A 65-year-old Japanese woman was admitted to our hospital for the evaluation of rapidly progressive renal dysfunction. At the age of 60 years (April 2000), hypertension was detected, and treatment with amlodipine was started. Subsequently, proteinuria (41 mg/dl) was noted, and serum creatinine (Cre) was 0.94 mg/dl. On September 3, 2005, edema of the bilateral lower extremities was noted with exacerbation of hypertension (200/110 mm Hg). She was admitted to hospital 2 days later on September 5.
On admission, her height was 154 cm, her weight was 48.2 kg, her blood pressure was 152/92 mm Hg, and her temperature was 35.9°C. No enlarged lymph nodes were palpable. Inspiratory and expiratory sounds were normal on auscultation. Both neurological examination and cutaneous examination revealed no abnormalities. There was pitting edema of the bilateral lower extremities. Laboratory findings are shown in table . Urea nitrogen was 41 mg/dl, and Cre was 2.7 mg/dl. CRP was 0.1 mg/dl, and the erythrocyte sedimentation rate was 53 mm/h. Soluble interleukin-2 receptor was elevated to 1,680 U/ml (normal range: 250–590). Urine sediment contained 6–10 erythrocytes per high-power field. Examination of a 24-hour urine specimen revealed excretion of 1.51 g of protein.
Computed tomography showed a normal liver and spleen with no lymphadenopathy. Both kidneys were small with a long axis of 9 cm bilaterally (fig. ). Echogenicity of the renal cortex was increased on ultrasonography (fig. ). Scintigraphy with 67Ga-citrate only showed positive uptake by the kidneys.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [154.0, 'cm'], 'weight': [48.2, 'kg']}",20.32383,19.30764,21.34002,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 154.0 cm, which is 154.0 cm * 1 m / 100 cm = 1.54 m. The patient's weight is 48.2 kg. The patient's bmi is therefore 48.2 kg / (1.54 m * 1.54 m) = 20.32383 kg/m^2."
2534,6,Body Mass Index (BMI),physical,decimal,pmc-4402179-1,Extracted,"A 49-year-old retired male was admitted to the physical therapy outpatient clinic with severe back pain. From the history, it was learned that he had an acute back pain in the morning with no trauma. On the day before presentation, he had suffered a witnessed nocturnal attack, of which he had no recollection. The patient was oriented normally on arrival and reported that he had not experienced any previous nocturnal attacks like this, which was confirmed by his wife. The attack was described by his wife as follows: he started to lock his jaw, stiffened, was sweating, convulsed, and became unconscious. The duration of the seizure was about 3 minutes. Following the seizure he was briefly postictal, during which time his wife noted decreased movement of his arms and lower extremities. She reported that after the seizure he slept again and, in the morning, he had a back pain. There was no history of trauma, previous falls, prior seizures, stroke, syncope, or steroid medication. In the absence of a history of trauma, an epileptic seizure was suspected. It was learned that he had a 23-year history of Type I diabetes mellitus. For the last 20 years, he had required Humulin R three times daily (11 IU/at morning, noon, and evening), and Lantus once a day (22 IU/at midnight). Further medical history was not relevant and the patient had no history of epilepsy. The patient was not using antiepileptic drugs (AED) or corticosteroids at that time. The cardiovascular and neurological examination results were normal. There were signs of a bitten tongue. The patient had complaints of dorsal vertebrae pain, which was determined by palpation on the dorsal vertebrae during physical examination.
Vital signs were noted as follows: blood pressure: 125/80 mm/Hg, heart rate: 75/min., temperature: 36.5°C, respiratory rate: 18/min., weight; 70 kg., and height: 1.78 cm. Basic blood examination was normal except for severely raised fasting blood glucose: 216 mg/dL (65–107 mg/dL), slightly raised urea: 54 mg/dL (15–44 mg/dL), ALP: 146 U/L (30–120 U/L), and hemoglobin A1c: 6.7% (4.0–6.5%). Thoracic magnetic resonance imaging (MRI) was applied to evaluate the severity of the injury. Acute phase compression fractures on T5 (loss of 50% of vertebral height) and on T6, T7, and T8 vertebrae were determined and an additional slightly increased risk of thoracic kyphosis was reported ().
For further evaluation, the patient was referred to the Neurology Department. In addition to basic studies, detailed investigations showed normal levels of parathyroid hormone, 25-hydroxy-vitamin D3, thyroid-stimulating hormone, free T3, free T4, cortisol, vitamin B12, and folate levels. Serum levels of calcium and phosphate were also within normal limits. Investigations for epilepsy were performed. An electroencephalogram (EEG) and a cerebral MRI showed no abnormalities. The patient was referred to the Orthopaedic Department, where he was treated conservatively. At the first follow-up examination, Dual Energy X-ray Absorptiometry (DEXA) was applied to rule out major osteoporosis due to diabetes. The T scores were as follows: femoral neck: −1.5, trochanter: −1.1, total: −1.2, lumbar (L) 1: −3.1, L2: −3.3, L3: −3.5, L4: −3.7, and total: −3.4. The DEXA reported osteopenia and osteoporosis on the right hip and in the lumbar spine, respectively. The osteopenia in the femoral region and osteoporosis in the lumbar region were treated with a single dose zoledronic acid 4 mg/5 mL intravenous infusion (for 1-year treatment), calcitonin 200 IU 1 × 1, and active vitamin D 0.25 mcg 1 × 1. Bed rest was applied for 3 weeks after the initial diagnosis, and then a thoracolumbar orthosis was used for 4 months (). The patient started taking bisphosphonate at the time of diagnosis, and still continues to date. After 2 months, the patient was able to walk confidently with assistance. He made a rapid recovery and minimal deformity and little disability remained. At the most recent follow-up (17 months from the initial diagnosis), he had no complaints of back pain. Written informed consent was obtained from the patient for publication of this case report and the accompanying images.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [1.78, 'cm'], 'weight': [70.0, 'kg']}",220931.7005,209885.1155,231978.2856,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.78 cm, which is 1.78 cm * 1 m / 100 cm = 0.0178 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (0.0178 m * 0.0178 m) = 220931.70054 kg/m^2."
2535,6,Body Mass Index (BMI),physical,decimal,pmc-3891032-1,Extracted,"A 62-year-old man was admitted due to his recent jaundice and abdominal distention. He was diagnosed about 2 years ago with gastric adenocarcinoma and he underwent radical subtotal gastrectomy. After surgery, he received five cycles of adjuvant chemotherapy with 5-FU and leucovorin. A physical examination showed his height to be 170 cm and the body weight was 68 kg. The condition of the chest and heart was normal. His vital signs were within normal limits. His sclera was deep icteric, but he showed neither hepatomegaly nor right upper quadrant tenderness. The neurological examination was normal. There were no specific findings on the occupational, familial and social histories. The laboratory tests on admission showed an elevated level of serum total bilirubin to 10.9 mg/dL (normal level: 0.3~1.2 mg/dL), a direct bilirubine of 8.5 mg/dL (normal level: 0~0.2 mg/dL), alanine aminotransferase of 374 U/L (normal level: 10~40 U/L), alkaline phosphatase of 480 U/L (normal level: 20~100 U/L) and lactate dehydrogenase of 2,133 U/L (normal level: 208~378 U/L). An abdominal and pelvic CT scan was performed to verify the biliary obstruction and metastatic lesions in the abdominal cavity, including the liver and biliary system. CT scan of the abdomen showed multiple metastatic nodules in the liver with no evidence of biliary tree obstruction (). The diagnosis of the patient was confirmed to be recurrent gastric cancer with advanced liver metastases and severe hepatic dysfunction. His performance status was estimated to be ECOG 2. Given his poor liver function, the patient was treated with oxaliplatin (130 mg/m2) on day 1 and capecitabine (1,000 mg/m2 orally twice daily) on days 1~14 of a 21-day cycle. After the first cycle of chemotherapy, his total bilirubin dropped to 4.5 mg/dL. After two cycles of chemotherapy, his total bilirubin and alkaline phosphatase decreased to near normal levels at 2.1 mg/dL and 116 U/L, respectively. No treatment-related grade 3 or above toxicities were noted during the first 4 cycles of treatment. He continued to well tolerate chemotherapy with excellent performance and normalization of all the liver enzymes ( and ). He displayed a major radiological response on the follow-up CT scans (); he has received 5 cycles of XELOX with ongoing clinical benefit.",What is the patient's body mass mass index (BMI)? Your answer should be in terms of kg/m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'height': [170.0, 'cm'], 'weight': [68.0, 'kg']}",23.52941,22.35294,24.70588,"The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 170.0 cm, which is 170.0 cm * 1 m / 100 cm = 1.7 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.7 m * 1.7 m) = 23.52941 kg/m^2."
2536,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2847727-1,Extracted,"A 32-year-old male presented with acute abdominal pain, reduced urine output and red urine since three days. No fever, vomiting or bowel or bladder symptoms were observed. The pain in the abdomen was diffuse and more as discomfort, which started following a jerk while the patient was traveling in a bus. No prior history of diabetes, hypertension or renal disease was reported.
Investigations conducted in a local hospital had revealed numerous red blood corpuscles (RBCs) and white blood corpuscles (WBCs) in urine sediment and 4 + proteinuria. Ultrasound showed moderate ascites. Plain computed tomography (CT) of the abdomen showed hepatomegaly with ascites. Serum creatinine measured the following day was high (4.0 mg/dl); hence, an opinion from a nephrologist was sought.
Upon examination, he was anxious and hemodynamically stable. The lungs were clear and abdominal distension and ascites was present. Pedal edema was absent. Following are the reports of the investigation carried out: hemoglobin, 17.6 g/dl; total leucocyte count, 20100 cells/m3; differential count polymorphs, 79%; lymphocytes, 17%; eosinophils and monocytes, 2% each; urine showed 3 + protein; 6-8 WBCs and numerous RBCs; arterial blood gas analysis pH, 7.31; bicarbonate, 10.8 meq/l; pCo2, 22.2 mmHg; blood urea nitrogen (BUN), 60 mg/dl; creatinine, 5.9 mg/dl; sodium, 131 meq/l; potassium, 5.1 meq/l; calcium, 8.6 mg/dl; phosphorus, 6.7 mg/dl; uric acid, 10.2 mg/dl; total bilirubin, 0.3 mg/dl; protein, 8.0 g/dl; albumin, 4.2 g/dl; serum glutamic-oxaloacetic transaminase (SGOT), 38 u/l; serum glutamic-pyruvic transaminase (SGPT), 25 u/l; alkaline phosphatase (ALP), 96 u/l.
We suspected intraperitoneal rupture of the urinary bladder because of the abrupt onset of symptoms. We performed catheterization of the urinary bladder, draining 3.5 l of hemorrhagic fluid. Abdominal distension began to regress and the patient started feeling relieved after this drainage. Cystogram showed leakage of the contrast into the peritoneal cavity []. Ascitic fluid creatinine and urea nitrogen approximated the values that are usually observed in urine samples rather than in blood (86 mg/dl and 425 mg/dl, respectively).
Following this confirmation, the patient underwent emergency laparotomy. A 5-mm tear was found in the dome of bladder, which was repaired in two layers. He was maintained on indwelling urethral and suprapubic Foley catheters. Within 24 h, the biochemical abnormalities in the patient improved to normal.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.2, 'g/dL'], 'Calcium': [8.6, 'mg/dL']}",8.44,8.018,8.862,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.2 g/dL. 
The concentration of Calcium is 8.6 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.2 g/dL)) + 8.6 mg/dL = 8.44 mg/dL.
The patient's corrected calcium concentration 8.44 mg/dL."
2537,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6037803-3,Extracted,"An 18-year-old girl presented with fatigue, anorexia, indigestion, constipation, and postprandial abdominal pain. She was diagnosed with cecal diverticulosis 5 years earlier, and Helicobacter pylori (HP)-positive gastric ulcer 1 year earlier. A previous UGI endoscopic examination showed no polyp in her stomach. On laboratory examination, WBC was 8,200/mm3, with polymorphonuclear cell 65%, hemoglobin 13.6 g/dL, and platelet count 205×103/mm3. Electrolytes levels showed sodium 142 mmol/L, potassium 4.4 mmol/L and chloride 106 mmol/L. The protein level was 7.4 g/dL, albumin 4.7 g/dL, calcium 9.3 mg/dL, phosphorus 4.7 mg/dL, cholesterol 167.9 mg/dL, glucose 99 mg/dL, BUN 10.1 mg/dL, creatinine 0.77 mg/dL, total bilirubin 0.35 mg/dL, AST 14 U/L, ALT 5 U/L, ESR 10 mm/hour, and CRP <0.3 mg/dL. UGI endoscopy revealed nodular gastritis in the antrum and a polyp of sessile type in the prepyloric area. Polypectomy was performed. The size of the polyp was 0.8×0.6×0.5 cm. She was negative to HP at the time of polypectomy. The pathological finding was HPP (). She was treated with medicines for her UGI mucosal lesions and the previous GI symptoms were resolved. Follow-up UGI endoscopy would be performed in one year.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.7, 'g/dL'], 'Calcium': [9.3, 'mg/dL']}",8.74,8.303,9.177,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.7 g/dL. 
The concentration of Calcium is 9.3 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.7 g/dL)) + 9.3 mg/dL = 8.74 mg/dL.
The patient's corrected calcium concentration 8.74 mg/dL."
2538,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6325030-1,Extracted,"A 79-year-old asymptomatic Caucasian male presented with progressive renal failure with abnormal serum creatinine (range of 1.82 to 2.18) in July 2012. Complete blood count (CBC) showed red blood cell count (RBC) of 3.36 x 108/uL, hemoglobin 10.9 g/dl, hematocrit 33.1%, mean corpuscular volume (MCV) 99 fL, mean corpuscular hemoglobin (MCH) 32.8 pg, mean corpuscular hemoglobin concentration (MCHC) 33.0%, red cell distribution width (RDW) 15.8% and white blood cell count (WBC) 4,000/uL, with differentials: neutrophils 50%, lymphocytes 37%, monocytes 8%, eosinophils 4%, basophils 1% and platelet count of 178,000/uL. Comprehensive metabolic profile (CMP) revealed: glucose 96 mg/dL, blood urea nitrogen 23 mg/dL, creatinine 2.18 mg/dL, sodium 140 mmol/L, potassium 4 mmol/L, chloride 107 mmol/L, carbon dioxide 25 mmol/L, albumin 4.4 g/dL, calcium 9.1 mg/dL, bilirubin (total) 0.8 mg/dL, phosphorus 3.3 mg/dL and magnesium 2.7 mg/dL. Computed tomography (CT)-guided needle biopsy of the left kidney showed severe lymphocytic inflammation mainly in the areas of tubular atrophy and interstitial fibrosis (Figure ).
Immunohistochemical staining showed atypical lymphocytes that were positive for CD20 and negative for CD5, CD10, CD19, CD22 and CD23. Molecular testing revealed an Ig heavy chain gene rearrangement; these findings were consistent with marginal zone B cell lymphoma. Furthermore, immunofluorescence (IF) microscopy demonstrated seven glomeruli with diffuse pseudo-linear staining of the glomerular capillary loops for albumin (1+). Glomerular staining for IgG, IgA, IgM, C3, C1q and kappa or lambda light chain was negative. Interstitium stained positive for fibrinogen, while protein casts were stained positive for IgA (3+), kappa light chain (3+) and lambda light chain (3+). By electron microscopy (EM), the glomerular basement membrane had a normal trilaminar structure, the mean thickness was within the normal range without electron-dense deposits or tubuloreticular inclusions and the majority of podocytes foot processes were intact (Figure ). No immune complexes were detected by IF or EM.
On serum protein electrophoresis (SPEP) and immunofixation, we found IgM kappa monoclonal gammopathy and serum M-protein level of 0.3 g/dL. Quantitative immunoglobulin testing was performed for IgG (699 mg/dL), IgA (51 mg/dL) and IgM (470 mg/dL). Serum free light chain (SFLC) showed kappa (37.9 mg/L), lambda (1.58 mg/L) and kappa/lambda ratio of 23.99. Urine protein electrophoresis (UPEP) showed a protein level of 91 mg/dL and M-spike of 18.1%. Bone marrow (BM) biopsy showed 30% BM involvement by clonal B cells, morphologically consistent with marginal zone B cell lymphoma. Positron emission tomography (PET) scan was found normal in 2012 and 2013. The patient was treated with five doses of weekly rituximab and one dose of rituximab-bendamustine combination, but renal function worsened and treatment was stopped in 2013. The patient was monitored closely without further treatment until 2017. PET scan (2017) showed a mild enlargement of the retroperitoneal lymph nodes (aortocaval from 1 x 0.8 to 1.4 x 1.2 cm, left periaortic from 1.4 x 0.5 to 1.3 x 1.0 cm) and a partially calcified subcarinal node from 3.1 x 1.1 to 3.5 x 1.5 cm (non-avid), and the spleen size increased from 12.2 to 14.2 cm in cubic centimeter dimension (Figure ). One dose of vincristine and prednisone was given at that time, but renal function declined further. The patient was offered bortezomib/dexamethasone or ibrutinib for further treatment consideration, which he declined.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.4, 'g/dL'], 'Calcium': [9.1, 'mg/dL']}",8.78,8.341,9.219,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.4 g/dL. 
The concentration of Calcium is 9.1 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.4 g/dL)) + 9.1 mg/dL = 8.78 mg/dL.
The patient's corrected calcium concentration 8.78 mg/dL."
2539,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7947728-1,Extracted,"A three-year-old Afghan boy was admitted to our hospital with a history of recurrent seizures since the age of two years. The first seizure was reported to be fever-induced at the age of four months. Cognitive and motor development was normal until the age of one, but thereafter neurodevelopmental decline was reported. He had been having generalized tonic-clonic seizures since the age of two years. The diagnosis of epilepsy was made in another center because of recurrent seizures and multiple antiepileptic drugs were started. He has been treated with levetiracetam, clonazepam, valproic acid, and pyridoxine treatments. The patient was admitted to our hospital from Afghanistan for further evaluation for recurrent seizures and hypocalcemia. He was born at full-term gestation after an uncomplicated pregnancy including an absence of polyhydramnios with a birth weight of 3500 gr from a consanguineous family (first degree cousins). His prenatal and natal history was uneventful. His family history was unremarkable. His family history was negative for epilepsy and neurological abnormalities, as well as any known renal, thyroid, or parathyroid disease. Physical examination revealed his growth parameters were within normal limits [height: 95 cm (25-50 p), weight: 15 kg (50-75 p)]. He did not show any dysmorphic or neurocutaneous features. He was conscious and had a speech delay. Bilateral horizontal nystagmus was prominent. He was hypotonic with normal reflexes. The rest of the physical examination was normal. Laboratory data included a serum Mg2+ level of 0.12 mmol/L (normal range: 0.7-0.86 mmol/L), calcium 4.7 mg/dL, phosphorus 6.2 mg/dL, alkaline phosphatase 222 U/L, parathyroid hormone 6 pg/mL (normal range: 11-67 pg/mL), 25-OH vitamin D3 60.1 ng/mL, sodium 139 mEq/L, potassium 4.24 mEq/L, albumin 3.2 g/dL, and uric acid 5.3 mg/dL. The urine fractional excretion of Mg2+ was 12% (normal range: <4%) with normal urine calcium/creatinine ratio. Laboratory examinations including acute phase reactants, serum glucose, and albumin levels, and liver and renal function tests were normal. The renal ultrasound did not show any medullary nephrocalcinosis. Electroencephalogram showed slow background activity without any epileptiform discharges and magnetic resonance imaging of brain showed mild diffuse cerebral and cerebellar atrophy ().
Laboratory examination revealed the characteristic combination of severe hypomagnesemia, hypoparathyroidism, and profound hypocalcemia. Clinical and laboratory findings together suggested the diagnosis of HSH as responsible for disruption in Mg2+ homeostasis. The genetic analysis of the patient revealed a novel, homozygous variant in the TRPM6 gene (NM017662.4: c.5473_5474insGCTTC (p.H18225Rfs*18) (p.His1825Argfs*18). This is a frameshift variant and based on American College of Medical Genetics and Genomics criteria this variant was classified as pathogenic. This is a null variant and is predicted to cause severe loss of gene function. TRPM6 gene sequence analysis was performed using MiSeq next generation sequencing platform, an Food and Drug Administration approved diagnostic system (Illumina Inc., San Diego, CA, USA). Sequences were aligned to the hg 19 genome within MiSeq Reporter software (Illumina Inc.). Visualization of the data was performed with IGV 2.3 (Broad Institute-www.software.broadinstitute.org) software (). Informed consent was obtained from the parents for genetic analysis. The parents were heterozygotes for the same variant.
Intravenous Mg2+ sulfate was administered at 50 mg/kg along with intravenous calcium for three days after which the serum Mg2+ increased and calcium levels normalized. The treatment was switched to oral Mg2+ sulfate 4x2000 mg (~533 mg/kg/d) but abdominal pain and diarrhea was significant. In addition, on this oral therapy, serum Mg2+ decreased to 0.2 mmol/L and convulsions re-occurred without hypocalcemia. The treatment was replaced with oral Mg2+ citrate and soon after switched again to Mg2+ carbonate because of persistent hypomagnesemia and gastrointestinal side-effects. Finally, Mg2+ oxide sachets were started and blood Mg2+ reached 0.78 mmol/L with high dose Mg2+ oxide (3x2 sachets ~ 150 mg/kg/d) (). Antiepileptic treatment was reduced. His muscle tone, cognitive development, and motor development improved. He has been stable on an oral maintenance dose of 2000 mg of Mg2+ oxide daily with borderline blood Mg2+ levels without hypocalcemia.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.2, 'g/dL'], 'Calcium': [4.7, 'mg/dL']}",5.34,5.073,5.607,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.2 g/dL. 
The concentration of Calcium is 4.7 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.2 g/dL)) + 4.7 mg/dL = 5.34 mg/dL.
The patient's corrected calcium concentration 5.34 mg/dL."
2540,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4421520-1,Extracted,"Mrs B, a 52-year-old female, presented to the hospital with chief complaints of vomiting, loss of appetite and swelling feet of 3 months duration. There was no history of oliguria, dysuria, haematuria or lithuria. She had no obstructive urinary symptoms. There was no fever or drug abuse prior to the onset of these symptoms. The patient denied any history of rash or joint pains. The family history was not significant. She had one child who was normal. Physical examination was unremarkable but for pallor and hypertension [blood pressure (BP) of 160/90 mmHg]. All peripheral pulses were well felt. Complete urine examination revealed trace protein and no red blood cells. Blood biochemistry showed serum creatinine 9 mg/dL (686.24 mmol/L), blood urea 180 mg/dL (128.52 mmol/L), serum sodium 138 mmol/L, serum potassium 4.4 mmol/L, serum calcium 8.8 mg/dL (2.2 mmol/L), serum phosphorus 4.9 mg/dL (1.58 mmol/L), serum bilirubin 0.8 mg/dL (13.68 µmol/L), serum aspartate amino transferase (AST) 13 U/L, serum alkaline phosphatase 140 U/L, plasma proteins 66 g/L, plasma albumin 40 g/L, haemoglobin 80 g/L, total leucocyte count 8.9 × 109/L and platelet count 350 × 109/L. Ultrasound examination showed a right kidney measuring 9.3 cm and a left kidney measuring 9.8 cm with a grade 2 echotexture. There were no cysts in any other organs. Computed tomography (CT) scan showed an altered echotexture in the renal cortices with sparing of medullary pyramids. The patient received two sessions of haemodialysis with blood transfusion. Subsequently, a renal biopsy was performed which showed features of glomerulocystic disease (). The patient subsequently was initiated on maintenance dialysis.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [40.0, 'g/L'], 'Calcium': [8.8, 'mg/dL']}",8.8,8.36,9.24,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 40.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 40.0 g Albmumin/10.0 dL = 4.0 g Albmumin/dL. The concentration value of 40.0 g Albmumin/L converts to 4.0 g Albmumin/dL. 
The concentration of Calcium is 8.8 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.0 g/dL)) + 8.8 mg/dL = 8.8 mg/dL.
The patient's corrected calcium concentration 8.8 mg/dL."
2541,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-8478360-1,Extracted,"An 82-year-old man was brought to our emergency department after he was found lying unresponsive on the floor of his house. At the hospital, the patient reported having decreased oral intake, nausea, malaise, abdominal discomfort and decreased urinary output. His medical history was significant for hypertension, type II diabetes mellitus, abdominal aortic aneurysm, hyperlipidemia, congestive heart failure, deep venous thrombosis, pulmonary embolism, and chronic back pain. His medications included ibuprofen, oxycodone, gabapentin, atorvastatin, losartan, carvedilol, furosemide, ticagrelor, apixaban, pioglitazone, insulin glargine, sitagliptin, tamsulosin and escitalopram. He had no known allergies.
On examination, vitals revealed a temperature of 36.8oC, blood pressure of 113/68 mmHg, pulse of 65 beats/minute and a respiratory rate of 18 breaths/minute. Physical examination was unremarkable except for bilateral lower extremity pitting edema. Laboratory findings included a hemoglobin of 11.6 g/dL (reference range [RR] 14 - 18 g/dL), serum creatinine of 11.6 mg/dL (RR; 0.7 - 1.3 mg/dL), blood urea nitrogen (BUN) of 119 mg/dL (RR; 7 - 18 mg/dL), serum potassium of 6.0 mMol/L (RR; 3.5 - 5.1 mMol/L), estimated glomerular filtration rate (EGFR) of 4 mL/min/1.73m2 (RR > OR = 60 mL/min/1.73m2), serum phosphorus of 3.9 mg/dL (RR; 2.5 – 4.9 mg/dL), serum calcium at 9.2 mg/dL (RR; 8.6 - 10.3 mg/dL), albumin at 3.7 g/dL (RR; 3.4 – 5 g/dL), serum uric acid at 10.5 mg/dL (RR; 2.6 – 6 mg/dL) and a serum creatinine phosphokinase (CPK) at 327 U/L (RR; 26 – 192 U/L). Two months earlier, his serum creatinine was at 1.06 mg/dL, BUN at 14 mg/dL and EGFR>60 ml/min/1.73m2. Spot urinalysis revealed clear light-yellow urine with a specific gravity of 1.010 without any protein. The urine did not show significant white blood cells, red blood cells and was also negative for nitrites and leukocyte esterase. No urine casts were identified, and no eosinophils were noted. A catheter was inserted and urine sample from the catheter showed a spot urine microalbumin to creatinine ratio at 287.6 mg/g. Serum complement C3 and C4 levels were normal. Renal ultrasound demonstrated increased echogenicity throughout the kidneys, likely related to intrinsic medical renal disease without any hydronephrosis or nephrolithiasis.
On the third day of the admission, a renal biopsy was performed which showed global sclerosis in 2/9 examined glomeruli without any significant changes in the mesangium. The glomerular basement membrane was unremarkable. The main findings were in the tubulointerstitial compartment which showed evidence of tubular damage and tubulitis (A-D). The tubules appeared simplified and lined by flattened cells. There were scattered inflammatory cells in the interstitium which were a combination of eosinophils and mononuclear cells and were associated with active tubulitis. Some of the tubules appeared to be dilated and contained hyaline casts but no myelomatous casts were seen. There was a moderate degree of thickening of the walls of the arterioles along with the small and medium sized arteries. Immunofluorescence demonstrated linear tubular basement membranes with positive staining for lambda light chain (3+). In contrast, kappa light chain stain was essentially negative (E and F). Electron microscopy (EM) revealed interstitial edema and inflammation without any immune complexes, fibrillary material, or light chain deposits in the tubulointerstitial compartment (). No proliferation of lysosomes or atypical lysosomes were identified in the damaged proximal tubules. Increased numbers of lysosomes, a few atypical, were seen in selected proximal tubules. These findings were found to be consistent with ATIN. This raised the suspicion for a monoclonal lambda light chain-related tubulointerstitial process.
The findings on the biopsy prompted us to pursue the workup for multiple myeloma. We obtained a plasma protein electrophoresis which showed a peak in the beta-1 globulin zone and a monoclonal lambda protein was identified by immunofixation. Serum free light chains showed an elevated lambda up to 9503 mg/L and an almost normal kappa of 24.53 mg/L. Bence Jones protein was present in the urine. Given the significant lambda light chain burden, a diagnosis of monoclonal lambda light chain-related ATIN was made. Bone marrow biopsy and aspirate showed a plasma cell neoplasm with lambda light chain restriction (A and B). Prussian blue stains of the biopsy revealed adequate iron storage (C). CD138 was positive in increased numbers of plasma cells representing approximately 50% of the marrow cellularity (D). Fluorescence in situ hybridization (FISH) analysis was also performed using a set of probes specific to multiple myeloma. Plasma cell enrichment was performed revealing various abnormalities including: 13q14 deletion (1R2G, 66.0%, normal < 11.9%), an atypical IgH gene rearrangement/partial gene deletion (1R, 64.8%, not seen in validation studies), and a gain in chromosome 1q (CKS1B) (3R2G 67.0%, normal < 8.6%). Counts for the remaining probes were within the normal reference range. No lytic lesions were seen on the bone survey. Laboratory tests were repeated showing a white blood cell count of 12.4 x 103 /μL (RR; 4.8 - 10.8 x 103/μL), red blood cell count of 2.7 x 106 /μL (RR; 4.63 - 6.08 x 103/μL), hemoglobin of 8.6 g/dL (RR; 14 - 18 g/dL), hematocrit 25.6% (RR; 42 - 52%), MCV 91.8 fL (RR; 79.0 - 92.2 fL), RDW 13.7% (RR; 11.5 - 15.0%), and platelets 182 x 103 /μL (RR; 150 - 450 x 103/μL). The diagnosis of multiple myeloma was hence confirmed.
During hospitalization, the patient received plasmapheresis and one cycle of CyBor-D (Cyclophosphamide, bortezomib and dexamethasone). At the time of discharge (day 20 of the admission) serum creatinine was at 6.2 mg/dL, BUN at 100 mg/dL and the EGFR at 9 ml/min/1.73m2. One week after discharge, lambda free light chain was noted to be 3107 mg/dL. The patient completed his second cycle of CyBorD as an outpatient but failed to return for scheduled follow-ups. He was readmitted to our hospital 2 months later for a community acquired pneumonia complicated with respiratory failure requiring intubation and pressor support. During this hospitalization, his mentation worsened; he had episodes of cardiac arrhythmias with worsening kidney function. The patient’s family decided to transfer him to hospice. At the time of writing our case report, the patient had already died ().","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.7, 'g/dL'], 'Calcium': [9.2, 'mg/dL']}",9.44,8.968,9.912,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.7 g/dL. 
The concentration of Calcium is 9.2 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.7 g/dL)) + 9.2 mg/dL = 9.44 mg/dL.
The patient's corrected calcium concentration 9.44 mg/dL."
2542,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4534955-1,Extracted,"A 16-year old man was admitted to the Department of Internal Medicine of Dongsan Medical Center with the chief complaint of hematochezia. He had suffered on 4–5 occassions from hematochezia and dizziness for 5 months. About 1 month prior to admission, he complained of a large amount of diarrhea (3–4 times a day) and swelling of the face and lower extremities. Eight years previously he underwent an operation for intestinal intussusception. Family history revealed that his father and younger sister also had pigmentation of the lips and oral mucosa, palms, and soles at birth ().
On physical examination, the patient appeared to be chronically ill. His blood pressure was 100/60mmHg, pulse rate 76/minute, respiration rate 20/minute, and temperature 36.9°C. The face was puffy and the conjunctiva was pale. There were multiple, dark blue colored pigmentations of the lips, buccal mucosa, palms, and soles () and especially onychodystrophy such as a longituidinally ridged, spoon-like deformity and distortion in all fingernails (), and pitting edema of the lower extremities. The other parts were normal.
The laboratory findings on admission were as follows: hemoglobin 5.9g%, hematocrit 19.0%, WBC count 9100/mm3) with 60% neutrophils, serum iron 6ug/dl, TIBC 174 ug/dl, ferritin Ong/ml, total protein 3.2g%, albumin 1.2g%, calcium 6.4mg%, inorganic phosphorus 5.0g%, sodium 142 m Eq/L, and potassium 3.3m Eq/L. Fecal occult blood test was positive.
The x-ray film of the upper GI tract, small intestine series and barium enema revealed variable sized, scattered, grouped, multiple polyps in the C loop of the duodenum, proximal jejunum, and from the rectum to the ascending colon (). Endoscopy of the upper GI tract and rectosigmoid showed red colored, variable sized, grouped, multiple polyps in the first portion of the duodenum to the distal (), and in the rectum at 12cm, 15cm, and 18cm from the anal verge.
The culture and semar of nail scrapings were negative for fungi.
The microscopic finding of specimens taken from rectal polyps showed hamartomatous polyps with cystic dilatation of glands and containing smooth muscle bundle supports, epithelial proliferation and infiltration of plasma cells, lymphocytes, and neutrophils (). The microscopic finding of specimens taken from duodenal polyps also showed Peutz-Jehgers polyps with columnar and goblet cells in the superficial portion and some inflammatory cell infiltration.
During admission, the patient was treated with blood transfusion, albumin infusion, and iron tablet medication, thereafter he was discharged with improvement. At present he is in good general condition with disappearance of the onychodystrophy, edema of face and lower extremities, and he showed improvement in laboratory tests during the OPD follow up check. His father and sister also revealed similiar findings of the upper GI tract, small intestine series, barium enema, and endoscopy without hypoproteinemia, hypokalemia, and onychodystrophy. The microscopic findings of rectal polyps showed hamartomatous polyps having smooth muscle fibers from muscularis mucosa and chronic inflammatory cell infiltration without cystic dilated glands (). The younger sister developed two segmental intestinal intussusceptions in the proximal and distal jejunum, one at a time, and underwent an operation recently.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [1.2, 'g/dL'], 'Calcium': [6.4, 'mg/dL']}",8.64,8.208,9.072,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 1.2 g/dL. 
The concentration of Calcium is 6.4 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.2 g/dL)) + 6.4 mg/dL = 8.64 mg/dL.
The patient's corrected calcium concentration 8.64 mg/dL."
2543,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2481241-1,Extracted,"A 52-year-old white male with O2-dependent COPD, hypertension, GERD, idiopathic gastroparesis, and chronic low back pain was noted to have persistent hypokalemia in the 2.7–3.3 meq/L range over more than 2 years. He complained also of chronic generalized weakness and fatigue. He denied nausea or vomiting, but did have occasional loose stools. The hypokalemia persisted despite discontinuation of diuretic treatment for hypertension and fludrocortisone that had been prescribed briefly for orthostatic hypotension. There was no improvement with aggressive oral potassium supplementation in amounts up to 120 meq per day. The patient's serum potassium level normalized on three occasions when he was hospitalized and given supplemental potassium (COPD exacerbations in 7/06 and 1/07, pseudoseizures in 7/07), but the hypokalemia promptly recurred after discharge from the hospital (Figure ). His medications were paroxetine, trazodone, pregabalin, sustained-release morphine, loratadine, isosorbide mononitrate, lisinopril, metoprolol, simvastatin, omeprazole, metoclopramide, potassium chloride, calcium/vitamin D tablets, alendronate, and mometasone, tiotropium, and albuterol inhalers. He smoked one-half pack of cigarettes per day and did not drink alcohol.
On physical examination, he was a chronically ill-appearing man wearing a nasal cannula. Height was 69 inches, weight 205 pounds. There were no cushingoid facies, buffalo hump, or abdominal striae. Vital signs were temperature 98.6 degrees, pulse 95, respiratory rate 14, blood pressure 128/73. There was no thyromegaly or lymphadenopathy. Lungs showed decreased breath sounds and mild expiratory wheezes bilaterally. Heart sounds were regular with no murmurs, rubs, or gallops. The abdomen was soft and non-tender, with no masses or organomegaly. Extremities showed no edema, clubbing or cyanosis. The neurologic examination revealed mild generalized muscular weakness (4+/5) and normal deep tendon reflexes.
Laboratory results include serum sodium 137 mg/dL, potassium 3.0 mg/dL, chloride 95 mmol/L, CO2 30.0 mmol/L, blood urea nitrogen 5 mg/dL, creatinine 0.8 mg/dL, calcium 9.3 mg/dL, phosphorus 4.1 mg/dL, albumin 3.6 g/dL, ferritin 126 ng/mL, hemoglobin 12.7 g/dL, white blood cell count 10.6 K/cmm, and platelet count 160 K/cmm. Serum aldosterone was 4.8 ng/dL (normal 4–31 ng/dL) and the plasma renin activity was 0.33 ng/mL/hr (normal 1.31–3.96 ng/mL/hr upright, 0.15–2.33 ng/mL/hr supine). Spot urine potassium was 8.6 mEq/L, urine sodium was < 10 mEq/L, and urine chloride was 16 mmol/L.
In the absence of a clear explanation for this patient's chronic hypokalemia, he was asked to give the details of his diet. He admitted to drinking 4 liters of Pepsi-Cola per day for the past several years. It was his habit to sip cola slowly but almost continuously, throughout the day. When hospitalized, he had stopped drinking cola and his potassium levels had temporarily normalized. In early May 2008, he decreased his cola intake to 2 liters per day, with a resultant increase in the serum potassium from 3.0 to 3.5 mg/dL (Figure ).","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.6, 'g/dL'], 'Calcium': [9.3, 'mg/dL']}",9.62,9.139,10.101,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.6 g/dL. 
The concentration of Calcium is 9.3 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.6 g/dL)) + 9.3 mg/dL = 9.62 mg/dL.
The patient's corrected calcium concentration 9.62 mg/dL."
2544,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6791640-1,Extracted,"A 71-year-old white man presented with hypertension and ileocolonic stricturing CD since 1974. He had undergone 3 surgeries including ileocecectomy and 2 small bowel resections in 1975, 1986, and 2007. Current medications include 6-mercaptopurine, amlodipine, metoprolol, vitamin D, calcium, and a multivitamin. He was previously treated with sulfasalazine and oral mesalamine. He sparingly required oral steroids throughout his life. In October 2018, he presented for a 5-month history of worsening watery diarrhea and unintentional weight loss. Stool studies, including Clostridium difficile, were negative. Colonoscopy to the neoterminal ileum revealed a Rutgeerts score of i3. He was started on oral budesonide as a bridge to biologic therapy.
After starting 9 mg of budesonide, the patient immediately began to experience weakness and muscle aches. Three weeks later, these symptoms progressed and he was unable to walk or lift his arms above his head. He presented to the hospital, and laboratory tests revealed magnesium 0.8 mg/dL, potassium 1.7 mmol/L, creatinine 1.52 mg/dL, creatine phosphokinase 15,913 IU/L, calcium 7.1 mg/dL, albumin 3.7 g/dL, aspartate aminotransferase 253 U/L, alanine aminotransferase 125 U/L, and lactate dehydrogenase 734 IU/L. Urinalysis showed 3+ blood and 0–3 red blood cells. Laboratory values 2 months before were unremarkable, despite having chronic diarrhea for several months (Table ). He was diagnosed with rhabdomyolysis. Intravenous fluids and electrolyte replacement were initiated. The patient felt that the onset of symptoms correlated with the initiation of budesonide, so the medication was held. Over the course of the week, his symptoms improved drastically and ultimately resolved, correlating with creatine phosphokinase and potassium improvement. He followed up 3 weeks later, asymptomatic and with normal laboratory values (Table ).","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.7, 'g/dL'], 'Calcium': [7.1, 'mg/dL']}",7.34,6.973,7.707,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.7 g/dL. 
The concentration of Calcium is 7.1 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.7 g/dL)) + 7.1 mg/dL = 7.34 mg/dL.
The patient's corrected calcium concentration 7.34 mg/dL."
2545,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,usmle-9340,Extracted,"A 69-year-old African American man is brought to the emergency department with sudden onset lower limb paralysis and back pain. He has had generalized bone pain for 2 months. He has no history of severe illnesses. He takes ibuprofen for pain. On examination, he is pale. The vital signs include: temperature 37.1°C (98.8°F), pulse 68/min, respiratory rate 16/min, and blood pressure 155/90 mm Hg. The neurologic examination shows paraparesis. The 8th thoracic vertebra is tender to palpation. An X-ray of the thoracic vertebrae confirms a compression fracture at the same level. The laboratory studies show the following:
Laboratory test
Hemoglobin 9 g/dL
Mean corpuscular volume 95 μm3
Leukocyte count 5,000/mm3
Platelet count 240,000/mm3
ESR 85 mm/hour
Serum
Na+ 135 mEq/L
K+ 4.2 mEq/L
Cl− 113 mEq/L
HCO3− 20 mEq/L
Ca+ 11.5 mg/dL
Albumin 4 g/dL
Urea nitrogen 18 mg/dL
Creatinine 1.2 mg/dL
Serum electrophoresis shows a monoclonal protein level of 38 g/L.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.0, 'g/dL'], 'Calcium': [11.5, 'mg/dL']}",11.5,10.925,12.075,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.0 g/dL. 
The concentration of Calcium is 11.5 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.0 g/dL)) + 11.5 mg/dL = 11.5 mg/dL.
The patient's corrected calcium concentration 11.5 mg/dL."
2546,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6037803-1,Extracted,"A 15-year-old girl presented with recurrent abdominal pain for 6 years. Initial laboratory workup revealed a white blood cell count (WBC) of 5,000/mm3 with 66% neutrophils, hemoglobin level of 12.7 g/dL, and platelet count of 202×103/mm3. Electrolytes levels showed sodium 143 mmol/L, potassium 4.6 mmol/L and chloride 108 mmol/L. The total protein level was 7.0 g/dL, albumin 4.1 g/dL, calcium 9.1 mg/dL, phosphorus 3.5 mg/dL, cholesterol 123.5 mg/dL, glucose 91 mg/dL, blood urea nitrogen (BUN) 7.7 mg/dL, creatinine 0.69 mg/dL, total bilirubin 0.50 mg/dL, aspartate aminotransferase (AST) 15 U/L, alanine aminotransferase (ALT) 7 U/L, amylase 52 U/L, lipase 52 U/L, erythrocyte sedimentation rate (ESR) 2 mm/hour, and C-reactive protein (CRP) <0.3 mg/dL. Trace elements panel was normal. UGI endoscopy showed gastric ulcer in the prepyloric area, verrucous gastritis in the body, and reflux esophagitis of grade A. Colonoscopy revealed no definite mucosal lesion, but a solitary polyp was noted in the rectum. Additionally, multiple cystic lesions were found on pelvic ultrasonography, but these were not considered the direct cause of her chronic abdominal pain. Medical treatment was administered for her UGI mucosal lesions. The rectal polyp was removed using cold snare. The size of polyp was 0.5×0.3×0.2 cm. Pathological examination of the excised polyp revealed that it was a tubular adenomatous type, which is known to be a precancerous lesion (). Her abdominal symptoms improved after polypectomy, although her chronic GI symptoms did not seem to be related to the polyp. Following the diagnosis, tumor marker tests (CA-125, αFP, β-HCG) were performed, and they were normal. The follow-up colonoscopy was performed in one year showed normal mucosal finding in the area of the previous polypectomy.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.1, 'g/dL'], 'Calcium': [9.1, 'mg/dL']}",9.02,8.569,9.471,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.1 g/dL. 
The concentration of Calcium is 9.1 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.1 g/dL)) + 9.1 mg/dL = 9.02 mg/dL.
The patient's corrected calcium concentration 9.02 mg/dL."
2547,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6284267-1,Extracted,"A 9-year-old male English Setter presented with a 6-month history of ulceration of the left upper eyelid as the only clinical finding (Fig. a). On examination, the lesion was round, elevated, and well circumscribed. A malignant eyelid tumour was suspected, and the lesion was excised for histopathological examination. A fine-needle aspirate was obtained from a popliteal lymph node from the left side. The popliteal lymph node was chosen, as the owner did not want any expensive diagnostic procedures and the popliteal lymph node was the easiest accessible. The dog was doing well and presented without fever, clinical signs of anaemia, or weight loss. A routine blood profile was unremarkable except for a haematocrit (packed cell volume, PCV) of 37%, which is borderline low. The blood test also showed a serum calcium: 2.43 mmol/L (ref 1.98–3.0 mmol/L), serum albumin: 31 g/L (ref 23–40 g/L), serum alkaline phosphatase: 53 U/L (ref 23–213 U/L), and serum creatinine: 91 µmol/L (ref 44–159 µmol/L). Serum sodium, potassium, chloride, and glucose were also within normal limits. C-reactive protein (CRP) was < 10 mg/L, which is also normal. The owner did not want additional examinations or treatments other than excision of the tumour and for this reason, a thoracic radiograph, abdominal ultrasound, and a full haematological profile were not performed. No systemic treatment was initiated, and 2 months after surgery an unremarkable full haematological profile was obtained. 19 months after the diagnosis the dog was still alive and doing well with no signs of relapse.
The specimen was fixed in 10% neutral buffered formalin immediately after surgical excision, processed and embedded in paraffin. Sections (4 µm) were prepared and stained with haematoxylin and eosin according to standard protocols. Furthermore, sections were routinely stained with periodic acid-Schiff (PAS), Gram stain, and Gomori’s methenamine silver stain (GMS) to detect microorganisms. Giemsa staining was performed to visualize the blood derived cells in the specimen.
Immunohistochemical stainings were performed on a Ventana Benchmark Ultra Platform (Ventana Medical Systems, Tucson, AZ, USA) according to manufacturer’s instructions. The following antibodies were used: CD3 [clone 2GV6, code 790-4341, rabbit anti-human, ready-to-use (RTU), Roche (Hvidovre, Denmark)], PAX-5 [clone SP34, code 790-4420, rabbit anti-human, RTU, Roche (Hvidovre, Denmark)], vimentin [clone V9, code 790-2917, mouse anti-human, RTU, Roche (Hvidovre, Denmark)], and Ki-67 (clone MIB-1, code M724001, mouse anti-human, 1:100, Dako). Positive and negative controls were performed according to the manufacturers’ instructions.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [2.43, 'mmol/L'], 'Albumin': [31.0, 'g/L']}",10.459,9.93605,10.98195,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 31.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 31.0 g Albmumin/10.0 dL = 3.1 g Albmumin/dL. The concentration value of 31.0 g Albmumin/L converts to 3.1 g Albmumin/dL. 
The concentration of Calcium is 2.43 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 2.43 mmol. To convert 2.43 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 2.43 mmol Calcium * 0.001 mol/mmol = 0.00243 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00243 mol Calcium * 40.08 g/mol = 0.09739 g Calcium. To convert 0.09739 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.09739 g Calcium * 1000.0 mg/g = 97.39 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 97.39 mg Calcium/10.0 dL = 9.739 mg Calcium/dL. The concentration value of 2.43 mmol Calcium/L converts to 9.739 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.1 g/dL)) + 9.739 mg/dL = 10.459 mg/dL.
The patient's corrected calcium concentration 10.459 mg/dL."
2548,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-8360739-1,Extracted,"A 13-year-old boy presented to the pediatric emergency department with bilateral leg pain after an unwitnessed fall onto the street from the sidewalk. There was no history of major trauma, syncope, or seizure. He had severe autism spectrum disorder (ASD) with poor verbal skills. On examination, he was crying and had tenderness over the bilateral knees and right ankle. The range of motion of the hip and knee was limited by pain. There were no bony deformities. Lower extremity X-rays revealed acute comminuted and impacted fractures of the bilateral distal femoral metaphyses with anterolateral apical angulation of the distal fracture fragments (Figures and ). Diffuse osteopenia was noted, but no other radiographic signs of rickets were seen, including metaphyseal widening, splaying, cupping, fraying, or prominence of the costochondral junctions on chest X-ray.
On physical examination, his height was at the 4th percentile (appropriate with his midparental target height at the 10th percentile). His weight was at the 52nd percentile and his body mass index (BMI) at the 87th percentile, meeting the criteria for overweight. His physical exam, apart from his limited lower extremity movement, was remarkable for a positive Chvostek sign, early Tanner stage 3 development with 8 cc testes descended bilaterally, and vertical fingernail ridges. Skin examination was negative for bruising, acanthosis, and striae. The differential diagnosis included vitamin D deficiency, malabsorptive disorder (i.e., celiac disease or inflammatory bowel disease), osteogenesis imperfecta, prolonged steroid use, renal failure, hypothyroidism, and juvenile osteoporosis.
Initial laboratory investigations revealed a serum calcium of 4.9 mg/dL with serum albumin of 4.4 g/dL. An ionized calcium of 0.61 mmol/L confirmed hypocalcemia. Parathyroid hormone (PTH) was elevated at 280.7 pg/mL and there was evidence of severe deficiency in both 25(OH)D (<4 ng/mL) and 1,25(OH)2D (17.8 pg/mL). Nutritional labs revealed a low vitamin A, vitamin B12, vitamin B6, and zinc as described in . There were notable coagulopathies, with deficiencies in factors II (73%), V (27%), and VII (37%). Other labs revealed an elevated alkaline phosphatase of 290 ug/L and normal thyroid function with a normal thyroid-stimulating hormone (TSH) of 1.137 uIU/mL, free thyroxine of 0.8 ng/dL, and total thyroxine of 6.1 ug/dL. Renal function showed normal creatinine (0.5 mg/dL) and blood urea nitrogen (9.0 mg/dL). Erythrocyte sedimentation rate was normal (<1 mm/hr) and a celiac screen was negative (tissue transglutaminase IgA antibody <2 U/mL with normal IgA of 120 mg/dL). Urine calcium-to-creatinine ratio was low at 0.01 mg/dL. An electrocardiogram revealed a prolonged QTc of 498 milliseconds.
The patient did not have a history of apparent numbness, weakness, muscle cramps, or bone pain. In the prior few months, however, he was noted to go down steps with two feet, one step at a time, and this had been a change in behavior. He was raised in the Northeast United States in New York and was of Hispanic ethnicity. His mother described him as a picky eater. On further dietary recall, he was noted to eat potato chips, French fries, corn, crackers, pizza without cheese, and chicken nuggets. He mainly drank ginger ale and apple juice. His lifestyle was sedentary with most time spent indoors or riding on the train. There was no personal or family history of metabolic bone disease. He had no history of prolonged steroid use.
Given his hypocalcemia, treatment was initiated with intravenous calcium gluconate 2 grams every 2-3 hours with a goal total calcium of greater than 8 mg/dL so that he would be stable for orthopedic surgery. After 48 hours of intravenous calcium treatment, he underwent bilateral antegrade nailing of the bilateral femurs. He was started on vitamin D3 50,000 international units once weekly. Postoperatively, enteral calcium carbonate of 100 mg/kg/day divided every 6 hours was ordered. However, due to his refusal to take enteral calcium, a nasogastric tube was placed and his dose was increased to 120 mg/kg/day divided every 8 hours. Total calcium levels continued to improve and enteral calcium was slowly weaned to 60 mg/kg/day divided twice daily. By the day of discharge, his calcium level had improved to 9.9 mg/dL and 25(OH)D concentration improved to 13 ng/mL. He was discharged to a rehabilitation center for further feeding therapy and physical therapy.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [4.9, 'mg/dL'], 'Albumin': [4.4, 'g/dL']}",4.58,4.351,4.809,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.4 g/dL. 
The concentration of Calcium is 4.9 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.4 g/dL)) + 4.9 mg/dL = 4.58 mg/dL.
The patient's corrected calcium concentration 4.58 mg/dL."
2549,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4964692-1,Extracted,"A 6-year-old boy presented with progressively increasing swelling over the body for 3 months, decreased urine output for 2 months; fever, cough, and respiratory distress for 6 days. There was no history of hematuria, dysuria, palpitations, chest pain, or jaundice. He had taken some treatment irregularly for these complaints, details of which were not known. On examination, he had severe respiratory distress due to pulmonary edema. His pulse rates were 155/min with all peripheral pulses well palpable; respiratory rates were 62/min with intercostal and subcostal recessions. He was anemic, hypertensive (blood pressure – 140/86, >99th centile) and had generalized anasarca and abdominal wall cellulitis. There was no jaundice, rash, arthritis, lymphadenopathy, or organomegaly. Systemic examination revealed bilateral basal crepts; there was tachycardia, but no murmur.
Investigations revealed anemia (hemoglobin [Hb] 6.3, microcytic hypochromic type), neutrophilic leukocytosis (total leukocyte count 14,800 with neutrophilia 87%) and renal dysfunction (blood urea 283 mg/dl, serum creatinine 3.9 mg/dl). The serum albumin levels were 1.6 gm/dl, cholesterol levels were 185 mg/dl and triglycerides of 472 mg/dl. The liver function tests were normal with a serum bilirubin of 0.3 mg/dl, alanine aminotransferase 14 IU/L and aspartate aminotransferase of 28 IU/L. The serum sodium levels were 143 mEq/L and potassium 5.9 mEq/L, total calcium 7.9 mg/dl, phosphates 3.6 mg/dl and SAP 181 IU/L. The venous blood gas showed mild acidosis (bicarbonate levels 16.7 mEq/L). The urine examination showed nephrotic range proteinuria with microscopic hematuria and 8–10 WBC/hpf. Radiology revealed pulmonary edema on chest radiograph and minimal pericardial effusion on echocardiography. A diagnosis of rapidly progressive glomerulonephritis with abdominal wall cellulitis was made, and the child started on intravenous antibiotics, furosemide and antihypertensives.
In view of worsening renal functions and hyperkalemia, hemodialysis was initiated. The child received two blood transfusions. Further investigations revealed that antinuclear antibody and anti-streptolysin-O-antibody were negative, complement levels (C3) were low and the serology was positive for hepatitis B (hepatitis B surface antigen, hepatitis B e antigen [HBeAg] and anti-hepatitis B core antibody [IgG anti HBc] positive; and anti-HBeAg negative; DNA titers for viral load could not be done due to nonavailability). The anti-hepatitis C virus and anti-human immunodeficiency virus (HIV) antibodies were negative. The renal biopsy showed features of collapsing glomerulopathy []. The light microscopy showed 18 glomeruli of which 10 showed glomerular capillary tuft collapse, three were segmentally sclerosed and five appeared unremarkable. The interstitium showed edema and a diffuse 30–40% of the tubulointerstitial compartment showed chronic parenchymal changes with blood vessels having mild medial sclerosis. Immunofluorescence showed nonspecific deposition of C3, IgM (2+), IgG, IgA. Hepatitis B antigen deposits were present in the glomerular tufts. Based on these findings and the serology report, a diagnosis of hepatitis B associated collapsing glomerulopathy was made. The child was started on lamivudine; was continued on diuretics and antihypertensives. After 2 weeks of antibiotic therapy the child improved and became dialysis independent. After 1 month of hospital stay the child was discharged on iron, calcium supplements, lamivudine and antihypertensives (amlodepine and furosemide). His blood urea and creatinine levels were 114 mg/dl and 1.9 mg/dl, respectively at discharge. At 6 months follow-up, the child was normotensive, with minimal edema and his kidney function test were urea of 86 mg/dl and creatinine 1.1 mg/dl. The serum albumin was still low (1.6 g/dl) and Hb had improved to 10 g/dl. Subsequently, the child has been lost to follow-up.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [1.6, 'g/dL'], 'Calcium': [7.9, 'mg/dL']}",9.82,9.329,10.311,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 1.6 g/dL. 
The concentration of Calcium is 7.9 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.6 g/dL)) + 7.9 mg/dL = 9.82 mg/dL.
The patient's corrected calcium concentration 9.82 mg/dL."
2550,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7522849-2,Extracted,"Case 2 involved a 52-year-old man who was admitted to our emergency department on 31 May 2015 with a 3-day history of upper abdominal pain with blood in the stool, accompanied by nausea and vomiting. Physical examination on arrival at our hospital revealed only tenderness in the lower right abdomen; the remaining physical examination was unremarkable. On laboratory testing, routine blood parameters were unremarkable except that the lymphocyte ratio (10.7%) and hemoglobin level (115 g/L) were slightly low, and liver and kidney function tests showed a low albumin level (27 g/L) and calcium level (1.82 mmol/L); blood coagulation parameters and the procalcitonin level were both unremarkable. Abdominal enhanced CT showed concentric changes from the ileocecal region to ascending colon (). Abdominal ultrasound (US) revealed concentric circles in the right abdomen. Finally, partial enterectomy was performed. Postoperative histopathologic examination showed angiolipoma of the terminal ileum. During the 3-year follow-up, the patient showed no recurrence.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [27.0, 'g/L'], 'Calcium': [1.82, 'mmol/L']}",8.335,7.91825,8.75175,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 27.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 27.0 g Albmumin/10.0 dL = 2.7 g Albmumin/dL. The concentration value of 27.0 g Albmumin/L converts to 2.7 g Albmumin/dL. 
The concentration of Calcium is 1.82 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.82 mmol. To convert 1.82 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.82 mmol Calcium * 0.001 mol/mmol = 0.00182 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00182 mol Calcium * 40.08 g/mol = 0.07295 g Calcium. To convert 0.07295 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.07295 g Calcium * 1000.0 mg/g = 72.95 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 72.95 mg Calcium/10.0 dL = 7.295 mg Calcium/dL. The concentration value of 1.82 mmol Calcium/L converts to 7.295 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.7 g/dL)) + 7.295 mg/dL = 8.335 mg/dL.
The patient's corrected calcium concentration 8.335 mg/dL."
2551,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7158116-1,Extracted,"The patient was a 47-year-old female with no history of trauma who developed bilateral hip pain 1 day prior to admission. She had a history of haemodialysis due to polycystic kidney disease. Upon physical examination, she demonstrated inability to move the hip joints and bilateral inguinal tenderness. Laboratory studies showed anaemia (haemogram 8.5 g/dL), a low normal albumin value (3.1 g/dL), a high parathyroid hormone level (907 pg/ml), hypocalcaemia (5.1 mg/dL), hyperphosphatemia (2.3 mmol/L), and elevated alkaline phosphatase activity (1228 U/dL). Hip X-ray (Fig. a) and CT (Fig. b, Fig. c) examinations showed bilateral femoral displaced fractures. Bone mineral density testing revealed osteoporosis (T = 3.0). She also had a history of hyperparathyroidism secondary to CKD and parathyroidectomy.
We promptly performed a multidisciplinary team consultation to make preoperative preparations and performed the surgery 4 days after admission. Considering her mobility and life expectancy, we performed concurrent bilateral hip hemiarthroplasty with cement prostheses (Fig. d). The operative findings included severe osteoporosis and displaced femoral neck fractures. Anti-osteoporosis medication was administered after surgery. Meanwhile, the patient continued maintenance haemodialysis. Three days after the operation, she could ambulate with a walker. The follow-up appointments at 3 and 6 months revealed that the woman had gradually regained her previous ability to walk.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.1, 'g/dL'], 'Calcium': [5.1, 'mg/dL']}",5.82,5.529,6.111,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.1 g/dL. 
The concentration of Calcium is 5.1 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.1 g/dL)) + 5.1 mg/dL = 5.82 mg/dL.
The patient's corrected calcium concentration 5.82 mg/dL."
2552,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6753394-1,Extracted,"We present a case of multiple bilateral rib fractures in association with sternal fracture and thoracic kyphosis who developed a severe acute respiratory insufficiency complicating the initial presentation of multiple myeloma.
A 56-year-old man presented to Hematological Department after he had been experiencing worsening back pain over the last five months, with easy fatigability, and progressive weight loss. He had no history of previous trauma.
Hypertension and mellitus diabetes, both under pharmacological treatment.
At intake, his blood pressure was 130/70 mmHg; pulse rate 70 beats/min; respiratory rate 14/min and body temperature 35.7 °C.
Blood chemical test results were as follows: creatinine 4.22 mg/dL; glomerular filtration rate 15 mL/min; calcium 15.9 mg/dL and hemoglobin 6.7 g/dL. Serum β2-microglulin level was elevated at 9.42 mg/L and serum albumin level was 2.7 g/dL. The diagnosis of Kappa -light chain Bence-Jones multiple myeloma was established on the basis of a bone marrow infiltration by 66% atypical plasmatic cells and a monoclonal component kappa in serum (86 mg/dL) and in urine with a proteinuria of 2.9 g/24 h. Urine was positive for Bence-Jones proteins
A radiographic bone survey of all major bones revealed, in addition to multiple bilateral rib fractures (4th to 11th), the presence of a sternal fracture and compression fracture at T9, T10, T11 and L1 vertebrae. The thoracic computed tomography (CT) scan confirmed a depressed pathological fracture of the sternum (Figure ).
With the results of the different tests, the patient was diagnosed with multiple myeloma. It was staged as Durie-Salmon stage IIIB and International Staging System IIIB. Subcutaneous fat biopsy was positive for amyloid.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.7, 'g/dL'], 'Calcium': [15.9, 'mg/dL']}",16.94,16.093,17.787,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.7 g/dL. 
The concentration of Calcium is 15.9 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.7 g/dL)) + 15.9 mg/dL = 16.94 mg/dL.
The patient's corrected calcium concentration 16.94 mg/dL."
2553,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6119788-1,Extracted,"A 72-year-old Japanese woman presented to our hospital for further examination because of a high fever, diarrhea, intermittent spotting into urine-absorbing pads, and constant fluid discharge from the vagina. The patient had been taking Lactobacillus preparation, potassium chloride, vitamin D analogue, vitamin B12, vitamin B complex, and iron sulfate for diarrhea and subsequent malabsorption. Warfarin was also prescribed for deep vein thrombosis of the lower limbs. She underwent radical hysterectomy and radiotherapy for the treatment of carcinoma of the uterine cervix 35 years previously. After the treatment of cervix cancer, she developed bilateral hydronephrosis and multiple episodes of ileus. Thus, right percutaneous nephrostomy, left nephrectomy, ileoascending anastomosis, and colostomy in the transverse colon were performed (Figure ). These treatments caused radiation colitis and short bowel syndrome, resulting in diarrhea, malabsorption, and protein-losing enteropathy.
Physical examination revealed anemia and leg edema. Laboratory examinations revealed anemia (red blood cell count, 266 × 104/mm3 and hemoglobin, 8.4 mg/dL), hypoproteinemia (total protein, 4.5 g/dL and albumin, 1.0 g/dL), hypokalemia (potassium, 2.5 mmol/L), hypocalcemia (calcium, 6.6 mg/dL), and hypophosphatemia (phosphorus, 2.1 mg/dL). A slight elevation in the C-reactive protein level was noted (1.73 mg/dL), whereas the white blood cell count was decreased (3180/mm3; neutrophil, 74.0%).
Although fistula formation was suspected as a cause of intermittent blood spotting and constant fluid discharge from the vagina, computed tomography (CT) scanning with contrast media, colonoscopy, and video capsule enteroscopy examinations were nondiagnostic. The patient accidentally slipped and fell on the floor and hit her hip. Subsequently, massive bleeding from the vagina occurred, and pelvic examinations by a gynecologist revealed enterovaginal fistulas. A colposcopy examination using a videoscope (GIF TYPE PQ260; Olympus) showed two fistulas with active bleeding (Figure A-C). Contrast medium (meglumine sodium amidotrizoate) was injected into the fistulas via the videoscope, and CT scanning confirmed the fistula formations between the ileum and vagina (Figure D,E). As the bleeding was uncontrollable, ileocecal resection was performed. Discharge of the blood and fluid resolved postoperatively.
Three months postoperatively, she presented with a low-grade fever. Urinalysis revealed bacteriuria, and Klebsiella pneumoniae and Serratia species were detected by urine culture. A CT scan showed fluid collection in the pelvic cavity (Figure A). Colonoscopy from the anus revealed mucosal edema (Figure B) and stricture (Figure C) of the sigmoid colon. After the injection of contrast medium, a fistula in the bladder was visualized (Figure D, arrowhead), in addition to the pooling of contrast medium in the descending colon (Figure D,E, arrows). Consequently, a colovesical fistula was diagnosed. The urinary tract infection because of the fistula was conservatively treated with an injection of cefmetazole. The patient has been free from infection-related symptoms for 4 months even after discontinuing the antibiotic treatment.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [1.0, 'g/dL'], 'Calcium': [6.6, 'mg/dL']}",9,8.55,9.45,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 1.0 g/dL. 
The concentration of Calcium is 6.6 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.0 g/dL)) + 6.6 mg/dL = 9.0 mg/dL.
The patient's corrected calcium concentration 9.0 mg/dL."
2554,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4177611-3,Extracted,"A 53-year-old Caucasian male presented with a one-month history of chest wall and back pain, and right-sided leg weakness and pain. Past medical history was significant for HIV infection and AIDS diagnosed about 27 years ago. He had a history of cytomegalovirus (CMV) retinitis, rectal condylomata, and toxoplasmosis, and he had been taking Atripla® over the last 2 decades. His CD4 count had been >1000/μl and HIV viral load undetectable. Computed tomography (CT) and magnetic resonance imaging (MRI) studies revealed enhancing soft tissue lesions involving the posterolateral right 8th rib and the posterior left 12th rib; fracture of the left posterior 7th rib; lytic lesions involving the thoracic (T) 4, T12, and lumbar (L)1 vertebral bodies, and a large lesion involving the right sacroiliac joint. CT guided biopsy of the right sacroiliac mass revealed plasma cell neoplasm with κ light chain restriction. His WBC was 8.65 × 109/L, hemoglobin 12 g/dl, platelet count 433× 109/L, serum creatinine 1.0 mg/dl, albumin 2.6 g/dl, and serum calcium 10.4 mg/dl. SPEP and IFE demonstrated an IgG κ M-protein at 1.64 g/dl. Bone marrow biopsy and aspiration revealed κ light chain restricted- plasma cells at 10%. FISH analysis showed 1 extra copy of 1q and a 13q14 deletion. The patient was diagnosed with MM (Stage III by International Staging System) with extensive medullary plasmacytoma. He continued his HAART and was treated with 6 cycles of VCd regimen (bortezomib, cyclophosphamide and dexamethasone). He also received a total of 30 Gy fractioned irradiation of the spine and the iliac crests. Due to the concern of possible progression in bony lytic lesions, his chemotherapy regimen was switched to VRd (bortezomib, lenalidomide and dexamethasone). After 3 cycles of VRd, the patient achieved a very good partial response. Because of the aggressiveness of his MM, the patient then underwent high dose chemotherapy and autologous hematopoietic stem cell transplant (HSCT). He received pegfilgrastin for stem cell mobilization and successfully collected 8.3 × 106 CD34+ cells/kg body weight with only one-day leukapheresis. He received high dose melphalan (200 mg/m2) conditioning and autologous HSCT. His HSCT was relatively uneventful. He had an appropriate count recovery, and restaging at 3 months post HSCT showed no evidence of M-protein in SPEP and UPEP.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.6, 'g/dL'], 'Calcium': [10.4, 'mg/dL']}",11.52,10.944,12.096,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.6 g/dL. 
The concentration of Calcium is 10.4 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.6 g/dL)) + 10.4 mg/dL = 11.52 mg/dL.
The patient's corrected calcium concentration 11.52 mg/dL."
2555,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5624136-1,Extracted,"23-year-old female presented to the Emergency Room with carpopedal spasms and tingling numbness in hands. Patient endorsed tingling sensation in hand since a month which was intermittent and unrelated to wrist movement. She denied history of preceding trauma and swelling in hands. There was no history of similar complaints in the past or any prior surgery. She denied complaints like nausea, vomiting, and diarrhea. Tingling in hands was not associated with paresthesia in other extremities and sensory or motor deficits. Patient was a known case of multidrug resistant tuberculosis and was being treated with the following drugs for two months: amoxicillin-clavulanate, ethionamide, intramuscular capreomycin, linezolid, and para-aminosalicylate (PAS) granules. Patient was afebrile and her initial vital signs were normal with a pulse of 78/min and blood pressure of 110/76 mm of Hg. On examination, flattening of chest wall on the left side was noted. Trail's sign was positive with a deviation of the trachea to the left side. On auscultation of lung fields, breath sounds were diminished on the left. These findings suggested presence of tuberculous fibrosis in the left lung. No other stigmata of TB were noted and rest of the physical examination was unremarkable.
Initial blood-work at the time of presentation revealed a low serum calcium level of 6.98 mg/dL. Patient was hospitalized and detailed investigations were done. Coexisting with hypocalcemia, other electrolyte abnormalities noted were as follows: serum sodium of 130 mEq/L, potassium of 1.8 mEq/L, chloride of 95 mEq/L, calcium of 6.98 mg/dL, and magnesium of 0.5 mg/dL. Serum albumin was 4 g/dL. Serum creatinine was normal and remained so throughout the course of hospitalization. The arterial blood gas evaluation showed metabolic alkalosis without respiratory compensation with pH of 7.5, HCO3 of 30 mEq/L, and PaCO2 of 30 mmHg. Routine urine examination revealed a 2–4 pus cells, 1-2 RBCs, and 1-2 epithelial cells, in the absence of proteinuria and glycosuria. Urine calcium/creatinine ratio was 0.49 (>0.2), which confirmed hypercalciuria. Urinary prostaglandin-E level was not performed as this assay is not readily available in our institute.
Vitamin D and serum parathyroid levels were found to be in the normal range, thus ruling out hypovitaminosis D and secondary hyperparathyroidism, respectively. Patient was treated symptomatically; injectable calcium, magnesium, and potassium were administered to correct electrolyte abnormalities. Due to the association of aminoglycoside antibiotics with alterations in electrolyte levels, capreomycin was discontinued. Subsequently, the electrolytes started to rise after two days of stopping capreomycin (). Patient was discharged once her symptoms resolved and the serum electrolytes were normalized. On follow-up, there were no complains of tingling sensations or carpopedal spasms and electrolytes remained to be in the normal range.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.0, 'g/dL'], 'Calcium': [6.98, 'mg/dL']}",6.98,6.631,7.329,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.0 g/dL. 
The concentration of Calcium is 6.98 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.0 g/dL)) + 6.98 mg/dL = 6.98 mg/dL.
The patient's corrected calcium concentration 6.98 mg/dL."
2556,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5646314-1,Extracted,"A 51-year-old male with a past medical history of HIV, COPD, and hypertension presented with a four-day history of fever, shortness of breath, and nonproductive cough associated with headache and reduced appetite. He had a 30-pack-year history of smoking cigarettes and had not been compliant with his HIV medications as well as trimethoprim-sulfamethoxazole. He had no history of nonsteroidal anti-inflammatory drug (NSAID), herbal drug, or cocaine use. He denied recent ill contacts, recent travel, or camping. On examination, he was in respiratory distress with blood pressure 143/95 mmHg, pulse 135 beats per minute, respiratory rate 24 breaths per minute, temperature 39.5 degrees Celsius, and sPO2 92% on room air and 98% on 2 litres nasal cannula. He had bronchial breath sounds in the left mid and lower lung fields with crackles, but no wheezing. His heart sounds were normal. Abdomen was soft and nontender, with normal bowel sounds. Other aspects of his examination were unremarkable.
His white cell count was 4.6 (4.5–11 × 103/uL); haemoglobin was 10.7 (12–16 g/dL); platelet was 246 (140–440 thou/cu mm); mean corpuscular volume was 94 (82–101 fl); Prothrombin Time (PT) was 12.9 (11–13.5 seconds); international normalised ratio (INR) was 1.0 (0.8–1.2); partial thromboplastin time (PTT) was 34 (25–35 seconds); HbA1c was 5.7% (4–5.6%); procalcitonin was 31.2 ng/mL (<0.15 ng/mL); thyroid stimulating hormone (TSH) was 0.705 (0.27–4.2 uIU·ml); sodium was 137 (135–145 mmol/L); potassium was 4.5 (3.3–4.6 mmol/L); chloride was 95 (101–110 mmol/L); BUN was 56 (6–22 mg/dL); creatine was 6.98 (0.6–1.17 mg/dL); calcium was 7.8 (8.6–10 mg/dL); albumin was 2.6 (3.8–4.9 g/dL); phosphorus was 5.5 (2.5–4.5 mg/dL); aspartate aminotransferase was 789 (14–33 IU/L); ALT was 235 (10–42 IU/L); anion gap was 22 (4–16); direct bilirubin was 3.3 (0–0.2 mg/dL); indirect bilirubin was 0.4 mg/dL (0.2–1.2 mg/dL); total bilirubin was 3.7 (0.2–1.0 mg/dL); alkaline phosphatase was 66 (40–129 IU/L); total creatine kinase was 51092 U/L (22–195 U/L), and urine was positive for myoglobin. His CD 4 count was 41 cells/ul, and HIV viral load was 34900 copies/mL.
Urine analysis with Alere BinaxNOW lateral flow immunochromatographic assay for Legionella antigen serogroup 1 was positive; urine pneumococcal antigen was negative; blood culture, respiratory culture, and urine culture were without bacterial growth; respiratory viral panel was reported negative for influenza, parainfluenza, rhinovirus, respiratory syncytial virus (RSV) virus, human metapneumovirus, H1, and H3.
His electrocardiogram showed sinus tachycardia. Chest X-ray (CXR) showed a homogenous consolidation in the left lower lung field (). CT chest showed consolidation in the left lingual with air bronchograms consistent with lobar pneumonia, without pleural effusion (Figures and ). Echocardiograph showed a left ventricular ejection fraction of 65%. Renal ultrasound showed normal sized kidneys with normal echogenicity without hydronephrosis.
He was diagnosed with Legionella pneumonia, rhabdomyolysis, and acute renal failure and started on levofloxacin and atovaquone. He became further oliguric, with rising creatine and BUN, with worsening respiratory status requiring intubation and ventilation in addition to dialysis which were commenced on the second day of admission. Azithromycin was added to his antibiotic regimen in the ICU. His maximum creatine was 13.04 mg/dL, and BUN was 153 mg/dL during his hospital course. His respiratory and renal function improved during his ICU stay. He was extubated after six days. With improvement in his urine output and renal indices; he no longer required dialysis. On discharge, after 28 days of hospital stay and seven days of ICU stay, his creatine was 2.6 md/dL, BUN 36 md/dL, total creatine kinase (CK) 69 U/L, aspartate aminotransferase (AST) 16 IU/L, alanine aminotransferase (ALT) 30 IU/L, direct bilirubin 0.1 mg/dL, indirect bilirubin 0.1 mg/dL, and total bilirubin 0.2 mg/dL. After three-weeks follow-up in the outpatient setting, his creatine was back to normal at 1.06 (0.6–1.17 mg/dL), with resolution of the chest X-ray consolidation (). Renal biopsy was not pursued in light of recovery of normal renal function.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [7.8, 'mg/dL'], 'Albumin': [2.6, 'g/dL']}",8.92,8.474,9.366,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.6 g/dL. 
The concentration of Calcium is 7.8 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.6 g/dL)) + 7.8 mg/dL = 8.92 mg/dL.
The patient's corrected calcium concentration 8.92 mg/dL."
2557,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,usmle-2638,Extracted,"A 17-year-old boy is brought to the physician by his father because of a 7-month history of fatigue, recurrent leg cramps, and increased urinary frequency. His pulse is 94/min and blood pressure is 118/85 mm Hg. Physical examination shows dry mucous membranes. Laboratory studies show:
Serum
Na+ 130 mEq/L
K+ 2.8 mEq/L
Cl- 92 mEq/L
Mg2+ 1.1 mEq/L
Ca2+ 10.6 mg/dL
Albumin 5.2 g/dL
Urine
Ca2+ 70 mg/24 h
Cl- 375 mEq/24h (N = 110–250)
Arterial blood gas analysis on room air shows a pH of 7.55 and an HCO3- concentration of 45 mEq/L.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [5.2, 'g/dL'], 'Calcium': [10.6, 'mg/dL']}",9.64,9.158,10.122,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 5.2 g/dL. 
The concentration of Calcium is 10.6 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 5.2 g/dL)) + 10.6 mg/dL = 9.64 mg/dL.
The patient's corrected calcium concentration 9.64 mg/dL."
2558,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-8383680-1,Extracted,"A 27-year-old woman with a past medical history of diabetes type 1 associated with latent autoimmune diabetes of adulthood diagnosed from the age of 11 years, ESRD secondary to diabetic nephropathy on hemodialysis (diagnosed in December 2017), bilateral diabetic retinopathy, ovarian cyst, hypertension, and anxiety was brought to the emergency department for evaluation of intractable abdominal pain, nausea and vomiting. These health issues started 2 days prior to emergency visit at the hospital. The patient has a history of multiple admissions with similar presentations. She was found to have large ascites.
It was observed that the patient was a young woman, anxious at the moment but alert and oriented × 3. She was pale but had no jaundice or lymphadenopathy. Her blood pressure was 218/108 mm Hg. Her cardiac and respiratory exam was unremarkable.
Abdominal examination showed abdominal distension, mild tenderness, and positive shifting dullness. The normal bowel sounds, no dilated veins and no palpable masses were found in the examination of the abdomen. Extremities exam was remarkable for bilateral +1 leg edema.
Her laboratory investigations revealed blood urea nitrogen (BUN) of 42 mg/dL, serum creatinine (Cr) of 6.1 mg/dL, serum calcium of 8.8 mg/dL and serum phosphorus of 4.8 mg/dL, white blood cell (WBC) of 12.0, hemoglobin (Hb) of 9.6, and platelets of 428. The patient’s international normalized ration (INR) on checking was within the normal range. Computed tomography (CT) scan of the abdomen/pelvis with intravenous and oral contrast was significant for moderate to be marked as abdominal ascites with hepatomegaly and a somewhat reticular pattern of enhancement suggesting possible cirrhosis. Hepatitis B and C serology had been negative in the previous admissions of the patient. Liver function test (LFT) of the patient was also conducted which was within normal limits. Therapeutic/diagnostic paracentesis was done and resulted as: fluid appearance of xanthochromia; fluid WBC of 892/µL; fluid red blood cell (RBC) of 5,120/µL; fluid polynuclear WBC of 0%; fluid mononuclear WBCs of 0%; fluid lymphocytes of 34%; fluid unclassified cell of 66%; fluid glucose of 134 mg/dL; fluid total protein of 5.7g/dL; fluid albumin of 2.0g/dL; fluid lactic dehydrogenase (LDH) of 226 IU/L; and fluid amylase of 25 IU/L. Serum albumin from December 12, 2018 was 2.7 g/dL. SAAG was calculated to be 0.7. Cytology showed chronic inflammatory and rare mesothelial cells, and no malignant cells were identified. Culture of ascitic fluid did not grow any organisms. With predominance of lymphocytic cells, ascetic fluid was sent for acid fast bacillus (AFB) and Gold QuantiFERON test was requested. All results were negative.
Hepatobiliary ultrasonographic (US) exam with Doppler did not show any finding suggesting portal vein thrombosis or Budd-Chiari syndrome.
In the previous admission, CT scan abdomen/pelvis showed a complex ovarian cyst and cancer antigen 125 (CA-125, U/mL) was slightly elevated. Repeat CT abdomen/pelvis and transvaginal ultrasound (TVUS) did not reveal any ovarian cyst. Echo did not show any elevation in right ventricular pressure with ejection fraction (EF) of 60%.
Based on the detailed workup, hepatic, cardiac, infectious and malignant causes for ascites were ruled out. The diagnosis of ascites of nephrogenic origin was made.
Because of her comorbidities and non-compliance with treatment, the patient was a poor candidate for intra-abdominal dialysis and renal transplant. The patient has been treated conservatively with salt/fluid restriction and intensive hemodialysis sessions with ultrafiltration. A gradual reduction in ascites was noted and abdominal girth had been reduced by about 40% with management. But because of her non-compliance with hemodialysis sessions, the patient keep presenting to the emergency room with the same complain.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [8.8, 'mg/dL'], 'Albumin': [2.7, 'g/dL']}",9.84,9.348,10.332,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.7 g/dL. 
The concentration of Calcium is 8.8 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.7 g/dL)) + 8.8 mg/dL = 9.84 mg/dL.
The patient's corrected calcium concentration 9.84 mg/dL."
2559,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2813130-1,Extracted,"Our patient was a 70 year-old male hypertensive who had been undergoing treatment (enalapril, 5 mg) for the last three years and was nondiabetic. He presented with lethargy, loss of appetite, constipation, confusion, and pain in the abdomen. Examination revealed a pulse of 76/min, blood pressure of 130/80 mm Hg, and no systemic abnormalities. Routine chemistry revealed; Hb 12 g/dL, TLC 6.1 × 109/L, DLC: N 64 %, L 24%, platelet 123 ×109/L, ESR 12/1st h, urea 87 mg/dL, creatinine 3.8 mg/dL (0–1.5 mg/dL), glucose 98 mg/dL, serum calcium 13.5 mg/dL (9.5–11.5 mg/dL), serum phosphorus 8.6 mg/dL (3.5–5.5 mg/dL), uric acid 6.6 mg/dL, LDH 292 U/L, total protein 7.0 g/dL, albumin 4.0 g/dL, bil 0.75 mg/dL, OT 35 U/L, PT 40 U/L, ALP 210 U/L. Urine: normal, 24 h urinary proteins 0.15 g/day, the 24 h urinary calcium 200 mg/dL, chest X-ray: normal, electrocardiography normal, the ultrasound was normal.
The patient was managed by continuous saline infusion, diuretics, hydrocortisone, and bisphosphonates. The level of serum calcium on the 10th day of treatment was 10.28 mg/dL, that of phosphorus was 3.94 mg/dL, and the creatinine level stabilized at 1.5 mg/dL.
The patient reported that he had been taking injection vitamin D, 6,00,000 IU (OSTA D3) every two weeks for the last two years for arthralgias and generalized body aches. He had received 35 injections of vitamin D to date, with a cumulative dose of 2,10,00,000 IU.
The PTH level was 15 ng/L (10–60 ng/L) and the 25-hydroxy vitamin D level was 302 nM (47–144 nM). The PSA was normal and the myeloma profile was negative. The serum calcium and renal functions remain normal on follow up.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.0, 'g/dL'], 'Calcium': [13.5, 'mg/dL']}",13.5,12.825,14.175,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.0 g/dL. 
The concentration of Calcium is 13.5 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.0 g/dL)) + 13.5 mg/dL = 13.5 mg/dL.
The patient's corrected calcium concentration 13.5 mg/dL."
2560,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-8571909-1,Extracted,"A 23-year-old girl underwent liposuction of the thighs and extensive autologous fat transfer of buttocks, breasts, and face on 7 October 2020. 6 h after the operation, she had a high fever, hypotension, chills, vomiting, and bilateral thigh bleeding. The patient was thereafter admitted to our emergency room at night. On physical examination, her body temperature was 39.7℃, heart rate was 135 beats/minute, and blood pressure was 83/39 mmHg. Several small scattered incisions from the liposuction and lipotransfer process were observed in the thighs, buttocks, breasts, and face. Besides, petechial skin lesions on the region of the back, lumbosacral, buttocks, posterior thighs with swelling and tenderness, and diffusely distributed erythematous lesions appeared at her toes and hands.
The patient’s laboratory data were notable for a white cell count (WBC) of 2.8 × 109 cells/L(normal:3.5–9.5 × 109/L), hemoglobin 49 g/L(normal:115–150 g/L), and decreased platelets at 49 × 109 cells/L(normal:125–350 × 109/L,). Blood coagulation studies revealed prothrombin time (PT) of 34.2 s(normal:9.8–12.1 s), activated partial thromboplastin time (APTT) of 131.6 s(normal:22.7–31.8 s), international normalized ratio (INR) 3.38(normal:0.79–1.14), D-dimers 70.40ug/ml(normal: < 0.55ug/mL), fibrinogen level was undetectable. Her potassium was 2.86 mmol/L(normal: 3.5–5.5 mmol/L), calcium was 1.57 mmol/L(normal: 2.25–2.75 mmol/L) and serum creatinine was 101umol/L(normal:46–92 umol/L). Liver function tests demonstrated albumin level was 13.5 g/L(normal:63.0–82.0 g/L); the total bilirubin level was 87.2 μmol/L(normal:2.0–22.0 μmol/L); the serum lactate level was 8.1 mmol/L (normal:0.5–1.6 mmol/L); the creatine kinase (CK) level was 918U/L(normal:30-135U/L), myocardial-bound creatine kinase (CK-MB) was 17U/L(normal:0-16U/L), muscle-type creatine kinase (CK-MM) was 901U/L(normal:0-137U/L)). An arterial blood gas analysis showed a potential of hydrogen (PH) of 7.37, a partial pressure of oxygen (PO2) of 165 mmHg, and a Partial Pressure of Carbon Dioxide (PCO2) of 29 mmHg. Cultures of blood, stool, and urine obtained before antibiotic therapy were negative.
She was additionally treated with vancomycin and imipenem, blood transfusion, massive fluid resuscitation, and a series of supportive therapy. During the next day, the patient’s condition worsened, a chest x-ray film showed massive infiltrations in both lungs. She was immediately admitted to the intensive care unit (ICU) and treated with continuous pumps of norepinephrine and metaraminol, imipenem, and vancomycin as empiric anti-infective, blood transfusions. On the second day after admission, the patient's condition deteriorated, and each test indicator continued to higher or lower than the normal range; CT showed pneumonia, pleural effusion, and gastric retention, and blood gas analysis suggested severe metabolic acidosis. Gastrointestinal decompression tube drainage gives about 1500 ml brown liquid.
She was in a state of persistent hyperthermia that her body temperature peaked at 40.1℃; On the third night after admission, the patient developed rapid heart rate (144 beats/min), shortness of breath (25 beats/min), and confusion; blood gas analysis indicated PH 7.31, PCO2 50 mmHg, PO2 43 mmHg, lactate 3.5 mmol/L, blood oxygen saturation(SpO2) 73%. Additionally, the patient’s urine was dark brown, and a large amount of exudation was drained from both thighs. Endotracheal intubation was performed with ventilator-assisted ventilation. On the 7th day after admission, bedside hemodialysis was performed because the patient's urine color continued to become dark, CK-MB, myoglobin, and infection indicators (C-reaction protein [CRP], Procalcitonin [PCT]) continued to rise. During the first 3 weeks after admission, a total of 3600 mL red blood cells, 1200 mL fresh frozen plasma, 4units(U) of platelet concentrate, 42U of cryoprecipitate coagulation factor, and large amounts of human fibrinogen and prothrombin complexes were used. The patient has gradually improved after positive and effective treatment, and the test indicators have gradually returned to the normal range (Additional file , which demonstrates the changes of patient’s body temperature and lab test indicators from day 1 through day 14 after admission).
Although the erythematous rush has subsided, peripheral ischemia appeared on her fingers and toes and gradually resulted in gangrene (Fig. ). What’s worse, her buttocks occurred necrotizing soft tissue infection. By the time her body was strong enough to withstand surgery and the gangrenous areas became demarcated, surgical amputation of fingers and toes gangrenous areas on the peripheral extremities was performed; both fingers and toes were secondly covered with split-thickness skin after firstly artificial dermis grafts; her buttocks were grafted with split-thickness skin after twice full debridement and treated with VSD (Fig. ). During the period, antibiotics (vancomycin, imipenem, teicoplanin, tigecycline, sulperazone, polymyxin, Linezolid, phosphonomycin) and antifungal drugs (Caspofungin, Fluconazole) were replaced according to the patient's sputum culture, wound secretion culture, and drug sensitivity.
Blood cultures were persistently negative for the growth of organisms, but Candida tropicalis was identified by the untargeted next-generation sequencing of sputum; Klebsiella pneumonia was identified by the untargeted next-generation sequencing of blood; Acinetobacter baumannii, Proteus mirabilis, and Klebsiella pneumonia were detected in the buttock subcutaneous effusion culture. The patient experienced desquamation of the hand on the 26th day after admission (Fig. ). The skin grafts survived and the function of both fingers and toes recovered well. She was discharged 2 months after admission and was in good health at the last follow-up (Fig. ).","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [1.57, 'mmol/L'], 'Albumin': [13.5, 'g/L']}",8.413,7.99235,8.83365,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 13.5 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 13.5 g Albmumin/10.0 dL = 1.35 g Albmumin/dL. The concentration value of 13.5 g Albmumin/L converts to 1.35 g Albmumin/dL. 
The concentration of Calcium is 1.57 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.57 mmol. To convert 1.57 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.57 mmol Calcium * 0.001 mol/mmol = 0.00157 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00157 mol Calcium * 40.08 g/mol = 0.06293 g Calcium. To convert 0.06293 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.06293 g Calcium * 1000.0 mg/g = 62.93 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 62.93 mg Calcium/10.0 dL = 6.293 mg Calcium/dL. The concentration value of 1.57 mmol Calcium/L converts to 6.293 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.35 g/dL)) + 6.293 mg/dL = 8.413 mg/dL.
The patient's corrected calcium concentration 8.413 mg/dL."
2561,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5757848-1,Extracted,"A 91-year-old female with a medical history of bilateral breast cancer, status post mastectomy and chemotherapy, iron deficiency anemia, hypertension, appendectomy, cholecystectomy, and dementia who lived in a long-term care facility. She had decreased appetite for several months, weight loss, intermittent nausea and vomiting, and was sedentary. Laboratory studies obtained at that time were significant for anemia, but with normal thyroid function studies. She had a 40 pack-year history of smoking, quit smoking over 27 years ago. Her home medications included: donepezil, metoprolol, hydralazine, Tylenol, colace, and cyanocobalamin.
The patient was admitted to our hospital with the diagnosis of FTT. Laboratory investigation revealed white blood cell (WBC) 16 K/uL, hemoglobin 8.4 g/dL, platelets 195 K/uL, international normalization ratio (INR) 1.24; complete metabolic panel shows serum sodium 135 mmol/L, potassium 3.7 mmol/L, chloride 103 mmol/L, bicarbonate 24 mmol/L, glucose 94 mg/dL, blood urea nitrogen 10 mg/dL, creatinine 0.6 mg/dL, calcium 7 mg/dL, total protein 4.7 g/dL, albumin 2 g/dL, alkaline phosphatase (ALP) 57 U/L, aspartate aminotransferase (AST) 10 U/L, alanine aminotransferase (ALT) 18 U/L, total bilirubin 0.2mg/dL. Evaluation with computed tomography (CT) scan of the chest and abdomen/pelvis revealed a right hepatic flexure mass invading the second portion of the duodenum and the right kidney (Figure ), with no clinical evidence of bowel obstruction. Carcinoembryonic antigen (CEA) 1090 ng/ml (reference- less than 3 ng/mL).
Surgical oncology team was consulted to evaluate the patient. On examination the patient had a nasogastric tube in place with bilious output, palpable non-tender mass in her right upper abdomen; the remainder the examination was unremarkable. The CT findings and management options were discussed with the patient, including a palliative care option. Patient opted for surgical intervention. After appropriate preoperative management, the patient was taken to the operating room for an exploratory laparotomy for en bloc resection of the mass for presumed colon cancer with invasion of duodenum and kidney. Intraoperatively, ascites was noted, the bowel was edematous, and the mass was fixed to the right retroperitoneum, kidney and duodenum; the overall findings suggested major resection would probably have a poor outcome. Therefore, gastrojejunostomy and ileocolic bypasses were created to prevent progression to clinical obstruction.
Postoperatively, the patient had an uneventful recovery. Operative findings were discussed with the patient and she decided to pursue palliative care management. She was discharged to her long-term care facility on postoperative day eight.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.0, 'g/dL'], 'Calcium': [7.0, 'mg/dL']}",8.6,8.17,9.03,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.0 g/dL. 
The concentration of Calcium is 7.0 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.0 g/dL)) + 7.0 mg/dL = 8.6 mg/dL.
The patient's corrected calcium concentration 8.6 mg/dL."
2562,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6106801-1,Extracted,"A 32-year-old primigravida presented to the Emergency Department (ED) during her 7th week of gestation with complaints of two weeks of progressively worsening intermittent lower abdominal pain. She denied any visual disturbances, headache, nausea, vomiting, constipation or diarrhea, vaginal bleeding, or uterine contractions. Her medical history was significant for a pituitary microadenoma (6.5 × 6 × 5 mm) diagnosed 12 months prior. At that time her serum prolactin was slightly elevated at 35 ng/mL (Ref: 3.34 - 26.72 ng/mL); however, other pituitary hormones were within the normal limits. There was no family history of parathyroid disease, hypercalcemia, nephrolithiasis, or other endocrinopathies except for hypothyroidism affecting her mother. Admission medications included daily prenatal vitamins.
On presentation to the ED, her review of systems was otherwise negative with no genitourinary or gastrointestinal or neurological symptoms. Her vital signs were within normal limits. Her physical examination was unremarkable.
Her blood tests demonstrated hypercalcemia (serum calcium 12.2 mg/dL [Ref: 8.6-10.3 mg/dL], ionized calcium 1.67 mmol/L [Ref: 1.15 - 1.33 mmol/L]), and hyperparathyroidism (PTH 135 pg/mL [Ref: 12-88 pg/mL]). Her serum albumin was 3.2 g/dL (3.5-5.7 g/dL), phosphorus 2.2 mg/dL (Ref: 2.5-5 mg/dL), and magnesium 1.5 mg/dL (Ref: 1.9-2.7 mg/dL). Other relevant labs included a 24-hour urinary calcium of 712 mg/24 hour (Ref: 100-300 mg/24 hr), 25-hydroxyvitamin D 18.5 ng/mL (Deficient if <20 ng/mL), 1,25-dihydroxyvitamin D 94.9 pg/mL (Ref: 19.9-79.3 pg/mL), and thyroid stimulating hormone (TSH) 0.43 uIU/mL (Ref: 0.45-5.33 uIU/mL). Renal ultrasound was unremarkable with no nephrolithiasis or hydronephrosis. Thyroid ultrasound revealed a 28 × 11 × 11 mm hypervascular, heterogeneous mass along the posterior margin of the left thyroid gland. A fine needle aspiration from the mass demonstrated scant cells and was reported as benign cytology. The FNA needle washout resulted in high levels of parathyroid hormone.
She was diagnosed with primary hyperparathyroidism and started conservative treatment with IV fluid and magnesium supplements with improvement in her serum calcium levels (11.4 mg/dL). Unfortunately the patient subsequently became symptomatic with nausea, vomiting, and maintaining serum calcium levels of 12 mg/dL despite sufficient hydration. She was started on aggressive hydration (lactated ringers at 125 ml/hr followed by normal saline at 125 ml/hr) continuously until the day of surgery. She received a total of 23 L of intravenous fluids over 10 days; however the serum calcium ranged between 10.6 and 11.6 mg/dL with most values at >11 mg/dL. Just prior to surgery, her serum calcium level was 10.7 mg/dL and her ionized calcium level was 1.38 mmol/L. She underwent left superior parathyroidectomy and the pathology was consistent with a 3.0 × 1.8 × 1.2 cm parathyroid adenoma (Figures and ). Intraoperative PTH measurement was not performed to reduce the time of anesthesia. Following surgery, her serum calcium and PTH levels normalized. She did not develop hypocalcaemia after surgery. In subsequent follow-up weekly visits after discharge, her serum calcium and PTH levels have been within the normal limits.
With her history of pituitary adenoma and a large parathyroid adenoma, multiple endocrine neoplasia type 1 (MEN1) was considered. However, direct DNA testing for MEN1, RET, AIP, and CDKN1B gene mutations were negative.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.2, 'g/dL'], 'Calcium': [12.2, 'mg/dL']}",12.84,12.198,13.482,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.2 g/dL. 
The concentration of Calcium is 12.2 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.2 g/dL)) + 12.2 mg/dL = 12.84 mg/dL.
The patient's corrected calcium concentration 12.84 mg/dL."
2563,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2396176-1,Extracted,"An 82-year-old man was found unresponsive on his backyard porch. His wife had gone to bed at 10 p.m. the evening before and did not realize he was missing until 6.30 a.m. the next morning. The ambient temperature was -10°C with a wind chill factor of -20°C. His past history included Alzheimer's disease, hypertension, hypothyroidism, a cerebrovascular accident in 1999 with a residual expressive aphasia, and surgery for prostate cancer. His medications included aspirin, olanzapine, alendronate sodium, and levothyroxine. He had an allergy to indomethicin.
He was flown by helicopter to the Level I trauma center. During prehospital resuscitation, he received intravenous lidocaine 100 mg, etomidate 30 mg, midazolam 5 mg, and 2 liters of warm 0.9% NaCl. As the aircraft landed, a pulse and blood pressure became unobtainable. He arrived on a backboard with a cervical collar in place, his trachea intubated, and a 20 gauge intravenous line infusing 0.9% NaCl. Cardiopulmonary resuscitation (CPR) was initiated (see Table ). An electrocardiogram (ECG) confirmed pulseless electrical activity (PEA) with a heart rate of 31 beats per minute. His lungs were clear to auscultation bilaterally. His pupils were fixed and dilated at 4 mm, and he had a rectal temperature of 25.5°C. He was severely cyanotic to his nipple line and in both upper extremities. A chest roentgenogram revealed the tracheal tube was in the proper position. He was given atropine 1 mg intravenously for his PEA, this was followed by 1 mg epinephrine intravenously. The patient converted to sinus rhythm, but within 90 seconds he went into ventricular tachycardia and subsequently into ventricular fibrillation; CPR was continued. Ventricular defibrillation attempts were withheld because of the critically low temperature of the patient. Two additional 16 gauge intravenous catheters and a left subclavian catheter were placed and warm 0.9% NaCl was instilled. A nasogastric tube and bilateral chest tubes were also placed to instill warm fluid. Laboratory examination revealed sodium 142 meq/liter, potassium 3.3 meq/liter, chloride 113 meq/liter, HCO3 19 mmol/liter, glucose 128 g/dl, lipase 28 U/liter, calcium 8.5 mg/dl, total bilirubin 0.9 mg/dl, alkaline phosphatase 57 U/liter, aspartate transaminase 35 U/liter, total protein 5.5 g/dl, albumin 2.8 g/dl, and lactate 3.0 mmol/liter. Arterial blood gas (ABG) was not drawn at this time. Thyroid stimulating hormone (TSH) and T4 levels were drawn (TSH was 9.02 micro-IU/ml (normal 0.10 to 5.0 micro-IU/ml) and his T4 was 1.6 mcg/dl (normal 4.5 to 13.2 mcg/dl), but the results were not available until after resuscitation). His temperature did not change after nearly 60 minutes of conventional warming therapies that included warm fluid instillation (intravenous, gastric, and intrapleural), use of a warming blanket, and CPR in a trauma room that was 27°C. The perfusion service was consulted and it was determined that the patient would benefit from rewarming by extracorporeal circulation.
A heparin bolus of 200 U/kg of body weight was given to target an activated clotting time of 300 seconds. Cannulation of the right common femoral artery and vein, using 20 French percutaneous femoral arterial and venous cannulas (Edwards Lifesciences, Irvine, CA) was achieved via surgical cutdown. The patient was placed on emergency percutaneous veno-arterial femoral-femoral bypass in the ED using a self-contained, portable cardiopulmonary bypass (CPB) support system (PBS Portable Bypass System, Medtronic, Inc., Minneapolis, MN) consisting of a portable centrifugal blood pump console with an external drive motor and heater unit. The pre-assembled perfusion circuit consisted of a Biomedicus centrifugal pump (Medtronic, Inc., Minneapolis, MN). CPB was initiated within 10 minutes of the decision for its use and 58 minutes after the arrival of the patient to the ED; the patient's core temperature was 25°C.
An initial venous blood gas drawn from the perfusion circuit revealed a pH of 7.16, pCO2 32 mmHg, pO2 60 mmHg (FIO2 1.0), sodium 148 meq/liter, potassium 2.8 meq/liter, calcium 1.04 meq/liter, HCO3 11 mmol/liter, a base excess of -15.0 mmol/liter, and a hematocrit level of 14.8%. The patient was stabilized at this temperature for 15 to 20 minutes prior to commencing core rewarming to provide the opportunity for reintroducing generalized perfusion and gas exchange prior to actively rewarming. Potassium was repleted, and the mean arterial pressure was maintained at 66 mmHg. Defibrillation attempts were withheld until the core temperature reached 35°C. Successful defibrillation was achieved after 120 minutes of core rewarming, at a core temperature of 34.9°C (Figure ). The patient was then transferred to the operating room for decannulation and repair of the femoral vessels under direct vision. His hemodynamic parameters were stabilized with a resultant ABG of pH 7.42, PaCO2 38 mmHg, PaO2 82 mmHg, and HCO3 24 mmol/liter, base excess 0 mmol/liter on 0.6 FIO2. He was transferred to the intensive care unit (ICU).
His hemodynamic support necessitated the use of large amounts of fluids and blood products secondary to a severe coagulopathy of hypothermia and subsequent vasodilation due to rewarming. He received 12 liters of crystalloid, 15 U of packed red blood cells, 20 U of platelets, and 2 U of fresh frozen plasma during the first 7 hours of his hospitalization. Twelve hours after admission prothrombin time was 16.1 seconds, partial promboblastin time was 32.6 seconds, and international normalized ratio was 1.23.
It was determined that he had sustained a myocardial infarction during his perihypothermic time interval (creatinine kinase 988 U/liter, creatinine kinase antibodies 109.6 ng/ml, CK-MB index 11.1 ng/ml, myoglobin 2323 ng/ml and troponin I 117.65 ng/ml). His ECG demonstrated occasional premature ventricular complexes, low-voltage QRS, non-specific ST and T wave abnormality, and a prolonged QT interval. However, transesophageal echocardiography 72 hours after admission revealed a normal global ventricular function, normal left ventricle, normal aortic, mitral and pulmonary valves, normal left and right atrial size, normal ventricular thickness, mild tricuspid regurgitation, mildly elevated right-sided pressures, and a small anterior pericardial effusion.
Five days after admission he underwent placement of a tracheostomy and gastric feeding tube. His mental status recovered to its premorbid state 10 days after admission, but he was physically debilitated. Three weeks after admission he was discharged to a long-term acute care hospital. Subsequently he was transferred to a nursing home where he was still residing 6 months after hospital discharge.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.8, 'g/dL'], 'Calcium': [8.5, 'mg/dL']}",9.46,8.987,9.933,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.8 g/dL. 
The concentration of Calcium is 8.5 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.8 g/dL)) + 8.5 mg/dL = 9.46 mg/dL.
The patient's corrected calcium concentration 9.46 mg/dL."
2564,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5434694-1,Extracted,"A 25-year-old man, with no comorbidities presented with sudden onset anasarca and oliguria of 2 days duration. He was diagnosed to have hemorrhoids by a local physician and was prescribed oral ciprofloxacin for 5 days with a cumulative dose of 5 g, 10 days before this admission. On investigation, routine blood and urine examination revealed the following results. Hemoglobin 11.7 g/dl, total leukocyte count 5700, neutrophils 80%, lymphocytes 15%, monocytes 3%, eosinophils 2%, platelets 2.2 lakhs/L, S. creatinine 3.6 mg/dl, urea 140 mg/dl, sodium 138 mmol/L, potassium 4.9 mmol/L, chloride 100 mmol/L, calcium 8.5 mg/dl, uric acid 8.0 mg/dl, phosphorus 4.7 mg/dl, total proteins 6.6 g/dl, albumin 3.8 g/dl, serum glutamic oxaloacetic transaminase 21 U/L, serum glutamic pyruvic transaminase 24 U/L, alkaline phosphatase 106 U/L, lactate dehydrogenase 840 IU/L. His urine analysis showed pH of 6.0 and bland sediment without any significant proteinuria, hematuria, eosinophiluria, or leukocyturia. Autoimmune workup including serum rheumatoid factor, antinuclear antibodies, anti-double-stranded DNA, antineutrophil cytoplasmic antibodies did not yield positive results. Serum complement levels were normal. HIV, hepatitis C virus, and hepatitis B virus infections were ruled out. His serum creatinine had increased to 5.8 mg/dl during next 2 days. A percutaneous renal biopsy [] was done, which showed ten glomeruli; the glomeruli were unremarkable. Twenty-five percent of tubules shown needle-shaped crystals occupying the entire luminal circumference. These crystals were refringent under polarized light. These intratubular Birefringent crystals [] showed a granulomatous response. The granuloma was composed of epithelioid cells. In addition, there was lymphocytic infiltrate in the interstitium. He was managed conservatively with intravenous fluids. His renal function improved during 10 days, and his serum creatinine was 0.9 mg/dl at discharge.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.8, 'g/dL'], 'Calcium': [8.5, 'mg/dL']}",8.66,8.227,9.093,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.8 g/dL. 
The concentration of Calcium is 8.5 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.8 g/dL)) + 8.5 mg/dL = 8.66 mg/dL.
The patient's corrected calcium concentration 8.66 mg/dL."
2565,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6961606-1,Extracted,"The patient was a 71-year-old man who presented with nausea, fatigue, and anorexia. He was referred to our hospital for investigation of these symptoms and abnormalities; as such, chest radiography was performed (). Laboratory examination revealed an elevated blood serum calcium level (12.3 mg/dL, serum albumin level 3.2 g/dL) and normal creatinine level, which did not indicate dehydration and renal dysfunction (). He did not take any hypercalcemia-inducing agents such as thiazide diuretics, theophylline, lithium, osteoporosis therapeutic drugs, and vitamin D supplements. Serum PTHrP level was elevated (11.7 pmol/L (reference value < 1.1 pmol/L)), although the intact PTH level was low (7 pg/mL (reference value 10-65 pg/mL)). Surprisingly, the serum calcitriol level was elevated (105 pg/mL (reference value 20-40 pg/mL)) although 25-OH vitamin D3 level was low (16 ng/mL (reference value > 20 ng/mL)). Integrated computed tomography and 18F-2-deoxy-2-fluoro-D-glucose (FDG) positron emission tomography (PET/CT) showed uptake of FDG by a left pulmonary hilar lesion and both ipsilateral mediastinal and subcarinal lymph nodes, because of which lung cancer with metastasis to the lymph nodes was highly suspected (Figures –). No other organs, including the bone, liver, and bilateral adrenal glands, showed FDG uptake. Head magnetic resonance imaging revealed no metastatic lesions. Based on the results of a bronchoscopic examination showing proliferation of large polygonal atypical cells with intercellular bridges in the bronchial submucosa (), the patient was diagnosed with stage IIIB lung squamous cell carcinoma (55% of tumor cells were positive for programmed cell death-ligand 1 expression). Lymphoma, granulomatous disease, and mycobacterial or fungal infections were ruled out based on the results of histopathological analysis. Pembrolizumab (200 mg/body every 3 weeks) was administered as the first-line treatment. In addition to anticancer treatment, calcitonin and intravenous 0.9% normal saline were first administered. Despite initial treatment for HCM, hypercalcemia did not improve. On day 28 from the initial treatment of HCM, systemic prednisolone (40 mg/day) was additively administered. Serum calcium level rapidly decreased thereafter and normalized (serum calcium 8.5 mg/dL, serum albumin 3.1 g/dL) on day 31. Serum PTHrP and calcitriol levels decreased simultaneously (PTHrP: 5.4 pmol/L; calcitriol: 65.4 pg/mL) in response to systemic prednisolone. Serum intact PTH levels were elevated to the normal range (47 pg/mL), indicating improvement of the negative feedback circuit to regulate serum calcium levels. However, lung cancer gradually progressed during two cycles of pembrolizumab, suggesting an inadequate therapeutic response to this immunotherapy. Respiratory failure developed, and the patient died on day 58. shows the clinical course of this patient.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.2, 'g/dL'], 'Calcium': [12.3, 'mg/dL']}",12.94,12.293,13.587,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.2 g/dL. 
The concentration of Calcium is 12.3 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.2 g/dL)) + 12.3 mg/dL = 12.94 mg/dL.
The patient's corrected calcium concentration 12.94 mg/dL."
2566,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5544981-1,Extracted,"A 67-year-old Japanese woman underwent OWHTO to treat SPONK that had occurred in the left medial femoral condyle (Fig. ). The patient reported the following history of the present illness. Pain in the left knee joint initially occurred at 1 year and 4 months before admission, without any particular trigger. Her former treating physician had provided conservative treatments such as oral administration of anti-inflammatory analgesics, rehabilitation including quadriceps muscle training, and guidance on the use of a cane to relieve weight bearing. However, this treatment was not successful in relieving her symptoms, and she was referred to our department for surgery. The patient had a history of hypertension and hyperlipidemia, and she had been taking oral candesartan and atorvastatin. The patient was a housewife with no noteworthy aspects related to social, family, or environmental history. On physical examination, the patient had a height of 157 cm, a body weight of 62 kg, and a body mass index of 25.2 kg/m2. She reported feeling pain in the medial joint space of the knee during walking, as well as during climbing or descending stairs. At the time of the first admission, her systolic/diastolic blood pressure was 165/97 mmHg. Table provides an overview of the patient’s pain scores in the knee joint, ROM of the knee joint, and knee joint function. Neurological examination revealed no abnormal findings. Similarly, laboratory findings at the time of the first admission did not indicate any abnormality: total protein 7.3 g/dl, albumin 4.6 g/dl, aspartate aminotransferase 22 U/L, alanine aminotransferase 18 U/L, lactate dehydrogenase 213 U/L, alkaline phosphatase 297 U/L, γ-glutamyl transferase 18 U/L, total bilirubin 0.6 mg/dl, Na 142 mEq/L, Cl 104 mEq/L, K 4.5 mEq/L, blood urea nitrogen 21.4 mg/dl, creatinine 0.56 mg/dl, Ca 9.7 mg/dl, inorganic phosphorus 3.7 mg/dl, leukocytes 5100/μl, erythrocytes 5.00 × 106/μl, hemoglobin 14.4 g/dl, hematocrit 43.6%, and platelets 263 × 103/μl.
The HAL-SJ treatment program was divided into five phases []. Phase 1 consisted of preoperative observation from the day of hospital admission until the day of surgery. The patient’s thigh circumference and lower leg length were measured preoperatively to adjust the HAL-SJ to the patient’s physical size, which would ensure appropriate training. We palpated the patient’s quadriceps muscles (vastus medialis, rectus femoris, and vastus lateralis) and attached electrodes to each muscle to detect the bioelectric potentials of the long axis along the belly of each muscle. We instructed the patient to perform knee extension and to contract her quadriceps. On the basis of these data, we instructed the patient to simulate the knee extension training, which would be performed postoperatively. Specifically, the patient sat with her lower leg hanging down naturally, and the height of the chair was adjusted so that the patient’s feet were not in contact with the floor. The patient performed ten knee extensions with HAL-SJ assistance, using the muscle that exhibited the largest bioelectric potential amplitude.
Phase 2 involved surgery (day of surgery). The patient underwent OWHTO (Figs. and ) using TomoFix (DePuy Synthes, Bettlach, Switzerland), artificial bone (OSferion60, β-tricalcium phosphate; Olympus Terumo Biomaterials, Tokyo, Japan), and biplanar osteotomy, as described by Takeuchi et al. []. The preoperative weight-bearing line (WBL) percentage [], calculated on the basis of an anteroposterior weight-bearing radiograph of the affected leg in full knee extension, was 29.6%. The surgery was planned with a target postoperative WBL percentage of 62.5%. The actual enlarged angle and distance of osteotomy were 5.5 degrees and 7 mm, respectively.
Phase 3 consisted of postoperative observation from day 1 to day 7 postoperatively. For postoperative rehabilitation, partial weight bearing was allowed after a non-weight-bearing period of 2 weeks, and full weight bearing began at 4 weeks postoperatively. The patient received rehabilitation training under the guidance of a physical therapist (ROM exercises and muscle-strengthening training) for 20–40 minutes each day, 5 days per week, from the first postoperative day until discharge. For ROM exercises, continuous passive motion training began on the first postoperative day for 1 hour per day and continued every day until discharge. On postoperative day 7, we attached electrodes to the quadriceps muscle to detect the bioelectric potential along the long axis of the rectus femoris muscle belly (Fig. ). Then, the patient was instructed to perform active knee extension exercises that involved contracting her quadriceps, thus simulating training with HAL-SJ (Fig. ).
Phase 4 consisted of HAL-SJ therapy from postoperative day 8 to discharge. The CVC mode of HAL-SJ serves to support the patient’s voluntary motion on the basis of voluntary muscle activity and the assistive torque provided to the knee joint []. In this study, we used the CVC mode, which allowed the operator to adjust the degree of physical support to maintain the patient’s comfort while gradually reducing support as training progressed. In addition to the regular rehabilitation program (Fig. ), the patient performed HAL-JS-assisted knee extension exercises while sitting, which consisted of five sets of ten repetitions per set, twice per week (Fig. ). The training was performed six times before the patient was discharged (postoperative days 8, 10, 15, 17, 22, and 24). The mean training duration, including the time required to put on the HAL-SJ, was 15.5 ± 1.4 minutes (15 minutes, 16 minutes, 17 minutes, 16 minutes, 13 minutes, and 16 minutes during training sessions 1, 2, 3, 4, 5, and 6, respectively). There were no adverse events related to the use of HAL-SJ, and the patient was discharged 30 days after the surgery.
Phase 5 consisted of post-HAL-SJ therapy observation from discharge until 3 months after the end of HAL-SJ therapy, during which the following indicators were assessed: EL, assessed as the difference between the maximum knee joint extension angle during passive exercise and that during active exercise; knee pain rated on the visual analogue scale (VAS); isometric knee extension muscle strength (IKEMS); active ROM before surgery, before and after HAL-SJ training, and at 1 and 3 months after the end of training; and the Japanese Orthopaedic Association (JOA) score [] before surgery, at discharge, and at 1 and 3 months after the end of training. Furthermore, we used lateral radiographs to measure the tibial slope angle (TSA) and Insall-Salvati ratio (ISR) as indicators of patellar tendon shortening before surgery and after implant removal at 1 year after the operation [] (Fig. ). Measurement of knee ROM was performed using goniometry, and the landmarks used in the measurements were the greater trochanter of the femur, proximal head of the fibula, and lateral malleolus. Goniometry was used because it has been reported that goniometric measurements of ROM are more reliable than visual observation, with an accuracy of up to 1.0 degree []. The maximal IKEMS of the operated leg was assessed with the patient in a sitting position, with the hips and knees flexed at 90 degrees. A μTas F-1 handheld dynamometer (Anima Corp., Tokyo, Japan) was fixed to the chair, and two measurements were recorded. Each trial lasted 3–5 seconds, with 30 seconds of rest between trials. The higher score of two valid trials was recorded. All measurements were performed by a single trained physical therapist to eliminate interobserver variability. The EL, VAS, IKEMS, and ROM results are shown in Table . The EL improved from 3 degrees preoperatively to 0 degrees at the end of the sixth HAL-SJ training session, but it returned to 3 degrees at 1 and 3 months after the end of the training. When we compared results obtained before training against those obtained after each of the six training sessions, we observed that three sessions produced improved EL and three sessions produced improved or relatively constant VAS scores immediately after training. However, for the other three sessions, the patient reported increased pain immediately after training, with the greatest increase in pain reported immediately after the first HAL-SJ training session, when the VAS score was 1.7 times higher immediately after training than before training. The EL improved after training sessions 1 and 3, when the patient reported increased knee pain (expressed as the VAS score). However, the EL did not change after training sessions 2 and 4, when the patient reported less knee pain (improved VAS score immediately after training). The patient did not refuse to undergo training because of increased pain. The IKEMS value was the largest preoperatively (17.6 kgf) and decreased to its lowest value (30% of the preoperative strength) before the first HAL-SJ intervention at 8 days after the operation. The IKEMS remained relatively constant throughout HAL-SJ training but recovered to the preoperative value during follow-up (18.7 and 16.6 kgf at 1 and 3 months, respectively, after completion of HAL-SJ training). The active ROM also recovered to the preoperative value by the end of the sixth HAL-SJ training session. Thereafter, the extension ROM did not change, but the flexion ROM was maintained or improved. The JOA score decreased from 60 points preoperatively to 55 points at discharge, but it improved with time, reaching 65 and 85 points at 1 and 3 months, respectively, after the end of HAL-SJ training. Whereas the TSA was maintained at 13.1 degrees before and after the surgery, the ISR decreased from 1.13 preoperatively to 0.97 postoperatively. At 6 months after surgery, the passive ROM was 0–135 degrees, and the JOA score was 90 points. There were no complications throughout the preparation, surgery, or rehabilitation process.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.6, 'g/dL'], 'Calcium': [9.7, 'mg/dL']}",9.22,8.759,9.681,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.6 g/dL. 
The concentration of Calcium is 9.7 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.6 g/dL)) + 9.7 mg/dL = 9.22 mg/dL.
The patient's corrected calcium concentration 9.22 mg/dL."
2567,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6395020-1,Extracted,"An 86-year-old male with no known past medical history presented to his primary care physician with complaints of sudden onset of right hip pain and progressive difficulty in walking for three weeks. He did not follow-up with any physician for over 30 years. He reported severe pain that was exacerbated by any physical activity and movement. His pain was minimally relieved with rest and radiated to bilateral lower extremities. Outpatient chest and right hip X-rays revealed multiple lytic lesions, suggestive of metastatic disease. The patient was admitted to the hospital for further workup. X-rays of the pelvis revealed multiple lytic lesions throughout the entire pelvis and bilateral femurs (Figures -). Laboratory tests were significant for the following: hemoglobin level of 9 g/dl, creatinine 2.8 mg/dl, calcium 13.5 mg/dl, albumin 2.7 g/dl, total serum protein 9.6 g/dl, globulin 7.1 g/dl, albumin to globulin ratio 0.3, free PSA 6.9ng/mL and total PSA 78.0 ng/mL. Urinalysis showed proteinuria and hematuria. Magnetic resonance imaging (MRI) of the spine revealed diffuse metastatic disease (Figure ). A bone scan showed multiple foci of increased activity throughout bilateral ribs, spinous processes of the lumbar spine, bilateral shoulders, left iliac wing and left acetabulum consistent with metastatic disease (Figure ). At this point, the working diagnoses included MM and metastatic prostate cancer. Urology proceeded with a prostate biopsy. Despite negative intra-operative frozen sections for prostate cancer, a bilateral orchiectomy was performed due to high clinical suspicion of prostate cancer. The aim of this procedure was to achieve early androgen deprivation to prevent spinal cord compression. The patient underwent the procedure without any complications. He was started on steroids for suspected spinal cord compression. Intravenous fluid hydration and zoledronic acid were administered for hypercalcemia. Subsequent laboratory tests showed improvement in calcium level. Serum creatinine level remained elevated between 2 mg/dl and 3 mg/dl. MM workup including serum protein electrophoresis, serum, and urine free kappa and lambda light chains were supportive of a diagnosis of MM: free kappa serum level 19.7 mg/dl, free lambda serum level 3099 mg/dl, free kappa urine 164 mg/L, free lambda urine 1500 mg/L, and free kappa/lambda urine ratio 0.11. Immunofixation was interpreted as monoclonal IgG lambda present. According to the Revised International Myeloma Working Group Diagnostic Criteria for MM, tissue evidence of >10% of bone or extramedullary plasmacytoma is necessary for a definitive diagnosis of MM. It was recommended by orthopedic surgeons that the patient be on bed rest indefinitely due to high fracture risk as a result of his bone frailty. The patient was given the option to proceed with bone marrow biopsy and appropriate treatment based on results. Radiation therapy to help with the pain was also recommended. After extensive discussion about all diagnostic, therapeutic and palliative options patient opted for comfort measures only. He did not want to pursue further diagnostic workup as his quality of life was expected to be severely diminished. The patient was eventually discharged to a nursing home for hospice care.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.7, 'g/dL'], 'Calcium': [13.5, 'mg/dL']}",14.54,13.813,15.267,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.7 g/dL. 
The concentration of Calcium is 13.5 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.7 g/dL)) + 13.5 mg/dL = 14.54 mg/dL.
The patient's corrected calcium concentration 14.54 mg/dL."
2568,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7829719-1,Extracted,"A 20-year-old male presented to the Nephrology Department of our hospital complaining of limb soreness, and after 5 mo, the patient began to develop proteinuria and edema in both lower extremities.
In February 2016, the patient developed limb soreness. The initial laboratory data were as follows: hemoglobin of 128 g/L and a platelet count of 398 × 109/L. Other values were as follows: Serum albumin was 29.4 g/L, alanine aminotransferase was 246.6 U/L, aspartate aminotransferase was 314.8 U/L, and creatine kinase was 4612.9 U/L. We considered that chronic rejection after transplantation resulted in myositis and liver damage, so the patient was treated with corticoid therapy by administration of oral methylprednisolone (32 mg/d). The outcome was favorable. However, after 5 mo, the patient began to develop proteinuria and edema in both lower extremities.
The patient diagnosed with T lymphoblastic lymphoma (stage IIIA, aaIPI 1) in September 2013 was treated with six cycles of hyper-CVAD and achieved complete remission. Then, he underwent syngeneic HSCT in June 2014 (Figure ), and had no kidney disease history before the transplant. The donor was his twin brother, and HLA matching at high resolution for the HLA-A, B, C, DRB1 and DQB1 loci revealed that the loci were completely consistent in the donor and recipient. Additionally, short tandem repeat analysis was performed on both the donor and recipient, and the results showed that the 20 loci were completely consistent (Figure and Table ). After transplantation, the patient used 8 mg glucocorticoids daily and then tapered off gradually, and he also received 3 mg sirolimus daily for 3 mo to prevent potential GVHD, which achieved good results.
The patient had a free medical history.
At admission, the patient’s temperature was 36.8 °C, the heart rate was 70 bpm, the respiratory rate was 16 breaths per minute, the blood pressure was 112/80 mmHg, and the oxygen saturation in room air was 99%. The clinical physical examination revealed moderate edema in both lower limbs without any other pathological signs.
The blood analysis results were as follows: Leukocyte count of 9.60 × 109/L, neutrophil count of 6.66 × 109/L, eosinophils at 0.20%, and hemoglobin of 132 g/L. The blood biochemistry results were as follows: Albumin of 15.7 g/L, total cholesterol of 9.45 mmol/L, calcium of 1.97 mmol/L, and alkaline phosphatase of 144.7 U/L. The thyroid function testing results were as follows: free triiodothyronine of 1.96 mmol/L, triiodothyronine of 0.61 nmol/L, thyroxine of 36.5 nmol/L, thyroglobulin of 39.30 ng/L, and free thyroxine of 9.51 pmol/L. Immunoglobulin G was 4.99 g/L, d-dimer was 1.48 mg/L, 25-hydroxyvitamin D was 7.50 nmol/L, blood kappa light chain was 0.866 g/L, and L light chain was 0.413 g/L. The patient had undergone testing for antinuclear antibody, rheumatism, hepatitis B virus antigen, hepatitis C, and syphilis, the results of which were all negative. Furthermore, his level of serum phospholipase A2 receptor (PLA2R) autoantibodies was 4.36 RU/mL (normal value < 20 RU/mL according to ELISA), which was also a negative result.
The electrocardiogram, chest X-ray, kidney, ureter and bladder ultrasonic imaging, and positron emission computed tomography/computed tomography results were all negative.
A percutaneous kidney biopsy was performed, which led to a diagnosis of glomerulonephritis with characteristics of MN (Figure ) on the basis of light microscopy, electron microscopy and immunofluorescence findings.
Light microscopy: Thirty-two glomeruli were observed. The number of glomerular cells was not increased, and the mesangial hypercellularity was mild. The mesangial matrix expansion was slight, and few intracapillary fibrin thrombi were observed. The capillaries were open, showing few microthromboses. Basement membrane thickening was observed, with a small number of capsule adhesions but no double contours or spikes. The renal tubular epithelial cells were basically normal. The lumen showed evidence of protein casts, red blood cell casts and few cellular casts. The interstitium showed little infiltration of inflammatory cells and no obvious fibrosis, and the wall of the arteriole was not thickened (Figure and ).
Electron microscopy: A large number of fibroblasts were seen in Bowman's space. There were few capillaries, and the opening was in acceptable condition. The endothelium was not hypercellular. The thickness of the basement membrane was approximately 300-500 nm. No clear mesangial area was seen, and only one podocyte showed lamellar vacuolar degeneration. There were epithelial electron dense deposits in the glomeruli (Figure and ).
Immunofluorescence (IF): Findings were as follows: IgG, diffuse granular immune reactant on the basement membrane (++++); IgA, diffuse granular immune reactant on the basement membrane (+); IgM, diffuse granular immune reactant on the basement membrane (+++); C1q, diffuse granular immune reactant on the basement membrane (++); C3, diffuse granular immune reactant on the basement membrane (++); C4, diffuse granular immune reactant on the basement membrane (++); Fibrinogen, diffuse granular immune reactant on the basement membrane (+) (Figure and ).","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [15.7, 'g/L'], 'Calcium': [1.97, 'mmol/L']}",9.84,9.348,10.332,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 15.7 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 15.7 g Albmumin/10.0 dL = 1.57 g Albmumin/dL. The concentration value of 15.7 g Albmumin/L converts to 1.57 g Albmumin/dL. 
The concentration of Calcium is 1.97 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.97 mmol. To convert 1.97 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.97 mmol Calcium * 0.001 mol/mmol = 0.00197 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00197 mol Calcium * 40.08 g/mol = 0.07896 g Calcium. To convert 0.07896 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.07896 g Calcium * 1000.0 mg/g = 78.96 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 78.96 mg Calcium/10.0 dL = 7.896 mg Calcium/dL. The concentration value of 1.97 mmol Calcium/L converts to 7.896 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.57 g/dL)) + 7.896 mg/dL = 9.84 mg/dL.
The patient's corrected calcium concentration 9.84 mg/dL."
2569,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4748919-1,Extracted,"A 14-year-old boy was admitted for the first time to our hospital, complaining of a chronic bellyache and diarrhea, intermittent fever, and occasional hematochezia lasting 1 year and 9 months. He experienced severe right lower abdominal pains, was diagnosed “appendicitis,” and received “appendicectomy” 4 months before hospitalization. In the last 2 months, he suffered from more frequent fever and hematochezia, obvious weight loss (from 40 to 30 kg), and skin nodules in four limbs and buttock, which ruptured and scabbed gradually (Figure ). He was diagnosed as IBD in local hospital, receiving mesalazine and prednisone (10 mg/day) for 1 month. He had no history of other diseases and no related family history. On physical examination, his lean appearance, superficial lymphadenopathy, and hepatosplenomegaly were noted.
Laboratory tests showed severe microcytic hypochromic anemia and hypoalbuminemia, with the hemoglobin (HGB) and serum albumin of 58 g/L (110–150) and 28 g/L (35–52), respectively. The patient suffered from decreased serum total calcium of 1.93 mmol/L (2.13–2.70) and 25-hydroxy vitamin D of 6.8 ng/ml (8–50), and elevated erythrocyte sedimentation rate (ESR) of 38 mm/hour (0–15) and C-reactive protein (CRP) of 40 mg/L (0–8). His serum ferrium, total iron binding capacity, transferrin saturation, and ferritin were all decreased. Fecal occult blood was positive, and no red and white blood cells were found in the stool. Salmonella typhi was positive from stool culture; Widal reaction was negative. T-SPOT.TB test (an assay used for tuberculosis diagnosis) was weakly positive; procalcitonin (PCT), G-test (a detection method for fungal infections), and antibodies to EBV and cytomegalovius were all negative. Autoantibodies related to IBD and autoimmune diseases were all negative. There were no evidence for tumor from bone marrow smear, tumor markers, and whole body diffusion-weighted imaging (DWI).
The abdominopelvic enhanced computed tomography (CT) scanning demonstrated bowel wall thickening, abnormally strengthening mucosal signals, and coarse serous membranes of terminal ileum, caecum, and ascending colon. Multiple enlarged abdominal lymph nodes, small intraabdominal effusions, and calcifications inside the liver and scrotum were also demonstrated. The previous colonoscopy showed ulcers and erosions; pathology showed chronic mucositis accompanied with exudation and necrosis. In order to identify his primary diagnosis, we performed skin biopsy and prepared to perform the second colonoscopy. Meanwhile, we continued his previous treatment and gave his symptomatic and supportive treatment.
However, he suddenly suffered from perforation in ileocecus (severe abdominal pain, tachycardia, and subdiaphragmatic free air). The emergency resection and anastomosis was successful, and the resected ileocecus was sent for pathology (Figure A). Several antibiotics and related treatment were added. However, on the third day after surgery, he experienced severe abdominal pain again, and excrement was found in his abdominal cavity drainage tube. Surgeons considered the second spontaneous perforation and performed the second operation. However, no gastrointestinal perforation was found, and it is incredible that there were still intestinal substances outflowing from the abdominal cavity drainage tube after surgery. His parents refused surgical treatment further; we continued medical conservative treatment.
The boy died from massive intestinal hemorrhea after a week. The pathological results of intestine and skin both showed diffuse heterotypic lymphoid cells infiltration; karyorrhexis and patchy necrosis could also be seen (Figure B–E). Combined with immunohistochemical staining (cluster of differentiation 2 (CD2)+, CD3+, CD5−, CD20−, CD4−, CD8−, CD30+ most, CD56±, T-cell restricted intracellular antigen 1 (TIA-1)+, granzyme B (GrB)+, T-cell receptor αβ (TCRαβ)−, TCRγδ−, and KI-67+ >50%; Figure ) and positive fluorescence in situ hybridization (FISH) for EBV-encoded early small ribonucleic acid (RNA) (EBER, Figure ) both in the intestine and skin, EBV-positive T/NK-cell LPD (tumor stage) was identified.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [28.0, 'g/L'], 'Calcium': [1.93, 'mmol/L']}",8.695,8.26025,9.12975,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 28.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 28.0 g Albmumin/10.0 dL = 2.8 g Albmumin/dL. The concentration value of 28.0 g Albmumin/L converts to 2.8 g Albmumin/dL. 
The concentration of Calcium is 1.93 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.93 mmol. To convert 1.93 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.93 mmol Calcium * 0.001 mol/mmol = 0.00193 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00193 mol Calcium * 40.08 g/mol = 0.07735 g Calcium. To convert 0.07735 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.07735 g Calcium * 1000.0 mg/g = 77.35 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 77.35 mg Calcium/10.0 dL = 7.735 mg Calcium/dL. The concentration value of 1.93 mmol Calcium/L converts to 7.735 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.8 g/dL)) + 7.735 mg/dL = 8.695 mg/dL.
The patient's corrected calcium concentration 8.695 mg/dL."
2570,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7187932-6,Extracted,"A 63-year-old male patient presented with pain in the right hip joint, which intensified after activity. MRI showed that signals from the right femoral neck, middle of the greater and lesser trochanters, and the mid femur were less homogeneous with the formation of a soft tissue mass and edema of the soft tissue. Emission CT showed that bone metabolism in the right femur and the left posterior ninth and tenth ribs was active. Routine blood tests revealed an HGB level of 135 g/L, total leukocyte count of 6.8 × 109/L, and platelet count of 106 × 109/L. Blood biochemistry revealed an ESR of 37 mm/hr (normal value, <22 mm/hr), serum globulin of 28.3 g/L, serum albumin of 33.1 g/L, serum creatinine of 74 μmol/L, serum calcium of 2.77 mmol/L, serum LDH of 299 U/L, and serum β2-MG of 3.9 mg/L. The serum IgG and serum kappa light chain was 17.37 g/L and 12.02 g/L, respectively. The serum EP and IEP also showed abnormally bowed arcs against IgG and anti-kappa light chain. Bone marrow (BM) aspirate demonstrated up to 13.2% dysplastic plasma cells, which were proved to be monoclonal plasma cells by flow cytometry. The pathology of the right femur puncture proved the malignant tumor; however, immunological labeling was not ideal and it was necessary to identify the plasma cell tumor and diffuse large B-cell lymphoma. Immunohistochemistry showed CK (-), Vim (-), CD5/6 (-), CK8/18 (-), P63 (-), CK18 (-), CD138 (-), Ki-67 approximately 20%, CD3 (-), CD5 (-), CD79a (+), CD20 (+), kappa (-), and lambda (-). In view of the current clinical diagnosis of MM, the VCD scheme (bortezomib 1.3 mg/m2 on days 1, 4, 8 and 11, cyclophosphamide 200 mg/m2 on days 1, 2, 3 and 4, and dexamethasone 20 mg on days 1, 2, 4, 5, 8, 9, 11 and 12;) was administered. After four cycles of chemotherapy, the levels of M protein, IgG heavy chain, and kappa light chain decreased significantly compared to before chemotherapy. However, the patient continued to suffer from pain in the right hip and MRI showed that the soft tissue mass near the right femur was larger than before. A biopsy was performed again and the immunohistochemical markers were supplemented. Finally, the diagnosis of diffuse large B-cell lymphoma was confirmed (). Thus, the ultimate diagnoses were MM with type of IgG-kappa (D-S stage IIIA and ISS stage II) and diffuse large B-cell lymphoma with the invasion of the paraplastic soft tissue (Ann-Arbor stage II and International Prognostic Index score 3). After two cycles of the R-EPOCH scheme (rituximab 600 mg on day 1, etoposide 50 mg/m2 on days 1–4, vindesine 0.4 mg/m2 on days 1–4, doxorubicin 9 mg/m2 on days 1–4; cyclophosphamide 750 mg/m2 on day 5, and prednisone 60 mg/m2 on days 1–5) combined with lenalidomide (25 mg on days 1–21), a reexamination showed that the size of the soft tissue mass had decreased significantly. The patient is still alive at present with a total survival time of more than 11 months.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [33.1, 'g/L'], 'Calcium': [2.77, 'mmol/L']}",11.654,11.0713,12.2367,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 33.1 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 33.1 g Albmumin/10.0 dL = 3.31 g Albmumin/dL. The concentration value of 33.1 g Albmumin/L converts to 3.31 g Albmumin/dL. 
The concentration of Calcium is 2.77 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 2.77 mmol. To convert 2.77 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 2.77 mmol Calcium * 0.001 mol/mmol = 0.00277 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00277 mol Calcium * 40.08 g/mol = 0.11102 g Calcium. To convert 0.11102 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.11102 g Calcium * 1000.0 mg/g = 111.02 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 111.02 mg Calcium/10.0 dL = 11.102 mg Calcium/dL. The concentration value of 2.77 mmol Calcium/L converts to 11.102 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.31 g/dL)) + 11.102 mg/dL = 11.654 mg/dL.
The patient's corrected calcium concentration 11.654 mg/dL."
2571,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2813133-1,Extracted,"A 26 year-old female patient presented a week postpartum with a history of fever, diarrhea of three days' duration, oliguria, edema of the legs, and bilateral lower limb motor weakness of one day's duration with no sensory or bladder involvement. There was no past history of diabetes, hypertension, or any similar illness. Clinical evaluation revealed pitting edema legs, normotension (blood pressure 130/80 mm Hg), paraparesis (grade 2/5 motor power), and no sensory or bladder abnormalities. Examination of the higher functions, cranial nerves, and cerebellar systems did not reveal any remarkable findings; there were no meningeal signs. Urine analysis showed 2+ proteinuria, a few RBCs, and occasional pus cells. The hemoglobin level was 12.5 g/dL, total leukocyte count was 6800 cells/cubic mm, and the platelet count was 75000/cubic mm. Renal function tests revealed severe renal failure (blood urea: 113 mg/dL, serum creatinine: 4 mg/dL, sodium: 159 meq/L, potassium: 6.9 meq/L). Liver function tests showed a total bilirubin: 0.5 mg/dL; direct bilirubin: 0.1 mg/dL, aspartate aminotransferase: 201 U/L, alanine aminotransferase: 158 U/L, alkaline phosphatase: 53 U/L, serum total protein: 5.2 g/dL, and albumin: 2.7 g/dL. Also observed were corrected serum calcium: 8.8 mg/dL, phosphorus: 4.5 mg/dL, serum CPK: 570 U/L, and serum lactate dehydrogenase: 112 U/L. Urine and blood cultures were sterile. Serum IgM antibodies for leptospira could be detected by enzyme linked immunoassay and the microagglutination test (MAT test) revealed significant antibody titers for Leptospira australis (1 in 100 titre). The kidneys were echogenic and bulky on ultrasonography while computed tomography of the brain showed an old infarct in the right frontoparietal area. Magnetic resonance imaging of the spinal cord was normal; nerve conduction studies were suggestive of bilateral crural radiculopathy.
Based on the above findings, the possibility was considered of leptospirosis manifesting with acute renal failure and paraparesis. The patient improved with antibiotics, hemodialysis, and physiotherapy support. She was discharged in an ambulatory state with improved renal function (serum creatinine: 1.2 mg/dL).","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.7, 'g/dL'], 'Calcium': [8.8, 'mg/dL']}",9.84,9.348,10.332,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.7 g/dL. 
The concentration of Calcium is 8.8 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.7 g/dL)) + 8.8 mg/dL = 9.84 mg/dL.
The patient's corrected calcium concentration 9.84 mg/dL."
2572,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2526448-1,Extracted,"In 1998, a 16-yr-old male patient visited our emergency center with a chief complaint of severe dyspnea. He was diagnosed with SAA at 11 yr of age. According to his medical record, his bone marrow was markedly hypocellular (<10% cellularity) without dysplastic features, and the Ham's and sucrose tests were negative. He received twice of ALG immunotherapies and supportive erythropoietin injections, but did not have any responses. He neither had an HLA-matched sibling stem cell donor nor found an unrelated stem cell donor despite continuous search. He was given oral oxymetholone and continuously had two pints of PRBC transfusion at a 1- to 2-week interval for five years while awaiting an HLA-matched unrelated stem cell donor. The total volume of PRBC (320-400 mL/pack) transfusion was approximately 96,000 mL during that period. Initial electrocardiography showed atrial fibrillation with a heart rate of 150/min. The chest radiography showed huge cardiomegaly with 80% of cardio-thoracic ratio and both pleural effusions (), and the erect and supine view of abdomen radiography showed a severe hepatomegaly. An echocardiographic examination presented 4% of left ventricular ejection fraction with severely dilated left ventricle and nearly akinetic cardiac wall movement. Laboratory tests showed 4.5 g/dL of hemoglobin, 20×109/L of absolute reticulocyte count, 2.7×109/L of white blood cell count (absolute neutrophil count, 0.3×109/L), 3×109/L of platelet count, 407 mg/dL of fasting blood glucose-level, and 68,800 ng/mL of serum ferritin.
We immediately admitted him to our intensive care unit. He received appropriate doses of oxygen, digitalis, diuretics, and a continuous intravenous infusion of insulin in addition to levothyroxine, calcium, and vitamin D of his previous prescriptions. Other laboratory tests showed 0.37 ng/dL of serum free thyroxine (normal range, 0.8 to 1.9 ng/dL), 142.2 mIU/L of thyrotropin (normal range, 0.4 to 4 mIU/L), 6.0 mg/dL of serum calcium level (normal range, 8.2 to 10.2 mg/dL), 13 pg/mL of intact PTH (normal range, 15 to 70 pg/mL), and 8.4% of hemoglobin A1C (normal range, 4 to 6%). These findings were suggestive of multiple endocrine dysfunctions including hypothyroidism, hypoparathyroidism with hypocalcemia, and diabetes. Liver function tests were 2.5 mg/dL of serum total bilirubin, 2.8 g/dL of serum albumin, prolonged prothrombin time of 16.4 sec (normal range, 11.1 to 13.1 sec) and 1.437 INR (normal range, 0.9 to 1.12), 35.1 sec of activated partial thromboplastin time (normal range, 25 to 38 sec), 649 IU/L of serum aspartate aminotransferase (normal range, 8 to 40 IU/L), and 539 IU/L of serum alanine aminotransferase (normal range, 5 to 40 IU/L). Ophthalmologic examination confirmed a cataract in both eyes. Generalized skin pigmentation was seen in his skin. Abdominal ultrasonography showed severe hepatomegaly with increased parenchymal echogenecity. Based on these findings, he was diagnosed with secondary hemochromatosis accompanied by multiple organ failures which resulted from iron deposition in body organs due to multiple PRBC transfusions. Based on some published reports that iron chelation plays a prominent role in hemochromatosis (, ), he received a 12-hr continuous intravenous infusion of deferoxamine (50 mg/kg/day) for five days at a 4-week interval. He received PRBC during deferoxamine treatment, if necessary. He also received innumerable units of platelet concentrates. Thereafter, he was frequently admitted to the medical intensive care unit through our emergency center because of the aggravated symptoms and signs of heart failure and diabetes-related complications, multiple cerebral and subdural hematomas, and seizure. Meanwhile, he was being given a 7-yr deferoxamine treatment. The frequency of his hospitalization was markedly being lowered, and his hematologic profiles () and heart size were beginning to nearly normalize after an approximately 4-yr deferoxamine treatment. His insulin requirement also decreased, and from then, a low-dose erythropoietin injection was initiated. Since then, he has only received outpatient care. He was noted to have completely normal ranges of peripheral blood cell counts, heart size, and liver functions two years ago. A defective expression of CD55/59 was not observed on either granulocytes or erythrocytes of peripheral blood. Since the event of complete response, his bone marrow aspirate and biopsy for the evaluation of bone marrow status has not been performed because of his strong refusal. He has not required any blood transfusions over the past four years (). He currently shows normal reference ranges of all hematologic and other laboratory tests.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [6.0, 'mg/dL'], 'Albumin': [2.8, 'g/dL']}",6.96,6.612,7.308,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.8 g/dL. 
The concentration of Calcium is 6.0 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.8 g/dL)) + 6.0 mg/dL = 6.96 mg/dL.
The patient's corrected calcium concentration 6.96 mg/dL."
2573,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,usmle-4379,Extracted,"A 75-year-old man with coronary artery disease and mitral valve stenosis status-post coronary artery bypass graft and mitral bioprosthetic valve replacement is evaluated in the intensive care unit. His postsurgical course was complicated by ventilator-associated pneumonia and bilateral postoperative pleural effusions requiring chest tubes. He has been weaned from the ventilator and has had his chest tubes removed but has required frequent suctioning to minimize aspirations. He has been dependent on a percutaneous gastrostomy tube for enteral nutrition for the past four weeks. He is currently on aspirin, carvedilol, atorvastatin, ceftazidime, and pantoprazole. He has a history of prostate cancer status post radical prostatectomy. His temperature is 96°F (35.6°C), blood pressure is 95/55 mmHg, pulse is 50/min, and respirations are 20/min. On physical exam, he is not alert and oriented but responds with moans when stimulated. His laboratory data are listed below:

Serum:
Na+: 145 mEq/L
Cl-: 110 mEq/L
K+: 3.4 mEq/L
HCO3-: 26 mEq/L
BUN: 10 mg/dL
Glucose: 112 mg/dL
Creatinine: 1.4 mg/dL
Thyroid-stimulating hormone: 10 µU/mL
Ca2+: 11.1 mg/dL
PO4-: 1.0 mg/dL
AST: 6 U/L
ALT: 10 U/L
Albumin: 2.5 mg/dL
Lactate dehydrogenase: 200 U/L (140-280 U/L)
Haptoglobin: 150 mg/dL (30-200 mg/dL)
1,25-(OH)2 D3: 10 pg/mL (15-75 pg/mL)
Parathyroid hormone: 9 pg/mL (10-60 pg/mL)

Leukocyte count: 10,000 cells/mm^3 with normal differential
Hemoglobin: 9 g/dL
Hematocrit: 30 %
Platelet count: 165,000 /mm^3

His electrocardiogram and chest radiograph are shown in Figures A and B.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [11.1, 'mg/dL'], 'Albumin': [2.5, 'mg/dL']}",14.298,13.5831,15.0129,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.5 mg/dL. We need to convert the concentration to g/dL. Let's first convert the mass of Albmumin from mg to g. The mass of Albmumin is 2.5 mg. To convert 2.5 mg of Albmumin to g, multiply by the conversion factor 0.001, giving us 2.5 mg Albmumin * 0.001 g/mg = 0.0025 g Albmumin. The volume units is dL so no volume conversion is needed. Hence, the concentration value of 2.5 mg Albmumin/dL converts to 0.0025 g Albmumin/dL. 
The concentration of Calcium is 11.1 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 0.0025 g/dL)) + 11.1 mg/dL = 14.298 mg/dL.
The patient's corrected calcium concentration 14.298 mg/dL."
2574,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5556615-1,Extracted,"An 18-month-old male child with steroid resistant nephrotic syndrome due to diffuse mesangial sclerosis rapidly progressed to end stage renal disease. He was initially started on hemodialysis followed by chronic peritoneal dialysis (PD). His chronic medications included lansoprazole, hydrocortisone, sevelamer, levothyroxine, amlodipine, epogen, ferrous sulfate, multivitamin, erythromycin, and albuterol. His main source of nutrition was a peptide-based formula that provided 1008 mg of calcium, 540 IU of vitamin D, and 30.4 mEq of potassium per day. The dialysate contained 2.5 mEq/l of calcium.
A year after being on PD, he developed persistent hyperkalemia (serum potassium 5.2 to 5.9 mEq/L) with increased doses of enalapril and was started on 0.5 g/kg of SPS. A month later, routine blood work noted improved serum potassium at 3.9 mEq/l, metabolic alkalosis (serum bicarbonate of 35 mEq/l), hypocalcemia (calcium of 6.1 mg/dl, serum albumin of 3.3 g/dl), and phosphorus of 3.7 mg/dL (). Intact PTH level had increased in the last month from 118.4 pg/ml to 180.4 pg/ml and 25(OH)-Vitamin D checked 6 months earlier was 33 ng/dL. On examination, heart rate was about 130/min and blood pressure was 102/58 mmHg. He had no tetany, normal deep tendon reflexes, a negative Chvostek sign, and no electrocardiogram (EKG) changes. He was started on 0.1 mcg of calcitriol weekly and 350 mg of calcium carbonate supplement three times a day (administered in between feeds). In a week his potassium was 4.7 mEq/L and calcium improved to 7.1 mg/dL. The following month, he had a potassium of 5 mEq/L, serum bicarbonate of 36 mEq/L, serum calcium concentration of 8 mg/dl (albumin of 3.7 g/dL), phosphorus of 2.4 mg/dl, and intact PTH level of 190 pg/ml. He had blood pressure of about 90/60 mmHg and enalapril was stopped. Sevelamer was decreased from 4.8 g to 3.2 g and SPS was discontinued.
A week later, he was noted to have a serum potassium concentration of 6.7 mEq/L, serum bicarbonate of 30 mEq/L, calcium of 8.3 mg/dl, and phosphorus of 3.3 mg/dL. He was started on 30 g of SPS (0.8 g of SPS per mEq of potassium in the formula) added to his formula for decanting. He was continued on calcium carbonate three times a day (administered with bolus feeds) and sevelamer was discontinued. Repeat serum potassium concentration was 5 mEq/L.
He had episodes of vomiting and diarrhea while being on SPS. About one week later, he had routine blood work done which was again notable for hypokalemia (serum potassium concentration of 1.7 mEq/L), persistent metabolic alkalosis (serum bicarbonate 35 mEq/L), and severe hypocalcemia (serum calcium of 4.8 mg/dL, albumin level of 3.3 g/dL). The serum phosphorus level was 4.8 mg/dL and magnesium 1.72 mg/dL. In the ED, he had a transient breath holding spell, heart rate of about 120/min and blood pressure of 114/55 mmHg, no tetany, normal deep tendon reflexes, and a normal EKG. He was treated with intravenous calcium and potassium. SPS was discontinued, calcium supplements were increased to 810 mg/day, and he was dialyzed on high calcium (3.5 mEq/L) dialysate fluid with 1 mEq/L of potassium. At the time of discharge his serum potassium concentration was 4.3 mEq/L, calcium concentration was 7.9 mg/dL, serum phosphorus level was 4 mg/dL, and magnesium level was 2.2 mg/dL. Most recently, he has maintained a stable calcium of about 9.4 mg/dL while off of SPS.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [9.4, 'mg/dL'], 'Albumin': [3.3, 'g/dL']}",9.96,9.462,10.458,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.3 g/dL. 
The concentration of Calcium is 9.4 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.3 g/dL)) + 9.4 mg/dL = 9.96 mg/dL.
The patient's corrected calcium concentration 9.96 mg/dL."
2575,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4871206-1,Extracted,"A 36-year-old Native American man with history of tobacco use was transferred from an outside hospital with a hyperacute presentation of hemoptysis and rapidly worsening respiratory distress. At the time of admission to our facility, he was intubated with an oxygen saturation of 88% and a pulse of 109 beats per minute. He was obtunded and sedated on a ventilator. Physical exam revealed decreased breath sounds bilaterally and mild generalized edema in his lower extremities. The patient had oliguria (~170 mL over 24 hours). Outside medical records indicated that he was diagnosed with streptococcal pharyngitis (testing methodology not stated) 2 weeks before admission and was prescribed penicillin. He had no history of recent travel, autoimmune or clotting disorders.
Abnormal laboratory findings on admission included white blood cell count 20 800/µL, hemoglobin 12.8 g/dL, hematocrit 39%, C-reactive protein 11.5 mg/dL, fibrinogen 566 mg/dL, glucose 125 mg/dL, calcium 8 mg/dL, phosphorus 5.8 mg/dL, magnesium 2.8 mg/dL, albumin 2.5 g/dL, globulin gap 5.3 g/dL. An arterial blood gas analysis revealed the following values: pH 7.29, pO2 58 mm Hg, pCO2 43 mm Hg (). Creatinine was 1.78 mg/dL with a blood urea nitrogen level of 52 mg/dL. Urinalysis showed proteinuria and hematuria with multiple dysmorphic red blood cells in the urine sediment. Antistreptolysin O (ASO) antibodies were elevated at 1270 IU/mL, suggesting recent infection with group A streptococcus. C3 (9 mg/dL) and C4 (8.9 mg/dL) were also measured.
A chest X-ray () noted bilateral airspace consolidation. An outside chest computed tomography scan showed diffuse centralized alveolar densities in both lungs suggestive of alveolar hemorrhage. Due to hemoptysis, a bronchoscopy was performed, which revealed a bloody lavage and erythematous mucosa in the main stem bronchi and subsegments. The bronchoalveolar lavage consisted predominantly of neutrophils with a few mononuclear cells. The culture had no growth. The patient was started on intravenous methylprednisolone (1 g/day) and plasmapheresis.
The patient’s renal function worsened in the first 3 days and was restored after 4 sessions of plasmapheresis during the first week (). The ASO levels showed progressive decline with each session of serum exchange (). Immunoassays including antinuclear antibody, anti–double stranded DNA, antiphospholipid, antiglomerular basement, and antineutrophil cytoplasmic antibodies were negative. Infectious process was ruled out by testing including chest X-ray, urinalysis, and blood, urine, and sputum cultures. The patient was in critical condition, and in the setting of the patient’s rapid improvement with the treatment, the likelihood of acute post-streptococcal glomerulonephritis (APSGN) was high. Therefore, lung and kidney biopsies were not performed as the risks outweighed the benefits at the time. Given the patient’s history of pharyngitis, clinical presentation, laboratory analyses, and response to immunosuppressive regimen, he was diagnosed with PRS secondary to streptococcal pharyngitis.
The patient’s pulmonary function gradually improved, and he was extubated on day 8. His edema cleared and the majority of his laboratory findings normalized by 11 days postadmission. He noted poor adherence to penicillin treatment after streptococcal pharyngitis. After full recovery, he was discharged to his home on day 12 with a tapering dose of steroids.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.5, 'g/dL'], 'Calcium': [8.0, 'mg/dL']}",9.2,8.74,9.66,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.5 g/dL. 
The concentration of Calcium is 8.0 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.5 g/dL)) + 8.0 mg/dL = 9.2 mg/dL.
The patient's corrected calcium concentration 9.2 mg/dL."
2576,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7890937-1,Extracted,"A 64-year-old man with a history of chronic obstructive pulmonary disease and ethanol abuse use presented to the emergency department with altered mentation. He was obtunded on arrival, unable to provide any additional history. Presenting vitals were notable for blood pressure of 150/93, pulse of 69 beats per minute, temperature of 97.3 °F (36.3 °C), respiratory rate of 18 BPM, and SpO2 95%. Physical exam revealed bilateral upper extremity tremors and obtundation. Pupils were symmetric and reactive to light, and he periodically tracked with his eyes. Neurological exam, including reflexes, was limited due to altered mental status. Cardiopulmonary exam was benign. Chest X-ray was notable for a normal cardiopulmonary silhouette. Electrocardiogram revealed normal sinus rhythm with a QTc interval of 409 ms. Computed tomography of the brain without contrast showed normal gray-white matter differentiation.
Laboratory evaluation revealed a sodium 143 mEq/L (135 – 145 mEq/L), potassium 3.0 mEq/L (3.6 – 5.1 mEq/L), chloride 105 mEq/L (98 – 110 mEq/L), bicarbonate 27 mEq/L (22 – 32 mEq/L), blood urea nitrogen 14 mg/dL (6 – 24 mg/dL), creatinine 1.11 mg/dL (0.64 – 1.27 mg/dL), undetectable blood ethanol level, blood glucose 95 mg/dL (67 – 99 mg/dL), calcium 12.8 mg/dL (8.5 – 10.5 mg/dL), ionized calcium 6.3 mg/dL (4.2 – 5.2 mg/dL), phosphorus of 2.2 mg/dL (2.4 – 4.8 mg/dL), and albumin 4.0 g/dL (3.5 – 5.0 g/dL). Initial management consisted of volume expansion with 3 L normal saline without improvement in mentation. Calcitonin was given on hospital day 2 and zoledronic acid was given on hospital day 3, but hypercalcemia persisted. Further labwork returned with intact parathyroid hormone (iPTH) 17 pg/mL (18 – 80 pg/mL), parathyroid hormone related peptide (PTHrP) 9 pg/mL (pg/mL 14 – 27), serum protein electrophoresis (SPEP) and immunofixation (IFE) without evidence of monoclonal protein, κ light chains 85.4 mg/L (3.3 – 19.4 mg/L), λ light chains 40.8 mg/L (5.7 – 26.3 mg/L), and β-2 microglobulin 3.75 mg/L (0.97 – 2.64 mg/L). The elevation of κ/λ ratio in the setting of a normal glomerular filtration rate prompted evaluation for a monoclonal gammopathy. Skeletal survey was negative for lytic lesions and bone marrow biopsy was negative for plasma cell dyscrasia. Finally, the following labs resulted: 25-hydroxy vitamin D > 150 ng/mL (30.0 – 100.0 ng/mL), 1,25-hydroxy vitamin D 36 pg/mL (18 – 72 pg/mL). The patient remained agitated and confused for the first 10 days of hospitalization, but mentation improved thereafter with calcium normalizing after 18 days. Upon recovery, he reported misunderstanding medication instructions and had been consuming 4 vitamin D 50,000 IU tablets daily.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [12.8, 'mg/dL'], 'Albumin': [4.0, 'g/dL']}",12.8,12.16,13.44,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.0 g/dL. 
The concentration of Calcium is 12.8 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.0 g/dL)) + 12.8 mg/dL = 12.8 mg/dL.
The patient's corrected calcium concentration 12.8 mg/dL."
2577,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5121444-1,Extracted,"A 70-year-old woman was presented with loin pain of 2 months and unable to stand and walk for 2 weeks, with no comorbidities. In her physical examination, there were blood pressure of 130/80 mmHg, body temperature of 37.3°C, a pulse of 86 bpm, and grade 3 motor weakness of lower limbs. Biochemical profile of the patient was identified as glucose 98 mg/dL, blood urea nitrogen 198 mg/dL, serum creatinine 3,5 mg/dL, uric acid 17,4 mg/dL total protein 9,8 gr/dL, serum albumin 4,0 gr/dL, calcium 6,5 mg/dL, phosphate 8,7 mg/dL, potassium 5,1 mmol/L, LDH 856 IU/L, white cell count 11 000 mm3/uL, Hb 5,7 gr/dL, Htc 17%, and platelet count 28 000/mm3. Arterial blood gas analysis was evaluated as metabolic acidosis (pH 7,22, HCO3 13 mEq/L, PCO2 27 mmHg, and PO2 96 mmHg). A radiography of the thoracal spine showed a compression fracture of the T12 vertebra. In serum protein electrophoresis, M-band was documented. Serum immunoglobulin Ig G was 5,6 g/dL. Serum and urine protein immunofixation revealed kappa light chain. Bone marrow aspiration smear showed abnormal plasma cells. Bone marrow biopsy showed plasma cells accounting for 90% of all cells; normal erythroid and myeloid cells were markedly suppressed. Immunohistochemistry examinations revealed kappa positive.
Our patient fulfilled clinical (acute renal injury) and laboratory criteria (hyperuricemia, hyperphosphatemia, and hypocalcemia) of TLS according to the Cairo and Bishop criteria []. The diagnosis of MM and spontaneous TLS were established. Medical treatment was initiated upon of TLS. The patient was treated with hydration, allopurinol, calcium gluconate, and sodium bicarbonate. After one week of initiating treatment, laboratory data showed glucose 117 mg/dL, blood urea nitrogen 48 mg/dL, serum creatinine 0,9 mg/dL, uric acid 3,2 mg/dL, serum albumin 3,5 gr/dL, calcium 7,8 mg/dL, phosphate 2,7 mg/dL, potassium 4,9 mmol/L, LDH 724 IU/L, white cell count 5300 mm3/uL, Hb 10,4 gr/dL, Htc 30,3%, and platelet count 40 000/mm3. Arterial blood gas analysis was normal.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.0, 'g/dL'], 'Calcium': [6.5, 'mg/dL']}",6.5,6.175,6.825,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.0 g/dL. 
The concentration of Calcium is 6.5 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.0 g/dL)) + 6.5 mg/dL = 6.5 mg/dL.
The patient's corrected calcium concentration 6.5 mg/dL."
2578,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4815244-1,Extracted,"A 67-year-old Caucasian woman was admitted to the emergency department with palpitations, and dizziness in the past 2 days. She complained of fatigue after minor effort, weight loss (11 kg in 3 years) without anorexia, and hand tremor. She had no complaints of dyspnea, orthopnea or chest pain. She had no heat intolerance nor increased frequency of bowel movements.
Our patient had a history of breast cancer diagnosed at the age of 37 and treated with right radical mastectomy and adjuvant chemotherapy. She underwent total thyroidectomy for nontoxic multinodular goiter [thyroid-stimulating hormone (TSH) 3.77 of μU/mL and free thyroxine (T4) of 1.53 ng/dL] with a dominant colloid nodule of 30 mm at the age of 60; the histological analysis confirmed multinodular adenomatous goiter weighing 66 g with no signs of malignancy. She was medicated with levothyroxine 100 μg/day since the surgery and had no follow-up. She smoked 20 cigarettes a day for the last 50 years.
At physical examination, our patient was conscious and oriented. Her temperature was 36.7 °C, she had a body mass index of 19.7 kg/m2, blood pressure of 122/76 mmHg, a heart rate of 130 bpm, and fine tremor at rest. She had no eye involvement. A cervical examination showed no palpable masses or adenomegaly. Pemberton’s sign was negative. The pulmonary sounds were normal and she had no cardiac murmur. She had no peripheral edema.
At admission, our patient had a hemoglobin level of 11.5 g/L (12–16); a normal white blood cell and platelet count; a normal liver panel; an albumin level of 32.6 g/dL (38–51); normal renal function and ionogram; corrected total calcium level of 9.6 mg/dL (8.1–10.4); B-type natriuretic peptide level of 442.2 pg/mL (<100); and a troponin I level <0.010 ng/mL. She had suppressed levels of TSH (0.000 μU/mL) and increased levels of free T4 3.22 ng/dL (0.70–1.48) and free triiodothyronine (T3) 8.46 pg/mL (1.71–3.71). In the electrocardiogram, she had sinus tachycardia of 117 bpm and incomplete right bundle branch block and left anterior fascicle block. Her chest roentgenogram showed normal cardiothoracic index, no pulmonary congestion, no mediastinal enlargement nor tracheal deviation.
She was admitted to the endocrinology department with a diagnosis of iatrogenic thyrotoxicosis. She was started on bisoprolol 5 mg and levothyroxine was stopped. Her heart rate remained under 100 bpm and her blood pressure was always normal. Her extremities’ rest tremor persisted. She showed no improvement on her free T4 and free T3 levels 10 days after levothyroxine treatment withdrawal (Table ). Her thyroglobulin levels were increased to 294 mg/mL (0–55). A cervical ultrasound scan revealed no thyroid remnant in the gland bed. Test results for anti-TSH receptor antibodies (TRAb) were positive – 19.7 U/L (<1.8) – and for anti-thyroperoxidase antibodies were negative – 0.6 U/mL (<5.61). Corporal scintigraphy with I-131 with single-photon emission computed tomography (SPECT) revealed an intrathoracic mass (60 × 40 mm) with increased radioiodine uptake and no increased uptake in the thyroid bed (Fig. ). A computed tomography (CT) scan of her neck and thorax confirmed a heterogeneous mass with 67 × 46 × 52 mm in the anterior mediastinum superiorly (Figs. and ).
The final diagnosis was Graves’ disease in mediastinal thyroid tissue. She was discharged with bisoprolol 5 mg/day and methimazole 10 mg/day.
Three months later, after achieving euthyroidism, she underwent surgical resection of the mass through a horizontal cervical incision. The thyroid tissue found in the superior mediastinum had cervical vascularization. There was no complication in the postoperative period. The histology showed hyperfunctional tissue with thyroid follicles of variable shape and form with papillary hyperplasia and some adenomatous areas; no signs of malignancy were found.
Our patient remained asymptomatic and with normal thyroid function under levothyroxine 88 μg/day (1.6 μg/kg) 5 months after surgery.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [32.6, 'g/dL'], 'Calcium': [9.6, 'mg/dL']}",-13.28,-12.616,-13.944,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 32.6 g/dL. 
The concentration of Calcium is 9.6 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 32.6 g/dL)) + 9.6 mg/dL = -13.28 mg/dL.
The patient's corrected calcium concentration -13.28 mg/dL."
2579,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4532131-1,Extracted,"A 55-year old female patient who had had a sub-total gastrojejunostomy seven years ago because of peptic ulcer was admitted to the local hospital on July 9, 1986 complaining of hematemesis, dizziness, and epigastric pain. Iced saline gastric lavage was done for massive hematemesis and two units of packed red blood cells and one unit of whole blood were given but massive bleeding continued. The patients was transferred to the Kang Nam Sacred Heart Hospital for further management.
Physical examination disclosed pallor. The blood pressure was 130/70, the pulse 140 beats per minute and the temperature 37.2°C. Distention of the neck veins was minimal. The lungs were clear on auscultation. The heart was not enlarged and no murmurs were audible. Examination of the abdomen was negative. Rectal examination revealed the presence of dark red stool.
The packed cell volume was 25 per cent and the leukocyte count was 14300 per cubic millimeter. Urinalysis revealed no abnormalities. An electrocardiogram showed sinus tachycardia. Chest film showed no abnormal finding. Laboratory data were as follows: total protein 4.0 g/dl, albumin 2.3 g/dl, GOT 16 IU/I, GPT 12 IU/I, cholesterol 68mg/dl, blood urea nitrogen 21.0 mg/dl, creatinine 0.6 mg/dl, sodium 135mEq/l, potassium 4.1 mEq/l, chloride 100 mEq/l, calcium 7.1 mg/dl, and phosphorus 2.8 mg/dl.
After admission, nasogastric tube lavage was done, which revealed coffee ground material and later bright red blood. As the patient became hypotensive and pale during the nasogastric tube irrigation, she was given 4 units of packed red blood cells, and 2 units of fresh frozen plasma. After the blood pressure had been stabilized by transfusion and iced saline gastric lavagean, emergency fiberoptic gastroscopy was performed. The stomach was in the state of subtotal gastrectomy with gastrojejunostomy. In the anastomotic area (at the jejunal side), a small vessel was exposed where some bleeding was noticed (). After the lesion was injected with epinephrine, a laser was used to photocoagulate the lesion. Multiple applications using a power setting of 60 watts and a duration of 0.5 sec were applied around and later to the center of the lesion and the bleeding was stopped ().
After laser therapy, the patient was under the fasting state for 2 days and treated with cimetidine and antacid. For two days, melena was presented. Then, a liquid diet was started and the patient’s general condition was improved during admission. She was discharged 10 days after laser therapy in good condition.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.3, 'g/dL'], 'Calcium': [7.1, 'mg/dL']}",8.46,8.037,8.883,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.3 g/dL. 
The concentration of Calcium is 7.1 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.3 g/dL)) + 7.1 mg/dL = 8.46 mg/dL.
The patient's corrected calcium concentration 8.46 mg/dL."
2580,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5836184-1,Extracted,"A 20-year-old male patient presented to the Emergency Department of our hospital with progressive abdominal pain and dyspnea during the previous 10 days, followed by cyanosis during the previous 3 days. His past medical history was uneventful. He denied alcohol intake, drug use, and transfusions. At admission, physical examination revealed a heart rate of 112 beats per minute, a blood pressure of 80/50 mm Hg, a respiratory rate of 22 breaths per minute, and a temperature of 36°C. The patient was icteric and showed central cyanosis. His abdomen was distended, and bowel sounds were hypoactive, with generalized tenderness, guarding, and rebound tenderness. Liver and spleen were not palpable. Blood count showed hemoglobin of 10.9 g/dL, a platelet count of 184 × 109, and a white cell count of 19.2 × 109, with predominance of neutrophils (84.9%). Coagulation screening tests showed a prothrombin time of 30.5 seconds, activated partial thromboplastin time of 37.1 seconds, and international normalized ratio of 2.77. Biochemical analysis showed a blood glucose of 69 mg/dL, serum creatinine of 2.45 mg/dL, blood urea nitrogen test 81.6, sodium 127 mmol/L, potassium 5.19 mmol/L, chloride 89 mmol/L, calcium 4.25 mmol/L, and phosphorus 3.8 mmol/L. Liver functions showed total bilirubin and direct bilirubin levels were 5.18 mg/dL and 3.47 mg/dL, respectively. Total protein was 6.44 mg/dL, serum albumin 3.24 mg/dL, serum alanine aminotransferase 573 U/L, serum aspartate aminotransferase 1,256 U/L, serum alkaline phosphatase value 456 U/L, and serum lactic dehydrogenase 6,744 U/L, and arterial blood gas analysis showed pH 7.29 and lactate 8.2 mmol/L. The patient initially received crystalloids, followed by packed red blood cells and fresh frozen plasma. Abdominal computed tomographic (CT) scan showed mild hepatomegaly, perihepatic and flank fluid, and multiple hypodense liver lesions suggestive of intrahepatic metastases or multifocal HCC (Fig. ). Transcatheter arterial embolization (TAE) was unavailable at the time of presentation. At emergency laparotomy, 2,800 mL of blood in the abdominal cavity were discovered; two actively bleeding liver tumors in segments III and VI, and multiple small nonbleeding tumors were observed (Fig. ). The liver did not show a cirrhotic aspect, and biopsy was taken. Suture plication and surgical perihepatic packing were performed. The patient was admitted to the Intensive Care Unit, under mechanical ventilatory support, with hemodynamic instability and coagulopathy. Despite the proper management, the patient had a fatal outcome 48 h after the surgical procedure. Histopathologic analysis reported HCC and absence of cirrhotic changes (Fig. ).","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.24, 'g/dL'], 'Calcium': [4.25, 'mmol/L']}",17.642,16.7599,18.5241,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.24 g/dL. 
The concentration of Calcium is 4.25 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 4.25 mmol. To convert 4.25 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 4.25 mmol Calcium * 0.001 mol/mmol = 0.00425 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00425 mol Calcium * 40.08 g/mol = 0.17034 g Calcium. To convert 0.17034 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.17034 g Calcium * 1000.0 mg/g = 170.34 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 170.34 mg Calcium/10.0 dL = 17.034 mg Calcium/dL. The concentration value of 4.25 mmol Calcium/L converts to 17.034 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.24 g/dL)) + 17.034 mg/dL = 17.642 mg/dL.
The patient's corrected calcium concentration 17.642 mg/dL."
2581,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7226549-2,Extracted,"A 76-years-old female patient was admitted to the Clinic of Nephrology in March 2018 for diagnostic evaluation of renal failure (serum creatinine, 198 µmol/l), anemia (hemoglobin, 102 g/l), and thrombocytopenia (75 G/l).
The clinical laboratory investigations revealed anemia (hemoglobin, 98 g/l) with low platelet count (95 G/l), serum creatinine 179 µmol/l, calcium 2.45 mmol/l, total protein 97 g/l, albumin 44 g/l, IgG 29.3 g/l, IgA 0.9 g/l, IgM 0.9 g/l, and proteinuria 6.4 g/24 h. Serum and urine immunofixation () revealed biclonal gammopathy IgG κ + IgG λ and the patient was referred to the clinic of hematology for further treatment of biclonal myeloma.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [44.0, 'g/L'], 'Calcium': [2.45, 'mmol/L']}",9.5,9.025,9.975,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 44.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 44.0 g Albmumin/10.0 dL = 4.4 g Albmumin/dL. The concentration value of 44.0 g Albmumin/L converts to 4.4 g Albmumin/dL. 
The concentration of Calcium is 2.45 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 2.45 mmol. To convert 2.45 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 2.45 mmol Calcium * 0.001 mol/mmol = 0.00245 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00245 mol Calcium * 40.08 g/mol = 0.0982 g Calcium. To convert 0.0982 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.0982 g Calcium * 1000.0 mg/g = 98.2 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 98.2 mg Calcium/10.0 dL = 9.82 mg Calcium/dL. The concentration value of 2.45 mmol Calcium/L converts to 9.82 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.4 g/dL)) + 9.82 mg/dL = 9.5 mg/dL.
The patient's corrected calcium concentration 9.5 mg/dL."
2582,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2561009-1,Extracted,"A 60-year-old Caucasian woman with a history of stage 5 chronic kidney disease presented with complaints of heaviness and pain in the medial aspect of left thigh, worsening over seven days. She denied any fever, chills or rigors. Past medical history was remarkable for coronary artery disease, hypertension, well controlled Type II diabetes mellitus diagnosed nine years ago, (hemoglobin A1C of 5.6, six months prior to presentation) and chronic kidney disease stage 5 (glomerular filtration rate: 12 ml/min/1.73 m2). Her medications included pioglitazone, furosemide, atenolol, lovastatin, lisinopril, isosorbide mononitrate and metolazone. Physical exam revealed some tenderness on the left thigh region but no edema or erythema. She had palpable pulses bilaterally. Rest of the physical exam was within normal limits. A doppler ultrasound performed on bilateral lower extremities was negative for deep vein thrombosis. Laboratory data revealed a white blood cell count 13.1 thousand/mm3, hemoglobin 8.6 mg/dl, blood urea nitrogen 52 mmol/l, creatinine 4.7 mmol/l (baseline creatinine around 5.0 mmol/l), calcium 10.4 mmol/l, albumin 2.2 gm/dl, phosphorus 8 mmol/l and a parathyroid hormone (PTH) level of 2138 pg/dl (with a level of 1381 pg/dL 6 months prior) On the fifth day of hospitalization, she started developing peridermal necrotic areas along with erythema and tenderness in her thigh (Figure ). She was initially started on vancomycin as the lesions were suspected to be secondary to local cellulitis. However the absence of fever and the presence of a markedly raised PTH levels along with the clinical picture of widespread necrosis with erythema made calciphylaxis a possibility. X-ray of left thigh was then obtained demonstrating extensive vascular calcifications (figures and Figure ) thus making calciphylaxis highly likely on our list of differential diagnosis. We did not perform biopsy of the plaques as biopsy of a calciphylactic tissue is known to precipitate ulceration and subsequent infection [,]. Patient was started on chronic renal replacement therapy and pain control and discharged home to be followed up as an outpatient. She presented back to the hospital because of worsening left thigh ulceration and related pain. Subtotal parathyroidectomy was then performed on this hospitalization because of very high concentration of parathyroid hormone. After parathyoidectomy, patient's calcium phosphorus product decreased from 80 to 30. Serum calcium and phosphorus had decreased to 8.2 mg/dl and 3.7 mg/dl respectively. On out patient follow up her serum intact parathyroid hormone level decreased to19 pg/ml over a 2 month period. Her skin lesions continued to progress and she complained of significant pain related to these lesions. We then performed a thorough literature review regarding various treatment options available for calciphylaxis and had detailed discussion with the patient regarding the same. Decision was made to try sodium thiosulfate. She was administered sodium thiosulfate therapy 3 times weekly (25 g intravenously over 30 to 60 minutes) following each hemodialysis session. Over the next 2 weeks patient had significant improvement in her pain symptoms and marked decrease in analgesic demand. She was then transferred to a nursing home with continued use of sodium thiosulfate along with each hemodialysis session. After 3 weeks patient was readmitted to the hospital with worsening skin lesions extending to involve her abdomen, buttocks and calf region in bilateral lower extremities. Patient was continued on sodium thiosulfate for 4 more weeks but her skin lesions continued to progress and deteriorate. Various other management options were again discussed with the patient and the decision was reached to keep her comfortable and her management was transferred to hospice care","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.2, 'g/dL'], 'Calcium': [10.4, 'mmol/L']}",43.123,40.96685,45.27915,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.2 g/dL. 
The concentration of Calcium is 10.4 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 10.4 mmol. To convert 10.4 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 10.4 mmol Calcium * 0.001 mol/mmol = 0.0104 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.0104 mol Calcium * 40.08 g/mol = 0.41683 g Calcium. To convert 0.41683 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.41683 g Calcium * 1000.0 mg/g = 416.83 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 416.83 mg Calcium/10.0 dL = 41.683 mg Calcium/dL. The concentration value of 10.4 mmol Calcium/L converts to 41.683 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.2 g/dL)) + 41.683 mg/dL = 43.123 mg/dL.
The patient's corrected calcium concentration 43.123 mg/dL."
2583,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4400567-1,Extracted,"A 61-year-old woman with history of Type 2 diabetes, hypertension and gout developed worsening hypertension and new-onset hematuria. Evaluation by her cardiologist showed hypochromic and microcytic anemia with hemoglobin 9.4 mmol/L (normal range 8.4–10.9 mmol/L) and AKI with serum creatinine 710.0 µmol/L (baseline <133 µmol/L). The patient was transferred to a tertiary referral hospital for further evaluation of AKI.
On physical examination, she appeared acutely ill. Temperature was 37.4°C, blood pressure 176/89 mm Hg, pulse 63 and respirations 21/min. Physical examination demonstrated normal heart sounds with no murmur, clear lungs, a soft, nontender, obese abdomen with no organomegaly and 2+ pitting edema of the lower extremities bilaterally. There was no skin rash. Laboratory data demonstrated sodium 138 mmol/L, potassium 4.7 mmol/L, chloride 106 mmol/L, bicarbonate 18 mmol/L, calcium 2.2 mmol/L, phosphorus 1.1 mmol/L, BUN 8.8 mmol/L, creatinine 790 µmol/L, glucose 12.5 mmol/L, total serum protein 61.0 g/L and albumin 31.0 g/L. Serum titers of antinuclear antibody, antidouble-stranded DNA, c-antineutrophil cytoplasmic antibody and antiglomerular basement membrane (GBM) antibodies were negative. Complement levels (C3 1.5 g/L, C4 0.4 g/L) were within normal limits. Serum and urine protein electrophoresis revealed no monoclonal spike. However, p-ANCA was >100 kU/L (normal <2.8 kU/L) and antimyeloperoxidase was >1:640 (normal <6 kU/L). Urinalysis showed proteinuria and microscopic hematuria with dysmorphic red blood cells. Proteinuria was 15.0 g/24 h. Renal ultrasonography showed the right kidney 10.4 cm and the left 11.2 cm in length. There was no history of alcohol abuse or smoking. She had poorly controlled Type 2 diabetes and hypertension for 10 years, complicated by neuropathy. She had no familial history of kidney disease. A percutaneous renal biopsy was performed to assess the cause of her rapidly progressive glomerulonephritis.
The renal biopsy specimen included two pieces of cortex containing nine glomeruli, four of which were globally sclerosed. There was mild increase in mesangial matrix and cellularity but no endocapillary proliferation. The GBM showed very rare spikes and rare holes (), segmental corrugation and split appearance. Two glomeruli had fibrinoid necrosis with fibrocellular crescents and segmental sclerosis with adhesions (). There was ∼40% interstitial fibrosis with proportional tubular atrophy and mild lymphoplasmacytic infiltrate. There was ATI involving ∼20% of tubular profiles with sloughing off of tubular epithelial cells. There were rare proteinaceous casts. There were no crystals or polarizable material. Arterioles were unremarkable. Interlobular arteries showed mild tortuosity without fibrinoid necrosis or inflammation.
Five glomeruli were present in frozen sections processed for immunofluorescence microscopy. There was 1+ (0 to 3+ scale) segmental granular capillary loop and mesangial staining for immunoglobulin G (IgG) () and 1+ C3 and equal 1+ kappa and lambda light chain staining in a similar pattern as IgG. There was no glomerular staining for IgA, IgM and C1q. There was no tubular basement membrane staining for any antisera. Immunofluorescence studies for subclasses of IgG, namely IgG1, IgG2, IgG3 and IgG4 were performed. There was dominant IgG4 segmental granular capillary loop and mesangial staining. IgG1, IgG2 and IgG3 were negative.
On electron microscopy, GBM showed normal thickness of lamina densa with occasional to scattered small to medium subepithelial deposits (), very rare small subendothelial deposits and rare mesangial deposits. There was ∼60% podocyte foot process effacement. There were no fibrin tactoids, tubuloreticular arrays and no increase in mesangial matrix or cellularity. There were no tubular basement membrane deposits.
Early membranous glomerulopathy (MG), with superimposed pauci-immune necrotizing crescentic glomerulonephritis (PNCGN) and focal ATI.
The patient was treated with hemodialysis and plasmapheresis × 5, and begun on immunosuppression with intravenous cyclophosphamide and prednisone. Her renal function did not recover and she remained on dialysis 6 months after the renal biopsy. Currently, she is being evaluated for renal transplantation.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [31.0, 'g/L'], 'Calcium': [2.2, 'mmol/L']}",9.538,9.0611,10.0149,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 31.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 31.0 g Albmumin/10.0 dL = 3.1 g Albmumin/dL. The concentration value of 31.0 g Albmumin/L converts to 3.1 g Albmumin/dL. 
The concentration of Calcium is 2.2 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 2.2 mmol. To convert 2.2 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 2.2 mmol Calcium * 0.001 mol/mmol = 0.0022 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.0022 mol Calcium * 40.08 g/mol = 0.08818 g Calcium. To convert 0.08818 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.08818 g Calcium * 1000.0 mg/g = 88.18 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 88.18 mg Calcium/10.0 dL = 8.818 mg Calcium/dL. The concentration value of 2.2 mmol Calcium/L converts to 8.818 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.1 g/dL)) + 8.818 mg/dL = 9.538 mg/dL.
The patient's corrected calcium concentration 9.538 mg/dL."
2584,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2500028-1,Extracted,"A 50-year-old man of Indian ancestry who was diagnosed with multiple myeloma three years earlier was evaluated in our hospital. His only other chronic medical issue was mild hypertension. His myeloma had progressed rapidly since diagnosis despite a variety of therapies over the years including systemic corticosteroids, cyclophosphamide, etoposide, cisplatin, stem cell transplantation, thalidomide, and for the most recent three months, bortezomib. Blood work and magnetic resonance imaging at a recent out-patient visit demonstrated pancytopenia as well as diffuse myelomatous bone marrow replacement throughout his pelvis and proximal femora (Figure ). At this time, he was being hospitalized due to extensive fluid retention in the abdomen and lower extremities as well as dyspnea. He stated that he had gained 15 pounds over the past two weeks. On initial examination, he was afebrile with a heart rate of 100 beats/minute and a blood pressure of 97/50 mmHg. His oxygen saturation was 96% while receiving oxygen at 3 liters/minute by nasal cannula. He had crackles at the bases of his lungs bilaterally. His cardiovascular exam was remarkable for 12 cm of jugular venous distension and tachycardia with a 2/6 systolic flow murmur at the left upper sternal border. His abdomen was distended with shifting dullness to percussion and a liver edge 4 cm below the right costal margin. His extremities were warm to touch with 3 + bilateral lower extremity edema as well as significant scrotal edema. Pertinent initial laboratory studies were remarkable for a hemoglobin of 9.1 g/dl, a platelet count of 10,000 per microliter, a blood urea nitrogen of 55 mg/dl, a creatinine of 1.0 mg/dl, an albumin of 3.6 g/dl, and a calcium of 13 mg/dl. The ECG demonstrated sinus tachycardia with normal voltage and diffuse T wave flattening. His chest X-ray demonstrated mild cardiomegaly and evidence of pulmonary edema. An echocardiogram conveyed a hyperdynamic left ventricle with normal wall thickness, no regional wall motion abnormalities, no valvular abnormalities and normal diastolic function. Thrice daily intravenous furosemide was administered for the first ten hospital days. Despite aggressive diuretic therapy, the patient's volume status worsened. On the eleventh hospital day, cardiac catheterization was performed (Table ). Based on the high output values obtained at catheterization, a thyroid panel was obtained which was unremarkable. In addition, he was given empiric thiamine replacement, placed on broad-spectrum antibiotics for possible sepsis, and was started on a continuous intravenous infusion of furosemide. His respiratory status continued to worsen and on hospital day number 14, he required intubation and mechanical ventilation for hypoxemic respiratory failure (Figure ). His volume status continued to worsen over the next 2 days despite the aforementioned therapy. As a last resort, it was decided to initiate therapy targeting the underlying myeloma on hospital day 17. Lenalidomide 25 mg and dexamethasone 40 mg daily were administered through the patient's nasogastric tube. Within 24 hours, a brisk diuresis was observed and he was successfully extubated on hospital day 19. Dexamethasone was discontinued per protocol after hospital day 20, though lenalidomide was continued. By hospital day 27, he had a net negative fluid balance of 15 liters and he was discharged out of the intensive care unit. Unfortunately, on hospital day 35 in the setting of his long standing refractory thrombocytopenia, he developed a massive upper gastrointestinal bleed that could not be controlled despite aggressive resuscitory efforts and died within hours.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.6, 'g/dL'], 'Calcium': [13.0, 'mg/dL']}",13.32,12.654,13.986,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.6 g/dL. 
The concentration of Calcium is 13.0 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.6 g/dL)) + 13.0 mg/dL = 13.32 mg/dL.
The patient's corrected calcium concentration 13.32 mg/dL."
2585,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-8546823-1,Extracted,"A 56-year-old woman visited the emergency department of an affiliated hospital with progressive upper abdominal discomfort, intermittent nausea, and abnormal vaginal bleeding, for 1 wk.
Initially, there was no apparent jaundice or changes in blood pressure. The patient denied any fever, dizziness, headache, or disturbance of consciousness at the beginning of the illness.
The patient had a history of Helicobacter pylori infection for more than 10 years. She had no relevant past interventions.
She denied family or psycho-social history.
The patient had stable vital signs: body temperature was 37.0 °C, blood pressure was 168/87 mmHg, heart rate was 74 bpm, and respiratory rate was 25 breaths/min, with obvious upper abdominal tenderness, slight rebound pain, and muscle tension.
Laboratory examination results were as follows: white blood cell count 26.5 × 109/L, neutrophil percentage 95%, C-reactive protein 109 mg/L, procalcitonin 4.35 ng/mL, serum amylase 1222.5 U/L, creatinine 172.3 µmol/L, urine amylase 1433.0 U/L, platelet 214 × 109/L, hemoglobin 156 g/L, albumin 26.8 g/L, alanine aminotransferase 19.5 U/L, aspartate aminotransferase 26.6 U/L, lactate dehydrogenase 457.3 U/L, ferritin 747 ng/mL, and 25-hydroxyvitamin D < 3 ng/mL. Serum calcium increased significantly to 4.72 mmol/L, with parathyroid hormone (PTH) rising to 366.90 pg/mL and carbohydrate antigen 125 to 142.5 U/mL. An overview of selected initial laboratory values is shown in Table .
Non-contrast enhanced computed tomography (CT) of the abdomen showed exudation around the pancreas (Figure and ). Ultrasound examination of the neck revealed an inferior thyroid nodule and mild hyperplasia of the parathyroid gland. Head magnetic resonance imaging (MRI) was performed, and abnormal signals were found in the bilateral fronto-parietal-temporal-occipital cortex-medullary junction area and bilateral paraventricular area, which were likely due to metabolic encephalopathy related to pancreatitis (Figure and ). A repeat non-contrast enhanced CT scan of the abdomen (Figure and ) and head MRI (Figure and ) showed a reduction in pancreatic exudation and abnormal head signals after effective treatment. Contrast enhanced CT of the neck (Figure and ) showed nodules located at the junction of the left lobe of the thyroid and parathyroid gland. MRI of the pelvis (Figure and ) suggested malignant lesions of the uterus and multiple uterine fibroids.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [26.8, 'g/L'], 'Calcium': [4.72, 'mmol/L']}",19.974,18.9753,20.9727,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 26.8 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 26.8 g Albmumin/10.0 dL = 2.68 g Albmumin/dL. The concentration value of 26.8 g Albmumin/L converts to 2.68 g Albmumin/dL. 
The concentration of Calcium is 4.72 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 4.72 mmol. To convert 4.72 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 4.72 mmol Calcium * 0.001 mol/mmol = 0.00472 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00472 mol Calcium * 40.08 g/mol = 0.18918 g Calcium. To convert 0.18918 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.18918 g Calcium * 1000.0 mg/g = 189.18 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 189.18 mg Calcium/10.0 dL = 18.918 mg Calcium/dL. The concentration value of 4.72 mmol Calcium/L converts to 18.918 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.68 g/dL)) + 18.918 mg/dL = 19.974 mg/dL.
The patient's corrected calcium concentration 19.974 mg/dL."
2586,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2526089-1,Extracted,"The patient, a 22-year-old male agriculturalist was admitted to our hospital in November 2006 with asthenia, weight loss, fever, diffuse enlargement of cervical lymph nodes and enlarged liver and spleen. The patient's temperature was 38.5°C and his blood pressure was 120/80 mmHg with a pulse of 96 beats per minute.
Initial laboratory studies included an erythrocyte sedimentation rate of 89 mm/hour, serum hemoglobin of 11.4 g/dl, white blood cell count of 13,690/mm3 (27% eosinophils), serum albumin of 2.4 g/dl, normal serum urea, creatinine, sodium and potassium. On admission, the patient had a total serum calcium level of 10.4 mg/dl (normal range 8.4 to 9.7 mg/dl; ~12 mg/dl when corrected for albumin), ionized calcium of 1.46 mmol/l (normal range 1.15 to 1.29 mmol/l) and phosphorus of 4.9 mg/dl (normal range 2.7 to 4.5 mg/dl). An aspiration of the cervical lymph node demonstrated P. brasiliensis.
Results of other laboratory tests performed to help assess the cause of the hypercalcemia were as follows: thyroid stimulating hormone 4.51 IU/ml (normal range 0.41 to 4.5 IU/ml); parathyroid hormone (PTH) 3.4 pg/ml (normal range 15 to 65 pg/ml); 1,25-dihydroxyvitamin D 49.4 pg/ml (normal range 15.9 to 55.6 pg/ml); and 24-hour urinary calcium 856.55 mg (normal range 100 to 300 mg/24 hours). Chest X-ray and bone scans were normal. A computed tomography scan of the chest and abdomen revealed no underlying malignancy. Other causes of hypercalcemia such as vitamin A and D intoxication, sarcoidosis, multiple myeloma, milk-alkali syndrome, adrenal insufficiency and immobilization were excluded on the basis of laboratory and clinical data.
Despite the administration of hydration with normal saline and furosemide therapy, the patient's calcium level increased to 1.59 mmol/l. Specific treatment for paracoccidioidomycosis was initiated with trimethoprim-sulfamethoxazole. At that time, prednisone (20 mg/day) was added to the regimen. On the 13th day of hospitalization, the ionized calcium level had decreased to 1.34 mmol/l and on the day of discharge from hospital this level was 1.26 mmol/l. The patient received follow-up examinations until May 2007 and during this time has been asymptomatic, with normal levels of serum calcium and 1,25-dihydroxyvitamin D (22.4 pg/ml).","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.4, 'g/dL'], 'Calcium': [1.59, 'mmol/L']}",7.653,7.27035,8.03565,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.4 g/dL. 
The concentration of Calcium is 1.59 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.59 mmol. To convert 1.59 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.59 mmol Calcium * 0.001 mol/mmol = 0.00159 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00159 mol Calcium * 40.08 g/mol = 0.06373 g Calcium. To convert 0.06373 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.06373 g Calcium * 1000.0 mg/g = 63.73 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 63.73 mg Calcium/10.0 dL = 6.373 mg Calcium/dL. The concentration value of 1.59 mmol Calcium/L converts to 6.373 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.4 g/dL)) + 6.373 mg/dL = 7.653 mg/dL.
The patient's corrected calcium concentration 7.653 mg/dL."
2587,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6612990-1,Extracted,"A 56-year-old man was referred to our internal medicine unit with abdominal pain, fatigue, and persistently elevated aminotransferases for 18 months. Three months earlier, he had been evaluated for numbness and weakness starting over the distal aspects of his four limbs and slowly progressing proximally over the last three years. Neurological examination performed at that time revealed walking difficulties and moderate muscle weakness in both lower and upper limbs (F = 3.5-4), generalized tendon areflexia, and mild sensory loss with stock and glove distribution. Electromyography/electroneurography (EMG/ENG) showed diffusely reduced motor and sensory nerve conduction velocity (mean motor nerve conduction velocity 22 m/s), with a dishomogeneous pattern, and absent F waves. Isolated hyperproteinorrachia (1.15 g/L) was found on cerebrospinal fluid (CSF) examination. The clinical, EMG/ENG, and CSF results were consistent with a diagnosis of CIDP, which was subsequently successfully treated with IV immunoglobulins.
On admission, the patient's temperature was 36°C, heart rate 125 beats per minute, blood pressure 110/80 mmHg, and oxygen saturation 94% while he was breathing ambient air. On physical examination, peripheral edema, bibasal pulmonary rales, hepatomegaly, and severe sensory and motor deficits located to the upper and lower limbs were noted. Laboratory data on admission showed the following values: aspartate aminotransferase (AST) 166 IU/L (normal range 17-59 IU/L), alanine aminotransferase (ALT) 64 IU/L (normal range 21-72 IU/L), gamma glutamyl-transferase 358 IU/L (normal range 15-73 IU/L), alkaline phosphatase 173 IU/L (normal range 38-126 IU/L), total bilirubin 1.28 mg/dL (normal range 0.20-1.30 mg/dL), albumin 2.8 g/dL (normal range 3.6-5.5 g/dL), lactate dehydrogenase 993 IU/L (normal range 313-618 IU/L), total serum calcium level 14.1 mg/dL (normal range 8.8-10.2 mg/dL), phosphorous 2.8 mg/dL (normal range 2.9-4.8 mg/dL), C-reactive protein 14.6 mg/dL (normal range < 1.0 mg/dL), and ferritin 1669 ng/mL (normal range 20-325 ng/mL). Viral markers for hepatitis B and C were negative. Serum intact PTH was low (4 pg/mL) (normal range 20-104 pg/mL). Moreover, anti-ganglioside antibodies (GD1bIgG and GM1IgG) were found in serum. Given the predominantly infiltrative pattern of altered liver function tests and the severe hypercalcemia with low serum intact PTH, imaging studies and further blood tests were performed to rule out cancer or metastases.
Whole body multidetector computed tomography (MDCT) scan showed a large hypoattenuating hepatic mass in the right lobe (maximum axial dimension 13 cm) characterized by heterogeneous peripheral enhancement, associated with secondary lesions located in the spleen and lung (more than 30 nodules); no evidence of bone metastasis was found (). The following magnetic resonance imaging, performed to confirm the diagnostic hypothesis from the previous CT study, showed typical findings of peripheral CHCC (). Alpha-phetoprotein was 247.8 ng/mL (normal value < 9 ng/mL), gastrointestinal cancer antigen (GICA) was 132 U/mL (normal value < 37 U/mL), and carcinoembryonic antigen (CEA) was 9.14 ng/mL (normal range 0-5 ng/mL). PTH-rP was markedly high (147 ng/mL; normal range 8.5-20.0 ng/mL).
Percutaneous ultrasound-guided biopsy of the hepatic tumor showed a mixed epithelial neoplasia comprising: (1) trabeculae and solid nests composed of large cells with pleomorphic nuclei and granular cytoplasm intermingled with (2) branching pseudoglandular structures composed of cuboidal/columnar cells with atypical nuclei. Nests and trabeculae showed strong immunohistochemical staining for cytokeratin 8/18 and HepPar1 while pseudoglandular structures stained selectively for cytokeratin 7 and cytokeratin 19 (). A diagnosis of “Stage IV CHCC associated to HHM and CIDP” was made.
The general status of patient rapidly worsened, and he became bedridden soon thereafter. After discussion with the patient about the prognosis of his disease, he declined further treatments and arrangements for hospice care were made prior to discharge.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.8, 'g/dL'], 'Calcium': [14.1, 'mg/dL']}",15.06,14.307,15.813,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.8 g/dL. 
The concentration of Calcium is 14.1 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.8 g/dL)) + 14.1 mg/dL = 15.06 mg/dL.
The patient's corrected calcium concentration 15.06 mg/dL."
2588,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-8383570-1,Extracted,"In April 2019 (April 27), a 28-year-old woman gravida 3/para 1 at 11 weeks of gestation with no previous known diseases, presented to the Obstetrics Department of the University Hospital of Brescia, Italy, with symptoms of general weakness, hyperemesis gravidarum and hypercalcemia. There was no family history of parathyroid disease, hypercalcemia, nephrolithiasis, or other endocrinopathies. At admission the physical examination revealed tachycardia, and serum calcium was 12.2 mg/dL. Thyroid ultrasound revealed an heterogeneous mass along the inferior margin of the left thyroid gland, measuring 8 mm. Laboratory investigations included total calcium level 11.95 mg/dL (normal range, 8.10 - 9.80), parathyroid hormone (PTH) 142 pg/mL (normal range, 11 - 67), phosphorus 1.8 mg/dL (normal range, 2.5 - 4.3), serum albumin 4.02 g/dL (normal range, 3.40 - 4.65), thyroid stimulating hormone (TSH) 0.083 mIU/L (normal range, 0.270 - 4.200) and fT4 22.80 (normal range, 9.30 - 17.00). Biochemical hyperthyroidism was interpreted as consistent with pregnancy-induced rise of beta human chorionic gonadotropin. A fine needle aspiration from the mass demonstrated scant cells, and it was reported as benign cytology. She was diagnosed with PHP. Conservative treatment with intravenous fluid (lactated ringers 500 mL/day and normal saline 1,000 mL/day) and furosemide 20 mg/die was started, monitoring blood pressure, daily diuresis and body weight. Meanwhile obstetric evaluation showed appropriate for gestational age fetal biometry. Neck computed tomography 4D showed a solitary adenoma of the parathyroid gland, measuring 6 × 2.9 × 11 mm ().
On May 15 (14 weeks of gestation), the patient underwent cervical exploration with left superior parathyroidectomy. The histopathology showed a benign adenoma (). The basal level of PTH was 151 pg/mL, within 10 min after the parathyroid adenoma was removed the PTH level decreased to 12 pg/mL. Intravenous glucose solution 5% (500 mL) with calcium gluconate 10% was started in the first 36 h after surgery and then was continued with oral calcium 1,000 mg two times a day. Total calcium level at the end of the intravenous calcium infusion was 8.88 mg/dL. Vitamin D supplementation (25,000 IU/week) for 6 weeks (and then one time a month) was also started and continued for 6 weeks. The postoperative period was uneventful; in particular she did not develop hypocalcemia after surgery. Her serum calcium and PTH levels normalized; on May 22, PTH was 31 pg/mL and total calcium level 8.99 mg/dL. She was discharged on May 30.
In subsequent weekly follow-up, her serum calcium and PTH levels have been within the normal limits. On October 30, at 38 weeks of gestation, the patient gave birth to a healthy female baby of adequate weight. Ethical approval was not required based on national laws regarding anonymized data.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.02, 'g/dL'], 'Calcium': [11.95, 'mg/dL']}",11.934,11.3373,12.5307,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.02 g/dL. 
The concentration of Calcium is 11.95 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.02 g/dL)) + 11.95 mg/dL = 11.934 mg/dL.
The patient's corrected calcium concentration 11.934 mg/dL."
2589,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6354123-1,Extracted,"A thirty-year-old Caucasian female was transferred to our medical center for further management of painful wounds of the abdomen, hips, and thighs. She had a past medical history of alcoholic hepatitis, diagnosed four months earlier with a liver biopsy that showed steatohepatitis and stage 3 fibrosis rather than cirrhosis, and morbid obesity (BMI = 56) status post Roux-en-Y gastric bypass done twelve years ago (unknown pre-surgical BMI). History was negative for diabetes mellitus, kidney dysfunction, autoimmune diseases, hyperparathyroidism or Warfarin intake.
Eight weeks after the onset of alcoholic hepatitis, the patient developed tender erythema on her abdomen, hips, and thighs, which evolved into painful firm subcutaneous nodules.
On admission to our hospital, vital signs were notable for temperature 36.7 °C (98.1 °F), blood pressure 98/41 mmHg, pulse 119 bpm, and respiratory rate 20/min. Physical examination showed woody, indurated, exquisitely tender erythematous plaques on the abdomen, hips, and thighs, with central stellate necrotic eschar and purpura (Figure ). She also had anterior abdominal wall edema and bilateral lower extremity pitting edema. Laboratory workup was significant for leukocytosis 24 × 109/L , with absolute neutrophil count 21.5 × 109/L , hemoglobin 7.2 g/dL, MCV 87.5 fL, total protein 6.1 g/dL, albumin 1.7 g/dL, AST 56 U/L, ALT 19 U/L, alkaline phosphatase 172 U/L, total bilirubin 1.8 mg/dL, PT 17.7 s, INR 1.6, APTT 37.3, BUN 15 mg/dL, creatinine 1.32 mg/dL, calcium 8.2 mg/dL, phosphorus 3.9 mg/dL, PTH 22 (normal), and 1,25 OH Vit D3 5.8 (low). The hypercoagulability panel showed low levels of Protein C 33 IU/dL (normal: 76-147), low normal levels of protein S 67 IU/dL (normal: 65-135), low antithrombin III levels, positive lupus anticoagulant and negative anticardiolipin. Wound biopsy showed dermal hemorrhage, dermal vascular occlusion, calcium deposition within the walls of large veins and the surrounding adipose tissue (Figure ). These pathologic findings, correlated clinically, were most consistent with non-uremic calciphylaxis in the setting of alcoholic liver disease.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [1.7, 'g/dL'], 'Calcium': [8.2, 'mg/dL']}",10.04,9.538,10.542,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 1.7 g/dL. 
The concentration of Calcium is 8.2 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.7 g/dL)) + 8.2 mg/dL = 10.04 mg/dL.
The patient's corrected calcium concentration 10.04 mg/dL."
2590,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7945673-1,Extracted,"A 22-year-old man with no previous past medical history was referred to the emergency department with severe hypocalcemia (Ca: 5 mg/dl) as well as spastic muscles in both upper and lower extremities. Also, he was opium-addicted and used 15 cc of daily methadone. He had severe bloodless diarrhea from 20 days before admission managed with serum therapy. His vital signs were in normal ranges. He was conscious, but he appeared to be pale. He did not have any positive history in terms of nausea, vomiting, cough, or dyspnea. However, he suffered from generalized muscle spasms and pain. There was not any positive finding during heart and lung examinations. His abdomen was nontender, but pitting edema (2+) was observed in the lower extremities. Chvostek's and Trousseau's signs were positive, and his electrocardiogram (ECG) revealed a prolonged QT interval (QT = 550 msec). Due to the high prevalence of COVID-19, lung high-resolution computed tomography (HRCT) was performed and the results were highly suggestive of COVID-19 infection ().
In the first hour of admission, intravenous infusion of 10% calcium gluconate was initiated promptly, and muscle spasms disappeared within four hours. Intravenous calcium administration was then continued based on plasma-calcium and ECG monitoring. The patient had a myoclonic-like seizure with an upward gaze on the first night of hospitalization, while the serum level of calcium was 8.9 mg/dl. The result of the requested brain CT was negative. Unfortunately, the seizure recurred, and intravenous diazepam was prescribed. On the third day of admission, the calcium concentration reached 9.1 mg/dl, and the QT interval was corrected (QT = 405 msec). Other laboratory data collected during the admission time were as follows: lactic acid dehydrogenase (LDH) of 1740 U/L, creatine phosphokinase (CPK) of 1840 U/L, potassium of 6.9 mEq/l, sodium of 142 mEq/l, blood sugar of 234 mg/dl, albumin of 3.2 g/dl, aspartate aminotransferase (AST) of 261 IU/L, alanine aminotransferase (ALT) of 110 IU/L, alkaline phosphatase (ALP) of 379 IU/L, parathyroid hormone (PTH) of 145 pg/ml, 25-hydroxy vitamin D of 32 ng/mL, blood urea nitrogen (BUN) of 19 mg/dl, and creatinine (Cr) of 1.2 mg/dl.
His laboratory findings favored rhabdomyolysis, and fluid therapy was started promptly with concurrent seizure as well as hypocalcemia management to avoid acute kidney injury. Unfortunately, the patient had a cardiac and respiratory arrest, and cardiopulmonary resuscitation (CPR) was implemented, and he was connected to a ventilator. However, on the fourth day of hospitalization, the patient could not be resuscitated after the second cardiac arrest attack.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [5.0, 'mg/dL'], 'Albumin': [3.2, 'g/dL']}",5.64,5.358,5.922,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.2 g/dL. 
The concentration of Calcium is 5.0 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.2 g/dL)) + 5.0 mg/dL = 5.64 mg/dL.
The patient's corrected calcium concentration 5.64 mg/dL."
2591,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2887526-1,Extracted,"A 23-year-old female in the 26th week of pregnancy (G5P3L1A1), presented with widespread erythema, edema and pustules over the abdomen, arms thighs, legs and buttocks of two weeks duration. []. She had similar lesions during three of her previous pregnancies which had started later around 30-32 weeks. The first was a pre-term delivery and the baby died soon after birth. During the second pregnancy, lesions were present only over the abdomen and she delivered a term live male baby. The third pregnancy resulted in intra-uterine death at term. The fourth pregnancy was terminated medically. There was no previous history of diabetes or hypertension.
Clinical examination revealed a toxic, febrile (temperature 39°C) patient with large erythematous, edematous plaques studded with pustules over the abdomen, arms, legs, and buttocks involving about 70% of the body with confluent erythema surrounding the plaques. The erythema and pustulation progressed in waves from the palms and soles to the forearms, abdomen, legs and trunk and finally involved the face and scalp. [] The mucosae and eyes were unaffected. Obstetric examination revealed a single live fetus with no anomalies on scanning.
Histopathology revealed parakeratosis, subcorneal neutrophilic pustules, acanthosis and regular elongation of rete ridges consistent with IH. [Figures and ]. Hematological parameters were as follows:
Leukocytosis of 13.3×109 /L with neutrophilia of 85%; hemoglobin of 11.3 g%; a raised erythrocyte sedimentation rate (ESR) of 52 mm/hr; hypoalbuminemia of 3.0 g/dL; fasting blood sugar of 293 mg/dL; post prandial sugar of 512 mg/dL; hypocalcemia of 7.7 mg/dL; glycosylated hemoglobin of 11.5% with ketone bodies in urine of 40 mg/dL. Serum cortisol and thyroid hormone levels were normal. Other liver and renal function tests were normal.
Prednisolone at a dose of 50 mg (1 mg/kg/d) was initiated along with insulin for 4 days. She was refractory to corticosteroids with worsening of diabetic control and showed disease progression. She was restless and complained of pain over the lesions. Cyclosporine was added at a dose of 150 mg (3 mg/kg/d) and steroids tapered to 20 mg over two weeks. Within three days of initiating cyclosporine, the intense red erythema had acquired a dusky hue but the waves of pustules continued their progression from the legs and hands to the abdomen and trunk and finally involving the face followed by exfoliation. The previous pregnancies were also associated with similar waves subsiding with the involvement of the face. Four days after cyclosporine, she developed pedal edema. Since serum albumin was low, two units of 20% salt free albumin were infused. There was dramatic control of disease progression following the addition of albumin with resolution of pedal edema. []. Her fluctuant blood sugar level was brought under control with insulin (60-0-25) units and later metformin at a dose of 250 mg thrice daily was added. This also helped to suppress her uncontrollable appetite. Potent topical corticosteroids and emollients were used to treat the erythematous and painful lesions over the palms. She was discharged in week 29, free of all lesions. She was followed-up every two weeks and an anomaly scan repeated at every visit (Ultrasound scan in the B mode and M mode to detect congenital anomalies and cardiac anomalies respectively were done). They did not reveal any lethal defects. She developed pustules on the abdomen, neck and legs at 30 weeks so the cyclosporine dose was increased to 200 mg/d.
Steroids were further tapered to 10 mg and remained so till delivery. She developed a fresh wave of pustules in week 36, followed by rupture of membranes and vaginal delivery of a female baby with gestational age 36 weeks with an Apgar score of 9 at five minutes. []. The baby had asymptomatic hypoglycemia (Random blood sugar-22 mg/dl), 10% dextrose infusions IV were started (260 ml in 24 hours), and random blood sugar monitored two-hourly. Two days after delivery, nasogastric feeds with Lactogen (formula) were started, 3 ml every three hours; this was increased slowly to 8 ml since the random blood sugar was 59 mg/dL. Sangu feeds with Lactogen were initiated and maintained at 18-20 ml/day. Nasogastric feeds were stopped as soon as the infant tolerated Sangu feeds.
IV dextrose was reduced to 50 ml/24 hrs and stopped prior to discharge. The baby also had polycythemia and developed hyperbilirubinemia (Total bilirubin 6.9 mg/dL; indirect 16.2 mg/dL), which was treated with fresh frozen plasma and phototherapy. Hypocalcemia was also observed (ionized calcium 0.781 mmol/L (Normal- 1.05-1.37). This was treated initially with slow IV infusion of calcium gluconate (3 ml); subsequently the infant was administered Calcium syrup, 2 ml once daily. The sacral area showed a small dimple.
Ultrasound scan of this area revealed a spina bifida occulta. The dermal sinus was not continuous with the spinal canal with conus, cauda equina, nerve roots and spinal canal being normal. The baby did not show any features of growth retardation or immunosuppression. Erythematous papules clinically suggestive of irritant dermatitis developed on the back since the baby was placed on a plastic sheet during phototherapy. This subsided with mild topical corticosteroids. In the mother, the waves of pustules waned the day after delivery with the skin acquiring a dusky hue. Cyclosporine was continued, the dose being tapered to 150 mg one week after delivery, and subsequently tapered by 50 mg every week. She continued to be maintained on insulin injections. Metformin 250 mg thrice daily was restarted five days after delivery since her blood sugar levels showed fluctuation. Since her serum albumin was low (2.3 g/dL), two units of 20% salt-free albumin were infused.
As noted previously, there was faster resolution of the lesions following the albumin infusion. Breast feeds were withheld while the patient was on cyclosporine and was started three days after withdrawal of cyclosporine. Live viral and bacterial immunization was postponed for the baby. Both the mother and baby continued to do well and were discharged 10 days after delivery []; the baby was on Sangu feeds with Lactogen (20 ml/day). The mother stopped cyclosporine after about two weeks after delivery on her own and started breast feeding three days later along with the formula feeds.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.0, 'g/dL'], 'Calcium': [7.7, 'mg/dL']}",8.5,8.075,8.925,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.0 g/dL. 
The concentration of Calcium is 7.7 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.0 g/dL)) + 7.7 mg/dL = 8.5 mg/dL.
The patient's corrected calcium concentration 8.5 mg/dL."
2592,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-8403091-1,Extracted,"A 6-year-old girl (height 110 cm, weight 20.3 kg) with no medical history had a fever 1 month before surgery. She visited a clinic and general hospital due to jaundice and malaise. At admission to the general hospital 2 weeks before surgery, she was diagnosed with acute hepatitis and was given liver protection drugs (Stronger Neo-Minophagen C, Lactulose, Vitamin K) and fresh frozen plasma, although her liver and coagulation function deteriorated during the course of treatment, along with decrease in platelet count. She was transferred to the pediatric intensive care unit (PICU) of our children's medical center for blood purification therapy 4 days before surgery.
On examination, she looked ill. Physical examination revealed the following: blood pressure 95/56 mm Hg, pulse rate 72 beats/min, respiratory rate 20 breaths/min with SpO2 of 99% on room air, body temperature 37.3 °C, and Glasgow Coma Scale (GCS) score of E3V4M6. Abdominal examination was unremarkable, with no hepatosplenomegaly. Examination of the eyes and skin revealed icterus.
Initial laboratory investigations revealed thrombocytopenia (hemoglobin 13.0 g/dL, white cell count 3.4 × 103/μL, platelet count 9.1 × 104/μL). Electrolytes were normal (Na 139 mmol/L, K 4.2 mmol/L, Cl 103 mmol/L, Ca 9.5 mg/dL, Mg 2.3 mg/dL, P 3.9 mg/dL). Her coagulation profile was prolonged (prothrombin time 23%, prothrombin time-international normalized ratio 2.36, activated partial thromboplastin time 63.7 s) and liver function tests were abnormal (albumin 4.0 g/dL, total bilirubin 18.76 mg/dL, direct bilirubin 13.17 mg/dL, venous ammonia 70 μg/dL, lactate 2.2 mmol/L). Infectious disease screening tests were negative. Computed tomography (CT) scan of her abdomen showed lower absorption in the liver compared to the spleen, suggesting ALF. Cranial CT scan and fundus examination were normal. Electroencephalogram (EEG) showed slow spindle waves with a frequency of 1–2 Hz, without laterality or triphasic waves (Fig. a). Daily plasma exchange and continuous hemodiafiltration were started for ALF with HE. Mannitol was administered to prevent cerebral edema. A day before surgery, GCS scores worsened to E1VTM1. Clinically, she was unresponsive to pain and auditory stimuli, and her EEG showed high voltage continuous slow waves with a frequency of 0.5–1 Hz, without lateralization (Fig. b). Assuming deterioration of HE, emergency LT was considered vital. After obtaining informed consent from her family, urgent living donor LT with an extended left liver graft from her mother was planned on the 5th ICU day.
General anesthesia was induced with fentanyl (50 mcg) and rocuronium (20 mg) and maintained with remifentanil and rocuronium infusions (0.1–0.4 mcg/kg/min and 7 mcg/kg/min, respectively), along with sevoflurane inhalation at 0.5%. A BIS Quatro Brain Monitoring Sensor (Medtronic plc, Dublin, Ireland) was placed on the frontotemporal region, and her electroencephalogram, including BIS values, 95% spectral edge frequency (SEF95), and suppression ratio (SR), was continuously recorded at each phase of liver transplantation by the BIS monitor until the end of anesthesia (Fig. , Fig. a–d). The durations of anesthesia and surgery were 708 min and 637 min, respectively. The graft volume was 254 g, graft volume/recipient standard liver volume (GV/SLV) was 46.1%, and graft-to-recipient weight ratio (GRWR) was 1.27%. Warm and cold ischemia times were 40 min and 51 min, respectively. BIS values ranged from 10 to 20 from the start of the operation to reperfusion (Fig. ). From reperfusion to the end of the operation, BIS values ranged from 10 to 80, and the variation in BIS values also increased. The frequency of EEG waveforms and BIS values seen with BIS monitoring gradually increased (Fig. ). She was re-admitted to the PICU after surgery, extubated on postoperative day (POD) 2 and discharged from the PICU on POD 7. Follow-up EEG on POD 5 showed low amplitude and fast waves with a frequency of 9–10 Hz, without laterality or paroxysmal waves (Fig. c). However, she spoke only a few words until POD 7. Two weeks postoperatively, she was newly diagnosed with hepatitis-associated aplastic anemia. Her immunosuppressant regimen was changed and continued for post liver transplantation prophylaxis and aplastic anemia. She was discharged after 4 months of hospitalization. The cause of liver failure in the present case remains unknown.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.0, 'g/dL'], 'Calcium': [9.5, 'mg/dL']}",9.5,9.025,9.975,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.0 g/dL. 
The concentration of Calcium is 9.5 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.0 g/dL)) + 9.5 mg/dL = 9.5 mg/dL.
The patient's corrected calcium concentration 9.5 mg/dL."
2593,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5883436-1,Extracted,"A 52-year-old retired military man on treatment for hypertension and a 25 pack-year smoking history, progressively developed difficulty in getting up from the squatting position, difficulty in chewing and swallowing food, hardening of both hands, generalized body pain, and swelling in all the limbs. He had considerable difficulty in using the squatting toilet as he required help to stand up after use. His sexual, bladder, and bowel functions were unaffected.
Significant examination findings included anasarca, hardened contractures of the thenar muscles of both hands, weak abduction of both shoulders, difficulty to stand up from squatting position, and early myopathic gait. Power was 3/5 in the bilateral proximal muscle groups and 4/5 in the bilateral distal muscles groups with preserved bilateral deep tendon reflexes and flexor plantar reflexes bilaterally; sensation and coordination were normal.
Laboratory investigations showed mild normocytic normochromic anemia, hypoalbuminemia 24 g/L, erythrocyte sedimentation rate – 79 mm in 1 h, C-reactive protein (CRP) – 85 mg/L (reference range <10 mg/L), and hypercalcemia (13.4 mg/dl) with suppressed intact parathyroid hormone; renal and liver functions were normal; urine protein loss was physiological; upper gastrointestinal endoscopy was unremarkable with normal duodenal biopsy; no evidence for malabsorption found; 25-hydroxy Vitamin D was low; 1,25 hydroxy Vitamin D assay was not available in our center. Serum angiotensin-converting enzyme (ACE) level mildly elevated but <2 times the upper limit of normal. Serum protein electrophoresis and free light chain assays excluded myeloma; complete autoimmune screen including antinuclear (ANA), antidouble strand DNA (anti ds-DNA), anti-histidyl-tRNA synthetase (anti-Jo1), anti-topoisomerase I (anti-Scl 70), and antiribonuclear proteins (u1RNP) antibodies were all negative. Hand X-ray showed diffuse faint calcification of the intrinsic muscles of the hands []. Whole body PET/CT was done to rule out an underlying malignancy. PET/CT showed symmetrical diffuse increased fluorodeoxyglucose (FDG) uptake in the multiple skeletal muscles predominantly involving bilateral gluteus muscles/bilateral external oblique abdominal muscles with associated fatty atrophy and calcification on CT []. Gluteal muscle biopsy was done which showed florid noncaseating granulomatous inflammation [].
A diagnosis of sarcoidosis was made given noncaseating granuloma in biopsy, mildly elevated serum ACE level, and hypercalcemia. The patient was initially given oral prednisolone 40 mg daily for 4 weeks; after that, he did not show any clinical improvement and therefore given 1 g methylprednisolone pulse therapy weekly for 8 weeks along with weekly methotrexate; he was reviewed after 12 weeks and had significant subjective improvement in pain, gait, proximal muscle function, and chewing but hand weakness remained the same. Serum calcium was normalized. His CRP levels were persistently elevated (86 mg/dL) and albumin remained low. The patient was explained about the guarded prognosis given extensive disease and discharged on oral methotrexate 15 mg once weekly, folic acid, hydroxychloroquine, and prednisolone 20 mg daily.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [24.0, 'g/L'], 'Calcium': [13.4, 'mg/dL']}",14.68,13.946,15.414,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 24.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 24.0 g Albmumin/10.0 dL = 2.4 g Albmumin/dL. The concentration value of 24.0 g Albmumin/L converts to 2.4 g Albmumin/dL. 
The concentration of Calcium is 13.4 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.4 g/dL)) + 13.4 mg/dL = 14.68 mg/dL.
The patient's corrected calcium concentration 14.68 mg/dL."
2594,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,usmle-7682,Extracted,"A 61-year-old woman visits the clinic with a complaint of new-onset episodic abnormal body movements. She says her husband noticed it twice in the past week. There were jerky movements for roughly 15 seconds during her last episode. She denies any recent trauma or fever. Her vital signs include: blood pressure 114/74 mm Hg, pulse 81/min, temperature 36.7°C (98.1°F) and respiratory rate 10/min. On physical examination, there is no evidence of focal neurological deficits. A basic metabolic panel is ordered which shows:
Sodium 141 mEq/L
Potassium 5.1 mEq/L
Chloride 101 mEq/L
Bicarbonate 24 mEq/L
Albumin 4.3 mg/dL
Urea nitrogen 11 mg/dL
Creatinine 1.0 mg/dL
Uric Acid 6.8 mg/dL
Calcium 8.9 mg/dL
Glucose 111 mg/dL
A contrast magnetic resonance imaging (MRI) of the head is shown in the provided image.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.3, 'mg/dL'], 'Calcium': [8.9, 'mg/dL']}",12.09656,11.49173,12.70139,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.3 mg/dL. We need to convert the concentration to g/dL. Let's first convert the mass of Albmumin from mg to g. The mass of Albmumin is 4.3 mg. To convert 4.3 mg of Albmumin to g, multiply by the conversion factor 0.001, giving us 4.3 mg Albmumin * 0.001 g/mg = 0.0043 g Albmumin. The volume units is dL so no volume conversion is needed. Hence, the concentration value of 4.3 mg Albmumin/dL converts to 0.0043 g Albmumin/dL. 
The concentration of Calcium is 8.9 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 0.0043 g/dL)) + 8.9 mg/dL = 12.09656 mg/dL.
The patient's corrected calcium concentration 12.09656 mg/dL."
2595,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3572805-1,Extracted,"The patient is a female whose age is 25 and undergoing medical treatment of Crohn's disease that is an inflammatory bowel disease after diagnosis of cryptogenic multifocal ulcerous enteritis and the nutrition team received the request to attempt high protein meal to improve hypoalbuminemia along protein-losing enteropathy.
The patient suffered from anemia continuously since when she was 4 years old, but could not find the specific reason for that, however, while implementing capsule endoscope to find the reason, the capsule was stuck at the upper part of ileum then the patient took small bowel resection. At that time, weight was normal by 49.4 kg (100% of IBW), but it decreased down to 37.0 kg (75% of IBW) by 25% for a year as weight loss continued, then reached the status of severe underweight at 33.3 kg (68% of IBW) at the time of hospitalization in 2010. She also suffered from ascites and subcutaneous edema with hypoalbuminemia (1.3 g/dL), however, abdominal discomfort and edema of face occurred from 2007 and diuretic was used to control ascites from 2009. She took the injection of albumin intermittently as the outpatient to improve hypoalbuminemia, but there was no effect.
The patient was in severe underweight that was included in 68% of IBW with 153 cm height and 33.3 kg body weight and in excessive malnutrition of protein-energy that marasmus was mixed at total protein by 2.7 g/dL and albumin by 1.3 g/dL from biochemical examination. Other blood test indices were 89 mg/dL for cholesterol, 7.5 for BUN, 0.28 Cr, 6.9 mg/dL for Ca, 33/19 IU/L for AST/ALT, 8.1 g/dL for hemoglobin, and 1.7 for CRP.
The foods for the patient were extremely restricted due to abdominal discomfort and the varieties were limited. In case of eating out, the symptoms of abdominal pain and diarrhea appeared and had meals at home most of the time. According to survey results of her dietary history, the patient consumed spinach and broccoli only after complete boiling and avoided the intake of other vegetables because she thought abdominal discomfort got worse if she had high-fiber foods. The patient appealed that abdominal discomfort occurred even when she consumed a bottle of vegetable juice little by little for a whole day. In case of ingesting fruits, she limited the quantity because she had burning feeling in her stomach because of sourness of the fruits. The patient also did not like the sweet taste of fruits, and there was nearly no intake of fruits. The patient had the meals mainly with rice and some fishes she could eat and intake of most nutrients such as calorie, carbohydrate, fat, protein, vitamin and minerals was very insufficient below 30-40% of required amount.
The foods the patient had were too limited considering her preference and abdominal discomfort. However, the motive and participation of the patient were willing to be induced to increase the intake by setting the goal of nutrition management so that she could minimize the supply of intravenous alimentation and increase oral feeding as much as possible considering that she was in the condition that could use gastrointestinal tract as an young female who were supposed to do social activities actively. First, low reside diet with low contents of dietary fiber was provided and supplementary snack was provided two or three times a day for the purpose of reducing discomfort and increase intake, although the amount was only slightly increased due to abdominal discomfort. Standard formula such as Ensure and Greenbia which have low contents of fiber as the nutritional supplementing beverage was recommended and tried, but the patient appealed the abdominal pain after ingesting them. And component nutrition solution (Monowell) that was produced for purpose of providing the nutrients to the patient of colitis was tried, but it could not be continued because she appealed abdominal discomfort. Despite the efforts of increasing oral feeding in various types, the intake was 800-900 kcal, 34 g protein (24-27 kcal/kg, 1 g/kg) a day falling into 40-50% of required intake, and it was insufficient to satisfy with the required intake though it increased comparing with the time of entering the hospital.
Because it was difficult to increase oral feeding, supplementation of calories and protein were required to increase the weight and improve hypoproteinemia. After discussion with the medical team, the use of protein supplement was suggested. The references of Umar & DiBaise [] and Braamskamp et al. [] that recommended 2.0-3.0 g protein/kg/day were referred for positive balance of protein in protein-losing enteropathy and the goal of nutrient supply was set to 40-50 kcal/kg and 2.5 g protein/kg considering the condition of excessive underweight. Nutrition intervention was implemented continuously to increase oral feeding by providing gruel or soup as the snack and insufficient protein from oral feeding was supplemented with protein supplement (Promax, >90% protein) ().
It was guided to take protein supplement with the meal by providing it twice a day for breakfast and dinner after discussion with the patient and instructed her to consume protein supplement with gruel, water and yogurt in the way that the patient could eat. Twenty g was provided a day when providing protein supplement at first, but actual intake stopped at degree of 1/2 and it was increased up to target goal 55 g slowly for about 2 weeks starting from intake of protein 10 g a day considering adaptability of the patient, and the adaptability was good for the period of increase without abdominal discomfort. Blood testing including BUN, Cr, and electrolytes was monitored monitored continuously to check load on kidney along intake of high protein meal (2.5 g protein/kg). The patient discharged from the hospital about 4 weeks after hospitalization, however, there was weight loss by 1.0 kg from 33.3 kg to 32.3 kg while ascites were controlled and stabilized after treatment and serum albumin was improved from 1.3 to 2.5. She discharged from the hospital in the condition without discomfort after increasing protein powder up to target amount.
After discharge, she visited the hospital regulary as the outpatient for about 10 months and was managed (total 8 times by every 2 weeks and one-two months after discharge). She kept 55 g (morning 30, lunch 5, dinner 20) of protein supplements for about 5 months and 35 g for about 2 months and 25 g along the improvement of the patient. Body weight increased gradually from 32.3 kg (65% of IBW) to 44.0 kg (89% of IBW) by about 36% for the period of continuous management () and serum albumin concentration was kept above 2.8 in average without the injection of albumin (). And, the performance status that the patient felt was improved from 4 points of 'very tired' to 2 points of 'a little tired' out of 5-points scale measurement and input of diuretic stopped owing to the improvement of edema and ascites from the time of 4th month after discharging from the hospital. During this period, the results of blood test such as BUN, Cr and electrolytes were within the normal range.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [1.3, 'g/dL'], 'Calcium': [6.9, 'mg/dL']}",9.06,8.607,9.513,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 1.3 g/dL. 
The concentration of Calcium is 6.9 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.3 g/dL)) + 6.9 mg/dL = 9.06 mg/dL.
The patient's corrected calcium concentration 9.06 mg/dL."
2596,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-8701011-1,Extracted,"A 93-year-old patient visited our hospital with hypokalaemia, malnutrition, and decreased renal function detected by a family physician.
Five years before her visit to the hospital, she had undergone bowel resection several times (). As a result, she had been suffering from diarrhoea for about three months, thought to be caused by SBS. The diarrhoea improved spontaneously and she had no abdominal symptoms. Then, one year before admission, watery diarrhoea appeared, and although antidiarrhoeal medication was prescribed, there was little improvement.
Her past history included colonic perforation, abdominal wall hernia with strangulated ileus, and resection of about 2 m 30 cm (59.1 inches) of the terminal ileum (). Five years prior to this admission, she was diagnosed with strangulated ileus, and the small intestine was resected, 7 cm from the terminal ileum and 50 cm from the ligament of Treitz (). At presentation, the patient’s blood pressure was 95/67 mmHg, heart rate was 59 beats per minute, SpO2 as 95%, and her temperature was 36.6 °C. On physical examination, normal breath sounds and heart sounds with mild systolic murmurs were observed. The abdomen was flat and soft. Murphy’s sign was negative, and there was no costovertebral angle tenderness. Lower leg oedema was observed. The results of blood tests were as follows: white blood cell count 15.30 × 103/μ (neutrophils 78.3%, lymphocytes 15.5%, monocytes 5.6%, eosinophils 0.4%, basophils 0.2%), red blood cell count 3.34 × 106/μ, hemoglobin 11.3 g/dL, hematocrit 33.2%, platelet count 27.9 × 104/μ, total bilirubin 1.6 mg/dL, aspartate aminotransferase (serum glutamic-oxaloacetic transaminase) 48 IU/L, alanine aminotransferase (serum glutamic-pyruvic transaminase) 37 IU/L, total protein 5.2 g/dL, albumin 2.5 g/dL, blood urea nitrogen 18.7 mg/dL, creatine 1.13 mg/dL, Na 143 mEq/L, K 1.7 mEq/L, Cl 99 mEq/L, Ca 5.0 mg/dL, P 2.8 mg/dL, Mg 0.8 mg/dL, and estimated glomerular filtration rate 34.1 mL/min/L. An abdominal computed tomography showed mild oedema of the colon, and no other obvious abnormalities (). No obvious organic abnormalities were noted on imaging, but the bowel was shortened because of repeated bowel resections. Colonic specimens showed only nonspecific inflammatory findings (a,b). We believe that this inflammatory finding was due to an imbalance between the protective and aggressive factors of the intestinal tract due to ageing.
After hospitalization, her electrolyte imbalance and renal function were improved by an infusion of magnesium and potassium, but the diarrhea persisted. A colonoscopy was performed and pathological specimens were taken. However, the colonoscopy, which was performed to evaluate diarrhea, did not reveal any specific findings. In addition, stool culture and histopathological examination did not reveal the exact cause. Taken together, this was likely to be de-adaptation of SBS, as a part of the clinical course. Since diarrhea and electrolyte abnormalities continued, we concluded that her bowel could not absorb nutrients, and therefore switched to central venous (CV) nutrition (delivered via a CV port), which improved her diarrhea. She was discharged in good general condition about one month after creation of the CV port.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.5, 'g/dL'], 'Calcium': [5.0, 'mg/dL']}",6.2,5.89,6.51,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.5 g/dL. 
The concentration of Calcium is 5.0 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.5 g/dL)) + 5.0 mg/dL = 6.2 mg/dL.
The patient's corrected calcium concentration 6.2 mg/dL."
2597,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7603875-1,Extracted,"A 62-year-old male visited our hospital and presented with a loss of appetite; epigastric discomfort; hair, eyebrow, and beard loss; diarrhea; taste loss; weight loss; and nail atrophy after oral administration of a traditional Chinese medicine >2 months prior. shows the patient’s hair loss and nail atrophy. He complained of watery stool five to eight times per day and a small amount of melena intermittently. Gastroscopy performed previously at the patient’s local hospital revealed atrophic gastritis and the pathology results suggested chronic gastritis. However, we did not view the report in detail. Doctors at the local hospital administered symptomatic treatment, but the patient unfortunately showed no improvement.
Therefore, the patient was admitted to our hospital. A colonoscopy revealed that the whole colonic mucosa was congested and edematous, with dense nodular hyperplasia. There were also numerous sessile or semipedunculated polypoid protuberances in the colon (). Gastroscopy showed that the mucosa of the gastric antrum and angle exhibited an uneven and nodular appearance, and the mucosa was congested and edematous (). Capsule endoscopy showed that partial small-intestinal mucosa was edematous and congested with villous atrophy (). Pathological examination showed local mucosal gland cystic dilatation with intraluminal fluid (). The serum IgE was 238.50 IU/ml (normal range 0–100 IU/mL), eosinophil count was normal, serum albumin was 31.6 g/L (normal range 40–55 g/L), serum calcium was 1.91 mmol/L (normal range 2.17–2.57 mmol/L), and other ions were within normal ranges. Antinuclear antibody (ANA), antimitochondrial antibody (AMA), smooth-muscle antibody, and antineutrophil cytoplasmic antibody were negative, and fecal occult blood was positive. Upon combining the clinical, endoscopic, and pathological features of the patient, a diagnosis of CCS was made.
After obtaining a definite diagnosis, prednisone 40 mg/d combined with mesalazine 1.0 g three times a day was administered orally. After treatment with prednisone and mesalazine, symptoms such as diarrhea were gradually improved. One month later, the patient underwent gastroscopy and colonoscopy again to assess the condition of the digestive tract and resect partial large-intestinal polyps, showing no obvious improvement in endoscopic findings ().","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [31.6, 'g/L'], 'Calcium': [1.91, 'mmol/L']}",8.327,7.91065,8.74335,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 31.6 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 31.6 g Albmumin/10.0 dL = 3.16 g Albmumin/dL. The concentration value of 31.6 g Albmumin/L converts to 3.16 g Albmumin/dL. 
The concentration of Calcium is 1.91 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.91 mmol. To convert 1.91 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.91 mmol Calcium * 0.001 mol/mmol = 0.00191 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00191 mol Calcium * 40.08 g/mol = 0.07655 g Calcium. To convert 0.07655 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.07655 g Calcium * 1000.0 mg/g = 76.55 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 76.55 mg Calcium/10.0 dL = 7.655 mg Calcium/dL. The concentration value of 1.91 mmol Calcium/L converts to 7.655 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.16 g/dL)) + 7.655 mg/dL = 8.327 mg/dL.
The patient's corrected calcium concentration 8.327 mg/dL."
2598,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5101375-1,Extracted,"A 28-year-old female with no past medical history, taking no medications or over-the-counter drugs, developed pain and stiffness in the metacarpophalangeal and proximal interphalangeal joints of both hands, two months after migrating from South Asia to United States. This was immediately followed by the development of a diffuse, erythematous, pruritic skin rash that quickly spread throughout the body. The patient was seen in an outpatient clinic, was diagnosed with an allergic illness, and received oral antihistamines. The symptoms did not improve and the patient deteriorated and developed fever, chills, cough, and dyspnea. She then presented to an outside hospital and was admitted with respiratory failure. After 14 days she was transferred to our hospital for further evaluation and treatment.
On arrival, vitals were temperature 39.2°C, blood pressure 90/54 mm Hg, heart rate 80/min, respiratory rate 22/min, and pulse oxygen saturation (SpO2) 98% on 2 L nasal cannula. Patient had a diffuse desquamating pruriginous rash (), periorbital edema and icterus, and bilateral lung crackles. Laboratory studies revealed anemia (hemoglobin 8.0 g/dL, N: 11.5–15.5 g/dL), hypoalbuminemia (albumin 1.8 g/dL, N: 3.5–5.0 g/dL), hypocalcemia (calcium 6.0 mg/dL, N: 8.5–10.5 mg/dL), and elevated liver enzymes (total bilirubin 2.9 mg/dL, N: 0.0–1.5 mg/dL; alkaline phosphatase 344 U/L, N: 40–150 U/L; ALT 639 U/L, N: 0–45 U/L; AST 1713 U/L, N: 7–40 U/L). Mycoplasma pneumoniae IgG and IgM antibodies were increased (1.32, and 1.44, resp., N < 0.91). Tuberculosis (TB) antigen and mitogen response were negative, as was the remainder of the infectious evaluation. The d-dimer levels were >35200 ng/mL, the maximum measurable limit. The serum ferritin level was 167357 ng/mL (N < 150 ng/mL). The rheumatoid factor (RF) and the anti-nuclear (ANA), anti-Sm, anti-ribonucleoprotein, anti-SSA, anti-SSB, anti-centromere, anti-Jo1, anti-ribosomal RNP, anti-chromatin, anti-PL4, anti-neutrophil cytoplasmic, anti-cardiolipin, and anti-Babesia antibodies were all negative.
Chest X-ray showed bilateral infiltrates (). Bone marrow biopsy revealed a hypercellular marrow with granulocytic hyperplasia, erythroid hypoplasia with maturation arrest of proerythroblast stage, increased histiocytes, and hemophagocytosis and increased cytotoxic T-lymphocytes. Immunostaining showed increased interstitial CD3 positive T-cells with strong Granzyme B reactivity and dim CD56 expression. Flow cytometry showed increased cytotoxic T-lymphocytes. Skin biopsy of the evanescent rash revealed hyperkeratosis and focal parakeratosis of the stratum corneum. Numerous apoptotic keratinocytes were appreciated in clusters and singly within the stratum corneum, suggestive of Still's Disease [, ].
The patient fulfilled all the four major and three of the four minor criteria as described by Yamaguchi et al. [] and was diagnosed with AOSD. Similarly, she fulfilled six out of eight criteria for the diagnosis of HLH []. The nonclassical pruritic rash [] was considered to be part of the atypical presentation of AOSD and not an allergic reaction, considering that patient had no medication history prior to admission.
The patient began treatment with oral azithromycin 500 mg daily and methylprednisolone 60 mg daily. The rash improved and fever subsided. When tapering the dose of methylprednisolone to 48 mg daily was attempted, the patient developed a high-grade fever to 40.5°C. She was transferred to the intensive care unit and received intravenous methylprednisolone 1000 mg for 3 days followed by anakinra 100 mg subcutaneous daily along with prednisone 40 mg twice daily (). After 6 more days she improved and was discharged home on cyclosporine 50 mg twice daily and prednisone 30 mg in the morning and 20 mg in the evening with a plan for a slow weekly taper.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [1.8, 'g/dL'], 'Calcium': [6.0, 'mg/dL']}",7.76,7.372,8.148,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 1.8 g/dL. 
The concentration of Calcium is 6.0 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.8 g/dL)) + 6.0 mg/dL = 7.76 mg/dL.
The patient's corrected calcium concentration 7.76 mg/dL."
2599,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5220425-1,Extracted,"A 65-year-old female with a history of mixed connective tissue disease and pulmonary fibrosis on azathioprine, hydroxychloroquine, and prednisone (osteoporosis previously on teriparatide) presented with a 1-month history of hypercalcemia. The patient initially presented to her rheumatologist with complaints of weakness, dizziness, confusion, and difficulty with ambulation. Laboratory workup during that visit revealed hypercalcemia at 12.0 mg/dL (normal: 8.7–10.7 mg/dL) and albumin of 3.2 g/dL (normal: 3.5–4.8 g/dL). Her hypercalcemia was attributed her teriparatide use and this medication was discontinued; however, when her symptoms persisted, she presented to her primary care physician who found a calcium level of 13.6 mg/dL. She was admitted to the hospital where a skeletal survey was negative for lytic lesions and serum electrophoresis (SPEP) showed no monoclonal band. Further testing determined that she had PTH-independent hypercalcemia; parathyroid hormone (PTH) was decreased at 6 pg/mL (normal: 10–65 pg/mL), PTHrP was normal at 14 pg/mL (normal: 14–27 pg/mL), calcifediol (25-hydroxyvitamin D) was decreased at 18 ng/mL (deficiency < 20 ng/dL; insufficiency: 20–29 ng/mL; optimal ≥ 30 ng/dL), and calcitriol (1,25-dihydroxyvitamin D) was elevated at 159 pg/mL (normal: 18–72 pg/mL). Repeat calcitriol and PTH were 197 pg/mL and 6 pg/mL, respectively. The patient was rehydrated with intravenous (IV) fluids, and she received calcitonin, leading to improvement of her calcium to 10.7 mg/dL at the time of discharge. After discharge, she developed symptoms of fatigue, polydipsia, and polyuria. She presented to her primary care physician who found a calcium level of 15.6 mg/dL and was again admitted to the hospital. Upon further questioning, the patient did report a twenty-three-pound weight loss during the preceding two-month span but denied any fevers, chills, or drenching night sweats.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.2, 'g/dL'], 'Calcium': [15.6, 'mg/dL']}",16.24,15.428,17.052,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.2 g/dL. 
The concentration of Calcium is 15.6 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.2 g/dL)) + 15.6 mg/dL = 16.24 mg/dL.
The patient's corrected calcium concentration 16.24 mg/dL."
2600,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3786287-1,Extracted,"A 65-year-old male patient, who had a 10-year history of hypertension and type II diabetes mellitus, presented with complaints of pain and a tingling sensation in both lower limbs over the previous year and in both upper limbs over the previous 6 months. He also had a history of weight loss and an intermittent low-grade fever during the previous 6 months.
On examination, the patient was pale, conscious, alert, and oriented with a pulse of 72 beats per minute and blood pressure at 140/90 mmHg. Nothing unusual was found on examination of the chest and cardiovascular systems. Abdominal examination revealed mild hepatomegaly without splenomegaly. Examination of the nervous system showed normal mental status (patient was conscious and well oriented in time, place, and person). Sensations were diminished below the knees in both lower limbs. Power in all of the muscles was 4/5. Fundoscopy revealed a grade 4 hypertensive retinopathy.
Investigations revealed pancytopenia and normocytic normochromic anemia with a hemoglobin of 6.8 g/dL; a total leukocyte count of 1.5×103/mm3; a differential leukocyte count with 23% neutrophils, 71% lymphocytes, 5% monocytes, and 1% eosinophils; a platelet count of 21,000/mm3; and a markedly raised erythrocyte sedimentation rate of 140 mm/hr. Biochemical investigations provided the following results: blood sugar, 92 g/dL; total bilirubin, 0.6 mg/dL; alkaline phosphatase/aspartate transaminase/alanine transaminase, 126/74/55 IU/mL; blood urea, 74 mg/dL; serum creatinine, 1.7 mg/dL; and serum uric acid, 11 mg/dL. The serum protein level was 10.0 g/dL, albumin level was 1.76 g/dL, and the albumin/globulin ratio was 0.2 (reference range, 0.9-2.0). Serum calcium levels ranged from 8.4 to 9.2 mg/dL on different occasions. The venereal disease research laboratory (VDRL), antinuclear antibody, and rheumatoid factor tests were negative, while C-reactive protein was raised. The Coombs test and the test for cold agglutinins were also negative. In addition, the serological markers for hepatitis B and hepatitis C were negative. The skull radiograph revealed multiple lytic lesions.
The chest radiograph showed cardiomegaly with prominent bronchovascular markings. Ultrasonography revealed mild hepatomegaly (15.5 cm in size), while the spleen and both kidneys were within normal limits. The wall of the rectum and sigmoid colon demonstrated thickening. Contrast enhanced computed tomography (CECT) revealed atrophy of the brain and multiple lytic lesions in the skull. The rectal wall was also edematous. There was mild hepatomegaly with the presence of minimal ascites. A clinical diagnosis of multiple myeloma was considered due to the presence of lytic bony lesions, increased total protein values, decreased serum albumin, and low albumin to globulin ratio.
Bone marrow aspiration, bone marrow biopsy, and serum protein electrophoresis were simultaneously performed to confirm the diagnosis of multiple myeloma. Bone marrow imprint smears were hypercellular with the presence of numerous bare nuclei, which were predominantly lymphoid cells with a few plasmacytoid cells (). The bone marrow biopsy revealed a hypercellular marrow with diffuse infiltration of a spectrum of lymphoid cells that were predominantly small lymphocytes, plasmacytoid lymphocytes, a few plasma cells, and mast cells (). The erythroid, myeloid, and megakaryocytic series were markedly suppressed. Therefore, a diagnosis of lymphoplasmacytic lymphoma was considered. Immunohistochemical staining revealed 2 populations of cells; the predominant population was strongly positive for CD20 (lymphocytic cells) ( inset) while the other population was positive for CD138 (plasmacytic cells). CD5 and CD23 were negative, which ruled out chronic lymphocytic leukemia/small lymphocytic lymphoma. The serum protein electrophoresis revealed the following: total protein, 10.5 g/dL (range, 6.4-8.1); albumin, 1.76 g/dL (range, 3.50-5.64); gamma globulin, 7.18 g/dL (range, 0.62-1.53); and albumin to globulin ratio, 0.2 (range, 0.9-2.0), with an M spike of 5.98 g/dL. Immunofixation electrophoresis revealed IgM kappa light chains. Thus, a final diagnosis of WM was established.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [1.76, 'g/dL'], 'Calcium': [9.2, 'mg/dL']}",10.992,10.4424,11.5416,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 1.76 g/dL. 
The concentration of Calcium is 9.2 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.76 g/dL)) + 9.2 mg/dL = 10.992 mg/dL.
The patient's corrected calcium concentration 10.992 mg/dL."
2601,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4508971-1,Extracted,"A 38-year-old Turkish male was admitted to our outpatient clinic for hypercalcemia. Before entering our clinic, hypercalcemia has been detected in another medical center. History revealed, that he took ace inhibitor in combination with thiazide diuretic for hypertension. Due to the complications, like hypopotassemia this medicine was replaced with calcium channel blockers. In his family history, none of his first degree relatives had hypertension. His father died at 47 years of age due to biliary tract cancer. His three children were diagnosed with West Syndrome. One of them died at the age of 13 months, while the other 9 months of age. His third child is 2 years old and living with the respiratory support equipment. He also has a 13-year-old healthy son. There is no other significant clinical data in his medical history.
On his physical examination: blood pressure—150/90 mmHg, pulse −74 per minute, rhythmic. His general clinical appearance was good. The other systemic and laboratory findings were the following: complete blood count and thyroid function tests were normal: serum Ca level: 10.9 mg/dl (8.8–10.2), inorganic P: 2.4 mg/dl (2.7–4.5), Mg: 2.3(1.6–2.6), albumine: 3.9 g/dl, parathormone (PTH): 200 pg/ml (12–88), Na: 138 mmol/l, K+: 2.8 mmol/l, glucose: 85 mg/dl, creatinine: 0.84 mg/dl, alanine transaminase: 24 U/l, white blood cells 8 ML, hemoglobin 14 g/dl, platelet 219 C-reactive protein 0.4 mg/dl (0–0.8), alkaline phosphatase 61 U/l (38–126), 25-OH vitamin D3 22 ng/ml (14–66). Calcium level in 24-h urine: 251 mg/day, inorganic P: 88 mg/day, and K+ value in spot urine: 66 mmol/l. Aldosterone level was measured after normalization of his serum potassium level (result: 26.9 ng/dl). Plasma renin activity was <0.15 ng/ml/h. The patient was detected for multiple endocrine neoplasia syndromes. Levels of catecholamine and its metabolites in 24-h urine were normal. In the low dose (1 mg) dexamethasone suppression test, serum cortisol level was suppressed to the normal range. Serum prolactin, thyroid-stimulating hormone, adrenocorticotropic hormone, growth hormone, insulin-like growth factor 1 and calcitonin were normal.
Thyroid ultrasound revealed a 24 × 14 × 12.5 mm hypoechoic nodular lesion at the upper posterior part of the right thyroid lobe, within the thyroid capsule (intrathyroidal parathyroid adenoma?). MIBI (Technetium (99mTc) sestamibi) scintigraphy of parathyroid glands was consistent with the ultrasound finding. Abdominal magnetic resonance imaging revealed 1.6 cm adrenal gland mass consistent with adenoma, cystic lesions in both kidneys with the largest (3 cm in length) in the right kidney and also on this side 11 mm lesion which may be consistent with angiomyolipoma. Pituitary magnetic resonance imaging was normal.
The patient was operated for parathyroid adenoma. At the 3rd day after the operation, serum Ca level was found to be 9.5 mg/dl, inorganic P—3.6 mg/dl and parathyroid hormone—62 pg/ml. Pathological examination of the surgery material revealed parathyroid adenoma. The patient post operatively was followed during the 2 months with spironolactone therapy for his hypertension. This medication was stopped soon after, due to its side effects like erectile dysfunction. Post-surgery, which was conducted for the lesion (1.6 cm) identified on the left adrenal gland revealed adrenal aldosterone producing adenoma. Follow up the adrenal surgery, his blood pressure came to normal ranges and hypokalemia were improved. Blood potassium and calcium levels were within normal ranges. Genetic screening revealed negative mutation of MENIN gene.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.9, 'g/dL'], 'Calcium': [10.9, 'mg/dL']}",10.98,10.431,11.529,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.9 g/dL. 
The concentration of Calcium is 10.9 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.9 g/dL)) + 10.9 mg/dL = 10.98 mg/dL.
The patient's corrected calcium concentration 10.98 mg/dL."
2602,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7391090-1,Extracted,"A 75-year-old Japanese male with end-stage renal disease due to antineutrophil cytoplasmic antigen (ANCA)-associated vasculitis had been receiving continuous ambulatory peritoneal dialysis (CAPD) for 9 years. He also had an implanted defibrillator (cardio-resynchronized therapy with defibrillator) to treat chronic heart failure resulting from a myocardial infarction. He had a poor appetite and general malaise without abdominal pain or fever. These symptoms gradually worsened, and he was hospitalized. At the time of admission, his blood pressure was 94/52 mmHg, his height was 165 cm, and his weight was 53 kg. At auscultation, no gallop rhythm was heard, and his extremities were not edematous. The laboratory parameters at the time of admission were as follows: white blood cells, 8080/μL; hemoglobin, 13.5 g/dL; platelets, 121 × 103/μL; total protein, 5.2 g/dL; albumin, 1.8 g/dL; lactate dehydrogenase, 309 U/L; glutamate oxaloacetate transaminase, 25 U/L; glutamate pyruvate transaminase, 19 U/L; blood urea nitrogen, 28 mg/dL; creatinine, 4.97 mg/dL; sodium, 125 mmol/L; potassium, 2.7 mmol/L; chlorine, 91 mmol/L; calcium, 6.8 mg/dL; phosphorus, 4.1 mg/dL; C-reactive protein, 0.092 mg/dL; procalcitonin, 0.21 ng/mL; BNP, 319 pg/mL; intact parathyroid hormone, 149 pg/mL; and β2-microglobulin, 23.4 μg/mL. Chest X-ray revealed bilateral free air in the abdomen (). Subsequent computed tomography of the abdomen revealed marked PP (Figures and ).
Peritonitis due to perforation of the digestive tract was suspected, but the possibility of perforation was considered very low because of the absence of abdominal pain, fever, and turbidity of dialysis drainage. Insufficient priming (air removal) at the time of peritoneal dialysis bag replacement was suspected, and the patient was instructed on how to perform sufficient priming. As a result, the free air in his abdominal cavity gradually disappeared ().","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [1.8, 'g/dL'], 'Calcium': [6.8, 'mg/dL']}",8.56,8.132,8.988,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 1.8 g/dL. 
The concentration of Calcium is 6.8 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.8 g/dL)) + 6.8 mg/dL = 8.56 mg/dL.
The patient's corrected calcium concentration 8.56 mg/dL."
2603,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7155848-2,Extracted,"A 27-year-old female presented at the Urology Center, Mansoura University on June 21th, 2015 with history of repeated vomiting, frequent urination and generalized bone ache. Her examination was unremarkable apart from pallor. Laboratory investigations showed white blood cells: 7.3 × 109/L without peripheral blood blasts, hemoglobin: 8.9 g/dL, platelets: 140 × 109/L, serum creatinine: 1 mg/dL, serum uric acid: 5.9 mg/dL, serum calcium: 13.1 mg/dL, serum phosphorus: 4.1mg/dL, serum albumin: 3 g/dL with normal levels of parathyroid hormone. Patient received dexamethasone and Lasix and kept hydrated for the treatment of hypercalcemia and she was referred to our Hematology Unit to rule out multiple myeloma on June 23rd, 2015. After admission, the patient developed acute onset weakness of both lower limbs with headache and diplopia. Ophthalmological examination showed bilateral severe papilledema and restricted lateral rectus movement in left eye. Neurological examination revealed abducent nerve palsy and paraparesis. Laboratory parameters showed WBCs: 3.2 × 109/L without peripheral blood blasts, hemoglobin: 8.7 g/dL, platelets: 125 × 109/L, creatinine: 0.7 mg/dL, uric acid: 5.8 mg/dL, serum calcium: 10.98 mg/dL, serum albumin: 2.9 g/dL. CT brain was free apart from multiple osteolytic lesions affecting the skull bone. CSF examination revealed no abnormal cells. Whole body skeleton CT showed multiple osteolytic lesions affecting the scanned bones (both iliac bones, sacrum, the scanned vertebrae, sternum and skull bones) (). MRI brain revealed heterogeneous signal intensity in diplopic space of skull bones with meningeal thickening and enhancement supporting leukemic infiltration. BMA showed the picture of ALL-L2 with 95% blast cells. Flow cytometry confirmed the diagnosis of B-ALL with a population of blast cells positive for CD10, CD19, CD20, CD22, CD34 and negative for CD3, CD4, CD8, CD5, CD14, CD64, CD79, IgM, MPO, CD13, CD33 and CD117. Patient started Hyper CVAD chemotherapy protocol with triple intrathecal twice weekly and cranial irradiation. Patient received course I, but unfortunately the patient had septic shock and transferred to ICU where she was expired on July12th, 2015.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.0, 'g/dL'], 'Calcium': [13.1, 'mg/dL']}",13.9,13.205,14.595,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.0 g/dL. 
The concentration of Calcium is 13.1 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.0 g/dL)) + 13.1 mg/dL = 13.9 mg/dL.
The patient's corrected calcium concentration 13.9 mg/dL."
2604,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6037803-2,Extracted,"A 13-year-old boy presented with abdominal pain and diarrhea. Laboratory examination revealed mild leukocytosis of 10,800/mm3 with polymorphonuclear cell 81%, hemoglobin level of 14.5 g/dL and platelet count of 174×103/mm3. Electrolyte levels were sodium 137 mmol/L, potassium 3.7 mmol/L and chloride 98 mmol/L. The total protein level was 7.5 g/dL, albumin 4.6 g/dL, calcium 9.3 mg/dL, phosphorus 4.5 mg/dL, cholesterol 154.1 mg/dL, glucose 105 mg/dL, BUN 11.9 mg/dL, creatinine 0.80 mg/dL, total bilirubin 1.38 mg/dL, AST 29 U/L, ALT 30 U/L, amylase 42 U/L, lipase 26 U/L, ESR 20 mm/hour, and CRP 19.19 mg/dL. The urinary ketone was 4+. On stool examination, occult blood and leukocyte were positive. Abdominal X-ray showed mild gaseous dilatation of the small bowel and abdominal ultrasonography showed reactive lymph nodes at ileocecal area, with mild splenomegaly. He was hospitalized and administered fluid therapy, but the GI symptoms did not subside. The stool was positive for Campylobacter coli, which was considered the cause of his diarrhea. It was resolved after therapy. UGI endoscopy was performed for his continuing upper abdominal pain. Acute gastritis and duodenitis were noted, and a solitary non-pedunculated polyp with hypervascularity was found beneath the gastroesophageal junction (GEJ) area. The biopsy sample of the polyp indicated that it was hyperplastic type. There was no difference in the size and external feature of the polyp on follow-up endoscopy 6 months later. Polypectomy was performed. The size of polyp was 1.0×0.9×0.8 cm. The post-polypectomy pathological finding was the same as that seen earlier (). He was treated with medicines of his acute gastritis and duodenitis for about 2 months and his UGI symptoms did not recur. Follow-up UGI endoscopy was not performed yet.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.6, 'g/dL'], 'Calcium': [9.3, 'mg/dL']}",8.82,8.379,9.261,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.6 g/dL. 
The concentration of Calcium is 9.3 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.6 g/dL)) + 9.3 mg/dL = 8.82 mg/dL.
The patient's corrected calcium concentration 8.82 mg/dL."
2605,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4901012-1,Extracted,"A 51-year old man had a breakfast cooked with wild mushrooms that he had gathered one day earlier during summer vacation in August, 2010 at the Jujak mountain located on the province of Jeollanam-do, the southern area of Korea. He was a bus driver. He had no particular past medical or social history other than the occasional ingestion of wild mushrooms during recreational hiking. He was healthy before this admission. He did not have a history of trauma, infection, other known underlying cause, or medication use that could explain the occurrence of rhabdomyolysis. He shared the meal with his wife and son who did not eat any more mushrooms due to nausea after ingesting a single piece of mushroom. However, he ate the mushrooms without immediate symptom. Six hours later, he began to complain of vomiting, diarrhea, and myalgia. He visited a local hospital where his general condition worsened and systolic BP fell to 60 mmHg requiring dopamine treatment and endotracheal intubation. Twenty-eight hours after ingestion of the mushrooms, he was transferred to the intensive care unit of our hospital. At the time of admission, he was alert, but acute ill-looking. He complained of generalized myalgia, chest discomfort, palpitations, and dyspnea. Blood pressure was 80/56 mmHg, heart rate 121/min, respiratory rate 25/min, and body temperature 36.3oC. Oliguria was noted with no response to intravenous fluid and furosemide. Systolic murmurs were present on auscultation. Laboratory tests showed the following: hemoglobin 15.9 g/dL, hematocrit 45.9%, leukocyte count 20,740/μL with neutrophil 89.6%, platelet 253,000/μL, C-reactive protein (CRP) 8.36 mg/dL, blood urea nitrogen (BUN) 38.5 mg/dL, serum creatinine 2.84 mg/dL, serum osmolarity 314 mOsm/kg, sodium 140 mEq/L, potassium 4.7 mEq/L, chloride 100 mEq/L, ionized calcium 0.75 mmol/L, glucose 187 mg/dL, cholesterol 221 mg/dL, albumin 4.0 g/dL, aspartate aminotransferase (AST) 1,214 U/L, alanine aminotransferase (ALT) 343 U/L, total bilirubin 0.51 mg/dL, alkaline phosphatase 92 IU/L, creatine kinase (CK) 69,121 U/L, CK-MB > 500 ng/mL, lactate dehydrogenase (LDH) 2,196 U/L, troponin I 1.86 ng/mL, N-terminal pro brain natriuretic peptide (NT-pro BNP) 7,414 pg/mL, amylase 1,930 U/L, lipase 18 U/L, prothrombin time (PT) 10.2 seconds. (INR 0.86), activated partial thromboplastin time (aPTT) 28.2 seconds, urine osmolarity 341 mOsm/kg, sodium 22 mEq/L, potassium 59.2 mEq/L, chloride 14 mEq/L, creatinine 123.8 mg/dL, myoglobin 51.7 ng/mL, and fractional excretion of sodium 0.36%. Urine analysis showed pH 5.0, specific gravity 1.020, protein 2+, ketone 2+, blood 4+, RBC 5-9/high-power field, and WBC 0-1/high-power field. Blood and urine cultures were all negative for microorganism. Arterial blood gas analysis was pH 7.04, PaCO2 69 mmHg, PaO2 172 mmHg, and HCO3
- 18.7 mmol/L. Chest radiographs revealed mild cardiomegaly without lung lesion. Electrocardiogram (ECG) showed sinus tachycardia with QT prolongation. The enlarged left ventricle (LV), severe LV systolic dysfunction (ejection fraction 30%), and akinesia of LV mid to apex wall suggesting stress induced cardiomyopathy were noted on echocardiography. He received ventilator support, hemodynamic monitoring, continuous venovenous hemodiafiltration, and conservative care including intravenous fluid and electrolyte repletion. Seventy hours after ingestion of the mushrooms, BUN 41.9 mg/dL, serum creatinine 3.46 mg/dL, AST 3,271 U/L, ALT 1,254 U/L, total bilirubin 1.55 mg/dL, CK 121,397 U/L, CK-MB >500 ng/mL, LDH 6,102 U/L, troponin I 11.77 ng/mL, amylase 2,779 U/L, lipase 601 U/L, PT 42.1 seconds. (INR 3.34), and aPTT > 150 seconds. Blood pressure continued to decrease despite intravenous fluid and inotropics. Ventricular tachycardia developed, and he died due to cardiogenic shock 72 hours after ingestion of the mushrooms.
The leftover samples of the mushrooms that he had ingested were sent to Agricultural Microbiology Division, National Academy of Agricultural Science, Rural Development Administration, Suwon, Korea. Those were identified as R. subnigricans by their gross morphology (). Further examination by microscopy also confirmed the presence of spores from R.
subnigricans.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.0, 'g/dL'], 'Calcium': [0.75, 'mmol/L']}",3.006,2.8557,3.1563,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.0 g/dL. 
The concentration of Calcium is 0.75 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 0.75 mmol. To convert 0.75 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 0.75 mmol Calcium * 0.001 mol/mmol = 0.00075 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00075 mol Calcium * 40.08 g/mol = 0.03006 g Calcium. To convert 0.03006 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.03006 g Calcium * 1000.0 mg/g = 30.06 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 30.06 mg Calcium/10.0 dL = 3.006 mg Calcium/dL. The concentration value of 0.75 mmol Calcium/L converts to 3.006 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.0 g/dL)) + 3.006 mg/dL = 3.006 mg/dL.
The patient's corrected calcium concentration 3.006 mg/dL."
2606,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-8129002-1,Extracted,"On October 2014, a 54-year-old male with no significant past medical history presented to the hospital with bilateral lower extremity edema and chest pain. A clinical, historical and imaging assessment revealed no evidence of a secondary cause of his clinical presentation. On admission his blood pressure was 157/93 mmHg. Laboratory tests revealed hypoalbuminemia (1.1 g/dl), elevated D-dimer (5,250 ng/ml), creatinine (1.4 mg/dl), BUN (19 mg/dl), low calcium (7.7 mg/dl), and proteinuria with random urine protein/creatinine ratio 5,139 mg/g. An ultrasound and a CT of the abdomen with IV contrast ruled out DVT in both extremities and any compressing mass or thrombus in the inferior vena cava, respectively. The patient was treated with furosemide 20 mg p.o. daily without improvement. Kidney biopsy was performed, revealing global effacement of the epithelial cell foot processes, unremarkable glomeruli on light microscopy, focal loss of fenestration of the endothelial cells and signs of injury with mild ectasia and slight vacuolization of the tubules consistent with minimal change disease ().
The MCD was considered idiopathic and initially treated with mycophenolate and prednisone (80 mg p.o. daily) for 8 weeks without any improvement. In December 2014, the patient continued to have problems with anasarca and volume overload; he was given outpatient diuretics including furosemide, torsemide, and metolazone, and he initially lost weight. In January 2015, his 24-h urine protein went up to 12 g/day and he was started on cyclosporine 50 mg p.o. twice daily. After gaining 50 pounds through fluid retention, he was admitted to the hospital and treated with IV furosemide drip 20 mg/h along with IV albumin, metolazone, prednisone (40 mg) and cyclosporine (75 mg twice daily). The patient was also put on a low salt diet with fluid restriction and he lost 50 pounds of fluids during the 13 days of hospitalization. His serum albumin went up to 2.7 g/dl and creatinine improved to 1.0 mg/dl. However, proteinuria was not resolved. He was discharged with the following medications: cyclosporine (100 mg twice daily), prednisone (40 mg daily), and furosemide (80 mg daily).
In the following months, prednisone was tapered off and eventually discontinued while cyclosporine was increased to 125 mg twice daily. On a follow up visit in March 2015, laboratory tests revealed increased BUN (51 mg/dl) and creatinine (1.5 mg/dl), and low chloride (91 meq/l), potassium (3.1 meq/l), calcium (7.5 mg/dl), and albumin (1.5 g/dl). Subsequently, the patient lost his health insurance and discontinued cyclosporine. In June 2015, his BUN was 63 mg/dl and creatinine 2.0 mg/dl and he was treated with cyclosporine (200 mg twice daily), metolazone (5 mg daily) and torsemide (100 mg twice daily) for 30 days. The patient rapidly progressed to kidney failure (BUN 109 mg/dl and creatinine 6.27 mg/dl) and, in September, initiated hemodialysis thrice weekly given the patient's excess fluid overload and inability to control his metabolic status. The patient's daily ultrafiltration rate was up to 5 l/day. The patient continued to require significant fluid and electrolyte control and after 3 months on dialysis, was evaluated and listed for kidney transplantation and was placed on the waiting list. When the patient was placed on chronic dialysis, the patient (who has an extensive scientific engineering background) began to review the literature on MCD and proteinuria. Over time he developed a more comprehensive understanding of the pathophysiology of MCD and proteinuria. He developed a hypothesis and with a colleague who had access to a nutritional supplement process facility, began to evaluate possible treatment approaches. Together they developed and continue to produce this proprietary nutritional supplement (in a regulated sterile production facility). It was at this point that he, on his own began a supplement regimen to promote regrowth of the glycocalyx and prevent its degradation () in the presence of a balanced colloid and electrolyte environment. Due to poor nutrition and at the request of the patient, at the beginning of January 2016, he initiated standard IDPN therapy together with hemodialysis. He responded to the improved nutritional delivery and intermittent hemodialysis and his kidney indices improved after 2 weeks of treatment (BUN 70 mg/dl and creatinine 3.45 mg/dl) and at the end of April BUN was 19 mg/dl and creatinine 1.4 mg/dl. Therefore, hemodialysis was discontinued. However, proteinuria was still present (random urine protein/creatinine ratio was 5,919 mg/g) and serum albumin was low (2.0 g/dl). The patient received supportive care consisting of IV albumin thrice weekly and His serum albumin increased up to 5.0 g/dl on July 2016 and IV albumin was discontinued. Proteinuria progressively decreased from June (random urine protein/creatinine ratio 2,458 mg/g) and almost completely resolved at his last follow up visit on September 2016 (random urine protein/creatinine ratio 280 mg/g). The patient continued to administer himself supplements and, as of today, he has had no further relapses. On May 2020, his urine protein/creatinine ratio was 159 mg/g, and his kidney function was stable (BUN 25 mg/dl and creatinine 1.41 mg/dl). : Timeline for treatment and response. Chronic dialysis course.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [1.5, 'g/dL'], 'Calcium': [7.5, 'mg/dL']}",9.5,9.025,9.975,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 1.5 g/dL. 
The concentration of Calcium is 7.5 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.5 g/dL)) + 7.5 mg/dL = 9.5 mg/dL.
The patient's corrected calcium concentration 9.5 mg/dL."
2607,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3643327-1,Extracted,"A 35-year-old man presented with weight loss, anorexia, and painful right inguinal mass with referral pain to the testis. Physical examination revealed right inguinal firm and painful mass adhesive to the spermatic cord and new onset hydrocele. In medical history, he had brucellosis two years ago and had been treated with anti-brucellosis drugs. Sonography showed a solid hypoechoic mass measuring 16 × 11 mm in the right inguinal canal and normal sized, normal echoic right testis with localised fluid collection in the superio-lateral part of the right testis (epididymal cyst or hydrocele). In sonography, the left testis had normal size and echogenicity. He underwent biopsy of the right inguinal mass. During operation, we encountered a firm mass adhesive to spermatic cord vessels and vas deferens, so it was impossible to resect the mass completely; we then decided to do a biopsy from the mass.
The pathologist reported primary or metastatic adenocarcinoma, and then the patient underwent trans-inguinal radical orchiectomy with complete mass resection, according to the pathologist's report of metastatic adenocarcinoma of the spermatic cord; after the resection, the margin was free of tumor. Immunohistochemistry was positive for cytokeratin and Epithelial Membrane Antigen (EMA) and negative for Leukocyte Common Antigen (LCA), S100, desmin, vimentin, Neuron-Specific Enolase (NSE), thyroglobulin, Alpha-Fetoprotein (AFP), and Prostate-Specific Antigen (PSA). He was admitted with nausea, vomiting, and abdominal pain. Gastroenterologist consultation was done, after which upper gastrointestinal endoscopy and colonoscopy were recommended, both of which had normal result. PSA (free and total) was in normal range. Transrectal sonography revealed an area (13 × 17 mm) with non-homogeneous echogenicity in the peripheral side of the left prostate lobe and biopsy was done, which reported as normal prostatic tissue and one core was granulation tissue. Laboratory findings include: White Blood Cells (WBC) = 6700/μl [Polymorphonuclear Leukocytes (PMN) = 63%, Lymph = 27%), Hemoglobin (Hb) = 17.2 gr/dl, Platelet Count Test (PLT) = 217,000/μl, Fetal Bovine Serum (FBS) = 105 mg/dl, albumin = 4.9 g/dl, protein = 8.1 g/dl, Aspartate Aminotransferase (AST) = 25 U/L, Alanine Aminotransferase (ALT) = 58 U/L, calcium = 13 mg/dl, Na = 126 meq/L, K = 4.6 meq/L, Cr = 0.84 mg/dl, Urea = 24 mg/dl, Parathyroid Hormone (PTH) = 18 (NL:8-69) pg/ml, 2ME = 1/160, total bilirubin = 0.9 mg/dl, direct bilirubin = 0.28 mg/dl, Magnesium = 2.42 mg/dl (NL:1.8-2.6), Lactate Dehydrogenase (LDH) = 428 U/L, Alkaline phosphatase = 256 U/L. Wright = 1/160, Coombs Wright = 1/320. Hepatitis B Surface. Antigen (HbsAg), anti-Hepatitis C Virus Antibody (HCV Ab), and HIV Antibody (HIV Ab) all showed negative results. Thyroid function tests yielded normal results. Tumor markers including CA15-3, CA19-9, ß-Human Chorionic Gonadotropin (ß-hCG), and AFP were in normal ranges. Abdominopelvic computed tomographic (CT) scan showed severe distention in the stomach and jejunum. Serum 8 am basal fasting cortisol level was 29.01 ug/dl (Nl:6.2-19.4). Abdominopelvic sonography showed distention only in the gastrointestinal loops. Chest X-ray and brain CT scan were reported to be normal. Whole body bone scan was unremarkable. We consulted with infectious disease specialist who recommended starting anti-brucellosis therapy for the patient due to elevation of Wright's and Coombs Wright's tests. Therefore, we administered ofloxacin and rifampin for the patient.
In the hospital, his nausea and vomiting did not resolve and he developed a state of delirium and abdominal distention. In repeated physical examination, we found sinus tachycardia, tenderness, and guarding in abdominal examination. We sent for a surgical consultation, but before consultation his family got the patient released from the hospital. They took him to another centre and at that center with diagnosis of acute abdomen he had been underwent laparotomy. During operation, the surgeon noticed a small bowel loop with a stricture in the middle portion and a tumoral lesion in that area with serosal involvement. Small bowel tumor resection revealed small bowel adenocarcinoma with full thickness and vascular involvement and three nodes out of six lymph nodes were involved. Chemotherapy with Capecitabine-plus-Oxaliplatin (XELOX) regimen was started and continued at three-week intervals. At present, six months after the operation, he has a good general condition, without any metastatic symptoms and signs.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.9, 'g/dL'], 'Calcium': [13.0, 'mg/dL']}",12.28,11.666,12.894,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.9 g/dL. 
The concentration of Calcium is 13.0 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.9 g/dL)) + 13.0 mg/dL = 12.28 mg/dL.
The patient's corrected calcium concentration 12.28 mg/dL."
2608,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7550932-1,Extracted,"A 49-year-old male smoker presented to the emergency department complaining of chest pain
and progressive dyspnea for the past 4 days. The chest pain was constant, sharp,
nonradiating in nature noticed over both sides of the chest. The pain progressively worsened
over time and with deep inspiration. The patient has a 10 pack-year smoking history.
On arrival his heart rate was 119 beats/minute, respiratory rate 23 breaths/minute, blood
pressure 109/59 mm Hg, and peripheral capillary oxygen saturation of 84% on room air. Chest
examination revealed diminished breath sounds and increased resonance on the left thorax.
His jugular venous pressure measured up to 12 cm of H2O.
Laboratory results were significant for white blood cell count of 12 200/µL, absolute
neutrophil count of 10 300/µL, bands 8%, hemoglobin 16.1 g/dL, hematocrit 47%, platelets
247 000/µL, sodium 125 mEq/L, potassium 4.3 mEq/L, chloride 91 mEq/L, bicarbonate 24 mEq/L,
blood urea nitrogen 18 mg/dL, creatinine 0.99 mg/dL, glucose 114 mg/dL, albumin 2.7 g/dL,
and calcium of 8.1 mg/dL. Troponins were negative. Lactic acid was 1.7 mmol/L. A stat chest
X-ray revealed the entire left lung occupied by thin-walled bullae, left-to-right
mediastinal shift, heterogeneous opacification of the right upper lobe, and a 1-cm nodule in
the right mid-zone ().
Subsequently, computed tomography (CT) with contrast of the chest was obtained which
revealed giant bullae in the hemithorax, atelectasis of the left lower lobe, peripheral
pneumothorax in posterior medial sulcus as well as the anterolateral base of the hemithorax,
marked mediastinal shift to the right, and consolidation with bronchiectasis in the right
upper/middle/lower lobes ().
Thoracic Surgery was consulted for a video-assisted thoracoscopy for distinguishing the
etiology of tension from giant bullae versus undiagnosed chronic tension pneumothorax and
possible bullectomy. The patient was found to have tension giant bullae and underwent
bullectomy.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.7, 'g/dL'], 'Calcium': [8.1, 'mg/dL']}",9.14,8.683,9.597,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.7 g/dL. 
The concentration of Calcium is 8.1 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.7 g/dL)) + 8.1 mg/dL = 9.14 mg/dL.
The patient's corrected calcium concentration 9.14 mg/dL."
2609,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4805222-1,Extracted,"A 16-year-old male presented to our outpatient clinic with complaints of bilateral pain and swelling along his Achilles tendon in the past four weeks. He stated that the pain was usually worse during and after walking. He was a high school student and was not involved in any sport activity. A closer questioning revealed a transient hematuria which had occurred two weeks ago. Medical history was unremarkable otherwise. Family history was also negative for known diseases including cancers.
Physical examination revealed normal findings except for tenderness and swelling in the area where the patient complained of pain. The height of the patient was 172 cm (50th percentile) and his weight was 63 kg (50th percentile). Pubertal stage conformed to Tanner 4 according to Tanner staging. Blood pressure was 110/70 mmHg.
Total blood count was normal. Blood chemistry showed a serum calcium level of 14.4 mg/dL (N: 8.4-10.6 mg/dL), phosphate: 2.4 mg/dL (N: 2.3-4.7 mg/dL), alkaline phosphatase: 245 U/L (N: 40-360 mg/dL), magnesium: 0.8 mmol/L (N: 0.5-1.1 mg/dL), creatinine: 0.8 mg/dL, total protein: 7.7 g/dL, albumin: 4.1 g/dL, alanine aminotransferase: 15 U/L, and aspartate aminotransferase: 19 U/L. Serum glucose and prolactin levels were within normal limits. Urinary calcium/creatinine ratio was 0.2. Parathormone (PTH) level was 512 pg/mL (N: 5-65 pg/mL). Anteroposterior and lateral radiograms of both ankles were normal. A superficial ultrasonography performed using GE logic5P Doppler Sonography device and linear probe (7-12 MHz) revealed calcific nodules and increased Doppler signals surrounding the nodules, which were localized in both Achilles tendons on the longitudinal Doppler sections (). Renal ultrasonography was normal. Intravenous saline infusion (3000 mL/day), furosemide (1 mg/kg every six hours) and prednisolone (60 mg/day) were started. Neck ultrasonography revealed a 12x10 mm hypoechoic lesion near the left thyroid lobe, suggesting a parathyroid adenoma. The dual-phase 15 mCi Technetium-99m (99mTc) sestamibi scanning revealed increased activity in the left thyroid lobe, indicating parathyroid adenoma. On the second day of admission, it was observed that the hypercalcemia did not respond to medical treatment and the patient was admitted to pediatric intensive care unit due to severe hypercalcemia (calcium: 18 mg/dL). Serum calcium levels decreased to 13 mg/dL after intravenous calcitonin (0.8 IU/kg/d) was added to the treatment.
A minimally invasive parathyroidectomy was planned. On the day of surgery, serum PTH level was 1222 pg/mL. PTH level was measured intraoperatively 10 minutes after the left superior gland was excised and detected to be decreased more than 50% of the initial PTH level. The left inferior gland was apparently normal. Left superior parathyroid gland was excised guided by gamma probe.
On post-operative day 3, the laboratory data were: calcium: 9.9 mg/dL, phosphate: 3.9 mg/dL, alkaline phosphatase: 176 U/L, and PTH: 12.5 pg/mL. After parathyroidectomy, the swelling also resolved and the patient had some relief from his pain. On the follow-up visit two months after the surgery, the tenderness over the Achilles tendon and the flow pattern on Doppler examination had both disappeared.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [14.4, 'mg/dL'], 'Albumin': [4.1, 'g/dL']}",14.32,13.604,15.036,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.1 g/dL. 
The concentration of Calcium is 14.4 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.1 g/dL)) + 14.4 mg/dL = 14.32 mg/dL.
The patient's corrected calcium concentration 14.32 mg/dL."
2610,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4008916-1,Extracted,"A 65-year-old male, presented with low back ache of 4 months duration and unable to stand or walk of 1½ months duration, with no comorbidities. On evaluation the patient had medical research council grade 3 motor weakness of lower limbs, normocytic normochromic anemia with hemoglobin of 8.5 g/dL, and normal total count with neutrophilic preponderance and thrombocytopenia. X-ray dorsolumbar spine revealed D10 vertebral compression and MRI spine revealed a posterior epidural mass from D9 to D11 levels. Further, skull X-ray showed multiple lytic lesion. Bone marrow aspiration was performed, which showed 30% plasma cells of all nucleated cells with plasmablastic morphology. Serum electrophoresis showed M band, urine Bence Jones Protein was negative, deranged renal function with blood urea of 184 and serum creatinine of 4.5, serum calcium was 14.2, serum beta-2 microglobulin was 7000 μg/L and albumin 3.8. The liver function tests were normal. The patient was diagnosed as a case of multiple myeloma, International Staging System (ISS) Stage 3.[]
The patient was initially stabilized with palliative radiation to spine in view of low back ache and motor weakness. He was also treated for hypercalcemia with hydration, steroids, and diuretics. Bisphosphonates was not given. Back ache reduced, lower limb weakness improved from grade 3 to grade 2, calcium levels reduced to 9.2 mg/dl, and serum creatinine was 1.3 mg/dl.
In view of renal failure, bortezomib- and dexamethasone-based chemotherapy regimen was started. First cycle day 1, bortezomib 1.3 mg/m2 and dexamethasone 40 mg were given. After 48 h, the patient became irritable and disoriented. However, no fever was observed. Vitals were stable with moderate to severe dehydration, bilateral crepitations in mid and lower lung fields. Upon investigation, blood sugar was 109 mg/dl, blood urea 124 mg/dl, serum creatinine 3.9 mg/dl, serum sodium 138 mg/dl, potassium >6 mg/dl, serum uric acid 8.4 mg/dl, calcium 6.3 mg/dl, and phosphorous level of 4.1 mg/dl. Blood gas analysis showed metabolic acidosis. The patient satisfied clinical and laboratory criteria of tumor lysis syndrome according to the Cairo and Bishop criteria 2. The patient was treated with insulin, sodium bicarbonate, calcium gluconate, salbutamol nebulization, and Frusemide injection. As the condition of the patient deteriorated, he underwent hemodialysis. On postdialysis, the patient developed dyspnea and desaturated even with oxygen support. Repeat blood gas analysis showed severe metabolic acidosis. The patient was put on ventilator and other supportive treatment was given, but the patient subsequently deteriorated and expired.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.8, 'g/dL'], 'Calcium': [14.2, 'mg/dL']}",14.36,13.642,15.078,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.8 g/dL. 
The concentration of Calcium is 14.2 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.8 g/dL)) + 14.2 mg/dL = 14.36 mg/dL.
The patient's corrected calcium concentration 14.36 mg/dL."
2611,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5740581-1,Extracted,"In May 2016, a 47-year-old Caucasian woman was hospitalized for pain in the left knee resistant to common analgesics. She presented with a past history of epilepsy and gastroesophageal reflux disease. She was a hairdresser, and she smoked more than 20 cigarettes/day. She was married, and she had three healthy children. She had no family history of malignancy. She did not take any particular medication regularly. In 2014, she had undergone radical resection of a squamous cell carcinoma of the oropharynx (stage pT2, pN1), then received adjuvant radiotherapy. Her follow-up was uneventful until April 2016, when multiple bone metastases from a squamous cell carcinoma were histologically confirmed.
The patient’s oxygen saturation on admission was 96%, and her blood pressure and heart rate were normal at 124/82 mmHg and 95 beats/minute, respectively. Her oral temperature was 36.8 °C. The result of her physical examination was normal except for a bulky, painful lesion of the left knee and a solitary, painless, intramammary lesion of 4 cm in the right upper external quadrant (UEQ), without any skin retraction, associated with multiple fixed right axillary and supraclavicular lymph nodes.
The patient’s pH was 7.43, her partial pressure of arterial oxygen was 72 mmHg, and her partial pressure of arterial carbon dioxide was 36 mmHg. Laboratory tests revealed normocytic normochromic anemia (8.6 g/dl), hypoalbuminemia (26 g/dl), and severe hypercalcemia (3.31 mmol/L, ionized calcium 1.99 mmol/L). The patient’s renal and hepatic function was normal.
Whole-body computed tomography revealed multiple lymph node, peritoneal, splenic, lung, and bone metastases, as well as a solitary breast lesion in the right UEQ (Fig. ). A positron emission tomographic scan documented multiple visceral lymph nodes and bone metastases with a single hypermetabolic lesion of the right breast (Fig. ). Breast ultrasound confirmed the presence of a hypoechogenic tumor lesion of 4 cm in the UEQ that was associated with multiple axillary and infra-/supraclavicular adenopathies (Fig. ).
A percutaneous echo-guided biopsy of the breast lesion was performed. Histology revealed well- to moderately differentiated squamous tumor cells infiltrating the breast tissue without any in situ ductal or lobular component or desmoplastic reaction (Fig. ). Immunohistochemistry showed that the tumor cells were positive for anti-p40 and anti-p63 and negative for cytokeratins 7 and 20, hormone receptors, and human epidermal growth factor receptor 2, confirming the diagnosis of a BM from a squamous cell carcinoma (Fig. ).
Analgesic palliative radiotherapy was performed at the tibial bone metastasis. The patient’s hypercalcemia normalized after intravenous hydration and zoledronic acid administration. Her anemia was treated with a blood transfusion of 2 U of red cell concentrate. Considering the quick worsening of the patient’s clinical condition, best supportive care was initiated, and the patient died of acute respiratory insufficiency in June 2016 before any systemic antitumoral treatment was started.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [26.0, 'g/dL'], 'Calcium': [3.31, 'mmol/L']}",-4.334,-4.1173,-4.5507,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 26.0 g/dL. 
The concentration of Calcium is 3.31 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 3.31 mmol. To convert 3.31 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 3.31 mmol Calcium * 0.001 mol/mmol = 0.00331 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00331 mol Calcium * 40.08 g/mol = 0.13266 g Calcium. To convert 0.13266 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.13266 g Calcium * 1000.0 mg/g = 132.66 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 132.66 mg Calcium/10.0 dL = 13.266 mg Calcium/dL. The concentration value of 3.31 mmol Calcium/L converts to 13.266 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 26.0 g/dL)) + 13.266 mg/dL = -4.334 mg/dL.
The patient's corrected calcium concentration -4.334 mg/dL."
2612,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7535667-1,Extracted,"A 58-year-old female patient with chronic kidney disease (CKD) was treated with laser lithotripsy. After 20 days, her serum creatinine (SCr) had increased from 200 to 280.2 μmol/L, at which point she was admitted to the hospital. SCr continued to increase to 393.0 μmol/L over the course of the next 16 days. Upon admission, she was fatigued, weak, and consistently dizzy. Blood pressure (BP) was 106/63 mmHg. Blood chemistry showed albumin of 3.1 g/L, ALT at 19 U/L, AST at 22 U/L, SCr at 273.9 μmol/L, K+ at 2.94 mmol/L, Ca2+ at 1.63 mmol/L, and Mg2+ at 0.46 mmol/L. She was diagnosed with metabolic acidosis, hypocalcemia, hypokalemia, and hypomagnesemia, and was treated with intravenous calcium gluconate, oral potassium sodium hydrogen citrate granules, potassium, and magnesium aspartate. Three days after treatment, the patient still complained of dizziness and physical weakness. Her BP was maintained at 83–110/56–75 mmHg, her urine volume was 600–1000 mL/d, and her heart rate had a range of 90–100 beats/min. Since she suffered from hypotension, she was given oral midodrine (2.5 mg three times daily). She took midodrine for the first time at 19:00 pm, and felt intermittent involuntary tremors after 2 h. Tremors became more frequent after 6 h. There were no observations of salivation, urination, or biting of the tongue, and she was able to obey verbal commands. The patient reported that she could not control her arms to keep them still. Blood gas analysis indicated a pH of 7.46, with Ca2+ of 0.93 mmol/L. Despite continuous supplementary intravenous calcium, the symptoms were not relieved. After taking midodrine for the second and third time, the patient had a generalized myoclonic seizure and paresthesia, described as the sensation of crawling ants on her skin. She reported that the clonus was less painful if she lay down, and she was unable to walk by herself. There were no additional significant abnormalities in her brain CT scan or neurological examination, although she was dehydrated from hemodialysis. She was given oral diazepam to relieve anxiety, but this was also ineffective. After evaluating the patient's medicines and manifestations, a clinical pharmacist suggested that the myoclonus reflected a rare ADR of midodrine, and midodrine was withdrawn immediately. Since the patient's blood pressure was still low, intravascular rehydration and furosemide were given without an alpha-1-receptor antagonist. Her symptoms improved gradually, and myoclonus ceased a day after midodrine withdrawal, although her ionized calcium remained abnormal. Myoclonus did not recur during hospitalization, and the patient did not report any further symptoms at the outpatient clinic one month later. The event was evaluated as Naranjo Scale is 7, and we therefore suspect it to be an adverse drug reaction.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.1, 'g/L'], 'Calcium': [1.63, 'mmol/L']}",9.485,9.01075,9.95925,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.1 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 3.1 g Albmumin/10.0 dL = 0.31 g Albmumin/dL. The concentration value of 3.1 g Albmumin/L converts to 0.31 g Albmumin/dL. 
The concentration of Calcium is 1.63 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.63 mmol. To convert 1.63 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.63 mmol Calcium * 0.001 mol/mmol = 0.00163 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00163 mol Calcium * 40.08 g/mol = 0.06533 g Calcium. To convert 0.06533 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.06533 g Calcium * 1000.0 mg/g = 65.33 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 65.33 mg Calcium/10.0 dL = 6.533 mg Calcium/dL. The concentration value of 1.63 mmol Calcium/L converts to 6.533 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 0.31 g/dL)) + 6.533 mg/dL = 9.485 mg/dL.
The patient's corrected calcium concentration 9.485 mg/dL."
2613,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4318109-1,Extracted,"An 18-year-old female was referred to our hospital for evaluation of swelling of legs of 2 months duration. There was history of bone pain, polydipsia, and polyuria for the past 3 years. She was born of non-consanguineous marriage. Patient had delayed developmental milestones. She began to walk and speak at 3 and 5 years of age respectively. Patient had difficulty in night vision since 8 years of age and difficulty in distant vision since 9 years of age. She dropped out from school due to poor scholastic performance. Patient had not attained menarche. Her both younger siblings were normal. The family history was unremarkable.
On examination, her height and weight were 136 cm (<10th centile) and 58 kg respectively with a body mass index of 31.4 kg/m2. She had pallor with bilateral pitting pedal edema. Physical examination was notable for the absence of secondary sexual characters in the form of absence of axillary, pubic hair, and poor breast bud development. She had post axial polydactyly in both her legs, central polydactyly in her right hand and clinodactyly of left little finger [Figures and ]. Genital examination was normal. Her visual acuity was decreased to counting fingers at 1 m in both the eyes. Ophthalmic examination revealed features of retinitis pigmentosa []. Her psychological evaluation showed an IQ of 70.
Investigations revealed hemoglobin - 7.6 gm/dl, urea - 64 mg/dl, creatinine - 10.6 mg/dl, calcium - 7.0 mg/dl, inorganic phosphorus - 5.6 mg/dl, and serum albumin - 3.7 gm/l. Urine analysis revealed trace proteinuria with no active sediments. She had features of secondary hyperparathyroidism with serum alkaline phosphatase of 1157 U/l and intact PTH of 418.3 pg/ml. Her fasting and post prandial blood glucose were 57 and 87 mg/dl respectively. Ultrasound examination showed normal sized kidneys with increased echogenicity. Renal biopsy revealed interstitial fibrosis and tubular atrophy in 75% of the area examined suggestive of chronic interstitial nephritis [].
The combination of pigmentary retinopathy, polydactyly, mild mental retardation, obesity, and renal failure fits well with the diagnosis of BBS. Patient was initiated on hemodialysis. At present, she is on maintenance hemodialysis in a peripheral dialysis center.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.7, 'g/L'], 'Calcium': [7.0, 'mg/dL']}",9.904,9.4088,10.3992,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.7 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 3.7 g Albmumin/10.0 dL = 0.37 g Albmumin/dL. The concentration value of 3.7 g Albmumin/L converts to 0.37 g Albmumin/dL. 
The concentration of Calcium is 7.0 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 0.37 g/dL)) + 7.0 mg/dL = 9.904 mg/dL.
The patient's corrected calcium concentration 9.904 mg/dL."
2614,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7813405-1,Extracted,"A 35-year-old woman progressively developed abdominal pain, associated with severe lymphoedema of the legs, ascites and diarrhoea. She was not taking any medication and her medical history was unremarkable, except for a sphincterectomy and papillotomy for gallstones, a laparoscopic cholecystectomy and a left ovarectomy after ovarian torsion. She did not have any familial antecedents of similar findings.
She did not smoke and there was no alcohol consumption.
Laboratory results showed a potassium level of 2.4 mmol/L, a calcium level 1.45 mmol/L, an albumin concentration 14 g/L, uric acid 1.8 mg/dL, gammaglobuline 1.7 g/L, transferrin saturation 28%, ferritine level 7 µg/L, haemoglobin 95 g/L, mean corpuscular volume (MCV) 72 fL, platelets 63×109/L, white cell count of 1.600×109/L, absolute lymphocytes 2.151×109/L and vitamin B12 0.18 µg/L.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [14.0, 'g/L'], 'Calcium': [1.45, 'mmol/L']}",7.892,7.4974,8.2866,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 14.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 14.0 g Albmumin/10.0 dL = 1.4 g Albmumin/dL. The concentration value of 14.0 g Albmumin/L converts to 1.4 g Albmumin/dL. 
The concentration of Calcium is 1.45 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.45 mmol. To convert 1.45 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.45 mmol Calcium * 0.001 mol/mmol = 0.00145 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00145 mol Calcium * 40.08 g/mol = 0.05812 g Calcium. To convert 0.05812 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.05812 g Calcium * 1000.0 mg/g = 58.12 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 58.12 mg Calcium/10.0 dL = 5.812 mg Calcium/dL. The concentration value of 1.45 mmol Calcium/L converts to 5.812 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.4 g/dL)) + 5.812 mg/dL = 7.892 mg/dL.
The patient's corrected calcium concentration 7.892 mg/dL."
2615,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7016445-1,Extracted,"The patient is a 58-year-old Haitian Creole-speaking female with no significant past medical, psychiatric, or substance use history who was brought to her primary care doctor by her family following three weeks of headache and change in mental status, including paranoia and auditory hallucinations. The patient's family reported that she was in her usual state of health when she suddenly began to exhibit “bizarre behavior,” hiding in closets out of fear that people were going to “beat her up and kill [her],” and hearing voices of these threatening people. During this time, the patient also had symptoms of headache, joint pain, and constipation. Bloodwork completed by her family physician found her calcium to be 14.4 (normal 8.5-10.2) mg/dL, and she was subsequently transferred and admitted to the medical unit at our hospital.
After admission, the patient was found to have a total calcium of 14.4 mg/dL, ionized calcium of 7.2 (normal 4.64 to 5.28) mg/dL, parathyroid hormone (PTH) level of 759 (normal 10-65) pg/dL, albumin of 4 (normal 3.5-5.5) g/dL, and phosphorous of 2 (normal 2.5-4.5) mg/dL, concerning for a diagnosis of PHPT. No other medical cause for delirium was found; the patient had consistently stable vitals and negative workup for sepsis, HIV, syphilis, and toxicological causes. The patient was treated with IV fluids and calcitonin. Ultrasound of the neck found multiple nodules on the right thyroid gland consistent with parathyroid adenoma, confirming the diagnosis of primary hyperparathyroidism. The patient was managed medically until her surgery could take place, with calcium levels fluctuating between 10 mg/dL and 12.9 mg/dL. As workup was completed, our Psychiatry Consultation and Liaison (C/L) team was consulted to assess her mental status and recommend and manage pharmacotherapy for delirium. The patient's primary language was Haitian Creole, and as such, interviews were conducted utilizing a phone-translation service, with information often verified by her bilingual family members. As aspects of the Mini-Mental State Examination (MMSE) are based on ability to read and write in English, some components of the MMSE were not possible to assess using phone-translation and were excluded from scoring, as noted below.
Our initial evaluation was on hospital day 2, with calcium now corrected with medical intervention to 10.2 mg/dL. Our exam was significant for somnolence, unchanged auditory hallucinations and persecutory delusions, poverty of speech, fluctuation in attention, and poor concentration. The patient was oriented only to person and knew that she was in a hospital. She was guarded with the interviewer, expressing fear that her clinical team would reveal her location to the “people trying to get [her].” During her stay, she periodically endorsed suicidal ideation, with two attempts at self-asphyxiation with an IV cord. She also was often found by night staff hiding in her closet from “people coming to get [her].” She was diagnosed with delirium due to hypercalcemia, mixed-subtype.
Our C/L team recommended one-to-one (1 : 1) observation, frequent reorientation, and limiting the use of tethers (e.g., catheters), as well as other environmental maneuvers as part of the hospital's delirium protocol. Her psychosis was treated with olanzapine titrated to 15 mg daily, gabapentin 300 mg daily, and haloperidol 2 mg IM every four hours for agitation that impeded essential medical care. These interventions yielded no significant change in mental status or perceptual disturbances.
Six days before right hemithyroidectomy, the patient was evaluated by the C/L team with calcium level of 10.4 mg/dL, ionized calcium of 5.2 mg/dL, albumin of 3.5 g/dL, and PTH of 8 pg/dL. Her MMSE was scored 11/22, with some questions deferred due to language barrier. Patient lost points for date, season, and declined to answer location questions or copy a drawing of intersecting pentagons. There was no change in the patient's mental status exam at this time; she continued to have auditory hallucinations of voices stating they were going to “tie a rope around [her] neck.” She also expressed persecutory delusions that these people came to the hospital and tried to enter her room the night before.
Six days postsurgery, with calcium level of 7.7 mg/dL, albumin of 4.1 g/dL, and PTH of 91 pg/mL, the patient was found to have continued somnolence, fluctuating attention, disorientation to place and time, and a persecutory delusion that she would be “arrested.” She denied hallucinations or suicidal ideation at this time. She was found to have an MMSE score of 4/18, losing points for all time and place questions, attention, and 2/3 delayed word recall, again with some questions deferred due to language barrier.
Eleven days postsurgery, with calcium level of 8.8 mg/dL, albumin of 4 g/dL, and PTH of 63 pg/mL, the patient was found to have improved alertness and was oriented to person, hospital, day, month, and year but not to city or state, despite continued treatment with olanzapine, gabapentin, and haloperidol. She denied hallucinations but her persecutory delusion of being “arrested” remained, and the patient expressed feeling unsafe in the hospital. The patient exhibited echolalia as well as blunted affect. She continued to have some impairments but showed marked improvement, with MMSE score of 17/30. Points were lost for date, town, county, hospital floor, concentration, phrase repetition, writing a sentence, copying a picture, and 2/3 words remembered on delayed recall.
The patient was discharged on postoperative day 13, hospital day 29, to an outside inpatient psychiatric unit for management of continued psychosis with no further improvement of her MMSE. While the patient was no longer in our direct care, she sought sporadic treatment through our hospital system following discharge and some of her course is known. The patient was discharged after 6 days from inpatient psychiatric care with a medication regimen including olanzapine 10 mg and gabapentin 600 mg three times daily and attended one appointment with our outpatient psychiatry office. The patient was lost to follow-up for 4 months until she presented to our hospital again for symptoms of disorientation, drowsiness, and slowed gait. She was then admitted for a second time, 5 months after initial presentation, and was diagnosed with extrapyramidal symptoms from antipsychotic use. She was discharged the next day with symptom resolution on 20 mg propranolol daily. Her olanzapine was discontinued and an appointment with her psychiatrist was made. Unfortunately, our records show that the patient next sought out care again 3 months later, when her family called crisis outreach for bizarre behavior, auditory hallucinations, and persecutory delusions. She was admitted to a nonaffiliate inpatient psychiatric service 8 months after initial presentation, and her current clinical status is unknown.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [14.4, 'mg/dL'], 'Albumin': [4.0, 'g/dL']}",14.4,13.68,15.12,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.0 g/dL. 
The concentration of Calcium is 14.4 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.0 g/dL)) + 14.4 mg/dL = 14.4 mg/dL.
The patient's corrected calcium concentration 14.4 mg/dL."
2616,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7187932-2,Extracted,"A 49-year-old female was found to have a right breast mass during a routine health examination. Breast biopsy suggested right breast invasive carcinoma, as seen in . Immunohistochemistry showed C-erB-2 (-), CK5/6 (+), EGFR (+ +), ER (−), Ki-67 (+30%), nm23 (−), P53 (85%), P63 (−), and PR (−). The molecular subtype was Basal-like. At the same time, the serum EP and IEP showed abnormally bowed arcs against IgG and anti-kappa light chain. Routine blood tests revealed an HGB level of 83 g/L, total leukocyte count of 3.1 × 109/L, and platelet count of 34 × 109/L. Blood biochemistry revealed an ESR of 73 mm/hr (normal value, <22 mm/hr), serum globulin of 90.9 g/L, serum albumin of 35.8 g/L, serum creatinine of 41 umol/L, serum calcium of 1.96 mmol/L, serum LDH of 274 U/L, and serum β2-MG of 4.25 mg/L. The serum IgG and serum kappa light chain was 80.52 g/L and 27.26 g/L, respectively. Bone marrow (BM) aspirate demonstrated up to 25% dysplastic plasma cells, which were proved to be monoclonal plasma cells by flow cytometry. The diagnoses were MM with type of IgG-kappa (D-S stage III A and ISS stage II) and right breast invasive carcinoma. The patient’s breast cancer was treated with radical mastectomy and postoperative staging was right invasive ductal carcinoma (pT1bN0M0, stage I). Then the scheme of PAD (bortezomib 1.3 mg/m2 on days 1, 4, 8 and 11, doxorubicin 9 mg/m2 on days 1–4, and dexamethasone 20 mg on days 1, 2, 4, 5, 8, 9, 11 and 12, repeated every 28 days) was applied and the evaluation of the curative effect was partial remission (PR) after four cycles of PAD. Because of intractable severe anemia and thrombocytopenia, the patient refused the follow-up chemotherapy and began to receive 150 mg of thalidomide daily, outside the hospital. Telephone follow-ups revealed that the patient died of MM progression with pulmonary infection and respiratory failure in a local hospital. The patient’s post-diagnosis survival time was 29 months.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [35.8, 'g/L'], 'Calcium': [1.96, 'mmol/L']}",8.192,7.7824,8.6016,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 35.8 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 35.8 g Albmumin/10.0 dL = 3.58 g Albmumin/dL. The concentration value of 35.8 g Albmumin/L converts to 3.58 g Albmumin/dL. 
The concentration of Calcium is 1.96 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.96 mmol. To convert 1.96 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.96 mmol Calcium * 0.001 mol/mmol = 0.00196 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00196 mol Calcium * 40.08 g/mol = 0.07856 g Calcium. To convert 0.07856 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.07856 g Calcium * 1000.0 mg/g = 78.56 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 78.56 mg Calcium/10.0 dL = 7.856 mg Calcium/dL. The concentration value of 1.96 mmol Calcium/L converts to 7.856 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.58 g/dL)) + 7.856 mg/dL = 8.192 mg/dL.
The patient's corrected calcium concentration 8.192 mg/dL."
2617,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4813628-1,Extracted,"A 38-year old female came to our attention with seven years history of mild microcytic anemia, with recent worsening of her general state, for further investigations and a certain diagnosis establishment. Besides the anemic syndrome, treated repeatedly, but inefficient with oral iron therapy, her additional history revealed non-specific gastrointestinal symptoms, „labelled “ as irritable bowel syndrome and managed accordingly. The patient stated for intermittent episodes of diarrhea, without warning signs like pus or blood passage in the stool and apparently without a clear trigger for the abdominal disturbances. Diffuse abdominal pain, flatulence and weight loss completed the clinical picture. At admission to our clinic, the patient complained of weakness, fatigue, diarrhea, meteorism and abdominal cramps. The physical examination showed a ill-looking patient, pale and thin with a lower BMI (17,8 kg/m2). The abdominal examination revealed abdominal distension, without any palpable masses or organomegaly. The laboratory studies showed a moderate microcytic hypochrome anemia with a hemoglobin level of 8,6 g/dl, a normal leukocyte and platelet count. Routine biochemical tests evidenced a mild hypoproteinemia of 5,9 g/dl and hypoalbuminemia of 3,3 g/dl, a low ionized seric calcium of 3,2 mg/dl and a decreased level of circulating iron of 35 µg/dL. The other biochemical results were within normal ranges. The urine examination was normal, without urine protein loss. Viral hepatitis markers as well as HIV antibodies were negative. Coproculture showed no pre absence of germs, the coproparasitological examination excluded the presence of parasites. Complete colonoscopy with terminal ileum visualization reveal no mucosal abnormalities. Upper digestive endoscopy showed the loss of Kerckring folds in the descending duodenum, which is a characteristic feature for celiac disease (). Small-bowel biopsies were obtained from the second part of the duodenum and send for histopathologic interpretation. Abdominal ultrasound was performed, with no abnormalities. Based on the endoscopy findings, correlated with clinical and biological data, the diagnosis of celiac disease was strongly suspected and other possible differential diagnosis were ruled out: infectious diarrhea, intestinal parasitoses, inflammatory bowel disease, pancreatic insufficiency, malignancies. Positive serology was also detected and come along to support the diagnosis of celiac disease. IgA endomysial antibody level was 1/320 and the titre of Ig A antibodies directed against deamidated gliadin was elevated, over 142U/ml (normal value <7 U/ml). Histologic examination completed with immunohistochemical tests confirmed the diagnosis of gluten-sensitive enteropathy grade 3 C ( Oberhuber): complete villous atrophy, decreased number of caliciform cells and lymphoplasmocitary infiltration of lamina propria with raised intraepithelial lymphocyte count (). No signs of atypical lymphoid infiltrate was detected, excluding a possible superimposed malignancy. Immunohistochemistry examination recognized typical findings: CD3 positive within intraepithelial lymphocytes, CD4 positive in the small lymphocytes of lamina propria and CD8 positive in the small intraepithelial lymphocytes (,). The patient was started on a strictly gluten-free diet associated with parenteral iron supplementation, vitamins and minerals substitution. Clinical improvement was noted after a couple of days, with stool normalization and general status recovery. The histologic recovery consequently gluten withdrawal will be assess performing follow-up small-intestine biopsies within 6 to 12 months after starting the the gluten-free diet. The patient was advised to keep life-long the gluten-free diet, in order to achieve a good clinical outcome, regression of mucosal abnormalities and avoid the complications of celiac disease, especially T-cell lymphoma development.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.3, 'g/dL'], 'Calcium': [3.2, 'mg/dL']}",3.76,3.572,3.948,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.3 g/dL. 
The concentration of Calcium is 3.2 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.3 g/dL)) + 3.2 mg/dL = 3.76 mg/dL.
The patient's corrected calcium concentration 3.76 mg/dL."
2618,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-8418939-1,Extracted,"An African American female in her early 50s was admitted to the hospital for worsening abdominal pain. She complained of intermittent generalized abdominal pain that started one month before the presentation. Her pain was not worsened with any movements, not associated with food, and mildly relieved by acetaminophen. She never had similar pain before. She denied any fever, chills, fatigue, cough, shortness of breath, hemoptysis, muscle aches, weight loss, loss of appetite, change in bowel routine, melena or hematochezia, and vomiting. She also denied any skin nodules, rashes, or joint pains. She also denied any recent travels or sick contacts. Her past medical history included mitral valve prolapse. She was a homemaker. She denied any history of smoking, alcohol, or drug abuse. She was not taking any medications at home. She had a strong family history of breast and lung cancer.
On the initial presentation, vital signs were normal. Her physical examination was within normal limits except for mild right upper quadrant tenderness without rebound, guarding, or rigidity. There were no signs of lymphadenopathy, leg edema, skin rashes, or nodules. Initial laboratory analysis was significant only for abnormal liver enzymes- aspartate aminotransferase (AST) 67 U/L (normal 13-39 U/L), alkaline phosphatase (ALP) 185 U/L (normal 50-142 U/L), low albumin 3.13 gm/dL (normal 3.5-5.7 gm/dL), and low serum lipase of 6 U/L (normal 11-82 U/L). Serum calcium was 9.5 mg/dL (normal 8.6-10.8 mg/dL). The remainder of the complete blood count and metabolic panel were also normal. Mild polyclonal gammopathy was diagnosed via serum protein electrophoresis. Chest x-ray showed patchy air opacities bilaterally, and COVID-19 polymerase chain reaction (PCR) was negative. Computed tomography (CT) abdomen showed multiple subpleural nodules along with a complicated sub-hepatic cyst/abscess, bowel wall thickening, prominent gastro-hepatic and gastroduodenal lymph nodes. Interventional radiology was consulted for CT-guided pigtail catheter placement to drain a sub-hepatic abscess. Her abdominal pain improved after the sub-hepatic drainage. Fluid analysis was unremarkable for infection or hepatic sarcoidosis. The patient also underwent esophagogastroduodenoscopy (EGD) and colonoscopy for concern of Inflammatory bowel disease based on CT findings, which were grossly normal. The histopathologic results from gastric biopsy-confirmed chronic non-caseating granulomatous gastritis (Figure ), negative for Helicobacter pylori infection, fungal or mycobacterial stains.
Subsequent CT-thorax was done, which revealed bilateral reticulonodular opacities and multiple nodules in bilateral lungs (Figure ). All the infectious workups, including human immunodeficiency virus (HIV), hepatitis A, hepatitis B, hepatitis C, and Quantiferon Gold test for tuberculosis, were negative. Influenza/RSV, group B streptococcus screen, respiratory cultures, fungal cultures, and mycobacterial cultures from sputum were negative. Blood cultures were also negative. Serum beta-D glucan test was negative as well. Tumor markers - CA 19.9 and alpha-fetoprotein were unremarkable. Pulmonology was consulted, and the patient had bronchoscopy with left upper lobe transbronchial biopsy.
Based on the laboratory data and clinical findings, a presumed diagnosis of sarcoidosis was made. Since she did not have any specific symptoms like dyspnea, nausea, vomiting, and her abdominal pain had improved after the drainage, she was not started on immunosuppressive agents. She was ready to be discharged. The risks, adverse effects, and benefits of starting Prednisone for the presumed diagnosis of sarcoidosis were discussed with the patient. She elected to wait for lung biopsy results and have a pulmonary function test (PFT) during an outpatient pulmonary clinic visit. The patient did follow up outpatient and had a mild restrictive disease on PFT. The lung biopsy results revealed poorly formed noncaseating granulomas (Figure ) and intra-alveolar hemorrhage. Stains for fungal and acid-fast organisms were negative. She did not receive any specific therapy as she remained asymptomatic. Repeat PFTs after three months showed significant improvement in the restrictive process.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.13, 'g/dL'], 'Calcium': [9.5, 'mg/dL']}",10.196,9.6862,10.7058,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.13 g/dL. 
The concentration of Calcium is 9.5 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.13 g/dL)) + 9.5 mg/dL = 10.196 mg/dL.
The patient's corrected calcium concentration 10.196 mg/dL."
2619,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7557114-1,Extracted,"A 43-year-old female presented to the emergency department with acute onset of abdominal pain for the last 12 hours. The pain was located in the epigastric region and the left upper quadrant of the abdomen, 8/10 in intensity, sharp in nature, radiating to back associated with two episodes of non-bilious and non-bloody vomiting, no aggravating or relieving factors. The patient medical history was significant for ulcerative colitis. Her past surgical history was significant for three cesarean sections. She reported that she used to drink alcoholic beverages occasionally (one to two times per month) but stopped drinking five years ago. She denied any history of smoking or any other toxic habits. Her only medication was oral sulfasalazine two grams per day past 18 months. She denied any known allergies. The patient denied using herbal or weight losing medication
Her initial vitals were a pulse rate of 94 bpm, blood pressure of 126/86 mmHg, respiratory rate of 17 breaths per minute, and temperature of 98.6˚F. On physical examination, the abdomen was soft with tenderness in the epigastric region, and bowel sounds were normal. Her initial labs showed an alanine aminotransferase (ALT) of 62 units/L (5-40 units/L), aspartate transaminase (AST) 164 units/L (9-36 units/L), alkaline phosphatase 98 units/L (42-98 units/L), total bilirubin 1.5 mg/dL (0.2-1.2 mg/dL), conjugated bilirubin 0.5 mg/dL (0.0-0.3 mg/dL), serum lipase 419 U/L (<60 U/L), serum ethanol level <10 mg/dL (<10 mg/dL), serum triglyceride level 88 mg/dL (45-150 mg/dL), serum calcium 8.7 mg/dL (8.5-10.5 mg/dL), albumin 3.8 g/dL (3.2-4.8 mg/dL), blood urea nitrogen (BUN) 11 mg/dL (6-20 mg/dL), and serum creatinine 0.5 mg/dL (0.5-1.5 mg/dL). Ultrasound of the abdomen showed a normal size and texture of liver, normal gallbladder with no gallstones, and bile duct was 3 mm in size. A CT of the abdomen with oral contrast showed findings suggestive of AP without any pancreatic necrosis or pseudocyst formation, no pancreatic duct, or common bile duct dilatation (Figure ).
Initially, during admission, sulfasalazine was continued as maintenance therapy for ulcerative colitis with no improvement in symptoms. The patient continued to complain of abdominal pain and nausea. Later on, sulfasalazine was discontinued and the patient started feeling better. Two days after discontinuation of sulfasalazine, she was able to tolerate a clear liquid diet, and shortly after her diet was advanced to regular. Symptoms had resolved by day 5, and the patient was discharged safely.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.8, 'g/dL'], 'Calcium': [8.7, 'mg/dL']}",8.86,8.417,9.303,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.8 g/dL. 
The concentration of Calcium is 8.7 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.8 g/dL)) + 8.7 mg/dL = 8.86 mg/dL.
The patient's corrected calcium concentration 8.86 mg/dL."
2620,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4003442-1,Extracted,"The patient is a 6-year-old boy who is referred to our hospital with complaints of fever, malaise, anorexia, nausea, and vomiting from 4 weeks ago. During this period, the patient had lost 7 kg and his nausea, vomiting, and anorexia had gradually worsened. Before referral to us, he had several referrals as outpatients and two hospitalizations with no definite diagnosis of his illness. The physical examination showed only lethargy and pallor and no other signs including lymphadenopathy and hepatosplenomegaly.
Initial laboratory studies were as follows: Na: 141 mmol/L, K: 3.6mmol/L, BUN: 18, Cr: 0.8mg/dl, Ca: 15.8mg/dl, P: 2.8mg/dl, uric acid: 5.8 mg/dl, LDH: 587 U/L, Mg: 1.4mg/dl, Alkaline phosphatase: 305U/L, Alb: 4gr/dl. Complete blood count included: WBC: 7.4×109 /L (lymphocyte: 72%, PMN: 26%), HB: 7.1gr/dl, PLT: 90×109 /L. Arterial blood gas analysis was as follows: PH: 7.47, PCO2: 31mmHg, HCO3: 22 mEq/L.
Blood count was normal 16 days prior to our visit. In peripheral blood smear no other abnormal point was seen except microcytic anemia, and mild thrombocytopenia. Chest X-ray was normal. In abdominal ultrasound, liver and spleen size were normal and there was sand in inferior pole of right kidney. Despite severe hypercalcemia, there were no significant electrocardiographic changes. The corrected QT interval (QTc) was in the normal range and echocardiography was normal. Serum levels of PTH and 1,25-(OH)2 Vitamin D were 7 pg/ml (10-65 pg/ml) and 15 pg/ml (20-70 pg/ml), respectively, but it was impossible to measure PTHrP. Bone marrow aspiration was performed for the patient due to anemia, thrombocytopenia, prolonged fever, and weight loss. Bone marrow smears showed ALL with L1 morphology. Flowcytometry of bone marrow was also consistent with early pre B-ALL phenotype. Cytogenetic analysis of bone marrow was normal and showed 46, XY karyotype. Bone marrow samples analysis for t (9; 22), t (12; 21), t (1; 19), and t (4; 11) using PCR method were negative.
Patient was hospitalized in pediatric intensive care unit for treatment and close monitoring of severe hypercalcemia. Aggressive hydration with normal saline was started with two times of the maintenance. Pamidronate 1 mg/kg IV infusion over 4 hours and furosemide 1 mg/kg IV every 6 hours was started. After 12 hours of treatment onset, regarding the serum calcium level increment from 15.8 to 17 mg/dl, dexamethasone (2 mg every 12 hours) was added to the previous treatment. Since serum calcium level was 16 mg/dl, 36 hours after treatment, the patient underwent emergency hemodialysis, and then calcium level became normal. Pamidronate and furosemide were discontinued and regarding the diagnosis of ALL, the patient was undergone chemotherapy protocol ALL IC-BFM 2002. Dexamethasone was continued and calcium remained within normal limits and the patient's clinical symptoms, including nausea, vomiting, weakness and lethargy resolved. Bone marrow aspiration on day 15 showed complete remission with less than 5% blasts (M1 marrow). Chemotherapy was continued for 24 months and the patient is now in complete remission, 25 months after treatment discontinuation.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.0, 'g/dL'], 'Calcium': [15.8, 'mg/dL']}",15.8,15.01,16.59,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.0 g/dL. 
The concentration of Calcium is 15.8 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.0 g/dL)) + 15.8 mg/dL = 15.8 mg/dL.
The patient's corrected calcium concentration 15.8 mg/dL."
2621,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6620230-1,Extracted,"We report a case of a 37-year-old male with PWS who suffered from ESKD. At 3 years of age, he started overeating and developed obesity. At 5 years of age, PWS was suspected based on the patient’s body type, facial expression, and overeating. Dietary restriction was instructed; however, at 17 years of age, he was diagnosed with type 2 DM (T2DM). At 30 years of age, a diagnosis of PWS was confirmed by genetic testing. At age 32 years, he suffered from nephrotic syndrome, and diabetic retinopathy was diagnosed at the same time.
By June 2015, renal function had continuously deteriorated and his serum creatinine reached 8.9 mg/dL (eGFR at 5.0 mL/min/1.73 m2). Therefore, the patient was admitted to the hospital for initiating RRT. At admission, physical examination revealed: 150.8 cm height, 80.3 kg BW, BP 112/64 mmHg, HR 110/min, SO2 99% (room air). He showed systemic edema and urine volume decreased to 800 mL/24 h. The patient’s IQ was inferred 40–60. Blood chemistry showed: TP 6.4 g/dL, albumin 2.4 g/dL, CRP 10.9 mg/dL, BUN 83 mg/dL, UA 6.4 mg/dL, Na 136 mEq/L, K 5.4 mEq/L, Cl 110 mEq/L, Ca 7.1 mg/dL, P 12.7 mg/dL and HCO3− 14.7 mEq/L. Complete blood count was: WBC 16,770/μL, RBC 354 × 104/μl, Hgb 8.1 g/dL, Ht 27.6%, MCV 78 fl, MCH 22.9 pg, MCHC 29.3% and Plt 54.2 × 104/μl. Urinalysis showed massive proteinuria (4839 mg/24 h) without hematuria or pyuria. He had been receiving insulin injection 4 times a day. Random blood glucose level was 156 mg/dL and HbA1c was 6.8%.
After admission, restricted fluid intake, nutritional management, and temporary HD was performed 6 times for 2 weeks since massive edema prevented insertion of PD catheter. The reasons for choosing PD were as follows: vessels in his both forearms looked premature for creating A-V fistula at that time, suspecting intolerance in hemodialysis session for long hours and difficult cessation of fluid and food intake which are necessary for hemodialysis. Negative aspect of PD was specifically considered as a difficulty in maintaining sanitary in inlet of PD catheter. In either modality, family burden for supporting his dialysis was also considered.
Substantially his body weight decreased to 64 kg (− 16 kg from admission; BMI 28.4 kg/m2) and a catheter for PD was inserted using the non-stylet method under general anesthesia combined with epidural anesthesia at the 14th day of admission. We selected the JBS-2 semi-long PD Catheter with the exit site placed in the left upper abdomen (Fig. ). The catheter position was not ideally located initially but it functioned well for the following PD session after the surgery (Fig. ). From the third postoperative day, nocturnal intermittent PD (NIPD) was started. Since he could not sufficiently understand the procedure of PD, instructions for PD as well as insulin self-injection were provided to his father. He was discharged at the day 35 of hospitalization.
At the 2nd, 5th, 7th, and 13th month after NIPD introduction, a subcutaneous tunnel infection occurred (Fig. ). Since additional antibiotic therapy could not terminate infection, he underwent subcutaneous pathway diversion and PD catheter replacement for three times consequently. However, that was the last infection episode and infection-free PD was observed until the present time for next 27 months. With regard to the dialysis modality, NIPD was chosen first because he desired to continue his daytime job for handicapped person. At the 7th month after NIPD introduction, the treatment was switched to continuous cycling PD (CCPD) and 7.5% icodextrin solution (Extraneal™, Baxter, Tokyo, Japan) was added daytime because urine output gradually decreased, and ultrafiltration volume became insufficient. At the 10th month after NIPD introduction, glucose concentration in peritoneal dialysate increased from 1.5 to 2.5% (Reguneal™, Baxter, Tokyo, Japan). “Hybrid dialysis”, which combined daily PD with once-a-week HD, was started by creating A-V fistula at the 16th month after NIPD introduction. Owing to this “hybrid dialysis”, adequate ultrafiltration volume was maintained for following 17 months. Dialysis efficiency has been checked by blood tests and chest X-ray once a month and revealed adequate dialysis without major problems; accordingly, BUN level was below 50 mg/dL and serum potassium level below 5 mEq/L. Blood sugar was well maintained by daily intensive insulin therapy with oral dulaglutide initially and then this regimen was successfully replaced with once-weekly GLP-1 agonist associated with once a day ultralong-acting insulin finally. HbA1c had been maintained under 7% since NIPD introduction. His maximum body weight without overhydration reached to 71 kg (BMI 31.6 kg/m2) during this period. Finally, he lost his A-V fistula twice and returned to PD (CCPD) alone at the 38th month of NIPD introduction because of difficulty in creating another vascular access. For evaluating efficacy of PD, serum β2-microglobulin level was monitored every 2 months and revealed between 34 and 40 mg/L during the latest CCPD alone period.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.4, 'g/dL'], 'Calcium': [7.1, 'mg/dL']}",8.38,7.961,8.799,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.4 g/dL. 
The concentration of Calcium is 7.1 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.4 g/dL)) + 7.1 mg/dL = 8.38 mg/dL.
The patient's corrected calcium concentration 8.38 mg/dL."
2622,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3236148-1,Extracted,"A 64-year-old man with a history of hypertension, chronic kidney disease, and liver failure secondary to hepatitis C, with status post liver transplant 13 years priorly, was brought in by ambulance to the emergency department for acutely altered mental status. The patient had been in his usual state of health, until he told his family 3 hours before that he “felt sick.” The family incidentally found him on the floor, confused and lethargic, and immediately called the ambulance.
Upon arrival, the patient had a temperature of 96.4°F; pulse, 117 beats per minute; blood pressure, 151/93 mmHg; respiratory rate, 22 breaths per minute; and oxygen saturation of 100% on nonrebreather. The patient was known to have a history of recurrent episodes of hepatic encephalopathy, and his last episode of hepatic encephalopathy was in the prior 3 months, which was treated and controlled with lactulose. The patient's family stated that the patient had run out of lactulose 4 days before presentation. Other than lactulose, the patient was compliant with all of his home medications, including amlodipine, buproprion, cyclosporine, hydrocodone, lasix, methocarbamol, and ramipril. The patient had no known history of seizure, recent illness, brain trauma, or recent surgical procedures.
Physical examination showed a male in no acute distress with a Glasgow Coma Scale of 12 (eyes, 4; verbal, 3; motor, 5). There were no signs of trauma found on his body. His pupils were equally round and reactive to light, and his neck was supple and soft with a cervical collar in place. Cardiopulmonary examination was unremarkable except for tachycardia. Abdominal examination was unremarkable. Because he was not following commands, the neurologic examination was limited. However, the patient was able to move all extremities equally and pulses were distally equal to all extremities. There was no posturing or clonus noted, and Babinski was downgoing in both feet.
Fingerstick glucose level was 210 mg/dL and bedside hemoglobin level was 13.1 g/dL. Noncontrast head and cervical spine computed tomography revealed no acute pathologic lesion. Chest radiography also showed no acute pathologic lesion. Laboratory tests showed white blood cell counts of 5.5 K/mm3 with 60% neutrophils, hematocrit of 36.5%, and platelets of 115 K/mm3. Electrolyte and liver function results were as follows: sodium, 141 mmol/L; potassium, 3.5 mmol/L; chloride, 104 mmol/L; bicarbonate, 22 mmol/L; calcium, 9.3 mg/dL; blood urea nitrogen, 71 mmol/L; creatinine, 1.9 mg/dL; total bilirubin, 2.1 mg/dL; aspartate aminotransferase, 128 U/L; alanine aminotransferase, 124 U/L; alkaline phosphatase, 231 U/L; albumin, 4.0 g/dL; lipase, 30 U/L; prothrombin time, 14.5 seconds; INR, 1.09; and ammonia, 501 μmol/L (reference range, 15–55 μmol/L). Toxicology serum screen results were negative for acetaminophen, salicylate, and ethanol. Urine toxicology screen results were positive only for opiates. Venous blood gas was pH 7.44.
Owing to the patient's obtunded condition and inability to protect his airway, the patient was electively intubated and given midazolam drip for sedation. The patient was admitted to the intensive care unit (ICU) for monitoring with a presumed diagnosis of hepatic encephalopathy. While administration of empiric antibiotics was started in the emergency department, it was discontinued after an infectious etiology was deemed unlikely and culture results were negative. Results of a magnetic resonance imaging brain scan were also negative, including no evidence of infarct.
During the ICU stay, the patient was readministered lactulose, and ammonia levels decreased to117 μmol/L by hospital day 2 and to 78 μmol/L by hospital day 4. Despite discontinuation of sedation, the patient remained unresponsive. A neurologist was consulted and a bedside electroencephalogram (EEG) revealed findings consistent with status epilepticus. However, the patient had no clinical manifestations of status epilepticus, leading to a diagnosis of nonconvulsive status epilepticus. A phenytoin load was immediately administered, while a midazolam infusion was restarted, ultimately leading to EEG resolution of the status epilepticus. The patient did not immediately improve neurologically during the hospitalization stay and was ultimately transferred to another facility for continued treatment and rehabilitation.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.0, 'g/dL'], 'Calcium': [9.3, 'mg/dL']}",9.3,8.835,9.765,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.0 g/dL. 
The concentration of Calcium is 9.3 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.0 g/dL)) + 9.3 mg/dL = 9.3 mg/dL.
The patient's corrected calcium concentration 9.3 mg/dL."
2623,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6256140-1,Extracted,"A seven-year-old girl, with a generalized erythematous squamous rash, was admitted to 2nd Pediatric Clinic, Emergency County Hospital Craiova (medical record no. 7885) in February 2015, being transferred from a county hospital.
Personal physiological antecedents. Fourth child, due time birth, natural childbirth, birth weight = 2200 g, Apgar score 8, breastfed until 4 months, correctly diversified after 4 months, weaned at 7 months, at present being fed with adult food. Normal psychomotor development.
Personal pathological antecedents: chicken pox at four years old.
Heredo-collateral antecedents: healthy parents, 3 healthy brothers, an aunt, related to her mother, with psoriasis.
Anamnesis. The onset was 2 weeks before, with an erythematous rash at the abdominal level. She went to the dermatologist who recommended a local treatment with Fluocinolone ointment and magistral prescription with salicylic acid, urea and jelly. The rash generalized: squamous patches appeared and subsequently she was admitted to our clinic.
When admitted: no fever, weight= 20 kg, fair general state, erythematous rash in patches, erythematous plaques covered with silvery, thick, easily exfoliating, not painful, non-pruriginous squamae, with the presence of Auspitz signs and white spots, at the level of scalp, earlobes, retro-auricular, anterior and posterior torso, abdomen, lower and upper limbs; pustules surrounded by red skin at the axillary, genital and inguinal level. Pulmonary – normal, normal heartbeat, CF=98/min, supple abdomen, liver 1 cm below costal margin, based-flared thorax, tooth caries (Fig.).
Investigations. Hemogram: Hb= 12.2g%, Tr= 236000/mm3, L= 16000/mm3, NS=62%, Ly=32%, M=6%, VSH= 7/14 mm after 1/2 hours, fibrinogen= 397 mg/dl, CRP= 0.4 mg/l, creatinine= 0.4 mg/dl, uric acid = 3.53 mg/dl, glycemia= 82 mg/dl, calcemia= 8 mg/dl, total serical proteins= 6.5 g/dl, sideremy= 103 mg/dl, GOT= 19 U/l, GPT= 14 U/l, negative coproparasitary examination, normal urine summary examination, ASLO= 116.86UI. Immunogram: IgA= 76.67 mg/dl, (N=70-400), IgG= 865.5 mg/dl (N=700-1600), IgM= 167.2 mg/dl (N=100-230), pharyngeal exudate: absent streptococcus, staphylococcus, nasal exudate: present staphylococcus aureus, sensitive to: Biseptol, Linezolid, Gentamicin, Vancomycin, resistant to: Penicillin, Clarithromycin, Oxacillin. Normal abdominal ultrasound.
Dermatologic examination: psoriasis vulgaris in patches and plaques. Cutaneous biopsy / histopathological examination - microscopic examination: epidermis with orthokeratosis, large areas of hypo- and agranulocytosis, acanthosis, mild perivascular chronic inflammatory infiltrate in the dermis. The HP aspect most probably suggests psoriasis vulgaris (Fig., Fig.).
The patient received a local treatment recommended by the dermatologist, with magistral prescription with salicylic acid, ihtiol, vitamin A, vitamin E, Advantan cream – applied once per day and Diprosalic scalp application.
Starting with the 3rd day of the treatment, the patient presented progressive desquamation of the squamae. She was discharged after 7 days, without squamae (Fig.). Discharge diagnosis: Psoriasis vulgaris in patches and plaques. Nasal staphylococcus aureus. Hypocalcemia. Hypoproteinemia. Tooth cavities. Weight hypotrophy.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [8.0, 'mg/dL'], 'Albumin': [6.5, 'g/dL']}",6,5.7,6.3,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 6.5 g/dL. 
The concentration of Calcium is 8.0 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 6.5 g/dL)) + 8.0 mg/dL = 6.0 mg/dL.
The patient's corrected calcium concentration 6.0 mg/dL."
2624,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-8387076-1,Extracted,"A 29-year-old man from a rural area of Mexico suffered many years of physical abuse during his childhood. He had a seizure at age 24. Approximately 4 years later, he developed confusion, weakness, fatigue and diarrhea, so his mother brought him to the United States for medical care. Ten days following the onset of his symptoms and 8 days after his arrival in the United States, he was brought to an urban outpatient clinic in the Southwest United States. In the clinic at 14:00, his temperature was 36.7o C, pulse rate 100 beats/minute, blood pressure 90/50 mm Hg, respiration rate 20 breaths/minute, hematocrit 16.3% (RR: 42-52%), and white blood cell (WBC) count 12,500/mm3 (RR: 4,500-11,000/mm3). An intravenous infusion of normal saline was started and the patient was sent to a large public hospital emergency department.
On arrival in the emergency department at 16:42, the patient’s pulse rate was 84 beats/minute, blood pressure 112/70 mm Hg and respiration rate 16 breaths/minute. He had a grade 2/6 systolic ejection murmur and yellow stool with gross blood in it. He was unable to cooperate for detailed interviewing or physical examination because of “altered mental status”. His hematocrit was 17.3%, hemoglobin 4.8 g/dL (RR: 14-18 g/dL), and WBC count 11,100/mm3. Chest x-ray showed patchy bilateral peripheral nodular infiltrates and pleural effusions.
The following morning, at 07:00, an order was written to transfuse 2 units of red blood cells over 1 hour each as soon as possible. The patient’s hemoglobin was 4.4 g/dL, hematocrit 14.9%, mean corpuscular volume (MCV 52.3 fL (RR: 80-100 fL), WBC count 15,500/mm3, bilirubin 0.3 mg/dL (RR: 0.1-1.2 mg/dL), alkaline phosphatase 150 U/L (RR: 35-110 U/L), alanine aminotransferase (ALT) 8 U/L (RR: 5-40 U/L), aspartate aminotransferase (AST) 12 U/L (RR: 5-40 U/L), lactate dehydrogenase (LDH) 285 U/L (RR: 120-300 U/L), albumin 2.3 g/dL (RR: 3.9-5 g/dL), blood urea nitrogen 11 mg/dL (RR: 10-20 mg/dL), creatinine 0.3 mg/dL (RR: 0.4-1.3 mg/dL), calcium 7.7 mg/dL (RR: 8.6-10.3 mg/dL), and creatine phosphokinase (CPK) 25 U/L (RR: 35-345 U/L). A hematology consultant obtained further blood tests showing hemoglobin 4.6 g/dL, hematocrit 16.5%, MCV 52.9 fL, WBC count 9,400/mm3 (58% segmented neutrophils, 1% bands, 14% lymphocytes, 4% monocytes, 22% eosinophils), folate 4.9 ng/mL (RR: 2.5-20 ng/mL), vitamin B12 419 pg/mL (RR: 250-1000) pg/mL), normal hemoglobin electrophoresis, and normal thyroid functions tests. Peripheral blood smear showed hypochromasia, microcytosis, teardrop cells, target cells, red blood cell fragments, anisocytosis, poikilocytosis and markedly increased platelets. The hematology consultant recommended parenteral iron instead of transfusion. The order for transfusion was rescinded, although the patient had already been premedicated for it. He was transferred from the emergency department to an inpatient unit where he passed two loose yellow foul-smelling stools with no blood in them.
The next morning, hospital day 3, the medicine resident who took over the patient's management noted confusion as a new problem. The medicine resident ordered a computed tomography scan of the head, which showed no abnormalities, and at 16:30, performed lumbar puncture. Opening pressure was 20 cm H2O. The cerebrospinal fluid was clear. Approximately 45 minutes following the lumbar puncture, the patient was found on the floor, unresponsive, with cyanosis, shallow respirations and fecal incontinence. He was given an ampule of 50% dextrose intravenously and supplemental oxygen at 6 L/minute. He became responsive, but remained confused. At 17:45, the patient ceased breathing and the cardiac arrest team was summoned. Despite full cardiopulmonary resuscitative efforts, the patient could not be revived.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.3, 'g/dL'], 'Calcium': [7.7, 'mg/dL']}",9.06,8.607,9.513,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.3 g/dL. 
The concentration of Calcium is 7.7 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.3 g/dL)) + 7.7 mg/dL = 9.06 mg/dL.
The patient's corrected calcium concentration 9.06 mg/dL."
2625,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3354861-1,Extracted,"A 7-year-old boy presented to the Pediatric Surgery Out-patient department with umbilical hernia. He had growth retardation and was referred to us for endocrine evaluation. The child was born post term at 10 months of gestation (birth weight: 3.5 kg). There was no h/o prolonged neonatal jaundice, hoarse cry, feeding or sucking difficulty. Growth retardation, recurrent upper respiratory tract infections, and delayed developmental milestones were present from infancy. Umbilical hernia was diagnosed when the child was evaluated at the age of 5 years.
On examination, the child was short (height 99 cm; < fifth percentile; –4.02 Standard Deviation, height age 4 years). Upper segment to lower segment ratio was 0.811. He had a large head circumference (53 cm), coarse facial features, depressed nasal bridge, delayed eruption of permanent teeth, joint stiffness with flexion deformity of elbow and distal interphalangeal joints. There was hepatosplenomegaly, umbilical hernia, mild mental retardation (Intelligence Quotient: 58.22), normal fundus examination, bilateral normal hearing and no corneal clouding [Figures and ].
On investigation, he was found to be normoglycemic and had normal renal function (S. creatinine 0.4 mg/dl). The other findings were as follows: hemoglobin (Hb) 12.1 gm %; S. calcium 9.3 mg/dl; S. albumin 4.2 g/dl; S. phosphorus 4.4 mg/dl; S. alkaline phosphatase 172 U/l. He had no evidence of metabolic acidosis.The thyroid function tests were normal [thyroid stimulating hormone (TSH) 0.931 mIU/l; T4 level 134 nmol/l] [Figures –].
USG abdomen revealed hepatosplenomegaly with umbilical hernia. Echocardiography (ECHO) study revealed normal findings. We could neither measure urinary glycosaminoglycan (GAG) levels nor perform iduronate sulfatase enzyme activity assay, as they are not done at our center and are also not available at most other centers. Our diagnosis of mucopolysaccharidosis II (Hunter syndrome) in this case was confirmed from his history, clinical examination and skeletal survey.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.2, 'g/dL'], 'Calcium': [9.3, 'mg/dL']}",9.14,8.683,9.597,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.2 g/dL. 
The concentration of Calcium is 9.3 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.2 g/dL)) + 9.3 mg/dL = 9.14 mg/dL.
The patient's corrected calcium concentration 9.14 mg/dL."
2626,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5477883-1,Extracted,"A 37-year-old woman presented with recent constitutional upset and a year-long history of swelling of her face and hands. Her past medical history included pre-eclampsia. Her father had suffered from focal segmental glomerulosclerosis and her brother underwent renal transplantation for reflux nephropathy. Examination revealed peri-orbital oedema and hypertension (140/100 mmHg). Her pulse rate was 58 beats/min.
Investigations included haemoglobin 11.6 g/l, white cell count 6.2 × 109/l, sodium 137 mmol/l, potassium 3.6 mmol/l, creatinine 148 μmol/l, estimated glomerular filtration rate (GFR) 37 ml/min/1.73 m2, urea 7.6 mmol/l, cholesterol 9.8 mmol/l, alkaline transferase 97 IU/l, alanine transaminase 45 IU/l, alkaline phosphatase 89 IU/l, albumin 45 g/l, calcium 2.37 mmol/l and glucose 4.9 mmol/l. Hepatitis, Epstein-Barr and cytomegalovirus serologies were negative.
Urinalysis was normal. A 24-h urine collection identified 0.30 g of protein and a creatinine clearance of 58 ml/min. Ultrasonography revealed her kidneys to measure 11 cm on the left and 10 cm on the right. A small pericardial effusion was evident on echocardiography, with no left ventricular hypertrophy. Magnetic resonance angiography revealed patent renal arteries.
A renal biopsy was undertaken. Twenty-two glomeruli were available for analysis, with no evidence of focal lesion or glomerulonephritis. Further, light microscopy, immunohistochemistry and electron microscopy were unremarkable.
At this point the patient described myalgias. Thyroid function tests showed a free thyroxine (FT4) concentration of <3 pmol/l and a thyroid stimulating hormone (TSH) concentration of >75 mu/l, consistent with severe hypothyroidism. Creatine kinase was elevated to 3454 IU/l, but urinary myoglobin was not detected. She was commenced on levothyroxine 100 mcg. Her blood pressure (110/70 mmHg), serum creatinine (94 μmol/l), creatine kinase and cholesterol (4.2 mmol/l) all normalized.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [45.0, 'g/L'], 'Calcium': [2.37, 'mmol/L']}",9.099,8.64405,9.55395,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 45.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 45.0 g Albmumin/10.0 dL = 4.5 g Albmumin/dL. The concentration value of 45.0 g Albmumin/L converts to 4.5 g Albmumin/dL. 
The concentration of Calcium is 2.37 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 2.37 mmol. To convert 2.37 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 2.37 mmol Calcium * 0.001 mol/mmol = 0.00237 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00237 mol Calcium * 40.08 g/mol = 0.09499 g Calcium. To convert 0.09499 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.09499 g Calcium * 1000.0 mg/g = 94.99 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 94.99 mg Calcium/10.0 dL = 9.499 mg Calcium/dL. The concentration value of 2.37 mmol Calcium/L converts to 9.499 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.5 g/dL)) + 9.499 mg/dL = 9.099 mg/dL.
The patient's corrected calcium concentration 9.099 mg/dL."
2627,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7253654-1,Extracted,"A 67-years-old male resident of Wuhan with laboratory-confirmed SARS-CoV-2 infection was admitted to the author's center on Feb 10. He had dyspnea for half a month, accompanied by fatigue and mild diarrhea. The patient had a history of coronary artery bypass, and chronic pulmonary diseases including obsolete pulmonary tuberculosis, chronic bronchitis, and emphysema. Body temperature and blood pressure were 37.2°C and 149/85 mm Hg, respectively at admission, while respiratory rate and pulse were normal. The breath sounds of both lungs were thick, and dry and wet rales could be heard at the lung base. The heart boundary was enlarged to the left and down, and murmurs could be heard.
The main abnormalities in laboratory findings at admission were as follows: glutamic-pyruvic transaminase (GPT) 63 U/L, albumin 32.8 g/L, lactate dehydrogenase (LDH) 535 U/L, leukocyte count 15.96 × 109/L, neutrophil 12.86 × 109/L, lymphocyte 2.04 × 109/L, procalcitonin 0.10 ng/mL, D-dimer 3.53 μg/mL FEU, glucose 7.43 mmol/L, and C-reactive protein (CRP) 45.8 mg/L.
He was given high flow intranasal oxygen inhalation with oxygen concentration 100%. However, he still had obvious shortness of breath, 87% pulse oxygen saturation (SpO2), and poor consciousness. Thus he was transferred to intensive care unit (ICU), where invasive ventilation was used for him during the whole hospitalization, maintaining SpO2 at about 95%. Other treatment included prone position ventilation, vasoconstrictor, antibacteria, and antiviral therapy. His blood pressure could be maintained at about 110/60 mm Hg with noradrenaline (NE) pumped in.
Subcutaneous emphysema was found in his left neck 5 days after admission (Feb 15), and the area of subcutaneous emphysema gradually increased. Five days later, extensive subcutaneous emphysema could be seen in the neck, bilateral chest walls, abdomen wall, bilateral groin area, and scrotum.
He underwent mobile X-ray 10 days after admission (Feb 20) for assessing SARS-CoV-2 pneumonia, as chest CT was unavailable for him. The chest radiograph revealed extensive air-space opacities in bilateral lungs, with lower lung involvement more serious than upper lung (Fig. ). Subcutaneous emphysema, mediastinal emphysema, and a small amount of pneumothorax on both sides (10–20% compression of lung) could also be seen. Chest closed drainage was thus performed for him immediately.
The main abnormalities in laboratory findings during his hospitalization were as follows: leukocyte count 3.12 to 20.44 × 109/L, neutrophil 2.94 to 19.24 × 109/L, lymphocyte 0.18 to 0.32 × 109/L, hemoglobin 109.0 to 131.0 g/L, platelet count 40.0 to 140.0 × 109/L, potassium 5.09 to 6.20 mmol/L, calcium 1.78 to 1.94 mmol/L, total protein 46.7 to 59.4 g/L, albumin 21.1 to 30.3 g/L, GPT 55 to 76 U/L, glutamic oxaloacetic transaminase (GOT) 102 to 104 U/L, total bilirubin 20.4 to 22.4 μmol/L, direct bilirubin 11.2 to 13.8 μmol/L, urea 12.10 to 16.00 mmol/L, hypersensitive CRP 202.0 to 216.8 mg/L, D-dimer 1.61 to >21.00 μg/mL FEU, prothrombin time 15.9 to 18.1 seconds, prothrombin activity 55.0% to 71.0%, international normalized ratio 1.24 to 1.49, fibrinogen 3.95 to 5.55 g/L, activated partial thromboplastin time (APTT) 42.9 to 80.9 seconds, fibrinogen degradation products 6.7 to 9.3 μg/mL, creatine kinase MB isoenzyme 4.3 to 208.3 ng/mL, myoglobin 198.2 to >1200.0 ng/mL, high sensitive cardiac troponin I 39.5 to 361.6 pg/mL, interleukin-6 472.20 pg/mL. The platelet, lymphocyte, and albumin continued to decrease until death, while GPT, GOT, APTT, and myoglobin continued to increase.
Sinus bradycardia (heart rate 30–45 bpm) was observed 11 days after admission (Feb 21). Echocardiography was performed immediately, showing left ventricular enlargement with ejection fraction 20%. Coagulation function was even worse for him, and a small amount of blood oozed from nose and mouth during prone position. There was still gas emerging from the thoracic drainage tube. Extensive subcutaneous emphysema was even worse than before. As his blood pressure dropped to 78/45 mm Hg, NE was increased to 1.5 μg/kg min, accompanied with rapid fluid infusion. However, the blood pressure and heart rate did not rise. The increase of lactate (up to 4.0 mmol/L) suggested aggravation of respiratory failure.
The heart rate slowed down to 20 bpm, and blood pressure could not be detected on the twelfth day after admission (Feb 22). Adrenaline, noradrenaline, and dobutamine were immediately given. However, the heart rate and respiration stopped, and the ECG showed a straight line, and clinical death was declared.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [30.3, 'g/L'], 'Calcium': [1.94, 'mmol/L']}",8.552,8.1244,8.9796,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 30.3 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 30.3 g Albmumin/10.0 dL = 3.03 g Albmumin/dL. The concentration value of 30.3 g Albmumin/L converts to 3.03 g Albmumin/dL. 
The concentration of Calcium is 1.94 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.94 mmol. To convert 1.94 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.94 mmol Calcium * 0.001 mol/mmol = 0.00194 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00194 mol Calcium * 40.08 g/mol = 0.07776 g Calcium. To convert 0.07776 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.07776 g Calcium * 1000.0 mg/g = 77.76 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 77.76 mg Calcium/10.0 dL = 7.776 mg Calcium/dL. The concentration value of 1.94 mmol Calcium/L converts to 7.776 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.03 g/dL)) + 7.776 mg/dL = 8.552 mg/dL.
The patient's corrected calcium concentration 8.552 mg/dL."
2628,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3775019-1,Extracted,"An 83-year-old male presented with barking cough with greenish expectoration, shortness of breath (grade III MMRC) and wheezing for 3 days. For last 3 years he has been under treatment for recurrent exacerbations of bronchial asthma, required multiple admissions at various hospitals and was suspected to have brittle asthma. He was a diabetic and hypertensive and a lifelong non-smoker. He had undergone left pneumonectomy 40 years ago for pulmonary tuberculosis. On general examination he was conscious, alert, afebrile, pulse was regular, 120 per minute, BP was 130/80 mm Hg. He had tachypnoea with respiratory rate of 28/min and had hypoxia with SpO2 of 89% on room air. Examination of respiratory system revealed shift of trachea to left, audible stridor which increased on lying down, absent air entry on the left side and conducted sounds on the right side. Arterial Blood Gas analysis showed; pH–7.28, pCO2–53 mm Hg, pO2–75.1 mm Hg, HCO3–22.1.
2D Echocardiography showed normal LV function, Mild RV dysfunction, dilated RA/RV (TAPSE: 1.24 cm), mild TR and plethoric IVC. CBP, Serum sodium, potassium, and magnesium, were normal. Serum calcium-6.8 mg/dl, phosphate-2.7 mg/dl, parathyroid hormone-179.4 pg/ml, Vit D-3.58, and serum albumin-2.7 mg/dl.
Patient was given intravenous hydrocortisone, calcium gluconate infusion, and NIV-BiPAP support. CT scan of Neck and Chest were done which showed left post-pneumonectomy status, thickening and calcification of left pleura, tortuous trachea with acute angulation at the thoracic inlet, gross shift of mediastinum to the left, multiple spiculated lesions with surrounding fibrosis (granulomas) in anterior and posterior segments of RUL, multiple calcified pretracheal lymph nodes and compensatory hyperinflation of right lung []. In view of worsening of arterial blood gas values and respiratory failure, he was intubated and mechanically ventilated. Fibreoptic bronchoscopy showed severe narrowing of trachea during inspiration and near total closure during expiration suggestive of tracheomalacia []. Similar dynamic airflow obstruction was visualized up to segmental bronchi, though of progressively lesser severity. Patient was considered unsuitable for invasive surgical procedures in view of poor general condition, high risk for anesthetic complications, and generalized debility. He was unsuitable for placement of stent due to long segment tracheobronchial involvement. He refused further invasive procedures. Long length tracheostomy tube (Portex 8.0) was placed with tip of tracheostomy tube 2 - 3 cm from the level of carina as checked with FOB post-placement. Patency of lower trachea was maintained and chest radiography showed well-aerated right lung. He was discharged with tracheostomy used as interface for BiPAP ventilator with no requirement of supplemental oxygen.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.7, 'g/dL'], 'Calcium': [6.8, 'mg/dL']}",7.84,7.448,8.232,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.7 g/dL. 
The concentration of Calcium is 6.8 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.7 g/dL)) + 6.8 mg/dL = 7.84 mg/dL.
The patient's corrected calcium concentration 7.84 mg/dL."
2629,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7506996-1,Extracted,"A 35-year-old male current smoker (22.5 pack-years) visited our hospital with facial oedema and persistent productive cough. Upon admission to our hospital, physical examination revealed a height of 170 cm, body weight of 51 kg, body temperature of 37.0°C, heart rate of 108 bpm, blood pressure of 107/64 mmHg, and oxygen saturation of 99% (room air, rest). Analysis of chest auscultation revealed attenuated respiratory sounds in the upper right lung field. The laboratory findings were as follows: white blood cells, 9000/mm3 with 63.9% neutrophils and 24.2% lymphocytes; haemoglobin, 9.2 g/dL; albumin, 3.4 g/dL; lactate dehydrogenase (LDH), 341 IU/L; calcium, 9.4 mg/dL; C-reactive protein, 3.32 mg/dL; carcinoembryonic antigen, 122.7 ng/mL; and pro-gastrin-releasing peptide, 2850 pg/mL. Chest radiography and high-resolution computed tomography (HRCT) showed a right hilar lung mass in the right upper lobe with pleural dissemination and multiple hilar, para-tracheal and subcarinal lymphadenopathies. Fluorodeoxyglucose-positron emission tomography with CT showed positive accumulation (maximum standardized uptake value = 14.3) in these thoracic lesions with high-uptake lesions in multiple bones (skull, sacrum, and right acetabulum). The target lesions were decided by Response Evaluation Criteria in Solid Tumours version 1.1 (RECISTv1.1).
Pathological examinations of the right S3 lung tumour under bronchoscopic guidance revealed proliferation of small round cells focally with prominent nucleoli and larger nuclei in sheets, nests, or cords with necrotic foci. The observations such as prominent nucleoli and larger nuclei were unusual, as these were not included in the descriptions of any categories of the World Health Organization classification of NSCLC based on histological types. Thus, the observations from the present case were indicative of SCLC. Immunohistochemistry (Bond MAX Immunostainer, Leica Microsystems) results showed that the tumour cells were diffusely positive for thyroid transcription factor-1 (Dako), cytokeratin markers (AE1/AE3; Dako, and CAM5.2; Becton Dickinson), and synaptophysin (Dako) and negative for chromogranin A (Dako), CD56 (Leica Biosystems), nuclear protein in the testis (Cell Signalling Technology), and SMARCA4 (Epitomics) (Fig. ). The tumour proportion score of programmed death-ligand-1 (PD-L1) was 1%–24% according to the 22C3 IHC pharmDX assay (Dako). Molecular analyses revealed no mutations or rearrangements of EGFR, ALK, or ROS1.
The patient was initially treated with two cycles of combined chemotherapy with cisplatin and etoposide, but the thoracic lesions aggravated. The chemotherapy regimens for SCLC were considered ineffective; hence, NSCLC regimens were employed after second-line treatment considering the patient's atypical pathological and clinical characteristics of SCLC. Carboplatin along with paclitaxel (protein-bound) was used as the second-line therapeutic regimen for. After two cycles of chemotherapy with carboplatin plus paclitaxel (protein-bound) and palliative radiation therapy (right upper lobe: 30 Gy/10 fr and right ilium: 30 Gy/10 fr), the sites of radiotherapy showed response. However, multiple new bone metastases were evident.
The subject was treated with nivolumab as a next-line treatment. A week after initiating nivolumab, the patient appeared febrile (38–39°C) with pain in the right chest. Chest HRCT performed on day 15 after nivolumab administration showed a marked increase in pleural effusion in the right lung and chest wall dissemination of the tumour (Fig. ).
HPD was considered to have been caused by treatment with nivolumab. The patient's Eastern Cooperative Oncology Group performance status score had rapidly deteriorated from 1 to 3, necessitating switching of the treatment regimen to docetaxel and ramucirumab. However, tumour progression was uncontrollable, and the patient died due to respiratory failure, 27 days after docetaxel and ramucirumab administration.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.4, 'g/dL'], 'Calcium': [9.4, 'mg/dL']}",9.88,9.386,10.374,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.4 g/dL. 
The concentration of Calcium is 9.4 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.4 g/dL)) + 9.4 mg/dL = 9.88 mg/dL.
The patient's corrected calcium concentration 9.88 mg/dL."
2630,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4531955-1,Extracted,"A 16-year-old boy had been in good health until June 21, 1996, when he finished a trip. On the next day, June 22, he developed bloody diarrhea with diffuse abdominal pain and was treated conservatively at a local clinic. A few days later, he developed oliguria, hematuria and acute renal failure with anemia and thrombocytopenia. He had a transfusion and underwent hemodialysis twice, and then was referred to our hospital on July 4, 1996.
The patient had no history of childhood illness and his familly history revealed no specific illnesses.
On admission day, he had a mild fever, malaise, diffuse abdominal pain, chest discomfort, anuria, gross hematuria and epistaxis. On examination, the patient was moderately developed and nourished. His vital signs were as follows: blood pressure, 180/110 mmHg; pulse rate, 80 beats per minute and regular; respirations, 20 per minute; temperature 37.2°C. Jaundice was not present. He had a skin rash over his entire body (scarlatiniform and petechial) (, ), periorbital edema, cervical lymphadenopathy and severe tenderness in the right costovertebral area.
The hemoglobin level was 81 g/L, the white blood cell count (WBC) was 7.9×109 cells/L (polymorphoneutrophil 0.88, lymphocyte 0.06, monocyte 0.03) and the platelet count was 40×109/L. Other values were as follows: blood urea nitrogen (BUN), 21.1 mmol/L; serum creatinine, 1,001 μmol/L; serum aspartate aminotransferase (AST), 1.01 μkat/L; and serum alanine aminotransferase (ALT), 0.33 μkat/L. The stool occult blood was positive. Urinalysis showed albumin 3+, 1 to 4 WBC and many RBC per high power field, and bile 2+. The reticulocyte was 0.051. The blood chemistry showed the following results: lactate dehydrogenase (LDH), 22.3 μkat/L; serum total protein, 52 g/L; serum albumin, 33 g/L, calcium, 2.00 mmol/L, phosphorus, 2.19 mmol/L, total bilirubin, 11.9 μmol/L; peripheral blood smear showed anisocytosis, polychromatosis and schizocytosis which suggested hemolytic anemia. At a local clinic, prothrombin time (PT) was 26.1 sec, activated partial thromboplastin time (aPTT) was 150 sec, fibrinogen was 2.3 g/L and fibrin degradation products (FDP) were positive. Upon admission to our hospital, PT was 13.7 sec (79%), aPTT was 29 sec, fibrinogen was 3.5 g/L, FDP was 80 mg/L and D-dimer test was positive. These findings suggested disseminated intravascular coagulation. An antistreptolysin titer was 54.2 Todd units. Antinuclear antibody was negative. C3 was 0.85 g/L. C4 was 0.27 g/L. Direct and indirect Coombs’ tests were negative. Anti-platelet antibody was negative. Immunoglobulin G, A, and M were 6.11 g/L, 1.14 g/L, and 1.51 g/L, respectively. The blood culture and stool culture were negative. The cytomegalovirus (CMV) antibody, rubella antibody, HIV antibody, Hantan virus antibody, leptospira antibody, and rhickettsia antibody were all negative. The EBV-IgM antibody was positive. Eighteen days after this result, early antigen (EA)-IgG antibody was negative and Heterophil antibody had a low titer of 1:14, but the Epstein-Barr nuclear antigen (EBNA) and EBV-IgG antibody were positive.
On his chest X-ray, there was pleural effusion in the left side. On abdominal ultrasonography, the size of both kidneys was about 12 cm, the cortical echogenecity of the kidney was increased and there were splenomegaly and ascites. The electrocardiogram showed myocardial ischemia and there was a moderate degree of pericardial effusion on cardiac echocardiography.
On the second day in hospital, therapy with hemodialysis and antihypertensives had been commenced. On the 3rd day, his fever and skin rash subsided. On the 4th day, the hemoglobin level was 68 g/L, BUN was 24.2 mmol/L, serum creatinine was 1,238 μmol/L, platelet count was 50 × 109 /L, urine ouput was below 50 ml/day and aspirin (100 mg/day) therapy was started. From the 7th day, plasma exchange using 10 units of fresh frozen plasma was done five times on alternate days. On the 11th day, urine output was increased to more than 1,000 ml per day. On the 15th day, BUN, serum creatinine and LDH were decreased to 11.0 mmol/L, 406 μmol/L, and 2.55 μkat/L, respectively, and gross hematuria disappeared. On the 17th day, BUN was 6.8 mmol/L and serum creatinine was 226 μmol/L. Plasma exchange and hemodialysis were stopped. Prior to the patient’s discharge, on the 29th day, renal function had markedly improved; BUN was 6.0 mmol/L; serum creatinine was 122 μmol/L; creatinine clearance, 0.86 mL/s; urine protein, 1.0 g/d; on urinalysis albumin (−), WBC 0 to 1, and RBC 5 to 9 per high power field. Other values had also improved; the hemoglobin level, 101 g/L; reticulocyte, 0.001; platelet count, 190×109 /L; total bilirubin, 5.1 μmol/L; AST, 0.31 μkat/L; ALT, 0.17 μkat/L; blood pressure was 140/90 mmHg ().
This patient recovered by hemodialysis, plasmapheresis, antihypertensive medication and aspirin, and was treated with an antiplatelet agent after discharge.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [33.0, 'g/L'], 'Calcium': [2.0, 'mmol/L']}",8.576,8.1472,9.0048,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 33.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 33.0 g Albmumin/10.0 dL = 3.3 g Albmumin/dL. The concentration value of 33.0 g Albmumin/L converts to 3.3 g Albmumin/dL. 
The concentration of Calcium is 2.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 2.0 mmol. To convert 2.0 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 2.0 mmol Calcium * 0.001 mol/mmol = 0.002 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.002 mol Calcium * 40.08 g/mol = 0.08016 g Calcium. To convert 0.08016 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.08016 g Calcium * 1000.0 mg/g = 80.16 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 80.16 mg Calcium/10.0 dL = 8.016 mg Calcium/dL. The concentration value of 2.0 mmol Calcium/L converts to 8.016 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.3 g/dL)) + 8.016 mg/dL = 8.576 mg/dL.
The patient's corrected calcium concentration 8.576 mg/dL."
2631,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7232960-1,Extracted,"A 48-year-old man from Northeast Nuevo Leon State presented with a history of a painless scrotal mass that progressively increased in size during the last 3 months. He denied dysuria, urethral discharge, weight loss, fever or diaphoresis. He has worked as a farmer for the last 20 years and his medical history was relevant for chronic alcohol consumption during the last 10 years (200 g/week) and a recent diagnosis of primary adrenal insufficiency treated with a daily dose of 10 mg of prednisone and fludrocortisone 0.1 mg per day in the past year. Vital signs were stable. Further examination revealed a hard and heterogeneous tumor in the posterior aspect of the right testis. Inguinal lymphadenopathy, local hyperthermia, skin lesions or color change were not present. Laboratory results showed a hemoglobin concentration of 13.1 g/dL, leukocytes 8.09 x109/L, platelets 199 x109/L, glucose 96 mg/dL, sodium 138 mmol/L, chlorine 100 mmol/L, potassium 4 mmol/L, calcium 8.4 mg/dL, urea nitrogen 16 mg/dL, creatinine 1.0 mg/dL, C-reactive protein 1 mg/L, alanine aminotransferase 36 UI/L, aspartate aminotransferase 30 UI/L, total bilirubin 0.8 mg/dL and albumin 3.8 g/dL. Color flow doppler testicular ultrasonography was performed and two nodular masses in the tail of the right epididymis with increased vascular flow were found (). An epididymectomy was performed and histologic examination revealed a granulomatous epididymitis with scattered coccidioidal spherules present within the granulomas (). The diagnosis of disseminated coccidioidomycosis was made and systemic antifungal therapy was initiated with fluconazole 400 mg once daily for 12 months. As the diagnosis of disseminated coccidioidomycosis usually relies on the histopathological identification, further serological tests or culture were not performed. Alterations in the lungs compatible with current pulmonary coccidioidomycosis were not found on the chest CT-scan. Involvement of other organs was systematically excluded in our patient as well, however, further evaluation for adrenal insufficiency will be carried out after discharge.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.8, 'g/dL'], 'Calcium': [8.4, 'mg/dL']}",8.56,8.132,8.988,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.8 g/dL. 
The concentration of Calcium is 8.4 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.8 g/dL)) + 8.4 mg/dL = 8.56 mg/dL.
The patient's corrected calcium concentration 8.56 mg/dL."
2632,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2972238-1,Extracted,"A 58-year-old man was admitted to our hospital with a 6-month history of frequent watery diarrhea (10-20 times per day), intermittent hematochezia, and a weight loss of 13 kg. Two months after onset of symptoms, he noticed pigmentation in the palms and hair loss. He had a negative family history of gastrointestinal disease and congenital disease. On physical examination, the patient was found to have marked alopecia, brownish macular pigmentation over the palms and soles, and onychodystrophy of the fingernails. The remainder of the physical examination was unremarkable.
Initial laboratory data showed that his albumin level was 31.2 g/L (normal range 35-55 g/L), serum potassium 3.1 mmol/L (normal range 3.5-5.5 mmol/L) and serum calcium 1.7 mmol/L (normal range 2.1-2.6 mmol/L). Other blood parameters, including thyroid hormones, parathyroid hormone and immunoglobulins, were within the normal range. The chest radiograph was negative. Esophagogastroduodenoscopy, video capsule endoscopy and colonoscopy were performed for further evaluation of the gastrointestinal tract and they identified various sizes of generalized gastrointestinal polyps (Figures , and ). Histological examination of the biopsy specimens obtained from the stomach and the colon showed adenomatous polyp and inflammatory polyp respectively. Thus, a diagnosis of CCS was made. We started corticosteroid therapy for him with oral prednisone (40 mg per day for 2 weeks and then reduced the dosage to 30 mg per day and lasted it for 10 days), but then we discontinued it because the clinical situation of the patient became better. At the same time, the patient was treated with nutritional supplementation by parenteral and enteral nutrition. His situation improved gradually after two months of treatment. The frequency of diarrhea decreased to 2 times per day, the weight increased by 5 kg, and the hair and fingernails regrew, but the levels of serum calcium (1.9 mmol/L) and albumin (30.6 g/L) were still lower than the normal range. He returned home for home nutritional support by enteral nutrition.
Two months later, he was admitted to our hospital for the second time with frequent diarrhea (7-8 times per day) and a weight loss of 7 kg. Laboratory data showed that his serum albumin level was 28.2 g/L and serum calcium 1.7 mmol/L. His chest radiograph showed fractures of the left sixth and seventh ribs (Figure ). Since the patient had not suffered from any load or trauma in the chest, this concomitant complication initially led us to presume that there was a possibility of rib metastasis of a malignant tumor. Emission Computed Tomography (ECT) was performed and it showed no increased tracer uptake in the skeletal system. Bone densitometry tests on vertebrae lumbales and caput femoris were normal. Further examination for checking bone metastasis was not performed because of the patient's financial situation, and his examinations and clinical features indicated no definite malignant tumor. Since his nutritional status was poor and he had no complain of pain in chest, orthopedic surgeons and chest surgeons advised us to supply calcium and nutrition for him and to restrict his chest wall movement. After one-month treatment, which was similar to our previous treatment except for the corticosteroid therapy, his clinical condition markedly improved again. His serum albumin level increased to 35.2 g/L and calcium to 1.9 mmol/L. However, the rib fractures persisted.
After one-month of home nutritional support, he was admitted to our hospital for the third time to improve his nutritional status. His chest radiograph revealed aggravating multiple rib fractures (Figure ). Since he did not complain of chest pain and respiratory distress when walking or resting, we consulted the orthopedic surgeons and chest surgeons again and received the same treatment recommendations. After one-month combination therapy, based on nutritional support, his weight increased by 4.5 kg, but hypocalcaemia (calcium level, 1.9 mmol/L), hypoalbuminemia (albumin level, 30.9 g/L) and multiple rib fractures still persisted.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [30.9, 'g/L'], 'Calcium': [1.9, 'mmol/L']}",8.343,7.92585,8.76015,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 30.9 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 30.9 g Albmumin/10.0 dL = 3.09 g Albmumin/dL. The concentration value of 30.9 g Albmumin/L converts to 3.09 g Albmumin/dL. 
The concentration of Calcium is 1.9 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.9 mmol. To convert 1.9 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.9 mmol Calcium * 0.001 mol/mmol = 0.0019 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.0019 mol Calcium * 40.08 g/mol = 0.07615 g Calcium. To convert 0.07615 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.07615 g Calcium * 1000.0 mg/g = 76.15 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 76.15 mg Calcium/10.0 dL = 7.615 mg Calcium/dL. The concentration value of 1.9 mmol Calcium/L converts to 7.615 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.09 g/dL)) + 7.615 mg/dL = 8.343 mg/dL.
The patient's corrected calcium concentration 8.343 mg/dL."
2633,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6779941-2,Extracted,"A 59-year-old man was refered to our hospital with anemia in 2006. The laboratory findings were as follows: WBC, 4.0×109/L; Hb, 7.9 g/dL; PLT, 330×109/L; TP, 8.5 g/dL; Alb, 3.2 g/dL; compensated Ca, 8.9 mg/dL; IgG, 4,135 mg/dL; IgA, 55 mg/dL; IgM, 42 mg/dL; and beta 2-microglobulin, 5.1 mg/L. Serum creatinine level was within the normal range, and proteinuria was not recognized. The serum protein electrophoresis showed an M-peak in the gamma fraction, although serum immunofixation test was not performed. The BM aspirate showed myeloma at that time; hence, he was initially diagnosed with symptomatic IgG myeloma. He was treated with two cycles of VAD therapy [28 days cycles of vincristine (0.4 mg/kg) with doxorubisin (9 mg/m2) by continuous intravenous infusion for 4 days, and dexamethasone (40 mg/kg) by intravenous infusion for 4 days] as an induction treatment, by which he achieved partial response. The patient had his first recurrence in 2009 and received BD therapy consisting of Bor and Dex [] and achieved a very good partial response. In 2014, enlargement of the mediasinum without any symptoms was noted on a chest X-ray. The CT showed a mediastinal mass (), slight enlargement of the post-peritoneal lymph nodes, and moderate splenomegaly. The biopsied specimen obtained from the mediastinal mass exhibited diffused infiltration of small- to medium-sized atypical lymphocytes with plasma cell differentiation (). On immunohistochemical staining, the atypical lymphocytes were positive for CD20 (), whereas atypical lymphoplasmacytes and plasmacytes were positive for CD138 (). The serum immunofixation test demonstrated dual monoclonal bands of IgG-kappa and IgG-lambda. BM aspirate revealed diffuse infiltration of small lymphocytes, lymphoplasmacytes, and plasmacytes. G-banding of the BM aspirate resulted in 46 and XY. FISH analyses for IgH-BCL1, chr 13q del, and chr 6q del were negative. MYD88 L265P mutation was also negative. Furthermore, reconfirmation of BM aspirate obtained in 2006 revealed that the neoplastic cells were composed of atypical small lymphocytes, lymphoplasmacytes, and plasmacytes. Therefore, the precise diagnosis was revised from IgG myeloma to IgG LPL after re-evaluation. After local radiation therapy (36 Gy/17 Fr), the mediastinal tumor disappeared, and the patient had no symptoms at that time. The patient was followed under close observation without administering any systemic chemotherapy. He has not received chemotherapy for 10 years after BD therapy and is alive 13 years after the initial diagnosis.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.2, 'g/dL'], 'Calcium': [8.9, 'mg/dL']}",9.54,9.063,10.017,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.2 g/dL. 
The concentration of Calcium is 8.9 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.2 g/dL)) + 8.9 mg/dL = 9.54 mg/dL.
The patient's corrected calcium concentration 9.54 mg/dL."
2634,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-8684889-1,Extracted,"A 60-year-old heterosexual man presented with 75 lb weight loss, dysphagia, jaw pain/swelling, hypotension and acute kidney injury. Medical history was significant for emphysema, hypertension, stroke, alcohol withdrawal seizure, alcohol abuse and cigarette smoking. He worked as a landscaper.
On presentation vitals were: 37.5°C, 68/48 mmHg, 95 beats/min, respiratory rate 22/min, oxygen saturation 99% on room air. Physical exam revealed halitosis, poor dentition, diffuse lower gum swelling and erythema. Soft palate showed exophytic growth (Figure ).
Abdominal exam was unremarkable. Serum chemistries showed sodium 139 mEq/L, chloride 102 mEq/L, bicarbonate 30 mEq/L, blood urea nitrogen 43 mg/dl, glucose 94 mg/dl, calcium 8.7 mg/dl, creatinine 2.3 (baseline 1.1 mg/dl), albumin 1.5 g/dl, alkaline phosphatase 574 U/L, lactic acid 2.9 mmol/L, Hb 10.8 g/dl with normal MCV, RDW, decreased RBC 3.87 x 106/ul (normal > 4.2), normal WBC 5000/ul, platelets 167,000/ul, normal bilirubin and ALT. CT neck (Figure ) showed soft palate asymmetry with thickening.
Piperacillin-tazobactam was started in addition to chlorhexidine empirically to provide coverage for any deep-seated bacterial infection of the oral mucosa while providing anaerobic coverage. ENT did soft palate biopsy which on GMS stain showed numerous round to oval yeast forms present intracellularly within the histiocytes and in the extracellular subepithelial tissue consistent with histoplasmosis (Figure ).
HIV-1/HIV-2 antigen/antibody screen was negative. Piperacillin-tazobactam was switched to amphotericin B. CD4 count was 36 cells/ul, CD8 count was normal, CD4:CD8 0.1 (normal: 1-3.6). Given a low CD4 count, he was started on azithromycin and sulfamethoxazole-trimethoprim for prophylaxis. Further testing revealed HIV RNA viral load (negative), HTLV-1/HTLV-2 DNA PCR (negative), hepatitis panel testing for hepatitis A, B and C (negative), vitamin B12 (normal), folate 3.7 ng/ml (low), reticulocyte count 2.2%, lactate dehydrogenase (normal), haptoglobin (normal), iron studies showed elevated ferritin, low iron, elevated transferrin saturation (anemia of chronic inflammation), copper (normal), zinc levels 37 mcg/dl (low), SPEP/UPEP (no monoclonal protein; diffuse hypergammaglobulinemia seen), IgA 467 mg/dl (high), IgG 2160 mg/dl (high), IgM 252 mg/dl (high), free light chain ratio (normal). Anti-nuclear antibody (ANA) 1:160, anti-CCP (cyclic citrullinated peptide) IgG 3.3 U/dl (high). Rapid plasma reagin (RPR) (negative), cytomegalovirus PCR (negative) and Epstein-Barr virus PCR were negative. Ultrasound abdomen showed no organomegaly. Bone marrow biopsy showed granulomas consistent with a diagnosis of histoplasmosis.
The patient subsequently developed upper gastrointestinal bleeding, so an EGD was performed which showed multiple 3-5 mm nodules in the second part of the duodenum (Figure ) which were biopsied.
Pathology showed duodenitis with fungal organisms on Gomorri-Methenamine Silver (GMS) stain compatible with histoplasmosis (Figure ).
CMV immunostain and AFB stain were negative. Colonoscopy showed diverticulosis, a 1 cm clean-based ulcer in the sigmoid colon (Figure ) which on biopsy showed the presence of histoplasma (Figure ).
The patient was then switched to oral itraconazole and discharged home on the same along with azithromycin, sulfamethoxazole-trimethoprim and folic acid.
Four months later, the patient had gained 10 lbs of weight, his dysphagia had resolved, and he was continuing his itraconazole therapy. His CD4 count now was 55/ul. Repeat low CD4+ T-cell count satisfied the criteria for the diagnosis of ICL.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [1.5, 'g/dL'], 'Calcium': [8.7, 'mg/dL']}",10.7,10.165,11.235,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 1.5 g/dL. 
The concentration of Calcium is 8.7 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.5 g/dL)) + 8.7 mg/dL = 10.7 mg/dL.
The patient's corrected calcium concentration 10.7 mg/dL."
2635,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7222535-1,Extracted,"A 59-year-old man presented with complaints of fatigue, respiratory distress, orthopnea and failure to thrive. He had a history of multiple rib fractures (2nd-10th on the right side and 2nd-11th on the left side) due to excessive body massage 1 year previously, leading to bilateral flail chest. He also had diarrhea (2–3 times per day), weight loss of approximately 15 kg over 2 years and onychodystrophy involving the finger and toe nails. He had undergone left hemicolectomy 1 year prior for multiple gastrointestinal polyps at another hospital and was diagnosed with CCS based on histopathological examination. He had no family history of polyposis. Since that time, he has been treated with nutritional supplementation, antibiotics (levofloxacin and cefepime) and corticosteroids (hydroprednisone) for 6 months.
On clinical examination, the patient was malnourished, emaciated and had loss of finger and toe nails. He could not lay down to sleep. He had a partial arterial oxygen pressure of 58 mmHg and an oxygen saturation (SpO2) of 88% with nasal oxygen. He had paradoxical chest movements on both sides due to flail chest and pseudarthrosis.
On colonoscopy, we found more than 100 colonic polyps diffusely distributed, starting at 17 cm from the cecum up to the anus with inflamed mucosa and few erosions in the size range of 0.8–1.5 cm (Fig. ). Histopathological evaluation of the colonic biopsy revealed multiple adenomatous polyps, mild atypical hyperplasia and inflammatory granuloma (Fig. a and Fig. b). On immunohistochemical analysis, IgG staining was present but staining for IgG4 was negative. Computed tomography (CT) of the chest showed multiple fractures of the 2nd-10th ribs on the right side and the 2nd-11th ribs on the left side (Fig. ). Laboratory investigations showed a serum albumin concentration of 31 g/L (normal range, 40–60 g/L), serum calcium concentration of 2.04 mmol/L (normal range 2.25–2.75 mmol/L), serum phosphorous concentration of 14 mmol/L, serum ferritin concentration of 225 ng/ml, highly sensitive C-reactive protein (hsCRP) concentration of 5.48 mg/L, and an erythrocyte sedimentation rate (ESR) of 7 mn/h. The T-spot/TB test yielded 176 + 28FC /10S6MC. Evaluation of tumor markers showed a carcinoembryonic antigen (CEA) level of 5.17 ng/ml with the absence of alpha-fetoprotein (AFP), CA19–9, and CA242. The kidney androgen-regulated protein (KAP) level was 7.55 mg/dL, and the results of the human lipoarabinomannan assay (for tuberculosis) were normal. The serum immunoelectrophoresis test was negative, the immunoglobulin 4 (IgG4) concentration was 5940 ng/mL, Ig alexin was normal. Analysis of antinuclear antibodies (ANAs) revealed the patient was PCNA(+) and anti-ENA(−). Analysis of bone metabolism showed a β-CTX (β-Crosslaps for bone resorption) concentration of 0.621 ng/mL, a T-25-OH-vitaminD concentration of 7.4 ng/mL, and a parathyroid hormone (PTH) concentration of 94.2 pg/mL. The patient had severe osteoporosis and osteomalacia.
We continued his nutritional supplementation and antibiotics but stopped his steroid treatment due to the rib fractures. He underwent open reduction and internal fixation twice (anterior and posterior separately) using a titanium alloy fixator and a nickel-titanium memory alloy embracing fixator for chest wall reconstruction (Fig. ). The surgeries were done in two sessions because the first operation took a long time and the patient could not tolerate the prolonged anesthesia. The fixations were done using two bilateral curved incisions one on either side. We mainly retracted the muscles during the fixation and muscle cutting was performed only at few places. Postoperatively, he developed respiratory muscle weakness and respiratory failure due to which he required prolonged ventilator support. Tracheostomy and bronchial lavage were performed to provide ventilator-assisted breathing after operation. He recovered gradually and remained on the invasive ventilator for 3 months (2 months in hospital and 1 month at home). His hospital stay was 2 months. Subsequently, he received nutritional support at home and household noninvasive ventilator support for 6 months. At last follow-up (6 months after discharge), the patient’s body weight had increased by 20 kg and the patient showed improvement in his symptoms (Fig. ).","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [31.0, 'g/L'], 'Calcium': [2.04, 'mmol/L']}",8.896,8.4512,9.3408,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 31.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 31.0 g Albmumin/10.0 dL = 3.1 g Albmumin/dL. The concentration value of 31.0 g Albmumin/L converts to 3.1 g Albmumin/dL. 
The concentration of Calcium is 2.04 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 2.04 mmol. To convert 2.04 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 2.04 mmol Calcium * 0.001 mol/mmol = 0.00204 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00204 mol Calcium * 40.08 g/mol = 0.08176 g Calcium. To convert 0.08176 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.08176 g Calcium * 1000.0 mg/g = 81.76 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 81.76 mg Calcium/10.0 dL = 8.176 mg Calcium/dL. The concentration value of 2.04 mmol Calcium/L converts to 8.176 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.1 g/dL)) + 8.176 mg/dL = 8.896 mg/dL.
The patient's corrected calcium concentration 8.896 mg/dL."
2636,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4177611-1,Extracted,"A 58-year-old African American female presented with a three-month history of fatigue, poor appetite, lack of energy, and 40 lbs weight loss. Her past medical history was significant for hysterectomy and uncontrolled diabetes. Physical examination demonstrated hepatomegaly with liver palpable 2 fingerbreadths below the right costal margin. There was no palpable lymphadenopathy. Laboratory tests showed a white blood cell count (WBC) of 2.31 × 109/L, hemoglobin 9.4 g/dl, platelet count 281 × 109/L; creatinine 0.8 mg/dl, serum calcium 8.9 mg/dl, total protein 8.2 g/dl, and albumin 2.51 g/dl. SPEP and immunofixation (IFE) revealed 3.22 g/dl of broad-based protein band in the gamma zone and 0.73 g/dl of monoclonal immunoglobulin G (IgG)- kappa (κ) M-protein. Bone skeletal survey showed no lytic lesions. Bone marrow aspirate and biopsy showed increased number of plasma cells (15% on biopsy) with no light chain restriction. HIV screening test was positive, confirmed with Western blot analysis. The CD4 count was 15/μl and HIV viral load 934,811 copies/ml. She was diagnosed with HIV-associated polyclonal hypergammaglobulinemia with concomitant monoclonal gammopathy. She was referred to the infectious disease clinic and was started on HAART.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.51, 'g/dL'], 'Calcium': [8.9, 'mg/dL']}",10.092,9.5874,10.5966,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.51 g/dL. 
The concentration of Calcium is 8.9 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.51 g/dL)) + 8.9 mg/dL = 10.092 mg/dL.
The patient's corrected calcium concentration 10.092 mg/dL."
2637,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7725568-1,Extracted,"A 59-year-old male with a significant history of chronic alcoholism presented to the emergency room after an upper arm fracture on light gardening. X-ray of the shoulder showed a spiral fracture of the proximal diaphysis of the humerus with displacement and angulation of the distal fractured bone (). During the orthopedic surgery evaluation, the patient reported dyspnea on exertion and increasing abdominal girth. These alarming symptoms prompted a referral to cardiology for preoperative clearance. The patient got admitted for the pre-op workup. His past medical history was significant only for chronic alcohol abuse. He denied smoking and use of illicit drugs. His family history was noncontributory and negative for bone or liver disease. His vitals on admission were the following: temperature of 97.1, blood pressure of 160/65 mmHg, respiratory rate of 18 breaths per minute, and pulse rate of 60 beats per minute. Pertinent physical findings included mildly enlarged liver on palpation, grade IV/VI systolic murmur at the aortic area, and scattered basilar rales. There was no splenomegaly, jaundice, or lymphadenopathy.
Laboratory workup showed hemoglobin 11.8 g/dL, white blood count 5,700/mm3, platelets 115,000/mm3, BUN 14 m/dL, creatinine 0.62 mg/dL, calcium 8.7 mg/dL, albumin 2.7 g/dL, total proteins 8.4 g/dL, prothrombin time 14 seconds (control 10-13 seconds), activated partial thromboplastin time 34 sec (control 27-37 seconds), alkaline phosphatase 172 IU/L, ALT 71 IU/L, AST 107 IU/L, LDH 224 IU/L, total bilirubin 1 mg/dL, alpha-fetoprotein 8.7 ng/mL, hepatitis C antibody reactive, and hepatitis C viral load of 1,626,714. Computerized tomography (CT) scan of the shoulder () showed an oblique comminuted fracture of the proximal humerus shaft as reported on X-ray in the emergency room. However, the fracture appeared to traverse through an ovoid lucency measuring approximately 5.5 × 2.8 cm within the proximal humerus shaft (). No discrete tumor or soft tissue mass was seen but was likely obscured by hemorrhage from the fracture. CT scan of the abdomen and pelvis (Figures –) revealed cirrhosis with portal hypertension, showing four liver lesions, with the largest measuring 3.1 cm, typical of HCC and another one hypoattenuating large lesion, measuring 5.8 × 5.2 cm, atypical for HCC. Staging scans did not reveal metastatic disease in the chest.
The differentials considered based on radiological features were a primary bone tumor or metastasis of an unknown primary or hepatocellular carcinoma. The patient underwent an open reduction and internal fixation of the right humerus with a bone biopsy at the fracture site with no postoperative complications. The biopsy results showed the presence of HCC (Figures and ). The patient was recommended to start radiation to the humerus and sorafenib after recovery from surgery.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.7, 'g/dL'], 'Calcium': [8.7, 'mg/dL']}",9.74,9.253,10.227,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.7 g/dL. 
The concentration of Calcium is 8.7 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.7 g/dL)) + 8.7 mg/dL = 9.74 mg/dL.
The patient's corrected calcium concentration 9.74 mg/dL."
2638,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2323011-1,Extracted,"A 81-year-old man with an adenocarcinoma of the prostate diagnosed one year earlier presented with a five month history of gradually progressive complaints of dyspnea. At the time of diagnosis of the prostate cancer, there had been no signs of metastases and since it was an asymptomatic grade 2 prostate cancer in a man of advanced age, a watchful waiting policy was followed. The medical history revealed hypertension and a transurethral resection of the prostate six years before presentation. The patient complained of dyspnea, progressive peripheral edema, orthopnea, and painful knees and thighs which made walking extremely difficult. There had been weight loss of ten kilograms over six months, with associated loss of appetite. No thoracic pain, hemoptysis or other pulmonary or cardiac complaints were present. The patient had been a heavy smoker for fifty years.
On admission his blood pressure was 150/80 mmHg with an irregular pulse of 96 per minute, temperature 36.2°C, and he had a normal central venous pressure. The heart sounds were normal. Percussion and auscultation of the left lower lung revealed dullness with diminished breath sounds. These signs were indicative of pleural effusion. The liver was not enlarged. There was pitting edema especially at the lower extremities, but also of both hands, which were also noted to be remarkably large. Percussion of, and axial pressure on, the vertebrae was not painful. The patient refused rectal examination because of painful earlier experiences.
Laboratory examination revealed the following data: ESR 35 mm in the first hour (normal: <7), CRP 134 mg/l (normal <10), hemoglobin 6.3 mmol/l (normal: 8.9–10.7) with a MCV of 82 fl (normal: 80–100), leukocytes 8.6 × 109/l (normal: 4.5–10.0) with 90% neutrophilic granulocytes (normal 40–70), normal blood platelets, electrolytes and liver enzymes. Creatinine was 77 μmol/l (normal: 64–108), alkaline phosphatase was elevated at 285 U/l (normal: 40–120), calcium was 1.95 mmol/l (normal: 2.15–2.68) with an albumin of 23.9 g/l (normal: 35–50 g/l) and a normal phosphate. Blood gas analysis showed a chronic compensated respiratory acidosis with an oxygen saturation of 80%.
Electrocardiography showed atrial fibrillation with a left bundle branch block, similar to earlier ECGs. Chest X-ray revealed a large amount of pleural fluid on the left side and an enlarged heart without signs of vascular redistribution. There were no signs of tumor or pulmonary metastasis on chest X-ray.
Analysis of the pleural fluid was performed. A total amount of 4.5 liters was evacuated. Cytological and biochemical analysis showed only lymphocytosis with no signs of malignancy or bacterial infection. Auramin and Löwenstein cultures were negative. An echocardiography showed good left ventricular function. Ultrasound investigation of the abdomen showed a dilated inferior caval vein without other abnormalities. The entire presentation was compatible with right-sided heart failure in a patient with probable pulmonary hypertension. On Computed Tomography Angiography (CTA) there were no pulmonary embolisms visible but a large amount of pleural fluid was seen in the left pleural cavity.
Because of the elevated alkaline phosphatase, the bone pains and the previously diagnosed prostate cancer, skeletal scintigraphy was performed. It showed a 'super scan', meaning there was diffuse uptake throughout the entire skeleton. This was judged as fitting diffuse skeletal metastasis of the prostate cancer [Figure ]. However the prostate specific antigen was within the normal range at 1.4 μg/l (normal < 4.4)
With the remarkably large hands in mind, additional investigations were carried out [Figure ]. A bone marrow examination showed no marrow disease nor malignancy. X-ray of the hands, humeri, femora and pelvis revealed extensive subperiosteal bone appositions compatible with generalized hypertrophic osteoarthropathy [Figure ]. Repeat of the earlier performed CTA indeed now showed a fluid-containing cavity in the lower left lobe surrounded by a large amount of pleural fluid at that side suggestive of a lung cancer. Bronchoscopy confirmed this diagnosis. The left main bronchus was stenotic with tumor totally occluding the left lower lobe and almost occluding the left upper lobe. Histological examination was not possible due to technical difficulties during the procedure. The diagnosis of incurable bronchial carcinoma with hypertrophic osteoarthropathy was made with the prostate cancer as an ""innocent"" bystander. Since the patient was rapidly deteriorating palliative care was given. The patient died several weeks after admission. Post mortum examination confirmed the clinical diagnosis. There was a large undifferentiated non-small cell lung carcinoma with a diameter of 10 cm and extension in the adventitia of the esophagus and lymphatic metastasis in the hili and mediastinum. Three liters of tumor-positive pleural fluid and extensive hypertrophic osteoarthropathy was seen without distant metastasis.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [23.9, 'g/L'], 'Calcium': [1.95, 'mmol/L']}",9.104,8.6488,9.5592,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 23.9 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 23.9 g Albmumin/10.0 dL = 2.39 g Albmumin/dL. The concentration value of 23.9 g Albmumin/L converts to 2.39 g Albmumin/dL. 
The concentration of Calcium is 1.95 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.95 mmol. To convert 1.95 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.95 mmol Calcium * 0.001 mol/mmol = 0.00195 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00195 mol Calcium * 40.08 g/mol = 0.07816 g Calcium. To convert 0.07816 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.07816 g Calcium * 1000.0 mg/g = 78.16 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 78.16 mg Calcium/10.0 dL = 7.816 mg Calcium/dL. The concentration value of 1.95 mmol Calcium/L converts to 7.816 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.39 g/dL)) + 7.816 mg/dL = 9.104 mg/dL.
The patient's corrected calcium concentration 9.104 mg/dL."
2639,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3420507-1,Extracted,"A 41 year old man was admitted to University Hospitals Case Medical Center for a two-week history of constitutional symptoms including arthralgias, night sweats, decreased appetite, dyspnea on exertion, and shortness of breath. Past medical history was significant for hypertension, thalassemia minor, hypogonadism, and recent history of uveitis.
Laboratory findings at admission included the following: WBC 3.6 × 109/L, RBC 5.52 × 1012/L, Hgb 11.1 g/dL Hct 33.1% MCV 60 fL, and Plt 193 × 109/L. Chemistry tests performed one week before admission were normal except for a low albumin at 2.7 g/dL and calcium at 7.9 mg/dL. Notable abnormal laboratory findings during admission were elevated C-reactive protein at 4.0 mg/dL, sedimentation rate at 69, LDH 218 U/L, and Beta 2 microglobulin 8.0 mg/dL. Serum protein electrophoresis revealed a monoclonal IgG lambda paraprotein 0.8 g/dL. Angiotensin-converting enzyme was elevated at 156 U/L. Testing for viral infections including hepatic function tests, hepatitis B, HIV, parvovirus, and Epstein-Barr virus serology was negative. Serology for mycoplasma and syphilis was negative. Blood cultures failed to grow organisms. Studies for rheumatologic disorders were negative including an ANA panel, rheumatoid factor, and ANCA.
CT, MRI, and PET scans revealed extensive adenopathy and abnormal PET uptake within the lymph nodes of the neck, supraclavicular region, chest, abdomen and pelvis, and pericardial thickening suspicious for a lymphoproliferative disease. MRI of the orbits was unremarkable except for mild prominence of the optic disks. EKG and echocardiogram were unremarkable.
A bone marrow biopsy was performed to investigate the cause of the paraproteinemia and revealed a hypercellular bone marrow (80%) with 5% mature-appearing plasma cells, normal trilineage hematopoiesis, mild erythroid hyperplasia, and microcytosis consistent with thalassemia minor (not shown). The plasma cells were lambda restricted by in situ hybridization staining. Flow cytometry performed on the marrow identified a small population of clonal plasmacytic cells that were surface light chain weakly lambda(+), CD19(+), HLA-DR(+), CD38bright, CD138(−), CD45(+) moderate to strong, CD20(−), CD5(−), and CD10(−) (not shown). The CD20(+) cells were not clonal. The phenotype was felt to be most consistent with a lymphoma with plasmacytic differentiation rather than a plasma cell dyscrasia [].
Shortly thereafter, a cervical lymph node biopsy was performed that revealed an effaced lymph node with a dimorphic morphologic picture, . A portion of the node demonstrated a diffuse proliferation of small lymphocytes with plasmacytoid features (Figures , , , , and ). The majority of cells in this region of the lymph node were CD20(+) with many lambda(+) plasmacytic cells. Flow cytometry revealed a small weakly lambda(+) CD19(+) cell population similar to that observed in the bone marrow (not shown). The findings were felt to be that of a lymphoma with plasmacytic differentiation, most likely a marginal zone lymphoma with extensive plasmacytic differentiation (P-MZL).
Other regions of the lymph node demonstrated a diffuse proliferation of histiocytic cells with pale staining cytoplasm and bland nuclei (Figures , , and ). Only very rare giant cells were observed ( (d)). Immunohistochemical staining revealed that the cells were CD68(+), CD1a(−), S100(−), CD31(+) weak, and lysozyme (+). By flow cytometry, an abnormal monocytic/histoicytic population was not identified. AFB and GMS were negative and culture of the lymph node did not grow bacteria or fungi. The exact significance of the histiocyte proliferation was unable to be determined from the biopsy.
The patient was subsequently started on prednisone with improvement of his symptoms and was discharged from the hospital with a follow-up appointment two weeks later. However, he expired suddenly at home three days after discharge. An autopsy was performed by the Summit County (Ohio) Medical Examiner.
Autopsy findings demonstrated extensive myocardial and peripancreatic adipose tissue infiltration by histiocytic cells similar to that observed in the antemortem lymph node biopsy, . The cardiac involvement was most impressive and also the cause of the patient's demise. The infiltrate was also seen focally in skeletal muscle, lymph nodes, and lung. Only rare multinucleated Touton-like giant cells were seen. There was no necrosis or caseation. The immunohistochemical profile of the histiocytic infiltrate in the postmortem sample was similar to that seen in the antemortem lymph node biopsy although S100 was focally, weakly positive (not shown). The pattern of infiltrate, the morphology, and the phenotype of the cells were diagnostic for Erdheim-Chester disease [–]. Lymphoma was not clearly evident in postmortem tissue sections.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.7, 'g/dL'], 'Calcium': [7.9, 'mg/dL']}",8.94,8.493,9.387,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.7 g/dL. 
The concentration of Calcium is 7.9 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.7 g/dL)) + 7.9 mg/dL = 8.94 mg/dL.
The patient's corrected calcium concentration 8.94 mg/dL."
2640,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3114796-1,Extracted,"A 78-year-old female, presenting with progressive shortness of breath and general weakness was admitted to our hospital on March 15, 2010. She experienced palpitations and tachycardia, and mild chest tightness when palpitations occurred. Her history was significant for primary cancer of the appendix with ovarian metastases, and was status post a debunking operation in December of 2006, complicated by chronic right leg lymphedema. She had been taking warfarin as prescribed by the cardiovascular surgery department for deep vein thrombosis of the right leg.
On admission, her blood pressure was 148/96 mmHg, heart rate 114 beats/min, respiratory rate 26 breaths/min, and temperature 37.8°C. Laboratory studies revealed: white blood cell (WBC) count, 17200/uL (neutrophil-segment 89.1%); hemoglobin, 7.6 gm/dL; platelet count, 455000/uL; NT-proBNP, 6776 pg/mL; PT, 143s (INR >10); blood urea nitrogen (BUN), 33 mg/dL; creatinine, 0.77 mg/dL; Na 131 mmol/L; K 2.5, mmol/L; Ca 8.4 mg/dL; Mg, 2.4 mg/dL; and albumin 1.7 g/dL. The thyroid function tests were normal. Artery gas analysis showed hypoxia (pH, 7.4; PCO2, 36.9 mm Hg; PO2, 75.7 mm Hg; HCO3, 23.4 mmol/L; SaO2, 95%). The elevated PT and INR suggested warfarin overdose. We prescribed VitK1 1 ample per-12h and transfused frozen fresh plasma 12 units per-day. Three days later, the PT was normalized, 21s (INR2.0).
As admitted, her chest radiograph revealed cardiomegaly with pulmonary edema and blunting of the left costophrenic angle (Figure ). Echocardiography revealed normal left ventricular systolic function with an ejection fraction of 70%, dilatation of the left atrium, right ventricle, and ascending aorta, moderate tricuspid valve regurgitation, mild pulmonary, mitral, and aortic valve regurgitation, and pericardial effusion; no valvular stenosis problem was identified. Chest CT was performed in consideration of an organic lesion, such as a pulmonary embolism or malignancy. A large bulging pouch-like lesion below the aortic arch greater than 6x6 cm in size and a fluid collection in the pericardium (relative high density) was found (Figure , ). Results were consistent with a pseudoaneurysm in the aortic arch and hemorrhage into the pericardium.
Thoracic endovascular aneurysm repair (TEVAR) was successfully performed by a cardiovascular surgeon one day later. Clinical presentation including serial CXR (Figure ) and patient status showed dramatic improvement. The procedure was successful, and the patient was discharged 2 weeks later in good condition. At follow-up in the cardiovascular surgery department she remained in stable condition.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [1.7, 'g/dL'], 'Calcium': [8.4, 'mg/dL']}",10.24,9.728,10.752,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 1.7 g/dL. 
The concentration of Calcium is 8.4 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.7 g/dL)) + 8.4 mg/dL = 10.24 mg/dL.
The patient's corrected calcium concentration 10.24 mg/dL."
2641,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3354861-2,Extracted,"A 6-year-old girl presented to the Pediatric Surgery department with umbilical hernia. It was found that she also had corneal opacity. The child had growth retardation and was referred to us for endocrine evaluation. She was born at term (birth weight: 2.9 kg). There was no h/o prolonged neonatal jaundice, hoarse cry, or feeding difficulty. Umbilical hernia and recurrent rhinorrhea were present since neonatal period. Growth retardation, delayed developmental milestones, and facial dysmorphism were present from infancy. Eruption of teeth started after 1 year of age. Opacities in eye were noticed by parents in the second year. She had difficulty in speech and could speak short sentences but not clearly.
On examination, the child was short (height 85 cm; < fifth percentile; –5.15 Standard Deviation; height age 2.5 years) and had upper segment to lower segment ratio of 41:46 (short trunk dwarfism). She had a large head circumference (54 cm), coarse facial features, depressed nasal bridge, cloudy cornea, joint stiffness with flexion deformity of elbow. There was hepatosplenomegaly, umbilical hernia and mild mental retardation (Intelligence Quotient: 56.11). Slit-lamp examination confirmed corneal clouding. Hearing assessment revealed bilateral normal hearing. Other examinations revealed normal findings.
On investigation, she was found to be normoglycemic and had normal renal function (S. creatinine 0.7 mg/dl). Her other findings were as follows: Hb 11.1 gm %; S. calcium 9.1 mg/dl; S. albumin 4.0 g/dl; S. phosphorus 4.4 mg/dl; S. alkaline phosphatase 177 U/l. Arterial blood gas analysis and thyroid function tests were normal [Figures and ].
We could neither measure urinary GAG levels nor assay for α-l- iduronidase (IDUA) enzyme activity, as they are not performed at our center and are also not available at most other centers. Our diagnosis of mucopolysaccharidosis I (Hurler–Schei disease) in this case was confirmed from her history, clinical examination and skeletal survey.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.0, 'g/dL'], 'Calcium': [9.1, 'mg/dL']}",9.1,8.645,9.555,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.0 g/dL. 
The concentration of Calcium is 9.1 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.0 g/dL)) + 9.1 mg/dL = 9.1 mg/dL.
The patient's corrected calcium concentration 9.1 mg/dL."
2642,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6348891-1,Extracted,"A 63-year-old female presented with epigastric pain, loss of appetite, abdominal bloating, regurgitation, and episodic projectile vomiting of five-year duration. These symptoms were aggravated particularly after meals. Her bowel opening was normal. The patient had lost 20 kilograms over five years. The patient had a background history of hypothyroidism for which she was on thyroxine replacement therapy. She was clinically euthyroid. She had undergone a vaginal hysterectomy for uterovaginal prolapse at the age of 39 years. There was no significant family history for bowel disorders.
On physical examination, she had a body mass index of 13. She was pale. There were peripheral stigmata of chronic malnutrition and vitamin B12 deficiency. She had a distended abdomen, visible peristalsis, and hyperacute bowel sounds. There was no clinically demonstrable free fluid in the abdomen. She had anaemia (haemoglobin-8.9 g/dl, haematocrit-27.3%, mean corpuscular volume-97.4 fl, mean corpuscular haemoglobin-31.6 pg, mean corpuscular haemoglobin concentration-325 g/l, and red cell distribution width-58.4 fl), with normal platelet (402 × 103/μl) and leucocyte (8.07 × 103/μl) counts. Blood picture showed macrocytic red cells and hypersegmented neutrophils. Abnormal chemical pathological investigations comprised of elevated C-reactive protein (20.1 mg/l), hypoproteinaemia (59 g/dl), hypoalbuminaemia (25.3 g/l), hypovitaminosis B12 (160 pg/ml), and hypocholesterolaemia (total cholesterol-125.5 mg/dl, HDL-32 mg/dl, LDL-66.3 mg/dl, and triglycerides-136.4% with normal VLDL-27.2 mg/dl). Serum ionized calcium was 2.41 mmol/l. Serum iron studies favoured anaemia of chronic disease (serum iron-95 μg/dl, total iron binding capacity-138 μg/dl, iron saturation-40.8%, and ferritin-238 μg/l). She was biochemically euthyroid (TSH-4.65 mIU/l). Ultrasonography was suggestive of subacute small intestinal obstruction with distended first part of the duodenum filled with fluid. Multiple tortuous small bowel loops were noted around the pancreas with increased peristalsis. Large bowel was distended with gas. There was no bowel wall thickening, mass lesions, or free fluid in the abdomen. Computed tomography (CT) of dual slice contiguous axial sections of the abdomen obtained after intravenous, oral, and rectal contrast administrations demonstrated mild dilatation of the first and second parts of the duodenum with no evidence of significant obstruction to distal passage of oral contrast. The stomach was not distended. A focal calcification of the segment VII of the liver was noted, which was likely to be an incidental finding. There was no CT evidence of an annular pancreas or superior mesenteric artery syndrome. A spiral CT was repeated after one week. It showed markedly distended proximal bowel loops involving the duodenum and the proximal jejunum. No definite transition point was identified. There was a whirl appearance seen in the mesentery and superior mesenteric venous branches around the superior mesenteric artery raising the suspicion of a possible midgut volvulus. Mild mesenteric engorgement was also seen. No definite CT evidence of diverticuli was seen. Upper gastrointestinal (UGI) endoscopy revealed multiple duodenal diverticuli with a small hiatus hernia. Barium meal and follow-through study revealed a slightly distended duodenum without evidence of obstruction or persistent narrowing. Magnetic resonance enterography revealed multiple dilated small bowel loops with loss of valvulae in the right side of the abdomen (). There were numerous outpouchings arising from the small bowel.
However, with unexplained weight loss, we wanted to exclude a gastrointestinal malignancy and intestinal tuberculosis. We opted for laparotomy out of diagnostic laparoscopy and laparotomy. Multiple large diverticuli were noted extending from the first part of the duodenum to the proximal ileum (). Diverticuli were measuring from 0.5-12.0 cm. There was macroscopic evidence of diverticulitis. There was gross gastric dilatation. Proximal small bowel was dilated without a definitive transition point. The rest of the terminal ileum and colon were normal macroscopically. Small bowel was not surgically resected because she was not a suitable candidate for a primary anastomosis as she had nutritional deprivation and the risk of short gut syndrome. We closed the abdomen without any surgical interventions. Because of macroscopic evidence of diverticulitis, intravenous cefuroxime 750 mg 8 hourly and intravenous metronidazole 500 mg 8 hourly were administered for 7 days and were converted to oral cefuroxime 500 mg 12 hourly and oral metronidazole 400 mg 8 hourly for another 21 days. She had an uneventful postoperative period. She received complementary parenteral nutrition with amino acids, electrolytes, dextrose, and lipid injectable emulsions followed by standard polymeric formulae containing whole proteins. Soluble fibres were gradually introduced to her diet. She received a high-calorie diet, initially 125% of the daily calorie requirement followed by 150% of the daily calorie requirement after one month. Thousand international units of vitamin B12 was administered intramuscularly every other day for five days, and oral vitamin B complex 1 mg three times a day was continued for six months, with folate and micronutrient replacement. Iron-rich food and standard formulae were used to supplement micronutrients such as selenium and zinc for six months. She had a remarkable recovery with no recurrence of symptoms following 10 months follow-up.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [25.3, 'g/L'], 'Calcium': [2.41, 'mmol/L']}",10.835,10.29325,11.37675,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 25.3 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 25.3 g Albmumin/10.0 dL = 2.53 g Albmumin/dL. The concentration value of 25.3 g Albmumin/L converts to 2.53 g Albmumin/dL. 
The concentration of Calcium is 2.41 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 2.41 mmol. To convert 2.41 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 2.41 mmol Calcium * 0.001 mol/mmol = 0.00241 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00241 mol Calcium * 40.08 g/mol = 0.09659 g Calcium. To convert 0.09659 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.09659 g Calcium * 1000.0 mg/g = 96.59 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 96.59 mg Calcium/10.0 dL = 9.659 mg Calcium/dL. The concentration value of 2.41 mmol Calcium/L converts to 9.659 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.53 g/dL)) + 9.659 mg/dL = 10.835 mg/dL.
The patient's corrected calcium concentration 10.835 mg/dL."
2643,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2782212-1,Extracted,"A 48-yr old female patient was admitted to our hospital because of generalized weakness and right flank pain for several months. She was diagnosed with hypercholesterolemia by biochemical tests, and had rouleaux formations on the peripheral blood smear analysis that was done at a local private clinic (). In order to continue her further evaluation and management, she was transferred to the department of internal medicine of Gyeongsang National University Hospital. She did not complain of any other abdominal pain or tingling sensation on her extremities. According to her past medical history, she was diagnosed as autoimmune thyroiditis and primary hypothyroidism in 1992 and began to take levothyroxine 100 µg daily. However, she took the medicine irregularly and then was lost to follow-up. In 1998, she revisited the of endocrinology and metabolism outpatient department with complaints of generalized weakness and fatigue. She still had hypothyroidism as well as uncontrolled diabetes mellitus and dyslipidemia. Thereafter, she took levothyroxine 100-150 µg daily in combination with a low fat diet and regular exercise therapy. After one month, her thyroid function test revealed the following results; TSH 61.13 mU/L, total T4 61 nM/L, total T3 1.4 nM/L, total cholesterol 8.0 mM/L, triglyceride 9.6 mM/L, HDL cholesterol 0.83 mM/L, and HbA1c 6.6%. After this, she started taking simvastatin and gemfibrozil, but not oral hypoglycemic agents because at this time the fasting blood glucose level was 8.7 mM/L. Thereafter, she did not keep scheduled visit. We could not find any skin symptoms or signs from her medical record. She denied smoking or alcohol intake and took no drugs except levothyroxine irregularly. One sister among the 5 siblings in her family was diagnosed with dyslipidemia (her lipid profiles performed on December 2002 were total cholesterol 8.30 mM/L, LDL cholesterol 4.32 mM/L, HDL cholesterol 1.37 mM/L and, triglyceride 3.7 mM/L). In addition, one of the patients brother has type 2 diabetes mellitus, but he did not have the dyslipidemia.
On the physical examination, her waist circumference and hip circumference was 33 inch and 37 inch (W/H ratio, 0.87) respectively, and the body mass index (BMI) was 26.2 kg/m2. Diffuse goiter with firm consistency was palpated on her anterior neck. Her breathing was clear, and hepatosplenomegaly or tenderness was not found upon abdomen palpation. Several yellowish skin nodules were observed on both her elbows and thighs ().
On admission, her laboratory findings were as follows; hemoglobin 12.2 g/dL, RBC volume 32%, WBC 5,100/µL, platelet 210,000/µL, postprandial 2 hr blood glucose 14 mM/L, total protein 99 g/L, albumin 44 g/L, total bilirubin 13.6 µM/L, ALP 61 IU/L, AST 24 IU/L, ALT 28 IU/L, BUN 3.7 µM/L and, creatinine 97.5 µM/L. Her serum electrolytes were sodium 124.1 mM/L, potassium 3.5 mM/L, chloride 90 mM/L, calcium 2.5 mM/L, and phosphorus 0.9 mM/L. The urinalysis was normal. Lipid profiles were as follows; total cholesterol 18.1 mM/L, triglyceride 61.64 mM/L, HDL 3.0 mM/L, and LDL 2.54 mM/L. Amylase and lipase levels were normal. The thyroid function tests, determined by a radioimmunoassay method (Immunotech, A Beckman coulter company, France), revealed that she has chronic autoimmune thyroiditis and primary hypothyroidism; TSH 72.69 mU/L (normal range; 0.17-4.05 mU/L), free T4 0.22 ng/dL (normal range; 0.95-2.23 ng/dL), free T3 0.46 pg/mL (normal range; 1.60-3.80 pg/mL). Glycosylated hemoglobin A1c was 9.4%. The excreted protein amount in 24 hr collected urine was 413.7 mg/day. On the second day after admission, a creamy and clouded layer was found in her fasting whole blood that had been placed in the refrigerator for 30 min. The concentration of lipoprotein (a) measured by a rate rephelometry method (Beckman, CA, U.S.A.) was 9 mg/dL. Lipoprotein electrophoresis findings indicated that the patient had type V hyperlipoproteinemia (). Apolipoproteins determined by a single radial immunodiffusion method (Hitachi 7050 chemistry analyser, Japan) were as follows; apolipoprotein C-II 42.0 mg/dL (normal range: 1.5-3.8 mg/dL), apolipoprotein C-III 100 mg/dL (normal range: 5.4-9.0 mg/dL), and apolipoprotein E 27.0 mg/dL (normal range: 2.8-4.6 mg/dL).
We carried out urinalysis and abdominal computed tomography to evaluate her right flank pain and tenderness. Although fatty liver was observed on the abdominal computed tomography, there was no abnormality noted that could be causing pain. Consultation with the rehabilitation department concluded that the patient had fibromyalgia.
The patient was diagnosed as hypothyroidism and type 2 diabetes that presented as hyperlipidemia, and she began to take glimepiride, voglibose, levothyroxine (100 µg daily), and fenofibrate (200 mg). Also, she began to visit the rehabilitation department to help releave her pain. She was then discharged when the blood glucose level and pain have been controlled. She has visited the outpatient department for regular check-ups. She has taken fenofibrate for two months. Currently, the level of both TSH and lipid concentration in blood have returned to the normal values (). Also, the patient's yellowish skin nodules have disappeared ().","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [44.0, 'g/L'], 'Calcium': [2.5, 'mmol/L']}",9.7,9.215,10.185,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 44.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 44.0 g Albmumin/10.0 dL = 4.4 g Albmumin/dL. The concentration value of 44.0 g Albmumin/L converts to 4.4 g Albmumin/dL. 
The concentration of Calcium is 2.5 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 2.5 mmol. To convert 2.5 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 2.5 mmol Calcium * 0.001 mol/mmol = 0.0025 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.0025 mol Calcium * 40.08 g/mol = 0.1002 g Calcium. To convert 0.1002 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.1002 g Calcium * 1000.0 mg/g = 100.2 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 100.2 mg Calcium/10.0 dL = 10.02 mg Calcium/dL. The concentration value of 2.5 mmol Calcium/L converts to 10.02 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.4 g/dL)) + 10.02 mg/dL = 9.7 mg/dL.
The patient's corrected calcium concentration 9.7 mg/dL."
2644,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4897161-1,Extracted,"A 33-month-old girl presented with edema and proteinuria. Following clinical diagnosis of NS, she was treated with prednisolone (60 mg/m2/day) for 4 weeks, but NS has been persistent. When the patient was transferred to our hospital, physical examination revealed generalized edema, but no evidence of thromboembolism. Her vital signs were stable, with a blood pressure of 103/66 mmHg. Her weight was 12 kg (25th–50th percentile) and her height was 91 cm (25th–50th percentile). Laboratory studies revealed a white blood cell count of 8.38×109/L, hemoglobin level of 15.9 g/dL, hematocrit level of 46.1%, and platelet count of 284×109/L. Biochemistry showed the following: total protein, 5 g/dL; albumin 2.5 g/dL; total cholesterol, 235 g/dL; blood urea nitrogen, 11 mg/dL; creatinine, 0.3 mg/dL; calcium, 8.7 mg/dL; phosphorus, 5.7 mg/dL, and normal electrolyte level. Prothrombin time and activated partial thromboplastin time were both within normal range. Urinalysis revealed proteinuria of 4+ and the spot urine protein-to-creatinine ratio was 31.23 g/g Cr. Test results for antinuclear antibody and antineutrophil cytoplasmic antibody were negative, and the IgG, IgA, and IgM levels were 391.0 mg/dL, 82.0 mg/dL, and 142.0 mg/dL, respectively. Ultrasonography revealed normal-sized kidneys with diffuse increased renal parenchymal echogenicity. Renal biopsy revealed a collapsing variant of focal segmental glomerulosclerosis (FSGS) ().
To manage the patient's steroid-resistant NS, high-dose intravenous methylprednisolone (MP) pulse therapy at a dose of 30 mg/kg was administered every 2 days. Angiotensin-converting enzyme inhibitor and intermittent albumin replacement followed by diuretics were also prescribed. After the first dose of MP, she complained of intermittent left lower leg pain, which was assumed to be a side effect of MP. After the third round of MP, her lower leg pain became continuous, progressed to both legs, and caused her to stop walking. The skin on the dorsum of her feet was pale and cold and capillary refill was slow. The dorsalis pedis pulse, posterior tibialis pulse, and popliteal pulse were palpable but not strong. Emergency Doppler ultrasonography of her lower extremities revealed turbulent flow in both her femoral and popliteal arteries. Magnetic resonance angiography showed multifocal segmental luminal occlusion of the common iliac arteries, external iliac arteries, and popliteal arteries (). The lumen of the common femoral arteries and superficial femoral arteries were relatively patent with distal flow reconstitution. The hemostasis study was as follows: thrombin time, 19.9 seconds (control, 17.0 seconds); fibrinogen, 362 mg/dL (reference, 180–380 mg/dL); D-dimer, 0.48 µg/mL (reference, 0–0.4 µg/mL); plasminogen activator, 86% (reference, 70%–140%); factor VIII, 214% (reference, 52%–190%); antithrombin (AT)-III activity, 91% (reference, 80%–120%); protein C, 243% (reference, 70%–140%); and protein S, 97% (reference, 65%–116%). Test results for anticardiolipin and anti-β2-glycoprotein-I antibodies were all negative. The factor V Leiden (1691G>A) mutation was absent.
TEC was suspected, and MP pulse therapy was discontinued and heparinization started, followed by mechanical thrombectomy of both iliac arteries and popliteal arteries using Forgarty balloon catheters. Thrombus cultures were obtained during mechanical thrombectomy despite the absence of clinical infection. Staphylococcus hominis subspecies hominis (S. hominis subsp. hominis) was isolated, which was found to be ampicillin-resistant and vancomycin-susceptible. Since peripheral blood culture results were negative, systemic antibiotics were not administered. Anticoagulant treatment was continued for 8 months with warfarin. Two months later, a follow-up Doppler ultrasonography of her lower extremities showed patent lumen and intact flow patterns in the common femoral arteries, superficial femoral arteries, and popliteal arteries. The severity of proteinuria, which was consistent with NS, persisted despite various combinations of oral steroids, cyclosporine A, tacrolimus, and rituximab. The patient's renal function deteriorated and progressed to end-stage renal failure, and renal replacement therapy of peritoneal dialysis was started 22 months after TEC onset.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.5, 'g/dL'], 'Calcium': [8.7, 'mg/dL']}",9.9,9.405,10.395,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.5 g/dL. 
The concentration of Calcium is 8.7 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.5 g/dL)) + 8.7 mg/dL = 9.9 mg/dL.
The patient's corrected calcium concentration 9.9 mg/dL."
2645,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2559825-1,Extracted,"A 2 year and 11-month-old mestizo boy was admitted to the Hospital Infantil del Estado de Sonora (Children Hospital of Sonora State, Mexico) with muscle cramps, fine tremors on hands and feet for the last 2 days. His mother reported chronic diarrhea for the last year with 6 hospitalizations because of diarrhea and dehydration. During physical examination, upper abdominal distention was observed (Figure ), in addition to hypotrophic arms and legs and positive Chvostek's and Trousseau's signs. His weight and height were less than the fifth percentile for his age.
Blood count showed hemoglobin 101 g/L, white blood cells 8500/mmc, platelets 472,000/mmc, GVS 26 mm/h and reticulocytes 3%. Microcytic and hypochromic anemia was evident, with hematocrit 30%, mean globular volume 73 fL, serum iron 41 μg/dL and ferritin under 5 μg/L. Serum laboratory tests revealed hypocalcemia with total calcium of 5.7 mg/dL, sodium 133 mEq/L, potassium 3.2 mEq/L, chloride 103 mEq/L, glucose 82 mg/dL, AST 71 U/L, ALT 44 U/L, albumin 2.5 g/L, and C-reactive protein 0.5 mg/L. Billirubins, urine examination, and serial stool analyses for infectious etiologies, were negative.
The patient's tetany resolved after replacement of calcium and additional analyses were performed. IgA and IgG anti-gliadin antibodies as well as IgA anti-transglutaminase were positive, with index values of 3.5, 35.7 and 26.8, respectively. Index value was defined as the ratio of the absorbance of the test serum divided by the cut-off value []. Additionally, there was IgA reactivity to maize prolamins (zeins). The diagnosis of CD was confirmed by inflammatory cells infiltrate in the small intestinal mucosa and lymphocytes in the surface epithelium on duodenal biopsy, in a Marsh IIa/IIb classification (Figure ). After initiation of a gluten-free diet and lactose-free milk (at the beginning), mineral and vitamins supplements, the patient's symptoms completely resolved within 6 weeks. The clinical and nutritional response to the gluten-free diet was excellent. In a 2-month follow-up period, he presented normal blood counts and serum biochemical analyses. Additionally, his weight and height were in the 75 percentile for his age, antibodies titers were normal and there were no further episodes of tetany or diarrhea over 4 years follow up period.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.5, 'g/L'], 'Calcium': [5.7, 'mg/dL']}",8.7,8.265,9.135,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.5 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 2.5 g Albmumin/10.0 dL = 0.25 g Albmumin/dL. The concentration value of 2.5 g Albmumin/L converts to 0.25 g Albmumin/dL. 
The concentration of Calcium is 5.7 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 0.25 g/dL)) + 5.7 mg/dL = 8.7 mg/dL.
The patient's corrected calcium concentration 8.7 mg/dL."
2646,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4258353-1,Extracted,"A 66-year-old man was diagnosed 28 years ago to have diffuse scleroderma which manifested as diffuse skin tightness, telangiectasias, dysphagia, arthralgias, and Raynaud's phenomena. Disease had been quiet over many years with no worsening in any of his symptoms and no evidence of cardiac, pulmonary, or renal involvement. Thus, the patient was not receiving any specific treatment for scleroderma.
Few months prior to presentation, patient noticed change in his condition with fatigue, weight loss (20 kilograms in 4 months), and generalized feeling of not being well. At that time, patient did not seek any medical attention. Two weeks before presentation, patient developed progressive abdominal distention resulting in significant discomfort. Medical evaluation at presentation revealed normal vital signs, palor, and fluid in the abdomen, in addition to the findings of chronic scleroderma (diffuse tight skin, fish mouth appearance, and telangiectasias). There were no palpable masses or enlarged lymph nodes. Lungs were clear, heart exam was within normal limits with no murmurs or rubs, and there was no evidence of peripheral edema.
Patient underwent abdominal fluid tap. A sample of the ascitic fluid was sent for analysis. It revealed inflammatory cells with no suspicious malignant cells. Two weeks later, ascites recurred. At that time, patient was admitted to the hospital for full workup. Complete blood count revealed anemia with hemoglobin 10.9 g/dL and borderline white blood cell count (4.4 × 103/µL) and platelet count (176000/µL). Lab tests also revealed hypercalcemia (10.3 mg/dL) with low albumin (31 g/L) and elevated globulin (50 g/L) levels. Thyroid function tests were normal. Renal parameters were also within normal limits. Patient underwent Echocardiography to assess cardiac function and rule out heart disease as the cause of ascites. Echocardiography revealed mild concentric hypertrophy, mild mitral valve and tricuspid valve regurgitation, and a mean pulmonary artery pressure of 35 mm Hg. Computed tomography of the chest, abdomen, and pelvis, performed to screen for malignancy, revealed marked abdominal and pelvic ascites with no masses or enlarged lymph nodes. Ascitic tap was repeated and fluid was sent again for analysis. Results revealed inflammatory cells with no malignant cells and negative culture results. Patient was started on spironolactone 50 milligrams daily and furosemide 40 milligrams daily.
Multiple myeloma was suspected based on anemia, hypercalcemia, and hyperglobulinemia, in addition to symptoms of weight loss and fatigue. Protein electrophoresis was done and showed monoclonal gammopathy. Immunofixation revealed IgA kappa pattern (). Results of bone marrow biopsy revealed 45% plasma cells. Immunohistochemistry studies revealed a pattern consistent with multiple myeloma (strong expression of CD 138 in tumor cells).
A diagnosis of multiple myeloma was thus established. Further studies were obtained for disease staging. Beta-2-microglobulin level was 7.9 mg/L. X-ray skeletal series revealed osteopenia but no lytic lesions. Magnetic resonance imaging (MRI) of the abdomen, performed to assess the liver and spleen, failed to demonstrate any evidence of extramedullary hematopoiesis and thus failed to provide a clear explanation for ascites in this patient.
Patient was started on chemotherapy (Bortezomib, dexamethasone, and zoledronic acid). After six cycles of treatment, there was a major improvement in his disease condition with amelioration of anemia and normalization of globulin levels. Patient continued to have abdominal and pelvic fluid collection. However, the time interval separating the required abdominocentesis procedures increased gradually from around two weeks to around four weeks, suggesting a decrease in the quantity and rate of fluid collection. No change was noted in his scleroderma symptoms, neither worsening nor improvement.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [10.3, 'mg/dL'], 'Albumin': [31.0, 'g/L']}",11.02,10.469,11.571,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 31.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 31.0 g Albmumin/10.0 dL = 3.1 g Albmumin/dL. The concentration value of 31.0 g Albmumin/L converts to 3.1 g Albmumin/dL. 
The concentration of Calcium is 10.3 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.1 g/dL)) + 10.3 mg/dL = 11.02 mg/dL.
The patient's corrected calcium concentration 11.02 mg/dL."
2647,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2775026-1,Extracted,"A 77-year-old Caucasian man with a history of type II diabetes and hypertension presented with confusion. Other symptoms included general fatigue, anorexia, weight loss, nausea and occasional vomiting that extended over a period of 2 months. He was afebrile and physical examination revealed an enlarged non-tender liver with an irregular border. Blood tests showed a white blood cell count of 14470 K/μl, Neu 82%, urea 100 mg/dl (normal range, 17-50), creatinine 1.4 mg/dl (normal range, 0.7-1.4), calcium 12.6 mg/dl (normal range, 8.6-10.2), phosphorus 2.9 mg/dl (normal range, 2.7-4.5), albumin 3.6 g/dl (normal range, 3.5-5.5), aspartate aminotransferase (SGOT) 77 U/L (normal range, 5-40), alanine aminotransferase (SGPT) 49 U/L (normal range, 5-40), alkaline phosphatase (ALP) 563 U/L (normal range, 64-280), gamma-glutamyl transferase (γGT) 500 U/L (normal range, 11-49), and plasma ammonia 44 μg/dl (normal range, < 75). The rest of blood routine biochemistry was unremarkable. Parathyroid hormone (PTH) was suppressed at 1.55 pg/dl (normal range, 8-76) and carcinoembryonic antigen 19-9 (CA 19-9) was elevated at 223 U/ml (normal range, <37). Computer tomography (CT) revealed a large multinodular mass in the right lobe of the liver consistent with neoplastic disease (Figure ) and smaller nodules in the right lung. Brain CT was normal, bone scan with 99mTc-MDP showed no evidence of metastatic bone disease, and parathyroid scan with 99mTc-MIBI double phase was unremarkable. A liver surgical biopsy confirmed the diagnosis of CC (Figure ). Neoplastic cells stained positively for cytokeratin 7 and 19.
The patient was treated with intravenous hydration, furosemide, ibandronate, and calcitonin, with calcium levels and consciousness state normalizing within 48 hours. He declined chemotherapy and was discharged home, from where he was readmitted 4 weeks later with relapsed hypercalcemia and progressively worsening confusion. A repeat CT scan showed significant expansion of the liver mass. Treatment of hypercalcemia resulted again in rapid restoration of his consciousness level. However, overall prognosis was poor and the patient died due to progressive disease within 3 months of diagnosis.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.6, 'g/dL'], 'Calcium': [12.6, 'mg/dL']}",12.92,12.274,13.566,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.6 g/dL. 
The concentration of Calcium is 12.6 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.6 g/dL)) + 12.6 mg/dL = 12.92 mg/dL.
The patient's corrected calcium concentration 12.92 mg/dL."
2648,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3063533-1,Extracted,"The patient, a 55 yr old female with Type 2 diabetes mellitus for the last 14 years, on insulin for 2 years, pre-sented with the complaint of sudden onset weakness of all four limbs for five days. She had a preceding history of severe muscle cramps and paraesthesia for about a month. History revealed that the patient had severe generalised weakness twenty days back, for which she had been admitted in a local hospital and had improved symptomatically (though some amount of muscle pain persisted) with intravenous fluid and injectable medications, the details of which could not be gathered. The onset of quadriparesis was acute, noticed on getting up in the morning, five days prior to admission in our institute. There was no history of unusually high carbohy-drate intake, cold exposure, excessive exertion or alcohol intake the previous night. She denied unexplained sweating, tremors, heat intolerance, prolonged vomiting, or any drug intake over a prolonged period of time. General examination revealed carpopedal spasm, hypertension(160/100 mm Hg) and mild pallor. Neurological examination revealed bilater-ally symmetrical weakness (Gr 1/5) of all four limbs and generalized hyporeflexia. Muscles of the eyes, face, tongue, pharynx, larynx, diaphragm and sphincters were not involved. Higher functions, cranial nerves and sensory system were intact. Plantar was bilaterally flexor. Apart from mild hepatomegaly, systemic examination was normal.
Investigations revealed hypokalemia(1.3 mEq/l), hypocalcemia (corrected 5.8 mg/dl) and hypomagnesemia (1.1 mg/dl) with normal sodium and chloride levels. Routine blood examination was normal. Fasting and post prandial plasma glucose was 171mg/dl and 309mg/dl respectively with an HBA1c of 9.5%. Serum osmolality was normal.
Urinary ketones were negative. Liver function tests were slightly deranged with AST of 71 mg/dl and ALT of 186 mg/dl. Serum protein was 7.09mg/dl, albumin - 3.2 mg/dl, globulin - 3.8mg/dl, serum bilirubin -0.5mg/dl. Serum creatinine was 1.l mg/dl and microalbuminuria was present. CPK and LDH were within normal limits. Thyroid profile was normal. Serum phosphorus was normal and PTH was 50.3 pg/ml(normal–10 to 55 pg/ml). 24 hour urinary calcium was 61mg (normal - 100 to 300mg/24hrs). Urinary potas-sium excretion was 53 mEq/L /day (normal-25-120 mEq/L/day). Blood gas analysis revealed metabolic alkalosis. Electrocardiogram, ultrasound abdomen, plain picture abdomen, X-ray cervical spine and chest X-ray were normal. MRI of brain, spine and abdomen were also normal.
Initially, the patient was treated with injectable potas-sium, magnesium and calcium preparations. Normalization of serum potassium and calcium was achieved only after total correction of magnesium level. There was gradual improve-ment in muscle power after 24 hours of therapy. Complete recovery was achieved after five days of treatment, following which she was shifted to oral preparations. Glycemic control was achieved using insulin and hypertension was controlled with Amlodepin 5 mg. She was discharged after two weeks on oral calcium(l gm daily) and advised to take diet rich in potassium and magnesium. On subsequent follow up at one and three months, she was asymptomatic with normal electrolyte levels and good glycemic control.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [5.8, 'mg/dL'], 'Albumin': [3.2, 'g/dL']}",6.44,6.118,6.762,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.2 g/dL. 
The concentration of Calcium is 5.8 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.2 g/dL)) + 5.8 mg/dL = 6.44 mg/dL.
The patient's corrected calcium concentration 6.44 mg/dL."
2649,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2803990-1,Extracted,"A 46-year-old Kirghiz female was admitted with the previous diagnosis of seronegative arthritis and inflammatory bowel disease. Various nonsteroidal anti-inflammatory drugs, prednisone, sulfasalazine, and two courses of anti-TNF alpha were prescribed earlier by her physician for symptomatic treatment.
At admission to our clinic, she presented with depressive symptoms and anxiety. She complained of weight loss (loss of 15 kg over a period of 1 to 2 months), diarrhea, weakness, and fatigue. She was severely cachexic with a significantly lower BMI (12.11 kg/m2). Physical examination revealed bilateral swelling of knee joints, skin rashes over the lower legs and the presence of pitting after applying pressure to pretibial areas. Movements of involved joints were painless and there was no definite restriction in the range of movements. The liver was palpated 1 cm below the costal margin in the right upper quadrant. Splenomegaly and enlargement of lymph nodes were not noticed.
Complete blood count at admission showed the following values: Hb: 11.2 g/dL, Hct: 32.6%, WBC: 7.500/mm3, Plt: 351.000/mm3. The erythrocyte sedimentation rate was 4 mm/h, and the level of C-reactive protein was 13.6 mg/L. The routine biochemical tests revealed hyponatremia (126,6 mmol/L, normal: 135-145), hypokalemia (2.59 mmol/L, normal: 3.5-5.5), low ionized calcium (3.18 mg/dL, normal: 4.2-5.4), magnesium (1.37 mg/dL, normal: 1.9-2.7) and phosphate concentrations (1.2 mg/dL, normal: 2.6-4.5), severe hypoproteinemia (4.78 g/dL, normal: 6.4-8.3), hypoalbuminemia (1.2 g/dL, normal: 3.5-5.5), elevated levels of alkaline phosphatase (298 U/L, normal: 38-155) and gammaglutamyl transpeptidase (127 U/L, normal: 7-32). The other biochemical results were within normal limits and routine urine examination was normal. The patient had a 24-hour urinary protein collection, which showed a 24-hour protein measurement of 67.50 mg. This was confirmed on a repeat sample. Thyroid function tests showed FT3 level of 0.62 pg/mL at the lower limit of the normal range (normal: 0.60-1.95), decreased FT4 level of 4.40 ng/dL (normal: 5.00-11.50) and normal TSH concentration of 1.14 μIU/mL (normal: 0.30-4.00). The concentrations of PTH (230 pg/mL, normal: 10-65) and 25-hydroxyvitamin D (4 ng/mL, normal: 10-40) were also measured. Electrophoresis of alkaline phosphatase isoenzymes revealed elevated levels of liver isoenzyme. To view the status of hypothalamic-pituitary-adrenal function synachten test was performed, which excluded the possibility of adrenal insufficiency. The serological tests for various infectious agents (HBsAg, anti HBC, anti HIV 1+2, Treponemal tests, Brucella Ig G/M antibody levels, TORCH titers) were found to be negative. Ig G, A, M levels were within normal limits. AMA, c-ANCA, p-ANCA, anti-LKM-1 were not detected. She was found to have positive ANA in a titer of 1/80 with granular and homogeneous pattern. Positive IgA endomysial antibody (1/80 titer) and IgG antigliaden antibody (98.50 RU/ml) levels were also detected.
Radiographs of involved joints revealed no evidence of bony erosions, chondrocalcinosis or deformity. Findings on electrocardiogram, echocardiogram, and chest radiograph, and magnetic resonance cholangiopancreatography images were all normal. Abdominal ultrasonography displayed enlarged liver (155 mm in maximum cranial-caudal extent) and increased echogenicity of the liver parenchyma (Grade 1). On thoracoabdominopelvic computed tomographic examination multiple mesenteric lymph nodes, with a largest diameter of 18 × 10 mm, were detected. DEXA scan of the lumbar spine and right hip showed low bone mineral density (BMD) with a total T score of - 5.7 and 4.9, respectively.
To examine the upper part of the gastrointestinal system esophagogastroduodenoscopy was done, which revealed grade 1 esophagitis, hypotonic LES, gastritis, erosive bulbitis and hyperemia in the postbulbar duodenum. To confirm the initial diagnosis of inflammatory bowel disease colonoscopy was performed. Findings other than nonspecific hyperemia of the ileal mucosa were not present. Multiple biopsies were obtained from both upper and lower gastrointestinal tract at the time of endoscopic evaluation. CD was histologically confirmed by duodenal biopsies, which revealed total villous atrophy of duodenal mucosa and regenerative hyperplasia. Increased cellularity of plasma cells and lymphocytes in the lamina propria and surface epithelium were observed. Histological examination of the excised tissue also revealed amorphous eosinophilic deposition in the lamina propria and in the wall of some vessels and glands, which was previously found typical for amyloid (Figure ). However, congo-red and crystal violet staining prosedures and immunohistochemical studies showed no amyloid protein. Neither kappa nor lambda monoclonality was detected in lymphoplasmocytoid cells, immunohistochemically. Loose light-green staining of the deposition by trichrome staining was the unique positive finding (Figure ). In the light of these findings, collagenous sprue due to long-standing celiac disease was the last diagnosis, histologically. Specimens obtained from terminal ileum revealed chronic inflammation and subtotal villous atrophy of ileal mucosa.
Our patient suffered from anorexia and poor oral intake. To increase caloric intake to gain weight total parenteral nutrition was administered by cyclic infusions. After several days diarrhea improved. She was asked to avoid taking gluten and her complaints abated and did not persist.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [1.2, 'g/dL'], 'Calcium': [3.18, 'mg/dL']}",5.42,5.149,5.691,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 1.2 g/dL. 
The concentration of Calcium is 3.18 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.2 g/dL)) + 3.18 mg/dL = 5.42 mg/dL.
The patient's corrected calcium concentration 5.42 mg/dL."
2650,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2728607-1,Extracted,"Ms. JB, a 66-year-old Caucasian woman, was admitted to our inpatient geriatric psychiatry unit from her long term care (LTC) facility because of behavioral disturbances associated with her dementing illness. She was resistant to care, was having persistent vocalization, and was hallucinating. Functionally, she required full assistance with all her ADLs. Her past medical history included early-onset dementia of Alzheimer's type, severe, hyperlipidemia, hypertension, and dysphagia. The patient did not have a history of psychiatric illness including anxiety, psychosis, substance abuse, or psychiatric hospitalizations.
Her medications at admission to our unit were multivitamins, citalopram 20 mg po daily, simvastatin 40 mg po daily, Vitamin D3 1000 IU po daily, calcium carbonate 600 mg po bid, valproic acid sprinkles 375 mg po twice daily, docusate 100 mg po twice daily, and risperidone 0.5 mg po twice daily.
Our review of record, indicates that the patient was being treated with citalopram, valproic acid sprinkles, and risperidone for the behavioral disturbances associated with her dementia. It is unclear exactly as to when the valproic acid sprinkles was started, but it appears that the patient was taking this drug for at least the last month prior to her hospitalization.
On admission examination, the patient was noted to be perseveratively calling out and crying. Her vital signs were stable, and she was uncooperative to the examination. She was underweight, at 66 inches in height, 99 lbs in weight, and body mass index (BMI) = 16 kg/m2. Despite her history of hypertension, her blood pressure (BP) on admission was low at 96/57 mm hg. She was noted to have a dysconjugate gaze. She had marked jerking movements of her upper extremities consistent with myoclonus. Muscle tone was increased, and it was difficult to assess for cogwheeling, as patient was unable to voluntarily relax her extremities. Myoclonus in her lower extremities was also noted when her feet were dorsiflexed. She was disoriented to time, place, and person and was unable to participate in a formal cognitive testing.
Laboratory examination on admission revealed a low serum albumin of 3.4 gm/dL. Her ammonia level was low normal at 4 umol/L. Her valproic acid level was 39 mg/L, a level generally considered to be subtherapeutic for patients with seizure disorders. Sodium was 143 meq/L, potassium was 3.7 meq/L, chloride was 104 meq/L, bicarbonate was 33 meq/L, blood urea nitrogen (BUN) was 12 mg/dL, serum creatinine was 0.7 mg/dL, glucose was 91 mg/dL, serum calcium was 8.5 mg/dL, aspartate transamisase (AST) was 7 iu/L, and alanine transaminase (ALT) was 21 iu/L. Vitamin B12, folate, and thyroid stimulating hormone (TSH) levels were normal. Urinalysis was unremarkable. Complete blood count (CBC) was normal with a white cell count of 8100/cmm, a hemoglobin level of 13.7 gm/dL, and a hematocrit of 41.2%.
Following the initial evaluation, the VPA dose was decreased and then discontinued, with complete resolution of her myoclonus. Quetiapine was started and titrated to 25 mg po at noon and 12.5 mg po at 5 pm for agitation. Because of her late afternoon agitation, risperidone 0.5 mg was increased from twice a day to 0.5 mg po three times a day, with the additional dose given in the early afternoon. Her restlessness, agitation, vocalizations, hallucinations and resistance to care were significantly decreased from admission on this medication regimen. She was discharged back to her long term care facility in a stable state.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.4, 'g/dL'], 'Calcium': [8.5, 'mg/dL']}",8.98,8.531,9.429,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.4 g/dL. 
The concentration of Calcium is 8.5 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.4 g/dL)) + 8.5 mg/dL = 8.98 mg/dL.
The patient's corrected calcium concentration 8.98 mg/dL."
2651,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3741976-1,Extracted,"A 51-year-old male was admitted to the local hospital after a hump-nosed viper bite on his hand while weeding his garden. Since the viper was brought alive by the neighbors, primary care physician was able to make a positive identification of the snake as Merrem's hump-nosed viper (Hypnale hypnale). The patient had severe pain and swelling in the hand. The next day his urine output was reduced and he was transferred to a tertiary care institute for hemodialysis. On admission, patient was conscious and rational, febrile, and he was in pain. He was pale and mildly icteric. He had marked swelling and redness in his right hand with blistering at the bite site.
His pulse rate was 92 beats per minute and blood pressure was 118/78 mmHg. On auscultation of the heart, S1 and S2 were heard in normal intensity with no murmurs. Respiratory system examination was normal except for few fine basal crepitations. Abdominal examination was normal with no organ enlargement or free fluid. Neurological examination was normal with no ophthalmoplegia or other cranial nerve paralysis.
His investigation results were as follows: white cell count, 12,700 (80% neutrophils); platelet count, 40,000/μl; hemoglobin, 9.9 g/dl; International normalized ratio, 1.46; activated partial thromboplastin time, 43 s; serum creatinine, 1,040 μmol/l; Na, +130 mmol/l; K+, 5.4 mmol/l; erythrocyte sedimentation rate, 10 mm/Hr; C-reactive protein, 1 mg/L; aspartate transaminase, 54 u/l; alanine transaminase, 42 u/l; serum bilirubin, 22.7 μmol/l; total protein, 52 g/l (albumin 33 g/l). Peripheral blood smear revealed marked red cell fragmentation, polychromasia and reduced number of platelets indicating disseminated intravascular coagulation. Serum calcium, 7.7 mg/dl; serum phosphate, 3.1 mg/dl; creatine phosphokinase, 122 u/l; urine microscopy showing 10-12 pus cells and 1-2 red cells per high power field with no casts. Protein was present in urine in trace amounts. Abdominal ultrasound scan revealed enlarged and globular kidneys suggestive of acute renal parenchymal disease. Venom-induced acute tubular necrosis was suspected.
He was commenced on hemodialysis. After 12 sessions of hemodialysis, he was dialysis dependent and renal biopsy was performed 8 weeks after the viper bite. The biopsy revealed patchy areas of tubular atrophy with interstitial edema and patchy interstitial chronic inflammation suggesting subacute interstitial nephritis. There was no evidence of acute tubular necrosis possibly because biopsy was performed very late after the onset of AKI. Glomeruli were normal.
Ten weeks after the viper bite, the patient's renal functions and urine output were improved. He was discharged from the hospital to be reviewed in clinic as an outpatient. At the time of discharge, he had a serum creatinine of 1.9 mg/dl and serum potassium of 3.9 mmol/l.
Eighteen weeks after the initial viper bite, he was admitted with sudden onset bilateral lower limb weakness. There was no respiratory muscle paralysis. Both lower limbs had grade two muscle power and upper limbs grade four. Reflexes were diminished and Babinski sign was negative. There was no objective sensory loss.
During this admission, he was found to have acidotic breathing. Arterial pH was 7.31 and PCO2 18 mmHg, PO2 121 mmHg, and HCO3
− 10.3 mmol/l. His serum potassium level was 7.0 mmol/l with sodium 130 mmol/l and chloride 114 mmol/l. ECG showed tall tented T waves suggestive of hyperkalemia. Serum creatinine was 114 μmol/l with an estimated glomerular filtration rate of 76 ml/min. He was given intravenous calcium gluconate, nebulized with salbutamol and started on insulin-dextrose infusion until an urgent hemodialysis was arranged. There was no history of use of angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), or diuretics like spironolactone.
Blood anion gap was normal at 5.7 mmol/l. Urine pH was 5.0. Urinary electrolytes were as follows: Na+ 77 mmol/l, K+ 16 mmol/l, Cl− 84 mmol/l, pH 5.0, serum osmolality 300 mosm/kg, urine osmolality 380 mosm/kg, and urinary anion gap was 9 mmol/l. Transtubular potassium gradient (TTKG) was 1.80.
Presence of hyperchloremic metabolic acidosis and hyperkalemia with normal serum creatinine level was suggestive of type IV renal tubular acidosis. The ability to lower the urine pH to 5.0, positive urinary anion gap, and the low TTKG (less than five) were all supportive evidence for type 4 renal tubular acidosis.
Patient had a good response to fludrocortisone 100 μg twice daily with the correction of hyperkalemia and the metabolic acidosis. He was discharged while on fludrocortisone with serum potassium of 4.3 mmol/l. Three weeks later, fludrocortisone was stopped as serum potassium was 3.5 mmol/l and he was closely observed for the development of hyperkalemia or acidosis. Eight weeks after discharge, he had potassium of 4.2 mmol/l without any potassium-lowering drug therapy.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [33.0, 'g/L'], 'Calcium': [7.7, 'mg/dL']}",8.26,7.847,8.673,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 33.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 33.0 g Albmumin/10.0 dL = 3.3 g Albmumin/dL. The concentration value of 33.0 g Albmumin/L converts to 3.3 g Albmumin/dL. 
The concentration of Calcium is 7.7 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.3 g/dL)) + 7.7 mg/dL = 8.26 mg/dL.
The patient's corrected calcium concentration 8.26 mg/dL."
2652,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6696828-1,Extracted,"A 3-year-old African-American boy presented to the emergency department with his mother for complaints of decreased urine output, decreased intake of both solids and liquids, and increased fussiness for 2 weeks. The patient had also been vomiting and refusing to walk for 3–4 days. During the earlier portion of this 2-week illness, the patient did have rhinorrhea and cough which had resolved upon this visit. Prior to this emergency department visit, over the last 14 days, the patient had been diagnosed with viral illness and thrush, having been treated with intravenous fluids and nystatin upon two different visits to our emergency department and a local urgent care. The mother denied any fever, rash, or diarrhea in the child over the last several weeks. His only known sick contact was an older brother with recent rhinorrhea and cough.
Significant medical, psychiatric, and surgical history for this child included ASD without any development of spoken language to this point, hydronephrosis with bilateral ureteropelvic junction repairs, and intra-abdominal tests with bilateral orchiopexy. Immunizations were up to date, no routine medications were given to the patient, and family history was noncontributory. The boy lived at home with his mother and three siblings, and there was no concern for abuse, neglect, or exposure to drugs and alcohol in the home. His mother was particularly concerned that recent decreased urine output may be related to his history of hydronephrosis, prompting her to bring him to the emergency room again.
In the emergency department, the patient was ill-appearing on examination with dry oral mucosa and hypoactive bowel sounds. However, he had an otherwise normal physical examination, was not in any acute distress, and had normal vital signs. He was given two boluses of normal saline causing spontaneous urine output. An electrolyte panel was obtained showing low calcium at 6.0 mg/dL, low K+ at 2.9 mg/dL, and low albumin at 3.2 mg/dL. Alkaline phosphatase was elevated at 644. The patient was admitted to the children’s hospital and treated with fluids including potassium and calcium replacement overnight. Other laboratory tests obtained in the emergency department were normal including viral panel, blood cultures, complete blood count, C-reactive protein, urinalysis, and additional electrolytes.
On day 2, vitamin D and parathyroid hormone (PTH) levels were obtained and found to be critically abnormal with a vitamin D level of 7.6 ng/mL (normal 20–100 ng/mL) and a PTH of 912 (normal 8–97). Urine calcium was also obtained and found to be low at less than 5 mg/dL. X-rays of the patient’s wrists were obtained () and showed radial and ulnar metaphyseal fraying and cupping suggestive of rickets. Chest films were within normal limits. Given the patients symptoms including refusal to walk, labs including low vitamin D, serum calcium, urine calcium and high PTH, and the patient’s wrist films, he was diagnosed with hypocalcemic rickets secondary to malnutrition. His mother endorsed extremely picky eating since beginning table food as an infant, often having extreme difficulty convincing him to eat anything other than crackers, potatoes, and juice. Renal disease was deemed less likely to be the cause of his acute illness as a renal ultrasound showing stable hydronephrosis was obtained along with normal creatinine and urine output once fluids were administered.
During the remaining week-long hospitalization, the patient’s electrolytes and vitamin D levels were trended and he received supplementation of fluids, calcium, vitamin D, magnesium, and eventually protein via total parenteral nutrition (TPN) once it was felt his electrolytes were stable. He was discharged home with continued calcium carbonate (1000 mg twice daily) and vitamin D (4000 IU daily) supplementation and instructed to follow-up with his outside primary care provider and endocrinologist.
One month after discharge, our team followed up with the mother and patient. He had continued taking vitamin D and calcium supplements at prescribed doses. His protein intake had increased as his electrolytes continued to normalize. To our surprise, our patient’s symptoms of autism spectrum disorder had also improved. Prior to supplementation, at the time of diagnosis, the patient had 18 failed Modified Checklist for Autism in Toddlers (M-CHAT) items, with only 8 failed items following treatment of rickets. The patient had also begun speaking 3–4 words as opposed to biting and scratching to communicate. He had returned to not only walking but also began running. Previously, he had not interacted with other children. He had begun interacting and playing with his siblings and their friends. The patient did not begin a new therapy regimen during this time or have any significant life changes outside of improved nourishment that would explain the improvement in his social responsiveness and other symptoms of ASD.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.2, 'g/dL'], 'Calcium': [6.0, 'mg/dL']}",6.64,6.308,6.972,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.2 g/dL. 
The concentration of Calcium is 6.0 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.2 g/dL)) + 6.0 mg/dL = 6.64 mg/dL.
The patient's corrected calcium concentration 6.64 mg/dL."
2653,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7569613-1,Extracted,"A 60 years old Caucasian woman was admitted to the Emergency Department of our Hospital because of ascites and abdominalgia. Twenty years earlier she was diagnosed with breast cancer, subjected to mastectomy and then treated with several chemotherapy lines, including the inhibitor of vascular endothelial growth factor A Bevacizumab, hormonal therapy and local radiotherapy. About 5 months before the admission, she developed seizures and sudden cognitive impairment, with loss of contact: a MRI revealed cranial and cerebral metastasis. An antiepileptic drug Levetiracetam was started as well panencephalic radiotherapy was given for five days. Chemotherapy was also administered with resolution of symptoms and regression of metastasis. One month before the hospitalization, she developed lower limb deep vein thrombosis, so she started fondaparinux as anticoagulation therapy. The patient continued its oncological follow-up schedule of a stage IV breast cancer, with multiple liver, pleural, pulmonary and bone metastasis, treated with Palbociclib, anti-CDK4 and 6 antagonist and Fulvestrant, an estrogen receptor antagonist. At two follow-up visits during the 4 weeks prior to admission to the Emergency Department because of low circulating serum magnesium levels, magnesium and potassium salts supplementation was reported and then suspended due to the appearance of abdominal pain. She was sent to the Emergency department by the oncologist because of abdominalgia associated to nausea and vomiting. She has been treated with a proton pump inhibitor for at least 6 months because of heartburn, regurgitation, and symptoms related to gastroesophageal reflux disease. An abdominal ultrasound highlighted abundant ascites. She was vigilant and collaborating, without alteration on neurological exam. Her vital parameters were normal, and laboratory tests showed mild anemia (Hemoglobin 10.6 g/dl, hematocrit 32%), no renal (creatinine 0.4 mg/dL) or hepatic (GOT 21 U/L; GPT 13 U/L; total bilirubin 0.4 mg/dL, albumin 3.2 g/dL) impairment and a moderate increase in C reactive protein (63 mg/L; normal values < 5 mg/L). Plasma sodium (135 mEq/L), potassium (3.9 mEq/L), chloride (98 mEq/L), calcium (8.2 mg/dL) and phosphate (4.0 mg/dL) concentration were normal, whereas magnesium levels were at the lower limit (1.8 mg/dL). Within the normal range was also pH and bicarbonate. Coagulation was normal, except for a significant increase of d-dimer. On physical examination, she had ascites and abdominalgia without breathing impairment. She felt nausea and vomit; symptomatic therapy with metoclopramide was given and a parenteral nutrition infusion with Olimel N4 (1500 ml/day, Glucose 112,5 g, Lipids 45 g, Amino-acids 38 g, Nitrogen 6 g; sodium 21 mEq/L, potassium 16 mEq/L, Mg 2.2 mEq/L, osmolarity 760 mOsm/L) was started. She was treated parenterally with loop of Henle diuretic therapy, furosemide associated with potassium sparing diuretic canrenoate, associated to water restriction. An abundant diuretic response and the reduction of ascites was observed in the 48 hours following, with a significant weight loss and an almost complete resolution of the abdominalgia. No changes in blood pressure or heart rate were measured. She suddenly presented confused and disoriented. She was not able to attempt a simple order and she complained headache. Her blood pressure was still normal and the neurological exam did not show any focal or lateral abnormality. Ammonium blood levels were normal (37 uM/L, normal values between 10-50). An urgent cerebral tomography was performed, showing a diffuse cerebral edema (,ABC). Patient neurological condition rapidly got worse, till vigil coma, with loss of interaction ability, while her vital parameters (blood pressure, heart rate and peripheral oxygen saturation) remained normal. Treatment with intravenous desametasone (8 mg twice a day) and mannitol (mannitol 18%, 100 ml four times per day followed by 50 ml four times per day), associated with magnesium sulphate (40 mEq in saline solution 250 ml per day in 6-hour infusion period) was immediately started and continued for three days. A cerebral MRI was urgently performed showing diffuse increase in signal alteration of the periventricular, deep and sub-cortical white matter in parieto-occipital region of the two sides, as from leukoencephalopathy, also in relation to post-radiotherapy modifications. venous thrombosis of the distal segment of the transverse sinus and of part of the left sigmoid sinus ().
She continued subcutaneous Fondaparinux at anticoagulating dose (7,5 mg/die) while Palbociclib and Fulvestrant were discontinued. Anti-edema (desametasone and mannitol) treatment as well magnesium sulphate infusion were continued. Her clinical condition rapidly improved with resolution of the acute episode.
A brain MRI was performed after 10 days, showing less but still persistent bilateral parieto-temporal-occipital vasogenic edema, partial resolution of the cerebral vein thrombosis, but evidencing the presence of few micro-haemorrhages in left temporal and parietal site ().
Patient neurological status completely recovered and after 2 weeks, she was discharged with the diagnosis of PRES.
At a MRI brain scan, performed the following month, a reduction of the vasogenic edema but a persistent even if reduced left transverse sinus thrombosis (). After a month, she was admitted to the hospital because of severe respiratory distress due to pneumonia and after three days she passed away.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [8.2, 'mg/dL'], 'Albumin': [3.2, 'g/dL']}",8.84,8.398,9.282,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.2 g/dL. 
The concentration of Calcium is 8.2 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.2 g/dL)) + 8.2 mg/dL = 8.84 mg/dL.
The patient's corrected calcium concentration 8.84 mg/dL."
2654,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2685790-1,Extracted,"A 14 year old boy was referred to hospital with 2 days history of back and calf pain. He had developed sudden onset of palpable purpuric rash on his extensor surfaces of lower extremities especially bilateral ankles on admission. There was no history of recent drug exposure, immunization, or upper respiratory tract infection. He denied recurrent attacks of abdominal pain and fever. Family history for FMF was negative. Physical examination showed a temperature of 38.3°C, respiratory rate of 48/min, pulse rate 128/min. He was hypertensive at 140/100 mmHg. In auscultation, lungs were clear and the heart sounds were normal. Abdominal palpation was normal. There were symmetric palpable purpuric rash on his lower extremities.
Laboratory tests showed an erythrocyte sedimentation rate (ESR) of 45 mm/h (normal: <20 mm/h), C-reactive protein of 3.74 mg/dl (normal: < 0.3 mg/dl), hemoglobin 10.7 g/dl, hematocrit 32.3%, white blood cell count (WBC) 11900/mm3 with normal differential count, platelet count 340000/mm3, serum urea 66 mg/dl, serum creatinine 1.8 mg/dl, albumine 3.5 g/dl, total cholesterol 106 mg/dl, triglycerides 57 mg/dl, calcium 8.7 mg/dl, sodium 140 mEq/L, potassium 4.7 mEq/L, chloride 107 mEq/L, alanine aminotransferase 23 U/l, aspartate aminotransferase 16 U/l. Serum complement-3 (C3) and complement-4 (C4) were decreased (85.4 mg/dl, 6.6 mg/dl, respectively). Serum immunglobulin (Ig) levels were normal. The anti-streptolysin – O titer was 100 Todd unit and throat culture was negative for group A B-hemolytic streptococcus. Antinuclear antibody, anti ds DNA, antineutrophil cytoplasmic antibody, anticardiolipine antibodies were negative. Urinalysis revealed macroscopic hematuria and proteinuria with a 24-h urinary protein excretion of 55 mg/m2/h. The fecal occult blood testing was positive. Renal ultrasonography (US) showed increased echogenicity (grade 2) in bilateral kidneys. A skin biopsy showed a leucytoclastic vasculitis and deposition of IgA. Renal doppler US was normal. Renal magnetic resonance angiography (MRA) to rule out PAN revealed normal results. Based on these clinical findings, the patient was diagnosed as having HSV with renal, skin and probable gastrointestinal tract involvement. A diagnosis of FMF was suspected because of the absence of occult blood in the stool and normal mesenteric MRA. Since there are reports of increase frequency of MEFV mutation in patients with HSV, we performed DNA analysis in our patient and found that he was compound heterozygote, carrying M694V/E148Q.
On the second day of hospitalization, He had periorbital and pitting pretibial edema. Respiratory examination revealed bibasilar crackles. His urine output decreased from 1.1 to 0.6 cc/kg/h and serum urea and creatine levels were increased (105 mg/dl, 3.5 mg/dl, respectively). We showed that serum urea and creatinine levels in figure . Echocardiography showed pericardial effusion (3 mm), minimal mitral regurgitation and increased inferior vena cava index and inferior vena cava collapsibility index.
The renal biopsy specimen consists of two portions of renal cortex and medulla. Forty glomeruli and many arteries are available for examination on multiple sections. The glomeruli are not significantly enlarged. They show variable, mostly segmental, expansion of the mesangial matrix associated with mild segmental mesangial hypercellularity. 25–30% of 40 glomeruli show crescents and/or necrotizing lesions (figure ). Another glomeruli show neutrophilic infiltration five glomeruli are available for examination by immunofluorescence. The mesangium contains peripheral membranous granular deposits of IgG (2+), IgA (3+), C3 (3+).
On the fifth day at hospitalization, hemodialysis was initiated for treatment of RPGN. Intravenous pulse methlyprednisolone was given (30 mg/kg, six consecutive days), followed by oral prednisolone and cyclophosphamide (2 mg/kg/day) for crescentic and necrotizing glomerulonephritis, in addition to Colchicine for FMF.
Clinical symptoms and renal failure resolved with intermittent hemodialysis therapy (total 20 cycles, twice a week). On one and half month after hospitalization, his abnormal serum and urinary findings resolved.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.5, 'g/dL'], 'Calcium': [8.7, 'mg/dL']}",9.1,8.645,9.555,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.5 g/dL. 
The concentration of Calcium is 8.7 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.5 g/dL)) + 8.7 mg/dL = 9.1 mg/dL.
The patient's corrected calcium concentration 9.1 mg/dL."
2655,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3014835-1,Extracted,"A 39-year-old man presented to the acute medical team with generalised weakness, vomiting, constipation, and abdominal pain. He had no chest pain or shortness of breath. The patient had no prior cardiac history. He had a 40-pack year smoking history, but he was not known to be hypertensive and there were no other risk factors for coronary artery disease. Blood pressure on admission was 105/55. On clinical examination the patient appeared dehydrated. He had a Glasgow Coma Score (GCS) of 13 and was unable to give a clear history at the time of presentation. There was mild epigastric tenderness but without rigidity or guarding. Heart sounds were normal, and there was no evidence of cardiac failure. There were no other significant findings or untoward features.
Blood testing revealed acute renal failure; urea was 21.7 mmol/L and creatinine was 338 μmol/L. His plasma adjusted calcium was 5.75 mmol/L and his albumin was 38 g/L, and parathyroid hormone was suppressed at 9 ng/L (normal range: 15–65 ng/L). Chest radiography revealed no features of malignancy or left ventricular failure, and a myeloma screen was negative. Thyroid function tests were also normal.
The ECG at presentation () revealed abnormal ST morphology in leads II, aVF, and V2-V3. These changes were minimal, and thrombolysis was not indicated.
The patient underwent initial resuscitation with intravenous fluids, and subsequently intravenous pamidronate was administered to correct the hypercalcaemia. His condition improved rapidly, and he was subsequently able to provide a detailed history. This revealed that he had been taking an over-the-counter calcium carbonate supplement: Tums. He had been ingesting extremely large quantities, up to 112 g calcium carbonate daily, for six months. This medication had initially been taken for indigestion. The patient was unaware of the detrimental effects these supplements could have on his health. Repeating a review of systems did not elicit any other significant symptoms, and there were no features suggestive of malignancy. Blood pressure recording on the ward at discharge was 128/70. An ECG following reversal of the hypercalcaemia () showed resolution of the ST segment elevation.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [38.0, 'g/L'], 'Calcium': [5.75, 'mmol/L']}",23.206,22.0457,24.3663,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 38.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 38.0 g Albmumin/10.0 dL = 3.8 g Albmumin/dL. The concentration value of 38.0 g Albmumin/L converts to 3.8 g Albmumin/dL. 
The concentration of Calcium is 5.75 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 5.75 mmol. To convert 5.75 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 5.75 mmol Calcium * 0.001 mol/mmol = 0.00575 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00575 mol Calcium * 40.08 g/mol = 0.23046 g Calcium. To convert 0.23046 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.23046 g Calcium * 1000.0 mg/g = 230.46 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 230.46 mg Calcium/10.0 dL = 23.046 mg Calcium/dL. The concentration value of 5.75 mmol Calcium/L converts to 23.046 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.8 g/dL)) + 23.046 mg/dL = 23.206 mg/dL.
The patient's corrected calcium concentration 23.206 mg/dL."
2656,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7427458-1,Extracted,"A 79-year-old male with a past medical history of CMML diagnosed 4 years prior, anemia related to CMML and CKD receiving erythropoiesis-stimulating agent, hypertension, and chronic kidney disease stage 3 (baseline creatinine 1.8 mg/dL) presented with one day of decreased urination and an unintentional 20 pound weight loss and fatigue over the preceding three months.
The patient’s blood pressure was 141/84 mmHg, pulse 104 beats per minute, respiratory rate 16 respirations per minute, SpO2 96%, and temperature of 36.6°C. The physical exam did not reveal any abdominal tenderness to palpation but did reveal splenomegaly. There was no palpable cervical, supraclavicular, axillary, or inguinal lymphadenopathy.
Laboratory evaluation was significant for profound leukocytosis, 88.5 × 103 cells per mm3, with 24.0% monocytes compared to his baseline WBC 4.5–7 × 103 cells per mm3 over the preceding 4 years. Additional laboratory abnormalities were significant for uric acid 19.8 mg/dL and creatinine 2.94 mg/dL as well as potassium 4 mmol/L, phosphorus 4 mg/dL, calcium 9.2 mg/dL, and albumin 3.2 g/dL. Urinalysis was significant for protein 200 mg/dL, 20/LPF granular casts, and 7/LPF hyaline casts. A renal ultrasound measured the left kidney as 10.2 cm long, with at least two cysts the largest at 3.5 cm, and without hydronephrosis. The right kidney measured as 10.5 cm long, with one cyst at 2 cm, and also without hydronephrosis. The CT of the chest, abdomen, and pelvis identified splenomegaly with a splenic diameter of 14.6 cm. No renal calculi were appreciated. Also visualized were several borderline subcentimeter retroperitoneal and pelvic lymph nodes.
Peripheral blood smear was performed and revealed a myeloid predominance with left shift and a small blast population (0.6%) as well as monocytic phenotypic aberrance (see ). Subsequently, a bone marrow biopsy was performed which identified 20–25% of CD 34+ blasts and morphologic features consistent with AML with monocytic differentiation (see and ). Flow cytometry showed prominent monocytes which demonstrated loss of expression of HLA-DR and CD14 as well as coexpression of CD56. Next generation sequencing (NGS) revealed a pathogenic mutation in the NPM1 gene.
With presenting hyperuricemia and acute on chronic kidney injury, he received one dose of rasburicase 3 mg IV given concern for early TLS with concomitant initiation of daily allopurinol. He commenced cytoreduction with hydroxyurea 1000 mg twice daily and after 48 hours, his white blood cell count and uric acid down-trended to 48.5 × 103 cells per mm3 and 5.5 mg/dL respectively. Creatinine also trended down to 1.98 mg/dL.
Due to the patient’s performance status and age, hematology offered reduced-intensity therapy consisting of azacitidine with or without venetoclax or best supportive care rather than intensive induction chemotherapy. Ultimately, the patient elected for home hospice services and passed away 10 days later.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.2, 'g/dL'], 'Calcium': [9.2, 'mg/dL']}",9.84,9.348,10.332,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.2 g/dL. 
The concentration of Calcium is 9.2 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.2 g/dL)) + 9.2 mg/dL = 9.84 mg/dL.
The patient's corrected calcium concentration 9.84 mg/dL."
2657,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4655285-1,Extracted,"An 83-year-old woman visits our hospital with complaint of a one-week history of worsening lower back pain. She felt lower back pain 3 months ago, occasionally radiating along right leg. She had taken medication for hypertension, diabetes mellitus, and dyslipidemia for several years. She underwent abdominal ultrasonography in our hospital 8 and 3 years ago, and she was suspected to have mild and moderate fatty liver, respectively. She denied alcohol drinking and cigarettes smoking for her entire life. Her family history was uneventful. She admitted for further evaluation.
On admission, her blood pressure was 140/90 mmHg. Height and body weight were 149 cm and 47.3 kg, respectively. Body mass index was 25.8 kg/m2. In physical examination, there was direct tenderness on sternum, right ribs, and thoracic and lumbar spine. Hypoesthesia on L4/5 dermatome was noted. At left occiput, a 3 cm-sized, fixed, and round mass was palpated without tenderness. She said that it seemed to be felt about 3 months ago. Breath sound was clear without adventitious sound, and heart beat was regular without murmur. There were no abnormal findings in abdomen. There was no palpable lymph node. The remaining examinations are unremarkable.
In laboratory examinations, total leukocyte count was 7,440/mm3, the level of hemoglobin was 11.3 g/dL, and platelet count was 245,000/mm3. In chemistry battery, creatinine was 1.2 mg/dL, uric acid was 5.5 mg/dL, total protein was 7.0 g/dL, albumin was 3.9 g/dL, AST was 38 IU/L, AST was 26 IU/L, total bilirubin was 0.2 mg/dL, alkaline phosphatase was 135 IU/L, and serum total calcium was 9.0 mg/dL. In lipid battery, total cholesterol was 130 mg/dL, triglyceride was 75 mg/dL, HDL cholesterol was 40 mg/dL, LDL cholesterol was 82 mg/dL, and HbA1c was 6.2%. In serologic test, hepatitis B surface antigen, hepatitis B core antibody, and hepatitis C antibody were negative; and hepatitis B surface antibody was positive. Serology for HIV and syphilis were negative.
In whole spine magnetic resonance image (MRI), 3 cm-sized metastatic lesions were revealed in T12 and L5 body to right pedicle, respectively. Also, small nodular lesions at T3, 9, 10, and 3 cm-sized occipital lesion were observed. To find primary cancer, chest computed tomography (chest CT) and abdominopelvic CT (AP-CT) were performed. In chest CT, multiple bone metastases were shown in sternum, right clavicle, right 11th rib, and thoracic spines. However, there was no abnormal finding to suspect primary cancer. In AP-CT, small round nodule was observed in liver segment 8, which was measured by 2.5 cm, showing faint arterial enhancement and delayed washout (). Also, moderate degree of fatty liver was suspected concordantly with her previous findings in ultrasonography. However, there were no features of cirrhosis such as surface nodularity, ascites, or splenomegaly. Also, there was right ovarian cystic tumor without mural nodules or calcification. It was measured by 3 cm compared to 1.4 cm 8 years ago. Liver MRI and α-fetoprotein (AFP) were checked due to the typical enhancing pattern observed in AP-CT. Carbohydrate antigen 125 (CA-125) also was checked due to right ovarian cystic tumor despite the fact that it did not show hot-uptake in PET-CT. In liver MRI, hepatic mass (<3 cm) showed low signal intensity on T1WI, high signal intensity on T2WI, diffusion restriction positive, arterial enhancement, delay washout, and defect on hepatobiliary phase in segment 8 (). The level of AFP was elevated to 12230 ng/mL, and the level of CA-125 was in normal range. HCC was identified; however, it was a small solitary HCC with T2 intrahepatic stage in modified International Union Against Cancer (UICC) staging system. There was no other intrahepatic metastasis. Because the liver lesion or ovarian lesion was too small to conclude it as the primary cancer of the disseminated bone metastases, further evaluation with positron emission tomography-computed tomography (PET-CT) was planned. PET-CT image showed fluorodeoxyglucose (18F-FDG) hot-uptakes in hepatic segment 8 (max standardized uptake value: 3.7), multiple bone metastases at right scapula, sternum, cervix—thoracic—lumbar vertebrae, bilateral ribs, left occipital bone, and right mandible. However, no other abnormal 18F-FDG uptakes were shown except liver and bone lesions. No lung metastasis and lymph node metastasis were suspected.
Because it is very unusual clinical finding that the diffuse and extensive musculoskeletal metastases were derived from small solitary HCC or ovarian cystic mass, we planned tissue biopsy at bone metastatic site to confirm the primary cancer. Brain MRI was taken to biopsy at occipital mass; brain MRI showed lobulating, enhancing skull mass in left occiput (3.5 × 2.5 cm), with destruction of bone and intracranial extension (). Incisional biopsy from occiput mass was done, and it revealed metastatic HCC with Edmondson Steiner grade 4/4 (). Finally, HCC with multiple bone metastases, modified UICC T2N0M1, IV-B stage was diagnosed. The patient needs two times of resuture due to the wound dehiscence at the incision site.
After diagnosis, the cause of HCC was searched again. However, antinuclear antibody, anti-neutrophil cytoplasmic antibody, anti-liver kidney microsomal antibody, anti-mitochondrial antibody, anti-smooth muscle antibody were all negative findings. Immunoglobulin G was in normal range (1461 mg/dL), serum ceruloplasmin was 32.7 mg/dL, and ferritin was 79.24 ng/mL. Although there was a suspicion of fatty liver and associated NAFLD, we did not perform liver biopsy because the patient would not have additional benefit from it.
With regard to the advanced stage and patient's poor performance status, conservative treatment with radiation therapy on L5 (39 Gy in 13 fractions) was done. After 1 month from the completion of radiotherapy, she complained of right chest pain and increased occipital mass, additional radiotherapy on metastatic lesion of left occiput and right 11th rib was done. After 3 months from then, PET-CT was reevaluated due to the aggravating lower back pain. Although there was little change in primary cancer in hepatic segment 8, the previous bone metastases were aggravated significantly and multiple new bone metastatic lesions were developed. She wanted supportive care and was transferred to hospice.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.9, 'g/dL'], 'Calcium': [9.0, 'mg/dL']}",9.08,8.626,9.534,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.9 g/dL. 
The concentration of Calcium is 9.0 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.9 g/dL)) + 9.0 mg/dL = 9.08 mg/dL.
The patient's corrected calcium concentration 9.08 mg/dL."
2658,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6091430-1,Extracted,"A 56-year-old female was referred to the nephrologist due to apparently chronic kidney disease (CKD), diagnosed on a routine laboratory check-up. The patient was asymptomatic, Past medical record was contributory for three normal pregnancies. There was no background of alcohol intake, tobacco consumption, drug abuse, or medication exposure. There was a family history of CKD (). Physical examination was unremarkable. Abnormal blood tests were as follows: Haematocrit 37%; haemoglobin 11.9 g/dL; bicarbonate 21 mEq/L; urea 78 mg/dL (normal value 20-50 mg/dL); serum creatinine 2 mg /dL; uric acid 6.4 mg/dL; creatinine clearance 42 ml/min; proteinuria 0.2 g/day; urinary sodium excretion 188 mEq/day; urine pH: 6, urinary density 1015. Urinary sediment was unremarkable. HIV, HCV, and HBV were negative; C3, C4, and CH50 were within normal limits. ANA, p-ANCA, c-ANCA, antiglomerular basement membrane antibody, and antiphospholipid antibodies were reported as negative. Renal sonogram disclosed two kidneys, normal in shape and size. A kidney biopsy was performed. Light microscopy disclosed 30 glomeruli: 6 completely obliterated, 8 presented peripheral sclerosis of the glomerular tuft with adhesions between parietal and visceral epithelial cells of Bowman's capsule, and 6 depicted mild mesangial expansion (). Tubular atrophy and interstitial fibrosis were 30%. Blood vessels showed mild intimal sclerosis in arterioles. Immunofluorescence was negative. Electron microscopy: diffuse effacement of podocyte foot processes existed with microvillous transformation. Basal membrane was normal. Tubules were normal. Pathology report was as follows: focal and segmental glomerulosclerosis with moderate interstitial fibrosis and tubular atrophy. Patient was started on enalapril 5 mg twice a day and simvastatin 10 mg/day and on appropriate diet.
She was lost to follow-up. Sixteen months later the patient returned to the nephrologist due to asthenia, fatigue, and cramps. Blood pressure was 110/70 mmHg. Significant blood test results were as follows: Haematocrit 32%; haemoglobin 9.2 g/dL; potassium 5.5 mEq/L; bicarbonate 19 mEq/L; serum calcium 9.5 mg/dL; serum phosphate 6.2 mg/dL; serum magnesium 2.2 mg/dL; urea 111 mg/dL; serum creatinine 3.78 mg/dL; uric acid 8.1 mg/dL; albumin 4.3 g/dL; creatinine clearance 21 ml/min; proteinuria 0.29 g/day; urinalysis was unremarkable. Urine pH was 7 and urinary density 1010. A renal magnetic resonance imaging was noncontributory. The patient was prescribed erythropoietin 2000 U every other day, enalapril 5 mg bid, calcium carbonate 2 g/day, sodium bicarbonate two tea spoons daily, and polystyrene calcium sulfonate. Six months later the patient was started on hemodialysis (creatinine clearance 12 mL/min). A genetic study disclosed the insertion of a cytosine nucleotide in the VNTR (Variable Number Tandem Repeats) region of the MUC-1 gene, consistent with a mutation of the mucin-1 gene previously reported []: cDNA NM_001204286.1, protein NP_001191215.1, SNaPshot. The diagnosis of ADTKD-MUC1 (Autosomal Dominant Tubulointerstial Kidney Disease-Mucin-1) was finally made. The laboratory results of the patient's daughter revealed mild proteinuria and normal kidney function (). A kidney biopsy revealed mild tubulointerstitial disease and focal and segmental glomerulosclerosis in 2 out of 16 glomeruli. She was started on enalapril and nephroprotection and genetic counseling was given to her.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.3, 'g/dL'], 'Calcium': [9.5, 'mg/dL']}",9.26,8.797,9.723,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.3 g/dL. 
The concentration of Calcium is 9.5 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.3 g/dL)) + 9.5 mg/dL = 9.26 mg/dL.
The patient's corrected calcium concentration 9.26 mg/dL."
2659,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4608639-1,Extracted,"A 69-year-old African-American man presented with a 1-month history of progressive generalized weakness, fatigue and anorexia. The patient denied a history of constipation, polyuria or polydipsia, nausea or vomiting. He also did not ingest any nonsteroidal anti-inflammatory drugs. The patient was known to have longstanding hypertension with stage 2 chronic kidney disease due to hypertensive/vascular disease. He recently had sustained left rib fractures following a motor vehicle accident. His home medications included extended-release nifedipine, dutasteride, tamsulosin, ferrous sulfate and acetaminophen with codeine on a PRN basis. The patient was not on a diuretic. He did not take any over-the-counter medication. Specifically, he took no calcium-containing antacids.
On examination, the patient was alert and oriented ×3. Blood pressure was 120/70 mm Hg without any orthostatic changes demonstrable while on a saline infusion begun in the emergency room 1–2 h before. His home medications for his hypertension were discontinued on admission because of the observed relative hypotension. Cardiac, respiratory, abdominal and neurologic examinations were normal. There was no peripheral edema. Skin turgor was poor. The patient had reproducible left-sided chest pain associated with his recent motor vehicle accident. No other skeletal pain could be elicited on exam.
Initial blood work demonstrated a serum creatinine concentration of 433.2 μg/l, a serum calcium concentration of 4.38 mmol/l, a serum phosphorus concentration of 1.06 mmol/l and a normal serum albumin level of 40 g/l. His serum creatinine and calcium concentrations were noted to be 123.8 μg/l and 2.35 mmol/l, respectively, 5 months prior to hospitalization. In addition, the patient presented with a serum bicarbonate concentration of 32 mmol/l and a serum potassium concentration of 2.5 mmol/l. His hypokalemic metabolic alkalosis was confirmed by a venous blood gas.
The workup to elucidate the etiology of his hypercalcemia revealed his intact PTH level to be appropriately suppressed to 0.95 pmol/l (normal range: 1.06–6.9 pmol/l) and his PTH-related peptide level to be 27 ng/l (normal range: 14–27 ng/l). 25-hydroxy vitamin D and 1,25 vitamin D levels were 92.4 nmol/l (within normal range) and <19.2 pmol/l, respectively (low). The patient demonstrated 7 g of proteinuria by a urine protein-to-creatinine ratio. The urine analysis by dipstick, however, revealed only 1+ proteinuria. A serum protein electrophoresis revealed 2 abnormal bands within the beta and gamma regions, and assays for free light chains were elevated for both kappa and lambda and demonstrated an elevation of his kappa/lambda ratio.
A renal sonogram revealed normal-sized kidneys with bilateral renal cysts, and there was no evidence of hydronephrosis. A CT scan of the chest abdomen and pelvis without intravenous contrast was remarkable for numerous lytic lesions in the midsternum, in the right and left ribs, in the upper and lower thoracic and lumbar spine as well as in his scapulas. A subsequent bone marrow biopsy demonstrated a plasma cell dyscrasia with a CD38 monoclonal kappa plasma cell population.
The initial hypercalcemia, metabolic alkalosis and hypokalemia were treated with intravenous saline and potassium chloride supplementation. No intravenous furosemide was utilized. Within 3 days, his hypokalemic metabolic alkalosis totally resolved (serum potassium concentration 4.6 mmol/l and serum bicarbonate concentration 21 mmol/l). On day 5 of his hospitalization, chemotherapy was begun with bortezomib and dexamethasone. Although calcitonin and zoledronic acid were administered shortly after admission, he remained hypercalcemic until the 6th day of hospitalization. With continued therapy for his underlying malignancy, he remained normocalcemic, and his renal function returned to its baseline level 5 months after discharge.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [40.0, 'g/L'], 'Calcium': [4.38, 'mmol/L']}",17.555,16.67725,18.43275,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 40.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 40.0 g Albmumin/10.0 dL = 4.0 g Albmumin/dL. The concentration value of 40.0 g Albmumin/L converts to 4.0 g Albmumin/dL. 
The concentration of Calcium is 4.38 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 4.38 mmol. To convert 4.38 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 4.38 mmol Calcium * 0.001 mol/mmol = 0.00438 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00438 mol Calcium * 40.08 g/mol = 0.17555 g Calcium. To convert 0.17555 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.17555 g Calcium * 1000.0 mg/g = 175.55 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 175.55 mg Calcium/10.0 dL = 17.555 mg Calcium/dL. The concentration value of 4.38 mmol Calcium/L converts to 17.555 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.0 g/dL)) + 17.555 mg/dL = 17.555 mg/dL.
The patient's corrected calcium concentration 17.555 mg/dL."
2660,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7407036-1,Extracted,"A 22-year-old female (height 1.72 cm, weight 40 kg, and body mass index 13.5 kg/m2) was admitted to our emergency room while receiving cardiopulmonary resuscitation for 45 minutes. Rhythm upon arrival was ventricular fibrillation. Since return of spontaneous circulation could not be achieved by all medical measures provided, the patient was immediately transferred to the catheter laboratory. Extracorporeal cardiopulmonary resuscitation via venoarterial extracorporeal membrane oxygenation (va-ECMO) was established. Due to severe left ventricular (LV) dysfunction, an Impella® pump was added to ensure sufficient LV output. Subsequently, percutaneous coronary angiogram was performed and showed no coronary disease (). The patient's history was noticeable for anorexia nervosa (AN) with several hospitalizations for renutrition, at the last several months prior to emergency admission. During the last few days prior to sudden cardiac death and after excessive caloric restriction, our patient began to increase her caloric intake to improve her nutritional state to avoid complications at an upcoming doctor's appointment. Prior to admission, our patient was an outpatient; did not receive medical refeeding or preventive treatment with supplementation of vitamins, phosphorus, or micronutrients; and did not had a history of binge episodes.
Initial blood analysis showed a severe electrolyte disorder with potassium depletion (1.38 mmol), hypocalcemia (ionized calcium 1.75 mmol/l), hyponatremia (117 mmol/l), hypochloremia (54 mmol/l), hypophosphatemia (0.28 mmol/l), and hypoproteinemia (total protein 30.2 g/l; albumin 28.9 g/l). In addition, laboratory data indicated a high level of lactate (18 mmol/l) combined with a normal pH of 7.38. Initial sugar levels were elevated (blood glucose 430 mmol/l). The first performed echocardiogram confirmed severe LV dysfunction. In the electrocardiogram, a sinus tachycardia and prolongation of the corrected QT interval were detected (660 ms) (). Electrolytes were substituted. Transient anisocoria and simultaneous severe coagulopathy under va-ECMO therapy led to a cranial computed tomography (CT), showing small bilateral subdural hematoma (). Most likely, the patient had aspirated during resuscitation; therefore, calculated antibiotic therapy with ampicillin/sulbactam was given. After initiating inodilatative support with levosimendan, cardiac output significantly improved within the next 24 hours. The Impella® pump and va-ECMO were subsequently removed on day 3. After the patient's respiratory situation had stabilized, extubation took place on day 5. Neurological assessment 10 days after admittance showed a mild difference in reflexes such as vertical saccade. Cranial magnetic resonance imaging (MRI), performed on day 16, revealed unchanged small bilateral subdural hematoma (). Subsequent cardiac MRI performed after 2 weeks showed a recovered LV ejection fraction and no signs of myocarditis (). The patient was dismissed after 3 weeks of hospitalization without neurological deficit to a psychiatric care station for further treatment of AN.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [28.9, 'g/L'], 'Calcium': [1.75, 'mmol/L']}",7.902,7.5069,8.2971,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 28.9 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 28.9 g Albmumin/10.0 dL = 2.89 g Albmumin/dL. The concentration value of 28.9 g Albmumin/L converts to 2.89 g Albmumin/dL. 
The concentration of Calcium is 1.75 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.75 mmol. To convert 1.75 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.75 mmol Calcium * 0.001 mol/mmol = 0.00175 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00175 mol Calcium * 40.08 g/mol = 0.07014 g Calcium. To convert 0.07014 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.07014 g Calcium * 1000.0 mg/g = 70.14 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 70.14 mg Calcium/10.0 dL = 7.014 mg Calcium/dL. The concentration value of 1.75 mmol Calcium/L converts to 7.014 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.89 g/dL)) + 7.014 mg/dL = 7.902 mg/dL.
The patient's corrected calcium concentration 7.902 mg/dL."
2661,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3183691-1,Extracted,"A 50-year-old nondiabetic, nonalcoholic and nonsmoking woman presented to our outpatient department with a history of difficulty in climbing stairs and lifting objects above her head for 2 1/2 months, and difficulty in lifting her head over off the pillow and keeping her head straight for 1 1/2 month. The weakness progressed rapidly and resulted in her being bedridden during the 15 days prior to presentation. There was no history of diplopia, dysphagia, dysarthria, drooling of saliva, deviation of the angle of the mouth, exertional fatigue, cold intolerance, hypertrophy of muscle, skin rash or joint pain. The past history was unremarkable; she never had jaundice. She denied recent use of any medicine or exposure to toxin.
Physical examination revealed an afebrile bedridden patient with a pulse rate of 72/min and blood pressure of 122/76 mm Hg. She had bilaterally symmetrical quadriparesis with muscle power of grade 3 in the lower limb and grade 4 in the upper limb (proximal weakness more than distal); and truncal and neck muscle weakness (both flexor and extensor muscle groups). All deep tendon reflexes were normally elicited with normal contraction and relaxation phases. Sensory, cerebellar and cranial nerve examinations were unremarkable. Abdominal examination revealed firm, nontender hepatomegaly, palpable up to 2 cm below subcostal margin in the midclavicular line. Cardiac and respiratory examinations were unremarkable. We decided on a working diagnosis of subacute-onset symmetrical quadriparesis without bowel and bladder involvement with the possibility of inflammatory muscle disease.
Laboratory test showed hemoglobin of 12 g/dL (normal range, 12-15.8 g/dL), erythrocyte sedimentation rate of 24 mm/h (normal range, 0-20mm/h), and a total leukocyte count of 7600/μL (normal range, 5000-8000/μL) with a differential of polymorphs of 42% (normal range, 40/70%), lymphocytes of 50% (normal range, 20-50%), eosinophils of 4% (normal range, 0-6%) and monocytes 6% (normal range, 4-8%). Blood urea and sugar (random) were 20 mg/dL (normal range, 5-20mg/dL) and 110 mg/dL (normal range, 75-125 mg/dL), respectively. Serum tests showed a total protein of 6.4 g/dL (normal range, 6-8.5g/dL), albumin of 3 g/dL (normal range, 3.2-5.5g/dl), aspartate aminotransferase of 240 IU/L (normal range, 0-45u/l), alanine aminotransferase of 146 IU/L (normal range, 0-50 IU/L), total bilirubin of 1.2 mg/dL (normal range, 0.1-1.2g/dL), alkaline phosphatase of 152 (normal range, 0-160 u/l), calcium of 9.4 mg/dL (normal range, 8.7-10.2 mg/dL), elevated creatinine kinase of 1972 IU/L (normal range, 40-150 IU/L) and elevated lactate dehydrogenase of 470 IU/L (115-220 IU/L). Renal function test, thyroid function test, urinalysis, electrocardiogram and chest x-ray were normal. Autoantibodies like anti-ds-DNA, anti-Jo, anti-neutrophilic cytoplasmic antibody were negative; however, antinuclear antibody was positive. The alpha-fetoprotein level was elevated. ELISA tests for HIV, rheumatoid factor, HBsAg, anti-HCV and anti-HAV were negative. Abdominal ultrasound showed a 4.8×3.6×4-cm heteroechoic solid mass in the left lobe of the liver (). Computed tomography of the abdomen showed a solitary hypodense mass in the left lobe of the liver (segments 2 and 3) without any lymph node enlargement (). An electromyograph of the deltoid and vastus lateralis showed low-amplitude, short-duration polyphasic motor unit potentials on voluntary contraction, positive sharp waves on rest and incomplete interference pattern with early recruitment; these findings were concluded as being a myopathic pattern. Sensory and motor nerve conduction studies revealed normal results. A muscle biopsy from the thigh muscle showed myofibrillar necrosis with macrophage infiltration in regenerating fiber and lymphocytic infiltration in the endomysium, suggesting myositis (). Ultrasound-guided biopsy of the hepatic mass showed poorly differentiated HCC. On viewing these findings, we made the diagnosis of HCC with polymyositis (PM).
Oral prednisolone was started at a dose of 1 mg/kg and a left lobe hepatic lobectomy was done. The patient showed improvement in power: grade 4+/5 in the lower limb and grade 5/5 in the upper limb; truncal and neck muscle weakness also showed marked improvement for 2 months. The creatinine kinase level was reduced to normal (), while the level of alpha-fetoprotein was also reduced on follow-up at the clinic. Two months later, the patient was again admitted to ICU with acute-onset dyspnea, pleuritic chest pain and hemoptysis and diagnosed as having pulmonary embolism. Unfortunately, the patient died on the day of admission; her attendants denied autopsy.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.0, 'g/dL'], 'Calcium': [9.4, 'mg/dL']}",10.2,9.69,10.71,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.0 g/dL. 
The concentration of Calcium is 9.4 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.0 g/dL)) + 9.4 mg/dL = 10.2 mg/dL.
The patient's corrected calcium concentration 10.2 mg/dL."
2662,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6962441-1,Extracted,"A 43-year-old woman visited the emergency room for oliguria. She was followed up in the hospital for type I diabetes mellitus, chronic kidney disease due to diabetic nephropathy, hypertension and heart failure with dilated cardiomyopathy. She had a history of volume depletion due to diarrhea and a decrease in urine volume. At the time of arrival, level of consciousness was drowsy and the Glasgow coma scale was 14. Physical examination revealed dehydration, including decrease in skin turgor, and tongue dehydration. The vital signs were blood pressure 110/60mmHg, pulse rate 104 beats/min, respiratory rate 20 breaths/min, and body temperature 36.2℃. In the chest auscultation the cardiac sound was normal without murmur and the breath sound was normal. Abdominal examination revealed no specific findings such as tenderness, and no pitting edema was observed in the lower extremities. Complete blood cell count examination revealed hemoglobin 8.3 g/dL; hematocrit 27.7%; WBC 12,070/mm3; and platelet count 195,000/mm3. The initial laboratory values were: serum sodium 134mEq/L; potassium 4.2mEq/L; calcium 8.71mg/dL; phosphorus 4.28mg/dL; magnesium 1.89mg/dL; serum urea nitrogen 46.7mg/dL; creatinine 6.86mg/dL; albumin 2.49 g/dL; total bilirubin 0.12mg/dL; AST/ALT 6.7/3.8 IU/L; glucose 235mg/dL; lactic acid 8.21mg/dL; alkaline phosphatase 68 IU/L; NGAL 739 ng/mL; ammonia 77 ug/dL; Pro-BNP >35,000 pg/mL; and CRP 3.95mg/dL. Arterial blood gas analysis revealed pH 7.14; pCO2 24mmHg; pO2 121mmHg, and tCO2 8.3mL/dL. The serum IgA was 109 mg/dL; ASO 32U; C3 92mg/dL; C4 35mg/dL; FANA negative; and ANCA negative. In the urine analysis, the specific gravity of urine was 1.007; pH 5.0; urine protein 2+; blood 3+; RBC 1–4/HPF; and WBC 5–9/HPF. Urine creatinine level was 14.9mg/dL, and urine protein was 6.78mg/dL. In the immune serum test, the HBs Ag/Ab, Anti-HCV Ab, Anti-HIV Ab, and VDRL results were all negative. Due to persistence of oliguria, continuous RRT was started. On the ninth hospital day, her mentation changed from alert to stupor mentation. The Glasgow coma scale (GCS) changed from 15 to 5. Brain images showed normal findings (). The following laboratory values were obtained: serum sodium 138mEq/L; potassium 4.5 mEq/L; calcium 8.26mg/dL; phosphorus <0.41mg/dL; magnesium 1.96 mg/dL; serum urea nitrogen 21.4mg/dL; creatinine 1.45 mg/dL; albumin 2.32 g/dL; glucose 209 mg/dL; and CRP 2.75mg/dL. After phosphate intravenous replacement, 0.25–0.5mmol/kg monobasic potassium phosphate (Phosten, JW, Korea) for 6 days, and administration of phosphate-containing replacement solution Phoxilium(containing phosphate at 1.2 mmol/L; Baxter Gambro, Deerfield, IL, USA) use, the phosphate level increased to 2.97mEq/L and mental state returned to alert (). On the 29th day of continuous RRT, normal urine volume was recovered with decrease in serum creatinine level. On the 33rd day, serum creatinine level decreased to 2.08mg/dL, subsequently RRT was stopped. At the time of discharge, serum creatinine and phosphorus level were 1.82mg/dL and 2.75mg/dL, respectively with alert mentation. The patient is still on outpatient follow-up.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.32, 'g/dL'], 'Calcium': [8.26, 'mg/dL']}",9.604,9.1238,10.0842,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.32 g/dL. 
The concentration of Calcium is 8.26 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.32 g/dL)) + 8.26 mg/dL = 9.604 mg/dL.
The patient's corrected calcium concentration 9.604 mg/dL."
2663,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3090653-1,Extracted,"A 46-year-old man presented to the emergency department with pleuritic chest pain, a swollen and painful right knee, and weight-bearing difficulty. Accompanying this was hip and back pain after a fall. This occurred on a background of unexplained progressive weight loss of 40 kilograms over the past 2 years, poor appetite, fever and drenching night sweats, increased susceptibility to infection, and intravenous drug use. He had a 16-year history of hepatitis C (HCV; genotype 3), which remained untreated due to noncompliance and poor clinic attendance. He had been a well-built professional boxer of 96 to 100 kilograms for most of his adult life; however, his admission weight was 60.61 kilograms. This was a loss of approximately 63% of his total body weight. His relevant medical history includes postoperative pulmonary embolism, disc prolapse, mild depression, and a family history of adult polycystic kidney disease. The relevant surgical history includes osteomyelitis and amputation of the third digit of the right hand, and multiple fracture repairs. Systems review was unremarkable. He has a complicated social history including a troubled upbringing, intravenous heroin use up to 1 gram per day, experimentation with most illicit drugs, a significant criminal history, and participation in an opiate substitution programme. He does not smoke tobacco or drink alcohol.
On examination, the patient appeared acutely unwell, although vital signs were normal. He appeared cachectic, had sunken eyes, reduced skin turgor, poor dentition, extensive tattoos, and had track marks in the cubital fossae and groin. There was rib and mediastinal tenderness with no masses. Right upper quadrant abdominal tenderness was noted on palpation, with hepatomegaly 6 centimetres below the costal margin. Nontender lymphadenopathy was present in the upper left jugular nodes and bilaterally in the groin. A warm, right knee effusion was also apparent. There were no signs suggestive of infective endocarditis or chronic liver disease. Respiratory, cardiovascular, thyroid, and neurological examinations were unremarkable.
Initial blood biochemistry revealed a noncritical normocytic normochromic anaemia (haemoglobin 102 g/L), raised CRP, elevated calcium (2.57 mmol/L), and low albumin (23 grams/L). A thyroid function test detected 18 picomols/L of free T4 (normal range 7–17 pmols/L). This was assumed to be a transient reactive elevation rather than the cause of such significant weight loss. Liver function tests, blood cultures, electrolytes, renal function, coagulation profile, α-fetoprotein, vasculitic screen, iron studies, vitamin B12, urate, and globulins were all within normal ranges. Hepatitis C serology was reactive with an IgG response. forth generation antigen/antibody assay was performed twice, four weeks apart, to determine HIV positivity; however, both tests returned negative. The patient's history revealed that previous HIV tests were also negative, and as such a Western blot analysis was not performed. Hepatitis B serology was consistent with immunisation. Polymerase chain reaction found the patient to be reactive to cytomegalovirus (CMV), and Epstein Barr virus (EBV), but human herpes virus 8 was not detected. Although blood IL-6 levels could have been used as a marker of systemic inflammation, C-reactive protein was chosen instead as per hospital policies. A computerized tomography of the chest and abdomen found enlarged para-aortic lymph nodes and lytic lesions in T8 and T9. There was no splenomegaly, and the liver architecture was unchanged.
A computerized tomography pulmonary angiogram, chest X-ray, and cardiac troponin I were requested to exclude pulmonary embolism, rib fracture and pneumothorax, and myocardial infarction. All were normal. The right knee joint was aspirated, and fluid analysis showed methicillin sensitive Staphylococcus aureus which was treated as septic arthritis with intravenous flucloxacillin and vancomycin. Following spiking fevers over the next few weeks in hospital, a transoesophageal echocardiogram was performed to exclude infective endocarditis from a septic arthritis-induced bacteraemia.
At this point, the patient was clinically suspected to have lymphoma or multiple myeloma, and further investigations undertaken were to exclude either. β-2 microglobulin and LDH levels were normal, no monoclonal band was detected on serum and urine protein electropheresis, and flow cytometry showed normal subpopulations of B cell and T cell lineages. A bone scan showed further destructive thoracic lesions but did not confirm its extent. Magnetic resonance imaging confirmed T8 to T11 osteomyelitis with epidural involvement indenting on, but not compressing, the spinal cord. Lymphoma and multiple myeloma were excluded by bone marrow biopsy.
The diagnosis of multicentric plasmacytic Castleman's disease was histologically confirmed by an excision biopsy from an inguinal lymph node. Macroscopically, the specimen was a circumscribed ovoid nodule measuring 30 × 22 × 10 mm with a central blackish area. Microscopically, no malignant cells, Reed Sternberg cells, or their variants were seen. This was confirmed by two separate laboratories. Also noted were distinct hyaline deposits, prominent paracortical expansion by sheets of plasma cells, and subcapsular and interfollicular neutrophilic bodies. HHV-8 was not detected in this sample.
A four-week rituximab regime was chosen as the primary treatment for this patient. Steroid treatment was also being considered as adjunct therapy.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [23.0, 'g/L'], 'Calcium': [2.57, 'mmol/L']}",11.661,11.07795,12.24405,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 23.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 23.0 g Albmumin/10.0 dL = 2.3 g Albmumin/dL. The concentration value of 23.0 g Albmumin/L converts to 2.3 g Albmumin/dL. 
The concentration of Calcium is 2.57 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 2.57 mmol. To convert 2.57 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 2.57 mmol Calcium * 0.001 mol/mmol = 0.00257 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00257 mol Calcium * 40.08 g/mol = 0.10301 g Calcium. To convert 0.10301 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.10301 g Calcium * 1000.0 mg/g = 103.01 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 103.01 mg Calcium/10.0 dL = 10.301 mg Calcium/dL. The concentration value of 2.57 mmol Calcium/L converts to 10.301 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.3 g/dL)) + 10.301 mg/dL = 11.661 mg/dL.
The patient's corrected calcium concentration 11.661 mg/dL."
2664,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6789385-1,Extracted,"A 45-year-old man was hospitalized for intense burning sensation in the lower limbs and hands.
A 45-year-old man was hospitalized at the First Affiliated Hospital of Guangxi Medical University for pain in the sternum and ribs. According to the International Staging System, the patient was diagnosed with stage II MM (λ type) and stage III disease according to the Durie-Salmon Staging system. A chemotherapy protocol was followed, consisting of bortezomib (1.3 mg/m2 on days 1, 4, 8, and 11, and every 21 d thereafter), cyclophosphamide, and dexamethasone. Numbness of limbs began on the fourteenth day after the second cycle of chemotherapy. The patient began to complain of intense painful and burning sensation in the lower limbs and hands, loss of tactile sensation, and pain bilaterally in the distal parts of the thighs and bilaterally in the distal parts of the wrist joint. Gabapentin and pregabalin did not improve his symptoms.
Nothing to declare.
He have been smoking 20 cigarettes a day for more than 20 years.
The pain and tactile sensation of distal wrist joints of both upper limbs and ankle joints of both lower limbs had decreased. Knee-jerk and ankle reflexes were absent.
The blood testing results were: Hemoglobin, 139.8 g/L (normal range, 130-175.00); creatinine, 54 µmol/L (59-104); creatinine clearance, 81 mL/min (85-125); calcium, 2.13 mmol/L (2.080-2.600); albumin, 40.7 g/L, and globulin, 24.3 g/L. The 24-h urine analysis showed a total protein of 84.6 mg/24 h (0.0-120.0). Serum lactate dehydrogenase was 247 U/L (109-245) and beta-2 microglobulin was 3.03 µg/mL (0.0-120.0). Serum immunoelectrophoresis showed no M protein band. Serum free light chain assay showed free light chain κ of 11.11 mg/L and free light chain λ of 21.69 mg/L. Folic acid and vitamin B12 levels were normal. Bone marrow had 3% plasma cells.
CSF pressure was 124 mmH2O, CSF protein was 931.1 mg/L (150-450), and CSF cell count was 0 × 106/L. CSF syphilis antibody and Cryptococcus neoformans were negative. Paraneoplastic antibodies in CSF and serum were negative, which included anti-Hu, Yo, Ri, CV2, Ma2/Ta, amphiphysin, ANNA3, Tr, PCA2, and GAD.
Nerve conduction studies: The sensory conduction velocity and amplitude of the median nerve and ulnar nerve were normal bilaterally, and the motor conduction velocity and amplitude were also normal. The latency and occurrence rate of F wave in the median nerve and bilateral ulnar nerve were normal bilaterally. The latency of F wave in the tibial nerve was prolonged bilaterally and the rate of occurrence was normal. The tibial nerve H reflex could not be induced bilaterally. The sensory potentials of both superficial peroneal nerves and both sural nerves could not be induced. The conduction velocity and amplitude of the common peroneal nerve and the tibial nerve were normal. No spontaneous potential was found in the right anterior tibial electromyography. The time limit was prolonged, the amplitude was increased, and the multiple waves were normal. No spontaneous potential was found in the left anterior tibial muscle, bilateral gastrocnemius muscle, or right medial femoral head muscle. The time limit, amplitude, and multiple waves were normal, and the maximum force was mixed. There was no spontaneous potential in the EMG of the right first interphalangeal muscle and the right biceps brachii. The time limit, amplitude, and multiple waves were normal, and the maximum force was mixed.
Mild to moderate multiple sensory neuron damage could be considered.
The imaging findings are presented in Figure .","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [40.7, 'g/L'], 'Calcium': [2.13, 'mmol/L']}",8.481,8.05695,8.90505,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 40.7 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 40.7 g Albmumin/10.0 dL = 4.07 g Albmumin/dL. The concentration value of 40.7 g Albmumin/L converts to 4.07 g Albmumin/dL. 
The concentration of Calcium is 2.13 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 2.13 mmol. To convert 2.13 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 2.13 mmol Calcium * 0.001 mol/mmol = 0.00213 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00213 mol Calcium * 40.08 g/mol = 0.08537 g Calcium. To convert 0.08537 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.08537 g Calcium * 1000.0 mg/g = 85.37 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 85.37 mg Calcium/10.0 dL = 8.537 mg Calcium/dL. The concentration value of 2.13 mmol Calcium/L converts to 8.537 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.07 g/dL)) + 8.537 mg/dL = 8.481 mg/dL.
The patient's corrected calcium concentration 8.481 mg/dL."
2665,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-8565699-1,Extracted,"We present a case of a 38-years old Caucasian man, a worker, admitted to the department of internal diseases, due to profound deficiency of both total blood protein and albumin, which were incidentally detected by analysis of outpatient laboratory tests, during the diagnosis of ribs’ pain. In the interview, the patient reported a degenerative disease of the lumbar spine (L5-S1 discopathy confirmed by the outpatient MRI), nicotinism and acute pancreatitis on the toxic background 7 years ago.
He also complained of the ribs’ pain, lasting for about 7 months, varying in severity and recurrent swelling of the left knee. At the time of admission, the patient did not present lower limbs edema nor reported any other complaints.
The man denied diarrhea, abdominal pain, fever, vomiting, weight loss, cough, hemoptysis, skin rash, frequent infections nor urinary disorders in the past few years.
The patient consumed normal meals, including meat products, defecated once a day without pathological admixtures and denied alcohol consumption for last 7 years.
During the physical examination at admission, the patient was in good general condition, except for ribs’ tenderness on both sides, no other abnormalities were found. His Body Mass Index (BMI) was 20.
Initial laboratory tests showed in serum: low albumin concentration 1.7 g/dL, hypoproteinemia 2.8 g/dL, hypocalcemia (Ca total 1.7 mmol/L, Ca corrected 2.16 mmol/L), slightly elevated alkaline phosphatase (194 IU/L) and parathyroid hormone level (189 pg/mL), vitamin D deficiency (13.3 ng/ mL), lymphopenia (0.7/uL) with normal other morphological values (Hb 16.6 g/dL, WBC 7.73 x 109/L, PLT 412 000/uL), inflammatory parameters within normal levels, liver and kidney function tests and indicators of the coagulation system. His immune electrophoresis and biochemical investigations’ profiles are summarized in and .
The ultrasonography of the abdomen and thyroid, gastroscopy and colonoscopy, aside from small amount of free liquid in abdominal cavity and gastroesophageal reflux, showed no significant abnormalities. The endoscopic image of the duodenum was normal, no villous atrophy was found. The test for Helicobacter pylori was negative.
In computed tomography of the chest a fracture of 7 ribs, with visible healing features, was described (6-8 and 11 on the right side and 9-11 on the left side). The patient denied the chest trauma and was unable to determine when and how the fractures occurred.
In the myelogram, granulocyte derived cell line dominated in the bone marrow, while the activity of the erythroblast and lymphocyte cell line was slightly reduced. There were no blasts or plasma cells in the smear. Further studies ruled out proteinuria and HIV infection, but showed a significant Ig deficiency within all classes, except IgE, a deficiency in all of the lymphocytes subpopulations and moderately elevated fecal 1-antitrypsin levels in the feces. The conducted stool tests were three times negative for parasites and the calprotectin level was within normal limits.
Moreover, further tests showed: presence of HLA DQ2.2 haplotype (both HLA DQ2.5 and DQ8 haplotypes were absent), negative TG2 antibodies in the IgG class and weakly positive TG2 antibodies in the IgA class 0.83 AU/mL (TG2 IgA <0.8 negative, TG2 IgA > 0.8 positive), which with a significant deficiency of immunoglobulins in this class, brought about a suspicion of CD. After about 3 months, a new gastro-duodenoscopy with biopsy from duodenum confirmed the diagnosis of CD: irregular shape of the villi in duodenum and Marsh IIIA stage lesions in histopathology ( and , ). The patient was enrolled in a GFD and about 2 weeks after exclusion of gluten from diet, we observed a significant increase of serum albumin to 2 g/dL and total protein to 3.4 g/dL. The man was afterwards directed in a good condition for further care under control of outpatient gastroenterological clinic.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [1.7, 'g/dL'], 'Calcium': [1.7, 'mmol/L']}",8.654,8.2213,9.0867,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 1.7 g/dL. 
The concentration of Calcium is 1.7 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.7 mmol. To convert 1.7 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.7 mmol Calcium * 0.001 mol/mmol = 0.0017 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.0017 mol Calcium * 40.08 g/mol = 0.06814 g Calcium. To convert 0.06814 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.06814 g Calcium * 1000.0 mg/g = 68.14 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 68.14 mg Calcium/10.0 dL = 6.814 mg Calcium/dL. The concentration value of 1.7 mmol Calcium/L converts to 6.814 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.7 g/dL)) + 6.814 mg/dL = 8.654 mg/dL.
The patient's corrected calcium concentration 8.654 mg/dL."
2666,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,usmle-5364,Extracted,"A 46-year-old woman presents to her primary care doctor to request a referral to ophthalmology. Her vision has been steadily declining over the past two years, and she thinks she needs a prescription for glasses. She further complains that her lips and feet feel numb. Her medical history is notable for medullary thyroid cancer status post total thyroidectomy. Her periods are regular. She enjoys a diverse diet and takes levothyroxine. Her blood pressure is 110/70 mmHg, pulse is 80/min, and respirations are 12/min. She is alert and oriented. Her pupils are equal, round, and reactive to light, but appear opacified. Extraocular movements are intact, albeit slow. Her visual acuity is decreased bilaterally. The remainder of her physical exam is unremarkable. Her basic metabolic panel is shown below:

Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.9 mEq/L
HCO3-: 25 mEq/L
BUN: 10 mg/dL
Glucose: 110 mg/dL
Creatinine: 0.8 mg/dL
Thyroid-stimulating hormone: 1.5 µU/mL
Ca2+: 7.0 mEq/L
Phosphorus: 6.5 mEq/L
Albumin: 3.6 mg/dL

The patient's electrocardiogram is shown in Figure A.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.6, 'mg/dL'], 'Calcium': [7.0, 'mEq/L']}",17.22512,16.36386,18.08638,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.6 mg/dL. We need to convert the concentration to g/dL. Let's first convert the mass of Albmumin from mg to g. The mass of Albmumin is 3.6 mg. To convert 3.6 mg of Albmumin to g, multiply by the conversion factor 0.001, giving us 3.6 mg Albmumin * 0.001 g/mg = 0.0036 g Albmumin. The volume units is dL so no volume conversion is needed. Hence, the concentration value of 3.6 mg Albmumin/dL converts to 0.0036 g Albmumin/dL. 
The concentration of Calcium is 7.0 mEq/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mEq to mg. The mass of Calcium is 7.0 mEq. To convert from 7.0 mEq to mg mmol, first convert from mEq to mmol. The compound, Calcium, has a valence of 2, and so divide the valence by the value of mEq to get, 7.0 mEq/(2 mEq/mmol) = 3.5 mmol Calcium. To convert 3.5 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 3.5 mmol Calcium * 0.001 mol/mmol = 0.0035 mol Calcium. The mass of Calcium is 0.0035 mol. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.0035 mol Calcium * 40.08 g/mol = 0.14028 g Calcium. To convert 0.14028 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.14028 g Calcium * 1000.0 mg/g = 140.28 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 140.28 mg Calcium/10.0 dL = 14.028 mg Calcium/dL. The concentration value of 7.0 mEq Calcium/L converts to 14.028 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 0.0036 g/dL)) + 14.028 mg/dL = 17.22512 mg/dL.
The patient's corrected calcium concentration 17.22512 mg/dL."
2667,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7155813-1,Extracted,"An 18-year-old African American female with no past medical history and no known drug allergies presented initially to an outside hospital with complaints of fatigue and generalized weakness. She was found to have a hemoglobin of 4.5 g/dL at that time. Testing revealed signs of hemolytic anemia, and she was treated with steroids, intravenous immunoglobulin (IVIG), and transfusions. Once her anemia stabilized, she was discharged home on steroids. She returned to the same hospital a few weeks later again with fatigue and now with new symptoms of severe back pain. Testing again showed anemia. Magnetic resonance imaging (MRI) of her spine was done for the back pain, and the results showed marrow abnormalities and a possible infarct of the L4 vertebrae. These abnormal findings directed physicians to perform a bone marrow biopsy which resulted several days later as DLBCL, activated B-cell type. The bone marrow morphology showed that the bone marrow spaces were almost entirely replaced by diffuse intermediate/large atypical appearing cells with a marked decrease of normal trilineage hematopoiesis. Immunohistochemical (IHC) stains on the biopsy demonstrated positivity for cluster of differentiation 20 (CD20), CD79a, PAX5, B-cell lymphoma 2 (BCL2) (weakly), BCL6, MUM1 (30%), Ki67 (65%). IHC testing resulted as negative for CD3, CD10, CD34, terminal deoxynucleotidyl transferase (TdT), myeloperoxidase (MPO), CD30, CD117, and cyclin D1. Fluorescence in situ hybridization (FISH) testing for BCL2, BCL6, and MYC was attempted on the sample but was unsuccessful due to inability to hybridize. Positron emission tomography (PET) scan () had been done at the outside hospital, and results had shown diffuse osseous uptake in the axial and appendicular skeleton with no other sites of uptake. Based on these results, it was determined that she had PBML. At that time, she was transferred to our facility for evaluation by a bone marrow transplant oncologist.
On arrival, patient’s labs showed: white blood cell (WBC) of 12.8 × 109/L, hemoglobin of 9.6 g/dL, hematocrit of 27.9%, platelets of 209 × 109/L, sodium of 137 mmol/L, potassium of 4.3 mmol/L, chloride of 107 mmol/L, bicarbonate of 25 mmol/L, glucose of 148 mg/dL, blood urea nitrogen of 16 mg/dL, creatinine of 0.64 mg/dL, phosphorus of 4.4 mg/dL, calcium of 8.4 mg/dL, albumin of 2.3 g/dL, total bilirubin of 1.2 mg/dL, aspartate aminotransferase (AST) of 32 U/L, alanine aminotransferase (ALT) of 38 U/L, uric acid of 1.8 mg/dL, lactate dehydrogenase (LDH) of 496 U/L, prothrombin time (PT) of 15.4 s (international normalized ratio (INR) of 1.25), activated partial thromboplastin time (aPTT) of 32 s, fibrinogen of 677 mg/dL, and D-dimer of 3.59 µg/mL. Infectious workup was negative except for a positive hepatitis B core Immunoglobulin G (IgG) antibody. Hepatitis B virus deoxyribonucleic acid (DNA) polymerase chain reaction (PCR) testing was then performed and resulted as undetectable. Entecavir 0.5 mg daily was used throughout and after treatment as hepatitis B reactivation prophylaxis. Baseline cerebrospinal fluid (CSF) testing showed normal cell counts and negative cytology. At this time, the decision was made to treat the patient with rituximab, cyclophosphamide, doxorubicin, vincristine, dexamethasone, and alternating with methotrexate and cytarabine as per the R-Hyper-CVAD protocol. She underwent four cycles of this regimen, with several complications. Complications included anemia requiring frequent transfusions, vertebral compression fracture of T9 with significant pain and debility, several episodes of neutropenic fever, pericardial effusion without tamponade, and a superior sagittal thrombus treated with 6 months of anticoagulation with apixaban. Some of these complications did result in delays in her treatment. The patient also completed six treatments of prophylactic intrathecal chemotherapy with methotrexate throughout the course of therapy.
After completion of all her treatments, the patient underwent another bone marrow biopsy as well as another PET scan (). Both showed evidence of a CR. At the time of this writing, the patient is 1 year out from the time of her diagnosis. She is continuing to do well except for a stable mild leukopenia (WBC of 3.93 × 109/L). She has not shown any signs of relapse.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.3, 'g/dL'], 'Calcium': [8.4, 'mg/dL']}",9.76,9.272,10.248,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.3 g/dL. 
The concentration of Calcium is 8.4 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.3 g/dL)) + 8.4 mg/dL = 9.76 mg/dL.
The patient's corrected calcium concentration 9.76 mg/dL."
2668,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7238301-1,Extracted,"A 61-year-old male with a past medical history of type 2 diabetes mellitus (T2DM),
hypertension, and hyperlipidemia presented to the office for a regular follow-up.
Vital signs were as follows: blood pressure 124/72 mm Hg, heart rate 78 bp,
respiratory rate 12 bpm, and temperature 98.3 F. The patient was asymptomatic.
Family history included T2DM in both parents and cardiovascular disease in his
mother, but no history of congenital diseases or malignancies. He denied smoking,
alcohol abuse, or illicit drug intake. Home medications consisted of amlodipine,
valsartan, atorvastatin, pioglitazone, metformin, insulin detemir, liraglutide, and
dapagliflozin. Patient took no calcium, vitamin D supplementation, and no proton
pump inhibitors (PPIs) or histamine H2-receptor antagonists. No known allergies to
medications were reported. Patient stated he had been properly hydrating himself. He
denied palpitations, fatigue, abdominal pain, polyuria, impaired concentration,
constipation, dysuria, flank pain or a history of nephrolithiasis, weight loss,
night sweats, dyspnea, cough, and rash. He also denied smoking, drinking alcohol, or
using recreational drugs. Physical examination was unremarkable, and vital signs
were within normal levels. There was no evidence of dehydration. Patient underwent
laboratory testing the day prior to being seen. Results were significant for calcium
11.1 mg/dL, albumin 4.7 g/dL, blood urea nitrogen (BUN) 21 mg/dL, creatinine
0.91 mg/dL, chloride 101 mmol/L, and fasting glucose 139 mg/dL. Careful history
revealed that, the evening prior the blood draw, the patient experienced an unusual
episode of sudden-onset epigastric burning and took six chewable tables of Tums
200 mg calcium (500 mg). Patient denied taking Tums on a regular basis and had not
had any in weeks. Patient was asked to refrain from ingesting Tums or any other
over-the-counter antacid medication and increase oral hydration. Given the mild
elevation in calcium and the lack of palpitations or tachycardia, an
electrocardiography was not ordered. Five days later, he went for repeat blood work.
By this time, calcium normalized to 9.3 mg/dL, thus ruling out hyperparathyroidism.
Ionized calcium and parathyroid hormone intact were 4.8 mg/dL and 54 pg/mL,
respectively. Urine protein electrophoresis and serum protein electrophoresis did
not detect any monoclonal proteins. Of note, patient never had an event of
hypercalcemia, either before or after this episode.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.7, 'g/dL'], 'Calcium': [11.1, 'mg/dL']}",10.54,10.013,11.067,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.7 g/dL. 
The concentration of Calcium is 11.1 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.7 g/dL)) + 11.1 mg/dL = 10.54 mg/dL.
The patient's corrected calcium concentration 10.54 mg/dL."
2669,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,usmle-9509,Extracted,"A 67-year-old man comes to the physician for a follow-up examination. He has had lower back pain for several months. The pain radiates down the right leg to the foot. He has no history of any serious illness and takes no medications. His pain increases after activity. The straight leg test is positive on the right. The results of the laboratory studies show:
Laboratory test
Hemoglobin 14 g/d
Leukocyte count 5,500/mm3 with a normal differential
Platelet count 350,000/mm3
Serum
Calcium 9.0 mg/dL
Albumin 3.8 g/dL
Urea nitrogen 14 mg/dL
Creatinine 0.9 mg/dL
  Serum immunoelectrophoresis shows an immunoglobulin G (IgG) type monoclonal component of 40 g/L. Bone marrow plasma cells return at 20%. Skeletal survey shows no bone lesions. Magnetic resonance imaging (MRI) shows a herniated disc at the L5.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.8, 'g/dL'], 'Calcium': [9.0, 'mg/dL']}",9.16,8.702,9.618,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.8 g/dL. 
The concentration of Calcium is 9.0 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.8 g/dL)) + 9.0 mg/dL = 9.16 mg/dL.
The patient's corrected calcium concentration 9.16 mg/dL."
2670,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4421631-1,Extracted,"A 70-year-old woman with a history of hypertension and osteoporosis presented with progressive renal insufficiency, abnormal fatigue for several months and increasing shortness of breath during exercise. Five months previously, an invasive ductal breast carcinoma (pT2, pTis, pN0, cM0 and R0) had been diagnosed, and the patient underwent breast-conserving tumour resection, followed by adjuvant radiotherapy and treatment with a non-steroidal aromatase inhibitor. On admission, the patient appeared to be in a good general condition (weight 53 kg, height 168 cm and BMI 19 kg/m2) and seemed only slightly affected. Vital signs were normal (blood pressure 130/60 mmHg and heart rate 80 bpm), and physical examination was unremarkable. The patient’s medication included letrozole, calcium and vitamin D3. Previous administration of alendronate had been stopped before admission. Laboratory testing showed impaired renal function with a creatinine of 297 μmol/L and an estimated glomerular filtration rate (GFR) of 14 mL/min/1.73 m2. Serum calcium level was significantly elevated (3.6 mmol/L) in the presence of slightly lowered serum albumin (31 g/dL). A blood count showed normocytic anaemia (haemoglobin 11,5 g/dL), leucocytopaenia (2840/μL) and a normal platelet count; a differential blood count revealed significant lymphocytopaenia (227/μL). Further biochemical tests demonstrated hyperphosphataemia (2.4 mmol/L) but normal values for parathyroid hormone and C-reactive protein. Urinalysis showed signs of prevailing tubulointerstitial nephritis with minor leucocyturia, predominant tubular proteinuria and mild haematuria.
A diagnostic work-up was performed to establish the cause of hypercalcaemia and bicytopaenia and to identify the underlying renal disease. A skeletal scintigraphy ruled out bone metastatic disease, and abdominal ultrasound did not show any isolated metastases or a tumour mass. Renal ultrasound demonstrated kidneys of normal size with hyperechoic parenchyma and hypoechoic pyramids as well as signs of nephrocalcinosis. Computed tomography of the chest revealed two new very small nodular lesions in both upper lobes; however, there was no notion of enlarged intrathoracic lymph nodes. Spirometric testing was within the normal range (FEV1 85%, VCin 99%, FEV1/VCin 90% and pO2 84 mHg). Subsequent bronchoscopy showed a macroscopically normal bronchial system, and bronchoalveolar lavage did not reveal suspicious cells or any infectious pathogen but a lymphocytic cell profile with an elevated T4/T8 ratio of 5.5. A renal biopsy was performed: histopathology displayed a few moderate epithelioid cell granulomas with interstitial nephritis, slight nephrocalcinosis and moderate focal tubular atrophy, suggesting sarcoid nephropathy (A and B). Bone marrow biopsy demonstrated impaired haematopoiesis with slight siderosis, moderate plasmocytosis and surprisingly also an epithelioid cell granuloma (C), consistent—although non-specific—with manifestation of sarcoidosis. Immunophenotyping of the bone marrow revealed CD138/CD19-positive plasma cells, but no light chains or any other B- or T-cell clonal disease. Revision of a lymph node biopsy, previously performed for staging of the breast cancer, also revealed an epithelioid cell granuloma (D). Further laboratory testing was negative for immunological antibodies, including antinuclear antibodies and c- and p-ANCAs, but showed elevated serum levels for angiotensin-converting enzyme (137 U/L, normal < 52). Echocardiography demonstrated moderate left ventricular hypertrophy with normal systolic function and slight diastolic dysfunction.
Altogether, a diagnosis of sarcoidosis with renal, pulmonary, bone marrow and lymph node involvement was made, while cardiac manifestation was suspected. Treatment with prednisolone resulted in significantly improved renal function within several days, normalized calcium and phosphate values, and led to a haemoglobin and leucocyte count within the normal range. Follow-up studies 3 months later showed an almost normal serum creatinine level of 108 μmol/L with an estimated GFR of 46 mL/min/1.73 m2, a normalized ACE level and regressive pulmonary lesions.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [31.0, 'g/dL'], 'Calcium': [3.6, 'mmol/L']}",-7.171,-6.81245,-7.52955,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 31.0 g/dL. 
The concentration of Calcium is 3.6 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 3.6 mmol. To convert 3.6 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 3.6 mmol Calcium * 0.001 mol/mmol = 0.0036 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.0036 mol Calcium * 40.08 g/mol = 0.14429 g Calcium. To convert 0.14429 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.14429 g Calcium * 1000.0 mg/g = 144.29 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 144.29 mg Calcium/10.0 dL = 14.429 mg Calcium/dL. The concentration value of 3.6 mmol Calcium/L converts to 14.429 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 31.0 g/dL)) + 14.429 mg/dL = -7.171 mg/dL.
The patient's corrected calcium concentration -7.171 mg/dL."
2671,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6007257-1,Extracted,"A 55-year-old female patient was examined in the emergency department with abdominal pain that had been persistent for ~10 days and having been aggravated for the last 3–4 days. Her past history was notable for diabetes mellitus (DM) for ~25 years. Additionally, she had undergone a coronary by-pass operation 10 years ago and a left infrapatellar amputation 4 years ago. Chronic renal failure had been diagnosed 2 years ago and she had been receiving hemodialysis treatment three times a week for the last 1 year. She had no history of abdominal trauma. Laboratory tests resulted with; White Blood Cell: 15 100/mm3, Hemoglobin: 8.5 g/dL, C-reactive protein: 40 mg/dL, Urea: 37.9 mg/dL, Creatinine: 2.25 mg/dL, Albumin: 2.4 g/dL, Sodium: 134 mmol/L, Potassium: 3.1 mmol/L, Calcium: 7.9 mg/dL, Glucose: 329 mg/dL and other biochemical parameters were normal. The abdomen was diffusely tender, and she also had guarding and rebound tenderness during the physical examination. Blood temperature was 38.7°C. An abdominal ultrasonography (US) showed diffuse intraabdominal free fluid collection. On an abdominal computed tomography (CT) there were free fluid collections in all abdominal quadrants; there also existed intraabdominal minimal free air images. There were air-fluid images in the splenic parenchyma (abscess?, perforation?) (Fig. a). The radiology department reported that it may be a gastrointestinal perforation. Based on the current findings, the patient was urgently operated according for a preliminary diagnosis of acute abdomen. Intraabdominal seropurulent fluid of ~2000 ml was aspirated perioperatively. There were diffuse fibrin matrixes in the entire peritoneum. No intestinal perforation was noted during exploration. There was a perforated abscess pouch with a size of ~8 × 6 cm2, which expanded posteriorly from splenic hilus and partly contained necrotic foci (Fig. b). Splenectomy and drainage were performed and the abdominal cavity was irrigated with abundant isotonic saline. Patient was postoperatively monitored in intubated state at intensive care unit. No proliferation occurred in her blood culture. Escherichia coli was isolated from the abscess culture, however, and Meropenem 500 mg I.V. (three times a day) and Metronidazole 500 mg I.V. (three times a day) treatment was commenced as recommended by the infectious diseases department. Her dialysis program was maintained according to blood parameters. The patient died on postoperative Day 25 due to septic shock and multiple organ failure. Histopathologic examination revealed suppurative inflammation and abscess formation of the splenic tissue (Fig. ). Informed consent was obtained from her son who participated in this case.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.4, 'g/dL'], 'Calcium': [7.9, 'mg/dL']}",9.18,8.721,9.639,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.4 g/dL. 
The concentration of Calcium is 7.9 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.4 g/dL)) + 7.9 mg/dL = 9.18 mg/dL.
The patient's corrected calcium concentration 9.18 mg/dL."
2672,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4532051-1,Extracted,"A 49-year old man was admitted to our hospital because of painless swelling of both testes and multiple bone pain. Five months before admission, he noticed a slight enlargement of the right testis. The enlargement of the right testis progressed slowly and, a few weeks later, the left testis was enlarged also.
On admission, he showed an acutely-ill looking appearance and was slightly thin. The vital signs were within normal range. There were no abnormal findings in skin and hair. He had slightly pale conjunctivae and anicteric sclerae. Peripheral lymph nodes were not palpable. His breath sound was clear and no adventitious sound was heard. His heart beat was regular and no murmur was heard. On abdominal palpation, liver, spleen or kidney were not palpable.
Both testes were nearly the same in size and were palpable as nontender, hard, movable masses. The size of the right and left testes were about 10 cm×15 cm and 10 cm×12 cm in diameter, respectively. Bony tenderness was prominent especially on both thighs.
Laboratory findings were as follows; Complete blood counts were hemoglobin 9.5 gm/dl, hematocrit 28%, leukocyte 14,000/mm3 and platelet 140,000/mm3. Blood chemistry tests showed Ca 11.7 mg/dl, P 6.4 mg/dl, total protein 9.5 g/dl, albumin 2.9 g/dl, LDH 509 IU/I, BUN 55 mg/dl, creatinine 7.1 mg/dl, IgG 3,460 mg/dl, IgM 64 mg/dl, IgA 43 mg/dl, IgD 1.1 mg/dl. He had proteinuria (5,905 mg/24 hours) and creatinine clearance was measured as 9 ml/min. Serum protein electrophoresis showed M-peak in γ-region and M-component was measured as 43.4%. Serum Immunoelectrophoresis showed monoclonal gammopathy in IgG, k band. Urine PEP and IEP showed kappa type light chain (M-peak). Radiologic examination revealed multiple punched-out osteolytic lesions in the skull. Bone marrow aspiration showed 65% plasma cell infiltration. Bone marrow biopsy revealed hypercellular marrow packed with immature plasma cells. Testis ultrasonography showed heterogeneous hypoechogenicity. Testicular needle biopsy showed diffuse infiltration of atypical large lymphoid cells with feature of poorly differentiated plasma cell nature between seminiferous tubules and inside of them as well (). Immunohistochemical studies revealed positivity for L26 (CD20) and Ig k predominance on infiltrating neoplastic plasmacytoid cells ().
The patient was initially treated with combination chemotherapy of vincristine, melphalan and prednisolon. After the 2nd cycle of treatment, the testicular enlargement was not decreased and multiple bone pain was aggravated. Palliative radiotherapy was given on both testes with some improvement. After that, he was treated with combination chemotherapy of vincristine, adriamycin and dexamethasone. One month later, however, numerous soft tissue nodules newly appeared on the left forearm, both lower legs, and chest wall. Somewhat later, follow-up chest x-ray showed multiple, variable sized round opacity in both whole lung fields with pleural effusion. The patient had a rapidly progressive downhill course and died 6 months after initial diagnosis.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [11.7, 'mg/dL'], 'Albumin': [2.9, 'g/dL']}",12.58,11.951,13.209,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.9 g/dL. 
The concentration of Calcium is 11.7 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.9 g/dL)) + 11.7 mg/dL = 12.58 mg/dL.
The patient's corrected calcium concentration 12.58 mg/dL."
2673,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4851541-1,Extracted,"A 6-year-old boy was admitted to our department due to vomiting, weakness, polyuria, polydipsia, irritability and weight loss in the last few weeks. The patient is the third child of the fourth pregnancy, one of which ended up with abortion. He was born at term, through Cesarean section, weighting 3400 g. Down syndrome was suspected clinically at birth and confirmed by karyotyping (47XX, t21).
The body weight on admission was 14.5 kg and the body height was 93 cm (20th and 5th percentile for sex and age in Down syndrome, respectively) ().
Typical features of Down syndrome were present, including typical facies and generalized hypotonia. A 3/6 heart murmur was heard on auscultation, and transthoracic echocardiography revealed a low grade aortic regurgitation. The rest of his physical examination was unremarkable.
Laboratory studies revealed red blood cell count 2.14 × 1012/l, Hb 6.1 gr/dL, Htc 17.5%, platelet count 272000/mm3, white blood cell count 7800/mm3, ESR 60 mm/h, CRP 26 mg/l, urea 12.7 mmol/1, creatinine 160 umol/1, Na 136 mEq/L, K 2.7 mEq/L, Cl 108 mEq/L, Ca 9.8 mg/dL, ionised Ca 1.28 mmol/1, Mg 1.0 mmol/1, total serum proteins 59.6 g/l, albumins 32.3 g/l, fasting blood glucose 5.6 mmol/l, cholesterol 6,1 mmol/l, triglycerides 2.3 mmol/l and alkaline phosphatase 49 U/l. Results of the capillary blood gas analysis were as follows: pH 7.25, PCO2 26 mmHg, HCO3 14 mEq/L.
Routine urine analysis showed mild proteinuria (+) and negative glucose. Urine microscopy showed 15 erythrocytes/hpf, 20 leucocytes/hpf and 20-30 bacteria/hpf; specific gravity was 1.005, and urinary pH was 7.0. Urine culture resulted positive for E. Coli.
Urinary uric acid was low at 774.0 umol/24h (normal values 1480-4430 umol/24h) as was citrate 21 mg/24h (normal value >115mg/24h). The urine calcium to creatinine ratio was 1.2 mmol/mmol (normal value < 1.1 mmol/mmol). In the view of normal anion gap hyperchloremic metabolic acidosis, alkaline urine and hypokalemia the diagnosis of dTRA was made.
Additional analysis searching for etiology of dTRA revealed serum 1,25-dihydroxyvitamin D 1.2 ng/ml (normal values 10.8-54 ng/ml), parathyroid hormone 27.2 pg/ml (normal values 6.5-36.8 pg/ml), free serum T4 2.20 pmol/l (normal values 10.3-25.8 pmol/l) and thyroid-stimulating hormone >1000.0 mU/l (normal values 0.54-4.21 mU/l). Prolactin was 163.9 ng/mL (normal values 3.2-20 ng/mL), while other hormonal profiles such as adrenocorticotropic hormone, luteinizing hormone, follicle-stimulating hormone and growth hormone were normal. Anti-thyroid peroxidase (TPO) antibody was >1000.0 IU/ml (normal value <50 IU/ml) and Thyroglobulin (hTg) was 3.41 ng/ml (normal values 0.2-70.0 ng/ml). Hence, Hashimoto thyroiditis as a possible cause was postulated. Moreover, antinuclear antibodies (ANA) test resulted negative.
The renal ultrasound showed hyper-echoic regions in the renal medulla consistent with bilateral nephrocalcinosis grade I (), also confirmed by abdominal CT (). Brain magnetic resonance imaging revealed pituitary enlargement ().
Treatment and follow up
Intravenous rehydration was started. The bicarbonate deficit was calculated, and KCl was added after the patient had his first urinary void. Blood gas analysis after 12 hours revealed increasing pH, HCO3 and K values. Packed red blood cells were then administered. The patient was put on potassium citrate and thyroid hormone substitution therapy. Also, intravenous antibiotherapy and oral ferrous supplements were started to treat urinary tract infection and anemia, respectively. On follow-up after six months, no evidence of metabolic acidosis and a nearly normal serum potassium level (3.4 mEq/L) were found. Urinary random analysis was normal. Patient’s weight was 16 kg and his height 98 cm (25th and 10th percetile, respectively). His thyroid hormone profile was within normal range. Also, prolactin, cholesterol, triglycerides and complete blood count analysis were normalizing. The patient is on regular follow-up.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [32.3, 'g/L'], 'Calcium': [9.8, 'mg/dL']}",10.416,9.8952,10.9368,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 32.3 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 32.3 g Albmumin/10.0 dL = 3.23 g Albmumin/dL. The concentration value of 32.3 g Albmumin/L converts to 3.23 g Albmumin/dL. 
The concentration of Calcium is 9.8 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.23 g/dL)) + 9.8 mg/dL = 10.416 mg/dL.
The patient's corrected calcium concentration 10.416 mg/dL."
2674,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,usmle-6933,Extracted,"A 32-year-old woman presents to the office with complaints of frothy urine and swelling in her body that started 6 days ago. She says that she first noticed the swelling in her face that gradually involved other parts of her body. On further questioning, she gives a history of rheumatoid arthritis for 2 years. She is taking Penicillamine and Methotrexate for the past 6 months. Vitals include: blood pressure 122/89 mm Hg, pulse rate 55/min, temperature 36.7°C (98.0°F), and a respiratory rate 14/min. On examination, there is generalized pitting edema along with some subcutaneous nodules on the dorsal aspect of the forearm.
Urinalysis
pH 6.6
Color light yellow
RBC none
WBC 1–2/HPF
Protein 4+
Cast fat globules
Glucose absent
Crystal none
Ketone absent
Nitrite absent
24 hours urine protein excretion  4.8 g
    Basic metabolic panel
Sodium 141 mEq/L
Potassium 5.1 mEq/L
Chloride 101 mEq/L
Bicarbonate 22 mEq/L
Albumin 3.2 mg/dL
Urea nitrogen 17 mg/dL
Creatinine 1.3 mg/dL
Uric Acid 6.8 mg/ dL
Calcium 8.9 mg/ dL
Glucose 111 mg/dL
A renal biopsy is ordered which shows diffuse capillary and glomerular basement membrane thickening.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.2, 'mg/dL'], 'Calcium': [8.9, 'mg/dL']}",12.09744,11.49257,12.70231,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.2 mg/dL. We need to convert the concentration to g/dL. Let's first convert the mass of Albmumin from mg to g. The mass of Albmumin is 3.2 mg. To convert 3.2 mg of Albmumin to g, multiply by the conversion factor 0.001, giving us 3.2 mg Albmumin * 0.001 g/mg = 0.0032 g Albmumin. The volume units is dL so no volume conversion is needed. Hence, the concentration value of 3.2 mg Albmumin/dL converts to 0.0032 g Albmumin/dL. 
The concentration of Calcium is 8.9 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 0.0032 g/dL)) + 8.9 mg/dL = 12.09744 mg/dL.
The patient's corrected calcium concentration 12.09744 mg/dL."
2675,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6639584-1,Extracted,"A 61-year-old female with colonic and perianal Crohn's disease, a chronic nonhealing wound in the perineum, a 4-month history of anal squamous cell carcinoma treated with combination chemoradiation presented to her family physician with a 10-day history of diffuse paresthesia and numbness on October 6, 2016, approximately 5 weeks following discharge from the local cancer center.
Originally diagnosed with Crohn's disease at 19 years of age, she had undergone 4 previous bowel resections with the last one at the age of 49. She presented with a perineal mass on May 6, 2016 and began outpatient mitomycin C and 5-fluorouracil with daily radiation treatments directed to the pelvis and anal canal on June 27. She completed 18 of 30 radiotherapy fractions as an outpatient but was admitted to the local cancer center on July 23 for management of pain associated with radiation desquamation and significant metabolic abnormalities including dehydration, hypotension, and hypomagnesemia related to a high-output ileostomy. Her radiotherapy was completed on August 10 and at discharge on August 30, she was using loperamide 2–4 mg orally b.i.d. and psyllium b.i.d. p.r.n. to regulate her ostomy output, was on morphine 15 mg orally every 4 h and 10 mg orally every 1 h p.r.n. for pain control and a variety of oral supplements (vitamin D 2,000 IU daily, zinc 50 mg daily, selenium 50 mg daily, calcium 1,000 mg daily, centrum multivitamin b.i.d.).
After presenting on October 6, she was found to have several electrolyte and fluid imbalances including hypomagnesemia (0.41 mmol/L), hypokalemia (3.1 mmol/L), elevated serum creatinine (123 mmol/L; estimated glomerular filtration rate [eGFR] 41 mL/min/1.73m2), total calcium 1.82 mmol/L (albumin 37 g/L), and her symptoms were successfully managed in the emergency department with a 2-g intravenous bolus dose of magnesium sulfate (Fig. ). There she was prescribed 75 mg (3 mmol) of elemental magnesium orally twice daily as magnesium glucoheptonate 1,500 mg/15 mL b.i.d. and calcium carbonate 500 mg b.i.d. Subsequent monitoring indicated an increase in her magnesium concentrations over the course of the next month, but she continued to empty her ostomy approximately 12 times per day and her serum creatinine (151 mmol/L; eGFR: 32 mL/min/1.73m2) indicated prerenal renal insufficiency.
On November 8, home subcutaneous normal saline infusions (1 L over 8–12 h overnight) were started and her psyllium and loperamide therapy were increased to 4 mg q.i.d, while she continued magnesium glucoheptonate 1,500 mg magnesium orally b.i.d. Over the next 10 weeks, her eGFR improved, stabilizing in the 40–50 mL/min/1.73m2 range, her magnesium glucoheptonate was titrated up to 3,000 mg (150 mg [6 mmol] orally t.i.d. in response to dropping magnesium concentrations [0.49 mmol/L on November 22]), and Codeine Contin was added and titrated up to 100 mg b.i.d. Despite this, over the next month, her magnesium concentrations showed a downward trend and on January 23, 2017, her magnesium was 0.46 mmol/L and she received a 2-g intravenous bolus dose of magnesium sulfate in the emergency department on January 25. She continued to have high ostomy output (i.e., 300–400 mL every 2–3 h) and on February 1, pantoprazole 40 mg daily was added, cholestyramine was prescribed in place of psyllium, stool cultures were collected (subsequently Clostridium difficile negative), and she was booked for upper endoscopy/ileoscopy to evaluate for recurrence of Crohn's disease.
While her family physician was arranging intermittent intravenous magnesium sulfateboluses at the hospital-based infusion clinic, her magnesium level continued downward to 0.43 mmol/L and she received 2 g of magnesium sulfate intravenously in the emergency department on February 24 and 26. After receiving a third dose of 2 g magnesium sulfate intravenously at the infusion clinic on March 2, she was electively admitted to the Inpatient Gastroenterology Service to expedite the investigation of her high-output ileostomy/hypomagnesemia and there received another dose of intravenous magnesium sulfate. Endoscopy showed mild gastritis, ileostomy and computed tomography enterography ruled out recurrent Crohn's disease, and her urine magnesium level was <0.40 mmol/L ruling out renal losses. Radiation enteritis was the presumed diagnosis on discharge (March 6) and no changes were made to her medications except pantoprazole was discontinued. Three weeks later (March 27), her magnesium was 0.55 mmol/L and another dose of magnesium sulfate 2 g was administered at the infusion clinic. On April 21, a consultant nephrologist suggested adding magnesium sulfate to her home subcutaneous fluid. While the feasibility of this recommendation was being explored, the patient had an emergency department visit on June 2 for general weakness and required two further 2-g bolus doses of magnesium sulfate at the infusion clinic on May 24 and July 5.
On July 19, 2017, the patient returned to the family medicine clinic to discuss initiating home subcutaneous magnesium sulfate supplementation. The patient agreed and was instructed to add magnesium sulfate 1 g (i.e., 4 mmol elemental Mg2+; 5 mL 200 mg/L magnesium sulfate) to her 500 mL normal saline infusion on 2 consecutive days, take 1 day off, then repeat the dose on the following 2 consecutive days. The clinic registered nurse instructed the patient on how to prepare and administer the infusion overnight. One week later, on July 25, her magnesium level was 0.88 mmol/L. She tolerated the infusions well with only a minor burning sensation and no significant side effects. After 2 more doses, her next magnesium level on July 31 was 0.87 mmol/L. During the following week, she took 2 serial doses followed by 3 days off and her next magnesium level on August 8 was maintained at 0.86 mmol/L. As shown in Figure , subsequent subcutaneous magnesium infusions on 2 days on a 3-days-off schedule were successful in maintaining magnesium concentrations >0.7 mmol/L for the next 6 weeks.
Due to a continued high output from her ileostomy (i.e., 300 mL, 12–15 times per day), the patient was assessed at the GI Malnutrition Clinic on September 22. Tethering of the bowel secondary to radiation, abnormal motility related to multiple previous surgeries, and bacterial overgrowth were suspected. She was started on a course of cyclical ciprofloxacin 500 mg b.i.d. and metronidazole 500 mg b.i.d., 2 weeks on and 1 week off, and restarted pantoprazole 40 mg twice daily. Her other therapies were unchanged.
The patient continued to tolerate the subcutaneous magnesium infusions well. However, on October 10, during a preoperative medical treatment for perineal wound closure, she complained of a 1-day history of pain and erythema on the left side of her abdomen where she last had her infusion, chills, and had a temperature of 38.0°C. She was treated for a presumed early cellulitis with a 7-day course of oral cephalexin.
In follow-up at the Malnutrition Clinic on November 3, the patient reported emptying her ileostomy less frequently and was advised to continue the cyclical antibiotics. As her magnesium was 0.67 mmol/L and renal function was stable (eGFR = 50 mL/min/1.73m2), she continued subcutaneous magnesium infusions but switched to oral magnesium glycinate 2,000 mg (200 mg [8 mmol] elemental magnesium) 2 tablets three times daily from magnesium glucoheptonate. Between November 21 and December 7, the patient was admitted to hospital for elective closure of her perineal wound. At her third visit to the Malnutrition Clinic (January 12, 2018), her weekly magnesium concentrations were noted to be between 0.73 and 0.92 mmol/L and she was advised to reduce the frequency of magnesium infusions to 2 days on 4 days off and to start a trial of cutaneous magnesium lotion.
On follow-up, at the Malnutrition Clinic on May 18, her subcutaneous magnesium infusions were stopped as her ileostomy output was <2 L per day and her magnesium levels were consistently >0.7 mmol/L. For the next 4 months, she consistently maintained magnesium levels above 0.7 mmol/L with oral magnesium glycinate therapy. However, she still required ongoing subcutaneous parenteral saline 500 mL daily to maintain fluid status. As of the time of writing in March 2019, her most recent magnesium was 0.77 mmol/L and she remains off subcutaneous magnesium supplementation.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [37.0, 'g/L'], 'Calcium': [1.82, 'mmol/L']}",7.535,7.15825,7.91175,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 37.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 37.0 g Albmumin/10.0 dL = 3.7 g Albmumin/dL. The concentration value of 37.0 g Albmumin/L converts to 3.7 g Albmumin/dL. 
The concentration of Calcium is 1.82 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.82 mmol. To convert 1.82 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.82 mmol Calcium * 0.001 mol/mmol = 0.00182 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00182 mol Calcium * 40.08 g/mol = 0.07295 g Calcium. To convert 0.07295 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.07295 g Calcium * 1000.0 mg/g = 72.95 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 72.95 mg Calcium/10.0 dL = 7.295 mg Calcium/dL. The concentration value of 1.82 mmol Calcium/L converts to 7.295 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.7 g/dL)) + 7.295 mg/dL = 7.535 mg/dL.
The patient's corrected calcium concentration 7.535 mg/dL."
2676,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3639672-1,Extracted,"A 45 year-old Hispanic male presented to the emergency department (ED) with complaints of weakness and myalgias for the preceding month with worsening on the days prior to admission. Physical exam was grossly unremarkable and vital signs were stable. He was found to be anemic with hemoglobin of 7.8 g/dL. In addition he had a platelet count of 73,000/mL. Other pertinent laboratory findings included a blood urea nitrogen (BUN) of 41 mg/dL, creatinine of 2.6 mg/dL, calcium 12.3 mg/dL and ionized calcium level was 1.59. Total protein was 7.6 g/dL and albumin was 4.1 g/dL. The patient's chest radiograph showed increased vascular markings and reticulonodular opacifications (see ). Computed tomography (CT) scans of chest also revealed diffuse ground-glass nodular opacities, with numerous poorly defined nodules measuring 3–10 mm in diameter both (see ). A skeletal survey revealed punched-out defects consistent with multiple myeloma (MM). The patient underwent a Technetium (Tc) 99 bone scan, which revealed diffuse activity in the lung with significant lighting up of the pulmonary parenchyma, consistent with metastatic pulmonary calcification (see ).
A subsequent serum protein electrophoresis revealed elevation of the free lambda light chain to 14,400 mg/L (normal range 5.71–26.3 mg/L). A bone marrow biopsy revealed massive plasmacytosis. The patient underwent standard therapy for his anemia and hypercalcemia and was seen by the oncology and nephrology services. Once discharged the patient was eventually lost in followup due to medical noncompliance. Our last search indicated that the patient has expired due to hypoxia and noncompliance with the hemodialysis sessions.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.1, 'g/dL'], 'Calcium': [12.3, 'mg/dL']}",12.22,11.609,12.831,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.1 g/dL. 
The concentration of Calcium is 12.3 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.1 g/dL)) + 12.3 mg/dL = 12.22 mg/dL.
The patient's corrected calcium concentration 12.22 mg/dL."
2677,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6823037-1,Extracted,"A 61-year-old man arrived at the emergency department reporting abdominal pain, persistent nausea, and vomiting for three weeks. It was localized to the upper-mid abdomen and was constant, dull, and 5-7 out of 10 in intensity and non-radiating. The pain was predominantly diurnal and aggravated with food intake but did not relieve with eructation, vomiting, bowel movements, or change in position. The pain was associated with nausea, followed by nonbilious, nonbloody vomiting unrelated to eating. He had not attempted to treat the symptoms with medications. He reported a 25-pound unintentional weight loss in the last month but denied fever, jaundice, change in the color of his urine or stool, chest pain, cough, shortness of breath, diarrhea, constipation, urinary symptoms, or fatigue.
Abdominal pain associated with nausea and vomiting is a common presenting symptom for patients seeking evaluation in the emergency department. A multitude of disorders affecting various organ systems such as the gastrointestinal tract, cardiovascular, endocrine, metabolic, CNS, renal, hematological, malignant and nonmalignant processes may be associated with such symptoms. A comprehensive history and physical examination need to be conducted to identify potential etiologies to the underlying processes.
The patient’s medical history was positive for atraumatic and intermittent back pain for the past six months. Lower back pain that persisted mostly during day-time worsened with a change in position. Family history was pertinent for high blood pressure and diabetes in both mother and brother. The patient denied taking any medications, herbal, or nutritional supplements. He denied smoking, alcohol intake, or drug use. He had not been sexually active for many years and did not have a history of sexually transmitted infection. The patient was originally from Latin America, but had not traveled outside the US in the past several years and had not seen a physician for the last 20 years. He lived alone and worked as a laborer. On physical examination, the patient appeared to be in no pain. The temperature was 97.1 °F, heart rate 81 beats per minute, blood pressure 140/88 mmHg, respiratory rate 20 breaths per minute, and oxygen saturation 100% at room air. Oral mucosa was dry. Sclera was anicteric. No conjunctival pallor was noted. The abdominal examination demonstrated normal bowel sounds, mild diffuse tenderness to deep palpation, which was most prominent over the epigastric region. There was no rigidity, guarding, or organomegaly. Murphy sign was negative. No abdominal bruits were noted. CVA tenderness was not elicited. Cardiac, respiratory, skin, musculoskeletal, and neurologic examinations were unremarkable.
Initial laboratory investigations revealed white cell count 8.5 k/uL (4.0-10.5), hemoglobin 12.1 g/dL (13.5-18.0), platelet count 203 k/uL (150-450), glucose 161 mg/dl (70-105), creatinine 10.8 mg/dl (0.7-1.3), blood urea nitrogen 65 mg/dl (7-25), bicarbonate 30 mg/dl (21-32), calcium 9.2 mg/dl (8.6-10.3), lipase 31 U/L (11-82), albumin 3.8 g/dl (3.5-5.0), globulin 3.0 g/dl, and total protein 6.8 g/dl (6.0-8.3). Hemoglobin A1c was 8.35. Urinalysis demonstrated trace leukocyte esterase, protein 30 mg/dl, and trace blood on dipstick. Microscopic analysis revealed no white blood cells, red blood cells, casts, crystals or bacteria.
The most remarkable finding on laboratory studies was the significantly reduced glomerular filtration rate. Given the history of nausea and vomiting over the past 2-3 weeks and the presence of elevated serum bicarbonate, it is likely that volume depletion and prerenal azotemia contributed to his kidney failure. On the other hand, the absence of hypotension or significant tachycardia made it unlikely that hypovolemia was the sole cause of his renal failure. The presence of mild proteinuria could be consistent with intrinsic renal disease. Elevated blood glucose and HbA1c suggested the possibility of diabetic nephropathy, which is the most common cause of end-stage renal disease, but it is highly unlikely that unrecognized diabetic nephropathy was the primary cause of renal failure in this case.
Abdominal ultrasonography showed normal-sized kidneys with normal cortical thickness, no hydronephrosis or evidence of urolithiasis, and no masses. The right kidney measured 11.7 cm longitudinally and the left kidney measured 12.3 cm longitudinally. Liver, spleen, gallbladder, and bile ducts were normal in size and appearance. A non-contrast computed tomography (CT) scan (Figure ) of the abdomen obtained in the emergency room confirmed normal size kidneys (arrows) and nonspecific bilateral perinephric stranding (arrowhead) and descending and sigmoid colon diverticulosis.
The patient initially received 2 L of intravenous crystalloid that was stopped when he developed dyspnea and jugular vein distension. His urine output over 12 hours was 1 liter. His vital signs remained stable, but the physical examination was consistent with a hypervolemic state. Creatinine levels decreased from 10.8 to 10.1 mg/dL.
The minimal improvement in kidney function with volume expansion excluded prerenal azotemia as the main cause of kidney failure. The imaging studies effectively ruled out the possibility of obstructive uropathy. The most striking feature of his imaging studies was the absence of gross evidence of chronic kidney damage such as decreased kidneys, increased echogenicity, decrease in cortical thickness, or cyst formation. A number of chronic kidney diseases, such as diabetic nephropathy, amyloidosis, HIV nephropathy, and autosomal dominant polycystic kidney disease, can be associated with preserved, or even enlarged kidney size despite advanced kidney failure. Alternatively, the imaging findings were consistent with an acute process or subacute process, resulting in a significant reduction in renal function over the span of 2 to 3 weeks before admission but unchanged kidney size. Such acute and subacute processes might include acute tubular necrosis, acute allergic interstitial nephritis, acute crystal-induced nephropathy, acute glomerulonephritis, monoclonal gammopathy of renal significance, and myeloma cast nephropathy as possible differentials. Further serological workup for HIV, hepatitis viruses, serum protein electrophoresis, quantification of urine protein excretion, urine protein electrophoresis, measurement of serum complements, and tests for ANA and antineutrophil cytoplasmic antibodies including anti-PR3 and anti-MPO antibodies were obtained.
Spot urine protein/creatinine was 1.96 g/day. Serum protein electrophoresis showed a small abnormality in gamma fraction. Serological studies for anti-PR3 and anti-MPO antibodies and ANA were negative. Serum complements were within the normal range. Hepatitis screen and HIV serology were also negative.
Despite only trace urine protein detected on the dipstick, spot urine protein to creatinine ratio indicates the presence of substantial proteinuria. This finding associated with the abnormality detected on serum protein electrophoresis was indicative of potential paraproteinemia-related kidney disease. On subsequent serum immunofixation and serum-free light chain assay, he was found to have a very elevated serum kappa free light chains 1240 mg/dl (normal range: 0.3300 to 1.94 mg/dl) and kappa/lambda ratio 816 (normal range: 0.2600 to 1.65).
Severe renal failure in the presence of very high levels of free light chains is diagnostic of monoclonal gammopathy. To accurately assess the characteristics of the monoclonal gammopathy, the patient underwent bone marrow and renal biopsies. Bone marrow biopsy (Figure ) depicted sheets of plasma cells (arrows) comprising up to 80% of marrow cells in some areas.
Renal biopsy (Figure ) demonstrated tubules containing casts of glassy to slightly granular proteinaceous material (arrow). The tubular epithelium appeared attenuated and flattened in some area (arrowhead) consistent with cast nephropathy.
The diagnosis of IgD MM with myeloma cast nephropathy was confirmed. Skeletal survey was obtained, which was normal. The patient’s urine output remained stable and he did not require hemodialysis.
The patient received one cycle of cyclophosphamide 1,692 mg intravenously with subcutaneous bortezomib of 2.4 mg and dexamethasone 40 mg intravenously. Acyclovir of 200 mg daily was initiated for Varicella zoster prophylaxis. The patient was discharged after the first cycle of chemotherapy. His creatinine level has decreased to 7.3 mg/dl by the day of discharge from 10.5 mg/dl on admission. He has since completed three cycles of chemotherapy and his creatinine level has improved significantly to 1.5 mg/dl.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [9.2, 'mg/dL'], 'Albumin': [3.8, 'g/dL']}",9.36,8.892,9.828,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.8 g/dL. 
The concentration of Calcium is 9.2 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.8 g/dL)) + 9.2 mg/dL = 9.36 mg/dL.
The patient's corrected calcium concentration 9.36 mg/dL."
2678,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4363681-1,Extracted,"A 40-year-old female patient was admitted with right upper quadrant and epigastric pain and extremity weakness of 15-day duration. She had mild tenderness in the epigastrium and right upper quadrant. No rebound was detected. Physical examination revealed motor power grade 5/5 in the upper and lower limbs. Deep tendon reflexes were normal. Otherwise, there were no other neurological deficits. The only remarkable finding of the physical examination was a nodule in the right lobe of the thyroid.
Laboratory findings were as follows: aspartate transaminase: 11 U/L (8–40); alanine transaminase: 2 U/L (5–35); alkaline phosphatase: 99 U/L (104–338); serum calcium (Ca): 11 mg/dL (8.0–10.0); phosphor: 5.7 mg/dL (2.5–4.5); albumin: 4.3 g/dL (3.5–5.2); parathormone (PTH): 1906 pg/mL (15–65); free T3: 2.49 pg/mL (2.5–3.9); free T4: 1.1 ng/dL (0.61–1.12); thyroid stimulating hormone: 0.57 uIU/mL (0.34–4.2).
Ultrasound examination of the thyroid showed 27 × 35 × 75 mm left thyroid lobe and 22 × 31 × 63 mm right thyroid lobe. A nodule completely filling the left thyroid lobe containing both heterogeneous necrotic and calcified areas was observed on the ultrasound. Parathyroid scintigraphy showed the left thyroid compatible with parathyroid adenoma (). Multiple millimetric stones in the gallbladder were shown on the abdominal ultrasound. Plain abdominal radiography on admission showed a visible gallbladder with calcium density. Abdominal CT showed millimetric radiopaque stones in the gallbladder () and ultrasound showed an acoustic shadow consistent with gallstones. Since the patient had never received radiopaque agents, a diagnosis of LB was made. Cholecystectomy and parathyroidectomy were performed on the patient. The postoperative course was uneventful. Histological examination of the gallbladder showed chronic cholecystitis. The postoperative course was uneventful, and the patient was discharged on postoperative day 4. During the follow-up, PTH at 48 pg/mL, serum phosphor at 4.7 mg/dL, and calcium at 8.7 mg/dL returned to normal levels. The weakness gradually improved. The diagnosis was confirmed by pathological evaluation.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [4.3, 'g/dL'], 'Calcium': [11.0, 'mg/dL']}",10.76,10.222,11.298,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.3 g/dL. 
The concentration of Calcium is 11.0 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.3 g/dL)) + 11.0 mg/dL = 10.76 mg/dL.
The patient's corrected calcium concentration 10.76 mg/dL."
2679,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4020506-1,Extracted,"An 84-year-old male patient was admitted to the emergency department with a complaint of generalized weakness and reduced consciousness for two days. He had a history of Alzheimer's disease for one year and he had taken donepezil 5 mg daily for two months. He had no other diseases and he had not taken any other medications. He had no history of trauma, convulsion, previous fall, or alcohol intake.
The patient's physical examination revealed apathy, loss of cooperation, and decreased muscle strength. His temperature was 36.8°C, blood pressure 140/90 mm/Hg, and pulse rate 88 bpm. He had bilateral moderate pretibial edema.
Laboratory studies revealed the following: urea: 128 mg/dL; creatinine: 6.06 mg/dL; aspartate aminotransferase: 93 U/L; CK: 3613; calcium: 8.1 mg/dL; phosphorous: 4.9 mg/dL; sodium: 149 mmol/L; potassium: 4,3 mmol/L; albumin: 3.7 g/dL; lactate dehydrogenase: 349 U/L; hemoglobin: 14.2 g/dL; fT3: 3.5 (N: 1.71–3.71 pg/mL); fT4: 1.35 (N: 0.7–1.48 ng/dL); TSH: 2.04 (N: 0.35–4.94 uIU/mL). Urinary dipstick analysis was 1+ positive for protein and 3+ positive in the Haem test. Urinary sediment showed a few red blood cells and 2-3 leukocytes per high-power field. Arterial blood gases analysis was PH: 7.44, PCO2: 23 mmHg, PO2: 151 mmHg, SO2: 99.5%, and HCO3: 19 mmol/L.
The patient's renal function tests were performed by other health centers before two months and they were completely normal. His renal ultrasound evaluation was normal. The patient was evaluated by a neurologist and there was no neurologic pathology other than Alzheimer's disease. Echocardiography was performed and ejection fraction was 60%, left ventricle was concentric hypertrophic, and a minimal pericardial effusion was reported. The patient was admitted to the nephrology ward with a diagnosis of ARF. Donepezil was discontinued. There was no indication for emergent hemodialysis. Intravenous hydration therapy was given. The patient's renal function tests improved gradually and were normal after 12 days of the treatment. He was discharged with complete recovery.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.7, 'g/dL'], 'Calcium': [8.1, 'mg/dL']}",8.34,7.923,8.757,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.7 g/dL. 
The concentration of Calcium is 8.1 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.7 g/dL)) + 8.1 mg/dL = 8.34 mg/dL.
The patient's corrected calcium concentration 8.34 mg/dL."
2680,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3741440-1,Extracted,"A 40 year-old-female
Altered mentality
This previously healthy 40-year-old female was transported to the emergency room by her neighbors, who heard her moaning in her house. She lived alone, and 1 month prior to her admission, she developed the paranoid idea that her water was poisoned, and did not drink any water or beverages since then.
Non-contributory
Non-contributory
Her blood pressure was 100/60 mmHg, pulse rate 106/min, respiration rate 16/min, and body temperature 36.5℃. She looked chronically ill, and her skin and mucosa were extremely dehydrated. There was no evidence of trauma. A chest examination revealed a regular heart beat and clear breathing sounds. The abdomen was soft and flat with no palpable mass.
She was light, drowsy and disorientated. Her pupils were intact and reactive. The Glasgow Coma Scale was 11. No cranial nerve problem or peripheral nerve dysfunction was found.
White blood cell count 21,900/mm3 (4000-10,000/mm3), hemoglobin 11.2 g/dL(men 13-17 g/dL: women 12-16 g/dL), hematocrit 51%(men: 42-50%: women 36-44%), and platelets 207,000/mm3 (150,000-400,000/mm3). Her coagulation profile showed an international normalized ratio of 1.71 (1.2 below) and activated partial thromboplastin time of 177.4 sec (24-33 sec). Laboratory chemistry showed blood urea nitrogen 208mg/dL (8.0-20 mg/dL), creatinine 4.90mg/dL(0.6-1.2mg/dL), serum osmolality 452mOsm/L(289-302mOsm/L), protein 7.5 g/dL (6.5-8.2mg/dL), albumin 4.5 g/dL(3.5-5.1 g/dL), ionized calcium 4.6mg/dL (4.2-5.4mg/dL), magnesium 4.5mg/dL (1.9-2.5 mg/dL), serum sodium 172mEq/L(135-145mEq/L), potassium 4.4mEq/L(3.5-5.5mEq/L), chloride 127mEq/L(98-110 mEq/L), total CO2 21mEq/L (24-31mEq/L), aspiratetransaminase 22 IU/L (0-40 IU/L), alanine aminotransferase 16 IU/L (0-40 IU/L), total bilirubin 1.1mg/dL(0.2-1.1 mg/dL), myoglobin 1,949 ng/mL (28-72 ng/mL), creatine phsphokanase 389 IU/L (190 below IU/L), anti-diuretic hormone 8.95 pg/mL(0.0-6.7 pg/mL), adrenocorticotropic hormone (ACTH) 111 pg/mL(10-60 pg/mL), and cortisol 71 g/mL (morning 9.4-26.1/evening 1.8-12.7 g/mL). Breathing room air, the arterial blood gas analysis revealed pH 7.422, PaCO2 35.4mmHg, PaO2 106mmHg, and bicarbonate 22.6mEq/L. Urinalysis showed specific gravity was >1.030, urine pH 5.0, urine osmolality 698mOsm/L (300-900mOsm/L), and urine sodium/potassium/chloride34/85.6/8mEq/L.
Brain computerized tomography (CT) was normal.
She was diagnosed with uremic encephalopathy due to severe prerenal acute renal failure. Her estimated water deficit was 5.94 L. We started intravenous dextrose for 4h, but the changein serum sodium was minimal (171mEq/L). We therefore started hemodialysis to treat the uremic encephalopathy. The dialysate sodium level was 150mEq/L. After dialysis, the serum sodium decreased to 160mEq/L, potassium was 4.2mEq/L, chloride 124 mEq/L, and total CO2 23mEq/L. After a second dialysis treatment, the sodium was 150mEq/L and she became alert without neurological sequelae. We continued an intravenous dextrose fluid infusion with oral hydration, and the sodium level normalized on day 3 of hospitalization (). After discharge, her sodium and chemistry profile remained normal.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [4.6, 'mg/dL'], 'Albumin': [4.5, 'g/dL']}",4.2,3.99,4.41,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.5 g/dL. 
The concentration of Calcium is 4.6 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.5 g/dL)) + 4.6 mg/dL = 4.2 mg/dL.
The patient's corrected calcium concentration 4.2 mg/dL."
2681,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3499991-1,Extracted,"A 52-years old man presented to our clinic with chest and back pain lasting for 3 months. On the chest radiography, pleural fluid was detected in left hemithorax (). On thorax CT, it was also detected that there were lytic bone lesions at level of 11th and 12th ribs and pleural thickening at paravertebral site on the left. In laboratory evaluations, following findings were observed: hemoglobin: 7.1g/dl.(14–18), white blood cells:11.26 × 103/μL(4.8–10.8), platelets: 787 × 103/μL., creatinine: 3.1mg/dl.(0.6–1.1).Uric acid: 6.1 mg/dl (2.6–6), calcium: 14.7mg/dL (8.8–10.6), total protein:10.7g/dL (6.4–8.3), albumin: 1.8g/dL (3.5–5.2). Serum protein electrophoresis revealed a hypoalbuminemia (21.1%; range; 55.8–66.1) associated with an increase in γ globulins (42.1%; range; 11.1–18.8). IgG-Kappa monoclonal paraproteinemia was detected in immunofixation tests (IgG: 4460mg/dL. reference interval, 850–1330; Kappa: 1640mg/dL, reference interval, 630–1350). ß-2 microglobulin was found as 2.71 mg/dlL (reference interval: 1.42–3.21). Bence-Jones protein was found to be negative in 24-hours urine collection. A thoracentesis was performed, which revealed serofibrinous fluid with a protein level of 6.3gr/dl and white blood cell count of 6.65 × 103μL consisting of lymphocytes (80%) and neutrophils (20%).
Bacterial and micobacterial culture tests of pleural fluid were reported as negative. Biopsy was performed on the mass at rib, which was reported as CD138(+), CD20(−) plasmocytoma. Pleural fluid flow cytometry was performed by using FACSCalibur flow cytometer (Becton-Dickinson, Erembodegem, Belgium). In the flow cytometry, CD56, CD38 and CD138 found to be positive, while CD19 was negative. Bone marrow biopsy was reported as CD38 (+) and CD20(−) atypical plasma cell infiltration. T(4;14), 17p13,1 (p53 gene) and 13q14,3(Rb gene) was found as negative by FISH method.
The patient was scheduled for VAD (vincristine, doxorubicin, dexamethasone) chemotherapy, biphosphonate therapy and involved-field radiotherapy.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [1.8, 'g/dL'], 'Calcium': [14.7, 'mg/dL']}",16.46,15.637,17.283,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 1.8 g/dL. 
The concentration of Calcium is 14.7 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.8 g/dL)) + 14.7 mg/dL = 16.46 mg/dL.
The patient's corrected calcium concentration 16.46 mg/dL."
2682,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5563946-1,Extracted,"A 40-year-old white man with a disease history of KTWS diagnosed since birth presented with iron deficiency anemia, his hemoglobin (Hb) level was 9 g/dL, and complaints about episodes of hematuria and weakness. The remarkable findings of a physical examination were port-wine stains and varicose veins on his limbs and part of his torso (Figs. , , and ), and hypertrophy of both lower extremities: status after amputation of the digits of his left foot and soft tissue resection of plantar surface with auto-skin plastic; and arteriovenous fistula in both legs. MRI and Doppler studies showed: splenomegaly (size 20 × 12 cm) since 1998; multiple hemangiomas in spleen, liver, and bladder; hepatomegaly since 2009 (Figs. , and ); and varicose mesenteric veins. A CT scan in 1998 revealed phleboliths in his pelvis around his colon and bladder. Dynamic renal scintigraphy in 2016 showed slowed excretion due to minor disorder of vascularization of both kidneys with weakened renal function. Laboratory results displayed pancytopenia consisting of normochromic normocytic anemia (Hb, 9 g/dL), neutropenia (1.24 × 103/uL) and thrombocytopenia (107 × 103/uL). Biochemical tests revealed low 25-hydroxyvitamin D (10.67, normal range 30 to 100 ng/ml), fibrinogen (1.1, normal range 1.8 to 3.6 g/l), calcium (1.95, normal range 2.08 to 2.65 mmol/l), and normal creatinine and parathyroid hormone (PTH) level. Hypoalbuminemia (27, normal range 35 to 52 g/l), hyperlipidemia (2.31, normal range < 1.7 mmol/l), and proteinuria (6.85 g/L) described the main criteria for nephrotic syndrome. During hospitalization he received multiple transfusions of red blood cells, perindopril, amlodipine, atorvastatin, allopurinol, and Vigantoel (vitamin D3).","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [27.0, 'g/L'], 'Calcium': [1.95, 'mmol/L']}",8.856,8.4132,9.2988,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 27.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 27.0 g Albmumin/10.0 dL = 2.7 g Albmumin/dL. The concentration value of 27.0 g Albmumin/L converts to 2.7 g Albmumin/dL. 
The concentration of Calcium is 1.95 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.95 mmol. To convert 1.95 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.95 mmol Calcium * 0.001 mol/mmol = 0.00195 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00195 mol Calcium * 40.08 g/mol = 0.07816 g Calcium. To convert 0.07816 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.07816 g Calcium * 1000.0 mg/g = 78.16 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 78.16 mg Calcium/10.0 dL = 7.816 mg Calcium/dL. The concentration value of 1.95 mmol Calcium/L converts to 7.816 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.7 g/dL)) + 7.816 mg/dL = 8.856 mg/dL.
The patient's corrected calcium concentration 8.856 mg/dL."
2683,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-8580185-1,Extracted,"An 81-year-old woman with a past medical history of hypothyroidism and Parkinson's disease complicated by dementia and dysphagia, with a feeding PEG tube that was placed six years prior to presentation, presented to the emergency room (ER) with hematemesis and melena. Her symptoms started one day prior to admission. The patient was also complaining of abdominal pain, however, there was no associated dysphagia, change in bowel habits, or bleeding from other sites. She did not have a history of GI bleeding nor was she taking aspirin or anti-coagulants.
In the ER, the patient was tachycardic and hypotensive, but afebrile. Her complete blood count (CBC) was significant for a white blood cell (WBC) count of 12.17 x 10(3)/uL, a slightly dropped hemoglobin of 10.4 g/dL from her baseline of 11.6 g/dL, and a normal platelet count. The basic metabolic panel was only significant for hypocalcemia of 5.5 mg/dL with serum albumin of 2.2 gm/dL. Liver function test, partial thromboplastin time (PTT), prothrombin time (PT), and international normalized ratio (INR) were all normal. She was given three units of packed red blood cells and was started on a proton pump inhibitor (PPI), but given the recurrent hematemesis and decreased level of consciousness, she was intubated for airway protection and was placed on mechanical ventilation.
Esophagogastroduodenoscopy (EGD) was done, which showed Los Angeles (LA) grade D esophagitis and a non-bleeding gastric ulcer. Moreover, the PEG tube balloon tip was displaced and trapped in the duodenal bulb causing GOO (Figure ) with resultant severe reflux esophagitis. The balloon tip was retracted to the gastric wall and fixed. The patient was continued on a PPI and was extubated the day after. Tube feeding was resumed, and the patient was discharged on a daily PPI.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.2, 'g/dL'], 'Calcium': [5.5, 'mg/dL']}",6.94,6.593,7.287,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.2 g/dL. 
The concentration of Calcium is 5.5 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.2 g/dL)) + 5.5 mg/dL = 6.94 mg/dL.
The patient's corrected calcium concentration 6.94 mg/dL."
2684,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7187932-3,Extracted,"A 65-year-old male presented with pain in the left leg and waist. CT imaging showed a circular and milled vitreous nodule in the left lower lung, which was recommended for puncture and the destruction of the lumbar vertebra and rib bone, which suggested metastasis or MM. Magnetic resonance imaging (MRI) showed multiple areas of destruction in the vertebral body and appendages of T12-L5, S1, S2, and S3. Puncture pathology of the left lung tissue and lumbar paravertebral soft tissue showed moderately differentiated adenocarcinoma (EGFR no mutation, ALK-negative) () and plasmacytoma, respectively. Bone marrow (BM) aspirate demonstrated up to 17% dysplastic plasma cells, which were proved to be monoclonal plasma cells by flow cytometry. Routine blood tests revealed an HGB level of 93 g/L, total leukocyte count of 5.7 × 109/L, and platelet count of 98 × 109/L. Blood biochemistry revealed an ESR of 97 mm/hr (normal value, <22 mm/hr), serum globulin of 33.2 g/L, serum albumin of 33.1 g/L, serum creatinine of 217 μmol/L, serum calcium of 2.21 mmol/L, serum LDH of 109 U/L, and serum β2-MG of 8.55 mg/L. The serum IgG and serum kappa light chain was 19.76 g/L and 8.65 g/L, respectively. The serum EP and IEP also showed abnormally bowed arcs against IgG and anti-kappa light chain. Positron emission tomography-CT imaging showed irregular nodules in the lower lobe of the left lung consistent with peripheral lung cancer and multiple irregular osteolytic bone destruction in the whole body consistent with changes in MM. The diagnoses were MM with type of IgG-kappa (D-S stage III B and ISS stage III) and moderately differentiated adenocarcinoma in the left lung. The patient first underwent wedge lobectomy. The postoperative staging was moderately differentiated adenocarcinoma (pT1N0M0, stage I).
Then, the PD scheme (bortezomib 1.3 mg/m2 plus dexamethasone 20 mg on days 1, 4, 8, and 11) was applied and the evaluation of the curative effect was PR after four cycles of PD. Postoperative review in July 2014 suggested pleural metastasis. So the PD and GP schemes (gemcitabine 1000 mg/m2 on days 1 and 8 plus cisplatin 20 mg/m2 on days 1–3) were administered alternately. After alternating the four cycles of PD and GP schemes, the efficacy of MM and lung cancer was evaluated as very good PR and PR, respectively. The patient then alternately received the other two cycles of PD and GP regimens. On the fourth-month post-treatment follow-up, the disease began to progress with metastasis to the liver and the biopsy revealed recurrent adenocarcinoma of the lung. The patient’s condition became progressively worsened; he gave up treatment and began experimenting with traditional Chinese medicine and eventually died of lung cancer progression with respiratory failure. The patient’s post-diagnosis survival time was 38 months.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [33.1, 'g/L'], 'Calcium': [2.21, 'mmol/L']}",9.41,8.9395,9.8805,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 33.1 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 33.1 g Albmumin/10.0 dL = 3.31 g Albmumin/dL. The concentration value of 33.1 g Albmumin/L converts to 3.31 g Albmumin/dL. 
The concentration of Calcium is 2.21 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 2.21 mmol. To convert 2.21 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 2.21 mmol Calcium * 0.001 mol/mmol = 0.00221 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00221 mol Calcium * 40.08 g/mol = 0.08858 g Calcium. To convert 0.08858 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.08858 g Calcium * 1000.0 mg/g = 88.58 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 88.58 mg Calcium/10.0 dL = 8.858 mg Calcium/dL. The concentration value of 2.21 mmol Calcium/L converts to 8.858 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.31 g/dL)) + 8.858 mg/dL = 9.41 mg/dL.
The patient's corrected calcium concentration 9.41 mg/dL."
2685,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7417050-1,Extracted,"A 26-year-old woman was referred by her general practitioner (GP) to the gastroenterology outpatient clinic. She had been fit and well until the onset of symptoms and her only regular medication was the combined oral contraceptive pill. She had not had any previous abdominal surgery, and her obstetric history included one previous pregnancy with uncomplicated vaginal delivery 7 years previously. Furthermore, she did not have a history of asthma/eczema/hay fever/atopy. Her family history was unremarkable. She does not smoke and rarely drinks alcohol.
Her symptoms included intractable dull abdominal discomfort with intermittent spasms of more intense pain, lasting for 1–2 minutes. For the pain she had been using over-the-counter analgesia to little avail but found some relief from holding a hot-water bottle against her abdomen. This was associated with an abrupt onset of change in bowel habit, from chronic constipation to passing watery stools up to 5 times per day. She had not experienced any tenesmus, urgency, incomplete emptying, dyschezia or nocturnal symptoms. She also described feeling nauseated but had not vomited. She had frequent episodes of dyspepsia, which was largely relieved by twice-daily PPI, initiated by her GP. There was no objective evidence of any weight loss, but she had a reduced appetite and had been only able to tolerate smaller portion sizes over the past few months.
On examination, she did not display any peripheral stigmata of anaemia or chronic disease. She did not have any rashes, joint effusions or ocular signs. Abdominal examination revealed striking erythema ab igne, but no overlying skin blistering or desquamation. She had left iliac fossa tenderness with a degree of voluntary guarding, but no other features of peritonism. There was no clinically palpable hepatosplenomegaly or supraclavicular lymphadenopathy, and bowel sounds were normal on auscultation.
Full blood count (FBC) performed before clinic in early June by her GP revealed: haemoglobin (Hb) 140, total white cell count (WCC) 19.4, eosinophils 12.94, faecal calprotectin (FCP) 83, erythrocyte sedimentation rate (ESR) 2, C-reactive protein (CRP) 5.4, adjusted calcium 2.25, and albumin 48, while IgA endomysium antibodies (EMA) was negative. On the day of her clinic appointment in late June, further investigations were arranged and these revealed: Hb 149, WCC 15.8, eosinophils 8.16, renal and liver profile all within normal limits, rheumatoid factor (RhF) negative, ESR 2, CRP 4.5, complement C3 1.19, complement C4 0.18, c-ANCA/p-ANCA both negative, ANA negative, and immunoglobulin screen showing IgA slightly low at 0.71, and IgG and IgM both normal, while serum electrophoresis showed no specific electrophoretic abnormalities.
CT of the abdomen/pelvis was carried out the day after clinic and showed thickened segments of the distal ileum including the terminal ileum, with no small bowel dilatation. Moderate volume ascites was also detected.
Stool microbiology including pathogenic ova/cysts/parasites, rotavirus antigen, Clostridium difficile toxigenic antigen, Cryptosporidium oocysts, Campylobacter culture, Salmonella, Shigella and E. coli 0157 was all negative.
Gastroscopy performed in early July was macroscopically normal to the second part of the duodenum (D2). Unfortunately, only one duodenal biopsy was taken due to poor tolerability of the procedure, but the histology was essentially normal, without excess infiltration of eosinophils.
We did not perform a bone marrow biopsy or screen for PDGFRA, BCR-ABL and JAK2 mutations.
The first step in the management of this patient was to exclude parasitic/enteric infection and obtain relevant information to rule out hyper-eosinophilic syndrome or haematological causes of raised peripheral eosinophilia. Usually, eosinophilic gastroenteritis is diagnosed by confirmatory histopathology.
After excluding infection, we decided to cautiously initiate a reducing regime of prednisolone 30 mg once daily for 2 weeks to be reduced by 5 mg weekly thereafter. This was started before endoscopic evaluation was undertaken due to the severity of the patient’s symptoms and the low clinical suspicion of other pathology.
The patient was reviewed on a fortnightly basis. Unfortunately, the patient was unable to have sedation for her gastroscopy and the procedure was abandoned due to poor tolerance. The colonoscopy was cancelled for similar reasons. Abdominal ultrasound scan (USS) 3 months after the initial CT revealed complete resolution of the ascites and a normal appearance of the distal ileum. Over a 2-month period, the peripheral eosinophil count fell from 12.94 to 0.01. The patient was appropriately followed up.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [2.25, 'mg/dL'], 'Albumin': [48.0, 'g/L']}",1.61,1.5295,1.6905,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 48.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 48.0 g Albmumin/10.0 dL = 4.8 g Albmumin/dL. The concentration value of 48.0 g Albmumin/L converts to 4.8 g Albmumin/dL. 
The concentration of Calcium is 2.25 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.8 g/dL)) + 2.25 mg/dL = 1.61 mg/dL.
The patient's corrected calcium concentration 1.61 mg/dL."
2686,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2813653-1,Extracted,"A 47-year-old male presented at an outside hospital with painful right hip that was diagnosed as synovitis of the hip. A CT scan of the hip that included the abdomen detected bilateral adrenal masses. At presentation he was totally asymptomatic and other than large palpable bilateral abdominal flank masses had a totally negative physical examination. The patient underwent the following investigations: hemoglobin 149 g/L, red blood cells 5.37×1012/L, WBC 6.1×109/L, serum creatinine 87 μmol/L (reference range, 65-129 μmol/L) serum calcium 1.95-2.25 g/L (reference range, 2.10-2.55 g/L), serum albumin 35 g/L (reference range, 42-48 g/L), serum phosphorus 0.57-1.27 mmol/L (reference range, 0.7-1.45 mmol/L), alkaline phosphatase 64-96 U/L (reference range, 40-115 U/L), total proteins 109 g/L (reference range, 65-81 g/L), and urine total protein of 1.22 g/L. The hormonal profile consisted of 24-hour urine normetanephrines of 2.88 μmol/day (reference range, 0-3.43 μmol), urine metanephrines of 0 μmol/day (reference range, 0-1.49), urine 3-methoxy-tyramine 1.34 μmol/day (reference range, 0-2.06), synthetic ACTH stimulation testing revealed a normal adrenal cortical reserve (base line serum cortisol, 301 nmol/L that increased to a peak of 564.7 nmol/L at one hour following intramuscular administration of 250 μg of 1-24 synthetic ACTH), urine cortisol of 45 μg/day (reference range, < 100 μg/day), urine aldosterone <33 nmol/day (reference range, 8-83 nmol/day), supine renin of 2.17 μg/L/h (reference range, 0.15-2.33 μg/L/h), and serum dehydroepiandrosterone sulfate of 0.7 μmol/L (reference range, 1.2-8.71). Imaging data consisted of an ultrasound of the abdomen/pelvis (not shown) that revealed large bilateral adrenal masses, a CT of the abdomen ( without contrast and following contrast administration) and an MRI abdomen (not shown) that showed massive bilateral adrenal masses, displacing the kidneys inferiorly, but that was otherwise negative. A skeletal survey (ribs, clavicle, scapulae, skull, spine, long bones of upper and lower extremities, pelvis), whole body bone scan and MRI spine showed no findings suggestive of multiple myeloma. Ultrasound-guided fine needle aspiration biopsy of the right adrenal mass () and a core-needle biopsy () showed morphological findings consistent with the diagnosis of plasmacytoma. Immunohistochemical staining data (Figures and ) supported the diagnosis of plasmacytoma. Flow cytometry analysis of the adrenal tumor revealed an abnormal CD38+ cell population that exhibited monoclonal cytoplasmic kappa light chain expression, but negative for CD45, cytokeratin and lambda light chain (). A bone marrow aspirate showed normocellular pattern with no evidence of multiple myeloma. Bone marrow flow cytometry for leukemia/lymphoma markers was negative. A distinct monoclonal protein band accounting for 44.6% of total serum proteins and 87.9% total gamma globulins was shown on serum protein electrophoresis. (). Immunofixation electrophorisis of urine specimen demonstrated free kappa light chain (Bence Jones proteins) ().
At initial treatment the patient received chemotherapy consisting of two cycles of vincristine, Adriamycin and dexamethasone (VAD) followed by two cycles of etoposide, dexamethasone, Ara-C and cisplatinum (EDAP). A follow-up CT scan showed no change in the size of the bilateral adrenal lesions nor was there a change in the immunological studies of serum and urine. Two years following initial presentation the patient received two consecutive autologous hematopoietic stem cell transplantation (HSCT) procedures using high dose melphalan. Starting 6 months pos-HSCT through a last follow-up at 50 months, serial periodic serum protein electrophoresis and immunofixation showed abrogation of a previously noted monoclonal band. Urine electrophoresis and urine immunofixation also turned out to be negative for Bence-Jones proteins. A last CT scan of the abdomen done at 47 month follow-up () revealed that both adrenal tumors had regressed substantially and demonstrated findings of calcification and fibrosis. A follow-up skeletal survey at 47 months showed normal findings. At 50 months follow-up the patient was alive and well.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [35.0, 'g/L'], 'Calcium': [952.25, 'g/L']}",95225.4,90464.13,99986.67,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 35.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 35.0 g Albmumin/10.0 dL = 3.5 g Albmumin/dL. The concentration value of 35.0 g Albmumin/L converts to 3.5 g Albmumin/dL. 
The concentration of Calcium is 952.25 g/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from g to mg. The mass of Calcium is 952.25 g. To convert 952.25 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 952.25 g Calcium * 1000.0 mg/g = 952250.0 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 952250.0 mg Calcium/10.0 dL = 95225.0 mg Calcium/dL. The concentration value of 952.25 g Calcium/L converts to 95225.0 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.5 g/dL)) + 95225.0 mg/dL = 95225.4 mg/dL.
The patient's corrected calcium concentration 95225.4 mg/dL."
2687,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,usmle-8562,Extracted,"A 65-year-old man comes to the physician because of increasing swelling of the legs and face over the past 2 months. He has a history of diastolic heart dysfunction. The liver and spleen are palpable 4 cm below the costal margin. On physical examination, both lower limbs show significant pitting edema extending above the knees and to the pelvic area. Laboratory studies show:
Serum
Cholesterol 350 mg/dL (<200 mg/dL)
Triglycerides 290 mg/dL (35–160 mg/dL)
Calcium 8 mg/dL
Albumin 2.8 g/dL
Urea nitrogen 54 mg/dL
Creatinine 2.5 mg/dL
Urine
Blood 3+
Protein 4+
RBC 15–17/hpf
WBC 1–2/hpf
RBC casts Many
Echocardiography shows concentrically thickened ventricles with diastolic dysfunction. Skeletal survey shows no osteolytic lesions.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.8, 'g/dL'], 'Calcium': [8.0, 'mg/dL']}",8.96,8.512,9.408,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.8 g/dL. 
The concentration of Calcium is 8.0 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.8 g/dL)) + 8.0 mg/dL = 8.96 mg/dL.
The patient's corrected calcium concentration 8.96 mg/dL."
2688,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4415489-1,Extracted,"A 43-year-old man presented to the gastroenterology department with colicky abdominal pain, microcytic hypochromic anemia, and fatigue. At colonoscopy, a tumor was seen in the ascending colon, as shown in .
His FBC was as follows: WBC: 17.7 × 109/L (normal: 4.0–11.0), NE: 15.9 × 109/L (normal: 2.0–7.5), LY: 0.7 × 109/L (normal: 1.5–4.0) MO: 0.8 × 109/L (normal: 0.2–0.8), HB: 98 g/L (normal: 130–180), MCV: 66.9 FL (normal: 76–100), MCH: 19.5 pg (normal: 27–32), MCHC: 291 g/L (normal: 310–360), RDW: 20 (normal: 10–15.7) crea: 198 μmol/L (normal: 58–110), urea: 11.0 mmol/L (normal: 2.5–7.8), bili: 8 μmol/L (normal: 0–21), ALT: 23 (normal: 3–53), ALP: 75 IU/L (normal: 30–130), albumin: 23 g/L (normal: 35–50), Ca: 2.45 mmol/L (normal: 2.20–2.60), and globulin: 20 g/L (normal: 18–36).
A CT scan of the thorax, abdomen, and pelvis showed a large soft tissue mass extending from the right iliac fossa into the pelvis with involvement of the adjacent small bowel loops. There was extensive bowel wall thickening of the caecum and ascending colon as shown in , extending over a length of approximately 20 cm, with the wall measuring up to 4.5 cm in thickness. Regional and mesenteric nodes were demonstrated and there was a suspicion of right juxtadiaphragmatic pulmonary and umbilical deposits. A subsequent dedicated skeletal survey was negative for lytic lesions.
CT scan pictures to follow as shown in .
The fragments of colonic mucosa showed extensive infiltration by large cells with eccentric nuclei and prominent nucleoli as shown in . Frequent mitotic figures were noted and the Ki67 proliferation index was 100%. The cells expressed plasma cell associated markers including CD138 and IRF4 as shown in though they lacked CD19 and showed strong expression of CD56 as shown in . There was no evidence of EBV. FISH identified a MYC rearrangement. The differential included plasmablastic lymphoma or soft tissue plasmacytoma though the presence of strong CD56 and lack of EBV favoured the latter. A subsequent bone marrow biopsy confirmed the diagnosis of myeloma with neoplastic plasma cells identified by flow cytometry (CD19−CD56++CD27−CD45−) and a multifocal infiltrate of plasma cells identified with similar blastic morphology as shown in . A c-MYC rearrangement was detected by FISH on the primary tissue biopsy and there was no evidence of other recurrent cytogenetic abnormalities.
The patient was then referred to the haematology department where serum protein electrophoresis was performed, but no monoclonal band was detected. IgG: 5.7 g/L (normal: 6–16), IgA: 2.5 g/L (normal: 0.80–4), IgM: <0.25 g/L (normal: 0.40–2.30), free kappa chains which were normal 15.6 mg/L (normal: 6.7–22.4), free lambda chains: 20.2 (normal: 8.3–27), SFLCR: 0.77 (normal: 0.31–1.56), within normal limits, and UBJ: negative, and urinary protein immunofixation did not detect a light chain band.
Consider the following: ESR: 47 mm/hr (normal: 3–15), ferritin: 55 μg/L (normal: 30–365), CRP: 162 mg/L (normal: 0–10), and LDH: 1415 IU/L (normal: 313–618).
The patient tested negative for HIV and EBV.
The bone marrow biopsy showed a normocellular marrow with active trilineage hematopoiesis.
There was a focal infiltrate of large blastic cells and a neoplastic plasma cell population was identified by flow cytometry. The features were consistent with plasma cell myeloma.
From the flow cytometry the plasma cells were 1.8% of leucocytes, of which 90% had a neoplastic phenotype CD19−, CD56++, CD27−, and CD45−.
Unfortunately the patient died of a pulmonary embolism before treatment could be commenced. Postmortem examination showed extensive tumour deposits in the abdominal cavity. The appearance in the abdominal cavity was consistent with disseminated myelomatous involvement. The plasma cell myeloma had put an increased risk for the development of pulmonary embolism and therefore would have also contributed indirectly to the cause of death. Patients with newly diagnosed multiple myeloma, prior to having received therapy, seem to be at increased risk for venous thromboembolic disease and pulmonary embolism as discussed by Auwerda et al. [].","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [23.0, 'g/L'], 'Calcium': [2.45, 'mmol/L']}",11.18,10.621,11.739,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 23.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 23.0 g Albmumin/10.0 dL = 2.3 g Albmumin/dL. The concentration value of 23.0 g Albmumin/L converts to 2.3 g Albmumin/dL. 
The concentration of Calcium is 2.45 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 2.45 mmol. To convert 2.45 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 2.45 mmol Calcium * 0.001 mol/mmol = 0.00245 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00245 mol Calcium * 40.08 g/mol = 0.0982 g Calcium. To convert 0.0982 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.0982 g Calcium * 1000.0 mg/g = 98.2 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 98.2 mg Calcium/10.0 dL = 9.82 mg Calcium/dL. The concentration value of 2.45 mmol Calcium/L converts to 9.82 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.3 g/dL)) + 9.82 mg/dL = 11.18 mg/dL.
The patient's corrected calcium concentration 11.18 mg/dL."
2689,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-8571802-1,Extracted,"A 54-year-old female with a history of (Global Initiative for Chronic Obstructive Lung Disease stage 3 and group D) multiple COPD exacerbations and one with endotracheal intubation, without home oxygen, 16 pack-year cigarette smoking, and marijuana abuse came to the emergency department for worsening shortness of breath with nonproductive cough, myalgia, and watery diarrhea for three days. Other systems were normal.
At presentation, she was afebrile, with a heart rate of 112 beats per minute, respiratory rate of 30 breaths per minute, and saturation of 95-98% on 3 L of oxygen on nasal cannula. Bilateral wheezing with few crepitations was noted on the bilateral bases of the lungs. The rest of the examination was unremarkable. Labs at the time of admission showed leukocytosis of 15.6 × 109/L (reference range: 4.5-11 × 109/L) with a left shift of neutrophils at 88.3% and relative lymphopenia at 4.5% (0.7 × 109/L). The chemistry panel was near-normal with the following findings: Na+/K+ of 139/3.9 mmol/L, Cl- of 97 mmol/L, elevated HCO3 of 32 mEeq/L, and normal anion gap of 10. Blood urea nitrogen (BUN)/creatinine ratio was 13.0/0.66 mg/dL, with a slightly elevated glucose level of 173 mg/dL. Furthermore, calcium, phosphorus, and magnesium levels were 8.9 mg/dL, 5.3 mg/dL, and 1.9 mg/dL, respectively. Liver function tests showed total bilirubin of 0.5 mg/dL, aspartate transaminase of 14 U/L, alanine transaminase of 13 U/L, alkaline phosphatase of 119 U/L, total protein of 5.9 g/dL, albumin of 3.7 m/dL, and elevated bicarbonate of 35.7 mEq/L. Moreover, urine toxicology was positive for cannabinoids. Polymerase chain reaction (PCR) test for coronavirus disease 2019 (COVID-19) was negative, and influenza, mycoplasma, and Legionella antigen tests were also negative. Lactate dehydrogenase was elevated at 322 U/L (reference range: 125-220 U/L), and total creatine kinase was 43 U/L. D-dimer was 414 ng/mL with a normal coagulation profile with prothrombin time (PT) of 12.8 seconds and activated partial thromboplastin time of 31.3 seconds. PT/international normalized ratio was 1.09. Chest X-ray showed hyperinflation with mild perihilar congestion without any evidence of consolidation and no significant changes compared with the prior study. Computed tomography (CT) without contrast revealed mildly hyperinflated lungs with mild emphysematous changes predominating in the apices, along with scattered small areas of fibrotic changes. No convincing lung consolidation or acute infiltrate pleural effusion was noted, with normal mediastinum, heart size, and unremarkable hila with pericardial effusion (Figure ).
Arterial blood gas (ABG) on 2 L of oxygen via nasal cannula showed pH of 7.299, pCO2 of 75 mmHg, pO2 of 72.9 mmHg, HCO3- of 35 mmol/L, and oxygen saturation of 96%. Sequential Organ Failure Assessment (SOFA) score was less than 2 (less than 9 implies <33.3% mortality), and PaO2/FiO2 ratio was 260. She was admitted to the hospital for acute hypoxic and hypercapnic respiratory failure secondary to COPD exacerbation and was started on methylprednisolone along with albuterol and ipratropium nebulization and intravenous ceftriaxone and azithromycin. Her clinical course worsened on days two and three of admission with tachypnea, fatigue, as well as occasional and multiple episodes of desaturation of up to 86% on 2 L of oxygen via a nasal cannula. She was switched to bilevel positive airway pressure (BiPAP) with inspiratory positive airway pressure/expiratory positive airway pressure of 15/5 mmHg, with a respiratory rate of 15 breaths per minute and FiO2 of 40% due to worsening respiratory status. Two repeat PCR tests for COVID-19 were negative. Blood culture sent at the time of admission grew two organisms later identified as E. faecium and P. agglomerans.
She was fairly compliant with BiPAP, and on day four of admission, she started improving clinically and reported feeling comfortable on 2-3 L of oxygen via a nasal cannula with on and off BiPAP (approximately six to seven hours) during the night. Her ABG on BiPAP with FiO2 of 40% oxygen also showed improvement with pH of 7.339, pCO2 of 63.7 mmHg, pO2 of 87.2 mmHg, HCO3- of 33 mmol/L, and oxygen saturation of 97%. Antibiotic sensitivity analysis of E. faecium and P. agglomerans revealed that both were sensitive to ceftriaxone. Therefore, ceftriaxone and azithromycin were continued for five days, with a continued tapering dose of steroids.
Of note, another set of blood cultures sent on the day of admission and on days two and three during deterioration showed no growth in the subsequent follow-up. On day six of admission, the patient improved significantly and was discharged home with home oxygen therapy with proper instructions regarding the medication and oxygen therapy. On the two-week follow-up at the medical clinic, she reported remarkable improvement in respiratory symptoms and was using oxygen during nights with the occasional need for inhaler use.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [8.9, 'mg/dL'], 'Albumin': [3.7, 'g/dL']}",9.14,8.683,9.597,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.7 g/dL. 
The concentration of Calcium is 8.9 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.7 g/dL)) + 8.9 mg/dL = 9.14 mg/dL.
The patient's corrected calcium concentration 9.14 mg/dL."
2690,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4246622-1,Extracted,"A 61-year-old male was admitted to The Second Affiliated Hospital of Zhejiang University Medical College (Hangzhou, Zhejiang, China) due to pain and weakness of the lower limbs that had been present for one year and a recurrent fever that had persisted for one month. One year previously, the patient had experienced pain and bilateral weakness of the muscles of the lower legs, and walking became limited. Several days later, a recurrent low to moderate fever developed and scattered red spots were visible on the extensor skin of the lower legs, with no pruritus or pain upon compression. The skin biopsy revealed erythema nodosum. The patient was administered 10 mg prednisone three times a day and the symptoms were attenuated. At 11 months prior to the present admittance, the pain and weakness of the lower limbs got worse, with involvement of the thighs and lower legs. Magnetic resonance imaging, electromyography and a biopsy of the muscle of the right thigh were performed, which diagnosed polymyositis. The condition was treated with 80 mg intravenous methylprednisolone per day and 10 mg oral methotrexate per week. Following attenuation of the symptoms, the dosage of methylprednisolone was gradually reduced.
Four months prior to admittance, the patient experienced exacerbation of the weakness in the lower limbs. A positron emission tomography/computed tomography (PET-CT) scan was performed two months later, which showed multiple regions of elevated fluorodeoxyglucose metabolism in the lymph nodes, lungs, liver, spleen and bones (). One month after the scan, the patient developed a high fever of 39.2°C, with no chill or cough. This raised temperature did not decrease subsequent to treatment with antibiotics (intravenous cefperazone-sulbactam, 3 g every 8 h) and, therefore, 10 mg methylprednisolone per day was administered to control the polymyositis and diclofenac potassium (50 mg, every 12 h) was administered to control the fever. No abnormal cells were found in bone marrow smears. Two lymph node puncture biopsies were performed, but the pathology showed granulomatous inflammation in each sample. Upon admission, the symptoms of nonchalance and confusion were identified, along with poor orientation and calculation abilities, and a bad memory. An enlarged lymph node could be palpated in the right lingual area. The muscles of the lower limbs were atrophied. The myodynamia of the lower limb was grade IV and the myodynamia of the upper limbs was grade V, according to Lovett’s myodynamic grading criterion (). No other positive signs were found. A routine blood test showed a white blood cell count of 7.0×109/l (normal range, 4.0–10.0 ×109/l), a hemoglobin level of 94 g/l (normal range, 110–160 g/l), a platelet level of 285×109/l (normal range, 100–300×109/l) and a neutrophil count of 80.2% (normal range, 50–70%). The blood biochemistry results were as follows: Albumin, 23.4 g/l (normal range, 35.0–52.0 g/l); serum globulin, 45.8 g/l (normal range, 15.0–30.0 g/l); alkaline phosphatase, 1,169 U/l (normal range, 30–120 U/l); γ-glutamyl transpeptidase, 293 U/l (normal range, 9–64 U/l); aspartate aminotransferase, 59 U/l (normal level, <35 U/l); lactate dehydrogenase, 280 U/l (normal range, 140–271 U/l); calcium, 3.87 mmol/l (normal range, 2.08–2.60 mmol/l); blood urea nitrogen (BUN), 13.20 mmol/l (normal range, 2.80–7.20 mmol/l); creatine, 152 μmol/l (normal range, 53–133 μmol/l); uric acid, 749 μmol/l (normal range, 208–428 μmol/l); β2-microglobulin, 16.55 mg/l (normal range, 1.00–3.00 mg/l); and C-reactive protein, 100.9 mg/l (normal level, <6.0 mg/l). The erythrocyte sedimentation rate was 70.00 mm/h (normal level, <20 mm/h), the rheumatoid factor level was 15.8I U/ml (normal level, <15.0I U/ml), and the tests for antinuclear antibodies (ANA), anti-neutrophil cytoplasmic antibodies (ANCA), anticardiolipin antibodies and cyclic citrullinated peptide antibodies were all negative. The parathyroid hormone (PTH) level was 4.96 pg/ml (normal range, 15.00–60.00 pg/ml). A hypercalcemic crisis was diagnosed and a fluid infusion of 20 mg intravenous furosemide, 100 IU intramuscular salmon calcitonin and 10 mg intravenous dexamethasone per day was administered.
Following treatment, the patient’s memory and orientation improved, and the calcium level decreased to 2.86 mmol/l the next day. A chest CT scan showed bilateral pulmonary exudation and pneumonia was indicated, therefore, antibiotics (400 mg/day moxifloxacin and 100 mg/day fluconazole) were administered. Subsequent to the attenuation of the symptoms, a biopsy of the right lingual lymph node was performed, which showed peripheral T-cell lymphoma, not otherwise specified (NOS). The disease stage was IVB according to the Ann Arbor staging system (), and chemotherapy consisting of 1.3 g cyclophosphamide, 60 mg liposomal doxorubicin and 40 mg vinorelbine on day 1, and 15 mg dexamethasone on days 1–5 was administered. Following two courses of chemotherapy, the result of a B-mode ultrasound and CT scan showed that the patient achieved partial remission.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [23.4, 'g/L'], 'Calcium': [3.87, 'mmol/L']}",16.839,15.99705,17.68095,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 23.4 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 23.4 g Albmumin/10.0 dL = 2.34 g Albmumin/dL. The concentration value of 23.4 g Albmumin/L converts to 2.34 g Albmumin/dL. 
The concentration of Calcium is 3.87 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 3.87 mmol. To convert 3.87 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 3.87 mmol Calcium * 0.001 mol/mmol = 0.00387 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00387 mol Calcium * 40.08 g/mol = 0.15511 g Calcium. To convert 0.15511 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.15511 g Calcium * 1000.0 mg/g = 155.11 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 155.11 mg Calcium/10.0 dL = 15.511 mg Calcium/dL. The concentration value of 3.87 mmol Calcium/L converts to 15.511 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.34 g/dL)) + 15.511 mg/dL = 16.839 mg/dL.
The patient's corrected calcium concentration 16.839 mg/dL."
2691,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3279325-1,Extracted,"A 69-year-old man presented with recurrent bilateral pleural effusions of unclear etiology. He had undergone thoracocentesis more than 25 times over the last 2 years and had bilateral pleurodesis multiple times without success. Pleural fluid studies and a pleural biopsy were negative for malignancy or infection. He had no history of chest trauma, thoracic surgery, tuberculosis, lymphoma, cancer or significant exposure to asbestos. His renal, hepatic and cardiac function had been normal. He had smoked one-half pack cigarettes a day for 40 years and quit a year ago. He reported a chronic cough, exertional dyspnea, severe anorexia and weight loss of 30 kilograms in last 3 months. Due to his intractable pleural effusions of undetermined etiology, he was admitted for a lung biopsy and ligation of thoracic ducts.
The physical examination revealed a man with mild shortness of breath. He had generalized edema, decreased breath sounds over the lung bases and a normal cardiac examination. He was afebrile with normal respirations, a pulse of 86 beats per minute and blood pressure of 145/79 mm of Hg. White blood count was 8700 cells/mm3, hemoglobin was 10 g/dL, serum creatinine was 1.1 mg/dL and serum calcium was 8.8 mg/dL. Serum protein was 3.7 g/dL with albumin of 2.7 g/dL. Liver function tests were normal. Urinalysis showed 30 mg/dL protein in a spot sample. C-reactive protein was elevated at 50 mg/L. Anemia work up was consistent with anemia of chronic disease with normal serum B12 and folate levels. A chest x-ray showed bilateral pleural effusions. Echocardiogram showed normal left ventricular ejection fraction of 60% and there were no features of cardiac amyloidosis. Computed tomography of the chest and abdomen showed multiple calcified mediastinal lymphadenopathy and pleural effusions with atelectasis of the lung bases, but no obvious parenchymal lung lesions ().
Pleural fluid was exudative with a white count of 212 cells/mm3 with 88% lymphocytes. Fluid triglycerides were elevated at 277 mg/dl, lactate dehydrogenase was 133 IU/L and fluid protein was 2800 mg/dL. The fluid was negative for infection, plasma cells or other tumor cells. Histopathology of biopsy of the right lung revealed pulmonary amyloidosis, mostly in a perivascular pattern, seen as hyaline deposits on Hematoxylin & Eosin stain (). Apple-green birefringence was noted on Congo-red stain under polarized light. Mass spectroscopic subtyping revealed AL-kappa amyloid deposits.
Serum protein electrophoresis showed total protein of 3.3 g/dL with albumin 1.6 g/dL but absence of M-protein. Serum and urine immunofixation revealed presence of kappa free light chains. Serum free light chain analysis showed kappa free light chains of 47.2 mg/dL (ref 0.33–1.95 mg/dL) and a kappa to lambda light chain ratio of 41.4 (ref 0.26–1.65). Urine protein electrophoresis showed 24-hour urine protein of 1201 mg with M-protein of 40%. A bone marrow biopsy revealed 25% plasma cells comprised predominantly of kappa-expressing cells (). A skeleton survey did not show any lytic or blastic lesions.
Our patient met the diagnostic criteria for MM based on bone marrow biopsy showing more than 10% plasma cells, monoclonal protein in the serum and urine, and presence of a myeloma-related organ dysfunction in the form of anemia. The etiology of his intractable effusion was felt to be pulmonary amyloidosis secondary to multiple myeloma. He did not have features of amyloidosis elsewhere such as cardiac failure, hepatomegaly, nephrotic syndrome and peripheral neuropathy. He was started on melphalan and bortezomib. His pleural effusions persisted despite thoracic duct ligation. His hospital course was complicated with acute renal failure, severe anasarca, deep vein thrombosis, congestive heart failure, myocardial infarction and sepsis. The diagnosis of MM as the cause of his intractable pleural effusion was terminal as the patient expired within a few weeks of diagnosis.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [1.6, 'g/dL'], 'Calcium': [8.8, 'mg/dL']}",10.72,10.184,11.256,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 1.6 g/dL. 
The concentration of Calcium is 8.8 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 1.6 g/dL)) + 8.8 mg/dL = 10.72 mg/dL.
The patient's corrected calcium concentration 10.72 mg/dL."
2692,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7456633-1,Extracted,"An 85-year old Caucasian female presented to our facility from home with three days of nausea, vomiting, and abdominal pain. Past medical history includes hypertension, diverticulosis and osteoarthritis. Symptoms came on spontaneously, with no aggravating or alleviating factors. She vomited twice prior to presentation, with nonbloody and nonbilious vomitus. She described her abdominal pain as generalized, dull and aching in nature, and constant over these three days. She experienced one week of constipation, and denied any diarrhea, melena, or hematochezia. Additionally, she endorsed generalized weakness, body aches (most notably in her legs), and intermittent headache that had been persisting for about four weeks.
On presentation, her physical exam consisted of a blood pressure of 173/78 mmHg but otherwise normal vital signs, normal neurologic examination, and tenderness to palpation in the left lower quadrant. Initial laboratory workup revealed an elevated white blood cell count of 12,300/ul of blood with 51% lymphocytes on differential, low sodium at 127 milliequivalents per liter, potassium at 3.5 milliequivalents per liter, chloride at 95 milliequivalents per liter, creatinine at 0.42 milligram/deciliter, AST at 88 U/L, ALT 99 U/L, alkaline phosphatase at 119 U/L, total bilirubin at 0.8 mg/dL, calcium at 7.8 mg/dL, and albumin at 3.2 g/dL. Lipase was normal at 60 U/L, serum osmolality was 250 milliosmoles/kilogram of water, urine osmolality was 280 milliosmoles/kilogram of water, thyroid stimulating hormone and serum cortisol at 5 AM was normal at 2.0 milliunits/liter and 16 ug/dL respectively. Computed tomography (CT) of the head revealed no acute abnormalities (Figure )
CT of the abdomen and pelvis revealed an enlarged spleen measuring 17.8 cm as well as diverticulitis of the descending and sigmoid colon with colonic wall thickening and surrounding inflammation (Figure ).
Intravenous metronidazole and levofloxacin were started for suspected diverticulitis. The day after admission, she developed left arm weakness and magnetic resonance imaging (MRI) of the brain was ordered. The findings of the MRI were nonspecific, described as mild T2 hyperintensity in the periventricular white matter with non-specific changes (Figure ).
After two days, the patient began to experience lower extremity weakness and was unable to walk without assistance. The following day, she had right facial droop and was alert with dysarthria and incomplete right lid closure. On exam, she had diffuse motor weakness of bilateral upper and lower extremities, intact sensation, and absent deep tendon reflexes. Neurology was consulted and lumbar tap was ordered. Cerebrospinal fluid (CSF) was clear and colorless and analysis revealed albumin 100 mg/dL, albumin (MS) 2950 mg/dL, IgG 22 mg/dL, no oligoclonal bands, white blood cells 1/mm3, and red blood cells 1/mm3, with an opening pressure of 6 cm H2O.
Additionally during hospital stay, the cause of the patient’s splenomegaly and lymphocytic leukocytosis were evaluated by examining peripheral blood. Flow cytometric immunophenotypic analysis of the same showed 48% small kappa clonal B-cell population expressing Cluster of differentiation (CD) 19 and moderate CD20; the sample was negative for CD5, CD10, CD25 and CD103. About 27.5% neutrophils with <0.1 % myeloblasts were identified. These findings are consistent with B-cell, non-Hodgkin lymphoma cells. The patient received intravenous immune globulin (IVIG) for five days as well as supportive care with physical and occupational therapy for treatment of Guillain-Barré Syndrome. Her strength improved and she was ultimately discharged to inpatient rehab with subsequent oncology follow up.
After discharge, she experienced B symptoms including fatigue, fever, and sweats. She was later seen outpatient by oncology, bone marrow biopsy was performed, and she was ultimately diagnosed splenic marginal zone lymphoma. She was started on rituximab. On follow up evaluation several months later and after several infusions of rituximab, she was noted to have complete resolution of these B symptoms and splenomegaly.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.2, 'g/dL'], 'Calcium': [7.8, 'mg/dL']}",8.44,8.018,8.862,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.2 g/dL. 
The concentration of Calcium is 7.8 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.2 g/dL)) + 7.8 mg/dL = 8.44 mg/dL.
The patient's corrected calcium concentration 8.44 mg/dL."
2693,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,usmle-9971,Extracted,"A 76-year-old woman presents to the physician for a follow-up examination. She had a hemoglobin level of 10.5 g/dL last month. She complains of mild dyspnea with exercise. She reports exercising daily for the past 30 years. She is relatively healthy without any significant past medical history. She occasionally takes ibuprofen for knee pain. She denies a prior history of alcohol or tobacco use. Her temperature is 37.1°C (98.8°F), the pulse is 65/min, the respiratory rate is 13/min, and the blood pressure is 115/65 mm Hg. The examination shows no abnormalities. Laboratory studies show:
Laboratory test
Hemoglobin 10.5 g/dL
Mean corpuscular volume 75 μm3
Leukocyte count 6500/mm3 with a normal differential
Platelet 400,000/mm3
Serum
Iron 35
Total iron-binding capacity 450 μg/dL
Ferritin 8
Ca+ 9.0 mg/dL
Albumin 3.9 g/dL
Urea nitrogen 10 mg/dL
Creatinine 0.9 mg/dL
Serum protein electrophoresis and immunofixation show a monoclonal protein of 20 g/L (non-IgM). Marrow plasmacytosis is 5%. A skeletal survey shows no abnormalities.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.9, 'g/dL'], 'Calcium': [9.0, 'mg/dL']}",9.08,8.626,9.534,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.9 g/dL. 
The concentration of Calcium is 9.0 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.9 g/dL)) + 9.0 mg/dL = 9.08 mg/dL.
The patient's corrected calcium concentration 9.08 mg/dL."
2694,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3728493-1,Extracted,"A 49-year-old Caucasian male was admitted for vasculitis. For more than 10 years, he was addicted to heroin, recently substituted by Methadone. He denied intravenous drug abuse. During the past 6–12 months, he had experienced loss of physical performance due to aching legs, decreasing muscle strength, weight loss, malaise, and fatigue. He had virtually no outdoor activities, and his preferred diet was white bread with chocolate butter. One week before admission, he noticed nonulcerating, painful purpuric rash on both legs (). There had been no fevers, ear-nose-throat manifestations, lung symptoms, abdominal pain, Raynaud's phenomenon, mucosal bleedings, or ulcerations. The patient did not take any medications apart from methadone, and had no exposures to insects or any travels abroad. On physical examination, he appeared in a poor condition, slightly anemic, blood pressure 125/92 mmHg, temperature 37,4 Celius, peripheral pulse 100 beats/min, respiratory rate 18/min, weight 65 kg, and height 179 cm. He presented with reduced locomotor function due to painful legs, calves in particular. A palpable, purpuric rash and confluent ecchymoses were noted on both legs, most pronounced at the medial aspects of thighs and lower legs (). There were scattered purpuric elements on the buttocks, but no proximal lesions. Walking and even mild physical exercise resulted in severe worsening of pain and progression of purpura into ecchymoses (). During the following days, suggilations appeared in the soles ().
B-hemoglobin was 5,2 mmol/L, and mean corpuscular volume (MCV) was 111 μ³ (80–100). The white blood cell and platelet counts were normal. C-reactive protein (CRP) was 87 (<10) mg/L. Creatinine and liver function tests were normal, except for slightly increased alkaline phosphatases, 138 U/L (35–105). Coagulation screening was unremarkable, and albumin was 35 g/L. Creatine kinase and urine analyses were normal. S-IgA was 3,76 g/L (0,70–3,65), and there were normal levels of IgG and IgM. There was no M-component. He tested negative for hepatitis B and C, human immunodeficiency virus (HIV), cryoglobulin, IgM-rheumatoid factor, anti-nuclear antibodies (ANA), anti-neutrophil cytoplasmic antibodies (ANCA, proteinase-3, and myeloperoxidase), and phospholipid antibodies. Complement levels were normal. There were no opacities on Chest X-ray. Blood cultures were negative. A skin biopsy showed erythrocyte extravasation and follicular hyperkeratosis, but no vasculitis, complement or immunoglobulin deposits ().
Additional analyses revealed low 25-hydroxy-vitamin D, <6 mmol/L (50–160), ionized calcium, 116 mmol/L (1,19–1,29), S-folate, <3,4 nmol/L (5,0–30,0), elevated parathyroid hormone, 13,1 pmol/L (1,10–6,50), and normal S-cobalamin. Ascorbate in serum was barely detectable, <3,0 μ/L (26,1–84,6).
Replenishment with vitamins C and D, folic acid, and calcium and adjustment of his dietary habits were followed by rapid and sustained recovery. One month later, serum levels of calcium and vitamins were normal with S-ascorbate at 30,5 μ/L.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [35.0, 'g/L'], 'Calcium': [116.0, 'mmol/L']}",465.328,442.0616,488.5944,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 35.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 35.0 g Albmumin/10.0 dL = 3.5 g Albmumin/dL. The concentration value of 35.0 g Albmumin/L converts to 3.5 g Albmumin/dL. 
The concentration of Calcium is 116.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 116.0 mmol. To convert 116.0 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 116.0 mmol Calcium * 0.001 mol/mmol = 0.116 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.116 mol Calcium * 40.08 g/mol = 4.64928 g Calcium. To convert 4.64928 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 4.64928 g Calcium * 1000.0 mg/g = 4649.28 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 4649.28 mg Calcium/10.0 dL = 464.928 mg Calcium/dL. The concentration value of 116.0 mmol Calcium/L converts to 464.928 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.5 g/dL)) + 464.928 mg/dL = 465.328 mg/dL.
The patient's corrected calcium concentration 465.328 mg/dL."
2695,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5654079-1,Extracted,"A 55 year old woman was referred to our Endocrinology Department in June 2006 for further investigation of multiple severe hypoglycemic attacks. She complained of sweating, tachycardia, palpitations, weakness, confusion and described episodes of hypoglycemic coma occurring in the last two months. She had severely limited physical activity because of hypoglycemia-related symptoms at minimal efforts. She had gradually gained weight (12 kg in the last two months) because of increased food intake to correct hypoglycemia.
The patient had been previously diagnosed and treated for high blood pressure.
Physical examination showed an overweight patient (BMI=29kg/m2). She had normal blood pressure (with antihypertensive treatment), normal pulse rate and body temperature. The abdomen was soft but with painless hepatomegaly. Physical examination of the cervical region revealed a mild goiter with normal consistency and no regional adenopathy.
Laboratory tests showed the presence of hypoglycemia (30mg/dl) associated with an increased value of plasma insulin (16µU/ml). Normal insulin level for glycemia under 45mg/dl must be below 6µU/ml. The calculated ratio of glycemia/insulinemia in our patient was 1.87 instead of the normal value of less than 0.25.
In a patient without previous treatment with insulin and sulfonylurea, failure to suppress endogenous insulin secretion in the presence of hypoglycemia is the hallmark of an insulinoma.
We also found elevated liver enzymes (ALT=47iu/l, AST=72iu/l, GGT=133iu/l). Decreased serum albumin (2.8g/dl) and prolonged prothrombin time indicated hepatic failure.
Abdominal CT revealed a 1.5cm mass localized at the head of pancreas and multiple tumors disseminated in both liver lobes (). Thoracic CT scan did not find any abnormal aspects suggestive of metastases. In order to establish the etiology of hepatic masses an ultrasound – guided liver biopsy was performed. Histological examination showed hepatic tissue with tumoral areas presenting an aspect of neuroendocrine carcinoma (). The immunohistochemistry study confirmed the neuroendocrine origin of the hepatic tumors (, , , ) showing tumoral cells with focal and diffuse expression for Chomogranin A, Synaptophysin and CD57; anti-Vimentin was positive in rare tumoral cells like Cytokeratin 18; anti-CD34 showed a denser vascular network; anti-Ki67 antibody displayed a nuclear expression in rare tumoral cells ( ~5%).
These findings established the diagnosis of malignant insulinoma with liver metastases.
Biochemical evaluation also revealed a mild elevation of total calcium 10.4mg/dl (normal upper range of serum calcium:10.2 mg/dl), normal serum phosphorus level of 4mg/dl (normal range: 2.5-4.5mg/dl) and increased alkaline phosphatase 405iu/l (normal range: 80-285iu/l).
In order to investigate the source of hypercalcemia, more tests were performed. We measured the PTH that revealed a mild elevated level of 71.2pg/ml (normal range: 10-69pg/ml) and 24 hour urinary calcium which was 180mg/dl (normal range between 100-300mg/24h).
Hypercalcemia with high PTH suggested the diagnosis of primary hyperparathyroidism.
Anterior neck ultrasound revealed a multinodular goiter with multiple nodules under 1cm, but did not give any information about parathyroid glands. A cervical CT was performed but it didn’t reveal any pathological parathyroid findings.
The coexistence of primary hyperparathyroidism and an enteropancreatic tumor (malignant insulinoma) suggested the presence of multiple endocrine neoplasia type 1 (MEN 1). Because of the high frequency of pituitary adenomas, especially prolactin-secreting ones among MEN 1 patients, we measured serum prolactin but we found a normal level: PRL=11.7ng/ml (normal ranges: 3-18 ng/ml).
In order to evaluate the presence of a pituitary adenoma we performed a cerebral CT scan which didn’t reveal any pathological aspects for the pituitary gland. We also considered the normal aspect of both adrenal glands on the abdominal CT in order to exclude an adrenal tumor, possibly associated with MEN 1.
We started treatment and recommended a daily 250-300g of carbohydrate intake in eight meals (every 2-3 hours). In order to improve glycemic control, we administered verapamil 240 mg/day, but no result was obtained.
The patient was referred to the surgical department but because of the magnitude of liver tumors and coexistence of liver dysfunction, surgical intervention was not an option. Impaired liver function was also a contraindication for hepatic artery embolization.
We decided to start medical treatment with a somatostatin analog. Our first option was long-acting lanreotide, 30mg at two weeks, but without response in terms of glycemic values. Instead, octreotide acetate 0.15mg/day (0.05 mg subcutaneously every 8 hours) was more effective, reducing both the frequency and severity of hypoglycemic episodes. We recommended that glucagon be available for the patient’s emergency use.
Because of the general condition of the patient and the absence of advanced features of hyperparathyroidism, parathyroid surgery was not performed; we administered biphosphonate therapy as specific inhibitor agents of bone resorption (alendronate 70mg, once a week) associated with moderate dietary calcium restriction to 1000 mg/day and adequate hydration.
After two months (in August 2006) the symptoms were more difficult to control even with double doses of Octreotide (0.30mg/day subcutaneously).
Laboratory tests showed a worsening situation: glycemia=20mg/dl, insulinemia=190,7µU/ml; glycemia/insulinemia ratio=9,53, ALT=63iu/L, AST=117iu/L, GGT=272iu/L and a total level of calcium (11.1ng/dl).
Abdominal CT revealed a progression of the pancreatic tumor (2.5cm) and increased number and dimension of liver metastases ().
We considered the disease as being progressive and a chemotherapeutical regimen with doxorubicin (100mg/day IV every 21 days) was instituted. After three months of chemotherapy no improvement was seen in biochemical or hormonal parameters. Moreover, CT exam showed a progression of hepatic masses and the presence of multiple sub pleural metastases. We decided to stop doxorubicin administration.
The patient died in December 2006 at home, probably in a hypoglycemic coma.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [2.8, 'g/dL'], 'Calcium': [10.4, 'mg/dL']}",11.36,10.792,11.928,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.8 g/dL. 
The concentration of Calcium is 10.4 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.8 g/dL)) + 10.4 mg/dL = 11.36 mg/dL.
The patient's corrected calcium concentration 11.36 mg/dL."
2696,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2930305-1,Extracted,"A one-year-three-month old female child, residing in Mumbai, was admitted in our hospital on 9 January, 2009, with complaints of high grade fever off and on, not associated with rigors, for the past one month. On examination, pallor was present along with ecchymosis and petechial rashes over the abdomen. She had hepatosplenomegaly. In the other systems, no abnormality was detected. Her hemoglobin was 5.7 gm%, TLC 16,400/cu.mm., with neutrophils 44%, lymphocytes 50%, and monocytes 6%. Platelet count was 8,000/cu.mm. Serum protein was 7 mg (albumin 4 and globulin 3), total bilirubin 1.1 mg/dl with direct bilirubin of 0.1 mg/dl. ALT 31, AST 13, and alkaline phosphatase was 337 IU/l, serum BUN 7 mg%, serum creatinine 0.7 mg%, serum sodium 138 mEq/l, potassium 4.1 mEq/l, calcium 8.9 mg%, and phosphate 4 mg%. She was diagnosed as a case of severe anemia with hepatosplenomegaly and acute lymphatic leukemia – CALLA positive. She was given chloroquine on admission and later two bottles of platelets were transfused. Antibiotics (Amikacin and Piperacillin-Tazobactam), Prednisolone (10 mg), Vincristine (0.36 mg), and Methotrexate (8 mg) were started. On 19 January, her hemoglobin increased to 7.7 gm%, TLC reduced to 7600/cu.mm, with neutrophils 27%, lymphocytes 68%, and monocytes 5%. The platelet count increased to 22,000/cu.mm. Two more bottles of platelet transfusion was given and the other medicines were continued.
On 27 January, she suddenly developed loose motions without abdominal pain. Stool was sent for culture along with blood culture in trypticase soy broth. After 24 hours, from the blood culture bottle, subcultures were peformed on MacConkey agar (MA) and blood agar (BA) plates and incubated at 37°C overnight. The stool was directly plated on MA and Xylose lysine deoxycholate agar (XLD). Pure non-lactose fermenting colonies with irregular margins grew on both the MA plates. They were oxidase positive and motile, and were identified as Pseudomonas aeruginosa by standard biochemical tests.[] Thus the same organism was isolated from the blood and stool cultures. Antibiotic susceptibility was carried out using the Kirby-Bauer disk diffusion method on a Mueller Hinton agar, according to CLSI guidelines.[] It was susceptible to amikacin, ofloxacin, piperacillin, and imipenem, and resistant to ceftazidime. The stool isolate, in addition, was susceptible to norfloxacin and resistant to nalidixic acid. On 27 January her complete blood count was by Hb 10.1 gm/dl, TLC 1100/cu.mm., P2, L8, Blasts90, Platelets 7,000/cu.mm.
She developed left facial palsy on 28 January and also developed perianal and gluteal abscesses.
On 29 January, she was put on amikacin, meropenem and metronidazole. Although the diarrhea subsided after five days, the stool cultures repeatedly grew P.aeruginosa. On 2 February, two stool samples were again sent for culture and both grew Pseudomonas aeruginosa in pure culture, with the same antibiotic susceptibility pattern, but the blood culture sent on the same day did not show any growth. On 12 February also, the stool culture grew Pseudomonas aeruginosa, susceptible only to amikacin. Blood cultures were further sent on 9, 16, and 20 February and 2 March. None of them showed any growth. Stool cultures were further sent on 20 February, 2 and 5 March, and they did not grow any pathogenic bacteria. She was given another bottle of platelet transfusion and was discharged on 9 March. At discharge, her condition was stable.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [8.9, 'mg/dL'], 'Albumin': [4.0, 'g/dL']}",8.9,8.455,9.345,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.0 g/dL. 
The concentration of Calcium is 8.9 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.0 g/dL)) + 8.9 mg/dL = 8.9 mg/dL.
The patient's corrected calcium concentration 8.9 mg/dL."
2697,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6874932-1,Extracted,"A 61-year-old woman presented with symptoms of intractable nausea and vomiting for 10 days. Her past medical history included permanent hypothyroidism and hypoparathyroidism from subtotal thyroidectomy due to a huge multinodular goiter 2 years earlier. Her thyroid condition was well controlled with levothyroxine 600 μg per week. She was also prescribed with 2,400 mg of elemental calcium and 1 μg of alfacalcidol per day. On the last follow-up, 2 months prior to this visit, she was in good health with normal calcium and thyroid function levels. A thorough medical history review discovered that she had been taking different preparations of over-the-counter alfacalcidol, 0.25 μg to 1 μg/tablet for 6 weeks. She also increased the daily calcium supplement up to 4,800 mg of elemental calcium per day to control her tingling sensation. On physical examination, the patient was drowsy and moderately dehydrated. Her vital signs and neurological examination were unremarkable. Laboratory investigations showed profound hypercalcemia, mild hypophosphatemia and azotemia: serum calcium 17.08 mg/dL (8.5–10.5), phosphate 2.1 mg/dL (2.5–4.5), albumin 3.5 mg/dL and creatinine 2.0 mg/dL. Her venous pH was 7.46 and electrolytes showed mild hypokalemia and metabolic alkalosis: sodium 135 mEq/L potassium 3.4 mEq/L, chloride 95 mEq/L, and bicarbonate 29 mEq/L. Low levels of intact PTH 6.07 pg/mL (15–65), 25-OH vitamin D 19 ng/mL (>20) with a normal level of 1,25(OH)2 vitamin D 25.4 pg/mL (19.9–79.3) and normal levels of PTHrP were shown. Her thyroid function test was normal: FT4 1.35 ng/dL (0.80–1.80) and TSH 2.52 μIU/mL (0.35–4.10). The electrocardiography (ECG) showed sinus rhythm with normal QTc interval (410 ms). Her amylase and lipase levels were not elevated. The presumptive diagnosis of CAS was proposed from her triad of hypercalcemia, metabolic alkalosis, and renal insufficiency. She responded well to intravenous hydration with isotonic normal saline (4 L/d), subcutaneous calcitonin (200 IU q 8 h) and discontinuation of calcium and vitamin D supplements. Her clinical symptoms and serum calcium level returned to normal within 2 days of treatment. The patient was discharged on the 4th day of hospitalization and was prescribed with 2,000 mg of calcium carbonate and 0.5 μg of alfacalcidol daily. During the follow-up after 6 months, she did not have experienced episode of hypercalcemia and her renal function returned to baseline level.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Albumin': [3.5, 'g/dL'], 'Calcium': [17.08, 'mg/dL']}",17.48,16.606,18.354,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.5 g/dL. 
The concentration of Calcium is 17.08 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.5 g/dL)) + 17.08 mg/dL = 17.48 mg/dL.
The patient's corrected calcium concentration 17.48 mg/dL."
2698,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-8705311-1,Extracted,"An 18-year-old adolescent female was evaluated at 15 weeks’ gestation for history of persistent emesis for four weeks, extreme fatigue and red colored urine for one day. There was no history of fever, diarrhea, abdominal pain, or urinary tract infection.
Past medical history was unremarkable for diabetes mellitus, rheumatoid arthritis, or other autoimmune diseases. She was not known to have hyperthyroidism in the past. Pregnancy had been uneventful except for persistent episodes of emesis for past one month. There was no prior history of mood symptoms or altered mental status. There was no history of heat intolerance, diarrhea, or weight loss. There was no recent history of usage of corticosteroid, loop or thiazide diuretic, strenuous exercise, vaginal bleeding, vaginal discharge of grape-like vesicles, seizures, alcohol intake, and carbohydrate load. Family history was notable only for type 2 diabetes in the father. There was no known family history of autoimmune diseases, thyroid disorders, hypokalemia, and periodic paralysis. There was no consanguinity.
Vital signs upon presentation showed blood pressure (BP) 142/87 mm Hg, pulse 120 beats per minute, oral temperature 38.9 °C (102.02 °F), respiratory rate 18 per minute, and oxygen saturation of 97%. Her height was 172.7 cm and weight was 109 kg (240 lb 4.8 oz). Physical examination was remarkable for an overweight female who was awake but slow to respond. There was no goiter and ophthalmopathy. There was mild scleral icterus. There was no tremor or pretibial edema.
Serum beta-human chorionic gonadotropin (hCG) level was 246,000 mIU/mL and sonogram confirmed the presence of a single viable intrauterine fetus of approximately 15 weeks gestation with expected uterine size. Renal function test showed sodium 127 mmol/L, potassium 2.5 mmol/L, bicarbonate 33 mmol/L, blood urea nitrogen (BUN) 123 mg/dL, serum creatinine 4.2 mg/dL (MDRD estimated glomerular filtration rate (eGFR) 17 mL/min/1.73 m2), calcium 9.5 mg/dL, phosphorus 2.7 mg/dL and magnesium of 1 mg/dL. Liver function test showed aspartate aminotransferase 140 IU/L, alanine aminotransferase 203 IU/L, total bilirubin 2.9 mg/dL, ammonia 55 µmol/L, and serum albumin 3.1 gm/dl. Renal function test two months prior to pregnancy showed normal serum creatinine of 0.8 mg/dL (MDRD eGFR 113 mL/min/1.73 m2) and normal electrolytes (serum sodium 138 mmol/L, potassium 3.9 mmol/L, bicarbonate 24 mmol/L, calcium 9.4 mg/dL, phosphorus 3.9 mg/dL, and magnesium was not available) Serum creatine kinase was normal at 121 U/L (normal 0–180 U/L). Urine sodium was <10 mmol/L, urine creatinine 84 mg/dL, urine potassium 28 mmol/L and urine osmolality was 344 mOsm/kg. Fractional excretion of sodium was 0.4%. Urinalysis showed 1+ proteinuria, no microscopic hematuria, 5 white cells per high power field, no ketonuria, pH 5, specific gravity of 1.015, and negative nitrites and leukocytes. Plasma renin activity was 14 ng/mL/h (normal 0.5–4 ng/mL/h, upright) and serum aldosterone was 13 ng/dL (normal 4–31 ng/dL, upright). Blood and urine cultures were negative. Other extensive investigations for infectious etiologies were also negative. Urine for Chlamydia and Neisseria was negative. SARS-CoV-2 DNA PCR from the nasopharyngeal swab was negative. Other labs were notable for undetectable thyroid stimulating hormone (TSH) level < 0.030 mIU/L (reference 0.4–5 mIU/L), total T3 238 ng/dL (reference 87–178 ng/dL), and free T4 > 6.99 ng/dL (reference 0.6–1.2 ng/dL). Computed tomography of the head showed no acute intracranial abnormalities.
Initial management included administration of intravenous fluids (IVF), propranolol, potassium iodide, propylthiouracil (PTU), and hydrocortisone. A presumptive diagnosis of hyperemesis gravidarum with thyroid storm and AKI secondary to persistent emesis was made. She met criteria for thyroid storm due to elevated serum free T4 and total T3 with undetected TSH, along with pyrexia, tachycardia, icterus, and altered mental status. Her clinical condition improved somewhat after receiving PTU, propranolol, and hydrocortisone as heart rate, blood pressure, and free T4 began to decrease. Her mental status improved and she became more alert and engaged in conversation. Given tachycardia and hypertension, she was started on propranolol 60 mg every 4 hours which was later converted to 160 mg daily.
Other thyroid studies showed thyroid peroxidase antibody 0.3 IU/mL (reference < 9 IU/mL), TSH receptor antibody (TRAb) < 0.90 (reference < 1.75 IU/L), and undetected thyroid stimulating immunoglobulin (TSI) of < 0.10 (reference ≤ 0.54 IU/L). Given negative TRAb, Graves’ disease was highly unlikely. Serum free T4 normalized in ten days, TSH in two weeks and total T3 in five days. Given pregnancy, further modalities including radioactive iodine uptake study were not pursued, given risk of fetal hypothyroidism, mental retardation, and increased risk of malignancy. Partial molar pregnancy was initially considered due to presentation of thyroid storm, however, the beta-hCG level was trending down and the patient did not show any signs of pre-eclampsia. Thyroid sonogram showed normal sized thyroid with homogenous thyroid texture and without increased vascularity, making Grave’s disease unlikely. Investigations for AKI included renal sonogram which showed right kidney measuring 12.8 cm in length and left kidney measuring 12.6 cm in length with bilateral normal cortical echogenicity without evidence of hydronephrosis or nephrocalcinosis. Hepatic sonogram showed gallbladder sludge. A chest X-ray was normal without pulmonary edema or cardiomegaly. Electrocardiogram showed normal Q-T interval. Echocardiogram was normal with ejection fraction of 65%. Cardiac enzymes were normal.
PTU was later changed to methimazole as she was no longer in the first trimester of pregnancy and as she demonstrated signs of liver insufficiency. Anti-emetics and IVF were discontinued after few days as the patient was able to tolerate well by mouth. Hydrocortisone was discontinued after two days. Subsequently, propranolol was discontinued along with methimazole, as the beta-hCG mediated hyperemesis was thought to be the likely etiology of thyroid symptoms. Her vital signs, including BPs, remained stable and her thyroid levels returned to normal without anti-thyroid drugs. Serum beta-hCG at discharge was 175,557 mIU/mL. Given decreasing level of hCG without other signs or symptoms of gestational trophoblastic disease, molar pregnancy was unlikely. She was discharged without any thyroid medications.
During the hospitalization, her serum potassium remained around 2.4–2.9 meq/L along with serum bicarbonate 30–38 meq/L despite resolution of emesis. Serum magnesium remained low, as well as with values ranging from 1–1.4 mg/dL. Twenty-four hour urine collection showed a urine calcium of 0.04 mg/kg/day. Random urine calcium to creatinine ratio was also low at 0.005. She required multiple intravenous potassium and magnesium supplements. Discharge serum potassium and magnesium was 3.5 meq/L and 1.2 mg/dL, respectively. She was discharged on magnesium oxide 400 mg daily and potassium chloride 10 meq twice daily. BUN and serum creatinine slowly improved with intravenous hydration. Kidney biopsy was not performed and renal replacement therapy was not required. Discharge BUN and serum creatinine was 15 mg/dL and 0.97 mg/dL (MDRD eGFR 90 mL/min/1.73 m2), respectively. Due to the persistent hypokalemia, alkalosis, hypomagnesemia and hypocalciuria despite resolution of emesis, a genetic testing by next generation sequence analysis was done which showed that the patient was homozygous in the SLCA123 (NM_001126108.2) gene for a known sequence variant designated c.2581C>T (p.Arg861Cys) (Prevention Genetics, Marshfield, WI, USA). No further in vitro functional studies were performed, hence the exact functional implication of this variant was unknown. However, to determine the pathogenicity of this variant, in silico tests were performed using SIFT, PolyPhen-2, FATHMM and MutationTaster. The resulting prediction utilizing these in silico tools was “Pathogenic”. At 37 weeks gestation, a healthy infant of 3.5 kilograms was born vaginally without any perinatal complications. The serum creatinine remained stable at 0.7 mg/dL after delivery (MDRD eGFR 132 mL/min/1.73 m2).","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [9.5, 'mg/dL'], 'Albumin': [3.1, 'g/dL']}",10.22,9.709,10.731,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.1 g/dL. 
The concentration of Calcium is 9.5 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.1 g/dL)) + 9.5 mg/dL = 10.22 mg/dL.
The patient's corrected calcium concentration 10.22 mg/dL."
2699,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7211338-1,Extracted,"A 57-year-old white man presented with a 3-month history of new-onset, severe, bi-frontal headaches and a 13.6 kg (30-lb) weight loss. Local emergency room evaluation revealed a negative computed tomography (CT) scan of his head. Laboratory findings included an elevated erythrocyte sedimentation rate (ESR) of 80 mm/hour and C-reactive protein (CRP) of 55.3 mg/L. He was discharged with pain control.
During follow-up with his local primary provider, his headache persisted and bilateral jaw pain and left facial numbness had developed. He was started on prednisone 60 mg/day for presumed GCA with partial improvement in his headache. Bilateral temporal artery biopsies were performed 3 days later and were negative. Prednisone was subsequently discontinued. Two weeks later his headache progressed and right eye horizontal diplopia and perioral numbness developed. Magnetic resonance imaging (MRI) of his brain was performed and interpreted as normal. He was admitted for pulse-dose steroids (1000 mg daily for 3 days) which led to resolution of visual symptoms and was discharged on prednisone 60 mg/day. Tapering below 50 mg/day was unsuccessful due to rising inflammatory markers, symptom progression, and return of diplopia. Severe left hip pain developed for which plain radiographs were obtained but negative for fracture or avascular necrosis.
On referral to our institution he continued to have ongoing headache and left jaw numbness despite 6 weeks of high-dose glucocorticoids (80 mg/day). Left hip pain had worsened to the point of wheelchair dependency. His past medical history was remarkable for atrial fibrillation for which he was receiving warfarin 2 mg/day and diltiazem 240 mg/day. Social history was notable for lack of tobacco or alcohol use and absence of known environmental exposures during his employment as an office manager. Aside from prostate cancer in his father, our patient’s family history was negative for other pertinent diagnoses of additional malignancies or autoimmune conditions. Laboratory evaluation noted an ESR 72 mm/hour, CRP 53 mg/L, hemoglobin 11.1 g/dL, leukocytes 5.2 × 109/L and platelets 110 × 109/L, international normalized ratio (INR) 2.3, creatinine 1.04 mg/dL, calcium 11.6 mg/dL, alanine aminotransferase 106 U/L, aspartate aminotransferase 64 U/L, alkaline phosphatase 360 U/L, total bilirubin 1.2 mg/dL, total protein 5.1 g/dL, and albumin 3.4 g/dL. Previously obtained autoimmune serologies were negative for antinuclear and extractable nuclear antigens as well as rheumatoid factor, anti-cyclic citrullinated peptide, myeloperoxidase, and proteinase-3 antibodies.
His vital signs demonstrated a heart rate of 95 beats per minute, blood pressure of 94/44 mm Hg, respiratory rate of 12 per minute, oxygenation saturation of 96%, and weight of 144 kg with body mass index (BMI) of 48.6 kg/m2. An examination was notable for a Cushingoid appearance and morbid obesity. Evaluation of adenopathy and splenomegaly was limited due to body habitus. Pertinent cardiovascular findings included irregularly irregular pulse without murmurs. Upper and lower arterial pulses were normal and symmetric. Common superficial temporal artery palpation was without tenderness or nodularity. Trace pitting edema was noted to the ankle bilaterally. Breath sounds were equal and symmetric without wheezing or rhonchi. Aside from scattered bruising at site of venipuncture, no cutaneous abnormalities were noted. A neurologic examination showed normal speech without language deficits. Visual acuity was 20/20 bilaterally. Cranial nerves 2–12 were assessed and normal except for mild esotropia of his right eye and hypoesthesia to light touch and pinprick over the left mandibular region of the left trigeminal nerve. The remaining dermatomes evaluated showed normal sensation. Reflexes were normal and symmetric throughout and toes were down-going bilaterally. No ataxia was observed. A musculoskeletal examination demonstrated normal range of motion of upper extremities without deficit. Marked pain was noted on passive and active range of motion of his left hip.
Given the persistent headache despite high-dose glucocorticoids and atypical features, alternative etiologies were suspected. The local MRI of his brain was reviewed and evidence of abnormal enhancing soft tissue involving Meckel’s cave bilaterally with extension through the foramen ovale was noted (Fig. a). The differential diagnosis for infiltrative process in Meckel’s cave included sarcoidosis as well as primary or secondary neoplastic lesions such as meningioma, nasopharyngeal carcinoma, schwannoma, neurofibroma, and lymphoma [, ]. The presence of constitutional symptoms and elevated inflammatory markers suggested a secondary process with associated intracranial involvement. As such, positron emission tomography (PET)-CT was obtained. This demonstrated extensive hypermetabolic lesions throughout the axial and appendicular skeleton, including the skull base, as well as fluorodeoxyglucose (FDG)-avid lymph nodes above and below the diaphragm (Fig. c). MRI of his left hip revealed diffusely abnormal marrow signal suggestive of infiltrative disease. A cervical lymph node biopsy demonstrated evidence of diffuse large B cell lymphoma and staging bone marrow biopsy revealed a hypercellular marrow (90%) with diffuse large B cell lymphoma involving 70% of the total cellularity (Fig. ). Initiation of high-dose methotrexate (3.5 g/m2), rituximab (375 mg/m2), cyclophosphamide (750 mg/m2), hydroxydaunorubicin (50 mg/m2), Oncovin (vincristine; 2 mg), and prednisone (255 mg) (MR-CHOP; 21-day cycle) resulted in interval improvement in his headache and visual symptoms (Fig. b, d).
Ten months after initial diagnosis and 4 months after completion of his sixth cycle of MR-CHOP, our patient re-presented with bilateral lower extremity weakness and PET-CT showed recurrence of disease with evidence of neurolymphomatosis of multiple cervical, thoracic, and sacral nerve roots. Intrathecal cytarabine (50 mg) was given and ibrutinib (140 mg/day) was initiated, resulting in initial findings of improved strength and subsequent decreased nerve root FDG-avidity.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [11.6, 'mg/dL'], 'Albumin': [3.4, 'g/dL']}",12.08,11.476,12.684,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.4 g/dL. 
The concentration of Calcium is 11.6 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.4 g/dL)) + 11.6 mg/dL = 12.08 mg/dL.
The patient's corrected calcium concentration 12.08 mg/dL."
2700,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-2813541-1,Extracted,"A seven year-old female child presented in July 2007 with a 12 h history of bloody urine, vomiting, agitation, and restlessness following a scorpion sting; health care services confirmed that the culprit species was Hemiscorpius lepturus. Examination revealed that she had a tender and erythematic area with local edema on the right leg (4 × 6 cm); the patient was conscious. Her temperature was 39.6°C, pulse was 125/min; blood pressure was normal (100/60 mmHg). At the time of admission, hematology revealed hemoglobin = 10.2 g/dL, white blood cells = 24,000/mm3, and platelets = 175,000/mm3; urinary analysis showed 3+ hemoglobinuria and microscopic hematuria without proteinuria. Serum creatinine (SCr) and blood urea nitrogen (BUN) levels were normal (0.4 and 25 mg/dL, respectively); other blood chemistry results were unremarkable. Coomb's test was negative and the G6PD level and peripheral blood smear were normal. At this time, the patient received polyvalent antivenom, cefazoline, and 20 meq/L sodium bicarbonate in dextrose water.
During the first week, SCr and BUN levels gradually rose (8.6 and 100 mg/dL, respectively), but the hemoglobin level and platelet count dropped to 8 g/dL and 47,000/mm3 respectively. A blood smear showed fragmented erythrocytes and burr cells; total serum protein level was 5.9 g/dL, albumin level was 3.3 g/dL, calcium level 9.2 mg/dL, phosphorus level 6.2 mg/dL, and lactate dehydrogenase 16358 IU/L. Urinary analysis showed 3+ proteinuria, 3+ hemoglobinuria, and erythrocyte casts. Prothrombin time and partial thromboplastin time were normal (12 and 32 seconds, respectively). A sonogram of the urinary tract was normal. Bone marrow aspiration revealed essential hypercellular marrow with increased megakaryocytes, erythroid hyperplasia, and a shift to the left in myelopoiesis. She received packed cell, fresh, frozen plasma and platelets several times. Also, hydrocortisone (10 mg/kg/day) was added and hemodialysis was performed. In the second week, platelets rose to normal levels (248,000/mm3) but the lactate dehydrogenase level dropped to 1430 IU/L. We did not do renal biopsy but the combination of microangiopatic hemolytic anemia, thrombocytopenia, and acute renal failure led us to diagnose hemolytic uremic syndrome in this child. After one month, she was discharged with a SCr level of 6.7 mg/dl on an every-other-day dialysis program.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [9.2, 'mg/dL'], 'Albumin': [3.3, 'g/dL']}",9.76,9.272,10.248,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.3 g/dL. 
The concentration of Calcium is 9.2 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.3 g/dL)) + 9.2 mg/dL = 9.76 mg/dL.
The patient's corrected calcium concentration 9.76 mg/dL."
2701,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5024499-1,Extracted,"A 57-year-old Caucasian woman with a four-year history of monoclonal gammopathy of undetermined significance (MGUS) complained of several weeks of dry mouth, polydipsia and episodes of confusion. Her serum calcium was 14.4 mg/dL when tested at the office of her primary care physician (PCP) and sent to the emergency department (ED) where her exam was remarkable only for dry mucous membranes. Initial labs were notable for Ca 14.4 mg/dL, albumin 5.0 g/dL, PTH 7 pg/mL, and Cr at 1.94. CBC was notable for mild pancytopenia with WBC 3.5 (th/cmm) with normal differential, Hgb 11.7 g/dL, Hct 34.2 (%), and PLT 145,000 (th/cmm). She received a bolus of normal saline and was subsequently admitted to inpatient service. Initially, the patient’s hypercalcemia was attributed to milk-alkali syndrome and her calcium supplements were discontinued. The patient was managed only with IV hydration. The patient’s serum calcium trended down to 10 mg/dL at the time of discharge.
There was a concern for a neoplastic process, particularly myeloma, given her history of MGUS. The patient underwent bone marrow biopsy at the time of discharge, which was remarkable for non-necrotizing granulomas with no findings suggestive of plasma cell dyscrasia or other neoplasms. (Fig. ) Two weeks later, the patient’s repeat calcium was 12.7 mg/dL despite adequate fluid intake. The patient was admitted for further evaluation of hypercalcemia and bone marrow granulomas. An extensive hypercalcemia workup was unrevealing. Malignant and infectious etiologies of granulomatous disease in this patient were investigated. Results from repeat SPEP, UPEP, and serum free light chains were unchanged from baseline values. PTHrp was undetectable. PET scan showed no FDG avid lesions. Infectious workup for granulomas was negative. The patient’s hypercalcemia was attributed to the granulomas given exclusion of other potential causes. As a result, a workup for sarcoidosis was pursued, which was notable for elevated ACE 126 and urinary calcium of 256 mg/24 h (Table ). Chest X-ray and chest CT revealed no intrathoracic lymphadenopathy or pulmonary parenchymal findings (Fig. ). There was no evidence of sarcoidosis in any other organ.
The patient underwent a rapid prednisone taper over 9 days. After discontinuation of prednisone, she developed hypercalcemia again. She was then treated with a slow prednisone taper for four months with normalization of serum calcium levels. A follow-up bone marrow biopsy 5 months later (1 month after 4-month course of slow prednisone taper) showed partial resolution of granulomas without malignancies. (Fig. ) At her follow-up PCP visit, two years after her initial presentation, the patient was overall asymptomatic with normal serum calcium, ACE, and CBC.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [14.4, 'mg/dL'], 'Albumin': [5.0, 'g/dL']}",13.6,12.92,14.28,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 5.0 g/dL. 
The concentration of Calcium is 14.4 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 5.0 g/dL)) + 14.4 mg/dL = 13.6 mg/dL.
The patient's corrected calcium concentration 13.6 mg/dL."
2702,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4421235-1,Extracted,"The mother was a 40-year-old primigravida with a 3-year history of essential hypertension. She was treated with olmesartan medoxomil (Olmetec® Munich, Germany), a single daily dose of 20 mg, and her hypertension was well controlled with this regimen. Her conception was assisted by IVF. At 33 weeks of gestation, a severe degree of oligohydramnios was diagnosed by ultrasonographic evaluation. Two doses of celestone chronodose were administered, and an emergency caesarean was performed. A premature female baby was delivered, with a weight of 1.980 g, length 45 cm and occipital–frontal circumference 30.5 cm. The Apgar score was 1′/9 and 2′/10. Shortly after the birth, the newborn presented respiratory distress syndrome, and was intubated and ventilated with oxygen supplementation; the newborn received two doses of sulfactant. Unclosed Botal's duct was detected until the second day of life. Oligoanuria was also observed on the first and second postnatal days. On the third day post-birth, renal ultrasonography revealed two kidneys of normal size with increased echogenicity, while on the fifth postnatal day, the plasma creatinine level was 3.1 mg/dl. The neonate was transferred from the maternity hospital to the neonatal intensive care unit at the Children's Hospital for further assessment and management. On admission, the newborn suffered from breathing difficulty and acute renal failure and was on nCPAP 21% O2. On several occasions, her blood pressure was detected as normal to low (≈70/40 mmHg). Dolichocephaly with cranial and facial asymmetries, light dysplasia of the external ear, equestrian figures of the feet, wide anterior fontanel and dilatation of celebral ventricles were also detected. All of these facial characteristics were likely closely related to the severe degree of oligohydramnios. On brain ultrasonography, IHV of first degree on both sides and increased periventricular echogenicity were recorded, as well as a small asymmetry of lateralis ventricle of brain L>R. Repeated renal ultrasonography confirmed the previously reported findings of increased echogenicity on two otherwise normal kidneys. Muscular tone and neonatal reflexes were normal for the age of gestation, but wide anterior fontanel and sutures were detected. Laboratory findings on admission were as follows: Hb 11.5 g/dl, Ht 35%, WBC 13.3 × 103/μl (PMN46%, L32%, M13%), PLT 223 × 103 μl, glucose 80 mg/dl, urea 201 mg/dl, creatinine 2.8 mg/dl, uric acid 12.9 mg/dl, urine spot for FENa 13%, SGOT 16 U/l, SGPT 17 U/l, γ-GT 56 U/l, ALP 114 U/l, Ca 9.7 mg/dl, P 7.4 mg/dl, Mg 2.8 mg/dl, K 3.9 mmol/l, Na 134 mmol/l, Cl 88 mmol/l, UA 12.6 mg/dl, total bilirubin 3.1 mg/dl, direct 0.93 mg/dl, CPK 64 IU/l, LDH 342 IU/l, total protein 4.4 g/dl, albumin 2.8 g/dl, CRP 0.43 mg/l, plasma aldosterone 872 ng/dl (normal 19–141 ng/dl) and renin 507 pg/ml (normal 40– 220 pg/ml).
During hospitalization, several challenges were observed regarding the treatment and follow-up. CPAP was continued for 3 days post-admission followed by diffuse O2 for the next 24 h. Following a conservative approach, meticulous fluid and electrolyte adjustment resulted in a gradual improvement of renal function so that by Day 19 after birth, the plasma creatinine level was 0.9%. Plasma creatinine levels during the first 2 weeks of postnatal period and at 1 year of life are displayed in Figure . The acute renal failure event and severe degree of oligohydramnios were both attributed to the mother's antihypertensive therapy and are related to the temporarily reduced fetal GFR. One month post-admission, the baby was discharged from the unit in good condition with urea 25 mg/dl, plasma creatinine 0.8 mg/dl and renal trasonographic findings compatible with normal sized kidneys and normal parenchyma echogenicity. At the latest follow-up examination, the baby (1 year old) was well developed and normotensive (BP 105/60 mmHg). Renal function tests showed 35 mg/dl and 0.5 mg/dl plasma urea and creatinine levels, respectively. The eGFR was 65 ml/min/1.73 m2.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [9.7, 'mg/dL'], 'Albumin': [2.8, 'g/dL']}",10.66,10.127,11.193,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.8 g/dL. 
The concentration of Calcium is 9.7 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.8 g/dL)) + 9.7 mg/dL = 10.66 mg/dL.
The patient's corrected calcium concentration 10.66 mg/dL."
2703,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6440327-1,Extracted,"A 51-year-old married male presented with complaints of swelling over lower limbs, face, and abdomen along with frothy urine for last 1 month. There was no history of preceding fever, sore throat, joint pain, rash, or hematuria. There was no past history of similar complaints, hypertension, diabetes, chronic analgesic or other drug abuse, blood transfusion, or any high-risk sexual behavior.
On admission, he was conscious, cooperative, and oriented to time, place, and person. He was afebrile; had a pulse rate of 82 beats/min, regular, normal volume; and had blood pressure of 126/82 mmHg with a respiratory rate of 18 breaths/min. There was the presence of facial puffiness and pitting pedal edema. On per abdomen examination, there was generalized abdominal distention with fullness of flanks, and on percussion, there was shifting dullness confirming the presence of ascites. His respiratory and cardiovascular examination was unremarkable. He had multiple purplish, well-circumscribed, and pedunculated skin lesions over face, chest, abdomen, and back. [] Also, on the trunk was presence of many café-au-lait spots of more than 1.5 cm in diameter.[] Ophthalmological examination revealed two Lisch nodules in iris in the left eye and three in the right eye. There was a history of similar skin lesions in patient's father and paternal grandfather although no history of renal disease was present. The diagnosis of NF-1 was made as per the National Institute of Health Criteria [].
His laboratory investigations showed hemoglobin 13.7 g/dl, white blood cell (WBC) 10,500/mm3 and platelets 3.61 lakhs, creatinine 0.98 mg/dl, urea 48 mg/dl, sodium 135.3 mEq/l, potassium, 4.81 mEq/l, calcium (Ca) 6.1 mg/dl with corrected Ca of 7.6 mg/dl, proteins 4.5 g/dl, albumin 2.1 g/dl, globulins 2.40 g/dl, total cholesterol 371 mg/dl, random blood glucose 87 mg/dl, serum antinuclear and antidouble-stranded DNA antibodies by ELISA were negative, C3 148 mg/dl (N 90–207 mg/dl), and C4 47.2 mg/dl (N 17.4–52.2 mg/dl). ELISA for HIV and hepatitis B and C was nonreactive. Urine routine and microscopic analysis revealed the presence of proteinuria 4+, red blood cell 40–50/HPF, WBC nil, and no cellular casts. Twenty-four-hour urinary proteins were 5.1 g.
Ultrasound abdomen examination revealed the presence of ascites with fused kidneys present on the right side with preserved corticomedullary differentiation.
A percutaneous kidney biopsy was performed under ultrasound guidance. Kidney biopsy pathological findings revealed the presence of 12 glomeruli with two glomeruli showing segmental mesangial sclerosis along with occasional synechiae formation with normal capillary membrane thickness and unremarkable Bowman's capsule. There were mild interstitial mononuclear cellular infiltration and mild tubular degeneration. [Figure and ] Immunofluorescence examination showed fine granular C1q (+3/+4) and IgG (+2) positivity across 70%–80% of the mesangial regions of all glomeruli with negative IgA, IgM, and C3. [Figure and ] Therefore, a diagnosis of C1q nephropathy was made.
The patient was started on treatment with prednisolone 1 mg/kg/day (50 mg) and telmisartan 20 mg once a day. Patient achieved complete remission after 14 weeks of steroid therapy with complete resolution of facial and pedal edema with 24 h urinary protein reduced to 280 mg and hence steroid dose was subsequently tapered. After 5 months of treatment, the patient is still in complete remission and at present is on 20 mg of prednisolone.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [7.6, 'mg/dL'], 'Albumin': [2.1, 'g/dL']}",9.12,8.664,9.576,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.1 g/dL. 
The concentration of Calcium is 7.6 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.1 g/dL)) + 7.6 mg/dL = 9.12 mg/dL.
The patient's corrected calcium concentration 9.12 mg/dL."
2704,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3230026-1,Extracted,"A 56-yr-old man with liver cirrhosis caused by the hepatitis B virus visited our hospital on December 30, 2008 for evaluation of weakness in his lower legs of 1-week duration. He first experienced discomfort and myalgia in his lower legs, which worsened over time and made him unable to walk. He had undergone a percutaneous coronary intervention 10 yr previously at the local hospital and had taken simvastatin (20 mg/day) regularly since then. He was diagnosed with Child-Pugh C cirrhosis due to hepatitis B virus a year ago and followed-up at the same hospital with stable liver function in a compensated state. Ten days before visiting our hospital, he was switched from simvastatin to fluvastatin (20 mg/day) by his doctor, as the patient was concerned about his liver disease. In addition to fluvastatin (20 mg/day), his medications included aspirin (100 mg/day), betaxolol (10 mg/day), candesartan (16 mg/day), lactulose (30 mL/day), and entecavir (0.5 mg/day) without diuretics or fibrates. His medical history was significant for no alcohol use and 10 pack-years of smoking, but he had quit smoking 10 yr previously.
The patient's blood pressure was 122/76 mmHg, his temperature was 36.8℃, his pulse was 63 beats/min, weight was 98 kg, and his body mass index was 29.8 kg/m2. He had mild tenderness of the lower extremities but all other assessments were unremarkable. Laboratory findings included sodium 125 mM/L, potassium 5.1 mM/L, chloride 97 mM/L, phosphorus 3.1 mg/dL, CO2 24.4 mM/L, serum creatinine 1.0 mg/dL, blood urea nitrogen 21 mg/dL, glucose 176 mg/dL, calcium 8.3 mg/dL, phosphorus 3.1 mg/dL, aspartate transaminase 1,303 IU/L (normal < 40), alanine transaminase 354 IU/L (normal < 40), alkaline phosphatase 145 IU/L (normal 40 to 120), total bilirubin 4.6 mg/dL, direct bilirubin 1.4 mg/dL, protein 8.0 g/dL, albumin 2.7 g/dL, and uric acid 3.5 mg/dL. His hematocrit was 38.5%, platelet count was 80,000/µL, and white blood cell count was 11,100/µL, with 18.5% lymphocytes, 69.7% polymorphonuclear leukocytes, 10.% monocytes, 1.4% eosinophils, and 0.2% basophils. His prothrombin time (PT) was 1.78 INR (40.7%) and activated partial thromboplastin time (aPTT) was 36.5 seconds. His total serum creatine kinase (CK) was 36,804 IU/L (normal 50 to 250 IU/L) and his CK-MB was 157.0 ng/mL (normal < 5 ng/mL). Thyroid function test was within normal limits. Urinalysis revealed no red or white blood cells, positive dipsticks for protein, occult blood, bilirubin and urobilinogen, but negative for glucose. A 99mTc-diphosphonate scintigram bone scan showed increased uptake over all extremities and muscles of the thorax and abdomen ().
The patient was diagnosed with fluvastatin-induced rhabdomyolysis. Treatment with fluvastatin, betaxolol and candesartan was discontinued, and he received massive hydration and urine alkalization. He was treated with intravenous sodium bicarbonate (100 mEq in 1,000 mL of half-normal saline at a rate of up to 500 mL/h or 50 mEq/h) titrated to a urine pH > 6.5. He was administered a 20-80 mg dose of intravenous furosemide to maintain diuresis. The extent of rhabdomyolysis progressed despite supportive treatment. His CK concentration was increased to 166,160 IU/L, and renal failure occurred. He underwent continuous renal replacement therapy on day 7, but his renal function did not recover and hepatic function worsened, with PT prolonged to 3.8 INR (18%) and total bilirubin increased to 24.5 mg/dL (). He died due to rhabdomyolysis complicated by hepatic failure on day 15.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [8.3, 'mg/dL'], 'Albumin': [2.7, 'g/dL']}",9.34,8.873,9.807,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.7 g/dL. 
The concentration of Calcium is 8.3 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.7 g/dL)) + 8.3 mg/dL = 9.34 mg/dL.
The patient's corrected calcium concentration 9.34 mg/dL."
2705,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3811713-1,Extracted,"A 48-year-old woman.
Incidentally found bilateral adrenal masses.
The patient had been diagnosed with hypertension 3 years prior, and had been receiving carvedilol 25 mg as prescribed by a private clinic. However, the patient's blood pressure (BP) had not been under control for about 3 months prior to the visit at our hospital. A year prior, the patient's menstrual cycle had become irregular and her weight had increased by 5 kg in the last year. The patient had visited our hospital due to the identification of bilateral adrenal masses from abdominal CT during a routine health examination.
Nothing specific except hypertension.
Nothing specific.
At the time of the visit to our hospital, the patient's height was 150 cm, weight was 53.8 kg, BP was 145/95 mm Hg, pulse rate was 72 beats per minute, respiratory rate was 20 times per minute, and body temperature was 37.1℃. She had an alert mental state, no visible signs for acute or chronic illness and no abnormal findings for skin, sclera and conjunctiva. Examination of the head and neck revealed a moon face, while a buffalo hump deformity was observed upon thoracic examination. There was no specific finding on the abdominal examination and no edema of extremities was identified. The patient had no accompanying muscle weakness or sensory deterioration.
The peripheral blood test performed at the time of visit to the hospital showed the following; white blood cell, 6,450/mm3; hemoglobin, 12.9 g/dL; hematocrit, 41.6%; and platelet, 289,000/mm3. The serum biochemical assay showed the following; calcium, 9.4 mg/dL; phosphorus, 3.3 mg/dL; total protein, 7.0 g/dL; albumin, 4.2 g/dL; aspartate aminotransferase, 21 IU/L; alanine aminotransferase, 19 IU/L; alkaline phosphatase, 43 IU/L; blood urea nitrogen, 10 mg/dL; creatinine, 0.7 mg/dL; sodium, 144 mEq/L; potassium, 3.4 mEq/L; and chlorine, 102 mEq/L.
The hormone test indicated that the morning baseline blood cortisol was 15.7 µg/dL and ACTH was less than 5 pg/mL. The 24-hour urine free cortisol excretion increased to 198.7 µg/day (normal range, 23 to 135). In addition, the following were in the normal range; metanephrine, 63 µg/day (normal range, 52 to 341); normetanephrine, 176 µg/day (normal range, 88 to 444); epinephrine, 3.1 µg/day (normal range, 0 to 20); norepinephrine, 28.9 µg/day (normal range, 15 to 80); and vanillylmandelic acid, 5.4 mg/day (normal range, 0 to 8). The 24-hour urine creatinine was 0.5 g/day (normal range, 0.8 to 1.8) and the creatinine clearance was calculated to be 122.4 mL/min (normal range, 75 to 125), indicating that the urine sampling was done relatively well. The plasma aldosterone concentration was 7.5 ng/dL and plasma renin activity was 0.4 ng/mL/hr, indicating that the aldosterone/renin activity ratio was 18.7 and there was no finding of primary aldosteronism.
The serum cortisol after an overnight 1 mg dexamethasone suppression test was 14.5 µg/dL, which was not suppressed. The low-dose dexamethasone suppression test demonstrated that the 24-hour urine free cortisol excretion increased to 397.8 µg/day and the blood cortisol concentration increased to 21.1 µg/dL, so we diagnosed the patient's condition as Cushing Syndrome. In the high-dose dexamethasone suppression test, the urine free cortisol excretion and blood cortisol concentration were not suppressed ().
Bilateral adrenal tumors were identified on adrenal CT, with one sized 2.8×2.0 cm on the right side and the others sized 2×2.3 cm and 1.7×1.4 cm, respectively, on the left side (). There were no abnormal findings from the Sella MRI.
Adrenal vein sampling (AVS) was done in order to identify the location of a functional tumor secreting cortisol in between the bilateral adrenal tumors. AVS was conducted without an ACTH stimulus on the day after the high-dose dexamethasone suppression test. The blood cortisol concentration was measured by sampling the blood twice from catheterization to the femoral vein and bilateral adrenal veins ().
When the bone density was measured by dual energy X-ray absorptiometry, osteopenia was found based on the finding that the T score of lumber spine was -2.1, T score of femoral neck was -1.0 and T score of the total hip was -0.7.
As the adrenal vein cortisol measured from AVS was eight times higher than that of the inferior vena cava, it was determined that the AVS was done selectively. The blood cortisol concentration was measured as high from the bilateral adrenal veins with AVS. Therefore, we diagnosed the patient with Cushing Syndrome induced by bilateral cortisol-secreting adenomas. To treat the patient, we removed all of the bilateral adrenal tumors by laparoscopic bilateral adrenalectomy. Immediately after the surgery, the patient was discharged because there was no specific complication while implementing supplementary therapy with prednisolone and fludrocortisone, and we had discontinued the antihypertensive agent as the BP had improved to 120/80 mm Hg at the 2-month follow-up observation. At 5 months postoperatively, the blood cortisol concentration was 5.0 µg/dL, ACTH was 19.0 pg/mL, the plasma aldosterone concentration was 15.0 ng/dL, and the plasma renin activity was 3.0 ng/mL/hr, indicating no evidence of recurrence. The patient is currently under follow-up study as an outpatient while receiving prednisolone 5 to 2.5 mg and fludrocortisone 0.1 mg.
A single mass was found on each of the adrenal glands and their sizes were 2.6×2.3×1.7 cm for the left side mass and 2.6×2.5×1.6 cm for the right side mass. Based on the visual findings, the left mass was in the shape of a dumbbell with a narrowed mid-part, showing a light brown cross-section, and the right mass had a brown cross-section ().
From the optical microscopic findings, the bilateral adenomas were composed of large round vacuolar cells of consistent shape and size, and with good differentiation, whereas the normal tissues of the adrenal cortex around the adenoma were atrophic. As an atypical nucleus and necrosis, hemorrhage, or reverse differentiation were not found, the findings were appropriate for adrenal adenoma ().","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [9.4, 'mg/dL'], 'Albumin': [4.2, 'g/dL']}",9.24,8.778,9.702,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.2 g/dL. 
The concentration of Calcium is 9.4 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.2 g/dL)) + 9.4 mg/dL = 9.24 mg/dL.
The patient's corrected calcium concentration 9.24 mg/dL."
2706,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3830302-1,Extracted,"A 27-year-old male patient, presented with the complaint of pain in legs and difficulty while walking for past 4 months. He also complained of pain and stiffness in the lower back for the same time. Patient could walk only with support for the past 1 month. There was no history of any trauma to the back. No history suggestive of bladder involvement, no positive or negative sensory symptoms. Patient was on antidepressant medication for the last few years and housebound for the past few months. Patient's examination revealed no features suggestive of spinal cord involvement; however, power in both lower limbs was grade four out of five in the proximal and distal muscles. No features suggestive of sensory involvement were seen. His systemic examination was unremarkable.
Investigations revealed hemoglobin 14.9 g/dl, total leucocyte count 6800/μl, platelets 212,000/μl, blood urea 20 mg/dl, serum creatinine 0.73 mg/dl, serum sodium 142 mEq/l, serum potassium 3.4 mEq/l, serum chloride 108 mEq/l, serum calcium 9.5 mg/dl, serum phosphorus 2.7 mg/dl, serum alkaline phosphate 2347 U/L, serum albumin 5.1 g/dl. Urine examination was unremarkable. Plasma parathyroid hormone (PTH) was 754.0 pg/ml and serum 25-hydroxyvitamin D3 (25[OH] D3) was 4.60 (normal > 20). His X-ray skull showed salt and pepper appearance [], X-ray pelvis showed loosers zones with marked subperiosteal resorption in the region of pubic rami [], X-ray hand showed resorption of the terminal phalanges with the presence of a cortical cyst in the metacarpal []. X-ray lumbosacral spine showed osteoporotic changes with central collapse of lumbar vertebrae and biconvex disc spaces []. His computerized tomography (CT) neck with contrast was normal, sestamibi scan showed diffuse uptake in the bones, with no evidence of parathyroid adenoma discernible in the parathyroid scan.
A diagnosis of vitamin D deficiency with a secondary hyperparathyroidism with normocalcemia was made. He was given vitamin D and calcium supplementation and his general condition improved over the next few months. Power in musculature improved with resolution of pain. His serum showed PTH levels, after 9 months, of 59.0 pg/ml and calcium 8.9 mg/dl. X-rays skull, hand and pelvis showed remarkable improvement with resolution of salt and pepper appearance, regression of osteopenic changes and cortical cyst in a span of 11 months [Figures –].","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [9.5, 'mg/dL'], 'Albumin': [5.1, 'g/dL']}",8.62,8.189,9.051,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 5.1 g/dL. 
The concentration of Calcium is 9.5 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 5.1 g/dL)) + 9.5 mg/dL = 8.62 mg/dL.
The patient's corrected calcium concentration 8.62 mg/dL."
2707,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4377810-1,Extracted,"A 43-year-old man with a history of hypertension and ESRD of unknown etiology presented with acute onset of severe nausea, vomiting and abdominal pain of a 1-day duration. There was no history of abdominal trauma, alcohol abuse, hepatobiliary disease, hypertriglyceridemia or intake of medications known to cause pancreatitis. He had been on hemodialysis thrice weekly for 1 year.
On presentation, the patient was afebrile, blood pressure was 156/77 mmHg and pulse 105 b.p.m. He appeared awake and in distress due to the abdominal pain. The remainder of the physical examination was significant for diffuse abdominal tenderness with mild guarding. Laboratory evaluation showed a white blood count of 12 200/mm3 with 81% neutrophils. Serum creatinine, albumin and calcium were 107 ηmol/L, 41 g/L and 3.87 mmol/L, respectively. Serum amylase and lipase were 428 and 1020 U/L, respectively. Liver transaminases, total bilirubin and serum triglycerides were in normal range. Pancreatic protocol contrast-enhanced computed tomography (CECT) with a radiographic contrast agent revealed necrotizing pancreatitis. The patient was admitted to the intensive care unit and managed with empiric antibiotics, intravenous fluids and nutritional support. Intact parathyroid hormone (iPTH) was <0.3 ng/L suggestive of primary hypercalcemia. On further inquiry about particular eating habits, the patient disclosed an almost daily consumption of pieces of chalk >2 years. He reported having developed a strong craving for pieces of chalk (composed mostly of calcium carbonate (CaCO3) with minor amounts of silt and clay), and was eating up two full boxes every day (100–150 g of CaCO3 daily). The patient had daily hemodialysis treatments with low-calcium bath (1.25 mmol/L). Over a period of the following 10 days, his clinical status improved and his calcium had normalized to 2.55 mmol/L. CECT with intravenous contrast agent showed improvement of pancreatic necrosis. At follow-up 4 weeks later the patient was asymptomatic and his serum calcium remained normal (2.5 mmol/L).","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [3.87, 'mmol/L'], 'Albumin': [41.0, 'g/L']}",15.431,14.65945,16.20255,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 41.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 41.0 g Albmumin/10.0 dL = 4.1 g Albmumin/dL. The concentration value of 41.0 g Albmumin/L converts to 4.1 g Albmumin/dL. 
The concentration of Calcium is 3.87 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 3.87 mmol. To convert 3.87 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 3.87 mmol Calcium * 0.001 mol/mmol = 0.00387 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00387 mol Calcium * 40.08 g/mol = 0.15511 g Calcium. To convert 0.15511 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.15511 g Calcium * 1000.0 mg/g = 155.11 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 155.11 mg Calcium/10.0 dL = 15.511 mg Calcium/dL. The concentration value of 3.87 mmol Calcium/L converts to 15.511 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.1 g/dL)) + 15.511 mg/dL = 15.431 mg/dL.
The patient's corrected calcium concentration 15.431 mg/dL."
2708,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6124168-7,Extracted,"A 12-year-old male with CGCG of the jaw post presented to our care after resection of a 2-cm lesion with recurrence.
Treatment was initiated with denosumab 60 mg, which was determined based on shared-decision making with family, who had concerns that higher doses may affect growth and bone quality during formative pubertal/developmental years. The patient received a single dose of medication then developed paresthesia and back pain 1 month later. Pretreatment calcium was 9.9 mg/dL, PTH 63 pg/mL, and 25 OH D 20.2 ng/mL while he was on supplementation with vitamin D 1000 units daily. On laboratory evaluation for his acute symptoms, the patient was found to have secondary hyperparathyroidism with a serum calcium of 6.3 mg/dL (albumin of 4.6 g/dL), PTH of 292 pg/mL, and 25 OH D 23.4 ng/mL. Calcium 600 mg three times a day was started along with ergocalciferol 50,000 units weekly. Denosumab was held and paresthesia and back pain have improved. The most recent calcium level was 9.6 mg/dL (albumin of 4.6 g/dL) and family is considering restarting treatment with denosumab at lower doses.
Table is a summary of the characteristics of the seven cases discussed herein.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [9.6, 'mg/dL'], 'Albumin': [4.6, 'g/dL']}",9.12,8.664,9.576,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.6 g/dL. 
The concentration of Calcium is 9.6 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.6 g/dL)) + 9.6 mg/dL = 9.12 mg/dL.
The patient's corrected calcium concentration 9.12 mg/dL."
2709,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4384674-1,Extracted,"A 58-year-old woman was admitted to our department for diagnostic workup of acromegalic features. She had noticed the enlargement of her face, hands, and feet 8 years prior to her visit, and these were associated with hyperhidrosis, a thicker and deeper voice, and decreased libido. At that time, she had also undergone uvulectomy because of obstructive sleep apnea that had caused severe snoring. The snoring continued after surgery, albeit much more infrequently.
On admission, the patient's blood pressure was 120/80 mm Hg. She had a heart rate of 86 per minute, a respiratory rate of 20 per minute, and a body temperature of 36.5℃. During physical examination, the facial enlargement with frontal bossing was noticed, as was the disproportionate enlargement of the tongue, nose, lips, hands, and feet (). Hypertrichosis was seen, especially in the lower extremities. Soft tissue swelling was noted, and the skin folds were thickened.
A complete blood count revealed a plasma hemoglobin level of 10.0 g/dL. The serum protein level was 10.5 g/dL (reference range, 6 to 8) and the serum albumin level was 2.5 g/dL (reference range, 3.5 to 5.2), reflecting a reversed albumin/globulin (A/G) ratio. Serum creatinine and calcium levels were 0.63 mg/dL (reference range, 0.70 to 1.40) and 8.6 mg/dL (reference range, 8.6 to 10.2), respectively. Thus, the serum calcium level corrected for hypoalbuminemia was 9.2 mg/dL. The fasting plasma glucose level was 109 mg/dL and the 2-hour postprandial plasma glucose level was 280 mg/dL. Hemoglobin A1c was 7.8% and the C-peptide level was 4.8 ng/mL. The thyroid-stimulating hormone level was 1.5 µU/mL (reference range, 0.4 to 5.0) and the free thyroxine level was 1.3 ng/dL. Basal levels of adrenocorticotropic hormone, prolactin, luteinizing hormone, follicle-stimulating hormone, and estradiol were 23.0 pg/mL, 6.8 ng/mL, 17.1 mIU/mL, 44.4 mIU/mL, and 10.0 pg/mL, respectively, which were all within normal ranges. Serum levels of IGF-1 and human growth hormone (hGH) were elevated to 898 ng/mL (age-adjusted reference range, 71 to 284) and 42 ng/mL (reference range, <16.0), respectively , ).
Because these laboratory findings strongly suggested acromegaly and associated diabetes mellitus, we performed a 75g oral glucose tolerance test (OGTT) to confirm GH hypersecretion (). To confirm the presence of a GH-secreting pituitary adenoma, we performed magnetic resonance imaging of the sella turcica. It revealed a 1.0×0.6-cm pituitary adenoma on the left side of the pituitary gland ().
The markedly reversed A/G ratio and anemia led us to suspect a monoclonal gammopathy such as MM. A peripheral blood smear revealed a red blood cell rouleux formation (). Protein electrophoresis (PEP) and immunofixation electrophoresis (IFE) of serum samples revealed a monoclonal gammopathy (M peak 4.9 g/dL) of immunoglobulin G (IgG)-λ type; PEP and IFE of urine samples were inadequate because of low urinary protein. The patient's serum IgG level was elevated to 5,860.0 mg/dL, and the κ and lambda free light chain ratios were 7.16 and 34.50 mg/L, respectively. To confirm the diagnosis of MM, we performed bone marrow aspiration and biopsy with plasma cell phenotyping. Neoplastic plasma cells were observed on bone marrow aspirate and touchprint slides (), and packed bone marrow with neoplastic plasma cells (35.6% of the clonal plasma cells) was observed in the bone marrow biopsy specimen (). In an attempt to find myeloma-related organ damage, we took simple X-rays of the entire body, and they did not reveal any osteolytic lesions. According to the diagnostic criteria for symptomatic MM, one should exhibit more than one of the parameters reflecting myeloma-related organ dysfunction (). Because the M peak was >3 g/dL and the proportion of monoclonal plasma cells in the bone marrow was >10% without myeloma-related orgam damages, the patient was diagnosed with asymptomatic (smoldering) MM. However, it is of note that her serum hemoglobin level was at the cutoff value for diagnosis of symptomatic MM and that her serum calcium level was slightly below the cutoff (). In accordance with the treatment guidelines for asymptomatic MM, we planned close follow-up, with deferral of chemotherapy until the disease became symptomatic.
To treat the GH-secreting pituitary adenoma, the patient underwent tumor resection via a transsphenoidal approach. There were no immediate postoperative complications. Three days after surgery, the serum IGF-1 level was measured and the 75 g OGTT was repeated. Although the serum hGH level was lower than it had been before surgery, the results indicated incomplete remission immediately after surgery (). However, after the surgery, the patient exhibited clinical improvements in acromegalic features, such as decreased skin thickness and reduced size of the extremities. She also claimed that the frequency of snoring and daytime drowsiness had decreased dramatically. Therefore, we decided to closely monitor the clinical and biochemical responses to the removal of the GH-secreting pituitary adenoma and to continuously determine the need for further treatment.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [8.6, 'mg/dL'], 'Albumin': [2.5, 'g/dL']}",9.8,9.31,10.29,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.5 g/dL. 
The concentration of Calcium is 8.6 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.5 g/dL)) + 8.6 mg/dL = 9.8 mg/dL.
The patient's corrected calcium concentration 9.8 mg/dL."
2710,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3683454-1,Extracted,"A 64-year-old Caucasian female with a history of Noonan's syndrome presented with sudden onset of coffee ground emesis and without any history of black tarry stool. She was recently treated for severe erosive gastritis during her last hospital admission, and an endoscopy done during that admission suggested Los Angles Class C erosive gastritis with an otherwise normal stomach and duodenum. Her past medical history is significant for a history of hypercoagulability, bilateral lower extremity deep venous thromboses, extensive bilateral pulmonary embolism, hyperlipidemia, hypertension, and dextrocardia. She complained of vague upper abdominal discomfort, and on further clinical examination, her epigastric region was soft, and distended and demonstrated no rebound. She was hemodynamically stable. Blood laboratory investigations revealed the following: white count 21.2 × 109/L (3.9–11.1), hemoglobin 14.9 gm/dL, hematocrit 43.7%, platelets 322,000, sodium 145 mEq/L, potassium 2.8 mEq/L, chloride 83 mEq/L, bicarbonate 49 mEq/L, BUN 32 mg/dL, creatinine 1.90 mg/dL, glucose 188 mg/dL, calcium 11.9 mg/dL, albumin 4.3 g/dL, total bilirubin 0.3 mg/dL, alanine aminotransferase (ALT) 11 U/L, aspartate aminotransferase (AST) 27 U/L, and alkaline phosphatase of 80 U/L. The patient underwent a CT scan of the abdomen and pelvis that showed marked gastric dilatation with extensive circumferential gas (pneumatosis) and portal venous gas suspicious for gastric ischemia. The likely etiology for these findings was the presence of gastric outlet obstruction (Figures , , , and ). On review of her history and comparing previous scans, there was no evidence of any prior hepatobiliary disease or prior endoscopic retrograde cholangiopancreatography. An upper gastrointestinal endoscopy showed severe mucosal congestion, submucosal hemorrhage, and bluish and purple areas with ulcers in the gastric body. Unlike the prior endoscopy, now the pylorus was visible only on retroflexion, and the scope could not be advanced into the pylorus due to looping related to the abnormal anatomy. She underwent exploratory laparotomy and was found to have one thick anomalous congenital band with blood vessels in it that was found to be the cause of gastric outlet obstruction. A patent gastrojejunostomy was created to bypass the gastric outlet obstruction, along with a feeding jejunostomy. The patient tolerated the procedure well and her symptoms completely resolved without the need for gastric resection. She was discharged home on postoperative day six.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [11.9, 'mg/dL'], 'Albumin': [4.3, 'g/dL']}",11.66,11.077,12.243,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.3 g/dL. 
The concentration of Calcium is 11.9 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.3 g/dL)) + 11.9 mg/dL = 11.66 mg/dL.
The patient's corrected calcium concentration 11.66 mg/dL."
2711,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4519607-1,Extracted,"We present a 62-year-old female with ESRD due to hypertension. She commenced maintenance HD in October 2001. Her past medical history included primary hypertension, paroxysmal atrial fibrillation, atherosclerosis of the carotids and the abdominal aorta, and chronic congestive heart failure. The procedure of HD was 3 times per week and 4 h each time. Her body weight was 46 kg and the ultrafiltration volume was around 2.5–2.7 kg each time. During HD, the occurrence of hypotension was frequent. The blood pressure was 120/70 mm Hg before HD and dropped to 80/60 mm Hg after HD. She became anuric after maintenance HD for 2 years. In August of 2008, she was admitted to our department because she developed mild, diffuse abdominal pain in combination with nausea and vomiting. Three months prior to admission, she had several episodes of abdominal pain, each time occurring after HD. Her abdominal pain began and became more severe after HD (usually in the situation of hypotension). However, repeated blood tests did not show any abnormal results and an abdominal X-ray ultrasound was also normal. On admission, her physical examination showed that her blood pressure was 120/70 mm Hg, a heart rate of 76 beats/min and a body weight of 43 kg; she had dry skin and complained of thirst. An abdominal examination revealed that she had decreased bowel sounds with a mild tenderness to deep palpation, especially in the lower right quadrants. A stool examination for occult blood was negative. Laboratory findings included blood urea 30.9 mmol/l, serum creatinine 749 umol/l, serum amylase 34 IU/l, calcium 2.2 mmol/l, phosphate 2.3 mmol/l, albumin 30 g/l, iPTH 130 pg/ml, hemoglobin 114 g/l, and a white blood cell count of 11.1 × 109/l. The rest of her laboratory examination (including disseminated intravascular coagulation, C-reactive protein, erythrocyte sedimentation rate, and tumor biomarkers) was within normal limits. Stool cultures for bacteria, fungus and tubercle bacillus were all negative. The echo examination showed that her left ventricular ejection fraction was 56%. A plain abdominal film in the erect position disclosed abdominal distention with small fluid levels of the small intestine. No free air and mass were noticed anywhere in the peritoneal cavity. An enhancement CT showed intestinal dilatation indicating a mesenteric ischemia; there was no evidence of a tumor, severe intestinal infection or obstruction. The patient was initially treated with intravenous antibiotics (rocephin 2.0 g once daily). Her medical condition did not improve in the following days. A CT angiography (CTA) was then performed, and the result showed that she had a portal vein thrombus with a normal superior mesenteric vein and a mesenteric artery stenosis suspecting NOMI (fig. , fig. , fig. , fig. ). After her CTA examination, she was treated with subcutaneous low-molecular-weight heparin (fraxiparine 5000 anti-Xa IU/ml, subcutaneously once and twice every other day). The patient refused to undergo an endoscopic examination. Thereafter, we recommended decreasing her ultrafiltration volume to less than 2 kg each time in order to avoid episodes of hypotension during or after HD; she was treated with intravenous prostaglandin E1 10 μg/day, and the abdominal pain gradually declined after 2 weeks. She was later discharged.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [2.2, 'mmol/L'], 'Albumin': [30.0, 'g/L']}",9.618,9.1371,10.0989,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 30.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 30.0 g Albmumin/10.0 dL = 3.0 g Albmumin/dL. The concentration value of 30.0 g Albmumin/L converts to 3.0 g Albmumin/dL. 
The concentration of Calcium is 2.2 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 2.2 mmol. To convert 2.2 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 2.2 mmol Calcium * 0.001 mol/mmol = 0.0022 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.0022 mol Calcium * 40.08 g/mol = 0.08818 g Calcium. To convert 0.08818 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.08818 g Calcium * 1000.0 mg/g = 88.18 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 88.18 mg Calcium/10.0 dL = 8.818 mg Calcium/dL. The concentration value of 2.2 mmol Calcium/L converts to 8.818 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.0 g/dL)) + 8.818 mg/dL = 9.618 mg/dL.
The patient's corrected calcium concentration 9.618 mg/dL."
2712,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-6031073-1,Extracted,"A 57-year-old African American male with past medical history of coronary artery disease, systolic heart failure, alcohol abuse, and stage-IV sarcoidosis on long-term oral prednisone at 10 mg daily for over two years presented with massive hematemesis and melena that started the night before his arrival to the Emergency Department. Upon physical examination, the patient appeared pale and was noted to have tachycardia, hypotension, and hematochezia. He denied any recent alcohol intake, chest pain, abdominal pain, and abdominal or rectal trauma. Vital signs consisted of a blood pressure of 84/33 mmHg, heart rate of 118 bpm, room air saturation of 92%, and temperature of 98.8 degrees Fahrenheit (37.1 degrees Celsius). He was admitted to the medical ICU for hypovolemic shock secondary to massive bleeding that required immediate endotracheal intubation for airway protection. An initial blood work showed a hemoglobin count of 13.9 g/dL, white blood cell count of 18.7 K/UL, platelet count of 159 K/UL, sodium of 140 mmol/L, potassium of 3.8 mmol/L, chloride of 101 mmol/L, bicarbonate below 10 mmol/L, calcium of 2.2 mmol/L, albumin of 2.7 g/dL, CRP of 233 mg/L, ESR of 36 mm/hr, BUN of 17 mg/dL (6.07 mmol/L), creatinine of 1.5 mg/dL (132.6 Umol/L), lactic acid of 17.0 mmol/L, BNP of 1140.63 pg/ml, total bilirubin of 0.4 mg/dL, troponins of 0.020 ng/mL, and CK-MB of 408 ng/mL. Resuscitation was initiated with administration of isotonic solutions, blood transfusions, and initiation of vasoactive medications, and pantoprazole drip was provided. An initial urgent endoscopy revealed a bleeding Dieulafoy lesion, which was immediately clipped. Acute kidney injury was addressed with aggressive fluid resuscitation as evident by increase in BUN of 33 mg/dL (11.78 mmol/L) and creatinine of 2.9 mg/dL (256.33 Umol/L). CT scan of abdomen performed to rule out ischemic colitis in the setting of progressive abdominal distention showed a diffuse pericolonic inflammation most pronounced at the rectosigmoid colon. Repeat endoscopy showed multiple ulcerated lesions of the gastric mucosa () with a biopsy that revealed necrotic debris with acute leukocytic exudate and numerous variably sized, 90-degree angulated fungal hyphae favoring mucormycosis (). Intravenous liposomal amphotericin-B (5 mg/kg/day at 60 kg weight) was started at a dose of 300 mg daily. Due to deterioration of renal function on the second day, treatment was switched to oral suspension of posaconazole at a dose of 400 mg twice a day for a total of 6 days (of note, no levels of posaconazole were drawn during hospital course). Repeat CT scan of the abdomen showed mild-to-moderate hydroureter with hydronephrosis and bladder wall thickening Figures and . Cystoscopy showed distorted anatomy of bladder lumen with multiple mounds of tissues all throughout the bladder most notable in the trigone with failure to locate ureteral orifices. Random biopsies taken from the bladder tissue also showed necrotic debris with active inflammatory and numerous variably sized angulated fungal hyphae consistent with Mucorales species. Once bladder biopsy confirmed Mucor spp, treatment was switched from posaconazole to intravenous isavuconazonium sulfate at a dose of 372 mg every eight hours for 48 hours as loading dose and then to an oral dose of 372 mg daily. Unfortunately, no sensitivity of the isolate to the newer triazoles was available. Surgical approach was considered; however, given patient's frail state and multiple comorbidities, such approach was deferred. Hydronephrosis significantly improved after placement of bilateral nephrostomy tubes. In addition, continuous bladder irrigation with amphotericin-B was given for localized bladder infection for a total of 5 days. A three-way Foley catheter was inserted for continuous amphotericin-B bladder irrigation where 200 ml of medication was administered via catheter; then, the catheter was clamped for 90 minutes and drained to gravity every six hours. After three weeks of systemic treatment with antifungals, a third endoscopy showed only inflammatory changes with a pathologic report, in which mucormycosis was no longer appreciated. His kidney function improved and remained stable after clamping and removal of his nephrostomy tubes. The patient completed 6 months of therapy with 372 mg of oral isavuconazonium sulfate per day. He is currently at home with resolution of his symptoms and no clinical evidence of relapse after 12 months since completion of his treatment.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [2.2, 'mmol/L'], 'Albumin': [2.7, 'g/dL']}",9.858,9.3651,10.3509,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.7 g/dL. 
The concentration of Calcium is 2.2 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 2.2 mmol. To convert 2.2 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 2.2 mmol Calcium * 0.001 mol/mmol = 0.0022 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.0022 mol Calcium * 40.08 g/mol = 0.08818 g Calcium. To convert 0.08818 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.08818 g Calcium * 1000.0 mg/g = 88.18 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 88.18 mg Calcium/10.0 dL = 8.818 mg Calcium/dL. The concentration value of 2.2 mmol Calcium/L converts to 8.818 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.7 g/dL)) + 8.818 mg/dL = 9.858 mg/dL.
The patient's corrected calcium concentration 9.858 mg/dL."
2713,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5065917-1,Extracted,"Our patient was a 65-year-old man who received PD for 12 years due to a 20-year history of type 2 diabetes mellitus (DM). He was under long-term follow-up at Taichung Veterans General Hospital in Taichung, Taiwan. He had also received type A aortic dissection repair 15 years previously. He presented with poor appetite and a weight loss of 3 kg in 6 months, starting in January 2015. His serum albumin had dropped to 3.2 g/dL. His PD regimen was 1.5%*2L*2 + 2.5%*2L*2 + Icodextrin*2L*1 and the amount of daily ultrafiltration was 1000 ml. Weekly creatinine clearance was 65 L, and Kt/V was 1.6. The result of the peritoneal equilibrium test was at a high-average level. Blood urea nitrogen was 91 U/L and serum creatinine was 13.1 mg/dL. Even while taking three tablets of calcium acetate (667 mg) with each meal, his calcium level was 8.8 mg/dL, phosphate was 7.7 mg/dL, and intact parathyroid hormone was up to 675 pg/mL. He experienced peritonitis three times during the PD period (all cultures grew Staphylococcus aureus). Due to no apparent cause for his poor nutrition and poor appetite, we performed abdominal computed tomography (CT) to rule out EPS. Unsurprisingly, CT disclosed diffuse thin calcifications of the serosal surface of the small intestinal loops (arrow, ). We reviewed the patient’s kidney, ureter, and bladder (KUB) x-ray from three months before the CT, and noted EPS in the wall of small intestine (arrow, ). Therefore, EPS was diagnosed by the radiologists due to cachexia, very low serum albumin, low clearance of the peritoneum, and diffuse calcifications of the intestinal serosal surface. Moreover, there was abdominal dissection with diffuse calciphylaxis (arrowhead in , arrow in ), as well as skin ulcers over the lower extremities. For the diffuse calciphylaxis, we changed to sevelamer, two tablets per meal. For the EPS, the PD was changed to hemodialysis with low-calcium dialysate and exchange of 2 L of dialysate every two weeks. We also prescribed prednisolone 30 mg per day and colchicine 1 mg per day. However, questions were raised about the use of tamoxifen for EPS, as this seems to be contraindicated in a patient in a state of calciphylaxis. However, this dilemma has seldom been discussed in the current literature.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [8.8, 'mg/dL'], 'Albumin': [3.2, 'g/dL']}",9.44,8.968,9.912,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.2 g/dL. 
The concentration of Calcium is 8.8 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.2 g/dL)) + 8.8 mg/dL = 9.44 mg/dL.
The patient's corrected calcium concentration 9.44 mg/dL."
2714,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7444888-1,Extracted,"A 77-year-old male patient presented to emergency department with complaints of shortness of breath and pain, discoloration, and swelling of the left leg. Vital signs on presentation were heart rate 110 per minute, blood pressure 155/85 mmHg, oxygen saturation 96% on room air, and temperature 36 degree Celsius. The patient had bilateral crackles on lung exam and absent left dorsalis pedis and posterior tibial pulses and foot was swollen, discolored, and cold. Electrocardiogram showed sinus tachycardia 110 per minute.
On initial laboratory evaluation, the following values were noted: hemoglobin 12.1 g/dl (reference: 12-16 g/dl), hematocrit 38.2% (reference: 36%-46%), white blood cells 41 K/mm3 (reference: 4.5-11 K/mm3), platelets 534 K/mm3 (reference: 140-440 K/mm3), potassium 4.1 meq/L (reference: 3.5-5 meq/L), glucose 126 mg/dl (reference: 70-105 mg/dl), creatinine 0.61 mg/dl (reference: 0.6-1.30 mg/dl), blood urea nitrogen 8 mg/dl (reference: 7-23 mg/dl), lactic acid 1.1 mmol/L (reference: 0.5-2.2 mmol/L), troponin 0.136 ng/ml (reference: less than 0.03 ng/ml), D-dimer 2.77 (reference: less than 0.5), prothrombin time 14.8 seconds (reference: 12.2-14.9 seconds), international normalized ratio (INR) 1.2 (reference: less than 1), partial thromboplastin time 39.8 seconds (reference: 21.3-35.1 seconds), lactate dehydrogenase (LDH) 392 U/L (reference: 140-271 U/L), C-reactive protein (CRP) 301 mg/L (reference: less than 10 mg/L), ferritin 1,396 ng/mL (reference: 12-300 ng/ml), procalcitonin 0.60 ng/ml (reference: less than 2 ng/ml), aspartate transaminase 134 U/L (reference: 13-39 U/L), calcium 8.5 mg/dl (reference: 8.6-10.3 mg/dl), and albumin 2.7 mg/dl (reference: 3.5-5.0 mg/dl). Chest X ray showed bilateral hazy infiltrates. CT angiography of the abdomen and aorta with Iliofemoral runoff showed thrombus within the mid left superficial femoral artery and occluded left anterior tibial artery, left posterior tibial artery, and left peroneal artery with no flow to the foot (Figure ).
Covid-19 was diagnosed on the basis of reverse transcription polymerase chain reaction (RT-PCR) testing. Echocardiogram showed an ejection fraction of 60%. The patient was placed on air-borne precautions and was started on ceftriaxone, azithromycin, hydroxychloroquine, and therapeutic anticoagulation with heparin. He underwent thrombectomy of left common femoral artery, profunda femoris, superficial femoral artery, popliteal artery, anterior tibial artery, posterior tibial artery, and peroneal artery.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [8.5, 'mg/dL'], 'Albumin': [2.7, 'g/dL']}",9.54,9.063,10.017,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.7 g/dL. 
The concentration of Calcium is 8.5 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.7 g/dL)) + 8.5 mg/dL = 9.54 mg/dL.
The patient's corrected calcium concentration 9.54 mg/dL."
2715,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5484213-1,Extracted,"A 55-year-old woman was hospitalized in the nephrology unit of Huriez Hospital, Lille, in January 2016. She had no previous history of any major disease. She had been diagnosed a superficial spreading type melanoma of the right thigh in March 2015, with BRAF V600E mutation. In September 2015, a CT-scan detected a pulmonary metastasis. She was then treated with encorafenib (450 mg once a day per os), a new BRAF inhibitor, and binimetinib (45 mg twice a day per os), a MEK inhibitor.
The treatment started in November 2015, when serum creatinine concentration was 0.77 mg/dL. In January, the laboratory testing measured a serum creatinine concentration of 2.8 mg/dL, prompting transfer to our nephrology department. On arrival the patient's BP was 130/70 mm Hg, and her heart rate and temperature were 88 bpm and 37.6 °C, respectively. She weighed 74 kg. She only complained of having experienced joint pain in the previous few weeks, but examination revealed no arthritis. Otherwise, examination results were completely normal. She did not present any rash or skin lesions on the previous days. Her recent medical history did not record new events. Three days before she arrived, she took ibuprofen 200 mg twice a day. She did not take any other medication.
The patient's serum creatinine concentration was 2.8 mg/dL, with blood urea 114 mg/dL, sodium level 133 mmol/L, and potassium level 5 mmol/L. Albumin level was 33 g/L and calcium level 8.4 mg/dL. C-reactive protein level was 1.23 mg/dL. She had a leucocyte count of 11,000/mm3 including 8700 polynuclear neutrophils and 1500 lymphocytes without polynuclear eosinophils.
Urine analysis showed a 1 g/day proteinuria, without leucocyturia or hematuria.
Serum protein electrophoresis was normal. Plasma tests for antineutrophil cytoplasm antibody and antiglomerular basement membrane antibody were negative. The test for antinuclear antibodies was negative.
A kidney biopsy was performed. Light microscopy revealed 6 glomeruli, including one that was globally sclerotic, with endocapillary proliferation in half of them. Four showed extracapillary proliferation with a granulomatous reaction. Several arterioles exhibited acute necrotizing arteritis with fibrinoid necrosis and a perivascular infiltrate that had a granulomatous appearance with palisading epithelioid macrophages. Major tubular necrosis was also present. Immunofluorescence was weakly positive for C1q and C3 staining, with focal and segmental endomembranous deposits. It was strongly positive for fibrinogen in the crescents. Immunostaining for kappa, lambda, IgG, IgA, and IgM was negative.
Electron microscopy, in one glomerulus without crescent, showed podocytes with cytoplasmic swelling and vacuolization. There was also focal interdigitating foot-process effacement. We did not find any debris or deposit in the subendothelial space.
Encorafenib and binimetinib were then stopped the 5th of January. The patient's serum creatinine decreased subsequently to 1.5 mg/dL at the beginning of February with a proteinuria stable at 1.2 g/24 hour. The patient did not receive steroids.
Starting March 2016, she was subsequently treated with pembrolizumab, an immunotherapy targeting program cell death 1. From March to July 2016, serum creatinine level was around 1.1 mg/dL, and there was a resolution of proteinuria. However, there was neither improvement nor worsening of the cancer lesions with pembrolizumab. Therefore, in July 2016 dabrafenib and trametinib, alternative BRAF and MEK inhibitors were introduced, and pembrolizumab was stopped. In October 2016, serum creatinine was 1.0 mg/dL and urine analysis showed no proteinuria.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [8.4, 'mg/dL'], 'Albumin': [33.0, 'g/L']}",8.96,8.512,9.408,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 33.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 33.0 g Albmumin/10.0 dL = 3.3 g Albmumin/dL. The concentration value of 33.0 g Albmumin/L converts to 3.3 g Albmumin/dL. 
The concentration of Calcium is 8.4 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.3 g/dL)) + 8.4 mg/dL = 8.96 mg/dL.
The patient's corrected calcium concentration 8.96 mg/dL."
2716,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-7350402-1,Extracted,"A 29-year-old pregnant woman (primipara; gestational age: 20 weeks) presented to hospital with a history of erythema, pustules, and itching since 1 month. The patient sought medical assistance at The First Hospital of Jilin University following 2 weeks of aggravation of symptoms. There was no family history of similar complaints. A physical examination showed widespread distribution of pin-sized pustules with erosions over an annular erythematic base over the torso and extremities (>40% of the body) (). Laboratory parameters were as follows: leukocyte count, 14.17 × 109/L; neutrophils, 87%; erythrocyte sedimentation rate, 34 mm/hour (reference range, 0–20 mm/hour); serum C-reactive protein level, 117 mg/L (reference range, 0–3.5 mg/L); serum calcium level, 1.82 mmol/L (reference range, 2.11–2.52 mmol/L); total protein level, 49.0 g/L (reference range, 65.0–85.0 g/L); and albumin level, 23.1 g/L (reference range, 40.0–55.0 g/L). The patient was prescribed a once-daily regimen of dexamethasone 5 mg and gamma globulin 30 g, together with antibiotics to prevent infection. Moreover, we administered supplemental calcium to correct electrolyte abnormalities.
Skin biopsy of the lesions showed spongiform pustules under the stratum corneum, acanthous hyperplasia and hypertrophy, spongy edema, and dilation of superficial dermal vessels. The perilesional areas showed moderate infiltration of lymphocytes and neutrophils (). These findings were consistent with IH. All symptoms, except for pruritus, were alleviated with active treatment. Subsequent administration of topical agents and systemic UVB irradiation alleviated the itching. After 5 days, we replaced dexamethasone with methylprednisolone (60 mg once daily) because dexamethasone may have adverse effects on the fetus. Two days later, the patient developed pustules over the neck and under the breast folds. The lesions showed rapid exacerbation. Therefore, the dosage of methylprednisolone was increased to 80 mg once daily. However, the patient experienced recurrence of severe symptoms. Based on the patient’s condition, 150 mg cyclosporine was administered twice daily along with 100 mg thalidomide once daily. The patient and her family members were fully informed about the teratogenic effects of thalidomide before prescribing this drug. After detailed discussion, the patient and her family members consented to the use of this drug and signed the notification of drug use. The dosage of methylprednisolone was adjusted to 70 mg (administered intravenously). However, there was no significant improvement in symptoms. Itching and repeated appearance of new skin lesions was distressing for the patient. Ultrasound assessment of the fetus showed that the biparietal diameter was 5.5 cm, the femur length was 3.7 cm, cardiac activity was 148 times/minute; and gestational age was 22 weeks.
After detailed counseling, the patient and her family members voluntarily consented to termination of pregnancy. Subsequently, the dosage of cyclosporine was reduced to 125 mg twice daily, and avermectin A (Chongqing Huabang Pharmaceutical Co., Ltd., Chongqing, China.) (20 mg once daily) was prescribed. After 3 days, there was a new eruption of erythematosquamous plaques and herpetiform pustules, and the symptoms continued to persist. Despite various treatment regimens, the skin lesions were not fully alleviated and there was appearance of new skin lesions. Ultimately, ethacridine lactate was used for induction of labor. After using rivanol (Guangxi Hefeng Pharmaceutical Co., Ltd., Hechi City, China) for 44 hours, the patient gave birth to a dead female infant with a length of 26 cm and a weight of 420 g. The dead infant’s skin showed no erythema or herpetic lesions. Thereafter, intravenous methylprednisolone 40 mg was administered twice daily for 3 days. After the abortion, there was gradual alleviation of skin lesions with no new eruptions. The original lesions dried up and started falling off. There was flattening of papules with residual brownish pigmentation. Methylprednisolone was gradually tapered off and the patient was discharged 8 days after the procedure. However, the symptoms recurred 15 days post-discharge and the patient was readmitted. On re-initiation of treatment, the skin lesions subsided and the patient was subsequently discharged. One month after her delivery, her skin was normal, except for residual pigmentation. Her skin showed complete recovery 3 months postpartum.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [1.82, 'mmol/L'], 'Albumin': [23.1, 'g/L']}",8.647,8.21465,9.07935,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 23.1 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 23.1 g Albmumin/10.0 dL = 2.31 g Albmumin/dL. The concentration value of 23.1 g Albmumin/L converts to 2.31 g Albmumin/dL. 
The concentration of Calcium is 1.82 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 1.82 mmol. To convert 1.82 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 1.82 mmol Calcium * 0.001 mol/mmol = 0.00182 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00182 mol Calcium * 40.08 g/mol = 0.07295 g Calcium. To convert 0.07295 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.07295 g Calcium * 1000.0 mg/g = 72.95 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 72.95 mg Calcium/10.0 dL = 7.295 mg Calcium/dL. The concentration value of 1.82 mmol Calcium/L converts to 7.295 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.31 g/dL)) + 7.295 mg/dL = 8.647 mg/dL.
The patient's corrected calcium concentration 8.647 mg/dL."
2717,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-5626297-1,Extracted,"The patient was a 62-year-old woman with a 24-year history of Crohn disease who had undergone multiple intestinal resections. Although gastrointestinal symptoms were recently minimal with administration of anti-TNF-α antibody and antidiarrheal drugs, she had made frequent trips to the hospital and received regular SFO administration to treat anemia. Over the course of treatment, she experienced numbness of her legs and was diagnosed with tetany due to hypocalcemia (serum calcium level approximately 6.0 mg/dL). Oral or intravenous calcium replacement therapy temporarily improved both her serum calcium level and numbness, but the patient's tetany and hypocalcemia recurred frequently and she had to be rehospitalized many times. She was then referred to our hospital for a further examination and treatment of hypocalcemia.
On admission, her height was 152 cm (decreased by a few centimeters over the past few years) and her body mass index was 12.7 kg/m2. She had severe kyphosis. She had smoked 10 cigarettes per day for 42 years, did not consume alcohol regularly, and had no allergies. Family history was negative for electrolyte and mineral disorders. She showed malnutrition and laboratory analysis was remarkable for a low serum albumin level of 2.3 g/dL. Serum mineral concentrations were as follows: adjusted serum calcium 8.6 mg/dL after correction with calcium gluconate, calcium L-aspartate hydrate, and alfacalcidol; potassium 3.3 mEq/L; phosphate 1.1 mg/dL; and magnesium 0.8 mg/dL (Table ). Bone scintigraphy revealed multiple uptakes in the ribs, spine, pelvis, and leg joints (Fig. ). Because serum mineral levels could not be maintained without calcium supplements and alfacalcidol, as shown in Fig. , administration of these drugs was resumed.
Assuming that one cause of her multiple mineral imbalances was hypomagnesemia, we first attempted to treat magnesium deficiency. Intravenous magnesium replacement followed by oral administration improved the deficiencies, not only of magnesium, but also partially of calcium and phosphate. Further investigation revealed that the level of FGF23 was extremely high (314 pg/mL); we then became aware of the patient's history of regular administration of intravenous SFO prior to our consultation. Because it has been reported that SFO can lead to hypophosphatemia via elevation of FGF23, we discontinued the SFO. Following this, the patient's FGF23 concentration gradually decreased, and multiple serum imbalances normalized despite reducing calcium and vitamin D replacement (Fig. ). Magnesium replacement and discontinuation of intravenous SFO alone resulted in normalization of serum mineral balance as well as improved bone mineral density at the femoral neck (Table ). Our case report was waived from the ethical approval or institutional review board of Hokkaido University Hospital, based upon their policy to review all intervention and observational study except for a case report. The patient provided informed consent for the publication of her clinical data. The presented data are anonymized and risk of identification is minimal.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [8.6, 'mg/dL'], 'Albumin': [2.3, 'g/dL']}",9.96,9.462,10.458,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 2.3 g/dL. 
The concentration of Calcium is 8.6 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 2.3 g/dL)) + 8.6 mg/dL = 9.96 mg/dL.
The patient's corrected calcium concentration 9.96 mg/dL."
2718,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-4208431-1,Extracted,"A 24-year-old woman was admitted for severe malnutrition and dehydration in the context of anorexia nervosa that was diagnosed one year ago. During this time, she had been hospitalized during 4 months with a transitory gain of six kilograms. She was treated with serotonin reuptake inhibitor and denied taking illicit drug or potentially harmful products. On admission, she presented hypotension (90/50 mmHg), sinus bradycardia (40 bpm), slight hypoglycemia (3.9 mmol/L), and hypothermia (35.7°C). She measured 160 cm and her body weight was 36 kg, corresponding to a body mass index (BMI) of 14 kg/m2. At physical examination she was oriented but lethargic and slightly jaundiced. The abdomen was slightly tender without ascites. The liver was not enlarged.
Laboratory data at admission demonstrated the following: glycemia (3.5 mmol/L), Na+ 137 mmol/L (N: 136–144), K+ 3.7 mmol/L (3.6–4.6), total Ca2+ 2.34 mmol/L (N: 2.2–2.52), Mg2+ 1.10 mmol/L (N: 0.65–1.05), P2− 1.22 (N: 0.8–1.5), and osmolality 289 mOsm/kg. Platelets were at 144 G/L (N: 150–350), hemoglobin was at 133 g/L (N: 120–160), and leucocytes were at 6.6 G/L (N: 4–11). The liver function tests was abnormal with a factor V at 33% (N: >70%). Serum aminotransferase levels were increased as follow: AST 208 U/L (N: 11–42), ALT 341 (N: 9–42), and total bilirubin 65 μmol/L (N: 7–25). The vitamin C was normal at 78 umol/L (N: 17–85) as was the thiamine at 208 umol/L (N: 65–200).
She was treated with serotonin reuptake inhibitor and denied taking illicit drug or potentially harmful products. Her treatment was stopped, but laboratory tests continued to deteriorate.
After one week, the laboratory routine tests revealed abnormal hematological tests with hemoglobin at 114 g/L, leucopenia at 2.5 G/L, and thrombocytopenia at 52 G/L. Additional investigations included prealbumin: 121 mg/L (N: 223–380) and albumin: 36 g/L (N: 35–48). Electrolytes remained normal. Renal and thyroid functions were unremarkable. Liver tests were as follows: AST 1088 U/L, ALT 1868 U/L, GGT 138 U/L, PA 102 U/L, and total bilirubin 66 μmol/L. INR was at 1.02 and factor V at 85%. Additional laboratory tests were performed to exclude all possible causes of liver injury. Hepatitis A, B, C, and E, CMV, and HIV tests were negative. Autoantibodies were absent; iron studies and ceruloplasmin were normal. At abdominal ultrasound the liver appeared normal with no ascites. Portal and hepatic veins were unremarkable. Thus, a diagnosis of acute liver injury associated with anorexia nervosa was considered the most plausible diagnosis.
A careful and progressive refeeding was performed, but liver transaminases remained abnormal. Thus, 10 days after hospital admission, a liver biopsy was performed by the transjugular route.
At histology, architecture of the liver was normal without fibrosis. Portal tracts and biliary and vascular structures were normal. Cytoplasm of hepatocytes was clarified and some acidophil bodies were found predominant in the centrilobular region. In addition, ceroid pigments at the apical pole of the hepatocytes were observed ().
An electron microscopy study was also performed in a fragment of liver biopsy, which showed features that strongly suggested a phenomenon of autophagocytosis: the density of glycogen particles in the hepatocytes was very low, consistent with cytoplasm clarification on PAS staining at the optical microscopy. In addition, the number of both mitochondria and rough endoplasmic reticulum appeared to be reduced. This observation contrasts with an increased number of Golgi bodies and smooth endoplasmic reticulum as well as primary and secondary lysosomes containing digested material (). Eight weeks after admission, with progressive refeeding the test returned back to normal ().","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [2.34, 'mmol/L'], 'Albumin': [36.0, 'g/L']}",9.699,9.21405,10.18395,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 36.0 g/L. We need to convert the concentration to g/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of g/dL. This will result to 36.0 g Albmumin/10.0 dL = 3.6 g Albmumin/dL. The concentration value of 36.0 g Albmumin/L converts to 3.6 g Albmumin/dL. 
The concentration of Calcium is 2.34 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 2.34 mmol. To convert 2.34 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 2.34 mmol Calcium * 0.001 mol/mmol = 0.00234 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.00234 mol Calcium * 40.08 g/mol = 0.09379 g Calcium. To convert 0.09379 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.09379 g Calcium * 1000.0 mg/g = 93.79 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 93.79 mg Calcium/10.0 dL = 9.379 mg Calcium/dL. The concentration value of 2.34 mmol Calcium/L converts to 9.379 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.6 g/dL)) + 9.379 mg/dL = 9.699 mg/dL.
The patient's corrected calcium concentration 9.699 mg/dL."
2719,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3190009-1,Extracted,"A 58-yr-old man visited the orthopedic surgery department of a local clinic in January 2008, with a 10-day history of lower back pain and tingling sensation of the left gluteal region and thigh. At the local clinic, spinal magnetic resonance imaging (MRI) was performed, and the clinician suspected a bone tumor. The patient was then transferred to the Hematology/Oncology Department of Eulji University Hospital for further evaluation. The patient had no history of trauma. In addition to the back pain and tingling sensation of the gluteal region and thigh, the patient complained of urinary symptoms, including hesitancy, mild voiding difficulties, and residual urine sensation. A physical examination revealed lower back tenderness, but other findings were normal.
The patient's peripheral white blood cell count was 3,990/µL, hemoglobin and platelet counts were 12.5 g/dL and 225,000/µL, respectively. Blood chemistry tests yielded the following results: total protein, 7.2 g/dL; albumin, 4.3 g/dL; AST, 25 U/L; ALT, 43 U/L; alkaline phosphatase, 88 U/L; total bilirubin, 0.6 mg/dL; calcium, 9.1 mg/dL; phosphorus, 4.3 mg/dL; blood urea nitrogen (BUN), 21 mg/dL; and creatinine, 1.0 mg/dL. Blood electrolyte analysis yielded the following results:sodium, 139 mmol/L; potassium, 4.1 mmol/L; and chloride, 103 mmol/L. Tumor markers detected included alpha-fetoprotein (AFP), 8.1 ng/mL; carcinoembryonic antigen (CEA), 1.49 ng/mL; carbohydrate antigen 19-9 (CA 19-9), 21.29 IU/mL; and prostate specific antigen (PSA), 62.40 ng/mL.
Spinal MRI revealed an osteolytic extension lesion with cortical pinning on the left half of the L3 vertebra, including the left transverse process (). Abdominal and chest computed tomography (CT) revealed an enhancing lesion of the prostate gland. Multiple metastatic lymphadenopathies were discovered in the paraaortic, aortocaval, and common iliac lymph nodes as well as in the left pelvic wall. A whole body positron emission tomography-computed tomography (PET-CT) was performed (). In the prostate gland, the standardized uptake value (SUV) was 3.45 for the lesion showing fructose-1,6-bisphosphate (FDP) uptake; maximum SUV was 4.57 for the lesion showing FDP uptake in the L3 vertebral body and transverse process; and SUV was 2.87 for the lesion showing FDP uptake in the left iliac bone. Multiple lesions showing FDP uptake were observed in the paraaortic, aortocaval, prevertebral, and left common iliac regions, with an SUV range of 2.27-4.1.
A prostate biopsy was performed under transrectal ultrasonographic guidance, and adenocarcinoma was confirmed in the pathologic review (). Because of the patient's severe back pain, decompression surgery of the L3 vertebra and a biopsy of the lesion were performed. The biopsy results characterized the lesion as a plasma cell neoplasm ().
Blood analysis yielded the following values: serum beta 2 microglobulin, 0.17 mg/dL; serum IgG, 1,436.6 mg/dL (reference interval: 870-1,700 mg/dL); IgA, 445.9 mg/dL (reference interval: 110-410 mg/dL); and IgM, 123.62 mg/dL (reference interval: 35-220 mg/dL). Serum protein electrophoresis showed an M-peak in the gamma fraction (serum M-protein was 217 mg/dL), and immunofixation electrophoresis revealed the presence of biclonal gammopathy (IgG kappa and IgA lambda). Urine immunofixation electrophoresis showed a dark band for kappa antisera (). In the 24-hr urine samples, the total protein was 151.2 mg/day and urine protein electrophoresis indicated tubular proteinuria with Bence-Jones proteinuria. Immunohistochemical staining of the bone marrow was performed with CD138, kappa, and lambda, and the bone marrow was positive for CD138 and kappa staining. Bone marrow plasma cells (CD138 positive cells) comprised 7.2% of nucleated cells (). Plain radiographic examination of the whole body did not show any abnormalities other than that in the L3 vertebra. Finally, we diagnosed the patient with multiple myeloma showing biclonal gammopathy accompanied by stage IV prostate cancer (due to an ischial bone metastatic lesion).
We started radiation therapy on the L3 vertebra plasma cell neoplasm, with a total dose of 3,940 cGy, and androgen deprivation therapy with bicalutamide (50 mg/day) and goserelin (3.78 mg/month) as well as bisphosphonate (90 mg/month) for prostate cancer treatment. After 27 months, we performed a whole-body PET-CT (), which revealed no abnormal FDP uptake in the intra-abdominal lymph nodes, prostate gland, and left iliac bone. Left vertebral body SUV uptake increased to SUV 3.10, but this change was considered as a post-radiotherapy change. PSA decreased to 0.05 ng/mL, which was within the reference interval. Follow-up serum protein electrophoresis revealed an M-peak (serum M-protein was 260 mg/dL) and immunofixation electrophoresis revealed the presence of biclonal gammopathy (IgG kappa and IgA lambda). The patient was administered 10 mg amitriptyline to control the neurologic pain in the left thigh and gluteal region. Nineteen months later, the neurologic pain disappeared, and medication was discontinued. The patient is doing well without evidence of tumor recurrence at 37 months after the initial diagnosis and treatment.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [9.1, 'mg/dL'], 'Albumin': [4.3, 'g/dL']}",8.86,8.417,9.303,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 4.3 g/dL. 
The concentration of Calcium is 9.1 mg/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 4.3 g/dL)) + 9.1 mg/dL = 8.86 mg/dL.
The patient's corrected calcium concentration 8.86 mg/dL."
2720,7,Calcium Correction for Hypoalbuminemia,lab test,decimal,pmc-3830317-1,Extracted,"A 42-year-old woman presented with acute onset lower limb paralysis associated with severe proximal muscle pain. These symptoms were not associated with respiratory difficulty, dysphagia, dysarthria or sensory symptoms and there was no associated backache, fever, rash or constitutional symptoms. She had a 2 year history of hypertension, which was poorly controlled despite treatment with a combination of nifedipine, atenolol and losartan. She was treated by a general practitioner and at initial diagnosis of hypertension had undergone biochemical evaluation including serum electrolyes, which had been within normal limits. She experienced two similar, but short lasting episodes of weakness in the preceding year, but had not been investigated. Three days prior to admission she had been given Frusemide as add on therapy by her general practitioner due to uncontrolled hypertension. Her blood pressure on admission was 160/100 mmHg. Clinical examination favored an acute onset myopathy with symmetric flaccid paralysis of lower limbs (muscle power - 3/5) with normal muscle power (5/5) in the upper limbs.
Initial work-up revealed severe hypokalemia (potassium - 2.0 mmol/l) with an elevated creatine kinase (CK) of 11347 IU (16-190) and increased lactic dehydrogenase of 856 IU/l (240-480). Patient's urine was positive for myoglobin with a high urinary myoglobin 4,170 μg/l. Serum creatinine was 130 μmol/l. In addition, patient had high urinary potassium of 19.45 mmol/24 h with metabolic alkalosis (pH - 7.540, HCO3-38 mmol/l, base excess - 15 mmol/l and PCO2-44 mmHg).
The other biochemical values on initial evaluation were as follows; serum aspartate aminotransferase - 244 IU/l (up to 35 IU/l); alanine aminotransferase - 193 IU/l (2-40); Sodium - 145 mmol/l; blood urea - 45 mg/dl; calcium - 0.9 mmol/l (1.12-1-32); phosphorus - 2.7 mg/dl (2.7-4.5); magnesium - 1.4 mg/dl (1.58-2.55); fasting blood glucose 110 mg/dl and the total protein was 7.6 g/dl with albumin 3.2 g/dl. Thyroid function tests were normal with a free T4 level of 1.02 ng/dl and thyroid-stimulating hormone 3.2 μIU/ml.
Based on the above findings, patient was diagnosed as having hypokalemic paralysis and rhabdomyolysis. Treatment was initiated by oral and intravenous supplementation of potassium and after 10 days, muscular strength and CK levels had returned to normal. Conduction studies and electromyography, which were performed after the correction of hypokalemia, were normal.
The coexistence of hypertension, hypokalemia with high urinary potassium loss in association with metabolic alkalosis raised the possibility of primary aldosteronism (PA), which lead to further hormonal evaluation. Aldosterone levels were 22,600 ng/dl (normal, 3.6-24.0 ng/dl) and the plasma renin activity (PRA) value was below the detection limit of our method (0.2 ng/ml/h). Aldosterone/renin ratio (ARR) was 113,000 ng/ml per ng/ml/h (<10). Abdominal ultrasound did not reveal adrenal lesions, but abdominal computed tomography scan showed a 20 mm × 16 mm hypodense mass in the medial limb of the right suprarenal gland []. She underwent right sided adrenalectomy and pathological examination of the gland confirmed a 20 mm adrenal adenoma. Post-operatively the patient was normokalemic without spiranolactone and the PRA was 0.52 ng/ml/h; aldosterone was 1.3 ng/dl with a reduced ARR of 2.5 (<20) ng/ml per ng/ml/h. After 4 weeks of discharge, her BP was normal without any antihypertensives and she was normokalemic with normal muscle strength.","Using the Calcium Correction for Hypoalbuminemia formula, what is the patient's corrected calcium in mg/dL? Your may set your normal albumin concentration to be 4 g/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Calcium': [0.9, 'mmol/L'], 'Albumin': [3.2, 'g/dL']}",4.247,4.03465,4.45935,"To compute the patient's correct calcium level in mg/dL, the formula is  (0.8 * (Normal Albumin (in g/dL) - Patient's Albumin (in g/dL))) + Serum Calcium (in mg/dL).
The patient's normal albumin level is 4.0 g/dL.
The concentration of Albmumin is 3.2 g/dL. 
The concentration of Calcium is 0.9 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Calcium from mmol to mg. The mass of Calcium is 0.9 mmol. To convert 0.9 mmol of Calcium to mol, multiply by the conversion factor 0.001, giving us 0.9 mmol Calcium * 0.001 mol/mmol = 0.0009 mol Calcium. To convert from mol Calcium to grams, multiply by the molar mass 40.08 g/mol, which will give 0.0009 mol Calcium * 40.08 g/mol = 0.03607 g Calcium. To convert 0.03607 g of Calcium to mg, multiply by the conversion factor 1000.0, giving us 0.03607 g Calcium * 1000.0 mg/g = 36.07 mg Calcium. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 36.07 mg Calcium/10.0 dL = 3.607 mg Calcium/dL. The concentration value of 0.9 mmol Calcium/L converts to 3.607 mg Calcium/dL. 
Plugging these values into the formula, we get (0.8 * (4.0 g/dL - 3.2 g/dL)) + 3.607 mg/dL = 4.247 mg/dL.
The patient's corrected calcium concentration 4.247 mg/dL."
2721,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7025968-1,Extracted,"A 39-year-old female patient, who had black stool twice without obvious inducement 3 days ago, accompanied by dizziness, and no other symptoms such as abdominal distension, abdominal pain, cold, and fever. After symptomatic treatment in the local hospital, the condition did not improve, so came to our hospital for further treatment and was hospitalized with gastrointestinal bleeding. Physical examination: T 36.7 °C, P 78/min, R 20/min, BP 99/62 mmHg, moderate anemia (Hb 85 g/L), no other abnormal signs and previous history of other diseases. After admission, through the preliminary examination of abdominal CT scanning, the results showed that hepatic cysts, small calcifications in the left lobe of the liver, and gallbladder inflammation, but no abnormalities in the intestinal tract. Subsequently, through electronic gastroscopy and enteroscopy, the results of the gastroscopy showed that patchy erythema could be seen in the gastric antrum, while in other parts of the stomach, the mucosa was smooth, the folds were intact, and the gastric peristalsis was good, which was diagnosed as superficial gastritis. The enteroscopy showed that, when the electronic enteroscope was inserted into the end of the ileum, a small amount of brown liquid could be seen, the intestinal mucosa was smooth, and the ileocecal valve is good. While a lot of coffee-like liquid could be seen in the colon cavity, but no bleeding site was found. At this time, we discussed and evaluated the relevant research results and case data, and highly suspected the possibility of intestinal vascular disease. In order to make a clear diagnosis and locate the bleeding site, further capsule endoscopy was performed (the whole photography time of capsule endoscopy was 11 h and 30 min). After the capsule endoscopy was swallowed, it was sent to the duodenum under the gastroscope, and entered the colon in 3 h and 27 min. Fortunately, some gains were obtained, at 48 min, there were a lot of fluid and blood clots in the upper and middle segment of the jejunum could be seen, but the entire field of vision was poorly blurred and no bleeding point was still found (). Through the results of capsule endoscopy, we were full of confidence in the previous judgment, and initially positioned the bleeding site in the jejunum.
After a week of treatment through nutritional support, rehydration and correction of anemia, the patient still had recurrent and intermittent black stool, and her condition was not very stable. Therefore, we decided to explore by laparotomy []. Based on the results of capsule endoscopy, the dark black part of the jejunum was found, and then the jejunum was cut at about 5 cm above it for intraoperative enteroscopy. The bleeding spot was finally found (located at about 10 cm from jejunum to the ligament of Traitz) and then the hemostasis was stopped by suture. Finally, it was diagnosed as jejunal telangiectasia complicated with bleeding (). After hemostasis during the operation, a thorough and careful exploration of other intestines was performed, and no other bleeding sites were found. After operation, the patient's condition was stable and the symptoms of hematochezia and anemia were controlled through symptomatic treatment.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [78.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 78.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2722,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4248619-1,Extracted,"A 42-year-old male was hospitalized in July 2008 with dizziness and mild dyspnea lasting two months. He also complained of intermittent febrile sensations and night sweats. His medical history revealed three open heart surgeries before admission. The patient underwent open mitral commisurotomy with mitral valve stenosis in 1986. After five years, he underwent mitral valve replacement with a Carbomedics prosthetic valve (CarboMedics, Inc.; Austin, TX, USA) in 1991. In 2005, his tricuspid valve was also replaced with a St. Jude Medical prosthesis (St. Jude Medical Inc.; Minneapolis, MN, USA) due to severe tricuspid regurgitation. He also had a history of atrial fibrillation and cardiac liver cirrhosis. The patient was a stock farmer and had buried cattle afflicted by brucellosis one year before this admission.
Upon admission, his vital signs showed a blood pressure of 130/70 mm Hg, pulse rate of 106 beats/min, respiratory rate of 22 breaths/min and body temperature of 37.5℃. Irregular heartbeats without murmurs were heard on auscultation and his electrocardiogram showed atrial fibrillation with a rapid ventricular response rate of 112 beats per minute. Laboratory studies revealed anemia and leukopenia with a hemoglobin level of 6.9 g/dL, a total white cell count of 2600/mm3 (66% neutrophils, 22% lymphocytes, 11% monocytes) and a platelet count of 191000/mm3. The C-reactive protein level of 5.76 mg/dL was elevated. The peripheral blood smears showed normocytic hypochromic erythrocytes with some fragmented cells.
Transesophageal echocardiography (TEE) demonstrated a very small echogenic mass (3×8 mm) attached to the inferomedial portion of the prosthetic mitral valve annulus (; ) which was not seen on the last TEE. The function of the prosthetic mitral valve and tricuspid prosthetic valve was normal. Under suspicion of infective endocarditis, six blood cultures were drawn for the first 48 hours and inoculated into an automated system (BACTEC; Becton Dickinson, Sparks, MD, USA). Because gram-negative coccobacilli were isolated from the initial blood culture after two days of incubation, an empirical antibiotic regimen of ceftriaxone (2 g/day) and gentamicin 3 mg/kg/day was started. The serum (tube) agglutination test against Brucella species showed a positive titer of 1:1280. The isolates of the automated hemoculture system were identified as Brucella species after six days and further identification of Brucella strains revealed B. abortus.
A diagnosis of BE on the prosthetic mitral valve was considered in this patient and specific antibiotics were started. The patient was given a triple combination therapy consisting of oral doxycycline 100 mg twice a day, oral rifampin 600 mg once daily and an intramuscular injection of streptomycin 1000 mg once daily. After 12 days of treatment, his fever recurred and streptomycin was switched to intravenous gentamycin (5 mg/kg/day). Although surgery was initially planned, the patient refused reoperation at that time. Therefore, he was treated with antibiotics alone under close follow-up. After 12 days of treatment, the blood cultures were negative. Three weeks after treatment, the follow-up echocardiography demonstrated no vegetations in the prosthetic mitral valve (). After seven weeks of hospitalization, he was discharged with oral doxycycline 200 mg/day. Doxycycline was maintained for one year and his Brucella titers decreased to <1:160. The patient has been regularly followed in the outpatient clinic. At present, five years after discharge, the patient remains free of symptoms.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [106.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 106.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2723,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-2803953-1,Extracted,"A white British, 78-year-old previously healthy female, non-smoker and with no known pulmonary disease, was admitted with collapse and shortness of breath with arterial oxygen saturations of haemoglobin of 80% on room air. The background included a history of persistent dry cough for 3 months without any other complaint or systemic symptoms. Her past medical history comprised of type 2 diabetes, increased uric acid and ongoing pain in the right knee. Her medication history consisted of gliclazide, allopurinol and diclofenac. The patient denied any recent travel or contact with animals (even pets). Physical examination revealed central cyanosis, tachypnoea, bilateral reduction in breath sounds and right-sided bronchial breathing. Cardiac examination was normal. There were no adenopathy noted. Arterial blood gases analysis on 5 litres of O2 per min showed mixed acidaemia. Serum biochemistry revealed raised urea (15.1 mmol/L) and creatinine (114 umol/L) levels consistent with acute kidney injury, positive D-dimmer's levels and increased CRP (48.2 mg/L). Chest radiography showed a loss of volume in the right lung (Figure ) and an electrocardiogram demonstrated normal sinus rhythm with a heart rate of 94 bpm, left axis deviation and an old inferior myocardial infarction. At this time the patient was started on treatment for both a possible community acquired pneumonia (benzyl penicillin and clarythromycin) and for pulmonary thromboembolism (therapeutic doses of Dalteparin). The patient was stable for 48 hours but then her oxygen requirements increased progressively. Contrast-enhanced chest CT scan and CT pulmonary arteriography with venous phase imaging failed to demonstrate any evidence of pulmonary artery thrombus. However thrombus, with associated fibrosis and volume loss, was seen to affect one of the right lower lobe pulmonary veins (Figure ). An echocardiogram was performed which showed a normal sized left ventricle with good function, normal aortic and mitral valves. The right heart although poorly visualized, appeared to be mildly enlarged with moderate function. The patient was started on methylprednisolone 1 g once a day and transferred to the intensive care unit (ICU).
The patient continued to deteriorate over the next 24 hours following admission to the ICU. She developed biochemical and electrocardiographic evidence of an acute anterior-lateral myocardial infarction and aspirin, clopidogrel and simvastatin were added to her anticoagulation therapy. Unfortunately the patient's oxygen requirements continued to increase and she was ventilated, initially supported by biphasic positive airway pressure (BIPAP) and then subsequently by invasive mechanical ventilation. Over the next eight days, despite maximal therapy she continued to deteriorate and died from multiple organ failure.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [94.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 94.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2724,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6647130-1,Extracted,"A 51-year-old Chinese woman presented with 16-month history of proteinuria and hypertension (160/90 mmHg) which was noticed during a routine examination. She was treated with Valsartan and blood pressure was controlled around 120/70 mmHg. Three months before admission, her urinary protein excretion was 2.12 g/d, serum albumin 36.4 g/L (normal range: 40–55 g/L), and serum creatinine 0.72 mg/dl (normal range: 0.50–1.50 mg/dl). One month before admission, her urinary protein excretion increased to 4.6 g/d, and serum creatinine increased to 1.16 mg/dl.
The patient was discovered Hepatitis C virus (HCV) infection 3 months prior to her admission, but not knowing how she got the infection. HCV-RNA was negative at that time and she did not receive any antiviral treatment. Family history was of no significance.
On admission, her blood pressure was 131/84 mmHg, temperature 36.7 °C, heart rate 75/min, and respiratory rate 18/min. There was mild edema around the eyelid, and there was no organomegaly. Other physical examinations were normal.
After admission, urine dipstick revealed proteinuria 2+. Urine sediment analysis revealed red blood cell 6 to 8 cells per high power field without white blood cell. Urinary protein excretion was 4.03 to 4.49 g/24 h. The urine albumin creatinine ratio was 2512.42 mg/gCr (normal range: < 30 mg/gCr). Her serum total protein was 58.4 g/L (normal range: 65–85 g/L), albumin was 35.3 to 29.7 g/L, and serum creatinine was 0.87 mg/dl to 1.03 mg/dl with estimated glomerular filtration rate (eGFR) of 64.33 to 63.39 ml/min/1.73m2. Her white blood cell (WBC) was 6.10 × 109 cells/L (normal range: 3.5–9.5 × 109 cells/L), hemoglobin was 101 g/L (normal range: 115–150 g/L) and platelet was 196 × 109 cells/L (normal range: 125–300 × 109 cells/L). Serum anti-HCV antibody was still positive and serum HCV-RNA was undetectable. Serum cryoglobulin was negative. She was negative for hepatitis B surface antigen (HBsAg), anti- human immunodeficiency virus (HIV) and Treponema pallidum antibody (TP-Ab). Other laboratory data revealed serum immunoglobulin (Ig) G was 5.42 g/L (normal range: 7.23–16.85 g/L), IgA was 1.37 g/L (normal range: 0.69–3.82 g/L), and IgM was 0.60 g/L (normal range: 0.63–2.77 g/L). Serum C3 level was 0.674 g/L (normal range: 0.60–1.50 g/L), and C4 level was 0.154 g/L (normal range: 0.12–0.36 g/L). Serum and urine immunofixation electrophoresis (IFE) did not identify monoclonal immunoglobulins. Anti-nuclear antibodies, anti-neutrophil cytoplasmic antibodies and anti- phospholipase A2 receptor (PLA2R) antibodies were all negative. Echocardiography and abdominal ultrasound were normal.
The patient underwent the first renal biopsy on February 26th, 2018. Direct immunofluorescence (IF) examination of frozen renal tissue revealed IgG +++, IgM +, C3 +++, C1q trace, C4d +++, κ++, λ++++, IgG1 +, IgG2 ++, IgG3 +++, IgG4 +, which were deposited along the capillary wall and mesangial area of the glomeruli (Fig. a-f). Light microscopic examination showed that 10/47 glomeruli were globally sclerosed. Other glomeruli showed a MPGN pattern with severe mesangial cell and matrix proliferation with nodular lesions, thickening of the capillary wall and double contour formation (Fig. g). Congo red staining for amyloid was negative. Electron microscopic examination revealed electron-dense deposits in the mesangial, subendothelial and subepithelial area. Subendothelial edema was observed in segmental capillary loops (Fig. h). Hence the pathological diagnosis was immune-complex mediated MPGN due to polyclonal immunoglobulins deposition.
To explore the etiology and pathogenesis of MPGN, the differential diagnosis and further examinations were performed. Autoimmune diseases were excluded as the absence of antoantibodies and relevant clinical manifestations. The anti-HCV antibodies were positive in the serum, but the serum HCV-RNA was negative, as were the serum cryoglobulin, serum C3 and C4 and HCV antigen staining on the renal tissue, excluding the diagnosis of HCV related MPGN. Other chronic infections were not identified. According to the IF findings by dominant IgG3 and λ light chain, monoclonal gammopathy associated MPGN was suspected. Bone marrow aspiration smear revealed 1.5% plasma cells. Bone marrow biopsy showed a few plasma cells with normal change. CD38 positive cells accounted for 0.28% of bone marrow cells, but no evidence of monoclonal light chain restricted expression as determined by flow cytometry and fluorescent in situ hybridization (FISH). She was treated with olmesartan 40 mg/d, ramipril 10 mg/d, amlodipine 10 mg/d and metoprolol 25 mg/d, blood pressure was controlled around 120/70 mmHg. She did not receive any anti-HCV treatment.
Six months after renal biopsy, her proteinuria increased to 5.57 g/d, with serum albumin 31.8 g/L, serum creatinine 1.29 mg/dl. Therefore, mycophenolate mofetil and tripterygium wilfordii were prescribed. One month later, her proteinuria decreased to 2.47 g/d with a serum albumin 27.7 g/L, serum creatinine 0.97 mg/dl. However, her serum creatinine increased to 1.96 mg/dl, and a repeated renal biopsy was performed 9 months later in November 19th, 2018.
IF examination of frozen renal tissue revealed IgG ++++, C3 +++, C1q negative, C4d +++ (immunohistochemistry), κ trace, λ++++, IgG1 negative, IgG2 negative, IgG3 +++,IgG4 negative, which were deposited along the capillary wall and mesangial area of the glomeruli (Fig. a-f). Light microscopic examination showed that 2/20 glomeruli were globally sclerosed. Other glomeruli showed a MPGN pattern(Fig. g). More prominent tubular atrophy and interstitial fibrosis than the first time, with focal loss of brush border of the tubular epithelial cells. There was moderate interstitial infiltration of lymphocytes, monocytes and a few eosinophils. Electron microscopic examination revealed electron-dense deposits in the mesangial, subendothelial and subepithelial area. (Fig. h). The patient was diagnosed with proliferative glomerulonephritis with monoclonal IgG3λ deposition (PGNMID). Further testes showed serum free κ chain was 16.8 mg/L (normal range: 3.30–19.40 mg/L), free λ chain was 25.3 mg/L (normal range: 5.71–26.3 mg/L), and the κ/λ ratio was 0.664 (normal range: 0.26–1.65). Serum and urine IFE were still negative for monoclonal immunoglobulin. Repeated serum anti-HCV antibody detection was negative without anti-HCV treatment.
Therapy and follw-up: The patient was treated with prednisone (40 mg/d) and cyclophosphamide (100 mg/d), her serum creatinine decreased to 1.47 mg/dl and remained stable until March 2019. Then she suffer an episode of herpes zoster, cyclophosphamide was discontinued, and the patient’s serum creatinine increased to 2.54 mg/dl.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [75.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 75.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2725,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-9340,Extracted,"A 69-year-old African American man is brought to the emergency department with sudden onset lower limb paralysis and back pain. He has had generalized bone pain for 2 months. He has no history of severe illnesses. He takes ibuprofen for pain. On examination, he is pale. The vital signs include: temperature 37.1°C (98.8°F), pulse 68/min, respiratory rate 16/min, and blood pressure 155/90 mm Hg. The neurologic examination shows paraparesis. The 8th thoracic vertebra is tender to palpation. An X-ray of the thoracic vertebrae confirms a compression fracture at the same level. The laboratory studies show the following:
Laboratory test
Hemoglobin 9 g/dL
Mean corpuscular volume 95 μm3
Leukocyte count 5,000/mm3
Platelet count 240,000/mm3
ESR 85 mm/hour
Serum
Na+ 135 mEq/L
K+ 4.2 mEq/L
Cl− 113 mEq/L
HCO3− 20 mEq/L
Ca+ 11.5 mg/dL
Albumin 4 g/dL
Urea nitrogen 18 mg/dL
Creatinine 1.2 mg/dL
Serum electrophoresis shows a monoclonal protein level of 38 g/L.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [68.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 68.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 0.
The patient's Well's score for pulmonary embolism is 0."
2726,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7783511-1,Extracted,"We present the case of a 62-year-old gentleman, who was brought into the emergency department (ED) by ambulance with a history of dry cough, low grade fever, worsening shortness of breath for 4 days, and pleuritic sounding chest pain, which was different to when he had a pulmonary embolism approximately ten months ago. His past medical history included type II diabetes mellitus, peripheral vascular disease, treated malignant neoplasm of the base of tongue, diverticular disease, essential hypertension, and previous provoked pulmonary embolism. Before admission, he was living independently with his wife. His exercise tolerance was restricted to 10 yards with the assistance of a walking stick. He was an exsmoker and used to smoke 5 cigarettes a day but stopped smoking a few years previously.
On admission, he was pyrexial with a temperature of 38.2°C, oxygen saturations 98% on 28% FiO2, blood pressure 73/35 mmHg, and pulse rate 92 bpm. Initial treatment included oxygen 28% FiO2 via a venturi mask and fluid resuscitation for hypotension. Physical examination revealed bibasal crepitations on auscultation of chest and a swollen and tender right leg. Initial investigations revealed deranged biochemical markers () and opacification affecting the right midzone of the lung ().
Initial laboratory workup summarised in .
In view of the clinical presentation and raised d-dimer, a computed tomography pulmonary angiogram (CTPA) was performed which reported right upper lobe consolidation with subtle peripheral ground glass opacification in the left upper lobe and both lower lobes, suggestive of early COVID-19 infection (). Moreover, his troponin I levels were markedly elevated and electrocardiogram (ECG) showed ST segment depression and T-wave inversion in the anterolateral chest leads. A transthoracic echocardiogram showed moderately impaired left ventricular systolic function with an akinetic and rounded apical septal wall.
On account of the history, examination, and investigations, he was treated as suspected COVID-19, community-acquired pneumonia (CURB-65 score = 2, moderate severity), COVID-19 myocarditis, and sepsis, leading to multiorgan failure. In view of poor physiological reserve and comorbidities, the ceiling of care was decided to be ward level care and noninvasive ventilation if needed. However, he began to improve clinically, became normotensive, and was able to be weaned off oxygen day 3 after admission. By that time, his swab detected SARS-CoV-2 RNA which confirmed the diagnosis of COVID-19.
Following initial improvement, he suddenly developed a new, increased oxygen demand, requiring titration of humidified oxygen up to 10 litres. Chest physiotherapy helped him bring up copious volumes of thick sputum, and he was stable for most of the day with oxygen saturations of 93%. Later that day, he suddenly deteriorated and becoming cyanotic and critically unwell. Oxygen saturations were 80% on 15 litres nonrebreathe mask, and he was significantly tachypnoeic with a respiratory rate of 40/minute. An urgent portable chest X-ray revealed a large right-sided pneumothorax causing mediastinal shift ().
An intercostal drain was inserted on an emergency basis and the patient improved slightly over the next 24 hours though he still required oxygen via a high flow nasal cannula system to maintain oxygen saturations of 92% or more. Despite the chest drain and the addition of thoracic suction, the lung did not reexpand. He continued to deteriorate rapidly, was unable to tolerate further pleural procedures, and died.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [92.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 92.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3 + 1 =  4.
The patient's Well's score for pulmonary embolism is 4."
2727,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3546274-1,Extracted,"In May 2009, a 30-year-old woman came to the emergency room (ER) with a five-day history of acute progressive dyspnea on exertion (NYHA class III). In 2007, ductal carcinoma in situ was diagnosed by biopsy during pregnancy. In 2008, after a full-term delivery, findings on fluorodeoxyglucose positron emission tomography computed tomography (CT) and ultrasound of the right breast revealed diffuse microcalcification and skin thickening of the right breast, and metastatic axillary lymph nodes. The patient refused further management and was lost to follow up until the ER visit.
On admission, the patient's blood pressure was 126/76 mm Hg, heart rate was 120 beats per min, respiratory rate was 18 breaths per minute, and body temperature was 36.7℃. A chest radiograph showed that the lung field was clear. Results of arterial blood gas analysis in room air indicated hypoxemia: pH 7.446, pCO2 28.2 mm Hg, pO2 44.3 mm Hg, HCO3 19.1 mmol/L, SaO2 76.8%. D-dimers were elevated to 2.59 µg/mL (normal, <0.39 µg/mL) with an elevated troponin I level to 0.24 ng/mL (normal, <0.04 ng/mL) and a brain natriuretic peptide of 774 pg/mL (normal, <100 pg/mL). Diffuse enlargement of the right breast with skin thickening and many enlarged axillary lymph nodes consistent with locally advanced breast cancer was observed on CT.
On the second day of admission, the patient was consulted with the cardiology department for possible preoperative cardiac evaluation. An electrocardiogram showed an S1Q3T3 pattern with inverted or flattened T waves in leads V1 through V4. A transthoracic echocardiogram showed normal left ventricular systolic function with right ventricular enlargement and free wall hypokinesia sparing the apex. In addition, the echocardiogram showed typical findings of acute pulmonary thromboembolism with a D-shaped left ventricle, moderate tricuspid regurgitation, and moderate pulmonary hypertension with an estimated right ventricular systolic pressure of 61 mm Hg.
Other laboratory tests showed the following results: white blood cell 7,900/mm3 with normal differential counts, hemoglobin15.4 g/dL, platelets 144,000/mm3, alanine aminotransferase 50 IU/L (normal, 0 to 40 IU/L), aspartate aminotransferase 218 IU/L (normal, 0 to 40 IU/L), total bilirubin 1.4 mg/dL (normal, 0.2 to 1.2 mg/dL), C-reactive protein 0.81 mg/dL (normal, 0 to 0.30 mg/dL), prothrombin time (PT) international normalized ratio (INR) of 1.36 (normal, 0.8 to 1.2), activated partial thromboplastin time (aPTT) of 45.7 seconds (normal, 27.0 to 45.0 seconds), fibrinogen of 196 mg/dL (normal, 200 to 400 mg/dL), and fibrin degradation products (FDP) of 1 : 2 positive (normal, negative). A peripheral blood smear showed increased numbers of schistocytes and reticulocytes consistent with MAHA ().
We measured serum vascular endothelial growth factor (VEGF) and interleukin 6 (IL-6) in view of preexisting information on VEGF, a critical angiogenic molecule and IL-6, a multifunctional cytokine promoting tumor growth. Serum VEGF levels were 26.9 pg/mL on the second day in the hospital and 9.5 pg/mL on the third day in the hospital (normal, 88.7 to 1,048.7 pg/mL); IL-6 levels were 50.3 pg/mL and 25.6 pg/mL on the second and third days, respectively (normal range, 0.4 to 8.6 pg/mL).
Anticoagulation therapy with enoxaparin was startedunder the clinical diagnosis of submassive acute pulmonary thromboembolism. While no evidence of pulmonary thromboembolism was observed on pulmonary CT angiography (), an echocardiogram showed acute right ventricular pressure overload (), and a perfusion lung scan showed multiple small wedge-shaped perfusion defects throughout both lungs (). Therefore, with a diagnosis of PTTM based on clinical and laboratory findings, the patient was transferred to the intensive care unit and received 1 mg/kg enoxaparin subcutaneously, 0.05 mg/kg dexamethasone intravenously, and 2 mg warfarin sodium orally.
On the third day of admission, repeated transthoracic echocardiogram showed additional significant right ventricular pressure overload with an estimated right ventricular systolic pressure of 60 mm Hg. Abnormal liver function was the result of either passive congestion or hepatic metastasis, although the initial CT did not show definite systemic metastasis. The patient was scheduled to undergo surgical breast biopsy and appropriate chemotherapy, however, her general condition showed rapid deterioration, and she died within 48 hours of admission.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",5.5,5.5,5.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3.0 + 1.5 = 4.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 4.5 + 1 =  5.5.
The patient's Well's score for pulmonary embolism is 5.5."
2728,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8443390-1,Extracted,"A 56-year-old man presented to the emergency room with progressively worsening shortness of breath and chest discomfort of one week duration. He had associated nonproductive cough for one week but denied any calf pain, leg swelling, hemoptysis, recent travel, recent surgeries, fever, or chills. His past medical history was notable for hypertension that was well controlled on lisinopril. He was also prescribed with 50 mg of clomiphene citrate 2 years ago due to low testosterone. He did not take any other medications and denied any smoking history. He denied any family history of blood clots or bleeding disorders.
On physical examination, his temperature was 97.8 F, respiratory rate was 26 breaths/min, blood pressure was 109/58 mm Hg, heart rate was 134 beats/min, and SpO2 was 96% on 6 liters nasal cannula. He had normal heart sounds without any murmurs and rubs and had clear lungs. He had trace pedal edema bilaterally without any calf tenderness. Laboratory results include leukocytes of 15.4 × 109/L, hemoglobin of 15.8 g/dL, platelets of 207 × 109/L, creatinine of 2.2 mg/dL, and troponin I <0.05 ng/ml initially, but later plateaued at 0.10 ng/ml.
Electrocardiogram on admission showed sinus tachycardia and incomplete right bundle branch block with S1Q3T3 pattern. Computed tomography angiography (CTA) of chest revealed acute large volume pulmonary embolism in bilateral main pulmonary arteries, lobar, and segmental branches of all lobes with mild right heart strain (as shown in ). Venous Doppler showed acute deep vein thrombosis in the right lower extremity involving the popliteal and posterior tibial veins. Echocardiogram was done which revealed a systolic ejection fraction of 55–65% with mildly decreased right ventricular systolic function.
The patient was started on a high flow nasal cannula initially for respiratory distress and then eventually was weaned to room air. He was started on heparin drip for anticoagulation that was later switched to rivaroxaban. Since clomiphene citrate (CC) was thought to be a contributing factor for pulmonary embolism, it was stopped, and he was referred to follow-up with a hematologist to evaluate for prothrombotic risk. His further workup for hypercoagulable disorders including anticardiolipin antibodies, factor V Leiden mutation and prothrombin gene mutation has been negative. He was also recommended to have age-appropriate screening for malignancy.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [134.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 134.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2729,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6764554-1,Extracted,"A 60-year-old Chinese male presented to the hospital with acute shortness of breath and lower limb swelling. He has a past medical history of stroke disease, chronic kidney disease, and ischaemic cardiomyopathy with a mildly reduced left ventricular ejection fraction of 45%. His cardiovascular risk factors include diabetes mellitus, hypertension, and hyperlipidaemia.
Clinical examination revealed bibasal crepitations with bilateral pitting oedema. The blood pressure on admission was 150/87 mmHg with sinus tachycardia with a heart rate of 129 beats per minute.
Initial arterial blood gas (ABG) on admission () revealed Type 2 respiratory failure, while chest X-ray done showed bilateral pulmonary congestion.
He was initially started on non-invasive ventilation and intravenous frusemide and glyceryl trinitrate infusion. Despite initial clinical improvement, the patient became increasingly restless with worsening hypoxaemia and decision was made for intubation and mechanical ventilation. However, he suffered a pulseless electrical activity cardiac arrest peri-intubation with a low-flow time of 20 min before return of spontaneous circulation (ROSC).
He was started on our institution’s protocolized post-cardiac arrest care bundle () which included continuous rSO2 monitoring and TTM with mild induced hypothermia at 33°C. An oesophageal probe was inserted for core body temperature monitoring. Initial ABG post-ROSC revealed a Type 2 respiratory failure with pH 7.14, pCO2 54, pO2 110, HCO3 18, and SaO2 97%. Patient was sedated and paralyzed and ventilator settings were optimized to correct the respiratory acidosis. Patient was ventilated with a tidal volume of 7 mL/kg predicted body weight and at a ventilator rate of 28 breaths per minute. Initial cerebral oximetry revealed an rSO2 66% (left) and 67% (right).
Post-resuscitation SpO2 was maintained above 94% and mean arterial pressure (MAP) was constantly above 80 mmHg without the need for inotropes or vasopressors. However, it was subsequently noted that the cerebral rSO2 had decreased to 33% (left) and 35% (right) and a repeat ABG showed resolution of the respiratory acidosis with pH 7.3, pCO2 33, pO2 138, HCO3 16, and SaO2 99%.
Ventilator settings were immediately adjusted and the minute ventilation reduced by lowering the ventilator rate to aim for mild therapeutic hypercapnia with a target pCO2 of 50–55 mmHg. PEEP was reduced from 12 cmH2O to avoid an excessively high intrathoracic pressure which may impede cerebral venous drainage. Patient was also started on dobutamine infusion to improve the global and cerebral perfusion as the central venous oxygen saturation (ScvO2) of 62% reflected a systemic oxygen delivery/consumption mismatch, while a Pcv-aCO2 gap of 14 mmHg suggested a low-flow state. The above interventions resulted in an improvement in cerebral rSO2 to 55% (left) and 51% (right) ().
Patient was cooled for 24 h and then gradually rewarmed. A repeat transthoracic echocardiogram revealed severe global hypokinesia with a left ventricular ejection fraction of 26%.
He was subsequently extubated after 6 days in the cardiac intensive care unit with improvement in Glasgow coma scale score and underwent rehabilitation in the general ward. On discharge, he had a cerebral performance category of 1 and is now on follow-up in the outpatient clinic.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [129.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 129.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2730,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5295575-1,Extracted,"A 34-year-old male patient was admitted with complaints of cough and fever for 2 weeks. He had history of similar complaints in the past in the form of frequent episodes of cough with expectoration for which he was hospitalized and treated with intravenous (IV) antibiotics. He had no history of dyspnea, chest pain or pedal edema. General physical examination was unremarkable except for grade I clubbing. Clinical examination revealed blood pressure of 118/84 mm Hg in right upper limb in supine position with pulse rate of 96/min, regular, normal volume with a normal character with no radio-radial or radio-femoral delay and all peripheral pulses equally palpable. The jugular venous pressure was raised 2 cm above the angle of Louis with a prominent c-v pattern. The apical impulse was in the fifth intercostals space medial to the midclavicular line. The S1 was normal, and S2 was narrowly split with loud P2 component. There was pan-systolic murmur along the left lower sternal border radiating all over the precordium. On systemic examination, respiratory system showed barrel-shaped chest with anteroposterior and transverse diameter ratio of 1, widely spaced ribs and increased resonance to percussion, and breath sounds decreased in intensity symmetrically with prolonged expiration. Rest of the examination was normal. On investigations, total leukocytes were 14,200/mm3, polymorphs 72%, lymphocytes 22%, monocytes 4%, eosinophils 2%, hemoglobin 15.1 g%, platelets 211,000/mm3, ESR 14 mm first h and fasting blood sugar was 98 mg%. Blood culture was negative for any growth. Sputum culture showed streptococcus pneumonia sensitive to amoxicillin, and patient was treated accordingly. On chest radiography, there were bronchiectatic changes. Electrocardiogram showed normal sinus rhythm with heart rate of 102 and right axis deviation. In lead II, III and aVF, P-wave was tall and peaked with maximum P-wave amplitude > 7 mm and larger than QRS complex in lead II (). P-wave axis was +82°. This was referred as Himalayan P-waves suggestive of right atrial enlargement. Precordial leads showed slow R-wave progression with right ventricular strain pattern (). The 2D transthoracic echocardiography revealed enlarged right atrium and right ventricle with severe tricuspid regurgitation, pulmonary arterial hypertension and preserved ejection fraction. So these findings were consistent with sequelae of COPD. The findings of bronchiectasis were confirmed on HRCT chest as evident by cystic bronchiectasis with bronchial wall thickening and mucous plugging (). The bronchial dilation was also seen, lack of bronchial tapering and visibility of airways within 1 cm of the pleural surface, i.e., abutting the mediastinal pleural surface ().",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [102.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 102.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2731,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7370690-1,Extracted,"A 50-year-old male who had a past medical history of HIV with unknown cluster of differentiation 4 (CD4) lymphocyte count and not compliant with his medications was brought in by emergency medical services (EMS) after he was found in his room covered in feces and looking disheveled. They brought him to Brookdale University Hospital and Medical Center emergency room. His initial vital signs showed a temperature of 100 ºF, blood pressure of 143/91 mmHg, heart rate of 105 beats per minute, respiratory rate of 20 per minute. He was noticed to have disseminated, vesicular-pustular rash all over his body at different stages of healing and crusted skin eruption on his anterior neck and submandibular area (Figures -).
Patient’s neurological exam revealed that he was alert and oriented to self only, had a right-sided upper and lower facial droop. The patient also had impaired hearing on the right side. The muscle strength was 5/5 throughout. The patient had normal reflexes and the sensation was intact. The remainder of his physical exam did not show any other abnormal findings. Computerized tomography of the head without contrast showed no acute intracranial pathology. Subsequently, the patient had a lumbar puncture done in the emergency room which revealed a cloudy cerebrospinal fluid (CSF) with a white blood cell count of 849 cells/uL with lymphocyte predominance (72%), glucose of 39 mg/dl and protein of 364 mg/dl. Serum electrolytes, liver enzymes, and coagulation profile were all within normal limits. CSF sample was sent for a varicella-zoster polymerase chain reaction (PCR) test as well. His chest X-ray was clear without any infiltrates. His initial laboratory investigations are summarized in Table .
A presumptive diagnosis of disseminated VZV with encephalitis was made according to the patient's skin lesions and CSF analysis. Therefore, he was started on intravenous acyclovir at 10 mg/kg every eight hours and admitted to the general medical floor under contact and airborne precautions. Patient’s varicella zoster PCR from the CSF sample came back positive. Patient mental status improved rapidly within 48 hours of treatment and he became alert and fully oriented. On eye exam, the patient had diplopia with right gaze, and it was determined that he had a right sixth cranial nerve palsy. He had deficits in right sided cranial nerves VI, VII, and VIII evident by impaired right eye abduction, right sided facial weakness, as well as impaired hearing. This constellation of findings is likely secondary to Ramsay Hunt syndrome with multiple cranial nerve involvement. Intravenous acyclovir was continued, and the patient started taking prednisone 50 mg orally for five days for the treatment of Ramsay Hunt syndrome. He was also found to have otitis externa and was prescribed ciprofloxacin with dexamethasone otic drops. Magnetic resonance imaging of the brain without contrast found nonspecific white matter lesions in the high left frontal lobe measuring approximately 8 mm but otherwise no mass, hemorrhage, or acute infarct (Figure ).
The patient’s mental status came back to his baseline on day three. The patient’s rash had crusted on day six hence the isolation precautions were discontinued. He started ambulating without any difficulty and facial paralysis resolved by day eight. He was safely discharged home after nine days of hospital stay with oral acyclovir 400 mg tablets three times daily for 21 days and prednisone 50 mg tablets daily for three days.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [105.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 105.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2732,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7299603-1,Extracted,"Patient 1: a 52-year-old woman, non-diabetic, non-hypertensive, was referred to the emergency with a history of large-volume, frank hematemesis (four episodes in 3 days). Positive history included recurrent cough for the past 1 year and low-grade fever for 3 months. No history of dysphagia, jaundice, abdominal distension, pain abdomen or altered sensorium. No history of chronic medications (oral anticoagulants or anti-platelets), analgesic intake or any substance abuse. She had received four units of packed red cells at an outside facility prior to admission. She was conscious, oriented, hemodynamically labile (heart rate: 110/min; BP: 86/60 mm Hg) with mild fever (99°F). General survey revealed obvious pallor. All other system examinations were within acceptable limits. Her hemoglobin (Hb) was 7.3 gram%, total leukocyte count (TLC) was 6400 cells/mm3, total bilirubin was 1.31 mg/dl and total protein was 4.75 gram%. An urgent UGI endoscopy revealed an opening in the posterior wall of the lower third of the esophagus, with a diverticulum. Inflammatory changes were noted in the diverticulum (). Contrast-enhanced computed tomogram (CECT) revealed erosion of the pouch into the thoracic aorta (), and a diagnosis of AEF with acute UGI hemorrhage was made.
The patient was resuscitated with packed red cells and definitive surgical management was emergently undertaken. A left posterolateral thoracotomy was performed, and pus was found in the pleural cavity and posterior mediastinum. After debridement of the chest cavity, partial bypass was instituted by cannulating the aortic arch in between the left common carotid artery and the left subclavian artery, and connecting this via the cardiopulmonary bypass machine to another cannula in the descending thoracic aorta just above the diaphragm (). The aorta was cross-clamped above and below the suspected fistulous region and opened longitudinally. A 2 × 2 cm opening was seen in the wall of the aorta, adjoining the esophagus (), and this was internally repaired with a Dacron patch (), and the aorta was primarily closed. The esophageal opening was debrided and then repaired with interrupted polypropylene sutures, superimposed with a vascularized intercostal muscle pedicle (). Bypass was successfully discontinued and a gastrostomy and jejunostomy were created. She remained on broad-spectrum antibiotics and the rest of her postoperative course was uneventful.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2733,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7822652-1,Extracted,"A 44-year-old gravida 6 para 4 postpartum woman presented to the emergency department (ED) complaining of substernal chest pain. That afternoon, she experienced sudden-onset severe left-sided chest pain radiating to her back and shoulder. She had been discharged four days prior after induction of labor for chronic hypertension with an uncomplicated vaginal birth. Her medical history was notable only for hypertension, for which she took metoprolol. She was maintained on metoprolol with good blood pressure control for the duration of her pregnancy and after induction. The day prior to admission she was under significant emotional distress after her infant was hospitalized with hyperbilirubinemia.
In the ED, the patient was afebrile, her blood pressure was 164/101 mm Hg, her heart rate was 60 beats per minute, and she was breathing 16 breaths per minute. Her cardiovascular examination was unremarkable with normal heart sounds with no murmurs, rubs, or gallops and no jugular venous distension. Her lungs were clear, her abdomen was soft, and she had no extremity edema. Her complete blood count and comprehensive metabolic panel results were within normal limits. Her initial troponin I was 0.41 ng/mL (reference range, <0.04 ng/mL), and her electrocardiogram (ECG) () was significant for ST elevation in leads V2-V5 consistent with an anterior ST-segment elevation myocardial infarction (STEMI). Her chest X-ray showed normal mediastinum, no signs of cardiomegaly, and clear lungs.
Given the concern for acute coronary syndrome (ACS), the patient was emergently taken to the cardiac catheterization lab. Her coronary angiogram showed haziness of the midleft anterior descending (LAD) artery followed by an abrupt change in arterial caliber extending to the distal LAD and diagonal branches (). There was no clear visualization of a dissection flap, but there was a visible long segment of diffuse vessel narrowing in the mid to distal LAD highly suspicious for coronary dissection. Contrast flow in the distal vessel was normal (TIMI 3), and there were no luminal changes with the administration of intracoronary nitroglycerin. There was no angiographic evidence of atherosclerotic disease in any of her coronary arteries, and no evidence of narrowing in the coronary arteries outside of the LAD. Her chest pain was resolved during the procedure, and her ECG showed normalization of her ST elevation. Given the patient's hemodynamic stability, normal blood flow in the distal LAD, resolution of chest pain, and suspicion for dissection, she was managed conservatively.
She was started on IV nitroglycerin for hypertension, metoprolol, and dual antiplatelet therapy with aspirin and clopidogrel and then transferred to the coronary care unit for close observation. Her transthoracic echocardiogram showed normal left ventricular function with an ejection fraction of 68% and hypokinetic septal and apical walls in the distribution of the LAD. Her repeat ECG () showed the expected evolution of her STEMI with QS waves and T-wave inversions seen in leads V2-V5. She was weaned off the nitroglycerin and transitioned to captopril and nifedipine for strict blood pressure control and safety with breastfeeding.
She remained chest-pain free during the course of the hospitalization and underwent a repeat angiogram to evaluate for the progression of disease given the diagnostic uncertainty. Her repeat angiogram on day 6 of hospitalization showed complete resolution of the LAD lesion () consistent with dissection. Compared to the initial angiogram, the area of haziness was no longer present, and the vessel tapered appropriately towards the apical LAD. However, a new tubular narrowing with abrupt vessel caliber change () was noted in the midposterior descending artery (PDA), compared to her initial angiogram () with normal flow and no clear dissection flap. This event was concerning for a new dissection event. The patient was asymptomatic throughout her hospitalization and was discharged home with close obstetric, primary care, and cardiology outpatient follow-up.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [60.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 60.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2734,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7478664-1,Extracted,"A 45-year-old man, who was diagnosed with gastric SET detected on endoscopy during a routine medical examination, was referred to our hospital in August 2016 for further evaluation. He was symptom-free and presented no specific abdominal symptoms such as pain, vomiting, heartburn, dysphagia, or change in bowel habits. He had no history of medication or family history of malignant disease or autoimmune disorder.
In the physical examination, his blood pressure was 110/70 mmHg and heart rate was 80 bpm. The abdomen was soft and flat, and no palpable mass was observed. His laboratory results were normal for the following parameters: leucocyte count, 8900/mm3; hemoglobin level, 14.3 g/dL; and platelet count, 226,000/mm3. His liver function tests were normal. Serum IgG4 or other immunoglobulin levels were not measured because there was no reason to suspect IgG4-RD at that time.
Endoscopy with endoscopic ultrasonography (EUS) was performed. In endoscopic vision, a 3 × 3 cm fixed, round, hard mucosal lesion was detected on the greater curvature of the upper gastric body (Fig. ). Endoscopic biopsy showed only mild chronic gastritis. EUS revealed a mainly hypoechoic, oval with sharp margins intramural lesion developing from the muscularis propria and measuring 29.4 × 16.4 mm at its largest diameter (Fig. ). Abdominal computed tomography (CT) showed a well-defined heterogeneously enhancing wall mass at the greater curvature of the upper gastric body (Fig. ), most likely to be a malignant gastrointestinal stromal tumor (GIST). No lymphadenopathy was noted.
Laparoscopic wedge resection was performed using Endo GIATM iDrive purple 60 mm (Covedien, New Haven, CT, USA). The postoperative course was uneventful, and the patient was discharged on the fourth postoperative day.
Histopathological examination of the lesion revealed a tan whitish-colored firm mass, measuring 3 × 2.8 cm, protruding from the submucosa and subserosa. On cut section, it appeared white-gray in color (Fig. ). Microscopically, storiform dense fibrosis and dense lymphoplasmacytic infiltration of plasma cells were identified by hematoxylin and eosin staining (Fig. A and B). On immunohistochemical staining, the tumor stained negative for anti c-kit protein and SMA; thus, GIST could be ruled out. Besides, we found IgG and IgG4-positive plasma cells in a ratio of IgG4/total IgG 40%, and a number of IgG4-positive plasma cells at approximately 60/high powered field (HPF), which indicated that the lesion could be an IgG4-related inflammatory mass (Fig. C and D).
The patient is presently followed up annually in our clinic. In April 2019, the latest follow-up date, the patient did not have any problems and showed no signs of recurrence on endoscopy and abdominal CT examination.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2735,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6243302-1,Extracted,"A 66-year-old white female with a 50 pack-year smoking history presented to our tertiary hospital with acute massive haemoptysis. She had recently moved interstate, with no patient data available in our hospital system. The patient also reported anorexia and weight loss of approximately 3 kg in the past 6 months. On examination, she was afebrile, pulse rate was 90 beats min–1, respiratory rate was mildly increased at 22 breaths min–1 and blood pressure was slightly elevated at 150/90 mmHg. On auscultation of the chest, fine rales over the right lung base were noted. Laboratory results showed normal white blood cell count at 7300 cells l–1 (3.5–11 × 109 cells l–1), C-reactive protein 14 mg l–1 (< 5 mg l–1) and haemoglobin 100 g l–1 (110–165 g l–1). Her initial chest X-ray showed an opacity in the right lower lobe (RLL) contiguous with the right hemidiaphragm (). A CT pulmonary angiogram demonstrated a 2.8 cm solid enhancing nodule in the posterobasal segment of the RLL with a density measuring 35 HU, with a 7 mm central focus of dense calcification (); also noted were hyperdense endobronchial material in the RLL, which was thought to represent fresh blood. A suspicion of lung cancer was raised, especially in view of heavy smoking history and reported weight loss. Positron emission tomography revealed increased 18F-fludeoxyglucose (FDG) uptake [maximum standardized uptake value (SUVmax) of 5] within the RLL nodule; the report described the finding as concerning for malignancy, with the differential diagnosis of an inflammatory pseudotumour (). A subsequent bronchoscopy was complicated owing to active bleeding from the RLL bronchus. The transbronchial biopsy showed no malignant cells, acid-fast bacilli or fungi.
Upon targeted questioning, the patient disclosed having had a complicated cholecystectomy 3 years ago, performed at another hospital, with attempted laparoscopic cholecystectomy converted into an open laparotomy owing to gallbladder rupture with intraperitoneal spillage of gallstones; this was complicated by the formation of post-operative subphrenic abscess, which was surgically drained. The relevant externally performed images have been retrieved, including a CT scan of the abdomen (). The patient further admitted to occasional episodes of minor haemoptysis of about two spoonfuls over the past 2 years, associated with right-sided mild chest pain, which she did not seek medical attention for.
As the RLL mass was the presumed cause for the repeated episodes of haemoptysis, a thoracotomy was recommended and the patient underwent a RLL wedge resection. A firm rhomboid-shaped calculus measuring 11 × 7 × 8 mm () that dislodged from the specimen was confirmed to be a gallstone. Pathological examination additionally found abundant bile pigment (25%) surrounded by microorganisms, extensive interstitial fibrosis and hyalinization. Further biochemical analysis of the calculus revealed the presence of 85% cholesterol. Post-operative recovery was uneventful, and the patient was discharged from the hospital in a satisfactory condition 1 week after the surgery.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [90.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Surgery in the previous 4 weeks': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 90.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 0 + 1 = 1.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1 + 1 =  2.
The patient's Well's score for pulmonary embolism is 2."
2736,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8011470-1,Extracted,"This patient was a 35-year-old Hispanic female with no past medical history who presented to the emergency department primarily for evaluation of heavy vaginal bleeding, bruises on her skin, and fatigue. Vaginal bleeding had started three days prior to presenting to the hospital. The patient had initially thought that she may be pregnant because the onset of her cycle was late by approximately 15 days. The bleeding improved prior to presenting to the hospital but was still much heavier than her usual periods. At the time of heaviest bleeding, the patient reported changing pads every few hours and occasionally passing clots the size of a quarter. Associated symptoms included fatigue, weakness/malaise, abdominal pain, dizziness, and easy bruising. Review of systems was otherwise negative.
Further evaluation revealed that she did not have any bleeding disorders, abortions, or previously late/missed periods in the past. As for obstetric history, the patient had two prior pregnancies that had both gone to full term with vaginal delivery. Family history was also unremarkable for any hereditary bleeding disorders, cancers, or other pertinent medical diagnoses. The patient was not taking any medications at time of hospitalization. Surgical history was unremarkable. Regarding social history, she reported cigarette smoking in the past but had quit for several years, occasional alcohol use, and no current or past illicit drug use. Lastly, the patient had been isolating at home with her partner and their two children.
Physical examination at time of presentation revealed the following vital signs: temperature 36.5 Celsius, pulse of 60, respiratory rate 16, pulse oximetry 100% on ambient air, and blood pressure of 110/66. She remained afebrile and never required supplemental oxygen. In general, the patient appeared tired but was not lethargic or somnolent. Examination of the skin revealed multiple non-palpable purpura on her torso and both upper and lower extremities (Figures , ).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [60.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 60.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 0.
The patient's Well's score for pulmonary embolism is 0."
2737,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8582768-1,Extracted,"A 48-year-old white male presented to the clozapine clinic for routine follow-up and monitoring. The past medical history was significant for schizoaffective disorder; tobacco use disorder; constipation; vitamin D deficiency; and metabolic syndrome characterized by obesity, dyslipidemia, and prediabetes. Current medications included clozapine 150 mg by mouth at bedtime, aspirin 81 mg by mouth daily, docusate 100 mg by mouth twice daily, and cholecalciferol 2000 units by mouth daily. He tried and failed multiple antipsychotics prior to initiation of clozapine 4 years ago. His mental health had been stable since initiating clozapine, and he resides in a group home. He gained 9.5 kg the year after clozapine was initiated, and then weight stabilized. He had difficulty controlling his diet at the group home and ate what was prepared for him. Despite lifestyle education, he continued to visit the vending machine frequently for soda (2 cans per day), candy bars (1 per day), and chips (1 bag per day). He was referred to a dietitian but was unable to successfully implement dietary changes. He did not have access to exercise equipment at his group home and did not walk outside due to inclement weather. He was referred to an exercise program located in the same facility as the clozapine clinic but did not attend the appointments. Metformin initiation for weight management and prediabetes was recommended at several appointments, but he declined because he preferred not to take more medications. He smoked half a pack of cigarettes per day and was not interested in smoking cessation services.
His resting BP was elevated at his past 2 appointments (136/84 and 136/86 mm Hg), so the nurse at his group home had been recording daily BP readings in a log. His BP log revealed an average BP of 138/86 mm Hg. Pertinent vital signs and fasting laboratory results from the appointment were as follows: height: 5 feet, 10 inches; weight: 104.5 kg; BMI: 33 kg/m2; BP: 138/88 mm Hg; pulse: 79 bpm; hemoglobin A1c = 6%; TC = 225 mg/dL; LDL = 136 mg/dL; triglycerides = 395 mg/dL; HDL = 27 mg/dL; clozapine level = 132 mcg/L; norclozapine level = 135 mcg/L; white blood cell count = 8.4 thousand cells/mcl; and absolute neutrophil count = 5.1 thousand cells/mcl.
Clozapine is considered high risk for causing increases in weight, lipids, BG, and BP. This patient had already tried and failed multiple antipsychotics, and his mental health had been stable for 4 years on clozapine. Switching to an antipsychotic with lower liability for metabolic AEs is likely not a feasible option for this patient. Lifestyle interventions are a first-line treatment approach, but the patient had been unsuccessful with altering his diet, exercising, or attempting smoking cessation. Therefore, medically treating the metabolic AEs was necessary.
Hydroxymethylglutaryl-CoA reductase inhibitors (statins) are considered the cornerstone of treatment for lipid lowering due to evidence demonstrating they can prevent ASCVD. There are 4 categories of patients that may benefit from statin therapy, including those with clinical ASCVD, LDL ≥190 mg/dL, diabetes aged 40 to 75 years, and estimated 10-year ASCVD risk score ≥7.5%. An online ASCVD risk estimator can be located at . Individuals with an ASCVD risk score of 7.5% to <20% are considered intermediate risk for a cardiovascular event, and a moderate-intensity statin can be initiated if risk enhancers favor it. Examples of risk-enhancing factors include but are not limited to metabolic syndrome, chronic kidney disease, inflammatory disease (rheumatoid arthritis, psoriasis, HIV), ethnicity (eg, South Asian ancestry), and persistently elevated triglycerides (≥175 mg/dL). Individuals with an ASCVD risk score ≥20% are considered high risk, and statin initiation should be considered with a goal to reduce LDL by at least 50%. Moderate-intensity statins are expected to lower the LDL by 30% to 49% and high-intensity statins by ≥50% ().
Statins are most effective for lowering LDL, but they can also lower triglycerides (22% to 45%) and increase HDL (5% to 10%). Fibrates and niacin are effective for reducing triglycerides but have a mild LDL-lowering effect, and there is not enough evidence to routinely support their use as add-on medications to a statin. Adding a fibrate or omega-3 fatty acids to a statin is recommended for patients with persistently elevated severe hypertriglyceridemia (≥500 mg/dL) to prevent pancreatitis. Fenofibrate is preferred over gemfibrozil in patients being treated with a statin due to lower risk of myopathy. The dose of the statin is another important consideration. The largest percentage of LDL lowering is achieved with the initial dose., Each doubling of the statin dose should then lead to an additional 4% to 7% reduction in LDL., Clinical experience indicates that starting statins at a low dose and titrating up does not lead to the same level of LDL lowering as starting at a moderate- to high-intensity dose. Initiation of a lower intensity statin may be considered if there is a history of statin intolerance.
Stage 1 hypertension is defined as systolic BP 130 to 139 or diastolic BP 80 to 89 mm Hg. Stage 2 hypertension is defined as BP ≥140/90 mm Hg. At least 2 resting BP readings obtained on 2 separate occasions should be used to estimate the BP. A log of home BP readings can provide a more accurate estimation of BP if proper techniques are used. For primary prevention of cardiovascular disease in adults, nonpharmacologic therapy and treatment with an antihypertensive is recommended for individuals with stage 2 hypertension or stage 1 hypertension and a 10-year ASCVD risk of 10% or higher. Initiation of 2 antihypertensive agents from different classes is recommended for individuals with stage 2 hypertension. A BP target of <130/80 mm Hg is recommended. Thiazide diuretics, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), and calcium channel blockers (CCBs) are first-line treatments for hypertension due to evidence demonstrating that they reduce clinical events. There is inadequate evidence to support beta blockers as a first-line treatment for hypertension in the absence of certain cardiovascular comorbidities, such as heart failure or ischemic heart disease. Patient-specific factors, such as comorbidities, concurrent medications, age, race, and medication adherence, should be taken into consideration when selecting an initial antihypertensive.
The optimal treatment for hypertension in individuals with metabolic syndrome has not been clearly defined. Thiazide diuretics can increase insulin resistance and accelerate conversion to diabetes mellitus.,, They can also worsen dyslipidemia., The European Society of Cardiology and the European Society of Hypertension guidelines list metabolic syndrome as a possible contraindication for use of thiazide diuretics. The ACC/AHA guidelines note that small increases in BG levels are possible but also state there are no data available demonstrating deterioration in cardiovascular outcomes in patients with metabolic syndrome who are treated with thiazide diuretics. When no compelling indications or contraindications are present to help guide treatment selection, preference may be given to an ACE inhibitor, ARB, or CCB in patients with metabolic syndrome to help avoid increases in BG. Age and race can also help with treatment selection. Thiazide diuretics and CCBs are preferred in Black adults without heart failure or chronic kidney disease because they are more effective than ACE inhibitors or ARBs. Older adults may also respond better to thiazide diuretics and CCBs due to a declining number of nephrons and lower plasma renin levels.
Using an average BP of 138/86 mm Hg, the patient in this case had a 10-year ASCVD risk score of approximately 17.5%, placing him into a statin benefit group. His known risk-enhancing factors included metabolic syndrome, characterized by persistently elevated triglycerides, obesity, and elevated BP. He also smoked cigarettes. Lifestyle modifications continued to be encouraged, and a risk-benefit discussion about statin therapy was conducted. He was willing to initiate a statin and was started on atorvastatin 20 mg by mouth daily. A moderate-intensity statin was appropriate based on his 10-year ASCVD risk score. His triglycerides were elevated but not enough to warrant addition of a nonstatin therapy. His BP readings in the clinic and at home indicated he had stage 1 hypertension, and his 10-year ASCVD risk score was greater than 10%. The patient did not have any compelling indications or contraindications to help guide selection of an antihypertensive. Given his age, race, and history of metabolic syndrome, initiation of an ACE inhibitor, ARB, or CCB may be most appropriate. After review of the potential AEs associated with each medication class, the patient elected to start amlodipine 5 mg by mouth daily.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [79.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 79.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2738,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7746889-2,Extracted,"A 36-year-old woman, case of pseudomyxoma peritonei, ASA physical status II, hypothyroid, who underwent total peritonectomy, near total gastrectomy, total abdominal hysterectomy, bilateral salpingo-oophorectomy, omentectomy, splenectomy, appendicular stump revision, loop sigmoid colostomy, and an accidental inferior vena cava rent which necessitated inferior vena cava repair, with bilateral intercostal drain placement followed by HIPEC with Doxorubicin 20 mg and Mitomycin-C 20 mg for 45 min. The PCI was 26 and a CC-0 was achieved. Noradrenaline infusion was started during CRS, requirement increasing up to 0.6 µg/kg/min during IVC repair, which was gradually tapered. Coagulopathy correction was started intra-operatively due to massive blood loss (9.4 L), abnormal coagulation parameters and oozing in the surgical field. Fluid management was goal directed as in case 1. The HIPEC phase was shortened to 45 min because of hemodynamic instability.
On shifting to the surgical ICU, patient had a HR of 93/min, MAP: 81 mm Hg, with cold clammy extremities, oropharyngeal temperature of 34.4 °C and noradrenaline infusion ongoing at 0.16 mcg/kg/min. Serum potassium in arterial blood was 2.61 mmoL/L. Subsequently, she developed tachycardia (HR 160/min), hypotension and required fluid boluses (500 mL crystalloid, 250 mL 4% albumin). After 45 min of shifting, patient had cardiac arrest, CPR was given and ROSC was attained after 20 min. Fluid resuscitation and coagulopathy correction was continued in the post-operative period including crystalloids, albumin, blood, and fresh frozen plasma. She was weaned from mechanical ventilation gradually and trachea was extubated on POD 6, required HFNC for 4 days and was shifted to ward on POD 11.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [93.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 93.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 =  1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2739,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7297475-1,Extracted,"A 79-year-old woman with stage IV colon cancer, metastatic to the lungs and the adrenal glands, presented to the emergency department with dry cough and worsening dyspnea on exertion of 1-day duration. She was diagnosed with colon cancer in 2015 and underwent left-sided colectomy and then was treated with adjuvant chemotherapy (5-fluorouracil [5-FU] for a total of 6 cycles). In 2018, she developed left lower extremity edema and was diagnosed with deep venous thrombosis of the left femoral vein and left great saphenous vein and was placed on rivaroxaban. Extensive workup showed metastatic disease to the lungs, adrenal glands, and pelvic lymph nodes. Biopsy of one of the nodes confirmed adenocarcinoma of the colon. She was started on the combination of capecitabine 1000 mg twice a day (day 1 to day 14 every 21 days) and bevacizumab 7.5 mg/kg (day 1 every 21 days) and received the first dose of bevacizumab 1 week after starting capecitabine; she has never been on those drugs before. Less than 24 hours after the bevacizumab dose, she started having a dyspnea on exertion that was worsening and was associated with a dry cough and fatigue.
She was tachycardic and tachypneic on admission (heart rate was 122 bpm, respiratory rate was 24 breaths/min). Her blood pressure was 163/110 mm Hg. Her Sao2 was 84% on room air. She was placed on noninvasive positive pressure ventilation for respiratory distress with minimal improvement on oxygen delivery therapies. Stat arterial blood gas showed acute hypoxic respiratory failure (pH of 7.26, Pco2 of 47, Po2 of 248, HCO3 of 21). She was subsequently intubated and required intensive care.
Her admission blood work was significant for mild leukocytosis (white blood cell count of 13.42/μL, with 82% neutrophils) (see ). Chest radiograph showed bilateral basilar opacities (see ). Computed tomography (CT) of the chest with intravenous contrast redemonstrated bilateral airspace opacities with a slight central distribution (see ).
She was started on broad-spectrum antibiotics due to suspicion of multifocal pneumonia. All cultures and gram stains for infectious etiologies including common bacteria, fungi, legionella, viruses, and Pneumocystis were negative. Intravenous antibiotics were discontinued when cultures came back negative; patient received antibiotics a total of 5 days. Bronchoscopy and bronchoalveolar lavage (BAL) were performed, and cytological examination of BAL fluid sample showed rare mildly atypical cells; it favored reactive mesothelial cells, histiocytes, and bronchial cells in a background of marked acute inflammation. Cultures of BAL were negative for bacteria, mycobacteria, or fungal pathogens. Pneumocystis jiroveci was not detected by polymerase chain reaction. Transthoracic echocardiogram showed a left ventricular ejection fraction of 55%, a grade I diastolic dysfunction, and moderate pulmonary hypertension. On day 6 of hospitalization, the patient was started on intravenous methylprednisolone 60 mg given every 8 hours with the aim to treat presumed interstitial pneumonitis. Subsequently, the patient’s condition improved significantly, and she was extubated within 2 days of corticosteroid therapy initiation. Post-extubation, bilevel positive airway pressure–assisted ventilation was used as needed and she was subsequently transitioned to daily oral prednisone 40 mg. Arterial blood gas analysis on 3 L nasal cannula then showed a pH of 7.54, Pco2 of 38, Po2 of 159 and an oxygen saturation of 98%. Chest radiograph on discharge showed partial resolution of the bibasilar opacities (see ). Eventually, the patient was discharged after 3 weeks on therapeutic subcutaneous enoxaparin and long-term oxygen therapy as needed with a gradual taper of steroid. She eventually signed a Do Not Resuscitate/Do Not Intubate form and was put on hospice care. No further chemotherapy was administered.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [122.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 122.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3.0 + 1 =  4.0.
The patient's Well's score for pulmonary embolism is 4.0."
2740,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8452543-1,Extracted,"A 58-year-old gentleman with a history of hypertension, hyperlipidemia, obesity, rheumatoid arthritis (RA), tobacco abuse, and opiate abuse on methadone presented to the emergency department (ED) with a worsening nonproductive cough and shortness of breath of four days duration. His symptoms were associated with generalized myalgia, fatigue, diaphoresis, and non-bloody diarrhea. He denied sick contacts but was employed as a maintenance manager with a focus on air conditioner repair.
To note, he was originally diagnosed with osteoarthritis in the context of bilateral knee pain, associated swelling, and morning stiffness, however, was subsequently diagnosed with RA that was managed with chronic daily prednisone (30 mg) for three years before transitioning to adalimumab, a tumor necrosis factor-alpha (TNF-a) inhibitor. He received his first infusion one week prior to the hospital presentation.
In the ED the patient was afebrile, normotensive (132/82 mmHg), but markedly tachycardic (157 beats per minute), tachypneic (30 breaths per minute), and hypoxic to 72% on room air. There was a minimal improvement with nasal cannula and nonrebreather, and the patient was initiated on heated high flow nasal cannula (55 L; 100% FiO2) with improved saturation to 95%. Physical examination revealed an obese gentleman with cushingoid features (buffalo hump, abdominal striae) and bilateral lower limb pitting edema. Cardiac examination was unremarkable and pulmonary auscultation revealed bilateral decreased breath sounds in the lower lobes. Joints evaluation revealed mild bilateral knee swelling and effusions without additional joint deformities. Laboratory diagnostics demonstrated mild leukocytosis with a slight neutrophilic predominance, but no evidence of anemia or thrombocytopenia. The metabolic panel was notable for an elevated blood urea nitrogen, creatinine (baseline < 1), and transaminitis with elevated inflammatory markers (Table ). Urinalysis was unremarkable with the exception of microscopic hematuria. Nasopharyngeal swab for COVID-19 RNA polymerase chain reaction (PCR) and urinary legionella antigen were positive. Diagnostic imaging included a chest radiograph that demonstrated extensive consolidation throughout the left lung field with air bronchograms involving the upper lobe, lower lobe, lingula, and right upper lobe (Figure ). Chest CT was negative for pulmonary embolism but revealed complete opacification of the left lung fields with diffuse pneumonia and associated air bronchograms, trace pleural effusion, and multiple ground glass alveolar infiltrates involving the right upper, middle, and lower lobes (Figure ).
The patient was admitted to the intensive care unit (ICU) for acute hypoxic respiratory failure in the setting of COVID-19 and Legionella pneumonia and initiated on dexamethasone (10 mg, daily; 10 days), remdesivir (daily; 5 days), azithromycin (500 mg, daily; 14 days), and ceftriaxone (1 g, daily, 7 days). It took 18 days to wean him to room air and prior to discharge, repeat COVID testing was negative. He was discharged on prednisone 30 mg daily for his RA and sulfamethoxazole-trimethoprim (Bactrim double strength, DS 800-160 mg) thrice weekly for pneumocystis carinii pneumonia (PCP) prophylaxis.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [157.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 157.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2741,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8642122-1,Extracted,"A 69-year-old man presented to the emergency room with two weeks of exertional dyspnea, unable to ambulate greater than 50 feet. Cardiopulmonary examination showed blood pressure of 131/82 mmHg, heart rate of 77 beats/min, a laterally displaced point of maximal impulse, bilateral dependent lung crackles, and bilateral lower extremity pitting edema. Medical history included uncontrolled hypertension, uncontrolled hyperlipidemia, peripheral artery disease, 50 pack-year smoking history, and alcohol use disorder. No history of recreational drug use was reported. Patient had no prior surgical history. The differential diagnosis for the etiology of clinical heart failure in this patient included ischemic cardiomyopathy, alcoholic cardiomyopathy, hypertensive heart disease, and heart failure with preserved ejection fraction.
On admission, a 12-lead electrocardiogram showed sinus rhythm with QS waves in leads V2-V4. Laboratory studies showed troponin I of 0.04 ng/ml and brain natriuretic peptide of 2498 pg/ml. Transthoracic echocardiography (TTE) showed left ventricular ejection fraction of 30%-35% with moderate to severe global hypokinesis. Given patient’s high likelihood of coronary artery disease, he underwent coronary angiography for workup of his cardiomyopathy, which revealed a diffusely diseased left anterior descending coronary artery (LAD) with worst stenosis up to 70%-80% (Figure -).
Patient was deemed not a candidate for coronary bypass graft surgery (CABG) by cardiothoracic surgery; thus, PCI with intravascular ultrasound (IVUS) guidance was performed. The LAD lesion was crossed using a Choice PT wire (Boston Scientific, Marlborough, Massachusetts, USA) and predilated using multiple compliant balloons with good expansion. A 3.0 x 28 mm drug-eluting stent (DES) was implanted in the distal LAD, 3.5 x 38 mm DES in the mid-LAD, and 3.5 x 28 mm DES in the proximal LAD with a very good final angiographic result (Figure ). The IVUS was used prior to stent implantation for lesion characterization and vessel sizing and post-stenting to confirm adequate stent expansion and apposition without any edge dissection. However, there was an occlusion of a septal perforating artery due to being jailed by the LAD stent struts (Figure ). We opted not to intervene on this septal branch to avoid disruption of LAD stent struts. Moreover, the patient did not have any clinical signs or symptoms from losing this septal branch. He did well and was subsequently discharged on appropriate medical therapy.
Six-month post-PCI, TTE showed improved left ventricular ejection fraction to 55%, but thinning of the midanteroseptum and midinferoseptum was noted (Figure -). No ventricular septal perforation was detected after evaluating the defect on multiple views with color Doppler.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [77.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 77.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 0.
The patient's Well's score for pulmonary embolism is 0."
2742,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7307622-1,Extracted,"A 25-year-old female presented with complaints of shortness of breath, giddiness, and generalized weakness. She had a history of recurrent abortions at the gestational age of 2–3 months twice. Currently, she was 4 months gravida and was sent to us for two-dimensional (2D) echocardiography by her treating gynecologist.
On examination, her blood pressure was 100/70 mmHg; pulse rate was 94/min; and oxygen saturation by pulse oxymeter was 88%. There was no evidence of cyanosis or clubbing. On cardiovascular examination, apex beat was present in the left 5th intercostal space in midclavicular line, parasternal heave present, P2 palpable, and S1 loud.
Ejection systolic murmur was present in the pulmonary area. Her electrocardiography was done, which revealed incomplete RBBB but no other significant abnormality [].
A 2D transthoracic echocardiogram was performed in the usual manner with a Vivid T8 General Electric (Milwaukee, Wisconsin, USA) ultrasound system and a 3 MHz transducer. It showed situs solitus of the atria, AV concordance, D-loop ventricles, and ventriculoarterial concordance. There was a complete absence of interatrial septum, dilated right atrium, and right ventricle associated with morphologically normal AV valves attached at the same level at crux [ and ].
There was no evidence of any ventricular septal defect or patent ductus arteriosus. There was no cleft in mitral leaflets, no mitral regurgitation, mild tricuspid regurgitation (TR), and significant pulmonary arterial hypertension measured by TR jet velocity [Figures and and Supplementary Videos –].
On the basis of echocardiographic findings suggestive of SA, significant pulmonary hypertension, and arterial desaturation, the patient was sent for cath study followed by further management.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [94.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Surgery in the previous 4 weeks': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 94.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 0.
The patient's Well's score for pulmonary embolism is 0."
2743,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5313357-1,Extracted,"A 44-year-old female presented with vaginal bleeding along with exertional chest discomfort. Vitals signs at the time of presentation were insignificant except for pulse 101 beats per minute with the normal electrocardiogram. However, she had no any past history of cardiovascular disease. Gynecological evaluations revealed cervical cancer (squamous cell carcinoma, stage IVB) which instigated further investigations and evaluations. Whole body positron-emitting tomography computed tomography (PET-CT) () revealed right ventricular mass possibly malignancy or tumor thrombus with enlarged lymph node in left inguinal area and retroperitoneum without other distant metastasis. For further evaluation of tachycardia and dyspnea occurred a week before visiting the hospital, transthoracic echocardiography () and pro B-type natriuretic peptide measurement were performed. Pro B-type natriuretic peptide was within the normal range but transthoracic echocardiography revealed right ventricular mass doubtful of malignant mass or tumor thrombus. Hence, she was referred to Department of cardio-thoracic surgery for further evaluation and management. She underwent total bypass surgery and removal of the mass. Histopathology revealed the mass to be a metastatic lesion from the cervical squamous carcinoma. Postoperatively, the patient received 175 mg/m2 paclitaxel (Genexol, Samyang, Seoul, Korea) and 50 mg/m2 of cisplatin for 12 cycles with 3 weeks apart. Until 9th cycle of chemotherapy, there was no relapse of disease which was confirmed by abdomen CT. She then underwent additional 3 cycles of chemotherapy as laboratory test and serum squamous cell carcinoma antigen level (5.2 ng/mL, normal <12.5 ng/mL) reported normal. A contrast enhanced CT was done after additional 3 cycles which unfortunately showed suspicious of newly metastatic lesion in the bladder. She tolerated the chemotherapy well till the 7th cycle only when she started complaining dyspnea on mild exertion. However, echocardiography was normal. Two months after completing 12th cycle, she started to suffer from the dyspnea again. CT scan of chest was performed, which confirmed the increased extent of focal filling defect (thromboembolism) in right pulmonary artery. Echocardiography showed newly developed severe pulmonary hypertension with right ventricular dysfunction. She was then treated with the intravenous heparin because of which she developed severe per vaginal bleeding. Unfortunately, she died of pulmonary embolism fourteen months and 4 weeks from the diagnosis of cardiac metastasis.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [101.0, 'beats per minute'], 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Immobilization for at least 3 days': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 101.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3.0 + 1 =  4.0.
The patient's Well's score for pulmonary embolism is 4.0."
2744,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6396799-1,Extracted,"A 67-year-old woman presented to our hospital with a 2-day history of pain and a feeling of coldness in her right hand. In her past medical history she had not received any treatment for dyslipidemia. There is no other medical history or smoking history. Upon physical examination she had no heart murmur or leg edema; her blood pressure was 154/96 mm Hg (left brachial), and oxygen saturation of peripheral artery was 96% at room air. Her right hand was pale and the right radial artery was pulseless. An electrocardiogram (ECG) showed sinus rhythm at 79 bpm. The serum D-dimer level was slightly increased (2.18 µg/mL). Computed tomography (CT) scan confirmed thromboembolism in the distal part of the right brachial artery, left pulmonary artery and right kidney infraction (). Cerebral infraction and stenosis of the main cerebral artery were not detected by the head magnetic resonance imaging (MRI)/magnetic resonance angiography (MRA).
Doppler sonography of right upper limb revealed the disappearance of blood flow at the distal part of the brachial artery, and collateral circulation to the radial artery from the brachial artery. In this case, multiple thromboemboli occurred in both the systemic and pulmonary circulation. Thus, we suspected paradoxical thromboembolism. Transesophageal echocardiogram and venous ultrasonography findings showed the presence of a PFO and DVT (). Thus, we diagnosed paradoxical embolism due to PFO. Photoplethysmogram (PTG) of her right hand was very slow on admission (). The condition of her right upper limb had been relieved from 2 days previously due to the development of collateral circulation. Therefore, we thought that neither emergency operation nor catheter intervention for thrombectomy was necessary in this patient. We started treatment with urokinase (UK) 240,000 U/day intravenous injection (IV) and unfractionated heparin (UFH) continuous IV (target activated partial thromboplastin time (APTT) 60 - 80 s). As her condition and the serum D-dimer level were improving we started catheterization at day 7 after admission (); however the thrombus still remained in the brachial artery. Although her pain was relieved, her right hand was still cold and PTG of the right hand at day 7 was slow. For her outpatient care, based on the viewpoint of providing rapid anticoagulant therapy within the therapeutic range, having longest periods of initial intensive therapy we chose treatment using ribaroxaban (15 mg, two tablets twice daily) (). Three weeks after discharge from the hospital, her right hand had become warm and the serum D-dimer level and PTG were normalized (). From that time, we changed ribaroxaban to the maintenance dose (15mg, one tablet once daily). Three months after discharge, Doppler sonography and MRA of her right arm confirmed the achievement of reperfusion of her brachial artery ().",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [79.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 79.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3 + 1.5 = 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2745,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8223078-1,Extracted,"A 56-years-old woman with history of hypertension, decompensated diabetes mellitus, was referred to our hospital with critical limb ischemia (CLI) presenting rest pain and ulcer on the left leg and negative COVID-19. On physical examination, her blood pressure was 160/90 mmHg with 130 b/m. Auscultation of the abdomen revealed a mesogastrium systolic bruit. Electrocardiogram showed signs of ST segment depression without thoracic pain. Coronary angiography was positive for severe coronary artery disease with no indication to treatment. Duplex ultrasound (DUS) revealed widespread irregularities of the aortic wall with monophasic wave on right common femoral artery and direct flow on the left femoral axis; diffuse disease of both superficial femoral arteries (SFA) with distal occlusion in the left side.
CT-scan showed atherosclerotic disease on infrarenal abdominal aorta with focal dissection, occlusion of right common iliac artery origin and short dissection of the left common iliac artery origin not hemodynamically significative ().
The presence of ulcers in the left leg was the indication to address the left SFA throughout an antegrade percutaneous homolateral access with drug eluting balloon (DEB) angioplasty in the proximal SFA (6.0 × 60 mm Luminor®; iVascular, Vascular S.L.U., Barcelona, Spain) and distal stenting (5.0x80mm iVolution; iVascular) (). The final result was a complete lesion healing in the left foot at three weeks ().
After two months of the index procedure, the patient was readmitted due to gangrene of the right foot and asymptomatic COVID-19 infection. The control CT showed a similar vascular pattern on the right side with no significant difference with the previous CT. At this stage, the rapid and aggressive right foot lesions evolution was the indication to address vascular lesions in the right axis.
The intervention was carried under general anesthesia with surgical exposure of both common femoral arteries employed as remote accesses for multilevel endovascular intervention. The first step consisted of aorto-iliac repair (aortic dissection and right common iliac occlusion) using an AFX aortic endograft (Endoogix Inc., Irvine, CA, USA); stenting of the right common iliac artery (balloon expandable stent - Isthmus 10 × 39; CID SpA, Saluggia, Italy).
During the same operation, the right SFA disease was addressed with a DEB (Luminor 5 × 200 iVascular) (). The multiple intervention determined the increase of the distal flow and the reappearance of dorsalis pedis pulse. After two days, the patient was asymptomatic for right foot pain and underwent to right foot minor amputation. The patient was discharged after a week with double antiplatelet therapy. CT angiography performed after two months confirmed the proper positioning of the aortic stent-graft with good patency of iliac-femoral axis and right foot ulcers healing ().",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [130.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 130.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2746,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4070354-1,Extracted,"A 77-year-old Japanese woman was admitted to our hospital because of fever of unknown origin. She had developed general fatigue and a slight fever 2 weeks before admission. Headache and a fever higher than 38°C had developed 3 days before admission, and oral cefditoren pivoxil prescribed at another hospital had been ineffective. She had a 2-year history of polymyalgia rheumatica and chronic gastritis. She had initially been treated with 15 mg/day of prednisolone for the polymyalgia rheumatica. Her dosage of prednisolone was tapered with improvement of her symptoms, and she had been treated with prednisolone (5 mg/day) and famotidine (20 mg/day) for 1 year before admission. She had no other medical or family history and did not smoke or drink alcohol. Physical examination on admission revealed a height of 156 cm, weight of 49 kg, temperature of 40.2°C, heart rate of 120 beats/min, and blood pressure of 116/62 mmHg. No obvious abnormalities of the chest or abdomen were found with the exception of slight right flank pain. Neurological examination also showed normal findings; her Glasgow Coma Scale (GCS) score was maximal at 15 (E4V5M6). She was ambulatory; no symptoms suggesting agnosia, agraphia, or any other higher brain dysfunction were observed on admission. In addition, finger perimetry showed no obvious visual field deficits. Laboratory findings showed a high WBC count (20,200/mm3), platelet count (40.4 × 104/mm3), and CRP level (10.02 mg/dl). Chest X-ray, abdominal X-ray, and electrocardiographic findings were normal. Urinalysis revealed pyuria with markedly increased WBCs and gram-negative bacilli, suggesting a urinary tract infection. Intravenous administration of ampicillin (6 g/day) was begun immediately after admission. On day 4, her body temperature remained higher than 38°C despite improvement in the WBC count (18,300/mm3) and CRP level (3.91 mg/dl). On the same day, E. coli was revealed in urine and blood culture specimens taken on admission. Although the E. coli was sensitive to ampicillin, we substituted ceftriaxone (2 g/day) for ampicillin on day 4 based on the results of the antibiotic sensitivity test.
On day 5, her body temperature dropped to 37.5°C. However, she began to drop her spoon frequently during meals and complain of difficulty in donning her shirt. On day 6, she complained of difficulty in seeing. Although she did not exhibit severe palsy or ataxia, she could no longer eat a meal, change her clothes, or walk by herself without nursing care. She was considerably confused, and it was difficult to evaluate her neurological function precisely. Her level of consciousness sharply deteriorated thereafter, and her GCS score dropped to 9 (E2V3M4). Her WBC count and CRP level on day 6 were 15,600/mm3 and 3.63 mg/dl, respectively. Electrolyte, thyroid hormone, and blood glucose levels were normal. Plain brain CT on day 6 showed debris in the right lateral ventricle and a tumor-like lesion in the left posterior lobe (Figure A). Contrast-enhanced MRI on day 6 revealed a tumor-like lesion in the left posterior lobe with ring-like enhancement on T1-weighted imaging (Figure B). On diffusion-weighted imaging, this lesion also showed homogenous high intensity, which seemed to be connected with the left lateral ventricle, and obvious debris was present in both lateral ventriculi (Figure C). Based on these findings, we considered that ventricular rupture of a brain abscess was the most probable cause of her deterioration. The size of the abscess was 1.6 × 1.8 cm. Subsequent abdominal contrast-enhanced CT on day 6 showed a unilocular right renal cyst with heterogeneous and high-density content, suggesting a renal cyst infection (Figure A). Abdominal ultrasonographic findings were inconclusive for a cyst infection. Contrast-enhanced chest CT showed no remarkable findings. Further laboratory and transthoracic echocardiographic diagnostics excluded potential risk factors for brain abscess, such as human immunodeficiency virus infection, fungal infection, endocarditis, and pulmonary hypertension. We immediately consulted with neurosurgeons and decided to manage the right occipital lesion with intravenous meropenem administration (6 g/day). Her consciousness gradually improved thereafter; her GCS score recovered to 12 (E3V4M5) on day 9. She was slightly confused and showed impaired orientation, but her ability to converse with us had improved. Brain MRI on day 9 revealed no remarkable changes in the size of the abscess. No signs of high intracranial pressure or hydrocephalus were present either clinically or radiographically. Cerebrospinal fluid (CSF) analysis on day 9 revealed a slight increase in leukocytes (64/mm3), including 23/mm3 (36%) lymphocytes and 41/mm3 (64%) neutrophils with no atypical cells, as well as high total protein (517 mg/dl) and low glucose (21 mg/dl) levels. Microscopy of CSF smear samples with methylene blue staining, India ink capsule staining, and Gram’s staining detected no bacteria or fungi. The CSF culture was sterile. On day 12, her body temperature remained below 37.5°C, but her WBC count (14,900/mm3) and CRP level (4.01 mg/dl) remained high. Additionally, her right flank pain persisted despite antibiotic therapy. MRI on day 12 showed no deterioration of the brain abscess. Based on these findings, we concluded that CT-guided drainage was needed to manage the renal cyst infection. The drainage procedure was performed on day 13, and E. coli from the aspirated pus showed the same sensitivity to antibiotics as did the E. coli from the blood and urine on admission. The patient showed good progress thereafter. The drainage catheter was removed on day 20. Her GCS score recovered to 15 on day 22. On day 30, she showed almost normal activities of daily life, although she still experienced difficulty in seeing. Her WBC count and CRP level normalized, and enhanced brain MRI showed a dramatic decrease in the abscess size (Figure D). Moreover, abdominal enhanced CT on day 35 showed that the right renal cyst had decreased in size (Figure B). Formal perimetry was performed by an ophthalmologist on day 35 and showed obvious right inferior quadrantic hemianopsia. Moreover, transesophageal echocardiography using contrast medium on day 35 showed no cryptic abnormalities, including intracardiac right-to-left shunting or small vegetations. Intravenous administration of meropenem was terminated on day 42, and no deterioration was observed even in the absence of oral antibiotics. Following rehabilitation, she was discharged from the hospital on day 60 with right inferior quadrantic hemianopsia as an aftereffect. She has been followed up for 6 months since discharge, and no recurrence of the brain abscess or renal cyst infection has been observed.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2747,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8136881-1,Extracted,"An 86-year-old woman with a history of atrial fibrillation, aortic stenosis, and hypertension presented to the emergency department due to altered mental status. She was lethargic, confused, and was not answering questions appropriately for the past four days. On arrival, she was afebrile, and her vitals included a pulse of 139 beats per minute, blood pressure of 110/79 mmHg, and a respiratory rate of 16 breaths per minute with saturation of 96% on room air. Physical exam was significant for a slow to respond female, orientated to self, who was able to follow commands with no focal neurological deficit. Her skin was warm and well-perfused with normal capillary refill, with no rashes or petechiae. The cardiovascular exam was significant for tachycardia, an irregular heart rhythm, and a systolic murmur heard best at the right upper sternal border. She had lower extremity pitting edema bilaterally. Her lab results were notable for elevated white blood cell count (WBC) 25.2 x 103 μL (3.9-11.3 x 103 μL), hemoglobin 11.0 g/dL (11.3-15.1 g/dL), platelets 58.0 x 103 μL (165-366 x 103 μL), troponin 0.164 ng/mL (<0.010 ng/mL), lactic acid 2.5 mmol/L (0.5-2.0 mmol/L), and a basic chemistry panel was within normal limits. The urinalysis was remarkable for the presence of WBCs, leukocyte esterase, and bacteria with a urine culture pending. Additionally, two sets of blood cultures were obtained. Her electrocardiogram was significant for atrial fibrillation with a rapid ventricular rate (RVR). She was started on ceftriaxone for probable UTI and was admitted to the hospital for further management. Further diagnostics included lower extremity Doppler ultrasound, which revealed deep venous thrombosis (DVT). A bedside echocardiogram indicated right ventricular strain, and the N-terminal proB-type natriuretic peptide level was elevated at 8,215 pg/mL (<449 pg/mL). Due to concern for possible pulmonary embolism in the setting of known DVT, the patient was started on a continuous heparin infusion. A transthoracic echocardiogram revealed severe aortic valve calcification with new aortic insufficiency. Blood and urine cultures returned positive for Aerococcus urinae. A transesophageal echocardiogram further confirmed moderate to severe aortic regurgitation with findings suggestive of infective endocarditis (IE), see Figures , .
Antibiotics were expanded to include gentamicin with ceftriaxone for IE, and surgical evaluation was consulted. Given she was a high-risk surgical candidate, surgery intervention was not offered at this time unless evidence of further clinical decompensation. Additional surgical recommendations included re-evaluation after completion of antibiotic course. She was therefore discharged on intravenous antibiotics to complete a total of six weeks of treatment with ceftriaxone and two weeks of gentamicin. Soon after completion, the patient returned due to worsening thrombocytopenia that had previously improved upon discharge. On readmission, repeat labs were most notable for worsening thrombocytopenia, leukocytosis, acute kidney injury, and hyperkalemia. The patient was in atrial fibrillation with RVR and physical exam concerning for decompensated heart failure. Despite administration of broad-spectrum antibiotics and heart rate control, the patient continued to decline, and her clinical picture was consistent with cardiogenic shock. In addition to respiratory distress, the patient went into ventricular fibrillation arrest. Due to the patient's wishes to not be intubated or resuscitated, she was made comfortable and passed away.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [139.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False}",7.5,7.5,7.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 139.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 = 6.0.
The patient not been diagnosed with pulmonary embolis (PE), but the patient has previously been diagnosed with deep vein thrombosis (DVT), we increase the current total by 1.5 so that 6.0 + 1.5 = 7.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 7.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 7.5.
The patient's Well's score for pulmonary embolism is 7.5."
2748,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4780201-1,Extracted,"A 68-year-old male patient 17 years after heart transplant was referred to our outpatient clinic for a regular follow-up. The patient was transplanted by biatrial method due to end-stage heart failure following a viral infection in July 1997. The Donor was a 37-year-old male without known risk factors. Postoperative course was uneventful under immunosuppression therapy with cyclosporin with no rejection episodes. The patient's post-HTx history included well controlled hypertension, mild chronic kidney disease, and prostatic hypertrophy.
Physical examination revealed good overall clinical condition, with normal blood pressure of 140/90 and a regular heart rate of 85/min. Standard laboratory findings were within reference ranges except for creatinine level of 1.5 mg/dL and GFR of 45 mL/min. Standard ECG demonstrated a regular sinus rhythm of 85 bpm, QRS duration within normal range and no ST segment deviation or T-wave abnormalities. Echocardiography revealed normal left ventricular function with EF of 60% and mild left ventricular hypertrophy of the graft that was noted during follow-up. Coronary angiography (2 years prior) showed normal coronary arteries without features of graft vasculopathy. Last myocardial biopsy performed in 2013 showed no signs of cellular rejection (ACR Grade 0 R). Standard graded cycle ergometry exercise test limited by exhaustion was performed (target HR was not used). Resting heart rate (82 beats/min) and BP values (140/84 mmHg), slowly increased up to 100 beats/min and 185/90 mmHg, respectively over 7 min. Maximal workload achieved was 75 W. During recovery phase a delayed HR recovery was noted, with HR gradually returning to its baseline value over 9 min.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [85.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 85.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2749,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4432902-1,Extracted,"A 36-year-old Caucasian female attended the accident and emergency department with right-sided chest pain. The pain was described as dull and aching, with a pleuritic nature. It was sited diffusely over the right anterior and lateral chest wall and was reproducible on palpation. The pain had increased in severity over the preceding 6 weeks and at the time of admission was associated with mild dyspnea. Prior to presentation, the patient reported no weight loss, fevers or night sweats. Her family history and past medical history were unremarkable. However, she was a cigarette smoker (10 pack-year history).
On examination, the patient was pale and tachypnoeic. Her observations demonstrated a borderline tachycardia at 92 beats per minute and pulse oximetry of 92% on room air. On examination of the respiratory system, there was decreased expansion, dullness to percussion and decreased breath sounds over the right hemithorax. There was no jaundice, digital clubbing, skin changes or palpable lymphadenopathy. The breast examination was unremarkable.
Initial laboratory findings demonstrated a leukocytosis (white blood cells 18.6 × 109/L) and neutrophilia (neutrophils 15.9 × 109/L), anemia (hemoglobin 9.8 g/dL), thrombocytosis (platelets 518 × 109/L), hypercalcemia (corrected calcium 2.81 mmol/L), and raised C-reactive protein (117 mg/L).
A chest radiograph revealed complete opacification of the right hemithorax with mild mediastinal shift to the left side (). This was further characterized by a contrast enhanced computed tomography (CT) scan of the thorax, abdomen and pelvis which showed a large loculated right pleural effusion with associated right lung collapse, significant multifocal right-sided pleural thickening, and multiple pulmonary nodules on the left. No abnormalities were seen below the diaphragm, save for some simple renal cysts. Appearances were reported to be likely in keeping with pleural and pulmonary metastases ().
The patient went on to have an ultrasound guided Seldinger chest drain inserted. Seven hundred twenty milliliters of heavily blood stained pleural fluid drained and was sent for analysis: pH 6.99, protein 52 g/L, and LDH 642 IU/L. Cytological analysis did not detect any malignant cells. The microscopy and subsequent culturing was unremarkable.
Considering the patient’s young age and the radiological findings, our provisional diagnosis was malignancy with a likely primary of breast, ovary, lymphoma or lung. With this in mind our patient went on to have an ultrasound examination of her breasts, which revealed some areas of benign breast changes but no focal suspicious appearances. Transvaginal ultrasound demonstrated an anteverted uterus, endometrial thickness of 5 mm and normal ovaries.
Despite chest drain insertion and the initial volume drained, we were subsequently unable to remove a significant volume of pleural fluid from the right hemi-thorax. The patient was referred to a tertiary center with cardiothoracic facilities where video-assisted thoracoscopic surgery (VATS) was performed. This allowed successful evacuation of the septated pleural effusion and the opportunity to perform pleural biopsies.
The histological diagnosis was confirmed by both conventional examination demonstrating the characteristic tumor cells with cords and nests, and immunohistochemistry with expression of MNF116 and CK7, D2-40, CD31 and CD34 antibodies ().
Post-operatively our patient recovered well and was referred for specialist oncological input which she received at a quaternary London cancer center. Although an effective treatment for pleural PHE has yet to be established, Pinet et al [] have reported the case of an aggressive pleural PHE which had a complete response to treatment with carboplatin and etoposide. Our patient received weekly cycles of paclitaxel, a mitotic inhibitor, which has also demonstrated a clinical response in case reports [], for a 3-month period. Unfortunately, during this time she required frequent admissions for pain control and sadly passed away 6 months after her diagnosis.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [92.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Surgery in the previous 4 weeks': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 92.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
2750,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3542936-1,Extracted,"A 53-year-old man was brought in by ambulance with the chief complaint of multiple “fainting” episodes. He was reported by the paramedics to be hypotensive and tachycardic prior to arrival. His past medical history was significant for hypertension, chronic renal insufficiency, and gouty arthritis. On presentation to the emergency department, the patient appeared critically ill with generalized pallor, perioral cyanosis, with a heart rate of 133 beats per minute (bpm), blood pressure of 130/106 mm Hg, and oxygen saturation of 100% on 15 L O2 via a nonrebreather mask. His exam was significant for grunting, otherwise clear bilateral breath sounds, rapid but regular heart tones, weak femoral pulses, and symmetric, non-edematous lower extremities.
Shortly after arrival, a bedside ultrasound was performed, demonstrating a thrombus in the right ventricle (RV) and inferior vena cava (IVC) (Figures and ). The patient lost cardiac motion during the ultrasound, and cardiopulmonary resuscitation (CPR) was initiated with return of spontaneous circulation within one minute. He was emergently intubated, and his postintubation oxygen saturation was noted to be 60%, despite 100% FiO2 and confirmation of adequate tube placement. A repeat bedside ultrasound was performed with visualization of an enlarged right ventricle (), and an EKG demonstrated a new right bundle branch block (), highly suspicious for a massive pulmonary embolus. Shortly thereafter, the patient again lost pulses requiring CPR and 1 mg IV epinephrine, with subsequent return of spontaneous circulation in three minutes. The patient's blood pressure was maintained on a continuous infusion of epinephrine, and bolus dosing of alteplase (tPA) was being prepared while a CT angiogram (CTA) of the thorax was ordered. The CTA confirmed the diagnosis of bilateral massive pulmonary emboli (PE) (), and alteplase was administered at a bolus dose of 0.6 mg/kg over 2 minutes followed by a heparin infusion and admitted to the ICU without further hemodynamic decompensation.
The patient's course was complicated by bilateral pneumothoraces, acute renal failure, and subconjunctival hemorrhage. However, he was ultimately extubated and discharged home with full neurologic recovery, and a repeat CTA chest demonstrated resolution of pulmonary thrombi (). A deep venous thrombosis (DVT) in the left distal popliteal vein with an aneurismal dilation of the popliteal vein was diagnosed during his inpatient stay, thought to be related a recent flare of gouty arthritis. The patient is currently awaiting outpatient work-up for possible coagulopathy and continues on warfarin anticoagulation.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [133.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Surgery in the previous 4 weeks': False}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 133.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
2751,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5018319-1,Extracted,"A 75-year-old gentleman with a past medical history of diabetes (DM), hypertension (HTN), prostate cancer status postprostatectomy, and end stage renal disease (ESRD) on hemodialysis was admitted from his dialysis center for an elective thrombectomy of his clotted left upper extremity arteriovenous graft (AVG). This finding had prompted insertion of a right subclavian permacath two weeks prior to admission. The patient was afebrile, with a blood pressure of 110/70, heart rate of 70 bpm, and an oxygen saturation of 97% on room air. On cardiovascular exam, he had normal S1 and S2 with no appreciated murmurs, rubs, gallops, jugular venous distension, or lower extremity edema. His basic lab panel was unremarkable and no leukocytosis was noted. He was originally scheduled for thrombectomy of the graft by vascular surgery but then was found to have asymptomatic Mobitz-I AV block on EKG which prompted cardiac evaluation. During this evaluation, a transthoracic echocardiogram (TTE) was significant for a prominent echodensity in the right atrium (RA). A subsequent transesophageal echocardiogram (TEE) demonstrated a serpiginous, highly mobile, elongated, oscillating echodensity measuring 8.4 cm × 0.5 cm prolapsing across the tricuspid valve orifice, probably consistent with thrombus [Figures , , and ]. The thrombus was seen attached to the anterolateral aspect of the right atrium at what appeared to be the site of microtrauma ensuing from the tip of the deep seated permacath. Intravenous heparin was immediately started and the patient was boarded for direct thrombolysis via EKOS catheter which was inserted through a 7 French sheath into the left subclavian graft. A Wholey wire was advanced into the right ventricle (RV) and the EKOS catheter was placed through the dialysis line into the RA and through to the RV. An alteplase bolus of 5 mg was administered and was continued as a drip at a rate of 2 mg/hr for 10 hours.
A follow-up TEE upon discontinuation of local thrombolytics showed resolution of the thrombus []. The patient was then started on warfarin. The hypercoagulability workup came back negative except for an elevated homocysteine level of 27 μm/L (3.2–10). Our patient remained hemodynamically stable throughout his admission without suspicion of PE. Permacath was removed two weeks later.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [70.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 70.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2752,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7027063-1,Extracted,"A 23-year-old female Chinese university student presented to the emergency department with acute onset dyspnoea, chest pain, palpitations and dizziness for 2 days. Her vital signs included a blood pressure of 105/79 mmHg with a pulse rate of 110 beats per minute, a respiratory rate of 16 per minute and oxygen saturation of 94% on room air. Initially she was treated in ED with full dose anti-coagulation for suspected pulmonary embolism overnight while awaiting CTPA the next morning. Further examination demonstrated an incidental finding of a continuous machinery cardiac murmur best heard at the left parasternal border, loudest in systole (5/6), and 3/6 in diastole with a palpable thrill across the precordium. There was no relevant past medical history or significant family history. Her medical check-up performed during her application for an Australian student visa was unremarkable.
Electrocardiogram (ECG) showed sinus tachycardia. Laboratory results demonstrated negative high sensitivity troponin I and positive D-Dimer (1.12 mg/LF). Computed tomography pulmonary angiography (CTPA) was negative for pulmonary embolism, with no other abnormalities noted.
Transthoracic echocardiography (TTE) was subsequently performed for investigation of the new continuous murmur – other conditions apart from an SVA which can present with continuous murmurs include; patent ductus arteriosus, coarctation of the aorta, coronary arteriovenous fistulas and an aortopulmonary window. TTE showed normal left and right ventricular size and systolic function. To the unwary eye, the colour flow at the RV inflow view may appear like tricuspid regurgitation. However, the continuous wave Doppler clearly demonstrated a continuous wave form throughout systole and diastole (Fig. , Videos and ). Additionally, a significant left-to-right shunt was detected on the colour Doppler between the right coronary sinus and the right atrium (Fig. , Video ). Interestingly, Doppler echocardiography detected diastolic flow reversal in the thoracic descending aorta which is more commonly seen in severe aortic regurgitation (Fig. ).
The patient then underwent transoesophageal echocardiography (TOE) which showed a rupture of the right sinus of Valsalva aneurysm with shunting into the right atrium (Fig. , Video ). The left-to-right shunt in the right atrium was directed towards the centre of the tricuspid valve, imitating significant tricuspid regurgitation. The tricuspid valve itself was normal in structure and function. A small saccular aneurysm of the right coronary sinus was seen extending into the junction between the right atrium and ventricle. A trileaflet aortic valve was noted with no regurgitation. There were no associated atrial or ventricular septal defects.
CTPA images were retrospectively reconstructed which visualised the SVA and shunt, likely originating from the right coronary sinus into the right ventricle (Fig. ).
Since the patient had an acutely ruptured SVA, a surgical repair was proposed given significant left-to-right shunting and to prevent RV overload. She underwent open-heart surgery with excision of the aneurysm and pericardial patch repair of the right coronary cusp-SVA fistula (Fig. ). At routine outpatient follow-up 4 weeks later, she reported no further symptoms, resolution of her cardiac murmur and successful repair on repeat transthoracic echocardiography.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2753,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6693239-1,Extracted,"We report the case of a 32 year-old male patient who presented to our Emergency Department with acute onset of unbearable epigastric pain after severe emesis following food ingestion. The pain was radiating to his chest and back and increases by any movement. Due to severe pain and dyspnea, the patient was unable to lay supine insisted on remaining sitting up for the examination. He had an episode of hematemesis after the start of pain. His medical, family, and psychosocial history were irrelevant. He had no previous surgeries performed. Physical examination revealed an anxious patient who looked pale, and dehydrated. His vital signs were, a temperature of 37.5 C, heart rate of 103 beats/minute, and the rest were unremarkable. Examination of the cardiopulmonary system was unremarkable. Upon examining the abdomen, the epigastric area was tender with guarding in the upper abdomen but soft at the lower part. No rigidity was appreciated.
His laboratory investigations showed leukocytosis, WBC was 22 × 109/L. An electrocardiogram was done and showed sinus tachycardia. The chest (Fig. ) and abdominal x-rays (Fig. ) showed tiny air collection in the paraspinal space on the left side above the diaphragm, but no free air under the diaphragm and no evidence of pleural effusion.
He was admitted to the Intensive care Unit and underwent CT of the abdomen and pelvis, which revealed air around the distal esophagus with apparent thickening of the wall of the esophagus, the air was noted at the gastroesophageal junction with air bubbles in the gastro-hepatic ligament in the abdomen. A large intramural hematoma is noticed within the gastric fundus and basal infiltration of the left lung. Features were highly suggestive of rupture of the distal esophagus at the gastroesophageal junction with pneumo-mediastinum (Fig. ).
The diagnosis of Boerhaave’s Syndrome was made. Intravenous antibiotic and fluid hydration were initiated. With signs of peritonitis, hematemesis, and impending shock, he was intubated and taken for laparoscopic abdominal exploration with the possibility of thoracic exploration. As a result, Thoracic surgery team was consulted and involved in the course of management of the case.
Upon entering the abdominal cavity, a generous hematoma was identified in the gastrosplenic ligament and filling the left upper quadrant area. No signs were indicating the presence of an abscess collection, nor a mass. Followed by dissecting through the pars flaccida on the right side of the stomach. The left side dissection initiated by cutting the greater omentum using a smart bipolar (Ligasure) device. The left crus of the diaphragm was identified, and the anatomy of the gastroesophageal.
(GE) junction was elaborated. We identified a 2 cm longitudinal perforation within the lower third of the esophagus at the posterolateral wall (Fig. ). We continued the circumferential dissection of the esophagus, preserving the Posterior Vagus nerve. A 38-French gastric calibration tube was carefully advanced across the GE Junction into the stomach. The edges of the esophageal perforation were cleaned, and primary repair was performed with interrupted 2–0 polyglactin (Vicryl) stitches, (Fig. ). Then, an omental patch was sutured over the perforation area (Additional file 1: Video S1).
A feeding jejunostomy was inserted to gain enteral access for postoperative nutritional support, and a nasogastric tube was advanced into the stomach under intraoperative guidance. Drains were placed intrabdominal and posterior mediastinal.
The patient was then shifted to the Intensive Care Unit. He was kept on the ventilator post-op and extubated the following day. He was kept on antibiotics and was started on jejunostomy feeding.
On postoperative day three, he was transferred to the regular surgical floor. Over a week duration, his leukocytosis resolved. On postoperative day 4, the patient was started on a clear fluid diet, which was well tolerated. One week postoperative, a CT scan of the abdomen-pelvis (Fig. ) was performed and confirmed the absence of fluid collections and contrast leak. He was discharged home on postoperative day eight but represented in the emergency room after 2 days with upper back and chest pain that aggravated with respiration. Examination of the chest revealed, left lower chest crepitations. He was afebrile and had a normal leukocyte count. A chest x-ray was done showing pleural effusion, for which he was re-admitted for further management. Upon admission, a repeat CT scan of the abdomen did not show any signs of contrast leakage and confirmed a left basal pulmonary consolidation and minimal left-sided pleural effusion. Pleural tapping with fluid analysis was performed, and he was managed with antibiotics and chest physiotherapy, which facilitated the resolution of the pleural effusion. He was discharged home in good condition after a week of hospitalization.
He was reassessed in the surgical clinics and was doing very well with no complains. An upper endoscopy was performed 2 months after the surgery and confirmed normal esophageal and stomach anatomy.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [103.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 103.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 1.5 + 1 = 2.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2754,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7860222-1,Extracted,"A 33-year-old, previously healthy Swiss male was admitted to our hospital with 10-day history of fever and chills, accompanied by epigastric discomfort, nausea, and malaise. The patient had first presented to a regional hospital, where symptomatic treatment was initiated without lasting effect. Persisting fever and new-onset emesis led to presentation at our tertiary hospital. He worked as a haulier.
Past medical history was not significant, and he neither smoked nor drank alcohol on a regular basis. The patient had just returned from a week-long holiday in Austria, where among other activities he had visited a children’s zoo. His wife and 2-year-old daughter did not experience any illness.
On clinical examination, the patient presented with a temperature of 36.8 °C, blood pressure 90/59 mmHg, heart rate 100/minute, and oxygen saturation 98%. A small inguinal lymph node was noted. The rest of the clinical examination was unremarkable.
Laboratory examination at admission revealed a markedly elevated C-reactive protein (CRP) of 404 mg/l. The complete blood count showed a normal leukocyte count with neutrophilia of 86% and a left shift (17% band forms, increasing to 37% the following day). There was slight anemia (hemoglobin 130 g/l) and normal thrombocyte count (245 G/l). The transaminases [aspartate transaminase (AST) 95 U/l, alanine transaminase (ALT) 104 U/l] and alkaline phosphatase (156 U/l) were elevated 2–3-fold the upper limit of normal. Bilirubin (27 µmol/l) and international normalized ratio (INR) were slightly elevated with low albumin (28.5 g/l), indicating incipient impairment of liver synthesis function. Creatinine (87µmol/l) and pancreas amylase (33 U/l) were within the normal range. Antinuclear antibodies (ANA) were unremarkable. Leukocyturia (46/µl) and microhematuria (479/µl) were noted and interpreted as likely para-infectious changes in the absence of clinical evidence of urinary tract infection.
Treatment with doxycycline p.o. 100 mg bid was initiated on the assumption of an intracellular pathogen, and the fever disappeared within 3 days.
Aerobic and anaerobic blood cultures and serological tests for Epstein–Barr virus and cytomegalovirus taken at the regional hospital 5 days after onset of symptoms were negative. Further serology testing was negative for human immunodeficiency virus (HIV), hepatitis B, C, and A virus, cytomegalovirus, as well as influenza A and B virus. Due to the history of animal contact, serological tests for Coxiella burnetii, Brucella, Leptospira interrogans, Francisella tularensis, Bartonella henselae, and Rickettsia rickettsii/conorii and typhi were added, all of which came back negative.
A conventional abdominal ultrasound scan with contrast-enhanced ultrasound (CEUS) revealed disseminated small, hypoechoic liver lesions (Fig. a), partially with hyperechoic rim (Fig ), measuring up to 1.8 cm in diameter. CEUS was performed for its superior sensitivity in the demarcation of liver abscesses, indicating stage IV pyogenic liver abscesses [].
A computed tomography (CT) scan confirmed multiple, partially confluent hypodense lesions of the liver consistent with the diagnosis of abscesses (Fig. ). It also demonstrated bilateral small, nodular pulmonary lesions and slightly larger consolidations in the right apex (1.2 cm) and lingula (1.1 × 2.2 cm2), as well as hilar and mediastinal lymphadenopathy. Transthoracic echocardiography was normal.
Blood cultures taken on day 1 of admission remained without growth. On day 7, the patient underwent a percutaneous ultrasound-guided biopsy of one of the liver lesions, while under treatment with doxycycline. The histopathological examination revealed granulocytic inflammatory infiltrates and abscess formation. No microorganisms could be detected in Gram, periodic acid–Schiff (PAS), diastase-PAS, Grocott, and Ziehl–Neelsen stains.
Aerobic and anaerobic cultures of the liver abscess material obtained by biopsy remained without growth, including mycobacterial cultures. Accordingly, the Gram stain of the liver aspirate showed no microorganisms. Eubacterial PCR of the liver biopsy tissue with 16S ribosomal DNA (rDNA) sequencing finally revealed the presence of Aggregatibacter aphrophilus.
At an outpatient follow-up visit 1 month after hospital discharge, the patient was asymptomatic with normal inflammatory markers and liver function tests. The ultrasound scan found that the liver abscesses had completely resolved (Fig. b), with no residual splenomegaly. A repeat echocardiography showed no abnormalities, specifically no signs of endocarditis. Doxycycline was stopped after a total of 6 weeks of treatment.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 100.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2755,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-9091,Extracted,"A 61-year-old Caucasian woman presents to her physician for a routine checkup. She has primary hypertension and rheumatoid arthritis. She currently does not report any relevant symptoms, such as weight change, increased or decreased appetite, sleep or mood problems, gastrointestinal symptoms, fever, or night sweats. Her medications include valsartan 160 mg, hydrochlorothiazide 25 mg daily, and methylprednisolone 28 mg every other day. According to her diary, her blood pressure varies from 130/80 to 120/60 mm Hg. In the past year, she had humeral and tibial fractures from a self-height fall and stepping over a fence, respectively, that occurred 6 months apart. She is in menopause and is not on hormone replacement therapy. Currently, she does not smoke but has a 10-pack-year history of smoking. She consumes alcohol occasionally. She weighs 56 kg (123.5 lb), and her height is 169 cm (5 ft 7 in). She does not report a family history of any cancer. Her father died after a myocardial infarction at the age of 63. She performs daily household activities but is not engaged in either aerobic or strength training. She mainly consumes vegetables, cereals, and dairy products. Her blood pressure is 125/80 mm Hg, heart rate is 67/min, respiratory rate is 14/min, and temperature is 36.5°C (97.7°F). Her physical examination is unremarkable.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [67.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 67.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2756,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7682127-1,Extracted,"A 23-year-old man was referred from another hospital with a history of a dry cough, fever (> 39 °C), and malaise, mostly at noon and at night. The symptoms started after he developed a self-limited skin and soft tissue infection on his left hand two weeks ago. Initially, he was hospitalized for 3 days under suspicion of COVID-19 infection. Empiric antibiotic therapy with piperacillin-tazobactam was started after his admission. Transthoracic echocardiography revealed floating vegetation (35–40 mm) on the tricuspid valve. Prior to transfer to our clinic, he also complained of blood-stained sputum and two episodes of diarrhoea and vomiting. The patient originally came from Romania, is a construction worker, and denied intravenous drug abuse. However, he admitted to having contact with a patient with active pulmonary tuberculosis in the past.
On physical examination at admission, his vital signs showed a blood pressure of 128/60 mmHg, a heart rate of 112 bpm, oxygen saturation of 97% on room air and a subfebrile temperature (37.5 °C). Cardiac auscultation revealed a grade III/VI holosystolic murmur over the tricuspid valve. There were also bilateral rales and crackles audible at the base of the lungs and right basal dullness on percussion. Examination of his extremities and skin revealed bilateral ankle pitting oedema and an isolated left-hand oedema with concomitant swelling of the third metacarpal-phalangeal joint. Neurological examination was unremarkable.
Initial investigations included laboratory tests and blood culture sets. An electrocardiogram showed a sinus rhythm without signs of underlying ischaemia or atrioventricular block. An initial full blood count revealed mild leucocytosis, neutrophilia, left deviation, and microcytic anaemia (Table ). High levels of C-reactive protein and procalcitonin suggested a bacterial infection. In addition, the patient presented with a concomitant acute kidney injury (creatinine 1.5 mg/dl, BUN 112 mg/dl). Liver function tests showed elevated levels of alkaline phosphatase and gamma-GT and low levels of cholinesterase (Table ). Empirical antibiotic therapy with ampicillin, flucloxacillin and gentamicin, according to the current European Guidelines for the empirical treatment of native valve endocarditis, was administered []. A throat swab for the SARS-CoV-2-RNA PCR test was reported to be negative.
After admission, we performed transoesophageal echocardiography (Fig. , Additional file : Video 1), which demonstrated 25 × 15 mm vegetation on the septal leaflet of the tricuspid valve without evidence of severe tricuspid regurgitation. The other valves presented no vegetation or severe regurgitation. The left ventricular ejection fraction was normal, and intracardiac thrombi were not observed. Further relevant echocardiographic findings revealed a normal right ventricular function and pulmonary arterial systolic pressure of 30 mmHg. A small ventricular left-to-right shunt due to a ventricular septal defect was observed on colour Doppler (Fig. , Additional file : Video 2).
In addition, a CT scan of the thorax and abdomen demonstrated bilateral disseminated multiple septic pulmonary emboli and concomitant pneumonic infiltrates as well as mild bilateral pleural effusions (Fig. ). On the CT abdomen scan, no additional organ emboli or abscess formations were found. A coronary CT angiography showed no evidence of calcium plaques suggestive of coronary artery disease or malformations. Although this patient did not present neurological symptoms, a brain CT was obtained, which showed normal findings. A CT scan of the left hand revealed a soft-tissue infection or phlegmon without bone involvement.
After admission, at least two blood culture sets were reported to be positive for methicillin-sensitive Staphylococcus aureus (MSSA). The final diagnosis of S. aureus bacteraemia and isolated right-sided endocarditis was based on two major criteria according to the modified Duke criteria for endocarditis []. We continued administering flucloxacillin, following the current guidelines []. Clarithromycin was started because of atypical pneumonic infiltrates on CT, and a course of 10 days of ceftazidime was also added to the antibiotic regimen due to concern about a Pseudomonas sp. infection. Previously, the initial antibiotic therapy with gentamicin was stopped in consideration of his acute kidney injury. A therapeutic intravenous anticoagulation with unfractionated heparin was begun after the diagnosis of septic pulmonary emboli.
Furthermore, a second transoesophageal echocardiography was performed 10 days after starting antibiotic therapy (Fig. ). Fortunately, it showed diminished vegetation (16 × 7 mm) on the septal leaflet of the tricuspid valve, without any evidence of further valve lesions. The left-to-right shunt due to the ventricular septal defect was stable without haemodynamic significance. In consensus with our endocarditis team, including a cardiac surgery evaluation, we decided on conservative management of the isolated right-sided endocarditis.
During hospitalization, the patient gained weight and there was an increase in peripheral oedema and anasarca, and increased levels of creatinine, BUN, and hypoalbuminemia were noted on laboratory tests (Table ). In addition, urine diagnostic tests revealed macrohematuria, albuminuria, high levels of A1-microglobulin, and a high protein-creatinine ratio, suggesting acute tubular injury (Table ). Autoantibodies and C3 complement tests were conducted, which revealed a low C3 level and a negative ANCA titre (Table ). In consideration of these findings, we suspected glomerulonephritis associated with S. aureus infection and decided to not perform a renal biopsy. Instead, we administered diuretic therapy with amiloride and hydrochlorothiazide to treat the anasarca symptoms. In addition, relevant proteinuria was observed on his 24-h urine protein test (Table ). Consequently, we started a regimen of corticosteroids with prednisolone therapy (1 mg/kg BW) for 4 weeks, and then it was tapered weekly, showing a gradual improvement in the patient’s proteinuria and oedema (Table ).
After an acute episode of massive haemoptysis, we stopped the intravenous anticoagulation and performed an urgent bronchoscopy (Fig. ). It showed tracheobronchitis with diffuse bleeding in segment 8 of the lower right lobe requiring an endobronchial tamponade for 24 h to stop the bleeding. Subsequently, the patient underwent a revision bronchoscopy for extraction of the endobronchial tamponade. It showed abundant purulent bronchial secretions without signs of de novo active bleeding. Acid-fast stain tests, Pneumocystis jirovecii, and respiratory viruses (RSV-RNA, Influenza A, B) were negative in the bronchoalveolar lavage. Although the gamma-interferon test was positive for a latent tuberculosis infection, we considered it an isolated finding not relevant to diagnose active pulmonary tuberculosis. Haemoptysis episodes are more likely due to multiple septic pulmonary emboli and concomitant S. aureus pneumonia, as previously found on the patient’s CT-thorax scans.
Further investigations related to explaining the microcytic anaemia revealed an iron deficiency (iron 33 µg/dL, ferritin 116 mcg/dL, transferrin 78 mg/dL). However, this finding might be explained as a combination of nutrition deficiency, recurrent haemoptysis, and inflammatory systemic disease due to acute infective endocarditis. His other parameters were at normal levels without suspicion of haemolysis or vitamin B12 deficiency.
Prior to discharge, a thorax CT scan revealed remission of the pneumonic infiltrates and septic emboli after two weeks of antibiotic therapy (Fig. ). After 4 weeks of hospitalization, considerable improvement of renal function, proteinuria, and inflammatory markers was observed. The patient was discharged with combined antibiotic therapy of flucloxacillin and clarithromycin at 4 weeks.
At follow-up, one month after discharge, the patient presented with a good recovery of renal function and proteinuria (Table ). Laboratory tests were unremarkable. Additionally, transoesophageal echocardiography showed no more relevant vegetation of the tricuspid valve only some mild regurgitation (Fig. ). However, an aneurysmal transformation of the ventricular septal defect (5 mm) located infravalvular to the septal leaflet of the tricuspid valve was found (Fig. , Additional file : Video 3). The left-to-right shunt was not haemodynamically significant (systolic velocity of 5.5 m/s) without involvement of the aortic valve or aorta (Fig. ). After surgical evaluation, conservative management, including endocarditis prophylaxis, was continued. The patient was scheduled for further echocardiographic follow-up and cardiac catheterization to determine the invasive haemodynamic parameters.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [112.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",7,7,7,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 112.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 = 6.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 6.0.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 6.0 + 1 = 7.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 7.0.
The patient's Well's score for pulmonary embolism is 7.0."
2757,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8289448-1,Extracted,"A 37-year-old white male presented to the Emergency Department with acute chest pain and breathlessness causing marked reduction in exercise tolerance. He denied loss of consciousness, cough, or other infective symptoms and had no symptoms of deep vein thrombosis. He did not have a personal or family history of venous thromboembolism nor any identifiable risk factors. He had been prescribed fluoxetine 60 mg once daily orally and promethazine 25 mg at night orally for low mood and insomnia and suffered mechanical back pain, but otherwise did not have any significant comorbidities. He is a non-smoker, drinks alcohol within recommended limits, denies recreational drug use, and works as a light technician.
On examination, the patient was febrile (temperature 37.8 °C), hypoxic (oxygen saturation 92% on room air), tachypneic (respiratory rate 24 breaths/minute), tachycardic (heart rate 120 beats/minute), and normotensive (blood pressure 132/84 mmHg). He was alert but appeared pale, with normal heart sounds and no murmurs heard. Auscultation of the chest was normal, and his abdomen was described as soft and nontender. There were no abnormalities on neurological examination. Electrocardiography (ECG) showed sinus tachycardia, right axis deviation, ischemic changes in the anterior leads, and the S1Q3T3 phenomenon.
Initial laboratory results are presented in Table . Assessment of d-dimer was not performed—we assume because clinical suspicion of VTE was sufficiently high to proceed directly to imaging and empirical treatment. Arterial blood gas sampling performed on room air revealed pO2 7.6 kPa, pCO2 7.6 kPa, hydrogen ion concentration 32 nmol/L, base excess 0.7 mmol/L, lactate 1.36 mmol/L, and oxygen saturation 92%. The patient routinely tested negative on severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) polymerase chain reaction (PCR) during admission, and there was no indication for other microbiological/serological testing.
The patient was treated for presumed pulmonary embolism with subcutaneous tinzaparin 17,000 IU/mL and proceeded to computed tomographic pulmonary angiography (CTPA). CTPA confirmed major pulmonary embolus, with associated acute right heart strain and dilation of the pulmonary trunk. The patient was transferred to the medical high-dependency unit for monitoring and continued treatment with tinzaparin. Echocardiogram confirmed the CTPA findings, demonstrating a dilated right heart with impaired right ventricular function and very mild tricuspid regurgitation.
The doctor in training responsible for his care at this point also requested a computed tomography (CT) scan of the abdomen and pelvis routinely to screen for malignancy. CT abdomen and pelvis was also documented in the management plan by two different consultant physicians. The same doctor in training then reviewed the patient 48 hours later and documented in the case notes at that time that National Institute for Health and Care Excellence (NICE) guidance dated March 2020 stated “not to offer further investigations for malignancy in patients with unprovoked PE unless relevant clinical signs or symptoms.” Despite this, the patient proceeded to CT scan without any symptoms or signs to suggest malignancy. The rationale for proceeding to CT scan is not documented in the medical notes and will be addressed in the discussion of the case.
CT revealed extensive thrombus extending from the proximal left external iliac vein into the left common iliac vein and along the inferior vena cava (IVC) to the level of the renal veins (Fig. ). The report also noted some prominent paraaortic nodes at the level of the renal veins and suggested these may be reactive. The solid abdominal organs appeared normal, and a small left-sided pleural effusion was noted. Due to unexplained lymphadenopathy, an astute clinician advised testicular examination. The patient did not self-examine regularly but denied testicular symptoms. Clinical examination was unremarkable, but he proceeded regardless to ultrasound examination. Ultrasound showed several hypoechoic and heterogeneous lesions identified within the right testis, the largest measuring 1.7 cm (Fig. ). There was some vascularity within these lesions with appearances suggestive of testicular malignancy. The testicle did, however, appear normal in size, which would support the clinical examination findings.
Following discussion with the local Urology service, assessment of tumor markers was performed, which revealed elevated lactate dehydrogenase (LDH) at 449 U/L (reference range 0–250 U/L) with beta human chorionic gonadotropin (hCG) and alpha fetoprotein (AFP) within the normal range. The differential diagnosis was metastatic testicular cancer of germ cell origin or lymphoma. Tissue diagnosis would be required to confirm the diagnosis and guide treatment; however, orchidectomy was complicated by the need for anticoagulation in the context of significant thromboembolic disease.
Following multidisciplinary discussion, the patient was discharged to continue anticoagulant treatment with tinzaparin with a plan for delayed orchidectomy following reduction in clot burden. On the advice of the Haematology service, tinzaparin was changed to subcutaneous enoxaparin because of subtherapeutic anti-Xa levels following discharge. The dose was adjusted on several occasions; at the time of writing, the patient continues on enoxaparin 140 mg twice daily. Other medications administered were co-codamol 30/500 orally on an as-required basis for treatment of pain, allopurinol 300 mg once daily orally to reduce risk of spontaneous tumor lysis syndrome, and the patient’s preadmission medications: fluoxetine 60 mg once daily orally and promethazine 25 mg once daily orally, all of which were continued long term. The duration of anticoagulation had not yet been determined at time of discharge, pending cancer treatment and follow-up in due course.
Unfortunately, repeat imaging 20 days after presentation showed progression of the IVC thrombus and persistent pulmonary artery filling defects, corresponding to pulmonary embolism. IVC filter insertion was performed to facilitate right orchidectomy, which revealed 35-mm seminoma (Fig. ) with invasion of the rete testis and hilar soft tissue.
Orchidectomy was complicated by scrotal hematoma, which was surgically evacuated. A repeat CT scan showed that aortocaval adenopathy had increased in volume from previous scans. Following multidisciplinary discussion, the patient’s disease was staged as stage 2A seminoma and the decision taken to proceed to adjuvant radiotherapy (30 Gray in 15 fractions) which was completed in December 2020. Less than 1 month later, abdominal CT imaging was repeated to assess burden of thrombus prior to IVC filter removal. This unfortunately showed multiple pulmonary and hepatic metastases. The decision was taken to proceed with bleomycin, etoposide and platinum (cisplatin) (BEP) chemotherapy, of which the patient completed four cycles in April 2021. Repeat CT showed good response to chemotherapy, and the patient remains well. He continues on therapeutic anticoagulation with enoxaparin and awaits specialist review by Haematology services to determine the duration of treatment.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3.0 + 1 =  4.0.
The patient's Well's score for pulmonary embolism is 4.0."
2758,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3079609-1,Extracted,"A 52 year old man was admitted to our clinic with shortness of breath and tachycardia. His past medical history included replacement of the mitral valve (biprosthesis 29 Sorin) and interposition of a valved conduit (25 mm Shelhigh) between the left ventricle and the pulmonary artery with a diagnosis of c-TGA, right atrioventricular valve (AV) insufficiency and pulmonary stenosis two years prior to presentation. His postoperative course was complicated by mediastinitis (blood cultures and exudate of the surgical wound were positive for methicillin-resistant Staphylococcus aureus), which required long-term antibiotic treatment and debridement of necrotic sternal fragments without success. Eventually, an omentoplasty (release of the greater omentum, sparing both vascular pedicles and short gastric vessels, with tunneling to the anterior mediastinum via upper midline laparotomy) was performed, sternum was closed with Robicsek type closure and the wound with a subcutaneous tissue and skin. The patient was discharged one month after the surgery. Upon presentation, his physical examination revealed a high grade systolic murmur at the right upper sternal border, decreased breath sounds and fine rales at lung bases, hepatomegaly and peripheral oedema. His blood pressure was 100/60 mmHg and his heart rate was 102 beats per minute. Cardiomegaly and bilateral pleural effusions were observed on chest x-ray. Echocardiographic examination revealed evidence of significant narrowing at the left ventricular-to-pulmonary artery (LV-PA) conduit (peak systolic instantaneous gradient of 130 mmHg), along with significant narrowing (a peak gradient of 29 mmHg and a mean gradient of 20 mmHg) and moderate regurgitation of the right AV bioprosthetic valve. The right atrium was dilated. Upon reviewing these findings, reoperation, in order to replace the prosthetic AV valve and the LV-PA conduit, was planned.
A median sternotomy was performed. Omentum was prepared carefully and protected with warm compresses (Figure ). The right atrial pressure was 20 mmHg. Cardiopulmonary by-pass (CPB), utilizing femoral venous and arterial cannulation, was performed. Mitral bioprosthesis was replaced with a 29 mm St. Jude mechanical valve. On inspection, it was evident that the narrowing was at site of the previous ventriculotomy. No evidence of degeneration was observed at the valved conduit therefore the conduit was excised prior to the valve. After enlarging the original ventriculotomy, a 24 mm polytetrafluoroethylene (PTFE) tube graft was interposed between the LV and proximal conduit just below the valve. Normal sinus rhythm was reestablished, and CPB was discontinued without the need for inotropic support. Omentum was placed in the mediastinum and reattached (Figure ). Sternum was closed with conventional sternal closure. Post-operative right atrial pressure was 10 mmHg. Wound healing was uneventful and the patient was discharged on post-operative Day 11. At the time of writing, he is at home, with satisfactory activity for his age and no signs of recurrent infection.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [102.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 102.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2759,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5390442-1,Extracted,"A 61-year-old Caucasian man presented to our emergency department with 20 pounds of unintentional weight loss over 2 months followed by a 2-week history of worsening shortness of breath, epigastric tenderness, and bilateral pitting leg edema. He had no symptoms of fever, cough, phlegm production, diaphoresis or night sweats. He had a 40 pack-year smoking history and 40-year history of alcohol misuse, but no significant past medical history or family history of significant medical illness. Later in the course of his current presentation, he admitted to 6 months’ history of intermittent abdominal pain and diarrhea. He had attributed this to his use of alcohol and he did not seek medical care.
On physical examination, he was emaciated and afebrile with a heart rate of 118 beats per minute and a blood pressure of 103/70 mmHg. His jugular venous pressure was elevated at 5 cm above the sternal angle. His abdomen was not distended but tender to light palpation in the epigastrium. He was not jaundiced. Leg pitting edema was noted from his feet up to the distal thirds of his tibia bilaterally. Auscultation of the lung fields revealed significantly decreased air entry at the base of the right lung. His oxygen saturation on room air was found to be 85%. With supplemental oxygen delivered by nasal prongs at 2L/minute he maintained an oxygen saturation of 94%.
The admission blood work is presented in Table . Results showed an elevated leukocyte count of 24.0 × 109/L, predominately neutrophils, elevated thrombocyte count of 894 × 109/L and low hemoglobin 79 g/L with a hematocrit of 27%. Liver enzyme test results revealed elevated alkaline phosphatase 197 U/L, elevated gamma glutamyl transferase (ϒGt) 121 U/L, international normalized ratio (INR) elevated at 1.4 and C-reactive protein (CRP) elevated at 262.5 mg/L. There was a significant drop in his albumin level, at 24 g/L. Serology results did not demonstrate any evidence of hepatitis B infection. Additionally, no evidence of hepatitis B immunity was found. Hepatitis C antibodies were non-reactive.
The admission chest X-ray, Fig. , revealed a large right lung pleural effusion with near complete opacification associated with mass effect and mild mediastinal shift toward the left hemithorax. A thoracentesis removed 1.5 L of yellow cloudy fluid from the right hemithorax in the emergency room. The pleural fluid analysis revealed an exudative effusion with a fluid lactate dehydrogenase of 256 U/L, nucleated cell count of 14.3 × 109 with 86% being neutrophils, and fluid to serum amylase ratio of 1:2. Light’s criteria were assessed and consistent for exudative effusion, Table . The serum effusion albumin gradient (SEAG) was measured at 5g/L (serum albumin 24g/L – effusion albumin 19g/L), which is consistent with exudative effusion. The fluid was also sent for Gram stain and microbiological culture.
Our patient was admitted to the internal medicine ward and piperacillin-tazobactam 3.375 g intravenously every 6 hours was initiated. A right-sided Wayne catheter chest tube was inserted with ultrasound guidance the following day; however chest X-rays post chest tube insertion did not show any significant decrease in effusion size. An esophagogastroduodenoscopy (EGD) and colonoscopy were performed to help determine the cause of the patient’s anemia. The EGD did not identify a source of bleeding, but the colonoscopy revealed an impassable diverticular stricture encountered at 25 cm from the sigmoid colon.
A computed tomography (CT) scan of our patient’s thorax demonstrated a tiny gas and fluid collection in the right lobe of the liver, suggestive of decompressed hepatic abscess with extension through the right pleural space and into the right lower lobe of the lung, Fig. . A CT scan of his abdomen confirmed a ruptured intrahepatic abscess extending across the diaphragm into the right pleura and into small right lower lobe abscesses. Furthermore, a complicated sigmoid colon diverticulitis with a fistula to the rectum was also seen, Fig. .
At this time, the general and thoracic surgery services were consulted. A decision was made to request the interventional radiology service to place a percutaneous drain to clear the remaining intrahepatic abscess. During the procedure, fluoroscopic contrast was instilled into the abscess drain and was found to track through the right hemidiaphragm into the right lung pleural space and bronchi, Fig. . This resulted in a sudden drop in the patient’s oxygen saturation, which resolved when the contrast was evacuated from the bronchi. A new chest tube was inserted to drain the remaining pleural fluids. Despite the intrahepatic drain and two chest tubes in situ, the patient’s pleural effusions failed to drain completely. The thoracic surgery team subsequently decided that lung decortication and exploratory bronchoscopy was indicated for the patient. The microbiological culture of the pleural fluid grew penicillin-sensitive Streptococcus anginosus, but our patient’s antibiotic regimen was not changed in order to maintain coverage for possible anaerobic and Gram-negative enteric microbes.
Our patient was taken to the operating room, where bronchoscopy revealed clear airways with no perforations. A thoracotomy was then performed to expose the pleura, which was found to be markedly thickened. The pleura were incised and a large amount of gelatinous material was removed from the pleural cavity. Extensive decortication of the right lung resulted in significantly improved intraoperative lung inflation. A biopsy of the lung abscess was also taken. Four chest tubes were placed intraoperatively to ensure effective drainage of the pleural cavity. Our patient tolerated the procedure well and substantial lung re-expansion was observed on chest X-rays in the days following the procedure. A subsequent drain check performed by an interventional radiologist, showed a residual cavity in the right lobe of the liver and that the fistula to the pleural space was still patent. However, no continuity to the lung abscess or bronchi was observed. General surgery also opted not to surgically remove the fistula as it was felt that it would close on its own given the effective drainage that had been achieved.
Ten days following his operation, our patient was discharged home with his hepatic abscess drain still in situ and with a 21-day course of ciprofloxacin 500 mg and metronidazole 500 mg, both orally and twice daily. An abscess check performed 3 weeks later found that the abscess had resolved without complications and the percutaneous drain was removed.
The general surgery service re-assessed our patient approximately 1 month post-discharge from hospital. Our patient reported he was feeling well and denied experiencing any abdominal pain or other concerning gastrointestinal symptoms. Because of this complex diverticulitis with an increased the risk of future bacterial seeding, a lower anterior resection of the affected colon and rectum was offered to the patient. Our patient agreed to have this procedure performed laparoscopically, however significant adhesions were found intraoperatively in the pelvis preventing easy mobilization of the sigmoid colon. Subsequently, the operation was converted to an open laparatomy. The segment of colon containing the fistula was identified and resected. A tension-free end-to-end anastomosis was then created without difficulty. Our patient tolerated the procedure well and was discharged from hospital 5 days following the operation. At follow-up appointments at 1 week and 1 month following his discharge, our patient again reported that he was feeling well and denied experiencing any abdominal pain or other gastrointestinal symptoms.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [118.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 118.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2760,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3976158-1,Extracted,"A 20-year-old Chinese woman first visited our hospital when she was 28 weeks pregnant. She was mentally retarded with typical features of trisomy 21. She had regular menstrual cycles before pregnancy. She had dyspnea, chest pain and fatigue with mild physical exertion. She also had trouble lying down in a supine position.
During the examination, her electrocardiogram showed sinus tachycardia and right atrial and right ventricular hypertrophy. Her heart rate was 115 beats per minute. Her symptoms were suggestive of an unrepaired ECD. She had severe left and right common valve insufficiency. Color flow imaging and pulsed wave Doppler demonstrated bidirectional cardiac shunting with dominant left-to-right shunting. Her left and right heart pressures were nearly equal. Based upon the natural history of an unrepaired ECD, we suspected that our patient had severe pulmonary hypertension.
Because of the extreme high risk of mortality for our patient, the obstetrician, cardiologist and anesthesiologist of our hospital offered to terminate the pregnancy. Our patient’s family refused the advice and insisted on continuing the pregnancy. Our patient was also advised to stay in our hospital for close monitoring and proper treatment, and again her family refused our advice.
Our patient returned at 33 weeks and six days of pregnancy because of lower abdominal pain accompanied with vagina fluid outflow for two hours. Her physical examination on admission showed a temperature of 35°C, pulse of 130 beats per minute, blood pressure at 140/80mmHg, respiration 33 breaths per minute (provided with 5L oxygen per minute), severe dyspnea, cyanosis, lower extremity edema, grade three to six heart murmur at her left intercostal space, and grade two to three systolic murmur at the apex of her heart. Her oxygen saturation was 19.4%.
Her baby was in breech presentation. The fetal heart rate was 120 beats per minute. Our patient had regular uterine contractions with an interval of three to four minutes. Her cervical dilation was 10cm with rupture of the fetal membranes. An ultrasound showed that her fetus was in the left sacral anterior position with a biparietal diameter of 72mm and femur length of 56mm. The amniotic fluid index was 20mm. An analysis of the fetal blood gas showed 48.8mmHg carbon dioxide and 22.1mmHg oxygen, with pH 7.15. A male baby was delivered by gentle traction. The weight of the baby was 1110g. His one-minute Apgar score was 5. His five-minute Apgar score was 10. Our patient died 10 minutes after delivery. When her heart stopped beating, standard cardiopulmonary resuscitation was performed. Our patient was not on a ventilator. The premature infant had a normal human karyotype and had intrapartum asphyxia and hypospadias deformity. The baby was treated at the Neonatology department of our hospital and discharged two months later with a body weight of 2055g. The baby does not have congenital heart disease.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [130.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 130.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2761,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7641022-1,Extracted,"A 55-year-old male, previously known to be healthy, presented to the emergency department with a 30-minute history of oppressive chest pain radiating to the upper extremities. Upon arrival, his vital signs were as follows: Blood pressure, 112/76 mmHg; pulse rate, 84 beats per minute; and peripheral oxygen saturation on room air, 96%. The patient did not have any family history of coronary artery disease or any other risk factors such as smoking or alcohol abuse. The physical examination was completely normal with no S3 or S4 sounds documented. Electrocardiography (ECG) before securing venous route showed ST segment elevations in leads V1 to V5 and aVL ().
The patient underwent an immediate cardiac catheterization which revealed an ectatic proximal left anterior descending (LAD) coronary artery with critical (90–99%) stenosis at the mid segment, mild ostial disease (20%) in the circumflex artery, and mild ectasia in the right coronary artery (). A drug-eluting stent was successfully inserted in the LAD without any residual stenosis (). Left ventriculogram showed an ejection fraction of 60–64% with a hypokinetic anterior myocardial wall. The results of a biochemical blood analysis performed upon presentation were significant for elevated troponin T levels of 11294 pg/mL and creatine kinase myocardial band (CK-MB) of 876 IU/L. His haemoglobin, white blood count, platelet count, liver function tests, thyroid function tests, lipid levels, fasting blood sugar, prothrombin time, activated partial thromboplastin time, fibrinogen, and D-dimer were all within normal limits. Patient showed prompt recovery and had a good follow-up course.
Four days prior to the event of myocardial infarction, the patient was complaining of 3-day history of acute polyarthritis and morning stiffness in the MCP joints of both hands that improves within 2 hours. No pain or other systemic symptoms were reported. Work-up to rule out reactive arthritis or new onset inflammatory arthritis showed a strongly positive anti-CCP of 500 u/ml (Normal <20), negative rheumatoid factor (RF), negative Brucella serology, and an elevated C-Reactive Protein (CRP) of 46 mg/dL. The patient did not report taking any non-steroidal anti-inflammatory drugs (NSAIDs) or pain-killer pending the blood tests and did not initiate any disease-modifying anti-rheumatic drugs (DMARDs) except after recovery of the acute myocardial infarction (AMI) event. The patient did not meet RA diagnostic criteria after a 6-month period of follow-up.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [84.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 84.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2762,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3391843-1,Extracted,"A 40-year-old (45-kg weight) previously healthy woman was admitted to the intensive burn care unit approximately 90 min after an assault chemical burn following conjugal violence. The total burned surface area was estimated at 35% (neck, face, head, arms, thorax, abdomen, and left leg), third degree []. There were severe bilateral eyes and ears lesions. Injury was due to sulfuric acid (battery acid, pH measured at 0.9). As the patient and relatives were in panic, irrigation with water was not performed at the scene of the accident but was started immediately after the arrival in the burn center. The emergency medical team began fluid resuscitation (Parkland's formula), and orotracheal intubation was performed on-site after evidence of the severity of facial burns. The patient was sedated for hospital transfer and presented the following vital signs: arterial blood pressure 70/30 mmHg, pulse 110 bpm, SpO2 >90% with normal lung auscultation.
The admission electrocardiogram and chest X-ray examination did not reveal significant abnormalities. Laboratory investigations mainly revealed a profound metabolic acidosis with a pH at 6.92, PaCO2 42 mmHg, total bicarbonate 8.6 mEq/l, base deficit 23.4 mEq/l, sodium 148 mEq/l, potassium 4.1 mEq/l, chloride 117 mEq/l, calcium 6.1 mg/dl, and phosphorus 15.1 mg/dl. The lactate level was within the normal range: 1.7 mmol/L. Renal function was initially preserved (serum creatinine 0.83 mg/dl), with no evidence for rhabdomyolysis. Blood coagulation tests on admission were disturbed, with fibrinogen 117 mg/dl, activated partial thromboplastin time (APTT) 69 s, and International Normalized Ratio (INR) 2.23. Platelets count was 169 000/mm3. Metabolic acidosis was progressively corrected by the administration of a total of 300 mmol of sodium bicarbonate over 14 h and of 140 mmol of lactate from Hartmann's solution over the first 24 h . The adjustment of the ventilator settings was complicated by the progressive development of a thoracic rigidity secondary to the chemical burns.
During the ICU stay, the patient developed several complications. Mechanical ventilation was required for 40 days, and a percutaneous tracheostomy had been performed after 1 month. The hemodynamic condition required mild inotropic support (maximal dose of dobutamine, 5 μg/kg/min) for a period of 15 days. Echocardiography demonstrated a moderate alteration of the left ventricular function. While urine output was maintained during the first week, continuous venovenous hemofiltration had to be started after this interval and was continued for 7 weeks. The patients also developed multiple episodes of wound-related sepsis treated by adapted antimicrobial therapy. In addition, iterative surgery was required with a total of 15 procedures for excision and grafting. After 5 months, the patient left the intensive care unit for rehabilitation.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 =  3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2763,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-1486,Extracted,"Three days after delivering a baby at 36 weeks' gestation by lower segment transverse cesarean section due to abruptio placentae, a 29-year-old primigravid woman develops fever, chills, and a heavy feeling in her breasts. She also has nausea and abdominal pain. Her temperature is 39.3°C (102.7°F), pulse is 101/min, and blood pressure is 110/70 mm Hg. Examination shows full and tender breasts and mild lower limb swelling. Abdominal examination shows diffuse tenderness with no guarding or rebound. Pelvic examination shows foul-smelling lochia and marked uterine tenderness. Laboratory studies show:
Hemoglobin 11.3 g/dL
Leukocyte count 16,300/mm3
D-dimer 130 ng/mL(N < 250 ng/mL)
Serum
Creatinine 1.2 mg/dL
Pelvic ultrasonography shows an empty uterus.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [101.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 101.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 =  6.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 6.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
2764,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8028090-1,Extracted,"A 76-year-old Japanese woman who was being treated for rectal cancer consulted our outpatient clinic with 1-week history of productive cough and fever. She was a never smoker. Two years earlier, she had undergone rectal cancer resection (moderately differentiated tubular adenocarcinoma, stage IIB, T4aN0M0). Two months prior to the consultation, she started chemotherapy with FOLFOX6 (fluorouracil [5-FU], oxaliplatin) + bevacizumab for peritoneal dissemination and liver metastasis from the rectal cancer. After the third course of FOLFOX6 with bevacizumab therapy, she noted fever as high as 39.0 °C without any other symptoms. Physical examination at that time showed a body temperature of 39.1 °C, blood pressure of 138/82 mmHg, heart rate of 85 bpm, respiratory rate of 20 breaths per minute, and intact level of consciousness. The totally implantable central venous port was palpable on the subclavicular region, without skin inflammation. Although her eosinophil count had increased form 171 to 607/µL, it rapidly decreased to 324/µL 3 days later. Her high-grade fever resolved within a few days without any medications. She then underwent her fourth course of chemotherapy with FOLFOX6 + bevacizumab; the high-grade fever recurred but resolved spontaneously within a few days.
After careful observation, the fifth course of chemotherapy was administered; there was recurrence of high-grade fever, along with productive cough and chest discomfort. These symptoms persisted. Physical examination at this time revealed coarse inspiratory crackles on the back. Blood tests revealed a white blood cell count of 5660/µL, eosinophil count of 736/µL hemoglobin of 12.5 g/dL, platelet count of 288,000/mL, and C-reactive protein of 9.92 mg/dL. The laboratory data showed liver dysfunction (aspartate transaminase [AST] 15 IU/L, dysfunctionalanine transaminase [ALT] 19 IU/L, lactate dehydrogenase [LDH] 236 IU/L, alkaline phosphatase [ALP] 401 IU/L, and gamma-glutamyl transpeptidase [γ-GTP] 21 IU/L). Serum surfactant protein-D (SP-D) was 250 U/L and KL-6 was 538 U/L (normal range: 0–499 U/mL). Urine antigen tests for Legionella and Streptococcus pneumonia were negative. Bilateral subpleural-predominant areas of consolidation were visible on chest x-ray and thoracic computed tomography (CT) images (Fig. ). At this point, we highly suspected bacterial pneumonia, rather than interstitial pneumonia, and tazobacterium/piperacillin (TAZ/PIPC) (12.5 g per day) for 5 days was administered. However, her symptoms and the findings on the chest x-ray and CT images gradually worsened (Fig. ). On physical examination, auscultation of the chest showed early inspiratory coarse crackles. Blood laboratory tests showed a white blood cell count 8960/µL, eosinophil count of 8.8% (788/µL), red blood cell count of 3,310,000/µL, hemoglobin of 10.0 g/dL, hematocrit of 30.8%, platelet count of 349,000/µL, AST of 13 IU/mL, ALT of 10 IU/mL, LDH of 353 U/mL (normal range 106–211 U/mL), C-reactive protein of 4.2 mg/dL, carcino-embryonic antigen (CEA) of 5.5 ng/mL; SP-D was 287 U/L and KL-6 was 1409 U/L.
To rule out interstitial pneumonia and opportunistic infections, fiberoptic bronchoscopy was performed. Bronchoalveolar lavage (BAL) fluid analysis showed lymphocytes at 17.0%, eosinophils at 4.0%, neutrophils at 5.0%, alveolar macrophages at 74.0%, and total cell count of 1.90 × 105/mL. The CD4/CD8 ratio of the BAL fluid was 1.6 (normal range 2.0–3.0). PCR for Pneumocystis jirovecii was negative, and no specific pathogen was identified in the BAL fluid. Cytomegalovirus antigenemia was absent. Cell pathological examination of BAL cells showed no evidence of malignancy.
A clinical diagnosis of interstitial pneumonia as an adverse effect to chemotherapy was then suspected. The drug-induced lymphocyte stimulation test (DLST) was positive for oxaliplatin but negative for 5-FU and bevacizumab. Because the chest CT findings were similar to those of nonspecific interstitial pneumonia (NSIP) and cryptogenic organizing pneumonia/bronchiolitis obliterans with organizing pneumonia (COP/BOOP), prednisolone at 30 mg daily (0.5 mg/kg/day) was started, and chemotherapy was temporarily discontinued. Her productive cough gradually decreased, and the consolidation seen on chest x-ray and thoracic CT scans improved gradually (Fig. ). Moreover, the eosinophilia and increased serum SP-D and KL-6 improved. The clinical course of the presenting case is shown on Fig. . After 3 months of treatment with tapering doses of prednisolone, there was no recurrence of interstitial pneumonia.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [85.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3.5,3.5,3.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 85.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 =  1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 1.5 + 1 = 2.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 2.5 + 1 =  3.5.
The patient's Well's score for pulmonary embolism is 3.5."
2765,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7792005-1,Extracted,"Patient is a 32-year old previously healthy Thai female without a history of malaria and not taking any medication before the disease episode. Two weeks prior to admission she had travelled to a malaria endemic forested area in Kanchanaburi Province, Thailand for camping and hiking with friends and her 6-year-old son. Eight days prior to admission she developed a high-grade fever with headache and chills without localizing symptoms. She had a history of poor appetite, nausea and reduced oral intake without vomiting or diarrhoea. On admission, she had a fever of 39.8 °C, a pulse rate of 78 beats per minute and a blood pressure of 90/60 mmHg. Her weight was 49 kg which were 1 kg lower from her base line of 50 kg. Her consciousness was normal, conjunctivae were not pale and sclerae were not icteric. She had no cold or clammy skin and her capillary refill time was less than 2 s. The liver span was 10 cm in the mid-clavicular line and the spleen was normal in size on palpitation.
Initial complete blood count revealed anaemia with 31% haematocrit, as well as thrombocytopenia of 74,000/µL. Liver function tests revealed mild elevated aspartate aminotransferase and alanine aminotransferase of 60 U/L and 86 U/L, respectively. Blood sugar, creatinine, glucose-6-phosphate dehydrogenase (G6PD) enzyme activity and urinary analysis were normal. Microscopic examination of a peripheral blood film showed an asexual stage P. vivax parasitaemia of 69,800 parasites/µL and the diagnosis was confirmed by a positive polymerase chain reaction (PCR) for P. vivax. In patients breathing spontaneously, inferior vena cava (IVC) collapsibility index measured by transthoracic echocardiogram is a predictor of fluid responsiveness when the value was more than 42% []. In this patient, IVC collapsibility index was 46%, which is predictive of a positive fluid responsiveness. She was admitted to the Hospital for Tropical Diseases and given 600 mg chloroquine orally and started on 5% dextrose in 0.9% Sodium Chloride infusion at a rate of 80 mL/h. After 10 h and infusion of 800 mL fluids, the patient complained of postural faintness while getting out of bed. At that moment, she had an upright blood pressure of 77/46 mmHg and a pulse rate of 103 beats/min which increased to 90/50 mmHg in the supine position. Her urine output was 0.5 to 1 mL/kg per an hour. After lying down, she had good consciousness, warm extremities and capillary refill less than 2 s. Her IVC collapsibility index was 31%. Twelve-lead electrocardiogram showed sinus tachycardia with a normal QTc interval.
She was initially diagnosed with severe Plasmodium vivax and given intravenous artesunate 2.4 mg/kg promptly followed by intravenous artesunate in the same dose after 12 h, which was repeated every 24 h for 5 days. Intravenous ceftriaxone was also started to cover potential concomitant bacterial septic shock awaiting blood culture results. Blood cultures obtained before start of antibiotics, however, remained without growth after which antibiotic therapy was discontinued on the 3rd day of admission. After transferring the patient to the intensive care unit, 400 mL normal saline was given over 1 h. After the fluid bolus, her blood pressure was 88/56 mmHg and her pulse rate was 74 beats/min in the supine position with falling to 77/50 mmHg and 72 beats/min while standing, and IVC collapsibility index of 16%, compatible with non-responsiveness to fluid resuscitation. Table details her haemodynamic profiles during hospital admission. This prompted the start of intravenous norepinephrine at a dose of 0.13 µg/kg/min to maintain a blood pressure of 90/50 mmHg in an upright position. Her plasma lactate assessed at that moment was 1.8 mmol/L (normal value: < 2 mmol/L). Her morning serum cortisol on the next day was 32 µg/dL (normal level: > 6 µg/dL) making a diagnosis of primary or secondary adrenal insufficiency unlikely, and corticosteroids were not started. Haemodynamic monitoring by an ultrasound cardiac output monitor (USCOM) in the supine and upright position before receiving norepinephrine showed a marked drop in cardiac index from 3 L/min/m2 in the supine position to 1.9 L/min/m2 after standing for 3 min, despite adequate hydration. The upright positional drop in cardiac output in the upright position was explained by an absence of an increase in stroke volume, and an insufficient increase in heart rate (Table ). This orthostatic hypotension persisted until 3 days after microscopically confirmed parasite clearance, necessitating continued vasopressor support with norepinephrine (Table ) (Figs. , , , , and ). Orthostatic intolerance only resolved completely at the 12th day of follow up. After recovery, the patient received radical treatment with a 14-day course of (0.25 mg/kg daily) primaquine.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [78.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 78.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2766,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3209597-1,Extracted,"A 73-year-old woman was referred to our hospital for surgery due to tuberculosis spondylitis and concomitant ankylosis. Her blood pressure was 110/70 mmHg, and her electrocariogram showed a normal sinus rhythm with a heart rate of 60 beats per minute. She was underwent surgery without immediate complication. However, twenty days after surgery, the patient complained of dyspnea; the arterial oxygen saturation was decreased to 82%, the D-dimer and B-type natriuretic peptide were increased to 9.73 ug/mL and 2,042 pg/mL, respectively. For evaluation of hypoxia, the transthoracic echocardiogram was perfomed and revealed right side cardiac chamber enlargements without right ventricular dysfunction. The peak pulmonary arterial pressure was increased to 59 mmHg. Furthermore, a 2.2 × 2.4 cm homogenous non-mobile echogenic mass was found within the right atrium (). Because of this finding, we performed a transesophageal echocardiogram that showed the right atrial mass was actually a prominent crista terminalis (). Subsequent chest computed tomography (CT) and magnetic resonance imaging (MRI) revealed findings consistent with a pulmonary embolism (), deep vein thrombosis, and a prominent crista terminalis without any definite right atrial abnormal mass ().",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [60.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 60.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 3 + 1.5 =  4.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
2767,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7405995-1,Extracted,"A 60 years old man with a history of newly diagnosed proteinuria was admitted to our hospital with a two months history of fatigue, with trace lower extremity edema. The patient had arthralgias of both knees and hands that had not changed in intensity. There was no hystory of rash, cough, sinus symptoms, chest pain or gastrointestinal complaints. He had long standing nocturia, and increased urinary frequency, but no dysuria. He had undergone routine cholecystectomy 4 months prior to current presentation. On admission, physical exam revealed man in good condition, with trace lower extremity edema, and normal cardiac, pulmonary and abdominal exam, no ascites or hepatosplenomegaly was detected. There was no rash, livedo reticularis, joint effusions or synovitis. He was afebrile, with blood pressure of 110/60 mmHg, heart rate 80 beat /min. Laboratory exam revealed a white blood count (WBC) of 6,15 x109/L (4-109/L), red blood count (RBC ) was 5,32 1012/L (4,30-5,70 x 10 12/L), normal hemoglobin 170 g/L (135-175 g/L), platelet count 254 x109/L (150-400 x 109/L, APTT 32,5 sec (27,4-37,7 sec), and INR 0,85 (0,80-1,20). Erytrocyte sedimentation rate was mild elevated 48 mm/hr, as was the value of iron 37,2 μmol/L (9-31,3 μmol/L). Urinalysis revealed 3+ proteine, no nitrites or glucose. Evaluation of urine sediment revealed several granulated casts, with 20-25/μl RBC, 8-10 /μl WBC. Renal function was normal with serum creatinine 86 μmol/L (63 -109 μmol/L). Urine protein was quantified at 10,68 gr/24h (<150 mg/24 hours), Bence-Jones proteins were not detected in urine specimen. Serum total protein and albumin were respectively of 46,0 g/L (62,0-82,0 g/L) and 17,0 g/L (35,0-50,0 g/L). The total cholesterol was 7,6 mmol/L (<5,3 mmol/L), and triglyceride of 1,82 mmol/L (0,4-0,9 mmol/L). A diagnosis of nephrotic syndrome was confirmed. Our patient received no drugs; no features of acute or chronic infections were found. The investigating for secundary causes of this membranous glomerulonephritis included: anti-double stranded deoxyribonucleic acid (anti-dsDNA) antibodies and antinuclear antibodies (ANA), titers for antineutrophil cytoplasmic antibodies (ANCA), complement levels and tests for cryoglobulins and rheumatoid factor, thyroid hormone, were negative or normal. Serologies for hepatitis A, B, C and HIV, were nonreactive. Measurement of tumor markers Ca -125 showed mild elevated 37,7 U/ml (0-35 U/ml). Thoracoabdominal tomography, stool for fecal occult blood, prostate – specific tumor markers (PSA) were normal or negative. Chest x ray showed no evidence of infiltrate, vascular congestion or cardiac enlargment (the chest radiography was normal). By ultrasound the right kidney’s longitudinal diameter was 13,8 cm and left kidney 14,2 cm, with no pelviectasis, but mild increases parenhimal echogenicity. No renal venous thrombosis was faund on the Doppler sonography. Renal biopsy showed that this was caused by membranous nephropathy. It showed glomeruli with thickening of the capillary walls and capillary loops. There was no mesangial hypercellularity and 40% of interstitium was fibrous. Imunofluorescence showed strong granular IgG along the capillary wall. No IgA deposition and complement were seen.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 0.
The patient's Well's score for pulmonary embolism is 0."
2768,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8601395-1,Extracted,"A 56-year-old male, with a past medical history of diabetes mellitus type 2, hypothyroidism, and celiac disease. He had a history of reactive abdominal and left axillary lymphadenopathy, which was diagnosed by imaging 18 months ago and was stable after repeated scans. He was diagnosed incidentally with latent tuberculosis with a positive QuantiFERON test and was started on rifampicin. Three weeks after starting rifampicin, the patient presented to the emergency department with chest pain. It was centrally located, sudden in onset, squeezing in nature, and with no radiation. The pain lasted for nearly 20 minutes. It was not associated with shortness of breath, hemoptysis, or cough. The patient mentioned that he had a weight loss of around 5 kg over the last couple of months. He had no history of immobility, travel history, or surgical interventions.
The patient was not in distress. Vitally: temperature 37.1 °C, blood pressure (BP) 119/67 mmHg, heart rate (HR) 91 beat per minute, saturation 96% on room air, body mass index (BMI) 27.2. Physical examination was remarkable for mild hepatomegaly, multiple, small, and enlarged lymph nodes in the axillary and inguinal area, with being the largest in the left axilla measuring 1.5 cm. Lower limbs examination revealed stiffness in the left calf but no asymmetry, redness, or tenderness. An electrocardiogram (ECG) was done, showing new changes (T-wave inversion in III, aVF, V3, mild ST-segment depression in V3-V6), along with an old right bundle branch block (Figure ). Chest X-ray showed no obvious pulmonary infiltrates/consolidation, the costophrenic angles were clear, and no apparent cardiomegaly. The patient’s D-Dimer has elevated at 8.01 mg/L FEU and positive troponin at 235 ng/L (normal range max approximately 13 ng/L). All other hematological and biochemical results were within the normal range. Given the clinical scenario with ECG and lab results, CT pulmonary angiography was done, indicating a filling defect seen in bilateral pulmonary arteries extending into the main segmental branches and draped over the bifurcation of the main pulmonary artery, consistent with saddle PE (Figure ). The patient was started on enoxaparin 80 mg BID. Ultrasound Doppler of lower limbs confirmed evidence of DVT, noted at the left, distal saphenofemoral vein (SFV), and popliteal vein levels, showing partial thrombus in the lumen with the partial flow. Extensive thrombophilia and autoimmune workup perturbing antinuclear antibody, antineutrophil cytoplasmic autoantibody, rheumatoid factor, C3, C4, homocysteine levels, factor V Leiden, lupus anticoagulant, protein C, protein S, antithrombin activity, anticardiolipin, IgM and IgG, and anti-B2 glycoprotein IgG, were all negative. Thyroid-stimulating hormone (TSH) was 2.55 mIU/L (normal range: 0.30-4.20) and free T4 of 15.1 pmol/L (normal range: 11-23).
Due to the history of weight loss and lymphadenopathy, an underlying malignancy was of concern; therefore, a repeat PAN CT scan was done. This showed mild hepatosplenomegaly with mildly enlarged upper abdominal lymph nodes and left axillary lymph nodes, which are unchanged since June 2020. An ultrasound-guided core needle left axillary lymph node biopsy was organized and done. The biopsy results showed reactive lymphoid follicles and an unremarkable inter-follicular zone. The biopsy was negative for TB and mycobacterial cultures were negative after 42 days. The patient also underwent a whole-body positron emission tomography (PET) CT, which showed reactive left axillary lymph nodes. No other hypermetabolic lymph nodes were seen. There was no sign of lymphoma or any other fluorodeoxyglucose (FDG)-avid malignancy on PET CT.
After discussion with infectious disease specialists and hematologists, the patient was started on isoniazid and pyridoxine for latent TB. The patient was already on anticoagulation with dabigatran after ruling out malignancy. The patient will be closely followed up in the infectious disease clinic due to the side effects and drug interactions of his current regimen.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [91.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 91.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3 + 1.5 = 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2769,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8459806-1,Extracted,"A 28-year-old male was referred to the emergency department of our hospital presenting with severe headache that occurred five hours ago when he was driving a car. The headache was of sudden onset and associated with intermittent vomiting. Non-contrast head computed tomography (CT) scan performed in the local hospital showed diffused hyperdensity in anterior and posterior fissure, Sylvian fissure, and around the brainstem, indicating the diagnosis of subarachnoid hemorrhage (SAH) (Figures -). Twelve months ago, the patient suffered right-sided weakness. Brain magnetic resonance imaging (MRI) performed in the other hospital demonstrated acute ischemic stroke in the left frontal lobe. The hemiparesis has recovered completely and he has been taking aspirin 100 mg per day ever since. The patient has no other remarkable past medical history.
The patient was admitted to the Department of Neurology for further management. On admission, he was afebrile and drowsy, with heart rate of 69 beats/min, respiration rate of 22 breaths/min, and arterial blood pressure of 129/65 mmHg. A 3/6 pansystolic apical murmur was heard by auscultation. Neurological examination revealed neck stiffness. On day two after admission, digital subtraction angiography (DSA) was performed for evaluation of intracerebral aneurysm. But no aneurysm or cerebral vascular malformation was found on the initial DSA (Figures , ). Results of the laboratory test were unremarkable except for a slightly elevated white blood cell count (11.9 * 109/L). The electrocardiography (ECG) showed nodal tachycardia. Brain MRI performed on day four revealed a previous infarction in the left frontal lobe (Figures , ). Transthoracic echocardiography (TTE) showed a dilated heart and detected a left atrial mass measuring 5.09 * 3.34 cm in size attached to the lower part of interatrial septum, oscillating with heat contraction (Figure ). Moderate-to-severe mitral regurgitation and mild tricuspid regurgitation were observed too (Figure ). A diagnosis of left atrial myxoma was considered.
The patient was transferred to the Department of Cardiac Surgery and underwent atrial tumor resection soon. A gray, polypoid, colloid-like left atrial mass of 6 * 5 * 2.4 cm in size was excised. No residual tumor tissue was detected by transesophageal echocardiogram (TEE). Pathological examination confirmed the diagnosis of atrial myxoma (Figure ). The patient’s symptoms improved in the following two weeks. On day 24 after onset, brain CT angiography (CTA) was performed in order to re-evaluate intracerebral aneurysm, but there was no aneurysm or any other vascular malformation found (Figure ). On day 28, the patient was discharged with no residual neurological symptoms.
We have followed the patient for one year. He remains asymptomatic since discharge. At six months after discharge, TTE was performed revealing no recurrence of the cardiac tumor. And at 12 months, no abnormality was found by a repeated brain CTA (Figure ).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [69.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 69.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2770,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3002912-1,Extracted,"57-year old man presented to emergency department of regional hospital with chest pain, which started after walking in the morning. Dull pain was localized in the middle of his chest and was accompanied with nausea, fatigue and difficult breathing.
He had no history of heart problems, but was a former smoker and had elevated cholesterol levels. During last summer, he noticed varicose veins on right groin and was wearing elastic bandage. He had no history of cardiovascular disease, took no medications, had no known allergies and was in good physical condition. His father died at the age of 80 due to cerebrovascular insult and his mother had pulmonary embolism at the age of 74.
Since chest pain, dyspnea and fatigue didn't subside he called an ambulance. Upon arrival to emergency department he was pale and hypotensive (102/60 mmHg), heart rate was 100 b.p.m. and respiratory rate 22 breaths/min. Oxygen saturation was 95% while breathing 100% oxygen. His body temperature was 36.6 C°. Beside varicose veins on right groin, his physical examination was unremarkable.
On 12-lead ECG there was sinus rhythm with incomplete right bundle branch block, ST segment elevations up to 3 mm in precordial leads V1-V4 and negative T wave in lead III (Figure ).
On the basis of ECG changes and clinical presentation, acute ST segment elevation myocardial infarction (STEMI) was suspected. After receiving aspirin 500 mg, morphine 5 mg i.v., thiethylperazine, unfractionated heparin 5000 IU i.v. and nitroglycerin sublingually, he was immediately transferred to our University medical center for primary coronary intervention (PCI). In case of STEMI, quick referral from local hospital or directly from the field, to catheterisation laboratory is a standard of care in Slovenia. That is why no further diagnostic procedures, which would delay transport to PCI were performed in regional hospital.
The coronaroangiography reveled normal ascending aorta, coronary arteries without atherosclerotic lesions and acute occlusion, however there was a small separate conus artery arising from aortic root with embolic occlusion (Figure , additional file ). The affected artery was too small to attempt PCI.
On admission to medical intensive care unit (ICU) his first blood tests were available. His white blood cell count was slightly elevated (13.4 109/L), so were troponin I (0.128 μg/l - cut off 0.1 μg/l) and D-dimmer (1172 μg/l - cut off 350 μg/l). 4 hours after the onset of symptoms brain pro-BNP concentration was still normal (332.8 ng/l - cut off 500 ng/L). Lactate concentration was not elevated. Arterial blood gas analysis while breathing 6 liters of oxygen via bi-nasal catheter showed pH 7.41, carbon dioxide pressure of 4.3 kPa, oxygen pressure of 17.3 kPa, bicarbonate concentration of 19.9 mM and BE -3.7 mM.
Transthoracic echocardiography reviled good left ventricular systolic function without segmental contraction defects. Right cardiac chambers were enlarged, paradoxical movement of interventricular septum was noted but contractility of right ventricle was not impaired and right heart pressure was estimated to be 40 mmHg + central venous pressure.
With bedside transesophageal echocardiography pulmonary embolism was confirmed; thrombi were seen in both pulmonary arteries (Figure , additional file ); right to left intra-atrial communication was diagnosed after contrast application (Figure , additional file ).
At the time of diagnosis of pulmonary embolism he was hemodynamically stable. He received continuous infusion of unfractionated heparin and was soon transferred to step down telemetry unit. Maximal troponin I value of 3.08 μg/l was reached 24 h after admission. ST segment elevations of precordial leads returned to baseline and inverse T waves appeared on leads V1-V3. Ultrasound of lower extremity veins reveled right popliteal vein thrombosis. In a few days heparin infusion was substituted for warfarin and he was discharged.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 100.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3 + 1.5 = 4.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2771,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7279948-1,Extracted,"On March 5, 2020, a-58-year-old woman was transferred to our intensive care unit (ICU) due to acute hypoxemic respiratory failure. The patient was previously diagnosed with COVID-19 on a screening test for throat discomfort 12 days earlier. The patient lived in Daegu, the epicenter of COVID-19 in Korea, and had acquired the infection through community spread. Seven days before ICU admission, the patient was diagnosed with pneumonia and started lopinavir/ritonavir 400 mg/100 mg tablets twice a day and supplemental oxygen was started 3 days ago. Vital signs on presentation to the ICU were: blood pressure 145/90 mmHg, pulse rate 90/min, respiratory rate 32/min, and body temperature 36.9°C. Arterial blood gas analysis showed pH 7.383, partial pressure of carbon dioxide (pCO2) 33.5 mmHg, partial pressure of arterial oxygen (PaO2) 83.9 mmHg, and bicarbonate (HCO3-) 19.5 mmol/L on high-flow nasal cannula (fraction of inspired oxygen [FiO2], 0.95; flow rate, 50 L/min). The patient was intubated and placed on mechanical ventilation with elaborate lung-protective strategies. The PaO2 improved to 229.1 mmHg on FiO2 0.9, and we initiated intravenous methylprednisolone 60 mg. A chest radiograph showed bilateral, multifocal, patchy consolidations in the lungs (). The C-reactive protein level was 22.9 mg/dL. Nasopharyngeal and oropharyngeal swabs as well as sputum specimens were obtained for retesting at our hospital and reported positive for infection with the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by real-time reverse-transcriptase–polymerase-chain-reaction (RT-PCR) assay.
From the evening on Day 1 of hospitalization, the patient's body temperature began to increase, reached approximately 40°C on Day 2, and was followed by tachycardia and desaturation (). The fever was refractory to repeated administration of antipyretics. The body temperature increased up to 41.6°C, heart rate to 156 per min, and oxygen saturation decreased to 88% on FiO2 of 1.0. Nitric oxide (NO) inhalation was initiated and raised to 40 ppm, and injection of methylprednisolone 60 mg was repeated. However, arterial blood gas analysis showed PaO2 of 77.6 mmHg, and the troponin I level increased to 6.22 ng/mL. Considering extracorporeal membrane oxygenation (ECMO) as the last resort for treatment, we applied a surface cooling device (Arctic Sun®) with a target temperature of 37°C. From an initial core temperature of 41.8°C, the target temperature was rapidly attained within 4.5 hours. PaO2 was markedly improved to 318.2 mmHg, and tachycardia resolved after a few hours. The norepinephrine requirement that had increased up to 16 µg/min during the shock phase was tapered off. Echocardiography on Day 4 showed mid-to-apical-segment akinesia and depressed left ventricular systolic function with an ejection fraction of 26%. The patient was extubated on Day 6 and TTM was stopped on Day 9. Other treatment details including antibiotics and steroid use are summarized in . On Day 12, SARS-CoV-2 RT PCR results converted negatively in all nasopharyngeal, oropharyngeal, and sputum specimens. Supplemental oxygen was discontinued on Day 16, and the patient's cardiac function was confirmed to have recovered on Day 19 with an ejection fraction of 54%. A coronary computed tomographic angiography was also normal. A chest radiograph on Day 22 showed considerable improvement compared to the previous ones ().",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [156.0, 'per min'], 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 156.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2772,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-10143,Extracted,"A 22-year-old woman presents to the emergency department feeling lightheaded and states that her heart is racing. She does not have a history of any chronic medical conditions. She is a college sophomore and plays club volleyball. Although she feels stressed about her upcoming final exams next week, she limits her caffeine intake to 3 cups of coffee per day to get a good night sleep. She notes that her brother takes medication for some type of heart condition, but she does not know the name of it. Both her parents are alive and well. She denies recent illness, injuries, or use of cigarettes, alcohol, or recreational drugs. The pertinent negatives from the review of systems include an absence of fever, nausea, vomiting, sweating, fatigue, or change in bowel habits. The vital signs include: temperature 36.8°C (98.2°F), heart rate 125/min, respiratory rate 15/min, blood pressure 90/75 mm Hg, and oxygen saturation of 100% on room air. The laboratory results are within normal limits. The ECG is significant for a shortened PR interval and widened QRS.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [125.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 125.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2773,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6180849-1,Extracted,"A 54-year-old male patient presented to the emergency department complaining of fatigue and increasingly limited mobility in his right arm. According to his records, the patient had fallen 10 days previously and hit his head and right shoulder. Right-sided subcutaneous facial haematoma and a contusion mark on the right shoulder were observed during physical examination. The examination showed a moderately limited range of motion in the right shoulder. A CT scan of the head and an X-ray of the cervical spine and right shoulder were performed. The CT scan of the head and the X-ray of the cervical spine showed no signs of injury, and the X-ray of the right shoulder was interpreted as normal. Besides a history of smoking and excessive drinking, the medical history was unremarkable. Laboratory examination showed a slightly elevated C-reactive protein inflammatory marker (22 mg l–1), anaemia (red blood cell count = 3.02 × 1012 l–1, haemoglobin = 105 g l–1), thrombocytopenia (platelet count = 46 × 109 l–1), low haematocrit (31%) and an alcohol blood concentration of 55 mmol l–1. As no major injury was found, the patient was discharged. 2 weeks later, the patient returned to the emergency department complaining of fatigue, diffuse arthralgia and myalgia, with severe pain in his right shoulder. The skin on his right upper arm was swollen, reddened and painful to palpation, and his right axillary lymph nodes were enlarged. On examination, the patient had a pulse of 92 beats min–1, blood pressure of 68/38 mmHg, oxygen saturation of 97% and a temperature of 36°C. Laboratory examination showed an elevated C-reactive protein of 129 mg l–1, a white cell count of 11.6 × 109 l–1, red blood cell count of 2.09 × 1012 l–1, haemoglobin of 70 g l–1, a haematocrit of 21% and a gamma glutamyl transferase of 1.36 μkat l–1. The patient was hospitalized and diagnosed with right upper arm cellulitis and probable sepsis. An emergency ultrasound examination of the upper arm showed a collection of thick fluid with the presence of gas bubbles and a free fragment of the cortical bone (). At this point, the shoulder X-ray image that was taken during the patient’s first visit to the hospital was re-examined, and a clavicle fracture in the distal third of the clavicle was diagnosed (). In order to assess the anatomical relations between the collection of fluid and its adjacent structures and to better evaluate the extent of bone involvement, we immediately performed an MRI on a Signa scanner 1.5 T (General Electric Medical Systems, Milwaukee, WI). The imaging protocol was performed using a short tau inversion–recovery sequence (coronal plane), a T
2 fast relaxation fast spin-echo (FSE) fat-saturated sequence (axial plane) and a T
1 FSE sequence (coronal plane) before i.v. application of the paramagnetic contrast media, and afterwards with a T
1 FSE fat-saturated sequence (coronal, axial plane). The MRI confirmed osteomyelitis of the clavicle and moderate right-sided pleural effusion (). Apart from these MRI findings, the X-ray of the lungs also showed radiological signs of possible infiltration of the right lower lobe.
Empirical therapy began with 2 g 6 h–1 of i.v. floxacillin and, after Streptococcus pneumoniae and E. coli grew in the blood cultures, 2 g 6 h–1 of i.v. cefotaxime was added to the therapy. No bacteria were isolated from the right pleural punctuate and uroculture. A thorough physical examination revealed a deep 1 × 2 cm wound on the patient’s left fourth toe, exposing the underlying tendon. The wound showed no signs of infection, but polybacterial flora grew on the smear taken from the wound, in which the presence of E.coli was identified. The patient was not a suitable candidate for immediate operation owing to abnormal haemostasis (prothrombin time = 68.9 s; international normalized ratio= 2.45) and profound anaemia (treated with supportive therapy with three ampoules of phytomenadione intramuscular and six units of concentrated thrombocytes i.v.), until 2 days later, at which point surgical debridement and drainage were performed. A day prior to the surgery, there was a spontaneous discharge from the clavicle area of approximately 500 ml of pus. E. coli grew on a smear of the intraoperative right clavicular wound and a clavicle tissue sample.
Despite surgical treatment, the patient’s condition deteriorated rapidly during the next 48 h with the development of acute respiratory distress syndrome and cardiac arrest with asystole. After successful cardiopulmonary resuscitation and the return of spontaneous circulation, systemic inflammatory response syndrome developed with multiple organ failure. The patient’s condition deteriorated rapidly, and he passed away the following day.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [92.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 92.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 3 + 1.5 =  4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2774,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4412089-1,Extracted,"A 43-year-old woman was admitted for the evaluation of a 25 kg weight loss resulting in severe protein malnutrition due to intentional calorie restriction (300 Kcal/day) for six months. She had no previous medical or surgical history and was not receiving medications. The patient believed that she developed an “autoimmune disease” that improved with self-induced calorie restriction. On presentation, the patient weighed 30.1 kg (BMI 11), temperature 98.6°F, heart rate 75 bpm, and blood pressure 105/68 mmHg. She was markedly cachectic with temporal wasting, scaphoid abdomen, and normal liver span without stigmata of cirrhosis. She was normally oriented and asterixis was absent. Her admission laboratory testing revealed AST (2895 U/L), ALT (1868 U/L), alkaline phosphatase (460 U/L), bilirubin (2.9 mg/dL), albumin (3.7 g/dL), INR (1.9), amylase 188, lipase 322, CPK 535, normal TSH, negative viral hepatitis and autoimmune serologies, ceruloplasmin (17 mg/dL), and elevated 24-hour urine copper (117 mcg). Abdominal ultrasound revealed a heterogeneous liver with patent vessels. A slit lamp exam failed to reveal Kayser-Fleischer rings. Psychiatry consultation diagnosed a somatic delusional disorder. She did not fit the DSM-IV TR diagnostic criteria for anorexia nervosa. Five days after the initiation of oral refeeding and intravenous vitamin K, laboratory testing revealed AST (221 U/L), ALT (539 U/L), alkaline phosphatase (373 U/L), bilirubin (1.3 mg/dL), and INR (1.43). During her initial refeeding period, she had occasional episodes of bradycardia, hypothermia, hypotension, and EKG changes with inverted T waves and prolonged QTc. On hospital day 9, her transaminases were improving but still 5–7 times the upper limit of normal and a liver biopsy was performed. The liver biopsy revealed mild non-specific acute hepatitis with intrasinusoidal and mild centrilobular perivenular fibrosis, focal necroinflammatory foci, acidophil bodies (long arrow), and increased mitotic figures in the hepatic lobules (short arrow) (). Dry copper weight was 53.8 ug/g. ATP7B PCR gene testing was negative for Wilson's disease.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [75.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 75.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2775,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8579618-1,Extracted,"A previously healthy 50-year-old man who was a smoker was referred to the emergency department with progressive dry cough and dyspnea for 1 month. He had been prescribed antiallergic and antitussive medications by a family doctor; however, they were ineffective. The patient had no family history of cardiopulmonary disease or malignancy. Physical examination and blood tests in the emergency department were non-diagnostic. Electrocardiography revealed negative T waves, and echocardiography was suggestive of pulmonary hypertension. Enhanced computed tomography (CT) revealed no apparent pulmonary embolism. He was prescribed a bronchodilator and corticosteroid under a diagnosis of cor pulmonale due to chronic obstructive pulmonary disease; however, his symptoms did not alleviate. The patient was admitted to our hospital two days later.
His vital signs on admission were as follows: oxygen saturation, 94%; pulse rate, 100 beats per minute; body temperature, 37.1 °C; blood pressure, 130/93 mmHg; and respiratory rate, 18 breaths per minute. Physical examination revealed right cervical lymphadenopathy, with the affected lymph node measuring 10 mm in size. Laboratory findings were as follows: 95.7 (normal: < 18.4) pg/mL of brain natriuretic peptide, 6.9 (normal: < 1.0) µg/mL of D-dimer, 134 (normal: 124–222) U/L of lactate dehydrogenase, 1.77 (normal: < 0.15) mg/dL of C-reactive protein, 8.7 (normal: < 5.0) ng/mL of carcinoembryonic antigen, and 19.4 (normal: < 2.1) ng/mL of cytokeratin-19 fragment.
Chest radiography revealed bilateral hilar lymphadenopathy (Fig. A). Enhanced CT showed no pulmonary embolism or deep vein thrombosis; however, right cervical, bilateral hilar/mediastinal, and upper abdominal lymphadenopathy was observed (Fig. B–D). Moreover, septal thickening and ground-glass opacities were predominantly detected in the lower lung lobes (Fig. E).
Electrocardiography showed negative T waves in precordial leads (Fig. A), and echocardiography indicated pulmonary hypertension with normal left ventricular function (Fig. B, C).
We suspected PTTM because of the subacute course, pulmonary hypertension without apparent etiology, elevated tumor marker levels, and diffuse lymphadenopathy. The primary cancer origin could not be determined using CT or tumor markers. Echo-guided needle biopsy of the right cervical lymph node was performed on day 1. Stamp cytology of the biopsy revealed atypical cells of epithelial origin. On day 2, a transbronchial lung biopsy was performed. On day 3, an interim report regarding the pathological findings of cervical lymph node biopsy revealed adenocarcinoma with signet ring cell carcinoma (SRCC) (Fig. A, B). Therefore, gastric cancer was suspected; however, upper endoscopy performed by a trained gastrointestinal endoscopist showed no mucosal abnormalities and a fully distensible gastric wall (Fig. C). Colonoscopy results were also normal. On day 4, the patient started receiving edoxaban (60 mg/day) for probable hypercoagulability due to PTTM. On day 5, the reported results of cervical lymph node biopsy with immunohistochemical staining were consistent with those of gastric cancer (Fig. D, E). The pathological findings of transbronchial lung biopsy were unremarkable. At this time, the patient’s status was stable without any apparent changes.
On day 6, his dyspnea mildly progressed, and oxygen delivery was initiated at 2 L/min via a nasal cannula. On day 7, after consultation with gastroenterologists at our institution, administration of imatinib (200 mg/day), prednisolone (30 mg/day), and tegafur/gimeracil/oteracil plus oxaliplatin (SOX) therapy was initiated. On day 8, the patient’s hypoxia suddenly worsened, and he subsequently died.
An autopsy was performed, and macroscopic examination showed no abnormalities in the gastric wall (Additional file a); however, lymphadenopathy surrounding the stomach was detected. Macroscopic pulmonary thromboembolism was not observed. Multiple serial sections of the whole stomach were prepared. Microscopically, two gastric cancer lesions of pure SRCC that measured 15 12 mm and 8 8 mm were identified in the pyloric region (Fig. A–C and Additional file b and c). Although these lesions were within the lamina propria, multiple lymphovascular invasions separate from the two superficial lesions were observed in the layers from the submucosa to the subserosa (Fig. D). Multiple lymph node metastases surrounded the stomach. No findings of Helicobacter pylori-associated gastritis were observed. Moreover, tumor emboli and thickened epithelial cells of the small pulmonary arteries were consistent with PTTM (Fig. E). Carcinomatous lymphangiomatosis was also observed (Fig. F). Examination of organs other than those mentioned above showed no tumor cell in the viscera or vascular system.
The final diagnosis was PTTM in occult early gastric cancer that was undetectable on upper endoscopy.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 100.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
2776,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8286635-1,Extracted,"A 44-year-old female with past medical history significant for anxiety, seizure disorder, hypothyroidism, and multiple provoked and unprovoked DVTs and PE for which she took 75 mg oral dabigatran twice daily presented to the ED with fatigue and shortness of breath. According to the patient, she was unable to walk from her bed to the bathroom without feeling winded. She also had sharp chest pain whenever she took a deep breath with pain radiating to the right side of her neck. She presented with similar symptoms and was admitted to the hospital two days prior and was diagnosed with a DVT of the left lower extremity and PE of the right pulmonary artery. She was discharged home after one night in stable condition with a prescription for 150 mg twice daily dabigatran, which was double her previous dosage.
She had been taking her dabigatran for the last five years; however, over the past two months, she had multiple interruptions in taking it as she was instructed to stop taking dabigatran four days prior to and following a recent spinal surgery that was rescheduled multiple times. She also occasionally uses marijuana, smokes half a pack of cigarettes most days for the past 10 years, and drinks alcohol a couple of times a month. She denied oral contraceptive use.
A complete review of systems was performed and was significant for left inner thigh pain that was slowly worsening in the last few days. Vital signs obtained were oxygen saturation of 99% on room air, blood pressure 142/95 mmHg, temperature 37.2°C, pulse 98 beats per minute, and respiratory rate 18 breaths per minute. She often required deep breaths between words when talking. She was not in acute distress, however. Her physical exam was significant for tachycardia, tachypnea, and tenderness to palpation over the left thigh with no obvious deformities, swelling, or rashes seen.
Differential diagnosis included but was not limited to PE, acute coronary syndrome, pneumothorax, aortic dissection, pericarditis, pneumonia, pleurisy, and gastro-esophageal reflux. The initial diagnostic workup was remarkable for leukocytosis and elevated troponin (Table ). A d-dimer was not obtained as the patient's pre-test probability of having a PE was too high, meaning we would have obtained a computed tomography angiogram (CTA) of the chest regardless.
Computed tomography angiogram was significant for bilateral PE in the distal left main pulmonary artery extending into the left lower lobe pulmonary artery branches as well as distal right main pulmonary artery extending into the upper and lower lobes. The heart was at the upper limit of normal size (Figure ).
An echocardiogram demonstrated preserved left ventricular function with an ejection fraction of 55% and was significant for a right ventricular systolic pressure of 57 mmHg and left pleural effusion. Bilateral lower extremity ultrasound re-demonstrated extensive left lower extremity DVT from left common femoral, superficial femoral, popliteal, and deep calf veins. The electrocardiogram demonstrated sinus tachycardia.
In consultation with hematology, a heparin drip was initiated. The patient was subsequently admitted to the medical floor. The patient was not a candidate for ekosonic endovascular system (EKOS) due to oral anticoagulation and showed an elevated international normalized ratio (INR). She was bridged to warfarin due to the patient's preference for no longer being on dabigatran. Hematology suggested that clot formation was likely secondary to medication non-compliance (intermittent medication use) rather than the failure of dabigatran. The patient’s hospital course was complicated by multiple episodes of hematemesis as well as hematochezia that were addressed and resolved. She was ultimately bridged to warfarin and discharged home with oxygen as well as follow-up with hematology.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [98.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 98.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 3 + 1.5 =  4.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
2777,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8558788-1,Extracted,"A 4-year-old girl with a history of eczema and absence seizures treated with ethosuximide presented with persistent fever, migratory joint pain, joint swelling, and hematuria. She was last at her baseline state of health 3 months prior to presentation, after which she experienced recurrent fevers and was hospitalized three times for pneumonia and impetigo. She then developed arthralgia, joint swelling, abdominal pain, fever, sore throat, cough, and change in behavior, prompting admission to a referring hospital. She was diagnosed with acute otitis media, started on ciprofloxacin, and transferred to our hospital for further management.
At admission, her temperature was 37.5°C, heart rate was 115 beats/min, respiratory rate was 20 breaths/min, and blood pressure was 121/84 mmHg. She appeared uncomfortable and was “not herself” according to her mother. Physical examination revealed diffuse polyarthritis and tender generalized lymphadenopathy. There were no appreciable skin rashes, mucosal changes, cardiac murmurs, or pleurodynia. She did not have any history of travel outside the United States, toxic exposures, or contact with other sick children. Family history was significant for SLE in her paternal grandmother’s sister. There was no family history of consanguinity.
Admission laboratory studies were significant for anemia (hemoglobin 10.5 g/dL, range: 11.5–14.5 g/dL), elevated erythrocyte sedimentation rate (ESR; >145 mm/h, range: 0–20 mm/h), elevated C-reactive protein (1.12 mg/dL, range: 0.0–0.9 mg/dL), and a positive Direct Coombs test. White blood cell count (9.1 × 103/µL, range: 4.0–12 × 103/µL), platelets (267 × 103/µL, range: 150–450 × 103/µL), and thyroid-stimulating hormone (1.34 UIU/mL, range: 0.66–4.75 UIU/mL) were within normal limits. HIV and tuberculosis testing were negative. Urinalysis was notable for 30 mg/dL of protein as well as 15 red blood cells per high-power field. Quantitative urine protein-to-creatinine ratio was 1790 mg/g (nephrotic range > 3500 mg/g).
 The calcium-to-creatinine ratio was 0.07 (normal range <0.2).
 There was no microbial growth on urine cultures. Creatine kinase was within normal limits. Serum complement studies were notable for low C3 (48 mg/dL, range: 86–166) and low C4 (6 mg/dL, range: 9.7–36). C1q immune complex binding protein was high (61 mcg Eq/mL, range ⩽ 25). She was also positive for both lupus anticoagulant and anticardiolipin antibodies. Recent outpatient rheumatology labs revealed an ESR of 77 mm/h, elevated antinuclear antibodies (ANA; >1:1280), as well as positive anti-double-stranded DNA (dsDNA), anti-Smith and anti-ribonucleoprotein antibodies. Unfortunately, her symptoms worsened before she could follow up on these results in clinic.
Brain magnetic resonance imaging (MRI) with arterial and venous phase contrast was done due to abnormal behavior; no intracranial pathology or vascular abnormalities were present. Abdominal ultrasound revealed grade 2 pelviectasis in both kidneys, mild distension of the right renal pelvis, slight hepatomegaly, increased mesenteric echogenicity, trace pelvic free fluid, and no masses.
 A bone marrow biopsy—performed due to her arthralgias and lymphadenopathy—showed mildly hypocellular bone marrow with no blasts or other pathology. To further investigate the hematuria and proteinuria, a kidney biopsy was done, which revealed mild mesangial hypercellularity and immune complex membranous glomerulonephritis with full house IgM/C3-dominant staining on immunofluorescence and reticular aggregates on electron microscopy, consistent with Membranous Lupus Nephritis Class V ().",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [115.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 115.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2778,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6820897-1,Extracted,"A 59-year-old Caucasian male with no history of heart disease presented with shortness of breath with reported medical history of chronic obstructive pulmonary disease and tobacco use. He was treated for a COPD exacerbation without complications. On day 6 of his hospitalization, at approximately 12 a.m., he developed acute onset substernal, non-radiating chest pain with associated nausea. He denied previous history of similar symptomatology. At the time of event, he was hypertensive with a blood pressure of 190/110 mmHg, tachycardic at a rate of 150 beats per minute, tachypnic with a respiratory rate of 24 breaths per minute, saturating at 97% on three liters nasal cannula. He was actively being monitored on telemetry. At the time of symptom onset, he was found to have Torsades de pointes (figure ) with progression to atrial fibrillation.
EKG obtained during the event demonstrated new onset atrial fibrillation with rapid ventricular response and significant ST elevations in the anterolateral leads that was significantly different when compared to admission EKG (figures -).
He was subsequently started on a heparin and nitroglycerin drip, along with an amiodarone drip and transferred to the intensive care unit for close hemodynamic monitoring. His symptoms resolved shortly after. A repeat EKG revealed resolution of ST elevations (figure ).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [150.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 150.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3.0 + 1.5 = 4.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2779,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-2803897-1,Extracted,"A 59-year old Caucasian female admitted to medical service for syncope and anemia. Initial evaluation revealed left lower quadrant abdominal pain and passage of maroon-colour stool which had been present for two days prior to the admission.
She has a past medical history which is significant for undefined hypercoagulable disorder characterized by 2 episodes of pulmonary embolism, hypothyroidism, Riedel's thyroiditis for which she had thyroidectomy, depression and obsessive-compulsive disorder. She was on the following medications- Coumadin, Synthroid, and Klonopin.
Physical examination revealed a middle-aged woman who was afebrile, tachycardic with heart rate of 136 beats per minute and orthostatic hypotension [supine blood pressure - 113/85 mmHg and 80/60 mmHg in sitting position].
Pulmonary examination was normal
Abdominal examination revealed a mildly but diffusely tender abdomen with grossly heme positive stool on rectal examination.
Initial laboratory work-up showed the following:
Complete blood count- white cell count 17,300/mm3, hematocrit 27.6%, platelet 167,000/mm3
Coagulation profile- PT 51.4 seconds, PTT 46.5 seconds, INR 15.3
Biochemical profile was normal
In view of abdominal pain and lower gastrointestinal bleeding, a computerized tomography scan of the abdomen and pelvis was ordered which revealed a mass within the small bowel associated with thickened small bowel wall and mesenteric lymphadenopathy [fig ].
She had the anticoagulation reversed with fresh frozen plasma and her INR quickly corrected to 1.4. She also had 2 units of blood transfused which raised the hematocrit to 28.1. She underwent laparotomy about 36 hours into the admission. Operative findings include a 5 cm mass in the mid jejunum with associated mesenteric lymphadenopathy [fig ]. The affected jejunal segment was resected and a side-to-side anastomosis was done. She had an uneventful post-operative course and was discharged home on post-operative day 5.
Pathology showed amyloidoma associated with ulceration and extensive recent and organizing hemorrhage. Congo red staining of the tumor was done and apple-green birefringence under polarized light was demonstrated [fig ]. Adjacent bowel proximally and distally to the tumor did not stain with Congo red.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [136.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 136.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2780,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3514371-1,Extracted,"A 55-year-old Iranian man was hospitalized due to left flank pain for five years before admission as well as dysuria, urinary frequency, and a decrease of urinary force and caliber. He had a negative history of diabetes mellitus, hypertension, cardiovascular disease, malignancy and drug abuse. He mentioned a history of recurrent febrile urinary tract infections, which had been treated medically. On admission he was ill-looking. His temperature was 38.6°C. His blood pressure was 120/80mmHg. His respiratory rate was 16 breaths per minute and his pulse rate 83 beats per minute. Lung, cardiovascular, genital, rectal and neurological examinations were normal. His blood test results at admission showed a white blood cell count of 8200/μL, hemoglobin 14.5g/dL and platelet count of 233,000/μL. A urine analysis and culture showed no infection. An ultrasound study of his left kidney revealed a hypoechoic heterogeneous mass in the upper pole measuring 62×54mm. The clinical impression was a renal tumor or xanthogranulomatous pyelonephritis. He underwent a left radical nephrectomy. During the operation, the mass was seen attached to his descending colon and psoas muscle. The specimen was sent to the pathology ward. Gross examination showed an ill-defined yellowish rubbery solid mass, measuring 7×7×3cm, that occupied the superior pole and mid portion of his kidney (Figure ). Macroscopic examination had revealed that the lesion extended to the renal sinus and perinephric fat.
Histological examination revealed diffuse infiltration of sheets of Periodic Acid Schiff-positive histiocytes into the renal parenchyma. These cells had granular acidophilic cytoplasms (Figure ) and some of them showed round concentric layered intracytoplasmic Michaelis-Gutmann bodies (Figure ). The histiocytes had infiltrated the renal sinus and perinephric fat. The immunohistochemical stainings showed strong reactivity for CD 68 (Figure ), and vimentin and negative immunoreaction for pancytokeratin, CD 10, cytokeratin 7, E-cadherin, CD 15, α-methylacyl-coenzyme A racemase and tyrosine-protein kinase Kit (C-kit). The final diagnosis was renal parenchymal malakoplakia.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [83.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 83.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2781,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6819342-1,Extracted,"The patient was a 60-year-old male who was referred to our institution for an intra-abdominal lesion. Abdominal computed tomography performed at a local hospital revealed a huge intra-abdominal mass. The patient had symptoms of vague abdominal discomfort and fatigue, which persisted for > 4 months. Six years earlier, he had visited an orthopedic clinic at another institution with a chief complaint of a painless mass in his right thigh. He was suspected of having a liposarcoma by clinical magnetic resonance imaging (Fig. ). The patient received wide local excision of the mass, and the maximum tumor diameter was 11 cm. The final pathological findings were myxoid liposarcoma with negative resection margins, stage IIIB according to the AJCC 8th edition []. The immunohistochemical findings were S-100(−) and CD34(−), and the positive rate of Ki67 was 1–2%. The patient was treated with adjuvant radiotherapy (200 cGy, 30 times), but lost up to follow-up after 2015. He had no significant medical or family history.
On physical examination, his blood pressure was 130/90 mmHg, heart rate was 90 beats/min, body temperature was 36.8 °C, respiratory rate was 20 breaths/min, and oxygen saturation at room air was 100%. The abdomen was moderately distended and rigid, without signs of peritonitis. A computed tomographic scan of his abdomen confirmed the presence of a heterogeneous enhancing mass lesion in the right mid-to-lower abdomen extending to the pelvic cavity (Fig. ). Positron emission tomography showed no distant metastasis, including in both lung fields (Fig. ). Core needle biopsy was not performed owing to the history of myxoid liposarcoma [], and we decided to perform an exploratory laparotomy for both diagnosis and treatment. His breath sounds were normal, and there were no significant findings from review of other systems. The results from laboratory examination were normal, including those for blood chemistry, routine blood tests, and tumor markers.
The patient was taken to the operating room for an exploratory laparotomy. A mid-line abdominal incision was made, and there was no evidence of ascites and peritoneal or distant metastasis in the abdominal cavity. The tumor was a multi-lobulated gelatinous mass (Fig. ) originating from the small bowel mesentery, 25 × 20 cm in size, so we performed wide local excision including small bowel resection and anastomosis. The patient was transferred to the general ward after operation and discharged 8 days after the surgery without immediate complications. At a follow-up appointment, the patient was in good condition without any symptoms and was transferred to a medical oncologist for further treatment. He is currently undergoing doxorubicin-based chemotherapy (75 mg/m2, every 3 weeks, eight cycles).
Histopathological examination of the intra-abdominal tumor revealed paucicellular with monomorphic, stellate, or fusiform-shaped cells in the myxoid parenchyma that were diagnosed as metastatic myxoid liposarcoma (Fig. ). Expert pathologist with 15 years of experience described the pathologic results for this study. The immunohistochemical findings were S-100(−), CD34(−), p53(−), desmin(−), SMA(−), EMA(−), CD31(−), HMB45(−), PanCK(−), and vimentin(+), and the positive rate of Ki67 was 5–7%. Finally, translocation t (12;16)(q13;11.2) FUS-DDIT3 was demonstrated by molecular analysis to confirm diagnosis of myxoid liposarcoma.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 90.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2782,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8012067-1,Extracted,"An 80-year-old female presented with a past medical history of hypertension, type II diabetes mellitus, transient ischemic attack, and end-stage renal disease due to diabetic nephropathy. She had been anuric and on hemodialysis for four years. She presented to the emergency department accompanied by her son due to generalized weakness, dyspnea on exertion, and mild confusion for the past three days. She had missed her last hemodialysis session and denied any chest pain. Her home medicines included aspirin, atorvastatin, amlodipine, carvedilol, hydralazine, and ergocalciferol. Her blood pressure was 131/58 mmHg with an irregularly irregular heart rate of 87 beats per minute. Physical examination demonstrated lethargy, confusion, and volume overload. Laboratory work-up was significant for a potassium level of 8.6 mEq/L and creatinine of 12.2 mg/dL. Repeat potassium was 8.7 mEq/L. Calcium level was normal, and blood gas results were as follows: pH of 7.28, pCO2 of 32 mm Hg, pO2 of 99 mmHg, and HCO3 of 12.8 mmol/L. ECG showed sinus arrest with ectopic atrial rhythm and intermittent junctional escape beats (Figure ). She was admitted to the intensive care unit for close monitoring of her rhythm and neurologic status.
She had been in sinus rhythm prior to this presentation.
The patient was given intravenous calcium gluconate, insulin, glucose, and bicarbonate infusion along with potassium-binding resin. Repeat potassium was 8.0 mEq/dL, pH was 7.31, and HCO3 was 16.0 mmol/L. There was no improvement in her neurologic status. The nephrology service was consulted and emergent hemodialysis was pursued to manage severe hyperkalemia and metabolic acidosis. Potassium level improved to 5.3 mEq/L, pH to 7.39, and HCO3 to 23 mmol/L after the first hemodialysis. Her symptoms improved after two hemodialysis sessions, and hyperkalemia and acidosis resolved. ECG was obtained, which showed normal sinus rhythm with non-specific ST-T wave abnormality (Figure ).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [87.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 87.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2783,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7430549-1,Extracted,"A 31-year-old male with a past medical history significant for hepatitis C, IV drug use, and nicotine dependence presented with severe back pain that started one month ago. He reported that the pain started suddenly while he was trying to get out of his vehicle and progressed to the point where he could not to lay flat or sit down. His pain was located in the middle and lower back, radiating to his abdomen, and both lower extremities. He denied any numbness, tingling, weakness, or decreased sensation of the lower extremities. He also denied urinary/stool incontinence, fever, or chills. There was no pertinent prior history of back trauma or surgery. The patient admitted to abusing IV heroin daily and sharing needles with his fiancée. Upon admission to our facility, vital signs were within normal range except for a heart rate of 115 beats per minute (bpm). On physical examination, significant tenderness was noted at the middle and lower spine. No obvious bony deformity or skin abnormalities were noted. Neurological examination was normal except for decreased power 3/5 in bilateral lower extremities. Extensive laboratory work-up was done revealing a white blood cell count of 10.7 x 109 cells per liter, hemoglobin 12.8 g/dl, with the rest of the work-up within normal range including lactic acid, urinalysis, creatinine, glucose, liver function, and serum electrolytes. CT of the abdomen and pelvis with contrast revealed marked irregularity of the endplates at the L3-L4 level and mild irregularity of the endplates at the L4-L5 level suggestive of osteomyelitis/discitis with no evidence of a paraspinal fluid collection (Figure ).
Core biopsy of the superior endplate of L4 and adjacent disc material was done and sent for microbiology and pathology review. In addition, blood cultures were obtained. The patient was started on vancomycin and piperacillin-tazobactam. His bone culture came back positive for Lactobacillus species; however, blood cultures remained negative. Infectious disease was consulted and recommended switching antimicrobial coverage to ampicillin. He then developed a rash prompting a switch from ampicillin to clindamycin. Clinical improvement was noted after starting antibiotics, and the patient was discharged on six weeks of oral clindamycin.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [115.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 115.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2784,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6380140-1,Extracted,"A 49-year-old woman presented to the emergency department with worsening dyspnea and generalized edema for 10 days. Her past, personal, and family histories were unremarkable. On physical examination, her temperature was 36.6°C, blood pressure was 194/112 mmHg, pulse was 120 beats/min, and respiratory rate was 24 breaths/min. Oxygen saturation was 100% under ambient air. Expiratory wheezes bilaterally and crackles at the left base were noted. A grade 2/6 systolic murmur was heard at the left upper sternal border and apex, radiating to the axilla. Generalized anasarca with pitting edema over the bilateral upper and lower extremities was noted.
An electrocardiogram showed sinus tachycardia and left ventricular hypertrophy with a strain pattern. A chest X-ray revealed cardiomegaly and patchy airspace consolidations with infiltrations in the right lung field []. A transthoracic echocardiogram showed a global left ventricular hypertrophy and hypokinesia with an ejection fraction of 22%. Pertinent laboratory results revealed normocytic anemia and elevated serum B-type natriuretic peptides levels of 2,440 pg/mL, with normal liver function, kidney function, and electrolyte status. Medications with intravenous nitrite, furosemide 20 mg twice daily, and oral anti-hypertensive heart failure medications including bisoprolol 0.625 mg once daily, perindopril 5 mg once daily, sustained-released nifedipine 30 mg twice daily, and spironolactone 25 mg twice daily were prescribed. An abdominal sonography was performed to evaluate the underlying causes of secondary hypertension, which demonstrated a huge lobulated heterogeneous mass (approximately 7.7 × 6.4 × 9.3 cm3) at the lower pole of the right kidney and a mass (approximately 4.2 × 3.2 cm) over the left suprarenal area. The masses were confirmed through magnetic resonance imaging []. Moreover, a urine catecholamine analysis revealed elevated levels of dopamine (991.7 μg/day, normal range 138–540 μg/day) and norepinephrine (104.1 μg/day, normal range 10–80 μg/day) with a normal epinephrine (7.6 μg/day, normal range 0–24 μg/day) level. The medication of bisoprolol was shifted to labetalol 200 mg twice daily. The patient underwent computed tomography-guided biopsy of the pulmonary nodule, left laparoscopic adrenalectomy, and right laparoscopic radical nephrectomy. Grossly, a renal tumor extended into major vein and invaded perirenal fat and peri-pelvic fat tissue. The adrenal gland was a brown tumor mass. Histopathological analysis confirmed the diagnoses of clear cell RCC of the right kidney (Fuhrman nuclear grade II) with metastasis to the lung. To exclude the possibility of neuroendocrine differentiation, which impacts the overall prognosis of RCC, immunohistochemical staining for the neuroendocrine feature, including chromogranin-A and synaptophysin, was performed and revealed negative results.[] Moreover, based on the WHO Pathology and Genetics of Tumors of Endocrine Organs, few foci revealed spindle cell change, nuclear hyperchromasia, and necrosis of tumor cells, indicating biologically aggressive behavior (atypical) pheochromocytoma of the left adrenal gland [].[] Genetic analysis of the patient revealed no mutation in the coding region of von Hippel-Lindau (VHL) gene. Target therapy with sunitinib was initiated. The blood pressure was 146/86 mmHg 1 month after surgery. One year later, a chest X-ray revealed a normal heart size without visible airspace consolidations [], and an echocardiography demonstrated normal left ventricular systolic function. Possibly due to the residual tumor, pre-existing hypertension, or sunitinib-related hypertension, the patient is presently under target therapy for her RCC and takes oral antihypertensive medications with stable disease.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3.0 + 1 =  4.0.
The patient's Well's score for pulmonary embolism is 4.0."
2785,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5883383-1,Extracted,"A 75-year-old Caucasian man presented to his local hospital with malaise, fever, and nausea for five days. He had a bio prosthetic aortic valve replacement for mixed aortic valve disease 12 years ago; further significant past medical history included placement of a permanent pacemaker for complete heart block, right total hip replacement, hypertension and benign prostatic hyperplasia (BPH). The patient had no history of smoking, alcohol consumption or illicit drug use. The patient had no recent surgeries or dental work, and the review of systems was unremarkable. The physical exam revealed vital parameters of HR 97 bpm regular, BP 134/87, the temperature of 101.5°F, respiratory rate of 18 per minute and oxygen saturation of 96% on room air. On precordial auscultation, a systolic and a diastolic murmur were heard in the aortic area, mild bi-basal crackles, but no jugular venous distention or peripheral edema. The rest of the physical exam was unremarkable. The labs showed a normal white cell count (WCC) of 9.9 × 10
6/L, elevated C-reactive protein to 214.9 mg/L (normal <5 mg/l) and a hemoglobin of 11.2 g/dl), the other labs were unremarkable. His mid-stream urine showed WCC < 20; red cell count (RCC) of 20–50 and it grew mixed organisms, all considered part of the normal flora. Chest X-ray, CT scan of the brain, thorax, abdomen, and pelvis did not show any source of infection.
The patient was empirically commenced on IV piperacillin-tazobactam and vancomycin. Blood cultures collected at the time of admission grew
Aerococcus urinae in both bottles. A repeat set of blood cultures corresponding to a spike of fever in the following 24 hours also grew
Aerococcus urinae in both bottles; all cultures were sensitive to ampicillin (MIC 0.064 mg/L) and gentamicin (MIC 2 mg/L).
A trans-thoracic echocardiogram showed mild aortic regurgitation and mitral regurgitation with no clear vegetation, however, trans-esophageal echocardiogram (TOE) showed normal left ventricular function with moderate aortic regurgitation due to large mobile vegetation on the bio-prosthetic aortic valve. There was no peri-valvular abscess or features of the paravalvular abscess noted (See
). Pacemaker lead and right-sided valves were not involved.
Clinical presentation, echocardiographic findings, and positive blood cultures fulfilled Duke’s criteria (Hoen
et al., 1996) for IE. The patient was managed as prosthetic aortic valve endocarditis from
Aerococcus urinae with IV amoxicillin 2 grams every 4 hours, and gentamicin 1 mg/kg twice daily as per hospital guidelines for IE. IV antibiotic therapy for six weeks in total with possible surgery for prosthetic valve replacement was planned (Truninger
et al., 1999).
Despite prompt initiation of appropriate antibiotic treatment and intensive clinical monitoring, the patient failed to improve this hospitalization and developed sudden pulmonary edema and worsening aortic regurgitation on repeat transthoracic echo and unfortunately died due to rapid deterioration before surgery. As per family’s wishes, an autopsy was not performed.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [97.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 97.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2786,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6150749-1,Extracted,"A 36-year-old female with past medical history significant for schizophrenia presented to the hospital after experiencing arthralgia for nine days followed by an evanescent rash for three days accompanied by persistent high-grade fever. Her symptoms were associated with pleuritic chest pain. The rash was non-pruritic and non-painful spreading over the neck, trunk, and all four extremities. The patient was diagnosed with schizophrenia five years before to her admission, and has been receiving olanzapine 20 mg daily for the last six months. She admitted noncompliance with her medication recently, due to developing diabetes mellitus and weight gain while being on olanzapine.
In the emergency department, her initial vital signs were as follows: temperature, 103.7°F (39.8°C); blood pressure, 111/55 mmHg; heart rate, 141 beats/minute; and respiratory rate 22 breaths/minute. The patient looked anxious and diaphoretic. Skin examination revealed salmon-like, blanchable, maculopapular rash of various shapes and sizes, most prominent over bilateral extremities. Soft, tender and mobile lymph nodes were palpated in the left cervical and left submandibular chains. Joint examination revealed reduced range of motion of both shoulders, right elbow, left wrist and right third proximal interphalangeal (PIP) joints. Her cardiac and pulmonary examination discovered no abnormalities.
Table describes the laboratory examination results at the presentation.
On admission radiograph of the chest revealed normal cardiac silhouette without any pleural effusions or pulmonary infiltration. Vancomycin and ceftriaxone were empirically started which were discontinued soon after the admission because the symptoms were not consistent with a bacterial infection, the patient then was managed symptomatically with acetaminophen and intravenous fluids. Over the next 36 hours, the patient continued to have spiking fevers with negative blood/urine cultures. Abdominal ultrasound revealed hepatomegaly and echocardiogram revealed trace pericardial effusion. On hospital day three, empiric gatifloxacin was started. Spiking fever persisted on following days four, five and six. Numerous lab studies including blood cultures and urine culture were performed to rule out infectious possibilities, e.g., antibody assays for rubella, mumps, cytomegalovirus, Epstein-Barr virus, parainfluenza, Coxsackievirus, adenovirus, influenza, human herpesvirus 6, parvovirus B19, hepatitis B and hepatitis C, Mycoplasma pneumoniae, Chlamydia pneumoniae, Borrelia burgdoferi, Quantiferon test, Pneumococcal and Legionella urinary antigens, Chlamydia, Mycoplasma and HIV. All of which proved to be negative. Lymph node biopsy has been done, reactive benign lymphadenopathy was reported. Infectious diseases consultation advised initiation of vancomycin despite lack of infectious source.
Table describes laboratory examination as per rheumatology consultation.
Based on Yamaguchi criteria, the patient was diagnosed to have AOSD, hence steroids with 50 mg Solu-Medrol intravenously started. Over the next four days, fever, rash and arthralgia resolved and serum ferritin levels decreased to 1085.2 ng/mL. The patient was discharged apyretic, in good clinical condition on oral prednisone and advised to follow up in outpatient clinic.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [141.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 141.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2787,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-2912233-1,Extracted,"A 41-year-old male with compartment syndrome of both lower legs and thighs was transferred to our intensive care unit (ICU) (hospital B) after emergency decompressive fasciotomy in another hospital (hospital A) the previous day (fig. ).
On admission to hospital A the previous day the patient had presented with severe muscle pain in the legs and a 2-week history of flu-like illness and sore throat with fever up to 39°C, which had been treated with moxifloxacin for several days. On initial physical examination signs of massive dehydration were present (heart rate 102/min; blood pressure 65/50 mmHg, temperature 37.1°C).
Extensive fluid resuscitation was initiated (15 L on hospital day 1). Previous medical history was unremarkable. The patient was working as a policeman and had been to Italy three weeks prior to admission. He reported playing in a football tournament one week previously.
Blood biochemistry indicated severe hemoconcentration (hemoglobin 22.3 g/dL, hematocrit 60.4%), hypoproteinemia (serum total protein 2.3 g/dL) and acute kidney failure (creatine 1.6 mg/dL, blood urea nitrogen 37 mg/dL). Markers of inflammation were only slightly altered (white blood cell count 15,900/μL, C-reactive protein 1.2 mg/dL, procalcitonin < 0.5 μg/L) and not suggestive of sepsis. Platelet count was normal. Differential blood count indicated no sign of hematologic disorders. Electrolytes were normal (sodium 133 mmol/L, potassium 4.6 mmol/L). Parameters of cholestasis and aminotransferases were not altered (bilirubin 0.7 mg/dL, alkaline phosphatase 66 U/L, gamma-glutamyl transferase 60 U/L, aspartate aminotransferase 32 U/L and alanine aminotransferase 39 U/L). Arterial blood-gas analysis showed the following: pH 7.06, pCO2 43 mmHg, pO2 91 mmHg, bicarbonate 11.9 mmol/L, anion gap 11.6 mmo/L. Creatine kinase was normal (124 U/L) on hospital day 1 and rose to over 7000 U/L on day 2 (day of admission to our ICU).
Chest radiography indicated a small right-sided pleural effusion. Echocardiography and abdominal ultrasound did not reveal any pathological findings. Lower extremity duplex sonography was performed showing no signs of venous thrombosis. The electrocardiogram was normal.
Although blood chemistry did not indicate an inflammatory constellation, an initial diagnosis of suspected sepsis with unknown focus was made (differential diagnosis: necrotizing fasciitis). Antibiotics (meropenem, clindamycin, penicillin) were administered. Measurement of pretibial compartment pressure and thigh compartment pressure by direct manometry revealed 100 mmHg and 44 mmHg, respectively. Decompressive fasciotomy of both lower legs and both thighs was performed and the patient was transferred to our ICU (hospital B) on hospital day 2 for further treatment.
On arrival to our ICU the patient was sedated, the trachea was intubated (since the fasciotomy) and the lungs were mechanically ventilated (controlled ventilation, respiratory rate on ventilator 20/min, PEEP 8 cmH2O, mean airway pressure 13 cmH2O, FiO2 0.65). Signs of protracted hypovolemic shock (arterial pressure 95/50 mmHg, heart rate 120 bpm, norepinephrine administration 0.13 μg/kg/min) were present. Laboratory tests on admission to our ICU showed the following: hemoglobin 12.9 g/dL, hematocrit 37.4%, white blood cell count 19,620/μL, platelet count 174,000/μL, creatine 1.5 mg/dL, blood urea nitrogen 21 mg/dL, C-reactive protein 2.1 mg/dL, procalcitonin 0.8 μg/L, sodium 138 mmol/L, potassium 5.2 mmol/L, bilirubin 0.2 mg/dL, alkaline phosphatase 20 U/L, gamma-glutamyl transferase 18 U/L, aspartate aminotransferase 147 U/L and alanine aminotransferase 54 U/L), lactate 4.6 mmol/L, blood gas analysis: pH 7.37, pCO2 32 mmHg, pO2 77 mmHg, bicarbonate 19.1 mmol/L, anion gap 5.6 mmo/L. Creatine kinase was 7,624 U/L (maximum value on hospital day 4: 29,195 U/L).
Invasive hemodynamic monitoring using the transpulmonary thermodilution technique (PiCCO-2-device, Pulsion Medical Systems AG, Munich, Germany) was initiated. The preload parameter, global end-diastolic volume index (GEDVI) was then 459 mL/sqm (n: 680-800 mL/sqm) despite previous aggressive fluid resuscitation. Moreover, stroke volume variation (SVV; a dynamic parameter that can be assessed in patients with sinus rhythm and controlled ventilation) indicated intravascular hypovolemia and volume responsiveness (SVV 19%; n: < 10%). Further extensive fluid resuscitation and norepinephrine administration was initiated (fig. ). On the following days, the patient continued to require catecholamine therapy to maintain a mean arterial pressure above 65 mmHg. Although the patient produced only 300 mL of urine on the first day at our ICU, hemodialysis was not required as urinary flow rate increased markedly and creatine and blood urea nitrogen values declined (maximum values: creatine 1.7 mg/dL, blood urea nitrogen 37 mg/dL) after fluid resuscitation.
Extensive tests for possible causes of hypovolemic shock and compartment syndrome were initiated. Cultures from blood, urine, pleural fluid, wound smear and central venous and arterial line catheters were tested for bacteria, fungi and mycobacterium, but were found to be sterile. Serological tests for HIV 1&2 and Leptospira as well as Influenza A/B-RNA testing by PCR were negative. Tests for antinuclear antibodies and antibodies to DNA did not reveal pathological results. Histopathology, enzyme histochemistry and electron microscopy after muscle biopsy showed normal muscle fibers without signs of muscle necrosis, myolysis, myositis or fasciitis. On electromyography no pathologic spontaneous activity was seen. The mitochondrial respiratory chain enzymes (complexes I-IV) showed normal activity. Serum IgG, IgA and IgM values were normal (727 mg/dL, 108 mg/dL and 57 mg/dL, respectively).
The antibiotic therapy started in hospital A (meropenem, clindamycin, penicillin) was continued for five more days. Then the patient was treated with piperacillin/tazobactam for another 6 days. The patient was treated with hydrocortisone (288 mg/day) for suspected septic shock for the first 6 days.
Over the following days the hypovolemic shock and edema gradually subsided under volume management (volume resuscitation with crystalloid fluid) based on transpulmonary thermodilution data and norepinephrine administration (fig. ). In three surgical procedures the fascias of both lower legs and thighs were completely closed.
Regarding hemodynamic stabilisation, in parallel to improving GEDVI and SVV through volume loading, the extra-vascular lung water index (EVLWI) also increased (20 mL/kg; n = 3-7 mL/kg), decreasing the pO2/FiO2-ratio. There were also clinical and radiological signs of pulmonary edema developing on hospital day 4. Therefore a more restrictive volume balance including the application of diuretics was initiated resulting in markedly improved gas exchange. The tracheal tube was removed on hospital day 11 and the patient was transferred to a normal ward on hospital day 14. Serum protein immunoelectrophoresis then indicated paraprotein of the IgG kappa type. A diagnosis of idiopathic SCLS (Clarkson's disease) was made retrospectively. Two weeks after transfer to the normal ward the patient was discharged to rehabilitation.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [120.0, 'bpm'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 =  3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2788,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8086747-1,Extracted,"A 38-year-old female patient presented to the ED with a 12-hour history of sharp, pleuritic, right-sided chest pain. The pain was worse with movement and was not associated with any shortness of breath or respiratory symptoms. She was otherwise healthy and had no history of, or risk factors for coronary artery disease or venous thromboembolism. One day prior to her presentation, she had received dry-needling treatment through a physiotherapy clinic for an unrelated back pain.
On presentation to the emergency department, she looked well. Her heart rate was 101, blood pressure was 105/69, respiratory rate was 18 and oxygen saturation was 98% on room air. Physical examination revealed slightly reduced air entry on the right with auscultation. Electrocardiogram (ECG) showed moderate voltage criteria for LVH and no ST changes. Cardiac enzymes were not measured. Point of care ultrasound (POCUS) was used to investigate a possible pneumothorax and revealed normal lung sliding on the left (Video ), but absent lung sliding and the presence of a lung point on the right (Video ). There was no evidence of other lung pathology or a pericardial effusion on ultrasound. A subsequent chest radiograph showed a small to moderate-sized right-sided pneumothorax with 2.2 cm of parietal pleural separation (Figure ).
Using procedural sedation, a 9 French Cook catheter was placed in the right hemithorax. Placement was confirmed with a chest radiograph which also demonstrated re-expansion. The patient did have a transient episode of atrial flutter following chest tube placement. Her vital signs returned to normal and no treatment was required.
The patient returned to the ED two days after initial presentation for reassessment. Upon return, she was in no apparent respiratory distress. Her heart rate was 80, blood pressure 116/83, respiratory rate 20 and oxygen saturation 92% on room air. She had good air entry bilaterally and a repeat chest radiograph showed re-expansion with no evidence of pneumothorax. The chest tube was removed, and the site sutured with no further complications.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [101.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 101.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2789,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6218346-1,Extracted,"A 39-year-old man visited the emergency room with a dizziness and balance impairment that occurred 6 hours before. At the time of admission, the patient showed alert consciousness, but neurological examinations showed the signs of cerebellar dysfunction. Finger to nose, heel to shin and rapid alternating movement test showed that cerebellar function was impaired on the left side, with intact function of the right side. Blood pressure was 150/80 mmHg, and pulse rate was 88 beats/min with normal sinus rhythm of electrocardiography. He had no underlying disease and no medication use. Routine laboratory tests of blood and electrolytes, were within normal ranges. He initially denied any trauma, but remembered severe pain when he underwent a cervical chiropractic manipulation about two weeks prior. Upon imaging, skull and cervical spine radiographs were normal. Brain computed tomography (CT) showed normal cerebellar parenchyma (). But magnetic resonance (MR) imaging (MRI) revealed acute infarction in the left PICA territory (). Gradient echo image suggested blood clot in left PICA (). MR angiography revealed complete occlusion of left VA with retrograde blood flow ().
Transfemoral cerebral angiography revealed the occlusion of left VA at V1/2 junction. And it showed the retrograde blood flow to the left VA to the V2 segment (C1 level) and also showed the occlusion of left PICA (). After angiography, the patient was admitted to a neurological intensive care unit, and he received antiplatelet therapy with the use of Aspirin® 100 mg/day (Bayer AG, Leverkusen, Germany). There was no embolic source in the heart transthoracic echocardiogram and heart CT. And doppler ultrasonography did not reveal atherosclerosis of both internal, external carotid arteries. So it is unlikely that the infarction was caused by cardiac thrombosis or other vascular abnormalities.
At 1 month later, axial CT imaging showed the change to the chronic phase of left PICA infarction (). And in neck CT subtraction angiography, previously obstructed VA flow was partially improved at V1/2 level (). Maximum intensity projection image from enhanced CT suggested suspicious dissected wall of left VA ().
Three weeks later, he was discharged without sequelae and was regularly followed up with at an outpatient clinic using antiplatelet agents. During a follow-up at 3 months, brain and neck CT angiography showed low density in left PICA territory but showed more improved state of VA dissection at the left V1/2 junction with focal stenosis remained compared to the previous study ().
MRI vessel wall study was not performed at the first time so we did not prove the intravascular thrombosis directly. However, it could be diagnosed as a dissection because he was relatively young and healthy person and was improved so fast by only medical treatment.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [88.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 88.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2790,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7180307-1,Extracted,"A 70-year-old man presented to a local hospital for treatment of a cough with bright
red blood, which he had experienced for 1 month. A pulmonary infection was initially
considered, and anti-infection treatment was provided, but the effect was poor. The
patient then visited the outpatient department of our hospital for treatment. A
chest computed tomography (CT) examination showed a shadow in the upper lobe of the
left lung (). The
patient was initially believed to be suffering from a pulmonary infection, but the
symptoms did not greatly improve after antibiotic treatment. Because an abnormal
lesion in the upper left lobe was found on a chest CT examination, we planned to
screen for lung cancer after considering the patient’s advanced age and symptoms. On
admission, the patient’s rectal temperature was 37.4°C and his heart rate was 88
beats/minute. The respiratory rate was 20 breaths/minute and blood pressure was
180/100 mmHg. A pulmonary exam showed clear bilateral breath sounds without rales or
rhonchi. No obvious abnormalities were detected during pulmonary and abdominal
examinations. Laboratory examinations showed that the patient had a white blood cell
count of 3.96 × 109/L with 61.6% neutrophils, a hemoglobin level of 131
g/L, and a platelet count of 278× 109/L. His erythrocyte sedimentation
rate was 22 mm/hour (slightly increased) and a t-cell spot test for tuberculosis
infection was negative. Electrolytes, creatinine levels, liver function, and urine
analysis results were normal. No acid-fast bacilli were found in a sputum smear, and
growth of normal respiratory flora was detected in the sputum culture. A CT scan
performed on admission showed that, below the pleura of the upper lobe of the left
lung, there was a patchy, dense shadow approximately 2.7 × 2.2 cm in size, with
rough edges, adjacent pleural traction, and localized thickening (). Additionally, a
bronchial shadow was observed in the lower portion of the lesion.
The patient was still coughing up sputum with dark blood. On the second day after
admission, emergency electronic bronchoscopy was performed after the necessary blood
samples were taken. Bronchoscopy showed that the bronchial mucosa in the upper lobe
of the left lung was swollen and no new organisms were found. Bronchoalveolar lavage
fluid collection and transbronchial biopsy were performed in the upper lobe of the
left lung (posterior apex segment), and these showed nonspecific inflammation and no
evidence of a malignant tumor. Percutaneous pulmonary needle biopsy was then
performed under CT guidance, and tissue samples were collected for cytological
acid-fast staining and pathological examinations. The morphological features of the
tissue samples were characterized by a multifocal centrilobular distribution of
fibromyxoid polyps of granulation tissue in the lumen of distal airspaces and small
bronchioles. This finding was associated with mild lymphocytic bronchiolitis and
alveolar septal infiltration of lymphocytes and plasma cells (), which was consistent with the
appearance of organizing pneumonia. Therefore, the diagnosis of focal COP was
made.
After the diagnosis of focal COP, the patient was started on intravenous ceftazidime
and oral prednisone. When the patient had no hemoptysis and airway secretions were
reduced, ceftazidime was discontinued. The initial dose of prednisone was
0.5 mg/kg/day. After 4 weeks, this dose was gradually reduced according to the
condition, and the total course of treatment was 6 months. After treatment, the
patient visited the clinic and complete resolution of his respiratory symptoms and
nearly complete resolution of the mass on chest CT were observed ().
This was an individual case report with no involvement in clinical or animal
research. The requirement for ethical permission was waived according to the
statements regarding the application of ethical permission by the Ethical Committee
of the First Affiliated Hospital of Nanchang University. Written consent was
obtained from the patient for publication of his medical data, including images.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [88.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 88.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 0 + 1 = 1.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.
The patient's Well's score for pulmonary embolism is 1."
2791,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8114250-1,Extracted,"A 51-year-old man with a past medical history of type 2 diabetes mellitus and hypertension, presented with complaints of fever, myalgia and dry cough for 8 days. No history of chronic obstructive pulmonary disease (COPD) and asthma. He denied smoking history. He tested positive for COVID-19 by reverse transcription polymerase chain reaction (RT-PCR), and he was initially treated elsewhere with remdesivir, dexamethasone and antibiotics (co-amoxiclav and doxycycline). On arrival, the patient was conscious, oriented, and febrile (temperature: 101°F) with a pulse rate (PR) of 106/min and blood pressure (BP) of 140/90 mm Hg. Arterial blood gas (ABG) analysis showed metabolic acidosis and type-I respiratory failure. He was hypoxic (SpO2: 86% on room air) and started on high-flow oxygen at 15 L/min.
His initial investigations revealed severe hyperglycemia (random blood sugar: 493 mg/dL (70–140 mg/dL)), hyperkalemia (6.4 meq/L (3.5–5.5 meq/L)), azotemia (urea: 101 mg/dL (7–20 mg/dL), creatinine: 1.3 mg/dL (0.9–1.3 mg/dL)), and leucocytosis (27,700 cells/mm3 (4000–11,000 cells/mm3)). Urine ketones were positive and serum ketones level was elevated, he was started on insulin infusion. Chest X-ray revealed bilateral patchy consolidations. Inflammatory markers were elevated (lactate dehydrogenase (LDH): 529 U/L (105–333 U/L), ferritin: 2783.4 ng/mL (20–250 ng/mL), interleukin-6 (IL-6): 329.4 pg/mL (5–15 pg/mL), and C-reactive protein (CRP): >199 mg/L (<10 mg/L)).
Due to worsening hypoxemia, he was intubated on the same day of admission and was started on volume control ventilator support. Because of persistent hypoxia, computed tomography scan (CT-scan) chest () done on sixth day of admission revealed PM, pneumopericardium with an extension of air into the fascial planes of the neck and subcutaneous and intermuscular planes of the chest, dense consolidation in the left lower lobe and intraparenchymal septated cavity. He was started on Meropenem, Targocid and voriconazole, and PM was managed conservatively. He had methicillin-resistant Staphylococcus aureus bacteremia, and bronchial wash cultures grew Klebsiella pneumoniae, antibiotics and antifungals were continued. Repeat X-ray done on eighth day of admission showed features of adult respiratory distress syndrome (ARDS), consolidation, subcutaneous emphysema and resolving PM ().
His condition further deteriorated, and he went into septic shock for which he was started on inotropes. Because of the need for prolonged ventilator support, he underwent tracheostomy. The patient’s inflammatory markers continued to remain high, and he remained haemodynamically unstable, requiring inotropes and mechanical ventilation. Despite aggressive management, his condition deteriorated, and he died due to his disease on tenth day of hospitalisation.
A 77-year-old man with a history of hypertension presented with complaints of shortness of breath (SOB) for 1 week. No history of fever, cough or chest pain, and no history of COPD and asthma. He denied smoking history. COVID-19 RT-PCR done elsewhere initially was negative. CT-scan chest done on the day of admission showed multiple confluent areas of ground-glass opacities and crazy paving pattern with a severity score of 26. On arrival in emergency room (ER), he was afebrile and hypoxic (PR: 96/min, BP: 120/80 mm Hg, temperature: 98.4°F, SpO2: 89% on room air). Physical examination was notable for bilateral crepts. ABG revealed type-I respiratory failure, and he was started on high-flow oxygen at 10 L/min. Baseline labs were notable for leucocytosis (16,300 cells/mm3) and hyponatremia (124 meq/L).
Inflammatory markers were elevated (LDH: 311 U/l, ferritin: 1403.8 ng/mL, IL-6: 177.8 pg/mL, CRP: >199 mg/L). Blood and urine cultures were sent, and he was started on dexamethasone, enoxaparin, remdesivir and antibiotics (co-amoxiclav and doxycycline). CT chest with pulmonary thromboembolism (PTE) protocol ( and ) was done on day 5 to rule out pulmonary embolism. It did not show evidence of pulmonary embolism, compared to the previous CT, lower lobe consolidation and PM was a new finding. In view of worsening hypoxia and increased work of breathing, he was intubated on the same day and was started on volume control ventilator support. Hyponatremia was managed with dietary and fluid modifications. PM was managed conservatively, and serial X-rays showed resolving PM and pneumopericardium ().
During the course of hospital stay, he had fluctuating haemodynamics requiring inotropes, and antibiotics were escalated to Meropenem and Targocid for new-onset fever. He developed acute kidney injury secondary to sepsis, severe metabolic acidosis and was dialysed. On the 16th day of admission, he had supraventricular tachycardia and was reverted to sinus rhythm with synchronised shock, and he was continued on anti-coagulants, inotropes and ventilator support. Despite aggressive management, his condition deteriorated, and he died due to multi-organ dysfunction syndrome and refractory hypoxemia on 17th day of hospitalisation.
This 53-year-old lady with a history of type 2 diabetes mellitus and dyslipidemia, presented with complaints of fever and headache for 5 days. She denied a history of cough, chest pain, giddiness, urinary or gastrointestinal symptoms. No history of COPD, asthma and smoking. She had come in contact with a COVID-19 positive patient. COVID-19 RT-PCR was positive.
She was conscious, oriented, febrile (PR: 88/min, BP: 110/80 mm Hg, temperature: 101.4°F) at the time of presentation. She was maintaining SpO2 of 98% on room air. Physical examination was unremarkable. Baseline labs were notable for hypokalemia (3.2 meq/L), and inflammatory markers were mildly elevated (ferritin: 301.5 ng/mL and CRP: 13.6 mg/L). She was started on dexamethasone, remdesivir and enoxaparin.
During the hospital stay, she had worsening hypoxia for which she was started on oxygen support via nasal prongs. CT chest () done on ninth day of admission revealed no evidence of pulmonary embolism, multiple patchy areas of ground-glass opacities with intralobular septal thickening and subpleural fibrotic bands, moderate PM extending into the subcutaneous planes of the neck with a severity score of 16. She was managed conservatively and continued on anti-coagulants. A repeat chest X-ray () showed resolution of PM. She improved clinically, maintaining oxygen saturation (SpO2) >96% on room air, and was discharged home on 15th day of admission.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [106.0, 'beats per minute'], 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 106.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2792,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8061133-1,Extracted,"A 46-year-old female presented to the primary care outpatient clinic with excruciating back pain radiating down to the lower extremities bilaterally along the inner calves. The patient presented to the office four weeks prior for back pain and was diagnosed with sciatica. She was prescribed tizanidine and tramadol to help alleviate her symptoms. Her past medical history was notable for chronic low back pain due to osteoarthritis diagnosed in 2017. She originally attributed her worsening pain to recently starting a new job where she was responsible for lifting a significant amount of weight, however, she reported that her back pain continued to worsen and described the pain as different from the previous pain. Additionally, the patient reported new onset urinary incontinence, numbness, and tingling in her inner thighs and calves. She reported that tramadol and tizanidine relieved her symptoms in the beginning, however, stopped providing any relief. The pain was described as constant and unrelieved by position or specific motions. She described the pain as sharp and tingling in nature. She reported the pain severity as a 9/10 at rest and after walking or movement, a 10/10.
Past medical history was significant for type 2 diabetes diagnosed in January 2020, essential hypertension diagnosed in July 2017, chronic back pain and osteoarthritis of the lumbar spine diagnosed in 2017, and iron-deficiency anemia diagnosed in August 2017. The patient had a cholecystectomy in 2015 without complications. The patient reports compliance with her medications: ergocalciferol (vitamin D2) 1,250 mcg capsule po once weekly, esomeprazole magnesium 40 mg po, losartan 100 mg tablet po daily, gabapentin 300 mg po daily, and ozempic 0.5 mg subcutaneous pen injection once weekly. Family history is significant for several family members having malignancy as illustrated below in Table .
At arrival the patient was afebrile (98.4℉) and hypertensive (161/80), with a regular heart rate of 91, respiratory rate of 18, and oxygen saturation of 100%. Physical exam revealed a healthy-appearing, well-nourished patient in significant pain. Musculoskeletal exam revealed pain along the lumbosacral spine with all range of motion (ROM), pain with movement and reduced ROM by 80% (great difficulty with getting out of chair). Neurological exam was significant for sensory deficits along the inner thigh. Considering the new onset urinary symptoms and change in intensity and description of pain from prior encounters an urgent MRI was ordered, the imaging results are displayed in Figure .
The patient was called and informed of her diagnoses and was instructed to immediately report to the nearest ED. Upon arrival to the ED, lab work and CT scan without contrast were ordered and neurosurgery was consulted (Table ). CT scan confirmed a gently lobulated soft tissue mass arising from the right psoas muscle extending into right L3 neural foramen resulting in CES. The CT scan also determined that unlike the infiltrative changes seen in the recent MRI, there was no definitive destructive osteoblastic or osteolytic changes evident.
Neurosurgery confirmed the diagnosis of CES and performed a laminectomy of L3. Additionally the tumor was removed and sent to pathology. Upon removal the tumor was described to be a very hemorrhagic, soft, and rubbery tissue that was highly attached to the dura. The biopsy was sent to pathology and the patient was discharged postoperative day one. Biopsy results confirmed the presence of a plasma cell neoplasm with the pathology report shown in Table below. The differential diagnosis for the patient remained plasmacytoma versus multiple myeloma.
Three days after discharge the patient followed up at her primary care office, where she reported a significant improvement in her symptoms. The patient’s back pain had improved drastically with only minimal residual urinary incontinence. Additional testing was ordered by medical oncology to assess for any additional neoplasms. After thorough evaluation no additional masses were found, kidney function remained adequate, and baseline anemia unchanged. Therefore, the final diagnosis of a plasmacytoma was confirmed.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [91.0, 'beats per minute'], 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 91.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
2793,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6188774-3,Extracted,"A 74-year-old male patient with a history of arterial hypertension, noninsulin dependent diabetes mellitus medicated with oral hypoglycemic agents, ischemic cardiopathology with stent placement, nonoliguric chronic kidney failure, and cryptogenic liver cirrhosis required a liver transplant and subsequently suffered portal vein thrombosis requiring anticoagulation. The patient sought consultation after 3 days of passing liquid stools, together with emesis. He denied having fever spikes and, on that date, consulted the emergency ward of this institution, to which he was admitted feeling alert, with AT: 130/64, heart rate: 108 beats per minute, and SO2: 97% on room air. Upon physical examination, the patient was alert, tachypneic, and being with dry mucous membranes. Admission laboratory results are shown in . A ketonemia test was requested and the result was positive. The clinical presentation was interpreted as dehydration secondary to gastrointestinal losses and euglycemic diabetic ketoacidosis. Reanimation was started with crystalloids, a continuous insulin infusion pump, and the administration of intravenous bicarbonate. After 48 hrs, the patient presented DKA resolution criteria.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [108.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 108.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 =  3.0.
The patient not been diagnosed with pulmonary embolis (PE), but the patient has previously been diagnosed with deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3.0 + 1.5 = 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2794,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5991278-1,Extracted,"A 26-year-old male with a history of hypertrophic cardiomyopathy (HOCM) and intravenous drug abuse (IVDA) presented with generalized body ache, fever, and shaking chills. His fever was 103°F, heart rate was 112 beats/minute, he had no cardiac murmur, but he did exhibit tender scattered macular lesions of the palm and soles of the feet (Janeway lesions).
Laboratory studies revealed a white blood cell (WBC) count of 16.8K/μL (n = 3.9-11 K/μL) with 88% neutrophils, lymphocytes of 2% (n = 21%-51%), a platelet count of 90K/μL (n = 160-392K/μL), an erythrocyte sedimentation rate (ESR) of 77 mm/h, an elevated C-reactive protein (CRP) of 202 mg/L (n > 3 mg/L), and blood cultures positive for methicillin-sensitive S. aureus (MSSA; three or four bottles positive persisted for 4 days) [].
The Chest X-ray (CXR) showed bilateral pulmonary nodules, while the chest computed tomography (CT) confirmed peripheral bilateral, nodular, cavitating septic emboli []. The transthoracic echocardiogram (TTE) showed a 2.7 cm × 0.7 cm vegetation on the tricuspid and a 0.8 cm × 0.9 cm vegetation on the posterior mitral valve leaflets. The transesophageal echocardiogram (TEE) also showed a vegetation at the insertion of the papilla extending into the left ventricle (e.g., 1 cm × 0.4 cm) with mitral regurgitation [].
On the sixth hospital day, the patient became lethargic and developed blurred vision. The brain CT scan revealed an acute embolic infarction involving the right occipital lobe accompanied by marked mass effect []. When his cognitive function worsened over the next 24 h, a follow-up CT scan revealed a large 6-cm acute hemorrhagic stroke involving the right parietal/occipital lobe, nearly obliterating the right lateral ventricle [].
The patient underwent successful endovascular embolization of the ruptured right occipital mycotic aneurysm; no craniotomy was required. After completing 6 weeks of nafcillin 2 g (IV) q4h (selected for its CNS penetration), he fully recovered.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [112.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 112.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2795,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-1808,Extracted,"A 38-year-old woman, gravida 2, para 1, at 32 weeks' gestation comes to the physician because of a 1-day history of dyspnea and left-sided chest pain that is worse when she breathes deeply. One week ago, she returned from a trip to Chile, where she had a 3-day episode of flu-like symptoms that resolved without treatment. Pregnancy and delivery of her first child were uncomplicated. She has no history of serious illness. Her temperature is 37.2°C (99°F), pulse is 118/min, respirations are 28/min and slightly labored, and blood pressure is 110/76 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 91%. Examination shows jugular venous distention and bilateral pitting edema below the knees that is worse on the left-side. There is decreased breath sounds over the left lung base. The uterus is consistent in size with a 32-week gestation. The remainder of the examination shows no abnormalities.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [118.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Hemoptysis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 118.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
2796,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-5165,Extracted,"A 72-year-old man presents to the ED complaining of worsening abdominal pain over the last few hours. He also reports nausea, but denies fever, vomiting, or changes in the appearance of his bowel movements. His medical history is significant for type 2 diabetes mellitus, hypertension, coronary artery disease, stroke, atrial fibrillation, and peptic ulcer disease. Due to his recurrent bleeding peptic ulcers, he does not take warfarin. His surgical history is significant for an appendectomy as a child. His medications include metformin, lisinopril, metoprolol, and omeprazole. He has a 50-pack-year history of smoking. His temperature is 37.6 C (99.7 F), blood pressure is 146/80 mm Hg, pulse is 115/min, and respiratory rate is 20/min. On physical exam, he is in acute distress due to the pain. Pulmonary auscultation reveals scattered wheezes and decreased air entry. His heart rate is irregularly irregular, with no murmurs, rubs or gallops. Abdominal exam is significant for decreased bowel sounds and diffuse tenderness.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [115.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 115.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2797,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6374917-1,Extracted,"An 88-year-old African American male with a history of CLL on ibrutinib and hypertension, presented to the emergency department with a 2-day history of palpitations accompanied by chest discomfort, shortness of breath and fatigue. The patient reported no previous history of palpitations or chest pain. He denied similar symptoms before and has no exercise intolerance, paroxysmal nocturnal dyspnea, orthopnea or shortness of breath before this presentation. He was taking 420 mg of ibrutinib for one month prior to his presentation beside amlodipine 5 mg daily for his hypertension He denied tobacco, illicit drugs, and alcohol use. Cardiopulmonary examination revealed irregularly irregular heart rhythm with a rate of 125, bilateral crepitations noted on chest auscultation with bilateral limb edema. Clinical examination was not consistent with infectious etiology.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [125.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Surgery in the previous 4 weeks': False, 'Previously documented Deep Vein Thrombosis': False}",7,7,7,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 125.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 6.0 + 1 =  7.0.
The patient's Well's score for pulmonary embolism is 7.0."
2798,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7952841-1,Extracted,"A 28-year-old healthy male with no significant past medical history presented with a cough, worsening shortness of breath, and chest pain for 2 days. He described his chest pain as intense sharp, stabbing pain in the chest with breathing. Review of systems was positive for mild headache and nausea. He was diagnosed with COVID-19 infection a month ago via nasopharyngeal reverse transcription polymerase reaction (RT-PCR) at an outside facility after being exposed at work. He had mild symptoms of COVID-19 initially, which included loss of smell, change in taste, dry cough, fatigue, and headache. He completed a 14-day quarantine period without requiring any supplemental oxygen and was treated symptomatically. He denied any fevers, chills, heat or cold intolerance, blurry visions, or any other related symptoms. The patient reported no history of tobacco, alcohol, or recreational drug abuse.
On physical examination, he was found to be alert and oriented. Vitals signs showed a blood pressure of 107/72 mm Hg, a pulse of 103 beats per minute, temperature was 98.4 °F, respiratory rate of 36 per minute, and oxygen saturation of 87% on room air. The patient was put on 2 L of supplemental oxygen immediately. Pupils were about 4 mm bilaterally and reactive to light. On auscultation, he had dual heart sounds with no murmurs noted. Breath sounds were bilaterally equal. The abdomen was soft and nontender, with active bowel sounds. No focal neurological deficits were noted. The investigations are presented in .
Electrocardiogram showed accelerated junctional rhythm with retrograde conduction with nonspecific T wave changes. Chest X-ray showed patchy bibasilar opacities, right greater than left. Computed tomography angiogram of chest was negative for pulmonary emboli but revealed tree-in-bud opacities predominantly in the right lung (). The vasculitis panel was ordered, which was negative. Abdominal ultrasound showed mild hepatomegaly with normal common bile duct diameter. The acute hepatitis panel was sent, which returned negative.
He was started on antibiotic treatment for community-acquired pneumonia. A transthoracic echocardiogram showed left ventricular dysfunction with an ejection fraction of 30% without evidence of clinical heart failure. The patient was diagnosed with myocarditis secondary to post COVID-19 viral infection and he was started on guideline-directed medical therapy with metoprolol, lisinopril, and low-dose aspirin.
On the night before discharge, day 7 of his admission, the patient developed sudden onset of polyuria, polydipsia, and increased thirst. His documented 24-hour urine volume was 2.5 L before he developed the complaints. At the time of these complaints, his urine output was approximately 7 L within 24 hours and the serum sodium level increased to 153 mEq/L. His urine studies revealed a low urine osmolality (93 mOsm/kg) and urine sodium of 16 mOsm/kg. On the administration of 2 µg of desmopressin, the patient improved clinically and symptomatically. He had a decreased urine output, increased urine osmolarity, urine sodium, and improved serum sodium levels ().
A magnetic resonance imaging of the brain was performed, which did not reveal any pituitary mass, acute hemorrhage, or malignancy. A diagnosis of diabetes insipidus as a sequelae of COVID-19 viral infection was made. Apart from close monitoring for serum sodium levels and urine output, the patient’s desmopressin dose was optimized and hydrochlorothiazide was also administered. He was discharged home after 16 days of hospitalization on desmopressin 0.3 mg thrice daily and hydrochlorothiazide 12.5 mg daily with close follow-up with endocrinology, nephrology, cardiology, and primary care physician. After 2 weeks, the patient followed-up with the primary care physician and his inflammatory markers, electrolytes, and brain natriuretic peptide were all within normal limits. His urine output was controlled on medications and therefore, his follow-up will continue till recovery.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [103.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 103.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2799,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6213679-1,Extracted,"A 28-year-old female was referred to the ophthalmology department with progressively worsening sudden diminution of vision OD for 15 days prior to presentation. Visual deterioration was preceded by severe frontal headache accompanied with an episode of vomiting. She was 1-year postpartum at presentation and had history of irregular menstrual cycles with menorrhagia for 7 months. There was no history of oral contraceptive drug intake. At presentation, her blood pressure was 118/80 mm Hg; pulse rate was 80 beats/min, regular with good volume and best-corrected visual acuity (BCVA) was hand movements with inaccurate projection of rays (PR) – OD and 6/18 with accurate PR – OS. The rest of the general physical and systemic examination was normal. She had bilateral upper eyelid retraction [], lid lag in down-gaze with decreased convergence and no proptosis. On pupillary examination, right-sided relative afferent pupillary defect (RAPD) was present. Color vision and contrast sensitivity were deranged in both the eyes. Bilateral optic discs were hyperemic and swollen with blurred margins, however, macula was normal in both the eyes [Fig. -]. The visual fields OD were grossly limited on confrontation. Visual field testing OS demonstrated a constricted pattern with a biarcuate type field defect []. Intraocular pressure was 14 mm Hg OD and 12 mm Hg OS. Flash visual evoked potential (VEP) waveforms were absent OD and delayed OS (P100: 133 ms). Thyroid stimulating hormone (TSH) was markedly decreased (0.01 μIU/ml) with significantly increased levels of free T3 (15.18 pg/ml), free T4 (3.65 ng/dl), and anti-thyroid peroxidase autoantibody (anti-TPO, 217.17 IU/ml). Thyroid scan revealed features of diffuse toxic goiter []. Coagulation profile, D – dimer, serum homocysteine levels, contrast-enhanced computed tomography (CT) of the brain [], and magnetic resonance imaging (MRI) of the brain, also showing the orbital structures and optic nerve [Fig. and ] were normal. There were no radiological features suggestive of thyroid orbitopathy. Magnetic resonance venography (MRV) of the brain demonstrated dural venous thrombosis involving left transverse and sigmoid sinus with minimal cerebral edema []. In view of sudden onset diminution of vision, RAPD, severe headache and neuroimaging findings, a working diagnosis of CVT, papilledema, and auto-immune hyperthyroidism was made. Treatment with mannitol [100 ml, intravenous (IV) three times a day (TDS)], oral glycerol [four teaspoonful four times a day (QID)], oral acetazolamide (250 mg QID), enoxaparin 0.6 ml subcutaneously twice a day (BD), oral warfarin 5 mg once a day (OD), oral carbimazole 20 mg TDS, and oral cholecalciferol 60,000 U once a week, was initiated. After 1 week of initiation of this treatment, oral prednisolone in a dose of 40 mg was added and gradually tapered as documented in . demonstrates the sequential follow-up of the patient on treatment.
Repeat MRI of the brain at 12 weeks was normal [Fig. and ]. BCVA remained 6/9 OD and 6/6 OS at subsequent follow-up, the last being at 15 months after the initial presentation []. The optic disc swelling decreased over time [Fig. and ]. The free T3 and T4 levels gradually normalized over a period of 1 year, oral carbimazole was stopped after 14 months, oral warfarin continued at 1.5 mg for 8 months and the patient was advised periodic monitoring of her thyroid function tests and coagulation profile under the supervision of an endocrinologist.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Previously Documented Pulmonary Embolism': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2800,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4763473-1,Extracted,"A 45-year-old man with a history of diabetes was admitted with cough, polyuria and polydipsia of one week’s duration. The patient had no medical history of hypertension and myocardial infarction. Upon physical examination, the patient was found to have a body temperature of 38.2°C, a respiratory rate of 23 breaths/min, a pulse rate of 106 beats/min and a systolic/diastolic blood pressure of 112/82 mmHg. A few moist crackles were apparent in the patient’s lungs.
Laboratory studies revealed a white blood cell count of 23.02 × 109 cells/l with 88.6% neutrophils, and the following blood levels: alanine aminotransferase (ALT), 233 U/l (range 0–40); creatinine (Cr), 243.1 μmol/l (range 44–133); creatine kinase (CK), 36 762 U/l (range 26–174); plasma glucose, 49.1 mmol/l; fasting C-peptide, 0.01 ng/ml (range 0.7–1.9); two-hour postprandial C-peptide, 0.15 ng/ml; glycosylated haemoglobin (HbA1c), 8.4%; and C-reactive protein (CRP), 33.7 mg/l (range 0–5). The patient’s creatine kinase-MB (CK-MB) concentration was > 500 ng/ml, and his troponin I concentration was > 180 ng/ml. Arterial blood gas analysis results showed the following: pH, 7.299; PO2, 16.80 kPa; PCO2, 4.01 kPa; base excess (BE), –10.8 mmol/l.
A chest X-ray revealed a pneumonia infection of the lower right lung. An ECG showed ST-segment elevation in leads II, III, aVF and V7–V9 (). Echocardiography revealed decreased left ventricular systolic function (ejection fraction: 32%) with left ventricular inferior and posterior wall motion abnormalities. Coronary angiography indicated no luminal narrowing in the left main coronary artery, circumflex or right coronary arteries, although atherosclerosis was apparent in the left anterior descending artery, with stenosis of 30% (). Intravascular ultrasound results showed a local plaque load of 43% in the middle of the anterior descending artery, with a minimum vessel lumen area of 7.34 mm2 (). Thus, myocardial infarction induced by coronary atherosclerosis and plaque rupture was excluded.
From the above findings, the patient was diagnosed with SIRS and MODS, which included acute inferior and posterior wall myocardial infarction with acute heart failure, fulminant diabetes, acute liver dysfunction, acute kidney dysfunction and rhabdomyolysis. The patient received a series of powerful treatments, including insulin intravenous infusion, antiplatelet therapy and anticoagulation therapy with aspirin, clopidogrel and low-molecular-weight heparin, diuretics, urine alkalisation, and anti-inflammatory antibiotic therapy.
The patient’s condition improved after treatment for one week; each organ regained normal function and the patient was discharged in a good clinical state after a total hospitalisation of 14 days. The follow-up visit in out-patient service one month after discharge showed that the patient’s blood test, ECG and echocardiography results were all normal.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [106.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 106.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2801,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-10162,Extracted,"Three days into hospitalization for a fractured distal femur, a 33-year-old man develops dyspnea and confusion. He has no history of a serious illness. He is unable to answer any questions or follow any commands. His blood pressure is 145/90 mm Hg, the pulse is 120/min, the respiratory rate is 36/min, and the temperature is 36.7°C (98.1°F). His oxygen saturation is 90% on 80% FiO2. On examination, purpura is noted on the anterior chest, head, and neck. Inspiratory crackles are heard in both lung fields. Arterial blood gas analysis on 80% FiO2 shows:
pH 7.54
PCO2 17 mm Hg
PO2 60 mm Hg
HCO3− 22 mEq/L
A chest X-ray is shown.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3.0 + 1.5 = 4.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2802,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8223853-1,Extracted,"A 29-year-old man was admitted to our hospital in August 2018, complaining of worsening generalized weakness and dyspnea.
The patient could hardly walk without oxygen mask, presenting with cyanosis and clubbing fingers for 16 mo, and progressive dyspnea for 1 mo.
The patient denied any history of pulmonary and cardiac disorders, and alcohol abuse. When he was 10 years old, his height was 125 cm (-2.5 SD compared to age and sex matched boys). Further investigation found multiple pituitary hormone deficiency (low thyroxin and thyroid-stimulating hormone, low cortisol and adrenocorticotropin hormone at 8 am, and low IGF-1 levels). Hypopituitarism was diagnosed based on laboratory findings. Magnetic resonance imaging showed aplasia of the pituitary gland, interrupted pituitary stalk, and ectopic posterior bright spot (Figure ). A diagnosis of pituitary stalk interruption syndrome was made. Levothyroxine 50 μg per day and hydrocortisone 20 mg per day were started. His poor compliance made him take these medicines occasionally. To achieve ideal height, his recombinant human GH (rhGH) treatment was started at the age of 14 years, and lasted for 5 years. At the age of 23 years, he was diagnosed with nonalcoholic fatty liver disease. It gradually deteriorated to cirrhosis in the following 6 years.
The patient was 187 cm in height, 105 kg in weight, and 117 cm in waist circumference. His BMI was 30 kg/m2. Oxygen saturation was 78% on room air, and could increase to 92% with oxygen mask. His blood pressure was 128/79 mmHg and resting heart rate was 66 bpm with a regular rhythm. Physical examination revealed acanthosis nigricans, barrel chest with clear bilateral respiratory sounds, cyanotic lips, and clubbed fingers (Figure ). Hepatomegaly was palpable 4 cm beneath the xiphoid and 8 cm beneath the right costal margin. Splenomegaly was also palpable. Gynecomastia (Tanner stage IV) and prepubertal testicular size of 3 mL could be observed.
Laboratory results indicated multiple pituitary hormones deficiency. Pulmonary function test showed decreased infiltration of oxygen from pulmonary alveoli into the blood. Common causes for cirrhosis, especially hepatitis B virus infection, were ruled out by serological evaluation (Table ). Activated partial thromboplastin time and international normalized ratio were within normal range, but prothrombin time was 14.9 s (normal range: 11-13 s).
Gastric varices were observed by gastroscopy (Figure ). Abdominal ultrasound showed cirrhosis and hypersplenotrophy without ascites (Figure and ). There was no evidence of an intracardiac shunt on echocardiography, and the ejection fraction was 52%. Transthoracic contrast echocardiography revealed opacification of the left chambers of the heart by micro-bubbles five heartbeats after the appearance of microbubbles in the right atrium, suggesting intrapulmonary shunting (Figure ). 99mTc-macroaggregated albumin perfusion lung scan demonstrated intrapulmonary arterio-venous right-to-left shunting with a shunt rate of 64.4% (Figure , top).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [66.0, 'bpm'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 66.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2803,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7239248-1,Extracted,"An 80-year-old woman was referred to our hospital due to dyspnea on exertion and malaise for the past 2 days. Past medical history was unremarkable and she did not take any medication.
Physical examination on admission showed a Glasgow Coma Scale of 15, blood pressure 138/68 mmHg, pulse rate 81/min, oxygen saturation 92% on ambient air and a tympanic temperature of 38.1°C (101°F). Auscultation of the lungs revealed normal breathing sounds. The patient's skin was warm without signs of oedema or dehydration.
Laboratory results showed lymphopenia of 0.54 × 109/L, C-reactive protein of 12 mg/L and slightly elevated lactate dehydrogenase (LDH) of 277 U/L. Arterial blood gas analysis revealed a partial pressure of oxygenof 8.5 kPa while breathing ambient air. Serum sodium on admission was 122 mmol/L with an osmolality of 253 mOsm/kg. An overview of laboratory results is provided in .
Computed tomography (CT) of the chest showed bilateral ground-glass opacities in all lobes of the lung, highly suggestive of COVID-19 pneumonia. After 12 h, the initially taken nasopharyngeal swab proved to be positive for SARS-CoV-2 in the polymerase chain reaction (PCR) analysis. The patient was admitted to the COVID-19 isolation ward with oxygen therapy.
After infusion of 1.000 mL of crystalloid, serum sodium fell to 115 mmol/L and a re-evaluation was made: urine chemistry revealed a urine osmolality of 789 mOsm/kg and a urine sodium of 71 mmol/L. On the basis of hypo-osmolar hyponatraemia, a decreased serum urea level of 3.3 mmol/L, normal thyroid stimulating hormone (TSH) levels together with a high urine osmolality as well as a urine sodium >30 mmol/L in this euvolaemic patient not taking diuretics, the diagnosis of SIADH due to COVID-19 pneumonia was made. Fluid restriction, low-dose loop diuretics and concomitant substitution of ongoing fluid losses were initiated. During the further course of hospitalization, serum sodium levels rose continuously.
Concerning COVID-19 pneumonia, the patient was administered hydroxychloroquine 400 mg twice daily as a loading dose followed by 200 mg twice daily for 4 days as well as azithromycin 500 mg once daily for 5 days. The demand for oxygen supply decreased during hospitalization and the patient’s general state of health improved significantly.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [81.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 81.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2804,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-612,Extracted,"A 65-year-old man comes to the emergency department because of sudden, worsening pain in his right calf and foot that started 30 minutes ago. He also has a tingling sensation and weakness in his right leg. He has had no similar episodes, recent trauma, or claudication. He has type 2 diabetes mellitus and was diagnosed with hypertension 20 years ago. His sister has systemic sclerosis. He works as an office administrator and sits at his desk most of the day. He has smoked one and a half packs of cigarettes daily for 30 years. Current medications include metformin and lisinopril. His pulse is 110/min, respirations are 16/min, and blood pressure is 140/90 mm Hg. His right leg is pale and cool to touch. Muscle strength in his right leg is mildly reduced. Pedal pulses are absent on the right.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 = 6.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
2805,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8630548-1,Extracted,"A 27-year-old male patient, from Mornag, a rural area of Tunisia, without any medical history, presented to the Habib Thameur Hospital emergency room with massive upper gastrointestinal bleeding. On admission (day one) in August 2020, physical examination revealed diffuse mucocutaneous pallor, lesions of old scarifications in the left upper limb, a Glasgow Coma Score (GCS) of 15/15, tachycardia of 105 beats per minute, hypotension of 80/50 mmHg without signs of peripheral hypoperfusion. Abdominal examination revealed slight epigastric tenderness and enlarged spleen without hepatomegaly or skin signs of hepatocellular failure. The rectal digital examination came back stained with melena.
Laboratory investigation showed signs of hypersplenism including decreased count of white blood count of 2870 cells/mm
3, thrombocytopenia of 46,000 cells/mm
3, and normochromic normocytic anemia of 5.6 g/dL. Minor signs of hepatocellular insufficiency were also displayed including a low rate of prothrombin ratio of 60% and hypocholesterolemia of 2.87 mmol/L. He had neither cholestasis nor cytolysis. Albuminemia was normal at the value of 36 g/L. Acute kidney failure was noted (urea of 11.6 mmol/L) with a normal blood electrolytes. Anti-hepatitis C virus antibody, hepatitis B surface antigen and hepatitis B core antibody were all negative.
On day two, the patient was stabilized following fluid resuscitation and blood transfusion of two red blood cell concentrates. The patience was treated with a proton-pump inhibitor (omeprazole) and octreotide. Upper gastroduodenoscopy showed the presence of oesophageal varices with massive active bleeding, moderate hypertensive gastropathy and gastric varicose veins (
). Four elastics with a first kit of ligature were put in place but did not allow the control of bleeding. Five supplementary elastics in a second ligature kit allowed a reduction in bleeding but without total control of the haemorrhage.
An abdominal ultrasound (US) concluded the presence of multiple multiloculated cystic formations evoking hydatic cysts type CE2 of the WHO classification of segments I, IV, and V with the largest cyst measuring 40 mm (
 and
). A portal cavernoma with a dilated splenic vein and splenomegaly of 22 cm was described. Hepatic veins were permeable with a normal caliber. Diagnosis of multiple liver hydatidosis was retained based on the epidemiological context and the typical aspect in abdominal US.
After a week, the patient had a cataclysmic re-bleeding causing refractory hemorrhagic shock and disseminated intravenous coagulation leading to death.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [105.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 105.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2806,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8240585-1,Extracted,"In August 2015, an 83-year-old HIV-negative, non-smoker Caucasian man was diagnosed with T3N2M0 small cell lung carcinoma. He went into complete remission after six cycles of carboplatin/etoposide and thoracic radiation (30 Gy with daily fractions of 3 Gy).
In December 2016, a stage I (pT1N0M0) right lower lobe lung adenocarcinoma was discovered and treated with lobectomy. The tumour had no EGFR, BRAF or KRAS mutation and no ALK, ROS1, RET rearrangement; only a copy number variation of MET gene (two to three copies). In April 2017, a neurological impairment revealed a frontal brain metastasis. The patient was treated with radiotherapy associated with methylprednisolone initially at 100 mg/day and then reduced to 50 mg/day.
In June 2017, he presented dry cough and shortness of breath associated with self-reported fever. Two days after the first symptoms, he was admitted to hospital. At admission, he had fever (38.2°C), blood pressure was 108/61 mm Hg, regular pulse of 79 bpm, respiration of 18 cycles/min, and 95% SpO2 with 2 L/min of oxygen supplementation. There was no recent chemotherapy, and no immunosuppressive treatment other than corticosteroids.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [79.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Surgery in the previous 4 weeks': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 79.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2807,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-2924353-1,Extracted,"A 50-year-old Caucasian alcoholic man presented to the emergency department with generalized weakness lasting 10 days and a history of weight loss. He had no other complaints. His history was significant for excessive alcohol intake and cachexia. At the emergency department, the patient was weak but alert, appeared ill and was very pale. The clinical exam revealed: a temperature of 35.9°C, blood pressure 60/38 mm Hg; a heart rate of 95 beats per minute, a respiratory rate of 23 breaths per minute, bilateral ankle edema, buccal candidiasis, and a faint systolic murmur. The neurological exam was normal, except for psychomotor slowing and a fine tremor. Laboratory results showed: hemoglobin 42 g/l, platelet count 23 G/l, WBC 4.9 G/l (normally distributed), C-reactive protein 21 mg/l (N < 5), hypoalbuminaemia and cholestasis. Other laboratory tests were normal. A chest radiograph showed cardiomegaly and pulmonary vascular redistribution with bilateral pleural fluid accumulation. Computed tomography (CT) imaging excluded aortic dissection, massive pulmonary embolism, pericardial fluid and retroperitoneal hematoma. After blood, urine and pleural fluid had been collected for culture, he was empirically treated intravenously with amoxicillin/clavulanate 2.2 g four times a day and ciprofloxacin 200 mg twice a day for presumed septic shock. A transthoracic echocardiography, that was performed because of the systolic murmur and the hemodynamic instability, showed evidence of tricuspid valvular involvement with several large vegetations of approximately 2.5 cm in diameter, severe valvular regurgitation, and a reduced ejection fraction (45%) (Figure ). As no pathogen could be isolated from blood cultures after 60 hours of incubation, we considered all agents of culture-negative endocarditis as possible etiology. Investigations for HACEK microorganisms, and serologic studies for Bartonella spp., Brucella spp. and Coxiella burnetti were negative; PCR of the blood and pleural fluid for Tropheryma whipplei was positive. The PCR technique described by Meibach et al. in 2003 was used []. Having diagnosed Tropheryma whipplei right heart endocarditis, we switched the antibiotic regimen to ceftriaxone 2 g once daily. Favorable clinical changes kept him from requiring surgery, and he returned home after 25 days with a combined treatment of doxycycline 100 mg twice a day, hydroxychloroquine 200 mg and sulfamethoxazole-trimethoprim 160/800 mg three times a day for a minimum of one year. The blood levels of doxycycline and hydroxychloroquine were measured every other month and doses adapted to therapeutic levels (doxycycline: > 5 μg/ml, hydroxychloroquine 1 +/- 0.2 mg/l). At a one-year follow-up he had completely recovered, gained weight and all his laboratory values were back to normal. A control echography performed after one year (Figure ) confirmed the treatment success.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [95.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 95.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
The patient's Well's score for pulmonary embolism is 3."
2808,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5473192-1,Extracted,"A 19-year-old healthy Caucasian man (AB), with no past medical history, presented to the emergency department with acute onset generalized muscle weakness, more pronounced in his lower extremities. AB described going to bed in his normal state of health. Upon awakening the following morning, he started experiencing severe weakness with inability to sit up in bed; requiring full assistance for activities of daily living. AB reported two episodes of similar presentation at the age of 12 years and most recently three months prior to this presentation. Muscle weakness during previous presentations was described as mild, transient, and self-limited, resolving in a matter of days. Also noted at time of presentation was a history of 40 lbs weight loss over two months in spite of increased appetite. AB denied palpitations, heat intolerance, dysphagia, dysphonia, dyspnea, and change in bowel movements. The remaining review of systems was negative. AB has never smoked and denied use of diuretics, laxatives, alcohol, or recreational drugs. Patient denied use of any prescribed or non-prescribed medications. There was no known history of radiation or thyroid toxin exposure. Family history was negative for periodic paralysis or thyroid disorders.
Physical examination revealed a cachectic male who appeared his stated age, with blood pressure: 100/54 mmHg, pulse: 110 beats per minute, temperature: 98.7°F, respiratory rate: 16 breaths per minute, and oxygen saturation: 97% on room air. He was alert, oriented, and in no acute distress. Head exam was significant for temporal muscle wasting bilaterally, lid lag, orbital lag, and mild exophthalmos. Neck exam showed diffuse symmetric enlargement of thyroid gland with firm consistency and lack of bruit. Cardiopulmonary and abdominal examinations were unremarkable. Neurologic exam was positive for brisk and symmetric patellar reflexes and fine tremors in bilateral hands with extension. Strength was 4/5 in all muscle groups of bilateral lower extremities. The remaining neurological examination was unremarkable.
Initial serum potassium on presentation to the emergency department was 1.9 mEq/L (3.5–5.1 mEq/L), with normal acid-base status that was confirmed on repeat testing. Previous serum potassium less than a month prior to this presentation was 4.9 mEq/L. Serum phosphorus: 3 mg/dL (2.5–4.5 mg/dL), magnesium: 1.7 mg/dL (1.6–2.3 mg/dL). Electrocardiogram showed sinus tachycardia with a ventricular rate of 108 beats per minute.
An initial clinical diagnosis of periodic hypokalemic paralysis was made. Treatment began with 20 mEq of intravenous potassium chloride (KCl) as well as 40 mEq of oral potassium in the emergency department and was then started on a normal saline infusion with 10 mEq/L of potassium. His serum potassium was checked four hours later and was 3.4 mEq/L. Re-examination at four hours was significant for complete resolution of lower extremity weakness with no change in the rest of his physical examination.
Serial measurements of his serum potassium level while in the hospital showed rapid improvement of his potassium with level of 4 mEq/L on hospital day 2. Initial thyroid-stimulating hormone level (TSH) returned at <0.02 mU/L (0.47–4.68 mIU/L), free thyroxine (T4) level: 5.5 ng/dL (0.8–2.2 ng/dL), and total triiodothyronine (TT3): 539 ng/dL (80–206 ng/dL).
Thyrotoxicosis was diagnosed, and the patient was given propranolol 10 mg PO three times a day (TID) as well as methimazole 10 mg PO TID. The patient’s thyroid-stimulating immunoglobulin level was elevated at 382% (<140%) and thyroid peroxidase antibody was 4 IU/mL (<9 IU/mL). Ultrasonography of the soft tissue of the neck showed mildly prominent thyroid gland with marked increased vascularity. The patient was discharged home with the diagnosis of TPP secondary to new onset Graves’ disease. At six week post-discharge follow-up, AB’s weight had returned to normal and there had been no more episodes of muscle weakness or paralysis. His physical exam was remarkable for improved exophthalmos, lid lag, and orbital lag, and mild symmetric thyroid gland enlargement with absence of bruit. Repeat thyroid function tests at that time were as follows: TSH:<0.02 mU/L, free T4: 1.8 ng/dL, and TT3: 209 ng/dL.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2809,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7380793-1,Extracted,"A 54-year-old female patient presented with dry cough and generalized weakness for 20 days, throat discomfort, and breathlessness for 2–3 days, after being referred from a local hospital.
In the preceding 6 months, she was admitted thrice with complaints of persistent dry cough and discharged each time with a diagnosis of acute exacerbation of bronchial asthma. There was no history suggestive of GERD, esophagitis, or aspiration pneumonia. She gave no history of fever, chills, or night sweats. She is a homemaker with no h/o smoking or tobacco addiction. She also never complained of chest pain, heart burn, dysphagia, odynophagia, nausea, vomiting, or weight loss.
On general examination, her vitals were stable. Systemic examination also did not reveal any abnormality except for scattered bilateral expiratory rhonchi.
ENT examination revealed only the posterior pharyngeal wall congestion. Her hemoglobin was 8.9 g%, total leukocyte count (TLC) 14,200/mm3, N73 L13 E05 B01, platelet count 223,000/mm3, RBS 94 mg%, S. creatinine 0.87 mg%, S. bilirubin 0.83 mg%, ALT 10.8, AST 15.3, alkaline phosphatase 86.9 unit/L, S. protein 6.4 g%, and S. albumin 3.4 g%. Urine routine examination was normal.
Chest X-ray showed clear lung fields [], and ECG showed sinus rhythm with no ST-T changes.
Throat swab culture sensitivity reported non-pathogenic, normal upper respiratory tract flora. Sputum for AFB was negative. She was treated with antibiotics, antihistaminics, bronchodilators, and steam inhalation, and discharged after 5 days with advice for follow-up.
She got readmitted the very same evening with paroxysmal cough and shortness of breath. She was conscious, oriented, and afebrile. Her pulse was 132/min and the blood pressure was 160/100 mmHg. She was dyspnoeic and having a respiratory rate of 28/min with SpO2 of 94% on room air. On systemic examination, she had tachycardia with bilateral crepitations and diffuse rhonchi.
Blood reports showed hemoglobin 10.2 g/dL, TLC 15,900/mm3, and N87% L10% M3%. The chest X-ray repeated next morning revealed right paratracheal soft tissue opacity with clear lung fields [].
A CECT thorax [] was planned because of her persistent cough, absence of any significant findings on general systemic or ENT examination, and the new finding of a right paratracheal opacity. CECT thorax revealed an enhancing wall thickening of the esophagus with paraoesophageal fat stranding, mediastinal lymphadenopathy, and subsegmental right lobe atelectasis suggestive of a probable esophageal malignancy.
Upper GI endoscopy [] showed a normal oropharynx, an irregular, friable, circumferential growth in the esophagus from 16 to 26 cm, and the GE junction at 35 cm distance from incisor teeth. Stomach and duodenum were normal. Histopathological examination revealed a moderately differentiated SCC of the esophagus []. CECT abdomen and bronchoscopy was normal.
In view of inoperability, she was referred to medical oncology with T3N1M0, Grade 2 SCC at lower one-third of esophagus and received concomitant radiation and chemotherapy.
She completed her radiotherapy and chemotherapy and is on regular follow-up in oncology.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [132.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 132.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2810,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7443033-1,Extracted,"A 47-year-old male, with a 10-year history of T2DM, presented to the emergency department (ED) with several days of sore throat, dyspnea, nonbloody emesis, abdominal pain, and poor oral intake. He denied any fever, chills, cough, chest pain, or diarrhea. He had a urinary tract infection (UTI) 2 weeks prior, which had resolved with a course of antibiotics. Over several months, he had made significant changes in his diet which resulted in a 60 lb weight loss. The patient reported that he was following an Atkins or ketogenic diet. In addition to diet control, he had been on metformin and empagliflozin started approximately 5 months ago. His last hemoglobin A1c was 76 mmol/dl (9.1%). Of note, one month prior to this presentation, he presented to the emergency department with weakness, intermittent chest discomfort, and shortness of breath with an anion gap of 21, a bicarbonate level of 13 mmol/L, a pH level of 7.22, and 3+ urinary ketones with a glucose level of 7 mmol/L (127 mg/dl). Cardiac workup was negative, lactate was normal, and liver enzymes and D-dimer were within normal limits. The patient was given 1 L fluid bolus with some improvement. Findings were attributed to a keto diet. The patient was discharged with recommendations to increase carbohydrate intake for 2 weeks and repeat electrolytes. His use of empagliflozin was not identified on his medication list in the emergency department nor was it mentioned in the ED notes. His repeat labs one week later did result in closure of his anion gap to 10. When this second presentation to the emergency department 24 days later, he was afebrile, tachypneic with a respiratory rate of 30, and tachycardic with a heart rate of 130 beats per minute, blood pressure was 160/89 mmHg, and SpO2 was 100% on room air. Other than respiratory discomfort, the exam only showed mild abdominal discomfort to palpation. Labs were significant for an anion gap of 28, a pH level of 6.94, with a bicarbonate level of 5 mmol/L, 3+ urinary ketones, a beta-hydroxybutyrate level of 8.9 mmol/L, and a glucose level of 14.9 mmol/L (269 mg/dl), as well as acute kidney injury with a creatinine level of 107 umol/L (1.21 mg/dl). His glutamic acid decarboxylase antibody assay ordered during this admission eventually returned negative. His C-peptide was 0.77 nmol/L (2.3 ng/ml). Cardiac workup was negative. CT scan did reveal possible aspiration pneumonitis. The patient was diagnosed with diabetic ketoacidosis, received several litres of fluid, started on insulin drip, and admitted to the medical ICU. With closure of anion gap, on the following day, the patient was transitioned to insulin basal bolus regimen, and metformin was eventually restarted. His empagliflozin was stopped indefinitely. Hospital course was also complicated by development of a new UTI, and the patient was treated with ceftriaxone/cephalexin. Finally, he was deemed medically stable for discharge with plans to follow up with endocrinology and his primary care provider.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [130.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 130.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2811,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8033466-1,Extracted,"A 62-year-old man presented with a 2-year history of dyspnea and a feeling of chest
compression during activity, and had also experienced shortness of breath with edema of the
lower extremities for 2 months. He was receiving loop diuretic therapy. He had received a
pacemaker implant 2 years earlier because of complete atrioventricular block, and the
pacemaker had been replaced due to pacemaker pocket infection 2 months ago. He developed
atrial fibrillation 1 month before pacemaker replacement surgery, which persisted to date.
He had experienced hypertension for 3 years, with good blood pressure control, and had
chronic bronchitis for over 10 years.
His vital signs were normal. Physical examination revealed signs of jugular venous
engorgement, a small amount of bilateral lung rales and low breath sound in both sides,
reflux heart murmur, and positive hepatic jugular venous reflux. His heart rate was 80
beats/minute and irregular. There was pulse deficit. Both lower extremities had pitting
edema.
N-terminal-pro B-type natriuretic peptide serum levels were significantly above the normal
range, fluctuating between 2000 to >4000 pg/mL. An electrocardiogram indicated atrial
fibrillation with left bundle branch block (). A chest radiograph showed bilateral pleural
effusion. The echocardiogram revealed an enlarged four-chamber (LV end-systolic diameter
4.8 cm and end-diastolic diameter 6.0 cm, left atrial diameter 4.5 cm) with normal LV
thickness (1.0 cm) and diffuse reduction of wall motion (LV ejection fraction 37% by
Simpson’s method) (),
color Doppler showed ingravescence of mitral and tricuspid regurgitation. Transesophageal
echocardiography showed patent foramen ovale. Coronary angiography showed no severe coronary
artery stenosis. 99mTc-sestamibi myocardial perfusion imaging showed dilated
cardiomyopathy with LV insufficiency (). Pulmonary function tests confirmed chronic obstructive pulmonary
disease (COPD). A pulmonary ventilation perfusion scan showed a small pulmonary embolism in
the posterior basal segment of the lower lobe.
The patient’s symptoms of edema and dyspnea improved after treatment with an
angiotensin-converting enzyme inhibitor (perindopril), beta-blocker (metoprolol tartrate),
aldosterone antagonist (spirolactone), and loop diuretic (torasemide). The patient also
received anticoagulation with dabigatran for atrial fibrillation and pulmonary embolism.
The patient’s sister (67 years old) had been diagnosed with DCM several years earlier and
had undergone pacemaker implantation because of complete atrioventricular block. The current
patient was accordingly diagnosed with FDCM because both he and his sister met the criteria
of idiopathic DCM in at least two closely related family members. Both patients both showed III atrioventricular block, probably because cardiomyopathy
involves the conduction system. The patient, his sister (both with confirmed DCM), and his
son (aged 34 years; healthy, with no record of dilated heart) all received genetic testing,
which revealed the same heterozygous DES mutation. None of the three
individuals showed any abnormal skeletal muscle symptoms. Mutation analysis (see below)
identified a c.1010C>T mutation in the DES gene, causing an alanine to
valine substitution at position 337 in the desmin protein in all three individuals (), which confirmed the FDCM
diagnosis. The pedigree is shown in .
Gene sequencing was carried out as follows. Peripheral blood was collected from the patient
and his family members and DNA was extracted using a blood DNA extraction kit (Tiangen,
Beijing, China), according to the manufacturer’s instructions. Targeted gene capture
sequencing was performed by MyGenostics (Beijing, China). Genomic DNA samples were
fragmented and prepared for standard Illumina library construction. Biotinylated capture
probes were designed for the exons of 94 genes related to cardiomyopathy and sequenced using
an Illumina HiSeq 2000 Next-Generation Sequencing platform (Illumina, San Diego, CA, USA)
and bioinformatics analyses (MyGenostics). Data analysis was performed according to
MyGenostics protocols. Clinically relevant variants from the patient, his sister, and his
son were confirmed by Sanger sequencing.
Informed written consent was obtained from the patient prior to publication of this report
and ethical approval was provided by the Biomedical Ethics Committee of Beijing Friendship
Hospital, Capital Medical University (No. 2019-P2-211-01).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 3 + 1.5 = 4.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
2812,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7868231-1,Extracted,"A 53-year-old woman known to have operated ovarian cancer with right salpingo-ovariectomy and adjuvant chemotherapy 1 year ago, history of deep vein thrombosis (DVT) on long-term anticoagulation and iron deficiency anaemia. She was hospitalised for a scheduled laparotomy for the treatment of her cancer where she underwent extensive abdominal and pelvic organ resections that included peritonectomy, splenectomy, hysterectomy, left annexectomy, appendectomy, colectomy, infracolic omentectomy and diaphragm scraping. In the immediate postoperative phase, she presented with abrupt aphasia. On physical examination, blood pressure was 100/60 mm Hg, heart rate 108 bpm, cardiopulmonary auscultation within normal limits, no heart failure signs, aphasic patient, oxygen saturation 98% on 12 L oxygen mask on lying position. ECG found normal sinus tachycardia with no conduction or ischaemic changes. Sodium 137 mmol/L, potassium 3.8 mmol/L, creatinine 46 µmol/L, glomerular filtration rate 109 mL/min and haemoglobin 107 g/L.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [108.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 108.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 =  3.0.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3.0 + 1.5 = 4.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2813,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7328697-1,Extracted,"The patient was a 49-year-old female with a past medical history of rheumatic heart disease status following two mitral valve replacements each with a mechanical prosthesis. She presented to the emergency department with a complaint of worsening fatigue, shortness of breath, epigastric pain, nausea, and vomiting. The patient also reported a history of jaundice and dark urine. Other significant past medical history included sick sinus syndrome with a pacemaker in situ, hepatitis B infection, and hyperlipidemia. On physical examination, blood pressure was 157/76 mm Hg, heart rate was 77 beats per minute, temperature was 97.7°F, respiratory rate was 18/minute, and oxygen saturation was 98% on room air. Scleral icterus and conjunctival pallor were noted. Her neck was supple without masses or bruits and skin was without rashes or lesions. Cardiac auscultation was significant for a crisp mechanical S1 click with a soft 2/6 systolic murmur in the left lower sternal border. Lungs were clear to auscultation bilaterally without rhonchi, rales or wheezes. The abdomen was soft with epigastric and right upper quadrant tenderness noted; no Murphy’s sign, guarding, or rebound tenderness; and positive normoactive bowel sounds. Laboratory studies are shown in Table .
Electrocardiogram (EKG) and chest x-ray were within normal limits. Computed tomography angiogram of the chest revealed no pulmonary embolism, thoracic aortic aneurysm, or dissection. Abdominal ultrasound showed cholelithiasis with pericholecystic fluid, but no gallbladder wall thickening or focal tenderness. Common bile duct diameter was measured as 4 mm with no intrahepatic bile duct dilation.
The patient had a history of elevated liver function tests in a hepatocellular pattern. She also had a history of positive hepatitis B surface antigen. A total bilirubin of 6.9 mg/dL was higher than her usual baseline. A magnetic resonance cholangiopancreatography (MRCP) of the abdomen was unremarkable except for chronic cholecystitis (Figures , ).
A hepatitis panel was also checked along with other viral antibodies (Table ). The findings were not consistent with a reactivation of hepatitis B infection.
Given the patient's significant cardiac history, a trans-thoracic echocardiogram (TTE) was performed that revealed mildly depressed biventricular systolic function (left ventricular ejection fraction 45%-50%), prosthetic mitral valve well seated, but at least mild paravalvular insufficiency. Subsequently, a transesophageal echocardiogram (TEE) showed normal left ventricular systolic function (ejection fraction 55%), a well-seated mitral valve prosthesis with a significant PVL and likely moderate mitral regurgitation with some pulmonary flow reversal, and no pericardial effusion (Figure ).
Cardiac catheterization revealed normal coronary arteries, mild left ventricular systolic dysfunction, mitral regurgitation secondary to multiple PVLs, and normal cardiac output/index.
Given these findings, hemolytic anemia was suspected. This was further evaluated with a hemolysis panel (Table ).
These findings were suggestive of hemolytic anemia. The differential diagnosis was of hemolysis occurring either secondary to mechanical shearing due to valvular pathology or an autoimmune etiology. Serum protein electrophoresis, immunoglobulin levels, as shown in Table , and direct Coombs test were unremarkable, eliminating autoimmune etiology as the cause for hemolysis. Cardiothoracic surgeons did a third time re-operation, a right mini-thoracotomy Heartport mitral valve re-replacement with a mechanical valve was performed without complications. A post-operative TEE demonstrated a normally functioning prosthesis with no PVL, and low normal left ventricular systolic function (ejection fraction 50%). The hyperbilirubinemia resolved, with a total bilirubin of 0.9 mg/dL at discharge. Hemoglobin improved to 12.7 g/dL at the 6-month follow-up.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [77.0, 'beats per minute'], 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 77.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2814,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6426093-1,Extracted,"We report a 28-year-old man who was suffering from carcinoma of tongue and underwent hemimandibulectomy and post-operative radiotherapy. A histological diagnosis of squamous cell carcinoma was made. Three months later, he presented with multiple episodes of syncope to the emergency department. ECG showed CHB and a broad complex escape with left bundle branch block morphology (Figure ). These episodes were sudden in onset with no preceding symptoms. On physical examination, the patient had bradycardia with a regular heart rate of 32/min and normal blood pressure. On auscultation the chest was clear and there were no murmurs heard. Routine blood investigations were normal with normal serum creatinine 1.1 mg/dL (0.6–1.4 mg/dL) and normal serum sodium and potassium of 4.1 meq/dL (3.5–5.5 meq/dL). Echocardiography was performed which showed normal left ventricular ejection fraction and no valvular abnormalities. However, there were hyperechoic areas and hypertrophy of interventricular septum and the posterolateral wall of left ventricle as well (Figure ). The patient was paced using a temporary pacemaker as the patient was symptomatic with multiple episodes of syncope and had CHB on ECG with escape rate of 32 on ECG. The chest X-ray showed a large solitary nodule in the right upper zone. A positron emission tomography (PET) scan was performed and was suggestive of multiple metastasis in the interventricular septum, the right atrium, and the LV wall along with a large pulmonary metastasis (Figure and D). The patient also developed paraneoplastic syndrome in the form of hypercalcaemia with serum calcium of 14 mg/dL (normal range: 8.5–10.2 mg/dL) which resolved on administering fluids and zoledronic acid intravenously. However, the CHB persisted despite normal calcium levels, so a decision to implant a permanent pacemaker was taken. The patient was then taken up for permanent pacemaker implantation and an active fixation lead was positioned into the low septal position in order to avoid metastatic site on the mid septal region. An active fixation lead was chosen as it is the institutional protocol to use active fixation lead (Figure ). A sensed R wave of 7 mV was achieved with a pacing threshold of 0.6 mV indicating a good position. Post-procedural ECG showed a ventricular paced rhythm. On the fifth day post-pacemaker implantation, the patient had massive haemoptysis. Crystalloids, and blood were transfused, but the patient succumbed before he could be taken up for bronchial artery embolization.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [32.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3.5,3.5,3.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 32.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 1.5 + 1 = 2.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 2.5 + 1 =  3.5.
The patient's Well's score for pulmonary embolism is 3.5."
2815,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7716385-1,Extracted,"A previously healthy 77-year-old female, a nonsmoker, was admitted to the hospital after a month of malaise, tiredness, dizziness, dyspnea, severe headache, and anorexia.
Recently, her general practitioner diagnosed her with arterial hypertension and started administering the diuretic bendroflumethiazide. She received no other medications, no corticosteroids, and no anticoagulants. Her chest X-ray revealed emphysematous lungs without apical bullae.
Upon arrival at the hospital, her blood pressure was 190/50 mmHg, pulse 40-50 bpm, serum-Na 114, and serum-K 3.2 mmol/L. Electrocardiogram (ECG) showed third-degree atrioventricular block and narrow, nodal escape rhythm. CT cerebrum was without any acute changes. Echocardiography was normal. Height was 165 cm, weight 55 kg, and BMI 20 kg/m2.
Bendroflumethiazide was withdrawn, the Na-deficit slowly corrected, and electrolyte derangements were abolished, but the atrioventricular (AV)-block persisted. After implantation of a pacemaker, the blood pressure fell to 160/70 mmHg, she was administered amlodipine, the blood pressure normalized, and the symptoms disappeared. This supported the theory that arterial hypertension with a very high systolic pressure and a wide amplitude was due to initially unnoticed bradycardia and the electrolyte derangements to treatment with the thiazide, conjointly causing the symptoms of the patient.
A dual-chamber (DDD) pacemaker was implanted without immediate complications. Two screw-in electrodes (helical active fixation leads) were inserted via the left subclavian vein. Puncture of the subclavian vein was guided by venography and fluoroscopy, the needle pointing towards the intersection of the clavicle and the first costa (Figure ).
The vein was punctured in the second attempt, with no aspiration of air, Seldinger technique using two peel-away-sheaths with a diameter of 9 and 7 French to introduce a guidewire into the right atrium and two pacemaker electrodes.
The atrial lead was repositioned a couple of times before good values were obtained on the lateral wall of the right atrium, where it was secured. The ventricular electrode was placed in the apex of the right ventricle. During the implantation, severe problems were not encountered, neither when searching for venous access, nor when fixing the leads.
Later the same day, her chest X-ray showed bilateral apical pneumothorax; it measured 15 mm on the left side, 10 mm on the right side (Figure ).
She was administered high flow oxygen on a nasal cannula. The patient stayed clinically stable and experienced no breathing problems, no pleuritic chest pain, and no pericardial signs or symptoms.
The following day, the left pneumothorax had diminished to 7 mm, the right pneumothorax was unchanged, but there was a small effusion in the right costophrenic angle (Figure ).
This was confirmed by fluoroscopy (Figures -). The atrial electrode seemed to respect the atrial wall (Figure ).
Repeated chest X-ray, fluoroscopy, and echocardiography did not show perforation of the right atrium, and there was no pericardial effusion, no ECG changes, and the pacemaker values remained fine with nonconclusive falls in sense and impedance. The atrial lead parameters at implantation and the following day were: capture 0.8/1 V (duration 0.4 ms); sense 4/2.4 mV, and impedance 400/342 Ohms.
The following day the left pneumothorax had diminished to 5 mm, but the changes on the right side were the same (Figures -). This led to the decision to replace the atrial electrode, even though the position was unchanged (Figure ).
The atrial electrode was repositioned; the tip was moved to the right atrial appendage without complications. Echocardiography remained normal.
Two weeks later, the chest X-ray had normalized (Figure ). The pacemaker was functioning well, and the patient felt fine under the circumstances.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [4050.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 4050.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2816,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7288206-1,Extracted,"A 53-year-old male with history of alcohol abuse presented with new-onset seizure/syncope, six painless maroon stools, and coffee-ground emesis. The patient admitted to frequent diclofenac use and ketorolac injections. He did not have a history of varices. Vital signs demonstrated tachycardia (heart rate 111 beats/min) and hypotension (79/59 mmHg). Physical exam revealed pale conjunctiva, dry mucous membranes, and maroon colored stool. He was found to be anemic with a hemoglobin of 7.9 G/dL and had an elevated INR of 1.2. He was transfused two units of packed red blood cells and was started on a pantoprazole drip.
Once stabilized, initial EGD revealed an island of tissue growth in the mid-esophagus and a bleeding duodenal ulcer that was injected with epinephrine, cauterized with gold probe and clipped. Biopsy of the esophageal lesion was deferred to outpatient follow-up given the severity of the patient's presenting condition. He had no further signs of gastrointestinal bleeding. Two weeks later, a repeat EGD was performed. Biopsies were taken of the stomach mucosa and mid-esophageal mass (see ). Gastric biopsy demonstrated mild chronic gastritis without dysplastic changes or Helicobacter pylori. Esophageal biopsy demonstrated findings consistent with squamous papilloma (see Figures and ).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [111.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 111.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2817,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6681851-1,Extracted,"A 78-year-old Caucasian woman presented with the complaint of acute-onset shortness of breath associated with right-sided chest pain. She had a past medical history significant for type II diabetes mellitus, hypertension, colon cancer status post colon resection about 18 years ago, subdural hematoma 2 years ago, persistent non-valvular atrial fibrillation, idiopathic thrombotic purpura (currently on romiplostim), combined systolic and diastolic heart failure, pulmonary arterial hypertension and seizure disorder. Her home medications included diltiazem, metoprolol, furosemide, metolazone and levetiracetam. Her weight was 194.2 lb (88.1 kg) and height was 167.6 cm (5 ft 6 in). Her vital signs on arrival were: heart rate of 103 beats per minute, blood pressure of 143/60 mm Hg and temperature of 97.4 °F (26.3 °C). On physical exam, she was not in acute distress and was alert, awake and oriented to person, place and time. Her lungs were clear to auscultation bilaterally and the heart was tachycardic and irregular in rhythm. The patient was noted to have mild bilateral lower extremity edema. Her hemoglobin was 8 g/dL, hematocrit was 25.8% and platelets were 62,000/µL. Prothrombin time (PT) was 11.5 s, INR was 1.06 and activated partial thromboplastin time (aPTT) was 25.2 s which were increased from her baseline. The D-dimer level was 659 ng/mL. All other routine lab works including cardiac enzymes were unremarkable. An electrocardiogram (ECG) revealed atrial fibrillation with rapid ventricular response with a low-voltage QRS and a ventricular rate of 120. Chest X-ray revealed a small left basilar pleural effusion. Computed tomography (CT) angiogram of the chest showed a right lower lobe segmental PE, moderate cardiomegaly and a dilated main pulmonary artery, suggestive of underlying pulmonary arterial hypertension (). Lower extremity duplex was negative for deep vein thrombosis bilaterally. A transthoracic echocardiogram revealed an ejection fraction (EF) of approximately 40%. She was treated with diltiazem 30 mg twice a day and metoprolol tartrate 50 mg two times a day; her arrhythmia subsequently converted to normal sinus rhythm. The patient was placed on a therapeutic-dose of enoxaparin and her symptoms resolved by hospital day 2. The patient was subsequently started on a loading dose of apixaban 10 mg twice a day for 7 days and was discharged with instructions to start a maintenance dose of 5 mg twice a day afterwards as per the package insert guidelines [].
Seven days later, the patient returned to the emergency department with a new onset of progressively worsening shortness of breath which started a day after her hospital discharge. Her vital signs on arrival were within normal limits. Her hemoglobin was 11.3 g/dL, hematocrit was 34.3% and platelet count was 930/µL. She had an INR of 2.33 and prothrombin time of 25.6 s which were elevated compared to previous levels. The troponins were within normal limits and B-type natriuretic peptide (BNP) was 3,132 pg/mL. Her creatinine was 1.4 mg/dL with a glomerular filtration rate of 36 mL/min/1.73 m2. An ECG revealed atrial fibrillation, left axis deviation, low-voltage QRS with ventricular rate of 89. Chest X-ray although showed persistent left basilar opacity, there was an enlargement of the cardiac silhouette. A bedside echocardiogram was done and revealed similar EF to prior echocardiogram but also revealed a large pericardial effusion. An official transthoracic echocardiogram confirmed the large pericardial effusion without any signs indicative of cardiac tamponade (). A pericardiocentesis was performed and 300 mL of hemorrhagic fluid was removed and a pericardial catheter was placed. Analysis of the pericardial fluid revealed numerous acute inflammatory cells and no malignant cells, bacteria, fungi or acid fast bacilli. A repeat echocardiogram showed resolution of the pericardial effusion. The pericardial drain was removed and 2 days later the patient decompensated, became septic requiring intubation, pressors and antibiotic therapy. A CT scan of the chest showed a left-sided pleural effusion and a new pericardial effusion (). A chest tube was subsequently placed and drained 800 mL of fluid. Fluid analysis of the pleural fluid showed cloudy, red fluid with 32,000 red blood cells, 4,843 total nucleated cells, 23% monocyte/macrophage count and 73% segmented granulocytes. The patient was no longer requiring pressors and the chest tube was removed. There was a worsening left pleural effusion and a drainage catheter was placed by cardiothoracic surgery. An echocardiogram 6 days later showed the pericardial effusion to have completely resolved. Apixaban was resumed and the patient was discharged to a skilled nursing facility.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [103.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 103.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2818,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5986674-1,Extracted,"A 28-year-old male physician with no significant past medical history except for asthma, for which he takes albuterol and cetirizine, presented to a cardiology clinic with shortness of breath and palpitations for the last 3 months. The patient reported feeling ‘the heart rubbing against the chest while leaning forward’. He denied chest discomfort or other cardiac symptoms. After auscultating his own chest, he heard a murmur for which he sought medical advice. Physical exam was normal except for a low-grade holosystolic murmur best heard at the left lower sternal border, tachycardia and tachypnea with a respiratory rate of 25. Electrocardiogram (ECG) showed sinus tachycardia with a heart rate of 112 beats per minute and right axis deviation. Transthoracic echocardiogram (TTE) revealed an RV mass (approximately 3 × 2 cm) attached to the interventricular septum by a small pedicle, dilated right heart chambers, moderate tricuspid regurgitation, and severe pulmonary hypertension (systolic pulmonary artery pressure > 60 mmHg) (Fig. ). Cardiac magnetic resonance (MR) confirmed the presence of a well-circumscribed non-obstructive mass (2.4 × 1.9 × 1.2 cm) that appeared not to invade the surrounding cardiac structures located in the RV outflow tract, inferior to the pulmonary valve (Fig. ). The patient denied a family history of cardiac tumors.
The patient underwent open heart surgery with median sternotomy and total cardiopulmonary bypass. Right ventriculotomy was performed, and the incision was extended superiorly and inferiorly. Traction sutures were placed on the right ventricle in order to improve exposure. A large and soft RV mass obstructing the RV outflow tract was identified in the right ventricle attached to the anterosuperior and septal leaflets of the tricuspid valve and partially attached to the interventricular septum. Based on the surgeon’s decision, the mass was partially excised without compromising the integrity of the tricuspid valve (Fig. ). TEE was used to evaluate the valve function and revealed mild tricuspid regurgitation. The patient had uneventful surgical recovery and was discharged following a 5-day hospitalization period.
The pathology report of the resected mass (two specimens) confirmed the diagnosis of myxoma. The first specimen consisted of three fragments of tissue measuring 1.3 × 1 × 0.5 cm in aggregate. One portion of tissue had a tan–white base with tan–red tissue attached and projecting from the base. Another portion of tissue was predominately tan–red with focal yellow tissue, reminiscent of adipose tissue. The third portion of tissue was tan–red. The second specimen was an aggregate of pink–tan to gray–white, rubbery, ragged, and soft tissue fragments measuring 3.5 × 3.5 × 1.5 cm. Sectioning revealed a gray–white to yellow–green, rubbery and friable cut surface. No firm areas were identified. Microscopically, the majority of the first specimen consisted of fibrin clot. There was a fragment of bland polygonal to spindle-shaped cells within a myxoid matrix. Factor VIII showed focal positivity within the bland cells and was positive in capillaries. CD34 was positive in capillaries. No entrapped cores of elastic tissue were seen on Verhoeff-Van Gieson stain (elastin stain). Trichrome stain showed no laminated elastic fibers within the matrix. The morphologic and immunohistochemical findings were compatible with cardiac myxoma. The microscopic examination of the second specimen showed myxoma cells with an oval nucleus which were forming ring structures around small thin-walled blood vessels. An accompanying mononuclear inflammatory cell infiltrate was present. Hemosiderin-laden macrophages were also present. A myxoid background was focally present. The majority of the tissue showed secondary changes of fibrosis and calcification which obscured the underlying nature of the lesion. The myxoma was attached to a portion of benign cardiac muscle.
Two weeks after surgery, a follow-up TTE showed a residual RV mass (approximately 2 × 1.5 cm) attached to the interventricular septum.
Five months after surgery, the patient presented to the emergency department with right-sided pleuritic chest pain and upper abdominal discomfort. The patient took 15 airplane flights over the previous 2 months, some of which were very long. He was tachypneic (22 breaths/min), and his ECG showed sinus tachycardia with a heart rate of 118 bpm and right bundle branch block (RBBB). Serum D-dimer was elevated (0.9 mg/l). His chest X-ray was normal. A chest computerized tomography (CT) scan revealed multiple emboli in the right lower lobe segmental and subsegmental pulmonary arterial branches, as well as peripheral airspace disease in the right lower lobe suggestive of pulmonary infarction (Fig. ). Venous Doppler ultrasound of the legs showed bilateral patent and compressible venous systems and no evidence of thrombus. TTE and transesophageal echocardiogram (TEE) were done and reported dilation of the inferior vena cava (IVC), right atrium and right ventricle and a mass (approximately 2 × 1.5 cm) attached to the base of the RV wall just below the insertion of the anterior tricuspid leaflet (Fig. ). The tricuspid jet was insufficient to calculate pulmonary pressure. Cardiac MR showed a small residual tissue (9 × 9 mm) adjacent to the interventricular septum and another residual tissue (7 × 9 mm) attached to the RV free wall (Fig. ). The patient was diagnosed with PE, due to either tumor emboli or thromboemboli, and was started on warfarin. On further follow-up (20 months following PE), he had no recurrent PE.
Informed consent was obtained from the patient for being included in the study.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [118.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 118.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3.0 + 1.5 = 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2819,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8196367-1,Extracted,"A 68-year-old woman with no medical history was discovered at home, lying on the floor for an unknown number of hours and her core temperature was 26°. No medication was found lying around. On admission, she presented with a severe cardiogenic shock. The mean blood pressure was 30 mm Hg with a sinus bradycardia of 31 per minute and the arterial lactate was 2.5 mmol/L. Cardiac ultrasonography showed a global hypokinesia of the left ventricle. She had acute respiratory distress, with oxygen saturation of 93% requiring high-flow nasal oxygen. Laboratory investigations revealed an increased sodium level (157 mmol/L), a KDIGO (kidney disease improving global outcomes), three acute kidney injury (uremia was at 342 mg%, creatinine 3.95 mg/dL), and a mild rhabdomyolysis (CPK at 280 U/L, myoglobin at 3880 ug/L). The initial PT was 51%, fibrinogen rate was 6.7 g/L, and blood platelets were 248 G/L. A DIC (disseminated intravascular coagulopathy) was present with raised D-dimers (4.93 ug/mL) and fibrin monomers at 24.6 ug/mL. The International Society on Thrombosis and Hemostasis (ISTH) score was 4. Initial care consisted in tracheal intubation, mechanical ventilation, external and internal rewarming (COOLGUARD 3000™ device), and continuous venovenous hemofiltration. Blood pressure quickly stabilized after initiation of norepinephrine perfusion. Complete warming occurred within 8 hours and sedation could be stopped. After awakening, the patient assessment revealed acute left leg ischemia and right hemiparesis. A whole-body CT scanner showed a constituted left Sylvian stroke, multiple tiered blood clots along the aorta, and in the left iliac artery (). A surgical embolectomy and preemptive fasciotomy were performed, and the patient was initiated on anticoagulation. On day 3, the abdominal examination revealed a generalized contracture with a CT scan showing a diffuse hepatic and bowel portal gas, with multiple arterial thromboses. End of life decision was taken in view of the possible poor outcome and the patient died after treatment withdrawal.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [31.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 31.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 3 + 1.5 = 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2820,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6488774-1,Extracted,"The patient was a 90-year-old male with a past medical history of coronary artery
disease, diabetes mellitus, benign prostatic hyperplasia, atrial fibrillation, and
hepatocellular cancer came for the evaluation of weakness. His home medications
included aspirin, metoprolol, tamsulosin, glipizide, glucophage, eliquis, and
acarbose. He quit smoking 5 years prior to admission and had a 30-pack-year smoking
history, occasionally drank alcohol, and did not use any recreational drugs. He
denied abdominal pain, nausea, vomiting, or diarrhea. He also reported no recent
sickness exposure or travel.
At 1 month prior to admission, he underwent magnetic resonance imaging (MRI) of his
abdomen following complaints of abdominal pain. This revealed a mass in his right
inferior hepatic lobe measuring 8 cm. Later, a computed tomography–guided biopsy of
the mass demonstrated the scirrhous variant of hepatocellular cancer. As the patient
was not considered to be a surgical candidate, he was started on sorafenib for his
hepatocellular cancer.
He was admitted to the hospital for an evaluation of weakness 1 week later. A
physical examination revealed that the patient was of thin build, not in respiratory
distress, afebrile with a temperature of 97°F, a heart rate of 87 beats per minute,
a blood pressure of 108/60 mmHg, a respiratory rate of 12 breaths per minute, and an
oxygen saturation of 94% on 2 L of oxygen via a nasal cannula. A chest examination
indicated that he had bilateral bronchial breath sounds, while a cardiovascular
examination confirmed that his heart sounds were normal. His abdomen was soft upon
palpation, with hepatomegaly noted, and his neurological examination was
unremarkable.
Laboratory analysis performed 1 week prior to starting sorafenib and subsequent
values after sorafenib discontinuation are shown in and are notable for hyponatremia.
Further work-up of hyponatremia, including serum osmolarity, serum uric acid, urine
sodium, urine specific gravity (1.021), thyroid-stimulating hormone, serum cortisol,
and total protein, is shown in .
Our initial assessment concluded that sorafenib induced hyponatremia, so the drug was
discontinued. After starting the patient on 3% saline, his sodium levels improved
slowly. Other common causes of hyponatremia were excluded, supporting our initial
assessment that this was a rare case of hyponatremia secondary to sorafenib. Because
the patient was a poor candidate for any intervention for his hepatocellular cancer,
he was accepted to hospice.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [87.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 87.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
2821,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5406044-1,Extracted,"A 66-year-old male patient presented with a past medical history of rheumatic heart disease and mitral stenosis for more than 10 years and has been taking oral warfarin anticoagulation. Sixteen days before admission, he had abdominal distension, nausea, and fever, with a Tmax of 39°C. Thirteen days earlier, the abdominal distention had become worse. An enema was performed, and the antibiotics moxifloxacin and levofloxacin were administered successively. Six days before admission, the patient developed difficulties eating, and received parenteral nutrition. On the morning of admission, the patient had dyspnea, with a respiratory rate (RR) of 30/min, and he came to the emergency room of our hospital.
The patient's vital signs were as follows: T: 36.8°C, heart rate (HR): 156 bpm, RR: 28/min, blood pressure (BP): 91/63 mm Hg, and SpO2: 99%. The breathing sound of the bilateral lower pulmonary field was low, and scattered wet rales could be heard. The laboratory examination results were as follows: hemoglobin (HGB) 84 g/L, white blood cell (WBC) count 8.51×109/L, neutrophil% (NEUT%) 83.2%, and potassium (K) 3.1 mmol/L; other results, including the complete blood count, liver function, renal function, and electrolytes, were normal. The patient was admitted to the intensive care unit (ICU) ward, and cefoperazone/sulbactam was prescribed. The patient had symptoms of gastrointestinal bleeding (GIB) during the night with hematochezia and positive occult blood in both his stool and gastric juice. The HGB was reduced to 65 g/L. Three days after admission, the patient received an examination by gastroscopy, and a jejunum nutrition tube was inserted. The gastroscopic results showed multiple lesions in the horizontal part of the duodenum, and a biopsy was performed (Fig. ). The pathological examination suggested inflammatory exudates, and acute and chronic inflammation of the small intestinal mucosa. Fungal hyphae were seen in the inflammatory exudates, which were considered mucor (Fig. ).
Due to the continuous gastrointestinal bleeding, an interventional therapy of artery embolization was performed on day 5 to stop the bleeding. The gastroduodenal artery proximal to the right gastroepiploic artery was embolized. The patient still had hematochezia after the intervention. A positron emission tomography-computer tomography (PET-CT) and an abdominal computer tomography angiography (CTA) examination were performed, but no obvious bleeding site was found.
Because of the ineffectiveness of the variety of hemostatic methods, laparotomy and intraoperative gastroscopy exploration were performed on day 6. During the operation, we observed adhesions of the jejunal wall 15 cm from the Treitz ligament with the surrounding small mesentery. There was a hard, palpable mass 5 cm in size. After decomposition of the adhesion, the site of chronic perforation could be observed in the jejunum wall. The site of the GIB was the proximal jejunum. The perforation site and the distended proximal jejunum were resected. A drainage tube was placed near the anastomosis, and a jejunum fistula tube was placed 50 cm from the anastomosis. The abdominal drainage fluid was collected for a pathogen culture.
The results of the culture returned on postoperation day (POD) 4 suggested Candida albicans, Klebsiella pneumoniae, and Acinetobacter baumannii. Caspofungin was prescribed for antifungal therapy. Cefoperazone/sulbactam, minocycline, and vancomycin were used for empirical antibiotic therapy. The patient's temperature returned to normal. Minocycline, vancomycin, and caspofungin were terminated on POD 11. The cefoperazone/sulbactam was withdrawn, and the abdominal drainage tube was removed on POD 14.
Heparin anticoagulant therapy was initiated on POD 17 for the rheumatic heart disease. Melena reappeared. The patient's HGB decreased to 86 g/L. Heparin was stopped, and the patient received a blood transfusion. The hematochezia did not improve. The plasma fungal D-glucan (G test) was 112.80 pg/mL. The pathologists re-examined the ulcer lesion of the surgical specimen and found degenerative fungal hyphae. The morphology and specific staining suggested it was a mucor infection (Fig. ). Oral mycostatin and intravenous amphotericin B (Amp B) were initiated on POD 26. Amp B was initiated at a dose of 5 mg daily, which was gradually increased to 20 mg daily. The patient had a fever, abdominal distension, and an increase in bilirubin, with a total bilirubin (TBil) of 36.2 mol/L and a direct bilirubin (DBil) of 26.7 mol/L. We considered these results adverse effects of Amp B, and gradually reduced the dose to 15 mg/d. After 20 days of medication, we withdrew the Amp B and used the single drug mycostatin. During the drug treatment, the patient's gastrointestinal bleeding gradually stopped, and the temperature remained normal. Six weeks after the operation, the patient was transferred from the ICU to the general surgery ward to continue the treatment of oral mycostatin until drug withdrawal. The total course of antifungal treatment with Amp B and mycostatin was 4 weeks. Nine weeks after the operation, the jejunal fistula tube was removed. The patient's body temperature was normal, and there was no evidence of gastrointestinal bleeding. The patient was discharged.
Four days after discharge, the patient again developed nausea, vomiting, and left abdominal pain with a body temperature up to 38.9°C. The following day, the patient developed abdominal distension. After an enema, about 1000 mL of loose stool was discharged. Subsequently, the patient had diarrhea approximately 8 times a day, with a total of approximately 1000 mL. The patient complained that he was thirsty. One week after discharge, the patient had delirium, weak breathing, confusion, and oliguria. He was re-admitted to the hospital, and septic shock was considered. Anti-infection therapy and active drug treatment were ineffective, and the patient was declared dead.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [156.0, 'bpm'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 156.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 =  3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2822,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8511584-1,Extracted,"A 77-year-old man with a medical history of type 2 diabetes mellitus (DM), peripheral neuropathy, and chronic obstructive pulmonary disease was admitted to the intensive care unit (ICU) of Bangladesh Medical College Hospital with complaints of high-grade fever and unconsciousness. The patient was first brought into the emergency department and eventually shifted to the ICU based on the patient’s condition. The attendant reported that the patient received his first dose of the Moderna vaccine just 2 days ago, and he was stable before vaccination. However, after 12 hours of vaccination, he developed fever, went unconscious after 36 hours, and was admitted to this hospital 48 hours after the vaccine.
On examination, the patient was found febrile and unconscious with a Glasgow Coma Scale of 8/15 where the score for eye-opening, motor response, and verbal response were 3, 3, and 2, respectively. His pulse rate was 106 beats/min, and his respiratory rate was 30 breaths/min. At the time of admission, the duty doctor found his blood pressure 90/60 mm Hg. The patient’s initial oxygen saturation recorded 80% on room air, which became 97% with 10 L of oxygen. No meningeal irritation or focal neurological deficits were noted. Plantar flexion was found. Notably, on admission, a chest X-ray was unremarkable, and COVID-19 was negative by reverse transcription-polymerase chain reaction test. The patient had no known neurological or psychiatric history except mild peripheral neuropathy due to DM. Besides, he had never used tobacco, alcohol, or any other harmful substances in his lifetime. As a regular medication, he was taking antidiabetic medicine along with H2 blocker and multivitamins.
Several laboratory tests were conducted on the first day of admission. The results were significant for erythrocyte sedimentation rate (ESR) of 80 mm in 1st hour, hemoglobin 8.20 g/dL, white blood cell 35.93×109/L, neutrophil 33%, lymphocyte 61%, platelets 75.00×109/L, C-reactive protein (CRP) 101.5 mg/L, random blood sugar 8.3 mmol/L, blood urea 73.2 mg/dL, serum creatinine 1.19 mg/dL, serum albumin 34.9 gm/L, lactate dehydrogenase 399 U/L, and troponin I 860.1 ng/L. The electrocardiogram report showed transient ST elevation with T wave inversion in the lead III (v1 and aVL) and ST depression in leads I and II (v4, v5, v6, and aVL) ().
On the second day, arterial blood gas (ABG) and thyroid-stimulating hormone (TSH) tests were performed, and the results were ABG (PH, 7.22; PCO2 [partial pressure of carbon dioxide], 64.3 mm Hg; PO2 [partial pressure of oxygen], 122 mm Hg) and TSH 0.34 µIU/mL. A non-contrast computed tomography scan of the brain revealed mild cerebello-cerebral atrophy of the brain (). Lipase 332.9 U/L, calcium 7.62 mg/dL, D-dimer 8,782 ng/mL, and prothrombin time 14.90 seconds were found on the third day of hospital admission.
However, after being admitted into ICU, the consciousness level improved almost 24 hours later, and the fever subsided 36 hours later. Then, another 30 hours later, the doctor shifted the patient to the critical care unit (CCU) due to cardiac abnormalities. In the CCU, patient was found to have upper abdominal tenderness.
Noticeably, on the 5th day of admission, the patient’s high-sensitivity troponin I was reduced to 144.6 ng/L along with his D-dimer (7,989 ng/mL). The Doppler echocardiogram report showed mild tricuspid regurgitation with mild pulmonary hypertension, impaired diastolic function with suitable left ventricular systolic function (left ventricular ejection fraction: 61% at rest). All the above investigations indicated that the patient was diagnosed with acute encephalopathy, NSTEMI, and acute pancreatitis (AP). During the hospital stay, he was treated conservatively with injection methylprednisolone, injection enoxaparin, intravenous (IV) antibiotic, and other supportive treatment. Finally, he was discharged after satisfactory improvement on the 10th day of hospital admission. On discharge, his vitals were pulse 78 beat/min, blood pressure 110/70 mm Hg, and SPO2 (blood oxygen saturation) 95% with 4 L of oxygen.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [106.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 106.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2823,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7403899-1,Extracted,"This is the case of a 57-year-old Colombian obese woman who was admitted to the emergency department complaining of abdominal pain, urinary symptoms, and fever. Her medical history was positive for systemic arterial hypertension, type 2 diabetes mellitus, and nephrolithiasis. Ten days before the symptoms' onset, she underwent a dental procedure for tooth decay. In the beginning, she was treated in another facility for ketoacidosis, renal failure, and bacterial urinary tract infection, developing pneumonia as well. She required renal replacement therapy and received a course of antibiotics including aminopenicillins, carbapenems, and glycopeptides.
During hospitalization, the patient suddenly presented right calf pain; a duplex ultrasound was requested evidencing deep venous thrombosis of soleal and peroneal veins. She complained as well of dyspnea, chest pain, and palpitations, raising the suspicion of pulmonary embolism (Wells' criteria: 4.5 points). Thoracic CT angiography showed thrombosis of the pulmonary trunk and both main branches, and the initial transthoracic echocardiography (4 days after admission) reported left ventricle diastolic dysfunction with impaired relaxation, trivial mitral regurgitation, mild right ventricle dilation, mild tricuspid regurgitation, and an intermediate probability of pulmonary hypertension (PSAP 40 mmHg) with no other findings. Systemic thrombolysis with streptokinase was the chosen treatment for the high-risk pulmonary embolism; subsequently, she was started on enoxaparin with bridge therapy to warfarin.
After thrombolysis, the patient remained febrile with chest discomfort despite antibiotic treatment suggesting dialysis catheter-related infection or bacterial endocarditis. A transesophageal echocardiogram was carried out, revealing a mitral valve mass considered as a bacterial vegetation, and therefore, she continued receiving vancomycin. For exploring therapeutic alternatives, she was transferred to our hospital and stayed in the intensive care unit for one month. Her vital signs were normal (36.8°C, 95 beats per min, 20 breaths per min, 132/55 mmHg, SpO2 94% on room air), but she was pale and cardiopulmonary auscultation was positive for S3 sound. No heart murmurs, abnormal breath sounds, or jugular ingurgitation was detected.
Laboratory analysis demonstrated leukocytosis (13.010 cells/μL), moderate anemia (7.4 g/dL), mild thrombocytopenia (146.000/μL), and increased C-reactive protein levels (17 mg/L, normal concentrations up to 5 mg/L). Moreover, renal function was severely compromised (creatinine 5.3 mg/dL and blood uremic nitrogen 42 mg/dL) and arterial blood gases showed metabolic acidosis (pH of 7.37, HCO3 13.9 mmol/L, PCO2 24 mmHg, SaO2 87%, and base excess -10.6). Urine cultures were positive for IRT-resistant Escherichia coli and azole-sensitive Candida albicans, while no germs could be isolated on blood cultures. Consequently, fluconazole was added to the antibiotic regimen.
Transesophageal echocardiogram (16 days after admission) demonstrated preserved left ventricular dimensions and ejection fraction. Mitral valve exhibited a rounded image of 10 × 10 mm with hyperrefringent edges and hypoechogenic content within the anterior ring, corresponding to A1 and A2 segments (). This lesion did not compromise the valve function nor obstructed the left ventricle outflow tract. The rest of the valves, cavities, and vessels were normal, except for a small left pleural effusion. The density of the mass and the absence of any other imaging features compatible with endocarditis (i.e., highly and asynchronously mobile pedicled mass) supported the diagnosis of a blood cyst. Contrast echocardiogram with sulfur hexafluoride microbubbles was not available in our institution.
Aside from the mass, she did not fulfill any other Duke's criteria and blood cultures were negative. Besides, there was no valvular regurgitation that supported the diagnosis of a leaflet aneurysm and the cyst remained the same size in transesophageal echocardiogram despite anticoagulation, being less likely that it corresponded to a thrombus adhered to the valve in a patient with no predisposing factors. Researchers have highlighted elsewhere that echogenicity is the key to differentiate other entities (infections, neoplasms, and thrombi) from blood cysts as the last exhibit a homogenous hypoechogenic content []. Unfortunately, we could not obtain the initial transthoracic echocardiogram for reviewing and confirming that the mass was not present at that point.
After 10 days of antifungals, the inflammatory response completely resolved and the antibiotic course was not extended as bacterial endocarditis was disregarded. The patient did not present any bleeding or embolic events and was discharged without any disability. Unfortunately, she did not attend to the Outpatient Clinic but, in a telephone follow-up, no recurrence of cardiovascular symptoms was reported.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [95.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",7,7,7,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 95.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 3 + 1.5 =  4.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 6.0 + 1 = 7.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 7.0.
The patient's Well's score for pulmonary embolism is 7.0."
2824,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6919399-1,Extracted,"A 28-year-old woman presented to our center complaining of a sudden onset of right-side lower abdominal pain with slight vaginal bleeding. She had undergone a thawed ET with two embryos 23 days before, following IVF. She had a history of right salpingectomy for an ectopic pregnancy during ovulatory cycle downregulation for IVF–ET 1 year previously. On physical examination, she was hemodynamically stable with a blood pressure of 97/65 mm Hg and heart rate of 80 bpm. A physical examination demonstrated a distended abdomen with diffuse abdominal pain that was maximal in the right iliac fossa with rebound pain and signs of peritonitis. Transvaginal sonography demonstrated one intrauterine gestational sac with an uneven mass measuring about 9.2 × 5.0 cm at the right adnexa (Fig. ). The intrauterine gestational sac measured 1.0 × 1.1 × 0.8 cm with a yolk sac about 0.3 cm in diameter (Fig. ). Ultrasonographic evidence of hemoperitoneum was present, with a large amount of free fluid within the pouch of Douglas (Fig. ). The patient underwent emergency laparoscopy that confirmed a ruptured right interstitial pregnancy and hemoperitoneum (Fig. ). This ectopic pregnancy tissue was removed and effective hemostasis achieved. The amount of hemoperitoneum was approximately 1.0 L, which was evacuated followed by peritoneal lavage. Histopathology of the tissues confirmed a tubal stump pregnancy. Medical treatment of progesterone and estrogen was used to prevent abortion of the intrauterine pregnancy. However, on day 10 after the operation, the patient had an incomplete abortion and underwent uterine curettage.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2825,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6813375-1,Extracted,"A 51-year-old male patient was admitted to the emergency department with massive hematochezia, hypotension, and abdominal pain. The patient reported intermittent hematochezia for 3 days. His medical history was remarkable for hypertension only. There was no history of radiation therapy or recent abdominal surgery.
On initial clinical observation, the patient was hemodynamically unstable. The systolic blood pressure was 90 mmHg, heart rate was 110/min, and temperature was 36.8 °C. His abdomen was soft and flat, but there was tenderness in the left upper quadrant. Because initial hemoglobin value in the emergency room was 7.3 g/dl (normal range, 13.5–17), immediate transfusion and emergency endoscopy were performed to identify bleeding sites and perform hemostasis. An esophagogastroduodenoscopy showed no upper gastrointestinal pathology to account for bleeding, and colonoscopy revealed hematic residues but no detected lesion (Fig. ). As soon as endoscopy was completed, abdominal pelvic computed tomography (AP-CT) scan was performed with IV contrast. AP-CT scan showed that the distal jejunum and its mesentery were tortuous and the end of the mesentery was ring-shaped suggesting an intra-abdominal intussusception (Fig. ).
Because of unresponsive transfusion for low blood pressure and continuous hematochezia, an emergency laparotomy was performed. Intraoperative laparoscopic findings showed typical intussusception in which one small bowel infiltrated the other small bowel (Fig. ).
Gross and histopathologic examination after resection confirmed GIST to be the leading point causative of the intussusception. Grossly, the mass was within the small bowel wall, covered with epithelial mucosa, and measuring 3.7 × 2.5 × 2.5 cm. A centrally located and depressed ulcerative lesion was identified overlying the tumor (Fig. ). On cut section, a relatively well-demarcated, firm and fibrotic, and light gray, lobulated mass was identified. The mass involved the entire small bowel wall, extending from the mucosa to the subserosa without penetrating the serosal surface. Overall, monotonous and multifocal hemorrhagic foci were identified, with no dominant focus of bleeding (Fig. ).
On light microscopic examination, hypercellular and hypocellular areas were identified with mostly hypercellular component showing nodular appearance under low magnification. Under high magnification, spindle cells showed elongated nuclei with vesicular chromatin and inconspicuous nucleoli forming short fascicles (Fig. ). The ulcerative area showed neutrophilic inflammatory exudate and extravasated erythrocytes, confirming heavy bleeding within the ulcerative focus.
Immunohistochemically, the tumor was strongly positive for c-kit (CD117), showing diffuse and cytoplasmic reactivity (Fig. ). DOG1 (also known as ANO1, anoctamin 1) stain was also positive in our case, which is sensitive and relatively specific for GIST, confirming the diagnosis.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2826,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6060943-1,Extracted,"A 65-year-old African-American female with medical history of hypertension, type 2 diabetes mellitus, rheumatoid arthritis, and a 45-pack-year smoking history presented to the ED complaining of sudden onset, pressure-like non-radiating chest pain that occurred at rest, it was associated with diaphoresis; and there were no relieving or provocative factors. The pain persisted till she arrived to ED. On physical examination, she was alert, oriented, and in acute distress. Her vital signs were temperature 36.3°C; pulse 37 bpm; blood pressure 81/54 mmHg (mean arterial pressure 63); respiratory rate 16 bpm; and O2% of 95% on 4 L/min oxygen through nasal cannula. Her initial electrocardiogram showed new-onset atrial flutter with ST-segment depression in lead I and V2–V4 []. This was suspicious for a posterior infarct.
She was taken to the cardiac catheterization laboratory urgently. Selective coronary angiography revealed patent left main, left anterior descending, and right coronary artery, but total occlusion of the left circumflex artery at its origin due to thrombus. An aspiration thrombectomy of the left circumflex coronary artery was performed using a 6-French JL4 guiding catheter, a 0.014 mm × 190 cm Cougar guide-wire, and a Fetch catheter. Images following the intervention revealed no ulcerated lesions or residual disease, with thrombolysis in myocardial infarction (TIMI) 3 flow was present immediately on withdrawing the catheter [].
The patient became chest-pain free, and her blood pressure normalized; however, she remained in atrial flutter during her hospital stay. Anticoagulation was initiated following a negative hypercoagulable workup. A transesophageal echocardiogram (TEE) was performed (to rule out atrial thrombus and other etiologies of coronary embolism) followed by electric cardioversion which failed to convert her to normal sinus rhythm. She was discharged home with anticoagulation therapy and planned for elective outpatient atrial flutter ablation procedure.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [37.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Surgery in the previous 4 weeks': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 37.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 0.
The patient's Well's score for pulmonary embolism is 0."
2827,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6833381-1,Extracted,"A 56-year-old man with a history of smoking was admitted to the emergency department
for treatment of a femoral fracture. Falling from a height had led to a slight
disturbance of consciousness. Brain computed tomography (CT) revealed a laceration
in the right temporal lobe of the brain and subarachnoid bleeding. Neurosurgical
consultation showed no abnormalities. Chest CT showed changes indicating hypostatic
pneumonia in both lungs. The patient had no history of hypertension, diabetes
mellitus, or heart disease. The results of laboratory tests were within normal
limits. The patient did not undergo routine anticoagulant therapy before surgery
because of the subarachnoid haemorrhage.
On the third day of hospitalisation, the patient was scheduled to undergo surgery for
internal fixation of the femoral fracture. In the operating room, peripheral
intravenous access was established in the right upper limb, and standard monitors
were placed. The Allen test was performed, and the left radial artery was then
cannulated for continuous blood pressure monitoring. The monitors showed a blood
pressure of 124/76 mmHg, heart rate of 108 bpm, and oxygen saturation of 95%.
Considering the patient’s anxiety, the anaesthesiologist administered 70 µg of
dexmedetomidine intravenously over 10 minutes. For anaesthetic induction, the
patient received midazolam (4 mg), sufentanil (50 µg), etomidate (15 mg), and
cisatracurium (12 mg). After intubation, the anaesthesiologist auscultated the chest
and confirmed good bilateral air entry. Anaesthesia was maintained with remifentanil
(0.1–0.2 µg/kg/minute), sevoflurane (2%) in an air–oxygen mixture, and
dexmedetomidine (0.4 µg/kg/h). Cisatracurium (5 mg) was administered at 1-hour
intervals to maintain muscle relaxation. Considering the intraoperative application
of vasoactive drugs, the anaesthesiologist inserted the central venous line through
the right internal jugular vein.
Approximately 1 hour after the surgery was started, the anaesthesiologist noticed
that the patient’s end-tidal carbon dioxide (ETCO2) had decreased from 35
to 15 mmHg within a few seconds. The oxygen saturation decreased to 80%, and the
blood pressure dropped to 80/50 mmHg. However, no significant change in the airway
pressure was noted. The anaesthesiologist immediately adjusted the mechanical
ventilation to manual ventilation and auscultated the bilateral breath sounds. The
heart rate gradually increased to 140 bpm, and an electrocardiogram showed atrial
fibrillation. The central venous pressure increased to 28 cmH2O.
Intravenous administration of ephedrine (6 mg) was repeated, and 100% oxygen was
administered via the endotracheal tube; this was followed by administration of
epinephrine (10 µg). However, these protocols did not improve the patient’s
haemodynamics. Instant arterial blood gas analysis (ABGA) showed hypercapnia (). Emergency TEE
demonstrated mobile echogenic densities in the right pulmonary artery and
enlargement of the right atrium, and these findings were suggestive of APE (see
Supplemental Video 1). Multidisciplinary consultation started immediately. The
following treatment was administered: epinephrine (0.05 µg/kg/minute) and
norepinephrine (0.03 µg/kg/minute), which were administered continuously;
methylprednisolone (200 mg); and 5% sodium bicarbonate liquid (100 mL).
The patient was transferred to the intensive care unit, and the operation was
postponed. A follow-up lower extremity Doppler study indicated intraluminal
obstructions in the left superficial femoral vein and popliteal vein.
Echocardiography suggested slight enlargement of the right heart, a severe increase
in the pulmonary artery pressure, and moderate mitral regurgitation. The D-dimer
level was high at 36.25 µg/mL (reference range, 0.0–0.3 µg/mL). These results
further supported the diagnosis of APE noted on TEE. Considering his history of
subarachnoid haemorrhage, the patient could not undergo anticoagulation with heparin
or thrombolysis therapy for APE. We recommended placement of an inferior vena cava
(IVC) filter to prevent APE recurrence after a multidisciplinary risk–benefit
discussion when the patient’s haemodynamic parameters became temporarily stable.
Unfortunately, the patient and his family members refused the IVC implantation, and
the patient was discharged.
The patient provided written informed consent for publication of this case report.
Approval by an ethics committee was unnecessary because of the nature of this study
(case report).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [140.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",7.5,7.5,7.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 140.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 =  6.0.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 6.0 + 1.5 = 7.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 7.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 7.5.
The patient's Well's score for pulmonary embolism is 7.5."
2828,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3424648-1,Extracted,"A 98-year-old woman suffered a left-sided femoral neck fracture caused by a fall and presented for a hip hemiarthroplasty. Her medical record shows paroxysmal atrial fibrillation, hypertension, recurrent complaints attributed to cardiac decompensation, a cardiac murmur and hypoxemic chronic obstructive pulmonary disease (COPD), global initiative for chronic obstructive lung disease (GOLD) classification stage II (moderate severity), for which she received supplemental oxygen therapy at home. Her symptoms of dyspnea have remained constant over the last few weeks. She had contracted pulmonary tuberculosis in the past and had recently been treated with an antibiotic and prednisolone because of recurrent pneumonia and COPD exacerbation. Over the last few years the number of falls she sustained had increased.
Additional medication consisted of a loop diuretic, calcium channel inhibitor, nebulized combination of a β2-agonist and an anticholinergic agent, and acetaminophen. She took no antiplatelet drugs or vitamin-K antagonists.
On physical examination she had a respiratory frequency of 17 per minute, peripheral oxygen saturation (SpO2) 92% with nasal administration of O2 at two liters per minute. Blood pressure was 144/72 mmHg and heart rate 81 beats per minute (bpm). A cardiac murmur was heard over the chest. Electrocardiography showed a normal sinus rhythm.
The transthoracic echocardiogram revealed a moderate aortic valve stenosis and a hypertrophied left ventricle with a good systolic function.
Because of the patients advanced age, aortic valve stenosis and the kind of surgery required, we formulated a plan to pursue a hemodynamic situation within normal limits for this patient with minimal impact on pulmonary and cerebral function. We decided to provide adequate regional anesthesia by CSA.
We undertook this procedure starting an hour before surgery at the postanesthesia care unit (PACU) with monitoring of pulse, ECG, and blood pressure. In a complete sterile manner with the patient in a sitting position we introduced an 18-gauge Tuohy needle (Perican; B. Braun Melsungen AG, Melsungen, Germany) in the midline at the level of the spinous process of the third and fourth lumbar vertebrae. After we punctured the duramater and observed a free flow of spinous fluid, we introduced a 20 gauge, 104 cm catheter (Perifix Softtip; B.Braun), and five centimeters intrathecally. This catheter was connected to an antimicrobial filter (Perifix; B.Braun), flushed with normal saline (NaCl 0.9%), and fixed to the patients back with adhesive film and tape. This procedure using these materials describes the standard operating procedure to introduce an intrathecal catheter for CSA in our institution.
Approximately 45 minutes before surgery we administered 0.5 mL of a 0.5% isobaric bupivacaine solution (2.5 mg; AstraZeneca, London, United Kingdom). Fifteen minutes later we administered another 0.25 mL (1.25 mg) of this solution. To assess the extent of sensory blockade a refrigerated metal “hammer” was used. The patient was able to adequately report cold sensation while touching the skin of the thorax, abdomen, and upper legs on both sides of the body, moving in a craniocaudal direction. Five minutes after having administered the second dose of the local anesthetic agent we tested sensory blockade and determined it to be symmetrically at the level of the eleventh thoracic dermatome and below. After this we introduced a urinary catheter and placed the patient in the right dependent position and surgery commenced.
An hour after the second dose of bupivacaine we administered a third dose of 0.5 mL (2.5 mg) and another hour later a fourth dose of 0.5 mL. Upon completion of the surgery and 50 minutes after the last dose of bupivacaine, we removed the spinal catheter. Immediately prior to removing the catheter we injected 10 mL of normal saline to reduce the risk of developing PDPH and the patient was transported to the PACU.
During surgery all monitored physiological variables stayed within normal values. We administered 500 mL of a colloidal solution and 250 mL of normal saline. The course of surgery was as planned. Blood loss was 500 milliliters.
Fifteen minutes after removal of the catheter her blood pressure decreased to a minimum of 75/35 mmHg with a heart rate of 80 bpm. After administration of up to a total of 350 μg of phenylephrine, her pulse slowed to 60 bpm and blood pressure improved. Examination revealed an unexpected symmetric sensory blockade at the third thoracic dermatome and below. She reported no pain and was unable to move her legs and feet.
Besides frequent hemodynamic monitoring, sensory blockade was monitored every 15 minutes. We considered requesting a magnetic resonance imaging scan to rule out an epidural hematoma being a deleterious side effect of introducing or removing neuraxial catheters. Fortunately 130 minutes after the first occurrence of high sensory blockade and hypotension, sensory blockade finally regressed to a level below the sixth thoracic dermatome. Thereafter motor and sensory blockade regressed swiftly.
Pain after regression of the blockade was successfully treated with fragmented doses of intravenous morphine.
The patient was discharged on the fifth day after surgery after an otherwise uneventful hospital stay. She never complained about headaches.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [81.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 81.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 =  1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2829,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4100447-3,Extracted,"A 38-year-old African American female went to a community hospital for difficulty in breathing. A week before, she had an acute onset of difficulty in breathing, which was associated with occasional lightheadedness. Later, she had difficulty with performing her activity of daily leaving due to the shortness of breath. The patient has history of iron deficiency anemia and depression. She was on birth control pills, which she had been taking for the past 18 years. She is neither smoker nor substance abuser. At the time of presentation, she denied chest pain, lightheadedness, diaphoresis, headache, or dizziness. The initial vitals were blood pressure of 129/49 mmHg, respiratory rate of 15 breaths per minute, pulse rate of 75 beats per minute, and oxygen saturation of 95% on room air. She was afebrile. The cardiopulmonary, neurologic, and musculoskeletal exam was unremarkable. The laboratory workup did not reveal any electrolytes abnormalities; however, her pro-BNP was 1193 pg/mL (normal: 50–92 pg/mL) and troponin was 0.02 ng/mL (normal: 0–0.10 ng/mL). An electrocardiogram showed normal sinus rhythm with T-wave inversions in inferior leads and V1-V3 without ST-segment changes. A CT-thorax showed large bilateral pulmonary emboli in the pulmonary arteries. At this time, the patient was transferred to our hospital for further management. The echocardiogram revealed preserved left ventricular ejection fraction, hypokinetic RV with RV/LV >1 and severe pulmonary hypertension (right ventricular systolic pressure of 73 mmHg) (). A lower extremity ultrasound with Doppler showed acute occlusive and nonocclusive deep vein thrombosis in left popliteal and right common femoral vein, respectively.
These findings were suggestive of submassive PE, which was treated with ultrasound accelerated thrombolysis. The right heart catheterization showed systolic pulmonary artery pressure of 51 mmHg. The catheters were placed in both pulmonary arteries and 13 mg of alteplase, along with heparin, was delivered over 16 hours with heparin drip. The patient tolerated the thrombolysis procedure without complication. The patient was discharged on oral rivaroxaban after the resolution of presenting symptoms. Three days later, the echocardiogram showed left ventricular ejection fraction of 65%, without the evidence of right ventricular strain (RV/LV < 1) or elevated right ventricle systolic pressure (). The RVSP was 35 mmHg. Refer to for data summary.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [75.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 75.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3 + 1.5 = 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2830,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8079180-1,Extracted,"A 66-year-old Japanese woman visited a local hospital with the chief complaint of malaise for two days. She presented with subcutaneous hemorrhage in both forearms; therefore, she was referred to the hematology department of our hospital. She had no remarkable medical history except pneumonia. Physical examination revealed a body temperature of 37.1°C, blood pressure of 136/86 mmHg, pulse rate of 85 beats per minute, and oxygen saturation of 99% in ambient air. She had no palpable lymphadenopathy, and chest auscultation revealed no rales or murmur. Her abdomen was soft, without palpable hepatosplenomegaly. Laboratory test results were as follows: hyperleukocytosis (white blood cell count: 97,800 cells/µL), differential count (blasts, 51.0%; neutrophils, 31.5%; monocytes, 2.5%; metamyelocytes, 5.5%; lymphocytes, 5.0%; basophils, 4.5%), anemia (hemoglobin level: 7.6 g/dL), thrombocytopenia (platelet count: 6.5 × 104/μL), and hyperfibrinolysis (elevated d-dimer level: 12.4 µg/mL; fibrin/fibrinogen degradation products: 26.9 µg/mL; elevated lactate dehydrogenase level, 1,398 IU/L). According to the bone marrow examination, blasts accounted for 30.4% of cells and presented with delicate nuclear folds and a high nucleus-to-cytoplasm ratio. The size of the blasts ranged from medium to large, and some presented with cytoplasmic nucleoli and granules. Most blasts were myeloperoxidase negative, although some were positive (). We were unable to morphologically classify blasts using the FAB classification. Flow cytometry CD45 gating revealed that the blasts expressed CD34, CD13, CD33, and CD117. G-banding of tumor cells and T cells in peripheral blood samples revealed the t(7;7)(p15;p22) translocation [20/20] () and 46, XX [20/20], respectively; thus, the novel translocation was observed. She was diagnosed with AML and the t(7;7)(p15;p22) translocation. She was first treated with cytoreductive therapy with hydroxyurea. However, hydroxyurea failed to improve hyperleukocytosis, and on hospital day 25, she presented with subcutaneous bleeding around both eyelids secondary to severe disseminated intravascular coagulation (DIC). On day 26, she developed sudden dyspnea and hypoxia. Chest computed tomography revealed bilateral shadows in the lung, which was highly suggestive of leukostasis of the lungs. She required a respirator. On day 27, chemotherapy comprising idarubicin and cytarabine was started, but on the following day, she developed oliguria, which was suggestive of renal failure due to tumor lysis syndrome (TLS) and sepsis. She required hemodialysis. On day 37, hematological remission was confirmed by bone marrow examination. On day 48 of her hospital stay, she died of multiple organ failure secondary to severe infection and gastrointestinal bleeding.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Heart Rate or Pulse': [85.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Surgery in the previous 4 weeks': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 85.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2831,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8189296-1,Extracted,"A 54-year-old male was admitted from pre-admission clinic for investigation of new-onset hypoxia. He was planned to have an endoscopy for investigation of weight loss, abdominal pain, and diarrhoea. He had additionally reported a history of intermittent palpitations and exertional dyspnoea.
Background medical history included hypertension, obesity, type 2 diabetes mellitus, gastro-oesophageal reflux disease, and previous traumatic splenectomy. He was a lifelong non-smoker.
Physical examination revealed oxygen saturation of 81% on room air improving to 87% on 4 L via nasal cannula. There was no orthodeoxia. Lung auscultation was unremarkable. There was a Grade 3/6 pansystolic murmur at the left sternal edge associated with jugular venous pressure elevated to the angle of the jaw, with prominent ‘v’ waves and no peripheral oedema.
Resting electrocardiogram showed sinus rhythm, rate of 71 beats per minute, normal axis, and no ischaemic changes. Chest X-ray showed clear lung fields. An arterial blood gas on room air showed hypoxia with a mild respiratory alkalosis and elevated alveolar-arterial (A-a) oxygen gradient (). Haemoglobin and renal function were normal. Computed tomography (CT) pulmonary angiogram on admission revealed normal lung parenchyma and a left posterior basal segmental pulmonary embolism without evidence of right heart strain, the size of which was thought to inadequately account for the hypoxia. Pulmonary function testing showed a mild restrictive pattern with FEV1 2.44 L (70% predicted), FVC 3.22 L (73% predicted), FEV1/FVC 75.90% (99% predicted), and carbon monoxide transfer coefficient 4.38 mL/(min*mmHg*L) (103% predicted), although there was variable performance in testing.
Transthoracic echocardiogram (TTE) showed the normal left ventricular size and systolic function. There was mild bi-atrial dilatation along with mild right ventricular dilatation (44 mm basal diameter) with hyperdynamic systolic function. Tricuspid annular plane systolic excursion was 30 mm. Tricuspid valve leaflets were noted to be thickened, immobile and retracted, not coapting in systole with free-flowing tricuspid regurgitation, which in the setting of a morphologically normal mitral valve was pathognomonic for carcinoid heart disease (, Video 1 and ). The pulmonary valve had a normal appearance and mild regurgitation. Twenty-four hour urinary 5-hydroxyindoleacetic acid was elevated at 260 µmol/24 h (normal range 0–30), whilst chromogranin A was 156 ng/mL (normal range 0–104).
A TTE bubble study (Video 2) was performed due to radiographically normal lungs, the small size of the pulmonary embolism, and patient reluctance for a transoesophageal echocardiogram (TOE), which were strongly positive within three cardiac cycles suggesting shunt at the cardiac level. However, the passage of bubbles appeared to originate from the pulmonary veins which was suspicious for pulmonary shunting.
Dedicated digital subtraction pulmonary angiography () was therefore performed which excluded pulmonary arteriovenous fistula and large pulmonary embolism but revealed early filling of the left atrium confirming an intracardiac shunt. The patient eventually agreed to a TOE (, ) with bubble study (, Video 3) which confirmed a long tunnel patent foramen ovale with an aneurysmal interatrial septum. There was evidence of the significant right to left shunting on colour Doppler at rest in the supine position.
68-Gallium DOTATATE PET () and CT imaging identified a 27 mm × 36 mm × 57 mm avid retroperitoneal para-aortic lymph node and avid right testicular mass. Percutaneous biopsy of the retroperitoneal mass revealed a well-differentiated neuroendocrine (carcinoid) tumour WHO Grade 1.
Prior to excision biopsy of the right testicular tumour, consideration of surgical tricuspid valve replacement combined with PFO closure was declined by the patient. Given marked resting hypoxia, need for surgery and undetermined diagnosis and prognosis, percutaneous closure of the patent foramen ovale was considered appropriate.
Pre-procedural right heart catheterization demonstrated a right to a left atrial pressure gradient (). The PFO was successfully closed under fluoroscopic guidance with a 30 mm Amplatzer PFO Occluder device (). Pre-procedural arterial oxygen saturation of 82% improved to 88% immediately post-procedure. There were no procedural complications.
The patient underwent an inpatient orchidectomy with histopathology of the right testicle confirming a primary well-differentiated neuroendocrine (carcinoid) tumour. The patient was commenced on somatostatin analogue therapy. He was discharged a week following PFO closure with arterial oxygen saturation of 92% on room air. He has had durable relief of his symptoms. Repeat TTE showed no residual flow across the interatrial septum. The patient continues to decline consideration of tricuspid valve surgery.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [71.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 71.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2832,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6919952-1,Extracted,"A 36-year-old Caucasian female with no significant past medical history presented to the Emergency Department (ED) with a several month history of shortness of breath, pleuritic chest pain, and nonproductive cough. Two weeks before this admission, she presented to the hospital after a mass in her left breast had eroded and broke through her skin. A core biopsy at that time had confirmed an estrogen-receptor-positive (ER +), progesterone receptor-positive (PR +), and human epidermal growth factor receptor-2 positive (HER2 +) Grade 4 left invasive ductal cell carcinoma of the left breast with perineural and lymphatic invasion, for which she had not yet initiated treatment. The patient presented to the ED due to worsening exertional shortness of breath and severe, non-radiating, pleuritic chest pain.
There was no surgical history and family history was significant for a history of prostate cancer in her uncle. Social history was negative for tobacco use, ethanol use, or illicit drug use.
On exam, she was lethargic, tired, tachycardic to the 140s, tachypneic, febrile at 101° F, and hypoxic to 87% on room air, requiring oxygen via nasal cannula. The cardiovascular, pulmonary, and neurological examinations were grossly normal. The entire left breast was firm and had extensive skin thickening with a reddish discoloration. Overlying erythema, necrotic tissue, and foul-smelling purulent discharge were present (Figure ). There was significant left axillary lymphadenopathy.
Significant laboratory values drawn on the day of admission are listed below in Table .
An electrocardiogram was nonischemic in nature and troponins were nondetectable. A Doppler ultrasound of the bilateral lower extremities was negative for deep venous thrombosis (DVT).
A computed tomogram (CT) scan of the chest with contrast did not reveal a pulmonary embolism but did reveal bilateral pulmonary nodules, basal consolidation, and bilateral axillary, left supraclavicular, and hilar adenopathy. There was abnormal skin thickening of the left breast, along with a 4.2 x 1.9 cm mass-like thickening involving the left pectoralis muscle (Figure ). A CT of the abdomen and pelvis with contrast showed diffuse hepatic masses concerning for metastases. The patient was treated with antibiotics for possible pneumonia.
Mammography confirmed a poorly defined a 6 - 7 cm mass extending into the left breast with a Breast Imaging-Reporting and Data System (BI-RADS®) assessment category of 5. F-18 fluorodeoxyglucose positron emission tomography and computerized tomography (FDG PET/CT) scan revealed an abnormal uptake in the T10 vertebra, along with diffusely intense uptake in the liver, left pectoralis minor muscle, left supraclavicular, bilateral hilar, and axillary and retroperitoneal lymph nodes, all concerning for metastasis (Figure ).
At this time, she was found to be in tumor lysis with a lactate dehydrogenase (LDH) level of 937 U/L, uric acid 13.4 mg/dL, potassium 6.5 mEq/L, phosphorus 4.7 mg/dL, and creatinine 1.4 mg/dL. An ultrasound of the kidneys was negative for obstructive uropathy. Aggressive supportive measurements with high-flow intravenous fluids and rasburicase were initiated. With the eventual resolution of her pneumonia and improvement of renal function, allopurinol was initiated for prophylaxis. With clinical and laboratory improvement, one dose of chemotherapy, including an HER-2 targeting agent, was administered before she was discharged for further outpatient management.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [140.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 140.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2833,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4442258-1,Extracted,"A 60-year-old Caucasian man presented with 2 weeks of back pain with drenching night sweats 20 days after undergoing laparotomic sigmoidectomy for severe diverticulitis. One week after his discharge, the patient developed right sided lower back pain and severe drenching night sweats that prompted him to change his clothing and bed sheets multiple times every night. The patient described the pain as a 7/10 throbbing, sharp pleuritic pain that was better in supine position and was initially responsive to nonsteroid anti-inflammatory drugs. The patient experienced mild shortness of breath on exertion. He denied any nausea, vomiting, chest pain, or chills or fevers. He had a 12-pound weight loss starting 3 weeks prior to presentation. His medications were silodosin, atorvastatin, diazepam, docusate, and as needed acetaminophen, naproxen, and oxycodone. Patient never smoked and lived an active life prior to his surgery.
On physical examination he was afebrile, resting in bed comfortably. Heart rate was 100 beats/minute, blood pressure was 144/91 mmHg, respiratory rate was 20 breaths/minute, and oxygen saturation level was 97% on room air. He had no palpable lymph nodes and had bibasilar dullness to percussion with decreased breath sounds. Auscultation of the heart revealed tachycardia, but regular and normal heart sounds. The right lower back was tender to palpation. The abdominal surgical scar was intact with no signs of inflammation.
The laboratory findings were hemoglobin level: 13.1 mmol/L; white blood cell count: 10.4 × 103/mL; platelet count: 354 × 103/mL; troponin: 0.01 ng/mL. Basic metabolic profile values were all within normal limits. Our initial differential diagnosis list included PE, pneumonia, pericarditis, and pneumothorax. As the patient presented with pleuritic back pain after recent surgical intervention, PE was very high on our differential diagnosis. Chest radiography revealed bilateral basilar opacities and no pneumothorax. CT imaging of the chest demonstrated PE involving the main pulmonary arteries (). Transthoracic echocardiogram showed no sign of pericardial effusion.
Therapy was initiated with subcutaneous enoxaparin injections. The back pain resolved after the first day, but night sweats continued. Further diagnostic workup showed elevated erythrocyte sedimentation rate (ESR): 53 mm/h, C-reactive protein (CRP): 19.34 mg/dL, normal thyroid-stimulating hormone, and normal procalcitonin. CT of abdomen and pelvis was performed to rule out abdominal abscess and showed postsigmoidectomy state with intact anastomosis. MRI of the spine revealed no epidural mass or collection. Based on clinical guidelines the patient was discharged home on 3 months of rivaroxaban treatment []. Patient's night sweats completely resolved after discharge, verified by a 3-month follow-up visit and by a 9-month follow-up call.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [100.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 100.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 =  1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2834,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3743340-1,Extracted,"A 57-year-old woman was admitted to the emergency department for diffuse maculopapular rashes on the whole body and anaphylactic shock. She had been complaining of sudden- onset of abdominal pain, dyspnea, pruritus, and urticaria. On physical examination, it revealed tenderness, guarding, and rigidity all over the abdomen. Her blood pressure was 90/60 mmHg, heart rate 118/min, and temperature 37.0°C. Blood test analysis was normal and subsequent leucocytosis with eosinophil dominance. Hydration, hydrocortisone, and antihistamines were used to treat the possible anaphylactic reaction. The patient received oxygen as supportive treatment. The patient recovered after emergency medications and then abdominal computed tomography (CT) revealed a splenic cystic lesion measuring about 9’ 6 cm2 in diameters and containing floating membranes. The anterior wall of the cyst showed discontinuity at a point []. Diffuse pelvic and minimal perisplenic fluid were detected. Our fundamental concerns were to preserve the spleen. Then, the patient underwent a laparoscopic partial cystectomy and omentoplasty, since the spread of the disease into the peritoneal cavity of lesions was strong contraindications for a radical surgical approach. At the time of laparotomy, the cyst's outer membrane was seen ruptured []. The postoperative course was uneventful, and the patient was discharged 10 days after the surgery. We applied albendazole, 10 mg/kg/day for 6 months, and the patient was followed up with CT that displayed no recurrence of the disease during a follow-up of 6 months []. She is still symptom-free in the 12-month follow-up.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [118.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 118.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2835,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4908703-1,Extracted,"A 78-year-old female with a past medical history significant for breast cancer and moderate COPD presented to Emergency Department with syncope. Nine months prior to admission, she underwent left total mastectomy for invasive ductal carcinoma and was started on Tamoxifen 20 mg daily. Home medications included GB 50 mcg once daily, Salbutamol, calcium and a multi-vitamin. GB was started 3 months prior to her presentation for syncope.
The day prior to admission, she received an IV vitamin infusion consisting of a mixture of thiamine, folic acid, multivitamin and magnesium sulfate at a naturopath clinic. Shortly after completion of the IV infusion, she developed emesis and took 2 tablets of dimenhydrinate. The following day, she reported dizziness as she walked across the kitchen and passed out after sitting in a chair. The patient reported no palpitations, chest discomfort, nausea, warm sensation or diaphoresis prior to the syncope event. She was not witnessed to have any seizure like activity and when she regained consciousness, reported immediate awareness of surroundings with no neurological deficits, no tongue biting, bowel or urinary incontinence. There was no previous history of syncope and no family history of sudden cardiac death. Her initial blood pressure in the ambulance was 70/50 mm Hg. Hemodynamics normalized after administration of intravenous fluid and her symptoms resolved. Oxygen saturation was above 97 % and telemetry revealed normal sinus rhythm with a heart rate of 77. Precordial examination was unremarkable with regular normal heart sounds and no murmurs. In the Emergency Department, blood tests including complete blood count (CBC), serum electrolytes (potassium, calcium, magnesium), glucose, creatinine and thyroid stimulating hormone were normal. Electrocardiogram (ECG) showed a corrected QT interval using Fridericia (QTcF) and Bazett’s formula (QTcB) of 603 and 631 ms respectively (Fig. ) and she was admitted to the cardiology service for further investigation of the etiology for her QT prolongation.
Prior to starting Tamoxifen her QTcF and QTcB were 439 and 440 ms respectively (Fig. ), however no ECG was obtained after initiation of Tamoxifen and prior to starting GB. Her last dose of Tamoxifen and GB were the day of admission with both medications discontinued at presentation.
An echocardiogram revealed that her left ventricular ejection fraction was >60 % with no valvular or regional wall motion abnormalities. Serial electrocardiograms demonstrated corrected QTcF and QTcB respectively of 603 and 631 ms day 0, 496 and 514 ms day 1, and 446 and 455 ms on day 2 and 442 and 460 ms on day 3 (Fig. ). There were no arrhythmias seen on telemetry. Syncope was felt to be secondary to orthostatic changes and she was discharged on day 3 after admission.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [77.0, 'beats per minute'], 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 77.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
2836,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7507911-1,Extracted,"A 44-year-old Arab female with no history of cardiovascular disease presented to the emergency department with acute onset of epigastric and retrosternal chest pain associated with vomiting. There were no other associated symptoms. Clinically, she was conscious, with blood pressure of 91/77 mmHg and pulse rate 110 beats/min. Cardiovascular examination revealed muffled heart sounds with no murmur. Her abdomen was soft with diffuse tenderness, and other systemic examinations were unremarkable. She had a past medical history of four cesarean sections, excision of fibroadenoma of the breast, right salpingectomy for ectopic pregnancy and tonsillectomy.
The 12 lead electrocardiographic (ECG) ruled out cardiac ischemia. High sensitive cardiac troponins were negative. Chest X-ray was remarkable for cardiomegaly. Transthoracic echocardiography (TTE) confirmed large pericardial effusion with echocardiographic signs of cardiac tamponade. She underwent successful pericardiocentesis under echocardiographic guidance and drained about 800 cc of serosanguinous fluid. She was investigated to identify the possible causes of the pericardial effusion, including malignancy, infectious, or connective tissue disease, but all were negative.
A repeat transthoracic echo showed normal study, and she was discharged. After 6 months, she presented with severe central and right-sided chest pain associated with shortness of breath (SOB), orthopnea and hemoptysis of acute onset. The 12 lead ECG ruled out cardiac ischemia. High sensitive cardiac troponins were negative. TTE showed large encysted pericardial effusion. The anterior pericardial space showed multiple masses []. Saline contrast study revealed filling of this space from the RA. The contrast persisted for some time after its clearance from the right heart cavity [].
The transesophageal echocardiography (TEE) confirmed the same encysted pericardial effusion. The space adjacent to the RA showed effusion with multiple masses. Color flow showed multiple bidirectional flow between the RA and this space through multiple tears []. Agitated contrast saline injection showed well-defined multiple communications with the RA confirming the diagnoses of RAPA, with masses inside RA [].
Computed tomography (CT) and magnetic resonance imaging of the chest confirmed the diagnosis of pseudoaneurysm of the RA that communicates freely with the RA. The pseudoaneurysm contained multiple filling defects, probably representing clots. There were bilateral pleural effusion and multiple peripheral lung lesions typical of pulmonary embolism. She was offered surgery but refused as she was seeking a second opinion.
Unfortunately, after a few days in the hospital, she developed severe central chest pain associated with SOB. An urgent CT of the chest showed the right hemothorax and expanding RAPA. She agreed to emergent operative treatment.
The operation was performed through median sternotomy and femorofemoral bypass. There were pericardial adhesions. The pseudoaneurysm was in the form of a thin membrane containing blood with several well-formed clots, and it was communicating with the RA through a 3 cm opening. The right atrial defect was directly sutured, and biopsies were taken from the atrial wall, the pericardium, and the pleura. She had an uneventful postoperative course and discharged home after 10 days. The right atrial biopsy showed EHE with atypical cells and mitotic figures. EHE is a rare vascular tumor, classified as an intermediate malignancy that sometimes metastasizes and may recur.[]
Further investigations showed liver and lung metastases, and she received multiple courses of chemotherapy and radiotherapy. One month later, she presented with nonspecific chest pain and SOB. TTE and contrast CT demonstrated the presence of pericardial hematoma with three points of communication between RA and the hematoma sac. The hematoma was extending over the right ventricular outflow tract (RVOT) with nonsignificant compression of the right ventricle.
She underwent re-exploration operation, and several points of communications were found between the RA and the hematoma from the suture line of the previous operation. Specimens were taken from multiple sites in the mediastinum, including the pericardium, and histopathology showed that all the specimens were involved by the same tumor with the same morphology EHE. However, the disease progressed rapidly, and she passed away after 9 months of the diagnosis.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",6.5,6.5,6.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3.0 + 1.5 = 4.5.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 4.5 + 1 = 5.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 5.5 + 1 =  6.5.
The patient's Well's score for pulmonary embolism is 6.5."
2837,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3493811-1,Extracted,"An 83-year-old woman presented with progressive exertional chest pain and dyspnea. She was an active smoker (1 pack per day during 50 years) with a past medical history of depression requiring pharmacotherapy. The patient's blood pressure was 145/48 mm Hg with a pulse rate of 62 beats per minute. Cardiac murmur was not auscultated on physical examination. Although her initial electrocardiography (ECG) showed sinus rhythm without ST segment changes, after 2 hours of observation, T-wave inversions on lead V2, V3 and V4 were recorded (). Troponin I level was not elevated throughout her admission. The patient was treated for an acute coronary syndrome and her symptoms were relieved with intravenous nitroglycerin. Coronary angiography demonstrated a marked capillary blush draining into the left ventricular (LV) cavity due to extensive multiple microfistulae arising from the left anterior descending artery (LAD), left circumflex artery and right coronary artery (RCA) producing a left ventriculography (). The left main coronary artery (LMCA) was severely dilated (up to 10 mm) and the LAD was diffusely calcified with a 40% narrowing at the proximal LAD. RCA was also markedly dilated with a discrete 30-40% luminal narrowing at the posterior descending artery and posterior lateral artery bifurcation. Echocardiography demonstrated concentric LV hypertrophy, normal LV chamber size and normal LV systolic function without the regional wall motion abnormality. She remained asymptomatic and was discharged on a beta-blocker and angiotensin converting enzyme (ACE) inhibitor. Two months later, the T-wave inversions at V2, V3 and V4 were normalized.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [62.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 62.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2838,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8613055-1,Extracted,"A 42-year-old male patient presented to the emergency department with severe retrosternal chest pain radiating to the left arm for two hours. The pain was associated with sweating and vomiting. Patient was a febrile with no cough, no dyspnea and no other cardiac symptoms. The patient is smoker (I pack/day for 20 years), no hypertension, or diabetes mellitus. He has a past history of right nephrectomy due to renal stones.
On examination the patient was conscious, oriented with heart rates of 80 beats/minute, respiratory rate of 17 cycle/minute, and blood pressure= 118/80 mmHg. Normal oxygen saturation (SpO2= 100%), normal jugular venous pressure and no carotid bruits. Chest: normal vesicular breathing. Heart: normal first and second sounds with no additional sounds. Abdomen: soft, no organomegaly, no bruit at renal artery site auscultation. Lower limbs were intact with normal pulse and no edema.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Surgery in the previous 4 weeks': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 0.
The patient's Well's score for pulmonary embolism is 0."
2839,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-2822321-1,Extracted,"A 53-yr-old man was hospitalized in April 2002 because of a sudden motor weakness in his left extremities, dysarthria, right eye visual disturbance, and headache. A diagnosis of nephrotic syndrome had been made elsewhere in 3 weeks before admission, based on clinical manifestation, blood, and urinary abnormalities and focal segmental glomerulosclerosis was confirmed by percutaneous renal biopsy. Also he had been diagnosed with alcohol-associated liver cirrhosis (Child-Pugh Classification A) from abdominal ultrasonography and healthy HBV carrier in 7 months before admission. After diagnosis of focal segmental glomerulosclerosis, he had been treated with diuretics, angiotensin converting enzyme (ACE) inhibitor, prednisolone 1 mg/kg/day, and lamivudine with a dosage of 100 mg/day for the prevention of flare up of viral hepatitis. He had no history of hypertension or diabetes. He had been a 30-pack year smoker and a heavy alcoholic, but quitted smoking and alcohol several months before. On admission, his general appearance revealed that he was acutely ill with bilateral pedal edema. His blood pressure was 120/80 mmHg, pulse rate 120/min, respiratory rate 24/min, and body temperature 37℃. Cardic examination showed normal findings. He had no evidence of systemic thromboembolism, deep vein thrombosis, or cervical bruit. Neurological examination revealed drowsy mentality with a left-side motor weakness, and decreased sensory perception on the left side. He was also exhibited dysarthria and right eye visual disturbance. However, the high cortical function was normal.
The initial MR and MR angiography of the brain showed a recent infarction in the right middle cerebral artery territory and the head of the caudate nucleus, no blood flow signal intensity in the right internal carotid artery (, ).
Laboratory data showed leukocytosis (2.49×103/µL) and hematocrit of 31.9% with hemoglobin of 10.9 g/dL, and platelet of 230×103/µL. The serum sodium level was 136 mEq/L, potassium 4.1 mEq/L, blood urea nitrogen 33 mg/L, serum creatinine 1.0 mg/L, and total serum protein 3.3 g/dL with albumin 1.2 g/dL. Urinalysis revealed 4+ albuminuria and 24-hr urine protein over 7.8 g/day. The serum cholesterol level was elevated at 539 mg/dL. The liver function tests, prothrombin time, and activated partial thromboplastin time were normal. The fibrinogen concentration and antithrombin III level were normal. The concentration of free protein S was 35.0% (normal 70-140%). Plasminogen and platelet aggregation test were not performed. The negative HBe Ag, undetectable HBV DNA, and HBs Ag seroconversion after lamivudine therapy were demonstrated. The C3 and C4 were in normal ranges. Anticardiolipin (IgM) was 4.9 MPL unit/mL (normal <12 MPL unit/mL). After the admission, supportive care for the cerebral infarction was initiated and he received anticoagulation therapy later. Hospital course was uneventful with a mild degree of residual left-side motor weakness at discharge. Two months after discharge, remission of nephrotic syndrome occurred on medication with steroid, angiotensin II receptor blocking agent. At present, 1 yr after discharge, serum albumin level is 4.6 g/dL with serum cholesterol 158 mg/dL and negative albuminuria on tapered dose of prednisolone 7.5 mg every other day (QOD).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2840,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7799191-2,Extracted,"A 53-year-old woman, active smoker, with a history of dysthyroidism, was admitted to the Emergency Unit with chest pain and dyspnoea. She complained of having had a fever, a cough, and had suffered from myalgia and diarrhoea for the previous 15 days.
On admission, the patient was suffering from a lateral chest pain. On auscultation, crackles were audible up to the mid zone on both sides. Her oxygen saturation in breathing ambient air was up to 85%.
In the presence of lateral chest pain, a blood test and an electrocardiogram (ECG) were performed, that showed D-dimer >20 000 ng/mL, and a sinus tachycardia at 105 b.p.m., with s1q3T3 pattern, and T-wave inversions in the right precordial leads.
The S1Q3T3 pattern shows the presence of an S-wave in lead I (indicating a rightward shift of QRS axis) with Q-wave and T inversion in lead III ().
The major suspicion of PE led to a CTPA that confirmed the diagnosis and showed pulmonary lesions of COVID-19 infection.
The patient was transferred to ICU, and a TTE was done on arrival. The echography showed an RV/LV ratio of 2, an abnormal septum motion with an elevation of the RV systolic pressure (RVSP) at 68 mmHg, atrial septal aneurysm with patent foramen ovale.
Intravenous UFH was started with a target between 2 and 3 times the control activated partial thromboplastin time (aPTT).
Twenty-four hours later, the patient presented with respiratory distress and oxygen saturation of 85% under 15 L/min O2 with tachypnoea, but without haemodynamic failure.
A systemic thrombolysis was performed according to the standard protocol of 10 mg over 15 min, then 90 mg over 120 min.
Follow-up: Favourable clinical evolution and on breathing ambient air 48 h later. She was discharged from hospital on Day 9 under Rivaroxaban 15 mg twice a day and then at Day 22, Rivaroxaban 20 mg once a day for at least 6 months.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [105.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 105.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2841,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5458001-1,Extracted,"A 43-year-old woman, with postliver transplant (2008) secondary to primary sclerosing cholangitis-related cirrhosis, maintained on tacrolimus, presented to our hospital with 4-day history of sore throat and fever and 2-day history of skin rash. On examination, patient was found to be febrile with temperature of 38.2 celsius, B.P 100/80 mmHg, respiratory rate (R.R) 24/min, and heart rate (H.R.) 130/min. Oxygen saturation on room air was 85%. Systemic examination revealed congested eyes, pharyngeal erythema, maculopapular skin rash involving face, upper limbs, and trunk. Chest examination revealed decreased breath sounds on the right basal area and crackles on the left side posteriorly till the mid-zone. Basic laboratory work-up was as follows: WBC: 9.8 × 103/μL, neutrophil: 7.7 × 103/UL, lymphocyte: 0.9 × 103/UL, BUN:2.80 mmol/L, creatinine: 88 μmol/L, Na: 129 mmol/L, K: 4 mmol/L, Cl: 99 mmol/L, HCO3: 18 mmol/L mmol/L, bilirubin T: 7.6 μmol/L, albumin: 28 gm/L, ALT: 50 U/L, AST: 84 U/L, ALP: 268 U/L, INR: O.9, CRP: 53, ESR: 29 and tacrolimus level: 3.4. Hepatic transaminases showed progressive increase over 2 days. Ultrasound of abdomen and liver was normal. A CT pulmonary angiogram was ordered due to the presence of tachypnoea, tachycardia and drop in oxygen saturation. It did not show any evidence of PE but showed bilateral basal lung infiltrates more on the right side with associated two large size basal lung cysts (Fig. ) .
Patient was admitted as a case of viral exanthemata fever and bronchopneumonia with airborne precautions and was treated with intravenous antibiotics and fluids. The respiratory viral panel came negative. Viral serology results were positive for CMV Ab IgG, EBV nuclear antigen IgG, EBV capsid antigen IgG, rubella IgG Ab, measles IgG Ab, and measles IgM Ab. Autoimmune serologies and tuberculosis work-up were negative. On day 2 of admission, patient's skin rash started to fade from the face and patient showed clinical improvement with regard to fever and constitutional symptoms. Bronchoscopy with bronchoalveolar lavage to evaluate lung infiltrates and cystic lung disease showed negative work-up for acid-fast bacilli, Pneumocystis jiroveci pneumonia, and fungi. Measles virus PCR in serum was reported positive. She was managed with fluids and supportive measures. The patient improved clinically with the fading of skin rash gradually and normalization of liver enzymes over the next 5 days and was discharged home.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [130.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 130.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2842,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-854,Extracted,"A 38-year-old primigravid woman at 34 weeks' gestation comes to the emergency department because of progressive shortness of breath for 3 hours. At a prenatal visit 2 weeks earlier, she was diagnosed with gestational hypertension. Amniocentesis with chromosomal analysis was performed at 16 weeks' gestation and showed no abnormalities. The patient has been otherwise healthy, except for a deep venous thrombosis 2 years ago that was treated with low molecular weight heparin. Her current medications include methyldopa and a multivitamin. She appears anxious. Her pulse is 90/min, respirations are 24/min, and blood pressure is 170/100 mm Hg. Crackles are heard over both lung bases. Pelvic examination shows a uterus consistent in size with a 32-week gestation. Examination of the heart, abdomen, and extremities shows no abnormalities.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 90.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2843,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4921103-1,Extracted,"A 62-year-old woman had undergone emergency surgery for a giant ovarian tumor rupture at another hospital in December 2013. A duodenal perforation occurred after surgery but improved with conservative treatment. She had undergone long-term nasogastric tube placement for 4 months because she was on a mechanical ventilator and did not receive proton pump inhibitors (PPIs). Thereafter, the patient experienced dysphagia, and a video fluoroscopic examination of her swallowing revealed the reflux of contrast medium from the stomach to the esophagus in February 2014. An esophagogastroduodenoscopy (EGD) revealed circumferential reflux esophagitis (grade D) and a stricture located 25 to 40 cm from the incisor teeth. She received medical treatment with fasting and PPIs. She underwent an EGD again in March 2014. The reflux esophagitis had improved somewhat, but the esophageal stricture located 33 cm from the incisor teeth had worsened, making it difficult to pass the nasal endoscope. Thereafter, balloon dilatation was attempted, but the stricture did not improve and she was referred to our hospital in April 2014. She had a history of bronchial asthma.
Upon admission, she had a height of 152.5 cm, a weight of 41.6 kg, a body mass index of 17.8, a blood pressure of 108/58 mmHg, a temperature of 36.4 °C, and pulse rate of 74 beats/minute, with no significant physical findings. Laboratory findings showed a hemoglobin level of 11.9 g/dL, a serum glutamic oxaloacetic transaminase level of 54 U/L, and a serum glutamic pyruvic transaminase level of 119 U/L, indicating mild anemia and liver dysfunction.
An upper gastrointestinal series revealed a severe stricture measuring 85 mm along the longitudinal axis from the middle to lower thoracic esophagus (Fig. ). An EGD showed a cicatricial stricture beginning 25 cm from the incisor teeth, making it difficult to pass the endoscope through the esophagus (Fig. ). A contrast-enhanced chest computed tomography (CT) scan examination revealed marked wall thickening from the middle to lower thoracic esophagus (Fig. ). FDG-PET/CT showed a slight accumulation of isotope in the esophagus, and while a malignant disease could not be completely ruled out, a diagnosis of esophagitis seemed more probable. Although a 24-h pH monitoring test is necessary for the diagnosis of gastroesophageal reflux disease (GERD), this test was not performed because the pH catheter was not expected to pass through the esophagus because of the severe stricture. The clinical course and the above findings led to a diagnosis of benign esophageal stricture caused by reflux esophagitis.
Because endoscopic balloon dilatation did not improve the stricture, a thoracoscopic esophagectomy was performed []. The patients were placed in a prone position after intubation using a single-lumen endotracheal tube and a bronchial blocker tube. Only the left lung was ventilated, and a pneumothorax in the right chest was created using 6 mmHg of CO2 gas. Five trocars were inserted into the right thoracic cavity. The 12-mm trocar inserted into the ninth intercostal space on the inferior scapular angle line was used for a flexible endoscope. The anterior pleura and the posterior pleura of the upper posterior mediastinum were incised around the esophagus, and the upper esophagus was mobilized. Lymph node dissection was not performed because the patient had been diagnosed as having a benign esophageal stricture. The arch of the azygos vein was divided, and the right bronchial artery was preserved. Next, the anterior pleura and the posterior pleura of the middle and lower posterior mediastinum were incised around the esophagus. When the middle and lower esophagus was also mobilized, a severe fibrotic change between the esophagus and the descending aorta was observed. This fibrotic change seemed to be similar to the change in a case that had received chemoradiation therapy (Fig. ). Finally, the upper esophagus was transected using a stapler device, and the thoracic esophagus was successfully mobilized. At the end of the thoracoscopic procedure, a single 32-Fr chest tube was inserted. The patient was then placed in a supine position. The stomach was mobilized, and a gastric tube was created. An antethoracic route was chosen because the patient had a BMI of 17.8 kg/m2 and was treated with total parenteral nutrition, which posed a surgical risk. An anastomosis between the cervical esophagus and the gastric tube was performed using a circular stapler in the neck, and a tube jejunostomy was created.
The gross pathological findings showed a circumferential stricture with white scar formation from the lower esophagus to the cardia. Histologically, the infiltration of inflammatory cells, mainly neutrophils, lymphocytes and plasma cells, and fibrosis were observed. Erosion and ulceration were seen, but there were no malignant findings (Fig. ).
Her postoperative course was uneventful, and she was discharged on day 19. At present, 1 year and 8 months after surgery, she is attending an outpatient clinic.
Esophageal strictures have a variety of causes. Makuuchi classified esophageal strictures into functional and organic strictures. The former included esophageal achalasia, diffuse spasm, vigorous achalasia, and nutcracker esophagus, while the latter included malignant neoplasms, reflux esophagitis, esophageal web, and postoperative anastomotic stricture. It was also described that most esophageal strictures caused by reflux esophagitis occur at the lower end of the esophagus []. The majority of esophageal strictures are malignant, and benign esophageal strictures are rare. Recently, the use of PPIs has decreased the number of patients with benign esophageal strictures. The incidence of esophageal stricture is 1.1 among 10,000 persons, and 68 % of esophageal stricture cases are peptic. GERD, hernia, ulcer, and heavy drinking increase the risk of stricture []. Also, patients with esophagitis reportedly have an eight times higher risk of stricture [].
The mechanism of stricture formation arising from reflux esophagitis is considered to be as follows: gastric acid reflux causes inflammation in the lamina propria which is then disrupted, leading to stricture formation []. In addition, esophageal stricture caused by long-term nasogastric tube placement has also been reported, and according to the report, the use of a nasogastric tube for more than 2–4 weeks should be avoided []. The present patient had reflux esophagitis, had undergone long-term nasogastric tube placement, and did not receive PPIs, placing her at a high risk for stricture.
Malignant transformation has to be taken into account in esophageal strictures associated with reflux esophagitis. The reflux of digestive juice is widely known to cause the development of Barrett’s esophagus, eventually leading to Barrett’s esophageal cancer, and controlling the reflux of digestive juice to prevent malignant transformation is of primary importance. In this case, the clinical course and the findings of CT and FDG-PET/CT led to a diagnosis of benign esophageal stricture caused by reflux esophagitis. Postoperatively, the resected specimen revealed no malignant findings and the preoperative diagnosis was proven to be correct.
van Boeckel and Siersema previously described an algorithm for treatment selection. According to their report, endoscopic dilatation is successful in more than 80–90 % of cases, but recurrence occurs within 1 year in one third of cases. At the time of recurrence, the combination of dilatation and steroid injection or stenting should be considered. Surgery should be a last-resort treatment option [].
Surgery for benign esophageal stricture can be classified into two types. In cases where endoscopic dilatation can be performed, antireflux surgery, such as a Toupet, Belsey, or Nissen procedure, is performed following stricture dilatation. In cases where the stricture cannot be dilated, an esophagectomy and reconstruction are performed. In addition, surgery is indicated in (1) patients in whom stricture dilatation is not useful, (2) patients with frequent aphagia, (3) patients with intractable refractory esophagitis, and (4) patients with aspiration pneumonia, etc. []. In the present case, surgery was performed because the patient was refractory to endoscopic treatment and had reflux esophagitis (grade D), and the extended length of the stricture persisted even after conservative treatment.
The present case was characterized by an 85-mm-long segment of stenosis extending from the middle to lower thoracic esophagus. As described above, most strictures associated with reflux esophagitis are usually localized at the lower end of the lower esophagus and are found at a distance of 1 to 4 cm from the gastroesophageal junction [, ]. A search of PubMed using the keywords “esophagus,” “stricture,” and “benign” yielded five articles on benign stricture caused by the reflux of digestive juice describing the length of the stricture [–] (Table ). None of the severe strictures measured >8 cm in length in these reports. Accordingly, the present case appears to be relatively rare.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [74.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 74.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 =  1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2844,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7333050-1,Extracted,"A male in his sixties with a past medical history of non-insulin-dependent type 2 diabetes mellitus, chronic obstructive pulmonary disease without the use of home oxygen, hypertension, and hypothyroidism was initially brought to the hospital by EMS after being found unresponsive at home by neighbors. Prior to the collapse, the patient reported having symptoms of dizziness, cough, fatigue, and an inability to keep his balance for one day. However, he did not have any of the typical suspicious symptoms, which correlate with COVID-19. He denied having dyspnea, myalgia, gastrointestinal symptoms, travel history, sick contacts, headaches, visual changes, loss of consciousness, palpations, or chest pain.
Upon admission, the patient was awake, alert, and oriented. His vitals were a temperature of 101°F, blood pressure of 137/82 mmHg, heart rate of 72 bpm, respiratory rate of 18 breaths per minute, and pulse oxygen saturation of 99% via a 6 L nasal cannula. His skin was dry and pale. Rale was heard on bilateral lower lung fields. Initial testing revealed that creatine kinase levels were greater than 5,000 U/L. The patient also had mild elevations in aspartate aminotransferase and alanine aminotransferase. Furthermore, lactic acid and leukocyte count were within normal range. There were no premature neutrophils (bands) present, and rapid flu testing was negative. Admission chest X-ray was unremarkable for acute changes when compared to studies from previous admission ().
The patient was admitted to the medical floor and was started on ceftriaxone and azithromycin for presumed pneumonia vs. bronchitis leading to a presumed chronic obstructive pulmonary disease exacerbation. The patient had a one-time read of fever on admission; vitals and labs were relatively stable during the first forty-eight hours. On day 2 of admission, the patient remained stable and asymptomatic with no changes on physical exam. However, fifty-two hours after admission, he became febrile with a temperature of 101.7°F, and his oxygen saturation declined to 88% on room air and 92% via a 6 L nasal cannula. Notably, he was found to be diaphoretic but able to talk in full sentences. Physical exam revealed new wheezing sounds in the bilateral lung bases. Given his deteriorating conditions, it was decided to test the patient for COVID-19 given the rapid spread of the virus nationwide. Prior to this point, the patient did not have any of the typical criteria that were identified in current papers or guidelines from the Centers for Disease Control and Prevention, besides a low-grade fever. At this point, necessary samples were taken (respiratory viral panel, COVID-19, rapid strep, and throat culture) and appropriate isolation was initiated. Arterial blood gas was obtained while the patient was on room air, which showed 45% partial pressure of oxygen (PaO2) and 84% saturation. Due to concerns for additional complications including differential such as a pulmonary embolism, the patient was sent for a CT angiography of the chest (Figures and ), which was negative for pulmonary embolism but did show findings consistent with COVID-19-positive patients [–].
Due to an increased risk of aerosolization while on BiPAP, the patient was placed on 50% high-flow nasal cannula (HFNC) which improved his saturations to 98% and PaO2 to 102 mmHg, while still maintaining a low threshold for possible intubation. He maintained a stable respiratory status for several days, including ambulation without becoming symptomatic/desaturating. Respiratory status was stable for approximately four days while the patient was on HFNC, with saturation maintaining above 92%, without signs of acute distress. However, the patient continued to spike fevers intermittently, with a maximum temperature of 103.2°F. Oxygen requirements on HFNC decreased on day 3 from 50% to 35%, where he was able to maintain his SaO2 above 94%. The SARS-CoV-2 test was positive. On day 5 and after this clinical improvement, he developed acute hypoxemic respiratory failure requiring intubation and transfer to the intensive care unit (ICU). He was found to have acute respiratory distress syndrome (ARDS) secondary to COVID-19 (). The ventilation setting was adjusted for the management of ARDS, which improved oxygenation; however, the patient remained hypercapnic. Noticeably, the patient's blood pressure declined and required pressors. Plaquenil and Kaletra were initiated 6 days after admission.
On day 10, which was approximately four days into his ICU stay, the patient developed cardiac arrest and later died.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [72.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 72.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2845,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7243065-1,Extracted,"The case we report here is of a 76-year-old African American female who presented with a complaint of gradually progressive, continuous fatigue which has limited her daily activities. There were no significant aggravating or alleviating factors for her tiredness. She denied any associated palpitations, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, chest pain, cough, hemoptysis, pedal edema, blurry vision, abdominal pain, fever, chills, or night sweats, or any changes in weight, appetite, mood, or sleep patterns. Her past medical history was significant for syncope, hypertension, stage III chronic kidney disease, diverticulosis, hypothyroidism, and obesity. The patient also recalled an unprovoked syncopal episode 15 years ago that led to the diagnosis of second-degree atrioventricular heart block. Her medications at the time of initial presentation included aspirin (81 mg) and Synthyroid (25 mcg) daily. The patient was referred to the cardiology clinic for evaluation of Mobitz II, second-degree heart block. Her family history was significant for sudden cardiac death. Her son died at the age of six years, while her brother died suddenly at the age of 48 years. Her sister, 64 years old, has Mobitz type II, second-degree atrioventricular block that is treated with a pacemaker.
On general physical examination, her blood pressure was 164/80 mmHg while heart rate was 48 beats per minute and regular. The temperature, respiratory rate, oxygen saturation, and weight were within normal limits. Cardiac examination revealed unremarkable S1 and S2 heart sounds with no associated murmurs, rubs, or gallops. The point of maximal impulse was not displaced. She had clear breath sounds bilaterally. Abdominal, musculoskeletal, and neurologic examinations were unremarkable. Initial blood tests including complete blood count, basic metabolic panel, thyroid function tests, and Lyme serology were normal. Baseline electrocardiogram was normal except for a Mobitz type II, second-degree atrioventricular block (Figure ). The patient was advised to monitor blood pressure periodically and keep a record of it. A follow-up appointment was scheduled for further investigations at the outpatient cardiology clinic.
Transthoracic echocardiogram estimated an ejection fraction of 60%-65% along with traces of mitral and tricuspid regurgitation and mild left ventricular dilatation with no evidence of diastolic dysfunction. On further follow-up, the patient underwent stress echocardiography due to the physician’s concern of significant family history of sudden cardiac death. She developed frequent premature ventricular contractions in couplets and triplets before reaching peak exercise intensity, which led to termination of the stress test. Because of the second-degree atrioventricular block and an abnormal stress test, left heart catheterization with selective coronary angiography was scheduled. The procedure was performed without any complications. Left ventricular systolic pressure was 160 mmHg, left ventricular end-diastolic pressure was 16 mmHg, and the aortic pressure was 159/59 mmHg. On angiography, the left ventricle revealed a large calcium deposit on the anterior wall but there was no evidence of coronary artery disease. To assess for infiltrative cardiomyopathy, the patient underwent cardiac MRI which revealed normal left ventricular global and segmental function with an ejection fraction of 65%. There was no evidence of myocardial scarring or infiltrative process. She was discharged with outpatient cardiac telemetry and Holter monitor.
The patient returned to the clinic two months later with a complaint of persistent fatigue described as tiredness and weakness. Her Holter monitor revealed intermittent complete heart block with the heart rate occasionally dropping to 28 beats per minute during day time. In order to avoid sudden death due to atrioventricular heart block, she was scheduled for a dual-chamber pacemaker implant. The procedure was successful, and the patient recovered without any adverse health effects.
In order to reach a conclusive diagnosis, the patient agreed upon genetic testing for inherited arrhythmias. Following genetic counseling, she underwent RhythmNext genetic testing (Ambry Genetics, Aliso Viejo, CA). The test revealed that the patient was heterozygous for the p.E203K pathogenic mutation in LMNA gene which is consistent with the diagnosis of LMNA-related cardiomyopathy. Due to the rarity of E203K mutation, the severity of the disease for this patient was unpredictable on the basis of the genetic test result. LMNA E203K mutation was subsequently found in her sister as well. The patient's daughter and another sister, both of whom are healthy, tested negative for this mutation.
At the latest follow-up, the patient's fatigue had subsided. She had not suffered from any adverse or unanticipated events due to her pacemaker implant. She was compliant with her medications which comprised of aspirin (81 mg once daily) and Synthyroid (25 mcg once daily). Intracardiac cardioverter-defibrillator implantation for primary prophylaxis of fatal arrhythmias was also discussed with the patient.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [48.0, 'beats per minute'], 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Immobilization for at least 3 days': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 48.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2846,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6048603-1,Extracted,"A 23-year-old African American female with no known past medical history presented to
the emergency department with 3 days history of nonproductive cough and runny nose.
Review of systems was otherwise negative denying chest pain, dizziness, palpitation,
or syncope. The patient was not taking any medications. She had no recent travel or
positive family history. On physical examination, the patient appeared comfortable.
She was afebrile with blood pressure of 107/74 mm Hg, heart rate of 45/minute, and
oxygen saturation of 99% on ambient air. The patient had mild pharyngeal edema but
no jugular venous distension. Auscultation of the heart revealed slow heart rate,
but it was regular with normal first and second heart sounds having no murmurs.
Auscultation of bilateral lungs revealed clear breath sounds. There were neither
skin rash nor pedal edema.
Admission electrocardiogram (ECG; ) showed CHB characterized by AV dissociation with narrow QRS
escape rhythm, atrial rate of 90/minute, and ventricular rate of 45/minute. Chest
X-ray was unremarkable. Complete blood count and chemistry panel were within normal
limits. Troponin, erythrocyte sedimentation rate, and thyroid panel were also within
normal limits. Urine toxicology was negative. Lyme IgM antibody, antinuclear
antibody, and rheumatoid factor were also negative.
The patient was admitted to the cardiac care unit in the diagnosis of CHB with
profound bradycardia at rest. Throughout her hospital stay, the patient remained
asymptomatic. She occasionally switched to apparent 2:1 heart block on the
telemonitor as shown in . Her average systolic blood pressure was around 100 mm Hg, and her
average heart rate was 40 to 50 beats per minute. The patient’s heart rate
fluctuated along with her physical activity, the lowest being 32/minute during sleep
and the highest being 116/minute during exertion. Transthoracic echocardiogram
revealed normal left ventricular systolic and diastolic function without major
valvular or structural abnormalities. Exercise stress test was performed to assess
the patient’s chronotropic competency to physical activity. The patient achieved
Bruce protocol stage 3 without any symptoms. She exercised for 10 minutes and
achieved metabolic equivalent 12.4. The maximum heart rate during exercise was
139/minute, and she remained in junctional escape rhythm with CHB throughout the
exercise and recovery. is her resting ECG showing CHB with isorhythmic AV dissociation
mimicking 2:1 block, atrial rate being around 80/minute, and ventricular rate being
around 40/minute.
Her hospital course was uneventful, and the patient was discharged with an outpatient
cardiology appointment. She was also scheduled to receive a loop recorder
implantation.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [116.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 116.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2847,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8442808-1,Extracted,"A 12-year-old right-handed male child presented to the emergency department due to altered mental status (AMS). He further complained of low-grade fever, body pains, cough, and headache for five days. He described his headache as worse in the morning and associated with nausea and vomiting for the past three days. He denied any significant past medical or surgical history. On examination, he was afebrile, oriented but complained of severe headache. His pulse was 89/min, his respiratory rate was 15/min, his blood pressure was 136/88mmHg, and he maintained a saturation of 98%. A neurology consult was given. Cranial nerve examination was normal. Fundoscopic investigation revealed papilledema. Initial MRI of the brain was suggestive of a right temporoparietal large hemorrhagic lesion (Figure ).
MRI of the brain with magnetic resonance venography (MRV) revealed massive cerebral venous thrombosis involving sigmoid, lateral, and jugular venous sinuses (Figure ).
Nasal swab polymerase chain reaction (PCR) was positive for COVID-19. He denied any family history of thrombotic disease or usage of any medications leading to the prethrombotic condition. Table shows the investigation done at the time of admission.
Further, hypercoagulability profiles including protein C, protein S, homocysteine, antithrombin III, factor V Leiden, anticardiolipin antibodies, prothrombin gene mutation within normal range. Factor VIII activity was found abnormal at 248% (normal range 50-150%). He was admitted to the ICU and was started on enoxaparin 1mg/kg twice a day for anticoagulation. His neurological status improved through his hospital stay. The patient was discharged on anticoagulation treatment for 90 days. Monthly follow-up was normal and managed conservatively.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [89.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 89.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
The patient's Well's score for pulmonary embolism is 3."
2848,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4660829-1,Extracted,"An 80-year-old white man was admitted to our emergency department (DEA) presenting with dyspnea; this symptom appeared 2 weeks before and worsened a few days prior to hospital admission. He did not present other symptoms or signs; in particular he did not report thoracic pain or unilateral extremity swelling. He had no previous episodes of VTE, major trauma, immobilization or any other risk factors, such as obesity, cancer or family history suggestive of inherited thrombophilia.
His main predisposing factor for VTE was advanced age. His medical history included arterial hypertension, previous left varicectomy and right saphenectomy. On examination, his systolic blood pressure was 130/80 mmHg and pulse rate was 100 beats per minute. His respiratory rate was 24 breaths/minute and arterial oxyhemoglobin saturation was 90 % at room air. His oral temperature was 36 °C and his mental status was preserved. Chest auscultation did not reveal pathological lung sounds. An electrocardiogram (ECG) showed a normal sinus rhythm with inversion of T waves in leads V3 to V6 (Fig. ) not detected in previous recordings (Fig. ). Arterial blood gas analysis revealed a mild hypoxemia with respiratory alkalosis. His chest X-ray was normal. No supplemental oxygen was administered.
Laboratory findings on admission revealed a high serum D-dimer level (6987 ng/L), elevated high-sensitivity cardiac troponin concentration (137 ng/l) and increased serum level of pro-B-type natriuretic peptide (pro-BNP; 6166 ng/L), while renal (creatinine 1.53 mg/dl and glomerular filtration rate 43 ml/minute/1.73m2) and liver function were normal. The focused assessment with sonography for trauma (FAST) scan performed in DEA showed a moderate right ventricular (RV) dilation and hypokinesia with flattening of his interventricular septum and dilated inferior vena cava.
Together, these findings led to the suspicion of PE, subsequently confirmed by a CT pulmonary angiography (Fig. ).
According to the simplified PE Severity Index (sPESI; Table ), an extensively validated prognostic tool for predicting death and adverse outcome events in patients with PE, our patient had a score of 0. This data, in combination with the hemodynamic status of our patient, signs of RV dysfunction and cardiac laboratory biomarkers, allowed us to classify our patient as having an intermediate to low risk of early mortality.
Given the diagnosis of bilateral PE and encouraged by the results of the EINSTEIN PE trial [], we decided to start therapy with rivaroxaban (15 mg, twice daily). In the following days the patient showed a progressive improvement of clinical status and laboratory tests. His troponin levels decreased from 905 ng/L on day 2 to 26 ng/L on day 4, pro-BNP from 6166 ng/L on day 1 to 543 ng/L on day 4 and D-dimer from 6987 ng/L to 1385 ng/L (Table ). Furthermore, his partial pressure of oxygen (pO2) increased from 68.9 to 136.4 mmHg and the following parameters remained in the normal range; pH, partial pressure of carbon dioxide (pCO2) and fraction of inspired oxygen (FiO2). Supplemental oxygen was not administered.
Five days after starting therapy, we performed another echocardiography showing a normalized RV function: ejection fraction (EF) of 55 %, systolic pulmonary artery pressure (PAPs) of 30 mmHg, and tricuspid annular plane systolic excursion (TAPSE) of 26 mm.
Seven days after starting treatment, the patient underwent a CT pulmonary angiography that revealed a significant improvement of filling defects in the lower lobes (Fig. ).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 100.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2849,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3543541-1,Extracted,"A 22 year old female presented in the emergency department with complaints of fatigue, malaise, dizziness, shortness of breath, and abdominal distension for the last 5 days. She had a full-term normal vaginal home delivery 10 days back and the baby expired 6 days after the birth. There was no history of fever, abdominal pain, or post partum hemorrhage.
On examination pulse was 110/min, blood pressure was 80/60 mmHg. Pallor, icterus, cyanosis, clubbing, lymphadenopathy were absent. Pitting edema was present in both lower limbs.
Respiratory system revealed bilateral pleural effusion, evident by absent breath sounds, and stony dullness on the bilateral lower axillary area. Abdominal examination revealed ascites with no hepatosplenomegaly. CNS and CVS were normal. On gynecological examination Labia majora were edematous and vaginal mucosa was congested and friable. There was no evidence of bleeding or foul smelling lochia. On bimanual examination, uterus was tender, bilateral fornices were nonpalpable and nontender.
On laboratory examination Hb 11.6 gm/dL, hematocrit 35%, and total leukocyte count of 64,030/m3 with polymorph 83%, lymphocyte 4%, and promyelocyte 13%, ESR 58 mm, general blood picture was normocytic normochromic. CRP was >150 mg/L. Renal and Liver Function Test and blood sugar were normal. HIV and HbsAg were nonreactive. On ultrasound there was fluid collection in peritoneal cavity and mild hepatomegaly. On ascitic fluid examinations, total cell count were 3200/mm3 with 60% RBC, 37% lymphocyte, and 3% polymorphs. On Gram staining gram positive rods were present and culture was positive for clostridia; differentiation of clostridium species could not be done due to unavailability of laboratory facility for different clostridia subspecies. Ascitic fluid AFB staining was negative, pleural fluid was exudative in nature and culture was sterile for gram staining and AFB. Blood culture was negative. Urine culture showed E. coli.
Patient was shifted in intensive care unit and administered fluid vasopressors, fresh frozen plasma, and intravenous antibiotic (piperacillin/tazobactam, gentamicin, and clindamycin). Patient gradually improved and her vitals became stable. Her TLC fall to 6200/mm3 gradually over 3 weeks. Patient improved clinically and was discharged.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 = 6.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 6.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
2850,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7236106-1,Extracted,"A 70-year-old female patient with a one-year history of diabetes insipidus was transferred to the Emergency Department of our hospital due to confusion and hypotension (minimum of 70/44 mmHg, maintained by dopamine). She also had fever (maximum of 39.3 °C), chills, and cough with a small amount of white phlegm that lasted for 2 days. The patient fainted 6 months ago and fell, and the head computed tomography (CT) at that time demonstrated left frontal and occipital fractures accompanied by frontotemporal lobe cerebral contusion, subarachnoid and subdural haemorrhage (Fig. a), and incidental pituitary micro adenoma (Fig. b). She had menopause at 48 years old.
On examination, her body temperature was 37.9 °C, heart rate was 98 bpm, respiratory rate was 23 bpm, and blood pressure was 95/67 mmHg (maintained by dopamine). Whole body physical examination showed that she had dry skin, chapped lips, pale areola, and sparse pubic and armpit hairs. On chest examination, coarse crackles were heard in both lung bases. All other physical examination results were within normal limits.
Infectious work-up showed elevated neutrophil count (7.8 × 109/L) and percentage (88%) as well as procalcitonin (PCT) at 0.291 ng/mL. Respiratory syncytial virus was positive, and other viruses were negative. Chest CTshowed bilateral pulmonary congestion, interstitial fibrosis, pleural effusion, and adjacent pulmonary atelectasis versus pneumonic infiltrates. Other laboratory examinations at admission revealed that the patient had yellow urine with a specific gravity of 1.015 and a volume of 4000 ml. Serum electrolyte examination showed potassium at 2.59 mmol/L, sodium at 125 mmol/L, calcium at 1.83 mmol/L, and phosphorus at 0.44 mmol/L. Laboratory adenohypophysis function examinations documented decreased thyroid, sex and adrenal hormones (Table ). Pituitary MR imaging performed on the day of admission revealed enlarged sella measuring 15 mm × 10 mm × 9 mm with heterogenous high signal on coronal T2 weighted image (Fig. a) and central low signal with peripheral rim enhancement on post contrast T1 weighted coronal (Fig. b) and sagittal (Fig. c) images causing mild compression on the optic chiasm, which is suggestive of acute pituitary apoplexy []. Thus, the patient was emergently managed for both pituitary apoplexy and pulmonary infection and was treated by hormone replacement therapy (adrenocortical hormone and levothyroxine sodium tablets), antibiotics (moxifloxacin and ganciclovir), ambroxol, and doxofylline.
Cardiac examination at admission showed elevated repeated brain natriuretic peptide precursor (Pro-BNP), C-reactive peptide (CRP), high sensitivity C-reactive peptide (hs-CRP) and troponin T (cTnT) levels (Table ). ECG revealed T-wave inversion on the inferior and anterior walls and an extended QT interval (QT/QTc 780/762 ms) (Fig. a). Emergency bedside TTE showed left ventricular ballooning, apical dyskinesia, and abnormal diastolic function (LVEF being 36% by Simpson’s method) (Fig. a b c), which was considered Takotsubo cardiomyopathy. Coronary angiography (CAG) performed 2 days later found no significant coronary arterial stenosis (Fig. ), but left ventricular angiogram demonstrated the typical apical LV wall motion abnormalities and a peculiarly shaped LV (a round bottom and narrow neck), resembling the type of bottle used in Japan for trapping octopus (Figs. ). Therefore, the patient was diagnosed with Takotsubo cardiomyopathy and treated with angiotensin converting enzyme inhibitor (ACEI), β-blocker and L-carnitine.
At 3 days after treatment, the patient’s vital signs were stable, her body temperature was 36.14°C, her heart rate was 62 bpm, her respiratory rate was 18 bpm, and her blood pressure was 124/72 mmHg.
At 10 days after treatment, Pro-BNP and cTnT levels were reduced to 500.8 pg/mL and 0.01 ng/mL, respectively (Table ). ECG revealed that the T-wave inversion partially recovered, and the QT interval returned to normal, with QT/QTc being 440/350 ms (Fig. b). TTE showed recovered LV apical ballooning and normal wall motion at 10 days after treatment (Fig. d).
Thirteen days after treatment, the patient suffered new abdominal pain, and her examination showed positive Murphy’s sign. Routine blood tests showed elevated neutrophil counts (8.86 × 10 []/L) and percentages (83%). Re-examination of Pro-BNP at the same time showed normal Pro-BNP levels. Her abdominal ultrasound was suggestive of acute cholecystitis. Thus, the patient was managed conservatively with antibiotics, and symptoms of acute cholecystitis resolved after 3 days.
At 2 months after treatment, there were no left ventricular apical ballooning or wall motion abnormalities, with LVEF at 63% by Simpson’s method (Figs. e and f).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [98.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 98.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2851,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8374986-1,Extracted,"A 90-year-old woman presented to the emergency department complaining of chest pain and syncope. Her medical history included chronic kidney disease (stage G4) and heart failure with preserved ejection fraction. Arrhythmia, atrial fibrillation, or atrial flutter had not been previously detected. On admission, her blood pressure (149/77 mmHg) and heart rate (68 b.p.m.) were stable, physical examination revealed no heart murmur. Electrocardiogram showed normal sinus rhythm and a complete right bundle branch block, with significant ST depression in the V3–V6 leads. Bedside transthoracic echocardiogram showed diffuse hypokinesis of the left ventricular wall with an ejection fraction of 20%; no evidence of apical thrombi, severe mitral regurgitation, and ventricular septal rupture were observed. Troponin I level was slightly elevated, at 0.039 ng/mL (normal, <0.034 ng/mL). Subsequently, the patient’s blood pressure gradually decreased, and, as cardiogenic shock was expected, catecholamines (noradrenaline 0.2 γ) were initiated, and emergency coronary angiography was scheduled for suspected ACS. Before the procedure, 200 mg aspirin and 300 mg clopidogrel were administered, in addition, 8000 units of unfractionated heparin (∼200 units per kg) were administered by intravenous bolus.
An intra-aortic balloon pump was inserted via the left common femoral artery in the catheter laboratory. The first angiogram of the left coronary artery showed filling defect in the proximal ascending aorta ( and Video 1). A guiding catheter was inserted into the left coronary artery, and the angiogram revealed no enhanced area at the LMCA or the left anterior descending coronary artery (LAD) (). IVUS revealed a large thrombus ( and Video 2), extending from the ascending aorta to the proximal LAD, without dissection of the coronary artery or the proximal ascending aorta ( and Video 3). Thus, the patient was diagnosed with ACS of the LMCA caused by a floating thrombus in the ascending aorta. Although we performed thrombectomy several times, the thrombus could not be completely removed. Consequently, we deployed a drug-eluting stent, and a final Thrombolysis in Myocardial Infarction flow grade of 3 was obtained. The patient’s vital signs were stable after the intervention. Contrast-enhanced computed tomography (CT) confirmed a large abnormal low-density area; thus, a large thrombus in the left coronary cusp without aneurysm was suspected. Additionally, contrast-enhanced CT confirmed that the ascending aorta was not dissected (). We suggested surgical repair to remove the thrombus; however, the patient and her family opted for palliative care without invasive surgical intervention, as she was a nonagenarian. Therefore, antithrombotic (warfarin) and dual antiplatelet therapy (aspirin and clopidogrel) were initiated, together with unfractionated heparin by continuous intravenous infusion (therapeutic dosing targeting 2.0–3.0 times the activated partial thromboplastin time). Unfortunately, her general condition gradually worsened, and she died of heart failure and multiple organ failure on Day 7 of hospitalization after the percutaneous intervention. The family denied an autopsy request.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [68.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 68.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
2852,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6011133-1,Extracted,"A 64-year-old white male with no prior medical history presented to his primary care physician for routine follow-up. There was no history of hypertension. During work-up for elevated liver transaminases, he was found to have hepatitis C. Before initiation of Harvoni, he underwent CT imaging of the abdomen with contrast which found a 5 × 6.7 × 7 cm right adrenal mass (). On physical examination, he was afebrile with a pulse of 47 and normotensive at 118/68. His abdominal exam was nontender, nondistended, without masses, or hernias. Review of systems was negative for abdominal pain, hypertension, weakness, palpitations, headache, diaphoresis, or weight gain. He was a current smoker with a 33 pack-year history. He had no history of endocrine disease. His family history was significant only for a father with pancreatic cancer. His remaining laboratory values were within normal values including a normal potassium value. The patient was seen by the endocrine service for evaluation, and biochemical work-up revealed that the ACTH level was 9.1 pg/ml (nl 7.2–63.3); AM cortisol was normal at 10.01 mcg/dl, and 24-hour urine metanephrines was less than 50 mcg (nl).
On CT imaging, the right adrenal mass contained scattered calcifications with small regions of fat. It enhanced in a peripheral globular fashion with central progression. The absolute contrast washout of 22.9% was indeterminate for adrenal adenoma (). The mass was noted to abut but did not appear to invade the adjacent liver, right kidney, and inferior vena cava. There was no adenopathy or free fluid. There was no evidence of metastatic disease.
Due to the size and atypical features of the mass, right adrenalectomy was performed. An open thoracoabdominal approach was chosen due to the patient's low lying costal margin, the size of the mass, and retrocaval extension of the mass medially towards the vertebral body. The patient recovered well postoperatively and was discharged four days after surgery. The resected specimen weighed 126 grams and measured 7.5 × 6.5 × 4.7 cm on gross pathology (). Within the specimen was a 6.4 × 5.5 × 4.7 cm intraparenchymal nodule, which on histologic examination proved to be a cavernous hemagioma (). The patient has had no evidence of recurrence for nearly 18 months.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [47.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 47.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2853,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7501600-1,Extracted,"An ambulance was called to a 65-year-old Caucasian male with dyspnea and deteriorating consciousness. His son confirmed that the patient had ingested 125 g of Arvalin® (containing 5 g of ZnP) a few hours prior to hospital admission. The patient’s past medical history included chronic alcoholism and depression and his only regular medication was alprazolam (0.5 mg/day). Paramedics performed gastric lavage and aspired a black-colored fluid with garlic-odor from the respiratory tract, on site. Peripheral venous access was obtained and oxygen was administered through a reservoir mask due to low oxygen saturation (SpO2: 92%). Subsequently, the patient started wheezing and was administered 120 mg intravenously (iv.) methylprednisolone. He also vomited and since the vomit was dark-colored and upper gastrointestinal tract bleeding could not be completely excluded, 1 g tranexamic acid was given iv.
The patient was then admitted to the emergency unit with the following parameters: 142/80 mmHg blood pressure, 74/min cardiac rate, 88% SpO2, and a Glasgow Coma Scale of 9. Due to impaired levels of SpO2 and consciousness, endotracheal intubation (ETI) was initiated. The patient received assisted mechanical ventilation but his spontaneous breathing persisted (fraction of inspired oxygen 0.4; pressure support 12 cmH2O) and his SpO2 normalized. Due to agitation, the patient was sedated with midazolam (5 mg/h) then a central venous catheter was inserted into the right jugular vein.
The laboratory test showed low calcium and potassium levels, elevated C-reactive protein (CRP), and low white blood cell count (WBC). Aspartate aminotransferase (AST) and gamma-glutamyl transferase (GGT) were slightly elevated, while the patient’s alanine aminotransferase (ALT) was within the normal range. Elevated creatinine and low glomerular filtration rate (GFR) levels indicated moderate kidney impairment (Table ).
The patient’s urine sample was positive for benzodiazepine; however, quantitative analysis was not carried out, based on the clinical symptoms.
Arterial blood gas results indicated global respiratory insufficiency, mixed acidosis with a moderately elevated anion gap (Table ).
Since physical examination upon admission had revealed dull percussion notes and muffled breath sounds on the right side of the thorax, as well as extensive abdominal pain, imaging was carried out. Chest X-ray and chest CT scan revealed extended alveolar infiltration of the patient’s lungs (Figs. and ).
Abdominal CT scan showed the thickening of the jejunal wall (Fig. ).
Electrolyte replacement was carried out via administration of intravenous crystalloid solutions (20 mmol potassium chloride (8.4%), 1000 mg calcium gluconate in 1500 ml Isolyte® [Fresenius Kabi] iv. and 1500 ml Sterofundin B® [B. Braun Melsungen] iv.). A single dose of 30 g charcoal via nasogastric tube (NG-tube) was given. Due to the observed lung infiltration and the patient’s elevated CRP level (114.9 mg/l), ceftriaxone (2 g per day) was empirically administered and continued for 7 days (Tables and , Fig. ).
Since the patient’s initial liver functions were slightly elevated (Table ), presumably as a consequence of chronic alcohol intake, daily doses of 600 mg ALA (Thiogamma Turbo-Set®) and 2 × 600 mg N-acetylcystein (NAC) iv. were given for 6 and 7 days, respectively. Our assumption regarding the patient’s impaired liver functions was justified by the low levels of pseudocholinesterase (ChE-PS) found on the second, third, fifth, and sixth days of care (Table ).
By the third day of the patient’s care, his potassium level had risen to 6.14 mmol/L (Table ). He received diuretics (furosemide 6 × 10 mg and 1 × 5 mg) and glucose-insulin solution (Actrapid® 10 IE with 500 ml of Glucose B Braun® [50 mg/ml]) iv. as well as polystyrene sulfonate (1 × 50 ml) via NG-tube, whereupon his potassium level declined to a normal level. The patient’s initially moderately impaired kidney functions significantly worsened, then gradually returned to their original levels by the end of the first week (Table ). Since the patient’s respiration became spontaneous and adequate, an attempt to remove the endotracheal tube was made. However, a few hours later tachycardia, and respiratory insufficiency occurred, therefore ETI was required again (Table ).
On day 6, the patient developed fever and microbiological testing from blood samples was carried out. After terminating the administration of ALA, the patient’s AST and ALT levels rose slightly, then the next day, his GGT level rose substantially (Table ).
Although still well below the normal range, the ChE-PS level had increased almost threefold (CHE-PS: 2026 U/L) by day 6 of the patient’s care, and continued to do so until day 14.
On day 7, his CRP level also began to rise (151.5 mg/L) (Table , Fig. ) By the evening, the patient developed non-sustained ventricular tachycardia. Since the arrhythmia did not cause cardial instability, no specific treatment was given. No pathological signs were detected on the chest X-rays made on days 7 and 8 (Fig. b). Nevertheless, suspecting the possibility of a beginning respiratory infection, after consulting with an infectologist specialist, iv. ciprofloxacin (2 × 400 mg per day) was initiated.
On day 8, the patient’s blood culture was found to be positive for Acinetobacter spp. (104 germ count) and sensitive to ciprofloxacin. In spite of the prevailing bacteremia and rising CRP, symptoms of sepsis did not occur, the patient’s procalcitonin level (0.25 μg/L) did not increase, and the administration of vasopressors was not required. On day 9, a second attempt was made for extubation. Due to inadequate expectoration, the patient developed dyspnea, therefore ETI was needed again. The same day a tracheostoma was inserted.
Over the next days, the patient’s hepatic enzymes and CRP level showed a slow, gradual improvement (Table , Fig. ).
On day 11, trickling bleeding appeared through the tracheostoma, which ceased after the administration of tranexamic acid (1 × 1 g iv.).
The patient became agitated on day 14 therefore tiapride (1 × 100 mg iv.) and clonazepam (1 × 1 mg iv.) were given. During his psychiatric examination, the patient non-verbally verified his depression and suicidal attempt. He accepted the offered psychiatric treatment and the initiation of paroxetine (1 × 20 mg/day). Further neurological or psychiatric symptoms could not be detected.
By the end of the second week of the patient’s care, there were no radiological, and laboratory signs (WBC = 11.97G/L, CRP = 53 mg/L) of a respiratory infection (Fig. c). The awoken patient, with stable vital functions, was transferred to the psychiatry department of our hospital.
During his psychiatric care, oral antidepressants were added (cinalozepam 1 × 40 mg per os to paroxetine 1 × 20 mg per os) and the patient began participating in psychotherapy.
While in psychiatric care, bronchoscopy was performed, mucopurulent sputum was aspirated, and subacute mucosal inflammation was detected. The microbiological examination of the sputum revealed the presence of ciprofloxacin-sensitive Acinetobacter spp., with a germ count of 104.
The patient’s clinical status gradually improved. His tracheostoma was removed on the 20th day following hospital admission and his inflammatory markers decreased to normal (WBC, 6.38 G/L) or almost normal (CRP, 5.7) levels by the 41st day of his inpatient care at the hospital. After 1 month of psychiatric inpatient care, the patient had recovered and was discharged.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [74.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 74.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 0.
The patient's Well's score for pulmonary embolism is 0."
2854,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4691597-1,Extracted,"A 41-year-old Hispanic male was brought to our hospital ED after having a witnessed tonic-clonic seizure on the street. His past medical history was significant for polysubstance abuse (heroin, cocaine, benzodiazepines, and methadone) and chronic liver disease (hepatitis C). He had history of multiple admissions to our institution for opiates detoxification. On arrival to ED his vital signs were as follows: blood pressure of 98/63 mmHg, heart rate of 118 beats/minute, respiratory rate of 48 breaths/minute, temperature of 37.5°C, and an oxygen saturation of 90% while receiving oxygen by a non-rebreather mask. Emergency Medical Services (EMS) staffing reported finding a bag of K2 at the scene. Physical examination was remarkable for bilateral rales on lung auscultation. Old needle puncture areas were found over his arms and legs, without erythema. Pupils were equal with positive light reflex. While in ED, he was combative and developed another tonic-clonic seizure episode. Endotracheal intubation was performed and he was placed on mechanical ventilation. Remarkable laboratory findings included a white blood cell (WBC) count of 29.5 K/mm3 (4.8–10.8), a bicarbonate level of 15 mmol/L (24–31), a lactic acid level of 4.4 mmol/L (0.5–2.2), and a urine toxicology screen positive for opiates, benzodiazepines, and methadone. Creatine kinase (CK) level was 5,590 U/L (25–215), and troponins were mildly elevated at 1.45 ng/mL (<0.1). Creatinine, coagulation, and liver function profiles were within normal limits. Arterial blood gas (ABG) while on mechanical ventilation and receiving FIO2 of 100% showed a pH of 7.14 (7.35–7.45), a pCO2 level of 79 mmHg (34–45), and a paO2 level of 77 mmHg (80–100). Initial chest X-ray (CXR) showed bilateral infiltrates (). Electrocardiogram (ECG) showed sinus tachycardia without ST-segment or T-wave abnormalities ().
He was admitted to the intensive care unit (ICU) with the diagnosis of acute hypoxemic/hypercapnic respiratory failure presumptively secondary to drug overdose. He required propofol, fentanyl, and midazolam to achieve adequate sedation and ventilatory synchrony. Empiric intravenous antimicrobial therapy consisting of piperacillin/tazobactam (3.375 grams every 6 hours) was initiated for the possibility of aspiration pneumonitis. While in ICU, CK and troponin levels continued to increase to 18,589 U/L and 8.76 ng/mL, respectively. A new transthoracic echocardiogram (TTE) showed markedly decreased left ventricular ejection fraction of 30% (55–65), with severe global and segmental hypokinesis and no vegetations or valvular dysfunction. Given the echocardiographic and CXR findings as well as the elevated troponin levels, therapy for acute congestive heart failure probably secondary to a non-ST-segment elevation MI was initiated with low-molecular weight heparin, β-blockers, aspirin, clopidogrel, diuretics, statins, and angiotensin-converting enzyme (ACE) inhibitors. Repeated CXR after 24 hours showed near resolution of bilateral infiltrates (). Blood, urine, and respiratory cultures were negative and antimicrobials were discontinued. He was extubated on day 4 of ICU admission but required reintubation because of severe agitation and hypoxemia, which were thought to be a clinical component of a possible withdrawal syndrome. His ICU course was further complicated by fevers, new bilateral infiltrates on CXR, and persistently elevated FIO2 requirements. TTE was repeated, showing a remarkable improvement of left ventricular ejection fraction (63%), with a complete resolution of wall motion abnormalities. He was successfully extubated on day 11 of ICU admission, after being treated for acute respiratory distress syndrome (ARDS) secondary to ventilator-associated pneumonia.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [118.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 118.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2855,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5798186-1,Extracted,"A 33-year-old white man presented to our hospital with sudden onset pleuritic chest pain and dyspnea of 1 day’s duration. The chest pain started when he was lifting a heavy trash bag and described the pain as sharp, constant, and radiating to his back. He also complained of diffuse body aches and chills but denied any fever, cough, hemoptysis, or weight loss. He denied any history of dental caries, recent travel, or exposure to sick contacts. He had no significant past medical history and was not taking any routine medications. He smoked half a pack of cigarettes a day for the past 10 years and denied any alcohol or illicit drug use. He worked as a waste collector in a garbage disposal firm.
At the time of presentation, he was: alert; oriented in time, place, and person; afebrile with a temperature of 37.06 °C (98.7 °F); tachycardic (heart rate of 110 beats/minute); and tachypneic (respiratory rate of 18/minute) with a blood pressure of 126/78 mmHg. An oral examination revealed normal dentition. A cardiopulmonary examination showed normal S1 and S2 with no murmurs and clear lung fields to auscultation bilaterally. An abdominal examination revealed a soft, non-tender abdomen with no organomegaly. A neurological examination showed intact cranial nerves and sensory system, and his muscle strength was 5/5 in all limbs with normal tone. Deep tendon reflexes were normal. An initial laboratory workup showed mild leukocytosis with white blood cell (WBC) count of 13,700 cells/mm3, elevated inflammatory markers of erythrocyte sedimentation rate (ESR) 48 mm/hour and C-reactive protein (CRP) 84 mg/dl, and moderately elevated serum transaminases of aspartate aminotransferase (AST) 634 U/L and alanine aminotransferase (ALT) 326 U/L. A basic metabolic panel was within normal limits. Three sets of cardiac enzymes done 8 hours apart were normal. An electrocardiogram was obtained which showed sinus tachycardia and diffuse ST segment elevations. A chest radiograph showed normal bilateral lung fields and normal cardiac silhouette. Computed tomography (CT) of his chest (Fig. ) ruled out aortic dissection but showed pericardial effusion. A transthoracic echocardiogram showed normal left ventricular systolic function with ejection fraction of 55% and a small pericardial effusion with no signs of tamponade physiology.
He was diagnosed as a case of acute pericarditis with minimal pericardial effusion. He was discharged home on indomethacin and was asked to follow up in the out-patient clinic. Two weeks later, when he was seen in our out-patient clinic, he complained of worsening dyspnea and chest pain. He was readmitted to hospital and an urgent transthoracic echocardiogram was obtained, which showed moderate to large pericardial effusion and tamponade physiology with right ventricular diastolic collapse and dilated inferior vena cava (Fig. ). An emergency pericardiocentesis was done and approximately 550 ml of purulent pericardial fluid was drained. The pericardial fluid was sent for culture, cell analysis, and cytology. Pericardial fluid WBC count was 15,376 cells/mm3 with 98% segmented neutrophils. A Gram stain of the pericardial fluid showed Gram-positive cocci in chains. He was started on broad-spectrum antibiotics with intravenously administered vancomycin (dosed on trough concentration) and piperacillin-tazobactam (3.375 g every 8 hours). Pericardial fluid cultures grew alpha hemolytic streptococci which were characterized as S. intermedius by matrix-assisted laser desorption/ionization time-of-flight mass spectroscopy (MALDI-TOF MS). S. intermedius was susceptible to penicillin and ceftriaxone. Anaerobic, fungal, and acid-fast bacilli cultures were negative. Pericardial fluid cytology was also negative for any malignant cells. Extensive workup with CT abdomen, CT chest, urine analysis, urine culture, and blood culture to look for source of infection failed to identify any other focus of infection. Human immunodeficiency virus (HIV) and tuberculosis QuantiFERON testing were negative. Antibiotics were deescalated to intravenously administered ceftriaxone (2 g every 24 hours) as per culture sensitivity.
His hospital course was complicated with the development of a pulmonary embolism for which he was started on an intravenously administered heparin infusion. However, within a few days of starting heparin, there was a steady decline in his platelets count. Heparin-induced thrombocytopenia (HIT) was suspected and heparin infusion was stopped. Our patient was started on argatroban infusion at a rate of 140 mcg/minute. HIT antibodies and serotonin release assay were sent which came back positive. He was subsequently transitioned to orally administered warfarin with target international normalized ratio (INR) range of 2 to 3. However, with the course of time, he did not have complete resolution of symptoms with persistence of chest pain and dyspnea. Hemodynamic and echocardiographic features were consistent with development of constrictive pericarditis. Surgical pericardiectomy with median sternotomy approach was performed which revealed thickened pericardium (Fig. ). He reported improvement in his symptoms after pericardiectomy. He was discharged home in a stable condition and received a total of 7 weeks of intravenously administered ceftriaxone. Six months post-discharge he reported complete resolution of his symptoms. A repeat echocardiography was normal and showed resolution of pericardial effusion.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2856,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5087259-1,Extracted,"A 49-year-old Caucasian woman presented to emergency department with sudden onset of right fronto-temporal throbbing headache for 1 day. It started as 3/10 in severity and then progressed to 10/10 in about half hour. The headache was associated with right eye pain, nausea, multiple episodes of vomiting, photophobia, and phonophobia as well as chills but no fever. She denied any vision changes, dizziness, speech difficulty, focal weakness, rash, joint pains, neck pain, or rigidity. The patient was previously healthy with no history of chronic medical problems except recurrent sinus infections as well as environmental allergies. Her medications included fexofenadine and oral combined contraceptive pills (OCPs), which she has been taking regularly for 10 years for menorrhagia. She had neither personal nor family history of blood clots, bleeding disorders, or any malignancy. She never smoked but used to drink alcohol socially. The patient had no history of abortion or difficulty getting pregnant. She had three pregnancies; last one was at the age of 35 with no complications. Her mother had three miscarriages while being on phenobarbital for epilepsy. Physical examination showed normal vital signs with blood pressure of 127/70 mm Hg, pulse 88 beats/min, temperature 98.2°F (36.8°C), respiratory rate 14 per min, and oxygen saturation 99% on room air. She was alert, oriented to time, place, and person, and in no distress; cardiopulmonary examination revealed clear breath sounds bilaterally without wheezes or rhonchi, and normal heart sounds with no murmurs, gallops, or rubs. Abdominal exam showed no tenderness, masses, or organomegaly, and she had no edema of the lower extremities. Detailed neurological examination showed intact cranial nerves 2–12 and round, reactive pupils to light and accommodation with normal fundi. She had normal and symmetric motor power in both upper and lower extremities, intact sensation, and no focal neurologic deficit.
Complete blood count was abnormal for leukocytosis of 18.6 K/µL with higher lymphocyte differential count of 21% and no bands. Complete metabolic panel and coagulation studies were within normal limits. Infectious workup including blood cultures was negative. The patient was given ketorolac and hydromorphone, but failed to relieve her headache; so computed tomography (CT) of the head without contrast was done that showed venous sinus thrombosis involving the posterior sagittal sinus and extending into the dominant right transverse sinus (). CT head with contrast was done for confirmation (); it showed occlusive thrombus within the posterior superior sagittal sinus, extending inferiorly into the dominant right transverse sinus, sigmoid sinus, and superior right internal jugular vein. The diagnosis of cerebral venous sinus thrombosis was made based on the patient's presentation and CT findings. Her OCPs were stopped. Anticoagulation was started with low-molecular-weight heparin (LMWH) that was switched to warfarin with an international normalized ratio (INR) target range of 2.0 to 3.0. She received warfarin for 3 months and then switched to low-dose aspirin. Further workup during her hospital stay including carotid artery Doppler and transthoracic echocardiogram was negative. Follow-up CT head 3 months after the initial diagnosis showed complete recanalization of the occluded cerebral sinuses and veins.
Three weeks after completion of anticoagulation, the patient underwent testing for prothrombotic conditions, including protein S, protein C, and antithrombin deficiency; antiphospholipid syndrome; prothrombin G20210A mutation; and factor V Leiden; all were negative.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [88.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 88.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2857,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8482717-3,Extracted,"A 33-year-old male with a history of salvage treatment for relapsed acute myeloid leukemia who recently was admitted with influenza pneumonia and complicated UTI presented with a fever. He was undergoing chemotherapy with high-dose cytarabine for AML with last dose received one month prior to infection. A SARS-CoV-2 RT-PCR test was administered which returned a positive result. The patient was subsequently admitted. Upon admission, blood pressure was 129/81 mmHg, heart rate 94 beats per minute, respiratory rate 17 breaths per minute, body temperature 37.2°C, pulse 94 beats per minute. Labs included an elevated ferritin of 6753 ng/mL and D dimer of 53 420 ng/mL. After three days of hospitalization, clinical symptoms improved and he was discharged home with instructions on oxygen saturation monitoring.
One week later, the patient returned with persistent fatigue, fever, and intermittent shortness of breath since he was discharged. He has had a productive cough of clear sputum and central chest discomfort. He denies any abdominal pain, diarrhea, blood in the stool or urine, and experiences no burning during urination. During this time, body temperature was 38.1°C, blood pressure 110/69 mmHg, heart rate 103 beats per minute, pulse 103 beats per minute, and oxygen saturation at 94%. Imaging revealed worsening left basilar consolidation suspicious for pneumonia ( and ). He was administered 10 mg of intravenous dexamethasone, 2000 mg of intravenous cefepime, 250 mg of oral azithromycin every 24 hours, and 800 mg–160 mg oral sulfamethoxazole/trimethoprim. The following day, the patient reported feeling better with resolving symptoms of fatigue and shortness of breath. He still however had intermittent episodes of dyspnea. After a 10 day hospital course, his symptoms gradually improved and he was asymptomatic for >72 hours. He was then discharged with instructions on self-isolation.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [103.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 103.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 =  3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3.0 + 1 =  4.0.
The patient's Well's score for pulmonary embolism is 4.0."
2858,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7478520-1,Extracted,"A 64-year-old man with a 50 packs per year smoking history, COPD on three-liter (L) home oxygen, and right lung cancer status post resection 25 years prior to admission presented to the emergency room with worsening shortness of breath, non-productive cough, wheezing, and generalized weakness for the past few weeks. At presentation, vitals were notable for blood pressure of 165/98 mm Hg, tachypnea (RR 22/minute), and oxygen saturation of 92% on 3 L of nasal cannula. On physical examination, he was dyspneic, cachectic appearing with diminished breath sounds more on left hemithorax, and bilateral diffuse wheezing. Laboratory workup was unremarkable. Chest radiograph revealed bullous changes involving both upper lobes and particularly the left hemithorax. Mild blunting of the left costophrenic angle from a small left pleural effusion or pleural thickening was also seen (Figure ).
Given his respiratory distress and radiographic findings concerning for a pneumothorax, a CT of the chest was performed and pneumothorax was ruled out. On CT scan, we noted that giant bullae compressed the left lower lung lobe (Figures , ). These radiological findings were consistent with VLS that had initially mimicked a pneumothorax. Our patient was not deemed a candidate for lung volume reduction surgery. He improved modestly with oral prednisone and scheduled nebulizer treatments.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [22.0, 'beats per minute'], 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 22.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2859,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7038555-2,Extracted,"A 12-year-old White male, who had also been diagnosed with SCD in childhood, sought treatment for a 20-day history of non-productive cough and lower limb oedema, which had evolved to anasarca, together with a new onset of hypertension. He had previously experienced one episode of pain and had undergone one transfusion. He reported no reduction in urine volume and no recent history of skin infection or tonsillitis. On physical examination, he was found to be pallid (+ 3/+ 4) and hypertensive (blood pressure, 160/90 mmHg), with a heart rate of 112 bpm, a respiratory rate of 36 breaths/min, and oxygen saturation of 92% on room air.
Blood tests performed at admission to the emergency room revealed the following: haemoglobin, 5.9 g/dl; haematocrit, 17.8%; haptoglobin, < 10 mg/dl; negative result on the Coombs direct antibody test; reticulocyte fraction, 4.26%; no schistocytes; lactate dehydrogenase, 970 U/L; indirect bilirubin, 0.65 mg/dl; leucocyte count, 17,330 cells/mm3; neutrophil count, 13,100 cells/mm3; lymphocyte count, 1700 cells/mm3; platelet count, 622;000 cells/mm3; and urea, 45 mg/dl. He also showed signs of hyperfiltration, with a serum creatinine concentration of 0.65 mg/dl, and an eGFR, as determined with the Schwartz formula, of 140.0 ml/min/1.73 m2, although no hydroelectrolytic or acid-base disorders were identified. An urine sample obtained at submission was found to contain 20 leucocytes/field and > 100 erythrocytes/field; 24-h proteinuria was 12.5 g. Metabolic analysis of the blood samples showed the following: total proteins, 6.1 g/dl; albumin, 2.6 g/dl; globulins, 3.1 g/dl; total cholesterol, 211 mg/dl, low-density lipoprotein, 118 mg/dl; high-density lipoprotein, 66 mg/dl; triglycerides, 133 mg/dl; C4, 25 mg/dl (normal range, 10–38 mg/dl); C3, 106 mg/dl (normal range, 73–149 mg/dl); C-reactive protein, 2.1 mg/dl (normal range, < 5 mg/dl). The serology was negative for HIV, hepatitis B, and hepatitis C. Tests for antinuclear factor, anti-DNA, rheumatoid factor, and antineutrophil cytoplasmic antibodies were also negative. Serum protein electrophoresis showed hypoalbuminaemia. Blood and urine cultures were negative. A chest X-ray showed cardiomegaly and signs of mild pulmonary congestion. Ultrasound of the kidneys and urinary tract showed that the kidneys were normal in size and appearance.
The patient underwent renal biopsy. Light microscopy showed 43 glomeruli with diffuse endocapillary hypercellularity (numerous lymphocytes and neutrophils). Synechiae were observed in 10% of the glomeruli in Bowman’s capsule. There was also occasional splitting of the glomerular basement membrane, as well as overall expansion of the mesangial matrix (Fig. b). There were no changes in the tubules, interstitium or arterioles. Immunofluorescence showed deposition of C3 (2+/3+) and lambda light chains (1+/3+), with a granular pattern, distributed throughout the capillary loop—the so-called “starry sky” pattern—consistent with a diagnosis of APIGN.
Treatment with a diuretic and an anti-proteinuric agent (angiotensin-converting enzyme inhibitor) was instituted, and the patient evolved to clinical improvement, including normalisation of blood pressure and a significant reduction in the level of proteinuria (24-h proteinuria, 1.34 g) after 10 days. Renal function was preserved. The patient left outpatient treatment after 18 months. In the final evaluation, he still presented no proteinuria or haematuria, although the signs of hyperfiltration persisted, his serum creatinine concentration being 0.5 mg/dl and his Schwartz-derived eGFR being 182 ml/min/1.73 m2. Evolution of laboratorial tests are available in Fig. .",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [112.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 112.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2860,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-546,Extracted,"A 67-year-old man comes to the physician for a follow-up examination. He feels well. His last visit to a physician was 3 years ago. He has chronic obstructive pulmonary disease, coronary artery disease, and hypertension. Current medications include albuterol, atenolol, lisinopril, and aspirin. He has smoked one pack of cigarettes daily for 18 years but stopped 20 years ago. He had a right lower extremity venous clot 15 years ago that required 3 months of anticoagulation therapy. A colonoscopy performed 3 years ago demonstrated 2 small, flat polyps that were resected. He is 175 cm (5 ft 9 in) tall and weighs 100 kg (220 lb); BMI is 32.5 kg/m2. His pulse is 85/min, respirations are 14/min, and blood pressure is 150/80 mm Hg. Examination shows normal heart sounds and no carotid or femoral bruits. Scattered minimal expiratory wheezing and rhonchi are heard throughout both lung fields.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [85.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 85.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2861,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6388901-1,Extracted,"A 69-year-old woman developed abdominal discomfort 3 days prior to presentation, when she noticed a copious amount of bleeding in a toilet after defecation. The bleeding continued regardless of defecation and urination. She was not experiencing fever, nausea, appetite changes, hematochezia, haematuria, diarrhoea, dysuria, abdominal pain or recent medication changes. Her previous medical history included a total hysterectomy with unilateral salpingo-oophorectomy for stage 1 cervical cancer at the age of 42. Her current medications did not include anticoagulants or antiplatelets. On physical examination, she appeared comfortable and her body mass index was 26. The temperature was 35.3°C, the heart rate 87 beats per minute, the blood pressure 147/83 mm Hg and the respiratory rate 16 breaths per minute. There was no inguinal lymphadenopathy. On the pelvic exam, a reddish, hard, fixed, papillary, subcutaneous mass measuring 2 cm with gross bleeding was identified at the 2 o’clock position on the wall of the vaginal vestibule. It was difficult to properly examine the bleeding source externally due to the copious amount of bleeding. The bleeding could not be controlled by simple application of the pressure. The remainder of the examination was unremarkable.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [87.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 87.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2862,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7350083-1,Extracted,"A 58-year-old male with history of stage 4 adenocarcinoma of the lung, type 2 diabetes mellitus, and hypertension was sent to the ED by his oncologist a day after initiating chemotherapy; the patient's chief complaints were generalized weakness and dyspnea. He had a new chemotherapy port and had completed 5 weeks of radiation therapy.
The patient reported weakness, shortness of breath, decreased appetite, polydipsia, polyuria, and chronic leg swelling. The patient denied fever, headache, chest pain, cough, nausea, vomiting, diarrhea, abdominal pain, dysuria, unexpected weight loss, and sick contacts.
The patient reported the following medications: empagliflozin 10 mg once daily, insulin aspart 100 U TID, insulin lispro 0-18 U QID, sitagliptin 100 mg once daily, dexamethasone 4 mg QID, alprazolam 0.25 mg TID, famotidine 20 mg BID, omeprazole 20 mg once daily, furosemide 40 mg once daily, lactulose 10 g TID PRN, losartan 25 mg once daily, temazepam 15 mg nightly PRN.
The patient's initial vitals in the ED were BP 76/50 mmHg, heart rate 103, respiratory rate 20, temperature 97.3°F, and oxygen saturation of 100% on room air. The patient was alert and oriented to person, place, time, and situation. The BMI was 21 kg/m2. He appeared lethargic and ill. The cardiovascular exam showed tachycardia with a gallop and S3. The lungs were clear to auscultation bilaterally. The abdomen was soft, nontender, and nondistended and had normal bowel sounds. The skin was warm and dry without rashes. The extremities showed 3 to 4+ pitting edema to the midcalf bilaterally. A portacath was in place over the patient's left anterior chest wall and showed no overlying signs of infection.
A CBC showed pancytopenia (). A CMP showed an anion gap of 20 and glucose of 113 g/dL (). The lactic acid was 1.4 mmol/L, Mg 2.2 mg/dL, procalcitonin 0.05 ng/mL, and proBNP 496 pg/mL. The result of a serum acetone level was large. A urinalysis showed marked glucosuria and ketonuria (). Swabs for influenzas A and B were both negative. Peripheral blood, portacath, and sputum cultures were drawn. Legionella and Streptococcus pneumoniae urinary antigens were negative. A nasal swab for MRSA was positive.
An EKG showed an incomplete right bundle branch block but was otherwise unremarkable. A chest X-ray showed a rounded cavitary lesion in the left lung, a nodularity in the right midlung (both masses consistent with previous lung cancer diagnosis), and a left-sided VAD in good position.
Day 1: in the ED, the patient received a weight-based fluid bolus of 3 liters of lactated ringers. A norepinephrine drip was started for hypotension. Empiric vancomycin and piperacillin-tazobactam were started in addition to an insulin drip at 6.9 U/hr. The patient was admitted to the ICU. The patient's intravenous (IV) fluids were switched from lactated ringers to D5NaCl 0.45% at 250 cc/hr. The recorded intake was 870 mL and output was approximately 1,400 mL, resulting in a net fluid balance of -530 mL.
Day 2: the anion gap closed, and the insulin drip was replaced with a sliding scale and basal insulin per protocol. The K was 3.3 mEq/L and repleted with 40 mEq KCl. Hydrocortisone was added for stress dose steroids. The patient's IV fluids were switched back to lactated ringers. The patient remained on a norepinephrine drip for blood pressure stabilization. The cultures reported no growth to date. The recorded intake was 950 mL and output was 1,780 mL, resulting in a net fluid balance of -830 mL.
Day 3: the patient reported feeling better but was transfused 1 unit of packed RBCs for Hb 6.9 g/dL. The K was 2.9 mEq/L and replaced with 40 mEq KCl. The patient's IV fluids were stopped. Midodrine was added while norepinephrine was weaned. The cultures reported no growth to date.
Day 4: the patient continued to report feeling better. The K was 3.0 mEq/L and replaced with 40 mEq. The cultures reported no growth to date.
Day 5: the patient continued to improve. The Mg was 1.9 mg/dL and replaced with 2 g of MgSO4. The K was 2.7 mEq/L and repleted with 40 mEq KCl. The cultures reported no growth to date. The patient was transferred from the ICU to the general medical floor.
Day 6: the patient continued to improve clinically, and the electrolytes stabilized. The patient elected for comfort care and was discharged home with hospice.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [103.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",7,7,7,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 103.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 =  6.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 6.0 + 1 =  7.0.
The patient's Well's score for pulmonary embolism is 7.0."
2863,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4530922-1,Extracted,"A 56-year-old male was brought to the emergency department by paramedics for a syncopal episode and inability to move his lower extremities. He complained of abdominal pain and inability to move his legs beginning five hours prior to arrival. He awakened from a nap that afternoon and experienced numbness in both legs, which progressed to paralysis. At baseline, he was ambulatory without any history of weakness and was last ambulatory hours prior. He endorsed occasional pain in his legs when walking at baseline.
He also complained of abdominal pain with nausea and vomiting for two days. He had a history of alcohol use and reported dark-colored emesis and last bowel movement three days prior. On review of symptoms the patient denied any history of headache, dizziness, chest pain, back pain, trauma, fevers, or extremity weakness. He walked longer than a mile the day prior. History from the patient’s wife revealed that he had an episode of altered level of consciousness while on the couch and that finding combined with his abdominal pain and paralysis prompted her to call 911. The patient’s past medical history was significant for hypertension, peripheral arterial disease, and myocardial infarction 10 years prior. His past surgical history included “abdominal stents” and a left carotid stent. His social history was significant for a 25-pack/year history of smoking and daily alcohol. His medications included atenolol and ranitidine.
Physical exam showed an oral temperature of 36.7°C, blood pressure 107/65mmHg, heart rate 99 beats/minute and a respiratory rate of 30 breaths/min, with oxygen saturation on 15L non-rebreather mask of 94%. His weight was 72.5kg and he appeared older than his stated age. He was alert, cooperative and in moderate distress, primarily complaining of pain and cramping in his lower extremities and repeatedly asking staff to straighten out his legs although they were already lying straight and motionless on the gurney. His head exam was unremarkable with the exception of a dry oropharynx. Cervical spine, cardiac, and lung exams were unremarkable. His abdomen was firm and diffusely tender to palpation with generalized rebound and guarding. An irreducible left inguinal hernia was present. He had vomiting, and placement of a nasogastric tube revealed 1.5 liters of coffee-ground emesis. Lower extremities were thin, cool, and without any palpable or Dopplerable pulses in bilateral femoral, popliteal or pedal distribution. There was trace non-reproducible sensation to the mottled lower extremities, and no sensation distal to the ankles. Motor exam was significant for lower extremity paralysis.
Laboratory data consisted of sodium 121mEq/L (135–145), potassium 6.8mEq/L (3.3–4.8), chloride 89mEq/L (101–111), CO2 18mEq/L (25–34), BUN 31mg/dL (8–26), creatinine 1.5mg/dL (0.5–1.3), and blood glucose 367mg/dL (70–115). White blood cell 19.1thous/mcL (4.0–10.5), hemoglobin 12.8g/dL (13.5–16.9), lipase 107U/L (22–51), hematocrit 38.8% (39.5–50.0), and platelets 165thous/mcL (150–400). There was a left shift in the neutrophils 16.2thous/mcL (85%) (2.0–8.1). Alkaline phosphate 88IU/L (26–110), AST 84IU/L (8–40), ALT 38IU/L (0.0–60), total bilirubin 1mg/dL (0.0–1.4), total protein 5.4g/dL (6.1–8.2), albumin 2.6g/dL (3.2–5.5). Lactate 7.2mmol/L (0.7–2.1). ABG showed pH of 7.25 (7.38–7.42), pCO2 31.6mmHg (36–42), pO2 123.6mmHg (80–104), bicarbonate 13.5mmol/L (21–27). PT was 17.3sec (9.5–12.3), PTT 45.9sec (24.1–35.1), and INR 1.62 (0.87–1.14). B-type natriuretic peptide 1,950pg/mL (<100). Troponin 2.75ng/mL (<0.03).
Chest radiograph was unremarkable. Electrocardiogram (ECG) showed sinus rhythm at 95 beats/minute with ST elevation inferiorly, anteriorly and laterally (). Bedside ultrasound to evaluate the abdominal aorta was limited. Vascular surgery was consulted prior to CT for concern of a vascular catastrophe. Cardiology was consulted for the patient’s ECG findings consistent with myocardial infarction. The patient went for a non-contrast head CT that was unremarkable and a CT angiogram of the chest, abdomen and pelvis, which was significant for the abdominal aorta with no contrast opacification 2.2cm superior to the bifurcation (), high-grade stenosis of the right common iliac artery, complete occlusion of the left common iliac artery, stents in the celiac artery and superior mesenteric artery (SMA), evidence of occlusion of the proximal SMA and inferior mesenteric artery (IMA), hepatic, splenic, bilateral renal infarctions, left inguinal hernia, bowel obstruction, pneumatosis intestinalis with evidence of ischemic bowel, and aspiration in the right lower lung. General surgery was consulted.
The cardiology service stated that the patient was not a candidate for cardiac catheterization and to start anticoagulation and low-dose aspirin if there was no contraindication or planned surgery. They also recommended thrombolytics for the diffuse thrombotic disease. The patient did have an echocardiography study that revealed an ejection fraction of 35% and multiple regional wall motion abnormalities. General surgery recommended comfort measures as he was not a surgical candidate. Vascular surgery commented that bypass would be futile and if patient survived, would be a candidate for extra-anatomical axillo-bifemoral bypass in the future. The patient was admitted to the medical intensive care unit for broad-spectrum antibiotics and a heparin drip and succumbed to his illness the following day.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [99.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Surgery in the previous 4 weeks': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 99.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 3.
The patient's Well's score for pulmonary embolism is 3."
2864,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7052551-1,Extracted,"In August 2016, a 64-year-old male patient presented to our department with the chief complaints of persistent, mild lower abdominal pain, diarrhea, and fever for more than 10 d.
The patient’s maximum body temperature was 39.8 °C. He was diagnosed with infective diarrhea by a local doctor and transferred to our hospital department.
The patient denied any notable medical history, except hypertension.
The patient stated that he had a history of drinking and smoking for 10 years.
At presentation, the patient’s body temperature was 37.1 °C. His heart rate was 72 beats/min. His respiratory rate was 20 breaths/min, and his blood pressure was 121/74 mmHg. His abdomen was soft and flat, with no tenderness.
Laboratory tests yielded the following results: Hemoglobin, 116 g/L; C-reactive protein, 99.3 mg/L; erythrocyte sedimentation rate, 73 mm/h; 24-h urinary protein, 0.21 g; and normal levels of blood urea nitrogen (1.98 mmol/L) and creatinine (70 µmol/L). The serum and urinary β2-microglobulin concentrations were 0.62 mg/dL and 2.31 mg/dL, respectively. The urinary kappa and lambda light chain concentrations were 10 mg/dL and 5.21 mg/dL, respectively. A fecal occult blood test was positive. All other laboratory parameters were within normal limits.
Abdominal computed tomography (CT) showed thickening of the colonic wall, with threadlike calcifications of the mesenteric vein in the transverse colon (Figure ). No obvious obstruction point was observed. A subsequent colonoscopy revealed purple-blue mucosa extending from the ascending colon to the transverse colon. Multiple circumferential and deep ulcers were observed along the colonic wall, with sparing of the rectum (Figure ).
Histological examination with hematoxylin and eosin staining showed obvious thickening and calcification of the vein walls. Eosinophil infiltration of the lamina propria was also seen (Figure ). Masson trichrome staining of the biopsy material revealed dense perivascular and mucosal collagen degeneration (Figure ). Congo red staining highlighted amyloidosis in the venous walls (Figure ).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [72.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 72.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2865,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5111284-2,Extracted,"Twenty-seven years old, Male.
At 01:10 on January 22, 2016, the patient visited emergency department and was presented with blurred vision and ophthalmalgia accompanied by myalgia.
He often had nausea since he started to work in the factory in September, 2015. However, this symptom subsided by taking some foods. Although he felt dizziness, he worked as night shift from 21:00 to 9:00 on January 20. In the morning of January 21, he had blurred vision shortly before he got off work. He also thought that the symptom was caused by his own fatigue. He went to sleep in his home and waked up at the evening of January 21. At that time, he felt blurred vision as well as both eye ball pain. Moreover, he had weakness accompanied by mild myalgia. He called his manager and said that he could not attend to work today. He took a cold medicine and went to sleep again. When he waked up at midnight of January 22, he had difficulty to distinguish objects. Until then, he could not hear that his coworker who had had similar symptoms was admitted to hospital.
No specific past medical history.
No specific hobby history, no specific drug history, the unmarried state.
0.5 pack × 8 years = 4 pack-years.
Beer, 2 bottles per week.
He was a migrant worker from China. He could speak Korean and communicate with other workers. He did not work any kinds of specific work in china. After he immigrated to South Korea, he worked lathe operators during 3 months. He quitted that job and started working at the same factory where the patient 1 has worked since September, 2015. He has worked as a shiftwork employee who manufactures the mobile phone parts by using the CNC machines. He used air-gun to remove remaining “alcohol” on aluminum plate without proper personal protectors like her. Sometimes, the solvent was spattered to his eyes. He rubbed his eyes to remove the solvent using his hands which were wetted with the solvent. He also did not know that what kinds of the solvent, “alcohol” he has been exposed in the factory.
No specific family history.
In emergency room, initial vital signs were as follows: blood pressure 130/80 mmHg, pulse 112 beats/min, respiration 20 breaths/min, body temperature 36.1 °C. His both eyes indicated mydriasis.
He was transferred to ophthalmologist who performed a special ophthalmologic test following visual acuity test, pupil examination, fundus examination. His visual acuity was as follows: right (hand motion perception), left (finger count 10 cm). Both pupils were dilated without light reflex (right 5.5 mm, left 6.4 mm). In addition, blurry optic disc margin with swollen optic disc was showed by funduscopy.
At afternoon on January 22, he received MRI orbit to find the cause of decreased visual acuity and spinal tapping to exclude the neurologic problems. MRI orbit showed bilateral tram track sign like T2 signal hyperinstensities with enhancement along the both retrobulba intraorbital segment of both optic nerve. After that, he was admitted in general ward under the ophthalmology department. The ophthalmologist diagnosed him with both optic neuritis and treated with steroid.
On January 23, he and his guardian spoke to the ophthalmologist that his coworker having visual disturbance was admitted in other hospital and diagnosed with methyl alcohol induced toxic optic neuropathy. The ophthalmologist requested a re-consultation with a specialist of emergency medicine. On January 24, he was transferred to ICU under the emergency medicine department. He received ABGA and was started hemodialysis treatment, leucovorin infusion per intravenous and 40% ethanol (Vodka) per oral treatment (loading dose 1.8 ml/kg, maintenance 0.5 ml/kg/h). The initial ABGA (pH 7.356, pCO2 26.8, pO2 121.8, Base excess -9.0, Bicarbonate 14.7) and serum electrolyte results (Na+ 139, K+ 3.5, Cl− 105, tCO2 8 mEq/L, anion gap 19) were confirmed that he had increased anion gap metabolic acidosis with respiratory compensation. On January 25, the follow up ABGA (pH 7.473, pCO2 32.1, pO2 99.2, Base excess 0.0, Bicarbonate 23.0) showed that he recovered from metabolic acidosis. On January 24–26, he was treated with hemodialysis once a day. On January 24–27, he was treated per oral ethanol treatment, too. On January 25, the neurologist had an exam about him to find neurologic deficits. Additionally, brain MRI and EEG were taken, which did not show any specific abnormality.
On January 26, patient’s urinary and blood samples were collected by recommendation of the specialist of occupational and environmental medicine in the hospital where his coworker was admitted. His urinary methyl alcohol concentration was 46.8 mg/L. On January 27, he was transferred to general ward. On February 1, he was finally diagnosed with bilateral optic neuropathy due to methyl alcohol intoxication. He discharged to home with ophthalmologic dysfunction, although he recovered other conditions such as metabolic acidosis and myalgia.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [112.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 112.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2866,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3527234-1,Extracted,"The patient, a 32 year old female, had ingested approximately 12.5 g of 70% oxalic acid mixed in a glass of water in an attempt at deliberate self harm. Immediately after ingestion, she experienced abdominal pain and profuse vomiting and was brought to the local rural hospital within 2 hours of ingestion. After intravenous access was established and an initial assessment was done, she was immediately transferred to the regional hospital. On arrival, 4 hours after ingestion, she was found to be drowsy but alert (Glasgow coma scale 15), but with a pulse rate (PR) of 50/min and a blood pressure (BP) of 80/60 mmHg. Oxygen saturation on air (SpO2) was 92%. Immediate volume resuscitation was done and the patient required inotropic support during the first 24 hours. Vomiting continued throughout the day, with two episodes of blood stained vomitus.
Her urine output was maintained subsequently, but by the 3rd day she developed worsening generalized oedema with a reduction of urine output to approximately 20 ml/hr. There was gradual elevation of serum creatinine (S.Cr) levels (up to 704 umol/dl) and blood urea (BU) levels (up to 43.5 mmol/dl). She was transferred to our hospital on the 3rd day after oxalic acid ingestion. On admission, she was febrile (temperature 99.6°C), nauseous, with stable vital parameters (PR 82/min, BP 120/80 mmHg, SpO2 99% on air) and mild tachypnoea. There was generalized oedema with bilateral fine basal crepitations in the lungs. S.Cr level was 493 umol/dl, with serum potassium (S.K+) of 4.8 mEq/l and a white blood cell (WBC) count of 22,500/ul with 87% neutrophils. Urinalysis revealed active sediment (70–80 red cells, 1–2 pus cells/hpf). Arterial blood gases (ABG) showed a metabolic acidosis, with a pH of 7.328, PaCO2 of 33.2 mmHg, PaO2 of 84.2 mmHg, BE of −6.2 and a HCO3 of 18.9 mmol/L.
The patient underwent hemodialysis on the 3rd day, with symptomatic improvement. Post dialysis ABG revealed a respiratory alkalosis (pH of 7.479, PaCO2 of 34.9 mmHg, PaO2 of 91.9 mmHg, BE of 2.5 and a HCO3 of 26.2 mmol/L). The urine output remained low and she required a second dialysis on the 7th day. Urine output increased by day 9, but the S.Cr level remained high.
Renal biopsy was performed on the 8th day revealed acute tubulointerstitial nephritis associated with diffuse moderate acute tubular damage with refractile crystals seen in some tubules (Figure
). This was reported as being consistent with oxalic acid poisoning. After day 9, the renal functions and urine output gradually improved. No further dialysis was required. She was prescribed antacids and mucoprotective agents and upper gastrointestinal symptoms settled. Blood picture was reported as mild normochromic normocytic anemia (Hb: 9.1 g/dl) with normal WBC and platelets. She was transferred back to the local hospital on 12th day and subsequently discharged on day 14.
On follow up (Day 28), she was asymptomatic with a normal S Cr. Level (114umol/L).
The clinical course of the patient is presented in Figure
.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [50.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 50.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2867,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-4202,Extracted,"A 45-year-old woman presents to clinic for an employment physical. She has no current complaints. She has no significant past medical history, does not smoke or drink alcohol, and leads an active lifestyle. Upon further questioning, you discover that she is a second generation immigrant from Brazil and frequently returns to South America to visit family. Vital signs are as follows: T 37 C, BP 110/70 mmHg, HR 70, and RR 14. On physical exam, you note a widely-split S2 heart sound. An EKG is performed (Figure A).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [70.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 70.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2868,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7450474-1,Extracted,"A 40-year-old Asian woman, non-smoker, housewife, presented in December, 2018 with progressive shortness of breath, initially only during physical exertion (i.e, walking upstairs) which later started occurring even at rest and a non-productive cough of three years duration which worsened in the ten days preceding presentation. She also complained of chest tightness during this presentation. She did not have a history suggestive of orthopnea or paroxysmal nocturnal dyspnea, swelling of her legs and/or body, fever, blood mixed sputum, chest pain or joints pain. She did not have exposure to patients with pulmonary tuberculosis. She had presented to an ophthalmologist 3 years back due to pain and redness of both eyes and was later diagnosed with bilateral granulomatous uveitis. She was treated with topical steroid for the same duration with intermittent intervals of as long as 2–3 months.
On examination, she was afebrile with a blood pressure of 130/80 mmHg in the right arm and heart rate was 80/minute. She had clubbing of her digits. Examination of peripheral pulses revealed absent pulse over the left radial and brachial arteries and feeble pulse over the right radial and brachial arteries, and bilateral carotid arteries. Carotid bruit was heard on the left side. Her oxygen saturation at room air was only 76% and required 4 liters/minute of oxygen to maintain 92% saturation (Normal >95%). Her jugular venous pressure was not raised and there was no pedal or sacral edema.
Laboratory parameters with normal ranges in parenthesis, are as follows:
Complete blood count: white cell count 4.2 (4–10) × 10^9/L; neutrophils 78%; lymphocytes 20%; red blood cells 4.6 (4.2–5.4) × 10^12/L; haemoglobin 13.3 (12–15) g/dL; platelets 244 (150–400) × 10^9/L.
Biochemistry: random blood sugar 126 (65–110) mg/dL; urea 29 (17–45) mg/dL; creatinine 0.9 (0.8–1.3) mg/dL; sodium 139 (135–145) mmol/L and potassium 4.3 (3.5–5) mmol/L.
Hepatic panel: bilirubin total 0.8 (0.1–1.2) mg/dL and direct 0.5 (0–0.4) mg/dL; alanine transaminase 39 (5–30) units/L; aspartate transaminase 45 (5–30) units/L; alkaline phosphatase 103 (50–100) IU/L; albumin 2.6 (3.5–5) g/dL
Erythrocyte sedimentation rate (ESR) was elevated at 45 mm/hr and c-reactive protein (CRP) was 4 mg/L (Normal < 10 mg/L). Angiotensin converting enzyme (ACE) levels were elevated at 186 u/L (Normal < 52 u/L); rheumatoid factor and anti-nuclear antibodies by indirect immunofluorescence were negative. Sputum examination did not reveal any organisms including acid fast bacilli. Sputum analysed by gene Xpert also did not detect
Mycobacterium tuberculosis. The electrocardiogram was normal. Echocardiography showed moderate tricuspid regurgitation with moderate pulmonary arterial hypertension with a normal systolic function.
Chest X-ray (
) revealed bilateral reticulo-nodular infiltrates involving the middle and lower zones and some parts of the upper zones. No changes were noted compared to a radiograph done three years ago. The pulmonary function test showed a restrictive pattern. High resolution computed tomography (CT) of the chest (
) showed diffuse ground glass changes with interlobular septal thickening with mosaic attenuation and multiple enlarged calcified mediastinal and hilar lymph nodes (separate image of mediastinal section could not be retrieved). Bronchoscopy with trans-bronchial lung biopsy revealed non- caseating granulomatous inflammation with characteristic ‘asteroid bodies’ (
 and
), and was negative for malignancy and tuberculosis. Hence the diagnosis of sarcoidosis (pulmonary and ocular) was made.
The findings of abnormal pulse led us to do a CT angiogram of aorta and its branches.
 shows stenosis of the left subclavian artery with almost complete block at the distal part as well as the proximal left axillary artery. Though images not available for the report, there was stenosis of right axillary, brachial artery and its branches, with sparing of abdominal aorta up to the lower extremities. This was suggestive of large vessel vasculitis in the upper extremities, Takayasu arteritis (Type I).
With the diagnosis of sarcoidosis with coexisting Takayasu arteritis, she was treated with prednisolone 60 mg once daily (1 mg/kg/day) along with supportive treatment including oxygen, chest physiotherapy, bone protection with calcium and vitamin D, and thromboembolism prophylaxis with daily 60 mg of subcutaneous enoxaparin. Ophthalmology examination showed bilateral granulomatous uveitis and was treated with topical prednisolone drops. She dramatically improved over 3–4 days and required only 1 liter/minute of oxygen support. Pneumococcal vaccination was administered. She was later discharged on domiciliary oxygen with a tapering prednisolone dosage.
After four weeks of discharge, while she was still on 30 mg of prednisolone, she developed blurring of vision. Ophthalmologic examination showed increased intraocular pressure with findings suggestive of Secondary glaucoma, probably steroid induced. Topical steroid was stopped and since oral steroid was to be tapered off quickly, azathioprine 50 mg/day was started as a steroid sparing immunosuppressant. Glaucoma was treated with topical timolol (0.25% twice daily) and oral acetazolamide (500 mg followed by 250 mg twice daily), and she responded well over the course of 2 weeks.
The patient is still on regular follow up (after 15 months of diagnosis) and is currently asymptomatic. She does not require oxygen and does not have symptoms of vasculitis (carotidynia, headache, lightheadedness, vertigo, tingling, numbness, limb claudication, cyanosis, arthralgias and skin lesions like erythema nodosum). She is currently taking azathioprine 50 mg/day, prednisolone 10 mg/day with calcium and vitamin D supplements. She is also on regular follow up every 3 months with a pulmonologist.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2869,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5646351-1,Extracted,"A 59-year-old female with a past medical history of obesity (body mass index 51 kg/m2), autoimmune hepatitis, and osteoporosis presented to the emergency department (ED) complaining of right calf pain and swelling. She had no history of previous venous thromboembolic disease. The patient stated that the pain started after watching television for eight continuous hours. The following day, she noted persistent right calf pain. However, she was particularly engaged in national convention coverage and watched television continuously for approximately eight more hours. She recalls that she did not take any breaks from watching the convention; in fact she states she only moved from the chair once to go to the bathroom. After two days of mild throbbing pain and swelling, she decided to have family members drive her to the ED. After obtaining a history from the patient, she disclosed that she was having occasional dizziness and dyspnea on exertion.
The patient has a history of immune hepatitis which had been stable for years, treated with Imuran. Her surveillance liver function tests have been within normal limits for a while and she did not need adjustments of her medications. Her other medical history included hiatal hernia, sleep apnea requiring nighttime continuous positive airway pressure (CPAP) machine, and osteoporosis. She had no previous surgeries other than a left wrist surgery 20 years previously. She never smoked and she does not drink alcohol. The family history was notable for Paget's Disease. She denied any family history of thromboembolism, bleeding, or clotting disorders. Other than Imuran and Fosamax, the patient did not take any other medications.
Initial vital signs showed blood pressure of 115/70 torr, heart rate of 125 beats per minute (bpm), respiratory rate of 18 breaths per minute, and temperature of 97.1 F, with oxygen saturation of 96% on room air. Her pain score was 5/10 and she was anxious. On physical exam, the patient appeared mildly anxious with obvious swelling of her right calf. There was moderate right calf tenderness with +1 pitting edema. Extremity pulses were normal bilaterally. On cardiac examination, there were no murmurs. Breath sounds were diminished bilaterally. Diagnostic studies revealed a significantly elevated d-dimer at 13.28 ug/ml, glucose of 131 mg/dL, BUN of 21 mg/dL, troponin of < 0.02 ng/dL, b-type natriuretic peptide (BNP) of 39 pg/mL, and arterial pH of 7.47 and PaO2 of 74 on room air (RA). Liver function tests were normal, with an alanine aminotransferase (ALT) of 18 units/L and an aspartate aminotransferase (AST) of 25 units/L, consistent with good control of her autoimmune hepatitis. Her international normalized ratio (INR) was 1.0. Ultrasound revealed occlusive thrombus to right popliteal and right posterior tibial vein (see ). A Computed Tomography Angiography (CTA) of the chest was positive for bilateral pulmonary emboli (see ): specifically right upper lobe, right middle lobe, and left lower lobe segmental thrombi. After two liters of intravenous (IV) 0.9% normal saline, her heart rate came down to 91 bpm. Anticoagulation was initiated in the ER with IV heparin. She had a 2D echocardiogram that revealed mild right ventricular dysfunction, mild tricuspid regurgitation, and an elevated pulmonary artery pressure of 25–30 mmHg at rest. The pulmonary/critical team was consulted and given that the patient had normal troponin, BNP, and oxygenation on RA, thrombolytics were withheld. Additionally, the patient's tachycardia improved with IV fluids.
It is uncertain, however, whether the evidence of mild right heart strain was acutely due to the pulmonary emboli or if these findings were chronic and due to the patient's body habitus and sleep apnea. Her general stability and response to IV fluids would suggest the latter.
The patient was hemodynamically stable upon leaving the emergency department for the Intensive Care Unit (ICU). She was transitioned over to a novel anticoagulant rivaroxaban the following day (hospital day number 1) and was discharged home three days later without complications.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [125.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",7.5,7.5,7.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 125.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 = 6.0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 6.0 + 1.5 = 7.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 7.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 7.5.
The patient's Well's score for pulmonary embolism is 7.5."
2870,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5624155-1,Extracted,"A 43-year-old male patient presented to the emergency department with a 20-day history of fever, predominantly at nights and headaches. His previous medical history is unremarkable; he only referred to a 20-year history of smoking and denied use of intravenous or recreational drugs, any prior sexually transmitted diseases, or blood transfusions. At presentation, the patient had a blood pressure of 109/75 mmHg, heart rate 87 bpm, respiration rate 24 breaths/minute, temperature 38.5°C, and oxygen saturation of 70% at atmospheric pressure. Physical examination revealed pale skin and mucosa; tongue and soft palate had lesions consistent with oral candidiasis and congestive pharynx. Pulmonary fields revealed decreased sounds without crackles or wheezing and painful hepatomegaly and extremities with hyperchromic nodular lesions on both ankles, suggestive of Kaposi sarcoma. Due to these findings, initial blood tests included HIV serology that came out positive; CBC: Hb 11.1 g/dL, hematocrit 33.8%, WBC 7,100/mm3, lymphocytes 3%, and neutrophils 95%; IgE 788.2 UI/ml; VSG 77 mm/hr; TGO 91 UI/L; TGP 66 UI/L; and DHL 2250 UI/L. Chest X-ray revealed disseminated infiltrates in both lungs. Medical management was initiated with omeprazole, metamizole, and oxygen with nasal prongs 3 L/min. On day 2 of hospitalization, the bronchoscopy fluid examination resulted positive for C. albicans and negative for other pathogenic bacteria and fungi. However, we decided to start dexamethasone 6 mg IV, trimethoprim/sulfamethoxazole 160/800 mg, nebulization with ipratropium, and budesonide due to high suspicion of P. jirovecii infection. On day 3 of hospitalization, HIV infection was confirmed with a viral load of 531,000 copies/ml and CD4+ T-cell count of 11 cells/mm3. Other studies were performed including a PPD (negative test 0 mm) and anticytomegalovirus serology (IgG positive). On day 4 of hospitalization, the infectious disease division started ART with ritonavir/lopinavir, tenofovir, and emtricitabine. During the subsequent days, the patient showed clinical improvement. However, on day 13, his clinical condition declined with progressive dyspnea, severe dysphagia, and abdominal pain. Auscultation showed basal rales in both lungs; a new chest X-ray demonstrated no changes compared with the previous one. New blood tests included CBC: Hb 14.5 g/dl, hematocrit 44%, VCM 90 fL, platelets 284,000 × 103, WBC 18,400/mm3, neutrophils 89%, and lymphocytes 5%. Serum electrolytes, glucose, BUN, and creatinine had no alterations. He developed dysphagia and episodes of oxygen desaturation partially corrected with nasal prongs. On day 19 of hospitalization, due to continuous episodes of low oxygen saturation, a chest CT-scan was ordered (), showing generalized lung involvement and mediastinal adenopathy (Video 1 in Supplementary Material ).
Supplementary Video 1 showed digitalized CT-scan of the thorax in coronal sectioning.
Later that day, an endoscopy showed chronic reflux esophagitis (Grade D of the Los Angeles Classification System), with ulceration (Figures and ). On day 23 of hospitalization, dyspnea worsened; oxygen supply was administered with continuous positive airway pressure (CPAP). A pulmonary biopsy was performed on day 24, which reported CMV pneumonia (Figures and ); the patient was transferred to the intensive care unit (ICU) due to persistent hypoxemia and was started on methylprednisolone 500 mg IV (maintained for 2 days) and ganciclovir 500 mg IV, and ART was changed to efavirenz, emtricitabine, and tenofovir, to decrease pill intake (1 pill/day). Intravenous sedation was initiated and oxygen supply was maintained with CPAP. The patient had 2 episodes of heart failure that required management with furosemide and nitroglycerin. He developed fever and respiratory distress with episodes of delirium treated with antipsychotics; we suspected the development of IRIS due to a paradoxical worsening of his condition despite being treated with ART and ganciclovir. Therefore, we started methylprednisolone and thalidomide 100 mg/day for immunosuppression and immunomodulation, respectively. After 17 days in the ICU, the oxygen requirements began to drop and the mental status improved. He remained hemodynamically stable with clinical and radiological improvemt. A new viral load reported 12,800 copies/ml. A new CBC reported hemoglobin 8 g/dL, hematocrit 26.4%, MCV 29 pg., platelets 366,000, WBC 7,400 mm3, neutrophils 86%, and lymphocytes 6%. Patient was discharged from the hospital after 45 days of treatment ().",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [87.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 87.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
2871,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4100447-5,Extracted,"A 72-year-old African American female came to the hospital complaining of shortness of breath. The patient stated that the dyspnea started to progress over three days limiting her activity of daily living. The symptoms would worsen with exertion. She denied any chest pain, lightheadedness, diaphoresis, nausea, or vomiting. Her medical history includes hypertension, chronic obstructive lung disease, and dyslipidemia. At the time of presentation, the vital signs were blood pressure of 136/66 mmHg, heart rate of 75 beats per minute, respiratory rate of 18 breaths per minute, oxygen saturation of 95% on room air, and no fever. The cardiopulmonary, extremities, and neurologic exam was unremarkable. An electrocardiogram revealed normal sinus rhythm without significant abnormal findings. An initial laboratory workup showed pro-BNP level of 603 pg/mL (normal: 50–92 pg/mL), troponin of 0.02 ng/dL (0–0.10 ng/mL), and D-Dimer at 2072 ng/mL (normal: 200–232 ng/mL). A CT-scan of thorax with contrast revealed saddle pulmonary embolus of the right and left main pulmonary artery with extensive emboli (). An emergent echocardiography showed normal ejection fraction with hypokinesia of right ventricular free wall. There was an evidence of moderate pulmonary hypertension (RVSP of 58 mmHg). Based on these findings, a submassive PE was diagnosed (). The ultrasound with Doppler of the lower extremity showed no evidence of deep vein thrombosis.
For the treatment, the patient was taken for right heart catheterization for the placement of UAT in the main pulmonary arteries. The UAT catheters were placed in both pulmonary arteries, and heparin and 0.5 mg/hr of alteplase were delivered to each artery for 12 hours. There were no complications. Two days later, repeated echocardiogram showed marked improvement in right ventricle function (RV/LV < 1) and right ventricle systolic pressure (45 mmHg) (). The patient denied exertional dyspnea and could ambulate without limitations. She was discharged to home with oral rivaroxaban. Refer to for data summary.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [75.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Surgery in the previous 4 weeks': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 75.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2872,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6878683-1,Extracted,"A 45-year-old caucasian woman with past medical history significant for generalized anxiety and major depression disorder presented with influenza-like symptoms including fevers and neck stiffness of 1-week duration. She worked as an accountant and had no tobacco smoking or alcohol history. Her family history was significant for depression in multiple members as well as stroke in a grandmother and gastric cancer in a grandfather. She is married with two children, who are healthy. Home medications consisted of amlodipine, cholecalciferol, clonazepam, duloxetine, and prazosin, and lamotrigine which was started 17 days prior to admission for recurrent major depression. She had been on all her other medications for years. Lamotrigine was held upon admission. Initial laboratory data were significant for: acute anemia with hemoglobin (Hgb) of 10.8 gm/dL; thrombocytopenia (platelet count of 95,000/mm3); transaminitis with aspartate aminotransferase (AST) of 151 U/L, alanine aminotransferase (ALT) of 59 U/L, alkaline phosphatase of 164 U/L with initial normal bilirubin level; elevated inflammatory markers with ferritin of 29,101 ng/mL, lactate dehydrogenase (LDH) of 1101 U/L, and D-dimer of 62,365 ng/mL; and normal white count. Initial vital signs revealed fever of 38.8 °C and tachycardia of 120 beats per minute with normal blood pressure of 110/64. A physical examination revealed a mildly anxious woman with no focal neurologic deficits, sinus tachycardia, clear lung fields, no palpable splenomegaly or lymphadenopathy, and a maculopapular rash on her trunk and bilateral lower extremities. Imaging included a chest X-ray which showed no obvious pneumonia and abdominal ultrasound (US) which showed hepatomegaly with increased echogenicity thought to be fatty liver and spleen size of 11–12 cm. A computed tomography (CT) scan of her chest was also done which revealed bibasilar opacifications thought to be atelectasis and small bilateral pleural effusions. A lumbar puncture performed in the Emergency Department had a normal cell count, protein level of 38 mg/dL, and glucose of 60 mg/dL with negative cerebral spinal fluid (CSF) bacterial culture and meningitis panel.
She was admitted for management of sepsis and acute hypoxic respiratory failure. She was started on broad spectrum antibiotics with intravenously administered vancomycin, ceftazidime, and metronidazole, which she remained on for 4 days. Hematology was consulted for evaluation of acute cytopenias and coagulopathy. Further studies included a peripheral blood smear which was notable for band neutrophils with prominent toxic granulation, anisocytosis, and poikilocytosis but normocytic red blood cells, thrombocytopenia with normal platelet morphology, and no schistocytes or fragmented red blood cells to suggest a microangiopathic process. An extensive infectious disease and autoimmune workup was also initiated. Given the constellation of findings that included severe hyperferritinemia > 50,000 ng/mL, coagulopathy with elevated prothrombin time (PT)/partial thromboplastin time (PTT), up-trending liver function tests (LFTs), and low fibrinogen with markedly elevated D-dimer and LDH, there was a high suspicion for an excessive immune activation process such as HLH. A bone marrow biopsy was performed (Fig. ) and other HLH studies including serum triglycerides (which was initially mildly elevated at 185 mg/dL but quickly up-trended to > 3000 mg/dL), NK cell activity (by flow cytometry which was normal), and soluble interleukin-2 (IL-2) receptor, and a germline mutation panel was sent.
As her clinical course evolved with rapidly rising ferritin (> 100,000 ng/mL) and worsening LFTs and creatinine, as well as the development of multiorgan failure (Fig. ) requiring transfer to a monitored unit, a decision was made to start empiric treatment for HLH per the HLH-94 protocol [, ]. The protocol entails an 8-week induction therapy of etoposide (150 mg/m2 twice weekly for 2 weeks and then weekly) and dexamethasone (initially 10 mg/m2 for 2 weeks followed by 5 mg/m2 for 2 weeks, 2.5 mg/m2 for 2 weeks, 1.25 mg/m2 for 1 week, and 1 week of tapering) []. Intrathecal methotrexate is given for patients with suspected central nervous system (CNS) involvement. At the time of the decision to start HLH-directed therapy, bone marrow biopsy results were available showing a hypercellular marrow with no evidence of hematologic malignancy but two foci of hemophagocytosis (Fig. ). In addition, an infectious disease workup did not identify a likely cause of fever, including extensive viral, bacterial, and fungal tests which included blood and urine cultures, gastrointestinal (GI) pathogen panel, herpes simplex virus (HSV) polymerase chain reaction (PCR), human immunodeficiency virus (HIV) PCR, cytomegalovirus (CMV) PCR, coccidioidomycosis, Histoplasma, QuantiFERON, Cryptococcus, and parvovirus serologies which were all negative. Of note, Epstein–Barr virus (EBV) PCR was detectable at 6633 deoxyribonucleic acid (DNA) IU/mL; however, the infectious disease specialists felt this to be more reflective of asymptomatic viremia in the setting of an excessive inflammatory state rather than the trigger. Furthermore, EBV staining in the bone marrow was negative by in situ hybridization. An autoimmune workup was also unremarkable and CT imaging revealed no overt malignancy.
The morning after dexamethasone was started our patient experienced a witnessed ventricular fibrillation arrest. The Code Blue (critical medical emergency) team was activated and was able to achieve a return to spontaneous circulation, during the Code Blue our patient was intubated for airway protection. Her intensive care unit (ICU) course was complicated by acute renal failure requiring intermittent dialysis, progressive transaminitis, and an acute drop in left ventricular ejection fraction with a transthoracic echocardiogram showing Takotsubo cardiomyopathy. HLH-directed therapy as per HLH-94 regimen [, ] was continued while she was intubated and in the ICU. She began to show clinical improvement 2 days after the first etoposide dose, and a gradual decline in ferritin, white blood cell (WBC) count, and liver enzymes began at this time as well (Fig. ). She continued to show clinical improvement, allowing for extubation and downgrade from the ICU 1 week after initiation of HLH therapy. Improvement in renal dysfunction was delayed relative to liver enzymes and WBC count, requiring the start of hemodialysis as well as dose reduction in etoposide; however, her renal function eventually returned to baseline with discontinuation of dialysis after 8 days. Soluble IL-2 receptor which had been elevated to 10,270 pg/mL initially (reference range < 1033 pg/mL) also returned to normal.
She was able to complete the remainder of the 8-week HLH-94 protocol, of note, no intrathecal methotrexate and hydrocortisone was given as there was no evidence of CNS involvement []. Laboratory parameters continued to improve including resolution of her significant hyperferritinemia, transaminitis and leukocytosis. Her cardiac function also normalized with ejection fraction improvement to 70% from 36% after her cardiac arrest. At time of discharge after a hospital course that spanned 44 days, she was referred to a Bone Marrow Transplant clinic for consideration of allogeneic transplant. At that time, germline mutation testing came back showing no known pathogenic variants. Due to her complete response and sustained resolution of symptoms currently 9 months since time of admission, a transplant has not been deemed to be indicated, although she is being closely monitored at regular intervals for any signs of recurrence. Lamotrigine had been held since her initial presentation.
Clinical data are from University of California San Diego clinical laboratories; germline sequencing for hereditary HLH-associated genes (ADA, AP3B1, BL0C1S6, BTK, CD27, IL2RA, IL2RG, ITK, LYST, MAGT1, MVK, PNP, PRF1, RAB27A, SH2D1A, SLC7A7, STX11, STXBP2, UCN13D, WAS, XIAP) was performed at ARUP Laboratories (Salt Lake City, UT, USA).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2873,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6023673-1,Extracted,"This patient was a 55-year-old man who had consulted at a local hospital for incidentally discovered AF. After being treated with amiodarone for a year, his electrocardiogram (ECG) remained abnormal. Then, he was transferred to the cardiovascular department of our hospital. He had no symptoms such as chest congestion, dizziness, or fatigue, nor did he exhibit symptoms of metabolic syndromes as tachycardia, trembling, or hyperhidrosis. Radiofrequency ablation was performed to treat his AF. The ECG recovered, but the laboratory tests showed TSH 8.9 mU/L (RR, 0.27–4.2), FT3 6.61 pmol/L (RR, 3.6–7.5), and FT4 33.47 pmol/L (RR, 12–22). He ignored the suggestion to consult an endocrinologist. Three months later, the AF recurred, so he received radiofrequency ablation again. Nine months after the patient was discharged from the cardiovascular department, he was referred to our outpatient division for tachycardia, tremors, and thermophobia. At that time, the hormonal examination implied thyrotoxicosis, with a positive result for the TSH receptor antibody (FT3 34.34 pmol/L, FT4 > 100 pmol/L, TSH 0.755 mU/L, TRAb 15.28 IU/L). After administration of thyrozol 10 mg twice a day for 4 months, his symptoms resolved, and his thyroid hormone levels returned to within normal ranges; however, his TSH level was markedly increased. It was suggested to the patient that he should consult an endocrinologist for further examination of the inappropriate secretion of TSH due to central hyperthyroidism. On physical examination at admission, the patient was 172.0 cm tall and weighed 73 kg (body mass index, 24.7 kg/m2). His blood pressure was 135/80 mm Hg, and his pulse was 75 beats/min. The thyroid gland was diffusely enlarged, and ultrasonography of the thyroid revealed a rich vascular supply with a nodule located in the left lobe. Fine needle inspiration biopsy suggested the nodule was benign. The computer perimetry suggested a defective visual field. Magnetic resonance imaging (MRI) of the sella region revealed a pituitary tumor measuring 2.3 × 1.7 × 2.2 cm3 in the sella, involving the cavernous sinuses and extending into the suprasellar cistern (Fig. ). Based on these data, we diagnosed the patient with TSH-producing pituitary macroadenoma and central hyperthyroidism. One week after diagnosis, in May 2014, total resection of the pituitary macroadenoma was performed through transsphenoidal neurosurgery. Upon immunohistochemical examination, the resected pituitary adenoma cells exhibited positive staining with the TSH and PRL antibodies, and the percentage of positive Ki-67 was less than 2%, suggesting that the tumor was benign (Fig. ). After surgery, his TSH levels and thyroid hormone levels remained within the normal ranges. His serum thyroid hormone levels increased beyond the normal ranges 1 year later (TSH 0.223, FT3 11.56, FT4 36.36), although no residual tumor was apparent on the MRI. Positive results were obtained for TRAb, and both TgAb and TPOAb were elevated beyond their normal ranges (TRAb 5.62 IU/L, TgAb 32.79 IU/L, TPOAb 14.13 IU/L). The patient was administered thyrozol 10 mg/day, and his thyroid function tests remained clinically acceptable during 3 years of follow-up. Repeated pituitary MRIs showed a possible mass in the pituitary, suggesting tumor recurrence. In addition, recent ultrasonography showed that the thyroid nodule remained the same size.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [75.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 75.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2874,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8543350-1,Extracted,"A 21-year-old male was admitted to our hospital as a transfer from another hospital to receive a high level of care due to ascites, abdominal pain, and nausea for 4 days. The patient and his family had no previous disease. On admission, he complained of dyspnea, abdominal distention with the presence of shifting dullness. The patient's workup was consistent with decompensated liver cirrhosis. His vital signs were as follows: Glasgow Coma Scale score, 15 (eyes, 4; verbal, 5; and motor, 6); body temperature 36.8°C; pulse 98 beats/min; blood pressure 125/80 mm Hg; respiration 26/min; and saturation of peripheral oxygen, 96% with 3 L/min oxygen through the nasal cannula. Initial labs showed WBC 10.5 g/L, RBC 6 T/L, hemoglobin 128 g/L, PLT 37 g/L, total bilirubin 33.9 μmol/L, albumin 27.8 g/L, AST 815 IU/L, ALT 1332 IU/L, prothrombin time (INR) 2.28, APTT time (s) 33.8, D-Dimer 15,811 ng/mL, Fibrinogen 2.79 g/L. Cirrhosis workup for chronic liver disease was negative, including viral and autoimmune etiologies. Abdominal ultrasound confirmed the presence of ascites, and a diagnostic paracentesis revealed a serum ascites protein 15.2 g/L, Rivalta negative, and no evidence of spontaneous bacterial peritonitis. Abdominal computer tomography demonstrated hepatomegaly with the absence of blood in the HV whereas the portal vein was patent at this time. CT imaging also showed enlarged caudate lobe, hepatic parenchymal perfusion disorders, plenty of abdominal fluid, and bilateral pleural fluid (Fig. ). Based on this information, BCS was suspected. Further workup, including JAK2 mutation, Factor V Leiden, antiphospholipid antibody syndrome, was negative despite the significant decrease of antithrombin III, protein S, and protein C (Table ). The patient was initiated on 80 mg low molecular weight heparin subcutaneously per day, simultaneously, underwent paracentesis for ascites and thoracentesis for pleural effusion. However, the patient grew increasingly abdominal distension with simultaneous continuing to have significant ascites and began to display asterixis. Within 48 h, the patient developed hepatic encephalopathy stage II with blood ammonia level was 91 µ/dL (normal range, 20–80), INR 2.74. Interdisciplinary consultation on the patient for urgent shunt placement was progressed because emergency orthotopic liver transplantation was unfeasible due to a lack of liver donor as well as financial constraints. Angiography was performed and demonstrated no thrombosis of the IVC. There was neither a normal-appearing HV nor any collateral veins to the IVC. In this case, the HV is entirely occluded and inaccessible to either recanalization or the creation of a TIPS. We decided to employ a DIPS without intravascular ultrasound (IVUS). After accessing the right transjugular, the liver was probed with the puncture needle from the IVC just below the origin of the HV. The guiding needle (Colapinto) was advanced through the liver parenchyma and rotated until an accessed right branch of the portal vein was verified by contrast injection. A guidewire and catheter were then put into the portal vein and a portal venogram illustrated the flow of hepatic parenchyma. The intrahepatic tract was dilated using an Evercross 8.0 dilatation balloon. The 10-French sheath was then passed through the intrahepatic tract to the portal vein. Two 9 mm × 8 cm Protégé stents were placed spanning from the portal vein to the IVC on the first day of treatment (Fig. ). Post-stenting venogram demonstrated excellent flow through the stented segment. After that patient's mentation began to improve and INR trended down. The daily volume of pleural effusion was significantly decreased; thus, his dyspnea was improved. On the 9th day, imaging of abdominal CT-scanner showed recurrent HV thrombosis occurred and trans-shunt thrombectomy whilst he has continued on low molecular weight heparin; therefore, he was transitioned to oral rivaroxaban for long-term anticoagulation therapy. After postprocedure for 2 weeks, his mentation returned to normal, his abdominal distention resolved. The liver function of the patient was markedly recovered and discharged. At 3-month follow-up, the patient has returned to work with normal liver function test, exception for PLT 127 g/L and INR 1.3. His DIPS is patent by ultrasound and CT-scanner of the abdomen (Fig. ).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [98.0, 'beats/min'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 98.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2875,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7418849-1,Extracted,"A 60-year-old man presented to hospital with progressive bilateral lower limb weakness, urinary retention and constipation.
Eighteen days prior, he developed fever and cough 1 day after returning from a flight from South America. His symptoms persisted, and he also developed loss of taste (dysgeusia) and smell (anosmia). A nasopharyngeal swab for SARS-CoV-2 PCR was positive (AusDiagnostics) on day 7 of his illness. He did not receive any specific treatment (antiviral or immune modulatory) for COVID-19. His respiratory symptoms resolved after 13 days. On day 16, he developed acute urinary retention and required insertion of a bladder catheter. Over the next 2 days, he reported progressive lower limb stiffness, difficulty walking and constipation, prompting his visit to the emergency department.
His medical history included well-controlled hypertension and hypercholesterolaemia for which he takes an angiotensin receptor blocker/calcium channel blocker and a statin, respectively. He was an ex-smoker and worked for the aviation industry. He had been involved in repatriation flights from South America to Australia. Several of his colleagues were also diagnosed with COVID-19 after returning on the same flight.
On presentation to the emergency department, the patient was noted to have normal observations and was afebrile. His respiratory rate was 16 breaths per minute, oxygen saturation of 97% on room air, blood pressure of 154/88(110) mm Hg, heart rate of 85 beats per minute and temperature of 36.7°C. Clinical examination revealed increased tone, hyperreflexia and reduced proprioception of the lower limbs. The patient also exhibited patchy paresthesia bilaterally to the level of the umbilicus. There was decreased anal tone on digital rectal examination. There was no clinical evidence of major head or spinal trauma and the remainder of his cranial nerve and general neurological examination was unremarkable. These findings were consistent with an upper motor neuron lesion. The patient was admitted to hospital for further evaluation and treatment.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [85.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 85.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2876,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5400470-1,Extracted,"A 35-year-old woman visited the emergency department with a 2-day history of increasingly worsening abdominal pain. She had no history of serious illnesses. Physical examination showed that her blood pressure was 113/72 mmHg, pulse was 97 b.p.m., and body temperature was 37.7 °C. She presented with epigastralgia (sometimes intermittent abdominal colics without muscle guarding). Laboratory examination showed that her haemoglobin level was 13.0 mg/dl, haematocrit level was 39.2%, white blood cell count was 10 870 mm–3 (74.6% segmented neutrophils) and C-reactive protein level was 0.07 mg/dl. An enhanced computed tomography (CT) scan of her abdomen showed the presence of a large intraluminal mass located in the transverse colon with signs of intussusception (Fig. a and b). There were no findings of intestinal ischaemia. Abdominal findings indicated no peritonitis or ischaemic change; therefore, colonoscopy was performed to release the intussusception and diagnosis the lead point lesion. There was an oval-shaped, 4-cm mass in the transverse colon, indicating ileocecal-type intussusception (Fig. ). The clinical impression was that intussusception was due to a non-epithelial tumour, such as a gastrointestinal stromal tumour, which could be pushed back into the ileum easily using pressurized air. It was difficult to obtain a biopsy given its movement.
Two days later, a laparoscopic-assisted operation was performed. Her intussusception was almost improved. There was no movable caecum or intestinal oedema; the laparoscopic-assisted operation was performed uneventfully. The ileocecal segment was resected, and functional end-to-end anastomosis was performed.
Results of the histopathological examination showed a 3.5 × 4.5 cm IFP composed of oedematous stroma containing spindle-shaped stromal cells, lymphoid nodules and eosinophils (Fig. a and b). Results of immunohistochemical analysis indicated that the spindle cells were negative for smooth muscle actin, C-kit, desmin and CD34 (Fig. a–d). A diagnosis of IFP of the ileum was made.
The patient has had no specific post-operative complications; she was discharged 11 days post-operatively. There was no recurrence at the 8-month follow-up.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [97.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 97.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2877,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5330003-1,Extracted,"M.S., a previously healthy 13 years old girl injured as a result of gunshots and grenade blast. She sustained injuries to her face and extremities. She was initially treated by a primary care physician of the IDF. The nearest hospital to the place of admission was a civilian hospital located about one hour drive away. While waiting for the ambulance for evacuation, resuscitation efforts were started. GCS was 15; she was restless due to severe pain. Systolic blood pressure could not be measured and the heart rate was 163 beats per minute. Her injuries included: 1. Active hemorrhage from open large wounds on the right knee (Mangled extremity severity score (MESS) 8). 2. Open fractures of left elbow and right thigh 3. Active hemorrhage from the left forearm and RT. Knee due to gunshot wounds. 4. Open superficial wounds on the forehead, right eye and face. Interventions included: Arterial tourniquet to the left forearm that was converted to hemostatic dressing during the secondary survey and a C-A-T tourniquet was applied to the right thigh. Dressing with antibiotic ointment to the wounds on her face was also applied. A peripheral intravenous catheter was established and adult dose of tranexamic acid (1 g) was administered in 500 ml of Hartmann solution. The IV line was pulled out by the restless patient and in order to assure a secure and rapid line for resuscitation a tibial intra-osseous catheter (B.I.G produced by PerSys Medical) was established. Due to severe hemorrhagic shock one unit of FDP (distributed as a powder, produced by LyoPlas in Germany) (250 ml about 5.5. ml/kg) was reconstituted and then administered. Intra-osseous Morphine was also administered for pain control. No colloids, or other blood products were administered until hospital arrival. No laboratory workup was performed until after arrival to hospital. Upon arrival to the hospital, oxygen saturation was 98%, the blood pressure was 106/80 and the heart rate was 127 beats per minutes. During her 3 weeks hospitalization surgical repairs of her open fractures were performed. Since her return to her homeland M.S. was lost to follow up.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [163.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 163.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 =  3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2878,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3318239-1,Extracted,"An 84-year-old man was discharged from hospital following an admission for cellulitis of his left calf treated with a 10-day course of clindamycin. The following day he returned to hospital with acute onset abdominal and back pain. The pain had started during the night, and was not associated with vomiting or gastrointestinal disturbance. His co-morbidities included atrial fibrillation, congestive cardiac failure, ulcerative colitis, type 2 diabetes mellitus and antiphospholipid syndrome with a past history of recurrent deep vein thromboses; he was receiving maintenance warfarin therapy. On examination he was apyrexial, BP 200/132, HR 68, BM 9.1, chest was clear, there was mild to moderate epigastric tenderness with normal bowel sounds and mild resolving cellulitis of the right calf. Admission blood tests showed Hb 10.3, WCC 12.9, Plts 303, INR 6.8, Ur 8.7, Cr 111, Na 144, K 4.1, CRP 75, Ca 2.02. Electrocardiogram demonstrated a paced rhythm and chest X-ray was consistent with slight fluid overload, cardiomegaly and interstitial shadowing. The initial impression was possible gastro-oesophageal reflux disease. However tenderness was a prominent feature on examination, and in view of his co-morbidities it was important to rule out sepsis or malignancy.
Warfarin was withheld, vitamin K administered, and intravenous fluids given. A CT of the chest, abdomen and pelvis was performed (Figure ) which revealed subtle, non-specific bilateral adrenal enhancing lesions, the differential diagnosis for which included metastases, infection, granulomatous disease or haemorrhage. By now the INR had normalized to the target of 2–3, however he had ongoing abdominal pain, nausea and lethargy. He was hypotensive, with abdominal distension and normal BMs despite diabetic medication having been withheld. Response to a synacthen test was flat: Time 0, 95 nmol/L; Time 60 min, 113 mmol/L; Time 90 min, 132 mmol/L. A CT with adrenal protocol was performed to better characterize the lesions (Figures and ) and confirmed the diagnosis of bilateral adrenal haemorrhage. Adrenal hormone replacement therapy with hydrocortisone (20/10/10 mg) was commenced, anti-glycaemic agents withheld, and bowel movements were closely monitored. He showed a good response to this therapy, although his diabetic and warfarin control needed ongoing review. Management of the haemorrhage was conservative.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [68.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 68.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
The patient not been diagnosed with pulmonary embolis (PE), but the patient has previously been diagnosed with deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3 + 1.5 = 4.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2879,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8589525-1,Extracted,"A 78-year-old male patient (height: 173 cm, weight: 74 kg, and BMI: 24.7) referred to a public hospital for acute abdominal pain from three days ago after seven days of dyspnea and coughing. He had a history of coronary heart disease and percutaneous coronary intervention 6 years ago. His drug history was metoprolol 25 mg tablets twice per day (bid), Nitrocontin 6.4 mg tablets twice per day (bid), and aspirin 80 mg tablets once daily. The patient reported no history of trauma to his abdomen and no history of substance or alcohol abuse. At presentation, the pulse rate was 105 beats per minute (BPM), the blood pressure (BP) was 80/60 mm Hg, the body temperature (BT) was 38.7°C, and the respiratory rate (RR) was 20 breaths/min. The baseline electrocardiography (ECG) showed tachycardia with sinus rhythm and without myocardial infarction (MI) or other arrhythmias. The main symptom was a sudden onset of generalized abdominal pain with periumbilical predominance with 10/10 intensity. He claimed obstipation along with nausea and vomiting in this period. He could not eat during these three days. He suffered from coughing, dyspnea, and tachypnea before onset of the abdominal pain.
He was visited two times in outpatient centers and prescribed with pantoprazole 40 mg once daily, hyoscine 10 mg q8h, and painkillers (Advil) before referring to our hospital. On the last hours of the third day, he was admitted to the COVID-19 emergency department. On the examination of the abdomen, the main findings were abdominal distention with no audible bowel sound and also generalized abdominal tenderness and rebound tenderness. He had an obvious abdominal guarding. Digital rectal examination showed an empty rectal ampulla with no sign of mucosal sloughing. Respiratory sounds were nearly normal.
Main laboratory data were positive specific COVID-19 polymerase chain reaction (PCR) (based on a nasopharyngeal swab). Leuckocytosis (WBC = 11.200) and prerenal azotemia (BUN = 120 mg/dl and CR = 2.5 mg/dl) were seen in the patient. The results of the laboratory are presented in .
Plane abdominal series radiographies and computed tomography (CT) of the chest were performed. A CT scan of the chest showed no definite findings of COVID-19 and cardiomegaly. There was no pleural effusion (Figures and ), but ascites and dilated small bowel loops could be seen in the few available axial cuts of the abdomen (Figures and ).
Supine abdominal X-ray showed prominent dilated small bowel loops and the absence of a completely visible colon. Both findings were in favor of small bowel obstruction (). Multiple air fluid levels were visible in the small bowel loops in upright abdominal X-ray, pointing at small bowel obstruction ().
After initial resuscitation with 2 liters of lactated ringer's solution and antibiotic therapy with empiric wide-spectrum prophylactic antibiotics (ceftriaxone 2 gr stat and metronidazole 500 mg stat), diagnostic laparotomy was performed. Massive brownish ascites and gangrenous small bowel and colon starting from 15 cm of ligamentum of Treitz to the middle part of the transverse colon were seen. Tissue decay has happened, and the intestine was about to perforate (). These findings corresponded to acute mesenteric ischemia due to complete occlusion of the superior mesenteric artery for at least several hours. No therapeutic procedure could be performed, and the abdomen was closed. He died a couple of hours later in the intensive care unit (ICU).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [105.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 105.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2880,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4283384-1,Extracted,"A 57-year-old unemployed African American woman with poorly controlled hypertension, congestive heart failure, and polysubstance abuse (including crack-cocaine) presented after one month of progressive nonproductive cough and dyspnea and two weeks of anorexia and fatigue. EMS was summoned to her home after she complained of increasing dyspnea. Her oxygen saturation measured 70% on room air. She was taken to Baylor University Medical Center at Dallas and admitted. Blood pressure was 187/99 mmHg, heart rate 84 beats per minute, respirations 28 breaths per minute, and temperature 98.0 degrees Fahrenheit. Initial laboratory values were significant for hemoglobin 12.4 g/dL; platelets 254 K/uL, creatinine of 1.7 mg/dL; glucose 237 mg/dL; and B-type natriuretic peptide 394 pg/mL (reference range 0–100 pg/mL). Liver function tests included aspartate aminotransferase of 103 U/L (reference range 5–35 U/L); alkaline phosphatase 129 U/L (reference range 38–126 U/L); and albumin 2.9 g/dL (reference range 3.5 to 4.8 g/dL). She had no recent long trips and she was not taking any current medications.
Physical examination found diffuse rales, rhonchi, wheezing, and generalized abdominal tenderness. No lower extremity swelling was noted. Her body mass index was 31.8 kg/m2. Chest X-ray showed cardiomegaly and bilateral pulmonary infiltrates suggesting pneumonia. Pelvic sonogram found a large mass suggestive of a fibroid uterus, posterosuperior to the bladder (). A nasal swab was positive for H1N1 influenza by PCR. She was placed on empiric antibiotics and BiPAP; however, her respiratory function continued to decline. Thirteen days after admission, she experienced sudden cardiopulmonary arrest and died.
Autopsy found a normally developed, moderately obese woman. An oral endotracheal tube was well positioned. A 1275-gram, 14.8 × 14.2 × 9.4 cm subserosal pedunculated tan-white uterine nodule extended from the fundus and filled the entire pelvis with extension into the lower abdominal cavity. A vein from the surface of the nodule anastomosed with an adjacent small bowel mesenteric vein (). The myometrium also contained smaller intramural and subserosal nodules ranging in size from 0.7 cm to 2.2 cm in diameter. Cut sections of all nodules were whorled and tan-white. Multiple laminated and focally adherent hilar and peripheral intravascular thrombi were present in all lobes of both lungs. Posterior leg dissection found thrombi in bilateral posterior tibial veins and deep gastrocnemius veins.
Microscopically, the myometrial nodules consisted of smooth muscle fascicles with areas of interstitial hyalinization (). No coagulation necrosis or mitotic figures were identified; and the masses were classified as leiomyomas. Sections from the leg veins and lungs showed laminated thrombi () with focal endothelial organization (). Additional autopsy findings included cardiomegaly (485 grams) with atherosclerotic and hypertensive cardiovascular disease and diffuse alveolar damage. Postmortem studies to investigate for hypercoagulability, including MTHFR (methylenetetrahydrofolate reductase), prothrombin G20210A, and factor V Leiden mutations, were performed and were negative.
The cause of death was pulmonary thromboembolism due to DVT associated with a very large uterine leiomyoma and probably contributory to death was obesity. The manner of death was natural.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [84.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 84.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
The patient not been diagnosed with pulmonary embolis (PE), but the patient has previously been diagnosed with deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3 + 1.5 = 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2881,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4316229-1,Extracted,"A 39-year-old male office worker without a previous history of specific diseases and symptoms underwent a scheduled colonoscopy as part of a medical check-up. The patient underwent colonoscopy in another institute 3 years ago, and did not experience any specific symptoms from the use of sodium phosphate bowel purgative (Solin oral solution, Korea Pharma Co. Ltd., Seoul, Korea) as a colonic cleansing agent. Other examinations also indicated no abnormal findings.
One day prior to the colonoscopy, the patient received a dose of PEG agent (Colyte powder, Taejoon Pharma Co. Ltd., Seoul, Korea). About 5 minutes later, he experienced a generalized rash, itching, swelling and tingling feeling in his arms, dizziness, dysphagia, and dyspnea, and therefore, he visited our emergency room (ER). The patient did not have a history of chronic diseases (e.g., diabetes, hypertension, tuberculosis, and hepatitis), or any allergic disorders such as bronchial asthma and food allergies. He had been smoking for over 10 years and drinking at least once per week. In addition, no specific family history was noted, including any known occurrence of CRC.
Within 30 min, the patient was transferred to the ER by ambulance. When admitted to the ER, he was in a state of shock, with a blood pressure of 41/31 mmHg, heart rate of 102 beats/min, respiratory rate of 28 breaths/min, and body temperature of 36.0℃. Even though the patient showed acute symptoms, he was still conscious. No specific findings were noted on chest and abdominal examinations. The liver and spleen were not palpable. Blood tests revealed leukocytes, hemoglobin, and platelet levels of 6,700/mm3 (92.9% neutrophils, and 0.0% eosinophils), 15.5 g/dL, and 238,000/mm3, respectively, which were all within normal ranges. Electrolyte tests showed that sodium, potassium, and chloride levels were 141 mEq/L, 3.1 mEq/L, and 106 mEq/L, respectively.
Other results on biochemical and urine analyses were found to be within normal ranges. In arterial blood gas analysis, levels of pH, pCO2, pO2, and bicarbonate were 7.427, 35.2 mmHg, 84.0 mmHg, and 23.2 mEq/L, respectively. Cardiac enzyme tests revealed a CK-MB level of 0.7 ng/mL and a Troponin I level of 0.012 ng/mL, both of which were within normal ranges. The heart rate was found to be 82 regular sinus rhythms per minute on electrocardiography, and no significant findings were revealed on chest and abdominal radiography. The patient was interviewed completely and thoroughly several times regarding food allergens, medications, exercise, and occupational exposure to hazardous substances that can cause anaphylaxis. However, no cause other than the administration of the PEG agent could be identified.
As anaphylactic shock by PEG was suspected, oxygen was supplied via a nasal cannula at a rate of 4 L/min. Although the patient was administered with 1 L of saline as well as an intravenous injection of 0.1 mg of epinephrine (epinephrine injection solution, Daihan Pharm Co., Seoul, Korea), 3 mg of piprinhydrinate (Plakon®, Yungjin Pharm Co., Seoul, Korea), and 125 mg of methylprednisolone (Salon®, Hanlim Pharm Co., Seoul, Korea), his hypotension was not alleviated after 10 minutes. Therefore, 1 mg of epinephrine was dissolved in 0.5 L of glucose injection solution (5%) and then injected with the constant rate of 1 µg/min. Most symptoms (e.g., difficulty in breathing, hives, itching, and other symptoms) improved 1 hour after treatment, and vital signs returned to normal (blood pressure, 120/78 mmHg; heart rate, 92 beats/min; respiratory rate, 20 breaths/min). The continuous injection of epinephrine and oxygen supply were subsequently discontinued. In order to confirm whether the PEG agent was responsible for the anaphylaxis, a skin prick test was planned but not performed because the patient firmly refused to undergo the test owing to a fear of experiencing another anaphylactic shock.
Three hours after admission to the ER, the patient only showed edema on both arms, but all other symptoms were attenuated or they disappeared. After 20 hours, his vital signs were stable and no further evidence of exacerbation and recurrence were noted. The patient was informed about the possibility of anaphylaxis caused by the PEG agent, and advised to avoid such substances in the future. After discharge, no evidence of recurrence or after-effects was observed on subsequent outpatient follow-ups.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [92.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 92.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2882,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8044679-1,Extracted,"A 39-year-old male was referred to our hospital's neurology department because of severe headache and numbness in the left side of his body with a partial seizure that lasts 1–2 min for 3–4 times a day. The complaint started two weeks before hospital admission and progressively worsened. He had been healthy until two months before. Recently, the patient presents complaining of several weeks of cough with generalized weakness and poor oral intake. He was a non-smoker and denied using illicit drugs or another relevant medical history. He had no family history of TB and denied contact with a person with a TB infection.
On admission, he appeared well: bodyweight, 52 kg; height, 162 cm; temperature, 36.5 °C; blood pressure, 120/80 mmHg; pulse, 72 beats/min; respirations rate, 24/min; oxygen saturation, 98% while breathing ambient air. The neurology examination showed a hemisensory syndrome and 4/5 as the muscle strength score on the upper and lower extremity, respectively, in the left side of the body. All of the cranial nerve examination results were normal.
A computed tomography (CT) scan of the head showed a hypodense lesion in the right parietal lobe. Chest radiograph showed uniform-sized small nodules randomly distributed diffusely throughout the lungs (). Laboratory results found HIV antibody test was positive using ELISA (enzyme-linked immunosorbent assay), and acid-fast bacilli from sputum produced positive results. His CD4 count was 84 cells/μL. We, therefore, diagnosed the patient with miliary TB.
The patient was treated daily with three tablets of a fixed-dose combination of antituberculous treatment consisted of isoniazid (225 mg), rifampicin (450 mg), ethambutol (825 mg), and pyrazinamide (1200 mg), and also streptomycin injection 15 mg/kg. He also received intravenous dexamethasone 0.4 mg/kg per day and mannitol and then tapered-off. Valproic acid was also given for his focal seizure. The symptoms began to improve within three days after he received the anti-TB agents, and he was discharged without any complications on day 10. We postponed the ARV (antiretroviral) therapy within two weeks after starting the Anti-TB medication.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [72.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 72.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2883,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7879510-1,Extracted,"A 66-year-old African American female presented complaining of five days of difficulty swallowing, swelling of the back of her tongue, painful bloody oral white plaques, and cough productive of blood-streaked sputum. Associated symptoms included chills and the onset of right hand swelling and pain of the right knee.
Her past medical history included rheumatoid arthritis, obesity, type 2 diabetes mellitus, crystal-proven gout, vitamin D deficiency, stage III chronic kidney disease, macrocytic anemia, hypertension, and two episodes of tonsillitis treated with antibiotics in the last two years. She had been diagnosed with RA (ANA+, RF+, CCP-) two years earlier and treated with renally dosed MTX (10 mg) weekly and daily folic acid supplementation with a 1 mg dose. Sulfasalazine 500 mg every 12 h had been added four months prior to presentation to improve disease control. The patient reported taking her last dose of MTX two weeks prior to presentation—she had been advised by a pharmacist to hold MTX when she began a course of amoxicillin clavulanate for a toenail infection. Other medications included metformin, glipizide, hydrochlorothiazide, carvedilol, amlodipine, clonidine, hydralazine, allopurinol, and vitamin D. She denied smoking, alcohol use, or use of recreational drugs.
On physical exam she had a temperature of 38 °C (100.4 °F), a heart rate of 124 beats per minute, and relative hypotension with a blood pressure of 101/77 mmHg. Physical exam revealed dry mucous membranes, severe mucositis, oral candidiasis, active synovitis of the right wrist, and right knee tenderness. She was awake, fully oriented, and had no neurological symptoms.
Laboratory work-up showed pancytopenia, macrocytosis, acute kidney injury, a high serum folate level of 20 ng/ml and a vitamin B12 level of 127 pg/mL (Table ). Right knee arthrocentesis revealed urate crystals. On admission, medication toxicity was suspected, and methotrexate, allopurinol, sulfasalazine, and metformin were held, while folic acid and vitamin D were continued. She was treated with fluids and broad-spectrum antibiotics for tonsillitis due to febrile neutropenia. Prednisone treatment for a gout flare was initiated. During this hospitalization she was additionally diagnosed with pernicious anemia (positive intrinsic factor antibody and negative parietal cell antibody) and received vitamin B12 injections (1000 μg daily for a week) for repletion.
Throughout the patient’s hospital course, no fevers recurred. Blood and synovial fluid cultures were sterile. No focus of infection was identified other than oral candidiasis, which was treated with fluconazole for 7 days. Broad spectrum antibiotics were discontinued. By day 4, mucositis began to improve to the point that the patient could tolerate a liquid diet. Pancytopenia persisted, however, with a platelet nadir of 49,000/uL, and leucovorin (10 mg every 6 h) was added to her regimen on day 6. By day 7, significant improvement in mucositis had occurred, pancytopenia was resolving, and she was discharged home with leucovorin, weekly B12 injections, prednisone, insulin and antihypertensives. Four days post-discharge, the WBC count was 13,900 cells/uL, the platelet count was 688, 000/uL (Table ), and the patient had resolution of all her symptoms. Subsequently, prednisone was discontinued and etanercept was started after a negative purified protein derivative (PPD) skin test. No complications occurred during ten months of follow-up. The macrocytosis persisted with an MCV of 105, likely due to inadequate vitamin B12 replacement, as a recent vitamin B12 level was only 248 pg/ml. In follow-up, the patient reported satisfaction with her new treatment and denied adverse effects.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [124.0, 'beats per minute'], 'Hemoptysis': True, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 124.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 1.5 + 1 = 2.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2884,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5903405-1,Extracted,"A 38-year-old lady presented with 2 day history of constant, central chest pain radiating down both arms. She was feeling breathless, nauseous and vomited once a few hours later. She was a cocaine-user and had inhaled cocaine on the day that the pain started. She came into the hospital as her pain did not settle despite codeine (included in her previous regular prescriptions). Her past medical history included asthma, anxiety and possibly hypermobility syndrome but there was no formal diagnosis of the latter. She was a smoker and drinking alcohol occasionally.
On arrival to the hospital, she was hemodynamically stable (Blood pressure = 125/75 mmHg and heart rate = 115 bpm). Her electrocardiogram (ECG) showed sinus rhythm with significant ST elevation and Q waves in I, avL, V2-5 (Fig. ). Troponin T was 4135 ng/l (normal < 14) and 6 h later reduced to 3941 ng/l. In view of the late presentation of her ST Elevation Myocardial Infarction (STEMI) with ECG evidence of completed infarct she was not considered for emergency angiography and percutaneous intervention. She was initially treated with aspirin, clopidogrel, fondaparinux, morphine, diazepam and glyceryl trinitrate infusion. Tirofiban was added later due to chest pain recurrence (BR = 105/73 mmHg, HR = 103 bpm) and urgent coronary angiography was arranged. Her echocardiogram prior to coronary angiography showed mildly dilated left ventricle with severe left ventricular systolic dysfunction and EF < 25%. Most contractility was seen in the basal segments. Coronary angiography showed an extensive spiral CAD from the ostium of the left anterior descending artery to the distal vessel including all diagonal branches (Figs – and submitted cines). The left main stem, circumflex and right coronary arteries were normal (Fig. ). Following discussion between two Interventional Cardiologists it was felt that there was no percutaneous coronary intervention option and opted for medical management in the first instance. Due to the late presentation of her STEMI and the fact that at the time of coronary angiography the patient was pain-free, it was elected not to pursue urgent coronary artery bypass. Pregnancy was excluded. It was acknowledged that there was a possible but unconfirmed diagnosis of hypermobility syndrome which could potentially increase the risk of CAD. However, there was a temporal relationship of the chest pain with the cocaine abuse which was the most important factor. The patient vomited after the onset of the pain and there was no particular history of emotional upset prior to the onset of the chest pain to suggest possible hypertension spike which might had contributed to the dissection. The patient was started on furosemide, ramipril, eplerenone, ivabradine instead of betablockers due to asthma and she improved over the next few days. Uptitration of her medications proved difficult because of hypotension and she was discharged on Day 9.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [115.0, 'beats per minute'], 'Previously Documented Pulmonary Embolism': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 115.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2885,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-2816202-1,Extracted,"A 51-year-old white male was presented to an outpatient clinic with left renal colic. A renal ultrasound revealed a renal mass in the left kidney. The patient was referred and admitted to surgical clinic of Russian Scientific Center of Roentgen-Radiology and Rosmedtechnology on June 03, 2008 with admission diagnosis: ""Primary-multiple synchronous cancer, cancer of right kidney T2N0M0, cancer of left kidney T2N0M0"".
The patient worked as an electronics engineer. He was not under any medical care and did not take any medications. He has a history of 20 pack-years of tobacco smoking. His regular alcohol consumption was about 10 standard drinks per week.
At initial presentation, the patient (height = 178 cm; weight = 94 kg; BP 130/80 mmHg, pulse 74 per minute, T-36.6°C) was awake and oriented and did not complain on any pain or discomfort. Peripheral lymph nodes were not unremarkable; skin was normal. Abdomen was soft, non-tender. Kidneys, liver, and spleen were not palpable. External genital organs: no changes. Per rectum: no changes. CBC, biochemical panel and UA were unremarkable. No changes on ECG and chest radiograph were noted.
Contrast CT of the kidneys showed a hypoechogenic 80 × 60 mm mass with irregular margins in the middle-lower segment of the right kidney. The mass distorted major calyces, renal pelvis, and the contours of the right kidney and accumulated a contrast. A similar 70 × 55 mm mass was revealed in the upper segment of the left kidney with deformation of anterior-lateral contours of the left kidney and was adjacent to the spleen and to the upper calyx of the left kidney without involving the calyx. Calyces and renal pelvis of the left kidney were not enlarged (Figure and Figure ). No changes were noted in organs of abdominal cavity.
Ultrasound of the abdomen and kidneys yielded similar changes. Bilateral lesions of the kidneys and mostly extrarenal location of the lesion in the left kidney were crucial in determining a possibility of organ-saving operation on the left kidney.
Angiography revealed that each kidney is supplied with one main vessel at the level of upper margin of L2. After contrasting of the right renal artery in the middle and lower segments an oval mass was found with arcuate pressing of vessels in the lower segment of the right kidney. Selective contrasting of the left kidney revealed avascular mass on the external contour of the left kidney with deformation of the kidney contour in the upper and middle segments. Calyces and renal pelvises of both kidneys were unchanged.
Fine needle aspiration cytology of the renal masses showed renal cell carcinoma, clear cell type in the left kidney and renal cell carcinoma, possibly chromophobe type in the right kidney.
However, histological study of biopsy specimens concluded that the tumor of the right kidney is presented by adenocarcinoma that probably has metastatic origin; the tumor of the left kidney is renal cell carcinoma (Figure , ).
Colonoscopy, esophagogastroduodenoscopy, ultrasonography of the thyroid gland and transrectal ultrasonography have been performed in order to locate the primary tumor. Ultrasonography of the thyroid gland showed that while the shape and size of the thyroid gland were normal, the structure of the gland was heterogeneous. Right lobe: a 12 mm node with distinct margins in the lower pole. Left lobe: two nodes 6 mm and 20 mm with distinct contours and two hypoechogenic nodes 7 mm and 14 mm with indistinct, rough contours and foci of calcification. Cervical lymph nodes were unremarkable. The first fine needle aspiration cytology of the described thyroid nodes showed erythrocytes, groups and layers of follicular epithelium with proliferation and dysplasia, colloid, connective tissue fragments, but no malignant cells.
In order to exclude a primary tumor of the lungs a CT scan of the chest has been performed. The CT scan showed metastatic lesions in both lungs. Serial CT with IV contrast revealed two lesions 5 mm in the S1 segment of the left lung; a 5 mm lesion in the S6 segment and a 2-3 mm lesion in S8 segment of the right lung. Lumens of the trachea and large bronchi were traced. Structures of the mediastinum were intact.
Considering specific ultrasound changes of the thyroid gland and absence of a primary tumor in other glandular organs, a second puncture biopsy of the thyroid gland has been performed. Cytology smears showed complexes of moderately polymorphic cells that constitute papillary structures of papillary cancer. Histological study showed that among abundance of erythrocytes there is a group of hemosiderophages and a complex of cells with polymorphic nuclei and single mitosis that represent papillary structures of papillary cancer.
Thus, the final diagnosis has been established: ""Primarily-multiple synchronous cancer: cancer of the left kidney T1N0M0, cancer of the thyroid gland T2N0M1, metastatic lesions of the right kidney and lungs"". On the clinical conference following plan of the treatment has been approved: 1) a resection of the left kidney; 2) thyroidectomy; 3) performing an immunotherapy with subsequent radioiodine therapy. According to the plan of the treatment, the resection of the left kidney was performed on October 01, 2008. Histological study showed a malignant node that had renal cell carcinoma structure with clear cell and papillary components; the node was removed within normal tissues (Figure. ).
The postoperative period proceeded without complications, the wound healed through primary intention; stitches were removed on 11th day of hospitalization. The patient was discharged from the hospital on 12th day.
Thyroidectomy was performed on December 11, 2008. On operation, enlargement of cervical lymph nodes up to 15 mm was found. The postoperative period proceeded without complications.
Thus, renal biopsy raised clinical suspicion for thyroid cancer and then helped to diagnose it. After iodine radiotherapy, the lesion in the right kidney has been stabilized in its growth. Lungs and bone metastases regressed. The size of cervical lymph nodes reduced. At present the patient feels well.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [74.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 74.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2886,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-5643,Extracted,"A 29-year-old G1P0 woman at 32 weeks gestation comes to the office for a prenatal appointment. She reports an increase in white, thin, and malodorous vaginal discharge. She now uses a panty liner and says she has become more embarrassed during her workout classes due to the smell. She denies fever, abdominal pain, dysuria, itching, or urinary frequency. The patient reports good fetal movement. She has maturity onset diabetes of the young, which is well controlled on antiglycemics. She had a tonsillectomy as a child. The patient exercises 4 days a week with weight lifting and yoga. She denies tobacco, alcohol or illicit drug use. During the past 8 months, she has been sexually active with multiple partners, both male and female following a breakup with a long-term boyfriend. The fundal height is 31 cm. The fetal heart rate is 155/min. Pelvic examination reveals a nontender, closed cervix with thin, gray vaginal discharge and no leakage of fluid. No vesicles, ulcers, or abnormal lesions are seen. Microscopy of the vaginal fluid is show in Figure A. Cultures are pending.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [155.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 155.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2887,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6641677-1,Extracted,"A 28-year old Korean woman presented to the emergency department after a witnessed syncopal episode on July 2017. She had epigastric discomfort and experienced dyspnea on exertion upon climbing stairs 2 days before admission. On the day of admission, she had transiently lost consciousness while complaining of dizziness. Her previous medical history was unremarkable. History of smoking tobacco, alcohol, or drug abuse was denied. Upon further inquiry, she admitted to having taken oral contraceptive pills for 5 days before going on a trip.
On admission, she was alert and oriented but lethargic with initial blood pressure of 78/38 mm Hg, a pulse rate of 116/minutes, and oxygen saturation 76% while breathing ambient air. Cardiac examination showed regular tachycardia with accentuated S2 sound and wheezing, crackles were present in the lower lung field. Abdominal findings were unremarkable. There was no leg edema. Her electrocardiogram revealed sinus tachycardia, normal axis, and normal intervals. Arterial blood gas analysis results were as follows: pH 7.46, pCO2 31.2 mm Hg, pO2 39.4 mm Hg, and bicarbonate 21.9 mmol/L. D-dimer was elevated to 10.1 μg/ml (reference range < 0.5 μg/ml). The complete blood count, electrolyte, glucose, prothrombin time, activated partial thromboplastin time, renal-, and liver-function tests were within normal range. A contrast-enhanced computed tomography (CT) scan was performed. There was near total occlusion of both main pulmonary arteries and upper, middle, and lower lobar pulmonary arteries that were consistent with acute pulmonary thromboembolism and deep vein thrombosis was seen at the left popliteal vein (Fig. ). Echocardiography showed dilated right ventricle with dysfunction, D-shaped left ventricle and inferior vena cava dilatation without plethora.
The patient was transferred to the intensive care unit (ICU) for close monitoring. She was hemodynamically stabilized after aggressive fluid resuscitation without need for thrombolysis or embolectomy, and supplemental oxygen was discontinued after several days. Anticoagulation treatment with low-molecular weight heparin was initiated and she was successfully discharged on hospital day 5 after switching to a direct oral anticoagulant (DOAC), rivaroxaban 15 mg every 12 hours.
Thrombophilia study for the patient showed the following results: PC 103 IU/dl (reference range 70–130 IU/dl), PS 75 IU/dl (reference range 70–130 IU/dl), and AT III 95% (reference range 80–120%), all levels within normal range. Lupus anticoagulant, anticardiolipin antibodies, and prothrombin G20210A gene mutation were negative. Homocysteine level was 6.59 μmol/L (reference range 4–15 μmol/L) and factor VIII level 164% (reference range 52–192%) were within normal range. Multiplex PCR was carried out using SNaPshot system to screen for FVL. Screening for FVL showed heterozygous mutation (1691G > A), confirming the diagnosis for massive VTE due to FVL mutation. The patient's family was counselled, and further investigations were done for the patient's father, mother, and brother. The patient's mother was found to have FVL mutation, but other family members were found to be normal (Fig. ).
Rivaroxaban was tapered down to a dose of 20 mg once daily after an initial 21-day course of higher dose therapy. Follow-up chest CT at 6 months of anticoagulation therapy showed no evidence of remnant pulmonary thromboembolism. After 12 months of anticoagulation therapy, rivaroxaban was discontinued. The patient is under close surveillance and has not had a subsequent thromboembolic event after discontinuation of rivaroxaban.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [116.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 116.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
2888,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6446015-1,Extracted,"A 67-year-old man was admitted with a fever and skin rash, which developed 2 days prior to admission. He had a previous history of diabetes and hypertension. He has been living in a rural area, and regularly works on his farm. On the physical examination, multiple erythematous macules on his neck, trunk, and both proximal extremities were observed and two pea-sized eschars were found on his left axilla and right upper abdomen (). There were no palpable masses suggesting lymphadenopathy around the eschars. The laboratory findings revealed a white blood cell count of 4,500/mm3, platelet count of 137,000 /mm3, and elevated liver enzyme (aspartate aminotransferase/alanine aminotransaminase 857/614 [IU/L]) and C-reactive protein (>8 mg/dL; normal range <0.5 mg/dL) levels. A serologic test for O. tsutsugamushi using an indirect immunofluorescence assay antibody was positive (quantitative value 1:80). Antibodies for the Hantaan virus and leptospira were negative. An electrocardiogram (ECG) revealed sinus rhythm (75 beats/min) with non-specific flattening of the T waves in the inferior leads. His clinical symptoms and laboratory findings gradually improved with oral doxycycline (200 mg/day), and he was discharged on the 5th hospital day. Oral doxycycline was additionally administered for 2 more days after discharge (7 days, totally).
One week after discharge, he was referred with a complaint of dyspnea for 3 days. His D-dimer level was elevated at 20.636 ug/ml FEU, and his troponin I and N-terminal pro brain natriuretic levels were normal. An arterial blood gas analysis on room air revealed the following: pH 7.45, partial pressure of carbon dioxide (PaCO2) 34 mmHg, partial pressure of oxygen (PaO2) 84 mmHg, and oxygen saturation 97.5%. A serologic antibody test for O. tsutsugamushi was markedly elevated at >1:10,240. His fibrinogen and protein C antigen levels had mildly decreased to 193 mg/dL (normal range, 200–400 mg/dL) and 69% (normal range, 72–160%), respectively. His antiphospholipid antibodies (immunoglobulin G [IgG] and IgM) were negative. An ECG revealed sinus rhythm (79 beats/min) without any definite change compared to the previous ECG. Chest computed tomography revealed multifocal contrast filling defects along both pulmonary arteries (). There was no evidence of deep vein thrombosis (DVT) on duplex ultrasonography of the lower extremities. On transthoracic echocardiography, the right ventricular systolic pressure was mildly elevated at 44 mmHg without any significant right ventricular dysfunction. The symptoms improved with anticoagulation using unfractionated heparin for 7 days and he was discharged with an oral non-vitamin K anticoagulant (rivaroxaban) on the 9th hospital day. A followed up serologic antibody titer on the day of discharge revealed the O. tsutsugamushi antigen level had decreased to 1:5,120.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [79.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 79.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 0.
The patient's Well's score for pulmonary embolism is 0."
2889,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8296797-1,Extracted,"A 20-year-old woman was admitted to the emergency room due to the second stage of labour on gravida two parity one 29 weeks of gestational age, singleton lives intrauterine, mother with superimposed pre-eclampsia with severe features and history of uncontrolled thyroid disease. Patient was diagnosed as hyperthyroidism since 5 years before admission, but never took adequate treatment. She had bad antenatal care and did only once visit to the midwife without any written data, but she was told that her blood pressure was high and given nifedipine 10 mg once per day without her taking the medicine. During this pregnancy, she had no history of screening for hyperthyroidism, neither does she took any medicine to lower her thyroid levels. The patient came to emergency room by herself due to regular contraction 6 hours before admission. The patient was in agitation state of consciousness, she had Glasgow Coma Score of 12 consisted of 3 for eye opening response score, 4 for verbal response score and 5 for motoric response score. Her blood pressure in the emergency room was 220/120 mm Hg, and her heart rate 156 times/min. She had fever with temperature of 38.4°C and an increased respiratory rate of 40 times/min with oxygen saturation 95% in room air.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [156.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 156.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2890,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5168471-1,Extracted,"An otherwise healthy 18-year-old woman was referred to our outpatient clinic because of a 2-week history of sore throat, high fever, and mild neck tenderness. Ten days before, she had been diagnosed with acute pharyngotonsillitis and had started a 7-day amoxicillin/clavulanic acid course (1 g bid), obtaining only partial relief of the throat pain. On examination, the patient was febrile (38.2°C); neck palpation revealed tender lymph nodes in the right anterior cervical chain. The tonsils were enlarged but not erythematous; breath sounds were diminished over the right lung base. Examination of the abdomen revealed slight splenomegaly. The diagnostic suspicion was oriented toward infectious mononucleosis and, after the collection of blood samples for laboratory tests, the patient was discharged home with the prescription of paracetamol. Laboratory tests showed neutrophilic leukocytosis (white blood cells count 11.56 × 109/L, neutrophils 93%), low platelet count (61.00 × 109/L), and elevated C-reactive protein (25.9 mg/dL). Serological tests for EBV, CMV, and HIV were negative. An unexpectedly high procalcitonin value (294 ng/mL) raised the suspicion of bacterial sepsis and elicited an urgent hospitalization in our internal medicine ward for diagnostic and therapeutic management. On presentation, the patient was alert, hypotensive (BP 100/60 mmHg), and tachycardic (115 bpm); body temperature was 38.7°C; respiratory rate was 17, with oxygen saturation of 97% on room air. A chest X-ray showed a faint retrocardiac opacity and raised the suspicion of a community acquired pneumonia. After drawing two sets of blood culture (aerobic, anaerobic), an empirical treatment with intravenous ceftriaxone and azithromycin was started. Two days later, the patient was still febrile and mildly lethargic, with toxic appearance. Blood cultures grew gram negative bacilli, and amikacin was added to ceftriaxone. The next day, Fusobacterium necrophorum, an anaerobic gram negative rod, was identified as responsible for the bloodstream infection, and the antibiotic treatment was changed to intravenous metronidazole and meropenem. Based on this microbiological finding, a neck ultrasound exam was performed, showing a nonoccluding parietal thrombosis of the right internal jugular vein. Diagnosis of Lemierre's syndrome was ultimately confirmed by a contrast enhanced CT scan of the neck and the thorax. This showed a small right parapharyngeal abscess, thrombosis of the right internal jugular vein (), and multiple peripheral lung nodules, expression of septic embolization (Figures , , and ). Anticoagulation with subcutaneous enoxaparin was prescribed (4,000 UI bid); subsequently, the patient was transferred to the High Dependency Unit for haemodynamic monitoring. Five days later, the body temperature became steadily normal and blood tests showed a sharp decline of procalcitonin (2.11 ng/mL) and C-reactive protein (2.3 mg/dL), an increase of platelet count (428.00 × 109/L), and the negativization of microbial cultures. The patient was discharged home after a 2-week course of intravenous antibiotic treatment. She received an outpatient oral treatment with metronidazole and amoxicillin/clavulanic acid for 14 days and a 3-month course of enoxaparin, experiencing an uneventful recovery. A control CT scan showed the complete resolution of lung opacities and pleural effusion (Figures , , and ).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [115.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 115.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2891,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6404278-1,Extracted,"A 69-year-old Filipino man with history significant for hypertension and hyperlipidemia presented to his primary care physician with hematuria with weight loss of 1 month’s duration. He did not have any flank pain, burning on urination, or increased urinary frequency. He did not endorse any symptoms of fatigue or night sweats. His only medication was atenolol for his hypertension. He did not smoke tobacco, drink alcohol, or do any recreational drugs. He was unemployed at time of interview. He did not have any family history of cancer. His vital signs were within normal limits. On physical examination, he was well appearing and in no acute distress. He had no palpable mass and had an otherwise normal cardiovascular, respiratory, and neurologic examination. Laboratory work showed normal cell counts and normal electrolytes; the results of his kidney and liver function tests were normal. A computed tomography (CT) – intravenous pyelogram was performed as a diagnostic work-up for his hematuria, which demonstrated a large mass in the left collecting system and proximal ureter. He was seen by urology with plans for surgical resection 1 month later. Three weeks later he was admitted to the Emergency Department with nausea and vomiting. He was tachycardic to 110 beats per minute but maintained a normal blood pressure. His laboratory results were notable for hemoglobin to 12.1. His sodium was 134. At that time, a CT scan of his abdomen and pelvis showed interval enlargement of the left renal mass. An ureteroscopy with biopsy was performed, which showed necrotic tissue with rare crushed degenerating atypical cells. A screening chest CT scan was also obtained which showed a small 3 mm nodule in the lower lobe of his left lung. A follow-up interventional radiology-guided left kidney biopsy showed a cellular neoplasm with sheets of pleomorphic round cells with hyperchromatic nuclei, irregular nuclear outlines, and inconspicuous nucleoli with scant and delicate cytoplasm which is consistent with SCC. The tumor cells were positive for the neuroendocrine markers synaptophysin and CD56 with focal staining for chromogranin and dot-like positive staining for cytokeratin (AE1/AE3), supporting the diagnosis of SCC (Fig. ). A bone scan did not show any metastatic lesions. Shortly afterwards, he developed dizziness and an MRI of his brain was obtained revealing a 1.6 cm partially hemorrhagic round mass with surrounding edema in the midline superior vermis potentially representing metastatic disease. An additional 4–5 mm hemorrhagic metastatic focus was seen in the right occipital convexity. The cerebellar mass was resected and probably represented a renal origin due to the absence of lung masses along with clinical and radiographic correlation. He was started on whole brain radiation therapy during his in-patient stay. An out-patient oncology referral was made but he was unable to establish care due to frequent hospitalizations. He had several hospital admissions for nausea and vomiting and continued to decline functionally. He developed chronic hyponatremia during these hospitalizations which were attributed to SIADH. He originally presented with sodium of 119 and was stabilized to a sodium level of 128 with the use of salt tablets. He declined chemotherapy when it was offered by the oncology team during in-patient consultation due to poor quality of life and functional status; he died within 8 months of presentation at his nursing facility. The cause of his death was unknown. An autopsy was not performed.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2892,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4593884-1,Extracted,"A 62 year-old-man suffering from obesity, diabetes mellitus, hyperlipidemia, and nonalcoholic liver cirrhosis was referred to the emergency department due to fever, chills, and progressive swelling of his left arm. The patient’s spouse mentioned that 36 hours prior to his admission he underwent acupuncture needle insertion along the anterior medial aspect and radial side of his left hand. The patient used to work as an assistant hatchery manager at an inland fish farm that cultivated fish for commercial use. The patient denied any injury prior to his illness. Thirty hours prior to his admission he complained of generalized weakness and fever. During the day prior to his admission his condition worsened rapidly with progressive swelling of his left arm. His physical examination upon hospital admission was remarkable for severe disorientation, his vital signs showed a blood pressure of 88/50 mmHg, 124 beats per minute, 38 breaths per minute, and O2 saturation at room air of 82%. The physical findings were suggestive of necrotizing fasciitis with severe edema, ecchymoses, hemorrhagic bullae, and progressive tissue necrosis of two fingers (). His laboratory studies were compatible with multi-organ failure with acute renal failure, rhabdomyolysis, disseminated intravascular coagulation, and elevated liver enzymes. The patient was treated with ceftriaxone, penicillin, and clindamycin pending culture results. The patient underwent surgical debridement with fasciotomy and amputation of 2 necrotic fingers within 24 hours of his arrival to the emergency department. Blood and wound cultures grew V. vulnificus. Antimicrobial susceptibility showed that the bacterium was susceptible to third-generation cephalosporins, fluoroquinolones, tetracyclines, aminoglycosides, and extended-spectrum penicillins. Clindamycin and penicillin were stopped and he was treated with ceftriaxone to complete two weeks of treatment. Biochemical and molecular characterization identified the bacterium as a biotype 3 strain, the main biotype responsible for human disease in Israel. In the first two weeks of his stay he received hemodialysis treatment for severe kidney failure with complete recovery of kidney function. During the 3rd week he suffered from septic shock. The patient was treated with meropenem, vancomycin, vasopressors, and mechanical ventilation. Blood cultures grew Pseudomonas aeruginosa that was susceptible to meropenem. The patient required skin grafts due to extensive skin loss and underwent tracheostomy due to failed weaning from mechanical ventilation. He also suffered from critical illness polyneuropathy. His condition improved gradually and after 72 days of hospital stay he was referred to a rehabilitation facility where he stayed for another 2 months.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [124.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 124.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 = 6.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 6.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
2893,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7358196-1,Extracted,"A 72-year-old Caucasian (white) man with a history of diffuse large B-cell lymphoma (DLBCL), immunoglobin M (IgM) monoclonal gammopathy of undetermined significance (MGUS), and chronic back pain secondary to osteoarthritis presented with dyspnea and a left pleural effusion. His social history was notable for a 60 pack-year cigarette smoking, and he had cut down to five cigarettes a day after diagnosis of non-Hodgkin’s lymphoma (NHL). He denied any significant past alcohol abuse, illicit drug abuse, or prescription drug abuse and reported consuming a beer or two on rare social occasions. Our patient was adopted so he is unaware of any past family history in regard to his parents. His brother has high blood pressure; otherwise he reported no other known malignancy or cardiopulmonary disease in the family. He worked as a mechanic and retired 20 years ago. He denied any known environmental exposures or allergies. Home medications included a daily probiotic, florastor 250 mg 2 tablets once daily, and acetaminophen/oxycodone – 325 mg/5 tablets once a day as needed for severe back pain. Our patient explained that he took opiate pain medication two to three times a week. Seven years prior, a bone marrow (BM) biopsy had revealed DLBCL, stage IVB, and he achieved complete remission (CR) with rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone (R-CHOP). Two years prior, he was diagnosed with monoclonal IgM kappa MGUS and BM biopsy revealed B-cell lymphoma with plasmacytic differentiation (10% of the marrow cellularity). The differential diagnosis at this time included LPL and marginal zone lymphoma. Given that he was asymptomatic at this time, he was monitored without treatment.
In the Emergency Department (ED), his vital signs were a pulse of 88 beats per minute, his blood pressure was 145/62, and temperature was 98.7 degrees Fahrenheit. His oxygen saturation was 95% on room air and he was mildly tachypneic with a respiratory rate of 24 breaths per minute. At physical examination, he appeared well, he was well nourished, awake, and in no apparent distress. An ear, nose, mouth and throat examination showed clear nasal mucosa and normal mouth mucosa. His head was atraumatic/normocephalic. His heart rate was normal, with a regular rhythm, heart sounds were S1, S2, and there were no murmurs, rubs or gallops. There were rales in his left lung base without wheeze or rhonchi. His abdomen was soft, non-distended, and non-tender. His lumbar spine showed a mild reduction in range of motion. He showed superficial bilateral inguinal lymphadenopathy. He was alert and oriented × 4, with no focal deficits, and no motor or sensory deficits. His CN II-XII were intact, extremities showed no cyanosis or edema, and his skin was dry, intact, with no rash. Our patient was given one ipratropium bromide/albuterol nebulizer treatment and two doses of morphine 1 mg for back pain. During the admission, our patient received tramadol 50 mg once for back pain and required no other medication. His complete blood count showed a white blood cell count of 6.2 × 109/L, hemoglobin of 13.8 g/dL, platelet count of 156 × 109/L with normal differential. The complete metabolic panel showed sodium of 141 mEq/L, potassium of 3.8 mEq/L, blood urea nitrogen of 18 mg/dL and creatinine of 1.0 mg/dL, glucose of 95 mg/dL, calcium of 9.2, albumin 3.8 g/dL, aspartate aminotransferase of 23 IU/L, and alanine aminotransferase of 32 IU/L, alkaline phosphatase of 46, and total bilirubin of 0.6. The urinalysis was within normal limits with no evidence of hematuria, pyuria, nitrates were not detected, and there were no bacteria. A computed tomography scan of his chest (Fig. ), abdomen, and pelvis showed layering left pleural effusion and para-aortic retroperitoneal lymphadenopathy extending to the iliacs and superficial inguinal nodes. Pleural fluid (PF) cytology was positive for malignant cells consistent with B-cell lymphoma and positive for MYD88 L265P mutation.
PF flow cytometry showed monoclonal kappa B-cell population with moderate CD19, CD20, CD22, and CD38 expression (Fig. ).
Inguinal lymph node biopsy showed lymphoplasmacytic, monoclonal B-cell population, CD20-positive, CD5-negative, CD10-negative B-cells, consistent with LPL/WM (Fig. ).
In comparison to his BM biopsy 2 years prior, the current study shows an increase in marrow involvement by B-cell lymphoma with plasmacytic differentiation. The findings in conjunction with IgM monoclonal paraprotein favor LPL, and the positive MYD88 L265P mutation analysis supports this impression. Congo red stain was negative for amyloid (Fig. ).
The pleural effusion recurred post-thoracentesis and 420 mg ibrutinib was initiated, but due to intolerance with nausea and vomiting, required a dose reduction to 240 mg. He achieved a lasting CR as defined by National Comprehensive Cancer Network (NCCN) guidelines []. Seven months after initial presentation to the ED, he remains in CR and is tolerating a reduced dose of imantinib without any side effects.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [88.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 88.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
2894,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6586102-1,Extracted,"A 29-year-old man with past medical history of Addison’s disease and hypothyroidism who recently relocated to the USA from Puerto Rico presented to the emergency department (ED) with chief complaints of fatigue, palpitations, and light headedness.
He was previously maintained on twice daily hydrocortisone and daily levothyroxine supplementation but had been off his medications for 5 days. He denied chest pain or shortness of breath. He also denied tremors, easy fatigability, weight gain, hoarseness of voice, or changes in bowel habit. Of note, he reported a childhood history of recurrent seizures due to hypocalcemia and had since been on calcium and vitamin D supplementation. He had no family history of autoimmune disease and review of systems was otherwise unremarkable. His knowledge about his medical condition was limited.
On physical examination, he was in no acute distress. He was hypotensive with BP 89/67 and tachycardic with pulse rate of 115 bpm. Other vital signs were normal. Chvostek sign was negative and there was no thyromegaly on neck palpation. Oral examination showed multiple hyperpigmented lesions on the dorsum of his tongue () and multiple deformed and pitting finger nails in both hands (). The remainder of the physical examination was unremarkable.
Basic metabolic panel revealed hyponatremia with Na 129 meq/L (136–145) and potassium of 4.8 meq/L (3.5–5.1). He was also severely hypocalcemia with ionized calcium of 0.96 mmol/L (1.15–1.33). Fasting blood glucose was normal. Thyroid function test showed elevated thyrotropin level at 5.807 uIU/mL (0.450–5.330) with normal free thyroxine level at 0.94 ng/dL (0.58–1.64). AM cortisol was markedly reduced at <1 mcg/dL (6.7–22.6). ACTH was markedly elevated at 785 pg/mL (7–69) and direct renin was also very elevated at 390 pg/mL (2.5–45.7). Parathyroid hormone was markedly reduced at <6 pg/mL (12–88). Complete blood count was normal, as was coagulation profile.
ECG also showed sinus tachycardia with no ischemic changes.
The patient was given intravenous saline and double his normal dose of his steroids. His levothyroxine dose was continued at 75 mcg daily while intravenous and oral calcium were given to correct hypocalcemia. His symptoms gradually improved, and he was discharged home on hydrocortisone 20 mg in the morning and 10 mg at night with fludrocortisone 0.1 mg daily and levothyroxine 75 mcg daily.
On follow-up in clinic 2 weeks later, patient was noted to be doing well. Patient education regarding medication adherence and stress dosing to avoid potentially life-threatening adrenal crisis and the importance of medic alert bracelets was reinforced. The patient was classified as having APS type 1 because of the presence of hypoparathyroidism, Addison’s disease, and chronic muco-cutaneous candidiasis, and promptly referred to the endocrinologist for continuity of care ().",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [115.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 115.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2895,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7934718-1,Extracted,"A 37-years-old pregnant woman, gravida 2 para 1, consulted our emergency clinic at 16 2/7 weeks of amenorrhoea for abdominal pain, which started 2 days before. Her pregnancy was spontaneously conceived. She was initially treated with cefuroxime prescribed by her gynaecologist who suspected cystitis, but failed to improve. In our service, she had problem of acute left pelvic pain irradiating to the back and left thigh. The patient denied having had vaginal bleeding, urinary or digestive symptoms. She did not have any relevant medical history, except for a normal vaginal delivery 16 months earlier.
On clinical examination, her heart rate was 84 beats/min, blood pressure was 100/55 mm Hg with a temperature of 37.3°C. The abdominal wall was tender without guarding nor rebound. On pelvic examination, there was a small quantity of blood in the vagina, and no adnexal mass was palpable on bimanual examination. The uterus was measured at 17 cm, as expected for the gestational age.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [84.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 84.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2896,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8482808-5,Extracted,"A 41-year-old African American male with no significant past medical history presented with complaints of fever, loss of appetite, myalgia, non-bloody, non-bilious vomiting, and shortness of breath for three days duration. On admission, his temperature was 98.9 ⁰F, BP 122/72, HR 87, RR 25, and saturating 87% on RA. Physical examination was notable for bilateral diffuse crackles throughout the lungs. CXR showed diffuse and patchy bilateral infiltrates. CT scan showed bilateral multi-lobar peripheral dominant ground-glass opacities (Figure ). Both SARS-CoV-2 antigen and RT-PCR were tested positive. Rapid influenza B antigen was also positive. His inflammatory markers were elevated. He was transferred to the intensive care unit for increasing oxygen requirements. He required mechanical ventilation and was also started on pressor support due to hypotension. His blood culture was positive for fusobacterium necrophorum caused by dental erosion as seen on the physical examination. He was given ceftriaxone and metronidazole for five days. He received remdesivir for five days, dexamethasone for 10 days, and oseltamivir for 10 days. He also received convalescent plasma for COVID 19. He developed multiorgan failure in the ICU with worsening renal and liver function. The patient expired due to cardiac arrest on the 20th day of admission.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [87.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 87.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2897,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-9796,Extracted,"A 59-year-old patient comes to the emergency department accompanied by his wife because of severe right leg pain and numbness. His condition suddenly started an hour ago. His wife says that he has a heart rhythm problem for which he takes a blood thinner, but he is not compliant with his medications. He has smoked 10–15 cigarettes daily for the past 15 years. His temperature is 36.9°C (98.42°F), blood pressure is 140/90 mm Hg, and pulse is 85/min and irregular. On physical examination, the patient is anxious and his right leg is cool and pale. Palpation of the popliteal fossa shows a weaker popliteal pulse on the right side compared to the left side.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [85.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 85.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 3.
The patient's Well's score for pulmonary embolism is 3."
2898,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-1609,Extracted,"A 22-year-old man comes to the physician because he has been increasingly worried and stressed in recent weeks. He started a marketing job three months ago, which involves traveling between Washington and California several times a year. Two months ago, he was supposed to fly to Seattle, but he experienced nausea, palpitations, sweating, and shortness of breath and was unable to board the plane, causing him great embarrassment. He had never been on a plane before; his parents died in a plane crash when he was younger. A week ago, he called in sick when he was supposed to go on a business trip. He worries that he will lose his job. He is otherwise well and has no history of serious illness. He takes no medications. His temperature is 37.2°C (99°F), pulse is 85/min, respirations are 12/min, and blood pressure is 130/80 mm Hg. Physical examination shows no abnormalities. On mental status examination, he is alert and cooperative. His speech is normal and his thought process is organized. His memory, attention, and concentration are intact.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [85.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 85.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2899,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8187023-1,Extracted,"A 25-year-old male with American Society of Anesthesiologists class III physical status and body mass index (height 167 cm, weight 65 kg) 23.3, was admitted for surgery for squamous cell carcinoma (SCC) of tongue.
The patient had been diagnosed with hemophilia 15 y ago. The previous medical history had no other abnormalities. Three months before being admitted, the patient had visited another hospital with complaints of intense pain on right tongue lesion. The patient had severe hemophilia A and required red blood cell transfusion because of bleeding after a swap test and incisional biopsy. The bleeding stopped within 30 min following an injection of factor VIII concentrate. Histological examination of the swab specimen revealed an atypical squamous cell carcinoma. The patient was then transferred to the Oral and Maxillofacial Surgery Department, Seoul National University Dental Hospital for surgery.
On examination using CT and MRI, an ulcerative lesion of 2.9 × 1.5 cm sized was seen on the right mid posterolateral border of tongue (). On clinical examination, the tumor showed endophytic growth, and the depth of the ulcer was >10 mm. Enhanced computational tomography (CT) image () revealed the depth of invasion to be 19 mm, and a suspicious metastatic lymph node was observed on the right level IIa. Due to swab test, there was prolonged bleeding and oozing on the swab site. The Human papillomavirus (HPV) infection status was tested using intraoral mucosal swab and the result showed HPV16 (−), HPV 18 (−), other high risk (−). After the swab test at the outpatient department, as hemostasis was not achieved the patient was moved to the day-surgery unit. Hemostasis was then achieved by application of bipolar electrocauterization, Surgicel® (Ethicon SARL, Puits-Godet 20, Swizerland) (oxidized regenerated cellulose); gauze biting was also performed. After discharge, factor VIII concentrate injection was needed again due to the swab site bleeding. The patient was scheduled to undergo partial glossectomy, selective neck dissection, and reconstruction with a lateral arm free flap.
A preoperative electrocardiogram (ECG) showed normal sinus rhythm and the chest radiography was unremarkable. Preoperative hemoglobin (Hb), hematocrit (Hct), and platelet count was 10.5 g/dl, 32.1, and 401 × 103/µl respectively. The coagulation profile showed that the prothrombin time (PT) international normalized ratio (INR) was 0.95, which was within the normal range of 0.8 to 1.2, and the activated partial thromboplastin time (aPTT) was 48.3 s, which was longer than the normal range of 26.7 to 36.6 s. The activity of coagulation factor VIII was reduced by 11%.
According to the answers of the consultation with the Hematology Department at Seoul National University Hospital, the patient was preoperatively injected with monoclonal antibody-purified factor VIII concentrate (GreenMono®, GC Pharma, Yongin, Republic of Korea, 2892 International Unit [IVS]) 1 h before the surgery. Twelve hours after the initial injection, another injection of the same amount of GreenMono® was administered. Thereafter, the injection was administered at every 12 h interval. Considering the extent of reconstructive surgery, the administration was recommended for 7 to 14 d so as to achieve sufficient hemostasis. In case of insufficient hemostasis after the injection of GreenMono®, 500 mg of tranexamic acid was recommended every 8 h.
General anesthesia was induced after routine monitoring (pulse oximetry, end-tidal CO2, ECG lead II with continuous ST-segment analysis, and noninvasive blood pressure monitoring) in the patient. His preoperative blood pressure (BP) was 121/65 mmHg, heart rate (HR) was 102 beats/min, body temperature was 36.1℃, and oxygen saturation (SpO2) was 100%. After sufficient preoxygenation, anesthesia was induced with lidocaine (30 mg), propofol (120 mg), and cisatracurium (16 mg). Nasotracheal intubation with an endotracheal tube (right angle endotracheal tubes, cuffed, 7.0 mm) was performed using fiberoptic bronchoscopy. Anesthesia was maintained with an O2/air mixture (fraction of inspired oxygen 50%) and adjusted for desflurane (4.5–8% vol). The patient was maintained on volume-controlled mechanical ventilation with a mean arterial pressure of 60–80 mmHg for a normal and regular heart rate. An additional neuromuscular blocker was administered, as needed. The tidal volume was 6–8 ml/kg, and positive end-expiratory pressure (5 cmH2O) was utilized. The respiratory rate was adjusted to maintain the partial pressure of end-tidal CO2 at 30–35 mmHg. Invasive BP monitoring and arterial blood gas analysis (ABGA) were performed with the catheter in the left dorsalis pedis artery. ABGA was performed every two hours after the surgery began ().
Non-invasive continuous monitoring of total hemoglobin (SpHb; Masimo, Irvine, CA, USA) was also performed. Though this is not as accurate as the laboratory hemoglobin, it is used to identify relative numerical changes due to the serial measurements obtained. The initial value was 11.1, and 10.1 was the lowest value measured.
Central catheterization of the right femoral vein was performed to gain venous access because of the known bleeding tendency. During the reconstruction procedure, when the systolic blood pressure dropped to less than 120 mmHg, ephedrine 5–10 mg was injected twice, followed by dopamine, which was continuously injected for 275 min at a rate of 3.2–10 mcg/kg/min. This permitted maintaining the systolic blood pressure of 130–150 mmHg.
The routine surgical field was draped with povidoneiodine in the orofacial and neck areas. The tongue lesion was grossly marked with a surgical marking pen. Partial glossectomy was performed for a 1 cm safety margin (). Muscular bleeding during partial glossectomy was controlled using bipolar electrocautery. Frozen biopsies were performed around the marked margin. While waiting for the biopsy result, selective neck dissection was initiated. The internal jugular vein, carotid artery, vagus nerve, and spinal accessory nerves were isolated and preserved. Right levels I, II, III, and IV lymphatic chains were resected (). Meticulous bleeding control was performed using electrocautery, vascular tying, and collagen sponge. The right side of the retromandibular vein branch and facial artery were isolated for vessel anastomosis. After confirmation of negative frozen biopsy results, lateral arm fasciocutaneous free flap harvesting was initiated. Skin incision and subcutaneous dissection were performed up to the junction of the radial collateral arteries. The branch and veins of the distal part of the posterior radial collateral artery were clamped and cut. The lateral arm fasciocutaneous free flap was transferred to the tongue to fit the defective region. The flap inset was closed with 4-0 Dafilon. Vessel anastomosis was performed using a microscope. The anastomosis of the posterior radial collateral artery with the facial artery and that of vena comitans with the retromandibular vein branch was performed via the end-to-end mode (). All surgical sites were closed layer by layer, and the surgery was completed by suction drain and pressure dressing.
The surgery was uneventful. At the end of the surgery, 125 mg of methylprednisolone mixed with 50 ml of normal saline was injected. The total anesthesia time was 535 min, and the total surgery lasted for 500 min. During the operation, 5500 ml of crystalloid was administered and the total urine output was 2350 mL. The estimated blood loss was 400 ml. Following recovery at recover room for 40 minutes in the intubated state, the patient was transferred to the intensive care unit (ICU) and after 11 h, was transferred to the recovery room for extubation. The oxygen was supplied as 5 L/min through the T-piece. Oral and endotracheal tube suction was performed with routine monitoring. During the leakage test, the oxygen saturation was maintained at 99%. After extubation, the patient was monitored, and oxygen support by a reservoir bag mask was provided.
Monoclonal-antibody-purified Factor VIII Concentrate (GreenMono®) 6000IU (3000IU Bis in die, bid) was used on the day of surgery. From the first postoperative day (POD) and up to the next 15 days, 3000 U (1500 U bid, 8:30am, 8:30pm) were administered daily and then discontinued. On POD 18, a total of 1500 IU of GreenMono® was used before and after dental scaling, #26 distal caries resin restoration, #28, and #38 surgical extraction. No additional hemostatic agents, such as tranexamic acid, were used. Following administration of GreenMono® after the surgery (), the aPTT level was rarely out of the normal range, and there were no bleeding-related symptoms or complications. The patient was discharged without any postoperative complications on POD 25.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [102.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 102.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3.0 + 1 =  4.0.
The patient's Well's score for pulmonary embolism is 4.0."
2900,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8301283-1,Extracted,"An 82-year-old male presented to ED with sudden onset of drowsiness and hypotension. Previous medical history was significant for hypertension, dyslipidaemia, obesity, liver steatosis, benign prostatic hyperplasia and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection two months earlier. Current medication included furosemide, clopidogrel, perindopril, indapamide, metformin, silodosin, and iron.
At admission, the patient was normotensive (blood pressure (BP): 115/70 mmHg), but tachycardic (heart rate (HR): 120 bpm); had a respiratory rate of 22 cpm and showed signs of poor peripheral perfusion. He had otherwise normal cardiac and pulmonary examination, no signs of deep venous thrombosis such as unilateral leg swelling or calf tenderness. Arterial blood gas (ABG) revealed respiratory alkalemia, hypoxemia and hyperlactacidemia (pH 7.50, pCO2 29mmHg, pO2 48mmHg, SatO2 87%, lactate 3.8mmol/L). He started fluid-challenge and oxygen therapy, while further workup was ordered.
On re-evaluation, his BP dropped (70/41 mmHg), maintained tachycardia (110 bpm) and hypoxemia (pO2 50 mmHg). Electrocardiography showed sinus tachycardia with 120bpm.
Bedside ultrasound was performed showing right ventricular (RV) overload, severe systolic disfunction and free wall hypokinesis with apical sparing on echocardiography (McConnell sign) (Video ).
A subsequent computerized tomography pulmonary angiogram (CTPA) was obtained confirming bilateral massive pulmonary emboli and infarction of superior lobe of the left lung. Laboratory workup was significant for high troponin 3056.16 ng/L (range 37.50-80.35), N-Terminal Pro-Brain Natriuretic Peptide (NTproBNP) concentration 1778 pg/mL (ref range <125 pg/mL), D-dimer 17436 ng/mL (range 45.0-250.0).
He started fibrinolytic treatment with alteplase 100 mg over two hours and norepinephrine.
He was admitted to the coronary intensive care unit.
Twenty-four hours later his systolic blood pressure (SBP) was 105-120 mmHg, HR 75 bpm and lactates 1 mmol/L. Bedside ultrasound showed no right heart overload, tricuspid annular plane systolic excursion 20 mm, good left ventricle systolic function and no inferior vena cava (IVC) distention with inspiratory collapse.
He was discharged 11 days later with hemodynamic stability, with no dyspnea on exertion or hypoxemia.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2901,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,trec-ct-2021-21,Extracted,"The patient is a 57-year-old man with abdominal pain and vomiting. The pain started gradually about 20 hours ago in the epigastric and periumbilical regions, radiating to his back. He drinks around 60 units of alcohol per week and smokes 22 cigarettes per day. He is healthy with no history of allergies or using any medications. His family history is positive for type 2 diabetes (his father and sister). He lives alone and has no children. The abdomen is tender and soft. His bowel sounds are normal. His heart rate is 115/min and blood pressure 110/75 mmHg. The lab results are remarkable for leukocytosis (19.5), urea of 8.5, high CRP (145), high amylase (1200) and Glc level of 15. Cross-sectional imaging was negative for obstructive pancreatitis.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [115.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 115.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2902,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-7121,Extracted,"A 67-year-old man comes to the office due to pain in the lower part of his calves on his afternoon walk to get the mail. The pain is relieved by rest. It started slowly about 6 months ago and has become more painful over time. He has a history of hypertension, hyperlipidemia, diabetes mellitus, and smoking. Medications include hydrochlorothiazide, atorvastatin, metformin, and a multivitamin that he takes daily. The patient does not smoke and only drinks socially. Today, his blood pressure is 145/90 mm Hg, pulse is 75/min, respiratory rate is 17/min, and temperature is 37.6°C (99.6°F). On physical exam, he appears mildly obese and healthy. His heart has a regular rate and rhythm, and his lungs are clear to auscultation bilaterally. Examination of the legs shows atrophic changes and diminished pedal pulses. A measure of his ankle brachial index (ABI) is 0.89.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [75.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 75.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 3.
The patient's Well's score for pulmonary embolism is 3."
2903,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5941729-1,Extracted,"A 70-year old female with cigarette smoking history of 50 pack years, presented with chronic cough and weight loss. CT scan of chest demonstrated a 4.7-cm right lower lobe lung mass. She was subsequently diagnosed with Stage Ib adenocarcinoma of lung and received right lung resection. Eighteen months later she developed recurrent disease in the lung and was treated with concurrent chemoradiation. Afterwards, she progressed with metastatic subcarinal, mediastinal and hilar lymphadenopathy. PET-CT and MRI of brain did not reveal extra-thoracic metastasis. Patient underwent biopsy of the mediastinal mass, which confirmed metastatic adenocarcinoma. There was no mutation in epidermal growth factor receptor gene, or translocation in anaplastic lymphoma kinase gene in her tumor. She progressed through several lines of treatment including paclitaxel plus carboplatin then vinorelbine alone. Thereafter she was referred to medical oncology clinic of our cancer center, and nivolumab treatment was recommended.
Four days after her first dose of nivolumab, patient presented with acute shortness of breath and chest pain. Initial work up, including infectious, was unremarkable except for mildly elevated creatinine kinase of 40 mg/dl. Electrocardiogram showed sinus tachycardia with heart rate of 124 beats/min, blood pressure was 98/55 mm Hg and patient was afebrile. A CT angiography of chest showed no pulmonary embolism or pneumonitis but new-onset large pericardial effusion of 2.4 cm thickness (Fig. ). Patient was admitted to cardiology service, transthoracic echo confirmed large pericardial effusion; posteriorly 2.1 cm, anteriorly 1.6 cm without features of tamponade. Patient was started on colchicine and fluid resuscitation for her hypotension, with symptomatic improvement. Follow-up echocardiogram showed persistent pericardial effusion. Given unclear etiology of her pericardial effusion and likely immune-related adverse event (irAE) of nivolumab, patient was started on prednisone 1 mg/kg/day. She continued to receive nivolumab treatment every 2 weeks. Follow up echocardiogram and computed tomographic scan (Fig. ) after 4 weeks showed complete resolution of pericardial effusion and her prednisone was slowly tapered off. One week after her prednisone was discontinued, she presented again with sub-sternal chest discomfort, shortness of breath and bilateral ankle edema. Echocardiogram showed recurrence of moderate to large pericardial effusion measuring 2.8 cm posteriorly and 1.2 cm anteriorly without tamponade. She was hospitalized for observation of any hemodynamic instability. Her recurrent pericardial effusion was likely irAE from nivolumab, hence nivolumab treatment was stopped and patient was started on prednisone 1 mg/kg/day. Significant clinical improvements was noted and follow up echocardiogram after 3 weeks showed complete resolution of her pericardial effusion. Nivolumab was resumed 1 week after while maintaining patient on low dose prednisone. Patient tolerated nivolumab well and a follow up echocardiogram 4 weeks later did not show any recurrence of pericardial effusion. The timeline of nivolumab treatment related to the development of pericardial effusion and the use of steroid is depicted in Fig. .",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [124.0, 'beats per minute'], 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Previously documented Deep Vein Thrombosis': False}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 124.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3.0 + 1 =  4.0.
The patient's Well's score for pulmonary embolism is 4.0."
2904,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4043629-1,Extracted,"A 44-year-old male patient was admitted to a local hospital one week subsequent to first presenting with symptoms of dyspnea and shortness of breath accompanied by dizziness, without severe chest pain, amaurosis or syncope. The electrocardiogram (ECG) demonstrated acute anteroseptal, right ventricular myocardial infarction, ventricular escape and a third degree atrioventricular block (AVB; ). Echocardiography showed mild mitral regurgitation and indicated that the cardiac structure, systolic function and wall motion were without abnormalities. The left ventricular ejection fraction was 65%, and the levels of troponin (Tn) were significantly increased. The patient was treated with an antiplatelet agent, an anticoagulant agent, vasodilators and a plaque stabilizer, and was transferred to the Northern Jiangsu People’s Hospital (Yangzhou, China) upon stabilization of the condition. The patient had previously been healthy, with a history of smoking (smoking index, 20 packs/year), but no history of hypertension, diabetes, hyperlipidemia, alcoholism or coronary heart disease. Furthermore, the patient had no recent history of upper respiratory tract infection or gastroenteritis virus.
The results of the physical examination of the patient were: Body temperature, 36.5°C; heart rate, 62 bpm; respiratory rate, 18 breaths/min; and blood pressure, 120/70 mmHg. The patient was conscious, exhibited no lip cyanosis and had a soft neck with no jugular vein engorgement. Clear breath sounds were heard from both lungs, with no rales and the patient exhibited a negative hepatojugular reflux. In addition, no abnormal precordial bulge was observed and the apex beat was at the fifth intercostal space, 0.5 cm medial to the left midclavicular line. The heart rate was regular. No pathological murmurs or pericardial friction rubs were identified on auscultation and the patient was negative for any peripheral vascular signs. The abdomen was soft, with no tenderness or rebound tenderness, and no pitting edema was observed on either of the lower extremities.
The Tn level was 0.053 ng/ml (normal range, 0–0.034 ng/ml). Urinalysis, thyroid function, liver and kidney function were normal, as were the levels of blood glucose, blood lipids and electrolytes. Four days following admission to hospital, coronary angiography was conducted. This revealed normal openings and a running area without calcification in a right-dominant type coronary system in which: the left main coronary artery was without stenosis and had a forward flow of thrombolysis in myocardial infarction (TIMI) level 3; the left anterior descending had no significant stenosis and a forward flow of TIMI level 3; the left circumflex had no significant stenosis and a forward flow of TIMI level 3; the first obtuse marginal openings had visible plaques and a distal blood flow of TIMI level 3; and the right coronary artery had no significant stenosis, a forward flow of TIMI level 3 and no collateral circulation. On the basis of the imaging results, the diagnosis was coronary atherosclerosis. Six days following admission to hospital, the cardiac MRI revealed small, long T2 signals on the left anterior ventricular wall, which indicated slight edema (). The patient was prescribed bed rest to improve myocardial metabolism, traditional Chinese medicine to alleviate heart qi deficiency, and symptomatic treatment. The repeat ECG at 1 week after patient discharge was identified to be normal () and the symptoms of the patient had improved. Therefore, the patient was discharged.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [62.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 62.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2905,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7944024-1,Extracted,"A previously healthy 30 years old man, with no medical history, was admitted to the emergency room after a car accident: rollover by his car.
The physical examination on his admission was as follows: hearts rate of 145 beats/minute, blood pressure of 80/30 mmHg, with no signs of external bleeding, medullar trauma or limb fracture, the respiratory rate was 25 cycles/min, and pulse oximetry 75% on ambient air, 85% on high concentration mask with ronchis on the right side. The Glasgow Coma Scale GCS was 10/15 (eyes opening response 2/4, verbal response 3/5, and motor response 4/5) with contracted pupils, and no localization signs.
At this moment a decision to put the patient on mechanical ventilation was taking with inspiratory fraction of oxygen at 100%, tidal volume og 6 mL/kg and pression end expiratory pressure at 3mBar, with pulse oximetry at 93%.
The complete blood count showed the following: hemoglobin 12 g/dl, platelets 350000/mL, prothrombin time 80%, fibrinogen 3.5 g/l, white blood cells 7500/mL, eosinphils 55%, normal renal function : creatinine 0.8 mg/dl, urea 0.30 g/L.
After hemodynamic stabilization by fluid restitution with 500 mL of saline serum, and introduction of norepinephrine 1 mg/h, the full-body computerized tomography CT scan was performed, and it showed no internal bleeding, pneumothorax or medullar trauma, and showed on the thoracic level where it showed a well limited rounded formation of regular contours containing a hydro-aeric level related to a ruptured hydatid cyst ().
After ruling out the possibility of a hemorrhagic, hypovolemic shock, the diagnosis of anaphylactic shock due to post-traumatic rupture of hydatid cyst was maintained, norepinephrine was switched with epinephrine with a dose of 2 mg/h, and we gave him 500 mg of hydrocortisone with improvement in the hemodynamic state.
The patient was admitted to the operating room the next day for cyst removal by open thoracotomy ().
In the postoperative period, Albendazole was started with a dose of 400 mg/day.
The evolution was favorable; he was extubated in the immediate post-operative period and referred to the thoracic department.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [145.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 145.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2906,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7793183-1,Extracted,"We describe the case of a 79-year-old woman, with a history of atrial fibrillation, who had undergone left atrial appendage (LAA) closure device implantation due to contraindication for anticoagulation because of a previous subdural haemorrhage. She was admitted for elective mitral valve replacement due to asymptomatic severe primary mitral regurgitation caused by anterior veil prolapse. An echocardiogram performed a month before showed a left ventricular ejection fraction (LVEF) of 56% and normal LV diameters. CT-angiography prior to surgery showed absence of coronary lesions. On admission, cardiac auscultation revealed a systolic murmur in mitral focus at the apex. Lung auscultation was normal. Prior to the surgery, the patient was on acetylsalicylic acid 100 mg/day. Cardiac surgery was uneventful. Since valve repair was not considered feasible, a Magna Ease biological mitral valve was implanted, maintaining the LAA closure device. Intra-operative transoesophageal echocardiography showed normal functioning of the prosthesis and extracorporeal circulation was concluded. Only low doses of noradrenaline (0.05 μg/kg/min) were required after extracorporeal circulation.
On arrival to the intensive care unit (ICU), the patient presented with cardiogenic shock: she presented cold extremities and oliguria, systolic blood pressure was 80 mmHg and blood analysis showed metabolic acidosis and elevated serum lactate; therefore, requiring vasoactive agents (noradrenaline at 0.1 μg/kg/min and dobutamine at 5 μg/kg/min). An electrocardiogram (ECG) revealed atrial flutter with a rapid ventricular rate (150 b.p.m.), which was electrically cardioverted. An ECG performed after cardioversion showed inverted T waves in precordial leads () and pulmonary congestion was evidenced on chest X-ray (). The findings of an echocardiogram showed severe LV dysfunction (LVEF 20%) with mid to distal diffuse hypokinesia that was more severe in the anterior and septal walls, which were almost akinetic. Contractility was much better in all basal segments (, Video S). Mitral prosthesis function was normal. Owing to a suspected coronary complication secondary to cardiac surgery, the patient underwent urgent coronary angiography, which showed absence of significant coronary lesions (, Video S). Troponin I levels were elevated to 0.12 ng/mL (normal value <0.08). Her haemodynamic status was compromised for the following 48 h, during which time vasoactive drugs (noradrenaline ranging from 0.1 to 0.2 μg/kg/min and dobutamine ranging from 5 to 7 μg/kg/min, adjusted to haemodynamic status) and intra-aortic balloon counterpulsation were needed. Daily echocardiographic evaluations showed similar images that resembled the first one, with severe LV dysfunction and regional WMA in the mid to distal segments. After 48 h, the haemodynamic status of the patient suddenly improved, leading to progressive suspension of supportive measures; echocardiography at 48 h showed partial recovery of LV systolic function, with an LVEF of 45–50% and mild paradoxical septal motion (, Video S). The electrocardiographic changes also reverted (). Altogether, the clinical picture of the patient was interpreted as a stress cardiomyopathy occurring in the postoperative period of mitral valve replacement surgery. After 1 week, the patient was discharged. Treatment at discharge was acetylsalicylic acid 100 mg/day. One month later, she was asymptomatic and had low to normal LVEF (50%).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [150.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 150.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2907,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8165845-1,Extracted,"A 14-year-old girl presented to the Endocrinology Department of the First Affiliated
Hospital of Xi'an Jiaotong University with palpitations, chest tightness, and
shortness of breath that developed during military training. The patient was an
apparently normal girl when she was delivered at full-term. Her parents are
non-consanguineous, and her mother had no history of taking medications during
pregnancy that could cause fetal malformations. There was no family history of
chronic illnesses, including hypertension.
Physical examination showed that the patient was 171 cm tall with a weight of 75 kg
and a body mass index (BMI) of 25.65 kg/m2. Her blood pressure, pulse,
and respiratory rate were 160/100 mmHg, 74 beats/minute, and 18 breaths/minute,
respectively.
The patient had Tanner stage II breast development and female infantile external
genitalia with a hymenal ring and vaginal dimples. Results of laboratory evaluations
are given in .
Laboratory analysis revealed normal levels of potassium and aldosterone. Plasma
adrenocorticotropic hormone (ACTH) was markedly elevated, cortisol was at the lower
limit of normal, and levels of follicle-stimulating hormone (FSH), luteinizing
hormone (LH), and progesterone were increased. Levels of testosterone,
dehydroepiandrosterone sulfate (DHEAS), and estradiol were substantially decreased.
Dual-energy X-ray absorptiometry indicated that the patient had low bone mass (Z
score: −3.7).
Trans-abdominal pelvic ultrasound revealed the cryptorchidism in the bilateral
inguinal region and the absence of a uterus and ovaries. A computed tomography scan
of the adrenal glands showed thickening of the left adrenal junction ().
After detailed physical examination and laboratory evaluations, diagnoses of renal
hypertension, primary aldosteronism, pheochromocytoma, Cushing’s syndrome,
hyperthyroidism, and pseudoaldosteronism (Liddle syndrome) were excluded, and the
patient received treatment for hypertension of nifedipine controlled-release tablets
30 mg three times per day.
Because the karyotype of the patient was 46,XY and cryptorchidism was found, the
patient was referred to the urology department for bilateral cryptorchidectomy with
a diagnosis of “abnormal sexual differentiation, grade 3 hypertension (low risk).”
After surgery, she attended the gynecological endocrine clinic for sex hormone
replacement therapy.
Considering the high levels of plasma FSH, LH, and progesterone; low levels of
estradiol, testosterone, and DHEAS; the physical examination results; and the
history of hypertension, a diagnosis of 17OHD was made. Genetic testing results
showed a heterozygous mutation of CYP17A1 gene: c.1169C>G (p.
Thr390Arg), c.985_987delTACinsAA (p. Tyr329fs). Because her BMI was 25.65
kg/m2, a glucose tolerance test and insulin release test were
performed, and the results indicated hyperinsulinemia. Therefore, the final
diagnosis was (1) congenital adrenocortical hyperplasia 46,XY 17OHD, (2)
hyperinsulinemia, (3) vitamin D deficiency, and (4) low bone mass.
Following consultation with the patient and her parents, the decision was made to
maintain the female gender identity. The patient received estrogen replacement
therapy to promote development of secondary sexual characteristics, prevent
osteoporosis, and improve long-term outcomes.
Under the guidance of endocrinologists, oral hydrocortisone was prescribed to inhibit
abnormally elevated ACTH, reduce aldosterone secretion, and decrease blood pressure
(hydrocortisone: 20 mg and 10 mg at 8:00 am and 4:00 pm, respectively). Calcium
carbonate D3 was given to supplement vitamin D and calcium levels. The
patient was regularly followed by the gynecology, endocrinology, and orthopedics
departments. One month later, the hydrocortisone dosage was reduced (10 mg at 8:00
am and 4:00 pm).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [74.0, 'beats/minute'], 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 74.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2908,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8383679-1,Extracted,"A 68-year-old man presented with constant non-radiating chest tightness that was relieved with nitroglycerin. No cough, shortness of breath, or hemoptysis were noted. He had history of diabetes mellitus, hypertension, chronic kidney disease, peripheral vascular disease and stage IV lung cancer (cT2, N0, M1) with metastases to the left jugular lymph nodes. On examination, temperature was 37.5 °C, oxygen saturation was 94% on room air, respiratory rate (RR) was 19/min, heart rate (HR) was 80 beats per minute (bpm) and BP was 114/52 mm Hg. Chest, abdominal and cardiovascular examinations were unremarkable. No lower extremities edema was noted. Five days prior to presentation, patient received gemcitabine 2,280 mg and vinorelbine 57 mg. EKG showed ST-segment depression in leads V3-V5. Serum troponin I was 21.6 ng/mL, total white blood cell count (TWBC) was 5,600/µL, hemoglobin was 9.2 g/dL, platelet count was 161,000/µL, serum potassium (K) was 4 mEq/L, serum magnesium (Mg) was 2.3 mg/dL and serum creatinine was 2.2 mg/dL (estimated glomerular filtration rate (eGFR) was 40 mL/min (baseline creatinine 1.3 mg/dL)). Chest X-ray was normal. The patient was admitted to the intensive care unit (ICU) with a working diagnosis of non-ST-segment elevation myocardial infarction (NSTEMI) and managed with aspirin, clopidogrel, metoprolol, simvastatin and heparin bolus followed by infusion (due to reduced GFR). Chest pain resolved with medical treatment and troponin I trended down to 4.98 ng/mL over 3 days. No invasive revascularization (percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG)) was done and gemcitabine and vinorelbine were held for 3 weeks.
For a 1-month period, the patient remained chest pain-free for 1 month, thereafter, a second cycle of gemcitabine was administered, followed by a third cycle 1 week later. Four days after receiving the third cycle of gemcitabine, he was found somnolent and confused, in atrial fibrillation (AF) with rapid ventricular response, and HR of 150 bpm. He was found to have significant neutropenia, septic shock, severe acute kidney injury and significant lactic acidosis. He then had cardiac arrest with pulseless electrical activity and passed away.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
2909,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6673679-1,Extracted,"A 66-year-old female patient sought medical care complaining of pain and numbness in the extremities for 1 month, which progressed to lower limb weakness preventing her from walking. Her family also referred some episodes of mental confusion. Initial laboratory workup included total blood cell count, which showed normal erythrocyte and platelet counts, but leukocytosis (white blood cell count = 21.200/mm3 (reference value [RV]: 5,000–10,000 leukocytes/mm3) with marked eosinophilia (28% of eosinophils, RV: < 5%). Serum determination of glucose, TSH, free T4 and vitamin B12 were normal. Serology for HIV, HTLV I and HTLVII were negative. The chest x-ray was normal. The lumbar spine computed tomography (CT) showed degenerative changes. The electroneuromyography (EMG) showed subacute peripheral neuropathic process with motor and sensory impairment: severe distal axonal sensory impairment was predominant in upper and lower limbs; and severe proximal, middle, and distal axonal motor involvement in the left upper limb and was more pronounced in the lower limbs and right upper limb.
During ambulatory diagnostic investigation, the patient came to the emergency service complaining of diffuse abdominal pain with nausea and vomiting associated with skin lesions that appeared on her hands and feet. Physical examination showed an ill-looking patient, presenting mental confusion (coma Glasgow scale = 14) with blood pressure of 167/100 mmHg, a pulse rate of 120 beats per minute (bpm), and room air oximetry of 99%. Thoracic and abdominal examinations were unremarkable. Muscle strength was grade III/IV in the upper limbs (predominantly distal), and grade I in the lower limbs. The skin showed the presence of livedo reticularis over the trunk and palpable purpura on the tips of the toes and hands. Slight lower limb edema was present. Medical past history included hypertension, asthma, and allergic rhinitis regularly medicated. With these clinical features, the diagnosis of systemic vasculitis, most probably Eosinophilic Granulomatosis with Polyangiitis (formerly Churg- Strauss Syndrome) (EGPA) was considered, and the patient was hospitalized and prescribed a single dose of ivermectin before daily prednisone 60 mg, followed by ceftriaxone because of a suspected infection. The laboratory workup is shown in .
The anti-neutrophil cytoplasmic antibody ANCA (ELISA) was positive to myeloperoxidase (MPO) and negative to PR3. ANA was positive until titration of 1/160 showing a nuclear centromeric pattern, and complement fractions C3 and C4 were normal. Serology for hepatitis B, hepatitis C, and syphilis were negative. Cerebrospinal fluid examination revealed a colorless sample with 1 leukocyte and 26 red blood cells, protein of 28.8 mg/dL (RV: 30-40 mg/dL), glucose of 61 mg/dL (concomitantly with normal glycemia), and a negative Pandy reaction. The culture of blood samples, urine, and cerebrospinal fluid (CSF) were negative for bacterial growth. The urinalysis showed proteinuria; occult blood, leukocyturia; 173.000/mL, hematuria 278.000/mL, but no cylindruria. The electrocardiogram (ECG) showed sinus tachycardia. Doppler echocardiography evidenced a thickened aortic valve with slight insufficiency. The paranasal sinuses computed tomography (CT) showed involvement of the left frontal, right sphenoid, and bilateral ethmoid sinuses. The chest CT showed tenuous mosaic attenuation of the lung parenchyma more pronounced in the bases; the presence of non-calcified nodules scattered bilaterally ranging in size between 5 and 10 mm; and a hiatal hernia. The abdominal CT disclosed the presence of pneumoperitoneum of unknown origin.
The patient persisted with the complaint of epigastric abdominal pain but no signs of distension or peritoneal irritation were observed. The gastrointestinal transit was normal. The upper endoscopy revealed the presence of esophageal moniliasis and multiple acute superficial gastric ulcers, the biopsy of which revealed a chronic gastric ulcer edge in pyloric mucosa, Helicobacter pylori negative. These findings were interpreted as compatible with a tamponade gastric micro perforation. Because of steady clinical appearance, a proton-pump inhibitor was chosen instead of the surgical approach. Skin biopsy of the palmar injury showed sub epidermal necrosis with fibrin and erythrocytes. Neutrophilic vasculitis was depicted, showing vessel wall necrosis with red blood cell leakage permeated by eosinophils.
After the initiation of corticosteroid therapy, an improvement in mental status was observed as well as a decrease in the eosinophils count, creatine phosphokinase, and C-reactive protein determinations, and also a slight improvement in muscle strength. With the diagnosis of EGPA, the patient was referred to a specialized clinic for supplementary immunosuppressive therapy.
One month after the hospital discharge, she returned complaining of generalized pain and a burning sensation throughout the body. She denied fever, chest pain, breathlessness, or headache. On examination she was pale. Blood pressure was 130/82 mmHg, pulse rate of 92 bpm, room air oximetry of 92%. Neurological examination revealed a distal symmetrical weakness (members distal muscle strength grade I and proximal grade III). The presence of scarring necrotic lesions on toes was noted. Four hours after admission, the patient presented sudden dyspnea, mental confusion, worsening of muscular weakness, pallor, and cold sweating, progressing to cardiac arrest and death. Recent laboratory workup showed a mild anemia (hemoglobin = 11.6 g/dL, RV: 13-15 g/dL). The remaining blood cell count, renal function, electrolytes, hepatic enzymes, CRP, CK, CK-MB and troponin I were all normal. The electrocardiogram showed a recent right bundle branch blockage. The acute clinical failure was interpreted as a pulmonary embolism. An autopsy was performed.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2910,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7350973-1,Extracted,"A 50-year-old man was referred to our emergency department for vomiting, fever and loss of appetite for a week. He also reported cough and atypical chest pain towards the top of his sternum. Asthenia and arthromyalgia were also present. He denied contact with anybody suspicious for COVID-19. His vital parameters were: blood pressure 135/70 mmHg, heart rate 74 bpm, respiratory rate 14 breaths/min, and peripheral oxygen saturation 96%.
Blood gas analysis revealed: pH 7.4, pCO2 40 mmHg, pO2 73.9 mmHg, P/F 352, and alveolar–arterial gradient 26 (expected value for age: 17). The electrocardiogram showed sinus rhythm with a mean heart rate of 70 bpm. The patient’s medical history was characterized by depression and tobacco consumption, treated with paroxetine, olanzapine, trazodone and lorazepam.
On physical examination, the patient was alert and collaborative, with no neurological deficits. The abdomen was painless and bowel function was regular. Lung auscultation revealed a slightly reduced vesicular murmur in the right basal region. Heart sounds were normal. There was no oedema in the lower limbs or pain on palpation.
Blood examination revealed: white blood cells (WBC) 7700×109/l, neutrophils 5.2×109/l, lymphocytes 1.8×109/l, D-dimer 1.5 mg/l, INR 1.0, aPTT ratio <0.8, platelets 202×109/l, LDH 468 U/l, AST 83 U/l, ALT 30 U/l, C-reactive protein 1.55 mg/dl, procalcitonin 0.2 ng/ml and creatinine 0.9 mg/dl.
Lung ultrasound showed minimum pleural effusion in the right basal field, while a round pleural-based consolidation was present with some B lines in the right field (). A chest CT scan was therefore performed and showed filling defects compatible with non-occlusive thromboembolism at the level of the apico-dorsal segmental branch of the upper right lobe and of the subsegmental branches of all right lobes and of lower lung lobes on the left. There was also complete occlusion of a peripheral subsegmental vessel to the dorsal segment of the lower right lobe ( and ). Small ground-glass opacities were evidenced in the parailary lung field near the upper right lobe. A modest pleural film was seen on the right (). There was no mediastinal lymphadenomegaly. The nasopharyngeal swab was positive for SARS-CoV-2 infection. A subsequent angiogram with echo colour Doppler did not reveal any venous thrombosis in the limbs. The patient underwent anticoagulant therapy.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [74.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 74.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2911,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5965129-1,Extracted,"A 52-year-old morbidly obese male presented to the Emergency Department (ED) with a chief complaint of syncope. The morning of presentation he reported feeling lightheaded with shortness of breath and blurry vision upon standing. He next remembered waking up on the floor. He reported worsening shortness of breath over the prior three days. Additionally, he reported experiencing a dull, constant, pressure-like sensation over the left side of his chest that had begun the night before. Initially, the patient denied any medical conditions other than morbid obesity; however, several hours into his stay we learned that he had a history of a deep vein thrombosis (DVT) with a PE after a knee arthroscopy two years earlier.
His temperature was 36.5 degrees Celsius, heart rate of 114 beats per minute, blood pressure of 137/91 mmHg, respiratory rate of 18 breaths per minute, and pulse oximetry of 94% on room air. His weight was 181 kilograms (body mass index of 59). The patient was awake, alert, conversing appropriately, and in no apparent distress. He was noted to be tachycardic but was well perfused, with no signs of cyanosis and a capillary refill less than two seconds. His lungs were clear to auscultation bilaterally without an increase in work of breathing. Other than venous stasis changes, his lower extremities appeared normal.
His electrocardiogram showed sinus tachycardia at 103 beats per minute with a S-wave in lead I, Q-wave in lead III, and small ST-elevations in V1–V3. His initial troponin was above the normal limit at 0.17 ng/mL [0.00–0.03 ng/mL]. The patient’s metabolic panel was notable only for an elevated glucose of 206 mg/dL [85–125mg/dL]. His complete blood count was normal except for an elevated white blood cell count of 12.3 thous/MCL [4–10.5 thous/MCL]. D-dimer was >1000ng/ml [<500 ng/ml]. A computed tomography pulmonary angiogram was ordered to rule out PE ( and ). It demonstrated a central saddle embolism and multiple occlusive and nonocclusive lobar, segmental, and subsegmental pulmonary arterial emboli bilaterally. Right heart strain and pulmonary hypertension were evidenced by enlargement of the main pulmonary artery and straightening to leftward bowing of the interventricular septum, indicating significant clot burden.
Pulmonary critical care and interventional radiology teams were consulted and after evaluating the patient, the decision was made to not start heparin and instead immediately take the patient for thrombectomy. The patient underwent clot aspiration and catheter-directed intra-procedural tissue plasminogen activator (tPA) administration into each pulmonary artery. Post-thrombectomy angiogram demonstrated significant improvement, but showed persistent areas of clots. Following the procedure, the patient became hypotensive and hypoxemic requiring vasopressors and continued intubation.
The following day the patient had bilateral pulmonary artery EKOSTM catheters (EkoSonic® Endovascular System designed for the treatment of PE) placed for continuous tPA administration.
On hospital day three, his pulmonary artery angiogram demonstrated no visible thrombus and the EKOSTM catheters were removed. The patient remained in the intensive care unit (ICU) intubated, sedated, and receiving anticoagulants. On hospital day 4, he had sustained hypoxia and then suffered a cardiac arrest but had return of spontaneous circulation after cardiopulmonary resuscitation. This event was thought to be due to a recurrent PE, and thus an inferior vena cava filter was placed the following day.
On hospital day 14, he was extubated and transferred out of the ICU. The patient returned to his baseline mental status without any breathing difficulties or chest pain. On hospital day 20, he was transferred to a skilled nursing facility for rehabilitation. At time of discharge, he was neurologically intact and required minimal assistance with activities of daily living.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [114.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 114.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3.0 + 1.5 = 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2912,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5649679-1,Extracted,"An 82-year-old male patient presented with chest tightness and shortness of breathing for 10 days. His past medical history included hypertension and old pulmonary tuberculosis. He suffered from productive cough for weeks and was referred to our center because of the worsening symptoms of dyspnea and lower leg edema noted over the past few days. On presentation, his consciousness was alert. Body temperature was 37.8 °C. Pulse was 136 per minute regular. Blood pressure was 164/90 mmHg. Oxygen saturation was 88%. Auscultation revealed decreased breathing sounds at left lung field and sonorous rhonchus at right lung field. X-ray of the chest showed left pneumothorax with collapse of left lung, and ground glass opacities in right lung field (), more in favor of inflammatory process at that time. He was admitted under the impression of right lung pneumonia with left pneumothorax and received chest tube insertion and empiric antibiotics treatment. However persistent air leak noted, he then received a chest CT for further survey. A chest CT showed nodular lesions over bilateral lung, with diffuse bone, left lower neck (), left suparclavicular, mediastinum, as well as right hilar () and lower abdominal lymph nodes metastases. Unknown primary malignancy with bilateral lung metastases, diffuse bony metastases with left supraclavicular and left neck lymph node metastases was impressed and further tissue proof for possible underlying malignancy was recommended. For this reason, an echo guided biopsy with left neck lymph node biopsy was arranged for further study because the surgical intervention was not recommended for the patient due to poor lung function while patient declined bronchoscopy biopsy either. A subsequent neck lymph node biopsy revealed metastatic adenocarcinoma, while immunohistochemical stain for thyroid transcription factor -1(TTF-1), and cytokeratin 20 (CK20) are all negative. Serum tumor markers were examined in an attempt to identify the primary lesion, revealing a PSA level of > 1,000 ng/mL (normal < 4.0 ng/mL) while CEA 2.7 ng/mL (normal < 5.0 ng/mL). Digital rectal examination showed an enlarged and hardened left prostate lobe. An abdomen CT disclosed 4.3 × 3.0 cm ill defined heterogenous mass lesion at lower lobe of prostate () with regional and non-regional lymph nodes () and bony metastases. The urologist was consulted, and transrectal ultrasonography (TRUS) showed irregular urinary bladder wall thickening with enlargement of prostate, hypoechoic nodule with increased vascularity in left peripheral zone of prostate. Meanwhile the patient refused further tissue proof due to his poor general condition. The pathologist was informed of the elevated serum PSA and further clinical data, then an additional immunohistochemical staining of the left neck lymph node biopsy with P504S was performed as was compared to the regular H&E stain (), the neoplastic cells expressed P504S diffusely (), a metastatic adenocarcinoma of prostatic origin was confirmed. However his condition went downhill rapidly, and after thoroughly discussion with the patient and his family, they decided to receive hospice care and refused further intervention.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [136.0, 'beats per minute'], 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Previously documented Deep Vein Thrombosis': False}",5.5,5.5,5.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 136.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 4.5 + 1 =  5.5.
The patient's Well's score for pulmonary embolism is 5.5."
2913,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5732123-1,Extracted,"Our patient was a 54-year-old man who was originally diagnosed with a gastric SMT in 2008. He underwent an annual follow-up by upper GI endoscopy at another hospital but was referred to our hospital for further examination and treatment in September 2016, during which his main clinical symptoms were epigastric soreness, general malaise, and melena. He had an unremarkable family history.
On admission, he measured 161.6 cm tall and weighed 58 kg and his pulse was 115 beats/min, and blood pressure was 69/43 mmHg. There were no significant findings on abdominal examination, but laboratory analysis revealed a hemoglobin level of 5.6 g/dl. Other hematological and biochemical parameters were within normal limits. Chest X-ray, electrocardiography, and echocardiography results were normal. On admission, because he had advanced anemia and low blood pressure, he received blood transfusion (480 ml). On upper GI endoscopy, an SMT was identified with an associated ulcer on the anterior wall of the lower body of the stomach (Fig. ). There was an extrinsically compressing mass on the anterior wall of the greater curvature and the posterior wall of the stomach (Fig. ). However, no active bleeding from the SMT or ulcer was observed.
We diagnosed lipoma without malignancy based on the biopsy of the SMT and ulcer. Endoscopic ultrasound (EUS) confirmed a high-echoic submucosal lesion in the antral wall that extended to the stomach body (Fig. ), and computed tomography (CT) and magnetic resonance imaging confirmed a fat-containing mass spanning entire gastric walls of the stomach antrum and body, but excluding the lesser curvature, with a mass protruding on the anterior wall of the greater curvature (Figs. and ). CT images revealed no metastasis to lymph nodes or to other organs, and the serum tumor markers CEA and CA19-9 were within the normal limits.
Based on our findings, we suspected a giant gastric lipoma and proceeded to perform a standard total gastrectomy. We considered the execution of resection of the stomach, but we decided to perform total gastrectomy because the range of the tumor was unclear and the risk of recurrence could not be determined. The specimen was opened along the greater curvature, revealing a mucosal surface that was smooth and diffusely elevated by the submucosal mass, but with no involvement of the lesser curvature (Fig. ). There was a compressing lesion associated with an ulcer on the anterior wall of the lower body. The gross pathology was of a yellowish adipose tissue with no fibrous capsules.
Gastric lipomatosis was confirmed by a histological examination of the resected specimen. Microscopy revealed adipocyte proliferation without nuclear atypia and mature adipocytes replacing the submucosal and muscle layers of the stomach. Lipomatosis was present only in the fundic gland zone, and there was no intestinal metaplasia or atrophic gastritis. Multiple hyperplastic polyps were observed on the mucosa overlying the area of diffuse lipomatosis. Immunostaining was negative for MDM2, CDK4, and p16. Moreover, there was no evidence of malignancy in the fatty lesion.
The patient recovered well following surgery and was discharged on the postoperative day 14. At the latest follow-up, he was continuing to do well and showed no evidence of recurrence in other organs.
Gastric lipomas are characterized by smooth, sharply marginated, and oval or spherical submucosal masses comprising well-differentiated adipose tissues surrounded by a fibrous capsule [–]. In contrast, gastric lipomatosis is characterized by multiple gastric lipomas or diffuse infiltration of mature adipose tissues into the gastric submucosal or subserosal layers. GI lipomas are extremely common benign colonic tumors, whereas gastric lipomatosis is particularly rare [, –].
Approximately, 90–95% of lipomas are submucosal, and the rest are subserosal []. Most gastric lipomas are small (4–9 cm) and asymptomatic, occur on the posterior wall of the antrum, and are incidentally detected on radiographic or endoscopic examination of the upper GI tract. Smaller lesions are rarely symptomatic, but large tumors can present with symptoms of gastric ulcer, including epigastric pain, nausea, vomiting, and upper GI tract bleeding. Indeed, the most frequent clinical manifestation is GI bleeding, which is due to the ulceration of the overlying mucosa in 50% of the patients [, ]. When a large lipoma is present, venous stasis is probably the single most important factor underlying mucosal ulceration, which may lead to acute, and sometimes severe, upper GI hemorrhage. Several authors have reported anemia as the primary indicator of large gastric lipomas [–]. In the present case, we suspect that a part of the tumor rapidly increased in size and led to the collapse of the mucosal surface with subsequent ulceration and bleeding.
CT is an excellent diagnostic tool because it allows the diagnosis of lipoma based on tumor fat density, precluding the need for an endoscopic biopsy. Indeed, a homogeneous mass with a fat density ranging between − 70 and − 120 Hounsfield units is considered pathognomonic of gastric lipoma []. Histologically, GI tract lipomas typically have well-differentiated adipose tissue structures. If a large submucosal tumor is detected on an endoscopic or upper GI examination, then a CT scan can be used to confirm the diagnosis and to inform therapy decisions. However, EUS is the most useful diagnostic tool for assessing neoplasia originating from the submucosa. In the present case, EUS showed a submucosal hyperechoic and homogeneous mass and diagnosed lipoma.
Although conservative treatment is preferred for asymptomatic solitary lipomas, surgical intervention should be considered for symptomatic lipomas associated with ulcers or non-fatty elements. Endoscopic polypectomy is an option for submucosal lesions that are smaller than 3 cm, but larger broad-based tumors have a higher risk of perforation using this approach. In our case, we decided to treat the patient by total gastrectomy for three main reasons: first, a large and symptomatic lipoma was present at surgery; second, although biopsy suggested lipoma, we could not completely exclude malignancy; and third, anastomotic leakage and tumor recurrence were possible if partial resection was performed.
Eight reports of gastric lipomatosis exist in the literature, of which five describe a detailed pathology (Table ) [, , , –]. According to these reports, lipomatosis in the upper stomach can occur with multiple organ involvement or with multiple types of lipomatosis. However, no tumor has been reported in any other organ when lipomatosis occurs in the lower stomach. Most previous cases have reported multiple lipomas, and this is only the second case of gastric lipomatosis presenting as a diffuse lipoma []. In our case and in that by Jeong et al. [], the cases not only had similar specimens and histological findings but were also diagnosed as diffuse-type lipomatosis. In our case, it was noteworthy that the lipomatosis was present only in the fundic gland zone, without intestinal metaplasia or atrophic gastritis. Furthermore, multiple hyperplastic polyps were observed on the mucosa overlying the diffuse lipomatosis. We hypothesize that a relationship exists between hyperplastic polyposis and lipomatosis in some cases.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [115.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 115.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2914,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5685213-1,Extracted,"A 33-year-old male presented to our hospital with a history of sudden-onset, pleuritic, right-sided chest pain of 2 days’ duration. It was not associated with fever, cough, dyspnoea, wheeze or haemoptysis. There was no history of swelling in the lower extremities, weight loss or anorexia. There was no history of any significant comorbidities. He was a smoker (8 pack-years). He had no history of drug abuse.
On examination, his temperature was 37.2°C, pulse was 77 beats⋅min−1, respiratory rate was 22 breaths⋅min−1, blood pressure was 112/66 mmHg and oxygen saturation measured by pulse oximetry was 98% on room air. There was no pallor, clubbing, pedal oedema, icterus or lymphadenopathy. The breath sounds were absent in the infrascapular and infra-axillary areas on the right side. No adventitious sounds were heard on either side of the chest. The remaining systemic examination was unremarkable.
Investigations revealed a haemoglobin level of 16.4 g⋅dL−1, and total leukocyte count of 8870 cells⋅mm−3 with a differential count of 62% neutrophils, 28% lymphocytes, 7% monocytes, 2% eosinophils and 1% basophils. The platelet count was 160 000 cells⋅mm−3. Creatinine, electrolytes and liver function tests were normal. The ECG was unremarkable and cardiac enzymes were within normal limits. Chest radiograph () showed a mild, right-sided pleural effusion, blunting of the left costophrenic angle, no shift of mediastinal position and no lung parenchymal opacities.
He was subjected to a diagnostic thoracentesis, which showed 6.5 g·L−1 protein (corresponding serum proteins were 7.3 g·L−1), and lactate dehydrogenase (LDH) concentration was 820 U⋅L−1 (corresponding serum LDH was 563 U⋅L−1) and that of glucose was 7 mmol⋅L−1. The erythrocyte count was 2 700 000 cells⋅µL−1, and leukocytes count was 3400 cells⋅µL−1 with 53% neutrophils, 42% lymphocytes and 5% monocytes. The Gram stain and cultures were sterile. There were no acid-fast bacilli seen in smears and real-time PCR for Mycobacterium tuberculosis was negative. The cytological examination showed no malignant cells.
He was treated with antibiotics and analgesics. 48 h after admission, the patient complained of severe, left-sided chest pain in the night. It was nonradiating and not associated with sweating, nausea or vomiting. There was no haemodynamic compromise and the patient was normoxaemic. There were reduced breath sounds in both infrascapular and infra-axillary areas. An ECG was performed ().
Serial cardiac enzymes were normal. Chest radiography was also repeated ().
The patient had a bout of cough associated with mild haemoptysis and fever of up to 38°C. The possibility of PE was entertained. The revised Geneva score for the assessment of the clinical probability of PE was 5, suggesting that there was an intermediate probability of an embolism. Therefore, a D-dimer test was ordered and the level was found to be 3.6 mg⋅L−1 (normal range 0.09–0.33 mg⋅L−1). In line with the diagnostic algorithm for patients with suspected, not high-risk PE proposed by the European Society of Cardiology [], the patient was subjected to computed tomographic pulmonary angiography (CTPA), which showed filling defects in the both lower and upper lobar arteries, right middle lobe, and lingular arterial branches consistent with an acute PE. There was no right ventricle enlargement seen in the four-chamber view of the heart by CTPA, which was suggestive that there was no right ventricular dysfunction ().
The patient was found to be in PESI class I. This, combined with there being no signs of right ventricular dysfunction on CTPA and normal troponin levels, was suggestive of a low risk of adverse early outcome. He was given enoxaparin 7 days, followed by dabigatran. Blood and sputum cultures were eventually found to be sterile. The autoimmune/vasculitis screen was negative. Gradually, over the next few days, the patient’s fever subsided and his chest pain resolved completely. He was continued on dabigatran and a repeat chest radiograph at the last follow-up showed a complete resolution of the pleural effusion on left side with a residual blunting of right costophrenic angle (). A pleural fluid acid-fast bacillus culture showed no growth of any organism after 6 weeks of incubation.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [77.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 77.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 1.5 + 1 = 2.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2915,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4144077-1,Extracted,"The patient was a 34-year-old Japanese woman (gravida 1, para 1) whose previous personal and family medical histories were unremarkable. During this pregnancy, the patient's physical findings, cervical length, laboratory data, urinalyses, and fetal growth determinations were all within normal ranges; glucosuria or ketonuria was not detected.
At 23 weeks and 6 days of gestation, physical findings, fetal growth, cervical length, laboratory data, and urinalysis were all within normal range. Two days later, the patient thought she had caught a cold because of the onset of malaise and thirst. At 24 weeks and 3 days of gestation, she presented with complaints of nausea and lumbago. Upon examination, the fetal heartbeat and movement were positive. The physician on duty at the time of admission initially diagnosed the condition as poor physical condition due to the common cold. However, 5 h later, the patient went into labor, and the gestational sac and fetal head appeared, resulting in emergent hospitalization and a subsequent premature delivery.
Upon admission, the patient was 166 cm tall, weighing 72.7 kg (before pregnancy, 63 kg), and had a body temperature of 36.9°C and a blood pressure of 156/74 mmHg. A physical examination revealed labored breathing and cold extremities. A stillborn infant (592 g, female) was soon delivered. The associated blood loss was minimal, and uterine contraction was good; the placenta and umbilical cord (130 g) appeared normal. Soon after delivery, the patient's vitals were normal, apart from a blood pressure of 129/69 mmHg and a slight tachycardia, with a pulse of 113 beats/min. The patient had no lower abdominal pain but complained of epigastric pain.
The results of laboratory tests on blood collected during labor were examined () and confirmed an extreme hyperglycemia, with a blood glucose level of 950 mg/dL. Her urinary sugar and ketones were markedly elevated. The labored breathing observed during delivery became more severe, and the patient developed clouded consciousness, leading to management in the intensive care unit (ICU).
After admission, the patient's white blood cell count, serum amylase levels, blood urea nitrogen levels (BUN), and blood creatinine levels were elevated, leading to a diagnosis of sepsis, acute renal failure, and acute pancreatitis associated with diabetic acidosis. Following a diagnosis of coma due to diabetic ketoacidosis (DKA), acute renal failure, acute pancreatitis, and sepsis, insulin therapy (regular insulin, 7 U/h) and antimicrobial therapy (meropenem trihydrate) were initiated in conjunction with adequate hydration. The patient's laboratory findings and blood gas data improved with this treatment (), and she regained consciousness 24 h after admission to the ICU. Abdominal computed tomography (CT) was performed, revealing a CT severity index of 2 ().
Despite elevated postadmission blood glucose levels, the patient's glycated hemoglobin (HbA1c) levels remained normal. However, C-peptide blood levels of 0.1 ng/mL indicated depleted insulin levels; antibodies against insulin, glutamic acid decarboxylase (GAD), and islet antigen-2 were not detected. Despite marked elevations of C-reactive protein and white blood cell levels, the patient's blood cultures were negative and she was afebrile. A search for factors contributing to DKA involved two investigations of possible viral infection (). The findings revealed elevated Coxsackie A9, B1, and B3 antibody titers. With the patient's consent, human leukocyte antigen (HLA) typing was performed; the findings showed HLA-DRB1∗0405-DQB1∗0401. The condition met all the diagnostic criteria of fulminant type 1 diabetes [] and was diagnosed as such.
The patient was discharged 13 days postpartum and her insulin levels remain depleted, 1 year later. The patient has required regular insulin (42 U/day) administration, with her blood glucose levels varying within the range of 150–250 mg/dL; occasional hypoglycemic episodes preclude higher insulin doses. The patient's HbA1c levels have recently been maintained at approximately 8%.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [113.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 113.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2916,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6824746-1,Extracted,"An 80-year-old man had already been diagnosed stage V chronic kidney disease for 2 years but did not receive renal replacement therapy. Otherwise, he had no history of foreign travel and familial problems. This time, he visited our emergency room due to high fever and chills for a day. Abdominal fullness, anorexia, and weight loss had also developed for 3 months before this visit. The physical examinations revealed a tachycardia of 114 beats per minute, fever of 38.4°C, and diffuse abdominal tenderness. The blood sampling showed leukocytosis, azotemia, and increased serum procalcitonin level (Table ). The urine analysis revealed the pyuria, suggesting the complicated urinary tract infection. The abdominal plain film showed mixed osteoblastic and osteolytic changes: cortical thickening, sclerosis with coarsened trabeculae, and flame-shaped lucent lesion in the pelvic bone with right site predominantly (Fig. ).
Considering the image results and other clinical symptoms such as anorexia and weight loss, the differential diagnosed of the bone lesion is crucial for the patient. The blood chemistry results on the second day, showed only mild elevation in alkaline phosphatase (ALP) and inorganic phosphorus, while highly elevated parathyroid hormone but decreased corrected calcium was noted, favor secondary hyperparathyroidism due to chronic renal function insufficiency (Table ). On the third day after admission, we check the serum tumor markers of leading causes for bone metastasis in the male patients, such as carcinoembryonic antigen and squamous cell carcinoma antigen for lung cancer and prostate-specific antigen for prostate cancer, and all of 3 markers showed normal or mild elevation (Table ). Monoclonal globulin elevation was not identified in serum screening as well (Table ).
Otherwise the abdominal plain film, the skull X-ray plain film was performed on the second day after admission and demonstrated no osteolytic lesions (Fig. ). We arranged gallium-67 tumor scan and Tc-99m methylene diphosphonate bone scan on the third day and disclosed no lesions throughout the entire body except for the pelvic bones (Fig. ).
The patient was diagnosed as asymptomatic PDB based on the pelvic X-ray and elevated ALP level without extended high-risk bone involvement on bone scan, and complicated urinary tract infection of Pseudomonas aeruginosa. He received intravenous hydration and piperacillin 4 g and tazobactam 0.5 g injection every 12 hours, which led to the clinical improvement of his urinary tract infection after 7 days treatment. We shifted to ciprofloxacin 500 mg orally once per day for another week and discharged the patient. A week later, the patient visited our outpatient department with complete recovery from infection and had no symptom of PDB such as bone pain, arthritis, deformity, or fracture.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [114.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 114.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2917,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3510284-1,Extracted,"A 51-year-old male was admitted to our hospital with high grade fever, severe right-sided chest pain and dyspnea for five days. He had a history of poorly controlled type 2 diabetes mellitus. The patient appeared severely ill. On admission, his body temperature was 38.2℃, pulse rate was 93 per minute, respiration rate was 18 per minute and blood pressure was 120/90 mm Hg. Auscultation of the chest revealed decreased breath sound and inspiratory crackle at the right lower lung field. There was tenderness on palpation and percussion of his right lower chest wall. Initial laboratory evaluation showed white blood cell count of 22,300/µL with 88% segmented neutrophils, hemoglobin of 11.9 g/dL, platelets of 317,000/µL and C-reactive protein of 37.8 mg/dL. His plasma glucose was 438 mg/dL and hemoglobin A1C was 11%. He was negative human immunodeficiency virus. Chest X-ray showed right lower zone consolidation with pleural effusion and peripherally multiple nodular opacities (). Further imaging with contrast enhanced helical computed tomography of the chest showed embolic occlusion of the azygos vein (). Long vascular computed tomography did not show lower extremity deep vein thrombosis but showed intramuscular abscess on both lower legs (). Initial empiric antibiotic therapy was started on ceftriaxone 2.0 g intravenously every twelve hours. The patient underwent a diagnostic thoracentesis with removal of serosanguinous fluid that was an exudative pleural effusion, negative bacterial and acid-fast stains and cytology. The pleural fluid cell count demonstrated a red blood cell count of 140/µL (per cubic millimeter), a white blood cell of 1,520/µL with 95% neutrophil and adenosine deaminase was normal. The patient's blood, sputum and pleural fluid cultures yielded oxacillin-sensitive S. aureus. Ceftriaxone was discontinued on day 3 of the admission. Nafcillin at 500 mg intravenously every four hours and isepamicin at 200 mg intravenously every twelve hours was begun. Transthoracic echocardiography revealed normal left ventricular function with no vegetation, valvular regurgitation and other signs of endocarditis.
With appropriate antibiotic therapy, the patient's clinical condition had been improved and subsequent chest X-ray showed gradual resolution of pneumonia and parapneumonic effusion. His diabetes was controlled well starting insulin therapy. After taking one month of antibiotics, a repeat chest computed tomography revealed complete resolution of septic embolism in the azygos vein without anticoagulant therapy ().",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [93.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Immobilization for at least 3 days': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 93.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2918,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8161910-1,Extracted,"A 37-year-old previously healthy man presented due to fever with chills and rigors, arthralgia and myalgia for 5 days duration. Symptoms were associated with headache, photophobia and recurrent episodes of vomiting. He did not report urinary, respiratory or bowel symptoms to suggest a focal infection. His past medical and surgical history was unremarkable but he admitted to bathing in a stream 1 week prior to admission.
He was febrile without pallor or icterus and did not have any rashes or lymphadenopathy. Examination revealed a Glasgow Coma Scale of 15/15 and neck stiffness. Blood pressure and pulse rate were 120/70 mmHg and 88 beats/minute, respectively. The rest of the examination, including nervous system, was unremarkable.
Investigations revealed a neutrophil leukocytosis and a high C-reactive protein (Table ). Examination of cerebrospinal fluid (CSF) revealed high protein, normal glucose and predominant polymorphonuclear cells. Blood, urine and CSF bacterial cultures and CSF viral studies were negative. He had raised serum creatinine level on admission which normalized during the next 48 h. Non-contrast computerized tomography of the brain, chest radiograph and ultrasound scan of the abdomen were normal.
The patient was managed as bacterial meningitis with intravenous ceftriaxone (2 g, twice daily) intravenous dexamethasone (8 mg, three times daily). Considering the history of high-risk exposure to possible contaminated water, serum leptospirosis microscopic agglutination test (MAT) was performed, yielding a positive titer of 1/5120. The serovar was identified as Leptospira borgpetersenii sv. Tarassovi (strain bakeri).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [88.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 88.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2919,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8607555-1,Extracted,"A 13-year-old spayed female domestic shorthair cat was presented to the Veterinary Teaching Hospital of the University of Padua with a recent history of weight loss, progressive dyspnoea, respiratory crises and multiple episodes of regurgitation in the previous week. According to the owners, the cat also experienced difficulty in eating and drinking.
On physical examination, the patient had decreased muscular masses with a reduced body condition score (BCS 4/9), mucus membranes appeared slightly pale with capillary refill time of 2 s. The patient exhibited marked tachypnoea (65 breaths/min), with inspiratory dyspnoea and bilateral reinforced respiratory sound with stridors and wheezes on thoracic auscultation, and slight bradycardia (140 bpm).
Diagnostic workup included haematology, biochemistry and urinalysis, which were within normal limits, and serum protein electrophoresis that revealed a slight decrease in the albumin fraction and an increase in the α2- and β1-globulin fractions.
Head, neck and thoracic x-rays performed under sedation revealed a soft tissue 2.6 × 2.2 cm mass that displaced the larynx dorsally. Moreover, a mild pulmonary interstitial pattern was observed bilaterally.
The laryngeal mass was inspected under sedation by oral cavity examination and sampled for cytology through a trans-oral fine needle aspiration. Cytology revealed a highly pleomorphic cell population. Cells were polygonal or elongated in shape, organized in small groups or individually, with abundant, lightly basophilic cytoplasm that often showed one large, intensely eosinophilic, perinuclear body. Nuclei were round to irregular in shape with granular chromatin and prominent nucleoli. Anisocytosis and anisokaryosis were marked. Additionally, macrokaryosis and multinucleated cells as well as cellular cannibalism were frequently observed (Fig. ). Based on the cytological findings, diagnosis of a malignant, poorly differentiated neoplasm was made. Based on cytomorphology, the differential diagnoses included a poorly differentiated carcinoma and a poorly differentiated soft tissue sarcoma.
Following the cytology results, a contrast-enhanced CT scan of the head, thorax and abdomen was performed for staging purposes and for surgical planning. CT findings showed an ill-defined, moderately contrast enhancing (pre-contrast HU: 36, post-contrast HU: 96) mass surrounding and largely invading the larynx. Both retropharyngeal lymph nodes appeared markedly enlarged and necrotic (Fig. ). No further tomographic changes in distant organs were detected.
The extension of the tumour and its location were not amenable to conservative surgery with complete surgical margins. Due to poor prognosis owners declined further investigations and opted for symptomatic treatment with meloxicam 0.6 mg/kg daily.
After a partial remission of clinical signs over a period of 10 days, the patient showed progressive deterioration of clinical conditions and severe respiratory sings and was euthanized 1 month after first clinical presentation. Euthanasia was performed under general anaesthesia using a combination of a curariform-like agent, a narcotic, and a local anaesthetic.
On post-mortem examination, two distinct, bilateral laryngeal masses were found. Both tumour masses arose from the mucosa of the cuneiform process of the arytenoid cartilage, and protruded in the laryngeal inlet dramatically reducing the lumen. The larger mass measured 2.8 × 2 cm and extended caudally involving the vocal cords, whilst the smaller was located more cranially involving the aryepiglottic fold. Both masses were well demarcated, exophytic, with firm texture, smooth, with white-tan colour on cut surface (Fig. ). Mild hyperaemia of the surrounding structures was observed and no other alterations were found on necropsy.
Both laryngeal masses were sampled, formalin fixed, routinely processed and haematoxylin and eosin stained for histological examination.
All sections were characterised by an infiltrative neoplastic population that expanded the laryngeal submucosa and extended deeper involving the arytenoid cartilage. Neoplastic cells were observed in poorly demarcated, partially encapsulated nodules, in which they were arranged in nests and cords supported by a moderate to abundant fibrovascular stroma. Cells were moderately preserved, oval to elongated in shape, with mostly distinct borders and a variable amount of pale eosinophilic cytoplasm, with scattered basophilic granules and an occasional large (up to 20 μm), brightly eosinophilic, glassy round to oval body, mainly located in the perinuclear area. Nuclei were round to oval, occasionally indented, with coarsely stippled chromatin and one prominent nucleolus. Histological criteria of malignancy, including anisocytosis, anisokaryosis, and macrokaryosis, were marked. Multinucleated cells (up to 6 nuclei per cell), and cellular cannibalism were frequently observed, while mitotic figures were 4 per 10 high power fields (HPFs; diameter of the field of view = 0.55 mm; HPF = 237 mm2; 40× magnification, Nikon Eclipse Ci-L, Nikon Instruments, Japan). Lymphocytic infiltration of the tumour mass and peripheral aggregates of lymphocytes with rare histiocytes were also present (Fig. ).
Based on histology, a diagnosis of undifferentiated malignant laryngeal tumour was made and any possible cellular origin of the tumour between epithelial, mesenchymal, or neuroendocrine was included. In order to further investigate the tumour phenotype, an immunohistochemistry (IHC) panel including pancytokeratin (PanCK), cytokeratin 5/6 (CK 5/6), and cytokeratin 8/18 (CK 8/18) as epithelial markers, p63 and calponin as myoepithelial markers, vimentin as mesenchymal marker, neurofilaments and chromogranin as neuroendocrine markers was performed, while CD3 and CD20 were included to better characterise the lymphocytic infiltrate. All antibodies included in the IHC panel were previously tested in cats (Table ).
Virtually all neoplastic cells showed a strong and diffuse membranous and cytoplasmic immunolabelling for PanCK. In addition, the same cells also showed a diffuse cytoplasmic positivity that ranged from mild to intense for CK 5/6, while mild cytoplasmic positivity for CK 8/18 was observed in scattered neoplastic cells. Occasionally, tumour cells showed a nuclear immunolabelling for p63. Interestingly, aggregates of p63-positive cells were observed specifically adjacent to, and palisading on connective stromal septa. Calponin immunoreactivity was only observed in stromal cells and on vessel walls. Vimentin expression was limited to tumour stromal cells, infiltrating inflammatory cells (lymphocytes and histiocytes) and blood vessels. Immunolabelling for neurofilaments was only observed in the peripheral nerves within tumour nodules, whilst chromogranin was negative. Lymphocytic aggregates at the periphery of the tumour had an equal distribution of CD3+ and CD20+ cells, whilst tumour infiltrating lymphocytes were mainly CD3+ (Fig. ).
In the light of the IHC results, the tumour was deemed an undifferentiated laryngeal carcinoma.
In order to better clarify the content of the large cytoplasmic vacuoles that were consistently observed in both cytological and histological samples, a periodic acid-Schiff reaction (PAS) was performed. However, both on cytological and histological samples, cytoplasmic vacuoles were PAS-negative.
Neoplastic tissue was then excised from paraffin and processed for transmission electron microscopy (TEM) examination. Ultrastructural results confirmed the presence of pleomorphic neoplastic cells with cytoplasmic vacuolations. Moreover, the presence of cytoplasmic, non-membrane bound, electron-dense deposits was also observed (Fig. ). TEM results therefore confirmed the diagnosis of undifferentiated laryngeal carcinoma, with the presence of cytoplasmic accumulations of electron-dense material that was compatible with the eosinophilic bodies observed both on cytology and histopathology.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [140.0, 'bpm'], 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 140.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2920,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5348219-1,Extracted,"A 31-year-old female with a past medical history of eczema and asthma was admitted to a tertiary care hospital for evaluation of significant weight loss and malnutrition. She was diagnosed with celiac disease based on the serological studies. A peripherally inserted central catheter (PICC) was inserted for poor intravenous access which was found to be close to the tricuspid valve area on confirmatory chest x-ray. The PICC was removed after three days as it was complicated by axillary vein thrombosis, and anticoagulation was started.
Two weeks after discharge, she presented to our emergency department due to fever, dyspnea, and leg swelling. Vital signs were: pulse of 112/min, blood pressure of 127/101 mmHg, respiratory rate of 47/min, temperature 97.5°F, and oxygen saturation was 100% on 4L oxygen. A physical examination revealed reduced air entry with crackles bilaterally on chest auscultation and no audible heart murmurs. Complete blood counts revealed white blood cell count of 8.10k/µL, hemoglobin of 7.8g/dL, and platelets of 95k/µL. The complete metabolic panel was within normal limits. NT ProBNP was >35,000pg/mL. A chest x-ray showed worsening left-sided pleural effusion and consolidations bilaterally. Computed tomography of the chest with contrast showed pulmonary embolism on the right side with small clot burden and cavitary right upper and right middle lobe pulmonary nodules. A transthoracic echo showed large mobile echodensity (2.65 cm x 1.52 cm) on the tricuspid valve with regurgitation (Figure ).
The vegetation was attached to the tricuspid leaflet which was attached to the right ventricular free wall. The vegetation was globular, homogeneous, and moved freely between the right atrium and right ventricle. She was started empirically on intravenous vancomycin and meropenem. The patient went into respiratory distress requiring intubation. Blood cultures revealed methicillin-susceptible Staphylococcus aureus (MSSA), and the antibiotics were narrowed to oxacillin. She had a long and complicated hospital course. Her blood cultures remained positive for seven days despite appropriate antibiotics. A repeat echocardiogram showed a reduced size of the vegetation, and, therefore, surgery was not considered. She was given a total of six weeks of antibiotics. She followed up one and six months after discharge, and she was doing well. A repeat echocardiogram six months after discharge showed tricuspid valve with no vegetation and no regurgitation. The patient agreed to participate and was explained the nature and objectives of this study, and informed consent was formally obtained. No reference to the patient's identity was made at any stage during data analysis or in the report.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [112.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",7.5,7.5,7.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 112.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 = 6.0.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 6.0 + 1.5 = 7.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 7.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 7.5.
The patient's Well's score for pulmonary embolism is 7.5."
2921,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8287425-1,Extracted,"A 31-year-old female, a mother of 2, originally from Mtubatuba in KwaZulu-Natal,
presented to the King Edward VIII Hospital Acute Medical Unit with a 2-month history
of progressive dyspnoea (New York Heart Association (NYHA) grade 4)
 and generalised body swelling. She reported that her abdomen became enlarged
within a few days before her presentation.
She reported no chest pain, palpitations, constitutional symptoms, nor rheumatic
heart disease as a child. She was HIV-infected, diagnosed in 2019, and was currently
on a tenofovir, emtricitabine, and efavirenz fixed-dose regimen of anti-retroviral
therapy (ART). She also reported a previous history of pulmonary TB infection
diagnosed on sputum testing in 2012, for which she had completed 6 months of anti-TB
therapy. She reported no prior hospital admissions and related that she had regular
menses, no history of pregnancy losses, nor a current or previous hormonal
contraceptive history. She is of sober habits with no use of traditional or herbal
treatment.
On examination, she was clinically fluid overloaded. She had mild pallor, no
jaundice, no clubbing, and was acyanotic. She had minimal lower limb swelling –
grade 1. She had no stigmata of advanced HIV infection or had any features
consistent with chronic liver disease. She had distended pulsatile neck veins, with
a markedly raised JVP (confirmed by a positive abdominal-jugular reflex) to the
angle of the jaw – with notable CV waves. She was tachycardic (112 beats/min) with a
pulse that was irregularly irregular in rhythm, consistent with atrial fibrillation
(AF). Her blood pressure was within normal limits. She had a right-sided S3 gallop
(possible pericardial knock) with a grade 3/6 pansystolic murmur of tricuspid
regurgitation at the left sternal boarder with no clinical signs of pulmonary
hypertension (no loud pulmonic component of second heart sound (P2), no parasternal
heave and no loud P2). She was in respiratory distress with a tachypnoea (24
breaths/min); however, maintaining an oxygen saturation of 96% on room air. No
crepitations were heard on auscultation of her chest. Her abdomen was grossly
distended with ascites (notably out of proportion to the lower limb peripheral
oedema) together with a tender right upper quadrant. At this point, we entertained a
differential diagnosis that explored the presentation of disproportional ascites to
peripheral oedema.
Our considerations therefore included the following:
right heart failure (RHF) secondary to post-TB bronchiectasis with cor
pulmonale,
CP,
intra-abdominal malignancy or disseminated TB,
restrictive cardiomyopathy,
hepatic outflow obstruction,
chronic liver disease,
superior vena cava syndrome, and
right atrial myxoma.
Laboratory investigations () revealed liver function tests, suggesting a predominantly
infiltrative pattern.
Her chest radiograph showed patchy lower lobe pulmonary opacification with small
bilateral pleural effusions – not amenable to pleurocentesis, with no pericardial
calcifications being noted ().
Her echocardiogram showed right atrial dilation with evidence of a thrombus, with
mild to moderate tricuspid regurgitation. The cardiac contractility was mildly
impaired with a significant septal bounce. The IVC appeared to be dilated with a
spontaneous echo-contrast noted. There was respiratory variation, with a preserved
left ventricular ejection fraction of 47%.
The abdominal ultrasound confirmed gross ascites with hepatomegaly measuring 16 cm
with no focal lesions. The portal vein diameter was 1.2 cm (reference
range = 0.7–1.5 cm). A Doppler ultrasound of the IVC and HV showed notable sludging,
suggesting a thrombus within the aforementioned vessels.
A computed tomography (CT) scan of the abdomen and chest confirmed CP – pericardial
thickening and calcifications were demonstrated. The right atrium was enlarged with
early reflux into the IVC which was attributed to the features of RHF (arrows in
).
The final diagnosis made was that of an HIV-infected patient on ART with a previous
history of treated pulmonary TB now presenting with features suggestive of:
CP with a possible BCS (acute 2-week history of rapidly enlarging abdomen
with sludge/thrombus in both HV and IVC) associated with AF.
The patient was continued on ART and started on anti-coagulation in the form of
Clexane® 60 mg BD subcutaneous and warfarin 5 mg daily orally once
the AF was detected. She was also commenced on anti-TB treatment before referral to
the cardiothoracic department.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [112.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 112.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2922,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8113932-1,Extracted,"A 49-year-old male patient was admitted to the Department of Nephrology, The First
Hospital of Jilin University, Changchun, Jilin Province, China on 2 August 2018 with
oedema, hypoproteinaemia and proteinuria during the previous 15 days. At 1 month
before admission, he had a cough and blood in the sputum. Chest computed tomography
(CT) imaging showed a 53 mm × 38 mm tumour in the upper left lobe. His blood test
results were as follows: white blood cell count, 15.28 × 109/l; albumin,
40.2 g/l (normal range: 40‒55 g/l). His renal function was normal and he had no
history of urinalysis abnormalities or kidney dysfunction. Additionally, urinalysis
performed 10 days before surgery was negative for haematuria and proteinuria. The
patient immediately underwent wedge resection and lymph node dissection in June 2018
and biopsies revealed lung adenocarcinoma with T2N1M0 stage according to the TNM
classification.
On 17 July 2018, urine analysis showed microscopic haematuria (red blood cell [RBC]:
147/per field at high power magnification [HP]) and proteinuria (protein 3+). The
24-h urine analysis revealed proteinuria of 19.38 g/day (normal range:
<0.2 g/day) and serum albumin was 31.5 g/l (normal range: 40‒55 g/l). The patient
received the first cycle of chemotherapy (1000 mg pemetrexed + 140 mg nedaplatin;
intravenous [i.v.] infusion) in July 2018 followed by 800 mg pemetrexed + 450 mg
carboplatin i.v. infusion every 21 days for three further cycles (cycles 2–4). Two
weeks following the first cycle of chemotherapy, the proteinuria had reduced to
5.62 g/day (normal range: <0.2 g/day), urine analysis showed microscopic
haematuria (RBC: 2992/HP) and proteinuria (protein 3+), the serum albumin level was
28.6 g/l (normal range: 40‒55 g/l), the serum creatinine (Scr) level was 92.8 µmol/l
(normal range: 54‒106 µmol/l) and multi-deformation of RBCs accounted for 80%,
suggesting glomerular haematuria. His blood pressure was 150/84 mmHg and his pulse
rate was 76/min. Ultrasound examinations of the heart and lung were normal. The
patient had a 1-year history of hypertension and a history of smoking; and had
undergone a kidney biopsy in August 2018 due to lower limb oedema, proteinuria (5.62
g/day) and hypoalbuminaemia (albumin: 28.6 g/l; normal range: 40‒55 g/l).
Histological analysis of the kidney biopsy suggested lgAN. The kidney biopsy
specimen contained 10 glomeruli and immunofluorescence staining showed C3 and IgA
deposition in mesangial areas. Staining for IgG, C4 and C1q was negative ( and ). Transmission electron
microscopy demonstrated a small number of high electron-dense deposits in the
subepithelial region (). After the patient completed the second and third cycles of
chemotherapy (pemetrexed + carboplatin) from 1 October 2018 to 16 November 2018, the
urine analysis results were PRO±/RBC 23.3/HP, proteinuria decreased to 1.02 g/day
(normal range: <0.2 g/day) and Scr was 95.3 µmol/l (normal range:
54‒106 µmol/l).
The symptoms of oedema were improved during chemotherapy. No immunosuppressants or
steroids were used during treatment. The follow-up showed that the 24-h urine
protein and urinary RBC count were reduced. Kidney disease was gradually relieved
with chemotherapy and the proteinuria was 1.02 g/day after three cycles of
chemotherapy. After four cycles of chemotherapy, the urine protein levels returned
to normal and the lower limb oedema had resolved, suggesting complete remission.
This patient is followed up regularly after discharge (). At the latest follow-up on 9 June
2020, there was no evidence of lung malignancy recurrence, renal function was normal
and urine protein was negative.
The patient provided verbal informed consent for publication of the case. All patient
details have been de-identified.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [76.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",3.5,3.5,3.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 76.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 1.5 + 1 = 2.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 2.5 + 1 =  3.5.
The patient's Well's score for pulmonary embolism is 3.5."
2923,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4107435-1,Extracted,"An 87-year-old man with a history of atrial fibrillation with CHA2DS2-VASc score of 5, heart failure with preserved ejection fraction, and hypertension presented to the emergency room with weakness, decreased oral intake, and mild cough. Consent for publication of this case report was obtained from the patient’s wife. Five months earlier, the patient started dabigatran etexilate 150 mg orally twice-daily for thromboembolic prophylaxis of atrial fibrillation [which is the dose approved by the US Food and Drug Administration (FDA) for patients with normal or mildly impaired renal function—the 110 mg dose is not available in the US]. One week prior, the patient was seen by his primary care physician for increased lower extremity edema and found to have atrial fibrillation with a rapid ventricular response averaging 120 beats per minute. The serum creatinine (Cr) at the time was measured at 1.20 mg/dL [estimated glomerular filtration (eGFR) = 57 mL/min/1.73 m2 as reported by the hospital laboratory based on the isotope dilution mass spectrometry (IDMS)-traceable Modification of Diet in Renal Disease [MDRD] study equation]. The daily doses of verapamil, metoprolol, and furosemide were increased from 120 to 240, 25 to 100, and 40 to 60 mg, respectively. Two days prior to presentation, the patient fell while getting out of bed, but did not seek medical attention. On the day of admission, the patient was too weak to stand and vomited three times, prompting his family to seek emergency medical care. The last dose of dabigatran was reportedly taken 2 days prior to admission.
On initial evaluation, the axillary temperature was 95.7 °F, blood pressure 102/48 mmHg, ventricular rate 36 beats/min with atrial fibrillation (Fig. ), and oxygen saturation 96% on 2 L/min of supplemental oxygen. On examination, the patient was ill appearing but in no acute distress. The patient had 10 cm of jugular venous distension with monophasic waves and hepatojugular reflux. There were bibasilar crackles present on lung examination. Cardiac auscultation revealed a bradycardic, irregular rhythm, normal first heart sound with a physiologically split second heart sound, and a III/VI systolic murmur loudest at the upper sternal border. The abdomen was benign without organomegaly. There was 3+ pitting edema of the extremities with normal pulses bilaterally.
Upon arrival to the emergency department 2 L of intravenous (IV) normal saline and 1 mg of IV glucagon were administered. A chest X-ray revealed a right lower lobe infiltrate (Fig. ), cultures were obtained, and treatment was initiated with ceftriaxone and levofloxacin. Laboratory studies were notable for acute renal failure and hepatic dysfunction, which likely developed in the setting of septic shock from pneumonia, potentially compounded by recently increased diuretic therapy and bradycardia in the setting of uptitration of nodal blockade (Table ; Fig. ). In conjunction, laboratory studies revealed electrolyte disturbances, elevated serum lactate, and profound coagulopathy (Table ; Fig. ). The patient received 10 units of IV insulin, 50 g of IV dextrose, 2 g of IV calcium gluconate, and 50 mEq of IV sodium bicarbonate to manage hyperkalemia. Computed tomography of the head, neck, and cervical spine did not show evidence of acute hemorrhage or fracture.
On admission to the cardiac intensive care unit, the heart rate was irregular at 48 beats/min and the blood pressure was 90/50 mmHg. The patient rapidly developed worsening hypoxia and was placed on 70% oxygen at 35 L/min delivered by high flow nasal cannula. During a phlebotomy, the patient became acutely unresponsive with a loss of palpable pulses. The cardiac monitor revealed progressive bradycardia to less than 30 beats/min. The patient received approximately 2.5 min of chest compressions with return of spontaneous circulation, was intubated, and placed on mechanical ventilation.
The patient did not demonstrate any overt signs of active bleeding at any point during the hospitalization. On admission, the hematocrit was 43.5%, consistent with the patient’s baseline value. In the setting of receiving a total of 4.5 L of IV normal saline during the first day of hospitalization, the hematocrit dropped to a nadir of 33.9%, but gradually improved without infusion of red blood cells to 38.3% on day of discharge. However, taking into account the history of a recent fall, need for central venous access, and presence of multi-organ failure in the elderly gentleman with possible need for dialysis, the decision was made to reverse the coagulopathy. A reversal strategy was pursued that attempted to counteract both dabigatran toxicity and the potential for decreased hepatic synthesis of clotting factors given concern for hepatic injury in the setting of an acute transaminitis. The patient’s history of heart failure and acute renal failure limited the amount of high volume blood products that could be administered and more concentrated forms of coagulation factor replacement were considered. A total of 4 units of fresh frozen plasma (FFP), 15 mg of vitamin K (initially 5 mg orally, then 10 mg IV), and 5,020 international units (IU) of IV inactivated prothrombin complex concentrates (PCC; Profilnine®, Grifols Biologicals, Inc, Los Angeles, CA, USA) were administered on the first day of hospitalization (Fig. ). The prothrombin time (PT) and partial thromboplastin time (PTT) peaked in the first 24 h and then gradually returned to normal (Fig. ). Coagulopathy was further measured using the thrombin time at 7, 24, and 26 h after admission and was >150 s (normal range 15–30) at all three measurements. A diluted thrombin time (one part patient plasma to three parts normal plasma) was measured at 24 and 26 h and was 125.0 and 113.1 s, respectively (Table ). The hepatic transaminases and renal function also peaked on the first day with an alanine aminotransferase (ALT) of 4,590 U/L, aspartate aminotransferase (AST) of 4,965 U/L, and Cr of 3.07 mg/dL (eGFR ≤20 mL/min/1.73 m2). Thereafter, the patient’s Cr, transaminases, and coagulation parameters trended downward over the course of 10 days (Fig. ).
The patient was stabilized and treated for pneumonia in the intensive care unit for 7 days. The patient was extubated on day 5, had no signs of bleeding, and was discharged home on hospital day 19. On hospital day 5, the patient’s international normalized ratio (INR) was 1.8 (see Fig. for trend) with a PTT of 46.9 s, at which time an unfractionated heparin infusion was started for stroke prevention secondary to atrial fibrillation given a CHA2DS2-VASc score of 5 (indicating a high yearly risk of stroke), and concern that the patient was unable to reliably take oral medications in the setting of acute illness and deconditioning. However, the patient regained ability to take oral medications more quickly than anticipated and was, therefore, started on warfarin on hospital day 7. On the day of discharge, the Cr was 0.70 mg/dL (eGFR ≥60 mL/min/1.73 m2) with a PTT of 41.3 s and INR of 1.8 on warfarin. The ALT and AST were last measured on hospital day 10 at 271 and 32 U/L, respectively.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2924,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6587655-1,Extracted,"A 68-year-old Taiwanese man with a history of gouty arthritis, hyperlipidemia, and adrenal insufficiency presented in our ED after 1 month of dyspnea and low back pain. He had no history of recent surgery or illicit substances use; however, previous frequent intravenous and/or intramuscular drug injections over shoulders and buttocks for gout attacks by local clinicians were mentioned. The patient denied smoking history and had no other notable medical record except low dose prednisolone prescribed. He also denied any recent invasive procedures or surgeries. The patient had consulted another hospital for similar symptoms before this visit. He was admitted and given serial examinations—an abdominal computed tomography (CT) scan and a TTE—but only a sternal fracture with a closed perifocal hematoma was found. During admission, the patient was diagnosed with Oxacillin-sensitive S aureus (OSSA) bacteremia, but no vegetation was detected using cardiac imaging. He was discharged with an uneventful course on his first admission.
The patient's persistent dyspnea and low back pain worsened, and he returned to our ED again 2 weeks later. On presentation, the patient was afebrile and had a pulse rate of 132 beats/min, a respiratory rate of 20 breaths/min, and a blood pressure of 117/87 mm Hg. A physical examination showed bilateral crackles, a right-side wheeze on chest auscultation, and a palpable fluctuant, non-tender mass (3 × 3 cm) over the anterior chest wall. There was no heart murmur and no skin rash over the chest wall. The patient's abdomen was soft without hepatosplenomegaly. His lower legs were not swollen, and they had no skin rash. No visible erythematous changes over hand (Janeway erythema) nor painful spots over fingers (Osler's nodes) being detected. The patient's laboratory data revealed the following: White blood cell count = 17.2 × 109/L (normal: 3.4–9.1 × 109/L) with 76% polys and 16% bands; platelet count = 32 × 109/L (normal: 138–353 × 109/L); prothrombin time = 14.3 s (control: 9.4–12.5 s); C-reactive protein = 270.0 mg/L (normal: 0–8 mg/L); blood glucose = 259 mg/dL (normal: <140 mg/dL); blood urea nitrogen = 62 mg/dL (normal: 7–21 mg/dL); serum creatinine = 1.8 mg/dL (normal: 0.7–1.5 mg/dL); alanine aminotransferase = 58 U/L (normal: 0–54 U/L); lactate = 7.2 mmol/L (normal: 0.7–2.1 mmol/L); D-dimers (fibrin degradation product) > 3500 ng/mL; fibrinogen = 546.8 mg/dL (normal: 30–400 mg/dL). Arterial blood gas measured in the ED revealed severe metabolic acidosis (pH, 7.28; PaCO2, 19.2; PaO2, 226; HCO3−, 8.9; BE, −18, SaO2, 100%) under an FiO2 1.0 concentration (non-rebreathing mask). No pyuria or hematuria was detected. An initial chest radiograph in the ED revealed no significant findings, and the electrocardiogram showed sinus tachycardia. A blood specimen was obtained for culturing and intravenous antibiotic agents (piperacillin and levofloxacin) were empirically initiated.
Because the patient's hemodynamic status and oxygen saturation rapidly deteriorated during observation in the ED, computed tomography of both chest and abdomen was arranged to detect a possible infection focus. A hypodense lesion with a peripherally enhanced wall and bone involvement was found in his sternal region (Fig. A), and multiple septic emboli lesions were found in his bilateral lung fields (Fig. B). Moreover, there was a paraspinal hypodense lesion with a peripherally enhanced wall and air-trapping over the T11 level. There was also one linear fracture line on T11 (Fig. A), and an L2 compressed fracture with a small anterior paraspinal abscess with gas density (Fig. B). CT-guided percutaneous drainage from the T11-T12 paraspinal space was done on day 2, and only minimal pus-like fluid was obtained for culture.
Because of the septic pulmonary emboli, TEE was done on day 3; it showed an oscillating mass (1.56 cm in size) over the anterior and septal leaflets of the tricuspid valve and moderate tricuspid regurgitation (Fig. ). The mitral, aortic, and pulmonary valves were intact, and there were no intracardiac shunts, either ASD (atrial septal defect) or PFO (perforation of foramen ovale) being found. Cardiovascular and chest surgeons were consulted immediately for emergency surgical intervention, but the family did not wish to pursue aggressive interventions and the patient eventually expired on day 4. OSSA was isolated from the blood culture and pus-like aspirate. The diagnosis was right-sided IE complicated with sternal abscesses, septic pulmonary emboli, and lumbar spondylodiscitis.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [132.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 132.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2925,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5984920-1,Extracted,"A 45-year-old Caucasian woman presented with abdominal pain, nausea, and vomiting for 17 h. At 22 h prior to admission, she went out to dinner and drank one glass of wine. A few hours after the meal, she developed epigastric and left upper quadrant abdominal pain that was moderate, persistent, cramping, and aching; the pain radiated to her left middle back and arm without exacerbating or alleviating factors. The pain was associated with nausea, vomiting, and she could not tolerate any oral intake. She felt thirsty and had polyuria and positional lightheadedness. She reported no fever, chills, chest pain, cough, sputum production, dysuria, hematuria, diarrhea, hematochezia, and melena.
On further questioning, the patient shared that she had a history of gestational glucose intolerance 6 years ago, and has had occasional impaired fasting glucose of 81–107 mg/dL for the past 6 years. She began following an American Diabetes Association (ADA) diet 2 years ago and lost 25 lb. Additionally, she had a past medical history of supraventricular tachycardia, irritable bowel syndrome, social alcohol use, cholecystectomy, and thyroid papillary adenocarcinoma status post partial thyroidectomy complicated by postsurgical hypothyroidism. Home medications included metoprolol tartrate, levothyroxine, and meloxicam. The patient reported no family history of diabetes.
Temperature 97.7 °F, pulse 130 bpm, respiratory rate 28 bpm, BP 134/71 mmHg, weight 87 kg, height 1.68 m, BMI 31 kg/m2, SpO2 99% on room air.
The patient was in moderate distress. There was no acanthosis nigricans. Cardiovascular system revealed tachycardia. A pulmonary exam revealed tachypnea, accessory muscle usage with moderate respiratory distress. Abdominal exam revealed central obesity, normoactive bowel sounds, left upper quadrant and epigastric tenderness to palpation, no rigidity or guarding. No costovertebral angle tenderness.
CBC: WBC 25.9 × 109/L, hemoglobin 14.7 g/dL, hematocrit 45.8%, platelet 386 × 109/L, MCV 100.2 µm3. BMP: sodium 135 mmol/L, potassium 7.4 mmol/L, chloride 89 mmol/L, bicarbonate 5 mmol/L, BUN 37 mg/dL, creatinine 1.27 mg/dL, glucose 931 mg/dL, eGFR 46 mL/min.
Liver chemistry: Total bilirubin 0.2 mg/dL, AST 23 U/L, ALT 54 U/L, ALP 138 U/L, total protein 7.5 g/dL, albumin 4.5 g/dL. Calcium 8.7 mg/dL, phosphate 1.4 mg/dL, magnesium 2.1 mg/dL. VBG: pH 6.92. Repeated ABG 2 h later: pH 7.21, pCO2 16 mmHg, pO2 129 mmHg, HCO3− 6.4 mmol/L, SaO2 98% on 2 L/min oxygen by nasal cannula. Beta-hydroxybutyrate 28 mmol/L, lactic acid 4.0 mmol/L. Urinalysis showed urine ketones 80 mg/dL, leukocyte esterase negative, urine culture no growth. HbA1c 6.4%. Lipid profile: triglycerides 89 mg/dL, total cholesterol 144 mg/dL, LDL 91 mg/dL, HDL 35 mg/dL. TSH 3.12 mIU/mL, free T4 1.26 ng/dL. Troponin I < 0.01 ng/mL.
Ultrasonography of the abdomen revealed mild hepatic steatosis, incidental mild to moderate right-sided hydronephrosis, status post cholecystectomy. ECG on admission: sinus rhythm, HR 126 bpm, peaked T waves at lead V2–V6 consistent with hyperkalemia, no ischemic changes.
All procedures performed in this study were in compliance with the ethical standards of the institutional and/or national research committee and with the 1964 Declaration of Helsinki and its later amendments or comparable ethical standards. Informed consent was obtained from the individual participant for being included in the study.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [130.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 130.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2926,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7434270-2,Extracted,"A 46-year-old gravida 11 para 9 woman with history of hypertension and an uncomplicated caesarean section four months prior arrived complaining of sudden onset of mid to lower back pain and cramping that radiated to her upper abdomen and chest with associated shortness of breath with exertion. Physical exam showed a tachycardic, moderately anxious female without back or abdominal tenderness on palpation. Her initial vital signs were documented as follows: heart rate 130 beats per minute; blood pressure 116/82 mmHg; respiratory rate 16 breaths per minute; temperature 36.3°C (97.4°F); and O2 saturation 100%.
A FAST exam was negative for free fluid, and her initial labs were unremarkable. Despite fluid resuscitation, she remained tachycardic. Blood pressure readings were obtained in both of her upper extremities and a 20 mmHg difference was noted, increasing the concern for dissecting aortic aneurysm. A computed tomography (CT) of the chest with IV contrast showed a splenic abnormality vs colonic gas. At that time, a subsequent CT of abdomen and pelvis with oral contrast was obtained that revealed a large amount of fluid within the greater peritoneal cavity and lesser sac. General surgery was consulted and vascular SAA was identified and coiled. During her hospital course she remained stable. She was discharged on day three postoperatively and has not had any other complications to date.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [130.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 130.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2927,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7580365-1,Extracted,"A 26 years old G2P1L1 at 31 weeks of pregnancy complaints of shortness of breath and palpitation since 4-5 months and raised blood pressure since 24 weeks of gestation. She gives history of neck swelling since last 2 years and had taken some thyroid medication for 6-7 months but left medication 4 months back on her own. She had history of previous caesarean section done for non progress of labor 6 years back.
On examination patient was dyspnoeic, respiratory rate was 22/min, pulse 130/min, BP 140/80, with saturation of 88% at room air. Systemic examination revealed exophthalmos and diffuse thyroid swelling of 3*3cm was seen. Respiratory examination revealed normal vesicular breath sounds. Systolic murmurs were heard at aortic and mitral area and per abdominal examination revealed uterus corresponding to 28-30 weeks, with single live intrauterine fetus in longitudinal lie not in labour without scar tenderness.
On Investigation, her complete blood count, renal function test, LDH, serum uric acid, cardiac markers and LFT were normal. Her thyroid function was grossly deranged. fT3, fT4 and TSH were 37 pg/ml, 106 pg/ ml and 0.001 uIU/ml respectively. Maternal TRAb couldn't be sent due to unavailability of facility. ECHO suggestive of mild MR, moderate TR, moderate PAH, LVEF 60-65%, <50% collapsibility of left ventricle with inspiration.
She was started with Propyl thiouracil 100 mg TDS; Labetalol 200 mg TDS; Hydrochlorothiazide 12.5 mg. OD; Propranolol 20 mg BD, and Iron and Calcium tablets. Two doses of dexamethasone were given for fetal lung maturity. Patient had significant improvement in term of shortness of breath and palpitation after initiation of treatment.
During her 5th day of course of treatment, she had Preterm Prelabor Rupture of Membrane (PPROM), and IV antibiotics was started to prevent maternal and fetal infection. On subsequent day, she progressed into labor. The patient was counselled regarding the mode of delivery and its possible risk. VBAC (vaginal delivery after caesarean) was counselled with short 2nd stage of labor to be aided by instrumentation. Caesarean section was deferred due to possible intra operative and postoperative complication like supra ventricular tachycardia, atrial fibrillation and thyroid storm. With careful monitoring, patient delivered a healthy female baby weighing 1.705 kg vaginally without instrumentation.
The baby was evaluated by neonatologist. Baby was then handed over to the mother. Her TFT was sent after 72 hrs. Mother was evaluated during postpartum period. Antithyroid drug was continued and she was discharged on 4th postpartum day with advice to follow up in Medicine OPD. Patient is currently on antithyroid medication and is asymptomatic and regularly on follow up in medicine OPD.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [130.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 130.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2928,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-999,Extracted,"Five days after undergoing a pancreaticoduodenectomy for pancreatic cancer, a 46-year-old woman has 2 episodes of non-bilious vomiting and mild epigastric pain. She has a patient-controlled analgesia pump. She has a history of hypertension. She has smoked one pack of cigarettes daily for 25 years. She drinks 3–4 beers daily. Prior to admission to the hospital, her only medications were amlodipine and hydrochlorothiazide. Her temperature is 37.8°C (100°F), pulse is 98/min, and blood pressure is 116/82 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 96%. Examination shows a midline surgical incision over the abdomen with minimal serous discharge and no erythema. The abdomen is soft with mild tenderness to palpation in the epigastrium. The remainder of the examination shows no abnormalities.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [98.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 98.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2929,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7385038-1,Extracted,"The patient was a 44-year-old man who had gone to a regional hospital with worsening dyspnea on exertion and lower extremity edema approximately 2 months prior to admission. He was referred to our hospital for diagnosis and treatment. The patient did not have an obvious history of occupational or incidental exposure to asbestos. The physical examination at admission revealed jugular distension and lower extremity edema. His blood pressure was 120/58 mm Hg and heart rate was 120 beats/min. Transthoracic echocardiography and computed tomography showed massive pericardial effusion, with a maximum diameter of 53 mm at the apex of the pericardial sac and a large tumor (95 × 99 mm in diameter) occupying the lateral to posterior pericardial space (A, B). The tumor showed heterogeneous contrast enhancement, and its border was unclear. Computed tomography showed lymphadenopathy of the mediastinal and subcarinal lymph nodes. Coronary angiography revealed that feeding vessels of the tumor extended from the circumflex artery (). Thoracentesis and pericardiocentesis were performed; however the signs/symptoms of tamponade remained. Cytological findings of the pericardial fluid specimen was grade II and was negative for malignant cells. After a preoperative discussion, our team decided upon a surgical intervention for the definitive diagnosis and to reduce the tumor mass as much as possible to improve the patient’s symptoms. A median sternotomy and pericardiotomy were performed, and the bloody pericardial effusion was removed. The pericardium was thickened. The large tumor was adherent to the epicardium and pericardium and extended from the lateral to posterior side (A). We performed a blunt dissection of the adhesions. The margins between the tumor and epicardium were unclear and most of the tumor was bluntly dissected. Some of the pericardium with adhesions to firm tumor tissue was removed, and the opened pericardium was not repaired so that pericardial fluid could drain to the thoracic space to alleviate cardiac tamponade. Only the tissue that included the feeding vessels was ligated and cut with an Endo GIA surgical stapler (Medtronic, Minneapolis, Minnesota, United States) in order to cut and ligate safely. Cardiopulmonary bypass was not needed for removal of the large tumor, which was resected as much as possible. We resected the large tumor by dividing it into sections. The weight of the resected tumor was 480 g (B). The histopathological diagnosis of the resected tumor specimen was malignant mesothelioma, sarcomatoid type (). The pericardial fluid obtained at surgery showed grade V cytology. It showed irregularly shaped nuclei and numerous mitotic divisions, and the cells were identified as malignant cells. The patient’s symptoms improved and his early postoperative course was uneventful. Postoperative computed tomography showed reduction of the tumor mass (A). We recommended adjuvant therapy for the patient because of his young age and he and his family agreed to proceed. At 3 weeks after surgery, he was administered carboplatin and pemetrexed; however, the tumor progressed. The tumor was irradiated, with a temporary reduction in size. However, 2.5 months after surgery, the tumor regrew and compressed the left ventricle (B). Heart failure developed. Chemotherapy was discontinued because of hematotoxicity. Despite maximum radiotherapy, the tumor started to increase in size. The patient was transferred to hospice care for palliative therapy and died 7 months after surgery.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",5.5,5.5,5.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3.0 + 1.5 = 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 4.5 + 1 =  5.5.
The patient's Well's score for pulmonary embolism is 5.5."
2930,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5422740-1,Extracted,"A 56-year-old male patient treated on a clinical trial for bronchopulmonary carcinoid tumors metastatic to the orbit was hospitalized due to complaints of polyuria, polydipsia, weakness, and visual changes. He had experienced polyuria and polydipsia for the past few weeks, and weakness and visual changes over the past few days. One month prior he had been treated for hypertensive urgency with lisinopril and Toprol XL. No previous history of type 2 diabetes mellitus was present. His recent oncology treatment history was significant for focal irradiation of orbital metastases. On admission, his blood pressure was 134/70 mm Hg with a heart rate of 97 beats/min. The rest of the physical examination revealed dry skin, moon face appearance with red cheeks, purple-colored striae on the skin, muscle wasting, and muscle weakness, which was suspicious for Cushing syndrome. A buffalo hump was not present (Fig. ).
His laboratory examination results were notable for hyperglycemia (venous blood glucose 615 mg/dL) and metabolic alkalosis (pH 7.54; bicarbonate 32.5 mmol/L [normal: 22–26]) without ketonuria. Other values were as follows: glycated hemoglobin (HbA1c) 9.7%; potassium 2.7 mmol/L (normal: 3.5–5.1); sodium 149 mmol/L (normal: 136–145); lactate 4.9 mmol/L (normal: 0.5–2.2), and blood urea nitrogen 23 mg/dL (normal: 7–20). Blood cultures and urinalysis were negative for evidence of infection. No EKG abnormalities were present.
Based on these clinical and laboratory findings, the patient was diagnosed with HHNS. Following intravenous hydration, potassium replacement, and regular insulin infusion (0.1 IU/kg/h), the patient reported immediate symptomatic improvement. On suspicion of Cushing syndrome, an endocrine workup was started, which included measurement of serum cortisol and plasma ACTH. The values were as follows: serum cortisol 40.5 mg/dL (8: 00 a.m.; normal: 5–25) and plasma ACTH 112.3 pg/mL (normal: 7.2–63.3), confirming the diagnosis of Cushing syndrome. It is unclear whether the emergence of Cushing syndrome represents active secretion of ACTH from the tumor due to disease progression, although a recent CT scan showed stable disease with central tumor necrosis. A more intriguing possibility is that the ACTH contained within the tumor was passively released, i.e., liberated into the circulation from dead or dying neuroendocrine cells due to recent irradiation of the patient's orbital metastases.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [97.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 97.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2931,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5725403-1,Extracted,"A 65-year-old male presented to the emergency department due to acute onset of left hemiparesis, spastic dysarthria, gaze preference to the right and left hemineglect while waiting for radiotherapy for his underlying disease of right parotid gland carcinoma in the hospital. He was alert, oriented, and able to follow commands. He had a National Institute of Health Stroke Scale of 12. His hemodynamic status was stable with a blood pressure of 110/68 mmHg and pulse rate of 74 bpm. He did not complain of chest discomfort. Computed tomography (CT) of the brain revealed subtle signs of acute ischemic stroke in the right-middle cerebral artery territory (Figure A). CT angiogram showed occlusion at proximal to mid M1 segment of the right-middle cerebral artery (Figure B). Intravenous recombinant tissue plasminogen activator (rtPA) was administered with standard dose of 0.9 mg/kg at 2 h 35 min after onset. During the thrombolytic administration, an electrocardiogram was performed and showed ST elevation in leads II, III, and aVF (Figure D). Initial cardiac troponin I was 137.4 pg/mL (<34.2 pg/mL) and creatine kinase-MB (CKMB) was 27 U/L (0–24 U/L). Due to the active cardiac condition and large infarct core from the CT perfusion the neuro-interventionist decided not to perform mechanical thrombectomy after intravenous thrombolytic despite the large vessel occlusion. The emergency coronary angiography was performed and revealed total occlusion at mid left circumflex artery. Percutaneous coronary intervention (PCI) with drug eluting stent placement was performed. Thrombolysis in myocardial infarction (TIMI) grade flow of 3 (complete perfusion) was achieved after the cardiac intervention. The follow-up electrocardiogram showed resolution of the ST-segment elevation (Figure E). Serial cardiac enzyme following next 5 h revealed an elevation of both serum cardiac troponin I and CKMB of 4,643 pg/mL and 325 U/L, respectively. An echocardiogram revealed mild basal to mid inferoposterior wall hypokinesia with normal left ventricular ejection fraction of 62%. He was admitted to the coronary care unit for 1 day and then transferred to the stroke unit. The neurological deficits were unchanged. A follow-up CT scan at 24-h post-thrombolytic therapy revealed an ischemic stroke in the right-middle cerebral artery territory involving in right insular cortex, right lentiform nucleus, and right-frontal region (Figure A′).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [74.0, 'bpm'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 74.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2932,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8432438-1,Extracted,"A 35-year-old male with no known past medical history presented to the emergency department with complaints of three-day history of fever, sore throat, and a skin rash. He had developed acute-onset watery diarrhea one week before this presentation. Infection workup for diarrhea was unremarkable and he was empirically prescribed oral metronidazole 400 mg three times a day along with oral rehydration solution. Subsequently, diarrhea resolved in two days; however, four days later, he noticed flu-like symptoms, malaise, and fatigability. These symptoms were followed by an abrupt appearance of a maculopapular rash involving the torso and bilateral lower extremities prompting his visit to the emergency department. He denied the use of any other medications except for metronidazole. A review of other systems was unremarkable. On examination, he had a low-grade fever of 100.4°F, blood pressure of 105/65 mmHg, heart rate of 100 per minute, and respiratory rate of 18 breaths per minute, with an oxygen saturation of 98% on room air.
The patient was in obvious physical distress due to pain. Bilateral conjunctivae were infected. The oral cavity showed multiple ulcers on the tongue and buccal mucosa. The neck was supple with no cervical or axillary lymphadenopathy. Lungs were clear on auscultation bilaterally. He had tachycardia with normal S1 and S2. His abdomen was mildly tender in all four quadrants without hepatosplenomegaly, rigidity, or guarding. He was alert and oriented without any gross focal neurological deficits. Skin examination was remarkable for maculopapular rash involving the face, neck, torso, abdomen, back, perineal area, as well as the bilateral upper and lower extremities. There were areas of desquamation specifically involving the upper and lower back, left eyelid, and genitalia.
Laboratory investigations revealed the following results: hemoglobin 14 g/dL, white blood cell count 3,500/µL, platelets 129,000/µL, neutrophils 88%, lymphocytes 10%, eosinophils 1%, sodium 130 mol/L, potassium 4.89 mmol/L, chloride 92.1 mmol/L, blood urea nitrogen 58 mg/dL, serum creatinine 1.21 mg/dL, blood glucose 200 mg/dL, total bilirubin 0.45 mg/dL, alanine aminotransferase 41.2 U/L, alkaline phosphatase 67 U/L, and creatine kinase 674 U/L. Infectious workup for diarrhea done one week ago including stool for ova and parasites, viral polymerase chain reaction panel, stool leukocytes, and stool culture was negative. Further viral tests including hepatitis A antibody, hepatitis B surface antigen, hepatitis C antibody, and human immunodeficiency virus antibody were negative. The CT scans of the chest, abdomen, and pelvis did not identify any pathology.
He was started on supportive therapy with aggressive intravenous fluids for volume replacement. Metronidazole was stopped and intravenous dexamethasone was started along with empirical broad-spectrum antibiotics, topical steroids, and emollients. Although the plan was to perform a skin biopsy, it was deferred due to the patient’s and his family’s refusal. His clinical condition continued to worsen with rapidly progressing desquamating skin and mucosal lesions despite aggressive supportive therapy. On the third day of hospitalization, he became hemodynamically unstable and was transferred to the intensive care unit (ICU) where he developed septic shock requiring vasopressor support. The patient’s condition worsened rapidly. Skin lesions (macules and papules) extended to the distal parts of the upper and lower extremities (Figures , ), chest, upper and lower back, and genitalia. Lesions on the back transformed into bullae, which eventually sloughed off (Nikolsky sign) (Figure ). He also developed mucosal ulcers in the oral cavity (Figure ) and penile urethra. Based on the history and clinical examination, TEN caused by metronidazole was diagnosed. He did not respond to supportive therapy in the ICU and eventually developed cardiac arrest.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 100.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2933,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8327866-1,Extracted,"A 22-year-old unmarried, unemployed male, resident of urban Chandigarh, was admitted in the surgical emergency in mid-December 2019 with complaints of acute onset of chest pain (which worsened during inspiration), breathlessness, and intermittent pain in the right lower abdomen for the last one week and fever for two days. History revealed regular use of heroin for the last five years and use was predominantly via injections for the last two years; if unable to procure heroin, he would chase Smack once or twice a month. He would share injection equipment and use tap water as a re-constituent. The place of injection would largely be empty and dirty parking lots and public toilets. Urine drug screen revealed the presence of morphine and cannabis. Initial assessment revealed a pulse rate of 94/min, blood pressure 120/76 mmHg, and an axillary temperature of 101° F. The chest auscultation was unremarkable. His past medical record revealed hepatitis C seropositivity.
Initial blood investigations revealed the following: hemoglobin 12 g/dl, total leucocyte count 7300/mm3 (differential count: neutrophil 67%, lymphocyte 32%, monocyte 7%, and eosinophil 4%), platelet 2,73,000/mm3, bilirubin (total: 0.7 mg/dl; conjugated: 0.2 mg/dl), and total protein 7.1 gm/dl. He was seronegative for both hepatitis B and human immunodeficiency virus (HIV1&2). Electrocardiogram was unremarkable. A chest radiogram revealed right-sided pleural effusion. Ultrasonogram (USG) whole abdomen, done as a part of acute abdomen work-up on the same day, showed mild splenomegaly, right-sided loculated pleural effusion (2.8 cm wide, with thick septations), and appendicolith.
He was diagnosed with pleural effusion and acute appendicitis. He was treated with empirical antibiotic therapy (ciprofloxacin and metronidazole) and intravenous fluids. After one day, 10 F pigtail catheter was placed in the right pleural space under USG guidance. Pleural fluid investigations revealed the following: sugar 17 mg/dl, protein 5.7 mg/dl, adenosine deaminase 53 IU/L, and cell count 680/cmm (polymorphonuclear cells: 60%, lymphocytes: 40%). The report was indicative of exudative effusion, possibly of infective origin. Real-time polymerase chain reaction for tuberculosis was negative. Culture and sensitivity report of the pleural fluid showed Burkholderia cepacia with intermediate sensitivity to cefoperazone-sulbactam and resistance to ceftazidime, ciprofloxacin, levofloxacin, and meropenem. But the antibiotic regime was not changed as the patient showed clinical improvement.
After five days, the pigtail catheter was removed, and the patient was discharged on ciprofloxacin and metronidazole (to be continued for another five days). There was a temporary resolution of fever and breathlessness. History obtained in the emergency ward revealed past treatment in a private de-addiction service with buprenorphine assisted therapy, to which he was poorly adherent. He was admitted subsequently to the addiction psychiatry ward for buprenorphine reinduction. Then the chest pain reappeared. A chest radiogram was repeated, which revealed minimal right-sided pleural effusion. After consultation with pulmonary medicine, the patient was kept under observations, with a fortnightly repeat of chest radiogram. The pain was controlled by buprenorphine. However, the level of effusion remained unchanged, and an intermittent mild right-sided chest pain, radiating to back, continued. But he did not experience breathlessness or fever. After 25 days, he was discharged on 14 mg buprenorphine and was referred to pulmonary medicine OPD. On serial monitoring with chest radiogram, the effusion gradually reduced and finally resolved in another month.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [94.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 94.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2934,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6794146-1,Extracted,"A 71-year-old man presented to the emergency department at Mater Dei Hospital (Malta) with 4-day history of colicky lower abdominal pain, without nausea or vomiting, and an inability to open bowels despite passing flatus. He also complained of a cough productive of greenish sputum and worsening shortness of breath. On examination, he was afebrile with a blood pressure of 179/80 mm Hg, pulse of 90 beats per minute, and peripheral oxygen saturation of 92% on room air. There were bilateral fine chest crepitations on auscultation. He had lower abdominal tenderness on deep palpation but no signs of peritonism. Bowel sounds were sluggish and no hernias were identified clinically.
Urgent laboratory investigations revealed a normal white blood cell count (4.52 × 109/L), microcytic anemia (hemoglobin, 13.1 g/dL; mean cell volume, 94.4 fL), acute kidney injury (urea, 25.8 mmol/L; creatinine, 225 µmol/L; estimated glomerular filtration rate (eGFR), 30 mL/min/1.73m
2
), and serum potassium of 5.65 mmol/L. His international normalized ratio (INR) was 2.71, C-reactive protein 88.6 mmol/L, and lactate 0.4 mmol/L. A chest X-ray identified a chronic left sided pleural effusion with fibrotic changes in the right lower lung zone. Evidence of a healed left seventh rib fracture and a large hiatus hernia were also present. On abdominal X-ray, multiple dilated loops of small bowel were noted.
His past medical history was remarkable for hypertension, congestive cardiac failure, cerebrovascular accident, right subclavian vein thrombosis, left carotid endarterectomy, right pulmonary empyema, left sided pneumothorax with surgical emphysema following fifth and sixth rib fractures in 2011 (requiring chest drain), and traumatic left 6 to 12th rib fractures in 2014. He was also an exsmoker and exhibited alcohol misuse. His medications included warfarin (dose adjusted according to INR), folic acid 5 mg daily, lactulose 15 mL daily, simvastatin 10-mg nocte, and bumetanide 0.5 mg daily.
A noncontrast computed tomography (CT) scan of the abdomen and pelvis showed distended jejunal loops containing air/fluid levels likely resulting from herniated jejunum between the left chest wall and left diaphragm (
). No obvious masses or large bowel pathology were noted. A combination of coamoxiclav and clarithromycin (doses titrated according to renal function) were started for his respiratory infection. He was subsequently consented for an urgent exploratory laparotomy for possible subacute small intestinal obstruction secondary to a diaphragmatic hernia. During laparotomy, small bowel and omentum were seen herniating through a small defect in the left posterior hemidiaphragm. The contents of the sac were reduced and a Meckel's diverticulum was found inside the sac, characteristic of a Littre's hernia (
). This was later confirmed on histology and was found to be 55 mm in length and 35 mm in diameter without malignant features or ectopic elements. The diaphragmatic defect was closed with nonabsorbable polypropylene 0 sutures and the Meckel's diverticulum stapled and excised. The small bowel was milked retrogradely and its contents emptied through a nasogastric tube. A nonsuction drain was placed in the left paracolic gutter.
Postoperatively, the patient made a steady recovery. Regular chest physiotherapy was performed and thromboembolic deterrent (TED) stockings applied. The drain was removed 4 days later and antibiotics stopped after 9 days. He was deemed fit for discharge home 10 days into his admission.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 90.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 =  1.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2935,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3184045-1,Extracted,"A 42 year old woman with SLE for the past 12 years and end stage renal disease requiring peritoneal dialysis was admitted to the hospital for congestive heart failure. Her SLE was controlled on hydroxychloroquine and prednisone 10 mg daily for the past 5 years. Prior to admission, she had a long-standing IV/VI systolic murmur, and a transthoracic echocardiogram revealed severe mitral regurgitation with a left ventricular ejection fraction of 35%. A subsequent transesophageal echocardiogram showed mild mitral valve thickening without vegetations and normal aortic, tricuspid, and pulmonic valves. Three months later as she was approaching the date for her elective mitral valve repair, she was admitted with 3 days of progressive dyspnea and severe, left sided chest pain radiating to her back. Physical examination showed a thin woman without hypotension or hypoxia. Her heart rate was 95 bpm and she had the same systolic murmur. She also had bilateral pulmonary crackles. She had a diffuse hyperpigmented mottled rash over her extremities, back, and trunk without stigmata of endocarditis.
She had the following lab results with normal ranges shown in brackets when values were abnormal: a hemoglobin of 8.2 g/dL [11.5 - 16.0 g/dL], white blood cell count 8.4 K/mm3, platelets 240 K/mm3, creatinine phosphokinase 95 U/L, myoglobin 3.4 ng/mL, cardiac troponin I 0.26 ng/mL. Electrolytes were normal and her blood urea nitrogen was at baseline of 53 mg/dL [10-20 mg/dL]. The ferritin level was 2055 ng/mL [10 - 29 ng/mL]. The EKG was unchanged from before. She had a loculated effusion within the minor fissure without pneumonia.
A new transesophageal echocardiogram revealed severe aortic insufficiency with destruction of the right coronary and non-coronary cusps, severe mitral insufficiency with destruction of the anterior leaflet, a fistula between the aorta and left atrium, and a left ventricular ejection fraction of 35%. In the operating room, it was clear that the right ventricle and right atrium were enmeshed in a dense inflammatory ""phlegmon"" extending to the aortic root. The right coronary and non-coronary cusps of the aortic valve were replaced by vegetations. The anterior mitral leaflet showed a large vegetation containing pus down to the head of the papillary muscle. The patient required an aortic valve replacement, mitral valve replacement, and reconstruction of the superior vena cava, dome of the left atrium, right atrium, and intra-atrial septum.
Valve tissue was sent for pathology and microbiologic analysis. The patient was started on vancomycin and ciprofloxacin. The post-operative course was uneventful: she remained afebrile and was easily extubated on day 3. Gram stain of the valvular tissue demonstrated no white blood cells and no organisms; cultures for bacteria (retained for 14 days), fungi and mycobacteria were all negative. Histopathologic examination of the valves revealed extensive fibrin, neutrophils, and calcification suggestive of infective endocarditis (Figure ). Fungal and acid fast stains were negative. The patient was discharged on doxycycline for presumptive culture-negative endocarditis. Serologies for Coxiella burnetii and Brucella melitensis were negative. At follow-up four months later she had no bacteremia, and a repeat transthoracic echocardiogram revealed normal appearing aortic and mitral bioprostheses. Tests for Legionella were not performed during the initial evaluation though a urine Legionella antigen was negative at follow-up five months later.
The valve tissue was sent for broad-range polymerase chain reaction (PCR) amplification to Unite des Rickettsies, Faculte de Medecine, Universite de la Mediterranee in Marseille, France for the following agents: Bartonella species, T. whipplei, C. burnetii, Mycoplasma species, fungi, Streptococcus/Enterococcus species, and Staphylococcus species which were all negative. In addition, immuno-histochemistry for Bartonella species and C. burnetii were also negative.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [95.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 95.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 =  1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2936,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6235639-1,Extracted,"A 67-year-old male chronic smoker with medical history significant for chronic obstructive pulmonary disease was admitted for imaging guided biopsy of a 1.2 cm left lower lobe lung nodule found recently on a computed tomography (CT) scan of the chest. The nodule was highly suspicious for primary lung malignancy. The patient was placed in a prone position and lung parenchyma in the posterior lateral left chest was visualized. Under CT guidance, a 19-gauge guide was advanced into the left lower lobe and two separate 20-gauge core biopsy specimens were obtained from the mass. There was no hemorrhage or immediate post procedure complication. However, towards the end of the procedure, the patient started complaining of sudden onset of chest pain and became unconscious. No palpable pulses were identified. A code blue was called and cardiopulmonary resuscitation was begun according to Advanced Cardiovascular Life Support guidelines. The patient subsequently demonstrated ventricular fibrillation which responded to defibrillation shock and epinephrine. The patient had three cycles of chest compressions, one dose of epinephrine, and a shock of 200 J. He was successfully resuscitated and intubated for mechanical ventilation. A CT scan of the chest was obtained immediately after the resuscitation and it demonstrated development of a small anechoic area in the left cardiac ventricle consistent with air embolus (Figure ).
The vital signs recorded at the time were as follows: blood pressure of 130/80 mmHg, pulse rate of 90 beats per minute, respiratory rate of 18 breaths per minute, and normal oxygen saturation of 92% on room air. The patient was admitted to the intensive care unit. Bedside transthoracic echocardiogram (TTE) did not reveal evidence of an air embolus. Additionally, no cardiac wall motion abnormalities were noted. The patient remained hemodynamically stable for 24 hours, and he was successfully weaned off from the mechanical ventilator next day and discharged home in a stable condition.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [90.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 90.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
2937,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5654361-1,Extracted,"A 37-year-old white male with a 20-year history of intravenous drug abuse was admitted after experiencing fever and chills for the past month, with progressive worsening. He had been treated with antibiotics twice for suspected pneumonia. Acute delirium onset led to hospitalization. The patient had no history of chest pain or haemoptysis, but cough and fever were reported.
At admission, the patient appeared septic and had a systolic heart murmur. Clinical examination revealed the following: respiration rate, 32/min; blood pressure, 132/64 mmHg; pulse, 122/min; and temperature, 39.8°C. Table presents the results of admission laboratory tests. Chest X-ray showed left-sided pneumothorax and pleural effusion, and findings consistent with pulmonary congestion and pneumonia. Thoracic computed tomography (CT) revealed multiple septic emboli in the lungs, pleural effusion and a small left-sided pneumothorax. Within 24 h post-admission, S. aureus grew in repeated blood cultures.
Based on these findings, right-sided native valve endocarditis (NVE) due to S. aureus was suspected. Following established guidelines [, ], the patient was started on empiric antibiotic treatment with 2 g cloxacillin 6 times daily and 320 mg gentamicin once daily. The patient was considered clinically unstable and was transferred to a university hospital the day after admittance.
Transthoracic echocardiogram (TTE) and transoesophageal echocardiogram (TEE) revealed aortic endocarditis with vegetations, aortic valve destruction, Grade 4 aortic insufficiency and small mitral insufficiency, but no signs of mitral valve vegetations. Infective endocarditis was diagnosed based on the modified Duke criteria [, ], as the patient met two major criteria (S. aureus growth from two blood cultures and endocardial involvement evidenced on echocardiogram) and three minor criteria (intravenous drug use, fever and vascular phenomena with septic pulmonary infarcts). However, there were no signs of right-sided endocarditis to explain the septic embolization to the lungs.
CT scan revealed right-sided thrombi in the ileofemoral vein segment. The patient exhibited severe cardiac decompensation despite intensive medical treatment, and thus underwent open heart surgery with biological aortic valve insertion 1 week after hospitalization. Postoperatively, the patient exhibited pleural effusion despite repeated pleural fluid drainage, and large amounts of pericardial fluids, generalized oedema, and clinical signs of right ventricle cardiac failure with pulmonary congestion.
Two weeks postoperatively, reinvestigation of previous CT scans showed rapid contrast filling in the inferior caval vein (Fig. a) as well as the right common iliac vein (Fig. b), almost simultaneously with the abdominal aorta. Recent CT scans showed dissolution of most of the right-sided, ileofemoral deep vein thrombus. Right groin palpation revealed fremissement. Doppler ultrasound demonstrated an unusually large arteriovenous (AV) fistula localized between the cranial part of the superficial femoral artery and the femoral vein. Flow in the fistula was estimated as 11.2 l/min.
Endovascular treatment of the AV fistula was performed in the following day. The contralateral femoral artery was accessed, angiography showed the fistula (Fig. a) and a stent-graft (Fluency, Tempe AZ, USA) was implanted in the cranial part of the right superficial femoral artery, covering the fistula (Fig. b). Treatment eliminated the arterial phase contrast filling in the veins. The patient recovered rapidly and was discharged 1 month later, after a total hospital stay of almost 8 weeks. Intravenous antibiotic treatment (cloxacillin and ciprofloxacin) continued until discharge. After discharge, he received oral trimethoprim sulfamethoxazole for another 4 weeks. At last follow-up, he showed no signs of recurrent infections, but was still intermittently abusing drugs.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [122.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Immobilization for at least 3 days': False, 'Previously Documented Pulmonary Embolism': False}",7.5,7.5,7.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 122.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 = 6.0.
The patient not been diagnosed with pulmonary embolis (PE), but the patient has previously been diagnosed with deep vein thrombosis (DVT), we increase the current total by 1.5 so that 6.0 + 1.5 = 7.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 7.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 7.5.
The patient's Well's score for pulmonary embolism is 7.5."
2938,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7498957-1,Extracted,"A 57-year-old female with family history of mitral valve prolapse presented to the hospital
with altered mental status, preceded with 1 week of fatigue, generalized weakness, episodes
of nonbloody vomiting, and diarrhea. Patient denied chest pressure, chest pain, fever, or
history of intravenous drug use. On presentation, vitals were within normal limits except
for heart rate of 135 beats per minute. Physical examination showed a thin, dry, lethargic
female with Janeway lesions over palms and soles (white arrows, and ), Osler nodes (red arrow, ), and splinter hemorrhages (). The heart rhythm was
regular, and no murmurs were appreciated. Laboratory findings were significant for white
blood cell count of 17 000/mm3 (normal 3700-11 000/mm3), hemoglobin of
11.7 g/dL (normal 12.0-16.7 g/dL), platelets 89 000/mm3 (normal 135 000-400
000/mm3), and point of care troponin of 0.28 ng/mL (normal 0.00-0.034 ng/mL).
Electrocardiogram (EKG) showed sinus tachycardia with nonspecific ST-wave changes. Blood
cultures were drawn, and patient was started on intravenous fluids and empiric intravenous
antibiotics (ceftriaxone and vancomycin). Follow-up troponin returned at 0.85, and heparin
drip was initiated. Patient was chest pain free. Serial EKG revealed persistent sinus
tachycardia without ST-segment changes. Computed tomography (CT) scan of brain showed
subacute infarcts in the cerebral hemispheres, and CT scan of chest and abdomen also showed
infarctions in the kidney and spleen. Heparin drip was stopped at that time. Transthoracic
echocardiogram (TTE) was ordered, and cardiology was consulted. Blood cultures turned
positive for methicillin-sensitive Staphylococcus aureus. TTE showed an
ejection fraction (EF) of 55% without vegetations. On day 3 of hospitalization, patient
experienced chest pain, with repeat EKG showing new diffuse ST-segment elevation and PR
depression consistent with pericarditis. Patient was treated with nonsteroidal
anti-inflammatory drugs with symptomatic relief. Repeat TTE was requested and showed EF of
35% to 40% with severe diffuse hypokinesis of the apical wall and a possible vegetation on
mitral valve. Transesophageal echocardiogram (TEE) was scheduled on day 4, confirming EF of
30% to 35% with severe hypokinesis and medium-sized, 1.3 cm (L) × 1.0 cm (W), mobile
vegetation on the atrial aspect of the tip of the anterior leaflet of mitral valve
associated with moderate to severe mitral valve regurgitation (red arrow, ). Cardiothoracic surgery was
consulted. Post TEE, patient developed shortness of breath and decompensated rapidly into
cardiogenic shock. Patient was placed on vasopressor support. Troponin trended up to 49.50
ng/mL. An emergent cardiac catheterization revealed no signs of atherosclerotic coronary
artery disease but a 100% occlusion of the proximal left anterior descending (LAD) artery
suspicious for a septic embolus (blue arrow, ). Patient was transferred to cardiac
intensive care unit for further stabilization. The following day, patient underwent
successful mitral valve replacement with coronary artery bypass grafting (CABG; left
internal mammary artery to LAD). Gross specimen showed vegetations involving the mitral
valve leaflets (). Patient
did well in the postoperative period and was discharged to a rehabilitation center 2 weeks
later in stable condition with 6 weeks of intravenous antibiotics (cefazolin 2 g
intravenously every 8 hours) from the date of the surgery, metoprolol tartrate, furosemide,
and potassium chloride.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [135.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 135.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2939,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6687317-1,Extracted,"A 40 year-old male with no known past medical history presented with palpitations that started within one hour after smoking marijuana. The palpitations were associated with substernal chest pain, which was non-radiating, not pleuritic, and not related to change in position. The patient denied dizziness or syncope. Exercise tolerance at baseline was more than 1 mile. At time of presentation, his heart rate was 190 beats per minute, blood pressure was 117/57 mmHg, respiratory rate was 18 per minute, and he was afebrile. Electrocardiography revealed the rhythm to be AVNRT (). The patient spontaneously converted to normal sinus rhythm with premature ventricular complexes (). Bloodwork revealed no electrolyte abnormalities and the patient was euthyroid. Urine toxicology was positive for marijuana use and negative for other illicit drugs. Mild troponin elevation was noted, with values of 0.018, 0.213, and 0.138 ng/mL (normal value < 0.010 ng/mL). The levels were attributed to demand ischemia. The patient underwent AVNRT ablation without complications.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [190.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 190.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2940,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5999392-1,Extracted,"A 44-year-old female with no significant past medical history presented with a one-day history of pleuritic chest pain and dyspnea. She denied any history of fever, chills, nausea, and vomiting. In the emergency room, she had a temperature of 35.1°C, heart rate of 107 per minute, respiratory rate of 22 per minute, and blood pressure of 70/35 mmHg; she was alert but lethargic, and no focal neurological deficit was noted. Laboratory evaluation revealed hemoglobin of 12.7 gm/dl, white blood cell (WBC) count of 16.08 k/cumm with neutrophilia, normal renal function and elevated troponin (0.321 ng/ml, normal 0.000-0.028). An electrocardiogram (EKG) showed sinus tachycardia, low voltage, PR suppression and ST changes consistent with acute pericarditis. Echocardiogram showed normal left ventricular systolic function with calculated ejection fraction of 70%, small pericardial effusion without tamponade physiology. Computed tomography (CT) (Figure ) demonstrated a moderate pericardial effusion in a patient with a normal heart size, moderate pleural effusions and marked peribronchovascular ground glass opacifications (representative of pulmonary edema).
Her hypotension persisted despite aggressive fluid resuscitation, and she was started on vasopressors norepinephrine and epinephrine to maintain mean arterial pressure >65. Blood cultures were ordered, and she was started on broad-spectrum antibiotics consisting of vancomycin 1.5 gm IV every eight hours (~15 mg/kg), piperacillin-tazobactam 4.5 gm IV every eight hours and levofloxacin 750 mg IV once daily. Further evaluation revealed C-Reactive protein of 13.8 mg/dl (normal <0.6 mg/dl), random serum cortisol level of <1.0 mcg/dl collected at 09:00 AM (normal A.M. specimens 3.7-19.4 mcg/dl). She was diagnosed with acute pericarditis and was started on Ibuprofen 800 mg every eight hours along with hydrocortisone 100 mg IV every eight hours for adrenal insufficiency. Patient clinically improved after starting steroids and vasopressors were weaned. As her infectious workup was negative, antibiotics were stopped. She was thought to have stress-induced relative adrenal insufficiency likely secondary to viral pericarditis; she was discharged home after 11 days, with a tapering dose of hydrocortisone over four days and was advised to closely follow up with primary care physician and cardiologist.
Three weeks later, she presented to local emergency room with complaints of persistent nausea, vomiting, chills, and weakness. In the emergency room, she had a temperature of 33.1°C (91.5°F), heart rate of 103 per minute, respiratory rate of 25 per minute, and blood pressure of 49/23 mmHg; she was alert but lethargic, and no focal neurological deficit was noted. Laboratory evaluation revealed hemoglobin of 11.9 gm/dl, WBC count of 23.37 k/cumm with neutrophilia. Comprehensive metabolic panel showed hyponatremia (130 mmol/L, 135-147), hypokalemia (3.4 mol/L, 3.5-5.0), and elevated creatinine of 2.9 mg/dl (normal 0.6-1.1 mg/dl). Further workup revealed elevated troponin (0.165 ng/mL, normal 0.000-0.028) and low 8:00 AM serum cortisol level of <1.2 mcg/dl (normal A.M. specimens 3.7-19.4 mcg/dl). EKG showed sinus rhythm with frequent supraventricular premature complexes, low QRS voltage and nonspecific ST and T wave changes. Her hypotension persisted despite aggressive fluid resuscitation, and she was started on vasopressors norepinephrine and dopamine to maintain mean arterial pressure >65. Echocardiogram showed loculated pericardial fluid adjacent to the right ventricle with echocardiographic evidence of tamponade. Emergent pericardiocentesis yielded 250 ml of straw color fluid. Blood pressure improved after the procedure.
The pericardial fluid contained 3.287 k/cumm WBC mainly polymorphonuclears but negative cultures (aerobic, anaerobic, acid-fast bacilli smear and fungal cultures). After the urgent pericardiocentesis, she was still noted to have a small effusion and ultimately pericardial drain was placed. Unfortunately, her hospital course was complicated by left-sided pneumothorax with thoracostomy tube placement. Repeat echocardiogram showed normal right ventricular size, normal systolic function with resolved pericardial effusion seen earlier. Endocrinology was consulted for further workup and management of adrenal insufficiency of unclear etiology. Table below shows results of the endocrine evaluation, with notable findings of mildly elevated thyroid-stimulating hormone (TSH) at 6.1 mcIU/ml with normal free T4 likely suggesting sick euthyroid syndrome.
Rheumatology was consulted for further evaluation of pericarditis, and further workup was negative for Lyme disease antibody, rheumatoid factor, antinuclear antibodies (ANA), Immunoglobulin G (IgG) antibody, smith antibody, parvovirus B19 IgG and Immunoglobulin M (IgM) antibody, human immunodeficiency virus (HIV), and compliments levels were normal. Interferon-gamma release assay (TB Gold) testing was negative. The patient was initially started on IV stress dose steroids, but following clinical stabilization, hydrocortisone was switched to a physiological dose of 15 mg in AM and 10 mg in PM. She was discharged with advice for follow-up with an endocrinologist in one month.
Upon follow-up at one month, she has done well as a whole except for complaint of increased appetite and weight gain of 20 lbs since her hospitalization. Unfortunately, ACTH level was not done before the commencement of steroids during her admission, complicating the differentiation of primary and secondary adrenal insufficiency. She did not need mineralocorticoid replacement, therefore, she was diagnosed with secondary adrenal insufficiency rather than primary adrenal insufficiency. Pituitary magnetic resonance imaging (MRI) showed mildly heterogeneous enhancement within a normal-sized pituitary gland, no discrete mass was identified. Due to significant weight gain, the dose of hydrocortisone was reduced from 22.5 mg to 20 mg PO daily (15 mg in AM and 5 mg in PM). Unfortunately, the patient was lost to follow-up.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [107.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 107.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2941,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-5053,Extracted,"A 24-year-old woman presents to the emergency department for chest pain and shortness of breath. She was at home making breakfast when her symptoms began. She describes the pain as sharp and located in her chest. She thought she was having a heart attack and began to feel short of breath shortly after. The patient is a college student and recently joined the soccer team. She has no significant past medical history except for a progesterone intrauterine device which she uses for contraception, and a cyst in her breast detected on ultrasound. Last week she returned on a trans-Atlantic flight from Russia. Her temperature is 98.4°F (36.9°C), blood pressure is 137/69 mmHg, pulse is 98/min, respirations are 18/min, and oxygen saturation is 99% on room air. Physical exam reveals an anxious young woman. Cardiac and pulmonary exam are within normal limits. Deep inspiration and palpation of the chest wall elicits pain. Neurologic exam reveals a stable gait and cranial nerves II-XII are grossly intact.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [98.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 98.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2942,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6205872-1,Extracted,"A 53-years-old female with the history of morbid obesity status post-Roux-en-Y gastric bypass surgery presented with a chief complaint of dyspnea on exertion and intermittent substernal chest pain. The patient reported that for the past two months she would feel very short of breath during early 10-15 minutes of exercise, however, with continued exertion her symptoms resolved. The patient then began to develop intermittent substernal chest pain, not associated with exercise, which prompted her to present to the emergency department. On further history, the patient stated that she has had dyspnea on early exercise after massive weight loss since bariatric surgery, but her symptoms worsened after she moved to high altitude in Albuquerque two months ago. The patient had undergone bariatric procedure five years prior to presentation and subsequently lost 100 pounds with an 18-point drop in body mass index (BMI).
On emergency department visit, the patient’s physical exam revealed resting bradycardia with a heart rate (HR) of 55 beats per minute (BPM) and blood pressure at 89/54. The patient was of normal weight with a BMI of 24. The patient denied any history of tobacco abuse, excessive consumption of alcohol or drug use. She also denied being on any negative ionotropic drugs.
Electrocardiogram (EKG) revealed non-specific ST waves changes (Figure ).
High sensitivity troponin I was within normal range (<0.017). Given EKG changes and a strong family history of coronary artery disease (CAD), the patient underwent EKG exercise stress test per the Bruce protocol.
The patient’s resting HR was 68. Stage I of exercise patient’s heart rate was 81. The patient did not experience a significant rise in heart rate until later part of stage III of exercise at 10.4 metabolic equivalents (METs) where her rate increased to 133 beats per minute. The patient did not achieve target HR until stage IV of exercise when her HR did increase to 148 which was 88% of age-predicted HR. Notably, the patient did experience profound dyspnea during the test, which improved once she reached HR of 133 at the ninth minute during stage III of exercise (Table ) (Figure ).
The patient’s resting bradycardia, hypotension, and delay of appropriate heart rate response during exercise stress testing prompted patient’s chart review. Comparison of resting heart rate before and after significant weight loss revealed a marked difference. Prior to bariatric intervention, the patient’s heart rate averaged in the 80s. After 100 lb weight loss and the decrease in BMI of 46% the patient’s heart rate dropped significantly, averaging in the 50s. The patient’s blood pressure followed a similar trend (Figures , ).
Retrospective chart review also revealed that approximately one year after a Roux-en-Y procedure and 100 pounds of weight loss, the patient presented to her primary care clinician complaining of light-headedness and hypotension at home. This was deemed to be due to “dehydration” related to gastric bypass surgery. Reviewing multiple clinic visits prior to presentation, the patient suffered from a dizzy feeling intermittently for four years prior to presenting to our facility, wherein she had just recently moved to Albuquerque, New Mexico at an elevation of >5,000 feet.
Ultimately, the patient’s chest pain was determined to be due to gastroesophageal reflux disease (GERD) and a large hiatal hernia as a complication of her bariatric intervention. However, her dyspnea on exertion was determined to be secondary to the delayed chronotropic response due to overwhelming cholinergic tone and less sympathetic tone at baseline due to hormonal changes associated with massive weight loss. The patient was counseled about her condition with the plan to follow her symptoms in subsequent clinic visits.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [148.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 148.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2943,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3586573-1,Extracted,"A 56-year-old male was admitted to our hospital with aggravated dyspnea over the previous 24 hours. He had a past medical history of right upper lobectomy for lung adenocarcinoma two years before. The pathologic stage was T3N1Mo (TNM stage IIIA), and adjuvant chemotherapy with vinca alkaloid (vinorelbine) had been followed postoperatively. However, newly-developed brain metastasis and metastatic nodules in the superior segment of the right lower lobe, had been diagnosed six months after the lung resection. He had undergone a whole brain radiation therapy and concurrent palliative chemotherapy with variable sequential regimens (pemetrexed, erlotinib, gemcitabine/cisplatin, and docetaxel) till six months before the re-admission. During the subsequent follow up the patient had shown a stable clinical course.
The patient was incidentally detected with right superior pulmonary vein thrombosis on follow up chest computed tomography, five months before the re-admission, and complained intermittent right arm swelling at this time. For the pulmonary vein thrombosis, he had been taking 2.0 mg to 2.5 mg of warfarin for five months. Prothrombin times (International Normalized Ratio, INR) had been usually controlled within 1.8 to 3.3 (INR target range: around 2.0), and he had not been prescribed other drugs that affect vitamin K metabolism during the previous six months. At the initial physical examination, the patient was looking very acutely-ill and markedly dyspneic. He did not present other respiratory symptoms like cough and hemoptysis. His vital signs were as follows: blood pressure 130/80 mmHg, pulse rate 115 beats/min, respiratory rate 40/min and body temperature 36.1°C. Auscultation revealed diffuse inspiratory crackles over both lungs. Results of laboratory investigations are shown in Table . There was no evidence of renal or hepatic dysfunction or autoimmune diseases. Any infection, heart failure, and platelet dysfunction were not suspect from the laboratory findings.
A chest X-ray revealed increased bilateral pulmonary infiltrations, and chest computed tomography showed newly developed extensive ground-glass attenuations with crazy-paving appearance on whole lung fields (Figure ). Ceftriaxone (2.0 g, once daily) and levofloxacin (750 mg, once daily) were empirically administered to prevent pneumonia. Warfarin was discontinued, and 10 mg vitamin K and 10 fresh frozen plasmas were administered intravenously. The deranged INR and activated partial thromboplastin time (aPTT) were corrected to 1.43 and 33 seconds respectively on the following day.
Since the patient’s oxygenation was not improved, despite maximum oxygen therapy through facial mask, endotracheal intubation and mechanical ventilation had to be started. Bloody secretions through the endotracheal tube were observed, and a flexible bronchoscopy was performed. Fresh blood on the whole bronchial system was observed, without any other endobronchial lesions (Figure ). The bronchoscope was wedged into sub-segmental bronchi, and we confirmed the diagnosis of DAH by finding bronchoalveolar lavage (BAL) to become progressively more hemorrhagic. A cytopathological analysis with iron stains was not performed in the bronchoalveolar lavage (BAL) fluid. All cultures of sputum, BAL fluid and blood did not reveal any causative pathogens. The patient showed pure DAH confined to the lungs, and there was no evidence of disseminated intravascular coagulation or hemorrhagic events occurring elsewhere in the body.
In spite of maximal ventilatory supports (pressure control mode, a pressure support of 20 mmHg, at a rate of 20 breath/min, PEEP of 14 cmH2O and a FiO2 of 1.0), the patient remained severely hypoxemic (pH 7.36, PaCO2 42.3 mmHg, PaO2 48.4 mmHg and SaO2 79.3%). Since the patient had very small safety margin in the remaining lung parenchyma, we decided to perform ECMO, instead of prone position, nitric oxide inhalation, and recruit maneuver.
A veno-venous type ECMO (EBS, Capiox® Emergency Bypass System, Terumo Inc., Tokyo, Japan) was applied to the patient on the day of hospitalization, with a 21-Fr drainage cannula from the left femoral vein and a 17-Fr return cannula into the right internal jugular vein (Figure A). ECMO was instituted without heparinization due to risk of alveolar hemorrhage. During ECMO, INR and aPTT of the patient were maintained within 1.25 to 1.43 and 21 to 33 seconds, respectively. Mechanical ventilatory care was minimally maintained (pressure control mode, a pressure support of 10 mmHg, at a rate of 10 breaths/min, a positive end-expiratory pressure of 10 cmH2O, and a FiO2 of 0.3) for lung protective strategy. Arterial blood gas analysis showed improved oxygenation and undisturbed gas exchange (Table ), one hour after the application of ECMO. On day 5 after ECMO application, chest radiography showed diffuse pulmonary infiltrations were resolving (Figure B), and the oxygenation was improved, thus ECMO was removed. The duration of ECMO was 126 hours, and there was no complication associated with the procedure. An exchange of the oxygenator membrane was not needed, even though we did not use heparin. We performed extubation without tracheostomy 3 days after ECMO removal. the patient was discharged 42 days after the extubation and remained free from respiratory symptoms. We did not prescribe warfarin due to the concern of recurrent fatal DAH and the absence of symptoms of pulmonary or peripheral venous thrombosis. The patient has been controlled recently and is doing well.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [115.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",7,7,7,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 115.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 6.0 + 1 =  7.0.
The patient's Well's score for pulmonary embolism is 7.0."
2944,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6601163-1,Extracted,"A 30-year-old female was admitted for nausea, vomiting, and altered mental status. The patient had a past medical history of treatment-naïve Hepatitis C and remote intravenous drug abuse that was complicated by MRSA tricuspid valve (TV) endocarditis. She underwent a bioprosthetic TV replacement 16 months previously, however, suffered a heroin relapse 6 months later that was complicated by recurrent endocarditis; she was medically managed with 6 weeks of intravenous gentamycin, cefazolin, and rifampin. She was doing well until this presentation and taking no medications.
Her vital signs upon presentation were significant for fever of 40.5°C, blood pressure 70/30 mmHg, heart rate 134 b.p.m., and respiratory rate of 34 breaths per minute with appropriate oxygen saturation. Physical exam was remarkable for jugular venous distention of 10 cm and grade II/VI holosystolic and diastolic murmurs at the left lower sternal border. Skin had a livedo reticularis appearance with numerous tattoos. Electrocardiogram revealed sinus tachycardia with rightward axis deviation and right atrial enlargement. Admission labs were significant for white blood cell count of 23.4 × 109/L (3.7–11.0 × 109/L), platelet count of 37 000/µL (150–400 × 103/µL), lactic acidosis of 6.9 mmol/L (0.5–2.2 mmol/L), PT INR of 1.8 (0.9–1.3), D-dimer >35 200 ng/mL (<500 ng/mL), and fibrinogen 234 mg/dL (200–400 mg/dL). The patient was empirically started on vancomycin and piperacillin-tazobactam due to concern for septic shock; blood cultures subsequently grew MRSA and piperacillin-tazobactam was discontinued. Transthoracic and transoesophageal echocardiograms demonstrated thickened bioprosthetic TV leaflets with severe stenosis (peak/mean gradient 20/14 mmHg) and regurgitation and a large mobile echodensity consistent with vegetation (Figure). Chest computed tomography demonstrated numerous subpleural nodules concerning for embolic phenomena.
She was supported with aggressive volume resuscitation, maximal doses of three vasopressors (norepinephrine 50 mcg/min, epinephrine 50 mcg/kg/min, and vasopressin 0.04 units/min), and continuous venovenous haemodialysis due to acute renal failure with haemodynamic improvement by hospital day 3. However, her skin lesions progressively worsened and, by hospital day 5, included (i) violaceous discolouration of distal nose and ears, (ii) large purpuric plaques on arms and legs, most severe distally and of all digits, and (iii) haemorrhagic bullae scattered within purpuric plaques with large areas of grey discolouration suggestive of necrosis (Figure). Our leading differential diagnosis was vasopressor-induced skin necrosis given her significant exposure to vasopressors. However, the exposure was not prolonged and the appearance of the rash was atypical. The haemorrhagic appearance of the rash raised a concern for a vasculitic process such as catastrophic anti-phospholipid syndrome, levamisole-mediated vasculitis given a history of substance abuse, or antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis in light of significant renal dysfunction. The differential also included cryoglobulinaemia or a viral-mediated process such as Hepatitis B or human immunodeficiency virus (HIV) given a history of untreated Hepatitis C and previous intravenous drug abuse. Finally, our differential included PF given a severe septic state with profound coagulopathy and thrombocytopenia despite no evidence of underlying liver dysfunction at baseline. Further work-up noted: C3 86 mg/dL (86–166 mg/dL), C4 14 mg/dL (13–46 mg/dL), negative lupus anticoagulant, serum levamisole, cryoglobulins, and negative serologic testing for active Hepatitis B, HIV, and anti-neutrophilic cytoplasmic antibodies. Function of protein C was 45% (76–147%), protein S 31% (59–131%), and antithrombin 54% (84–138%). Factor VIII: C of 441 suggested appropriate liver synthetic function. This constellation of findings was consistent with PF with secondary bullae formation and skin necrosis.
On hospital day 7, intravenous human protein C concentrate (Ceprotin) was initiated with 100 units/kg bolus followed by 50 units/kg infusion every 6 h. With this, skin lesions rapidly improved and thrombocytopenia resolved (Figure). Blood cultures remained positive on repeated cultures and ultimately cleared following transition from vancomycin to ceftaroline on hospital day 16. She was taken to the operating room on hospital day 19 with findings notable for obstructive vegetation involving all three TV leaflets, abscess cavity around the annulus, and vegetations extending into the right ventricle and subvalvular space. She underwent debridement and removal of the infected valve (FigureA) followed by bioprosthetic TV replacement. Movat staining showed a pericardial tissue valve with marked acute inflammation and fibrinous vegetation (FigureB). Gomori methenamine silver stain showed bacterial cocci which on Gram stain revealed Gram-positive cocci in clusters.
Post-operatively she did well though remained dialysis dependent. Dry gangrene of her left foot and several right toes persisted. For this, she has followed with Vascular Surgery. She was ultimately discharged to a skilled nursing facility after completion of ceftaroline for 6 weeks for rehabilitation given a prolonged hospital stay. She has been seen in follow-up and is doing well.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [134.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 134.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2945,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-8510,Extracted,"A 58-year-old woman with breast cancer presents to her primary care physician for referral to a medical oncologist. She denies any personal history of blood clots in her past. Her past medical history is significant for preeclampsia, hypertension, polycystic ovarian syndrome, and hypercholesterolemia. She currently smokes 1 pack of cigarettes per day, drinks a glass of wine per day, and she currently denies any illicit drug use, despite a history of cocaine use. The vital signs include: temperature 36.7°C (98.0°F), blood pressure 126/74 mm Hg, heart rate 111/min and irregular, and respiratory rate 17/min. On physical examination, she has a grade 2/6 holosystolic murmur heard best at the left upper sternal border, bilateral bibasilar crackles on the lungs, and a normal abdominal examination. At her follow-up with the oncologist, they subsequently plan to start the patient on a highly emetic chemotherapeutic regimen.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [111.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Surgery in the previous 4 weeks': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 111.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2946,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4797165-1,Extracted,"A 37-year-old, active Caucasian man was admitted to our hospital’s acute medical unit with a 1-week history of erythematous painful swelling of his right elbow and arm. He had no history of fever and rash. His systemic review was generally unremarkable. He worked as an engineer but also did judo tutoring in the evenings. He was normally fit and well, had no family history of thrombosis, and had not undergone surgery recently or in the past. He was not on any regular medication, denied any current or previous history of recreational drug use, and had no known history of drug allergy.
After a routine judo training session, he noticed acute onset of a red, swollen, and painful right arm. He presented to his general practitioner (GP), who made a diagnosis of cellulitis with possible trauma-related musculoskeletal injury. He was subsequently commenced on analgesics and antibiotics. About 1 week later, he attended a follow-up examination with his GP, who immediately referred him to the hospital because he showed no improvement. On admission, his temperature was 37.3 °C, his blood pressure was 124/74 mmHg, his pulse rate was 80 beats/minute, his respiratory rate was 16 breaths/minute, and his oxygen saturation was 96 % on room air.
His physical examination revealed noticeable swelling and redness from his right elbow to his shoulder as well as mild erythema and tenderness of the affected area. No superficially engorged vein was noted on his chest. All of his systemic examinations were essentially within normal limits. All of his blood workup results, including the coagulation profile, were unremarkable, except for a slightly elevated C-reactive protein level of 26 mg/l (normal range <5 mg/l).
The working differential diagnoses of possible olecranon bursitis and right arm cellulitis to rule out DVT were made. The patient was then commenced on parenteral antibiotics and low molecular weight heparin pending further investigations. The x-rays of his right elbow, right arm, and chest showed no abnormalities; however, venous Doppler ultrasonography revealed a right axillary DVT with extension into the cephalic and brachial veins.
Thrombophilia screening was performed, and the patient was started on warfarin with a plan to discharge him to home with community-based anticoagulant clinic follow-up. While waiting for discharge, he was moved to a medical outlier ward on the diabetes ward due to bed pressures. The consultant on the ward reviewed the patient’s case and made a diagnosis of PSS, and an urgent requests for consultation was sent to the vascular surgical team for review of further management.
The vascular team organized catheter-directed thrombolysis (CDT) to clear the patients’ extensive thrombosis. A prethrombolysis venogram (Fig. ) with extensive thrombosis showed marked reduction in thrombus load within the axillary and subclavian veins after a postlysis venogram (Fig. ) was performed. Following thrombolysis, an early thoracic outlet decompression via a transaxillary first rib resection was undertaken to reduce the risk of recurrent thrombosis and long-term morbidity. The BMJ Best Practice treatment guideline for thoracic outlet syndrome [] provides a good illustration of this procedure. The patient had an uneventful postoperative recovery. He was subsequently anticoagulated and was discharged to home with a target international normalized ratio of 2–3. A few weeks after his surgical procedure, the patient was followed in the outpatient clinic. The swelling of his right arm had completely almost resolved. The patient reported no postoperative complications.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
The patient's Well's score for pulmonary embolism is 3."
2947,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-9365,Extracted,"A 42-year-old woman presents to her family physician with a headache. The patient reports that the symptoms started about 2 hours ago when she woke up and have not improved. She states the pain is moderate, throbbing, tight in character, and is located in the occipital region bilaterally. The patient denies any visual and audio disturbances, nausea, and vomiting. She recalls 2 similar headaches in the past month. She has no other relevant medical history. Current medications are alendronate and a daily multivitamin. The patient works long hours as a corporate attorney. A review of systems is significant for mild photophobia. Her temperature is 37.0°C (98.6°F), the blood pressure is 110/70 mm Hg, the pulse is 70/min, the respiratory rate is 18/min, and the oxygen saturation is 98% on room air. On physical exam, the patient is alert and oriented. There is moderate tenderness to palpation diffusely over the upper posterior cervical muscles and occipital region of the scalp. The remainder of the physical exam is normal. Laboratory tests are normal. Urine pregnancy test is negative.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [70.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 70.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2948,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8412003-1,Extracted,"A 67-year-old man, a known Jehovah's witness, presented to our tertiary care setup with progressive worsening of fatigue, anorexia, dull generalized abdominal pain with frequent bloating and constipation, and unintentional 55 pounds weight loss over two months. Associated with these changes was increasing shortness of breath with the slightest exertion, two months preceding the worsening fatigue. In the emergency department, the patient was febrile with 100.7F, blood pressure being 89/60 mmHg, tachypnea with a respiratory rate of 23 breaths per minute, resting tachycardia to 110 beats per minute, and low oxygen saturation to 90% on room air which worsened to 86% on minimal exertion. On physical exam, the patient appeared tired, had scleral icterus, triceps wasting, dry mucous membranes, and abdominal tenderness to palpation over all quadrants, most pronounced in the epigastrium and right upper quadrant.
Complete blood count and comprehensive panel were obtained on initial labs, which were significant for hemoglobin of seven grams per deciliter (g/dl) and borderline normocytic anemia with poikilocytosis and occasional target cells, normal leukocyte and platelet count; elevated blood urea nitrogen to creatinine ratio and severe hypercalcemia to 14.2 milligrams per deciliter. Given hypoxia at room air, the patient was sent for computed tomography (CT) of the chest showed submassive pulmonary embolism with extension to segmental and subsegmental vessels bilaterally. In the emergency department, the patient was given boluses of normal saline with calcitonin, zoledronic acid, therapeutic low molecular weight heparin, and oxygen delivery optimized with the nasal cannula. The patient was admitted to the medicine floor for further optimization. Given the concern of malignancy or chronic inflammatory process, CT abdomen/pelvis obtained showed large heterogenous mass extending from gallbladder's fundus and invading liver parenchyma with peripheral enhancement and central hypo-enhancement with contrast measuring 105 x 145 x 154 mm in anteroposterior and craniocaudal dimensions suggestive of a tumoral mass with extensive necrosis or liver abscess. There were also perihepatic ascites, and a satellite lesion in the left hepatic lobe measuring 12 x 13 x 15 mm noted on imaging (Figures , ).
Given systemic signs, the patient was started on broad-spectrum antibiotics, and cultures were sent. Interventional radiology was consulted for pigtail drains, and around 300 mL output was obtained, which was sterile with no bacterial growth, serosanguineous, and exudative by nature. Biopsy was also sent from the invasive mass of the gall bladder. Antibiotics were discontinued after successive negative blood cultures, but low-grade fever persisted. MRI liver was also obtained after interval placement of pigtails to delineate the mass further, which confirmed the aforementioned findings demonstrating large centrally necrotic heterogeneous mass and nodularity along with the omentum anteriorly with soft tissue signals representing peritoneal carcinomatosis, making it metastatic carcinoma of the gall bladder. Few porta hepatis nodes were measuring up to a centimeter on the short axis (Figures , ).
Pathology results resulted in neoplastic cell proliferation with intercellular bridges and focal individual cell keratinization, with rare keratin pearls. Core biopsy did not show any glandular or hepatic parenchyma component. Immunohistochemical stains showed diffusely positive staining on neoplastic cells for p63, CK5/6, CK17, and CK19, while negative for hepatocyte, glypican-3, and arginase-1, supporting the diagnosis of squamous cell carcinoma (Figure -D).
Given the current diagnosis, oncology, general surgery, and radiation oncology were taken on board. General surgery deemed the mass inoperable in this particular setting. Oncology recommended a trial of dose modified gemcitabine and cisplatin regimen versus dose reduced gemcitabine regimen for the patient. Given the severe risk of myelosuppression and the patient's attestation as Jehovah's witness and thus refusal of blood transfusion and considerable anemia below seven g/dl during the hospital course, oncological treatment was deferred. Radiation oncology scheduled the patient for palliative radiation for local control and tumor burden alleviation, but the patient opted for a hospice course.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3.0 + 1 =  4.0.
The patient's Well's score for pulmonary embolism is 4.0."
2949,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5998282-1,Extracted,"48-year-old woman with recently diagnosed stage IV sigmoid adenocarcinoma with liver metastasis was started on FOLFOX (folinic acid, 5-fluorouracil, and oxaliplatin) therapy. She had no known history of hypertension or migraines. Bevacizumab was held initially due to concerns of rectal bleeding; however, it was added back into her third cycle of chemotherapy. She responded well to her treatment, and a repeat CT abdomen/pelvis after 3 months of starting chemotherapy showed interval decrease in the size of the tumor. After the addition of bevacizumab in the third cycle of FOLFOX, she started having high blood pressure (BP) readings with a range of 160–180 mmHg systolic BP. About a week after the sixth cycle of FOLFOX, which included the fourth dose of bevacizumab, she started complaining of a headache. Her headache was mainly frontal in location, throbbing in nature, continuous and radiating behind her eyes. She explained this headache as the worst headaches of her life, prompting a visit to the emergency department (ED). A non-contrast CT scan of her head was performed and found to be unremarkable. She was managed with supportive care with acetaminophen and metoclopramide with partial relief of headache, and discharged home. Two days later, while driving, she had a tonic-clonic seizure and was brought to the ED.
On examination, vital signs included BP ranging from 170s to 190s systolic and 80s to 95s diastolic, temperature: 100 F, pulse: 110/min, oxygen saturation: 99% on ambient air, and respiratory rate of 18/min. Physical examination in the ED was pertinent for confusion and agitation, rest of the physical examination was unremarkable. An initial laboratory workup including complete blood count, blood chemistry, coagulation studies, urinalysis, toxicology screen, lumbar puncture was negative. Radiographic imaging including non-contrast CT head was also negative. She was started on an antiepileptic regimen, levetiracetam for seizure prophylaxis. Electroencephalography (EEG) was unremarkable. Brain MRI () showed hyperintense T2 signal intensity in both occipital lobes involving the gray-white matter consistent with PRES syndrome.
She was initially observed in the neuro-critical care unit. Intravenous hydralazine was given for persistently elevated BP, which was later switched to oral amlodipine once she started taking oral diet resulting in good BP control. Her symptoms resolved by the third day of hospitalization and she was discharged on amlodipine for hypertension and levetiracetam as seizure prophylaxis. A repeat MRI one week after presentation showed resolving gray-white matter changes (). Later on, FOLFOX was continued while bevacizumab was held. She did well on chemotherapy with good control of her BP and didn’t report any recurrent headaches. Repeat MRI after one month of the initial presentation showed complete resolution and seizure prophylaxis was discontinued.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2950,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5813769-1,Extracted,"A 46-year-old woman presented to our hospital because of general fatigue. Blood counts showed severe anemia (serum hemoglobin = 2.8 g/dL) and pelvic MR imaging revealed multiple uterine leiomyomas. Otherwise, her physical examination, laboratory tests including blood electrolytes, renal and liver function tests, pulmonary function tests, chest radiographs, electrocardiogram, and transthoracic echocardiography were within normal limits. Her anemia was treated with ferritin and her hemoglobin increased to 11.0 g/dL within 2 months. Total hysterectomy under general anesthesia was scheduled for her uterine leiomyomas. On admission, her body weight was 61 kg, height 1.54 m, blood pressure (BP) 106/64 mmHg, and heart rate 78 beats/minute. She had no history of hypertension.
Prior to surgery, she received 0.5 mg of atropine and 2 mg of midazolam intramuscularly. In the operation room, she was monitored by electrocardiography, noninvasive arterial BP measurements, and a pulse oximeter. Her BP was 161/76 mmHg and heart rate 75 beats/minute before induction of general anesthesia, which was induced with propofol, remifentanil, and rocuronium. Following tracheal intubation, she was ventilated with 50% oxygen and 50% nitrous oxide and sevoflurane, and intermittent doses of fentanyl (total 0.2 mg) were administered intravenously. The operation was uneventful, lasting 1 h and 56 min. Postoperatively, she regained full consciousness and complained of wound pain after extubation. Postoperatively, pain control was achieved with intravenous fentanyl (total 0.2 mg), and she was transferred to the ward.
After her transfer to the ward, 30 mg of pentazocine hydrochloride and 50 mg of hydroxyzine pamoate were administered intravenously in response to further complaints of wound pain. Her BP ranged between 146/84 and 166/100 mmHg in the ward. Two hours after she had been transferred to the ward, she became less responsive; 4 h later she had six episodes of tonic-clonic seizures lasting from 30 s to 2 min and lost consciousness. She was given 5 mg of diazepam intravenously; this terminated the seizures. Even though she was receiving 10 L/minute oxygen by face mask her oxygen saturation remained low at 90%, she was therefore admitted to the ICU. On admission to the ICU, her Glasgow coma scale was 6/15 (motor 3, eyes 2, verbal 1). Her respiration was labored with a rate of 18 per minute and stridor, suggesting upper airway obstruction. Her BP was 112/60 mmHg, heart rate 102 beats/minute, body temperature 36.7°C, and her pupils were 2.5 mm in diameter, equal, and reactive. Initial arterial blood gas analysis while receiving 12 L/minute oxygen administered by a face mask showed a pH of 7.19, PaCO2 of 46 mmHg, PaO2 of 125 mmHg, HCO3
− of 17.6 mmol/L, and standard base excess of −10.6 mmol/L. A chest radiograph showed diffuse, slightly increased opacity in both lungs. Brain CT images taken an hour after the seizures occurred showed symmetrical, slightly hypodense areas predominantly in the subcortical white matter of both occipital lobes.
Based on the aforementioned clinical features and neuroradiological findings, PRES was suspected. The patient was intubated and received mechanical ventilator support while being sedated with midazolam and fentanyl. By 20 min after intubation, her acidosis had improved dramatically, her arterial blood pH being 7.43. To prevent seizures, 250 mg of phenytoin and 800 mg of valproate per day were administered. Phenytoin was administered until the fourth and valproate until the 20th day after the event. On the day after admission to the ICU, the PaO2/FiO2 ratio was over 500. On brain MR imaging performed 15 h after the seizures had occurred, T2- and diffusion-weighted images revealed symmetrical, increased signal intensity in both parietooccipital lobes (Fig. a, b). The lesions showed increased signal intensity on apparent diffusion coefficient map images (Fig. c). MR angiography was not suggestive of atherosclerotic changes. After stopping sedation, she regained consciousness and was extubated. She was found to have no neurological deficit except for visual disturbance with hand motion. Her vision had recovered fully by the fourth postoperative day and she was transferred to the ward on the sixth postoperative day. All abnormal findings on brain MR imaging had completely resolved 7 weeks after surgery (Fig. a, b and c).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [78.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 78.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 =  1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2951,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8374965-1,Extracted,"A 60-year-old male patient (hypertensive, dyslipidaemic, and ex-smoker) on optimal medical treatment for stable angina for 5 months (aspirin, beta blocker, isosorbide-5-mononitrate, ramipril + hydrochlorothiazide combination, and high dose statin) presented to our outpatient department with the history of crescendo angina for 1 week associated with two episodes of rest angina in prior 12 h. Clinical examination was unremarkable with pulse rate of 64/min and blood pressure of 130/80 mmHg. Electrocardiogram (ECG) showed normal sinus rhythm, normal QRS axis, normal progression of R waves in precordial leads associated with 0.5–1 mm downsloping ST depression in anterior leads (V1–V6) with biphasic T waves. He was admitted in coronary care unit. Echocardiography showed normal left ventricular systolic function with ejection fraction of around 50% but hypokinesia in the mid and apical segments supplied by the LAD. The quantitative test for high sensitive cardiac troponin T (Elecsys, Roche) assessed on admission was elevated and was 84 ng/L (>5 times of normal). After reloading with 150 mg of non-enteric coated aspirin, a continuous infusion of unfractionated heparin was started (bolus of 5000 units with maintenance dose of 12 units/kg/h) with plan for coronary angiography within 24 h. Coronary angiogram done next morning revealed predominantly single vessel disease with a long 90% lesion from proximal to mid-LAD resulting in TIMI2 flow ( and Video 1A and B). After loading with 60 mg of prasugrel, during angioplasty of LAD, serial dilatations with 2.5 mm non-compliant (NC) and cutting balloon failed to dilate a point in proximal LAD completely. Hence, rotablation [Rotational Atherectomy System (Boston Scientific, Natick, MA, USA)] with 1.5 mm burr (burr artery ratio of 0.5:1) at 1 50 000 rpm was undertaken ( and Video 2) to modify the lesion. An angiogram after rotablation showed good distal flow in LAD with non-flow limiting Type B dissection in mid-LAD and significant lesion from mid to distal LAD (). Following rotablation, the same point in proximal LAD could not be dilated completely with a 3 mm cutting balloon () necessitating repeat rotablation with an upsized 1.75 mm burr. Unfortunately, 1.75 mm burr was not available on shelf due to use on the same day in the adjacent Cath lab and high-pressure OPN balloon/lithotripsy balloon or laser atherectomy is not available in our hospital. At this point, an option for bailout emergency bypass surgery was given to the patient but he refused with request to try other options. Hence after consultation with the cardiothoracic surgeon, it was decided that if we failed in addressing the lesions in mid and distal LAD along with the Type B dissection with stents, then the patient would be sent for bailout bypass surgery to which the patient also agreed. Following this, stenting of the lesions in distal and mid-LAD were attempted and successfully done with 2.5 mm × 20 mm and 2.75 mm × 16 mm drug-eluting stents which expanded completely at 12 and 14 atm pressure, respectively. A check angiogram done by withdrawing the wire from LAD showed TIMI3 flow with non-flow limiting type A dissection and significant residual stenosis in proximal LAD (Video 3). As the risk of occlusion of Type A dissection is negligible and patient remained asymptomatic, he was shifted to our post-intervention coronary care unit where subsequently heparin infusion was started to maintain APTT to two times above normal. The 1.75 mm rota burr became available next day but by this time 24 h had passed and the patient was totally asymptomatic. Hence, a decision was taken to defer rotablation to allow the dissection to heal over next 4 weeks before reintervention (as per recommendation of the company and European expert consensus on rotational atherectomy)., He was switched to low molecular weight heparin (injection enoxaparin 1 mg/kg body weight twice daily) for next 7 days with plan to discharge thereafter. As patient had dissection in proximal LAD just adjacent to a significant residual calcified lesion in background of non-STEMI (a highly prothrombotic state), we decided to give enoxaparin under supervision in hospital to ensure compliance and also watch for any bleeding complication as patient was also on dual antiplatelet therapy (aspirin and prasugrel). However, on the 9th day (around 36 h after stopping anticoagulation), the patient developed acute chest pain with ST-elevation in anterior leads () and immediate angiogram showed 100% occlusion of proximal LAD at the site of dissection with significant residual lesion ( and ). Injection abciximab was started intravenously (bolus of 0.25 mg/kg body weight with maintenance dose of 0.125 μg/kg/min for 12 h). The cardiothoracic surgeon was informed for bailout bypass surgery if required. Failing with a choice floppy wire, the LAD was crossed carefully with a Whisper wire. After failing to pass a thrombosuction catheter, a 1.5 mm balloon passed freely without any resistance to distal LAD confirming intraluminal position of wire. Dilatation with a 2.75 mm compliant balloon resulted in TIMI3 flow in LAD with no significant thrombus burden at the site of occlusion. Following this, rotablation was done with a 1.75 mm burr at the maximum recommended speed of 1 50 000 rpm by gentle pecking motion with each run not exceeding 15 s, avoiding deceleration of more than 5000 rpm and monitoring for slow flow/perforation after each run. Every precaution was taken not to ablate the recently implanted stent just distal to the undilated calcified segment. Henceforth, three runs of focal rotablation were done () and procedure completed without any final polishing run. Following rotablation, the lesion in proximal LAD showed complete expansion with a 3 mm NC balloon. A 3 mm × 28 mm drug-eluting stent was deployed in proximal LAD at 14 atm pressure overlapping 5 mm with the distally deployed stent resulting in TIMI3 flow ( and ) and significant resolution of ST segment in anterior leads on ECG (). The patient was discharged after 72 h with predischarge ejection fraction of around 45% [ecosprin 100 mg, prasugrel 10 mg, ramipril + hydrochlorothiazide (5 + 12.5 mg), sustained-release metoprolol 50 mg, atorvastatin 80 mg, and pantoprazole 40 mg] and he is asymptomatic at 6 months of follow-up with near-normal ejection fraction of around 50%.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [64.0, 'beats per minute'], 'Previously Documented Pulmonary Embolism': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 64.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2952,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7780431-2,Extracted,"The second patient was a 72-year-old woman. In her medical history, a functional endoscopic sinus surgery was performed because of persisting sinusitis, and she had tympanostomy tubes placed because of recurrent otitis media with effusion. There were no cardiovascular risk factors. She was admitted to the internal medicine department with complaints of increased fatigue, dizziness, and persistent fever for 2 months. Clinical examination showed a blood pressure of 130/76 mmHg, a heart rate of 74 b.p.m., and a JVP of 6 cm above the sternal angle. A diastolic murmur was noticed and lung auscultation was normal. Initial laboratory results showed an elevated erythrocyte sedimentation rate of 114 mm/u (0–30), a slightly elevated white blood cell count of 10.99 × 10E3/µL (3.65–9.30), and a CRP level elevated up to 122 mg/L (<5.0). Serum creatinine level was 0.61 mg/dL (0.55–0.96). Computed tomography (CT) scan of the sinuses showed a bilateral maxillary sinusitis, CT scans of thorax and abdomen were negative. TOE showed normal atria and ventricles with a normal systolic function. A tricuspid aortic valve was seen with moderate aortic valve regurgitation, thickened leaflets and an additional structure at the level of the left and RCC. There was a maximal gradient of 32 mmHg and a mean gradient of 17 mmHg across the valve. The thickening of the aortic sinus continued to the base of the anterior mitral leaflet and a moderate mitral valve insufficiency was seen. Pulmonary valve and tricuspid valve were normal ( and Video 2). Although blood cultures remained negative, a tentative diagnosis of infective endocarditis was made and treatment for endocarditis was started with ampicillin (6 × 2 g), oxacillin (6 × 2 g), and gentamycin (1 × 450 mg). On a new ultrasound an expansion of the thickening was seen (aortomitral continuity 17 mm × 9 mm; RCC 9 mm). Antibiotic therapy was empirically switched to vancomycin (1.8 mg/day continuous infusion) and gentamycin (600 mg/day) and patient was scheduled for surgery (20 days after initial antibiotic therapy). Coronary artery imaging was not performed prior to surgery. Intraoperative findings did not show endocarditis, but a massive infiltration of the ventricular side of the right and left coronary cusp was seen, expanding towards the apex in the interventricular septum, between pulmonary artery and aortic base, and towards the base of the mitral valve. An aortic valve replacement was performed with a 23 mm biological valve. Mitral valve replacement was not performed. The procedure was uneventful. Due to a persistent third-degree AV block, a dual-chamber pacemaker was placed on the 11th postoperative day. Anatomopathological findings of the valve showed a valvular and subvalvular pseudotumour caused by GPA, with necrotizing granulomas (). Microscopic findings of the myocardial biopsy showed a mixed inflammatory process as well as necrosis and multiple, small necrotizing granulomas. The patient was discharged on postoperative Day 15; however, on postoperative Day 26, she was readmitted because of a persisting fever. Investigations showed inflammatory blood result with an elevated erythrocyte sedimentation rate of 87 mm/h (0–30), CRP of 157 mg/L (<0.5), and white blood cell count of 13.41 × 10E3/µL (3.65–9.30). There was a positive ANCA result with slightly elevated anti-MPO titer up to 5.8 IU/mL. Therapy with Methylprednisolone (32 mg daily) was started, resulting in a good clinical and biochemical response. Two weeks later, Cyclophosphamide was started (6 cycles of 500 mg, with 2 weeks interval), followed by a maintenance therapy of Azathioprine (50 mg, twice daily) and a corticoid tapering schedule (10% per month). With this therapy no GPA-activity was seen: patient had no complaints, inflammatory markers and kidney function remained normal. Cardiac evolution initially showed a thickening at the level of the left coronary cusp with a mild paravalvular regurgitation. After 4 years of follow-up, no evolution of the aortic regurgitation and no more GPA activity were noted.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [74.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 74.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2953,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4612483-1,Extracted,"A 63-year-old Caucasian male with a past history of supraventricular tachycardia and recurrent deep vein thrombosis, who had been non-compliant with his daily Rivaroxaban® 20 mg, presented with pleuritic chest pain and was found to have a right lower lobe pulmonary embolus. The patient was subsequently restarted on Rivaroxaban® and discharged. He presented again 5 days later with left arm weakness and was found to have multiple areas of punctuate infarctions of both cerebral and cerebellar hemispheres, more confluent within the right frontal lobe on magnetic resonance imaging (MRI) of the brain ( and ). He has been compliant with his Rivaroxaban® since the previous hospital discharge 5 days prior. The patient was admitted and subsequently started on unfractionated heparin. On admission, his vital signs were blood pressure 138/93, heart rate 65 beats per minute, respiratory rate 16, and oxygen saturation 97% on room air. Cardiopulmonary examination revealed regular rate and rhythm, without murmurs, rubs, or gallops and clear lungs on auscultation. Neurologic examination revealed intact cranial nerves, preserved strength in all extremities with an exception of mild dysmetria in the left upper extremity and an NIH score of 1. Electrocardiogram revealed normal sinus rhythm, non-specific ST changes, and a premature ventricular contraction. Transthoracic echocardiogram was notable for normal left ventricular function with mild tricuspid regurgitation and stage 1 diastolic dysfunction. Transesophageal echocardiogram was negative for intracardiac thrombus. The echocardiography with agitated saline contrast revealed microbubbles of moderate opacity entering the left atrium from the left lower pulmonary vein indicative of a grade 2 intra-pulmonary arteriovenous shunt (). There was no atrial septal defect or patent foramen ovale. Unfractionated heparin was continued, and the patient was transferred to a tertiary care center for embolization of the shunt. There, he developed recurrent cerebral infarctions while anticoagulation was temporarily held. Computed tomography of the abdomen and pelvis was done for persistent abdominal pain, and noted an omental mass, and subsequent exploratory laparotomy revealed an adenocarcinoma within the omentum with nodular peritoneal implants. The patient was placed on weight-based Enoxaparin® and discharged home with scheduled outpatient chemotherapy. Embolotherapy of the intrapulmonary shunt was deferred given this new diagnosis of malignancy.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [65.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 65.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2954,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3407666-1,Extracted,"A 27-year-old Greek male patient was presented to the outpatient clinic of the Pulmonary Medicine Department of our hospital due to relapsing episodes of fever spikes (up to 38.7°C) accompanied by general fatigue and discomfort. He was initially treated with a course of oral antibiotics (b lactam plus macrolide) with poor clinical response. He was then transferred to our department for further evaluation. He reported a hospitalization 2 years ago due to fever of unknown origin, which subsided after a short course of high doses of corticosteroids. Nonetheless, he failed to recall any further details regarding the etiology of his hospitalization. He was a current light smoker (5 pack-years) and reported no exposure to illicit drugs, environmental, and occupational allergens or toxic fumes, chemicals, and dust. On physical examination, he was febrile with general fatigue and discomfort; however, he reported no dyspnea, tachypnea (respiratory rate 12 breaths/min), or palpitations (heart rate within normal range-70 bpm). He had no hypoxaemia (partial pressure ofoxygen 84 mm Hg) on arterial blood gas analysis. He had no clubbing, skin lesions, cervical lymphadenopathy, or joint swelling. Auscultation of the lungs mild end-inspiratory crackles in both lower lung zones. Cardiovascular, abdominal, and neurological system examinations were unremarkable.
Laboratory tests were performed and divulged microcytic iron deficiency anaemia (Hct: 35.9%, Hgb: 11.9 g/dL, MCV: 69.7, Fe: 19 mg/dL). Ferritin, B12, and folic acid levels were within normal range. The erythrocyte sedimentation rate was 65 mm·h−1. The rest of the physical examination and routine laboratory tests, including white blood cell count and differential, red blood cell count, liver and renal function, and serum C-reactive protein, were normal. Gross and microscopic urinary analysis revealed neither hematuria nor renal red blood cell casts, while his 24-hour urine protein levels were within normal range (60 mg/dl). His chest X-ray showed alveolar infiltrates in both lower lobes. Patient was then commenced on intravenous course of broad spectrum of antibiotics (piperacillin/tazobactam plus moxifloxacin) coupled with oseltamivir 75 mgr twice daily, which was discontinued three days after the sputum smear was negative for H1N1.
Laboratory tests for collagen vascular disease and vasculitis, including antinuclear (ANA), antiextractable nuclear antigens (ENA), antineutrophil cytoplasm (ANCA), and antiglomerular basement membrane antibodies, were also negative. The tuberculin skin test was negative. His HIV test was also negative, while his hepatitis B and C antibody titers were within normal range. The patient had a positive Mayer stool test for erythrocytes raising a suspicion for inflammatory bowel disease, but his further gastrointestinal workup (gastroscopy and colonoscopy) excluded any source of bleeding. In particular, gastroduodenal biopsies were performed and findings were inconsistent with both inflammatory bowel disease and malignancy as well as celiac disease. Regarding the latter specific antibodies against transglutaminase (ATA), both IgA and IgG isoforms were also negative.
Pulmonary function tests (PFTs) were performed and showed normal FVC (91%), FEV1 (92%), and FEV1/FVC ratio (84.1%) and a strikingly elevated DLCO (120% of the predicted normal value) indicative of alveolar hemorrhage.
Patient was then subjected to high-resolution computed tomography (HRCT) showing diffuse bibasilar ground-glass opacities consistent with alveolar hemorrhage (). Diagnosis of DAH was confirmed by BAL demonstrating increased numbers of hemosiderin-laden macrophages (>40% of total number of macrophages). BAL fluid specimens were negative for routine bacterial, mycobacterial, fungal, and viral as well as Pneumocystis stains and cultures. Due to the patient's continuously worsening clinical condition (onset of dyspnoea, ESR and CRP increase to 187 mm/h and 15.91 mg/L, constant decrease of haemoglobin levels), a VATS biopsy from the right middle lobe was employed to address the cause of the alveolar haemorrhage. Extensive pathologic evaluation of the lung specimen divulged hemosiderin-laden alveolar macrophages and absence of any specific pathology such as granulomas or evidence of vasculitis/capillaritis. Immunofluorescence microscopy of frozen tissue samples, using a panel of antibodies against complement and immunoglobulins was without notice of immune complexes that would drive a diagnosis towards a specific cause. Taking into consideration the above data, we came up with the diagnosis of IPH.
Treatment with high doses of oral prednisone (0.75 mg/kg of weight) as a monotherapy was adopted for 6 weeks and gradually tapered to 0.5 mg/kr for another 6 weeks and 20 mgr for another 6 weeks leading to a profound improvement of symptoms (dyspnoea) as well as imaging and laboratory findings including complete resolution of bilateral areas of ground-glass opacities () as well as a significant incline of his haemoglobin levels and decrease of his CRP and ESR titers, respectively. The patient is now followed for almost 3 months, on an outpatient basis, in good clinical condition, free of disease relapses, afebrile, and hemodynamically stable on 10 mgr/day of oral corticosteroids. Due to high incidence of relapses, the patient is under close monitoring.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [70.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 70.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2955,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6890309-1,Extracted,"In September 2018, a 63-year-old woman was admitted to our hospital due to progressive dyspnea over the past month. Vital signs: weakness, blood pressure 88/50 mm Hg, respiratory rate 28 bpm, heart rate 146 bpm, and temperature 36.5°C, as well as oxygen saturation 88%. Electrocardiography (ECG) showed the obvious ST-segment elevation in the leads I, aVL, and V1–3 (Fig. A and B). Laboratory tests revealed the elevated level of cardiac troponin T (576.7 ng/L; reference range: 0–14 ng/L). Emergent coronary angiography demonstrated 95% distal occlusion of the left main coronary artery (LMCA), 95% ostium occlusion of the left anterior descending coronary artery (LAD) and left circumflex coronary artery (LCX), and the abnormal changes in the aortic valves (Fig. C and D). We then performed the contrast-enhanced computed tomography (CT) scan promptly, which showed the compression of mediastinal soft tissues on the LMCA, LAD, and LCX, as well as the proximal superior/inferior vena cava and the right main pulmonary artery, resulting in severe stenosis of these arteries and veins (Fig. E–G). Venous collateral circulation dilatation due to severe stenosis of the inferior vena cava was observed (Fig. H). Further inquiry revealed that the patient complained of a cough 5 months ago in the local hospital, and CT scan showed pulmonary nodules; she received left pulmonary nodulectomy. The pathological examination indicated PEH (immunohistochemical staining: ERG+, CD31+, CD34±, CAMTA1+, TFE3−, EMA+/−, CK−, TTF1−, P63−, Ki67+). She did not undergo further therapy after the pulmonary nodulectomy. Unfortunately, the patient deteriorated rapidly into multi-organ failure and eventually died.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [146.0, 'beats per minute'], 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 146.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2956,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3686071-1,Extracted,"A 32-year-old male presented with a sudden onset of massive rectal bleeding. He had a history of KTS since childhood. He had multiple admissions for bleeding, presenting mainly as hematuria that started at the age of 11. He also had one episode of self-limited rectal bleeding four years prior to this presentation. His medications were multivitamins with iron supplement.
At the time of admission, physical examination was remarkable for blood pressure of 55/29 mm Hg, HR of 135 per minute, respiratory rate of 22 per minute, and normal temperature. He appeared pale and diaphoretic. Cardiopulmonary examination was unremarkable except for tachycardia and tachypnea. His abdomen was soft and nontender, with active red blood oozing from his rectum. He was noted to have extensive varicose veins over the right leg and scrotum and his right leg was larger than the left one.
Laboratory studies showed Hg 7.1 g/dL (normal 13–17 g/dL), hematocrit 22.9% (normal 38.6–49.2%), MCV 80.6 fl (normal 80–100 fl), MCH 24.9 pg (normal 26–34 pg), platelets 148 k/mL (normal 150–450 k/mL), AST 522 IU/L (normal 0–40 IU/L), ALT 257 IU/L (normal 0–50 IU/L), alkaline phosphatase 39 IU/L (normal 40–129 IU/L), bilirubin 1.7 mg/dL (normal 0-1 mg/dL), and INR 1.7 (normal 0.8–1.2).
Kidneys, ureters, and bladder (KUB) X-ray revealed multiple small rounded calcifications throughout the lower abdomen (). Computed tomography (CT) scan of the abdomen and pelvis showed marked wall thickening in the left colon, sigmoid colon, and the rectum (Figures and ). The patient underwent upper endoscopy which was within normal limits. Subsequent colonoscopy showed long, large, and dilated tortuous veins throughout the colon, with large amount of red and clotted blood extending to the ascending colon (Figures and ).
He underwent angiography which showed hypervascularity of one of the superior mesenteric artery branches supplying the right colon. This area was embolized, but the patient continued to bleed and subsequently underwent rectosigmoid resection.
Grossly, the resected left colon and rectum showed extensive mucosal varicoses with nodular changes (). Almost the entire mucosa was cobblestone in appearance with multiple polypoid areas. The wall was markedly thickened, and the mucosal surface was reddish-pink in color (Figures and ). The serosal surface showed markedly dilated veins with prominent varices (Figures and ). Histological examination of the resected area showed extensive venous malformations and dilated lymphatics with focal thrombosis consistent with KTS (). Postoperative course was complicated by hemoperitoneum, worsening coagulopathy, peritonitis, sepsis, and right leg deep venous thrombosis (DVT). He had an inferior vena cava (IVC) filter placed. He was sent to an operative room three times for hemoperitoneum evacuation and wound dehiscence closure. Patient required intubation, mechanical ventilation, and vasopressors multiple times during his hospitalization because of the sepsis and respiratory failure. He required transfusion of a total of 50 units of blood (33 units on the first day of presentation), 18 units of fresh frozen plasma, 26 units of platelets, and 10 units of cryoprecipitate. He expired after 2 months of hospitalization.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [135.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",7.5,7.5,7.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 135.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 =  6.0.
The patient not been diagnosed with pulmonary embolis (PE), but the patient has previously been diagnosed with deep vein thrombosis (DVT), we increase the current total by 1.5 so that 6.0 + 1.5 = 7.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 7.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 7.5.
The patient's Well's score for pulmonary embolism is 7.5."
2957,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6446494-1,Extracted,"A 24-year-old man was brought to the emergency department of a hospital, by his office-colleagues, complaining of sudden onset of chest pain and dyspnea at rest, for the last one hour. It was not associated with sweating, palpitations, cough, hemoptysis, syncope, giddiness, leg pain, pedal edema, fever, rash, or any bleeding manifestations.
History of calf pain, trauma, surgery, prolonged immobilization, long-haul air travel, bleeding diathesis or any other co-morbidity was not reported by the patient. The patient also denied having any addiction history. Family history was found to be insignificant.
On admission, the patient’s heart rate was 114/min, and blood pressure was 106/90 mmHg. His respiratory rate was 22/min, and O
2 saturation rate was 82% at room air. BMI was 20.76 kg/m
2. There was no murmur or gallop on cardiovascular examination. Air entry was reduced in the left infra-axillary region. Also, the detailed examination (including Homan’s and Moses sign) was performed and was deemed unremarkable. Electrocardiogram (ECG) showed tachycardia with S
1Q
3T
3 pattern, and chest X-ray was suggestive of obliteration of left costo-phrenic angle. The D-Dimer (17.31 ug/ml) was elevated, 34 times above the normal upper limit (0.5 ug/ml).
CT-Pulmonary Angiogram (
) was suggestive of a massive pulmonary thromboembolism. The pulmonary trunk was dilated to ~30 mm. There was a non-lumen occluding circumferential filling defect in the main pulmonary trunk, with maximum thickness of 4.5 mm. A large partial-lumen occluding filling defect was noted in the left main pulmonary artery, which was extending further into the hilar branch, occluding the lumen completely. Another larger complete lumen occluding filling defect was noted in the right main pulmonary artery. These filling defects were extending into the segmental and sub-segmental branches of the lateral segment of the right middle, lingual and bilateral lower lobe. The RV: LV ratio was 2:1. All four pulmonary veins were normal, and there was no evidence of mediastinal pathology.
On admission, the patient also underwent a bilateral arteriovenous Doppler study, which was suggestive of a partially-lumen- occluding thrombus in the proximal part of left popliteal vein and a completely lumen-occluding thrombus at the left saphenopopliteal junction, approximately 14 cm long. The veins of both legs showed arterialized waveforms.
On 2D echocardiography, right atrium and right ventricle was mildly dilated with grade I, tricuspid regurgitation (TR) and pulmonary arterial systolic pressure by TR jet was 55 mmHg suggestive of moderate pulmonary artery hypertension. No regional wall motion abnormality was observed and left ventricular ejection fraction was 60%.
The coagulation profile was within normal limits. All other blood investigations i.e. hemogram, serum electrolytes, renal and liver function tests were within normal range. The patient had mild hyperuricemia with serum uric acid level being 7.4 mg/dL (Normal: 3.5 – 7.2 mg/dL). Cardiac enzymes (Creatine PhosphoKinase-MB and Troponin T) were mildly elevated. Trop I levels testing was not available at our centre and hence, was not done.
Although it was a clear case of massive VTE, the underlying etiology of such an event could not be extrapolated. Since the patient was a 24-year-old man, without any risk factors or comorbidities, the final diagnosis of unprovoked VTE was made.
The patient was thrombolysed with Injection Alteplase infusion (100mg IV, over two hours) with Injection Enoxaparin 60 mg given subcutaneously every 12 hours. After which, the patient developed hypotension which was treated with inotropic support. Although he had tachycardia post-thrombolysis for the next two days, his blood pressure returned to normal on the third day. 48-hours after giving thrombolytic treatment, the left lower limb venous doppler was done which was suggestive of a partial-lumen occluding the thrombus in popliteal vein extending from saphenopopliteal junction to mid-leg approximately 10 cm long. The CT-pulmonary angiogram was not repeated (post-thrombolysis), due to financial constraints; however, the patient improved drastically. He was shifted to general ward on day 4 post admission. Tab Rivaroxaban 15 mg (12 hourly, orally) was prescribed for the next three weeks. The patient was discharged successfully on the 15
th day of admission. One week after discharge, the patient was advised Tab. Rivaroxaban 20 mg, once daily. The patient was most satisfied with the treatment and the recovery he’d made, but this was not recorded in a form of any official questionnaire (but he had mentioned this verbally).
The patient had followed up in our center for the first three months, following which relocated to Uttar Pradesh, India (his hometown). He experienced no side effects of Rivaroxaban. At three months of post discharge, a lower limb doppler was repeated which showed more than 50% reduction in size of the obstructing thrombus as compared to the previous one done at admission. Post three months of discharge, the patient has not returned back yet and has been lost to follow up.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [114.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 114.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
The patient not been diagnosed with pulmonary embolis (PE), but the patient has previously been diagnosed with deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
2958,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-4381,Extracted,"A 65-year-old man arrives to the emergency department (ED) complaining of pain and swelling in his right leg. The patient reports he recently underwent a total hip replacement. His past medical history is significant for hypertension and diabetes. His current medications include aspirin, lisinopril, metformin, and atorvastatin. On arrival, his temperature is 99°F (37.2°C), blood pressure is 135/82 mmHg, pulse is 88/minute, and oxygen saturation is 99% O2. He denies chest pain or shortness of breath. On physical exam, his right leg appears moderately erythematous, swollen, and is tender to palpation. Other physical exam findings are negative.

A complete blood count (CBC) was performed with the following findings:

Hemoglobin: 13.0 g/dL
Leukocyte count: 6500/mm^3
Platelet count: 150,000/mm^3

The appropriate anti-coagulation therapy is started. Seven days later the patient arrives back to the ED complaining of crushing substernal chest pain. An electrocardiogram is performed and is shown in Figure A.

A CBC was performed with the following findings:

Hemoglobin: 13.5 g/dL
Leukocyte count: 8500/mm^3
Platelet count: 58,000/mm^3
INR: 2.5
aPTT: 34 seconds
Fibrinogen level: 200 mg/dL
Troponin T: 0.2 ng/mL

On physical exam, the right leg is again swollen and tender to palpation. However, a new lesion has also formed, as shown in Figure B.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [88.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 88.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 3 + 1.5 =  4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2959,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-2803799-1,Extracted,"A 66-year-old Caucasian man was admitted to our surgical department with the diagnosis of a rectal cancer 8 cm from the anal verge. He had a colonoscopy due to the presence of blood in his stools for a month prior to his admission. Endoscopy revealed a polypoid lesion of the rectum and the pathology diagnosed an adenocarcinoma.
From his medical history, we ascertained that he had pulmonary tuberculosis at the age of 25 years, cholocystectomy at the age of 61 and that he currently had ischemic heart disease. The patient had no history of tobacco smoking and no allergies. Laboratory tests were normal. Preoperative staging was negative on abdominal and chest computed tomography scans. The patient did not receive neoadjuvant therapy.
A laparoscopic low anterior resection was performed with an end-to-end anastomosis. The operation was converted to an open laparotomy due to technical problems in the completion of the anastomosis and the intraoperative observation of oozing from the presacral fascia. Microscopic examination of the specimen revealed a moderately differentiated adenocarcinoma of the rectum with adequate resection margins and no metastases in the 16 resected lymph nodes. By World Health Organisation classification, this was a T3N0 M0 tumor.
The immediate postoperative course was uneventful. On the fourth postoperative day, the patient developed abdominal pain and dyspnea. Physical examination revealed tachycardia (130 beats per minute), hypertension (systolic blood pressure of 210 mmHg) and fever (38.1°C). The patient had a normal blood count and hypoxia was diagnosed on arterial blood gases (saturation 88%, PO2 56 mmHg). He received intramuscular analgesics (pethidine 75 mg four times daily) and intravenous antibiotics (piperacillin-tazobactam 4.5 gm and metronidazole 500 mg three times daily).
The patient underwent an emergent laparotomy on the same day. Anastomotic rupture with fecal peritonitis was diagnosed. Intraperitoneal lavage and a loop ileostomy were performed. Two drain catheters were placed in the pelvis next to the anastomosis and the abdomen was left open for a delayed closure using the Bogota bag technique. Intraoperatively, the patient suffered a cardiac arrest and he was successfully resuscitated. He was transferred to the intensive care unit (ICU) and mechanically ventilated. He was hemodynamically unstable.
On the seventh day, the patient underwent a second laparotomy, and then returned to the ICU. Due to persistent hyperpyrexia, tachycardia and metabolic acidosis unresponsive to supportive measures, the patient was taken back to the operating theatre for a third laparotomy. Exploration of the peritoneal cavity was negative. We performed peritoneal lavage and three drains were placed in the pelvis. Using the Bogota bag technique, the abdominal wall was left open. The patient was transferred to the ICU again.
Five days later, we detected intestinal content in one of the drain catheters - the patient was hemodynamically stable but his condition was not improving. At that time, abdominal hypertension developed (21 mmHg) accompanied by acute renal failure. It was decided that the patient should undergo another exploratory laparotomy some days later. Fecal peritonitis and pseudomembranes were recognized and a peritoneal lavage with warm saline was performed. The anastomosis was taken down and the rectal stump was closed. Omentum was placed in the lesser pelvis. A proximal sigmoidostomy was performed along with reconstruction of the loop ileostomy. Two drains were placed in the pelvis. The abdominal fascia was left open with skin closure. The patient was intubated and transferred back to the ICU.
The patient developed multi-organ dysfunction requiring mechanical ventilation, inotropic support and renal replacement therapy in his 40 days in the ICU. 17 days after the last laparotomy, he was tracheostomized and was transferred to a hospital ward after 75 days in the ICU. He was on a T-piece and receiving enteral feeding through a Levin tube. Multiple broad-spectrum antibiotics were administered. He was discharged from the hospital and transferred to a rehabilitation center after 3 months of supportive therapy. At that time, he had neither clinical nor laboratory signs of infection, his tracheostomy had closed and he had restarted oral food intake.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [130.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 130.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 =  3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3.0 + 1 =  4.0.
The patient's Well's score for pulmonary embolism is 4.0."
2960,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-9582,Extracted,"A 63-year-old man with a history of stage 4 chronic kidney disease (CKD) has started to develop refractory anemia. He denies any personal history of blood clots in his past, but he says that his mother has also had to be treated for deep venous thromboembolism in the past. His past medical history is significant for diabetes mellitus type 2, hypertension, non-seminomatous testicular cancer, and hypercholesterolemia. He currently smokes 1 pack of cigarettes per day, drinks a glass of wine per day, and he currently denies any illicit drug use. The vital signs include: temperature 36.7°C (98.0°F), blood pressure 126/74 mm Hg, heart rate 87/min, and respiratory rate 17/min. On physical examination, the pulses are bounding, the complexion is pale, but breath sounds remain clear. Oxygen saturation was initially 91% on room air, with a new oxygen requirement of 2 L by nasal cannula. His primary care physician refers him to a hematologist, who is considering initiating the erythropoietin-stimulating agent (ESA), darbepoetin.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [87.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Immobilization for at least 3 days': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 87.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
2961,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7585967-1,Extracted,"A 64-year-old male patient presented to our emergency department with newly perceived chest pain. He had undergone aortic bioprosthesis replacement due to infective endocarditis and single vessel coronary by-pass for second obtuse marginal artery stenosis eight months ago. The initial examination identified ongoing anginal chest pain along the mid-sternal region for two and half hours. His blood pressure was 100/60 mm Hg, and his pulse was 70 beats/min. His cardiac troponin T blood levels were higher than normal. Thus, the patient was diagnosed with non-ST-elevation acute coronary syndrome and underwent emergency coronary angiography. During the coronary angiography, severe stenosis was detected in the left main coronary artery (LMCA), the left anterior descending (LAD), and the left circumflex (CX) arteries (). We intended to perform coronary revascularization via a percutaneous coronary intervention. However, immediately after this procedure, we realized that there was a pulsatile variability in the severity of the coronary stenosis () and a silhouette of a round-shaped mass under the aortic valve. Left ventriculography revealed an LVOT pseudoaneurysm ( and ). Then, we selectively imaged the LVOT pseudoaneurysm ( and ) to evaluate its suitability for percutaneous closure. The patient immediately underwent computed tomography (CT), which clearly revealed the nature of the pseudoaneurysm and its compressive effect on the LMCA, LAD, and CX (). He was given percutaneous or surgical closure options. The patient chose surgery, and unfortunately he died after surgery from sudden cardiac arrest.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [70.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 70.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2962,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3985204-1,Extracted,"A 25-year-old woman with no past medical or surgical history was brought to the Emergency Department (ED) after being kicked by a horse in her chest. The patient was found to have a midsternal fracture with underlying hematoma on computed tomography (CT) chest (see ). Her blood pressure was 102/67 mm hg, her heart rate was 58/min, and her respiratory rate was 18/min, and oxygen saturation was 99% while breathing room air. Her white blood cell count was normal and her hemoglobin was 14.1 gm/L. The creatinine phosphokinase 494/L (normal 38/L–174/L) and troponin level was 3.74 μg/L (0.00–0.08 μg/L). These were felt to be secondary to a blunt cardiac contusion. Her elevated cardiac enzymes reverted back to normal within 48 hours.
The patient's electrocardiogram (EKG) on admission revealed normal sinus rhythm with rate of 65 bpm (beats per minute) with first-degree atrioventricular block (AV Block) and left anterior hemiblock as depicted in . The patient was admitted to the coronary care unit (CCU) for observation. 13 hours after her injury, she developed a third-degree AV block along with left bundle branch block with the rate of 55 bpm (see ). At that point, she was totally asymptomatic with normal hemodynamic parameters. A cardiology consultant was obtained and felt that the patient's AVB was likely secondary to the substernal hematoma causing mechanical compression of the AV bundle. A 2D echocardiogram was normal with no evidence of cardiac injury with a normal with an ejection fraction of 70%. She was kept in CCU and within seventy-two hours, her rhythm converted to normal sinus rhythm with rate of 85 bpm and first-degree AV block and left anterior hemiblock as depicted in . She was discharged home in a stable condition with an outpatient followup with her primary care physician. A four-week followup revealed that the EKG is in normal sinus rhythm with the rate of 56 bpm (see ).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [58.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 58.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2963,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-2769308-1,Extracted,"A 72-year-old, Turkish, Caucasian female patient was referred immediately to our surgery department after extravasation was found during barium enema procedure. The patient presented with complain of nausea, vomiting and intermittant cramping abdominal pain. Her vital signs included temperature of 37.4°C, blood pressure of 110/70 mmHg, pulse rate of 82 beats/min, respiratory rate of 24 breaths/min. On physical examination, the abdomen was distended and tenderness was noted to direct and rebound palpation with guarding in all quadrants. Routine hematological and biochemical investigations were within normal limits except for raised total leucocyte count (12,800/mm³). Plain X-ray of abdomen revealed dilation of rectum, sigmoid and descending colon with barium which occupied the abdomen intraperitoneally. A chest X-ray did not reveal any pneumoperitoneum.
Immediate fluid resuscitation and intravenous antibiotics were initiated. The patient underwent surgery after the diagnosis of acute abdomen was made. Exploratory laparotomy revealed perforation of the colon with a diameter of 10 cm, located 15 cm above the peritoneal reflection and barium covering the colon segments and the omentum. After an effective abdominal washout, sigmoid colon resection with Mikulicz colostomy was performed, followed by omentectomy because barium on the omentum could not have been removed by washout. Oral diet was given 24 hours after removing the nasogastric tube on the third postoperative day. On the ninth day of her hospitalization, the patient was discharged with complete recovery with a plan to close the colostomy 8 weeks later.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [82.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 82.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2964,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7750352-1,Extracted,"A 15-year-old male patient presented to an external center with headache and swelling that started in his left eye and occurred in his right eye and forehead on the next day. The laboratory tests performed in the external center showed a white blood cell (WBC) value of 15 600/mm3 and a C-reactive protein (CRP) value of 5.6 (normal: 0–0.5) mg/dL. A diagnosis of acute frontal sinusitis was made with an examination and the laboratory findings, and oral amoxicillin-clavulanate treatment was initiated at a dosage of 60 mg/kg/day. Netilmicin sulfate eye drops and sodium fusidate ophthalmic ointment treatment was initiated because of conjunctivitis. The patient, whose headache and swelling in the left eye and forehead continued during treatment, presented to our hospital when his symptoms did not regress.
At the time of presentation, the patient’s vital findings were as follows: body temperature: 36.8°C, blood pressure: 110/70 mm Hg, apical heartbeat: 74 beats/min. On physical examination, his oropharynx was hyperemic, there was periorbital edema and 2x2 cm of local swelling infraorbitally, hyperemia and local increase in the heat (). There was marked postnasal purulent discharge and tenderness on the frontal region with palpation. The initial laboratory findings were as follows: WBC: 8.99 (74.5% neutrophil, 16% lymphocyte, 7.7% monocyte), hemoglobin (Hb): 15 g/dL, hematocrit (Hct): 42.2%, mean corpuscular volume (MCV): 92.9 fL, platelets (Plt): 333 000, CRP: 102 (normal: 0–8) mg/dL, erythrocyte sedimentation rate (ESR): 52 mm/h. Routine biochemical tests were found to be normal.
Treatment with intravenous ceftriaxone (75 mg/kg/day) and teicoplanin (a loading dosage of 16 mg/kg/day on the first day and a maintenance dosage of 8 mg/kg/day subsequently) was initiated with a prediagnosis of Pott’s puffy tumor as a complication of frontal sinusitis. The paranasal sinus CT revealed increased mucosal thickness and appearance of a collection and a sclerotic lesion (osteoma?) in both frontal sinuses (with a size of 42x28 mm with lobulated contours in the widest part in the coronal plane extending to the left ethmoid cells on the left side), and an erosion in the anterior wall of the frontal sinus adjacent to the lesion described (). On the second day of hospitalization, the patient was consulted by Opthalmology and Otorhinolaryngology clinics. The opthalmology consultation resulted as follows: “Full vision, eye movements are free and painless in all directions, no cell was observed in the anterior camera on biomicroscopic examination and bilateral fundi are natural.” The patient was assessed by the otorhinolaryngology department and it was thought that excision of the mass, which was thought to be an osteoma, would be appropriate, because it eroded the anterior wall of the frontal sinus, and the sinusitis that developed was complicated by the development of subperiostal abscess (Pott’s tumor). In the follow-up, the edema around the patient’s eye and forehead reduced, and his headache improved. He was discharged with oral antibiotherapy after treatment with IV ceftriaxone and teicoplanin for 10 days. Following outpatient follow-up with antibiotherapy, the patient was hospitalized by the otorhinolaryngology department for surgery, mass excision was performed, and a histopathologic examination of the tissue obtained was found to be compatible with osteoma. Written consent was obtained from the patient who participated in the study and from his family.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [74.0, 'beats/min'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 74.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2965,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7596015-1,Extracted,"A 32-year-old nulliparous woman presented into Emergency Room with colicky abdominal pain that lasted 48 h. Additionally, she had diarrhea, abdominal distension, nausea, vomiting, dry cough, nasal congestion, headache, and fever. She was taking antibiotics for H. pylori gastritis. Her medical history included endometriosis. She was taking oral contraceptives intermittently. She had right oophorectomy at age 22 due to endometrioma, and right salpingectomy at age 25 due to ectopic pregnancy. In-vitro fertilization and embryo transfer failed at age 29.
On physical examination: BP 80/60 mmHg. HR 120 bpm. RR 22 bpm. Temp. 39 °C. Her abdomen was diffusely distended, absent bowel sounds, generalised tenderness, without rebound. Vaginal examination was unremarkable. Rectal exam showed liquid stool. Leucocytes 18,000/μL. PaO2/FiO2 ratio 370. Abdominal CT scan with IV contrast showed small bowel diameter of 5 cm with air-fluid levels and transition point at 5 cm from the ileocecal valve (). PCR was positive for C. difficile as well as Influenza AH1N1.
Patient was admitted in the Intensive Care Unit. She was kept NPO. A nasogastric tube was placed, and 2 L of enteric fluid were drained. She was started on Vancomycin 500 mg QID and Oseltamivir 75 mg BID by nasogastric tube, as well as Tigecycline 50 mg BID IV. The organ failure resolved within 48 h.
On her second hospital day, laparoscopic exploration was performed. Small bowel was diffusely dilated, and extensive intra-abdominal and pelvic adhesions were seen. The point of obstruction was at the terminal ileum next to the ileocecal valve. That segment of bowel was severely stenosed. Ileal obstruction was induced by many blue-black nodules (). On the surface of the parietal and visceral peritoneum, many lesions were visualized and biopsied ().
Due to the complexity of the case, it was converted to midline laparotomy since the exposure was not adequate to perform the surgery safely. Extensive lysis of adhesions was done. At this point, right ileocolectomy was performed. Using a 60 mm stapler, ileo-transverse anastomosis was done. No complications were reported.
Patient's recovery was uneventful. She was started on total parenteral nutrition (TPN) on postoperative day (POD) 0. On POD 1, she had bowel sounds and slowly recovered her bowel function. On POD 4, she was stared on liquid diet. Her diet was slowly progressed and the TPN weaned. By POD 8, she was tolerating soft diet, having bowel function, and no signs of active infection. She was discharged home.
The macroscopic pathological examination consisted of a 20 cm long ileum segment and a 6 cm cecum and colon segment. The external surface was light brown, with congestive areas. The luminal surface had hematic material and showed a variable diameter secondary to stenotic areas, with purplish areas of hemorrhagic appearance. Cross sections showed small dilated cystic areas in relation to fibrosis and mural bleeding.
Microscopically, we found multiple foci along the enterocolonic wall of glandular and tubular structures, lined by epithelial cuboidal-columnar cells without atypia, surrounded by endometrial stroma with lymphoplasmacytic inflammatory infiltrate, focal hemorrhage, and hemosiderin-laden macrophages. There was important vascular proliferation as well as extensive subserosal fibrous bands. Immunostains for Estrogen Receptor and PAX8 were positive, which confirmed the endometrial nature of the lesions. The diagnosis of enterocolonic transmural endometriosis with serosal adhesions was established ().
Definite diagnosis was ileal obstruction secondary to transmural endometriosis. At one-year follow-up, patient remains asymptomatic. She has been referred to Gynecology for further treatment of endometriosis.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2966,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3987413-1,Extracted,"A 22 years old lady was admitted because of progressive dyspnea, severe abdominal protrusion and lower extremity edema. She had experienced gradual abdominal pain and dyspnea at rest since one week before admission. Ovarian hyperstimulation had been performed for primary infertility by Clomiphen and Human chorionic gonadotropin (HCG) for 3 months. Her gynecologist had stopped these medications, but as her symptoms aggravated, she was admitted to ICU. She denied any previous cardiovascular disease. Her physical examination exhibited BP 90/60, PR:108, RR 24/min normal jugular venous pressure, reduced breathing sounds in both lung bases , normal cardiac sounds, marked abdominal protrusion, tender abdomen and 2 + lower extremity edema .
Paraclinical work up revealed: Hb: 12.8 g/dl; Hct: 48; WBC: 24000/mm3 BUN, Creatinine and liver function test were normal and ß-HCG was 25400pg/mm3 Chest X-Ray showed bilateral plural effusion. Abdominopelvic ultrasonography demonstrated bilateral enlarged multi-cystic ovaries and massive ascites. Because of patient’s dyspnea and poor echo window, she underwent transesophageal echocardiography that exhibited a large thrombus in right ventricular apex (). Color Doppler study of both lower extremities and pelvic veins failed to show any thrombus in venous system, and spiral chest Computed Tomography Scan showed normal pulmonary vasculature and no evidence of pulmonary thromboembolism. Dose-adjusted heparin was started with concurrent supportive care. Follow up echocardiographic study revealed gradual disappearance of right ventricular thrombus. She was finally discharged after 10 days in good general condition.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [108.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 108.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 =  3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2967,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8278137-1,Extracted,"A 54-year old female, with no metabolic disorders or previous surgeries reported, and medical history of chronic obstructive pulmonary disease of 12 years of evolution, treated with nebulized salbutamol as needed. The relatives reported she had mild to moderated headache the last four days, balance impairment, and generalized weakness, although the presence of neurological symptoms associated to COVID-19 such as anosmia and dysgeusia were denied. She was admitted to emergency room with sudden loss of consciousness with the following vital signs: BP (110/80 mmHg), HR (80 bpm), BF (18 bpm), body temperature (36.1℃), and a Glasgow Coma Scale (GCS) of 6 points (eye opening: 2 points, verbal response: 2 points, and motor response: 2 points) so we started airway management. The cranial computed tomography (CT) scan revealed cerebrovascular disease (CVD) characterized by acute intra-axial hemorrhage in the left cerebellar hemisphere associated with peripheral edema, which obliterated cortical subarachnoid spaces and cisternae of the posterior fossa and bulges the tentorium (); hemorrhage extended into the fourth ventricle, which were displaced and compressed to the contralateral direction (). Likewise, the hemorrhage extended to the choroid plexuses of the supratentorial ventricles and led to obstructive hydrocephalus. The cortical subarachnoid spaces and supratentorial basal cisterns were obliterated (). Measurement of laboratory parameters showed high leucocyte and neutrophil counts, whereas lymphocyte and monocyte counts decreased. She also presented high serum levels of glucose, total cholesterol, indirect bilirubin, gamma glutamyl transferase (GGT), creatinine kinase myocardial band (CK-MB), fibrinogen, D-dimer, and procalcitonin. There was no concluding evidence of COVID-19 in chest CT scan (CO-RADS III) (), and then the presence of SARS-CoV-2 mRNA was confirmed by RT-PCR in nasopharyngeal swabs. Urgent right-sided precoronal ventriculostomy was performed. The patient presented clinical findings concurring with brain death immediately after postoperative period, and she died 24 hours later because of cardiopulmonary arrest.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [80.0, 'bpm'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2968,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4276298-1,Extracted,"A 29-year-old multiparous female at 35 weeks and 6 days of gestational age arrived at our obstetrical triage unit in extremis with the chief complaint of abdominal pain. She was transported to the hospital by her male partner who provided the history. The abdominal pain was of abrupt onset approximately 1.5 hours prior to arrival and was mainly epigastric in origin. The partner observed a single episode of emesis en route and the gradual onset of confusion. The patient's prenatal course had otherwise been unremarkable. A physical examination revealed a lethargic and confused gravid female in apparent distress. The fundal height was 35 cm and the abdomen was diffusely tender. There was evidence of involuntary guarding and an absence of rebound tenderness. The systolic blood pressure was 60 mmHg as determined by palpation, pulse was 150 beats per minute, and body temperature was 38.2°C. She was able to localize pain and respond to simple commands. The obstetric history was significant for two prior uncomplicated spontaneous vaginal deliveries, one at term and one late preterm. An ultrasound study of the abdomen was performed at the bedside and showed a singleton fetus with a fetal heart rate of 70 beats per minute and free peritoneal fluid. The cervix was 3 cm dilated by digital examination, the membranes were intact, and there was no evidence of significant vaginal bleeding.
Two large bore intravenous lines were placed and aggressive fluid replacement was undertaken with normal saline. The systolic blood pressure improved modestly to 70/30. The fetal bradycardia persisted despite aggressive volume replacement, oxygen supplementation via nasal cannula, and position changes. An emergent exploratory laparotomy with cesarean delivery under general anesthesia was performed for the indications of suspected intra-abdominal hemorrhage and nonreassuring fetal heart tones. At the time of initial evaluation, the most likely cause of the patient's symptoms was assumed to be uterine rupture. A Pfannenstiel incision was used to access the abdomen. Upon entering the peritoneal cavity, 1500 mL of hemoperitoneum was encountered. A viable female infant was delivered through a low transverse hysterotomy and transferred to the neonatologist for resuscitation. The hysterotomy site was closed and the abdomen and pelvis were packed with laparotomy sponges to control the hemorrhage and identify the source of bleeding. The packs were removed from the pelvis in a stepwise fashion. The uterus and accompanying pelvic structures were intact and were not the source of hemorrhage. Upon removing the packs from the upper abdomen, brisk bleeding was encountered following removal of the packs in the left upper quadrant. An intraoperative consultation was obtained from a general surgeon who created a midline vertical incision extending to the xiphoid. The lesser sac was opened revealing copious blood clot and a peripancreatic hematoma. Heavy bleeding from this area was encountered stemming from the spleen. A splenectomy and distal pancreatectomy were performed with cessation of bleeding. Intraoperatively, she received six units of packed red blood cells, four liters of crystallized fluids, four units of fresh frozen plasma, and one pack of pooled platelets after an estimated three-liter blood loss. She received two prophylactic doses of Cefazolin. Her abdomen was closed after a Jackson Pratt drain was placed, and she was transferred to the Intensive Care Unit.
Postoperatively, broad spectrum antibiotics were administered empirically for 6 days for leukocytosis and persistent fever to 38.2°C. A discrete source of infection was not identified. Appropriate vaccinations were administered to Haemophilus influenza, seasonal influenza, pneumococcus, and meningococcus. She was discharged home in stable condition on hospital day 8 with one week of oral antibiotics. The patient's long-term course was complicated by a pancreatic fistula that resolved with conservative management. Final pathology revealed a 165-gram spleen measuring 10.8 × 6.8 × 4.5 cm with a large aneurysm of the main splenic arterial branch.
The neonate was born with APGARS 0 and 2, an arterial blood gas pH of 6.507, pCO2 of 176, and a base excess of −29.4. The neonate was resuscitated, intubated, and given head cooling measures for suspected hypoxic ischemic encephalopathy. An MRI of the head showed multiple brainstem infarcts. The neonate had multiple procedures performed to include tracheostomy and percutaneous gastrostomy. The infant was with severe neurologic impairment at one year of age.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [150.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 150.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2969,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4005217-1,Extracted,"A 33-year-old Caucasian male was transferred to our hospital from outside facility with acute renal impairment. The patient had no significant past medical history other than gastroesophageal reflux disease (GERD) and he was not known to be on any medication. He has history of tobacco use (rubbing and snuffing) for 20 years and drinks 3 cans of beer per week.
Patient presented with the chief complaint of bilateral lower extremities edema and generalized muscle weakness and cramps. These symptoms were noticed two days prior to the admission. Two months prior to the admission, the patient had also complained of tiredness and constipation. He had not been sleeping well at night. He denied being in unusual stress situation. He was also feeling colder than other people around him. Prior to the admission, the patient noted a weight gain of 10 pounds in 2 days. Patient denied any history of seizure, trauma, or fall recently although he mentioned that he had been doing a lot of snow shoveling over the past two weeks before admission.
On presentation, the patient had a body temperature of 36.6°C, pulse of 78 per minute, respiratory rate of 20, and blood pressure of 193/115 mm Hg. The patient was obese with a body mass index of 38.1 Kg/m2. On physical examination, he was alert and oriented. His conjunctivas were clear and pupils were equal, round, and reactive to light and accommodation. An enlarged, rubbery thyroid was palpable. Chest was clear on auscultation bilaterally and S1/S2 was normal with no murmur. Abdomen was soft and nontender. Pitting edema was noted in lower extremities bilaterally with slight muscle tenderness. No evidence of dehydration was found. No lymphadenopathy was noted. No motor or sensory disturbances were noted.
Blood tests showed a creatinine of 1.54 (reference: 0.62–1.27 mg/dL). His GFR was 52 (reference: >59 mL/min/1.73 m2). Blood urea nitrogen (BUN) was 13 (reference: 8–26 mg/dL). His CK was 7200 (reference: 48–222 U/L). Sodium was 141 (reference: 136–145 mmol/L), potassium was 4.2 (reference: 3.5–5.1 mmol/L), and chloride was 99 (reference: 96–111 mmol/L). Urine electrolytes were also measured. Fractional excretion of sodium (FENa) was 0.88 pointing towards prerenal cause of renal impairment.
His TSH was 145.7 (reference: 0.3–5.9 μlU/mL). TSH with free T4 reflex was 117.13 (reference: 0.3–5.9 μIU/mL) and thyroxine free (free T4) was <0.3 (reference: 0.6–1.1 ng/dL). Thyroid peroxidase (TPO) antibody was 150 (reference: <40 IU/mL).
Liver function tests showed an aspartate aminotransferase (AST) of 148 (reference: 8–48 U/L), alanine transaminase (ALT) of 82 (reference: 7–55 U/L), and lactate dehydrogenase (LDH) of 239 (reference: 98–192 U/L). Lipid panel showed cholesterol of 365 (reference: <200 mg/dL), high-density lipoprotein (HDL) of 42 (reference: >39 mg/dL), and triglyceride (TG) of 257 (reference: <150 mg/dL).
White blood cell (WBC) count was 6.9 (reference: 3.5–11 103/μL). Erythrocyte sedimentation rate (ESR) was 12 (reference: 0–15 mm/hr). C-reactive protein (CRP) was 0.27 (reference: <0.8 mg/dL). B-type natriuretic peptide (BNP) was 20 (reference: <100 pg/mL). Hemoglobin (HGB) was 12.3 (reference: 13.1–17.3 g/dL). Ferritin was 515 (reference: 24–336 ng/mL). Serum iron was 93 (reference: 50–160 μg/dL). Total iron binding capacity (TIBC) was 333 (reference: 260–400 μg/dL). Iron saturation was 28 (reference: 20–50%). Urine analysis was negative for hematuria and proteinuria.
Ultrasound of thyroid showed a small thyroid that was hypoechoic and heterogeneous with diminished vascularity. These findings, although nonspecific, are suggestive of prior episodes of thyroiditis or long standing hypothyroidism. Ultrasound of kidney was unremarkable. Transthoracic echocardiogram (TTE) was within normal limit.
The patient was started on levothyroxine at 125 mcg and aggressive hydration. The patient was initially given IV fluids at a rate of 200 mL/hr for 8 hours in addition to the oral hydration. The fluids were subsequently tapered off. His creatinine decreased to 1.44 mg/dL and his CK decreased to 5409 U/L after a day of treatment. Leg edema and muscle cramps started improving rapidly after a day of treatment. At the time of presentation, the patient was also given IV hydralazine 10 mg to lower his blood pressure. He was subsequently continued on hydralazine 25 mg every six hours to manage his hypertension. Patient's condition continuously showed improving trend over a 2-day period after which he was discharged.
On follow-up after four months, the patient's creatinine decreased to 0.9 mg/dL and his GFR was >60 (reference: >59 mL/min/1.73 m2). His TSH was 0.469 (reference: 0.3–5.9 μlU/mL). TSH with free T4 reflex was 6.22 (reference: 0.3–5.9 μIU/mL). His HGB was 15.3 (reference: 13.1–17.3 g/dL). His AST level was 47 (reference: 8–48 U/L).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [78.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 78.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
The patient's Well's score for pulmonary embolism is 3."
2970,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4058584-1,Extracted,"A 16-year-old adolescent female presented to the ER with sudden onset abdominal pain, lasting for six hours. Her last menstrual period was 18 days back. The patient did not have previous diseases or surgery.
On physical examination she presented tachycardia (pulse rate 115 beats per minute), tachypnea (respiratory rate 22 breaths per minute), and hyperpyrexia (37.8°C) with abdominal distention and severe rigidity on the lower quadrants on palpation. Blood pressure (BP) was 85/60 mmHg and she was anxious but alert and oriented.
Laboratory investigations showed mild leukocytosis, slight elevation of C-reactive protein (CRP) (192 mg/L), and discrete anemia (hemoglobin 10 g/dL). Urine output was 26 cc/h and serum; β-human chorionic gonadotropin (βhCG) level was below 4 UI/L. Gynecological examination excluded abnormalities of the external genital structures in a virgin patient.
Transabdominal USS revealed a moderate amount of fluid in the abdomen and in the pouch of Douglas and a complex right adnexal mass with signs of peripheral vascularization ().
An abdominal CT study was indicated and performed using a 64-row scanner (LightSpeed VCT, General Electric Medical System, Milwaukee, WI, USA), before and after the injection of iodinate contrast medium (Iomeron 350 mg/mL, Bracco Imaging, Milan, Italy).
The unenhanced CT scan () showed a low-attenuation fluid within the peritoneum surrounding spleen and part of liver with extension to the pouch of Douglas and to the periuterine area, where a round hypodense image was detected. The fluid showed progressively increasing attenuation values from the upper abdomen to the pelvis and it appeared clearly hyperdense in the pouch of Douglas (60–65 Hounsfield units, HU). These findings were suggestive for the presence of hemoperitoneum. A dynamic CT scan revealed thickened cysts with enhancing walls, such as a corpus luteum cyst. The arterial phase showed a cloud-like extravasation from the cyst, indicating the presence of active bleeding (). The CT study excluded other diseases of the intra-abdominal organs, such as the uterus and left adnexae.
After fluid resuscitation, the patient became haemodynamically stable and the subsequent emergent laparoscopy confirmed a bleeding corpus luteum as the cause of the hemoperitoneum.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [115.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 115.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2971,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8312776-1,Extracted,"A 30-year-old woman with a past medical history of tobacco use presented to our facility with worsening shortness of breath on exertion, dry cough, and pleuritic pain. Outpatient treatment with antibiotics and nebulizers did not relieve her symptoms. She then presented to the emergency room (ER). In the ER, she was in no apparent distress; her blood pressure was 122/75 mmHg, heart rate 90 beats per minute, respiratory rate 18 breaths per minute, temperature 98.2°F, and pulse oximetry was 95% on room air. Heart and lung examinations were normal.
Laboratory tests revealed white blood cell count of 15.6 × 103/uL (reference range: 4.5-11.0 × 103/uL), hemoglobin 12.1 g/dL (reference range: 13.2-17.5 g/dL), platelet count 410 × 103/uL (reference range: 140-450 × 103/uL), blood urea nitrogen 19 mg/dL (reference range: 5-25 mg/dL), creatinine 0.95 mg/dL (reference range: 0.61-1.24 mg/dL), and troponin 0.01 ng/mL (reference range: <0.04 ng/mL). Chest X-ray showed no evidence of pneumonia or pleural effusion (Figure ).
Given the persisting symptoms despite outpatient medical management and clear chest X-ray, she underwent computed tomography (CT) of the chest with contrast showing bilateral lower lobe pulmonary emboli (Figures , ) and a 4.5 cm mass in the right atrium (Figure ).
Intravenous unfractionated heparin was started. A subsequent transthoracic echocardiogram confirmed a 3.76 cm × 4.95 cm mass in the right atrium (Video , Figures , ).
A discussion was held with the cardiothoracic surgery team. The patient underwent surgical excision of the right atrial mass the following day. An intraoperative transesophageal echocardiogram revealed the massive right atrial mass with a stalk attached to the interatrial septum (Video ). Pathology of the mass confirmed right atrial myxoma (Figure ). The patient was discharged four days later to a rehab facility in a stable condition.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 90.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2972,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5819632-1,Extracted,"A 72 years old male with past medical history of chronic healed lower extremity ulcers due to lymphedema was brought to the hospital for evaluation of fever and altered mental status. On admission, vital signs showed temperature 39.1 °C, heart rate 92 beats/min, and respiratory rate 22 breaths/min. Physical examination was remarkable for pallor, systolic murmur along the aortic area. Lungs were clear to auscultation. Abdomen was soft, non-tender, and no organomegally was detected. Examination of the extremities showed multiple healed wounds along both the lower extremities without evidence of infection. His right ankle was swollen and mildly tender to palpation with no erythema or warmth. Labs were remarkable for lactic acid 3.8 g/dL, white cell counts (WBC) 12.3 × 109/L, hemoglobin 6.5g/dL, procalcitonin 54.96 ng/mL, and C-reactive protein (CRP) 19.2 mg/dL. Two sets of blood cultures were obtained. Fluid resuscitation and broad-spectrum antibiotics were initiated. Later his blood culture grew streptococcus G. Given the newly discovered heart murmur, transthoracic echocardiogram (TTE) was obtained and showed a medium sized, 1.0 cm (length) × 1.0 cm (width), irregular, partially calcified, mobile mass on the left ventricular aspect with appearance consistent with vegetation. Subsequently, transesophageal echocardiogram (TEE) was performed and confirmed aortic valve vegetation (). No other obvious source for bacteremia was identified. Patient underwent right ankle magnetic resonance imaging (MRI) which was negative for osteomyelitis or septic arthritis or abscess. Given the patient’s severe microcytic anemia, iron studies were obtained and confirmed severe iron deficiency anemia. He received 4 units of packed red blood cells (PRBCs) during his hospital stay. His low hemoglobin prompted further workup including computed tomography (CT) of the abdomen and pelvis which revealed circumferentially thickened segment of descending colon adjacent to the splenic flexure with localized invasion into the sigmoid colon. Such finding was highly suspicious for primary colonic cancer. CT of the chest showed multiple bilateral pulmonary nodules measuring 1.6 cm most compatible with metastatic disease. Colonoscopy showed a friable lesion that was partially occluding the lumen and biopsy of the lesion confirmed a diagnosis of adenocarcinoma (, ). Patient was discharged on intravenous (IV) ceftriaxone to complete 6 weeks of antibiotics coverage for IE and follow-up was planned with colorectal surgery.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [92.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 92.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3 + 1 =  4.
The patient's Well's score for pulmonary embolism is 4."
2973,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7086115-1,Extracted,"Our patient is a 28-year-old male with a past medical history of EGE, duodenal ulcers, and stricture who presented to the hospital with chief complaints of 3 episodes of dizziness and melena for one day. The patient reported that before coming to the hospital, he was shopping at a mall, where he experienced dizziness and then had a dark black colored bowel movement. The patient recently came from Canada. He denied any other past medical history or any past surgical history. He reported allergy to peanuts. His home medications included prednisone, montelukast, and pantoprazole daily.
On admission, his vitals were obtained and he was found to be tachycardic with a heart rate of 150. Initial lab workup done in the emergency department showed hemoglobin (hgb) of 9.3. Soon after admission, the patient had an episode of large volume hematemesis >1.5 L and brief loss of consciousness for which a code rapid response was called. Between days 1 and 2, his hgb dropped from 9.3 to 5.7. The Patient was initially stabilized by intravenous crystalloids and was transferred to the ICU. The patient received blood transfusions and his hgb improved significantly. The patient was managed conservatively with continuous monitoring in the ICU. Emergent endoscopy (EGD) revealed high-grade duodenal stenosis, severe pyloroduodenal deformity and a duodenal ulcer with a visible vessel. Two clips were deployed blindly during the EGD (figure -).
Epinephrine could not be injected due to hard and fibrotic tissue around the duodenal stenosis. The Interventional radiology (IR) service was consulted. The patient was taken for angiography which revealed active bleeding from a branch of the gastric artery. Coiling and subsequent embolization were done by the IR service. The patient received 5 units of RBCs total and continued on pantoprazole intravenous twice daily. For his known duodenal stricture, surgery was consulted with a recommendation of no acute surgical intervention in the hospital was provided. On discharge, he was sent home with pantoprazole and prednisone and close follow up with gastroenterology, surgery and primary care doctor.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [150.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 150.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 1.5 + 1 = 2.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2974,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6842506-1,Extracted,"A 72-year-old Dutch female presented to the emergency department with fever and concomitant confusion. Three years before this admission, a symptomatic MM was diagnosed for which melphalan, prednisolone and bortezomib were initiated. Eighteen months before presentation lenalidomide in combination with dexamethasone was given for relapse of her MM, and 2 months later cyclophosphamide was added to this regimen. Six months later she progressed and received third line therapy consisting of bortezomib, thalidomide and dexamethasone. Four months before this presentation the MM was regarded refractory to bortezomib and immunomodulatory drugs, thus immunotherapy with weekly daratumumab in combination with prednisone was offered. Although amyloidosis was suspected due to proteinuria, no confirmation by fat tissue biopsy was performed. One year before presentation an echocardiography showed no structural abnormalities of valves or heart. At admission, no (septic) shock was present with vital signs showing mild tachycardia (100 beats per minute), blood pressure of 110/60 mmHg, temperature of 37.2 °C and respiratory rate of 15 per minute. History revealed fever, pollakisuria and confusion since 2 days. At physical examination no cardiac murmur, no signs of systemic major emboli, normal pulmonary auscultation and no signs for an acute abdomen or heart failure were found. No infusaport was in situ. Laboratory investigations showed mildly elevated leukocyte count (10.9 × 109/L) together with elevated C-reactive protein (127 mg/L). Kidney function, electrolytes and liver enzymes were normal. Immunoglobulin gamma was 31.4 g/L, which was stable over time and hypo-albuminaemia was also stable at 11 g/L. Electrocardiogram was unchanged when compared to 1 year earlier, without signs of arrhythmia, AV-blocks or myocardial ischemia. Pulmonary X-ray was normal. Urine tests were compatible with a urinary tract infection with positive nitrite and leukocytosis. Dipstick screening showed also signs of albuminuria and microscopic hematuria, which were not investigated further at this point. Intravenous amoxicillin with clavulanic acid (1000/200 mg 4 times daily) was initiated corresponding to Dutch guidelines for urinary tract infections. Hydrocortisone (100 mg bolus followed by continuous infusion of 100 mg per 24 h) was initiated because of suspected tertiary adrenal insufficiency due to prolonged use of prednisolone. One day after admission the results of urine culture confirmed bacterial growth of Escherichia coli. In contrast, all four blood cultures showed growth of M. morganii. Ciprofloxacin (200 mg 2 times daily) was added due to the penicillinresistance of the Morganella species. There was no evident portal of entry for the M. morganii, though no specific work-up was done.
Two days after admission, the patient acutely deteriorated with hemodynamic instability. Under the diagnosis of septic shock gentamicin (4 mg per kg) and once more hydrocortisone (100 mg bolus injection) were administered without improvement of hemodynamic status after 1 h. Transthoracic echocardiography showed severe aortic regurgitation and a mobile structure, 10 by 10 mm, attached to left or non-coronary cusp, strongly suspective of vegetation (Fig. ). These findings led to the diagnosis of bacterial endocarditis of the native aortic valve. Half an hour after diagnosis, the patient died due to ongoing hypoperfusion and refractory shock.
At autopsy, vegetation with gram-negative rods in the native aortic valve was observed, consistent with a diagnosis of M. morganii-endocarditis. Additional staining for amyloid confirmed advanced light-chain (AL) amyloidosis in heart, kidneys and spleen. The aortic valve itself contained patchy amyloid depositions near the adherent vegetation (Fig. ). These observations led to our hypothesis that the patient became susceptible to IE caused by the opportunistic pathogen M. morganii due to valvular endothelial damage related to amyloid depositions and a severely compromised immune system.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [100.0, 'beats per minute'], 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 100.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
2975,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6831222-1,Extracted,"A 57-year-old Hispanic male with a medical history of human immunodeficiency virus (HIV) infection, hepatitis C virus (HCV) infection, HIV related neuropathy and chronic degenerative disease of lumbar spine presented to the emergency room (ER) complaining of dark brown-to-red colored urine and bilateral lower extremity and lower back pain for 2 days before his presentation. He was in his normal state of health before the onset of symptoms. The patient denied any fever, chills, shortness of breath, chest pain, dizziness, recent trauma or immobilizations and there was no seizure activity or extreme exertion reported. He never had these symptoms before. His home medications included dolutegravir-abacavir-lamivudine (Triumeq) and omeprazole 40 mg taken occasionally for stomach discomfort. Triumeq was started 2 months prior to his presentation. He was allergic to penicillin. He was a former illicit drug user and former smoker, having stopped both habits more than 20 years ago since date of presentation. Review of systems was pertinent only for dark urine, lower back pain and bilateral lower limbs pain. Initial vital signs showed a temperature of 98.4°F (36.8°C), blood pressure 142/89 mm Hg, pulse rate 109 beats per minutes and respiratory rate 16 breath per minute, with a pulse oximetry saturation of 97% while breathing on room air; body mass index (BMI) was 21.8 kg/m2. Physical examination showed a cachectic male, with a warm and dry skin, conjunctiva was clear. Head and neck exam did not show any relevant findings. Lungs were clear to auscultation. Heart examination showed a regular rhythm, S1 and S2 were present; no murmurs or rub were noted. Abdomen was soft, nontender and nondistended; no organ distention or palpable masses were noted. Musculoskeletal examination revealed tenderness of lumbar spine and both lower extremities, with no signs of trauma. Neurological examination was grossly intact.
Initial investigations included a computerized tomography (CT) of the abdomen and pelvis without contrast material, which was grossly unremarkable. Initial laboratories are shown in Table . Significant analysis included a complete blood count with a red blood cell (RBC) of 4.32 MIL/μI, Hemoglobin was 16.1 g/dL, Hematocrit 47.5%, white blood cell (WBC) 14,000/μI. Basic metabolic profile showed a Potassium of 4.3 mEq/L, blood urea nitrogen (BUN) 30 mg/dL, Creatinine 1.2 mg/dL, estimated glomerular filtration rate (e-GFR) was 49 mlLmin/1.73m2. Liver function test showed an Aspartate Transaminase (AST) of 2,270 units/L, alanine transaminase (ALT) of 342 units/L and total bilirubin was within normal limits. Serum CK was 98,061 units/L (normal 20–200 units/L). Lactic acid was 2.3 mg/dL. Blood ethanol was <10. Urine toxicology screen was negative for recreational drugs. Urine analysis was red and turbid on gross examination; specific gravity was 1.030. Urine protein was more than 300 mg/dL, bilirubin was moderate elevated and blood was reported as large. Nitrates were positive and microscopy showed many bacteria and few mucous casts. Crystal examination revealed few amorphous phosphate crystals and pathological casts were significant for few fine granular casts. Blood and urine cultures were negative. The human leucocyte antigen (HLA)-B5701 was negative. His CD4+ cell count was 816 cell/microliter and performed HIV polymerase chain reaction (PCR) showed an undetectable viral load.
Given the severe rhabdomyolysis, the patient was started on high infusion rate intravenous fluid therapy with sodium chloride 0.9%. He was admitted to the intensive care unit (ICU) for further management; dolutegravir-abacavir-lamivudine (Triumeq) was held in view of severe rhabdomyolysis. In the ICU, the patient remained stable and intravenous fluid therapy was continued. His CK levels trended down from 98,061 units/L to 10,000 units/L on day 3 (see Table and Fig. ) and continued to decrease to 838 units/L on the day of discharge (hospital day 7). Follow-up in the clinic 1 week after discharge revealed that patient symptoms improved significantly and repeated CK levels were 179 units/L. In subsequent clinic visits, the patient was started on emtricitabine, elvitegravir, tenofovir, and cobicistat (Genvoya) and he remained stable with no further episodes of rhabdomyolysis noted. The Naranjo Scale[ (see Table ) (Adverse Drug Reaction Probability Scale, developed to help standardize assessment of causality for all adverse drug reactions) score was 6 in our patient (1 point for previous conclusive reports of this reaction, 2 points for the adverse event appearing after the suspected drug was administered, 1 point for improvement after the drug was discontinued, 2 points for no alternatives causes that could on their own have caused the reaction).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [109.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 109.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2976,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8331174-1,Extracted,"A 60-year-old female presented to the emergency department in our hospital with acute bilateral eye vision loss. Her past medical history included an undocumented splenectomy, diabetes mellitus, and hypothyroidism. Two weeks prior to the onset of visual symptoms, she reported flu symptoms, including fever, myalgia, and dry cough. The patient neglected these symptoms and did not benefit from any treatment. Fifteen days later, the patient presented with a sudden drop in visual acuity in the left eye without pain, eye redness, or headache which became blinding after 24 hours with involvement of the contralateral eye after four days, associated with right hemibody weakness. Her admission parameters were as follows: pulse 94 beats per minute (bpm), blood pressure 135/88 mmHg, temperature 38.2°C, and oxygen saturations were 85% on room air.
Her neurological examination on admission revealed complete bilateral blindness with no perception of light. Pupil responses to light were abolished with horizontal nystagmus and unremarkable fundoscopic findings. No other obvious abnormal findings in cognitive function, cranial nerves, or neck rigidity were demonstrated. Motor system examination revealed normal bulk in all four limbs. There was hypotonia, most marked on the right side. Power was grade 4/5 in the right hemibody and 5/5 in the left side. There was no involuntary movement or seizures. Plantar reflexes showed bilaterally Babinski signs. All modalities of sensation were conserved. Clinical examination of other systems revealed no abnormalities She presented with breathlessness a few hours after her admission to the neurology department. She was then transferred to the intensive care unit following clinical deterioration and continued increasing oxygen requirements where she was started on non-invasive ventilation.
The patient had magnetic resonance imaging (MRI) (1.5 Tesla) of the brain and orbits with and without contrast, which revealed right parietal nodular signal abnormality in the posterior limb of the internal capsule (Figures -)"". No intramedullary abnormal signal or enhancement was present.
Biochemical and cytological studies of the cerebrospinal fluid (CSF) showed an elevated protein count (1.41 g/L) and normal glucose without pleocytosis. No oligoclonal band was found in the CSF analysis. Blood and CSF cultures were negative. SARS-CoV-2 ribonucleic acid (RNA) in the CSF was not detected. She tested negative for myelin oligodendrocyte glycoprotein immunoglobulin G (MOG-IgG) and serum aquaporin-4 IgG antibodies. The serum paraneoplastic panel was assessed at the Mayo Clinic, and the serum angiotensin-converting enzyme (ACE) levels were normal. Blood tests showed a highly elevated C-reactive protein (CRP) at 300 mg/L with marked hyperleukocytosis (15,510/μl). Other laboratory results, such as copper, B12, and zinc levels, were checked and were within the reference range. Her nasopharyngeal swab reverse transcription-polymerase chain reaction (RT-PCR) was negative for SARS-CoV-2. COVID serology was positive for immunoglobulin M (IgM) and IgG antibodies. Other serological tests for syphilis, human immunodeficiency virus (HIV), human T-cell leukemia virus, types 1 and 2 (HTLV I/II), Epstein-Barr virus, cytomegalovirus, and hepatitis B and C were all negative. Serum ferritin (42.92 μ/L) and interleukin-6 levels (7.8 pg/mL) were normal. They were only measured on Day 5 of her admission (15 days after symptom onset). The patient reported no family history of cancer. Computed tomography (CT) imaging of the thorax, abdomen, and pelvis was done to assess possible malignancy, which was negative. The patient received seven sessions of plasmapheresis and motor physiotherapy sessions, with the prevention of thromboembolic complications by anticoagulant therapy. Her clinical evolution was stationary. A second control by encephalic and medullar MRI was performed and showed stability of the lesion load with disappearance of contrast enhancement with optic atrophy (Figure ).
During her stay in intensive care, she benefited from an immunoglobulin cure (0.40 g/kg per day for five days) associated with corticosteroids. The evolution was marked by the remission of the respiratory discomfort, an improvement in the motor deficits on the right side (5/5 proximal, 4/5 distal), and the persistence of blindness. The patient was then discharged with regular neurology follow-up.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [94.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 94.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2977,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-4982,Extracted,"A 50-year-old man presents to his primary care physician for management of a lung nodule. The nodule was discovered incidentally when a chest radiograph was performed to rule out pneumonia. The nodule is 8.5 mm in size and was confirmed by CT. The patient is otherwise healthy, has never smoked, and exercises regularly. The patient works in a dairy factory. He has had no symptoms during this time. His temperature is 97.6°F (36.4°C), blood pressure is 122/81 mmHg, pulse is 83/min, respirations are 12/min, and oxygen saturation is 98% on room air. Physical exam including auscultation of the lungs is unremarkable.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [83.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 83.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2978,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3946053-1,Extracted,"A 57-year-old Brazilian woman was referred to our hospital because of an increase in abdominal girth in February 2003. She said she was overweight, and had noted a rapid increase in abdominal girth during the last year. Her menarche occurred at the age of 15, she always had regular periods, and had used oral contraceptives for two years. She had eight pregnancies, producing eight children, and underwent tubal ligation at the age of 29. Her menopause occurred at the age of 46, and she never used hormonal therapy. She underwent an appendectomy and cholecystectomy, respectively, at the ages of 16 and 29, and had arterial hypertension and dyslipidemia. She denied the use of tobacco, alcohol or illicit drugs. Physical examination revealed pale skin, a temperature of 36.1°C (97°F), a respiratory rate of 25 breaths/minute, a pulse rate of 100 beats per minute, blood pressure at 180/140mmHg; normal cardiac and respiratory sounds; her abdomen was distended and tense, and her abdominal circumference measured 134cm (Figure A), with dullness to percussion and superficial dilated veins. Examination of her breasts, vulva and vagina did not reveal abnormalities. Her lower limbs showed moderate swelling. She was admitted to the gynecological ward for accurate diagnosis and treatment. Laboratory tests revealed hematocrit 29%, hemoglobin 9.2g/dL, leukocytes 7000 cells/μL, platelets 478,000/μL, CA-125 374.8IU/dL, and normal levels of carcinoembrionic antigen (CEA) as well as of alpha fetal protein. The chest radiograph showed an upward compression of her diaphragm, and abdominal ultrasonography study showed a voluminous cystic abdominal-pelvic mass with thick walls, strongly suggestive of an ovarian tumor (Figures A, B). Abdominal ultrasound (US) images showed a normal aspect of the liver, bile ducts, portal and supra-hepatic veins, as well as normal spleen and kidneys. The cystic mass had rough septa and voluminous solid components, occupying the entire abdominal cavity with extrinsic compression of the liver and spleen; discrete blood flux within the tumor and high resistance peripheral blood flow. Computed tomography (CT) images of the abdomen and pelvis revealed a conspicuous and well delineated tumor with heterogeneous attenuation coefficient, predominantly liquid and with coarse septa and some solid internal irregularities. The huge tumor displaced her uterus to the left, compressed her abdominal contents, and extended up to her diaphragm (Figures D-F). As the main hypothesis was a giant adnexal complex mass, in addition to the high possibility of malignant origin, the surgical option was open laparotomy. Procedures included the intact removal of the right ovarian tumor along with her normal right fallopian tube, left adnexal resection, total hysterectomy, omentectomy, para aortic and pelvic lymph node dissection to stage the disease, and sampling of lymph nodes and of the ascitic fluid for routine tests and cytopathological evaluations. Accentuated excess of skin and subcutaneous tissue was observed after removal of the mass (Figure B). The extra-large (42×40×28cm) tumor, weighing 40kg, had a smooth external surface, and the inner aspect was multilocular, with mucinous and serous fluid areas (Figures C-F). The histopathological diagnosis was a well-differentiated mucinous cystadenocarcinoma (Figure ). The staging was 1A (tumor limited to one ovary, no ascites present containing malignant cells, no tumor on the external surface, and capsule intact). The immediate postoperative period was in the Intensive Care Unit (ICU), for close hemodynamic, ventilatory and renal function monitoring and fluid and electrolytes control. She underwent six cycles of chemotherapy (three weeks apart) with paclitaxel plus cisplatin, with no side effects, and was under close surveillance on the outpatient section of Clinical Oncology. The option for intravenous chemotherapy in this setting was based on two major concerns. The very large abdominal cavity made it difficult to treat with intraperitoneal chemotherapy with platin, and the persistence of elevated CA-129 after the cytoreduction. The levels of CA-125 were 374.8 and 222IU/mL (before and after the cytoreductive surgery), and post chemotherapy control was 7.1IU/mL. Actually, carboplatin is the best option because of its less toxic effects; however, cisplatin was the standardized drug in our hospital at the time of her admission. She has been under specialized follow-up for more than 10 years, asymptomatic and with normal imaging and laboratory parameters, including the CA-125 marker.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [100.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",5.5,5.5,5.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 100.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 3 + 1.5 = 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 4.5 + 1 =  5.5.
The patient's Well's score for pulmonary embolism is 5.5."
2979,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5331635-1,Extracted,"A 52-year-old man was diagnosed with uraemia at a local hospital in February 2013. He was treated using haemodialysis while in the hospital and with peritoneal dialysis after discharge. His serum creatinine concentration was 1000 μmol/L, showing two reduced renal volume. The patient was also diagnosed with chronic obstructive pulmonary disease, grade 3 hypertension (high-risk), and cardiac insufficiency. Starting in June 2015, the patient reported experiencing epigastric pain during the peritoneal dialysis, which was exacerbated during inspiration, relieved during dialysis fluid removal, and absent during non-dialysis periods. The dialysis fluids were smooth and accompanied by floccule.
On November 17, 2015, the patient experienced bloody ascites, swelling of both lower limbs, and asthma after playing sports and was admitted to our hospital. A physical examination revealed a body temperature of 38.0 °C, a respiratory rate of 22 breaths/min, a pulse of 110 beats/min, and blood pressure of 130/63 mmHg. The patient showed clear consciousness, but he exhibited facial signs of chronic anaemia, distension of the jugular vein, barrel chest, mild swelling of both lower limbs, wheezing in both lungs, an expanded heart boundary on two sides, abdominal wall tension, positive pressure at the navel, and no rebound tenderness. Laboratory testing revealed a white blood cell count of 3.4 × 109/L, a procalcitonin level of 2.69 ng/mL, a B-type natriuretic peptide level of 460 pg/mL, a prothrombin time of 14.5 s, and a D-dimer level of 2,127 ng/mL. Routine testing of the peritoneal fluid revealed a slightly muddy appearance with a specific gravity of 1.018, weak positive results in the Rivalta test, a white blood cell count of 510 × 106/L (mononuclear cells: 40%, multinuclear cells: 60%), a red blood cell count of 2,980 × 106/L, and positive results for coagulability.
The patient’s peritoneal fluid was submitted for culturing, and the patient received initial treatment using intravenous cefazolin, which was changed to intraperitoneal ceftazidime and vancomycin on November 19. On November 23, the patient’s body temperature was 36.5 °C. He reported that his chest congestion and stomach ache were relieved, and the dialysis fluid appeared smooth and clear. The patient and his relatives insisted that he be discharged, despite our informing them that the culture results were incomplete, the infection might not be controlled, and the patient might experience recurrence of the peritonitis and septicopyaemia. Unfortunately, a telephone follow-up with the patient’s relatives revealed that he had not received continued treatment after his discharge and had died in February 2016. The cause of death was multiorgan failure.
On November 19, 2015, the patient’s peritoneal fluid was aseptically collected into aerobic blood culture bottles (BD, USA) and sent to a clinical laboratory, where it was cultured using the BactecTM 9120 blood culture system (BD, USA). After culturing for 51.76 h, a positive result was observed, and the culture fluid was directly smeared to identify gram-positive bacilli. The fluid was also transferred to blood agar (Zhengzhou Autobio) and chocolate agar plates (Tianjin Jinzhang), which were incubated at 35 °C with 5% CO2. There were no visible colonies after 24 h of culturing, although both plates exhibited small light-brown colonies after 48 h of culturing. The colonies were positive in the catalase test. After 72 h on the chocolate agar plate and 6 days on the blood agar plate, the colonies were dry, cracked, elevated, and light brown in colour (Figs. and ). Figures and show that the colonies were confirmed to be gram-positive bacilli with positive, weak acid-fast staining. Additional testing using the MicrolexLT/SH mass spectrometer (Bruker) identified the strain as G. rubropertincta with a score of 1.702. However, a 16S rRNA sequence analysis was also performed at the Shanghai Sangon Company, using the following primers: 27 F (5′-GAGTTTGATCCTGGCTCAG-3′) and 1492R (5′-AAGGAGGTGATCCAGCCGCA-3′) []. After Blast alignment, we observed that the bacteria were 99% similar to the sequence of G. terrae EY-T12 (GenBank: KR476419.1). The phylogenetic tree of the 20160601 isolate is shown in Fig. .
An antimicrobial susceptibility testing was performed using the E-test (Zhengzhou Autobio), in which in the McFarland and M-H plates (Tianjin Jinzhang) are adjusted to 0.5 and incubated at 35 °C with 5% CO2 for 48 h. The results from the patient described in this report and from those in previous studies are summarized in Table . The strains in the previous studies were also tested using the E-test after 48 h of incubation. The isolate from the present report was resistant to ceftazidime and susceptible to penicillin, ampicillin, amikacin, erythromycin, ceftriaxone, imipenem, gentamicin, and vancomycin.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2980,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8106123-1,Extracted,"A 16 year-old female Gravida 1 para 1 presented to the emergency department with no past medical and surgical history. According to her history, she developed intermittent fever and chills, right upper quadrant pain, and urinary retention for the last 2 weeks; she underwent normal vaginal delivery one week ago. She was hospitalized in another province for these complaints. The presenting complaints were diffuse abdominal pain, abdominal distention, and continuous fever from the last three days with vomiting and constipation for the last two days. The vital signs were BP 133/97 mmHg, RR 20/m, PR 136/m, temperature 39 C0, and SpO2 90%. On physical examination, the patient looked ill with a distended abdomen, generalized tenderness, rebound tenderness, and guarding. Fluid thrill and shifting dullness was positive. Bowel sounds were not audible on auscultation. Blood workup showed TLC 21,000/mm3 (normal 4000–11,000), neutrophil 89% (normal 40–75), Hb 8.2 g/dl (normal 11.5–16.5), serum creatinine 0.86 mg/dl (normal 0.6–1.2), total bilirubin 0.71 mg/dl (normal 0.1–1.2), SGOT 20 IU/ml (normal 0–40), SGPT 34 U/L (normal 5–40), alkaline phosphatase 109 IU/L (normal 40–240), and blood group AB + ; the HbsAg, anti HCV Ab, and HIV were negative. She was initially received by the emergency doctor and was diagnosed with “postpartum sepsis” because she was having signs and symptoms of sepsis. Ultrasound showed distended bowl loops floating in free fluid in the peritoneal cavity. Erect chest X-ray showed no air under the right hemidiaphragm. CT with contrast was performed revealing gross ascites suggesting peritonitis but the cause of the ascites was unclear.
An exploratory laparotomy was performed after initial management with a hollow viscous perforation in mind. Biliary peritonitis was found with about 4 L of bile-stained fluid in the peritoneal cavity; the stomach, small intestine (distended), and colon were normal. A perforation of about 7–8 mm was found on anterolateral wall of supra duodenal segment of CBD below the junction of cystic duct and common hepatic duct as shown in Fig. . Gall bladder and the rest of biliary tree was normal without any calculus. An intra-operative cholangiogram was not available so a 10 French feeding tube was passed to the duodenum through a perforation to confirm the distal obstruction that passed without any resistance. Peritoneal lavage with warm normal saline, cholecystectomy, and CBD repair over a T-tube was thus performed. The post-operative stay was uneventful, and the patient fully recovered and was discharged on the 7th post-operative day. The T- tube was removed on the 15th post-operative day after the cholangiogram showed no filling defects and normal contrast flow to the duodenum. The patient did well after one year of follow up.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [136.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 136.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2981,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4192414-1,Extracted,"A 57-year-old female was referred to our hospital because of dyspnea worsening for 2 days. She had no hypertension, diabetes, or prior spontaneous abortion. At presentation, physical examination revealed that arterial pressure was 140/90 mmHg, heart rate was 110 beats/min, and respiration was 20 breaths/min. Mild pitting edema was noted in the right lower extremities. She was found to have both a lupus anticoagulant and antibodies to beta2-glycoprotein I of IgG, type. IgG and IgM anticardiolipin antibodies, antinuclear antibodies, double-stranded DNA antibodies, and venereal disease research laboratory tests were negative. Procoagulant work up including protein C, protein S, antithrombin, urine homocystine assays were normal. Factor V leiden mutation was not seen. The twelve lead electrocardiogram demonstrated sinus tachycardia and non-specific ST-T segments changes in precordial leads. A chest radiography showed mild cardiomegaly (cardiothoracic ratio, 0.55). Color Doppler and duplex-scan ultrasonography of the lower limbs presented deep venous thrombosis in right common femoral vein, superficial femoral vein, and popliteal vein. Transthoracic echocardiography (TTE) showed a dilated right ventricle associated with severely depressed systolic function ( and ). Computed tomography (CT) with contrast confirmed a diagnosis of pulmonary embolism via the disclosure of clots at the bifurcation of the common pulmonary artery and in its main branches (). In additions, the aortic valve mass, located at the non-coronary cusp, resembling papillary fibroelastoma was discovered incidentally during chest CT (). Its margin was smooth, and internal contour was homogeneous comparatively. However, the aortic mass was not diagnosed initially with TTE due to poor acoustic windows. Four hours later, her vital signs were unstable; heart rate was 110 beats/min, blood pressure was 90/60 mmHg, and she was breathing at a rate of 26/min. Because of persistent right ventricular dysfunction and progressive clinical deterioration, thrombolytic therapy were immediately performed. After initial treatments, a repeat echocardiography the following day revealed clear improvement in the right ventricular (RV) dysfunction with normal RV dimension. Subsequently, a transesophageal echocardiogram (TEE) was performed for evaluation of the aortic valve, revealing a 1 cm sized mobile cylindrical mass in the aortic valve. It attached without stalk to the non-coronary cusp annulus of the aortic valve and to extend into the ascending aorta. The aortic valve was tricuspid, without dystrophic calcification, and had no functional abnormality. In addition, there was no intracardiac shunt such as patent ductus arteriosus or atrial septal defect. The aortic valve mass was initially considered as a thrombus according to the presence of deep vein thrombosis and pulmonary embolism. After 2 weeks anticoagulation, however, a repeat TEE revealed that there was still a mass over 1 cm long at the non-coronary cusp of the aortic valve (, and ). Because a size change of the mass was not found after 2 weeks anticoagulation, we concluded that the aortic valve mass was thought to be a papillary fibroelastoma rather than thrombus. Therefore, surgical resection was considered as the best treatment option in this patient with mobile mass to prevent fatal embolic complications and to confirm pathologic findings. The following day, operation was performed under cardiopulmonary bypass. Aortic valve mass was easily removed and the valve was preserved. Gross inspection of cardiac mass showed a red-colored gelatinous lobulated mass measuring 1.4 × 0.9 cm. In the surgeon's opinion, the aortic mass was suggested as a diagnosis of organized thrombus. The histology of specimen revealed an organized thrombus with no evidence of papillary fibroelastoma ().
Postoperative CT showed complete removal of the thrombus (). She was diagnosed with antiphospholipid antibody syndrome based on her clinical presentation and laboratory findings. We repeated the lab tests after 12 weeks, which confirmed the diagnosis of antiphospholipid antibody syndrome.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
2982,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7299603-2,Extracted,"Patient 2: a 48-year-old hypertensive, non-diabetic gentleman, presented to the emergency with one episode of massive hematemesis. There was no history of dysphagia, jaundice, abdominal distension, pain abdomen or altered sensorium. Past history was significant for percutaneous coronary intervention with two drug-eluting stents performed 3 years ago, for which he was on aspirin. He had normal mentation, his BP was 90/60 mm Hg and his heart rate was 120/min. A general survey revealed pallor and rest of the systemic examination was normal. His Hb was 6.1 gram% and TLC was 6300 cells/mm3. Liver function tests, coagulation parameters, renal function and electrolytes were normal. Chest X-ray was unremarkable. He was initially resuscitated with intravenous fluid, packed red blood cells and a proton-pump inhibitor infusion. An urgent UGI endoscopy revealed a large depressed ulcer with a red spot located in the middle third of the esophagus. A diverticulum was seen in the lower end of the ulcer (). An endoscopic clip was applied to the margin for ease of identification. CECT thorax revealed a 6 cm saccular thoracic aortic aneurysm distal to the left subclavian artery, eroding into the esophagus ().
Surgery was emergently undertaken. A posterolateral thoracotomy was performed, and the aneurysmal segment of the aorta was seen originating 6 cm distal to the left subclavian artery. A partial bypass circuit was created, similar to the one described earlier. After cross-clamping the aorta both proximally and distally, the aneurysm sac was opened (). The aneurysmal segment of the aorta was replaced with a Dacron graft, taking care to preserve as many intercostal arteries as possible, while suture ligating the others (). The esophageal opening of the fistula was debrided and repaired with interrupted polypropylene sutures, superimposed with a vascularized intercostal muscle pedicle. The patient was successfully separated from the partial bypass, and a gastrostomy and jejunostomy were created. He was placed on broad-spectrum antibiotics postoperatively. He recovered well and had an uneventful post-operative course.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2983,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7575203-1,Extracted,"A 36-year-old woman who was 16-weeks pregnant with no known past medical history was brought to the hospital by her sister for 2 weeks of headaches and insomnia, followed by vivid hallucinations and bizarre delusions. Her vital signs at arrival were significant for a heart rate of 104 bpm, temperature of 97.60 F, blood pressure of 111/64 mmHg and a respiratory rate of 18 breaths per minute saturating of 100% on room air. She was agitated, disoriented and speaking incoherently. Her cardiac and respiratory exams were normal. Neurological evaluation was limited as the patient was agitated and non-cooperative. Her deep tendon reflexes were +2 in bilateral upper and lower extremities. She was moving all extremities and reacted to pain stimuli. EKG on admission was significant for sinus tachycardia at 110 bpm []. CT scan of the head which was negative for any intracranial bleeding or intracranial masses. Arterial blood gas analysis, thyroid function testing, blood cultures and urine analysis were noncontributory [].
On day 2 of admission, the patient experienced refractory generalized tonic-clonic seizures necessitating endotracheal intubation for airway protection. Evaluation with an MRI of the brain, MRA and MRV of the cerebral circulation did not reveal any intracranial pathology. Cerebrospinal fluid analysis showed lymphocytic pleocytosis []. Electroencephalography (EEG) demonstrated an extreme delta brush pattern consistent with ANMDARE. ANMDARE antibody and glial fibrillary acidic protein antibody positivity confirmed the diagnosis of ANMDARE. During her seizure episodes the patient demonstrated rhythmic oral grimacing and intermittent adduction of bilateral lower extremities. These findings correlated with the delta brush pattern seen on EEG. The patient required four anti-epileptic agents (phenobarbital, levetiracetam, clobazam, and lacosamide) to suppress the seizures. NMDARE was subsequently treated with 5 cycles of plasmapheresis, a course of stress dose methylprednisolone*, IVIG and rituximab.
During the course of her stay, telemetry identified sinus node dysrhythmias. Episodes of sinus tachycardia alternating (HR ~ 110–125 bpm) [] with sinus bradycardia (HR ~ 30–35 bpm) [] and sinus arrest (longest pause ~ 7 secs) [] related and unrelated to vagal stimuli (ultrasound fetal monitoring). A transvenous pacemaker was placed through the right internal jugular vein [].
Once ANMDARE was diagnosed, evaluation for a potential precipitating cause was undertaken. MRI of the abdomen demonstrated a left ovarian complex cystic structure measuring 32 × 33 mm. Given the association between teratomas and ANMDARE, bilateral oophorectomy was performed. Pathology identified hair and sebaceous secretions in the cyst and confirmed the diagnosis of ovarian teratoma. Despite treatment and oophorectomy patient currently remains dependent on the ventilator with poor neurological recovery at 32 weeks of gestation. Her sinus node dysrhythmia recovered in 8 days precluding the need for the placement of a permanent pacemaker.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [104.0, 'bpm'], 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 104.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2984,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8041535-1,Extracted,"A 60-year-old Japanese woman with no medical history was admitted to the emergency department of another hospital with a chief complaint of severe left lateral pain. She had no family history of endocrine disease including pheochromocytoma. Abdominal computed tomography revealed a left 5.7 cm adrenal mass with a large retroperitoneal hemorrhage (), and the patient was transferred to our hospital for multidisciplinary treatment.
She was 149 cm tall and weighed 49 kg. On presentation, her vital signs and physical findings were as follows: body temperature of 37.3°C, pulse rate of 106 bpm, blood pressure of 193/115 mmHg, respiratory rate of 18/min, and Glasgow Coma Scale score of 15. These findings strongly suggested that her pain was caused by a ruptured pheochromocytoma. Laboratory tests revealed that her white blood count was 28180/μL, hemoglobin was 11.2 g/dL, and hepatic enzymes were normal. However, her creatinine (Cre) and estimated glomerular filtration rate (eGFR) were 1.03 mg/dL and 43 ml/min/1.73 m2, respectively, which indicated decreased renal function. After arriving at our hospital, her blood pressure suddenly dropped to 62/44 mmHg. Ongoing hemorrhage was suspected because of sudden hypotension. Under a presumptive diagnosis of active bleeding from a ruptured left adrenal tumor suspected of pheochromocytoma, we decided to perform TAE to prevent the further deterioration of hemodynamics. Angiography was performed using a right femoral approach and showed that the tumor blood flow was supplied from a branch of the left adrenal artery. Thereafter, TAE was selectively performed for the left inferior adrenal artery by using gelatin sponge particles and coiling. No further tumor vascularity was demonstrated by subsequent contrast injection. Her hemodynamics stabilized after TAE, and systolic blood pressure ranged from 150–170 mmHg. After admission, she was treated with intravenous nicardipine and oral doxazosin. Intravenous phentolamine was not administered to this patient because phentolamine was not available in our hospital.
On the second day of admission, hormonal assays were performed and showed markedly elevated levels of plasma metanephrine at 952 pg/mL (reference range <130 pg/mL), plasma normetanephrine at 3150 pg/mL (reference range <506 pg/mL), urinary metanephrine at 6.64 μg/mg Cr (reference range <0.2 μg/mg Cr), and urinary normetanephrine at 7.22 μg/mg Cr (reference range <0.3 μg/mg Cr). On the third day of admission, abdominal computed tomography was performed and showed a significant resolution of the retroperitoneal hematoma. She was discharged on day 11 after TAE without any symptoms. At discharge, the systolic blood pressure was improved to 130 mmHg or less by oral doxazosin 4 mg/day alone. On the day after discharge, an iodine-131 metaiodobenzylguanidine (MIBG) scan was performed, and results showed only a significant left adrenal uptake.
She was followed up at an outpatient clinic, and computed tomography or magnetic resonance imaging confirmed that the tumor size had spontaneously and gradually decreased. The tumor sizes were 3.1, 2.8, and 1.3 cm one month, three months, and five months after discharge, respectively (). Tumor shrinkage prompted us to resect the tumor laparoscopically (). Six months after TAE, laparoscopic left adrenalectomy was successfully performed with proper preoperative treatment by 7 mg/day of doxazosin. Pathological findings confirmed the diagnosis of an adrenal pheochromocytoma (). The gross appearance of the resected tumor was 13 mm × 12 mm × 11 mm in size and was yellow and tan in color. Pathological examination revealed coagulative necrosis in the tumor, and the cytoplasm of the tumor cells was immunohistochemically positive for chromogranin A, synaptophysin, and S100. The Ki67 labeling index was <1%. A score of five was obtained from the grading system for adrenal pheochromocytoma and paraganglioma (histological pattern; large and irregular cell nest, one point; cellularity, high, two points; vascular or capsular invasion; presence, one point; and catecholamine type and noradrenaline type, one point) []. She was graded as moderately differentiated.
Doxazosin was stopped after surgical resection, and her blood pressure was stable. Plasma metanephrine and normetanephrine levels decreased to 21 and 78 ng/L, respectively, at three months postoperatively. Urinary metanephrine and normetanephrine levels also showed a significant decrease. At the half-year follow-up, her postoperative course was uneventful without any recurrence of pheochromocytoma, and levels of plasma metanephrine and normetanephrine remained within normal ranges.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [106.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 106.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2985,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8326605-1,Extracted,"A 55-year-old man was diagnosed with dilated cardiomyopathy and treated with optimal pharmacological therapy, including an angiotensin-converting enzyme inhibitor, a β-blocker, furosemide, and spironolactone. At age 62 years, a cardiac resynchronization therapy defibrillator (CRT-D) and tolvaptan were introduced for worsening HF and complete left bundle branch block. Despite optimal medical therapies, he was admitted to our hospital three times between the ages of 65 and 66 years due to HF exacerbations, and multidisciplinary interventions by doctors, nurses, pharmacists, nutritionists, and physiotherapists were initiated. During this period, we repeatedly recommended transcatheter mitral valve repair for severe functional regurgitation, but he declined. Adaptive servo-ventilation was introduced to relieve dyspnea, but rather was discontinued due to the discomfort caused by wearing the device. A month after discharge, his HF symptoms of dyspnea at rest, malaise, insomnia, and appetite loss recurred, and a fourth hospitalization was required.
Physical examination revealed lip cyanosis, jugular venous distention, liver swelling, bilateral leg edema, and a systolic murmur with the Levine scale grade of III/VI at the apex. His blood pressure was 82/68 mm Hg, his heart rate was 102 bpm and regular, his respiratory rate was 24/min, and his peripheral oxygen saturation was 96% on room air. A chest X-ray on admission revealed significant cardiomegaly with pulmonary congestion (). A 12-lead electrocardiogram (ECG) revealed sinus tachycardia with biventricular pacing, which was unchanged compared to the previous findings (). A transthoracic echocardiogram revealed severe left ventricular dysfunction with a reduced ejection fraction of 21% and marked dilatation of the chambers (left ventricular end-diastolic diameter of 72 mm and left atrium diameter of 61 mm). Severe functional mitral regurgitation, with an effective regurgitant orifice of 0.62 cm2, was also observed (). Laboratory studies revealed a brain natriuretic peptide level of 864 pg/mL, deterioration of renal function, a blood urea nitrogen level of 33.1 mg/dL, and a serum creatinine level of 1.45 mg/dL ().
The clinical course during hospitalization was shown in . We initiated a continuous infusion of dobutamine 3γ and furosemide 100 mg/day based on a diagnosis of an HF exacerbation complicated by organ dysfunction. In addition, his oral pre-hospitalization medications were continued, including enalapril 2.5 mg, carvedilol 5 mg, tolvaptan 15 mg, furosemide 40 mg, spironolactone 25 mg, and empagliflozin 10 mg. Despite continuous infusion of dobutamine and furosemide, laboratory data 3 days after admission revealed worsening organ dysfunction (aspartate aminotransferase level of 101 U/L, alanine aminotransferase level of 121 U/L, blood urea nitrogen level of 61 mg/dL, and serum creatinine level of 2.23 mg/dL). Furthermore, his respiratory rate increased, and shortness of breath during conversation was observed. With informed consent from the patient and his family, we decided to initiate oral opioids, which had been approved by the internal ethics committee.
We first prescribed oral codeine phosphate hydrate 60 mg/day, but this failed to relieve his symptoms. We then switched to oral immediate-release hydromorphone 1 mg. Since he often experienced dyspnea after meals as well as insomnia, hydromorphone was regularly administered as a prophylactic before meals and at bedtime. In dose titration, oral extended-release hydromorphone 4 mg once daily and oral immediate-release hydromorphone 2 mg as rescue administration relieved his symptoms and improved his ability to perform activities. No side effects were observed after opioid administration, his systolic blood pressure was approximately 80–100 mm Hg, his heart rate was approximately 90 bpm, his respiratory rate was less than 20/min, and excessive respiratory depression was not induced. In addition to symptom alleviation, his urine volume increased, and his general condition and blood examination findings gradually improved. Introducing cardiac rehabilitation by physiotherapists and foot bath therapy we previously reported, furosemide infusion was withdrawn on hospital day 25, and dobutamine was withdrawn on hospital day 42. Treatment with HF medications and oral extended-release hydromorphone was continued, and he was discharged to home on hospital day 54. After discharge, he continued to take hydromorphone in addition to optimal medical treatment, and received continuous infusions of dobutamine and furosemide three times a week at an outpatient clinic.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [102.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 102.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 = 6.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 6.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
2986,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7110679-1,Extracted,"A 38-year-old female, gravida 3 para 2 at 33 weeks of gestation, was hospitalized for preeclampsia with severe features. A viable neonate had been expeditiously delivered yet the patient’s post-partum blood pressures remained severely elevated ranging from 230/130 mmHg to 280/170 mmHg. She had no antenatal care but reported a history of uncomplicated hypertension during her prior pregnancies and tobacco abuse which was stopped 8 months prior. At the bedside, she complained of mild headaches but denied visual disturbances or upper abdominal pain. She was alert and well oriented with a pulse of 80 bpm. There was no hyperreflexia, clonus, papilledema, peripheral edema or signs of pulmonary edema. Her examination was otherwise unremarkable including the absence of renal bruits. Apart from an elevated random urine protein to creatinine ratio of 0.7, the laboratory investigations were within normal limits including serum creatinine, electrolytes, platelet count, liver function and coagulation studies. There were no laboratory features of hemolysis. She was treated with multiple anti-hypertensives over the next 72 h including oral nifedipine, labetalol and clonidine as well as intravenous infusions of labetalol, nicardipine, hydralazine. Magnesium was used for eclampsia prophylaxis. Of note, a single dose of intravenous enalapril was given with a subsequent 60% increase in serum creatinine that returned to baseline within 24 h of discontinuation. Renal artery dopplers (Fig. ) were performed which revealed greater than 60% stenosis of the proximal left renal artery and at least 60% stenosis of the distal right renal artery. Computerized tomography angiography showed approximately 50% stenosis of the proximal left renal artery without stenosis of the right renal artery (Fig. ). At this juncture, in the setting of recalcitrant severe preeclampsia and the mortality risk of impending eclampsia, an invasive strategy for better evaluation and possible intervention was deemed net beneficial. Renal angiography showed 50% stenosis of the left proximal renal artery for which balloon angioplasty and stenting was performed (Fig. ). The right renal artery demonstrated less than 50% stenosis with an insignificant hemodynamic gradient, thus was not stented. Following revascularization, the patient’s blood pressure improved, ranging from 180/100 mmHg to 160/90 mmHg within 48 h, on dual oral antihypertensive therapy. She was ultimately discharged to titrate further anti-hypertensive therapy as an outpatient.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 0.
The patient's Well's score for pulmonary embolism is 0."
2987,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8538014-1,Extracted,"A 45-year-old female patient with a medical history of hypothyroidism, atopic dermatitis, and a heterozygote factor V mutation and no history of kidney disease presented with a seven-day history of swelling of lower limbs, palms, and eyelids accompanied with abdominal distension and foamy urine. She did not indicate shortness of breath, fever, flank pain, or dysuria. Four days before the onset of symptoms, the patient received the first dose of BNT162b2. Other than mild tenderness at the injection site and transient diarrhea, there were no other immediate significant adverse effects. At the time of admission, the patient was afebrile. Her blood pressure and heart rate were 126/65 mmHg and 72 beats/minute, respectively, with a normal respiratory rate, and she was maintaining oxygen saturation on room air. Physical examination revealed pitting edema in bilateral lower extremities extending to the level of thighs, swelling in both hands and around the eyelids, and abdominal ascites. Laboratory tests revealed proteinuria in the nephrotic range, hypoalbuminemia, and dyslipidemia (Table ). Her serum creatinine level was within the normal range, and she was negative for common-associated viral infections and autoimmune diseases. Polymerase chain reaction and serology testing for severe acute respiratory syndrome coronavirus 2 were negative. In addition to proteinuria, urinalysis revealed the presence of granular casts.
Consequently, chest radiograph showed bilateral pleural effusion, transthoracic echocardiography revealed a normal ejection fraction of 62%, and ultrasonography revealed that both kidneys were normal in size, outline, and echotexture.
During hospitalization, the patient was initiated on furosemide (40 mg b.i.d.) and the signs of anasarca started to improve. Her renal function tests remained stable. Histopathological examination of percutaneous renal biopsy specimens (Figures , , ) led to the diagnosis of MCD.
The furosemide dose was later reduced to 40 mg/day p.o., and peripheral edema gradually disappeared in parallel with a loss of 8 kg. She was discharged with a treatment plan including prednisolone (60 mg/day), vitamin D, calcium, pantoprazole, and trimethoprim/sulfamethoxazole for Pneumocystis pneumonia prophylaxis. Follow-up at three weeks after discharge was planned to conduct renal function tests and measurement of urine protein level.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [72.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 72.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
The patient's Well's score for pulmonary embolism is 3."
2988,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-2827159-1,Extracted,"A 72-year-old Caucasian woman presented with squeezing chest pain. The pain had started 30 minutes previously and was associated with nausea, vertigo, shortness of breath and weakness. Her history was significant for hypertension and coronary artery disease. Two years before admission, she had undergone coronary angiography because of angina, which revealed three-vessel coronary disease. The examination was followed by repeated angioplasty with stent implantation. A drug-eluting stent had also been applied. The first intervention had been complicated by a haematoma at the femoral puncture site.
On physical examination, the patient had a blood pressure of 130/60 mmHg and a heart rate of 65 beats per minute. The lung and heart sounds were clear on auscultation. Her weight was 60 kg, her height was 156 cm and her body mass index was 24.65 kg/m2. An electrocardiogram showed normal sinus rhythm without signs of myocardial ischaemia. Laboratory testing was significant for haemoglobin at 11.4 g/dL, blood urea nitrogen at 10.45 mmol/L and creatinin at 131 μmol/L. The creatinin clearance calculated with the Cockroft-Gault equation was 26.47 mL per minute. There was no elevation of cardiac troponin-I and creatine phosphokinase-MB isoenzyme levels.
After admission, her symptoms soon subsided. Repeated electrocardiography did not show signs of ischaemia, and the troponin-I value remained in the normal range. A diagnosis of unstable angina was established. The patient received early conservative treatment with the following pharmacotherapy: 2 × 60 mg enoxaparin subcutaneously, 75 mg clopidogrel, 100 mg aspirin, 50 mg metoprolol, 20 mg atorvastatin, 0.2 mg per hour transdermal nitroglycerin, 80 mg valsartan and 12.5 mg hydrochlorothiazide.
On the fifth day of her hospital stay, an exercise stress test was performed on a bicycle ergometer where she reached 3.9 metabolic equivalent and no ischaemic response occurred. A few hours later, she experienced pain in the left side of her abdomen. On examination, a palpable, growing tender mass was detected in the lower left quadrant. An abdominal ultrasound scan demonstrated a rectus sheath haematoma with a depth of 20 mm and a width of 40 mm. The upper margin of the haematoma was at the umbilicus, the lower reached the pubic bone. As continued haemorrhage was suspected, the patient underwent surgical exploration with haematoma evacuation, and received a blood transfusion. She remained on a reduced dose of enoxaparin (1 × 60 mg). Since she was febrile and showed a decreasing haemoglobin level, on the 9th postoperative day a computed tomography (CT) scan was performed. This showed a recurrence of the rectus sheath haematoma (Figure ) and its extension in the abdominal wall. A second haematoma evacuation was performed. Subsequently, no recurrence of bleeding was observed, but the patient developed an ascending superficial thrombophlebitis on the left lower limb, which was treated with ligature. She was finally discharged in good health.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [65.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 65.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 3 + 1.5 = 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2989,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3789027-1,Extracted,"A 54-year-old female (weight, 46 kg; height, 153 cm), was transferred to Tri-Service General Hospital on account of an unexpected large pancreatic tumor. The clinical history of the patient included paroxysmal headaches, mildly elevated blood pressure (BP), diaphoresis and occasional palpitations. The patient was previously diagnosed with ventricular arrhythmia by cardiovascular departments in numerous hospitals, without any other significant findings. The patient was not administered regular treatment for the headaches or hypertension as the symptoms were considered insignificant. One month prior to surgery, the patient underwent a detailed health checkup and an abdominal mass was identified using abdominal sonography. A large, well-encapsulated pancreatic tail tumor, measuring 9 cm in length, was observed on abdominal computed tomography (). The patient was consequently transferred for surgical intervention.
On admission, mildly elevated BP (138–160/80–90 mmHg) with a heart rate (HR) of 70–90 beats per minute (bpm) was noted. The ECG revealed a normal sinus rhythm with two ventricular premature contractions (VPCs). Other laboratory tests showed no significant abnormalities. An exploratory laparotomy with a resection of the tumor was scheduled. Thoracic epidural anesthesia was initially performed without adverse events, followed by general anesthesia. When the pancreas was approached, no any abnormal lesions were identified, with the exception of a bulging mass from the retroperitoneal region. The mass originated from the adrenal gland and presented as a capsulated, vessel-rich tumor. The systolic BP surged to 260 mmHg abruptly with fluctuations and the HR increased to 150 bpm during the manipulation of the tumor. The concentration of the anesthesia was increased along with an additional administration of 100 μg intravenous (i.v.) fentanyl. The fentanyl was ineffective and 5 mg i.v. labetalol was administered twice. However, the hypertensive crisis remained. The surgeon made a temporary stay of surgery until the vital signs were under control and then the tumor was removed.
The BP dropped (75/50 mmHg) once the tumor was removed. Aggressive fluid replacement and vasopressors were administered until the patient was hemodynamically stable. The endotracheal tube was then removed. At one day post-surgery, the patient was completely asymptomatic and no sequelae were identified. The pathological report confirmed a diagnosis of pheochromocytoma () and the patient was discharged five days later.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [150.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 150.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3.0 + 1 =  4.0.
The patient's Well's score for pulmonary embolism is 4.0."
2990,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4421423-1,Extracted,"A 57-year-old white male presented to the emergency room complaining of decreasing urinary output in the last 3 days and referring anuria in the last 24 h. He had no other urinary and obstructive complains, and denied fever, malaise, skin rash or any other symptoms. He denied smoking or alcohol drinking and reported mild hypertension controlled with losartan 50 mg/day.
The relevant information from his previous history was the diagnosis of hepatitis C 11 years before. Seven months before the present condition, he was treated with peginterferon alfa-2a and ribavirin, and the treatment was finished 10 days before his admission. HCV viraemia was negative since the third treatment month. In the physical examination, he was in good general health and well hydrated with normal skin colour. Blood pressure was 140/90 mmHg, heart rate was 80 per minute, temperature was 36.6°C and respiratory rate was 22 breaths/min. In the examination, the only abnormality found was +/4 ankle oedema.
The initial laboratory work-up disclosed normal CBC (haematocrit 40.9%, haemoglobin 14.0 g/dL and 5420 leucocytes). Blood urea nitrogen was 68 mg/dL, serum creatinine was 2.3 mg/dL (increasing to 3.2 mg/dL the following day), serum potassium was 5.7 mg/dL and serum bicarbonate was 21 mEq/mL. Urine examination disclosed 40 red blood cells, ++++ proteins, hyaline and granular casts, and tubular cell debris. The protein/creatinine ratio was 29. Liver function tests, albumin, RNI, C3, C4, P and C ANCA, antinuclear and anti-DNA antibodies, rheumatoid factor, and serum proteinogram were all within the normal range. Anti-hepatitis B virus and anti-HIV were negative, and anti-HCV antibodies were present. Urinary ultrasound disclosed normal sized kidneys and prostate gland without obstruction signs, and a renal biopsy was performed.
He was first found to have anti-HCV antibodies in 1997 and a positive HCV PCR along with altered ALT (180 U/L) and AST (84 U/L) at that time that led to a liver biopsy showing chronic persistent hepatitis. In 2004, a new biopsy disclosed chronic hepatitis with fibrous portal expansion, increased septal lymphocytes and moderate piecemeal necrosis, without iron deposition (Metavir classification A2F2). The virus was found to be 3a genotype, and before treatment onset, the number of viral copies was 33.000 UI/mL. In March 2008, peginterferon alfa-2b (180 μg/week) and ribavirin (500 mg twice/day) were initiated and kept for 6 months. By the third month of treatment, HCV viral copies were no longer detectable by PCR and remained so until its end. The laboratory work-up upon treatment end disclosed normal LFTs, serum creatinine 0.78 mg/dL, and normal urinary chemistry and sediment.
Before the renal biopsy result was available, the differential diagnosis included rapidly progressive glomerulonephritis and acute vasculitis leading to a methylprednisolone pulse of 1000 mg/day (3 days) followed by prednisone 60 mg/day. In the biopsy, there were 17 glomeruli in the optic microscopy slides, slight mesangial expansion, focal acute tubular necrosis normal vessels and collapsing glomerulopathy (). In the immunofluorescence slides, there were 11 glomeruli and absence of immunoglobulins, fibrinogen and complement deposition. At Day 7, after the steroid pulse, urine output started to increase, but he remained dialysis dependent for 12 days. Thereafter, renal function improved continuously reaching a normal serum creatinine and protein/creatinine ratios after 4 and 18 weeks, respectively. Diuresis, serum creatinine, protein/creatinine ratios and steroid doses are shown in . Steroids were tapered down over 6 months and discontinued. Renal function and protein/creatinine ratio remained normal thereafter. Also, 12 months after completing the peginterferon plus ribavirin therapy, HCV PCR remained negative.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 3 + 1.5 = 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2991,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7220020-1,Extracted,"A 26-year-old woman without medical history presented to the ED due to abdominal pain for approximately 12 hours. The patient reported no tobacco use, and her only prescribed medication was the etonogestrel/ethinyl estradiol intravaginal ring. The patient had been evaluated earlier in the day at an urgent care facility; the urgent care provider then sent the patient to the ED for an apparent abnormal urinalysis (UA). In the ED, she was complaining of mid-epigastric and right upper quadrant abdominal pain along with continued nausea. She also noted back pain, a headache, and bilateral upper extremity numbness since that morning. She noted her bilateral upper extremity numbness and headache had become intermittent. She denied any associated diarrhea, constipation, dysuria, fever, chills, recent travel, or trauma.
The patient’s vital signs included the following: temperature 98.0º Fehrenheit; heart rate 76 beats per minute; respirations 18 breaths per minute; blood pressure 129/53 millimeters of mercury; and pulse oximetry 98% on room air. On physical exam, she exhibited moderate tenderness to palpation of the right upper quadrant and epigastric area. The remainder of the physical exam was unremarkable.
There were no considerable lab abnormalities except for “small” bilirubin noted on the UA. Urine pregnancy test was negative. The patient had a computed tomography (CT) of the abdomen/pelvis with intravenous (IV) contrast, which demonstrated an extensive thrombus within the superior mesenteric vein, extending into the main portal vein, intrahepatic portal veins, and distal splenic vein (). She was administered IV heparin 5800 units bolus and a continuous IV heparin infusion of 18 units per kilogram per hour. She was then transferred to a tertiary care center.
At the tertiary care center, the patient was maintained on the heparin infusion until she was later transitioned to rivaroxaban. The patient underwent extensive hematologic testing including the following: protein C; protein S; anti-thrombin III; alpha fetoprotein, homocysteine; factor 5 gene mutation; prothrombin gene mutation; anti-cardiolipin antibody IgG and IgM by ELISA; anti-beta2-GP I antibody; JAK2 V617F mutation; and mutation in exon 12 of JAK2. No abnormalities were detected. The patient also had normal venous Doppler studies of the bilateral upper and lower extremities. Ultimately she was discharged home on hospital day 3 on rivaroxaban 15 milligrams twice daily with hematology follow-up and discontinuation of hormonal contraception.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [76.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 76.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
2992,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7410512-1,Extracted,"A 66-year-old African American male with a past medical history of hypertension, alcohol use, and asthma presented with facial swelling. He was discharged two months prior for a similar event related to lisinopril. On initial presentation, the patient's vitals were significant for heart rate of 104 beats per minute, respiratory rate of 30 breaths per minute, blood pressure of 190/100 mmHg, and oxygen saturation of 99% with a non-rebreather mask at 15 liters. Physical exam was significant for moderate to severe respiratory distress, inspiratory stridor, and subcostal and intercostal retractions. Lungs were clear to auscultation. The patient was otherwise alert and oriented. Arterial blood gas showed pH 7.447, pCO2 39, pO2 197, and HCO3 27 on 60% FiO2. His initial metabolic panel was significant for sodium 104 mmol/L, potassium 2.6 mmol/L, chloride 66 mmol/L, blood urea nitrogen (BUN) 5 mg/dL (baseline 20 mg/dL), and creatinine 0.6 mg/dL (baseline 1.0 mg/dL). Glucose was 165 mg/dL. Magnesium and phosphorus were 1.1 and 2.1 mg/dL, respectively. Serum uric acid was low at 2.7 mg/dL. Complete blood count showed no leukocytosis or anemia. Urinalysis had a specific gravity of 1.010, moderate blood, and 15-29 red blood cells. Urine electrolytes were notable for a sodium of 48 mmol/L and osmolality of 217 mOsm/kg. Serum osmolality was 215 mOsm/kg. Urine and serum toxicology were negative for any substances. Alcohol level was negative.
Due to concern for airway protection, the patient was intubated and admitted to the intensive care unit. Initial chest x-ray held concern for infectious process, but antibiotics were stopped after infectious workup was negative. The patient was given two units of fresh-frozen plasma, famotidine, and Benadryl, and started on methylprednisolone 60 mg every six hours for angioedema. Lisinopril was held at this time. For his hyponatremia, the patient's labs were suspicious for syndrome of inappropriate antidiuretic hormone (SIADH) and a one-liter fluid restriction was initiated with nephrology consult. Thyroid and adrenal workup to rule out other causes of SIADH was unremarkable. A CT chest scan was done to evaluate for malignancy as a cause of SIADH, but did not demonstrate overt suspicious lung pathology (Figure ). The patient's hyponatremia appropriately corrected over the course of one week and was 130 mmol/L upon discharge. Lisinopril was discontinued and marked as an allergy for the patient. On follow-up approximately nine months later, the patient's sodium had corrected and remained within normal limits.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [104.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 104.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2993,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7881412-1,Extracted,"A 61-year-old man with past medical history of chronic obstructive pulmonary disease for 20 years and hepatic hydatid cyst surgery for 4 years ago presented to the emergency department of Taleghani hospital; a teaching referral hospital in Tehran, Iran, with recurrent abdominal pain aggravated by ingestion, obstructive jaundice, lower limbs edema and abdominal distention. On admission, he denied systemic symptoms like fever, chills and malaise. His vital signs were as follows: blood pressure 120/75 mmhg, heart rate 85 beats per minute, respiratory rate 16 per minute and O2 saturation 95% breathing room air. Before admission, his clinical scenario suggestive of biliary involvement made physicians proceed with an outpatient abdominopelvic ultrasound which revealed heterogeneous parenchymal echo pattern of liver with a large amount of ascites indicating the presence of concurrent cirrhosis and a heterogeneous 5.2x4.5cm cystic lesion with sharply defined but irregular borders in liver segment VIII. Common bile duct was reported dilated in proximal part and some sludge was detected in gallbladder. Serum aminotransferases demonstrated an elevation of about 3 times the upper limit of normal. Blood tests revealed a remarkable increase in ALP level up to 5 times the upper limit of normal. A total bilirubin level of 8.9 mg/dl was reported of which direct bilirubin 6.1 mg/dl was. Serum CA19-9 level was normal. Further evaluations by abdominopelvic CT scan were in line with ultrasonographic study. A CT scan revealed moderate ascites, increased gastrointestinal wall thickness, moderate generalized dilation of intra hepatic ducts, common bile duct and common hepatic duct with heterogeneous intraluminal filling defects and a 5.4x4cm-cystic lesion in right liver lobe adjacent to the scar of previous surgery with few calcified foci in its wall. An enlarged gallbladder with a dense layer in the neck suggestive of biliary sludge was also seen. Hydatid cyst treatment by albendazole 400 mg/BD started and he was transferred to the referral hospital for further evaluation and management of choledocholithiasis and cirrhosis. At the first day of admission, he was clearly jaundiced and his vital signs were stable. Ascites analysis revealed a high SAAG and low protein fluid with negative cytology for malignancy suggestive of cirrhosis necessitating a secondary work up.
Given biliary obstruction, the patient underwent an ERCP. Duodenoscopy was then performed Common bile duct was measured 20mm with multiple large filling defects. We then performed dilation with balloon TTS 12-15 and more than 20 pigmented stones, sludge and pus were extracted by balloon. Finally, a 7cm, 10Fr-plastic stent was inserted. Another abdominopelvic CT scan was demanded as presented in -.
In spite of biliary stent placement, he continued to remain icterus. We decided to proceed with another ERCP. The procedure revealed more than 30 pigmented stones and hydatid cysts membranes in common bile duct which were extracted completely. An extracted stone has been disclosed in . Given the patient’s clinical picture, laboratory results, imaging and ERCP findings in addition to negative secondary work -ups for cirrhosis, we suspected a diagnosis of hydatid cyst with cystobiliary fistula formation resulting in a portal hypertension and cirrhosis. Portal hypertension is said to be one of the rare complications of hydatid cyst. It has been reported in cases afflicted by cysts involving liver hilum making a compression on porta hepatis or invading inferior vena cava. Portal hypertension in the mentioned case is suggested to come out of a durable cystobiliary communication and its resultant biliary cirrhosis (,).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [85.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 85.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
The patient's Well's score for pulmonary embolism is 3."
2994,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8342832-1,Extracted,"Written informed consent was obtained from the patient. A 26-year-old primigravida with a body mass index (BMI) of 25.71 kg/m2 (weight 70 kg, height 165 cm) presented to our delivery suite in Manchester at 32-weeks with a 2-week history of dyspnea on exertion, orthopnea, and palpitations. She was known to have SS. Her syndrome consisted of a supra-valvular mitral ring, a parachute MV, mild LV outflow tract obstruction with Co-A, and a BAV. The mitral ring, LV outflow tract obstruction, and the Co-A were repaired at the age of three by open heart surgery, which was followed by a dual chamber pacemaker insertion for complete heart block. The BAV and the parachute MV were not repaired. This was followed by balloon dilatation of the aorta for re-coarctation at the age of 12. She remained asymptomatic following this till the end of the second trimester of pregnancy.
On presentation to our unit, she had a heart rate (HR) of 100 beats/min, blood pressure (BP) of 136/88 mmHg, respiratory rate (RR) of 28 breaths/min with oxygen saturations (SpO2) 90–92% on room air. Auscultation revealed bilateral crepitations along with a mid-diastolic murmur and a diagnosis of acute pulmonary edema was made. Arterial blood gas (ABG) revealed a pH – 7.48, partial pressure of carbon dioxide (pCO2) – 23.5 mmHg, partial pressure of oxygen (pO2) – 90.76 mmHg, base excess of 4 mmol/L with a lactate of 3 mmol/L. Her hemoglobin was 12.2 g/dl, serum potassium (K+) was 3.6 mmol/L, and serum magnesium (Mg+) was 0.65 mmol/L. Her N-terminal pro-B-type natriuretic peptide (NT-pro BNP) levels were 1,020 pg/ml. Her chest X-ray was suggestive of pulmonary edema and electrocardiogram (ECG) showed a sinus tachycardia with P mitrale.
She was transferred to the coronary care unit and the treatment instituted included oxygen, intravenous (IV) furosemide 20 mg, 5 mg of IV diamorphine, and oral bisoprolol 2.5 mg. Fluid balance was monitored using strict input and output monitoring with a urinary catheter, and oral potassium chloride and IV magnesium were supplemented to maintain K+ > 4 mmol/L and Mg+2 > 0.7 mmol/L.
Pacemaker check revealed an appropriately functioning dual chamber DDD device. Cardiotocography as part of fetal monitoring revealed a normal trace. A trans-thoracic echocardiogram (TTE) revealed:
1) A BAV with mild AS with a velocity of 2.5 m/s across the valve and a mean gradient of 25 mmHg
2) A normal LV size (LV diastolic diameter of 4.4 cm), with an ejection fraction of 48%, with mildly impaired systolic function
3) Parachute MV with chordal attachment to single papillary muscle, MV area of 1.12 m2, mean gradient of 8 mmHg across MV, moderate MV stenosis with mild-moderate regurgitation
4) Severely dilated left atrium (LA-volume/body surface area of 49 ml/m2)
5) A normal aortic root, with a normally functioning repair (velocity across the aorta was 2.4 m/s) with no diastolic tail
6) A mildly dilated well-functioning right ventricle (base RV of 4.3 cm and mid RV of 3.8 cm with preserved RV fractional area of change > 40%), mild tricuspid regurgitation (vena contracta width of 3 mm, max velocity of 3.4 m/s) with estimated mean pulmonary artery (PA) pressure of 56 mmHg with a moderately dilated right atrial volume of 67 ml.
Her case was discussed at the multi-disciplinary cardiology, obstetric, anesthetic team meeting. In view of her on-going symptoms, limited mobility, and detection of a severely dilated LA and raised PA pressure on TTE, the team decided to administer tinzaparin 4500 IU subcutaneously for thromboprophylaxis.
Despite medical management for the next 72 h, she complained of dyspnea on minimal exertion. She required 2 L of oxygen to maintain saturations of 97% (94% on air) but was able to lie almost flat without significant difficulty. A repeat ABG on oxygen, revealed a pH – 7.42, pCO2 – 30.5 mmHg, pO2 – 93.33 mmHg, base excess of 2 mmol/L with a lactate of 1.6 mmol/L. As thromboembolism remains one of the most common direct causes of death in pregnancy in the United Kingdom (UK), on a risk-benefit basis, based on her symptoms and dependence on oxygen, the team decided to rule out pulmonary embolism (PE) with a computerized tomography with pulmonary angiography (CTPA), which was reported back as normal.
In view of her symptoms and significant pulmonary hypertension, a decision was made to deliver her by category (Cat) 3 C-section in accordance with The Royal College of Obstetricians and Gynaecologists’ guidelines for classification of urgency of C-section (Cat 1: Immediate threat to life of woman or fetus, Cat 2: Maternal or fetal compromise, which is not immediately life-threatening, Cat 3: Needing early delivery but no maternal or fetal compromise, Cat 4: At a time to suit the woman and maternity team). Maternal steroids were administered to accelerate fetal lung maturity. After discussion with the patient of the potential risks and benefits of general anesthesia (GA) compared with neuraxial anesthesia, it was decided to perform the surgery under combined spinal-epidural (CSE) anesthesia. The decision process incorporated the patient’s preference to stay awake and witness the delivery of her baby along with partner in the operating theatre.
In theatre, a 16 gauge (G) peripheral cannula was inserted and the patient had ECG, SpO2, and invasive BP monitoring was established in theatre via a radial artery catheter. Baseline HR was 86 beats/min and BP was 100/58 mmHg. A 12-h interval between the last dose of prophylactic tinzaparin and administration of CSE anesthetic was followed in accordance with The European Society of Anesthesiology guidance []. CTG was monitored during and after the CSE insertion and was normal at all times.
With the patient in the sitting position, using an aseptic technique, the epidural space initially was detected with a 16 G Tuohy needle using a loss-of-resistance to saline technique at the L3–4 intervertebral space and an epidural catheter threaded into the epidural space. A test dose of 5 ml of 0.1% bupivacaine was given to rule out intrathecal catheter placement. This was followed by a subarachnoid injection at L4–5 interspace of 7.5 mg of hyperbaric bupivacaine and 300 ug diamorphine with a 25 G pencil point needle. The patient was positioned supine with left uterine displacement and 500 ml of compound sodium lactate (CSL) solution commenced along with a phenylephrine infusion 100 μg/ml at the rate of 30 ml/h. Within 12 min, a bilateral block to cold up to T8 to S5 dermatomes was established. To augment the block height, 5 ml of 0.75% ropivacaine was administered via the epidural catheter. Once the block height to T4 dermatome with cold spray was confirmed, C-section was commenced, and a female infant weighing 2.3 kg was delivered. APGAR scores of 5 at 1 min and 8 at 5 min were recorded. Oxytocin 5 IU was given as an IV infusion over 20 min to avoid tachycardia and hypotension. Pacemaker was kept on throughout the C-section. Patient was hemodynamically stable throughout, blood loss recorded during the C-section was 700 ml, and the procedure was completed uneventfully in 45 min. The phenylephrine infusion was weaned off gradually. Her epidural was removed at the end of the surgery to facilitate thromboprophylaxis following C-section. Tinzaparin 4,500 IU was administered subcutaneously 4 h after removal of epidural and continued for 10 days post-operatively. She stayed in our cardiac intensive care unit for 24 h, then stepped down to our obstetric high dependency unit over the next 48 h, and was discharged uneventfully from the hospital on the 7th post-operative day.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [100.0, 'beats per minute'], 'Previously Documented Pulmonary Embolism': False, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 100.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
2995,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8127029-1,Extracted,"A 69-year-old woman with repaired TOF suffering from recurrent haemoptysis was referred to our institution for further investigations. She underwent palliation in 1962 (age 12) with a classic right-sided BTT shunt and TOF repair in 1967 (age 17) with closure of the VSD, relief of the RV outflow tract obstruction, and closure of the BTT shunt. Over the course of the years, she developed atrial fibrillation for which she was started on oral anticoagulation. In 1993, she had a first episode of massive haemoptysis which was treated conservatively. In 2002, computed tomography (CT) indicated a stellate nodule in the right upper lung lobe. Over the next years the lesion remained stable on axial follow-up imaging. In 2019, after new episodes of haemoptysis, this time with progressively worsening dyspnoea, a positron emission tomography–CT was performed showing isotope accumulation in the lesion of the right upper lung lobe (). She underwent a bronchoscopy that showed mucosal swelling in the right upper lobe. Cytology indicated acute inflammation without evidence of malignancy.
On physical examination, the right-sided radial pulse was absent and blood pressure (BP) not measurable. Blood pressure and heart rate taken on the left arm were 112/45 mmHg and 78 b.p.m., respectively. Respiratory rate was 22 per minute. The second heart sound was pronounced with a grade 3/6 systolic and 2/4 diastolic murmur at the second intercostal space on the left. C-reactive protein was normal (2.9 mg/L) and N-terminal B-type natriuretic peptide slightly elevated (733 ng/L). The electrocardiogram showed atrial fibrillation with inferolateral ST depression and Q-waves in V1–V2–aVR (). Transthoracic echocardiography indicated a moderately dilated RV with normal systolic function, a peak/mean gradient of 53/32 mmHg across the pulmonary valve with severe pulmonary valve regurgitation ().
A diagnostic cardiac catheterization was performed but no arteriovenous connections were seen and the BTT shunt was not patent. Right atrial pressure was 14 mmHg, RV systolic pressure 56 mmHg, systolic pulmonary artery pressure 33 mmHg, and mean pulmonary artery pressure 21 mmHg. The RV was dilated with severe pulmonary valve regurgitation. A bronchoscopy with EndoBronchial UltraSound (EBUS) in order to perform EBUS guided biopsy was performed. A rope-like structure was seen through the bronchoscope, but we were unable to take a biopsy ().
After multidisciplinary discussion, the findings appeared to be most consistent with chronic inflammation due to a foreign body with secondary chronic inflammation, rather than vasculitis or a granulomatous infection, and the patient underwent a thoracotomy with lobectomy of the superior lobe of the right lung. The foreign body was removed without any resistance nor bleeding. Pathology indicated diffuse necrotizing granulomatous inflammation around the rope-like structure ( and ) which appeared to be the old suture around the BTT shunt that had caused a chronic inflammatory reaction invading the right upper bronchus and causing haemoptysis. The patient remained stable after the procedure. She left the hospital after a couple of days. The postoperative course was uncomplicated. After 3 months, she underwent percutaneous pulmonary valve replacement. After the surgical intervention, given a CHA2DS2 VASc score of 6/9, a HAS-BLED score of 5 and the fact that the most likely source of haemoptysis was removed, she was started on edoxaban 60 mg once daily.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [78.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 78.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 =  1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 1.5 + 1 = 2.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 2.5.
The patient's Well's score for pulmonary embolism is 2.5."
2996,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4010044-1,Extracted,"A 74-year-old Caucasian female presents to the emergency department of a local community hospital with a chief complaint of diarrhea for the past 3-4 days and a productive cough. All other review of systems was documented as negative. Her medical history was positive for hypertension, TIA, and an unspecified cardiac condition requiring a pacemaker. Her home medications included Bumetanide, digoxin, atorvastatin, carvedilol, lisinopril, and oral potassium supplement. Surgical and social histories were noncontributory. All history was obtained from the patient who was reported as alert and oriented for the duration of the emergency room stay.
On initial presentation, her vital signs were as follows: a blood pressure of 131/84, pulse of 108, respiratory rate of 20, temperature of 38.6, and a pulse oximetry of 94% on room air. She was reported to be in a new onset atrial fibrillation with a rapid ventricular rate. The rest of her examination was positive for the tachycardia with an irregularly irregular rhythm and 2+ pitting edema bilaterally in her lower extremities.
The initial electrocardiogram confirmed an atrial fibrillation with a rate of 112 beats per minute and other nonspecific changes. A posterior-anterior and lateral chest radiograph showed no acute process and stable pacemaker hardware. Initial complete blood count revealed a leukocytosis at 11.9 K/uL (3.8–10.6 K/uL), hemoglobin of 8.2 g/dL (12.0–15.0 g/dL), hematocrit of 25.9% (36–46%), and a platelet count of 42 K/uL (150–450 K/uL). Serum sodium measured 133 mmol/L (135–145 mmol/L), potassium of 5.1 mmol/L (3.5–5.0 mmol/L) with no mention of sample hemolysis, bicarbonate of 18 mmol/L (24–32 mmol/L), and an anion gap of 12. Kidney function testing had a creatinine level of 2.0 mg/dL (0.6–1.2 mg/dL) and a BUN of 41 mg/dL (10–25 mg/dL) with no reported history of kidney failure. She had a lactic acidosis with a lactate of 4.8 mmol/L (0.4–1.8 mmol/L) and the digoxin level was just above therapeutic range at 2.1 ng/ml (0.8–2.0 ng/ml). Troponin I was elevated to 0.11 ng/ml (<0.10 ng/ml) on presentation. Total bilirubin was elevated at 1.8 mg/dL (0–0.3 mg/dL) and the INR was 2.14 (0.80–1.20). Urine sample was nitrite positive with few bacteria reported on microscopic exam, 0–5 WBC/HPF (<10), and 10–20 RBC/HPF (<3). There were also 0–5 squamous cells/HPF and 0–10 granular casts/HPF.
Overall, this patient presented with a new onset atrial fibrillation with a rapid ventricular rate, acute anemia without signs of active bleeding, non-ST segment elevation myocardial infarction (NSTEMI), acute renal failure, and an elevated bilirubin and INR. Suspected etiology was initially hypovolemia from sepsis confounded by further volume loss via diarrhea. An abdominal ultrasound was performed and was negative for acute pathology. Blood and stool cultures were obtained and a stool for Clostridium difficile was negative.
Treatment in the emergency department consisted of fluid resuscitation with 0.9% normal saline (NS) boluses, for a total of 3L of NS in the emergency department as well as 2 units of packed red blood cells were transfused. She received 2 liters of oxygen via nasal cannula and was given 1 gram of intravenous ceftriaxone for UTI. Her four-hour repeat troponin was elevated to 1.97 ng/ml (<0.10 ng/ml) and the lactic acid elevated to 6.0 mmol/L (0.4–1.8 mmol/L). Thyroid studies were ordered and not found to be a contributing factor to the new atrial fibrillation with rapid ventricular rate with a thyroid stimulating hormone (TSH) of 5.72 uIU/ml (0.35–5.50 uIU/ml) and free T4 of 0.88 ng/dL (0.59–1.17 ng/dL). She remained in the emergency department approximately five hours before a bed was available in the step-down intensive care unit.
The antibiotics were switched to intravenous cefepime 2 grams every eight hours, 250 mg of oral vancomycin every eight hours, and 500 mg of intravenous metronidazole every eight hours on the floor. She was seen by cardiology, nephrology, gastroenterology, hematology, and infectious disease specialists. General surgery was consulted for possible abdominal etiology of sepsis per documentation. CT abdomen without contrast revealed a low density lesion within the spleen, mesenteric edema, questionable bowel wall thickening of the ascending colon, and a right pleural effusion with bilateral patchy consolidations. General surgery opted to continue antibiotics at that time without immediate surgical intervention.
Labs were repeated the following morning. Her lactate had elevated to 11.2 mmol/dL (0.4–1.8 mmol/L) despite resuscitation. The leukocytosis elevated to 17.4 K/uL (3.8–10.6 K/uL), potassium to 5.4 mmol/L (3.5–5.0 mmol/L), bicarbonate of 7 mmol/L (24–32 mmol/L) with anion gap of 23 (8–16). Troponin I elevated to 2.88 ng/ml (<0.10 ng/ml), Cr. to 2.3 mg/dL (0.6–1.2 mg/dL), and INR >19.2 (0.80–1.20). The patient had developed disseminated intravascular coagulation (DIC), likely secondary to sepsis. Transfusion of four units of fresh frozen plasma and six units of platelets were initiated. Hydrocortisone 25 mg intravenously every 6 hours and intravenous Vitamin K 10 mg were administered. The patient ultimately went into acute respiratory failure from the fluids and blood products she received, was intubated by anesthesia, and moved to the intensive care unit. She also became hypotensive and required a continuous infusion of norepinephrine, subsequently developed oliguria, and a right femoral dialysis catheter was placed in case she would later require dialysis. Her blood cultures came back positive for gram positive cocci identified as Staphylococcus lugdunensis. Infectious endocarditis was suspected and nafcillin was started. A transthoracic 2D echo was performed and showed large vegetation on the posterior leaflet of the mitral valve. Transesophageal echocardiogram confirmed this finding and further identified additional vegetation on the anterior leaflet of the mitral valve measuring 0.4 cm. The posterior vegetation measured 1.8 cm and was noted to be very mobile. At this point, the CT findings were thought to be secondary to septic emboli.
The laboratory abnormalities began to improve the following day and she was started on rifampin in addition to the nafcillin with all other antibiotics discontinued. Her leukocytosis, lactate, troponin, and creatinine began to trend down, but the decision was made to transfer the patient to a local tertiary center affiliate for the definitive care of pacemaker removal where she was accepted to the medical intensive care unit.
The patient had a 24-day course between the two facilities. Her DIC resolved and she was still in the atrial fibrillation with a controlled ventricular rate during her stay. On hospital day 10, the pacemaker and its leads were removed out of concern, it was the source of infection. It was reported to be implanted on 1/15/2010 and was a Biotronik Cyclos DR with one lead in the right atrium and another in the right ventricle. The leads were sent to lab for tip cultures. The right atrial lead showed rare S. lugdunensis, while the right ventricle lead revealed few S. lugdunensis that was susceptible to nafcillin. A temporary transvenous pacemaker was immediately replaced; however, this pacemaker was found not necessary and subsequently removed 48 hours later. The patient was still on intravenous naficillin and rifampin and was finally extubated on hospital day 11. Repeat blood cultures were negative for growth after 5 days on hospital days 11, 19, and 20. The discharge summary reported that the nafcillin was discontinued because she began to develop rashes. She was discharged on oral warfarin for her atrial fibrillation. Her kidney function returned to baseline with creatinine of 1.2 mg/dL (0.6–1.2 mg/dL). Subsequent transthoracic echo cardiograms revealed that the mitral valve vegetations were improving. She was discharged to a sub-acute rehab facility with continued intravenous nafcillin therapy and outpatient followup with cardiology and infectious disease.
The patient returned to the original community hospital's emergency department three days after discharge with chief complaint of mental status changes. She was found to have bright red blood per rectum and an anemia of 6.0 g/dL (12.0–15.0 g/dL) with a hemoglobin level of 9.0 g/dL (12.0–15.0 g/dL) reported from the tertiary facility at discharge. The decision was made by family to make the patient not to resuscitate (DNR) status with no desired intubation or mechanical ventilation. The patient was only oriented to person at this time and incapable of making her own medical decisions. She was placed in hospice care and expired two days later.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [108.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 108.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
2997,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-8621,Extracted,"A 35-year-old G4P1 woman presents for follow-up after her 3rd miscarriage. All 3 miscarriages occurred during the 2nd trimester. Past medical history is significant for systemic lupus erythematosus (SLE) and a deep vein thrombosis (DVT) in her right lower leg 3 years ago. Her current medication is hydroxychloroquine. The patient denies any tobacco, alcohol, and illicit substance use. Her vitals include: temperature 36.8℃ (98.2℉), blood pressure 114/76 mm Hg, pulse 84/min, respiration rate 12/min. Physical examination reveals a lacy, violaceous discoloration on her lower legs.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [84.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 84.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
The patient not been diagnosed with pulmonary embolis (PE), but the patient has previously been diagnosed with deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
2998,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8404589-1,Extracted,"A 50-year-old male known smoker, smoking 7-8 cigarettes/day for the last 10 years presented with complaints of intermittent hemoptysis for last 2 years. He denied any history of low-grade fever, loss of appetite, night sweats, weight loss, chest pain, trauma, or breathlessness. There was no history of exposure to any drugs (antiplatelets, anticoagulants) or bleeding disorder. His sputum for acid-fast bacilli (AFB) was negative. Diagnostic evaluation for his symptom on the previous occasions at other hospitals was inconclusive with a normal reported chest X-ray and computed tomography (CT) scan exam. Fiberoptic bronchoscopy findings reported blood in right and left main bronchial system. Presently, his physical examination revealed a temperature of 37°C, pulse rate of 82/min, blood pressure of 142/84 mmHg, respiratory rate of 12/min, oxygen saturation of 98%, normal respiratory sounds, and a normal chest X-ray. Laboratory investigations revealed a normal blood value including normal platelet count and coagulation parameters. His transthoracic echocardiography revealed normal right and left ventricular functions without any evidence of mitral stenosis/right-sided infective endocarditis or pulmonary hypertension. High-resolution CT scan showed localized pocket of air density medial to bronchus intermedius on axial [] and coronal sections [] suggesting accessory cardiac bronchus. No lung tissue was associated with accessory cardiac bronchus. Subsequent fiberoptic bronchoscopy confirmed accessory cardiac bronchus originating medially from bronchus intermedius opposite to the right upper lobe bronchus, whose lumen was partially obscured by small a clot. Bronchial and pulmonary angiography revealed no abnormality in tracheobronchial tree or pulmonary drainage.
A right thoracotomy was performed and accessory cardiac bronchus was identified. ACB extended 3 cm toward pericardium without any associated lobule. It was resected with preservation of vagus nerve. Bronchus intermedius was closed in two layers. Subsequent pathological examination revealed a tubular structure ending blindly with cartilage rings, inflamed and ulcerated mucosa with the collection of neutrophils and fibrous tissue. Hemoptysis was attributed to this inflamed vascularized accessory cardiac bronchus. The patient is asymptomatic currently with no recurrent hemoptysis at 6-month follow-up.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [82.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Surgery in the previous 4 weeks': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 82.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 0 + 1 = 1.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 1.
The patient's Well's score for pulmonary embolism is 1."
2999,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4644769-1,Extracted,"A 14-year-old male adolescent patient was admitted to the Gyeongsang National University Hospital on 3 December 2012 because of a 3-day history of high fever, general myalgia, and dry cough. He complained of a 1-day history of pain on the right lower side of the chest. The patient appeared pale and ill. His temperature was 38.5℃, pulse was 100 beats/min, and blood pressure was 100/60 mmHg. Physical examination revealed slightly decreased breath sounds at the right lung base and a continuous murmur with a thrill over the left subclavicular and left upper sternal border. He has been heard about the heart murmur and he complained of exertional dyspnea over the past 2-3 months. However, these signs of cardiac problems have not been evaluated. He had no cutaneous symptoms and no lymphadenopathy. However, the liver and spleen edges were palpable to be 5 and 3 cm below the costal margin, respectively. The patient had no pharyngotonsillitis or oral ulceration. There was no evidence of insect bites. A tuberculin skin test was negative. Increased pulmonary vascular markings were apparent, but obvious consolidations were not found on chest x-ray on the admission day (). Echocardiography showed a large patent ductus arteriosus (7 mm with a left-to-right shunt), mitral valvular regurgitation (Δp=48 mmHg), dilated left ventricular internal dimension, and pericardial effusion. However, valvular anomaly or vegetation was not observed. The leukocyte count was 14.3×109/L (85% polymorphonuclear neutrophils with left-shift maturation), the hemoglobin level was 8.4 g/dL, the platelet count was 240×109/L, and the C-reactive protein level was 162 mg/L. The antistreptolysin O titer was 260 IU/mL. An antibody test for mycoplasma was negative. Polymerase chain reaction tests with respiratory specimens for respiratory viruses and Mycobacterium tuberculosis were negative. Bacterial culture of a throat swab and urine and stool samples were negative. Three consecutive blood cultures (blood was drawn >12 hours apart from different sites) were performed.
Considering the possibility of infective endocarditis, the patient was treated with ampicillin/sulbactam, vancomycin, and gentamicin. After administration of antibiotics, the fever gradually subsided and the patient's general condition improved. However, on the third day of hospitalization, the patient complained of right lower chest pain aggravation. To rule out pulmonary embolism, chest computed tomography and lower-extremity venography computed tomography were performed. Pneumonia and pleural effusion were notified without evidence of embolism (). Bloody and turbid, neutrophil-dominant exudate (red blood cell count>1,000/high power field, white blood cell count>1,000/high power field, polymorphonuclear neutrophils 69%, lymphocytes 14%, monocytes 12%, pH 7.5, glucose 102 mg/dL, protein 6.2 mg/dL, lactate dehydrogenase 1,100 U/L, and no bacteria) was removed by thoracostomy due to progressively increase in the amount of fluid. On the seventh day of hospitalization, F. tularensis was finally confirmed in all blood cultures by incubation for an extended period for the identification of fastidious bacteria; we did not suspect tularemia until the pathogen was identified. Another challenge we encountered was identification of the route of exposure to the pathogen. However, the patient had not been traveling, camping or hunting or exposed to arthropods or hay. He had not eaten any game or skinned any animals. The patient was treated with gentamicin for an additional 3 weeks. Echocardiography before discharge revealed disappearance of the pericardiac effusion and marked improvement in the mitral valvular regurgitation. He will be scheduled to undergo surgery for patent ductus arteriosus.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [100.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 100.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 0.
The patient's Well's score for pulmonary embolism is 0."
3000,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6970509-1,Extracted,"The patient is a 32-year-old male with history of inflammatory ileocolonic Crohn's disease (CD) status after ileocecectomy with perianal involvement, Type 1 arthropathy with synovitis of the bilateral knees, essential hypertension, recurrent cellulitis, and obesity, who presented to our institution for ustekinumab therapy. At that time, he reported a three-day history of right knee pain and swelling. He reported that this initial presentation was similar to past arthropathy flares. The patient had a known history of spondyloarthropathy, best explained as an extraintestinal manifestation of his active CD. The patient noted development of intermittent fevers and chills as well. During his ustekinumab infusion, the patient had acute worsening of his knee pain with sudden extension into the right calf, ankle joint, and foot. He also reported tightness and tenderness to palpation of the posterior right calf. This specifically, as well as the development of systemic symptoms, differed from his prior Type 1 arthropathy symptoms in the affected extremity.
Upon presentation to the Emergency Department, his pain had progressed in severity with associated nausea. The affected extremity had also developed erythema and had become exquisitely tender to palpation. He denied cough, shortness of breath, abdominal pain, headache, lightheadedness, or dizziness. The patient was tachycardic to 136 beats per minute and febrile to 38° Celsius. He was treated with analgesics, with notable labs including WBC of 14.4 × 103/μL, K+ of 3.3 mEq/L, Cr of 0.63 mg/dL, and CK 21 units/L. Blood draw and knee joint aspiration for cultures were both negative. Empiric antibiotic therapy was started, and Orthopedics was consulted for concern of compartment syndrome. The patient was not found to have developed compartment syndrome and maintained distal pulses identifiable on Doppler. The affected extremity remained warm and appeared well perfused. Radiographs of the lower extremity were unremarkable. Ultrasound venous duplex was completed to evaluate for deep vein thrombosis (DVT) given the development of erythema and systemic symptoms, and was negative. On ultrasound, soft tissue swelling of the posterior calf with incidental Baker's cyst in the medial aspect of the calf, measuring 6.8 × 4.0 cm, was noted in addition to small joint effusion. Further evaluation with lower extremity MRI showed evidence of complex fluid in the right semimembranosus-gastrocnemius bursa with edema suggestive of extravasation of fluid from rupture of Baker's cyst (). There was no evidence of osteomyelitis. A CT pelvis was performed to rule out other causes of lower extremity edema.
The patient was maintained on acetaminophen and oxycodone for pain control. Orthopedics recommended weight bearing and range of motion as tolerated, and antibiotics were discontinued. Rheumatology was consulted and recommended outpatient intra-articular cortisone injection for persistent swelling and pain. The patient was continued on his home doses of prednisone and oral methotrexate. Upon 2-month follow-up in the inflammatory bowel disease (IBD) clinic, the patient had not pursued outpatient cortisone injection. He reported complete resolution of the acute symptoms related to rupture of Baker's cyst, which he treated conservatively with acetaminophen. At the time of follow-up, he reported persistent pain related to his known Type 1 arthropathy in the bilateral knees, which he described as predominantly stiffness without swelling.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [136.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 136.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 = 6.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
3001,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8184328-1,Extracted,"A 46-year-old Caucasian woman presented to the emergency department pale and clammy, complaining from the day before of a syncopal episode, hypotension, diarrhea, and left shoulder tip pain which in the immediate hours before hospitalization spread to the whole abdomen. The patient also complained from the day before of widespread arthromyalgia and slight fever. No history of trauma was reported.
Her past surgical history included a laparoscopic sleeve gastrectomy performed for obesity (pretreatment BMI 37.5) about a year earlier. At presentation, the patient had a BMI of 25.3.
At the preliminary examination, she was alert and oriented, tachycardic at 100 beats per minute, and normotensive and had a temperature of 35.8°C. She was eupnoeic with an oxygen saturation of 99% on air. Examination of the abdomen revealed generalized guarding at palpation, worst in the left hypochondrium. The hemoglobin level at arrival was 7.7 g/dl (12-17.5), and she received a transfusion of 1 unit of red blood cells. Diffuse free fluid in the abdomen was seen on the patient's Focused Assessment with Sonography for Trauma (FAST) ultrasound. Reverse transcriptase-polymerase chain reaction (RT-PCR) was positive for SARS-CoV-2 infection.
The routine admission blood test revealed a liver function test partially deranged with normal bilirubin, alkaline phosphatase, and gamma glutamic transpeptidase, but abnormal alanine aminotransferase 69 IU/L (0-45) and aspartate aminotransferase 130 IU/L (0-35). At presentation, the coagulation values were PT INR 1.12 (0.8-1.2), APTT sec. 25 (17-35), and APTT ratio: 0.9 (0.8-1.2). The platelets were 168 × 10 · e3/μL (130-400).
The rest of her routine biochemical investigation was unremarkable, and neither portal hypertension nor liver steatosis was documented either clinically or macroscopically.
Chest and abdominal CT scan revealed parenchymal thickening areas associated with frosted glass opacity halo in both lower lobes of inflammatory significance (lung score 2), voluminous splenic subcapsular hematoma with a maximum thickness of 57 mm, and abundant hemoperitoneum (Figures and ).
During this investigation, the patient became increasingly unstable with blood pressure 75/45 mmHg and cardiac frequency > 100 pulse rate per minute and mildly anxious, which is why the patient, in accordance with the literature, had an emergency (rather than laparoscopic) laparotomy within 2 hours of presentation. This revealed 2 L of free blood in the peritoneal cavity and a bulky blood clot attached to the lower pole of the broken spleen [].
Choice in the surgical approach was not conditioned by COVID-19 infection, even though previous research has shown that laparoscopy may lead to aerosolization of blood-borne viruses. Currently, there is no evidence to indicate that this effect is seen with COVID-19, nor that it would be limited to minimally invasive surgery procedures [].
On the first postoperative day, the patient was transferred to a COVID-19 surgical unit where she needed antibiotic treatment with azithromycin and oxygen low-flow therapy for a week.
Both acute-phase and convalescent serum analyses provided no evidence of other acute viral infections beyond SARS-CoV-2. The postoperative course was complicated by a wound infection, and the patient was discharged on day 20 after therapy.
At macroscopy, the pathology report demonstrated that the spleen had a normal size with a weight of 182 g, the capsule was torn on multiple sides, and several subcapsular hemorrhages and hematomas were documented with a variable range from 4.5 cm to 2 cm (). The larger one was on the anterior surface of the spleen and compressed the parenchyma behind and probably led to the spleen capsule rupture. At microscopy, the white pulp showed normal compartmentalization of B and T lymphocytes, demonstrated also by immunohistochemistry (CD3 and CD20), and the red pulp showed sinuses normal in size but increased in number, with a slight decrease in chordal tissue and capillaries (Figures –). We also performed a novel immunohistochemistry marker SARS-CoV/SARS-CoV-2 (COVID-19) spike antibody in the spleen of our patient to eventually demonstrate SARS-CoV-2 presence in the tissue.
The case shows the effective use of the multidisciplinary hospital team to diagnose and manage what was a potentially life-threatening event.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [100.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 100.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3002,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8221132-1,Extracted,"A 77-year-old female patient with a past medical history of chronic obstructive pulmonary disease, hypertension, hyperlipidemia who presented to our emergency room (ER) due to worsening of respiratory distress. Four days prior to admission, the patient was hospitalized for management of community acquired pneumonia and upper gastrointestinal (GI) bleed and was later discharged to a rehab center. During a physical therapy session at the rehab facility, the patient developed severe shortness of breath and was found to be hypoxic with an oxygen saturation (SpO2) of 75%, she was placed on a nasal cannula. Presenting vitals in the ER showed a blood pressure of 152/83 mmHg, pulse 137 bpm, respiratory rate of 18/min and SpO2 97% on a 15 litre nonrebreather, and the patient was found to be COVID-19 positive using the RT-PCR test. Initial computed tomography (CT) of the chest pulmonary embolism protocol found multiple small bilateral pulmonary emboli as well as elevated right ventricular to left ventricular ratio of 1.4 indicating right heart strain (). The patient was noted to have expressive aphasia and left sided flaccid paralysis, and an initial CT scan of the head without intravenous (IV) contrast showed no evidence of acute intracranial abnormality. A magnetic resonance imaging (MRI) of the head with and without gadavist intravenous (IV) contrast () done later on Day 1 found a large acute right middle cerebral artery (MCA) territory infarct. The patient was started empirically on IV dexamethasone, antibiotic therapy, aspirin, atorvastatin, and therapeutic enoxaparin. On Day 2, a CT angiography of the head and neck with IV contrast showed an abrupt vessel cut off of the right internal carotid artery at the level of the supraclinoid right ICA, and nonvisualization of the distal right internal carotid artery as well as the right M1 due to a non-occlusive thrombus ().
The patient was transferred to an acute care facility, and a transthoracic echocardiogram () showed moderately dilated right ventricle with moderately reduced systolic function, right atrial thrombus in transit and hypermobile atrial septal aneurysm. The thrombus was managed with thrombectomy using the Inari FlowTriever device () and was started on continuous IV infusion of unfractioned heparin. On day 3, a venous doppler of the lower extremities showed a thrombus in the right femoral vein of the distal thigh, gastrocnemius veins, posterior tibial, and peroneal veins. At this point, COVID-19 related hypoxic respiratory symptoms were mild and required only nasal cannula for supplemental oxygen. Patient remained hemodynamically stable until day 10 her condition was complicated by an upper GI bleeding in the form of melanotic bowel movement, she subsequently underwent esophagogastroduodenoscopy (EGD) and found a clot in the anterior bulb, which was treated with epinephrine, clot removal and cautery of a non-bleeding vessel. She was then treated with pantoprazole IV infusion and transfused two units of packed red blood cells (PRBC), while anticoagulation therapy was held. An interdisciplinary decision was made to restart anticoagulation on day 13. On Day 18, the patient had a hemorrhagic conversion of right middle cerebral artery ischemic infarct which was detected on CT of the head (), and heparin infusion was discontinued. Neurosurgery evaluated the patient and she was deemed not a candidate for any surgical intervention. Given her grave prognosis, the patient was transitioned to hospice care on Day 20.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [137.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",7.5,7.5,7.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 137.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 =  6.0.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 6.0 + 1.5 = 7.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 7.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 7.5.
The patient's Well's score for pulmonary embolism is 7.5."
3003,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8559745-1,Extracted,"A 55-year-old man with a weight of 76 kg and height of 178 cm, suddenly experienced a nontraumatic loss of consciousness after a cough attack at an upright position as reported by a witness. Two months prior, he was diagnosed with pulmonary tuberculosis and had been receiving antituberculosis treatment. On arrival, the patient was unconscious with a Glasgow coma scale score of 6, blood pressure of 169/89 mm Hg, regular heart rate of 85 beats/minute, respiratory rate of 18/minute, body temperature of 36.5°C, SaO2 of 82% at room air, and capillary blood sugar of 110 mg/dL. Auscultation of the lungs revealed an inspiratory crackle at the left lung field. After rapid intravenous access and oxygenation, the patient was sedated, the trachea was intubated, mechanical ventilation was initiated, and conservative treatment was maintained in the intensive care unit. Urgent computed tomography (CT) of the brain was performed and showed multiple air shadows in both hemispheres and the right cerebral vessels (). These lesions suggest air embolism. Twelve hours later, a magnetic resonance imaging (MRI) of the head was performed and showed a diffuse ischemic stroke in the right and left frontoparietal cortical areas and multiple hypointense signals, which were consistent with cerebral air embolism ().
The brain perfusion images were normal. The chest CT performed at the emergency department showed pulmonary tuberculosis cavity associated with the destruction of parenchyma in the left upper lobe (). There was no evidence of cerebral hemorrhage. The diagnosis of cerebral gas embolism after sudden cough was retained, and immediate treatment was started including 100% oxygen and cardiovascular support while the patient was placed in a supine position. The transthoracic echocardiography was performed, and no patent foramen ovale was found. A lumbar puncture was performed to seek for tuberculous meningoencephalitis. The cerebrospinal fluid analysis was normal. Hyperbaric oxygen therapy was considered, but the patient’s condition was too unstable to support transfer to the hyperbaric oxygen center. One day later, his neurological status deteriorated. The patient died on the fourth day with multiple organ failure. No autopsy was performed based on his family’s wishes.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [85.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 85.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 1.5 + 1 = 2.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 2.5.
The patient's Well's score for pulmonary embolism is 2.5."
3004,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6727588-1,Extracted,"A 49-year-old woman (89.9 kg, 167.1 cm, body mass index: 32.3 kg/m2) without any past medical history, including heart failure, asthma, allergies, or immediate hypersensitivity reaction to any type of iodinated radiocontrast material, visited our hospital for a self-paid medical imaging health check-up-package which includes the MRI-upper abdomen imaging and low-dose computed tomography (LDCT) of chest. Her initial non-contrast LDCT of chest showed unremarkable finding (Fig. A). Two hours after LDCT, she underwent abdominal MRI after an injection of 15 mL (0.1 mL/kg body weight) of gadobutrol (Gadovist, Bayer Inc., Toronto, Canada). Ninety minutes after the injection of gadobutrol, she was found to have dyspnoea and cyanosis. Her vital signs were as follows: blood pressure 127/77 mmHg, pulse rate 100 bpm, respiratory rate 35/min, and oxygen saturation 60% by pulse oximetry.
At emergency room, physical examinations showed diffuse wheezes and use of accessory muscles of respiration. The chest radiograph (Fig. A) showed bilateral alveolar infiltrates and hilar haze suggestive of acute pulmonary oedema. Laboratory tests showed a serum creatinine of 0.4 mg/dL, a D-dimer of 899 ng/mL, and a Brain Natriuretic Peptide (BNP) of 35.4 pg/mL. The repeated chest computed tomography scan showed multiple ground glass attenuation and consolidation in bilateral lungs (Fig. B). An echocardiography revealed no impaired left ventricular function or valvular defect. The initial arterial blood gas analysis showed a pH of 7.45, a partial pressure of carbon dioxide of 28.7 mmHg, and a partial pressure of oxygen (PaO2) of 48.6 mmHg, which was remarkable for severe oxygenation impairment with a PaO2/FiO2 ratio of 121.5 (FiO2: 40%). Under a diagnosis of MRI contrast-induced ARDS, she was transferred into intensive care unit (ICU) where BiPAP ventilation with a 15/5 cm H2O pressure support was administered. Her hypoxaemia improved to a PaO2 level of 85 mmHg after the use of BiPAP ventilation. In addition, she received intravenous dexamethasone 5 mg immediately at emergency room and then switched to methylprednisolone injection with a maintenance dose of 1.5 mg/kg daily. During the ICU course, the patient got improvement from respiratory distress and hypoxaemia. The repeated chest radiograph on day 3 (Fig. B) revealed rapid resolution of airspace infiltrates in bilateral lungs. The patient was weaned successfully from BiPAP ventilation on day 4 and she was discharged with resolution of pulmonary infiltrates (Fig. C) on day 6.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 100.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3005,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8319662-1,Extracted,"A 66-year-old woman presented to the emergency department with complaints of shortness of breath and chest pain for the preceding 2 days.
She had a history of rheumatoid arthritis (RA) and systemic lupus erythematous (SLE), taking oral prednisolone (6 mg/day) and hydroxychloroquine (200 mg/day). She was a housewife and frequently worked with potting soils in her garden. She also had orange-coloured sputum (Figure ). Her vital signs upon admission were as follows: temperature, 36.1°C; blood pressure, 109/69 mmHg; pulse rate, 111 beats/min; respiratory rate, 30/min; and oxygen saturation, 96% on 9 L/min of oxygen mask with reservoir bags. She had clear consciousness. She had coarse crackles bilaterally.
Laboratory findings were as follows: white blood cell count 30,510/μl (neutrophils 99.5%), haemoglobin 10.1 g/dl, platelet count 5.0 × 104/μl, lactate dehydrogenase 341 U/L, urea nitrogen 30 mg/dl, creatinine 1.21 mg/dl and C-reactive protein 41.06 mg/dl. Blood gas analysis showed the following: pH 7.397, pCO2 34.4 torr, pO2 46.5 torr and HCO3
− 21.8 mEq/L (with room air).
Her chest x-ray showed consolidation in the upper and middle lung fields bilaterally (Figure ). Computed tomography (CT) of the chest showed consolidation of the right upper, middle and lower lobes and the left upper, and atelectasis of the left lower lobe (Figure ). Sputum Gram stain showed very few epithelial cells and some neutrophils, but not satisfactory to estimate causative bacteria. Both the BinaxNOW™ pneumococcal and Legionella urinary antigen test (Abott) were negative.
We suspected severe pneumonia and started with intravenous levofloxacin (500 mg q24h) and meropenem (500 mg q6h) empirically. Given her history of RA and SLE, and immunosuppressive state, we thought that viral/fungal infections, alveolar haemorrhage and interstitial pneumonia were important differential diagnoses. Thus, she underwent BAL by bronchoscopy under intubation. The colour of BALF was also orange (Figure ) and the cellular pattern was neutrophil predominant (90.0%) suggestive of bacterial infection. But, Gram stain of the BALF results was negative. Cytology of BALF revealed numerous neutrophils and a few macrophages which were not hemosiderin-laden. Because it has been clinically suggested that the colour of sputum obtained from patients with pneumonia caused by L. pneumophila is orange, we suspected non-pneumophila Legionella species pneumonia. We switched meropenem to azithromycin (500 mg q24h) and increased levofloxacin to maximum dose (750 mg q24h) targeting Legionella species pneumonia. Acid-fast bacillus cultures of sputum resulted negative. Two sets of blood cultures were negative. Polymerase chain reactions (PCR) for Pneumocystis, cytomegalovirus and SARS-CoV-2 were all negative. On the fifth day, mass spectrometry analysis of colonies obtained by culturing in BCYEα medium from BALF identified the presence of Legionella longbeachae.
On the sixth day, her respiratory condition deteriorated and contrast-enhanced CT showed exacerbation of ground-glass opacity (GGO) without pulmonary thromboembolism. We suspected organizing pneumonia secondary to L. longbeachae and started high-dose pulse intravenous steroid treatment with 1 g methylprednisolone for 3 days followed by prednisolone 1 mg/kg (60 mg/day) alongside levofloxacin that was administered 21 days in total. The following days she recovered gradually and she was extubated on Day 12. Eventually, consolidation and GGO improved on her chest CT of Day 23 and she was discharged home without oxygen on Day 34.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [111.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 111.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3006,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7384707-1,Extracted,"Our patient is an 80-year-old gentleman presented to the emergency department (ED) after a sudden onset of a near-syncope episode accompanied by diaphoresis and lightheadedness while at rest. His pertinent medical history was significant for coronary artery disease (CAD) status post coronary artery bypass grafting (CABG), peripheral artery disease (PAD), hypertension, dyslipidemia, and chronic kidney disease (CKD). He was admitted to our hospital three months ago as his PAD was worsening that required left above the knee amputation and was subsequently discharged to the acute inpatient rehabilitation service. He subsequently recovered well and was discharged home after six weeks of rehabilitation. Emergency medical service (EMS) arrived at his house after the near-syncope episode without loss of consciousness, fall, chest pain, palpitation, dyspnea, fever, chills, nausea, vomiting, or bowel habit changes. Initial blood pressure was 80/40 mmHg and heart rate of 50 beats per minute. His symptoms had completely resolved upon EMS arrival, but it was determined to bring the patient to the ED for further evaluation.
His vital signs in the ED were as follows: temperature 99.3°F, blood pressure 109/61 mmHg, heart rate 103 beats per minute, respiratory rate 18 breaths per minute and pulse oximetry saturation at 97% on room air. Physical examination was overall benign, and further review of systems was unremarkable. Initial laboratory findings were significant for lactic acid 3.0 mEq/L, creatinine 1.59 mg/dL, calculated glomerular filtration rate (GFR) 42 mL/minute, cardiac troponin <0.10 ng/mL, and cardiac b-type natriuretic peptide (BNP) 46 pg/mL. Electrocardiography (EKG) showed sinus tachycardia. Chest x-ray (CXR) showed normal size heart, no evidence of pulmonary vascular congestion, and negative for active pulmonary diseases (Figure ). The patient’s episode of near syncope was thought to be related to hypovolemia or potential rate control medication side effects. He was given one liter of normal saline and was admitted to the general medicine floor for further observation. His creatinine and lactic acid levels normalized with fluid resuscitation. The patient remained to be hemodynamically stable overnight.
On day 2 of hospitalization, a code blue was activated due to the sudden onset of pulseless electrical activity (PEA) arrest as the patient was found to be unresponsive in bed. He was hemodynamically stable and saturating well on room air prior to the code activation. He also denied chest pain, diaphoresis, or dyspnea. Emergent high-quality cardiopulmonary resuscitation (CPR) began according to the advanced cardiovascular life support (ACLS) protocol as the return of spontaneous circulation (ROSC) was later achieved. The patient was intubated, sedated, and transferred to the cardiac surgical unit (CSU) for further management. EKG during the code blue revealed findings that were concerning for anterolateral myocardial infarction (Figure ). The patient was taken to the cardiac catheterization laboratory for an urgent exploration of the coronary arteries as troponin levels were trending upwards to possibly explain for the PEA arrest. Catheterization showed patent bypass grafts along with a hyperdynamic left ventricular systolic function. He remained to be stable overnight.
On day 3 of hospitalization, an echocardiogram was ordered that revealed right ventricular dysfunction with pulmonary hypertension. Urgent CT with contrast showed extensive bilateral central pulmonary emboli with multiple filing defects distally in the right and left pulmonary arteries extending to the pulmonary artery branches to all lobes of the lung (Figure ). Interestingly, he maintained adequate arterial oxygen saturation (SaO2) on 40% of the fraction of inspired oxygen (FiO2) and positive end-expiratory pressure (PEEP) of 5 cm H2O. His blood pressure remained to be stable despite multiple vasoconstrictors, and central venous pressure (CVP) was moderately elevated per the pulmonary artery catheter. There was no evidence of cardiogenic shock or lactic acidosis. He had a low clinical indication for urgent tissue plasminogen activator (tPA) after considering the risk and benefits and was instead treated with therapeutic intravenous (IV) heparin. The presenting chief complaint of the near-syncope episode along with the later in-hospital PEA arrest was thought to be related to the hidden extensive bilateral PEs. He remained to be hemodynamically stable overnight.
On day 4-5 of hospitalization, vasoconstrictors were begun to wean off as his blood pressure appeared to be improving. He had maintained stable SaO2 as FiO2 was further downtitrated to 30%. CVP remained to be in acceptable range per the pulmonary artery catheter. He continued to receive therapeutic heparin treatment. The code status of the patient was changed to do not resuscitate (DNR) by family members after the palliative care team was consulted to discuss goals of care.
On day 6 of hospitalization, the patient suddenly became hypotensive despite multiple vasoconstrictors, bradycardic, but remained SaO2 of 96% on FiO2 of 40%. He went into asystole and unfortunately past away as no resuscitative measures were attempted due to DNR status.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [103.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 103.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3007,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6060922-1,Extracted,"A 45-year-old African-American male presented to emergency department with complaints of fever and a pruritic inguinal rash. He had medical history of hypertension, diabetes mellitus, dyslipidemia, bilateral Stage 3 gluteal decubitus ulcer, and paraplegia after gunshot wound to the spine 26 years ago. Patient noticed reddish-brown itchy rash with odor in the groin for the past 4 days. He denied any cough, chest pain, dyspnea, palpitations, dysuria, diarrhea, nausea, or vomiting. Patient had a history of tobacco and alcohol abuse but no illicit drug abuse. Patient reported asymptomatic elevations in liver function tests (LFTs) with prior 7-day course of oral fluconazole for candiduria approximately a year ago, after which the drug was discontinued.
On admission, his vitals were remarkable for temperature of 102.4°F, pulse of 117 beats/min, and blood pressure of 170/106 mmHg. Physical examination revealed an elevated, erythematous, and tender rash in inguinal area with marks of skin excoriations consistent with intense pruritus. There was a bilateral Stage 3 sacral decubitus ulcer visible with no signs of infection. There were no signs of asterixis, spider angioma, or organomegaly. A sepsis workup including blood cultures, urine cultures, sputum cultures, lactic acid, and chest X-ray was ordered. His initial serum electrolytes, LFTs, comprehensive metabolic panel, and coagulation panel were all within reference range. Hematological investigations showed a leukocytosis of 21,000 white blood cell/uL (reference 4500–11,000) with normochromic and normocytic anemia. On the day of admission, his aspartate aminotransferase (AST) was 12 IU/L (reference 8–46 IU/L), alanine aminotransferase (ALT) 18 IU/L (reference 7–55 IU/L), alkaline phosphatase 100 IU/L (reference 45–115 IU/L), total bilirubin 0.9 (reference 0.1–1.2 mg/dL), and direct bilirubin 0.2 IU/L (reference <0.3 mg/dL).
A diagnosis of sepsis was made, likely due to inguinal candidiasis with superimposed bacterial cellulitis. Patient was started on IV normal saline, IV fluconazole 200 mg daily, and IV clindamycin. Cultures were reported negative, and the patient had no further febrile episodes. On day 3 of hospitalization, the patient developed ALF with an AST of 25000 IU/L (reference 8–46 IU/L), an ALT of 6500 IU/L (reference 7–55 IU/L), a GGT of 210 IU/L (reference 0–65 IU/L), an alkaline phosphatase of 130 IU/L (reference 45–115 IU/L), a total bilirubin 2.3 mg/dL (reference 0.1–1.2 mg/dL), and a direct bilirubin 0.4 mg/dL (reference <0.3 mg/dL). With an ALT/alkaline phosphatase ratio >5, this drug-induced liver injury (DILI) was classified as “hepatocellular.” Coagulation studies noted an international normalized ratio of 3.2 (0.8–1.1), a prothrombin time of 25 s (reference 11–14), and a partial thromboplastin time 28 s (reference 25–35). Hepatitis panel, Epstein–Barr virus, cytomegalovirus, and HIV tests resulted negative. He had no history of chronic liver disease (CLD). An abdominal ultrasound showed mild hepatomegaly. Considering the temporal association combined with no other probable etiologies for the patient's worsening ALF, DILI secondary to fluconazole was suspected, and fluconazole was stopped. Three days after stopping the drug, the LFTs [] and coagulation studies [] improved. The patient's prompt clinical recovery after withholding the drug corroborated our diagnosis of fluconazole-mediated ALF.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [117.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 117.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3008,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8294909-1,Extracted,"A 53-year-old man (height, 180 cm; weight, 76.6 kg), a heavy alcoholic, was admitted to a local medical center under the diagnosis of right acetabular and iliac wing fracture after falling from a tree. The patient was bedridden under conservative treatment. Three days later, he presented with abdominal pain and tenderness and was then transferred to our hospital for further evaluation and management. The systolic/diastolic blood pressure, heart rate on electrocardiogram, and body temperature were 160/94 mm Hg, 120 beats/min, and 37.5°C, respectively. Under the suspicion of dehydration and fracture-induced pain, fluid resuscitation was initiated with Hartmann solution and analgesics were administered. Nonetheless, the heart rate did not decrease. Hence, bisoprolol (5 mg per os) was administered once daily. Thiamine, haloperidol, and quetiapine were administered to treat alcohol withdrawal delirium. Every time the patient became responsive to verbal stimuli, he kept reporting abdominal pain. However, no pulmonary symptoms were present. Anteroposterior chest radiograph and transthoracic echocardiography (TTE) were normal. Abdominal CT revealed retroperitoneal and right iliacus hematoma. However, no injury was found in major vessels or organs. The laboratory findings showed increased levels of D-dimer (26.64 μg/mL), the normal range of which was < 0.1 μg/mL. Because he was immobilized after the injury with elevated levels of D-dimer, combined CT venography and CTPA was performed 7 days after the injury to rule out DVT and PTE; however, the results were negative.
Three days later (10 days after the injury), he presented to the operating room for open reduction and internal fixation of the pelvic bone fracture. Before anesthesia induction, the systolic/diastolic blood pressure, heart rate, and peripheral oxygen saturation (SpO2) were 142/92 mm Hg, 100 beats/min, and 100%, respectively. Anesthesia was induced with bolus administration of 130 mg propofol and continuous infusion of remifentanil at 0.1 μg/kg/min. Endotracheal intubation was facilitated with 50 mg rocuronium. The ventilator was set in the volume-controlled mode to deliver a tidal volume of 6 to 8 mL/kg at a respiratory rate of 10 to 12 breaths/min. The tidal volume and respiratory rate were adjusted to maintain end-tidal carbon dioxide concentration (EtCO2) between 33 and 35 mm Hg. Anesthesia was maintained with sevoflurane (1.5–2.0 vol%) in oxygen/air mixture (inspired oxygen saturation of 50%) to ensure bispectral index values between 40 and 60. The infusion rate of remifentanil (0.1–0.2 μg/kg/min) was adjusted to maintain blood pressure and heart rate within 20% of the baseline values. The right radial artery was catheterized for real-time monitoring of arterial blood pressure and arterial blood sampling. The right internal jugular vein was catheterized for real-time monitoring of central venous pressure, bolus administration of drugs, and continuous infusion of drugs. The results of arterial blood gas analysis after anesthesia induction were as follows: pH, 7.468; partial pressure of arterial carbon dioxide (PaCO2), 37.2 mm Hg; partial pressure of arterial oxygen (PaO2), 193.5 mm Hg; bicarbonate (HCO3−), 26.3 mmol/L; base excess, 2.6 mmol/L; hemoglobin, 8.2 g/dL.
At 10 minutes before the surgery, 100 μg phenylephrine was bolus administered twice at a 5-minute interval to ensure a systolic blood pressure of > 100 mm Hg. At the beginning of the surgery, phenylephrine was continuously infused at a rate of 0.2 μg/kg/min owing to the transient effects of its bolus administration. To compensate for intraoperative blood loss and preoperative dehydration, 6% hydroxyethyl starch, packed red blood cells, and fresh frozen plasma were administered at a rate of 8 to 10 mL/kg/min, and systolic blood pressure and heart rate were maintained between 90 and 100 mm Hg and between 100 and 110 beats/min, respectively. Ninety minutes after the surgery, systolic/diastolic arterial blood pressure and EtCO2 abruptly decreased from 100/60 to 30/15 mm Hg and from 29 to 13 mm Hg, respectively. The central venous pressure elevated from 10 to 29 mm Hg. The heart rate slightly increased from 105 to 115 beats/min. The normal sinus rhythm on the electrocardiogram turned into atrial fibrillation, after which bradycardia (49 beats/min) ensued. Under the impression of PTE, 3 cycles of cardiopulmonary resuscitation (CPR) were intermittently performed for 25 minutes until spontaneous circulation [systolic/diastolic blood pressure of 80–90/50 mm Hg and sinus tachycardia (115 beats/min)] was achieved (Fig. ). At the beginning of CPR, epinephrine and norepinephrine were infused at a rate of 0.1 μg/kg/min, and 3 mg epinephrine was bolus administered during CPR. Arterial blood gas analysis performed between the first 2 CPR cycles revealed hypercapnia (pH, 7.287; PaCO2, 55.8 mm Hg; PaO2, 98.7 mm Hg; HCO3−, 26.0 mmol/L; base excess, −0.6 mmol/L; hemoglobin, 8.8 g/dL). At the end of the last CPR cycle, the infusion rate of the fluid was reduced to 3 to 5 mL/kg/min, and a probe for transesophageal echocardiography (TEE) was inserted into the esophagus. TEE showed right ventricular dysfunction with paradoxical septal motion. However, no embolus was found in the main, right, and left pulmonary arteries. Intraoperatively, 500 mL of 6% hydroxyethyl starch, 1250 mL of packed red blood cells, and 450 mL of fresh frozen plasma were administered in total. The amount of blood loss and urine output was 700 and 100 mL, respectively.
Chest CT performed immediately after the surgery showed emboli in both the pulmonary arteries (Fig. ). The patient was taken back to the operating room and underwent surgical embolectomy under cardiopulmonary bypass with aortic cross-clamping and cardioplegic arrest. The incision was made in both the main pulmonary arteries, and emboli were removed (Fig. ). EtCO2 and central venous pressure were elevated from 20 to 31 mm Hg and reduced from 30 to 4 mm Hg, respectively, after weaning from cardiopulmonary bypass. Intraoperative TEE and postoperative TTE showed normalized right ventricular function and septal motion. Anticoagulation therapy with warfarin was commenced from the third postoperative day. The inferior vena cava filter was also placed. One month after the surgery, CTPA and CT venography revealed no DVT and PTE. The patient was then discharged from the hospital without any complications. The patient provided informed consent for the publication of this case.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 =  3.0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3.0 + 1.5 = 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
3009,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-3374,Extracted,"A previously healthy 24-year-old male is brought to the emergency department because of fevers, congestion, and chest pain for 3 days. The chest pain is exacerbated by deep inspiration. He takes no medications. His temperature is 37.5°C (99.5°F), blood pressure is 118/75 mm Hg, pulse is 130/min, and respirations are 12/min. He appears weak and lethargic. Cardiac examination shows a scratchy sound best heard along the left sternal border when the patient leans forward. There are crackles in both lung bases. Examination of the lower extremities shows pitting edema. Results of a rapid influenza test are negative. EKG shows diffuse ST-elevations with depressed PR interval. An echocardiogram shows left ventricular chamber enlargement with contractile dysfunction.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [130.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 130.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
3010,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7425628-1,Extracted,"A 54-year-old woman with a past medical history of anxiety, hypothyroidism and bipolar disorder presented to the emergency room (ER) for evaluation of a change in mental status for 2 days. Her bipolar disorder had been well controlled for many years on lithium and trifluoperazine. However, she was recently started on perphenazine due to a shortage of trifluoperazine. She was noted to be extremely agitated and dehydrated in the ER.
On arrival, she was afebrile with normal blood pressure and slightly tachycardic (90 bpm). For the agitation, she received two doses of Haldol 5 mg. Subsequently, she became catatonic with diffuse muscle rigidity. On examination, she was oriented to person but not to place, time or events.
Her blood pressure rose to 170/85 mmHg, her heart rate increased (122/minute) and her temperature rose to 105 F. Her cardiac, chest and abdominal examinations were unremarkable.
After admission, in the general ward, the patient complained of chest pain and ST-segment elevation was noted on EKG. () A rapid response was called. The patient was ultimately intubated and shifted to the cardiac unit where her coronary angiography was done, which came out normal. (). However, echocardiography showed her left ventricular ejection fraction (LVEF) to be 20–25%. Echocardiography showed good movement of the basal wall and severe hypokinesis of the rest of the walls consistent with Takotsubo cardiomyopathy. () She required the insertion of IABP and heparin infusion. Over time her blood pressure improved and IABP was removed subsequently.
During her second day in CCU, she was found to have left upper extremity swelling which required evaluation with doppler, which was suggestive of subclavian vein thrombosis. Heparin was stopped due to the suspicion of heparin-induced thrombocytopenia (HIT). HIT antibodies and serotonin release assay (SRA) were sent and she was started on argatroban. She became hypoxic for which a computed tomography with pulmonary embolism (CTPE) protocol was done showing pulmonary embolism. () HIT assay came back negative. The initial CT scan of the head was unremarkable. Therefore, an MRI brain was done which showed multiple infarcts. She ultimately tolerated extubation but was nonverbal and bedridden due to multiple infarcts.
Blood work was significant for elevated creatinine levels of 1.32 mg/dL, blood urea nitrogen of 10 mg/dL and creatinine kinase levels of 9529 U/L. Complete blood count and liver function tests were unremarkable. During the rapid response, EKG showed ST-segment elevation in precordial leads, an x-ray showed bilateral infiltrates, BNP was 747 pg/ml, and a creatine kinase level of 9876 U/L. Troponins elevated to 9.05 ng/ml. Right heart catheterization showed a wedge pressure of 23 mmHg, a mean pulmonary artery pressure of 36, and a cardiac output of 2.3 L/min. A left heart catheterization showed normal coronaries but LVEF of 20–25% by left ventriculography. Subsequent brain MRI showed acute infarction in the subcortical white matter of the high right parietal lobe, and possible subcentimeter bifrontal foci of acute infarction.
Because of fever and a change in mental status, meningitis/encephalitis was high on the differential. Lumbar puncture (LP) was unsuccessful as the patient was extremely agitated. She was started on vancomycin, ceftriaxone, ampicillin, and acyclovir. She was initially admitted to the progressive care unit (PCU) with a working diagnosis of CNS infection versus neuroleptic malignant syndrome. She was also started on dantrolene (skeletal muscle relaxant) and bromocriptine (dopamine agonist) which were later discontinued. Her repeat EKG showed a resolution of ST elevation. () The patient was ultimately discharged to a rehabilitation center after a prolonged hospitalization. A 6 month follow up revealed an uneventful recovery, and the patient had no further episodes of Takotsubo cardiomyopathy.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [122.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",7.5,7.5,7.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 122.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 = 6.0.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 6.0 + 1.5 = 7.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 7.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 7.5.
The patient's Well's score for pulmonary embolism is 7.5."
3011,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8204462-1,Extracted,"A 35-year-old nulliparous Arab woman with an 8-year history of primary infertility presented to our infertility center. During these 8 years, she was diagnosed with uterus didelphys with two cervices and no vaginal septum (Fig. ). She underwent hysterosalpingogram (HSG), three-dimensional ultrasound (3D US), and diagnostic laparoscopy, which proved the diagnosis (Fig. ). Hence, no magnetic resonance imaging (MRI) was done since the 3D US was enough to determine the sizes of both horns, which showed minor differences in dimensions.
She had no specific history, apart from her irregular period explained by the diagnosis of polycystic ovary syndrome (PCOS), was not a smoker, and did not consume alcohol. Her weight was 87 kg and her height 158 cm.
Her spouse was 44 years old, with uncontrolled type 2 diabetes, a recent history of coronary angioplasty and stents, and chronic hypertension.
They had three previous failed intracytoplasmic sperm injection (ICSI) trials outside our center years prior due to an indication for a male factor (oligo-astheno-teratozoospermia).
The couple was very anxious, depressed, and distressed at the first consultation, to which they brought a new semen analysis showing azoospermia.
The male, who had a medical condition, declined any intervention to extract the sperm surgically per recommendations from the anesthesiologists and cardiologists. A diagnosis of retrograde ejaculation was made, as well as a plan for isolation of the sperm from a urine sample after the preparation. Three vials of frozen motile sperm were obtained before embarking on the fourth IVF trial.
Four blastocysts were obtained from the first IVF/ICSI antagonist cycle in February 2018 (Table ), one of which (4AA) was transferred to the left uterus, and surplus freezing was done. The patient tolerated the procedure very well with no need for sedation or anesthesia. Her vital signs were normal (blood pressure 118/67 mmHg, heart rate 73 beats per minute, temperature 36.7 °C).
Both horns had a highly suitable endometrium, with a triple line with an average thickness of 10.3 mm. The left horn was chosen because it was more accessible to the left cervix at the moment of embryo transfer. It was planned to transfer one embryo, and the couple was counseled by our high-risk-pregnancy consultant to improve the obstetrics outcome for this uterine anomaly.
The first successful IVF journey ended with no need for cerclage and with no obstetrical complication by an elective C-section at 35 weeks for a baby girl of 2800 g weight, 46 cm length, 31.5 cm head circumference, and 7/10 Apgar score at delivery.
The couple visited our infertility center again in 2020 with the goal of conceiving a second child. The first child was with them, showing very good progress, normal development, and intelligence as per her parents. They extended their request to transfer one of the frozen embryos.
The endometrium was prepared by hormone replacement therapy (HRT) protocol for embryo transfer for the frozen embryo transfer (FET) cycle using 6 mg ethinyl estradiol daily starting from second day of period. Progesterone was added on day 14, when reaching triple-line endometrium with thickness of 11.1 mm. One blastocyst was thawed and survived. The initial decision was to transfer the embryo to the same horn (left) because of the previous successful transfer. The very deep and long vagina forced us to reach one of the cervices. The outer sheet of the embryo transfer catheter was used and showed that we were targeting the right horn.
Embryo transfer proceeded successfully and smoothly (Fig. ), in which the embryo was placed in the right uterus without changing or manipulating the anatomy, and the embryo was placed 1 cm from fundus. The patient tolerated the procedure well, and the couple was counseled properly.
Nine days later, her beta human chorionic gonadotropin (b-hCG) level was 258 mIU/ml. A single gestational sac with a viable pregnancy (positive heart beat) was observed in the right uterus, and the patient was referred to our high-risk-pregnancy specialist for follow-up. An elective C-section was performed at 34 weeks for a baby boy of 2650 g weight, 47 cm length, 31 cm head circumference, and 6/10 Apgar score at delivery.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [73.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Surgery in the previous 4 weeks': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 73.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3012,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8647775-1,Extracted,"A 72-year-old male with a past medical history significant for non-obstructive chronic artery disease (CAD), gastroesophageal reflux disease (GERD), prostate cancer post-resection presented to the emergency department (ED) with left-sided chest tightness, lightheadedness, and presyncope. He also reported mild exertional shortness of breath. His initial vitals were stable with a heart rate (HR) of 65 beats per minute and blood pressure (BP) of 112/66 mmHg. Initial labs including complete blood count, metabolic panel (K: 4.2, Mg: 2.1, Ca: 9.1) initial troponin, and chest X-ray were largely unremarkable. Coronavirus disease 2019 (COVID-19) reverse transcriptase-polymerase chain reaction (RT-PCR) was negative. Initial electrocardiogram (EKG) at 6:17 PM showed normal sinus rhythm, rate of 65 beats per minute without ST-T wave changes. He was admitted to the floor for further evaluation and management. It was noted that the patient did have a recent exercise stress test (with myocardial perfusion scan) as an outpatient which was negative for ischemic changes. He also had a recent echocardiogram which showed a normal ejection fraction (EF) of 60% with mild mitral regurgitation. Orthostatic vitals were checked and were negative (lying BP: 100/55 mmHg, seating BP: 99/54 mmHg, and standing BP: 100/61 mmHg). Overnight, he was noted to develop symptomatic bradycardia with HR on the cardiac monitor between 30-40 beats per minute (bpm).
Repeat EKG obtained in the morning showed sinus bradycardia with Mobitz type 1 (Wenckebach) heart block and progressive prolonged PR interval (Figure ). Telemetry also revealed Wenckebach's heart block (Figure ). Lyme titers were ordered and came back reactive and Western blot was positive for IgG (10/10 bands); however, negative for IgM consistent with Lyme infection that occurred more than a month prior. He was treated with IV ceftriaxone 2 g every 24 hours with the resolution of his heart block and bradycardia after a total of seven days of IV antibiotics (Figure ). He was eventually discharged home on doxycycline 100 mg p.o. for 21 days to complete 28 days total with recommendations to follow up with cardiology as an outpatient without needing pacemaker implantation.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [65.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 65.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3013,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6348079-1,Extracted,"A 73-year-old Caucasian woman with a medical history significant only for hypertension, presented to our emergency department complaining of intermittent subjective fever, anorexia, weakness, and fatigue for 2 weeks. Her subjective fevers were occurring almost nightly, and she had associated night sweats. Her weight was stable. She had a persistent non-productive cough. There was no sore throat or rashes. Her review of systems was negative for any other current symptoms. Her only medication was enalapril. Her family history was non-contributory.
She had been previously assessed by her family doctor for the same symptoms 2 weeks prior to this presentation. Routine investigations were unrevealing. At that time, she had left knee pain that developed after a hike the previous month. X-rays of her knee and femur were unremarkable. Her pain resolved within a week. No therapeutic interventions were undertaken at that time.
She had no sick contacts, no sexual partners, and no insect or tick bites. She had no known exposure to tuberculosis. She travelled to the Channel Islands 3 months before presentation. She had no animal exposures. She denied any history of injection drug use.
On initial examination, she appeared non-toxic. Her vital signs included a temperature of 38.6 °C, a heart rate of 96 beats/minute, blood pressure of 130/65 mmHg, and oxygen saturation of 99% on room air. There were no rashes and no lymphadenopathy was present. There were no signs of hyperthyroidism and the thyroid itself was normal in size without any nodules. Her jugular venous pulse was 2 cm above the sternal angle. She had normal heart sounds with no extra sounds or murmurs. There were no stigmata of endocarditis. Her lungs were clear with equal breath sounds bilaterally. An abdominal examination revealed a soft and non-tender abdomen. There was no hepatosplenomegaly, jaundice, or asterixis. Examination of her knees did not reveal any redness, warmth, effusions, or pain. A screening neurologic examination demonstrated grossly normal cranial nerves, full strength bilaterally, and normal reflexes, tone, and coordination. She was admitted for further investigation for her fever of unclear cause. Empiric piperacillin-tazobactam and intravenously administered saline were started on admission as acute bacterial infection was in the differential diagnosis.
Table displays the results of her laboratory investigations. A peripheral smear was unremarkable. Serum free light chains were normal. No monoclone was found on serum protein electrophoresis. Urine analysis was bland. Five sets of blood cultures, a urine culture, and Lyme serology were negative. A chest X-ray was normal. Computed tomography (CT) scans of her head, neck, chest, abdomen, and pelvis were all unremarkable. A transthoracic echocardiogram revealed a normal heart with no vegetations.
She had one further temperature of 39.4 °C while in hospital, without any clear infectious source. Once the blood cultures were known to be negative, piperacillin-tazobactam was stopped. There was an impression that her workup could be continued on an out-patient basis as immediately life-threatening causes of fever had been ruled out. She was discharged home after an 8-day admission in hospital with plan for out-patient follow up.
She was seen 1 month after discharge. She had no improvement in her symptoms and noted a recurrence of her left leg pain. Her C-reactive protein (CRP) was 207 mg/L. On examination, she had a large, warm, left thigh mass. An urgent ultrasound revealed a 4.5 × 6.8 × 11.6 cm spindle-shaped, well-defined soft tissue mass with internal vascularity (Fig. ). Magnetic resonance imaging (MRI) found that the mass met the femur but was not invading (Fig. ). An initial biopsy revealed a poorly differentiated malignant neoplasm.
She underwent a distal femur excision with distal Global Modular Replacement System (GMRS) reconstruction. Final pathology revealed a grade 3, pT2bN0M0 undifferentiated sarcoma with epithelioid morphology. She had no nodal involvement or distant metastases at this time. Her CRP fell to 28.42 mg/L within 8 days of surgical excision. She recovered well from her surgery with resolution of her constitutional symptoms. She subsequently was planned to receive radiation therapy.
Prior to receiving radiation therapy, a follow-up CT scan was done a couple months after her surgery. This revealed the presence of a new 4 mm pulmonary nodule in the lower lobe of her left lung that was not felt to be a metastasis. There was no other evidence of distant metastases. Given these results, adjuvant radiation treatment was begun. She received 6600 cGy given in 33 fractions to her leg.
Roughly 1 month following the end of her radiation therapy course, she re-presented to our emergency room with painless hematuria and a month-long history of non-productive cough associated with decreased energy. CT scans of her chest revealed 16 pulmonary masses, measuring up to 6.2 cm. A CT scan of her abdomen and pelvis revealed a solitary nonobstructive renal calculus, as well as a new 3.2 × 6.5 cm pelvic mass.
She was subsequently referred to radiation and medical oncology where a shared decision was made to pursue palliative management.
Figure provides a timeline of the above described case.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [96.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",6.5,6.5,6.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 96.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 3 + 1.5 = 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 4.5 + 1 = 5.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 5.5 + 1 =  6.5.
The patient's Well's score for pulmonary embolism is 6.5."
3014,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-5409,Extracted,"A 45-year-old woman presents to her physician with a four-month history of headache. Her headache is nonfocal but persistent throughout the day without any obvious trigger. She was told that it was a migraine but has never responded to sumatriptan, oxygen, or antiemetics. She takes amlodipine for hypertension. She does not smoke. She denies any recent weight loss or constitutional symptoms. Her temperature is 98°F (36.7°C), blood pressure is 180/100 mmHg, pulse is 70/min, and respirations are 15/min. She is obese with posterior cervical fat pads and central abdominal girth. Her neurological exam is unremarkable. In her initial laboratory workup, her fasting blood glucose level is 200 mg/dL. The following additional lab work is obtained and is as follows:

Serum:
Na+: 142 mEq/L
Cl-: 102 mEq/L
K+: 4.1 mEq/L
HCO3-: 24 mEq/L
BUN: 20 mg/dL
Glucose: 135 mg/dL
Creatinine: 1.3 mg/dL
Ca2+: 10.0 mg/dL
AST: 8 U/L
ALT: 8 U/L
24-hour urinary cortisol: 500 µg (reference range < 300 µg)
Serum cortisol: 25 µg/mL (reference range 5-23 µg/dL)
24-hour low dose dexamethasone suppression test: Not responsive
High dose dexamethasone suppression test: Responsive
Adrenocorticotropin-releasing hormone (ACTH): 20 pg/mL (5-15 pg/mL)

Imaging reveals a 0.5 cm calcified pulmonary nodule in the right middle lobe that has been present for 5 years but an otherwise unremarkable pituitary gland, mediastinum, and adrenal glands.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [70.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 70.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3015,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7522164-1,Extracted,"A 78-year-old male with a past medical history of hypertension, chronic kidney disease, chronic obstructive pulmonary disease, and atrial fibrillation with CHA2DS2-VASc score of 3 on rivaroxaban, presented to the hospital with complaints of left upper quadrant pain and chest pain. The patient was recently admitted with a concern for gastrointestinal bleeding, and rivaroxaban was held. Unfortunately, the patient left the hospital against medical advice at that time without further workup for gastrointestinal bleeding. The patient presented two days after leaving the hospital. On physical examination, the patient was alert and oriented. The abdomen was soft with mild left upper quadrant tenderness. Lungs were clear to auscultation without any crackles or wheezing. The patient had an irregular heart rhythm, and no murmurs were appreciated. The patient's vital signs were stable, except for his heart rate of 100 bpm. The patient underwent a stat computed tomography angiography of the chest, which was negative for aortic dissection and pulmonary embolism. Other laboratory workup showed hemoglobin 9.1 gm/dl (reference range 13-17 gm/dl), hematocrit 27.5% (reference range 41-50%), and lipase 170 U/L (reference range 0-160 U/L). The patient had an electrocardiogram (ECG), which showed atrial fibrillation with a ventricular rate of 112 bpm, right bundle branch block, ST-segment depression in lateral leads with ST-segment elevation in aVR (Figure ). His Troponin level was minimally elevated at 0.036 ng/ml (normal range below 0.04 ng/ml) with a brain natriuretic peptide (BNP) of 436 pg/ml (normal range below 100 pg/ml).
The patient was transferred for urgent cardiac catheterization after heparin drip initiation, which showed left-main thrombosis with extension into the left anterior descending artery (LAD) with 90% obstruction and left circumflex artery (LCX) leading to 100% occlusion without collaterals (Figure , ). The mid to distal right coronary artery (RCA) had minimal luminal irregularities. After insertion of the intra-aortic balloon pump (IABP) for hemodynamic support, the left main was engaged, and two 0.014 wires were crossed across the LAD and LCX lesions. Aspiration thrombectomy of LAD was performed that caused the distal embolization of the thrombus (Figure ). Repeat thrombectomy was done. Post-procedure there was TIMI grade 3 flow throughout the LCX (Figure ) without any evidence of thrombosis, dissection, or distal embolization. The patient transferred to the critical care unit. The heparin infusion and abciximab were continued, repeated ECG showed complete resolution of ST-segment elevation in aVR and depression in anterolateral leads (Figure ). The patient was subsequently taken off IABP support. The patient was stable without any chest pain and was discharged on rivaroxaban.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [100.0, 'bpm'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 100.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3016,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,trec-cds-2015-24,Extracted,"A 31 yo male with no significant past medical history presents with productive cough and chest pain. He reports developing cold symptoms one week ago that were improving until two days ago, when he developed a new fever, chills, and worsening cough. He has right-sided chest pain that is aggravated by coughing. His wife also had cold symptoms a week ago but is now feeling well. Vitals signs include temperature 103.4, pulse 105, blood pressure 120/80, and respiratory rate 15. Lung exam reveals expiratory wheezing, decreased breath sounds, and egophany in the left lower lung field.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [105.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 105.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3017,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3345141-1,Extracted,"A 40-year-old female presented with complaints of dyspnea and palpitation on exertion since 1 month prior to admission, which had been insidious in onset and progressive. There was no history of orthopnea or paroxysmal nocturnal dyspnea. There was a history of occasional retrosternal chest pain, nonradiating and anginal in character. On examination, she was pale, had a pulse of 88/min, which was regular, with average volume, blood pressure (BP) of 110/80 mm of Hg. Her jugular venous pulse (JVP) was normal; also, there were no signs of congestive cardiac failure (CCF). On cardiovascular examination, the apex was present in the 6th intercostal space (ICS) on the right side, lateral to mid clavicular line; right parasternal heave and diastolic shock were also present. First heart sound was loud and there was a wide, fixed split second heart sound. There was a mid diastolic murmur present at the apex and a systolic murmur present at the right parasternal area at the 3rd–4th ICS. There were no rales or wheeze on auscultation of lungs. There was no hepatomegaly or pedal edema.
A chest X-ray was done which showed a right-sided cardiac shadow with presence of cardiomegaly.
2D echocardiography revealed dextrocardia, situs inversus, concordant atrio-ventricular (AV) connection, large-size (12 mm) ostium secundum type of atrial septal defect (ASD) with bidirectional shunt []; dilated right atrium and ventricle; concordant ventriculo-arterial connection (aorta arises from the left ventricle and pulmonary artery arises from the right ventricle); intact interventricular septum; normal biventricular function; and mild to moderate tricuspid regurgitation. Mitral valve was thick, pliable with commissural fusion and doming of anterior mitral leaflet []. Moderate pulmonary regurgitation was present and mean pulmonary artery pressure was 35 mm of Hg. Mitral valve area was 1.60 cm []. Tricuspid, aortic and pulmonary valve were normal. There was no evidence of patent ductus arteriosus. Total anomalous pulmonary venous connection or coarctation of aorta. Mild to moderate pericardial effusion was present []. The patient also underwent an ultrasound examination of the abdomen which showed liver on the left side, confirming situs inversus [].
Pericardiocentensis was done. Pericardial fluid was straw colored and had a protein (albumin) content of 3.2 g/dl and showed lymphocytosis consistent with tubercular pericardial effusion. The patient was started on antitubercular treatment.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [88.0, 'beats per minute'], 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Immobilization for at least 3 days': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 88.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3018,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7010591-1,Extracted,"A 47-year-old female (body mass index, 30.5 kg/m2 (160 cm, 78 kg)) presented in a corresponding hospital with acute pain in the upper abdomen after gastric bypass and cholecystectomy 9 years earlier and loosing 40 kg weight afterward. At the first consultation in the emergency department, she complained of massive abdominal pain since the night before admission, which did not respond to analgesic drugs. Because of the patient’s history of bariatric surgery and the suspicion of SBO, a computed tomography (CT) scan was performed, which was inconclusive at the first look with multiple differential diagnoses. It showed a thickening of the wall of the ascending colon and a diverticulum of the duodenum with semisolid contents. The patient was then referred to our hospital for further treatment.
In our emergency department, the patient’s general condition was reduced because of pain and signs of diffuse peritonitis. The vital signs showed a blood pressure of 120/70 mmHg and an accelerated pulse (120 bpm), a respiratory rate of 25/min and a normal body temperature. The blood results showed a leukocytosis with only slightly elevated C-reactive protein (14 mg/l). The CT scan was reviewed and revealed the presence of retroperitoneal and parapancreatic fluid with some air bubbles, which could also be seen in an additional abdominal sonography. Further a thickening of the colon ascendens was found (). A perforated duodenal diverticulum was likely and suspected. The thickening of the ascending colon was interpreted as an accompanying colitis.
Attributable to the reduced condition of the patient with little response to opioids, signs of diffuse peritonitis and our interpretation of the imaging, we decided to perform an explorative transverse laparotomy in the upper abdomen. Although the right colic flexure was mobilized, the exposure of the duodenum was difficult and very limited. However, a hard resistance could be palpated. After a Kocher maneuver and exposing the duodenum and the pancreas dorsally, we were then able to dissect the duodenal diverticulum. The diverticular wall was incised and a biliary stone of the size of ~7 × 4cm was exposed and removed (). Sutures then reattached the duodenal wall. A T-drain was placed intraduodenally, an Easy-Flow drain paraduodenally ( and ). Postoperatively, the patient was admitted to the ICU for initial surveillance. An empiric intravenous antibiotic therapy with Piperacillin/Tazobactam was initiated. After one night, the patient could be transferred to the normal ward in stable condition.
The postoperative course was uneventful. Pain was controlled with basis analgesia and slowly she returned to a normal diet. Inflammatory markers were declining and antibiotics could soon be stopped. Ten days postoperatively, a fistulography showed a persistent retroperitoneal collection of 3 × 3 cm so the drains were left in situ. Two days later, the patient was discharged from the hospital in proper general condition but with extraduodenal drains still in place.
One week after dismissal, the patient felt well with normal appetite and a regular intestinal passage. The fistulography showed a significant reduction of the collection so the T-drain was removed. Two weeks later, she still felt irritated by the last remaining Easy-Flow drainage, which continued showing some turbid liquid and was therefore left in situ. Intestinal passage was unchanged and there were no signs of inflammation. Another 2 weeks later, the drain fell out by accident. Seven weeks postoperatively, still no signs of inflammation, we were able to finish our treatment.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [120.0, 'bpm'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3019,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5217592-1,Extracted,"A 30 year old G2P1001 sub-Saharan African female teacher at 11 weeks amenorrhea, presented to the Nkwen Baptist Health Center (Bamenda, North West Region of Cameroon) on the 15th of May 2016 with bilateral lower limb swelling and pain of 5 days duration. She had no known chronic illness and denied having a family history of VTE.
She reported being well till 2 weeks prior to presentation when she started experiencing abdominal pains; the pain was mainly in her lower abdomen, dull in nature, non-radiating, mild in intensity, was initially intermittent then became constant. It was associated with intermittent low grade fever. This prompted her to consult at a remote health center, where a urinalysis and malaria parasite test was done but their results were inconclusive. She was then cautioned to be having early pregnancy symptoms and placed on acetaminophen 3 g per day in three divided doses which she took for a week with no regression of symptoms. The persistent and progressively worsening pain now localized at the right lower quadrant prompted a second consultation at another health facility. This pain was still associated with low grade fever and now included; loss of appetite and intermittent postprandial vomiting. The attending physician on examination remarked right iliac fossa tenderness and rebound tenderness with a positive Rovsing’s sign. Presumptive diagnosis of acute appendicitis and differential of ovarian cyst in pregnancy were retained. An emergency surgery was booked. However, intra-operative findings revealed a normal appendix and ovaries.
Following surgery, lower abdominal pains persisted and she complained of a sudden onset of crampy constant pains in her right thigh. She was told to be having post surgery pain, for which she was then given analgesics. On day 3 post hospitalization she was discharged on analgesics, antibiotics and progesterone suppository. While at home, the pains persisted and 2 days later involved her left calf area. This was associated with bilateral lower limb swelling that was more on the right lower limb. The pain increased in severity making it difficult for her to walk. This prompted consultation at our health facility.
On arrival she was ill-looking and in painful distress. Her blood pressure was 122/76 mmHg, heart rate 94 beats/min, respiratory rate of 22 breaths/min, temperature 37 °C, O2 saturation at 97% and weight 58 kg. Her conjunctivae were pink and sclera anicteric, heart sounds were normal and lung fields clear. On examining the abdomen, a clean midline incision was seen and there was tenderness on deep palpation of the lower abdominal quadrants marked on the right. There was bilateral lower limb pitting oedema extending to the thighs with right lower limb more swollen than left. The limbs were mildly erythematous but there was no area of cracked skin or wound on both limbs that could have served as portal of entry for skin infection. Both lower limbs were warm tender.
Based on these we made a tentative diagnosis of bilateral lower limb deep venous thrombosis in early pregnancy with a possible pelvic vein thrombosis that was misdiagnosed for acute appendicitis. Our health facility was not equipped with the necessary tools and personnel to confirm our diagnosis and manage the patient. She was therefore referred to a tertiary care center about 40 km from our facility.
At the tertiary center compressive doppler ultrasound of the pelvis and lower limbs revealed pelvic and bilateral lower extremity veins seen with echoes in the right common iliac vein (Fig. ), right femoral vein, left femoral vein and left popliteal vein. There was decreased colour flow in these veins and decreased compressibility. These suggested DVT of the right common iliac vein, right femoral vein, left femoral vein and left popliteal vein and thus confirmed our diagnosis of bilateral lower limb and pelvic DVT.
Further laboratory testing showed the following: normal white cell count of 8100/µl, mild anaemia with haemoglobin of 9.8 g/dl, thrombocytosis of 532,000/µl, normal kidney function test (serum creatinine of 0.64 mg/dl and urea of 12.7 mg/dl), glycaemia of 85.9 mg/dl and normal serum electrolytes of: (Sodium 134 mmol/l, Potassium of 4.17 mmol/l and Chloride of 103 mmol/l). Cardiac echography and electrocardiogram done were all normal.
The patient was immediately started on low molecular weight heparin (LMWH) 80 mg subcutaneous route daily. After 5 days of treatment the patient’s symptoms had subsided and she was discharge and counter referred for continuation of care. We continued her daily LMWH injections and scheduled her for a repeat of the pelvic and lower limb ultrasound. Six weeks later there were no more echoes in the pelvic and lower limb veins (Fig. ). She continued daily LMWH till 12 weeks postpartum.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [94.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 94.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 3 + 1.5 =  4.5.
The patient not been diagnosed with pulmonary embolis (PE), but the patient has previously been diagnosed with deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
3020,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6075628-1,Extracted,"A previously healthy 27-year-old man presented with complaints of left calf pain and erythema of four days duration, which was preceded by a petechial rash of the bilateral lower extremities and left foot pain. He also reported low-grade fever (100.7 F) with associated chills. He was initially seen at a Level 1 trauma center where he underwent a Doppler investigation of the lower extremities with negative findings. Blood work at the time was reported normal. A worsening induration and swelling of the left lower extremity prompted him to seek further work-up. An inquiry into past medical and family history was non-contributory. He had a history of hernia repair and tonsillectomy. Social history was significant for recreational marijuana and cocaine use in the past. He was homosexual and reported being sexually active with one male partner and inconsistent contraception use. The patient denied weight loss, night sweats, recent travel, recent major illness or surgery, or steroid use. On admission, he was afebrile (98.8 F) and tachypneic (18 breaths per minute). A blood pressure of 132/75 mmHg, heart rate of 81 beats per minute, and oxygen saturation of 99% on room air were documented. The physical examination revealed a mildly enlarged spleen and confluent erythema of the bilateral lower extremities that were tender to touch. Blood work showed a normal white blood count of 7.33X109/L, hemoglobin of 15.6 mg/dl with marked thrombocytopenia, and platelet count of 51X109/L. An aspartate aminotransferase (AST) level of 289/L, alanine aminotransferase of 372/L, and direct bilirubin of 0.22 umol/L confirmed transaminitis. The D-Dimer level was 14,000 ng/ml. The venous duplex of the lower extremities showed extensive thrombosis in the left peroneal (Figure ) and thrombosis of the left popliteal (Figures -).
Computed tomography (CT) of the chest with contrast revealed borderline splenomegaly of size 13 cm. Extensive investigations eventually showed evidence of an active CMV infection with CMV-Immunoglobulin M (IgM) seropositivity (>240.0 AU/mL) and positive polymerase chain reaction (PCR). Serology was positive for the Epstein Barr virus (EBV) (368 U/mL). He received a platelet transfusion with symptomatic improvement. He was discharged home on Eliquis 5 mg twice daily; however, he returned to the hospital a week after with new symptoms. He reported right lower leg pressure-like pain that was exacerbated with walking. Doppler revealed right great saphenous vein superficial thrombophlebitis along with unchanged findings in the left leg. He was initially switched to Rivaroxaban 15 mg twice daily; and on clinical improvement, he was later discharged on Apixaban 5 mg twice daily.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [81.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 81.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3 + 1.5 = 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
3021,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7362665-1,Extracted,"A 61-year-old female former smoker presented with increasing dyspnea and productive cough with white expectoration for a few days. She denied fever, chest pain, palpitation, orthopnea, paroxysmal nocturnal dyspnea and edema. She had unintentional weight loss of 20 lbs along with loss of appetite. She had past medical history of bronchial-associated lymphoid tissue (BALT) lymphoma and was treated with rituximab. A positron emission tomography (PET) scan two months prior to the admission showed left lower lobe mass with obstruction of the left mainstem bronchus, and diffuse bilateral pulmonary nodules with moderate left pleural effusion. Subsequently, she received chemotherapy with obintuzumab and bendamustine.
On admission, she was afebrile, sinus tachycardia 110/min, normotensive, respiratory rate 25/min and oxygen saturation 96% on 2 L nasal cannula oxygen. There was neither jugular venous distension nor pedal edema. Cardiac auscultation revealed normal S1 and S2 without murmur or added sound. Lung auscultation revealed diminished breath sound over the left hemithorax. The rest of the physical examination was unremarkable.
Her electrocardiogram showed sinus tachycardia with the rate of 109/min. Complete blood count showed normocytic anemia with hemoglobin 9 g/dl which was stable compared to that two months ago. Blood chemistry was within normal limits. Chest X- ray showed opacification of the left hemithorax (Figure ).
Given these observed findings along with the elevated risk of thrombosis in active cancer, computed tomography (CT) pulmonary angiogram was performed (Figure ). CT chest ruled out pulmonary embolism but revealed a large filling defect within the left atrium, left inferior and superior pulmonary veins. It was suspected to be a thrombus since it was not reported on earlier PET scan. Apixaban was initiated given the concern for thromboembolism.
A transthoracic echocardiogram showed a 3 x 3 cm, mobile, echogenic mass in the left atrium best seen in the parasternal long axis view (Figure ). Her left atrial size was reported to be normal. Her left ventricular size and function were also within normal limit. Further evaluation with transesophageal echocardiogram (TEE) was considered. However, the patient did not provide consent for TEE after being informed about the risks of the procedure.
To offer the best characterization of soft tissue cardiac masses, cardiac magnetic resonance imaging (CMR) was performed (Figure ). It confirmed a bulky left lung mass suggestive of carcinoma invading the left atrium via the left pulmonary veins. There was bulky intraluminal tumor thrombus and extensive mediastinal invasion by tumor. CT-guided biopsy of left lung mass was suggestive of non-small cell lung carcinoma (NSCLC). A diagnosis of dual synchronous cancers, BALT lymphoma and NSCLC, adenocarcinoma to be exact, with cardiac invasion was made. As of now, we are not sure about the relationship between these two tumors. We do not know which one had invaded the left atrium. She continued to receive palliative chemotherapy. After discussion with the hemato-oncology, the anticoagulation was stopped due to the risk of internal bleeding.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Previously documented Deep Vein Thrombosis': False}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3.0 + 1 =  4.0.
The patient's Well's score for pulmonary embolism is 4.0."
3022,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7642566-1,Extracted,"A previously healthy 29-year-old female was transferred to the emergency department of the Second Affiliated Hospital of Zhejiang University School of Medicine because of left hemothorax with hemodynamic instability.
She had suffered from increased neck pain with shortness of breath and severe vomiting without hematemesis after eating fish two days before. The examination in a local hospital indicated a massive left pleural effusion on chest radiograph; however, no fishbone was found under laryngoscopy. Due to her rapidly decreasing blood pressure even after massive liquid infusion, the patient was quickly transferred to our hospital for further treatment.
The patient had a free previous medical history.
At the time of admission, the patient was in a light coma. Vital signs showed a heart rate of 129 beats/min and blood pressure of 69/35 mmHg.
Blood tests revealed that her hemoglobin was 46 g/L.
The enhanced chest computed tomography (CT) showed a pseudoaneurysm in the initial segment of the left vertebral artery and massive effusion in the mediastinum and the left thoracic cavity (Figure ).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [129.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 129.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3023,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5952454-1,Extracted,"A 46-year-old male without any known comorbidity presented with left flank pain and vomiting for 15 days. He also had intermittent fever for the past 1 week, but there was no hematuria, history of passage of stones, or lower urinary tract symptoms. On examination, the patient had fever (104°F) and tachycardia (110/min). The left flank was tender, and an ill-defined lump was palpable in the left flank. Ultrasonography done elsewhere revealed left nephromegaly, and the patient was referred to us with a provisional diagnosis of acute left pyelonephritis. Blood reports showed anemia (Hb 6.7 g/dL), leukocytosis (TLC 181 × 109/L), and thrombocytopenia (9 × 109/L). Serum creatinine was 0.6 mg/dl (normal: <1.4 mg/dL). He was further evaluated with contrast-enhanced computed tomography of the abdomen which was suggestive of non enhancing left kidney with filling defect in the renal vein []. Prothrombin time, activated partial thromboplastin time, thrombin time (TT), and plasma fibrinogen levels were normal. Peripheral smear examination showed blast cells. A subsequent bone marrow examination confirmed the diagnosis of an AML French–American–British (FAB) M1 []. Myeloblasts were 90%, with fine chromatin, 1–2 prominent nucleoli, and Auer rods. Flow cytometry showed AML with expression of CD13–25%, CD14, CD33–99%, CD117–41%, cytoplasmic myeloperoxidase–78%, negative for CD34 and human leukocyte antigen-antigen DR. In view of severe thrombocytopenia and hyperleukocytosis, nephrectomy was initially deferred. A cytoreductive therapy (hydroxyurea and cytarabine) was given for hyperleukocytosis along with adequate hydration, platelets, and appropriate antibiotics prophylaxis. Further evaluation with magnetic resonance imaging (MRI) showed RVT extending into inferior vena cava (IVC) for 2 cm with partial occlusion of IVC lumen. Heparin could not be started in view of persistent low platelets count. The TLC decreased to 60 × 109/L after 4 days of cytoreductive therapy. Tc-99m Diethylenetriaminepentaacetic acid scan revealed a nonvisualized left kidney. After platelet transfusion (single donor apheresis), the patient underwent left simple nephrectomy with IVC thrombectomy. Intraoperatively, a hard thrombus was present completely occluding the renal vein and extending into the IVC lumen for 2 cm []. He had satisfactory immediate postoperative recovery with adequate urine output till the 3rd postoperative day, and serum creatinine was 0.7 mg/dL. On the 4th postoperative day, there was sudden fall in urine output with mild swelling of the bilateral lower limb. His TLC was 39 × 109/L, platelet count was 20 × 109/L, and serum creatinine was 1.8 mg/dL. Lower limb Doppler showed no evidence of deep venous thrombosis. On the next day, limb swelling increased, urine output decreased, and serum creatinine rose to 2.1 mg/dL. Abdominal MRI showed extensive thrombosis of bilateral common iliac veins and infrahepatic IVC []. He was started on unfractionated heparin (UFH) as desperate measure in spite of low platelets. Hemodialysis was done for acute renal failure on the 6th postoperative day. The patient developed sudden cardiac arrest on the following day and could not be revived.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 =  3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3.0 + 1 =  4.0.
The patient's Well's score for pulmonary embolism is 4.0."
3024,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6177082-1,Extracted,"A 60-year old man with a past medical history of hypertension, presented with 3-months of progressive dyspnoea on exertion. He had no known cardiac history. Based on his complaints and abnormal chest X-ray, he was treated with ciprofloxacin for pneumonia. However, his symptoms were nonetheless becoming progressively worse. In addition, he began to have dizziness and worsening shortness of breath with minimal exertion. He reported three separate occasions of briefly losing consciousness after exertion, from which he awoke abruptly. A transthoracic echocardiography (TTE) performed at an outside institution revealed a left atrial mass.
On examination, he was afebrile with a blood pressure of 100/60 mmHg and a regular pulse rate of 81 beats per minute. Room air oxygen saturation was 93%. There were no signs of distress; the lungs were clear; no murmur or friction was audible over the heart. There were no overt signs of heart failure.
An electrocardiogram (ECG) revealed normal sinus rhythm with T wave inversions in the anterior precordial leads. Chest X-ray showed vascular congestion and small bilateral effusions blunting the costophrenic angles consistent with congestive heart failure. Laboratory findings included normocytic anaemia with haemoglobin level of 11.6 g/dL (normal 14–18), a thrombocytosis of 524 000/UL (normal 150 000–500 000), and normal white cell count. Serum creatinine was 1.4 mg/dL (normal 0.7–1.2), troponin I level was 0.24 ng/mL (normal <0.04), and B-type natriuretic peptide level was 1340 pg/mL (normal <100).
As shown in Figure , a transoesophageal echocardiography (TOE) revealed a large (3.4 cm × 4.5 cm) lobulated mass in the left atrium adherent to the intra-atrial septum, and another smaller mass in the right atrium, both highly suggestive for atrial myxoma. However, as seen in Figure (arrows) the mass consisted of multiple echo-lucent areas compatible with cystic elements inside the tumour. During diastole, the mass prolapsed from the left atrium into the mitral valve orifice creating severe functional mitral stenosis with a mean gradient of 11.6 mmHg across the mitral valve (, Video S1). Left ventricular ejection fraction was mildly reduced (45%).
The patient was promptly referred to cardiothoracic surgery, and he was hospitalized for an emergent surgery. Upon his admission, he developed rapid atrial fibrillation. Preoperative coronary angiography revealed a 60% stenosis of the proximal left anterior descending (LAD) artery which was found to be haemodynamically significant by fractional flow reserve (FFR).
The patient underwent robotic-assisted surgical excision of the atrial masses. After a standard median sternotomy, cardiopulmonary bypass was obtained, and the left atrium was approached. The mass was close to the mitral valve but arising from the superior and medial aspects of the atrial septum with a broad base, so wide excision of the atrial septum was necessary to excise the tumour. Once the left atrial mass was removed, the right atrium was opened, and another separate mass was noted, occupying the entire septum anteriorly all the way to the orifice of the coronary sinus. This second mass also required a wide excision afterwards the intra-atrial septum and the right atrial wall had to be reconstructed using bovine pericardium patches. A single coronary artery bypass grafting to the LAD was performed. The patient tolerated the procedure well.
On gross pathology, the excised tumours measured 4.5 and 4.0 cm, had a smooth and multilobulated surface with a white colour and gelatinous texture (Figure A). Microscopically, the tumours consisted mostly of conventional myxoma histology, characterized by classic stellate and fusiform myxoma cells in myxoid stroma (Figure ). A significant amount of each tumour volume (∼20%) showed evidence of glandular differentiation that manifest through formation of small and large cystic glandular elements measuring up to 1.4 cm (Figure and C). The content of the glands was mucin which was confirmed using special studies. No cytologic atypia or mitotic activity was found.
The post-operative period was uneventful. The atrial fibrillation resolved spontaneously. On post-operative echocardiography, the left atrium appeared normal, and there was no obstruction of mitral inflow. There was no transit of agitated saline bubbles across the septum. The patient was discharged home on the 10th post-operative day. Two-months post-operatively, the patient was feeling well.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [81.0, 'beats per minute'], 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Immobilization for at least 3 days': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 81.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3025,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7336594-1,Extracted,"A 74-year-old Caucasian male presented to the ED with worsening shortness of breath and elevated blood pressure. On presentation, he was markedly tachypneic and in severe respiratory distress. Vital signs include an elevated blood pressure of 165/114 mmHg, a pulse of 122 beats per minute, a temperature of 99.1°F and a respiratory rate of 28/minute. On physical examination, the patient was in acute distress, diaphoretic, and using accessory muscles of respiration. Lung auscultation revealed diffuse rales. Regular rate and rhythm with no accessory heart sounds were appreciated on precordial auscultation. The patient was put on a non-rebreather mask with mild improvement in the respiratory status and subsequently intubated and transferred to the intensive care unit on mechanical ventilation.
The patient’s medical history was significant for obstructive sleep apnea with noncompliance to positive airway pressure therapy due to discomfort. He had grade 1 left ventricular diastolic dysfunction on an echocardiogram 8 months ago with normal biventricular size and function. He took a trip to Florida with his wife and noticed body aches, constant non-productive cough, headaches, fatigue, and fevers with a temperature of 101°F since his return 10 days prior. He reported sick contact at his vacation, which prompted him to get checked for viral pathogens and get a chest x-ray. The patient was diagnosed with COVID-19 8 days prior to presentation and was followed by the Cleveland Clinic’s distance health service with daily phone encounters while he was in isolation at home. His chest x-ray had shown left perihilar opacity and he was provided with doxycycline.
The differential diagnosis included viral pneumonia, bacterial pneumonia, PE, and COVID-19 acute respiratory distress syndrome (ARDS).
Laboratory work revealed hemoglobin of 17.3 g/dL, white blood cell count of 16,400/uL, elevated liver enzymes with ALT 336 U/L and AST 309U/L. C-reactive protein was elevated to 11.9 mg/dL, D-dimer elevated to 4,300 ng/mL, IL-6 was elevated to 52 pg/mL and ferritin was elevated to 5440 ng/mL. Electrocardiogram (EKG) was insignificant for any acute abnormality, troponin T was elevated to 0.0770 ng/mL and proBNP was elevated to 1312 pg/mL. Arterial blood gas analysis revealed acute hypoxemic respiratory failure with a P: F of 220 on 80% fractional inspired oxygen (FiO2). Chest x-ray revealed bilateral hazy opacities. The patient was kept in airborne precautions. Blood and urine cultures were drawn. The tracheal aspirate was sent for bacterial pneumonia workup. A point of care lower extremity ultrasound revealed left femoral deep venous thrombosis (Figure ).
Low tidal volume lung-protective ventilation was maintained with a high positive end-expiratory pressure (PEEP) and a low fraction of inspired oxygen (FiO2) strategy. The patient was initiated on hydroxychloroquine and azithromycin based on anecdotal data. The patient was a candidate for tocilizumab therapy but was avoided in the setting of abnormal liver function. His P: F ratio suddenly started to decrease along with the elevation of troponin T and pro-BNP. Suspicion of myocarditis, as well as a PE, were high on the differential. As multimodality imaging was limited due to strict precautions to prevent spread, transthoracic echocardiography was performed revealing a normal left ventricular size and systolic function but with a moderately dilated right ventricle with impaired right ventricular (RV) systolic function, severe hypokinesis of basal and mid RV walls and septum with normal contractility of distal RV wall and apex (Video ).
The pattern of RV wall motion was consistent with acute RV strain and a positive McConnell’s sign (Video ).
The patient was started on a heparin infusion. The patient’s acute inflammatory markers trended down with medical therapy and his ARDS improved. Troponin T also returned to baseline after 48 hours.
Hospital course was complicated by the development of ventilator-associated pneumonia and after being on the ventilator for 14 days. the patient was successfully extubated. The patient is currently recovering on the medical floor.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [122.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 122.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
3026,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7255560-1,Extracted,"A 58-year-old female with a past medical history of bipolar disorder presented to the emergency department with acute onset of dyspnea, upper respiratory symptoms, restlessness, and agitation. According to the family, the patient had been on lithium therapy for the past nine years. There was no family history of any endocrine or renal diseases. On examination, her blood pressure was 156/76 mmHg, respiratory rate of 23/min, saturation 91% on room air, and a pulse rate of 101/min. The chest was clear on auscultation with no added sounds. Blood work showed a hemoglobin of 12.1 g/dL (normal: 14 - 17 g/dL), hematocrit - 45.2% (normal: 41% - 51%), WBC - 13 K/uL (80% neutrophils) (normal: 3.3 - 8.7 K/uL), platelets - 170 K/uL (normal: 147 - 347 K/uL), calcium - 9.4 mg/dL (normal: 9 - 10.5 mg/dL), blood urea nitrogen (BUN) - 26 mg/dL (normal: 8 - 20 mg/dL), creatinine - 1.1 mg/dL (normal: 0.7 - 1.3 mg/dL), sodium - 151 mmol/L (normal: (136 - 145 mmol/L), and lithium - 0.9 (therapeutic range (0.8 - 1.2). Respiratory pathogen viral polymerase chain reaction (PCR) was positive for influenza.
The chest X-ray was normal (Figure ). MRI brain did not reveal any underlying pathology (Figure ). Due to increasing agitation, she was intubated for airway protection and started on Tamiflu for influenza. She was transferred to the intensive care unit for further management. On day two of follow-up, the patient was found to have hypotonic polyuria with a 24-urine output of 7L, urine osmolality of 316 mOsm/kg, with serum sodium of 151 mEq/L and serum osmolality of 327 mOsm/kg (Table ). As her serum osmolality (327 mOsm/kg), and serum sodium (151 mEq/L) were above the threshold for maximal arginine vasopressin (AVP) secretion, a water deprivation test was not performed. Thus, we performed a desmopressin challenge test on day two. After desmopressin injection, her urine osmolality increased to 485 mOsm/kg, which was approximately 35% increase from baseline, less than 50% increase indicating partial nephrogenic diabetes insipidus (Table ). As lithium could not be discontinued in the patient (she had difficulty controlling bipolar disorder per psychiatry), she was started on amiloride for lithium-induced partial nephrogenic diabetes insipidus. On day three of follow-up, she was extubated. Subsequently, her hypernatremia resolved in the next three days with amiloride therapy. Serum sodium normalized to 141 mmol/L and urine output decreased to 2340 ml/24 hours. She was subsequently discharged to a long term care facility.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [101.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 101.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3027,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4664787-1,Extracted,"A 39 year-old gentleman presented to the Emergency Department with a two-day history of pleuritic chest pain, lethargy and associated symptoms of progressively increasing shortness of breath (now occurring with minimal exertion). This occurred on a background of more long-standing non-specific lethargy. There was a history of a recent long-haul flight from Nigeria to Ireland one week previously. At presentation, he exhibited a tachycardia of 116 beats per minute, blood pressure of 131/94 mmHg, and a respiratory rate of 22 breaths per minute.
An electrocardiogram revealed a sinus tachycardia with symmetrical T wave inversion in praecordial lead V3. Arterial blood gas analysis showed a PaO2 of 7.5 kPa, PaCO2 of 3.8 kPa, pH 7.47, and an oxygen saturation of 89%. A D-dimer assay performed at triage was significantly elevated at 10.5 mg/L. Given the working diagnosis of probable pulmonary embolus (high-risk pretest probability), therapeutic low-molecular-weight heparin (Enoxaparin 120 mg subcutaneously) was administered prior to emergent Computed Tomographic Pulmonary Angiography (CTPA).
Two hours later, while awaiting emergent CTPA, the patient collapsed and was found to be in cardiac arrest. Cardiopulmonary resuscitation was promptly initiated for pulseless electrical activity (PEA). Intubation with a cuffed oroendotracheal tube (COETT) was achieved without interruption of chest compressions. Despite primary confirmation of COETT placement, end-tidal CO2 was not detected initially. Subxiphoid ultrasound—performed during brief interruption of chest compressions—did not reveal a dilated right side of heart. Despite this, given the overall clinical picture at this juncture, a presumptive diagnosis of massive or saddle pulmonary embolus was made.
Along with conventional ACLS adrenaline therapy, rtPA (alteplase) 50 mg was promptly administered. Despite continuing high quality chest compressions and a gradual rise in quantitative end-tidal CO2, no cardiac output was detected after twenty minutes. A decision was taken to administer a second bolus of rtPA (alteplase) 50 mg. Ten minutes subsequent to this and following on-going advanced life support, return of spontaneous circulation (ROSC) was achieved with an initial non-invasive blood pressure of 144/50 mmHg.
Standard post-ROSC resuscitation care was instituted and this gentleman was admitted to the intensive care unit. A CTPA demonstrated multiple bilateral pulmonary emboli. He was continued on Enoxaparin and bridged to Warfarin once critical care stability was achieved. No major (or minor) bleeding was observed during this gentleman's hospital stay. The patient ultimately recovered to hospital discharge with a Glasgow Outcome Score of 4, secondary to watershed cerebellar infarcts.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [116.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 116.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3.0 + 1.5 = 4.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
3028,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8501896-1,Extracted,"A 66-year-old male with bipolar disorder and hypertension presented to the Emergency Room due to decreased level of consciousness 14 days after a COVID-19 diagnosis through real-time reverse-transcriptase polymerase chain reaction. He had been discharged from the hospital two days ago due to an atrial flutter and mild respiratory COVID-19 symptoms, with lung imaging showing 10-20% of ground-glass opacities. Vital signs at the present admission were 84 beats per minute with a sinus rhythm, blood pressure of 128/80 mmHg, and 94% oxygen saturation on room air. On physical examination, the patient was afebrile, with a Glasgow Coma Scale of 14, not oriented in time and space, with hyperreflexia and globally decreased strength. He presented no signs of meningism, no abnormal gait, no focal deficit, and no signs of respiratory distress nor hemodynamic instability. Laboratory testing revealed leukocytosis with normal differential, normal electrolytes, normal d-dimers, C-reactive protein of 5.9 mg/dl, creatinine of 3.49 mg/dl, urea of 175 mg/dl and serum lithium of 2.3 mEq/L, which was suspected to be the cause of his obnubilation. Brain computerized tomography (CT) only showed signs of microangiopathy, with no acute process explaining his mental state alteration (Figure ).
He was admitted to the hospital for further investigation and lumbar puncture was postponed due to the fact that the patient was taking anticoagulants because of his recent episode of arrhythmia. Lithium was suspended as it was hypothesized that his altered mental state could be caused by lithium intoxication. Despite his improvement of renal function and serum lithium level on the following days, the patient presented a worsening of his neurological status. His Glasgow Coma Scale decreased to 11 and he presented myoclonic movements in upper and lower limbs. Further investigation revealed a suppressed thyroid stimulating hormone (TSH), with normal anti-thyroid peroxidase (TPO), T3 and T4. Cerebrospinal fluid (CSF) showed no evidence of infection in the central nervous system (CNS). CSF analysis was clean, with glucose of 85 mg/dl, proteins of 10 mg/dl and normal leukocytes with predominant mononuclear cells. CSF testing was negative for tuberculosis, cryptococcosis and syphilis. There were identical IgG oligoclonal bands in CSF and plasma serum indicated systemic inflammation. Electroencephalogram (EEG) showed moderate cortical encephalopathy. Magnetic resonance imaging (MRI) revealed discrete ectasia of the supratentorial ventricular system, associated with slight erasure of the paramedian brain gyri, which may be associated with some degree of normal pressure hydrocephalus and also mild to moderate cerebral volumetric reduction (Figure ). Furthermore, in the T2 and T2/fluid-attenuated inversion recovery (FLAIR) sequences, there were rare foci of hypersignal in the periventricular and deep white substance, related to incipient microangiopathy.
By the fifth day after admission, the patient was hemodynamically stable, recovered his renal function and was breathing comfortably in room air. Despite the improvement of his general condition, his neurological status kept declining. Considering that other causes of primary CNS affection (such as meningitis, fungi infection, tuberculosis, autoimmune encephalitis and syphilis) were excluded, it was hypothesized that the patient’s impaired neurological status was due to a COVID-19-related encephalopathy. Based on previous studies reporting improvement of neurological condition of COVID-19 patients after corticosteroid treatment, pulse therapy with methylprednisolone 500 mg IV for three days was started on day five after admission. A significant improvement in his neurological condition was seen on the first day of therapy. He was discharged five days after the start of methylprednisolone with a complete recovery of his mental status. In an outpatient consult two weeks post-discharge, the patient remained with significant neurological improvement, but complaining of transitory aphasias and lapses of memory, happening three times a week and lasting for a few seconds. His new EEG had no abnormalities.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [84.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Surgery in the previous 4 weeks': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 84.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 0.
The patient's Well's score for pulmonary embolism is 0."
3029,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8349278-1,Extracted,"A 23-year-old male presented to the emergency department (ED) with a chief complaint of diarrhea for the last one week. On examination, his vital signs were as follows: temperature, 101.8 F; blood pressure, 125/76 mmHg; pulse rate, 126/min; and respiratory rate, 24/min. His blood oxygen saturation was 85% at room air and 95% with 5 L oxygen via nasal cannula. His body mass index (BMI) was 25.1 kg/m2. Chest examination revealed decreased breath sounds with bilateral crackles in the lower part of lung fields and normal first and second heart sounds.
Initial laboratory investigations revealed these results: white blood cell count (WBC), 7700/ul with lymphopenia; prothrombin time (PT), 16.6 seconds; international normalized ratio (INR), 1.4; activated partial thromboplastin time (APTT), 38.5 seconds; D-dimer, 3.85 mcg/mL, serum lactate dehydrogenase (LDH), 402 U/L; and C-reactive protein (CRP), 3.63 mg/dl. Arterial blood gas (ABG) analysis showed a pH of 7.53, paCO2 of 33 mmHg, paO2 of 62 mmHg, serum HCO3− level of 27.6 mmol/L, and alveolar-arterial (A-a) oxygen gradient of 46.5 mmHg.
A chest X-ray () showed patchy bilateral pulmonary opacities. The patient's clinical presentation of shortness of breath and hypoxia together with elevated D-dimer levels prompted a chest CT to rule out pulmonary embolism. The chest CT demonstrated notable diffuse bilateral ground glass opacities () and arterial embolism in the pulmonary arteries supplying the right middle and lower lobes.
Reverse-transcription polymerase chain reaction (RT-PCR) for COVID-19 ribonucleic acid (RNA) conducted on a nasopharyngeal swab sample of the patient revealed a negative result. However, the patient was still considered to have clinical COVID-19, given he had typical features of COVID-19 such as hypoxia, shortness of breath, elevated D-dimer, pulmonary embolism, and ground glass opacities on chest CT. Thereby, dexamethasone (6 mg) for COVID-19 and apixaban for pulmonary embolism were initiated. Decision was made to hold remdesivir since COVID-19 was not confirmed in this patient.
During further questioning, the patient reported productive yellowish cough during the last month coupled with anorexia and significant weight loss of 15 pounds. The insidious onset of the long-lasting symptoms and the radiological features characterized by ground glass opacities seen in Pneumocystis pneumonia as opposed to patchy and peripheral ground glass opacities of typical COVID-19 pneumonia () prompted further investigation for potential occult immunodeficiency. The fourth-generation Ag/Ab combination human immunodeficiency virus (HIV)-1/2 immunoassay showed a positive result for HIV-1 antibody and negative for HIV-2 antibody. Repeat PCR tests for COVID-19 on day 3 and day 5 of hospitalization were negative as well. Thereafter, IV trimethoprim-sulfamethoxazole 400 mg every 8 hours was started for possible Pneumocystis pneumonia (PCP) given the new diagnosis of HIV. Dexamethasone was switched to prednisone 40 mg oral twice a day.
Bronchoscopy was performed on day 4 of hospitalization, and bronchoalveolar culture, Gram stain, acid-fast bacilli (AFB) stain, silver stain, and Pneumocystis jirovecii PCR were performed on the specimen obtained. Cells obtained via bronchial washing were negative for malignancy, and no fungal elements were visualized by methenamine silver stain. No acid-fast bacilli were detected on AFB staining, and neither any Mycobacterium species was isolated in the mycobacterial culture. HIV viral load was 1.4 million copies/ml, and total cluster of differentiation 4 (CD4) count was <20 cells/mcl. Treatment with oral emtricitabine/tenofovir and oral dolutegravir was, thus, initiated.
PCR for Pneumocystis jirovecii on material obtained via BAL revealed a positive result. The patient's presentation of chronic symptoms as opposed to acute presentation of COVID-19 patients together with a positive HIV test, high viral load, low CD4 count, and positive PCR for Pneumocystis jirovecii contributed to establishing the diagnosis of Pneumocystis pneumonia. After one more week of continued treatment with IV antibiotics and prednisone, the patient's condition improved and he was discharged with instructions for home oxygen therapy and prescription for apixaban, trimethoprim-sulfamethoxazole (800 mg/160 mg), prednisone, dolutegravir, and emtricitabine/tenofovir.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [126.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 126.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3030,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3310787-1,Extracted,"A 38-year-old Japanese man with seronegative RA, diagnosed in the year 2004 by using the American College of Rheumatology (ACR) 1987 criteria, had received sulphasalazine and methotrexate (MTX) therapies before he visited our institute and was started on regular low-dose prednisolone therapy. Despite these therapies, his RA disease activity remained high (tender and swollen joints at the knees and ankles; patient global assessment score, 48/100 mm; C-reactive protein (CRP), 3.37 mg/dL; erythrocyte sedimentation rate (ESR), 48 mm/hour; matrix metalloproteinase-3, 1531 ng/mL; Disease Activity Score 28-ESR, 4.57). The patient was obese (175 cm, 95 kg, BMI (body mass index): 31.0); however, he neither had a history of other medical problems (no viral infection and a non-carrier) nor had he ever received surgical intervention. He did not require intra-articular steroid injection. IFX at a dose of 3 mg/kg (total dose, 285 mg) was introduced in addition to MTX (10 mg weekly), prednisolone (5 mg daily), and folic acid (5 mg weekly). He suffered no immediate adverse effects and experienced excellent pain relief in his knees and ankles the day after his first infusion of IFX, but six days after infusion he presented with a fever of 40°C, chills, and polyarthralgia including the knees and ankles that persisted for two days, and he was admitted to hospital.
At admission (day 0, eight days after his first infusion), his body temperature was 40.6°C and he was tachycardic (107 beats/minute) with 104/68 mmHg blood pressure. His heart sounds were normal and he had no visible rash. The affected joints (knees, ankles, and right wrist) were swollen, painful, and warm. There was no evidence of a primary source of infection. Laboratory data showed marked acute inflammation (CRP, 31.0 mg/dL; white blood cells, 19,200/mm3) and pre-disseminated intravascular coagulopathy and shock (prothrombin time (PT), 62.2%; activated partial thromboplastin time (APTT), 45.1%; fibrinogen, 804 mg/dL; serum fibrin/fibrinogen degradation products (FDP), 14.7 μg/mL). Findings from chest computed tomography (CT) (Figure ), urine smears, and cultures were all normal, and he had no symptoms involving the abdomen or pelvis. Fluid drawn from the knees was purulent and its smear revealed numerous gram-positive cocci arranged in chains, which were subsequently identified as S. pneumoniae at day five. He was clinically diagnosed with bacterial septic polyarthritis. Emergency surgical joint lavage and drainage was then performed at the knees, along with needle aspiration and lavage of the ankles and right wrist just after admission (day 0). He was treated with intravenous antibiotic therapy with cefazolin (2 g twice daily at days 0 and one) and vancomycin (1 g once daily at days one and two). At day two, a whole body CT showed auxocardia and hydrothorax, but no pneumonia or other abnormal findings (Figure ). Two blood cultures taken at day 0 revealed penicillin-sensitive S. pneumoniae (minimal inhibitory concentration of penicillin G ≤ 0.03 μg/mL) with no penicillin-resistant strains at day two. He was switched to ceftriaxone (2 g twice daily at day two and thereafter for a total of 29 days). He made a rapid and sustained recovery with intensive rehabilitation. He was discharged on day 37 with 10 mg weekly of MTX, when he returned to his preadmission state (Figure ).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [107.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 107.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
3031,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-8907,Extracted,"A 23-year-old woman presents to the emergency department complaining of nausea, vomiting, and abdominal pain. She has a 10-year history of type I diabetes mellitus treated with lispro and glargine. Upon questioning, she mentions that she stopped taking her insulin 3 days ago due to recent malaise and decreased appetite. She denies recent weight change, illicit drug use, or sexual activity. She does not take any other medications and she does not use tobacco products or alcohol. Upon physical examination she is afebrile. Her blood pressure is 105/70 mm Hg, pulse is 108/min and respiratory rate is 25/min. She appears lethargic, with clear breath sounds bilateral and a soft, nontender and nondistended abdomen.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [108.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 108.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3032,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5107853-1,Extracted,"A man aged 28 years was admitted to our clinic with symptoms of shortness of breath, cough, numbness, pain, and coldness in the lower extremity. His medical history showed that he had heart failure and he had a pacemaker. Approximately 15 days before presenting to our clinic, he had symptoms of fatigue, cough, sore throat, and fever. In the physical examination, he was found to have 130/70 mm Hg blood pressure, 20/min respiratory rate, 37°C body temperature, 108/min pulse rate, and bilateral, crepitant rales in his lungs, and bilateral lower extremity pulses were not detected.
The laboratory examination revealed the following values: glucose 146 mg/dL (100–125 mg/dL), blood urea nitrogen (BUN) 18 mg/dL (9–23 mg/dL), serum creatinine (CRE) 1.4 mg/dL (0.6–1.2 mg/dL), total protein 6.4 gr/dL (5.7–8.2 gr/dL), albumin 3.8 gr/dL (3.2–4.8 gr/dL), amylase 159 IU/L (28–100 IU/L), alkaline phosphatase 94 IU/L (35–105 IU/L), alanine aminotransferase (ALT) 24 IU/L (0–32 IU/L), aspartate aminotransferase (AST) 36 IU/L (0–33 IU/L), lactate dehydrogenase (LDH) 4121 IU/L (135–214 IU/L), creatinine kinase (CK) 908 IU/L (26–192 IU/L), gamma glutamyl transferase 62 IU/L, sodium 132 mEq/L (135–145 mEq/L), potassium 4.2 mEq/L (3.5–5.5 mEq/L), erythrocyte sedimentation rate 18 mm/hr, CRP 154 mg/L (0–8 mg/L), white cell count 15 000 mm3/μL, neutrophil 89%, lymphocyte 3%, hemoglobin (Hb) 13 gr/dL (13–17 gr/dL), Htc 41% (36–48%), and platelet count 280 000/mm3 (150 000–400 000/mm3). Arterial blood gas was metabolic acidosis (pH 7.29, PO2 76 mm Hg, PCO2 34 mm Hg, HCO3 18 mEq/L). Abdominal computerized tomography (CT) angiography was performed to test for thromboses, which revealed a thrombosis in the infrarenal aorta (), and thorax CT angiography revealed pleural effusions of 2.8 cm in the right hemithorax and 1.6 cm in the left hemithorax, prevalent ground-glass areas in the parenchyma of both lungs, and reticulonodular infiltrates showing nodule formation, which were dominant in the upper lobe of the left lung but prevalent in both lungs.
Patient was presented with instantaneous severe lower limb pain, coolness, paleness, and absence of pulses and CT angiography confirmed infrarenal aorta thrombosis. Therefore, we decided to perform emergency surgery. Under local anesthesia bilateral common femoral artery exposed and femoral embolectomies were performed after the administration of heparin, and a large amount of fresh thrombus material was retrieved. Immediately after femoral circulation was restored. After the operation the patient was transferred to intensive care unit.
In the postop laboratory evaluations the following results were obtained: glucose 139 mg/mL, BUN 41 mg/dL, CRE 4 mg/dL, ALT 103 IU/L, AST 641 IU/L, CK 11915 IU/L, LDH 2625 IU/L (135–225 IU/L), sodium 129 mEq/L, potassium 6.0 mEq/L, INR 2.2, leucocyte count 17000/mm3, Hb 10 gr/dL, Htc 30, and Plt 187 000 mm3 (lymphopenia presence 3%). Urinalysis was not performed because the patient was anuric. Enoxaparin treatment was initiated due to thrombosis. Empirical moxifloxacin treatment was given owing to the prediagnosis of pneumonia. No growth was reported in the blood culture. The patient was diagnosed as having anuric acute kidney injury (AKI), Kidney Disease: Improving Global Outcomes (KDIGO) stage 3 and taken into hemodialysis after catheterization. Autoantibody analysis was requested because of the AKI etiology and the results (P-ANCA, C-ANCA, anti-Ds DNA, and ANA) were negative with negative components and negative rheumatoid factor. In the analyses requested to evaluate thrombosis, anti-thrombin III and protein C values were normal, protein S 50% (55–160) was slightly low, and anticardiolipin and antiphospholipid antibody results were negative. Serum Legionella pneumophila was negative in the patient who had hyponatremia (sodium 129 mmol/L) and pneumonia.
PCR analysis conducted on nose and throat swap samples was positive for H1N1. Oseltamivir was added to the patient's treatment. Four units of erythrocyte suspension were given upon a decrease in the patient's Hb value. Fever was detected in the follow-up examination conducted two weeks after the initiation of treatment and cultures were taken from the patient. Piperacillin-tazobactam was added to the treatment. On the 17th day of hospitalization, the patient had sudden shortness of breath and the following clinical values: blood pressure 80/30 mm Hg, body temperature 37°C, respiratory rate 30/min, and pulse 108/min, and rales were present in his lungs. Growth of Acinetobacter baumannii was observed in a blood culture. Arterial blood gas was respiratory and metabolic acidosis (pH 7.11, PCO2 65 mm Hg, PO2 45 mm Hg, and HCO3 15 mEq/L). The patient was evaluated to have sepsis and was intubated and connected to mechanical ventilation, and inotrope treatment was initiated. Despite the inotrope treatment, the patient was hypotensive and died on the 17th day of treatment.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [108.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 108.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 = 6.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
3033,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5095088-2,Extracted,"A 60-year-old man with a history of hypertension, variant angina, and hyperthyroidism developed high fever, cough, sputum, myalgia and dyspnea 4 days before admission. He was admitted to our hospital with a presumptive diagnosis of community-acquired pneumonia and treated with empirical antibiotic therapy comprising piperacillin–tazobactam and levofloxacin (Fig. ). His systolic blood pressure was 100 mm Hg, heart rate 126 beats/min, respiratory rate 36/min, and body temperature 39 °C. The initial laboratory findings were as follows: WBC 14,500/mm3, platelets 237,000/mm3, CRP 302.6 mg/L, BUN 29.8 mg/dL, and creatinine 1.18 mg/dL. Liver function tests were within normal ranges. The initial O2 saturation was 85% and he received O2 (5 L/min) via facial mask. On day 3, his chest X-ray findings were worse and his oxygen requirement was increased. The patient was transferred to the ICU and treated with a non-invasive positive pressure ventilator. However, his severe hypoxemia was not improved (SaO2 = 94% with FiO2 100% and respiratory rate = 45/min), and he was intubated. On ICU day 2, his severe hypoxemia was not improved despite mechanical ventilation (i.e., PaO2/FiO2 = 67.6 with a PEEP of 15 cm H2O), and his heart rate increased to 151 beats/min (SAPS II, 36). We decided to apply VV ECMO, and started CRRT for fluid management. The initial ECMO settings were as follows: blood flow 5.0 L/min, sweep gas flow 4.5 L/min, and FiO2 1.0. On ECMO day 4, a PCR test for HAdV in a sputum sample taken at the time of admission was positive; based on this finding, the patient was administered cidofovir 5 mL/kg/week. The cell differential in the BAL fluid was as follows: neutrophils 43%, lymphocytes 34%, macrophage 22%, and eosinophils 1%. All tests of the BAL specimen for bacteria and viruses were negative. Although his blood gas oxygenation and chest X-ray showed an initial improvement during the early period of VV ECMO support, they were again worse on ECMO day 7 (Fig. ). Therefore, we started treatment with methylprednisolone 2 mg/kg q 24 h, which was then tapered slowly. We attempted to maintain a conservative fluid strategy (Table ) and the PaO2/FiO2 ratio and chest X-ray findings began to improve from ECMO day 9. On ECMO day 12, a tracheostomy was performed and ECMO and CRRT were removed on ECMO day 24. His net fluid balance was +10,219 mL (+425.8 mL/day) throughout the ECMO treatment (Fig. ). The patient was transferred to a general ward on ICU day 32 and finally discharged home. At his 1-year follow-up assessment, the patient was ambulatory and able to perform light housework.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [151.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 151.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3034,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6906696-1,Extracted,"A 26-year-old female presented, walking, to the emergency department with a 2 week history of abdominal pain radiating to the back. This was associated with a 2 day history of nausea and vomiting following an alcohol binge. On one episode the vomitus was noted to be blood stained. She had no prior medical, surgical or family history. She consumed alcohol regularly and had a binge on the two days prior. She consumed Non-Steroidal Anti-Inflammatory Drugs (NSAID) chronically and had an eight-pack-year history of smoking.
On arrival she had a blood pressure of 124/64 mmHg and was tachycardic with a heart rate of 118bpm. She had a temperature of 37 °C. Her urine dipstick and pregnancy tests were negative. On examination she had epigastric tenderness but her abdomen was soft and she had no signs of peritonitis. Her cardiovascular, respiratory and central nervous system examinations were unremarkable. She had no malaena or blood on rectal examination.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [118.0, 'beats per minute'], 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 118.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3035,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-10095,Extracted,"A 57-year-old woman presents to an outpatient clinic with lower extremity weakness and lower back pain. The patient says that her symptoms began 2 weeks ago when she was working in her garden and have progressively worsened to the extent she currently is unable to walk on her own. She describes the pain as sharp, severe and descending bilaterally from her lower back to her lateral ankles along the posterior surface of her thighs and legs. She also states that she has had several episodes of urinary incontinence for the past couple of days. The patient denies having any similar pain or incontinence in the past. No other significant past medical history. Current medications are alendronate 5 mg orally daily and a daily multivitamin. Her temperature is 37.0℃ (98.6℉), the blood pressure is 110/70 mm Hg, the pulse is 72/min, the respiratory rate is 15/min, and oxygen saturation is 99% on room air. On physical examination, the patient appears to be in significant distress. Strength is ⅗ in her thighs bilaterally and ⅖ in the legs bilaterally left greater than right. Muscle tone is decreased in the lower extremities. The patellar reflex is 1+ bilaterally and plantar reflex is 0+ bilaterally. Fine touch and pain and temperature sensation are decreased in the lower extremities bilaterally, left greater than right. Saddle anesthesia is present.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [72.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 72.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3036,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8387082-1,Extracted,"A 38-year-old male presented to the emergency department with worsening chronic right lumbar pain associated with legs and scrotum edema. He also had itchy and erythematous cutaneous lesions on the abdominal wall over the last 8 months, with no remission despite numerous therapeutic attempts, and complained of diffuse mild to moderate abdominal pain. He denied weight loss, fever, or night sweats. He was a smoker, and his past medical history included unilateral (right) polycystic kidney disease with functional renal exclusion and a left vicariant kidney (he was waiting for a right nephrectomy) and pulmonary tuberculosis in 2003. He frequently used diclofenac, paracetamol, caffeine, and carisoprodol for his chronic lumbar pain.
On admission, he had a good general appearance, no signs of respiratory distress, no alterations in skin color. His heart rate was 95 bpm, blood pressure 166 x 104 mmHg, and room air oximetry were 96%. There were eczematous desquamating skin lesions on his thighs and legs. There were no enlarged lymph nodes. Chest auscultation revealed decreased breath sounds and dullness to percussion at the right lung base. On abdominal palpation, the liver was enlarged, palpable up to 5 cm below the costal margin and was slightly tender. His legs had 2+ symmetrical pitting edema extending from his feet to just above his knees. Laboratory workup revealed mild anemia (Hb 10.8 g/dl), normal white blood cell, and platelet count. The hepatic enzymes, bilirubin, creatine kinase, lactate dehydrogenase, uric acid, and electrolytes were within the normal range. However, the creatinine was 1.47 g/dL (RR: 0.70 - 1.20 g/dL) and the creatinine clearance estimated by the CKD-EPI equation was 69 mL/min/1.73m2. C-reactive protein (32 mg/L; RR: < 3 mg/L) and erythrocyte sedimentation rate (46 mm/1h) were increased. HIV, HCV, syphilis, and Hepatitis B virus serologies yielded negative results. The rheumatoid factor and antinuclear antibodies were negative, and the complement was normal. Urinalysis revealed 1+ of protein and 150 x 103 red blood cells/mm3.
Abdominal computed tomography (CT) showed a large, contrast-enhanced mass (10 x 8 x 4cm) involving the abdominal infrarenal aorta and the iliac arteries and compressing the inferior vena cava with dilated iliac veins and the left ureter (), raising the hypothesis of the lymphoproliferative disease. The liver had normal size but had a heterogeneous attenuation.
The chest CT showed a diffuse pleural thickening in the right hemithorax with a small loculated pleural effusion, and enlarged mediastinal and peri-esophageal lymph nodes.
The patient was admitted with the working diagnosis of a lymphoproliferative disease for a confirmatory diagnostic workup. A double J ureteral stent was placed in the left ureter. A CT-guided biopsy of the right pleural thickening was performed, which lacked a precise diagnosis. The patient was submitted to a laparoscopic-guided biopsy of the peri-aortic mass. This biopsy showed a fibro-connective tissue exhibiting fibrosis, obliterating phlebitis, and moderate mixed inflammatory infiltrates with few eosinophils, histocytes, and small lymphocytes and frequent plasma cells (
).
The immunohistochemical examination () showed an increased number of IgG4 positive plasma cells. The IgG4/IgG ratio of 30% and approximately 80 IgG4 positive-plasma cells per high-power field (HPF) in areas of more density. This examination, together with the morphological and clinical findings, is highly suggestive of IgG4-RD.
The patient was started on 1.0 mg/kg/day of prednisone for 2 weeks and then tapered for 0.6 mg/kg/day for two months, and to 20 mg/day for 3 months, afterward. The outcome was favorable and he gradually recovered his previous health status. The abdominal and lumbar pain ceased in about 3 weeks after starting treatment, his hemoglobin level returned to normal and his inflammatory markers decreased. Five months after initiation of corticotherapy, a new abdominal CT scan was done (), and the initial contrast-enhanced mass had almost disappeared, but it showed an inferior vena cava thrombosis extending to bilateral external iliac veins. He was started on warfarin. The double J ureteral stent was removed, and the patient remains asymptomatic with a good urine output with no renal function impairment. At the closure of this manuscript, he was asymptomatic and taking only 5 mg/day of prednisone.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [95.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 95.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3 + 1.5 = 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
3037,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3956996-1,Extracted,"A 46-year-old female underwent abdominal computed tomography (CT) imaging at a private clinic due to mild right upper quadrant abdominal discomfort and back pain during the previous 2 weeks. She was referred to our hospital to evaluate the cause of IVC dilatation shown by abdominal CT (). The patient had no history of hypertension or diabetes mellitus and no family history of aortic, collagen, vascular or congenital heart disease. She had latent hepatitis B virus infection and her mother died of hepatocellular carcinoma. Ultrasonography of the liver showed hepatic vein dilatation without obstruction or thrombus in either the hepatic vein or IVC. The abdominal CT showed prominent dilatation of the IVC and hepatic vein with no evidence of liver disease such as cirrhosis, hepatocellular carcinoma or Budd-Chiari syndrome. Her vital signs included blood pressure of 107/64 mmHg, pulse of 60 beats per minute, respiration of 20 breaths per minute, and body temperature of 36.5℃. During the physical examination, cardiac auscultation revealed no definite murmurs and her electrocardiography demonstrated no apparent ST segment or T wave abnormalities. The blood chemistry analyses were within normal limits, including N-terminal pro-B natriuretic peptide, coagulation studies with fibrinogen, antinuclear antibody, complete blood cell count, and liver enzymes. Her heart size was normal on chest X-ray. Transthoracic echocardiography was performed to evaluate right side heart abnormalities. Dilated IVC with diminished inspiratory collapse was observed (expiration 24.3 mm, inspiration 21.4 mm) using a subxiphoid approach to view the IVC along the longitudinal axis (). Spontaneous echo contrast was present in the dilated IVC without flow obstruction including the entry from the RA. The hepatic vein was dilated mildly (13.2 mm), but the flow through the hepatic vein was normal (). Tricuspid regurgitation (TR) was mild and showed normal right ventricular (RV) systolic pressure (). Normal pulmonary artery (PA) pressure without regurgitation or stenosis () and normal flow of the superior vena cava were observed. The RV size and its contractility were normal with a normal degree of tricuspid annulus displacement toward the apex in the systole (1.75 cm). Additionally, we observed normal left ventricle (LV) size and LV systolic function (ejection fraction = 68%) without regional wall motion abnormalities. Normal RA pressure, RV pressure, and PA pressure were observed (), and the RA pressure was decreased with an inspiratory effort (-2 mmHg). As the patient had no symptoms or abnormal signs, we observed her and plan to follow-up annually with echocardiography.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [60.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 60.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3038,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4165973-1,Extracted,"A 30-year old, gravida 1, para 0, woman at 24th week of pregnancy presented with right lower quadrant pain, fever and nausea. Axillary body temperature and pulse rate were 37.3oC and 104/min, respectively. Abdominal examination revealed tenderness, guarding, and rebound tenderness at the right side of the uterus. White blood cell count was 19,500 cells/mm3 with 92.8% neutrophils.
The sonographic examination did not reveal any findings consistent with acute appendicitis exception for periceaceal fluid and it showed a normal intrauterine pregnancy. With a preoperative diagnosis of acute appendicitis, a laparotomy was done via a paramedian incision in the right side of the abdomen. Appendix was erythematous and appendicectomy was performed.
The histopathological examination of the appendix revealed acute appendicitis with extensive deciduosis of the appendiceal wall of all the three layers. There were also glandular structures among the decidua which were positive with cytokeratin 7, while the adjacent appendicial mucosa was negative. The diagnosis was endometriosis and decidiosis of appendix and acute appendicitis. The patient was discharged with antibioteraphy without further complaints.
One month later, at 28 weeks’ pregnancy, the patient came again with left lower quadrant pain, high fever and vomiting. Her temperature and pulse rate were 38.5oC and 110/min, respectively. At physical examination, the patient had 7 months of pregnant uterus and acute abdominal findings consisting of mainly left lower quadrant tenderness. Laboratory results showed a white blood cell count of 23, 800 cells/mm3. A pelvic sonogram revealed a normal intrauterine pregnancy at 28 weeks and free fluid between the intestinal structures and a 5 cm complicated left ovarian cystic mass compatible with tubo-ovarian abscess. At laparotomy with a median subumbilical incision, a small amount of purulent free fluid and extensive pelvic deciduosis covering all the pelvic peritoneal surfaces with left tuboovarian abscess was observed. The abscess was drained and left salpingectomy was performed.
Papillary excrescences were observed protruding into the lumen of the mass and ovarian biopsies were obtained. The abdominal cavity was washed with warm saline solution and a drain was placed in the Douglas pouch for drainage which was removed 3 days later. Early postoperative recovery was uneventful but on the 5th postoperative day the patient had uterine contractions and tocolytic therapy was initiated with nifedipine. She gave birth to a 1400 gr healthy male baby with spontaneous vaginal delivery.
Histo-pathological examination revealed ovarian endometriosis with marked decidual changes and hemosiderin-laden macrophages as well as moderate amount of polynuclear leukocytosis in cyst wall. The final pathological report confirmed infected endometrioma with deciduosis. Postoperatively patient received tazocin antibiotherapy for 3 weeks and discharged from the hospital without further complications. At the second postpartum month she was completely recovered and her baby was doing well without any complications related to prematurity.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 =  3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3039,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8364437-1,Extracted,"A 74-year-old female patient came in for a follow-up with an extensive past medical and surgical history. During the visit, her vital signs were as follows: blood pressure, 133/83 mmHg; heart rate, 88 beats/min; temperature, 97.5°F; respiratory rate, 16/min; and body mass index, 27.16. Her medications were the following: vitamin D, potassium, magnesium, aspirin 81 mg/day (calcium supplement), glucosamine capsule, and prednisone 20 mg as needed.
Past medical history: The patient has a past medical history of skin cancer, endometrial cancer, and Schneiderian papilloma of the right mastoid.
Past surgical history: The patient had undergone a bilateral hip replacement, hysterectomy, hemorrhoidectomy, breast lump resection, tubal ligation, resection of Schneiderian papilloma (June 2018), and excision of skin cancer from the right leg (December 2019).
In 2014, the patient presented with right-sided hearing loss. In 2017, her right tympanic membrane was perforated, with blood and abnormal tissue protruding from the eustachian tube orifice. Right ear tympanostomy tubes were placed, which helped. The tube eventually fell out, and the tympanic membrane healed. She had a recurrence of middle ear effusion, for which a computed tomography (CT) scan of the right temporal area was performed. The CT images with and without contrast showed complete opacification of the right middle ear cavity and mastoid air cells.
Because of the opacification of the middle ear and the mastoid air cells, an audiogram was recommended to test the extent of hearing loss. The results demonstrated mild sloping profound sensorineural hearing loss of the right ear with a conductive component at 2 kHz and mild sloping profound sensorineural hearing loss of the left ear. The pure tone averages were 60 dB in the right ear and 28 dB in the left ear. The word recognition scores were 36% on the right and 92% on the left. The fiber-optic examination revealed blood draining from the right eustachian tube orifice. The magnetic resonance imaging (MRI) results showed extensive fluid throughout the mastoid air cells and the middle ear with some relative enhancement.
She underwent right trans-temporal craniotomy and partial resection of the mass in January 2018. Histopathology was performed on the excised mass, which was reported as an ELST. In May 2018, a follow-up MRI revealed the recurrence of the lesion, and on physical examination, the lesion was protruding through the eardrum associated with otorrhea. In June 2018, a re-resection of the lesion was done, and this time, the eardrum, malleus, incus, and external canal bones were removed. There was a portion along the petrous bone and carotid artery where the tumor could not be removed, and the tumor extended from the middle fossa dura to the sigmoid sinus.
The patient then underwent radiation therapy (60 Gy in 30 fractions). In November 2019, the patient developed right facial palsy, which was treated with two weeks of prednisone without resolution. A follow-up MRI showed a new 5-mm nodule in the right nasopharynx. There was no radiographic reoccurrence of the tumor in the right temporal bone/fossa, and there was no evidence of facial nerve involvement.
In January 2020, the patient underwent a right-sided nasopharyngeal eustachian tube biopsy. The biopsy specimen was sent and processed in the pathology department, and the report showed a low-grade papillary neoplasm consistent with an ELST origin. The patient was scheduled for a follow-up MRI and CT in the next six months. The details about how the biopsy specimen was processed and the histopathological diagnostic features of ELST are discussed in the Methods and Materials sections below.
Methods and materials
The biopsy specimen was processed by fixing in formalin and embedding in paraffin before sectioning and fixing on glass slides. After the slides were processed and ready, they were stained with hematoxylin and eosin (H&E). In addition to H&E, some selected slides were also stained with periodic acid Schiff.
An immunohistochemistry (IHC) study was performed using the EnVision method. The process of immunostaining implies the selective recognition of antigens (proteins) in the tissue sections of cells by utilizing the fundamental rationale of antibody binding particularly to the antigens in the biological tissue. The antibodies that were used for IHC in this case of ELST were cytokeratin 7 (CK-7), pan-keratin, cytokeratin 20 (CK-20), cytokeratin 19 (CK-19), vimentin, glial fibrillary acid protein (GAF), thyroglobulin, and Ki-67. The slides were boiled under high pressure with citrate buffer (0.01 mole/L, pH 6.0) for the purpose of antigen retrieval. The proper positive and negative controls were also performed.
Histopathology
Low Power
Morphologically, at low power, the specimen showed mostly papillary and focally glandular architecture. The neoplastic proliferation of the tumor cells comprised columnar and focally cuboidal cells with round to oval nuclei that show mild to moderate pleomorphism with abundant extracytoplasmic mucin (Figures , ). As mentioned above, the tumor cells were generally columnar or cuboidal and cohesive, often with distinct cell boundaries. Above the basement membrane and underneath the luminal cells was a layer of conspicuous myoepithelial cells. The epithelial cells have a clear-pale cytoplasm, luminal, central, and uniform nuclei. In the case of infected and old healing lesions, inflammatory infiltrates were often present next to neoplastic cells along with granulation tissue.
High Power
On higher magnification, a single layer of columnar to cuboidal cells lined the papillary and glandular structures. Moderate to mild pleomorphism, rare mitotic activity, and necrosis were not observed. On the other hand, multiple acinar configurations with infiltrative growth patterns and desmoplastic responses were seen (Figure ). Unconventional microscopic features that were not observed in our case of ELST but may be present in others include intermittent thyroid-like hypercellular regions with cystic glandular spaces filled with colloid substances, areas of hemorrhage, and necrosis with cholesterol clefts, mitotic figures, and structures that appear similar to choroid plexuses papillomas.
Immunochemistry
As described in the Methods and Materials sections, an IHC study was performed. CK-20, which highlights papillary growth, was negative, whereas CK-7 immunostaining was positive as evident in Figures , .
Diagnostic modalities for an ELST
Radiography
In this case of ELST, both CT and MRI were used as the imaging diagnostic tools. The CT scan and MRI results showed opacifications in the middle ear and the mastoid air cells in 2018, during the initial presentation of the patient. After partial resection of the lesion, the patient developed a nasopharyngeal mass along with middle ear effusion, which was diagnosed through a CT scan and MRI in January 2020.
The CT scan and MRI techniques are widely used to diagnose ELST []. The CT scan images usually show a lytic temporal bone mass that typically extends into the posterior cranial cavity, which may present as a cerebellopontine angle tumor. In most cases, the tumor center rests at or near the temporal bone at the posterior medial surface [,].
Angiography and Audiogram
Apart from the imaging modalities, the most sophisticated procedure to diagnose an ELST in clinical practice is angiography. Compared to an angiography, an audiogram is a noninvasive test that was performed in this case of ELST. The audiogram showed that the patient had significant hearing loss in the right ear and moderate hearing loss in the left ear because of an invading ELST. A fiber-optic examination was also performed, which showed blood draining into the eustachian tube.
Angiography was not performed on this patient. However, according to previous angiography results in the literature, the tumor can have a dual blood supply from intra- and extra-cranial sources, making it extremely vascularized. A jugulotympanic paraganglioma is another entity that can mimic ELST because both of these tumors are highly vascularized and can carry potential bleeding risks [].
Differential Diagnosis of ELST
Intrinsic temporal bone neoplasms are included in the differential diagnosis for ELSTs, with paragangliomas being the most common. Meanwhile, metastatic papillary thyroid carcinoma, metastatic renal cell carcinoma, and choroid plexus papilloma are histologically similar to ELSTs. The ELSTs are papillary cystic structures lined with a simple cuboidal or columnar epithelium and are heavily vascularized. Clear cells, as well as siderophages and cholesterol clefts, are visible (vacuolated cells). Nuclear pleomorphism is minimal, and mitoses are uncommon [,].
Staging
There are no universally accepted staging recommendations. Bambakidis et al. suggested the system described in Table [].
Schipper et al. defined type A tumors as those with no temporal bone destruction or dura invasion, type B as those with signs of osseous labyrinth infiltration and sensorineural hearing loss, and type C as those that have invaded the sigmoid sinus and jugular bulb [,].
The patient in this case underwent resection for a tumor that extended into the sigmoidal sinus and middle cranial fossa. If we follow the proposed staging system, then it is obvious that the tumor was an aggressive one, and the patient presented as stage III at the time of treatment.
Treatment
Complete resection with negative margins is the treatment of choice for ELST, but in advanced cases, this may not be possible. As the patient presented as ELST stage III, the only universally accepted treatment of choice is complete resection of the neoplastic tissue, which is recommended. Because of the complexity and advanced stage of the disease, the tumor was only partially resected. Under general anesthesia, she underwent a trans-temporal craniotomy and a partial resection of the lesion, along with resection of the eardrum, malleus, incus, and external canal bones. There were portions along the petrous bone, carotid artery, middle cranial fossa, and sigmoid sinus where the tumor could not be removed.
After the surgical resection, adjuvant radiotherapy and chemotherapy were administered with subsequent follow-ups. In January 2020, her follow-up MRI results showed a 5-cm lesion in the nasopharynx that was biopsied and confirmed as a reoccurrence of the ELST. The relapse of the ELST after resection confirms the aggressive nature and high recurrence rate of this condition.
Because the tumor relapsed, follow-up CT scans and MRIs were scheduled every six months, and close monitoring was recommended. From the patient's past medical and surgical history, she developed the ELST after the resection of the Schneiderian papilloma. Schneiderian papillomas are mostly benign, non-aggressive neoplasms that arise from the sinonasal mucosa. The development of ELST from a Schneiderian papilloma is quite rare. The pathological variants, classification, differentials diagnoses, etiological factors, clinical features, and treatment modalities of ELST and Schneiderian papillomas are elaborated in detail in the Discussion section.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [88.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 88.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
3040,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8201668-1,Extracted,"Our patient is a 20-year-old Filipino male diagnosed with SLE 6 months prior and was started on hydroxychloroquine. The patient presented to the emergency department after sudden onset of dyspnea, pleuritic chest pain, generalized fatigue, dry cough, fevers and chronic progressive rash. His review of systems was negative for sick contacts, recent travel, engagement in high-risk sexual activity, intravenous drug use, was a lifetime nonsmoker, and did not consume alcohol. On evaluation, vitals were notable for normal blood pressure (118/72 mmHg), tachycardia (118 beats per minute), tachypnea (respiratory rate 22 breaths per minute), and fever (100.8 °F). His cardiovascular exam was unremarkable for murmurs, elevated jugular venous pressure, splinter hemorrhages, or lower extremity edema. No cyanosis, clubbing, scleral icterus, organomegaly, or lymphadenopathy was appreciated. The skin examination showed no oral ulcers or alopecia, but demonstrated hyperpigmented to violaceous, scaly plaques with excoriated papules involving the bilateral extremities, back, and chest worsened as shown in Fig. . A prior skin punch biopsy of a similar rash (Fig. ) showed lichenoid dermatitis with features of interface changes and chronic inflammation suggestive of cutaneous SLE. This rash had improved from his index presentation following treatment with hydroxychloroquine, though not fully resolved. Laboratory data on admission revealed the following: leukopenia, anemia, and non-nephrotic range proteinuria without active urinary sediment on urine microscopy. There was evidence of acute myocardial injury with elevated cardiac biomarkers along with an elevated N-terminal pro-brain natriuretic peptide. Additionally, inflammatory biomarkers were elevated with hypocomplementemia, positive antinuclear antibody (ANA) with anti-Smith, ribonucleoprotein, chromatin, SS-A, double-stranded DNA, perinuclear anti-neutrophil cytoplasmic antibodies (pANCA), and myeloperoxidase positivity. Comprehensive laboratory evaluation for additional workup and the reference ranges is shown in Table . His electrocardiogram and telemetry monitoring demonstrated normal sinus rhythm with diffuse < 1 mm ST-segment elevations in leads without any ischemic changes. Initial chest x-ray showed no acute cardiopulmonary process. Further infectious evaluation demonstrated positive blood cultures for methicillin-sensitive Staphylococcus aureus (MSSA) with a likely skin source from aggressively scratching a purulent lesion on the right anterior thigh. Initial transthoracic echocardiogram showed normal LVEF with all other normal parameters. Given concerns for sepsis secondary to presumed cellulitis, in the setting of SLE flare, he was treated with broad spectrum intravenous (IV) antibiotics and corticosteroids (methylprednisolone 1 g/kg for three days) before his transfer to our institution. Given concerns for endocarditis with persistent fevers on arrival, repeat transthoracic and transesophageal echocardiograms demonstrated mildly reduced LVEF 45% with no valvular pathology. MSSA bacteremia resolved within 72 h of intravenous antibiotics (cefazolin 2 g IV every 8 h), but the patient later developed a rapid cardiopulmonary decline on hospital day #5 with worsening dyspnea, pleuritic chest pain, and hemoptysis. A repeat chest x-ray (Fig. ) and CT chest (Fig. ) were obtained demonstrating dense pulmonary bilateral pleural effusions with dense consolidations, pulmonary nodules, possible pulmonary emboli within the left subsegmental pulmonary artery branches, and pericardial effusions. A repeat transthoracic echocardiogram demonstrated a severely reduced LVEF 25%, moderate global hypokinesis, and small pericardial effusion without evidence of tamponade (Fig. ). Other abnormal findings included elevated right atrial pressures (15 mmHg) and mild pulmonary hypertension (43 mmHg) with a normal left atrial pressure, right ventricular systolic function, left ventricular diastolic function, and valvular function. Given clearance of bacteremia with IV antibiotics, cardiogenic shock was favored over septic shock. Intravenous vasopressors (norepinephrine, 0.4mcg/kg/min IV infusion) for shock, diuretics, amiodarone drip for atrial fibrillation with a rapid ventricular response, heparin drip for submassive pulmonary emboli, high-dose corticosteroids (solumedrol 500 mg IV every 12 h) and hydroxychloroquine 400 mg daily for SLE related co-activity were initiated. A cardiac MRI (CMR) was subsequently pursued to clarify the cause of myocarditis, which demonstrated a LVEF of 25% and moderate global hypokinesis with worsening pericardial effusions (Fig. ). Unfortunately, the patient’s poor respiratory reserve and tachycardia limited our ability to perform late gadolinium enhancement. With his continued clinical decline potentially requiring escalating hemodynamic support, he was transferred to a medical center with advanced heart failure treatment capabilities.
The differential etiologies leading to a precipitous cardiopulmonary decline in our SLE patient included infectious causes, autoimmune causes including an overlapping ANCA vasculitis, ischemic etiologies, septic cardiomyopathy, metabolic, and other toxic causes such as hydroxychloroquine-induced cardiomyopathy. An extensive infectious work-up included negative viral and fungal serologies, negative surveillance blood cultures, and respiratory cultures as listed in Table . The lack of arthritis, thrombocytopenia, and alveolar hemorrhage with ongoing systemic features better fit SLE, than overlapping ANCA vasculitis. In the absence of any other etiology to explain such a dramatic decline, a diagnosis of SLE myocarditis was most likely. Echocardiogram was repeated on hospital day #7 at the outside institution, which showed interval worsening of LVEF 10% with global hypokinesis, moderate concentric hypertrophy (LV mass index: 143.2 g/m2), and moderate pericardial effusion. Other echocardiogram parameters were normal. In addition to aforementioned therapy for SLE, medical management of his heart failure was instituted with angiotensin receptor neprilysin inhibitor (sacubitril/valsartan 24–26 mg twice daily), b-blocker (carvedilol 6.25 mg twice daily), digoxin 0.125 mg daily, amiodarone 200 mg daily, and mineralocorticoid receptor antagonist (spironolactone 12.5 mg daily). Following a relative improvement in hemodynamics, an endomyocardial biopsy was performed on hospital day #10 to elucidate the etiology of decompensation. Concurrently, a right and left heart cardiac catheterization and coronary angiogram were performed for a comprehensive cardiac workup, which revealed normal right and left-sided filling pressures, no evidence of pulmonary hypertension, normal cardiac output and index, and non-obstructive coronary artery disease. Later, his endomyocardial biopsy demonstrated extensive myocardial degeneration with architectural disarray, neoangiogenesis, and perivascular inflammation (Figs. , ) suggestive of myocarditis. Notably, there were no granulomas, giant cells, or cytoplasmic vacuolization. Additionally, a repeat skin biopsy of a thigh lesion performed earlier revealed lichenoid interface dermatitis with vacuolization, and chronic inflammation (Fig. ) with diffuse immunofluorescence demonstrated a granular deposition of IgA, IgG, C3, and fibrin (full house pattern) at the dermoepidermal junction. These pathological results of skin and endomyocardial biopsies further supported systemic SLE. The patient rapidly improved as his echocardiogram on the day of discharge (hospital day #12) showed improved LVEF 45% with improving pericardial effusion and normal left ventricular mass, and wall thickness. He was weaned off vasopressors and discharged on medical therapy for heart failure, oral prednisone 20 mg daily, hydroxychloroquine 400 mg daily, trimethoprim-sulfamethoxazole double-strength 800/160 mg twice daily for cellulitis, and cefazolin 2 mg IV daily MSSA bacteremia.
At one month follow-up in rheumatology clinic, the patient was started on additional steroid-sparing therapy with monthly infusions of cyclophosphamide (750 mg/m2) given systemic SLE with cutaneous manifestations. After completing four cycles of cyclophosphamide and steroid taper, cardiac MRI was repeated after 3 months to assess interval activity. His severely impaired LVEF and pericardial effusions were resolved with no evidence of myocardial scarring or evidence suggesting active SLE on LGE and edema sequences. Echocardiogram after 6 months also showed normal LVEF > 55%, left ventricular diastolic function and mass, wall motion, and global longitudinal strain similar to his baseline findings. Laboratory evaluation showed a significant improvement in his inflammatory markers and cytopenias (leukopenia and anemia) shown in Table . His SLE is currently treated with mycophenolate mofetil 100 mg bid (transitioned from cyclophosphamide given favorable side effect profile with potentially long-term therapy) for maintenance therapy with a prednisone taper (60 mg daily for three weeks, taper by 10 mg every two weeks down to 10 mg daily), hydroxychloroquine 400 mg daily, and aforementioned heart failure guideline-directed medical therapy. His functional status is classified as New York Heart Association (NYHA) class I with continued clinical recovery (Table ).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [118.0, 'beats per minute'], 'Hemoptysis': True, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Immobilization for at least 3 days': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 118.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 1.5 + 1 = 2.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 2.5.
The patient's Well's score for pulmonary embolism is 2.5."
3041,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5804339-1,Extracted,"A 52-year-old female presented to the emergency department (ED) resuscitation unit with a 5-day history of progressive shortness of breath and productive cough of green sputum. She described some brief episodes of hot and cold spells but had no documented fever or rigors. She was too tachypnoeic to further offer any history. Vitals on presentation were as follows: pulse oximeter reading of 78% on room air, heart rate (HR) of 110 bpm, blood pressure of 85/60 mmHg, respiratory rate of 37 breaths per minute, and temperature of 35.4°C. Initial management was commenced by the ED physicians.
A brief collateral history was obtained from her daughter. The patient was visiting Ireland on holiday and had arrived 6 days ago from Minnesota, USA. Her past medical history included chronic migraine, genital herpes, and zika virus infection, which was acquired 2 months ago during a visit to Mexico and was treated supportively. She was an ex-smoker with 10-year pack history, and her alcohol intake was described as moderate by her daughter. Her medications included hydrocodone, topiramate, and gabapentin all of which she had been on for more than 2 years. She had no history of staying in motels, cruise ships, exposure to birds, purchase of new pets, sick contact, intravenous drug usage, or tick bites.
Her chest radiograph () showed multiple foci of consolidation representing multifocal pneumonia or possible pulmonary infarcts secondary to multiple pulmonary emboli.
Blood results () showed a CRP of 516 mg/L, urea of 28 mmol/L, creatinine of 163 μmol/L, and D-dimer of 1400 ng/ml and a mixed respiratory metabolic acidosis with type 2 respiratory failure on arterial blood gas. Microbiology on call was contacted, and she was commenced on broad spectrum coverage with piperacillin-tazobactam, clarithromycin, vancomycin, and oseltamivir. Bilevel positive airway pressure (BIPAP) as a form of noninvasive ventilation was commenced, with ICU involvement.
An urgent CT-pulmonary angiogram was arranged () and showed no acute pulmonary emboli, extensive multifocal consolidations, and most likely reactive mediastinal lymphadenopathy.
Her arterial blood gases continued to deteriorate, and 3 h after admission she was severely acidotic. She was intubated and moved to the ICU. Her initial ICU management was based around a working diagnosis of acute respiratory distress syndrome secondary to severe CAP.
The Infectious Disease (ID) team was consulted the following morning, and her antibiotics were further rationalised to ceftriaxone to cover invasive S. pneumoniae; vancomycin to cover resistant S. pneumoniae and community acquired MRSA; ciprofloxacin to cover atypical pneumonia including legionellosis; and oseltamivir for influenza. Twenty-four hours after her admission, blood cultures result came back positive for S. pneumoniae, and she was deescalated to high-dose ceftriaxone therapy.
Forty-eight hours after admission, she developed severe pulmonary oedema, and her troponin T reached a peak of 20,643 ng/L and proBNP of 68,543 pmol/L. An urgent angiogram demonstrated no coronary artery disease. Echo showed posteroapical akinesia with an ejection fraction of 40–45% with no valvular abnormality. The working diagnosis of cardiomyopathy with myocarditis secondary to S. pneumoniae was established by the cardiology and ID team.
Seventy-two hours after admission, she was anuric with worsening renal function despite optimal fluid management. She was commenced on continuous venovenous haemofiltration (CVVH). Despite these complications and the development of multiorgan failure, she responded to the antibiotic regime and was successfully extubated with no further requirement for invasive ventilation or CVVH. She developed extensive critical illness myopathy and is currently undergoing rehabilitation.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3042,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6741371-1,Extracted,"A 71-year-old male with a history of gastric MALT lymphoma status post H. pylori treatment and confirmed eradication presented with progressively worsening shortness of breath and productive cough. He had noticed the dyspnea two months prior to presentation and reported exertion as the main trigger. There was no nausea, vomiting, diarrhea, constipation, fever, chest pain, or appetite changes. However, he reported a 13-pound unintentional weight loss over six months. The patient has a past medical history that is significant for chronic obstructive pulmonary disease (COPD) with chronic respiratory failure requiring supplemental home oxygen, heart failure with preserved ejection fraction, and deep vein thrombosis. The patient is an active smoker with more than 50 pack-year tobacco use. He has no history or risk factors of tuberculosis. There was no history of alcohol use or illicit drug use. Medications prior to admission were furosemide, lisinopril, pantoprazole, tiotropium bromide monohydrate inhaler, and albuterol inhaler.
The patient was diagnosed with gastric MALT a year prior to the current presentation and underwent eradication of H. pylori infection with amoxicillin, clarithromycin with a proton pump inhibitor with resolution of the gastric tumor.
On physical examination, his temperature was 36.8 °C, his blood pressure was 121/72 mm Hg, his pulse rate was 78 beats per minute, and his respiratory rate was 18 breaths per minute. He had scattered wheezing and decreased breath sounds over the right lung base. The rest of the examination was unremarkable. A chest X-ray with posteroanterior and lateral views revealed a large right pleural effusion which was confirmed on thoracic ultrasonography (Figures -).
The patient underwent thoracentesis with the removal of 750 milliliters of exudative fluid based on Light’s criteria (Table ). Cytologic assessment of the pleural fluid revealed 90% lymphocytes with no malignant cells. The pleural effusion recurred within three days and the pulmonary team elected to pursue medical pleuroscopy, pleurodesis, and pleural biopsy for further evaluation and prevention of further recurrence. The procedure was followed by chest tube placement which was removed four days later.
The biopsy of the right pleura demonstrated fibroadipose tissue with multiple poorly defined lymphoid aggregates (Figure ). The lymphocytes within these aggregates were small in size, with predominantly round nuclear contours, condensed chromatin, no identifiable nucleoli, and moderate amounts of pale-staining cytoplasm. Focally, the lymphocytes displayed a so-called “monocytoid” appearance, a histologic finding typical of marginal zone lymphoma. By immunohistochemistry, the majority of the lymphocytes were cluster of differentiation (CD)20-positive B-cells, with few infiltrating small CD3-positive T-cells. Flow cytometric immunophenotyping performed on a concurrent pleural fluid specimen identified a monotypic B-cell population that expressed CD19, CD20, CD22, and kappa surface light chains, but not CD5 or CD10. Given the patient’s known history of gastric extranodal marginal zone lymphoma, the morphologic and immunophenotypic findings in the pleural biopsy and pleural fluid were interpreted as representing pleural involvement by extranodal MALT lymphoma.
The patient responded to pleurodesis with minimal recurrence of the pleural effusion after chest tube removal and improvement in dyspnea (Figure ). However, the hospital course was complicated with a complete heart block. In light of advanced disease and multiple comorbidities, the patient declined any intervention and elected to pursue comfort care measures. He was discharged to home with hospice care.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [78.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 78.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3.0 + 1 =  4.0.
The patient's Well's score for pulmonary embolism is 4.0."
3043,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8702235-1,Extracted,"A 41-year-old woman presented to the emergency department with worsening generalized edema and dyspnea for a month. She was diagnosed with Graves’ disease at a primary clinic 18 months ago. Methimazole was prescribed for 10 months and has been discontinued for 8 months after restoration to normal thyroid function. However, Graves’ disease relapsed and methimazole was resumed since last month. Despite treatment, worsening pedal edema and dyspnea brought her to the emergency room.
At presentation, her blood pressure was 116/73 mmHg, heart rate 91 beats/min, respiratory rate 20/min, and body temperature 36.2 °C. Physical examination revealed exophthalmos, a diffuse goiter, irregular heartbeats with grade 3/6 systolic murmur at the left lower sternal border, and grade 3 pitting edema at both lower legs. Chest radiographs showed cardiomegaly with a cardiothoracic ratio of 0.56 (Fig. A) and small amount of fluid shift on bilateral decubitus views. An electrocardiogram (ECG) demonstrated AF at a rate of 87 bpm. Laboratory test revealed suppressed thyroid-stimulating hormone (TSH, 0.007 μIU/mL), elevated levels of free thyroxine (T4, 37.63 pmol/L) and anti-TSH receptor antibody (27.12 IU/L), and negative anti-thyroid peroxidase (anti-TPO Ab, 21.23 IU/mL) and anti-thyroglobulin (anti-TG Ab, 14.70 IU/mL) antibodies. The levels of liver enzymes were mildly increased (aspartate aminotransferase, 50 IU/L; alanine aminotransferase, 45 IU/L) and N-terminal pro-brain natriuretic peptide was also elevated to 1007 pg/mL. Technetium-99m thyroid scan showed bilateral diffuse enlargement of thyroid gland and intense homogeneous radiotracer uptake, consistent with Graves’ disease (Fig. B). Transthoracic echocardiography was performed to assess the etiology of HF and demonstrated severe tricuspid regurgitation (TR) associated with incomplete systolic coaptation of tricuspid valve due to dilated right ventricle (RV) (Fig. A, B), moderate resting pulmonary hypertension with pulmonary artery systolic pressure of 59 mmHg (Fig. C, D), normal left ventricular (LV) dimension, normal LV systolic function with ejection fraction of 59%, borderline elevation of LV end-diastolic pressure with E/E′ ratio of 12.5, and preserved RV systolic function. She underwent enhanced chest computed tomography to identify the presence of pulmonary thromboembolism as a cause of RHF, which showed bilateral pleural effusion, minimal ascites, and no evidence of pulmonary embolism. Generalized edema and dyspnea were gradually improved with administration of furosemide, propranolol, and methimazole. After 6 months, euthyroid state was restored. In addition, follow-up ECG showed spontaneous conversion to normal sinus rhythm. Echocardiography revealed scanty TR with normalization of RV dimension and pulmonary artery systolic pressure of 27 mmHg (Fig. ). Diuretics and beta-blocker were discontinued and methimazole was gradually tapered. She has been doing well and thyroid hormone levels have been maintained within the normal range for 6 months.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [91.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 91.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3044,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8272681-1,Extracted,"A 77-year-old Caucasian male with a past medical history of MG presented to the emergency room (ER) with complaints of dysphagia for one week. The patient was first diagnosed with MG five years ago and has been maintained on prednisone 7.5-milligram tablet daily and pyridostigmine 60-milligram tablet six times daily. The dysphagia was associated with non-specific arthralgia, intermittent fevers, chills, and fatigue. The remaining review of systems is negative. He is compliant with medications. He received the first and second doses of Moderna COVID-19 vaccine approximately five and one weeks prior to presentation. In the ER, vitals were notable for tachypnea (20 breaths per minute), tachycardia (110 beats per minute), and hypoxia (Pox 91% on room air). An electrocardiogram showed sinus tachycardia. Chest x-ray was negative for any infiltrates, effusions, or consolidations. Labs were significant for acute renal failure (due to poor oral intake). The septic workup was negative. He was admitted to the neuro floor with MG exacerbation. He was started on pyridostigmine 60 milligrams every four hours, prednisone 7.5 milligrams daily, and intravenous (IV) immunoglobulin (Ig) 35 grams daily for five days. His acute renal failure resolved with adequate IV hydration. Over the next few days, the patient's oxygen requirement normalized, but the dysphagia persisted. On day six of admission, he acutely decompensated with another crisis of MG manifested by lethargy and flaccidity. An arterial blood gas analysis (ABG) confirmed acute hypercapnic respiratory failure for which the patient was intubated and transferred to the medical intensive care unit (MICU). He was started on prednisone 10 mg (which was gradually increased in 48-hour intervals to 40 mg), another two IVIg were given on days 9 and 10. Serial negative inspiratory force (NIF) readings were obtained, with improvement from -20 to more than -40 and subsequent successful extubation. The MG crisis was attributed to the second dose of the Moderna COVID-19 vaccine.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3045,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7977182-1,Extracted,"A 23-year-old Caucasian male presented to a rural hospital with a 1-week history of left lower limb pain, edema, and pallor. His symptoms commenced 1 week prior to hospital admission, starting with pain in the entire left lower limb, and then edema, with the thigh worse than the lower leg, and finally pallor of the entire left lower limb. He denied any trauma, history of thromboembolic disease, shortness of breath, chest pain, alcohol consumption, smoking history, recreational drug use, or family history of hypercoagulable disorders. Past medical history included type 2 diabetes mellitus, which was managed with oral gliclazide MR 120 mg once daily and oral metformin XR 1000 mg once daily. He has no other significant medical history or family history and was not on any other regular medications. He was unemployed and lived in a rural town with a friend. On clinical examination, his left thigh was more swollen than his lower leg, with associated tenderness and pallor. The left femoral, popliteal, tibial and dorsalis pedis pulses were palpable. His lower-limb neurological examination was normal, with intact sensation and 5/5 power in all movements bilaterally. He had a heart rate of 85 beats per minute, blood pressure of 120/70 mmHg, oxygen saturation of 98% on room air, respiratory rate of 16 breaths per minute, and was afebrile at 36.5 ℃. Initial assessment with computed tomography (CT) angiography demonstrated no significant arterial disease. He was then found to have extensive DVT over the entire length of the left lower limb on venous Doppler ultrasound (US), involving the left fibular, soleus, and gastrocnemius veins up to the popliteal vein, femoral vein, common femoral vein, and external iliac vein (Fig. ). He had normal renal function, serum urea, electrolyte levels, creatine kinase, calcium, magnesium, phosphate, and full blood examination. He had elevated serum C-reactive protein at 59 mg/L (normal range <10), a slightly elevated fibrinogen at 5.0 g/L (normal range 1.5–4.0 g/L), and mildly high gamma-glutamyl transferase of 107 U/L (normal range <65 U/L) and alkaline phosphatase of 135 U/L (normal range 30–110 U/L). Otherwise, his coagulation profile and liver function test were normal. Plasma D-dimer was 12.62 µg/ml fibrinogen-equivalent units (normal range <0.50). The initial impression of the clinical picture was phlegmasia alba dolens. He was given an intravenous heparin loading dose of 5000 units and then commenced on an intravenous heparin infusion at a rate of 1080 units per hour, titrated according to the activated partial thromboplastin time (target range of 60–85 seconds) and transferred to the vascular surgery unit of a metropolitan hospital for further management.
Further investigation with CT pulmonary angiogram and CT venography of the abdomen and pelvis showed bilateral interlobar and segmental pulmonary emboli, and compression of the left common iliac vein with an extensive thrombus of the left common iliac, internal, and external iliac veins, consistent with MTS (Figs. and ). The Interventional Radiology team subsequently inserted a temporary Cook Celect Platinum inferior vena cava (IVC) filter via the right internal jugular vein. The left common iliac vein was cannulated, and venography showed an extensive thrombus across the left common femoral, external, and common iliac veins. AngioJet mechanical thrombectomy, thrombolysis using 200,000 units of urokinase, angioplasty, and stenting of the left common femoral, external, and common iliac veins, using two Cook Zilver Vena venous self-expanding stents of 16-mm diameter and 63-mm length each were all performed successfully (Fig. ). On discharge from hospital, he wore left lower limb compression stockings, and the heparin infusion was switched to subcutaneous therapeutic enoxaparin 60 units twice per day. Oral anticoagulation was not used because of its slightly higher risk of future thrombosis, when compared with enoxaparin. He received intravenous heparin infusion for 4 days. His IVC filter was removed 10 weeks later without complication.
Therapeutic enoxaparin was continued until a follow-up appointment at the hematology clinic 4 months later. His thrombophilia screen was overall negative, with a negative prothrombin gene mutation, normal protein C, protein S, lupus anticoagulant, anti-beta-2 glycoprotein 1, and anticardiolipin antibody. He had marginally low antithrombin at 73% (normal range 80–120%); however, this may have been related to the presence of thrombosis or heparin therapy at the time of testing, rather than an underlying genetic disorder. Factor V Leiden will be tested at his next appointment. He was advised to remain on anticoagulation until next follow-up and was switched from therapeutic enoxaparin to oral apixaban 5 mg twice per day because of convenience of use despite a slightly higher risk of future clots. He has had no recurrent thrombosis of his lower limb and has a follow-up due in 4 months.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [85.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 85.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3 + 1.5 = 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
3046,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-4215,Extracted,"A 45-year-old male presents to the emergency room complaining that he has been coughing up blood-tinged sputum. Since this morning, the patient reports he has coughed up around 1/4 cup of ""phlegm"" mixed with blood. A review of systems is also notable for fatigue and night sweats that began two nights ago, but he denies any recent changes in weight. His past medical history is significant for hypertension, chronic sinusitis, and childhood asthma. His current medications include metoprolol and amlodipine. He is a smoker with a 20 pack-year history. The patient’s temperature is 99°F (37.2°C), blood pressure is 126/76 mmHg, pulse is 72/min, and respirations are 14/min with an oxygen saturation of 98% O2 on room air. A physical exam is notable for oral ulcers. A chest radiograph is performed and is shown in Figure A.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [72.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 72.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 0 + 1 = 1.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.
The patient's Well's score for pulmonary embolism is 1."
3047,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-4826,Extracted,"A 78-year-old female is brought to her primary care doctor by her daughter after developing worsening cough, shortness of breath, and shaking chills over the past 3 days. The patient's cough has not produced any sputum. She also complains of alternating feelings of being 'hot then cold.' Whenever she coughs or breathes deeply, she experiences a severe sharp pain in her chest. The patient lives at home with her daughter and is otherwise healthy. Her past medical history is significant for hypertension treated with losartan and hyperlipidemia managed with atorvastatin. The patient does not have a history of tobacco use. Vital signs recorded in the office are as follows: T 38.7, HR 101, BP 135/78, RR 16, and SpO2 94%. Physical exam is significant for crackles in the right upper lung field. The patient is transferred to the local emergency department for further evaluation and management and a chest radiograph is obtained (Figure A).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [101.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 101.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3.0 + 1.5 = 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
3048,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-1337,Extracted,"A 55-year-old man comes to the physician for a routine health visit. He feels well except for occasional left-sided abdominal discomfort and left shoulder pain. He has smoked 1 pack of cigarettes daily for 20 years. He does not drink alcohol. His pulse is 85/min and his blood pressure is 130/70 mmHg. Examination shows a soft, nontender abdomen. The spleen is palpated 5 cm below the costal margin. There is no lymphadenopathy present. The remainder of the examination shows no abnormalities. Laboratory studies show:
Hemoglobin 12.2 g/dL
Hematocrit 36 %
Leukocyte count 34,000/mm3
Platelet count 450,000/mm3
Cytogenetic testing of his blood cells is pending.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [85.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 85.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 0.
The patient's Well's score for pulmonary embolism is 0."
3049,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5358130-1,Extracted,"Fifty-one-year-old Caucasian female was admitted to our hospital with complaints of fever and chills for three days and low back pain for two days. Past medical history included recent spinal abscess followed by implantation of spinal nerve stimulator, mitral valve prolapse and GERD. Her medications included omeprazole and acetaminophen as needed for chronic back pain. On physical examination, patient appeared sick. Vital signs: BP 80/50 mmHg, Pulse 120/min, respiratory rate 24/min. No skin lesions; neck was supple. Jugular veins were distended up to angle of the ear with prominent ‘a’ and ‘v’ waves. Her P2 was loud; No murmurs or gallop; lung fields were clear with normal vesicular breath sounds. Abdomen was soft and non tender. She had increased warmth and tenderness at the level of D10 - D12 vertebrae. Neurological examination was normal. Her labs revealed WBC count of 15,000 with bandaemia of 20%, lactic acid of 45 mgs%. Her EKG revealed sinus tachycardia. Serial troponin levels were normal. She was treated with broad spectrum antibiotics, intravenous fluids and dopamine as infusion. Her blood culture was positive for Staphylococcus aureus. Her echocardiogram revealed small left ventricle with ejection fraction of 65%, flattened interventricular septum, normal left atrium (LA), bowing of the interatrial septum to the LA, right atrial (RA) and RV enlargement with severe hypokinesia of RV (). Estimated RV systolic pressure was 75 mmHg. She also had TEE to look for any vegetation. There was no vegetation. Her echo examination 8 months ago was normal. High resolution Chest computerized tomography (CT) revealed normal lungs and CT angiogram revealed no evidence of pulmonary embolism. The patient underwent left and right heart catheterization10 days later. Coronary arteries and LV function were normal. RA pressure 6 mmHg, RV, 36/11 mmHg, pulmonary artery 36/11 mmHg, mean 24 mmHg, indicating significant improvement of pulmonary hypertension. Echo on the next day revealed markedly improved RA and RV dilatation (). Patient had a full recovery on discharge.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Hemoptysis': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
3050,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5004600-1,Extracted,"Paramedics brought a 65 year old female patient to our department of emergency medicine as she was in a reduced general condition. The patient was severely obese (body mass index: 41 kg/m²), fully conscious (GCS: 15) and complained about nausea, vomiting, left-sided abdominal pain, severe weakness and a slight cough. The patient denied having dyspnoea and thoracic pain.
Two years prior to admission, pulmonary embolism resulted in cardiopulmonary resuscitation. After successful resuscitation, a splenectomy due to a traumatic two-stage splenic rupture was performed. The postoperative course in the intensive care unit was complicated by an angioneurotic edema and blood stream infection with Serratia marcescens, which was cured by ceftriaxone and piperacillin/tazobactam but resulted in prolonged weaning. The patient had fully recovered during the past 2 years after discharge from hospital.
Her further history included mild hypertension, recurrent upper gastrointestinal and urogenital bleeding following various anticoagulation treatments, which was based on esophagitis (stage IV, Savary and Miller), and diverticulosis of the descending and sigmoid colon. Consequently, she was receiving rivaroxaban 20 mg 1x1, torasemid 5 mg 1x1, ramipril 5 mg 1x1 and esomeprazole 40 mg 1x1. All vaccinations had been administered as recommended for splenectomised patients [] including vaccination for Streptococcus pneumoniae (Pneumovax®).
On admission, she displayed tachypnea (25/min), tachycardia (116/min), a slightly impaired oxygen saturation (91%), normal blood pressure (112/76 mmHg) and fever (39.0 degree Celsius).
Auscultation of the lungs was normal. Palpation of the abdomen enhanced the pain in the left part of the abdomen, suggestive for diverticulitis. No skin pathologies were observed. Apart from a sinus tachycardia, the electrocardiogram was normal. In particular, there was no link to myocardial infarction of pulmonary embolism.
The patient received intravenous paracetamol (1 g) and 1000 ml electrolyte-solution, which normalized the fever, tachypnea and tachycardia. We additionally administered 40 mg of pantoprazole.
Blood gas analysis revealed normal findings except for reduced oxygen saturation (81%), which lead to oxygen administration (4 l/min). Urine examination excluded a urinary tract infection.
We performed a chest X-ray and computed tomography of the abdomen, which did not reveal any sign of a causative pathology. Laboratory analyses revealed no leucocytosis, normal lactate, elevated C-reactive protein (63 mg/l; normal: <5 mg/l), an elevated creatinine-level (1.5 mg/dl; normal <0.95 mg/dl) and marginalized positive troponin (123 µg/dl; normal <100 µg/dl). INR (1.27) was slightly impaired and PTT was normal. The patient was referred to our intensive care unit.
Two hours after admission to hospital, we started intravenous administration of 4 g ceftriaxone on suspicion of a highly feverish infection of unknown origin, accompanied by another 1,000 ml electrolyte-solution.
Twenty minutes after administration of ceftriaxone, the patient’s condition deteriorated. Vomiting and diarrhoea preceded a generalized cyanosis. Oxygen saturation dropped, the patient became drowsy and short of breath while circulation still remained stable.
We suspected a potential allergic reaction and administered subcutaneous adrenaline (0.5 mg), prednisolone (250 mg) and increased oxygen therapy, which primarily stabilized the patient.
Re-evaluation for cardiac enzymes revealed no increase in troponin levels and assessment for pulmonary embolism showed only slightly elevated d-dimers (1.1 mg/dl; normal: <0.5 mg/l).
Within 30 minutes, livid spots appeared on her skin which increased in size and number. The patient’s condition now required intubation, mechanical ventilation and additionally, continuous increase of intravenous noradrenalin application. Despite excellent oxygenation in blood gas analysis, cyanosis persisted. Four hours after admission to hospital, the patient died.
Eight hours after collection, blood cultures became positive for Streptococcus pneumoniae (serogroup: 12F), and confirmed the differential diagnosis of OPSI retrospectively.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [116.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 116.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3051,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5889371-1,Extracted,"A 74-year-old lady presented to our emergency department following 3 days’ history of watery diarrhoea and feeling generally unwell. She had been ‘off legs’ for 3 days and was not improving hence called the GP for a home visit. She was referred to the hospital as a case of severe sepsis for medical admission and pre-alerted into Resus by paramedics. She denied any cough, cold, or urinary symptoms. She had a past medical history of hypertension and CKD and was on Ramipril and Atorvastatin. She was at reasonably normal baseline health and 3 days back started with watery diarrhoea. There was no history of recent travel and no vomiting or per rectal bleed. On examination, she looked unwell, still responding to verbal commands, hypotensive at 80/50 mmHg, and tachycardic at 110 beats per minute with a temperature of 38.5 °C. She was hypoxic on air, with saturations of 90% on high flow oxygen. She had evidence of peripheral cyanosis and delayed capillary refill time. Her chest was clear and abdomen was soft, with no guarding or rigidity. Her Glasgow coma scale was 14 (E3V5M6). Her venous blood gas revealed metabolic acidosis with a lactate of 14.
With a working diagnosis of severe sepsis of unknown source, she was started on broad-spectrum intravenous antibiotics and fluids. As there was no improvement in her haemodynamic status, a referral to the intensive care team was made for inotropic support.
While all of these were being done, she was noticed to have a tender bruise on her leg; however, she denied any trauma or fall. On examination, she had a large area of blackish discolouration and vesicle formation on the posteromedial aspect of the left thigh (Fig. ), which was tender on palpation. The area looked suspicious of necrotising fasciitis. Her antibiotics were changed as per the microbiology advice to Tazocin and Clindamycin. A urinary catheter was inserted to monitor her fluid balance. An urgent referral to the surgical and orthopaedic team was made for definitive management of surgical debridement. Her initial blood results showed a white cell count of 13.1 and neutrophilia at 11.7. She had a CRP of 439, CPK of 4187 and an AKI stage 3 with urea at 15.2, creatinine of 291 and e-GFR of 13. Serum electrolytes showed a sodium of 137, potassium of 3.4 and chloride of 101.
She underwent debridement of necrosed tissue within few hours of arrival into the emergency department. She subsequently stayed in the intensive care unit and had a further debridement and above-knee amputation of the affected limb (Figs. and ). On the second surgery, she was found to have necrotic tissue extending up to the pelvis. A subsequent pus culture report confirmed group A Beta haemolytic streptococci as the causative organism. The blood culture showed no growth, and faeces culture was negative and showed no evidence of Salmonella, Shigella, Camplylobacter or Escherichia coli. MRSA was not isolated and there was no evidence of C-difficile in the stool.
She eventually died after about 48 h of hospital stay despite an early diagnosis and prompt surgical debridement.
Although necrotising fasciitis is a rare condition, each one of us may still come across a case in our clinical practice. As a learning point from this case, we would like to highlight the importance of a thorough clinical examination of patients with sepsis with no obvious source. As in this patient, the presenting complaint was diarrhoea, which was actually a manifestation rather than a cause for sepsis and clearly had a hidden diagnosis, which could have been missed if the patient was not adequately exposed.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Surgery in the previous 4 weeks': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3052,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3492424-1,Extracted,"A 61-year-old man experienced sudden onset of right lower chest pain before visiting the emergency room. The chest pain began 2 days ago and was aggravated the next day, followed by blood tinged sputum. He smoked 1 pack of cigarette every day for 13 years and had no other identified cardiovascular risk factor. He was diagnosed with chronic hepatitis B virus infection 30 years ago. He had been taking tadalafil for 2 years, usually once a week for erectile dysfunction. He denied taking any other medications.
Approximately 15 hours before developing chest pain, he took one dose of tadalafil before attempt of sexual contact. Afterwards he had sexual intercourse with two different women with time interval of about 8 hours. Few hours after the second sexual intercourse he experienced sudden onset of right lower chest pain. The pain aggravated the next day and hemoptysis occurred the day afterwards which led him to visit the emergency room.
His initial blood pressure was 123/99 mm Hg, heart rate 69 beats/min, respiration rate 20 frequencies/min, body temperature 36.8℃, oxygen saturation 96%. The mental status was oriented. Auscultation revealed no heart murmur but breathing sound was decreased on his right lower lung field. There was no pitting edema or clubbing seen in the four limbs. The chest X-ray showed ill-defined density in the right lower lung zone with blunted costophrenic angle (). Electrocardiography revealed Q wave in lead III and aVF and poor R progression. D-dimer was increased to 0.6 µg/mL (normal, less than 0.4) and chest computed tomography was performed with suspicion of acute pulmonary thromboembolism. Thrombus was seen at right ascending and descending subsegmental pulmonary arteries along with wedge-shaped lesion in right lower lobe. Small amount of right pleural effusion was also noted (). Blood analysis showed normal concentrations of protein C (98%), protein S (83%), antithrombin III (97%), factor XI (124%) and elevated concentrations of factor VIII (222%). Tests for lupus anticoagulants, factor V Leiden mutation and anticardiolipin antibodies were also negative. The patient was treated with anticoagulation therapy of 80 mg of enoxaparin (1 mg/kg) subcutaneous injection every 12 hours and oral warfarin. When the warfarin dosage was adjusted to keep prothrombin international normalized ratio between 2 and 3, enoxaparin was no longer used. Oral anticoagulation was maintained for 6 months and the patient made full recovery confirmed by chest computed tomography.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [69.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 69.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 1.5 + 1 = 2.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 2.5.
The patient's Well's score for pulmonary embolism is 2.5."
3053,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7396098-1,Extracted,"A 38-year-old obese male presented to the emergency department (ED) for worsening dyspnea and palpitations over the past three days. Earlier in the day, he described feeling like his heart was “jumping out from his chest.” His occupation requires him to sit for long periods and he endorsed that for the past week, he had progressively worsening pain in his legs. He is a former smoker; however, he quit three years ago.
Vitals on presentation were a temperature of 36.8°C, blood pressure of 80/60 mmHg, pulse rate of 148 beats/minute, respiratory rate of 26 breaths/minute, and oxygen saturation of 83% on ambient air which improved to 97% on a non-rebreather mask. Chest auscultation was notable for bilateral crackles, wheeze, and stridor.
Laboratory abnormalities included thrombocytopenia (117 k/μl), elevated D-Dimer (20.0 μg/ml), elevated aPTT (151.9 s), elevated lactate dehydrogenase (463 U/L), and a positive RT-PCR for SARS-CoV-2. EKG showed sinus tachycardia with rightward axis deviation. Chest X-ray (see ) demonstrated patchy infiltrates peripherally in the right upper lung and left mid to lower lung with mild elevation of right hemidiaphragm. Computed tomography angiography (CTA) done a few hours later (see Figures and ) showed extensive prominent multifocal acute bilateral pulmonary embolism and findings consistent with viral pneumonia.
He was given heparin IV 5,000 units in the ED as prophylaxis for DVT as per hospital protocol; however, he was subsequently switched to a one-time subcutaneous injection of enoxaparin 100 mg. Enoxaparin was held as the patient's aPTT levels were noted to be elevated. However, on day three, he was started on the oral anticoagulant, apixaban 10 mg twice daily. After a seven-day hospitalization, he was clinically stabilized and discharged on home oxygen along with instructions to continue oral anticoagulation for three months and follow up as an outpatient.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [148.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",7.5,7.5,7.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 148.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 = 6.0.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 6.0 + 1.5 = 7.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 7.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 7.5.
The patient's Well's score for pulmonary embolism is 7.5."
3054,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8040190-1,Extracted,"A 52-year-old woman was admitted to our hospital’s emergency department with a fever for 13 d and no cough, abdominal pain, nausea, or diarrhea.
The patient did not have chronic diseases, such as hypertension, diabetes, or cardiovascular disease.
The patient underwent hysterectomy 2 decades ago.
The patient had no remarkable personal and family history. She does not take drugs in daily life.
The patient’s vital signs were as follows: Blood pressure, 133/74 mmHg; pulse, 78 beats per minute and regular; blood glucose, 6.0 mmol/L; and temperature, 39.2 °C. On physical examination, her abdomen was soft, with no tenderness, rebound pain, or percussion pain in the liver or kidney areas.
Routine blood test results showed the following: White blood cell (WBC) count, 12.24 × 109/L; percentage of neutrophilic granulocytes, 85.6%; hemoglobin concentration, 93 g/L; platelets, 358000/mL; and C-reactive protein, 138 U/mL. The blood chemistry examination, glycosylated hemoglobin, coagulation profile, and extractable nuclear antigens were within normal limits. Urinalysis showed urinary protein 1+, urinary WBC 3+, and nitrite negativity, and bacteria were not found in the urine or blood.
First, we considered the possibility of an infectious disease, but the site of infection was unclear. The patient underwent blood tests, X-ray of the chest, abdominal ultrasound, and urine tests to investigate the infection site. Chest X-ray revealed normal findings.
Around the left kidney, abdominal ultrasound showed a visible, liquid, dark area. To distinguish whether there was a perirenal abscess, hematoma, or tumor, the patient underwent a contrast-enhanced computed tomography (CT) scan, which showed atrophy of the left kidney. The left renal capsule had a crescent-shaped, low-density shadow, and the CT value of the contrast-enhanced scan without enhancement was 53 HU, with no enhancement observed on the contrast-enhanced scan (contrast agent, iodohydril; CT value, 100 HU) (Figures and ). The perirenal fat was blurred, and exudation was visible with no sign of calculi, malignancies, instrumentation, or trauma (Figures -). Inflammation was considered to be secondary to rupture of the left kidney and extravasation of urine.
Under ultrasound guidance, a pigtail catheter was inserted into the hematoma, and 150 mL in total of fluid was drained and used for the bacterial test. The appearance was hemorrhagic, thick, and brown, indicating a Gram-negative bacterial infection, which was then proved to be caused by Klebsiella pneumoniae (Table ) 3 d later. We considered the source of inflammation to be the hematoma, which had existed for a long time and led to chronic infection according to the normal urine and blood culture results.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [78.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 78.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3055,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5515777-1,Extracted,"We present the case of a male Caucasian patient, aged 37 years, splenectomized for spherocytosis since the age of 4, with no prophylaxis of meningococcal, and pneumococcal infections through vaccination, that was brought to the emergency room for fever, diarrhea, vomiting, rash skin, myalgia, anuria, and marked alteration of his general condition. At the time of admission, on physical examination, the following changes were noticed: facial erythema, purpura on the legs (see Fig. ), cyanosis of the extremities, jaundice, left basilar crackles, heart rate of 130 beats per minute, blood pressure of 140/100 mm Hg, hepatomegaly, and anuria. The laboratory investigations that were performed revealed the following alterations (at admission and in evolution) that are presented in Table .
Peripheral smear revealed normochromic normocytic red blood cells, as well as microspherocytes and spherocytes, frequent polychromatophilic macrocytes; erythrocytes with Howell–Jolly bodies (splenectomy), rare dacryocytes (teardrop cells), and schistocytes. Polymorphonuclears with vacuolated cytoplasm are present (toxic appearance), diplo-, encapsulated, and intra- and extracellular gram-positive cocci. Bone marrow sample was harvest and on hematoxylin-eosin stain an increased number of activated macrophages with prominent hemophagocytosis of hematopoietic elements was revealed. Blood cultures and urine cultures were positive for S pneumoniae, resistant to benzylpenicillin, chloramphenicol, erythromycin, trimethoprim/sulfamethoxazole, tetracycline, cefotaxime, and intermediate resistance to ceftriaxone, imipenem, sensitive to ofloxacin, vancomycin, moxifloxacin, quinupristin/dalfopristin, levofloxacin, linezolid, rifampicin, sparfloxacin, pristinamycin, amoxicillin, and telithromycin. Viral, parasitic etiologies were excluded, as well as rheumatic diseases, malignant tumors, which may be involved in secondary HLH.
A cardiac ultrasound was performed and revealed no suggestive images of infectious endocarditis or valvular heart disease. Initially, the chest radiography revealed no changes, but in evolution, it showed bilateral alveolar condensation and left pleural effusion.
The case was interpreted as sepsis due to a multidrug-resistant S pneumoniae associated with consumption coagulopathy (bleeding at venepuncture site and epistaxis), acute liver failure, acute renal failure by myoglobinuria, and HLH. In evolution, acute respiratory failure occurred, for which endotracheal intubation of the patient was performed.
The treatment was started with infusions of macromolecular solutions, hydro-electrolytic rebalancing, packed red blood cells, fresh frozen plasma, and antibiotics – initially, with ultrabroad-spectrum antibiotics, meropenem 2 g/day associated with linezolid 2 × 600 mg/day, thereafter treatment continued with linezolid associated with moxifloxacin 400 mg/day according to antibiogram results, dexamethasone, etoposides 150 mg/m2/day, 3 days, anidulafungin, intravenous immunoglobulin, and daily hemodialysis sessions throughout hospitalization. The evolution was unfavorable with coma, Glasgow Coma Scale of 3, and quadriplegia, the occurrence of bronchopneumonia required endotracheal intubation. During hospitalization, the patient was anuric. Patient death occurred on day 15 of hospitalization. Hematoxylin-eosin and immunohistochemically stainings of liver biopsies taken during the anatomopathological examination revealed the following changes: massive infiltration of portal tract and sinusoids by mononuclear cells. The CD68 stain shows numerous large, irregularly shaped CD68+ cells as being macrophages, cells that are localized both in the portal tract and sinusoids, and with an increased phagocytic activity on lymphocytes, erythrocytes, and polynuclear cells. On CD8 stain, numerous CD8+ lymphocytes were revealed. The conclusion was: the described aspect is in concordance with the diagnosis of hemophagocytic lymphohistiocytosi. Autopsy examination also revealed bilateral renal papillae necrosis secondary to myoglobinuria, and the presence of hemophagocytosis in bone marrow, and lymph nodes Figs. –.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [130.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 130.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3056,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5376942-1,Extracted,"A 68-year-old Chinese female was diagnosed with genotype 1b chronic hepatitis C in 2006 when she was noted to have mildly deranged liver function test with alanine aminotransferase (ALT) of 62. The likely source of HCV infection was blood transfusion in 1988 at the time of left mastectomy. Liver biopsy in 2007 showed mild fibrosis (Grade 3, Stage I). Her comorbidities included type 2 diabetes diagnosed in 1997 complicated by mild diabetic retinopathy, hypertension, dyslipidaemia, atrial fibrillation, laparoscopic cholecystectomy in 2013 for gallstone disease, and previous breast cancer cured in 1988.
Due to concerns regarding the safety and efficacy of interferon, she declined therapy and was followed annually in Hepatitis Clinic. She did not drink alcohol. A FibroScan in February 2016 demonstrated liver stiffness measurement of 12.4 KPa consistent with established cirrhosis. She had normal liver synthetic function and no evidence of portal hypertension. Her baseline blood tests included normal platelet of 230 × E9/L, haemoglobin 126 g/L, albumin 34 g/L, bilirubin 5 umol/L, and creatinine 75 umol/L ().
In view of the degree of liver disease she was offered treatment with VIEKIRA PAK through a national early access scheme. Potentially interacting medications including felodipine and atorvastatin were stopped, and she started 12 weeks of VIEKIRA PAK without ribavirin on 21 March. Her other medications including Penmix 30 50-unit mane, 40-unit nocte, NovoRapid 12 units at lunchtime, cholecalciferol, losartan, and dabigatran 110 mg bd were continued.
One week later, she presented acutely to hospital with a two-day history of fever, cough, headache, and palpitation and VIEKIRA PAK was suspended on admission. Her observations were temperature of 37.8°C, HR 128/min, BP 144/80, and oxygen saturation of 92% on 2 L of oxygen. Jugular venous pressure was not elevated, heart sounds were dual with no murmur, she had crepitations at the right lung base, and abdomen was soft and nontender without peripheral oedema. She had no evidence of meningism or petechiae. Chest X-ray showed pulmonary interstitial changes in the right lung without frank consolidation (). ECG showed fast atrial fibrillation at a rate of 129/mins with T wave flattening in leads II, avF, V4, V5, and V6 (). She was admitted to the ward with the provisional diagnosis of community acquired pneumonia and was started on intravenous cefuroxime and erythromycin. Due to worsening hypoxaemia, respiratory fatigue, tachycardia, and development of acute kidney injury she was admitted to the Critical Care Unit for intensive support. Over the next 24 hours, she rapidly improved and was transferred back to the respiratory ward. Echocardiogram (ECHO) on 30 March revealed normal left ventricular and right ventricular size and function, with only mild tricuspid regurgitation and trivial aortic regurgitation. She continued to improve. She was discharged after 5 days in hospital on a further 10-day course of oral amoxycillin and roxithromycin with the diagnosis of community acquired pneumonia.
She was reviewed in outpatient clinic 3 weeks later. She was asymptomatic and returned to normal activities with no restrictions. Postdischarge blood tests were normal (). Given good recovery, she was restarted on VIEKERA PAK. She represented unwell with fever, cough, shortness of breath, headache, and back pain 4 days later. Her temperature was 38°C, heart rate was 104/mins, BP was 127/58, and oxygen saturation was 96% room air. Chest X-ray on admission showed bilateral pulmonary infiltrate more prominent on the right (). Computed tomography (CT) noncontrast head scan excluded intracranial haemorrhage as a cause for headache. The respiratory service restarted empiric cefuroxime, roxithromycin, and oxygen support. She was in fast atrial fibrillation and required stat dose of 300 mg intravenous amiodarone to manage her heart rhythm. She continued to deteriorate rapidly. She became increasingly hypoxaemic and developed lactic acidosis and oliguria. She was again transferred to the Critical Care Unit for presumed systemic sepsis. She initially received continuous positive airway pressure (CPAP) but due to fatigue was intubated and ventilated. Despite fluid resuscitation and inotropic support, anuric renal failure ensued and she was commenced on Continuous Veno-Venous Haemodiafiltration (CVVHDF). A high resolution CT of the chest demonstrated widespread interstitial oedema, ground glass opacities, moderate bilateral pleural effusions with atelectasis of upper and lower lobes, and increased lung attenuation suggesting cellular infiltrate related pneumonitis (). Repeat ECHO performed showed normal biventricular function with mild atrial regurgitation, moderate mitral regurgitation, and severe tricuspid regurgitation in the context of moderately dilated right ventricle. Autoimmune and vasculitis screen including antinuclear antibodies, antineutrophil cytoplasmic antibody (ANCA), anti-Sjögren's-syndrome-related antigen A (Anti-SSA/Ro), and rheumatoid factor were negative. Cryoglobulins and complement levels were not performed.
Reviewing results from her first admission, urinary legionella and pneumococcus were negative, and nasal pharyngeal viral polymerase chain reaction (PCR) panel and serial blood cultures were sterile. Repeat sputum and tracheal aspirates and pleural fluid aspirates had no evidence of bacterial, viral, or fungal infection. Given the similar presentations on rechallenging her with VIEKIRA PAK, a provisional diagnosis of drug induced interstitial pneumonitis was made and high dose corticosteroid therapy instituted. She received 500 mg intravenous methylprednisone daily for 4 days and clinical improvement was prompt. She was discharged home with normal gas exchange and renal function 7 days after admission. At the most recent follow-up nine months out from discharge, she remained clinically well with compensated liver disease.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [128.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 128.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
3057,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8548719-1,Extracted,"A 58-year-old male who had no previous smoking history consulted an oncologist because of pulmonary nodules revealed by physical examination in July 2019. The diagnosis was stage IV (cT4bN3M1b) adenocarcinoma. EGFR mutation analysis showed mutations in exon 18 G719X and exon 20 S781I. He received 40 mg of afatinib orally every day beginning on July 27, 2019, with the treatment being well-tolerated with mild diarrhea. After 1 month, a partial response was obtained, hence the patient continued receiving afatinib therapy. However, the patient was admitted to the hospital on October 9, 2019 due to shortness of breath, fever without chills, and cough for 1 week. shows the patient’s lung lesions at partial response, and shows the lung inflammation. Physical examination showed cyanosis of the lips, short-breath, respiratory rate 26 per min, pulse 110 per min, crepitus sounds in both lungs, expecially in the lower lungs. Blood examination showed a white blood cell count of 9.7 × 109/L, neutrophil percentage of 80.6%, brain natriuretic peptide (BNP) of 29 pg/ml, procalcitonin (PCT) of 0.117 ng/ml, and C-reactive protein (CRP) of 161.71 mg/L. Blood oxygen was 93% and arterial partial pressure of oxygen was 62 mmHg when admission. Serum albumin 33.2 g/L, blood urea nitrogen (BUN) 5.6 mmol/L, creatinine (Cr) 75 µmol/L, electrocardiogram showed sinus tachycardia. The glucan (G) test, galactomannan (GM) test, and sputum culture were all negative. The suspected diagnosis for the pulmonary inflammation was infection. The patient’s afatinib was discontinued and he was administered empiric antibiotics instead. At the same time, he received 40 mg of methylprednisolone daily to reduce inflammatory exudation. The patient’s shortness of breath and cough progressively worsened, and type I respiratory failure occurred 3 days later. The patient was transferred to the intensive care unit for respiratory support therapy and received broad-spectrum antibacterial therapy. The patient died from respiratory failure 9 days after admission. showed the episodes according to the order of occurrence for case 1.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3.0 + 1 =  4.0.
The patient's Well's score for pulmonary embolism is 4.0."
3058,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7850465-1,Extracted,"A 53-year-old man presented to the emergency room of the Xiangya Hospital on December 19, 2017, with intermittent chest tightness, palpitation, and dyspnea. The patient had repeated bleeding in the joints since childhood. He underwent quantitative coagulation factor (FVIII) testing at a local hospital, and the diagnoses were as follows: severe hemophilia A, baseline factor VIII (FVIII) level <1%. Multiple follow-ups showed negative results for FVIII inhibitors; fresh frozen plasma and cryoprecipitate had been infused during previous bleeding episodes. Due to the improved financial situation in the past 20 years, the patient received occasional infusions of plasma-derived concentrates of FVIII/recombinant FVIII at irregular intervals. The patient had an approximately 16-year history of diabetes and had his blood sugar controlled through dietary restrictions and oral hypoglycemic agents, such as metformin and gliclazide. He had an approximately 3-year history of hypertension and kept his blood pressure (BP) in check through the intermittent use of therapeutic drugs, such as irbesartan and amlodipine. The patient had been hospitalized thrice in the past 5 years, owing to gastrointestinal bleeding (duodenal ulcer). The patient had no history of hepatitis C. He was a light smoker and a mild drinker.
The family and friends notified that the patient experienced chest tightness, palpitation, and dyspnea after consuming a large amount of alcohol on December 17, 2017; the symptoms were slightly relieved after administering “nitroglycerin.” December 18, his chest tightness and dyspnea significantly exacerbated. He was admitted to the emergency room of the People’s Hospital of Ningxiang, and his electrocardiogram showed ST-segment depression. The patient had hypotension and shock during the examination, which rapidly progressed to respiratory and cardiac arrest and loss of consciousness. He was administered immediate cardiopulmonary resuscitation and was managed using anti-shock therapy, tracheal intubation, assisted ventilation, and symptomatic and supportive treatment. During this period, the patient received FVIII 2000 IU once. Other specific treatments were not available. Following the stabilization of his condition, the patient was transferred to the emergency ICU on December 19. His physical examination findings were as follows: height, 170 cm; weight, 60.0 kg; BMI, 20.8 kg/m2; body temperature, 37.1°C; pulse, 112 beats/min; respiratory rate, 23 breaths/min; BP, 147/87 mmHg. The patient was managed by tracheal intubation, continuous oxygen supply, and assisted ventilation. He appeared to have moderate anemia, a heart rate of 112 beats/min, and metronomic heartbeats. Widespread moist rales were heard in both the lungs, the abdomen was soft and non-tender, and the liver and spleen were not enlarged. Joints of the right lower limb were deformed, and movement was impaired. Joints of the remaining limbs were normal. There was mild edema in the lower limbs. Pathological signs were not observed. Laboratory examination results were as follows: 1) complete blood count: white blood cells (WBC): 10.5×109/L, hemoglobin (Hb): 81 g/L↓, red blood cell (RBC): 2.69×1012/L↓, platelets: 214×109/L; 2) coagulation function: APTT, 34.4 s; FVIII: C, 160% (after FVIII infusion); FVIII inhibitor (-); 3) myocardial enzymology: lactate dehydrogenase (LDH), 393 U/L↑; creatine kinase, 210.2 U/L; creatine kinase-MB, 25.2 U/L↑; Troponin I quantification, 9.49 ng/mL↑; myoglobin, 180.00μg/L↑; brain natriuretic peptide (BNP), 15,712 pg/mL↑; C-reactive protein (CRP), 182 mg/L↑; procalcitonin (PCT), 2.22 ng/mL↑; 24 h blood glucose, 7.5–13.5 mmol/L; 4) electrocardiogram: II, III, aVF, V4–V6, significantly depressed ST segment (); 5) bedside chest radiography: diffuse exudative changes in both the lungs (cardiogenic pulmonary edema).
Following discussions among a multidisciplinary team (MDT) including the physicians from the hemophilia center, a cardiologist, and an ICU physician, the diagnoses were as follows: 1) hemophilia A (severe); 2) coronary heart disease (CHD), acute NSTEMI, acute pulmonary edema (cardiogenic), class IV cardiac condition; 3) Type I respiratory failure; 4) hypertension (stage 2, very-high-risk group); and 5) Type 2 diabetes. The MDT developed a management plan after considering that the patient had hemorrhagic disease with the concomitant thrombotic disease. The physicians at the hemophilia center formulated the factor VIII replacement therapy regimen: 1600–1800 IU of FVIII, Q12h (target activity: 50–60%); the cardiologists formulated the treatment regimen for acute NSTEMI: aspirin tablets (100 mg, Qd) + enoxaparin sodium injection (4000 IU, Qd×3 days), isosorbide dinitrate (10 mg, continuous injection), metoprolol tablets (6.25 mg, Q12h), and atorvastatin tablets (20 mg, Qd). As the patient had acute NSTEMI, intervention treatment (PCI) was not necessary at that time; the ICU physicians formulated the following treatment plan: insulin for blood sugar control, assisted ventilation, antibiotics, organ function preservation, and symptomatic and supportive treatment.
Following the above treatment, the patient’s condition improved significantly after 1 month, by which time he was able to walk independently and was discharged from the hospital. Based on the medication order, the patient was continuously treated with FVIII 600 IU prophylaxis twice a week and clopidogrel and atorvastatin tablets after discharge to prevent the recurrence of cardiovascular events.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [112.0, 'beats per minute'], 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 112.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
3059,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3971557-3,Extracted,"A 37-year-old man with a liver abscess was referred to our department for management after the implantation of an IVC filter. The patient's family history was unremarkable, and the patient had not complained of chest pain, dyspnea, or lower back pain. His physical examination showed a regular pulse rate of 80 beats/min, blood pressure of 90/50 mmHg, and a normal temperature of 36.8°C. The patient did not demonstrate any obvious murmur or rales, but his laboratory tests revealed an increased D-dimer concentration (3.6 μg/mL); the patient did not show any findings suggestive of congenital thrombotic disease. Contrast-enhanced CT and catheter-based venography demonstrated a small, polyp-like thrombus at the site of the infrarenal IVC (), in absence of any IVC malformation. The patient was administered an anticoagulant therapy involving unfractionated heparin, and the IVC thrombus was completely resolved approximately 2 weeks later. He was discharged after removal of the filter.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3060,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4323061-1,Extracted,"A 17-year-old female presented at the emergency department following a 7-day history of worsening sore throat, fever, headache, and vomiting and a 4-day history of developing neck pain. Her illness initially started with fever, headache, and sore throat with subsequent loss of appetite. The headache was reported to fluctuate in severity and was described more like a migraine, although it was relieved slightly by paracetamol. The sore throat was severe enough to affect her intake of food, as she was unable to swallow solids, but liquids were unaffected. The patient reported vomiting following the onset of the illness, although this only initially occurred after eating and there was no blood or bile present. The vomiting subsided in the following days due to decreased intake of food. However, one more episode of vomiting occurred the day before admission which was reported to be bilious. The patient had previously been seen by her general practitioner and at the emergency department on two previous occasions (four and three days before admission). She was discharged on all occasions with the diagnosis of a self-limiting viral illness. Subsequently, she developed a left-sided neck pain, radiating down the lateral margin of her neck (ranked as 6/10 for severity) and was admitted to the emergency department via an ambulance.
On admission, there was swelling of the left neck and pain on movement, although there was no photophobia, and on examination she had a negative Kernig's and Brudzinski sign. Her temperature was 39.9°C, respiratory rate was 18 breaths/min, blood pressure was 105/44 mmHg, and heart rate was 137 bpm. The patient's blood results showed evidence of liver dysfunction with decreased albumin of 28 g/L, raised alkaline phosphatase of 178 U/L, raised alanine transaminase of 50 U/L, raised bilirubin of 28 μmol/L, and raised gamma-glutamyl transferase of 200 U/L. They also showed a raised C-reactive protein (CRP) of 241 mg/L, reduced haemoglobin of 105 g/L, reduced red blood cell count of 3.54 × 1012/L, and a reduced haematocrit of 0.32. The absolute neutrophil count was raised at 8.50 × 109/L; however, the absolute lymphocyte count was reduced at 0.40 × 109/L, whilst the white cell count was within the normal range at 9.2 × 109/L. Platelet count was also normal at 212 × 109/L. Chest X-ray, computerised tomography (CT) neck, CT pulmonary angiogram, and ultrasound of the neck were performed. The chest X-ray () showed prominent vascular appearances to the hilar contours, but no obvious paratracheal hilar lymphadenopathy. There was also a slight increase in perihilar bronchovascular markings. A second chest X-ray was performed 4 days later to look for an infective focus in the chest; none was found (not shown). The CT scan of the neck with contrast showed a thrombus within the left jugular vein (). The thrombus did not extend into the venous sinuses in the brain or into the mediastinum. The CT pulmonary angiogram showed no evidence of pulmonary embolism or lung pathology. Ultrasound of the neck () showed left neck soft tissue swelling, reactive lymphadenopathy, and left internal jugular vein thrombosis. At this point a diagnosis of Lemierre's syndrome was made. Blood cultures were taken on admission and were returned negative five days later. A second set of blood cultures were repeated at this time, with these also returned as negative. However, it is noteworthy that these blood cultures were taken after the patient had received antibiotic therapy in the community as well as after admission to the emergency department.
The patient was given benzylpenicillin (2.4 g IM) and paracetamol (1 g PO) by the ambulance crew prior to admission, before being commenced on intravenous co-amoxiclav (1.2 g tds) and oral clarithromycin (500 mg bd) as well as therapeutic low molecular weight heparin (dalteparin 10000 units S/C od). Following the diagnosis of Lemierre's syndrome one day after admission, the antibiotic regimen was switched to IV clindamycin (1.2 g tds) and IV metronidazole (500 mg tds), whilst the IV co-amoxiclav was continued. These were changed to oral amoxicillin (1 g tds) and oral metronidazole (400 mg tds) 9 days after admission. She was also started on warfarin (5 mg PO od), 9 days after admission and continued receiving therapeutic dalteparin as from admission.
At discharge, 11 days following admission on the Infectious Diseases ward, her CRP levels had fallen to 6.4 mg/L, and the liver enzyme results had improved, although were not yet within the normal ranges. The patient was asymptomatic on discharge. Her course of antibiotics ended 11 days after discharge and she continued to take warfarin for 3 months, subject to the advice of the haematology department. The patient attended a follow-up outpatient appointment eight weeks later. Her inflammatory markers and liver enzymes had fallen to within the normal range and there was no fever, sore throat, or neck swelling.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [137.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 137.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
3061,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6854395-1,Extracted,"A 37-year-old male patient with a background of hypertension was admitted to our emergency department with sudden dizziness and left limb weakness. Non-jet vomiting occurred before transfer to our hospital for further management, and the vomitus was gastric content. He reported no trauma, fever, or coma, he was a non-smoker, and he had no history of drug use or cardiac events. The patient was immediately subjected to a non-contrast computed tomography (CT) scan of the brain, which revealed hemorrhage in the occipital and parietal lobes. The diagnosis of intracerebral hemorrhage (ICH) was made. He developed sudden onset chest tightness, shortness of breath, and occasional chest pain behind the sternum around 48 h after emergency hematoma evacuation. The pain was stuffy in nature and did not radiate to other places. His symptoms continued to worsen gradually, until breath sounds were observed when the patient was sitting up. There were no severe symptoms of dyspnea, cough, hemoptysis or sputum (a characteristic pink frothy sputum is often produced).
The patient’s medical history was only hypertension; he had not been treated regularly, and the blood pressure control was unknown. There was no other history of illness or medication.
The patient had warm extremities with hemodynamically stable blood pressure maintained at 128/73 mmHg and a heart rate of 77 beats per minute (bpm) on initial assessment. He was breathing smoothly on room air with clear lungs. His cardiac examination was normal and did not show any murmurs or gallops.
The physical examination was unremarkable, except for the low left limb muscle tension and the third limb muscle strength. The physical examination was carried out when the patient suffered from chest tightness. On further examination, his heart rate was faster than 100 bpm and his blood pressure had risen to 150/90 mmHg; other general conditions were stable. However, when the patient was breathing in a sitting position, auscultation revealed abnormal breath sounds, which manifested as obvious bilateral bubbling rales in the lower part of the lungs.
The serum level of creatine kinase (CK) was 837 U/L (reference range, 38-174 U/L), that of CK isoenzyme was 26 U/L (reference range, 2-25 U/L), lactate dehydrogenase (LDH) was 269 U/L (reference range, 109-245 U/L) and hydroxybutyrate dehydrogenase (HBDH) was 249 U/L (reference range, 72-182 U/L) at admission; other blood values were within the normal range. When the symptoms of chest tightness worsened, the patient’s blood was immediately checked for any sign of heart failure (HF). The laboratory examination showed the concentration of N-terminal pro b-type natriuretic peptide (NT-proBNP) was 493 pg/mL (reference range, < 85 pg/mL). Myocardial enzyme levels, including cTnI, did not exhibit normal values after serial determination: the cTnI level was increased to 0.175 ng/mL in the resting state (reference range, < 0.06 ng/mL), the CK level was 660 U/L, the CK-MB level was 26 U/L, LDH was 298 U/L, and HBDH was 271 U/L. Repeated measurements 5 d later showed the values had decreased: CPK, 49 U/L; CK-MB, 12 U/L; LDH, 231 U/L; and HBDH, 187 U/L (Figure ).
On admission, the emergency cerebral CT image revealed cerebral hemorrhage in the occipital and parietal lobes (Figure ), while the initial 12-lead ECG (Figure ) revealed a normal sinus rhythm and a regular rate within the normal range; however, T wave inversions and ST segment in leads V5 and V6 were already observed.
We made another ECG at the onset of chest tightness. It is notable that the ECG demonstrated extensive depression of the ST segment and T wave inversion, suggestive of myocardial injury. At this time, there was a prolongation of the corrected QT interval (QTc, 487 ms) (Figure ). But at this time, the chest radiograph showed no bilateral patchy opacities that are typical of pulmonary edema and consistent with the breath sounds when the patient was in a sitting position (Figure ).
In sum, the working hypothesis of a non-ST elevation myocardial infarction (NSTEMI) could be established. Further cardiological investigations, including coronary arteries with CT angiogram (CTA) of the coronary arteries, were needed to make a definite diagnosis. Considering the patient was in acute stage of ICH, coronary angiography was not timely completed.
A coronary CTA and echocardiogram (ECHO) were made at 72 h after the initial symptoms when the patient’s chest discomfort disappeared. The ECHO revealed normal sized chambers with an ejection fraction of 60% and showed no significant valvular abnormality or any wall motion abnormality (Figure ). Coronary arteries did not reveal any sign of obstruction or significant narrowing (Figure ). Another 12-lead ECG was made 11 d after the patient’s symptoms improved, by this time, the patient had returned to the same state as at admission with the recovery of ICH, but the QTc interval was now prolonged (QTc, 424 ms).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [100.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 100.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3062,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-9329,Extracted,"A 55-year-old man recovering from knee replacement surgery complains of breathlessness in the postoperative ward. He has been confined to bed for the past 5 days and is under observation. He felt a sudden difficulty in breathing and called for the ward nurse. He says that he is unable to take deep breaths and has a sharp pain on the right side of his chest with each inspiration. His temperature is 37.5°C (99.8°F), the pulse is 111/min, the respirations are 31/min, and the blood pressure is 85/55 mm Hg. He experiences pain in his right calf on dorsiflexion. There are no other prominent findings on physical examination. His chest X-ray does not show anything significant. The ECG reveals sinus tachycardia.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [111.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 111.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 =  6.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
3063,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7675879-1,Extracted,"A 78-year-old Caucasian male with non-ischemic dilated cardiomyopathy, who had
received a cardiac resynchronization therapy device (a CRT-D) 2 years earlier at our
center, was brought to our clinic in an emergency situation for an electric storm
(ES) with repeated shock delivery. ES is the sequela of a state of cardiac
electrical instability leading to multiple episodes of ventricular arrhythmia in a
short period of time and is commonly defined as the occurrence of at least three
sustained episodes of appropriate ventricular tachycardia, ventricular fibrillation
or ICD shock during a 24-h period.
During the 2 years after biventricular implantation of an implantable
cardioverter-defibrillator (ICD), the patient referred moderate improvement in
general conditions, corresponding to an increase in the ejection fraction from 28%
to 34% with functional improvement from III to II New York Heart Association (NYHA) class. Medical therapy included bisoprolol 5 mg, ramipril 10 mg, furosemide 75 mg,
and aldactone 25 mg. During periodic checks of the device, no significant
ventricular arrhythmias had emerged that required anti-tachycardia therapy with
shock delivery or anti-tachycardia pacing (ATP), or that fell within the window of
monitoring, except for rare ventricular triplets. About 10 days before the current
hospitalization, the patient experienced fever, which after 2 days was associated
with anosmia and ageusia, in the absence of cough, dyspnea, or other symptoms. SpO2
by percutaneous pulse oximetry was constantly around 95%, which was similar to
levels prior to the febrile episode. On the advice of his general practitioner, home
therapy with HCQ was initiated (400 mg BID on day 1, followed by 200 mg BID for a
total period of 6 days), 5 days before admission.
Upon arrival at the emergency department, blood pressure was 130/70 mmHg, heart rate
80 bpm, temperature was 36.8 °C, and oxygen saturation was 96% while breathing
ambient air. The patient had cold sweats and was clearly agitated. Blood glucose was
within normal limits. Arterial gases, lactate and electrolytes were within normal
ranges. Blood tests revealed high levels of hs-troponin T, creatine kinase-MB, and
NT-proBNP (), and
a slight increase in creatinine (1.3 mg/dL, corresponding to creatinine clearance of
46.37 mL/ min by Cockcroft-Gault formula). Tisdale score, which at the last visit 2
months earlier was 5 (low risk) was 11 (high risk). Chest X-ray did not detect any
notable pulmonary changes and confirmed regular placement of the leads. A 12-lead
electrocardiogram (ECG) revealed a sequential biventricular pacemaker rhythm (). Interrogation of
the device revealed, during the last 6 hours, the presence of numerous episodes of
sustained and non-sustained ventricular tachycardia (VT), which in three occasions
reverted with ATP and on eight occasions with shock delivery of 41 Joules (). In addition, the
device showed functionality parameters within normal limits and superimposable on
previous control visits with 98% of correct biventricular stimulation.
The patient was admitted to the intensive care unit, sedated with propofol,
intubated, and administered intravenous metoprolol and magnesium sulfate.
Nasopharyngeal swab was positive for SARS-CoV-2 by reverse transcription polymerase
chain reaction (RT-PCR), and did not have a very high viral load of 27
cycle-threshold, while the search for common cardiotropic infectious agents was
negative. Echocardiographic examination revealed deterioration of cardiac
contractility, in the absence of specific contractile deficits, with an ejection
fraction that had decreased to levels seen prior to implantation of the
biventricular ICD. Urgent coronary angiography showed no evidence of obstructive
coronary artery disease. Upon arrival at the emergency department, while checking
the biventricular ICD, an ECG was also done in the absence of pacing, with the
observation of spontaneous electrical activity, highlighting a QTc of 483 ms; at
electrocardiogram (ECG) performed 2 months earlier, the QTc was 446 ms (). The only change in
therapy was the introduction of HCQ, and after consultation with an infectious
disease specialist the drug was discontinued (it had been administered for a total
of 6 days). This was followed by progressive improvement in the QTc and parallel
regression of ventricular arrhythmias. On the second day, therapy with propofol was
stopped, and on the fourth day therapy with oral beta-blockers was restarted.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3064,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7410440-1,Extracted,"A 60-year-old male patient was admitted with myalgia and fatigue for 2 days. The patient had no fever, cough, sore throat, chest tightness, and shortness of breath.
The patient had no previous history of chronic diseases such as kidney disease, hypertension, and an endocrine disorder; muscle diseases such as muscular dystrophy and neuromuscular disorders; or a statin class of drug use that could lead to muscle breakdown. There was no trauma and no history of medication. The patient reported no alcohol intake and smoking.
Blood pressure was 120/70 mmHg, respiratory rate 18/minutes, heart rate 93/minutes, temperature 36.7°C, and arterial oxygen saturation 98% in room air. The patient was conscious and had a clear mind. He was in a regular heart rhythm without any obvious murmur. There were obvious moist crackles during auscultation of inferior lobes in the lung.
Routine blood test results were as follows: white blood cells, 2.91 × 109/L; neutrophils, 55.7%; lymphocytes, 30.2%; total number of lymphocytes, 0.88 × 109/L; C-reactive protein (CRP), 35.1 mg/L; potassium, 4.3 mmol/L; sodium, 138 mmol/L; urea, 21 mg/dL; D-dimer, 210 ng/mL; alanine aminotransferase (ALT), 52 U/L; aspartate aminotransferase (AST), 117 U/L; lactate dehydrogenase (LDH), 575 U/L; ferritin, 428 ng/mL; international normalized ratio, 1.07; prothrombin time, 11 minutes; total bilirubin, 0.5 mg/dL; and direct bilirubin, 0.2 mg/dL. Cardiac acute damage marker values such as creatine kinase myocardial band (CK-MB: 3.80 U/L) and troponin (13.6 pg/mL) were among normal reference values at the time of hospital admission.
The patient’s baseline serum creatinine (Cr) level was 0.91 mg/dL and baseline serum CK level was 4,267 U/L. Changes in CK, CRP, AST, ALT, LDH, ferritin, and D-dimer during the patient’s hospitalization are presented in .
Blood tests for rapid detection of influenza A, influenza B, respiratory syncytial virus, adenovirus, hepatitis A, and hepatitis B were all negative. Electrocardiogram was normal; no significant cardiac arrhythmia was detected.
The patient, who was admitted with frequent complaints of myalgia and fatigue, was diagnosed in the emergency department. Considering the clinical features, physical examination, and chest radiography, the patient was hospitalized with the diagnosis of suspected viral infection. However, considering COVID-19 infection to the epidemic area, atypical pneumonia virus infection had to be ruled out. On the same day, a chest computerized tomography (CT) scan was performed, and small ground-glass nodules were seen, suggesting viral pneumonia scattered across the two lungs (). Two days later, a real-time reverse transcription–PCR (RT-PCR) analysis of the patient’s throat swab sample indicated SARS-CoV-2 infection.
We hospitalized the male patient diagnosed with COVID-19. When we evaluated according to the WHO classification, we found that our patient had severe pneumonia. During hospitalization, hydroxychloroquine (first day 2 × 400 mg loading + 4 days 2 × 200 mg maintenance), oseltamivir (2 × 75 mg, 5 days), and azithromycin (first day 1 × 500 mg loading + 4 days 1 × 250 mg) therapy were used as recommended in the COVID-19 guidelines. The patient was quickly treated with a combination of IV fluids and sodium bicarbonate for alkalization. After five days of treatment, the patient’s clinical condition deteriorated, and the patient’s respiratory rate was 30 breaths/min; severe respiratory distress developed, and SpO2 was ≤ 93% on room air. Favipiravir (first day 2 × 1,600 mg loading + 4 days 2 × 600 mg) antiviral treatment was added to the treatment of the patient, who was thought to develop severe pneumonia. The length of hospital stay of our patient was 10 days between April 9, 2020 and April 19, 2020. After 11 days of treatment, the patient’s symptoms improved significantly, and he recovered with a negative RT-PCR test.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [93.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 93.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3065,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8555752-1,Extracted,"A 39-year-old female presented to a regional Australian hospital with a three-day history of polydipsia, polyuria and fatigue. This was on a background of a previous stroke suffered 11 years ago, resulting in left-sided hemiplegia and epilepsy. Patient was not a known diabetic.
Vital signs on initial presentation included tachycardia to 160 beats per minute and mild hypotension of 110/80 mmHg. Abdomen was soft non-tender. Patient also had a strong ketotic breath. Venous blood gas was done which showed a pH of 7.36, lactate of 2.5, blood glucose of 44, and ketones of 6.5. Urine microscopy was also performed which showed 500 leukocytes, 80 erythrocytes and 10 epithelial cells. Impression of the patient at the time of admission was that the patient’s urinary tract infection had unmasked undiagnosed diabetes mellitus in the form of diabetic ketoacidosis (DKA).
Patient was commenced on intravenous fluid resuscitation, insulin infusion and intravenous antibiotics (piperacillin-tazobactum and gentamycin). Patient was admitted to the intensive care unit for ongoing care.
During the patient’s stay in intensive care, patient’s diabetic ketoacidosis resolved and insulin infusion was ceased on day 2 of admission. However, the patient remained tachycardiac to 116 beats per minute with an oxygen requirement of 4 litres on nasal prongs so a CT pulmonary angiogram was performed. An occlusive thrombus was found in the right lower lobar artery with CT evidence of right heart strain. Patient was then commenced on therapeutic anticoagulation (Figure ).
On day 4 of admission, patient remained tachycardic despite therapeutic anticoagulation and then became febrile. A computed tomography (CT) scan of abdomen and pelvis was done to rule out pyelonephritis given the known urinary tract infection (Figure ). CT found a large left staghorn calculus with an obstructed infected left kidney. An additional finding included emphysematous left pyelonephritis with soft tissue gas in the left retroperitoneum and left flank/posterolateral soft tissues in keeping with necrotising fasciitis.
Later that day the patient was reviewed by the local general surgery team. Abdomen was soft with significant left flank tenderness and oedema but no crepitus. There was also a skin tear and bruising at the left flank (Figure ).
Given the aetiology of the necrotising fasciitis, the patient was discussed with urology at a tertiary hospital. Discussions centred on whether debridement of necrotising fasciitis should occur at the current treating hospital or whether the patient should be transferred for definitive source control and wound debridement. Given the massive pulmonary embolism and that the patient was relatively stable, decision was made for patient to be transferred for definitive management rather than subject her to two general anaesthetics and procedures.
The patient was then urgently transferred to a tertiary hospital for ongoing care. On the day of transfer, patient underwent a left open nephrectomy with extensive debridement of left flank and groin. Findings included a large pus-filled retroperitoneal cavity extending to the left gluteal region, an atrophic friable left kidney filled with pus and calculus. Vac dressing was applied to the open wound. The patient was subsequently taken back to theatre the following day for further debridement of necrotising fasciitis. Day 2 post nephrectomy, the patient was again taken back to theatre for a relook and debridement and faeces was found in the abdominal cavity. Upon exploration, two colonic perforations were found near the splenic flexure where the kidney had been removed. An omental patch was performed and a loop ileostomy was formed. After this, a total of five relooks and debridements were performed. Eventually, edges of the flank wound were able to be closed with suture repair but a defect in the central portion of the wound remained. This was closed with a split-thickness skin graft performed by plastic surgery.
Approximately two months after the initial presentation, the patient was transferred back to the regional hospital for a two-week stint of rehabilitation after which she was discharged home.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [160.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 160.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3066,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7768872-1,Extracted,"A 36-year-old man with a history of traumatic brain injury, followed by depression and maintenance therapy with antidepressant drugs but without other relevant medical history, presented to our emergency department after a few days of experiencing shortness of breath, fever, and cough. Physical examination initially revealed hypotension (blood pressure 96/65 mmHg), tachycardia (heart rate 116 beats per minute), tachypnoea (respiratory rate 29 breaths per minute), impaired oxygenation (oxygen saturation 84% on room air), hyperglycaemia (blood glucose 375 mg/dL), and fever (temperature 38.6°C). The patient was immediately started on supportive oxygen via mask, and his saturation increased to 95% on 6 L of oxygen. On general examination, the patient was conscious and oriented (Glasgow Coma Score 15) and appeared tired and unwell, without other significant physical findings. By Day 5, the clinical condition of the patient had not improved markedly, and his clinical picture and laboratory values began to worsen, with sinus tachycardia (164 beats per minute), tachypnoea (respiratory rate 30 breaths per minute), fever (temperature 38°C), and his oxygen saturation remained 95% on room air.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [116.0, 'beats per minute'], 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Immobilization for at least 3 days': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 116.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3067,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7069872-1,Extracted,"A seventy-five-year-old man was admitted to hospital with a 2-day history of rash. Eight days before admission, he was prescribed oral dicloxacillin 1000 mg three times a day as treatment for folliculitis in the scalp. In the same period, he had been bicycling more than 100 km during a week. After 1 week, a sudden eruption of generalized erythematous rash with white cutaneous pustules developed in the face spreading to the rest of the body. He also began to feel fever chills. Dicloxacillin was discontinued, and treatment with prednisolone 12.5 mg once daily and fexofenadine 180 mg twice daily was initiated. He was known with a past medical history of hypertension and allergic rhinitis and was bypass operated twice, but he had no previous history of psoriasis or other skin conditions. He had a warning registration in the medical journal for a contrast agent due to generalized pruritus.
Physical examination revealed tachycardia (heart rate 160/min), blood pressure 156/79 but normal respiratory frequency and saturation. By admission, no fever was present. Examination of the skin revealed a generalized erythematous skin eruption where the skin had been exposed to sunlight, leaving the skin under his watch and clothes (shorts area) completely uninvolved with a sharp boundary to exposed skin (Figure ). Dozens of white pinhead sized pustules were seen on the chest (Figure ). The pustules spread within few days to involve shoulders, abdomen, upper back, and legs. There was no involvement of mucous membranes.
Laboratory studies revealed leukocytosis (leukocytosis of 25.1 × 109/L, neutrophils 22.8 × 109/L) and C-reactive protein (CRP) of 145 mg/L but with normal liver and kidney function. During admission, fever developed (38.9 Celcius) and the infection counts increased (CRP 193, leukocytes 26.8). A skin biopsy from the chest was not fully representative of the clinical diagnosis. It was described as acute folliculitis showing spongiosis with neutrophil exocytosis and papillary edema, and inflammation with lymphocytes, macrophages, and neutrophils. The patient was treated with topical corticosteroids and systemic prednisolone 25 mg for a few weeks with good response, and upon checkup two weeks later, he had recovered completely.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [160.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 160.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3068,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5701362-2,Extracted,"A 68-year-old female non-smoker was referred to our emergency department due to progressive dyspnea. On physical examination, she exhibited tachypnea (20 breaths per minute) and her oxygen saturation was 85%, her pulse was regular at 91 beats per minute, and her blood pressure was 116/70 mmHg. Chest CT revealed a 36-mm mass with a cavity in the right S9 (Fig. ), and a 10-mm nodule in the right S6. CT also revealed right middle lobe atelectasis due to bulky hilar and subcarinal lymph nodes (Fig. ). Concomitantly, a bilateral pulmonary thromboembolism was identified. Transthoracic echocardiography revealed normal a left ventricular function; the right ventricle was dilated with moderate tricuspid regurgitation and her systolic pulmonary artery pressure was elevated (estimated pressure: 55 mmHg); these findings were considered to have been caused by bilateral pulmonary thromboembolism. Ulthrasonography of the lower extremity veins revealed right fibular vein thrombus. Her serum D-dimer, BNP and CEA levels were elevated to 8.0 μg/mL (normal range: <1.0), 332.5 pg/mL (normal range: <18.4) and 14.6 ng/mL (normal range: <5.0), respectively.
Enhanced CT performed 1 week after the administration of intravenous heparin and oral edoxaban tosilate hydrate, which were administered immediately after the detection of the bilateral pulmonary and right fibular vein embolisms, revealed that the pulmonary artery and right fibular venin thrombus had disappeared. Subsequently, the pathological analysis of a bronchoscopy specimen led to a diagnosis of adenocarcinoma harboring an EGFR exon 19 deletion. Based on these results, she was clinically diagnosed with T3N2M0, stage IIIA adenocarcinoma. As lung cancer associated with pulmonary thromboembolism was taken into consideration, EGFR-TKI treatment was proposed as the first-line systemic therapy and afatinib (40 mg/day) was prescribed after receiving her informed consent. In spite of requiring a dose reduction to 30 mg due to grade 3 diarrhea, she became asymptomatic at 2 months after the initiation of treatment. Chest CT revealed the marked response of both tumors and lymph node metastases with the disappearance of the middle lobe atelectasis (Fig. ). Her serum CEA level decreased to within the normal range (1.4 ng/mL).
We planned surgery to remove the residual lesions. Three days after the discontinuation of afatinib and after receiving her informed consent, we performed right middle and lower lobectomy with systemic mediastinal lymph node dissection. Her postoperative course was uneventful. Complete resection was achieved, with a negative bronchial margin. A histological examination showed the prominent proliferation of fibroblasts accompanied by lymphocytes and histiocytes (Fig. ). However, residual viable tumor cells were found in a small area of the primary lesion (Ef.2a, Fig. ) because an immunohistochemical examination revealed a few small clusters of atypical cells that were positive anti-pancytokeratin (AE1/3) and thyroid transcription factor 1. There were no malignant cells in the dissected lymph nodes. Down-staging from clinical stage IIIA to pathological stage IA was established. We did not identify an exon 20 point mutation (T790 M) in any of these specimens.
Although afatinib therapy was continued after the operation, she developed spinal cord compression due to 5th cervical vertebral cortical bone metastasis with the onset of neck pain at 8 months after the operation. Direct surgical decompression with tumor debulking and spinal stabilization was performed, followed by radiotherapy. An exon 20 point mutation (T790 M) was found in the resected specimens. Thus, osimertinib is now being prescribed. She is currently alive at 15 months after surgery (18 months after the initial diagnosis).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [91.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",7,7,7,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 91.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 3 + 1.5 = 4.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 6.0 + 1 =  7.0.
The patient's Well's score for pulmonary embolism is 7.0."
3069,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-5179,Extracted,"A 65-year-old woman presents to the emergency department with shortness of breath. She is an immigrant and does not speak English, but it is clear she is struggling to breathe. You observe the patient struggling to breathe and coughing up large amounts of mucous. A phone call to her home nurse reveals that she has a past medical history of diabetes for which she is not currently taking her medications. She also states the patient recently recovered from a long flight back from her native country where she was visiting a relative in prison. Her temperature is 99.1°F (37.3°C), blood pressure is 167/108 mmHg, pulse is 112/min, respirations are 25/min, and oxygen saturation is 78% on room air. A chest radiograph is obtained as seen in Figure A. Physical exam reveals a distressed woman who is not cooperative with the exam secondary to her discomfort.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [112.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 112.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 3.0 + 1 = 4.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.0.
The patient's Well's score for pulmonary embolism is 4.0."
3070,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-4809,Extracted,"A 64-year-old man presents to the emergency department with sudden onset of pleuritic chest pain and dyspnea on exertion. He has a history of lung cancer and is currently being treated with outpatient chemotherapy. His temperature is 98.9°F (37.2°C), blood pressure is 111/64 mmHg, pulse is 130/min, respirations are 25/min, and oxygen saturation is 90% on room air. Initial laboratory values in the emergency department are seen below.

Hemoglobin: 8.2 g/dL
Hematocrit: 26%
Leukocyte count: 7,700/mm^3 with normal differential
Platelet count: 157,000/mm^3

A CT angiogram demonstrates a blood clot in the pulmonary vasculature. The patient is started on heparin and he is admitted to the ICU.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [130.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 130.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 3.0 + 1 =  4.0.
The patient's Well's score for pulmonary embolism is 4.0."
3071,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6234785-2,Extracted,"A 67-year-old Greek woman, a retired high-school teacher, presented to our department after an evaluation for fatigue, mass effect, epigastric discomfort in liver cirrhosis, and hypothyroidism. Her past medical history was also remarkable for arterial hypertension. She was on double anti-hypertensive medication and she was also receiving levothyroxine 100 μG once daily. She was a heavy tobacco smoker (>1pack/day) for 35 years and a social alcohol consumer. She was afebrile at the time of admission. Her neurological examination was normal; her blood pressure was 145/97 mmHg, her pulses were 95 beats/minute, and her temperature was 36.4 °C. Her mother died from breast cancer.
Laboratory testing revealed results that are shown in Table . A CT scan revealed a large invasive mass in the anatomical area of ​​her left adrenal gland, well circumscribed, measuring 7 × 7 × 9 cm; it extended to the upper pole of her left kidney and the inner hilum of her spleen without infiltration of the above organs, which showed marked heterogeneous enhancement after intravenous infusion of a contrast agent, which posed a differential diagnosis problem with possible pheochromocytoma (Fig. ).
Further laboratory testing of post-prandial plasma cortisol and plasma testosterone levels gave normal results, mimicking a nonfunctional left ACC. Elective open adrenalectomy was scheduled without any complications and the postoperative pathology record was consistent with a pseudocyst, without evidence of malignancy (Figs. and ). She has had an uneventful course 1 year postoperatively.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [95.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 95.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3072,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7676789-1,Extracted,"A 20-year-old Black male, Division 1 collegiate basketball player presented to a student health urgent care clinic with an insidious two-day history of complaint of dry cough, sore throat, and myalgias, as well as chest pain starting one day prior to evaluation. He described his chest pain as an “achy pressure,” radiating down his right arm, intermittent and worse with deep inspiration and laying supine. He denied smoking cigarettes or marijuana but did vape frequently. He had no recent injury, chest exercises, or concern for musculoskeletal injury, or history of deep vein thrombosis (DVT) or PE. The most recent airplane flight was approximately three hours long and greater than six weeks prior to presentation. He had no leg swelling. He had a remote history of right knee arthroscopic meniscus repair seven months prior. He had a history of acid reflux controlled through diet. His vital signs were normal (pulse 79 beats per minute, blood pressure 111/88 millimeters of mercury, respiratory rate 15 breaths per minute, temperature 36.8° Celsius, oxygen saturation 99%). Due to concern for cardiopulmonary pathology, he was sent to the emergency department (ED) for further evaluation.
On arrival to the ED, his vital signs were again normal. He appeared acutely ill and in mild distress. There was no edema to the lower extremities and he did not report leg pain to the emergency providers. His physical exam was otherwise unremarkable. Complete blood count, basic metabolic panel, and troponin were found to be within normal limits. Additional lab work included elevated D-dimer of 592 nanograms (ng) per milliliter (mL) (normal <232 ng/mL). A D-dimer was ordered because of the patient’s status as an athlete. PERC may not have applied due to concern that his presenting heart rate may have been above his baseline. Electrocardiogram and plain chest radiography at the time were normal. A point-of-care echocardiogram showed no evidence of right heart strain and no pericardial effusion.
Given his concerning presentation and abnormal lab work, computed tomography (CT) angiography of the chest was performed demonstrating PE involving the right posterior basal segmental pulmonary artery with associated hemorrhage vs developing pulmonary infarct (). He was started on heparin infusion and admitted for further evaluation. After diagnosis of PE was made, the admitting hospitalist noted that there was tenderness along his posterior knee and distal thigh, as well as pain with active and passive range of motion of his knee. These exam findings were not noted in the initial provider’s documentation.
During his hospital course he underwent venous duplex imaging, which was negative for lower extremity DVT, and transthoracic echocardiogram was normal. His oxygen saturations remained above 97% and his highest documented heart rate was 79 beats per minute. His hypercoagulability workup was negative except for equivocal lupus anticoagulant. No clear provoking factors were identified, as his surgery was over six months prior to presentation, and he had no recent team flights or travel in the prior one month. His chest pain and shortness of breath improved on day two of his hospital stay. He was transitioned to apixaban for anticoagulation and discharged home with precautions not to participate in contact sports.
At his three-month follow-up with hematology/oncology, he was found to have a persistently elevated D-dimer and underwent repeat CT angiography of his chest. The CT showed focal right lower lobe opacity consistent with scarring but no residual PE. He was no longer experiencing chest pain or shortness of breath. Additional hypercoagulability workup including protein C, S, and cardiolipin antibody, and beta-2 glycoprotein was negative as well. The PE was ultimately determined to be provoked from either his airplane travel six weeks prior or his arthroscopic meniscus repair seven months prior. He was taken off of anticoagulation and cleared for participation in contact sports. He was instructed to take 81 milligrams aspirin on days of team travel if on a bus or plane. He was able to make a full recovery and returned to competitive Division I basketball.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [79.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 79.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3 + 1.5 = 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
3073,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3485910-2,Extracted,"A 64-year-old female with a history of breast cancer presents to the ED with acute shortness of breath and chest pain. She states that the disease has been “stable” and that she has not received chemotherapy in the past three years. She appears acutely ill with blood pressure of 74/58 mm Hg, heart rate 120 beats per minute, respiratory rate 30 breaths per minute, temperature 98 F, and pulse oximetry 94% on room air. Rales are auscultated, but it is difficult to hear heart tones. An EKG reveals a low voltage tracing without ischemic changes. Portable chest radiography demonstrates an enlarged cardiac silhouette and scattered lung opacities.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Immobilization for at least 3 days': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3074,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8725212-1,Extracted,"A 65-year-old Caucasian man with a history of tobacco dependence presented with a brief
episode of dizziness while standing in line at the bank, which was immediately followed by
witnessed loss of consciousness for 30 seconds. The dizziness was only “seconds-long” and
immediately preceded “passing out.” He reported one previous episode of syncope last summer
while “walking in the heat,” which also was sudden without any prodromal or other associated
symptoms. His review of systems was negative for seizures, angina, orthostatic hypotension,
stroke, or trauma. Over the past 3 months, he experienced an 18.1 kg weight loss with
anorexia and constipation. The patient was a retired construction worker, had smoked 50
pack-years, and drank alcohol, but denied intravenous drug use.
On physical examination in the emergency department (ED), the patient was afebrile, with a
presenting heart rate of 63 beats per minute (bpm), blood pressure range of 134/73,
respiratory rate of 20 breaths per minute, and normal oxygen saturation of 98% on room air.
There was no evidence of orthostatic hypotension based on blood pressure and heart rate
measurements in the supine, sitting, and standing positions. The patient appeared thin and
chronically ill with temporal-wasting, barrel chest, mild egophony of the right lung base,
and a scaphoid abdomen. There was no evidence of dry mucus membranes, delayed capillary
refill, heart murmur, jugular venous distension, lymphadenopathy, clubbing, cyanosis, edema,
or neurological deficits. In addition, there was no evidence of gastrointestinal bleeding,
scleral icterus, or jaundice.
Laboratory studies were notable for white blood cell count of 16.9 K/mm3,
hematocrit of 28% with normal mean corpuscular volume (MCV), platelets of 650
K/mm3, albumin of 2.6 g/dL, normal glucose and corrected calcium, and negative
cardiac enzymes. There were no other electrolyte or biochemical laboratory abnormalities
with respect to liver and renal function. A chest radiograph showed a right peri-hilar
mass-like dense opacity concerning for malignancy (). Electrocardiogram (ECG) revealed
bradycardia, variable junctional and ectopic atrial rhythms, ventricular bigeminy, QT
prolongation, low voltage, T-wave abnormalities, and short PR interval (). Additional rhythm strips in the ED showed
ventricular bigeminy followed by a witnessed episode of worsening bradycardia (heart rate in
the range of 30-35 bpm) with associated near syncope.
Chest computed tomography (CT) revealed a large cavitating necrotic mass in the right
middle lobe contiguous with the mediastinum, invading the superior vena cava and right
atrium with surrounding patchy consolidation (). Echocardiogram showed an extrinsic
pericardial mass at the right atrial roof () with an atrial mass measuring 5.0 × 4.4 cm (). Bronchoscopy showed erythema and
compression within the right bronchus intermedius and external compression of the right
upper lobe bronchus ().
Endobronchial biopsy revealed invasive well-differentiated squamous cell carcinoma and a
clinical picture consistent with stage IIIB disease ().
Unfortunately, the patient missed several chemotherapy appointments to treat his lung
cancer. He did not maintain regular follow-up and we do not know whether he had recurrent
episodes of syncope. On hospital readmission 6 months later, the patient developed atrial
fibrillation and flutter (with frequent ventricular ectopy) and electrocardiographic
evidence of right atrial enlargement (, ), a right
pleural effusion, and hypoxemic respiratory failure. The patient eventually expired from
progressive lung cancer opting for comfort care rather than continued medical treatment.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [63.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Surgery in the previous 4 weeks': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 63.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
3075,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5506470-1,Extracted,"A 74-year-old female retired healthcare worker presented with abdominal pain and vomiting following a left inguinal hernia repair performed 7 days priorly. Symptoms began two days after her surgical procedure. Patient had a seven out of ten nonradiating, diffuse abdominal pain localized to the epigastric region described as burning in nature. It was accompanied by fever, nausea, and postprandial vomiting, which was clear and mucoid in nature, sometimes containing food particles. She did not have bowel movements since her inguinal hernia repair. Upon further inquiry, the patient mentioned that she had a decrease in appetite for all types of food for the past 6 months and began limiting her intake to liquids because they were easier to tolerate. The patient also noticed changes in stool caliber and noted an unintentional weight loss of 25 pounds in a one-month span. The patient stated that laboratory tests were unremarkable. A stool exam was not ordered since patient had no complaints of diarrhea. She had an esophagogastroduodenoscopy performed four months priorly due to similar symptoms and the results were essentially normal. The patient has a history of osteoarthritis. Surgical history includes umbilical hernia, a hysterectomy in 2012, and a left inguinal hernia in 2015. Family history includes diabetes mellitus and breast cancer. Patient is a retired home healthcare worker who resides in Grenada six months out of the year and frequently visits the United States. Patient has no other significant medical conditions and denies use of tobacco, alcohol, or illicit drugs. In review of systems, the patient complains of feeling dizzy and experienced a severe bout of malaise beginning around the time she began to lose weight. However, no signs of fever, pruritus, or erythema were noted. The patient was asked about any distinctive food choices or habits and she states that she plants and consumes her own vegetables in rural Grenada.
Upon examination, the patient was an elderly female of the appropriately stated age; she appears apathetic and fatigued. The patient was malnourished and in mild distress with vital signs reading: blood pressure of 135/90 mmHg, a pulse of 110 bpm, a temperature of 99.8°F, and a respiratory rate of 18 breaths per minute. Lungs were clear to auscultation bilaterally and normal S1 and S2 sounds were heard with regular rate and rhythm. The abdomen was soft, nondistended, tender to light, and deep palpation in the umbilical area but no masses or organomegaly was felt. Bowel sounds were normoactive in all 4 quadrants and a surgical scar from umbilical hernia was noted. Patient's left inguinal surgical site was tender to touch with mild swelling and no drainage.
The abdominal X-ray and CT were ordered and suggested evidence of ileus and dilated stomach with small bowel distended up to 4.5 cm diameter without identifiable obstruction, respectively. No organomegaly or lymphadenopathy was noted. Upper GI follow-through was performed and impressions identified jejunal mural abnormality with thickening and loss of normal mucosal pattern, suggestive of broad region of infection or inflammation. Laboratory examination revealed an unremarkable absolute eosinophil count and blood percentage ().
Patient presented with an elevated white blood cell count of 11,000/mm3 which rose to 16,000 mm3, following days of admission which is related to the infected surgical site (). Tumor markers for CA-19-9, CEA, and CA-125 were also measured and were within normal limits to rule out malignancy.
The patient was admitted for possible small bowel obstruction which was worked up with conservative treatment. Patient was placed on a regimen of nothing by mouth (NPO), lactated ringer 1000 mL intravenously at 125 mL/hr, NGT tube for intermittent decompression, and ketorolac 20 mg subcutaneously every 6 hours for pain. Another esophagogastroduodenoscopy was performed and the impression revealed duodenal mucosal thickening and diffuse redness. Biopsies were also taken: one sample from the antrum of the stomach and three samples from the duodenum which were submitted in formalin with the largest fragment measured up to 0.5 × 0.3 × 0.2 cm. Microscopic examination samples in the nonfundic type of gastric mucosal biopsy showed numerous parasites in the lumen of the glands (Figures and ). Parasite sections were noted in cross-sectional views and in other areas showing in long sections, which were identified as Strongyloides stercoralis. Eosinophils were identified in the infiltrate at 200x to 600x magnification, but a count was not taken. The diagnosis was confirmed with a stool ova and parasite, revealing rhabditiform larvae, which typically measure 200 to 300 microns by 10 to 20 microns [].",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [110.0, 'bpm'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 =  3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3076,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-2767142-1,Extracted,"A 36-year-old Iranian man was admitted to our emergency department on 31 August 2006, presenting with epigastric and retrosternal pain of two and a half hours duration. His detailed medical history revealed that he had no risk factors for coronary artery disease, however, BD had been diagnosed 10 years earlier and he was on colchicine 1 mg/day. Oral aphthous ulcers were exacerbated during coronary artery events. Eye examination was normal. He had an episode of thrombophlebitis of his left leg in 2004 and had been taking warfarin but had discontinued the medication.
Medical examination revealed blood pressure of 130/70 mmHg and heart rate of 85 beats/minute and the patient was pale and perspiring. Chest auscultation revealed no abnormalities. His electrocardiogram (ECG) revealed normal sinus rhythm with ST segment elevation on II, III and aVF and reciprocal ST segment depression on V1-V6. Laboratory tests showed elevation of plasma total creatine phosphokinase (CPK) and CPK-MB activities. There were no findings consistent with coagulation and fibrinolysis disorders. He was diagnosed as having an acute inferior wall myocardial infarction, therefore nitroglycerin, heparin, aspirin and beta blocker therapies were started immediately followed by thrombolytic therapy with streptokinase within 1 hour. After 40 minutes, his chest pain was relieved and there was a significant reduction of ST segment elevation along with increased cardiac enzyme levels. A transthoracic echocardiogram showed mild apical hypokinesia and a left ventricular ejection fraction of 50%.
On the third day of hospital admission, he underwent coronary angiography. Coronary angiography revealed an 8 mm giant aneurysm of the proximal left anterior descending artery, an 8 mm aneurysm of the proximal left circumflex coronary artery (Figure ) and a 9 mm aneurysm of the proximal right coronary artery (Figure ). Based on clinical evidence, electrocardiogram and coronary angiography, we considered that the acute myocardial infarction in our patient was due to a coronary aneurysm. Therefore, we did not attempt any coronary intervention and decided to continue with medical therapy including azathioprine, colchicine, prednisolone, aspirin, beta blocker, nitroglycerin and enalapril. On 25 November 2006, the patient experienced another episode of chest retrosternal pain which lasted for 7 hours. His ECG revealed significant ST segment depression on V1-V6. Cardiac enzymes did not rise so he was diagnosed with unstable angina. No changes in ECG were noticed after 5 days. The patient was not adhering to drug therapy and when his coronary events occurred drug therapy was restarted. The next episode of retrosternal pain occurred on 28 February 2007 and lasted for 5 hours. His ECG showed tall T waves on precordial leads. Laboratory tests showed elevation of plasma total CK and CK-MB activities. He was diagnosed with an acute anterior wall myocardial infarction. Medical treatment was started but since he had received thrombolytic therapy 5 months earlier, streptokinase was not administered. The echocardiogram showed septal, apical and anterior wall hypokinesia with an estimated left ventricular ejection fraction of about 25-30%. He was discharged 10 days later with his previous medication plus digoxin, warfarin, frusemide, and spironolactone. On 2 August 2007, he experienced another bout of retrosternal pain that lasted for 7 hours. ECG showed ST segment elevation on precordial leads. Laboratory tests showed elevation of plasma total CK and CK-MB activities. This time, a new anterior myocardial infarction was diagnosed, medical treatment was started and azathioprine was switched for pulse cyclophosphamide 10 mg/kg, but the patient then discharged himself. At the time of writing, the patient is well with pulse cyclophosphamide every 2 months and prednisolone 7.5 mg/day, but unfortunately, he is non-compliant to drug therapy and so it was not possible to switch him to oral medication.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [85.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Immobilization for at least 3 days': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 85.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3077,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7263131-1,Extracted,"A 74-year-old man with a medical history of hypertension presented with dyspnea that had worsened during the past 3 weeks. He had been experiencing mild dyspnea on exertion for the past 6 months. On admission, he had a cough but denied other symptoms. His vital signs were as follows: respiratory rate, 20 bpm; temperature, 36.7°C; pulse, 77 bpm; and blood pressure, 130/70 mmHg. Arterial blood gas analysis revealed a partial oxygen pressure of 65 mmHg, partial carbon dioxide pressure of 39 mmHg, pH of 7.44, and oxygen saturation of 93% while resting in room air. Laboratory data included a D-dimer level of 0.44 µg/mL (reference range, 0.00–0.50 µg/mL) and an N-terminal B-type natriuretic peptide level of 15 pg/mL (reference range, 0–500 pg/mL). A chest radiograph indicated no active lesions in the lung (). Contrast-enhanced chest CT was performed to exclude pulmonary thromboembolism or other lung disease and revealed no evidence of filling defects in vessels, thus suggesting pulmonary thromboembolism. Transthoracic echocardiography indicated a mean pulmonary arterial pressure of 47 mmHg (reference range, 10–22 mmHg). On further evaluating the chest CT through the bone setting, however, we identified several hyperdense linear lesions in both peripheral pulmonary arteries that could not be identified using the lung or soft tissue windows, and this raised suspicion for PCE (). We confirmed that the patient had undergone PVP with a diagnosis of vertebral compression fracture at another hospital 14 months previously. During hospitalization, his symptoms resolved slightly after starting treatment with diuretics.
This study was a case report involving only one patient and only involved observation of the clinical effects. Therefore, approval by an ethics committee was not required. We obtained verbal consent from the patient for publication of this case report and images.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [77.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 77.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3078,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7325392-1,Extracted,"Our patient, a 78-year-old man, came from a nursing home to the emergency department with progressively worsening shortness of breath and nonproductive cough of two days' duration. He denied any fever, chills, nasal discharge, chest pain, or any abdominal complaints. He had been admitted to a hospital one month back (during the peak of COVID-19 pandemic in Detroit) with a runny nose, low-grade fever, and shortness of breath. At that time, he had tested positive for COVID-19, had been given a hydroxychloroquine course (for five days), and discharged to the nursing home, with stable oxygen requirements, on 4 L of oxygen through the nasal cannula. He had not required any mechanical ventilation or intensive care monitoring during hospitalization.
His past medical history included hypertension, diabetes, obesity (body mass index of 35), atrial fibrillation (with a CHA2DS2-VASc score of 4), renal failure secondary to diabetic nephropathy post-renal transplant (15 years back), and interstitial lung disease (ILD). The etiology of fibrotic changes in the lung was thought to be drug-induced (sirolimus); however, the changes had been stable over the last three years and he had been off the drug for the past few years. There had been no history of any thrombotic events including deep vein thrombosis or pulmonary embolism in the past. He denied any use of alcohol, tobacco, or any illicit drugs. His medications included insulin, tacrolimus, warfarin, and multivitamins. He denied any recent dose adjustment of warfarin. All his medications had been continued and no changes in anticoagulation had been made during the recent hospital discharge.
During the current presentation, he was afebrile with a heart rate of 120/min, blood pressure of 120/80 mmHg, respiratory rate of 24/min, and 90% oxygen saturation on 4 L of the nasal cannula. He had coarse breath sounds bilaterally, was using accessory muscles of respiration, and his pulse was irregular with tachycardia. The patient was immediately tested for COVID-19 with a nasopharyngeal swab, which was negative. However, based on the current clinical presentation, the possibility of a false-negative test result, and his recent COVID-19 infection, he was immediately placed on contact and airborne precautions for possible COVID-19 pneumonia. His chest X-ray showed bilateral opacities suggestive of multifocal pneumonia (Figure )
Electrocardiogram indicated atrial fibrillation without rapid ventricular response. He was given metered-dose inhaler breathing treatments, supplemental oxygen through the nasal cannula, and was started on vancomycin and cefepime. Blood cultures and other lab work were obtained (Table ). He was found to have mild normocytic normochromic anemia, prolonged prothrombin time, activated plasma thrombin time, elevated international normalized ratio (INR), and hyperglycemia. The inflammatory markers including C-reactive protein (CRP), ferritin, and D-dimer were elevated with mild high sensitivity troponin elevation.
A comparison of inflammatory markers during current and previous admission is shown in Table .
The patient was started on high dose of methylprednisolone intravenously. Since his INR was supratherapeutic, warfarin was held. However, within the next 24 hours, the respiratory status of the patient worsened, necessitating higher oxygen requirements. An arterial blood gas analysis showed pH 7.402/PCO2 40.2/PO2 70.2 and oxygen saturation of 90% at 6 L of nasal cannula. A decision was made to start the patient on high-flow nasal cannula and transfer him to intensive care unit. In the next two hours, his repeat arterial blood gas analysis showed pH 7.31/PCO2 55.7/PO2 60.7, which was suggestive of hypoxemia and carbon dioxide retention, and a decision for tracheal intubation and mechanical ventilation was taken.
Since the patient was on tacrolimus, there was also concern for opportunistic infections or superimposed bacterial pneumonia; however, the infectious workup including respiratory culture, viral panel, blood cultures, fungal cultures, streptococcal antigen, and pneumocystis stain of sputum came back negative. Although clinical suspicion for COVID-19 pneumonia was high given his history, clinical presentation, and imaging, repeat testing of nasopharyngeal secretions for COVID-19 was still negative. False-negative results of RT-PCR for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have been reported in studies [,]. No additional experimental therapy (including remdesivir, tocilizumab) was administered for COVID-19 pneumonia as he did not meet the criteria for starting treatment based on the hospital protocol followed at the time.
Lung imaging with a CT scan was obtained (Figure ), which showed multifocal ground-glass opacities concerning for multifocal pneumonia superimposed on previous fibrotic changes. In addition, there were multiple segmental pulmonary emboli on the right side of the lung (Figure ).
Two-dimensional echo did not show any evidence of right heart strain, regional wall motion abnormalities, or thrombus. The estimated ejection fraction was 55-60%. At that time, a repeat INR was also obtained, which was found to be 3, and the patient was started on enoxaparin therapeutic anticoagulation dosing (1 mg/kg twice daily). Lower extremity Doppler was negative for deep vein thrombosis. Thrombophilia workup was not done given the acute onset of the embolus and was planned for later in the outpatient setting.
Over the next few days, his ventilator requirements decreased, and he did well with a spontaneous breathing trial and was subsequently extubated after a total intubation duration of five days. His oxygen requirement also decreased over the next few days although he continued to require oxygen through a nasal cannula. He was subsequently transferred to the medical floor and then discharged a week later. Given he had supratherapeutic INR on presentation with unclear etiology, new multiple pulmonary emboli while on warfarin, and based on recent guidelines supporting the use of direct oral anticoagulants (DOACs) in atrial fibrillation, it was decided that he will be started on apixaban on discharge [].",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3.0 + 1.5 = 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
3079,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3671823-1,Extracted,"A 41-year-old previously healthy female was admitted to the Department of Neurology, Taizhou People’s Hospital in March 2012, for two transitory episodes of syncope during a 5-h period. The patient had an unhealthy lifestyle of physical inactivity. No urinary and fecal incontinence, general fatigue, chest pain, breathing difficulty, hemoptysis or fever were observed during the course of disease. Following admission, physical examinations revealed a body weight of 75 kg, body height of 159 cm, body temperature of 36.0°C, pulse of 80 bpm, respiratory rate of 23 bpm and blood pressure of 120/60 mmHg. The patient had a slightly haggard expression, no cyanosis of the lips and no jugular vein distention. Bilateral respiratory movements were identical and vocal fremitus was equal. Dullness was heard in the right lower lung on percussion. Breath sounds were diminished and no moist rales were heard. The patient’s heart rhythm was regular, P2>A2 (pulmonary second sound was higher than aortic second heart sound) and there was no edema in the lower extremities.
A complete blood test revealed a white cell count of 11.21×109 cells/l and the percentage of large white blood cells was 57.2%. Biochemical tests revealed 1.4 mmol/l triglycerides, 0.75 mmol/l high-density lipoprotein and 3.61 mmol/l low-density lipoprotein. Blood gas analysis revealed a pH of 7.471, 61.1 mmHg PaO2, 23.5 mmHg PaCO2 and 18.2 mmol/l HCO3− (under the condition of a low flow rate of oxygen inhalation). Chest radiographs revealed pulmonary hilar enlargement and a broadened shadow on the right superior pulmonary artery. An electrocardiogram revealed a flat V1–V3 T wave and magnetic resonance angiography of the head revealed ∼60% luminal stenoses of the right posterior cerebral artery and the left external carotid artery.
After admission, ‘reflex syncope’ was suspected and the patient was administered oral calcium antagonists (Nimotop 30 mg qd) and intravenous Alprostadil for injection (Alprostadil 10 μg qd) to boost the cerebral circulation, without effect. A further episode of syncope occurred during the 18 h after admission and the patient was transferred to the Department of Respiratory Medicine for a D-dimer assay, which indicated a value of 1,200 μg/l. An enhanced chest computed tomography (CT) scan revealed filling defects in the right main pulmonary and left inferior pulmonary arteries, as well as bilateral pleural effusion (). Color ultrasonography of the heart revealed a dilated right ventricle and right heart overload, severe tricuspid regurgitation and severe pulmonary hypertension and the systolic pulmonary arterial pressure was 130 mmHg (). The patient was finally diagnosed with MPE.
Following confirmation, the patient underwent interventional mechanical thrombectomy combined with local and systematic thrombolytic therapy with low-dose urokinase.
Following the above therapies, digital subtraction angiography (DSA) of the deep veins of the lower limbs and the inferior vena cava demonstrated unobstructed blood flow, with no apparent thrombosis. A 4–5F double J tube was inserted through the right femoral vein to the main pulmonary artery for DSA of the pulmonary artery, to confirm the filling defect in the right main pulmonary artery (). An exchange guide wire was then inserted to coordinate with the tube for twists and drags to disintegrate the embolus. Following disintegration of the embolus, 500,000 units urokinase were injected into the tube for thrombolysis over 30 min. Subsequent DSA of the pulmonary artery indicated an improvement in the filling defect compared with before treatment (). The patient’s condition was significantly alleviated and the anoxia was reduced. A blood gas assay performed 2 h after surgery indicated a pH of 7.51, 72 mmHg PaO2, 29 mmHg PaCO2 and 23.1 mmol/l HCO3− (under the condition of a low flow rate of oxygen inhalation).
A postoperative intravenous drip of low-dose urokinase (200,000 units) was initiated and the patient was also treated with 5,000 units low-molecular-weight heparin, administered subcutaneously once every 12 h for three consecutive days. Warfarin (2.5 mg) was administered orally once every 12 h on a daily basis. The prothrombin time (PT) and international normalized ratio (INR) were monitored; when the PT and INR were twice and 2.5 times their respective normal levels, warfarin therapy was administered singly, plus anti-infective, supportive and oxygen therapies.
Three days after surgery, the patient demonstrated a distinctly improved mental condition with no further syncopal attacks. An enhanced chest CT scan 10 days after surgery revealed evident improvement of the thrombosis in the right main pulmonary artery and left inferior pulmonary artery branch, as well as disappearance of the pleural effusion, compared with the previous chest CT scan (). Color ultrasonography revealed a significant decrease of pulmonary artery pressure and right heart load; the systolic pulmonary arterial pressure was 71 mmHg. The patient was discharged from hospital 26 days after admission, with continued daily administration of 2.5 mg warfarin. Based on the monitoring of PT and INR, the doctor suggested discontinuation of warfarin 3 months after hospital discharge. The study was approved by the Ethics Committee of Taizhou People’s Hospital, Jiangsu, China and according to the Declaration of Helsinki. Written informed consent was obtained from the patient.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 0 + 1.5 = 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3080,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8474797-1,Extracted,"We report the case of a 41-year-old male who presented to our outpatient department with minor symptoms, including dyspnea during heavy activities. The patient did not have a history of fever, weight loss, malaise, or carotid tenderness but had a 1-year-old history of dyspnea on exertion. The patient never had any previous indications of autoimmune diseases or infections. Approximately 17 years earlier, at the age of 24, the patient experienced a frequent loss of consciousness during exercise. He had no history of hypertension, diabetes, smoking, dyslipidemia, or obesity. The patient was diagnosed with dilated cardiomyopathy a year ago, and echocardiography showed that all chambers were dilated with a left ventricular ejection fraction (LVEF) of 39%. The patient had received an angiotensin-converting enzyme inhibitor, a beta-blocker, and spironolactone and had good compliance and functional outcomes as the patient has presently been classified as New York Heart Association functional class I. Physical examinations revealed blood pressure of < 120/80 mmHg and a heart rate of 60 beats per minute (bpm) because of the optimal medical treatment he had received since last year. The patient had left carotid bruit and an enlarged heart with a grade IV/VI holosystolic murmur on the apex radiating to the axilla. Chest X-ray showed cardiomegaly, and electrocardiography revealed sinus rhythm with a heart rate of 64 bpm, poor R wave progression, and left ventricular hypertrophy (LVH) (Fig. ). Transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) showed eccentric LVH with reduced ejection fraction and some hypoechoic lesions resembling cysts at the anterior, anteroseptal, and anterolateral walls, suggestive of myocardial detachment. Both ventricles were dilated with reduced LVEF (31%). A severe functional mitral regurgitation secondary to increased left ventricular end diastolic volume and mild aortic regurgitation due to aortic root dilatation and uncoaptation of the left coronary cusps were detected. Moreover, TTE and TEE data obtained last year showed similar results. The patient underwent cardiac computed tomography (CT), which revealed a large calcified LSVA protruding into the left ventricular anteroseptal, anterior, and anterolateral walls, causing MD. The patient had no plaque, stenosis, or intimal wall thickness on the coronary arteries. CT angiography (CTA) showed diffuse calcification from the aortic arch and main branches of the aorta, extending to the descending thoracic and abdominal aortae. The patient had mural thickness at the left carotid artery as a sign of active disease, and no calcification or thickness was observed on either renal artery on CTA. We performed duplex ultrasonography to assess the involvement of aortic branch arteries. A long-diffuse-homogenous-concentric type IV plaque was detected along the left common carotid artery without the participation of other aortic branch arteries. The venereal disease research laboratory test, treponema pallidum hemagglutination assay, anti-hepatitis B surface antigen, anti-human immunodeficiency virus (anti-HIV), and anti-streptolysin titer O were nonreactive; inflammatory markers were slightly increased, including the C-reactive protein (CRP) (0.51 mg/dL) and erythrocyte sedimentation rate (ESR) (25 mm/h).
The patient was diagnosed with TA with MD complicating LSVA and dilated cardiomyopathy and received the treatment for chronic heart failure treatment: a beta-blocker, an angiotensin-converting enzyme inhibitor, and a mineralocorticoid antagonist, which were administered at the optimal dose. The patient has also received a high-dose steroid (40-mg methylprednisolone) as the initial therapy for TA and aspirin (81 mg, daily). Later, azathioprine (50 mg, b.i.d.) was added to further reduce inflammation. The symptoms and signs were improved, and inflammatory markers decreased after 3 months of therapy. Follow-up ESR was 17 mm/h, and the CRP level decreased to 0.3 mg/dL. The patient experienced no adverse events owing to the medications.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [60.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 60.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3081,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3174929-1,Extracted,"A 64-year-old Swiss Caucasian man patient with weak urinary flow and an elevated serum prostate-specific antigen (PSA) level of 130 μg/L was diagnosed with adenocarcinoma of the prostate on the basis of a biopsy (Gleason grade G3, Gleason score 4 + 4 = 8). A chest X-ray obtained for further staging showed a solitary node 9 mm in size in the left lower lung lobe. A computed tomographic scan of the patient's abdomen and skeletal nuclear scintigraphy revealed no further suspicious malignancies. Leuprolide acetate therapy delivered as a monthly dose was initiated. After two months of therapy, his serum PSA level decreased to 7 μg/L, and a chest X-ray showed complete regression of the lung node. A second dose of leuprolide acetate delivered every three months was applied. Two months later the patient was admitted to the hospital because of progressive proximal muscle weakness of six weeks' duration; slight, intermittent proximal muscle pain; dyspnea; and oliguria. He was treated with irbesartan and hydrochlorothiazide (CoAprovel® 150/12.5 mg Sanofi Pharma Bristol - Myers Squibb SNC, 174 Avenue de France F - 75013 Paris, France) because of arterial hypertension and tamsulosin (Pradif T® Boehringer Ingelheim GmbH, Dufourstrasse 54 CH 4002 Basel, Switzerland) because of weak urinary flow. He did not drink alcohol but smoked one pack of cigarettes per day. At the time of admission, the patient was alert, his body temperature was 38.6°C, his blood pressure was 140/80 mmHg, his heart rate was 80 beats/minute, his breathing rate was 20 breaths/minute, and his oxygen saturation level was 85% while breathing ambient air. He had edema in his lower legs. Painless muscle weakness prevented him from standing or sitting. He had normal strength in both his hands and his feet, but active lifting of his head, legs, and arms was barely possible while he was supine, and his speech was slurred. His reflexes, eye movements, and cranial nerve function were normal. He had no skin lesions. A chest X-ray showed right lung infiltration consistent with aspiration pneumonia. No signs of lung fibrosis were observed. His electrocardiogram was normal. His laboratory values were as follows: hemoglobin 148 g/L, leukocyte count 14.7 × 109/L, erythrocyte sedimentation rate 14 mm/hour, creatine kinase 121,530 U/L, C-reactive protein 39 mg/L, creatinine 51 μmol/L, BUN 6.4 mmol/L, sodium 122 mmol/L, and potassium 4.3 mmol/L. His serum 25-OH vitamin D level and thyroid gland function were normal, and his human immunodeficiency virus test was negative. MRI of his legs showed edema of the proximal muscles, particularly of both adductors. A biopsy of adductor muscle tissue was performed. Histological and immunohistochemical tests (inflammation marker, membrane attack complex, and major histocompatibility complex class I) showed signs of muscle necrosis (Figure , Figure ) and diffuse muscle infiltration of T lymphocytes (Figure ), but no signs of an autoimmune process. Additional serological tests for hepatitis B, hepatitis C, anti-nuclear antibodies, anti-neutrophil cytoplasmic antibodies, anti-double-stranded DNA antibodies, anti-mitochondrial M2 antibodies (anti-Mi2), anti-signal recognition particle (anti-SRP) antibodies, anti-Jo-1 antibodies and anti-polymyositis/scleroderma antibodies (anti-PM-Scl) all yielded negative results.
The patient was rehydrated with bicarbonate solution until his jugular veins were distended, and therapy with intravenous furosemide, ceftriaxone, methylprednisolone (500 mg/day), calcium, vitamin D, and alendronate was initiated. The patient's proximal muscle weakness declined within three days. Within four days, his serum creatinine level rose to 190 μmol/L, which was accompanied by oliguria, and his serum creatine kinase level dropped from a maximum of 169,910 U/L to 34,897 U/L. His steroid therapy was modified to oral prednisone 80 mg/day. Seven days later he could walk again with support, and his urine output and serum creatinine level had normalized. After 28 days, his prednisone treatment was tapered back to 35 mg/day, but within four days his serum creatine kinase rose again from 547 U/L to 1548 U/L without clinical deterioration. His prednisone dosage was increased to 70 mg/day, and his serum creatine kinase declined to normal (246 U/L) within six weeks. The patient was discharged from the hospital free of symptoms after undergoing orchiectomy on the 45th day following his initial admission. His serum creatine kinase and serum creatinine were normal, and he was prescribed prednisone 50 mg/day. After his discharge from the hospital, prednisone was tapered to 20 mg/day and his serum creatine kinase level rose slightly without clinical relapse. Nine months after discharge his prednisone therapy was stopped without a subsequent increase in his creatine kinase level. At his 12-month follow-up examination, the patient was in good clinical condition and had normal laboratory values, including PSA.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
3082,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6393102-1,Extracted,"A 32-year-old man was admitted for a spontaneous oppressive left side chest pain with a left arm irradiation for 2 days. He had a history of HME diagnosed in the childhood, with multiple leg exostosis resections and a leg-length inequalities correction. No genetic testing was available. He was a tobacco and cannabis smoker (13-pack-years). At admission, clinical exam did not reveal any sign of acute respiratory failure but a slight decrease in breath sounds in the left lung. Blood pressure was 130/80 mmHg, cardiac rate: 62 per minute, Sa02: 98%. Standard blood analysis and ECG were normal. A chest X-ray identified a left pneumothorax extending on axillary line and 2 dense opacities, 1 is located near the left fifth rib and the other being located near the right sixth rib (Fig. A). A chest computed tomography (CT) was performed and confirmed the left side pneumothorax and multiple costal exostoses (Fig. B–D). One exostosis was developed from the anterior arch of the left fifth rib with an intra-thoracic involvement and had a contact with the pneumothorax. Furthermore, CT-scan revealed bilateral paraseptal emphysema with an apical predominance.
Given clinical and radiological presentations, a conservative management was first proposed, resulting in a progressive and spontaneous improvement. The patient was discharged from hospital after 2 days management. Chest X-ray performed 2 weeks later exhibited complete resolution of the pneumothorax. Pulmonary function tests identified: forced expiratory volume in the first second (FEV1) 93% of predicted value, FEV1/forced vital capacity (FVC) 92%, RV 179% pred. The Alpha-1-antitrypsin level was normal.
Several weeks after this event, a surgical management of rib exostoses was proposed in order to prevent any pneumothorax recurrence. Surgery was performed by left-sided video-assisted thoracoscopy (VATS) and revealed exostoses of the left-sided fourth and fifth ribs with tight pulmonary adherences. A partial resection of the left-sided fourth and fifth ribs exhibiting intrathoracic exostosis lesions as well as a resection of 2 small emphysematous bullae were performed (Fig. ). Due to double exostoses withdrawal, an early pulmonary hernia occurs and was taken care with a Vicryl plate to filling the anterior parietal defect.
Histological examination demonstrated emphysematous bullae and exostosis of the fourth and fifth ribs, with no sign of malignant transformation.
Written informed consent was obtained from the patient for publication of this case report.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [62.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 62.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3083,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-2415356-1,Extracted,"A 34-year-old healthy woman with a twin pregnancy at 31 weeks and 6 days was admitted to our hospital with premature uterine contractions. She had no history of previous pregnancy, allergy or smoking. Vaginal examination revealed the presence of pooled amniotic fluid on a sterile speculum. Preterm PROM was diagnosed and a ritodrine infusion was started at a dose of 0.10 to 0.3 mg/minute, given in 1000 ml of normal saline, for 24 hours. At 24 hours, uterine contractions were arrested successfully, the ritodrine infusion was tapered and oral ritodrine was begun with 2 mg every 2 hours. She was also given dexamethasone (two 12 mg doses) to improve fetal lung maturation. Over the next 24 hours she became increasingly breathless with a tachycardia of 140 beats/minute, blood pressure of 110/70 mmHg, bilateral basal crackles and temperature of 37.6°C. Cardiotocography (CTG) revealed no signs of fetal distress. Pulmonary edema was diagnosed clinically and ritodrine administration was stopped, while she responded to a bolus of intravenous furosemide. Antibiotic treatment (amoxicillin/clavulanic acid 1000 mg/100 mg four times a day intravenously and erythromycin 1 g four times a day intravenously) was started to prevent possible intrauterine infection and nadroparin calcium (2850 IU once daily subcutaneously) was added for venous thomboprophylaxis. On the suspicion of an intrauterine infection an uneventful Cesarean section was performed 48 hours later, under spinal anesthesia, and the patient delivered healthy twins (Apgar score: 9 and 8 at 1 minute and 10 at 5 minutes for both neonates). As Cesarean section requires a T4 sensory level, 1.5 liters of normal saline was administered intravenously prior to surgery and 1 liter during surgery.
A few hours after delivery the patient became acutely dyspnoeic with a respiratory rate of 35 breaths/minute and bilateral rhonchi. Blood pressure was 75/45 mmHg. The electrocardiogram showed a sinus tachycardia of 123 beats/minute. In spite of treatment with oxygen via nasal spectacles (15 liters/minute), her arterial blood gas analysis showed a severe hypoxemia with cyanosis (pH 7.46, PaO2 6.25 kPa, PaCO2 3.99, bicarbonate 22 mmol/L). The patient was intubated and transferred to the intensive care unit (ICU). A chest X-ray (Figure ) revealed bilateral pulmonary edema with pleural effusions while a spiral computed tomography (CT) scan of the thorax supported the above findings and excluded any case of pulmonary embolism. A noradrenaline infusion was started at a low rate (2 μg/minute) during initial resuscitation to support blood pressure; noradrenaline infusion was gradually reduced and stopped after 90 minutes as the patient's hemodynamics stabilized. Central venous pressure was 12 mmHg under mechanical ventilatory support. An echocardiogram showed good biventricular function with normal chamber dimensions while there was no elevation in cardiac enzymes. Duplex ultrasound scanning of the lower extremities revealed no thrombosis of the femoral and popliteal veins.
During her first day in the ICU the patient developed fever (38.8°C), leucocytosis (17 × 109/liter) and mild coagulopathy (platelets 110 × 109/liter, activated partial thromboplastin time 47 seconds, fibrinogen 140 mg/dl). A serologic examination of pleural fluid was performed and revealed no signs of exudate. Extensive cultures (blood, sputum and vagina) remained negative, while C-reactive protein (CRP) was increased (15 mg/dl). After the third day of treatment, the patient made a quick recovery with complete resolution of the pulmonary edema and she was extubated 1 day later.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [140.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 140.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3084,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7816498-1,Extracted,"A 62-year-old woman with a history of congestive heart failure, coronary artery disease, diabetes mellitus type 2, and recent coronary artery bypass graft (CABG) presented to the emergency department with acute weakness, dizziness, and malaise.
Past surgery history was significant for a two-vessel coronary artery bypass graft involving the left internal mammary artery to the left anterior descending artery and the left radial to obtuse marginal artery nine days prior to presentation. In the perioperative period she received three heparin boluses at 40u/kg based on a weight of 66.7 kg as well as a heparin infusion dosed between 16u/kg/hr-26u/kg/hr. for 3 days. She had no family history of hematological disorders or hypercoagulability. She was on low-dose aspirin. Her complete blood count (CBC) was normal prior to CABG including platelet count of 268 x 10P3P/μL (normal 150–379 x 10P3P/μL) and at hospital discharge was 174 x10P3P/μL with post-operative hematocrit of 36% (normal 37.5–51%).
On physical examination she was afebrile, hypotensive with systolic blood pressure in the 70s, and in rapid atrial fibrillation with heart rate 120–130 s. She denied abdominal pain and had a benign abdominal examination. Laboratory data revealed white blood cell count 10.7 x 10P9/PL (normal 3.4–10.8 x 10P9/PL), hematocrit 19%, and platelet count of 49 x10P3P/μL. Complete metabolic panel and lactate were normal. Troponin was elevated at 0.21 ng/mL (normal 0.00–0.07 ng/mL. Chest x-ray was normal. A limited beside echocardiogram demonstrated no pericardial effusion. She received intravenous fluid resuscitation and transferred to the intensive care unit for further evaluation.
Upon arrival to the intensive care unit, she received 2 units of packed red blood cells with appropriate increase to hematocrit 25% post-transfusion and 1 unit of platelets with increase to 73 x10P3P/μL. Further laboratory evaluation was negative for hemolysis with normal lactate dehydrogenase 292 U/L (normal 119–226 U/L) and haptoglobin 98 mg/dL (normal 34–200 mg/dL). A disseminated intravascular coagulopathy (DIC) panel demonstrated d-dimer of > 40.00 μg/ml (normal <=0.49 μg/ml), normal fibrinogen 214 mg/dL (normal 175–475 mg/dL), international normalized ratio (INR) 1.4 (normal 0.9–1.1), protime (PT) 16.7 s (normal 12.0–14.4 s), partial thromboplastin time (PTT 37.3 s (normal 22.0–35.0 s), normal thrombin time (TT), and normal red blood cell morphology.
To evaluate for bleeding, a computed tomography (CT) angiogram of the chest, abdomen, and pelvis was ordered and demonstrated filling defects suggestive of right atrial thrombus, splenic vein.
thrombosis with splenic infarct, and mild to moderate associated hemoperitoneum. She denied abdominal trauma. Surgery service was consulted and concerned about splenic hemorrhage. Hematology was consulted to evaluate the etiology of spontaneous splenic vein thrombosis with associated hemorrhagic infarction.
Unfortunately, on the day of Hematology evaluation (post-operative day 10) she developed left-sided weakness and balance changes concerning for stroke and an MRI revealed infarct involving the distribution of the right anterior cerebral artery. A transesophageal echocardiogram revealed large immobile thrombus in the right atrium with a second thrombus adjacent to this which was mobile and.
arising from the left tricuspid valve annulus, large thrombus in the left atrial appendage, and absence of a patent foramen ovale (Fig. ). She was not a candidate for thrombolytic therapy due to thrombocytopenia. She was calculated to have a 4Ts score of 7. A heparin PF4 IgG antibody was.
markedly positive with 3.290 OD. Serotonin release assay was not performed due to the high probability of HIT evidenced by the markedly positive PF4 IgG and 4Ts score of 7. Together these predictive tools indicate a 72% likelihood ratio and 99% posttest probability of HIT []. Lower extremity ultrasound was negative for thrombosis while upper extremity ultrasound showed cephalic vein thrombosis. The patient was diagnosed with heparin-induced thrombocytopenia with thrombosis (HITT).
Given extensive thrombosis in HIT, anticoagulation was cautiously started with bivalirudin. Our organization utilizes direct thrombin inhibitor (DTI) levels to monitor and adjust bivalrudin dosing. Given the presence of hemoperitoneum prior to bivalruin dosing, bivalrudin was started at 10.01 mg/hr. and titrated to 12.012 mg/hr. based on DTI levels and a dose of 0.13–0.156 mg/kg/hr. at a weight of 77 kg. DTI levels were maintained at goal between 60 and 90 s throughout therapy. She remained clinically stable from the intrabdominal hemorrhage and transitioned to warfarin anticoagulation. Platelets recovered to 108 x10P3P/μL four days after starting alternative anticoagulation and greater than 150 x10P3P/μL nine days after therapy for HITT initiated. The patient had repeat transthoracic echocardiogram after 3 months of warfarin anticoagulation with the resolution of intra-cardiac thrombi. She continues on long-term anticoagulation for atrial fibrillation.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [130.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 130.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 =  3.0.
The patient not been diagnosed with pulmonary embolis (PE), but the patient has previously been diagnosed with deep vein thrombosis (DVT), we increase the current total by 1.5 so that 3.0 + 1.5 = 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
3085,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6176874-1,Extracted,"A 56-year-old woman presented with sudden onset central chest pain and shortness of breath on a background of PCI and stenting for worsening angina 3 weeks before.
On examination, the patient was dyspnoeic with a heart rate of 100 beats/min and blood pressure of 110/70 mmHg. Normal S1 and S2 heart sounds were present on auscultation. An electrocardiogram was performed, which showed normal sinus rhythm with ST-elevation in leads I and aVL. The patient was haemodynamically stable on presentation; however, the condition of the patient deteriorated and a dobutamine infusion was commenced at a rate of 5 ug/kg/min. The patient was then transferred for primary PCI. The patient was on aspirin and clopidogrel 75mg along with atorvastatin 40 mg at night.
The patient had a 10 pack-year smoking history; however, they had not smoked for the past 10 years. Background medical history was significant for hyper-cholesterolaemia and a spontaneous intracranial bleed 4 years previously.
A coronary angiogram was performed that confirmed a LAD/D1 occlusion caused by a stent thrombosis. Thrombus aspiration and stenting was performed with good result and TIMI 3 flow. Clopidogrel was switched to ticagrelor following the procedure.
Despite successful intervention, the patient remained persistently hypotensive and an echo revealed a reduced ejection fraction of 10–15% with anterior apicoseptal hypokinesis, a dilated left atrium and moderate functional mitral regurgitation. Dobutamine requirements increased to 10 μg/kg/min, and the decision was made to insert an IABP and Swan Ganz catheter for management of the persistent hypotension in the setting of a reduced ejection fraction. This was done percutaneously via the right groin. Unfractionated heparin was commenced at 1000 IU/h.
Over the next 48 h, the patient’s condition improved with a reduction in ionotropic requirements and stable renal function. Due to this marked improvement in haemodynamic parameters, the decision to remove the device was made.
At the time of removal, however, it was noticed that there was blood within the helium tubing suggesting device perforation. The pump was removed without difficulty to 10 cm, at which point significant resistance was encountered suggesting balloon entrapment. Right lower limb pulses were not palpable, however, Doppler signals were present distally.
The vascular surgery team was contacted and a computed tomography angiogram was performed, which showed the tip of the balloon to lie within the distal right common iliac artery (Figures ). Unfractionated heparin was re-commenced at 1000 IU/h.
The patient was brought to the operating theatre for cut down and removal under general anaesthesia.
A transverse incision was made in the right groin and extended inferiorly to form a T shape. A femoral arteriotomy was performed after achieving proximal and distal control of the common femoral artery. The existing arterial puncture site with catheter in situ was extended transversely, and the balloon was extracted without difficulty. On inspection following removal, a significantly sized solid thrombus was visible within the lumen of the balloon (Figure ).
A Fogarty catheter was used to perform an iliac embolectomy, which resulted in the removal of a small clot. The arteriotomy site was closed uneventfully as was the skin. The Swan Ganz catheter was left in situ. Good distal pulses were present following the procedure.
Testing of the balloon post-removal showed a number of small holes and a very solid thrombus that could not be fragmented with finger pressure (Figures and )
The patient encountered no post-operative complications from the surgery and was discharged home. Management of heart failure in the setting of a reduced ejection fraction is ongoing.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [100.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 100.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 3 + 1.5 = 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
3086,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-314,Extracted,"Twelve hours after undergoing an exploratory laparotomy for a perforated duodenal ulcer, a 36-year-old man has shortness of breath. He has asthma well controlled with an albuterol inhaler. His father died of lung cancer at 62 years of age. He has smoked one pack of cigarettes daily for 14 years. He does not drink alcohol. He appears uncomfortable. His temperature is 37.4°C (99.3°F), pulse is 98/min, respirations are 19/min, and blood pressure is 122/76 mm Hg. Examination shows reduced breath sounds over the left lung base. Cardiac examination shows no abnormalities. There is a clean, dry surgical incision over the midline of the abdomen. Bowel sounds are hypoactive. The calves are soft and nontender. His hemoglobin concentration is 12.9 g/dL, leukocyte count is 10,600/mm3, and platelet count is 230,000/mm3. An x-ray of the chest in supine position is shown.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [98.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 98.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 =  1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3087,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3966445-1,Extracted,"A 32-year-old overweight male with recently diagnosed type 2 diabetes presented to an urban, university hospital ED with a chief complaint of palpitations, shortness of breath, light-headedness, and “feeling ill.” He had seen his primary care physician twice in the previous weeks for similar symptoms, and he had started an exercise program to address his new-onset diabetes. After an unsuccessful attempt to see his primary care physician again that day, the patient came to the ED for care. The triage nurse charted the patient’s chief complaint as “chest pain with shortness of breath for one week increased with exertion” and recorded a heart rate at 140. The remaining vital signs at triage were a blood pressure of 128/71 mm/Hg, respirations of 28, and a temperature of 35 degrees C. Room air pulse oximetry was recorded at 95%. At the time of his arrival, the ED was over 250% of capacity (patients/beds), and the institution was on ambulance diversion. Since all 40 licensed ED beds were occupied, the patient was placed on a gurney in one of several narrow hallways within the ED. Twenty patients were already receiving hallway care when the patient presented to the ED, and another 40 were in the waiting room. The triage nurse immediately performed an electrocardiogram (EKG) per ED policy, which was immediately reviewed by an attending physician on duty at that time. This physician noted there was no ST-elevation myocardial infarction (STEMI) on the EKG and, at the request of a nurse, wrote orders for a basic lab panel. As it was the end of shift, this physician had no further involvement with the patient and did not mention his/her involvement to the next attending. On average, attending physicians in this ED screen as many as 25 patient EKGs for STEMI while providing direct supervision to an additional 30 patients during a 10-hour shift.
Four hours after triage, the patient was formally evaluated by an off-service PGY1 (post-graduate year one) resident. The resident was aware that an attending physician had already viewed the EKG and ordered labs. The resident charted the results, including the comments from the EKG, and performed a history and physical. The prior attending was off-shift, thus the resident presented the case to a new attending physician. At that time the ED remained crowded, with all its resources overwhelmed. The oncoming attending physician had immediately become overwhelmed with critically ill and injured patients and was repeatedly confined to the resuscitation room with medical or trauma codes. During the first 2 hours of the shift, this new attending physician performed over 10 initial EKG screenings. At 5 hours post-arrival, the resident was able to present the case to the new ED attending physician, who then examined the patient in the hallway. The history obtained by the resident noted the patient never actually had chest pain, and this was confirmed by the attending physician. The point-of-care glucose was 463 mg/dL, and the initial diagnostic impression was probable hyperglycemia with dehydration. Because the patient was in the hallway, there was no formal location to maintain his paper records, and the EKG was no longer available for review. This attending physician did know that, per ED policy, a patient with dyspnea and chest pain would have automatically received a triage EKG and assumed it had been reviewed by the prior attending physician. If the initial screening review of the EKG had been concerning, the patient would have been moved out of the hallway to a monitored licensed bed, or “doubled up” in the central treatment area of the ED. Six hours after presentation the patient’s laboratory studies returned with results consistent with the initial impression of possible mild diabetic ketoacidosis (DKA) and dehydration. The blood glucose was 417 mg/dL, bicarbonate 19 mmol/L, and an anion gap of 15. Venous blood gas pH was 7.34. PCO2 was mildly decreased. Other labs were within normal limits. The patient was treated with 3 liters of IV normal saline, as well as 5 units IV and 5 units subcutaneous regular insulin. A chest radiograph was performed and was normal. Oxygen saturation was checked multiple times and ranged from 95 to 98% saturation on room air.
After therapy, the patient’s glucose decreased to the 200 mg/dL range, and a repeat chemistry panel showed normal bicarbonate with no anion gap. The patient’s heart rate ranged from 66 to 114 for much of the stay in the ED, and by time of discharge was normal. The dyspnea had improved. The patient passed an oral trial of fluids, felt improved, and wanted to return home. Because this was a new onset DKA, albeit mild, an informal discussion was held with the hospitalist about admission. The hospitalist, based on the quick resolution of symptoms and patient’s access to his primary care physician, recommended outpatient management. The patient was then discharged home with the final diagnosis of hyperglycemia, mild DKA, dyspnea secondary to metabolic acidosis, and dehydration. A more aggressive regimen for his diabetes was prescribed, and home equipment for self-monitoring ordered. Close follow-up with his primary care doctor was specified. The patient was discharged 8 hours after arrival in the ED. Discharge vital signs were 154/86 mm/Hg, heart rate 94, respiratory rate 20, temperature 37 degrees C, and 98% room air saturation. He never occupied a licensed ED bed and was never on a cardiac monitor, as these were all in use.
Two days later, the patient developed severe shortness of breath; therefore, 911 was called and EMS activated. The patient had a cardiac arrest en route to the same hospital from which he was discharged two days earlier. Resuscitative efforts were unsuccessful, and the patient expired. An autopsy was performed and showed multiple acute and chronic pulmonary emboli as the primary cause of death. The initial EKG was retrospectively interpreted by a cardiology attending physician as showing “right axis deviation, multiple ST and T-wave changes suspicious for anterior ischemia.” The autopsy did not show coronary artery disease or evidence of myocardial infarction.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [140.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 140.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3088,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6590859-2,Extracted,"Case 2 presentation
The patient is a 62-year-old African American male with an unknown past medical history who was brought by EMS after being found down at his home without heat by his neighbor.
On physical examination, his vital signs were: rectal temperature was 28.5 °C, heart rate 94 bpm, respiratory rate 22 breaths/min, and blood pressure 170/100 mmHg. On presentation, his Glasgow Coma Scale was 8 (E4 V1 M3). He was found to be non-responding verbally, pupils were reactive to light, lungs clear to auscultation, the heart had regular rate and rhythm. He was intubated in the emergency department.
Initial laboratory with blood gas analysis showed a metabolic and respiratory acidosis with the following pH 7.103; pCO2 65.6 mmHg; pO2 514.9 mmHg; HCO3 20.0 mmHg on the following ventilator settings: tidal volume 450 mL, respiratory rate 18 breaths/min, fraction of inspired oxygen (FiO2) 100% and positive end-expiratory pressure (PEEP) of 5 cmH2O. Other laboratory findings were the following: sodium 165 mmol/L, potassium 3.0 mmol/L, chloride 122 mmol/L, carbon dioxide (CO2) 18 mmol/L, glucose 182 mg/dL, blood urea nitrogen (BUN) 86 mg/dL, creatinine 1.83 mg/dL, AST 92 U/L, ALT 56 U/L, lipase 300 U/L, creatinine kinase 1,661 U/L, troponin 0.02 ng/mL, white blood cell count (WBC) 29.50 x 103 cmm, hemoglobin 5.4 g/dL, platelets 225 x 103 cmm, PT 17 sec, INR 1.5, APTT 36.4 sec, lactic acid 6.3 mmol/L. Urine drug screening was negative for any substances and alcohol level was <10 mg/dL. Initial EKG showed atrial fibrillation with premature ventricular complexes, left axis deviation, lateral injury pattern. Initial chest x-ray showed diffuse opacities on bilateral lung fields consistent with aspiration pneumonitis or infection.
The patient was admitted to the Intensive Care Unit (ICU) for rewarming with IV fluids and Bair Hugger (3M temperature management system). He developed multifactorial shock and was started on vasopressors, blood transfusion, and antibiotics. An echocardiogram was done 2 days after admission for shock investigation which demonstrated moderate left ventricular hypertrophy, anteroseptal and anterior akinesis with global hypokinesis, ejection fraction 25% with suspicion of apical thrombus and left atrial enlargement (Figure ).
Outcome and Follow-up
The patient was later started on anticoagulation after anemia resolved but anticoagulation was later held as he developed a psoas hematoma. He had 2 subsequent echocardiograms including a transesophageal echocardiogram during hospitalization that were concerning for apical thrombus. The patient was later discharged to a nursing home facility after 80 days of hospitalization with multiple complications.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [94.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 94.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3089,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7681755-1,Extracted,"The patient is a 24-year-old African-American female with a past medical history of tuberous sclerosis, gestational hypertension, stable renal angiomyolipoma, and recent pneumothorax, most recently three months prior to admission. She presented with a four-week history of productive cough. The cough was described as occurring intermittently throughout the day, productive of light-yellow colored sputum, and being associated with rhinorrhea and sinus congestion. She reported her uncle as a sick contact, who was being treated for an upper respiratory infection at the time she developed symptoms. The patient endorsed shortness of breath with mild exertion. The patient also complained of increased urinary frequency and dysuria that had started three days prior to admission; however, she denied any complaints of headaches, fever, chest pain, weakness, changes in vision, nausea, vomiting, or changes in bowel habits. The patient admitted to actively smoking tobacco and smokes approximately five cigarettes daily.
On presentation to the emergency department, the patient was not in respiratory distress. Her vital signs showed a blood pressure of 148/77 mmHg, heart rate of 74 beats per minute, temperature of 98.3 degrees Fahrenheit, and oxygen saturation of 97% on room air. The patient’s physical examination was significant for absent breath sounds in the right basilar and anterior-mid lung field compared to the left with no wheezes or rales. Her examination was otherwise benign. Her laboratory studies are shown in Table .
She was evaluated further with a chest X-ray (Figure ), computed tomography (CT) of the chest, abdomen, and pelvis (Figure ), which was compared to her CT chest from her visit three months prior to her current admission (Figure ), and magnetic resonance image (MRI) of the abdomen (Figure ). The summary of imaging impressions is given in Table .
The patient was determined to have developed a recurrent spontaneous pneumothorax as a result of her cough. She received a dose of albuterol-ipratropium nebulizer therapy and a one-time 500 mg oral dose of levofloxacin followed by a chest tube placement. The patient’s pneumothorax ultimately resolved. Upon removal of the chest tube three days later, the patient was discharged to her home in stable condition, with advice to follow-up regularly with the medical team in the outpatient clinic.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [74.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 74.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3090,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8517785-1,Extracted,"A 68-year-old female presented to the emergency department with melena.
The melena started a day before she consulted us. She had no past history of chronic abdominal symptoms suggesting the presence of celiac disease.
The patient had a history of hypertension and hyperlipidemia.
She had no significant personal and family history.
Her body temperature was 36.4 ºC, blood pressure was 128/85 mmHg, and heart rate was 98 bpm with sinus rhythm. She had mild abdominal tenderness, but there was no obvious hepatosplenomegaly or lymphadenopathy. Digital rectal examination revealed melena.
Laboratory tests indicated a hemoglobin level of 11.3 g/dL, blood urea nitrogen level of 26.0 mg/dL, and creatinine level of 1.64 mg/dL. Her serum lactate dehydrogenase level was 232 U/L (106- 211 U/L) and soluble interleukin-2 receptor level was 213 U/mL (145- 519 U/mL) (Table ).
Urgent esophagogastroduodenoscopy (EGD) showed an ulcerative lesion with fresh blood clots in the transverse part of the duodenum (Figure ). Based on the location and shape of the lesion, we suspected not only a peptic ulcer, but also an ulcer caused by vascular malformation or malignancy. Therefore, we decided to interrupt the endoscopy and perform contrast-enhanced computed tomography (CT) scan, which showed slight localized contrast enhancement on the wall of the transverse part of the duodenum in the early phase of contrast injection (Figure ). No vascular lesions were observed, and there was no extravasation of contrast agent in the delayed phase. EGD was immediately resumed again for further observation of the lesion. When we removed the blood clots, a protruding vessel was seen at the base of the ulcer, which was coagulated using hemostatic forceps (Coagrasper; Olympus Corp., Tokyo, Japan) (Figure ).
Following this hemostatic treatment, the patient was discharged from the hospital without re-bleeding. The lesion that caused the bleeding was suspected to be a malignant tumor of the duodenum based on its location. EGDs, including forceps biopsies from the ulcerative lesion, were performed three times after the initial hemostatic treatment. While the first and second biopsies revealed no malignancy, the third biopsy showed findings suggestive of malignant lymphoma. On pathological evaluation, diffuse proliferation of atypical medium-sized lymphoid cells was seen in the entire mucosa, along with a few intraepithelial lesions (Figure and ). No necrosis was observed. Immunohistochemical analysis revealed that the cells were positive for CD3 and CD56, and negative for CD4, CD5, CD8, CD20 and EBER (Figure -).
At this point, MEITL was suspected, and examinations for systemic lesions were subsequently performed. No abnormal lymphocytes were found on iliac bone marrow examination. 18Fluorodeoxyglucose (18FDG) positron emission tomography/CT (18FDG-PET/CT) showed nodular FDG accumulation in the wall of the transverse part of the duodenum, consistent with the findings of contrast-enhanced CT (Figure ). There was no abnormal FDG accumulation in the systemic lymph nodes or other parts of the gastrointestinal tract. The results of total colonoscopy and random biopsies of the gastrointestinal tract were unremarkable.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [98.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': True, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 98.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
3091,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4815390-1,Extracted,"A 21-year-old young woman presented with a chief complaint of swelling of bilateral lower extremities, more on the left side than the right, for 2 days prior to seeking medical attention. One month before, she described a similar swelling of her right lower extremity that lasted for about 1 week which spontaneously improved. She has one child of 4 years of age and has been taking oral contraceptive pills for 2 years. She had a history of thrombocytopenia of which cause has not yet been determined. She has no known underlying cancer. She has no history of miscarriage. Upon admission, she was fully conscious and alert. Her weight and height were 96 kg and 170 cm, respectively. Her initial blood pressure, heart rate, respiratory rate, and body temperature were 112/82 mmHg, 108 bpm, 20 bpm, and 37.9 c, respectively. She had swelling of both lower extremities more pronounced on the left side. After an initial assessment, color Doppler ultrasonography was done and revealed acute deep venous thrombosis. She was positive for lupus anticoagulant which suggested that antiphospholipid syndrome was the cause of her extensive thrombosis. Further, CT venography revealed partial thrombosis of the entire inferior vena cava (IVC) down to the common and external iliac veins and common femoral veins []. A ventilation-perfusion lung scintigraphy was requested to evaluate for pulmonary embolism. Imaging was carried out with Vertex V60 EPIC HP Gamma Camera System (ADAC Laboratories, USA) using a LEGP collimator. For the ventilation study, the patient inhaled 20 mCi of Tc-99m diethylenetriamine-pentaacetic acid aerosol and 6-view images of the lungs were obtained for 300 k counts per view. Immediately after the ventilation study, the lower extremity ascending RNV was done by injecting 3 mCi of Tc-99m macroaggregated albumin intravenously at the superficial vein of each feet with elastic bandages tied around both ankles. Anterior and posterior scintigraphic imaging started at the ankle level with the gamma camera moving proximally up to the upper abdomen at a speed of 20 cm/min. Then, immediately after the venogram was acquired, the 6-view perfusion lung images were obtained for 1200 k counts. A postexercise scan of the lower extremities was also done after the patient performed alternate leg raising for about 15 min during the time the perfusion lung scintigraphy was being acquired. The RNV revealed the absence of radiotracer activity in the deep venous system of bilateral lower extremities with the radiopharmaceutical shunting into numerous superficial collateral veins at the calves, thighs, pelvis, and the anterior abdominal wall. There was diminished radiopharmaceutical activity in the IVC with shunting into the paravertebral veins.[] The postexercise scan revealed that there was retention of the radiopharmaceutical in both calves and faintly along the deep veins of the thighs and the iliac veins. These findings mirror that of the contrast-enhanced CT which indicate extensive thrombosis in the deep veins of both lower extremities up to the iliac veins and the IVC []. Upon examination of the lung scintigraphy, a large mismatched perfusion defect at the left lower lobe was seen which suggested pulmonary embolism. It was noticed that there is radiopharmaceutical activity accumulation in the upper abdomen which was seen in only the perfusion scan but not in the ventilation scan []. A SPECT/CT of the lung and upper abdomen was performed to better characterize these lesions and revealed that there was increased radiopharmaceutical uptake in segment 4 of the liver or the quadrate lobe []. The SPECT/CT of the lung also more clearly revealed the perfusion defect at the superior and basal segments of the left lung with no corresponding opacity on the CT image, which further consolidates the diagnosis of pulmonary embolism (image not shown).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [108.0, 'bpm'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 108.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
3092,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8260197-1,Extracted,"A 46-year-old male with a past medical history significant for remote IVDU and treated hepatitis C virus (HCV), presented with shortness of breath, fatigue, and intermittent low-grade fever for one month. He denied any recent headache, cough, or diarrhea. He also denied any recent IVDU. On presentation, he was febrile at 101 F and had tachycardia at 112 bpm. Cardiovascular examination revealed a holosystolic murmur at the apex. Laboratory workup was remarkable for leukocytosis 35,000 per mm3 with 89% neutrophils. Liver and kidney function tests were normal. HIV screening test was negative. The right upper quadrant ultrasound was negative for cirrhosis. Alpha-fetoprotein was negative. Due to high suspicion of infective endocarditis, the patient was started empirically on intravenous vancomycin. An echocardiogram showed mitral valve vegetation with regurgitation (Figure ). Blood culture grew Rothia mucilaginosa. The patient was discharged to a subacute care facility with six weeks of intravenous vancomycin.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [112.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 112.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3093,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8121203-1,Extracted,"A 58-year-old male with no prior medical problems, who was leading an active lifestyle, presented to our emergency department with progressively worsening shortness of breath and abdominal distension for one month. His breathlessness had gradually worsened to the point where he felt winded even upon getting out of bed. He also reported intermittent abdominal discomfort associated with a decrease in appetite for a similar duration. Initially, the patient sought medical attention from his primary care physician and was started on treatment for community-acquired pneumonia without any significant improvement. He denied any fever, chills, night sweats, or weight loss. Review of systems was unremarkable including bowel habits, which were regular.
The patient had been a nonsmoker his entire life but had secondhand exposure to smoking from his wife. His alcohol consumption was limited only to social occasions and he denied any illicit drug use. He had no known allergies, nor did he take any daily medications. Family history was not significant for any malignancies. No recent travel was reported and by occupation, he was a tailor.
On examination, the patient was found lying comfortably in bed. Vital signs were significant for a pulse rate of 106 beats per minute, respiratory rate of 17 breaths per minute, and oxygen saturation of 98% on 2 liters of oxygen via nasal cannula. He was normotensive and afebrile. No cyanosis, clubbing, rash, or lymphadenopathy was noted. Respiratory examination revealed decreased air entry and dullness on percussion on the right side of the chest. His abdomen was distended, non-tender with a palpable liver and spleen, and he was noted to have shifting dullness. The rest of the examination was within normal limits. Laboratory data are summarized in Table .
Upon admission, a chest x-ray showed a near-complete opacity of the right hemithorax secondary to a large pleural effusion (Figure ). A bedside thoracocentesis was performed and 600 milliliters of whitish milky pleural fluid was drained (Table ). The pleural fluid analysis was consistent with chylothorax. A computed tomography (CT) scan of the abdomen and pelvis with contrast revealed a large soft tissue mass in the region of the pancreatic head with extensive diffuse lymphadenopathy and minimal perihepatic ascites (Figure ). Further review of imaging revealed soft tissue deposits in the anterior abdomen and pelvis with peritoneal enhancement concerning for peritoneal carcinomatosis. The initial impression was pancreatic adenocarcinoma with peritoneal seeding. An oncology consultation was requested and a biopsy of the peritoneum was advised due to ease of access. An ultrasound-guided biopsy of the peritoneal lesion with analysis of the peritoneal fluid (Table ) and a CT-guided placement of a right chest pleural drainage catheter was performed by interventional radiology. Analysis of the peritoneal pathology specimen revealed a mature B-cell neoplasm reported as a grade 2 follicular lymphoma (Figure ), and immunophenotype stains revealed CD20+, CD79A+, CD10+, BCL-2+, BCL-6+, CD5-, CYCLIN D1-, CD3-, CD43-, AE1/AE3-. Cytology from the previously obtained pleural fluid also demonstrated lymphomatous infiltration. Due to persistent right pleural effusion, embolization of the thoracic duct was attempted without success. The patient was eventually transferred to a tertiary center under thoracic surgery service for further management of the high output chylothorax. He eventually was enrolled in the lymphoma program of the tertiary care center and started on chemotherapy.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [106.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 106.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
3094,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7798777-1,Extracted,"A 75-year-old female presented to the emergency department with dyspnoea. She had been treated for recurrent lower respiratory tract infections by the general practitioner (GP) with oral antibiotics (12 cases in the past 14 months). Her relevant medical history included chronic kidney disease stage 3 (baseline creatinine 80–110 µmol/L), polymyalgia rheumatica requiring long-term steroids, asthma and chronic back pain. The pneumonia diagnosis was confirmed by a chest radiograph and CT showing multifocal nodular consolidation in the right lower lobe with cavitations and blood cultures were taken that grew Staphylococcus aureus.
Her medical history otherwise included depression, hypercholesterolaemia, gastro-oesophageal reflux disease, spondylosis, glaucoma, hypertension, lacunar stroke, transient ischaemic attack, vitamin B12 deficiency and vascular dementia.
Her long-term treatment included hydromorphone, paracetamol, topiramate, paracetamol–codeine–doxylamine, doxylamine, colecalciferol, aspirin, duloxetine, pantoprazole, prednisolone, docusate, macrogol, hydroxocobalamin, salbutamol and denosumab.
On presentation, she was initially afebrile, heart rate of 95 bpm, respiratory rate of 25 breaths per minute and oxygen saturation of 96%. On examination, there were crackles on the right base, dual heart sounds with no murmurs and no peripheral stigmata of infective endocarditis. She was subsequently treated for pneumonia and urinary tract infection with intravenous piperacillin–tazobactam. The working diagnosis was S. aureus bacteraemia secondary to a pulmonary source.
The patient was transferred to the closest tertiary hospital as the eventual need for further investigations, including a trans-oesophageal echo, was anticipated in the context of S. aureus bacteraemia. The treatment of her bacteraemia was eventually changed to intravenous flucloxacillin (2 g four times daily) once sensitivities were confirmed. Flucloxacillin was planned to continue for a further 5 weeks via peripherally inserted central catheter (PICC) on an 8 g/24 hours infuser that was monitored via hospital in the home (HITH).
Four weeks into the HITH treatment, the patient developed nausea and was investigated with blood results that showed worsening renal function associated with HAGMA. She was subsequently referred back to the regional hospital. Her heart rate was 105 bpm, respiratory rate of 20 breaths per minute and O2 sat 98% on room air. At that point, HAGMA was attributed to an acute kidney injury (AKI). Following adequate fluid resuscitation, HAGMA and AKI persisted. She was investigated for the AKI with a renal ultrasound which was negative and there were no eosinophils found in the urine. Interstitial nephritis secondary to flucloxacillin use was considered as another reason for her AKI but was deemed unlikely. The treatment plan was to commence sodium bicarbonate 840 mg once daily following consultation with the renal team. Ultimately, further investigations for the AKI were completed at the tertiary hospital. The HAGMA was suspected to be caused by the concurrent use of flucloxacillin and paracetamol. As a result of this, flucloxacillin was changed to cefazolin and the patient transferred again to a tertiary facility pending further investigations as well as suspected pulmonary embolism following reports of chest pain.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [105.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 105.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3095,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6940160-1,Extracted,"A 79-year-old Chinese Han man with a history of squamous cell carcinoma of the esophagus was treated with surgical excision 3 months before admission. He denied having any family history of digestive disease.
He presented with progressive dysphagia and esophageal metallic stent placement (20 × 70 mm, the upper edge was 24 cm from the incisors) for anastomotic stenosis (27.5 cm from the incisors) 1 month before. At this time, he was transferred to our emergency department due to hematemesis and tarry stool. Abdominal computed tomography (CT) revealed only postoperative changes in esophageal cancer and esophageal metallic stent, which was placed close above the aortic arch (Fig. ). Upon arrival at the intensive care unit, the patient vomited approximately 500 mL of fresh blood. On physical examination, he was oriented and diaphoretic with a pale conjunctiva. He had no heart murmur, clear breathing sounds, and an old operative scar over the left chest, and the abdomen was soft without tenderness. Blood pressure (BP) was 72/56 mmHg, heart rate was 108 beats/min, respiratory rate was 28 breaths/min, and oxygen saturation was 91% in room air. Hemoglobin level was 6.8 g/dL. Large volumes of blood products were rapidly transfused, including 7.5 units of packed cells and 340 mL of fresh frozen plasma, and noradrenaline were administered simultaneously. When the patient's BP reached 90/60 mmHg, gastroscopy demonstrated large quantities of fresh blood and blood clots in the esophagus and stomach, so the source of the bleeding could not be identified. A vascular rupture was highly suspected. CT angiography (CTA) of the aorta was performed, which disclosed an aortic arch with possibly localized rupture (Fig. ). A cardiovascular surgeon performed an emergent angiography of the aorta, which showed bleeding from the wall of the aortic arch, so a diagnosis of AEF was confirmed, and an long covered stent (26 × 200 mm) was implanted (Fig. ) for thoracic endovascular aortic repair (TEVAR). The patient underwent fasting and received antibiotic treatment (intravenous cefodizime [2.0 g] once every 12 hours for 2 weeks and then replaced with intravenous combination of levofloxacin [0.5 g] once a day and piperacillin-tazobactam [4.5 g] once every 12 hours for another 2 weeks). The patient recovered well and was admitted to the department of gastroenterology on post-admission day 2. On post-admission day 9, esophagogastroduodenoscopy showed neither endoleakage nor peptic ulcer, and a jejunal feeding tube was established to provide enteral nutrition. Re-hematemesis occurred abruptly and massively on post-admission day 26, and the patient eventually died. The son of the patient provided informed consent for the publication of the case.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [108.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",5,5,5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 108.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 3.0 + 1 = 4.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 4.0 + 1 =  5.0.
The patient's Well's score for pulmonary embolism is 5.0."
3096,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-2830976-1,Extracted,"A 63-year-old Japanese woman was diagnosed with IMF in 1994 and was since treated with hydroxycarbamide. She was admitted to our hospital on January 22, 2008, with melena. On admission, her consciousness was clear. Her physical status was moderate and her nutrition was good. She had a blood pressure of 104/56 mmHg and a heart rate of 74 beats/min. Anemia was observed on her palpebral conjunctivae, and jaundice was observed on her bulbar conjunctivae. The laboratory findings were as follows: hemoglobin 7.5 g/dl, platelets 144 × 109/L, white blood cells 2.52/μl, total protein 7.0 g/dl, and albumin 3.9 g/dl. Her peripheral blood smear pattern showed a possible presence of myeloproliferative disease such as immature myeloid cells, teardrop-shaped cells, and giant platelets.
A liver chemistry revealed the following (Table 1, Additional file ): aspartate aminotransferase to alanine aminotranferase (AST/ALT) of 17/17 IU/l, alkaline phosphatase (ALP) of 771 IU/l, lactate dehydrogenase (LDH) of 525 IU/l, and T-Bil and D-Bil markers of 2.63/0.76 mg/dl. Hepatitis B and C virus markers were negative. On palpation, her abdomen revealed a markedly enlarged spleen. A contrast-enhanced computed tomography (CT) scan showed mild hepatomegaly and a markedly severe splenomegaly with dilatation of the splenic vein. An emergency endoscopy showed esophagogastric varices (Li F2 Cb RC (+), Lg-cf F1 RC (-)) (Figure ). A white thrombus was detected on the middle of the esophageal varices.
The first endoscopic variceal ligation (EVL) with one rubber band was carried out successfully on the first day of her admission. Another endoscopic ligation was performed for the remaining varices 41 days after her admission (Figure ). In order to eradicate the cause of her varices, the extramedullary hematopoiesis was treated by chemotherapy (hydroxycarbamide, prednisolone and melphalan). After the chemotherapy, her splenomegaly improved without the recurrence of esophagogastric varices (Figure and Figure ).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [74.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 74.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
3097,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8645413-1,Extracted,"A 48-year-old man presented to the emergency department with shortness of breath and a productive cough that had been gradually worsening for the past one week. He had a history of protein S deficiency and numerous associated deep vein thromboses and pulmonary emboli requiring placement of an inferior vena cava filter and long-term anticoagulation. On arrival to the emergency department, he had a heart rate of 101, respiratory rate of 31, blood pressure of 153/110 mmHg, and oxygen saturation of 89% on room air. Physical examination showed lower extremity edema and labored breathing.
Laboratory workup was significant for creatinine of 1.47 mg/dL (normal range 0.60–1.30 mg/dL). A respiratory pathogen screen, severe acute respiratory syndrome coronavirus (COVID-19) PCR testing, and troponin were negative. An electrocardiogram (EKG) showed sinus tachycardia without evidence of ischemia. Computed tomography (CT) of the chest showed pulmonary emboli with involvement of the right middle and lower lobar arteries, a moderate pericardial effusion, and a large, nearly occlusive thrombus in the superior vena cava (SVC) with extension into the right atrium and bilateral brachiocephalic veins. Extensive venous collateralization was also evident and thought to be indicative of obstruction in venous return (Figures and ). The patient was treated with supplemental oxygen and a heparin infusion.
Vascular surgery determined that the patient's SVC thrombus was likely acute on chronic as it was present but not noted on previous imaging. An initial echocardiogram showed a moderate effusion without evidence of tamponade. However, serial echocardiograms demonstrated increasing size of the effusion with development of right ventricular dilation and collapse. Pericardiocentesis was performed with drainage of 400 mL of chylous-appearing fluid ().
Analysis of the pericardial fluid showed 91,000 red blood cells/μL; 26,248 nucleated cells/μL with 62% neutrophils, 36% lymphocytes, and 2% monocytes; protein of 4.8 gm/dL; albumin 2.1 gm/dL; lactate dehydrogenase 373 U/L; glucose 158 mg/dL; amylase 20 U/L; lipase 25 U/L; cholesterol < 200 mg/dL; and triglycerides of 2,726 mg/dL. Gram stain and culture of the fluid were negative for organisms. Cytology was negative for malignancy. Given the results of the pericardial fluid analysis, it was determined that the chylous pericardial effusion was likely due to lymphatic obstruction secondary to subclavian vein thrombus.
The patient was treated with therapeutic doses of enoxaparin for anticoagulation during hospital admission. After pericardiocentesis, he was monitored with serial echocardiograms which showed gradual reaccumulation of his pericardial effusion without evidence of tamponade. A repeat CT of the chest showed worsened venous obstruction with complete occlusion of the left subclavian vein. Vascular and cardiothoracic surgery teams decided that the best treatment option was definitive management of the patient's thrombus as a pericardial window would result in continuous effusion. Despite a high risk of causing pulmonary embolism, the patient underwent catheter-assisted thrombolysis directed at the left subclavian thrombosis.
Following the procedure, a repeat CT angiogram of the chest showed a decrease in clot burden. The patient clinically improved and was discharged without further operative intervention. He was found to have only trace pericardial effusion on echocardiography with no residual symptoms at one-year follow-up.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [101.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Hemoptysis': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 101.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
3098,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6625292-1,Extracted,"A 24-year-old primigravida, booked case in our hospital, was a known case of rheumatic heart disease (RHD) and had mitral valve replacement (MVR) with a mechanical valve at 19 years of age and was on regular follow-up. During her first trimester, she was switched over from warfarin to low molecular weight heparin (LMWH). During the second trimester, she was restarted on warfarin, her heart rate (HR) was 50/min and electrocardiogram (ECG) revealed sinus rhythm. She was anemic and was treated with oral and parenteral iron. After 30 weeks of gestation she was lost to follow-up. At 37 weeks, she presented with draining per vaginum. Her HR was 36–40/min and blood pressure (BP) was 100/60 mmHg. Though she was asymptomatic, ECG revealed CHB. The cardiologist placed a temporary pacemaker through the right internal jugular vein (IJV) and set the HR at 80/min in VVI (ventricular pacing, ventricular sensing, inhibition response) mode. She was posted for emergency cesarean delivery due to nonprogression of labor and cephalo-pelvic disproportion (CPD). On preoperative assessment, she had dyspnea at rest and continuous new-onset cough. Her HR was 80/min paced, BP was 160/100 mmHg, and auscultation revealed bilateral crepitations with fall in room air SpO2 from 98 to 92%, suggestive of cardiac failure. Presuming that the failure was secondary to HR of 80/min as the patient was asymptomatic with HR 40/min, after discussion with cardiologist, HR was reset at 50/min. She was treated with propped-up position, O2, IV Frusemide (40 mg). ECG revealed good valvular function, biventricular functions, and moderate pulmonary artery hypertension. Hemoglobin at this stage was 8.6 g%, prothrombin time (PT) with International Normalized Ratio (INR) was 2.9, and other investigations were normal. Though it was an emergency, we had few hours for optimization as the continuous fetal HR monitoring was reassuring. Our anesthetic challenges and concerns were: (1) MVR status; (2) CHB on temporary pacemaker; (3) warfarin-induced coagulopathy; (4) ongoing treatment for cardiac failure; (5) fresh frozen plasma (FFP) and packed red blood cells (PRBC) transfusion may result in further volume overload; (6) temporary pacemaker; and (7) Issues regarding insertion of another central venous catheter when the temporary pacemaker was in situ. The patient was optimized over a period of 3 h with 2 units of FFP and IV Frusemide (40 mg) during transfusion. Patient improved symptomatically, and was taken up for cesarean delivery. Preoperatively, she received antiaspiration and infective endocarditis prophylaxes. In the operation theater, she was attached to ASA standard monitors. Pre-induction, left IJV was catheterized under ultrasound guidance with 7-Fr central venous catheter (CVC) [] and left radial artery was cannulated. Paced HR was 50/min, CVP was 19 mmHg, and IBP was 106/56 mmHg. She was pre-oxygented with 100% oxygen. Rapid sequence induction was achieved with IV Glycopyrrolate (0.2 mg), thiopentone (250 mg), succinylcholine (100 mg), and she was intubated with 7-mm ID cuffed ETT, confirming with capnography. Anesthesia was maintained with O2/N2O/isoflurane/vecuronium/morphine with controlled ventilation. Bipolar diathermy was used. The baby was delivered with APGAR scores of 8/10 and 9/10 at first and fifth minute, respectively. Uterus contracted well with oxytocin infusion. Intraoperative blood loss was 800 ml, 2 units FFP, and 1 unit PRBC were transfused to maintain MAP of 60–70 mmHg. Postoperatively, there was no excessive blood loss and the patient was bridged with therapeutic dose of LMWH 8 h later. She was extubated on first postoperative day. Later permanent pacemaker (PPM) was placed and set in VVI mode (HR, 70/min). She was restarted on oral anticoagulants and was doing well at the time of discharge.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [50.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 50.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 0 + 1 = 1.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.
The patient's Well's score for pulmonary embolism is 1."
3099,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8313005-1,Extracted,"A 71-year-old Caucasian male with a past medical history of chronic constipation, depression, hypertension, and hypothyroidism presented to the emergency department complaining of severe abdominal pain that began suddenly the day prior. The pain, described as being constant, sharp, and “crampy,” was initially localized to the left upper quadrant but had progressed to involve the entire abdomen just prior to presentation. The patient also complained of fevers and rigors throughout the day, with a sublingual temperature check at home showing 100.5 degrees Fahrenheit, leading the patient to start acetaminophen. There was no reporting of nausea, vomiting, or diarrhea. Vitals on presentation included a temperature of 98.1 degrees Fahrenheit, a heart rate of 91 beats per minute, a blood pressure of 140/86 mmHg, a respiratory rate of 16 breaths per minute, and an oxygen saturation of 99% on room air. Physical examination revealed diffuse abdominal tenderness that was worst at the upper left quadrant, guarding of the entire abdomen, and rebound tenderness. Laboratory tests were significant for an elevated white blood cell count of 22.6 x 10⁹/L with a neutrophil predominance (18.7 x 10⁹/L). The levels of lipase and lactic acid were found to be within normal limits, with readings of 13 U/L and 1.0 mmol/L, respectively. Other laboratory values were also found to be grossly normal. A CT scan of the abdomen and pelvis with IV contrast disclosed multiple foci of regional and upper abdominal peritoneal free air secondary to perforated jejunal diverticulitis without a drainable fluid collection (Figure ). The patient was initially started on IV fluids, IV acetaminophen, and IV piperacillin-tazobactam. After the results of the CT scan came back, the patient was taken to the operating room for an exploratory laparotomy, which showed approximately 75 cm of jejunum, which was tan-brown and hemorrhagic with areas of suppurative yellow material. The affected area was then excised with establishment on a primary anastomosis. Intraluminal examination of the resected bowel showed areas of induration with multiple diverticular tracts impacted with fecal material. The perioperative course was unremarkable with the remainder of the patient’s hospital stay consisting of an uncomplicated two days of observation.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [91.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 91.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3100,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5776405-1,Extracted,"In February 2009 a 53-year-old female patient was admitted to the University Hospital in Freiburg, Germany for further evaluation. The patient was initially diagnosed with autoimmune hepatitis/primary biliary cholangitis (AIH/PBC) overlap syndrome (positive for anti-nuclear antibodies, antibodies to smooth muscle cells, antibodies to pyruvate decarboxylase E2 subunit, and to soluble liver antigen) in 1989. Since histology and clinical chemistry showed that the AIH component was predominant without cholestasis, the prescribed therapy was a combination of corticosteroids and azathioprine.
In 2006 the patient was previously admitted in the Hospital of Norden, Germany with the first episode of acute variceal bleeding with hemodynamic instability. Banding of varices was performed. Sonography of the abdominal organs showed signs of liver cirrhosis including enlarged spleen. No other abnormalities were found. Within the following 3 years she bled three times per year from these varices. In 2008 she had two episodes of bleeding from rectal varices which were treated with rubber band ligation. Medical therapy of portal hypertension with propranolol was initiated but had to be stopped even at the low dose of 20 mg twice daily due to intolerable cardiovascular side effects (i.e., bradycardia and hypotension). The patient was regularly monitored in the liver transplant center of the University Hospital in Hannover (Medizinische Hochschule Hannover). She was waitlisted for liver transplantation and the implantation of TIPS was scheduled. She was referred to our hepatological unit in order to check whether the application of an inhibitor of the enzyme phosphodiesterase-5 could be an option to lower portal pressure and reduce the risk for bleeding from esophageal varices.
The patient was in a good clinical condition upon admission. The physical examination findings were normal except for the palpable liver and minor bilateral varicose veins of the lower extremities. Examination of heart and lungs was unremarkable. No bipedal edema was present. There were no signs of hepatic encephalopathy. Blood pressure was 154/86 mmHg and the heart rate was 78/min. ECG and echocardiography findings were normal except for a slight tricuspid valve insufficiency. Systolic pulmonary artery pressure was not increased (26 mmHg). Laboratory results showed no pathological values except a slight increase in total bilirubin (1.6 mg/dL) and thrombocytopenia of 105.000/μL, establishing the case as Child A cirrhosis (i.e., normal bilirubin, normal serum albumin, normal INR, no ascites, no hepatic encephalopathy). In esophago-gastro-duodenoscopy scarring transformation of two ligated varices was observed. Three small varices of grade 1-2 were visible. At this point, the daily medication consisted of azathioprine 75 mg, prednisolone 5 mg, pantoprazole 20 mg, and calcium 500 mg.
To test the effect of a PDE-5-inhibitor on portal hemodynamics in February 2009 10 mg of Vardenafil were administered orally. Wedged hepatic vein pressure (WHVP) and free hepatic vein pressure (FHVP) were measured in triplicate before and one hour after the drug administration. The HVPG, defined as WHVP - FHVP, decreased by 14% from 10.5 to 9.0 mmHg. Duplex sonography showed an increase in portal flow by 28% (0.97 L/min to 1.24 L/min) 60 min after drug intake. Systemic blood pressure changed from 130/87 to 121/75 mmHg one hour after drug administration, while heart rate changed from 65 to 61/min. Portal flow monitored by flow-sensitive 3D magnetic resonance imaging increased by 16 % (0.85 L/min to 0.99 L/min). Maximal flow velocity remained constant, at 24 cm/s in duplex sonography and 17 cm/s in 3D MRI. No relevant effect was observed on systemic blood pressure. Visualization of the portal venous system by MRI (Figure ) confirmed the duplex sonographic findings of a prograde blood flow in the portal vein and the two main intrahepatic branches and a recanalized umbilical vein originating from the left main branch of the portal vein.
We discussed an experimental therapeutic approach of the application of a PDE-5-inhibitor with the patient. The patient was informed that this was an off-label use and gave written informed consent. After having verified that the PDE-5-inhibitor Vardenafil decreased HVPG and that it led to an increase of portal venous blood flow confirmed by two independent methods we decided to start a long-term therapy with 5 mg Tadalafil/day, as this PDE-5-inhibitor has a longer half-life than Vardenafil. In June 2009 an HVPG one hour after oral administration of 5 mg Tadalafil of 10.5 mm Hg was measured. Portal venous blood flow remained elevated at 1.21 L/min. Systemic blood pressure showed no clinically relevant changes (124/79 mmHg, heart rate 88/min to 127/77 mmHg, heart rate 64/min) in the acute setting. The next evaluation was performed in October 2009 wherein after 10 mg Tadalafil the HVPG decreased by 15% from 12.0 to 10.0 mm Hg. Portal venous blood flow remained markedly elevated (1.28 L/min in Duplex sonography and 0.99 L/min as measured by MRI). In March 2010 HVPG was 10.5 mm Hg, while portal venous blood flow remained about 30% higher than the initial reading as verified by the two methods. Notably, the flow in the umbilical vein was not influenced by the PDE-5-inhibitor. The results of the measurements are shown in Table . No relevant changes in heart rate or blood pressure occurred. In April 2010 a second-grade esophageal varix was injected with acryl-glue prophylactically. In March 2011 the last measurement of portal blood flow using duplex sonography and the MRI method was performed. It showed that the portal venous blood flow remained constant at a level above than at the start of treatment. Further invasive portal pressure measurements were not performed.
The clinical course of the patient remained stable. The portal venous blood flow determined by duplex sonography was constant within the range of 1.2 and 1.4 L/min. Endoscopic monitoring every six months showed scarring in the distal esophagus and with no signs of new esophageal varices. The varices remained closed by thrombosis. Two episodes of upper gastrointestinal bleeding occurred in 02/2016 and 04/2016. Upper endoscopy excluded bleeding from varices or portal hypertensive gastropathy. The bleeding from the small visible erosions in the duodenum was attributed to NSAID use which the patient had taken due to headache. After administration of a proton pump inhibitor no further bleeding occurred. In 12/2016 portal flow was quantified to be 1.06 L/min. However, this was measured with a different sonographic device. The next sonographic examination in 09/2017 with the original device revealed a constant portal blood flow of 1.29 L/min.
Figure shows the distal aspect of the esophagus with visible scars caused by sclerosing and banding, with the old varices remained thrombosed. Figure shows an abdominal computer tomographic angiography. The portal vein (solid arrow) was perfused in a prograde direction, the diameter was enlarged. There were collateral veins at the splenic hilus and an enlarged left ovarian vein (dashed arrows).
The patient continued the daily intake of 5 mg Tadalafil. Other medications consisted of 75 mg Azathioprine per day and 2.5 mg Prednisone per day. Because of the stable clinical condition the patient is no longer on the list of liver transplant candidates. During the time of follow-up the number of varicose veins of the lower extremities increased and a local therapy was suggested.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [78.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 78.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3101,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-6441,Extracted,"A 50-year-old man is brought to the emergency department due to chest pain and shortness of breath for the last 2 hours. He describes the chest pain as squeezing in nature and radiating towards his left arm. It is associated with nausea and sweating. He has a similar history in the past, which is mostly aggravated with strenuous activities and relieved with sublingual nitroglycerin. He has a history of uncontrolled diabetes and hypercholesterolemia for the last 10 years. His last HbA1c was 8.0 %. His blood pressure is 150/90 mm Hg, pulse rate is 90/min, respiratory rate is 20/min, and temperature is 36.8°C (98.3°F). Oxygen saturation in room air is 98%. ECG shows ST-segment elevation in leads I, II, and aVF. He is being prepared for coronary angioplasty.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 90.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3102,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8616652-1,Extracted,"Mrs. M.F. (22-year-old, unemployed, Gravida 3, Para 1011) (history of one full term normal vaginal delivery and one termination of pregnancy during the first trimester) was admitted at the emergency unit at 8 weeks of pregnancy with severe pelvic pain of abrupt onset extending to the whole abdomen and radiating to the shoulder. The onset was 4 days prior to admission and there was neither trauma history nor vaginal bleeding. She fainted despite medication with paracetamol and a drip of amino acid pack administered by a community nurse at home to alleviate the pelvic pain and fatigue. She then went to a community health centre where ultrasonography revealed a 9-week-old intrauterine viable foetus with a massive peritoneal effusion (). From there, she was referred to our emergency unit.
Clinical assessment on admission revealed hemoperitoneum with shock (blood pressure: 72/56 mmHg; pulse rate: 120 pulsations/minute, respiratory rate: 28 cycles/minute, positive paracentesis). Our working diagnosis was a ruptured ectopic pregnancy with massive hemoperitoneum and shock. A very improbable associated intrauterine pregnancy was nevertheless evoked. The haemoglobin level was 6 grams/decilitre. Preoperative workup was unremarkable. The mainstay of management was emergency laparotomy under general anaesthesia with blood transfusion (only 1 pint of whole blood out of the 3 requested due to lack of means to afford). Laparoscopy was impossible because equipment was not available. Findings were as follows: hemoperitoneum (about 2000 millilitres), an increased and soft uterus (like 10 weeks of pregnancy), a ruptured left tubal (ampullary) pregnancy with contralateral corpus luteum, and bilateral tubo-ovarian adhesions (). A total left salpingectomy was carried out followed by a cleansing of the abdominopelvic cavity. The uterus was handled very gently. Progesterone (7α-hydroxyprogesterone caproate) was administered prior to the surgery (1 gram via intramuscular route) and during the five postoperative days (500 milligrams/day via intramuscular route). Postoperative course was uneventful until day five during which she had an uneventful complete spontaneous abortion. The patient was discharged in a good condition 7 days after the surgery with iron supplementation (100 milligrams of ferrous sulphate twice a day for 3 months) because of a haemoglobin level of 8 grams per decilitre. She was seen 6 weeks later, and the attending physician found than she had fully recovered. During that visit, her opinion was asked and she complained of the late diagnosis by the nurse who attended her at home and of the expensiveness of management at the University Teaching Hospital. Six months later, she was still fine but had light periodic pelvic pains.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3103,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7752485-1,Extracted,"A 69-year-old man was admitted to the hospital because of anorexia and fever. He had suffered an acute middle cerebral artery territory stroke 45 days previously and underwent treatment. The only medications he was taking were for stroke (aspirin 100 mg, cilostazol 100 mg, atorvastatin 80 mg, and rabamipide 100 mg). On the initial physical examination, his vital signs were as follows: blood pressure, 162/79 mm Hg; pulse rate, 104 beats/min; respiratory rate, 20 breaths/min; and temperature, 37.8°C. He had severe dysarthria and right extremity weakness due to the stroke. No malar rash, oral ulcers, jugular venous distension, or lymphadenopathy were observed. Bilateral fine crackles were detected on chest auscultation, and his abdomen was soft but there was no organomegaly. Multiple pinkish reticulated patches were observed on the lower leg. The results of initial laboratory tests were as follows: white blood cell (WBC) count, 17 630/μL (4000-10 000/μL); hemoglobin, 9.1 g/dL (13.0-17.0 g/dL); blood urea nitrogen, 24.3 mg/dL (6-20 mg/dL); creatinine, 1.52 mg/dL (0.6-1.2 mg/dL); C-reactive protein, 153.5 mg/dL (0.0-5.0 mg/dL); MPO–ANCA, 100.0 U/mL (0-4.9 U/mL); and PR3–ANCA, negative. The urinalysis revealed the following findings: protein, 2+; blood, 2+; red blood cells, 5-9/high power fields (HPF); and WBC, 5-9/HPF. Serum/urine protein electrophoresis and immunofixation showed nonspecific findings (Table ). Pulmonary interstitial fibrosis was noted on a chest X-ray (CXR). Brain magnetic resonance imaging revealed no evidence of a newly developed infarction, but the hemorrhagic transformation of the left MCA infarction lesion was detected (frontoparietal lobes, basal ganglia, and insular region). His baseline serum creatinine was 0.71 mg/dL, which increased to 1.52 and 2.24 mg/dL on days 1 and 3 of admission, respectively. A percutaneous renal biopsy was performed on day 7 of admission. Seven fibrocellular crescents out of 17 glomeruli were observed on light microscopy (Figure ). Some were associated with fibrinoid necrosis, and numerous neutrophils were detected in the capillary lumen. In addition, a few small vessels with neutrophil infiltration and fibrin deposition were evident, indicating acute necrotizing vasculitis (Figure ). Most of the interstitial area was infiltrated by numerous plasma cells and several neutrophils. The possibility of crescentic glomerulonephritis, associated with plasma-cell proliferative disease or IgG-related disease, was considered. Kappa and Lambda in situ hybridization revealed a positive staining pattern, indicating polyclonality (Figure ). In addition, IgG4-positive plasma cells were up to 200/HPF in the interstitial area. Unlike IgG4-tubulointerstitial nephritis, there was no sclerosing lymphoplasmacytic inflammation or apparent obliteration of the tubules. Therefore, the patient was diagnosed with microscopic polyangiitis having pauci-immune crescentic glomerulonephritis with fibrinoid necrotizing vasculitis. A bone marrow (BM) aspiration and biopsy showed a normocellular marrow with no increase in plasma cells (1.8% of all nucleated cells), and no evidence of BM involvement by monoclonal plasma cells. His Birmingham vasculitis activity score was 27. Serum creatinine peaked at 3.1 mg/dL. He received three pulses of methylprednisolone (500 mg/day) followed by prednisone (1 mg/kg/day) and cyclophosphamide (1.5 mg/kg/day). After treatment, his serum creatinine improved to 2.3 mg/dL, and the microscopic hematuria disappeared. Furthermore, his fever and skin lesions improved. He was discharged with prednisolone 40 mg/day (1 mg/kg/day), peroral cyclophosphamide 50 mg/day, and his renal function remained stable until 2 months after discharge. No side effects were observed due to the immunosuppressive agents. The dose of azathioprine was maintained, and the dose of prednisolone was tapered to 30 mg/day. He was subsequently lost to follow-up and died 16 months later due to pneumonia.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [104.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 104.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3104,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3607879-1,Extracted,"A 27 year old male, non-smoker and non alcoholic, resident of Punjab, India, presented to the outpatient department complaining cough and hemoptysis for two month. Cough was present off and on with mild specks of blood initially. One day prior to presentation patient had hemoptysis of around 400 ml fresh blood. There was no associated fever, weight loss, or decreased appetite. There was no history of close contact with any tubercular patient. He had taken four drug antitubercular therapy (ATT) for about one month, prior to visiting us but without any improvement. The reason for starting ATT and the exact dose was not clear as the patient did not have any written records.
The patient was a thin man with a marked pale complexion. Patient’s height, weight, and BMI were 165 cm, 52 kg and 19.1, respectively. Blood pressure, heart rate and respiratory rate were 116/76 mmHg, 110 per minute and 20 per minute, respectively. Chest examination revealed occasional crepitations bilaterally. The remaining part of the systemic examination was unremarkable.
Lab investigations showed severe microcytic, hypochromic anemia (Hb = 5 g/dl). Blood total leukocyte count was 8.9 × 109/L with 58% polymorphs 40% lymphocytes and 2% eosinophils. The platelet count was 210 × 109/Liter of blood. Coagulation profile, renal and liver function tests were normal. Urine examination did not reveal albuminuria or hematuria. Sputum examination for Acid Fast Bacilli and Tuberculin skin test were negative. Elisa for HIV was non-reactive. Arterial blood gas analysis revealed pH 7.4, PaO2 82.3 mm Hg, PaCO2 42 mmHg, HCO3- 23 mEq/L. Chest radiograph on the day of admission showed bilateral diffuse alveolar infiltrates over middle and lower zones, while X- ray taken one month back was normal. Flexible fiberoptic bronchoscopy revealed normal airways. Bronchoalveolar lavage showed numerous hemosiderin laden macrophages.
Antinuclear, anti-neutrophil cytoplasmic (p-ANCA and c-ANCA), and anti-glomerular basement membrane antibodies were negative. C3 and C4 levels were normal. Echocardiography and electrocardiography provided normal findings. After excluding secondary causes of diffuse alveolar hemorrhage, diagnosis of idiopathic pulmonary hemosiderosis (IPH) was done. Since an association between celiac disease (CD) and IPH has been previously described, a workup for CD was also performed. IgA tissue transglutaminase (TTG) titre was 178 IU/L (normal: ≤10 IU/L). Upper GI endoscopy on gross examination did not reveal any significant abnormality. Duodenal biopsy showed partial villous atrophy, increased numbers of intra-epithelial lymphocytes (70 IELs per 100 epithelial cells), and infiltration of the lamina propria with plasma cells, confirming the diagnosis of celiac disease (Figure and ). On reviewing the history of the patient, he reported a vague abdominal discomfort after feeds since childhood but never significant enough to warrant any treatment. The discomfort used to subside on its own in 1 to 1.5 hours and he used to pass one formed stool per day.
At admission the patient was given empirical antibiotics and blood transfusion. There was a marked clinical response to blood transfusion. After the diagnosis of associated Celiac Disease, the patient was started on Gluten free diet (GFD). He was discharged after one week. At the time of discharge the patient was asymptomatic and his Chest X-ray revealed resolution of earlier noted shadows. He did not have fever or recurrence of hemoptysis during the hospitalization. Over a follow up period of one year, on GFD, the patient has gained twelve kg weight. There has not been any recurrence of pulmonary symptoms and his hemoglobin level is normal (11.8 g/dl). His abdominal symptoms, which were present since early childhood, also disappeared on GFD. Chest x-ray after one year is normal.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 1.5 + 1 = 2.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 2.5.
The patient's Well's score for pulmonary embolism is 2.5."
3105,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4279256-1,Extracted,"A 61-year-old male presented from his primary care physician's clinic to the emergency department (ED) with a complaint of worsening shortness of breath at rest for the past two days, which was exacerbated by talking. He had associated symptoms of fever, chills, chest pain, and nonproductive cough. His past medical history was significant for stage III, T2N2 metastatic squamous cell lung cancer of the right upper lobe which was diagnosed in 2012. The patient had received three-week cycles of carboplatin and paclitaxel (4 cycles) and then weekly cycles for five weeks. The patient also received concurrent external beam radiation, which was discontinued at patient request after receiving 58 Gy. The patient also was found to have new paratracheal lymph node a year later and one month prior to this presentation on CT scan of chest. The patient underwent endobronchial ultrasound (EBUS) guided needle aspiration of station 7, which was positive for malignancy. The patient had a history of smoking of 90 pack year. The patient was also edentulous and was not wearing dentures.
On examination, the patient was having tachycardia and was hypotensive with pulse of 148 beats per minute and blood pressure of 67/38 mm hg. He was hypoxic with oxygen saturation of 84% on room air, had tachypnea with respiratory rate of 24/min, and was febrile with a temperature of 101.8°F (38.8°C). He was chronically ill in appearance with use of accessory muscles for breathing. Oropharynx was dry with dentures noted. Jugular venous distension was present in the angle of the jaw. Breath sounds were significant for decreased air entry in the right lower base and expiratory wheezes bilaterally. Heart sounds were distant with no murmurs or rubs. There was bilateral pitting edema in his lower extremities.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [148.0, 'beats per minute'], 'Hemoptysis': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Previously documented Deep Vein Thrombosis': False}",7,7,7,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 148.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 6.0 + 1 =  7.0.
The patient's Well's score for pulmonary embolism is 7.0."
3106,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3596659-1,Extracted,"A 27-year-old male presented with an episode of syncope while playing soccer. During the episode of syncope, a pulse was detected and sphincter function was preserved. He had experienced pre-syncope three times during resting status over the most recent 2 months. He had no history of hypertension and diabetes mellitus. He had no family history of sudden cardiac death or syncope. Also, he did not take any medication.
A physical examination revealed that blood pressure was 130/80 mm Hg and heart rate was 78 beat per minute. Other physical examinations were normal. Baseline electrocardiography (ECG) showed a sinus rhythm with frequent PVC and non-sustained polymporphic VT (). QT interval was 370 ms. PVC morphology, which triggers polymorphic VT is uniform and identical to that of isolated PVC. Initiation of polymorphic VT is not related to the fixed coupling interval. There was no QT interval prolongation, ST elevation on the precordial lead, and abnormal notch at QRS wave. Holter monitoring showed frequent PVC greater than 40% a day and frequent non-sustained polymorphic VT, and there was no diurnal variation in their occurrence (). He felt no specific symptoms during polymorphic VT. A laboratory blood study including serum electrolytes showed no abnormalities. An exercise test using a treadmill showed no changes of PVC and non-sustained polymorphic VT frequency. Isoproterenol infusion did not change in corrected QT interval and PVC frequency. There was no remarkable structural heart disease on the echocardiography except for borderline left ventricular dysfunction (left ventricular ejection fraction=52%). Coronary angiography involving right ventricular angiography was normal and coronary spasm was excluded using the provocation test with ergonovine. A cardiac MRI after catheter ablation also showed no remarkable finding involving the right ventricle.
We thought that isolated PVC triggered polymorphic VT and then ablation of the PVC could abolish the genesis of polymorphic VT. Using activation mapping with an adjustable Lasso catheter (Biosense Webster, Diamond Bar, CA, USA) via the SL1 sheath (St. Jude Medical, Daig Division, Minnetonka, MN, USA), which was positioned at the right ventricular outflow tract (RVOT), a discrete potential was detected at the pulmonary artery just above the pulmonary valve, the free wall side of RVOT (). The local potential preceded the QRS onset by 60 ms and showed relatively high amplitude and reversal of polarity (). Radiofrequency ablation was done just above the pulmonary valve with the temperature setting of 60℃. After radiofrequency delivery for 3.2 seconds, PVC was abolished. There was no PVC or non-sustained VT on the ECG and Holter ECG (). Symptoms of vague chest discomfort improved and there was no PVC free of medication after a 2 month follow up visit.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [78.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 78.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3107,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8173423-1,Extracted,"Nonproductive cough for 2 mo.
The patient was a 21-year-old Han Chinese man. He had no history of smoking, but he suffered from a nonproductive cough for 2 mo, accompanied by a low-grade fever (ranging from 37.4-37.8 ℃) and night sweats; however, he denied hemoptysis, chills, weight loss, dyspnea, and other symptoms. Then he developed paroxysmal chest stabbing pain for 1 wk.
The patient had no known history of a past illness.
The patient had no known personal and family history.
Physical examination showed normal auscultation of both lungs, oxygen saturation of 98%, blood pressure of 126/75 mmHg, a temperature of 36.5 ℃, respiratory rate of 20 times per minute, and pulse of 88 beats per minute. He had no clubbing, a pale complexion, or cyanosis.
Laboratory inspection revealed a white blood cell (WBC) count of 10.01 × 109/L with 79.10% neutrophils, and serological detection for Mycobacterium tuberculosis (M. tuberculosis) antibody was positive. The erythrocyte sedimentation rate (ESR), procalcitonin (PCT), and Fungitec G test results were normal.
Computerized tomography of the chest demonstrated increased lung texture and multiple patchy enhanced densities of both lungs, especially in the upper lobes, with no obvious adhesion to the pleurae. There were no abnormities in the bronchi under the broncho fiberscope.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [88.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 88.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3108,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6967328-1,Extracted,"A 68-year-old man (165 cm, 74 kg) was scheduled for transurethral resection of a bladder tumor using 5-ALA. He had been receiving amlodipine 5 mg and azilsartan 20 mg every morning orally for hypertension. His blood pressure was maintained around 130/70 mmHg. Since he had been diagnosed with pyogenic spondylodiscitis in the fourth/fifth lumber disk region in his forties, general anesthesia was preferred. During the pre-operative examination, chest X-ray, electrocardiogram, and laboratory test findings were normal.
The patient took only amlodipine besylate on the morning of the surgery. Three hours before anesthesia induction, 5-ALA 20 mg/kg (Alaglio, Chugai Pharmaceutical, Tokyo, Japan) was administrated orally. Just before anesthesia induction, the patient’s blood pressure was 98/61 mmHg and his heart rate 82 beats/min. Anesthesia was induced with propofol 100 mg, rocuronium 50 mg, fentanyl 100 μg, and remifentanil 0.4 μg/kg/min. After 5 min, just before tracheal intubation, his blood pressure decreased to 47/32 mmHg. There were no observed changes in his electrocardiogram, such as ST-T changes or arrhythmia. Although we used phenylephrine at a total dose of 0.2 mg and ephedrine at a total dose of 10 mg over 10 min, hypotension persisted at 50/33 mmHg. Wheezing and erythema were not observed. Administration of 100 mL hydroxyethyl starch bolus for a few minutes was unsuccessful in increasing blood pressure. Transthoracic cardiac ultrasonography revealed normal systolic function, no asynergy, and normal size of the inferior vena cava. Bolus administration of noradrenaline at a total dose of 30 μg over 6 min slightly increased blood pressure to 65/39 mmHg. Arterial blood gas analysis revealed the following: pH, 7.350; HCO3− concentration, 23.2 mmol/L; base excess, 2.3 mmol/L; and lactate concentration, 1.7 mmol/L. Following this, bolus administration of adrenaline at a total dose of 30 μg over 9 min elevated the blood pressure from 53/26 to 127/49 mmHg. We decided to perform surgery under continuous administration of adrenaline. Anesthesia was maintained with sevoflurane and remifentanil. The patient’s blood pressure and heart rate ranged from 72/31 to 94/40 mmHg and from 70 to 85 beats/min, respectively, under the administration of adrenaline at 0.01–0.07 μg/kg/min. On completion of the surgery, he was transferred to the intensive care unit under intubation. Twelve minutes after admission to the intensive care unit, he was extubated as his blood pressure had stabilized at 142/56 mmHg under the administration of adrenaline at 0.03 μg/kg/min. Ten minutes after extubation, adrenaline infusion was discontinued. Although his lactate concentration was 5.3 mmol/L at this time, it decreased to 2.7 mmol/L after 3 h. His blood pressure and heart rate were stable during his intensive care unit stay. The patient was then transferred to the general ward on day 1 postoperatively. He was discharged without any complications 6 days postoperatively. Three months later, dermatologists performed a skin-prick test on him for propofol, rocuronium, and 5-ALA, the results of which were negative. Five months later, he received TUR-Bt under general anesthesia without 5-ALA for recurrence of tumor. Although we used propofol and rocuronium, severe hypotension did not occur.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [82.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 82.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3109,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5324248-1,Extracted,"A 24-year-old Caucasian man was hospitalised in March 2015 for renal transplantation. He had a history of spina bifida, neurogenic bladder with Bricker ileal conduit complicated by chronic renal failure requiring haemodialysis since 2011; and atopy, comprising respiratory allergy to pollens and house dust mites (asthma and rhinitis), contact allergy to latex (angioedema following inflation of a toy balloon), and vancomycin drug allergy.
The patient was undergoing renal transplantation for the first time. Surgery was performed in a latex-free operating room. General anaesthesia was induced by intravenous (IV) administration of propofol (150 mg IV push), ketamine (35 mg IV push) and sufentanil (20 µg IV push). Tracheal intubation was performed without complication and the patient received antibiotic prophylaxis by cefoxitin (2 g IV). Forty-five minutes after induction, thymoglobulin immunosuppression (12.5 mg/h of 5 mg/mL in 50 mL 5% dextrose to be administered over 8 h) was initiated. Within 3 min of the start of the thymoglobulin infusion, the patient experienced hypotension of 56/35 mmHg and extreme bradycardia (43 bpm) secondary to hypoxia, requiring resuscitation with external cardiac massage (for less than 1 min) and administration of adrenaline (0.1 mg IV push) (Table ). The thymoglobulin infusion was stopped immediately (at which point 0.625 mg had been infused). The patient concomitantly presented with generalised erythroderma and bronchospasm. He was subsequently managed in the intensive care unit and the operation was deferred. A favourable course was observed in response to adrenaline 2 mg/h, despite another episode of bronchospastic respiratory distress several hours later than required terbutaline nebulisation. A tryptase assay performed 1 h after onset of anaphylactic shock was elevated to 182 µg/L (normal 10.5 µg/L) confirming the anaphylactic origin of the shock. Histamine was also elevated to 234 nmol/L (normal < 10 nmol/L).
To explore the origin of the shock, the patient was hospitalised for allergy testing in September 2015. A clinical interview retrospectively revealed a history of atopy with asthma and allergic rhinitis and contact hypersensitivity to rabbits triggering asthma and facial oedema. Skin tests were performed. Positive (histamine dihydrochloride 10 mg/mL equivalent to 1% or 5.43 mmol/L, Stallergenes, France) and negative (glycerinate solution) controls were included. Skin prick tests (SPTs) were carried out and interpreted according to international guidelines []. The results were read after 10 min and the largest diameter was recorded. A skin reaction of ≥3 mm was considered positive. The histamine positive control response was small (wheal of 2 mm). SPTs and intradermal tests (using a sterile solution of the suspected drug serially diluted in phenolated saline) were negative for all medications used during induction of anaesthesia []: sufentanil, propofol, and ketamine at 10−3, 10−2, and 10−1 dilutions; suxamethonium, rocuronium bromide, and cisatracurium besylate at 10−3 and 10−2 dilutions; and atracurium besylate and mivacurium chloride at 10−1 dilution. An intradermal test for colloid (Voluven®) was negative at 10−3, 10−2, and 10−1 dilutions. In contrast, a SPT for thymoglobulin was positive, with an 8 mm wheal at a dilution of 10−6. Additional SPTs were performed using commercial standardised extracts and prickers (Alyostal Prick®, Stallergenes, France). The panel included the following allergenic extracts at 100 IR/mL or 100 IC/mL: rabbit, hamster, guinea pig, and horse epithelia, and latex (a known allergen for this patient). The SPTs for rabbit and horse epithelia were positive at 5 mm; the test for latex was also “positive” but was only 2 mm. A blood sample was taken for measurement of specific IgE (ImmunoCap system, ThermoFisher, Uppsala, Sweden). IgE for quaternary ammonium and suxamethonium were <0.10 kU/L and specific IgE for penicillin and cefaclor were negative. Specific IgE to rabbit dander and rabbit serum proteins were elevated at 10.2 and 2.22 kU/L, respectively. IgE specific to rabbit meat was 0.13 kU/L.
On the basis of clinical and laboratory data, we concluded that the patient had experienced a grade IV anaphylactic reaction to thymoglobulin due to rabbit protein allergy. All medications containing rabbit proteins will be permanently contraindicated for this patient and an allergy card was issued. To date, the patient has not been transplanted.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [43.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 43.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3110,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6181536-1,Extracted,"A 29-year-old man (height = 180 cm, weight = 60 kg) was admitted to our hospital due to sudden onset of palpitation, chest tightness, mild fever, and night sweats, accompanied with bilateral double lower extremities adynamia and paralysis for 5 days, but no obvious syncope and edema. Examination on admission revealed a normal heart rate of 96 beats/minute (bpm) and blood pressure of 120/80 mmHg. On cardiac auscultation, 3/6 grade systolic murmur (Levine Scale) was heard between the third and fourth ribs at the left margin of sternum. The sensory below the sternum was dysfunctional. Muscle strength on both legs was at 1/6 levels (Lovett Scale), and tendon reflex diminished. Electrocardiography showed a sinus rhythm with pulmonary P-wave. An X-ray image of the chest showed discrete and scattered miliary nodules over both lungs, and cardiac silhouette was enlarged. Magnetic resonance imaging (MRI) (Fig. ) showed an erosive space-occupying lesion located between the first and third thoracic vertebrae, which resulted in stenosis of the spinal canal and thinning of the spinal cord. Transthoracic echocardiography (TTE) (Fig. ) showed a huge mobile mass (72 × 58 mm) in the RA and myxoma was considered. The left ventricular ejection fraction was 60%. The remaining physical examination findings were unremarkable, and laboratory tests were normal, except for the accelerating erythrocyte sedimentation rate. There was no family history of heart disease, including tumors and other cardiovascular problems. The preliminary diagnosis was thoracic vertebra tumor and cardiac myxoma. To treat the incomplete paraplegia caused by thoracic vertebra tumor erosion, the operation including resection of thoracic vertebral lesions, decompression, and internal fixation with nail-rod must be carried out immediately. A multiple disciplinary team consisting of cardiologist, orthopedist, sonologist, and anesthesiologists, was created. Fatal complications of cardiac myxoma, such as intracardiac obstruction and pulmonary embolism, were assessed. Informed consent of critical illness was signed by the patient's legal representative.
The patient did not receive premedication before anesthesia. On arrival in the operating room, peripheral venous access was established on the dorsum of the hand, and continuous electrocardiogram and pulse oximetry monitoring were instituted. Invasive arterial blood pressure (IBP) was measured in the left radial artery, and the central venous pressure (CVP) was measured in the right femoral vein. Anesthesia induction was carried out with intravenous injection of midazolam 4 mg, penehyclidine hydrochloride 1 mg, etomidate 16 mg, and sufentanil 50 μg. Cisatracurium 12 mg was used to facilitate tracheal intubation. Maintenance of compound anesthesia consisted of 2% sevoflurane in an air–oxygen mixture, and remifentanil was continuously injected intravenously at 0.2 μg/kg/min. Intermittent bolus dose of 5 mg cisatracurium was administered for muscle relaxation. After anesthesia induction, hemodynamic parameters were stable at the supine position: heart rate of 80 bpm, IBP of 110/65 mmHg, and CVP of 8 mmHg. However, after the patient was turned to the prone position on the level of the standard operating table (lying on a pair of bolsters, unpressurized abdomen), the patient's heart rate increased gradually to 130 bpm, IBP dropped to 70/45 mmHg, and CVP increased to 22 mmHg. Moreover, the jugular vein was filled observably. Emergency treatment was carried out immediately against the symptoms of right heart failure. Fluid infusion was restricted and vasoactive drugs were used to maintain appropriate arterial blood pressure. Dopamine at 5 to 10 μg/kg/min and norepinephrine at 0.03 to 0.05 μg/kg/min were continuously injected intravenously, keeping the mean arterial pressure above 70 mmHg during the operation. During the 3 hours of surgery, blood volume supplementation totally consisted of sodium chloride 500 mL, hydroxyethyl starch 500 mL, fresh-frozen plasma 600 mL, and suspended red blood cells 2 U. Total blood volume loss was 600 mL, and urine output was 500 mL. After the operation, anesthetic drugs were stopped, and the patient was returned to the supine position. At this moment, his hemodynamic status was stabilized gradually with a heart rate of 84 bpm, IBP of 130/88 mmHg, and CVP of 10 mmHg. Dopamine and norepinephrine intravenous titration was suspended. When the patient recovered spontaneous respiration and responded to verbal commands, tracheal extubation was performed. After ventilated with 100% oxygen via a facemask in 5 min, the patient was transferred to the post-anesthesia care unit. Evaluation of spinal function was performed on the second postoperative. The muscle strength of the left leg was 4/6 levels, and the right leg was 3/6 levels; meanwhile, the superficial sensibility was considered dysesthesia. Furthermore, hemodynamic parameters were stable at the ward.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [96.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 96.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 3 + 1.5 =  4.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
3111,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5358245-1,Extracted,"A 40-year-old male wasa truck driver without family history and admitted with progressively worsening shortness of breath from 2 years ago. He had history of acute PE 10 years ago and treated with anticoagulant therapy whichwas stopped by himself after 6 months.Physical examination revealed blood pressure 100/60 mmHg, pulse rate 110 beats/minute, respiration rate 24 breaths/minute, jugular venous distention, and pitting edema in both lower extremities. Blood tests revealed D-dimer 6.04 µg/mL, pro-BNP 6963 pg/mL, and platelet 97×109/L. Artery blood gas analysis (room air) revealed pH 7.47, PCO2 23 mmHg, PO2 67 mmHg, and O2saturation 92%. In addition, factor V Leiden was negative and protein C and S levels, anticardiolipin antibodies and lupus anticoagulant were within normal limits. Electrocardiogram showed sinus tachycardia, right axis deviation, and right ventricle hypertrophy. Chest X-ray revealed enlargement of the right ventricle and both main pulmonary arteries, as well as bilateral pleural effusion. Initial transthoracic echocardiography (TTE) showed enlarged right chambers with right overload and severe tricuspid regurgitation (), and a massive thromboembolus (4.35×2.85 cm) in the enlarged pulmonary artery () with severe pulmonary hypertension(). Chest computed tomography (CT) revealed eccentric filling defect in the central and both main pulmonary arteries (). CT venogram showed diffuse thrombus from the suprarenal to the femoral vein. Therefore, CTEPH was diagnosed. The patient has been considered pulmonary thromboendarterectomy but he refused to undergo surgery and received anticoagulant therapy of heparin for 3 weeks. Then follow-up inferior vena cava venogram revealed that the thrombus had disappearedand the patient’s symptom mild improved.He was discharged with warfarin and prostacyclin analogue therapy. 3 months later,follow-upTTE and chest CT showed there was no significant improvement.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
3112,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5907393-1,Extracted,"We describe a case of a 29-year-old man with a history of IDU who presented to the hospital with fever and chills a few days after an inadvertent needle stick while injecting heroin. Avoiding medical care at first, he eventually came to the Emergency Department when he developed swelling around the punctured skin over the inferior aspect of the left cubital fossa. Upon initial evaluation, he had a temperature of 37.3°C, heart rate of 104 per minute, and respiratory rate of 38 per minute. The inferior aspect of the left cubital fossa was warm, erythematous, and with a 3.5 cm × 3.5 cm well-circumscribed area of fluctuance and induration. Laboratory evaluation revealed a hemoglobin of 10.9 gm/dl and white blood cell count of 10.6 k/cumm with a neutrophilic predominance but no immature granulocytes. His absolute neutrophil count was 9.1 k/cumm (normal 1.5–6.5 k/cumm). The comprehensive metabolic panel showed normal renal function and transaminases but elevated total bilirubin (4.5 mg/dl). His chest radiograph showed patchy infiltrates throughout the mid and upper right lung field with possible small right pleural effusion. Blood and sputum cultures were ordered, and he was started on broad-spectrum antibiotics consisting of vancomycin 1.5 gm IV every 8 hours (∼15 mg/kg), piperacillin-tazobactam 4.5 gm IV every 8 hours given as an extended infusion, and levofloxacin 750 mg IV once daily. He underwent incision and drainage of the cubital abscess. His antibiotics were tailored to oxacillin 2 gm IV every 4 hours as blood and sputum cultures revealed growth of methicillin-susceptible Staphylococcus aureus. On hospital day 6, his condition rapidly deteriorated due to sepsis (persistent fevers, tachycardia, and hypotension with rising white blood cell count), and a new 4 cm × 3 cm area of fluctuance was noticed on the left superior pectoralis region. He was transferred to the intensive care unit. A transesophageal echocardiogram (TEE) revealed a multilobed lesion on the superior and septal leaflets of the tricuspid valve, with lesion dimension approximating 3 cm on the superior cusp. CT of the chest with intravenous contrast demonstrated extensive bilateral cavitary lung lesions likely reflecting septic emboli, reactive mediastinal and hilar lymphadenopathy, and a large left-sided pleural effusion. A loculated component along the left upper lung insinuated through the chest wall into the left pectoralis muscle, raising the possibility of empyema necessitans (Figures and ).
Incision and drainage was performed with subsequent indwelling catheter placement for drainage of pectoralis major EN. For the left-sided pleural effusion, a chest tube was placed and it drained serosanguinous fluid. The cardiothoracic surgery service evaluated the patient and recommended ongoing antibiotic therapy with close clinical and radiographic surveillance. CT of the chest, when repeated, showed no interval change in multiple bilateral cavitary lesions, and a surveillance TEE done two weeks later identified persistent tricuspid vegetations with minimal regurgitation. As the CT of the chest was stable and the patient was clinically improving, surgery to replace the tricuspid valve was deferred with plans to treat the patient with six weeks of oxacillin.
The patient completed six weeks of intravenous oxacillin and was later started on suppressive antibiotic therapy with oral dicloxacillin 500 mg twice daily given the fact that he had high disease burden and had not undergone surgical intervention. Follow-up transesophageal echocardiogram (TEE) done soon after completing six weeks of antibiotic treatment showed that the tricuspid valve lesions had stabilized, if not minimally regressed in size, but tricuspid insufficiency had progressed to a moderate range. Magnetic resonance (MR) cardiac imaging reconfirmed sclerosis/thickening of the tricuspid valve leaflets, with moderate-to-severe tricuspid valve regurgitation. Surveillance radiography with CT of the chest showed that the cavitary lesions throughout the lungs had resolved. Unfortunately, at this point, the patient was lost to follow-up.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [104.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Surgery in the previous 4 weeks': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",4.5,4.5,4.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 104.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 4.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.5.
The patient's Well's score for pulmonary embolism is 4.5."
3113,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7872592-2,Extracted,"A 54-year-old male with a history of diabetes, hypertension, hyperlipidemia, hypothyroidism, coronary artery disease, and a DVT, who had not been on anticoagulation at the time due to gastrointestinal bleeding, presented to the ED with fever, chills, body aches, and chest tightness as well as worsening bilateral calf pain. The patient reported feeling ill for the prior 10 days with progressively worsening symptoms of fatigue, fever, myalgias, and diarrhea. The patient was a hospital employee and tested positive for COVID-19 four days prior to the ED visit. Upon arrival to the ED he was found to be hypoxic to 90% on room air, tachypneic with a respiratory rate of 20 breaths per minutes, tachycardic with a heart rate of 102 beats per minute, afebrile with oral temperature of 98.7 degrees Fahrenheit, and blood pressure of 125/75 millimeters mercury. On physical exam the patient was ill-appearing with increased work of breathing, decreased breath sounds bilaterally, and bilateral calf tenderness to palpation. Laboratory evaluation showed an elevated D-dimer of 465 ng/ml (with a normal cutoff value of 229 ng/ml). A point-of-care lower extremity duplex compression ultrasound demonstrated turbulent blood flow in the right lower extremity ().
A right calf vein thrombosis was noted distal to the trifurcation. (This was an incidental finding as calf vein imaging is not part of the compression ultrasound protocol.) A CTA was negative for PE but showed bilateral peripheral ground-glass opacities. The patient was placed on supplemental oxygen, started on enoxaparin and admitted to the hospital. He was admitted for four days with improvement and discharged home on anticoagulation. The patient returned to the ED five days later with worsening shortness of breath, hypoxia, and chest pain. A CTA again demonstrated no PE. D-dimer at that time was 31,876 ng/ml. During the second admission, a subsequent comprehensive ultrasound demonstrated a persistent calf vein thrombosis, and the patient’s D-dimer continued to downtrend but was significantly higher than on the prior visit. Radiology did not comment on the turbulent flow finding; however, upon retrospective review of these images, the patient continued to have turbulent flow in the deep venous system of the lower extremity. His oxygen requirements continued to escalate along with the deterioration of his hemodynamics. A repeat bedside echocardiogram showed evidence of right heart strain with an enlarged right ventricle, septal bowing, and low tricuspid annular plane systolic excursion. He was given tissue plasminogen activator for a suspected massive PE, without significant improvement and ultimately expired in the intensive care unit.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [102.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",7.5,7.5,7.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 102.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 = 6.0.
The patient not been diagnosed with pulmonary embolis (PE), but the patient has previously been diagnosed with deep vein thrombosis (DVT), we increase the current total by 1.5 so that 6.0 + 1.5 = 7.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 7.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 7.5.
The patient's Well's score for pulmonary embolism is 7.5."
3114,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6485830-1,Extracted,"Our patient is a 54-year-old female with a past medical history of hypothyroidism and very severe obesity (BMI 48 kg/m2). She underwent laparoscopic gastric sleeve surgery in the year 2012. Results were non-satisfactory in terms of weight loss with a difference of 6 kg/m2 in BMI post-procedure. So after six years, she underwent a laparoscopic biliopancreatic diversion with a duodenal switch. She had an uneventful postoperative recovery period. An upper gastrointestinal (GI) study contrast post-procedure did not reveal any evidence of obstruction or leak. The patient was discharged home two days after the procedure. A few days later, she started experiencing three episodes of nausea with brown-colored vomitus. She was found to be septic, with a heart rate of 110 beats per minute and temperature of 100.2oF. Her white blood cells count was 12/mm3.The source of infection was presumed to be intraabdominal considering her symptoms. Computed tomography (CT) of the abdomen and pelvis showed mildly dilated proximal small bowel loops. The patient was started on empiric antibiotic therapy with ceftriaxone 1 gm intravenous (IV) daily and metronidazole 500 mg IV every eight hours. Symptoms did not improve, so she was taken back to the operating room for diagnostic laparoscopy. Partial small bowel obstruction was noted along with ischemia of a segment of the ileum that was part of the duodenoileostomy due to mesenteric dissection. She underwent an open revision of the small bowel anastomosis with resection and anastomosis for the obstruction revision of the duodenoileostomy. Her hospital stay post-surgery remained uneventful. Diet was advanced gradually throughout the hospital course and a week later, the patient was discharged home with outpatient follow-up. Three weeks after that procedure, she noticed a productive cough with thick, yellow, foul-smelling phlegm and shortness of breath. She saw her primary care physician. A chest X-ray performed showed a right lung infiltrate with a right-sided pleural effusion. She was started on treatment with augmentin 500 mg/125 mg every eight hours. Her symptoms became worse so she came to the emergency room. Her vitals showed blood pressure 129/79 mmHg, heart rate 86 beats per minute, respiratory rate 20 breaths per minute, and temperature 98.6oF. Pulse oxygen saturation was 97% on room air. Mild leukocytosis was evident (white blood cells count 11.4/mm3 with no bands or left shift). A chest CT showed loculated, right-sided hydropneumothorax with almost total collapse of the right lung (Figure ).
There was a fistulous connection evident, extending from the surgical anastomosis in the stomach/bowel in the right upper quadrant through the right hemidiaphragm to the right hemithorax. These CT scan findings were new as compared to a CT scan obtained for this patient six months prior to the duodenal switch when she presented to the emergency department for non-specific left-sided chest pain. To analyze the anatomy of the fistula further, an upper gastrointestinal fluoroscopic contrast study was performed that showed a large fistula from the distal stomach prior to the duodenal bulb opening to the right pleural cavity (Figure ).
Consultations from gastroenterology and cardiothoracic surgery teams were obtained. Chest tube drains were placed with the plan of eventually performing a video-assisted thoracoscopic surgical decortication. Post-procedure CT showed patent chest tubes draining the right pleural cavity. The drained fluid was exudative in nature as per Light’s criteria (fluid lactate dehydrogenase > 12,000 u/L and total protein ratio = 0.7) and culture from the right lung empyema grew Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Candida albicans. An infectious disease consultation was placed at this time. The patient was started on levofloxacin 750 mg IV daily for two weeks as per the sensitivity result obtained for Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa. Micafungin 100 mg IV daily was started for the infection with Candida albicans. This was later switched to Diflucan 400 mg IV daily for a total of two weeks. Repeat cultures from the draining fluid were negative toward the end of the second week.
For treatment of the fistula, the patient was transferred to another facility for esophagogastroduodenoscopy (EGD) and possible clipping of the fistula due to the unavailability of that particular service in our hospital. As a result, there was a delay of 16 days from admission to the treatment of the fistula. When the EGD was performed, it showed that there was no anastomotic leak from the previous surgery. No evidence of any stricture was identified at the previous anastomosis. A small fistulous tract was noted in the distal part of the antrum likely secondary to ulcer formation that was noted in very close proximation to the fistula tract. An endoscopic clipping was performed. A post-procedure contrast study performed on the same day revealed complete closure of the fistulous opening. The patient was transferred back to our facility after the procedure. An upper GI contrast study performed two days later showed residual leakage from the distal stomach to the right upper quadrant. A repeat EGD was performed along with fulguration of a fistulous opening with argon beam coagulation and repeat orthoscopic clip application with complete obliteration of the fistula tract. This was confirmed by an upper gastrointestinal contrast study showing no persistent fistulous communication between the post-bulbar duodenum and pleural space (Figure ).
After confirmation of fistula obliteration, a video-assisted thoracoscopic surgery was performed followed by the washout of the right pleural space with the placement of a right-sided chest tube. The patient was discharged home after the procedure and has been followed by multidisciplinary teams on an outpatient basis.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [86.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': True, 'Hemoptysis': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",4,4,4,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 86.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 =  1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be present and so one point is incremented to the score, making the current total 3.0 + 1 = 4.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 4.0.
The patient's Well's score for pulmonary embolism is 4.0."
3115,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-1618827-1,Extracted,"A 41 year-old Caucasian female patient was referred to us by general practioner (G.P.) with 2-day history of the migratory abdominal pain. Initially, the pain was constant and dull in the peri-umbilical region, which later became sharp and localised in the right iliac fosssa. She also complained of four episodes of vomiting and loss of appetite. She occasionally felt pain in her right shoulder. There was no history of even trivial trauma. In the past, she had 3 episodes of pulmonary embolism following hysterectomy and she had been on warfarin for the prophylaxis since then. She used to take tylex (paracetamol and codeine), pantoprazole, tramadol, senna, migraleve, zimovane and fentanyl citrate lozenges as her regular medications. She had 35-pack year history of smoking. On examination, she was afebrile (however, temperature of 37.8°C noticed by General Practitioner 6 hours before presentation in the Casualty) but tachycardic with pulse rate of 134/minute. There was no bruising or haematoma in the abdominal wall. The abdomen was distended with marked tenderness in the right lower quadrant. There were guarding and rebound tenderness in the right iliac fossa. The rectal examination revealed tenderness in the right pelvic wall. The urine dipstick was positive for the ketones and trace of protein. The pregnancy test was negative. The blood investigations showed haemoglobin of 10.8 gm/dl with reduced haematocrit of 32%, White Blood Cells of 11.8 × 109/l and INR of 2.2. The blood biochemistry did not reveal any abnormality.
The clinical diagnosis of acute appendicitis was made. She was scoring 8 according to modified Alvarado scoring system []. The decision for appendectomy was made and the consent was given for the emergency appendectomy. Through the Lanz incision, about 200 ml of haemorrhagic fluid was aspirated from the peritoneal cavity. The appendix and the mesoappendix were looking normal. The appendectomy was performed. Intra-operatively, there were several blood clots present, so the incision was converted to the formal transverse infra-umbilical laparotomy incision. The large, 10 × 15 cm2 size blood clot was evacuated from the pelvis. Despite thorough search for the active bleeding site, we could not find any cause for active bleeding. The final diagnosis of the spontaneous intra-peritoneal bleeding secondary to warfarin was made. The abdomen was closed with the low suction drain, which drained about 200 ml of the serosanguinous fluid over next 2 days. 2 units of fresh frozen plasma were transfused in the immediate post-operative period. The warfarin was stopped after the operation. The patient was re-warfarinised on 8th post-operative day and was followed up in the surgical and the haematology clinics. At 2 weeks follow up visit in surgical clinic; patient was doing well without any complaints and complications. The histology of the appendix confirmed normal appendix without any inflammation.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [134.0, 'beats per minute'], 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 134.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3116,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5165135-1,Extracted,"A 65-year-old man with a remote history of possible PE and current tobacco use presented with swelling, erythema, and warmth of his right lower extremity for three to four weeks (). He denied cough, hemoptysis, shortness of breath, chest pain, recent travel, prolonged immobilization, or history of malignancy. Approximately ten years ago he was diagnosed with a PE at an unrecallable hospital and did not receive anticoagulation. The events surrounding this self-reported PE could not be verified.
Five weeks before presentation, the patient went to the Emergency Department with low back and right buttock pain radiating down to the mid-posterior right calf and was diagnosed with sciatica. Two weeks later, he returned with pleuritic chest pain and exertional dyspnea, thought to be secondary to costochondritis; he left against medical advice. Three weeks later, on the day of admission, he was evaluated by his primary care physician, who obtained a lower extremity venous Doppler study that showed extensive DVT in his right lower extremity ().
The patient's medications included bupropion, cholecalciferol, ibuprofen, prazosin, simvastatin, vitamin A, and over-the-counter supplements including DIM. He had used over-the-counter testosterone supplements for six months but discontinued them 13 months before hospitalization. Prior to his hospitalization, he used DIM one tablet daily for three to four months. He did not know the dose, but a common dose is 100 mg per tablet. He had a 60 pack-year smoking history, with cessation for five years prior to resumption one year ago. He had a documented weight loss of 7 kg over one month, but he endorsed a recent increase in exercise, including skiing and weight lifting. Colonoscopy four months earlier found a benign polyp. Prostate specific antigen was less than 3 ng/mL a year before and during hospitalization.
Physical examination revealed a heart rate of 104 beats per minute, blood pressure 123/81 mmHg, respiratory rate 16 breaths per minute, temperature 36.1°C, and oxygen saturation 96% on room air. The right leg was mildly swollen with erythema and warmth. The rest of the examination was unremarkable. Chemistry panel, complete blood count, hepatic function panel, and coagulation studies were normal. PE-protocol computed tomography (CT) of the chest (Figures and ) showed bilateral pulmonary artery filling defects with marked involvement of the right middle lobe branch with associated probable infarction. He was treated with anticoagulation and counseled on tobacco dependence. Five months later, a lower extremity venous Doppler study found chronic DVT in the right lower extremity ().",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [104.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 104.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
3117,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-2740172-1,Extracted,"A 47 year-old Asian female was transferred to the authors’ institution from another hospital with a subacute history of shortness of breath, bilateral lower extremity swelling, pleuritic chest pain, cyanosis, episodic loss of consciousness and hypotension. Two years prior to admission she had underwent an abdominal hysterectomy for uterine fibroids, which were complicated by symptomatic anemia from associated menorrhagia. Two months prior to admission, she sustained a brief loss of consciousness, then two weeks before admission she developed gradual onset of pleuritic chest pain and lower extremity edema. One day prior to admission, she complained of some shortness of breath and a non-productive cough. There were no known risk factors or family history of thromboembolism. She had no other significant past medical, surgical or obstetric history. She was a non-smoker, non-alcoholic and denied use of illicit substances. She had no history of drug allergy.
On the day of admission, she developed dizziness at home and fell to the ground. Her family helped her to bed wherein she had a witnessed four-minute period of loss of consciousness. She was taken by ambulance to an outside hospital where she appeared cyanotic and hypotensive with a weak pulse, was immediately sedated, endotracheally intubated and started on intravenous norepinephrine. Physical examination, prior to intubation, revealed a dusky blue skin suggestive of cyanosis. She had a tachycardia with pulse rate of 110 per minute, hypotension with systolic blood pressure of 70 mmHg and tachypnea with respiratory rate of 34 breaths per minute. There was teeth clenching and hypersalivation. An electrocardiogram and serum troponin levels were normal, her initial arterial blood pH was 7.25 with a PCO2 of 2.93 kPa (22 mmHg) and a PO2 of 67.46 kPa (506 mmHg) on an inspired fraction of oxygen of 1.0. The leukocyte count was 12.9 x 103 /μL with 81% neutrophils and 16.2% lymphocytes. Other hematologic and coagulation parameters were within the normal range. The serum bicarbonate was 14.6 mmol/L while other serum chemistries, renal and liver function tests were unremarkable. A computed tomography (CT) scan of the head was normal. A venous duplex ultrasound scan showed the presence of a right lower extremity proximal deep venous thrombosis (DVT) extending to the groin and she was commenced on intravenous standard unfractionated heparin.
Later that day the patient was transferred to our hospital where a pulmonary embolism protocol computed tomography (CT) scan of the thorax and pelvis (, , ) and a repeat transthoracic echocardiogram were performed (). Because of the positive venous duplex ultrasound finding of a DVT, a D-Dimer was not requested.
The patient was seen by a pulmonologist who made a differential diagnosis of an intracardiac tumor thrombus versus a thromboembolism-in-transit, and advised a surgical opinion. Because of delays in obtaining a concensus on appropriate surgical management from the cardiothoracic, vascular and gynecologic surgeons together with the need for further imaging studies, ongoing hypotension, presumed transient complete occlusion of the tricuspid valve and a confirmed deep venous thrombosis, the patient was initially thrombolysed intravenously with 100 mg of tissue plasminogen activator to treat any life-threatening component of venous thrombosis. Following this, the patient’s hemodynamic indices improved only slightly. The next day, the patient underwent a joint procedure with single stage median sternotomy and exploratory laparotomy, extraction of an inferior vena cava, common iliac vein and right atrial tumor thrombus, and included bilateral salpingo-oophorectomy. The histopathology of the tumor was consistent with leiomyoma ().
Post-operative transoesophageal echocardiogram and CT showed complete removal of the intravascular lesion with minimal residual pelvic mass. There were no complications and the patient was subsequently taken off pressors, extubated and discharged to follow-up on oral anticoagulation.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
Because the patient has previously been diagnosed for pulmonary embolism (PE) and deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
3118,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7205380-1,Extracted,"A 39-year-old female presented to the emergency department with complaints of shortness of breath. She had a significant history of intravenous (IV) drug abuse and stated she had last used heroin one day prior. She had also been hospitalized at an outside facility a month prior for sepsis secondary to methicillin-resistant Staphylococcus aureus (MRSA) bacteremia and tricuspid valve endocarditis. At that time she was treated with IV antibiotics and discharged on linezolid, but she did not complete the full treatment course. The patient had also been diagnosed with a pulmonary embolism during that hospitalization and was discharged on apixaban. She had taken her last dose of apixaban the day before presenting to the ER for this admission. Review of systems was significant for pleuritic chest pain, a cough with no sputum production that also exacerbated chest pain, nausea and vomiting for the past week.
Initial vitals were as follows: temperature 102°F, pulse rate 145 beats per minute, respiratory rate of 35 breaths per minute and oxygen saturation of 98% on room air. Physical exam revealed track marks that were present on the left neck. Chest auscultation revealed that the patient was tachycardic with an early systolic murmur at the left sternal border and shallow but clear breath sounds bilaterally. Old scarring from an abscess on the right thigh and track marks were present behind the right knee.
Initial workup revealed an elevated lactic acid of 3.1 mmol/L, leukocytosis with white blood cell count of 22.4 k/cmm, elevated D-dimer, an elevated B-type natriuretic peptide (BNP) 2,229 pg/ml, a mildly elevated troponin of 0.093 ng/ml that trended to 0.085 ng/ml and finally 0.054 ng/ml. Cultures were drawn, and the patient was started on vancomycin and piperacillin/tazobactam. A transthoracic echo revealed a 1.3-cm vegetation on the posterior leaflet of the tricuspid valve confirmed with a transesophageal echocardiogram. The CT revealed multiple occlusive emboli in her pulmonary artery involving the right lobar segment and segmental branches of lower limbs bilaterally, along with extensive airspace disease with cavitations that were possibly septic. Blood cultures grew Serratia, and the patient’s antibiotics were optimized to piperacillin/tazobactam, rifampin, and linezolid due to concerns over possible non-clearance of previous MRSA infection.
The patient was initially started on a heparin drip while cardiothoracic surgery planned to operate on her to remove the vegetation. The patient’s white count steadily trended down and vitals became more stable. Unfortunately, the heparin Xa unfractionated level was low (initially 0.16 IU/ml), indicating subtherapeutic anticoagulation. On day 1, the patient received a total of 6,021 IU of heparin at an average infusion rate of 18 IU/kg/hr. On day 2, the patient received a total of 47,632.8 IU of heparin at an average infusion rate of 23 IU/kg/hr. On day 3, the patient received a total of 60,143.1 IU of heparin at an average dose rate of 31 IU/kg/hr. On day 4, the patient received 66,900 IU of heparin at an average dose rate of 35 IU/kg/hr. And on day 5, the patient received 71,716.8 IU at an average dose rate of 38 IU/kg/hr. The patient received 40 IU/kg bolus of heparin per hospital standards with every infusion change (approximately every six hours). Despite the increasing titration of heparin, the highest anti-Xa level was no more than 0.27 IU/ml. On the sixth day of admission, the patient started complaining of increasing right-sided chest pain and CT chest showed a worsening area of probable infarct in the right lung. With concern for increasing lung infarction in the setting of subtherapeutic anticoagulation, heparin was stopped and subsequently the patient was started on argatroban. The following morning (day 7), the fibrinogen level dropped significantly to 50 from 650 mg/dl. There was a significant concern for DIC, but clinically the patient showed no signs of active bleeding or clinical worsening.
In the setting of sepsis from an uncontrolled source (infective endocarditis), a sudden drop in fibrinogen levels alerted all providers to a possible coagulopathic state of DIC. Of note, the patient had no clinical signs of DIC and the platelet levels were regularly above the 400,000 k/cmm. In the interest of precaution, the patient had argatroban therapy held. Six hours later, the DIC panel showed a fibrinogen of 470 mg/dl and platelets remained above 400,000 k/cmm. Low molecular weight heparin was started. Four-hour post-administration Xa level was not therapeutic at 0.23 IU/ml. For that reason, low molecular weight heparin was stopped, and the patient was started on bivalirudin. The patient is currently scheduled for surgical resection of the vegetation by cardiothoracic surgery.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [145.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 145.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3119,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7568137-1,Extracted,"A 57-year-old woman was admitted to the hospital with one week of worsening, nontraumatic back pain. The patient reported a history of chronic back pain secondary to her sedentary occupation. The pain had significantly worsened from baseline approximately seven days prior to admission. Before arrival, the patient was prescribed a lidocaine patch without significant relief. The pain did not radiate and was appreciated at the level of the thoracic spine. The pain intensity, 10/10, was aggravated by motion and relieved with rest, and to some degree, with hydromorphone. The patient's past medical history was significant for COPD, hyperlipidemia, depression, bipolar disorder, anxiety, GERD, irritable bowel syndrome, and distant history of the intravenous drug abuse with heroin in her youth. The patient's home medications included: albuterol inhaler, BREO ellipta, cyclobenzaprine, acetaminophen, ibuprofen, aspirin, docusate, ondansetron, ranitidine, and a lidocaine patch. The review of systems was otherwise negative.
On physical examination, no skin changes were detected over the patient's back. The spine was tender to palpation in the paraspinal area and tender to percussion at the midline. The neurologic examination performed at the bedside did not show any gross or focal neurologic signs. The lungs were clear to auscultation bilaterally. Heart tones were clear, without rubs, murmurs, or gallops. The rest of the physical exam was unremarkable. No skin tracks or other signs of intravenous drug abuse were detected during the physical exam.
The Emergency Department vital signs observed an oral temperature of 98.3°F, a blood pressure of 147/100 mmHg, a pulse of 96/min, and respirations of 20/min. O2 saturation was 98% on room air. During her time in the emergency department, blood pressure was normalized.
The laboratory assay revealed aWBC count of 26.100 leukocytes/μl with 78% neutrophils, an elevated lactate of 2.4 mmol/l, a sodium level of 118 mEq/l, a chloride level of 78 mEq/l, CRP >320 mg/l, an ESR 75 mm/h, and a creatinine level of 1.9 mg/dl which was three times more than her baseline. Urinalysis was normal. Chest X-ray done on admission showed hypoinflation with areas of linear airspace disease representing atelectasis and a small left pleural effusion.
The patient was admitted to the hospital with a diagnosis of sepsis with a concern for spinal infection, hyponatremia, and acute kidney injury. She was prescribed broad-spectrum antibiotics (ceftriaxone, vancomycin, and metronidazole) and normal saline. Infectious Diseases and Neurosurgery services were consulted.
An MRI was performed revealing (1) a large posterior SEA extending from the lower cervical spine into the upper lumbar spine causing moderate spinal canal narrowing with mild cord compression in the lower thoracic spine without abnormal signal to suggest cord edema or ischemia, (2) extensive cellulitis and myositis involving the paraspinal musculature of the cervical and lower lumbar spine, (3) small left paraspinal abscesses of the lumbar region, and (4) large right cervical paraspinal abscesses and a left psoas muscle myositis with a 2 cm left psoas abscess ().
Neurosurgery service deferred an open surgical procedure and recommended a guided aspiration of the abscess for diagnosis and culture. Antibiotics were adjusted to cefepime and vancomycin. A lumbar puncture was not deemed necessary.
The ultrasound-guided percutaneous aspiration of the right neck paravertebral abscess yielded only 3 cc of highly viscous purulent fluid. The patient was transferred to the intensive care unit for close postprocedure monitoring. A 2D echocardiogram performed on the day of admission did not show any definite vegetation on the cardiac valves. Cultures obtained from the cervical abscesses grew pan-sensitive Staphylococcus aureus. The patient's antibiotic therapy was adjusted to nafcillin.
The patient remained stable after procedure with no exacerbation of her neurologic status and a diminishment in the intensity of her back pain.
As her clinical status improved, the patient was discharged to a skilled nursing facility to complete a 12-week course of nafcillin.
Six weeks after initiation of the antibiotics course, the patient's leukocyte count decreased to 10.9, and the basic metabolic panel were within normal limits. A repeat MRI performed eight weeks after initiation of antibiotic therapy showed resolution of previously seen paraspinal abscesses and phlegmonous changes. A repeat physical exam did not show any focal neurologic changes, and the patient's back pain was back to baseline.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [96.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 96.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3120,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5721960-1,Extracted,"A 31-year-old woman presented for evaluation of pain in the left forearm, right hand, right knee, right hip, and lower back following a fall sustained 3 days prior to presentation. She had a past medical history notable for end-stage renal disease (ESRD) for which she has been receiving maintenance hemodialysis for the past 15 years, hypertension, diabetes, and congestive heart failure. She was wheelchair bound due to disabling peripheral neuropathy and chronic leg pain. She reported that she had fractured her left wrist about 3 weeks prior to presentation. She also experienced femoral fracture about a year ago, that was managed conservatively.
Physical examination revealed a blood pressure of 153/81 mm Hg and pulse rate of 101 bpm. There was moderate swelling and tenderness over the right distal femur with limited range of motion of the right knee due to pain. Left forearm splint due to previous fracture was in place. Tenderness was also noted over tip of the right index finger. There was no distal neurovascular deficit in the extremities. Medications included aspirin of 81 mg per day, lisinopril of 40 mg per day, carvedilol of 25 mg twice a day, sevelamer carbonate of 800 mg thrice a day with meals, and insulin regimen. The patient reported non-compliance with medications, diet, and hemodialysis treatment.
Initial laboratory values were significant for hemoglobin of 8.5 g/dL (12–15 g/dL), white blood cell count of 6.2 thou/mm3 (4–10 thou/mm3), platelet count of 222 thou/mm3 (150–450 thou/mm3), blood urea nitrogen of 36 mg/dL (6–20 mg/dL), and creatinine of 5.72 mg/dL (0.4–0.9 mg/dL). Serum intact PTH was found to be significantly elevated at 1735 pg/mL (15–65 pg/mL (goal 150–300 pg/mL for ESRD)) with serum calcium level of 9.5 mg/dL (8.4–10.2 mg/dL) and phosphate of 5.7 mg/dL (2.7–4.5 mg/dL). Serum 25-hydroxy vitamin D level was 24 ng/mL (>20 ng/mL).
X-ray of the right lower extremity showed diffusely decreased osseous mineralization and a comminuted distal femoral fracture (). Similarly, X-ray of the left upper extremity revealed significant diffuse osteopenia, and X-ray of the right hand showed findings concerning for possible fracture of the distal phalanx of the index finger just proximal to the subungual tuft versus aggressive erosion at this site was reported for the right hand (). Computed tomography (CT) scan of the abdomen and pelvis showed remarkable diffuse severe demineralization of the bones, with florid changes of renal osteodystrophy, prominent subligamentous resorption in the sacroiliac joints bilaterally, and widespread brown tumors ().
With normal serum calcium, high serum phosphate together with severely high PTH level, and history of non-compliance with medications and the dialysis treatment, the diagnosis of secondary (renal) hyperparathyroidism was made. Chart review revealed a history of long-standing severe hyperphosphatemia in the past explaining the presence of severe hyperparathyroidism despite current mild hyperphosphatemia (possibly now evolving toward more autonomous PTH secretion).
Typical imaging stigmata of hyperparathyroidism including diffuse demineralization, insufficiency fractures, and brown tumors supported the diagnosis in this young woman.
Her fractures were managed with non-operative treatment given her poor baseline functional status and severe hyperparathyroidism. The patient refused surgical parathyroidectomy. A high-dose phosphate binder (i.e. sevelamer carbonate) and also an oral calcimimetic (i.e. cinacalcet) were started for management of hyperphosphatemia and hyperparathyroidism. We reinforced compliance with low phosphate diet, medications, and hemodialysis treatment.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [101.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 101.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 =  6.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
3121,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8489796-1,Extracted,"A 36-year-old African American woman with a past medical history of systemic lupus erythematosus (SLE), a recent novel coronavirus infection severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2, COVID-19) not requiring supplemental oxygen and treated with intravenous steroids, and hypertension presented to the hospital with acute nausea, vomiting, and fever. The patient had recently been admitted for fatigue from SLE and was discharged on hydroxychloroquine, mycophenolate, and prednisone taper to a rehabilitation facility to continue physical therapy one month prior. On discharge from the rehabilitation facility, the patient reported, she was not prescribed prednisone. She reported she had been tapering down every two weeks from a starting dose of 80 mg and had reached 30 mg daily. After a few days on 30 mg, she ran out of pills and was unable to get a new prescription. After she was without prednisone for three days, she started having nausea and vomiting and was unable to tolerate any oral intake. She endorsed diarrhea and fatigue but denied subjective fever, chills, weight loss, abdominal pain, melena, hematochezia, hematemesis, joint pain, joint swelling, oral sores, hair loss, and facial rash.
The patient had no past psychiatric history. The patient’s medications were amlodipine, calcium carbonate-vitamin D3, hydroxychloroquine, mycophenolate, nystatin powder, pantoprazole, and prednisone (the last dose was three days prior to admission). The patient had no known drug allergies. Her only past surgery was a cesarean section. The patient reported working virtually as a court clerk and performing all her activities of daily living independently. Due to generalized weakness after her hospital admission for a lupus flare and COVID-19 infection, she reported using a walker when walking long distances. She denied using tobacco, alcohol, and any illicit drugs. She reported a family history of hypertension in multiple family members.
On physical examination, her temperature was 38.9 °C (102.0 °F), blood pressure was 146/97 mm Hg, heart rate was 111 beats per minute, respiratory rate was 18 breaths per minute, and oxygen saturation was 94%. The patient appeared tired but was alert, oriented, and well-developed. The rest of the exam was insignificant.
Pertinent laboratory data on admission are included in Table . Transaminases, bilirubin, and lipase were all within normal limits. Due to concerns for sepsis, the patient was admitted to the inpatient hospital medicine service, where she was restarted on her home prednisone at 30 mg daily and empirically started on ceftriaxone. Workup revealed a morning cortisol level of 3.0 mcg/dL and negative blood and urine cultures. The patient’s symptoms improved on steroids, and her symptoms were attributed to adrenal insufficiency.
On her third day of admission, the patient became tachycardic and altered with elevated mood, decreased need for sleep, distractibility, hyper-religiosity, and inappropriate smiling and laughing. Due to concern for corticosteroid-induced mania, she was started on valproic acid 500 mg twice a day and clonazepam 1 mg at bedtime as needed for insomnia. Her prednisone was not discontinued due to her initial presentation of adrenal insufficiency but was decreased to 20 mg daily. Physical exam revealed no focal neurologic deficits. CT and MRI of the brain showed no acute abnormalities and no evidence of lupus cerebritis. Lumbar puncture showed low protein, elevated lymphocytes, and immunoglobulin G within normal limits. While cerebrospinal fluid analysis showed a lymphocytic pleocytosis, the low protein, lack of focal neurologic deficits on an exam, unremarkable MRI, and acute onset of symptoms following steroid resumption were more consistent with a diagnosis of substance-induced mood disorder rather than aseptic meningitis or other neurologic manifestations of lupus.
The patient returned to her baseline mental status with valproic acid within 24 hours. As she had previously been on 80 mg of prednisone, the dose was increased from 30 mg to 40 mg daily to allow for a more gradual steroid taper and prevent adrenal insufficiency. She was discharged with the plan of decreasing her valproic acid dose in parallel with her steroid taper. Although the goal was to discontinue valproic acid after she was off steroids, the patient ran out of valproic acid three months after discharge while still on prednisone (15 mg daily). She had been referred to psychiatry upon discharge to manage her valproic acid taper and was seeing a psychiatrist. However, she was not given refills at her previous psychiatry appointment for unknown reasons. Although she had a psychiatry appointment scheduled during the same month that she ran out of valproic acid, in a visit to the emergency department two months later, she reported she had not resumed her valproic acid. During that encounter, she reported she had not experienced further psychiatric symptoms while off valproic acid and had continued her steroid taper.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [111.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 111.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3122,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8212532-1,Extracted,"An 89-year-old caucasian female presented to the emergency department at an outside hospital with a 12-hour history of right medial thigh pain that radiated to the right buttocks and down the right leg. She reports that she was in the attic that morning when she stepped over a box and felt a sharp pain in her groin. The patient also reported the appearance of small bulge in her groin that had disappeared prior to her presentation. The patient’s medical history was significant for atrial fibrillation and transient ischemic attack. She also had a history of breast cancer 30 years ago and is now cancer free. Current medications were significant for Eliquis 2.5 mg twice daily. Surgical history was significant for laparoscopic cholecystectomy, double mastectomy, and total abdominal hysterectomy. There was no pertinent family history relating to this case. She has had two pregnancies and has two living children, which were born via standard vaginal delivery. Socially, the patient is widowed, retired, lives at home, and does not smoke or drink alcohol.
Physical examination revealed a pleasant frail female in no acute distress. Her heart had a regular rate and rhythm, and her lungs were clear to auscultation bilaterally. She exhibited mild distention of the abdomen and no peritoneal signs. Neurologically, she was intact with no focal deficits; her sensation and strength were intact and equal on both sides. She had no lymphadenopathy, edema, or cyanosis. Blood pressure was 158/70, pulse was 80 with regular rate and rhythm, and temperature was 97.8℉. BMI was 16.46 kg/m2. Inguinal and femoral hernias were not found on light or deep palpation. Rectal examination revealed no frank blood, fissures, or palpable masses. Complete blood count, basic metabolic panel, hepatic function panel, magnesium, phosphorus, and prothrombin time and international normalized ratio (PT-INR) were all within normal limits. CT scan of the abdomen and pelvis identified a loop of small bowel in the right obturator canal that appeared to be causing a small bowel obstruction (Figs. and ).
Patient was made nil by mouth, given Rocephin 1 g intravenous and Flagyl 500 mg intravenous, and taken to the operating room emergently for diagnostic laparoscopy with transabdominal extraperitoneal obturator hernia repair, and possible small bowel resection. On initial laparoscopic exploration, several loops of dilated bowel were visualized. A loop of bowel was found within the right obturator canal, was reduced, and displayed an obvious transition point. The bowel was pink and appeared healthy; therefore, resection was not performed (Fig. ). A flap of peritoneum was dissected back to expose the pelvic floor and obturator hernia. A piece of polypropylene mesh was placed over the entire inguinal floor to include the obturator foramen. The pelvic floor was reperitonealized. Postoperatively, she resumed her normal diet without nausea or vomiting and began passing flatus. She was discharged on postoperative day 2 without any complications with five tablets of Roxicodone PO 5 mg for pain control. Because of the out-of-town location of the patient’s home address, further follow-up was not possible.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 80.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3123,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7255072-1,Extracted,"Our patient is a 29-year-old caucasian, non-smoker woman who initially presented to the hospital due to a sudden onset of blurry vision of the right eye. Her past medical history was significant for obesity status post gastric sleeve surgery, menorrhagia, and iron deficiency anemia. She had a long history of iron deficiency anemia due to menorrhagia since she was 12 years old and had sleeve gastrectomy five years ago. Furthermore, she was treated with oral and intravenous (IV) iron infusion during her pregnancy to control her anemia. Over the past few months, she had been experiencing heavy periods lasting around six days that soaked through multiple pads and tampons a day. She was offered an intrauterine device (IUD) by her gynecologist but declined and elected to use an estrogen and progestin transdermal patch for contraception.
Her visual changes started when she was driving her car the day before admission that was accompanied by a throbbing headache along with photophobia, phonophobia which were not relieved by Ibuprofen or sleep. Her symptoms did not resolve after 12 hours; thus, she decided to present herself to the Emergency Department (ED) for further evaluation. In the ED, besides the complaints of blurry vision and headache, she denied any weakness, numbness, tingling, ataxia, similar prior episodes of visual changes, history of migraine, or alleviating factors. She noted persistent fatigue throughout this period but denied any dizziness, lightheadedness, shortness of breath, or chest pain. She denied any active bleeding on admission. The review of systems was otherwise negative. Her initial vital signs were: temperature of 99.6°F, blood pressure of 128/64 mmHg, respiratory rate 20 breaths per minute, heart rate 111 beats per minute, and oxygen saturation 99% on room air. Physical examination revealed a well-developed, well-nourished woman who was conversational, alert, and oriented. She had normal speech, language, funds of knowledge with intact recent and remote memory. Her visual field was normal by quadrant. Extraocular muscles were intact without gaze deviation, nystagmus, or ptosis. Pupils were equal and reactive to light. Normal motor strength and sensation were present throughout the body with negative Babinski sign. Cranial nerves 2-12 were intact. The rest of the physical examinations were unremarkable. Pertinent laboratory findings were hemoglobin 7.8 g/dL, hematocrit 26.1%, MCV 57.5 FL, MCHC 29.7%, RDW 17.2%, iron 11 ug/dL, iron-binding capacity 395 ug/gL, iron saturation 3%, ferritin <1 ng/mL, and platelet 364k/UL. The electrocardiogram showed normal sinus rhythm. CT head without contrast was concerned for a non-hemorrhagic left occipital lobe infarction in the posterior cerebral artery distribution [Figure ]. CT angiographic examination demonstrated no focal high-grade intracranial stenosis, occlusion, or vasculitis. MRI of the brain revealed an abnormal increase in signal density on the FLAIR sequence that was consistent with an acute left posterior artery occlusion [Figure ]. MRA of the brain and neck were subsequently unremarkable for any stenosis, occlusions, or dissections. Transthoracic echocardiogram revealed a small patent foramen ovale that was deemed to be clinically insignificant. She was treated with permissive hypertension, started on atorvastatin, clopidogrel without aspirin due to the history of gastric sleeve. She remained stable overnight.
On day 2 of hospitalization, her vital signs remained to be stable without new neurological findings on physical examination. Her hemoglobin level decreased from 7.8 g/dL to 6.8 g/dL. Later on during the day, the Rapid Response Team alert was activated due to an acute onset of left-sided numbness without other interval changes found on the rest of the neurological examination. She scored two on the National Institutes of Health Stroke Scale (NIHSS). CT scan of the head without contrast ruled out intracranial hemorrhage. MRI of the brain with and without contrast showed no interval changes to the left occipital lobe infarction. Repeat Hemoglobin was found to be 7.2 g/dL. It was then believed that the low hemoglobin level was the most likely cause of her acute ischemic stroke. She was treated with two units of packed red blood cell transfusion (PRBC) along with IV iron infusion with the goal of 1000 mg of the iron supplement per day for her underlying IDA. The patient reported an improvement of her symptoms a few hours later after the treatment began as her numbness and blurry vision both had resolved. She tolerated the blood transfusions well without complications.
There were no interval changes on day 3-7 of hospitalization. She was also started on daily folic acid. Atorvastatin was discontinued as hypercholesterolemia was the unlikely cause of her infarction given low LDL. Hemoglobin A1c was 5.4%. Hemoglobin levels remained to be greater than 8.5 g/dL status post the two units of PRBC transfusion. She had completed a total of five days course of iron transfusion. An intravaginal ultrasound was performed that did not reveal any endometrial abnormalities. Biopsy of the endometrium revealed benign proliferative endometrium, as well as a normal endocervix. The estrogen and progestin transdermal patches were discontinued as well. She was subsequently discharged home and was instructed to follow up with an outpatient hematologist for iron transfusion and hypercoagulable workup to assess whether it could be related to the CVA. Finally, she was also advised that the safest hormonal option would be a progesterone IUD for contraception as it has the least amount of systemic absorption.
She was followed closely by a hematologist in the outpatient setting. Hypercoagulable workup that included protein C activity, protein S antigen, PT/INR, PTT, peripheral blood smears, cardiolipin IgA, IgM, IgG, beta2-glycoprotein I IgA, IgM, IgG, factor V Leiden, prothrombin gene analysis was completely unremarkable. She also has been receiving intermittent iron transfusions, and her hemoglobin was closely monitored. Her hemoglobin levels were stable, with the most recent value of 12.0 g/dL. There were no reported residual neurological deficits.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [111.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 111.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3124,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-10027,Extracted,"A 65-year-old man, known to have chronic obstructive lung disease for the last 3 years, presents to the emergency department with a cough, breathing difficulty, and increased expectoration for a day. There is no history of fever. His regular medications include inhaled salmeterol and inhaled fluticasone propionate. He was a chronic smoker but quit smoking 2 years ago. His temperature is 37.1°C (98.8°F), the pulse rate is 88/min, the blood pressure is 128/86 mm Hg, and the respirations are 30/min. On physical examination, the use of the accessory muscles of respiration is evident and the arterial saturation of oxygen is 87%. Auscultation of the chest reveals the presence of bilateral rhonchi with diminished breath sounds in both lungs.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [88.0, 'beats per minute'], 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 88.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3125,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7387071-3,Extracted,"A 53-year-old man with past medical history significant for hypertension and prior smoking presented to the emergency department (ED) with complaints of fever, dyspnea, and cough that had started four days prior to presentation. He reported the fever had been progressively worsening since onset with a max temperature of 103°F at home. He also reported myalgias, fatigue, and decreased appetite. He mentioned that one of his coworkers had tested positive for COVID-19 after having similar symptoms.
His triage vitals were significant for a temperature of 37.6°C, a respiratory rate of 24 breaths per minute, a heart rate of 118 beats per minute, a blood pressure of 135/87 mmHg, and an oxygen saturation of 79% on room air. On physical examination, the patient was awake, alert, oriented, and in no distress. Lung sounds were clear and equal bilaterally with no signs of respiratory distress. There was no increased work of breathing. The patient spoke in full sentences; however, he did have to pause during longer sentences. His skin was pink, warm, and dry with moist mucosal membranes. His abdomen was soft and nontender.
Labs and a chest x-ray were ordered in addition to blood cultures and COVID-19 testing. His labs were significant for leukocytosis 13.6 x 103 cells/mm3, D-dimer 1.30 mg/L (normal <0.49), hyponatremia 134 mEq/L (normal 135-145), lactic acid 2.4 mmol/L (normal <1), AST 86 units/L, lactate dehydrogenase (LDH) 746 units/L (100-190), and procalcitonin 0.43 ng/mL (<0.05). His chest x-ray demonstrated a mild perihilar interstitial infiltrate or edema pattern.
During his clinical course in the ED, the patient had improved oxygenation on 6 L nasal cannula to 92% saturation. Empiric antibiotics and intravenous fluids were started for suspected sepsis. The patient was admitted to the hospital for acute hypoxemic respiratory failure requiring supplemental oxygen. On day 2 of hospitalization, the ICU team was consulted by the hospitalist and infectious disease for evaluation for increased respiratory effort. The follow-up chest x-ray also revealed increasing alveolar infiltrate, and the patient’s COVID-19 test was positive. On evaluation by the ICU, the patient endorsed worsening difficulty breathing, particularly with movement despite receiving 15 L via nonrebreather (NRB) mask. He was tachycardic to 105 beats per minute, had an oxygen saturation of 90% on 15 L NRB mask, and labored respirations at a rate of 23/min. His breath sounds were diminished bilaterally.
The decision was made to transfer the patient to the ICU for observation. His respiratory distress progressed, and the patient was intubated and sedated for mechanical ventilation. The patient’s urine output declined since admission to the ICU with concern for acute tubular necrosis possibly secondary to a thrombotic event. On day 4 of hospitalization, the decision was made to empirically start heparin drip (titrated to an activated partial thromboplastin time value 1.5 to 2.5 times the mean normal value) after the patient remained anuric. On day 9 of hospitalization, the patient was found to have a left lower extremity DVT in the posterior tibial vein despite empiric therapeutic level heparinization (Figure ). He was eventually deemed a poor candidate for long-term anticoagulation for bleeding risk and had an inferior vena cava (IVC) filter deployed. The patient was discharged on hospital day 36 to a long-term acute care hospital after remaining afebrile for three consecutive days.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [118.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",6,6,6,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 118.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 4.5.
The patient not been diagnosed with pulmonary embolis (PE), but the patient has previously been diagnosed with deep vein thrombosis (DVT), we increase the current total by 1.5 so that 4.5 + 1.5 = 6.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 6.0.
The patient's Well's score for pulmonary embolism is 6.0."
3126,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-6761459-1,Extracted,"A 32-year-old woman living in North Carolina but under the care of a local physician in Washington DC for symptoms attributed to chronic Lyme disease presented to George Washington University Hospital with fever, shortness of breath, and increasing confusion. Two years prior to the current presentation, the patient had been given a diagnosis of chronic Lyme disease after she developed multiple symptoms including confusion, photophobia, arthralgia/ myalgia, headaches, constipation, and seizures. A computed axial tomography (CT) scan of the chest at the time showed patchy infiltrates and she underwent a bronchoscopy, which did not detect any abnormality including negative acid-fast bacilli smear and culture. Subsequent imaging showed resolution of those infiltrates. She was treated with multiple oral regimens including rifabutin, pyrimethamine, leucovorin, metronidazole and ivermectin. One year prior to her current presentation she had a subclavian CVC implanted for administration of intravenous antibiotics including meropenem, clindamycin, and tigecycline. Most recently, she had completed a three-week course of ciprofloxacin and meropenem every other day, ending several weeks prior to her presentation. After development of her current symptoms, she sought treatment in an emergency department in North Carolina, where she was diagnosed with pneumonia and treated with azithromycin without improvement. She then traveled to Washington, DC for evaluation by her local physician, and subsequently presented to our institution.
In the emergency department the patient was noted to be febrile to 39.5°C, blood pressure 125/73 mmHg, heart rate 85 beats/minute. Physical exam revealed fatigued appearance with decreased breath sounds bilaterally, and a CVC with port access in the left chest wall without evidence of infection. Laboratory studies revealed leukocytosis (white blood count 11,370 cells/mL, 85% neutrophils). Contrast CT chest showed bilaterally symmetric opacification with bronchovascular distribution and innumerable pulmonary nodules (). Multifocal pneumonia due to septic emboli was suspected, and vancomycin plus piperacillin-tazobactam were started. A trans-thoracic echocardiogram (TTE) found no evidence of valvular vegetations. No other foci of infection were apparent on physical examination. After 72 hours anaerobic blood culture bottles (BACTEC Plus Aerobic/F, Becton Dickinson, Sparks, Maryland) revealed growth of beaded Gram-positive, acid-fast rods suggestive of mycobacterial species.
After lengthy discussion with the patient and her family, the CVC was removed. Culture of initial blood cultures and the CVC tip revealed growth of M. goodii. The patient’s antibiotics were empirically changed to azithromycin 500 mg intravenously daily, ciprofloxacin 400 mg intravenously every 12 hours, and meropenem 1 g intravenously every 8 hours. The patient clinically improved on this regimen. The patient returned to North Carolina before the identification and sensitivities of the mycobacterial species was available. Therefore, she was empirically switched to an oral regimen of trimethoprim/ sulfamethoxazole 800 mg/160 mg twice daily, azithromycin 250 mg once daily, and ciprofloxacin 500 mg twice daily for two-weeks from time of line removal. The patient was counseled extensively to avoid future placement of a CVC in the absence of a clear medical indication. Blood cultures drawn after CVC removal were negative at the time of her discharge but subsequent to discharge also grew M. goodii. The patient cancelled her follow-up appointment in our Infectious Diseases clinic and she was lost to follow-up.
The mycobacterial isolate was sent to Quest Diagnostics Labs (San Juan Capistrano, California) for the beta subunit of RNA polymerase (rpoB) and 16S rDNA sequencing which revealed the organism to be genetically consistent with M. goodii with an identity match of 99.86%. Sensitivity testing showed the organism to be resistant to clarithromycin (MIC >16 mcg/mL), intermediate to cefoxitin (MIC 32 mcg/mL), and susceptible to both ciprofloxacin (MIC 1 mcg/mL) and trimethoprim/sulfamethoxazole (MIC 0.5/9.5 mcg/mL).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [85.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 85.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is not reported in the patient note and so we assume that this is absent for the patient, keeping the score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3127,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4124661-1,Extracted,"A 29-year-old female German law student was referred to our outpatient department (OPD) with a two-week history of severe frontal headache and high-grade fever reaching 41°C (106°F). Upon her first presentation, diarrhea, bloody discharge or abdominal cramps were denied. She did not report any weight changes or high-risk sexual behaviour. She had no previous history of diseases and was not on any medication. Paracetamol had relieved pain and fever for up to eight hours.
Her travel history was remarkable for a three-month sojourn to Delhi, India, where she had completed an internship in an upper-class neighbourhood and from which she had returned three weeks prior to presentation. During the last months, she had not taken any antibiotics and was not on malaria prophylaxis. Before travelling, she had received all recommended vaccinations including for typhoid fever (Ty21a) and hepatitis A. Her clinical examination was unremarkable. Routine laboratory tests showed a mild thrombocytopenia of 112Gpt/L (150 to 300) whilst leukocyte counts were not elevated. Her rapid malaria test results were negative. Serum antibodies against typhoid fever (O and H antigens, cutoff 1:200), Serum antibodies against typhoid fever (O and H antigens, cutoff 1:200), human immunodeficiency virus (HIV), herpes simplex virus (HSV) 1/2, dengue fever, and hepatitis C could not be detected. Stool microscopy, stool culture and specific antigene assays were unremarkable for pathologic bacteria, viral antigens, worms or protozoa. As she had no fever at the time of presentation, the attending physician did not take blood cultures.
However, she returned to the OPD five days later as her fever and headaches had not ceased. She then also complained of a non-productive cough, bone and muscle pain, abdominal discomfort and constipation. Blood cultures were taken and she was admitted to the gastroenterology ward.
On clinical examination, we saw a deterioration in the young woman’s general and nutritional condition. Her body temperature was 38.3°C (101°F); her heart rate was 90/min with a blood pressure of 115/70mmHg. There was no lymph node swelling. Her sclera were white and without suffusions. Her chest examination result was unremarkable. Her abdomen was slightly tense with reduced bowel sounds. There was no liver or spleen enlargement. Her laboratory test results were remarkable for elevated C-reactive protein (CRP) 142mg/L (<5); aspartate aminotransferase (ASAT) 8μkat/L; alanine aminotransferase (ALAT) 5μkat/L (both <0.6); lactate dehydrogenase (LDH) 17μkat/L (2.2 to 3.5); a decreased thrombocyte count of 109/μL and a cholinesterase activity of 58μkat/L (71 to 181). There was no eosinophilia, and microscopic differentiation showed normal leucocyte values (4.8Gpt/L (4.0 to 9.0), neutrophils 66.6%, lymphocytes 27.5%, monocytes 5.5%, eosinophils 0.0%, basophils 0.4%). Her chest X-ray revealed milky opacities of the basal parts of the lung as well as a prominent scoliosis (Figure ). A urinary tract infection was ruled out. Stool microscopy and culture were again negative. A calculated antibiotic regimen with intravenous ciprofloxacin 500mg twice daily was initiated and switched to an oral formula after three days. Her antibody test results (including the Widal test) were again negative.
Five days later, three out of four blood cultures returned positive for Salmonella enterica serovar typhi. The pathogen was found to be sensible to all tested antibiotics including beta-lactams, fluoroquinolones and cotrimoxazole. Chloramphenicol sensibility was not tested. On the same day, the fever decreased and the headaches resolved. Repeated stool controls were negative for Salmonella spp. The patient was discharged after seven days in an improved condition. In order to control Salmonella carriage further, stool controls were performed by German health authorities. Only one out of six stool samples turned out to be positive for Salmonella typhi. Up to now, the patient remains healthy and has not experienced any typhoid relapse.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 90.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3128,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8677986-1,Extracted,"A 45-year-old man (occupation: medical doctor) visited a university hospital with a chief complaint of fainting 1 day back. He had no history of medical problems and was not taking any medications. He had hiked 4 to 5 times a week for 2 years. Syncope occurred while hiking on a cold winter night (temperature: −8°C). He fainted while resting for a while in a standing position after hiking at a fast speed for an hour. The witness reported that he lost consciousness for about 1 minutes, and no head strike or seizure-like activity was observed. Upon awakening from syncope, the patient had no syncope recollection. After syncope, the patient did not have any illnesses or symptoms, such as headache, cognitive deficits, or somnolence. He had no prior episodes of syncope or fainting.
At the time of examination (the day after the syncope), his blood pressure was 122/77 mm Hg, and his resting heart rate was 75 beats per minute. Electrocardiogram, 24 hours ambulatory electrocardiogram monitoring, echocardiogram, tilt table test, and exercise tolerance test showed no abnormal findings. In addition, in conventional brain and chest computed tomography and brain MRI, no abnormalities were observed. All blood test results, such as electrolyte level, hemoglobin level, erythrocyte sedimentation rate, and C-reactive protein level, were normal. In the physical examination, he did not show any neurological symptoms, including motor, sensory, or cognitive deficits (Mini-Mental State Exam: full marks, no patient's subjective symptoms). The deep tendon reflex was normoactive in all the extremities. Based on the patient's history and examination results, the cardiologist diagnosed the patient with transient loss of consciousness due to syncope. In addition, considering that syncope occurred during excessive physical activity at cold temperatures, the possibility of vasovagal syncope was thought to be high.
DCE scans were acquired using a 3T system (Skyra, Siemens Healthcare, Erlangen, Germany). In addition to the patient, a DCE scan was obtained from a healthy control participant (42-year-old man) who volunteered for the study. Seven pre-contrast sets of DCE-MRI (echo time= 1.92 ms, repetition time= 5.46 ms, the field of view = 230 × 135 mm2, matrix size of 256 × 150, and slice thickness of 3 mm), followed by an additional 114 sets under the intravenous injection of contrast agent were imaged in axial view. The permeability (Ktrans) of the mid-slice was calculated using the Patlak model.[
Here, t indicates the time step, τ indicates the variable of integration, Vp indicates the volume of plasma, and Ct (t) and Cp (t) indicate the temporal variation of the concentration of the contrast agent in the tissue and plasma, respectively. A circular region of interest (ROI) with an inner diameter of 1 to 2 cm was located at the superior sagittal sinus, which has higher consistency and plausibility compared to the internal carotid artery or the arterial vessel closest to the lesion.[ In the axial image where the body and crus of the fornix were presented, 10 round random ROIs of 2 cm diameter (dotted circles in Fig. ) were selected (5 in each hemisphere) to quantify the overall averaged Ktrans of the brain. ROIs were depicted, including sulci in which the bright blue colored lines (BBB disruption) are presented.
For the quantitative analysis, in each ROI of the healthy control participants and the patients, the T2 and Ktrans values were measured. The differences in the measured values between the healthy controls and patients were compared using an independent t-test. Statistical significance was set at P < .05.
In the conventional MRIs of the healthy control and the patient, no lesions were observed (Fig. A, 1B). In addition, in the Ktrans map of DCE MRI of healthy control participants, no specific abnormal findings were observed (Fig. C). However, in the patient, bright blue-colored lines were observed within the sulci throughout the cerebral cortex (Fig. D). These findings indicate disruption of the BBB of vessels in the overall cerebral sulci. In the quantitative analysis, the averaged T2 intensity (within 10 randomly selected ROIs) of healthy control and patient was 403.95 ± 24.91 (AU) and 404.50 ± 24.21 (AU), which was not statistically different (P = .9625). Here, the average Ktrans of healthy controls within 10 randomly selected ROIs was 0.000156 ± 0.000099 (minutes−1) and 0.001067 ± 0.000806 (minutes−1) for the patient. The average Ktrans of the patient was 6.86 times higher than that of the healthy controls, and the difference was statistically significant (P = .003409).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [75.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 75.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3129,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-235,Extracted,"A 25-year-old man is brought to the emergency department by his girlfriend for a nosebleed. Pinching the nose for the past hour has not stopped the bleeding. For the past several months, he has had recurring nosebleeds that resolved with pressure. He has no history of hypertension or trauma. He has asthma that is well controlled with an albuterol inhaler. He has intermittent tension headaches for which he takes aspirin. His temperature is 37.9°C (100.2°F), pulse is 114/min, and blood pressure is 160/102 mm Hg. Physical examination shows active bleeding from both nostrils. Pupil size is 6 mm bilaterally in bright light. The lungs are clear to auscultation. The hemoglobin concentration is 13.5 g/dL, prothrombin time is 12 seconds, partial thromboplastin time is 35 seconds, and platelet count is 345,000/mm3.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [114.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 114.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3130,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4145377-1,Extracted,"A fifty-five-year-old normotensive, nondiabetic, male smoker presented with progressively increasing soft tissue swelling in the left upper arm with intractable pain which was increasing at night for last 3 months. He also complained of weakness of left upper limb and difficulty to move the part of the limb distal to the swelling. There was history of significant weight loss, loss of appetite, and extreme fatigue, but no fever. There was no respiratory symptom or any history of contact with the patient with smear positive pulmonary tuberculosis.
General examination of the patient revealed anaemia and clubbing but no superficial lymphadenopathy. His axillary temperature was 37°C, respiratory rate 16 breaths/minute, pulse rate 84 beats/minute, and blood pressure 110/70 mmHg. Systemic examination revealed no abnormality except a tender soft tissue swelling located in the midhumerus of left side, firm in consistency, irregular in shape, and 7.5 cm × 5 cm in size with indistinct margins. Skin overlying the swelling was reddened, warm, edematous, and nodular with prominence of superficial veins but had no discharging sinus. Movements of the shoulder joints were normal. Movement of the part of the limb distal to the swelling was restricted. Biceps, triceps, and supinator jerks were absent in left side. But there was no sensory loss.
Complete hemogram and blood biochemistry including serum calcium (9.1 mg/dL) and alkaline phosphatase were normal. Chest X-ray (CXR) posteroanterior (P.A.) view showed a spiculated nodule in the left midzone with an osteolytic lesion in middle of the left humerus (). Fine needle aspiration cytology (FNAC) of the osteolytic lesion revealed sheets, clumps, and dense malignant cells having hyperchromatic, pleomorphic nuclei with inconspicuous nucleoli and squamoid differentiation at places on the hemorrhagic background. Few cells showed individual keratinization, suggestive of metastatic squamous cell carcinoma (). Contrast enhanced computed tomography (CECT) scan of thorax showed a spiculated nodule in left upper lobe with osteolytic lesion in the midhumerus on the left side (). CT-guided FNAC of the left lung nodule showed clusters of malignant epithelial cells with nuclear pleomorphism, hyperchromasia, distinct nucleoli, moderate amount of cytoplasm, and distinct cell boundary, suggestive of nonsmall cell carcinoma and squamous cell variety. (). Ultrasound of the abdomen revealed no abnormality. 99mTcRadionuclide bone scan revealed an increased uptake of radiotracer over the midhumerus on left side only, suggestive of metastatic bony lesion to left humerus (). So, the final diagnosis was squamous cell carcinoma of upper lobe of left lung with osteolytic metastasis to left humerus, that is, stage IV disease of bronchogenic carcinoma. Palliation of the symptoms was the only option. With consultation of the radiotherapy department of our institution, palliative radiotherapy (total dose: 30 Gy in 10 fractions) was given to the osteolytic lesion of the left midhumerus with an aim to relieve the pain and reduce the size of the lesion. First cycle of chemotherapy comprising of cisplatin + etoposide was given intravenously following radiotherapy. Although chemoradiotherapy was a very good option for palliation of the malignant bone pain, in our patient, size of the primary lung tumour was gradually increasing (as evidenced by serial CXRs) and pain of the osteolytic lesion of left humerus was not relieved, though the size of the lesion reduced marginally. As a whole, therapeutic benefits on primary and metastatic tumours were very poor, probably due to squamous cell histology which is a chemo- and radiotherapy resistant variant of lung cancer. On the other hand, the part of the limb distal to the metastatic lesion was totally nonfunctioning. This is why below shoulder amputation of the left upper limb was planned. Preoperative magnetic resonance imaging (MRI) of left upper extremity showed destructive and expansile osteolytic lesion in the junction of upper and midthird of the shaft of the left humerus, marrow edema, and surrounding soft tissue infiltration (). After first cycle of chemotherapy amputation of upper limb was done in the department of orthopaedics, and histopathological examination of resected specimen showed metastatic squamous cell carcinoma of the bone (). He succumbed to his illness after second cycle of chemotherapy.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [84.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Surgery in the previous 4 weeks': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 84.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 0 + 1 =  1.
The patient's Well's score for pulmonary embolism is 1."
3131,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3416741-1,Extracted,"A 43-year-old Pakistani woman presented for gynecologic surgery for an ovarian mass. Seventeen years prior, she had an emergency TV replacement with a St Jude bileaflet tilting disc prosthetic valve for bacterial endocarditis of her TV. The reasons for choosing a mechanical valve at that time are not known. Anticoagulation with warfarin without an antiplatelet agent was maintained and managed largely by our patient along with her primary care doctor. After her TV replacement she had three episodes of TV thrombosis, for which she received thrombolytics. Two of these episodes occurred during the discontinuation of warfarin and initiation of heparin or low molecular weight heparin for pregnancy, necessitating the termination of her pregnancies. Her international normalized ratio on admission was at a therapeutic level of 2.5; heparin was initiated with a goal prothrombin time of 80 seconds and warfarin discontinued for the gynecologic surgery. A preoperative echocardiogram showed a mean gradient across the TV of 5 mmHg.
Our patient underwent an exploratory laparotomy, oophorectomy, removal of an ovarian mass and a cystotomy repair. The surgery was four hours long and she had 400 cm3 of blood loss. Heparin was off for a total of 13 hours. On postoperative day one, our patient complained that she could not hear the click of her mechanical valve. She was hemodynamically stable with a heart rate of 105 beats per minute. Doppler echocardiography showed a mean TV gradient of 18 mmHg (Figure ). A transesophageal echo showed the St Jude valve to be stuck in the open position. This was confirmed by fluoroscopy (Figure and ).
Thrombolytics were not an option as she was in a recent postoperative state. She was maintained under close observation and serial echocardiograms showed that the gradients across her TV remained stable. Limited blood testing did not show any disorders in blood coagulation. Ten days after her initial surgery, when it was deemed safe to be placed on bypass, her St Jude TV was removed and a bioprosthetic valve was placed in the TV position. The explanted prosthesis showed fibrin and pannus that involved both discs (Figure ). Our patient tolerated the procedure well and went home in stable condition.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [105.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",8.5,8.5,8.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 105.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 =  6.0.
The patient not been diagnosed with pulmonary embolis (PE), but the patient has previously been diagnosed with deep vein thrombosis (DVT), we increase the current total by 1.5 so that 6.0 + 1.5 = 7.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 7.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 7.5 + 1 =  8.5.
The patient's Well's score for pulmonary embolism is 8.5."
3132,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8343428-1,Extracted,"A 57-year-old gentleman presented to a peripheral centre with sudden onset palpitations associated with dizziness and profound sweating. Two episodes of VT were documented and needed direct current (DC) cardioversion due to haemodynamic instability. After 3 h, he was referred to our emergency on intravenous (IV) amiodarone infusion at 1 mg/min (after initial loading dose of 150 mg).
He had history of Type 2 diabetes mellitus and Grave’s disease for last 10 years (on oral hypoglycaemic drugs and tablet carbimazole 10 mg thrice daily). He had no past history suggestive of cardiac illness but the family history was significant for sudden cardiac death (SCD) in two siblings at ages of 55 and 59 years. However, the patient had not undergone any work-up for familial SCD.
At presentation, he had a pulse rate of 60/min and BP of 120/84 mmHg with no other significant clinical findings. In our emergency, he had another episode of monomorphic VT (with haemodynamic compromise) that was DC cardioverted.
The 12-lead electrocardiogram (ECG) during VT showed ventricular rate of 190 beats/min with left bundle branch block pattern, left axis deviation, and QRS transition in lead V6 with notching in QRS complexes, all suggestive of right ventricle (RV) free wall origin (). This was similar in morphology to the ECGs recorded in the peripheral centre. ECG during sinus rhythm showed epsilon waves in leads V1–V3 and inferior limb leads. Leads V1–V3 also showed T-wave inversion along with terminal activation duration of 60 ms (). These findings favoured a diagnosis of arrhythmogenic right ventricular cardiomyopathy (ARVC).
His blood sugar, serum electrolytes, and thyroid profile were normal. High-sensitivity cardiac-specific troponin T (Elecsys Troponin-T-hs, Cobas®, Roche diagnostics) (hs-cTnT) was mildly raised (). Patient was reloaded with IV amiodarone 150 mg for breakthrough VT and continued the infusion at 1 mg/min for a total of 6 h followed by 0.5 mg/min for 48 h. After 24 h, the IV infusion was overlapped with oral amiodarone (200 mg tablet thrice daily for 10 days followed by 200 mg twice daily for 5 days, making a cumulative dose of 10.1 g) followed by 200 mg once daily thereafter as per recommendations. He was also started on oral carvedilol (50 mg) daily.
Echocardiography showed dilated RV and RV outflow tract (RVOT) (diameter—34.7 mm), RV fractional area change of 20.3%, and RV global strain (free wall + septum) of −14.8%. The left ventricular (LV) dimensions and function were normal. Patient met all major non-histological modified task force criteria for diagnosis of ARVC. Automated implantable cardioverter-defibrillator (AICD) for secondary prevention was planned as per European guidelines.
As part of protocol in our institute to assess COVID-19 status of all emergency patients warranting admission, reverse transcription-polymerase chain reaction (RT-PCR) assay for COVID-19 on nasopharyngeal swab was done which turned out positive with a cycle threshold (Ct) value of 25.4. His laboratory investigations showed high erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), raised neutrophil to lymphocyte ratio (NLR), interleukin 6 (IL-6), D-dimer, and B-Type natriuretic peptide (BNP) ().
We monitored his inflammatory markers, D-dimer, and NLR along with hs-cTnT twice weekly and BNP every 2 weeks. These parameters showed a surge during the first 4 weeks ( and ). Holter monitoring (for 24–72 h) and RT-PCR for COVID-19 were also done at weekly intervals. RV origin multi-morphic ventricular premature contractions (VPCs) along with couplets and non-sustained VT episodes were noted () with highest burden during the 4th week (). The RT-PCR was also persistently positive for COVID-19 till 4th week. The Ct value for first 3 weeks suggested increasing viral RNA load (Ct value is inversely proportional to the viral RNA load) followed by a decline starting from 4th week (). No QT prolonging antiviral drug like hydroxychloroquine or azithromycin was given to the patient. At the end of 4th week, the thyroid profile reassessed was within normal limits and amiodarone 200 mg once daily was continued.
From 5th week onwards, the inflammatory markers started subsiding, mirrored by a similar decrease in the levels of hs-cTnT, BNP, and 24 h VPC burden ( and ). RT-PCR for COVID-19 became negative during the 6th week (assessed twice at 48 h interval). By this time, the inflammatory markers, BNP, and hs-cTnT had also returned to normal range and the VPC burden had become insignificant ( and ). No respiratory symptoms or fever were noted during these 6 weeks.
Following this, cardiac magnetic resonance imaging (MRI) was done, which revealed grossly dilated RV [end-diastolic volume = 114.3 mL/m2 (ULN 110 mL/m2)] with global hypokinesia, reduced RV ejection fraction (20.5%), and dilated RVOT (3.6 cm). Prominent trabeculations in RV apex along with focal outpouchings in RV free wall were also noted ( and Videos 1 and 2). The RV mid-cavity free wall, inferior, and apical segment showed late gadolinium enhancement (LGE) suggestive of myocardial fibrosis. The LV basal and mid-cavity (anterior and inferior septal segments) along with mid-cavity (inferior and inferolateral segments) showed T2W hyperintensity due to myocardial oedema which colocalized with selective subepicardial LGE suggestive of myocarditis in evolution with replacement fibrosis ().
After the systemic hyperinflammatory phase had subsided and the patient became COVID negative, a single-chamber AICD was implanted (Fortify Assura™ ICD, St. Jude Medical, Minnesota, USA) at the end of 6th week. Amiodarone, carvedilol, carbimazole, and oral hypoglycaemic drugs were continued in the post-intervention phase along with broad-spectrum IV antibiotics for 72 h.
A transient surge of inflammatory markers and hs-cTnT along with the VPC burden was noted in the post-operative phase ( and ). However, the patient’s total leucocyte count and serum procalcitonin levels were normal together with sterile blood and urine cultures, ruling out any infectious aetiology. All the deranged parameters spontaneously returned to baseline within 1 week. He was discharged thereafter on tablet amiodarone 200 mg once daily, carvedilol 25 mg twice daily, and ramipril 5 mg once daily as per guidelines along with anti-thyroid and anti-diabetic drugs. At follow-up of 6 weeks, the patient is asymptomatic and euthyroid without any recurrence of symptoms or AICD interventions.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [60.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 60.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3133,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8554358-1,Extracted,"Chest pain, nausea and vomiting × 3 d.
A 25-year-old male patient with no prior medical history presented to the emergency department with chest pain, nausea and vomiting × 3 d. He described sharp, intermittent chest pain that is sub sternal, radiating to the back and left arm for last 3 d. His pain is worse upon leaning forward and worse with deep inspiration. He also had multiple episodes of nausea and vomiting with an episode of coffee-ground emesis. Patient reported long-term abuse of hydrocarbon containing inhalant (PC keyboard dust off) for the last 1 year. He used to huff 2 cans of dust off at the same time to achieve a hallucinogenic effect along with marijuana use. One week prior to admission, he reported increased use (10 cans/d).
History of intracranial aneurysm rupture in father.
The patient’s heart rate was 112 bpm, respiratory rate was 15 breaths per minute, blood pressure was 114/73 mmHg and oxygen saturation on room air was 99%. His body mass index (BMI) was 37 kg/m2. Cardiac examination revealed a regular rate and rhythm, and no jugular venous distention with mild chest wall tenderness. Erythematous, non-scaling lesions were noted on the chest wall, arm and lips. Abdominal examination revealed right upper quadrant and bilateral flank tenderness.
Initial laboratory evaluation showed leukocytosis (WBC-19.6 bil/L), acute kidney injury (Cr-3.4 mg/dL, BUN-54 mg/dL), elevated transaminases (AST-161 U/L, ALT-77 U/L), troponin-1.63 (ng/mL) peaked at 2.06 (ng/mL), CK-3000 ng/mL, CKMB-45 ng/mL. Urine drug screen was positive for cannabinoids. Initial electrocardiography (EKG) showed sinus tachycardia with diffuse inferolateral ST elevation, concerning for acute myopericarditis (Figure ).
Echocardiogram showed left ventricular (LV) ejection fraction (EF) of 40% to 45% with severe aortic root dilation (5.0 cm) and trivial pericardial effusion. Given patient’s elevated troponins, cardiac catheterization was performed. Coronary angiogram showed no evidence of coronary artery disease (Figure ). Working diagnosis of myocardial infarction with non-obstructive coronary arteries (MINOCA) was established and cardiac magnetic resonance imaging (CMR) was performed to evaluate the etiology further.
CMR showed borderline LV function with edema in the mid and apical LV suggestive of myocardial inflammation (Figure and ). No delayed enhancement was seen in the myocardium or in the pericardium (Figure and ). There was no evidence of pericardial effusion.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [112.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 112.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3134,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-4793133-1,Extracted,"A 74-year-old normotensive, nondiabetic, male smoker (30-pack years) presented with progressively increasing shortness of breath, cough, white, mucoid expectoration, and retrosternal and right sided parasternal, oppressive chest pain for last 2 months. Chest pain and shortness of breath were increased in severity on exertion and were associated with palpitation, but there is no history of sweating, orthopnoea, paroxysmal nocturnal dyspnoea, unconsciousness, and convulsion. There was no radiation of chest pain. Chest pain was suddenly increased for last five days and the patient was admitted in the emergency department with a suspicion of acute myocardial infarction (AMI). There was no history of fever, hemoptysis, leg swelling, and facial puffiness. History of significant weight loss and anorexia were present. There was no history of household contact with the patient of sputum smear positive tuberculosis. The patient received formoterol + tiotropium metered dose inhaler (2 puffs once daily with spacer) and oral doxofylline (400 mg twice daily) for last five years, as he suffered from chronic bronchitis predominant chronic obstructive pulmonary disease (COPD) which resulted in persistent breathlessness, cough, and expectoration.
General survey revealed anemia and clubbing, but there was no cyanosis, edema, and engorged neck vein. There were multiple cervical and supraclavicular enlarged lymph nodes on left side, which were hard in consistency, discrete, nontender, and fixed to underlying structure, but not fixed to overlying skin, and there was no discharging sinus. His temperature was 37°C, respiratory rate 24 breaths/minute, pulse rate 120 beats/minute, regular blood pressure 94/64 mmHg, oxygen saturation in capillary blood (SpO2) 96% @ room air, and FiO2 0.21.
Examination of respiratory system revealed no abnormality, except vesicular breath sound with prolonged expiration on both sides, bilateral crackles, mainly over the bases of the lungs, and occasional wheezes. Examination of other system was normal. Complete hemogram showed anemia with hemoglobin concentration of 7.1 g/dL. Blood biochemistry was normal. Electrocardiogram (ECG) showed atypical ST segment elevation and T wave inversion in lateral chest leads (Lead V4, Lead V5, and Lead V6). Initial rapid troponin-t-test was inconclusive, but repeat one after 12 hours of first test was negative. Sputum for acid fast bacilli and Gram stain was negative, and pyogenic culture of sputum showed no growth. Chest X-ray posteroanterior (PA view) showed cardiothoracic ratio was more than 0.5; that is, size of the cardiac silhouette was increased, but lung parenchyma was normal. Contrast enhanced computed tomography (CECT) of thorax showed a large, nonhomogenous mass lesion in right lower lobe which invaded the left atrium and was compressing the adjacent ventricular walls (). There was also mediastinal and hilar lymphadenopathy. CT-guided fine needle aspiration cytology (FNAC) showed discrete clusters of malignant epithelial cells which showed nuclear pleomorphism, hyperchromasia, high nucleocytoplasmic ratio, pale cytoplasm, and ill-defined cell boundary—suggestive of non-small-cell carcinoma, possibly squamous cell variety (). FNAC of left sided supraclavicular lymph nodes showed metastatic squamous cell carcinoma. Sputum for malignant cell was negative and fibre optic bronchoscopy did not show any abnormality. Echocardiogram showed a large echogenic mass of 15 × 12 mm, attached to the roof of the left atrium adjacent to right pulmonary venous openings, encroaching to interatrial septum, an extension of the tumour from adjacent lung parenchyma. Ejection fraction was 66%. Ultrasound of abdomen and CECT scan of brain were normal. Hence the diagnosis was a non-small-cell carcinoma of lower lobe of right lung with invasion of the left atrium and compression of adjacent ventricular wall (T4 disease) with contralateral supraclavicular metastatic lymphadenopathy (N3 disease). First cycle chemotherapy regimen comprising intravenous cisplatin (100 mg on day 1) and etoposide (100 mg on days 1, 2, and 3) was given, but unfortunately he died just after completion of first cycle.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Immobilization for at least 3 days': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 120.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
3135,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5809623-1,Extracted,"A 24-year-old primigravida woman presented to the obstetric emergency department at 35 weeks of gestation complaining of bilateral vision loss. There was nothing abnormal with her previous medical history and she had no history of previous ophthalmologic disorders. The patient reported a mild headache that has been going on for the past 2 days.
Clinical examination showed an important peripheral edema. Vital signs were as follows: pulse rate 105 beats/min, blood pressure 186/115 mmHg, respiratory rate 20 breaths/min, temperature 36.9 °C, and oxygen saturation 98% on air. Visual acuity in the two eyes was finger-counting at less than 1 m. Her pupils were equal and reactive to light. Neurologic examination showed exaggerated deep tendon reflexes.
Proteinuria dipstick was 3+. Laboratory tests revealed anemia at 103 g/L, thrombocytopenia with platelets count at 97 × 109/L and elevated liver enzymes (GOT 82 U/I, GPT 78 U/I, alkaline phosphatase 168 U/I). The remaining laboratory tests, including electrolytes, creatinine, bilirubin, and coagulation tests, were within normal limits.
A bedside ultrasound was performed by an anesthesiologist trained in bedside focused ultrasonography using a 7.5-MHz linear probe (mindray DC 70 Shenzhen, China). Sagittal and transverse planes of the right and left globe were obtained by asking the patient to close her eyelids and then applying ultrasound gel to the inside and outside of a sterile sheath covering the probe as it was gently placed on each eyelid. To measure the optic nerve sheath diameter (ONSD), the placement of the probe was adjusted to view the entry of the optic nerve into the globe. We used an electronic caliper and an axis perpendicular to the optic nerve 3 mm behind the lamina cribosa. The Mechanical Index and Thermal Index were reduced to 0.2 and 1, respectively.
Sonographies detected in the right and left eye a hyper-echoic stripe extending to the optic nerve head, but not across it. The point of fixation of the retina at the optic nerve head was respected. When the patient was also asked to look in various directions with her eyelids closed, the hyper-echoic line undulated with the associated ocular movements, which was suggestive of retinal detachment (RD). The ONSD was measured at 6.9 mm in the right eye (Fig. a) and 6.6 mm in the left eye (Fig. b), suggesting an elevated intracranial pressure. The patient tolerated the sonogram without pain or complications.
Obstetric ultrasound revealed an intra-uterine fetus with a heart rate of 140 beats/min and a fetal biometry consistent with a 34-week gestation.
Based on these findings, the patient was diagnosed with severe preeclampsia complicated by hemolysis, elevated liver enzymes and low platelets (HELLP) syndrome, bilateral RD and cerebral edema. Therefore, the patient underwent an urgent cesarean section delivery under spinal anesthesia and was immediately administrated an intravenous Magnesium Sulfate and Nicardipine infusion which were maintained 24 h after delivery. Blood pressure was then controlled with Methyldopa 500 mg 6 hourly and Amlodipine 10 mg 12 hourly.
Magnetic resonance imaging (MRI) performed 24 h after delivery showed T2 hyperintensities on flair indicating parieto-occipital and temporal distribution of vasogenic edema. A dilated fundoscopic examination using an ophthalmoscope performed by an ophthalmologist subsequently confirmed the diagnosis of bilateral exudative retinal detachments.
During 1 week, a daily ocular sonogram was performed. The ONSD was back to a normal range after arterial blood pressure control. The RD regressed but it was difficult to objectify it.
Within 3 weeks of delivery, her visual acuity had returned to normal without any further treatment. At that time, the slit lamp examination was normal.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [105.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 105.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient did not have an immobilization for at least 3 days but the patient had a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3136,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-5225336-1,Extracted,"A 66-year-old male who was a long standing inmate in a forensic psychiatric hospital presented to the Emergency Department with a complaint of abdominal distention. The patient denied any nausea or vomiting but reported a decreased appetite which he attributed to abdominal discomfort. His last bowel movement was five days ago. The patient also endorsed dysuria. A computerized tomography (CT) scan of the abdomen and pelvis was performed prior to ED arrival and the images were brought with patient.
The patient had a past medical history notable for paranoid schizophrenia, bipolar disorder, latent tuberculosis, and ascending aortic aneurysm. There was no known history of liver disease. The patient's medications included clozapine, fluphenazine, lithium, paroxetine, lorazepam, and haloperidol. He had no known drug allergies and had no recent medication changes. Complete review of systems was otherwise negative. The patient had no history of previous surgeries, did not smoke, drink, or consume illicit drugs, and had a noncontributory family history.
On initial presentation to the ED his vital signs were heart rate (HR), 104; blood pressure (BP), 147/101; respiratory rate (RR), 22; pulse oximetry, 93% on room air; and temperature, 36.4 degrees Celsius.
On examination of the patient, his oral mucosa was noticeably dry. His cardiac exam was unremarkable with normal S1 and S2, no murmurs, rubs, or gallops, and 2+ pulses in all four extremities and his lungs were clear to auscultation bilaterally. The patient's abdomen was firm and grossly distended and was noted to resemble a full-term pregnant patient. Dilated superficial veins were noted on the abdomen and palpation revealed mild, diffuse tenderness without rebound or guarding. The patient was awake, alert, and orientated to time, date, and environment.
Labwork was notable for sodium of 115 mmol/L and a serum osmolality of 251 mOsm/kg. The potassium level was 5.2 mmol/L, chloride 80 mmol/L, bicarbonate 21 mmol/L, creatinine 1.58 mg/dL, lactic acid 1.5 mmol/L, troponin T < 0.01 ng/mL, and lithium level 1.0 mmol/L. The patient was mildly anemic with a hemoglobin of 11.5 g/dL, while his remaining complete blood count (CBC) was unremarkable with a white blood cell (WBC) count of 9.44/L and platelets of 318/L. An electrocardiogram was obtained during the ED evaluation () which showed a sinus tachycardia of 105 beats per minute, QRS 98s, QTc 415 ms, and peaked T waves in the precordial leads.
Upon review of the CT, large dilated loops of colon were noted up to 12 cm (Figures and ).
During the ED course, the acute care surgical service was consulted for further management. A rectal exam was performed by the resident physician with a plan for disimpaction immediately following. The patient was positioned on his left side. Soft stool was found on rectal exam. During the rectal examination, the nurse in the room noted that the patient was apneic and a code was called. The patient was unresponsive for less than one minute prior to the nurse noticing his status change. The patient had no new complaints prior to his arrest.
Unfortunately, the patient was not on a cardiac monitor at this time. Upon immediately placing the patient on a monitor, a bradycardic rate was noted. Following a pulse check, the patient was then found to be in pulseless electrical activity. Cardiopulmonary resuscitation (CPR) was started and advanced cardiac life support (ACLS) protocol was followed including intubation. Initial bedside ultrasound showed no cardiac activity. Following multiple rounds of CPR and ACLS medications, return of spontaneous circulation (ROSC) was obtained. The patient then again went into PEA with a bradycardic rhythm but ROSC was again obtained and remained. A postarrest arterial blood gas was notable for pH 6.84, pCO2 100 mmHg, and pO2 94.5 mmHg. The patient was then admitted to Intensive Care Unit (ICU) on epinephrine, norepinephrine, and vasopressin infusions. At time of ICU admission the patient was in a normal sinus rhythm of 98. Eight days later the patient expired following confirmation of anoxic brain injury and a decision made to provide comfort care.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [104.0, 'beats per minute'], 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 104.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 1.5 + 1.5 = 3.0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.0.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3137,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7772108-1,Extracted,"An 81-year-old man, who was an ex-smoker, presented to our emergency department with acute onset of shortness of breath, non-productive cough, and swelling of bilateral lower extremities. His past medical history was significant for chronic obstructive pulmonary disease and hypertension. He used an albuterol metered-dose inhaler prior to the presentation but his symptoms did not improve. On initial evaluation, the patient had a heart rate of 179 beats per minute (bpm), blood pressure of 172/118 mmHg without pulsus paradoxus, and a respiratory rate of 26 per minute. He had good mental status and was speaking full sentences. There was no jugular venous distention. His lung exam was normal. A heart exam revealed tachycardia without murmur. He had mild bilateral pitting edema of both legs without signs of infection or inflammation. His blood test was unremarkable. Initial ECG (electrocardiogram) showed atrial flutter characterized by a rapid ventricular rate and 2:1 atrioventricular block as demonstrated in Figure .
We administered a 20 mg bolus of diltiazem to the patient intravenously and his heart rate decreased to 90 bpm. Point-of-care ultrasound (POCUS) showed a large pericardial effusion without ultrasonographic signs of tamponade or signs of pulmonary edema. Computed tomography (CT) of the chest illustrated the large pericardial effusion and led to the discovery of a new mass in the upper left lung, consistent with a lung tumor (Figure ). Several hours later, while awaiting admission, he became tachypneic and was intubated due to impending acute respiratory failure, despite negative tamponade physiology on previous imaging. The interventional radiologist performed pericardial drainage. Cytology from the pericardial effusion revealed squamous cell carcinoma. The patient was diagnosed with malignant pericardial effusion caused by advanced-stage squamous cell lung cancer. Unfortunately, his hospital course was complicated by septic shock, and eventually, death.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [179.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2.5,2.5,2.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 179.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 1.5 + 1 =  2.5.
The patient's Well's score for pulmonary embolism is 2.5."
3138,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-3226617-1,Extracted,"Over the last year, a 40-year-old man had complained of weekly episodes of facial flushing, diaphoresis, irritability,and diarrhea, which were triggered by emotional stress or exercise. He also presented with chest discomfort and had lost 6 kg. He had poorly controlled essential hypertension that had lasted over the last six years. On examination, his systolic blood pressure was 160 mm Hg, his diastolic blood pressure was 110 mm Hg, his heart rate was 110 beats/min, and his body mass index was 32 kg/m2; he did not present with postural hypotension. A small goiter without nodules and a slight lid retraction were noted. He had no facial flushing or hand tremor. During the chest discomfort investigation, the chest X-ray revealed an anterior mediastinal enlargement.
A thoracic computed tomography (CT) scan revealed a homogeneous mass with no adjacent structure invasion or calcification at the topography of the thymus enlargement (). Goiter was also detected but did not extend to the intrathoracic compartment. A carcinoid syndrome caused by a primary neuroendocrine tumor was suspected.
The patient´s exams depicted normal values of urinary 5-hydroxyindoleacetic acid (2.8 and 3.1 mg/24 h, normal values-NV 2-6), urinary metanephrines (1.0 and 0.09 mcg/mg creatinine, NV <1.2), serum calcitonin (7.3 pg/mL, NV <11.5), negative tumoral markers β-hCG and alpha-fetoprotein. Thyrotoxicosis was diagnosed from the following fluoroimmunoassay measurements: total T3, 371 ng/dL (NV 40–180 ng/dL); total T4, 20.9 mcg/dL (NV 4.5–12 mcg/dL); free T4, 4.9 ng/dL (NV 0.7–1.5 ng/dL); and a suppressed TSH<0.03 mUI/L (NV 0.4–4.5 mUI/L). Serum antiperoxidase and antithyroglobulin antibodies measured by fluoroimmunoassay were positive (859 and 72 U/mL, NV<35 U/mL), with levels of TSH-receptor antibody (TRab) of 49% (radioimmunometric assay NV<8%). Ultrasound thyroid imaging revealed a 43.2 g homogeneous hypoechogenic goiter, which did not have nodules and was limited to the neck.
Therefore, Graves' disease was diagnosed, and a thymus growth was then attributed to hyperplasia caused by Graves' disease.
Methimazol (20 mg/day) was initiated, and after four months of treatment, symptoms had improved, and thyroid hormones had normalized. Goiter and TRab values had reduced. After six months of thyroid hormonal control, a new CT revealed marked thymus shrinkage ().
After 24 months, the patient was in remission of Graveś disease, with negative TRab values and a normal thoracic CT scan. Graveś ophthalmopathy was never presented.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Previously documented Deep Vein Thrombosis': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 110.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3139,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-9122,Extracted,"A 61-year-old man presents to the urgent care clinic complaining of cough and unintentional weight loss over the past 3 months. He works as a computer engineer, and he informs you that he has been having to meet several deadlines recently and has been under significant stress. His medical history is significant for gout, hypertension, hypercholesterolemia, diabetes mellitus type 2, and pulmonary histoplasmosis 10 years ago. He currently smokes 2 packs of cigarettes/day, drinks a 6-pack of beer/day, and he endorses a past history of cocaine use back in the early 2000s but currently denies any drug use. The vital signs include: temperature 36.7°C (98.0°F), blood pressure 126/74 mm Hg, heart rate 87/min, and respiratory rate 18/min. His physical examination shows minimal bibasilar rales, but otherwise clear lungs on auscultation, grade 2/6 holosystolic murmur, and a benign abdominal physical examination. However, on routine lab testing, you notice that his sodium is 127 mEq/L. His chest X-ray is shown in the picture.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [87.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': False, 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': False, 'Malignancy with treatment within 6 months or palliative': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are repoted to be absent and so the total score remains unchanged, keeping the total score at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 87.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3140,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,usmle-4760,Extracted,"A 46-year-old woman presents to the emergency department with 1 day of painful leg swelling. She is otherwise healthy and takes only oral contraceptive pills. The patient does not regularly follow up with her primary doctor and is generally not medically compliant. Her temperature is 98.0°F (36.7°C), blood pressure is 122/78 mm Hg, pulse is 70/min, respirations are 13/min, and oxygen saturation is 99% on room air. Lower extremity examination shows mild calf swelling on her left leg, but otherwise is unremarkable. An ultrasound is performed as seen in Figure A.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [70.0, 'beats per minute'], 'Immobilization for at least 3 days': False, 'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 70.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 3.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 3.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 3.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.
The patient's Well's score for pulmonary embolism is 3."
3141,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7676801-1,Extracted,"A 56-year-old male with history of multiple myeloma status post-bone marrow transplant on suppressive therapy, hypertension, and peripheral neuropathy presented to the emergency department (ED) after a syncopal episode, where he was found in the bathtub by his family with his eyes rolled back. Upon initial examination, the patient complained of mild chest pain. Upon arrival to the ED, the patient was found to be tachycardic with a pulse of 108 beats per minute, tachypneic with 24 breaths per minute, a blood pressure of 95/68 millimeters mercury, and oxygen saturation of 100% on room air. An electrocardiogram (ECG) demonstrated ST elevations in V1 through V3 with reciprocal changes in the inferior leads ().
High-sensitivity troponins were obtained and were elevated to 0.20 nanograms (ng) per milliliter (mL) (reference range: normal <0.04 ng/mL). The patient was taken to the cardiac catheterization laboratory where he underwent percutaneous coronary intervention (PCI), which did not reveal severe coronary artery disease () but did show hyperdynamic left ventricle with an ejection fraction >70% on ventriculography, tachycardia, and low left ventricular end-diastolic pressure indicating low filling pressures with suspicion for reduced preload. This was concerning for hypovolemia or pulmonary embolus.
Computed tomography angiography (CTA) of the chest was obtained showing submassive PE as well as right ventricular strain with a right ventricle to left ventricle ratio of 1.2 suggestive of cor pulmonale ().
It was later reported after cardiac catheterization that the patient had had increased bilateral leg swelling and discomfort as well as dyspnea on exertion for several weeks preceding his presentation to the ED, which he attributed to his neuropathy following chemotherapy. The patient was started on a continuous heparin infusion, and repeat ECG demonstrated resolution of anterior ischemic changes. Venous duplex ultrasound of the bilateral lower extremities was obtained on hospital day two and demonstrated a partially occlusive venous thrombus in the left popliteal, peroneal, and posterior tibial veins. The patient underwent catheter-assisted thrombolysis on hospital day three. He was started on apixaban 10 milligrams (mg) twice daily for the first week, followed by 5 mg twice daily, and discharged home in stable condition.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [108.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'Immobilization for at least 3 days': True, 'Surgery in the previous 4 weeks': True, 'Clinical signs and symptoms of Deep Vein Thrombosis': True, 'Malignancy with treatment within 6 months or palliative': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Previously Documented Pulmonary Embolism': False}",8.5,8.5,8.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are reported to be present and so three points are added to the score, making the current total 0 + 3 = 3. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 3.
The patient's heart rate is 108.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 3 + 1.5 = 4.5.
Because the patient has had an immobilization for at least 3 days and the patient had a surgery in the past 4 weeks, the score increases to 4.5 + 1.5 =  6.0.
The patient not been diagnosed with pulmonary embolis (PE), but the patient has previously been diagnosed with deep vein thrombosis (DVT), we increase the current total by 1.5 so that 6.0 + 1.5 = 7.5.
Hemoptysis is not reported in the patient note and so we assume that it is missing from the patient, keeping the total score at 7.5.
Malignany with treatment within 6 months or palliative is reported to be present and so one point is added to the score, making the total score 7.5 + 1 =  8.5.
The patient's Well's score for pulmonary embolism is 8.5."
3142,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7593723-1,Extracted,"A 55-year-old male without prior medical history presented to the emergency department (ED) with dry cough, sore throat, mouth sores, and myalgias for a week. He was afebrile with stable vitals. Physical examination revealed vesicular lesions on the buccal mucosa and the sublingual area, with posterior pharyngeal erythema, but no edema or midline shift. The lungs were clear. He worked as a taxi driver but denied obvious sick contacts. Chest X-ray (CXR) revealed increased vascular markings, especially at the left base (). 12 lead ECG showed sinus rhythm with normal axis, right bundle branch block, and inverted anterior T waves without other changes. Nasal swabs for coronavirus and influenza were obtained, and he was discharged home with instructions for self-quarantine for 14 days. Nasopharyngeal swab turned positive for SARS-CoV-2 on RT-PCR assay in two days.
The patient returned to the ED a week later, with worsening shortness of breath over 24 hours. He was afebrile, with a blood pressure of 143/80 mmHg and a resting heart rate of 88 beats per minute, respiratory rate of 38 per minute, and with oxygen saturation of 88% on 4 liters by nasal cannula. CXR revealed bilateral patchy infiltrates consistent with multifocal pneumonia, right greater than left lung field, and he was intubated with the diagnosis of COVID-19 pneumonia (). Laboratory data revealed an unremarkable complete blood count and basic metabolic panel, AST, and ALT of 216 U/L and 159 U/L, respectively. He was stabilized on assist control (AC) ventilation with tidal volume (TV) of 400 mL, positive end expiratory pressure (PEEP) of 12 mmHg, and FiO2 of 40%. On these settings, his arterial PaO2 was 99%. He was maintained on midazolam drip for sedation. Azithromycin 250 mg once daily and hydroxychloroquine 200 mg Q12 hours were started.
The next day, he became febrile to 102F, and broad-spectrum antibiotics were added to cover for possible bacterial superinfection. Laboratory values were notable for leukocytosis of 14000/μL, creatinine of 1.8 mg/dL, ferritin of 1181 ng/mL, CRP of 163 mg/L, ESR of 90 mm/hr, fibrinogen of 736 mg/dL, and D-dimer of 2.74 μg/mLFEU. His LFTs and ventilator requirements remained stable on hospital day 2.
On hospital day 3, he became progressively hypotensive, tachycardiac, and hypoxic. He quickly escalated to requiring maximum doses of norepinephrine, epinephrine, vasopressin, and phenylephrine. Despite increased ventilator support with FiO2 of 100%, PEEP of 14 mmHg, and TV 500 mL, his arterial blood gas (ABG) was notable for a pH of 6.86, pCO2 of 84 mmHg, PaO2 of 63%, and bicarbonate of 17 mg/dL. His peak inspiratory airway pressure was 25 cmH2O and plateau pressure of 24 cmH2O. Laboratory data showed worsening leukocytosis to 22,000/μL, creatinine of 3.1 mg/dL, AST of >7000 U/L, ALT 4828 U/L, troponin T < 0.01, CKMB 25.3 ng/mL, NT-pro-BNP of 8244 pg/dL, CRP of 31.6 mg/dL, ferritin 47,646 ng/mL, and D-dimer of >20 μg/mL/FEU (). Repeat CXR showed persistent bilateral patchy opacities (). Bedside 12 lead ECG revealed evidence of RV strain (). Bedside echocardiogram revealed severe right ventricular dilation, moderate tricuspid regurgitation, and severely reduced right ventricular function with global hypokinesis ventricle apical sparing, a.k.a. McConnell's sign (94% specificity for the diagnosis of APE) [] (Movie ). Given hemodynamic instability, a decision was made to proceed directly with systemic thrombolytic therapy in the form of tissue plasminogen activator (alteplase) (TPA) 100 mls at 50 mL/hr. He was then initiated on a heparin infusion as per standard DVT/PE protocol. Over the next day, there was a steady improvement in his hemodynamics. He unfortunately suffered acute oliguric kidney injury and required CVVHD.
By day 5, the patient was weaned off vasopressors. By day 10, he was extubated to nasal cannula. By day 14, at the time of submission, he was discharged to acute rehabilitation facility on room air and apixaban 2.5 mg twice daily given hemodialysis requirement. Repeat CXR and ECG are shown in Figures and , respectively.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False, 'Surgery in the previous 4 weeks': False, 'Previously Documented Pulmonary Embolism': True, 'Pulmonary Embolism is #1 diagnosis OR equally likely': True, 'Malignancy with treatment within 6 months or palliative': False, 'Immobilization for at least 3 days': True, 'Heart Rate or Pulse': [88.0, 'beats per minute']}",3,3,3,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 88.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has had an immobilization for at least 3 days but the patient did not have a surgery in the past 4 weeks, the score increases to 0 + 1.5 = 1.5.
Because the patient has been previously diagnosed for pulmonary embolism (PE), but the patient has never been diagnosed for deep vein thrombosis (DVT), we increase the current total by 1.5 so that 1.5 + 1.5 = 3.0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 3.0.
The patient's Well's score for pulmonary embolism is 3.0."
3143,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7802725-1,Extracted,"A 79-year-old woman with a medical history of hypertension and mild Alzheimer’s dementia presented with acute onset loss of consciousness in the community. She was a passenger in a car and found to be unresponsive, with a family member reporting absence of a palpable pulse. She was presumed to have had a cardiac arrest and received 2 min of cardiopulmonary resuscitation in the community before the return of spontaneous circulation was noted. Paramedics arrived, and she was transported to a regional secondary hospital, triaged as a cardiac arrest. She was unresponsive with a Glasgow Coma Scale (GCS) of 3 and intubated on arrival. On arrival, she was in sinus rhythm with a heart rate of 84 beats/min. Her blood pressure was 140/110 mm Hg. The blood glucose reading was 6.7 mmol/L. Her neurological deficits were difficult to determine as she was unresponsive, but there was no obvious focal neurology. On examination, her lung fields were clear and she had dual heart sounds. There was no evidence of an infective aetiology on further history and examination. She was transferred to a tertiary hospital on the same day for further work-up in light of her ongoing reduced level of consciousness. The patient was extubated 24 hours later, with her GCS improving to 13–14 over the next day.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Hemoptysis': False, 'Surgery in the previous 4 weeks': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Malignancy with treatment within 6 months or palliative': False, 'Immobilization for at least 3 days': False, 'Heart Rate or Pulse': [84.0, 'beats per minute'], 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 84.0 beats per minute. The heart rate is less than 100 bpm, and so the score remains unchanged, keeping the total score at 0.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 0.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 0.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 0.
The patient's Well's score for pulmonary embolism is 0."
3144,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-8523197-1,Extracted,"The patient reported in our case is a 36-years-old, tall and thin (height: 185.5 cm, weight: 70.3 kg, BMI: 20.4) male without a significant past medical history. Social history revealed a 30 pack-year cigarette smoking, the patient quit smoking five years before the presentation.
The patient reported left-sided back pain for three days. He went the next day after the pain started to a chiropractor and underwent spinal manipulation of his back to relieve his back pain. He described a significant improvement in his back pain after that. However, he suddenly developed shortness of breath at rest and left-sided chest pain a day later, and he presented to the emergency department for evaluation.
At presentation, the patient was afebrile, tachycardic with a heart rate of 105, normotensive with normal oxygen saturation (96% on room air). Chest x-ray showed a moderate left-sided hydropneumothorax (Figure ).
Chest CT scan with contrast was then done and showed moderate left-sided hydropneumothorax with moderate pneumothorax component and moderate pleural fluid component (Figure ). It also showed mild right-sided apical paraseptal blebs (Figure ).
After that, a left-sided chest tube was inserted with immediate drainage of 700 cc of bloody output. It was then placed on negative 20 mmHg suction. A chest x-ray confirmed a good chest tube placement with decreased left hydropneumothorax (Figure ).
The patient was then monitored with daily chest x-rays. Chest CT angiogram was performed on hospitalization day two that was negative for vascular aneurysms, dissection, or extravasation. It also showed significant improvement in left-sided hydropneumothorax with a small residual pneumothorax and significantly decreased residual pleural fluid (Figure ).
On day two of hospitalization, chest tube drainage of 300 cc of the bloody component was noted. No further drainage on hospital day three. Therefore, the chest tube was clamped and then removed.
A morning chest x-ray on hospital day four showed a new small left apical pneumothorax, this was treated with high flow oxygen therapy (Figure ).
On the day of discharge, the patient was feeling well and denied any more shortness of breath or chest pain. The last chest x-ray on the day of discharge showed stable left-sided pleural effusion and trace left-sided pneumothorax (Figure ).
Four days after discharge from the hospital, the patient followed with his primary care physician, who repeated a chest x-ray, and this showed only a persistent small left pleural effusion with no more left-sided pneumothorax (Figure ).",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False, 'Surgery in the previous 4 weeks': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Malignancy with treatment within 6 months or palliative': False, 'Immobilization for at least 3 days': False, 'Heart Rate or Pulse': [105.0, 'beats per minute'], 'Previously Documented Pulmonary Embolism': False}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 105.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3145,8,Wells' Criteria for Pulmonary Embolism,risk,decimal,pmc-7543135-5,Extracted,"A 34-year-old Caucasian female waitress at a local restaurant presented with
complaints of worsening dyspnea, productive cough with yellow phlegm, nausea,
vomiting, generalized weakness, and diarrhea for 2 weeks duration. She was
prescribed azithromycin 10 days prior to this presentation without any improvement
in her symptoms. She denied any sick contacts or travel abroad. She is a current
cigarette smoker and also started vaping CBD/THC oil a year ago. She admits vaping
CBD/THC oil bought from a local dispensary 2 days prior to her symptom initiation.
On physical examination, the patient was in respiratory distress with vital signs of
temperature 100.8 °F, HR 136 beats per minute, BP 123/88 mm Hg, RR 22 breaths per
minute, and oxygen saturation of 88% on room air. Physical examination was
significant for decreased breath sounds throughout the lung fields. Laboratory
workup was significant for leukocytosis, elevated ESR, CRP, and urine drug screen
was positive for cannabinoids/THC (). Extensive infectious workup
including sputum studies urine and serum studies were negative (). CXR showed
bilateral interstitial infiltrates and CTA of the chest with and without contrast
confirmed bilateral upper lobe ground glass patchy infiltrates (). She was diagnosed with acute
hypoxic respiratory failure likely from VALI secondary to vaping CBD/THC oil. The
patient was started on IV methylprednisolone 60 mg daily and then transitioned to
oral prednisone 40 mg daily. A repeat CT chest with contrast 6 days after steroid
initiation showed interval improvement of patchy bilateral infiltrates with a small
residual superior segment of right lower lobe ground glass opacity (). She was
discharged home with a tapering course of steroids for a total to 2 weeks.",What is the patient's score of Wells' criteria for Pulmonary Embolism? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False, 'Surgery in the previous 4 weeks': False, 'Previously Documented Pulmonary Embolism': False, 'Pulmonary Embolism is #1 diagnosis OR equally likely': False, 'Malignancy with treatment within 6 months or palliative': False, 'Immobilization for at least 3 days': False, 'Heart Rate or Pulse': [136.0, 'beats per minute']}",1.5,1.5,1.5,"
The criteria for the Wells' Criteria for Pulmonary Embolism score are listed below:

1. Clinical signs and symptoms of DVT: No = 0 points, Yes = +3 points
2. PE is #1 diagnosis OR equally likely: No = 0 points, Yes = +3 points
3. Heart rate > 100: No = 0 points, Yes = +1.5 points
4. Immobilization at least 3 days OR surgery in the previous 4 weeks: No = 0 points, Yes = +1.5 points
5. Previous, objectively diagnosed PE or DVT: No = 0 points, Yes = +1.5 points
6. Hemoptysis: No = 0 points, Yes = +1 point
7. Malignancy with treatment within 6 months or palliative: No = 0 points, Yes = +1 point

The total score is calculated by summing the points for each criterion.
   
The Well's score for pulmonary embolism is currently 0.
Clinical signs and symptoms of DVT are not reported and so we assume that this is missing from the patient, keeping the current total at 0. Whether Pulmonary Embolism is the #1 diagonsis or is equally likely to being the #1 diagnosis is not reported and so we assume this statement is false, keeping the total unchanged at 0.
The patient's heart rate is 136.0 beats per minute. The heart rate is more than 100 bpm, and so the score is increased by 1.5, making the total score, 0 + 1.5 = 1.5.
Because the patient has not had an immobilization for at least 3 days, and the patient did not have a surgery in the past 4 weeks, the score remains at 1.5.
Because the patient has no previous diagnosis of pulmonary embolism (PE) or deep vein thrombosis (DVT), the score remains at 1.5.
Hemoptysis is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
Malignany with treatment within 6 months or palliative is reported to be absent and so the total score remains unchanged, keeping the total score at 1.5.
The patient's Well's score for pulmonary embolism is 1.5."
3146,9,MDRD GFR Equation,lab test,decimal,pmc-7654560-1,Extracted,"A 49-year-old male patient without any significant past medical history presented to our hospital with problems of not voiding his bladder and back pain. The patient reported his back pain began four days ago when he was at work and tried to lift a 100 lb instrument. The patient went to see a chiropractor, but there was no improvement with his back pain. He then started to experience left thigh and buttock pain along with the back pain for which he took eight ibuprofen tablets a day (1600 mg) for four days before presenting to the hospital. He denies taking ibuprofen for any other pain that he experienced in the past.
While in the emergency room, the initial labs revealed creatinine of 32mg/dL, BUN of 175mg/dL, Na of 128 mEq/L, K of 4.5mmol/L, Cl of 90mEq/L, Co2 of 17.0mEq/L, anion gap of 21, Ca of 7.9mEq/L, and a total creatine kinase of 1315 micromoles/L. His liver function tests (LFTs) were also elevated - serum aspartate aminotransferase (AST) was 104 units, and alanine aminotransferase (ALT) was 281 units. His urinalysis showed 3+ blood and 2+ protein but 0-5 red blood cells. Left lower extremity Doppler ultrasound was negative for deep vein thrombosis (DVT). CT scan of the abdomen was unremarkable. There was fatty infiltration of the liver and thickening of the bladder wall, and diffuse soft tissue edema involving the left hip. The patient was given ondansetron hydrochloride (Zofran® Injection) 4 mg intravenously (IV) Q6H PRN for nausea, oxycodone hydrochloride (Roxicodone®) 5 mg PO Q4H PRN for pain, morphine sulfate 2 mg IV Q2H PRN for severe back pain, hydralazine hydrochloride (Apresoline® Injection) 10 mg IV Q4H PRN for hypertension, ceftriaxone sodium 1 gm/ (sodium chloride) 100 mls at 200 mls/hr IV Q24H at 1900 SCH for cystitis, and sodium bicarbonate 150 meq/ (dextrose) 1,150 mls at 150 mls/hr IV, Q7H40M SCH. Acute kidney injury and metabolic acidosis was the impression on evaluation in the ED.
Later the patient was moved to the telemetry unit to be followed up with the hospitalist. The patient was monitored by an internist, and a nephrology consultation was requested. On the following day, during the nephrology consultation, the patient's laboratory values were as shown in Tables -. The patient's vitals are mentioned in Table . CT scan and renal ultrasound of the kidneys were ordered. CT scan of the abdomen was unremarkable. The nephrologist's recommendation was to continue the patient on the IV fluids with bicarbonate and avoid nephrotoxins. The nephrologist closely monitored the patient, and the plan was to place the patient on temporary dialysis if the kidney function doesn't show improvement.
On a subsequent day on follow up with the internist, the kidney function tests were not improving; upon discussion with the nephrologist, a temporary dialysis catheter order was placed. On the same day, an interventional radiologist placed a right internal jugular vein (IJV) temporary dialysis catheter, and the patient went for the first round of hemodialysis treatment, after which the creatinine level went down to 18 mg/dl. Urinalysis was positive for protein and red blood cells, and the labs of creatine phosphokinase (CPK) 1315 micromoles/L pointed towards rhabdomyolysis. The next day during the nephrology consultation, it was recommended to go for the second round of hemodialysis. The patient's lab showed phosphorus of 11.60 mg/dL, leading to sevelamer 800 mg PO TID initiation. The patient underwent another four rounds of hemodialysis, and the kidney function tests showed a creatinine level of 11.92 mg/dL.
The patient subsequently went through hemodialysis for the seventh time, but his kidney function had not yet returned to the normal level. The nephrologist ordered a tunneled dialysis catheter to be placed on the patient to be able to receive outpatient dialysis once he is discharged, which was also placed by an interventional radiologist. His labs were checked again, and the results showed that his CPK, hyponatremia, and hyperkalemia were resolving to normal, but the creatinine stayed stable at a high level of 10.6 mg/dL. Due to the lack of improvement in the kidney function tests towards normal range, the nephrologist ordered a renal biopsy. A day later, a kidney biopsy was done (Figure ), which showed acute interstitial nephritis with very minimal chronicity, and the patient was started on prednisone 60 mg once a day. Because of the lack of improvement on the kidney function test to normal levels, the patient was declared to have end-stage renal disease and was discharged with the outpatient dialysis treatment program and to follow up with the nephrologist.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [49, 'years'], 'creatinine': [10.6, 'mg/dL'], 'sex': 'Male'}",5.20865,4.94822,5.46908,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 49 years old. The concentration of Creatinine is 10.6 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 10.6^(-1.154) * 49^(-0.203) * 1 * 1=5.20865.
Hence, the patient's GFR is 5.20865 mL/min/1.73m²."
3147,9,MDRD GFR Equation,lab test,decimal,pmc-5541172-1,Extracted,"A 71-year-old lady presented with an abnormal ECG finding during a scheduled primary care appointment. She was asymptomic and had a history of type 2 diabetes mellitus, essential hypertension, and dyslipidemia. During the consultation, the ECG reading showed premature ventricular contraction at a 1:1 ratio (ventricular bigeminy) with a heart rate of 46/min (). Her ECG from the previous year () showed non-specific changes, possibly related to early left ventricular hypertrophy. The recorded vital signs were as follows: blood pressure, 159/74 mm Hg; heart rate, 62/min; and respiratory rate, 18 breaths/min. On physical examination, heart murmurs were not audible and other findings were unremarkable. The laboratory findings were: glycated hemoglobin, 7.1%; urea, 10.0 mg/dL; creatinine 1.0 mg/dL; Na+, 137 mEq/L; and K+, 3.6 mEq/L. In order to rule out secondary causes that could have led to the changes in the ECG, various blood investigations were ordered. An urgent appointment was scheduled a week later to review these results. The patient was also advised to seek urgent medical attention if she felt palpitations or giddiness. During the second consultation, a week later, the repeat ECG showed atrial flutter with a 3:1 atrioventricular block (). All the results of the blood investigations were normal (thyroid stimulating hormone, 4.26 µIU/mL; Na+, 135 mEq/L; K+, 4.4 mEq/L; corrected Ca2+, 8.9 mg/dL; PO4-, 0.32 mg/dL; hemoglobin, 12.9 g/dL; and white blood cell count, 7.4×103/µL), except for an elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels (88 mm/h and 9.8 mg/L).
Urgent transthoracic echocardiography revealed a dilated left atrium and ventricle without any myocardial hypokinetic changes. A large echogenic mass measuring 3.1×4.1 cm was identified at the left atrium (). The mass was solid and appeared pedunculated, arising from a stalk at the endocardium. The patient had a left ventricular ejection fraction of 54%. The patient was immediately referred to a tertiary care cardiology clinic where a second transthoracic echocardiography was performed. An imaging diagnosis of left atrial myxoma was confirmed. The tumor measured approximately 2.9×3.1 cm. A paroxysmal atrial fibrillation pattern was observed on the ECG. Warfarin treatment was initiated while aiming for a target international normalized ratio between 2 and 3. Currently, the patient is jointly cared for by the primary care physician and a multidisciplinary team that is helping to manage the anticoagulation therapy. The patient is unwilling to undergo surgery to remove the tumor.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [71, 'years'], 'creatinine': [1.0, 'mg/dL'], 'sex': 'Female'}",54.65583,51.92304,57.38862,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 71 years old. The concentration of Creatinine is 1.0 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.0^(-1.154) * 71^(-0.203) * 1 * 0.742=54.65583.
Hence, the patient's GFR is 54.65583 mL/min/1.73m²."
3148,9,MDRD GFR Equation,lab test,decimal,pmc-4891606-1,Extracted,"A 73-year-old woman, with a past medical history of hypertension, diabetes mellitus for 40 years, and chronic kidney disease stage 5, because of diabetic nephropathy, presented to the emergency department with dyspnea (NYHA IV). The patient had the following vital signs: blood pressure: 155/63 mmHg; pulse: 93 beats per minute; respiratory rate: 28 breaths per minute; and her body temperature was 36.0℃. On physical examination, the patient had no notable findings, other than bilateral expiratory rales and neck vein distention. No heart murmurs or pericardial friction rub were heard. An electrocardiogram was within normal limits. A chest X-ray revealed marked cardiomegaly and pulmonary edema. Laboratory tests showed the following: white blood cell count: 10300/mm3, hemoglobin: 8.3 g/dL, platelet count: 250000/mm3, blood urea nitrogen: 63 mg/dL, creatinine: 4.4 mg/dL, brain natriuretic peptide: 483 pg/mL, creatine kinase isoenzyme MB: 2.0 ng/mL, and troponin-I: 0.10 ng/mL. The patient received emergency hemodialysis because of pulmonary edema refractory to medical therapy, including high-dose furosemide infusion. After stabilizing the patient’s volume status by regular hemodialysis, she received coronary angiography for the evaluation of ischemic heart disease on the 19th day of admission. The patient took aspirin (300 mg) and clopidogrel (300 mg) loading dose 12 hours before the procedure.
Exploration was performed via the right femoral artery. When the 0.025-inch straight guidewire (45 cm, Terumo, Tokyo, Japan) for a 4 French sheath was advanced, some resistance was felt. We then checked the fluoroscopy and found that the guidewire was introduced into the circumflex iliac artery (). We promptly pulled the guidewire back from the circumflex iliac artery and advanced it into the abdominal aorta under fluoroscopic guidance. After the 4 French sheath was inserted, we checked the femoral angiography. Neither perforation nor dissection from the circumflex iliac artery was shown (). The external iliac artery and circumflex iliac arteries were intact, there were no changes in the patient’s vital signs, and no abdominal symptoms were found, therefore, we continued the coronary angiography without incident.
Coronary angiography revealed significant stenosis in the middle and distal segments of the right coronary artery and the middle segment of the left anterior descending artery. After 7000 IU of heparin was administered intravenously, we performed a PCI at the middle and distal right coronary artery and the mid-left anterior descending artery with an activated clotting time (ACT) of more than 300 seconds, without any immediate complications. Because the ACT remained prolonged, the sheath removal was performed 12 hours after PCI without any acute complications. Fourteen hours after PCI, the patient complained of a right abdominal pain, with mild swelling of her right abdomen. Her blood pressure abruptly dropped to 80/40 mmHg. We started hydration with normal saline and performed a transfusion of 2 pints of packed red blood cell because of an abrupt drop of hemoglobin from 9.3 to 7.3 g/dL over 12 hours. After hydration and transfusion, her blood pressure returned to 110/70 mmHg. The sheath site was clear with no evidence of bleeding, hence, we performed an abdominal computed tomography angiography to identify other causes of the bleeding, which revealed a right lateral abdominal wall hematoma about 5 cm in diameter (). The right circumflex iliac artery was located in the hematoma, but there was no evidence of active extravasation of contrast media. The patient’s vital signs remained stable after hydration and transfusion, so we decided to closely observe her. However, the patient still complained of abdominal pain and ecchymotic patches appeared on her abdomen 3 days after the procedure (). Next, the patient underwent intermittent hemodialysis with minimal use of heparin and had her hemoglobin checked daily. After 5 days, her abdominal pain resolved and the ecchymosis gradually improved. There was no evidence of further hemoglobin changes. The patient was discharged uneventfully after 26 days of hospitalization (7 days after PCI). She was discharged on aspirin (100 mg), clopidogrel (75 mg), rosuvastatin (10 mg), losartan (50 mg), and carvedilol (6.25 mg). No further complications were evident, after one year of follow-up.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [73, 'years'], 'creatinine': [4.4, 'mg/dL'], 'sex': 'Female'}",9.83203,9.34043,10.32363,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 73 years old. The concentration of Creatinine is 4.4 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 4.4^(-1.154) * 73^(-0.203) * 1 * 0.742=9.83203.
Hence, the patient's GFR is 9.83203 mL/min/1.73m²."
3149,9,MDRD GFR Equation,lab test,decimal,pmc-7748311-1,Extracted,"The patient was an 82-year-old man, who had a history of hypertension for the past 20 years; his highest recorded blood pressure was 180/110 mmHg, and he took his oral antihypertensive drugs including telmisartan, irregularly. He also had a history of coronary heart disease for >10 years, and was taking oral antiplatelet drugs (aspirin) irregularly. He had experienced a sudden decrease of urine volume for the past 2 days, with abdominal distension and pain, followed by edema of both lower limbs, mental disorder, loss of appetite, and occasional cough and sputum; however, there was no fever or chills.
The patient was admitted to the emergency department of our hospital, and no urine output was noted after urethral catheterization. Following preliminary investigations, he was transferred to the Nephrology department, where physical examination revealed the following: temperature: 36 °C, heart rate: 105 beats per minute, respiratory rate: 21 breaths per minute, and blood pressure: 145/76 mmHg. The patient was unconscious, and patchy ecchymosis were visible in both arms, forearm, and right groin. The conjunctiva and lips were pale, and the respiratory sounds in both lungs were poorly audible; no wet rales were noted. The heart rhythm was irregular with well audible heart sounds, and the abdomen was distended. Muscular atrophy was noted in both lower limbs with visible tremor in the upper limbs, and the muscle power was of level 4.
The patient underwent the following tests in hospital on an emergency basis: total protein: 61.73 g/L, potassium: 6.00 mmol/L, sodium: 130.00 mmol/L, chloride: 96.00 mmol/L, anion gap: 23.90 mmol/L, urea: 65.05 mmol/L, creatinine: 756.00 μmol/L, and glucose: 6.70 mmol/L. In addition, blood analysis revealed: leukocyte count: 4.45 × 109/L, neutrophils: 71.70%, lymphocytes: 18.90%, red blood cell count: 3.17 × 1012/L, hemoglobin: 103.00 g/L, hematocrit: 0.30, and platelet count: 66.00 × 109/L. The myocardial enzyme levels were as follows: troponin T: 115 ng/L and myoglobin: 354.70 ng/mL. The initial diagnosis in the emergency department was that of acute renal failure, and he was accordingly transferred to the Department of Nephrology. He was finally diagnosed with acute renal injury, atrial fibrillation, coronary artery atherosclerotic heart disease (grade III cardiac function), lung infection, old cerebral infarction, level 3 hypertension (high risk), prostatic hyperplasia (after prostatectomy), urethral stricture, and Parkinson syndrome.
He was administered diuretics, intravenous immunoglobulin, anti-infectives, and nutritional support at the Nephrology department.
On day 22 of admission, his blood pressure suddenly dropped to 86/55 mmHg, with a heart rate of 107 beats per minute, dyspnea, anuria (urine volume <100 mL/d), abdominal distention, cold extremities, and blood stasis. At this time, he was considered to have shock and insufficient organ perfusion, and was administered rehydration to improve cardiac output. However, the symptoms did not improve after administration of 500 mL of fluid. The symptoms of dyspnea worsened with further decline in blood pressure.
The critical-ultrasound specialists were urgently requested to perform the protocol of critical consultation ultrasonic examination (CCUE) at the bedside to evaluate the circulatory and respiratory functions (Tables and ). The ultrasound examination revealed: a cardiac output of approximately 3.08 L (although the ejection fraction was approximately 65%), widening of the inferior vena cava (Fig. ) and a low degree of variability with breathing, suggestive of volume overload, increased pulmonary artery pressure with right heart volume expansion (Fig. ), suggestive of right heart failure, diffuse B-lines in the entire lung, suggestive of severe pulmonary edema (Figs. and ), and contradictory motion of the interventricular septum, manifested by a rapidly expanding right ventricle squeezing the left ventricle, which results in left ventricular diastolic restriction (Fig. ).
All the above 5 conditions were indicative of volume overload. Excessive circulating fluid had aggravated the right heart failure and pulmonary edema. Therefore, under the guidance of bedside ultrasound, reverse fluid resuscitation was immediately instituted. Bedside continuous renal replacement therapy (CRRT) was initiated to promote a negative fluid balance. A volume of 800 mL of fluid was removed in 24 hours with CRRT. On the 2nd day, his blood pressure increased to 110/80 mmHg, and the tissue perfusion improved slightly. The CCUE protocol of critical ultrasound was repeated, and CRRT was administered based on the findings. We ensured that the daily fluid output exceeded input. A total volume of 3500 mL of fluid was removed within 72 hours. We can observe that the following time, with the increase of reverse fluid resuscitation, the patient's cardiac load were significantly improved, manifested as the increase of inferior vena cava variability and cardiac output, and the decrease of blood pressure and heart rate. In addition, lung ultrasound (LUS) showed that pulmonary edema also improved significantly, which may be related to the decrease of pulmonary capillary pressure.
The circulation stabilized, dyspnea improved, urine output was restored without support and creatinine levels were reduced to 352 μmol/L. The third session of bedside ultrasound showed a marked reduction of B-lines in both lungs, and A-lines appeared in the anterior thoracic region, and the LUS score was decreased (Table ), suggesting significant improvement of pulmonary edema. Echocardiography showed that the diameter of the left atrium, right ventricle, and right atrium had decreased, while left ventricular end-diastolic volume and inferior vena cava variability had increased (Table ). This suggested an improvement in his condition, with attainment of stability.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [82, 'years'], 'creatinine': [352.0, 'µmol/L'], 'sex': 'Male'}",14.61908,13.88813,15.35003,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 82 years old. The concentration of Creatinine is 352.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 352.0 µmol. To convert 352.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 352.0 µmol Creatinine * 1e-06 mol/µmol = 0.00035 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00035 mol Creatinine * 113.12 g/mol = 0.03959 g Creatinine. To convert 0.03959 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.03959 g Creatinine * 1000.0 mg/g = 39.59 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 39.59 mg Creatinine/10.0 dL = 3.959 mg Creatinine/dL. The concentration value of 352.0 µmol Creatinine/L converts to 3.959 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.959^(-1.154) * 82^(-0.203) * 1 * 1=14.61908.
Hence, the patient's GFR is 14.61908 mL/min/1.73m²."
3150,9,MDRD GFR Equation,lab test,decimal,pmc-8143807-2,Extracted,"Case 2 was a 37-year-old male with a PMH of SUD who presented to the ED in June 2020. He had reportedly been given naloxone from EMS after using opioids and reported not feeling well. He was uncooperative and shouting on arrival and complained of possible assault, noting right hip and back pain. His initial creatinine was 4.33 mg/dL and potassium was 6.9 mmol/L, which prompted reassessment for compartment syndrome. Examination with the patient standing showed edema and erythema of the right buttock. The left buttock, although less edematous, was also tense. Given those findings, he was transferred for emergent surgery evaluation. Additional laboratory studies included a CK of 218,142 U/L and a UDS positive for fentanyl, cocaine, cannabinoids, and amphetamines. He subsequently had CT imaging of his head, chest, abdomen and pelvis, which was remarkable for left lateral gluteal and pelvic musculature swelling, as well as edema of the right anterior abdominal musculature and right gluteus that were presumed to be secondary to blunt injury. He was taken to the OR that evening for left gluteal fasciotomy and was started on hemodialysis. On hospital day two, his right buttock was noted to be firm and he was taken back to the OR for right-sided gluteal fasciotomy. He also had renal recovery and was discharged on hospital day 18.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [37, 'years'], 'creatinine': [4.33, 'mg/dL'], 'sex': 'Male'}",15.4948,14.72006,16.26954,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 37 years old. The concentration of Creatinine is 4.33 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 4.33^(-1.154) * 37^(-0.203) * 1 * 1=15.4948.
Hence, the patient's GFR is 15.4948 mL/min/1.73m²."
3151,9,MDRD GFR Equation,lab test,decimal,pmc-8177963-1,Extracted,"This is a 75-year-old man with a past medical history of diabetes mellitus and hypertension. He had a history of 6 months of an intense left flank pain. Physical exam was unremarkable. An abdominal ultrasound described a left renal mass. Computed tomography (CT) showed a 7.3 × 5 cm mass in the descending colon infiltrating the left kidney, iliopsoas muscle and retroperitoneum. No distant metastases were observed ().
Laboratory tests showed increased serum creatinine (2,0 mg/dl) and glycosylated hemoglobin (8,8%) levels. Carcinoembryonic antigen was normal (2.8 ng/ml). A urine culture was positive for Escherichia coli.
Surgery was decided due to high suspicion of a symptomatic locally advanced colorectal neoplasm. Intraoperatively, a tumoral mass was founded, involving the descending colon, left kidney, lateral abdominal wall and retroperitoneum. A left segmental colectomy with primary colonic anastomosis, left partial nephrectomy and retroperitoneum soft tissue resection was performed. Postoperative recovery was uneventful. Patient was discharged on postoperatory Day 6.
Pathology described a big mass of 8.5 × 5.3 × 3.5 cm infiltrating the pericolic adipose tissue and the colonic mucosa. Microscopically, an extensive chronic inflammatory reaction was observed involving the colonic wall, renal tissue and muscle, corresponding mainly to macrophages and Michael–Gutman bodies (), compatible with malakoplakia.
During follow-up, patient reported resolution of symptoms and no major deterioration in renal function was observed.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [75, 'years'], 'creatinine': [2.0, 'mg/dL'], 'sex': 'Male'}",32.73497,31.09822,34.37172,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 75 years old. The concentration of Creatinine is 2.0 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.0^(-1.154) * 75^(-0.203) * 1 * 1=32.73497.
Hence, the patient's GFR is 32.73497 mL/min/1.73m²."
3152,9,MDRD GFR Equation,lab test,decimal,pmc-4365362-1,Extracted,"A 62-year-old right-handed male with chronic renal failure due to chronic glomerulonephritis began to experience difficulty with speech and swallowing and was admitted to our hospital one month after the onset of these symptoms. At the age of 35, he had proteinuria and was diagnosed with nephrotic syndrome and kidney injury. He was diagnosed with possible membranoproliferative glomerulonephritis (MPGN) based on the results of a renal biopsy (see below). His systolic blood pressure was kept in control within 125–140 mmHg. The patient's medications included amlodipine, carvedilol, furosemide, doxazosin, and sodium hydrogen carbonate. He had no history of smoking or any other toxic habits. His parents and siblings had been free from strokes, migraines, and dementia.
On admission, the patient's blood pressure was 160/82 mmHg and his pulse rate was 62 beats/min and regular. He was alert and did not have any mood disorder, migraines, scalp alopecia, or spinal osteoarthritis. A neurological examination showed left facial palsy, dysarthria, and dysphagia (pseudobulbar palsy). The Mini-Mental State Examination score was 27 of 30.
Peripheral blood cell counts and biochemical studies showed moderate anemia (hemoglobin, 9.6 g/dL; hematocrit, 28.7%), impaired kidney function (blood urea nitrogen, 69 mg/dL; creatinine, 3.63 mg/dL; urinary protein excretion, 1.04 g/day), dyslipidemia (LDL-cholesterol, 89 mg/dL; HDL-cholesterol, 32 mg/dL; triglycerides, 183 mg/dL), and hyperhomocysteinemia (24.5 nmol/mL). No abnormality was detected in his antinuclear antibody, anticardiolipin antibody, fibrinogen, d-dimer, protein C, protein S, antithrombin III, or antineutrophil cytoplasmic antibody (ANCA) levels.
Cerebral MRI demonstrated diffuse T2 hyperintense areas in the periventricular and subcortical white matter involving bilateral temporal poles and the external capsule (). On diffusion-weighted images, a hyperintense area was observed at the right frontal lobe, indicating a recent infarct. T2*-weighted images showed multiple microbleeds in the bilateral basal ganglia and subcortical areas. MR angiograms did not show any abnormal findings.
Since he had severe white matter lesions, including the temporal pole, which is characteristic of CADASIL [], we performed a mutational analysis of the NOTCH3 gene after he provided informed consent. Genomic DNA was extracted from peripheral blood leukocytes of the patient. Polymerase chain reaction- (PCR-) mediated direct sequencing demonstrated that no mutation was found in exons 3 and 4, which are hot spots in CADASIL. Then, we examined all other exons and splice sites of the NOTCH3 gene, and G to C transversion was detected in exon 24, c.4039G>C. It changed the codon 1347 from GGG to CGG, resulting in a p.Gly1347Arg substitution (). The DNA mutation numbering is based on the cDNA sequence (GenBank accession number NM_000435.2), with +1 corresponding to the A of the translational initiation site. The patient was heterozygous for this missense mutation. We did not find any other mutations or splice variants. The c.4039G>C change was absent in the database of common gene variations in the Japanese population (JSNP), in the Human Gene Mutation Database (HGMD), in the Single Nucleotide Polymorphism database of the NCBI, and in 30 unrelated Japanese controls, who were examined after providing consent according to the ethics code of the Kyushu University Hospital.
The p.Gly1347Arg substitution was present in the EGF-like repeat domain 34 of the Notch3 extracellular domain. According to in silico analysis, this substitution was predicted to be “probably damaging” with a score of 0.999 using polymorphism phenotyping-2 (PolyPhen-2, ) [], and it was also predicted to be “deleterious” with a score of −4.930 as determined by Protein Variation Effect Analyzer (PROVEAN, ) [], thus indicating an adverse effect on the structure and function of the protein.
The renal biopsy specimens that had been obtained 28 years earlier showed mesangial cell proliferation with widening of the matrix in almost all glomeruli and an irregular thickened glomerular basement membrane with a “double contour” appearance (Figures and ). In the immunofluorescence studies, the staining of immunoglobulins G, A, M, and C3 was granular and located along the glomerular capillary loop (). Electron-dense deposits were confirmed in the subendothelial space by electron microscopy (). These findings were consistent with the findings of MPGN. On the other hand, severe hyaline changes of the arterioles were observed, especially from the efferent and afferent arterioles to glomerular arterioles (). Granular deposits were also found in many places in the thickened subendothelial basement membrane or the basement membrane-like material of the arterioles, similar to the findings of GOM by electron microscopy (). These findings were consistent with CADASIL, whereas the loss of medial vascular smooth muscle cells (VSMCs) was not observed in the patient at that time.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [62, 'years'], 'creatinine': [3.63, 'mg/dL'], 'sex': 'Male'}",17.10213,16.24702,17.95724,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 62 years old. The concentration of Creatinine is 3.63 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.63^(-1.154) * 62^(-0.203) * 1 * 1=17.10213.
Hence, the patient's GFR is 17.10213 mL/min/1.73m²."
3153,9,MDRD GFR Equation,lab test,decimal,pmc-6803094-1,Extracted,"A 25-year-old man presented to the emergency department with sudden onset paraplegia and pain in the lower extremities. His medical history included Crohn’s disease, managed with sulfasalazine. He was otherwise healthy, worked as a tradesman, and was competing in fitness championships. There was no history of trauma to the back or abdomen. Earlier in the morning, while lifting a 10 kg object at work, he experienced sudden onset of bilateral leg pain and felt the urge to defecate. While in the bathroom, he lost power in his lower extremities and was found on the floor by his coworkers. Vital signs were stable upon ambulance crew arrival. The patient presented with abdominal and bilateral leg pain in addition to numbness and paralysis of the legs. He had faecal incontinence and had soiled his clothes and the floor. During ambulance transport, he received intravenous crystalloid fluids, ondansetron and a total of 25 mg of intravenous morphine.
On arrival to the resuscitation room at Skåne University Hospital in Malmö, the patient was still complaining of pain, now primarily localised to the perianal region, and persistent paraplegia. His vital signs were within normal range, except blood pressure that was elevated at 180/90 mm Hg. His legs were pale, cold and numb with flaccid paralysis. Femoral and distal peripheral pulses were impalpable. Sensory loss extended distally from the umbilical level, whereas examination above the umbilical level was normal. Bedside ultrasonography revealed no free intra-abdominal fluid and the aorta appeared normal. On log-rolling, there was no sign of trauma or midline tenderness on palpation of the spine. Rectal examination revealed total loss of sphincter tone and sensation in the perianal area. Bedside arterial blood gas showed metabolic acidosis with pH 7.2, base excess −13 mmol/L, lactate 6.2 mmol/L, an elevated creatinine at 155 µmol/L and otherwise unremarkable. More analgesia was given.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [25, 'years'], 'creatinine': [155.0, 'µmol/L'], 'sex': 'Male'}",49.45422,46.98151,51.92693,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 25 years old. The concentration of Creatinine is 155.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 155.0 µmol. To convert 155.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 155.0 µmol Creatinine * 1e-06 mol/µmol = 0.00015 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00015 mol Creatinine * 113.12 g/mol = 0.01697 g Creatinine. To convert 0.01697 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01697 g Creatinine * 1000.0 mg/g = 16.97 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 16.97 mg Creatinine/10.0 dL = 1.697 mg Creatinine/dL. The concentration value of 155.0 µmol Creatinine/L converts to 1.697 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.697^(-1.154) * 25^(-0.203) * 1 * 1=49.45422.
Hence, the patient's GFR is 49.45422 mL/min/1.73m²."
3154,9,MDRD GFR Equation,lab test,decimal,pmc-4652317-1,Extracted,"A 24-year-old man was admitted to our hospital with the signs of advanced chronic renal failure (CRF) in 2006. In his past history, he had developed kidney and bladder stones since he was 5-year-old. In his family history, his sister exhibited an elevated urine Ox concentration and his brother presented with kidney stones and renal failure. Unfortunately, they refused to cooperate with physicians to perform required tests until transplantation. Immediately in 1st day of admission, blood urea nitrogen (BUN) and serum creatinine (Cr) were determined 165 and 16.5 mg/dl, respectively, and also protein and glucose were detected in urine. The diagnostic findings indicate shrunken hyper-echogenic kidneys with hydronephrosis. Multiple stones with different sizes were observed in calyces of both kidneys. The bladder wall was thickened (4.7 mm), and urinalysis did not reveal any crystals. The patient underwent hemodialysis (HD) three times per week for 4 months. Four months after admission, the patient underwent bilateral nephrectomy. Based on the findings obtained in bilateral radical nephrectomy, chronic pyelonephritis with nephrolithiasis was confirmed. Microscopic examination revealed glomerulosclerosis and tubulointerstitial fibrosis. About 2 years later (September 2008), the patient underwent living kidney transplantation with a diagnosis of ESRD. The primary graft function was acceptable? but 3 days after transplantation, the urine output suddenly dropped to 30-50 cc a day. Therefore, a renal biopsy was taken. Tissue sections containing glomeruli and tubules were obtained. The following histopathological data were gathered: The glomeruli showed no conspicuous changes, mild to moderate atrophy with mononuclear inflammatory cells and occasional eosinophilic infiltration of interstitium, some tubules contained marked Ox crystals, and some contained granular and white blood cells casts. Following the acute rejection, anti-thymocyte globulin (ATG) was administered for the patient. After few days of ATG administration, the drug was discontinued because of fever. The possibility of PH1 was considered when a lot of Ox crystals were observed in the renal allograft biopsy and also by ruling out the other causes of hyperoxaluria. Therefore, pyridoxine therapy was commenced (dose, interval, and route of admin).
In January 2009, the patient's serum Cr and BUN levels were 4.8 and 38 mg/dl, respectively. The patient's computed tomography (CT) scan and radiography demonstrated cardiomegaly, bilateral pleural effusion with congestion, and calcification at the right pulmonary hilum and parenchyma. The molecular diagnostic polymerase chain reaction test revealed the persistence of cytomegalovirus. After few months, the patient refused to continue the treatment and finally he died 1-year later.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [24, 'years'], 'creatinine': [16.5, 'mg/dL'], 'sex': 'Male'}",3.61309,3.43244,3.79374,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 24 years old. The concentration of Creatinine is 16.5 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 16.5^(-1.154) * 24^(-0.203) * 1 * 1=3.61309.
Hence, the patient's GFR is 3.61309 mL/min/1.73m²."
3155,9,MDRD GFR Equation,lab test,decimal,pmc-8591455-1,Extracted,"Our patient is a 73-year-old man with diabetes, hypertension, coronary artery disease, congestive heart failure, and chronic renal insufficiency (creatinine 1.4 mg/dL) who presented with a nonhealing wound on his left lateral heel and a toe pressure of 4 mm Hg (Society of Vascular Surgery Wound, Ischemia, and Foot Infection score 2-3-0, stage 4). His diabetes was poorly controlled (A1c 8.8), and he had recently started empagliflozin in addition to metformin and insulin. Empagliflozin and metformin were held on the morning of surgery, and he underwent left femoral endarterectomy with common and external iliac stenting and left femoral to below-knee bypass using the ipsilateral saphenous vein.
His postoperative course initially followed the expected trajectory, but early in the morning of postoperative day 2, he developed acute-onset delirium with severe metabolic acidosis (pH 7.2, PaCO2 of 19 mm Hg, bicarbonate of 8.9 mmol/L, and base deficit of 16.7 mmol/L with anion gap 24 mEq/L). Surprisingly, serum lactate was only mildly elevated (3 mmol/L). He was hypotensive requiring volume resuscitation and low-dose pressor support, despite brisk urine output. Workup did not demonstrate evidence of bleeding, infection, or cardiac event to explain his clinical condition. His serum glucose was relatively normal (170-200 mg/dL), but his urinalysis was significant for high urinary glucose and ketones (>500 mg/dL and 80 mg/dL, respectively). Of note, he had not received any insulin on postoperative day 1 given normal glucose levels.
The treating intensivist was familiar with the risk of euglycemic DKA with SGLT-2 inhibitors and started the patient on an insulin drip, resulting in normalization of the severe acidosis. The patient’s blood pressure and mental status also improved with fluids and correction of the DKA. He was transitioned from insulin drip to subcutaneous insulin the following day, and the remainder of his hospital course was unremarkable. He was discharged home on postoperative day 7 without further complication.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [73, 'years'], 'creatinine': [1.4, 'mg/dL'], 'sex': 'Male'}",49.67659,47.19276,52.16042,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 73 years old. The concentration of Creatinine is 1.4 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.4^(-1.154) * 73^(-0.203) * 1 * 1=49.67659.
Hence, the patient's GFR is 49.67659 mL/min/1.73m²."
3156,9,MDRD GFR Equation,lab test,decimal,pmc-3808169-1,Extracted,"At an initial visit in September 2006, a 46-year-old white male presented with edema, blood pressure indicative of hypertension (144/94 mmHg), heart rate of 76 beats per minute, and creatinine of 1.4 mg/dL (123.76 μmol/L). He had experienced sudden onset of edema in his feet and legs 5 weeks prior to this initial visit, which caused him serious concern. At a height of 5 feet 8 inches (172.72 cm) and weighing 235 lbs (105.75 kg; up about 35 lbs [15.75 kg] from his usual weight), his body mass index was 35.7. He had not been on any medication regimen. Laboratory values included 24-hour urinary protein at >7,500 mg/dL (750.0 g/L) and cholesterol at 307 mg/dL (7.9513 mmol/L; low-density lipoprotein, 224 mg/dL [5.8016 mmol/L]). He was negative for cancer screening, hepatitis B and C panel, antinuclear antibody, rheumatoid factor, and rapid plasmid reagin. He was started on olmesartan medoxomil-hydrochlorothiazide 40/25 mg for hypertension and proteinuria and simvastatin 40 mg for elevated cholesterol.
The patient was scheduled for a kidney biopsy for nephrotic range proteinuria in October 2006, which resulted in a diagnosis of idiopathic membranous glomerulopathy. Lisinopril 40 mg twice daily was added to his medication regimen. At this time, his creatinine was at 1.3 mg/dL (114.92 μmol/L).
The patient’s membranous glomerulopathy progressed from October 2006 to July 2009, as revealed by laboratory results. During this period, he remained on an angiotensin receptor blocker (olmesartan medoxomil-hydrochlorothiazide) and angiotensin-converting enzyme inhibitor (lisinopril) treatment regimen. Since no improvement was observed, he then received cyclosporine A for 6 months, to which he was relatively adherent. No improvement was observed 3 months after initiation of cyclosporine A, so prednisone was added. Three months later, he developed shingles and was admitted to the hospital due to what was felt to be complications of cyclosporine A plus prednisone. Both cyclosporine A and prednisone were tapered off after the patient requested all immunosuppressive medications be stopped. Three months later, he agreed to be treated with mycophenolate, which he received for approximately 12 months but only during the last 3 months did he take it as prescribed.
The patient was agreeable to trying Acthar (80 USP U/mL) and received treatment from September 2009 to October 2010; his laboratory values during this period are summarized in . Acthar was self-administered subcutaneously at an initial dose of 40 U every 72 hours. After 3 months, the dose was increased to 80 U every 72 hours. In April 2010, his urinary protein levels rose to 9,520 mg/dL (952.0 g/L), and he required additional antihypertensive therapy. By July 2010, his urinary protein had dropped to 2,948 mg/dL (294.8 g/L). Thus, it took approximately 10 months of Acthar treatment to improve his urinary protein levels. By October 2010, his urinary protein levels had decreased further to 1,628 mg/dL (162.8 g/L). As shown in , in addition to the decline in urinary protein levels, the patient experienced decreases in creatinine and albumin levels, an increase in creatinine clearance, and modest weight gain while receiving treatment with Acthar.
Acthar treatment was stopped in October 2010 for several reasons. First, one year of ACTH treatment has been shown in European studies to be sufficient for resolving proteinuria.– In addition, the patient’s laboratory results indicated clinically significant improvement in his signs of membranous nephropathy. Finally, the patient reported that his quality of life had improved, and he was not experiencing any symptoms of membranous nephropathy. He felt well and was able to return to his previous lifestyle.
The laboratory results since halting Acthar are also shown in . Urinary protein levels continued to decline overall, from 407 mg/dL (40.7 g/L) in December 2010, with slight elevation to 451 mg/dL (45.1 g/L; still within normal range) in March 2011, to 189 mg/dL (18.9 g/L) in September 2011. His protein to creatinine ratio was 0.58 in January 2012, and at that time his medications were limited to an angiotensin-converting enzyme inhibitor (lisinopril) and angiotensin receptor blocker (olmesartan medoxomil-hydrochlorothiazide). As of May 1, 2012, his blood pressure was 124/78 mmHg, he weighed 199 lbs (89.55 kg), his heart rate was 81 beats per minute, and there was no evidence of edema. Current medications include olmesartan medoxomil-hydrochlorothiazide 40/12.5 mg once daily, lisinopril 40 mg once daily, and simvastatin 40 mg once daily.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [46, 'years'], 'creatinine': [1.4, 'mg/dL'], 'sex': 'Male', 'Race': 'White'}",54.55901,51.83106,57.28696,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 46 years old. The concentration of Creatinine is 1.4 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.4^(-1.154) * 46^(-0.203) * 1 * 1=54.55901.
Hence, the patient's GFR is 54.55901 mL/min/1.73m²."
3157,9,MDRD GFR Equation,lab test,decimal,pmc-3697147-1,Extracted,"A 53-year-old white male was admitted for acute kidney injury and hyperkalemia 21 months after liver transplantation for hepatitis C. He had a past medical history of human immunodeficiency virus (HIV), recurrent hepatitis C after transplant (grade 2, stage 2), and stage 3 chronic kidney disease (CKD). Approximately 2 weeks prior to admission, he was converted as an outpatient to a protease-inhibitor (atazanavir) based highly active antiretroviral therapy (HAART) regimen. He presented to clinic with nausea, vomiting, a serum creatinine (SCr) of 6.3 mg/dL (baseline 1.7 mg/dL), potassium of 6.7 mEq/L, and an FK trough level > 30 ng/mL. He was subsequently admitted for hydration, treatment of hyperkalemia, and telemetry monitoring. Despite sodium polystyrene administration, hydration, and withholding of tacrolimus, and HAART, on hospital day 2, SCr remained at 6.2 mg/dL, potassium was 6 mEq/L, and FK was >30 ng/mL. Due to the magnitude of renal impairment, lack of knowledge of the precise quantitative FK level, and unpredictability of tacrolimus clearance in the presence of atazanavir use, the decision was made to initiate phenytoin as a means to induce drug metabolism. Phenytoin was administered orally at a dose of 200 mg twice daily. FK concentration decreased to 22.3 ng/mL the day after phenytoin initiation and then to 11.7 ng/mL the next day. Phenytoin was continued for 3 days, and the patient was discharged 3 days after admission with a SCr of 3.9 mg/dL and potassium level within normal range. HAART therapy was reintroduced at discharge and at an outpatient visit 2 days later tacrolimus was reinitated. SCr eventually returned to near-baseline at 1 week after discharge, and has remained stable ever since.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [53, 'years'], 'creatinine': [6.2, 'mg/dL'], 'sex': 'Male', 'Race': 'White'}",9.51897,9.04302,9.99492,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 53 years old. The concentration of Creatinine is 6.2 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 6.2^(-1.154) * 53^(-0.203) * 1 * 1=9.51897.
Hence, the patient's GFR is 9.51897 mL/min/1.73m²."
3158,9,MDRD GFR Equation,lab test,decimal,pmc-5051059-1,Extracted,"RF is a 66-year-old male with a history of ischemic cardiomyopathy. The patient had a HeartMate II LVAD placed 3 years prior to presentation for medically refractory heart failure. He was on warfarin and aspirin for his LVAD with goal INR of 1.5–2.0. He presented to the emergency department with light-headedness and hematochezia for several days. He had no prior history of GIB. His physical examination and vital signs were unremarkable. His INR was 2.8, creatinine was 2.3 mg/dl, and hemoglobin was 10.4 from baseline of 12 to 13 g/dl. His last screening colonoscopy was 4 years prior and was reportedly unremarkable. He was admitted for close monitoring, serial laboratory testing, and gastroenterology consultation. He underwent esophagogastroduodenoscopy revealing a gastric ulcer with a clean base with no evidence of active bleeding. A colonoscopy revealed a likely malignant tumor in the cecum, diverticulosis, and nonbleeding colonic angiodysplastic lesions []. The cecal mass was biopsied; it appeared to be actively bleeding and uncontrollable endoscopically. These findings were relayed to the emergency general surgery team.
He was taken emergently to the operating room. A midline laparotomy was undertaken and he was found to have a cecal mass that was perforated into a retroperitoneal abscess. The right colon was mobilized to the hepatic flexure and the abscess cavity was debrided. A right colectomy was performed with a stapled side-to-side ileocolonic anastomosis. A drain was placed in the abscess cavity, fascia was closed, and the skin and subcutaneous tissues were packed with gauze.
Final pathology showed no evidence of malignancy. It revealed a transmural defect of 1.0 cm × 0.5 cm with organizing hematoma and acute on chronic inflammation. Cytomegalovirus testing was negative. There was focal re-epithelialization, thus making bleeding diverticulum a possible diagnosis.
The patient's postoperative course was complicated by prolonged ileus necessitating total parenteral nutrition and pelvic abscess that required percutaneous drain placement. The patient additionally had bacteremia and fungemia. The patient's postoperative complications eventually resolved, and he was discharged to home with home health.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [66, 'years'], 'creatinine': [2.3, 'mg/dL'], 'sex': 'Male'}",28.59148,27.16191,30.02105,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 66 years old. The concentration of Creatinine is 2.3 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.3^(-1.154) * 66^(-0.203) * 1 * 1=28.59148.
Hence, the patient's GFR is 28.59148 mL/min/1.73m²."
3159,9,MDRD GFR Equation,lab test,decimal,pmc-6545665-1,Extracted,"A 60-year-old Hispanic female with multiple comorbid conditions including
hypertension, type 2 diabetes mellitus, chronic kidney disease stage III with a
baseline creatinine of 1.3 mg/dL, baseline chronic obstructive pulmonary disease not
on home oxygen, and HIV on highly active antiretroviral therapy (HAART) therapy for
more than 10 years, compliant with her medications, visited emergency room with
nausea, vomiting, and inability to maintain a good oral intake. She also complained
of progressive fatigue over the past several weeks with no relieving factors. Her
HAART medications included tenofovir/emtricitabine with fosamprenavir. Her initial
workup revealed a serum creatinine of 1.6 mg/dL, phosphorus of 1.4 mg/dL, with rest
of her blood work in normal limits. Fractional urinary phosphorus excretion was
calculated at 40% despite low phosphorus levels indicating renal loss. Oral
phosphate repletion was started; however, tenofovir was continued as per Infectious
Disease recommendations. She was subsequently discharged with oral phosphorus
supplementation and was advised to follow-up with her primary care physician within
1 week. Before she could follow-up with her primary care physician, she was
readmitted with progressive fatigue, loss of appetite, and 1 episode of confusion at
home. Workup revealed very low serum phosphorus levels of 0.7 mg/dL. Intravenous
phosphorus was initiated for repletion, and after consultation with Nephrology and
Infectious Disease specialties, it was decided to stop tenofovir and monitor her
serum phosphorus levels. Before discharge, fractional urinary phosphorus excretion
showed improvement with a drop to 15%. Her symptoms improved and she was discharged
home. shows the
time course of tenofovir-associated hypophosphatemia in this patient.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [60, 'years'], 'creatinine': [1.6, 'mg/dL'], 'sex': 'Female', 'Race': 'Hispanic'}",32.87932,31.23535,34.52329,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 60 years old. The concentration of Creatinine is 1.6 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.6^(-1.154) * 60^(-0.203) * 1 * 0.742=32.87932.
Hence, the patient's GFR is 32.87932 mL/min/1.73m²."
3160,9,MDRD GFR Equation,lab test,decimal,pmc-6795349-1,Extracted,"A 56-year-old female with a past medical history significant for hypothyroidism, hyperlipidemia, and seropositive rheumatoid arthritis diagnosed in 2014 presented to the nephrology clinic upon referral for evaluation of acute kidney injury, proteinuria, and hematuria. The patient first presented to her primary care physician in July 2017 due to a flu-like illness accompanied by nausea, stomach upset, and dark urine. She was prescribed a two-week course of ciprofloxacin by her primary care physician for a presumed urinary tract infection and then prescribed a two-week course of trimethoprim-sulfamethoxazole due to persistent symptoms.
In August 2017, the patient presented to the emergency department with persistent nausea, vomiting, fatigue, and anorexia. Laboratory workup at this visit revealed an elevated creatinine of 1.79 mg/dL from a baseline creatinine of 0.75 mg/dL in February 2017. The patient received intravenous (IV) fluids and ondansetron. Further workup was non-contributory, and the patient was subsequently discharged to home with a follow-up appointment with her primary care physician. The following month, the patient presented to the emergency department with similar symptoms and was admitted to the hospital. Her creatinine upon presentation was 2.00 mg/dL, which improved to 1.56 mg/dL with IV fluids. She was discharged to home the following day with a plan to follow up with outpatient nephrology.
The patient presented to the nephrology clinic in September 2017 with persistent generalized fatigue, malaise, nausea, and occasional vomiting. She reported that her lack of energy affected her ability to perform her job. The patient’s medications included levothyroxine 75 mcg daily, methotrexate 7.5 mg per week, etanercept 50 mg subcutaneous every week since January 2016, simvastatin 20 mg daily, famotidine, folic acid, vitamin D and biotin. Vital signs revealed a temperature of 37°C, a pulse of 72 beats per minute, a blood pressure of 130/92, and a respiratory rate of 18. Physical examination did not reveal any abnormalities. Initial laboratory workup was significant for a blood urea nitrogen (BUN) level of 29 mg/dL (normal 7-20 mg/dL), creatinine level of 1.67 mg/dL (normal 0.6-1.0 mg/dL) and a urine protein/creatinine ratio of 3.30 (normal <0.5) (Table ). Additional workup revealed a positive antinuclear antibody, anti-SSA (Sjögren’s syndrome antigen A) antibody, anti-SSB (Sjögren’s syndrome antigen B) antibody, and anti-histone antibody (Table ).
The patient agreed to a kidney biopsy for further evaluation, and the renal specimen was examined under light microscopy, electron microscopy, and immunofluorescence. Under light microscopy, four out of 14 glomeruli were globally sclerotic and at least six showed fibrocellular crescents, most of which were circumferential. There was moderate interstitial fibrosis and associated tubular atrophy as well as chronic inflammation involving approximately 30-40% of the cortex (Figure ). Under immunofluorescence, some of the 14 glomeruli showed crescentic formation and the glomerular walls and mesangium, as well as some vessels, had granular staining of IgG (3+), IgA (2+), IgM (2+), C3 (2+), kappa (3+) and lambda (2 to 3+) light chains (Figure ). Electron microscopy of the specimen revealed crescentic changes, highly distorted capillary tufts, extensive foot process effacement on the capillary surface, and scattered electron densities predominantly in the intramembranous and mesangial areas and rarely in the subendothelial and subepithelial areas (Figures , ).
The biopsy results were significant for crescentic necrotizing glomerulonephritis with moderate interstitial fibrosis and moderate atherosclerosis. The patient was diagnosed with crescentic glomerulonephritis, attributed to etanercept in the clinical context as a diagnosis of exclusion. The etanercept was subsequently discontinued and the patient was prescribed steroids and mycophenolate mofetil. The patient was closely followed up in the clinic and her creatinine gradually improved after stopping etanercept and beginning steroids and mycophenolate mofetil (Figure ). Her most recent laboratory results showed a near-normal creatinine level.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [56, 'years'], 'creatinine': [1.67, 'mg/dL'], 'sex': 'Female'}",31.73547,30.1487,33.32224,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 56 years old. The concentration of Creatinine is 1.67 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.67^(-1.154) * 56^(-0.203) * 1 * 0.742=31.73547.
Hence, the patient's GFR is 31.73547 mL/min/1.73m²."
3161,9,MDRD GFR Equation,lab test,decimal,pmc-7403899-1,Extracted,"This is the case of a 57-year-old Colombian obese woman who was admitted to the emergency department complaining of abdominal pain, urinary symptoms, and fever. Her medical history was positive for systemic arterial hypertension, type 2 diabetes mellitus, and nephrolithiasis. Ten days before the symptoms' onset, she underwent a dental procedure for tooth decay. In the beginning, she was treated in another facility for ketoacidosis, renal failure, and bacterial urinary tract infection, developing pneumonia as well. She required renal replacement therapy and received a course of antibiotics including aminopenicillins, carbapenems, and glycopeptides.
During hospitalization, the patient suddenly presented right calf pain; a duplex ultrasound was requested evidencing deep venous thrombosis of soleal and peroneal veins. She complained as well of dyspnea, chest pain, and palpitations, raising the suspicion of pulmonary embolism (Wells' criteria: 4.5 points). Thoracic CT angiography showed thrombosis of the pulmonary trunk and both main branches, and the initial transthoracic echocardiography (4 days after admission) reported left ventricle diastolic dysfunction with impaired relaxation, trivial mitral regurgitation, mild right ventricle dilation, mild tricuspid regurgitation, and an intermediate probability of pulmonary hypertension (PSAP 40 mmHg) with no other findings. Systemic thrombolysis with streptokinase was the chosen treatment for the high-risk pulmonary embolism; subsequently, she was started on enoxaparin with bridge therapy to warfarin.
After thrombolysis, the patient remained febrile with chest discomfort despite antibiotic treatment suggesting dialysis catheter-related infection or bacterial endocarditis. A transesophageal echocardiogram was carried out, revealing a mitral valve mass considered as a bacterial vegetation, and therefore, she continued receiving vancomycin. For exploring therapeutic alternatives, she was transferred to our hospital and stayed in the intensive care unit for one month. Her vital signs were normal (36.8°C, 95 beats per min, 20 breaths per min, 132/55 mmHg, SpO2 94% on room air), but she was pale and cardiopulmonary auscultation was positive for S3 sound. No heart murmurs, abnormal breath sounds, or jugular ingurgitation was detected.
Laboratory analysis demonstrated leukocytosis (13.010 cells/μL), moderate anemia (7.4 g/dL), mild thrombocytopenia (146.000/μL), and increased C-reactive protein levels (17 mg/L, normal concentrations up to 5 mg/L). Moreover, renal function was severely compromised (creatinine 5.3 mg/dL and blood uremic nitrogen 42 mg/dL) and arterial blood gases showed metabolic acidosis (pH of 7.37, HCO3 13.9 mmol/L, PCO2 24 mmHg, SaO2 87%, and base excess -10.6). Urine cultures were positive for IRT-resistant Escherichia coli and azole-sensitive Candida albicans, while no germs could be isolated on blood cultures. Consequently, fluconazole was added to the antibiotic regimen.
Transesophageal echocardiogram (16 days after admission) demonstrated preserved left ventricular dimensions and ejection fraction. Mitral valve exhibited a rounded image of 10 × 10 mm with hyperrefringent edges and hypoechogenic content within the anterior ring, corresponding to A1 and A2 segments (). This lesion did not compromise the valve function nor obstructed the left ventricle outflow tract. The rest of the valves, cavities, and vessels were normal, except for a small left pleural effusion. The density of the mass and the absence of any other imaging features compatible with endocarditis (i.e., highly and asynchronously mobile pedicled mass) supported the diagnosis of a blood cyst. Contrast echocardiogram with sulfur hexafluoride microbubbles was not available in our institution.
Aside from the mass, she did not fulfill any other Duke's criteria and blood cultures were negative. Besides, there was no valvular regurgitation that supported the diagnosis of a leaflet aneurysm and the cyst remained the same size in transesophageal echocardiogram despite anticoagulation, being less likely that it corresponded to a thrombus adhered to the valve in a patient with no predisposing factors. Researchers have highlighted elsewhere that echogenicity is the key to differentiate other entities (infections, neoplasms, and thrombi) from blood cysts as the last exhibit a homogenous hypoechogenic content []. Unfortunately, we could not obtain the initial transthoracic echocardiogram for reviewing and confirming that the mass was not present at that point.
After 10 days of antifungals, the inflammatory response completely resolved and the antibiotic course was not extended as bacterial endocarditis was disregarded. The patient did not present any bleeding or embolic events and was discharged without any disability. Unfortunately, she did not attend to the Outpatient Clinic but, in a telephone follow-up, no recurrence of cardiovascular symptoms was reported.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [57, 'years'], 'creatinine': [5.3, 'mg/dL'], 'sex': 'Female', 'Race': 'Hispanic'}",8.34036,7.92334,8.75738,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 57 years old. The concentration of Creatinine is 5.3 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 5.3^(-1.154) * 57^(-0.203) * 1 * 0.742=8.34036.
Hence, the patient's GFR is 8.34036 mL/min/1.73m²."
3162,9,MDRD GFR Equation,lab test,decimal,pmc-8133129-1,Extracted,"A 51-year-old male was diagnosed with glomerulonephritis by renal biopsy 25 years ago, and developed into chronic renal failure (uremia period), then received allogeneic kidney transplantation 2 years later. Cyclosporine A, azathioprine and a small dose of prednisolone were used to inhibit the immune response and reduce the rejection. The serum creatinine was lower than 2.3 mg/dL in the first 10 years after transplantation. Renal insufficiency began 15 years after transplantation. Other accompanying symptoms gradually appeared, including increased serum creatinine level, decreased urine volume, facial and lower extremities edema, hypertension, proteinuria, etc. There was little improvement of renal function after methylprednisolone shock therapy and renal nutrition treatment. The patient's condition worsened to uremia 15.5 years after transplantation and began regular hemodialysis. 21 years after transplantation, CT scan showed that there was a convex growth cyst-solid mixed mass in the cortex of the transplanted kidney. The volume was about 1.5 cm × 1.0 cm × 0.5 cm (Fig. A), which was increased to 2.5 cm × 1.5 cm × 1.5 cm in the 22nd year after transplantation. Considering that the transplanted kidney had lost its function and ruling out the possibility of tumor metastasis to surrounding tissues and distant organs, the patient received ICAN under general anesthesia.
The brief procedures of the operation were as follows. First, we exposed the transplanted kidney outside the peritoneum through an incision at the outer edge of the right lower rectus abdominis. We observed that the kidney adhered tightly to the surrounding tissues and could not be separated completely. Considering that sharp separation or forced dissection may cause serious damage to the surrounding organs or renal pedicle vessels, we decided to use ICAN. The inflammatory adhesive renal capsule was cut longitudinally along the long axis of the kidney, and separated with a vascular clamp in order to find out the space between the renal capsule and the cortex. The index finger was then extended into the space, and blunt separation was performed in the anterior, posterior, upper, and lower directions of the involved kidney. The adhesion of the renal pedicle at the hilum of the kidney was very light, therefore we cut the renal capsule at the renal hilum after bluntly separating in the loose plane under the renal capsule. Then the renal pedicle arteries and veins were together clamped, ligated, and cut, and the ureter was exposed and cut. Finally, the transplanted kidney was removed completely. During the operation, we had paid great attention to avoid massive hemorrhage caused by avulsion of the renal pedicle and antibiotics had been prophylactically used to prevent infection. The patient received regular hemodialysis treatment after the operation.
Gross observation showed that the transplanted kidney had atrophic changes. The tumor is located in the cortex of the transplanted kidney, with a convex growth, about 2.5 × 1.5 cm in diameter, and an intact capsule. After longitudinal incision, it was found that the tumor was multilocular cystic with a thick wall and granular inner surface (Fig. B, C). Histopathological examination revealed locally acquired cystic disease-associated renal cell carcinoma with focal hemorrhage, degeneration, fibrosis, and necrosis (Fig. ). The patient recovered well and was discharged 6 days after the operation. At the 12th month postoperation, no residual tumor or recurrence was found by imaging, and the creatinine level of the patient was about 3.5 mg/dL under hemodialysis treatment. The patient planned to have second kidney transplantation 6 months later, so we recommend that the immunosuppressive drug regimen be adjusted to mycophenolate mofetil because of the potential toxicity of cyclosporine A to the kidney.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [51, 'years'], 'creatinine': [3.5, 'mg/dL'], 'sex': 'Male'}",18.55867,17.63074,19.4866,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 51 years old. The concentration of Creatinine is 3.5 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.5^(-1.154) * 51^(-0.203) * 1 * 1=18.55867.
Hence, the patient's GFR is 18.55867 mL/min/1.73m²."
3163,9,MDRD GFR Equation,lab test,decimal,pmc-7584298-1,Extracted,"An 82-year-old woman presented to our hospital’s emergency department with new onset confusion. Her past medical history includes type 2 diabetes mellitus, hypertension, hyperlipidemia, and age-related osteoporosis on intravenous (IV) bisphosphonate yearly.
Six weeks prior to this admission, she was treated for pyelonephritis at a different hospital. At that time, laboratories were notable for a total calcium of 12.8 mg/dl (ref range, 8.4-10.5 mg/dl), albumin 3.6 g/dl (ref range, 3.5-5.3 g/dl), creatinine 1.6 mg/dl (ref range, 0.50-0.90 mg/dl), phosphorus of 2.7 mg/dl (ref range, 2.5-4.5 mg/dl), alkaline phosphatase (ALP) of 150 U/L (ref range, 35-105 U/L), parathyroid hormone (PTH) intact of 7 pg/ml (ref range, 15-65 pg/ml), and 25-hydroxy vitamin D level of 28.1 ng/ml (ref range 30-80 ng/ml). A 1,25-dihydroxy vitamin D level was not checked. CT of the abdomen without contrast revealed fatty infiltration predominantly of the right lobe of the liver and two hypodense lesions, one at hepatic segment V (largest diameter of 8 cm) and another at hepatic segment VI (largest diameter of 3.4 cm). On the day of discharge, she had a calcium level of 10.6 mg/dl and a creatinine of 0.89 mg/dl. She was discharged with oral ciprofloxacin and 800 units of cholecalciferol daily in addition to her regular outpatient medications.
On presentation to our hospital, her initial vitals were temperature 98.3˚F, heart rate of 81 beats/minute, respiratory rate of 18 cycles/minute, blood pressure of 142/65 mmHg, and oxygen saturation of 100% on ambient air. Physical examination was notable for a cachectic, non-toxic appearing woman with altered mentation. Otherwise, physical examination was unremarkable. Initial laboratory data were notable for a blood urea nitrogen (BUN) of 19 mg/dl, creatinine of 1.5 mg/dl, calcium level of 16.7 mg/dl, albumin of 3.4 g/dl ref (3.9-4.9 g/dl), hemoglobin of 9 g/dl, mean corpuscular volume (MCV) of 79 fl, and ALP of 175 U/L. Bilirubin, aspartate transaminase (AST), and alanine aminotransferase (ALT) were normal. CT head was negative for any acute pathology.
A work-up for hypercalcemia showed a low serum intact PTH of 8 pg/ml (ref range 15-65 pg/dl) and a low parathyroid hormone related peptide (PTHrP) of <2 pmol/L. 1,25 dihydroxy vitamin D was elevated at 81 pg/ml (ref range 19.9-79.3 pg/dl). The patient was admitted and treated for vitamin D dependent hypercalcemia with IV 0.9% sodium chloride infusion, subcutaneous calcitonin, and zoledronate infusion. Calcium levels were closely monitored and gradually trended down. Serum immunofixation did not identify a monoclonal band, and both serum and urine protein electrophoresis were normal.
CT of the abdomen was performed and showed two adjacent hypoenhancing large masses in the right hepatic lobe with central areas of hypodensity/necrosis: one at segment V measuring approximately 8.8 × 7.1 × 5.7 cm, while the other at segment VI measuring 6 × 5.8 × 5.3 cm (Figure ). Alpha-fetoprotein (AFP) and carcinoembryonic antigen (CEA) levels were normal. Because the initial impression was concerning for hepatocellular carcinoma, a triphasic CT scan of the liver was done but provided no definitive diagnosis. Viral hepatitis serologies were also negative. A CT of the chest was unremarkable.
Percutaneous liver biopsy under ultrasound guidance was then pursued. Histology, immunohistochemistry (Figure ), and fluorescent in situ hybridization (FISH) report (Figure ) showed diffuse proliferation of atypical cells positive for CD10, BCL-2, and BCL-6 with low C-myc positivity, consistent with large B cell lymphoma. The patient was evaluated by the inpatient oncology team for chemotherapy. She was discharged five days later and is currently receiving rituxan-cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone (R-CHOP regimen).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [82, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Female'}",33.24516,31.5829,34.90742,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 82 years old. The concentration of Creatinine is 1.5 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.5^(-1.154) * 82^(-0.203) * 1 * 0.742=33.24516.
Hence, the patient's GFR is 33.24516 mL/min/1.73m²."
3164,9,MDRD GFR Equation,lab test,decimal,pmc-3741982-1,Extracted,"A 54-year-old male was seen in our nephrology clinic for progressive increase in his serum creatinine from 1.38 to 3.66 mg/dl over 9 months. There was no history of fever, diarrhea, steatorrhea, urinary tract symptoms, renal stones, or use of nephrotoxic agents. His past medical history included hypertension for 15 years, type 2 diabetes for 11 years, obstructive sleep apnea, depression, and treated cellulitis. He had undergone a duodenal switch procedure for morbid obesity (body mass index >50 kg/m2) 20 months earlier. Subsequently, he had lost more than 100 kg of body weight, and there was significant improvement in the control of blood pressure, sleep apnea, and blood sugar. His serum creatinine was 1.38 mg/dl and urinalysis was normal at the time of surgery.
His clinical examination was unremarkable. Laboratory investigations showed hemoglobin of 9.9 g/dl, white cell count of 6.9 × 103/μl, blood urea nitrogen of 51.82 mg/dl, and serum creatinine of 3.66 mg/dl. Serum electrolytes, calcium, phosphate, and bicarbonate were within normal limits. Urinalysis showed 5-10 white cells/hpf and 1-2 white cell casts without any proteinuria or hematuria. Ultrasound of kidneys showed normal sized kidneys with a few small bilateral calculi without any evidence of obstruction. Doppler of renal arteries was normal.
In view of progressive unexplained increase in creatinine, a kidney biopsy was done. The kidney biopsy [Figures and ] demonstrated 13 glomeruli of which six were globally sclerosed. The remaining glomeruli were histologically normal. The tubular interstitial compartment showed foci of tubular damage with deposition of translucent crystals of different shapes which are predominantly intraluminal with few intracellular and focal interstitial distributions. Under polarized light, the deposits appeared strongly birefringent forming fan-like, sheaf-like, or irregular shapes consistent with calcium oxalate crystals. There was an associated mild interstitial inflammation with moderate interstitial fibrosis and tubular atrophy. Blood vessels exhibited moderate arteriosclerosis and arteriolar hyalinosis. The immunofluorescence was negative and electron microscopy did not show any electron dense deposits but did reveal tubular damage with intratubular crystal deposition. His 24-h urinary oxalate level was found to be significantly elevated at 98.7 mg/day (normal range upto 40 mg/day). Urinary calcium and citrate were undetectable.
A diagnosis of oxalate nephropathy secondary to enteric hyperoxaluria post-duodenal switch operation was made and he was started on low-oxalate, low-fat diet, with high-fluid intake (>3 liters per day). In addition, he was prescribed calcium citrate 1000 mg tid with meals as an oxalate binder. He was also started on cholestyramine 4 g twice daily and repeat urine oxalate improved markedly to 63 mg/day and his serum creatinine stabilized.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [54, 'years'], 'creatinine': [3.66, 'mg/dL']}",17.42228,16.55117,18.29339,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 54 years old. The concentration of Creatinine is 3.66 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.66^(-1.154) * 54^(-0.203) * 1 * 1=17.42228.
Hence, the patient's GFR is 17.42228 mL/min/1.73m²."
3165,9,MDRD GFR Equation,lab test,decimal,pmc-4329376-1,Extracted,"A 68-year-old female was admitted to the hospital because of a 5-day history of left pleuritic chest pain. She had no other relevant medical history except for a ten-year history of hypertension. On admission, her blood pressure was 146/70 mm Hg and her body temperature was 36.9℃. Physical examination was unremarkable, and urinalysis did not reveal any abnormal findings. Laboratory findings were as follows: hemoglobin 11.7 g/dL, hematocrit 32.7%, blood urea nitrogen (BUN) 6.9 mg/dL, serum creatinine 0.74 mg/dL, sodium 130 mEq/L, potassium 3.9 mEq/L, total protein 5.6 g/dL, albumin 3.9 g/dL, and total cholesterol 167 mg/dL. According to chest X-ray, a pleural effusion was present in the left lower lobe. The pleural fluid (PF) was exudative, and PF analysis showed a pH of 7.4, total protein of 5800 mg/dL, albumin of 3200 mg/dL, lactate dehydrogenase of 679 IU/L, and glucose of 92 mg/dL. In addition, the white blood cell (WBC) count was 3879/mm3 with 99% mononuclear cells, and adenosine deaminase (ADA) was shown to be 104.0 IU/L in the PF. Pleural biopsy and pleural cytology were negative for malignancy. Based on the exudative characteristics and the high ADA level in the PF, pleural tuberculosis was suspected and anti-tuberculosis treatment was started. Treatment comprised rifampicin 600 mg/day, isoniazid 300 mg/day, ethambutol hydrochloride 1200 mg/day, and pyrazinamide 1500 mg/day.
During the 4-week anti-tuberculosis therapy regimen, the patient developed nausea, vomiting, general weakness, and edema. Urinalysis revealed 4+proteinuria with a few transitional epithelial cells, some coarse granular casts, and many mucous threads. According to a 24-h urine collection, protein and albumin values were 9.2 and 6.2 g/day, respectively. Laboratory findings were as follows: hemoglobin 12.1 g/dL, WBC 5490/mm3, BUN 33.2 mg/dL, serum creatinine 1.36 mg/dL, creatinine clearance 39 mL/min, total protein 5.6 g/dL, albumin 2.4 g/dL, serum aspartate aminotransferase 282 IU/L, alanine aminotransferase 282 IU/L, normal total bilirubin, and a total cholesterol of 283 mg/dL. Antinuclear antibody and P-anti-neutrophil cytoplasmic antibody (ANCA) and C-ANCA were all negative with normal serum complement levels.
According to a renal biopsy, MCD was present with focal thinning of the glomerular basement membrane (). Non-sclerotic glomeruli were normocellular without mesangial expansion, and the tubules showed minimal atrophy and mild focal tubular injury. Additionally, the interstitium was widened by minimal fibrosis, and no depositions of immunoglobulins or complement components were observed in the glomeruli. Electron microscopy showed the podocyte foot processes to be diffusely effaced ().
Due to toxic hepatitis, rifampicin and isoniazid were discontinued, but ethambutol hydrochloride and pyrazinamide were maintained. Moxifloxacin was added after 1 week, and isoniazid was added after 2 weeks. The pleural tuberculosis was well controlled with isoniazid, ethambutol hydrochloride, and moxifloxacin thereafter.
When her diagnosis was confirmed to be MCD, we determined to use steroid therapy at first. However, she was afraid of adverse effects of steroid treatment and asked us to observe closely. Moreover, we found out that heavy proteinuria was developed after using anti-tuberculosis agents. In addition, hepatitis also occurred after anti-tuberculosis agents started, and then we had to stop rifampicin and isoniazid agents. Fortunately, she improved spontaneously without steroid use only after quitting rifampicin. Therefore, we observed and followed up continuously. Her nausea, vomiting, and general edema improved and her body weight recovered from 68 kg to 63 kg at 3 weeks after rifampicin discontinuation, and a random urine protein-to-creatinine ratio was 0.14 at 8 weeks (). Furthermore, her serum albumin and cholesterol levels were shown to be 3.9 g/dL and 180 mg/dL, respectively, 8 weeks after stopping rifampicin.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [68, 'years'], 'sex': 'Female', 'creatinine': [1.36, 'mg/dL']}",38.66685,36.73351,40.60019,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 68 years old. The concentration of Creatinine is 1.36 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.36^(-1.154) * 68^(-0.203) * 1 * 0.742=38.66685.
Hence, the patient's GFR is 38.66685 mL/min/1.73m²."
3166,9,MDRD GFR Equation,lab test,decimal,pmc-7501118-1,Extracted,"A 15-year-old girl with a recent diagnosis of Crohn’s disease was admitted to Emma Children’s Hospital with complaints of right lower quadrant abdominal pain, nausea, anorexia, and reduced urine output with anuria for the last 8 h. She had no fever and no diarrhea. She had lost 5 kg in weight during the past month but put on again 1.5 kg in the last week.
On admission, her blood pressure was mildly elevated to 127/90 mmHg (95–99th percentile), with a heart rate of 90 BPM. Her height was 155 cm and weight 41.5 kg. On physical examination, she was well appearing, with right lower quadrant and bilateral flank tenderness. She had no rash, no edema, and normal capillary refill. Laboratory tests showed a hemoglobin of 10.5 mg/dL (5.2 mmol/l), thrombocytosis of 930,000 per microliter, leukocytosis of 12,300 per microliter, with an absolute neutrophil count of 9800 per microliter, and normal eosinophil count (40 per microliter). C-reactive protein was 38 mg/L. Serum creatinine was elevated to 2.5 mg/dL (220 micromol/L), blood urea nitrogen was normal (10.3 mg/L, i.e., 3.7 mmol/L). Albumin was 3.8 g/dL (38 g/L), phosphorus 5.1 mg/dL (1.65 mmol/L), sodium 135 mmol/L, and potassium 4.1 mmol/L. Blood gases were normal with a bicarbonate of 24 mmol/L.
Her urine sediment was positive for leukocytes (244 per microliter) and epithelial cells, with no RBC, casts, or crystals. There was moderate proteinuria with a protein/creatinine ratio of 0.9 mg/mg (104 mg/mmol). Urine sodium was < 20 mmol/L, and urine urea 43 mmol/L, with fractional excretions of 0.6% and 43%, respectively. Urine osmolality was 118 mOsmol/kg. Abdominal ultrasound showed stable ileocecal inflammation and normal renal size and structure. Urine culture was sterile.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [15, 'years'], 'creatinine': [2.5, 'mg/dL'], 'sex': 'Female'}",26.02991,24.72841,27.33141,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 15 years old. The concentration of Creatinine is 2.5 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.5^(-1.154) * 15^(-0.203) * 1 * 0.742=26.02991.
Hence, the patient's GFR is 26.02991 mL/min/1.73m²."
3167,9,MDRD GFR Equation,lab test,decimal,pmc-6656662-1,Extracted,"A 62-year-old woman with a history of stage IIIa chronic kidney disease (CKD) was referred to our hospital for rapidly worsening renal function with hyperkalemia and metabolic acidosis. Her baseline creatinine level was 1.5 mg/dL but had increased to 5.62 mg/dL over a period of 4 mo.
She has noticed bilateral lower-extremity edema and dyspnea on exertion 2 wk prior to the presentation. She denied any hemoptysis, chest pain, nausea, or vomiting. She had two episodes of epistaxis about a month prior to admission. She had two admissions over the prior 6 mo for hypertensive encephalopathy and influenza pneumonia with hypoxemic respiratory failure. There was no history of any invasive vascular procedures, use of radio-contrast agents, or treatment with anticoagulants or thrombolytic agents.
Her relevant medical history included poorly controlled hypertension, hyperli-pidemia, transient ischemic attack (TIA), diastolic heart failure, reactive airway disease, nephrolithiasis status post-lithotripsy, and osteoarthritis with nonsteroidal anti-inflammatory drug usage.
She reported no family history of renal disease or thrombosis. She was a non-smoker and not a current alcohol user.
Her vitals were within normal limits and physical exam was normal except for bilateral lower-extremity edema and diminished breath sounds at the lung bases.
Laboratory examination revealed normocytic normochromic anemia, serum eosino-philia (10%), hyperkalemia, metabolic acidosis, elevated creatinine (5.2 mg/dL), and elevated blood urea nitrogen (69 mg/dL). Urinalysis showed few red blood cells (RBCs), granular casts, and microalbuminuria and was negative for eosinophil and red cell casts. Serology was positive for antineutrophil antibody, anti-cardiolipin IgM antibody, and c-ANCA; 1:320.
Liver function tests, troponins, creatinine kinase, serum magnesium, calcium, HbA1c, complement levels (C3, C4), serum immunoglobulin levels, coagulation studies including prothrombin time, protein C, S levels/activity, antithrombin III activity, and lupus anticoagulant were within normal limits. Additionally, D-dimer was positive, and factor V Leiden mutation was negative.
Her perinuclear ANCA, atypical pANCA, anti-histone antibodies, anti-double-stranded DNA antibodies, anti-glomerular basement membrane antibodies, myeloma panel (serum and urine protein electrophoresis and immunofluorescence), viral panel (hepatitis B, C; HIV serology), and urine toxicology tests were negative.
A retroperitoneal ultrasound showed diffuse cortical thinning suggestive of medical renal disease but negative for obstructive uropathy. Non-contrast-enhanced com-puted tomography of the chest, abdomen, and pelvis was unremarkable except for diffuse atherosclerotic changes in the aortic arch. An electrocardiogram showed normal sinus rhythm, without any significant ischemic changes. A transthoracic echocardiogram showed a normal ejection fraction and was negative for atrial myxoma, vegetation, or intracardiac thrombi.
She was clinically volume overloaded and had no oliguria. She responded well with good urine output to intravenous diuretics. Hyperkalemia and metabolic acidosis were improved upon initial medical management. In the background of rapidly worsening renal function with a positive titer of ANCA and history of epistaxis, ANCA-associated vasculitis was suspected; thus, she was started on pulse therapy of IV methylprednisolone 1 g/d. A renal biopsy was postponed to day 4 after admission due to relative contraindications such as aspirin usage, poorly controlled hyperten-sion, and the patient’s inability to assume a prone position due to body habitus. Once she was medically optimized, an interventional radiologist performed the renal biopsy under anesthesia. She was discharged with prednisone 60 mg because the biopsy report was not yet available at the time of discharge.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [62, 'years'], 'creatinine': [5.2, 'mg/dL'], 'sex': 'Female'}",8.38144,7.96237,8.80051,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 62 years old. The concentration of Creatinine is 5.2 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 5.2^(-1.154) * 62^(-0.203) * 1 * 0.742=8.38144.
Hence, the patient's GFR is 8.38144 mL/min/1.73m²."
3168,9,MDRD GFR Equation,lab test,decimal,pmc-5398301-1,Extracted,"A 76-year-old man was admitted in June 2014 due to progressive deterioration of renal function, loss of appetite, and asthenia. Nine months prior to his admission (September 2013), he was diagnosed with effort angina and infrarenal abdominal aortic aneurysm. At the beginning of October 2013, he was found to have unprovoked PE for which he had received oral warfarin, delivering a prothrombin time-international normalized ratio (PT-INR) of 1.7 to 2.1 (reference range: 0.9-1.2) with a favorable clinical course. He had no history of renal disease, and steady serum creatinine (sCr) levels ranging between 0.96 and 1.12 mg/dL (reference range: 0.63-1.03 mg/dL) were noted until mid-December 2013. His sCr level was 1.89 mg/dL in mid-March 2014 and increased to 7.33 mg/dL in early June 2014. Therefore, he was referred and admitted to our hospital for further examination. His medical history included a diagnosis of acute myocardial infarction at 58 years of age. He had been a smoker for more than 40 years but denied the use of any drugs.
At the time of admission, the patient was alert and had a temperature of 36.4°C, a heart rate of 89 beats/min, and a blood pressure of 176/94 mm Hg. His physical examination revealed livedo reticularis on the soles of his toes and a blue-purple discoloration of all toes bilaterally (), whereas his feet were warm to the touch and the peripheral pulse remained intact. Laboratory examinations revealed the following: blood urea nitrogen (BUN), 64 mg/dL (reference range: 8-20 mg/dL); sCr, 7.23 mg/dL; white blood cell count, 9800/µL (reference range: 3900-9800/µL); eosinophils, 1092/µL (reference range: 0-400/µL); platelet count, 166 × 103/µL (reference range: 130-369 × 103/µL); erythrocyte sedimentation rate (ESR), 59 mm/h (reference range: 0-10 mm/h); serum albumin, 3.5 g/dL (reference range: 6.9-8.4 g/dL); triglycerides, 203 mg/dL (reference range: 40-185 mg/dL); low-density lipoprotein (LDL) cholesterol, 129 mg/dL (reference range: <139 mg/dL), fibrinogen, 410 mg/dL (reference range: 129-271 mg/dL); fibrin/fibrinogen degradation products, 13.5 µg/mL (reference range: 0-5 µg/mL); D-dimer, 5900 µg/L (reference range: 0-1500 µg/L); PT-INR, 1.76; C3, 104 mg/dL (reference range: 86-160 mg/dL); C4, 45 mg/dL (reference range: 17-45 mg/dL); and C-reactive protein, 0.49 mg/dL (reference range: 0-0.14 mg/dL). Tests for anti-neutrophil cytoplasmic antibodies, anti-glomerular basement membrane antibodies, hepatitis B virus surface antigen (HBsAg), anti-HBsAg antibodies, and antibodies to the hepatitis C virus were all negative. His urine was trace positive for protein, 2+ for occult blood, and contained 0.09 g of protein in a 24-hour specimen, whereas his creatinine clearance was 3.9 mL/min. The urinary excretion of β2-microglobulin and N-acetyl-beta-d-glucosaminidase was 22 856 µg/L (reference range: <200 µg/L) and 5.4 U/g·Cr (reference range: 0.9-2.4 U/g·Cr), respectively. A computed tomographic scan revealed a calcified thoracic aorta without a dimensional disorder and an infrarenal aortic aneurysm with a maximum diameter of approximately 4.4 cm. Diagnostic noncontrast-enhanced T2-weighted half-fourier-acquired single-shot turbo spin ecocho (HASTE) magnetic resonance imaging subsequently revealed hypointense areas and bright signals, which were suggestive of an atheromatous plaque consisting of lipids and fibrous tissues, respectively, in the abdominal aorta (). Oral warfarin was discontinued on admission, and the patient was subjected to empirical treatment with pravastatin at a dose of 10 mg/day combined with limaprost alfadex at a dose of 30 µg/day. A 5-mm-deep punch biopsy was performed on clinical day 7 within the territory of livedo reticularis on the lateral aspect of the left first toe. Typical biconvex needle-shaped empty spaces, suggestive of cholesterol clefts, were observed within the lumen of the arteriole in the subcutis (). A diagnosis of CES was made based on pathological and imaging findings as well as clinical manifestations.
Due to the elevated D-dimer level of 10 600 µg/L confirmed on clinical day 8, the decision was made to resume anticoagulation therapy despite our failure to detect deep venous thrombotic lesions using ultrasonography. The patient was treated with intravenous heparin and then switched to warfarin 2.5 mg/day on clinical day 30. Oral prednisolone (PSL) at a dose of 20 mg/day was also initiated on clinical day 22, resulting in the amelioration of eosinophilia and cutaneous manifestations within a few days and the subsequent stabilization of sCr levels at approximately 4.3 mg/dL. His elevated blood pressure was also controlled at approximately 120-130/70-80 mm Hg with irbesartan (100 mg/day) and amlodipine besilate (5 mg/day). However, sCr levels started to increase when PSL was tapered to 5 mg/day. The patient developed general fatigue, appetite loss, decline in urine output, and progressive swelling in both legs without any calf pain at the end of September 2014, with an elevated sCr level of 8.07 mg/dL, and was readmitted for further examinations. Similar to his initial admission, a laboratory analysis at this point revealed mild hypoalbuminemia (3.6 g/dL), whereas echocardiography and chest radiograph findings did not support the concurrent presence of heart failure. The relationship between deteriorated cutaneous manifestations and recurrent eosinophilia of 1365/µL resulted in the diagnosis of relapsed CES. The patient received hemodialysis (HD). After the resumption of an increased dose of PSL (15 mg/day) and the addition of a transient session of LDL apheresis (LDL-A) to the therapeutic regimen, his cutaneous manifestations improved and eosinophilia disappeared; however, severely deteriorated renal function did not recover, and he was finally started on a periodic HD program with favorable volume control ().","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [76, 'years'], 'creatinine': [8.07, 'mg/dL'], 'sex': 'Male'}",6.52681,6.20047,6.85315,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 76 years old. The concentration of Creatinine is 8.07 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 8.07^(-1.154) * 76^(-0.203) * 1 * 1=6.52681.
Hence, the patient's GFR is 6.52681 mL/min/1.73m²."
3169,9,MDRD GFR Equation,lab test,decimal,pmc-7583596-1,Extracted,"Herein, we present the case of a 37-year-old male RDEB patient admitted to our hospital. He had no genetic history, and no genetic tests were performed after admission. The patient experienced chronic blistering and erosion soon after his birth, continuing to admission to the hospital, resulting in scarring, contraction, and dactylosymphysis of the limbs. Repeated transplantation of cultured skin had been performed to treat skin defects. Chest radiography revealed cardiomegaly, and computed tomography showed narrowing of the abdominal aorta (the diameter was 12 mm at the bifurcation of the renal artery (normal—16 mm) and 13 mm at the splenic artery (normal—21 mm)), hepatomegaly and splenomegaly (). At 31 years old, squamous cell carcinoma (SCC) was detected at his skin ulcer, and he underwent radical surgery for recurrent SCC nine times. At 32 years old, there was marked deterioration of renal function and congestive heart failure. A renal biopsy was not performed because of the high risk to the patient, but a nephrologist diagnosed him with renal amyloidosis. His serum total protein level was 7.5 g/dL (normal 6.5–8.0 g/dL). The serum albumin level was 2.5 g/dL (normal 3.5–5.0 g/dL). The serum aspartate transaminase (AST) level was 12 U/L (normal <40 U/L). The serum alanine transaminase (ALT) level was 10 U/L (normal <35 U/L). The serum lactate dehydrogenase level was 110 IU/L (normal 100–230 IU/L). The serum C-reactive protein (CRP) level was 13.47 mg/dL (normal <0.30 mg/dL). The serum amyloid A (SAA) level was 1250 µg/mL (normal 0–8 µg/mL). The serum immunoglobulin G level was 2040 mg/dL (normal 800–1800 mg/dL). The serum rheumatoid factor level was 2 U/mL (normal <20 U/mL). Serum IL-1α and IL-1β levels were measured, but IL-1α levels were below the detection limit, and IL-1β was not significantly elevated, as compared with the normal control, which was partially due to the sensitivity of the system. The serum IL-18 level was 512.1 pg/mL (healthy control: 90.8 pg/mL), and the IL-17A level was more than five-time higher compared to healthy controls (data not shown). The serum creatinine level was 4.65 mg/dL (normal 0.60–1.40 mg/dL). The 24-h urinary protein level was 2.24 g/day (normal 0.02–0.06 g/day). Two years after the deterioration of his renal function, he started treatment with artificial hemodialysis. At 37 years old, he died due to the progression of emaciation. This study was approved by the ethics committee of Mie University (#2684).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [37, 'years'], 'creatinine': [4.65, 'mg/dL'], 'sex': 'Male'}",14.27093,13.55738,14.98448,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 37 years old. The concentration of Creatinine is 4.65 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 4.65^(-1.154) * 37^(-0.203) * 1 * 1=14.27093.
Hence, the patient's GFR is 14.27093 mL/min/1.73m²."
3170,9,MDRD GFR Equation,lab test,decimal,pmc-6374990-1,Extracted,"A 39-year-old female presented with complaints of generalized abdominal distension, weight loss, swelling of legs, and muscle weakness extant for several weeks. Her past medical history was significant for a well-controlled HIV infection of 6 years on highly active anti-retroviral therapy, hypertension, ESRD secondary to HIV-associated nephropathy, and secondary hyperparathyroidism. She was a non-smoker and had no history of alcohol or drug abuse. Her initial renal biopsy revealed collapsing focal glomerular sclerosis, microcystic dilation of renal tubules, lymphocytic interstitial infiltrates, and interstitial fibrosis. She received chronic cycler-assisted peritoneal dialysis (PD) for 5 years and was well controlled clinically regarding uremic and volume status with no abnormalities regarding color, viscosity, or volume of exchanges. Subsequently, she was transitioned to intermittent hemodialysis (HD) due to personal preferences. A few weeks after the transition to intermittent HD, ascites of unclear etiology developed, ultimately requiring repeated large-volume paracentesis with ~ 5 – 7 L ascitic fluid removals every other week.
There were no associated symptoms of coughing, palpitations, or shortness of breath. She was chronically anuric. Vital signs showed blood pressure of 160/80 mmHg, heart rate 74 beats/min (regular), respiratory rate 16/min and temperature 36.9 °C. Oxygen saturation was 98% on ambient room air. Her physical examination was remarkable for moderate ascites and edema of the lower extremities. Otherwise neurological, respiratory, and cardiovascular examinations were normal without organomegaly and without clinical stigmata or symptoms of chronic liver disease or heart failure.
Laboratory investigations showed normocytic, normochromic anemia with a hemoglobin of 10 g/dL and uncorrected serum calcium of 8.6 mg/dL. Other labs were as follows: CD4 T-cell count: 600/mm3, HIV viral load: 986 copies/mL (reference: < 40 copies/mL), serum creatinine: 10.3 mg/dL, aspartate aminotransferase: 13 U/L (normal range: 5 – 34 U/L), alanine aminotransferase: 17 U/L (5 – 45 U/L), bilirubin: 0.4 mg/dL, prothrombin time INR: 1.01, serum albumin: 2.3 mg/dL, serum amylase: 105 IU/L (27 – 130 U/L), serum lipase: 40 IU/L (8 – 78 U/L). Her tumor antigens (Ag) were within reference range for cancer antigen (CA) 15-3 and CA19-9. CA 125 levels were repeatedly elevated (197 – 416 U/mL (normal: < 34.9 U/mL)), but no further follow-up was obtained. Analysis of the ascites fluid showed an albumin level of 1.5 g/dL and protein of 3.5 g/dL. The serum-to-ascites albumin gradient was < 1.1 excluding portal hypertension as a cause of ascites. The culture of peritoneal fluid was negative for acid-fast bacilli. There were no fungi seen by calcofluor white stain. Histoplasma Ag and Aspergillus Ag were negative. The pancreas was reported normal on computed tomography. Her β-2 microglobulin was elevated to 47.30 mg/L (normal: 0.80 – 2.3). Serum protein electrophoresis showed hypoalbuminemia and decreased total protein, with minimal monoclonal M-component only (IgG-κ 0.30 g/dL in the γ zone). Immunofixation electrophoresis showed polyclonal immunoglobulins (Ig) with polyclonal light chains. κ and λ light chains were increased to 66.86 mg/dL (normal: 0.33 – 1.94) and 18.55 mg/dL (normal: 0.57 – 2.63), respectively, yielding a ratio of 3.6 (normal: 0.26 – 1.65) (). Ascitic fluid analysis showed a marked increase in plasma cells with an abnormal κ : λ ratio, i.e., > 5 : 1.
Liver biopsy was essentially normal, hence an omental biopsy was performed which on immunohistochemistry showed similar findings as the ascitic fluid with predominant κ and faint λ staining (). Multiple myeloma work-ups with skeletal surveys revealed no focal osseous lesions, apart from the osseous changes of hyperparathyroidism. Accordingly, the diagnosis of omental EMP with malignant ascites was established. Omental resection and radiation were offered to the patient, but she refused further intervention. Two years of follow-up, she remained stable without any further complication, apart from requiring regular paracenteses.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [39, 'years'], 'creatinine': [10.3, 'mg/dL'], 'sex': 'Female'}",4.18448,3.97526,4.3937,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 39 years old. The concentration of Creatinine is 10.3 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 10.3^(-1.154) * 39^(-0.203) * 1 * 0.742=4.18448.
Hence, the patient's GFR is 4.18448 mL/min/1.73m²."
3171,9,MDRD GFR Equation,lab test,decimal,pmc-7570767-3,Extracted,"A 56-year-old male presented to the ED with fever, hypotension, and altered mental status. His nursing home stated he was unusually drowsy with episodes of oxygen desaturation down to 60% with shallow breathing and unresponsiveness. His medical history was significant for hypertension, congestive heart failure, and schizoaffective disorder. On presentation, the temperature was 37.8 C, the blood pressure 67/42 mmHg, the pulse 76 beats/min, the respiratory rate 20 breaths/min, and oxygen saturation 60% on ambient air. He was unresponsive to painful stimulation. Labs were notable for thrombocytopenia (77k/µL), absolute lymphopenia (0.49k/µL), blood urea nitrogen of 53 mg/dL, and creatine of 1.9 mg/dL. Initial chest X-ray () revealed bilateral patchy infiltrates in middle and lower lung fields consistent with pneumonia. Norepinephrine drip and fluids were given for management of hypotension. Given his low oxygen saturation, he was intubated for mechanical ventilation and admitted to the critical care floor. Nasopharyngeal swab for SARS-CoV-2 RT-PCR was negative. On hospital day 3 of admission, another nasopharyngeal swab was sent and returned positive for SARS-CoV-2. On day 7, he was extubated following a spontaneous breathing trial with oxygen saturation 99% on 4 L of nasal cannula. At the time of writing, during day 8, he had symptomatic improvement while saturating at 96% oxygen on ambient air.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [56, 'years'], 'creatinine': [1.9, 'mg/dL'], 'sex': 'Male'}",36.85312,35.01046,38.69578,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 56 years old. The concentration of Creatinine is 1.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.9^(-1.154) * 56^(-0.203) * 1 * 1=36.85312.
Hence, the patient's GFR is 36.85312 mL/min/1.73m²."
3172,9,MDRD GFR Equation,lab test,decimal,pmc-6323504-2,Extracted,"A 64-year-old male presented from clinic after routine lab monitoring showed new AKI and hyperkalemia. He was asymptomatic other than fatigue with no prior history of kidney disease. Past medical history was significant for hypertension, gout, and cholangiocarcinoma diagnosed in 2003. His cancer was in remission after chemotherapy and surgical interventions including complete excision of the extrahepatic biliary tree, Roux-en-Y hepaticojejunostomy, and cholecystectomy. He developed chronic pancreatitis and insulin-dependent diabetes postoperatively. Pertinent medications included losartan, triamterene-hydrochlorothiazide, and insulin. Admission vitals were notable for BP 165/71 and he was euvolemic on physical exam.
Laboratory workup revealed stage 3 nonoliguric AKI with serum creatinine of 4.61 mg/dL elevated from a stable baseline of 0.94 mg/dL. Supporting labs included elevations in potassium (5.4 mEq/dL), phosphorus (6.9 mg/dL), uric acid (10.5 mg/dL) and low bicarbonate (16 mEq/L), normocytic anemia (hemoglobin 9.9 g/dL), and hypoglycemia (blood sugar 32 mg/dL). CA19-9 was elevated to 51, but this was stably elevated and not felt secondary to signify recurrent disease. His hemoglobin A1C was 5.4%. Urine analysis showed 2-3 WBC/hpf. The etiology of his AKI was unclear but AIN was considered given his use of triamterene and leukocytes on urine microscopy.
Subsequent renal biopsy showed severe, chronic active interstitial nephritis, severe interstitial fibrosis and tubular atrophy, and oxalate nephropathy (). The oxalate nephropathy was believed secondary to enteric hyperoxaluria due to fat malabsorption from chronic pancreatitis and Roux-en-Y bypass. Followup 24-hour urine collection showed high oxalate excretion (90 mg) with low calcium (53 mg) and citrate (<28 mg) consistent with hyperoxaluria. 24-hour fecal fat was elevated at 26.3 g suggesting pancreatic insufficiency. Intermittent hemodialysis was initiated. He was started on a low oxalate diet with supplementation of pancrelipase, calcium citrate, and potassium citrate. Serum oxalate improved from 11.0 μmol/L to 7.9 μmol/L with these interventions. Serum creatinine peaked to 5.37 mg/dL before plateauing with cessation of dialysis. After further education and diet changes, his creatinine improved and plateaued to 3.57 mg/dL two years after admission.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [64, 'years'], 'creatinine': [3.57, 'mg/dL'], 'sex': 'Male'}",17.32225,16.45614,18.18836,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 64 years old. The concentration of Creatinine is 3.57 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.57^(-1.154) * 64^(-0.203) * 1 * 1=17.32225.
Hence, the patient's GFR is 17.32225 mL/min/1.73m²."
3173,9,MDRD GFR Equation,lab test,decimal,pmc-5487311-1,Extracted,"A 63-year-old Vietnamese male with end stage renal disease due to IgA nephropathy received an expanded criteria deceased donor kidney transplant (DDKT) in 2012 (5 antigen mismatch, 5% panel reactive antibody, PRA). He received induction with alemtuzumab and solumedrol and was maintained on tacrolimus and mycophenolate mofetil. There were no surgical complications or episodes of acute rejection in the post-transplant period. Allograft function stabilized with a serum creatinine (Cr) of 1.8 mg/dL. His past medical history was notable for incarceration in Vietnam, prior hepatitis B exposure with protective anti-Hepatitis B surface antibody, positive tuberculin skin test (TST) and a non-calcified nodule on chest X-ray (CXR). He had been in the United States for twenty years prior to his transplant. He did not receive isoniazid (INH) prophylaxis before undergoing kidney transplant. At one-year post-transplant, he was admitted with fever, palpitations and 3 cm non-tender submental lymph node. Labs were notable for acute kidney injury (AKI) with Cr of 3 mg/dL and urinary retention that resolved with urinary catheter placement and treatment for an enlarged prostate. CXR revealed bilateral pleural effusions and a large pericardial effusion. Fine needle aspiration of the lymph node and pericardial fluid grew Mycobacterium tuberculosis (MTB). He received anti-tubercular therapy (ATT) with 2 mo of Rifampin, INH, Pyrazinamide and Ethambutol (RIPE) and 4.5 mo of INH and Rifampin (IR). His treatment course was complicated by transaminitis with reactivation of hepatitis B leading to end stage liver disease. He was treated with tenofovir with resolution of transaminitis. Patient completed 6.5 mo of ATT and has been cured of TB. His kidney transplant failed three years later due to BK nephropathy, and he was initiated on hemodialysis.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [3.0, 'mg/dL'], 'sex': 'Male', 'Race': 'Asian'}",21.24095,20.1789,22.303,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 63 years old. The concentration of Creatinine is 3.0 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.0^(-1.154) * 63^(-0.203) * 1 * 1=21.24095.
Hence, the patient's GFR is 21.24095 mL/min/1.73m²."
3174,9,MDRD GFR Equation,lab test,decimal,pmc-7886295-1,Extracted,"Renal dysfunction was diagnosed in a 70-year-old man who visited our hospital for a medical checkup. His serum creatinine level and creatinine clearance rate were 8.78 mg/dL (normal range: 0.53–1.02 mg/dL) and 8 mL/min (normal range: 80–180 mL/min), respectively. He was diagnosed with Bence–Jones protein λ-type multiple myeloma based on the presence of 40% plasma cells in his bone marrow (10% or more of plasma cells is considered definitive of the disease) and Bence–Jones proteinuria (M proteinuria of 4.8 g/day). Additionally, the diagnosis of symptomatic multiple myeloma (International Staging System stage 3) was based on the presence of renal dysfunction. Renal biopsy revealed cast nephropathy known as myeloma kidney, in which large amounts of Bence–Jones proteins formed casts that blocked the tubules (). BD therapy was initiated with concurrent VACV for herpes zoster prophylaxis. We administered a reduced dose VACV of 500 mg three times a week because of the patient’s renal impairment, based on the drug information on VACV provided in the UpToDate database. His renal function was monitored twice per week during therapy. Six weeks later, during his second course of BD therapy, the patient was hospitalized because of impaired consciousness. He displayed no other symptoms during hospitalization.
On admission, his vital signs were as follows: Glasgow Coma Scale score, E2, V4, M4; body temperature, 36.5°C; blood pressure, 145/79 mmHg; pulse rate, 73 beats/min; respiratory rate, 15 breaths/min; and SpO2, 96%. His vital signs were normal, and there were no remarkable neurological abnormalities except for disturbance of consciousness. summarizes the results of patient’s blood test on admission. The results, including renal function, were unchanged. Brain magnetic resonance imaging and cerebrospinal fluid analysis—cell counts 1/µL, protein 40 mg/dL, glucose 98 mg/dL, reference blood glucose level 125 mg/dL—revealed no abnormalities. There was no new electrolyte, endocrine hormone abnormality, or suggestion of epilepsy. Therefore, we suspected drug-induced disturbance of consciousness and suspended the BD and VACV therapy. Three days after discontinuing the drugs, his level of consciousness returned to normal, and the BD therapy was restarted after 20 days of drug interruption. The Naranjo score for estimating the probability of adverse drug reactions was 7 points. In this scoring system, ≥ 9 points indicate “high probability for adverse reactions” and 5–8 points indicate “probability for adverse reactions”. In all Japan, the laboratories do not have facilities to measure ACV/CMMG levels. Though his blood level of ACV could not be measured, the clinical diagnosis was ACV neurotoxicity based on his response to the suspension of the therapy, the high Naranjo score, and the lack of other contributing factors. We theorized that ACV blood levels gradually increased over the long-term administration of oral VACV owing to renal dysfunction. illustrates his clinical course.
The patient underwent 9 cycles of BD therapy and achieved complete remission. We administered 250 mg of famciclovir for herpes zoster prophylaxis, three times a week, between cycles 4 to 9. One year after the end of treatment, he remained in remission. His creatinine level recovered and remained stable at 4–5 mg/dL in response to the treatment. He did not exhibit any sequelae of ACV encephalopathy.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [70, 'years'], 'creatinine': [8.78, 'mg/dL'], 'sex': 'Male'}",6.0213,5.72023,6.32237,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 70 years old. The concentration of Creatinine is 8.78 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 8.78^(-1.154) * 70^(-0.203) * 1 * 1=6.0213.
Hence, the patient's GFR is 6.0213 mL/min/1.73m²."
3175,9,MDRD GFR Equation,lab test,decimal,pmc-5438010-1,Extracted,"A 63-year-old white male, with a history of end-stage renal disease secondary to granulomatosis with polyangiitis (GPA), received a living donor kidney transplant in 1996. His past medical history included hypertension, coronary artery disease, gout, dyslipidemia, and obstructive sleep apnea. He was maintained on cyclosporine, with trough levels ranging from 80 to 100 µg/L, mycophenolate mofetil 500 mg 3 times a day, and prednisone 5 mg daily. In addition, the patient was on amlodipine, metoprolol, allopurinol, and lisinopril. Baseline creatinine was 1.5 – 1.7 mg/dL. There was no family history of rheumatoid arthritis (RA). Kidney biopsy done 3 years post-transplant was unremarkable.
10 years post-transplant he developed bilateral shoulder pain, subjective muscle weakness, and stiffness with an elevated erythrocyte sedimentation rate (ESR) above 100 mm/hg and was diagnosed with polymyalgia rheumatica (PMR). He was treated with prednisone 60 mg daily, which was gradually decreased to 40 mg daily with symptomatic improvement. Further attempts to decrease steroid dose were unsuccessful, as symptoms of muscle weakness and myalgias recurred. The patient was referred to our institution for further evaluation. Detailed musculoskeletal examination showed symmetrical synovitis over the proximal interphalangeal, metacarpophalangeal joints, and wrists. He had boutonniere and swan neck deformities of both hands and bilateral lower extremities edema. Cardiopulmonary and abdominal examinations were normal. Relevant laboratory results included serum creatinine 1.6 mg/dL, elevated inflammatory markers and rheumatoid factor (). IgG antibody against cyclic citrullinated peptide was weakly positive at 21 U/mL (< 5 µ/mL). Urine analysis was positive for albumin (300 mg/dL) without blood; protein to creatinine ratio was 6.8 g/g of creatinine.
Hand X-rays showed medial subluxation of the first metacarpophalangeal joints bilaterally with scattered poorly-defined erosions. Feet X-rays revealed erosions at the tarsometatarsal joints. Based on clinical presentation, laboratory, and radiologic findings, the patient was diagnosed with RA with PMR features. Based on the clinical symptoms and laboratory findings, the patient met the 1987 American College of Rheumatology (ACR) classification criteria and the 2010 ACR classification criteria for the diagnosis of rheumatoid arthritis. The patient denied a family history of autoimmune diseases.
The patient underwent transplant kidney biopsy for evaluation of proteinuria. Light microscopy showed moderate interstitial fibrosis and tubular atrophy in a pattern which was attributed to cyclosporine exposure accompanied by mild scattered interstitial lymphoplasmacytic infiltrate and scattered tubulitis. Glomeruli demonstrated basement membrane spikes on silver Jones-stained sections, and direct immunofluorescence showed diffuse and global fine granular staining in peripheral capillary loops for IgG (1+) and C3. Electron microscopy showed subepithelial and intramembranous electron-dense deposits consistent with immune complexes, with rare subendothelial and scattered mesangial deposits also identified. In all, biopsy findings were consistent with membranous nephropathy (MN). There was no histological evidence of relapse of GPA.
The patient underwent thorough work-up for other autoimmune diseases and malignancy considering the strong association of MN with these conditions. Antinuclear antibody, anti-double-stranded deoxyribonucleic acid antibody, complement (C3, C4, and CH-50) levels, antineutrophil cytoplasmic antibodies (P-ANCA, C-ANCA), prostate specific antigen, hepatitis panel, colonoscopy, CT of the chest, abdomen, and pelvis were all unremarkable.
The patient was started on methotrexate, while mycophenolate mofetil was discontinued and prednisone dose was tapered down to 10 mg daily. He remained on cyclosporine. After 4 – 6 weeks of therapy, joint pains and stiffness improved, but creatinine increased to 3.6 mg/dL. Repeated kidney transplant biopsy results were consistent with previous findings. Given the lack of alternative explanations for acute worsening of kidney function, methotrexate was discontinued and mycophenolate mofetil was restarted at the dose of 750 mg twice a day. Kidney function improved. Approximately 3 weeks later, he presented with profound fatigue, synovitis over the proximal interphalangeal and metacarpophalangeal joints, and elevated inflammatory markers. Prednisone dose was increased to 40 mg daily and the patient was started on abatacept at the dose of 1,000 mg IV infusion every 4 weeks (weight: 120 kg), together with discontinuation of cyclosporine. 2 weeks after initiation of abatacept, his symptoms of myalgia, fatigue, and arthritis significantly improved. Prednisone was gradually tapered down to the current dose of 5 mg. Renal function stabilized (). 7 years post initiation of abatacept, his creatinine is 1.5 mg/dL, and urine protein to creatinine ratio is 0.4 g/g of creatinine, while rheumatoid arthritis continues to be in remission (). The patient remained on abatacept, 1,000 mg IV infusion every 4 weeks, mycophenolate mofetil 750 mg daily and prednisone 5 mg daily. Plain film radiographs repeated 5 years post original diagnosis showed no new joint erosions in hands or feet.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Male', 'Race': 'White'}",47.2675,44.90412,49.63088,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 63 years old. The concentration of Creatinine is 1.5 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.5^(-1.154) * 63^(-0.203) * 1 * 1=47.2675.
Hence, the patient's GFR is 47.2675 mL/min/1.73m²."
3176,9,MDRD GFR Equation,lab test,decimal,pmc-4541743-1,Extracted,"A 51-year-old Korean man was admitted to our hospital because of severe left flank pain, hematuria, and oliguria for 3 days. Additional complaints included epigastric discomfort and generalized weakness, but he denied fever or emesis. He had a medical history of hypertension for 1 year and TAO for 10 years with intermittent claudication. He had undergone amputation of both of his great toes 10 years prior because of gangrenous change due to TAO. At that time, lower extremity angiography showed that the flow of the right distal portion of the popliteal artery and the proximal portion of the tibiofibular artery were remarkably decreased by occlusion. The left superficial femoral artery was also occluded from its origin, at which collateral arteries had developed (Fig. ). He took beraprost for TAO but had not stopped smoking tobacco products. He had smoked approximately 1 pack per day for 30 years. Four years later, he underwent repeat angiography of his abdominal aorta and lower extremities because of worsening claudication. Occlusion of his left superficial femoral artery, bilateral tibial, and peroneal arteries had progressed. He had never been diagnosed with diabetes mellitus, collagen disease or cardiac disease.
Upon presentation, his blood pressure was 180/100mmHg, and his body temperature was 36.4°C. He complained of severe tenderness in his left costovertebral angle area. Raynaud’s toe, skin nodules and phlebitis were not observed.
Laboratory findings showed the following: white blood cell count (WBC) 9700/uL, hemoglobin (Hb) 12.7g/dL, platelets 201×103/uL, serum creatinine 14.02mg/dL, creatinine clearance 3.6ml/minute/1.73m2 according to the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula, β2 microglobulin 19.80mg/L, phosphorus 5.48mg/dL, intact parathyroid hormone (PTH) 329.5pg/mL, creatine phosphokinase (CPK) 74U/L and lactate dehydrogenase (LDH) 1687IU/L. Urine sediment contained 0 to 2 WBC and 3 to 5 red blood cells (RBC) per field. Urine protein electrophoresis revealed no paraprotein bands. The blood lipid profile, coagulation tests, protein C, protein S activity, complement fractions, antinuclear antibodies, rheumatoid factor, anti-Scl-70, anticardiolipin and antiphospholipid, and antineutrophil cytoplasmic antibodies were all negative or within normal limits. Electrocardiography and echocardiography were normal.
Contrast-enhanced abdominal computed tomography (CT) demonstrated left kidney enlargement (9.3cm) with a multifocal infarcted area and a shrunken right kidney (7.6cm). Neither renal artery was visualized (Fig. ).
Abdominal and lower extremity angiography was performed to examine his abdominal aorta and lower extremity arteries. The vascular status in both lower limbs and the viscera had worsened. His superior mesenteric artery, inferior mesenteric artery, both renal arteries, left common iliac artery, and left superficial femoral artery were not visualized, and the arteries below both his knees were occluded. Collateral vessels were well developed in his lower extremities. During examination, a stent was inserted into his left common iliac artery (Fig. ). Upper extremity angiographic CT showed no abnormal findings. His ankle-brachial index was 0.82 on the right and 0.61 on the left.
Renal failure associated with TAO progression was diagnosed. He started continuous ambulatory peritoneal dialysis (CAPD) and stopped smoking tobacco products. He was discharged with a daily oral anticoagulant, warfarin. Two months after discharge, he complained of postprandial abdominal pain without muscle guarding, preventing him from eating and resulting in an approximately 10kg weight loss. Upper gastrointestinal endoscopy revealed gastric mucosal atrophy; a follow-up contrast-enhanced abdominal CT showed colitis of the hepatic flexure and transverse colon, which was consistent with ischemic colitis. His vessel status had not changed compared with that at the prior examination (Fig. ). He changed his dialysis modality from CAPD to hemodialysis, which improved his pain. He recently reported abdominal pain with hypotension; however, after a decrease in his hypertension medications and an increase in body weight, his pain resolved.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [51, 'years'], 'creatinine': [14.02, 'mg/dL'], 'sex': 'Male', 'Race': 'Asian'}",3.74157,3.55449,3.92865,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 51 years old. The concentration of Creatinine is 14.02 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 14.02^(-1.154) * 51^(-0.203) * 1 * 1=3.74157.
Hence, the patient's GFR is 3.74157 mL/min/1.73m²."
3177,9,MDRD GFR Equation,lab test,decimal,usmle-8091,Extracted,"A 53-year-old woman presents to the emergency room with severe chest pain radiating to the back. She was diagnosed with acute aortic dissection. A few hours into the resuscitation, she was having oliguria. Laboratory findings show a serum creatinine level of 5.3 mg/dL.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [53, 'years'], 'creatinine': [5.3, 'mg/dL'], 'sex': 'Female'}",8.46447,8.04125,8.88769,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 53 years old. The concentration of Creatinine is 5.3 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 5.3^(-1.154) * 53^(-0.203) * 1 * 0.742=8.46447.
Hence, the patient's GFR is 8.46447 mL/min/1.73m²."
3178,9,MDRD GFR Equation,lab test,decimal,pmc-7963429-1,Extracted,"A 9-year-old boy was admitted to the Shenzhen People's hospital with kidney failure. The laboratory results are shown in Table . Samples and medical history were collected with the full informed consent of the patient and his parents in accordance with the declaration on the human genome prepared by the United Nations Educational Scientific and Cultural Organization. This study was approved by.
Urine analysis revealed the sample was occult blood + and protein ++. Serological analysis revealed elevated urea nitrogen, creatinine, and cystatin C (26.55 mmol/L, 719.0 μmol/L, and 3.56 mg/L, respectively). In addition, the CT examination of the urinary system revealed that the patient's left and right kidneys were 53 × 22 mm and 61 × 27 mm, respectively, indicating bilateral renal atrophy (Figure ). In addition, except for continuous nocturia, there were no obvious abnormalities on physical examination. In terms of treatment, the patient began continuous peritoneal dialysis after admission to relieve renal deterioration.
The patient had occasional chest tightness, palpitations (heart rate 113 bpm), no dyspnea, chest pain or discomfort, and exercise was not restricted under normal conditions. Hypertension, hyperlipidemia, pulmonary hypertension, and no atrial fibrillation. The results of echocardiography indicated a slight increase in left ventricular diameter (left ventricular end-diastolic diameter 56 mm and end-systolic diameter 34 mm), with a left ventricular ejection fraction of 60%. Mitral thickening and prolapse with severe regurgitation and tricuspid thickening and prolapse with mild regurgitation were also observed. The shape of the aortic sinus was acceptable, with an internal diameter of 34 mm. The calculated Z-value of the internal diameter of the aortic sinus was 3.1. The echocardiographic manifestations of the patient are shown in Figure .
The parents of the patient were not consanguineous and were in good health. The parents had a negative family history of heart and kidney disease. The mother had no special pregnancy history, and the patient was delivered naturally at term, with a birth weight of 2.9 kg, and no history of neonatal asphyxia or infection. No obvious abnormalities were detected in the outer court genetic metabolic screening and microarray comparative genomic hybridization analysis (Affymetrix Cytogenetics whole genome––2.7 M array).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [9, 'years'], 'creatinine': [719.0, 'µmol/L'], 'sex': 'Male', 'Race': 'Asian'}",9.95769,9.45981,10.45557,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 9 years old. The concentration of Creatinine is 719.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 719.0 µmol. To convert 719.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 719.0 µmol Creatinine * 1e-06 mol/µmol = 0.00072 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00072 mol Creatinine * 113.12 g/mol = 0.08145 g Creatinine. To convert 0.08145 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.08145 g Creatinine * 1000.0 mg/g = 81.45 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 81.45 mg Creatinine/10.0 dL = 8.145 mg Creatinine/dL. The concentration value of 719.0 µmol Creatinine/L converts to 8.145 mg Creatinine/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 8.145^(-1.154) * 9^(-0.203) * 1 * 1=9.95769.
Hence, the patient's GFR is 9.95769 mL/min/1.73m²."
3179,9,MDRD GFR Equation,lab test,decimal,usmle-8312,Extracted,"A 44-year-old woman presents with increased thirst and frequent urination that started 6 months ago and have progressively worsened. Recently, she also notes occasional edema of the face. She has no significant past medical history or current medications. The patient is afebrile and the rest of the vital signs include: blood pressure is 120/80 mm Hg, heart rate is 61/min, respiratory rate is 14/min, and temperature is 36.6°C (97.8°F). The BMI is 35.2 kg/m2. On physical exam, there is 2+ pitting edema of the lower extremities and 1+ edema in the face. There is generalized increased deposition of adipose tissue present that is worse in the posterior neck, upper back, and shoulders. There is hyperpigmentation of the axilla and inguinal areas. The laboratory tests show the following findings:
Blood
Erythrocyte count 4.1 million/mm3
Hgb 12.9 mg/dL
Leukocyte count 7,200/mm3
Platelet count 167,000/mm3
Fasting blood glucose 141 mg/dL (7.8 mmol/L)
Creatinine 1.23 mg/dL (108.7 µmol/L)
Urea nitrogen 19 mg/dL (6.78 mmol/L)
Urine dipstick
Glucose +++
Protein ++
Bacteria Negative
The 24-hour urine protein is 0.36 g.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [44, 'years'], 'creatinine': [1.23, 'mg/dL'], 'sex': 'Female'}",47.4319,45.0603,49.80349,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 44 years old. The concentration of Creatinine is 1.23 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.23^(-1.154) * 44^(-0.203) * 1 * 0.742=47.4319.
Hence, the patient's GFR is 47.4319 mL/min/1.73m²."
3180,9,MDRD GFR Equation,lab test,decimal,pmc-4818873-1,Extracted,"A 20-year-old Sri Lankan man diagnosed with end-stage renal failure associated with childhood steroid-resistant nephrotic syndrome underwent a renal transplant. His altruistic donor had ABO and human leukocyte antigen compatibility within acceptable limits. The patient was not sensitized and had received massive doses of immunosuppressants, including steroids, cyclosporine, tacrolimus, azathioprine, mycophenolate, and cyclophosphamide. He had severe growth retardation with height (1.45 m) and weight (26 kg) well below the third percentile, lack of secondary sexual characteristics, and cushingoid features. He had severe hypertension causing end-organ damage, retinopathy, and left ventricular hypertrophy. Control of his blood pressure had been challenging before the transplant.
He received induction immunosuppression keeping with local induction protocol (intravenous basilixumab 20 mg, cyclosporine 20 mg/kg/day, mycophenolate mofetil 25 mg/kg/day, and intravenous methylprednisolone 1 g). His cold and warm ischemia times were 60 and 24 minutes, respectively. Following surgery, he was managed in a high-dependency unit for monitoring and support. Standard immunosuppressive therapy was commenced thereafter.
The patient had poor urine output and became anuric 4 h after the transplant. Ultrasound-guided renal biopsy was carried out by a trainee nephrologist on the second day after the transplant to assess graft failure. Before the patient’s biopsy, his hemoglobin level was 117 g/L, his platelet count was 178,000/μl, his creatinine level was 563 μmol/L, and his international normalized ratio (INR) was 1.1. We used real-time ultrasound to guide the biopsy and a Bard® 18-gauge spring-loaded disposable gun (Bard Biopsy Systems, Tempe, AZ, USA) to collect tissue. With two firings of the gun, we obtained two tissue cores. The patient’s blood pressure before the biopsy was 160/100 mmHg, but postbiopsy it rose to 220/120 mmHg. Immediately after the procedure, the patient complained of severe suprapubic pain, and gross hematuria with clots was noted. Urgent surgical review was sought, and bladder irrigation was started via a cystostomy. The patient’s volume depletion was treated with crystalloids and packed red blood cell transfusions. His blood pressure was controlled with intravenous nitroglycerin and labetalol. Within a couple of hours, we were able to control the patient’s bleeding. However, he had three further episodes of bleeding amounting to 500–750 ml per episode, which was massive in relation to his body weight. Twelve units of blood were transfused in total to control his hypovolemia over the course of 60 h. Fortunately, the patient did not develop massive transfusion syndrome. His highest INR was 1.3, his longest activated partial thromboplastin time was 39.4 seconds, and his lowest platelet count was 130,000/μl. We did not obtain a thromboelastogram before the surgery, and desmopressin was not used preoperatively, in keeping with the local protocol.
A duplex ultrasound scan showed the presence of an iatrogenic, slender AVF (2–3 mm in width and 25 mm long) in close proximity to the biopsy tract (Fig. ), as well as a small, perinephric hematoma (not shown). The flow of the AVF was as great as 150 ml/minute and resulted in poor diastolic flow in the rest of the kidney. The pulsatile flow and high resistivity index of 1.0 presented a clinical picture similar to that of acute rejection (Fig. ). We planned to selectively embolize the feeding vessels of the AVF; however, the interventional radiology department of the National Hospital of Sri Lanka was experiencing technical difficulties, and selective embolization was possible only on the following morning. The patient developed another torrential bleed of 1250 ml in the evening on day 2, and an emergency graft nephrectomy appeared to be the only way to stop his bleeding. His skin was opened through the existing surgical incision, and we observed a profusely bleeding biopsy tract (Fig. ). A minor perinephric hematoma of about 100 ml was observed. The patient’s bladder was distended with clots and close to rupture. We were well aware of the anatomy of the AVF, which was slender. We decided to control the bleeding using local pressure (that is, by suturing the tract).
We used a #0 polyglactin 910 filament to suture the bleeding AVF with an encircling knot cutting through the renal parenchyma. The patient’s bleeding resolved, and pulsatile flow in the area surrounding the sutured segment (15 % of the surface area of the kidney) was absent. Suturing was hindered by edema of the surrounding parenchyma, as tight sutures tend to cut through the parenchyma. We evacuated clots via a cystostomy and inserted a suprapubic drain. The patient did not experience any further bleeding. A repeat duplex study showed obliteration of the AVF and change of the flow patterns (from monophasic to biphasic), suggestive of acute tubular necrosis (Fig. ). A renal biopsy confirmed the radiological diagnosis, and the patient was recommenced on hemodialysis. His urine output improved by day 16 posttransplant, and his creatinine levels reached a baseline of 116 μmol/L by day 20. He was discharged on day 22, and at his 18-month follow-up he was doing well, with a creatinine level of 108 μmol/L. His height, secondary sexual characteristics, and quality of life had improved. A repeat duplex scan done 6 weeks after the biopsy showed no features of AVF and excellent perfusion of the graft (Figs. and ).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [20, 'years'], 'creatinine': [108.0, 'µmol/L'], 'sex': 'Male', 'Race': 'Asian'}",74.04679,70.34445,77.74913,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 20 years old. The concentration of Creatinine is 108.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 108.0 µmol. To convert 108.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 108.0 µmol Creatinine * 1e-06 mol/µmol = 0.00011 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00011 mol Creatinine * 113.12 g/mol = 0.01244 g Creatinine. To convert 0.01244 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01244 g Creatinine * 1000.0 mg/g = 12.44 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 12.44 mg Creatinine/10.0 dL = 1.244 mg Creatinine/dL. The concentration value of 108.0 µmol Creatinine/L converts to 1.244 mg Creatinine/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.244^(-1.154) * 20^(-0.203) * 1 * 1=74.04679.
Hence, the patient's GFR is 74.04679 mL/min/1.73m²."
3181,9,MDRD GFR Equation,lab test,decimal,pmc-2858848-1,Extracted,"A 75-year-old male patient was emergently admitted to the hospital with gross hematuria, generalized abdominal pain, and oliguria of about 3 days' duration. He had undergone multimodal treatment for muscle-invasive bladder cancer (stage T2, urothelial cancer with sarcomatous differentiation) with transurethral resection (TUR) of the bladder tumor and 6 adjuvant cycles of cisplatin-based cytotoxic chemotherapy (gemcitabine+cisplatin) (), because he desired bladder preservation and had a strong fear of urinary diversion. One year after TUR, a follow-up CT scan showed bladder tumor recurrence with a focal irregular margin of the bladder wall, suggestive of perivesical invasion. So he underwent TUR of the bladder cancer (stage T2, urothelial cancer with squamous differentiation) () with adjuvant chemotherapy (methotrexate, vinblastine, Adriamycin, and cisplatin).
At 10 months after the operation, he presented with acute illness with vague abdominal pain. He was febrile at 39℃. He did not have a history of recent pelvic trauma, instrumentation, pelvic radiation, infravesical obstruction due to benign prostatic hyperplasia, or episodes of acute urinary retention. On the physical exam, the abdomen was markedly distended with muscular guarding and rebound tenderness. The urinary sediment contained many white blood cells and red blood cells. The blood test showed marked leukocytosis with an acute phase inflammatory reaction. The serum creatinine (Cr) level was elevated to 5.8 mg/dl with biochemical features of acute renal failure [K 5.7 mmol/l, Na 126 mmol/l, serum blood urea nitrogen (BUN) 53 mg/dl, BUN/Cr ratio 9:1]. The spiral CT showed a large bladder tumor extending into the perivesical space with a focal bladder wall disruption. The bladder tumor was nearly in contact with the anterior rectal wall without clear demarcation. Also, both kidneys showed moderate hydronephrosis.
We therefore first suspected an invasive bladder tumor with a rectovesical fistula and performed sigmoidoscopy and plain film cystography with retrograde contrast media injection through an indwelling urethral catheter. Sigmoidoscopy showed no signs of fistula opening within the site of 70 cm from the anal verge except for a mild segmental mucosal edema. Plain film cystography showed a refractory bowel pattern to paralytic ileus and left lateral wall irregularity with a suggestive sinus tract, but no evidence of intra- or extraperitoneal contrast media extravasation (). Despite many imaging studies, it was difficult for us to identify the cause of the acute peritonitis and biochemical features of acute renal failure. So we finally performed CT cystography with the patient in the prone position with 50 ml megluatmine iothalamate mixed in 500 ml of normal saline. The CT cystography showed the highly attenuated fluid in the peritoneum via a disrupted left lateral bladder wall and small bowel loop pooling with contrast media (). However, there was no direct communication between the urinary bladder and the rectum. Considering the patient's age, poor general condition, and performance status, we decided to manage him conservatively with broad-spectrum antibiotics and indwelling catheters. A 8.5 Fr pigtail drain catheter was inserted into the right pelvic area under the guidance of fluoroscopy in addition to percutaneous nephrostomy catheters for adequate urine drainage. After the insertion of the intraperitoneal drain catheter, 150 ml of turbid, yellowish urine with pus was drained. Culture of the drained intraperitoneal fluid confirmed Enterococcus as the causative pathogen. After intervention, the patient's serum creatine level and white blood cell count returned to normal values in 4 days. The patient was discharged home with successful peritonitis resolution on hospital day 28th but died 3 months later as the result of acute renal failure.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [75, 'years'], 'creatinine': [5.8, 'mg/dL'], 'sex': 'Male'}",9.58086,9.10182,10.0599,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 75 years old. The concentration of Creatinine is 5.8 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 5.8^(-1.154) * 75^(-0.203) * 1 * 1=9.58086.
Hence, the patient's GFR is 9.58086 mL/min/1.73m²."
3182,9,MDRD GFR Equation,lab test,decimal,pmc-7772176-1,Extracted,"A 76 year-old-man with DM controlled on metformin was admitted for a decline in his overall well-being. His friends reported he had become fatigued, forgetful, less involved, missed medications, and had lost some weight. He reported passing foul-smelling dark urine but denied dysuria, frequency, fevers, chills, or rigors. He denied abdominal pain, nausea, vomiting, or a history of recent urinary bladder instrumentation.
On admission, his oral temperature was 98°F, blood pressure was 166/94 mmHg, pulse was 66 beats per minute and the respiratory rate was 18 breaths per minute. His physical examination was unremarkable, and he was alert and oriented to person, place and year. Complete blood count was normal, but serum creatinine was 1.7 mg/dl. Other electrolytes, including sodium, were normal. His glycosylated hemoglobin was 5.6%. Computed tomography (CT) of the brain showed moderate to severe small vessel ischemic changes but no acute abnormality. Rapid plasma reagin (RPR) was negative, and vitamin B12 and thyroid-stimulating hormone levels were normal. Urinalysis revealed pyuria and urine culture grew > 100,000 CFU/mL Escherichia coli and Klebsiella pneumoniae. Blood cultures obtained on admission were negative. CT images of the chest, abdomen, and pelvis performed to rule out malignancy showed diffuse bladder wall thickening with air seen circumferentially within the bladder wall (Figures -).
Based on his clinical presentation, microbiologic and radiologic findings, he was diagnosed with emphysematous cystitis, a rare complication of lower urinary tract infection. He was initially treated with empiric intravenous piperacillin/tazobactam then discharged to a nursing facility on ertapenem (Escherichia coli strain was an extended spectrum beta-lactamase producer). A urinary catheter was inserted for effective bladder drainage, and he completed a total of 14 days of antibiotic therapy. After completion of antibiotic therapy, a repeat CT of the abdomen and pelvis showed complete resolution of the bladder wall emphysematous changes.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [76, 'years'], 'creatinine': [1.7, 'mg/dL'], 'sex': 'Male'}",39.38173,37.41264,41.35082,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 76 years old. The concentration of Creatinine is 1.7 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.7^(-1.154) * 76^(-0.203) * 1 * 1=39.38173.
Hence, the patient's GFR is 39.38173 mL/min/1.73m²."
3183,9,MDRD GFR Equation,lab test,decimal,pmc-4804144-1,Extracted,"Mild proteinuria had been incidentally detected in a 22-year-old woman during a regular health check-up 2 years prior to presentation. She visited a local clinic for a follow-up check. She took medication to treat hyperlipidemia for 1 year and did not take any other drugs including diuretics or laxatives. She was admitted to our hospital for evaluation of persistent mild proteinuria.
The prenatal course was unremarkable. On physical examination, her height was 153 cm, her body weight was 49 kg and her blood pressure was 100/60 mm Hg. No edema was found, and normal muscle strength and reflexes were noted. The rest of the physical examination was unremarkable. The laboratory examination revealed blood urea nitrogen of 10.9 mg/dL, creatinine of 0.68 mg/dL, sodium of 137 mmol/L, potassium of 2.59 mmol/L, chloride of 94.7 mmol/L, magnesium of 2.05 mEq/L, and bicarbonate of 31.2 mEq/L. Serum levels of IgG, IgA, IgM, C3, and C4 were normal. Anti-nuclear antibody was negative. Urinalysis showed a specific gravity of 1.007, trace protein, pH 8.0, and no red blood cells. The spot urine protein/creatinine ratio was 0.95 g/g creatinine. Abdominal sonography revealed normal-sized kidneys, without nephrocalcinosis or stones. Plasma renin activity was elevated at 27.98 ng/mL/hr (normal range, 0.50 to 1.90 ng/mL/hr in a supine position), but serum aldosterone was 13.2 pg/mL within normal limits (normal range, 1 to 16 pg/mL in a supine position). The urine prostaglandin E2 level was elevated at 2,815 ng/day (normal range, 400 to 620 ng/day). These findings suggested BS or pseudo-BS/GS caused by vomiting or diuretics.
Light microscopy of renal biopsy demonstrated 14 glomeruli, two of which were globally sclerotic. Most glomeruli appeared moderately increased in size and cellularity due to prominence of the mesangium and JGA. Five glomeruli showed marked enlargement with hyperplasia () and hypergranulosis of the JGA (). The mesangium was diffusely expanded due to mild to moderate increase in cells and matrix (). There was moderate tubular atrophy and interstitial fibrosis with infiltration of lymphocytes. The interlobular arteries and arterioles displayed mild to moderate intimal fibrous thickening and medial sclerosis. Immunofluorescence revealed weak positive (1+) staining for IgG, IgA, and fibrinogen and trace (+/–) of staining for C3 and lambda in the mesangium (). Electron microscopy revealed mild increase in the mesangial cells and matrix with rare small mesangial electron-dense deposits and hyperplastic juxtaglomerular cells with increased electron dense renin and progranules ().
Genetic analysis revealed a homozygous deletion of exon 1–14 and heterozygous deletion of exon 15–19 in the CLCNKB gene (). Her father had heterozygous deletion of exon 1–14 (), and her mother had heterozygous deletion of all examined exons of the CLCNKB gene (). However, her parents displayed no renal symptoms or abnormal renal function.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [22, 'years'], 'creatinine': [0.68, 'mg/dL'], 'sex': 'Female'}",108.19691,102.78706,113.60676,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 22 years old. The concentration of Creatinine is 0.68 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.68^(-1.154) * 22^(-0.203) * 1 * 0.742=108.19691.
Hence, the patient's GFR is 108.19691 mL/min/1.73m²."
3184,9,MDRD GFR Equation,lab test,decimal,pmc-4519609-1,Extracted,"A 62-year-old woman who provided written and signed consent to publish this case report was admitted to our institution with a history of diabetes mellitus type II, hypertension, and chronic kidney disease secondary to diabetic nephropathy and a hysterectomy 15 years earlier. She presented with weakness, malaise, and loss of appetite. Complete blood count analysis revealed the following: white blood cell count 10.1 × 109/l; hemoglobin level 113 g/l; mean corpuscular volume 84 fl; mean corpuscular hemoglobin level 31 pg/cell, and platelet count 264. Further blood tests revealed the following: glucose level 7.8 mol/l; urea nitrogen level 28.1 mg/dl; creatinine 877 mol/l; sodium 134 mol/l, and potassium 3.5 mol/l. Four days after admission, the patient underwent hemodialysis with unfractionated heparin. Six days after the administration of heparin, she became febrile and was treated with the antibiotics vancomycin and amikacin. That was on day 6 after holding the heparin, which was promptly day 2 after vancomycin treatment had been initiated. Two days after commencing the vancomycin, her platelet count started to drop gradually, decreasing to 21 × 109/l over 8 days, which was day 16 since heparin was held. The HIT test was ordered by the nephrologists. Thereafter, a hematologist was consulted for the persistent thrombocytopenia, as heparin had already been stopped 16 days ago. Because her platelet count slightly regenerated (from 21 to 25 × 109/l), no additional steps were taken other than avoiding heparin, as the patient was scheduled to undergo permacath insertion for hemodialysis the next day. The following day, the platelet count dropped to 19 × 109/l. The patient was treated with steroids to increase the platelet level for the permacath insertion. Both platelet transfusion (owing to the possible HIT diagnosis) and heparinoid anticoagulants (owing to the urgency of the permacath insertion surgery) were avoided.
Because her platelet count continued to drop to 10 × 109/l over the next 24 h, methylprednisolone was given while waiting for the HIT test result. Because the platelet drop occurred following the fever and the vancomycin administration, a secondary ITP that could have been caused by DITP was considered. The next day, the patient developed a swollen, hot, and tender right leg. Doppler ultrasound revealed extensive progressive lower limb deep vein thrombosis. An inferior vena cava filter was inserted on the same day. The HIT test result was revealed positive result. Her platelet count rose to 23 × 109/l following the administration of methylprednisolone. She was labeled a HIT case, and the pretest probability 4Ts score was an intermediate score.
Bivalirudin (Angiomax) was started, but the deep vein thrombosis advanced to acute phlegmasia cerulea dolens requiring above-the-knee amputation. The leg had become gangrenous with continuous blood oozing caused by both the low platelet count and the anticoagulant drugs. Hemoglobin levels had also dropped to 8.6 g/dl because of the continuous bleeding, requiring the transfusion of 2 units of blood. Intravenous immunoglobulin (IVIG) was commenced to treat the DITP, and the platelet count started to increase. On the fourth day of IVIG treatment, the patient developed right thalamic lacunar infarction. The IVIG treatment was continued for 4 weeks along with bivalirudin. The platelet count responded well to the IVIG treatment, reaching 98 × 109/l after 6 days but dropping to 26 × 109/l over 4 weeks. The amputation site started to bleed again and developed an infection that required debridement. During her long-term admission, the patient received four different courses of vancomycin on days 13, 16, 34, and 75, at doses of 500–1,000 mg, along with 240 mg of amikacin, based on the findings from the blood and wound cultures. The patient was also treated with other antibiotics during the course of treatment, including ceftriaxone on day 26, marine, and linezolid on day 52. Romiplostim, which was the third and a U.S. Food and Drug Administration-approved ITP treatment, was administered promptly when IVIG was stopped. In response to romiplostim treatment, the platelet count increased promptly to the normal values, and the bleeding stopped. The patient, however, developed a third thrombosis in her right iliac vein. The next dose of romiplostim was administered on time, 1 week later, when the patient had been hematologically stabilized, i.e., no more bleeding occurred and a normal cell count was achieved. Bivalirudin was replaced by warfarin because of the normalized platelet count as well as the recurrent thrombosis events and the need for hemodialysis. The patient developed septicemia from the amputation site, which caused delayed healing and infection. The wound site was debrided several times, but no improvement was noted. The amputation site showed positive results on several swab cultures, but antibiotic treatment was ineffective. The patient was kept on conservative management strategies until her death after 3 months. Although vancomycin was suspected as the cause of her thrombocytopenia, no vancomycin antibody test was available in our laboratory to confirm the findings in this patient. No malignancy screening tests were conducted because she was not suspected to have a malignancy, and no postmortem autopsy was performed because it was considered unacceptable based on religious factors in her community.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [62, 'years'], 'creatinine': [877.0, 'mol/L'], 'sex': 'Female'}",4.74E-07,4.50E-07,4.97E-07,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 62 years old. The concentration of Creatinine is 877.0 mol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from mol to mg. The mass of Creatinine is 877.0 mol. The mass of Creatinine is 877.0 mol. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 877.0 mol Creatinine * 113.12 g/mol = 99206.24 g Creatinine. To convert 99206.24 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 99206.24 g Creatinine * 1000.0 mg/g = 99206240.0 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 99206240.0 mg Creatinine/10.0 dL = 9920624.0 mg Creatinine/dL. The concentration value of 877.0 mol Creatinine/L converts to 9920624.0 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 9920624.0^(-1.154) * 62^(-0.203) * 1 * 0.742=4.7378e-07.
Hence, the patient's GFR is 4.7378e-07 mL/min/1.73m²."
3185,9,MDRD GFR Equation,lab test,decimal,usmle-379,Extracted,"A 66-year-old white man comes to the physician because of a 10-day history of fatigue and lower leg swelling. Over the past 6 months, he has had a 3.6-kg (8-lb) weight loss. He has chronic bronchitis and uses an albuterol inhaler as needed. He has smoked one pack of cigarettes daily for 44 years and drinks one alcoholic beverage daily. His temperature is 37°C (98.6°F), pulse is 88/min, and blood pressure is 120/75 mm Hg. He appears thin. Examination shows 2+ pretibial edema bilaterally. Cardiopulmonary examination shows no abnormalities. Laboratory studies show:
Hemoglobin 11.2 g/dL
Leukocyte count 8500/mm3
Platelet count 130,000/mm3
Serum
Urea nitrogen 23 mg/dL
Glucose 77 mg/dL
Creatinine 1.6 mg/dL
Albumin 1.8 mg/dL
Total cholesterol 475 mg/dL
Urine
Blood negative
Glucose negative
Protein 4+
WBC 0–1/hpf
Fatty casts numerous
An x-ray of the chest shows a right upper lobe density. A CT scan of the chest shows a 2.5 x 3.5 x 2-cm right upper lobe mass.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [66, 'years'], 'creatinine': [1.6, 'mg/dL'], 'sex': 'Male', 'Race': 'White'}",43.46265,41.28952,45.63578,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 66 years old. The concentration of Creatinine is 1.6 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.6^(-1.154) * 66^(-0.203) * 1 * 1=43.46265.
Hence, the patient's GFR is 43.46265 mL/min/1.73m²."
3186,9,MDRD GFR Equation,lab test,decimal,pmc-7929522-1,Extracted,"A 71-year-old male with PMHx of HTN, type-2 diabetes and known right bundle branch block, presented to the emergency department with dyspnea and fatigue. Four days prior to presentation the patient had noticed a decreased appetite with associated lower extremity edema. Patient denied recent travel, no sick contacts and no recent changes in medications. Review of systems were pertinent for subjective fever, no chills or cough.
Initial vital signs included temperature of 98.2 F, heart rate of 45 bpm, blood pressure of 169/90 mmHg, respiratory rate of 22 bpm and oxygen saturation of 98% on RA (room air). Physical exam was unremarkable. CXR showed bilateral opacities and initial labs were pertinent for a potassium 4.6 mmol/L, creatinine of 1.8 mg/dL, magnesium of 2.0 mg/dL, troponin-I of 0.16 ng/mL and brain natriuretic peptide (BNP) of 1028 pg/mL. WBC was 11.09 K/uL, Hgb 13.4 g/dL and platelet count of 190 K/uL. Initial venous blood gas (VBG) showed pH of 7.30, pO2 23.7 mmHg, pCO2 45.6 mmHg, HCO3− 21.6 mmol/L and lactic acid of 5.7 mmol/L. Patient had mildly elevated initial ferritin level at 299.4 ng/mL and elevated C-reactive protein (CRP) at 41mg/L. Both levels were significantly elevated within 48 hours, 740.0 ng/mL and 277 mg/L respectively. Initial EKG showed sinus rhythm with right bundle branch block (RBBB), second-degree type II atrioventricular block (AVB) and prolonged QT interval (), which differed from prior EKG 6 weeks ago, that showed sinus rhythm with RBBB and QTc was 433 ms. Transthoracic echocardiography (TTE) at that same time reported an ejection fraction (EF) of 49 % and CT coronary angiography 10 months prior showed non-obstructive coronary artery disease.
Shortly upon presentation, the patient developed acute respiratory failure, followed by profound bradycardia and cardiac arrest. Cardiopulmonary resuscitation was initiated and return of spontaneous circulation was achieved after 2 minutes of chest compression and administration of 1mg of IV epinephrine. Patient was intubated and a transvenous pacemaker was placed. Differential diagnosis included, but was not limited to acute hypoxic respiratory failure due to COVID-19 (given pandemic state in Brooklyn, NY) and progression of AV conduction abnormalities causing hemodynamic and respiratory collapse. The patient was admitted to the medical intensive care units (MICU) for further management.
On the following day, once the pacing rate was decreased to 40 bpm, we were able to appreciate a high degree AV block with an uncorrected QT interval at > 700ms (). Bedside TTE was performed and showed an EF 45% and global hypokinesis with minor regional wall motion abnormalities. Given persistence of conduction abnormalities and significant new QT prolongation without readily identifiable reversible causes a decision was made to proceed urgently with biventricular pacemaker implantation despite repeat COVID-19 PCR results x2 being reported as negative ().
Patient was extubated on the day following pacemaker implantation, remained hemodynamically stable and was downgraded to the internal medicine service. He completed a course of doxycycline for presumed community acquired pneumonia and safely discharged with outpatient cardiology follow up.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [71, 'years'], 'creatinine': [1.8, 'mg/dL'], 'sex': 'Male'}",37.38076,35.51172,39.2498,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 71 years old. The concentration of Creatinine is 1.8 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.8^(-1.154) * 71^(-0.203) * 1 * 1=37.38076.
Hence, the patient's GFR is 37.38076 mL/min/1.73m²."
3187,9,MDRD GFR Equation,lab test,decimal,pmc-6321693-1,Extracted,"A 63-year-old Japanese woman was referred to our department because of an abnormal shadow at the left side of her chest wall on computed tomography. She had undergone total hysterectomy and radiotherapy for cervical carcinoma 4 years prior. One year after the first surgery, three metastatic lung nodules appeared at the upper lobe of her right lung, the lower lobe of her right lung, and the lower lobe of her left lung. Wedge resection for upper and lower lobe of her right lung was initially performed via three-port thoracoscopic surgery. Then, wedge resection for the lower lobe of her left lung was performed via eighth intercostal single incisional thoracoscopic surgery. After the surgery, an intrathoracic chest wall mass developed which increased in size gradually. Her gynecologist introduced her to our department for surgical resection of the mass. Her family, including her parents and two sisters, had been healthy and had no inheritable diseases. She had no symptom, drug history, tobacco smoking history, or psychosocial history, and she was a social drinker. She had not received any medications since the mass developed and until admission to our hospital. She had undergone an operation three times as mentioned above and had been a carrier of type B hepatitis.
After her admission to our department, her general condition was good, and there were three operative scars at both sides of her chest and lower abdomen. Her chest sounds were clear and there was no neurological abnormality. She was 151.1 centimeters tall and weighed 49.8 kilograms. Her heart rate was 77/minute, blood pressure was 135/87 mmHg, and body temperature was 36.1 °C. The laboratory findings were white blood cells 5.25 × 103/μL, hemoglobin 12.7 g/dL, and platelets 156 × 103/μL. A liver function test revealed: albumin 4.6 g/dL, aspartate aminotransferase 15 U/L, alanine aminotransferase 13 U/L, and total bilirubin 0.3 mg/dL. A renal function test revealed blood urea nitrogen 13.6 mg/dL and creatinine 0.79 mg/dL. An electrolyte test revealed sodium 143 mEq/L, potassium 3.8 mEq/L, and chlorine 106 mEq/L. A tumor marker test revealed carcinoembryonic antigen 3.4 ng/mL and squamous cell carcinoma antigen 0.80 ng/mL. Another test revealed positive reaction to type B hepatitis surface antigen and C-reactive protein < 0.1 mg/dL. Computed tomography demonstrated a gradually increasing low-density mass measuring 2.0 × 1.8 cm in diameter (Fig. ). Magnetic resonance imaging demonstrated a low-intensity mass in T1-weighted imaging and a high-intensity mass in T2-weighted imaging (Fig. ). The mass was thought to be a singular cyst; however, this type of cyst was rare and the mass was increasing. Therefore, dissemination of cervical carcinoma could not be excluded, and surgical removal of a part or tissue of the mass was performed.
In the right lateral position, thoracoscopic excision of the mass was done with two ports (3 mm and 2 cm access ports) by two general thoracic surgeons (Fig. ). First the 3 mm port was set at the sixth intercostal space on the inframammary line. Most of her left lung was attached to her chest wall; therefore, the second port was set above the cyst and lysis of adhesions was done. After the lysis, the cystic mass was found adhering to the upper lobe of her left lung. The adhesion of the mass to her lung was not strong and could be separated without injury to the visceral pleura. Therefore, the mass was thought to derive from the chest wall pleura and was resected by adhesiolysis.
The mass was a unilocular cyst containing mucinous fluid. On microscopic examination, the cyst was lined with a single layer of cuboidal epithelium (Fig. ); immunohistochemistry showed positive staining of calretinin and D2-40 (Fig. ). Thus, the cyst was diagnosed as mesothelial cyst derived from the chest wall pleura. Five years after the surgery, our patient had no evidence of cyst or cervical carcinoma on computed tomography.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [0.79, 'mg/dL'], 'sex': 'Female', 'Race': 'Asian'}",73.50454,69.82931,77.17977,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 63 years old. The concentration of Creatinine is 0.79 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.79^(-1.154) * 63^(-0.203) * 1 * 0.742=73.50454.
Hence, the patient's GFR is 73.50454 mL/min/1.73m²."
3188,9,MDRD GFR Equation,lab test,decimal,pmc-4519001-1,Extracted,"A 76-year-old Caucasian man with a history of type 2 diabetes, chronic kidney disease (CKD) stage 3A, essential hypertension, hypothyroidism, antiphospholipid antibody syndrome, prior cerebellar strokes, and prostate cancer (Gleason 10) with widespread metastasis to the bone presented with non-oliguric severe AKI 3 weeks after receiving simultaneous therapy with denosumab (120 mg subcutaneous injection once) and abiraterone (1 g per day orally). The patient had failed prior antineoplastic therapy with leuprolide acetate, bicalutamide, and nilutamide. On admission, his serum creatinine (SCr) was elevated at 5.7 mg/dL from a baseline of 1.2 mg/dL (Fig. ). His active outpatient medications consisted of rosuvastatin (40 mg daily), benazepril, metoprolol tartrate, metformin, warfarin, low-dose prednisone (started concomitantly with abiraterone), and levothyroxine. The patient had been on statin therapy for more than 1 year and the dose had not been recently modified. The patient denied prior episodes of myopathies, rhabdomyolysis, or AKI. His physical exam was unremarkable. Further blood work showed hyperkalemia, mild metabolic acidosis, hypocalcemia, mild transaminemia (predominantly AST), and creatine kinase (CK) of 44,476 IU/L (Table ). Urine studies revealed dipstick proteinuria (100 mg/dL), large dipstick blood, only a few normomorphic erythrocytes, and negative culture. All serologic work-up (ANA, PR3- and MPO-ANCA, anti-GBM antibodies, ENA panel, C3, C4, RF) and viral studies (HBV, HCV, CMV, EBV, Influenza A/B, Parainfluenza, Adenovirus, RSV) were negative or normal. Thyroid function tests were normal. Kidney sonogram and Doppler studies were negative for hydronephrosis and renal vein thrombosis, respectively. On admission, abiraterone therapy was discontinued and no further doses of denosumab were administered. Subsequently, the patient underwent kidney biopsy that was consistent with severe acute tubular injury with presence of myoglobin casts, confirming the diagnosis of rhabdomyolysis-induced AKI (Figs. and ). The patient responded well to intravenous isotonic fluids and discontinuation of denosumab, abiraterone, and rosuvastatin. CK levels normalized by day 25 of hospitalization and the SCr at the time of hospital discharge was 3.1 mg/dL (Fig. ). After hospital discharge, the patient resumed all prior medications, including rosuvastatin, except for denosumab and abiraterone. His successive antineoplastic therapy consisted of enzalutamide. Kidney function returned to baseline 12 months after discharge and he had no recurrent episodes of rhabdomyolysis.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [76, 'years'], 'creatinine': [5.7, 'mg/dL'], 'sex': 'Male', 'Race': 'White'}",9.74885,9.26141,10.23629,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 76 years old. The concentration of Creatinine is 5.7 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 5.7^(-1.154) * 76^(-0.203) * 1 * 1=9.74885.
Hence, the patient's GFR is 9.74885 mL/min/1.73m²."
3189,9,MDRD GFR Equation,lab test,decimal,pmc-6425374-1,Extracted,"A 74-year-old woman with a history of SLE on hydroxychloroquine without known renal involvement, chronic kidney disease stage (CKD) IIIa, heart failure with reduced ejection fraction, hypertension, and type 2 diabetes mellitus (T2DM) presented to the emergency department with progressive chest “heaviness” which had started several days prior to admission. In addition, she complained of swelling in both feet and at least three-pound weight gain.
Upon admission she was afebrile, blood pressure ranged 150-180/70-80 mm Hg, heart rate was about 50 bpm, and oxygen saturation was above 95% on room air. She was a well-developed, nonobese woman in no significant distress and nontachypneic. Pertinent physical exam findings included no jugular venous distention, no crackles audible at base of lungs, heart with regular rate and rhythm with no extra sounds or murmurs, nondistended abdomen, trace peripheral leg edema, and no visible rashes. Laboratory tests were significant for sodium 129 mEq/L, potassium 4.2 mEq/L, chloride 98 mEq/L, CO2 20 mEq/L, BUN 46 mg/dL, and creatinine 3.4 mg/dL. Her baseline creatinine based on the most recent reading one month prior to admission was 1.1 mg/dL. Urinalysis was significant for a specific gravity of 1.006, RBC 142, and WBC 8 per HPF. No casts of dysmorphic cells were seen. Proteinuria was 2+, and a random urine protein-to-creatinine ratio was 1.48.
Her creatinine continued to rise rapidly, and by day 6 of hospitalization it was 6.4 mg/dL. Due to these findings, a renal biopsy was performed. Up to 21 glomeruli were present per tissue section, and two of them showed global sclerosis. Two other glomeruli showed segmental sclerosis and the remaining glomeruli were open. There was global diffuse marked mesangial sclerosis and hypercellularity, and there was no obvious endocapillary cell proliferation or inflammatory cell infiltrate. Three of the open glomeruli also displayed segmental or circumferential predominantly cellular crescent. There was multifocal chronic tubulointerstitial injury characterized by atrophic tubules, interstitial fibrosis, and mild mononuclear inflammatory cell infiltrate, all which accounted for about 20-40% of the cortical tissue area. Figures and are biopsies seen in light microscopy with the former showing mesangial proliferation and the latter demonstrating a crescent on silver stain. Immunofluorescent staining showed marked IgA and C3 mesangial deposition, weak linear IgG staining of the glomerular basement membrane, and absence of C4 and C1q which was consistent with IgA nephropathy. There are also changes suggestive of diabetic nephropathy, in keeping with the clinical history of diabetes. These changes include thickened lamina densa and linear IgG of the glomerular basement membrane and mesangial sclerosis. Immunofluorescent staining positive for IgA and C3 is seen in Figures and , respectively. Staining for C4 and C1q was both negative with the latter seen on . In addition, electron microscopy showed uniform thickening of lamina densa of glomerular basement membrane, marked mesangial sclerosis, and hypercellularity, and some electron dense deposits were identified in the mesangial areas and subepithelial location which can be seen in Figures and . Ultimately, given the histological findings, the biopsy was diagnosed as mesangial proliferative glomerulonephritis with crescent formation. Findings were not comparable with lupus nephritis, especially the immunofluorescent findings. The significant mesangial IgA staining raised the likelihood of IgA nephropathy.
Her serologic work-up included anti-dsDNA antibody (1:80), ANA (1:320), and normal serum complement levels. With these biopsy results in the setting of worsening kidney function, she was diagnosed with immune complex RPGN secondary to IgAN.
She subsequently received intravenous methylprednisolone 500 mg daily for three days and five rounds of plasmapheresis. Unfortunately, her renal function continued to deteriorate, and she was started on hemodialysis. She was discharged with instructions to take prednisone 60 mg daily for one month with a taper. Her clinical symptoms showed mild improvement, however, there was no significant recovery in kidney function, and she was declared to have end-stage renal disease (ESRD).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [74, 'years'], 'creatinine': [3.4, 'mg/dL'], 'sex': 'Female'}",13.20265,12.54252,13.86278,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 74 years old. The concentration of Creatinine is 3.4 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 3.4^(-1.154) * 74^(-0.203) * 1 * 0.742=13.20265.
Hence, the patient's GFR is 13.20265 mL/min/1.73m²."
3190,9,MDRD GFR Equation,lab test,decimal,pmc-5670091-1,Extracted,"A 66-year-old Caucasian male inpatient was transferred from the neurological ward to the emergency department (critical care unit) of the same hospital because of decreased consciousness. His medical history included poorly controlled type 2 diabetes mellitus, atrial fibrillation and cardiovascular disease.
The patient had been admitted to the department of cardiology 17 days earlier because of a myocardial infarction. He underwent successful percutaneous coronary intervention and felt well during the first days of hospitalisation. The patient developed focal pontine stroke [National Institutes of Health Stroke Scale (NIHSS) 7] 12 days later and was subsequently transferred to the neurology ward for further care. The patient experienced moderate dysarthria, some degree of hemiparesis and limb ataxia but was otherwise alert and responsive. However, reduced general condition with moderately severe disability kept the patient bedridden and necessitated intensified nursing care, including assistance with drinking and personal care, including bodily functions (modified Rankin scale 4). The patient was transferred to the emergency department 5 days later because of progressive loss of consciousness. Figure highlights the medically relevant events that occurred during hospitalisation.
On admission to the emergency department, the patient was stuporous (Glasgow coma scale 10; eye response 3, motor response 4, verbal response 3), had elevated body temperature (38.5 °C) and low blood pressure (95/50 mmHg) and appeared to be dehydrated. Laboratory findings included severe hypertonic hypernatraemia (164 mmol/l), hyperglycaemia (322 mg/dl), excessive glucosuria (3935 mg/dl) and impaired kidney function (creatinine 2.1 mg/dl). Chest X-ray (posterioranterior) showed patchy consolidations in upper lung fields. Table gives a summary of laboratory test results, the patient’s medical history and a list of his medications.
Diagnostic work-up primarily focused on the differential diagnosis of hypernatraemia as it was the predominant laboratory finding and considered the cause of impaired consciousness.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [66, 'years'], 'creatinine': [2.1, 'mg/dL'], 'sex': 'Male', 'Race': 'White'}",31.75628,30.16847,33.34409,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 66 years old. The concentration of Creatinine is 2.1 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.1^(-1.154) * 66^(-0.203) * 1 * 1=31.75628.
Hence, the patient's GFR is 31.75628 mL/min/1.73m²."
3191,9,MDRD GFR Equation,lab test,decimal,pmc-6309397-1,Extracted,"A 45-year-old male with a history of hypertension and chronic kidney disease (CKD) diagnosed concomitantly 2 years ago presented with acute onset rash [] and diffuse joint pains for 2 weeks. His previous medical records revealed a baseline serum creatinine (S. Cr.) of 1.6–1.7 mg/dL. He denied any blood transfusions, intravenous drug abuse or high-risk sexual behavior. His medications included amlodipine and telmisartan. His blood pressure was 132/96 mm Hg, pulse rate 76/min and he had a diffuse erythematous maculopapular rash on the extensor surface of his lower extremities. His ankle joints were swollen, and movements were painful. He had 2+ bilateral pitting edema. His fundus examination was normal.
Initial laboratory investigations revealed hemoglobin of 9.4 g/dL with a normal platelet and white cell count. His S. Cr. was 1.9 mg/dL and electrolytes were normal. His liver enzymes were normal and serum albumin was 2.9 g/dL. His initial urinalysis showed 3 + protein, 6–10 red blood cell/hpf and 4–6 white blood cell/hpf. His ESR was mm in 1st hour 38 and C-reactive protein was normal. An ultrasound revealed normal sized kidneys and chest X-ray was normal. His 24 h urine showed protein excretion of 3.1 g. His anti-nuclear antibody (ANA), HBsAg and HIV antibody tests were negative. Complements C3 and C4 were both low at 0.63 and 0.03 g/L, respectively. His anti-HCV antibody was positive with an HCV RNA viral load of 4133209 IU/ml and HCV genotype 3a. Complement cryoglobulin and cryocrit was undetectable.
An ultrasound-guided kidney biopsy was performed which showed enlarged glomeruli, with a global increase in mesangial matrix and cellularity, along with lobular accentuation. There was thickening of glomerular basement membranes and double contouring []. Few hyaline thrombi were seen within the capillary lumen. Interstitium showed mild edema with foci of chronic mononuclear inflammatory infiltrate. Immunofluorescence showed strong granular staining for C3, IgG and IgM along the capillary wall and in mesangial areas. Electron microscopy (EM) could not be done. A diagnosis of immune-complex mediated MPGN pattern was made.
The patient was started on DAA drugs-sofosbuvir 400 mg and daclatasvir 60 mg once daily for 12 weeks. Telmisartan was increased to 40 mg twice a day. A repeat HCV RNA test done after 6 weeks was undetectable. His S. Cr. gradually decreased to 1–1.2 mg/dL range with spot urine protein: creatinine ratio being 0.3–0.5 mg and continued to be stable at 12-month follow-up. Repeat quantitative HCV RNA testing done at 6 months and 1 year follow-up continues to be in the undetectable level.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [45, 'years'], 'creatinine': [1.9, 'mg/dL'], 'sex': 'Male'}",38.52603,36.59973,40.45233,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 45 years old. The concentration of Creatinine is 1.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.9^(-1.154) * 45^(-0.203) * 1 * 1=38.52603.
Hence, the patient's GFR is 38.52603 mL/min/1.73m²."
3192,9,MDRD GFR Equation,lab test,decimal,pmc-4421387-1,Extracted,"A 50-year-old normotensive and non-diabetic man of Asian origin was admitted for investigation of anaemia and progressive renal impairment. Anaemia and renal dysfunction had been noticed 6 years ago (haemoglobin 7.6 g/dL, serum creatinine 137 μmol/L and creatinine clearance 52 mL/min) during consultation at another hospital after which the patient was lost to follow-up. There were no urinary symptoms or previous history of nephrolithiasis, urinary tract infections, flank pain or dark coloured urine. He denied taking any regular medication including non-steroidal anti-inflammatory agents.
On examination, he looked extremely pale. Blood pressure was 110/60. There was no lymphadenopathy, organomegaly or signs of cardiac decompensation. The laboratory findings are summarized in Table .
He had severe normochromic anaemia, anisopoikilocytosis, granulocytopenia and thrombocytopenia. Subsequent work-up confirmed intravascular haemolysis as evidenced by increased serum LDH, reduced haptoglobin and haemosiderinuria. The direct antiglobulin (Coomb’s) test was negative implying that haemolysis was of non-immune origin. A bone-marrow biopsy was carried out that showed marked erythroid hyperplasia, dyserythropoietic features and reduced iron stores. No malignant cells were seen. Diagnosis of PNH was made by the Ham test indicating complement-mediated red blood cell lysis. Flow cytrometric studies were not performed.
Serum biochemistry revealed moderately severe renal impairment with a creatinine clearance of 28 mL/min/ 1.73 m2. This was associated with a low-grade proteinuria of 0.68 g/day. Urine was negative for the Bence-Jones protein, and serum electrophoresis did not show any monoclonal band. ANA was negative, and there was no hypocomplementaemia. Ultrasonography showed unobstructed, normal-sized echogenic kidneys with decreased corticomedullary differentiation. A renal biopsy was performed. The predominant finding was that of widespread haemosiderosis involving the proximal tubular cells (Figure ) that gave a blue tinge to the specimen on application of Perls’ Prussian blue stain. This was associated with interstitial fibrosis and tubular atrophy affecting ∼30% of the core. Glomeruli and blood vessels were normal and immunofluorescence was negative.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [50, 'years'], 'creatinine': [137.0, 'µmol/L'], 'sex': 'Male', 'Race': 'Asian'}",46.51892,44.19297,48.84487,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 50 years old. The concentration of Creatinine is 137.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 137.0 µmol. To convert 137.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 137.0 µmol Creatinine * 1e-06 mol/µmol = 0.00014 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00014 mol Creatinine * 113.12 g/mol = 0.01584 g Creatinine. To convert 0.01584 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01584 g Creatinine * 1000.0 mg/g = 15.84 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 15.84 mg Creatinine/10.0 dL = 1.584 mg Creatinine/dL. The concentration value of 137.0 µmol Creatinine/L converts to 1.584 mg Creatinine/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.584^(-1.154) * 50^(-0.203) * 1 * 1=46.51892.
Hence, the patient's GFR is 46.51892 mL/min/1.73m²."
3193,9,MDRD GFR Equation,lab test,decimal,pmc-4400505-1,Extracted,"A 44-year-old Asian man with end-stage renal disease of unknown cause underwent renal transplantation from a deceased donor. The renal allograft had a main superior renal artery and an accessory inferior renal artery. He received immunosuppression with thymoglobulin, tacrolimus, mycophenolate mofetil and prednisone. His sCr decreased from 4.7 mg/dL pre-operatively to 2.0 mg/dL throughout the first month. Approximately 4 months post-transplantation, he had an episode of acute allograft dysfunction—sCr increased to 3.8 mg/dL—associated with increased blood pressure requiring an additional anti-hypertensive drug. On physical exam, no bruit was detected overlying the allograft. A CDU demonstrated a 10.5 cm renal allograft with normal echogenicity and two patent main renal arteries both with normal velocities. Evaluation of the intra-renal segmental arteries showed ‘parvus tardus’ waveforms but normal resistive index. A renal allograft biopsy revealed mild acute tubulointerstitial cellular rejection. After treatment with steroids, sCr decreased to 2.2 mg/dL and blood pressure improved. Five months post-transplantation, his blood pressure worsened and sCr rose up to 2.9 mg/dL. A second renal allograft CDU of the superior-pole intra-renal segmental arteries showed parvus tardus waveforms and low-normal resistive index (0.47–0.50). Angle-corrected peak velocities in the main superior renal artery were normal, from 73 to 85 cm/s. The inferior pole resistive index was normal (0.61) without parvus tardus waveform and the corresponding inferior accessory renal artery peak systolic velocity was not elevated (28 cm/s). A kidney allograft biopsy showed patchy mild interstitial inflammation associated with areas of atrophy, but no evidence of segmental or global glomerulosclerosis, glomerulitis, proliferation, necrosis or crescents. Focal intimal sclerosis was observed in the interlobular arteries and mild to moderate arteriolosclerosis was present. A non-contrast magnetic resonance angiography was performed using inversion-recovery pulses to enhance arterial inflow and three-dimensional balanced steady-state free precession acquisition (INHANCE®) [, ]. This imaging study showed focal narrowing of the superior main renal artery 2 cm distal to the anastomosis with mild post-stenotic dilatation (). The inferior accessory artery was grossly normal, but assessment was limited by the small caliber of this vessel. X-ray angiography with CO2 confirmed a 15 mm-long stenosis, 8 mm distal to the anastomosis in the superior main renal artery (). The peak systolic gradient of 100 mmHg was consistent with a very tight stenosis. Angioplasty was performed with excellent angiographic results and no residual pressure gradient. A decision was made not to use a stent due to the difficulty of deployment in the area of stenosis. The inferior accessory artery was normal. A post-angioplasty renal allograft CDU showed improved arterial waveforms and resistive index. The patient was continued on aspirin and clopidogrel was started. The sCr decreased to 1.8 mg/dL and his blood pressure improved. He is currently maintained on low doses of blood pressure medications.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [44, 'years'], 'creatinine': [1.8, 'mg/dL'], 'sex': 'Male', 'Race': 'Asian'}",41.19388,39.13419,43.25357,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 44 years old. The concentration of Creatinine is 1.8 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.8^(-1.154) * 44^(-0.203) * 1 * 1=41.19388.
Hence, the patient's GFR is 41.19388 mL/min/1.73m²."
3194,9,MDRD GFR Equation,lab test,decimal,pmc-6701887-1,Extracted,"A 40-year-old female with no significant past medical history who was seen by her primary care physician for fatigue and workup revealed low hemoglobin, so she was asked to go to the emergency department (ED) for further evaluation. The patient has been complaining of fatigue, nausea, diarrhea, dysuria, and urinary frequency for more than seven days prior to presentation. On physical examination, the patient was pale, had mild abdominal tenderness, and left flank fullness was felt. Labs were repeated in the ED and were remarkable for a hemoglobin of 6.5 g/dL (down from 10 g/dL three months prior), white blood cell (WBC) count of 18 x 109/L, creatinine of 1.87 mg/dL (baseline is 1 mg/dL) with blood urea nitrogen (BUN) of 24 mg/dL. Urinalysis was remarkable for numerous WBC, positive bacteria, and nitrite. The patient received one unit of packed red blood cells and was started on ceftriaxone for urinary tract infection (UTI). No source of active bleeding was identified.
Gastroenterology team was consulted for the anemia, and they performed esophagogastroduodenoscopy (EGD) which was normal. Subsequently, they performed a colonoscopy which detected a fistula opening with surrounding nodularity close to the splenic flexure of the colon with a small amount of pus noted coming out of it (Figure ).
Shortly after, the patient spiked a fever of 102.7F. C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were both elevated. Based on the colonoscopy findings and the new fever, a computed tomography (CT) scan of the abdomen and pelvis with contrast was performed and it revealed chronic left kidney pyelonephritis with multiple contiguous abscesses in the inferior left kidney with a staghorn calculus concerning for XGP; it also showed the fistula between the left kidney and the splenic flexure of the colon (Figures -). The patient underwent exploratory laparotomy, takedown and repair of renocolic fistula, partial omentectomy, and left nephrectomy by urology and general surgery teams. The patient had an uncomplicated postoperative course and was discharged home on postoperative day six with stable hemoglobin of 8 g/dL.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [40, 'years'], 'creatinine': [1.87, 'mg/dL']}",29.82075,28.32971,31.31179,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 40 years old. The concentration of Creatinine is 1.87 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.87^(-1.154) * 40^(-0.203) * 1 * 0.742=29.82075.
Hence, the patient's GFR is 29.82075 mL/min/1.73m²."
3195,9,MDRD GFR Equation,lab test,decimal,pmc-4255995-1,Extracted,"A 79-year-old Thai woman with a history of CKD stage 5 (serum creatinine level 4.5–5.0 mg/dl), dyslipidemia and anemia of chronic disease presented with fatigue, low-grade fever and a productive cough for the last 2 months. She denied any history of tuberculosis infection. Her current medication was manidipine hydrochloride (10 mg/day) and furosemide (20 mg/day). Physical examination revealed fever, fine crepitation in both lungs and multiple discrete small pustules on her face, trunk and extremities (fig. ). Laboratory findings showed a hemoglobin level of 9.2 g/dl, a white cell count of 21,060/mm3 with 91.2% neutrophils, and a platelet count of 210,000/mm3. An anti-HIV test was negative. Radiography of the chest revealed diffuse reticulonodular infiltration of both lungs. Sputum examination was positive for acid-fast bacilli and Mycobacterium tuberculosis complex DNA was detected by polymerase chain reaction. Skin scrapings from pustules of the right thigh were positive for acid-fast bacilli and M. tuberculosis complex DNA was detected by polymerase chain reaction. She was diagnosed with pulmonary and cutaneous miliary tuberculosis. Blood cultures identified M. tuberculosis complex 50 days later. She was started on an initial therapy of isoniazid (300 mg/day), rifampicin (450 mg/day), ethambutol (800 mg/day) and pyrazinamide (1,500 mg/day). The pustules subsided after 3 weeks of treatment and pulmonary symptoms improved after 5 weeks of treatment.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [79, 'years'], 'creatinine': [4.5, 'mg/dL'], 'sex': 'Female', 'Race': 'Asian'}",9.42793,8.95653,9.89933,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 79 years old. The concentration of Creatinine is 4.5 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 4.5^(-1.154) * 79^(-0.203) * 1 * 0.742=9.42793.
Hence, the patient's GFR is 9.42793 mL/min/1.73m²."
3196,9,MDRD GFR Equation,lab test,decimal,pmc-7478927-1,Extracted,"A 69-year-old female with a recent diagnosis of BCR/ABL+ CML, type 2 diabetes mellitus, hypertension, and coronary artery disease presented to the ED with complaints of shortness of breath (SOB). The patient reported her SOB started worsening over the last couple of days prior to admission. She denied any orthopnea or paroxysmal nocturnal dyspnea. She also reported dizziness (positional), palpitations, poor oral intake due to poor appetite, and nausea. The patient reported several episodes of coffee-ground emesis and black tarry stools for the last couple of days. She denied any hematemesis or bright red blood per rectum (BRBPR). She also endorsed easy bruising and episodes of blurry vision. Initial vital signs in the ED showed a heart rate of 105 beats per minute, blood pressure of 89/55, and 85% saturation on 4L nasal cannula. Lung exam revealed crackles with decreased breath sounds, muffled heart sounds, and no murmurs.
Lab results were as follows: hemoglobin of 7.9 g/dL, hematocrit of 25.6%, platelets of 379 K/mm3, WBCs of 105.2 K/mm3, and peripheral smear (Figure ) showed neutrophils of 46%, bands of 10%, lymphocytes of 10%, monocytes of 4%, metamyelocytes of 21%, myelocytes of 9%, and blasts of 1%.
Complete metabolic profile showed Na (sodium) of 134 mmol/L, K (potassium) of 7.3 mmol/L, bicarbonate of 19 mmol/L, BUN (blood urea nitrogen) of 103 mg/dL, creatinine of 3.4 mg/dL, glucose of 208 mg/dL, AST (aspartate aminotransferase) of 17 U/L, ALT (alanine aminotransferase) of 12 U/L, uric acid of 15.2 mg/dL, proBNP (pro b-type natriuretic peptide) of 1,135 pg/mL, troponin of <0.015 ng/mL, and procalcitonin of 1.3 ng/mL. COVID-19 screen was negative. Blood culture showed no growth after five days. Immunoglobulins were within normal limits. RF and ANA screen was negative. P-ANCA and C-ANCA were negative. C3 and C4 were within normal limits.
Chest X-ray (Figure ) showed air space disease, left side pleural effusion, and a boot-shaped heart concerning for pericardial effusion. Transthoracic echocardiography showed a large pericardial effusion of 2 cm circumferentially surrounding the heart with focal strands. There were no echo signs of frank tamponade (Figure ).
Bedside pericardiocentesis was performed and 900 cc of frank bloody fluid was removed. A drain was left in place for subsequent removal of 400 cc on day 2 and 250 cc on day 3. Pericardial fluid analysis revealed the following: negative gram stain/culture, bloody appearance, 2,300,000 RBCs, and 64,420 WBCs with polymorphonuclear neutrophils (PMNs) of 94%, lymphocytes of 2%, and monocytes of 2%. Pericardial cytology shows infiltration by CML (Figure ).
The patient was treated in the critical care unit for multifocal pneumonia, severe sepsis, and acute renal failure requiring hemodialysis (HD). The patient's hemodynamics improved after pericardiocentesis, and a total of 1,550 cc of bloody pericardial fluid was removed. WBCs decreased to 85k with hydroxyurea. Tyrosine kinase inhibitors (TKIs), such as nilotinib, were not started due to prolonged QTc (550 ms) and resistant atrial fibrillation. The patient was instructed to follow up with the outpatient hematology/oncology service to start chemotherapy once stable.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [69, 'years'], 'creatinine': [3.4, 'mg/dL'], 'sex': 'Female'}",13.39149,12.72192,14.06106,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 69 years old. The concentration of Creatinine is 3.4 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 3.4^(-1.154) * 69^(-0.203) * 1 * 0.742=13.39149.
Hence, the patient's GFR is 13.39149 mL/min/1.73m²."
3197,9,MDRD GFR Equation,lab test,decimal,pmc-5673475-1,Extracted,"A 38-year-old female patient was transferred to our tertiary care center from another hospital with an overdose of approximately 12-14 grams of labetalol with alcohol. Her past medical history is unremarkable. In a suicidal attempt, she ingested the labetalol prescribed to her husband one-two hours prior to presenting to the hospital.
At the time of presentation at the outside hospital, she was hypotensive at 54/33 mm of Hg and her heart rate was approximately 60 beats/minute. Her physical exam was within normal limits and her mentation was intact. Serum creatinine was 1.1 mg/dl (83.3 µmol/L), CO2 was low at 18 mmol/L, acetaminophen/salicylate was undetectable, creatinine phosphokinase levels were normal, and serum lactate and serum labetalol levels were not obtained.
Initial therapy at the outside hospital included fluid boluses, glucagon, calcium gluconate, and dopamine infusion. The patient remained hypotensive and anuric, so after consultation with the poison center, norepinephrine was added. After three-four hours, her urine output and blood pressure improved, so norepinephrine was discontinued, and she was transferred to our center.
Upon arrival at our center, she was six hours post-ingestion and was on dopamine only. Her blood pressure was 84/37; she remained alert and was in no acute distress. Her creatinine was 2.63 mg/dl (200 µmol/L). On arrival, dopamine was switched to norepinephrine and eventually discontinued, as her urine output and blood pressure remained stable and the abdominal ultrasound was within normal limits. Over the next few days, her urine output improved, but her serum creatinine continued rising, reaching 5.4 mg/dl (411.8 µmol/L) by day five.
Causes such as myoglobinuria and interstitial nephritis were excluded in our patient by urinalysis, which showed muddy brown casts. Acute tubular necrosis is the possible diagnosis but as the patient was asymptomatic and non-oliguric, a renal biopsy was not performed. She was asymptomatic throughout her stay and maintained good urine output. She was managed conservatively, needing dialysis, and was discharged once her serum creatinine started decreasing. She did not keep her two-week follow-up appointment.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [38, 'years'], 'creatinine': [1.1, 'mg/dL'], 'sex': 'Female'}",55.5877,52.80831,58.36709,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 38 years old. The concentration of Creatinine is 1.1 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.1^(-1.154) * 38^(-0.203) * 1 * 0.742=55.5877.
Hence, the patient's GFR is 55.5877 mL/min/1.73m²."
3198,9,MDRD GFR Equation,lab test,decimal,pmc-8510665-1,Extracted,"An 83-year-old man with a past medical history significant for coronary artery disease, hyperlipidemia, hypertension, and chronic kidney disease presented to the emergency department with a 6-week history of worsening bilateral lower extremity swelling and 1 week of increased shortness of breath. He also endorsed dyspnea on exertion and a weight gain of 8 pounds in the past 2 weeks. Of note the patient did not have a prior history of congestive heart failure (CHF) and previous echocardiograms revealed normal heart function.
Approximately 3 weeks prior to presentation, the patient underwent preoperative testing at a different facility in preparation for primary hip arthroplasty. Nuclear stress test at the time showed multivessel coronary artery disease, left ventricular ejection fraction of 40% and abnormal myocardial perfusion. Echocardiogram revealed the presence of severe left ventricular hypertrophy with an abnormal strain pattern and an inferobasilar aneurysm. The patient was then scheduled at that facility for a coronary angiogram but was deferred due to elevated creatinine. His anti-hypertensives losartan and chlorthalidone were discontinued at discharge due to the elevated creatinine. The patient was directed to follow up with his cardiologist whom he scheduled an appointment in 4 weeks’ time.
In the time between the preoperative testing and presentation to our hospital, the patient reported initially feeling well. He endorsed a healthy lifestyle with the ability to exercise and walk miles without any difficulty. He was employed as a physical education teacher. As the lower extremity swelling worsened, he started to develop shortness of breath limiting his activity level which prompted his visit to the emergency room.
On arrival to our hospital, the patient’s vital signs were all within normal limits and his blood pressure was well controlled despite the recent discontinuation of some of his anti-hypertensives (). Physical examination exhibited leg edema, crackles on auscultation and flat neck veins. Laboratory results showed an elevated brain-type natriuretic peptide (BNP) (1,761 ng/L), troponin (0.31 ng/mL), blood urea nitrogen (BUN) (55 mg/dL) and creatinine (3.46 mg/dL) (). According to medical records, his baseline creatinine ranged 1.4 - 1.8 mg/dL. Urine analysis revealed hematuria and proteinuria suggesting nephrotic syndrome (). Electrocardiogram (EKG) displayed low-voltage normal sinus rhythm. Repeat echocardiogram at our hospital confirmed the severe left ventricular hypertrophy with reduced ejection fraction of 46-50% but also revealed a strain pattern suggestive of cardiac amyloidosis.
The patient underwent laboratory investigation for amyloidosis due to the echocardiogram findings. Total urine protein was elevated (1.19 g/L) and positive for monoclonal free lambda light chains (Bence-Jones protein). Serum protein electrophoresis (SPEP) showed markedly decreased total protein, hypoalbuminemia, hypogammaglobulinemia and increased alpha-2-globulin. It also revealed a monoclonal protein peak migrating in the beta-globulin region making up 0.21 g/dL of the total 0.67 g/dL, a second monoclonal protein peak migrating in the gamma globulin region making up 0.10 g/dL of the total 0.22 g/dL with markedly increased free lambda light chains and markedly decreased kappa/lambda ratio.
Diagnostic testing for amyloidosis was initiated with a fat pad biopsy that upon Congo red staining was indeterminate for amyloid deposition. Bone marrow biopsy of the left iliac crest showed extensive interstitial infiltrate of atypical plasma cells (80-90%) in the form of diffuse sheets that is consistent with multiple myeloma. An X-ray skeletal survey was negative for any osteolytic lesions. The patient was scheduled for positron emission tomography (PET) on a later date at an outpatient center.
The patient was initially started on a daily dose of 40 mg intravenous dexamethasone. Once the multiple myeloma diagnosis was confirmed with bone marrow biopsy, the patient received two rounds of “CyBorD” chemotherapy treatment: cyclophosphamide, bortezomib and dexamethasone. CHF medications and diuretics were administered to manage volume overload secondary to cardiac amyloidosis. As treatment progressed, serial labs indicated increased uric acid production (12.3 mg/dL) that was treated with one-time rasburicase and managed thereafter with allopurinol. He also received “Granix” (tbo-filgrastim) to reduce the duration of severe neutropenia while undergoing chemotherapy. After 9 days of initial hospitalization, the patient was scheduled for a third chemotherapy session and discharged to home.
Seven days later, the patient presented again to our facility with continued symptoms of worsening dyspnea and generalized edema. Additionally, he tested positive for a urinary tract infection and was started on antibiotics. Blood work revealed acute on chronic kidney disease with significantly worse creatinine of 5.40 mg/dL compared to previous admission. He was promptly started on hemodialysis. Next morning, the patient became hypoxic and hypotensive requiring transfer to the intensive care unit where vasopressors, inotropes and bilevel positive airway pressure (BiPAP) were initiated. Shortly thereafter, the patient went into cardiac arrest and resuscitation efforts were unsuccessful.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [83, 'years'], 'creatinine': [3.46, 'mg/dL'], 'sex': 'Male'}",17.03615,16.18434,17.88796,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 83 years old. The concentration of Creatinine is 3.46 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.46^(-1.154) * 83^(-0.203) * 1 * 1=17.03615.
Hence, the patient's GFR is 17.03615 mL/min/1.73m²."
3199,9,MDRD GFR Equation,lab test,decimal,pmc-7983145-1,Extracted,"A 38-year-old female was admitted to the emergency ward with altered sensorium and anuria. She had off and on constitutional symptoms of disease such as general malaise, myalgia, polyarthralgia (mainly involved knee, elbow, and ankle joints), anorexia, weight loss, headache, and pyrexia from the last 4 years. She also had a history of recurrent blood-stained nasal discharge, epistaxis, nasal crusting, nasal ulceration, cough, breathlessness, stridor, and wheeze from the last 3 years. She had a history of pedal edema 3 months back. She also complained of diminution of vision with redness of eyes from 3 months. The patient had a history of ulcers on lips and tongue from the past 4 days and decreased frequency of urination from 3 days. There is no history of hematuria, hemoptysis, or cardiovascular manifestations. On examination, her vitals were deranged; she had tachycardia (120/bpm) and hypotension (100/60 mm of Hg). She also had pallor and bilateral pedal edema. There was high suspicion of GPA with acute renal failure or rapidly progressive glomerulonephritis associated with systemic small-vessel vasculitis. Keeping these two main diagnoses in mind, the investigations were ordered accordingly.
It is based on a combination of clinical manifestations of systemic disease, positive ANCA serology, and histological evidence of necrotizing vasculitis, necrotizing glomerulonephritis, or granulomatous inflammation of affected organs such as skin, lung, or kidney.
A trucut biopsy was taken from the right kidney of the patient and detailed analysis was done. On light microscopy, there was focal segmental necrotizing glomerulonephritis involving more than 60% glomeruli associated with extracapillary proliferation with pauci-immune crescent formation. Electron microscopic examination showed fibrinoid deposition in the glomerular basement membrane. In biochemistry, serum sodium (159 mmol/L) and serum potassium levels (17 mmol/L) were deranged. In kidney panel, serum urea (155.8 mg/dL) and serum creatinine levels (8.9 mg/dL) were highly increased suggesting severe form of disease.
On performing ANCA serology, her serum showed a predominantly diffuse, granular cytoplasmic ANCA (c-ANCA) staining pattern on indirect immunofluorescence. By direct enzyme-linked immunosorbent assay, there were high titers of ANCA directed against proteinase-3 (PR-3). PR-3 (1:100 with 1+ intensity) was highly raised and confirmed the diagnosis of granulomatosis with polyangiitis associated with c-ANCA positivity.
The patient underwent two sessions of hemodialysis with a 2-day interval with packed red cell transfusion. Following that, serum urea and creatinine levels were controlled. Due to high levels of circulating c-ANCA autoantibodies, TPE was planned in addition to the standard therapy. GPA comes under category I, Grade 1A; American Society for Apheresis guidelines 2016.[] TPE sessions were started on the 4thday of admission. A total of seven cycles was performed with 1.3 total plasma volumes exchanged on every alternate day. Fresh frozen plasma (FFP) and normal saline were used as replacement fluids. During the third cycle of TPE after 5 units of FFP transfusion, the patient developed allergic reaction in the form of severe itching all over the body. To treat allergic reaction, oral pheniramine maleate 5 mg and injection hydrocortisone 100 mg intravenous (i.v.) were given, and after 20 min, procedure was restarted and completed successfully. Rest six cycles of TPE was done uneventfully. Simultaneously, standard induction therapy was also started that comprised of combination of cyclophosphamide (500 mg, i.v.) and methylprednisolone 1000 mg, i.v. daily for 3 days followed by oral prednisolone 60 mg daily for at least 4 weeks. Mesna 200 mg slow i.v. over 2 h was also given to prevent cyclophosphamide-induced hemorrhagic cystitis. Regular monitoring of full blood count, serum proteins, renal function, liver function, urine cytology, and clinical symptoms were done. After seven cycles of TPE, the patient was improved clinically as indicated by her renal function tests and ANCA serology and hence TPE was stopped. The patient's recovery was faster due to the timely intervention of TPE along with standard immunosuppression therapy. The total hospital stay of patient was 18 days which was lesser in comparison to the patient who were treated with standard therapy alone. After that, the patient was on maintenance therapy with azathioprine (2 mg/kg/body weight) at least for 12 months and advised for monthly follow-up.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [38, 'years'], 'creatinine': [8.9, 'mg/dL'], 'sex': 'Female'}",4.97909,4.73014,5.22804,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 38 years old. The concentration of Creatinine is 8.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 8.9^(-1.154) * 38^(-0.203) * 1 * 0.742=4.97909.
Hence, the patient's GFR is 4.97909 mL/min/1.73m²."
3200,9,MDRD GFR Equation,lab test,decimal,pmc-6600126-1,Extracted,"On November 6, 2018, a 68-year-old female patient was admitted to the emergency room with altered level of consciousness. At the time of admission, her blood pressure was 80/60 mm Hg, pulse rate was 112 beats/min, respiratory rate was 24 breaths/min and body temperature was 34.9°C. She had chronic kidney disease (stage 4) and an 18-year history of type 2 diabetes mellitus treated with insulin over the past 10 years. She had been admitted for acute pyelonephritis in February 2015, December 2016 and August 2018. Following the three admissions, she resided in a nursing hospital. The patient was a non-smoker and had no previous history of pulmonary disease. On admission, her blood results showed an elevated white blood cell (WBC) count (18 990/uL), a low hemoglobin (8.3 g/dL) and normal platelets (317 000/uL). The patient’s blood urea nitrogen level and serum creatinine (Cr) level were markedly elevated (160 mg/dl and 11.59 mg/dl, respectively). Despite fluid resuscitation and catecholaminergic therapy, the patient deteriorated and developed septic shock with metabolic acidosis (lactate: 5.9 mmol/L; blood pH: 6.965; and bicarbonate: 5.5 mmol/L). Urine microscopy showed many WBCs per high power field, and the urine dipstick test was positive for nitrite. She was transferred to a medical intensive care unit and received continuous renal replacement therapy and antibiotics at a dose adjusted for renal impairment (piperacillin/tazobactam 2.25 g every 6 hours). On November 23, 2018, the patient developed dyspnea, and a chest X-ray examination showed atelectasis in the upper lobe of the right lung.
Urine cultures showed more than 100 000/ml of Escherichia coli, but no bacteria grew in the blood culture. On November 23, 2018, chest computed tomography (CT) scan showed partial atelectasis in the right upper lobe (RUL) and prominent wall thickening and enhancement in the proximal portion of the RUL bronchus (Fig. ). There was no evidence of other pulmonary diseases like bronchiectasis. On November 26, 2018, bronchoscopy showed inflammation of the RUL bronchus accompanied by necrosis (Fig. ). Acid fast bacilli (AFB) stain, Mycobacterium tuberculosis (MTB) DNA detection with polymerase chain reaction (PCR) technique and the culture for MTB were all negative. Bronchoscopic biopsy showed fungal infection with necrosis and yeast-like fungus with positive periodic acid–Schiff (PAS) stain (Fig. ).
Candida albicans grew from the endobronchial aspirate (WBC: >25; epithelial cell: <10). The EBFI was treated with one dose of intravenous fluconazole 400 mg for induction followed by 200 mg once daily by mouth. The patient’s electrolyte imbalance and uremia worsened during hospitalization. We considered dialysis treatment, but the patient rejected it because of cost. She signed a do-not-resuscitate order and died on December 13, 2018.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [68, 'years'], 'creatinine': [11.59, 'mg/dL'], 'sex': 'Female'}",3.26205,3.09895,3.42515,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 68 years old. The concentration of Creatinine is 11.59 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 11.59^(-1.154) * 68^(-0.203) * 1 * 0.742=3.26205.
Hence, the patient's GFR is 3.26205 mL/min/1.73m²."
3201,9,MDRD GFR Equation,lab test,decimal,pmc-4127544-1,Extracted,"A 26-year-old man was referred to our emergency department; he complained about bilateral red eye associated with a loss of visual acuity (VA) starting 1 week ago. His medical history was remarkable for grade IV chronic kidney disease secondary to genitourinary malformation and under treatment with hemodialysis. He developed secondary hypertension, which was managed with oral antihypertensive drugs.
His VA was ‘hand motions’ in both eyes. The anterior segment examination revealed bilateral subconjunctival hemorrhage with no signs of intraocular inflammation. Dilated fundus examination evidenced serous retinal detachment with macular involvement (fig. ). No retinal tears were observed in the peripheral retina examination with scleral depression. However, curvilinear whitish lesions scattered throughout the peripheral retina were observed. Optical coherence tomography (OCT) scans confirmed the presence of subretinal fluid in the macular region (fig. ).
The patient was uncompliant to oral antihypertensive therapy and dialysis treatment. His blood pressure measured 180/110 mm Hg. A systemic workup was conducted with the only relevant finding of a significantly increased creatinine value (17 mg/dl). Oral antihypertensive therapy and dialysis were initiated in order to control the kidney failure and the arterial hypertension.
One week later, his VA improved to 0.3 in both eyes. Dilated fundus examination demonstrated a significant regression of the retinal detachment. After 2 weeks, his VA improved to 0.5 in both eyes, showing a subcomplete resolution of the exudative detachment in his right eye and a persistence of subretinal fluid in the macula and the inferior retina in his left eye (fig. ).
As the retina reattached, splinter hemorrhages and retinal vascular tortuosity were observed, thus supporting the hypertensive origin of the retinopathy. Likewise, the whitish areas remained unchanged (fig. ), especially in the retinal periphery. We assume that this might be secondary to ischemia of the underlying retinal pigment epithelium and the choroid. A longer follow-up could not be performed because the patient did not show up for his scheduled visits.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [26, 'years'], 'creatinine': [17.0, 'mg/dL'], 'sex': 'Male'}",3.43448,3.26276,3.6062,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 26 years old. The concentration of Creatinine is 17.0 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 17.0^(-1.154) * 26^(-0.203) * 1 * 1=3.43448.
Hence, the patient's GFR is 3.43448 mL/min/1.73m²."
3202,9,MDRD GFR Equation,lab test,decimal,usmle-1490,Extracted,"A 62-year-old man comes to the physician because of fatigue and swelling of the lower legs for 3 weeks. One year ago, he had an 85% stenosis in the left anterior descending artery, for which he received 2 stents. He was diagnosed with hepatitis C 5 years ago. He has type 2 diabetes mellitus and arterial hypertension. Current medications include aspirin, metformin, and ramipril. He does not smoke or drink alcohol. His temperature is 37°C (98.6°F), pulse is 92/min, and blood pressure is 142/95 mm Hg. Examination shows 2+ pretibial edema bilaterally. The remainder of the examination shows no abnormalities. Laboratory studies show:
Hemoglobin 10.2 g/dL
Leukocyte count 6500/mm3
Platelet count 188,000/mm3
Serum
Na+ 137 mEq/L
Cl− 105 mEq/L
K+ 5.2 mEq/L
Urea nitrogen 60 mg/dL
Glucose 110 mg/dL
Creatinine 3.9 mg/dL
Albumin 3.6 mg/dL
HbA1C 6.8%
Urine
Blood negative
Glucose 1+
Protein 3+
WBC 0–1/hpf
A renal biopsy shows sclerosis in the capillary tufts and arterial hyalinosis.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [62, 'years'], 'creatinine': [3.9, 'mg/dL'], 'sex': 'Male'}",15.74324,14.95608,16.5304,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 62 years old. The concentration of Creatinine is 3.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.9^(-1.154) * 62^(-0.203) * 1 * 1=15.74324.
Hence, the patient's GFR is 15.74324 mL/min/1.73m²."
3203,9,MDRD GFR Equation,lab test,decimal,pmc-8259465-1,Extracted,"A 39-year-old African American female with 20-year history of HIV infection and hypertension presented with complaints of abdominal pain and decreased urinary output of 2 weeks duration. She had sustained a mechanical fall 2 weeks prior to presentation and had taken ibuprofen for pain control. Initial evaluation revealed a serum creatinine 5.5 mg/dL. Her baseline serum creatinine 3 months prior to presentation was 0.91 mg/dL. Urinalysis showed 3+ proteinuria and microhematuria, without microscopic casts. Urine protein-to-creatinine ratio was > 10 g/g. CD4 count was 267/µL and HIV viral load by PCR revealed viremia with 1,220 copies/mL. She was compliant with antiretroviral therapy (ART) consisting of bictegravir, emtricitabine, and tenofovir alafenamide (Biktarvy), and lisinopril 10 mg daily for hypertension.
Non-contrast computed tomography (CT) scan of the abdomen and pelvis showed mild bilateral hydronephrosis, marked diffuse irregular bladder wall thickening and ascites. Bladder cystoscopy revealed no evidence of ureteral obstruction but showed diffuse nodules throughout the bladder wall; multiple bladder biopsies were obtained. Given her renal insufficiency, tenofovir was stopped and ART was changed to renally adjusted dolutegravir, rilpivirine, and lamivudine. Serologic workup, including complement C3 and C4, antinuclear antibodies, hepatitis C antibody, hepatitis B surface antigen, anti-neutrophil cytoplasmic autoantibody (ANCA) titers, and anti-GBM antibody, were negative. Serum protein electrophoresis was consistent with acute inflammatory stress response, with no evidence for a monoclonal protein. However, serum free κ light chains were elevated at 1,988 mg/L, with serum free κ/λ ratio 36.4. Urine immunofixation revealed monoclonal free κ light chains. Attempted bone marrow biopsy was unsuccessful. Diagnostic paracentesis was negative for malignancy. Hemodialysis was initiated on hospital day 6 because of progressive renal failure and uremic symptoms.
Bladder biopsy revealed high-grade plasmablastic lymphoma (). Histopathology showed large plasmablastic cells diffusely positive for CD138, MUM-1, and negative for PAX-5, CD20, BCL-6, and BCL-2. Cell proliferation marker Ki-67 approached 100%. Tumor cells were positive for EBER1. Additional immunostains revealed that the plasmablastic lymphoma cells were κ light chain-restricted and positive for CD56, CD10, and c-MYC. They were negative for λ light chain, CD30, and AE1/AE3.
Diagnostic kidney biopsy, performed 9 days after presentation, revealed focal atypical κ-restricted tubular casts with diffuse acute tubular injury and 30% interstitial inflammation and edema, consistent with κ light chain cast nephropathy (). There was no evidence of glomerular disease by light microscopy, immunofluorescence, or electron microscopy.
Chemotherapy was initiated 2 weeks after initial presentation with bortezomib and CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone). She received 1 dose of intrathecal methotrexate, cytarabine, and hydrocortisone followed by 3 doses of intrathecal methotrexate alone to prevent central nervous system (CNS) relapse, which is common in patients with HIV-associated lymphoma []. She was maintained on ART during this period and started on trimethoprim-sulfamethoxazole and acyclovir for opportunistic infection prophylaxis.
Seven weeks after initial presentation, renal function recovered, and hemodialysis was discontinued. Eleven weeks after presentation, the patient achieved complete remission by imaging (PET). Her chemotherapeutic induction regimen was then switched to bortezomib with ifosfamide, carboplatin, and etoposide (ICE) as CHOP is considered insufficient treatment for PBL []. Six months after presentation, repeat bladder biopsy showed no evidence of PBL and additional testing including PET and bone marrow biopsy were negative confirming complete remission. Seven months after presentation, she underwent modified BEAM (BCNU, etoposide, cytarabine, melphalan) followed by autologous hematopoietic cell transplant. At last follow-up 8 months after autologous hematopoietic cell transplant, her renal function remains stable (creatinine 1.07 mg/dL) with minimal proteinuria (urine protein-to-creatinine ratio 0.36 g/g), normal plasma free light chains, and improved HIV viral load (364 copies/mL). She tolerated chemotherapy well, except for peripheral neuropathy and onychodystrophy which were attributed to her chemotherapy.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [39, 'years'], 'creatinine': [5.5, 'mg/dL'], 'sex': 'Female', 'Race': 'Black'}",10.46116,9.9381,10.98422,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 39 years old. The concentration of Creatinine is 5.5 mg/dL. 
The patient is Black, so the race coefficient is 1.212.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 5.5^(-1.154) * 39^(-0.203) * 1.212 * 0.742=10.46116.
Hence, the patient's GFR is 10.46116 mL/min/1.73m²."
3204,9,MDRD GFR Equation,lab test,decimal,trec-ct-2021-72,Extracted,"The patient is a 16-year-old girl recently diagnosed with myasthenia gravis, class IIa. She complains of diplopia and weakness affecting in her upper extremities. She had a positive anti-AChR antibody test, and her single fiber electromyography (SFEMG) was positive. She is on acetylcholinesterase inhibitor treatment combined with immunosuppressants. But she still has some symptoms. She does not smoke or use illicit drugs. She is not sexually active, and her menses are regular. Her physical exam and lab studies are not remarkable for any other abnormalities.
BP: 110/75
Hgb: 11 g/dl
WBC: 8000 /mm3
Plt: 300000 /ml
Creatinine: 0.5 mg/dl
BUN: 10 mg/dl
Beta hcg: negative for pregnancy","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [16, 'years'], 'creatinine': [0.5, 'mg/dL'], 'sex': 'Female'}",164.5865,156.35717,172.81583,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 16 years old. The concentration of Creatinine is 0.5 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.5^(-1.154) * 16^(-0.203) * 1 * 0.742=164.5865.
Hence, the patient's GFR is 164.5865 mL/min/1.73m²."
3205,9,MDRD GFR Equation,lab test,decimal,pmc-3420770-1,Extracted,"A 50-year-old black woman was admitted to the hospital with dyspnea and left hemibody swelling (breast, thorax and upper and lower limbs). These symptoms had started eight days before the admission and had gradually become more severe.
The patient had a severe form of a rare, heterogeneous, congenital cyanotic heart disease with pulmonary artery atresia, ventricular septal defect, and multifocal circulation with multiple aortopulmonary collaterals (type C) [] with resulting heart failure (NYHA class III) and chronic respiratory failure with oxygen home therapy (3 L/min).
Recent transthoracic echocardiogram revealed large ventricular septal defect, ascendant aortic aneurismatic dilatation, biventricular hypertrophy, pericardial effusion, and pulmonary atresia, with left ventricular ejection fraction of 32%.
Furthermore, she was HIV-positive and had been on highly active antiretroviral therapy (HAART) for 5 years; recent examinations showed undetectable HIV viral load (HIV-VL) and CD4 cells count of 169 for cubic millimeter of blood.
There was no history of drug allergies, nor of previous central venous cannulation.
Daily medications included furosemide 40 mg, digoxin 125 mcg, acetylsalicylic acid 100 mg, lorazepam 1 mg, HAART (tenofovir 245 mg, emtricitabine 200 mg, nevirapine 200 mg).
On physical examination the patient showed central cyanosis, jugular venous distention at 45 degrees, superficial venous circulation on the anterior chest wall, left hemibody swelling (particularly of the upper limb), and digital clubbing (Figures and ).
Her body temperature was 37°C, pulse rate was 92 bpm, respiratory rate was 24/min, and blood pressure was 118/56 mmHg.
There was no superficial lymphadenopathy. Lung examination showed decreased breath sounds over the left posterior lower chest and bibasilar rales. There was a grade III/IV loud systolic murmur heard all over the precordium and moderate hepatomegaly on abdominal examination. Blood examination showed leukocyte count 6800 × 103/mcL [4500–11000], hemoglobin 13.7 g/dL [11.5–15.5], platelet count 241 × 103/mcL [150–450], urea 44 mg/dL [17–43], creatinine 0.62 mg/dL [0.51–0.95], aspartate aminotransferase 28 U/L [<35], alanine aminotransferase 19 U/L [<35], gamma-glutamyltransferase 104 U/L [<38], alkaline phosphatase 116 U/L [30–120], lactate dehydrogenase 466 U/L [<247], BNP 1278 pg/mL [<100]. The hypercoagulability study was negative for deficiencies including protein S, protein C, and antithrombin III. Serum homocysteine was normal. Neither factor V Leiden mutation nor prothrombin gene mutation was detected. Anticardiolipin antibodies and lupus anticoagulant were negative too.
The electrocardiogram showed normal sinus rhythm with right bundle branch block.
The chest radiograph showed marked cardiomegaly and aortic aneurismatic dilatation ().
High-resolution computer tomography (CT) of the chest showed global cardiomegaly with pericardial effusion, thrombosis of the left axillary, subclavian and brachiocephalic veins, left chest and left upper limb edema, ascendant aortic aneurismatic dilatation (4.8 cm), descendant aortic ectasia, pulmonary atresia, small caliber of the right pulmonary artery and mural thrombosis of the left lower aortopulmonary collateral.
Color Doppler Ultrasonography highlighted no compression and no variability in flow velocity of left axillary-subclavian veins and normal morphology and compressibility of lower limbs circulation.
CT of the abdomen and pelvis confirmed hepatomegaly and detected normal permeability of the caval and iliac-femoral venous sector.
The diagnosis was left axillary, subclavian and brachiocephalic veins thrombosis, left lower aortopulmonary collateral arterial thrombosis and left lower limb lymphedema.
Due to patient comorbidities and thrombosis extension, we decided not to carry out thrombolysis, angioplasty or stent placement. A treatment with low molecular weight heparin (LMWH) in full dose was started, followed by warfarin, in order to maintain INR between 2.0 and 3.0. The patient also underwent lymphatic drainage with resolution of the edema of the left hemibody after 8 weeks of treatment.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [50, 'years'], 'creatinine': [0.62, 'mg/dL'], 'sex': 'Female', 'Race': 'Black'}",123.49053,117.316,129.66506,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 50 years old. The concentration of Creatinine is 0.62 mg/dL. 
The patient is Black, so the race coefficient is 1.212.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.62^(-1.154) * 50^(-0.203) * 1.212 * 0.742=123.49053.
Hence, the patient's GFR is 123.49053 mL/min/1.73m²."
3206,9,MDRD GFR Equation,lab test,decimal,pmc-4518342-1,Extracted,"A four-year-old male patient presented with progressive left thigh swelling, lower abdominal swelling, both of six months' duration and inability to walk for four weeks prior to presentation.
Left thigh swelling started insidiously and became progressively bigger. It was initially painless but later became painful. There was history of intramuscular injection into the gluteal region, which developed into injection abscess for which child had incision and drainage though with insignificant improvement.
There was associated low grade fever, malaise and weight loss. About four weeks prior to presentation, he could no longer walk probably due to pain because power in both lower limbs was normal. No associated change in bowel habit.
Child had plain radiograph of the thighs that showed soft tissue swelling of the left thigh with no bony abnormality. Abdomino-pelvic ultrasound scan showed heterogeneous lower abdominal mass, more on the left side; bilateral hydronephrosis and relatively normal liver and spleen.
Computerised tomographic (CT) scan of the abdomen and pelvis done at this time revealed a heterogeneous soft tissue pelvic mass with no associated bony lesion. Enlarged and hydronephrotic kidneys were worse on the left than on the right. Normal liver and spleen with no metastases noted.
Tissue biopsy taken from the left thigh revealed “malignant round blue cell tumour most probably an embryonal rhabdomyosarcoma.”
He was admitted following histological diagnosis of embryonal rhabdomyosarcoma for commencement of chemotherapy. However while on admission, he developed acute renal failure secondary to obstructive uropathy. Urinary output started to reduce and he became anuric despite repeated renal challenges. There was generalised oedema and irritability.
Biochemical parameters then were deranged with Sodium of 109.7 mmol/L; HCO3 of 15.3 mmol/L; urea of 15.3 mmol/L; Creatinine of 583 µmol/L and Uric acid of 818 µmol/L.
The child then had right PCN for urinary diversion and antegrade pyelography. This was done using the standard ‘Seldinger’ technique of needle puncture, guide wire insertion and serial dilatation. It showed markedly dilated right ureter, which terminated abruptly in the pelvis. [] No contrast is seen flowing into the urinary bladder.
There was significant clinical and biochemical improvement following right percutaneous urinary diversion; generalised oedema got resolved and there was improvement in urinary output.
Percutaneous urinary diversion was also done for the left kidney, five days later. This significantly improved the biochemical parameters.
The child also had repeated blood transfusion for anaemia and work-up for commencement of chemotherapy.
Chemotherapy was instituted in a combination dose of Vincristine (1.5 mg/m²), Actinomycin D (1.5 mg/m²) and cyclophosphamide (250 mg/m²²).
There was significant reduction in both thigh and abdominal swelling after two courses of cytotoxic therapy. The child resumed passage of urine per-urethra at this time following which drainage through the nephrostomy tubes was stopped.
The child had taken the third course of cytotoxic drugs and there was sustained improvement as at the last clinic follow-up.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [4, 'years'], 'creatinine': [583.0, 'µmol/L'], 'sex': 'Male'}",15.06734,14.31397,15.82071,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 4 years old. The concentration of Creatinine is 583.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 583.0 µmol. To convert 583.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 583.0 µmol Creatinine * 1e-06 mol/µmol = 0.00058 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00058 mol Creatinine * 113.12 g/mol = 0.06561 g Creatinine. To convert 0.06561 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.06561 g Creatinine * 1000.0 mg/g = 65.61 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 65.61 mg Creatinine/10.0 dL = 6.561 mg Creatinine/dL. The concentration value of 583.0 µmol Creatinine/L converts to 6.561 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 6.561^(-1.154) * 4^(-0.203) * 1 * 1=15.06734.
Hence, the patient's GFR is 15.06734 mL/min/1.73m²."
3207,9,MDRD GFR Equation,lab test,decimal,pmc-5093871-1,Extracted,"A 78-year-old male with history of hypertension, dyslipidemia, and prosthetic aortic valve replacement presented to the emergency department with complaints of exertional shortness of breath for few days. Chest X-ray showed widened mediastinum. Subsequently, CT angiogram of the chest showed massively dilated ascending aorta with maximum diameter of 10.2 cm []. Transthoracic echocardiogram revealed normal ejection fraction with mild aortic insufficiency, well-functioning prosthetic aortic valve, and no aortic stenosis. His creatinine was 1.8 mg/dl, and he had received 150 ml of contrast for CT angiogram. It was necessary to evaluate his coronary arteries before surgery for AAA.
There were two options in this case: coronary CT angiography or conventional coronary angiography. Coronary CT angiography would require about 150 ml of contrast.[] A diagnostic coronary angiogram can be done using about 50 ml of contrast.[] Given his renal insufficiency, we decided to do conventional coronary angiography. Since the ascending aorta and root were extremely dilated, we knew it would not be possible to engage the coronaries using regular catheters and standard technique. Hence, telescopic technique was used. Amplatz left 3 (AL3) 7F (French) guide catheter (90 cm) was initially used, and nonselective injection of contrast was done to see the coronary ostium [ and ]. After that, a 5F multipurpose (MP) catheter (110 cm) was telescoped through 7F AL3 guide catheter to engage the ostium of the left main coronary artery [ and ]. Using this technique, images of coronaries were obtained, and it showed minimal luminal irregularities in major epicardial coronary arteries. Total of 50 ml contrast was used. The patient underwent successful surgery with aortic valve replacement and excision of aneurysm with graft placement. The most likely etiology of giant aortic aneurysm in our patient was atherosclerosis. However, we did not have any record of his previous aortic valve surgery, and we do not know if it was a bicuspid aortic valve. In that case, he could have had aortopathy associated with bicuspid aortic valve.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [78, 'years'], 'creatinine': [1.8, 'mg/dL'], 'sex': 'Male'}",36.67401,34.84031,38.50771,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 78 years old. The concentration of Creatinine is 1.8 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.8^(-1.154) * 78^(-0.203) * 1 * 1=36.67401.
Hence, the patient's GFR is 36.67401 mL/min/1.73m²."
3208,9,MDRD GFR Equation,lab test,decimal,pmc-7789149-1,Extracted,"A 54-year-old Chinese man presented with a 4-year history of multiple myeloma (IgAλ), proteinuria and hematuria. He had been receiving intermittent chemotherapy including TD (thalidomide and dexamethasone), TCD (thalidomide, cyclophosphamide and dexamethasone), PD (bortezomib and dexamethasone), PCD (bortezomib, cyclophosphamide and dexamethasone) and PDDT (bortezomib, doxorubicin, dexamethasone and thalidomide) for 3 years. The hematologic response was not available. He had persistent hematuria and proteinuria with normal serum creatinine (SCr). Then, his SCr increased to 1.64 mg/dl (normal range: 0.50–1.50 mg/dl) 11 months before admission, and 6.18 mg/dl 4 months before admission and went on hemodialysis. One month prior to presentation, he received one course of PTD (bortezomib, thalidomide and dexamethasone) chemotherapy. Then he was referred to our division in September 2017 to further evaluate the renal dysfunction.
He had a 10-month history of hypertension (160/100 mmHg) and was treated with nifedipine and metoprolol. Blood pressure was controlled around 130/80 mmHg. He also had a 50-year history of asthma. His family history was unremarkable. On admission, his medical examination revealed blood pressure 128/78 mmHg, heart rate 79 beats/min and respiration rate 18/min. He was pale, and wheeze was heard in both lungs. Hepatomegaly and splenomegaly were noticed.
After admission, complete blood count showed white blood cell (WBC) 4.1 × 109/L (3.5–9.5 × 109/L), hemoglobin 73 g/L (130-175 g/L) and platelet count 52 × 109/L (125–350 × 109/L). His SCr level was 5.58 mg/dl, calcium 2.14 mmol/L, serum albumin 34.5 g/L (40–55 g/L) and serum lactate dehydrogenase level 198 IU/L (100–240 IU/L). His urinalysis showed proteinuria 1+ and hematuria (12–15 red blood per high power field). Urine protein excretion was 1.19 g/d with 70.1% of albumin, 25.5% of low molecular weight protein and 4.4% of high molecular weight protein. Urine albumin creatinine ratio (ACR) was 1506.82 mg/gCr (< 30 mg/gCr), N-acetyl-glucosaminidase (NAG) 2 U/L (0–21), and α1-microglobulin 152 mg/L (0-12 mg/L). Kidney ultrasound showed enlarged kidneys (right kidney 13 cm, left kidney 14.1 cm) with increased echogenicity. Serum B-type natriuretic peptide (BNP) was 3359 pg/ml (< 100) and cardiac troponin I (cTnI) 0.05 ng/ml (0–0.03). Electrocardiogram was normal. Echocardiography showed enlarged left ventricle, left atria and right atria, left ventricle showed symmetrical hypertrophy, left ventricular ejection fraction was 65%, and there was severe mitral valve regurgitation and moderate tricuspid valve regurgitation. Systolic blood pressure of pulmonary artery was elevated (56 mmHg). Liver enzymes were normal. Monoclonal IgAλ plus free λ spike was identified in both serum and urine by immunofixation electrophoresis. Serum free light chain test was not done. His serum immunoglobulin (Ig) G level was 3.76 g/L (7.23–16.85 g/L), IgA level was 3.55 g/L (0.69–3.82 g/L), and IgM level was 0.24 g/L (0.63–2.77 g/L). Plasma C3 level was 0.566 (0.60–1.50) g/L, and C4 level was 0.195 (0.12–0.36) g/L. Hepatitis B surface antigen (HBsAg), anti-hepatitis C virus (HCV), antihuman immunodeficiency virus (HIV), Treponema pallidum antibody (TP-Ab), anti-nuclear antibodies, anti-neutrophil cytoplasmic antibodies, anti-glomerular basement membrane antibody and anti-phospholipase A2 receptor (PLA2R) antibodies were all negative.
To identify the cause of albumin-dominant proteinuria and acute kidney disease, the patient underwent renal biopsy on October 16th, 2017. Direct immunofluorescence (IF) examination of frozen renal tissue revealed IgA++ (Fig. a), λ++ (Fig. b) depositing along the glomerular capillary wall and tubular basement membrane, but not κ. Some intratubular casts showed strong staining for λ+++ (Fig. c) with negative κ. No significant deposits for IgG, IgM, C3 and C1q in the glomeruli. Light microscopic examination showed 5 glomeruli. The glomeruli revealed minimal mesangial proliferation (Fig. d) with some glomeruli showed ischemic change. Tubular epithelial cells exhibited focal loss of brush border and focal tubular atrophy. Periodic acid-Schiff (PAS) negative thick protein casts were noticed in the tubular lumens (Fig. e), the protein casts showed fibrillary structure on silver staining (Fig. f). Mononuclear cells were found in the center of the protein casts (Fig. g). These protein casts were Congo-red positive (Fig. h) and showed apple- green birefringence with polarized microscopy (Fig. i). A few protein casts were Congo-red negative. There was very little amyloid deposit in one artery, and no amyloid deposit in glomeruli or interstitia. On electron microscopy, the glomeruli were normal, and there were no deposits along the glomerular basement membrane or tubular basement membrane (Fig. j). Only one protein cast was found on electron microscopy but no amyloid fibrils were found on this protein cast.
The final diagnosis of this patient was multiple myeloma (IgAλ) with MCN with diffuse amyloid casts. He was maintained on chemotherapy and hemodialysis. He died 8 months after renal biopsy.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [54, 'years'], 'creatinine': [5.58, 'mg/dL'], 'sex': 'Male', 'Race': 'Asian'}",10.70893,10.17348,11.24438,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 54 years old. The concentration of Creatinine is 5.58 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 5.58^(-1.154) * 54^(-0.203) * 1 * 1=10.70893.
Hence, the patient's GFR is 10.70893 mL/min/1.73m²."
3209,9,MDRD GFR Equation,lab test,decimal,pmc-4635960-4,Extracted,"A 57-year-old male presented with fever (38.9°C), chest pain, cough, and progressive dyspnea. The patient exhibited tachypnea (34 breaths/min) and tachycardia (134 bpm). Auscultation revealed decreased breath sounds in both lung bases, with crackles on the left. A chest X-ray revealed bilateral pleural opacities and enlargement of the cardiac silhouette ( A). Echocardiography showed moderate pericardial effusion affecting the entire cardiac silhouette. Pericardiocentesis yielded 250 mL of exudative fluid. A CT scan of the chest showed pneumonia in the left lower lobe, bilateral pleural effusion, and moderate pericardial effusion ( B). Thoracentesis was performed and yielded 1,050 mL of exudative fluid. Laboratory tests yielded the following data: white blood cell count, 11.78 × 109 cells/L (84.3% neutrophils, 4.3% lymphocytes, and 9.1% monocytes); platelet count, 512 × 109/L; serum C-reactive protein, 31.27 mg/dL; serum creatinine, 0.94 mg/dL; serum sodium, 133 mEq/L; and serum potassium, 3.72 mEq/L. Examination of the pleural fluid showed a pH of 7.16, a glucose level of 4.5 mg/dL, proteins at 49.1 g/L, and an LDH content of 1,385 U/L. A urinary pneumococcal antigen test was positive. Pleural fluid culture was positive for S. pneumoniae. The patient was treated for four weeks with amoxicillin-clavulanate (2.2 g/8 h, i.v.) plus levofloxacin (500 mg twice a day), together with a nonsteroidal anti-inflammatory drug (ibuprofen, 800 mg/day), after which there was nearly complete resolution of the alterations seen on the chest X-ray and CT scan.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [57, 'years'], 'creatinine': [0.94, 'mg/dL'], 'sex': 'Male'}",82.71912,78.58316,86.85508,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 57 years old. The concentration of Creatinine is 0.94 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 0.94^(-1.154) * 57^(-0.203) * 1 * 1=82.71912.
Hence, the patient's GFR is 82.71912 mL/min/1.73m²."
3210,9,MDRD GFR Equation,lab test,decimal,pmc-6244097-1,Extracted,"A 32-year-old female that has been a HCV carrier for the past 10 years came to our clinic for hepatitis C treatment. She had not received any treatment for hepatitis C in the past. She also had a history of thalassemia minor and SCD, requiring frequent hospitalizations for sickle cell crisis and multiple blood transfusions. She had undergone splenectomy in childhood and denied illicit drug use, smoking, or alcohol abuse. At the time of her visit, she was taking folic acid only. Her baseline blood workup showed hemoglobin 8.4 g/dL, platelets 297 K/μL, creatinine 0.33 mg/dL, albumin 3.9 g/dL, INR 1.1, AST 94 IU/l, ALT 35 IU/l, ALP 96 IU/l, and total bilirubin 2.6 mg/dL. Hepatitis C viral load was 38,907 IU/mL with genotype 1a. Recent abdominal CT revealed a mildly nodular hepatic contour with hypertrophied left hepatic lobe, indicative of cirrhosis, with no evidence of ascites. The FibroTest revealed severe fibrosis with a score of F4. Hepatitis B surface antigen and HIV antibodies were checked, and both were negative. As the patient had not been previously treated for hepatitis C and had Child-Pugh class A liver cirrhosis with no serologic evidence of HBV and HIV coinfection, once-daily ledipasvir 90 mg/sofosbuvir 400 mg was initiated for 12 weeks. At the 4-week follow-up, the patient complained of mild headache and fatigue. Repeat blood workup showed hemoglobin 7.8 g/dL, AST 93 IU/l, ALT 49 IU/l, and total bilirubin 2.9 mg/dL, with an undetectable HCV load. Her treatment continued for the remaining 8 weeks, during which headache and fatigue resolved completely. At the end of the 12-week ledipasvir/sofosbuvir course, hemoglobin stabilized at 8.4 g/dL, and no increase in LDH, total bilirubin or retic count was noted. HCV viral load remained undetectable 3 months after treatment completion.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [32, 'years'], 'creatinine': [0.33, 'mg/dL'], 'sex': 'Female'}",230.95716,219.4093,242.50502,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 32 years old. The concentration of Creatinine is 0.33 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.33^(-1.154) * 32^(-0.203) * 1 * 0.742=230.95716.
Hence, the patient's GFR is 230.95716 mL/min/1.73m²."
3211,9,MDRD GFR Equation,lab test,decimal,pmc-7302721-1,Extracted,"A 77-year-old gentleman with a past medical history significant for hypertension, hyperlipidemia, chronic kidney disease and recent cerebrovascular accident presented to the emergency department with two weeks of intention tremors increasing in intensity to the extent that he was unable to walk. He also reported limited oral intake secondary to nausea over approximately the same period. Medication reconciliation was notable for omeprazole and furosemide. Vital signs in the emergency department were within normal limits, and physical exam was notable only for significant generalized tetany that worsened with intention. The patient’s electrocardiogram (EKG) revealed normal sinus rhythm with multiple premature atrial contractions (Figure ).
Initial laboratory results showed a creatinine of 1.18 mg/dL (which is at the patient’s baseline), sodium of 143 mmol/L, potassium of 3.3 mmol/L, phosphate of 2.5 mg/dL, calcium of 7.4 mg/dL and an undetectable magnesium level of <0.6 mg/dL. Additionally, parathyroid hormone was elevated to 79 pg/mL (reference range = 15-65 pg/mL).
In the emergency department, he was given 20 milliequivalents oral potassium replacement and one gram of intravenous magnesium sulfate with immediate improvement of his tetany. Omeprazole and furosemide were discontinued on admission, and causes of hypomagnesemia were evaluated. Both random urine and 24-hour urine magnesium testing did not reveal evidence of renal magnesium wasting. Furthermore, in the setting of recent occipital and cerebellar infarcts, magnetic resonance imaging of the patient’s brain was performed, which showed only encephalomalacia of the left occipital region from his prior ischemic stroke without evidence of an acute infarct as possible etiology (Figure ).
The patient required aggressive electrolyte replacement of magnesium, calcium, phosphate and potassium throughout his hospital course. He was asymptomatic at the time of discharge on hospital day 5 and was prescribed oral magnesium, calcium and vitamin D replacement. Discharge laboratory results were notable for stable creatinine, sodium of 139 mmol/L, potassium of 4.3 mmol/L, phosphate of 2.4 mg/dL, calcium of 8.4 mg/dL and a magnesium level of 1.8 mg/dL. Repeat magnesium level one week after discharge remained stable at 2.2 mg/dL. The patient remained on magnesium supplemental for a period of eight months after discharge before this was discontinued by his primary care physician. His measured serum magnesium level three months after discontinuation was within normal limits at 2.1 mg/dL.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [77, 'years'], 'creatinine': [1.18, 'mg/dL']}",59.85888,56.86594,62.85182,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 77 years old. The concentration of Creatinine is 1.18 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.18^(-1.154) * 77^(-0.203) * 1 * 1=59.85888.
Hence, the patient's GFR is 59.85888 mL/min/1.73m²."
3212,9,MDRD GFR Equation,lab test,decimal,pmc-3808806-1,Extracted,"An 83-year-old man was admitted to our unit for rapidly worsening renal function 3 weeks following angioplasty of the left internal carotid artery. During this 3-week period his serum creatinine increased from 2.0 to 5.4 mg/dl. The patient had suffered from hypertension within the last 20 years and had chronic kidney disease with unremarkable urinalysis and diffuse peripheral vasculopathy. At the time of admission, he was being treated with an angiotensin receptor blocker (ARB), a dihydropyridine calcium channel blocker, aspirin and rosuvastatin (20 mg/day), which was prescribed following the carotid angioplasty. At admission the patient was afebrile, eupneic and mildly hypovolemic, showed normal diuresis and had a blood pressure of 110/60 mm Hg and a heart rate of 88 bpm. Laboratory tests were normal except for elevated serum creatinine (5.4 mg/dl) and BUN (73 mg/dl). Urinalysis showed no active sediment with mild proteinuria (500 mg/day). ANA, ENA, C3, C4, CH50, ANCA, cryoglobulinemia, rheumatoid factor, serum and urine protein immunofixation and free light-chain concentrations were all within the normal range. Kidney ultrasonography showed elevated echogenicity of the parenchyma and an increased renal resistance index (0.76) in the absence of renal artery stenosis. The ARB was discontinued and the patient received intravenous crystalloids for the next 72 h. At this time, the possibility of atheroembolic renal disease was excluded since the recent carotid angioplasty was performed through a femoral artery catheter, during which both an ophthalmologic examination for retinal cholesterol crystal emboli and dermatological manifestations were negative and did not show eosinophilia. However, because renal function did not recover (serum creatinine: 5.9 mg/dl), an echo-guided biopsy of the left kidney was performed. Light microscopy showed interstitial edema with lymphocyte infiltrate associated with tubulitis (fig. ). Electron microscopy evaluation was negative. Immunofluorescence was aspecific and not consistent. Based on these results, a diagnosis of acute tubulointerstitial nephritis was made.
Since rosuvastatin was the most recently introduced drug, a possible relationship between the drug and AIN was considered. Thus, rosuvastatin was withdrawn, and oral prednisolone (1 mg/kg/day) was prescribed but rapidly tapered over a period of 4 weeks. The patient was discharged with conservative therapy, and after 8 weeks renal function values returned to baseline (serum creatinine 2 mg/dl, BUN 30 mg/dl, proteinuria 150 mg/24 h and urinalysis at polarized light microscopy was unremarkable).
One month later, the same ARB was reintroduced and, because of the high cardiovascular risk of the patient, a different statin (atorvastatin 20 mg/day) was prescribed. The patient is being regularly followed up at our outpatient service and, 6 months after the beginning of atorvastatin, has not shown any deterioration in renal functions.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [83, 'years'], 'creatinine': [5.4, 'mg/dL'], 'sex': 'Male'}",10.19255,9.68292,10.70218,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 83 years old. The concentration of Creatinine is 5.4 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 5.4^(-1.154) * 83^(-0.203) * 1 * 1=10.19255.
Hence, the patient's GFR is 10.19255 mL/min/1.73m²."
3213,9,MDRD GFR Equation,lab test,decimal,pmc-4164317-1,Extracted,"An 81-year-old Caucasian male presented to our hospital with a 10-day history of fever and non-productive cough. He also complained of abdominal pain, malaise, and weight loss.
His past medical history included hypertensive cardiomyopathy. He was diagnosed with nephrotic syndrome several months previously when a renal biopsy showed changes of membranous nephropathy stage III. Three months after this diagnosis, he was admitted to our hospital due to progressive worsening of renal function and persistent nephrotic syndrome. A laboratory test, chest radiograph, and an abdominal ultrasound scan ruled out secondary causes of membranous nephropathy and treatment with CBL 10mg and methylprednisolone 0.5mg/kg daily was started. Twenty-two days after the initiation of this treatment, he presented to our hospital with fever and non-productive cough and was admitted.
On initial assessment his temperature was 38°C, his blood pressure was 125/75mmHg, and his cardiac frequency was 105 beats per minute. His oxygen saturation level was 93%. There were no oral lesions. An examination of the lungs revealed widespread rhonchi. A cardiac examination demonstrated a regular rhythm and no murmurs. His abdomen was soft, not distended, but painful at the epigastrium.
His laboratory tests showed a white blood cell count of 2.3×109/L, neutrophils at 82%, a hemoglobin level of 11.8g/dL, platelets at 96×109/L, lactate dehydrogenase at 965U/L, a serum creatinine of 2.8mg/dL, urea at 164mg/dL, total proteins at 4.1g/dL, albumin at 2.6g/dL aspartate transaminase at 74U/L, alanine transaminase at 98U/L, gamma-glutamyltransferase at 255U/L, cholesterol at 219mg/dL, and triglyceride at 416mg/dL. His procalcitonin level was lower than 0.5ng/mL. Coagulation studies revealed no abnormalities. A urinalysis showed 14 to 16 red blood cells/high-powered field and 4g of protein. The urine culture was negative. Serology test results were negative for hepatitis C virus, hepatitis B virus, and human immunodeficiency virus. The polymerase chain reaction (PCR) assay for detecting CMV was positive with 31,400copies/mL.His chest radiograph showed a bilateral consolidation and pleural effusion (Figure ). His pulmonary angiography, ventilation-perfusion, and abdominal ultrasound scan did not show any abnormalities. A bronchoscopy procedure was rejected due to his respiratory conditions. So that cytology or immunohistochemical tests were not possible.The patient was treated with meropenem, levofloxacin and caspofungin on his admission. Signs of acute respiratory distress and necessity of non-invasive continuous positive airway pressure and hemodialysis marked the initial clinical evolution. Follow-up chest radiographs showed progression of the findings, with irregular, multifocal, patchy consolidation (Figure ). On the third day, treatment with vancomycin and ganciclovir was started as well. All antibacterial and antifungal drugs were administrated until his cultures were negative and a PCR assay for detecting CMV was positive. An intravenous infusion of 5mg/dl ganciclovir every 12 hours for 21 days was the specified treatment course. Viral load suppression during the first several weeks of antiviral therapy, associated with clinical and renal improvement, which allowed the stopping of hemodialysis, was finally observed. Viral load monitoring with weekly CMV-PCRs was performed for four weeks until the results were negative.
He was finally discharged after thirty days and continues to do well.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [81, 'years'], 'creatinine': [2.8, 'mg/dL'], 'sex': 'Male', 'Race': 'White'}",21.85724,20.76438,22.9501,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 81 years old. The concentration of Creatinine is 2.8 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.8^(-1.154) * 81^(-0.203) * 1 * 1=21.85724.
Hence, the patient's GFR is 21.85724 mL/min/1.73m²."
3214,9,MDRD GFR Equation,lab test,decimal,pmc-3731623-1,Extracted,"A 43-year-old man presented to the emergency department complaining of lower extremity edema for 2 weeks. The patient denied any pertinent past medical or family medical history; though he took metoprolol and hydrochlorthiazide for about 1 month a year earlier, he was not taking either of these agents at the time of presentation. He denied use of nonsteroidal anti-inflammatory agents and recreational drugs (including cocaine, heroin and phencyclidine). Initial physical examination was significant for elevated blood pressure (151/94 mm Hg) and pitting edema in both lower extremities. Initial laboratory analysis at presentation (table ) revealed renal failure (serum creatinine 2.6 mg/dl) and anemia (hemoglobin 10.8 g/dl, hematocrit 33.4% and mean corpuscular volume 85.4 fl). Urinalysis (random urine; table ) showed proteinuria, small blood and pyuria without bacteria. Proteinuria was confirmed on 24-hour urine collection that demonstrated nephrotic-range protein (25 g/24 h). Kidney ultrasound revealed enlarged kidneys bilaterally with multiple cysts and this was confirmed by computed tomography (CT) scanning (fig. ). A complete serologic evaluation, including hepatitis screen, was performed and was unrevealing (table ).
Initially, the patient was empirically treated with intravenous steroid pulse (methylprednisolone, 1 g daily for 3 days) and then switched to prednisone orally (1 mg per kilogram daily). A CT-guided kidney biopsy was performed and revealed immune complex glomerulonephritis with features of membranous nephropathy with crescent formation (fig. ). Despite treatment with oral prednisone (1 mg/kg), the patient's renal function declined and he became oliguric. Intermittent hemodialysis was initiated. In addition to oral steroid, treatment with mycophenolate (500 mg twice daily; escalated to 1,500 mg twice daily over 2 weeks) was started. Over a 5-month period, urine output increased in association with improvement in kidney function. Concurrently, serum albumin recovered to normal values and proteinuria decreased from 25 to 3 g daily. Because of persistent nephrotic-range proteinuria, cyclosporine 75 mg twice daily was added to his medication regimen. Over the ensuing 3 months, the patient manifested further improvement in physiologic parameters. Accordingly, prednisone dosage was reduced (10 mg orally per day) and mycophenolate mofetil (MMF) was maintained at 1,500 mg orally twice daily and cyclosporine at 75 mg orally twice daily. Hemodialysis was subsequently discontinued and the patient has been off dialysis with stable chronic kidney disease stage 3 (creatinine clearance 45 ml/min by 24-hour urine studies). He continues to be monitored closely in an outpatient setting for any changes in renal function. Immunosuppressive agents are being tapered.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [43, 'years'], 'creatinine': [2.6, 'mg/dL'], 'sex': 'Male'}",27.07477,25.72103,28.42851,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 43 years old. The concentration of Creatinine is 2.6 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.6^(-1.154) * 43^(-0.203) * 1 * 1=27.07477.
Hence, the patient's GFR is 27.07477 mL/min/1.73m²."
3215,9,MDRD GFR Equation,lab test,decimal,pmc-5472366-1,Extracted,"A 56-year-old African American male with history of prostate cancer had undergone open prostatectomy at an outlying hospital, which was followed by a complicated recovery due to wound dehiscence that ultimately led to Enterococcal bacteremia and endocarditis. He was started on intravenous gentamicin and ampicillin for 4 weeks while inpatient and then discharged to community nursing home to finish his course of antibiotics. One week later he presented to our tertiary care center with generalized weakness and recurrent falls. Vital signs on admission were blood pressure of 149/78 mmHg, respiratory rate 17/min, pulse 99 bpm, SaO2 95% on room air. Physical exam showed expiratory wheezing but otherwise unremarkable. Labs were significant for BUN 41 mg/dL, Cr 5.22 mg/dL, Na 136 meq/L, K 4.3 meq/L, troponin 0.03 ng/mL, WBC count was 14,000/mm3, Hb 8.4 g/dL, PLT 505/mm3. His baseline creatinine was normal. He was found to be in non-oliguric acute kidney injury likely secondary to gentamicin, so ampicillin and gentamicin were discontinued and patient was started on daptomycin. Electrocardiogram (ECG) showed normal sinus rhythm without any ST-T wave changes. A transthoracic echo was obtained on which echogenic mass was visualized on aortic valve leaflets measuring 1.99x1.67 cm with moderate aortic regurgitation (). Cardiothoracic surgery was consulted, they recommended aortic valve repair once renal function normalized. Three days later patient started to complain of left sided chest pain radiating down the left arm and left jaw. Stat ECG was obtained that showed ST segment elevation in I, aVL and V3-V6 leads consistent with anterolateral STEMI (). Emergent coronary angiogram showed 99% left anterior descending artery occlusion (). Due to the presence of persistent symptoms and ECG changes, a bare metal stent was placed. This acute coronary event was thought to be an embolic —phenomenon given the fact that he had just had a normal coronary angiogram 3 months prior. Unfortunately, patient's condition gradually deteriorated with worsening respiratory and renal function requiring mechanical ventilation and hemodialysis. Patient was on ventilator support for a few days. He continued dialysis through temporary dialysis catheter. His respiratory status improved gradually and he was extubated. Patient renal functions improved slowly as well and got discharged to rehabilitation facility He is being followed in cardiology office and continues to be stable.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [56, 'years'], 'creatinine': [5.22, 'mg/dL'], 'sex': 'Male', 'Race': 'Black'}",13.91447,13.21875,14.61019,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 56 years old. The concentration of Creatinine is 5.22 mg/dL. 
The patient is Black, so the race coefficient is 1.212.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 5.22^(-1.154) * 56^(-0.203) * 1.212 * 1=13.91447.
Hence, the patient's GFR is 13.91447 mL/min/1.73m²."
3216,9,MDRD GFR Equation,lab test,decimal,pmc-6499096-1,Extracted,"A 47-year-old man with a medical history of smoking and chronic hidradenitis suppurativa (HS) presented to the emergency department complaining of asthenia, vomiting, watery diarrhoea and a painful swelling in the left mandibular region that had started 3 weeks previously. He was self-medicated with ibuprofen 600 mg (4 times a day). He did not report fever, arthralgia or urinary symptoms.
HS had started 20 years previously with cervical, axillar and inguinal involvement. The patient had undergone plastic surgery of the right axilla and reported periods of exacerbation controlled with non-steroidal anti-inflammatory drugs (NSAIDs).
On examination, he was debilitated, normotensive and apyretic. Cardiac, pulmonary and abdominal evaluations did not show any alterations. Examination of the skin revealed confluent inflammatory nodules with purulent drainage (Hurley 3/3) in the gluteal area ().
Arterial blood gas revealed severe metabolic acidaemia (pH 7.22, HCO3 8.3). Laboratory findings reported normocytic anaemia (Hgb 6.7 g/dl; normal 13.5–18.0 g/dl), leucocytosis (13.87 K/μl; normal 4–10 K/μl), uraemia (322 mg/dl; normal 6–23 mg/dl) and elevated creatinine (20.55 mg/dl; normal 0.50–1.20 mg/dl), with low-normal albumin (3.5 g/dl; normal 3.5–5.2 g/dl) and hyperkalaemia (5.1 mmol/l; normal 3.4–5.0 mmol/l). The urinary study showed a protein to creatinine ratio of >4.00 mg/mg. An abdominal and renal ultrasound revealed splenomegaly (18 cm bipolar axis), kidneys with preserved dimensions and increased cortico-medullar differentiation and absence of hydronephrosis. The patient started urgent renal replacement therapy with haemodialysis and was admitted to the internal medicine department.
The patient maintained haemodialysis with no recovery of renal function. A 24-hour urine collection documented proteinuria of 18.7 g/day. A renal biopsy with immunostaining study was performed, revealing deposition of amyloid A in all 34 glomeruli and vascular walls with apple-green birefringence upon examination of Congo red-stained tissue under polarized light microscopy ().
AA was confirmed by immunohistochemical amyloid protein identification with DNA analysis. Infectious, autoimmune (including anti-nuclear antibody, rheumatoid factor, anti-Ds-DNA, anti-ANCA and anti-citrullinated peptide antibody) and monoclonal gammopathy (including serum protein electrophoresis, urine protein electrophoresis, immunofixation and serum free light chain assay) studies were negative. Inflammatory studies revealed an elevated erythrocyte sedimentation rate (ESR) of 119 mm/h, C-reactive protein (CRP) of 152.2 mg/l and serum amyloid protein (SAP) of 11.9 ng/l (normal 0.0–6.4 ng/l). Coagulation and cardiac studies (including NT-proBNP and troponin levels) were normal.
As the patient maintained watery diarrhoea without an infectious cause identified and to evaluate for another manifestation of amyloidosis, a colonoscopy with biopsy was performed and showed amyloid deposition () without signs of inflammatory bowel disease. A transthoracic echocardiogram and ECG did not reveal any alterations.
As HS is associated with inflammatory rheumatic diseases and an increased risk of malignancy, a mandibular and thoracoabdominal computed tomography (CT) scan was performed and revealed sclerosis with cortical periosteal reaction in the left mandibular branch, subchondral sclerosis in the right sacroiliac joint and hyperostosis at the proximal extremities of the clavicles and in some sterno-costal joints ().
A bone marrow biopsy with immunocytochemical study also documented deposits of amyloid A but no evidence of lymphoproliferative or plasmocytic disease.
Due to the association of HS with radiological multifocal (mandibular, sternoclavicular, sacroiliac, vertebral) osteoarticular findings, SAPHO syndrome was suspected. Therefore, 99mTc bone scintigraphy was performed and showed multifocal (sternocostoclavicular, sacroiliac joints, left mandibular branch) hypercaptation (). A mandibular biopsy documented no evidence of neoplastic disease.
The patient maintained confluent inflammatory nodules with purulent drainage (Hurley 3/3) in the gluteal area, and was medicated with doxycycline 100 mg. As the skin lesions worsened after 2 months, biological treatment with adalimumab was considered.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [47, 'years'], 'creatinine': [20.55, 'mg/dL'], 'sex': 'Male'}",2.44691,2.32456,2.56926,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 47 years old. The concentration of Creatinine is 20.55 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 20.55^(-1.154) * 47^(-0.203) * 1 * 1=2.44691.
Hence, the patient's GFR is 2.44691 mL/min/1.73m²."
3217,9,MDRD GFR Equation,lab test,decimal,pmc-2740182-1,Extracted,"A 78-year-old African American female was admitted with multiple painful ulcers on the lower extremities and possible septicemia. Her medical history included coronary artery disease, peripheral vascular disease, end-stage renal disease on hemodialysis for 7 months, insulin-dependent diabetes, hypertension, hypothyroidism, chronic obstructive pulmonary disease and asthma. Her surgical history included thyroidectomy and left upper extremity graft in October 2005 which failed to maturate and patient did not follow up. Patient was admitted in March 2006 for symptoms of worsening of lower extremity swelling and paroxysmal nocturnal dyspnea when her laboratory results showed BUN-141 mg/dl and creatinine-8.1 mg/dl. Patient underwent fistulogram which showed multiple high-grade stenosis. She had internal jugular catheter placed at the time and was started on daily hemodialysis. When she was discharged 6 days later, her BUN was 33 mg/dl and creatinine was 5.4 mg/dl. She was advised to follow with the dialysis center three times weekly, however patient remained noncompliant with intermittent dialysis. Since the September 2006 hospitalization as described on the case she was dialyzed regularly on Tuesday, Thursday & Saturday. She also had right lower extremity angiogram with an attempted right superficial femoral arterectomy and angioplasty which failed because of severely calcified vessels and multiple wound debridements in the past 3-4 months. Drug therapy included aspirin 81 mg daily, pentoxifylline 400 mg 3 times daily, lisinopril 40 mg daily, amlodipine 10 mg and minoxidil 2.5 mg daily, insulin 70/30 22 units every morning and 12 units every evening, atorvastatin 40 mg daily, albuterol and atrovent inhalers as needed, levothyroxine 150 mcg daily, PhosLo 2 caps 3 times daily, cinacalcet 30 mg daily, colace 100 mg twice daily, hydrocodone 500 mg as needed. Patient denied any exposure to tobacco, ethanol, and intravenous drug abuse. She had 2 children and lived with her son and daughter-in-law who are the primary caretakers. Family history included chronic kidney disease, hypertension, coronary artery disease and diabetes.
Six months prior to presentation, she was found to have significant hyperparathyroidism (serum intact parathormone of 1133 pg/ml [normal, 10-65]) and hypercalcemia of 11.1 mg/dl [normal, 8.5-10.5]. Meanwhile, she developed 7 × 4 cm ulcer on the posterior aspect of right calf after a burn which remained non-healing for more than 2 weeks. She complained of severe local pain and continued developing multiple ulcerations on both lower extremities. Wound care and pain management was attempted as outpatient. Admission followed due to worsening of ulcerations and poor pain control. On admission, physical examination revealed obese (Ht-154 cm, Wt-84 kgs, BMI-35) African American female in distress due to pain with marked abdominal adiposity, absent pedal pulses and extensive lesions on the hips, buttocks, and proximal thighs with surrounding erythema, induration and dark eschar ( & ). No other pertinent physical findings were present. Laboratory studies showed serum calcium of 8.6 mg/dl (normal, 8.5-10.5), serum phosphorous of 3.7 mg/dl (normal, 2.5-5.0), calcium-phosphorous product - 31.8, parathormone of 155 pg/ml (normal, 10-65), urea of 35 mg/dl (normal, 7-20) and creatinine of 4.3 mg/dl (normal, 0.8-1.3), alkaline phosphatase-145 IU (normal, 70-230 IU), and serum albumin-1.9 g/dl (normal, 3.5-5.5 g/dl).
X-ray of lower extremities revealed extensive arterial calcifications within the femoral, popliteal artery and smaller branches. Nuclear medicine scan of parathyroid showed adenoma of the right lobe. With significant multiple co morbidities of diabetes, peripheral vascular disease and end stage renal disease, we considered the possibilities of ischemic ulcers and superimposed infection. The patient underwent several investigations, including a lower extremity angiogram with an attempted right superficial femoral arterectomy and angioplasty which failed because of severely calcified vessels and multiple wound debridements in the past 3-4 months. Hypercoagulable state with cryoglobulinemia was also ruled out, with the results of protein C, protein S and antithrombin-3 being in the normal range.
A biopsy of the lower extremity ulcer demonstrated circumferential vascular mural calcification affecting small and medium sized blood vessels with degeneration of elastic fibers and absence of inflammation (). During her hospitalization, despite attempts to control deterioration (wound care, pain control, hemodialysis and parenteral antibiotics), leg wounds and general condition worsened over the next 3-4 weeks. She exhibited periodic disorientation. Upon multiple discussions with the family on different treatment options and overall poor prognosis, the patient’s family opted for comfort care under Hospice. Patient expired two days later.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [78, 'years'], 'creatinine': [4.3, 'mg/dL'], 'Race': 'Black'}",12.07332,11.46965,12.67699,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 78 years old. The concentration of Creatinine is 4.3 mg/dL. 
The patient is Black, so the race coefficient is 1.212.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 4.3^(-1.154) * 78^(-0.203) * 1.212 * 0.742=12.07332.
Hence, the patient's GFR is 12.07332 mL/min/1.73m²."
3218,9,MDRD GFR Equation,lab test,decimal,pmc-4779822-1,Extracted,"A 61-year-old male with a past medical history notable for diabetes mellitus, chronic kidney disease, hepatitis C, and right below-the-knee amputation due to peripheral vascular disease presented with acute nausea, vomiting, and altered mental status in the setting of chronic diarrhea. His diarrhea had been present for eight months and had been evaluated with a colonoscopy three weeks prior to presentation. The colonoscopy revealed four polyps, all of which were biopsied. Three polyps were tubular adenomas and one polyp in the sigmoid colon was carcinoid.
On admission, physical examination revealed him to be an ill-appearing African American male in moderate distress. He was alert and oriented but unable to recall specific details of his history. His temperature was 37°C, pulse 137 beats per minute, and blood pressure 117/76 mmHg. Examination of the oropharynx revealed dry mucous membranes. Cardiopulmonary exam revealed tachycardia with a regular rhythm and clear lungs to auscultation. He had tenderness to palpation in the right upper quadrant as well as right costovertebral angle tenderness. There was evidence of a right below-the-knee amputation with a well-healed stump.
Laboratory data on admission was notable for a white blood cell count of 15.3 k/uL with 86% neutrophils, hemoglobin of 8.7 g/dL (decreased from 10.4 g/dL six months prior), and platelet count of 64 k/uL (decreased from 253 k/uL six months prior). Haptoglobin was within normal limits making significant intravascular hemolysis unlikely. Serum creatinine was 14.6 mg/dL, which was increased from 3.8 mg/dL six months prior, and blood urea nitrogen was 141 mg/dL. There was an anion gap of 26 with lactic acid of 1.94 mmol/L. Urinalysis revealed 2+ protein, negative nitrites, trace leukocyte esterase, 2 red blood cells/hpf, 3 white blood cells/hpf, no casts, occasional bacteria, and no epithelial cells/hpf.
He was admitted to the medical intensive care unit for severe sepsis and acute renal failure. On admission, percutaneous blood cultures were collected in a sterile fashion and submitted to the microbiology lab in an aerobic bottle and an anaerobic bottle. A BacT/Alert 3D (BioMérieux, Inc., Durham, NC) automated microbial detection system was used to detect bacterial growth. Once growth was detected, the broth was plated on solid media. On hospital day one, two out of four bottles of percutaneous blood cultures grew an organism on anaerobic blood agar that was identified as Gram-positive rods on Gram stain. Vancomycin, ciprofloxacin, and metronidazole were started due to concern for polymicrobial infection. CT abdomen and pelvis without contrast revealed a 5 mm proximal to midureteral stone on the right with associated hydronephrosis, tiny (sub-2 mm) calculi in the bilateral collecting systems, and a small amount of free pelvic fluid along the bilateral paracolic gutters. On hospital day two, Vitek MS (BioMérieux, Inc., Durham, NC), an automated mass spectrometry microbial identification system, identified the Gram-positive organism as C. perfringens. Antibiotics were narrowed to ciprofloxacin and metronidazole. On hospital day three, a right percutaneous nephrostomy tube was placed. Placement of the nephrostomy tube returned grossly purulent urine. Gram stain of the right nephrostomy urine revealed Gram-variable rods. Ultimately, no bacteria grew from the right nephrostomy urine culture. Although no bacteria grew on urine culture, the Gram-variable rods are likely C. perfringens. The previously administered antibiotics likely disrupted the bacteria's cell wall affecting its Gram staining features. Clostridium species may stain as Gram-variable or even as Gram-negative rods as they are decolorized rapidly []. Moreover, with right-sided costovertebral tenderness on exam, right-sided nephrolithiasis with hydronephrosis on imaging, and purulent discharge on placement of his percutaneous nephrostomy tube, severe sepsis and bacteremia due to a urinary source are clinically supported. He was treated with ciprofloxacin and metronidazole for fourteen days. Ciprofloxacin and metronidazole were continued, as opposed to narrower coverage with penicillin, because of concern for polymicrobial infection. Surveillance blood cultures remained negative.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [61, 'years'], 'creatinine': [14.6, 'mg/dL'], 'sex': 'Male', 'Race': 'Black'}",4.17307,3.96442,4.38172,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 61 years old. The concentration of Creatinine is 14.6 mg/dL. 
The patient is Black, so the race coefficient is 1.212.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 14.6^(-1.154) * 61^(-0.203) * 1.212 * 1=4.17307.
Hence, the patient's GFR is 4.17307 mL/min/1.73m²."
3219,9,MDRD GFR Equation,lab test,decimal,pmc-7533627-1,Extracted,"We report a case of an 80-year-old man with a history of arterial hypertension and type 2 diabetes who uses an insulin therapy since 2012. The patient used to suffer from terminal renal insufficiency (stage 5) for 10 years treated with hemodialysis (3 sessions per week). Also, the patient had a long history with smoking (at a rate of 2 packs/day for 30 years) suspended 1 year ago. Eight months ago, the patient was admitted for pain and changes in color in the left lower limb. Evaluated by the vascular department, it was detected that there are many necrosis in his bilateral lower limbs. The patient was treated by surgical amputation of his left lower limb in March 2019, and nine months later, the patient’s right lower limb was amputated. Two months later, the patient was referred to our department because of a severe penile pain and necrosis. On clinical examination, there were necrotic ulcer and blackish discoloration of the glans (). The patient had a urinary tract infection, the urine culture found E coli, so he started antibiotic treatment for 10 days by quinolones (ciprofloxacin) 500 mg twice a day).
Due to a severe penile pain, the patient was programmed for partial penectomy (a) after taking his permission as well as that of his family. In the trans-surgery, the absence of vascular flow was observed in the penile arteries and in the deep dorsal vein (b).The following management was based on a daily wound care, debridement for the next 2 weeks and an antibiotic-based treatment for a second episode of urinary tract infection. So, he received imipenem 500 mg two times per 10 day. In the first postoperative days, the patient’s state shows recovery, but from the 14th day of this intervention, the surgical wound remained open with little serohematic secretion, as well as infected tissues shows poor progression that led to Fournier’s gangrene (a). Then, a total penectomy was performed through removing a part of his left scrotum (b). An arteriography was performed during his hospital stay in the vascular department which showed multiple vascular calcifications notably at the level of the internal iliac artery and its branches. During laboratory assessment, the creatinine and urea levels in the blood were higher than the laboratory values: Creatinine 78 mg/L, urea 82.2 g/L. The other results were like the following: Serum Ca was slightly decreased to 83 mg/Land serum phosphate was high reaching 55 mg/L. In addition to that, parathyroid hormone level was not recorded, and vitamin D was deficient lowering to10.8 ng/mL. Elevated inflammatory markers were noticed including C-reactive protein and leukocytes because of his urinary tract infection. Haemoglobin (Hb) was only 7.2 g/dL due to renal anemia by end-stage renal failure. The histopathological analysis found an advanced diabetic microangiopathy accompanied by significant calcium deposits in vessels lumen with intimal fibroblastic proliferation (a and b).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [80, 'years'], 'creatinine': [78.0, 'mg/L'], 'sex': 'Male'}",6.7179,6.382,7.0538,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 80 years old. The concentration of Creatinine is 78.0 mg/L. We need to convert the concentration to mg/dL. The mass units of the source and target are the same so no conversion is needed. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 78.0 mg Creatinine/10.0 dL = 7.8 mg Creatinine/dL. The concentration value of 78.0 mg Creatinine/L converts to 7.8 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 7.8^(-1.154) * 80^(-0.203) * 1 * 1=6.7179.
Hence, the patient's GFR is 6.7179 mL/min/1.73m²."
3220,9,MDRD GFR Equation,lab test,decimal,pmc-6997309-1,Extracted,"A 71-year-old Japanese man had undergone laparoscopic right living-donor kidney transplantation for end-stage renal disease due to chronic nephritis at the age of 65 years. His immunosuppression regimen included combination therapy with tacrolimus 1 mg/day, mycophenolate mofetil 1000 mg/day, and prednisolone 4 mg/day. Renal graft function remained stable without any episodes of rejection.
Six years after transplantation, he presented to our hospital complaining of abdominal pain. A colonoscopy revealed a near-circumferential mass at the rectosigmoid colon. The tumor proved to be adenocarcinoma (tub) by biopsy. The descending colon on the oral side of the tumor showed reddening and edematous changes circumferentially (Fig. a, b). The colitic region was observed through the normal mucous membrane from 8 to 30 cm on the oral side of the tumor. The most oral side of the reddening and edematous change was located at sigmoid-descending colon junction. Histological examination by biopsy revealed that the colonic mucosa of the colitic region showed only moderate colitis. There was no evidence of cytomegalovirus colitis. He had a previous history of hypertension but no cigarette smoking or drinking. His family history showed no remarkable findings.
On admission, his abdomen was flat and soft, and abdominal pain disappeared during fasting. No special signs were noted except for a healed surgery scar on his right abdominal wall. Laboratory tests showed no anemia, serum creatinine was 1.1 μmol/L, liver function was normal, and serum tumor markers (CEA, CA19-9) were within normal range. A barium enema examination showed a tumor measuring 45 mm in diameter at the rectosigmoid colon. No other colorectal lesions were observed (Fig. a, b). A subsequent computed tomography (CT) scan revealed a circumferential mass with irregular surface and contrast effect and wall thickening at the rectosigmoid colon. The transplanted kidney was located in the right pelvic cavity (Fig. a, b). No evidence of lymph node or distant metastasis was apparent. Conservative therapy of fasting and laxatives without a decompression tube improved his symptoms. Patient continued to take immunosuppressants during the fasting period. After 5 weeks of conservative therapy, a colonoscopy revealed the same findings as the previous test. Considering the long-term use of immunosuppressants and the persistence of the obstructive colitis, we decided to perform a two-stage operation and performed a laparoscopic Hartmann’s operation first. The patient took the immunosuppressant on the day of surgery and resumed taking it from the first day after the operation.
After induction of general anesthesia, the patient was positioned in the lithotomy position. Complete exploration of the abdominal cavity suggested that there was no liver or peritoneal carcinomatosis. The tumor was identified at the rectosigmoid colon location, and the transplanted kidney was also located in the right lower abdomen (Fig. a). To avoid the transplanted kidney, we inserted the right lower quadrant port more towards the midline than usual (Fig. b, c). Considering the effect of abdominal pressure on the transplanted kidney, the pneumoperitoneum pressure was set at 10 mmHg. The resections performed achieved complete tumor removal with tumor-free margins and tumor-specific mesorectal excision. We cut the superior rectal artery, preserved the left colic artery, and harvested the D3 lymph nodes. The distal rectum was transected intracorporeally and then a 6-cm left supraumbilical incision was made to remove the proximal colon. We dissected the proximal sigmoid colon and removed the tumor. Then, we confirmed the difference between normal mucosa and colitic region. Finally, a sigmoid colostomy was performed. The operation was completed successfully with an operating time of 206 min and blood loss of 60 mL. The specimen was a circumferential tumor measuring 90 × 40 mm. The mucosa except for the tumor in the specimen was normal (Fig. ). Histopathology revealed a well-to-moderately differentiated adenocarcinoma with invasion through the muscularis propria into pericolorectal tissues. The resection margins were free, and there were no lymph node metastases, indicating a tumor stage of pT3N0M0.
Postoperative course was uneventful. The patient needed time to learn the stoma application and discharged 30 days after surgery. At 3 months after the surgery, obstructive colitis still remained. At 6 months after the surgery, his obstructive colitis had improved (Fig. a, b), and we performed a laparoscopic colorectal anastomosis as the second stage.
After induction of general anesthesia, the colostomy was returned to the abdominal cavity. GelPort® (Applied Medical, Rancho Santa Margarita, CA) with three ports (12 mm, 5 mm, 5 mm) was attached where the colostomy was, and operation was started laparoscopically. There was a little adhesion in the abdominal cavity and the stump of the rectum was easily found. An anastomosis was performed using an autosuture device. The operating time was 80 min and blood loss was 5 mL.
The patient discharged hospital 4 days after second surgery with no postoperative complications. During 1 year of follow-up, no allograft rejection, complications, or recurrence was observed.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [71, 'years'], 'creatinine': [1.1, 'µmol/L'], 'sex': 'Male', 'Race': 'Asian'}",12129.9063,11523.41099,12736.40162,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 71 years old. The concentration of Creatinine is 1.1 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 1.1 µmol. To convert 1.1 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 1.1 µmol Creatinine * 1e-06 mol/µmol = 1.1e-06 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 1.1e-06 mol Creatinine * 113.12 g/mol = 0.00012 g Creatinine. To convert 0.00012 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00012 g Creatinine * 1000.0 mg/g = 0.12 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 0.12 mg Creatinine/10.0 dL = 0.012 mg Creatinine/dL. The concentration value of 1.1 µmol Creatinine/L converts to 0.012 mg Creatinine/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 0.012^(-1.154) * 71^(-0.203) * 1 * 1=12129.9063.
Hence, the patient's GFR is 12129.9063 mL/min/1.73m²."
3221,9,MDRD GFR Equation,lab test,decimal,pmc-6526544-1,Extracted,"A 64-year-old-man presented to the Emergency Department of Venizeleio Hospital, Heraklion, Crete, with a 3-day history of nausea, vomiting, and abdominal pain. His medical history included type 2 diabetes and hypertension. He had had type 2 diabetes for 10 years and was being treated at the time with vildagliptin, metformin, and dapagliflozin. Dapagliflozin was added 8 months prior to admission. He reported a weight loss of 3 Kg following the commencing of dapagliflozin, but his weight appeared stable during the last 3 months. The A1C was 7.1% one month before admission. The patient noted that he suffered from recurrent episodes of abdominal pain the last 2 months.
At presentation the blood pressure was 130/80 mmHg, heart rate 95 beats/min, temperature 36.8°C, and oxygen saturation 98% on ambient air. The patient appeared mildly dehydrated with a BMI of 26.5 kg/m2. The abdomen was soft with mild tenderness in the epigastrium and left upper quadrant. The remainder of the physical examination was normal.
An arterial blood gas analysis was performed and revealed metabolic acidosis pH 7.33, HCO3− 10.9 mEq/L, and PCO2 21 mmHg with an increased anion gap at 29 mmol/L. Plasma glucose was mildly elevated at 203 mg/dL. Serum lactate was 1.1 mmol/L, i.e., within normal range. The rest of laboratory investigation was as follows: white blood cells 7860/μL, hemoglobin 14.8 g/dL, serum urea 84 mg/dL, serum creatinine 1.33 mg/dL, Na+ 134 mmol/L, K+ 4.6 mmol/L, and Cl− 94 mmol/L. C-reactive protein level was moderately elevated at 8 mg/dL. Urinalysis showed glycosuria and ketonuria (glucose 4+, Oxone 4+). Measurement of serum ketones was not available.
The patient was diagnosed with euDKA possibly related to dapagliflozin use and was treated with intravenous fluids and insulin, with subsequent improvement of acid base disorders within the first 48 hours. He was also treated empirically with broad spectrum antibiotics. A computed tomography (CT) scan of the abdomen/pelvis with IV contrast was ordered to further evaluate the cause of the abdominal pain. The CT scan revealed ascending and transverse colonic dilatation proximal to a transition point in the splenic flexure and decompressed bowel distal to the obstruction, highly suspicious of colonic malignancy. Colonoscopy was then performed which showed splenic flexure cancer. The patient was transferred to the surgical clinic and underwent left hemicolectomy. He was discharged from the surgical clinic on the 9th postoperative day in good condition. Dapagliflozin was discontinued and basal-bolus insulin treatment was prescribed.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [64, 'years'], 'creatinine': [1.33, 'mg/dL'], 'sex': 'Male'}",54.13258,51.42595,56.83921,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 64 years old. The concentration of Creatinine is 1.33 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.33^(-1.154) * 64^(-0.203) * 1 * 1=54.13258.
Hence, the patient's GFR is 54.13258 mL/min/1.73m²."
3222,9,MDRD GFR Equation,lab test,decimal,pmc-4035682-1,Extracted,"A 32-year-old female was hospitalized and referred to the Kidney Center for refractory hypertension and nephrotic syndrome in the 23rd gestational week. Initially, superimposed preeclampsia was suspected. She had a 1-year history of essential hypertension before admission, which had been diagnosed as essential hypertension because no endocrinological or urinary sediment abnormalities had been detected at that time; plasma renin activity and serum aldosterone level had been 2.3 ng/ml/h (reference range 0.3–5.4 ng/ml/h in the standing position) and 170 pg/ml (reference range 38.9–307 pg/ml in the standing position), respectively. In the 5th gestational week, her blood pressure had been 170/108 mm Hg, despite receiving a combination of hydralazine hydrochloride and methyldopa. Proteinuria had been detected in the 12th gestational week. Laboratory data had been significant for proteinuria (9.8 g/day), hypokalemia (2.8 mmol/l), hypoalbuminemia (1.9 g/dl), hypercholesterolemia (274 mg/dl), and a fractional sodium excretion of 0.1%. Her blood pressure remained uncontrolled after admission despite receiving comprehensive medical therapy. This led to the development of congestive heart failure, with her body weight increasing from 46.5 to 62.8 kg, and acute renal injury, with creatinine levels increasing from 0.51 to 0.99 mg/dl. Eventually, she underwent surgical termination of the pregnancy in the 25th gestational week and delivered a viable fetus weighing 606 g.
After the procedure, the patient's acute renal injury and congestive heart failure improved for a short period following treatment with albumin and furosemide. However, she was still hypertensive with 140–150/80–90 mm Hg, and proteinuria persisted in the nephrotic range. Laboratory data still showed proteinuria (3.7 g/day), hypokalemia (serum potassium 2.8 mmol/l), and hypoalbuminemia (serum albumin 2.7 g/dl). The fractional excretions of sodium and urea were 1.3 and 51%, respectively. Free water clearance and electrolyte-free water clearance were −0.12 and 0.25 ml/min, respectively. The transtubular potassium gradient was 7.9, indicating the presence of aldosteronism. Plasma renin activity was increased (13 ng/ml/h; reference range 0.3–2.9 ng/ml/h in the supine position), and the serum aldosterone level was normal (133 pg/ml; reference range 22.9–159 pg/ml in the supine position) 20 days after pregnancy termination, prompting a suspicion of the presence of renovascular hypertension. Ultrasonography and magnetic resonance imaging detected a 5.5-cm left renal cystic mass with a partial solid component and early contrast enhancement at the lower renal pole (, online suppl. fig. S1 and S2). A final diagnosis of secondary hypertension due to a renin-secreting tumor (with a plasma renin activity of 7.3 ng/ml/h, a high serum renin level of 186 pg/ml, and a serum aldosterone level of 456 pg/ml) was made 40 days after pregnancy termination, and her blood pressure was controlled to 120–130/80–90 mm Hg with nicardipine and methyldopa. 100 days after pregnancy termination, the left kidney with the renal mass was excised by laparoscopic nephrectomy. The plasma renin activity and serum renin level normalized the day after surgery. However, proteinuria remained in the range of 1–2 g/day, although it showed a decreasing trend.
Figure presents the histopathological characteristics of the tumor lesion. The specimen was collected during left radical nephrectomy; the tumor measured 55 × 45 × 25 mm and was poorly circumscribed and unencapsulated. The cut surface was grayish-white to yellowish-white, with necrosis and hemorrhaging in the center. Microscopically, the tumor was composed of round or spindle-shaped cells containing polygonal nuclei with clear or eosinophilic cytoplasm. Mitotic activity and abnormal mitosis were not observed. Immunohistochemical staining for anti-renin antibody (AnaSpec, Inc., Fremont, Calif., USA) showed a punctate positivity in the perinuclear cytoplasm of some tumor cells. The tumor cells stained positive for α-smooth muscle actin and negative for cytokeratin (CAM5.2), epithelial membrane antigen, and melanoma-associated antigen (HMB-45). The unaffected renal parenchyma showed segmental glomerulosclerosis in 22% of the glomeruli (fig. ), which was observed mainly as segmental areas of sclerosis with capillary collapse on the vascular pole (fig. ). Smooth muscle cell proliferation was pronounced in the afferent and efferent arterioles near the vascular pole (fig. ). However, a segmental area of sclerosis was also observed on the urinary pole (fig. ). Moreover, collapses of the glomerular tufts and cell proliferation on Bowman's capsular epithelium were observed (fig. ). Thus, the histological findings exhibited mixed morphological variants and could not be categorized as any specific variant by the Columbia classification. Global glomerular sclerosis was observed in 2 of 94 glomeruli. Glomerular hypertrophy and occlusion of capillary lumens by swelling of the endocapillary cells were not observed. Glomerular endotheliosis was also not observed in the electron micrograph. Intimal thickening was observed in the small arteries; however, no onionskin lesions were present.
Written and signed informed consent was obtained from the patient for the publication of this case report with accompanying images.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [32, 'years'], 'creatinine': [0.99, 'mg/dL'], 'sex': 'Female'}",65.00301,61.75286,68.25316,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 32 years old. The concentration of Creatinine is 0.99 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.99^(-1.154) * 32^(-0.203) * 1 * 0.742=65.00301.
Hence, the patient's GFR is 65.00301 mL/min/1.73m²."
3223,9,MDRD GFR Equation,lab test,decimal,pmc-4748675-1,Extracted,"A 41-year-old HIV-positive man was admitted to our hospital because of fever and cough since 5 days. His medical history revealed intravenous drugs addiction, chronic renal failure and hepatitis C infection. He was started on HAART based on abacavir, lamivudine and efavirenz during the last year. On examination the patient was oriented. His temperature was 37°C, pulse rate of 100 beats per minute and 20 breaths per minute. Chest examination did not reveal rhonchi or crackles. No focal neurological deficit was evident. Relevant laboratory findings showed an hemoglobin level of 7 g/dl, total white cell count of 3,700 cells/mm3 and a normal platelet count. Renal dysfunction was evidenced by serum urea of 47 mg/dl and creatinine of 1.8 mg/dl. Ocular fundus examination was normal. The liver function test and lactate dehydrogenase level (LDH) were normal. A chest radiograph showed bilateral interstitial infiltrates []. Staining and culture of sputum samples were negative for bacteria, mycobacteria and fungi. Blood cultures for the same microorganisms were also negative. The CD4 T-cell count was 35 cells/µl and the plasma viral load was 203,906 copies/ml. Serologic testing revealed the presence of T. gondii IgG antibodies with a positive titer of 1:1024 and IgM negative by indirect immunofluorescence.
Fever and cough continued 7 days after admission to the hospital. On the eighth day a bronchoalveolar lavage (BAL) was performed. Cytological and microbiological examinations of the BAL were negative for bacteria, fungi, Pneumocystis jirovecii and Mycobacterium tuberculosis. Giemsa-stained smears of the BAL were negative for tachyzoite forms of T. gondii. An aliquote of the BAL fluid was assayed for T. gondii using the PCR technique for amplification of a fragment corresponding to the B1 gene. BAL specimens were positive by PCR for T. gondii. Treatment for T. gondii infection was initiated with sulfadiazine, pyrimethamine and folinic acid. Computed tomography (CT) scan of the brain showed marked cerebral atrophy without evidence of focal lesions.
He showed a marked improvement in clinical, radiological, and laboratory findings after the seventh day of therapy for T. gondii. He was discharged from the hospital after 15 days of admission in a good clinical condition.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [41, 'years'], 'creatinine': [1.8, 'mg/dL'], 'sex': 'Male'}",41.78866,39.69923,43.87809,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 41 years old. The concentration of Creatinine is 1.8 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.8^(-1.154) * 41^(-0.203) * 1 * 1=41.78866.
Hence, the patient's GFR is 41.78866 mL/min/1.73m²."
3224,9,MDRD GFR Equation,lab test,decimal,pmc-6990267-1,Extracted,"A 60-year-old Japanese woman was admitted to our hospital for evaluation of plaque psoriasis, which was initially diagnosed at the age of 25 years. Although she had used topical agents such as maxacalcitol and betamethasone, the skin lesion had persisted. Hemodialysis was started at the age of 39 years for chronic renal failure due to polycystic kidney disease. Four months before this admission, renal transcatheter arterial embolization was performed to treat enlargement of the kidneys, as reported previously []. Her skin lesions became worse three months later and the patient was admitted to our hospital. On admission, she was 147.0 cm tall and weighed 36 kg, with a blood pressure of 123/66 mmHg, heart rate of 70/min, and body temperature of 37.0℃. Raised, red and scaly patches, consistent with psoriatic plaques, were note on the skin of almost of all parts of the body (Fig. a, c). The psoriasis area and severity index (PASI) score was calculated to be 49.8 according to Fredriksson’s classification []. She had no pain or swelling of any joints. Laboratory tests showed that the leukocyte count was 4400/μL (76.5% neutrophils, 16.5% lymphocytes, and 1.8% eosinophils), hemoglobin was 11.0 g/dL, platelet count was 22.0 × 104/μL, urea nitrogen was 56.0 mg/dL, serum creatinine was 7.79 mg/dL, C-reactive protein (CRP) was 0.1 mg/dL, and matrix metalloproteinase-3 (MMP-3) was 91.5 ng/mL (normal range 36.9–121). In addition, liver function and electrolyte levels were normal. Computed tomography revealed polycystic kidneys and the metal microcoils used previously for embolization.
Secukinumab was started at a dose of 150 mg (half of the standard dose in consideration of her low body weight < 60 kg) by weekly injection. After four doses, treatment was changed to monthly injections. Her skin lesion was improved in after 2 weeks of secukinumab (Fig. b, d). PASI decreased to 14.8 after 2 weeks of treatment and to 0 after 6 weeks (Fig. ), and it remains at zero after 28 months. She had used topical maxacalcitol at the start of secukinumab. The topical maxacalcitol was discontinued after 8 week because of improvement of skin lesion. No adverse events were observed, including infections.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [60, 'years'], 'creatinine': [7.79, 'mg/dL'], 'sex': 'Female', 'Race': 'Asian'}",5.29228,5.02767,5.55689,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 60 years old. The concentration of Creatinine is 7.79 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 7.79^(-1.154) * 60^(-0.203) * 1 * 0.742=5.29228.
Hence, the patient's GFR is 5.29228 mL/min/1.73m²."
3225,9,MDRD GFR Equation,lab test,decimal,pmc-3778802-2,Extracted,"A 50 years old male patient with chronic renal failure since two years, on haemodialysis since 8months with blood pressure, developed hemorrhagic blister at the junction of buccal mucosa and alveolar ridge on right side. Over a period of 12 hrs it ruptured discharging thin clear blood mixed fluid and healed within four days without any scarring or other squeal.
On examination, there was solitary oval tense hemorrhagic bulla measuring about 2.5 × 2 cm present at the junction of buccal mucosa and alveolar ridge on right side. On manipulation it ruptured easily [].
Tzanck smear in both cases showed numerous RBC's and there was no acantholytic or multi-nucleated giant cell. Biopsy from case -1 of the ruptured blister revealed sub-epithelial split with minimal perivascular infiltrate. Biopsy could not be done in case -2, since the patient did not consent. Routine blood and urine tests including Bleeding and clotting time, Liver function test, Renal function test, thyroid function test, lipid profile, Ultra sound examination of abdomen and pelvis, chest – X ray were within normal limits in Case-1. In case-2, all the investigations were normal except for high blood pressure (130/90 mm Hg) and elevated serum urea and creatinine levels (50 and 2.5 mg/dl respectively).
Spontaneous onset, isolated nature, constant presence of blood in the blister fluid and rapid healing in the absence of an identifiable local cause or systemic disorder differentiates ABH from mucous membrane pemphigoid, bullous pemphigoid, bullous lichen planus, epidermolysis bullosa, dermatitis herpetiformis, linear IgA disease and oral amyloidosis. The classical history and morphology of lesions helped us to arrive at the clinical diagnosis of angina bullosa hemorrhagica in both the presenting cases.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [50, 'years'], 'creatinine': [2.5, 'mg/dL'], 'sex': 'Male'}",27.47416,26.10045,28.84787,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 50 years old. The concentration of Creatinine is 2.5 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.5^(-1.154) * 50^(-0.203) * 1 * 1=27.47416.
Hence, the patient's GFR is 27.47416 mL/min/1.73m²."
3226,9,MDRD GFR Equation,lab test,decimal,pmc-4421709-1,Extracted,"A 51-year-old female was hospitalized for shortness of breath on exertion for 2 days. She had no prior history or risk factors for kidney disease but was taking daily ibuprofen (1600–2400 mg p.r.n.) over the past 7 months for chronic neck pain. She had been smoking one pack of cigarettes daily for the past 35 years. Four weeks prior to admission, she developed fever and a cough productive of mucoid sputum. At that time, a chest radiograph revealed a 7-cm right middle lobar and hilar mass with right pleural effusion, and her serum creatinine (SCr) was 1.7 mg/dL. After completing a course of cefuroxime, a transbronchial biopsy of the lung mass and mediastinal lymph nodes revealed primary poorly differentiated lung adenocarcinoma with positive immunohistochemical staining for thyroid transcription factor-1 (TTF-1) and presence of the K-ras mutation.
On admission, her physical exam was normal except for decreased breath sounds at the right lung base with dullness to percussion and bilateral pedal oedema. No lymphadenopathy, flank mass or tenderness was appreciated. Laboratory work revealed microcytic anaemia (haemoglobin = 8.3 g/dL), a further elevation in SCr (= 2.8 mg/dL) and unremarkable urinalysis (1+ dipstick albumin, 1 red blood cell/high power field, no casts and spot urine protein:creatinine ratio = 0.88 g/g). Other laboratory results were unremarkable (serum calcium = 8.8 mg/dL, serum uric acid = 7.6 mg/dL, absolute eosinophil count = 800/mm3, normal complement C3 and C4 levels, urine sodium = 17 mEq/L, anti-nuclear antibody 1:400 speckled, and negative serum immunofixation). Her symptoms improved with blood transfusion and pleural drainage of 1000 mL serous fluid. She had a renal ultrasound () that showed enlarged kidneys (right 15.1 cm and left 15.4 cm), lack of corticomedullary differentiation with no pelvicalyceal dilatation or hydronephrosis.
A positron emission tomography scan (PET, ) done for staging showed increased tracer uptake in the right middle lobe of the lung (peak standard uptake value, SUV = 8.4), lymphadenopathy (left supraclavicular, paratracheal, mediastinal, subcarinal, retrocrural, paracaval, para-aortic and peripancreatic) and bilateral enlarged kidneys with heterogeneous uptake in the cortices (peak SUV = 8.5). An ultrasound-guided renal biopsy was performed to determine if the renal mass was due to renal cell carcinoma or metastases. We found sheets of tumour cells replacing ~70% of the renal interstitium () with positive TTF-1 staining and presence of intracellular lumina morphology similar to the lung adenocarcinoma. Three glomeruli with atrophic tubules were negative for all immunoreactants (IgG, IgA, IgM, C3, C1q, fibrinogen, albumin, κ and λ). Diffuse metastatic infiltration of both kidneys from primary lung adenocarcinoma (stage IV) was confirmed. She received one cycle of palliative non-nephrotoxic chemotherapy with paclitaxel 175 mg/m2 and gemcitabine 1000 mg/m2 (both administered on Day 1 and 8). Two weeks later, she had progression of renal failure (SCr = 4.5 mg/dL) and developed uraemic encephalopathy and pruritus (blood urea nitrogen = 129 mg/dL), and the family requested home hospice care.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [51, 'years'], 'creatinine': [4.5, 'mg/dL'], 'sex': 'Female'}",10.30381,9.78862,10.819,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 51 years old. The concentration of Creatinine is 4.5 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 4.5^(-1.154) * 51^(-0.203) * 1 * 0.742=10.30381.
Hence, the patient's GFR is 10.30381 mL/min/1.73m²."
3227,9,MDRD GFR Equation,lab test,decimal,usmle-6013,Extracted,"A 61-year-old woman presents to the emergency department with bloody vomiting for the last hour. She had been vomiting for several hours. Additionally, she states she felt a sudden onset of chest and epigastric pain when she noted blood in her vomit. In the emergency room, she endorses feeling lightheaded and denies difficulty breathing or coughing, and the pain is not worse with swallowing. On review of systems, she notes that she has been bruising more easily than usual over the last 3 months. The patient has a long history of alcoholism with recent progression of liver disease to cirrhosis. She has known esophageal varices and is on propranolol for prophylaxis. In the emergency room, the patient’s temperature is 98.2°F (36.8°C), blood pressure is 94/60 mmHg, pulse is 103/min, and respirations are 16/min. On exam, she is in moderate distress, and there is frank blood in her emesis basin. Cardiovascular and lung exams are unremarkable, and there is pain on palpation of her epigastrium and chest without crepitus. Initial labs are shown below:

Hemoglobin: 13.1 g/dL
Leukocyte count: 6,200/mm^3
Platelet count: 220,000/mm^3
Creatinine: 0.9 mg/dL

The patient is started on IV isotonic saline, pantoprazole, ceftriaxone, and octreotide.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [61, 'years'], 'creatinine': [0.9, 'mg/dL'], 'sex': 'Female'}",63.65377,60.47108,66.83646,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 61 years old. The concentration of Creatinine is 0.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.9^(-1.154) * 61^(-0.203) * 1 * 0.742=63.65377.
Hence, the patient's GFR is 63.65377 mL/min/1.73m²."
3228,9,MDRD GFR Equation,lab test,decimal,pmc-8136987-1,Extracted,"A 25-year-old man visited the emergency room because of sudden severe right flank pain. He was diagnosed with end-stage renal disease due to Alport syndrome and had been receiving maintenance hemodialysis 3 times a week for 4 hours per session since 2013. The last hemodialysis session was the previous day, and 1000 units of heparin were administered as an initial bolus dose followed by an infusion of 500 units per hour of heparin 3 times as a maintenance dose. He had no history of trauma or urological procedures except for a left renal biopsy to diagnose Alport syndrome 10 years prior. His blood pressure was well controlled by taking antihypertensive drugs and undergoing regular hemodialysis. The patient had no other symptoms or signs during hemodialysis. His vital signs at the emergency room were as follows: blood pressure, 160/100 mm Hg; heart rate, 77 beats per minute; body temperature, 36.5°C; and respiratory rate, 20 breaths per minute. Initial laboratory findings revealed white blood cell count 9080/mm3, hemoglobin 11.7 g/dL, hematocrit 35%, platelets 203,000/μL, blood urea nitrogen 26 mg/dL, creatinine 9.32 mg/dL, erythrocyte sedimentation rate 5 mm/hour, and C-reactive protein 0.9 mg/L. His prothrombin time and activated partial thromboplastin time were within the normal ranges. He complained of progressively worsening right flank pain, and his hemoglobin level also decreased to 10.1 g/dL. Contrast-enhanced computed tomography revealed a right perirenal hematoma with pseudoaneurysms (Fig. ). On renal angiography, multiple pseudoaneurysms were observed in the right renal artery branches, and embolization was performed (Fig. ). Post-embolization angiography revealed no pseudoaneurysms or contrast leakage.
The size of the perirenal hematoma slightly decreased on CT 10 days after embolization. He had no more abdominal pain, and his hemoglobin level did not change. The patient was discharged with instructions to maintain heparin-free hemodialysis. On outpatient blood tests 3 weeks later, his hemoglobin level was 11.6 g/dL, and he did not report any discomfort. After 3 months, we performed another CT scan, which confirmed that the perirenal hematoma and retrohemoperitoneum had completely resolved (Fig. ). The patient started using heparin again at the previous dose during hemodialysis. He had no recurrence of symptoms even after heparin was resumed during hemodialysis.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [25, 'years'], 'creatinine': [9.32, 'mg/dL'], 'sex': 'Male'}",6.92708,6.58073,7.27343,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 25 years old. The concentration of Creatinine is 9.32 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 9.32^(-1.154) * 25^(-0.203) * 1 * 1=6.92708.
Hence, the patient's GFR is 6.92708 mL/min/1.73m²."
3229,9,MDRD GFR Equation,lab test,decimal,pmc-6627500-1,Extracted,"A 68-year-old Japanese man was admitted to our hospital in winter due to disturbed consciousness and difficulty with body movements. Approximately two weeks prior, he had experienced fever and generalized edema. Thirteen days before admission, his family physician prescribed levofloxacin at 500 mg/day, furosemide at 20 mg/day, and spironolactone at 25 mg/day for seven days. The patient complied with this and became afebrile, and his edema disappeared. Two days before admission, his wife noticed that his speech was slurred, and he was only able to understand short and simple sentences. On the day of admission, he could not communicate and was unable to speak comprehensibly. He could not move by himself. His past medical history included cerebral palsy with lower limb atrophy, but he could walk using a frame. He had normal mental and intellectual development. He also had chronic kidney disease (CKD) at the stage of G4A3 due to nephrosclerosis and a horseshoe kidney, with a creatinine level of around 2.5 mg/dL. He had been treated with nifedipine, doxazosin, and febuxostat and did not use any over-the-counter supplements or illegal drugs.
Upon physical examination, his blood pressure was 65/40 mm Hg, his heart rate was 40 bpm, his respiratory rate was 20 breaths/min, and his body temperature was 27.9 °C. His consciousness was registered as E4V1M4 (E: Eye opening, V: Best verbal response, M: Best motor response) on the Glasgow Coma Scale. Accidental hypothermia was suspected, because his room had been cold and he had stayed there throughout the night. He was rewarmed immediately, and his body temperature increased to 35.7 °C, after which his vital signs became stable. However, his consciousness level remained abnormal, and he also showed myoclonus in both upper limbs. The deep tendon reflex of the biceps was normal. Laboratory findings showed a white cell count of 2700/μL, a hemoglobin level of 5.9 g/dL, a platelet count of 16.5 × 104/μL, albumin at 2.0 g/dL, aspartate aminotransferase at 137 U/L, alanine aminotransferase at 50 U/L, alkaline phosphatase at 288 U/L, γ-glutamyl transpeptidase at 13 U/L, blood urea nitrogen at 82.3 mg/dL, creatinine at 3.84 mg/dL, sodium at 142 mEq/L, calcium at 8.0 mg/dL, glucose at 101 mg/dL, thyroid-stimulating hormone at 9.29 μU/mL, free T4 at 1.03 ng/mL, and vitamin B1 at 3.9 g/dL. Antithyroid peroxidase antibody and antithyroglobulin antibody were undetectable. An arterial blood gas analysis did not show CO2 elevation and indicated mild metabolic acidosis. An electrocardiogram initially showed first-degree atrioventricular block, which became normal sinus rhythm after rewarming. Head-computed tomography and magnetic resonance imaging examinations showed no abnormalities, and an electroencephalogram showed generalized slowing waves. CSF was shown to have a cell count of 0/μL, a protein concentration of 68 mg/dL, and a glucose level of 65 mg/dL. Levofloxacin-associated encephalopathy and myoclonus were suspected based on the patient’s history of high levofloxacin dosages and present renal function.
The patient was treated through the administration of fluids and furosemide with the aim of levofloxacin being excreted in his urine. Although the patient produced more urine, his creatinine did not return to basal level, and his consciousness level did not improve. Hemodialysis was carried out on days 3 and 5 after admission, and his consciousness level improved and completely recovered by day 7 (). The myoclonus disappeared four days after admission. An electroencephalogram on day 15 showed no slowing waves. His Naranjo adverse drug reaction probability scale registered at 7 points, which indicated a probable relationship between his symptoms and adverse drug reactions to levofloxacin []. Sixteen days after admission, the patient was transferred to another hospital for rehabilitation. Later, we measured the concentration of levofloxacin in the reserved samples of plasma or CSF, obtained during hospitalization. The plasma concentrations of levofloxacin were 16.9, 16.2, 2.44, 0.61, and 0.71 μg/mL on days 1, 2, 4, 6, and 7 after admission, respectively (). The initial CSF concentration of levofloxacin was 6.81 μg/mL.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [68, 'years'], 'creatinine': [3.84, 'mg/dL'], 'sex': 'Male', 'Race': 'Asian'}",15.7297,14.94321,16.51619,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 68 years old. The concentration of Creatinine is 3.84 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.84^(-1.154) * 68^(-0.203) * 1 * 1=15.7297.
Hence, the patient's GFR is 15.7297 mL/min/1.73m²."
3230,9,MDRD GFR Equation,lab test,decimal,pmc-5385221-1,Extracted,"We present the case of a 33-year-old woman with a rapid deterioration of haemodynamic and neurological status. She is known with brittle diabetes mellitus type 1, treated with continuous subcutaneous insulin infusion and there is a history of gastroparesis. A report, given by relatives, stated that she went to a party 36 h earlier and complained of abdominal pain and vomiting afterwards. She presented to the ambulance team with a Glasgow Coma Scale score dropping from 13 to 3 in only 10 minutes. She had sinus tachycardia, absent peripheral pulses, blood pressure (BP) 99/52 mmHg, and temperature 307 Kelvin. Clinical examination revealed severe dehydration, respiratory distress with a respiratory rate of 40/min and bilateral diffuse rhonchi, PEARRL, minor neck stiffness, and no petechiae. She required urgent intubation. After intubation, her systolic BP decreased to 50 mmHg. Initial finger-stick found glucose to be above range of detection and ketonemia above 8 mmol/L. During transport to the hospital, a nonsustained ventricle tachycardia (NSVT) occurred. The patient was found to have a severe metabolic acidosis with a pH of 6.74, bicarbonate of 5.3 mmol/L, pO2 50.2 mmHg, and pCO2 39.9 mmHg. Further laboratory investigation showed a serum glucose of 106.8 mmol/L, a white blood cell count of 32.8 × 109/L, C-reactive protein 789.54 nmol/L, lactate 4.6 mmol/L, sodium 113 mmol/L, bicarbonate 6 mmol/L, potassium 6.7 mmol/L, calcium 2.0 mmol/L, phosphate 3.53 mmol/L, serum osmolality of 378 mOsm/kg, troponin I 0.463 μg/L, blood urea level of 47.8 mmol/L, and serum creatinine level 332.4 μmol/L. Urine toxicological screen was positive only for paracetamol (210.5 μmol/L) and not ethanolemia.
A presumptive diagnosis of diabetic ketoacidosis (DKA), sepsis, vasoplegia, and acute renal failure was made and the patient was treated with aggressive IV fluids (crystalloids), norepinephrine, 300 meq of sodium bicarbonate, calcium chloride, and 20 units of actrapid insulin IV bolus, along with an insulin drip (10 U/h).
Since the most common precipitating factor of DKA is infection, a computed tomography brain and abdominal scan, urine culture, and chest radiography were performed. All were negative for signs of infection. The chest radiography showed some mild pulmonary edema. Further evaluation included a lumbar puncture. Ceftriaxone and acyclovir were given empirically. Subsequently, the lumbar puncture came back negative.
Her condition progressively improved over the following days and she was successfully extubated. Renal function normalized over two days. Due to continuing abdominal pain, an abdominal laparoscopy was performed without any specific findings.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [33, 'years'], 'creatinine': [332.4, 'µmol/L'], 'sex': 'Female'}",13.96461,13.26638,14.66284,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 33 years old. The concentration of Creatinine is 332.4 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 332.4 µmol. To convert 332.4 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 332.4 µmol Creatinine * 1e-06 mol/µmol = 0.00033 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00033 mol Creatinine * 113.12 g/mol = 0.03733 g Creatinine. To convert 0.03733 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.03733 g Creatinine * 1000.0 mg/g = 37.33 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 37.33 mg Creatinine/10.0 dL = 3.733 mg Creatinine/dL. The concentration value of 332.4 µmol Creatinine/L converts to 3.733 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 3.733^(-1.154) * 33^(-0.203) * 1 * 0.742=13.96461.
Hence, the patient's GFR is 13.96461 mL/min/1.73m²."
3231,9,MDRD GFR Equation,lab test,decimal,pmc-6219210-1,Extracted,"A 53-year-old, non-diabetic, Chinese gentleman, presented with multiple episodes of bilateral lower extremities edema in 2012. There was no prior history of weight loss, skin rash, heart failure symptom or numbness over the lower extremities. Physical examination revealed a well-built gentleman with an elevated blood pressure reading of 160/90 mmHg. There was bilateral lower limbs edema but no organ enlargement was noted. Blood investigation showed normal full blood count, mildly impaired renal function with serum creatinine of 202 μmol/L and hypoalbuminemia without raised globulin level. Connective tissue disease screening was negative. 24 h urinary protein collection revealed proteinuria of 9 g per day Ultrasonography scan of the kidneys showed normal renal parenchymal echogenicity with bilateral kidneys’ size measuring at 9.5 cm and 9.6 cm respectively. Renal biopsy carried out showed AL amyloidosis with no evidence of free light chain deposition (as evidenced by the Congo red staining and negative for other specific staining). Extensive workup to look for other features of primary amyloidosis failed to show any association with systemic involvement (bone marrow aspiration and trephine biopsy, skeletal survey, echocardiogram, rectal biopsy was all reported negative). The only positive results was from the serum electrophoresis whereby it demonstrated the presence of IgG lambda paraprotein < 0.2 g/L migrating towards beta zone without any evidence of immunoparesis. The urine electrophoresis showed albuminuria of 14.1 g/L with mixed IgG lambda paraproteinuria of < 0.15 g/L. He was subsequently referred to hematologist for an opinion and was treated with 2 cycles of CTD (cyclophosphamide, thalidomide and dexamethasone) and VTD (bortezomide, thalidomide and dexamethaosone) with no resolution of the nephrotic syndrome. A repeated renal biopsy performed 3 years later showed no histological difference as compare with the first biopsy. A repeated systemic amyloidosis workup again showed inconclusive result. Bone marrow aspiration and biopsy repeated showed normal cellularity with presence of 2–3% plasma cells likely to be reactive in nature. Flow cytometry result showed 6% lymphocytes and 0.5% plasma cells with no aberrant plasma cells detected. He remains in overt proteinuria (7.8 g–10 g/dl) with a slowly creeping serum creatinine.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [53, 'years'], 'creatinine': [202.0, 'µmol/L'], 'sex': 'Male', 'Race': 'Asian'}",30.47373,28.95004,31.99742,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 53 years old. The concentration of Creatinine is 202.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 202.0 µmol. To convert 202.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 202.0 µmol Creatinine * 1e-06 mol/µmol = 0.0002 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.0002 mol Creatinine * 113.12 g/mol = 0.02262 g Creatinine. To convert 0.02262 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.02262 g Creatinine * 1000.0 mg/g = 22.62 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 22.62 mg Creatinine/10.0 dL = 2.262 mg Creatinine/dL. The concentration value of 202.0 µmol Creatinine/L converts to 2.262 mg Creatinine/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.262^(-1.154) * 53^(-0.203) * 1 * 1=30.47373.
Hence, the patient's GFR is 30.47373 mL/min/1.73m²."
3232,9,MDRD GFR Equation,lab test,decimal,pmc-4400567-1,Extracted,"A 61-year-old woman with history of Type 2 diabetes, hypertension and gout developed worsening hypertension and new-onset hematuria. Evaluation by her cardiologist showed hypochromic and microcytic anemia with hemoglobin 9.4 mmol/L (normal range 8.4–10.9 mmol/L) and AKI with serum creatinine 710.0 µmol/L (baseline <133 µmol/L). The patient was transferred to a tertiary referral hospital for further evaluation of AKI.
On physical examination, she appeared acutely ill. Temperature was 37.4°C, blood pressure 176/89 mm Hg, pulse 63 and respirations 21/min. Physical examination demonstrated normal heart sounds with no murmur, clear lungs, a soft, nontender, obese abdomen with no organomegaly and 2+ pitting edema of the lower extremities bilaterally. There was no skin rash. Laboratory data demonstrated sodium 138 mmol/L, potassium 4.7 mmol/L, chloride 106 mmol/L, bicarbonate 18 mmol/L, calcium 2.2 mmol/L, phosphorus 1.1 mmol/L, BUN 8.8 mmol/L, creatinine 790 µmol/L, glucose 12.5 mmol/L, total serum protein 61.0 g/L and albumin 31.0 g/L. Serum titers of antinuclear antibody, antidouble-stranded DNA, c-antineutrophil cytoplasmic antibody and antiglomerular basement membrane (GBM) antibodies were negative. Complement levels (C3 1.5 g/L, C4 0.4 g/L) were within normal limits. Serum and urine protein electrophoresis revealed no monoclonal spike. However, p-ANCA was >100 kU/L (normal <2.8 kU/L) and antimyeloperoxidase was >1:640 (normal <6 kU/L). Urinalysis showed proteinuria and microscopic hematuria with dysmorphic red blood cells. Proteinuria was 15.0 g/24 h. Renal ultrasonography showed the right kidney 10.4 cm and the left 11.2 cm in length. There was no history of alcohol abuse or smoking. She had poorly controlled Type 2 diabetes and hypertension for 10 years, complicated by neuropathy. She had no familial history of kidney disease. A percutaneous renal biopsy was performed to assess the cause of her rapidly progressive glomerulonephritis.
The renal biopsy specimen included two pieces of cortex containing nine glomeruli, four of which were globally sclerosed. There was mild increase in mesangial matrix and cellularity but no endocapillary proliferation. The GBM showed very rare spikes and rare holes (), segmental corrugation and split appearance. Two glomeruli had fibrinoid necrosis with fibrocellular crescents and segmental sclerosis with adhesions (). There was ∼40% interstitial fibrosis with proportional tubular atrophy and mild lymphoplasmacytic infiltrate. There was ATI involving ∼20% of tubular profiles with sloughing off of tubular epithelial cells. There were rare proteinaceous casts. There were no crystals or polarizable material. Arterioles were unremarkable. Interlobular arteries showed mild tortuosity without fibrinoid necrosis or inflammation.
Five glomeruli were present in frozen sections processed for immunofluorescence microscopy. There was 1+ (0 to 3+ scale) segmental granular capillary loop and mesangial staining for immunoglobulin G (IgG) () and 1+ C3 and equal 1+ kappa and lambda light chain staining in a similar pattern as IgG. There was no glomerular staining for IgA, IgM and C1q. There was no tubular basement membrane staining for any antisera. Immunofluorescence studies for subclasses of IgG, namely IgG1, IgG2, IgG3 and IgG4 were performed. There was dominant IgG4 segmental granular capillary loop and mesangial staining. IgG1, IgG2 and IgG3 were negative.
On electron microscopy, GBM showed normal thickness of lamina densa with occasional to scattered small to medium subepithelial deposits (), very rare small subendothelial deposits and rare mesangial deposits. There was ∼60% podocyte foot process effacement. There were no fibrin tactoids, tubuloreticular arrays and no increase in mesangial matrix or cellularity. There were no tubular basement membrane deposits.
Early membranous glomerulopathy (MG), with superimposed pauci-immune necrotizing crescentic glomerulonephritis (PNCGN) and focal ATI.
The patient was treated with hemodialysis and plasmapheresis × 5, and begun on immunosuppression with intravenous cyclophosphamide and prednisone. Her renal function did not recover and she remained on dialysis 6 months after the renal biopsy. Currently, she is being evaluated for renal transplantation.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [61, 'years'], 'creatinine': [790.0, 'µmol/L'], 'sex': 'Female'}",4.50195,4.27685,4.72705,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 61 years old. The concentration of Creatinine is 790.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 790.0 µmol. To convert 790.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 790.0 µmol Creatinine * 1e-06 mol/µmol = 0.00079 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00079 mol Creatinine * 113.12 g/mol = 0.08936 g Creatinine. To convert 0.08936 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.08936 g Creatinine * 1000.0 mg/g = 89.36 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 89.36 mg Creatinine/10.0 dL = 8.936 mg Creatinine/dL. The concentration value of 790.0 µmol Creatinine/L converts to 8.936 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 8.936^(-1.154) * 61^(-0.203) * 1 * 0.742=4.50195.
Hence, the patient's GFR is 4.50195 mL/min/1.73m²."
3233,9,MDRD GFR Equation,lab test,decimal,pmc-4616402-1,Extracted,"A 75-year-old Japanese woman was admitted to our hospital complaining of swelling of the right elbow and the wrist joint for a month. She had no history of orthopedic surgery, joint trauma, or intraarticular injections in those joints. She had a 17-year history of dermatomyositis after being diagnosed at 58 years of age, along with interstitial lung disease (ILD), pulmonary hypertension, chronic kidney disease, and Raynaud phenomenon. She had pulmonary tuberculosis at the age of 33, resulting in old inflammatory changes and volume loss in the left lung. Later, her dermatomyositis proved to be antisynthetase syndrome with antithreonyl-tRNA synthetase antibody. Antisynthetase syndrome is characterized by the existence of antibodies to aminoacyl-transfer ribonucleic acid synthetase enzymes, myositis, ILD, arthropathy, fever, Raynaud phenomenon, and mechanic's hands.
The patient had remained on corticosteroids for 17 years; at least 3 times she had received high-dose corticosteroid therapy, that is, 45–60 mg prednisolone (PSL) per day continued for 4 weeks and tapered, with or without pulsed methylprednisolone (P-MPSL). As for other immunosuppressants, methotrexate was only temporarily used 10 years before this event; they were never used after that time. Four years before her present admission, she experienced the last exacerbation of antisynthetase syndrome-associated ILD that required the high-dose PSL therapy and P-MPSL. Despite the therapy, her respiratory function worsened due to the progression of fibrosis, and she had to receive home oxygen therapy. The PSL was tapered gradually to 10 mg per day over the next 3 years. She was on 9.5 mg PSL per day at the time of admission. On physical examination, she was afebrile, and all other vital signs were within normal limits. Her right elbow, forearm, and wrist joint were swollen with tenderness. Erythema and warmth were noted on her right arm. No skin eruptions or nodules were found. The cardiopulmonary and abdominal findings were normal.
Laboratory examinations showed that white blood cell count was 9000/μL (normal range 3300–7600/μL, neutrophils 77%, lymphocytes 20%, monocytes 3%, and eosinophils 0%). Elevated serum levels of C-reactive protein (2.6 mg/dL, normal range <0.3 mg/dL) and creatinine (1.2 mg/dL, normal range 0.5–0.8 mg/dL, the estimated glomerular filtrating ratio was 34.0 mL/min) were shown. No other abnormalities were detected on laboratory testing. X-ray of her right elbow joint showed osteolysis and pathological fracture of the right olecranon (Figure ). Magnetic resonance imaging revealed fluid in her right elbow joint and forearm (Figure ). In addition, there were high-intensity lesions in the right olecranon, which suggested an osteomyelitis. M abscessus, identified by hps65 gene sequencing (100% homology), grew in blood and joint fluid cultures (BacT/ALERT system; Biomérieux, Marcy-l’É toile, France).
Breakpoint susceptibility testing was performed using the broth microdilution method with 10 drugs based on the recommendations of the Clinical and Laboratory Standards Institute M24-A2 (Table ). Sputum cultures were negative for mycobacteria. A surgical debridement of the right elbow joint, forearm, and wrist joint was performed. The extra fluid in the patient's right elbow joint and forearm was completely removed. We initiated a vancomycin treatment for the patient, empirically. Based on the culture reporting, we switched the antimicrobial treatment to clarithromycin, amikacin, and imipenem/cilastatin. This combination therapy was continued for 6 weeks. The daily PSL was maintained to prevent adrenal insufficiency.
The subsequent blood and joint fluid cultures became negative 1 week later. We placed a peripherally inserted central catheter in the right jugular vein for long-term intravenous antimicrobial therapy.
One month after the initiation of antimicrobials, the patient became febrile, and blood cultures turned positive for yeast-like fungi, which were identified as Candida albicans. The patient also had candida endophthalmitis. We added micafungin and later changed the micafungin to fluconazole based on the blood culture results. Although the subsequent blood cultures became negative for C albicans, a pleural effusion was increased with paroxysmal atrial fibrillation. The pleural fluid culture was negative. Two weeks later, the patient died due to respiratory failure possibly related to the disseminated candidiasis. An autopsy was not performed, per her family's request.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [75, 'years'], 'creatinine': [1.2, 'mg/dL'], 'sex': 'Female', 'Race': 'Asian'}",43.79549,41.60572,45.98526,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 75 years old. The concentration of Creatinine is 1.2 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.2^(-1.154) * 75^(-0.203) * 1 * 0.742=43.79549.
Hence, the patient's GFR is 43.79549 mL/min/1.73m²."
3234,9,MDRD GFR Equation,lab test,decimal,pmc-7957842-1,Extracted,"A 66-year-old male presented to the ED with a two-week history of subjective fever, dyspnea, and a productive cough of rusty sputum. The symptoms started insidiously and improved after a few days of onset only to progressively worsen, bringing the patient to the hospital. The patient has a past medical history of diabetes mellitus (DM), chronic kidney disease (CKD), hypertension (HTN), coronary artery disease, and heart failure with preserved ejection fraction. On initial exam, he was tachypneic with a respiratory rate of 32 breaths/min, febrile with a temperature of 39.7℃, pulse rate of 101 beats/min, and blood pressure of 146/84 mmHg, and he required 15 L of oxygen/min through a nonrebreather mask to maintain his oxygen saturation above 94%. Lung auscultation was significant for crackles at lung bases bilaterally. Chest radiograph at presentation showed bilateral patchy basal infiltrates (Figure ).
Laboratory work was significant for a creatinine level of 1.76 mg/dL, and the white blood cell count was 6,300 cells per cubic per millimeter with an absolute lymphocyte count of 1,800 cells per cubic millimeter, C-reactive protein of 143 mg/L, fibrinogen of 1026 mg/dL, D-dimer of 11.6 mcg/mL, and ferritin of 1071 ng/mL. Nasal swab for COVID-19 polymerase chain reaction (PCR) was positive. The patient was admitted to general medicine service; he received a loading dose of IV remdesivir 200 mg followed by 100 mg IV daily for five days. IV dexamethasone 6 mg daily was given for 10 days.
The admitting physician suspected cobacterial infection because of the history of rusty sputum and administered ceftriaxone 2 g IV for five days upon admission to general medicine. Urine Streptococcal pneumoniae antigen was reported to be positive a few hours after his admission. Blood culture revealed no growth, and chest CT performed two days after admission revealed bilateral consolidative infiltrates (Figure ).
Respiratory status improved slowly; he required 10 L of oxygen/min on day 5 and 5 L of oxygen/min on day 7 when he developed severe chest pain, which improved with nitroglycerine. An electrocardiogram revealed subtle ST segment depression in lead 3, and high sensitivity troponin I was elevated at 33.048 ng/L. An echocardiogram revealed an ejection fraction of 45% and hypokinetic anterior and lateral walls. Non-ST segment elevation myocardial infarction was diagnosed and managed conservatively with aspirin, clopidogrel, metoprolol, heparin, and atorvastatin with a plan for heart catheterization a few weeks after he recovered from his illness. The patient also developed acute kidney injury with a peak creatinine of 2.8 mg/dL, which recovered on conservative management to a baseline creatinine of 1.5 mg/dL. He also received a few doses of furosemide. He did not require intensive care admission, and his oxygen saturation was 98% on ambient air on day 10 but dropped to the low eighties with ambulation. He was discharged home on day 12 with home oxygen to be used with ambulation. Our patient had a follow up in the medicine clinic two weeks after his discharge, and he was very pleased that he recovered from COVID-19.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [66, 'years'], 'creatinine': [1.76, 'mg/dL'], 'sex': 'Male'}",38.93579,36.989,40.88258,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 66 years old. The concentration of Creatinine is 1.76 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.76^(-1.154) * 66^(-0.203) * 1 * 1=38.93579.
Hence, the patient's GFR is 38.93579 mL/min/1.73m²."
3235,9,MDRD GFR Equation,lab test,decimal,pmc-3621255-1,Extracted,"A 45-year-old white male was examined before related preemptive renal transplantation. The patient was regularly examined by ultrasound because of positive family history of ADPKD. His 69-year-old father had ESRD at 52 years because of polycystic kidneys. Father had not well compensated hypertension many years. His grandmother with polycystic kidneys developed renal failure at 77 years. His father had one sister and one brother with normal ultrasound finding at the age of 40.
ADPKD in the patient was first diagnosed on ultrasound at the age of 20. At this age he suffered from repeated renal colic caused by urate concrements. The stones passed spontaneously after hydration. He was on antihypertensive drugs ACE inhibitor and AT1 receptor blocker because of mild hypertension since the age of 25. The blood pressure was well compensated (repeatedly below 130/80 mm Hg). There was a mild dilatation of ascending aorta and mild mitral valve insufficiency on echocardiography. The renal function started to decline at the age of 30, with ESRD reached at the age of 45. His 40-year-old sister volunteered herself as a potential kidney donor. Results of her blood group and tissue-type identified her as a suitable donor with an optimal HLA match and negative cross-match. However an ultrasound scan revealed 2 cysts in her left kidney.
The paternal grandmother developed renal failure at 77 years and then was hemodialyzed. The diagnosis of ADPKD was based on incidental ultrasound finding of renal and hepatic cysts during examination before cholecystectomy at the age of 64. Kidney size was about 16 cm in diameter, there were multiple cysts about 3 centimeters and serum creatinine was 180 μmol/l. Computed tomography or magnetic resonance were not performed. Moderate renal insufficiency was present.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [45, 'years'], 'creatinine': [180.0, 'µmol/L'], 'sex': 'Male', 'Race': 'White'}",35.57184,33.79325,37.35043,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 45 years old. The concentration of Creatinine is 180.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 180.0 µmol. To convert 180.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 180.0 µmol Creatinine * 1e-06 mol/µmol = 0.00018 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00018 mol Creatinine * 113.12 g/mol = 0.02036 g Creatinine. To convert 0.02036 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.02036 g Creatinine * 1000.0 mg/g = 20.36 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 20.36 mg Creatinine/10.0 dL = 2.036 mg Creatinine/dL. The concentration value of 180.0 µmol Creatinine/L converts to 2.036 mg Creatinine/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.036^(-1.154) * 45^(-0.203) * 1 * 1=35.57184.
Hence, the patient's GFR is 35.57184 mL/min/1.73m²."
3236,9,MDRD GFR Equation,lab test,decimal,pmc-2938507-1,Extracted,"A 65-year-old male presented with an abrupt onset of sharp, burning, constant right lower abdominal pain after previously been feeling well. There was no history of trauma, fever, vomiting, diarrhea, chest pain, shortness of breath, syncope, dysuria, hematuria or melena. His past medical history included hypertension, atrial flutter and cardiomyopathy, and he had an implantable cardioverter/defibrillator (ICD). There was no prior history of abdominal aortic aneurysm in the patient or in his family. His past surgical history included an inguinal hernia repair. His medications included aspirin, valsartan, metoprolol and atorvastatin. He did not smoke, use alcohol or illicit drugs.
Physical exam showed vitals signs as follows: body temperature of 36.3°C, blood pressure of 140/82 mmHg, heart rate of 52 beats per minute, respiratory rate of 18 breaths per minute and pulsoximetry of 98% on room air. He was alert, but appeared in mild distress due to pain. His abdominal exam revealed tenderness to palpation in the right lower quadrant, with no rebound, guarding, distention or organomegaly. The remainder of the exam was normal.
The initial emergency department evaluation included an electrocardiogram that showed atrial flutter with a 4:1 block. Laboratory assessment revealed trace hematuria, no leukocytosis, creatinine of 1.3 mg/dL (normal range, 0.7–1.4 mg/dL), mildly elevated lipase to 85 U/L (normal range, 12–70 U/L), mild hyperglycemia and mildly elevated aspartate aminotransferase to 46 U/L (normal range, 7–40 U/L). The lactate and coagulation profiles were within normal limits. Lactate dehydrogenase was not ordered at presentation, but obtained 2 days after admission, and was elevated at 1,479 U/L (normal range, 100–220 U/L). Lactate dehydrogenase is present in the renal tissue and elevates in serum after kidney insult, and it is unknown whether this level correlates to the severity of the infarct.
Given the nature of the pain and the hematuria seen on urinalysis and the history of cardiomyopathy with atrial flutter, both nephrolithiasis and mesenteric ischemia were strongly considered as causes for this acute pain. Therefore, both non-contrast- and contrast-enhanced helical computed tomography (CT) images [Figures and ] were obtained, which showed extensive infarction involving the upper pole of the right kidney with multiple patchy infarcts into the lower pole, a patent right renal artery, but no visualization of the interparenchymal arterial branches within the mid and upper poles of the right kidney, suggesting arterial thromboembolic disease. There was poor opacification of the right renal vein, and, therefore, renal vein thrombus could not be ruled out. A 2-mm left renal calculus was also identified.
The urology and vascular surgery services were consulted, and both recommended conservative treatment with anticoagulation. In addition to normal saline and dilaudid for pain control, a heparin bolus of 80 mg/kg was given and an infusion at 18 mg/kg/h was initiated, with the patient being admitted to the general medicine service.
It was concluded his renal artery thrombosis was most likely embolic and a 2-D echocardiogram was ordered, which showed no intramural thrombus. He was discharged 5 days later, on coumadin. His creatinine, which was 1.3 mg/dL on admission, rose to 1.8 mg/dL and fell to 1.7 mg/dL by discharge. One month later, the creatinine levels had declined to 1.6 mg/dL.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [65, 'years'], 'creatinine': [1.6, 'mg/dL'], 'sex': 'Male'}",43.59756,41.41768,45.77744,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 65 years old. The concentration of Creatinine is 1.6 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.6^(-1.154) * 65^(-0.203) * 1 * 1=43.59756.
Hence, the patient's GFR is 43.59756 mL/min/1.73m²."
3237,9,MDRD GFR Equation,lab test,decimal,pmc-6682238-1,Extracted,"A 76-year-old Caucasian female with a past medical history significant for hyperlipidemia and poorly controlled hypertension was sent to the emergency department (ED) by her outpatient cardiologist due to abnormal labs. Her labs were most significant for a severe leukocytosis and hypokalemia. On her arrival to the ED, she was grossly asymptomatic but reported a two-week history of generalized fatigue and intermittent lightheadedness. On review of systems, she also endorsed a 10-pound weight loss over the prior six months and episodic generalized abdominal pain associated with nausea and vomiting over the prior year.
On exam, she was hypotensive to 83/42 millimeters of mercury with otherwise normal vital signs. She was awake, alert, in no acute distress, and in general was very comfortable and well appearing. She did not demonstrate any evidence of hypoperfusion on exam such as altered mental status, dizziness, or cold extremities. Her abdomen was soft and non-distended with only mild tenderness to palpation in the suprapubic region but no guarding or rebound. Her exam was otherwise notable for a diminished left radial pulse and bilaterally diminished dorsalis pedis pulses.
Routine investigations revealed a white cell count of 49.1/liters (L) (4.4–11.3×109/L) with a left shift and neutrophil predominance, potassium of 2.5 millimoles (mmol)/L (3.5–5.3mmol/L), sodium of 127 mmol/L (136–145mmol/L), blood urea nitrogen of 31 milligrams per deciliter (mg/dL) (6–23 mg/dL), creatinine of 1.53 mg/dL (0.50–1.05 mg/dL), C reactive protein of 31.44 mg/dL (<1.00) and lactate of 3.7 mmol/L (0.4–2.0 mmol/L). Her liver function tests were within normal limits. Urinalysis and chest radiograph were obtained for an infectious workup and were both unremarkable.
After a period of observation, an abdominal computed tomography (CT) was obtained given her history of chronic abdominal pain and persistent concern for infectious process with no clear source. The CT showed gallbladder wall thickening and edema with pericholecystic edema and a contained perforation of the gallbladder wall near the fundus ().
Interval CT angiogram showed severe atherosclerotic changes of the abdominal aorta and its branches with complete occlusion of the celiac artery origin and diminutive flow in its distal branches from collateral vessels, severe stenosis of the superior mesenteric artery, and mild stenosis of the inferior mesenteric artery. There was mild wall thickening of the ascending colon and transverse colon.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [76, 'years'], 'creatinine': [1.53, 'mg/dL'], 'sex': 'Female', 'Race': 'White'}",32.99916,31.3492,34.64912,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 76 years old. The concentration of Creatinine is 1.53 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.53^(-1.154) * 76^(-0.203) * 1 * 0.742=32.99916.
Hence, the patient's GFR is 32.99916 mL/min/1.73m²."
3238,9,MDRD GFR Equation,lab test,decimal,pmc-6688890-1,Extracted,"A 40-year-old Caucasian lady with a prior medical history of chronic kidney disease stage 4 with a recently diagnosed biopsy-proven focal crescentic glomerulonephritis (p-ANCA), chronic obstructive pulmonary disease, obstructive sleep apnea (OSA), diabetes mellitus type 2, hypertension and morbid obesity was transferred from outside hospital (OSH) with altered mental status, headaches and generalized tonic-clonic seizures. Given rapid clinical deterioration and progressive cognitive decline, she was transferred to our facility. Upon arrival, the patient’s Glasgow Coma Scale was 4, was hypoxic and required emergent endotracheal intubation.
After a recent diagnosis of focal crescentic glomerulonephritis, she had received three doses of 1 gm intravenous pulse methylprednisolone followed by oral prednisone(1 mg/kg/day) along with weekly outpatient rituximab intravenous infusions (375 mg/m2). The last and fourth dose of rituximab was 5 days before her presentation.
She was an active smoker with 15 pack years history, and family history was not relevant to her current presentation. Her physical examination was notable for obesity, intubated status, with reduced air entry in the posterior lung fields and trace pedal oedema. Blood pressure on presentation was 162/79 mm Hg. Her husband endorsed good compliance with medications and continuous positive airway pressure for her OSA. Laboratory studies showed serum creatinine of 2.2 mg/dL and blood urea nitrogen of 29 mg/dL. White cell count was 10.8 (1000/uL), haemoglobin was 12 gm/dL and platelets was 230 (1000/uL). Urine analysis showed 3+ protein, 40 RBCs and 4 WBCs. She underwent extensive serological work up 5 weeks prior and were relevant with her pauci-immune ANCA vasculitis. HIV, hepatitis B and C serologies were unremarkable. A lumbar puncture with cerebrospinal fluid (CSF) examination showed normal opening pressure, clear fluid, 0 WBCs, protein of 47 mg/dL and glucose of 131 mg/dL. An MRI showed cortical white matter changes suggestive of possible PML or PRES (Fig. ). CSF polymerase chain reaction (PCR) for herpes simplex virus (HSV) and John Cunningham virus (JCV) were negative. Flow cytometry and cytology were negative. Serum JCV PCR was negative. Brain biopsy deferred given clinical improvement.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [40, 'years'], 'creatinine': [2.2, 'mg/dL'], 'sex': 'Female', 'Race': 'White'}",24.72111,23.48505,25.95717,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 40 years old. The concentration of Creatinine is 2.2 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.2^(-1.154) * 40^(-0.203) * 1 * 0.742=24.72111.
Hence, the patient's GFR is 24.72111 mL/min/1.73m²."
3239,9,MDRD GFR Equation,lab test,decimal,pmc-7566983-1,Extracted,"A 46-year-old Caucasian male with minimal routine primary care presented to the emergency department after 24 hours of confusion, generalized fatigue, epistaxis, oral mucosal bleeding, and an ecchymotic rash on the chest and lower extremities. Past medical history was significant for IgG myeloma diagnosed one month prior, with m-protein of 4.8 g/dL by serum protein electrophoresis (SPEP), 14.1 mg/L kappa free light chains (FLC) and 1606.6 mg/L lambda FLC, and IgG of 5,680 mg/dL, IgA of 33 mg/dL, and IgM of 12 mg/dL by serum immunofixation (IFX). Concomitant renal and respiratory failure were also present at the time of diagnosis. He received one cycle of cyclophosphamide, bortezomib, and dexamethasone (CyBorD) but left the hospital against medical advice.
On admission, the patient was tachycardic, tachypneic, intermittently febrile, and had a leukocytosis of 15 x 103/µL. Chest radiography demonstrated patchy, consolidative opacities affecting the right middle and upper lung lobes (Figure ). Complete blood count was noteworthy for anemia and thrombocytopenia, with hemoglobin and platelet counts of 6.3 g/dL and 11 x 109/L, respectively. Complete metabolic panel was significant for hyponatremia of 121 mmol/L, corrected hypercalcemia of 15.2 mg/dL, albumin of 2.0 g/dL, and blood urea nitrogen (BUN) of 39 mg/dL with creatinine of 2.38 mg/dL, and lactic acid was 7.7 mmol/L. These findings showed electrolyte derangements and organ dysfunction consistent with multiple myeloma compounded by sepsis for which the patient was started on broad-spectrum antibiotics. Blood cultures obtained at this point would later return positive for Streptococcus pneumoniae. Repeat serum FLC revealed 5.3 mg/L kappa FLCs and 15,115.1 mg/L lambda FLCs, a significant increase from just a month prior. SPEP was significant for an m-protein of 6.89 g/dL. Serum IFX revealed an IgG of 6,609 mg/dL, IgA less than 40 mg/dL, and IgM less than 25 mg/dL. Peripheral blood smear demonstrated 1% blast cells and 4% circulating plasma cells raising the concern for development of acute plasmocytic leukemia. Flow cytometry was performed and later revealed CD38+ blasts at 0.77% and CD34+ plasma cells at 1.05%.
CT of the chest, abdomen and pelvis revealed numerous osteolytic bone lesions, consistent with multiple myleoma, throughout the pelvis (Figure ), thoracolumbar spine (Figure ), and proximal femurs. Hepatosplenomegaly (Figure ) was also seen on CT of the abdomen and pelvis possibly indicating extramedullary invasion of plasma cells.
Regarding the remainder of his hospital course, the patient was intubated and mechanically ventilated for increasing oxygen requirements. Multiple transfusions with packed red blood cells and platelets would be performed during this admission with neither anemia nor thrombocytopenia resolving. Lactic acid levels remained elevated two days after admission with vasopressor requirement. Additional laboratory studies included a fibrinogen of 109 mg/dL, D-dimer of 23.02 µg FEU/mL, partial thromboplastin time (PTT) of 48.5 seconds, and prothrombin time (PT) of 17.2 seconds, suggesting developing disseminated intravascular coagulation. Repeat serum creatinine had also increased to 3.69 mg/dL, with potassium of 6.6 mmol/L and phosphorus of 9.1 mg/dL; tumor lysis syndrome was suspected. At this juncture, the family was made aware of the patient’s requirement for continuous renal replacement therapy and poor overall prognosis; comfort measures were favored.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [46, 'years'], 'creatinine': [3.69, 'mg/dL'], 'sex': 'Male', 'Race': 'White'}",17.82994,16.93844,18.72144,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 46 years old. The concentration of Creatinine is 3.69 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.69^(-1.154) * 46^(-0.203) * 1 * 1=17.82994.
Hence, the patient's GFR is 17.82994 mL/min/1.73m²."
3240,9,MDRD GFR Equation,lab test,decimal,pmc-3741979-3,Extracted,"A 22-year-old male was admitted with history of oliguria and back pain of 1-week duration. He had received pantoprazole and paracetamol for 10 days as treatment for dyspepsia and body ache. On examination, there was no fever, BP was 140/80 mm Hg, blood urea was 123 mg/dl, and serum creatinine 10.7 mg/dl. Hemodialysis was started. Renal biopsy showed AIN with lymphocytic and eosinophilic infiltrations in the interstitium with normal appearing glomeruli. PPI was stopped and he was started on pulse methyl prednisolone for 3 days followed by oral prednisolone for 12 weeks. His renal function normalized after 8 weeks and remained at 0.9 mg /dl after 12 months.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [22, 'years'], 'creatinine': [10.7, 'mg/dL'], 'sex': 'Male'}",6.06202,5.75892,6.36512,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 22 years old. The concentration of Creatinine is 10.7 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 10.7^(-1.154) * 22^(-0.203) * 1 * 1=6.06202.
Hence, the patient's GFR is 6.06202 mL/min/1.73m²."
3241,9,MDRD GFR Equation,lab test,decimal,pmc-4421527-1,Extracted,"A 55-year-old Filipino man with a past medical history of hypertension, hyperlipidaemia, CKD (not taking activated vitamin D derivatives or phosphate binders) and coronary artery disease presented to a hospital in the Philippines with abdominal pain, nausea and post-prandial, non-bloody, non-bilious vomiting. His pre-hospitalization serum creatinine concentration was 3.0 mg/dL. An anterolateral ST segment elevation myocardial infarction was diagnosed, and emergent coronary angiography revealed 70% stenosis of the left anterior descending artery distal to a drug-eluting stent (DES) placed ~2 years earlier. A second DES was successfully placed, and he was discharged home on clopidogrel, aspirin, isosorbide mononitrate, metoprolol, rosuvastatin, imidapril and lansoprazole.
Four weeks prior to admission at our hospital, he was admitted to another hospital in the Philippines with intractable nausea and vomiting, fatigue, generalized weakness, constipation and a 30-lb weight loss. Symptomatic treatment was provided; on physical examination, he was noted to have a palpable left anterior neck mass. Serum chemistries showed markedly elevated serum calcium of 17.28 mg/dL and a serum creatinine of 3.8 mg/dL.
An abdominal ultrasound showed possible renal parenchymal disease, and an abdominal non-contrast computed tomography (CT) was normal except for two non-obstructing, hyper-dense foci (thought to represent stones) in the left kidney. In an attempt to treat hypercalcaemia, normal saline infusion (200 mL/h) and furosemide were begun. A narrow corrected QT (QTc) interval was observed, and he was transferred to the coronary care unit (CCU) for closer monitoring.
On the next day, the serum calcium was 14.29 mg/dL and a narrow QTc interval remained. Haemodialysis was recommended; during catheter insertion, the patient's pulse and blood pressure dropped. Atropine and a dopamine infusion were started, but the patient developed chest pain and non-sustained ventricular tachycardia followed by supraventricular tachycardia, which converted to normal sinus rhythm with intravenous amiodarone. On the same day, a neck ultrasound revealed a 4.5 × 1.2 × 1.2-cm soft tissue mass behind the left lobe of the thyroid as well as a cystic component in the inferior pole with no gross calcification.
The patient's serum calcium was 16.36 mg/dL the following day, with serum phosphorus 4.87 mg/dL. Haemodialysis was attempted, but the catheter malfunctioned. A tunnelled haemodialysis catheter was subsequently placed, but profuse bleeding at the site prohibited immediate use. In the interim, he was treated with additional normal saline, subcutaneous calcitonin and ibandronate, which lowered his serum calcium to 13.77 mg/dL. The serum creatinine increased to 4.99 mg/dL.
Approximately 3 weeks prior to admission at our hospital, he was found to have an elevated PTH of 496.2 pg/mL. Dual-energy X-ray absorptiometry demonstrated osteoporosis (spine T-score −3.28, hip T-score −2.70). A 201Tl/99mTc pertechnetate thyroid scan revealed a minimally enlarged thyroid (4.8 × 2.4 cm right lobe, 4.2 × 2.7 cm left lobe), but suboptimal radioactivity accumulation precluded parenchymal evaluation. Delayed static images of the neck after 99mTc-sestamibi injection showed abnormal radiopharmaceutical accumulation in the region of the superior and inferior left parathyroid glands suggestive of adenoma or hyperplasia. Surgical excision was recommended.
With continued hypotension requiring a continuous dopamine infusion, repeat coronary angiography was performed and showed the recently placed DES to be patent. Cardiology recommended 6 months of clopidogrel therapy before proceeding with parathyroid surgery. He was transferred out of the CCU 2 days later, and cinacalcet was started. The serum calcium initially decreased to 12.49 mg/dL (with serum phosphorus 2.9 mg/dL and serum creatinine 2.5 mg/dL), but increased to 14.69 mg/dL (with serum phosphorus 2.9 mg/dL and serum creatinine 2.6 mg/dL) 2 days later, after which his cinacalcet dose was doubled and another dose of intravenous ibandronate was given. An interdisciplinary care conference concluded that continued medical management of the patient's hypercalcaemia was ineffective. The family requested that the patient be transferred to our hospital for surgery.
In preparation for surgery, a contrast CT scan of the head, neck and thorax showed a 1.8 × 1.4 × 4.5-cm heterogeneously enhancing, well-defined mass lesion spanning the posterior aspect of the left thyroid lobe. Mild compression of the trachea with slight rightward deviation was present. Repeat PTH was 1142.89 pg/mL.
Approximately 1 week prior to admission at our institution, he received another dose of intravenous ibandronate and underwent haemodialysis, which lowered the serum calcium from 16.16 mg/dL (with the pre-dialysis serum creatinine 3.0 mg/dL) to 14.97 mg/dL. The following day, his total serum calcium was 17.28 mg/dL and he developed a fever; vancomycin was started for presumed tunnelled catheter infection. A new permanent haemodialysis catheter was inserted, and he underwent daily haemodialysis, which lowered his total serum calcium to 12.97 mg/dL. He was subsequently transferred.
Upon admission to our hospital, the patient's serum calcium was 15.0 mg/dL. The PTH was 1347 pg/mL and increased to 1890 pg/mL the following day. Ultrasound of the thyroid () showed a normal thyroid gland with a 3.7 × 1 × 1.3-cm left lobe and a 4.4 × 1.3 × 1.8-cm right lobe. A large, elongated, hypoechoic, hypervascular mass with internal cystic change measuring 5 × 1.7 × 1 cm was found behind the entire left lobe of the thyroid. Intravenous fluids, furosemide and subcutaneous calcitonin were begun. Serum calcium initially fell to 13.4 mg/dL (with serum phosphorus 4.8 mg/dL) but rose again to 15.7 mg/dL (with serum phosphorus 5.0 mg/dL), and haemodialysis was re-initiated.
Based on a working diagnosis of parathyroid carcinoma, the patient underwent the planned left parathyroidectomy with concomitant left thyroid lobectomy on the following day. Intraoperative PTH was 2462 pg/mL prior to incision, which decreased to 310 pg/mL immediately after removal and to 144.5 pg/mL within 10 min after removal. Gross pathologic findings included a 4-cm, in greatest dimension, portion of left thyroid with a 3.7 × 1.8 × 1.8-cm solitary abnormal parathyroid gland weighing 2 g. Microscopic examination () revealed a densely cellular proliferation of neoplastic chief cells demonstrating uniformly round, regular nuclei with smooth nuclear membranes, small variably prominent nucleoli and abundant granular cytoplasm. Features (as proposed by Schantz and Castleman in []) suspicious for carcinoma—thick tumour capsule, invasion into adjacent tissues, dense sclerosis within tumour and increased mitotic figures (>1/high-power field)—were noticeably absent.
One day after surgery, the PTH declined to 7 pg/mL and the serum calcium declined to 12.1 mg/dL (with serum phosphorus 3.5 mg/dL). His calcium continued to decline until 4 days after discharge with a total serum calcium of 8.2 mg/dL (with serum phosphorus 1.8 mg/dL) (). His serum calcium remained stable at 8.7 mg/dL ~6 months after discharge. He required no calcium or phosphorus supplementation.
The serum creatinine at admission to our hospital was 3.1 mg/dL. Ultrasound of the kidneys and bladder with Doppler revealed normal-sized kidneys (11.6 cm right long axis diameter, 11.4 cm left long axis diameter) exhibiting minimal bilateral pelviectasis. A minimally complex cyst with a septa measuring ~13 × 16 × 12 mm in diameter and a second small, simple cyst measuring ~8 × 10 × 9 mm in diameter were found in the left kidney. Numerous, scattered, echogenic foci were seen within the kidneys bilaterally, which may reflect small calcified renal stones. However, there was no evidence for obstruction. The patient has done well with a serum creatinine of 1.5 mg/dL ~6 months after discharge.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [55, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Male', 'Race': 'Asian'}",48.58868,46.15925,51.01811,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 55 years old. The concentration of Creatinine is 1.5 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.5^(-1.154) * 55^(-0.203) * 1 * 1=48.58868.
Hence, the patient's GFR is 48.58868 mL/min/1.73m²."
3242,9,MDRD GFR Equation,lab test,decimal,pmc-3999580-1,Extracted,"A 77-year-old woman presented with vomiting for 1 month and loss of 25% of body weight during that time. She had previously visited a general practitioner for vomiting. Abdominal X-ray in that clinic had indicated gastric dilatation. She was referred to our hospital for further examination.
On physical examination, her abdomen was bloated without tenderness. She was 143 cm tall and weighed 30 kg. Vital signs were: body temperature 36.8°C, pulse 65 beats per minute, respiratory rate 18 per minute, and blood pressure 90/60 mm Hg. Laboratory data on admission were as follows: white blood cell count 5,800/μl, red blood cell count 326 × 104/μl, hemoglobin 10.2 g/dl, platelets 35.1 × 104/μl, total protein 4.4 g/dl, albumin 2.1 g/dl, total bilirubin 0.38 mg/dl, aspartate aminotransferase 13 IU/l, alanine aminotransferase 6 IU/l, alkaline phosphatase 68 IU/l, γ-glutamyl transferase 12 IU/l, cholinesterase 99 IU/l, total cholesterol 103 mg/dl, blood urea nitrogen 17.1 mg/dl, creatinine 0.42 mg/dl, C-reactive protein 1.20 mg/dl, Na 134 mEq/l, K 3.61 mEq/l, Cl 97 mEq/l, CEA 4.7 ng/ml, and CA19-9 7.3 U/ml. Abdominal X-ray showed gastric dilatation. Computed tomography (CT) of the abdomen revealed a duodenal giant mass spreading from the bulb to the horizontal part of the duodenum (fig. ). Upper gastrointestinal radiography with Gastrografin revealed smooth taper shape of the duodenum. No tumor was clearly detected (fig. ). A villous tumor was observed in the duodenal bulb endoscopically, but the pyloric ring was not confirmable (fig. ). There were no appearances suggestive of malignancy. The tissue obtained from biopsy did not include malignant cells. Insertion of the endoscope into the second part of the duodenum was easy.
We diagnosed the mass to be a huge duodenal tumor, and laparotomy was therefore performed. About one third of the stomach was invaginated through the pylorus into the duodenum (fig. ). We in vain performed manipulative reduction by Hutchinson's maneuver. Gastrotomy followed by duodenotomy was performed and revealed a villous tumor measuring 12 cm in maximum diameter. The tumor was excised and pathological examination of the frozen section showed malignant cells composed of well-differentiated adenocarcinoma and undifferentiated carcinoma. The infrapyloric lymph node was positive for metastasis. Therefore, additional distal gastrectomy with lymphadenectomy was performed. The patient made an uneventful postoperative recovery.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [77, 'years'], 'creatinine': [0.42, 'mg/dL'], 'sex': 'Female'}",146.30348,138.98831,153.61865,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 77 years old. The concentration of Creatinine is 0.42 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.42^(-1.154) * 77^(-0.203) * 1 * 0.742=146.30348.
Hence, the patient's GFR is 146.30348 mL/min/1.73m²."
3243,9,MDRD GFR Equation,lab test,decimal,pmc-5634435-1,Extracted,"An 86-year-old woman with heart failure due to ischemic heart disease, polymyalgia rheumatica, idiopathic pulmonary fibrosis, non-dialysis-dependent chronic kidney disease and panic disorder was brought to the emergency room with a 2-month history of persistent daily high-grade fever (38.5 °C) and progressive dyspnea. She had been previously hospitalized for 15 days because of fever and dyspnea accompanied by a cough and hyaline sputum, when the laboratory work-up revealed a positive blood culture for Achromobacter xylosoxidans. At that time, there was no evidence of vegetation on a transthoracic echocardiogram (TTE), no abnormality on the abdominal ultrasound or on the chest and abdominal computed tomography (CT). Also, she had a normal urinalysis and a negative urine culture. HIV, hepatitis B and C serology, and antinuclear antibodies were negative. The patient received an 8-day course of intravenous trimethoprim-sulfamethoxazole according to the blood culture sensitivity tests, followed by a 6-day course of the same orally administered antibiotic. She was discharged without fever, but the dyspnea remained unchanged.
On the eighth day following the withdrawal of the antibiotic, the fever relapsed and the patient restarted empirical treatment with the same antibiotic. Despite this new regimen of antibiotic, she was readmitted with a high-grade fever, progressive worsening of dyspnea, and new skin lesions on the palms of her hands and soles of her feet. Over the previous 2 months, she had lost 5 kg (10% of her usual weight). She denied any previous diagnosis of malignancy, and any use of intravascular devices or immunosuppressive therapy. She was regularly using carvedilol, atorvastatin, and aspirin, besides the previously mentioned antibiotic when readmitted.
During the physical examination, she was pale, with tachycardia (pulse of 108 bpm), blood pressure of 98/60 mmHg and normal axillary temperature of 36.8 °C. A systolic and diastolic cardiac murmur in the aortic area, and a systolic murmur in the mitral area, were easily audible. Pulmonary auscultation detected Velcro-like crackles, which were consistent with pulmonary fibrosis. The abdominal examination was painless; the liver was palpable at the right rib cage; the spleen was not palpable; and there was no dullness on percussion over the Traube’s space. Multiple non-tender erythematous violaceous papules and macules were present in the patient’s palms, fingers, thumbs, and soles, which was consistent with Janeway’s lesions (). The patient had a total dental prosthesis and the oral cavity was free of lesions. Upon readmission, trimethoprim-sulfamethoxazole was withdrawn and three sets of blood cultures were sampled at different puncture sites at 12-hour intervals.
The initial laboratory work-up showed an elevated C-reactive protein level of 120 mg/L (reference value [RV]: <5 mg/L) and an erythrocyte sedimentation rate at 170 mm/h (RV: <20 mm/h), normocytic and normochromic anemia, thrombocytosis, a positive rheumatoid factor of 60 UI/mL (RV: <16 UI/mL) and a serum creatinine of 1.59 mg/dL (RV: 0·4-1.3 mg/dL), which was similar to the patient’s previous creatinine determination; normal complement levels (C3 and C4) and a positive qualitative cryoblobulin’s test. Urinalysis showed microscopic hematuria without erythrocyte dysmorphism and mild proteinuria. All blood culture sets were negative. A TTE was performed on the second day following readmission, which did not show any valvular vegetation. However, a left ventricular systolic dysfunction and aortic and mitral regurgitation were found.
During the first 2 days of hospitalization, the patient remained afebrile, but on the third and fourth day she presented an ongoing axillary temperature of 38.3 °C. Treatment with piperacillin-tazobactam was scheduled for a 6-week regimen. Another thoracic and abdominal CT was performed, ruling out any suspected site of infection or malignancies. A transesophageal echocardiography (TEE) showed a 4 mm vegetation on the non-coronary cusp of the aortic valve.
During hospitalization, the patient presented worsening signs of heart failure, including weight gain, sacral and lower limbs pitting edema, bilateral rales crackles, and hepatojugular reflux, which improved with diuretics and vasodilators titration. Furthermore, she presented five episodes of supraventricular tachycardia, which was treated with amiodarone. She completed a 6-week course of piperacillin-tazobactam along with improved clinical and laboratorial status. Her fever subsided after the 15th day of antibiotic treatment; the arrhythmia remained controlled and the heart failure became asymptomatic. She was discharged after 55 days of hospitalization for an outpatient clinical follow-up.
A signed informed consent for publication was obtained, and the manuscript is in accordance with the institution’s ethics committee.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [86, 'years'], 'creatinine': [1.59, 'mg/dL'], 'sex': 'Female'}",30.7841,29.24489,32.3233,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 86 years old. The concentration of Creatinine is 1.59 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.59^(-1.154) * 86^(-0.203) * 1 * 0.742=30.7841.
Hence, the patient's GFR is 30.7841 mL/min/1.73m²."
3244,9,MDRD GFR Equation,lab test,decimal,pmc-5789470-1,Extracted,"A 71-year-old Caucasian female with end-stage renal disease due to p-antineutrophil cytoplasmic antibodies-positive vasculitis underwent cadaveric kidney transplantation in April 2012. It is also important to emphasize that the patient had a previous history of moderate aortic stenosis with aortic valve area 1.5 cm2 but she rejected further diagnostics and treatment.
In May 2016, she presented to the emergency department with dyspnea, anasarca, and precordial oppressions. Signs of global heart failure were present and confirmed by the diagnostic imaging techniques. No bleeding tendency was present in patient's laboratory values– they included a red blood cell count 3.34 × 1012/L, Hg 91 g/L, platelet count 196 × 109/L, prothrombin time 0.98, international normalized ratio 1.02, and activated partial thromboplastin time 29.3 s. Cardiac enzymes were negative (creatine kinase –40 U/L, lactate dehydrogenase – low-density lipoprotein [LDH] 126 U/L, troponin 9 ng/L) and worsening of allograft function (creatinine 200 μmol/L, previously 153 μmol/L) was present. Thus, a double lumen CVC was placed in the right subclavian vein and intensified hemodialysis was commenced, the total of nine sessions. During the CVC insertion, the patient was restless and disorientated. The chest radiography revealed catheter tip in the right atrium and no signs of pneumothorax. However, due to further worsening of the symptoms-patient became hypotensive, dyspnoic, tachycardic, and agitated, she was immediately transferred to the Intensive Care Unit. There was no laboratory sign of bleeding (red blood cell count 3.42 × 1012/L, Hg 97 g/L, platelet count 186 × 109/L, LDH 110 U/L). Pulmonary angiography outruled pulmonary embolism or signs of pneumonia. However, in comparison to previous scans from June 2013, it revealed pericardial effusion 2 cm thick []. During the next 3 days, patients were stabilized with intravenous fluids without vasopressors, echocardiography was performed and showed concentric hypertrophy of the left ventricle, with ejection fraction 70%, and without regional hypocontractility. There was also pericardial effusion 2 cm thick and without repercussions on the blood flow, predominantly reclining the free surface of right atrium, with fibrin scar tissue covering the epicardium (differential diagnosis – spot of previous cardiac wall perforation, spontaneously recovered) []. With careful fluid administration and antibiotic treatment, the patient became hemodynamicaly stabile with good diuresis and stabile allograft function (creatinine after the discharge 147 μmol/L) without the need for dialysis treatment. Before the discharge, echocardiography was performed once more. The pericardial effusion was now in regression; it was 5–6 mm thick and without repercussions on the blood flow []. CVC was hence extirpated without further complications during the last outpatient clinic visit in June 2016.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [71, 'years'], 'creatinine': [200.0, 'µmol/L'], 'sex': 'Female', 'Race': 'White'}",21.30846,20.24304,22.37388,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 71 years old. The concentration of Creatinine is 200.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 200.0 µmol. To convert 200.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 200.0 µmol Creatinine * 1e-06 mol/µmol = 0.0002 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.0002 mol Creatinine * 113.12 g/mol = 0.02262 g Creatinine. To convert 0.02262 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.02262 g Creatinine * 1000.0 mg/g = 22.62 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 22.62 mg Creatinine/10.0 dL = 2.262 mg Creatinine/dL. The concentration value of 200.0 µmol Creatinine/L converts to 2.262 mg Creatinine/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.262^(-1.154) * 71^(-0.203) * 1 * 0.742=21.30846.
Hence, the patient's GFR is 21.30846 mL/min/1.73m²."
3245,9,MDRD GFR Equation,lab test,decimal,pmc-3304619-2,Extracted,"A 21-year old male presented with upper abdominal pain for 15 days accompanied by a gradually increasing abdominal girth and swelling of the feet with low grade fever for one week. On examination, he was normo-tensive and showed pitting pedal edema. There was a tender hepatomegaly extending three fingers below the costal margin in the mid-clavicular line. Shifting dullness was positive. Hematological investigations revealed Hb level of 9 g/dL and WBC of 7,500/mm3. The biochemical investigations showed a raised BUN of 65 mg/dL and serum creatinine of 1.5 mg/dL. Urine analysis revealed slight proteinuria. Liver functions tests showed a total bilirubin of 0.6 mg/dL, serum ALP of 247 IU/L, AST 40 IU/L and ALT 80 IU/L. Ultrasonography of the abdomen showed an abscess in the right lobe of liver on its postero-superior surface measuring 1.4×1×1 cm with internal echoes and moderate ascites. Color doppler scan was done which showed patent hepatic veins with normal hepatofugal flow. Hepatic IVC was seen displaced and compressed by the large abscess cavity but the flow was normal. Infra-hepatic IVC was dilated to 1.7 cm. The Doppler findings were suggestive of IVC obstruction due to the liver abscess with proximal dilatation. A contrast enhanced CT scan confirmed the findings of thrombus in the IVC (). The patient tested positive for amoebic antibody by indirect haemagglutination test. The patient was started on intravenous metronidazole and broad spectrum antibiotics. The liver abscess was aspirated twice under ultrasonic guidance within a period of two days yielding 500 mL and 360 mL of pus. The pus was thick, creamy and brownish in color and did not grow any organisms on culture. The ascites and pedal edema disappeared rapidly after the treatment. Doppler scan repeated four days later showed a decrease in the infra-hepatic IVC dilatation. Hepatic portion of the IVC was normal in caliber and fully patent in subsequent color doppler examination performed twelve days after the aspiration of pus. The biochemical renal parameters improved and two weeks after aspiration of the liver abscess, the BUN was 32 mg/dL and serum creatinine was 1.1 mg/dL. Patient was followed up for three months, and repeat ultrasonography done was essentially normal.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [21, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Male'}",59.07697,56.12312,62.03082,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 21 years old. The concentration of Creatinine is 1.5 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.5^(-1.154) * 21^(-0.203) * 1 * 1=59.07697.
Hence, the patient's GFR is 59.07697 mL/min/1.73m²."
3246,9,MDRD GFR Equation,lab test,decimal,pmc-5463665-1,Extracted,"A 39-year-old female with past medical history of deep vein thrombosis (DVT), chronic kidney disease stage-3 with biopsy-proven focal segmental glomerulosclerosis (FSGS), and tobacco abuse, presented to the emergency department (ED) with complaint of five-day pain in left medial thigh and popliteal region limiting her ambulation and sleep. Thirteen days before presenting to the ED, she was started on high dose prednisone (60 mg daily). A week after starting prednisone, she developed the above-mentioned symptoms along with pain and numbness in her left great toe and second toe. There was no history of chest pain, shortness of breath, palpitations or trauma to the leg.
She had a history of two episodes of unprovoked DVT and received prophylactic anticoagulation during her last two pregnancies. Hypercoagulable workup performed at outside hospital during that time was negative. There was no history of miscarriage or bleeding disorder. She did not have a history of atrial fibrillation or other heart disease. There was no family history of clotting disorders. She smoked half pack of cigarettes a day.
On physical examination, she was in no acute distress. Her blood pressure was 147/77 mm Hg, pulse 68/minute, temperature 37.3oC, respiratory rate 19/minute and oxygen saturation 100% at room air. Lungs were clear to auscultation. Cardiac examination revealed normal rate and rhythm with normal first and second heart sounds with no murmur. Femoral pulses were palpable bilaterally. Left dorsalis pedis and posterior tibial artery pulse were absent. There was tenderness to palpation in left medial distal thigh and popliteal region; however, no calf tenderness or cords were noted. There was no skin breakdown, rash, pedal edema, pallor on leg elevation or dependent rubor. Strength in bilateral lower extremities was normal.
A venous ultrasound (US) of the left lower extremity (LLE) revealed a superficial muscular branch thrombosis in the popliteal region but no evidence of DVT. Arterial US duplex of LLE revealed sub-acute thrombosis of left popliteal artery and tibio-peroneal artery. Ankle-brachial index was 1 on the right and 0.57 on the left. Electrocardiogram revealed no arrhythmias. Transthoracic echocardiogram revealed normal systolic and diastolic function with no valvular abnormalities.
Pertinent labs included creatinine 1.6 mg/dL, BUN 26 mg/dL, total urine protein/creatinine ratio of 1.8, serum albumin 3.1 g/dL and normal C3 and C4. Complete blood count revealed WBC of 10.7 × 103/μL, hemoglobin of 14.4 g/dL and platelets of 127 × 103/μL. Coagulation profile was normal with normal INR and aPTT. Hypercoagulability workup was negative with normal fibrinogen level, protein C, protein S activity and antithrombin III activity. Factor V Leiden mutation (R506Q), prothrombin G20210A mutation and methylene-tetrahydrofolate reductase (MTHFR) C677 T gene mutation were negative. Lupus anticoagulant, anti-phospholipid antibodies and anti-nuclear antibody (ANA) were negative.
She was started on tissue plasminogen activator (tPA) at 1 mg/hr along with continuation of prednisone and analgesia. There was some improvement of her symptom but little improvement in the occlusion of the arteries. She was started on anticoagulation with heparin bridged with warfarin. Her symptoms gradually improved and she was discharged home on warfarin and prednisone. She did not have recurrence of thrombosis in the following six months.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [39, 'years'], 'creatinine': [1.6, 'mg/dL'], 'sex': 'Female'}",35.88404,34.08984,37.67824,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 39 years old. The concentration of Creatinine is 1.6 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.6^(-1.154) * 39^(-0.203) * 1 * 0.742=35.88404.
Hence, the patient's GFR is 35.88404 mL/min/1.73m²."
3247,9,MDRD GFR Equation,lab test,decimal,pmc-5004031-1,Extracted,"A previously healthy 74-year-old Japanese female was hospitalized with unknown fever and high C-reactive protein (CRP) values in December 2015. On admission, she was 155 cm in height and 59.2 kg in weight and had temperature of 37.6°C, blood pressure of 118/64 mmHg, pulse rate of 71/min, respiration rate of 18/min, and SpO2 of 94% at room temperature. Physical examination revealed no specific findings. After admission, she developed herpangina-like aphthous ulcers at the palate, when significant monocytosis (absolute monocyte counts >5,000/μL) was first noted; however, monocytosis fluctuated (). Thereafter, a CT scan of the abdomen showed localized thickening of the intestinal wall () and colonofiberscopy (CF) revealed the presence of multiple ovoid punched-out ulcers at the terminal ileum and aphthous lesions at the ascending colon (). In addition, the patient also developed multiple erythematous rashes on her right thigh (). Given the diagnostic criteria of BD [], the rash was not typical erythema nodosum but was thought rather to be acneiform eruption. Ophthalmological studies showed no evidence of BD signs. Taken together, BD was suspected in this patient from fulfilling 2 major and 1 minor clinical features required in the diagnosis of BD []. Thereafter, from the second week of admission, the patient again developed a significant monocytosis (from 15% to >70% in PB, with absolute monocyte counts to a maximum of 23,900/μL) associated with urinary infection at the 5th week of admission (). These findings with subsequent bone marrow study confirmed a diagnosis of AMoL (Figures and ).
Blood results at the 5th week of admission, when AMoL was diagnosed, were as follows: white blood cells (33,200/μL) containing 15% blasts, 21% promonocytes, 19% mature monocytes, 1% myelocytes, 10% neutrophils, and 33% lymphocytes (). Flow cytometric data of a major cell population in PB were as follows: CD13+ (86.4%), CD14+ (80.0%), CD33+ (97.4%), CD34+ (0.8%), CD41+ (44.8%), CD56+ (32.4%), and HLA-DR+ (97.0%). Mature lymphocytes in PB consisted of mostly T cells (approximately 90%), whose markers were CD4+ (59.2%) and CD8+ (27.4%), respectively. By contrast, the hypercellular BM consisted of 33.2% blasts, 15.0% promonocytes, 33.6% mature monocytes, 6.8% granulocytes, 1.4% lymphocytes, 2.0% plasma cells, and 8.0% erythroblasts with an M/E ratio of 0.85 (). No significant abnormalities indicating MDS were noted. Flow cytometric results of the major cell population in BM were as follows: CD13+ (38.3%), CD14+ (26.0%), CD33+ (97.5%), CD41+ (45.5%), CD34+ (2.3%), CD56+ (38.0%), and HLADR+ (80.9%). Mature lymphocytes in BM were mostly T cells (approximately 90%) with a CD4/CD8 ratio of 0.54. Myeloperoxidase positive cells accounted for 10% of the mononuclear cells present in both the PB and BM, while alpha-naphthyl butyrate esterase (inhibited by sodium fluoride) positive cells comprised more than 60% of cells in both the PB and BM. These findings were compatible with the diagnostic criteria of AMoL (FAB M5b) []. In addition, the karyotypes of PB and BM cells were both 46, XX [20/20]. The other blood chemistry was uneventful except for high levels of CRP (15.75 mg/dL), with aspartate aminotransferase 13 U/L, alanine aminotransferase 14 U/L, lactate dehydrogenase 205 U/L, total bilirubin 0.76 mg/dL, total protein 6.9 g/dL, albumin 2.9 g/dL, blood urea nitrogen 23.4 mg/dL, creatinine 1.61 mg/dL, sodium 135 mmol/L, potassium 3.6 mmol/L, chlorine 97 mmol/L, and calcium 8.0 mg/dL.
Since the diagnosis of AMoL (FAB M5b) was confirmed, the biopsied tissues showing BD-like illness were reevaluated with immunostaining except for stomatitis lesions and were proved to have leukemic cell infiltrations. The intestinal ulcer-associated granulation tissues with vascularization and infiltration of cells were positive for lysozyme, CD13, CD14, and CD33 (Figures and ). Also the histopathology of skin rash showed that the infiltrating cells were positive for lysozyme, CD13, CD14, and CD33 (Figures and ). These findings confirmed that the lesions primarily thought due to BD-like illness were in fact AMoL-related. In addition, HLA-typing, performed to ascertain whether the patient had BD-related HLA types, detected the presence of A2/A24 and B52/B55 but not the BD-related HLA-B51 or B5 alleles [, ]. As shown in , the patient was initially treated with adalimumab for BD-like illness, following the successful report for a case of intestinal BD with trisomy 8 MDS by Kimura et al. []; however, after AMoL was confirmed, she was transferred to another hospital for intensive chemotherapy as a very high-risk patient.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [74, 'years'], 'creatinine': [1.61, 'mg/dL'], 'Race': 'Asian'}",31.28318,29.71902,32.84734,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 74 years old. The concentration of Creatinine is 1.61 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.61^(-1.154) * 74^(-0.203) * 1 * 0.742=31.28318.
Hence, the patient's GFR is 31.28318 mL/min/1.73m²."
3248,9,MDRD GFR Equation,lab test,decimal,pmc-5320692-1,Extracted,"A 42-year-old white man without pre-existing comorbidities was transferred to our unit on 8 September 2014. He was involved in a car crash on 30 August 2014 with traumatic hemorrhagic shock and an ISS of 28. Shock resuscitation according to Advanced Trauma Life Support (ATLS) guidelines and massive transfusion policy were immediately started []. Upon hemodynamic stabilization, a total body computed tomography (CT) scan confirmed unstable pelvic fractures and right flank mesenteric bleeding, without clear evidence of intestinal perforation. Damage control surgery of his pelvic fractures was performed by positioning external fixators [, ]. Transfer to our unit was then planned for definitive osteosynthesis.
On arrival he had fever and profuse diarrhea, leukocytosis, normal procalcitonin (PCT), elevated C-reactive protein (CRP), lactate 0.9 mmol/L, an Acute Physiology and Chronic Health Evaluation (APACHE) II score of 11, and a Sequential Organ Failure Assessment (SOFA) score of 3; his Predisposition, Infection, Response, and Organ Dysfunction (PIRO) score was 5 []. He wore a tracheostomy and was mechanically ventilated on analgosedation; he was left on parenteral nutrition and a minimal enteral feeding was started.
Chest X-rays detected a right basal infiltrate. Orthopedic surgery was postponed. After thorough microbiological sampling, immune chromatography for Clostridium difficile was negative, rectal swabs grew MDR Acinetobacter baumannii, whereas blood cultures yielded coagulase-negative staphylococci. His antibiotic therapy was modified as described here and in Table . As external fixators poured purulent secretions, on day 15 he underwent definitive pelvic osteosynthesis in spite of persistent fever and diarrhea (Fig. ). Septic shock ensued 24 hours after surgery, with oliguria, leukocytosis, PCT 4.39 ng/ml, CRP 46.6 mg/L, and lactate 1.17 mmol/L; his SOFA score rose to 6. After adequate fluid resuscitation, norepinephrine was added for persistent hypotension, based on data of hemodynamic monitoring (cardiac output and stroke volume variation using PiCCO Plus monitoring system) and trends of central venous saturation of oxygen (ScVO2). Low doses of steroids were prescribed for the first 3 days. Microbiological sampling included blood cultures, quantitative culture of tracheal secretions, and culture of urine []. Blood cultures were negative; urine and tracheal aspirate samples were positive for CRKP and MDR A. baumannii.
He had a short-lasting improvement, with fever, abdominal pain, and vomiting relapsing after a few days; a repeated CT scan of his abdomen revealed suprapubic and left ischiatic abscesses at surgical sites, as well as dilated bowel due to paralytic ileus. Surgical debridement was performed, followed by vacuum-assisted closure (VAC) therapy []. Intraoperative microbiological sampling revealed multiple CRKP isolates, with a worsened resistance profile, including colimycin (colistin) resistance. He improved and a control radiographic (RX) scan of his thorax was negative; bronchoalveolar lavage (BAL) sampling, however, confirmed persistence at low bacterial load of CRKP. After 21 days, colimycin was withdrawn. However, 4 days later, he had fever and severe leukocytosis; he relapsed with acute renal failure: creatinine 2.53 mg/dL and acute kidney injury (AKI) stage 2 according to the Kidney Disease: Improving Global Outcomes classification (KDIGO) []. His PCT levels rose above 100 ng/ml, his lactate was 3.3 mmol/L, and his SOFA score was 10. After further blood sampling for blood cultures and multiplex polymerase chain reaction (PCR; Magicplex™ Sepsis Test, Seegene), colimycin and anidulafungin were restarted with the addition of rifampicin (Table ). Multiplex PCR revealed A. baumannii and Candida albicans. To support septic shock recovery, two extracorporeal hemoperfusion devices were used: the Polymyxin B-Immobilized Cartridge (Toraymyxin® PMX 20-R, Toray Medical, Tokyo, Japan), allowing endotoxin removal and coupled plasma filtration adsorption (CPFA; CPFA® LYNDA®, Bellco, Mirandola, Italy), a hydrophobic resin with high affinity for many inflammatory mediators. Within 3 days, two Polymyxin B and three CPFA treatments were overall delivered. Clinical improvement ensued; his PCT fell to 19.25 ng/ml and serum creatinine to 1.82 mg/dL. Microbiological samples yielded: MDR A. baumannii and CRKP from tracheal aspirate, C. albicans and MDR A. baumannii from blood cultures, and A. baumannii and panresistant CRKP from wound swabs. In spite of septic shock reversal, he remained febrile with diarrhea and worsening anemia in the next 2 weeks. Control blood cultures (three lots) were persistently positive for C. Albicans, A. baumannii and CRKP. Ophthalmoscopy revealed retinal involvement, so that sequential therapy with liposomal amphotericin B was started. In the following weeks frequent vomiting ensued, impeding any enteral nutrition; his abdominal pain increased, paralleled by a palpable mass in his right flank. Colonoscopy revealed patchy serpiginous ulcers; a repeated CT of his abdomen revealed a periappendicular mass. Based on such data, after repeated multidisciplinary consults, an exploratory laparotomy was at last performed and an inflammatory pseudotumor of his right colon was diagnosed and resected with ileostomy. Soon after surgery, his blood cultures turned negative. Colimycin was interrupted. Once more, septic shock relapsed 4 days later. Leukocytosis, hypotension, PCT >100 ng/mL, renal failure, and lactate 4.0 mmol/L led to a SOFA score of 11; creatinine zenith was 4.73 mg/dL. Combination antibiotic therapy was modified (see Table ) and a single Polymyxin B extracorporeal hemoperfusion cycle was repeated. Blood cultures were persistently positive for CRKP. After interdisciplinary consultation, removal of pelvic synthesis media was anticipated. Shortly after surgery, he improved; 3 weeks later, microbiological and biochemical evidence of infection resolved, as well as gastric atonia. Combination therapy was continued for 56 days (Table ). He was transferred to the orthopedic ward after 146 days of ICU stay and later to rehabilitation. At present, he is doing well at home able to walk.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [42, 'years'], 'creatinine': [2.53, 'mg/dL'], 'sex': 'Male', 'Race': 'White'}",28.07484,26.6711,29.47858,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 42 years old. The concentration of Creatinine is 2.53 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.53^(-1.154) * 42^(-0.203) * 1 * 1=28.07484.
Hence, the patient's GFR is 28.07484 mL/min/1.73m²."
3249,9,MDRD GFR Equation,lab test,decimal,pmc-7542734-1,Extracted,"An 85-year-old menopausal woman was referred to our hospital for diagnostic evaluation of worsening dyspnea over 6 weeks. The patient had a history of chronic atrial fibrillation, hypertension, and chronic kidney disease (CKD) of uncertain etiology. She had a uterine fibroid diagnosed at 64 years of age. Pre-admission medication included amlodipine (10 mg/day), valsartan (40 mg/day), verapamil (120 mg/day), digoxin (0.125 mg/day), and rivaroxaban (10 mg/day).
Her vital signs were as follows: blood pressure 146/97 mmHg, heart rate 90 beats/min and irregular, and respiratory rate 21 breaths/min. Physical examination revealed a third heart sound, diminished breath sounds from the right lower lungs, and notable bilateral leg edema, but no remarkable jugular vein distention (JVD) was observed. A hard mass was palpable in the lower abdomen. The electrocardiogram revealed atrial fibrillation. Chest radiography revealed cardiomegaly and right-sided PE (Fig. a). Laboratory testing revealed elevated levels of serum creatinine (1.36 mg/dL, reference, 0.65–1.07 mg/dL) and brain natriuretic peptide (BNP) (183 pg/mL, reference: < 18.4 pg/mL). Hepatic and thyroid function, C-reactive protein levels, and urinalysis were within normal ranges.
Echocardiography demonstrated normal left ventricular (LV) cavity size and systolic function, with an ejection fraction of 54% and left atrial dilation (35 mL/m2) (Additional files and ). Doppler and tissue Doppler profiles for the assessment of LV diastolic function revealed a decreased septal e′ of 5.8 cm/sec and an elevated E/e′ of 17, indicating elevated LV filling pressure. In addition, continuous wave Doppler revealed a peak tricuspid regurgitation velocity of 2.6 m/s, consistent with a pressure gradient of 27 mmHg and an estimated right ventricular systolic pressure of approximately 35 mmHg. Echocardiographic evaluation of the right heart revealed almost normal systolic function; tissue Doppler of the free lateral wall (S′) = 9 cm/s (reference: ≥ 10 cm/s), tricuspid annular plane systolic excursion = 18 mm (reference: 16 ≥ mm), and fractional area change = 53% (reference: ≥ 35%), respectively.
Thus, a tentative diagnosis of heart failure with preserved ejection fraction (HFpEF) was made. The patient was administered oxygen at 3 L/min and treated with intravenous loop diuretics (furosemide 40 mg daily). On day 6, although diuretic treatment improved leg edema, PE remained unchanged (Fig. b).
A subsequent diagnostic workup of unexplained PE was performed. The patient underwent thoracentesis with drainage of 1240 mL of serosanguineous PE. PE analysis revealed lymphocyte-predominant exudates fulfilling Light’s criteria (Table ). Additionally, the serum-to-effusion albumin gradient was 0.3 g/dL (reference: ≤ 1.2 g/dL), further confirming the true exudative effusion. The adenosine deaminase activity in PE was 9.3 U/L. PE cytology, as well as the bacterial and mycobacterial cultures, were unremarkable.
Chest computed tomography revealed an absence of lung tumors or inflammatory infiltration after the removal of PE. Abdominal/pelvic computed tomography scan revealed bilateral inhomogeneous ovarian masses (Fig. ). Magnetic resonance imaging further characterized the right substantial mass and detected a trivial ascites (Fig. ). Axial and sagittal T2-weighted images demonstrated the peripheral hypointense mass, which contained hyperintense and multilocular areas in the central portion, mimicking a malignant ovarian tumor with a central necrosis or a degenerated subserosal fibroid. Gadolinium-enhanced axial imaging showed inhomogeneous enhancement correspondently on the peripheral solid portion, suggesting malignancy. In addition, screening tests for tumor markers revealed elevated CA-125 levels (382 U/mL, reference: < 35 U/mL). Repeated serial thoracentesis was ineffective, and PE reaccumulated within a week (Fig. c-f). Thus, we highly suspected of ovarian cancer with pleural dissemination. Nevertheless, a repeated cytological examination of PE revealed no evidence of malignancy, which led us to consider the possibility of MS.
On day 26, the patient underwent bilateral salpingo-oophorectomy (Fig. ). The resected masses exhibited yellow-to-tan fleshy cut surfaces, with hemorrhage and extensive hyaline degeneration. Histopathological examination revealed a mitotically active cellular fibroma (MACF) of the ovary. Spontaneous resolution of the right-sided PE was noted post-operatively after 7 days of follow-up, confirming a definitive diagnosis of MS. A follow-up echocardiography revealed no significant changes. The post-operative course was uneventful, and the patient made a full recovery and was discharged with no changes to her pre-admission medication regimen on day 33. She remained clinically stable upon subsequent follow-up.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [85, 'years'], 'creatinine': [1.36, 'mg/dL'], 'sex': 'Female'}",36.95439,35.10667,38.80211,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 85 years old. The concentration of Creatinine is 1.36 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.36^(-1.154) * 85^(-0.203) * 1 * 0.742=36.95439.
Hence, the patient's GFR is 36.95439 mL/min/1.73m²."
3250,9,MDRD GFR Equation,lab test,decimal,pmc-3236148-1,Extracted,"A 64-year-old man with a history of hypertension, chronic kidney disease, and liver failure secondary to hepatitis C, with status post liver transplant 13 years priorly, was brought in by ambulance to the emergency department for acutely altered mental status. The patient had been in his usual state of health, until he told his family 3 hours before that he “felt sick.” The family incidentally found him on the floor, confused and lethargic, and immediately called the ambulance.
Upon arrival, the patient had a temperature of 96.4°F; pulse, 117 beats per minute; blood pressure, 151/93 mmHg; respiratory rate, 22 breaths per minute; and oxygen saturation of 100% on nonrebreather. The patient was known to have a history of recurrent episodes of hepatic encephalopathy, and his last episode of hepatic encephalopathy was in the prior 3 months, which was treated and controlled with lactulose. The patient's family stated that the patient had run out of lactulose 4 days before presentation. Other than lactulose, the patient was compliant with all of his home medications, including amlodipine, buproprion, cyclosporine, hydrocodone, lasix, methocarbamol, and ramipril. The patient had no known history of seizure, recent illness, brain trauma, or recent surgical procedures.
Physical examination showed a male in no acute distress with a Glasgow Coma Scale of 12 (eyes, 4; verbal, 3; motor, 5). There were no signs of trauma found on his body. His pupils were equally round and reactive to light, and his neck was supple and soft with a cervical collar in place. Cardiopulmonary examination was unremarkable except for tachycardia. Abdominal examination was unremarkable. Because he was not following commands, the neurologic examination was limited. However, the patient was able to move all extremities equally and pulses were distally equal to all extremities. There was no posturing or clonus noted, and Babinski was downgoing in both feet.
Fingerstick glucose level was 210 mg/dL and bedside hemoglobin level was 13.1 g/dL. Noncontrast head and cervical spine computed tomography revealed no acute pathologic lesion. Chest radiography also showed no acute pathologic lesion. Laboratory tests showed white blood cell counts of 5.5 K/mm3 with 60% neutrophils, hematocrit of 36.5%, and platelets of 115 K/mm3. Electrolyte and liver function results were as follows: sodium, 141 mmol/L; potassium, 3.5 mmol/L; chloride, 104 mmol/L; bicarbonate, 22 mmol/L; calcium, 9.3 mg/dL; blood urea nitrogen, 71 mmol/L; creatinine, 1.9 mg/dL; total bilirubin, 2.1 mg/dL; aspartate aminotransferase, 128 U/L; alanine aminotransferase, 124 U/L; alkaline phosphatase, 231 U/L; albumin, 4.0 g/dL; lipase, 30 U/L; prothrombin time, 14.5 seconds; INR, 1.09; and ammonia, 501 μmol/L (reference range, 15–55 μmol/L). Toxicology serum screen results were negative for acetaminophen, salicylate, and ethanol. Urine toxicology screen results were positive only for opiates. Venous blood gas was pH 7.44.
Owing to the patient's obtunded condition and inability to protect his airway, the patient was electively intubated and given midazolam drip for sedation. The patient was admitted to the intensive care unit (ICU) for monitoring with a presumed diagnosis of hepatic encephalopathy. While administration of empiric antibiotics was started in the emergency department, it was discontinued after an infectious etiology was deemed unlikely and culture results were negative. Results of a magnetic resonance imaging brain scan were also negative, including no evidence of infarct.
During the ICU stay, the patient was readministered lactulose, and ammonia levels decreased to117 μmol/L by hospital day 2 and to 78 μmol/L by hospital day 4. Despite discontinuation of sedation, the patient remained unresponsive. A neurologist was consulted and a bedside electroencephalogram (EEG) revealed findings consistent with status epilepticus. However, the patient had no clinical manifestations of status epilepticus, leading to a diagnosis of nonconvulsive status epilepticus. A phenytoin load was immediately administered, while a midazolam infusion was restarted, ultimately leading to EEG resolution of the status epilepticus. The patient did not immediately improve neurologically during the hospitalization stay and was ultimately transferred to another facility for continued treatment and rehabilitation.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [64, 'years'], 'creatinine': [1.9, 'mg/dL'], 'sex': 'Male'}",35.86756,34.07418,37.66094,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 64 years old. The concentration of Creatinine is 1.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.9^(-1.154) * 64^(-0.203) * 1 * 1=35.86756.
Hence, the patient's GFR is 35.86756 mL/min/1.73m²."
3251,9,MDRD GFR Equation,lab test,decimal,pmc-4783551-1,Extracted,"A 60-year-old man presented with few days of jaundice, generalized fatigue, and dark urine. On admission, he had a bilirubin level of 836 μmol/L (normal < 24), direct bilirubin of >580 μmol/L (normal < 5), ALP of 235 U/L (normal 40–130), GGT of 340 U/L (normal < 60), AST of 236 U/L (normal < 45), ALT of 75 U/L (normal < 45), albumin of 21 g/L (normal 38–52), and serum creatinine of 135 μmol/L (normal 60–105). His creatinine 6 months earlier had been 80 μmol/L.
He had been taking flucloxacillin 500 mg daily intermittently for 3 months to treat skin folliculitis. He stopped the antibiotics 6 weeks prior to his presentation. There was no history of substance or alcohol abuse. He was on no other regular medications.
On Examination. He was afebrile and had BMI of 30, BP of 125/80, and heart rate of 70/min. His JVP was +2 cm above the sternal angle, with mild peripheral oedema, clear chest on auscultation, and nontender liver extending 3 cm below the costal margin.
The screen for viral and metabolic causes of hepatitis was unremarkable. An abdominal CT with contrast showed hepatomegaly with diffuse fatty changes but no biliary dilatation. The serum bilirubin continued to rise reaching a peak of 881 μmol/L on day 8. A liver biopsy was performed and showed panacinar steatosis, moderate steatohepatitis (NAFLD score 5/8), portal fibrosis, and cholestasis. An ERCP was normal. The diagnosis was flucloxacillin-induced hepatitis.
The patient's serum creatinine continued to rise and peaked at 581 μmol/L on day 16 despite adequate hydration and avoidance of nephrotoxins. In addition, the patient had persistent severe hypokalemia with serum potassium levels consistently <3 mmol/L despite the potassium replacement. Arterial blood gas was not suggestive of renal tubular acidosis with serum bicarbonate level of 26 mmol/L and pH of 7.46.
On day 3, his urine sodium was 33 mmol/L, urine potassium 42 mmol/L, and urine osmolality 420 mmol/kg. The transtubular potassium gradient was >10 and the serum potassium at the time of specimen collection was 2.7 mmol/L indicating renal cause for his hypokalemia. The urinary protein/creatinine ratio was slightly raised at 39 mg/mmol (normal < 23) and otherwise bland urine sediment. The urine output averaged 1.5 L per day from the day of admission.
A renal USS showed normal sized kidneys at 128 mm and 125 mm with no obstruction, normal echotexture, and perfusion; a renal biopsy was performed.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [60, 'years'], 'creatinine': [135.0, 'µmol/L'], 'sex': 'Male'}",44.82867,42.58724,47.0701,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 60 years old. The concentration of Creatinine is 135.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 135.0 µmol. To convert 135.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 135.0 µmol Creatinine * 1e-06 mol/µmol = 0.00014 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00014 mol Creatinine * 113.12 g/mol = 0.01584 g Creatinine. To convert 0.01584 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01584 g Creatinine * 1000.0 mg/g = 15.84 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 15.84 mg Creatinine/10.0 dL = 1.584 mg Creatinine/dL. The concentration value of 135.0 µmol Creatinine/L converts to 1.584 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.584^(-1.154) * 60^(-0.203) * 1 * 1=44.82867.
Hence, the patient's GFR is 44.82867 mL/min/1.73m²."
3252,9,MDRD GFR Equation,lab test,decimal,pmc-3970448-1,Extracted,"A 52-year-old woman presented to our hospital complaining of severe abdominal pain and nausea. She reported recurrent mild abdominal pain, bloating, nausea, occasional vomiting, and severe nonbloody diarrhea with 20 evacuations a day for one year. She had a 45 pound weight loss within six months. She denied any other symptoms suggestive of local or systemic infections, recent travels or sick contacts, changes in her diet habit, or medications within the last year.
Vital signs were within normal range. Physical exam revealed generalized abdominal tenderness with guarding and signs of dehydration. At the emergency department, the patient suffered from a cardiac arrest. She was successfully resuscitated and admitted to the intensive care unit. Laboratory investigations showed potassium 2.9 mMol/L, bicarbonate 17 mMol/L, blood urea nitrogen 7 mg/dL, creatinine 0.9 mg/dL, white blood count 12.1 × 10³/μL, hemoglobin 13.8 gm/dL, and albumin 2.4 gm/dL. CT scan of the abdomen showed ascending colon inflammation and evidence suggestive of perforation (Figures and ). She was treated conservatively without surgical intervention. A repeat abdominal CT scan revealed improving of the colonic inflammation and sealing of the perforation.
An extensive investigation for chronic diarrhea over the past year was performed, including serum thyroid stimulating hormone and stool cultures, Clostridium difficile toxin assay, ova, parasites, osmolality, and electrolytes that were unremarkable. Celiac disease was excluded by negative conventional serology tests (tissue transglutaminase antibodies, endomysial antibodies and antienterocyte antibodies) and the absence of a clinical response to a gluten-free diet. Management including an opioid-receptor agonist, corticosteroids, azathioprine, and antibiotic therapy failed to relieve her symptoms. Endoscopic biopsies from the stomach and colon showed inflammatory changes and lymphoid aggregation with no subepithelial collagen depositions. Helicobacter pylori testing of the specimens was negative.
She had been on olmesartan (20 mg/day) for hypertension for 3 years. Olmesartan associated enteropathy was suspected and the drug was discontinued and replaced by lisinopril. One month later, she had complete resolution of the abdominal discomfort and diarrhea. After 5 months, the patient continued to be asymptomatic with no gastrointestinal manifestations.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [52, 'years'], 'creatinine': [0.9, 'mg/dL'], 'sex': 'Female'}",65.75025,62.46274,69.03776,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 52 years old. The concentration of Creatinine is 0.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.9^(-1.154) * 52^(-0.203) * 1 * 0.742=65.75025.
Hence, the patient's GFR is 65.75025 mL/min/1.73m²."
3253,9,MDRD GFR Equation,lab test,decimal,pmc-4421704-1,Extracted,"A 76-year-old Hispanic female with a past medical history of hypertension, diabetes mellitus, hypercholesterolaemia and chronic kidney disease (stage IV; baseline creatinine 2.0 mg/dL) presented with a 3-day history of fever, productive cough and pleuritic chest pain. Physical examination was remarkable for decreased air entry in her right lung base. Chest X-ray revealed right lower lobe infiltrates, and the patient was treated for community-acquired pneumonia. She demonstrated symptomatic improvement after 3 days of intravenous antibiotics and was therefore discharged from the hospital on the third day. The patient was advised to complete the course of oral antibiotics and to be followed up as an outpatient in the clinic.
Two days later, she presented to the emergency department with worsening shortness of breath. On examination, her respiratory rate was 22 breaths/minute, pulse 98 beats/minute and blood pressure 154/80 mmHg. The patient’s oral temperature was 39°C, and she had diffuse bilateral crackles on her lung examination. Chest X-ray showed bilateral patchy infiltrates (). The patient was now started on intravenous vancomycin and ceftriaxone. The basic laboratory panel was suggestive of an acute-on-chronic renal failure with nephritic syndrome (). Her condition worsened over the next 24 h as she developed massive haemoptysis and severe hypoxaemia, requiring intubation. Posterior bronchoscopy revealed diffuse alveolar haemorrhage with bleeding predominantly in the lower lobes. Blood culture, respiratory culture and urine culture showed no growth, and no organisms were isolated from the bronchoalveolar lavage. Antinuclear antibody (ANA) was 1:80, and the remainder of the immunology panel was essentially normal (). In view of PRS, the patient was started on steroids (methylprednisolone pulse of 1 g for 3 days). By the third hospital day, haemodialysis had to be initiated for worsening renal failure and oliguria (creatinine 6 mg/dL). Repeat immunology panel was unchanged from the previous values, and therefore, a renal biopsy was performed. It revealed diffuse necrotizing and crescentic pauci-immune GN ().
The patient was treated with steroids, cyclophosphamide and a total of six cycles of plasmapheresis. Her clinical course was complicated with ventilator-associated pneumonia. After 20 days of intensive care treatment, her renal function improved. Haemodialysis was discontinued, and the patient was successfully extubated. Oral prednisone and cyclophosphamide were continued, and her creatinine plateaued at 2.7 mg/dL. Immunofluorescence (IF) testing for ANCAs was consistently negative at diagnosis and before the initiation of immunosuppressive therapy, and remained negative during follow-up.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [76, 'years'], 'creatinine': [2.0, 'mg/dL'], 'sex': 'Female', 'Race': 'Hispanic'}",24.22413,23.01292,25.43534,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 76 years old. The concentration of Creatinine is 2.0 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.0^(-1.154) * 76^(-0.203) * 1 * 0.742=24.22413.
Hence, the patient's GFR is 24.22413 mL/min/1.73m²."
3254,9,MDRD GFR Equation,lab test,decimal,pmc-6293897-3,Extracted,"A 49-year-old gentleman known to have T2DM since the last 12 years presented with pain and swelling of the right upper calf for last 3 weeks with acute worsening since 5 days without associated fever or systemic symptoms. The right upper calf had a localized, firm tender swelling without associated lymphadenopathy or skin changes. His fundus examination revealed a bilateral moderate nonproliferative diabetic retinopathy and grade 2 hypertensive retinopathic changes. He had diabetic nephropathy with proteinuria and bilateral distal symmetric polyneuropathy. Biochemical investigations revealed a poor glycemic control with plasma glucose levels of 423 mg/dl with an HbA1c of 10.2%. Further, he had total leucocyte counts of 7100/cu mm with subnephrotic range proteinuria (1.6 g/24 h), serum creatinine of 1.66 mg/dl, and hemoglobin of 6.6 g/dl. His ESR, at the end of the first hour, being normal was 65 mm and CPK levels were 38 U/l with no evidence of systemic infection. Venous Doppler was normal except for diffuse subcutaneous edema. MRI of the right lower limb showed areas of diffuse swelling and edema of the medial gastrocnemius muscle of the right leg with areas of patchy irregular enhancement on T2-weighted images without any evidence of focal abscess or collection [ and ]. The MRI features were consistent with a muscle infarction. He was conservatively managed with bed rest, analgesics, and insulin for glycemic control. He also required two units of blood transfusion. He recovered over a period of 8 weeks and was discharged in a stable condition.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [49, 'years'], 'creatinine': [1.66, 'mg/dL'], 'sex': 'Male'}",44.25104,42.03849,46.46359,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 49 years old. The concentration of Creatinine is 1.66 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.66^(-1.154) * 49^(-0.203) * 1 * 1=44.25104.
Hence, the patient's GFR is 44.25104 mL/min/1.73m²."
3255,9,MDRD GFR Equation,lab test,decimal,pmc-5609046-1,Extracted,"A 40-year-old male patient visited hospital with complaints of nausea, vomiting and gross hematuria for several days. Eleven years ago, he was diagnosed ESRD of unknown origin, and received a living related kidney transplantation from his father 1 year later. He underwent immunosuppressive agents based on cyclosporine, mycophenolate and corticosteroids. After KT, the patient was performed graft biopsy twice. The 1st biopsy result at 3 months after KT was consistent with acute interstitial nephritis and IgA nephropathy, and 2nd biopsy at 6 years after KT was acute cellular rejection IIb. The graft function had progressively declined to chronic kidney disease stage 4 at the latest visit of the outpatient clinic. At admission, he showed mild fever with body temperature 37.8 °C, and complained mild tenderness on graft kidney. Laboratory data showed white blood cell (WBC) 7400 /mm3, hemoglobin 8.2 g/dL, and platelet 258,000 /mm3, blood urea nitrogen 87 mg/dL, creatinine 11.2 mg/dL, sodium 141 mEq/L, potassium 5.0 mEq/L, and chloride 105 mEq/L. The urinalysis showed protein (++++), occult blood (+++), red blood cell (RBC) >100 /high power field (HPF), and WBC >100 /HPF. There were not decoy cells in urine cytology, and negative BK virus DNA by urine polymerase chain reaction (PCR). Abdominal sonography demonstrated a 7.9 cm-sized intra-pelvic hyperechoic mass causing obstructive pelvo-calyceal dilation of graft kidney (Fig. ). Abdominal magnetic resonance image showed a huge polypoid mass of graft kidney with pelvo-calyceal dilation, and there were a 3.3 cm-sized nodule in aortocaval chain and a 2.5 cm-sized nodule in right external iliac chain (Fig. ). There was no invasion to graft ureter orifice and bladder in cystoscopy (Fig. ). Whole body positron emission tomography (PET) showed a high uptake mass (standardized uptake value (SUV) max: 14.9) in graft kidney, and reactive lymph nodes with high uptake in right external iliac chain (SUV max: 9.6) and in aortocaval chain (SUV max: 10.1), and then it proved stage IV TCC (cT3N2M0, Fig. ). Sonography-guided percutaneous needle biopsy of the mass in the pelvis of graft kidney demonstrated a low grade urothelial carcinoma (Fig. ). Consecutively, radical nephroureterectomy of renal allograft was performed. The post-operative histopathology report confirmed as a low grade urothelial carcinoma of graft pelvis and ureter lumen, which invaded to perirenal fat and renal parenchyma with lymphovascular presence (T3Nx). The patient started with postoperative adjuvant concurrent chemo-radiation therapy and he returned to maintenance hemodialysis. Immunosuppressive agents were discontinued, and no tumor recurrence has been observed during the 24 months after the operation.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [40, 'years'], 'creatinine': [11.2, 'mg/dL'], 'sex': 'Male'}",5.09357,4.83889,5.34825,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 40 years old. The concentration of Creatinine is 11.2 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 11.2^(-1.154) * 40^(-0.203) * 1 * 1=5.09357.
Hence, the patient's GFR is 5.09357 mL/min/1.73m²."
3256,9,MDRD GFR Equation,lab test,decimal,pmc-7768448-1,Extracted,"A 72-year-old man was referred to our hospital from a suburban nephrology center because of prolonged fever and persistent enterococcal bacteremia. The patient was suffering from chronic renal failure, undergoing regular hemodialysis sessions three times per week through a permanent right internal jugular venous catheter. He was a chronic smoker with chronic obstructive pulmonary disease, and had been operated on for lung decortication because of amiantosis 18 years prior to admission (since then he was under methylprednisolone therapy). Furthermore, he had high blood pressure and single vessel coronary artery disease for which he was treated with successful angioplasty the previous year, and was compliant to antihypertension and anticoagulant therapy.
The patient had sought medical consultation 35 days before in the nephrology center where he was having hemodialysis, because he had high fever (up to 39 °C). Blood cultures were drawn and were processed in the nephrology center’s laboratory, resulting in the isolation of Enterococcus spp. from two culture vials with a susceptibility profile that included vancomycin: sensitive (MIC: 4 μg/mL), ampicillin: sensitive, daptomycin: sensitive, dalfopristin/quinopristin: resistant, gentamicin synergy: sensitive, ciprofloxacin: sensitive, and linezolid: sensitive. The patient received daptomycin and ciprofloxacin for 21 days. After the completion of antibiotic therapy he presented again with fever at the nephrology center, new blood cultures were drawn, and he started again receiving daptomycin. Two days later, during hemodialysis, he suffered from chills, and after completion of the session developed fever. In the next hemodialysis session, the same symptoms occurred (chills and fever), and gentamicin was added to his therapy. The nephrology clinic’s laboratory in the meantime isolated again Enterococcus spp. from the blood culture. He was treated with antibiotic lock therapy of the central venous catheter with gentamicin, and was referred to University General Hospital Attikon for further evaluation and treatment.
On the day of admission to our hospital, the following laboratory results were obtained: hemoglobin 10.4 g/dL, leukocytes 13,590/μL (Neutrophils 87%), platelets 295,000/μL, creatinine 3.8 mg/dL, C-reactive protein 61 mg/L, and procalcitonine 2.7 ng/mL. The physical examination was normal except for a holosystolic mitral valve murmur upon cardiac auscultation. Initially he continued the therapeutic regimen he had started at the nephrology center (antibiotics only on the haemodialysis days of Tuesday, Thursday and Saturday). On Tuesday and Thursday, he was receiving daptomycin 300 mg IV, and on Saturday the dose was 450 mg. On all haemodialysis days he was receiving gentamicin 240 mg IV before the haemodialysis session and gentamicin 80 mg IV after each session. On the first day at the hospital six blood cultures were drawn and two more on the following day, and all were incubated with the standard BACTEC system (Becton Dickinson, Sparks, NV, USA). On the second day of his hospital stay, five of the blood cultures were positive with Gram-positive coccus forming chains. On the third day, two more cultures were positive with the same coccus. The central venous catheter was removed on the third day of stay. The isolate from all seven blood culture bottles was identified as E. casseliflavus. The colonies in standard Columbia agar exhibited distinct yellow pigment, the coccus was positive for motility [], and the biochemical profile examined by Phoenix (Becton Dickinson, Sparks, NY, USA) and Vitek 2 (BioMerieux, Marcy-l’Etoile, France) matched E. casseliflavus. The antibiotic susceptibility phenotype included vancomycin: sensitive (MIC: 4 μg/mL), ampicillin: sensitive (MIC: 1 μg/mL), daptomycin: sensitive (MIC: 2 μg/mL), dalfopristin/quinopristin: resistant (MIC: 8 μg/mL), gentamicin synergy: sensitive (MIC: 16 μg/mL), ciprofloxacin: sensitive (MIC: 1 μg/mL), and linezolid: sensitive (MIC: 4 μg/mL). The MICs were determined by Vitek 2, Phoenix and E-tests while following the EUCAST breakpoints for all antibiotics (with the sole exception of the daptomycin MIC which was compared to the CLSI breakpoint). Furthermore, a multiplex PCR detecting vanA, vanB, vanC, vanD, vanE and VanG genes was performed and was positive for vanC, further corroborating the biochemical diagnosis []. The central venous catheter was cultured but there was no growth of any pathogen. The urine cultures were also negative.
The transesophageal echocardiogram was negative for vegetations and the fundoscopy was negative for Roth spots in the retina. A colonoscopy revealed numerous diverticula mainly in the sigmoid colon. CT scans of the head, thorax and abdomen were performed revealing a thrombus in the anterior vena cava near the distal end of the central venous catheter, and a pulmonary embolus at the lower lobe of the right lung involving the respective lobar artery and segmental branches.
After the fourth day in our hospital the patient’s antibiotic therapy was changed to a combination of ampicillin 2gr IV every 8 h and ceftriaxone 2gr IV every 12 h, which he received for a total of 6 weeks. He also received anticoagulant therapy for the pulmonary embolus. He was released from the hospital after a total stay of seven weeks, afebrile, with negative blood cultures.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [72, 'years'], 'creatinine': [3.8, 'mg/dL'], 'sex': 'Male'}",15.73727,14.95041,16.52413,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 72 years old. The concentration of Creatinine is 3.8 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.8^(-1.154) * 72^(-0.203) * 1 * 1=15.73727.
Hence, the patient's GFR is 15.73727 mL/min/1.73m²."
3257,9,MDRD GFR Equation,lab test,decimal,pmc-6910037-1,Extracted,"A 47-year-old male patient diagnosed with hypertension (since 1999), who was nondiabetic, and diagnosed with chronic kidney disease Stage V (~2012) on maintenance hemodialysis (MHD) (10/months) since February 2016 was admitted in our hospital for a second renal transplant. His blood group was O positive. The first renal transplant was done in June 2012. The donor was his 62-year-old mother of the same blood group. His histocompatibility workup before the first transplant included low-resolution HLA-A, B and DR typing of both patient and donor. HLA type of the patient was HLA-A*29, 68; HLAB*44, 44; and DRB1*07, 11. HLA type of the donor was HLA-A*03, 68; HLA-B*39, 44; and DRB1*07, 10 with a 3/6 match. His HLA antibody screen and complement-dependent cytotoxicity crossmatch was negative. No therapeutic plasma exchanges were done during stay and posttransplant, and he was on triple immunosuppressant (solumedrol + mycophenolate + tacrolimus). The patient was discharged and had no complaints until March 2014. A causal biopsy was done, and chronic active antibody-mediated rejection (AMR) with C4d positivity, thrombotic microangiopathy, and immunofluorescence IgA positivity suggestive of recurrent membranoproliferative glomerulonephritis was diagnosed. His serum creatinine level gradually increased to 5 mg/dl since then. He was managed on MHD and second renal transplant was planned, and histocompatibility workup was started. HLA antibody screen was done and found to be positive for HLA Class II. Panel reactive antibody showed HLA Class I 0% and II value 97%. Single-antigen bead (SAB) assay for HLA Class II showed multiple HLA Class II antibodies with varying mean fluorescent intensities (MFIs) (1017–17761). Since initially, only HLA-A, B, and DR typing was performed and that too only low-resolution and high-resolution HLA typing was done for HLA-DR and DQ to ascertain if these antibodies are de novo DQ/DR DSA. On analysis, it was clear that the patient had developed de novo DSA against HLA-DRB1*10:01 (DR10), MFI-2374 and DQB1*06:01 (DQ6), and MFI-15315.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [47, 'years'], 'creatinine': [5.0, 'mg/dL'], 'sex': 'Male'}",12.50233,11.87721,13.12745,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 47 years old. The concentration of Creatinine is 5.0 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 5.0^(-1.154) * 47^(-0.203) * 1 * 1=12.50233.
Hence, the patient's GFR is 12.50233 mL/min/1.73m²."
3258,9,MDRD GFR Equation,lab test,decimal,pmc-8053571-1,Extracted,"The patient was a 64-year-old Japanese man with no noteworthy medical or family history. He
experienced malaise and abdominal distention three weeks before admission, and chest
discomfort and orthopnea began five days before admission. The day before admission, he
visited the emergency department, presenting with arm and leg edema and right pleural
effusion seen on chest X-ray. Heart failure was suspected, and he was prescribed furosemide.
The next day, he visited the internal department of the general hospital. Plain computed
tomography (CT) revealed bilateral hydronephrosis and a retroperitoneal mass lesion. He was
then transferred to the urology department of our hospital as an emergency case. Blood tests
showed elevated soluble interleukin-2 receptor (sIL-2R) levels at 9334 IU/L, and he was
referred to our department with suspicion of malignant lymphoma.
On admission, he was fully conscious, his temperature was 35.7°C, pulse was 53 beats per
minute, blood pressure was 177/87 mmHg, and SpO was 98% on room air. He had no anemia in the foveal
conjunctiva and no jaundice in the ocular conjunctiva. Respiratory and cardiac sounds were
normal. The abdomen was flat and soft, and the liver and spleen were not palpable. Both
lower limbs had pitting edema. Inguinal lymph nodes were 3-cm in size and elastic, hard, and
smooth-textured on palpation bilaterally. No other superficial lymph nodes were palpated.
There were no abnormal neurological findings. His Eastern Cooperative Oncology Group
Performance Status (ECOG PS) was 2. He had no systemic B symptoms (fever, night sweats, or
weight loss).
Laboratory data on admission () showed a
markedly elevated creatinine (Cre) of 17.31 mg/dL, blood urea nitrogen (BUN) of 121 mg/dL,
potassium (K) of 7.3 mEq/L, and inorganic phosphorus (IP) of 10.1 mg/dL. Lactate
dehydrogenase (LDH) and sIL-2R were elevated to 666 IU/L and 9334 IU/mL, respectively. Plain
CT () showed a 9 cm × 5 cm retroperitoneal mass
causing bilateral hydronephrosis and partially kidney invasive lesion. It also showed
pleural effusions and right cardiophrenic and bilateral inguinal lymphadenopathies. Bone
marrow examination revealed no apparent tumor cell infiltration, and Giemsa banding showed a
normal 46,XY karyotype. Cytopathologic examination of pleural fluid showed invasion of large
abnormal lymphocytes.
On the second day in hospital, inguinal lymph node biopsy was performed (). Hematoxylin and eosin (H&E) staining showed
a diffuse pattern of involvement with medium to large abnormal lymphocytes, and loss of the
normal structure of lymphoid follicles. Immunostaining showed that the tumor was negative
for CD3 and Bcl-6, and positive for CD10, CD20, CD79a, Ki67, c-Myc, and Bcl-2. The positive
rate of Ki67, c-Myc and Bcl-2 was over 90% for each. Fluorescence in situ hybridization
(FISH) showed split signals at 8q24 (MYC) and 18q21 (BCL2)
(). Based on these findings, we diagnosed
high-grade B-cell lymphoma, with MYC and BCL2 and/or
BCL6 rearrangements. Ann Arbor stage was IV A and International
Prognostic Index was high-intermediate risk.
On the day of admission, right nephrostomy was performed for ureteral obstruction, but Cre
improvement was poor, and the patient required emergency hemodialysis from the 4th hospital
day. As diagnosis from the preliminary pathological report was diffuse large B-cell lymphoma
(DLBCL), we started half-dose CHOP therapy (cyclophosphamide 375 mg/m2, day 1;
doxorubicin 25 mg/m2, day 1; vincristine 0.7 mg/m2, day 1;
prednisolone 60 mg/m2, days 1–5) on the 23rd hospital day. Rasburicase was
administered to prevent tumor lysis syndrome. Urinary volume of 1000 mL/day was obtained on
the 25th hospital day, but despite this and removal of the ureteral obstruction, Cre and
24-hour urine collection creatinine clearance (Ccr) improved only to 2.4 mg/dL and 37
mL/min, respectively, and right renal dysfunction remained (). The patient was weaned off hemodialysis on the 30th hospital day. After
the first cycle of half-dose CHOP therapy, the treatment response was stable disease (SD)
with 47% tumor reduction (). Cre remained
approximately 2 mg/dL during treatment.
Pathological examination and FISH revealed the diagnosis of high-grade B-cell lymphoma,
with MYC and BCL2 and/or BCL6
rearrangements. Although Ccr was as low as 45 mL/min, we started DA-EPOCH-R therapy
(rituximab 375 mg/m2, day 1; doxorubicin 10 mg/m2, days 2–5;
vincristine 0.4 mg/m2, days 2–5; cyclophosphamide 750 mg/m2, day 6;
prednisolone 60 mg/m2, days 2–6; administered every 21 days) without initial dose
reduction on the 38th hospital day because more intensive treatment was considered necessary
for DHL/THL. No worsening of renal function was observed during the treatment, and the
patient completed the first cycle without any problems. The treatment response was partial
response (PR) with 64% tumor reduction, and we decided to continue the DA-EPOCH-R therapy.
On the third cycle, grade 4 neutropenia as categorized by the Common Terminology Criteria
for Adverse Events (CTCAE) was observed, and we therefore reduced dosages from the fourth
cycle onward by 20% in accordance with the protocol for DA-EPOCH-R therapy. The patient
completed six cycles of DA-EPOCH-R without any new CTCAE grade 2 or higher adverse events.
Ccr remained between 31 and 43 mL/min, with no further exacerbation. Plain CT after six
cycles of DA-EPOCH-R therapy showed the response was PR with 65% tumor reduction, although
contrast-enhanced CT was not possible due to renal dysfunction, and the accurate evaluation
was difficult. There was no indication of tumor enlargement, and we therefore decided to
monitor him as an outpatient and he was discharged on the 163rd hospital day. We scheduled
positron emission tomography-computed tomography (PET-CT) after discharge. However, 22 days
after discharge he presented diplopia. Head magnetic resonance imaging revealed swellings of
the bilateral abducens nerves and the left optic nerve. Cytopathologic examination of lumbar
puncture showed an invasion of large abnormal lymphocytes. He was readmitted, and we could
not perform PET-CT.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [64, 'years'], 'creatinine': [2.0, 'mg/dL'], 'sex': 'Male', 'Race': 'Asian'}",33.80609,32.11579,35.49639,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 64 years old. The concentration of Creatinine is 2.0 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.0^(-1.154) * 64^(-0.203) * 1 * 1=33.80609.
Hence, the patient's GFR is 33.80609 mL/min/1.73m²."
3259,9,MDRD GFR Equation,lab test,decimal,pmc-5312984-1,Extracted,"The patient is a 34-year-old Hispanic male with a BMI of 41 kg/m2 and a history of type 1 diabetes since age 17, who presented with diabetic nephropathy, retinopathy, and hypoglycemic unawareness. Overall glycemic control was poor, with a pretransplant hemoglobin A1c (HbA1c) of 9%. The average daily insulin dose was approximately 100 units. One and half years previously, a laparoscopic robotic-assisted living-donor kidney transplantation was performed. Considering the poor glycemic control and the uneventful postoperative recovery, the patient was offered minimally invasive pancreas transplantation. Preoperative lab data included: C-peptide at 0.7 nmol/L and creatinine at 1.6 mg/dL without hemodialysis.
The donor was a 21-year-old Hispanic male with BMI 25 kg/m2, who expired from a gunshot wound to the head. There was no cardiac downtime. The predonation HbA1c was 5.2% and flow cytometric and standard cross-matches were negative.
Ethical approval in this case report was waived by IRB at University of Illinois at Chicago because it was a medical activity that does not meet the DHHS definition of “research.” The patient was given informed consent, which explicitly explained that he may be the first patient who receives robotic pancreas transplantation in USA before operation.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [34, 'years'], 'creatinine': [1.6, 'mg/dL'], 'sex': 'Male', 'Race': 'Hispanic'}",49.72713,47.24077,52.21349,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 34 years old. The concentration of Creatinine is 1.6 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.6^(-1.154) * 34^(-0.203) * 1 * 1=49.72713.
Hence, the patient's GFR is 49.72713 mL/min/1.73m²."
3260,9,MDRD GFR Equation,lab test,decimal,pmc-7773467-1,Extracted,"A 76-year-old woman was transferred to our hospital after a 6-month history of progressive renal failure with bilateral hydronephrosis of unclear origin and normal cystoscopy.
At admission the patient complained of fatigue, bilateral leg oedema and a 10 kg weight loss. The patient denied any episode of macroscopic hematuria. Clinical examination found a patient in poor general condition with bilateral pitting edema of the legs. Temperature was 36.5°C, blood pressure 135/70 mmHg. The laboratory findings were as follows: serum creatinine was 601 μmol/l, urea 39.5 mmol/l, total protein 57.5 g/l, serum albumin 28 g/l, sodium 143 mmol/l, potassium 4.8 mmol/l. The sedimentation rate was 81 mm/h, C-reactive protein (CRP) 33 mg/l, hemoglobin 107 g/l, leukocyte count 7.2 G/l and platelets 333 G/l. Urinalysis showed microscopic hematuria with mild leukocyturia. Urine culture was sterile. Creatinine clearance was 4 ml/min. Proteinuria was present at 1.9 g/24 h, without paraproteins.
A native abdominal CT scan was performed showing bilateral hydro-uretero-nephrosis with massive dilatation of the upper ureters and of the renal pelvis (). The CT scan showed no signs of an obstructive abdomino-pelvic mass, of retroperitoneal fibrosis, urolithiasis or sloughed papillary necrosis. Bilateral ureteral catheterization using double J catheters was performed and the retrograde pyelography revealed that the bilateral hydronephrosis was due to a complete right ureteral stenosis and a partial stenosis on the left side (). As bilateral malignancy was considered in the differential diagnosis a small periprocedural ureteral biopsy was performed showing only nonspecific inflammation without tumoral cells.
In the following days, despite an improvement of diuresis (≈2000 ml/day) with double J catheters, no improvement of renal function occurred. The diagnostic workup was therefore completed with immunological tests showing high c-ANCA titers (1 : 1280) with anti-PR3 positivity. Thereafter, a kidney biopsy detected pauci-immune crescentic glomerulonephritis (). The ENT exam and a native pulmonary CT scan were normal.
Treatment with pulse methylprednisolone (4 × 1 gram) followed by oral prednisone in combination with monthly intravenous pulse cyclophosphamide (3 × 500 mg) was started. Renal function progressively improved in the following weeks and the creatinine stabilized at 140 μmol/l after 3 months, with negative c-ANCA. At the same time repeated ultrasounds showed a progressive regression of the hydro-uretero-nephrosis and the double J catheters were withdrawn. A follow-up CT scan at 3 months showed a complete regression of the hydronephrosis on the left side and a partial regression on the right side (). Of note this second CT scan, as the first one, showed no evidence of an obstructive abdomino-pelvic mass, of retroperitoneal fibrosis, urolithiasis or papillary necrosis.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [76, 'years'], 'creatinine': [601.0, 'µmol/L'], 'sex': 'Female'}",5.91399,5.61829,6.20969,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 76 years old. The concentration of Creatinine is 601.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 601.0 µmol. To convert 601.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 601.0 µmol Creatinine * 1e-06 mol/µmol = 0.0006 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.0006 mol Creatinine * 113.12 g/mol = 0.06787 g Creatinine. To convert 0.06787 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.06787 g Creatinine * 1000.0 mg/g = 67.87 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 67.87 mg Creatinine/10.0 dL = 6.787 mg Creatinine/dL. The concentration value of 601.0 µmol Creatinine/L converts to 6.787 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 6.787^(-1.154) * 76^(-0.203) * 1 * 0.742=5.91399.
Hence, the patient's GFR is 5.91399 mL/min/1.73m²."
3261,9,MDRD GFR Equation,lab test,decimal,pmc-4858726-1,Extracted,"A 48-year-old nonsmoking Filipino man with a medical history of hypertension, recurrent syncope, and chronic Hepatitis B previously treated with tenofovir and self-administered herbal agents complicated by chronic kidney disease attributed to drug-induced tubulointerstitial disease, presented for follow-up care and was admitted to the hospital for acute on chronic liver and kidney injury. Baseline and admission laboratory values are shown in . He was jaundiced but otherwise asymptomatic and non-oliguric. Urinalysis showed no proteinuria or haematuria and a spot urine protein to creatinine ratio was 0.6. Abdominal ultrasound demonstrated hepatomegaly without ascites, focal liver lesion, or biliary ductal dilatation; kidneys were slightly enlarged (12.4 and 12.8 cm in length) without stones, masses, or hydronephrosis. Echocardiogram showed sparkling left ventricular acoustic reflections and moderate left ventricular hypertrophy with normal ejection fraction and no restrictive physiology; electrocardiogram did not demonstrate any conduction abnormalities. Serum protein electrophoresis was negative for monoclonal gammopathy but urine protein electrophoresis demonstrated kappa light chains. Serum free kappa light chains were markedly elevated at 915 mg/dL with a kappa/lambda light chain ratio of 59.0. Liver function tests continued to trend upward despite optimal virologic response to entecavir which was started for Hepatitis B treatment, and his kidney function also continued to worsen.
Kidney biopsy showed amorphous deposits expanding the small artery walls and tubular basement membranes () staining positive for Congo Red (), with relative sparing of the glomeruli (). Immunofluorescence showed dominance of staining of the tubulointerstitial and vascular deposits for kappa light chain (). Electron microscopy demonstrated randomly arrayed straight 8–10 nm thick fibrils expanding the interstitium and surrounding interstitial capillaries and atrophic tubules (). Liver biopsy also showed Congo Red positive amorphous deposits in the blood vessel walls and within the hepatic sinusoids. Bone marrow biopsy was consistent with plasma cell neoplasm, demonstrating 50–60% atypical kappa predominant plasma cells by immunohistochemistry.
The patient was initiated on treatment with intravenous dexamethasone and bortezomib 0.7 mg/m2 and received five concurrent treatments of plasmapheresis. Over the ensuing month, he had a decrease in serum free kappa light chains, downtrending liver enzymes, and improvement in kidney function with serum creatinine nadir of 3.8 mg/dL from a peak level of 5.5 mg/dL. Unfortunately, he later suffered a witnessed syncopal episode followed by cardiac arrest resulting in his death.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [48, 'years'], 'creatinine': [3.8, 'mg/dL'], 'sex': 'Male', 'Race': 'Asian'}",17.08739,16.23302,17.94176,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 48 years old. The concentration of Creatinine is 3.8 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.8^(-1.154) * 48^(-0.203) * 1 * 1=17.08739.
Hence, the patient's GFR is 17.08739 mL/min/1.73m²."
3262,9,MDRD GFR Equation,lab test,decimal,pmc-4432416-1,Extracted,"A 59-year-old white female presented with an incidentally discovered increased serum creatinine of 2.7 mg/dL (236 μmol/L) from a baseline of 0.8 mg/dL (71 μmol/L) measured 5 years ago. Physical examination showed mild hypertension (145/70 mmHg). Cardiac and pulmonary examinations were unremarkable and no splenomegaly, hepatomegaly or peripheral lymphadenopathy were noted. Skin examination revealed a diffuse reddish-brown macular rash on her upper torso and legs, which had been unchanged for years. Urinalysis showed 3+ blood, no albumin, 2 white blood cells/high power field (HPF) and 1 red blood cell/HPF. Subsequent workup demonstrated a positive serum protein electrophoresis with 1.4 g/dL of a monoclonal protein identified as IgG kappa on immunofixation. The kappa/lambda-free light chain ratio was elevated at 48.97 (normal 0.26–1.65). Urine protein electrophoresis and immunofixation confirmed monoclonal-free kappa light chain quantified at 333 mg/24 h (30% of total proteins measured at 1092 mg/24 h). Past medical history was significant for SM diagnosed 7 years earlier by recurrent urticaria and skin rash, and a skin biopsy showed increased mast cells. A bone marrow biopsy at the time of diagnosis showed multiple paratrabecular and perivascular mast cell aggregates comprising 30–50% of the marrow space, as well as many fusiform mast cells. Both CD2- and CD25-positive mast cells (detected by immunohistochemistry) and the D816V kit mutation (detected by polymerase chain reaction on a paraffin block) were present, confirming SM diagnosis. Serum tryptase was elevated at 97.2 ng/mL (normal <1 ng/mL). She was classified as having ISM. Her symptoms were stable and managed with fexofenadine, cromolyn sulfate, aspirin and diphenhydramine over the next few years. A repeat bone marrow biopsy confirmed the diagnosis of SM, but there was no evidence of a myeloid/myelomonocytic neoplasm, plasma cell neoplasm or other lymphoproliferative disorders. She then underwent a kidney biopsy to determine the cause of renal insufficiency.
Light microscopic examination showed glomeruli with mild segmental mesangial expansion due to mildly increased cellularity and matrix but without overt mesangial nodules (A). Glomeruli were otherwise unremarkable. There was also widespread acute tubular injury, characterized by flattening of tubular epithelial cells and loss of brush borders (A). Rare intratubular casts showed fractured and/or metachromatic appearance. In addition, a single intratubular cast was surrounded by epithelioid cells, suspicious of syncytial cell reaction. The interstitium showed patchy focally dense mononuclear inflammatory cell infiltrates in the background of at least mild interstitial fibrosis and tubular atrophy. Congo-red stain was negative for amyloid deposition. Immunoperoxidase stain for CD117 (c-kit), a marker for mast cells [], showed scattered-positive cells, some in small clusters , notably with <15 cells, in close proximity to areas with dense mononuclear inflammatory cell infiltrates (B).
Immunofluorescence microscopy demonstrated bright (3–4+; on a scale of 0–4) linear staining of glomeruli, Bowman's capsules and tubular basement membranes for kappa light chain (C). The walls of some arteries and arterioles similarly showed diffuse bright staining for kappa light chains in an extracellular matrix pattern. There was no significant staining of glomeruli, vessels, tubular basement membranes or interstitium for lambda light chains (D) or other immunoreactants. Some tubular casts with fractured appearance were brightly positive for kappa light chains but not for lambda light chains.
On ultrastructural examination, there were diffuse finely granular, ‘powdery’, electron dense deposits with linear arrangement within the glomerular basement membranes (predominantly localized in intramembranous and focally towards the subendothelial aspect of the glomerular basement membranes) and tubular basement membranes (). We did not observe any obvious evidence of light chain proximal tubulopathy by light, immunofluorescence or electron microscopy.
Based on the characteristic linear staining of glomerular and tubular basement membranes and vascular walls for kappa light chain without lambda light chain detected by immunofluorescence microscopy and ‘powdery’ electron dense deposits along the glomerular and tubular basement membranes detected by electron microscopy, a diagnosis of monoclonal kappa LCDD was established. The presence of rare atypical intratubular casts, which brightly stained for kappa light chain, but not for lambda light chain by immunofluorescence microscopy, together with the presence of widespread acute tubular injury and rare possible syncytial cell reaction was interpreted highly suggestive of a concomitant light chain cast nephropathy (LCCN).
After her kidney biopsy results returned, the patient was started with bortezomib and dexamethasone. Urinary protein electrophoresis showed an initial decrease in M-spike from 333 mg/24 h (30% of total proteins) pre-treatment to 107 mg/24 h (6% of total proteins) after the first cycle of above chemotherapy and 81 mg/24 h (4.6% of total proteins) after the second cycle. Kappa/lambda free light chain ratios also decreased from 49 pre-treatment to 28 and 10 after the first and second cycles, respectively. However, serum M-spike increased after the third cycle to 379 mg/24 h (9% of total proteins) and serum creatinine, which had been 2.3 mg/mL (203 μmol/L) before her first cycle of treatment continued to rise to 4.6 mg/dL (407 μmol/L).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [59, 'years'], 'creatinine': [2.7, 'mg/dL'], 'sex': 'Female', 'Race': 'White'}",18.03704,17.13519,18.93889,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 59 years old. The concentration of Creatinine is 2.7 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.7^(-1.154) * 59^(-0.203) * 1 * 0.742=18.03704.
Hence, the patient's GFR is 18.03704 mL/min/1.73m²."
3263,9,MDRD GFR Equation,lab test,decimal,trec-cds-2016-3,Extracted,"A 75F with a PMHx significant for severe PVD, CAD, DM, and CKD presented after being found down unresponsive at home. She was found to be hypoglycemic to 29 with hypotension and bradycardia.  Her hypotension and confusion improved with hydration. She had a positive UA which eventually grew klebsiella. She had temp 96.3, respiratory rate 22, BP 102/26, a leukocytosis to 18 and a creatinine of 6 (baseline 2).  Pt has blood cultures positive for group A streptococcus.  On the day of transfer her blood pressure dropped to the 60s.  She was anuric throughout the day.  She received 80mg IV solumedrol this morning in the setting of low BPs and rare eos in urine. On arrival to the MICU pt was awake but drowsy.  On ROS, pt denies pain, lightheadedness, headache, neck pain, sore throat, recent illness or sick contacts, cough, shortness of breath, chest discomfort, heartburn, abd pain, n/v, diarrhea, constipation, dysuria.  Is a poor historian regarding how long she has had a rash on her legs.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [75, 'years'], 'creatinine': [6.0, 'mg/dL'], 'sex': 'Female'}",6.83625,6.49444,7.17806,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 75 years old. The concentration of Creatinine is 6.0 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 6.0^(-1.154) * 75^(-0.203) * 1 * 0.742=6.83625.
Hence, the patient's GFR is 6.83625 mL/min/1.73m²."
3264,9,MDRD GFR Equation,lab test,decimal,pmc-8173221-1,Extracted,"A 74-year-old male patient visited our hospital in October 2020 with a mass above the stoma that had persisted for 2 months. He had no history of abdominal pain, fever, or cough. In 2016, he underwent an abdominoperineal resection procedure for carcinoma located in the distal one-third of the rectum. He also had a history of open appendectomy. The patient was an active smoker, was on medication for diabetes, had no chronic obstructive pulmonary disease, and was not using any immunosuppressive drugs. He had also received chemotherapy (10 cycles of FOLFOX6) for carcinoma. There was no history of any other comorbidities. Family, psychosocial, and genetic histories were insignificant.
The patient's blood pressure was 140/90 mmHg, heart rate was 82 beats/min, respiratory rate was 20 breaths/min, and body temperature was 36.4°C during the examination. His body mass index was 27.5 kg/m2. Abdominal examination in the erect position revealed a mass with a diameter of ~5 cm protruding above the stoma. He had midline and gridiron incisional scars. There was a parastomal hernia at the outer edge of the rectus abdominis muscle. The hernia was soft and reducible to the abdominal cavity in the supine position.
Computed tomography (CT) examination revealed a parastomal hernia () with a diameter of 3 cm. Laboratory tests revealed a leukocyte count of 5.90 × 109/l, hemoglobin concentration of 65 g/l, neutrophil percentage of 61.8%, and platelet count of 149 × 109/l. Glycosylated hemoglobin A1c (HbA1c) level was 6.5%. The renal function test showed that creatinine was 79.2 μmol/l and urea was 7.21 mmol/l. Electrolytes and coagulation function were normal. There were no abnormalities detected in the electrocardiogram, chest X-ray, and echocardiogram. The diagnosis at admission was post-operative rectal cancer with a parastomal hernia.
Under general anesthesia, endotracheal intubation or a laryngeal mask and pre-operative indwelling urinary catheterization were applied to the patient, who was in a supine position. The surgeons were standing contralateral to the stoma with the monitor over the surgical site. The stoma was sealed with an adhesive incise drape. The surgical field was divided into right and left partitions using the sterilized surgical towel to prevent any potential contamination.
An incision of 1.2 cm through the skin and subcutaneous adipose tissue was made at the right iliac region. The incised subcutaneous tissue was separated using a pair of retractors to expose and dissect aponeurosis of the external oblique muscle. Hemostatic forceps were used to separate the internal oblique and transversus abdominis muscles. The primary extraperitoneal space was created using a finger. To create the preperitoneal space, 2 sets of 5-mm trocars were inserted at the site of surgical incision using the retrograde puncture technique (); the trocars were placed at ~5 cm to each side of the incision, and a 12-mm observation trocar was placed through the incision (). After successfully placing all three trocars, extrapneumoperitoneum was induced (11 mmHg CO2) for endoscope insertion.
The further extraperitoneal space was created under direct endoscopic guidance down to the pubic floor and up to the bladder, where it was easier to create. We then moved to the contralateral side of the abdomen; as the long midline incision in the abdomen made it very difficult to separate the peritoneum, the membrane was cut while avoiding damage to the tissue at the middle of the incision, thus weakening the abdominal wall. When performing cephalad dissection, we targeted the space between the rectus abdominis and posterior sheath. To create the space, we opened the lateral edge of the posterior sheath to penetrate the extraperitoneal space between the lateral and mid-abdomen. The TEP technique was used for this separation. The dissecting plane of the lateral space was the extraperitoneal space between the peritoneum and parietal plane. During separation, the peritoneum was dissected and observed to avoid damage to the bowel around the stoma. Through the space that was created by separation, we enlarged the extraperitoneal space within a 15- to 20-cm radius around the stoma, providing a large field for mesh placement ().
At the end of the procedure, the abdominal wall defect was closed with a 2-0 non-absorbable suture (). The peritoneum defect was secured using a 3-0 absorbable suture with the enterostomy loop positioned outside the peritoneum.
A 15 × 15-cm polypropylene mesh was cut in the middle and placed around the colostomy loop (), then sutured and fixed. After a careful re-examination, the surgical field was clean, and no drainage tube was placed. Then extrapneumoperitoneum was relieved to complete the operation.
The total operation time was 240 min while the peritoneal separation time was 115 min. The patient was discharged 48 h after the operation. At the 3-month follow-up, the patient had a regular oral intake and defecation, no pain around the stoma, no seroma formation, and no infection at the incision site. The follow-up abdominal CT scan showed no recurrence of the hernia ().","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [74, 'years'], 'creatinine': [79.2, 'µmol/L'], 'sex': 'Male'}",81.96181,77.86372,86.0599,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 74 years old. The concentration of Creatinine is 79.2 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 79.2 µmol. To convert 79.2 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 79.2 µmol Creatinine * 1e-06 mol/µmol = 8e-05 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 8e-05 mol Creatinine * 113.12 g/mol = 0.00905 g Creatinine. To convert 0.00905 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00905 g Creatinine * 1000.0 mg/g = 9.05 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 9.05 mg Creatinine/10.0 dL = 0.905 mg Creatinine/dL. The concentration value of 79.2 µmol Creatinine/L converts to 0.905 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 0.905^(-1.154) * 74^(-0.203) * 1 * 1=81.96181.
Hence, the patient's GFR is 81.96181 mL/min/1.73m²."
3265,9,MDRD GFR Equation,lab test,decimal,pmc-3741977-2,Extracted,"A 57-year-old man, known to have type 2 diabetes mellitus (on diet control) and dyslipidemia (on statins) presented to us with a history of anorexia, nausea, and fatigue for 2 weeks after intake of I. puli fruit juice for 5 days; he was oliguric. He had a normal hemogram, with serum creatinine: 9.3 mg/dl, serum cholesterol: 180 mg/dl. Urine analysis showed 1+ Protein, and microscopic examination of the urine sample showed plenty of oxalate crystals. He was initiated on hemodialysis and subsequently underwent a left percutaneous kidney biopsy which showed acute tubular necrosis with intra tubular calcium oxalate crystals. He needed six sessions of hemodialysis. His renal functions became normal in about 5 weeks’ time.
Similar cases have been reported in other hospitals of Kerala. All the patients had history of consuming I. puli juice and developed renal failure. None of the patients had history of renal failure before consuming the fruit juice. The details of these ten patients are given in . All the patients were male, age ranging from 38 to 72 years. Six patients had pre-existing problems like diabetes mellitus or hypertension. Eight out of 10 patients had plenty of oxalate crystals in urine; all the patients had severe renal failure with serum creatinine ranging from 5.5 to 12.3 mg/dl. Seven patients required hemodialysis in view of severe renal failure; the remaining three patients were treated conservatively and renal functions returned to normal. Kidney biopsy was performed in seven patients. All the patients showed acute tubular necrosis with polarizable tubular crystals consistent with oxalate crystals []. The time taken for Serum creatinine to reach the normal level ranged from 2 to 6 weeks.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [57, 'years'], 'creatinine': [9.3, 'mg/dL'], 'sex': 'Male'}",5.87444,5.58072,6.16816,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 57 years old. The concentration of Creatinine is 9.3 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 9.3^(-1.154) * 57^(-0.203) * 1 * 1=5.87444.
Hence, the patient's GFR is 5.87444 mL/min/1.73m²."
3266,9,MDRD GFR Equation,lab test,decimal,pmc-8278676-1,Extracted,"A 35-year-old woman with a history of hypertension, severe osteoporosis, and stage 5 chronic kidney disease due to lupus nephritis, was admitted to our emergency department for suspected uremic symptoms of nausea and general weakness. Her vital signs were normal, with a heart rate of 80 beats/min and blood pressure of 100/60 mmHg. However, her blood urea nitrogen (179.4 (reference range: 8–23) mg/dL) and serum creatinine (10.9 (reference range: 0.5–1.3) mg/dL) levels were markedly increased, with her serum inorganic phosphate level also higher than normal at 8.4 (reference range: 2.5–5.5) mg/dL. The patient was treated with emergent hemodialysis and a living-donor kidney transplantation, from her father, was planned.
During the pre-transplantation medical work-up, contrast-enhanced computed tomography (CT) of the abdomen revealed a heterogeneously enhancing mass, 1.7 cm in diameter, located in the upper pole of the right kidney (Fig. A). On follow-up magnetic resonance (MR) imaging, the mass presented high signal intensity on T2-weighted images, with heterogeneous enhancement in the right kidney (Fig. B and C). Based on findings of the MR imaging, a diagnosis of renal cell carcinoma, stage T1aN0, was made. As the right renal mass was small, with no associated symptoms, simultaneous right radical nephrectomy and kidney transplant was planned by the transplant surgeon and urologist. Open radical nephrectomy was performed via a subcostal incision; the patient was then positioned for the kidney transplant. Hematoxylin and eosin staining performed after nephrectomy revealed irregularly shaped vascular spaces of various sizes, with an anastomosing pattern (Fig. A). On immunostaining, the sample was positive for CD34, CD31, and ETS-related genes and for friend leukemia integration 1 transcription factor and negative for podoplanin, human herpes virus-8, and glucose transporter-1 on immunostaining (Fig. B–D). Based on these findings, a final diagnosis of anastomosing hemangioma was made. After kidney transplantation, good renal function was achieved, with no tumor recurrence.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [35, 'years'], 'creatinine': [10.9, 'mg/dL'], 'sex': 'Female'}",4.00688,3.80654,4.20722,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 35 years old. The concentration of Creatinine is 10.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 10.9^(-1.154) * 35^(-0.203) * 1 * 0.742=4.00688.
Hence, the patient's GFR is 4.00688 mL/min/1.73m²."
3267,9,MDRD GFR Equation,lab test,decimal,pmc-6176666-1,Extracted,"A 36-year-old gentleman presented to the nephrology department with 1 month history of renal dysfunction, generalised oedema, and decreased urine output, for which he had been initiated on haemodialysis elsewhere via a temporary jugular venous catheter. At presentation, he had fever and blood culture grew non-fermenting Gram-negative bacilli, suggestive of a catheter-related blood stream infection. The catheter was removed, he was given antibiotics according to sensitivity and admitted for renal biopsy after a week. Pre-biopsy lab parameters showed high creatinine (6.08 mg/dL), low haemoglobin (8.5 g/dL), and other lab parameters were normal.
For the biopsy, the patient was placed in prone position, lower pole cortex of the left kidney was selected under ultrasound guidance, depth and direction from the skin surface to lower cortex was determined, and overlying skin surface was marked. Renal biopsy was performed under local anaesthesia with free hand ultrasound-assisted biopsy. Two passes were made with 2.2 cm throw from a spring-loaded biopsy gun (18G × 16 cm, BARD Max Core, Bard Peripheral Vascular, Inc. AZ, USA). An adequate sample was obtained. After biopsy, patient was placed in supine position and complete bed rest was advised for next 12 h in the ward.
Three hours post-biopsy, the patient developed pain in left flank, tachycardia, and hypotension with a drop in haemoglobin (Hb 6.6 g/dL). He was resuscitated with IV fluid and oxygen. Urgent ultrasonography showed a large (300–400 mL) retroperitoneal haematoma posterior to the kidney. Blood transfusion was started. He was taken up for immediate catheter angiography. Initial catheter angiogram through right common femoral artery access in a biplane DSA machine showed no detectable arterial injury []. Selective angiograms of the left side intercostals (from T10 to T12) and lumbar arteries (from L1 to L3) also showed no abnormality. Haemorrhage from an accessory renal artery was considered less likely initially as an apparently complete nephrogram was noted on main renal artery angiogram. Pigtail abdominal aortogram also did not show any accessory renal artery. As the haemorrhage was large and the drop in Hb was significant, a CT scan angiogram (CTA) was planned to identify the source of bleeding. Patient was directly shifted to CT scan room with introducer sheath in the right common femoral artery. CTA showed an accessory left renal artery arising from aorta at L2–L3 disc level and supplying the lower pole of the left kidney. There were two separate nodular areas of contrast extravasations, one in the lower pole of the left kidney [] and another in the posterior pararenal space []. Patient was shifted back to DSA room. The accessory left renal artery angiogram showed a small pseudoaneurysm with arteriovenous fistula (AVF) in the lower pole of the kidney []. It was selectively cannulated with Progreat coaxial microcatheter (2.7 F, Terumo, Japan) and embolised with five 3 mm × 3 cm pushable coils (0.018, Cook Medical) []. The main renal artery was cannulated with a 4F cobra catheter and the capsular artery was selectively cannulated with a Progreat microcatheter. Angiogram showed a left testicular artery arising from the capsular artery [Figure and ]. Further selective angiogram of the testicular artery showed contrast extravasation corresponding to the CTA findings []. This testicular artery was embolised near the site of contrast extravasation with two 3 mm × 14 cm pushable coils (0.018, Cook Medical) []. The patient was closely monitored in the ward and did not show any further drop in Hb. He was discharged after 2 days in a stable condition and was advised to continue saline dialysis for the next 4–5 sessions. Ultrasound and Doppler of scrotum after 2 days showed good arterial flow without any infarct in the left testis. The kidney biopsy was reported as cortical parenchymal necrosis.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [36, 'years'], 'creatinine': [6.08, 'mg/dL'], 'sex': 'Male'}",10.53135,10.00478,11.05792,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 36 years old. The concentration of Creatinine is 6.08 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 6.08^(-1.154) * 36^(-0.203) * 1 * 1=10.53135.
Hence, the patient's GFR is 10.53135 mL/min/1.73m²."
3268,9,MDRD GFR Equation,lab test,decimal,pmc-5886906-1,Extracted,"A 36-year-old African-American woman presented to the ER with a 3-day history of vomiting, diarrhea, full-body arthralgias, myalgias, and bilateral TMJ stiffness and tenderness, along with severe persistent headache. She had been seen in urgent care 1 week prior to admission with complaints of fever, nausea, and diarrhea. Her medical history was significant for rheumatoid arthritis that had been in remission for 12 years. She was not currently on any maintenance therapy for this auto-immune disease. On arrival, vitals were recorded as BP of 125/89, HR of 92 bpm, RR of 18/min, Temperature of 98.3 °F, and 100% SpO2 on room air. Physical exam was significant for a malar rash, shown in Fig. , as well as a second subcutaneous rash on her arms that was erythematous and nodular seen in Fig. . In addition, she had bilateral knee effusions along with weakness and edema of the lower extremities.
Labs obtained in the emergency room showed an elevated creatinine level of 2.85 mg/dL (0.5–1.0 mg/dL), AST 1293 U/L (10–40 U/L), ALT 397 U/L (7–56 U/L), elevated phosphorus 8.3 mg/dL (2.0–4.5 mg/dL), and a low potassium level of 3.1 mmol/L (3.5–5.0 mmol/L). CPK was extremely high at 6270 U/L (22–198 U/L) and CRP at 9.244 mg/L (< 3.0 mg/L). The initial differential diagnosis included dermatomyositis/polymyositis/SLE with rhabdomyolysis. She was admitted to the medical floor and given a 3 L bolus of normal saline along with IV methylprednisolone.
Despite the initial treatment with fluid and steroids, the patient’s creatinine and lab values worsened over the next 24 h. Her creatinine rose to 3.59 mg/dL, BUN increased to 70 mg/dL (7–20 mg/dL), and phosphate jumped to 9.8 mg/dL. In addition, CPK elevated to 207,300 U/L along with an increase in AST and ALT to 1797 and 482 U/L, respectively. Clinically, the patient was also deteriorating; she had been anuric since admission despite fluid resuscitation. The patient was transferred to the ICU, and nephrology and rheumatology were consulted. She was started on a bolus of intravenous corticosteroids to treat rhabdomyolysis secondary to polymyositis after consultants’ review. The rheumatologist ordered a panel of auto-immune markers to include CRP, RF, ANA, dsDNA, Ribosomal P, SSA (anti-Ro), SSB (anti-La), snRNP, anti-smith, RNP, centromere B, SCL-70, and Jo-1. The results revealed that the CRP was 5.556 mg/L (< 3.0 mg/L); the RF was 121 IU/mL (< 15 IU/mL), ANA was greater than 8 IU/mL (< 8 IU/mL), DsDNA was 1 IU/mL (0 IU/mL), Ribosomal P was greater than 8 IU/mL (IU/mL < 8), SSA (anti-Ro) was greater than 8 IU/mL (< 8 IU/mL), SSB (anti-La) was less than 0.2 IU/mL (< 1 IU/mL), snRNP was less than 0.2 IU/mL (< 1 IU/mL), anti-smith was less than 0.2 IU/mL (< 1 IU/mL), RNP was 4.4 IU/mL (< 1 IU/mL), centromere B was less than 0.2 IU/mL (< 1 IU/mL), SCL-70 was less than 0.2 IU/mL (< 1 IU/mL), and Jo-1 was less than 0.2 IU/mL (< 1 IU/mL).
These lab values suggested a probable diagnosis of SLE. Diagnostic criteria for SLE are based on ACR (American College of Rheumatology) guidelines with a sensitivity of 85% and specificity of 95% in patients with 4 out of 11 criteria. This patient had arthritis, photosensitivity, renal involvement, blood disorders, elevated ANA, immunologic phenomena with anti-dsDNA, and a malar rash, giving her an ACR SLE score of 7/11, defining her as having SLE. The SELENA–SLEDAI scoring matrix is a way to assess SLE disease activity using 24 different disease descriptors. Scores of six or above on the SLEDAI grid are considered to be consistent with active disease requiring therapy. The patient had a lupus headache, arthritis, myositis, urinary casts, a rash, low complement levels, and leukopenia having a total of 25 points on the SELENA–SLEDAI scoring matrix. This was consistent with a significant degree of active SLE, and need for aggressive medical therapy.
A central line was placed to initiate hemodialysis to alleviate her acute kidney injury. Prompt hemodialysis corrected her electrolytes and improved her creatinine and BUN within 24 h. However, her CPK continue to escalate to 304,700 U/L and her anuria persisted. The intravenous corticosteroids were tapered and changed to oral preparations to prevent further fluid overload and edema. Hydroxychloroquine was started 1 week after ruling out G6PD deficiency and the risk of iatrogenic hemolysis.
Over the next week, with continued hemodialysis and steroid treatment, her laboratory and clinical picture improved. CPK levels dropped to within normal range, and creatinine and BUN levels remained consistent and improved (though not normalized) with hemodialysis every other day. Due to persistent oliguria, a renal biopsy was ordered to determine if rhabdomyolysis, SLE, or both were to blame. The biopsy showed muddy brown casts with permanent tubular atrophy, interstitial fibrosis, and massive amounts of myoglobin, implicating rhabdomyolysis, as shown in Figs. and , as the main culprit of the acute kidney injury.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [36, 'years'], 'creatinine': [2.85, 'mg/dL'], 'sex': 'Female', 'Race': 'Black'}",22.70514,21.56988,23.8404,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 36 years old. The concentration of Creatinine is 2.85 mg/dL. 
The patient is Black, so the race coefficient is 1.212.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.85^(-1.154) * 36^(-0.203) * 1.212 * 0.742=22.70514.
Hence, the patient's GFR is 22.70514 mL/min/1.73m²."
3269,9,MDRD GFR Equation,lab test,decimal,pmc-6188736-1,Extracted,"The patient was a 60-year-old man who was diagnosed with alcoholic liver cirrhosis and type 2 diabetes when he was 50 years old. His drinking history was 540–720 mL Japanese sake per day for 35 years, and his smoking history was 30 cigarettes per day for 30 years. His ascites increased in 2008 when he was 57 years old, and he repeatedly exhibited symptoms of hepatic encephalopathy. Due to the liver cirrhosis symptoms, the patient was treated with several medications including furosemide, spironolactone, lactulose, and total amino acid preparation. To prevent the complications of liver cirrhosis, coil embolization to a portal venous shunt was performed twice. The patient was admitted to our hospital in June 2012 because of slowly progressive renal impairment and nephrotic syndrome.
Upon admission, the patient's height and weight were 166 cm and 64 kg, respectively. His body temperature was 36.7°C and his blood pressure was 150/60 mmHg. His consciousness was clear. His abdomen was slightly expanded but exhibited no tenderness. The liver and spleen were not palpable. No rash or purpura was noted on the skin. Diabetic and/or hypertensive changes were not observed in the ocular fundus.
The laboratory findings on admission were hemoglobin level of 9.4 g/dL (normal range 13.5–17.6 g/dL), platelet count of 11x104/μL (normal range, 13.1–36.2x104/μL), prothrombin time measurement of 68% (normal range, 70–130%), total bilirubin level of 0.9 mg/dL (normal range, 0.3–1.2 mg/dL), NH3 level of 85 mg/dL (normal range, 30–80 mg/dL), blood urea nitrogen level of 41 mg/dL (normal range, 8–20 mg/dL), serum creatinine concentration of 1.77 mg/dL (normal range, 0.5–1.1 mg/dL), serum total protein level of 5.7 g/dL (normal range, 6.7–8.3 g/dL), serum albumin level of 2.1 g/dL (normal range, 3.5–5.2 g/dL), total cholesterol of 188 mg/dL (normal range, 120–219 mg/dL), and HbA1c of 5.8% (normal range, 4.3–5.8%). The serum levels of IgG were 1558 mg/dL (normal range, 870–1700 mg/dL), of IgA were 481 mg/dL (normal range, 110–410 mg/dL), of IgA1 were 398 mg/dL (normal range, 50–314 mg/dL), of IgA2 were 83 mg/dL (normal range, 10–156 mg/dL), and of IgM were 219 mg/dL (normal range, 35–220 mg/dL). The serum levels of free κ and λ light chains were 149.0 mg/L (normal range, 3.3–19.4 mg/L) and 106.0 mg/L (normal range, 5.7–26.3 mg/L). The serum free light chain ratio was within normal range. The serum level of complement factor C3 was 79 mg/dL (normal range, 65–135 mg/dL), of C4 was 17 mg/dL (normal range, 13–35 mg/dL), and of CH50 was 41.1 U/mL (normal range, 30–50 U/mL). All of the other serology findings including anti-nuclear antibody, hepatitis B virus surface antigen, hepatitis C virus antibody, anti-neutrophil cytoplasmic antibody, and anti-glomerular basement membrane antibody were negative. There was no M-spike on serum and urine protein electrophoresis. A serum test for a cryoglobulin precipitation was negative.
The urinary sediments showed many red blood cells in high power fields together with granular casts and dysmorphic red blood cells. The urinary protein excretion was 4.7 g/day. The 24-hour creatinine clearance was 45 mL/min. Computed tomography revealed liver deformity with moderate accumulation of ascites. The kidneys were normal in size and there were no signs of urinary tract obstruction.
The renal biopsy specimens contained a total 28 glomeruli, 12 of which were globally sclerotic. The degree of interstitial fibrosis/tubular atrophy was 50–60% of the total biopsy specimen identified. Moderate fibrous intimal hyperplasia was observed in the arcuate artery. Diffuse segmental double-contours of the glomerular basement membrane and mesangial cell hypercellularity were identified in nonsclerotic glomeruli, exhibiting a membranoproliferative glomerulonephritis-like pattern (). Some glomeruli showed moderate-to-severe endocapillary hypercellularity, accompanied by fibrocellular crescents (). Fluorescent immunostaining showed granular staining of IgA and C3, but not of IgG, IgM, or C1q, on glomerular capillaries and some mesangial areas (Figures –). Among the IgA subtypes, staining of IgA1 (GenWay Biotech, San Diego, CA, USA) was observed, but staining of IgA2 (GenWay Biotech) was not identified (Figures and ). With light chain immunostaining, only κ (SouthernBiotech, Birmingham, AL, USA) was identified and no λ staining (SouthernBiotech) was seen (Figures and ). On electron microscopy, the glomerular capillary walls showed double contours. Electron-dense deposits were found in the paramesangium and around the subendothelial space of the glomeruli (). No organized structure deposits were identified (). Based on these findings, this case was histologically diagnosed as diffuse membranoproliferative glomerulonephritis with monoclonal IgA1-κ deposits.
Because this case was accompanied by moderately advanced decompensated liver cirrhosis, there was a concern that the patient may have serious side effects due to aggressive treatment such as the administration of corticosteroids. Thus, supportive treatment based on medications such as RAS inhibitors/diuretics, in addition to dietary therapy including salt restriction/branched-chain amino acid administration, was selected. Although these treatments led to a modest decrease in the urinary protein excretion, the patient's renal dysfunction slowly progressed and finally resulted in end-stage renal failure and initiation of dialysis therapy.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [60, 'years'], 'creatinine': [1.77, 'mg/dL'], 'sex': 'Male'}",39.43776,37.46587,41.40965,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 60 years old. The concentration of Creatinine is 1.77 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.77^(-1.154) * 60^(-0.203) * 1 * 1=39.43776.
Hence, the patient's GFR is 39.43776 mL/min/1.73m²."
3270,9,MDRD GFR Equation,lab test,decimal,pmc-4508971-1,Extracted,"A 38-year-old Turkish male was admitted to our outpatient clinic for hypercalcemia. Before entering our clinic, hypercalcemia has been detected in another medical center. History revealed, that he took ace inhibitor in combination with thiazide diuretic for hypertension. Due to the complications, like hypopotassemia this medicine was replaced with calcium channel blockers. In his family history, none of his first degree relatives had hypertension. His father died at 47 years of age due to biliary tract cancer. His three children were diagnosed with West Syndrome. One of them died at the age of 13 months, while the other 9 months of age. His third child is 2 years old and living with the respiratory support equipment. He also has a 13-year-old healthy son. There is no other significant clinical data in his medical history.
On his physical examination: blood pressure—150/90 mmHg, pulse −74 per minute, rhythmic. His general clinical appearance was good. The other systemic and laboratory findings were the following: complete blood count and thyroid function tests were normal: serum Ca level: 10.9 mg/dl (8.8–10.2), inorganic P: 2.4 mg/dl (2.7–4.5), Mg: 2.3(1.6–2.6), albumine: 3.9 g/dl, parathormone (PTH): 200 pg/ml (12–88), Na: 138 mmol/l, K+: 2.8 mmol/l, glucose: 85 mg/dl, creatinine: 0.84 mg/dl, alanine transaminase: 24 U/l, white blood cells 8 ML, hemoglobin 14 g/dl, platelet 219 C-reactive protein 0.4 mg/dl (0–0.8), alkaline phosphatase 61 U/l (38–126), 25-OH vitamin D3 22 ng/ml (14–66). Calcium level in 24-h urine: 251 mg/day, inorganic P: 88 mg/day, and K+ value in spot urine: 66 mmol/l. Aldosterone level was measured after normalization of his serum potassium level (result: 26.9 ng/dl). Plasma renin activity was <0.15 ng/ml/h. The patient was detected for multiple endocrine neoplasia syndromes. Levels of catecholamine and its metabolites in 24-h urine were normal. In the low dose (1 mg) dexamethasone suppression test, serum cortisol level was suppressed to the normal range. Serum prolactin, thyroid-stimulating hormone, adrenocorticotropic hormone, growth hormone, insulin-like growth factor 1 and calcitonin were normal.
Thyroid ultrasound revealed a 24 × 14 × 12.5 mm hypoechoic nodular lesion at the upper posterior part of the right thyroid lobe, within the thyroid capsule (intrathyroidal parathyroid adenoma?). MIBI (Technetium (99mTc) sestamibi) scintigraphy of parathyroid glands was consistent with the ultrasound finding. Abdominal magnetic resonance imaging revealed 1.6 cm adrenal gland mass consistent with adenoma, cystic lesions in both kidneys with the largest (3 cm in length) in the right kidney and also on this side 11 mm lesion which may be consistent with angiomyolipoma. Pituitary magnetic resonance imaging was normal.
The patient was operated for parathyroid adenoma. At the 3rd day after the operation, serum Ca level was found to be 9.5 mg/dl, inorganic P—3.6 mg/dl and parathyroid hormone—62 pg/ml. Pathological examination of the surgery material revealed parathyroid adenoma. The patient post operatively was followed during the 2 months with spironolactone therapy for his hypertension. This medication was stopped soon after, due to its side effects like erectile dysfunction. Post-surgery, which was conducted for the lesion (1.6 cm) identified on the left adrenal gland revealed adrenal aldosterone producing adenoma. Follow up the adrenal surgery, his blood pressure came to normal ranges and hypokalemia were improved. Blood potassium and calcium levels were within normal ranges. Genetic screening revealed negative mutation of MENIN gene.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [38, 'years'], 'creatinine': [0.84, 'mg/dL'], 'sex': 'Male'}",102.26421,97.151,107.37742,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 38 years old. The concentration of Creatinine is 0.84 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 0.84^(-1.154) * 38^(-0.203) * 1 * 1=102.26421.
Hence, the patient's GFR is 102.26421 mL/min/1.73m²."
3271,9,MDRD GFR Equation,lab test,decimal,pmc-6563334-1,Extracted,"A 79-year-old Caucasian male, with a past medical history of atrial fibrillation on warfarin and metoprolol, and coronary artery disease on atorvastatin with previous coronary artery bypass grafting and placement of a dual-function pacemaker/ implantable cardioverter defibrillator (ICD), was on a motor boat in a remote location. The patient’s boat went over a wake of a larger boat passing by. He bounced off his seat in a vertical direction and subsequently landed on his tailbone. After the high impact fall, he complained of both immediate lower back and diffuse abdominal pain but did not seek out urgent medical help.
Two days after the initial incident, he started to become pale and diaphoretic; additionally, his ICD delivered three shocks over a 30-min period. He presented via ambulance service to a local community hospital in hemorrhagic shock with a blood pressure of 63/22 and heart rate of 118 beats/min. A primary survey was pertinently positive for hemodynamic instability and diffuse abdominal and lower thoracic spine tenderness.
He was resuscitated with 1 L of normal saline leading to an improvement of his pressure to 106/88. Initial laboratory investigations included a hemoglobin of 95 g/L, lactate of 6.1 mmol/L, creatinine of 129, and a supratherapeutic INR of 8.8. An initial non-contrast CT abdomen and pelvis showed moderate hemoperitoneum with sentinel clot in the left upper quadrant and pericolic gutter, as well as the area adjacent to the posterior wall of the stomach. An additional finding of a severely comminuted, minimally displaced burst fracture of the T10 vertebral body was noted (). Further interventions included INR reversal with 3 mg of Vitamin K and 3000 units of prothrombin complex concentrate, and administration of 2 units of packed red blood cells and 2 L of normal saline. Based on clinical severity, the patient was transferred to the trauma service at a tertiary-care Level 1 trauma center.
Primary survey revealed a protected airway, spontaneous and bilateral air entry, and hemodynamic stability with a blood pressure of 100/60 and a heart rate of 88 beats/min. His abdomen continued to be mildly distended and tender without peritoneal signs, however the patient reported it had improved since his original presentation to the local hospital. Repeat laboratory investigations revealed a stable hemoglobin of 94 g/L, and correction of his INR to 1.2. Given his stable condition, he underwent a CT RIPIT (Rapid Imaging Protocol in Trauma) [] and CT angiogram (CTA) of the abdomen and pelvis. His imaging revealed pseudoaneurysms of the left gastric artery measuring up to 6 mm with another 9 mm rounded area of increased attenuation along the lesser curve of the stomach (, ). No extravasation was seen. Decision was made to monitor the patient closely with serial abdominal exams and repeat imaging in 72 h, or sooner if the patient exhibited any signs of deterioration.
Over the next 72 h, the patient’s vital signs and abdominal exams, improved and his hematological profile remained stable. Given the patient’s CHADS score of 2, it was decided to hold therapeutic anticoagulation until the patient’s bleeding risk decreased, however deep venous thrombosis prophylaxis was initiated. A repeat CTA was performed to follow the evolution of the two pseudoaneurysms. The imaging study revealed unchanged pseudoaneurysms but noted the distal aspect of the left gastric artery was attenuated in keeping with a focal dissection and intramural thrombus. Secondary to the dissection, the patient was started on 81 mg of aspirin daily. Over the next few days the patient continued to improve clinically, and was discharged home. The patient lived outside of the local area, and arrangements for close follow up were made.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [79, 'years'], 'creatinine': [129.0, 'µmol/L'], 'sex': 'Male', 'Race': 'White'}",46.17371,43.86502,48.4824,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 79 years old. The concentration of Creatinine is 129.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 129.0 µmol. To convert 129.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 129.0 µmol Creatinine * 1e-06 mol/µmol = 0.00013 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00013 mol Creatinine * 113.12 g/mol = 0.01471 g Creatinine. To convert 0.01471 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01471 g Creatinine * 1000.0 mg/g = 14.71 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 14.71 mg Creatinine/10.0 dL = 1.471 mg Creatinine/dL. The concentration value of 129.0 µmol Creatinine/L converts to 1.471 mg Creatinine/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.471^(-1.154) * 79^(-0.203) * 1 * 1=46.17371.
Hence, the patient's GFR is 46.17371 mL/min/1.73m²."
3272,9,MDRD GFR Equation,lab test,decimal,pmc-8638927-1,Extracted,"A 63-year-old African American male presented with a two-day history of intermittent fever and shortness of breath; he complained of productive cough without specified sputum characteristics, concomitant abdominal discomfort, lower back pain, and watery diarrhea. His medical history was significant for heart failure with reduced ejection fraction, chronic kidney disease, type 2 diabetes, and obstructive sleep apnea. Ten years ago, the patient underwent a right kidney transplant due to poorly controlled hypertension and received post-transplant tacrolimus and mycophenolate immunosuppressive therapy. He lives by himself, and upon further investigation into his home environment, he reported having two air conditioning systems at least 40 years old. On admission, he was febrile, tachycardic, tachypneic, and hypoxic. Physical exam revealed dehydration signs and decreased breath sounds on the left upper and lower lung fields with positive rhonchi and bilateral pitting edema in lower extremities.
The metabolic panel was pertinent for elevated creatinine of 2.79 mg/dL from a baseline of 2.15 mg/dL; CBC was remarkable for leukocytosis with left shift and normocytic anemia with hemoglobin at 9.5 g/dL. Urinalysis revealed +3 bacteriuria and +3 hematuria. Urine Legionella antigen was positive. EKG showed atrial fibrillation with a rapid ventricular response, multiple premature atrial and ventricular complexes with prolonged QTc at 492. Chest x-ray showed cardiomegaly in addition to left upper lobe pneumonia with mild left pleural effusion (Figure ). Subsequent thorax/chest CT scan detected multifocal pneumonia notably concentrated in the left upper lobe with small left-sided pleural effusion, moderate cardiomegaly with trace pericardial effusion, and mediastinal, hilar adenopathy (Figure ).
The patient was started on 0.9% NaCl fluid resuscitation and azithromycin that later changed to the fourth-generation fluoroquinolone (moxifloxacin) due to possible drug interaction with tacrolimus. The nephrology team closely monitored and daily adjusted tacrolimus. Hydration was maintained cautiously to prevent the worsening of acute kidney injury. An echocardiogram revealed a 30% reduced ejection fraction, consistent with a previous echo. Cardiology followed up during hospital stay and recommended outpatient evaluation of automatic implantable cardioverter-defibrillator (AICD) placement. He was placed on BIPAP at night and nasal cannula oxygen at daytime. Due to concerns over mobility and restrictive life space in the home environment, physical and occupational therapy recommended subacute rehabilitation (SAR) placement. The patient completed eight days of moxifloxacin and was discharged to rehabilitation.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [2.79, 'mg/dL'], 'sex': 'Male', 'Race': 'Black'}",27.99286,26.59322,29.3925,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 63 years old. The concentration of Creatinine is 2.79 mg/dL. 
The patient is Black, so the race coefficient is 1.212.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.79^(-1.154) * 63^(-0.203) * 1.212 * 1=27.99286.
Hence, the patient's GFR is 27.99286 mL/min/1.73m²."
3273,9,MDRD GFR Equation,lab test,decimal,pmc-3568895-1,Extracted,"A 65-year-old male patient presented to our institution with lower urinary tract symptoms and elevated serum urea and creatinine levels. He was under followup for type II diabetes mellitus for the last 6 years and prostate cancer for the last 3 years. Maximal androgen deprivation therapy (GnRh analogue and nonsteroidal antiandrogen) was initiated 3 years ago, but the patient did not receive the treatment in a regular way. He had had 2 sessions of hemodialysis previously in emergency settings in another center. Blood tests at the time of first inspection were serum urea: 135 mg/dL, creatinine: 6.2 mg/dL, and prostate specific antigen: >153 ng/dL. Evaluation of the urinary tract revealed a maximal urinary flow rate of 6 mL/s, an international prostate symptom score (IPSS) of 29, and grade III dilation of bilateral kidneys and ureters on the sonogram. Invasion of the trigone and left ureteral orifice was observed, and right unit was double-j stented during cystoscopy. Diversion of the left unit with a percutanous nephrostomy was recommended, but was refused by the patient. Transurethral resection of the prostate (TUR-P) was performed after serum creatinine was stabilized at a level of approximately 3 mg/dL 1 month after stenting of the right collecting system. Patient was discharged with a serum creatinine level of 2.9 mg/dL and with conservative recommendations like increased oral hydration and low-protein diet. The patient was meticulously followed after the TUR-P with monthly routine blood biochemistry and PSA measurements and urinary ultrasound. Four months later, the patient applied with a sudden onset tachycardia. Laboratory analysis revealed serum hemoglobin, total calcium, ionized calcium, urea, creatinine, potassium, and glucose levels of 8.7 g/dL, 8.2 mg/dL, 4.7 mg/dL, 87 mg/dL, 3.61 mg/dL, 7.2 mmol/L, and 190 mg/dL, respectively. Coagulation panel and urine analysis were normal. There were wide QT interval and upright T waves in the Electocardiogram (ECG). Nephrologist suggested infusion of Ca and initiation of hemodialysis by these findings. The baseline and predialysis blood pressures of the patients were 147/85 mmHg and 150/90 mmHg, respectively.
A dialysis duration of 2.5 hours was scheduled in order to achieve the target uro-reduction rate of 30%. 1.2 m2 synthetic biocompatible membrane (Fresenius F6 polisulfone low flux fully synthetic biocompatible membrane) was employed. Dialysate bicarbonate value was set to 30 mEq/L. Heparin was not used as this was the first hemodialysis of the patient.
During dialysis, acute bilateral loss of vision developed in the patient and therefore the intervention was terminated. The highest and lowest systolic/diastolic blood pressures recorded during hemodialysis were 90/60 and 80/50 mmHg, respectively.
Ophthalmological inspection revealed that patient's vision was at the hand-motion level, the light reflexes were normal, there was no afferent pupillar defect, bilateral posterior segments, and bilateral intraocular pressures were normal. Findings suggested a central pathology, and the CT scan performed afterwards revealed large hypodense infarct areas in the bilateral occipital and parasagittal posterior region of right parietal lobes (Figures and ). Bilateral carotid artery doppler and echocardiography for differential diagnosis of thromboembolism were normal.
Patient was conscious, cooperating, and well oriented, and all deep tendon reflexes were found to be hyperactive in the neurological evaluation. Also a few days later right hemiparesis appeared in the patient. Therefore patient was accepted in the intensive care unit of the neurology department and received two times of 0,6 cc clexane and three times 10 mg dexametasone a day. Thus our purpose was to protect the ischemic penumbra with anticoagulant and anti-inflammatory effect.
Despite the recovery of hemiparesis, loss of vision continued during followup of the patient. Patient's loss of vision continued and did not recover throughout the followup.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [65, 'years'], 'creatinine': [3.61, 'mg/dL'], 'sex': 'Male'}",17.04721,16.19485,17.89957,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 65 years old. The concentration of Creatinine is 3.61 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.61^(-1.154) * 65^(-0.203) * 1 * 1=17.04721.
Hence, the patient's GFR is 17.04721 mL/min/1.73m²."
3274,9,MDRD GFR Equation,lab test,decimal,pmc-6275454-1,Extracted,"A 66-year-old African American man was referred for outpatient nephrology evaluation in October 2013 for chronic kidney disease, which had progressed to Stage 4 over several years.
His medical history included uncontrolled hypertension, hyperlipidemia, hyperthyroidism treated with radioactive iodine 10 years prior and obesity. Prescribed medications included amlodipine, lisinopril, levothyroxine and aspirin.
Physical examination revealed an obese man with body mass index 35.6 kg/m2, blood pressure of 162/90 mmHg and 2+ pitting edema of the lower extremities. The remainder of his examination was unremarkable.
The creatinine level declined from 2.2 to 2.7 mg/dL within a month. He had nephrotic-range proteinuria of 5.1 g/day as well as hematuria. Results for other analyses, including hepatitis B and C viral serologies, human immunodeficiency virus status, antineutrophilic cytoplasmic antibody, serum and urine protein electrophoreses, complement levels and renal ultrasound were unremarkable. His renal biopsy in December 2013 showed advanced-stage FGN.
Light microscopy of paraffin sections stained with hematoxylin and eosin, periodic acid–Schiff (PAS) and PAS-trichrome showed prominent mesangial expansion and widespread, segmental irregular capillary loop thickening. Two-thirds of the renal cortices showed interstitial fibrosis and tubular atrophy. A Congo red stain was negative.
Direct immunofluorescence (DIF) of the renal cortex showed strong smudgy-to-granular glomerular staining for IgG and the kappa light chains. Slightly weaker, moderate and weak glomerular staining was noted for C3 and the lambda light chains, respectively. Immunofluorescence with the IgG subclass antibodies revealed strong glomerular staining for IgG1, weak staining for IgG4 and no staining for IgG2 and IgG3 ().
Electron microscopy revealed abundant deposition of randomly arranged rigid fibrillary material in the mesangium and along the glomerular capillary loops within the thickened glomerular basement membrane. Fibril diameter was 19.0 ± 1.8 nm.
Three months after his biopsy-proven diagnosis, the patient agreed to a trial of treatment with repository corticotrophin (RC), which is approved for use in a nephrotic-range proteinuria. This medication was chosen in order to avoid the severe systemic immunosuppressive effects of alternative cytotoxic agents such as rituximab, particularly, at his level of progressed fibrosis and interstitial scarring.
He was started on RC 40 U/mL twice weekly for 2 weeks, after which the dose was increased to 80 U/mL twice weekly. We initially observed a rise in proteinuria, with a peak of 8.9 g/day 1 month into treatment, followed by a decline over the following several months with edema resolution and stabilization of the creatinine. After 6 months of treatment, the dose of RC was reduced to 40 U/mL twice weekly in order to minimize the potential adverse effects. Within 8 months of initiating RC treatment, proteinuria resolved to <1 g/day. The patient tolerated the therapy quite well and had no worsening of hypertension control, hypokalemia or hyperglycemia. He experienced mood swings and mild darkening of the skin, but surprisingly reported improved level of energy and memory. After 4 years of follow-up, he has attained partial remission, with complete resolution of nephrotic syndrome and stabilization of renal function completing 45 months of therapy.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [66, 'years'], 'creatinine': [2.7, 'mg/dL'], 'sex': 'Male', 'Race': 'Black'}",28.79914,27.35918,30.2391,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 66 years old. The concentration of Creatinine is 2.7 mg/dL. 
The patient is Black, so the race coefficient is 1.212.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.7^(-1.154) * 66^(-0.203) * 1.212 * 1=28.79914.
Hence, the patient's GFR is 28.79914 mL/min/1.73m²."
3275,9,MDRD GFR Equation,lab test,decimal,pmc-7868892-1,Extracted,"A 36-year-old previously healthy man presented to the emergency department with 2 days of worsening dyspnea. He had fever, cough, and fatigue during the week before presentation. His initial vital signs included temperature 39.2 °C, blood pressure 141/105 mmHg, respiratory rate 22 breaths per minute, heart rate 142 beats per minute, and oxygen saturation 92% on room air. Physical examination revealed mild crackles in both basal lung fields. He denied myalgia. Pertinent laboratory findings included the following: white blood cell count 5.7 × 103/μL (reference, 3.3–8.6 × 103/μL), lymphocyte count 11.7% (reference, 25–55%), platelet count 165 × 103/μL (reference, 158–348 × 103/μL), CRP 3.17 mg/dL (reference, 0.02 mg/dL or less), lactate dehydrogenase 220 U/L (reference, 124–222 U/L), CK 170 U/L (reference, 59–248 U/L), myoglobin 20 ng/mL (reference, 20–85 ng/mL), creatinine 0.7 mg/dL (reference, 0.65–1.07 mg/dL), D-dimer 0.7 ng/mL (reference, 1 ng/mL or less), and brain natriuretic peptide 3.9 pg/mL (reference, 18.4 pg/mL or less). Chest radiography showed patchy bilateral opacities in the lung parenchyma, and computed tomography of the chest showed bilateral ground-glass opacities. We treated the patient with oxygen inhalation, azithromycin, and ceftriaxone, and with antipyretics to control his high fever. On day 2 after admission, a reverse-transcriptase polymerase chain reaction assay detected the presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA by nasopharyngeal swab. The next day, his condition deteriorated, with hypoxemia. We started him on favipiravir [3600 mg on day 1 and 1600 mg per day on day 2 and subsequently, median treatment 14 days (IQR, 12 to 14 days)]. Anti-inflammatory agents, such as steroids and tocilizumab, were not administered during admission. On day 4 after admission, his condition continued to deteriorate, with fever, hypotension, and hypoxemia. He was administered midazolam, fentanyl, and rocuronium, and underwent endotracheal intubation. He was admitted to the intensive-care unit (ICU).
After ICU hospitalization, sedative therapy with dexmedetomidine was used for mechanical ventilation support. His condition continued to deteriorate, with high fever and high ventilatory requirements. High body temperature and CRP levels, systemic inflammatory response syndrome, and refractory hypoxemia (PaO2:FiO2 159 mmHg and FiO2 of 0.6 with PEEP 15 cmH2O) continued.
On hospital day 9, his laboratory examination revealed that CK and myoglobin levels started to increase (to 26,046 U/L and 3668 ng/mL, respectively) (Fig. ), and he developed muscle rigidity on the jaw and extremities in addition to tachycardia, tachypnea, and diaphoresis. Blood gas analysis showed that PaCO2 was 51 mm Hg (reference 35–45 mm Hg). His other laboratory examinations were normal: sodium, 144 mmoL/L (reference 138–145 mmoL/L); potassium, 4.7 mmoL/L (reference 3.6–4.8 mmoL/L); phosphorous, 3.2 mg/dL (reference 2.7–4.6 mg/dL); thyroid stimulation hormone (TSH), 0.94 (reference 0.34–3.8 μIU/mL); free triiodothyronine (FT3), 2.21 (reference 2–3.8 pg/mL); and free thyroxine (FT4), 1.04 (reference 0.8–1.5 ng/dL). Fatty-acid oxidation disorder was unlikely due to normal free carnitine [50.6 μmol/L (reference, 36–74 μmol/L)] and acyl carnitine [9.2 μmol/L (reference, 6–23 μmol/L)] levels. The patient was diagnosed with malignant hyperthermia associated with a late complication of COVID-19, although he had no hereditary predisposition to malignant hyperthermia or neuroleptic malignant syndrome. In addition to ongoing treatment, he received a total of a 3-L bolus of intravenous crystalloids. After fluid therapy, CK and myoglobin levels tended to decrease (to 14,047 U/L and 2179 ng/mL, respectively). However, on the next day, although he continued to receive fluid resuscitation, his CK and myoglobin levels were elevated again (to 18,205 U/L and 2612 ng/mL, respectively), and his high body temperature and CRP and ferritin levels persisted (Fig. ). On the other hand, compartment syndrome was unlikely because his color of skin and pulse of the extremities revealed no abnormalities. We started him on 20 mg dantrolene intravenously four times a day from 14 to 16 days after admission and 50 mg orally three times a day over the next 2 days. Consequently, his body temperature started to decrease, and he showed a decrease in CK, myoglobin, CRP, and ferritin levels (Fig. ). It was possible to extubate him on the 17th day after admission. His clinical condition continued to improve. After a negative SARS-CoV-2 test, we finally discharged him to his home on the 28th day after admission.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [36, 'years'], 'creatinine': [0.7, 'mg/dL'], 'sex': 'Male'}",127.60436,121.22414,133.98458,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 36 years old. The concentration of Creatinine is 0.7 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 0.7^(-1.154) * 36^(-0.203) * 1 * 1=127.60436.
Hence, the patient's GFR is 127.60436 mL/min/1.73m²."
3276,9,MDRD GFR Equation,lab test,decimal,pmc-5588616-1,Extracted,"A 21-year-old Japanese woman was admitted to our hospital because of proteinuria and hematuria. She had been diagnosed at birth with persistent cloaca and congenital esophageal atresia, and underwent enterostomy, cystostomy, and radical esophageal surgery, followed by repair of persistent cloaca and colostomy closure 2 years later. She was followed-up at the pediatric surgery and urology department, and developed with no major problems. Proteinuria and hematuria were detected at routine examination 7 months prior to admission for the first time. No urological problems were detected at a visit to the urology department 3 months before admission. She had mild edema before admission; however its onset had been gradual and it was therefore not clear when the edema had started.
On admission, the patient’s height was 158.6 cm, her weight was 53.0 kg, and her blood pressure was 101/80 mmHg. Physical examination revealed an abdominal midline operation scar and pretibial pitting edema. Urinary examination revealed a protein level of 3+ and 5–9 red blood cells per high-power field. Her urine protein/creatinine ratio was 3.38 g/gCr, blood urea nitrogen was 13.2 mg/dL, serum creatinine was 0.73 mg/dL, and serum albumin was 3.6 g/dL. Serum C3 was 25 mg/dL, C4 was 18.5 mg/dL, and 50% hemolytic unit of complement (CH50) was 13 U/mL. Chromosome G banding revealed a normal karyotype 46XX. Kidney ultrasound showed no kidney deformity. Kidneys size was normal.
A renal biopsy contained 24 glomeruli, all of which showed moderate to severe mesangial hypercellularity and increased homogenous materials in the mesangium. Which were positive with periodic acid-Schiff and were negative with methenamine silver (Fig. ). One glomerulus revealed fibrous crescent formation, and 11 showed segmental double contour of glomerular basement membrane. Immunofluorescence microscopy showed slight staining for fibrinogen, but no staining for IgG, IgA, IgM, kappa light chain and lambda light chain (Fig. ). Electron microscopy showed massive granular deposits in the mesangial area and some subepithelial area (Fig. ). According to these findings, we speculated fibronectin glomerulopathy as a diagnosis. Thus, we performed immunoassays using anti-human fibronectin antibodies. The staining with IST-4, which detects plasma and cell-associated fibronectin, was positive but no staining was observed with IST-9, which stains only cell-associated fibronectin (Fig. ). The mesangial deposits were therefore shown to comprise plasma fibronectin. The patient was finally diagnosed as fibronectin glomerulopathy.
Her family history was investigated further. Although her mother and younger sister had previously been detected to have proteinuria, their urine and blood tests were normal. Her father showed no urinary abnormalities and normal kidney function at his annual health examination. Given that no family history of renal disease could be identified, the current case was determined to be sporadic. The patient and her mother underwent genetic testing of the FN1 gene, which revealed no abnormalities.
Treatment with an angiotensin II receptor antagonist and a sodium-restricted diet were started. However, 10 months after the kidney biopsy, the patient’s proteinuria had increased and her renal function was deteriorated, with a urine protein/creatinine ratio of 9.52 g/gCr, serum creatinine 0.86 mg/dL. Her serum albumin decreased to 2.0 g/dL.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [21, 'years'], 'creatinine': [0.86, 'mg/dL'], 'sex': 'Female', 'Race': 'Asian'}",83.29525,79.13049,87.46001,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 21 years old. The concentration of Creatinine is 0.86 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.86^(-1.154) * 21^(-0.203) * 1 * 0.742=83.29525.
Hence, the patient's GFR is 83.29525 mL/min/1.73m²."
3277,9,MDRD GFR Equation,lab test,decimal,pmc-6534021-1,Extracted,"A previously healthy 55-year-old female without known comorbidities was admitted to the General Practice Clinic of Hospital Geral Dr. Waldemar Alcântara (HGWA). She complained of weakness, paresthesia, and a burning sensation in her lower limbs she had been feeling for three years along with macular hyperchromic lesions on the soles of her feet. The patient went to a dermatologist nine months prior to admission and was diagnosed with contact eczema. She was prescribed topical corticosteroids and a moisturizing agent. One month before hospitalization the patient had pain, hyperemia, and bullous lesions on her right foot, which ruptured spontaneously letting out a serous secretion. She improved after taking unspecified medication. Five days prior to admission the patient developed oliguria, lower limb edema, and abdominal pain - mainly in the hypogastrium - along with nausea and hyporexia. She went to an Emergency Unit and was found to have a serum creatinine (SCr) level of 21.94 mg/dL and a blood urea nitrogen (BUN) level of 260 mg/dL, which triggered her referral to the hospital cited above. A test run six months prior to her arrival at the hospital read SCr = 0.7 mg/dL and blood urea= 37.4 mg/dL. Upon admission, she was found to be generally well and hydrated, pale 2+/4+, eupneic, conscious and oriented. Her heart was normal on auscultation while crackles were heard bilaterally on the bases of her lungs. She had a flaccid distended abdomen on account of fat accumulation and complained of pain on her hypogastrium upon palpation. No evidence of visceromegaly was found. Her peripheral pulses were palpable, and she had lower limb edema 1+/4+ and hyperchromic scar tissue-like lesions on the soles of her feet (). Examination of the upper limbs revealed the interosseous muscles of her right hand were atrophied. Neurological examination showed she had predominantly distal paresis of the lower limbs (grade IV on the left and III on the right leg), grade IV paresis of the upper limbs, and anesthesia on the soles of her feet.
Lab tests performed upon admission () were negative for HIV, syphilis, and hepatitis B and C. Tests for cytoplasmic (c-ANCA) and perinuclear (p-ANCA) antineutrophil cytoplasmic antibodies were negative; ANCA was atypical; the test for cryoglobulins was negative. Serum protein electrophoresis showed polyclonal increases of alpha-1-globulin and gamma globulins. Ultrasound examination of the kidneys and urinary tract showed normal-sized kidneys with irregular contours (RK: 9.1 x 4.3 cm, LK: 9.2 x 5.0 cm) and good corticomedullary differentiation. Transthoracic echocardiogram showed good cardiac function (EF 61%) and no vegetation. Fat pad biopsy was negative for amyloidosis. Electroneuromyography revealed distal mixed axonal demyelinating sensorimotor polyneuropathy with a predominant axonal component and preferential involvement of the right leg, producing severe impairment of the lower limbs and moderate to mild dysfunction of the upper limbs, as seen in cases of infectious neuropathies (including Hansen's disease), uremia, and vasculitis.
The patient was started on hemodialysis three times a week. Neurological assessment showed she had multibacillary Hansen's disease (positive for bacilli agglomerates). The patient was prescribed polychemotherapy with rifampicin, dapsone, and clofazimine. The choice was made to prescribe prednisone 1mg/kg/day two weeks after the start of treatment for Hansen's disease, since the patient had signs consistent with RPGN; she was waiting to undergo a kidney biopsy, which was performed only after 27 days of steroid therapy. The pathology specimen was satisfactory and featured 22 glomeruli and two medium-caliber vessels. Ten glomeruli had global sclerosis and three had fibro-cellular crescents (). The other glomeruli had mild mesangial proliferation (); findings such as polymorphonuclear infiltration and subepithelial or mesangial deposits (humps) were not seen. Mild to moderate interstitial fibrosis (), acute tubular necrosis, and benign nephrosclerosis were also described. Immunofluorescence showed strong and diffuse labeling for C3 (3+ in 4+) in the mesangium, and barely positive results for IgA (1+ in 4+) in the mesangial compartment, following a pattern similar to that of C3 ( and ).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [55, 'years'], 'creatinine': [21.94, 'mg/dL'], 'sex': 'Female'}",1.63065,1.54912,1.71218,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 55 years old. The concentration of Creatinine is 21.94 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 21.94^(-1.154) * 55^(-0.203) * 1 * 0.742=1.63065.
Hence, the patient's GFR is 1.63065 mL/min/1.73m²."
3278,9,MDRD GFR Equation,lab test,decimal,pmc-4940515-1,Extracted,"A 64-year-old 87 kg man with a past medical history of hypertension for 10 years, type 2 diabetes for 13 years, painful diabetic neuropathy, mild depression, and recent diabetic foot infection (DFI) related hospitalization initially presents to the emergency room with a 2-week history of left lower extremity edema, redness, and pain that limits his normal daily activities. He has a lesion close to his small toe that is macerated and foul-smelling. His physical examination was notable for temperature 38.2°C, blood pressure 145/90 mmHg, heart rate 92 beats/minute, respiratory rate 19 breaths/minute, and 1+ lower extremity edema. His initial laboratory values which were ordered in emergency room include sodium 139 mEq/L, potassium 4.3 mEq/L, BUN 19 mg/dL, SCr 0.9 mg/dL, glucose 180 mg/dL, A1C 8%, WBC 15 × 103 cells/mm3, hemoglobin 12 g/dL, hematocrit 36%, and platelet count 290,000 cells/mm3.
According to a patient his home drugs include hydrochlorothiazide 25 mg/day, lisinopril 20 mg/day, glyburide 10 mg/day, metformin 1000 mg twice daily, olanzapine/fluoxetine, and aspirin 81 mg/day.
He was admitted to the hospital for the cleansing, irrigation, and surgical debridement of his ulcer. The surgical culture of ulcer specimen was positive for methicillin-resistant Staphylococcus aureus (MRSA) with following susceptibilities: Vancomycin (R), Clindamycin (S), linezolid (S), and Trimethoprim/sulfamethoxazole (S).
On the second day of admission he was started on IV linezolid 600 mg every 12 hrs and IV moxifloxacin 400 mg/day for the treatment of DFI. The first dose of antibiotics was uneventful. However, after the second dose of linezolid, he became severely nauseated for which he was given IV metoclopramide at 10 mg IV every 6 hrs.
After 12 hrs patient was constantly nauseated and febrile (38.7°C). He was confused, diaphoretic, and dyspneic. ECG showed tachycardia at pulse 104 bpm without ST or T wave abnormalities; blood pressure was 127/87 mmHg. He started to desaturate gradually (oxygen saturation 84%) and was maintained on oxygen therapy via high flow nasal cannula.
On the third day of the hospital, he continued to desaturate and remained febrile and hypertensive at 160/90 mmHg; blood and urine cultures were ordered and returned negative. An X-ray of the chest was clear. Complete blood count showed leukocytosis.
On neurologic examination, he was rigid asymmetrically in upper and lower extremities and right lower limb showed hyperreflexia with clonus. On neurological examination nuchal rigidity was negative, and both eyes were responsive to light; all signs of meningism were negative. Due to the rigidity of extremities, a blood creatine phosphokinase (CPK) level was checked, and it was 1856 mcg/L. Magnetic resonance imaging of the brain was normal. There was no evidence of epileptiform activity on a 12-hour continuous electroencephalography.
After ruling out all possible infections causes of aforesaid mentioned symptoms and giving the consideration on persistent muscle rigidity, high CPK levels, and causality of patient condition with the metoclopramide administration, a clinical diagnosis of the neuroleptic malignant syndrome was made and metoclopramide was stopped. The patient was treated with IV dantrolene 1 mg/Kg stat dose, carbidopa 25 mg/levodopa 100 mg PO, and baclofen 5 mg PO for rigidity. He was maintained on fluid and IV dimenhydrinate 100 mg q 4 hrs for nausea. Labetalol was used to normalize high blood pressure.
Twelve hours after the dantrolene treatment CPK levels were rechecked; it was 780 mcg/L and physical examination showed improvement in rigidity. However, the patient has still exhibited a high fever with diaphoresis, high blood pressure with labetalol deescalation, consciousness disturbance, and myoclonus. The repeat blood complete count showed leukocytosis. Blood culture was negative. In arterial blood gas analysis, pCO2 was 27.2 mmHg and pO2 was 69.6 mmHg, sO2 81.3%. He was maintained on oxygen.
Because physicians suspected that, despite the execution of NMS treatment, her persistent increase in blood pressure, hyperthermia, and clonus may have been linked to serotonin syndrome. This information, together with his negative workup, prompts the medical team for medication reconciliation. Thorough medication reconciliation revealed that patient was recently started on olanzapine/fluoxetine by a general practitioner 4 days ago and the last dose was taken by the patient 1 day before arriving at ER.
At this point, after the consultation of a clinical pharmacist, it was decided to discontinue linezolid and maintain the patient on fluid, labetalol 20 mg IV, as needed for the control of blood pressure and cyproheptadine hydrochloride 12 mg PO stat, followed by 4 mg every 6 hours for 24 hours. Clonazepam was given to control myoclonus. After 24 hours all of the patient's symptoms abated except slight fever and mild clonus and hyperreflexia. The patient was discharged from the hospital on the 7th day with a prescription of PO cyproheptadine, PO paracetamol, and PO TMP/SMX with moxifloxacin for DFI treatment.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [64, 'years'], 'creatinine': [0.9, 'mg/dL'], 'sex': 'Male'}",84.95475,80.70701,89.20249,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 64 years old. The concentration of Creatinine is 0.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 0.9^(-1.154) * 64^(-0.203) * 1 * 1=84.95475.
Hence, the patient's GFR is 84.95475 mL/min/1.73m²."
3279,9,MDRD GFR Equation,lab test,decimal,pmc-3657446-1,Extracted,"A thirty-nine-year-old African American female with no significant past medical history presented to the emergency department cachectic and “feeling sick” for two weeks with generalized fatigue, malaise, and productive cough with hemoptysis. Review of systems was positive for anorexia, unquantified weight loss, nausea, vomiting, and dizziness. She had no history of hypertension, hematologic disorders, or cancers in herself or in her family.
The clinical examination at the time of admission revealed severe pallor and oral candidiasis with the rest of the examination benign. Her mental status was normal and she was alert and oriented to person, place, and time. Medical research scale (MRC) grade was 4/5 in all extremities, likely secondary to deconditioning and severe anemia. The patient's vital signs were normal, including a blood pressure of 122/65 mm Hg.
On admission, laboratory analysis revealed severe abnormalities including blood urea nitrogen (BUN) of 138 mmol/L, serum creatinine of 22.3 μmol/L, hemoglobin of 4.9 g/dL, and hematocrit of 16.4% with a normocytic anemia. Arterial blood gas revealed pH 7.17, pCO2 18.8 mm Hg, pO2 143 mm Hg, and oxygen saturation of 99 percent on room air. The other laboratory parameters including white blood count, chemistry panel, platelets, and liver function tests were within normal limits. Urine toxicology screen and pregnancy tests were negative.
She was admitted to the intensive care unit and placed on droplet precautions until tuberculosis was ruled out. She was given 4 units of packed red blood cells after ruling out reversible causes of blood loss. Gynecologic history included eleven live births with poor antenatal care. During the hospital stay, the patient was diagnosed, for the first time, with new onset ESRD classified as Stage 5 chronic kidney disease. It had gone unchecked and the patient was unaware of any kidney issues. During this admission, She received multiple rounds of dialysis which brought her blood urea nitrogen and creatinine ratio (BUN/Cr) to near normal ranges over 3 days. Also, due to the patient's oral candidiasis her HIV status was checked. HIV ELISA and Western Blot were positive with a CD4 T lymphocyte count of 112 cells/μL and a viral load of 780,000 cells/mm3.
The patient was stable for the first 4 days until she had 2 seizures within 24 hours and became nonverbal, uncooperative, and encephalopathic. By this point, her BUN/Cr was brought down to 25/6.2 from the rounds of dialysis. Her blood pressure during the period of seizure was 152/96 mm Hg, which was thought to be secondary to the seizures, and electrolytes were within normal limits. She responded to painful stimuli, pupils were equally reactive, deep tendon reflexes intact, MRC rated 3/5, and there was no papilledema or neck stiffness. Keppra was started for seizure control.
Computed tomography (CT) without contrast showed white matter hypodensity in the posterior parietal-occipital lobes with the remaining findings within normal limits (). A CT performed the following day confirmed the presence of hypodense regions but with newly noted small hemorrhages within the parietal and occipital regions. Magnetic resonance imaging (MRI) without contrast revealed areas of T2 prolongation in the subcortical white matter, predominantly in the occipital and parietal regions with scattered foci of susceptibility artifact bilaterally in the occipital lobes. The largest focus measured 10 cm × 0.6 cm in the left occipital lobe (). A repeat MRI with gadolinium showed a stable image with no pathologic enhancement and the foci of hemorrhage remained stable ().
Given that PRES is a diagnosis of exclusion and based on clinical and radiographic findings, infectious causes of this acute change in mental status were ruled out. Cerebrospinal fluid analysis showed protein of 164 mg/dL, glucose of 49 mg/dL, 630 RBCs/mm3, 0 WBCs/mm3, and LDH of 37 U/L. No acid fast bacilli were seen. Polyomavirus, herpes simplex virus 1 and 2, cytomegalovirus, Epstein-Barr virus, Toxoplasma Gondii IgG, and VDRL were negative. Two sets of blood and urine cultures were negative. There were no further complications with mental status and her cognitive function recovered completely. The patient's vital signs, hemoglobin, and BUN/Cr were stable when she was discharged to home with follow up at the HIV and renal clinics.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [39, 'years'], 'creatinine': [22.3, 'µmol/L'], 'sex': 'Female', 'Race': 'Black'}",416.21461,395.40388,437.02534,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 39 years old. The concentration of Creatinine is 22.3 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 22.3 µmol. To convert 22.3 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 22.3 µmol Creatinine * 1e-06 mol/µmol = 2e-05 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 2e-05 mol Creatinine * 113.12 g/mol = 0.00226 g Creatinine. To convert 0.00226 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00226 g Creatinine * 1000.0 mg/g = 2.26 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 2.26 mg Creatinine/10.0 dL = 0.226 mg Creatinine/dL. The concentration value of 22.3 µmol Creatinine/L converts to 0.226 mg Creatinine/dL. 
The patient is Black, so the race coefficient is 1.212.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.226^(-1.154) * 39^(-0.203) * 1.212 * 0.742=416.21461.
Hence, the patient's GFR is 416.21461 mL/min/1.73m²."
3280,9,MDRD GFR Equation,lab test,decimal,usmle-4818,Extracted,"A 29-year-old woman presents to the emergency department with joint pain and a notable rash. She has had joint pain for the past 12 months but noticed the rash recently as well as generalized malaise. She states her joint pain is symmetric, in her upper extremities, and is worse in the morning. Her temperature is 97.6°F (36.4°C), blood pressure is 111/74 mmHg, pulse is 83/min, respirations are 14/min, and oxygen saturation is 98% on room air. Laboratory studies are ordered as seen below.

Hemoglobin: 10 g/dL
Hematocrit: 30%
Leukocyte count: 6,800/mm^3 with normal differential
Platelet count: 207,000/mm^3

Serum:
Na+: 140 mEq/L
Cl-: 101 mEq/L
K+: 4.9 mEq/L
HCO3-: 21 mEq/L
BUN: 30 mg/dL
Glucose: 120 mg/dL
Creatinine: 1.8 mg/dL

The patient is ultimately admitted to the hospital.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [29, 'years'], 'creatinine': [1.8, 'mg/dL'], 'sex': 'Female'}",33.26524,31.60198,34.9285,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 29 years old. The concentration of Creatinine is 1.8 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.8^(-1.154) * 29^(-0.203) * 1 * 0.742=33.26524.
Hence, the patient's GFR is 33.26524 mL/min/1.73m²."
3281,9,MDRD GFR Equation,lab test,decimal,pmc-5031831-1,Extracted,"Our patient was a 93-year-old Caucasian lady who presented with a three-day history of right upper quadrant abdominal pain, nausea, and vomiting. She had an episode of acute bronchitis two weeks before she presented to us, which was treated with Levofloxacin. A week after initiation of treatment for her acute bronchitis, the patient developed a purpuric rash involving both her lower extremities, which gradually progressed to involve her upper extremities as well. Upon further questioning, the patient revealed she had an episode of painless hematuria three days prior to the current presentation.
Her past medical history was significant for four-vessel coronary artery bypass grafting (CABG) in 1995, chronic atrial fibrillation on anticoagulation with warfarin, and hypertension and chronic kidney disease stage 3 with baseline creatinine in 1.3–1.5 range. Social history was unremarkable.
Physical exam revealed RUQ tenderness and a purpuric rash involving both upper and lower extremities.
Initial laboratory analysis showed leukocytosis with a white blood cell count of 21.2 k/mcl and creatinine of 3.39 mg/dL. Urinalysis showed hematuria and proteinuria with negative nitrites and leucocyte esterase. Urine eosinophils were negative. Liver function tests, lactic acid, procalcitonin, and cardiac enzymes were all within normal limits. An ultrasound of the abdomen showed findings suggestive of acute cholecystitis and no abnormalities in the renal anatomy. The general surgery team was consulted and the patient underwent a laparoscopic cholecystectomy.
The patient recovered well from her cholecystectomy and did not have any more episodes of abdominal pain; however, her kidney function continued to worsen progressively with creatinine peaking at 4.97 mg/dL. Her urine output became minimal and she began to show signs of volume overload on exam. An extensive work-up was done to evaluate the cause of her renal failure. Antinuclear antibodies (ANA), anti-neutrophil cytoplasmic antibodies (ANCA), anti-glomerular basement membrane antibody (anti-GBM Ab), serology for hepatitis B and C, and antistreptolysin O titres were all negative. Complement levels (C3 and C4) were low. IgA levels were normal. Rapid and progressive deterioration of the renal function prompted a renal biopsy, which showed an IgA nephropathy. A diagnosis of adult onset HSP was made based on the presence of nonthrombocytopenic purpura with renal biopsy showing IgA nephropathy ().
The patient was initiated on high dose intravenous methylprednisolone for 3 days followed by oral prednisone, but her renal function continued to worsen eventually requiring hemodialysis. Patient also developed multilobar pneumonia with hypoxemic respiratory failure. After much discussion with the patient and family, the patient did not want further dialysis and was discharged home on hospice. She passed away within a few days.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [93, 'years'], 'creatinine': [3.39, 'mg/dL'], 'sex': 'Female', 'Race': 'White'}",12.64706,12.01471,13.27941,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 93 years old. The concentration of Creatinine is 3.39 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 3.39^(-1.154) * 93^(-0.203) * 1 * 0.742=12.64706.
Hence, the patient's GFR is 12.64706 mL/min/1.73m²."
3282,9,MDRD GFR Equation,lab test,decimal,pmc-7455384-1,Extracted,"A 57-year-old man was admitted to the ED with complaints of syncope and weakness. We noticed that in his medical history, leeches were applied to treat the diabetic wounds on his feet two hours before he attended our clinic. After this, the leeches spontaneously detached but he observed bleeding from his bites and bleeding did not stop in spite of compression with tight bandages. A review of the patient’s past medical history revealed hypertension, diabetes mellitus, diabetic foot, ischemic heart disease and coronary artery bypass surgery.
Vital signs were as follows; fever: 36.6°C, blood pressure: 85/50 mmHg, heart rate: 112/min and respiratory rate: 28/min. Physical examination revealed tenderness in the whole abdomen. Ampulla was empty with rectal examination. There was an ulcerative lesion with size 5x3 cm on the site of the amputated first toe. Additionally, there were multiple bites due to leech therapy on both feet (Figure ).
Laboratory tests indicated the following: hemoglobin: 7.6 g/dL, white blood cells: 9370/mm3, platelets: 147000/mL, blood urea nitrogen: 29.1 mg/dL, creatinine: 1.98 mg/dL, glucose: 527 mg/dL, Na: 127 mmol/L, K: 6 mmol/L, CL: 94.5 mmol/L, C-reactive protein: 1.27 mg/dL and other routine blood tests and coagulation functions were all normal. Blood gas analysis revealed pH: 7.26, pO2: 86 mmHg, and bicarbonate: 20.2 mmol/L. Abdominal ultrasonography (USG) showed gas in the intrahepatic biliary ducts. No obstructive pathology was found to mesenteric blood flow on Doppler USG. CT without intravenous contrast was performed because of abnormal renal function tests. CT revealed gas near the stomach, among colon segments (pneumatosis cystoides intestinalis, PSI) and intrahepatic biliary ducts in central and left hepatic lobe (hepatic portal venous gas, HPVG) (Figure , Figure , respectively).
The patient was referred to another hospital that had an intensive care unit and started conservative treatment with antibiotics and intravenous fluid. Twelve hours after treatment, his general condition did not improve and signs of diffused peritonitis were observed on abdominal examination. The patient underwent exploratory laparotomy. Necrosis was found in the terminal ileum and the entire colon during laparotomy. Doppler USG detected low flow in the vessels supplying these necrotic segments. However, resection was decided due to necrosis of these segments. These necrotic intestinal segments were resected and an end-ileostomy was performed. He had an uneventful recovery and was discharged on the 17th postoperative day.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [57, 'years'], 'creatinine': [1.98, 'mg/dL'], 'sex': 'Male'}",35.01417,33.26346,36.76488,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 57 years old. The concentration of Creatinine is 1.98 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.98^(-1.154) * 57^(-0.203) * 1 * 1=35.01417.
Hence, the patient's GFR is 35.01417 mL/min/1.73m²."
3283,9,MDRD GFR Equation,lab test,decimal,pmc-6695237-1,Extracted,"A 54-year-old female, with a past medical history significant for a recent diagnosis of diffuse cutaneous systemic sclerosis, hypertension, and chronic kidney disease stage three, and a history of adrenal insufficiency presented to the emergency room due to generalized weakness. The patient reported that her weakness started in the lower extremities and had been progressively worsening with difficulty both standing up and sitting. She was unable to walk for the past week. She also reported unintentional weight loss of 70 pounds for the past nine months, inadequate oral intake, decreased urine output, accompanied by dry eyes and mouth, with erythematous non-pruritic and non-painful rash in the inner thighs and buttocks.
On admission, vital signs were only significant for a blood pressure of 160/80 mmHg. The physical examination was remarkable for loss of wrinkles, maculopapular rash, bilateral lower extremity with pitting edema up to the ankles, and skin breakdown in the inner thighs and sacral area. Neurological examination was normal except for decreased motor strength 3/5 in the upper extremities and 2/5 in the lower extremities. Laboratory work-up was significant for a hemoglobin level of 10.8 g/dl (normal 12-15.5 g/dl), potassium 5.8 mmol/L (normal 3.4-5.1 mmol/L), magnesium 1.5 mg/dl (normal 1.7-2.4 mg/dl), bicarbonate 14 mmol/L (normal 21-32 mmol/L), worsening creatinine 6.83 mg/dl (normal 0.51-0.95 mg/dl) (baseline creatinine 1.8-2.1 mg/dl, six months ago), and blood urea nitrogen (BUN) 107 mg/dl (normal 6-20 mg/dl). An electrocardiogram (EKG) showed a normal sinus rhythm with no other changes and her chest X-ray showed no abnormalities (Figure ). The initial treatment consisted of treatment for hyperkalemia with regular insulin 10 units, dextrose, and polystyrene sulfonate. The patient was admitted for further workup of kidney dysfunction and weakness. The rheumatology team recommended immunologic workup, kidney biopsy, and intravenous fluid resuscitation.
During the second day of hospital admission, the patient started to complain of sudden onset chest pain and shortness of breath. Her vital signs were significant for blood pressure 170/90 mmHg, 115 beats per minute, and tachypnea with an oxygen saturation of 89%. The patient was placed on 4 liters of oxygen via a nasal cannula. Her physical examination was remarkable for non-reproducible substernal chest pain, right lower lobe crackles, diffused wheezing throughout, and marked pitting edema in bilateral lower extremities up to the knee. Intravenous fluids were stopped, and a trial of albuterol inhaler was given, with no improvement. As part of the initial workup, the laboratory was remarkable for elevated troponin 0.07 ng/ml (normal <0.05 ng/ml), d-dimer 2.5 mg/l (normal <0.57 mg/l) and procalcitonin 19.9 ng/ml (normal<0.10 ng/ml). A new electrocardiogram (EKG) showed sinus tachycardia with no ischemic changes, and chest X-ray showed current ground-glass densities with interstitial opacities bilaterally (Figure ). The patient was transferred to the medical intensive care unit (MICU) for further care.
At arrival to the MICU, she was progressively getting worse and using accessory respiratory muscles. Her arterial blood gas (ABG) showed pH 7.20 unit (normal 7.35-7.45 unit), CO2 22 mmHg (normal 32-45 mmHg) and O2 54 mmHg (normal 83-108 mmHg) on 6 L through a nasal cannula. The patient was transitioned to bilevel positive airway pressure (BiPAP), but no improvement was achieved. Later, ABG with worsening acidosis and CO2 retention (PH 7.15 and CO2 45), a potassium level of 6.2 mmol/L (normal 3.4-5.1 mmol/L), BUN 150 mg/dl (normal 6-20 mg/dl), and creatinine 7.9 mg/dl (normal 0.51-0.95 mg/dl). The decision was made to proceed with intubation for ventilatory support; she was started on empiric antibiotics (ceftriaxone and azithromycin), intravenous heparin for suspected pulmonary embolism, and emergent dialysis for worsening uremia. Repeated chest X-ray after intubation showed worsening bilateral diffuse interstitial opacities concerning for different etiologies, including pleural effusion, pneumonia, or pulmonary hemorrhage (Figure ). Later during the day, a small amount of blood through the endotracheal tube (ETT) was noted, thereby intravenous heparin was held.
At this point, owing to the findings of worsening kidney function, fluid overload, and persistent hypertension with systolic blood pressure >200/100 mmHg, the primary diagnosis was SRC. Management includes starting the patient on angiotensin-converting enzyme (ACE) inhibitor. Further extensive investigations only showed lower levels of decreased hemoglobin 7.7 g/dl (normal 12-15.5 g/dl), low complement C3 40mg/dl (normal 79-152mg/dl), and high lactate dehydrogenase (LDH) levels of 625 U/L (normal 82-240 U/L). The peripheral smear showed mildly hypochromic anemia and rare polychromatophilic cells. Imaging included transthoracic echocardiogram that revealed concentric hypertrophy, ejection fraction 50%-55%, and grade one diastolic dysfunction. Bilateral lower extremities ultrasound gave no evidence of deep venous thrombosis. Computed tomography of the chest showed bibasilar atelectatic changes, no gross evidence of interstitial lung disease, and cardiomegaly (Figure ).
During the fourth day of hospitalization, the patient's condition worsened, with persistent moderate to large amounts of blood through the ETT with a significant drop in the hemoglobin to 5.7 g/dl (normal 12-15.5 g/dl) from which she received a unit of packed red blood cells. Bronchoscopy was later done, revealing moderate thick bloody secretions in the tracheobronchial tree consistent with pulmonary hemorrhage. Intravenous steroids were held to avoid the worsening of SRC. The kidney biopsy reported an acute thrombotic microangiopathy type pattern with severe vascular involvement, most consistent with scleroderma renal crisis associated with tubular necrosis (Figure ).
Ultimately, the patient was transferred to a tertiary scleroderma center, in which she significantly improved after supportive treatment and infusion with cyclophosphamide. The patient was successfully extubated and was transitioned to acute inpatient rehabilitation.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [54, 'years'], 'creatinine': [7.9, 'mg/dL'], 'sex': 'Female'}",5.31991,5.05391,5.58591,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 54 years old. The concentration of Creatinine is 7.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 7.9^(-1.154) * 54^(-0.203) * 1 * 0.742=5.31991.
Hence, the patient's GFR is 5.31991 mL/min/1.73m²."
3284,9,MDRD GFR Equation,lab test,decimal,pmc-6890156-1,Extracted,"A 60-year-old male was admitted with a chief complaint of palpitations, abdominal pain, and diarrhea. Palpitations were sudden in onset and woke up the patient from sleep and were persistent, which prompted him to seek medical attention. The patient was having diarrhea and abdominal pain for two days before the presentation. Past medical history was significant for polycystic kidney disease resulting in end-stage renal disease, bilateral nephrectomies with living unrelated kidney transplant that failed after 13 years, and he was on peritoneal dialysis for two years. Other history details include hypertension, diabetes, hyperlipidemia, and coronary artery disease with four-vessel coronary artery bypass grafting. Home medications include aspirin 81 milligrams (mg) daily, ticagrelor 90 mg twice a day, calcitriol 0.25 micrograms daily, carvedilol 6.25 mg twice a day, olmesartan 40 mg daily, vitamin d2 50,000 units weekly, and insulin sliding scale.
The vital signs in the ER were a temperature of 36.5 centigrade, pulse rate of 80 beats per minute (bpm), respiratory rate of 18 breaths per minute, and blood pressure of 123/76 mmHg. Physical examination revealed that the patient was in sinus rhythm, with no rubs or gallops or murmurs. Abdominal examination revealed a distended, tender abdomen with a peritoneal dialysis catheter in the left lower quadrant. The rest of the physical examination was unremarkable.
Investigations revealed electrocardiogram with 80 bpm in sinus rhythm, premature complexes, and nonspecific conduction delay as shown in Figure . Laboratory data showed hemoglobin 7.8 g/dL, white blood cell (WBC) count 7220 mm3, platelet count 150,000 mm3, sodium 131 mmol/L, potassium 4.3 mmol/L, bicarbonate 20 mmol/L, blood urea nitrogen 76 mg/dL, creatinine 12.92 mg/dL, albumin 2.8 g/dL, and troponin I 15.01 ng/mL. The peritoneal fluid effluent revealed peritoneal fluid WBC 14,309 cells/uL, with 89% predominant neutrophils. Peritoneal fluid Gram stain revealed >100 WBC, and no organisms were seen. The patient was started on treatment for peritonitis with empiric intraperitoneal vancomycin and ceftazidime. The patient underwent coronary intervention because of non-ST elevation myocardial infarction (NSTEMI) and had successful angioplasty of in-stent restenosis of ramus intermedius. The peritoneal fluid WBC count started to get better with 11,715 cells/uL on day 2,4502 cells/uL on day 3,1574 cells/uL on day four and got worse to 10,097 cells/uL on day 5. Peritoneal fluid culture grew E. avium in both aerobic and anaerobic bottles. Species identification was made by VITEK 2. Sensitivities were done using a broth microdilution technique. The sensitivities of E. avium to antibiotic are listed in Table .
The patient was initially treated with vancomycin and was changed to linezolid because of worsening peritoneal fluid cell count before the antibiotic sensitivities were available. The peritoneal dialysis catheter was removed, and the dialysis modality has been switched to hemodialysis because of refractory peritonitis. The patient was discharged on linezolid and completed the antibiotic course for a total of 14 days. He was followed up in the clinic after completion of antibiotics and was doing well without any signs and symptoms of recurrent infection. He was continued on hemodialysis three times a week as an outpatient for end-stage renal disease.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [60, 'years'], 'creatinine': [12.92, 'mg/dL'], 'sex': 'Male'}",3.97811,3.7792,4.17702,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 60 years old. The concentration of Creatinine is 12.92 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 12.92^(-1.154) * 60^(-0.203) * 1 * 1=3.97811.
Hence, the patient's GFR is 3.97811 mL/min/1.73m²."
3285,9,MDRD GFR Equation,lab test,decimal,pmc-6719473-1,Extracted,"A 78-year-old patient presented with acute shortness of breath. She was too breathless to give a detailed history, though she did indicate on specific questioning that she had passed little urine in the previous week. Cardiac and respiratory examinations were normal. SpO2 was 98% on 8 l/min oxygen, with respiratory rate 20/min, heart rate 72/min and BP 160/70 mmHg. Her ECG () which was available before her blood chemistry showed tall T waves, loss of P wave, broad QRS complex together with high take-off >2 mm, coved ST segment elevation and T wave inversion in V1 (Brugada type 1 pattern). CXR showed clear lung fields.
Suspecting hyperkalaemia, initial emergency treatment was with calcium gluconate 10 ml 10% IV, repeated twice, which led to narrowing of the QRS complex. Blood chemistry subsequently showed serum potassium 9.5 mmol/l with blood urea 72 mmol/l, serum creatinine 2200 µmol/l and H+ 120 nmol/l indicating advanced kidney injury and that her dyspnoea was likely due to acidosis. There were no recent blood results for comparison.
Subsequent treatment with dextrose and insulin, nebulised salbutamol and emergency dialysis lowered her serum potassium to 4.3 mmol/l. Her ECG had by this time returned to normal (). Further investigations showed that the cause of her kidney injury was obstructive uropathy due to bilateral pelviureteric junction obstruction. We assumed this was a late presentation of an idiopathic pelviureteric junction obstruction as there was no evidence of stone or tumour on her scan. She received dialysis for six days, bilateral nephrostomies and then ureteric stents. When last seen at the clinic nine months after her initial presentation she was still feeling tired but otherwise well with serum potassium 3.9 mmol/l, blood urea 23.7 mmol/l and serum creatinine 545 µmol/l.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [78, 'years'], 'creatinine': [2200.0, 'µmol/L'], 'sex': 'Female'}",1.31345,1.24778,1.37912,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 78 years old. The concentration of Creatinine is 2200.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 2200.0 µmol. To convert 2200.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 2200.0 µmol Creatinine * 1e-06 mol/µmol = 0.0022 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.0022 mol Creatinine * 113.12 g/mol = 0.24886 g Creatinine. To convert 0.24886 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.24886 g Creatinine * 1000.0 mg/g = 248.86 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 248.86 mg Creatinine/10.0 dL = 24.886 mg Creatinine/dL. The concentration value of 2200.0 µmol Creatinine/L converts to 24.886 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 24.886^(-1.154) * 78^(-0.203) * 1 * 0.742=1.31345.
Hence, the patient's GFR is 1.31345 mL/min/1.73m²."
3286,9,MDRD GFR Equation,lab test,decimal,pmc-4323074-1,Extracted,"A 65-year-old man with a history of acquired human immunodeficiency syndrome (AIDS) was in his usual status until three days prior to presentation, when he suddenly developed dizziness. He was seen in the emergency room at a public hospital in Indianapolis, where he was found to be persistently hypotensive. He was given intravenous fluid resuscitation and was hospitalized for further investigation. Human immunodeficiency virus (HIV) infection had been diagnosed 19 years before. The CD4 T-lymphocytes cell count at diagnosis was 525 cells per cubic millimeter, and the HIV viral load was 4500 copies per milliliter. The CD4 count one year to presentation was 248 per cubic millimeter, and the HIV viral load was 150,000 copies per milliliter. He had been noncompliant with his antiretroviral agents since the diagnosis of HIV infection. He also had a history of ischemic cardiomyopathy, atrial fibrillation, chronic orthostatic hypotension, diabetes mellitus, hepatitis B, hepatitis C, and end-stage renal disease for which he was receiving hemodialysis. The patient was taking didanosine, stavudine, and nevirapine for HIV intermittently. He was not on antiretroviral therapy on admission. Two days after admission, he developed severe abdominal pain followed by massive hematochezia. He subsequently developed hemodynamic instability which required the initiation of vasopressin and norepinephrine. An abdominal radiograph showed small bowel ileus and the colonic cutoff sign at the splenic flexure. A computer tomography scan of the abdomen showed diffuse colonic wall thickening. An emergent exploratory laparotomy revealed extensive colitis with necrosis which necessitated subtotal colectomy. On physical examination after surgery, the patient appeared critically ill. The temperature was 99.5°F (37.5°C), blood pressure 102/59 mm Hg, pulse 100 beats per minute, respirations 25 breaths per minute, and oxygen saturation 99% on FiO2 of 40%. His heart sounds were regular without murmurs and his lungs were clear to auscultation. There was a large abdominal midline incision. The abdomen was remarkably distended. There were three drainage tubes with serosanguinous fluid inside. A right sided colostomy was also in place. He had an arteriovenous fistula on the left arm. The remainder of physical examination was unremarkable.
Laboratory studies revealed a white blood cell count of 13,100 cells/mm³ with 12% band forms, hemoglobin of 8.0 g/dL, and platelets of 96,000 per cubic millimeter. Other abnormal laboratory values included potassium 4.7 mmol/L, bicarbonate 18 mEq/L, urea nitrogen 33 mg/dL, creatinine 4.5 mg/dL, aspartate aminotransferase 100 U/L, total bilirubin 5.5 mg/dL, and lactic acid 10.0 mmol/L. The CD4 count was 10 per cubic millimeter, and the HIV viral load was 630,000 copies per milliliter. The patient was started on intravenous vancomycin and piperacillin/tazobactam. Caspofungin was added after colectomy. The patient remained in a critical condition, requiring high doses of pressors. Three of four sets of blood cultures obtained on admission turned positive in anaerobic bottles. A gram stain of the blood cultures showed Gram-positive rods with spores (), which were identified as Clostridium paraputrificum by the available automated identification system (VITEK 2) in our laboratory. Tissue cultures of the necrotic ascending colon obtained during the extensive colectomy also yielded C. paraputrificum. Metronidazole was added to the initial antibiotic regimen and the patient demonstrated gradual clinical improvement. He was weaned off mechanical ventilation and was transferred to a rehabilitation facility on day 15 after admission.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [65, 'years'], 'creatinine': [4.5, 'mg/dL'], 'sex': 'Male'}",13.21933,12.55836,13.8803,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 65 years old. The concentration of Creatinine is 4.5 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 4.5^(-1.154) * 65^(-0.203) * 1 * 1=13.21933.
Hence, the patient's GFR is 13.21933 mL/min/1.73m²."
3287,9,MDRD GFR Equation,lab test,decimal,usmle-4195,Extracted,"A 65-year-old obese man presents to his primary care clinic feeling weak. He was in the military and stationed in Vietnam in his youth. His current weakness gradually worsened to the point that he had to call his son to help him stand to get on the ambulance. He smokes a pack of cigarettes every day and drinks a bottle of vodka a week. He has been admitted for alcohol withdrawal multiple times and has been occasionally taking thiamine, folic acid, and naltrexone. He denies taking steroids. His temperature is 98°F (36.7°C), blood pressure is 170/90 mmHg, pulse is 75/min, and respirations are 20/min. He is obese with a significant pannus. Hepatomegaly is not appreciable. Abdominal striae are present. His workup is notable for the following:

Serum:
Na+: 142 mEq/L
Cl-: 102 mEq/L
K+: 3.9 mEq/L
HCO3-: 25 mEq/L
BUN: 24 mg/dL
Glucose: 292 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 10.1 mg/dL
AST: 7 U/L
ALT: 14 U/L
24-hour urinary cortisol: 400 µg (reference range < 300 µg)
Serum cortisol: 45 pg/mL (reference range < 15 pg/mL)

A 48-hour high dose dexamethasone suppression trial shows that his serum cortisol levels partially decrease to 25 pg/mL and his adrenocorticotropin-releasing hormone (ACTH) level decreases from 10 to 6 pg/mL (reference range > 5 pg/mL).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [65, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Male'}",46.96857,44.62014,49.317,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 65 years old. The concentration of Creatinine is 1.5 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.5^(-1.154) * 65^(-0.203) * 1 * 1=46.96857.
Hence, the patient's GFR is 46.96857 mL/min/1.73m²."
3288,9,MDRD GFR Equation,lab test,decimal,pmc-7734887-1,Extracted,"Initial presentation
A 27-year-old male presented to a community emergency department in summer of 2016 in western Washington State complaining of lightheadedness and ""almost passing out."" The patient reported that he had been feeling generally fatigued over the past 48 hours. He was normally very active, hiking and rock climbing frequently, however he felt as though he had not been able to hike at his normal brisk pace. The day before his presentation, while finishing a long hike, he had become lightheaded and nearly lost consciousness, stating that he rapidly lowered himself to the ground. His girlfriend, who accompanied him, confirms that he did not fully lose consciousness. The patient cannot recall any preceding symptoms; he specifically denies having chest pain, palpitations, shortness of breath, headache, or any focal neurological deficits. Several seconds after the episode, the patient felt completely back to his recent baseline. He had no persistent lightheadedness.
Upon returning from the hike that day, the patient visited a local urgent care. He had no symptoms at the time and was noted to have dry mucus membranes on physical exam. His work-up there included complete blood count, comprehensive metabolic panel, and electrocardiogram, which were normal. The patient was diagnosed with dehydration and presyncope and was discharged to home.
At home, the patient rehydrated orally and went to bed. He awoke at 02:00 with recurrent symptoms so he drove to the emergency department.
Upon arrival, the patient was placed on a monitor in the triage room and was noted by the triage nurse to be in complete atrioventricular dissociation. During triage, the patient briefly lost consciousness, during which time the triage nurse noted an eight-second ventricular pause on the cardiac monitor. External pacer/defibrillator pads were placed and the patient was brought back to a trauma room. On initial physician interview, the patient noted continued lightheadedness but denied chest pain, palpitations, jaw or arm pain, nausea, edema, or shortness of breath. He also denied headache, focal weakness, and speech or coordination changes. He reported no fever or respiratory symptoms in the past week.
The patient had no past medical or surgical history. He received all routine pediatric vaccinations and screening studies. He was not prescribed any medications and denied using any supplements or alternative medical treatments. He had no known drug allergies. He had a family history of hypertension in his mother and coronary artery disease in his father, diagnosed in his 60s. There was also a family history of colorectal cancer in his father. He denied any known family history of sudden cardiac death or cardiac arrhythmias, although he admitted to not being well informed about his family history. The patient was a non-smoker, drank one to two alcoholic drinks per week, and denied recreational or intravenous drug use.
During the travel history, the patient did report having traveled extensively throughout the United States over the past year to participate in outdoor recreational activities. He recalled camping in the Northeast region two months ago, after which he had some low grade fever and a red rash on his right shoulder. He described the rash as circular and gradually enlarging. He did not recall any central clearing. The fever and rash spontaneously resolved and he did not seek medical attention for these. He had no further symptoms after that, up until 48 hours prior to his presentation to the emergency department.
A complete review of systems was obtained and was negative. Vital signs were blood pressure: 112/65; heart rate: 62; respiratory rate: 12; temperature: 98.5.
Physical exam revealed a fit-appearing young male who was mildly diaphoretic but was alert and fully oriented and in no acute medical distress. Cardiac exam demonstrated a borderline bradycardic rate. There were no murmurs, rubs, or gallops. There was no extremity edema and peripheral pulses were symmetric. There was no jugular venous distention. Breath sounds were clear to auscultation and symmetric. His abdomen was soft and non-tender. The remainder of the physical examination was without noted abnormalities. Notably, there was no rash, focal weakness, or joint tenderness or effusion. He had a normal neurologic exam.
An electrocardiogram was obtained rapidly after the patient’s admission to the emergency department. This showed atrioventricular (AV) dissociation with accelerated junctional rhythm. Axis was normal. There were no acute ST elevation or depression and no T wave abnormalities. See Figure for the ECG.
Complete blood count in the emergency department showed a white blood cell count of 8,500 per microliter (reference range 3,800-11,000 per microliter), hematocrit of 41.2% (reference range 39-50%), and a platelet count of 248,000 per microliter (150,000-400,000 per microliter). White blood cell differential was within the hospital laboratory’s established normal limits.
A comprehensive metabolic panel revealed a glucose of 97 mg/dL (reference range 65-99 mg/dL), creatinine of 0.80 mg/dL (reference range 0.7-1.30 mg/dL), blood urea nitrogen (BUN) of 15 mg/dL (reference range 7-18 mg/dL), sodium of 140 mmol/L (reference range 136-145 mmol/L), and potassium of 3.6 mmol/L (reference range 3.5-5.1). Transaminases and alkaline phosphatase were within normal laboratory reference ranges.
Urine toxicology screen was negative for any drugs of abuse.
A point-of-care troponin was not elevated outside of the reference range. A repeat troponin was checked 4.5 hours later and was also within normal limits.
Subsequent serial ECGs demonstrated periods of junctional rhythm slower than atrial rhythm, confirming third-degree heart block.
Intervention
The patient was given a 1-liter bolus of intravenous normal saline and was admitted to a cardiac telemetry floor. A transvenous pacemaker was placed. Blood was sent for serologic testing for Borrelia burgdorferi antibodies. He was started on empiric therapy with 2 grams of IV ceftriaxone given once daily on the presumption of Lyme carditis as well as maintenance IV normal saline.
Serial laboratory evaluation each morning consisted of a complete blood count and comprehensive metabolic panel. These laboratory studies did not fall significantly outside of reference ranges throughout the course of the patient’s hospitalization. Serial electrogardiograms were obtained and showed persistent complete atrioventricular block in the first three days of his hospitalization. Additional diagnostic studies that were ordered during the patient’s hospital stay included an echocardiogram, which revealed a normal left ventricular wall thickness, normal left ventricular ejection fraction of 55-60% (reference range 55-60%), and no significant valvular regurgitation or stenosis. There was no evidence of diastolic dysfunction to suggest infiltrative cardiomyopathy. There was no pericardial effusion. A thyroid stimulating hormone level was checked and was 1.210 microIU/mL (reference range 0.358- 3.740 microIU/mL).
Outcomes
The patient’s enzyme-linked immunosorbent assay (ELISA) and subsequent Western blot serology testing returned positive for Borrelia burgdorferi antibodies, suggesting active infection. He remained in the hospital for 10 days during which time his cardiac telemetry monitoring showed gradually lengthening intervals of Mobitz I second-degree heart block. Following seven days of treatment, there were no further intervals of third-degree heart block. Upon discharge from the hospital, pacemaker wire was removed. The patient followed up with a family medicine physician one week following his discharge. ECG done at that time showed normal sinus rhythm.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [27, 'years'], 'creatinine': [0.8, 'mg/dL'], 'sex': 'Male'}",115.95924,110.16128,121.7572,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 27 years old. The concentration of Creatinine is 0.8 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 0.8^(-1.154) * 27^(-0.203) * 1 * 1=115.95924.
Hence, the patient's GFR is 115.95924 mL/min/1.73m²."
3289,9,MDRD GFR Equation,lab test,decimal,pmc-5419245-1,Extracted,"A 28-year-old female was admitted to our hospital with history of gradually progressive pedal edema and weight gain of 4 kg since 4 months. There was no other complaint on presentation. The family history was insignificant. On physical examination, she had normal vitals along with normal systemic examination except bilateral pitting pedal edema. Ophthalmic examination including fundoscopy was unremarkable. Laboratory data on admission showed hemoglobin; 9.3 g/dl, mean corpuscular volume (MCV); 82.6 fl, white blood count (WBC); 9690/µl with a normal differential count. Additionally poikilocytosis and ‘target’ erythrocytes in peripheral blood smear was seen. Around 3.3 g/day proteinuria was also found, while hematuria was not existed. Serum blood urea nitrogen and creatinine were 24 mg/dl and 0.99 mg/dl respectively. Serum total proteins were 4.5 g/dl (serum albumin 2.5 g/dl). Liver function tests and lactate dehydrogenase levels, prothrombin time, and partial thromboplastin time were within normal limits. She had a raised total serum cholesterol (415 mg/dl) and triglycerides (402 mg/dl) levels. There was also high serum VLDL (80.40 mg/dl) and normal HDL-C (63 mg/dl). Coombs test and autoantibodies was negative. Serum complements consisting C3 and C4, was within the normal range. A renal biopsy was conducted to find the etiology of nephrotic syndrome. Light microscopy showed 22 glomeruli with variable affection and enlarged size (). Normal glomerular architecture was replaced by markedly dilated capillary lumina, which was filled with a lamellated, pink staining, fluid-like material. Mesangial matrix was focally increased and showed bubbly appearance. Capillary membranes showed craters on silver staining. Tubules showed moderate degeneration. Electron microscopy examination showed lipid deposition in the lamina densa of the basement membranes. The cystically dilated capillary loops revealed concentrically lamellated/myelinoid structures. Glomeruli were enlarged due to marked accumulation of amorphous lipid material in the capillary loops. Immunofluorescence examination of renal biopsy specimen was not done due to inadequate sample size. Finally, the evaluation of the plasma LCAT enzymatic activity revealed markedly decreased LCAT activity (10.1 nmol/ml/h; reference range, 80.9 ± 11.2 nmol/ml/h). We confirmed again the absence of corneal opacities or any kind of ophthalmic involvement. The patient was treated with a combination of gemfibrozil, atorvastatin, and telmisartan without any significant improvement in proteinuria at 2 months of follow-up.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [28, 'years'], 'creatinine': [0.99, 'mg/dL'], 'sex': 'Female'}",66.78914,63.44968,70.1286,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 28 years old. The concentration of Creatinine is 0.99 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.99^(-1.154) * 28^(-0.203) * 1 * 0.742=66.78914.
Hence, the patient's GFR is 66.78914 mL/min/1.73m²."
3290,9,MDRD GFR Equation,lab test,decimal,pmc-8201711-1,Extracted,"A 69-year-old man was admitted to our hospital on Jan 25, 2020 with a complaint of fever and abdominal pain for 1 days’ duration. The patient was diagnosed with hypertension and cerebral infarction 10 years ago, and also with a medical history of renal anemia and cholecystectomy. In 2014, the patient was diagnosed with IgA nephropathy by a renal biopsy and was treated with diet. In 2018, the patient progressed to chronic kidney disease stage 5 and underwent peritoneal dialysis for 2 years until this admission.
At the emergency department on Jan 25, 2020, his physical examination showed a body temperature of 38.6 °C, a blood pressure of 206/95 mmHg, a pulse rate of 85 beats/min, and a respiratory rate of 18 breaths/min. He complained tenderness and rebound pain in his abdomen, with pitting lower extremity edema. Redness or discharge was not found near the peritoneal catheter. Laboratory tests revealed a white blood cell count (WBC) of 13.9 × 109/L with 80.7% neutrophils, a hemoglobin (Hb) level of 74 g/L, a C-reactive protein (CRP) level of 96.7 mg/L, a procalcitonin (PCT) level of 3 ng/ml, a B-type natriuretic peptide (BNP) level of 939 pg/mL, an urea level of 25.27 mmol/L and a creatinine level of 924.2 μmol/L. Routine testing of the PD effluent revealed a yellow and muddy appearance with positive results in the Rivalta test, WBC count of 13,363 × 106/L (neutrophils: 98%). Peritoneal dialysis-associated peritonitis was diagnosed initially. The PD effluent was collected for bacterial culture.
Being admitted to the Nephrology ward later in the same day, another PD effluent was collected for bacterial culture before starting an empirical antibiotic therapy. Then, the patient was empirically treated with ceftizoxime intravenously (2 g bid iv) and intraperitoneal injection of teicoplanin (0.2 g qd ip) for 7 days. On Feb 1, a gram-positive bacterium was found from PD effluent culture. Therefore, teicoplanin (0.2 g qd iv) and imipenem (0.5 g qd ip) were administered based on the antimicrobial susceptibility testing for the next 4 days. Due to the low blood concentration of teicoplanin and intraperitoneal catheter removed on Feb 5, the treatment was adjusted to teicoplanin (0.4 g qd iv) and imipenem (0.5 g q12h iv). With the continuous treatment with teicoplanin and imipenem for 15 days, the infection symptom was improved with a normal body temperature of 36.6 °C, a PCT level of 0.7 ng/ml and a CRP level of 76.8 mg/L. Routine testing of the peritoneal fluid were within normal ranges. Peritoneal dialysis effluent culture and intraperitoneal catheter culture also showed negative result.
Thereafter, arteriovenous fistula angioplasty was performed for hemodialysis on Feb 15 and the patient developed fever (38 °C) and disturbance of consciousness on the first day after surgery. No cerebral hemorrhage and cerebral infarction were found by cranial Computed Tomography (CT). Considered the toxicity, imipenem was switched to biapenem. However, the patient’s symptoms and signs did not improve, and the laboratory test indicators gradually increased. On Feb 17, elevated PCT (0.801 ng/mL) and CRP (76.8 mg/L) was observed. Blood culture showed a negative result, and amikacin was given instead of biapenem for the treatment. On Feb 20, the patient still had a fever (37.8 °C) and thick sputum. Laboratory examination revealed a PCT of 1.34 ng/mL, a CRP of 58.5 mg/L, a ESR of more than 140 mm/h, a Hb of 45 g/L. The fecal occult blood test was positive and the blood culture was negative. High resolution CT of the thorax showed inflammatory manifestations including pulmonary cord, flocculent shadow and exudate. Unfortunately, the patient died on Feb 25 due to septic shock and multi-organ failure.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [69, 'years'], 'creatinine': [924.2, 'µmol/L'], 'sex': 'Male'}",4.96316,4.715,5.21132,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 69 years old. The concentration of Creatinine is 924.2 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 924.2 µmol. To convert 924.2 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 924.2 µmol Creatinine * 1e-06 mol/µmol = 0.00092 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00092 mol Creatinine * 113.12 g/mol = 0.10407 g Creatinine. To convert 0.10407 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.10407 g Creatinine * 1000.0 mg/g = 104.07 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 104.07 mg Creatinine/10.0 dL = 10.407 mg Creatinine/dL. The concentration value of 924.2 µmol Creatinine/L converts to 10.407 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 10.407^(-1.154) * 69^(-0.203) * 1 * 1=4.96316.
Hence, the patient's GFR is 4.96316 mL/min/1.73m²."
3291,9,MDRD GFR Equation,lab test,decimal,pmc-6863346-1,Extracted,"A 66-year-old woman presented with bilateral cramping thigh pain for three days. She had no antecedent history of trauma, infection, severe exercise, seizures, uncontrolled blood glucose or use of herbal medication. She had a history of coronary artery disease, heart failure, diabetes, hypertension, and hyperlipidemia. A month prior, she was admitted to the hospital for a non-ST elevation myocardial infarction (NSTEMI). Invasive strategy versus medical therapy was discussed. Given that she had diffuse disease which was not amenable to percutaneous coronary intervention (PCI), medical management with dual antiplatelet therapy (DAPT) was instituted. Her secondary prevention regimen included Ticagrelor 90 mg twice daily in addition to, her past medications: Aspirin, Nifedipine, Losartan, Simvastatin, Metoprolol and Furosemide 20 mg as needed. At discharge, her serum creatinine (SrCr) concentration was 1.44 mg/dl and serum creatinine-kinase (CK) concentration was 203 U/L.
On presentation, laboratory investigations were significant for a Sr Cr. of 2.93 mg/dL and CK of 22,000 U/L. She was diagnosed with acute on chronic kidney injury (underlying CKD stage II) and acute rhabdomyolysis with CK levels peaking close to ~40,000 U/L by hospital day 2. Urinalysis demonstrated 2+ proteinuria and 3+ hemoglobinuria, with only 3 RBC seen. She was started on aggressive intravenous (IV) hydration and simvastatin and ticagrelor were discontinued. Her symptoms resolved, CK levels promptly decreased [] and the Sr Cr. decreased to 2.3 mg/dl. On discharge, she was started on clopidogrel. During a follow up clinic visit, the patient was prescribed rosuvastatin and has remained without complications on follow up visit and laboratory checks.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [66, 'years'], 'creatinine': [2.93, 'mg/dL'], 'sex': 'Female'}",16.04388,15.24169,16.84607,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 66 years old. The concentration of Creatinine is 2.93 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.93^(-1.154) * 66^(-0.203) * 1 * 0.742=16.04388.
Hence, the patient's GFR is 16.04388 mL/min/1.73m²."
3292,9,MDRD GFR Equation,lab test,decimal,pmc-4677192-1,Extracted,"A 65-year-old male patient was admitted to the clinic with weakness and dark stool persisting for the last 3-4 days. He had hypertension (HT) and chronic renal failure (CRF) and no habit of smoking or alcohol consumption. He had no history of using anticoagulants or antiaggregant drugs. On physical examination, the patient appeared pale and tired. His skin turgor and tone were decreased. Blood pressure was 90/60 mmHg, pulse rate 120 beats/min, and body temperature 36.4°C. Lung examination was normal. Abdominal examination demonstrated mild epigastric tenderness and melena was identified by rectal examination. Initial laboratory values were as follows: glucose: 107 mg/dL, urea: 361 mg/dL, creatinine: 7.1 mg/dL, sodium: 139 mEq/L, potassium: 3.86 mEq/L, leukocyte: 21.300/mm3, hemoglobin: 7.8 g/dL, platelets: 100.000/mm3, prothrombin time: 12 sec, and INR: 1.05. Serum transaminase, bilirubin, and amylase-lipase values were within normal ranges. Crystalloid and colloid fluid replacement were promptly given intravenously, parenteral proton-pump inhibitor was initiated, and four units of erythrocyte suspension was administered. Following hemodynamic stabilization, the patient underwent upper gastrointestinal endoscopy (UGIE). A 9 mm sized ulcer, covered with fresh red clot, was observed at the anterior wall of the bulb. The clot was removed and oozing bleeding was seen at the base of the ulcer; epinephrine was then injected into the areas adjacent to the ulcer. A vascular lesion at the ulcer base was coagulated with argon plasma coagulation (APC) during the same session (Figures and ). Although there had been no evidence of clinical bleeding (no hematemesis or melena), hemoglobin and hematocrit values declined approximately 36 hours later from this intervention, and a second UGIE was carried out. On endoscopic examination, there was no bleeding from the ulcer. However, the posterior wall mucosa of the second part of the duodenum, at approximately 2 cm distal to the ulcer, was erythematous with no obstruction (). Postoperatively the patient developed nausea, vomiting, abdominal pain, and jaundice after the second endoscopic assessment. Serum total bilirubin and direct bilirubin values increased up to 23 mg/dL and 19 mg/dL, respectively. Plasma amylase level was 1389 U/L, and lipase level was 991 U/L. At the third day of admission, a final UGIE was performed to investigate the possible presence of a hematoma. The ulcer was stable but the mucosa of the second part of the duodenum was erythematous and was also significantly protruded towards the lumen, resulting in complete obstruction (). Upper abdominal magnetic resonance imaging (MRI) and computerized tomography (CT) demonstrated a mass with size 5.6 × 10.1 cm at the section corresponding to the second and third parts of the duodenum, consistent with an intramural hematoma causing complete obstruction of the lumen. The lesion compressed the bile ducts and the pancreatic duct resulting in dilation of the common bile duct and main pancreatic duct (Figures , , and ). Decompression with a nasogastric tube was performed and a conservative treatment modality was attempted (total parenteral nutrition, intravenous fluid, and careful observation). However, the patient did not respond to conservative treatment and his overall condition deteriorated rapidly with signs of sepsis developing. In response, ultrasonography-guided percutaneous hematoma drainage was performed. The patient's clinical parameters did not improve although the hematoma was drained. The patient died because of sepsis, septic shock, and multiorgan failure.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [65, 'years'], 'creatinine': [7.1, 'mg/dL'], 'sex': 'Male'}",7.81024,7.41973,8.20075,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 65 years old. The concentration of Creatinine is 7.1 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 7.1^(-1.154) * 65^(-0.203) * 1 * 1=7.81024.
Hence, the patient's GFR is 7.81024 mL/min/1.73m²."
3293,9,MDRD GFR Equation,lab test,decimal,pmc-5719915-1,Extracted,"An 82-year-old woman with no significant medical history presented with a 2-month history of abdominal pain and nausea. Vital signs were as follows: blood pressure, 130/80 mm Hg; heart rate, 72 beats/minute (bpm); respiratory rate, 20/minute; and body temperature, 36.4°C. She appeared chronically ill and the findings of a physical examination of the thorax, heart, and abdomen were unremarkable. Laboratory studies revealed a white blood cell (WBC) count of 8,110/μL (neutrophils, 78.5%; and lymphocytes, 17.5%) and a hemoglobin (Hb) of 11.5 g/dL. Serum biochemical values were as follows: blood urea nitrogen (BUN), 12 mg/dL; serum creatinine (Cr), 0.8 mg/dL; aspartate aminotransferase/alanine aminotransferase, 21/14 U/L; albumin, 4.0 g/dL; total bilirubin, 0.6 mg/dL; and amylase 2,460 U/L. Electrolyte levels were as follows: Na, 139 mmol/L; K, 4.0 mmol/L; and Cl, 102 mmol/L. Carbohydrate antigen 19-9 (CA19-9) levels were 37.0 U/mL.
An abdominal computed tomography (CT) scan revealed a 2-cm mass near the ampulla of Vater with mild dilation of the intrahepatic and common bile ducts as well as the pancreatic ducts (). There was no evidence of invasion of other organs. Both kidneys were normal sized without apparent abnormalities.
Endoscopic retrograde cholangiopancreatography with endoscopic ultrasound (EUS) revealed a 2-cm adenoma-like protruding lesion in the ampulla of Vater. EUS showed a well-defined isoechoic homogeneous mass without bile or pancreatic duct invasion (-). The mass was resected using a snare and a plastic stent was inserted into the bile duct; insertion of a plastic stent into the pancreatic duct failed. No specific complications, including severe bleeding or perforation, were observed (). Six hours post-procedure, the patient vomited 50 mL of blood and complained of abdominal pain. A second episode of hematemesis (<30 cc) occurred approximately 5 hours later. Immediately after the second episode, treatment with 1 g of tranexamic acid and 2 KU of hemocoagulase administered three times per day along with ceftriaxone (2 g intravenous) and a proton pump inhibitor for suspected bleeding at the resection site was initiated. Her vital signs were unremarkable. The WBC count was 7,090/μL, Hb was 10.1 g/dL, BUN was 14 mg/dL, Cr was 0.8 mg/dL, and amylase/lipase was 69/54 U/L. After the initial two episodes of hematemesis, no further hematemesis, melena, or hematochezia was observed and the patient’s vital signs remained stable. Her Hb level remained >10 g/dL. Four days after the papillectomy, the patient’s daily urine volume abruptly decreased to <100 cc and she complained of dyspnea. Her blood pressure was 103/86 mm Hg, heart rate was 134 bpm, respiratory rate was 30/minute, and body temperature was 37.0°C. Laboratory studies were as follows: Hb, 9.1 g/dL; amylase/lipase, 415/418 U/L; BUN/Cr, 73/3.9 mg/dL; and brain natriuretic peptide, 5,000 pg/mL. Venous blood gas analysis revealed the following: pH, 6.92: pCO2, 37 mm Hg; and HCO3, 7.6 mmol/L. Pulmonary edema was observed on a chest radiograph and continuous renal replacement therapy (CRRT) was performed to treat metabolic acidosis and pulmonary edema caused by acute renal failure. Although there were no signs of bleeding at that time, 2 units of packed red blood cells were transfused.
Approximately 10 hours after the CRRT was initiated, the patient was noted to have melena mixed with a small amount of hematochezia. Melena continued to occur 2–3 times/day with a total daily volume of 200–400 cc. Her vital signs were relatively stable: blood pressure, 120–175/65–100 mm Hg; heart rate, 90–120 bpm; respiratory rate, 20–25/minute; and body temperature, 36.0°C–37.8°C. The daily serum Hb level was 7.1–9.5 g/dL and the tranexamic acid with hemocoagulase were continued. The patient received a total of 13.5 g of tranexamic acid and 36 KU of hemocoagulase and received three additional units of packed red blood cells until the sixth day post-procedure, when no further signs of bleeding were observed. However, her daily urine output was nearly zero despite the CRRT. A contrast-enhanced abdominal CT scan was performed on day 12 to assess the cause of her anuric acute renal failure and showed normal-sized kidneys with enhancement of the renal medulla but not of the renal cortex, a finding consistent with acute RCN (). Histopathology revealed a villotubular high-grade adenoma with clear resection margins. Conventional hemodialysis was continued, but renal function did not improve and the oliguria persisted post-discharge. Presently, 6 months after the endoscopic procedure, she continues to undergo hemodialysis. Her most recent BUN/Cr was 22/6.1 mg/dL.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [82, 'years'], 'creatinine': [0.8, 'mg/dL'], 'sex': 'Female'}",68.67077,65.23723,72.10431,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 82 years old. The concentration of Creatinine is 0.8 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.8^(-1.154) * 82^(-0.203) * 1 * 0.742=68.67077.
Hence, the patient's GFR is 68.67077 mL/min/1.73m²."
3294,9,MDRD GFR Equation,lab test,decimal,pmc-6111013-1,Extracted,"An 82-year-old man developed cardiogenic shock followed by an acute right ventricular MI during colon cleansing with PGE-Asc before a colonoscopy for evaluation of prolonged anemia. He had no history of cardiovascular events, but had been taking an angiotensin receptor blocker for hypertension and had a long history of smoking. He had no other coronary risk factors, including family history, hyperlipidemia, obesity, and diabetes mellitus, and no history of an allergic reaction to any medicine or antigens. He had not previously undergone a colonoscopy. Based on the protocol for preparation for a colonoscopy in our hospital, the patient was instructed to take 24 mg of sennoside in the evening prior to digesting PGE-Asc in the morning. He was given the drug information document for PGE-Asc, which indicates that patients should swallow 1 L of MoviPrep in the first hour before drinking 0.5 L of water. However, the patient took 2 L of PGE-Asc in 1 h and did not hydrate. After 2 h, he developed nausea and soon became unconscious, after which his family called the emergency medical service.
On arrival of the emergency medical service, the patient was in a shock state, with a systolic blood pressure of 60 mmHg and a heart rate of 50 bpm. When he was brought to the emergency department of our hospital, he was still in shock and his vital signs were a respiratory rate of 25/min, oxygen saturation 98% with a 6-L/min reservoir mask, heart rate 50 bpm, systolic blood pressure 100 mmHg, and Glasgow Coma Scale E3V5M6. His peripheral skin was cold and wet, and the capillary refilling time was prolonged. He complained of nausea, but had no dyspnea or chest discomfort. Other findings on physical examination include normal breath sound without stridor and wheezing, no significant heart murmurs, no tenderness in the abdomen, and no skin rash. Laboratory data were as follows: white-cell count 12,900/µL, hemoglobin 11.0 g/dL (9.9 g/dL 17 days earlier), hematocrit 35.6% (32.3% 17 days earlier), creatinine kinase 119 U/L, urea nitrogen 20 mg/dL, creatinine 1.16 mg/dL, sodium 140 mEq/L, potassium 4.5 mEq/L, and troponin T 0.049 ng/mL. Arterial blood gas analysis under 6 L/min oxygen with a reservoir mask showed pH 7.181, PaCO2 36.7 mmHg, PaO2 262.6 mmHg, lactate 7.64 mmol/L, HCO3− 13.4 mmol/L, base excess − 14.9 mmol/L, and anion gap 20.1 mmol/L.
Soon after the initial examination, we found the patient had developed acute MI with ST elevation on an electrocardiogram, which revealed sinus bradycardia with ST elevations in II, III, aVF, V3R, and V4R. Cardiac ultrasound showed severe hypokinesis in the inferior wall of the left ventricle. Coronary artery angiography revealed total occlusion in the right coronary artery, 90% stenosis in the left arterial descending coronary artery, and 90% stenosis in the left circumflex coronary artery, and the patient underwent a percutaneous coronary artery intervention in the right coronary artery. The door to balloon time was 80 min and the maximum creatinine kinase level was 1432 U/L. After the intervention, shock improved within the day, and after 4 days, the patient underwent a colonoscopy with correct administration of PGE-Asc under careful monitoring and appropriate hydration in the Cardiac Care Unit. Because transparent fluid was drained before administration of 1 L of PGE-Asc, the drug was discontinued within 1 h. Progressive colon cancer in the cecum was found. Laboratory data on day 4 showed decreases compared with the day of admission of creatinine kinase, hematocrit, urea nitrogen, and creatinine levels to 128 U/L, 27.0%, 11 mg/dL, and 0.73 mg/dL, respectively. There were no adverse effects after taking the colon preparation. After a month, the patient underwent a colectomy at our hospital, and was transferred to another hospital for rehabilitation on day 74. A Naranjo score [] of 4 was obtained in this case (see the “”).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [82, 'years'], 'creatinine': [1.16, 'mg/dL'], 'sex': 'Male'}",60.27668,57.26285,63.29051,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 82 years old. The concentration of Creatinine is 1.16 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.16^(-1.154) * 82^(-0.203) * 1 * 1=60.27668.
Hence, the patient's GFR is 60.27668 mL/min/1.73m²."
3295,9,MDRD GFR Equation,lab test,decimal,pmc-5558125-1,Extracted,"Case 1: A 63-year-old, nonalcoholic, man with a medical history of hypertension treated with lisinopril, amlodipine, and nifedipine, and hyperlipidemia treated with lovastatin, presented with epigastric pain, early satiety, and involuntary 10-kg-weight-loss during the last 6 mo, and melena and dyspnea on exertion for 3 d. The vital signs were stable, with a blood pressure of 144/74 mmHg, and pulse of 87/min. The abdomen was soft, nontender, and without hepatosplenomegaly or palpable masses. Rectal examination revealed melena. The hemoglobin was 6.2 g/dL, blood urea nitrogen was 27 mg/dL, and creatinine was 1.40 mg/dL. He had 496000 platelets/mL, a normal international normalized ratio (INR), and normal partial thromboplastin time (PTT). He was transfused two units of packed erythrocytes.
EGD revealed a 13-cm-wide submucosal, yellowish, gastric mass primarily in the antrum, covered by smooth mucosa except for focal ulceration (Figure ), and exhibiting the pillow sign, of indentation of the mass with moderate pressure applied via a closed forceps[,]. Microscopic examination of multiple mucosal biopsies of the ulcer margin revealed superficial ulceration, granulation tissue, and no malignancy. Abdominal computerized tomography (CT) revealed a well-circumscribed, homogeneous, 13.4 cm × 8.4 cm × 8.2 cm mass, with attenuation characteristic of fat, arising from the gastric antrum and producing a mass effect on the proximal duodenum (Figure ). A 7-mm-wide lesion in the body of the pancreas was also suspected to be a lipoma based on its characteristic attenuation. The patient underwent laparotomy due to the recent bleeding of the giant lipoma. It was resected via subtotal gastrectomy extended by partial bulbar duodenectomy due to lipoma extension into duodenal bulb, with Billroth II reconstruction. Gross pathology revealed a homogeneous, soft, submucosal mass with a cut surface exposing yellowish, greasy tissue, measuring 14.5 cm × 8.7 cm × 7.5 cm (Figure ), which microscopically revealed lipoma (Figure ). Immunohistochemical staining revealed positivity for CD34 (Figure ), a finding highly consistent with a spindle cell variant lipoma[]. The patient was discharged 8 d postoperatively, and had no complications during 8 wk of follow-up.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [1.4, 'mg/dL'], 'sex': 'Male'}",51.1847,48.62546,53.74394,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 63 years old. The concentration of Creatinine is 1.4 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.4^(-1.154) * 63^(-0.203) * 1 * 1=51.1847.
Hence, the patient's GFR is 51.1847 mL/min/1.73m²."
3296,9,MDRD GFR Equation,lab test,decimal,pmc-7559648-1,Extracted,"On July 2012, a 63-year-old female came to the urology office with symptoms of intermittent left flank pain for 2 mo.
The pain was described to be localized at left fank. Neither precipitating factors nor exaggerating factors were mentioned. It occurred randomly without any special time or occasions, and can be suppressed by painkillers. Accompanying symptoms include vomiting and body weight loss, about 7 kg over 2 mo. She denied having visible red color urine, neither fever. Appetite was not changed. Neither specific travel histories nor cluster histories were mentioned.
She had uterine prolapse diagnosed 2 years before this episode, but did not have any interventions about it.
Her temperature was 35.9 °C, and heart rate was 74 bpm. Respiratory rate was 17 breaths per minute, and blood pressure was 127/81 mmHg. Oxygen saturation in room air was 98%. She ranked the pain subjectively 4 out of 10 on visual analog scale pain score. No knocking pain was examined at costovertebral angle, neither the tenderness on abdomen.
Normocytic anemia was seen on complete blood cell (White blood cell: 4 500/UL, Red blood cell: 3370000/UL, Hemoglobulin: 10.4 g/DL, Mean corpuscular volume: 93.5 FL). Mildly insufficiency was seen on renal functions tests (Creatinine: 1.4 mg/DL, Blood urea nitrogen: 16.2 mg/DL). Elevated Intact parathyrin (EIA/LIA) was 245 pg/ML. Free T4 (EIA/LIA) was 1.070 ng/DL, and TSH (EIA/LIA) was 1.5 UIU/ML. Tumor markers of carcino-embryonic antigen, CA-199, and alpha-fetoprotein were all within normal limits. Urine examination showed hematuria (red blood cell 5-10/HPF) and pyuria (white blood cell: 10-20/HPF). Urine cytology was gained, but no atypical cells were examined.
Left side hydronephrosis was evident on ultrasound. Intravenous pyelography showed a non-enhanced left kidney (Figure ) and then computed tomography urogram was arranged (Figure ) for comprehensive studies, which showed an enlarged lymph node close to the left renal pedicle and one irregularly ill-defined 4.2-cm width mass at the left renal pelvic.
Ureteroscopy was arranged and biopsy was done to this 4.2-cm mass at left renal pelvis. Pathology from the biopsy was proved to be high-grade (grade III) UC, which is invasive to lamina propria.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [1.4, 'mg/dL'], 'sex': 'Female'}",37.97905,36.0801,39.878,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 63 years old. The concentration of Creatinine is 1.4 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.4^(-1.154) * 63^(-0.203) * 1 * 0.742=37.97905.
Hence, the patient's GFR is 37.97905 mL/min/1.73m²."
3297,9,MDRD GFR Equation,lab test,decimal,pmc-6062773-1,Extracted,"A 60-year-old man with a history of acute myeloblastic leukemia status postallogenic HSCT 2 months prior, tonic-clonic seizures, coronary artery disease, polycystic kidney disease, and hypertension presented with fever, diarrhea, and abdominal pain. He had been taking tacrolimus 0.5 mg BID, and levetiracetam 500 mg BID. He was transferred to the intensive care unit for persistent hypotension and acute hypoxic respiratory failure requiring intubation. Initial vitals included a temperature 100.2°F, blood pressure 70/43 mm Hg, heart rate 89 beats per minute, respiratory rate 20 breaths per minute, and 92% on room air. Pertinent physical examination findings included pallor and right upper quadrant abdominal tenderness with a positive Murphy’s sign. Initial laboratory tests were normal except for hemoglobin 10.1 g/dL, hematocrit 29.1%, platelets 79 000/µL (130 000-450 000/µL), sodium 133 mmol/L (136-144 mmol/L), bicarbonate 20 mmol/L (22-32 mmol/L), blood urea nitrogen 21 mg/dL, creatinine 2 mg/dL, and albumin 3.4 g/dL (3.5-5 g/dL). Initial arterial blood gas showed pH 7.37, pCO2 30.9 mm Hg; pO2 66 mm Hg; and a base excess of −8. Blood cultures were positive for Pseudomonas aeruginosa.
He was diagnosed with septic shock and started on acyclovir, voricanazole, vancomycin, tobramycin, metronidazole, and cefepime for empiric coverage given his immunocompromised state. Later that day, vasopressors (norepinephrine, epinephrine, vasopressin, and phenylephrine) were initiated along with stress dose steroids (hydrocortisone 100 mg TID). Empiric antibiotics were adjusted to meropenem instead of flagyl and cefepime. That night, the patient became progressively acidotic (pH of 7.37 earlier to pH of 7.22); therefore, it was decided to initiate continuous renal replacement therapy.
The following day his tacrolimus level was 8.6 ng/mL (10-20 ng/mL) and creatinine was 2.2 (baseline = 1.8). The patient inadvertently received 15 mg intravenous tacrolimus instead of his scheduled 0.5 mg intravenous. Four hours later, a random tacrolimus level was 36.4 ng/mL. Tacrolimus was subsequently discontinued. Based on several case studies and literature review, phenytoin 200 mg BID was started for 4 doses and rifampin was started for 2 doses at 600 mg in order to potentially limit the patient’s tacrolimus toxicity. Levetiracetam was stopped during the administration of phenytoin; and rifampin was discontinued after 2 doses given its side effect profile. Sixteen hours postinjection, the tacrolimus level decreased to 26.4 ng/mL and to 9 ng/mL after 64 hours (). Creatinine decreased to 1.1 after 30 hours (). He was extubated 5 days later without any new neurological findings and his creatinine returned to baseline.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [60, 'years'], 'creatinine': [2.2, 'mg/dL'], 'sex': 'Male'}",30.6844,29.15018,32.21862,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 60 years old. The concentration of Creatinine is 2.2 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.2^(-1.154) * 60^(-0.203) * 1 * 1=30.6844.
Hence, the patient's GFR is 30.6844 mL/min/1.73m²."
3298,9,MDRD GFR Equation,lab test,decimal,pmc-5569917-1,Extracted,"A 16-year-old female presented with AKI (creatinine 324 µmol/L) and a 4-day history of vomiting without diarrhoea. Her only past medical history was acne, and Roaccutane had been commenced 1 month earlier; blood tests performed at that time were all normal. Her mother had been unwell with a diarrhoeal illness 2 weeks previously.
Blood tests on admission were consistent with a thrombotic microangiopathy (TMA): haemoglobin 9.9 g/dL, platelets 41 × 109/L, bilirubin 38 µmol/L, lactate dehydrogenase (LDH) 1865 U/L, reticulocytes 107 × 109/L and red blood cell fragmentation on the blood film; Coombs test was negative and coagulation was normal. Treatment with plasma exchange was commenced (total of eight exchanges) and thrombotic thrombocytopenic purpura (TTP) was excluded (ADAMTS13 activity 76%). The National Health Protection Agency (HPA) laboratory reported that immunoglobulin M (IgM) antibodies to E. coli O157 lipopolysaccharide (LPS) were positive, in keeping with acute STEC-HUS []. Levels of C3, C4, factor H and factor I were normal. Her renal function deteriorated and she required haemodialysis, as well as ventilatory and inotropic support in the intensive care unit (ICU) consequent to a hospital-acquired pneumonia. There was no recovery in renal function and she remained on haemodialysis. A kidney biopsy was performed 3 months later, showing features of TMA; immunofluorescence showed segmental C3 deposition in the glomerular tuft. Later, 10 months after presentation, she was admitted with seizures that were attributed to hypertensive encephalopathy (computed tomography of the brain and cerebrospinal fluid examination were normal) and she was again managed in the ICU for ventilatory support and blood pressure control.
She received a donor after brain death (DBD) renal transplant with a 1:1:0 human leucocyte antigen mismatch 18 months after her initial presentation. She received basiliximab and methylprednisolone at induction with maintenance tacrolimus, mycophenolate mofetil (MMF) and prednisolone. A transplant biopsy performed 7 days post-operatively due to delayed graft function showed borderline acute T-cell–mediated rejection and no evidence of TMA; she was treated with intravenous methylprednisolone, but her renal function deteriorated concurrent with a decrease in her platelet count and an increase in LDH, with a peak creatinine of 396 µmol/L. At Day 10 she developed MAHA and was treated with plasma exchange. Tacrolimus levels were therapeutic. The following day she had multiple generalized tonic–clonic seizures, severe headache, photophobia and blurred vision, which progressed to cortical blindness over the course of 4 h in the context of a blood pressure of 190/113 mmHg. Magnetic resonance imaging (MRI) of the brain was consistent with posterior reversible encephalopathy syndrome (PRES) (Figure A). She was admitted to the ICU for management of hypertension and treatment with eculizumab was commenced. The neurological symptoms resolved within 48 h and over the following 2 weeks the renal function improved and haematological parameters normalized. A transplant biopsy performed 15 days post-operatively demonstrated severe acute TMA and borderline acute T-cell–mediated rejection (Figure Bi–ii).
Subsequent genetic analysis identified a heterozygous rare genetic variant in C3: c.4855A>C p.(Ser1619Arg). The functional significance has not been assessed, however, the amino acid is well conserved, in silico analysis suggests that the variant is possibly deleterious and structural modelling (Figure C) demonstrates that this is in the same C3 domain as the variant c.4973T >C p.(Val1658Ala) demonstrated by Sartz et al. to be functionally significant [].
A transplant biopsy performed 3 months post-operatively for proteinuria (urine protein:creatinine ratio 243 mg/mmol) showed no significant abnormality. A fourth transplant biopsy was performed 5 months post-operatively because the creatinine rose from 130 to 180 µmol/L. This showed acute T-cell–mediated rejection (Banff IB) (Figure Biii) and she was treated with intravenous methylprednisolone. Immunofluorescence, including kappa and lambda, was negative. She remains on eculizumab, prednisolone, tacrolimus and MMF, and 3 years after transplantation she is well and creatinine is 157 µmol/L.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [16, 'years'], 'creatinine': [157.0, 'µmol/L'], 'sex': 'Female'}",37.29448,35.42976,39.1592,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 16 years old. The concentration of Creatinine is 157.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 157.0 µmol. To convert 157.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 157.0 µmol Creatinine * 1e-06 mol/µmol = 0.00016 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00016 mol Creatinine * 113.12 g/mol = 0.0181 g Creatinine. To convert 0.0181 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.0181 g Creatinine * 1000.0 mg/g = 18.1 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 18.1 mg Creatinine/10.0 dL = 1.81 mg Creatinine/dL. The concentration value of 157.0 µmol Creatinine/L converts to 1.81 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.81^(-1.154) * 16^(-0.203) * 1 * 0.742=37.29448.
Hence, the patient's GFR is 37.29448 mL/min/1.73m²."
3299,9,MDRD GFR Equation,lab test,decimal,usmle-1994,Extracted,"A 73-year-old man comes to the physician because of progressive fatigue and shortness of breath on exertion for 3 weeks. He has swelling of his legs. He has not had nausea or vomiting. His symptoms began shortly after he returned from a trip to Cambodia. He occasionally takes ibuprofen for chronic back pain. He has a history of arterial hypertension and osteoarthritis of both knees. He had an episode of pneumonia 4 months ago. His current medications include lisinopril and hydrochlorothiazide. He has no history of drinking or smoking. His temperature is 37°C (98.6°F), pulse is 101/min, and blood pressure is 135/76 mm Hg. Examination shows pitting edema of the upper and lower extremities. Laboratory studies show:
Hemoglobin 14.1 g/dL
Leukocyte count 6,800/mm3
Platelet count 216,000/mm3
Serum
Urea nitrogen 26 mg/dL
Creatinine 2.9 mg/dL
Albumin 1.6 g/L
Urine
Blood negative
Protein 4+
Glucose negative
Renal biopsy with Congo red stain shows apple-green birefringence under polarized light.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [73, 'years'], 'creatinine': [2.9, 'mg/dL'], 'sex': 'Male'}",21.4376,20.36572,22.50948,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 73 years old. The concentration of Creatinine is 2.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.9^(-1.154) * 73^(-0.203) * 1 * 1=21.4376.
Hence, the patient's GFR is 21.4376 mL/min/1.73m²."
3300,9,MDRD GFR Equation,lab test,decimal,pmc-3890728-1,Extracted,"A 46-year-old woman presented with general weakness that had lasted for several weeks. She was diagnosed with type 2 diabetes mellitus (DM) 15 years ago and began continuous ambulatory peritoneal dialysis (CAPD) three years ago. An abdominal sonography obtained before CAPD began revealed a normal liver. The patient received CAPD with four daily exchanges of 2 L each time and switched to three exchanges with 2.5% glucose and one with 4.25% glucose solution; this was required because the ultrafiltration capacity was not sufficient and she became volume overloaded. A peritoneal equilibrium test was not performed. The patient had insulin administered subcutaneously when she started the CAPD but changed to intraperitoneal insulin treatment combined with subcutaneous treatment two years later. Hyperlipidemia treated with simvastatin and fenofibrate were started one year previously but stopped three months later because the drugs caused rhabdomyolysis. Lipid profiles began to worsen and she had to resume with atovastatin but did not develop rhabdomyolysis. Plasma glucose was poorly controlled despite the combination therapy of subcutaneous and intraperitoneal insulin injections. Insulin doses increased from 102 units daily up to 110 units daily during the previous month. The patient was 158 cm tall and weighed 58 kg. When she visited our clinic, her body mass index was 23 kg/m2. Vital signs were a blood pressure of 130/80 mmHg, pulse rate 68/min, respiratory rate 20/min, and body temperature 36.6℃. Her abdomen was soft and mildly distended. The initial complete blood count was white blood cells 8,000/mm3 (neutrophils 70.7%, lymphocytes 18.5%, eosinophils 3.2%), hemoglobin 11.5 g/dL, hematocrit 33.3%, and platelet 288,000/mm3. Her blood chemistry values were, fasting glucose 293 mg/dL, blood urea nitrogen 46.6 mg/dL, creatinine 10.3 mg/dL, sodium 134 mEq/L, potassium 4.4 mEq/L, chloride 90 mEq/L, AST 119 IU/L, ALT 192 IU/L, alkaline phosphatase 850 IU/L, amylase 110 U/L, total protein 6.8 g/dL, albumin 4.0 g/dL, calcium 11.1 mg/dL, phosphorus 6.2 mg/dL, CPK 43 IU/L, LDH 468 IU/L, total cholesterol 450 mg/dL, and triglyceride 1,096 mg/dL. Hepatitis B antigen and hepatitis C antibody were negative. ANCA, anti-liver kidney microsome antibody, and anti-smooth muscle antibody were all negative. Sonography of the abdomen revealed an increased echogenicity of the liver. A CT scan of the abdomen showed extensive low attenuated lesions in the liver capsule, the parenchyma of the left hepatic lobe and a small nodular lesion in the capsular area of the right lobe of the liver (). The MRI findings were consistent with the CT findings. The hepatic subcapsular area showed bright signals in the on-phase T1weighted images, but a marked signal decrease in the off-phase T1-weighed sequences; these findings suggested that the subcapsular area was composed of fat tissue. Hepatic subcapsular steatosis due to high dose intraperitoneal insulin was suspected; the patient was changed from CAPD to HD. Insulin was given only subcutaneously after changing to HD. A CT scan performed two months after starting HD showed complete resolution of the hepatic subcapsular steatosis (). Laboratory values were also improved: AST 34 IU/L, ALT 81 IU/L, alkaline phosphatase 733 IU/L, total cholesterol 259 mg/dL, and triglyceride 177 mg/dL. The blood sugar has been well controlled insulin therapy could be discontinued. Six months after changing from CAPD to HD, oral hypoglycemic agents have been sufficient to maintain adequate plasma glucose levels. Furthermore, liver enzyme levels are within normal range; the total cholesterol level was 206 mg/dL, and triglyceride level 157 mg/dL without requirement for lipid-lowering agents.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [46, 'years'], 'creatinine': [10.3, 'mg/dL'], 'sex': 'Female'}",4.04658,3.84425,4.24891,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 46 years old. The concentration of Creatinine is 10.3 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 10.3^(-1.154) * 46^(-0.203) * 1 * 0.742=4.04658.
Hence, the patient's GFR is 4.04658 mL/min/1.73m²."
3301,9,MDRD GFR Equation,lab test,decimal,usmle-12510,Extracted,"A 77-year-old woman is brought to the emergency department from her nursing home because she was found down overnight. On presentation she was found to be delirious and was unable to answer questions. Chart review shows that she is allergic to cephalosporins. Her temperature is 102.2°F (39°C), blood pressure is 105/52 mmHg, pulse is 94/min, and respirations are 23/min. Physical exam reveals a productive cough. A metabolic panel is obtained with the following results:

Serum:
Na+: 135 mEq/L
Cl-: 95 mEq/L
K+: 4 mEq/L
HCO3-: 19 mEq/L
BUN: 40 mg/dL
Creatinine: 2.5 mg/dL
Glucose: 150 mg/dL

Based on these findings two different drugs are started empirically. Gram stain on a blood sample is performed showing the presence of gram-positive organisms on all samples. One of the drugs is subsequently stopped.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [77, 'years'], 'creatinine': [2.5, 'mg/dL'], 'sex': 'Female'}",18.67504,17.74129,19.60879,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 77 years old. The concentration of Creatinine is 2.5 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.5^(-1.154) * 77^(-0.203) * 1 * 0.742=18.67504.
Hence, the patient's GFR is 18.67504 mL/min/1.73m²."
3302,9,MDRD GFR Equation,lab test,decimal,pmc-3481392-1,Extracted,"A 27-year-old man visited the emergency room with hemoptysis. His blood pressure was 180/100 mm Hg, and he had tachycardia (110/min) and tachypnea (24/min). He had been a heavy smoker, but had never been diagnosed with hypertension. Laboratory data was as follows: white blood cell count 13150/µL; hemoglobin level, 11.3 g/dL; platelet count, 110×103/µL; serum urea nitrogen level, 32 mg/dL; and serum creatinine level, 3.11 mg/dL. His serum electrolyte levels were as follows: sodium, 120 mEq/L; potassium, 2.5 mEq/L; chloride, 80 mEq/L; calcium, 7.5 mg/dL; and phosphorus, 3.2 mg/dL. Urinalysis showed microscopic hematuria and proteinuria (+++). Total protein to creatinine ratio in spot urine was 6.08 mg/g. Pro-brain natriuretic peptide level was markedly increased. Chest radiograph () and computed tomography showed bilateral infiltration, suggesting alveolar hemorrhage. Renal ultrasound using a Doppler scan showed increased echogenicity in both normal-sized kidneys without renal artery stenosis. Goodpasture's syndrome, SLE, microscopic polyangiitis or PAN was strongly suspected.
On the second hospital day, his serum creatinine level increased to 4.65 mg/dL. Anti-nuclear antibody test was negative, complement levels were normal, plasma renin activity was 6.27 ng/L·s (reference, 0.28-0.69 ng/L·s), serum aldosterone level was 6.54 nmol/L (reference, 0.11-0.28 nmol/L), and serum parathyroid hormone level was 159.1 pg/mL (reference, 14-72 pg/mL). Peripheral blood smear (PBS) showed some helmet cells suggestive of micrcoangiopathic hemolysis. Fundoscopic examination showed cotton wool spots and splinter hemorrhage with papillary edema, consistent with hypertensive changes ().
On the third day, his serum creatinine level increased to 4.91 mg/dL. Steroid pulse therapy was administered because of a strong suspicion of immune-mediated pulmonary renal syndrome.
A renal biopsy and bronchoscopy were promptly performed. Bronchoscopic examination showed mild hyperemia in both bronchi, with red bronchial alveolar lavage fluid. Light microscopic examination of the renal biopsy showed proliferative endarteritis in interlobular arteries and fibrinoid necrosis and intramural thrombi of small arterioles without crescent formation or necrotizing lesions, consistent with hypertensive nephrosclerosis (). Steroid therapy was rapidly decreased and stopped. A trans-bronchial lung biopsy showed macrophage infiltration into alveolar spaces and goblet cell metaplasia in bronchial mucosa generally seen in heavy smokers. Vanillyl-mandelic acid, metanephrine, epinephrine, and norepinephrine in 24-h urine samples were within normal levels. Tests for anti-glomerular basement membrane antibody and anti-neutrophil cytoplasmic antibody (ANCA) were negative. An echocardiogram showed eccentric left ventricular hypertrophy with decreased systolic and diastolic dysfunctions and a dilated left atrium. In the further reports of the patient's renal biopsy, immunofluorescent studies showed fine granular deposition of C3 and C1q only within the vessel walls and electron microscopic examination showed focal effacement of the epithelial cell foot processes, focally swollen endothelial cell with irregularly thickened capillary basement membrane and normal mesangial basement membrane without deposition.
His serum creatinine level increased to 5.15 mg/dL on the fourth day, but he did not require dialysis. Serum creatinine level gradually decreased with strict blood pressure control and was 4.03 mg/dL at discharge. The patient last visited the outpatient clinic 10 months after discharge: his blood pressure was 120/80 mm Hg and well controlled with antihypertensive mediation, and his serum creatinine level was 1.98 mg/dL.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [27, 'years'], 'creatinine': [1.98, 'mg/dL'], 'sex': 'Male'}",40.74925,38.71179,42.78671,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 27 years old. The concentration of Creatinine is 1.98 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.98^(-1.154) * 27^(-0.203) * 1 * 1=40.74925.
Hence, the patient's GFR is 40.74925 mL/min/1.73m²."
3303,9,MDRD GFR Equation,lab test,decimal,pmc-2776156-1,Extracted,"Female, 22 years old, the first born to healthy, unrelated Dutch parents. She has one healthy sibling. At the age of 1 year she was evaluated because of growth failure, abnormal chest shape and limb shortness. Skeletal radiographs showed a small, narrow thorax, brachydactyly of the fingers, short and broad diaphyses, and wide metaphyses of the arms and legs, and short iliac bones with spiky protrusions. There was no history of respiratory difficulties. At 3 years of age she was admitted because of a respiratory infection. Blood gas revealed a metabolic acidose, serum creatinine was elevated, urinalysis showed proteinuria and her blood pressure was 200/170 mmHg. Her renal function deteriorated (serum creatinine 422 μmol/l, ureum 16.8 mmol/l) and at the age of 4 years CAPD was started. A renal transplant was performed when she was 5 years old and 5 weeks later bilateral nephrectomy was performed because of persistent hypertension. At the age of 12 years she developed progressive renal failure, as a result of chronic rejection, and she was transplanted for a second time. Until now, her renal function remained stable. Ophthalmic examination showed narrow blood vessels without clinical problems. At the age of 22 years she is living independently and working as a nurse with mildly impaired exercise tolerance. Physical examination at the age of 22 years showed a height below the third centile, a sitting height/height ratio above the 97th centile, a chest circumference below the third centile, a hand length below the third centile and a foot length below the third centile. The chest radiograph showed an abnormal position of both ribs and claviculae with a CTR of 0.53 (reference < 0.50; []). Pathological examination of the native kidneys showed that most of the glomeruli were totally sclerotic and the remainder showed capillary collapse. Periglomular fibrosis, tubular atrophy and dilatation with interstitial lymphocyte infiltration were seen.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [22, 'years'], 'creatinine': [422.0, 'µmol/L'], 'sex': 'Female', 'Race': 'White'}",11.47943,10.90546,12.0534,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 22 years old. The concentration of Creatinine is 422.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 422.0 µmol. To convert 422.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 422.0 µmol Creatinine * 1e-06 mol/µmol = 0.00042 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00042 mol Creatinine * 113.12 g/mol = 0.04751 g Creatinine. To convert 0.04751 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.04751 g Creatinine * 1000.0 mg/g = 47.51 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 47.51 mg Creatinine/10.0 dL = 4.751 mg Creatinine/dL. The concentration value of 422.0 µmol Creatinine/L converts to 4.751 mg Creatinine/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 4.751^(-1.154) * 22^(-0.203) * 1 * 0.742=11.47943.
Hence, the patient's GFR is 11.47943 mL/min/1.73m²."
3304,9,MDRD GFR Equation,lab test,decimal,usmle-2777,Extracted,"A 67-year-old man with chronic kidney disease comes to the physician because of worsening fatigue and shortness of breath on exertion for 6 months. He has a 20-year history of poorly-controlled type 2 diabetes mellitus. Current medications include metformin and insulin. His pulse is 105/min. Examination shows conjunctival pallor and bounding pulses. Laboratory studies show:
Hemoglobin 8.6 g/dL
Mean corpuscular volume 90 μm3
Reticulocyte count 0.5%
Serum
Ferritin 325 ng/mL
Urea nitrogen 45 mg/dL
Creatinine 2.2 mg/dL
The patient is prescribed a drug to treat the cause of his current symptoms.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [67, 'years'], 'creatinine': [2.2, 'mg/dL'], 'sex': 'Male'}",30.00469,28.50446,31.50492,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 67 years old. The concentration of Creatinine is 2.2 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.2^(-1.154) * 67^(-0.203) * 1 * 1=30.00469.
Hence, the patient's GFR is 30.00469 mL/min/1.73m²."
3305,9,MDRD GFR Equation,lab test,decimal,pmc-3423709-1,Extracted,"A 65-year-old male was presented in March 2009 with primary metastatic adenocarcinoma of pancreas (metastases in retroperitoneal and cervical nodes). He had a history of nephrolythiasis ten years ago and 5 months lasting history of hydronephrosis of the left kidney of grade III, caused by enlarged retroperitoneal lymph nodes. At presentation he was overweight with grade I renal impairment (creatinine 129 μmol/L). He complained of pain in the upper abdomen. Tumour marker CA 19-9 was elevated (> 12 000 IU); platelet count was 376 × 109/L.
In March 16 2009 he started the treatment with gemcitabine monotherapy in a weekly dose 1000 mg/m2. After 3 weekly doses he had less pain in the abdomen and tumour marker CA 19-9 halved (6163 IU). Platelet count was elevated (570 × 109/L). He complained of painful swelling in three digits of right hand and acrocyanosis. After the 4th dose of gemcitabine pain in digits increased and the patient was admitted to the local hospital. Raynaud’s syndrome was suspected. Criteria for paraneoplastic microthrombosis, which was suspected, were not met. At the beginning the patient was treated with acetylsalicylic acid. No improvement was recorded. On the control visit in our institution (May 05 2009) the patient complained of severe pain in five digits of both hands. The examination showed dry fingertips necrosis. Radial and ulnar pulses were normal. The Doppler ultrasound of both arms showed normal macrocirculation. Digital plethismography showed an absent signal on digits I, II and IV of the right and digits III and V of the left hand. Gemcitabine induced vasculitis causing ischemia was suspected and gemcitabine treatment was stopped. The patient was treated with the prolonged infusion of a prostacycline analogue iloprost trometamol (20 mg/day for three weeks) and analgesic therapy with NSARD and opioids. Digital changes in all but one of affected digits resolved at the next visit in June 24 2009. Ischemic changes of distal phalange of digit V of the left hand required the amputation. The patient died in August 2009 due to the progressive disease.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [65, 'years'], 'creatinine': [129.0, 'µmol/L'], 'sex': 'Male'}",48.03874,45.6368,50.44068,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 65 years old. The concentration of Creatinine is 129.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 129.0 µmol. To convert 129.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 129.0 µmol Creatinine * 1e-06 mol/µmol = 0.00013 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00013 mol Creatinine * 113.12 g/mol = 0.01471 g Creatinine. To convert 0.01471 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01471 g Creatinine * 1000.0 mg/g = 14.71 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 14.71 mg Creatinine/10.0 dL = 1.471 mg Creatinine/dL. The concentration value of 129.0 µmol Creatinine/L converts to 1.471 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.471^(-1.154) * 65^(-0.203) * 1 * 1=48.03874.
Hence, the patient's GFR is 48.03874 mL/min/1.73m²."
3306,9,MDRD GFR Equation,lab test,decimal,pmc-5471780-1,Extracted,"An 82-year-old man presented to his general practitioner with anorexia, abdominal distension, pain, and fever. His past medical history consisted of left nephrectomy for renal cell carcinoma at 66 years of age. He had been found to have simple hepatic cysts at 55 years of age, and received a follow-up examination from his general practitioner with CT. Plain CT scanning and US revealed enlargement of a simple hepatic cyst measuring 20 cm in diameter, right hydronephrosis, and gallstones in the compressed gallbladder (Fig. ). Laboratory analysis showed severe inflammation and renal dysfunction. Thus, he was referred and admitted to our hospital for further evaluation and treatment. Laboratory data on admission showed increased serum C-reactive protein (CRP) and creatinine levels: 34.0 and 1.61 mg/dL, respectively (Table ). Liver function tests and serum tumor marker levels were within the normal range, except for a slight elevation in alkaline phosphatase (385 IU/L, reference range: 115–359). Urinalysis showed no signs of urinary tract infection, and blood culture was negative. Although CT showed gallstones, acute cholecystitis was negative due to almost normal liver function tests. Therefore, we diagnosed the patient with an infected hepatic cyst complicated by urinary tract obstruction, and we prescribed intravenous drip infusion of cefoperazone sodium and sulbactam sodium (1 g, twice a day). Despite intravenous drip infusion of antibiotics, the patient's fever persisted. Thus, we inserted a drainage tube into the largest hepatic cyst with suspected infection under ultrasound guidance. About 3,800 mL of yellow, turbid fluid was drained. Cystography did not show any communication between the intrahepatic bile ducts. Then, 400 mg of minocycline hydrochloride in 40 mL of saline was injected for conglutination. The catheter was clamped and reopened after 24 h. Streptococcus parasanguinis was isolated from the cyst fluid. Cystic fluid carbohydrate antigen 19-9 (CA19-9) level was 264,338 U/mL (normal range for serum CA19-9 level: 0–35). However, neoplastic cells were not detected in the cystic fluid. We injected minocycline hydrochloride 2 more times, on days 4 and 12, after catheter insertion. After drainage, abdominal symptoms and fever resolved, and serum CRP and creatinine levels improved (Fig. ). The amount of daily drainage gradually decreased from approximately 1,000 mL to about 100 mL. Follow-up CT scan and abdominal US showed prominent regression of the hepatic cyst and relief of the ureteral obstruction (Fig. ). Thus, we removed the catheter 19 days after insertion. Regarding his gallstones, magnetic resonance cholangiopancreatography(MRCP) also revealed a common bile duct stone. Thus, we treated him by endoscopic retrograde cholangiopancreatography (ERCP), sphincterotomy, and stone removal. ERCP did not show any communication between the intrahepatic bile ducts. His asymptomatic gallstones were followed up without cholecystectomy due to his age. The patient was then discharged in excellent general condition 1 month after admission. He has since shown an uneventful course without reenlargement of the hepatic cyst.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [82, 'years'], 'creatinine': [1.61, 'mg/dL'], 'sex': 'Male'}",41.29113,39.22657,43.35569,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 82 years old. The concentration of Creatinine is 1.61 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.61^(-1.154) * 82^(-0.203) * 1 * 1=41.29113.
Hence, the patient's GFR is 41.29113 mL/min/1.73m²."
3307,9,MDRD GFR Equation,lab test,decimal,pmc-7171472-1,Extracted,"A 42-year-old male on peritoneal dialysis presented with abdominal pain and cloudy effluent of one-day duration. The patient denied any fever and denied any in advent breach in the technique while making peritoneal dialysis connections. Moreover, the patient denied history of diarrhea or constipation. The patient has been on peritoneal dialysis for five years and had no prior history of peritonitis. Past medical history was signification for diabetes, hypertension, hyperlipidemia, hyperparathyroidism, end-stage renal disease on peritoneal dialysis. Home medications included metoprolol 100 milligrams (mg) twice a day, nifedipine 60 mg extendedrelease daily, atorvastatin 80 mg daily, sevelamer 2400 mg three times a day with meals, calcitriol 0.5 micrograms (mcg) daily, gabapentin 100 mg daily at bedtime, cinacalcet 30 mg daily, insulin glargine 15 units daily, insulin sliding scale.
The vital signs on presentation were the temperature of 36.4 Celsius, pulse rate of 84 beats per minute, respiratory rate of 16 breath per minute, blood pressure of 158/95 mm Hg. Physical examination revealed abdominal tenderness with a peritoneal dialysis catheter in the right lower quadrant. There was no exit site drainage or redness along the tunnel and the rest of the physical examination was nonsignificant.
Laboratory analysis showed white blood count 10300 mm3, hemoglobin 11.2 gm/dl, platelet count 22300 mm3, sodium 138 mmol/l, potassium 4.5 mmol/l, bicarbonate 22 mmol/l, blood urea nitrogen 58 mg/dl, creatinine 11.6 mg/dl, albumin 3.3 g/dl. The peritoneal fluid effluent revealed peritoneal fluid white blood cells (WBC) 1837 cells/ul with 85% predominant neutrophils. Peritoneal fluid gram stain revealed >100 WBC, and no organisms were seen. The patient was started on empiric treatment for peritonitis with intraperitoneal vancomycin and ceftazidime. Later on, peritoneal fluid culture grew Citrobacter freundii in both aerobic and anaerobic bottles. The sensitivities of Citrobacter freundii were listed in done by VITEK 2 method.
The patient was treated with double antibiotic coverage of intraperitoneal ceftazidime and oral ciprofloxacin for three weeks. The repeat peritoneal fluid cultures after finishing the antibiotic course yielded heavy growth of C. freundii again. The sensitivities of Citrobacter freundii are listed in done. Another three weeks course of double antibiotic treatment (intraperitoneal ceftazidime and intravenous imipenem) was given, which failed to clear the organism. The symptoms resolved when peritoneal dialysis catheter was removed after failing two double antibiotic courses. Subsequently, he did not require a further course of antibiotics. The dialysis modality of the patient was then switched to hemodialysis and the patient continues to be hemodialysis dependent after two years of follow up.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [42, 'years'], 'creatinine': [11.6, 'mg/dL'], 'sex': 'Male'}",4.84322,4.60106,5.08538,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 42 years old. The concentration of Creatinine is 11.6 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 11.6^(-1.154) * 42^(-0.203) * 1 * 1=4.84322.
Hence, the patient's GFR is 4.84322 mL/min/1.73m²."
3308,9,MDRD GFR Equation,lab test,decimal,pmc-7872057-2,Extracted,"A 67-year-old White male with a history of stage IV metastatic melanoma receiving combination therapy with ipilimumab (anti-CTLA4) and pembrolizumab (anti-PD1) was admitted for altered mental status and AKI. He was diagnosed with CPI-induced autoimmune encephalitis and methylprednisolone 1 g IV daily was initiated. His serum creatinine peaked at 3.54 mg/dL (baseline 0.93 g/dL). No biopsy was obtained since his creatinine had improved. Two weeks after he completed a five-week course of GC treatment, he again recurred with AKI, Cr 2.26 mg/dL (from Cr 1.01 mg/dL). Kidney biopsy confirmed ATIN with focal non-caseating granuloma (negative for acid-fast and fungal stains) () and ATI (acute tubular injury). Due to relapsed CPI-ATIN, he was reinitiated on a shortened course of prednisone and infliximab and experienced complete renal recovery achieving baseline function with a Cr 0.97 mg/dL. He has no evidence of cancer recurrence and continues to be followed.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [67, 'years'], 'creatinine': [0.97, 'mg/dL'], 'sex': 'Male', 'Race': 'White'}",77.19875,73.33881,81.05869,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 67 years old. The concentration of Creatinine is 0.97 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 0.97^(-1.154) * 67^(-0.203) * 1 * 1=77.19875.
Hence, the patient's GFR is 77.19875 mL/min/1.73m²."
3309,9,MDRD GFR Equation,lab test,decimal,pmc-5582273-1,Extracted,"A 56-year-old man was admitted to the medical intensive care unit for acute hypoxemic respiratory failure. Initial chest X-ray showed bilateral extensive multifocal nodular pulmonary opacities. He had a temperature of 38.9°C, blood pressure of 82/54 mmHg, heart rate of 51 per min, and oxygen saturation of 91% on supplemental O2 (FiO2 of 95%) on admission.
For suspected severe sepsis from healthcare-associated pneumonia, he was started on vancomycin, piperacillin-tazobactam, and methylprednisolone 50 mg IV every 8 h. Laboratories showed pancytopenia with white blood cell (WBC) count of 1.6 × 103/μL, absolute neutrophil count (ANC) of 0.7 × 103/μL, hemoglobin of 11.3 g/dL, hematocrit of 36%, and platelet count of 99 × 103/μL. Creatinine was elevated at 1.07 mg/dL from a baseline of 0.38 mg/dL. Liver function tests were within normal range except for albumin of 1.8 g/dL. Urinalysis showed new onset microscopic hematuria and nephritic-range proteinuria (70.2 mg/dL). Serum ferritin was elevated at 7512 ng/mL (normal 26–388 ng/mL). Abdominal ultrasound showed splenomegaly (spleen size was 17.7 cm). Hematology, Rheumatology, and Nephrology services were consulted, but a renal biopsy was unable to be done due to critical status.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [56, 'years'], 'creatinine': [1.07, 'mg/dL'], 'sex': 'Male'}",71.49028,67.91577,75.06479,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 56 years old. The concentration of Creatinine is 1.07 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.07^(-1.154) * 56^(-0.203) * 1 * 1=71.49028.
Hence, the patient's GFR is 71.49028 mL/min/1.73m²."
3310,9,MDRD GFR Equation,lab test,decimal,pmc-6051099-1,Extracted,"A 71-year-old female with multiple myeloma status after 5 cycles of ixazomib, lenalidomide, and dexamethasone, chronic kidney disease stage III, previous stroke, hypertension, gout, and peripheral arterial disease presented to the hospital with generalized weakness, vomiting, and diarrhea as well as acute on chronic kidney injury in which serum creatinine and creatinine clearance (CrCl) were 3.3 mg/dl and 15 ml/min, respectively (baseline creatinine of 1.9 mg/dl with CrCl of 30 ml/min). Blood test showed thrombocytopenia with a platelet count of 84000/dl and anemia with hemoglobin of 12 g/dl. Regarding multiple myeloma, she was diagnosed with kappa light chain multiple myeloma with extensive lytic lesions in bones as well as renal dysfunction a few years ago. Diagnosis was made by bone marrow biopsy which demonstrated 80%–90% cellular marrow with 61% plasma cells. FISH study was abnormal for chromosome 1q, chromosome 13q, and 17p deletion. Based on patient's average CrCl of 30 ml/min, ixazomib was started at a dose of 3 mg on days 1, 8, and 15 of a 28-day treatment cycle along with lenalidomide and dexamethasone. After the second cycle of ixazomib, the patient had been having intermittent GI disturbances including diarrhea, and biweekly blood test revealed thrombocytopenia with a nadir of about 75000/dl (), which were both attributed to ixazomib. Ixazomib was held on admission due to significant vomiting, abdominal pain, and diarrhea. Clostridium difficile toxin and stool culture were negative, ruling out infectious causes. One week after admission, the platelet count decreased dramatically to 9000/dl from 84000/dl on admission. The patient also developed intravascular hemolysis evident by an elevated LDH level (1366 units/L), decreased haptoglobin level (10 mg/dl), elevated total bilirubin (1.6 mg/dl), and indirect bilirubin (1.3 mg/dl). Peripheral blood smear also showed profound schistocytes. Coomb's test was negative, and DIC was ruled out as the fibrinogen level was normal (521 mg/dl). Acute thrombocytopenia, Coomb's negative hemolytic anemia with profound schistocytes, and acute renal injury raised the concern for TMA. Given the high morbidity of TMA, the patient received fresh frozen plasma and underwent plasmapheresis while further workup was in progress. Normal ADAMTS13 activity ruled out TTP. Normal complement levels and negative stool culture made atypical HUS and HUS less likely. Plasmapheresis was stopped after 5 days due to lack of clinical improvement and negative workup for TTP. Approximately three weeks after the onset of TMA, the platelet count started to improve spontaneously with supportive management. The gradual and spontaneous improvement in the platelet count pointed suspicion away from malignancy-induced TMA and favored DTMA caused by cumulative toxicity of ixazomib, likely precipitated by acute renal dysfunction and hypoproteinemia from malnutrition and chronic diarrhea related to ixazomib side effect. The presentation of this patient was consistent with ixazomib-induced DTMA from cumulative toxicity as the clinical picture of TMA improved after stopping ixazomib, independently of plasmapheresis. Also, the lack of recurrence of TMA after stopping ixazomib supported the diagnosis in our case.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [71, 'years'], 'creatinine': [3.3, 'mg/dL'], 'sex': 'Female'}",13.7807,13.09166,14.46974,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 71 years old. The concentration of Creatinine is 3.3 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 3.3^(-1.154) * 71^(-0.203) * 1 * 0.742=13.7807.
Hence, the patient's GFR is 13.7807 mL/min/1.73m²."
3311,9,MDRD GFR Equation,lab test,decimal,usmle-10845,Extracted,"A 55-year-old African American male presents to his primary care physician with complaints of persistent back pain and fatigue over 12 months. Physical examination reveals a blood pressure of 190/150 mm Hg, and laboratory tests reveal hyperlipidemia and a serum creatinine level of 3.0 mg/dL. 4.5 g of protein are excreted in the urine over 24 hours. Renal biopsy shows eosinophilic, acellular material in the glomerular tuft and capillary walls that display apple green-colored birefringence in polarized light upon Congo red tissue staining.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [55, 'years'], 'creatinine': [3.0, 'mg/dL'], 'sex': 'Male', 'Race': 'Black'}",26.46361,25.14043,27.78679,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 55 years old. The concentration of Creatinine is 3.0 mg/dL. 
The patient is Black, so the race coefficient is 1.212.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.0^(-1.154) * 55^(-0.203) * 1.212 * 1=26.46361.
Hence, the patient's GFR is 26.46361 mL/min/1.73m²."
3312,9,MDRD GFR Equation,lab test,decimal,pmc-6712628-2,Extracted,"A 47-year-old Tamil woman from Northern Sri Lanka was referred by a peripheral clinic for further evaluation of elevated serum creatinine. She had been hypertensive for 5 years; she did not have a history of diabetes or ischemic heart disease. She was on treatment for hypertension and hypercholesterolemia with enalapril 5 mg daily and fenofibrate 200 mg daily. She did not have a history suggestive of renal disease, autoimmune disorder, or connective tissue disorder. She failed to recall any history of major trauma, dehydration, ingestion of drugs and/or toxins, or seizures within the last few weeks. She is a housewife and mother of two children. Similar to many Asian women, she did not consume alcohol and she did not smoke tobacco. She was married to a hospital clerk, and did not recall exposure to toxins. She was not living in an endemic area of chronic interstitial nephritis in agricultural communities (CINAC).
She had a blood pressure of 150/100 mmHg, with normal cardiovascular examination. She was not pale. She did not have any edema on examination. Her serum creatinine was 126 umol/L, with a blood urea of 3.2 mmol/L. Urine analysis revealed bland sediment with 100 mg/dL of protein, but no hemoglobin or myoglobin. A full blood count showed hemoglobin of 112 g/L, with a mean corpuscular volume of 98 fl. This raised the possibility of hypothyroidism. Further investigations showed a UPCR of 1.6, elevated serum lipids, TSH of > 100 U/L, and CK of 3980 U/L. Her liver profile showed alanine transferase (ALT) of 45 (reference range < 30), aspartate transferase (AST) of 56 (reference range < 30), and alkaline phosphatase (ALP) of 122 (reference range < 245), slight derangement. An initial diagnosis of fenofibrate-induced rhabdomyolysis was made, and fenofibrate was withdrawn from the treatment. She was initiated on management of rhabdomyolysis with alkaline diuresis. An ultrasound scan of her abdomen revealed normal-looking kidneys and no lymphadenopathy. Hepatitis B, hepatitis C, HIV, antinuclear factor, C3 level, and C4 level, were all within reference ranges. Urine myoglobin and urine hemosiderin deposits were negative. However, there was no change in her CK levels (3870 U/L) or creatinine (133 umol/L) levels after a lapse of 2 weeks, and we decided her elevated CK levels were unlikely to be due to fenofibrate-induced rhabdomyolysis. We assumed it was due to hypothyroidism and started an escalating dose of thyroxine at 25 μg/day, with increments of 25 μg each 2 weeks, up to 75 μg/day. A renal biopsy was not performed initially as rhabdomyolysis was not likely, and it was not performed later due to rapid resolution with thyroxine. An ultrasound plus duplex of her thyroid revealed a multinodular goiter with no prominent or vascular nodules. Her CK gradually dropped over the next 12 weeks, with her creatinine, to 93 umol/L. Her UPCR reduced to 0.6 after 6 months of treatment. At the end of 6 months of follow-up her renal function and thyroid functions normalized, and proteinuria was absent.
In both patients, thyroglobulin antibodies tests were not performed due to economic constraints. A summary of the investigations is given in Table . Figure gives a graphical representation of change of renal functions and CK levels with TSH.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [47, 'years'], 'creatinine': [126.0, 'µmol/L'], 'sex': 'Female', 'Race': 'Asian'}",38.06984,36.16635,39.97333,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 47 years old. The concentration of Creatinine is 126.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 126.0 µmol. To convert 126.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 126.0 µmol Creatinine * 1e-06 mol/µmol = 0.00013 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00013 mol Creatinine * 113.12 g/mol = 0.01471 g Creatinine. To convert 0.01471 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01471 g Creatinine * 1000.0 mg/g = 14.71 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 14.71 mg Creatinine/10.0 dL = 1.471 mg Creatinine/dL. The concentration value of 126.0 µmol Creatinine/L converts to 1.471 mg Creatinine/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.471^(-1.154) * 47^(-0.203) * 1 * 0.742=38.06984.
Hence, the patient's GFR is 38.06984 mL/min/1.73m²."
3313,9,MDRD GFR Equation,lab test,decimal,usmle-8710,Extracted,"A 74-year-old man returns to his physician to follow-up on laboratory studies obtained for anemia 2 weeks ago. He has no complaints. He has a 20-year history of hypertension and several years of knee osteoarthritis. He walks 2 miles a day. He does not smoke. He drinks alcohol moderately. He takes hydrochlorothiazide, losartan, and pain killers, including ibuprofen. The vital signs include: temperature 37.1°C (98.8°F), pulse 68/min, respiratory rate 12/min, and blood pressure 110/70 mm Hg. The physical examination shows no abnormalities. The laboratory studies show the following:
Laboratory test
Hemoglobin 10 g/dL
Mean corpuscular volume 75 μm3
Leukocyte count 5,000/mm3
Platelet count 350,000/mm3
ESR 18 mm/hr
Serum
Ferritin 5 μg/L
Iron 30 μg/L
Total iron-binding capacity 500 μg/dL
Calcium (Ca+) 9 mg/dL
Albumin 4 g/dL
Urea nitrogen 14 mg/dL
Creatinine 0.9 mg/dL
Monoclonal protein on serum electrophoresis is 12 g/L (non-IgM). Clonal bone marrow plasma cells comprise 4% of the total number of cells. Skeletal survey with magnetic resonance imaging reveals no pathologic findings.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [74, 'years'], 'creatinine': [0.9, 'mg/dL'], 'sex': 'Male'}",82.4875,78.36312,86.61187,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 74 years old. The concentration of Creatinine is 0.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 0.9^(-1.154) * 74^(-0.203) * 1 * 1=82.4875.
Hence, the patient's GFR is 82.4875 mL/min/1.73m²."
3314,9,MDRD GFR Equation,lab test,decimal,pmc-6375246-1,Extracted,"A 72-year-old female patient with end-stage renal failure, who had been undergoing dialysis for the previous 9 months, presented with headaches, lightheadedness, dizziness, balance disorders, vision disturbance, fatigue, memory disturbances, depression and anxiety.
She had undergone a total thyroidectomy 54 years previously, due to goitre. Hypothyroidism requiring thyrormone supplementation and marginal hypocalcaemia were since reported. Twenty-three years prior to the current admission, she developed hypertension and incipient renal insufficiency. The primary cause was considered to be renovascular disease, but her case was not pursued further. Her recovered follow-up data revealed that 15 years previously, she had a serum creatinine of 1.4 mg/dl, normal urinary sediment, serum calcium of 8.1 mg/dl and serum phosphate of 6.8 mg/dl, while receiving alphacalcidol at 1 mg/day.
Nine years prior to the present admission, while her serum creatinine was 1.8 mg/dl, she underwent a radionuclide study with 99mTc–Mag3 showing decreased renal perfusion and abnormal parenchymal function with reduced kidney size. Alphacalcidol was discontinued 5 years ago due to hypercalcaemia, when her serum creatinine had risen to 2 mg/dl. Her renal function gradually worsened and the patient finally reached end-stage renal failure. Renal replacement treatment with haemodialysis was initiated 9 months prior to admission. Intact parathormone (iPTH) measurements at that time were in the range 0–1 pg/ml.
On admission, the patient was drowsy and possessed a BP of 130/80 mmHg and temperature of 36.4°C. Physical examination revealed a mild systolic murmur at the heart apex that radiated to the neck, and a systole–diastolic murmur at the umbilical area and groin region. Neurological examination was remarkable for fixed, symmetrical pupils, normal pyramidal signs and reflexes, reduced muscle tone, a Parkinsonian tremor, impaired posture and gait. The patient was alert, but slightly disoriented with memory defects. Fundoscopy showed mild papillary oedema. Blood gases were within normal limits. The skull x-ray revealed discrete intracranial calcifications (). A CT scan of the head demonstrated the presence of numerous, symmetrically located calcifications in both frontal lobes, subcortical nuclei, the paraventricular region, brain fornix, as well as both cerebellar hemispheres (). Further radiological evaluation revealed extended calcification of arteries of various sizes ().","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [72, 'years'], 'creatinine': [2.0, 'mg/dL']}",24.49147,23.2669,25.71604,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 72 years old. The concentration of Creatinine is 2.0 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.0^(-1.154) * 72^(-0.203) * 1 * 0.742=24.49147.
Hence, the patient's GFR is 24.49147 mL/min/1.73m²."
3315,9,MDRD GFR Equation,lab test,decimal,pmc-4655807-1,Extracted,"A 61-year-old Caucasian female developed end-stage kidney disease (ESKD) secondary to membranoproliferative glomerulonephritis (MPGN) based on a native kidney biopsy in 2001, with no further information about IF or electron microscopy (EM). In December 2006, her serum creatinine (SCr) was 530 μmol/L and she underwent a preemptive unrelated living kidney transplantation. In 2014, she was found to have a random urine protein/gram creatinine (UPCR) of ∼452 mg/mmol and an SCr of 132 μmol/L, up from 106 μmol/L. Her workup for a lymphoproliferative disorder was negative, as was her serologic workup (see Table ). On biopsy, IF showed diffuse granular positivity for IgG, C3 and C1q. Deposits were composed of IgG3-kappa with no peritubular C4d. EM showed EDDs, mostly in the mesangium and subendothelial regions (please see Figures–). She received three cycles of bortezomib. UPCR was persistently elevated at 565 mg/mmol. She was later switched to Carfilzomib, as she developed acute kidney injury with SCr up to 247 μmol/L; after completion of therapy her SCr was 150 μmol/L.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [61, 'years'], 'creatinine': [150.0, 'µmol/L'], 'sex': 'Female', 'Race': 'White'}",30.61732,29.08645,32.14819,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 61 years old. The concentration of Creatinine is 150.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 150.0 µmol. To convert 150.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 150.0 µmol Creatinine * 1e-06 mol/µmol = 0.00015 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00015 mol Creatinine * 113.12 g/mol = 0.01697 g Creatinine. To convert 0.01697 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01697 g Creatinine * 1000.0 mg/g = 16.97 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 16.97 mg Creatinine/10.0 dL = 1.697 mg Creatinine/dL. The concentration value of 150.0 µmol Creatinine/L converts to 1.697 mg Creatinine/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.697^(-1.154) * 61^(-0.203) * 1 * 0.742=30.61732.
Hence, the patient's GFR is 30.61732 mL/min/1.73m²."
3316,9,MDRD GFR Equation,lab test,decimal,pmc-8284755-1,Extracted,"A 66-year-old male patient presented with a history of hypertension, diabetes mellitus, and concurrent renal and ureteral stones after receiving endoscopic management at another hospital about 1 month previously. Residual stones in the UPJ and lower calyx were noted in a kidney, ureter, and bladder radiograph (Fig. ) after the previous operation. The patient reported severe flank pain, and a second operation was considered to be necessary due to the deterioration of his renal function. According to the records of the previous operation, a tight connection between the UPJ stones and adjacent ureter mucosa made it difficult to push back to the renal pelvis, and the severe angulation made it difficult to reach the edge of the UPJ stones. Therefore, ureteroscopic lithotripsy had been performed for the distal stones with PCNL for the renal pelvis stones in the previous operation. Consequently, a residual UPJ stone about 2.8 cm in size and multiple small lower calyx stones were left with D-J stenting and percutaneous nephrostomy.
Laboratory studies, including tests for amylase, lipase, bilirubin, alanine, aspartate aminotransferases, and urine analysis were all within normal ranges. Computed tomography was performed to identify the relative positions of the UPJ stone, renal stones, and D-J stent to assess the pre-operative condition (Fig. ).
We placed the patient in the left decubitus position with his right flank upward, and the procedure was performed through 4 ports (Fig. ). An 11-mm trocar inserted 3 cm lateral to the umbilicus was used as the camera port using an open method. A 5-mm trocar (first working port) was placed in the subcostal area around the midclavicular line, and another 5-mm trocar (second working port) was placed 6 cm lateral to the camera port over the anterior axillary line. The third working port was a 5-mm assistant port over the midclavicular line 8 cm beneath the second working port. After reflection of the colon, the ureter was identified and mobilized, and the stone was located and extracted through a vertical ureterostomy. Using a stone grasper, the stone was extracted through the camera port (Fig. A and B). We then performed LA-RIRS after ureterolithotomy. We inserted a flexible ureteroscope through the third working port to perform a ureterostomy, and suctioned overflow normal saline from the outlet of the ureterostomy via the first port (Fig. A). Lower calyx stones were found and removed using a basket (Fig. B). The ureterostomy was closed as 2 layers with interrupted 4.0 Vicryl sutures to close the ureterostomy incision along the D-J stent. A 7-mm Jackson–Pratt drain was inserted through the second port. The total operation time from skin to skin was 1 hour and 27 minutes.
No complications were noted after the surgery, and the Jackson–Pratt drain was removed 3 days after the operation. The total hospital course was about 5 days.
A follow-up kidney, ureter, and bladder radiograph (Fig. ) were arranged 2 months after the operation, and no residual stones above 2 mm were found. Laboratory data measured during the same clinic visit showed a decline in creatinine from 1.63 to 1.1 mg/dL. The D-J stent was removed through cystoscopy after a radiograph in outpatient surgery. According to the Clavien Dindo classification, only a low grade II complication of a urinary tract infection was noted, which did not cause sepsis, and was treated with antibiotics.[ No high-grade complications occurred. A follow-up renal echo was performed 1 month after the D-J stent had been removed, which showed no obstructive nephropathy or significant residual renal calculi above 2 mm.
He is currently receiving regular follow-up of renal function, kidney, ureter, and bladder radiography, and renal echo every 6 months to 1 year.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [66, 'years'], 'creatinine': [1.1, 'mg/dL'], 'sex': 'Male'}",66.97357,63.62489,70.32225,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 66 years old. The concentration of Creatinine is 1.1 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.1^(-1.154) * 66^(-0.203) * 1 * 1=66.97357.
Hence, the patient's GFR is 66.97357 mL/min/1.73m²."
3317,9,MDRD GFR Equation,lab test,decimal,pmc-4241641-1,Extracted,"A 36-year-old African American female with a history of asthma, hypertension, pulmonary embolism and metastatic breast cancer presented with fever 1 day after the administration of a single intravenous 4-mg dose of zoledronate. She received vancomycin and piperacillin/tazobactam for 4 days and was discharged without antibiotics after she defervesced and showed negative culture results. She presented again 6 days later with anasarca and nonoliguric AKI. Her home medications consisted of gabapentin, promethazine, ranitidine, amlodipine, enoxaparin subcutaneously, albuterol inhaler and morphine. Her vital signs were a temperature of 36.6°C, a blood pressure of 141/91 mm Hg, a pulse of 102 beats/min and an oxygen saturation of 97% breathing room air. The physical examination was remarkable for anasarca, distended neck veins and decreased breath sounds throughout her right hemithorax. The laboratory data displayed mild leukocytosis, thrombocytosis, hemoglobin 8.8 g/dl and serum creatinine 556.9 µmol/l (6.3 mg/dl) [baseline 79.6 µmol/l (0.9 mg/dl)]. The urinalysis exhibited many granular casts and few white and red blood cell casts. A 24-hour urine collection revealed proteinuria of 3.5 g/24 h without a paraprotein. The complete serological workup was negative; this included HIV, parvovirus, cytomegalovirus, hepatitis B and hepatitis C serologies, rapid plasma reagin, antineutrophil cytoplasmic antibodies, antiglomerular basement membrane antibodies and normal serum complements. Renal ultrasound showed normal-sized kidneys and no hydronephrosis. Given our patient's overall good functional status despite her metastatic cancer, a kidney biopsy was performed 16 days after the exposure to zoledronate. Light microscopy of the biopsy specimen exhibited a total of 27 glomeruli, 2 of which were segmentally to globally collapsed with overlying hyperplasia and hypertrophy of the parietal epithelial cells, and microcystic dilation of the tubules. Additionally, there was evidence of mild interstitial infiltrate and moderate acute tubular injury (fig. ). Electron microscopy revealed podocyte foot process effacement without immune complex deposits (fig. ).
The patient's renal disease course (serum creatinine and proteinuria) is described in figure . She remained nonoliguric and did not require renal replacement therapy. Her serum creatinine peaked at 556.9 µmol/l (6.3 mg/dl) and proteinuria at 3.5 g/24 h (350 mg/mmol). After kidney biopsy results became available, the patient was started on low-dose lisinopril (2.5 mg daily) and no additional zoledronate therapy was given. Approximately 6 weeks after zoledronate exposure, her proteinuria decreased to 90.5 mg/mmol (0.8 g/g-1.73 m2) by urine protein-to-creatinine ratio, her serum albumin improved from 3.1 to 4.1 g/dl, and her serum creatinine improved to 141.4 µmol/l (1.60 mg/dl).
To expand on her cancer history, the patient was diagnosed with right breast carcinoma (estrogen/progesterone positive, human epidermal growth factor receptor 2 negative) about 8 years before the aforementioned presentation. She was treated with modified mastectomy and neoadjuvant chemotherapy (doxorubicin and cyclophosphamide) in addition to tamoxifen. The patient was then lost to follow-up until she presented 4 years later with metastases and was started on bevacizumab and paclitaxel. Four cycles were administered prior to discontinuing this regimen due to the development of proteinuria. Her proteinuria eventually improved to only trace on semiquantitative dipstick urinalysis. She was then treated with gemcitabine, vinorelbine tartrate and paclitaxel until her most recent presentation described above.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [36, 'years'], 'creatinine': [6.3, 'mg/dL'], 'sex': 'Female', 'Race': 'Black'}",9.09026,8.63575,9.54477,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 36 years old. The concentration of Creatinine is 6.3 mg/dL. 
The patient is Black, so the race coefficient is 1.212.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 6.3^(-1.154) * 36^(-0.203) * 1.212 * 0.742=9.09026.
Hence, the patient's GFR is 9.09026 mL/min/1.73m²."
3318,9,MDRD GFR Equation,lab test,decimal,pmc-7751079-1,Extracted,"A 72 year-old man with generalized fatigue was hospitalized at our Department of Diabetes Medicine because of rapidly worsening blood sugar control and an increased inflammatory response. He had a history of hypertension and type II diabetes mellitus.
Characteristics on admission were as follows: height, 173 cm, and body weight, 59 kg. Hematological findings at the time of the initial examination were as follows: white blood cell count, 10190/µL; neutrophils, 82.5%; C-reactive protein (CRP), 7.24 mg/dL; creatinine (Cr), 2.25 mg/dL; and hemoglobin A1c, 9.3%. These results indicated a high leukocyte count and inflammatory response, low renal function, and poor diabetes control.
Contrast-enhanced computed tomography (CT) showed localized dissection from the abdominal aorta to the right common iliac artery. He was suspected of having an infectious abdominal aortic aneurysm and was referred to our department ().
After admission, antibiotic therapy (vancomycin, ceftriaxone, and levofloxacin) was started for the suspected infectious aortic aneurysm. Consequently, the leukocyte count and CRP decreased steadily (CRP, 7.24 to 0.12). Blood culture tests were conducted multiple times, and all yielded negative results. However, the antibiotic therapy was continued for a total of 6 weeks, following which the inflammation resolved.
Contrast CT conducted 1 month later showed a penetrating aortic ulcer-like irregular inflow of contrast agent in the lumen of the aortic aneurysm. Furthermore, the aortic aneurysm had enlarged compared with the CT imaging on admission (descending aorta, 36–43 mm; suprarenal aorta, 37–44 mm; infrarenal aorta, 34–37 mm; and right common iliac artery, 31–35 mm), thus indicating the necessity for the treatment ( and ).
Because of his advanced age, poorly controlled diabetes mellitus, and renal dysfunction, staged surgery was considered adequate for treating his extensive aortic aneurysms. However, saccular aneurysm was observed to be growing rapidly. As the infection was controlled, a one-step treatment with a fenestrated stent graft was considered better.
Endovascular surgery was conducted in the supine position under general anesthesia. The common femoral arteries (FA) were exposed bilaterally. A 12-Fr safe sheath was placed in the right FA, and a 6-Fr sheath was placed in the left FA. A hybrid operating room (Trinias; Shimadzu Corporation, Kyoto, Japan) was used for angiography.
The Zenith TX2 Extension (ESBE-26-80-T-PF; Cook Medical Inc., Bloomington, IN, USA) was removed from the sheath. Based on the CT image, four fenestrations of 10, 13, 10, and 10 mm were created for the 7 mm celiac artery, 7 mm superior mesenteric artery (SMA), 5 mm left renal artery (RA), and 5 mm right RA, respectively.
To prevent endoleaks from the fenestrations, two 4/8 mm Tornado coils (MWCE-18S-4/8-TORNADO-LEF-081800; Cook Medical Inc.) were deployed at the portion sealing zone between the fenestrations for the celiac artery, SMA, and the saccular aneurysms (). Then, they were gathered into a 10 mm bundle and sutured with a single interrupted 6-0 polypropylene suture () to prompt thrombosis at the same site, thereby reinforcing attachment between the wall of the aorta and surrounding areas. To ensure that the fenestration site under fluoroscopy can be visualized more easily and that the fenestration opened in circular shape without deformation, the metal portions of Amplatz Goose neck snares (Medtronic, Dublin, IE) were sutured to the fenestrations for the SMA and left RA with 6-0 polypropylene sutures () and then re-inserted in the sheath.
A pigtail catheter and Radiofocus Guidewire (Terumo, Tokyo, Japan) were inserted through the right FA to replace the guidewire with a Lunderquist Extra-Stiff Wire Guide (Cook Medical Inc.) at the ascending aorta. The TX2 Extension (ESBE-26-80-TPF) fenestrated beforehand was inserted from the right FA and deployed after ensuring its position with the contrast image (). To completely exclude the thoracoabdominal aortic aneurysm, another TX2 Extension (ESBE-28-80-T-PF) was deployed. Endologix Powerlink® (EPL) stent (28-16-120BL; Endologix, Irvine, CA, USA) was inserted via the right FA and deployed to sit on the terminal aorta. An additional EPL Extension (28-28-75L0) was deployed and adjusted with a coda balloon (32 mm; Cook Medical Inc.) to bridge the gap between the EPL main body and the fenestrated TX2 Extension.
The final imaging procedure was conducted to ensure that there were no occluded branches or endoleaks so that the surgery could be completed. The operative time was 215 min, with a blood loss of 67 mL; 200 mL of contrast agent was used postoperatively, and the patient was extubated in the operating room and transferred to the intensive care unit. Oral tranexamic acid was administered postoperatively. Cefazolin was administered for 48 h as perioperative antibiotic therapy, and then, it was discontinued.
The postoperative course was favorable. According to CT conducted on day 7 postoperatively, no occlusions or endoleaks at the branches occurred. The patient was able to walk independently at the time of discharge on day 8 postoperatively (). The recent follow-up CT at 2 years and 4 months postoperatively indicated shrinkage and disappearance of the aortic aneurysms at the treated site. Furthermore, there were no recurrent findings of infection during the follow-up period.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [72, 'years'], 'creatinine': [2.25, 'mg/dL'], 'sex': 'Male'}",28.8125,27.37187,30.25313,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 72 years old. The concentration of Creatinine is 2.25 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.25^(-1.154) * 72^(-0.203) * 1 * 1=28.8125.
Hence, the patient's GFR is 28.8125 mL/min/1.73m²."
3319,9,MDRD GFR Equation,lab test,decimal,pmc-6283186-1,Extracted,"In spring of 2013, a 32-year-old woman sought medical attention at the Jilin University First Bethune Hospital with complaints of intermittent pruritus and fatigue. Liver function tests revealed significantly increased levels of γ-glutamyltransferase (γ-GT, 468 U/L) and alkaline phosphatase (ALP, 968 U/L). The patient was diagnosed with hypothyroidism 3 years ago due to the use of I31I therapy and was treated with euthyrox (250 mg/d). She had no hypertension, diabetes, special drug, hepatitis, or consumption of alcohol history, as well as no any family history. No positive signs were observed on physical examination. Serology for hepatitis virus A, B, or C was negative. Immunologic tests showed that serum antinuclear antibodies were positive (1:640), accompanied by increased concentrations of serum immunoglobulin M (IgM, 5.01 g/L) and the presence of an anti-mitochondrial M2 antibody (AMA-M2, >200 RU/mL); however, the anti-Ro (SS-A) and anti-La (SS-B) antibodies were negative. A liver biopsy showed stage II PBC (Fig. A and B). The patient was eventually diagnosed with PBC and was treated with ursodeoxycholic acid (UDCA, 250 mg/d). The cholestatic enzyme levels and symptoms of pruritus were significantly improved.
In April 2016, the patient visited our hospital because of repeated fatigue for 2 years. Liver and kidney function, serum glucose levels, and blood routine tests were normal. Laboratory tests mainly revealed that the level of serum potassium (2.42 mmol/L) was low. The patient was treated intermittently with potassium citrate. However, the therapeutic effect was not satisfactory, and the cause of low potassium was unknown.
In July 2016, the patient visited the superior hospital for further treatment. She weighed 43 kg, and her height was 155 cm. Blood tests showed the following: pH, 7.347; PaCO2, 33.1 mm Hg; HCO3−, 17.7 mmol/L; PaO2, 103 mm Hg; Na+, 141 mmol/L; K+, 3.4 mmol/L; Cl−, 113 mmol/L; Mg2+, 0.94 mmol/L; serum creatinine, 70 μmol/L. In addition, the plasma anion gap (AG) was normal: AG = [Na+] – [Cl− + HCO3−] = 141 – (113 + 17.7) = 10.3 mmol/L (normal, 10–14 mmol/L). Urine routine showed a pH of 7.5, and 24-hour urine analysis demonstrated that the urine potassium concentration was 94 mmol/24 h. The aldosterone renin ratio was normal. Baseline data of the patient are summarized in Table . An abdominal ultrasound showed evidence of cirrhosis and gallstones. Adrenal CT showed bilateral nephrocalcinosis and no tumor. Whole-body bone mineral density was 0.99 g/cm2 with a T score of −1.3. According to the patient's history and related test results, she was finally diagnosed with RTA in PBC and was then treated with a combination of UDCA, potassium citrate, calcium supplements and activated vitamin D. One year after the treatment, the patient's liver function remained stable, and the clinical symptoms were significantly improved.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [32, 'years'], 'creatinine': [70.0, 'µmol/L'], 'sex': 'Female'}",84.09451,79.88978,88.29924,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 32 years old. The concentration of Creatinine is 70.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 70.0 µmol. To convert 70.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 70.0 µmol Creatinine * 1e-06 mol/µmol = 7e-05 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 7e-05 mol Creatinine * 113.12 g/mol = 0.00792 g Creatinine. To convert 0.00792 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00792 g Creatinine * 1000.0 mg/g = 7.92 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 7.92 mg Creatinine/10.0 dL = 0.792 mg Creatinine/dL. The concentration value of 70.0 µmol Creatinine/L converts to 0.792 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.792^(-1.154) * 32^(-0.203) * 1 * 0.742=84.09451.
Hence, the patient's GFR is 84.09451 mL/min/1.73m²."
3320,9,MDRD GFR Equation,lab test,decimal,usmle-9236,Extracted,"Three days after admission to the intensive care unit for septic shock and bacteremia from a urinary tract infection, a 34-year-old woman has persistent hypotension. Her blood cultures are positive for Escherichia coli, for which she has been receiving appropriate antibiotics since admission. She has no history of any serious illness. She does not use illicit drugs. Current medications include norepinephrine, ceftriaxone, and acetaminophen. She appears well. Her temperature is 37.5°C (99.5°F), heart rate is 96/min, and blood pressure is 85/55 mm Hg. Examination of the back shows costovertebral tenderness bilaterally. Examination of the thyroid gland shows no abnormalities. Laboratory studies show:
  Hospital day 1 Hospital day 3
Leukocyte count 18,500/mm3 10,300/mm3
Hemoglobin 14.1 mg/dL 13.4 mg/dL
Serum
Creatinine 1.4 mg/dL 0.9 mg/dL
Fasting glucose 95 mg/dL 100 mg/dL
TSH   1.8 µU/mL
T3, free   0.1 ng/dL
T4, free   0.9 ng/dL
Repeat blood cultures are negative. A chest X-ray shows no abnormalities.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [34, 'years'], 'creatinine': [0.9, 'mg/dL'], 'sex': 'Female'}",71.67305,68.0894,75.2567,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 34 years old. The concentration of Creatinine is 0.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.9^(-1.154) * 34^(-0.203) * 1 * 0.742=71.67305.
Hence, the patient's GFR is 71.67305 mL/min/1.73m²."
3321,9,MDRD GFR Equation,lab test,decimal,pmc-7828748-1,Extracted,"A 47-year-old male patient with a history of hypertension, diabetes mellitus type 2, current smoker with one pack per day was admitted to our hospital with cough, congestion, shortness of breath, and fever for five days. On admission, he was found to be positive for COVID 19. His vital signs were the following: temperature 39.4° Centigrade, heart rate (HR) 124 beats/minute, blood pressure (BP) 160/110 mm Hg, oxygen saturation (SpO2) of 88% on room air, and 93% on 3L of oxygen via nasal cannula. Chest X-ray showed right pulmonary opacity mainly at the basal region with some streaky left retro cardiac opacities (Figure ).
He was able to talk in full sentences. Chest examination revealed bilateral basal crackles. Cardiac examination revealed normal heart sounds and regular rhythm, the abdomen was soft, non-tender with normal bowel sounds, and the examination of the nervous system did not reveal any abnormalities. He was started on prophylactic low dose molecular weight heparin (LMWH) subcutaneous injections, two units of convalescent plasma for COVID-19, parenteral remdesivir, and oral dexamethasone 6 mg per oral daily. Over the next seven days, the patient’s oxygen requirement increased gradually despite the treatment, and he ended up on continuous bilevel positive pressure support (BiPAP) with 100% fractional inspired oxygen (FiO2). On the ninth day of admission, his work of breathing continued to worsen even on BiPAP. His Chest x-ray showed worse diffuse bilateral airspace opacities, new pneumomediastinum, and subcutaneous emphysema (Figure ).
Laboratory findings were notable for leukopenia with white blood cell count of 3.7 per microliter (range: 4.5 to 11.0 X 109 /L), worsening serum creatinine of 1.23 mg/dl (admitted with serum creatinine of 0.8 mg/dl), d-dimer 827 ng/ml (normal less than 500 ng/ml), serum ferritin 1836 ng/ml (range: 20 to 250 ng/ml), lactate dehydrogenase 363 units/liter (normal range: 140 to 280 units/ liter) and C-reactive protein of 5.3 mg/liter (normal less than 10 mg/liter). He was subsequently intubated and transferred to the intensive care unit. Given large pneumomediastinum and initiation of invasive ventilation with high positive end-expiratory pressure (PEEP) ranging from 8 to 10 centimeter of water, chest tubes were also placed preemptively. An X-ray taken the next day incidentally showed free air under the diaphragm apart from the pneumomediastinum, subcutaneous emphysema, and bilateral chest tubes (Figure ) with similar findings in computed tomography (CT) of the chest (Figure ). However, a CT scan of the abdomen and pelvis did not reveal any evidence of bowel perforation but did show a large pneumoperitoneum (Figure ).
General surgery was consulted for the pneumoperitoneum. They recommended managing the patient conservatively due to the absence of evidence for bowel perforation on computed tomography imaging of the abdomen and pelvis. The patient’s abdomen started getting softer and less distended in the next few days. Pneumoperitoneum resolved after five days of diagnosis with the improvement of pneumomediastinum (Figure ).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [47, 'years'], 'creatinine': [1.23, 'mg/dL'], 'sex': 'Male'}",63.07419,59.92048,66.2279,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 47 years old. The concentration of Creatinine is 1.23 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.23^(-1.154) * 47^(-0.203) * 1 * 1=63.07419.
Hence, the patient's GFR is 63.07419 mL/min/1.73m²."
3322,9,MDRD GFR Equation,lab test,decimal,pmc-4553271-1,Extracted,"An 81-year-old man was admitted to the nephrology ward because of anorexia, weight loss, and acute on chronic renal failure. His past medical history was remarkable for atrophy of the left kidney, myocardial infarction, follicular type non-Hodgkin lymphoma treated with CHVmP/BV chemotherapy (19 years prior to the present admission), and prostate cancer treated with androgen deprivation (6 years prior to the present admission). The patient had a permanent suprapubic catheter that was changed at 6-weekly intervals. On admission, he was found to have extensive supra- and infradiaphragmatic lymphadenopathy, with encasement of the right ureter and hydronephrosis of the right kidney. An urgent nephrostomy had been performed. Biopsy of a palpable cervical lymph node later revealed diffuse large B-cell lymphoma.
During the hospitalization, a sudden purple discoloration of the suprapubic urine collection bag was noted (see ). The nephrostomy urine had a normal color. The patient had been constipated during the preceding days, for which he had been treated with macrogol laxatives. His other medications had not been changed and included enoxaparin, aspirin, bisoprolol, amlodipine, rosuvastatin, sertraline, and three-monthly injection of goserelin. The patient had no other complaints.
Vital parameters were normal. Physical exam showed right cervical lymphadenopathy and the presence of a nephrostomy with normal colored urine and a suprapubic catheter with obvious purple color of urine bag and tubing. Laboratory evaluation revealed renal insufficiency with creatinine of 1.49 mg/dL and blood urea nitrogen of 25 mg/dL (creatinine at admission, before the nephrostomy procedure, had been 6.36 mg/dL). Hemogram showed a mild normochromic normocytic anemia with hemoglobin of 10.5 g/dL; white blood cell differential count and platelets were normal. Liver function tests were within normal limits. Lactate dehydrogenase was elevated (505 U/L): this was attributed to the diffuse large B-cell lymphoma. The level of CRP was 25 mg/L (reference value < 5 mg/L). Analysis of the suprapubic catheter urine showed pyuria and trace hematuria. Urinary pH was 9.0. Urine culture came back positive for Pseudomonas aeruginosa and Enterococcus faecalis. Analysis of the nephrostomy catheter urine showed trace hematuria, with a pH of 6.0 and a negative culture. As the nephrostomy urine was sterile and the patient had no signs of urinary infection, no antibiotics were given. The purple discoloration gradually disappeared during the following week. At discharge, kidney function had improved back to baseline with creatinine of 1.20 mg/dL. The patient was subsequently treated with R-CVP chemotherapy, with remission after 6 cycles.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [81, 'years'], 'creatinine': [1.2, 'mg/dL'], 'sex': 'Male'}",58.1086,55.20317,61.01403,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 81 years old. The concentration of Creatinine is 1.2 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.2^(-1.154) * 81^(-0.203) * 1 * 1=58.1086.
Hence, the patient's GFR is 58.1086 mL/min/1.73m²."
3323,9,MDRD GFR Equation,lab test,decimal,pmc-3283759-1,Extracted,"A 74-year-old woman was admitted to the hospital for diarrhea and epigastric pain. She had a history of hypertension, diabetes mellitus, chronic kidney disease, dilated cardiomyopathy, and permanent AF for 5 years (). Echocardiography performed 3 months before admission revealed severe global left ventricular hypokinesia (ejection fraction=19% by Simpson's method) and an enlarged left atrium (left atrial volume index=40 mL/m2). Her medications included digoxin (0.125 mg daily), warfarin (2 mg daily), ramipril (10 mg daily), furosemide (40 mg daily), spinolactone (25 mg daily), and carvedilol (25 mg daily).
On examination, her heart rate was 41 bpm, and blood pressure was 110/70 mm Hg. Heart sounds were regular, and there were no murmurs or thrills. An electrocardiogram (ECG) revealed junctional rhythm at a rate of 35 bpm and a QRS duration of 136 msec (). Admission laboratory results showed severe hyperkalemia (serum potassium 8.3 mEq/L), high blood urea nitrogen (62.4 mg/dL), creatinine of 4.0 mg/dL, glucose of 248 mg/dL, and low sodium (131 mM) and hemoglobin (7.2 g/dL) levels. Arterial blood gas analysis on room air showed a pH of 7.400, pCO2 of 41.6 mm Hg, pO2 of 102.8 mm Hg, and HCO3- of 26.0 mmol/L.
The patient was immediately treated with intravenous calcium chloride, followed by intravenous glucose/insulin and a sodium bicarbonate infusion. On hospital day 2, the serum potassium level was 5.3 mEq/L and the ECG showed sinus bradycardia at a rate of 53 bpm with an 80 ms QRS duration (). On hospital day 3, the ECG revealed a normal sinus rhythm at a rate of 67 bpm, and the serum potassium level was within normal limits (4.3 mEq/L). The patient was discharged 6 days after admission, and the ECG at discharge showed normal sinus rhythm at a rate of 65 bpm with occasional premature ventricular complexes. At the 10 day and 1 month follow-ups, the ECG at an outpatient clinic had returned to AF and serum potassium levels were within the normal range.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [74, 'years'], 'creatinine': [4.0, 'mg/dL']}",10.94487,10.39763,11.49211,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 74 years old. The concentration of Creatinine is 4.0 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 4.0^(-1.154) * 74^(-0.203) * 1 * 0.742=10.94487.
Hence, the patient's GFR is 10.94487 mL/min/1.73m²."
3324,9,MDRD GFR Equation,lab test,decimal,pmc-6366143-1,Extracted,"The first patient is a 54-year-old Hispanic female with poorly controlled diabetes mellitus with a hemoglobin A1C of >10 since diagnosis in 2011. She was treated with oral agents and insulin shortly after diagnosis, given her poor glycemic control. She initially did not have overt DN, but gradually started developing albuminuria and renal function decline. Her serum creatinine first started rising to 123.79 μmol/L (1.4–1.6 mg/dL) over 2014–15 and her proteinuria rose from 1000 μg albumin/mg creatinine (1000 μg albumin/mg creatinine = 1 g albumin/g creatinine) to 2000–3000 μg albumin/mg creatinine. Her hyperglycemia remained persistent in spite of her medication regimen. She began to take nonsteroidal anti-inflammatory drugs (NSAIDs) a few times a month, but as her renal function declined, she was instructed to stop NSAID use in 2016–17. Urine protein:creatinine ratios were not obtained in the Kaiser Permanente (KP) system, so trends of albumin:creatinine ratio (ACR) were followed at the University of California Los Angeles Health System.
She was examined in KP’s ophthalmology clinic and was noted to have worsening glaucoma and proliferative DN. She started treatment with bevacizumab every 4 weeks as needed in January 2016. She required a monthly dose of 1.25 mg of bevacizumab over the next 13 months in either one or both eyes over a total of 10 separate visits, with the indication of proliferative diabetic retinopathy (DR). Thus the full dose administered was 12.5 mg of bevacizumab over 10 injections during this period. A notable increase in the slope of proteinuria was noted, with an increase in ACR to 4000 μg/mg and ultimately to 7000 μg/mg (see for trends of renal function decline and worsening proteinuria in this patient). The patient’s blood pressure did not rise beyond her usual range of 140–150 mmHg and, as such, it was not plotted.
It was noted that her renal function seemed to worsen more rapidly in the year after bevacizumab was started. A full serological workup was performed, but was unrevealing. Due to the more rapid than expected decline in renal function, a renal biopsy was performed. The biopsy showed nodular diabetic glomerulosclerosis and hypertensive nephrosclerosis without any histological features suggestive of other glomerular disease. The timing of proteinuria exacerbation corresponded with the first few months after starting intravitreal bevacizumab injections. The mechanism of renal function decline may be due to worsening proteinuria and acute tubular necrosis. Given the severity of the patient’s DR, a change to a less potent agent, like ranibizumab, was not immediately feasible. The patient was managed with renin–angiotensin–aldosterone system (RAAS) blockade with plans to add a non-dihydropyridine calcium channel blocker (i.e. verapamil or diltiazem) for proteinuria control, with continuing attempts to optimize hypertensive control.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [54, 'years'], 'creatinine': [1.4, 'mg/dL'], 'sex': 'Female', 'Race': 'Hispanic'}",39.1863,37.22698,41.14562,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 54 years old. The concentration of Creatinine is 1.4 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.4^(-1.154) * 54^(-0.203) * 1 * 0.742=39.1863.
Hence, the patient's GFR is 39.1863 mL/min/1.73m²."
3325,9,MDRD GFR Equation,lab test,decimal,pmc-8310551-1,Extracted,"This is a case of a 76-year-old Caucasian man with a known past medical history of chronic kidney disease stage IIIb and hypertension, who had been taking hydralazine, losartan, and hydrochlorothiazide for several years. He presented with complaints of shortness of breath, fatigue, weakness, and decreased oral intake for two weeks prior to admission. He denied any symptoms of arthralgia, myalgia, cough, and headache. Physical examination was relatively unremarkable; the patient did not have any signs of hypervolemia, the integumentary exam was normal with no visible rash, and lungs were clear to auscultation. His chest X-ray was negative for pulmonary edema or other acute processes. Serum troponin and D-dimer levels were within the normal limit. The patient was non-oliguric and was making around two liters of urine per day.
Other laboratory findings were consistent with an acute or chronic kidney injury. His serum creatinine was 6.5 mg/dL, up from his baseline of 1.6 mg/dL. Urinalysis was positive for microscopic hematuria with 10-20 red blood cells (RBC) per high power field (HPF) as well as an elevated protein/creatinine of 0.9. A serologic workup including antinuclear antibody (ANA), C3, C4, anti-glomerular basement membrane antibody (anti-GBM Ab), hepatitis B surface antigen (HBsAg), antibody to hepatitis B surface antigen (HBsAb), and hepatitis B core antibody (HBcAb) was unremarkable. However, the p-ANCA titer was high at 1:160. Serum and urine immunofixation electrophoresis were negative for monoclonal protein. Renal ultrasound was unremarkable. He was treated with IV fluids, and his aforementioned antihypertensives, which included hydralazine, were discontinued. Interestingly, he continued to have good urine output as well as improvement in his symptoms and his serum creatinine dropped to 4.8 mg/dL. Given the improvement of his renal function and clinical symptoms, he was discharged to close follow-up with the nephrology clinic and his hydralazine was resumed.
Follow-up blood work in two weeks showed worsening serum creatinine to 6.8 mg/dL. He had persistent microscopic hematuria. Repeat serologic workup revealed a p-ANCA titer of 1:320 and an elevated myeloperoxidase immunoglobulin G (MPO IgG) of 78 U/mL. The patient was readmitted to the hospital for further workup. A renal biopsy was obtained, which revealed pauci-immune glomerulonephritis, including crescent formation, segmental necrotizing inflammation on light microscopy, and absence of immune deposits on immunofluorescence (Figure ). Steroids and rituximab were initiated as treatment. Hydralazine, which was re-initiated at the time of discharge, was now discontinued on the suspicion of being an etiologic agent of AAV. However, there is a possibility that this was ANCA-associated vasculitis unrelated to hydralazine. Due to worsening kidney function, the patient was started on hemodialysis. He remained dialysis-dependent with no significant renal recovery.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [76, 'years'], 'creatinine': [6.8, 'mg/dL'], 'sex': 'Male', 'Race': 'White'}",7.95276,7.55512,8.3504,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 76 years old. The concentration of Creatinine is 6.8 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 6.8^(-1.154) * 76^(-0.203) * 1 * 1=7.95276.
Hence, the patient's GFR is 7.95276 mL/min/1.73m²."
3326,9,MDRD GFR Equation,lab test,decimal,usmle-690,Extracted,"A 72-year-old man develops reduced urine output and a serum creatinine concentration of 2.9 mg/dL three days after being hospitalized for acute diverticulitis. On admission, a complete blood count showed a hemoglobin concentration of 15.5 g/dL and a leukocyte count of 14,000/mm3. Urinalysis showed 2+ proteinuria, and serum studies showed a blood glucose of 145 mg/dL and a creatinine concentration of 1.2 mg/dL. A CT scan of the abdomen confirmed the diagnosis. Therapy with intravenous ketoprofen, piperacillin, and tazobactam was begun, and the patient was placed on bowel rest. He has a history of hypertension, chronic constipation, and type 2 diabetes mellitus. Prior to admission, his medications were insulin, metoprolol, and losartan. Today, his temperature is 37.7°C (99.9°F), pulse is 97/min, respirations are 12/min, and blood pressure is 135/87 mm Hg. The abdomen is soft on physical examination, and there is tenderness to palpation of the left lower quadrant. The remainder of the examination shows no abnormalities.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [72, 'years'], 'creatinine': [2.9, 'mg/dL'], 'sex': 'Male'}",21.49771,20.42282,22.5726,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 72 years old. The concentration of Creatinine is 2.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.9^(-1.154) * 72^(-0.203) * 1 * 1=21.49771.
Hence, the patient's GFR is 21.49771 mL/min/1.73m²."
3327,9,MDRD GFR Equation,lab test,decimal,pmc-8078049-1,Extracted,"An 80 year old male patient with renal impairment, non-smoker, known case of bladder cancer since 2007, missed follow-up since 2014, presented to outpatient clinic complaining of intermittent gross painless hematuria of two months duration, his Covid-19 polymerase chain reaction test was negative on admission, his serum creatinine was elevated (1.9 mg/dl), a non-contrasted computed tomography showed mild right-sided hydroureteronephrosis, bilateral cortical thinning, and diffuse bladder thickening ().
Intraoperatively, a urethral stricture and an enlarged prostate median lobe were seen, multiple growths on bladder neck, posterior wall, both right and left lateral wall more on the right side were seen, too.
After an optical urethrotomy for the stricture, and partial transurethral resection of prostate, an extensive transurethral resection of bladder tumor was done.
The right ureteric orifice could not be seen, a second look cystoscopy was planned in two weeks. The surgery was performed by an experienced senior urologist.
The histopathology showed high grade T1 transitional cell carcinoma consistent with T1N0M0 stage ().
On the second post-operative day, a new creatinine was same as baseline (1.9 mg/dl) and the patient was doing well so he discharged to home.
On the third postoperative day, at his home the patient started to feel hotness, chills and rigors, with no cough and no new urinary symptoms.
On the fifth postoperative day, a new Covid-19 test was done at another hospital and it was positive.
On the seventh postoperative day, he started to have shortness of breath, productive cough and generalized weakness, so he presented to another hospital and found to have raised creatinine (8 mg/dl), he was offered admission but he preferred to observe himself at home.
On the ninth postoperative day, he came to emergency department at our hospital and found to have serum creatinine of (9 mg/dl), a new computed tomography scan showed no new finding compared to the previous one ().
The nephrologist advised hemodialysis for the patient and to be admitted to intensive care unit, there were no available intensive care unit bed at our hospital, so he was transferred to another hospital where hemodialysis was performed for him.
One month after the procedure, the patient is still hospitalized under medical care due to Covid-19 infection and its complications.
This case has been reported in line with the SCARE 2020 criteria [].","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [80, 'years'], 'creatinine': [9.0, 'mg/dL'], 'sex': 'Male'}",5.69528,5.41052,5.98004,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 80 years old. The concentration of Creatinine is 9.0 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 9.0^(-1.154) * 80^(-0.203) * 1 * 1=5.69528.
Hence, the patient's GFR is 5.69528 mL/min/1.73m²."
3328,9,MDRD GFR Equation,lab test,decimal,pmc-4530922-1,Extracted,"A 56-year-old male was brought to the emergency department by paramedics for a syncopal episode and inability to move his lower extremities. He complained of abdominal pain and inability to move his legs beginning five hours prior to arrival. He awakened from a nap that afternoon and experienced numbness in both legs, which progressed to paralysis. At baseline, he was ambulatory without any history of weakness and was last ambulatory hours prior. He endorsed occasional pain in his legs when walking at baseline.
He also complained of abdominal pain with nausea and vomiting for two days. He had a history of alcohol use and reported dark-colored emesis and last bowel movement three days prior. On review of symptoms the patient denied any history of headache, dizziness, chest pain, back pain, trauma, fevers, or extremity weakness. He walked longer than a mile the day prior. History from the patient’s wife revealed that he had an episode of altered level of consciousness while on the couch and that finding combined with his abdominal pain and paralysis prompted her to call 911. The patient’s past medical history was significant for hypertension, peripheral arterial disease, and myocardial infarction 10 years prior. His past surgical history included “abdominal stents” and a left carotid stent. His social history was significant for a 25-pack/year history of smoking and daily alcohol. His medications included atenolol and ranitidine.
Physical exam showed an oral temperature of 36.7°C, blood pressure 107/65mmHg, heart rate 99 beats/minute and a respiratory rate of 30 breaths/min, with oxygen saturation on 15L non-rebreather mask of 94%. His weight was 72.5kg and he appeared older than his stated age. He was alert, cooperative and in moderate distress, primarily complaining of pain and cramping in his lower extremities and repeatedly asking staff to straighten out his legs although they were already lying straight and motionless on the gurney. His head exam was unremarkable with the exception of a dry oropharynx. Cervical spine, cardiac, and lung exams were unremarkable. His abdomen was firm and diffusely tender to palpation with generalized rebound and guarding. An irreducible left inguinal hernia was present. He had vomiting, and placement of a nasogastric tube revealed 1.5 liters of coffee-ground emesis. Lower extremities were thin, cool, and without any palpable or Dopplerable pulses in bilateral femoral, popliteal or pedal distribution. There was trace non-reproducible sensation to the mottled lower extremities, and no sensation distal to the ankles. Motor exam was significant for lower extremity paralysis.
Laboratory data consisted of sodium 121mEq/L (135–145), potassium 6.8mEq/L (3.3–4.8), chloride 89mEq/L (101–111), CO2 18mEq/L (25–34), BUN 31mg/dL (8–26), creatinine 1.5mg/dL (0.5–1.3), and blood glucose 367mg/dL (70–115). White blood cell 19.1thous/mcL (4.0–10.5), hemoglobin 12.8g/dL (13.5–16.9), lipase 107U/L (22–51), hematocrit 38.8% (39.5–50.0), and platelets 165thous/mcL (150–400). There was a left shift in the neutrophils 16.2thous/mcL (85%) (2.0–8.1). Alkaline phosphate 88IU/L (26–110), AST 84IU/L (8–40), ALT 38IU/L (0.0–60), total bilirubin 1mg/dL (0.0–1.4), total protein 5.4g/dL (6.1–8.2), albumin 2.6g/dL (3.2–5.5). Lactate 7.2mmol/L (0.7–2.1). ABG showed pH of 7.25 (7.38–7.42), pCO2 31.6mmHg (36–42), pO2 123.6mmHg (80–104), bicarbonate 13.5mmol/L (21–27). PT was 17.3sec (9.5–12.3), PTT 45.9sec (24.1–35.1), and INR 1.62 (0.87–1.14). B-type natriuretic peptide 1,950pg/mL (<100). Troponin 2.75ng/mL (<0.03).
Chest radiograph was unremarkable. Electrocardiogram (ECG) showed sinus rhythm at 95 beats/minute with ST elevation inferiorly, anteriorly and laterally (). Bedside ultrasound to evaluate the abdominal aorta was limited. Vascular surgery was consulted prior to CT for concern of a vascular catastrophe. Cardiology was consulted for the patient’s ECG findings consistent with myocardial infarction. The patient went for a non-contrast head CT that was unremarkable and a CT angiogram of the chest, abdomen and pelvis, which was significant for the abdominal aorta with no contrast opacification 2.2cm superior to the bifurcation (), high-grade stenosis of the right common iliac artery, complete occlusion of the left common iliac artery, stents in the celiac artery and superior mesenteric artery (SMA), evidence of occlusion of the proximal SMA and inferior mesenteric artery (IMA), hepatic, splenic, bilateral renal infarctions, left inguinal hernia, bowel obstruction, pneumatosis intestinalis with evidence of ischemic bowel, and aspiration in the right lower lung. General surgery was consulted.
The cardiology service stated that the patient was not a candidate for cardiac catheterization and to start anticoagulation and low-dose aspirin if there was no contraindication or planned surgery. They also recommended thrombolytics for the diffuse thrombotic disease. The patient did have an echocardiography study that revealed an ejection fraction of 35% and multiple regional wall motion abnormalities. General surgery recommended comfort measures as he was not a surgical candidate. Vascular surgery commented that bypass would be futile and if patient survived, would be a candidate for extra-anatomical axillo-bifemoral bypass in the future. The patient was admitted to the medical intensive care unit for broad-spectrum antibiotics and a heparin drip and succumbed to his illness the following day.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [56, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Male'}",48.41128,45.99072,50.83184,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 56 years old. The concentration of Creatinine is 1.5 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.5^(-1.154) * 56^(-0.203) * 1 * 1=48.41128.
Hence, the patient's GFR is 48.41128 mL/min/1.73m²."
3329,9,MDRD GFR Equation,lab test,decimal,pmc-4421438-2,Extracted,"The patient was a 34-year-old Caucasian man, without toxic habits, with chronic renal failure stage V due to membranous glomerulonephritis but he had no other remarkable medical history. He was studied for receiving a preemptive kidney transplantation but there were no contraindications.
Study of a possible living donor (the patient’s 71-year-old mother) was performed. No contraindications for donation were found but she carried an MGUS with two monoclonal proteins, IgG kappa and IgA lambda. A bone marrow examination showed 8% plasma cells. The M-protein concentration in the serum was 10 g/L and serum free light chains lambda and kappa were 14.4 and 16 mg/L, respectively, with a normal ratio.
Kidney transplantation was carried out in May 2007 with no complications and renal function progressively improved. The patient was discharged 1 week after the procedure. Currently, 36 months after the transplantation, the patient has a serum creatinine level of 1.8 mg/dL (159 μmol/L) and a 24-h urinary protein excretion of 200 mg.
Induction immunosuppressive treatment consisted of basiliximab, mycophenolate mofetil, prednisone and tacrolimus. Three months after transplantation, tacrolimus was switched to sirolimus for the same reasons as in Case 1. The patient is currently receiving sirolimus and mycophenolate mofetil.
The patient has developed no immunological or infectious complications and serum protein electrophoresis and serum immunofixation revealed no monoclonal proteins.
No complications have occurred in the donor and there is no evidence of MGUS progression. Renal function is normal.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [34, 'years'], 'creatinine': [1.8, 'mg/dL'], 'sex': 'Male', 'Race': 'White'}",43.40736,41.23699,45.57773,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 34 years old. The concentration of Creatinine is 1.8 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.8^(-1.154) * 34^(-0.203) * 1 * 1=43.40736.
Hence, the patient's GFR is 43.40736 mL/min/1.73m²."
3330,9,MDRD GFR Equation,lab test,decimal,pmc-5418030-2,Extracted,"A 51-year-old female presented in September 2016 with decreased urine output, generalized weakness, and decreased appetite. The patient was a known case of Type 2 diabetes mellitus for two years, hypertension for 30 years, cervical carcinoma (post-chemotherapy and radiotherapy, 22 cycles) diagnosed in 2012 with recurrence in 2015, and obstructive nephropathy with double J (DJ) stent in-situ on the right side since January 2016. On examination, the patient was afebrile with other systems within normal limits. Her total leucocyte count (TLC) was 12,400/mm3, blood urea was 69 mg/dl, serum creatinine was 3.7 mg/dl, and potassium was 5.1 meq/l. Liver function tests were within normal limits. Abdominal ultrasound showed moderate hydronephrosis of the right kidney and increased parenchymal echogenicity with diminished corticomedullary differentiation of the left kidney. Computed tomogram (CT) scan of the abdomen showed right kidney hydroureteronephrosis with DJ stent in situ, and the left kidney showed parenchymal atrophy with irregular margins. The patient was diagnosed as a case of acute chronic kidney disease with DJ stent blockage. The DJ stent was changed, and the pus was evacuated. Gram stain examination of the pus showed plenty of branching Gram-positive bacilli, along with Gram-negative bacilli (Figure ).
The specimen was processed similarly to Case 1. Escherichia coli was grown in aerobic culture, and Bifidobacterium sp. was cultured in anaerobic culture. The identification of Bifidobacterium sp. was done by both MALDI-TOF Vitek® MS and Vitek® 2. Escherichia coli was found to be extended spectrum beta-lactamase (ESBL)-positive and sensitive to piperacillin + tazobactam, cefoperazone + sulbactam, imipenem, meropenem, amikacin, gentamicin, tobramycin, chloramphenicol, and co-trimoxazole. Bifidobacterium sp. was found to be sensitive to penicillin, ceftriaxone, imipenem, meropenem, amoxicillin + clavulanic acid, piperacillin + tazobactam, and clindamycin and was resistant to metronidazole. The patient showed a good response to meropenem and recovered completely.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [51, 'years'], 'creatinine': [3.7, 'mg/dL'], 'sex': 'Female'}",12.91518,12.26942,13.56094,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 51 years old. The concentration of Creatinine is 3.7 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 3.7^(-1.154) * 51^(-0.203) * 1 * 0.742=12.91518.
Hence, the patient's GFR is 12.91518 mL/min/1.73m²."
3331,9,MDRD GFR Equation,lab test,decimal,usmle-4328,Extracted,"A 45-year-old with a past history of being admitted for alcohol withdrawal and acute alcohol toxicity presents to the emergency department with ataxia. He is stuporous and does not respond to questions appropriately, often yelling and falling down. On exam, the patient has visual impairment and cannot read the Snellen chart correctly. Figure A shows his retina on ophthalmologic exam. His electrolytes are Na 140, K 3.0, Cl 95, HCO3 15, BUN 27, Cr 1.2.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [45, 'years'], 'creatinine': [1.2, 'mg/dL'], 'sex': 'Male'}",65.47278,62.19914,68.74642,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 45 years old. The concentration of Creatinine is 1.2 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.2^(-1.154) * 45^(-0.203) * 1 * 1=65.47278.
Hence, the patient's GFR is 65.47278 mL/min/1.73m²."
3332,9,MDRD GFR Equation,lab test,decimal,pmc-7675750-1,Extracted,"A 56-year-old male with a history of obesity (body mass index = 35) and hyperlipidaemia presented to the emergency department with 1 day of dyspnoea and lethargy. He reported close contact with a COVID-19-positive coworker. He was in respiratory distress with measured oxygen saturation (SaO2) of 66%, hypotensive, and in rapid atrial fibrillation. He rapidly progressed to respiratory failure and shock requiring mechanical ventilation and three vasopressors.
Initial investigation included laboratory studies that were notable for white blood cell count 9.8 K/μL (66% neutrophils and 19% lymphocytes), haemoglobin 19.4 g/dL (declined to 15.2 g/dL after fluid administration), creatinine 2.0 mg/dL, B-type natriuretic peptide 790.0 pg/mL, troponin I 1.3 ng/mL, lactate 8.7 mmol/L, d-dimer 1961 ng/mL, C-reactive protein 4.1 mg/dL, and procalcitonin 1.4 ng/mL with unremarkable liver chemistries. An arterial blood gas (on 100% FiO2) demonstrated a pH of 7.25 and partial pressure of oxygen (PaO2) of 319 mmHg; the initial venous haemoglobin saturation drawn from the superior vena cava was 80% (on the same FiO2). His electrocardiogram (EKG) showed rapid atrial fibrillation and low voltage (Figure
). Transthoracic echocardiogram (TTE) revealed extreme concentric left ventricular (LV) hypertrophy (LVH) with a wall thickness of 2.0 cm, reduced biventricular function with LV ejection fraction (EF) of 20%, and a small pericardial effusion (Supporting Information, Video
A and 
B). A chest X-ray showed multifocal bilateral airspace disease, a general respiratory viral panel was negative, but the rapid Abbott ID NOW™ COVID-19 test resulted positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (later confirmed on the Cepheid Xpert® Xpress testing system).
The clinical presentation of acute respiratory failure with rapidly progressive shock and biventricular dysfunction suggested a diagnosis of COVID-19 FM. The discrepancy between the degree of LVH and low voltage on EKG hinted at significant myocardial oedema, further supporting this diagnosis. After a multidisciplinary discussion, the patient was cannulated on peripheral veno-arterial extracorporeal membrane oxygenation with a distal perfusion catheter. Repeat TTE, on admission to the intensive care unit, revealed an EF < 5%, and his arterial line waveform was non-pulsatile (Supporting Information, Video
A and 
B). A femoral Impella 2.5 (Abiomed U.S., Danvers, MA) was inserted for LV venting. The patient was treated with methylprednisolone 100 mg and tocilizumab 800 mg. Because of continued cardiac standstill, his methylprednisolone was readministered at increasing doses (200, 200, and 500 mg) for a total of 4 days. As his inflammatory markers briefly decreased (Figure
), tocilizumab was not re-dosed and no other COVID-19 targeted therapy was administered. Despite initial haemodynamic improvement, he developed oliguric kidney failure requiring continuous venovenous haemofiltration. As a result of retroperitoneal injury and haemorrhage, he was decannulated from VA-EMCO on hospital day (HD) 4 and transitioned to biventricular support with a ProtekDuo (LivaNova, London, UK) and axillary Impella 5.0; transoesophageal echocardiogram completed in the operating room noted improved LV function (EF 50%). TTE on HD 7 revealed further EF recovery to 65% (Supporting Information, Video
A and 
B), EKG exhibited return to sinus rhythm (Figure
), and arterial line tracings showed improved pulsatility; he was ultimately able to be weaned from both Impella (HD 10) and ProtekDuo (HD 12). Interestingly, he then developed severe vasoplegia, requiring high-dose vasopressor support, correlating with increasing markers of inflammation, and myocardial injury. Re-dosing tocilizumab at this time was considered but ultimately deferred because of clinical improvement. As of this writing, the patient has recovered from critical illness and is currently on the general medical floor awaiting discharge to a rehabilitation centre.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [56, 'years'], 'creatinine': [2.0, 'mg/dL'], 'sex': 'Male'}",34.735,32.99825,36.47175,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 56 years old. The concentration of Creatinine is 2.0 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.0^(-1.154) * 56^(-0.203) * 1 * 1=34.735.
Hence, the patient's GFR is 34.735 mL/min/1.73m²."
3333,9,MDRD GFR Equation,lab test,decimal,usmle-430,Extracted,"A 62-year-old man is brought to the hospital because of a 6-hour history of worsening upper abdominal pain, nausea, and vomiting. He is diagnosed with acute calculous cholecystitis and scheduled for cholecystectomy the next day. He has congestive heart failure, hyperlipidemia, and hypertension. Physical examination shows no abnormalities. Current medications include metoprolol and simvastatin. One month ago, spironolactone was added to his medication regimen. Preoperative serum studies show:
Na+ 138 mEq/L
K+ 6.1 mEq/L
Cl- 100 mEq/L
HCO3- 22 mEq/L
Urea nitrogen 13 mg/dL
Creatinine 1.0 mg/dL
An ECG shows normal sinus rhythm.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [62, 'years'], 'creatinine': [1.0, 'mg/dL'], 'sex': 'Male'}",75.71511,71.92935,79.50087,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 62 years old. The concentration of Creatinine is 1.0 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.0^(-1.154) * 62^(-0.203) * 1 * 1=75.71511.
Hence, the patient's GFR is 75.71511 mL/min/1.73m²."
3334,9,MDRD GFR Equation,lab test,decimal,usmle-2152,Extracted,"A 71-year-old, hospitalized man develops abnormal laboratory studies 4 days after starting treatment for exacerbation of congestive heart failure. He also has a history of osteoarthritis and benign prostatic hyperplasia. He recently completed a course of amikacin for bacterial prostatitis. Before hospitalization, his medications included simvastatin and ibuprofen. Blood pressure is 111/76 mm Hg. Serum studies show a creatinine of 2.3 mg/dL (previously normal) and a BUN of 48 mg/dL. Urinalysis shows a urine osmolality of 600 mOsm/kg and urine sodium of 10 mEq/L.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [71, 'years'], 'creatinine': [2.3, 'mg/dL'], 'sex': 'Male'}",28.17077,26.76223,29.57931,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 71 years old. The concentration of Creatinine is 2.3 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.3^(-1.154) * 71^(-0.203) * 1 * 1=28.17077.
Hence, the patient's GFR is 28.17077 mL/min/1.73m²."
3335,9,MDRD GFR Equation,lab test,decimal,pmc-8038922-1,Extracted,"A 47-year-old Caucasian female with a past medical history of major depressive disorder, chronic alcohol abuse, and an unspecified eating disorder was brought to the hospital by emergency medical services under the Florida Mental Health Act due to new-onset altered mental status. The patient had been found to be too weak to stand and her only reported oral intake had been alcohol with no food for an undefinable amount of time. Examination in the emergency room revealed a tangential thought process and poor responses to questioning. She believed she was in her home and the hospital staff were friends and family. She was found to be tachycardic with a heart rate of 131 beats per minute (bpm), blood pressure 105/75 mm Hg, respirations 16 breaths per minute with a 99% pulse oxygen level, and afebrile 37.3⁰C (99.1⁰F). On physical exam, the patient was noted to be cachexic and tremulous with a body mass index (BMI) of 15.9kg/m2. Horizontal nystagmus was noted. The rest of the physical exam was unremarkable. Laboratory analysis abnormalities showed leukocytosis 19.04 x 103/uL, hypokalemia with potassium 3.2 mmol/L, slight hypernatremia 146 mmol/L, creatinine 2.2 mg/dL, blood urea nitrogen (BUN) 59 mg/dL, glucose 144 mg/dL, and mild hypercalcemia 10.5mmol/L. Liver function was normal as well as albumin levels. Urine toxicology was negative and alcohol level was < 3 mg/dL. Patient met criteria for sepsis as she was tachycardic with acute kidney injury with elevated creatinine, leukocytosis, and an elevated lactic acid level of 4.97 mmol/L (normal 0.90-1.70 mmol/L) with altered mental status. Lipase levels were found to be elevated at 1234 unit/L. Chest x-ray and computed tomography (CT) head were unremarkable. She was admitted to the intensive care unit (ICU) with severe sepsis, altered mental status, acute kidney injury, and failure to thrive.
The patient was started on high-dose thiamine supplementation with close monitoring of electrolytes. She experienced persistent encephalopathy, ataxia, and nystagmus. The patient was retaining urine on bladder scan and a Foley catheter was placed with a urine sample sent for urinalysis. She was started on intravenous ceftriaxone. Magnetic resonance imaging (MRI) of the brain without contrast also showed no acute intracranial processes. The initial urinalysis returned positive and urine cultures were sent out. The urine culture was positive for Escherichia coli and antibiotics were adjusted according to the sensitivity panel. The patient did not show any improvement in mental status following completion of the antibiotic course. The patient continued to display fluctuating mental status, believing she was at home with her parents and, on rare occasions, understood that she was in the hospital. The patient also showed increased agitation in the late evenings where she was found to be combative and tearful. These episodes required extra nursing support with frequent reorientation. After discussion with Neurology and Psychiatry, it was determined the patient’s cognitive status was likely permanent and was classified as Korsakoff syndrome. As the primary team, multiple antipsychotics were attempted to stabilize her moods and agitation, including varying doses of haloperidol, ziprasidone, and quetiapine. Eventually we settled on a scheduled low dose of quetiapine, which showed only minimal improvement in patient’s mental status.
By this point, the patient had been hospitalized for over two months. There were multiple barriers making a safe discharge plan difficult to establish. We conversed with the patient’s sister and power of attorney (POA) regarding possible alternative treatments, including initiation of memantine. After discussing the risks and benefits, we agreed to initiate memantine. Notably, the patient’s sister reported a family history of alcoholism in both parents and a prodrome of altered mental status for a month-long period prior to their father’s death. The patient’s mother’s cause of death was unknown. The patient and her sister had last spoken one month prior to admission and her sister reported the patient was alert and oriented x4 at that time with no prior history of Wernicke’s or memory deficits.
A Folstein mini-mental state exam (MMSE) was first performed prior to initiation of the medication on which the patient scored an 18/30. Her primary deficits were in cognition and recall. She showed no deficits in attention, calculation, or language skills. She was started on a low dose of memantine 5 mg twice a day and observed. After one week of treatment, she appeared to have more frequent, intermittent episodes of clarity during which she was oriented to place and was able to recall she was in the hospital, however, she could not recall reasons for hospitalizations despite daily reorienting. She was consistently disoriented to time and self. Long-term memory including details regarding childhood and early adult life remained preserved. Nursing staff noticed she appeared to be calmer in the evenings and her mood appeared less labile. Her MMSE after one week of treatment with memantine was 19/30. During the remainder of her admission, we avoided making any changes to her quetiapine. Her memantine was increased to a maintenance dose of 10 mg twice a day with continued observation of her cognitive function and weekly MMSEs. Her mental status continuously fluctuated over the next few weeks, ranging between 18-22/30. After 119 days, she was deemed medically optimized for discharge to a long-term memory care facility.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [47, 'years'], 'creatinine': [2.2, 'mg/dL'], 'sex': 'Female', 'Race': 'White'}",23.92491,22.72866,25.12116,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 47 years old. The concentration of Creatinine is 2.2 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.2^(-1.154) * 47^(-0.203) * 1 * 0.742=23.92491.
Hence, the patient's GFR is 23.92491 mL/min/1.73m²."
3336,9,MDRD GFR Equation,lab test,decimal,pmc-6322530-1,Extracted,"A 57-year-old male presented with right side abdominal pain for two months. He had the history of right side pelvicaliceal calculus of 26 x 18 mm2 removed percutaneously by nephrolithotomy 10 years before the visit. He also had the history of recurrent renal calculi thereafter and managed accordingly. His laboratory investigations including complete blood counts, blood sugar, liver function tests, electrolytes, and lipid profile were within normal range. Serum creatinine (SCr) was 1.76 mg/dL. Urine examination showed proteinuria (+3) with microscopic hematuria and calcium oxalate dihydrate crystals. Ultrasonography (USG) showed 116 x 55 mm sized right kidney (RK) with multiple calculi in calyces, pelvis, and ureter along with 55 x 40 mm heterogeneous echogen ic mass with internal echoes adjacent to pelvis, and moderate hydroureteronephrosis. Computed tomography (CT) urography showed 47 x 52 x 47 mm sized well-defined lobulated heterogeneously enhancing mass lesion with calcification foci in interpolar region of RK extending up to pelvicalyceal system. Few calculi were observed in the mid and lower calyces and pelvis, the largest measured 11 x 13 x 16 mm. There was moderate right hydroureteronephrosis with multiple calculi measuring 8 x 9 x 16 mm in upper and 6 x 7 x 11 mm in mid-ureter. He was subjected to laparoscopic right radical nephroureterectomy and specimen was sent for histopathological examination.
Gross examination revealed RK weighing 310 g and 10 x 6 x 5.5 cm in size. Outer surface was covered with perinephric fat and fascia. Capsule was adherent at places, otherwise could be stripped off easily. Outer surface was granular, bosselated, and pinkish brown. One cortical cyst was found measuring 0.6 cm in diameter at upper pole. Cut section showed ill-defined corticomedullary differentiation and dilated pelvicalyceal system filled with tumor mass measuring 4.5 x 3.5 cm in size, grey white in color, irregular and friable with areas of necrosis, and hemorrhage extending up to pelvis. Few calculi were present in mid and lower calyces (). A cortical cyst measuring 0.6 x 0.6 cm was present at upper pole. Ureter also showed few calculi in upper and mid part. Multiple sections from the mass, renal parenchyma, and ureter were submitted for light microcopy. Sections were stained with Hematoxylin and Eosin. Immunohistochemistry for CEA and CK34β12 were conducted on the representative sections.
Microscopic examination from kidney tumor showed a malignant tumor comprising of cells arranged in glandular fashion. Individual cells were polygonal, moderately large, and had fine granular eosinophilic cytoplasm with well-defined borders, round vesicular nuclei, moderate to marked anisonucleosis with prominent nucleoli and coarse nuclear chromatin. Atypical mitotic figures were observed frequently. There was focal hemorrhage and necrosis in the tumor. The adjacent parenchyma showed focal calcification, tumor infiltration, and changes of acute tubular necrosis. No tumor infiltration was noted in ureter and vessels. Surgical margins were free from tumor infiltration (, ). The cyst showed features of simple epithelial cyst lined by flattened epithelial cells. CEA was positive and CK34β12 was negative (). Final diagnosis was adenocarcinoma of renal pelvicalyceal system (tubulovillous pattern).
On the last follow-up of one and a half years postsurgery, the patient was asymptomatic with normal renal function and had no recurrence.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [57, 'years'], 'creatinine': [1.76, 'mg/dL'], 'sex': 'Male'}",40.11196,38.10636,42.11756,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 57 years old. The concentration of Creatinine is 1.76 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.76^(-1.154) * 57^(-0.203) * 1 * 1=40.11196.
Hence, the patient's GFR is 40.11196 mL/min/1.73m²."
3337,9,MDRD GFR Equation,lab test,decimal,pmc-6376501-1,Extracted,"A 48-year-old woman, known case of diabetes mellitus for 8 years, on oral hypoglycemics with a well-controlled blood sugar, presented with the complaint of vomiting for 15 days, for which she went to various local GPs and hospitals but, she did not get any relief. Detailed workup was done to exclude possible causes like infectious, metabolic, drug-induced, or any other potential cause. Her vomiting was characterized by 2 to 3 episodes per day, non-projectile, without any blood, bile, or foul-smelling content (like undigested food). She also had a history of back pain for 6 years that aggravates on activity and numbness in feet. She also had a history of abdominal pain, polyuria, and polydipsia. She also gave the history of receiving multiple injections for back pain by some local physician in her residential area. On further investigation, it was found that she received vitamin D supplements 15 000 µg/d (equivalent to 600 000 IU/d) IM for 6 consecutive days a month back.
She is a known case of type 2 diabetes mellitus since 8 years, which was well-controlled with metformin; other than that, her past medical, surgical, and blood transfusion history was not significant.
On examination, she was conscious and oriented. Her vitals were BP was 130/70 mm Hg, pulse was 76 beats per minute, respiratory rate was 15 breaths per minute, and temperature was 98°F. Pallor, edema, and icterus were absent. No significant clinical findings were found in her respiratory, abdominal, and cardiovascular examinations. However, her central nervous system examination displayed a mild impairment in touch, pain, and vibration on the right side along with decreased pulsations of dorsalis pedis artery on the right side while there were diminished reflexes in both lower limbs. All the other common causes of long-term vomiting were excluded on the basis of clinical examination and lab findings.
Complete blood count reports showed hemoglobin of 11.8 g/dL with mean corpuscular volume (MCV) of 73 fL, but with normal white cells and platelet count. Blood biochemistry showed Serum Lipase of 17.7 U/L (normal = 10-190 U/L). Serum vitamin D3 levels were 155 ng/mL (normal = 30-80 ng/mL). Serum creatinine was 1.87 mg/dL (men = 0.7-1.5 mg/dL, women = 0.6-1.1 mg/dL), urea was 34 mg/dL (normal = 10-40 mg/dL), serum uric acid concentration was 5.3 mg/dL (men = 3.8-8.2 mg/dL, women = 2.8-6.1 mg/dL), and serum calcium was 15 mg/dL (men = 8.5-10.5 mg/dL, women = 8.2-10.4 mg/dL). Her serum parathyroid hormone level was 3.95 pg/mL (normal = 17-73 pg/mL). Liver function tests were well within the normal range. Chest radiograph and ultrasound of whole abdomen and pelvis were also normal.
She was started on intravenous fluids, intramuscular calcitonin 240 IU thrice daily and oral furosemide 40 mg twice daily for hypercalcemia, after which she started showing rapid clinical improvement. On her follow-up for next 10 days, she was monitored for serum calcium levels on regular basis as they optimized to baseline levels within a couple of weeks. She was prescribed with an anti-diabetic along with the counseling on calcium-restricted diet at the time of discharge; she is doing well.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'age': [48, 'years'], 'creatinine': [1.87, 'mg/dL']}",28.73722,27.30036,30.17408,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 48 years old. The concentration of Creatinine is 1.87 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.87^(-1.154) * 48^(-0.203) * 1 * 0.742=28.73722.
Hence, the patient's GFR is 28.73722 mL/min/1.73m²."
3338,9,MDRD GFR Equation,lab test,decimal,pmc-4421616-2,Extracted,"A 69-year-old woman with a history of atrial fibrillation, hypothyroidism and chronic kidney disease secondary to contrast-induced nephropathy was transferred for treatment of a pacemaker lead infection with MSSA.
On exam, the patient was afebrile with a blood pressure of 170/80 mmHg. A 3/6 systolic murmur was noted on cardiac exam. Her skin exam was negative for rash or embolic lesion. She had 2+ pitting edema in her lower extremities. Her laboratory exam was notable for a haemoglobin of 7.05 mg/dL and a serum creatinine of 3.23 mg/dL. Urine analysis showed protein 3+ and blood 2+ by dipstick; urine microscopy showed 30 dysmorphic RBCs/high-power field, many RBCs casts and several degraded cellular casts. Oval fat bodies and numerous maltese crosses were noted. A 24-h urine collection showed 3.6 g of protein. ANA, ANCA, cryoglobulin, C3, C4, HIV and hepatitis serologies were normal. A transesophageal echocardiogram showed a mobile echodensity present on the atrial side of the right ventricular pacemaker lead. A kidney biopsy was obtained on hospital Day 3.
Of 18 glomeruli present, 7 showed mild segmental hypercellularity, predominantly mesangial and occasionally endocapillary, with rare polymorphonuclear leukocytes. Two glomeruli were globally sclerotic, one was globally hypercellular, and the rest were unremarkable. There was moderate arteriosclerosis. Abundant eosinophilic casts without cellular reaction were present, predominantly in the medullary region. Immunohistochemistry for myoglobin A was negative. Mild tubular atrophy, interstitial fibrosis and chronic interstitial inflammation with occasional eosinophils were noted. (). Immunofluorescence revealed IgA, lambda and C3c deposition in the mesangium. Staining for IgG, IgM, kappa, C1q and albumin was negative ().
Electron microscopy showed that the glomerular basement membrane was within the normal adult range (0.36 μ). Mesangial electron-dense deposits were abundant. Subepithelial humps were not seen. There was mild epithelial foot process effacement (). A diagnosis of IgA-dominant focal proliferative glomerulonephritis was made.
The patient was started on i.v. oxacillin and underwent extraction of the infected pacemaker lead. Repeat blood cultures were negative for MSSA. Her creatinine decreased to 2.2 mg/dL after 1 week from initiation of the antibiotics. She was discharged on a 6-week course of i.v. oxacillin. At 1-month follow-up, the patient’s creatinine returned to baseline of 1.5 mg/dL. Her proteinuria resolved but she continued to have microscopic hematuria.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [69, 'years'], 'creatinine': [3.23, 'mg/dL'], 'sex': 'Female'}",14.2081,13.49769,14.91851,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 69 years old. The concentration of Creatinine is 3.23 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 3.23^(-1.154) * 69^(-0.203) * 1 * 0.742=14.2081.
Hence, the patient's GFR is 14.2081 mL/min/1.73m²."
3339,9,MDRD GFR Equation,lab test,decimal,pmc-5107662-1,Extracted,"A 55-year-old lady presented to our clinic, referred from the emergency department, with 4 weeks duration of intermittent right lower back pain, fatigue, and associated nausea. There was no associated dysuria, urinary urgency or frequency, or fevers; however, she reported possible hematuria in the guise of “orange” urine. She denied abnormal vaginal discharge, constipation, or recent trauma. She denied a history of prior urolithiases or recent urinary tract infections (UTIs). She had never smoked tobacco. She denied recent weight loss.
Her medical history was notable for stage 1B mixed clear cell-endometroid cancer of the uterus status post total abdominal hysterectomy, bilateral salpingo-oophorectomy, and bilateral pelvic/para-aortic lymph node dissection (0 of 22 lymph nodes positive) with adjuvant radiotherapy, 7 years before the current episode, with no evidence of recurrence. An abdominal and pelvis CT scan revealed severe right-sided hydroureteronephrosis, marked renal cortical thinning, and a 2.5 mm distal ureteral calculus (). The urinary bladder and the left renal unit appeared normal, and no lymphadenopathy was recognized. Urinalysis was negative for infection; however, four red blood cells per high-power field were appreciated. Creatinine was stable at 0.90 mg/dL. White and red blood cell counts were stable at 3700 cells per microliter and 13.2 gm per deciliter, respectively.
To better assess right renal function, the patient underwent an MAG-3 renogram that showed severely decreased right renal function with a split renal function of ∼20%, and an excretion half-life of >30 minutes. Subsequently, the patient was taken to the operating room for a right-sided diagnostic ureteroscopy and possible stone lithotripsy. Intraoperatively, however, no stones were observed, rather, a fleshy mass was observed in the distal ureter with proximal hydronephrosis (). Biopsies were obtained from the lesion and a plastic, double pigtail ureteral stent was left in place.
The histopathology demonstrated small round blue cells with hyperchromatic nuclei, most consistent with pure small cell carcinoma of the ureter. The immunohistochemical staining revealed positivity for synaptophysin that supported the neuroendocrine phenotype; staining for urothelial carcinoma (GATA 3 and p63), gynecologic cancer (PAX8), lymphoma (PAX5 and LCA), or sarcoma (Myogenin, CD31 and Desmin) was negative (). Given the findings, a full work-up for metastatic disease was initiated and included: (1) contrast-enhanced CT of the abdomen–pelvis revealed bulky retroperitoneal lymphadenopathy involving retrocaval/aortocaval/para-aortic nodes extending from the level of the ureteral lesion (L5–S1) to the right common iliac vessel bifurcation (), (2) contrast-enhanced CT of the head and chest was negative for metastatic disease, and (3) the Tc-99 bone scan was negative for bony involvement. The final clinic stage was cT3N2M0. The patient was started on Cisplatin–Etoposide neoadjuvant chemotherapy that the patient tolerated well except for minor hearing loss, with a plan for nephroureterectomy pending favorable clinical response. At 3 months of follow-up, she was doing well with lymphadenopathy reduction of 50% () and no evidence of disease progression.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [55, 'years'], 'creatinine': [0.9, 'mg/dL'], 'sex': 'Female'}",65.00585,61.75556,68.25614,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 55 years old. The concentration of Creatinine is 0.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.9^(-1.154) * 55^(-0.203) * 1 * 0.742=65.00585.
Hence, the patient's GFR is 65.00585 mL/min/1.73m²."
3340,9,MDRD GFR Equation,lab test,decimal,pmc-6735578-1,Extracted,"A 37-year-old male patient, a farmer, born and resident in a small town of northeast Brazil, sought medical attention complaining of recurrent episodes of gross hematuria alternating with brownish urine for 5 months. This symptom worsened 2 weeks ago, becoming continuous. Concurrently, he complained of asthenia, abdominal pain, nausea, and vomiting, which prevented him from exercising his daily activities. He denied the use of toxic substances or accidents with poisonous animals. The admission physical examination showed a well-looking patient, but pale, anicteric, and afebrile; no edema was evidenced. Pulse rate = 80 beats per minute, blood pressure = 130/70 mm Hg, respiratory rate = 18 breaths per minute, room air oximetry = 97%. Cardiac, pulmonary, and abdominal examination was normal. The initial laboratory tests showed the presence of uremia (BUN = 197 mg/dL and creatinine = 25.9 mg/dL), hyperkalemia (potassium = 8.6 mEq/L) with electrocardiographic changes, and bicytopenia (anemia with hemoglobin = 6.5 g/dL and platelet count = 51,600/mm3). The patient underwent hemodialysis, received packed blood red cells transfusion, and hyperkalemia was promptly treated. The urinary tract ultrasound was normal except for cortical enhanced echogenicity. Colored Doppler echography of the renal arteries and veins were normal. Proceeding the lab workup, urinalysis showed 76,000 leukocytes/mL, 93,000 erythrocytes/mL, but casts were absent; 24-hours proteinuria was 411 mg in a 2475 mL volume. Urine culture failed to show any bacterial growth. Serum total protein was 5.5 g/dL, albumin 3.2 g/dL and globulins = 2.3 g/dL. Hepatitis B antigen (HBsAg), antibodies to HIV, HCV and HBsAg, as well as antinuclear antibody (ANA) were negative; complement fractions C3 and C4 were normal. The search for schistocytes as well as direct and indirect Coombs was negative. Total bilirubin was normal but the lactate dehydrogenase was elevated (LDH = 940 U/L), reticulocytes count was reduced (0.3% and absolute = 8310/mm3) and myelogram showed slight hypercellularity with no atypical elements. Renal biopsy was not performed due to thrombocytopenia.
The patient was discharged and referred to chronic hemodialysis treatment and a follow up in an outpatient clinic.
One month later, the patient returned to the emergency department complaining of back pain and fever. Urinalysis showed marked leukocyturia and urine culture showed growth of more than 105 colony-forming units of Escherichia coli, and blood culture was positive for the same pathogen. Diagnosis of acute pyelonephritis was done and ceftazidime was initiated and lasted 14 days. On this occasion, BUN = 40 mg/dL, creatinine = 3.2 mg/dL, hemoglobin 7.7 g/dL, hematocrit = 22.8%; leukocytes = 10.100/mm3 and platelets = 50,400/mm3. Approximately 3 days after the end of antimicrobial therapy, the patient presented with asthenia, chills, and anorexia, progressing to right flank pain, fever (38 ºC), and gross hematuria. Although he had already lost 8 kg since the very beginning of symptoms, the patient still presented well-looking, anicteric but pale. Blood pressure was 88 × 62 mm Hg, pulse rate = 90 beats per minute, respiratory rate = 18 breaths per minute. Examination of the heart and lung remained unchanged, but costovertebral angle tenderness was detected on the right. The computed angiotomography of the abdomen showed signs of pyelonephritis in the right kidney with multiple small abscesses, homogeneous hepatomegaly, but no signs of renal arterial or venous thrombosis. New antibiotic regimen with cefepime and vancomycin was started. A new laboratory workup disclosed the recovery of renal function (BUN = 21 mg/dL and creatinine = 1.2 mg/dL) allowing the removal of the temporary dialysis catheter. Reviewing the whole case the diagnosis of paroxysmal nocturnal hemoglobinuria (PNH) was considered. Flow cytometry showed a CD55 negativity in 58% of granulocytes, CD59 negativity in 65% of granulocytes and CD14 negativity in 56,4% of monocytes. Red blood cells failed to express CD55 in 17,8% of cells and 12,3% of cells for CD59. Red blood cells results should be interpreted with caution, because the cytometry was undertaken after hemotransfusion. These results were consistent with the diagnosis of paroxysmal nocturnal hemoglobinuria (PNH). The patient received a packed red blood cells transfusion and 30 mg of prednisone daily aiming at hemolysis control. Joint evaluation with the urologist ruled out surgical intervention, opting for conservative treatment for 6 weeks. The patient presented a satisfactory outcome, weight gain, and fever defervescence. He was again discharged and was prescribed warfarin and folic acid.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [37, 'years'], 'creatinine': [25.9, 'mg/dL'], 'sex': 'Male'}",1.96673,1.86839,2.06507,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 37 years old. The concentration of Creatinine is 25.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 25.9^(-1.154) * 37^(-0.203) * 1 * 1=1.96673.
Hence, the patient's GFR is 1.96673 mL/min/1.73m²."
3341,9,MDRD GFR Equation,lab test,decimal,pmc-4376926-1,Extracted,"A 63-year-old female was admitted to our hospital on February 6, 2012, due to uncontrolled hypertension despite antihypertensive treatment. She had been treated with chronic HD (F15 dialyzer, 1.5 m2, polysulfone, Shandong Weigao, PR China) for end-stage kidney disease secondary to diabetic nephropathy 3 times a week for 3 months. The blood flow rate and dialysis time of each HD session was 200–220 ml/min and 4 h. The ultrafiltration volume was 1.0–1.5 liters for each session. Her postdialysis body weight was kept at 58–59 kg. She had had hypertension for 15 years and had been treated with telmisartan 80 mg b.i.d., lacidipine 4 mg b.i.d. and clonidine 150 μg t.i.d. Her blood pressure was controlled around 150/90 mm Hg. Erythropoietin (10,000 U q.w.) was used to treat anemia. Two months previously, the patient experienced headache and dizziness with a blood pressure of 235/120 mm Hg. Her postdialysis body weight was then adjusted to 55 kg in the next 2 weeks. However, there was no improvement of the blood pressure and she started to feel thirsty during the HD session. Meanwhile, the antihypertensive drugs were gradually increased to olmesartan (20 mg b.i.d.), benazepril (20 mg b.i.d.), nitrendipine (20 mg t.i.d.), arotinolol (10 mg b.i.d.), terazosin (2 mg b.i.d.), torasemide (40 mg q.d.) and clonidine (150 μg t.i.d.). Her symptoms were not relieved, and the systolic blood pressure maintained at about 180–200 mm Hg. Two days before her hospital admission, she presented with severe headache, objective vertigo, nausea and persistent vomiting, with a blood pressure in the 240/120 mm Hg. Her urine volume was about 400 ml/day on admission. The physical examinations at hospitalization showed that her blood pressure was 240/120 mm Hg without any postural change, and her pulse rate was 83/min with a regular rhythm. No abnormal finding was seen in her chest and abdomen. She had an arteriovenous shunt in the right forearm. There was no leg edema. Neurological findings showed that the bilateral Babinski sign was positive.
A blood analysis showed a white blood cell count of 8.6 × 109/l, hemoglobin of 106 g/l and a platelet count of 242 × 109/l. Her blood chemistry revealed a urea level of 13.6 mmol/l, creatinine 312 μmol/l, potassium 3.8 mmol/l, sodium 136 mmol/l, chloride ion 101 mmol/l, calcium 1.84 mmol/l and phosphate 1.65 mmol/l. The liver function was unremarkable. A CT of the head showed several lacunar infarctions and did not exhibit hemorrhage or masses. An ambulatory blood pressure measurement showed the average diurnal and nocturnal blood pressure to be 173/69 and 183/71 mm Hg, respectively, while the maximum and minimum blood pressure was 216/85 and 155/100 mm Hg. A color duplex ultrasonography of the renal artery did not suggest the presence of stenosis. A CT of the abdomen revealed mild hyperplasia of the left adrenal gland (fig. ). However, no abnormal results were found in the endocrinological analysis. The plasma renin activity was 0.37 ng/ml (normal range 0.05–0.79 ng/ml) and a plasma aldosterone concentration of 103.85 pg/ml (normal range 59.5–173.9 pg/ml). Her serum angiotensin I and II were 0.2 and 55.65 pg/ml (normal range 28.2–52.2 pg/ml), respectively. The serum cortisol was 318.1 μg/l (normal range 42–384 μg/l), and her plasma adrenocorticotropic hormone level was 13.9 pg/ml (normal range 10–80 pg/ml). She was treated intravenously with urapidil hydrochloride, and the blood pressure maintained at 160–240/70–130 mm Hg.
Two weeks after admission (February 24), NHD with a Rexeed 15UC dialyzer (1.5 m2, polysulfone membrane; Asahi Kasei, Japan) was initiated, with a blood flow rate of 150 ml/min and a dialysis time of 7 h on a t.i.w. regimen. Her postdialysis body weight stayed at roughly 54 kg. Erythropoietin was temporally held because of the extremely high blood pressure. After 3 months of NHD, all symptoms were remittent and her systolic blood pressure started to decrease by 10–20 mm Hg (fig. ). Erythropoietin was then used again, and the dosage was gradually increased to 10,000 U per week. Six months later, the pre-dialysis blood pressure was decreased to 140–160/90–100 mm Hg and the antihypertensive drugs were reduced to 4 kinds (olmesartan 20 mg b.i.d., nitrendipine 20 mg t.i.d., arotinolol 10 mg b.i.d. and clonidine 150 μg t.i.d.). The patient has been on NHD for over 2 years. The most recent blood biochemical parameters including hemoglobin, serum calcium and phosphate and parathyroid hormone were 100 g/l, 2.42 mmol/l, 1.8 mmol/l and 156.5 pg/ml, respectively.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [312.0, 'µmol/L'], 'sex': 'Female'}",13.16194,12.50384,13.82004,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 63 years old. The concentration of Creatinine is 312.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 312.0 µmol. To convert 312.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 312.0 µmol Creatinine * 1e-06 mol/µmol = 0.00031 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00031 mol Creatinine * 113.12 g/mol = 0.03507 g Creatinine. To convert 0.03507 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.03507 g Creatinine * 1000.0 mg/g = 35.07 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 35.07 mg Creatinine/10.0 dL = 3.507 mg Creatinine/dL. The concentration value of 312.0 µmol Creatinine/L converts to 3.507 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 3.507^(-1.154) * 63^(-0.203) * 1 * 0.742=13.16194.
Hence, the patient's GFR is 13.16194 mL/min/1.73m²."
3342,9,MDRD GFR Equation,lab test,decimal,pmc-4924496-1,Extracted,"The patient is a 45-year-old male who presented in 2009 with proteinuria, high serum creatinine and bilateral shrunken kidneys on ultrasonography (USG) and was diagnosed as ESRD. Etiology was presumed to be chronic glomerulonephritis – exact etiology was not known. The patient was put on continuous ambulatory peritoneal dialysis protocol before transplant and received a living-related kidney transplant from his brother in 2009 with excellent immediate graft function.
The patient's immunosuppression regimen comprised pulse steroid therapy followed by triple immunosuppression regime (prednisone, tacrolimus, and mycophenolate mofetil). No induction with anti-thymocyte globulin/monoclonal antibodies was given. During his 1st year posttransplant, he developed polycythemia which was managed with phlebotomy. After 1½ year, his serum creatinine reached 2.0 mg/dl. He was noted to have significant proteinuria of 4 g/day. His general physical and systemic examination was normal. The patient underwent a renal transplant biopsy to ascertain the cause of worsening creatinine and proteinuria.
The biopsy contained renal medulla and cortical parenchyma containing up to 7 viable glomeruli []. One glomerulus showed global sclerosis. Remaining glomeruli appeared variably enlarged and exhibited dilated capillary lumina. Two glomeruli showed segmental sclerosis with a monolayer of visceral epithelial cells overlying the sclerosed segments. There was remarkable global enlargement of visceral epithelial cells which contained abundant vacuolated cytoplasm, with few cells containing cytoplasmic basophilic debris. Tubular atrophy and interstitial fibrosis involved about 15–20% of sampled cortex. Patchy dense interstitial inflammation and mild interstitial edema with a few foci of moderate tubulitis affecting the nonatrophic tubules were noted. Patchy loss of tubular brush borders with epithelial simplification and luminal granular casts were seen. Few atrophic tubules were dilated and contained luminal hyaline/proteinaceous casts whereas few tubular lumina contained red blood cells (RBC‘s). Arteries appeared relatively unremarkable while arterioles showed focally marked hyalinosis. Focal RBC extravasation and interstitial inflammation were noted in the medullary parenchyma. Tissue for immunofluorescence showed up to 5 glomeruli, exhibiting segmental mesangial staining for IgM, and were negative for IgA, IgG, C3 and C1q.
The patient received pulse doses of methylprednisolone for cell-mediated rejection and was continued on immunosuppressive regime of prednisone, tacrolimus and mycophenolate mofetil, and olmesartan for proteinuria. Serum creatinine initially improved to 1.7 mg/dl. However, subsequent testing revealed worsening serum creatinine to 2.7 mg/dl. In view of renal biopsy showing visceral epithelial cells containing abundant vacuolated cytoplasm, patient was evaluated for alpha-galactosidase A enzyme activity. Levels of the enzyme was found markedly deficient in the recipient (7.00; enzyme normal limit >60). Diagnosis of FD was confirmed in the recipient. Further evaluation revealed normal electrocardiogram and normal echocardiography. There was mild acroparesthesias in the hands and feet of the recipient. The renal function of the donor continued to remain within normal limits (serum creatinine 0.8 mg/dl and urinary protein of <50 mg/24 h). The alpha-galactosidase level of donor was normal on evaluation.
A pedigree analysis showed recipient was second in birth order and had four more brothers. A second sibling, another brother, fourth in birth order, who was evaluated for infertility was found to have raised serum creatinine (serum creatinine of 4 mg/dl) with proteinuria of 5.8 g/24 h. He was evaluated for alpha-galactosidase activity which was found markedly decreased (12.10; normal enzyme activity level >60), and was diagnosed as FD with renal failure. The mother of the patient had died at around 55 years of age due to chronic kidney disease (CKD)/ESRD, the etiology of which was not known as she was not evaluated for it. The father is alive at the age of 90 years and is well. Three other brothers are not affected. His mother has three more siblings who are all alive and well with ages more than 75, but have not been evaluated for FD. The children of the patient are being evaluated for FD.
The patient is being planned for ERT. However, due to financial constraints has still not been started on ERT.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [45, 'years'], 'creatinine': [2.7, 'mg/dL'], 'sex': 'Male'}",25.68279,24.39865,26.96693,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 45 years old. The concentration of Creatinine is 2.7 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.7^(-1.154) * 45^(-0.203) * 1 * 1=25.68279.
Hence, the patient's GFR is 25.68279 mL/min/1.73m²."
3343,9,MDRD GFR Equation,lab test,decimal,pmc-5558125-2,Extracted,"Case 2: A 78-year-old, nonalcoholic, woman with a medical history of atrial fibrillation, peripheral neuropathy, hypertension, dyslipidemia, diabetes, chronic renal insufficiency, and hysterectomy for uterine fibroids, presented with melena for three days, associated with fatigue and orthostatic dizziness. Medications included warfarin, furosemide, metoprolol, diltiazem, atorvastatin, pioglitazone, amitriptyline, and glimepiride. Physical examination revealed stable vital signs, with a blood pressure of 124/67 mmHg, and pulse of 68/min. There was a heart murmur, and bilateral 3+ lower extremity edema. The abdomen was soft, and non-tender, with normoactive bowel sounds, and no organomegaly. Rectal examination revealed melena. The hemoglobin was 7.1 g/dL, INR was 4.9, platelet count was 306000/mL, and PTT was 42.5 s. The blood urea nitrogen was 44 mg/dL and creatinine was 1.8 mg/dL. An electrocardiogram revealed atrial fibrillation without acute ischemic changes.
She was transfused 2 units of packed erythrocytes and 2 units of fresh frozen plasma. Two-dimensional echocardiography revealed mild mitral valve regurgitation, moderate-to-severe right atrial dilatation, and severe tricuspid valve regurgitation. Abdominal CT revealed a submucosal, antral, gastric mass measuring 9.5 cm × 6.0 cm × 4.5 cm. EGD revealed a large, focally ulcerated, smooth, antral gastric mass, exhibiting the cushion sign (Figure ). Microscopic examination of multiple mucosal biopsies of the ulcer margin revealed superficial ulceration, granulation tissue, and no malignancy. The patient underwent surgery due to the recent bleeding of the giant lipoma. At laparotomy, the submucosal mass was excised by distal gastrectomy. Gross pathology of the resected mass revealed a relatively homogeneous, 9.0 cm × 6.0 cm × 4.5 cm, focally ulcerated, mass with a greasy, tan-yellow cut surface (Figure ), which microscopically was a lipoma (Figure and D). The patient was discharged 5 d postoperatively with no further GI bleeding[-].","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [78, 'years'], 'creatinine': [1.8, 'mg/dL'], 'sex': 'Female'}",27.21211,25.8515,28.57272,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 78 years old. The concentration of Creatinine is 1.8 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.8^(-1.154) * 78^(-0.203) * 1 * 0.742=27.21211.
Hence, the patient's GFR is 27.21211 mL/min/1.73m²."
3344,9,MDRD GFR Equation,lab test,decimal,pmc-4519605-1,Extracted,"A 43-year-old female patient developed end-stage renal disease due to chronic glomerulonephritis and underwent continuous ambulatory peritoneal dialysis (CAPD) for 2.5 years (started in January 2012). Her peritoneal dialysis regime included 2,000 ml of 1.5% peritoneal dialysis solution (Dianeal 1.5%, Baxter, International Inc.) with three exchanges daily (PD2) and 2,000 ml of 2.5% PDF overnight (PD2). Her daily peritoneal dialysis ultrafiltration volume was 500–800 ml and her urine output was 800–1,000 ml/24 h. The patient denied having had any systemic diseases or a history of allergic or infectious diseases. In general, her CAPD therapy went well during the past 30 months, and the peritoneal dialysis effluent was always clear.
From May 2014, the patient observed cloudy peritoneal effluent without abdominal pain or fever. The ultrafiltration volume was stable. An effluent cytological study and bacterial/fungal culture were demanded before the antibiotic application. The former showed a white blood cell (WBC) count of 630 × 106/l, with 80% polynuclear cells, while the latter was negative. Despite all treatments, such as peritoneal lavage, diagnostic antibiotic treatment by intraperitoneal injection of aminoglycosides (amikacin) combined with first-generation cephalosporins (cefazolin) for 14 days, the effluent was still turbid. The second peritoneal fluid culture was performed 10 days after the antibiotic application, which was, however, still negative; thus, a bacterial/fungal culture was demanded. Therefore, we changed the antibiotic regime of intraperitoneal injection of ceftazidime and vancomycin to 21 days. Intraperitoneal urokinase 5,000 IU/l was also added to each dialysate. There was still no improvement of the turbidness, but the ultrafiltration was always stable. The patient was hospitalized in July 2014.
Our 43-year-old patient weighed 65 kg and measured 165 cm (BMI 23.8). Her blood pressure was 140/80 mm Hg, with a heart rate of 80 bpm. There was no rash or purpura. Pulmonary auscultation was normal. Abdominal palpation revealed no tenderness, tension or rebound pain, and no lower extremity edema was found.
In July 2014, the complete blood count (CBC) revealed a WBC count of 3.8 × 109/l, with 32.2% eosinophils, and there were up to 500 × 106/l leukocytes in the peritoneal effluent, with 87% eosinophils. The absolute eosinophil count was 435/mm3 (before the antibiotic application). The peritoneal effluent culture showed no growth of aerobic or anaerobic bacteria, or fungi, and negativity for acid-fast stain. The patient remained asymptomatic, and the antibiotics were then stopped.
Given the fact that there was a significant elevation of eosinophils in the peritoneal effluent with a ratio of 87% and an absolute eosinophil count of >30/mm3 (up to 435/mm3), the patient was diagnosed with eosinophilic peritonitis (EP). The etiological examinations included repeated effluent bacteria, fungi, and Mycobacterium tuberculosis detection and cultivation; serum tumor markers, serum immunological markers like ANA, ENA and ANCA, and blood allergen tests were all negative. Chest and abdominal injected computed tomography did not reveal any sign of malignancy. However, there was a slight elevation in erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) (table ).
Ketotifen (1 mg daily p.o.) was given as anti-allergic treatment along with low-dose oral corticosteroid therapy. The patient commenced oral prednisone acetate with a daily dose of 20 mg. Over the next 24 h, her peritoneal dialysis effluent became clear. Prednisone acetate was rapidly reduced and stopped over a 2-week period, but 3 days after that, the peritoneal dialysis effluent turned turbid again. Thus, we restarted a low dose of prednisone acetate (20 mg daily p.o.), which was gradually weaned off and stopped over an 8-week period. During the therapy course, the patient had no complaint of abdominal pain, and the dialysis fluid remained clear. In September 2014, we reanalyzed the dialysis effluent cytology demonstrating that the polynuclear cell count decreased to 1 × 106/l, with no eosinophils (fig. ). The CBC showed a WBC count of 9.2 × 109/l, with 1.1% eosinophils.
In May 2014, the following examinations were performed: CBC: WBC 7.3 × 109/l with 12.8% eosinophils, Hgb 112/l, PLT 217 × 109/l; SGPT 14 IU/l, SGOT 17 IU/l, Alb 28 g/l, Scr 897 μmol/l; ESR 38 mm/h, CRP 1.12 mg/lRF 29 IU/ml, IgG 1,800 mg/dl, IgA 392 mg/dl; dialysis effluent cytology: WBC 630 × 106/l with 80% polynuclear cells; dialysis effluent culture: negative.
In July 2014, the following examinations were performed: CBC: WBC 3.8 × 109/l with 32.2% eosinophils, Hgb 100/l, PLT 202 × 109/l; SGPT 15 IU/l, SGOT 16 IU/l, Alb 20 g/l, Scr 856 μmol/l; ESR 42 mm/h, CRP 0.45 mg/lRF 29 IU/ml, IgG 574 mg/dl, IgA 81 mg/dl; dialysis effluent cytology: WBC 500 × 106/l with 87% eosinophils; dialysis effluent culture: negative.
In August 2014 (4 weeks), the following examinations were performed: CBC: WBC 8.99 × 109/l with 1.3% eosinophils, Hgb 91/l, PLT 242 × 109/l; SGPT 22 IU/l, SGOT 18 IU/l, Alb 17g/l, Scr 816 μmol/l; dialysis effluent cytology: WBC 60 × 106/l with 20% eosinophils; dialysis effluent culture: negative.
In September 2014 (8 weeks), the following examinations were performed: CBC: WBC 9.2 × 109/l with 0.9% eosinophils, Hgb 120/l, PLT 279 × 109/l; SGPT 18 IU/l, SGOT 17 IU/l, Alb 25 g/l, Scr 769 μmol/l; dialysis effluent cytology: WBC 1.0 × 106/l with no eosinophil; dialysis effluent culture: negative.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [43, 'years'], 'creatinine': [897.0, 'µmol/L'], 'sex': 'Female'}",4.15774,3.94985,4.36563,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 43 years old. The concentration of Creatinine is 897.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 897.0 µmol. To convert 897.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 897.0 µmol Creatinine * 1e-06 mol/µmol = 0.0009 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.0009 mol Creatinine * 113.12 g/mol = 0.10181 g Creatinine. To convert 0.10181 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.10181 g Creatinine * 1000.0 mg/g = 101.81 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 101.81 mg Creatinine/10.0 dL = 10.181 mg Creatinine/dL. The concentration value of 897.0 µmol Creatinine/L converts to 10.181 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 10.181^(-1.154) * 43^(-0.203) * 1 * 0.742=4.15774.
Hence, the patient's GFR is 4.15774 mL/min/1.73m²."
3345,9,MDRD GFR Equation,lab test,decimal,pmc-4722097-1,Extracted,"A 61-year-old woman was admitted with severe diarrhea and dehydration. She was a current smoker, with a history of 40 pack-years. Her medical history showed monoclonal gammopathy of undetermined significance and chronic kidney disease, for which she had been visiting the nephrology department of our hospital monthly and receiving medical treatment for 5 years. Three days after admission, she developed a fever and hypoxia, complaining of dyspnea. A chest radiograph showed no abnormalities, but thoracic computed tomography (CT) showed thickening of bronchial walls, suggesting bronchitis (Fig. ). Her respiratory distress progressed despite empirical antibiotic therapy. She was transferred to our section 25 days after admission. A chest radiograph showed infiltrative shadows and a cavity in the right middle lung field, while thoracic CT demonstrated consolidation along with obstructed bronchi. Distal portion of the obstructed bronchi showed cystic bronchiectatic lesions in the right upper lobe (Fig. ). Laboratory findings showed an elevated leukocyte count of 18,370 cells/mm3 (neutrophil 84.3%, lymphocytes 10.6%, monocytes 3.0%, eosinophils 1.8%, basophils 0.3%). C-reactive protein level, 9.86 mg/dL; procalcitonin (PCT) level, 0.72 U/mL; serum albumin, 1.7g/dL; lactate dehydrogenase, 295 IU/L; creatinine 1.35 mg/dL; and β-D-glucan, 236.9 pg/dL. The influenza antigen test was negative. Her IgG value was 1683 mg/dL and she was hepatitis B surface antigen negative, hepatitis C virus antibody negative, and human immunodeficiency virus antibody negative, with a CD4 positive cell count of 1044/μL. Her neutrophil function tests showed normal values. Considering the ineffectiveness of empirical antibiotic therapy and the elevated β-D-glucan level, a pulmonary fungal infection was suspected. Intravenous voriconazole was started. The patient underwent flexible bronchoscopy 27 days after admission, which revealed multiple, discrete whitish plaques involving the trachea and the right upper lobe bronchus (Fig. ). A biopsy under bronchoscopy showed chronic active inflammation with necrotic tissue, in which numerous filamentous fungal hyphae were seen. Aspergillus fumigatus was isolated from bronchial lavage fluid cultures. After administration of voriconazole, her symptoms and chest radiograph findings gradually improved. Thoracic CT showed remarkable improvement of the infiltrative shadows. The patient was discharged 70 days after admission.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [61, 'years'], 'creatinine': [1.35, 'mg/dL'], 'sex': 'Female'}",39.86712,37.87376,41.86048,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 61 years old. The concentration of Creatinine is 1.35 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.35^(-1.154) * 61^(-0.203) * 1 * 0.742=39.86712.
Hence, the patient's GFR is 39.86712 mL/min/1.73m²."
3346,9,MDRD GFR Equation,lab test,decimal,pmc-3921998-1,Extracted,"A 62-year-old man attended the diabetes outpatient clinic for his annual review visit. He had been diagnosed with type 2 diabetes mellitus 6 years earlier. His diabetes was complicated by diabetic nephropathy, background diabetic retinopathy and peripheral neuropathy manifested by reduced vibration sense in both feet. He also suffered from hypertension and dyslipidaemia. His medications at the time of review included an angiotensin converting enzyme inhibitor, an α-blocker, a statin, metformin and aspirin.
He was symptomatically well. Physical examination revealed a blood pressure of 155/83 mmHg, reduced vibration sense in his feet and palpable peripheral pulses. Laboratory tests revealed a HbA1c of 6.1%, lipid profile within goal range with total cholesterol 3.4 mmol/l, triglyceride 1.10 mmol/l, HDL 1.64 mmol/l and LDL 1.29 mmol/l. Serum creatinine was elevated at 120 mmol/l (58–110) and 24-h urinary protein 1.13 g.
After his physician review was complete, an electrocardiogram (ECG) was performed as part of his routine annual assessment (). The patient was recalled to the clinic room for further review as a result of the ECG findings. On questioning, he denied chest, arm or jaw pain or discomfort; shortness of breath; palpitations; nausea; indigestion or sweating. In view of the ECG changes, he was admitted for investigation and treatment of a suspected myocardial infarction.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [62, 'years'], 'creatinine': [120.0, 'mmol/L'], 'sex': 'Male'}",0.01837,0.01745,0.01929,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 62 years old. The concentration of Creatinine is 120.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from mmol to mg. The mass of Creatinine is 120.0 mmol. To convert 120.0 mmol of Creatinine to mol, multiply by the conversion factor 0.001, giving us 120.0 mmol Creatinine * 0.001 mol/mmol = 0.12 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.12 mol Creatinine * 113.12 g/mol = 13.5744 g Creatinine. To convert 13.5744 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 13.5744 g Creatinine * 1000.0 mg/g = 13574.4 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 13574.4 mg Creatinine/10.0 dL = 1357.44 mg Creatinine/dL. The concentration value of 120.0 mmol Creatinine/L converts to 1357.44 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1357.44^(-1.154) * 62^(-0.203) * 1 * 1=0.01837.
Hence, the patient's GFR is 0.01837 mL/min/1.73m²."
3347,9,MDRD GFR Equation,lab test,decimal,pmc-6375012-1,Extracted,"A 38-year-old female presented on March 2016 with breathlessness, oliguria, and edema of 1-week duration. She had polyarthritis on and off for 1 year and was diagnosed to have SLE, established with 4 out of 11 criteria of the American College of Rheumatology. She had a significant obstetric history of intrauterine death at 22 weeks during her second and third pregnancy, with histopathology of placenta showing a large area of placental infarct (25%) and normal umbilical vessels. Her blood pressure was 160/100, and peripheral edema was present.
Laboratory investigation showed urinalysis: 3+ proteinuria, plenty of red blood cells; spot urine protein creatinine ratio: 8.6; blood urea: 88 mg/dl; serum creatinine: 6.4 mg/dl; serum C3:21 mg/dl; serum C4:5 mg/dl; serum antinuclear antibodies, and anti-ds DNA: positive. Anticardiolipin and antiphospholipid antibodies (APLA): negative. Ultrasonogram of the abdomen showed normal-sized kidneys. Renal biopsy showed eight glomeruli with endocapillary proliferation and lobular accentuation of the capillary tuft []. Early cellular crescents were identified in two glomeruli with fibrous intimal proliferation of the arteries. Immunofluorescence was positive for IgG (+3), IgM (+2), IgA (+1), C3 (+3) over capillary walls and mesangium suggestive of diffuse profilerative glomerulonephritis, lupus nephritis (ISN/RPS Class IV – A). She was treated with pulse methylprednisolone 1 g/day for 3 days, followed by oral prednisolone 60 mg/day for 8 weeks and monthly intravenous cyclophosphamide 500 mg. In addition, she also received hydroxychloroquine (HCQS) 200 mg once daily and antihypertensives. She had dialysis-dependent renal failure for 2 months and was on twice-weekly hemodialysis (HD). At 3 months after onset of renal failure, she developed difficulty in opening both the eyes. Her blood pressure was 150/100 mm Hg. Neurological examination was normal except for bilateral eye ptosis []. Oral HCQS was stopped, and there were no improvement even after 1 week of discontinuing this drug. The cerebral contrast-MRI and chest X-ray were normal. Serum creatinine kinase was 140 U/L. Nerve conduction studies showed the decremental response of 15%–25% over facial muscles with no decremental response over limb muscles. The findings were consistent with neuromuscular junction disorder. Anti-AchR antibody was negative. She was treated with oral pyridostigmine 60 mg twice daily. Clinical improvement was seen within 48 h. Her renal failure also slowly improved and she was dialysis independent after 4 months of HD. Mycophenolate mofetil therapy was started at a dose of 1000 mg/day orally as a maintenance therapy for lupus nephritis along with oral prednisone after 6 months. Till the last follow-up, recently, her serum creatinine was 1.41 mg/dl with no recurrence of ocular symptoms.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [38, 'years'], 'creatinine': [1.41, 'mg/dL'], 'sex': 'Female'}",41.73948,39.65251,43.82645,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 38 years old. The concentration of Creatinine is 1.41 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.41^(-1.154) * 38^(-0.203) * 1 * 0.742=41.73948.
Hence, the patient's GFR is 41.73948 mL/min/1.73m²."
3348,9,MDRD GFR Equation,lab test,decimal,pmc-6078926-1,Extracted,"A 62-year-old man visited our hospital for a surveillance colonoscopy as part of a routine check-up. He underwent colonic polypectomy three years ago at another hospital and had not experienced hematochezia, diarrhea, abdominal pain, weight loss, or fever. Hypertension, diabetes mellitus, and stage 5 chronic kidney disease due to diabetic nephropathy were noted in his past medical story. He had been treated with hemodynamic dialysis, and the patient’s blood pressure was 160/91 mm Hg. His body temperature was 36.3°C, heart rate was 73 beats per minute, respiratory rate was 20 breaths per minute, and he was mentally alert. There was neither abdominal tenderness nor rebound tenderness. Bowel sounds were normal, and the liver and spleen were not palpable. Laboratory findings were as follows: white blood cell count, 5,940 cells/μL (neutrophils, 42.7%, eosinophils, 6.9%, lymphocytes, 46.6%); hemoglobin, 11.2 g/dL; platelet count, 164,000/μL; aspartate aminotransferase, 13 IU/L; alanine aminotransferase, 10 IU/L; alkaline phosphatase, 81 IU/L; total bilirubin, 0.4 mg/dL; total protein, 7.7 g/dL; albumin, 4.5 g/dL; blood urea nitrogen, 24.3 mg/dL; and creatinine, 5.56 mg/dL. The serum carcinoembryonic antigen level was 2.36 ng/mL, and the serum lactate dehydrogenase level was 404 U/L, both of which were within the normal range. Colonoscopy revealed four sessile polyps, 2−4 mm in size, one in the hepatic flexure, two in the proximal transverse colon, and one in the distal transverse colon. The polyps had a smooth surface, without nodularity or ulceration. Narrow band imaging (NBI) without magnification was performed on one of the four colon polyps. The pit pattern of the polyp showed dark or white spots of uniform size and was identified as type 1 according to NBI international colorectal endoscopic classification []. We removed two of the polyps with forceps and performed en bloc endoscopic mucosal resection with a snare for the other two polyps, after injecting saline into the submucosa (). Upon histological examination, all resected specimens showed atypical lymphoid aggregation composed of small- to medium-sized and mainly cleaved B-lymphoid cells, which stained positively for CD20 and Bcl-2 but negatively for CD3 and cyclin D1 (). The labeling index of Ki-67 was 10%. These findings were highly suspicious of lymphoma. After confirming the biopsy report of colon polyps, computed tomography (CT) was performed and demonstrated multiple lymph node enlargement. Subsequently, positron emission tomography-CT was performed sequentially to confirm the degree of involvement of the follicular lymphoma. The images showed moderate splenomegaly and numerous variably sized enlarged lymph nodes on both sides of the neck, both axillae, the mediastinum, abdominal aorta, celiac trunk, hepatoduodenal ligament, gastrohepatic ligament, and both inguinal regions (). A bone marrow study including aspiration and trephine biopsy was performed, which showed normocellular marrow and no evidence of bone marrow involvement of malignant lymphoma.
Excisional biopsy of the lymph nodes of the left side of the neck was performed for histopathologic confirmation. On immunohistochemical staining, CD20 and Bcl-2 were positive, whereas CD3, CD5, and cyclin D1 were negative (). The Ki-67 labeling index was 10%. Based on these findings, the diagnosis of grade 1 follicular lymphoma with a predominantly follicular pattern was made. The tumor was stage IIIA according to the Ann Arbor staging system []. The patient received five courses of combination chemotherapy, consisting of cyclophosphamide, vincristine, prednisone, and rituximab (R-CVP), which led to complete remission. Since then, maintenance therapy with rituximab has been initiated, and no recurrence has been reported for approximately 21 months.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [62, 'years'], 'creatinine': [5.56, 'mg/dL'], 'sex': 'Male'}",10.45602,9.93322,10.97882,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 62 years old. The concentration of Creatinine is 5.56 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 5.56^(-1.154) * 62^(-0.203) * 1 * 1=10.45602.
Hence, the patient's GFR is 10.45602 mL/min/1.73m²."
3349,9,MDRD GFR Equation,lab test,decimal,pmc-6031599-1,Extracted,"A 67-year-old male patient presented with a three-day history of diarrhea. He had received 14 months of dasatinib therapy (100 mg/day) for the treatment of CML, and He had chronic kidney disease. Physical examination revealed no fever and mild abdominal pain without any tenderness. At hospitalization, he had white blood cell (WBC) count of 19,430/mm3 (lymphocyte, 71%), hemoglobin (Hb) level of 8.0 g/dl, platelet count of 239,000/mm3, and a blood urea nitrogen/creatinine ratio of 85.2/3.08 mg/dl. On the 2nd day, his WBC count declined sharply to 8,720/mm3 (lymphocyte 20%), and he developed hematochezia without thrombocytopenia on 3rd day of admission. At this point, his blood and stool cultures tested negative. Dasatinib-induced hemorrhagic colitis was suspected, and a total colonoscopy revealed edematous and friable mucosa, along with a loss of vascularity from the cecum to rectum (). His symptoms did not improve upon the discontinuation of dasatinib and with conservative care. After 4 days of admission, biopsy tissue showed positive CMV-specific IHC staining, and a blood CMV real time quantitative polymerase chain reaction (RQ-PCR) also tested positive (760 copies/ml). His symptoms subsided following 19 days of ganciclovir (5 mg/kg IV q12hr) administration. Dasatinib was re-started subsequently, and the CMV colitis did not relapse (15 months).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [67, 'years'], 'creatinine': [3.08, 'mg/dL'], 'sex': 'Male'}",20.34967,19.33219,21.36715,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 67 years old. The concentration of Creatinine is 3.08 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.08^(-1.154) * 67^(-0.203) * 1 * 1=20.34967.
Hence, the patient's GFR is 20.34967 mL/min/1.73m²."
3350,9,MDRD GFR Equation,lab test,decimal,pmc-5295522-1,Extracted,"A 27-year-old African American female presented to the hospital after a sudden onset of severe retrosternal chest pain. Past medical history was insignificant for hypertension or diabetes mellitus. Patient has a history of smoking cigarettes, beginning at age 9, and frequent marijuana use. The patient was treated with morphine and Percocet for pain. Lab data and urine toxicology screen were negative for troponins and significant for marijuana, respectively. Urine drug screen was negative for cocaine and amphetamines. Drug screen was positive for opiates, but this result is most likely an artifact of morphine and Percocet treatment for chest pain. Initial laboratory findings included hemoglobin 12 g/dL, hematocrit 12.6%, platelets 223 × 103/μL, glucose 156 mg/dL, BUN 9 mg/dL, creatinine 0.8 mg/dL, sodium 135 mEq/L, potassium 4 mEq/L, chloride 101 mEq/L, and bicarbonate 18 mEq/L. In the emergency room, vital signs demonstrated a pulse rate of 98 beats/min, respiratory rate 22 breaths/min, blood pressure 132/89 mm Hg, temperature 98.1 °F, and oxygen saturation 100% on room air. The remainder of the physical examination was unremarkable. Initial electrocardiogram (ECG) demonstrated normal sinus rhythm, and the patient was admitted to telemetry for observation. The subsequent morning, the patient actively experienced chest pain and ECG changes. ECG demonstrated ST segment elevations in leads II and III, and T-wave inversions in V1-V3. Stat troponin level was found to be elevated at 11.07 ng/mL (< 0.30 ng/mL). The patient immediately underwent cardiac catheterization which demonstrated a 99% blockage of the left anterior descending artery and revascularization was performed (, ). Two-dimensional echocardiogram demonstrated a left ventricular ejection fraction of 40% with anterior wall akinesis. Transesophageal echocardiogram ruled out an apical mural thrombus, but confirmed the ejection fraction and wall akinesis from the previous echocardiogram. The patient was also found to have hyperlipidemia after the conduction of a lipid panel. Hypercoaguable state and vasculitis workup was negative.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [27, 'years'], 'creatinine': [0.8, 'mg/dL'], 'sex': 'Female', 'Race': 'Black'}",104.28261,99.06848,109.49674,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 27 years old. The concentration of Creatinine is 0.8 mg/dL. 
The patient is Black, so the race coefficient is 1.212.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.8^(-1.154) * 27^(-0.203) * 1.212 * 0.742=104.28261.
Hence, the patient's GFR is 104.28261 mL/min/1.73m²."
3351,9,MDRD GFR Equation,lab test,decimal,pmc-5337863-1,Extracted,"An 84-year-old Japanese man was admitted to our hospital for a detailed examination of an indolent swelling on his right back. He had noticed the swelling on the day of admission; its onset was unknown. He had a 9-year history of treatment with candesartan (4 mg/day), furosemide (20 mg/day), and warfarin (2 mg/day) for hypertension, chronic kidney disease, and atrial fibrillation, but he had no other remarkable medical history or family history. He was a nonsmoker and did not consume alcohol. Prior to admission, he had never presented with pain, fever, or night sweats.
On admission, his height was 159 cm, weight was 71 kg, body temperature was 36.8°C, and blood pressure was 132/76 mmHg. His heart rate was 66 beats/min and irregular. Physical examination revealed no significant abnormalities except for a painless elastic hard subcutaneous lump adjacent to the right side of the lumbar vertebrae. The lump was oval in shape and vertically long, measuring about 3 × 10 cm. His arterial blood oxygen saturation was normal at 98%. Both chest and abdominal radiographs showed normal findings. An electrocardiogram showed atrial fibrillation but no other abnormalities. Laboratory tests showed a low blood hemoglobin concentration of 12.7 g/dl (reference range, 13.5–18.0 g/dl), high international normalized ratio-prothrombin time of 1.73 (reference range, 0.85–1.15), high serum lactate dehydrogenase concentration of 270 U/L (reference range, 120–230 U/L), high C-reactive protein concentration of 0.66 mg/dl (reference range, 0.00–0.30 mg/dl), high blood urea nitrogen concentration of 34.8 mg/dl (reference range, 8.0–22.0 mg/dl), and high creatinine concentration of 2.35 mg/dl (reference range, 0.60–1.10 mg/dl). Because his renal dysfunction imposed a restriction upon the use of contrast agent, plain 3 T MRI of the abdomen, including the lumbar region, was performed. MRI of the abdomen revealed an oval-shaped lesion in the right psoas major muscle measuring 4 × 11 cm and exhibiting homogenous internal intensity (). This mass showed mildly high intensity on both T1- and T2-weighted imaging compared with the adjacent muscle, but its intensity on T2-weighted imaging was lower than that of water. The mass also showed high intensity on diffusion-weighted imaging, corresponding to the characteristics of an acute-phase hematoma, although the patient had no history of trauma that might have caused an intramuscular hematoma. Based on these findings, the oral warfarin administration was temporarily stopped on day 2 after providing the patient with information regarding the increased risk of cerebral infarction and obtaining his consent.
The patient underwent follow-up MRI on day 7 to ascertain whether this oval-shaped mass had changed with time, which is typically observed in hematomas. However, the internal intensity of the lesion was almost identical to that on admission, and the size of the lesion had slightly increased. Accordingly, a CT-guided needle biopsy was performed on day 9. Blood was not aspirated during the biopsy procedure, and a solid tissue specimen was obtained. Histopathological examination revealed diffuse infiltration of large, atypical cells with irregularly shaped nuclei among the striate muscle fibers (). These atypical cells lacked abnormal lymphoid follicle formation and were predominantly CD20-positive on immunostaining. These cells were also weakly BCL-2–positive but CD3-, CD5-, and CD10-negative. The pathological diagnosis was DLBCL. Plain CT of the neck, chest, and abdomen on day 15 showed no significant lymphadenopathy. We consulted with the hematologists of our institution regarding curative treatment, but they discouraged immunochemotherapy because of the patient's renal dysfunction. We proposed additional examinations including detailed analysis of the lymphoma tissue using flow cytometry and 18F-fluorodeoxyglucose positron emission tomography (F-FDG-PET), but the patient refused. He was discharged from our hospital on day 16 and lost to follow-up.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [84, 'years'], 'creatinine': [2.35, 'mg/dL'], 'sex': 'Male', 'Race': 'Asian'}",26.5581,25.23019,27.88601,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 84 years old. The concentration of Creatinine is 2.35 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.35^(-1.154) * 84^(-0.203) * 1 * 1=26.5581.
Hence, the patient's GFR is 26.5581 mL/min/1.73m²."
3352,9,MDRD GFR Equation,lab test,decimal,pmc-6879974-1,Extracted,"A 59-year-old woman was admitted to the hospital for asthenia, nausea, oliguresis and haemoptysis. In her medical history, in 1978 she underwent kidney transplant for polycystic kidney disease; despite this treatment she had IV stage KDOQI chronic kidney disease in hemodialysis treatment; she suffered from anemia, diffuse skin xerosis, multiple warts, osteodystrophy with osteonecrosis and osteoporosis. CT of the Chest revealed to the left upper pulmonary lobe a 10 mm nodular formation, with significant enhancement compatible with neoplastic lesion []. There was also a nodular lesion localized in the left lobe of thyroid identified as a parathyroid adenoma. PET–CT detected hypercaptation only in the pulmonary formation. Cytology performed with bronchoscopy was negative.
Laboratory data were as follows: PTH 570 pg/ml; Ca 12.20 mg/dl; P 1.8 mg/dl; Hb 10,6 g/dl; HCT 31,5 %; creatinine 4,16 mg/dl;
The patient underwent atypical lung resection; pathological examination was compatible with metastatic lesion from parathyroid carcinoma [].
After about a month, the patient underwent parathyroid scintigraphy that showed pathological hypercaptation of radionuclide in the lower pole of the thyroid left lobe and in paratracheal region []. Milder hypercaptation was present on the lower right lobe of the thyroid gland.
Laboratory data were as follows: PTH 1544.5 pg/ml; Ca 14 mg/dl; P 1.4 mg/dl; Hb 10,4 g/dl, creatinine 4,56 mg/dl.
The patient underwent left “en bloc” parathyroidectomy with adjacent structures and lymph nodes dissection near the left recurrent nerve.
Parathyroids appeared almost white, hard and increasing in size. The post-operative period was uneventful and the patient was discharged within 72 h after surgery. Pathological examination of parathyroid glands revealed neoplastic proliferation, capsule invasion and infiltration of muscles, adipose tissue and perithyroidal tissue; thyroid gland was not involved.
On immunohistochemical examination, the tumor cells were positive for TTF1, Cyclin D1 and P16. These results were consistent with parathyroid carcinoma.
After six months, no signs of local recurrence or metastases were observed.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [59, 'years'], 'creatinine': [4.56, 'mg/dL'], 'sex': 'Female'}",9.85175,9.35916,10.34434,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 59 years old. The concentration of Creatinine is 4.56 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 4.56^(-1.154) * 59^(-0.203) * 1 * 0.742=9.85175.
Hence, the patient's GFR is 9.85175 mL/min/1.73m²."
3353,9,MDRD GFR Equation,lab test,decimal,pmc-4655797-1,Extracted,"A 16-year-old Caucasian male presented to the hospital with a 3-week history of lower extremity and periorbital oedema. He also reported short-lasting episodes (few minutes) of blurred vision. Other than sports injuries he had been healthy. He had taken Isotretinoin 20 mg QD for ∼1.5 years for acne, but had stopped the medication. Parents and the extended family were healthy, and there was no history of hereditary kidney disease.
On presentation he had a blood pressure of 138/86 mmHg. The physical examination showed periorbital and lower extremity oedema, but was otherwise unremarkable. Laboratory results showed potassium 5.2 mmol/L, creatinine 0.9 mg/dL and mild haemolysis [haemoglobin 12.3 g/dL, platelets 315 000 G/L, haptoglobin not detectable, lactate dehydrogenase (LDH) 236 U/L]. Albumin was decreased (2.9 g/dL), and a spot urine revealed a proteinuria of 3.4 g/g creatinine. The dipstick was positive for blood and the urinary sediment showed few dysmorphic erythrocytes but no casts. Serology for ANA, ANCA, hepatitis, HIV and phospholipid antibodies was negative. Complement factors (C3, C4) were normal. The patient was referred to ophthalmology for short episodes of blurred vision, but neither the eye examination, MRI imaging studies of the head, nor a spinal tap showed any abnormalities. Fundus hypertonicus and lenticonus were ruled out. The patient did not report any hearing problems.
A renal biopsy was performed and showed a broadened and hypercellular mesangial field as well as a focal thickening and double contours of the peripheral basement membranes (A and B). Immunofluorescence microscopy showed mesangial and peripheral C3 and IgA deposits. Basement membrane lamellation was present in the electron microscopy (Figure). A presumptive diagnosis of IgA nephropathy with atypical features was made, and ramipril and furosemide were started (FigureA). Ramipril was replaced with candesartan, but proteinuria and serum creatinine continued to increase with a urinary protein-creatinine ratio (UPCR) of 5.4 g/g and a serum creatinine of 1.2 mg/dL. Steroids were started, and the UPCR dropped to 1.1 g/g. Since the patient developed Cushingoid features, steroids were replaced with IV cyclophosphamide. Due to recurrent neutropaenia, however, cyclophosphamide was substituted with mycophenolat mofetil; creatinine remained relatively stable at 1.6 mg/dL with an UPCR of 2.4 g/g.
When the serum creatinine increased to 2.2 mg/dL, a second kidney biopsy was performed 12 months after the first presentation, revealing isolated double contours and prominent FSGS with hyalinosis. The electron microscopy showed distorted capillary walls and expansion of the mesangium. The case was reviewed by several pathologists, and classified as membrane-proliferative glomerulonephritis with features of chronic thrombotic microangiopathy. However, candidate gene sequencing did not reveal mutations in F2, F5, CFH, CFI, MCP, ADAMTS13 and NPHS2.
In light of the pathological features of chronic thrombotic microangiopathy and persistent proteinuria, plasma exchanges with fresh frozen plasma were performed. This therapy led to transient normalization of haemolysis and a nearly 3-fold reduction of proteinuria. However, creatinine and proteinuria began to rise again, and rituximab 375 mg/m2 was administered. Finally, end-stage renal disease developed, and dialysis was initiated. As the family history for kidney disease was negative at that time, 3 years later, the patient received a living related donor transplant from his mother. During the next 4 years of follow-up, the patient developed neither haematuria, nor proteinuria. LDH returned to the reference range, while haptoglobin remained suppressed. A post-transplant biopsy 3 years after transplantation did not provide evidence of splitting of the GBM in the donor organ, nor of GBM thinning (309 ± 74 nm, reference value 320 ± 50 nm; C and D).
Seven years after the first contact, a maternal cousin of the patient presented at the age of 18 years with nephrotic-range proteinuria (4.8 g/g creatinine) as an incidental finding. Renal function was normal, and there were no features of haemolysis. The cousin did not report any eye or hearing problems. The kidney biopsy showed a mesangio-proliferative glomerulonephritis with mesangial sclerosis with IgM, IgG, C3 and C1q deposits. Therapy with an ACE inhibitor was initiated, while a trial of therapy with prednisolone had no effect.
Because of the co-occurrence, whole-exome sequencing was performed on selected family members (FigureB). We found a thymine-to-guanine substitution at nucleotide 665 (c.T665G, rs281874761) in exon 5 of the COL4A5 gene on the X chromosome, resulting in a phenylalanine-to-cysteine missense mutation at codon 222 (p.F222C). The mutation, confirmed by Sanger sequencing (FigureC), disrupts an amino acid sequence highly conserved down to zebrafish, and is not found in data from large-scale sequencing projects (1000 Genomes Project, Exome Sequencing Project, ExAC Browser). It is rated as damaging by several prediction softwares (PolyPhen2, SIFT, CADD). So far, the mutation has been identified in one previous report of a family with end-stage renal disease without signs of Alport syndrome []. This report did not contain any information on the presence of thrombotic microangiopathy. Whole-exome sequencing did not reveal any additional known or novel and potentially disease-causing mutations (defined as stop, splice, missense or frameshift mutations) of frequency <1% in large-scale sequencing data and predicted pathogenicity in COL4A5 or other genes causing known monogenic kidney diseases including complement factors ().","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [16, 'years'], 'creatinine': [2.2, 'mg/dL'], 'sex': 'Male', 'Race': 'White'}",40.12785,38.12146,42.13424,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 16 years old. The concentration of Creatinine is 2.2 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.2^(-1.154) * 16^(-0.203) * 1 * 1=40.12785.
Hence, the patient's GFR is 40.12785 mL/min/1.73m²."
3354,9,MDRD GFR Equation,lab test,decimal,usmle-10445,Extracted,"A 50-year-old female with a past medical history of hypertension comes to your clinic for a refill of her lisinopril medication. She is also taking lovastatin and hydrochlorothiazide. The patient's vital signs are as follows: HR 80, BP 150/100, and BMI 40. Physical exam is remarkable for a waist-to-hip ratio of 1.0 and the presence of diffuse dark patches on her skin (Figure A). Her fasting lab results are as follows: Sodium: 145 mmol/L, Potassium: 5.0 mmol/L, Chloride: 105 mmol/L, Bicarbonate: 25 mmol/L, BUN: 10 mg/dL, Creatinine: 1.0 mg/dL, Glucose: 200 mg/dL, Triglyceride: 200 mg/dL, LDL: 250 mg/dL, Total cholesterol: 300 mg/dL, HDL: 30 mg/dL, and Hemoglobin A1C: 7.0%.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [50, 'years'], 'creatinine': [1.0, 'mg/dL'], 'sex': 'Female'}",58.68823,55.75382,61.62264,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 50 years old. The concentration of Creatinine is 1.0 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.0^(-1.154) * 50^(-0.203) * 1 * 0.742=58.68823.
Hence, the patient's GFR is 58.68823 mL/min/1.73m²."
3355,9,MDRD GFR Equation,lab test,decimal,pmc-7969317-2,Extracted,"The patient was an 83-year-old man who had been undergoing hemodialysis since the age of 80, because of nephrosclerosis. He had a history of undergoing surgery for sigmoid and ascending colon cancer at the ages of 77 and 80, respectively. He was taking lanthanum carbonate 1500 mg/d, febuxostat 10 mg/d, epinastine 20 mg/d, nalfurafine 5.0 μg/day, and magnesium oxide 500 mg/d. Bicarbonate dialysate and a dialyzer with a polysulfone dialysis membrane were being used for hemodialysis. His medications and dialyzer membrane had not been changed for 12 months. Three months before admission, he had presented with generalized pruritus and had eosinophilia (18.5%, 1905 /μL). One day before admission, he presented with hypotension (systolic blood pressure of 60 mmHg) and dyspnea during his hemodialysis session. Therefore, he was referred to our department for further examination and treatment. On admission, his systolic/diastolic blood pressure was 107/74 mmHg and his body temperature was 36.7°C. A generalized pruritic skin rash was observed. Blood tests showed marked eosinophilia (39.5%, 6130 /μL), high serum troponin I concentration (154.9 pg/mL), and impaired renal function (serum creatinine: 10.15 mg/dL, blood urea nitrogen: 42 mg/dL). Serological tests were negative for myeloperoxidase-anti-neutrophil cytoplasmic antibody and antiparasite antibodies. No abnormalities were detected on thoraco-abdominal computed tomography. No findings other than mild left ventricular hypertrophy were noted on electrocardiography and echocardiography. Bone marrow examination revealed an eosinophil count of 27%, with no increase in the blast count.
On the basis of these findings, the patient was diagnosed with idiopathic hypereosinophilic syndrome, with involvement of the skin and heart. All his medications were stopped and his dialyzer membrane was changed from polysulfone to cellulose triacetate. However, his intradialytic hypotension and pruritus did not improve. Therefore, oral prednisolone was started at a dose of 30 mg (0.5 mg/kg) per day on the 9th day of hospitalization, and his intradialytic hypotension and pruritus were immediately ameliorated. On the 14th day of hospitalization, his eosinophil count and serum troponin I concentration had decreased to 0/μL and 31.6 pg/mL, respectively. He was discharged on the 27th day of hospitalization.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [83, 'years'], 'creatinine': [10.15, 'mg/dL'], 'sex': 'Male'}",4.92043,4.67441,5.16645,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 83 years old. The concentration of Creatinine is 10.15 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 10.15^(-1.154) * 83^(-0.203) * 1 * 1=4.92043.
Hence, the patient's GFR is 4.92043 mL/min/1.73m²."
3356,9,MDRD GFR Equation,lab test,decimal,pmc-6962441-1,Extracted,"A 43-year-old woman visited the emergency room for oliguria. She was followed up in the hospital for type I diabetes mellitus, chronic kidney disease due to diabetic nephropathy, hypertension and heart failure with dilated cardiomyopathy. She had a history of volume depletion due to diarrhea and a decrease in urine volume. At the time of arrival, level of consciousness was drowsy and the Glasgow coma scale was 14. Physical examination revealed dehydration, including decrease in skin turgor, and tongue dehydration. The vital signs were blood pressure 110/60mmHg, pulse rate 104 beats/min, respiratory rate 20 breaths/min, and body temperature 36.2℃. In the chest auscultation the cardiac sound was normal without murmur and the breath sound was normal. Abdominal examination revealed no specific findings such as tenderness, and no pitting edema was observed in the lower extremities. Complete blood cell count examination revealed hemoglobin 8.3 g/dL; hematocrit 27.7%; WBC 12,070/mm3; and platelet count 195,000/mm3. The initial laboratory values were: serum sodium 134mEq/L; potassium 4.2mEq/L; calcium 8.71mg/dL; phosphorus 4.28mg/dL; magnesium 1.89mg/dL; serum urea nitrogen 46.7mg/dL; creatinine 6.86mg/dL; albumin 2.49 g/dL; total bilirubin 0.12mg/dL; AST/ALT 6.7/3.8 IU/L; glucose 235mg/dL; lactic acid 8.21mg/dL; alkaline phosphatase 68 IU/L; NGAL 739 ng/mL; ammonia 77 ug/dL; Pro-BNP >35,000 pg/mL; and CRP 3.95mg/dL. Arterial blood gas analysis revealed pH 7.14; pCO2 24mmHg; pO2 121mmHg, and tCO2 8.3mL/dL. The serum IgA was 109 mg/dL; ASO 32U; C3 92mg/dL; C4 35mg/dL; FANA negative; and ANCA negative. In the urine analysis, the specific gravity of urine was 1.007; pH 5.0; urine protein 2+; blood 3+; RBC 1–4/HPF; and WBC 5–9/HPF. Urine creatinine level was 14.9mg/dL, and urine protein was 6.78mg/dL. In the immune serum test, the HBs Ag/Ab, Anti-HCV Ab, Anti-HIV Ab, and VDRL results were all negative. Due to persistence of oliguria, continuous RRT was started. On the ninth hospital day, her mentation changed from alert to stupor mentation. The Glasgow coma scale (GCS) changed from 15 to 5. Brain images showed normal findings (). The following laboratory values were obtained: serum sodium 138mEq/L; potassium 4.5 mEq/L; calcium 8.26mg/dL; phosphorus <0.41mg/dL; magnesium 1.96 mg/dL; serum urea nitrogen 21.4mg/dL; creatinine 1.45 mg/dL; albumin 2.32 g/dL; glucose 209 mg/dL; and CRP 2.75mg/dL. After phosphate intravenous replacement, 0.25–0.5mmol/kg monobasic potassium phosphate (Phosten, JW, Korea) for 6 days, and administration of phosphate-containing replacement solution Phoxilium(containing phosphate at 1.2 mmol/L; Baxter Gambro, Deerfield, IL, USA) use, the phosphate level increased to 2.97mEq/L and mental state returned to alert (). On the 29th day of continuous RRT, normal urine volume was recovered with decrease in serum creatinine level. On the 33rd day, serum creatinine level decreased to 2.08mg/dL, subsequently RRT was stopped. At the time of discharge, serum creatinine and phosphorus level were 1.82mg/dL and 2.75mg/dL, respectively with alert mentation. The patient is still on outpatient follow-up.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [43, 'years'], 'creatinine': [6.86, 'mg/dL'], 'sex': 'Female'}",6.55737,6.2295,6.88524,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 43 years old. The concentration of Creatinine is 6.86 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 6.86^(-1.154) * 43^(-0.203) * 1 * 0.742=6.55737.
Hence, the patient's GFR is 6.55737 mL/min/1.73m²."
3357,9,MDRD GFR Equation,lab test,decimal,usmle-9730,Extracted,"A 55-year-old man presents with bloody nasal secretions and shortness of breath. He reports he has lost 4 kg (8.8 lb) in the last two months with no changes in his diet. He has also been suffering from mild to moderate joint pain in the left knee for the last year. His past medical history is unremarkable. His vitals include: blood pressure 120/70 mm Hg, temperature 37.0℃ (98.6℉), pulse 70/min, respiratory rate 14/min. Physical examination is significant for nasal ulcers. Diffuse crackles are present over all lobes of the lung bilaterally. Laboratory findings are significant for the following:
Hemoglobin 12.9 g/dL
Hematocrit 37.7%
Leukocyte count 5500/mm3
Neutrophils 65%
Lymphocytes 30%
Monocytes 5%
Mean corpuscular volume 82.2 μm3
Platelet count 190,000/mm3
Erythrocyte sedimentation rate 35 mm/h
C-reactive protein 14 mg/dL
Creatinine 3.09 mg/dL
The patient is prescribed a corticosteroid nasal spray and oral antibiotics but returns in 2 weeks without any clinical improvement.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [55, 'years'], 'creatinine': [3.09, 'mg/dL'], 'sex': 'Male'}",21.10242,20.0473,22.15754,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 55 years old. The concentration of Creatinine is 3.09 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.09^(-1.154) * 55^(-0.203) * 1 * 1=21.10242.
Hence, the patient's GFR is 21.10242 mL/min/1.73m²."
3358,9,MDRD GFR Equation,lab test,decimal,usmle-945,Extracted,"A 47-year-old woman comes to the physician for a follow-up examination. She has type 1 diabetes mellitus, end-stage renal disease, and was recently started on erythropoietin for anemia. Her last hemodialysis session was yesterday. Current medications also include insulin, calcitriol, and sevelamer. She appears well. Her pulse is 68/min and regular, respirations are 12/min, and blood pressure is 169/108 mm Hg. Her blood pressure was normal at previous visits. Examination shows normal heart sounds. There are no carotid, femoral, or abdominal bruits. The lungs are clear to auscultation. Laboratory studies show a hemoglobin concentration of 12 g/dL, a serum creatinine concentration of 3.4 mg/dL, and BUN of 20 mg/dL.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [47, 'years'], 'creatinine': [3.4, 'mg/dL'], 'sex': 'Female'}",14.47703,13.75318,15.20088,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 47 years old. The concentration of Creatinine is 3.4 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 3.4^(-1.154) * 47^(-0.203) * 1 * 0.742=14.47703.
Hence, the patient's GFR is 14.47703 mL/min/1.73m²."
3359,9,MDRD GFR Equation,lab test,decimal,pmc-8637396-1,Extracted,"A 34-year-old Hispanic female was admitted with the chief complaint of a painful nonhealing abdominal wound for 2 weeks duration. The patient initially developed few scabs in the infra umbilical area which led to frequent itching and irritation. She used plain cotton gauze with vaseline ointment to treat them by herself. The scabs later turned into ulcers. Her past medical history was significant for ESRD, and she has been on continuous ambulatory peritoneal dialysis (CAPD) for 5 years, gastroesophageal reflux disease, obesity, anemia of chronic kidney disease (CKD), secondary hyperparathyroidism of renal origin, and coccidioidomycosis infection. Her chronic renal disease was from amphotericin B drug toxicity secondary to previous disseminated coccidioidomycosis treatment. The patient had a history of uncontrolled hyperparathyroidism with an intact parathyroid hormone level as high as 2400 picograms/milliliter (pg/mL) and an elevated phosphorus level of 10 mg/dL as an outpatient. These were values 6 months before the current hospitalization. This was difficult to control mainly because of financial constraints in getting the medications and nonadherence to prescribed phosphate binders. Home medications include sevelamer carbonate 3200 milligrams (mg) 3 times a day with meals. The patient lived at her parent’s home and has stopped working because of multiple medical issues. The patient denied any history of smoking, alcohol, or illicit drug use. Her peritoneal dialysis prescription was 4 daytime exchanges of 2-L peritoneal dialysate fluid, each bag composed of 2.5% dextrose and each exchange for 4 hours daily. Her weekly Kt/V was 2.1, with no residual kidney function.
Vital signs on presentation were, temperature of 98.6 Fahrenheit (F), pulse rate of 84 beats per minute (bpm), respiratory rate of 18 breaths per minute, blood pressure 117/59 mm Hg, and oxygen saturation of 99% on room air. Physical examination showed a morbidly obese female in mild distress due to abdominal pain. Abdominal examination revealed multiple tender indurated ulcers with surrounding erythema and black eschar in the lower abdomen section ( and ) along with skin ulceration with exposed subcutaneous tissue and granulation in lateral walls ( and ). The rest of the physical examination was non-significant.
Laboratory data revealed elevated white blood count (WBC) 21,000/mm3, hemoglobin 8.5 g/dL, platelets 526,000/mm3, sodium 131 mmol/L, potassium 3.4 mmol/L, blood urea nitrogen 59 mg/dL, creatinine 13.26 mg/dL, albumin 3.3 g/dL, calcium 8.6 mg/dL, phosphorus 8.3 mg/dL, parathyroid hormone 712 pg./mL, C reactive protein 129.8 mg/L, CAPD fluid was not positive for an infection, and blood cultures were negative for any infection. Computerized tomography (CT) abdomen and pelvis with and without contrast revealed anterior abdominal wall subcutaneous calcification. Parathyroid imaging by 29.2 mCi Technetium 99m Sestamibi scan revealed no abnormal radiotracer accumulation to suggest parathyroid adenoma.
To the patient was initially treated with empiric antibiotics until the infection was ruled out and was also started on sodium thiosulphate 25 g in sterile water intravenous infusion over 30 minutes, 3 times a week for 3 months. Due to unavailability of dermatologist and skilled surgeons, skin biopsy was not possible. The peritoneal dialysis regimen was intensified with the patient switching to continuous cycler peritoneal dialysis and doing 6 exchanges throughout the night with 2.5-L peritoneal dialysate fluid, each bag composed of 2.5 % dextrose and each exchange for 2.5 hours. The patient underwent 4-gland parathyroidectomy with implantation of half of the right superior parathyroid gland on the right forearm. The patient also received aggressive wound care daily. The calciphylaxis lesions healed completely in 3 months with intense peritoneal dialysis, sodium thiosulfate infusion for 3 months, and parathyroidectomy. The dialysis modality was never changed to hemodialysis during the management of calciphylaxis lesions.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [34, 'years'], 'creatinine': [13.26, 'mg/dL'], 'sex': 'Female', 'Race': 'Hispanic'}",3.21467,3.05394,3.3754,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 34 years old. The concentration of Creatinine is 13.26 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 13.26^(-1.154) * 34^(-0.203) * 1 * 0.742=3.21467.
Hence, the patient's GFR is 3.21467 mL/min/1.73m²."
3360,9,MDRD GFR Equation,lab test,decimal,pmc-3469072-1,Extracted,"A 62-year-old insulin-dependent diabetic female patient presented to our emergency department with pyrexia and left-sided renal colic. Her ultrasound kidney-ureter-bladder (KUB) examination revealed left-sided moderated hydronephrosis. A plain KUB film did not reveal any opacity at the course of the left ureter. The laboratory results were urea 64 mg/dL, creatinine 1.5 mg/dL, glucose 334 mg/dL, hemoglobin 11.6 g/dL, and white blood cells (WBC) 15.5 × 103. She underwent noncontrast CT of the abdomen which revealed one stone at the level of 05 vertebrae (7 mm) and a second one at the level of 03 vertebrae (6 mm) causing left-sided pelvicalyceal dilatation. She was then admitted and commenced on antibiotics. The next day under local anesthetic, she underwent placement of an open end 4.8FR-26 cm D-J stent (Cook ureteral stent) under fluoroscopy. A hydrophilic guide wire (Road Runner straight tip, Cook) was used for stent placement. On the first postoperative day, she developed gross hematuria and left-side abdominal tenderness, with a total urinary output of 430 cc. Hemoglobin level dropped to 7.6 g/dL and creatinine raised to 1.8 mg/dL. She then underwent a noncontrast CT of the abdomen which showed a large perinephric collection located inferior and posterior to the left kidney.
The patient was put to bed rest; 3 units of erythrocyte suspension and 2 units of fresh frozen plasma were administered. She was hemodynamically stable and urine cleared the third postoperative day. Diuresis was accomplished and creatinine levels normalized. The third postoperative day she underwent a second CT of the abdomen with intravenous contrast which showed a 12 × 8 stable perirenal hematoma pushing forward and medially the left kidney with the tip of the stent penetrating the renal parenchyma with no contrast extravasation from the collecting system of the kidney (). The fifth postoperative day the stent was repositioned in the renal pelvis under fluoroscopy. She was discharged the ninth postoperative day. Follow-up CT of the abdomen the first month after stent placement showed stabilization of the hematoma ().","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [62, 'years'], 'creatinine': [1.8, 'mg/dL'], 'sex': 'Female'}",28.51031,27.08479,29.93583,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 62 years old. The concentration of Creatinine is 1.8 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.8^(-1.154) * 62^(-0.203) * 1 * 0.742=28.51031.
Hence, the patient's GFR is 28.51031 mL/min/1.73m²."
3361,9,MDRD GFR Equation,lab test,decimal,pmc-6167512-1,Extracted,"A 79-year-old woman who had a 2-year history of diabetes mellitus and hypertension controlled with oral hypoglycemic and antihypertensive agents presented to the hospital due to altered mental status on the day of admission. The patient did not have any medical history, nor did she have a history of alcohol consumption and smoking.
On physical examination, body temperature was 36.0°C, blood pressure was 68/40 mmHg, pulse rate was 100 beats/min, and respiration was 22 breaths/min. The initial mental status was assessed as semicomatose, and auscultation of her lungs revealed coarse crackles throughout bilaterally. A chest radiograph showed cardiomegaly and bilateral patchy consolidations. Arterial blood gas analysis revealed a pH of 7.23, carbon dioxide tension of 14 mmHg, partial pressure of oxygen of 76 mmHg, bicarbonate level of 9.9 mmol/L, base excess of 19.1 mmol/L, oxygen saturation level of 92%, and lactic acid level of 12.0 mmol/L. Increased levels of serum ketones (1.3 mmol/L) and blood sugar (691 mg/dL) with elevated hemoglobin A1c (8.2%) were also observed. Initial laboratory findings revealed a hemoglobin level of 12.4 g/dL, white blood cell count of 25,240 /mm3 (neutrophils, 92.3%), platelet count of 11,000/mm3, blood urea nitrogen level of 105.0 mg/dL, creatinine level of 2.32 mg/dL, and C-reactive protein level of 22.95 mg/L (normal range, 0.0-5.0 mg/L).
Abdominopelvic computed tomography (CT) with enhancement revealed extensive intraosseous gas, which extended from the fifth lumbar (L) spine to the sacrum (S), indicative of emphysematous osteomyelitis (). In addition, gas-containing abscesses were observed in the epidural space (L3-S5), soft tissue, and muscles in the adjacent sacrum and L5 vertebrae (). CT findings also confirmed two liver abscesses (sizes of 3 cm and 2.2 cm, respectively) () Systemic septic emboli, such as multiple septic pulmonary emboli and multifocal cerebral embolic infarctions, were observed on CT and magnetic resonance imaging ( and ).
The patient was treated for presumed septic shock with diabetic ketoacidosis with intravenous ceftriaxone 2 g every 12 hours and metronidazole 500 mg every 8 hours. Although we initially planned urgent surgical decompression to release pus from the epidural and pelvic abscesses, aggressive surgical intervention could not be performed, because refractory shock and severe acidosis (serum lactic acid level, 15.0 mmol/L) developed rapidly. Despite the urgent addition of clindamycin and intravenous inotropic agents to meropenem without delay, the patient died of multiorgan failure from septic shock, 19 hours after admission.
After the patient died, on the second day after admission, two sets of blood cultures taken upon admission tested positive for gram-negative bacilli. On the third day, blood cultures showed non-resistant K. pneumoniae, susceptible to cefazolin, ceftriaxone, and ciprofloxacin on the standard disk diffusion method.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [79, 'years'], 'creatinine': [2.32, 'mg/dL'], 'sex': 'Female'}",20.25119,19.23863,21.26375,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 79 years old. The concentration of Creatinine is 2.32 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.32^(-1.154) * 79^(-0.203) * 1 * 0.742=20.25119.
Hence, the patient's GFR is 20.25119 mL/min/1.73m²."
3362,9,MDRD GFR Equation,lab test,decimal,pmc-3324215-1,Extracted,"A 14-year-old boy presented with right hydronephrosis. He had no complaints, and this was an unexpected finding detected by ultrasonography during his periodical health test. The boy had a past history of acute myeloblastic leukemia at 8 years of age. The disease was treated according to AML-BFM-93 protocol, which includes cytarabine, vepezide, daunorubicine, prednisolone, vincristine, adriomycin, cyclophosphamide, and tioguanine. A complete remission was achieved 4 years ago. No signs of renal lesion were recorded during and after chemotherapy. Previous yearly ultrasound examinations showed no alteration of the kidneys also. Having detected hydronephrosis, the patient was admitted for further examination and treatment to the Department of Urology.
Ultrasonography showed hydronephrosis on the right with anteroposterior diameter of pelvis reaching 50 mm, calyceal dilatation and parenchymal thinning. Ureter was not dilated. The left kidney seemed normal. Calculus obstructing the pyeloureteral segment was suspected on the first ultrasound test. However, no sign of urinary stone was detected on Doppler ultrasound, confirming accessory vessel extrinsic to pyeloureteral junction.
His general blood test and urinalysis were normal, and the serum concentration of creatinine was 59 μmol/L. Intravenous urography revealed normal left kidney, and no excretion of the contrast material was seen on the right side even on the late urograms. 99Tc-dimercaptosuccinic acid (DMSA) scan was made to assess differential renal function. It showed no renal uptake of DMSA on the right. No anatomical or functional lesion was found in the left kidney.
Nephrostomy was proposed as initial management with a little hope for some part of renal function to recover. The boy and his parents refused, willing for a definite procedure. The right retroperitoneoscopic nephrectomy was performed. Three renal arteries were found with the lower pole artery lying on pyeloureteral junction. The kidney was 10.5 × 5.5 cm of size, with slight atrophy of the parenchyma (). There were no intraoperative or postoperative complications. Histopathology revealed chronic tubulointerstitial nephritis. Glomeruli showed no significant changes. A rather copious infiltration of lymphocytes, several plasmocytes, and granulocytes were present in stroma. An obstruction of tubules with a prominent amount of small eosinophilic and periodic acid-Schiff (PAS) positive cylinders was found. Tubular epithelium was focally detached. There was a peritubular fibrosis around excretory tubules (). Special attention was focused on the search of BK nephritis, but no specific histological signs were found.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [14, 'years'], 'creatinine': [59.0, 'µmol/L'], 'sex': 'Male'}",160.10185,152.09676,168.10694,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 14 years old. The concentration of Creatinine is 59.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 59.0 µmol. To convert 59.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 59.0 µmol Creatinine * 1e-06 mol/µmol = 6e-05 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 6e-05 mol Creatinine * 113.12 g/mol = 0.00679 g Creatinine. To convert 0.00679 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00679 g Creatinine * 1000.0 mg/g = 6.79 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 6.79 mg Creatinine/10.0 dL = 0.679 mg Creatinine/dL. The concentration value of 59.0 µmol Creatinine/L converts to 0.679 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 0.679^(-1.154) * 14^(-0.203) * 1 * 1=160.10185.
Hence, the patient's GFR is 160.10185 mL/min/1.73m²."
3363,9,MDRD GFR Equation,lab test,decimal,pmc-7303541-1,Extracted,"A 63-year-old Asian male with prior history of kidney transplant 10 years ago due to end-stage renal disease secondary to hypertension presented with lower extremity edema for 2 weeks. A month post transplant, he had an episode of biopsy-proven rejection but no complications otherwise. His maintenance immunosuppression consisted of mycophenolate mofetil 750 mg oral twice daily, tacrolimus 3 mg oral twice daily, and prednisone 2.5 mg oral once daily. In addition, the patient had been on sertraline 200 mg oral once daily, nifedipine 10 mg oral once daily, and vitamin D3 1,000 U oral once daily. On examination, his vitals were stable, and examination was unremarkable except for 2+ pedal edema. Laboratory data showed a slowly rising serum creatinine over the past 6 months with current value of 2.3 mg/dL (baseline 1.5 – 1.8 mg/dL), a spot urine protein-to-creatinine ratio of 7.6 g/g of creatinine, and tacrolimus level of 4.7 ng/mL. BK virus PCR and donor-specific anti-HLA antibodies were negative. The patient had a spot urine protein-to-creatinine ratio of 0.9 g/g of creatinine 6 months prior. The transplant kidney biopsy showed focal mild interstitial fibrosis with tubular atrophy, glomeruli with lobulation of tufts, large endothelial cells with foamy cytoplasm (), glomerular capillary endothelial cells, and mesangial cells containing lamellar and dense cytoplasmic inclusions or myelin bodies (). No rejection or viral cytopathic effects, immune complex deposits, or fibrils were identified. The stains for polyomavirus and for C4d were negative. In addition to chronic transplant glomerulopathy, the diagnosis of glomerular phospholipidosis was entertained. The serum α-galactosidase A level was normal, 0.136 U/L (reference range: 0.074 – 0.457). Sertraline was discontinued and patient was switched to bupropion. The proteinuria declined to 2.3 g/g of creatinine with stabilization of serum creatinine at 6-months follow-up visit.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [63, 'years'], 'creatinine': [2.3, 'mg/dL'], 'sex': 'Male', 'Race': 'Asian'}",28.86277,27.41963,30.30591,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 63 years old. The concentration of Creatinine is 2.3 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.3^(-1.154) * 63^(-0.203) * 1 * 1=28.86277.
Hence, the patient's GFR is 28.86277 mL/min/1.73m²."
3364,9,MDRD GFR Equation,lab test,decimal,pmc-8270600-1,Extracted,"A 60-year-old Korean woman was admitted to our hospital for a renal biopsy. She had presented to the nephrology outpatient department due to edema 9 months earlier. She was diagnosed with T2DM and hypertension 5 years ago and took 4 mg glimepiride, 1000 mg metformin, 50 mg gemigliptin, 15 mg pioglitazone, 5 mg amlodipine, 100 mg losartan, and 25 mg carvedilol. The pioglitazone was withdrawn, while the other medicines were maintained, after the initial visit to our hospital. Her serum creatinine level had been gradually increasing (Fig. ) without significant changes in other laboratory findings. She denied symptoms and signs indicating deterioration of renal function, such as edema, oliguria, fever, chills, general weakness, malaise, arthralgia, myalgia, skin rash, and urine color changes during the 9-month follow-up. She also denied ingestion of known toxins, Chinese herbal medicines, drugs (including non-steroidal anti-inflammatory drugs), and nutraceuticals that can affect the serum creatinine level. Her hypertension and serum glucose were well controlled. She was admitted for renal biopsy and management of AKI.
Her initial vital signs were as follows: blood pressure, 120/80 mmHg; heart rate, 68 beats/min; respiratory rate, 18 breaths/min; and body temperature, 36.5°C. No lymph nodes were palpated on a neck examination. Heart sounds were normal and no wheezing or rales was heard in either lung field. No organomegaly was present in the abdomen, and bowel sounds were audible. No skin color changes on the torso or pitting edema were observed on the legs. Her blood urea nitrogen and serum creatinine levels were 29.7 mg/dL (range: 8.0–20.0 mg/dL) and 1.45 mg/dL (range: 0.51–0.95 mg/dL) on admission, whereas they were 14.1 and 0.53 mg/dL, respectively, 9 months before admission (Fig. ). The hematocrit and hemoglobin levels were 34% (range: 36%–48%) and 11.4 g/dL (range: 12–16 g/dL), respectively. Platelet and red blood cell counts were 232 × 109/L (normal range: 130–400 × 109/L) and 3.82 × 1012/L (normal range: 4.0–5.40 × 1012/L), respectively. The white blood cell count was 6.76 × 109/L (normal range: 4.0–10.0 × 109/L), with 63.5% segmented neutrophils (normal range: 50%–75%), 27.5% lymphocytes (normal range: 20%–44%), 6.7% monocytes (normal range: 50%–75%), and 1.9% eosinophils (normal range: 1.0%–5.0%). Other laboratory test results included sodium, 138 mmol/L (range: 135–145 mmol/L); potassium, 4.6 mmol/L (range: 3.3–5.1 mmol/L); chloride, 104 mmol/L (range: 98–110 mmol/L); glucose, 177 mg/dL (range: 70–110 mg/dL); HbA1c, 6.8% (range: 4.2%–5.9%); calcium, 9.0 mg/dL (range: 8.6–10.2 mg/dL; phosphorus, 3.9 mg/dL (range: 2.7–4.5 mg/dL); and total CO2, 28 mmol/L (range: 21–31 mmol/L). The C3 and C4 levels were 129.7 mg/dL (range: 90–180 mg/dL) and 34.8 mg/dL (range: 10–40 mg/dL), respectively. Urinalysis (dipstick test) revealed no protein or blood, and no red blood cells or white blood cells. The urine albumin creatinine ratio was 14.9 mg/g (range: 0–20 mg/g). The thyroid function test was within normal limits, and anti-neutrophil cytoplasmic antibodies and the anti-glomerular basement membrane antibody were negative.
Kidney ultrasound revealed normal-sized kidneys (right, 10.4 cm; left, 10.4 cm) and echogenicity without evidence of hydronephrosis or nephrolithiasis. A renal biopsy was performed on day 2 of admission. There was edematous interstitium, detachment of tubular epithelial cells, and lymphoplasmacytic infiltration into the interstitium (Fig. A). Tubulitis was indicated by tubular cell detachment and epithelial casts including numerous neutrophils were observed in the lumen of renal tubules and a few eosinophils were also observed among the increased interstitial inflammatory cell infiltrates (Fig. B). However, the glomeruli were normal (Fig. ). After the renal biopsy, we again enquired regarding the consumption of drugs, Chinese herbal medicines, and nutraceuticals that could evoke AIN on day 3 of admission. She disclosed that she had been ingesting an M charantia extract for 7 months to control her T2DM. She took about 600 mg almost every day in liquid form during the first 3 months, and had taken 1200 mg per day during the last 4 months. The M charantia extract was immediately withdrawn and 0.5 mg/kg/day of prednisolone was prescribed, and tapered, and then stopped after 3 months. Her serum creatinine decreased to 0.65 mg/dL after 3 months (Fig. ), while still using the other medicines.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [60, 'years'], 'creatinine': [1.45, 'mg/dL'], 'sex': 'Female', 'Race': 'Asian'}",36.83482,34.99308,38.67656,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 60 years old. The concentration of Creatinine is 1.45 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.45^(-1.154) * 60^(-0.203) * 1 * 0.742=36.83482.
Hence, the patient's GFR is 36.83482 mL/min/1.73m²."
3365,9,MDRD GFR Equation,lab test,decimal,pmc-2034390-1,Extracted,"A 46-year-old previously healthy male presented to Emergency Department with four days of primarily left-sided abdominal pain, low-grade fevers, nausea, and anorexia. His medical history was significant for poorly controlled diabetes and dyslipidemia. No history of abdominal surgery was reported. Two months prior to admission, the patient's serum hemoglobin A1C was markedly elevated at 10.7 and his serum lipid profile was quite abnormal (total cholesterol: 313, triglycerides: 287, HDL: 39, LDL: 217). On admission, the patient's home medications included atorvastatin (Lipitor®; 40 mg orally per day) and subcutaneous isophane/regular insulin (Insulin Novolin® 70/30) twice per day.
The patient's physical exam at presentation was significant for left lower quadrant pain and voluntary guarding. The patient's white blood count at that time was 18.1 × 109 cells/L (absolute neutrophil count: 13.6; 75.1%), hematocrit: 45.2%, serum glucose: 279, blood urea nitrogen (BUN): 31, and serum creatinine: 1.5. Serum electrolytes were as follows: sodium: 133, potassium: 4.2, chloride: 95, and CO2: 23 (anion gap 15). Urinalysis was positive for 2+ albumin, 1+glucose, 1+ ketones, 1+ bilirubin, and hyaline casts. Plain films of the abdomen were obtained in the Emergency Department. A spiral CT scan of the abdomen and pelvis with oral and IV contrast was subsequently performed to exclude colonic diverticulitis.
Abdominal plain films demonstrated multiple dilated loops of small bowel with air/fluid levels in the right abdomen (arrows in Figure ), consistent with small bowel obstruction, but also noted, unusually, to herald acute appendicitis. Intestinal malrotation was not considered in the differential diagnosis at that point. No pneumoperitoneum was evident.
Abdominal CT with oral and IV contrast was then performed, which demonstrated the majority of the small bowel positioned in the right abdomen, the cecum located in the left mid abdomen, and absence of the ligament of Treitz. The orientation of the superior mesenteric vessels was abnormal. These findings together were consistent with complete intestinal malrotation. No associated situs, caval, or other congenital anomalies were present and no evidence of volvulus was identified. A dilated, tubular, blind-ending structure was identified arising from the cecumin the left mid-abdomen (arrows in Figures ), with significant stranding in the adjacent fat, indicative of acute appendicitis.
Fluid resuscitation was initiated in the Emergency Department with Lactated Ringer's solution (125 cc/hr). Based on plain film findings of possible small bowel obstruction and absence of history of any abdominal surgery, an abdominal CT was performed, as discussed above.
After extensive review of the CT data for presurgical planning, the patient was taken to the operating room for laparoscopic exploration and appendectomy, where the imaging findings were confirmed and the appendix was found to be perforated. No surgical intervention to address the malrotation, such as Ladd's procedure, was performed. Pathologic examination of the excised appendix verified the diagnosis of acute gangrenous appendicitis with perforation. The patient's post-operative course was uneventful. The patient was treated perioperatively with a 5 day regimen of intravenous cefoxitin (1,000 mg every 6 hours) and as an outpatient with a 14 day course of oral levofloxacin (500 mg per day; Levaquin®).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [46, 'years'], 'creatinine': [1.5, 'mg/dL'], 'sex': 'Male'}",50.38357,47.86439,52.90275,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 46 years old. The concentration of Creatinine is 1.5 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.5^(-1.154) * 46^(-0.203) * 1 * 1=50.38357.
Hence, the patient's GFR is 50.38357 mL/min/1.73m²."
3366,9,MDRD GFR Equation,lab test,decimal,pmc-4376932-1,Extracted,"Our patient was a 54-year-old male who presented with anuria, fever, and lower-leg edema. On June 3, 2012, the patient visited the urology department of a local community hospital with macroscopic hematuria and dysuria. He was diagnosed with acute prostatitis and began treatment with levofloxacin hydrate, loxoprofen sodium hydrate, and cernitin pollen extract. However, his condition did not improve, and he subsequently developed lower extremity numbness, bilateral flank pain, and diarrhea, followed by anuria. On June 11, he visited another hospital in his community and was eventually transferred to our hospital on June 13 for inpatient treatment of possible acute kidney injury.
Physical examination on admission revealed the following: height 175 cm; body weight 80 kg; systolic and diastolic blood pressure values 179 and 102 mm Hg, respectively; pulse 98 beats/min (regular), and body temperature 37.9°C. The patient had a normal mental status despite persistent headache. His palpebral conjunctivae indicated signs of anemia. Radiographic images showed no abnormal findings. Both lower limbs were edematous. The results of clinical laboratory tests obtained on admission are summarized in table . Urinalysis showed high protein levels (3 g/l), blood (+++), pyuria, and a fractional sodium excretion rate of 20.3%. Hematological analyses of peripheral blood yielded a white blood cell count of 9.61 × 109 cells/l (neutrophils 85.0%, lymphocytes 8.5%), a red blood cell count of 3.44 × 1012 cells/l, a hemoglobin level of 100 g/l, the presence of fragmented red blood cells, and a platelet count of 90 × 109 cells/l. C-reactive protein levels were as high as 160,900 μg/l. The fibrinogen degradation product level was 1.168 g/l, the prothrombin time was 45.6 s, and the fibrinogen level was 4.1 g/l. These measurements resulted in a disseminated intravascular coagulation score of 6 points. Serum biochemistry tests yielded a blood urea nitrogen level of 58.1 mmol/l and a creatinine level of 2,044 μmol/l, suggesting significant renal impairment. The lactate dehydrogenase level was 765 IU/l, and the haptoglobin level was below 1.2 μmol/l. The patient had hypoproteinemia, as evidenced by a total serum protein level of 58 g/l and an albumin level of 24 g/l. Serum samples were negative for anti-nuclear antibodies as well as myeloperoxidase- and proteinase 3-specific antineutrophil cytoplasmic autoantibodies, although anti-GBM antibody levels were high at 230 ELISA units. Stool examination was negative for occult blood, intestinal pathogens, and verotoxins. Plain chest radiographs revealed no alveolar hemorrhage or other abnormal signs. On interview, the patient reported a history of cervical disc herniation diagnosed at the age of 52 years. He had no noteworthy family history and was not taking any medications on a regular basis at the time of admission to our hospital.
Changes in platelet counts, lactate dehydrogenase levels, and mean blood pressure over time during the 119-day hospital stay are schematically represented in figure , along with major therapeutic interventions. Computed tomography (CT) imaging conducted on admission indicated renal atrophy and ascites, but no collapse of the inferior vena cava. These findings negated the possibility of prerenal and postrenal failure and suggested an acute aggravation of chronic kidney disease rather than a typical acute kidney injury. Since the patient had not undergone regular medical checkups, it was not clear whether proteinuria had existed in the past. During the early hospitalization period, we administered γ-globulin, diuretics, and hemodialysis, under the assumption that the patient had either sepsis- or drug-induced acute kidney injury. Peripheral blood smears revealed the presence of fragmented red blood cells (hospital day 2), suggesting hemolytic uremic syndrome (HUS) resulting from food poisoning caused by Escherichia coli O-157:H7 or other pathogenic strains. However, the patient had no diarrhea and was negative for intestinal pathogens and verotoxins. Epistaxis developed on hospital day 4, platelet counts and hemoglobin levels decreased to 29 × 109 cells/l and 55 g/l, respectively, and the lactate dehydrogenase level rose to 1,253 IU/l. The patient's anemia was unresponsive to erythropoiesis-stimulating therapy, and frequent blood transfusions were required (i.e., a total of 16 units of irradiated red cell concentrates). His fever remained in the range of 38-39°C despite treatment with γ-globulin. The patient was diagnosed with TMA [thrombotic thrombocytopenic purpura (TTP) or HUS] based on the following findings: thrombocytopenia, hemolytic anemia evidenced by anemic signs and elevated lactate dehydrogenase levels, signs of renal impairment, fever, bleeding episodes (i.e., epistaxis), neuropsychiatric manifestations (i.e., headache), direct and indirect Coombs test results, and haptoglobin levels below 1.2 μmol/l.
Assays conducted several days later indicated an ADAMTS13 activity of 31.6% (reference range 70-120%), and ADAMTS13 inhibitors were negative. Serum factor H measured by the ELISA method was 0.473 g/l (the standard value of factor H ranges from 0.3 to 0.6 g/l). These findings led us to administer plasma exchange therapy with a total of 30 units of fresh frozen plasma, starting on hospital day 8. On hospital day 15, steroid pulse therapy (3 methylprednisolone doses of 1,000 mg/day) was initiated to lower the elevated anti-GBM antibody level. Following the completion of this 3-day course, the patient was given oral prednisolone at a starting dose of 50 mg/day, which was gradually tapered and discontinued. After this, platelet counts rose to 197 × 109 cells/l, and kidney biopsy was conducted on hospital day 22 (fig. ). Seventeen glomeruli examined by optic microscopy all showed destructive patterns with characteristic architecture ranging from atypical proliferative changes to global sclerosis. Renal arterioles, both afferent and efferent, showed extensive endothelial cell edema and swelling, indicative of glomeruloid changes. Renal tubules showed focal atrophy with massive lymphocyte infiltration. Congo red staining of the biopsy specimen was negative. Electron microscopy showed that the loss of glomerular structure observed under optic microscopy was the result of an extensive and dense extracellular deposition of fibrillar components, which were larger in diameter than amyloid fibers and aggregated to form large bundles. Immunofluorescence analysis for immunoglobulin G and third component (C3) deposits was not carried out because of glomerular collapse. Available findings supported the diagnosis of FGN involving severe glomerular destruction. On hospital day 29, a second course of steroid pulse therapy was started due to significantly decreased platelet counts.
On hospital day 46, the mean blood pressure values started to increase gradually. Although the target body weight was lowered and arotinolol hydrochloride and methyldopa hydrate were added to nifedipine and candesartan cilexetil, these measures did not achieve successful blood pressure control.
On hospital day 56, the patient had a mild seizure. T2-weighted fluid-attenuated inversion recovery (FLAIR) magnetic resonance scans of the bilateral cerebellum, occipital lobe, and parietal lobe showed multiple high-intensity areas, suggesting a diagnosis of reversible posterior leukoencephalopathy syndrome (fig. ). Despite antihypertensive therapy with imidapril hydrochloride, carvedilol, nifedipine, and nitroglycerin infusion, hypertension persisted, and the patient's headache continued. On hospital day 61, generalized convulsions recurred, and head CT images showed multiple hemorrhagic lesions in the right temporal, right parietal, and right frontal lobes (fig. ). Doses of intravenous hemostatic medications were increased, while antihypertensive agents were administered nasogastrically. Blood pressure levels gradually decreased with the increase in platelet counts, starting around hospital day 65. On hospital day 72, the patient started rehabilitation exercises. The patient recovered enough to walk with a cane (fig. ). He was transferred to a rehabilitation hospital on hospital day 119.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [54, 'years'], 'creatinine': [2044.0, 'µmol/L'], 'sex': 'Male'}",2.08101,1.97696,2.18506,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 54 years old. The concentration of Creatinine is 2044.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 2044.0 µmol. To convert 2044.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 2044.0 µmol Creatinine * 1e-06 mol/µmol = 0.00204 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00204 mol Creatinine * 113.12 g/mol = 0.23076 g Creatinine. To convert 0.23076 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.23076 g Creatinine * 1000.0 mg/g = 230.76 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 230.76 mg Creatinine/10.0 dL = 23.076 mg Creatinine/dL. The concentration value of 2044.0 µmol Creatinine/L converts to 23.076 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 23.076^(-1.154) * 54^(-0.203) * 1 * 1=2.08101.
Hence, the patient's GFR is 2.08101 mL/min/1.73m²."
3367,9,MDRD GFR Equation,lab test,decimal,pmc-6566467-1,Extracted,"A 76-year-old man was referred to the hospital in September 2016, due to bilateral edema in his lower extremities and general fatigue. He had pancreaticoduodenectomy against pancreatic cancer in November, 2015, and had Tegafur, Gimeracil, Oteracil Potassium as postoperative chemotherapy which was discontinued because of the occurrence of pancytopenia. From April, 2016, nivolumab treatment at the dose of 0.5 mg/kg was started and continued until July, three times in total, which improved his symptoms for a certain period. However, from the beginning of September, 2016, he re-developed edema and fatigue. At visit, his serum creatinine (SCr) level increased from 0.8–0.9 mg/dL to 3.08 mg/dL, and he was hospitalized for further investigation. His past medical history was not remarkable, except for the history of treatment against lung tuberculosis in his 20’s. Among his medication, rabeprazole 10 mg/day, Furosemide 10 mg/day, and spironolactone 25 mg/day were started recently. Other than that, he was taking levocarnitine 1500 mg/day and sennoside 24 mg/day. On physical examination, vital signs were unremarkable except for an increase of 5 kg in body weight in 4 months. His lungs were clear to auscultation, and bilateral pitting edema was noted in his lower extremities. His skin was dry, but no eruption nor rash were noted. Laboratory findings on admission are shown as . His SCr level was 3.08 mg/dL, and urinary protein or occult blood were both negative, although pyuria was evident without any eosinophil in urine cytology. Urinary excretion of β2-miroglobulin and α1-microglubulin were high. A renal ultrasound showed hyperechoic parenchyma of bilateral kidneys without an evidence of hydronephrosis or enlargement of the both kidneys. Gallium scintigraphy showed increased gallium-67 uptake in both kidneys, which was compatible with the inflammation of AIN. A percutaneous renal biopsy was performed. Of 15 glomeruli, six were collapsed; however, no increase of mesangial matrix nor hypercellularity were represented. There was severe interstitial inflammation along with tubulitis in some parts. Among infiltrate lymphocytes, CD3+ T-lymphocytes were dominant, and infiltration over the basement membrane of CD8+ lymphocytes were seen. Some nuclei of tubular epithelial cells were variably sized, massively enlarged, irregularly shaped, and abnormally hyperchromatic occasionally. These morphological findings were indicative of those of karyomegalic changes. These epithelial cells were positive for Ki-67 in immunostaining, which suggested the regenerative changes in renal tubular epithelium. Interstitial fibrosis and tubular atrophy were observed in approximately 20% of the cortical area, according to the result of the Masson-trichrome staining. Overall, the changes represented drug-induced tubulointerstitial nephritis with karyomegalic epithelial changes. After the discontinuation of nivolumab treatment, his renal function had recovered gradually from 3.08 mg/dL to SCr level 1.84 mg/dL in 5 months. His renal function continued to partially improve, to which SCr level 1.42 mg/dL, approximately 1 year after the discontinuation of nivolumab treatment.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [76, 'years'], 'creatinine': [3.08, 'mg/dL'], 'sex': 'Male'}",19.8356,18.84382,20.82738,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 76 years old. The concentration of Creatinine is 3.08 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.08^(-1.154) * 76^(-0.203) * 1 * 1=19.8356.
Hence, the patient's GFR is 19.8356 mL/min/1.73m²."
3368,9,MDRD GFR Equation,lab test,decimal,pmc-2771803-1,Extracted,"A 59-year-old woman was admitted to the hospital because of progressive dyspnea, peripheral edema, and general weakness. She had a six-year history of end-stage renal disease and peritoneal dialysis. She also had a history of diabetes mellitus, hypertension, and parathyroidectomy due to parathyroid adenoma. She denied alcohol use and corticosteroid use and had no history of tuberculous infection or tuberous sclerosis.
She was 156 cm tall and weighed 72 kg, with a body mass index of 29.6 kg/m2. Her blood pressure was 90/60 mmHg, and her pulse rate was 95 beats/min. Facial edema and neck vein distension were noted on physical examination. No palpable masses were found in the neck, trunk, or axillae. Respiratory examination revealed clear breathing sound bilaterally, with no crackles or wheezes. Heart sounds were decreased, but no murmur or pericardial rub was heard. Pitting edema was noted in both legs. The electrocardiogram was within normal limits. Laboratory examination showed evidence of end-stage renal disease, including blood urea nitrogen of 50.8 mg/dL and creatinine of 9.13 mg/dL. The other laboratory parameters, including autoantibodies, were unremarkable.
Chest radiography revealed cardiomegaly and bilateral obliteration of the costophrenic angles, indicating the presence of a pleural effusion (). TTE showed a small pericardial effusion and a diffuse, circumferential echogenic mass in the epicardium, suggesting massive fat infiltration. There were no significant abnormalities in systolic or diastolic function. The left ventricular (LV) ejection fraction was estimated to be 68% (). There was no evidence of right ventricular (RV) dysfunction, based on fractional area change.
The patient underwent high concentrative peritoneal dialysis and additional hemodialysis to control uremia and hypervolemia. Despite management over a two-week period, her symptoms and signs of hemodynamic instability failed to improve. Follow-up TTE revealed no residual pericardial effusion, but continued to show diffuse, massive fat infiltration. Moreover, the patient had pericardial thickening and adhesions, interventricular septum bouncing, inferior vena cava plethora, diastolic reversal of hepatic venous flow, and respiratory variations on transmitral inflow (), suggesting the presence of constrictive pericarditis. On tissue Doppler imaging, the average of the pulsed Doppler-derived E' velocity at the septal corner was 5 m/s (). Multislice CT of the heart confirmed thickened pericardium (7-11 mm) and diffuse, extensive fat infiltration of the whole pericardium, with a density similar to that of fat (). We measured the volume of the epicardial adipose tissue using 3-mm thick axial slices. We manually traced the epicardial fat in every slice, working from the aortic root to the apex. The number of manually traced slices was 37. The measured volume of epicardial fat in this patient was 487 mL.
Coronary angiography and left ventriculogram showed minimal intracoronary stenosis and normal systolic function, but also showed decreased normal inward systolic motion of the coronary arteries, caused by interference from massive surrounding fat tissues. Cardiac catheterization showed diastolic pressure equalization, ""dip and plateau"" feature on simultaneous right ventricular and left ventricular pressure tracings (), equalization of right atrium and left ventricular pressures on simultaneous right atrial and left ventricular pressure tracings, and marked x & y descent on right atrial pressure tracings (). These findings were compatible with constrictive pericarditis.
We therefore diagnosed this patient with constrictive pericarditis that may have been promoted by massive epicardial fat. We prepared the patient for pericardiectomy to improve hemodynamics, after consultation with the department of cardiac surgery. The patient developed sudden exacerbation of hemodynamic instability during preparation. Pericardiectomy could not be performed, and the patient expired.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [59, 'years'], 'creatinine': [9.13, 'mg/dL'], 'sex': 'Female'}",4.42156,4.20048,4.64264,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 59 years old. The concentration of Creatinine is 9.13 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 9.13^(-1.154) * 59^(-0.203) * 1 * 0.742=4.42156.
Hence, the patient's GFR is 4.42156 mL/min/1.73m²."
3369,9,MDRD GFR Equation,lab test,decimal,pmc-6091430-1,Extracted,"A 56-year-old female was referred to the nephrologist due to apparently chronic kidney disease (CKD), diagnosed on a routine laboratory check-up. The patient was asymptomatic, Past medical record was contributory for three normal pregnancies. There was no background of alcohol intake, tobacco consumption, drug abuse, or medication exposure. There was a family history of CKD (). Physical examination was unremarkable. Abnormal blood tests were as follows: Haematocrit 37%; haemoglobin 11.9 g/dL; bicarbonate 21 mEq/L; urea 78 mg/dL (normal value 20-50 mg/dL); serum creatinine 2 mg /dL; uric acid 6.4 mg/dL; creatinine clearance 42 ml/min; proteinuria 0.2 g/day; urinary sodium excretion 188 mEq/day; urine pH: 6, urinary density 1015. Urinary sediment was unremarkable. HIV, HCV, and HBV were negative; C3, C4, and CH50 were within normal limits. ANA, p-ANCA, c-ANCA, antiglomerular basement membrane antibody, and antiphospholipid antibodies were reported as negative. Renal sonogram disclosed two kidneys, normal in shape and size. A kidney biopsy was performed. Light microscopy disclosed 30 glomeruli: 6 completely obliterated, 8 presented peripheral sclerosis of the glomerular tuft with adhesions between parietal and visceral epithelial cells of Bowman's capsule, and 6 depicted mild mesangial expansion (). Tubular atrophy and interstitial fibrosis were 30%. Blood vessels showed mild intimal sclerosis in arterioles. Immunofluorescence was negative. Electron microscopy: diffuse effacement of podocyte foot processes existed with microvillous transformation. Basal membrane was normal. Tubules were normal. Pathology report was as follows: focal and segmental glomerulosclerosis with moderate interstitial fibrosis and tubular atrophy. Patient was started on enalapril 5 mg twice a day and simvastatin 10 mg/day and on appropriate diet.
She was lost to follow-up. Sixteen months later the patient returned to the nephrologist due to asthenia, fatigue, and cramps. Blood pressure was 110/70 mmHg. Significant blood test results were as follows: Haematocrit 32%; haemoglobin 9.2 g/dL; potassium 5.5 mEq/L; bicarbonate 19 mEq/L; serum calcium 9.5 mg/dL; serum phosphate 6.2 mg/dL; serum magnesium 2.2 mg/dL; urea 111 mg/dL; serum creatinine 3.78 mg/dL; uric acid 8.1 mg/dL; albumin 4.3 g/dL; creatinine clearance 21 ml/min; proteinuria 0.29 g/day; urinalysis was unremarkable. Urine pH was 7 and urinary density 1010. A renal magnetic resonance imaging was noncontributory. The patient was prescribed erythropoietin 2000 U every other day, enalapril 5 mg bid, calcium carbonate 2 g/day, sodium bicarbonate two tea spoons daily, and polystyrene calcium sulfonate. Six months later the patient was started on hemodialysis (creatinine clearance 12 mL/min). A genetic study disclosed the insertion of a cytosine nucleotide in the VNTR (Variable Number Tandem Repeats) region of the MUC-1 gene, consistent with a mutation of the mucin-1 gene previously reported []: cDNA NM_001204286.1, protein NP_001191215.1, SNaPshot. The diagnosis of ADTKD-MUC1 (Autosomal Dominant Tubulointerstial Kidney Disease-Mucin-1) was finally made. The laboratory results of the patient's daughter revealed mild proteinuria and normal kidney function (). A kidney biopsy revealed mild tubulointerstitial disease and focal and segmental glomerulosclerosis in 2 out of 16 glomeruli. She was started on enalapril and nephroprotection and genetic counseling was given to her.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [56, 'years'], 'creatinine': [3.78, 'mg/dL'], 'sex': 'Female'}",12.3633,11.74513,12.98147,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 56 years old. The concentration of Creatinine is 3.78 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 3.78^(-1.154) * 56^(-0.203) * 1 * 0.742=12.3633.
Hence, the patient's GFR is 12.3633 mL/min/1.73m²."
3370,9,MDRD GFR Equation,lab test,decimal,pmc-6210852-2,Extracted,"Urine sample of a 53-year-old female patient with colon carcinoma and bilateral hydroureteronephrosis yielded the growth of T. asahii on three occasions. The patient underwent hemicolectomy and was on chemotherapy. The patient had a urinary catheter throughout her stay in the hospital. The patient was on treatment with Amoxyclav, Linezolid, and Levofloxacin in appropriate dosages along with antacids and multivitamins. Her blood picture showed hemoglobin = 6.9 mg/dl, total leukocyte count = 13,600/ml, urea = 72 mg/dl, and creatinine = 4.2 mg/dl.
Wet mount of the urine sample revealed moderate number of pus cells and budding yeast cells with pseudohyphae []. Based on cultural and biochemical characteristics, the isolate was identified as T. asahii which is sensitive to voriconazole, fluconazole and resistant to Amphotericin-B, Itraconazole, and ketoconazole. Antifungal therapy with fluconazole was given, and urine sample sent for the culture after treatment which was found to be negative for the fungus.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [53, 'years'], 'creatinine': [4.2, 'mg/dL'], 'sex': 'Female'}",11.07093,10.51738,11.62448,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 53 years old. The concentration of Creatinine is 4.2 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 4.2^(-1.154) * 53^(-0.203) * 1 * 0.742=11.07093.
Hence, the patient's GFR is 11.07093 mL/min/1.73m²."
3371,9,MDRD GFR Equation,lab test,decimal,pmc-6062775-1,Extracted,"We present the case of a 70-year-old female who was sent to the hospital by her family physician for an elevated blood urea nitrogen of 84 g/dL and a creatinine of 6.1 mg/dL. Baseline values were normal 1 month prior. Her chief complaints were weakness, decreased appetite, bilateral lower extremity swelling, and discoloration for the past 3 weeks. She has a past medical history significant for SSc, diagnosed in 1980, Raynaud’s disease, hypertension, and neuropathy. Of note, she was recently started on mycophenolate mofetil at a dose of 500 mg twice daily for treatment of her SSc.
On physical examination, she was hypertensive to 164/72 mm Hg, had bilateral lower extremity edema, and skin changes limited to her hands and feet, consistent with lcSSc. Her urinalysis was positive for proteinuria and hematuria. Her complete blood count was significant for decreased hemoglobin of 8.6 g/dL. Her serologies were positive for ANA at 1:160, and MPO antibodies, at a level of 23.8 by ELISA (enzyme-linked immunosorbent assay). PR-3 antibodies, p-ANCA, and c-ANCA were negative. Renal biopsy demonstrated an acute necrotizing vasculitis superimposed on chronic changes related to her SSc. Light microscopy demonstrated 28 to 38 glomeruli of which 10% were globally sclerosed. The majority of the remaining glomeruli show prominent ischemic-type wrinkling of capillary walls (). Necrotizing vasculitis of the artery is seen, with prominent transmural necrosis and inflammatory infiltrate with prominent thickening of surrounding arterioles due to concentric hyperplasia (). Ten percent of glomeruli per section show crescents ().
Electron microscopy confirmed the absence of immune complexes as well as tubular epithelial necrosis and diffuse foot process effacement. Treatment was initiated with 8 sessions of plasma exchange with albumin, pulse steroids at a dose of 500 mg intravenous for 3 days, and rituximab at 1 g for 2 doses 2 weeks apart. The patient unfortunately remains hemodialysis dependent.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'age': [70, 'years'], 'creatinine': [6.1, 'mg/dL'], 'sex': 'Female'}",6.80168,6.4616,7.14176,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 70 years old. The concentration of Creatinine is 6.1 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 6.1^(-1.154) * 70^(-0.203) * 1 * 0.742=6.80168.
Hence, the patient's GFR is 6.80168 mL/min/1.73m²."
3372,9,MDRD GFR Equation,lab test,decimal,pmc-8402958-1,Extracted,"A 50-year-old male was referred to the Nephrology team for a renal transplant workup in March 2020. He had a history of diabetes and hypertension. He was diagnosed with obstructive uropathy in 2013 and subsequently developed end-stage renal disease with a baseline creatinine of three. He was managed successfully with medication till March 2020 when his renal functions deteriorated and he was offered a renal transplant.
As part of the pre-transplant workup, a CT scan of the abdomen, chest, and pelvis suggested multiple enlarged necrotic lymph nodes in the peripancreatic and portocaval areas. The largest node was found abutting the head of the pancreas measuring 23 mm x 18 mm (Figure ). The patient’s hemoglobin, white blood count, and C-reactive protein levels were 8.9 g/dL, 12,000/mm3, and 7.63 mg/L. The liver function tests were within the normal range. Unfortunately, the patient was lost to follow up.
The patient was re-admitted via the emergency department (ED) in December 2020 with fever, decreased urine output, and right sub-costal pain. Initial investigations revealed hemoglobin, white blood count, and C-reactive protein levels of 6.7 g/dL, 16,000/mm3, and 65.88 mg/L respectively. Liver function tests were normal. A CT scan of the abdomen suggested an interval increase in the size of the peripancreatic and portocaval lymph nodes. The patient's chest X-ray was performed, which was unremarkable.
He was subsequently referred for endoscopic ultrasound (EUS) guided biopsy of the peripancreatic lymph node mass. EUS was performed with a curvilinear scope. A necrotic lymph node mass was identified near the uncinate/head of the pancreas (Figure ). Multiple biopsies were taken with a 22G FNB Acquire needle. Histopathology suggested the presence of predominantly necrotic and scanty fibro collagenous tissue containing occasional granulomas. The granulomas were composed of epithelioid histiocytes and giant cells (Figure ). Mycobacterium tuberculosis-polymerase chain reaction (MTB-PCR) was positive confirming the diagnosis of TB.
The patient was commenced on anti-tuberculosis treatment. A repeat CT abdomen in March 2021 suggested interval reduction in the sizes of the centrally necrotic lymph nodes in peripancreatic and portocaval locations compared to the CT abdomen performed in December 2020, from 47 mm x 26 mm to 35 mm x 30 mm and 26 mm x 35 mm to 18 mm x 23 mm respectively (Figure ). Clinically the patient had improved significantly with no further episodes of pyrexia or abdominal pain. The blood tests improved as well, with hemoglobin, white blood count, and C-reactive protein levels of 13.9 g/dL, 8500/mm3, and 2.02 mg/L respectively. Renal transplantation is planned once the patient completes his treatment for TB.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [3.0, 'mg/dL'], 'age': [50, 'years']}",22.26123,21.14817,23.37429,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 50 years old. The concentration of Creatinine is 3.0 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.0^(-1.154) * 50^(-0.203) * 1 * 1=22.26123.
Hence, the patient's GFR is 22.26123 mL/min/1.73m²."
3373,9,MDRD GFR Equation,lab test,decimal,pmc-5206421-1,Extracted,"A 43-year-old female who received kidney transplantation from a living donor presented with renal dysfunction. Her history revealed purpura nephritis, which was diagnosed at the age of 2 years and culminated in end-stage renal disease at the age of 26 years. She was started on peritoneal dialysis from the age of 26 years, and she received kidney transplantation from her mother (living donor) at the age of 27 years. Her renal dysfunction steadily progressed from the age of 42 years, and she was referred to our department to investigate the cause of the renal dysfunction. She was given cyclosporine, azathioprine, and prednisolone. Physical examination was normal. Blood pressure was 152/95 mmHg, heart rate was 90 beats/min, body temperature was 36.7°C, and Body Mass Index (BMI) was 29.8. On laboratory examination, she had anemia (Hb, 6.6 g/dl), her serum creatinine (Cr) level was 1.88 mg/dl, and her urine was clear. CT revealed a large uterine mass compressing the distal ureter of the transplanted kidney and causing hydronephrosis ().
First, a 5 Fr ureteral stent was retrogradely placed in the transplanted ureter. However, a percutaneous nephrostomy was needed because the serum Cr levels and hydronephrosis of the transplanted kidney did not improve. Serum Cr and hydronephrosis immediately improved after the nephrostomy, but it was necessary to perform a simple hysterectomy to remove the nephrostomy tube. The hysterectomy was performed a month later, and the pathological diagnosis was uterine adenomyosis.
Two years after the hysterectomy, she experienced painful urination, fever, right abdominal pain, and right lower limb pain. Physical examination revealed right abdominal tenderness on the transplanted kidney. Her blood pressure was 120/85 mmHg, heart rate was 110 beats/min, and body temperature was 38.5°C. Her white blood cell count was 1.32 × 104/μl, C-reactive protein level was 14.4 mg/dl, and serum Cr level was 2.73 mg/dl. Urinalysis revealed pyuria. T2-weighed magnetic resonance imaging (MRI) of her pelvis demonstrated right psoas abscess in conjunction with the transplanted kidney (). Immediately, broad-spectrum antibiotics were administered. β-Streptococcus was isolated from the urine culture. The blood bacterial culture was negative. Her fever and abdominal pain were quickly alleviated, and T2-weighed MRI after 2 months revealed abscess improvement (). Immunosuppressive agent was not changed during the entire treatment course. No relapses have occurred after the completion of treatment.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [2.73, 'mg/dL'], 'age': [43, 'years']}",18.98962,18.04014,19.9391,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 43 years old. The concentration of Creatinine is 2.73 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.73^(-1.154) * 43^(-0.203) * 1 * 0.742=18.98962.
Hence, the patient's GFR is 18.98962 mL/min/1.73m²."
3374,9,MDRD GFR Equation,lab test,decimal,pmc-8225443-1,Extracted,"A 77-year-old Caucasian male with a past medical history of insulin-dependent diabetes mellitus, dyslipidemia, hypertension, and chronic kidney disease stage IIIa presented to the emergency department due to bilateral lower extremity pain. The patient was diagnosed and treated for lower extremity cellulitis. Due to pain of his lower extremities with ambulation, the patient requested an indwelling urinary catheter. Therefore, urinary catheter placement was performed on the patient's request. Prior to discharge to the skilled nursing facility, discontinuation of the indwelling urinary catheter was recommended multiple times to the patient, but he refused the catheter's removal. He was discharged to the skilled nursing facility after having completed his antibiotic course. He was to continue furosemide, gabapentin, and also nystatin cream for prophylactic prevention of fungal infection on his feet bilaterally.
Nearly three weeks after discharge to the skilled nursing facility, the patient was brought to the emergency department by emergency medical services due to signs of a possible stroke observed at the facility. He was demonstrating dysarthria, right-sided facial droop, and right-sided weakness. These symptoms were first noted about 2.5 hours prior to arrival. Computed tomography head showed no acute abnormality. The patient was not a candidate for alteplase due to an elevated INR.
Initial emergency department vitals showed a temperature of 38.3. After blood cultures were drawn, a single dose of one gram of ceftriaxone was given to the patient. Later that day, the patient's antibiotics were broadened to vancomycin and cefepime. On his physical exam, the patient's speech remained dysarthric, and he also exhibited a right-sided facial droop with right-sided weakness. The indwelling urinary catheter from his previous admission was still in place. His labs were remarkable for a creatinine level of 3.50, a blood urea nitrogen of 105, a potassium level of 5.2, and a serum bicarbonate of 17. His white blood cell count was within normal limits. Computed tomography angiography of the head and neck vessels was performed in the emergency department even with his acute on chronic kidney injury with a creatinine of 3.50. The computed tomography scans revealed a 50% to 70% stenosis of the left carotid artery and a less than 50% stenosis of the right carotid artery at the bifurcation. The patient underwent magnetic resonance imaging of the brain the following day, which revealed no signs of an acute stroke.
Upon returning to his hospital room after his magnetic resonance imaging scan, the patient was observed to be unresponsive with no palpable pulses. Cardiopulmonary resuscitation was started. Once return of spontaneous circulation was achieved, the follow-up electrocardiogram did not reveal any ST-segment or T-wave changes concerning for ischemia or infarction. Transthoracic echocardiogram with a bubble study revealed an ejection fraction estimated at 50% to 55% without any wall motion abnormalities and a negative bubble study. Alarmingly, the echocardiogram reported “a possible vegetation attached to the tricuspid valve with a separate possible vegetation attached to the Eustachian valve.” It also reported mild-to-moderate tricuspid regurgitation.
At this time, the patient's blood cultures returned positive for fungal growth. Urine cultures were drawn following the blood culture results, and those cultures also demonstrated fungal growth. The patient's blood and urine cultures were finalized as Candida lusitaniae, and the patient continued on micafungin 150 mg daily. As this organism is highly uncommon, multiple blood cultures were drawn. However, on 3 different days, the blood cultures resulted positive for C. lusitaniae.
As the days progressed, the patient displayed findings consistent with an anoxic brain injury. Therefore, the decision was made with the family to withdraw care, and the patient expired soon after.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [3.5, 'mg/dL'], 'age': [77, 'years'], 'Race': 'White'}",17.0697,16.21622,17.92319,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 77 years old. The concentration of Creatinine is 3.5 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.5^(-1.154) * 77^(-0.203) * 1 * 1=17.0697.
Hence, the patient's GFR is 17.0697 mL/min/1.73m²."
3375,9,MDRD GFR Equation,lab test,decimal,pmc-8373194-1,Extracted,"A 93-year-old female presented to the ED with complaints of two episodes of black, tarry stool over the previous 24 hours that turned lime-green in color when it contacted the water in the toilet bowl. She expressed personal concern for GI hemorrhage, as she had a similar episode of melena one year prior and was subsequently found to have a gastric ulcer thought to be secondary to non-steroidal anti-inflammatory drug (NSAID) use. The ulcer was treated with endoscopic ablation and the patient had been symptom free since that time. Further past medical history included hypertension and stage III chronic kidney disease. Her only home medications included a daily multivitamin and an omega-3 polyunsaturated fatty acid supplement.
A detailed history obtained in the ED revealed that she had eaten a fast-food hamburger and frozen beverage the evening prior to the onset of her perceived melanotic stool. Further questioning revealed that the hamburger bun and beverage were both dyed black in color as a promotional event by the fast-food restaurant in celebration of Halloween. She denied ongoing NSAID use that had seemingly contributed to her previously mild upper GI bleed (UGIB).
The patient was hemodynamically stable with a blood pressure of 132/79 millimeters of mercury, a heart rate of 74 beats per minute, a respiratory rate of 16 breaths per minute, and an oxygen saturation of 96% on room air. She denied abdominal discomfort. Serology testing showed a chronic and otherwise stable hemoglobin of 11.0 grams per deciliter (g/dL) (reference range 11.5–15.5 g/dL), a blood urea nitrogen (BUN) of 17 milligrams per deciliter (mg/dL) (8–28 mg/dL), a creatinine of 1.8 mg/dL (0.5–1.5 mg/dL), and a BUN to creatinine ratio of 9.4.
Digital rectal exam done in the ED revealed a bright, lime-green stool without obvious evidence of melena or hematochezia. A guaiac FOBT (gFOBT) was performed. Despite the grossly bright, lime-green appearance of the specimen, this turned dark green to black in color with a blue hue when developer was introduced. Appearance of occult blood in stool specimens is considered when a blue coloration is appreciated on the indicator card. However, given the duration of the patient’s symptoms, the absence of acute anemia, the lack of observed melena on digital rectal exam, and the history of recent ingestion of artificially dyed food, a false positive gFOBT was considered.
A shared decision-making discussion on inpatient observation vs close outpatient follow-up was done with the gastroenterologist, the emergency physician, and the patient. Given the absence of melena on digital rectal exam, a stable hemoglobin level near her baseline, and patient preference, she was felt to be reasonable for close outpatient follow-up. Further, she had a calculated Glasgow-Blatchford Bleeding Score of 1, which would suggest a predicted survivability without intervention at a sensitivity of 98.6%. Following a four-hour observation period, she remained asymptomatic and without observed melena. The patient was discharged home with close outpatient follow-up the next day.
A repeat hemoglobin level obtained 12 hours after ED discharge was unchanged at 11.2 g/dL. A one-year follow-up of the patient’s medical record from her primary physician showed no return visits to the ED, and no diagnostic or therapeutic colonoscopy had been performed. Her hemoglobin levels remained stable within her baseline range of 11.0 to 12.3 g/dL in the one-year period since ED discharge.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [1.8, 'mg/dL'], 'age': [93, 'years']}",26.25763,24.94475,27.57051,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 93 years old. The concentration of Creatinine is 1.8 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.8^(-1.154) * 93^(-0.203) * 1 * 0.742=26.25763.
Hence, the patient's GFR is 26.25763 mL/min/1.73m²."
3376,9,MDRD GFR Equation,lab test,decimal,usmle-2773,Extracted,"Several weeks after starting a new medication for rheumatoid arthritis, a 44-year-old woman comes to the physician because of painful ulcers in her mouth. Oral examination shows inflammation and swelling of the tongue and oropharynx and ulcers on the buccal mucosa bilaterally. Skin examination shows soft tissue swelling over her proximal interphalangeal joints and subcutaneous nodules over her elbows. Serum studies show an alanine aminotransferase level of 220 U/L, aspartate aminotransferase level of 214 U/L, and creatinine level of 1.7 mg/dL.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [1.7, 'mg/dL'], 'age': [44, 'years']}",32.64999,31.01749,34.28249,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 44 years old. The concentration of Creatinine is 1.7 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.7^(-1.154) * 44^(-0.203) * 1 * 0.742=32.64999.
Hence, the patient's GFR is 32.64999 mL/min/1.73m²."
3377,9,MDRD GFR Equation,lab test,decimal,pmc-5567081-1,Extracted,"The third case was a 4-year-old female of Indian descent who presented with renal insufficiency and hyperkalemia. Two months prior to our evaluation, she had been hospitalized for acute renal failure requiring dialysis while visiting India. While in hospital she had gastroenteritis and oliguric renal failure with concern for sepsis. She required hemodialysis and plasma transfusions for worsening bilateral pneumonia and ARDS that required intubation and mechanical ventilation. Lower respiratory tract cultures grew Acinetobacter baumannii, but blood cultures remained negative. She required hemodialysis for 2 weeks after which her renal function improved and the hemodialysis catheter was removed. Upon her return to the United States, she was evaluated by her primary care physician and referred to our hospital for hyperkalemia (6.6 mg/dL). The patient's laboratory findings at that time showed elevated Cr (3.4 mg/dL), hyponatremia (113 mEq/L), and increased WBC (19.8 × 103/mm3) but no anemia or thrombocytopenia. Family history was positive for maternal Hashimoto's thyroiditis but negative for renal disease. At the time of our evaluation, the patient's only medication was pantoprazole. Physical examination at our hospital revealed an afebrile child with a BP of 114/86 mm Hg. She appeared thin and anxious but the rest of her physical exam was unremarkable. UA revealed trace leukocytes but no hematuria or proteinuria. Her CBC showed anemia (Hgb 8.9 g/dL), increased WBC of 12.3 × 103/mm3, normal differential count, and thrombocytosis (775 × 103/mm3). BUN and Cr were 58 mg/dL and 1.8 mg/dL, respectively. Electrolytes revealed hyperkalemia (6 mEq/L) and hyperphosphatemia (6.6 mg/dL). C3 and C4 were normal. ANA and anti-double-stranded DNA autoantibodies were negative. Viral serological studies were positive only for rhinovirus/enterovirus (Table ). Renal ultrasound revealed that her right kidney had a duplicated collecting system. Renal biopsy was performed and LM showed 35 unremarkable glomeruli. Foci of mild tubulitis were seen. Interstitial fibrosis and tubular atrophy was approximately 50% with a moderate infiltrate of mononuclear leukocytes diffusely present in the interstitium (Fig. ). Direct IF was negative for all immunoreactants. EM showed mild podocyte foot process effacement. Definitive electron-dense deposits were not identified, but multiple TRIs were present (Fig. ). She was discharged home on antihypertensives (amlodipine and clonidine), erythropoietin, bicitra, and phosphate binders. Steroids were subsequently prescribed based on the biopsy diagnosis of acute and chronic tubulointerstitial nephritis. On her last follow-up, Cr was at 0.6 mg/dL, and she had normal electrolytes.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [0.6, 'mg/dL'], 'age': [4, 'years']}",176.70028,167.86527,185.53529,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 4 years old. The concentration of Creatinine is 0.6 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.6^(-1.154) * 4^(-0.203) * 1 * 0.742=176.70028.
Hence, the patient's GFR is 176.70028 mL/min/1.73m²."
3378,9,MDRD GFR Equation,lab test,decimal,pmc-4421368-1,Extracted,"A 67-year-old male patient who had been on CAPD therapy for end-stage renal disease secondary to type 2 diabetes mellitus. He had been on CAPD therapy for 3 years. He experienced two episodes of CAPD peritonitis secondary to Enterococcus spp and metycilline-sensitive Staphylococcus aureus in December 2007 and June 2008, respectively. All episodes were successfully treated with standard antibiotic therapy.
The patient presented to our hospital due to abdominal pain, tenderness, cloudy effluent and pruritus. His body temperature was 37.8°C. The abdominal examination showed diffuse abdominal tenderness and signs of peritonitis. The remaining physical examination was normal. On admission, haemogram showed white blood cell count 10.700/mm3 with 76% neutrophils and 6% eosinophils and haemoglobin 11.6 g/dL. Blood urea nitrogen was 72 mg/dL, and serum creatinine was 6.6 mg/dL. C-reactive protein was high (23.3 mg/dL). Peritoneal effluent leukocyte count was 1550/mm3 with 80% neutrophils and 10% eosinophils. S. stercoralis larvae were seen on centrifuged dialysate sediment with microscopic examination (Figure ). Stool examination was also positive for S. stercoralis larvae. The patient was treated with albendazole 400 mg orally for 1 month. The dialysate and stool cultures were negative. The patients' complaints disappeared and dialysate white blood cell count decreased to 100/mm3 4 days later without a need for catheter removal. We did not detect larvae in three stool samples and treatment finished at the end of the first month. Strongyloides larva was also not detected in stool samples 2 months after the therapy.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [6.6, 'mg/dL'], 'age': [67, 'years']}",8.44483,8.02259,8.86707,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 67 years old. The concentration of Creatinine is 6.6 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 6.6^(-1.154) * 67^(-0.203) * 1 * 1=8.44483.
Hence, the patient's GFR is 8.44483 mL/min/1.73m²."
3379,9,MDRD GFR Equation,lab test,decimal,pmc-6355299-3,Extracted,"A 70-year-old African-American female with a past medical history significant for non-ischemic cardiomyopathy, pulmonary hypertension, chronic kidney disease (CKD) stage III, and ankle fracture status post open reduction and internal fixation complicated by a wound infection, presented to our hospital with word-finding difficulty. Three weeks prior, the patient was hospitalized for a wound infection of her surgical site with wound cultures positive for pseudomonas and enterococcus. She subsequently underwent surgical debridement, incision and drainage, and was started on IV piperacillin/tazobactam 4.6g every six hours. She was later discharged to a subacute rehabilitation on IV vancomycin 1,250mg every 24 hours and cefepime IV 2g every 12 hours. At the rehabilitation facility, the patient’s daughter noted that the patient’s cognitive ability had continued to deteriorate since discharge from the hospital. The patient now had word-finding difficulty prompting an emergency department (ED) evaluation for a stroke. The vitals in the ED were within normal limits and the physical exam only remarkable for asterixis. Complete blood count showed anemia and mild leukocytosis and basal metabolic panel was remarkable for a blood urea nitrogen of 38mg/dL (ref range: 7-20mg/dL), bicarbonate of 19mEq/L (ref range: 23-29mEq/L), and a creatinine of 4.66mg/dL (ref range: 0.8-1.4mg/dL). CT, chest x-ray, ultrasound, and MRI did not identify any acute processes contributing to her presentation. An EEG suggested moderate diffuse cerebral dysfunction (encephalopathy) with possible structural or physiologic disturbances in the left hemisphere. Due to the high dose of antibiotic in the setting of chronic renal disease, there was a high suspicion for cefepime-induced neurotoxicity. Infectious disease switched the antibiotic regimen to IV meropenem 1g every 24 hours, and the patient experienced a drastic improvement in mentation. The patient was subsequently discharged back to subacute rehabilitation to finish her antibiotic course for wound infection.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [4.66, 'mg/dL'], 'age': [70, 'years'], 'Race': 'Black'}",11.24792,10.68552,11.81032,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 70 years old. The concentration of Creatinine is 4.66 mg/dL. 
The patient is Black, so the race coefficient is 1.212.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 4.66^(-1.154) * 70^(-0.203) * 1.212 * 0.742=11.24792.
Hence, the patient's GFR is 11.24792 mL/min/1.73m²."
3380,9,MDRD GFR Equation,lab test,decimal,pmc-7489871-1,Extracted,"A 55-year-old male with a past medical history of squamous cell carcinoma of the tongue, chronic kidney disease, gastroesophageal reflux disease, and severe alcohol use disorder presented to our institution for the evaluation of abnormal liver biochemistries and painless jaundice. The patient initially presented to the ED after suffering a fall at his home. Initial evaluation revealed diffuse jaundice. As such, lab work was obtained, which was significant for total bilirubin of 23.7 mg/dL (reference range: 0.1-1.2 mg/dL), direct bilirubin of 21 mg/dL (reference range: 0.1-0.3 mg/dL), alkaline phosphatase of 1,480 U/L (reference range: 44-147 IU/L), aspartate aminotransferase of 320 U/L (reference range: 5-40 IU/L), alanine aminotransferase of 180 U/L (reference range: 7-56 IU/L), white blood cell count of 40 x 109/L (reference range: 4.5-11.0 × 109/L), potassium of 5.4 mmol (reference range: 3.5-5 mmol/L), blood urea nitrogen of 51 mg/dL (reference range: 2.5-7.1 mmol/L), and creatinine of 5 mg/dL (reference range: 0.7-1.2 mg/dL). C-reactive protein was also elevated at 35 mg/dL (reference range: 0.1-1 mg/dL); however, lactic acid and procalcitonin were within normal limits at 2.3 mmol/L (reference range: 0.5-2.3 mmol/L) and 0.47 ng/mL (reference range: 0.10-0.49 ng/mL), respectively. Coagulation studies revealed an international normalized ratio of 1.2 and prothrombin time of 12 seconds (reference range: 11-13.5 seconds). The patient denied abdominal pain, fever, or chills, and vital signs were within normal limits. CT of the abdomen showed an enlarged liver and diffuse hepatic steatosis (Figure ).
On day one of admission, the patient was started on broad-spectrum antibiotics with cefepime and vancomycin. The etiology of his leukocytosis was unclear as extensive infectious workup was negative. Multiple sets of blood cultures did not show any growth, and there was no evidence of any abnormal collection on imaging. Urine analysis and X-ray chest were unremarkable. Despite the initiation of antibiotics, there was no improvement in white blood cell count, which peaked at 42 x 109/L on the fifth day of admission. The gastroenterology service was consulted, who determined that the most likely etiology was alcoholic hepatitis in the setting of underlying cirrhosis. Given the negative infectious, metabolic, and autoimmune workup, the patient underwent endoscopic ultrasound (EUS)-guided liver biopsy, which showed diffuse fibrosis and neutrophilic infiltration (Figures , ). The patient had an elevated Maddrey’s discriminant function score of 34, with an MELD (model for end-stage liver disease) score of 24.
The patient was subsequently started on prednisolone for the treatment of alcoholic hepatitis, with only mild improvement in liver function tests. Total bilirubin peaked at 24.9 mg/dL and was at its lowest on the second day of prednisolone treatment at 20.3 mg/dL. In light of abnormal liver biochemistries, he underwent magnetic resonance cholangiopancreatography (MRCP), which was negative for biliary obstruction. Esophagogastroduodenoscopy (EGD) was significant for candida esophagitis, along with portal hypertensive gastropathy (Figures , ). As such, steroids were discontinued. The patient was not a candidate for fluconazole given his liver injury and was started on micafungin which was later discontinued after learning of its potential hepatotoxicity. Because of the unusual presentation with such profound leukocytosis without evidence of sepsis, the hematology service was consulted to rule our possible hematologic malignancy. Bone marrow biopsy showed no evidence of myeloproliferative state. Janus kinase 2 (JAK 2) testing was negative, ruling out a myeloproliferative disorder. Unfortunately, the patient passed away on the 13th day of admission. Request for autopsy was declined; however, it was presumed that the patient expired as a result of alcoholic hepatitis.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [5.0, 'mg/dL'], 'age': [55, 'years']}",12.10969,11.50421,12.71517,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 55 years old. The concentration of Creatinine is 5.0 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 5.0^(-1.154) * 55^(-0.203) * 1 * 1=12.10969.
Hence, the patient's GFR is 12.10969 mL/min/1.73m²."
3381,9,MDRD GFR Equation,lab test,decimal,pmc-5831873-1,Extracted,"A 79-year-old woman with past medical history of stage IV non-small cell lung cancer (NSCLC), heart failure with preserved ejection fraction, and dyslipidemia presented to the emergency department with generalized weakness and fatigue. Patient was initiated on nivolumab 3 months prior to presentation as a second line treatment following failure of chemotherapy with carboplatin and pemetrexed, confirmed by progressive disease on PET/CT scan. Home medications included rosuvastatin, docusate sodium, and low-dose furosemide. Patient received nivolumab 240 mg every 2 weeks. Following her fourth dose, she started complaining of worsening generalized fatigue and progressive weakness. Upon outpatient evaluation, her creatinine was found to be elevated at 2.9 mg/dl from a normal baseline. Nivolumab and furosemide were held, and patient received intravenous fluid hydration in the clinic. A renal sonogram was unremarkable. Repeat blood work few days later showed improved renal function. However, the patient's functional status declined over the next few days limiting her out of bed activity. She was sent to the emergency department for further workup.
On admission, vital signs were within normal limits. Physical exam was unremarkable except for trace lower extremity edema bilaterally.
Initial blood work showed a sodium level of 137 meq/L, potassium of 2.4 meq/L, chloride of 116 meq/L, bicarbonate of 11 meq/L, BUN of 23 mg/dL, and creatinine of 1.67 mg/dL. Arterial PH was acidotic at 7.21 with a CO2 of 27 suggestive of nonanion gap metabolic acidosis with adequate respiratory compensation.
Urine analysis revealed few white blood cells and red blood cells but no casts. Urine studies demonstrated a urine PH of 6.5 and a urine anion gap of 22. The fractional excretion of sodium (FeNa) was calculated at 0.5%.
The clinical picture was suggestive of prerenal AKI (FeNa < 1%) and renal tubular acidosis (RTA). Gentle hydration with sodium bicarbonate drip was started, and the patient was given potassium supplementation.
On further investigation, the patient had a negative autoimmune workup except for an ANA of 1 : 320. SPEP, UPEP, free light chains, and hepatitis serology were negative. Thyroid function tests were within normal range.
The alkaline urine PH in the setting of a significantly low serum bicarbonate level suggested a distal-type RTA. After ruling out common etiologies of RTA, nivolumab was considered as the likely culprit for a drug-induced RTA.
On day 2 of hospitalization, repeat blood work revealed mild increase in serum bicarbonate to 13 meq/L and improved serum creatinine to 1.39 mg/dl. In the context of a suspected drug-induced RTA secondary to nivolumab irAE, the patient was started on dexamethasone 4 mg every 8 hrs and her fluid rate was increased to target administration of 3 mmol/kg/day of bicarbonate.
On day 4 of hospitalization, the serum bicarbonate increased to 19 meq/L and serum creatinine was back to baseline. Patient was transitioned to oral sodium bicarbonate and prednisone. Her functional status improved significantly, and she was discharged on day 6 of hospitalization. Her discharge labs revealed a sodium of 142 meq/L, potassium of 3.3 meq/L, chloride of 112 meq/L, bicarbonate of 21 meq/L, and creatinine at 0.95 mg/dL.
The patient was discharged home on oral bicarbonate and a prednisone taper.
Repeat labs 1 week after discharge were stable. Follow-up with nephrology and hematology was set up. However, the patient returned to the hospital with acute hypoxic respiratory failure due to massive pulmonary embolism secondary to heparin-induced thrombocytopenia and expired.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [0.95, 'mg/dL'], 'age': [79, 'years']}",56.74539,53.90812,59.58266,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 79 years old. The concentration of Creatinine is 0.95 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.95^(-1.154) * 79^(-0.203) * 1 * 0.742=56.74539.
Hence, the patient's GFR is 56.74539 mL/min/1.73m²."
3382,9,MDRD GFR Equation,lab test,decimal,pmc-7863463-1,Extracted,"We report the case of a 23-year-old male patient admitted to our hospital in June 2018. The patient had a 4-month history of foamy urine prior to admission. His medical report revealed proteinuria (+++), mild edema of the lower limbs, elevated serum creatinine (259 μmol/L) levels, and mild hypertension (145/78 mmHg). The patient had no prior history of renal problems.
The patient was hospitalized due to nephrotic syndrome and renal failure. Laboratory testing revealed the following: blood urea nitrogen (BUN), 7.1 mmol/L; serum creatinine (Scr), 282 μmol/L; urine albumin/creatinine (UACR), 2701.53 mg/g; urine protein/creatinine (UPCR), 3360 mg/g; urinary protein quantitative (24 h), 6.678 g; serum albumin, 34.3 g/L; serum uric acid, 561 μmol/L; total cholesterol, 7.63 mmol/L; low density lipoprotein, 5.18 mmol/L; hemoglobin (Hb), 130 g/L; anti-PLA2R, negative; parathyroid hormone (iPTH), 135.79 pg/mL; and homocysteine (HCY), 22.23 μmol/L. Interventricular septal thickness was found to be 12 mm using cardiac ultrasound. As renal ultrasound revealed renal cortex thinning and an unclear boundary of the renal cortex and medulla, renal biopsy was not performed.
After discharge, the patient was prescribed α-keto acid, atorvastatin calcium, and febuxostat tablets to control proteinuria and edema. Unfortunately, the patient’s proteinuria was not improved, and his serum creatinine levels rose rapidly (Table ). Prednisone (Starting dose 1 mg/kg) was administered for several months but was not effective as renal failure rapidly progressed. In March 2020, the patient started hemodialysis. In June 2020, the patient underwent renal transplantation. The transplantation was successful, and the patient has not shown any sign of proteinuria or hematuria since.
Eight years ago, the patient’s mother had manifested proteinuria, elevated serum creatinine levels (142 μmol/L), high blood pressure, and hyperuricemia. Angiotensin receptor blockers (ARBs) treatment was ineffective, and renal failure rapidly progressed. Peritoneal dialysis was initiated 3 years later (12/31/2014), and kidney transplantation was performed after another 2 years (03/03/2017). After transplantation, proteinuria was completely resolved; blood pressure and uric acid returned to normal; renal function improvement was also recorded (recent serum creatinine, 114 μmol/L) (Table ).
Given the patient’s familial history of renal failure, whole exome sequencing (WES) was performed. Genomic DNA from the patient, his mother, and a control was extracted from buccal swab samples, using a QIAmp DNA Mini Kit (Qiagen China Co., Ltd., Shanghai, China). Target capture sequencing was performed on the extracted DNA. All coding exons were enriched. Genetic analysis, variation annotation, and identification of candidate pathogenic mutations were performed. For our study, a total of 16 members of the patient’s family were recruited. Three individuals were affected in this pedigree, including the patient, his mother, and his maternal grandmother. Sequencing of exon 4 of autosomal INF2 revealed a nonsynonymous missense variant, wherein a C was substituted with T (c.640C > T), resulting in the p.Arg214Cys mutation (Figs. and ).
We conducted a review of the literature to compare the phenotypes of our patients with other patients reported to have been carrying the INF2 p.Arg214Cys mutation (Table ).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [282.0, 'µmol/L'], 'age': [23, 'years']}",24.48271,23.25857,25.70685,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 23 years old. The concentration of Creatinine is 282.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 282.0 µmol. To convert 282.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 282.0 µmol Creatinine * 1e-06 mol/µmol = 0.00028 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00028 mol Creatinine * 113.12 g/mol = 0.03167 g Creatinine. To convert 0.03167 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.03167 g Creatinine * 1000.0 mg/g = 31.67 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 31.67 mg Creatinine/10.0 dL = 3.167 mg Creatinine/dL. The concentration value of 282.0 µmol Creatinine/L converts to 3.167 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 3.167^(-1.154) * 23^(-0.203) * 1 * 1=24.48271.
Hence, the patient's GFR is 24.48271 mL/min/1.73m²."
3383,9,MDRD GFR Equation,lab test,decimal,pmc-7769497-1,Extracted,"A 52-year-old Caucasian male with a significant past medical history of COPD, diabetes mellitus type 2, essential hypertension and chronic back pain presented to the emergency room with diffuse abdominal pain. The patient reported associated abdominal swelling with 3 episodes of nausea and vomiting in the past day. The patient also reports having felt lightheaded for the past couple weeks and reports falling 2 weeks ago. On arrival, the patient was afebrile with a blood pressure of 60/40, heart rate of 74, respiratory rate of 14 and saturating 98% on room air. Labs obtained were significant for a Na:130, Glucose: 115, BUN:46, Cr:4.3 (baseline:0.8), WBC:20.9, blood cultures grew gram + cocci. The patient denies drinking alcohol, smoking cigarettes or consuming anything corrosive. After not responding to fluids, a central line was placed and Norepinephrine started. CT of the abdomen demonstrated air within the wall of the stomach, portal veins and perigastric veins at which point surgery was consulted. After admission to the ICU, a follow-up EGD demonstrated Emphysematous gastritis secondary to gastric mucosal necrosis particularly in the proximal stomach just below the GE junction. The patient had already been placed on Piperacillin/Tazobactam and Metronidazole before admission to the ICU and after blood cultures came back positive for gram + cocci, Vancomycin was added. The following day the patient continued to complain of severe pain and follow up CT abdomen/pelvis demonstrated interval gastric perforation with mild free air within the upper abdomen and fluid within the posterior gastric wall representing gastric necrosis with perforation along with interval development of mild pneumoperitoneum (Figures , ).
He was taken to surgery and underwent a subtotal gastrectomy with splenectomy due to becoming hypotensive during the procedure and the fear that attaching his distal esophagus to the jejunum at that point would result in poor perfusion. The decision was made to close him up and go back in a few days. Things became even more interesting when wound cultures taken during surgery came back positive for both yeast and streptococcus parasanguinis. Follow-up blood cultures were also positive for yeast. Micafungin was started at that point. He went back to surgery where his esophagus was found to have retracted into his chest, as well as his abdominal mesh being covered with pus. As much pus was cleared out as possible and was closed back up. In order to attach his esophagus to his jejunum, a thoracic surgical approach would need to be done for which the patient was not stable enough to perform. Peritoneal fluid cultures taken during the procedure grew yeast. With fungemia in his bloodstream, TPN had to be stopped. ID recommended stopping zosyn and adding meropenem. He remained intubated in the ICU where his family made the decision to compassionately extubate and make him comfort care. Culture wound results that had been sent for identification of the fungal species came back positive for Candida Glabrata.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [4.3, 'mg/dL'], 'age': [52, 'years'], 'Race': 'White'}",14.57695,13.8481,15.3058,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 52 years old. The concentration of Creatinine is 4.3 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 4.3^(-1.154) * 52^(-0.203) * 1 * 1=14.57695.
Hence, the patient's GFR is 14.57695 mL/min/1.73m²."
3384,9,MDRD GFR Equation,lab test,decimal,pmc-5695022-1,Extracted,"A 26-year-old man arrived at the emergency department with a seven-day history of hematemesis and melena. He had no previous medical history and did not drink alcohol or used any illicit drug or medication.
Physical examination on admission showed blood pressure of 100/60 mmHg, a temperature of 36°C (96.8°F), a pulse rate of 90/min, and a respiratory rate of 22/min; his height was 1.75 m, weight 98 kg, and BMI 32 kg/m2. He experienced pain with deep palpation in the epigastrium and no organomegaly or lymphadenopathy was identified. The left scrotal sac was enlarged and indurated and there was a mass in the left scrotum that was indistinguishable from the left testis and provoked displacement of structures of the penis and right testis (the right scrotum was empty). No inguinal lymphadenopathy was identified.
Laboratory tests revealed normal liver function. Hemoglobin was 9.13 g/dl, MCV was 87.9 fL, WBC was 11.9 K/uL, neutrophils were 9.81 K/uL, lymphocyte count was 1.59 K/uL, and platelet level was 252 K/uL. Serum glucose level was 106 mg/dl, BUN was 38 mg/dl, creatinine was 0.9 mg/dl, and calcium was 8.9 mg/dl. Serum alpha-fetoprotein (AFP) level was 17,090 ng/mL, lactate dehydrogenase was 1480 U/L (normal range: 91–180 IU/L), and human chorionic gonadotropin level was 287.4 IU/mL.
After resuscitation with crystalloid solutions, he underwent upper endoscopy. The gastroenterologist found abundant active bleeding, for which orotracheal intubation was decided to provide airway protection. The patient was transferred to the intensive care unit. A second upper endoscopy revealed a type 1 isolated gastric varix, treated with cyanoacrylate without complications ().
A scrotal US showed a large heterogeneous image in the left testicle area, with an echogenic and cystic solid component and flow presence with color Doppler assessment.
A contrasted CT scan of the thorax, abdomen, and pelvis showed a liver of normal size and density with multiple retrocrural, retroperitoneal, mesenteric, and left iliac metastatic lymphadenopathy which caused extrinsic compression of the portal vein along with splenic vein partial thrombosis with left-sided portal hypertension and perigastric and perisplenic collateral neovascularization (). A heterogeneous, well defined mass was found in the left testicle, 16.7 × 16.1 × 14.9 cm, with a solid component that was enhanced with the administration of contrast, as well as a cystic component. There was also invasion of the left spermatic cord.
The patient was extubated after surveillance and transferred to the Internal Medicine Department. We started chemotherapy with etoposide 100 mg/m2 and cisplatin 20 mg/m2, and seven days later the patient underwent a left radical orchiectomy by an inguinal approach with left hemiscrotectomy, without complications. Following this intervention, serum alpha-fetoprotein (AFP) level was reduced to 350 ng/mL, and the human chorionic gonadotropin level was 50 IU/mL.
A postoperative biopsy showed a pure testicular teratoma () with glandular formations and the presence of cartilage (a) and respiratory epithelium, with ciliated columnar cells alternating with goblet cells (b).
The patient was discharged after showing clinical improvement to receive ambulatory chemotherapy.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [0.9, 'mg/dL'], 'age': [26, 'years']}",102.00057,96.90054,107.1006,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 26 years old. The concentration of Creatinine is 0.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 0.9^(-1.154) * 26^(-0.203) * 1 * 1=102.00057.
Hence, the patient's GFR is 102.00057 mL/min/1.73m²."
3385,9,MDRD GFR Equation,lab test,decimal,pmc-4598801-1,Extracted,"A 17-year-old boy was followed up by pediatric nephrologist for bilateral cystic kidney disease, hypertension, and obesity since he was 13 years old. The diagnosis was an accidental finding during abdominal CT at the age of 13 to rule out appendicitis (BUN, 14; Cr, 0.77; electrolytes, WNL).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [0.77, 'mg/dL'], 'age': [17, 'years']}",133.12102,126.46497,139.77707,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 17 years old. The concentration of Creatinine is 0.77 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 0.77^(-1.154) * 17^(-0.203) * 1 * 1=133.12102.
Hence, the patient's GFR is 133.12102 mL/min/1.73m²."
3386,9,MDRD GFR Equation,lab test,decimal,pmc-5048039-1,Extracted,"A 42-year-old female with hypertension (HTN), ESRD, secondary to IgA nephropathy and a history of deceased donor renal transplant, presented with acute kidney injury (AKI). Her AKI was presumed to be prerenal due to ongoing gastroenteritis. Her S Cr was elevated to 3.3 mg/dL (from baseline of 2–2.2 mg/dL) and admission blood pressure (BP) ranged with 190/100–210/110 mmHg. She was on mycophenolic acid 360 mg QID, sirolimus 1 mg daily, prednisone 5 mg daily, and carvedilol 50 mg BID. Her renal transplant ultrasonography (USG) showed normal resistive indices (RI) with no hydronephrosis. An allograft biopsy was performed to rule out transplant rejection, as her S Cr continued to be elevated at 3.3 mg/dL even after 72 hours of hydration and negative GI workup. Her antihypertensive regime was adjusted with the addition of nifedipine, clonidine, and minoxidil and her blood pressure ranged within 140–160/80–95 during 48 hours prior to procedure. On postprocedure day 1, her blood pressure was again elevated (170–210/90–110 mmHg) and she had a noticeable drop in her hemoglobin (Hgb) from 10 g/dL to 8.5 g/dL. Her CT scans showed large subcapsular hematoma. Renal allograft angiography failed to show any active bleeding, an AV fistula, or any pseudoaneurysm formation. On postbiopsy day 2, her BP remained high and the S Cr peaked at 4.2 mg/dL prompting the drainage of subcapsular hematoma and a Jackson-Pratt (J/P) drain placement for continuous drainage. This resulted in significant improvement in blood pressure () and her IV antihypertensives were tapered off within 24 hours of drainage. Her S Cr improved to 3.1 mg/dL and her J/P drain was removed on day 5. She was soon discharged on PO antihypertensive regime. Her allograft biopsy showed moderate fibrosis with no evidence of antibody or cell mediated rejection or any other acute process.
Unfortunately, six weeks later she was readmitted with severe anemia (Hgb 6.4 g/dL), AKI (S Cr of 8.3 mg/dL), and hypertensive emergency (BP range of 190/90–210/110 mmHg). Her CT scans confirmed recurrence of the subcapsular hematoma. Again, renal allograft angiography failed to show any active bleeding or any AV malformations. This time, the hematoma was surgically drained to ensure the bleeding stopped after drainage. A J/P drain was again placed which was removed after 2 weeks. She required four sessions of hemodialysis treatments for this episode of AKI but her renal function stabilized at discharge with S Cr of 3.1 mg/dL and improved BP control (). A repeat USG at discharge showed complete resolution of hematoma. An overt cause for recurrence of hematoma was not elucidated by angiography. She was not on any anticoagulation and her coagulation profile was normal.
She was admitted again seven weeks later, for a large perinephric seroma with uncontrolled HTN (190/90–200/110 mmHg). The collection was drained emergently with an immediate and significant improvement in her BP (range 110–130/60–70) (). Her renal function remained at baseline and she had no acute kidney injury. She had no more recurrence of Page Kidney phenomenon and her antihypertensive regime is managed successfully as an outpatient.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [3.1, 'mg/dL'], 'age': [42, 'years']}",16.47749,15.65362,17.30136,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 42 years old. The concentration of Creatinine is 3.1 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 3.1^(-1.154) * 42^(-0.203) * 1 * 0.742=16.47749.
Hence, the patient's GFR is 16.47749 mL/min/1.73m²."
3387,9,MDRD GFR Equation,lab test,decimal,pmc-7454860-1,Extracted,"A 30-year-old man presented with a background of end-stage renal failure secondary to birth asphyxia and with a donation after brainstem death renal transplant (baseline creatinine 290 µmol/l), maintained on sirolimus and tacrolimus. This was the patient’s second transplant, the first being complicated by graft rejection, microangiopathic haemolytic anaemia and requiring graft nephrectomy in 2013. The current transplant had taken place >1 year before the current presentation, of which he had had one episode of BK viral nephropathy treated with CSs. He had been stable after this, with no significant infections. He presented with a 14-day history of feeling unwell with fevers, and a 5-day history of a cough, sore throat and difficulty breathing.
Initial oxygen saturation was 80% on room air, which improved to 100% on 35% oxygen via a venturi face mask. His blood pressure was 127/73 mmHg, heart rate 95 beats/min, temperature 38°C and respiratory rate 21 breaths/min. Chest X-ray (CXR) showed bilateral patchy consolidation, and nasopharyngeal swab (NPS) confirmed SARS-CoV-2. Blood tests revealed ferritin of 24617 µg/l, creatinine 519 µmol/l and CRP 92 mg/l.
Oxygen was titrated to keep his saturations >94%, and he was initiated on co-amoxiclav. After 2 days, with increasing oxygen requirements and progressive CXR consolidation, he was transferred to the ICU, where he was commenced on continuous positive airway pressure. The sirolimus was stopped, but he remained on tacrolimus. Ferritin at the time was 23 788 µg/l, CRP 73 mg/l and procalcitonin 17.27 μg/l (normal range <0.5 μg/l). Microscopy from blood cultures and urine cultures was negative, and CMV and EBV viraemias remained very low level. Given the increasing oxygen requirement and persistent inflammatory state, anakinra 200 mg i.v. was initiated (). A marked improvement in ferritin was seen within 2 days; CRP steadily decreased (), creatinine improved, and his respiratory effort stabilized. After 3 days of continuous positive airway pressure, he was weaned off and stepped down to the ward. Anakinra i.v. was stopped on day 10, when the ferritin was 4969 µg/l. He was discharged on day 12 with a creatinine of 371 µmol/l and CRP 7 mg/l and remained on tacrolimus.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [371.0, 'µmol/L'], 'age': [30, 'years']}",16.8169,15.97605,17.65775,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 30 years old. The concentration of Creatinine is 371.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 371.0 µmol. To convert 371.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 371.0 µmol Creatinine * 1e-06 mol/µmol = 0.00037 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00037 mol Creatinine * 113.12 g/mol = 0.04185 g Creatinine. To convert 0.04185 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.04185 g Creatinine * 1000.0 mg/g = 41.85 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 41.85 mg Creatinine/10.0 dL = 4.185 mg Creatinine/dL. The concentration value of 371.0 µmol Creatinine/L converts to 4.185 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 4.185^(-1.154) * 30^(-0.203) * 1 * 1=16.8169.
Hence, the patient's GFR is 16.8169 mL/min/1.73m²."
3388,9,MDRD GFR Equation,lab test,decimal,pmc-6913245-1,Extracted,"A 71-year-old male, with a medical history relevant for uncontrolled hypertension, diabetes mellitus type 2, and chronic kidney disease (baseline creatinine = 1.8 mg/dl), presented to the emergency department with abdominal pain, vomiting and loose stools. The patient denied any new-onset lower tract urinary symptoms, hematuria, fever, or flank pain. His laboratory tests were notable for leukocytosis of 12,000/cu.mm, serum creatinine of 1.9 mg/dl, and negative urinalysis. A CT scan done to rule out an intraabdominal process did not reveal any intraperitoneal pathology; however, a rightsided ureteral diaphragmatic herniation was seen, associated with mild-moderate hydronephrosis and significant blunting of calyceal fornices (Figures and ). The patient was counselled about his management options which included stenting of the ureter to relieve the obstruction or active surveillance of the hydronephrosis for which he opted. Serial ultrasounds performed every 6 months showed no progression of the hydronephrosis and no renal cortical thinning (). Follow-up on serum creatinine showed no change in his baseline levels and was in the 1.8–2 mg/dl range for over 18 months.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.9, 'mg/dL'], 'age': [71, 'years']}",35.11971,33.36372,36.8757,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 71 years old. The concentration of Creatinine is 1.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.9^(-1.154) * 71^(-0.203) * 1 * 1=35.11971.
Hence, the patient's GFR is 35.11971 mL/min/1.73m²."
3389,9,MDRD GFR Equation,lab test,decimal,pmc-3504257-1,Extracted,"Patient A is a 66-year-old woman with end-stage renal disease secondary to diabetes mellitus and hypertension who underwent cadaveric kidney transplantation. Upon discharge the patient's serum creatinine was 4.5 mg/dL, serum potassium was 3.8 mEq/L, and serum bicarbonate was 20 mEq/L. She was discharged home with maintenance immunosuppressive therapy with mycophenolate mofetil, tacrolimus, and prednisone and, furosemide (80 mg/day), sulfamethoxazole-trimethoprim (SMZ/TMP 400–80 mg/day), and sodium bicarbonate (1300 mg/day).
On post-op day 20, patient A's serum potassium was 5.9 mEq/L. At this time, she was started on metolazone (5 mg/day) and continued on furosemide, SMZ/TMP, and sodium bicarbonate. During a clinic visit on post-op day 53, patient A was taken to the emergency room with complaints of tremor, weakness, and palpitations. In clinic, she was found to have an elevated potassium level of 7.5 mEq/L. An EKG was performed and no changes were found. In the emergency room, she was treated with 30 grams of SPS, and her potassium level decreased to 4.8 mEq/L.
Following her visit to the ER, patient A was started on SPS to control her hyperkalemia (5 grams/week) for 3 weeks. She also continued taking furosemide (80 mg/day), metolazone (5 mg/day), SMZ/TMP (400–80 mg/day), and sodium bicarbonate (3.9 g/day). On post-op day 75, the patient was again found to have an elevated serum potassium level of 6.7 mEq/L. Patient A was instructed to take 45 grams of SPS and to return to the clinic the following day. Her potassium level decreased to 5.2 mEq/L and the patient was started on hydrochlorothiazide 25 mg daily. Her dose of SPS was increased to 15 grams per week and furosemide was cut in half (40 mg/day).
Several weeks later on post-op day 117, patient A was again admitted to the hospital from clinic for elevated potassium level of 6.8 mEq/L. Her serum creatinine was 2.3 mg/dL and serum bicarbonate was 20 mEq/L. She was treated with SPS (30 g), IV fluids, sodium bicarbonate (50 mEq), dextrose (25 g), and insulin (10 units), which brought her serum potassium level to 4.8 mEq/L. On post-op day 119, she was started on fludrocortisone 0.1 mg daily and her dose of hydrochlorothiazide was increased (50 mg/day). Metolazone and sulfamethoxazole-trimethoprim were discontinued and furosemide was decreased (20 mg daily).
Fludrocortisone was continued for five months. During this time, her serum potassium levels were within reference range of 3.5–5.5 mEq/L.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [2.3, 'mg/dL'], 'age': [66, 'years']}",21.21488,20.15414,22.27562,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 66 years old. The concentration of Creatinine is 2.3 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.3^(-1.154) * 66^(-0.203) * 1 * 0.742=21.21488.
Hence, the patient's GFR is 21.21488 mL/min/1.73m²."
3390,9,MDRD GFR Equation,lab test,decimal,pmc-4652317-3,Extracted,"A 15-year-old girl, who was suffered from ESRD since she was thirteen, was admitted to our hospital with dyspnea, chest pain, cellulitis, and osteomyelitis. Two months after admission, the patient had an operation with the diagnosis of septic knee arthritis. In the sonography performed 1 month later, renal stones were observed. The patient underwent HD and PD. Two days before transplantation, the BUN and Cr levels were 73 and 5.9 mg/dl, respectively. Before the operation, the patient had received methylprednisolone and vitamin B6. She underwent kidney transplantation from an independent living donor. Two days after transplantation, BUN and Cr levels were 24 and 1.4 mg/dl, respectively. The patient developed dyspnea and severe ascites and the urine volume decreased. Five days after transplantation, BUN and Cr levels increased (66 and 4 mg/dl, respectively). The leukocyte count also increased. Furthermore, renal transplant scintigraphy showed mild increased perfusion with reduced function of transplanted kidney with the evidence of dilated ureter (ureterovesical junction stenosis). Therefore, core needle biopsy of the transplanted kidney was done. Histopathologic view of the biopsy showed nonsignificant changes in glomeruli, moderate infiltration of lymphocytes accompanying edema in the interstitium, and marked Ox crystal deposition in some tubules and endarteritis consistent with type II acute T-cell-mediated rejection. Two months after transplantation, she developed avascular necrosis of the head of the femur. Finally, 9 months after transplantation, the nephrectomy was conducted due to graft failure. Renal transplant nephrectomy revealed excessive CaOx deposition. Subsequently, the peritoneal catheter was implanted which was functional for 1 month. At the end, she was again admitted with hyperkalemia and the patient died [Figures and ].","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [5.9, 'mg/dL'], 'age': [15, 'years']}",9.66345,9.18028,10.14662,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 15 years old. The concentration of Creatinine is 5.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 5.9^(-1.154) * 15^(-0.203) * 1 * 0.742=9.66345.
Hence, the patient's GFR is 9.66345 mL/min/1.73m²."
3391,9,MDRD GFR Equation,lab test,decimal,pmc-6993319-1,Extracted,"A 41-year-old woman was investigated in July 2016 for fatigue and loss of 10 kg over a few weeks. She was not taking any medication at this time and had no history of kidney disease. An abdominal computed tomography scan was performed in July, revealing a 13x13x10cm left adrenal mass of heterogeneous density with heterogeneous and prolonged enhancement after contrast agent administration. This mass was suggestive of ACC not associated with significant hormonal hypersecretion. Other lab results revealed plasma creatinine = 97 μmol/L, proteinuria = 0.7 g/g of urine creatinine, haemoglobin 9.9 g/dL, platelet 143 G/L.
Surgical procedure was planned in early-August, and no treatment was introduced.
At admission, she had stage 3 KDIGO AKI with plasma creatinine at 439 μmol/L and 0.99 g/24 h proteinuria. Urine sediment was normal. Blood pressure was 119/70 mmHg, there was no clinical sign of other organ involvement. She presented thrombocytopenia (67G/L) and mechanical hemolytic anemia: haemoglobin = 7.9 g/dL, reticulocyte = 175G/L, presence of schistocytes, Lactate Dehydrogenase (LDH) = 1058 UI/L and haptoglobin < 0.1 g/L. Extensive laboratory investigations were performed for the differential diagnosis of cytopenias. Antinuclear factors were negative, as were antibodies for antiphospholipid syndrome and scleroderma. ADAMTS 13 activity was 93%, complement investigations were normal (C4, C4, CH50, Factor I and H, anti-Factor H antibody).
The specific treatment of TMA consisted in daily plasma-exchange therapy of 60 mL/kg with plasma as replacement fluid. Intermittent hemodialysis was started on the same day. Left adrenalectomy was performed with splenectomy because of peroperative splenic decapsulation. A kidney biopsy was also performed.
ACC was confirmed by pathology, with a Weiss score at 6/9, Ki67 = 45% and 25 mitotic figures per 50 high-power field. The resection was total, and mesenteric lymphadenopathy was not metastatic, leading to stage III according to ENSAT classification. Renal pathology confirmed TMA. Twenty-six glomeruli were observed, of which 11 were ischemic with fibrin thrombi within glomerular capillary loops. Thrombi were present in interlobular arteries, arterioles and glomerular capillaries with fibrinoid deposit. No duplication of the glomerular basement membranes was found. There was moderate acute tubular necrosis with mild interstitial fibrosis and tubular atrophy (Fig. ).
Fourteen plasma-exchanges lead to correction of hemolysis, but the patient remained dialysis-dependent, and biological TMA reappeared a few days after plasma-exchange discontinuation. Owing to the isolated renal TMA, unfavourable renal prognosis according to pathology, kidney function evolution, and the lack of efficiency of terminal complement blockade in cancer-related TMA (CR-TMA), we decided not to escalate treatments and to undergo chronic hemodialysis.
Mitotane was started despite lack of pharmacokinetic knowledge on this treatment in hemodialysis patients, with a target plasma concentration between 14 and 20 mg/L. Eighteen months later, metastatic lesions occurred, leading to treatment by etoposide, doxorubicin and cisplatin. During all the follow-up, the patient remained anuric in hemodialysis and had persistent hemolysis with schistocytes, high LDH’s value and decreased haptoglobin. Twenty-four months after diagnosis, she died in a context of severe pneumonia.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [439.0, 'µmol/L'], 'age': [41, 'years']}",9.5884,9.10898,10.06782,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 41 years old. The concentration of Creatinine is 439.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 439.0 µmol. To convert 439.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 439.0 µmol Creatinine * 1e-06 mol/µmol = 0.00044 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00044 mol Creatinine * 113.12 g/mol = 0.04977 g Creatinine. To convert 0.04977 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.04977 g Creatinine * 1000.0 mg/g = 49.77 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 49.77 mg Creatinine/10.0 dL = 4.977 mg Creatinine/dL. The concentration value of 439.0 µmol Creatinine/L converts to 4.977 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 4.977^(-1.154) * 41^(-0.203) * 1 * 0.742=9.5884.
Hence, the patient's GFR is 9.5884 mL/min/1.73m²."
3392,9,MDRD GFR Equation,lab test,decimal,pmc-8567179-1,Extracted,"An 85-year-old woman with hypertension and chronic kidney disease (CKD) stage III (baseline creatinine approximately 1.70-1.80 mg/dL) presented to a hospital emergency department with 2 months of vaginal bleeding soaking 3 to 4 pads per day and dysuria. Hemoglobin was 9.4 g/dL and creatinine was 2.07 mg/dL on admission. Initial diagnostic computerized tomography (CT) of the abdomen and pelvis demonstrated marked endometrial thickening as well as bilateral mixed cystic and solid nodular masses inseparable from the uterus. In conglomerate the masses measured 13 × 9 × 9 cm (A-C). The patient had peritoneal metastases as well as extensive periportal and retroperitoneal lymphadenopathy.
Physical examination revealed pale clear tumor masses circumferentially filling the vaginal vault and approaching within 3 cm of the introitus; the tumor had parametrial extension but no rectal involvement. Vaginal biopsy was obtained and demonstrated high-grade carcinoma. Immunohistochemistry was positive for PAX-8, napsin A, pancytokeratin, and CK7. Stains were negative for WT-1 and CK20 and supported a diagnosis of clear cell carcinoma. CT chest was obtained to complete staging and was negative for pulmonary metastases. Work-up yielded a diagnosis of International Federation of Gynecology and Obstetrics stage IVB clear cell carcinoma of the endometrium. The patient was deemed not to be a surgical candidate and so was referred to radiation oncology for palliative radiation therapy.
Given her pain and bleeding, the patient was offered palliative radiation to the pelvis 20 Gy in 5 fractions or further dose escalation with lattice SBRT on a phase II clinical trial (NCT04553471). She consented to lattice SBRT and was simulated supine without intravenous contrast due to CKD. Iodinated KY jelly was placed intravaginally to help delineate the lower extent of the target volume. Planning target volume (PTV) 20 Gy (ie, PTV_2000) consisted of GTV_2000 with a 1-cm isotropic expansion, which was prescribed to 20 Gy in 5 fractions. PTV_6670 consisted of a geometric arrangement of spherical vertices, each with a diameter of 1.5 cm and a minimum of 4 cm of spacing from center-to-center, placed to achieve the desired rapid dose fall-off within GTV_2000. Each spherical vertex was prescribed to a dose of 66.7 Gy in 5 fractions as an SIB within GTV_2000. Specific care was taken to refrain from placing any high dose spheres within a vagina avoidance structure, which was designed by the treating radiation oncologist and located in the inferior third of the PTV_2000. A total of 7 high-dose spheres were placed within the superior two-thirds of GTV_2000, with appropriate separation from the surrounding organs-at-risk to ensure all clinical dosimetric planning guidelines were achieved. The volumetric-modulated arc therapy plan was delivered every other day. The patient tolerated treatment well with only grade 1 nausea, diarrhea, and fatigue, which were present before initiating lattice SBRT.
She was seen in a scheduled follow-up visit 4 days after the completion of therapy. Her gynecologic oncologist remarked on his examination that the vaginal tumor was “markedly diminished in size after radiation therapy but not gone.” He recommended proceeding with platinum-based chemotherapy, but the patient decided against initiation of chemotherapy at that time. Thirteen days after completion of radiation therapy, the patient was found down and bradycardic at home by emergency medical services after the reporting of seizure-like activity by her family. Family members also reported progressive weakness and diminished urine output for several days before this event. In the emergency room, the patient was noted to be minimally responsive and bradycardic with heart rate in the 20s and mean arterial pressure in the 30s, which improved with transcutaneous pacing, norepinephrine, and epinephrine drips. Admission labs are shown in .
Chest radiograph demonstrated dilatated pulmonary vasculature and bilateral lung opacities due to pulmonary edema. CT head was negative for acute intracranial pathology. CT abdomen and pelvis showed a smaller uterine tumor as well as extensive retroperitoneal, mesenteric, and pericardiophrenic lymphadenopathy and peritoneal metastases (). There was no evidence of obstructive nephropathy. Notably, the diagnostic CT was uploaded to the treatment planning system and the GTV_2000 was recontoured yielding a volume of 450 cm3, down from 625 cm3 at time of simulation (28% volume reduction).
The patient was treated with calcium gluconate, insulin-dextrose, albuterol, and sodium zirconium cyclosilicate for hyperkalemia and rasburicase for hyperuricemia. High-rate fluids titrated to a urine output of 100 cc/hr were administered to help with blood pressure, augment renal clearance, and prevent intrarenal crystallization during TLS. Renal dysfunction and metabolic derangements were progressive despite medical management, and the patient declined escalation of care with dialysis. The patient was discharged to home hospice 2 days after admission. She passed away at home.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [2.07, 'mg/dL'], 'age': [85, 'years']}",22.75832,21.6204,23.89624,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 85 years old. The concentration of Creatinine is 2.07 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.07^(-1.154) * 85^(-0.203) * 1 * 0.742=22.75832.
Hence, the patient's GFR is 22.75832 mL/min/1.73m²."
3393,9,MDRD GFR Equation,lab test,decimal,pmc-4752979-1,Extracted,"A 53-year-old CMV-seronegative man with hepatorenal polycystic disease who had been on hemodialysis for seven years underwent kidney transplant from a CMV-seropositive deceased donor in 2012.
The transplant was carried out without any surgical, immunological, or infectious complications. Immunosuppression was based on basiliximab induction therapy, followed by IV and then per os steroids tapered to a maintenance dose (oral prednisone 5 mg/die), tacrolimus (0.2 mg/kg/die to achieve trough level of 8–10 ng/mL for the first month and 5–8 ng/mL thereafter), and mycophenolic acid (720 mg/die). In view of the CMV R+/D− serological mismatch, the patient was given oral VGCV prophylaxis (900 mg/die based on renal function) for six months.
CMV pp65 antigenemia monitoring was negative during the patient's hospital stay and on discharge. He was discharged two weeks after transplant with serum creatinine up, 1.8 mg/dL. Serial outpatient follow-up showed a good kidney graft trend with serum creatinine up to 1.6 mg/dL at the one-month follow-up visit after transplant surgery. Laboratory tests 40 days after transplantation showed a serum creatinine increase to 1.9 mg/dL associated with raised blood immunosuppression levels (tacrolimus: 19.3 ng/mL). The patient reported diarrhea for several days. pp65 antigenemia monitoring now showed >300 cells and quantitative PCR assay of the viral genome showed 164,440 copies/mL.
The patient was admitted to hospital for further tests and treatment. On admission his general clinical status was good with normal vital parameters, no fever, and no diarrhea.
Chest X-ray and esophagogastroduodenoscopy (EGD) were negative. Biohumoral tests were normal except for serum creatinine, 2 mg/dL. Oral VGCV was suspended and IV GCV (5 mg/kg/12 h) initiated. Immunosuppression was adjusted with suspension of mycophenolic acid, also in light of his recent bowel symptoms, combined with reduced calcineurin inhibitor dose (to achieve tacrolimus trough level of 5 ng/mL).
Despite antiviral therapy, there was no reduction in CMV DNAemia. Ten days after the start of treatment, genetic screening for suspected drug resistance disclosed a mutation of the UL97 gene at codon C603W (substitution of cysteine for tryptophan) conferring resistance to VGCV and GCV []. Based on the algorithm recently confirmed in the Guidelines of the Transplantation Society [], GCV was suspended and antiviral therapy switched to foscarnet with dosage adjusted for the patient's weight and kidney function (6 g/die).
Foscarnet was infused at a concentration of 24 mg/mL with dilution prior to administration through a jugular venous catheter.
In light of several literature reports on the efficacy of mTOR inhibitors in GCV-resistant CMV infection [] our patient's immunosuppressive regimen was modified with the introduction of everolimus (trough level of 3–8 ng/mL) and a further reduction of tacrolimus dosage (trough level of 1–3 ng/mL). Mycophenolic acid was not used more.
Kidney function, blood count, and serum and urine electrolytes were monitored throughout treatment. Viral load was determined by PCR every three days.
Combination therapy with foscarnet and everolimus did not worsen kidney function. The patient presented three episodes of mild fever (up to 37.5°C) that resolved spontaneously. Calcium and magnesium supplementation were administered for transient hypocalcemia (7.5 mEq/L; range 9–10.7 mg/dL) and hypomagnesemia (1.1 mEq/L; range 1.4–1.85) with good response.
Two weeks after the start of foscarnet and everolimus combination therapy, the patient presented complete viral clearance (negative PCR) so foscarnet was suspended maintaining the immunosuppression regimen with everolimus (trough level of 3–8 ng/mL) and tacrolimus (trough level of 1–3 ng/mL). The patient was discharged with a serum creatinine level of 1.6 mg/dL. Subsequent PCR assays for CMV remained negative (<500 copies) and kidney function was stable (). The patient was monitored by DNA PCR testing every three months for two years. One year after transplant kidney function was 1.6 mg/dL with negative DNAemia.
One-year protocol kidney allograft biopsy disclosed no signs of CMV infection or graft rejection but only aspecific mild focal chronic parenchymal changes (Banff 2013 score: acute alterations: all negative; chronic alterations: interstitial fibrosis 2+, tubular atrophy 1+, arterial fibrointimal thickening, negative transplant glomerulopathy, and arteriolar hyalinosis; negative peritubular capillaries C4d deposition; CMV and BKV nephropathy, both negative). At three-year follow-up the patient's serum creatinine level is 1.3 mg/dL with persistently negative CMV infection. His immunosuppressive regimen remains unchanged.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'age': [53, 'years'], 'creatinine': [1.3, 'mg/dL']}",57.74567,54.85839,60.63295,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 53 years old. The concentration of Creatinine is 1.3 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.3^(-1.154) * 53^(-0.203) * 1 * 1=57.74567.
Hence, the patient's GFR is 57.74567 mL/min/1.73m²."
3394,9,MDRD GFR Equation,lab test,decimal,pmc-4531723-1,Extracted,"A 66-year-old man was admitted to Keimyung University Hospital because of decreased urine output and right upper quadrant pain. Seven years earlier, he had a Whipple’s operation for obstructive jaundice due to Ampulla of Vater cancer. At that time, the pathology report showed a moderately differentiated adenocarcinoma and biopsies of the regional lymph nodes showed no evidence of metastasis. At that time, renal function was normal and the urine contained no proteins or red cells. Two weeks before admission, the patient developed right upper quadrant dull pain, nausea, anorexia, myalgia, chills and fever. Four days prior to admission, he noticed gross hematuria, marked decrease in urine output and edema in lower extremities. On admission, his body temperature was 36.4°C and blood pressure was 110/60 mmHg. Daily urine output ranged 800–1200 mL. Face was puffy. He did not have icterus. His conjunctivae was slight anemic and revealed several petechial hemorrhages. Auscultation of the lung revealed bilateral basilar rales. No murmurs or frictions were heard. The liver was enlarged and tender. There was no splenomegaly or rash. There was marked costovertebral angle enderness. here was mild pretibial edema. Laboratory data on admission showed WBC 34,600/mm3, hemoglobin 8.3 g/dL, platelet count 95,000/mm3, BUN 16.4 mmol/L, serum creatinine 985,6 μmol/L, cholesterol 118 mg/dL, total bilirubin 3.4 mg/L, alkaline phosphatase 270 IU/L, SGPT 18 IU/L, and serum albumin 2.0 g/dL and creatinine clearance 2.5 ml/min. Urinalysis showed specific gravity 1.020, protein 2+, and urinary sediment containg two granular casts, many red blood cells and 10 white blood cells/HPF. The 24-hour urinary protein excretion was 2.4 gm and FENa was 1.7%. C3 level was 0.67 g/L (normal range: 0.8–1.2 g/L) and C4 level was 0.46 g/L (normal range: 0.2–2.5 g/L). Cryoglobulin was absent. The tests for hepatitis B and C, antinuclear antibody and rheumatoid factor were negative. Chest radiographs demonstrated bilateral perihilar pulmonary congestions. On admission, he was afebrile. He had obvious pulmonary edema as well as peripheral edema. Immediate hemodialysis resulted in a weight loss of 2 kg and respiratory improvement. Ultrasonographic examination of liver showed ill marginated cystic mass in left lobe. Computed tomography (CT) of the abdomen demonstrated 7×5cm sized multiple septated lower density lesions in medial segment of left lobe of the liver (). Numerous blood cultures were negative. Initially the patient was treated with diuretics, albumin infusions and antibiotics (sulbactam/cefoperazone and aztreonam). On the 15th day, percutaneous needle biopsy of the kidney was performed. Light microscopy showed 17 glomeruli with two global sclerosis. The glomeruli showed endo-and extracapillary proliferation (), with cellular crescents involving 25% of the glomeruli. The interstitium showed diffuse edema and no tubular necrosis. Immunofluorescent examination showed a diffuse granular staining with anti-IgG and anti-C3 along the capillary wall, and no staining with anti-IgM or anti-IgA (). Needle aspiration of the liver was performed on the 19th hospital day, with the drainage of greenish pus material. Culture of the liver aspirates later grew Pseudomonas aeruginosa. Ticarcillin was given. The patient improved substantially. The levels of BUN and serum creatinine declined progressively and stabilized at 5.7 mmol/L and 176 μmol/L, respectively, by the 25th hospital day. One month after admission, the laboratory findings were : BUN 5.5 mmol/L, serum creatinine 176 μmol/L, hemoglobin 8.1g/dL. WBC 5,430/mm3 and platelet count 208,000/mm3. The 24-hour urinary protein excretion was 4.4 g/day. Follow-up CT showed almost complete resolution of previous abscess in the liver. He was discharged on the 40th hospital day with the serum creatinine level of 167 μmol/L.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [985.6, 'µmol/L'], 'age': [66, 'years']}",4.60169,4.37161,4.83177,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 66 years old. The concentration of Creatinine is 985.6 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 985.6 µmol. To convert 985.6 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 985.6 µmol Creatinine * 1e-06 mol/µmol = 0.00099 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00099 mol Creatinine * 113.12 g/mol = 0.11199 g Creatinine. To convert 0.11199 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.11199 g Creatinine * 1000.0 mg/g = 111.99 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 111.99 mg Creatinine/10.0 dL = 11.199 mg Creatinine/dL. The concentration value of 985.6 µmol Creatinine/L converts to 11.199 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 11.199^(-1.154) * 66^(-0.203) * 1 * 1=4.60169.
Hence, the patient's GFR is 4.60169 mL/min/1.73m²."
3395,9,MDRD GFR Equation,lab test,decimal,pmc-4957720-1,Extracted,"A 40-year-old woman with ESRD, native kidney disease (NKD) being adult polycystic kidney disease, had been on twice weekly maintenance hemodialysis (MHD) and EPO therapy for 10 months. She underwent live unrelated renal transplantation in August 2013 and was on triple drug immunosuppression with tacrolimus, mycophenolate mofetil (MMF) and prednisolone, along with valgancyclovir prophylaxis for 3 months and cotrimoxazole prophylaxis for 6 months. In the early post-transplantation period, she had antibody-mediated and borderline cellular rejection, which responded to pulse steroid and plasmapheresis with her creatinine reaching 1.3 mg/dL. She was discharged with hemoglobin (Hb) of 12.1 g%. Nine months later, she presented with symptoms suggestive of anemia ongoing for the previous 3 months and she had received 22 units of packed red cell transfusions during this period. The Hb was 4.0 g%, while total leucocyte counts and platelet counts were normal. The serum creatinine at this presentation was 0.9 mg/dL. The peripheral blood smear showed normocytic and normochromic anemia with a reticulocyte count of 0.1%. The patient was advised after developing anemia to stop MMF for a brief period of time, but had no improvement.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [0.9, 'mg/dL'], 'age': [40, 'years']}",69.34704,65.87969,72.81439,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 40 years old. The concentration of Creatinine is 0.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.9^(-1.154) * 40^(-0.203) * 1 * 0.742=69.34704.
Hence, the patient's GFR is 69.34704 mL/min/1.73m²."
3396,9,MDRD GFR Equation,lab test,decimal,pmc-4421251-1,Extracted,"A 58-year-old woman with nephropathy caused by type 2 diabetes received a cadaveric renal transplant in May 2003. The function of the transplant was unproblematic. She had standard triple immunosuppression with cyclosporine, mycophenolate mofetil and methylprednisolone. Early on, the dose of mycophenolate was reduced to 500 mg daily due to the elevation of liver enzyme activities. The cyclosporine dose had stabilized at 150 mg and 175 mg every other day, divided into two daily doses, with which the blood cyclosporine level was in the upper target range of 90–140 ng/ml as tested by the fluorescence polarization assay. Other medications included bisoprolol, felodipine, telmisartan, furosemide, simvastatin, gabapentin, subcutaneous glargine and aspart insulin, and topical timolol and iopidine for glaucoma. In May 2006, allopurinol was started for hyperuricaemia. In August 2006, her blood cyclosporine level was 142 ng/ml while serum creatinine was 110 μmol/l.
In August 2006, an ophthalmologist detected severe neovascular glaucoma, and acetazolamide 125 mg t.i.d. was started. A week later, the patient reported having nausea and heartburn. In September, gastroduodenitis and oesophagitis were detected by gastroscopy. Pantoprazole 40 mg daily was started. In November 2006, on a routine control, a high cyclosporine level of 265 ng/ml was detected with slightly elevated serum creatinine (113 μmol/l). Cyclosporine concentration was controlled immediately and a high level of 239 ng/ml was again detected. The dose of cyclosporine was reduced to 150 mg daily. A week later, her cyclosporine level was still 187 ng/ml and slight tremor of the hands was noted as a possible sign of cyclosporine toxicity. Three weeks later, cyclosporine level was 220 ng/ml. The dose of cyclosporine was then reduced to 125 mg daily. Subsequently, the blood cyclosporine level started to gradually decrease and stabilized at the level of 99 ng/ml.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [113.0, 'µmol/L'], 'age': [58, 'years']}",44.26326,42.0501,46.47642,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 58 years old. The concentration of Creatinine is 113.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 113.0 µmol. To convert 113.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 113.0 µmol Creatinine * 1e-06 mol/µmol = 0.00011 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00011 mol Creatinine * 113.12 g/mol = 0.01244 g Creatinine. To convert 0.01244 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01244 g Creatinine * 1000.0 mg/g = 12.44 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 12.44 mg Creatinine/10.0 dL = 1.244 mg Creatinine/dL. The concentration value of 113.0 µmol Creatinine/L converts to 1.244 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.244^(-1.154) * 58^(-0.203) * 1 * 0.742=44.26326.
Hence, the patient's GFR is 44.26326 mL/min/1.73m²."
3397,9,MDRD GFR Equation,lab test,decimal,pmc-4421192-1,Extracted,"A 46-year-old Asian man with chronic kidney failure due to tuberculosis received a deceased donor kidney transplant in February 2000. He received triple immunosuppressive therapy consisting of tacrolimus, mycophenolate mofetil (MMF) and prednisolone. His subsequent course was uneventful until 2 years post-transplantation (February 2002) when a rise in serum creatinine to 2.1 mg/dL (190 umol/L) prompted a kidney biopsy. The biopsy showed severe polyomavirus nephropathy (PVN) stage B [], and BK virus (BKV) DNA was identified in urine and serum by PCR. Cyclosporin A and azathioprine were substituted for tacrolimus and MMF. Over the following 6 years, creatinine was stable at 2.1–2.3 mg/dL (190–200 umol/L); BKV DNA remained detectable in the serum at fluctuating low levels of 422–570 copies/mL (2.63–2.76 log10 copies/mL) on the seven occasions when it was measured over these 6 years. Regular urine cytology was performed in the first 2 years following the diagnosis of PVN with no malignant cells seen. In May 2007, urine examination showed a small number of red cells (20 × 106 RBC/L) and in December 2007 urine examination showed 600 × 106 RBC/L. Subsequent urine cytology revealed malignant cells; no definite ‘decoy cells’ were seen. The patient was referred to a urologist, and during cystoscopy urinary bladder biopsies were performed. These showed a high-grade urothelial carcinoma with invasion of the muscularis propria and a focal invasive micropapillary pattern. On immunohistochemistry, the tumour showed diffuse strong nuclear staining for Simian virus 40 (SV40) T-antigen (T-Ag) and P53 in >90% of cells (Figure ). No normal mucosa was present.
The patient underwent cystectomy with ileal conduit formation and removal of the left native kidney. Within the cystectomy specimen, residual high-grade urothelial carcinoma with invasion into perivesical fat and prominent lymphovascular space invasion was seen (Figure ). The tumour showed a predominant invasive micropapillary pattern. Elsewhere, the urothelium showed focal evidence of in situ carcinoma (Figure ). No polyomavirus nuclear changes were evident in the non-malignant urothelium, and there was no convincing cystitis. Diffuse strong expression of SV40 T-Ag was seen in both the invasive and in situ carcinoma (Figure ), whereas the non-malignant urothelium and atrophic native kidney were negative. P53 also showed diffuse strong nuclear staining in the malignant epithelium in both the in situ and invasive tumour, exactly mirroring the SV40 T-Ag staining (Figure ).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [2.1, 'mg/dL'], 'age': [46, 'years'], 'Race': 'Asian'}",34.17096,32.46241,35.87951,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 46 years old. The concentration of Creatinine is 2.1 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2.1^(-1.154) * 46^(-0.203) * 1 * 1=34.17096.
Hence, the patient's GFR is 34.17096 mL/min/1.73m²."
3398,9,MDRD GFR Equation,lab test,decimal,pmc-7155866-1,Extracted,"A 20-year-old female with no significant disease history presented with nausea, vomiting, fatigue and easy bruising to an urgent care. Patient was given antiemetics and subsequently sent home. Routine labs done during the encounter showed acute renal failure (creatinine 2.8mg/dL) with small amount of proteinuria and hematuria, elevated serum protein 11.3gm/dL while albumin was 2.6mg/dL, macrocytic anemia (Hb 8.1 g/dL and MCV 99 fL) with mild thrombocytopenia (platelets count 122 k/uL) and prolonged PTT (65 s). The patient was called back in and further questioning revealed that she had been having increased bleeding and easy bruising for the last 1 month. She would bleed every time when she brushed her teeth. She also stated that she lost about 30 lbs in the past few months. The patient was not in the usual age bracket for MM but workup was sent. Serum protein electrophoresis (SPEP) showed that a large protein spike is noted in the beta region. Urine studies showed elevated excretion of monoclonal lambda light chains 167mg/dL (normal 0.02 - 0.67), kappa/lambda ratio < 0.01 (normal 2.04 - 10.37), urine protein > 3 g. Urine IFE showed a monoclonal IgA heavy chain with associated lambda light chain and excess monoclonal free lambda light chains.
For elevated PTT mixing study was done which didn’t correct the PTT suggesting presence of inhibitor. No lupus anticoagulant was detected. Platelet function ADP and platelet function epinephrine were elevated. Factor X levels were low at 40% (normal 81-157%). Factor VIII and von Willebrand factor were at normal levels. Echo revealed normal EF of 67% and mild pulmonary HTN at about 46 mm Hg. Bone survey was negative for any lytic or blastic lesions. Renal biopsy showed acute tubular injury with atypical lambda chain casts consistent with light chain cast nephropathy. Bone marrow (BM) biopsy () revealed 90% plasma cells and FISH analysis showed 1q21 (CKS1B) mutation. The diagnosis of MM was made but certain characteristics of the patient suggested amyloidosis. Further workup was sent including Congo red stain of the BM sample which came out as negative. Abdominal fat pad biopsy and cardiac MRI are currently pending as outpatient. The patient was started on cyclophosphamide, bortezomib and dexamethasone during this admission. The patient’s renal function subsequently improved. She was discharged and given follow-up with an oncologist.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [2.8, 'mg/dL'], 'age': [20, 'years']}",21.54331,20.46614,22.62048,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 20 years old. The concentration of Creatinine is 2.8 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.8^(-1.154) * 20^(-0.203) * 1 * 0.742=21.54331.
Hence, the patient's GFR is 21.54331 mL/min/1.73m²."
3399,9,MDRD GFR Equation,lab test,decimal,pmc-8301726-1,Extracted,"Here, we report the case of a 60-year-old Caucasian male patient with a past medical history of diabetes mellitus type 2, coronary artery disease, atrial fibrillation, hypertension, obstructive sleep apnea, chronic kidney disease stage 3, and nonalcoholic steatohepatitis. The patient had a recent hospital admission due to a surgical C2-C3 epidural abscess which was treated with drainage and spinal C2-C5 laminectomy and fusion, initially manifesting as quadriparesis. Abscess cultures were positive for methicillin-sensitive Staphylococcus aureus, and he was completing his six-week treatment of intravenous (IV) cefazolin in a skilled nursing facility after hospitalization. Nearly 10 days after hospital discharge, the patient started developing diffuse abdominal pain, decreased appetite, poor oral intake, and diarrhea. He tested positive for C. difficile and was started on oral vancomycin. Two days after starting the antibiotic, his clinical status rapidly declined with worsening diarrhea, oliguria, and hypotension. Although he was initially transferred to a regular floor in another hospital, he was admitted to our ICU two days later with septic shock, respiratory failure, and acute kidney injury.
In the ICU, his workup at admission showed pH 7.061, PCO2 28 mmHg, PO2 127 mmHg, HCO3 7.9 mEq/L, creatinine 4.54 mg/dL, blood urea nitrogen 152 mg/dL, potassium 4.4 mEq/L, lactate 9.0 mmol/L, WBC 14.35 × 109/L with a neutrophil count of 88%. C. difficile stool antigen and toxin genes were positive confirming the results of the external facility. Admission CT of the abdomen and pelvis showed a marked diffuse colonic wall thickening with adjacent fat stranding, suggestive of colitis without dilated bowel (maximum right colon dilation of 4 cm) and nodular contour of the liver, suggestive of hepatic cirrhosis (Figures -). Upon arrival to our facility, the patient required immediate intubation and use of vasopressors; he was started on IV fluids, norepinephrine, and later on vasopressin. The antibiotic coverage for the septic shock was empiric use of IV vancomycin and piperacillin/tazobactam. CDI treatment was done with oral vancomycin 500 mg QID and IV metronidazole 500 mg TID. Nephrology was consulted for acute renal failure and the patient was dialyzed on the same day. General surgery was consulted; however, due his to critical condition and associated comorbidities, the patient was deemed to be a poor surgical candidate. Two days after admission to the ICU, the patient presented with worsening diarrhea with watery bloody stools. Another CT of the abdomen and pelvis (Figures -) showed a worsening of colitis inflammation/infection besides an improvement in the WBC count (8.42 × 109/L with a neutrophil count of 87.9%). Fidaxomicin was started, and within 24 hours of treatment, the patient had a rapid clinical stabilization with a reduction in diarrhea volume and a significant reduction in the use of vasopressors. The patient was extubated and transferred to the regular floor in four days. He completed a total of seven days of IV vancomycin and piperacillin/tazobactam and 15 days of IV metronidazole; fidaxomicin was continued for 10 days.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [4.54, 'mg/dL'], 'age': [60, 'years'], 'Race': 'White'}",13.29936,12.63439,13.96433,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 60 years old. The concentration of Creatinine is 4.54 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 4.54^(-1.154) * 60^(-0.203) * 1 * 1=13.29936.
Hence, the patient's GFR is 13.29936 mL/min/1.73m²."
3400,9,MDRD GFR Equation,lab test,decimal,pmc-4421284-1,Extracted,"This was a 51-year-old Caucasian man who had delivered renal stones (composed of uric acid and calcium oxalate) in 1995 and 2002; he was also suffering from a mild renal insufficiency (1.7 mg/dl serum creatinine, 150 μmol/l). In April 2005, while receiving nephrological consultation at a different hospital, he presented with a moderate renal insufficiency (3.5 mg/dl serum creatinine, 310 μmol/l); serum and urinary uric acid as well as blood pressure was normal, and a microscopic lithiasis was found at renal scan. He was treated with citrate, allopurinol and hydrochlorothiazide as well as a low calorie, low protein and low sodium diet. He lost 10 kg weight over 5–6 months, and diuretic therapy was stopped following a lipotimic episode. In January 2006, he was admitted to our hospital because of protracted nausea, vomiting and general fatigue over the previous 3 weeks. He showed signs of dehydration with orthostatic hypotension, severe hyponatraemia (114 mmol/l Na+) and metabolic acidosis (14 mmol/l HCO3−); we diagnosed advanced non-oliguric renal failure (12 mg/dl serum creatinine, 1060 μmol/l) and he began haemodialysis. Uricaemia was in the normal range or only slightly above the upper limit. He showed microscopic haematuria and light proteinuria, without crystalluria.
A percutaneous renal biopsy showed severe tubulointerstitial nephritis with birefringent needle-shaped crystalline precipitate in tubular lumen, tubular epithelium and interstitium. Extensive tubular atrophy, interstitial chronic inflammation and fibrosis, foreign body-type reaction, with no glomerular changes, were also observed (Figure ). During histological examination, we were unable to determine whether crystalline deposits were of uric acid or 2,8-DHA.
Because the clinico-pathological features and laboratory findings were inconsistent with uric acid nephropathy, we performed a biochemical and molecular biological evaluation for suspected APRT deficiency. A pathological presence of adenine in serum and urine was identified and APRT enzyme activity was absent. Molecular biological analysis of the amplified APRT gene revealed a homozygous 254 bp deletion–8 bp insertion in exon 3. These results confirmed that our patient had APRT deficiency []. Although a diet poor in purine content and allopurinol was given, there was no improvement in renal function.
The patient's parents were native to two areas from the middle portion of Italy and were not related; both had many siblings, some of which had left the country. Some of these relatives were offered screening by biochemical assay for the presence of adenine in urine and serum, by erythrocyte APRT activity and by molecular biological analysis of the APRT gene []. As showed in Figure , a first cousin was homozygous and a sister and two first cousins were healthy; all other relatives were carriers for the same APRT gene mutation. In heterozygotes, APRT enzymatic activity was reduced (Table ), but serum and urinary adenine concentrations were non-detectable.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [12.0, 'mg/dL'], 'age': [51, 'years'], 'Race': 'White'}",4.4774,4.25353,4.70127,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 51 years old. The concentration of Creatinine is 12.0 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 12.0^(-1.154) * 51^(-0.203) * 1 * 1=4.4774.
Hence, the patient's GFR is 4.4774 mL/min/1.73m²."
3401,9,MDRD GFR Equation,lab test,decimal,pmc-2566561-1,Extracted,"This is a 55 years old woman presented at our institute. We were so surprised at the first moment we saw this woman and we kept thinking what could be this bulge under her clothes (figure ), we thought she is hiding a bag under her clothes as it is a habit for some Egyptian farmers to keep precious things in a bag or big wallet fixed to a belt under their clothes, but then as she started to tell us about her medical history we discovered that this a huge incisionl hernia.
She had an operation 19 years ago – elsewhere – to remove a branched stone from her right kidney and admitted for two months into the hospital at this time as she had troubles with her surgical wound and she had repeated secondary sutures. She had repeated blood transfusions during and after that operation.
The hernia is in the right lumbar region, has a smooth surface, shows expansile impulse on coughing, there are some dilated veins on its surface, there is no tenderness, it has a uniform consistency, mobile, there are no pulsations, it contains large and small intestine, partially reducible, the defect is about 10 cm in diameter and there are no complications (figure , ).
This woman had left nephrectomy two years ago as a treatment for painful non functioning kidney (advanced hydronephrotic with immeasurable cortex with multiple stones inside) and she is living now with only functioning right kidney with serum creatinine 1.1 mg % and blood urea 38 mg %.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [1.1, 'mg/dL'], 'age': [55, 'years']}",51.5681,48.98969,54.14651,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 55 years old. The concentration of Creatinine is 1.1 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.1^(-1.154) * 55^(-0.203) * 1 * 0.742=51.5681.
Hence, the patient's GFR is 51.5681 mL/min/1.73m²."
3402,9,MDRD GFR Equation,lab test,decimal,pmc-7393746-1,Extracted,"A 52-year-old woman presented with intermittent left lower quadrant pain that had started in 2017. She was diagnosed with systemic lupus erythematosus 19 years ago and had been taking oral corticosteroids since then. Her past medical history also showed steroid-induced diabetes mellitus, hypertension, and hypothyroidism, which was treated with levothyroxine. Menopause occurred when she was in her thirties.
On her first visit to the emergency department in another tertiary hospital in May 2018, she underwent abdominal pelvic computerized tomography (APCT), which showed a multiloculated lesion on the left adnexa, with left ovary involvement and hydrosalpinx or pyosalpinx. Under the impression of a TOA, she was admitted and received conservative care including intravenous (IV) antibiotics for 15 days. However, the pain in her left lower quadrant persisted. She visited the emergency department for the second time in July 2018. APCT was performed again, which revealed a slightly increased multiloculated, rim-enhancing lesion compared with the previous APCT findings. Again, the impression was TOA; however, APCT showed a newly developed wall enhancement of the left ureter due to either secondary change or combined ureteritis. Because of persistent pain, she agreed to undergo surgery. On August 3, 2018, the patient underwent laparoscope-guided bilateral salpingo-oophorectomy. The pathology report showed chronic active inflammation with foam cell collection in her left ovary and both salpinges.
Because the surgery did not alleviate her pain, she underwent both APCT and magnetic resonance imaging in April 2019, which revealed a 7-cm irregular mass in her left adnexa and an infiltrative lesion in her uterus, suggestive of endometrial cancer. Imaging results also showed left ureter invasion by the left adnexal tumor. As prophylactic management, a left ureter stent was inserted. Furthermore, she underwent dilatation and curettage for diagnosis. Pathological examination showed chronic active inflammation with foam cell collection, consistent with the finding in the previous laparoscopic surgery.
The patient visited the emergency department of our hospital on May 20, 2019. She had sepsis and a body temperature of >39°C; blood culture revealed the presence of extended-spectrum beta-lactamase–producing Escherichia coli. The cervix culture taken at the emergency department also showed the presence of the same organism. Her initial blood urea nitrogen level was 45.6 mg/dL, and her creatinine level was 2.75 mg/dL, which implied septic postrenal acute kidney injury. For septic shock evaluation, she underwent APCT without contrast, which revealed newly developed mild hydronephrosis of the left kidney. The left adnexal mass remained the same as that seen in April 2019 (). We started initial shock management in the emergency department and conservative care including an IV antibiotic (meropenem) for bacteremia and left percutaneous nephrostomy (PCN) for left hydronephrosis and acute kidney injury.
After her recovery from septic shock, the patient underwent debulking surgery on June 4, 2019. During the surgery, severe adhesion in the pelvis involving the peritoneum, rectum, uterus, and left ureter was noted. Multiple hard and catheter-shaped foreign body–like materials were observed in the left parametrium and left pararectal space and near the left internal iliac artery. Caseous necrotic materials had spread deep into the left pelvic and paravaginal space. Total hysterectomy and debulking operation of the left pelvic mass, including left pelvic lymph nodes, were performed.
The final pathology showed foamy histiocyte aggregation and acute and chronic inflammation with numerous Michaelis-Gutmann bodies, consistent with malakoplakia (). According to the recommended treatment for malakoplakia, we continued IV administration of tazoperan after the surgery. After the culture from peritoneal fluid cytology showed ceftazidime-sensitive E. coli, we changed the antibiotic to ceftazidime 1 g twice a day.
However, her creatinine level increased gradually to 4.48 mg/dL after the surgery. A retrograde pyelogram showed patent left ureter and dye spillage from the right ureter. Right PCN was performed. A computerized tomography scan performed on postoperative day 9 showed recurrence of a 9-cm mass in her left pelvis. Hence, we again administered tazoperan. On postoperative day 21, the patient was referred to a general hospital for further conservative care with IV antibiotics.
On July 24, approximately 1.5 months after surgery, she underwent left PCN removal and right PCN clamping. On August 2, the patient returned to the emergency department with complaints of fever and right flank pain that had started on the previous day. She presented with right costovertebral angle tenderness and pyuria and was admitted to the urology department with a diagnosis of right acute pyelonephritis. On August 9, the anterograde pyelogram showed leakage at the right ureter, which was similar to the previous retrograde pyelogram finding. Right PCN exchange was performed. After conservative care with IV antibiotics, the patient was discharged on August 12. On September 10, direct ureteroneocystostomy was attempted; however, only right PCN exchange was performed because the ureter was short.
The patient has been closely followed up through outpatient visits to both urology and obstetrics and gynecology departments.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [4.48, 'mg/dL'], 'age': [52, 'years']}",10.31617,9.80036,10.83198,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 52 years old. The concentration of Creatinine is 4.48 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 4.48^(-1.154) * 52^(-0.203) * 1 * 0.742=10.31617.
Hence, the patient's GFR is 10.31617 mL/min/1.73m²."
3403,9,MDRD GFR Equation,lab test,decimal,pmc-6369133-1,Extracted,"A 20 yr old male patient was referred from a peripheral hospital to our institution intensive care unit having been operated on for perforated duodenal ulcer. He had presented with a long- standing history of peptic ulcer disease and had developed sudden onset of severe abdominal pain a day prior to admission. A plain radiograph done revealed free air under the diaphragm. Surgical intervention of a modified Grahams patch for a perforated duodenal ulcer was done. Post operatively, he was referred to due acute kidney injury(AKI).
At the ICU, his vital signs were an elevated heart rate of 140bpm, increased respiratory rate of 36 breaths per minute, low blood pressure of 80/50 mmHg and his temperature was 36.5°c. On examination, he had purulent discharge from his abdominal drain. His serum creatinine was elevated at 254 mmol/L (65–130) with an increased Blood Urea Nitrogen of 18.8 mmol/L (1.7–8.3). The arterial blood gas analysis (BGA): PH-7.354, PCO2 -3.57 kPa, PO2 – 8.26 kPa, HCO3 – 14.6 mmol/L, Base Excess- -9.6 mmol/l and SPO2 -91.3%. He was admitted with a diagnosis of hypovolaemic shock with intra-abdominal sepsis, compensated metabolic acidosis, and AKI. His initial management was intravenous fluids, empirical antibiotics: ceftriaxone, metronidazole and analgesics.
The patient was taken to theatre and intra operatively, 2 litres of purulent bilous material was found in the peritoneum and the previous repair had given way and there was now a large duodenal perforation with friable edges measuring approximately 1 cm in size at D1. A pyloric exclusion was done with a Roux-and-Y gastrojejunostomy and peritoneal lavage was done. Abdominal drains were left in-situ and he was taken back to the ICU.
The patient remained stable post operatively but was noted to have pus oozing from the incision site on post-op day three and on day four upon release of sutures he had a burst abdomen. He was also noted to be febrile with temperatures of 39 °C. An emergency laparotomy revealed a duodenal stump blow-out. Peritoneal lavage and repair of the duodenal stump was done and a “Bogota bag” as a method of temporary abdominal wall closure was chosen. He went to theatre twice weekly for peritoneal lavage and change of Bogota bag for an initial period of three weeks due to pus exudate from the abdomen and abdominal drains but as the effluent reduced, he went on demand basis. His clinical outlook was generally improving however the intra-abdominal infection persisted. The challenges we faced with the patient’s deranged physiology while in ICU are tabled as shown on .
shows the microbial profile that was grown and the antibiotic sensitivity patterns. These are most likely hospital acquired infections. His urinary cultures only once grew candida and all his tracheal aspirates grew nothing on culture. His antibiotic treatment changed from the empirical treatment with ceftriaxone and metronidazole and was tailored as per microscopy, culture and sensitivity results. Throughout his stay in the ICU he was put on H.pylori treatment, thromboprophylaxis, total parenteral nutrition and two hourly turning in bed to avoid bed sores.
After the fifteen laparotomies of which 12 were planned, the repair held and the intra-abdominal sepsis was controlled. The patient developed an entero-atmospheric low output fistula that was managed conservatively. He started passing stool ten weeks after his admission and he was allowed to feed orally as the parenteral nutrition was weaned off. Granulation tissue formed over his bowel and the low output fistula eventually closed. The patient was transferred from ICU to the ward having stayed there for ten weeks. The wound continued to be dressed in the ward for the next 2 months and healed with formation of a large ventral wall hernia. He was discharged home to be reviewed by the plastic surgery team at the surgical outpatient clinic to plan for reconstruction of the abdominal wall at a later time.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [254.0, 'mmol/L'], 'age': [20, 'years']}",0.00973,0.00924,0.01022,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 20 years old. The concentration of Creatinine is 254.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from mmol to mg. The mass of Creatinine is 254.0 mmol. To convert 254.0 mmol of Creatinine to mol, multiply by the conversion factor 0.001, giving us 254.0 mmol Creatinine * 0.001 mol/mmol = 0.254 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.254 mol Creatinine * 113.12 g/mol = 28.73248 g Creatinine. To convert 28.73248 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 28.73248 g Creatinine * 1000.0 mg/g = 28732.48 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 28732.48 mg Creatinine/10.0 dL = 2873.248 mg Creatinine/dL. The concentration value of 254.0 mmol Creatinine/L converts to 2873.248 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 2873.248^(-1.154) * 20^(-0.203) * 1 * 1=0.00973.
Hence, the patient's GFR is 0.00973 mL/min/1.73m²."
3404,9,MDRD GFR Equation,lab test,decimal,pmc-6323407-1,Extracted,"A 67-year-old Japanese man with hypertension, hyperlipidemia, and a history of smoking presented with claudication and leg numbness. He had no history of diabetes mellitus. His ankle brachial index (ABI) was low at 0.48 (right)/0.51 (left). Abdominal aortic bruit was audible in the epigastrium of the umbilicus area. Carotid and femoral bruits were not audible. Bilateral dorsal and dorsalis pedis arteries were impalpable. Computed tomography revealed that his whole aorta was severely calcified, and aortic arch aneurysm, infrarenal abdominal aortic aneurysm, and left internal iliac artery aneurysm were detected. Furthermore, suprarenal abdominal aortic stenosis with severe calcification was identified (Fig. ). The root of his right renal artery was totally occluded, and his right kidney was atrophied; the left kidney was not atrophic (Fig. ). His clinical course is presented in Figure . His initial serum creatinine (sCr) level was 1.97 mg/dL, but increased within 2 months. He was admitted to the hospital based on the suspicious of decreased renal blood flow leading to rapid progression of kidney dysfunction. On admission, his sCr was 4.83 mg/dL. Urinary examination revealed that proteinuria was ±0.24 g/gCr, and hematuria was not detected (main laboratory data are shown in Table ). Aortic and renal artery angiography was performed. There was severe suprarenal abdominal aortic stenosis; no significant stenotic lesion was detected in his left renal artery. The pressure gradient at the stenotic aorta was approximately 60 mm Hg. These results indicated that severe aortic stenosis caused renal ischemia, resulting in deteriorating renal function. Percutaneous plain balloon angioplasty was done with 8.0/40 and 10.0/40 mm balloons. After EVT to the stenotic aorta, his renal function was temporarily improved, but later worsened because of dehydration, the use of an angiotensin receptor blocker (ARB), and severe anemia. He required hemodialysis for a short period. After the dehydration and anemia were improved, and ARB was discontinued, his renal function stabilized with an sCr of approximately 2.0–2.5 mg/dL. Six months from his first admission to our hospital, reconstructive surgery to the suprarenal abdominal aortic stenosis and infrarenal abdominal aortic aneurysm was performed. The abdominal aorta was replaced with a 24-mm (4 branched J Graft, Japan Lifeline, Japan) and 20-mm (bifurcated J Graft, Japan Lifeline) artificial grafts. The celiac artery, superior mesenteric artery, and left renal artery were reconstructed with an artificial graft, while the bilateral internal iliac artery and right renal artery were sacrificed. After the operation, sCr was temporarily decreased at 1.69 mg/dL, but renal dysfunction progressed again after 3 weeks (sCr level 3.20 mg/dL). Because echography and computed tomography indicated stenotic anastomosis to his left renal artery, EVT to the anastomosis of the renal artery was performed. A 6.0/18 mm Palmaz Genesis (Cardinal health company, Japan) stent and a 3.5/18 mm BMX-J (Biosensors, Japan) stent were implanted via left radial artery (Fig. ). After EVT, his renal function markedly improved and his sCr level was 1.06 mg/dL. Urinary protein was not significantly increased after EVT. His blood pressure was decreased, and he did not require any blood pressure-lowering agents. His renal function has been preserved with an sCr of approximately 1.0 mg/dL for 6 months.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.06, 'mg/dL'], 'age': [67, 'years'], 'Race': 'Asian'}",69.68542,66.20115,73.16969,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 67 years old. The concentration of Creatinine is 1.06 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.06^(-1.154) * 67^(-0.203) * 1 * 1=69.68542.
Hence, the patient's GFR is 69.68542 mL/min/1.73m²."
3405,9,MDRD GFR Equation,lab test,decimal,pmc-5389244-1,Extracted,"A 46-year-old and 60 kg weight male patient was admitted in kidney transplant unit with a history of end-stage renal disease (ESRD) and on maintenance hemodialysis twice weekly since 21 months. He was having type 2 diabetes mellitus since 7 years and was on oral hypoglycemics. He was also hypertensive since 18 months and was on nifedipine retard 20 mg TID, clonidine 100 μg TID, metoprolol 50 mg OD, and furosemide 40 mg BID. During preoperative evaluation, the patient was New York Heart Association Class III having a history of breathlessness and dyspnea on exertion. Jugular venous pressure was raised. Mild ascites was present without evidence of organomegaly. His daily urine output was around 500 ml. His 12-lead electrocardiogram (ECG) showed left ventricular hypertrophy with strain pattern. Two-dimensional echocardiography revealed moderate mitral regurgitation, moderate tricuspid regurgitation, dilated left ventricle with global hypokinesia, and LVEF of 15% with moderate pulmonary artery hypertension (right ventricular systolic pressure = right atrial pressure + 44). Coronary angiography was normal. His routine blood investigations were within normal limits except hemoglobin of 8.7 g% and a serum creatinine of 6.9 mg/dl on preoperative visit. His creatinine value before starting of dialysis 21 months earlier was 9.4 mg/dl. His chest radiograph showed cardiomegaly with cardiothoracic ratio of 0.7. On airway examination, his mouth opening was 3 cm with normal dentition. He was Mallampati Class 2 with a full range of neck movements and a thyromental distance of 7 cm. All antihypertensive medications were continued as prescribed. Heparin-free hemodialysis was done 24 h before surgery. A written informed consent for surgery and anesthesia was obtained along with high risk of cardiovascular events and postoperative mechanical ventilation.
In the operating room, an 18-gauge intravenous (IV) cannula was secured in the right upper limb and 5-lead ECG, noninvasive blood pressure (NIBP), and pulse oximetry were attached, and baseline hemodynamic parameters were noted. A 20-gauge arterial cannula was secured in right radial artery under local anesthesia (LA), and FloTrac™ monitor for cardiac output monitoring was attached. A functioning brachiocephalic arteriovenous (AV) fistula was present in the left upper limb. Right internal jugular vein was cannulated under ultrasound guidance, after adequate LA infiltration for continuous central venous pressure (CVP) monitoring and vasopressor administration if required. His baseline IBP was 155/92 mmHg, heart rate (HR) of 64/min, oxygen saturation of 98% on room air, and CVP was 23 mmHg. Dobutamine and epinephrine infusions were kept ready for use. Under strict aseptic precaution, epidural was placed in left lateral position at T10–T11 interspace after adequate LA infiltration, with a 16-gauge Tuohy epidural needle using the loss of resistance technique. Correct placement of epidural catheter was confirmed by a negative test dose of 3 ml lignocaine 2% with 15 μg of epinephrine. A total of 15 ml of bupivacaine 0.5% with 50 μg fentanyl was given in epidural space in “graded” doses of 5 ml every 10 min while assessing the pulse, blood pressure changes, respiration, and keeping constant verbal command to the patient. IV dobutamine was started at the rate of 5 μg/kg/min after giving the first bolus of epidural and titrated according to IBP response. After 30 min of bolus doses, sensory level was T8 with adequate motor paralysis. A continuous epidural infusion at rate of 6 ml/h of 0.5% bupivacaine with 2 μg/ml was started for maintenance. Surgery was allowed to start, and IV infusion of propofol was started at the rate of 50 mg/h for sedation. Supplemental oxygen was given by Venturi mask (FiO2 0.5). Goal-directed fluid therapy was given based on pulse pressure variation. Cardiac output, cardiac index, and stroke volume variation were also considered during fluid therapy and inotropes titration. A total of 2 L of crystalloid and 200 ml of 20% albumin were given intraoperatively. One unit of packed red blood cell and 2 units of fresh frozen plasma were also given. Surgery lasted for 6 h and total loss was around 800 ml including 500 ml of ascites and 350 ml blood. At the time of release of cross-clamp, his IBP was 157/94 mmHg, HR was 67/min, and CVP was 12 mmHg. Urine output was adequate after release of cross-clamp. All vital parameters, blood gasses, blood sugar, and electrolytes remained within normal range throughout surgery. Epidural infusion was stopped on starting on skin closure. Renal transplant was completed uneventfully. Patient was shifted to postanesthesia care unit with vital near baseline and urine output at 250–300 ml/h. Postoperative analgesia was maintained by continuous epidural infusion of 0.125% bupivacaine with 2 μg/ml fentanyl at the rate of 6 ml/h along with IV paracetamol 1 g TID.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [6.9, 'mg/dL'], 'age': [46, 'years']}",8.65897,8.22602,9.09192,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 46 years old. The concentration of Creatinine is 6.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 6.9^(-1.154) * 46^(-0.203) * 1 * 1=8.65897.
Hence, the patient's GFR is 8.65897 mL/min/1.73m²."
3406,9,MDRD GFR Equation,lab test,decimal,pmc-8186344-1,Extracted,"A 53-year-old female presented to our Emergency Department (ED) in January 2021 with a six-day history of nausea, vomiting, diarrhea, and myalgias. Her relevant past medical history included liver transplant in 2010 due to alcoholic cirrhosis, hypertension, hypothyroidism, anxiety, and chronic kidney disease. She also reported that she had been diagnosed with and treated for COVID-19 infection three months prior to the current ED visit in October 2020. She was hospitalized at that time for encephalopathy due to her COVID-19 infection and was treated with remdesivir and convalescent plasma. No virus serotyping was done on this admission. She recovered and was discharged from the hospital after a seven-day course that did not involve admission to the intensive care unit or require any significant supplemental oxygen therapy beyond standard nasal cannula. She received a negative COVID-19 result approximately one month after discharge from the hospital in November 2020 and reported a full recovery in the interim. Her immunosuppression regimen was tacrolimus 1 mg twice daily, and her graft function since transplantation was stable with normal results on outpatient laboratory and radiographic monitoring.
During the present ED encounter (January 2021), she was stable from a hemodynamic and respiratory perspective with normal vital signs. Physical examination revealed no acute abnormalities, including normal lung examination. She received a positive COVID-19 result (SARS-CoV-2 Rapid PCR kit, Roche Diagnostics, Rotkreuz, Switzerland). The remainder of her laboratory workup revealed no significant derangements other than mild baseline renal insufficiency with a creatinine of 1.28 mg/dL.
Her nausea and vomiting were not intractable, and after consultation with the hospitalist service, no reason was identified for inpatient management, especially in light of lack of severe symptoms or pulmonary involvement. She was discharged from the ED and referred to our outpatient service for monoclonal antibody infusion therapy and was also instructed to follow up with her primary care and transplant providers.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [1.28, 'mg/dL'], 'age': [53, 'years']}",43.6208,41.43976,45.80184,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 53 years old. The concentration of Creatinine is 1.28 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.28^(-1.154) * 53^(-0.203) * 1 * 0.742=43.6208.
Hence, the patient's GFR is 43.6208 mL/min/1.73m²."
3407,9,MDRD GFR Equation,lab test,decimal,pmc-4018764-1,Extracted,"A 64-year-old female was admitted to our medical center due to recurrent episodes of pre-syncope. The patient denied any connection to postural changes, dyspnea, palpitations or urinary complaints, and she associated the episodes with prolonged standing and strenuous work at home.
The patient had undergone LAGB for morbid obesity 5 years prior to admission, with a weight reduction of ∼65 kg. The patient suffered from recurrent vomiting and GERD attributed to her tightened gastric band. The patient's past medical history was positive for ischemic heart disease, empty sella syndrome, primary hyperaldosteronism, polymyalgia rheumatica, fatty liver, osteoporosis, peptic ulcer disease and status post-deep vein thrombosis.
On physical examination an ejection type systolic murmur was heard, with radiation to the neck and a subtle bruit of both the carotid arteries.
Blood tests demonstrated: mild hypokalemia 3.2 (3.5–5 mmol/l), elevated creatinine 130 (60–106 micromol/l) and urea 9 (3.3–6.5 mmol/l), and normocytic anemia with hemoglobin 10.8 (12–16 g % female).
Electrocardiogram was remarkable for Q waves in leads I, aVL and V6. Chest X-ray (CXR) demonstrated a marked esophageal distention with an air fluid level (Figs and ).
During her hospitalization, the patient developed fever and desaturation, with a new infiltrate on CXR (Fig. ). She was diagnosed with pneumonia and was treated with antibiotics. Later on, after significant improvement, though still suffering from a barking cough (attributed to reflux), the patient left her bed and in an attack of severe coughing, lost consciousness, fell and became cyanotic. Repeated attempts to improve oxygenation failed until a naso-gastric tube was inserted with drainage of ∼1 l of non-bilious content, resulting in rapid improvement in the patient's condition. A repeat CXR revealed the naso-gastric tube in her esophagus. Repeated attempts to insert the NGT into her stomach failed, even with the aid of contrast media. The silastic band was then deflated, allowing for less restriction, and an endoscopy showed esophagitis but no obstruction.
On syncope workup, Doppler assessment of the carotid artery revealed no significant obstructions, and echocardiogram demonstrated a small left ventricular cavity with hyper contractile global systolic function, mild basal septal hypertrophy and LVOT obstruction with the pressure gradient increasing from 16 mmHg at rest to 120 mmHg during Valsalva (Fig. ).
In light of the echocardiographic findings, the patient's recurrent pre-syncope was attributed to LVOT obstruction exacerbated by Valsalva and hypovolemia (in a patient with recurrent vomiting) secondary to gastric banding. Adding to this chronic condition, acute infection and retching resulted in an acute and almost fatal exacerbation. This condition responded to esophageal decompression with resolution of the retching and relief from recurrent Valsalva. Treatment with β-blockers was initiated, diuretics were discontinued and the patient was referred to the cardiomyopathy clinic. On follow-up, several months later, the patient reported the resolution of pre-syncopal feelings though she had gained several pounds in weight.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [130.0, 'µmol/L'], 'age': [64, 'years']}",35.75711,33.96925,37.54497,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 64 years old. The concentration of Creatinine is 130.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 130.0 µmol. To convert 130.0 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 130.0 µmol Creatinine * 1e-06 mol/µmol = 0.00013 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.00013 mol Creatinine * 113.12 g/mol = 0.01471 g Creatinine. To convert 0.01471 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01471 g Creatinine * 1000.0 mg/g = 14.71 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 14.71 mg Creatinine/10.0 dL = 1.471 mg Creatinine/dL. The concentration value of 130.0 µmol Creatinine/L converts to 1.471 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.471^(-1.154) * 64^(-0.203) * 1 * 0.742=35.75711.
Hence, the patient's GFR is 35.75711 mL/min/1.73m²."
3408,9,MDRD GFR Equation,lab test,decimal,pmc-5139760-1,Extracted,"A 30-year-old woman was seen in the gastroenterology clinic of this hospital because of gastrointestinal bleeding. The patient had previously been healthy and took no medications. The patient was born in the eastern part of Turkey and was a farmer in a village.
Physical examination revealed ortostathic hypotension, melena and splenomegaly but the liver was not palpable. The remainder of the physical examination was normal. The patient’s white-cell count was 1.3 × 1012/L. A differential cell count revealed 50% polymorph nuclear cells, 42% bands, 4% lymphocytes, and 4% monocytes. The hemoglobin level was 9.9 g/dl, and the platelet count was 79.0 × 1012/L. The serum creatinine level was 0.55 mg/dl, albumin level 4.31 g/dl, aspartate aminotransferase level 16 U/L (normal range, 0 to 31), alanine aminotransferase level 16 U/L (normal range, 0 to 31), alkaline phosphatase level 206 U/L (normal range, 0 to 240), and total bilirubin level 0.25 mg/dl (normal range, 0.0 to 1.0). The international normalized ratio (INR) was 0.95.
Tests for hepatitis C antibody, hepatitis B surface antigen, hepatitis B core antibody and hepatitis D antibody were negative. Doppler ultrasonography of the abdomen revealed splenomegaly and dilated portal and splenic veins without intraluminal thrombus.
On upper gastrointestinal endoscopy, there were four columns of varices at the distal esophagus and were treated by endoscopic varices ligation. Additionally an ulcerous mass protruding between variceal columns was seen and an endoscopic esophageal biopsy was performed ().
The liver biopsy showed portal fibrosis and sinusoidal dilatation and the esophageal biopsy revealed SCC (, ). A thorax computerized tomography scan revealed the esopahageal mass and varices ().
The patient was diagnosed as having esophageal SCC with associated NCPF. She was transferred to a tertiary care hospital for possible esophageal surgery.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [0.55, 'mg/dL'], 'age': [30, 'years']}",129.78001,123.29101,136.26901,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 30 years old. The concentration of Creatinine is 0.55 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.55^(-1.154) * 30^(-0.203) * 1 * 0.742=129.78001.
Hence, the patient's GFR is 129.78001 mL/min/1.73m²."
3409,9,MDRD GFR Equation,lab test,decimal,pmc-5819634-1,Extracted,"An 81-year-old female presented to the emergency department (ED) complaining of progressive shortness of breath over the preceding few weeks. Other symptoms include weight loss of 30 lb over 5 months, pain in both knees and hips, as well as swelling and numbness in her right-hand fingers. Patient had been following regularly at the cardiology clinic. She had extensive past medical history significant for chronic kidney disease (CKD) stage III, hypertension, coronary artery disease and history of remote myocardial infarction complicated by right ventricular (RV) aneurysm with mural thrombus treated with warfarin therapy, and sick sinus syndrome managed with a pacemaker. She also had remote colon cancer treated with partial colectomy.
On arrival to the ED, she was afebrile, had tachypnea and tachycardia with stable blood pressure. Physical exam revealed fine crackles along the bases and absent pedal edema. She had wide spread hyper pigmented macules and papules over the back and extremities. Initial laboratory workup showed creatinine 2.84 mg/dL, hemoglobin (Hb) 8.2 g/dL, brain natriuretic peptide (BNP) 317 pg/mL and normal troponin level. Electrocardiogram (EKG) showed ST changes along the inferior leads with low voltage QRS (). Transthoracic echocardiography (TTE) revealed a large circumferential pericardial effusion with tamponade physiology (). Previously seen RV mural thrombus was not identified. Pericardiocentesis was performed with 700 mL of frankly bloody pericardial fluid drained, and a pigtail catheter was left in place for passive dependent drainage (). Pericardial fluid analysis showed a hemorrhagic exudate without evidence of infection or malignancy based on normal microbiology studies and cytology results.
Further tests showed an erythrocyte sedimentation rate (ESR) 109 mm/h, C-reactive protein (CRP) 10.5 mg/L and normal thyroid function test. She had positive serology for ribonucleoprotein antibodies at 1.9 consistent with a diagnosis of MCTD. Further serology tests were negative for anti-dsDNA, ribosomal P protein, anticentromere Ab, Sjogren’s syndrome A and B, Jo1 Ab and Scl-70 Ab.
Computed tomography (CT) scan of the chest, abdomen, and pelvis showed no evidence of malignancy, and tumor markers including CA19-9, CA125 and CEA were negative. Follow-up echocardiogram during admission showed rapidly re-accumulating pericardial effusion. Accordingly, she had a sub-xiphoid pericardial window placed and pericardial tissue biopsy revealed acute and chronic fibrinous pericarditis (). Patient responded to empiric therapy with intravenous prednisone. Prior to discharge, echocardiography showed left ventricular ejection fraction (LVEF) of 30-35% with only a trivial pericardial effusion. Given the high risk for recurrence of a pericardial effusion and lack of a mural thrombus, warfarin was held.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [2.84, 'mg/dL'], 'age': [81, 'years']}",15.95475,15.15701,16.75249,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 81 years old. The concentration of Creatinine is 2.84 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.84^(-1.154) * 81^(-0.203) * 1 * 0.742=15.95475.
Hence, the patient's GFR is 15.95475 mL/min/1.73m²."
3410,9,MDRD GFR Equation,lab test,decimal,pmc-2876914-1,Extracted,"A 56-year-old male weighing 60 kg was scheduled for live related allograft kidney transplantation. He was diagnosed to have end-stage renal disease and was on regular bi-weekly maintenance haemodialysis. The patient was on regular medications like antihypertensive drugs, calcium and phosphorous supplements. He had an adequate cardio-respiratory reserve with a normal chest X-ray, ECG and resting 2-D echocardiogram. All investigations, except an Hb level of 8.5 gm% and serum creatinine of 5.8 mg/dl, were within normal limits.
The patient was haemodialysed the previous day and premedicated with tablet alprazolam 0.25 mg orally the night before the operation and on the morning of surgery. The morning doses of antihypertensive drugs were also given with a few sips of water. His preoperative pulse rate, BP, RR, SpO2 were 80/min, 140/80 mm of Hg, 14/min and 98% respectively.
General anaesthesia was induced with fentanyl 100 μg, midazolam 1 mg, thiopentone 250 mg and atracurium 30 mg IV. Trachea was intubated with cuffed ETT of 8.5 mm ID and anaesthesia was maintained with O2: air (40:60), isoflurane 0.6-1% and atracurium infusion @ 0.5 mg/kg/hr. For invasive monitoring triple lumen CVP catheter was placed via the right internal jugular vein approach and right radial artery was cannulated. The surgery was proceeding uneventfully with continuous monitoring of pulse, SpO2 EtCO2, ECG, ST analysis, temperature, IBP, CVP and intermittent ABG analysis (which were all within normal limits). Vascular anastomoses were being done after clamping the external iliac artery and vein. The base line CVP of 8 mm Hg was raised up to 20 mm Hg by rapid infusion of normal saline (collapsible IV bags) with the help of pressure infuser bags and simultaneous 20% albumin infusion. This was done to achieve supranormal intravascular volume to ensure adequate perfusion to the new renal graft. Just after unclamping of the vascular clamps there was a sudden decrease in EtCO2 from 32mm Hg to 15mm Hg followed by decrease in the SpO2 from 98 to 66% with significant bradycardia (HR <45/min) and hypotension. Since there was a clinical suspicion of sudden air embolism (most probably due to entrainment of air in the IVC), immediate resuscitative measures including flooding of operative site with saline, head down with left lateral tilt (Durrant's position), IV atropine 0.6 mg, ventilation with 100% O2 and aspiration of air through distal lumen of CVP line were tried. No obvious air was seen on aspiration and SpO2 returned to 100% with normal EtCO2 tracing within a minute.
The surgery proceeded uneventfully with an adequate urine output. The trachea was extubated on the operating table and the patient was shifted to kidney transplant ICU for observation and further management. However, the surgeon was doubtful about entrainment of air into IVC as there was no leak around the anastomotic site. Subsequently we observed that one of the IV sets connected to the proximal lumen of CVP line had air in it and the IV fluid bag inside the pressure infuser bag was empty.
On retrospective analysis, it was realized that the self collapsible one litre NS bag was disconnected during the infusion and IV mannitol was connected in that line. Later, after the mannitol infusion, the same NS bag was reconnected and the pressure infuser bag was applied to it for the rapid infusion which resulted in air embolism as the saline infusion had finished unnoticed and the pressurized air entered through the central venous catheter leading to sudden fall in EtCO2, HR, BP and SpO2.
As this life threatening situation was immediately recognized due to standard monitoring protocols, the resuscitation measures were started. Left lateral tilt might have allowed the air bubble obstructing the RV outflow tract to be shifted to the superiorly placed right atrium, thereby, allowing the oxygenation and circulation to be restored. The drop in saturation level could have been attributed to overloading with IV fluids, but it would not have been as sudden as in our case. Moreover, the SpO2 in Durrant's position would have worsened in case of fluid overload. Hence fluid overload was unlikely in our case. We established this as the possible cause by simulating the same scenario in vitro.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [5.8, 'mg/dL'], 'age': [56, 'years']}",10.16623,9.65792,10.67454,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 56 years old. The concentration of Creatinine is 5.8 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 5.8^(-1.154) * 56^(-0.203) * 1 * 1=10.16623.
Hence, the patient's GFR is 10.16623 mL/min/1.73m²."
3411,9,MDRD GFR Equation,lab test,decimal,pmc-8267025-1,Extracted,"A 44-year-old female with past medical history of SLE and mechanical mitral valve replacement presented to the hospital with abdominal pain and black stools. She was prescribed mycophenolate mofetil, prednisone, and azathioprine for management of her SLE as an outpatient; however, the patient was only taking azathioprine due to issues with her insurance.
On presentation, the patient was found to have pancytopenia with platelets of 67 000 and acute renal failure (creatinine 3.0). She underwent a computed tomography (CT) scan of the abdomen and pelvis in addition to esophagogastroduodenoscopy (EGD). The patient’s CT scan showed a thickened gallbladder, which required no surgical intervention according to general surgery. Meanwhile, the EGD only revealed small erosions in her stomach. Rheumatology workup () was consistent with SLE flare as demonstrated by elevated dsDNA and low C3/C4. She was initiated on intravenous methylprednisolone for 3 days to treat for SLE flare. Her thrombocytopenia temporarily improved with the corticosteroids; however, her renal function continued to decline. Therefore, she underwent a renal biopsy that revealed class IV lupus nephritis with crescentic glomerulonephritis (IFTA [interstitial fibrosis/tubular atrophy] 20% to 30%), but it did not show any evidence of thrombotic microangiopathy (TMA) or features of ANCA-associated vasculitis. The patient was subsequently initiated on mycophenolate-mofetil and prednisone for treatment of lupus nephritis. She was transitioned from warfarin to a heparin drip during the biopsy for management of her mechanical valve. In the meantime, her thrombocytopenia continued to worsen to a platelet count of 11 000.
Her hospital course was soon complicated by acute encephalopathy. CT scan of the head was negative for acute intracranial pathology. Laboratory workup for pancytopenia () was unrevealing. Her low haptoglobin and high lactate dehydrogenase (LDH) are indicative of a hemolytic process, but are not markers for a specific etiology of hemolytic anemia, especially with a negative direct Coombs test. She was also noted to have high ferritin, high iron, low total iron-binding capacity, and high iron saturation, which may suggest underlying anemia of chronic inflammation but does not explain the acute drop in hemoglobin. Antiphospholipid syndrome was also considered, since the patient had positive antiphospholipid syndrome antibodies (); however, there were no signs of thrombosis on imaging including Doppler ultrasound of lower extremities. Last, while the patient was on heparin, her partial thromboplastin time and international normalized ratio were elevated but fibrinogen was normal with only mildly elevated d-dimer rendering disseminated intravascular coagulation less likely.
Rheumatology and hematology were consulted, and produced a differential diagnosis for the patient’s thrombocytopenia that included TTP, complement-mediated hemolytic uremic syndrome (CM-HUS), SLE-associated immune thrombocytopenic purpura (ITP), heparin-induced thrombocytopenia (HIT), and drug-induced thrombocytopenia from the mycophenolate mofetil. It was unclear whether her mental status changes were from uremia or a condition such as TTP, steroid-induced, or lupus-associated flare affecting the central nervous system. HIT assay returned negative and ADAMTS13 returned at 52%, which was less suggestive for TTP. Peripheral smear revealed few to moderate schistocytes with burr cells (); however, these schistocytes could be due to her mechanical valve rather than any active disease process. Furthermore, CM-HUS was less likely given that no TMA was found on renal biopsy. She was started on Rituximab in addition to another round of intravenous steroids to treat for possible SLE-associated ITP. Her renal function (creatinine 5.5) and azotemia (blood urea nitrogen 123) continued to worsen, which led to the patient being initiated on hemodialysis. She was transfused platelets without much response.
Although we initially thought TTP was less likely in the setting of a normal ADAMTS13, the treatments for ITP were unsuccessful, HIT assay returned negative, and she had been on mycophenolate mofetil without any drug-induced thrombocytopenia in the past. Thus, the patient was treated preemptively with PLEX for a TTP-like microangiopathy associated with her SLE. Her mycophenolate mofetil was held simultaneously in an attempt to rule out drug-induced thrombocytopenia from the differential. This resulted in an immediate improvement in her platelets, and her LDH normalized by the second session of PLEX. Mycophenolate mofetil was reinitiated because we reasoned that if this was drug induced from bone marrow suppression, such a stark improvement would not be seen over the course of a day. The patient continued to receive hemodialysis and PLEX on alternate days with improvement of platelets to >100 000 after 6 PLEX treatments. Her renal function improved during the hospital course to the point where she no longer required hemodialysis.
The patient underwent bone marrow biopsy to rule out any other potential causes for her pancytopenia. Her bone marrow biopsy showed cellular marrow with trilinear hematopoiesis, blasts <5%, and no evidence of acute leukemia, lymphoma, myelodysplasia, monoclonal B-cell population, or ring sideroblasts. The lymphoid cells were predominantly T-cells with a CD4:CD8 ratio of 1.27:1. No monoclonal surface light chain expression was demonstrated to suggest B-cell lymphoma. The kappa:lambda ratio was 1.78:1. The B cells were negative for CD5 and CD10. We concluded that her clinical course was consistent with SLE-associated TTP-like microangiopathic hemolytic anemia (MAHA) without a very low ADAMTS13.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [3.0, 'mg/dL'], 'age': [44, 'years']}",16.95209,16.10449,17.79969,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 44 years old. The concentration of Creatinine is 3.0 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 3.0^(-1.154) * 44^(-0.203) * 1 * 0.742=16.95209.
Hence, the patient's GFR is 16.95209 mL/min/1.73m²."
3412,9,MDRD GFR Equation,lab test,decimal,pmc-7890750-1,Extracted,"A 63-year-old Hispanic male with no past medical history presented to the ED for shortness of breath, dry cough, and worsening fatigue for approximately one-week duration. He was hypoxic on presentation saturating 88% on room air.
Chest X-ray demonstrated bilateral hazy infiltrates, greater in the left lung field (Figure ). Laboratory evaluation showed elevated inflammatory markers including a lactate dehydrogenase of 558 U/L, ferritin of 1218 µg/L, erythrocyte sedimentation rate 57 mm/h, C-reactive protein of 133.8 mg/dL, d-dimer of 0.6 µg/mL, elevated liver enzymes, serum creatinine of 0.9 mg/dL which later normalized to 0.4 mg/dL, and elevated white blood cell count 15,000/mm3. The severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) polymerase chain reaction testing was positive.
The patient was started on IV dexamethasone, ceftriaxone, azithromycin, and remdesivir. A nasal cannula at 3 L was not providing satisfactory oxygenation and the patient was switched to a nonrebreather at 10 L and then to bilevel positive airway pressure.
On day 3 of admission, the patient reported right lower extremity pain and was found to have absent dorsalis pedis and posterior tibial pulses. He was also in increased respiratory distress and tachypneic at which point he was placed on a high-flow nasal cannula. With concern for multiple arterial thrombi, a computed tomography angiogram (CTA) with iliofemoral runoff was ordered. The CTA demonstrated right middle and lower lobe pulmonary emboli, a large wedge-shaped region of hypoenhancement in the right kidney (Figure ) and smaller wedge-shaped regions of hypoenhancement within the left mid to lower kidney representing renal infarcts. The run-off showed moderate stenosis within the origin of the right peroneal artery and segmental occlusion of the left peroneal artery (Figure ).
The patient was given an IV heparin bolus and started on an IV heparin drip. The patient and family decided not to proceed with vascular surgical intervention. A 2D echo was obtained to look for a cardiac source of emboli and resulted normally. Transesophageal echocardiogram with a bubble study, though useful to rule out patent foramen ovale, was unable to be performed as the patient later became unstable and required intubation and mechanical ventilation for continued hypoxia on noninvasive modes of ventilation. No cardiac arrhythmias were observed during his hospital course.
A hypercoagulable workup was negative including anti-phospholipid antibodies; beta 2-microglobulin, anticardiolipin, and lupus anticoagulant. The patient was maintained on therapeutic anticoagulation with enoxaparin sodium.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [0.9, 'mg/dL'], 'age': [63, 'years'], 'Race': 'Hispanic'}",85.22678,80.96544,89.48812,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 63 years old. The concentration of Creatinine is 0.9 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 0.9^(-1.154) * 63^(-0.203) * 1 * 1=85.22678.
Hence, the patient's GFR is 85.22678 mL/min/1.73m²."
3413,9,MDRD GFR Equation,lab test,decimal,pmc-5872390-1,Extracted,"We present the case of a 41-year-old man who had been diagnosed with type 1 DM in junior high school. He was 168 cm tall and weighed 90.0 kg (body mass index, 31.9 kg/m2). His baseline serum creatinine (sCr) level was 79.6 μmol/L and his urinary protein level was 0.3 g/gCr. His blood pressure was well controlled with an aldosterone receptor blocker. DM control was poor (haemoglobin A1c 9.0–10.0%) under intensive conventional insulin therapy. His diabetic retinopathy was simple type. Pregabalin, duloxetine and mexiletine were also used for diabetic neuropathy. His family history was not significant except cerebral infarction in his grandmother. He initially visited a primary care unit because of general fatigue and high fever and was given oral levofloxacin. However, he later called an urgent care unit because of swelling and pain in his genitals. He was diagnosed with Fournier gangrene and admitted to our hospital (Fig. , clinical course). Table showed urinary, blood and culture examination on admission. Inflammatory markers were elevated (white blood cell count 25,700/μL with left shift and C reactive protein 28.8 mg/L). Renal function was slightly abnormal (Blood urine nitrogen 22.0 mg/dL, sCr 91.1 μmol/L) and proteinuria was detected. Blood culture was negative. Escherichia coli and Enterococcus faecalis were detected from wound culture. Free air was noted in his genital area via computed tomography (CT) scan (Fig. ). He underwent debridement and received tazobactam/piperacillin (PIPC/TAZ) 4.5 g every 8 h and intravenous VCM 1.5 g every 12 h. Because his trough VCM level was still low (9.24 μg/mL, 15–20 μg/mL is for complicated infections []) and sCr stable (83.1 μmol/L) on day 3, intravenous VCM increased to 1.5 g every 8 h. Thereafter, he developed pitting pedal edema, weight gain (10 kg), reduced urine volume (100 mL/day), increased sCr (416.4 μmol/L) and trough VCM level (80.48 μg/mL) on day 6, which suggested VCM-induced AKI. Urinary examination results, which included N-acetyl-beta-D-glucosaminidase of 32.0 U/L, α1-microgloblin of 25.7 mg/L, and β2-microgloblin of 1800 μg/L, were also consistent with AKI. CT scan showed no signs of hydronephrosis or renal atrophy (Fig. ). Gallium scintigraphy showed significant accumulation in both kidneys (Fig. ).
VCM and PIPC/TAZ were switched to ampicillin/sulbactam (ABPC/SBT), and frequent haemodialysis was performed on days 6–17, a total of seven times over 12 days (seven 4-h sessions with a blood flow rate of 120–150 mL/min and dialysate flow rate of 500 mL/min). Ethylene vinyl alcohol membrane was used on days 6 and 7, whereas polysulfone membrane was used on days 9, 11, 12, 14, and 17. His urine volume began to increase as his plasma VCM levels gradually decreased. A renal biopsy was performed on day 18 to rule out other renal disorders and evaluate for diabetic nephropathy. ABPC/SBT was switched to ciprofloxacin on day 13 because of a rash that developed mainly on his abdomen and back, and clindamycin was added on days 16–22. He was discharged on day 49 without haemodialysis and antibiotics (sCr, 145.0 μmol/L). Eight months later, his sCr was decreased to 109.6 μmol/L.
The specimen included 16 glomeruli with cortex (no medulla). Subcapsular and medullary ray fibrosis was found in 10% of the specimen on Masson staining (Fig. ). Glomeruli showed no sclerotic or inflammatory changes, but mild mesangial expansion without significant depositions of immunoglobulin or complement in immunofluorescence was found. Nodular lesions were not detected (Fig. ). Focal but severe AIN (Fig. ) and tubular epithelium injury with nuclear denudation or tubular dilatation (ATN) (Fig. ) were detected. Interstitial monocyte infiltration and tubulitis were mainly distributed in the medullary ray lesions (Fig. ). There were no obvious eosinophilic infiltrations or granular lesions in the specimen. Mild intimal fibrosis was found in some of the small interlobular arteries, and mild hyalinosis was also noted in an arteriole. In summary, the kidney biopsy showed that ATN and focal AIN with mild diabetic nephropathy.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [79.6, 'µmol/L'], 'age': [41, 'years']}",92.39968,87.7797,97.01966,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 41 years old. The concentration of Creatinine is 79.6 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 79.6 µmol. To convert 79.6 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 79.6 µmol Creatinine * 1e-06 mol/µmol = 8e-05 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 8e-05 mol Creatinine * 113.12 g/mol = 0.00905 g Creatinine. To convert 0.00905 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00905 g Creatinine * 1000.0 mg/g = 9.05 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 9.05 mg Creatinine/10.0 dL = 0.905 mg Creatinine/dL. The concentration value of 79.6 µmol Creatinine/L converts to 0.905 mg Creatinine/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 0.905^(-1.154) * 41^(-0.203) * 1 * 1=92.39968.
Hence, the patient's GFR is 92.39968 mL/min/1.73m²."
3414,9,MDRD GFR Equation,lab test,decimal,pmc-4365329-1,Extracted,"A 54-year-old white female presented with abdominal pain, nausea, vomiting, and diarrhea (five watery bowel movements every day) for 2 days. The patient states that she has been eating a regular diet and denied eating outside the home and did not have fever, and no one in the family had similar symptoms. Past medical history was positive for hypothyroidism and bipolar disorder and family history was negative for diabetes. One year prior to this presentation the patient had routine blood work with fasting blood glucose of 95 mg/dL. The patient reported polyuria and polydipsia for one month prior to this presentation but did not seek any medical attention.
On physical examination her blood pressure was 127/65 mmHg, heart rate 80 beat/min, and temperature 37°C. Her body mass index was 35 kg/m2. She was in mild distress and had no thyromegaly, clear lungs, regular heart without murmurs, soft abdomen but with generalized tenderness, and hyperactive bowel sounds throughout. The remainder of the physical exam was normal.
WBC 14.8 × 109/L with neutrophils 89%, hemoglobin 18.2 g/L, and platelets 241 × 109/L. Her chemistry shows sodium 132 mmol/L, potassium 3.9 mmol/L, chloride 99 mmol/L, bicarbonate 12 mmol/L, BUN 5.71 mmol/L, creatinine 53.3 μmol/L, calcium 2.35 mmol/L, phosphorus 1.55 mmol/L, magnesium 1.1 mmol/L, and blood glucose 18.76 mmol/L. Arterial blood gases show PH 7.25, Pco2 3.72 kPa, and Po2 9.58 kPa on room air. Lactic acid was 1 mmol/L, amylase 1.1 μkat/L, and lipase 0.27 μkat/L, and serum ketones were positive. Her hemoglobin A1C was 13.7%. Urinalysis was positive for glucose and ketones.
It was obvious from the labs that the patient had diabetic ketoacidosis (high blood glucose, low bicarbonate, and positive ketones) with anion gap of 21. The patient was admitted to the medical intensive care unit. Intravenous normal saline fluid bolus was given with maintenance intravenous fluid after that. She was kept on nothing per mouth and started on insulin drip with hourly blood glucose check and every four hours serum electrolytes (sodium, potassium, chloride, magnesium, and phosphorus) check.
CT scan of the abdomen showed mild distension of the proximal small bowel and tiny amount of free fluids with wall thickening of distended small bowel loops. She was started on ampicillin/sulbactam after getting blood cultures. Stool sample was sent for analysis and the results were negative leukocytes and negative clostridium difficile toxin. Therefore, we decided to stop the antibiotics at this point and treat her as viral gastroenteritis. Later on, the patient's symptoms have improved and her anion gap closed, so we started her on liquid diet (which she was able to tolerate). She was switched to subcutaneous insulin injections (as insulin glargine at bedtime and sliding scale insulin before each meal) and transferred to medical floor. Her blood cultures did not grow any bacteria, and stool culture was negative. Insulin autoantibodies were negative, c-peptide was lower than normal (0.34 ng/mL), and her glutamic acid decarboxylase autoantibodies were highly positive (>30 U/mL).
After having diabetic education including a dietitian consult in the hospital, the patient was discharged home on subcutaneous insulin treatment with a diagnosis of latent autoimmune diabetes in adult. The patient was encouraged to do regular exercise.
The patient was concerned about her new diagnosis and its possible complications which required counseling about the importance of taking care of her diabetes and how this would help prevent future complications.
The patient was very compliant with the discharge plan and checked her blood sugar before each meal and at bedtime. She followed up in the diabetic clinic on a biweekly basis to adjust her insulin dose. Three months later her hemoglobin A1C was 7.7%. The patient has not experienced any adverse or unanticipated events.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [53.3, 'µmol/L'], 'age': [54, 'years'], 'Race': 'White'}",111.43352,105.86184,117.0052,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 54 years old. The concentration of Creatinine is 53.3 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of Creatinine from µmol to mg. The mass of Creatinine is 53.3 µmol. To convert 53.3 µmol of Creatinine to mol, multiply by the conversion factor 1e-06, giving us 53.3 µmol Creatinine * 1e-06 mol/µmol = 5e-05 mol Creatinine. To convert from mol Creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 5e-05 mol Creatinine * 113.12 g/mol = 0.00566 g Creatinine. To convert 0.00566 g of Creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.00566 g Creatinine * 1000.0 mg/g = 5.66 mg Creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 5.66 mg Creatinine/10.0 dL = 0.566 mg Creatinine/dL. The concentration value of 53.3 µmol Creatinine/L converts to 0.566 mg Creatinine/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.566^(-1.154) * 54^(-0.203) * 1 * 0.742=111.43352.
Hence, the patient's GFR is 111.43352 mL/min/1.73m²."
3415,9,MDRD GFR Equation,lab test,decimal,pmc-4300580-1,Extracted,"A 39-year-old male patient presented with fever, left flank pain, nocturia, and daytime frequency. He was on intensive phase of antitubercular therapy for pulmonary tuberculosis. The left flank was tender on examination. Urine microscopy showed pyuria and hematuria. The serum creatinine was 1.82 mg%. Ultrasound showed a bulky left kidney with moderate hydroureteronephrosis. A left percutaneous nephrostomy was placed. He became afebrile and serum creatinine normalized after 48 h. The nephrostogram obtained subsequently showed central pooling of contrast in the excavated area [, white arrow] in the region of interpole papilla giving “egg-in-a-cup” appearance characteristic of papillary necrosis [].","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [1.82, 'mg/dL'], 'age': [39, 'years']}",41.68018,39.59617,43.76419,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 39 years old. The concentration of Creatinine is 1.82 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 1.82^(-1.154) * 39^(-0.203) * 1 * 1=41.68018.
Hence, the patient's GFR is 41.68018 mL/min/1.73m²."
3416,9,MDRD GFR Equation,lab test,decimal,pmc-3943372-1,Extracted,"A 71-year-old Asian woman presented with a two-day history of lower abdominal pain and vomiting, and was admitted to our hospital. She had undergone postoperative pelvic irradiation for the treatment of uterine cancer 10 years prior to the current admission. Upon admission, her vital signs were as follows: body temperature, 37°C; heart rate, 98 beats/min; and blood pressure, 176/70mmHg. Her lung and heart sounds were normal. An abdominal examination revealed tenderness, but no muscular tension was evident; bowel sounds were audible. No edema of her extremities was observed. She presented with hyperkalemia (potassium level, 8.1mmol/L), a serum creatinine (s-Cr) level of 9.9mg/dL and a blood urea nitrogen (BUN) level of 107.2mg/dL, indicating renal failure. A work-up of her arterial blood gasses indicated metabolic acidosis (pH7.256; concentration of bicarbonate, 12.3mmol/L). Urine microscopy showed white blood cells 3 to 5 cells per high-power field (hpf) ; red blood cells, 20 to 30/hpf; hyaline casts, 8 to 10/hpf; and the presence of mesothelial cells. A urine analysis showed a value of 3+ for both protein and blood; her urine did not contain myoglobin. An abdominal CT showed intraperitoneal fluid collection, with no other abnormalities (Figure ). After an initial evaluation, hemodialysis was initiated and a transurethral catheter was inserted.
Over the next three days, our patient’s s-Cr and BUN levels rapidly improved, and her daily urine output was good. Because her symptoms disappeared, the transurethral catheter was removed. However, four days after the removal of the transurethral catheter, her symptoms re-occurred; her s-Cr and BUN levels became elevated, and her urinary output gradually declined. At that time, we noted the presence of mesothelial cells in her urine (Figure ), leading to the suspicion of an intraperitoneal rupture of her bladder. Cystoscopy showed a diverticulum in the apex of her bladder and a possible fistula. After the transurethral catheter was re-inserted into her bladder, her symptoms alleviated, and her s-Cr and BUN levels returned to normal.
Our patient underwent surgery to close the fistula and subsequently received 10 hyperbaric oxygen therapy sessions. The transurethral catheter was removed after these therapies and her s-Cr and BUN levels remained normal; her urine output also remained similar to that prior to the transurethral catheter removal.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [9.9, 'mg/dL'], 'age': [71, 'years'], 'Race': 'Asian'}",3.87859,3.68466,4.07252,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 71 years old. The concentration of Creatinine is 9.9 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 9.9^(-1.154) * 71^(-0.203) * 1 * 0.742=3.87859.
Hence, the patient's GFR is 3.87859 mL/min/1.73m²."
3417,9,MDRD GFR Equation,lab test,decimal,pmc-4448518-1,Extracted,"A 103-year-old (body mass index [BMI]=27.2) African-American female from an assisted living home presented for left hip pinning of a femoral neck fracture following a fall from a wheelchair. Preoperative evaluation revealed an elderly women moaning in distress from severe excruciating left hip pain. After she was diagnosed with a left femoral neck fracture, she was scheduled for a hip pinning procedure under subarachnoid anesthesia. Past medical history was significant for hypertension, congestive heart failure, atrial fibrillation, osteoporosis, renal insufficiency, right lower extremity lymphedema with cellulitis, and peripheral vascular disease. She had a history of right tibial fracture and was taking furosemide, morphine, and enoxaparin. She had no history of known allergy.
Preoperative laboratory reports were significant for blood urea nitrogen (BUN) 35, creatinine (Cr) 1.75, hemoglobin (Hgb) 9.4, platelets 113, and international normalized ratio (INR) 1.1. Preoperative vital signs were blood pressure (BP) 120/70, heart rate (HR) 87. Blood gas analysis revealed a pH 7.39, CO240, PO285. In the operating room (OR) at 16:45, the patient was placed into the right lateral decubitus position. Approximately 500 ml of normal saline solution was given as preload prior to the spinal blockade. At 17:00 nasal cannula O2was administrerd, while maintaining good spontaneous ventilation and with 2 mg of midazolam injected intravenously. Following local skin infiltration, a 25G 5-inch Pencan brand spinal needle was used to access the subarachnoid space, with free flow of clear cerebrospinal fluid (CSF). Multiple attempts by an experienced, pain fellowship trained anesthesiologist were necessary to obtain CSF due to severe scoliosis and multiple bony osteophytes. Hyperbaric bupivacaine, 1.5 ml of 0.75% (11.25 mg), with 15 mcg of fentanyl was injected into the subarachnoidal space. Adequate analgesia was not reached for approximately 45 min, at which time she developed a dense sensory level of anesthesia to the T12 level. Once this level was obtained, the remainder of the procedure was uneventful. Postoperativly, the patient was comfortable, and she returned to full alert status after one and half hours. At the end of the surgery, she had BP 126/78, HR 91, RR 18, Temperature 37.0°C, SaO2100%. Laboratory results showed PT 10.8, INR 1.1, albumin 3.3, Na 138. She received 1.5 L of crystalloids and estimated blood loss was 100 ml, urine output 200 ml. She also received 1 unit of blood and 250 mL of red blood cells (RBC).","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [1.75, 'mg/dL'], 'age': [103, 'years'], 'Race': 'Black'}",32.20125,30.59119,33.81131,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 103 years old. The concentration of Creatinine is 1.75 mg/dL. 
The patient is Black, so the race coefficient is 1.212.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 1.75^(-1.154) * 103^(-0.203) * 1.212 * 0.742=32.20125.
Hence, the patient's GFR is 32.20125 mL/min/1.73m²."
3418,9,MDRD GFR Equation,lab test,decimal,usmle-2298,Extracted,"A 58-year-old female comes to the physician because of generalized fatigue and malaise for 3 months. Four months ago, she was treated for a urinary tract infection with trimethoprim-sulfamethoxazole. She has hypertension, asthma, chronic lower back pain, and chronic headaches. Current medications include hydrochlorothiazide, an albuterol inhaler, naproxen, and an aspirin-caffeine combination. Examination shows conjunctival pallor. Laboratory studies show:
Hemoglobin 8.9 g/dL
Serum
Urea nitrogen 46 mg/dL
Creatinine 2.4 mg/dL
Calcium 9.8 mg/dL
Urine
Protein 1+
Blood 1+
RBCs none
WBCs 9-10/hpf
Urine cultures are negative. Ultrasound shows shrunken kidneys with irregular contours and papillary calcifications.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [2.4, 'mg/dL'], 'age': [58, 'years']}",20.73492,19.69817,21.77167,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 58 years old. The concentration of Creatinine is 2.4 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 2.4^(-1.154) * 58^(-0.203) * 1 * 0.742=20.73492.
Hence, the patient's GFR is 20.73492 mL/min/1.73m²."
3419,9,MDRD GFR Equation,lab test,decimal,pmc-5505299-1,Extracted,"A 42-year-old white female was admitted to our institution for evaluation of right upper quadrant (RUQ) abdominal pain, which worsened with food and was accompanied by intermittent nausea and vomiting. She also reported dyspnea on exertion, fatigue and chronic palpitations. Past medical history included asthma, patent ductus arteriosus repaired in childhood and ill-defined thyroid disease.
Physical examination revealed a blood pressure (BP) of 136/88 mm Hg and a heart rate (HR) of 149 beats per minute (bpm); she was afebrile. Cardiovascular exam revealed an irregularly irregular rhythm, and pulmonary exam revealed mild expiratory wheezing. Abdominal exam was positive for RUQ tenderness. Chest radiograph displayed no acute pathology. Electrocardiogram revealed atrial fibrillation with rapid ventricular response at 149 bmp (). Laboratory investigations revealed a white blood cell count of 13,300/µL, creatinine of 0.78 mg/dL, troponin I of 0.05 ng/mL, TSH of < 0.1 mU/L and free T4 of 2.82 ng/dL. The patient received a loading dose of diltiazem 20 mg IV, and was initially placed on a diltiazem drip at 10 mg/h, and later transitioned to oral diltiazem with adequate HR control (). Further thyroid studies revealed a positive TSH-receptor and thyroid peroxidase antibodies suggesting Grave’s thyrotoxicosis; therefore, she was started methimazole.
The patient underwent a transthoracic echocardiogram, which was technically difficult and reported an ejection fraction of 55-60%, with mild to moderate mitral regurgitation (MR) and moderate to severe TR with dilated right heart chambers (), a new finding compared to a prior echocardiographic study few years earlier. Pulmonary artery systolic pressure was elevated at 52 mm Hg. She underwent a transesophageal echocardiogram () to further evaluate the valve abnormalities, and this revealed a myxomatous tricuspid valve with thickening and malcoaptation of the leaflets and moderate to severe TR; mild to moderate MR with mild thickening of the mitral valve leaflets was also noted. RUQ ultrasound revealed wall thickening of the gall bladder concerning for acute cholecystitis. She underwent uneventful laparoscopic cholecystectomy and was later discharged in stable condition on oral diltiazem for rate control and anticoagulation for atrial fibrillation, with outpatient follow-up of her thyroid abnormalities. Follow-up visit with her cardiologist few months later documented absence of cardiac symptoms, and no murmurs were reported on physical examination.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'creatinine': [0.78, 'mg/dL'], 'age': [42, 'years'], 'Race': 'White'}",80.99257,76.94294,85.0422,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 42 years old. The concentration of Creatinine is 0.78 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is female, so the gender coefficient is 0.742.
Plugging in these values will give us: 175 * 0.78^(-1.154) * 42^(-0.203) * 1 * 0.742=80.99257.
Hence, the patient's GFR is 80.99257 mL/min/1.73m²."
3420,9,MDRD GFR Equation,lab test,decimal,pmc-6534016-1,Extracted,"A 70-year-old Caucasian man with long-term type 2 diabetes mellitus, arterial hypertension, dyslipidemia, and past smoking habits was admitted in the nephrology department with unspecific complaints of weakness and weight loss (5 kg in 3 months) associated with a rapidly progressive renal failure. His outpatient medications were metformin, simvastatin and enalapril. There was no history of new medications, surgical interventions, or other medical procedures. On admission, he was afebrile with a normal blood pressure. The physical examination was unremarkable.
Initial laboratory studies showed normocytic and normochromic anemia (Hb 10.5 g/dL), mild thrombocytopenia with normal lactate dehydrogenase, serum creatinine of 7.64 mg/dL (ten days before the value was 4 mg/dL), with normal anion-gap metabolic acidosis, C reactive protein of 4.1 mg/dL, and erythrocyte sedimentation rate (ESR) of 100 mm/h. Urine sediment had no alterations. Urinary protein/creatinine ratio was 297 mg/g. Laboratory studies performed 3 months before showed no anemia (Hb of 13g/dL) and a serum creatinine of 1.2 mg/dL.
Renal ultrasound revealed normal kidneys and no dilation of the urinary system. Chest X-ray was unremarkable. Based on this presentation a rapidly progressive glomerulonephritis was suspected. Considering the severity of renal impairment, empiric therapy with pulse methylprednisolone followed by oral prednisolone (1 mg/Kg/day) was initiated before the additional laboratory evaluation was available.
Complementary studies revealed hypertriglyceridemia (201 mg/dL) and hypercholesterolemia (total cholesterol of 211 mg/dL and LDL of 105 mg/dL). Viral serologies were negative, peripheral blood cultures were sterile, and complement levels (C3 and C4), antinuclear antibodies, serum electrophoresis, and anti-neutrophil cytoplasmic antibodies were normal.
Kidney biopsy was performed ( and ). Light microscopy showed slit-like cholesterol clefts within arteries and arterioles lumen, with cellular inflammatory reaction and lumen occlusion. Glomerular basal membrane thickening and mesangial expansion was also present with interstitial fibrosis, lymphocytic infiltration, and tubular atrophy. Immunofluorescence revealed linear IgG deposit and albumin. Electron microscopy was not performed. These alterations were compatible with atheroembolic renal disease and diabetic nephropathy (stage IIb).
The patient showed a significant improvement with serum creatinine decreasing to 4.14 mg/dL at discharge. Prednisolone in tapering doses plus statin and antiagregation therapy with acetylsalicylic acid was prescribed.
Ten days later, he presented a sudden unilateral vision loss. Ophthalmological examination () revealed the presence of Hollenhorst plaques on retina and retinography confirmed the presence of retinal emboli. Clopidogrel was added to the previous therapeutic schema.
To better assess the extension of the vascular disease, a body tomography was performed, which revealed multiple vascular calcifications with irregular thrombosis in alternated aortic segments. Additionally, carotid ultrasound showed bilateral atherosclerotic disease, without major hemodynamic alterations.
Three months after the initial episode, the patient was asymptomatic, had a further improvement of renal function (serum creatinine of 1.4 mg/dL), and vision loss was also partially recovered.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [7.64, 'mg/dL'], 'age': [70, 'years'], 'Race': 'White'}",7.06958,6.7161,7.42306,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 70 years old. The concentration of Creatinine is 7.64 mg/dL. 
The patient is not Black, so the race coefficient is defaulted to 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 7.64^(-1.154) * 70^(-0.203) * 1 * 1=7.06958.
Hence, the patient's GFR is 7.06958 mL/min/1.73m²."
3421,9,MDRD GFR Equation,lab test,decimal,usmle-9949,Extracted,"A 30-year-old man who was recently placed on TMP-SMX for a urinary tract infection presents to urgent care with a new rash. The vital signs include: blood pressure 121/80 mm Hg, pulse 91/min, respiratory rate 18/min, and temperature 36.7°C (98.2°F). Physical examination reveals a desquamative skin covering both of his lower extremities. A basic chemistry panel reveal sodium 139 mmol/L, potassium 3.8 mmol/L, chloride 110 mmol/L, carbon dioxide 47, blood urea nitrogen 23 mg/dL, creatinine 0.9 mg/dL, and glucose 103 mg/dL.","Using the MDRD GFR Equation, what is the patient's Glomerular Filtration Rate (GFR) in terms of mL/min/1.73 m²? If the patient is black, please use the MDRD GFR Equation for Blacks. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'creatinine': [0.9, 'mg/dL'], 'age': [30, 'years']}",99.08013,94.12612,104.03414,"The patient's estimated GFR is calculated using the MDRD equation as:
GFR = 175 * creatinine^(-1.154) * age^(-0.203) * race_coefficient * gender_coefficient. The creatinine concentration is mg/dL. The race coefficient is 1.212 if the patient is Black and 1.0 otherwise. The gender coefficient is 0.742 if the patient is female and 1.0 otherwise.
The patient is 30 years old. The concentration of Creatinine is 0.9 mg/dL. 
The race of the patient is not provided, so the default value of the race coefficient is 1.0.
The patient is male, so the gender coefficient is 1.
Plugging in these values will give us: 175 * 0.9^(-1.154) * 30^(-0.203) * 1 * 1=99.08013.
Hence, the patient's GFR is 99.08013 mL/min/1.73m²."
3422,10,Ideal Body Weight,physical,decimal,pmc-3443612-1,Extracted,"We report the case of a 20-year-old Caucasian, nonsmoking female student, height 185 cm, weight 66 kg, who developed pain of the left pinna which is why she attended the otolaryngological ambulatory unit two days later (). The left pinna was found to be sore and reddish but without vesicles, which is why chondritis was diagnosed and amoxicillin and clavulanic acid prescribed. One day later she awaked with a peripheral facial nerve palsy on the left side and hypoesthesia of the left upper lip. The weeks before onset she had a lot of stress with her studies at the university but there was no fever, no vaccination, or infection. A few days before onset of the palsy she recognised dysesthesias of the parietal skull on the left side. The night before onset of the palsy she was exposed against the ventilator of an air condition for more than an hour. She was regularly taking loratadine.
Clinical neurologic examination on admission revealed slight hypoesthesia of the left upper lip, moderate peripheral facial nerve palsy, and generally reduced tendon reflexes. The left pinna showed an erythematous rash but no vesicles. Hearing and taste were normal and there was no vertigo, double vision, skew deviation, nystagmus, headache, hyposmia, or ataxia []. Blood chemical investigations revealed slight leucopenia but normal C-reactive protein. Ophthalmologic examinations excluded a zoster of the eye. Immediately after admission, she was treated with dexamethasone (40 mg intramuscularly) during two days followed by dexamethasone orally during another six days. Additionally, she received 750 mg acyclovir three times a day intravenously during eight days. For continuous pain periauricularly she received mefenamic acid and paracetamol with success.
At followup three days later she reported some transient vesicles at the left pinna, no longer visible at the visit, lid closure had improved, and there was recovery from the pinna's rash but only marginal voluntary innervation of the frontalis and lower facial muscles. Audiometry was normal. Followup six days after onset of the palsy showed complete lid closure but unchanged innervation of the other facial muscles. She reported neuralgiform pain in the left ear which is why gabapentin was prescribed with success. Eleven days after onset of facial palsy lid closure on the left side was complete. There were slight innervation of the frontal branch and only slight innervation of the left mouth corner. Nerve conduction studies 12 days after onset showed almost equal compound muscle action potential (CMAP) amplitude when recording from the orbicularis oculi muscle but >50% amplitude reduction on the left side when recording from the orbicularis oris muscle. Antibodies against the varicella zoster virus (VZV) were determined three times by means of an ELISA test. IgG antibodies against VZV were positive at all three determinations and IgM antibodies against VZV were negative at the first and positive at the second and third determination, which is why valacyclovir orally was given for seven days after discontinuation of acyclovir. Antibodies against other viruses and Borrelia burgdorferi were normal. Follow-up 6 weeks after onset showed further recovery of the palsy, such that it was no longer visible in the absence of emotional reactions. Nerve conduction studies confirmed the improvement such that the CMAP amplitude difference was only reduced to 30%.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [185.0, 'cm']}",75.01979,71.2688,78.77078,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 185.0 cm, which is 185.0 cm * 0.393701 in/cm = 72.83469 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (72.83469 (in inches) - 60) = 75.01979 kg.
Hence, the patient's IBW is 75.01979 kg."
3423,10,Ideal Body Weight,physical,decimal,pmc-4009655-1,Extracted,"A healthy 21-year-old, 69 kg, 170 cm primigravida presented at 38 weeks gestation for elective cesarean section due to fetal anomalies. A spinal anesthetic was performed in the sitting position with 10.5 mg of 0.75% hyperbaric bupivacaine, 10 mcg fentanyl and 200 mcg of morphine. After an uncomplicated intrathecal (IT) injection, she was positioned supine with left uterine displacement. A sensory block was present to T3 bilaterally.
The surgery proceeded uneventfully and a viable infant was delivered. Approximately 40 min after the IT injection, the uterus was externalized for hysterotomy repair. Shortly thereafter, the patient complained of right sided peri-oral numbness, dysphagia and dysarthria. Five minutes later she developed a constellation of neurologic symptoms including: Horizontal nystagmus of the right eye, right sided ptosis with facial droop and right upper extremity weakness with a “claw hand” (hand strength 2/5). Vital signs and mentation remained normal. She denied shortness of breath or chest pain. Differential diagnosis at that time included: High spinal, stroke or transient ischemic attack, air embolus, amniotic fluid embolus and seizure.
At the conclusion of surgery, the neurologic symptoms were unchanged. A non-contrast computed tomography of the head showed no intracranial pathology. Approximately, 90 min after the IT injection, her facial droop and ptosis began to resolve but the right upper extremity weakness persisted. All neurologic symptoms resolved within 120 min. A brain magnetic resonance imaging and a magnetic resonance angiography of the neck vessels were negative. An echocardiogram with agitated saline bubble study showed no right-to-left shunt, ruling out paradoxical embolus.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [170.0, 'cm']}",61.43709,58.36524,64.50894,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.92917 (in inches) - 60) = 61.43709 kg.
Hence, the patient's IBW is 61.43709 kg."
3424,10,Ideal Body Weight,physical,decimal,pmc-3049976-1,Extracted,"The 67-year old, male patient (164 cm, 70 kg) with chronic renal failure was supposed to undergo arteriovenous bridge graft of the upper arm for hemodialysis under high level thoracic epidural anesthesia. Patient history revealed that he underwent coronary bypass graft six years ago and was taking antihypertensive agents and insulin for hypertension and diabetes. Blood tests performed after hemodialysis on the day before the operation showed hemoglobin 11.3 g/dl, hematocrit 36.3%, glucose 202 mg/dl, Na 136 mmol/L, K 5.2 mmol/L, Cl 97 mmol/L, BUN 43 mg/dl, and creatinine 4.5 mg/dl. Test results on the day of the operation showed that the platelet count and coagulation profile (prothrombin time, International Normalized Ratio, activated partial thromboplastin time, fibrinogen) were in the normal ranges.
When the patient arrived at the operation room, blood pressure was 135/89 mmHg, and heart rate was 64 bpm. The high level thoracic epidural anesthesia was performed in the sitting position, and an assistant supported both shoulders of the patient so that the patient could lower his head to the maximum (). The first prominent spinous process of the cervical spine, which is the C6 spinous process, was identified []. Referring to that, local infiltration of 2% lidocaine 2 ml was performed in the middle line between the T1 and T2 spinous processes. Then, for the loss of resistance technique, a 5 ml glass syringe was connected to a 17-G Tuohy needle (ARROW®, Arrow International Inc., USA), and the needle was moved to the epidural space by the midline approach. When it moved into the 4.5 cm position from the skin, the plunge of the glass syringe was sucked inside, and the hanging drop method was performed at that position. As a result, the epidural space was positively identified, the loss of resistance technique to air was performed to verify that the loss of resistance was positive, and the drip infusion method showed that the normal saline was dropping at a rate of one drop per second or higher.
After that, an 18-G epidural catheter (ARROW®, Arrow International Inc., USA) was inserted through the Tuohy needle. The epidural catheter was inserted without particular resistance up to 3 cm inside the epidural space. After fixing the catheter, the patient's position was altered to the supine position, and 1% lidocaine 3 ml containing 1:200,000 epinephrine was injected through the catheter as the test dose. There was no change in blood pressure and heart rate at five minutes after the test injection. The sensory change on both upper arm medial sides was not accurately verified since the patient was unable to cooperate well. For epidural anesthesia, a mixture of 0.375% ropivacaine 15 ml and fentanyl 50 µg was injected through the epidural catheter. Pin-prick tests at 5, 10, 15 and 20 minutes after drug injection showed that pain had not been alleviated at all, and vital signs were not changed.
Judging that the epidural anesthesia failed, general anesthesia was performed under the agreement of the patient. To induce general anesthesia, 2% lidocaine 2 ml-propofol 2 mg/kg-atracurium 0.6 mg/kg was intravenously injected, and the anesthesia was maintained with O2-N2O-desflurane. The operation was carried out for 1.5 hours, and epidural anesthesia failure was reconfirmed when the patient complained of pain in the operated region in the recovery room. To find out the causes of the epidural anesthesia failure, iohexol 5 ml was injected through the epidural catheter and radiographic images were taken (). However, since the accurate position of the catheter was not found, cervical and thoracic computed tomography (CT) was performed after ensuring the patient that the hospital would cover the cost of the CT and receiving agreement from the patient and caregiver. CT findings revealed that the catheter had entered between T1 and T2 but failed to penetrate into the ligamentum flavum, proceeded along the T2 right lamina, and was eventually positioned within the erecter spinae muscle after converting the direction backwards ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [164.0, 'cm']}",60.50401,57.47881,63.52921,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 164.0 cm, which is 164.0 cm * 0.393701 in/cm = 64.56696 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.56696 (in inches) - 60) = 60.50401 kg.
Hence, the patient's IBW is 60.50401 kg."
3425,10,Ideal Body Weight,physical,decimal,pmc-4166791-1,Extracted,"A 90-year-old woman presented at our institution suffering from right hip joint pain that had been absent since an earlier visit when she was 83 years old. Her height was 153 cm and her body weight was 58 kg. She had a history of hypertension. The clinical course of her joint pain was as follows: she initially complained of continued right hip joint pain at the age of 83 years and 3 months. Therefore, non-steroidal anti-inflammatory drug (NSAID) administration and bisphosphonate (BP) treatment for osteoporosis were given. A mild thoracic vertebral compression fracture was also observed approximately 7 years earlier at the patient’s first visit. Osteoporotic treatment with BP had been continued since that time. Right hip bone mineral density (BMD) 7 years prior and at present were 0.915 (T score = -1.7) and 1.094 (T score = -0.1), respectively. Left hip BMD had risen from 0.702 (T score = -1.9) 7 years earlier to 0.755 (T score = -1.5) at present. During follow-up, she sometimes complained of mild hip joint pain. At the time of this report, her joint pain was substantially decreased.
Right hip range of motion (ROM) was slightly restricted at the patient’s first visit, but did not worsen over 7 years.
A right hip plain radiograph at age 83 showed joint space narrowing (Kellgren-Lawrence [KL] grading II) [] (Fig. ) that was diagnosed as radiographic OA. There was no acetabular dysplasia. At the age of 83 years and 8 months, plain radiographs revealed greater joint space narrowing, a band around the bone defect change-like osteonecrosis, and a concave shape to the right femoral head (Fig. ). The necrotic region of the femoral head had progressed a year after onset and was noticeably worsened at the age of 86 (Fig. , ). Ensuing radiographs showed progressive destruction of the femoral head and osteosclerotic change of the remaining joint line (Fig. ). In addition, radiographs retrospectively uncovered a laddering-shaped deformity in the right lateral proximal femoral head and a fracture-like line that were consistent with the necrotic region (Fig. , arrow).
The particularity of this case was that 1) the patient was initially diagnosed as having radiographic OA, 2) joint pain was markedly improved after a few months, 3) the femoral head degenerated over several years in the absence of joint pain, and 4) radiographic diagnosis changed based on the timing of disease progression.
The patient was informed that the data from her case would be submitted for publication and gave her consent.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.0, 'cm']}",46.04337,43.7412,48.34554,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.0 cm, which is 153.0 cm * 0.393701 in/cm = 60.23625 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.23625 (in inches) - 60) = 46.04337 kg.
Hence, the patient's IBW is 46.04337 kg."
3426,10,Ideal Body Weight,physical,decimal,pmc-8159644-1,Extracted,"The patient initially presented as an 18-year-old nulligravida with a chief complaint of 2 years of infertility and a known uterine septum. Gynecological history was significant for menarche at the age of 13, regular monthly menses, and a history of treated chlamydia. She had a history of congenital pulmonary stenosis treated with 2 angioplasties and hypertension managed with losartan. Her most recent echocardiogram showed an ejection fraction of 60-65% and no significant valvular disease.
On examination, she was 165 cm tall and weighed 58 kg with a BMI of 21 kg/m2. Her vital signs were normal. A pelvic exam showed an anteverted, 8-week size uterus. Transvaginal ultrasound revealed a uterus measuring 7.1 cm length × 8.1 cm width × 4.6 cm depth with normal appearing ovaries. On 3D transvaginal ultrasound, the uterine septum had a 2 cm deep indentation with an angle of 65° (). A hysterosalpingogram showed two uterine cornua with normal appearing and patent fallopian tubes (). Laboratory studies were unremarkable and included an estradiol level of 81 pg/mL, a follicle stimulating hormone level of 2.8 mIU/mL, a luteinizing hormone level of 11.1 mIU/mL, and a thyroid stimulating hormone level of 0.860 μIU/mL.
She conceived her first pregnancy spontaneously 2 months after the hysterosalpingogram was performed. Part of the uterine septum can be seen on an 18-week obstetrical ultrasound performed in this first pregnancy (). During her first pregnancy, she was diagnosed with preeclampsia with severe features at 37 weeks of gestation at an outside hospital. An ECV was performed, followed by induction of labor and an uncomplicated vaginal delivery.
The patient then conceived her second pregnancy spontaneously 4 months after her first delivery. She received prenatal care by an outside clinic that does not offer ECVs and was referred to our obstetrical triage unit for the procedure. On presentation to our hospital, she was a 20-year-old gravida 2 para 1001 at 37 weeks and 6 days of gestational age with confirmed breech presentation and a posterior placenta. The estimated fetal weight by ultrasound was 3003 grams, and maximum vertical amniotic fluid pocket was 5.7 cm. Risks and benefits of an ECV were discussed with the patient, and consent was obtained. At 38 weeks and 0 days, an ECV was performed in the operating room under epidural anesthesia with administration of 0.25 mg subcutaneous terbutaline. The fetus was in frank breech position with the fetal head in the maternal right upper quadrant and back facing up and to the maternal left. The fetal rump was elevated out of the pelvis while pressure was simultaneously applied to the fetal head to direct it towards the pelvis. The ECV was successful on the second attempt, and anti-D immune globulin was administered after the procedure.
After the ECV, the patient was discharged home and scheduled to return for induction of labor at 39 weeks 0 days. When she returned for induction of labor, breech position was again observed by ultrasound. An epidural was placed, ECV was performed again in the operating room easily and without complications, and the patient was transferred to labor and delivery for induction of labor. During labor, the patient was diagnosed with preeclampsia with severe blood pressures and started on magnesium sulfate for seizure prophylaxis.
A singleton male in cephalic position was delivered vaginally at 39 weeks 2 days of gestation weighing 3510 grams with Apgar scores of 8 at 1 minute and 9 at 5 minutes. After delivery of the fetus and placenta, there were retained membranes that did not deliver with gentle traction. Manual uterine exploration revealed membranes firmly adhered in the right cornu which was felt to have contracted around the membranes holding them in place. The membranes were removed manually with traction. Manual uterine exploration afterwards revealed a thick uterine septum consistent with previous 3D TVUS and hysterosalpingogram findings. The postpartum course was uncomplicated, and another dose of anti-D immune globin was administered on postpartum day 2 since the infant was Rh positive. The mother and infant were both discharged on postpartum day 2.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3427,10,Ideal Body Weight,physical,decimal,pmc-8191279-1,Extracted,"A 52-year-old male obese patient (weight 115 kg, height 181 cm), with history of hypertension, analgesics abuse due to chronic back pain, came to Emergency Department for repeated massive hematemesis episodes. Upon arrival, the patient was conscious, with slightly reduced response to painful stimulation and regularly reflexive pupils; vital signs were recorded: heart rate was 145 bpm, non-invasive blood pressure 80/45 mmHg, SpO2 86% in room air. Blood tests were performed, urinary catheter and indwelling arterial line for blood pressure monitoring and serial blood gas measurements were placed. After anamnesis excluded presence of active liver disease and esophageal varices, the patients signed the informed consent so that a gastric tube was gently positioned to drain blood from stomach, and immediately after a Sengstaken Blackmore tube to in an attempt to stop bleeding.
Emergency endoscopy was arranged and performed with locally sprayed 10% lidocaine and minimal sedation with midazolam 1 mg, resulting in failure to identify and control active source of bleeding with endoscopic treatment. Following the worsening of hemodynamic conditions and impossibility to stop bleeding, immediate surgical access was scheduled. Patient was moved to operatory room and, under vital parameters monitoring and 3 minutes preoxygenation in 100% oxygen, a rapid sequence induction was performed with etomidate 0.2 mg*kg-1, suxamethonium 1 mg*kg-1, and fentanil 100 mcg. Cricoid pressure (CP) was applied in order to decrease the risk of regurgitation. Before the procedure, patient was not carefully studied for airway management, due to urgent setting, but a Mallampati 3 score and slightly reduced neck movement were recorded. At a first direct laryngoscopy, no glottic structures were visible; a second attempt, after aspiration of blood and releasing of CP, showed a Cormack-Lehane 3 grade with partial view of lingual border of epiglottis.
Intubation was attempted blindly twice with styletted tube, unsuccessfully, whereas ventilation by face-mask was getting quickly worse. As the oxygen saturation was descending rapidly (spO2 60%), a number 4 classic LMA was placed after repeated mouth aspiration. Mask was inflated accordingly to manufacturers' instruction (25 ml of air) and manual ventilation was obtained via gentle but frequent insufflation with 100% Oxygen. Once saturation was fully recovered, considering emergency surgery and aspiration risk, the decision to intubate through LMA was taken.
Optical instruments (video/fiberoptical) were not available. We then inserted a 16 Fr standard nasogastric tube (NGT) blindly through LMA, finding indirect sign of passage in trachea in easy advancement without resistance and repeated free air aspiration. Then, we cut proximal tip of NGT and kept granting ventilation passing proximal end of NGT via holed catheter mount. Next, proximal part of LMA with glued connector was cut and removed to allow passage of a 7,5 mm endotracheal tube (ET) through LMA by railroading on NGT [].
Before removing the LMA, the ET cuff was inflated and position confirmed by capnography.
After successful intubation, surgery started and patient was successfully treated for duodenal ulcer. Vital parameters were stable throughout the operation, but blood and plasma transfusion were necessary according to blood test results. At the end of the surgery, the patient was moved to intensive care unit for postoperative monitoring and uneventfully extubated the day after using a safe extubation technique.[]","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [181.0, 'cm']}",75.89772,72.10283,79.69261,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 181.0 cm, which is 181.0 cm * 0.393701 in/cm = 71.25988 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (71.25988 (in inches) - 60) = 75.89772 kg.
Hence, the patient's IBW is 75.89772 kg."
3428,10,Ideal Body Weight,physical,decimal,pmc-3987429-1,Extracted,"Our patient was a 62-year-old male, 175 cm tall who complained about dyspnea on exertion (NYHA class III). The patient was on beta blocker, warfarin, and diuretic and his rhythm was atrial fibrillation. Transthoracic and transesophageal echocardiography was performed and severe mitral stenosis was established. Mitral valve area was 0.8 cm2 and no thrombus was found in the left atrium and its appendage. In addition, Wilkins score was 6 and systolic pulmonary artery pressure was 38 mmHg.
The patient was candidatedfor BMV.
Before attempting for valvulotomy, coronary artery status was determined. Selective coronary angiography demonstrated no significant obstruction in the coronary arteries. First, the right femoral vein was approached, but it could not be accessed; therefore, the left femoral vein was punctured. Then, the retrograde injection of the contrast media in the proximal of the right external illiac vein showed that the right femoral vein was occluded. Thus, we decided to continue the procedure from the left side.
Transseptal puncture of the interatrial septum was performed via the left femoral vein using Brocken Brugh needle. After dilatation of this puncture site, Inoue balloon 28 was used and graded inflation was done with 24, 26, and 28 cc. The mean transmitral valve gradient was declined from 16 mmHg to 3 mmHg and the left ventricudar injection revealed no mitral regurgitation. After all, the procedure was terminated without any complications.
The patient was discharged two days after the procedure with beta blocker and anticoagulant (warfarin) due to atrial fibrillation rhythm.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3429,10,Ideal Body Weight,physical,decimal,trec-ct-2021-54,Extracted,"A 57-year-old man was admitted to the clinic because of weight loss and persistent dry cough 4 months ago. Chest computed topography showed bilateral multiple infiltrates in the upper lobes and thickened bronchial walls. There is a documented positive serum MPO-ANCA in his medical record. Transbronchial biopsy revealed necrotic granulomas with multinucleated giant cells and the Wegener's granulomatosis was diagnosed for him. He is treating with corticosteroid and cyclophosphamides since 4 months ago. His Birmingham Vasculitis Activity Score (BVAS) is above 4 since the beginning of his disease. His last physical exam and lab study was performed yesterday and showed the results bellow:
A wellbeing, well-nourished man, non-icteric, cooperative and alert
Weight: 73 kg
Height: 177
BP: 120/80
HR: 90/min
RR: 22/min
Hgb: 13 g/dl
WBC: 8000 /mm3 (Neutrophil: 2700/mm3)
Plt: 300000 /ml
AST: 40 U/L
ALT: 56 U/L
Alk P: 147 U/L
Bill total: 1.2 mg/dl
ESR: 120 mm/hr
MPO-ANCA: 153 EU","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [177.0, 'cm']}",72.27568,68.6619,75.88946,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 177.0 cm, which is 177.0 cm * 0.393701 in/cm = 69.68508 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.68508 (in inches) - 60) = 72.27568 kg.
Hence, the patient's IBW is 72.27568 kg."
3430,10,Ideal Body Weight,physical,decimal,pmc-3193786-1,Extracted,"A 34-year-old male presented with recurrent carpopedal spasms of 4 years duration with perioral numbness, cramps, muscle twitching and generalized weakness for which he was evaluated 2 years back and found to have hypocalcemia, hyperphosphatemia, hypercalciuria, high PTH without AHO phenotype. He was given provisional diagnosis of PHP and started on calcium and 1α-calcidiol. Presently he reported for review. He was symptomatically improved with treatment. There was no family history of similar illness, or bony abnormality. On examination he was 184 cm tall with weight of 78 kg (BMI 23 kg/m2). He had no evidence of AHO phenotype. Latent signs of tetany in the form of positive Chvostek's sign and Trousseau's sign were present. We decided to re-evaluate him in view of late age of onset of symptoms, absence of AHO phenotype, and to confirm the diagnosis. His medications were stopped for 7 days. Investigations revealed normal renal parameters (serum creatinine, 88.4 μmol/L) and normal serum magnesium (0.86 mmol/L), 25(OH)D levels (137.2 nmol/L) and raised PTH (63 pmol/L). His computed tomography scan of the brain was normal. His bone mineral density (T score,0.5 at L1-L4 and –0.2 at femur neck) and thyroid function were normal (T3 0.87 ng/mL, T4 7.59 μg/dL, TSH, 2.20 mIU/L). In view of hypocalcemia with raised PTH three possibilities were entertained—idiopathic hypoparathyroidism with heterophile antibody against PTH, PHP1b, or PHP2. For the first possibility his serum was precipitated with polyethylene glycol (PEG) for detection of heterophile antibodies.[] His PEG precipitated serum PTH levels were also high (61.5 pmol/L). Modified Ellsworth Howard test[] was planned to differentiate between PHP1b and PHP2. Since this test was performed first time in this institute, it was planned in three subjects: one present case, one healthy age- and sex-matched control and another known case of postoperative hypoparathyroidism. The protocol starts with oral hydration with 200 mL water every 30 min starting at 0600 hours in the morning. Starting from 0830 hours, timed urine collection is done every 30 min and blood samples are collected at midpoint of each till 1100 hours. From 1000 to 1010 hours, teriparatide is infused intravenously in the dose of 5 units/kg (200 units maximum; conversion factor 20 μg = 67 units). Each sample is analyzed for phosphate, creatinine, and additional cAMP in urine samples. Basic parameters of all subjects are depicted in . The patient had blunted urinary cAMP response to exogenous PTH (recombinant 1-34) as compared to healthy control and patients with postoperative hypoparathyroidism []. However, our patient had normal tubular reabsorption of phosphate and percentage fall in the ratio of maximum rate of renal tubular reabsorption of phosphate to glomerular filtration rate (TmPO4/GFR) [] when compared to two other subjects, indicating normal phosphaturic response. In view of hypocalcemic tetany with raised PTH levels and blunted nephrogenous response to exogenous PTH, the patient was diagnosed as a case of PHP1b. He was continued with calcium and 1α-calcidiol.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [184.0, 'cm']}",78.61425,74.68354,82.54496,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 184.0 cm, which is 184.0 cm * 0.393701 in/cm = 72.44098 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (72.44098 (in inches) - 60) = 78.61425 kg.
Hence, the patient's IBW is 78.61425 kg."
3431,10,Ideal Body Weight,physical,decimal,pmc-3106396-1,Extracted,"A 48-year-old, 48 kg, 154-cm tall woman, ASA physical status II, posted for total abdominal hysterectomy and bilateral salpingo-oophorectomy, was scheduled for a combination of continuous lumbar epidural analgesia and general anaesthetic. The surgery was indicated for management of an ovarian tumour. She had a history of some psychiatric illness a few years back and was on medications, which were later discontinued, but details of the same could not be obtained owing to poor documentation. During location of the epidural space, the initial attempt resulted in a dural puncture, following which the epidural space was located at the immediate upper spinous interspace and anaesthesia proceeded uneventfully with endotracheal intubation. She was extubated on table, Inj morphine 3 mg administered through the epidural catheter for relief of postoperative pain, and was shifted to the postoperative ward without any major concerns.
Five hours later, she was found catatonic in bed with total loss of limb movements. Plantars were flexor and pupils normal. Eyes were half-open, mouth slightly open and the patient held this posture ignoring any verbal contact or external stimulus. She was actively resisting eyelid elevation and blinking in response to visual threat. The patient was haemodynamically stable and arterial blood gases (ABG), serum electrolytes, and blood glucose levels were unremarkable. In view of the previous dural puncture, egress of the epidurally administered morphine into the intrathecal space was considered and naloxone administered to antagonize its effects. In about an hour, the patient was fully conscious, oriented, and responding to oral commands. However, the patient was not vocalizing and was still keeping her mouth slightly open. Upon being instructed to close her mouth, the patient indicated that she was unable to do so and TMJ dislocation was considered. The Oral and Maxillofacial Surgeon was called to do a reduction of the TMJ. The patient’s jaw was placed in a bandage for 2 days with instructions to refrain from opening her mouth widely for several weeks and to support her jaw while yawning.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [154.0, 'cm']}",46.94889,44.60145,49.29633,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 154.0 cm, which is 154.0 cm * 0.393701 in/cm = 60.62995 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.62995 (in inches) - 60) = 46.94889 kg.
Hence, the patient's IBW is 46.94889 kg."
3432,10,Ideal Body Weight,physical,decimal,pmc-5695193-1,Extracted,"Our patient was a 15-year-old female resident in Inner Mongolia. She started to develop intermittent claudication 1 year prior to admission. She was also noted to have low-grade fever of 37.5°C, bilateral rash over her lower limbs, and apparent hair loss. Local hospital made the diagnosis of Erythema Nodosum and prescribed unclear regimen of thymosin and traditional Chinese medicine to treat the disease. Although the fever and rash resolved slowly, the claudication kept worsening gradually. One month ago, she could only climb up two floors and complained of decreased appetite, intermittent emesis, coughing white frothy sputum, and pitting oedema of lower limbs and eyelids. One week ago, she suddenly developed shortness of breath and hemoptysis. Chest computed tomography (CT) showed multiple infiltrates, ground-glass opacities, budding signs, and bilateral pleural effusions. Cardiac ultrasound revealed diffuse biventricular hypokinesia, left ventricular thrombosis, and moderate pulmonary arterial hypertension (56 mmHg). Left ventricular ejection fraction (LVEF) was 28%. Tricuspid annular plane systolic excursion (TAPSE) was 7 mm. Acute heart failure was diagnosed, and diuresis was initiated. Her discomforts slightly improved, and she was admitted to the Cardiac Care Unit in our hospital for further investigation. Past medical history and family history revealed nothing significant.
On admission, her height was 163 cm and weight was 57.5 kg. Her body mass index (BMI) was 21.6 kg/m2. Her blood pressure in the upper extremities were 160/110 mmHg (left) and 140/90 mmHg (right). The number could not be interpreted in the lower limbs. Her heart rate was 120 bpm of regular rhythm. Respiration rate was 25 per minute and oxygen saturation was 98% on room air. Physical examination revealed a 3/6 systolic murmur over the right cervical region, asymmetrical radial pulses, and disappearance of both dorsalis pedis artery pulses. Jugular vein distentions, bilateral rales in lung bases, liver enlargement, and pitting oedema of lower limbs were also noted. Blood tests revealed low albumin level of 23 g/L (33–52 g/L) and markedly increased BNP of 2009 ng/L (<300 ng/L). Twenty-four-hour urine albumin was 5.2 g with G/P 100% while antinuclear antibodies (ANA), anti neutrophilic cytoplasmic antibody (ANCA), high sensitivity C reactive protein (hsCRP), erythrocyte sedimentation rate (ESR) were normal. The 12-lead electrocardiogram showed normal sinus rhythm, left atrial overloading, and left ventricle enlargement. Echocardiography revealed multiple abnormalities: (i) enlargement of the entire heart, with left atrium diameter of 41 mm and left ventricular end diastolic diameter of 53 mm; (ii) mural thrombus of both ventricles. Two were in the left while one was in the right; (iii) diffuse hypokinesis of left ventricle and severe impairment of both ventricle's systolic and diastolic functions. The estimated LVEF was 12%; (iv) moderate pulmonary hypertension of 49 mmHg; (v) small amount of pericardial effusion (Figure
). Vascular ultrasounds detected multiple arterial stenosis, including right cephalic artery, common femoral arteries, and superficial femoral arteries. Thickening of the femoral arterial walls was also noted.
Rheumatology, pulmonology, and infectious diseases were consulted, and the following diagnoses were made: (i) acute decompensated heart failure; (ii) Takayasu arteritis. Our patient met four out of five diagnostic criteria of TA (age < 40 years old, symptoms of limb ischaemia, physical findings of decreased pulses, and unsymmetrical blood pressure, evidence of arterial stenosis provided by imaging); (iii) multiple ventricular thrombosis; (iv) pulmonary tuberculosis. This preliminary diagnosis was based on multiple infiltrates of her lungs and high incidence of tuberculosis in TA patients. Continuous intravenous nitroglycerin infusion, vigorous furosemide boluses, and oral beta blockers were administered to counter heart failure while low molecular weight heparin was injected subcutaneously for anticoagulation. Intravenous methylprednisolone 40 mg daily and cyclophosphamide 400 mg weekly were tailored to treat TA while an anti-tuberculosis regimen of oral isoniazid, rifampicin, ethambutol, and pyrazinamide was initiated at the same time. One week later, her symptoms began to resolve. Serum BNP and urine albumin excretion level gradually decreased while her ESR level raised up to 96 mm/h (<20 mm/h). After two weeks, repeated echocardiography showed her heart's dimensions returned to normal with LVEF 41%. Cardiac magnetic resonance imaging (MRI) detected small patches of delayed enhancement in myocardium of the ventricular septum and left ventricular inferior wall (Figure
). Both coronary arterial angiograms and Technetium sestamibi (99mTc-MIBI) static myocardial perfusion imaging were negative. Thoracic CT found her left lobe had greatly improved while multiple infiltrates and patches remained in the right lobe. Pulmonary embolism was suspected, and CT pulmonary angiogram found multiple emboli in the right pulmonary artery (Figure
). We gradually transitioned from low molecular weight heparin to warfarin and switched from intravenous methylprednisolone to oral prednisone before discharge. At her 2 month follow-up, we discontinued the warfarin as both echocardiography and computed tomography pulmonary angiography (CTPA) showed the complete dissolve of the thrombus. Both the morphology and function of her heart were normal. Her pulmonary lesions disappeared at her 4 month follow-up, and she remained on her steroid and anti-tuberculosis regime.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [163.0, 'cm']}",55.0985,52.34358,57.85343,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 163.0 cm, which is 163.0 cm * 0.393701 in/cm = 64.17326 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.17326 (in inches) - 60) = 55.0985 kg.
Hence, the patient's IBW is 55.0985 kg."
3433,10,Ideal Body Weight,physical,decimal,pmc-8079971-3,Extracted,"An 80-year-old man was admitted to our hospital for community-acquired pneumonia. He was treated with antibiotics and hospitalized for 8 days. His condition was complicated by diabetes mellitus and hypertension.
His body length was 158 cm, body weight was 63.7 kg, BMI was 25.5, serum albumin level was 2.6 g/dl, and PNI was 32.8 at discharge. He was started on Kracie ninjin'yoeito 7.5 g/day from the day of discharge. His grip strength, femoral circumference, SF-36 score, serum albumin level, and PNI were evaluated at discharge and 4 weeks later. Body weight increased to 65 kg at 4 weeks after discharge. As shown in , grip strength in his dominant right hand increased from 17 kg at discharge to 20 kg at 4 weeks after discharge. Right thigh circumference increased from 44 cm at discharge to 45.7 cm at 4 weeks after discharge. Corresponding SF-36 scores are shown in : PF 70.0 and 40.0, RP 68.8 and 100.0, BP 52.0 and 61.0, GH 52.0 and 72.0, VT 43.8 and 62.5, SF 37.5 and 100.0, RE 58.3 and 91.7, and MH 95.0 and 85.0. Serum albumin level was 4.3 g/dl, and PNI was 54.95 at 4 weeks after discharge.
Overall, the average changes in the component SF-36 scores from discharge in these three cases were as follows: PF −10.00 at 4 weeks and +5.00 at 12 weeks after discharge, RP +15.60 and +6.25, BP +9.50 and +35.5, GH +15.00 and +1.00, VT +9.35 and +15.65, SF +56.25 and 37.50, RE +20.90 and +12.50, and MH −5.00 and +22.50 () (1, 2).
The average change in grip strength at discharge was +1.75 kg at 4 weeks and +3 kg at 12 weeks after discharge. The corresponding change in femoral circumference was +1.35 and 4.5 cm, in serum albumin level was +1.4 and +0.85 mg/dl, and in PNI was +16.89 and +8.88 () (1, 2).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [158.0, 'cm']}",55.07095,52.3174,57.8245,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.20476 (in inches) - 60) = 55.07095 kg.
Hence, the patient's IBW is 55.07095 kg."
3434,10,Ideal Body Weight,physical,decimal,pmc-7968492-1,Extracted,"A 45-year-old man (height: 174 cm, weight: 82 kg) with no relevant medical history or known substance abuse had been working in a chemical plant producing and storing monochloroacetic acid for almost 20 years. The containers and pipes used for production, use, storage, and transportation of monochloroacetic acid in the factory are made of corrosion-resistant materials. However, they had not been inspected and maintained for a long time. On 17 October 2019, at 10 am, a glass tube ruptured as 80 % monochloroacetic acid, heated to 60 °C, was being delivered under pressure. The liquid sprayed the patient’s chest, left armpit, and right wrist. Although he immediately took off the clothes, redness, swelling, and the sensation of burning appeared in the affected area of the skin. The patient rinsed the acid off with water for 15 min and dried the skin with a towel. He then reported the accident and waited for assistance at his workplace. He complained of monochloroacetic acid mist and smell in the workshop and inhaled some of the vapours of the acid. Shortly thereafter, pain appeared in the area that previously was in contact with monochloroacetic acid, and dyspnoea and irritating dry cough developed. The patient was rushed to the local hospital in an ambulance, and during the ride, the skin was washed with a 4 % solution of sodium bicarbonate. Despite this treatment, the skin continued to show redness, ulceration, and blisters, and some areas turned dark brown. He arrived at the hospital approximately 2.5 h after the accident, and emergency debridement of necrotic areas was performed immediately. Shortly after, the patient developed lethargy, dyspnoea, and hypoxemia and was transferred to the Qilu Hospital for treatment the following day (18 October 2019). Upon admission, the patient’s vital signs were as follows: blood pressure (BP) 152/104 mmHg, heart rate (HR) 90 beats/min, respiratory rate (RR) 13 breaths/min, body temperature 37 °C, and oxygen saturation 95 % (with oxygen treatment at the rate of 5 L/min). The patient was conscious, lethargic, and developed dry heaving and blurred vision. Crepitations were audible over the lung base bilaterally. Heart rhythm was normal, the abdomen was flat and soft, and no abnormality was apparent. shows the laboratory findings on admission to the Qilu Hospital.
After administration of anti-tetanus immunoglobulin, the wound () was treated again by repeated rinsing with iodophor and saline and covering with antibacterial dressing. An intravenous infusion was initiated to maintain water-electrolyte balance and provide antibiotic treatment with cefoperazone/sulbactam and moxifloxacin. The patient also received daily intravenous infusions of 200 mg methylprednisolone as pulse therapy. Considering the large area of the burn and the long time during which monochloroacetic acid was absorbed, bedside continuous veno-venous haemofiltration (CVVH) was applied every other day to rapidly remove acid from the circulation and prevent acute renal failure. Patient’s lethargy gradually improved, and the level of consciousness returned to normal on the third day of treatment. The wound dressing was changed daily, and the patient did not have severe acidosis, oliguria, or anuria. However, he developed a cough with purulent yellow sputum and his temperature rose to 38.8 °C but dropped to normal after the administration of antibiotics. Six days after the admission (on 24 October), the patient’s condition was relatively stable, and laboratory tests improved (). Wheezing, coughing, and expectoration continued, however. shows the head, abdomen, and chest scan () revealed cerebellar infarction, a few ischemic degeneration foci in the brain, a few inflammation areas in both lungs, fibrous foci, a small amount of effusion in bilateral pleural cavity, and adjacent pulmonary tissue swelling, indicating monochloroacetic acid aspiration pneumonia. The patient therefore continued to receive antibiotics and started a regular terbutaline atomisation therapy to help expel the phlegm, and the patient was encouraged to cough out the sputum.
The patient remained stable until 5 November (see blood test findings in ). Methylprednisolone was discontinued and replaced with oral prednisone, which was gradually reduced. Given the stable condition of the patient, the burn department was contacted to arrange skin grafting. The patient was diagnosed with a 10 % third-degree burn. On 18 November, he underwent debridement and negative pressure suction of the upper limbs and left chest wall under general anaesthesia. Granulation and stale tissue on the wound surface were removed. Skin grafting was performed under general anaesthesia by rinsing the wound with hydrogen peroxide and sterile saline, and implanting the patient’s left anterior thigh full-thickness flap into the left upper limb and the left side of the chest wall. The wound healed perfectly (), and the patient was discharged on 4 December 2019. The results of the tests performed during a follow-up visit on 29 April 2020 were within the normal range.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [174.0, 'cm']}",69.55913,66.08117,73.03709,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 174.0 cm, which is 174.0 cm * 0.393701 in/cm = 68.50397 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.50397 (in inches) - 60) = 69.55913 kg.
Hence, the patient's IBW is 69.55913 kg."
3435,10,Ideal Body Weight,physical,decimal,pmc-7713855-1,Extracted,"An 18-year-old man (175 cm, 81 kg) with right hemifacial microsomia was scheduled for double-jaw surgery, correction with distraction osteogenesis, and mandibular anglectomy. Although he had no underlying medical history, he had undergone correction with distraction osteogenesis in 2006. At that time, the patient was classified as Cormack-Lehane grade 4, and oral intubation was performed with FOB. The patient reported a history of sleep apnea and heavy snoring, during the preoperative interview. His mouth opening was about 2.5-finger-breadth and neck extension was normal, during the preoperative physical examination. However, he had severe retrognathia and a class III Mallampati score. The thyromental distance was less than 6 cm. Moreover, an oral panoramic view X-ray showed narrowing of the nasopharyngeal airway, due to severe retrognathia (). According to El-Anwar et al. [], the mean depth (anteroposterior diameter) of the nasopharynx in normal adults is 21.8 ± 4.6 mm. However, the depth of nasopharynx in our patient was 15.5 mm, which was narrower than usual. We explained the possibility of a difficult airway and informed the patient about the special risks and procedures pertaining to performing an awake intubation procedure. Other preoperative laboratory examinations, chest X-ray, and electrocardiography revealed no abnormalities.
On the day of surgery, we prepared a Glidescope®; LMA, fiberoptic bronchoscope (Olympus Optical, Japan); a 0.035-inch-thick, 145-cm-long straight-tipped Angio Guidewire (Lunderquist-ring, Cook Critical Care, ); and a high-flow nasal cannula (Optiflow™). Nasotracheal intubation was required to secure space in the oral cavity for surgery; thus, we prepared nasotracheal tubes of various sizes. Non-invasive blood pressure monitoring, electrocardiogram, pulse oximetry, and bispectral index (BIS) measurement were performed in the operating room. The monitor showed an initial blood pressure of 140/84 mmHg, a heart rate of 58 beats/min and room air saturation of 98%. Lidocaine 4% was sprayed onto the tongue and oropharynx for topical anesthesia. Sufficient preoxygenation was provided with Optiflow™, at a flow rate of 20 L/min, to achieve an SpO2 of 100%. We started total intravenous anesthesia (TIVA) with 2% propofol and remifentanil administered at effect-site concentrations of 2.5 µg/ml and 1.5 ng/ml, respectively, with a target-controlled infusion pump. The SpO2 decreased to 96%, soon after the BIS was 42 and the patient fell asleep, but there was no further desaturation, after we raised the flow rate of Optiflow™ to 40 L/min. Since the left nostril was larger than the right nostril, owing to right-sided hemifacial microsomia, we decided to insert the FOB into the left nostril. After guiding the FOB into the left nostril of the patient, it passed into the trachea through the glottis, without any issue. We inserted the 145-cm-long, straight-tipped Angio Guidewire (Lunderquist-ring, Cook Critical Care) into the working channel of the FOB, till we could visualize the entrance of the guidewire into the carina (). We carefully removed the FOB and the guidewire remained in position. We also used the Glidescope® to confirm that the guidewire was still within the oral cavity and had passed through the vocal cord, and into the trachea (). The exchange catheter (1.6-mm internal diameter [ID], 2.7-mm outer diameter, CAEC, Cook Critical Care) was inserted over the Angio Guidewire and the Angio Guidewire was pulled out. A nasotracheal tube with 6.5 mm ID was advanced carefully over the exchange catheter into the airway without incidence. After removing the exchange catheter, the tracheal tube cuff was inflated, and proper positioning of the ETT was confirmed by auscultating both lungs and by confirming continuous positive end-tidal CO2. The monitor showed a blood pressure of 133/86 mmHg, heart rate of 95 beats/min, an SpO2 of 97%, and a BIS of 50 after intubation. An oxygenation level of 97% or higher was maintained throughout the procedure. After confirming proper intubation, we adjusted the effect-site concentration of propofol and remifentanil to 4.0 µg/ml and 2.5 µg/ml, respectively, and administered 80 mg of rocuronium intravenously. The time required for the administration of intubation to its confirmation was 16 min. The intra and postoperative periods were uneventful.
After the procedure, we provided a full explanation regarding this case report to the patient and obtained permission for the same.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3436,10,Ideal Body Weight,physical,decimal,pmc-7017684-2,Extracted,"A 42-year-old male (45 kg; 155 cm) with right Pancoast tumor severe pain (7/10 on NRS) from 5 months in dermatome distribution from C5 to T3, incompletely relieved on medical treatment. Right ESP block was given at T2 level in the sitting position. Following administration of 20 ml of 0.375% ropivacaine and 40 mg triamcinolone, pain was relieved in few minutes (1/10 on NRS) with sensory blockade from C3 to T5 on the right side. NRS score was noted for 24 h []. The patient was discharged with oral medications tapered. The patient was still pain-free without consumption of any other oral analgesics at the follow-up after 2 months.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [155.0, 'cm']}",52.35442,49.7367,54.97214,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (61.02366 (in inches) - 60) = 52.35442 kg.
Hence, the patient's IBW is 52.35442 kg."
3437,10,Ideal Body Weight,physical,decimal,pmc-5090078-1,Extracted,"A 17-year-old female with no medical history complained of general fatigue and bradycardia from three months before. Her height, body weight, and body mass index (BMI) were 161 cm, 45 kg, and 17.4 kg/m2, respectively. A physical examination indicated that the blood pressure and heart rate are 87/46 mmHg and 38 beats/min, respectively. Laboratory data indicated an elevation of hepatic enzymes (aspartate aminotransferase, 21 IU/L; alanine aminotransferase, 28 IU/L), hypoproteinemia (total protein, 6.1 g/dL; albumin, 3.9 g/dL), hypoglycemia (blood glucose, 67 mg/dL), and a decrease in free triiodothironene (FT3) and free thyroxine (FT4) levels (FT3, 0.87 pg/mL; FT4 0.87 ng/dL). Thyroid stimulating hormone (4.610 μIU/L) was normal. The total blood ketone level was high (114 mmol/L), but the levels of thiamin (2.7 μg/dL), cobalamin (548 pg/mL), folic acid (4.8 ng/mL), growth hormone (6.17 ng/mL), and adrenocorticotropic hormone (31.3 pg/mL) were within normal limits. An electrocardiogram showed bradycardia with junctional rhythm and prolonged QT interval (). A cardiac echocardiogram showed reduced left ventricular ejection fraction (LVEF 45%) with apical wall motion decline of both ventricles and both ventricles were dilated (LV diastolic dimension: LVDd 52 mm) (). A coronary angiogram showed no stenosis or obstruction, and cardiac magnetic resonance imaging (MRI) did not show late gadolinium enhancement. An endomyocardial biopsy revealed moderate vacuolar degeneration, hypertrophy, and attenuation of the myocardium as well as moderate interstitial fibrosis. Any inflammatory cell infiltrate, myocardial edema, or necrosis was not observed (). The patient was diagnosed with idiopathic dilated cardiomyopathy with sick sinus syndrome at the time.
An angiotensin-converting-enzyme inhibitor (perindopril) was prescribed without pacemaker implantation since the fatigue was clearly not related to the bradycardia. During the follow-up, cardiac echocardiographic findings after four months did not improve (LVEF 44%, LVDd 49 mm); her body weight reduced to 34.1 kg (BMI 13.6 kg/m2) after losing 16 kg in six months, and she was diagnosed with anorexia nervosa (AN) by a psychiatrist. The patient received nutritional counseling and appropriate psychotherapy to increase her caloric intake. One month later, her body weight increased to 43.5 kg (BMI 16.8 kg/m2), heart rate (HR) increased to 66 beats/min with sinus rhythm, and LVEF increased to 55%. One year later, her body weight increased to 54 kg (BMI 20.8 kg/m2), HR increased to 70 beats/min, and LVEF rose to 60%.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [161.0, 'cm']}",53.28748,50.62311,55.95185,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 161.0 cm, which is 161.0 cm * 0.393701 in/cm = 63.38586 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.38586 (in inches) - 60) = 53.28748 kg.
Hence, the patient's IBW is 53.28748 kg."
3438,10,Ideal Body Weight,physical,decimal,pmc-7505644-1,Extracted,"A 60-year-old male (height: 173 cm; weight: 70.9 kg) with a past history of rheumatoid arthritis was transferred to the ICU due to ARDS caused by H1N1 influenza virus infection. In a previous hospital, he was treated for influenza and possible secondary bacterial pneumonia for 18 days. However, oxygenation rapidly deteriorated two days before the transfer with the suspicion of ARDS. After the ICU admission, he was immediately intubated and the mechanical ventilation was started in an A/C mode with a tidal volume of 6.7 mL/kg of predicted body weight, peak inspiratory pressure of 24 cmH2O, positive end-expiratory pressure (PEEP) of 14 cmH2O, fraction of inspired oxygen 1.0, respiratory rate (RR) of 21 breaths/min, during which blood gas values were as follows: pH 7.35, PaO2 of 103 mmHg, and PaCO2 of 46 mmHg. Chest X-ray and CT showed diffuse bilateral infiltration with normal left ventricular function on cardiac echocardiography (Figure ).
Murray score was 3.25 (PaO2/FiO2 of 103, X-ray alveolar consolidation confined to 4 quadrants, PEEP of 14 cmH2O, compliance of 37 mL/cmH2O). In view of the deteriorating condition, we decided to start veno-venous ECMO using Cardiohelp (Maquet CP, Hirrlingen, Germany). Cannulation performed was with a 22-Fr cannula (PCKC-V, Toyobo, Japan) for drainage into his right atrium through the right femoral vein and with a 16.5-Fr cannula (CAPIOX EBS, Terumo, Japan) for blood infusion into the right internal jugular vein. The initial settings of ECMO begin at a flow of 42 mL/kg/min, speed of 3,000 rotations/min, fraction of delivered oxygen (FiO2) of 100%, and sweep of 2 L/min. The ventilator was changed to a lung-rest setting (PEEP of 10 cmH2O and pressure control of 8 cmH2O, RR of 15 breaths/min). In addition, he was empirically started on meropenem and azithromycin.
In the previous hospital, he was treated with methylprednisolone (1,000 mg/day) for two days. Additional methylprednisolone 1,000 mg was used for one day with subsequent steroid dosing (predonine 70 mg/day) in our hospital. The treatment of steroid pulse was performed because of suspected autoimmune disease or drug-induced pneumonia by methotrexate treatment. However, his blood test was finally negative for all autoimmune antibodies. Moreover, all bacteria and virus tests were negative. Therefore, the deteriorated patient’s oxygenation was considered to be suggestive of ARDS caused by influenza infection.
The multidisciplinary mobilization team with a physical therapist, nurse, medical engineer, and doctor evaluated the patient’s status and developed a daily plan of rehabilitation based on progressive mobilization protocol. On day 2, rehabilitation was limited to a passive range of motion due to the low conscious level (Richmond Agitation Sedation Scale [RASS] score: −2 to −4). Active mobilization was started from day 3 with patient consciousness alert (RASS score: −1 to 0). The patient was mobilized with sitting on the edge of bed and standing.
On day 4, mobilization level was elevated to standing two times in a day. On day 5, foot stepping was added to standing. On day 6 after the separation from ECMO, the patient was transferred from the bed to the chair with minimum assistance. On day 7 after extubation, the patient was ambulated in the ICU. Nutrition was started from day 2, and the intake protein increased to 1.3 g/kg on day 4 with calorie suppressed to 17.6 kcal/kg (Peptamen Intense®, Nestlé, Vevey, Switzerland). During mobilization in the ICU, the patient did not experience any hemodynamic, ventilatory, or cannulation trouble.
By using ultrasound, muscle mass was measured three times, and the median value was recorded for evaluation. Experienced examiner (N.N.) conducted the measurement with previously reported intra- and inter-observer reproducibilities [,]. The Rectus femoris cross-sectional area was measured between the anterosuperior iliac spine and the proximal end of the patella []. Diaphragm thickness was also measured by the ultrasound from the zone of apposition []. During the seven days of admission, the rectus femoris muscle mass decreased by 5.3%, 10.8%, and 13.0% on days 3, 5, and 7, respectively, compared with the ICU admission value (Figure ).
Diaphragm thickness remained unchanged (1.8 cm from day 1 through day 5) during five days of mechanical ventilation. The urinary titin, corrected with urinary creatinine, was measured using ELISA kit (27900 Titin N-Fragment Assay Kit, Immuno-Biological Laboratories, Gunma, Japan) to evaluate catabolism. Urinary titin level was much higher than the normal range (normal range: 1-3 pmol/mg Cr, urinary titin level in this patient: 24.1, 32.8, 38.0, 31.5, 38.4 pmol/mg Cr on days 1, 2, 3, 5, and 7, respectively), indicating ongoing catabolism. Blood urea nitrogen/creatinine (BUN/Cr) was also elevated to 34.6-63.6 (normal range: 10-20). In spite of the catabolism, the Medical Research Council (MRC) score was maintained at 59, 60, 58, and 60 on days 2, 3, 5, and 7, respectively. Furthermore, the patient did not experience ICU-acquired weakness [].
During ECMO, the patient’s tidal volume was reduced to 4.0-4.6 mL/kg, with peak inspiratory pressure of 18 cmH2O and PEEP of 10 cmH2O. His lung condition gradually improved. The bilateral infiltration of the X-ray was clearly disappearing. On day 4, oxygenation had significantly improved to PaO2/FiO2 of 183. On day 5, he was completely separated from ECMO. On day 6, he was liberated from mechanical ventilation. On day 7, he was discharged from the ICU. The functional status score for the ICU (FSS-ICU) was 31 out of 35 at discharge from the ICU.
On day 8, he was transferred to a ward with a Barthel index (BI) of 95 (stairs: need help). The six-minute walk test was 260 m (45% of normal value) on day 10 and 395 m (69%) on day 24 []. On day 22, chest X-ray showed normal lung fields (Figure ).
After steroid tapering in a ward, he was discharged directly home with a BI of 100 on day 27.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.0, 'cm']}",68.65362,65.22094,72.0863,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.0 cm, which is 173.0 cm * 0.393701 in/cm = 68.11027 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.11027 (in inches) - 60) = 68.65362 kg.
Hence, the patient's IBW is 68.65362 kg."
3439,10,Ideal Body Weight,physical,decimal,pmc-7344706-1,Extracted,"In 2005, a 30-year-old woman was admitted to the Department of Endocrinology, Poznan University of Medical Sciences, Poznan, Poland, with uncontrolled hypertension and obesity. On physical examination at admission, the patient was 163-cm tall and weighed 87 kg, with a body mass index (BMI) of 33 kg/m2. The mean arterial pressure in daily measurements was 140/105 mmHg. In the clinical examination, Cushing syndrome was suspected. In the hormonal evaluation, elevated cortisol concentration with the normal circadian rhythm of cortisol secretion was found.
Nevertheless, in a dexamethasone suppression test, the patient presented an elevated cortisol concentration after administration of 1 mg of dexamethasone (). Serum and diurnal urine concentration of Na, K, Ca, and phosphates were normal. The serum glucose profile is presented in .
Among the complications of hypertension, the patient revealed a hypertensive retinopathy of stage I/II.
We also performed dual-energy X-ray absorptiometry: T-score at L1–L4 lumbar spine was −1.57, and the patient was diagnosed with osteopenia.
Due to adrenocorticotropic hormone (ACTH)-independent hypercortisolemia, we performed diagnostic imaging; an adrenal computed tomography (CT) scan revealed the presence of moderately enlarged left gland presenting homogeneous absorption with no focal changes, whereas the right adrenal gland appeared normal. Magnetic resonance imaging (MRI) did not confirm any lesions in the pituitary gland. The biological and radiological data were highly suggestive of ACTH-independent Cushing’s syndrome. Surgical removal of the left adrenal gland was performed. Histopathology results showed micronodular adrenal hyperplasia. The patient was prescribed indapamide 1.5 mg once daily and perindopril 5 mg once daily. Moreover, sodium and potassium, calcium, and vitamin D3 supplementation were prescribed.
Despite surgical treatment, in 2010, the patient was admitted to the hospital due to recurrent uncontrolled hypertension. Her BMI was 35.8 kg/m², and mean arterial pressure in daily measurements was 155/120 mmHg. Skin hyperpigmentation was observed. The hormonal profile is presented in and the patient’s blood glucose level before treatment in 2010 is presented in .
Adrenal angiography did not show any focal changes. MRI of the sella region was therefore performed, revealing a hypointense pituitary tumor of 5 mm in diameter located in the left anterior pituitary lobe. These MRI findings were highly suggestive of pituitary microadenoma.
Trans-sphenoidal total resection of the pituitary tumor was performed. Upon immunohistochemical examination, the resected pituitary microadenoma cells exhibited positive staining for the ACTH antibody. The patient was prescribed perindopril 5 mg once daily, losartan 50 mg once daily, spironolactone 50 mg once daily, bisoprolol 5 mg once daily, indapamide 1.5 mg once daily, acetylsalicylic acid 75 mg once daily, desmopressin 0.1 mg twice daily, and hydrocortisone 20 mg–10 mg–0 mg daily.
Subsequently, in 2011, the patient was admitted to the Department of Surgery for a scheduled strumectomy due to multinodular struma, which had been diagnosed in 2010. During the physical examination, an enlarged and fibroelastic thyroid was identified. The serum concentration of thyroid-stimulating hormone (TSH), free triiodothyronine (fT3), and free thyroxine (fT4) were normal, indicating euthyreosis. The hormonal profile is presented in .
Ultrasound imaging demonstrated multiple nodules in both thyroid lobes, with the biggest solid nodule with calcification and hypoechoic outline measuring 1.17 × 1.82 cm.
The patient underwent a total strumectomy. Histological sections from the left lobe showed features of papillary thyroid carcinoma. The lesion was 1 cm in diameter with hyaline-fibrous capsule and calcification inside. Histopathology also revealed a multinodular struma of the right lobe. The patient was prescribed levothyroxine 100 µg (1 × 1), and she was qualified for iodine treatment.
In 2018, the patient was admitted to the Department of Gynecological Endocrinology Poznan University of Medical Sciences, Poznan, Poland, due to irregular menstrual cycle.
In the transvaginal ultrasonography, multiple small uterine fibroids were revealed. The endometrial thickness was 7 mm. The right ovary was enlarged by a cystic-solid, unilocular tumor with a size of 97 mm × 69 mm with central blood flow. There were no abnormalities in the left ovary revealed in the ultrasound examination.
Additionally, a hormonal analysis was performed ().
Due to ultrasound features and elevated Risk of Ovarian Malignancy Algorithm (ROMA) results, the patient was qualified for surgical treatment. Hysterectomy with bilateral salpingo-oophorectomy and retroperitoneal tumor excision were performed. Histopathology results have shown uterine glandular polyp (0.5 cm), serous superficial papillomas and superficial endometriosis in both ovaries, and female adnexal tumor of probable Wolffian origin (FATWO) located in the broad ligament of the uterus. The FATWO was 8 cm in diameter, contained a variable admixture of diffuse, solid, and sieve-like cystic areas filled with blood. Macroscopically, the tumor was soft and uncapsulated. Immunohistochemical examination revealed an interesting profile of this tumor: ER(+), PgR(+), AR(+), GATA3(+), calretinin(+), HBME(+), WT1(+), cytokeratins AE1/AE3(+), CK7(+), CKAE 1/3 (+), melan A(+), α-inhibin(+), CD99 (+), CEA mono(−), PAX8(−), TTF1(−), RCC(−), CK20(−), CD117(−), S100(−), EMA(−), HMB45(−), and Ki67 (5%).
Due to a history of multiglandular diseases: micronodular adrenal hyperplasia, pituitary adenoma, papillary thyroid carcinoma, and ovarian tumor, the patient was referred to genetic testing for mutations associated with multiple gland malignancy. We performed an analysis of 83 genes deletion/duplication (Invitae Multi Cancer Panel) in the whole blood sample. The Invitae Multi-Cancer Panel analyzes 83 genes associated with hereditary cancers across major organ systems, including: breast and gynecologic (breast, ovarian, uterine); gastrointestinal (colorectal, gastric, pancreatic); endocrine (thyroid, paraganglioma/pheochromocytoma, parathyroid, pituitary); genitourinary (renal/urinary tract, prostate); skin (melanoma, basal cell carcinoma); brain/nervous system sarcoma and hematologic (myelodysplastic syndrome/leukemia) cancers: AIP; ALK; APC; ATM; AXIN2; BAP1; BARD1; BLM; BMPR1A; BRCA1; BRCA2; BRIP1; CASR; CDC73; CDH1; CDK4; CDKN1B; CDKN1C; CDKN2A; CEBPA; CHEK2; CTNNA1; DICER1; DIS3L2; EGFR; EPCAM; FH; FLCN; GATA2; GPC3; GREM1; HOXB13; HRAS; KIT; MAX; MEN1; MET; MITF; MLH1; MSH2; MSH3; MSH6; MUTYH; NBN; NF1; NF2; NTHL1; PALB2; PDGFRA; PHOX2B; PMS2; POLD1; POLE; POT1; PRKAR1A; PTCH1; PTEN; RAD50; RAD51C; RAD51D; RB1; RECQL4; RET; RUNX1; SDHA; SDHAF2; SDHB; SDHC; SDHD; SMAD4; SMARCA4; SMARCB1; SMARCE1; STK11; SUFU; TERC; TERT; TMEM127; TP53; TSC1; TSC2; VHL; WRN; and WT1 gene mutations. We received positive results—pathogenic variant, exon 4. c.470T > C (p.Ile157Thr) heterozygous, with low penetrance identified in CHEK2, and a variant, exon 17. c.2484C > T (silent) heterozygous, of uncertain significance identified in KIT. Both mutations are not associated with MEN1 or MEN2 syndromes.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [163.0, 'cm']}",55.0985,52.34358,57.85343,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 163.0 cm, which is 163.0 cm * 0.393701 in/cm = 64.17326 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.17326 (in inches) - 60) = 55.0985 kg.
Hence, the patient's IBW is 55.0985 kg."
3440,10,Ideal Body Weight,physical,decimal,pmc-8494846-1,Extracted,"A 46-year-old Japanese man with a history of distal gastrectomy for gastric cancer visited our hospital on November 2011, because he wanted a more adequate dose of HD than the dialysis schedule (four hours twice a week) he was receiving at his facility at that time. The primary cause of his renal failure was ADPKD, and he started HD in October 2009. His dialysis schedule was 3 h twice a week until October 2011, when he suffered palpitations and shortness of breath due to congestive heart failure. His mother and young sister suffered from end-stage renal disease due to ADPKD. His height and weight were 175 cm and 72.1 kg, respectively, at the first visit to our hospital. His blood pressure was 201/122 mmHg. On physical examination, he had severe leg edema. Chest radiography revealed a high cardiothoracic ratio (55.9%), and his electrocardiogram showed no remarkable change. Extracellular fluid was gradually removed by ultrafiltration during his 5-h thrice weekly HD just after he started dialysis at our hospital on November 9, 2011. He subsequently recovered from this volume overload state. Four months after starting treatment, he became normotensive and had a lower cardiothoracic ratio.
He suffered from high fever and abdominal pain with serum C-reactive protein (CRP) 27.29 mg/dL soon after he started dialysis at our hospital. Abdominal magnetic resonance imaging (MRI) revealed an infected renal cyst with higher intensity on T1-weighted image (T1WI), T2-weighted image (T2WI), and diffusion-weighted image (DWI) compared with normal cysts, and that had a fluid–fluid level (Fig. ). The type of causative organism was not confirmed, because blood cultures obtained from him were negative. He was administered meropenem hydrate for 9 days followed by ciprofloxacin hydrochloride (CPFX) for 7 days on admission. He needed to receive CPFX for about 3 months after he was discharged from the hospital because of fever and abdominal pain with moderate serum CRP levels. The frequency of cyst infection episodes with fever, abdominal pain, and moderate serum CRP level were 10.0 days a month during his conventional HD period (November 2011 to April 2012). Following the initiation of 8-h thrice weekly nocturnal HD on May 2012 and until December 2019, the frequency of cyst infection episodes decreased to 1.5 days a month. Moreover, he attained a decrease and stabilization in levels of inflammatory markers and an improvement and maintenance of nutritional status compared with the conventional HD period (Fig. A, B).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3441,10,Ideal Body Weight,physical,decimal,pmc-7713794-1,Extracted,"A 70-year-old male (170 cm, 59 kg) was admitted for a cystic mass (10.4 × 7.9 × 7.6 cm) of the liver and decided to undergo right hepatectomy. The patient had a medical history of hypertension and diabetes mellitus. Pre-operative transthoracic echocardiography revealed a left ventricular ejection fraction of 44% and severe hypokinesia of the left ventricle. Coronary angiography showed no significant stenosis. Pulmonary function tests demonstrated a restrictive ventilation defect. Positron emission tomography-computed tomography (PET-CT) revealed pleural effusion and consolidation in the right lower lobe (). Laboratory findings were as follows: hemoglobin, 12.9 g/dl, white blood cell, 7,100 /μl, platelet, 339,000 /μl, C-reactive protein, 11.1 mg/dl.
The patient’s vital signs were stable prior to general anesthesia. General anesthesia was induced with 50 mg of propofol and rocuronium 50 mg and maintained with 0.2 μg/kg/ min of remifentanil and 5 vol% of desflurane. Tidal volume and respiration rate were set to 400 ml and 13 times/min, espectively. Positive end-expiratory pressure of 5 cmH2O was applied, and peak inspiratory pressure (PIP) was 20 cmH2O.
At four hours after the beginning of the operation, PIP abruptly increased to 32 cmH2O and a large amount of serous fluid was regurgitated through the endotracheal tube (ETT) (Figs. and ). However, hypoxia did not occur at FiO2 0.5. PaO2 and PaCO2 were within normal range and oxygen saturation was 100% during the entire intra-operative period. The endotracheal tube was exchanged for a 35 Fr left doublelumen endotracheal tube (DLT) and tracheal suction was performed continuously. Approximately 1,000 ml of yellowish fluid was regurgitated through the right side lumen of the DLT within 30 min. Right-sided thoracostomy was performed following hepatectomy, and 300 ml of pleural effusion was drained through the chest tube. Air leakage was observed through the chest tube during positive pressure ventilation. We could not detect and localize abnormal lesion with bronchoscopy. Any gross defect of diaphragm was not observed at operation field. The oxygen saturation of the patient had been consistently maintained at 100%.
Total operation time was 7 h and estimated blood loss was about 9,000 ml. Nine liters of crystalloid fluid, 550 ml of colloid fluid, 5 units of packed red blood cells and 10 units of fresh frozen plasma were infused. Urine output during the operation was 790 ml. Post-operational hemoglobin level decreased to 9.1 g/dl after the operation.
The patient was transferred to the intensive care unit (ICU) with intubated state. Laboratory findings of the drained fluid from chest tube and the DLT revealed that it was parapneumonic exudate (pH 7.12, glucose 37 mg/dl, protein 3.31 g/ dl, albumin 1.63 g/dl, lactate dehydrogenase 346 IU/L, cholesterol 18.2 mg/dl). The patient was diagnosed with pneumonia and treated with pleural drainage and antibiotics. The volume of fluid drained through the ETT and the chest tube gradually decreased. The patient was extubated on postoperative day 5 and discharged from the ICU ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3442,10,Ideal Body Weight,physical,decimal,pmc-5728880-1,Extracted,"A 46-year-old man who served as a government official first visited our hospital with complaints of 8-month history of involuntary movements during sleep time, and 3- month history of slow response and walking unsteady. He had begun feeling depressed without a known cause 8 months ago. At almost the same time, he had started to engage in involuntary movement such as kicks and grasps during nighttime sleep, with snoring and sleep apnea. He took diazepam tablets, but it did not work. Afterwards, he noticed excessive sweating and felt hot and cold waves. His maximum body temperature was 37.2°C; after he used nimesulide, the temperature dropped to 35.0°C and was subsequently increased, with difficulty. Moreover, he got terrible constipation at that point. He visited mental health centers and was diagnosed with “mild depression” without auxiliary examinations or treatment 4 months ago. About 3 months ago, his family noticed that he had lost approximately 20 kg in weight, choked when drinking, and exhibited slow response, visual hallucinations, and walking unsteady. He got frequent drops from bed during sleeping due to his substantial actions; meanwhile, gasping breath and sleep apnea fragmented his sleep. Eventually, he spoke seldom and seemed to be blunt with shuffling gait.
The patient did not have any relevant medical history. He denied having history of trauma, prior blood transfusions, intravenous drug use, and alcohol abuse (Table ).
The patient was the fourth individual in his large family to exhibit the same clinical manifestations. The other 3 members all died within a year after onset (Fig. , pedigree chart).
Eight months after the onset, he was taken to our hospital by his families. We did series of tests at that time.
The middle-aged man appeared dull. During check-up, he fell into “sleep” easily and soon was awakened in horror by his involuntary sleep movements or snoring. The skin and general examination were normal. Temperature: 36.5°C, respiratory rate 20/min, Blood pressure (lying): 165/109, Pulse: 115. Blood pressure (standing): 150/100 mm Hg, Pulse: 110. Weight: 77 kg. Height: 178 cm.
He exhibited severe cognitive impairments, particularly with respect to orientation, attention, calculation power, delayed memory, and visuospatial dysfunction (his Mini-Mental State Examination and Montreal Cognitive Assessment scores were 15/30 and 9/30, respectively).
He had slurred speech and dysarthria
Cranial nerves (CNs) I-VIII and XI-XII revealed no deficits. CN IX and X showed slowness of bilateral gag reflex, and limited symmetrical elevation of soft palate to phonation.
Muscle tone was normal. Muscle strength was 5/5 for all groups tested. Spontaneous and evoked myoclonus was evident.
Bilateral biceps reflex and bilateral triceps reflex were 3/4, and bilateral patellar reflex and bilateral Achilles reflex were 4/4. Hoffman sign and Babinski sign were absent. Frontal lobe signs palmomental and grasp were not elicited.
Touch, pin, vibratory, and proprioception sensations were normal. Romberg test was negative.
Coordination was inaccurate for finger/nose testing and heel/knee/shin testing; rapid alternating movements were clumsy.
Arm swing was absent. There was bradykinesia and postural instability. Rapidly progressive dementia, ataxia (dysarthria and gait instability), and myoclonus were typical signs in prion diseases.
Temperature monitoring revealed that the patient's body temperature fluctuated from 36.0°C to 37.8°C, and the loss of circadian rhythm was observed. Blood pressure monitoring indicated a steady high blood pressure of approximately 150/100 mm Hg and the loss of dipper-type blood pressure rhythm, with a heart rate that fluctuated approximately 100 beats per minute. A dynamic electrocardiogram revealed sinus rhythm with the incidental discovery of multifocal ventricular premature beat.
Blood examinations such as blood routine, coagulation function, liver and kidney function, electrolytes, myocardial enzyme, blood ammonia, homocysteine, folic acid, VitB12, microelement (calcium, cadmium, cobalt, chromium, copper, iron, lithium, magnesium, manganese, nickel, lead, thallium, zinc), thyroid function and antibodies, rheumatism biomarker, infection-related antibodies (hepatitis B virus, hepatitis C virus, syphilis, HIV), and tumor marker showed normal. Cerebrospinal fluid (CSF) examination (intracranial pressure was 200 mmH2O, cell number 1, glucose, chloride, protein, acetic acid, IgA, IgM, IgG, Oligoclonal bands, PCR for JC virus, EB virus, HSV-I virus, Mycobacterium tuberculosis) appeared normal and 14–3–3 protein was negative. Autoimmune encephalopathy related antibodies (N-methyl-D-aspartic acid receptor, contactin-associated protein 2, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid 1 receptor, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid 2 receptor, leucine-rich glioma inactivated protein 1, gamma-aminobutyric acid B), and paraneoplastic syndrome related antibodies (CV2/CRMP5, PNMA2, RI, Yo, Hu, Amphiphysin) in blood and CSF were all detected, but none of them indicates abnormity. Routine urinalysis and fecal analysis were normal. Hormone secretion detection demonstrated the abnormal secrete rhythmicity of prolactin and growth hormone.
Extensive θ activity and scattered slow waves are recorded in an electroencephalogram (EEG). Brain magnetic resonance imaging (MRI) revealed atrophy of the frontal and temporal. Polysomnogram (PSG) demonstrated the patient's obvious deprivation of total sleep time; neither spindle nor slow wave sleep was detected during his “fragmented sleep,” even when he showed snoring, mentalis relaxation, sleep apnea, and hyoxemia (Fig. ).
The nucleotides from 12742 to 13318 (GenBank accessionnumber U2918) of exon I in PRNP were amplified; then, polymerase chain reaction products were directly sequenced on an ABI 377 automatic sequencer. The results were analyzed using DNA Sequencing Analysis Software version 3.4.1 (Gene Codes Corp, Ann Arbor, Michigan). Genetic analysis found that the patient harbored a D178N/129M haplotype mutation in PRNP (a GAC→AAC homozygous mutation at codon 178 and a methionine polymorphism at codon 129).
The patient had been diagnosed with FFI and received treatment with drugs to improve brain metabolism, such as idebenone, ganglioside, and coenzyme Q10. During the follow-up by telephone, his wife told us that he got once improvement in his responsiveness soon after discharge; however, sudden death occurred 3 months later. The total disease course was 11 months.
The patient information involved in our manuscript has been obtained and informed consent was obtained from his legal representatives. All human studies have been approved by the appropriate ethics committee and have therefore been performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki and its later amendments.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [178.0, 'cm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3443,10,Ideal Body Weight,physical,decimal,pmc-7402981-1,Extracted,"A developmentally appropriate and previously healthy 15-year-old girl presented to the Emergency Department with a 4-day history of severe and persistent headache associated with a 1-day history of photophobia, altered mentality, and gait disturbance. No recent contributing history was noticed. She was afebrile but had tachycardia (111 beats/min) and hypertension (146/78 mmHg). She was 160 cm tall and weighed 51 kg. The initial neurologic examination revealed lethargic mentality with emotional lability, dysarthria, and an ataxic gait without lower-extremity weakness; however, no focal neurologic deficits or meningismus-related signs were apparent. She had no palpable lymphadenopathy or rash.
The initial work-up showed normal complete blood count, electrolyte, and chemistry panel, and thyroid function test findings. Pregnancy testing was negative. Brain magnetic resonance imaging (MRI) showed unremarkable results. Lumbar puncture revealed significant lymphocytic pleocytosis (WBC, 114/mm3; 86% lymphocytes); normal protein (21 mg/dL) and glucose (64 mg/dL) levels; and normal opening pressure. CSF meningitis and encephalitis panels were negative for multiple bacterial, viral, and fugal antigens, including herpes simplex virus (HSV)-1, varicella zoster virus, and Cryptococcus. Systemic infectious and rheumatologic evaluations were also negative. Pelvic computed tomography of a palpable mass found on an abdominal exam revealed a large cystic mass with a complex component (3.8 cm×4.9 cm×3.6 cm) in her right ovary, which was most likely a dermoid cyst or teratoma (). She underwent surgical resection of the ovarian tumor. Twenty-four-hour video/EEG monitoring revealed continuous diffuse background slowing and extreme delta brushes (), suggesting diffuse encephalopathy related to anti-NMDA receptor (NMDAR) encephalitis. No AED was administered. The antibody and NMDAR test results were positive in the CSF (1:40 titer) but negative in the serum. Anti-voltage-gated potassium channel (VGKC), anti-glutamic acid decarboxylase (GAD), antiperoxidase, antithyroglobulin, and paraneoplastic antibodies tested negative in the CSF and serum.
The patient was administered high-dose intravenous (IV) methylprednisolone 20 mg/kg daily for 5 days and IV immunoglobulin G (IVIG) 400 mg/kg daily for 5 days. Her aggressive activity, ataxic gait, and dysarthria symptoms continued to wax and wane since the first-line immune therapy. No significant improvement was observed on video/EEG monitoring. She was treated with IV rituximab (a monoclonal anti-CD20 antibody, 375 mg/m2/wk) as the second-line immune therapy. Her neurological symptoms and behavioral abnormalities improved significantly after IV rituximab therapy, while repeat MRI showed negative results; repeat CSF examination showed decreased anti-NMDAR antibody titer (1:20). Video/EEG findings became normal. She had no significant complications such as a serious infection or viral reactivation during the rituximab treatment. Final pathology of the ovarian mass showed a right cystic teratoma. She was discharged on day 19 with significant improvement in neurologic status and planned to continue active rehabilitation treatment. Presently, she is no longer taking antihypertensive drugs. At the 12-month follow-up, she reported continued improvement in her neurologic symptoms and a stable mood.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3444,10,Ideal Body Weight,physical,decimal,pmc-6329249-1,Extracted,"A 66-year-old male weighting 72 kg, with a height of 170 cm, was admitted to the Post Anesthesia Care Unit (PACU) after a laparotomic duodeno-cefalo-pancreasectomy. His comorbidities included hypertension, chronic obstructive lung disease and a history of deep vein thrombosis. His medications included fondaparinux (discontinued 24 h before surgery), atenolol and pantoprazole.
The anaesthesiologist planned an endovenous analgesia strategy. The positioning of an epidural catheter was considered an unacceptable risk due to the short discontinuation time of the fondaparinux.
The surgery was uneventful and the patient was extubated in the operating room. The analgesia was administered as follows: acetaminophen 1 g 8 hourly, ketoprofen 100 mg 6 hourly and tramadol 100 mg 6 hourly.
However, the patient complained of a pain described as ‘sharp’ during the first postoperative day. The pain intensity was evaluated with the numeric rating scale (NRS) and ranged from 8 to 10. The analgesic rescue therapy consisted of morphine boluses (total 30 mg); however the patient reported more nausea than pain relief after the administration of each bolus.
In order to provide analgesia we decided to execute a bilateral ESP block at T9 level. An informed consent for anaesthesia was obtained.
The ESP block was performed as described by Forero: the patient was placed in the semi-recumbent position and a high-frequency linear ultrasound transducer was placed transversally on the spinous process of the T9 vertebra. Afterwards, with a lateral movement of the probe, the transverse process was visualized and centred. The erector spinae muscle was identified by performing a 90° rotation of the probe on the deep plane. The ESP block was executed by injecting 20 ml of 2% ropivacaine. In the following 30 min the patient reported a satisfying analgesia (NRS 3). The patient requested further analgesics after 18 h of the block execution.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3445,10,Ideal Body Weight,physical,decimal,pmc-7322849-1,Extracted,"A 28-year-old Japanese woman had infertility, with G5 P1, but not antiphospholipid syndrome. Owing to protein S deficiency, she was treated with aspirin 100 mg per day and heparin therapy, which was discontinued because of a subchorionic hematoma at 12 weeks of gestation. At 16 weeks, she presented with proteinuria and edema in the lower extremities and was transferred to another hospital. A high dose of oral glucocorticoids (prednisolone, 40 mg) was initiated for presumed primary glomerulonephritis before 20 weeks of gestation with severe hypoalbuminemia (1.8 g/dL) and severe proteinuria (10 g/gCre) were suspected. In addition, 40 mg of nifedipine per day and 750 mg of methyldopa hydrate per day were administered for hypertension. Her condition failed to improve, and bilateral pleural effusion appeared. Therefore, she was transferred to our hospital at 21 weeks and 3 days of gestation.
Her medical history was unremarkable, except for infertility. Her birthweight was within the normal range (3260 g). Her height was 156 cm, blood pressure was not high at 128/91 mmHg, and she weighed 53.3 kg. She had remarkable edema in her lower extremities. She did not have sclerodactyly. Laboratory test results were as follows. Serum total protein and albumin levels were very low at 4.9 and 2.2 g/dL, respectively. Serum creatinine and uric acid were slightly high at 0.65 and 6.9 mg/dL, respectively, owing to her gestation. Serum total cholesterol, low density lipoprotein cholesterol, and triglycerides were 510, 329, and 439 mg/dL, respectively. C-reactive protein was 0.37 mg/dL, and urine protein content was 5.6 g/day, with no hematuria. Antinuclear antibody was low titer (1:40), and anti-centromere antibody was positive at 29.3 IU/mL. In addition, anti-dsDNA, anti-β2-glycoprotein I antibody, and anti-phospholipid IgG antibody, lupus anticoagulant were negative. Serum IgG, IgA, C3, and C4 levels were 131, 85, 64, and 10 mg/dL, respectively. Serum IgM and IgE levels were 139 and 133 mg/dL, respectively. Further, protein S activity was in the normal range (95%) in our hospital.
She met the criteria for nephrotic syndrome. However, it was difficult to diagnose primary nephrotic syndrome due to PE before 20 weeks without kidney biopsy. Therefore, we examined serum soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF) levels since the ratio of sFlt-1/PlGF (> 36) in pregnant women have been demonstrated as a predictor of PE []. The sFlt-1/PlGF ratio turned out to be very high (sFlt-1, 13,400 pg/mL; PlGF, 21.9 pg/mL; serum sFlt-1/PlGF ratio 611.9), so that we diagnosed her nephrotic syndrome because of PE, and we discontinued oral glucocorticoids. We used furosemide and human albumin solution, however, her fetal growth curve was lower than 2 standard deviation after 21 weeks (Fig. ) and, further, she had a reflux of uterine artery blood flow. Therefore, she had a cesarean section at 24 weeks 3 days. Five weeks after delivery, we performed a kidney biopsy. The core kidney tissue contained 21 glomeruli without global sclerosis. Two of the 21 glomeruli showed focal segmental sclerotic lesions, with epithelial cell hyperplasia and foam cells in the tubular poles (Fig. a, b). In addition, spike formations and bubbly appearances of the glomerular basement membrane were absent (Fig. c). In addition, hyaline arteriolosclerosis and intimal thickening in the interlobular arteries were not found (Fig. d).
Immunofluorescence (IF) staining demonstrated diffuse, linear, peripheral patterns of C4d, slight paramesangial patterns of IgM and negative results for IgG, IgA, C3, and C1q. Electron microscopy revealed diffuse subendothelial edema without electron-dense deposits. Further, diffuse foot process effacement was not observed (Fig. ). The histological diagnosis was severe glomerular endotheliosis with focal segmental glomerulosclerosis (FSGS) lesions. For the histology of the placenta, hemorrhagic infarction around the umbilical cord and syncytial knots were consistent with PE (Fig. ). As shown in her whole clinical course (Fig. ), 8 months after delivery, her proteinuria disappeared completely without anti-hypertensive agents, which was also compatible with PE. The neonate was diagnosed with respiratory distress syndrome, rickets, and retinopathy. His weight increased from 303 g to 2806 g 171 days after birth.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [156.0, 'cm']}",48.75993,46.32193,51.19793,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 156.0 cm, which is 156.0 cm * 0.393701 in/cm = 61.41736 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.41736 (in inches) - 60) = 48.75993 kg.
Hence, the patient's IBW is 48.75993 kg."
3446,10,Ideal Body Weight,physical,decimal,pmc-8556051-1,Extracted,"A 46-year-old Korean woman presented with a 1-month history of progressive generalized edema since November, 2020. She had a history of malignant melanoma on the left posterior side of the thigh that was treated with wide local excision on May 29, 2019. Because of metastasis to the left sentinel and inguinal lymph nodes, she received pembrolizumab 200 mg every 21 days for 1 year, from July 10, 2019 to July 3, 2020. During pemblizumab treatment, she was started on levothyroxine for hypothyroidism, presumably an immune-related AE of pembrolizumab. Four months after the cessation of pembrolizumab, she developed generalized edema, most notable in the periorbital area and both hands and legs, which gradually worsened. She denied taking any new medication or personal and family history of kidney disease. Her baseline observations on admission were as follows: height, 165 cm; weight, 70 kg; blood pressure, 140/80 mm Hg; heart rate, 74 bpm and regular; and temperature, 36.4°C. Clinical examination revealed grade 3 pitting edema in both lower legs. Four months before the onset of the edema, her blood pressure was 120/70 mm Hg, body weight was 65 kg, and body mass index was 23.88 kg/m2. Laboratory findings were as follows: white blood cell count 10,940/μL (reference range 3800–11,000/μL); hemoglobin 12.5 g/dL (reference range 11.2–15.0 g/dL); platelet count 208 × 103/μL (reference range 140–420 × 103/μL); total protein 5.71 g/dL (reference range 6.0–8.0 g/dL); albumin 2.84 g/dL (reference range 3.3–5.2 g/dL); blood urea nitrogen 5.4 mg/dL (reference range 6–26 mg/dL); creatinine 0.66 mg/dL (reference range 0.4–1.2 mg/dL); estimated glomerular filtration rate 105.9 mL/min per 1.73 m2; total cholesterol 238 mg/dL (reference range 0–200 mg/dL); urine red blood cells 6 to 10 cells/high power field (reference range 0–2 cells/high power field); and urine protein to creatinine ratio 3277 mg/g (reference range 0–150 mg/g). Urine dipstick for protein was negative before pembrolizumab treatment. Human immunodeficiency virus antigen and antibody results were negative. A contrast-enhanced computed tomography scan of the abdomen showed normal sized kidneys (right kidney: 9.6 cm; left kidney: 10.7 cm) and no evidence of vaso-occlusive processes in the renal arteries.
She underwent kidney biopsy for suspected glomerulonephritis. Light microscopic findings of biopsy specimens showed that up to 36 glomeruli, 2 glomeruli exhibited segmental sclerosis with atrophied tubules and fibrosis in the interstitium (Fig. A, B). Electron microscopy revealed wide effacement of the epithelial cell foot processes (Fig. C). Immunofluorescence microscopy showed no immune complexes or autoantibody deposition.
After ruling out other causes of secondary FSGS, she was diagnosed with FSGS caused by pembrolizumab. The patient was started on irbesartan and furosemide to treat high blood pressure, proteinuria, and edema. She did not resume treatment with pembrolizumab and immunosuppressive therapy was not applied. After 2 months, the features of nephrotic syndrome resolved and the urine protein-to-creatinine ratio decreased to 203 mg/g.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3447,10,Ideal Body Weight,physical,decimal,pmc-2946043-1,Extracted,"A 62-year-old man (weight, 59.5 kg; height, 162 cm; BMI, 22.7 kg/m2) was scheduled to undergo a subtotal gastrectomy with gastrojejunostomy. The patient had been diagnosed with hypothyroidism one year earlier and had been prescribed medication since then. No specific abnormal laboratory results were noted on the preoperative evaluation except a first degree AV block on the electrocardiograph.
Midazolam 2 mg was administered i.m. as premedication 30 minutes before anesthesia. In the operating room, the patient was monitored by an electrocardiogram, a noninvasive blood pressure monitor and pulse oximetry. The baseline blood pressure, heart rate, and SpO2 were within the normal range. Before induction, epidural catheterization was performed at the T6-7 interspace with a paramedian approach for continuous postoperative analgesia. There were no questionable signs suggesting a pneumothorax or pneumomediastinum during epidural catheterization. Anesthesia was induced with 100 mg of propofol and 40 µg of remifentanil. Facial mask ventilation was made easy with 100% O2. After an intravenous injection of 50 mg rocuronium, tracheal intubation was performed using a single lumen internal diameter (ID) 8.0 mm tube (Mallinckrodt medical. high volume low pressure. Athlone. Ireland) in one attempt without difficulty. The laryngeal grade was 1 and the tracheal tube was passed through trachea without resistance. The tube was fixed 23 cm from the level of the incisors and the cuff was inflated with 4 ml of air as a minimal volume to prevent a circle leak in this patient. Bilateral breath sounds were confirmed by auscultation. Anesthesia was maintained with isoflurane in air/O2 (FiO2 = 0.5) and supplemental continuous infusion of remifentanil. A nasogastric decompressive tube was not inserted into this patient. No other venous access including central venous line was made. The subtotal gastrectomy with gastroduodenostomy (Billoth I) under the diaphragm proceeded without an event. At the end of surgery, all anesthetic agents were discontinued and the residual neuromuscular blockade was reversed with pyridostigmine and glycopyrrolate. The tracheal tube was removed when the patient responded to verbal commands and showed sufficient spontaneous respiration and neuromuscular function (as ascertained by the nerve stimulator). There were no tinged signs of blood or tissue-like material on the removed tube. The patient remained in the post-anesthetic care unit (PACU) for 30 minutes event free and was then transferred to the general ward. During the 24 hour postoperative period, the patient's vital signs were stable without any specific incidents. On postoperative day 1, the patient complained of discomfort on the left lateral side of the neck without any dysphagia or dyspnea. On palpation, diffuse crepitus was felt on that site of the neck but no definite swelling was detected. Pulse oximetry revealed an oxygen saturation of 91% under room air breathing. Oxygen with a flow rate of 3 L/min was provided through a nasal cannula. The patient had already been placed on nil orally and intravenous antibiotics administration due to surgery. Arterial gas analysis before applying the oxygen showed the following: pH 7.44, PaO2 74.4 mmHg, PaCO2 34.2 mmHg and 95.8% of SaO2. Neck CT (), chest CT () and chest x-ray revealed emphysema of the left neck (), a retropharyngeal space and a pneumomediastinum. The patient was observed closely with an electrocardiograph and pulse oximetry. The patient showed no specific signs or symptoms over the subsequent 24 hours, and the oxygen saturation was maintained at 99-100%. Antibiotics were used for only two days, and a diet was also started. On postoperative day 6, the emphysema of the neck and retraopharynx had almost resolved, but a small amount of air still remained in the mediastinum (). He had an uneventful recovery and was discharged on postoperative day 8. Five days after discharge, the neck AP/lateral x-ray still showed slight emphysematous signs. However, the patient did not feel any discomfort.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [162.0, 'cm']}",58.69299,55.75834,61.62764,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (63.77956 (in inches) - 60) = 58.69299 kg.
Hence, the patient's IBW is 58.69299 kg."
3448,10,Ideal Body Weight,physical,decimal,pmc-7605781-1,Extracted,"A 31-year-old male professional Sumo wrestler presented with right hip pain associated with a limited range of motion (ROM). His height was 190 cm, and his weight was 200 kg (body mass index [BMI] 55.4 kg/m2). Physical examination revealed a positive flexion adduction internal rotation test, flexion abduction external rotation test and dial test. The lateral center-edge angle was 19°, and the Sharp angle was 46° with a double floor at the bottom of the acetabular fossa, increased tear-drop distance, and a pistol grip deformity on the well-centered anteroposterior (AP) pelvis radiograph (). A false profile view revealed that the vertical center anterior angle was 16° (). A modified Dunn view revealed that the alpha angle was 87°, suggesting cam morphology (). Three-dimensional computed tomography scan revealed an anterior inferior iliac spine (AIIS) morphology and a cam lesion (). On magnetic resonance imaging (MRI), a T2-weighted coronal view demonstrated a high signal intensity area in the anterosuperior labrum (). Proton-density fat suppression coronal view on MRI revealed increased cartilage width (), and T2 mapping showed an increasing T2 value, suggesting articular cartilage damage.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [190.0, 'cm']}",84.04734,79.84497,88.24971,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 190.0 cm, which is 190.0 cm * 0.393701 in/cm = 74.80319 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (74.80319 (in inches) - 60) = 84.04734 kg.
Hence, the patient's IBW is 84.04734 kg."
3449,10,Ideal Body Weight,physical,decimal,pmc-6751414-1,Extracted,"A 77-year-old man presented with a complaint of a lump on the upper abdominal wall for several weeks. His performance status (PS) was Grade 2 (Height, 168 cm; Weight, 58 kg; BMI, 20 kg/m2). He had a history of appendicitis that was operated upon. On physical examination, the tumor was located on the upper left side of the abdominal wall measuring around 5 cm with poor mobility and partial ulceration but without pain (Fig. ). At a nearby hospital, he had previously undergone physical examination and computed tomography (CT) for his symptoms. Advanced gastric cancer with invasion to the skin of the abdominal wall was suspected and, for more specific investigation and therapy, he was referred to our department. We obtained informed consent from all participants, and all procedures therapy were performed in accordance with the Declaration of Helsinki.
His blood investigation revealed the following: hemoglobin 8.7 g/dL, white blood cell count 6,060 /μL, platelets 321,000 /μL, prothrombin time-international nomarized ratio (PT-INR) 1.05, sodium 140 mmol/L, potassium 4.2 mmol/L, chlorine 105 mmol/L, creatinine 0.91 mg/dL, aspartate aminotransferase (AST) 13 U/L, alanine aminotransferase (ALT) 10 U/L, alkaline phosphatase 249 U/L, γ-guanosine triphosphate cyclohydrolase (γ-GTP) 14 U/L, LD 156 U/L, total bilirubin 0.8 mg/dL, C-reactive protein 0.41 mg/dL, carcinoembryonic antigen-S (CEA-S) 1.6 ng/mL, alpha-fetoprotein 1.83 ng/mL and carbohydorate antigen 19–9 (CA 19–9) <2 U/mL. There was moderate anemia but there was no organ failure and or elevation of tumor marker.
On Upper gastrointestinal endoscopy, a Type 3 tumor that measured around 40 mm was observed occupying from the angle of the stomach to the anterior wall of the antrum of the stomach (Fig. ).
On biopsy, the histological type was revealed as tubular adenocarcinoma (tub1) and immunostaining for HER2 was negative.
Thoracoabdominal enhanced CT revealed invasion of the tumor from the anterior wall of the stomach to the lateral region of the liver and infiltration from the abdominal wall to the skin. There was no evidence of metastasis or ascites (Fig. ).
On the basis of these findings, we diagnosed advanced gastric cancer (L-Less, Gre, type 3, 40 mm, tub1), cT4b (SI; liver, skin) N0M0 c Stage IIIA. Initially we anticipated chemotherapy considering that the patient's PS was Grade 2 and the defect of abdominal wall was too large for surgery. In addition, the patient did not want to undergo surgery. S-1+Cisplatin (SP) therapy was performed as first-line therapy every 3 weeks [].
Obvious shrinkage of the tumor invasion to the skin was observed, and we determined that PR was obtained at the end-point of 4th course of SP therapy. However, because of malaise (Grade 2), we had to set a 1-month interval. During the interval, the invasion to the skin gradually increased again; hence, another two courses of SP regimen were added with decreased dose. After six courses of SP therapy had been completed, PR was obtained again by the re-shrinkage of the skin tumor on physical examination and upper gastrointestinal endoscopy and CT (Fig. , ). At this point, the patient was not amenable to surgery or chemotherapy; hence, we adopted a “wait-and-see” approach. During this period, the skin tumor underwent re-growth gradually for which RAM/PTX therapy (3-week administration at 1-week intervals) was introduced as the second line chemotherapy, 2 months after the previous one []. Over the course of therapy, anemia (Grade 3) and neutropenia (Grade 2) were observed and we were compelled to skip one administration each of PTX in course 2 and 3but RAM dosage was completely administrated through all five courses (Fig. ). Throughout the second line of therapy, the skin tumor kept decreasing visually and enhanced abdominal CT revealed the shrinkage of the primary tumor and the invasion to the lateral area of the liver and skin. Similar findings were observed on gastrointestinal endoscopy; and hence, we determined that PR was obtained again (Fig. ). Since his general condition was observed have improved, we planned to perform surgery with the aim of reaching a chemotherapy-free status.
We performed open total gastrectomy with D2 lymph nodes dissection (Roux-en-Y reconstruction) with combined partial resection of the skin, abdominal wall, and liver. There were no findings of the peritoneal dissemination, metastasis to the liver, or ascites (Fig. ). The components separation method was performed for abdominal wall closure with the defect of the skin by exposure of the anterior sheath of abdominal rectal muscles and resection of partial aponeurosis of the right external abdominal oblique muscle.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.0, 'cm']}",64.12607,60.91977,67.33237,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg."
3450,10,Ideal Body Weight,physical,decimal,pmc-7544376-1,Extracted,"A 58-year-old obese woman presented to the emergency department of our hospital with recurrent episodes of constrictive chest pain during exercise within the last 2 weeks (de novo AP). She described similar symptomatology a few years ago, but she did not have any medical evaluation at that time. The patient denied shortness of breath during daily activities, dizziness, or syncope. Her past medical history revealed type 2 diabetes mellitus, arterial hypertension, and dyslipidemia, with an estimated 10-year risk of fatal cardiovascular disease of 3% according to SCORE risk chart. She was on chronic ambulatory medication with bisoprolol 5 mg quaque die (QD), perindopril 5 mg QD, atorvastatin 20 mg QD, and metformin 1000 mg bis in die with good medication adherence. There was no family history of cardiac diseases.
Focused clinical examination on admission revealed class I obesity (height = 156 cm, weight = 80 kg, body mass index = 33 kg/m2); blood pressure was 120/65 mm Hg, heart rate was 56 bpm, heart and lung sounds were normal with no audible cardiac murmurs, respiratory rate was 17 breaths/min and peripheral oxygen saturation was 98% in ambiental air.
Laboratory workup revealed impaired fasting glucose (112 mg/dL = 6.2 mmol/L), high values for total cholesterol (210 mg/dL = 5.43 mmol/L), LDL-cholesterol (157 mg/dL = 4 mmol/L) and tryglicerides (157 mg/dL = 1.76 mmol/L), high NTproBNP (1120 pg/mL) and normal myocardial necrosis markers, including serial determination of myoglobin (33–28 ng/mL, cut-off value 60 ng/mL), high-sensitive cardiac troponin I (23-8-13 ng/L, cut-off value 54 ng/L), and creatinkinase (CK/CK-MB = 61/21– 84/15–52/17 UI/L, cut-off value 280/22 U/l). Routine liver and kidney function blood tests were within normal range (serum creatinine: 0.85 mg/dL = 75 μmol/L, blood urea nitrogen: 15.85 mg/dL = 5.66 mmol/L, AST = 32 U/L, ALT = 47 U/L).
The resting ECG on admission during pain-free interval showed biphasic T-waves with terminal negative component (+/−) in leads V2 to V6, DIII, aVF and minimal ST depression in leads DI and aVL (Fig. ).
Transthoracic echocardiography revealed interventricular septum and anterior wall hypokinesia with preserved global left ventricular ejection fraction (55%) and mild mitral regurgitation.
We established the diagnosis of low-risk non-ST-segment elevation acute coronary syndrome with a Global Registry of Acute Coronary Events risk score of 92 points.
The patient was admitted to the cardiac intensive care unit and monitored with continuous telemetry. Following her presentation, the patient was immediately started on aspirin 300 mg loading dose followed by 75 mg QD orally, clopidogrel 600 mg loading dose followed by 75 mg QD orally, atorvastatin 80 mg QD orally, and a bolus of 5000 IU of unfractioned heparin. Keeping in mind that our patient presented ECG findings compatible with type A Wellens pattern, which is highly specific (89%) for critical LAD stenosis, the patient underwent cardiac catheterization the same day. Coronary angiography showed subocclusive dynamic obstruction of the LAD due to MB (Figs. and ). The ECG taken the next day showed diffuse T waves flattening (Fig. ).
The patient was managed conservatively. Her hospital course was uneventful and she was discharged on pharmacological therapy (clopidogrel, bisoprolol, amlodipine, atorvastatin, and metformin) with well-controlled symptoms on follow-up.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [156.0, 'cm']}",48.75993,46.32193,51.19793,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 156.0 cm, which is 156.0 cm * 0.393701 in/cm = 61.41736 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.41736 (in inches) - 60) = 48.75993 kg.
Hence, the patient's IBW is 48.75993 kg."
3451,10,Ideal Body Weight,physical,decimal,pmc-6503421-1,Extracted,"A 19 years old man was admitted to our hospital after a high energy motorcycle accident in February 2018. The patient presented with a severe varus deformity of the left thigh and an ipsilateral open fracture of the distal femur, without neurovascular injuries. Associated injuries were a left wrist trans-scaphoid trans-styloid perilunate fracture-dislocation and a right occipital condyle fracture. The patient height was 1,95 m and weight 115 kg. The patient had a previous motorcycle accident with a femoral diaphyseal fracture treated with an antegrade T2 Recon nail (StrykerTM) almost 2 years before the recent trauma. Anamnestic data revealed full weight bearing without aids and full return to everyday life at the latest follow-up outpatient evaluation (18 months after surgery). However, the patient referred dull pain at the fracture site at weight bearing, with radiographic signs suspect for hypertrophic nonunion (). Plain radiographs obtained at the emergency department showed a refracture of the femoral shaft in correspondence to the nonunion site with 145° nail angulation in the coronal plane. The distal locking screws were also bent (). A comminuted fracture of the distal femur (AO type 33 C3) was confirmed, occurring at the tip of the previously implanted nail. The patient was treated in the first hours with a damage control procedure. An external fixator bridging the knee joint was applied in order to gain length, axis and rotation at the distal femur fracture site (). Accurate debridement of the open fracture was carried out, classifying the lesion as Gustilo () type II open fracture after the procedure. Primary closure of soft tissue was achieved. After surgery the patient was kept under observation for three days in intensive care unit and transferred to our orthopedics and traumatology unit afterwards. Definitive treatment was scheduled on the seventh day after trauma.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.95, 'm']}",88.57489,84.14615,93.00363,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.95 m, which is 1.95 m * 39.3701 in/m = 76.77169 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (76.77169 (in inches) - 60) = 88.57489 kg.
Hence, the patient's IBW is 88.57489 kg."
3452,10,Ideal Body Weight,physical,decimal,pmc-2876915-1,Extracted,"A 46-year-old morbidly obese man, 168 cm tall and weighing 98 kg, was brought to the emergency department with a penetrating injury in back of neck []. He had sustained the injury in a personal brawl with a fellow truck driver. The offending instrument (screw driver) was in between the 7th cervical and 1st thoracic intervertebral space in situ. The patient was immobilised in lateral position by cotton roles and pillow since stabilisation by cervical collar was not possible. Patient was incoherent and inebriated with smell of alcohol but answered questions satisfactorily. His pulse rate was 100/min, blood pressure 140/84, regular respiration and; he was maintaining oxygen saturation of 100%. Neurological examinations did not reveal any motor deficit at that time. There were no obvious injuries in thorax and abdomen, confirmed by radiological investigations. X-ray of neck and chest showed the point of screwdriver, which was present between 7th cervical and 1st thoracic intervertebral space []. Chest radiograph of the thorax revealed absence of pneumothorax. Lateral position and stabilisation was maintained meticulously during examination and investigations. The neurosurgeon planned to operate in prone position. The anaesthesiologist team decided to establish airway, in lateral position, in which patient was immobilised. Patient was shifted to emergency operation theatre maintaining the lateral position. His medical problems included alcoholism and hypertension on irregular treatment. Preoperative examination revealed patient was full stomach having normal intact dentition and about two-finger mouth opening. Mallampati score was III. Difficult airway situation was compounded due to patient's inebriated state, obesity, full stomach and emergency nature of surgery. Difficult airway trolley was kept ready. Establishment of airway and prevention of any neurological damage were of prime concern. Three options were considered to secure airway - fibre optic intubation, use of laryngeal mask airway and direct laryngoscopy aided with flexible stylet. Since patient was uncooperative and under influence of alcohol, ‘awake’ fibre optic intubation was not possible. Using LMA was not preferable due to full stomach situation. Direct laryngoscopy with elective use of flexible stylet was finalized. ECG, pulse oximeter, non-invasive blood pressure, temperature and provision to measure end tidal carbon dioxide were attached to patient. After preoxygenation anaesthesia was induced by propofol 2 mg/kg body weight, fentanyl 1.5 μgm/kg body weight and succinylcholine 1 mg/kg body weight. After adequate anaesthetic conditions were reached, manual in line stabilisation was done. Direct laryngoscopy with (size four) Mcintosh laryngoscopic blade was performed and glottic view revealed Class 3 of Cormack and Lehane's classification. Intubation was aided with malleable 673 mm long stylet with outer diameter of 4 mm. Intubation was achieved in first attempt with size 8.0 disposable endotracheal tube []. Ventilation with normal peak pressure was easy.
Anaesthesia was maintained with oxygen, nitrous, halothane and vecuronium. Subsequently, patient was turned to prone position for surgical approach. Intraoperative ventilation and surgery were uneventful. Extubation and postoperative course was uneventful. Postoperative examination revealed no neurological deficit. Patient was cared in postoperative ward with uneventful recovery and discharge.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.0, 'cm']}",64.12607,60.91977,67.33237,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg."
3453,10,Ideal Body Weight,physical,decimal,usmle-6870,Extracted,"A 17-year-old man presents to his family physician for an evaluation about the size of his penis. He feels increasingly anxious during physical education (PE) class as he has noticed that the size of his penis is significantly smaller when compared to his peers. Based on the physical examination, he is Tanner stage 1. The weight and height are 60 kg (132 lb) and 175 cm (5 ft 9 in), respectively. The cardiopulmonary examination is normal; however, the patient has difficulty identifying coffee grounds by smell.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3454,10,Ideal Body Weight,physical,decimal,pmc-4720805-1,Extracted,"A 30-year-old male (height: 175 cm, body weight: 105 kg) presented with fever for 6 days, and abdominal pain and diarrhea for 2 days. He was admitted to the gastroenterology department of an outside hospital. He did not have any history of underlying disease and had recently stopped smoking. He worked for 2 weeks at another hospital where a patient diagnosed with MERS. His initial vital signs and results of initial laboratory examination were unavailable to us, because he was admitted to an outside hospital. However, according to information from that hospital, physical examination on admission to that hospital revealed normal vital signs (except for fever) and initial laboratory examination showed mild elevation of liver enzymes. In that hospital, he firstly underwent chest and abdominal radiographs and abdominal CT for further evaluation of abdominal pain. The initial chest radiograph, which was taken 6 days after the onset of fever, showed a patchy increased opacity in the left lower lung zone, retrocardiac area (). Abdominal CT showed no specific finding in abdominal and pelvic organs; however, a patchy area of consolidation with an air-bronchogram was detected in the left lower lobe of the lung, which was mainly peripherally located (). Conservative treatment with intravenous fluid was used for abdominal pain. Although he did not initially have any respiratory symptoms, he began coughing 9 days after the onset of fever. Because of this new respiratory symptom, occupational history, and a recent MERS outbreak in Korea, he underwent laboratory examination for MERS. A follow-up chest radiograph, which was taken 10 days after the onset of fever, showed newly developed patchy areas of ill-defined increased opacity in the right upper lung zone and increased extent of the previously detected consolidation in the left lower lung zone (). A chest CT scan performed on the same day showed multifocal patchy areas of nodular consolidations orgwith ground-glass opacity (GGO) halo and nodular GGO lesions in both upper lobes, which were mainly slightly peripherally located (). Moreover, this scan also demonstrated increased extent of mixed consolidations and GGOs with air-bronchograms in both lower lobes, mainly in the dependent area (). There was no pleural effusion or significant lymph node enlargement. Finally, he was diagnosed with MERS by testing the sputum by real-time reverse-transcriptase-polymerase chain reaction (rRT-PCR) (). For intensive care and management of MERS, he was transferred to a negative pressure room of our hospital on the day of diagnosis. Physical examination in our hospital showed fever (38.4℃) and elevated blood pressure (154/106 mm Hg). His vital signs on admission are summarized in . Laboratory examination on admission of our hospital showed normal white blood cell counts (5640/µL), and elevated serum aspartate aminotransferase (AST, 155 international unit [IU]/L), alanine aminotransferase (ALT, 77 IU/L), lactate dehydrogenase (904 IU/L), and C-reactive protein (CRP, 9.39 mg/dL).
He was administered antiviral agents (ribavirin, kaletra [ritonavir + lopinavir], and interferon-alpha) and antibiotics (tabaxin [piperacillin + tazobactam] and cravit [levofloxacin]). Daily follow-up radiographs were taken to evaluate disease progression. Fever disappeared after 2 days of treatment; although radiologic abnormalities remained on early follow-up radiographs, then their extent decreased after 5 days of treatment. After a week of treatment, he showed no symptom. Follow-up laboratory examination showed normalization of CRP (0.14 mg/dL), slightly deceased but remained elevated AST (131 IU/L), whereas increased ALT (142 IU/L). Finally, follow-up sputum tests by rRT-PCR (conducted twice) showed negative results, and he was discharged after 13 days in our hospital.
On the day of discharge (23 days after the onset of fever) he underwent chest radiograph and chest CT scan. The chest radiograph depicted markedly decreased extent of previous increased opacities in the right upper and left lower lung zones (). The chest CT scan showed markedly decreased extent of previously detected lesions with residual nodules or GGOs in both lungs, and developed traction bronchiectasis within retracted consolidation with volume loss in the left lower lobe, which suggested fibrosis ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3455,10,Ideal Body Weight,physical,decimal,pmc-3483496-1,Extracted,"A 37-year-old female patient (161 cm, 49 kg) was admitted with sickle cell syndrome (SCA), S/Beta (β) positive thalassemia. Hemoglobin electrophoresis showed an HbS count of 58.5%, HbA count of 23.5%, HbA2 count of 7%, and an HbF count of 11%. Due to Crohn's disease and liver dysfunction, the patient was scheduled for elective laparoscopic cholecystectomy (LC) to treat acute cholecystitis. It was decided to perform the operation with thoracic epidural anesthesia (TEA) due to severely impaired liver function and hematologic problems. The patient had been diagnosed as having Crohn's colitis ten years prior to our clinic admission, following several episodes of abdominal pain and bloody diarrhoea. The diagnosis had been confirmed by radiology, endoscopic examination and biopsy of the gastrointestinal tract. Azathioprine was also used for treatment of Crohn's disease. Seven years ago the patient underwent successful elective cesarean surgery. During the diagnosis of SCA disease, plasma exchange occurred 7 times. Examination of each system revealed no abnormality. The reports of hemoglobin (Hb) level and liver function tests are shown in and . Our patient was not given preoperative medication. Noninvasive monitoring (EKG, arterial blood pressure and pulse oximetry) was initiated on patient arrival. All data were recorded at 5 minutes intervals. During the monitoring, 500 ml of isolyte S was infused.
TEA was performed with a 20-G Tuohy needle and epidural catheter that was inserted 5 cm in the cephalic direction from T9/T10 for perioperative anesthetic management and postoperative
pain control. This was followed by a 15 ml injection of 0.5% bupivacaine through the catheter. Twenty-fifth minutes later, sensory blockage was established at T4. The patient received oxygen at a rate of 4 L/min through a facemask attached to an end tidal CO2 monitor. During the operation the patient was given a 10-25 microgram/kg/min propofol infusion for sedation, 2 mg midazolam for hypnotic, and 100 microgram fentanyl for shoulder pain. Shoulder pain was the main intraoperative problem observed in our patient. Surgery time was approximately 105 minutes with CO2 insufflations pressure ≤ 12 mmHg and was eventful. There was no need for intraoperative blood transfusion and our patient was taken to the intensive care unit without experiencing any problem during the surgical procedure. Throughout surgery, the patient remained hemodynamically stable with a pulse rate 64-78/min and a systolic blood pressure of 104-126 mmHg. After the operation during the 2nd and 4th hours, 0.5% bupivacaine was administered for postoperative pain control. The epidural catheter was removed after 24 hours. The patient was discharged from the hospital 3 days after surgery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [161.0, 'cm']}",53.28748,50.62311,55.95185,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 161.0 cm, which is 161.0 cm * 0.393701 in/cm = 63.38586 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.38586 (in inches) - 60) = 53.28748 kg.
Hence, the patient's IBW is 53.28748 kg."
3456,10,Ideal Body Weight,physical,decimal,pmc-3983423-1,Extracted,"A 52-year-old woman (height 160 cm, weight 47 kg) with a history of hyperthyroidism was scheduled for total radical thyroidectomy because of a gradual increase in the size of the thyroid nodules. The patient's previous medical history was unremarkable. Preoperative laboratory tests, including thyroid function test, and chest x-ray were unremarkable. An electrocardiogram (ECG) taken 1 month prior to surgery showed atrial fibrillation, and transthoracic echocardiography revealed normal left ventricular ejection fraction without regional wall motion abnormalities. She was not given premedication before surgery. In the operating room, non-invasive blood pressure monitoring, ECG (lead II) and a pulse oximetry monitoring were placed. Pre-anesthetic blood pressure was 120/70 mmHg, heart rate was 70 beats/min, and oxygen saturation was 95%. The ECG rhythm was same as preoperative state, suggesting atrial fibrillation is chronic. After preoxygenation, anesthesia was induced with propofol (3.5 µg/ml) and remifentanil (0.1 µg/kg/min) using target controlled infusion (TCI) pump (Orchestra® Base Primea, Fresenius Vial, Brezins, France) and she was intravenously given rocuronium 50 mg. After tracheal intubation, anesthesia was maintained using propofol and remifentanil TCI in an oxygen-air mixture (FiO2 = 0.5). After about 40 minutes, atrial fibrillation converted to the NSR (heart rate, 70 or so), which persisted. On postoperative day 4, the patient was discharged with NSR. One month later, the patient was still having NSR. The patient was lost to follow-up afterwards.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3457,10,Ideal Body Weight,physical,decimal,pmc-5067398-1,Extracted,"A 19-year-old man presented to the orthopedic surgery department with pain in the left buttock after military training which including running with hyper-flexion of hip for 3 hours, twice a day for 5 days. When he hyper-flexed his left hip joint, he felt and heard a crack. Initially about one week later, he referred to the local hospital because of persisting hip pain. On radiographic evaluation, he diagnosed as pelvic bone fracture and recommended for further evaluation. However, he refused to get more examination due to the alleviation of the hip pain. Although he got rest without any military training for the next six weeks, there was no improvement and tingling sense developed over the posterior aspect of left thigh. During the first consultation with the patient, he complained difficulty on sustained standing and sitting on a locked position.
His body weight, height, hip and lumbar T-score for dual-energy x-ray absorptiometry (DXA) scan were 76 kg, 183 cm, –0.7 and –0.1 respectively. On physical examinations, there was no limitation on range of motion of the left hip joint. Also he could walk without any pain except mild tenderness on the area distal from the ischial tuberosity. On the radiographs of the pelvis anteroposterior and frog leg view (), there was a 35×40×20 mm sized bony fragment, 15 mm distance from the left ischial tuberosity. After the patient admitted to our hospital, he had an examination of computed tomography () and magnetic resonance imaging for rule out pathologic conditions. There was a bony fragment at left ischial tuberosity, which was mainly from conjoined origin of biceps femoris and semitendinosus tendons without any bone marrow edema (). Overall, he diagnosed as old avulsion fracture at ischial tuberosity. He determined to get conservative treatment on condition of a gradual alleviation of the symptom. During the admitted 2 months, he just got rest and high intensity laser therapy. Thanks to the improvement except discomfort on running, he discharged and returned to his military unit.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [183.0, 'cm']}",77.70874,73.8233,81.59418,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 183.0 cm, which is 183.0 cm * 0.393701 in/cm = 72.04728 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (72.04728 (in inches) - 60) = 77.70874 kg.
Hence, the patient's IBW is 77.70874 kg."
3458,10,Ideal Body Weight,physical,decimal,pmc-5646301-2,Extracted,"A 42-year-old female with anxiety neurosis presented with urinary retention, perineal numbness, and gait disturbance owing to sacral pain. Her height was 160 cm, weight was 37.65 kg, and body mass index was 14.7 kg/m2 (weight loss) []. She complained of urinary retention 10 days after slipping and falling to the floor. Neurological examination revealed normal muscle power in her lower extremities, with decreased ankle jerk. Sensory disturbance was detected in the perineal region. Urinary retention was severe, with loss of bladder urgency. On the basis of the above findings, we diagnosed neurogenic bladder dysfunction.
Sagittal reconstructed CT revealed that the second sacral vertebral body was fractured and displaced into the sacral canal (). The sacral kyphotic angle was 107 degrees (). Axial reconstructed CT confirmed that sacral canal was narrowed by the protruding sacral vertebral body (). Sagittal and axial plane MRI revealed that sacral nerves were compressed by the angulated sacral vertebral body and lamina on T2-weighted images (Figures and ). We determined that the fracture was unstable and would subsequently become a sacral kyphotic deformity. Thus, we planned to perform decompression surgery with stabilization.
The first, second, and third sacral laminae were explored through a straight posterior midline approach. Laminectomy of the first, second, and third sacral laminae was performed using a burr. No hematoma was observed. The sacral nerve roots were not disrupted. We passed UHMWPE cables from the central laminectomy area to the third and fourth posterior sacral foramina using a sublaminar wire technique. We inserted bilateral S1 pedicular and S2AI screws and connected the rods. Finally, we tightened the UHMWPE cables to the rods (Figures and ).
The patient's perineal numbness improved immediately after surgery. One month after surgery, she was able to urinate, and, 3 months after surgery, her bladder function had completely recovered. Three months after surgery, implant infection occurred. We considered that the fracture became stabilized at that time. Thus, we removed all implants. Following the surgery, the infection was healed. One year after the surgery, she returned to normal daily life without a cane. One- and three-month postoperative follow-up sagittal reconstructed CT revealed a high-density area in the second sacral vertebral body (Figures and ). One-year postoperative follow-up sagittal reconstructed CT revealed that the second sacral vertebral body had united without any displacement (). The sacral kyphotic angle was 105 degrees and the sacral kyphotic deformity did not deteriorate ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3459,10,Ideal Body Weight,physical,decimal,pmc-6026813-1,Extracted,"An 18-year-old female patient presented to the dermatology clinic with recurring painful and tender boiles on her axillae, groin and neck. She had been suffering from these boiles for two years. Her family history was unremarkable for hidradenitis supprutiva (HS). Previous therapy included local antimycotic treatment (clotrimazole, econazole and ketoconazole), local antiinflammatory treatment with corticosteroids and systemic antibiotic treatment (doxycyclin, clindamycin, rifampicin and azithromycin). The patient is a known case of insulin resistance (laboratory findings: fasting blood sugar of 65 mg/dL (normal), high fasting insulin level of 20 mU/L and a positive glucose tolerance test with maximal 195 mg/dL after 1h and 144 mg/dL after 2h, HbA1c 5.9), consequently Metformin had been administered but discontinued after 12 months because of intolerable side effects (nausea). Cyproterone acetate was also prescribed in order to treat the polycystic ovarian syndrome (PCOS) and hyperandrogenism (DHEA Serum: 4397 ng/ml, free androgen index of 49, normal testosterone and tissue proteins).
On physical examination, the patient had normal vital signs, her body mass index (BMI) was 37.1 kg/m² (body height: 185 cm and body weight: 127 kg). She showed seborrhea of the scalp, the face and the upper back. Acanthosis nigricans was found in the axillae, abdominal, submammary, neck and in the groins. A mild form of hypertrichosis presented with growth of beard hair and narrowing the hairline border on the sides of the forehead.
There were multiple inflamed nodes on the neck, the intramammary and inframammary region, both axillae, inguinal folds and one sinus tract draining pus in her left axilla (). On the basis of the aforementioned clinical findings, the diagnosis of hidradenitis suppurativa Hurley stage II was made.
Antibiotic treatment with clindamycin 300mg bd and rifampicin 300mg bd was administered for 10 weeks. After completion of the prescribed course of antibiotic treatment, the remaining inflammatory lesions of HS on the above-mentioned areas had completely regressed. Then, a wide surgical excision of two inflamed deep-seated nodes, one sinus tract of 2.5 cm length and one atrophic scar in the left axilla was carried out ().
The histopathological examination yielded the following results: an expanded epidermis with deep-seated and expanded hair follicles, surrounded by massive infiltration consisting of neutrophils, plasma cells, lymphocytes, eosinophils and histiocytes. The epithelium of the hair follicles was degraded. In other nearby tissue, we found a moderately cell-rich scar tissue with extensive plasma cell collection surrounded by vascularity.
Subsequently, she was referred to the endocrinology clinic where congenital adrenal hyperplasia, Cushing syndrome and hypercortisolism were excluded.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [185.0, 'cm']}",75.01979,71.2688,78.77078,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 185.0 cm, which is 185.0 cm * 0.393701 in/cm = 72.83469 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (72.83469 (in inches) - 60) = 75.01979 kg.
Hence, the patient's IBW is 75.01979 kg."
3460,10,Ideal Body Weight,physical,decimal,pmc-7726185-2,Extracted,"Case 2 is the sister of case 1 who presented with headache, vomiting, blurred vision, and pulsatile tinnitus when she was 33 years old. She was 1.58 meters tall and weighed 54 kg (BMI 21.6). Neurological examination disclosed bilateral papilledema and decreased visual acuity (OD, 0.6; OS, 0.4). A lumbar puncture revealed a higher recumbent opening pressure of 400 mmH2O and the component of cerebrospinal fluid was normal. MRI disclosed partial empty sella. Other examinations were the same as case 1 and were also unremarkable. The patient was treated with acetazolamide and glycerol, from which her headache subsided and visual impairment receded partially. Eight years later, the patients complained of numbness of the left face. Ophthalmoscopic examinations revealed atrophy of papilla and loss of acuity which was the same as before. Hyperalgesia of the left face was found on physical examination. Lumbar puncture found that recumbent opening pressure was 260 mmH2O.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.58, 'm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.58 m, which is 1.58 m * 39.3701 in/m = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3461,10,Ideal Body Weight,physical,decimal,pmc-6713204-1,Extracted,"A 24-year-old male suffered a cardiorespiratory arrest at home's bathtub when returning from New Year's party. Cardiopulmonary resuscitation was unsuccessful and a forensic autopsy was ordered by the Magistrate on duty. According to the deceased's friends, he had taken AAS (stanozolol, testosterone, tamoxifen, mesterolone, and nandrolone) with intramuscular delivery in the previous 6 months (doses unknown). He had no family history of dyslipidaemia, premature atherosclerosis or cardiac events except for one episode of precordial pain some months before. There were no antecedents of illicit drugs consumption.
A forensic autopsy was performed, with a postmortem delay of 12 h, according to the guidelines of the Association for European Cardiovascular Pathology (AECVP) []. The corpse showed hypertrophy of skeletal musculature, with low amount of subcutaneous fat and several tattoos in shoulders, arms, thighs, and thorax (). The height was 178 cm and the weight 85 kg (body mass index, BMI: 26.8 kg/m2). On internal examination, there were multiorgan congestion and acute pulmonary edema. Mechanical trauma or asphyxia was ruled out.
On gross examination the heart showed cardiomegaly (420 g) being the expected heart weight in relation to body weight of 358 g (range 271–473 g) according to Kitzman et al. []. The ventricular thickness was within the upper normal ranges (left ventricular free wall 15 mm, ventricular septum 15 mm, right ventricular free wall 5 mm) (). Coronary arteries, with a right dominance, had a normal origin and course, showing severe atherosclerosis (>75% stenosis) with acute superimposed occlusive thrombosis at the left main trunk and left anterior descendant (LAD) (). The right and circumflex coronary arteries did not show alterations. Areas of scarring were located at the intersection between the posterior wall and the posterior third of the septum (postero-septal) (). Atrioventricular and sigmoid valves were normal. For histology, samples of ventricular myocardium (n = 14), coronary artery, brain, lung, liver and kidney were taken, fixed in formaldehyde solution 4%, buffered, paraffin-embedded sectioned at 3–6 µm thickness and stained with hematoxylin and eosin (HE) and Masson trichrome (heart). Acute myocardial infarction at the anterior third of the septum and the left ventricle (LV) anterior wall (), subacute myocardial infarction at apical septum and apical posterior LV wall (), myocytes hypertrophy () and small intramyocardial vessel disease () were detected. Furthermore, the macroscopic findings described in the coronary arteries were confirmed (). The rest of organs showed congestion and acute pulmonary edema.
The peripheral blood was obtained from femoral vein (adding potassium oxalate and sodium fluoride as preservatives) and stored refrigerated at 4 °C until the analysis. Blood and vitreous humor were used for routine ethanol and other volatiles screening by headspace gas chromatography with flame-ionization detector (HS-GC-FID) (Varian 3800CP; Varian, Inc., Walnut Creek, CA, USA) coupled with combipal autosampler (CTC Analytics, Zwingen, Switzerland). Blood was screened by cloned-enzyme donor immunoassay (CEDIA) (Indiko®; Thermo Fisher Scientific, Waltham, MA, USA) for the presence of cocaine, amphetamines, methadone, barbiturates, opiates and cannabis. Then, independently of the result obtained in the immunoassay, blood and vitreous humor were submitted to a broad toxicological analysis using gas chromatography (Agilent 6890N; Agilent Technologies, Santa Clara, CA, USA), with mass spectrometric (MS) detection (Agilent 5973; Agilent Technologies) in combination with high-performance liquid chromatography (HPLC) (Agilent Infinity 1260 G1311B, Agilent Technologies) with a diode-array detector (DAD) (Agilent Infinity 1260 G4212B; Agilent Technologies). Analysis of anabolic steroids in whole blood was performed using a method previously developed by Fabresse et al. [] using liquid chromatography (Vanquish UHPLC; Thermo Scientific, Waltham, MA, USA) coupled to high-resolution mass spectrometry (LC-HRMS) (Orbitrap Q-Exactive-Focus; Thermo Scientific).
Ethanol was quantified by HS-GC-FID (Varian 3800CP) using the official method of the National Institute of Toxicology and Forensic Sciences (NITFS). The column used was a DBWAX (30 m × 0.25 mm × 0.25 µm, Agilent J&W GC Columns; Agilent Technologies). To 200 µL of each specimen was added another 200 mL of saturated saline solution containing 1-propanol as internal standard. After stirring and waiting 15 min to reach the equilibrium 500 µL of headspace was injected into the chromatograph. Ethanol was positive in blood ((0.90 ± 0.05) g/L) and vitreous humour (0.84 g/L).
Blood and vitreous humor were submitted to systematic toxicological analysis by solid phase extraction (SPE). The pH of each sample 2.5 mL of blood and 2.5 mL of humor vitreous was adjusted to 6. The mixture was poured into Bond-Elut Certify™ columns (Agilent Technologies), and gently sucked through. Finally, the analytes were eluted with 3 mL of a freshly prepared mixture of chloroform:acetone (Vchloroform:Vacetone = 50:50) and then with a second mixture of dichloromethane:isopropanol:ammonia (Vdichloromethane:Visopropanol:Vammonia = 78:14:8). The elutes were collected and evaporated to dryness under a gentle nitrogen stream. The residue was reconstituted with 100 µL of methanol and transferred to a chromatographic vial.
Aliquots (2 µL) of the extracts were injected into a GC–MS system mentioned above. In this case, a VF-1 ms capillary column (methylsilicone gum, 30 m × 0.25 mm × 0.25 µm; Hewlett Packard, San Jose, CA, USA) was used. In parallel, 4 µL of each extract were injected into the HPLC-DAD system mentioned above. In this case, a gradient created by a mobile phase composed of aqueous phosphate 10 mmol/L buffer pH 3.6 and acetonitrile which allows to obtain the complete separation of the analytes on a C18 reversed phase column (250 m × 4.6 mm × 5 µm; Kinetex, Torrance, CA, USA).
No toxic substances were found in this routinely analysis.
One milliliter of methanol and 2 mL of sodium hydroxide 0.1 mol/L were added to 2 mL of whole blood, then the mixture after stirring was extracted twice with 2 mL of heptane. The sample was mixed for 15 min and then centrifuged at 3 500 rpm for 10 min. The upper organic layer was decanted into another tube and evaporated to dryness under a nitrogen steam. The sample was reconstituted with 100 µL of methanol containing 0.1% formic acid, vortex mixed for 10 s, and transferred into injection vials for analysis.
A six-point calibration curve was used over the range 1.0 to 100.0 µg/L for blood. The calibration levels were prepared spiking 2 mL of physiological serum with a standard solution containing stanozolol, nandrolone, tamoxifen, testosterone, and mesterolone and submitted to the same procedure as whole blood.
Chromatography was performed on a Thermo Vanquish UHPLC system and separation was carried out on a C18 Thermo column (100 m × 2.1 mm × 1.9 µm; Thermo Scientific) maintained at 30 °C. The mobile phase was composed of solvents A (aqueous 0.05% formic acid) and B (acetonitrile + 0.1% formic acid). The column was maintained at 35 °C and eluted with a gradient of 10% B (0–1.0 min), 10%–100% B (1.0–5.0 min), hold at 100% B (5.0–6.0 min); the column was finally set to 10% B (6.0–6.5 min) and hold at 10% B (6.5–9.0 min). The total runtime was 9 min at a flow rate of 0.40 mL/min. Compounds were detected using an Orbitrap mass spectrometer (Q-Exactive Focus; Thermo Scientific) equipped with a heated electrospray ionization source (HESI) operating in positive ionization mode (Sheath gas flow rate 60, Aux gas flow rate 5, Spray Voltaje 3.50, Capillary Temp 380 °C, S-lens 300, Aux gas heat Temp 300 °C). Data were acquired in PRM mode over a mass range of 100–400 m/z at the resolving power 35.000 with an isolation window of 3.0 m/z. Chromatographic data acquisition and quantification were performed using TraceFinder Forensic v4.1 software (Thermo Scientific).
Protonated molecular ions (M + H+) of steroids were identified with exact mass and retention time (±0.2 min). Mass error was <5 ppm for all analytes. No interferences were observed at the retention times. The method showed a good linearity in the range previously described in physiological serum. The lower limit of quantification for all compounds was 100 µg/L.
The results from the analysis of those anabolic steroids in blood are summarized in . Tamoxifen and mesterolone were not found and testosterone was below quantification level.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [178.0, 'cm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3462,10,Ideal Body Weight,physical,decimal,pmc-6395486-1,Extracted,"The patient that has been reported here was a 40-year-old male. Chief complains were an epigastric pain, abdominal bloating in postprandial time, and progressive increase of darkish color of his urine. The previous history of illness was not contributory to his present illness. Family history revealed that his uncle had colon cancer and lung cancer, however, a family history of hepatitis or jaundice or liver diseases could not be substantiated. The patient was a smoker and has been consuming about 10 cigarettes per day for the last 24 years. He was a social drinker and consuming about 350 mL of beer once a week. The patient reported no history of allergy. Also, there was no history of taking nutrient supplements. He has been working in recycling industry. There was no history of previous surgery or blood transfusion.
According to the history of present illness, the patient started taking oral Za ga-do Kowa® from January 2016 for his constipation. He began to feel heartburn from around March 2016 and then started to consume Ohta-Isan® and Gasuto-ru®. From early April 2016, he frequently felt malaise as well as epigastric pain. Around mid-April 2016, he noticed yellowish skin. From May 2016, the color of urine was found to be dark and brown. The stool color became somewhat whitish.
Along with time and mainly from mid-May 2016, the extents of malaise feelings became exacerbated. On May 17th, 2016, he noticed considerable nausea, noticeable loss of appetite, and increasing order of malaise. On May 19th, 2016, he was admitted to a clinic for his complaints. The local clinic referred him to our department on that day, and he was admitted to Imabari Saiseikai Hospital, Ehime, Japan.
On admission, physical examination revealed that his height was 168.7 cm and weight was 84.6 kg. He was conscious of admission. The skin and bulbar conjunctiva were icteric. However, there was no murmur at heart or lung. There were marks of insect bites on extremities. Also, acne was found on the back. Bowel sounds were normal. The abdomen was flat, soft and without any noticeable tenderness. Liver and spleen were not palpable. He had a blood pressure of 116/72 mm of Hg. Pulse rate was within normal range (88 beats per minute).
The laboratory findings on admission have been shown in and described below: aspartate trans-aminase (AST); 988 IU/I, alanine aminotransferase (ALT); 847 IU/I, alkaline phosphatase (ALP); 320 IU/I, gamma-glutamyl transpeptidase (-GTP); 126 IU/I, total bilirubin (T-bil); 11.88 mg/dl, direct bilirubin (D-bil); 7.77 mg/dl, PT-activation; 58%, lactate dehydrogenase (LDH); 386 IU/I, alpha fetoprotein (AFP); 73.9 ng/mL, carcinoembry-onic antigen (CEA); 2.8 ng/mL and PIVKA2; 30mAU/mL. The patient was negative for markers of acute infections (IgM type antibodies) against cytomegalovirus (CMV), herpes simplex virus (HSV), Epstein-Barr virus (EBV), hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV) and hepatitis E virus (HEV). The titers of anti-mitochondrial antibody titer [<20 (-ve)], anti-smooth muscle antibody (<20) and anti-LKM-1 antibody were negative. Serum mac-2 binding protein glycosylation isomer (M2BPGi) was 9.21 and serum hepatocyte growth factor (HGF) was 2.31 ng/mL.
Liver elastography showed VTQ: 4.0 m/s (3 times of average). This hardness corresponds to Inuyama classification F4 or more. (VTQ Reference standard value: F0 0.67 to 1.44 m/s, F1 0.81 to 1.63 m/s, F2 0.89 to 1.85m/s, F3 1.11 to 2.29m/s, F4 1.52 to 2.94m/s Multicenter 2012)). Fibro scan showed liver stiffness of 7.5kPa (just above the upper limit of normal).
Contrast CT showed the irregular atrophy of the interior ~ anterior compartment of the liver with features of fatty liver. Obvious space occupying lesion (SOL) could not be visualized in the liver. Volume rendering image of the liver revealed potato-like regrowth (potato-liver) (). Measurement of liver volume showed that it was 1428 mL in May 2016, 1007 mL in July 2016 and 1259 mL in November 2016. Along with the improvement of liver function, recovery of volume and augmentation of the anterior zone were seen.
The liver biopsy specimen revealed features of liver cell necrosis (multilobular hepatic necrosis) and infiltration of inflammatory cells containing relatively higher ratios of lymphocyte accumulation (). Partially bridging fibrosis, hyperplasia of cholangiole, and expansion of fibrous portal areas was also shown (). Vacuolation of the nucleus of liver cells (glycogen nucleus) were few and fatty depositions was negligible. Features of cholestasis and iron deposition could not be marked. The findings of liver biopsy were compatible with a diagnosis of DILI.
As all serum viral markers including hepatitis viruses (A, B, C, and E) were negative, we performed the drug lymphocyte stimulation test (DLST). DLST for Za ga-do Kowa® and Ohta-Isan® were positive, however, that for Gaster® was negative. Cinnamon and fennel are components common to Za ga-do Kowa® and Ohta-Isan®, and they showed borderline stimulation (). Drug-induced liver injury score (DDW-J 2004) was four points.
After admission, the patient stopped taking medicine. Subjective symptoms gradually disappeared. However, it was the sixth week after hospitalization, the liver enzyme rises and bilirubin re-elevation started. At one time PT became 45% and T-bil increased to 14.8mg/dL.
It presented a severe liver injury. After that, we were given ursodeoxycholic acid and late evening snack (LES) therapy. We continue treating in a protective way for liver, and the patient left the hospital after 15th week when the levels ALT and AST came below 100 IU/L, and the levels of serum bilirubin decreased to 4 mg/dL.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.7, 'cm']}",64.75993,61.52193,67.99793,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.7 cm, which is 168.7 cm * 0.393701 in/cm = 66.41736 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.41736 (in inches) - 60) = 64.75993 kg.
Hence, the patient's IBW is 64.75993 kg."
3463,10,Ideal Body Weight,physical,decimal,pmc-4234985-1,Extracted,"A 79-year-old Chinese man was admitted to our hospital complaining of episodes of repeated fever and some uncertain discomfort for 10 days. He had a nonproductive cough, but no chill, pharyngalgia, arthralgia, chest pain, dyspnea or diarrhea. He denied experience of trauma or drug abuse. He previously had been well but had a medical history of hypercholesterolemia and a long duration of two packs/day cigarette smoking. His father died from a sudden heart attack and he also had two brothers suffering from hypertension. On physical examination, he was 69 inches (1.73m) tall and weighed 178lb (81kg). He was febrile with a heart rate of 90 beats per minute, blood pressure 135/85mmHg, and respiratory rate 22 breaths per minute. Head and neck examinations were significant for pale conjunctivae and a left carotid bruit. His chest was clear to auscultation. His heart rhythm was regular with a nondisplaced apical impulse, an S4 gallop, no murmurs or rubs. His abdomen was benign, with no tenderness or masses. He had symmetrical palpable pulses in the femoral, popliteal and pedal arteries bilaterally without changes of skin appearance, temperature or sensations. Laboratory assessments revealed a high level of white blood cell count (20.7×109/L), neutrophils (85%), C-reactive protein (132mg/L), erythrocyte sedimentation rate (45mm/hour) and a low level of hemoglobin (94g/L). A lipid level test showed total cholesterol, triglycerides, high-density lipoprotein and low-density lipoprotein were 342, 280, 35 and 263mg/dL respectively. Liver and kidney functions, urine and stool tests were normal. A chest X-ray showed no recent infections. Conventional antibiotics using cefoxitin and levofloxacin were given for 10 days in the out-patient department and 4 days in our hospital for suspected sepsis, but his temperature still fluctuated and mostly remained above 38°C. However, bacteriological cultures of blood, urine, and sputum were negative. Immune markers like complements, interleukins, self-antibodies and globulins showed no abnormalities. Tumor and human immunodeficiency virus biomarkers were also negative. However, a brief scanning of computed tomography (CT) and magnetic resonance imaging (MRI) were done to search for the focus of the fever and suggested edemas and abnormalities around his left greater psoas and peritoneum, suggesting inflammatory changes. Ceftizoxime and clindamycin were regulated to use on advice from microbiologists and kept for another 2 weeks, but still without any conspicuous relief of symptoms. Based on the ambiguity of the CT and MRI done earlier, a contrast-enhanced computed tomographic angiography ([CTA], Figures a and b) was performed and demonstrated the existence of an 81.9mm×61.6mm PA, which originated from his left iliac arteries and covered the bifurcation of his left common iliac artery and proximal ends of both his internal and external iliac arteries.
The endovascular procedure was performed 1 day after the CTA. Heparin 4000IU was administered intra-arterially once access had been obtained. A 6-F artery sheath punctured his contralateral femoral artery. Then a 5-F Rösch inferior mesenteric catheter (Cordis) and 0.035 3mm “J” standard guide wire (Cook) were used together to enter his left common iliac artery. Hand injections of contrast demonstrated the existence of a huge PA (Figure a) and also identified both the rupture of PA and the proximal end of his left internal iliac artery (Figure b). Another catheter and guide wire were inserted through an ipsilateral femoral artery puncture. Via the catheter passway, metal coils (Cook: 8mm diameter, Figure c) were released and fixed at the distal end of his left internal iliac artery. Then the left femoral artery was exposed and a 14-F artery catheter (Cordis) was inserted. A 14mm×7cm Bard self-expandable polytetrafluoroethylene-covered Fluency stent (Boston Scientific) was placed after dilating with an 8mm×4cm angioplasty balloon. A selective left iliac arteriography (Figure d) 5 minutes after deployment of the stent graft confirmed complete exclusion of the PA and normal flow to the arteries of his ipsilateral lower extremity.
The postprocedural course went well. The patient received subcutaneous low-molecular-weight heparin, urokinase and prophylactic cefminox. Furthermore, he was given long-term medications for hypercholesterolemia with atorvastatin, aspirin and omega 3 cod liver oil. Initially there was eradication of fever. His subsequent clinical course was uneventful and he was discharged 7 days after the endovascular treatment. CTA performed after 30 days showed a well-expanded stent with no signs of a new PA (Figure ) and a decreasing and consolidated residual hematoma. He received oral administration of warfarin for 3-month anticoagulation, maintaining an international normalized ratio of 2.0 to 3.0. At 1.5-year clinical follow-up, his recovery was good.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.73, 'm']}",68.65362,65.22094,72.0863,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.73 m, which is 1.73 m * 39.3701 in/m = 68.11027 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.11027 (in inches) - 60) = 68.65362 kg.
Hence, the patient's IBW is 68.65362 kg."
3464,10,Ideal Body Weight,physical,decimal,pmc-6237942-1,Extracted,"A 20-year-old adult male who underwent BGS and double-switch operation (hemi-Mustard and Rastelli procedures) for CCT, subpulmonary VSD, and SVPS at the age of 3 years complained of intermittent chest tightness for years. At the outpatient clinic, he did not have cyanosed lips and clubbed fingers. A grade 3/6 systolic ejection murmur was heard over the left upper sternal border. Cardiac enzymes, chest radiogram, electrocardiogram, and echocardiography were inconclusive to achieve a diagnosis. On admission, he was 178 cm in height and 85 kg in weight. The pulse rate was 70/min, respiratory rate 20/min, and blood pressure 120/74 mm Hg. The hemoglobin level was slightly elevated (16.1 g/dL). Computed tomography angiography () and conventional angiography () showed a systemic vein draining from the left brachiocephalic vein into bilateral upper pulmonary veins, indicating the presence of LACV, which measured 8.0–12.7 mm in diameters. By cardiac catheterization, oxygen saturations of the left ventricle and ascending aorta were both 92%. The systolic pressure of the right ventricle and main pulmonary artery was 32 mm Hg and 19 mm Hg, respectively. The left ventricular end-diastolic pressure was 4 mm Hg. The mean pressure of the left brachiocephalic vein and right atrium was 14 mm Hg and 12 mm Hg, respectively. The mean pressure of the main pulmonary artery was 14 mm Hg. There was a pressure gradient of nearly 10 mm Hg between the left brachiocephalic vein (14 mm Hg) and the left atrium (4 mm Hg). After informed consent was obtained, transvenous coil occlusion was performed using a coaxial delivery system (), which is composed of a 5-Fr right coronary Judkins catheter serving as an outer supportive catheter (denoted by the Arabic numeral 1 in a triple circle inserted in the right upper corner in ), a 2.9-Fr microcatheter (Progreat, TERUMO, Cottontail Lane, Somerset, New Jersey, USA) serving as a middle advancing catheter (Arabic numeral 2 in ), and a 0.018-inch micro-coil inserted as a central detachable vascular plug (Arabic numeral 3 in ). Through this coaxial delivery system, five sets of Tornado Embolization Coil (Cook, Daniels Way, Bloomington, IN, USA) and one set of Complex Helical Fibered Platinum Coil-18 (Boston Scientific, La Garenne Colombes, Cedex, France) were steadily deployed more distally at the anticipated location. After occlusion, left subclavian venography showed complete occlusion of LACV (). Oxygen saturation of the ascending aorta increased to 98%. During the 24-month follow-up, oxygen desaturation and chest tightness did not recur.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [178.0, 'cm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3465,10,Ideal Body Weight,physical,decimal,pmc-6511931-1,Extracted,"A 52-year-old female presented with a sudden onset of right-sided numbness and weakness that was accompanied by a left temporal cluster-like headache. No fever or prodromal infection was found at disease onset.
The family and personal history was unremarkable.
On physical examination, the height and weight of the patient were 154 cm and 56 kg, respectively. Vital signs were normal, as were heart, lung and abdominal exami-nations. Neurological examination showed intact mental status, with normal speech and comprehension. Mild 4/5 right-sided hemiparesis was present with normal tone in both the arm and leg, though no other focal neurological deficits were found. After admission, she complained of discomfort and tingling in the right leg, after which a generalized tonic-clonic seizure for 3 min occurred before it was stopped by a bolus of intravenous diazepam.
Laboratory tests, including D-dimer, lactic acid, and serum autoantibody levels, as well as thyroid function and tumor markers indicated no apparent abnormalities. Glucose tolerance and lactic acid movement tolerance tests were normal. A lumbar puncture was performed, and her open intracranial pressure was 180 mm H2O. Cerebrospinal fluid (CSF) testing showed that cell counts and protein, glucose, chloride, monoclonal antibody, adenosine deaminase, and lactate dehydrogenas levels were within normal ranges.
MRI demonstrated a lamellar left parietal lobe lesion predominantly involving the cortex, with hyperintensity on both diffusion-weighted imaging and fluid-attenuated inversion recovery (Figure ). The apparent diffusion coefficient map revealed a preserved, isointense signal. No abnormalities were found by susceptibility weighted imaging or magnetic resonance angiography and venography (Figure ). Due to the stroke-like onset pattern and MRI features, further thrombophilia screening was performed and showed decreased protein S activity. A diagnosis of cortical venous thrombosis was first proposed. Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) was also considered but temporarily excluded because of the incomplete manifestation and lack of genetic evidence. Anticoagulation therapy was initiated, and follow-up was performed to maintain the international normalized ratio (INR) within the target range.
Two months later, the patient was readmitted for subacute cognitive impairment. She was unable to identify and communicate with family members; she also had difficulty understanding questions or instructions and instead responded by repeating the word ""nothing"". During hospitalization, a secondary generalized seizure occurred, initially with eyes gazing to the right and then convulsion developing, which lasted for approximately 10 s before self-alleviation. Neurological examination suggested transcortical sensory aphasia, with fully covered limb strength. Blood tests and CSF examination were normal; INR was 2.21. On repeated MRI, new lesions were identified in the left temporal lobe and were also detected 10 days later in the right temporal lobe on radiological follow-up (Figures and ). Although the MRI signal characteristics are consistent with the initial findings, the original lesion in the left parietal lobe had been alleviated, with cortical atrophy. We further conducted magnetic resonance spectroscopy (MRS), which revealed markedly elevated lactate (Lac) concentrations in the regions of interest in the left temporal lesion (Figure ). Mitochondrial encephalopathy was diagnosed, and genetic testing using peripheral blood was performed. However, DNA testing for frequent MELAS and myoclonic epilepsy with ragged red fibers syndrome mutations were negative. Because of the lack of symptoms of muscle weakness or pain, the patient declined our suggestion of performing a muscle biopsy. Anticoagulation therapy was terminated, and levetiracetam (1000 mg/d) was administered.
At 3 mo after her second admission, the patient was experiencing involuntary movement in her left limbs, with repetitive flexion/extension. An MRI scan showed a hyperintense signal abnormality in the right parietal lobe (Figure ). Brachial biceps biopsy was performed. Histopathology revealed no abnormalities, and no necrotic or regenerating fibers were observed; ragged-red fibers and intense succinate dehydrogenase activity were not detected. Nonetheless, complete sequencing of mitochondrial DNA samples extracted from the biopsied muscle revealed a heteroplasmic m.10158T>C mutation, with a heteroplasmy level of 69.6%, in the mitochondrial complex I subunit gene MT-ND3. In contrast, this mutation was not found in her peripheral blood cells.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [154.0, 'cm']}",46.94889,44.60145,49.29633,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 154.0 cm, which is 154.0 cm * 0.393701 in/cm = 60.62995 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.62995 (in inches) - 60) = 46.94889 kg.
Hence, the patient's IBW is 46.94889 kg."
3466,10,Ideal Body Weight,physical,decimal,pmc-7739354-1,Extracted,"A 26-year-old female elite rower (height 182 cm, weight 68 kg) presented with left anterior hip pain. She began rowing aged nine years and from the age of 15, trained up to 28 h a week. She complained of left anterior hip pain for 12 years and FAI (pincer) was diagnosed via X-ray and confirmed using magnetic resonance imaging. Arthroscopic surgery, performed four years prior to the present case study (modification of acetabular and removal of calcified hip labrum), did not alleviate symptoms. Her main complaint on presentation was persistent anterior hip/groin pain on rowing and other activities requiring lifting the knee towards the chest, e.g., cycling, climbing stairs, sitting in a low chair. Symptoms limited her training time and intensity, and participation in competitive rowing. Previous physiotherapy included treatment to the lumbar spine, soft tissue therapy and stretches to the low back/pelvis and hip restrictions.
The study was approved by the Faculty of Health Sciences, University of Southampton Ethics Committee (Ethics ID 6732, approved 3 July 2013) for case studies of hip and groin pain. The participant provided written informed consent.
Assessments were performed pre-intervention (0 weeks) and 16 weeks post-intervention. Both clinical and laboratory-based measures were used. Hip and groin outcome score (HAGOS) [,], a patient reported outcome measure recommended for the assessment of young-aged to middle-aged physically active individuals with hip and groin pain was the main outcome measure. The HAGOS consists of six separate subscales assessing pain, symptoms, physical activities and hip and/or groin-related quality of life (QOL) []. The test–retest reliability of the questionnaire was shown by the group that devised the HAGOS [] to be substantial, with intraclass correlation coefficients (ICC) ranging from 0.82–0.91 for the six subscales. Construct validity and responsiveness were confirmed with statistically significant correlation coefficients 0.37–0.73 (p < 0.01) for construct validity, and 0.56–0.69 (p < 0.01) for responsiveness []. The HAGOS, therefore, has adequate psychometric properties for the assessment of symptoms, activity limitations, participation restrictions and QOL in physically active, young-to-middle-aged patients with longstanding hip and/groin pain []. Active and passive hip flexion were measured in supine using a plurimeter placed on the distal thigh. The participant was asked to bring one knee towards their chest as far as possible. The plurimeter has a rotating dial, which allows easy reading of the angle of movement to the nearest 2° []. It has been shown that the measurement of hip flexion ROM are repeatable between practitioners (ICC 0.87) using a plurimeter []. For passive assessment, the assessor moved the lower limb into hip flexion until pelvic movement occurred. Any pain provocation was noted.
MCIs were identified using The Foundation Matrix, part of The Performance Matrix movement analysis system, Movement Performance Solutions Ltd., which is a battery of 10 multi-joint functionally relevant cognitive movement control tests that identifies MCIs. Failing a cognitive movement control test demonstrates a loss of choice about how a movement is achieved []. This test battery reveals the movement “choices” lost during postural and non-fatiguing tasks (low threshold recruitment) and in fatiguing load and speed tasks (high threshold recruitment). As these different loading/intensity environments are influenced by different physiological mechanisms, testing is suggested to inform about loss of movement choices and the presence of low movement coordinative variability across a spectrum of tasks. The ability to pass a battery of cognitive movement control tests in all planes of movement illustrates a desirable wealth of choice in movement options (high movement coordinative variability) []. The tests have been described by Mischiati [] and Test 1: Double knee swing was described, by Dingenen and McNeill [,]. The inter- and intra-rater reliability of this tool has been found to be acceptable []. The system reports the site (e.g., hip), direction (e.g., flexion) and threshold (low or high) of MCIs [,]. Reports produced by an inbuilt algorithm in the online system present MCIs that appear as areas of high risk, subsequently guiding clinical reasoning and development of a prioritisation plan for retraining. A movement control impairment score is given out of 50 (lower score indicates fewer MCIs). The Foundation Matrix is suggested to have clinical utility for the assessment of MCIs [] and the value of assessing movement within the world of movement health, injury prevention and rehabilitation has been presented by Dingenen []. The test battery is employed by therapists in clinical settings for the assessment of MCIs.
The retraining programme consisted of four therapist-led training weeks and a bespoke home exercise programme. At weeks 1, 2, 10 and 16, the athlete attended for five daily sessions (2 h a day contact time).
The Foundation Matrix report was used to develop the retraining programme (see : Results), focusing on high-risk areas and progressing to low risk areas. Priorities included retraining MCIs of the low back and pelvis, hip and foot. In this case study, six priorities for retraining were identified, reflecting the relevance of the MCIs to the provoking activity, symptoms and goals of the individual (see ).
Exercises included low threshold motor control recruitment retraining twice a day and high threshold strength and speed retraining up to four times per week. Strategies were directed at retraining the MCIs with either direction control retraining (co-ordination patterns) or muscle-specific retraining (muscle synergy recruitment) [,]. This cognitive stage represents an initial rehabilitation phase in a progression back to functional tasks. The retraining programme is detailed in the and involved cognitive strategies to influence both motor learning and elicit subsequent change to movement patterns and did not include manoeuvres that formed the tests of movement control.
Three progressive phases of learning a new skill were proposed by Fitts and Posner in 1967 []: cognitive phase, understanding of the required action; associative phase, practice of the programme learned in the cognitive phase; and autonomous phase, during which the performer learns to carry out the skill with little conscious effort. Bernstein [], also in 1967, proposed that freezing during motor learning (restricting joint ranges of motion and tightly coupling the motion of different joints) is prevalent mainly during the early stages of motor learning and gradually decreases as learning progresses. More recently, van Ginneken’s [] experimental paper suggests that conscious control is associated with the freezing of mechanical degrees of freedom during motor learning. This highlights the importance of cognitive input in the early stages of motor learning, and simple, single plane movement patterns. These strategies were implemented in the athlete’s early retraining programme.
This test examined the ability to actively control movements of the pelvis during hip flexion. The participant was seated on a couch (90° hip and knee flexion, feet unsupported, arms folded across chest) and instructed to lift one knee towards the chest, until the femur was 20° above horizontal (approximately 110° hip flexion), whilst keeping the low back/pelvic region still (). The task was repeated three times per side. Kinematics of the pelvis and lower limbs were obtained using a Vicon MX 3-dimensional motion capture system with 12 T-series cameras operated at 100 Hz (Vicon Motion Systems, Oxford, U.K.). Retro-reflective markers were attached bilaterally according to the Vicon plug-in gait model [], on the anterior super iliac spine (ASIS), mid-thigh, lateral femoral condyle, lateral tibia, lateral malleolus, calcaneus and dorsal aspect of the head of the first metatarsal. Additional markers were attached to the medial femoral epicondyle and medial malleolus during a static standing trial. An Aurion “Zerwoire” EMG system was used to obtain electrical activity of tensor fascia latae (TFL) and rectus femoris (RF) muscles. Electrodes were placed bilaterally following SENIAM (Surface ElectroMyoGraphy for the Non- Invasive Assessment of Muscles) guidelines []. EMG data were recorded at 1000 Hz via the motion capture system to allow for time synchronisation with kinematic data.
Kinematic and EMG post-processing and data reduction: Kinematics of the pelvis and femur were determined using a modified version of the Vicon plug-in gait model and Vicon Bodybuilder modelling software (Vicon, London, UK). This utilized the medial femoral epicondyle and medial malleolus markers, captured during the static standing trial to ensure correct alignment of the femur flexion axes. Post-processing of kinematic and EMG data was undertaken in Matlab 8.1 (The MathWorks Inc, Natick, MA, USA). Kinematic data were filtered using a low-pass fourth order zero-lag Butterworth filter at 10 Hz and cropped to the start and end of the seated hip flexion task (start defined as first notable increase in knee lift and hip flexion from static sitting, and end as the point where hip extension ceased following lowering of the leg onto the couch) through visual inspection of the kinematic waveform. Data were interpolated to 101 data points between the start and end of the task to time-normalize the data and allow averaging across the three repetitions. Hip flexion range of movement was defined as the maximum amount of hip flexion minus the start angle of the hip. EMG data were band-pass filtered using a band-pass fourth order zero-lag Butterworth filter between 10 Hz and 500 Hz, then rectified. Onset and termination of muscle activity was determined using the on/off methodology using visual interpretation of the filtered rectified EMG signal [] and the humeral angle where this occurred was noted. The time of muscle onset was subtracted from the time at which hip flexion commenced. A negative value indicated muscle activation commenced before initiation of hip flexion. Onset times were established for each trial then averaged across the three trials for each side, pre- and post-intervention.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [182.0, 'cm']}",72.30323,68.68807,75.91839,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 182.0 cm, which is 182.0 cm * 0.393701 in/cm = 71.65358 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (71.65358 (in inches) - 60) = 72.30323 kg.
Hence, the patient's IBW is 72.30323 kg."
3467,10,Ideal Body Weight,physical,decimal,pmc-4886904-1,Extracted,"A 40-year-old Japanese man was admitted to our hospital to undergo a laparoscopic cholecystectomy. An unknown hypokalemia [potassium (K) 2.7 mmol/L] was found and he was referred to our department presurgery. He had been hospitalized in another hospital for periodic paralysis due to unknown severe hypokalemia (K 1.7 mmol/L) 4 months prior. He and his father, who had died of a stroke, had been diagnosed with nephrocalcinosis in their 20s. None of his three siblings had any medical history. His physical and laboratory findings were as follows: height, 182 cm; weight, 81.5 kg; blood pressure, 120/78 mmHg. No abnormalities were observed in a physical examination. His audibility test was normal. In a blood examination, his serum creatinine level was elevated at 1.44 mg/dL (127.3 μmol/L). His serum K level was low, at 2.7 mmol/L, while his sodium (Na), chlorine (Cl), calcium (Ca), phosphorus (P) and magnesium (Mg) levels were all normal, at 144 mmol/L, 108 mmol/L, 8.7 mg/dL, 2.7 mg/dL and 2.6 mg/dL, respectively. The venous bicarbonate () level was at the lower limit of the normal range, at 22.8 mmol/L. His blood anion gap was normal at 13.2. His complete blood counts were all normal. The levels of immunoglobulins and complements were all within normal limits, and he tested negative for antinuclear, anti-SS-A and anti-SS-B antibodies. The plasma renin activity (normal: 0.1–2) and plasma aldosterone concentration (normal: 35.7–240) were 0.7 ng/mL/h and 141.1 pg/mL, respectively. The spot urinary pH was 7.5 and the fractional excretion of K was inappropriately normal, at 10.3%, even in a hypokalemic state. The urinary Ca/creatinine ratio (mol) was 0.70. The urinary anion gap was positive at 30.9 (=Na 67 mmol/L + K 13.9 mmol/L – Cl [minus sign] 50 mmol/L). Abdominal CT revealed medullary nephrocalcinosis in both kidneys. A bone mineral density test showed normal levels. We suspected dRTA and started a prescription of potassium aspartate and sodium/potassium citrate during the perioperative period. The level of serum K was corrected to within the normal range at 3.6 mmol/L. Black-pigmented stones in the patient's gallbladder were detected after a successful laparoscopic cholecystectomy.
After suspension of the prescription for 7 days, the hypokalemia became advanced (K 3.0 mmol/L), while metabolic acidosis was not evident ( 29.3 mmol/L). We performed ammonium chloride (NH4Cl), furosemide–fludrocortisone and HCO3− loading tests (Figures – ). The NH4Cl loading test demonstrated that the patient had dysfunction in both urinary acidification and net acid excretion under the acid loading condition (Figure A–C). In the furosemide–fludrocortisone loading test, the potential to secrete H+ into the lumina at distal nephrons with an enhanced negative charge was extremely weak (Figure A). In this test, instead of H+, the patient's K secretion increased sharply compared with a healthy control (Figure B). In the bicarbonate loading test, the patient's basal H+ secretion dysfunction was also demonstrated (Figure A); conversely, the tubular maximal reabsorption rate of () was elevated compared with the control (Figure B).
We performed comprehensive genetic testing for known causal genes of RTA in the patient using next-generation sequencing (NGS) technology based on the capturing method (Agilent Technologies). The genes SLC4A1 (encoding AE1), ATP6V1B1, ATP6V0A1, ATP6V0A4 (encoding the B1, a1 and a4 subunits of V-ATPase, respectively), SLC4A4 (encoding NBCe1-A), SLC34A1 (encoding NaPi-2a) and CA2 were all examined simultaneously. The detected mutations were narrowed down to those that might be disease-causing mutations according to the following two filters: one for novel variants that have not been reported previously or for variants with minor allele frequencies (MAFs) of up to 1% in the four single nucleotide polymorphism (SNP) databases [Human Genetic Variation Database (Japanese) [], 1000 Genomes [], ESP6500 [], Exome Aggregation Consortium []] and a second one for variants except for synonymous mutations if the variants are in the coding region. Consequently, only one mutation, which is a novel heterozygous mutation in ATP6V0A4 (exon 15, c.C1631T, p.S544L) was detected. As shown in Figure , the detected variants were validated with conventional Sanger sequencing and the result was consistent with that of the NGS diagnosis. Moreover, to confirm whether a large structural variant such as a large deletion or insertion exists as the second mutation, we performed the copy number variation (CNV) analysis for all the targeted genes by using CONTRA (). Briefly, this is CNV detection software using NGS data, and it calls copy number gains and losses for each target region by comparing the normalized sequencing depth from control samples. We used the sequence data from seven individuals as controls and did not find any large deletions or insertions in the patient. The results of CNV detection extracting the ATP6V0A4 region are shown in . There were no regions where relative sequencing depth was significantly changed compared with the controls, indicating that this patient did not have large deletions in ATP6V0A4, thus he was believed to be a heterozygous carrier of the ATP6V0A4 mutation. In addition, it was confirmed at the same time that other tested genes (SLC4A1, SLC4A4, ATPV1B1, ATPV0A1, etc.) did not have any CNVs.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [182.0, 'cm']}",76.80323,72.96307,80.64339,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 182.0 cm, which is 182.0 cm * 0.393701 in/cm = 71.65358 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (71.65358 (in inches) - 60) = 76.80323 kg.
Hence, the patient's IBW is 76.80323 kg."
3468,10,Ideal Body Weight,physical,decimal,pmc-8344329-1,Extracted,"In January 2020, a 70-year-old woman came to the China-Japan Union Hospital of Jilin University for the treatment of bilateral knee pain with limited movement that had been aggravated for approximately 1 year. She was 1.67 m tall, weighed 60.00 kilos, and with a BMI of 25.0. This patient was able to perform daily activities independently without assistance of others, but sometimes required the use of assistive devices. On physical examination, bilateral enlarged knees were seen, and the right lower extremity was 2 cm shorter than the left. A pronounced right genu varum was seen. When pressure is applied to bilateral distal femurs, proximal tibias and patella, significant unevenness of the bone surface can be felt. The right knee and left knee were passively flexed to 90° and 130°, respectively. And according to the manual muscle testing (MMT), the myodynamia of bilateral lower extremities was grade IV. In addition, this patient also had flexion contracture of the elbow joints, but it did not have a clear impact on quality of life.
X-ray examination revealed bilateral femoral condyles and proximal tibial dysplasia in this patient. Joint spaces of knees were narrowed, especially in the lateral left knee and medial right knee. The right varus angulation was 21.5°, and the femoral mechanical-anatomical angle (FMAA) was 11.3°. Bilateral knees with bone sclerosis were seen under the articular surfaces, joint surfaces were not smooth and had osteophytes, and a couple of loose bodies were seen in the left knee (Fig. ).
This patient reported a contagious disease history of smallpox in childhood, and her bilateral knees became deformed after healing. The variola virus was eradicated in China in 1961, and pitted facial scars were visible on her face, which were typical of previous smallpox infection. The woman presented with progressive pain in the bilateral knees 8 years ago and underwent loose body removal for left knee secondary arthritis 7 years ago. Additionally, she underwent debridement and antituberculosis therapy for tuberculosis of the lumbar spine 40 years ago and recovered well without the occurrence of complications after the operation. Laboratory results showed that the white blood cell count (WBC), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and procalcitonin (PCT) were normal. Lymphocyte percentage (44.0%), alkaline phosphatase (141.92 IU/L), γ-glutamyltransferase (95.45 IU/L), leucine aminopeptidase (46.62 IU/L), and glutamate dehydrogenase (10.47 IU/L) were slightly elevated, and the eosinophil count (0.03 × 109/L) was slightly decreased.
Based on physical examination, imaging and past medical history, the patient was considered to have bilateral knee osteomyelitis variolosa combined with secondary arthritis. The patient underwent right total knee arthroplasty (TKA) owing to persistent pain with limited motion in the knees, and the right knee was more severe than the left knee. Postoperatively, she was given intravenous antibiotic therapy with piperacillin sodium and sulbactum sodium for prevention of infection. The woman recovered well, the surgical incision healed primarily, and the knee underwent regular functional exercises.
This elderly woman fell at home on the 20th postoperative day, resulting in a tear of the right knee proximal surgical incision. The patient was treated conservatively on her own for more than 1 month, but the wound continued to extravasate and did not heal. When she was readmitted to our hospital on the 52th day postoperatively, physical examination revealed a sinus tract in the proximal part of the right knee, with red inflamed skin and visible yellowish-white fluid exudation. X-ray examination showed a stable surfacing prosthesis of the knee (Fig. ). Laboratory results showed that the WBC, CRP, ESR, PCT, and myeloperoxidase (MPO) levels were normal. The consequences of bacterial culture were methicillin-resistant coagulase-negative Staphylococcus (MRCNS). The bacteria were sensitive to vancomycin, gentamicin, and rifampicin and were resistant against clindamycin, levofloxacin, and penicillin.
The patient received extensive debridement under intravenous anesthesia on the third day of readmission. Fortunately, no evident infection or inflammatory tissue was seen in the articular cavity. The athroplasty was stable, the surrounding soft tissues were good, and there was no necrotic tissue. According to Tsukayama classification, the prosthetic joint infection was Type IIA. Therefore, we did not remove the knee prosthesis. Vancomycin anti-infective therapy was given postoperatively. Her surgical incision healing by second intention without recurrence of incision infection or sinus tract formation. At the 12-month follow-up, there was no recurrence of infection and no pain during movement. Under the correct guidance of the multidisciplinary rehabilitation programme, this elderly woman recovered good motor function of the right knee, and Hospital for Special Surgery (HSS) knee score was 88.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.67, 'm']}",58.72056,55.78453,61.65659,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.67 m, which is 1.67 m * 39.3701 in/m = 65.74807 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (65.74807 (in inches) - 60) = 58.72056 kg.
Hence, the patient's IBW is 58.72056 kg."
3469,10,Ideal Body Weight,physical,decimal,pmc-6416119-1,Extracted,"Sixty-three-year-old woman presented with multicentric left breast cancer requiring mastectomy. She is 69 inches tall with a weight of 215 pounds and a corresponding BMI of 31.8 kg/m2. She has a history of inferior pedicle breast reduction surgery performed 20 years ago (Fig. 1). Despite her previous reduction, she has a very large breast volume and footprint that will be difficult to replicate on the reconstructed left side. She desires nipple preservation and wants to keep her native right breast. We proceed with a left nipple-sparing mastectomy through her previous vertical limb and immediate prepectoral reconstruction using a full-height variable-projection tissue expander (width = 16 cm, height = 16.5 cm, projection = 6.8 cm, and volume = 850 ml) with anterior coverage using an acellular dermal matrix. Twelve weeks later, we exchange her tissue expander for the largest anatomical implant available, a full-height extra-projection 775 ml implant (width = 15.5 cm, height = 16 cm, and projection = 7.1 cm). She also undergoes a contralateral reduction of 300 g to achieve better symmetry. The final result is shown in Figure . Despite using the largest and tallest implant available and reducing the right breast by an additional 300 g, the entire upper pole of the left breast was depleted with significant size asymmetry between the breasts. We discussed multiple sessions of lipofilling to fill this defect but felt that an autologous flap would be more definitive. The LICAP flap was chosen to reconstruct the upper pole of the left breast. An intraoperative photograph is shown in Figure , where an extended flap is dissected based off the known perforators that arise anterior to the latissimus muscle at the level of the inframammary fold as previously described. This flap is rotated on its pivot point and used to reconstruct the upper pole of the breast by suturing it to the underlying pectoralis muscle. The final result 6 months after surgery is shown in Figure , where we have reconstructed the upper pole of her breast with the LICAP flap and have acceptable symmetry between the 2 sides. The patient is discharged the same day, and drains are removed on postoperative day 4.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [69.0, 'in']}",66.2,62.89,69.51,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 69.0 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (69.0 (in inches) - 60) = 66.2 kg.
Hence, the patient's IBW is 66.2 kg."
3470,10,Ideal Body Weight,physical,decimal,pmc-3611079-1,Extracted,"The patient was male, aged 50, 169 cm and 72 kg, and visited the hospital to undergo shoulder joint surgery with a damaged in the right rotator cuff. Although he had diabetes that was diagnosed ten years before, he did not undergo treatment for it; however, blood sugar level had been controlled. Preoperative endocrinologic evaluation revealed no abnormal findings. The patient sometimes complained of palpitations and underwent tests for that in another hospital, but no anomaly was found and he was being followed-up. Nonspecific ST-T wave change was found in the preoperative electrocardiograph. No specific findings were found in the chest radiograph or echocardiogram, and laboratory findings were normal. Premedication was not administered. Vital signs just before induction and after arriving in the operation room were as follows: blood pressure of 160/90 mmHg, heart rate of 70/min, and oxygen saturation of 97%, and electrocardiography showed normal sinus rhythm. Anesthesia was induced with pentothal sodium 300 mg, fentanyl 100 µg, and rocuronium bromide 50 mg, and the endotracheal tube (inner diameter 8.0 mm) was inserted orally. For maintenance of anesthesia, 50% N2O - O2, sevoflurane 3 vol%, and remifentanil 0.05 µg/kg/min were used. After vital signs were stabilized, concentration of sevoflurane was adjusted to 1.5 vol% and atropine sulfate 0.5 mg was intravenously injected just before changing the patient's position from supine to a sitting position (beach chair position 70-80°). One or two minutes after sitting position, heart rate was suddenly reduced from 80/min to 30/min or less, and blood pressure was 70/40 mmHg. But no electrocardiograhic changes were noted. Intravenous injection of atropine sulfate 0.5 mg was immediately given, but heart rate and blood pressure did not change. After stopping the administration of remifentanil and sevoflurane, 1 : 10,000 epinephrine 1 ml (10 µg) was intravenously injected, and the patient was moved to the supine position. Heart rate soon recovered to 90/min, and blood pressure returned to 120/60 mmHg. The results of the arterial blood gas analysis at that time were within normal range. Through the discussion with surgeons, we decided to postpone the operation. Detailed tests were performed a 24-hour electrocardiography and echocardiography, and the patient was suspected of having vasovagal syncope suspect. The head-up tilt testing and circulatory assessment diagnosed BJR as the cause. A sufficient amount of fluid was supplied and a β-sympatholytic was orally administered as the preventive treatment. Following preoperative administration of anticholinergic and sedative, anesthesia was induced well with desflurane and remifentanil. Afterwards, the operation was performed without any specific findings.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [169.0, 'cm']}",65.03158,61.78,68.28316,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 169.0 cm, which is 169.0 cm * 0.393701 in/cm = 66.53547 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.53547 (in inches) - 60) = 65.03158 kg.
Hence, the patient's IBW is 65.03158 kg."
3471,10,Ideal Body Weight,physical,decimal,pmc-7329962-2,Extracted,"Case 2: a 65-year-old female (153 cm, 39 kg) was diagnosed with recurrence of esophageal cancer and metastasis of lung and bone. She was receiving intravenous oxycodone which was gradually increased for 18 days to 4.5 mg/h for her pain due to metastasis of her right sacral bone. Femoral trochanteric fracture was diagnosed after tumbling on the floor and she was planned for intramedullary nailing. As her preoperative chest x-ray revealed narrowing of the trachea due to lung metastasis (Fig. a), regional anesthesia with spinal anesthesia was selected. Isobaric 0.5% bupivacaine 2 ml completely treated her pain due to both fracture and bone metastasis (no record of anesthesia level). Oxycodone was continued during the surgery (surgery time, 1 h 48 min) and continuous RR and end-tidal CO2 monitoring was applied in accordance with the standard monitoring of ECG, SpO2, and BP. No respiratory event was recorded throughout the surgery (Fig. b) with average RR of 18 ± 6/min.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.0, 'cm']}",46.04337,43.7412,48.34554,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.0 cm, which is 153.0 cm * 0.393701 in/cm = 60.23625 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.23625 (in inches) - 60) = 46.04337 kg.
Hence, the patient's IBW is 46.04337 kg."
3472,10,Ideal Body Weight,physical,decimal,pmc-2852812-1,Extracted,"A 66-year-old, 160 cm, 48 kg man was scheduled to undergo a total knee arthroplasty. His medical history revealed a ten-year history of diabetes mellitus (DM), uncertain hypertension history, and previous knee surgery. The patient suffered from occasional dyspnea and chest discomfort. An ECG showed a sinus bradycardia of 57 bpm and a 99-m Tc-MIBI scan was normal. Laboratory tests showed glucose 4+ on urinalysis, HbA1c 10.0%, and serum glucose around 200-300 mg/dL.
At the pre-anesthesia preparation room, ECG and pulse oximetry were applied and blood pressure (BP) was measured non-invasively at 5-min intervals. The initial BP was 104/56 mmHg with a heart rate (HR) of 57 bpm. Combined spinal-epidural anesthesia was administered using a 17-gauge Tuohy needle and 27-gauge Whitacre spinal needle at the level of the L3-4 interspace under standard aseptic conditions. Upon the first attempt, the epidural space was found using a loss of resistance technique, and clear cerebrospinal fluid (CSF) was obtained after spinal needle insertion. There were no paresthesias. A total of 2.0 mL of 0.5% tetracaine, mixed with saline, the patient's CSF, and epinephrine 1 : 200,000, was administered slowly to the patient. An epidural catheter was inserted without resistance and advanced 5 cm upward (by having the bevel of the needle pointed cephalad) and a sensory block to T12 was achieved by a pin-prick test. Then, BP dropped to 87/46 mmHg, and the sensory block was checked at T6. Ephedrine hydrochloride 12 mg and 20 mg was administered intravenously and intramuscularly, respectively. BP raised to 120/65 mmHg, and the patient was transferred to the operating room. In the operating room, BP was 147/69 mmHg and rose to 153/79 mmHg after turning a tourniquet on. Then, the patient complained of a sudden onset of a severe headache and became restless. The BP recorded at the onset of the headache was 190/123 mmHg, and HR was 75 bpm. No ECG changes were noted. Labetalol hydrochloride (10 mg) was injected, and, to sedate the patient, midazolam (2 mg) was injected, but the patient was still irritable. Then, thiopental sodium (100 mg) was injected via IV. BP was maintained around 160/65 mmHg for an hour before a sudden tachycardia of 140 bpm and BP of 200/97 mmHg was observed. Lidocaine (80 mg) was injected and isosorbide dinitrate infusion began due to ST depression. The patient was semi-comatose with asymmetric pupils. BP gradually decreased and was maintained around 105/60 mmHg. After taking a brain CT scan, the patient was transferred to the ICU.
The brain CT showed a large amount of SAH and an intraventricular hemorrhage (IVH) (), and a CT brain angiogram showed a 6-mm ruptured intracranial aneurysm at the anterior communicating cerebral artery (ACOM) and a 4-mm unruptured cerebral aneurysm at the left middle cerebral artery bifurcation ( and ). GDC coil embolization at the ACOM was performed, and external ventricular drainage was carried out. The patient was transferred to the ICU for observation.
The patient was semi-comatous without light reflex, and pupils were asymmetric. BP was maintained by infusing dopamine, vasopressin, and levophad. The patient fell into a coma, unable to maintain stable vitals, and died 17 days after the surgery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [160.0, 'cm']}",56.88197,54.03787,59.72607,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.99216 (in inches) - 60) = 56.88197 kg.
Hence, the patient's IBW is 56.88197 kg."
3473,10,Ideal Body Weight,physical,decimal,pmc-6295374-3,Extracted,"A 53-year-old man (body weight 100 kg; height 1.78 m; BMI 32 kg/m2) with a MELD score of 40 underwent LT for autoimmune cirrhosis with a graft derived from a female donor (body weight 86 kg; height 1.73 m; BMI=29 kg/m2). The liver graft weighed 2400 g, and the GRWR was 2.4%. A total hepatectomy preserving the native IVC was performed and the graft was implanted with LLCCA. Severe graft congestion was observed at reperfusion. Four abdominal pads were placed behind the right liver to restore adequate hepatic venous outflow as demonstrated by DUS (). Liver graft biopsy showed moderate macrovesicular steatosis. Surgery was completed by a skin-only closure. Three days later, repeated laparotomy was performed to remove the abdominal pads. The patient underwent re-transplantation for early graft dysfunction on postoperative day 10. No hepatic venous outflow was detected on DUS before re-transplantation. The patient died from multiorgan failure few hours after the re-transplantation.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.78, 'm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.78 m, which is 1.78 m * 39.3701 in/m = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3474,10,Ideal Body Weight,physical,decimal,pmc-3977502-3,Extracted,"A 43-year-old male (72 in, 200 lbs, BMI 27.1, nonsmoker) with a full thickness rotator cuff tear and impingement was treated with subacromial decompression and rotator cuff repair. On postoperative day 12, the patient presented with pain in the medial elbow. Surgical incisions were healing well; however, there was tenderness to palpation at his medial elbow with no other obvious findings. Patient was referred for duplex ultrasound, which demonstrated occlusive basilic vein thrombosis, as well as nonocclusive brachial vein thrombosis. He was treated with a course of aspirin 81 mg for 3 months. Elbow pain resolved within 3 weeks and he had excellent shoulder recovery at the latest follow-up 5 months after procedure.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [72.0, 'in']}",77.6,73.72,81.48,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 72.0 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (72.0 (in inches) - 60) = 77.6 kg.
Hence, the patient's IBW is 77.6 kg."
3475,10,Ideal Body Weight,physical,decimal,pmc-5324894-1,Extracted,"A post-mortem examination was carried out to determine cause of death of a 37-year-old man who died suddenly and unexpectedly without pre-existing heart disease. Height of the man was measured as 187 cm and his weight as 90 kg. External examination showed no sign of trauma. Autopsy results are discussed below. Left and right lungs weighed 600 g and 760 g, respectively. Left atrium and ventricle showed chamber dilation. Heart showed abnormalities, including dilated cardiomegaly (cor bovinum, 520g in weight) and giant mitral valve (17 cm in length). No atherosclerotic plaque was found in coronary arteries. No remarkable changes were seen in other organs. Histopathological examinations showed elastic degeneration in spongiotic area, minimal inflammatory elements in mitral valve, nodular fibrosis of chordae tendinae, nucleomegaly, thickening and disorientation of fibers, fibro-hyalinization, and focal mononuclear inflammatory and degenerative cardiomyopathic changes to myocardium (, ).
Study material for genetic screening of cardiomyopathies was selected from case database at the Department of Forensic Medicine, Near East University (NEU), upon a request from the local police department. After deoxyribonucleic acid (DNA) isolation process was performed by genetics department, samples were sent to GENetic DIAgnostic Network (GENDIA) for further DNA analyses. Next-generation sequence analysis of coding regions of 40 genes involved in cardiomyopathy and Sanger sequencing confirmation were conducted by GENDIA. Novel missense mutations were identified both in SGCD and TTN genes analyzed. A heterozygous SGCD:c.15G>C a variant with unknown significance (VUS) in exon 3 of SGCD gene, and a heterozygous TTN:c.21758T>C VUS in exon 89 of TTN gene were identified. The cause of death was determined to be sudden circulatory failure resulting from DCM/HCM. Primary genetic counseling was given to his ex-wife and two sons, who were the only family members available at that time.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [187.0, 'cm']}",81.33081,77.26427,85.39735,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 187.0 cm, which is 187.0 cm * 0.393701 in/cm = 73.62209 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (73.62209 (in inches) - 60) = 81.33081 kg.
Hence, the patient's IBW is 81.33081 kg."
3476,10,Ideal Body Weight,physical,decimal,pmc-3427809-1,Extracted,"A 54-year-old male patient with a height of 170 cm and weight of 77 kg visited a private hospital due to a headache and weakness in left muscle that started the day before his hospital visit. During the examination, the patient showed decreased consciousness, and internal hemorrhaging in the cerebral ventricle was observed in the CT scan, hence he was transferred to our hospital. When he arrived at the emergency room, the patient was semi-conscious and had difficulty in breathing, and his Glassgow coma scale (GCS) showed severe head trauma with a total score of 8 or lower. The head CT scan revealed worsened stage of hemorrhage in the cerebral ventricle, so he was immediately intubated and transferred to the ICU.
A day after entering the ICU, the hemorrhaging in the patient was still worsened according to the CT scan and he was in a semi-comatose state; therefore, an extra ventricular drainage (EVD) was done to decrease the pressure in the brain and hematoma aspiration was also carried out. In addition, an emergency tracheostomy was done at the same time since long term mechanical ventilation was expected. There were no premedications given to the patient. Preoperative vitals were a blood pressure of 150/80 mmHg, a heart rate of 100/min, a respiration rate of 24/min, a body temperature of 38℃, and a SpO2 of 97%. After administering 0.2 mg of glycopyrrolate, anesthesia was induced with 125 mg of thiopental sodium. After complete loss of consciousness, muscle relaxation was achieved with 8 mg of vecuronium. Alfentanil at a concentration of 1.0 mg was administered to minimize hemodynamic changes when replacing the tube and at the same time anesthesia was maintained with O2 supply of 1 L/min, air supply of 2 L/min, and 2.0 vol% of sevoflurane. Considering the difficulty in maintaining airway characteristics in head surgery, the previously intubated polyvinylchloride (PVC) plain tube was replaced with a reinforced tube. The patient's vitals immediately after intubation were blood pressure of 130/70 mmHg, a heart rate of 95/min, and a SpO2 of 98%. Starting from the EVD, the operation proceeded smoothly and the tracheostomy was done in 2 hours and 30 minutes. Ten minutes after starting the tracheostomy, the FiO2 increased to 1.0. While adjusting for bleeding around the tracheal cartilage with monopolar coagulation before inserting the tracheostomy tube, a fire of about 15 cm in size suddenly started perpendicular to the direction of the trachea. The supply of sevoflurane and 100% O2 was immediately stopped after the initiation of fire and manual ventilation was done at a FiO2 of 0.2. Normal saline was used to extinguish the fire and soon the condition was brought under control. The endotracheal tube (reinforced tube) was taken out, tracheostomy tube was intubated to maintain manual ventilation, and SpO2 was again increased to 98%. Vitals before and after the tracheostomy were stable except for the temporary decrease in SpO2. The condition of the tube after extubation was as follows: the part directly above the cuff had holes due to melting from the heat; the coil inside the tube had melted, and there was overall charring (). The operation was completed without occurrence of any further incident, and since the patient was still in a semi-coma state, he was transferred to the ICU while maintaining bag ventilation through the tracheostomy tube. In the ABGA conducted directly after being transferred to the ICU, the pH was 7.406; the pCO2 was 33.6 mmHg; the pO2 was 121 mmHg; the HCO3 was 20.7 mmHg, and oxygen saturation was 97.8%. There were no observable changes in the chest x-rays both, before and after the operation () and no irregularities were observed in the bronchial endoscopy. The patient showed no improvement in consciousness during continuous mechanical ventilation; therefore, 5 days after the surgery, the patient was transferred to another hospital as per the wishes of the guardian. There were no irregularities in the chest x-ray images and clinical symptoms after being monitored for 4 months post-surgery ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3477,10,Ideal Body Weight,physical,decimal,pmc-3337389-1,Extracted,"A 65-year-old woman (weight, 44 kg; height, 153 cm) was admitted to our hospital for an elective total thyroidectomy. She had been diagnosed with a papillary carcinoma of the thyroid. Her medical history included hypertension, minor depression, a cerebral infarction, and brain surgery. Her medications included aspirin, a calcium channel blocker, and antidepressant. The preoperative chest radiograph and electrocardiography revealed no abnormalities. Echocardiography revealed mild pulmonary hypertension. The blood tests were within the normal limits.
Her blood pressure, heart rate and SpO2 was 140/70 mmHg, 80 beats/min and 99%, respectively. General anesthesia was induced with thiopental 5 mg/kg and rocuronium 0.6 mg/kg. She was intubated without problems using a 7.0 mm oral endotracheal tube that was fixed 22 cm from the mouth. Anesthesia was maintained with air 1 L/min, O2 1 L/min, sevoflurane 1-2 vol% and a continuous infusion of remifentanil 0.01-0.05 µg/kg/min. Her vital signs, airway pressures, and end-tidal CO2 remained stable during surgery. The planned surgical procedure was performed uneventfully in 2 hours and 55 minutes. A total volume of 900 ml lactated Ringer's solution was administered. During surgery, the estimated blood loss was 200 ml and urine output was 300 ml. After reversing the muscle relaxant, the patient was extubated in the operating room after confirming her ability to obey commands and her full recovery of motor function as tested by the hand grip and head control.
On the way to the post-anesthesia care unit, the patient was unable to breath and became cyanotic. The initial blood pressure at the recovery room was 110/60 mmHg, heart rate was 90 beats/min, and SpO2 was 78%. The oral airway was maintained and manual bagging was started with 100% oxygen at 10 L/min but there was considerable resistance and adequate oxygenation could not be maintained. A decision was made to reintubate the patient with midazolam 2 mg and succinylcholine 2 mg/kg while inserting an arterial line catheter into the left radial artery. Direct laryngoscopy revealed no specific abnormalities, such as laryngeal edema or aspirate. The patient was intubated successfully with a 7.0-mm endotracheal tube and ventilated several times with a bag valve mask with less resistance. However, a large volume of pink, frothy fluid emerged from the endotracheal tube, prompting an interim diagnosis of pulmonary edema. Pulmonary auscultation revealed moist rales in the entire bilateral lung fields. Despite the continued manual ventilation and tracheal suction with 100% O2, the SpO2 remained at approximately 80%. The first arterial blood gas analysis was as follows: pH 7.40, PaCO2 30.4 mmHg, PaO2 35.0 mmHg, SaO2 66.8% at FiO2 1.0. A portable chest radiograph confirmed the typical pattern of pulmonary edema with symmetric bilateral infiltrates and a slightly enlarged heart (). As a treatment of pulmonary edema, morphine 3 mg and furosemide 20 mg were administered. After 10 minutes, spontaneous respiration was observed and the patient could reply to verbal commands.
The patient was transferred to the ICU for ventilatory support with a positive end-expiratory pressure (PEEP) of 7 cm H2O. The patient's SpO2 remained > 97% on 100% oxygen. The follow-up arterial blood gas analysis was as follows: pH 7.39, PaCO2 33.6 mmHg, PaO2 125 mmHg, SaO2 98.9% at FiO2 1.0. The cardiac enzyme studies and echocardiography were unremarkable. Extubation was attempted on the second postoperative day because her SpO2 remained at 100%, her breathing was spontaneous, and her chest radiograph had improved (). Immediately after extubation, however, the patient became cyanotic and hypoxia developed and she was reintubated. According to the advice of our cardiologist colleagues, repeated echocardiography and coronary angiography was performed, which suggested transient stress-induced cardiomyopathy. Dobutamine 5 µg/kg/min was infused. The patient was extubated successfully and weaned from the dobutamine infusion on the sixth postoperative day but still showed some degree of dyspnea on 3 L/min via nasal cannula. Otolaryngology consultation attributed the residual dyspnea and the initial upper airway obstruction to bilateral vocal cord dysfunction. Given the possibility of sudden respiratory arrest, the patient underwent a tracheostomy.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.0, 'cm']}",46.04337,43.7412,48.34554,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.0 cm, which is 153.0 cm * 0.393701 in/cm = 60.23625 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.23625 (in inches) - 60) = 46.04337 kg.
Hence, the patient's IBW is 46.04337 kg."
3478,10,Ideal Body Weight,physical,decimal,usmle-546,Extracted,"A 67-year-old man comes to the physician for a follow-up examination. He feels well. His last visit to a physician was 3 years ago. He has chronic obstructive pulmonary disease, coronary artery disease, and hypertension. Current medications include albuterol, atenolol, lisinopril, and aspirin. He has smoked one pack of cigarettes daily for 18 years but stopped 20 years ago. He had a right lower extremity venous clot 15 years ago that required 3 months of anticoagulation therapy. A colonoscopy performed 3 years ago demonstrated 2 small, flat polyps that were resected. He is 175 cm (5 ft 9 in) tall and weighs 100 kg (220 lb); BMI is 32.5 kg/m2. His pulse is 85/min, respirations are 14/min, and blood pressure is 150/80 mm Hg. Examination shows normal heart sounds and no carotid or femoral bruits. Scattered minimal expiratory wheezing and rhonchi are heard throughout both lung fields.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3479,10,Ideal Body Weight,physical,decimal,pmc-6567775-1,Extracted,"A 58-year-old Chinese man presented with a 4-year history of fatigue and disabling bone pain that was most prominent in the knees. He was admitted to our hospital in 2015. During the prior 4 years, his symptoms had been progressively worsening. He had been unable to climb stairs for the past 7 months. He had also recently been unable to get up from a supine position. The patient had no history of trauma or any familial inherited bone disorders. He had been diagnosed with type 2 diabetes 2 years previously and was undergoing treatment with metformin with a well-controlled glucose level. On physical examination, his height was 165 cm; it had previously been recorded at 167 cm. He had a waddling gait. Palpation revealed tenderness in the bilateral hypochondriac regions. Muscle strength was normal in all four limbs, although tendon hyper-reflexia was noted. A lump measuring 8 × 6 cm was found in the right palm (). The left lower limb was 2 cm shorter than the right limb, and the left lower extremity had an external rotational deformity. The remaining systemic examination findings were unremarkable.
Laboratory findings revealed severe hypophosphatemia, phosphaturia, an elevated serum alkaline phosphatase level, and an elevated serum intact FGF-23 level as measured by enzyme-linked immunosorbent assay (Kainos Laboratories, Tokyo, Japan). The percent tubular reabsorption of phosphate was 77% (reference range, 85% to 95%), and the maximal tubular renal phosphate reabsorption normalized for the glomerular filtration rate was 0.32 (reference range, 0.89 to 1.34). Serum protein electrophoresis findings were normal. The patient’s laboratory data are summarized in .
A pelvic radiograph revealed a fracture of the left femoral neck. Dual-energy X-ray absorptiometry (Lunar Prodigy; GE Medical Systems, Chicago, IL, USA) revealed low bone mineral density at L1–L4 (0.957 g/cm2; T-score, −2.0; Z-score, −1.5), the femoral neck (0.601 g/cm2; T-score, −3.6; Z-score, −2.3), and total hip (0.774 g/cm2; T-score, −2.9; Z-score, −2.1). Whole-body 99mTc-methylene diphosphonate bone scintigraphy showed focal increased uptake in multiple bones and joints (). Magnetic resonance imaging revealed an irregular mass located in the right palm (7.2 × 6.2 × 3.3 cm in maximum diameter). The lesion had low signal intensity on T1-weighted images and a heterogeneously isointense bright signal on T2-weighted images. The tumor was broadly attached to the flexor digital tendons. Abnormal signals were present in several metacarpal bones (I/II/V), exhibiting low signal intensity on T1-weighted images and a bright signal on T2-weighted images ().
The patient underwent surgical resection. During the operation, the surgeons observed that the tumor had penetrated the mesothenar and interosseous muscles. They excised both the tumor and related muscles. Histopathologic examination indicated that the tumor was an epithelioid vascular leiomyoma, categorized as a phosphaturic mesenchymal tumor, mixed connective tissue variant. Immunohistochemistry of the tumor showed positive staining for vimentin, CD68, CD34, smooth muscle actin, and caldesmon ().
One week after removal of the tumor, the patient’s serum phosphorus level was 0.95 mmol/L and his serum FGF-23 level had decreased dramatically. Significant amelioration of his symptoms was noted 2 weeks later, and he could walk without assistance. Three months later, he was asymptomatic and his serum phosphorus level was maintained within the reference range (). Dual-energy X-ray absorptiometry showed that his bone mineral density had increased by 66.98% at the lumbar spine and by 19.13% at the hip. At the time of this writing (40 months postoperatively), he was still asymptomatic, had no evidence of tumor recurrence, and was still undergoing follow-up.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3480,10,Ideal Body Weight,physical,decimal,pmc-7529567-1,Extracted,"A 59-year-old man was admitted to our hospital with abnormal findings on chest X-ray (Fig ). On physical examination, he weighed 63.0 kg and was 176 cm tall. The patient had diabetes for 20 years and suffered from diabetic retinopathy. He had unremarkable medical and family histories, but a smoking history of 90 packs per year. Chest CT revealed a 30 mm mass in the right upper lung lobe and mediastinal lymph nodes with advanced calcification (Fig ). Transbronchial biopsy resulted in a diagnosis of adenocarcinoma. [18F]-fluoro-2-deoxy-D-glucose (FDG) positron emission tomography (PET) showed increased tumor uptake, with a maximum standardized uptake value of 6.16, and slight FDG uptake in the mediastinal lymph nodes. No metastases were detected by brain magnetic resonance imaging or FDG-PET (Fig ). Mediastinal lymph node #4 had a short-axis diameter < 1 cm, but was considered potentially to be lymph node metastasis because of the slight accumulation of FDG-PET; therefore, preoperative adjuvant treatment was performed. HgbA1c of 10.5 indicated diabetes was poorly controlled and required treatment before surgery. Diabetic nephropathy did not coexist and blood calcium and phosphate concentrations were within the standard range. During diabetes treatment, he received neoadjuvant chemotherapy (pemetrexed (500 mg/m2) plus cisplatin (75 mg/m2). The patient achieved no significant radiological improvement with two courses of this regimen. Based on radiological findings, he was diagnosed with yc-T1cN0M stage 1A, and surgical treatment was planned. He underwent right upper lobectomy and dissection of the upper mediastinal lymph nodes (2R and 4R). The lymph nodes were firmly adherent to the surrounding tissue, the sidewall of the superior vena cava was firmly fused, and there was invasion of the vascular wall. Despite this, the lymph nodes and superior vena cava sidewall were removed. The chest drain tube was removed on postoperative day 3 and the patient was discharged on postoperative day 14. Macroscopically, the tumor was well circumscribed and most of the tumor was calcified (Fig ). There was no bronchial or pleural involvement within the tumor. Acinar adenocarcinoma tissue was mixed with calcified tissue and PBs were confirmed. Similar features were found in calcified lymph nodes. The tumor was diagnosed as p-T2aN2M0 stage 3A (Union for International Cancer Control eighth edition). Immunohistochemistry revealed tumor cells positive for parathyroid hormone-related proteins (PThrP) 1 and 2. Postoperative examination indicated PThrP levels were within the standard range.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [176.0, 'cm']}",71.37017,67.80166,74.93868,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 176.0 cm, which is 176.0 cm * 0.393701 in/cm = 69.29138 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.29138 (in inches) - 60) = 71.37017 kg.
Hence, the patient's IBW is 71.37017 kg."
3481,10,Ideal Body Weight,physical,decimal,pmc-3193693-2,Extracted,"A 19-year-old girl, of 58 kg weight and 165 cm height, presented with a large cyst in the right ovary. She was asymptomatic, and during a routine health check-up, abdominal ultrasound revealed a 9.0 × 6.3 × 5.2 cm cyst, which was unilocular with minimal internal echoes. Serum CA-125 was normal (21 ng/ml). The uterus and the left ovary were normal. The SILS cystectomy was done under general anaesthesia by the same surgical technique as described above. The cyst had minimal adhesions and was filled with serous fluid. The patient had an uncomplicated postoperative recovery and was discharged the next day.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3482,10,Ideal Body Weight,physical,decimal,pmc-7586384-1,Extracted,"A 20-year-old male presented to the emergency department with vomiting, excessive retching, and diarrhea after consuming organophosphate insecticide in a suicidal attempt. General physical examination revealed miosis, hyperhidrosis, and hypersalivation. On chest auscultation, bilateral crepitations were present. Gastric lavage was performed immediately. Complete atropinization was done followed by maintenance infusion of atropine for two days which was gradually tapered off. Pralidoxime was also given for 24 hours. The patient responded to the treatment. However, it was noticed that he is not having beard and moustache despite being 20 years of age (Figure ).
He expressed feeling of insecurity about physique, learning difficulties, and perceived rejection from peers. On further evaluation, he was tall with a height of 178 cm, weight 78 kg, and a BMI of 24.6 kg/m2. Axillary and chest hair were absent. Testes were firm in consistency with a volume of 2 ml bilaterally .Gynecomastia was present (Figure ).
Hormonal profile revealed high follicle-stimulating hormone (FSH) 45 mIU/ml (normal range = 1.5-12.4 mIU/ml), high luteinizing hormone (LH) 12.8 mIU/ml (normal range = 1.7-8.6 mIU/ml), and low testosterone 1.4 nmol/L (normal range = 9.9-27.8 nmol/L), suggestive of hypergonadotropic hypogonadism. Karyotype of peripheral blood mononuclear cells revealed 47, XXY karyotype, thus confirming the diagnosis of Klinefelter syndrome. The patient was started on testosterone replacement therapy, along with counseling and psychotherapy.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [178.0, 'cm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3483,10,Ideal Body Weight,physical,decimal,pmc-4770005-1,Extracted,"A 21-year-old male student presented with history of sudden onset of breathlessness, left-sided chest pain radiating to the upper abdomen with nausea, vomiting and hiccup of 4-h duration. There was no history of cough, fever and hemoptysis or other constitutional symptoms. He had history of blunt compressive trauma to the chest 15 days back. Initial chest X-ray (Fig. ) showed raised left hemi-diaphragm, so he was treated conservatively. He had no history of smoking, alcohol intake or any major illness in the past. On examination, he was fully conscious, oriented in time, place and person and of average build, moderately nourished with height of 165 cm and weight of 55 kg. He was afebrile, and his general physical examination was unremarkable with pulse rate of 112/min, blood pressure 112/68 mmHg, respiratory rate 22/min and saturation was 85 % on room air. Pallor, icterus, cyanosis, clubbing and pedal oedema were not present; J.V.O. not appreciated. Chest examination revealed fullness of intercostal spaces, diminished movements with a resonant note, absent breath sounds and vocal resonance on the left side. Arterial blood gas analysis on 6 l oxygen showed respiratory alkalosis with mild hypoxemia. A clinical diagnosis of left-sided pneumothorax was made. X-ray chest (Fig. ) revealed a well-defined encysted hyper-translucent opacity covering the whole left hemi-thorax with shift of mediastinum and heart to the right side suggestive of encysted pneumothorax. In view of persisting vomiting and hiccup, a nasogastric tube was inserted resulting in a large gush of air. Subsequent X-ray chest (Fig. ) showed a nasogastric tube in the left hemi-thorax; possibility of diaphragmatic hernia was considered confirmed by CT scan of the chest (Fig. ) which revealed a posterior left diaphragmatic defect with resultant herniation of the stomach, splenic flexure of the colon, spleen, omental fat, descending colon, left-sided transverse colon, bowel and mesentery into the left hemi-thorax. He underwent laparotomy which confirmed a large diaphragmatic hernia in the left side postero-lateral region with herniation of the spleen, splenic flexure of the colon and proximal stomach into the thoracic cavity. Reduction of the contents was easily possible, and closure of the defect was done. Further reinforcement was done using a polypropylene mesh. Post-operative course of the patient was uneventful. Follow up X-ray chest (Figs. and ) showed full expansion of the left lung.
The diaphragm is the major muscle of respiration. Diaphragmatic excursion and chest wall expansion increases the negative intra-thoracic pressure required for inhalation. The sequelae from diaphragmatic rupture and subsequent herniation of intra-abdominal contents are associated with significant morbidity and mortality. Diaphragmatic hernia can be divided in two categories: (1) Congenital hernias: occur because of embryological defects in the diaphragm, which the patient presented early in life; however, a subset of adults may present with congenital diaphragmatic hernia undetected during childhood. (2) Acquired hernias: Stem from all types of trauma with blunt forces seen in the majority of cases. Diaphragmatic hernias require a high level of suspicion as patients can be asymptomatic in up to 53 % from blunt trauma and 44 % from penetrating trauma. Chest X-ray detects only 33 % of hernias when interpreted by a trauma team leader at an initial evaluation. Of all the patients admitted for trauma, 3–5 % have diaphragmatic hernia [, ], with male to female ratio of about 4:1, mostly presenting in the third decade of life. Approximately 0.8 to 1.6 % patients with blunt trauma sustain a rupture of the diaphragm accounting for 75 % diaphragmatic hernias, out of which 69 % are left sided, 24 % are right sided and 15 % are bilateral. The left rupture is more common than the right (68.5 % vs 24.2 %) due to hepatic protection and increased strength of the right hemi-diaphragm. Children have equal rates of rupture on both sides due to laxity of liver attachments []. The most common cause of blunt trauma is motor vehicle accident, whereas penetrating injuries result from gunshot or stab wounds. Other causes include labour in women with prior diaphragmatic hernia repair [, ] and barotrauma during underwater dive in patients with history of Nissen fundoplications []. The probable mechanisms for rupture from blunt injuries are (1) shearing of stretched membrane, (2) avulsion of the diaphragm from the points of attachments and (3) sudden increase in the trans diaphragmatic pleuro-peritoneal gradient; the resting pressure difference between pleural (−5 to −10 cm H2O) and peritoneal (+1 to +10 cm H2O) cavities rises to 100 cm H2O with large cough and does not injure the diaphragm. Forces transmitted to the abdomen from blunt trauma can raise the pressure gradient to 1000 cm H2O. The pathophysiology of diaphragmatic hernia includes circulatory and respiratory depression secondary to decreased function of the diaphragm. Herniation of intra-abdominal contents into the thorax leads to pulmonary compression, shifting of mediastinum and cardiac compromise []. Clinical presentation includes marked respiratory distress, decreased breath sounds on the affected side, auscultation of bowel sounds in the chest, palpable abdominal contents upon insertion of a chest tube, paradoxical movements of the abdomen with breathing and abdomen being less full on palpation. Initial chest radiography detects 73 % of traumatic diaphragmatic hernias with an additional 25 % found on subsequent film []. Chest radiographic findings include [] (1) abdominal contents in the thorax with or without signs of focal constriction (collar sign), (2) nasogastric tube seen in the thorax, (3) elevated hemi-diaphragm (>4 cm higher on left) and (4) distortion of the diaphragmatic margin. CT chest findings include [, ] (1) direct visualization of injuries, (2) segmental diaphragm non-visualization, (3) diffuse thoracic herniation of the viscera, (4) peri-diaphragmatic active contrast extravasation and (5) collar sign. CT scan of the chest has 14–82 % sensitivity with 87 % specificity while sensitivity increased to 71–100 % with helical CT. The left side has higher sensitivity than the right. Ultrasonography scan [] (focussed assessment with sonography for trauma-FAST) reported decreased movements of the diaphragm, especially in patients who are on ventilator support. Diagnostic laparoscopy and/or video-assisted thoracoscopic surgery (VATS) is indicated in stable patients if isolated diaphragmatic tear is suspected. For traumatic rupture, initial resuscitation is done according to ATLS protocol with airway control being the most important treatment followed by surgical intervention (once the patient’s condition stabilizes) which depends on the timing of diagnosis. In the acute phase of trauma, abdominal approach is preferred while transthoracic approach is preferred in latent phase because the patient often has adhesion to intra-thoracic organs. However, high incidence of concomitant injuries requires emergency exploration in most cases. Early exploration should be done to ensure viability of the herniated contents; repair of the defect should be done preferably reinforced using a polypropylene mesh. Laparoscopic surgery [, ] is performed to assess diaphragmatic integrity; it is a minimally invasive procedure by which the diaphragm can be directly visualized to know whether an injury had occurred or not. The diaphragm can be repaired easily by laparoscopic technique [, ] in the absence of intra-abdominal injuries. The laparoscopy is helpful in penetrating thoracic and flank injuries with intra-peritoneal penetration. Follow-up and surveillance is important for recurrence which is reported to be very low though small defect have been reported at the repairing site. Outcome and prognosis is good in isolated diaphragmatic injuries without long-term disability; overall mortality has been reported to be in the range of 5.5–51 % with associated complicated intra-abdominal injuries. This case had a history of compressive blunt trauma to the chest, chest pain, and breathlessness and was initially diagnosed as pneumothorax; however, it was confirmed on nasogastric tube insertion and follow-up chest X-ray and CT scan as diaphragmatic hernia improved after laparotomy, with full expansion of the lung. The message here is that the possibility of diaphragmatic hernia should be kept in mind in patients coming to the emergency department with history of breathlessness under respiratory distress.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3484,10,Ideal Body Weight,physical,decimal,pmc-7520797-1,Extracted,"An 80-year-old woman with a past medical history of recurrent right cheek nodular melanoma and new lung metastasis previously on immunotherapy presented for worsening dysphagia and odynophagia for one month.
The patient initially developed dysphagia, odynophagia and associated malnutrition after 6 cycles of pembrolizumab. Immunotherapy was discontinued, and patient was started on prednisone slow taper with initial improvement of symptoms. However, after 2 mo, the patient developed throat swelling with hoarseness and new oxygen requirement.
The patient initially had a right cheek skin pigmented lesion diagnosed as nodular melanoma in July 2015. She subsequently underwent tumor resection, and sentinel lymph node biopsy showed 0/4 positive lymph nodes. She was then started on active surveillance. In December 2016, the patient noticed a lump near the right parotid gland, and positron emission tomography/computed tomography (PET/CT) showed 1 cm fluorodeoxyglucose (FDG) avid nodule in the subcutaneous tissue of her right lower cheek consistent with malignancy and a new 1 cm FDG avid right upper lobe lung nodule with a standardized uptake value (SUV) max of 4.5. Fine needle aspiration (FNA) of right lower cheek subcutaneous nodule revealed metastatic melanoma. The patient underwent right superficial parotidectomy, modified radical neck dissection, and excision of the right subcutaneous peri-mandibular facial mass in January 2017. In February, local radiation therapy and adjuvant Ipilimumab immunotherapy were started. However, the patient developed severe diarrhea and rash after 2 doses of ipilimumab, so ipilimumab was discontinued, and she resumed active surveillance again. In March 2018, PET/CT showed an increased right upper lobe lung mass of 3.5 cm × 3 cm with SUV max of 17.3, pembrolizumab and radiation therapy to right lung were initiated. Near resolution of right lung metastatic lesion was noted after 3 doses.
In October 2018, PET scan revealed metabolic activity in the right supraglottic area (Figure ). The patient was hospitalized and underwent direct laryngoscopy with biopsy which showed a developed posterior supraglottic mass with inflamed mucosa encroached over posterior supraglottic airway and generalized inflamed mucosa throughout lower pharynx. Biopsy showed friable purulent debris with focal multinucleated giant cells without any evidence of fungal, bacterial, acid fast organisms or melanoma cells, indicating a diagnosis of immunotherapy associated mucositis. Pembrolizumab was held and patient was started on prednisone 40 mg oral daily with improvement of symptoms, and she was discharged home with prednisone slow taper.
Past medical history was significant for depression, diabetes mellitus type 2, hypertension.
Height: 5’4.9” (165 cm); Weight 199.3 Lbs (90.4 kg); Body Mass Index 33.2 kg/m2. Physical examination detected copious amount of thick mucus in the oropharynx.
CT neck showed near complete occlusion of the airway due to tissue thickening of epiglottis and larynx (Figure ).
Direct laryngopharyngoscopy with biopsies of pharyngeal, supraglottic, and glottic mucosa showed impending airway obstruction with massive swelling of posterior supraglottic larynx and diffuse inflamed granular mucosa involving majority of supraglottic larynx and lower larynx.
Histologic analysis of tissue biopsies demonstrated fibrinopurulent exudate and granulation tissue with acute and chronic inflammation in left and right arytenoid tissues of the larynx and also epiglottic tissue (Figure ).
Tissue culture with Periodic acid-Schiff (PAS), Grocott-Gomori’s methenamine silver (GMS) stain, gram stain, Fite, Kinyoun, and Wright-Giemsa stains were negative for typical and atypical bacteria, acid-fast bacteria (AFB), and fungi.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3485,10,Ideal Body Weight,physical,decimal,pmc-5490092-1,Extracted,"A 54-year-old female (weight 55 kg, 160 cm) was referred by an orthopedic surgeon to our pain clinic for persistent low back pain radiating down to right leg. She had a history of low back pain associated with radiculopathy, which was more on the right side and radiated till the big toe for more than 6 weeks. The impression on the magnetic resonance imaging (MRI) revealed a right paracentral disc protrusion at levels L4-L5, L5-S1 causing thecal sac indentation, effacement of the right lateral recess and right exiting nerve root impingement. There was no associated lumbar canal stenosis and no evidence of facet arthropathy. She had been taking analgesics tablet diclofenac 650 mg, tablet pregabalin 75 mg, tablet nortriptyline 10 mg, and regular physiotherapy for the last 6 weeks. She even underwent an epidural steroid injection (ESI) through the caudal route with 4 ml of 0.5% bupivacaine, 1 ml of methylprednisolone, and 5 ml of normal saline at a tertiary care center 4 weeks back after which her symptoms improved marginally for a period of 1 week and then she again started with debilitating pain, not getting relieved with analgesics and other modes of conservative management. The complete motor and sensory examination of the patient revealed motor power of Grade V, i.e. the muscle can move the joint; it crosses through a full range of motion against gravity and resistance. The sensations were intact as elicited by pain, temperature, vibration, position sense, stereognosis, and two-point discrimination. All the superficial and deep tendon reflexes were intact with an SLR of 10° on the right side and 70° on the left side. The patient had full control over the bladder and bowel.
We hence planned, fluoroscopic-guided transforaminal ESI (TFESI) using clonidine as an adjuvant at levels L4-L5 and L5-S1 on the right side, after discussing both with the patient and the orthopedic surgeon.
After taking an informed written consent, an 18-gauge intravenous cannula was secured. All routine monitors (electrocardiography, noninvasive blood pressure, and oxygen saturation) were attached. The patient was positioned on the operating room table with a pillow underneath the abdomen in the prone position. Under fluoroscopic guidance, the standard safe triangle was identified with pedicle of the vertebrae forming one arm of the triangle, lateral border of vertebral body forming the second arm, and the hypotenuse being formed by the exiting nerve root. Under all aseptic precautions, the skin overlying the target area was anesthetized with 2 ml of 1% lidocaine. The level of the epidural injection was chosen depending on the MRI findings and physical examination as L4- L5 and L5-S1.
A 22-gauge spinal needle was then advanced under fluoroscopy aiming the needle at the superior and anterior part of the intervertebral foramen through the safe triangle. The needle placement was confirmed after injecting 1–2 ml of omnipaque, nonionic water-soluble contrast medium iohexol dye, demonstrating the contrast going through the foramen. Furthermore, the confirmation of the needle position with contrast dye reduced the possibility of misplacement or intravascular placement of the needle, which is always a risk in ESIs performed without fluoroscopy. The needle was advanced into the safe triangle, and its placement was then confirmed both by anteroposterior and lateral view. One milliliter methylprednisolone (40 mg) mixed with 0.5 ml clonidine (50 μg) and 1 ml bupivacaine 0.5% were given at each level (volume 2.5 ml).
After the completion of the procedure, the patient was transferred to the recovery area. The patient's hemodynamic parameters were monitored during and after the procedure. Assessment of pain relief and any motor or sensory deficit was checked immediately and then hourly after the procedure till discharge from the recovery area.
The patient was discharged after having met the following discharge criteria after 2 h:
The patient was able to walk unaided The patient was able to void her bladder without any difficulty.
She was assessed for any numb or weak feeling in her back or legs for a few hours after the injection.
After 24 h, the patient was discharged from the hospital, and there was a significant improvement in the pain with an improvement in the SLR to 60°.
Following instructions were given at the time of discharge:
To report any untoward incident To continue taking analgesics as advised To start back muscle strengthening exercises after 3 days if there was considerable pain relief.
Patient was then reassessed at 2 weeks, 1 month, and 3 months interval after the procedure. There was a significant improvement in the pain after single injection of TFESI using clonidine as depicted by the visual analog scale (VAS) score; there was a much reduced drug dose intake and an improvement in the daily life activities as stated by the patient.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3486,10,Ideal Body Weight,physical,decimal,pmc-7091521-1,Extracted,"A 45-year-old woman, madam CB, was referred to our emergency unit on 22 July 2018. The patient was referred on account of eclampsia, acute kidney injury, and HELLP syndrome at 33 weeks gestation.
The patient presented there with complaints of epigastric pain and blurred vision of a day's duration.
She was apparently well until a day prior to presentation when she had the above complaints, which became associated with tonic clinic seizures at home with tongue bite; hence, she was rushed to the hospital. At the hospital, she had another episode of tonic clinic seizures. She was stabilized and referred to KATH for further management. The patient was given antihypertensives and anticonvulsant before referral.
At KATH, the blood pressure was high with proteinuria of 3+; however, the SpO2 was 99% on room air. She looked very unwell, pale, and not jaundiced with good hydration. Her chest was clinically clear. She had epigastric pain. Symphysis-fundal height of 32 cm was consistent with the gestational age. Lie was longitudinal, and presentation was cephalic. Fetal heartbeat was present and normal. No contractions were felt. On pelvic examination, the vulva and vagina looked healthy. The cervical os was closed, and the cervix was 2 cm long, firm, and posterior. The patient had 500 mL of cola-like urine and bedside clotting of 15 min. Impression of eclampsia with HELLP syndrome with an unfavorable cervix was made. The patient had samples taken for FBC, BUE, creatinine, serum uric acid, and grouping and crossmatch for 4 units of whole blood and 8 units of FFP. She was then prepared for emergency CS after the bedside clotting was corrected with transfusion of 3 FFPs. Immediately postop, the patient was very stable with normal vital parameters. 4 h post-CS, the patient had abdominal distension was tympanic, severally pale, and jaundiced. The uterus was well contracted, and shifting dullness was negative. Her pulse was 116 with blood pressure of 164/112 mmHg.
The patient had made 30 mL of cola-like urine in 4 hours. No bleeding per vaginam was noted. She was continued with the haemotransfusion and the FFP, but unfortunately, her condition did not improve and she ceased breathing. Cardiopulmonary resuscitation was attempted for over 30 min but was unsuccessful; hence, she was declared dead. Her labs came later, and liver indices were all markedly raised.
General condition: body of a woman of normal posture. She is 1.60 m in height. She is 45 years old.
Postmortem findings established multiple petechial bleeds in the lungs, liver, and gastric mucosa. There was massive clotted blood collected in the gastrointestinal tract. The postmortem findings are summarised as follows (the cause of death):
Haemorrhagic shock
Ingestion of corrosive herbal preparation Disseminated intravascular coagulopathy
Test report:
Laboratory no.: GSA LAB No9: 121/FS4/2019
Request: screening for common poisons including herbal poisons
Description/specimen tested
Liver—110 g
Stomach and content—320 g
Both kidneys—165 g
Blood sample—10 mL
Method of analysis: chemical/chromatography
Sampling procedure: submitted by Central Police, Kumasi, Ashanti
Test results
Liver: common poison/drugs—phenolic compounds detected
Stomach content: common poisons/drugs—phenolic compounds detected
Kidney content: common poisons/drugs—phenolic compounds detected
Blood sample: common poisons/drugs—phenolic compounds detected
Remarks
The samples submitted for analysis tested positive for phenolic compounds. They are basic chemical compounds of plant origin, which have pharmacological effects on humans and animals. They are corrosive/toxic and harmful depending on the amount ingested.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.6, 'm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.6 m, which is 1.6 m * 39.3701 in/m = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3487,10,Ideal Body Weight,physical,decimal,pmc-7370336-1,Extracted,"A 48-year-old woman, Jehovah’s Witness, presents to the outpatient of pulmonology service, with 8-year history of chronic cough and dyspnea, along with a progressive deterioration of her functional class (NYHA IV), along with permanent requirement of oxygen therapy and decline in the quality of life. Computed tomography scan of the chest revealed interstitial lung disease (see and ). Rheumatoid factor was positive and anticardiolipin antibodies were in indeterminate range; rest of autoimmune profile was negative. The patient did not present with clinical features of autoimmune disease. A diagnosis of autoimmune featured interstitial lung disease was made; cyclophosphamide cycle was administered without improvement of symptoms. Lung biopsy was taken via video-assisted pulmonary wedge resection, under general anesthesia. Pathology showed a histologic pattern consistent with usual interstitial pneumonia. Due to failure of medical therapy, the patient was accepted as a transplant candidate. However, due to religious beliefs, the patient stated that she does not accept blood products. Pulmonary function tests revealed a forced vital capacity (FCV) of 1.33 (44%), a forced expiratory volume in one second (FEV1) of 1.10 (44%), FEV1/FVC ratio of 83%, partial pressure of oxygen (PO2) of 91.3 mmHg and partial pressure of carbon dioxide (PCO2) of 55.1 mmHg, diffusing capacity for carbon monoxide (DLCO) 8.1 mL/mmHg/min (31%), 6-minute walk distance of 422 meters (73%), and a minimal oxygen saturation of 76 % without oxygen therapy.
Several months later, and after meticulous case review held by the lung transplant board (anesthesia, thoracic surgery, pulmonology), abdominal organ transplant board, and ethics committee, the patient was admitted for single-lung transplantation. She signed an informed consent declining transfusion of blood components, however agreeing to continuous cell-saver use. In the case of major perioperative bleeding, the patient also accepted the use of a prothrombin complex concentrate (which has advantages over fresh frozen plasma as it allows rapid correction of coagulation factor deficits with less volume infusion) and desmopressin. Blood loss during surgery was planned to be restored with 5% lactalbumin, in order to reduce the use of crystalloids in the event of significant bleeding.
The patient’s anthropometrics were 71 kg weight and 160 cm height. Regarding general procedure information, length of the procedure was 135 minutes. Cold Ischemia time was 230 minutes; there was no need for ECMO support. Bleeding during the procedure was estimated at 300 mL. Pulmonary artery pressure (PAP) was continuously measured, achieving a mean PAP of 18 mmHg in average during surgery.
Regarding hemostatic perioperative management for this patient, recommendations established in the current literature within the “Patient Blood Management” at the time were taken into account. Since preoperative hemoglobin was within normal values (14.6 g/dL), no additional measures were taken to optimize erythropoiesis. To minimize bleeding in the intraoperative setting, blood preservation methods were used: prophylactic use of antifibrinolytics was planned preoperatively, using an initial bolus of tranexamic acid 1 g, followed by continuous infusion during surgery. Fluids were adjusted at 2 to 4 cc/kg/h and readjusted according to intraoperative hemodynamic and metabolic variables. Insensible fluid loss was restored infusing a total of 870 cc of Ringer’s lactate. Normothermia was maintained with the use of Blanketrol heating system, and electrocautery scalpels were used to obtain a thorough surgical hemostasis with the help of topical hemostatic agents (tissue sealant/Surgicel). The patient agreed to intraoperative closed-system cell salvage, as it did not represent a conflict with her religious beliefs. Bleeding during surgery was calculated as of 300 cc, from which 120 cc were reinfused postoperatively. Finally, during the postoperative period, a drainage thoracostomy was positioned for a better quantification of postoperative bleeding and adequate blood evacuation from the lung. Erythropoietin was initiated during hospitalization.
After surgery, the patient was admitted to the intensive care unit, early extubation was successfully achieved, and there was no need of vasopressors or inotropes. PaO2/FiO2 ratio of 480 mmHg. Chest radiography revealed right perihilar infiltrates. The previous findings suggested a primary graft dysfunction grade 1 (see and ). Intensive care unit length of stay was 4 days, and total hospitalization length of stay was 13 days. Hemoglobin levels decreased at the end of hospitalization (see ). The patient was discharged without further complications with hemoglobin levels of 10.6 g/dL, which was treated in the outpatient setting with subcutaneous erythropoietin 2000 IU 3 times per week as ordered by internal medicine and pulmonology physicians. Hemoglobin levels increased to 11.4 g/dL at 1-week follow-up.
Pulmonary function tests after LT revealed FVC of 1.88 (53%), FEV1 of 1.73 (59%), FEV1/FVC of 92%, 6-minute walk distance of 353 meters (67%), and a minimal oxygen saturation of 94% without oxygen therapy. The patient final hemoglobin level was 11.4 g/dL.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3488,10,Ideal Body Weight,physical,decimal,pmc-4455857-2,Extracted,"A 20-year-old female with a history of SLE presented for HCQ screening. She had been on HCQ therapy for 5 months at 400 mg per day. Her height was 68 inches and she weighed: 89.086 kg. The calculated dose of HCQ was 4.5 mg/kg per day. She noted visual loss OS for 5 months a few days prior to starting HCQ, while she was hospitalized with SLE flare. Her BCVA was 20/20 OD and 1/200 OS with normal eye pressures and an afferent pupil defect OS. The OD examination and FA was unremarkable (). Dilated fundus examination OS showed marked vascular attenuation, macular exudates along with neovascularization of the disk (NVD), neovascularization peripherally/elsewhere (NVE), and vitreous heme (). FA OS demonstrated diffuse vascular blockage, retinal non-perfusion, and leakage from NVE (). SD OCT of macula showed thinning of retinal layers OS with central macular thickness 227 μ OD and 128 μ OS (). Automated visual field testing revealed severe constriction of visual field OS ().
The patient was diagnosed with central retinal artery occlusion/ophthalmic artery occlusion (CRAO/OAO) with neovascularization. She received pan-retinal photocoagulation and an intravitreal injection of 0.05 cc (1.25 mg) bevacizumab OS. She was already on oral 81 mg aspirin daily as she was positive for lupus anticoagulant factor.
On follow-up, she had BCVA 20/20 OD and counting finger OS with normal IOP. Fundus examination showed regression of NVD, macular exudates, and vascular attenuation with pan-retinal photocoagulation scars (). FA revealed resolving vascular leakage OS without macular edema ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [68.0, 'in']}",63.9,60.705,67.095,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 68.0 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (68.0 (in inches) - 60) = 63.9 kg.
Hence, the patient's IBW is 63.9 kg."
3489,10,Ideal Body Weight,physical,decimal,pmc-8258038-1,Extracted,"A 36-year-old man was transferred to intensive care unit (ICU) at a tertiary centre after a 24-hour period of being intubated and ventilated secondary to worsening type 1 respiratory failure. The presentation was consistent with COVID-19 with correlating symptomology describing a 1-week history of persistent fever, dry cough and 3 days of coryzal symptoms. Radiographic features included lower/mid zone and multiple peripheral opacities described as moderate to severe disease status (). This was later confirmed with a positive SARS-CoV-2 PCR swab result returning 48 hours into admission.
Baseline biochemical markers were equally in keeping with a diagnosis of COVID-19. Admission bloods indicated a proinflammatory process with a raised C-Reactive Protein (CRP) (320 mg/L), ferritin (2020 µg/L), D-dimer (2262 ng/mL) and a lymphocytopaenia (0.7×109/L) in keeping with COVID-19. Furthermore, a concurrent neutrophilia indicating possible superimposed bacterial infection. During this admission, nutritional specific markers were collected indicating a normal Glycated Haemoglobin (HbA1c) and lipid profile as obtained within the first week of admission. Serum vitamin D—25-hydroxyvitamin D (25(OH)D) was further measured at week six indicating insufficient levels at 34 nmol/L.
Nutritional assessment was completed post transfer to the tertiary ICU and was conducted remotely in line with local guidance, which involved restricted access to the unit preserving PPE and footfall. Initial anthropometric data were collected using estimated weight/height (75 kg/1.75 m2) providing a Body Mass Index (BMI) 24.5 kg/m2 although later corrections with the patient indicated initial body weight to be 80–85 kg (minimum of 5 kg discrepancy) giving a BMI of ~26.1 kg/m2 (overweight category). Early nasogastric tube placement enabled enteral tube feeding whereby a number of predictive energy equations were used to estimate energy and protein requirements noting the limited guidance specific to patients with COVID-19. These included the use of the Penn State protocol (Mifflin-St.Jeor formula) which equated to 1631 kcal/day and using ESPEN recommendations of 15–20 kcal/kg during the initial ebb phase of disease which provided a range of 1125–1500 kcal/day (calculated based on initial estimated body weight of 75 kg). The latter equation was adopted as per department recommendations to help simplify the assessment process as part of the wider contingency planning for dietetic care. Ongoing assessment aimed to ensure continual re-evaluation of nutritional requirements and was later adjusted to reflect 20–25 kcal/kg in keeping with ESPEN recommendations. Protein requirements were initially estimated between 90 and 112.5 g protein/day based on 1.2–1.5 g protein of actual body weight.
Initially large volumes of sedation and paralysis were required. The use of propofol was factored into calculations of total energy provision, which initially exceeded 300 mg/hour, equivalent to over ≥350 kcal/day in the first week. When calculating baseline requirements, sepsis was the primary factor considered noting the patient had no significant medical history, no further comorbidities and was previously well nourished and physically active. The patient was not on any regular medications or over the counter supplements prior to admission.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.75, 'm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.75 m, which is 1.75 m * 39.3701 in/m = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3490,10,Ideal Body Weight,physical,decimal,pmc-8523197-1,Extracted,"The patient reported in our case is a 36-years-old, tall and thin (height: 185.5 cm, weight: 70.3 kg, BMI: 20.4) male without a significant past medical history. Social history revealed a 30 pack-year cigarette smoking, the patient quit smoking five years before the presentation.
The patient reported left-sided back pain for three days. He went the next day after the pain started to a chiropractor and underwent spinal manipulation of his back to relieve his back pain. He described a significant improvement in his back pain after that. However, he suddenly developed shortness of breath at rest and left-sided chest pain a day later, and he presented to the emergency department for evaluation.
At presentation, the patient was afebrile, tachycardic with a heart rate of 105, normotensive with normal oxygen saturation (96% on room air). Chest x-ray showed a moderate left-sided hydropneumothorax (Figure ).
Chest CT scan with contrast was then done and showed moderate left-sided hydropneumothorax with moderate pneumothorax component and moderate pleural fluid component (Figure ). It also showed mild right-sided apical paraseptal blebs (Figure ).
After that, a left-sided chest tube was inserted with immediate drainage of 700 cc of bloody output. It was then placed on negative 20 mmHg suction. A chest x-ray confirmed a good chest tube placement with decreased left hydropneumothorax (Figure ).
The patient was then monitored with daily chest x-rays. Chest CT angiogram was performed on hospitalization day two that was negative for vascular aneurysms, dissection, or extravasation. It also showed significant improvement in left-sided hydropneumothorax with a small residual pneumothorax and significantly decreased residual pleural fluid (Figure ).
On day two of hospitalization, chest tube drainage of 300 cc of the bloody component was noted. No further drainage on hospital day three. Therefore, the chest tube was clamped and then removed.
A morning chest x-ray on hospital day four showed a new small left apical pneumothorax, this was treated with high flow oxygen therapy (Figure ).
On the day of discharge, the patient was feeling well and denied any more shortness of breath or chest pain. The last chest x-ray on the day of discharge showed stable left-sided pleural effusion and trace left-sided pneumothorax (Figure ).
Four days after discharge from the hospital, the patient followed with his primary care physician, who repeated a chest x-ray, and this showed only a persistent small left pleural effusion with no more left-sided pneumothorax (Figure ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [185.5, 'cm']}",79.97254,75.97391,83.97117,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 185.5 cm, which is 185.5 cm * 0.393701 in/cm = 73.03154 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (73.03154 (in inches) - 60) = 79.97254 kg.
Hence, the patient's IBW is 79.97254 kg."
3491,10,Ideal Body Weight,physical,decimal,pmc-2879976-1,Extracted,"A 30-year-old Caucasian female patient was admitted to our Hospital in February 2009, due to prominent, localized loose and sagging skin of abdomen, with reduced elasticity and resilience which gave her prematurely aged appearance induced by prior cesarean section 6 years ago (Figures and ). One month after cesarean section due to prolonged labor, she noticed the development of loose, wrinkled skin of abdomen without any sign of inflammation. The patient was treated by her gynaecologist with topical emollients, but with no result. At that time, patient refused reconstructive surgery of the redundant abdominal skin and had second cesarean section 3 years ago due to prolonged labor.
On admission to our Hospital her height was 175 centimeters and weight was 60 kilograms, body mass index was normal (19,6). Lax, redundant folds in the lower part of the abdominal wall were not associated with papules or plaques and were on non-sun-exposed areas.The affected area has normal pigmentation and no associated scaling. There was a lack of cutaneous induration or sclerosis. Skin lesions were asymptomatic and lack clinical sings of inflammation. Loss of recoil due to impaired function of the elastic fiber network has led to pendulous skin which was most notable in abdomen. These findings were limited to the skin of abdomen and were primarily of major cosmetic concern to patient. Extracutaneous findings were absent. She had had no previous illnesses and without any subjective difficulties (e.g., pain, fever, weight loss). There was no family history of this disorder and skin lesions were not present at birth and developed during 2nd decade of life. There was no mucosal involvement. She was not taking any medication. History of chronic sun exposure was negative. She was non-smoker.
CL has been diagnosed based on the clinical picture and pathohistological appearance. On admission excisional biopsy of lax skin has been performed. Routine hematoxylin-eosin staining has revealed normal collagen fibers, without any inflammatory infiltrate. Histopathologic analysis of skin has shown characteristic histologic feature of CL such as a loss of dermal elastic fibers revealed by orcein stain. Diminished elastic tissue was revealed throughout the dermis, not extending into the subcutis. The remaining elastic fibers were disorganized, shortened and fragmented. There was no epidermal alterations or cellular infiltrate ().
There was no evidence of IgG and IgA deposits in lesional skin.The following diagnostic and laboratory tests have been performed during hospitalization. Obtained findings include the erythrocyte sedimentation rate, complete blood count with differential and platelet count—values were within normal limits. The following tests were normal as well (glucose, transaminases, electrophoresis, immunoelectrophoresis, C3, C4, ANA, bilirubin, total protein, blood urea nitrogen, creatinine, electrolytes, iron, cholesterol and triglyceride levels, urine analysis). Other laboratory findings were also regular (pharyngeal and nasal swabs, oral cavity mycological analysis, PPD, hemoccult test). A basic laboratory assessment of clotting was performed including a platelet count, prothrombin time, and activated partial thromboplastin time. Obtained echocardiogram and abdominal ultrasound were without significant changes. There were no radiological signs for pulmonary emphysema. Serum level of α
1-antitrypsin and tumor markers (CA 19-9, CEA, CA 125, CA 15-3, and CYFRA 21-1) was normal as well. A serum thyroid-stimulating hormone (TSH) level was normal. Additional laboratory findings include free T3 and free T4 levels, and antithyroperoxidase and antithyroglobulin antibodies. Patient was sent to a plastic surgeon to undergo abdominoplasty and reduction of subcutaneous fat (Figures and ). Wound healing was normal and there was no clinical sign of dehiscence.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [175.0, 'cm']}",65.96466,62.66643,69.26289,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (68.89768 (in inches) - 60) = 65.96466 kg.
Hence, the patient's IBW is 65.96466 kg."
3492,10,Ideal Body Weight,physical,decimal,pmc-3599738-1,Extracted,"A 25-year-old Caucasian Croatian man, American Society of Anesthesiologists (ASA) status 1, underwent elective surgery for removal of a retroperitoneal tumor suspected to be a sarcoma. The tumor had been discovered accidentally during a routine examination. Our patient had no history of previous medical conditions. His family history did not suggest a hereditary disorder. He had no symptoms that could be related to a neuroendocrine-secreting tumor such as hypertension, palpitations, sweating, headache, glucose intolerance or Cushing’s appearance. His height was 165cm, weight 55kg and body mass index (BMI) was 20.2kg/m2. Pre-operative laboratory findings, chest X-ray and electrocardiogram (ECG) results were normal; his blood pressure measured 120/70mmHg pre-operatively. Ultrasound and magnetic resonance imaging (MRI) results showed a large, well-demarcated retroperitoneal tumor mass in his upper abdomen localized between the aorta and vena cava, measuring approximately 9×6×4.5cm, leaning on the liver and pancreas and spreading towards, but not affecting, the right adrenal gland. Our patient received midazolam 7.5mg orally 30 minutes before he was taken to the operating room. After establishing intravenous access and placing standard anesthesia monitors (non-invasive measurement of blood pressure (NIBP), ECG, SpO2 (pulse oximetry), and temperature), an epidural catheter was inserted in the epidural space between T7 and T8 under local anesthesia. Its correct epidural placement was tested with 60mg of lidocaine (with no additional epinephrine) to exclude the possibility of intra-vascular or intra-thecal puncture. A mixture of 0.25 percent levobupivacaine 25mg and sufentanil 10μg were administered epidurally twice as a bolus dose to adjust the block level, before the induction of general anesthesia. The epidural analgesia was tested by loss of sensation to pinprick and cold, compared to an unblocked dermatome. To eliminate surgical stress during the resection in accordance with the localization of tumor as assessed by MRI, the aiming level of epidural analgesia was adjusted to be from T5 to T12. Induction of anesthesia was made with propofol 120mg, sufentanil 10μg, following rocuronium 50mg to facilitate endotracheal intubation. Our patient received an arterial line for invasive blood measurement and a central venous catheter in the right jugular vein for central venous pressure measurement. The anesthesia was maintained with sevoflurane, in a mixture of O2 and air (in 40:60 ratios). Epidural analgesia was maintained continuously with an infusion pump (mixture of 0.125 percent levobupivacaine 50mg with sufentanil 10μg in 50mL of saline, infusion rate 5 to 25mL/hour) and this block completely satisfied intra-operative analgesic demands.
During the surgical excision of the tumor, severe and unexpected hemodynamic changes occurred. Minimal tumor manipulation was followed with severe hypertension measuring 205/110mmHg and tachycardia up to 120 beats/minute. Due to the fact that the surgical manipulation did not affect the adrenal glands and that epidural anesthesia was tested as sufficient for the anticipated surgery and also proven to be effective for treating surgical stimuli until this change occurred, suspicion of the presence of a neurosecreting tumor was raised.
The levels of both anesthesia and analgesia were increased in order to rule out too light a level of anesthesia and, as a consequence, pain. A bolus dose of intravenous sufentanil (25μg) was given, along with increase of the sevoflurane minimum alveolar concentration (MAC) and infusion rate of epidural analgesia (for 15 minutes), but the hypertension and tachycardia could not be suppressed by these pharmacological measures.
Also, we tried to rule out the other most common causes of such hemodynamic changes. Based on our patient’s medical history we could rule out pre-existing cardiac conditions, autonomic nerve system dysfunctions or hormonal disorders such as thyroid storm. His body temperature did not rise so we ruled out the presence of malignant hyperthermia. Basic laboratory results did not suggest any severe electrolyte disorder. All the symptoms were reflecting high and unsuppressed catecholamine activity. The clinical symptoms diminished only after additional administration of intravenous urapidil 40mg, esmolol 20mg and MgSO4 (magnesium sulfate) 2g.
Due to a large intra-operative blood loss because of the tumor’s extremely high vascularization our patient received high volume replacement in the form of crystalloids (7500mL), colloids (2000mL), and multiple blood transfusions (red blood cells (RBC) 1400mL and fresh frozen plasma (FFP) 1000mL). Adequate central venous pressure and diuresis were maintained during the procedure.
After excision of the tumor, our patient developed hypotension, due to the ‘downregulation’ of the receptors, with a lowest blood pressure measurement of 65/35mmHg. The epidural infusion was immediately discontinued. This condition was treated with additional large volume replacement with crystalloids, colloids, and vasopressors (norepinephrine up to 0.25μg/kg/min) in order to achieve a mean arterial pressure (MAP) over 65mmHg. Additional hemodynamic stability was eventually restored after administration of a bolus dose of hydrocortisone 100mg intravenously, which eventually led to cessation of the vasopressor infusion 45 minutes later.
His post-operative course was unremarkable. After the surgery, our patient was admitted to our Intensive Care Unit (ICU) where he remained intubated and ventilated for two hours. He was hemodynamically stable, without vasopressor support. There were no episodes of hypertension or tachycardia reported. Analgesia was supplied by epidural catheter and our patient experienced no pain. He was transferred to the ward the next day and on the eighth post-operative day he was discharged from hospital. The final pathology report confirmed the presence of an extra-adrenal sympathetic paraganglioma (EASP).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3493,10,Ideal Body Weight,physical,decimal,pmc-7934134-1,Extracted,"A 17-year-old male presented to the outpatient department of cardiology at Rawalpindi Institute of Cardiology, Rawalpindi, Pakistan, after being referred from a local practitioner in Kashmir, for evaluation of a murmur that had been auscultated at the lower left sternal border. The patient presents with complaints of bluish discoloration of the body and difficulty in breathing for 5 years of age. The patient had a history of inconsistent follow-ups. The patient’s cyanosis was exacerbated during eating and lessened spontaneously. The patient’s dyspnea occurred mostly at night. Exertion was an exacerbating factor but the patient was reported that he altered his lifestyle (not taking active part in sports, taking rest after walking long distances, and walking less vigorously) accordingly to prevent exacerbation. History was not significant for any other complaints. The patient is a student of 10th grade and doing well in school. Family history is significant for consanguineous marriage of his parents. All his siblings were normal. On examination, a tall and lean male was sitting comfortably in the given settings. Anthropometry revealed his height to be 183 cm and weight to be 40 kg. Vitals were all normal. There was bilateral Grade 3 clubbing on both his fingers and toes [].
There was central cyanosis on the lips. Micrognathia was also noted [].
On precordial examination, the lateral diameter of the chest was lesser and not in proportion to anteroposterior diameter. Apex beat was found in fifth intercostal space in the mid-clavicular line. It was normal in character. Auscultation revealed normal heart sounds and a holosystolic murmur, Grade 3/6, heard at the lower left sternal border. Rest of history and examination was unremarkable.
Pediatrics department was also consulted. A provisional diagnosis of Pierre Robin sequence with VSD was made. The patient was prescribed oral bosentan, 62.5 mg once daily, sildenafil, 5 mg thrice daily, and spironolactone, 40 mg once daily. Echocardiography could not be attempted due to rib crowding. However, his computed tomography (CT) images revealed characteristic findings of TOF [Figures and ].
VSD correction with infundibular repair was attempted and the patient was subsequently discharged. He had no post-operative complications.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [183.0, 'cm']}",77.70874,73.8233,81.59418,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 183.0 cm, which is 183.0 cm * 0.393701 in/cm = 72.04728 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (72.04728 (in inches) - 60) = 77.70874 kg.
Hence, the patient's IBW is 77.70874 kg."
3494,10,Ideal Body Weight,physical,decimal,pmc-6966759-1,Extracted,"A 48-year-old man (height 168 cm, weight 80 kg) with gastric cancer was scheduled for laparoscopic gastrectomy. He was on maintenance dialysis for chronic renal failure. His medical history included coronary artery bypass grafting for angina. Blood tests were done a day before surgery and prior to maintenance hemodialysis showed mild hyperkalemia (serum K+ 5.4 mEq/L). Serum K+ was not rechecked after hemodialysis.
In the operating room, after placing a thoracic epidural catheter, we induced general anesthesia by intravenous administration of propofol 60 mg, fentanyl 100 μg, and rocuronium 70 mg. A central venous catheter was placed via the internal jugular vein. Anesthesia was maintained with oxygen (40 to 50%), air and desflurane (4 to 5%); and a continuous infusion of remifentanil (0.1–0.2 μg/kg/min). Bolus 1.5% lidocaine epidural infusion and intravenous fentanyl infusion were added as needed. Circulation was supported by continuous nicorandil infusion and bolus phenylephrine. In addition to standard monitors, continuous arterial pressure was monitored via the radial artery.
Surgery was performed in the reverse Trendelenburg position. An hour into surgery, his arterial blood gas (ABG) analysis showed hyperkalemia serum K+ =6.3 mEq/L (Table ). The patient had received K+ free infusion since arriving in the operating room until then. The cause for hyperkalemia was unclear at that point in time. In the surgical field, the liver was enlarged and had been retracted for optimal exposure.
ABG analysis during the third hour of surgery showed a further increase in serum K+ to 7.0 mEq/L (Table ). Hence, we initiated an infusion of 50% glucose at 5 mL/h with insulin at 0.2 U/h. As serum K+ remained high, we increased the ratio and volume of the infusion gradually to 50% glucose at 20 mL/h with 2 U/h of insulin. When the K+ level exceeded 7 mEq/L during the fifth hour of surgery, sodium bicarbonate (120 mg) was administered. We reported the hyperkalemia to surgeons and discussed to arrange an emergency postoperative hemodialysis. They did not report any abnormal changes that could be the cause of the hyperkalemia in the surgical field, including color changes to the liver. The K+ level continued to remain high despite remedial measures. From the eighth hour onwards, the lactate level also increased (Table ). The total surgical duration was 601 min, and anesthesia time was 743 min.
The patient received a total of 900 mL of normal saline and 500 mL of 5% albumin during the procedure. His estimated blood loss was 350 mL. The patient was hemodynamically stable throughout the operation, with no abnormal findings on electrocardiogram (ECG). After the conclusion of the surgery, the patient was extubated in the operating room and transported to the intensive care unit.
Immediate postoperative blood analysis showed a significant rise in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) (Fig. ), suggestive of liver damage, most probably due to intraoperative liver retraction. We initiated glycyrrhizin infusion for suspected liver damage. Serum K+ decreased marginally to 6.7 mEq/L (Table ) because of continuous glucose-insulin infusion, and thus an emergency postoperative hemodialysis was avoided. However, we resumed hemodialysis on the first postoperative day (POD 1). Serum K+ was 7.0 mEq/L (Table ) despite hemodialysis and so he received continuous hemodiafiltration from POD 1 to POD 4. Serum K+, AST, and ALT peaked on POD 1 and then improved gradually with the above treatment measures (Fig. ). However, the patient developed a high-grade fever (39 °C) on POD 5. Emergent computed tomography (CT) showed a low-density area in the left lobe of the liver (Fig. ), suggestive of hepatic infarction. Treatment with antibiotic agent was initiated for presumed infection of the infarcted liver. The patient responded well to treatment. He was discharged 27 days after surgery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.0, 'cm']}",64.12607,60.91977,67.33237,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg."
3495,10,Ideal Body Weight,physical,decimal,pmc-4610930-1,Extracted,"A 25-year-old male (height 167.7 cm, weight 52.2 kg) was admitted for surgical resection of a 5.0 × 1.8 cm right-cheek mass, suspected to be a lymphangioma. The patient had undergone a tonsillectomy under general anesthesia 8 years previously without any perioperative complication. The medical history indicated no drug or food allergies. Preoperative examinations of the patient were within normal limits. Therefore, anesthesia was applied according to the American Society of Anesthesiologists physical status classification 1.
The patient received no premedication prior to admission to the operating theater. The blood pressure upon arrival in the operating theater was 158/76 mmHg, with a heart rate of 80 beats/min (BPM), and with a peripheral oxygen saturation of 99% of room air. Anesthesia was induced using an injection of 50 µg fentanyl, 150 mg propofol and 50 mg rocuronium. Endotracheal intubation was performed using a cuffed oral right-angle endotracheal tube. Anesthesia was maintained using oxygen, air and desflurane. As a prophylactic antibiotic, 1 g cefazoline was administered intravenously immediately after completion of induction.
One hour after commencing surgery, the surgeon requested a reversal of the neuromuscular blockade to monitor patency of the facial nerve. Anesthesia was consequently maintained using desflurane alone. At this time, the blood pressure was 105/74 mmHg and the heart rate 92 BPM. We administered 1 mg atropine and 1.5 mg neostigmine intravenously to reverse neuromuscular blockade. After approximately 5 min, the blood pressure was decreased to 75/42 mmHg and the heart rate was 104 BPM. We administered 10 mg ephedrine intravenously. After 5 min, the blood pressure was 67/36 mmHg and the heart rate was 94 BPM. To manage persistent hypotension, 200 µg phenylephrine were administered, followed by a rapid infusion of lactated Ringer's solution. However, the non-invasive blood pressure decreased further to 57/36 mmHg and the heart rate rose to 138 BPM. As we asked the surgeon, there was no drug administration at surgical field.
Invasive blood pressure monitoring was applied to the left dorsalis pedis artery and additional venous access was established. The arterial blood gas analysis showed all parameters to be within normal limits. Continuous infusion of norepinephrine at 0.03 µg/kg/min was initiated. Consequently, the blood pressure was restored to 99/51 mmHg and surgery was resumed.
Because the patient was covered with a drape, clinical manifestation of anaphylaxis, including skin rash, could not be observed. Approximately 1 h after the hypotension event, a skin rash was detected over the entire body. There were no respiratory symptoms, including wheezing or increased airway pressure. The patient was suspected to be suffering from an anaphylactic reaction. A 10 µg bolus of epinephrine was given and a continuous epinephrine infusion was initiated at 0.03 µg/kg/min. The patient responded to the epinephrine and soon maintained hemodynamic stability; with a blood pressure of 110/52 mmHg and a heart rate of 78 BPM. Norepinephrine infusion was discontinued and epinephrine infusion was tapered to maintain the restored blood pressure. The patient was treated using 4 mg chlorpheniramine together with 5 mg dexamethasone to prevent delayed reactions and halt any further histamine release. After 1.5 h, the blood pressure was 110/46 mmHg without any inotropic or vasopressor support. The skin lesion was improved and no respiratory symptoms were detected throughout the completion of the surgery. The total operation time was 200 min and the anesthesia time 245 min. The total infused crystalloid, colloid, estimated blood loss and urine output were 1,300 ml, 500 ml, 50 ml, and 450 ml, respectively ().
The patient was transferred to the intensive care unit for close monitoring and was placed on ventilatory support. An hour after arrival, the patient was extubated uneventfully without any neurologic deficit. Blood tests were obtained for the tryptase level, which was elevated to 37.9 µg/L (normal range: 0-11 µg/L) and the total serum immunoglobulin E (IgE) level, which was increased to 675 Ku/L (normal range: negative). The patient was transferred to a general ward 1 day later and was discharged after 1 week without any complications. The consultant allergist recommended that allergen tests be conducted.
Skin-prick and intradermal tests were performed after 1 month to determine the cause of the anaphylaxis. The skinprick tests were negative for all agents, whereas the intradermal tests were positive for atropine (wheal of 4 × 4 mm for a stock concentration of 0.5 mg/ml; wheal of 4 × 4 mm with 1 : 5 dilution) (). The intradermal skin tests also demonstrated a positive result for rocuronium (wheal of 5 × 5 mm for a stock concentration of 10 mg/ml; wheal of 4 × 4 mm with 1 : 10 dilution). The patient was advised to completely avoid atropine and is currently receiving regular check-ups at the outpatient department of plastic surgery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [167.7, 'cm']}",63.85442,60.6617,67.04714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 167.7 cm, which is 167.7 cm * 0.393701 in/cm = 66.02366 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.02366 (in inches) - 60) = 63.85442 kg.
Hence, the patient's IBW is 63.85442 kg."
3496,10,Ideal Body Weight,physical,decimal,pmc-7746323-1,Extracted,"We describe the case of a 38-year-old man with HIV who has had a one-year history of blurring of vision, intermittent flashing lights and occasional transient visual obscurations with position change. He denied any headaches or tinnitus. A visit to the ophthalmologist led to a diagnosis of bilateral papilledema.
His past medical history was significant for hypertension, diabetes, hyperlipidemia and bipolar disease. His medications included emtricitabine-tenofovir 200/300 milligrams (mg) once daily, bupropion 150 mg daily, cimetidine 200 mg twice daily, hydrochlorothiazide 25 mg daily, losartan 100 mg daily, metformin 500 mg daily, atorvastatin 40 mg daily and quetiapine 200 mg daily.
On examination, his blood pressure (BP) was 122/77 mmHg, pulse of 85 beats per minute, weight of 231 pounds, with height of 71 inches and body mass index (BMI) of 31.1. Precordial chest examination did not reveal a cardiac murmur. His neurological examination was entirely normal. Funduscopic eye examination revealed bilateral optic disc edema with peri-papillary flame hemorrhages and cotton-wool spots (Figure ).
A magnetic resonance imaging (MRI) of the brain with and without gadolinium contrast, magnetic resonance venogram of the brain and MRI of the orbits with and without contrast gadolinium were all normal.
The cluster of differentiation (CD-4) white cell count was 1392 (>500 cells/cubic millimeter). Serum RPR titer was very high at 1:128 (<1:8). A lumbar puncture revealed an opening pressure of 20 cm of water (<25) in the lateral decubitus position. Cerebrospinal fluid (CSF) results are listed below (Table ).
The serum and CSF serology displays the typical signature of neurosyphilis. We have a high titer serum NT-test, RPR, and a positive CSF T-test, fluorescent treponemal antibody absorption test (FTA-ABS), and in this case two positive CSF NT-tests, RPR and venereal disease research laboratory (VDRL). CSF RPR is usually of low sensitivity. We believe our patient did not display a significant pleocytosis because he had received two empirical doses of intramuscular procaine penicillin from the HIV clinic two weeks prior to the lumbar puncture. Following the lumbar puncture, our patient received the standard therapeutic protocol for ocular syphilis; 1.2 million units of intramuscular procaine penicillin daily for 14 days plus probenecid 500 mg four times daily for 14 days. A repeat lumbar puncture is planned in three months in order to demonstrate a four-fold drop in serum NT-test titers, in this case the RPR. A lumbar puncture will also be performed four weeks after the last dose of procaine penicillin to assess CSF VDRL status.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [71.0, 'in']}",75.3,71.535,79.065,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 71.0 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (71.0 (in inches) - 60) = 75.3 kg.
Hence, the patient's IBW is 75.3 kg."
3497,10,Ideal Body Weight,physical,decimal,pmc-3420530-1,Extracted,"A 54-year-old woman was admitted to our hospital with fever, general malaise, and dyspnea. She had undergone bilateral breast augmentation surgery with silicone bags 5 years previously, with resurgery on the right side due to bag rupture 7 months before presentation. Seven days before admission, she became febrile and noticed dyspnea. She visited her family doctor and was diagnosed with pneumonia, but treatment with antibiotic therapy had no noticeable effect. She was then referred to our hospital for further examination and treatment.
The patient was 158 cm tall, weighed 46 kg, and blood pressure was 100/50 mmHg, heart rate was 74 beats/min, body temperature was 37.0°C, and respiratory rate was 30 breaths/min on admission. Inspiratory rales were heard at both lung bases.
The examination of the blood revealed severe thrombocytopenia with prolonged prothrombin time and high levels of fibrinogen degradation product (FDP) (). Chemical analysis revealed severe abnormal liver function with jaundice, mild renal insufficiency, and high C-reactive protein (CRP) level. Arterial blood gas levels on room air revealed hypoxemia with hypocapnia. All testing for autoantibodies yielded negative results. Blood culture was negative for bacteria. Computed tomography (CT) of the chest revealed nodular and macular shadowing in the right upper and middle lobes and left inferior lobe and ground-glass opacities in both inferior lobes (). Our patient saw an ophthalmologist, and there were no findings suggestive of uveitis.
We diagnosed interstitial pneumonia with hepatic dysfunction and disseminated intravascular coagulation (DIC) and initiated methylprednisolone pulse therapy (1 g/day for 3 consecutive days) for interstitial pneumonia and gabexate mesilate and antithrombin III for DIC. Antibiotic (Meropenem trihydrate 1 g/day, Azithromycin hydrate 500 mg/day) was administrated to cover the possibility of concomitant bacterial pneumonia. On day 4, respiratory status and interstitial opacity on CT were improved (). However, fever recurred on day 10 and respiratory status and CT findings were deteriorated on day 15 (). Methylprednisolone (1 g/day for 3 consecutive days) was again administered, followed by prednisolone (40 mg/day) to avoid recurring exacerbation of interstitial pneumonia. On day 18, bronchoscopy was performed to identify the cause of interstitial pneumonia. Transbronchial lung biopsy specimens revealed small cell infiltrations of lymphocytes, plasma cells, and neutrophils. Analysis of bronchoalveolar lavage fluid (BALF) revealed an increased number of lymphocytes (52.5%) and a high CD4/CD8 ratio (2.52). However, the cause of interstitial pneumonia remained unclear. Ziehl-Neelsen staining of tissue samples and sputum culture yielded negative results for Mycobacterium tuberculosis. Fever recurred on day 20 and liver biopsy was performed to identify the cause of fever. We considered the possibility of sarcoidosis based on elevated levels of angiotensin-converting enzyme (ACE) (63.0 IU/L) and lysozyme (11.8 mg/mL). On day 23, Liver biopsy confirmed Langhans' giant cell and noncaseating granuloma (). On day 34, CT was performed to followup the interstitial pneumonia and fever, revealing miliary nodules in both lung fields, typical of miliary tuberculosis, although interstitial shadows had disappeared (). On day 35, antituberculosis therapy (isoniazid, 300 mg/day; rifampicin, 450 mg/day; ethambutol, 750 mg/day; pyrazinamide, 1200 mg/day) was applied for miliary tuberculosis after acid-fast bacilli were detected in gastric fluid and sputum, and polymerase chain reaction testing for Mycobacterium tuberculosis yielded positive results. Ziehl-Neelsen staining obtained positive results in a liver specimen (), but negative results in a lung specimen. Fever subsided following antituberculosis therapy. On day 41, rifampicin was stopped due to leukocytopenia (while blood cell (WBC) count, 1550/mm3; neutrophils, 350/mm3), likely caused by rifampicin. On day 59, the WBC count was fully recovered, and rifampicin was restarted at a low dose (150 mg). Fever was again seen on day 64, and CT was performed on day 68. Although miliary nodules in both lung fields had almost disappeared (), sickly shadowing was newly apparent in both upper lobes (). These new lesions were considered highly likely to represent recurrent interstitial pneumonia and not exacerbation of miliary tuberculosis, because exacerbation occurred during treatment for tuberculosis. On day 68, methylprednisolone was restarted at 0.5 g/day for 3 days and the dose of prednisolone was increased to 40 mg/day. Thereafter, fever subsided and the sickly shadowing had disappeared by day 72 (). On day 70, we switched from rifampicin to levofloxacin, as leucopenia had again progressed. Prednisolone was gradually tapered to 30 mg/day, and the patient was discharged without recurrence of the disease on day 100 ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3498,10,Ideal Body Weight,physical,decimal,pmc-4579816-1,Extracted,"In March 2007, a 21-year-old female underwent a right salpingo-oophorectomy, partial omentectomy and appendectomy due to right ovarian cancer at the Department of Obstetrics and Gynecology, Ehime University Hospital (Toon, Japan). Pathological examination of the tumor revealed multiple mucinous cysts, lined by mucinous tumor cells. Although adenomatous and borderline malignant regions were identified in the tumor, partial areas of carcinoma were also present, which proliferated and invaded the stroma. Thus, the ovarian tumor was diagnosed as mucinous cystadenocarcinoma. After performing adjuvant chemotherapy with three 28-day cycles of carboplatin (2 AUC; days 1, 8 and 15) and paclitaxel (60 mg/m2; days 1, 8 and 15), follow-up care was conducted on an outpatient basis every 3 months.
At 2 years and 6 months post-surgery, follow-up contrast-enhanced computed tomography (CT) showed two low density areas in the spleen. Thus, 18F-fluorodeoxyglucose (FDG)-positron emission tomography (PET)/CT was performed and revealed two abnormal high uptake lesions in the spleen, which were 2.5 and 1.0 cm in diameter, with a maximum standardized uptake value (SUVmax) of 21.0 and 18.2, respectively. The PET/CT also showed an abnormal high uptake lesion in the lateral segment of the liver, which was 1.5 cm in diameter, with an SUVmax of 14.5 ().
In October 2009, the patient was referred to the Department of Hepatobiliary-Pancreatic and Breast Surgery of Ehime University Hospital due to a working diagnosis of splenic and hepatic metastases from right ovarian cancer. A splenectomy and partial hepatectomy were recommended and the patient was admitted. Contrast-enhanced CT was performed again prior to admission and showed a low-attenuation nodule in the lateral segment of the liver, in addition to two low-attenuation nodules in the spleen (). Hepatomegaly and splenomegaly were not indicated on the radiology report. Abnormal lesions in the lung and bilateral hilar lymphadenopathy were also not indicated. At the time of admission, the patient was 162.3 cm tall and weighed 93.3 kg. The body mass index was 35.4 and the patient exhibited no swelling of the superficial lymph nodes. Routine blood analysis showed that the complete blood count, and test results for liver function, renal function and electrolytes, including serum calcium, were within normal limits, with the exception of a slightly elevated level of C-reactive protein (1.20 mg/dl; normal range, 0.00–0.20 mg/dl) (). The serum levels of carcinoembryonic antigen, cancer antigen (CA)19-9, CA125 and α-fetoprotein were normal on admission, although the serum levels of CA19-9 (45 U/ml; normal range, <37 U/ml) and CA125 (56.8 U/ml; normal range, <35 U/ml) had been elevated prior to the previous surgery for right ovarian cancer. Electrocardiogram and chest X-ray results were normal ().
Due to the fact that the main differential diagnosis was splenic and hepatic metastases from right ovarian cancer, a laparoscopic procedure was performed. At the beginning of the laparoscopic procedure, an exploration of the abdominal cavity by a gynecologist was performed, which confirmed no abnormalities in the uterus or the adnexa of uterus, and no ascites or peritoneal dissemination. A cytological sample of peritoneal washing in the pouch of Douglas was obtained, and the presence of no malignant cells in the sample was confirmed the following day. The laparoscopic splenectomy and partial hepatectomy were then performed. Tumors were observed on the surface of the spleen (). Although a tumor was not observed on the liver, a 1.5-cm low echoic mass in segment 3 (Couinaud classification) () of the liver was confirmed by intraoperative ultrasonography. The whole spleen was removed after a 12-mm median incision for a port was widened by 4 cm. The weight of the spleen was 269 g. The weight of the resected liver specimen was 34 g. Macroscopically, yellow-whitish and elastic-hard nodules were found in the specimens on the sectional views (). Histopathological examination showed that these nodules contained no malignant cells and that a large number of non-caseating epithelioid cell granulomas formed these nodules (). Acid-fast bacillus was not detected using Ziel-Nielsen staining. Fungus was also not detected using periodic acid-Schiff staining and Grocott staining. Thus, the final diagnosis was of extrapulmonary sarcoidosis of the liver and spleen. Further post-operative laboratory studies showed no angiotensin-converting enzyme (ACE; 11.4 IU//l; normal range, 8.3–21.4 IU/l) or lysozyme (6.5 µg/ml; normal range, 5.0–10.2 µg/ml) abnormalities.
The patient recovered well with no further treatment, such as steroid therapy, and neither recurrence of sarcoidosis in any other organs nor recurrence and metastasis of right ovarian cancer have been observed for 2 years and 5 months since the surgery. At 5 years and 6 months post-surgery the patient remained alive.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [162.3, 'cm']}",54.46464,51.74141,57.18787,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 162.3 cm, which is 162.3 cm * 0.393701 in/cm = 63.89767 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.89767 (in inches) - 60) = 54.46464 kg.
Hence, the patient's IBW is 54.46464 kg."
3499,10,Ideal Body Weight,physical,decimal,pmc-3934786-1,Extracted,"A 43-year-old Caucasian woman was admitted to the hospital due to acute renal failure and proteinuria in the nephrotic range. She presented with a 3-month history of fatigue, anaemia and lymphadenopathy. Before admission, a CT scan was performed, which revealed lymphadenopathy of the neck as well as generalized abdominal and mediastinal lymphadenopathy. Lymph node excision showed reactive lymphadenopathy. No history of skin rashes, photosensitivity, joint swelling, hair loss or oral ulcers was identified. On physical examination, the patient's height was 170 cm, her weight 56 kg (BMI 19.4), she was afebrile and her blood pressure was 117/77 mm Hg.
Laboratory examinations revealed (table ) a white blood cell count of 3.2 × 109/l (reference range, 4–10 × 109/l), lymphocytes 13.5% (reference range, 10–50%), haemoglobin 102 g/l (reference range, 115–165 g/l), platelets 147 × 109/l (reference range, 150–350 × 109/l), total protein 71 g/l (reference range, 64–83 g/l), albumin 27 g/l (reference range, 35–50 g/l), lactate dehydrogenase 161 U/l (reference range, <250 U/l), haptoglobulin 1.85 g/l (reference range, 0.3–2.0 g/l), urea 12.6 mmol/l (reference range, 2.7–6.8 mmol/l), creatinine 174 μmol/l (reference range, 45–84 μmol/l), C-reactive protein <5 mg/l (reference range, <5 mg/l) and an increased erythrocyte sedimentation rate of 81 mm/h. Urine analysis showed proteinuria of 6.4 g/day and an active sediment containing dysmorphed red blood cells. Serum complement levels were low with a C3c of 0.2 g/l (reference range, 0.8–1.8 g/l), C4 0.02 g/l (reference range, 0.1–0.4 g/l), and CH50 14 U Eq/ml (reference range, 70–180 U Eq/ml). Antinuclear antibodies were elevated to 1:80 (reference range, <40-fold), anti-double-stranded DNA antibodies were not detectable and anti-C1q was 20 IU/ml (reference range, <15 U/ml). ANCA titres on immunofluorescence were increased up to 1:640 (reference range <1:20). Using enzyme-linked immunosorbent assay (ELISA), MPO-ANCAs were positive with 3,622 U/ml (reference range, <5 U/ml) and PR3-ANCAs were not detectable. Anti-SS-A/Ro52 were 22 U/ml (reference range, <10 U/ml) and anti-SS-A/Ro60 were >240 U/ml (reference range, <10 U/ml). Cryoglobulines were not detectable. Serologic tests for HIV, hepatitis B/C and cytomegalovirus were all negative. Epstein-Barr-virus IgG was positive, IgM was negative and EBNA1 IgG was positive.
Renal biopsy was performed on day 2, which revealed a diffuse, segmental, proliferative, immune-complex GN with crescents in 4 of 19 glomeruli corresponding to an LN class IV-S (A/C; fig. ). Immunofluorescence staining showed deposition of IgA, IgM, C1q, C3 and C5–9 in the mesangial area and peripheral capillaries. Electron microscopy revealed mesangial and peripheral electron-dense deposits without obvious structuring. Most of the peripheral deposits were located subendothelially, there were also some subepithelial deposits. Tubulo-reticular structures within one endothelial cell were found.
After renal biopsy, methylprednisolone pulses were initiated (500 mg/day for 3 days) followed by oral prednisone 50 mg/day and cyclophosphamide 1 g intravenously. However, the serum concentration of creatinine gradually increased, so that again methylprednisolone pulses (500 mg/day for 2 days) were repeated on day 13, and high volume plasma exchange was started for 5 consecutive days to eliminate MPO-ANCAs (fig. ). After the plasma exchanges, the MPO-ANCA levels were decreased to 104 U/l and renal function improved so that the patient was discharged on day 39. Cyclophosphamide therapy was continued with 500 mg intravenously every second week for 3 months, so that the patient received a cumulative dose of 3.5 g. The maintenance therapy with azathioprine had to be switched to mycophenolate mofetil due to gastrointestinal side effects. Eighteen months after starting treatment, the patient is still in remission. MPO-ANCAs are not detectable and renal function has recovered completely with a creatinine concentration of 88 μmol/l (reference range, 45–84 μmol/l) and a minimal proteinuria of 0.2 g/day – using a treatment regime consisting of mycophenolate mofetil 2 g, prednisone 7.5 mg and hydroxychloroquine 200 mg per day.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [170.0, 'cm']}",61.43709,58.36524,64.50894,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.92917 (in inches) - 60) = 61.43709 kg.
Hence, the patient's IBW is 61.43709 kg."
3500,10,Ideal Body Weight,physical,decimal,pmc-6769358-1,Extracted,"A 16-year-old boy with past medical history of type 1 truncus arteriosus, a very rare congenital cardiac malformation, and moderate-to-severe tricuspid insufficiency, who underwent several corrective surgical interventions (the last one in 2014), started amiodarone (200 mg/day) therapy in August 2015 due to paroxysmal supraventricular tachycardia. He was referred to Pediatric Endocrinology in October 2017 for thyroid dysfunction compatible with thyrotoxicosis; he had no personal or family history of thyroid disease and prior thyroid tests proved to be normal.
He complained of a more intense feeling of palpitations, fatigue and had a weight loss of 4kg in the previous 3 months (baseline height and weight: 167cm and 59.8kg, respectively) yet he denied heat intolerance, diarrhea or other symptoms; physical examination showed no relevant changes other than the known holosystolic murmur, loudest at the base. Laboratory assessment revealed: serum thyroid-stimulating hormone (TSH) <0.01 uUI/mL [reference values (RV): 0.47-3.41 uUI/mL]; serum free thyroxine (FT4) 2.83 ng/dL (RV: 0.89-1.37 ng/dL); serum free triiodothyronine (FT3) 7.92 pg/mL (RV: 2.25-3.85 pg/mL); negative antithyroid antibodies [thyroid peroxidase antibodies (TPOAb) <1.0 UI/mL (RV: <5.61 UI/mL), thyroglobulin antibodies (TgAb) <1.0 UI/mL (RV: <4.11 UI/mL) and negative TSH receptor antibodies (TRAb) (<1.0 UI/L)]. Thyroid function was reassessed at the moment of our evaluation (4 days later), which was found to be deteriorated as serum FT3 notably reached 19.76 pg/mL and serum FT4 3.61 ng/dL; serum TSH levels remained undetectable and thyroid autoimmunity negative. The thyroid ultrasound was normal: thyroid with globally hypoechogenic texture, with no solid nodules, no increase in vascularization and no latero-cervical adenopathies ().
The distinction between the two main AIT types could not be made clinically. Considering the potential iatrogenic effect of corticosteroid therapy on this adolescent heart disease, treatment has been promptly started with thiamazole 15 mg/day (0.25 mg/kg/day). In face of no significant improvement in thyroid function and slight changes in hepatic enzymes during the first couple of weeks, with alanine transaminase (ALT) elevation even attaining > 3-fold upper limit of normal (ULN), it was decided to replace amiodarone by sotalol 160 mg/day (in-hospital replacement on Pediatric Cardiology Department), maintaining a strict monitoring of thiamazole hepatotoxicity, without prompt dose increase. The patient kept fair control of both heart rhythm and rate. Thyroid hormone levels had then gradually improved (TSH 0.02 UI/mL, FT4 0.78 ng/dL, FT3 2.83 pg/mL) (), as well as liver enzymes. After 4 months of starting thiamazole the patient had gained 5kg, presenting sustained clinical and analytical enhance. Thiamazole dose was gradually decreased afterwards and treatment was completely discontinued 1.5 months later. The patient remained asymptomatic thereafter.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [167.0, 'cm']}",63.22056,60.05953,66.38159,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 167.0 cm, which is 167.0 cm * 0.393701 in/cm = 65.74807 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.74807 (in inches) - 60) = 63.22056 kg.
Hence, the patient's IBW is 63.22056 kg."
3501,10,Ideal Body Weight,physical,decimal,pmc-4532033-1,Extracted,"A 44-year-old woman was admitted to our hospital for the evaluation of Cushing’s syndrome. She was diagnosed as hypertension at a local clinic in 1986 but recieved no antihypertensive medication. She developed headache, nausea and vomiting in Feb, 1990 and was admitted to the department of neurosurgery with diagnosis of Rt. cerebellar hemorrhage. After discharge, she has been followed for treatment of hypertension. During the follow-up period, she was found to have the Cushingoid features and transferred to the Department of Internal Medicine for the evaluation of Cushing’s syndrome.
The family and other past medical history were not contributory.
On admission, blood pressure was 150/110 mmHg, pulse rate 78/min, body temperature 36.5°C, respiration rate 18/min and height was 164cm and body weight was 77kg.
On physical examination, she was shown to have central obesity. Her face was round and plethoric. She had pink conjunctivae and white sclerae.
On auscultation of the chest, breathing sounds were normal and the heart sound was regular without murmur. On examination of the abdomen, she was found to have striae. Further examination revealed no abnormal finding.
Laboratory studies included hemoglobin 12.7g/dl, WBC 6700/mm3 with 75% neutrophils and 23% lymphocytes, platelet 261,000/mm3, total protein 7.2g/dl, albumin 4.2g/dl, total bilirubin 0.7mg/dl, direct bilirubin 0.3mg/dl, ALT 17unit, AST 19 unit, alkaline phosphatase 65U/L, BUN 20mg/dl and creatinine 1.1mg/dl. The concentrations of Na, K, CI and Ca were normal. FBS was 116mg/dl and HbA1c was 3.1%. Urinalysis was normal.
The results of low and high dose dexamethasone suppression test were shown in .
Chest PA and skull series revealed no abnormal findings.
By her history and physical examination, we suspect she had Cushing’s syndrome and then measured 24hr urine free cortisol and performed low dose dexamethasone suppression test. After this study, high dose dexamethasone suppression test was done to differentiate the etiology of Cushing’s syndrome. The levels of plasma cortisol were not suppressed and plasma ACTH level was very low. Abdominal CT scanning was done under the impression of adrenocortical tumor but revealed no abnormal mass in the adreanal gland first. Therefore we performed pituitary fossa MRI to rule out Cushing’s disease associated with micronodular adrenal hyperplasia. MRI reveals atrophic pituitary gland with empty sella. At that time, we didn’t decide the treatment modality for this patient because of poor general condition.
Instead, follow-up study was recommended. Follow-up abdominal CT scan, 3 years after the first study, revealed 2cm-sized hypodense mass in the upper pole of lt, adrenal gland (). So, explorative laparotomy was done under the impression of lt, adrenal adenoma. At operation field, no abnormal adrenal mass was found but the surgeon performed lt, adrenalectomy. The cut surface of surgical specimen showed multiple black pigmented nodules with pale atrophic cortex ().
On the microscopic finding, pigmented micronodular dysplasia with cortical atrophy was found (, ).
After operation, her blood pressure was normalized, and follow-up hormonal levels were also improved.
We concluded that her Cushing’s syndrome resulted from primary pigmented nodular adrenocortical disease and we plan the contralateral adrenalectomy.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [164.0, 'cm']}",56.00401,53.20381,58.80421,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 164.0 cm, which is 164.0 cm * 0.393701 in/cm = 64.56696 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.56696 (in inches) - 60) = 56.00401 kg.
Hence, the patient's IBW is 56.00401 kg."
3502,10,Ideal Body Weight,physical,decimal,pmc-5440537-1,Extracted,"An 18-year-old girl was referred to our department of pediatric nephrology due to elevated serum creatinine level. She was born premature and dysmature (gestational age 31 weeks + 5 days, birth weight 1210 g) to consanguineous parents. She had a good start but a very low blood glucose level directly after birth (0.2 mmol/L); this was corrected with an intravenous glucose infusion, and there was no further hypoglycemia in the neonatal period. She had mild bilateral eyelid ptosis from birth. Psychomotor development was normal. During childhood, she had a history of recurrent airway infections and bronchitis, mild failure to thrive, and mild anemia for which she visited a general pediatrician regularly. At age 4 years, routine serum creatinine measurements were 58 μmol/L, with an estimated glomerular filtration rate (eGFR) of 60 ml/min/1.73 m2. The lower than expected eGFR escaped the attention of the local pediatrician, and it was only at age 15 years, during routine testing, that a mildly elevated serum creatinine was noted for the first time (106 μmol/L, eGFR 53 ml/min/1.73 m2). At age 18 years, the serum creatinine level had increased to 139 μmol/L (eGFR 48 ml/min/1.73 m2), and she was referred to our university hospital for further examination. At that time, she reported exercise intolerance and lightheadedness on rising in the morning. Physical examination showed a height of 1.56 m (−2 standard deviations [SD]), a weight of 60 kg (+1SD), and a supine blood pressure of 106/55 mmHg; results were normal for heart, lungs, and abdomen examination, and, with the exception of the eyelid ptosis, for the neurological examination. Her symptoms and signs, especially the exercise intolerance and eyelid ptosis, raised the suspicion of a mitochondrial disorder. Laboratory investigations showed normal values for serum lactate and electrolytes (Na+ 140 mmol/L, K+ 4.4 mmol/L, Ca2+ 2.2 mmol/L, Mg2+ 0.75 mmol/L, P3− 1.33 mmol/L). There was no proteinuria nor hematuria. Kidney size and structure were normal on the renal ultrasound images. In order to obtain a diagnosis, we performed a renal biopsy. Light microscopic examination revealed a few vascular sclerosed glomeruli with only discrete interstitial fibrosis. Electron microscopic examination revealed notable abnormal, fused mitochondria in the proximal tubules but not in the distal tubules (Fig. ). This prompted the performance of a muscle biopsy for further evaluation of a mitochondrial defect. However, muscle histology was normal, and extensive biochemical testing of the respiratory chain also did not show any evidence of a mitochondrial disorder []. Mutation analysis of mitochondrial DNA was performed in leucocytes and muscle tissue, but did not show any abnormalities. At that time, current techniques, such as whole exome sequencing, were not yet available, and so the patient was managed further by our department without a classifying diagnosis. At age 19 years, she fainted while her height was being measured during a routine visit to the outpatient clinic. She reported that she was increasingly suffering from dizziness, especially in the morning. Orthostatic blood pressure measurements were performed, showing severe orthostatic hypotension with preserved heart rate increase. Her blood pressure decreased from supine values of 116/76 mmHg (heart rate 54 bpm) to 56/30 mmHg (heart rate 84 bpm) after standing for 3 min. Upon asking, she reported that sweating was normal.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.56, 'm']}",48.75993,46.32193,51.19793,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.56 m, which is 1.56 m * 39.3701 in/m = 61.41736 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.41736 (in inches) - 60) = 48.75993 kg.
Hence, the patient's IBW is 48.75993 kg."
3503,10,Ideal Body Weight,physical,decimal,pmc-8382267-1,Extracted,"We describe the case of a 42-year-old man (75 kg, 177 cm), American Society of Anesthesiologists (ASA) II for smoking (20 pack-years) as the only history. He presented to the emergency department due to headache and one episode of vomiting. Headache initially was relieved by simple analgesia which subsequently became resistant to therapy. CT angiography demonstrated right intraventricular haemorrhage without a clear source of bleeding. MRI found a stable right thalamic haematoma probably originating from a leaking arterial-venous malformation. A cerebral arteriography performed the next day concluded that the haematoma probably originated from a branch of the right posterior cerebral artery. The neurologically asymptomatic patient was scheduled for an elective embolisation of the arterial-venous malformation under general anaesthesia 1 week later. The patient was fasted for at least 6 hours before anaesthesia and received no premedication. Standard monitoring included a three-lead ECG, non-invasive blood pressure, end-tidal partial pressure of carbon dioxide and peripheral pulse oximetry. To monitor the depth of anaesthesia, we used the SedLine Brain Function Monitor (Masimo). The bilateral SedLine electroencephalogram (EEG) Sensor was installed on the patient’s front (). The front electrodes were not visible on the operator’s X-ray screen (, ) and did not disturb at any moment the operator during the procedure. The cable of the sensor was conducted posteriorly with respect to the patient’s head and kept out the field of the radiological image (). Anaesthesia was induced and maintained with a target-controlled infusion (TCI) of propofol (Orchestra Base Primea, Fresenius Kabi) using the pharmacokinetic model of Schnider et al. Analgesia was assured with intermittent boluses of sufentanil 0.2 µg/kg. The lungs were normoventilated (end-tidal partial pressure of carbon dioxide, 4.6–6.0 kPa) with 50% oxygen–air mixture. Neuromuscular block was induced with rocuronium bromide 0.6 mg/kg and maintained with intermittent boluses of 0.2–0.3 mg/kg to obtain a deep neuromuscular block (post tetanic count of 2) measured with acceleromyography on the patients left thumb (IntelliVue NMT Module, Philips). After intubation an invasive arterial line was placed in the right radial artery. We used the Patient State Index (PSI) of the SedLine Brain Function Monitor to titrate the depth of anaesthesia targeting a PSI between 25 and 50. Relatively low calculated doses of propofol were necessary to maintain a stable depth of anaesthesia, with calculated effect-site concentrations of about 2.6 µg/mL () and a PSI of about 27 (). The neuroradiological intervention was uneventful but was ended after 2 hours without embolisation of the arteriovenous malformation as no source vessel could be identified. The target-controlled perfusion of propofol was stopped (local time 13:30, total perfusion time 2 hours and 18 min, total propofol dose 1043 mg) and 2 min later (local time 13:32) the patient received sugammadex intravenously (4 mg/kg) to reverse deep neuromuscular block with a train of four count of 0 (post-tetanic count was not done before reversal). Very rapidly thereafter without any stimulation the patient aroused from anaesthesia (local time 13:33) (). The patient was extubated 4 min after the injection of sugammadex with a propofol effect site concentration of 2.0 µg/mL () and a train of four ratio of 100%. After extubation (13:37) the patient displayed eye opening but had difficulty responding to questions (). During stable anaesthesia, the raw EEG showed a very slow and depressed brain activity with zero EMG activity and spectral edge frequencies (the frequency below which 95 precent of the total electroencephalogram power is located) of around 10 Hz for both hemispheres and a PSI around 27. The event of immediate arousal from anaesthesia was followed by a very steep increase in the PSI index (up to 80 and more) with an EMG activity of 80% and a spectral edge frequency of about 17 Hz (). Spectrogram analysis showed a monotonous content in the delta range in the first part followed by a complex and increasing electrical brain activity. The white bars indicate background artefacts due to movement.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [177.0, 'cm']}",72.27568,68.6619,75.88946,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 177.0 cm, which is 177.0 cm * 0.393701 in/cm = 69.68508 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.68508 (in inches) - 60) = 72.27568 kg.
Hence, the patient's IBW is 72.27568 kg."
3504,10,Ideal Body Weight,physical,decimal,pmc-6250748-1,Extracted,"A 53-year-old male diagnosed with OI type I was referred to our clinic for extraction of the remaining maxillary teeth and evaluation for full arch immediate load hybrid prosthesis. His clinical history included osteogenesis type 1, bipolar disorder, alopecia, and hypothyroidism. The patient presented with normal stature, measuring 170.18 cm and weighing 81.65 kg with characteristic blue sclerae of OI type I (Fig. ). Throughout his life, he has had multiple orthopedic fractures due to his OI. At the time of surgery, he was on Lamictal, Xarelto, Synthroid, lisinopril, and hydrochlorothiazide.
Extraoral, TMJ, intraoral soft tissue, and lymph node examinations produced no abnormal findings. An examination of the dentition revealed the maxillary teeth were in poor repair with a fixed bridge extending from site number 2 to site number 5 with site number 3 serving as the pontic abutment. Sites number 8, number 9, number 10, and number 11 have periodontal involvement as well as recurrent decay. He was edentulous on the posterior left maxillary arch. His lower dentition consisted of sites number 19 through number 27 with number 28 being edentulous and number 29 having a root fracture (Fig. ). The upper jaw had good ridge width with reproducible centric relation and centric occlusion. The patient was otherwise healthy apart from medical issues directly related to his OI.
Due to his significant gag reflex, he was unable to wear a removable prosthesis. Lengthy conversations regarding implant therapy and implant options were reviewed as well as risks with his OI. Options presented included no treatment, placement of fixtures to support a removable prosthesis, placement of fixtures to support a fixed hybrid, and placement of axial implants for fixed denture prosthesis. He elected for a fixed denture prosthesis. Our patient was apprehensive towards having full edentulation and implant placement completed all at once and decided to have the implants placed in stages (Table ).
The patient underwent implant therapy in stages under general anesthesia with immediate load protocol. Intravenous access was obtained, and the patient was anesthetized under general anesthesia by our anesthesiologist. Carpules of 2% lidocaine with 1:100,000 epinephrine, 4% articaine hydrochloride with 1:100,000 epinephrine (Septocaine), and 0.5% bupivacaine hydrochloride with 1:200,000 epinephrine (Marcaine) were used as needed. For each site, a 15 blade was used to make a sulcular incision from the mesial to the distal aspect of the tooth. A full thickness mucoperiosteal flap was elevated with a periosteal elevator exposing the buccal alveolus. Buccal bone was removed using a surgical fissure bur to allow for osteotomes and elevators to atraumatically elevate and deliver the teeth, while preserving lingual, mesial, and distal walls. Next, a straight elevator was positioned between the alveolus and the root surface. The tooth was elevated, and the periodontal ligament was separated from the alveolus. The tooth was extracted using a no. 150 upper universal forcep. The socket was curetted and irrigated with copious amounts of normal saline solution. A bone file and rongeur were used to smoothen the alveolus.
To deliver implants, all bony walls were checked with a perio probe to verify the depth. A series of osteotomy burs were used at 1000 RPM and 50 Ncm of torque with copious sterile normal saline irrigation. At each step, angulation was checked. Once the final osteotomy was completed, the site was checked to verify that all bony walls were stable. A NobelActive implant was torqued into position at greater than 30 Ncm followed by placement of a cover screw. In instances where grafting was necessary, the graft material was positioned to obliterate the bony defect using a periosteal elevator and curette to place in the bony voids. The gingival tissues were repositioned using an Adson Tissue Forcep. A tension-free closure was attained with a periosteal release technique. The sites were closed with interrupted 3-0 gut sutures. All procedures were accomplished without any further complications.
The standard immediate loading procedures were followed as the patient met the guidelines of a minimum torque value of 35 Ncm. All fixtures placed had intraoperative open tray impressions taken. Impressions were sent to the laboratory, and fabrication of a screw-retained temporary was completed. Temporaries were placed within 24 h of surgery and were torqued at 15 Ncm. Following a 6-month period of functioning in temporary prostheses, final impressions were taken via open-tray technique. He was placed in his final prostheses with no complications. Our patient settled on final prostheses consisting of a four-unit bridge cemented at sites number 3 through number 6; individual crowns placed at sites number 7, number 8, number 9, number 10, and number 11; and a screw-retained, three-unit bridge placed at sites number 12 through number 14 (Figs. , , , , and ). The restorative dentist placed a polymethyl methacrylate (PMMA) prosthesis on the left side, and our patient will transition to his final crowns once he is financially ready.
Regular hygiene visits show that our OI patient has greatly improved his overall home care routine. No areas of gingival inflammation were found. Probing depths have remained 2–4 mm with no bleeding or purulent drainage at the fixtures sites. There have been no issues with implant mobility, and all healing post-operatively was uneventful.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.18, 'cm']}",66.10009,62.79509,69.40509,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.18 cm, which is 170.18 cm * 0.393701 in/cm = 67.00004 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.00004 (in inches) - 60) = 66.10009 kg.
Hence, the patient's IBW is 66.10009 kg."
3505,10,Ideal Body Weight,physical,decimal,pmc-6320575-1,Extracted,"A 14-year-old White Italian boy came to our Emergency Unit with a headache that had worsened over 20 days together with blurred vision and diplopia over the previous 10 days. His past history was negative for significant morbidities. He reported a recent episode of fever associated with cough, which coincided with the onset of headache. For this respiratory infection he had started taking levofloxacin 500 mg once a day one week before coming to our attention but had stopped taking it after three days due to worsening headache. This headache was initially associated with daytime somnolence, myalgia and arthralgia. The somnolence and arthralgia underwent rapid and spontaneous regression, with subsequent appearance of blurred vision.
The physical examination revealed an alert adolescent with weight of 66 kg (75th -90th percentile) [], height of 169 cm (50th–75th percentile) [] and body mass (BMI) of 23.1 kg/m2 (85th–95th percentile) []. The general examination was normal. The neurological examination was normal except for a right eye abduction deficit. Eye examination showed a normal visual acuity (10/10) in both eyes with normal colour vision and pupillary light responses, but a fundus examination revealed severe bilateral papilloedema with elevated disc, hyperaemia, blurred margins and vessel tortuosity in both eyes (Fig. a-b). Lancaster red-green test confirmed a right abducens nerve palsy, and campimetry showed a restricted visual field with external right muscle deficiency on the right side. Cranial neuroimaging (CT and MRI) showed a normal brain parenchyma with no evidence of hydrocephalus, mass, structural lesion, or abnormal meningeal enhancement. MRI neuroimaging showed oedema of both optic nerves with a tapered appearance of the right optic nerve. Venography was not performed, but an angio-MRI of the cerebral circulation was normal. Visual evoked cortical potentials were normal. A 24-h Ambulatory Blood Pressure Monitoring was negative.
Blood tests showed high M. pneumoniae IgM (15.00 AU/ml, normal range 0–9) and normal M. pneumoniae IgG levels (3.89 AU/ml, normal range 0–9) suggesting a recent infection, with normal white blood cell indices and negative C-reactive protein. Clarithromycin was then prescribed for 14 days without any adverse effects.
Serological screening for Coxsackie, Parvovirus, ECHO virus, Adenovirus, Cytomegalovirus (CMV), Epstein-Barr Virus (EBV), Herpes Simplex Virus 1 (HSV1), and Herpes Simplex Virus 2 (HSV2) excluded recent infections. Thyroid function was normal. Antinuclear antibodies (ANA), anti-double stranded DNA (dsDNA), ENA screening and rheumatoid factor were negative.
During hospitalisation we observed a complete and spontaneous regression of headache and an initial spontaneous reduction in diplopia within a few days. Oral prednisone 50 mg/day (0.75 mg/kg/day) was administered for a week and ocular fundus was monitored.
Since severe bilateral papilloedema persisted one week after the first assessment, lumbar puncture was performed with the patient sedated and relaxed in lateral recumbent position. Opening cerebrospinal fluid (CSF) pressure measured with a standard manometer was 20 cm H2O and closing pressure was 19 cm H2O. These CSF pressure values have traditionally been considered borderline, but are within normal range according to a recent study in children [].
CSF biochemical tests and cultures were negative. HSV1, HSV2, VZV, HHV6, CMV, Neisseria, Haemophilus, Streptococcus pneumoniae, Streptococcus B group, Escherichia coli, Listeria and Cryptococcus neoformans, Parvovirus, Adenovirus, EBV DNA and Enterovirus and Parechovirus RNA PCR were negative. CSF oligoclonal bands were absent on CSF and blood tests.
Oral acetazolamide (1 g divided twice daily) was introduced to accelerate recovery. A gradual further improvement in diplopia was seen during hospitalisation (Fig. a-b). Ophthalmological, neurological and neurosurgical follow up was continued after discharge. The patient gradually improved, with complete resolution of the right abducens nerve palsy in one month and resolution of papilloedema in three months (Figs. and ). For this reason, acetazolamide was gradually reduced and stopped on resolution of the papilloedema (see Additional file ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [169.0, 'cm']}",65.03158,61.78,68.28316,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 169.0 cm, which is 169.0 cm * 0.393701 in/cm = 66.53547 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.53547 (in inches) - 60) = 65.03158 kg.
Hence, the patient's IBW is 65.03158 kg."
3506,10,Ideal Body Weight,physical,decimal,pmc-7666458-1,Extracted,"A 67-year-old Japanese man with weight of 80 kg, height of 162.2 cm, and body mass index (BMI) of 30.4 kg/m2 was referred to our hospital for examination of a pulmonary mass in the left upper lobe. He had suffered from traumatic right rib fractures 6 weeks before the referral. Chest computed tomography (CT) on admission demonstrated a mass 32 mm in diameter in the anterior segment of the left lung (S3) (Fig. a) without obvious swelling of hilar or mediastinal lymph nodes. The CT also showed right 3rd–5th rib fractures, which were almost healed, but the fractured ends projected into the chest cavity (Fig. b). Bilateral lung fields showed no emphysema or bullae. Fluorine-18-fluorodeoxyglucose positron emission tomography/CT demonstrated uptakes in the tumor of the left upper lobe and the site of the rib fractures (Fig. c), and no uptake was found in hilar or mediastinal lymph nodes. The clinical stage of the patient was judged to be cT2aN0M0 (stage 1B). He had no specific comorbidities except for obesity and no smoking history. The mass in his left lung was diagnosed as adenocarcinoma by transbronchial biopsy. Preoperative pulmonary function test showed a mild obstructive ventilatory impairment with a forced vital capacity (FVC) of 2.67 L (80% of predicted), a forced expiratory volume in one second (FEV1) of 1.84 L (68.0% of predicted), and 68.9% of FEV1/FVC.
After the induction of general anesthesia, a right-sided 37-French double-lumen endotracheal tube (DLT, BronchoCath®, Mallinckrodt Medical, Ireland) was inserted. The position of the DLT was adjusted using bronchofiberscopy. The patient received volume-controlled ventilation appropriated for the physique. The tidal volume during OLV was set to 200 mL, and the peak inspiratory pressure with this tidal volume was about 35 cmH2O. The patient was placed in the right decubitus position and underwent left upper lobectomy under three-port VATS. Approximately 2 hours after the start of the surgery and during the closure of the wound, the patient’s blood pressure suddenly decreased to 50 mmHg. The arterial oxygen saturation of pulse oximetry (SpO2) and heart rate remained stable. The blood pressure improved immediately after the intravenous injection of phenylephrine. After placing a chest drain tube in the surgical side, a few minutes after the transient hypotension, OLV was switched to two-lung ventilation as usual. The operation was completed with the operation time of 137 minutes. The patient was rotated to the supine position, and portable chest x-ray photography was performed in the operation room, which revealed a right-sided tension pneumothorax (Fig. ). The DLT was located in the proper position. Immediately, a chest drain tube was inserted into the right chest cavity. A little air leak was observed through the right-sided drain tube, which fortunately stopped spontaneously by the next day. The right-sided drain tube was removed on day 1 and the left-sided tube on day 2 after surgery. He left the hospital on the 8th postoperative day.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [162.2, 'cm']}",58.87409,55.93039,61.81779,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 162.2 cm, which is 162.2 cm * 0.393701 in/cm = 63.8583 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (63.8583 (in inches) - 60) = 58.87409 kg.
Hence, the patient's IBW is 58.87409 kg."
3507,10,Ideal Body Weight,physical,decimal,pmc-6966219-1,Extracted,"A 16-year-old boy was referred for endoscopy due to severe IDA and recurrent hematochezia. He was noted to have mild intellectual disability at the level of elementary school but denied diarrhea, constipation, weight loss, or growth restriction. He initially denied hematochezia but later explained that he defecated feces stained with fresh blood 2 to 3 times a month for several years. His mother recalled that the patient had hematochezia at age 6 which led him to be misdiagnosed with hemorrhoids. The patient did not receive regular health care but visited the clinic for cellulitis treatment upon the diagnosis of IDA.
The patient had a height of 177.5 cm and a weight of 76.1 kg. His vital signs were stable and abdominal examinations were unremarkable. Vascular engorgement was observed around the anus but no fissures were seen. A blood test showed a white blood cell count of 4,590/mm3, a hemoglobin level of 5.9 g/dL, a hematocrit of 23.2%, and a platelet count of 305,000/mm3. Mean corpuscular volume was determined to be 64.4 fL while ferritin level was at 3 ng/mL; these findings were suggestive of IDA. All other laboratory parameters were unremarkable.
Abdominal computed tomography (CT) showed a huge, dilated aberrant vein that drained both the splenic and left internal iliac veins (). This vein had developed most tortuously around the rectum. Congested small vessels around the rectum merged into the superior and middle rectal veins and drained into the left internal iliac vein. Additionally, the rectal mucosa showed prominent enhancement with associated thickening of the rectal walls. There was no evidence of arteriovenous malformations or fistulas. Doppler ultrasound of the liver demonstrated intact portal venous flow.
Colonoscopy was performed due to the suspicion of rectal varices based on the history and CT scan results. Colonoscopy showed numerous rectal polyps emerging up to 10 cm from the anus. Stalked or sessile polyps of various sizes were observed on the entire lumen of the rectum with some normal intervening mucosa. A few protruding vessels were identified. The polyp mucosa was covered with yellow-white fibrinous exudates and tortuous, dilated, superficial blood vessels were noted on their tips (). The entire colon and terminal ileum, except the rectum, were unremarkable. Biopsy specimens obtained from the tip of a polyp revealed diffused lymphocytic infiltration, crypt dilatation, mucinous infiltration of the crypt, and surface ulcerations (). These findings confirmed the cause of bleeding to be secondary to multiple rectal polyps.
Although the hugely dilated aberrant vein in the abdomen was considered a venous malformation, other abnormal findings were also noted in the systematic physical examination including subtle hypertrophy of the right upper extremity and light red-colored port wine stains on the trunk and the lateral aspect of the lower extremities (). Additionally, no prominent difference was observed in the thickness of the lower extremities despite macrodactyly on the right second toe. Taken together, the characteristic port wine stains, right upper extremity hypertrophy, and abdominal venous malformation meet the classic triad of KTS. Hence, KTS was diagnosed.
Various kinds of interventions, including radiologic and surgical treatment, were considered for the treatment of the abnormal abdominal vascularity found in this patient. However, his parents opted to postpone aggressive treatment, and he was therefore prescribed oral iron supplementation. The patient continues to have intermittent hematochezia but his hemoglobin level is maintained at 15.5 mg/dL with intermittent oral iron supplementation.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [177.5, 'cm']}",72.72844,69.09202,76.36486,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 177.5 cm, which is 177.5 cm * 0.393701 in/cm = 69.88193 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.88193 (in inches) - 60) = 72.72844 kg.
Hence, the patient's IBW is 72.72844 kg."
3508,10,Ideal Body Weight,physical,decimal,pmc-8077549-1,Extracted,"A 31-year-old man was seen in neuro-ophthalmology consultation for double vision and suspected internuclear ophthalmoplegia. He had a past medical history of chronic intermittent diarrhea starting 3 years prior to presentation. Following extensive investigations including multiple colonoscopies, his condition was diagnosed as irritable bowel syndrome and medically managed with cholestyramine and diphenoxylate/atropine daily. One year prior to presentation, he developed abdominal pain and leucocytosis for which he underwent a laparotomy for small bowel obstruction. The distal small bowel and cecum were resected, whereby the procedure revealed chronic ruptured appendicitis without any evidence of inflammatory bowel disease. A few months later, he underwent right nephrectomy due to possible congenital atrophic right kidney, discovered during the investigation of recurrent UTIs for a year. As a child, he had a normal developmental history and academic performance.
One year prior to presentation, he developed intermittent horizontal binocular diplopia that was present in all directions of gaze and had increased in duration 6 months prior. He saw an ophthalmologist who noted bilateral limitation of adduction of each eye and suspected internuclear ophthalmoplegia. He therefore underwent MRI of the brain, which was initially reported to represent advanced multiple sclerosis but after later review was interpreted as a diffuse leukoencephalopathy, as shown in Figure . A neuro-ophthalmology consultation was then requested to clarify the etiology of his double vision.
At the neuro-ophthalmology consultation, he appeared cachexic and weighed 46 kg and was 177 cm tall (BMI 14.7 kg/m2). He reported no family history of neurological or oculomotor syndromes except a grandfather with Parkinson disease. He had normal afferent visual function with a visual acuity of 20/20 in each eye and normal Humphrey visual field testing. Dilated fundus examination was normal. External examination revealed bilateral ptosis with recruitment of the frontalis muscles. There was a large exotropia of 40 prism diopters (PD) in the primary position. The exotropia was fairly comitant, measuring 35 PD in both left and right gaze. He had diffuse limitation of extraocular movements, as shown in Figure . Neurological examination revealed diffuse muscle atrophy, particularly in the proximal upper and lower limbs with relative sparing of his distal leg, forearm, and hand muscles. There was moderate weakness (4/5 on the Medical Research Council scale) in proximal upper and lower limb muscles, with normal distal strength. He had reduced vibration sensation at the big toes, which normalized by the ankle. Joint position sense was normal and sensation to pinprick was normal throughout. Nerve conduction studies and electromyography demonstrated a mixture of a diffuse predominantly axonal, but mixed axonal and demyelinating, sensory-motor peripheral neuropathy, along with evidence of a proximal myopathy (small motor unit potentials with early recruitment in proximal muscles).
He saw his gastrointestinal specialist and additional bloodwork including those measuring vitamin levels was performed. He was found to be anemic with a hemoglobin of 129 g/L (normal 140–180 g/L) and deficient in magnesium at 0.40 mmol/L (normal 0.70–1.10 mmol/L), calcium at 2.13 mmol/L (normal 2.20–2.62 mmol/L), 25-hydroxy vitamin D at 14 nmol/L (normal 25–200 nmol/L), and vitamin B12 at 212 pmol/L (normal 222–652 pmol/L). His parathyroid hormone levels were elevated at 9.9 pmol/L (normal 1.3–7.6 pmol/L), while his albumin was normal at 42 g/L. He continued supportive treatment and vitamin supplementation to correct these deficiencies. Diphenoxylate/atropine was discontinued due to low energy and fatigue, and he was started on loperamide 2 mg as needed up to twice daily.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [177.0, 'cm']}",72.27568,68.6619,75.88946,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 177.0 cm, which is 177.0 cm * 0.393701 in/cm = 69.68508 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.68508 (in inches) - 60) = 72.27568 kg.
Hence, the patient's IBW is 72.27568 kg."
3509,10,Ideal Body Weight,physical,decimal,usmle-525,Extracted,"A 54-year-old woman comes to the physician because she has not had her menstrual period for the last 5 months. Menarche occurred at the age of 11 years, and menses occurred at regular 28-day intervals until they became irregular at 30- to 45-day intervals with light flow 2 years ago. She does not have vaginal dryness or decreased libido. She had four successful pregnancies and breastfed all her children until the age of 2 years. There is no personal or family history of serious illness. Except when she was pregnant, she has smoked one pack of cigarettes daily for 30 years. She does not drink alcohol. She is 167 cm (5 ft 5 in) tall and weighs 92 kg (203 lb); BMI is 33 kg/m2. Her vital signs are within normal limits. Physical examination shows no abnormalities.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [167.0, 'cm']}",58.72056,55.78453,61.65659,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 167.0 cm, which is 167.0 cm * 0.393701 in/cm = 65.74807 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (65.74807 (in inches) - 60) = 58.72056 kg.
Hence, the patient's IBW is 58.72056 kg."
3510,10,Ideal Body Weight,physical,decimal,pmc-8102657-1,Extracted,"The patient was an 84-year-old man with a height of 176 cm and a body weight of 80 kg who was scheduled for minimally invasive posterior spine fusion (T9–L3) for the treatment of a lumbar compression fracture. He had a history of hypertension, atrial fibrillation, and chronic kidney disease and was taking amlodipine and apixaban (5 mg twice daily). Preoperative serum examination indicated moderate loss of kidney function, which was confirmed by a serum creatinine level of 1.05 mg/dL and an estimated glomerular filtration rate of 52 mL/min/1.73 m2. Preoperative coagulation tests indicated prolonged values for both APTT and PT-international normalized ratio (40.1 s and 1.7, respectively). Although temporary interruption of apixaban is commonly recommended for the perioperative period (usually 48–72 h before surgical procedures, such as spine surgery, with high bleeding risk) [], the patient continued apixaban until the night before surgery, according to the instruction of his cardiologist.
We considered it necessary to evaluate the residual anti-Xa effect of apixaban for the estimation of perioperative bleeding and potential need for transfusion; therefore, we implemented the use of ClotPro in combination with the conventional blood tests performed at our hospital’s central laboratory. ClotPro uses RVV as the reagent to activate coagulation. Because RVV specifically cleaves factor X to Xa, clotting time (CT) is prolonged by anti-Xa drugs, such as apixaban, in a dose-dependent manner [, ]. We examined blood cell count, PT, APTT, and plasma fibrinogen level at four time points: after anesthesia induction, at the end of surgery, on postoperative day (POD) 1, and on POD 6. We simultaneously performed the ClotPro assay, an ecarin chromogenic assay (ECA), to detect the effect of direct thrombin inhibitors such as dabigatran [], and a fibrinogen concentration assay. Blood samples for outsourced chromogenic anti-Xa assay were collected at the same time points.
Anesthesia was induced with propofol and rocuronium, and was maintained with desflurane and continuous infusion of remifentanil. The results of coagulation tests after anesthesia induction indicated delayed thrombin production (Table ) (Fig. ). All members of the surgical team recognized the residual effects of apixaban, and we prepared fresh frozen plasma for excessive bleeding. Fortunately, the volume of bleeding was 440 mL, and we did not perform a transfusion. Considering the balance of the risk of postoperative bleeding and the result of the RVV test on the morning of POD 1, which was in the normal range, we resumed apixaban at a decreased dose of 2.5 mg twice daily on POD 1. The CT for the RVV test on POD 6 was prolonged to 93 s, which was shorter than the preoperative value (167 s) (Table ). Although the patient had minor subconjunctival hemorrhaging after the resumption of apixaban, he was discharged without major bleeding or thrombotic complications.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [176.0, 'cm']}",71.37017,67.80166,74.93868,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 176.0 cm, which is 176.0 cm * 0.393701 in/cm = 69.29138 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.29138 (in inches) - 60) = 71.37017 kg.
Hence, the patient's IBW is 71.37017 kg."
3511,10,Ideal Body Weight,physical,decimal,pmc-2966711-1,Extracted,"A 70-year-old woman (height: 156 cm, body weight: 48 kg) with lower abdominal pain was admitted and associated symptoms were fever, nausea, vomiting and diaphoresis which started from the day previous to her admission. On abdominal computed tomography (CT), right ovarian cyst in size of 2.5 cm was found, and an acute appendicitis was diagnosed by an abdominal ultrasonography. An elective operation was scheduled under the collaboration of gynecology and general surgery.
In the patient's past medical history, she had taken digoxin, dilatrend, nitrate, telmisartan, and thiazide for 5 years because of hypertension, congestive heart failure, AF, and right coronary artery 90% stenosis on coronary angiography. An electrocardiogram before operation showed AF with ventricular response 90-100 times/min, left ventricular hypertrophy. Cardiomegaly and pleural effusion were found on chest X-ray. On transthoracic echocardiography (TTE), ejection fraction was 55% and left atrial enlargement, right atrial enlargement and eccentric hypertrophy with decreased mobility of the inferior wall of the left ventricle were shown. A moderate aortic valve insufficiency, aortic valve sclerosis, mild aortic stenosis, and severe posterior mitral valve leaflet calcification were also found and the width of mitral valve measured by pressure half-time was 1.92 cm2. A chronic cerebral infarction in the right posterior cerebral artery was found on brain CT with symptoms of dysarthria. Signs of dehydration on physical examinations with prerenal azotemia of FeNa 0.1% and serum creatinine of 1.7 mg/dl on blood test led us to start an fluid therapy. The serum creatinine was decreased to 1.3 mg/dl after the fluid therapy.
Glycopyrrolate 0.2 mg IM was premedicated at 30 minutes pre-operation. The patient's blood pressure (BP) was 130/50 mmHg, ventricular response 90-100 times/min, and arterial oxygen saturation 97% when she arrived at the operation room. A right radial artery was cannulated with great caution before the induction of anesthesia. The induction of anesthesia was initiated with injecting 2 ml of 2% lidocaine to reduce injection pain and propofol (Diprivan® AstraZeneca, UK) and remifentanil (Ultiva® GlaxoSmithKline, UK) were injected using a target-controlled infuser (Orchestra® Fresenius Vial, France). After confirming the patient's being unconscious, rocuronium 40 mg was injected and then endotracheal intubation was performed with close monitoring of arterial blood pressure. Ventilation with 100% O2 was given while central venous catheterization was placed in right jugular vein. After the induction of anesthesia, the patient's vital sign showed no hemodynamic disorder with systolic BP 130-150 mmHg, diastolic BP 40-60 mmHg, ventricular response approximately 100-110 times/min, and central venous pressure (CVP) 8-9 mmHg. The effect site concentration was injected as 2.5-3.0 µg/ml of propofol and and 2.0 ng/ml of remifentanil.
After the lower abdomen laparotomy at obstetrics and gynecology for the right ovary cystectomy, a small bowel infarction from jejunum to ileum was detected. The authors suspected a mesenteric arterial embolism based on the patient's previous medical history. A transesophageal echocardiology (SonoSite MicroMaxx, Bothell, USA) probe was immediately inserted and a spontaneous echo contrast (SEC or ""smoke"") in the left atrium (LA) and a 13 × 18 mm size thrombus in the LAA was detected (). The findings in TEE made a mesenteric arterial embolism highly suspicious for the cause of the small bowel infarction. A segmental resection and intestinal anastomosis were performed by the department of general surgery. No hemodynamic instability was observed through whole procedure of operation and the patient was transferred to the intensive care unit with endotracheal tube inserted. After confirming her awareness and the absence of any neurologic disorder, extubation was performed in intensive care unit. To minimize the risk of hemorrhage of the anastomosis site, anticoagulation was performed with caution under the collaboration of general surgery and cardiology. It was started with low molecular weight heparin 3 days after the operation and oral warfarin was added 5 days after the operation. After 4 weeks, cardioversion was successfully performed to turn into normal sinus rhythm.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [156.0, 'cm']}",48.75993,46.32193,51.19793,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 156.0 cm, which is 156.0 cm * 0.393701 in/cm = 61.41736 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.41736 (in inches) - 60) = 48.75993 kg.
Hence, the patient's IBW is 48.75993 kg."
3512,10,Ideal Body Weight,physical,decimal,pmc-6814111-1,Extracted,"A 40-year-old Japanese man experienced periumbilical pain since November 2013, and although the symptoms were mild, they were prolonged. He visited his family physician in January 2014, who noted mild tenderness in the lower left quadrant. The patient underwent an abdominal CT scan. CT revealed a low-density mass that measured 43 × 40 mm in size in the left abdomen. He was referred to the National Hospital Organization Tsuruga Medical Center in February. His past medical and family histories were unremarkable. On examination, the patient had a height of 179.0 cm, a body weight of 98.7 kg, and a body mass index (BMI) of 30.8 and did not present with anemia, icterus, edema, or malnutrition. His abdomen was flat and soft, with mild tenderness in the lower left quadrant on palpation; however, the mass could not be felt.
The laboratory results showed no abnormalities in his blood cell counts; however, an elevation in the serum alanine transaminase (ALT; 60 IU/L), γ-glutamyl transferase (γ-GTP; 108 IU/L), total bilirubin (T-Bil; 1.31 mg/dL), and total cholesterol (T-Chol; 229 mg/dL) levels was observed. The levels of epithelial tumor markers, such as carcinoembryonic antigen (CEA; 2.1 ng/mL), carbohydrate antigen 19-9 (CA19-9; 8.7 U/mL), and cancer antigen 125 (CA125; 11 U/mL), were within normal limits.
The patient underwent a contrast-enhanced CT examination 2 weeks after the CT examination conducted by his family physician because in the previous examination, the patient had not been administered a contrast agent. A low-density mass with an irregular outline and measuring 45 × 42 mm in size was detected in the left abdomen at the slightly cranial level of his umbilicus in the plain phase (Fig. ). The tumor was located in the peripheral part of the mesentery of the jejunum and partly compressed the adjacent jejunum. In the enhanced phase, the tumor lacked contrast. The peripheral artery was shown to be involved, indicating that the tumor developed in the mesentery of the jejunum; however, the adjacent jejunum showed good enhancement (Fig. ). The oral side of the jejunum did not show dilatation. A lymphatic cyst diagnosis was highly suspected.
The patient’s abdominal symptom passed without exacerbation, and a follow-up examination was conducted in March. One month later, he underwent a scheduled CT examination, and the mass did not appear to have increased in size (Fig. a). Enhancement revealed apparent invasion of the wall of the jejunum without ischemia of the adjacent jejunum or dilatation of the oral side of the bowel (Fig. b). Magnetic resonance imaging (MRI) showed intermediate intensity on T1-weighted imaging (T1WI) (Fig. ) and high intensity on T2-weighted imaging (T2WI) (Fig. ). Relatively low intensity was observed with enhancement using gadolinium diethylenetriaminepentaacetic acid (DTPA) contrast medium on T1WI (Fig. ). An accumulation of cystic lesions with a variety of sizes was clearly depicted on the coronal view on T2WI (Fig. ).
Because it was expected that depiction of the tumor would be made somewhat more difficult by its location and the body shape of the patient, we conducted a sonography examination in reference to the location and properties of the tumor determined by CT and MRI. The lesion showed a low echo; however, a clear image was not obtained.
CT performed by the previous physician and at our institution showed that the tumor was located in the peripheral part of the jejunal mesentery and exhibited slight enteric compression without dilatation of the oral jejunum but no rapid increase in size. The patient hesitated to agree to an immediate operation but did agree to a 1-month observation period. Permeation of the jejunal wall was shown by a second CT examination at our institution performed 1 month later, and from these findings, we highly suspected that the lymphangioma was invading the jejunal wall and thus decided to perform surgery.
We made a preoperative diagnosis of lymphangioma invading the jejunal wall, and with the patient’s informed consent, we performed an operation to relieve his symptoms and obtain a definitive diagnosis of the tumor in April.
The patient was placed in the supine position under general anesthesia. Small incisions were made along the superior and inferior border of the umbilicus and connected through the bottom of the umbilicus with an S-shape. The length of the wound was approximately 5 cm. We placed the Lapprotector™ (Model FF0707; Hakko Co., Ltd., Medical Device Division, Japan) in the umbilical wound and then attached the E·Z Access™ device (E·Z Access for FF07; Hakko Co., Ltd., Medical Device Division, Japan). A 12-mm trocar was placed through the E·Z Access device, and pneumoperitoneum was established with carbon dioxide (CO2) gas at 8 mmHg of pressure. An accessory trocar (5 mm) was placed on the right side of the 12-mm trocar through the E·Z Access device. Using forceps, we removed the omentum from the small intestinal front and found a soft yellowish mass in the mesentery of the jejunum that had invaded the wall of the jejunum (Fig. ). We removed the tumor from the body through the umbilical wound, resected the surrounding mesentery and part of the jejunum, and performed anastomosis in a functional end-to-end manner (Fig. ). The total operative duration was 94 min, and the intraoperative blood loss volume was 30 ml.
Macroscopically, the external surface of the mass had a whitish-yellowish and lobulated appearance. The tumor protruded from both sides of the mesentery leaves and was surrounded by the mesenteric peritoneum. The tumor measured 50 × 45 mm in size and was located in the peripheral part of the mesentery and adjacent to the jejunum (Fig. ). The small intestinal mucosal surface formed a hemispherical uplift approximately 24 × 20 mm in size adjacent to the mesenteric lesion without contraction (Fig. ). The cut surface of the mass after fixation by formalin revealed multicystic lesions of various sizes containing a café-au-lait-colored milky fluid similar to chyle (Fig. ). Histologically, the cyst wall showed an attenuated endothelial lining, surrounding rich adipose tissue and scattered smooth muscle fibers (Fig. ). In addition, small lymphoid aggregates also appeared focally. Immunohistochemical staining showed that the flat endothelial cells associated with the cysts were positive for the endothelial markers CD31 (Fig. ) and factor VIII-related antigen (Fig. ), partially positive for the lymphatic endothelial marker D2-40 (Fig. ) and the undifferentiated pluripotent stem cell marker CD34 (Fig. ), and negative for cytokeratin (AE1/AE3) (Fig. ) and the mesothelial marker calretinin (Fig. ). Dilated lymphatic ducts were observed in the tumorous lesion of the mesentery and adjacent to this lesion in the muscularis propria and submucosal layer of the small intestine. In the wall of the jejunum without tumor invasion, dilation of the lymphatic ducts was not observed. These findings were consistent with cystic lymphangioma.
The patient recovered successfully and was discharged from the hospital 9 days after the operation.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [179.0, 'cm']}",74.0867,70.38236,77.79103,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 179.0 cm, which is 179.0 cm * 0.393701 in/cm = 70.47248 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.47248 (in inches) - 60) = 74.0867 kg.
Hence, the patient's IBW is 74.0867 kg."
3513,10,Ideal Body Weight,physical,decimal,pmc-7642533-1,Extracted,"An 81-year-old Japanese man was referred to our hospital due to progressive gait disturbance and appetite loss.
His medical history included partial resection due to brain tumor, four times, starting when he was 74 years old, and 50-Gray radiation therapy when he was 77 years old, at another hospital. In addition, he was phlebotomized three times due to polycythemia vera when he was 81 years old, and was diagnosed with Alzheimer’s disease. He was given 90 mg of phenobarbital, 500 mg of hydroxycarbamide, and 5 mg of donepezil on a regular basis. He had no history of smoking or drinking alcohol, and no history of exposure to asbestos. He did not undergo regular medical exams. The patient was unemployed, and had no food or drug allergies. However, he needed full assistance for everyday life activities. He presented no family history of malignant disease.
The patient was 158 cm tall and weighed 52 kg. His vital signs were abnormal, with blood pressure of 94/77 mmHg, heart rate of 80 regular beats/min, body temperature of 36 °C, oxygen saturation of 97% in ambient air, and respiratory rate of 16/min; his glasgow coma scale score was 15 (E4V5M6) points. He complained of right hemiparesis, and manual muscle testing for the right half of the body had a grade of 2. On the other hand, nothing else abnormal was detected upon physical examination, including skin or neurological findings.
Routine laboratory examination revealed increased values of white blood cells, red blood cells, hemoglobin, hematocrit, aspartate transaminase, alanine aminotransferase, lactate dehydrogenase, alkaline phosphatase, gamma-glutamyl transpeptidase, C-reactive protein, and plasma glucose, and decreased values of creatine phosphokinase, creatinine, and sodium. However, other values were normal, including complete blood count, biochemistry, and tumor marker for diagnosing lung cancer (Table ).
An unenhanced head computed tomography (CT) scan revealed an 8 cm × 5.1 cm × 6.5 cm mixed-density mass at the left frontal lobe, accompanying a midline shift (Figure ). An unenhanced chest-abdomen CT scan revealed a 6 cm × 4.1 cm × 6.5 cm low-density mass in the left chest wall at the superior segment, namely S6 (Figure ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [158.0, 'cm']}",55.07095,52.3174,57.8245,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.20476 (in inches) - 60) = 55.07095 kg.
Hence, the patient's IBW is 55.07095 kg."
3514,10,Ideal Body Weight,physical,decimal,pmc-4173354-1,Extracted,"A morbidly obese 80-year-old female [weight 102.1 kg, height 157.5 cm, body mass index (BMI) of 41] presented with mouth pain, and multiple carious teeth were scheduled for teeth extraction with an alveoplasty. She had a past medical history of Cerebrovascular accident (CVA), transient ischemic attack (TIA), congestive heart failure (CHF), hypertension, and myocardial infarction (MI). Electrocardiogram (ECG) showed first-degree heart block, prolonged QT interval with anterolateral infarct. Echocardiograph (ECHO) showed an ejection fraction of 45–50%, left atrial enlargement, mild pulmonary hypertension, and trace mitral regurgitation.
Preoperative airway assessment revealed a Mallampati score of IV, three finger breadth mouth opening, slight limitation of neck movement, and loose carious teeth. With this assessment, the patient was predicted to be difficult to intubate. The anesthetic plan included management of the predicted difficult intubation with the GlideScope® with other usual backup planes for difficult intubation.
Anesthesia was induced with fentanyl 150 µg, lidocaine 100 mg, propofol 150 mg and succinylcholine 100 mg.
The GlideScope® blade tip was placed in the vallecula and the vocal cords and epiglottis were seen. A size 7 endotracheal tube (ETT) was mounted in the GlideRite® rigid stylet and then passed into the oral cavity for intubation. The endotracheal tube (ETT appeared to slide into the oropharynx with relative ease and the endotracheal tube was placed into the trachea. The stylet was removed, and positive EtCO2 and equal bilateral breath sounds was confirmed. A successful GlideScope® intubation was assumed.
As the surgeon began the procedure, he noticed that ETT had pierced and entered the tissue of the retromolar trigonum (the same space which holds the lingual nerve), and then proceeded to pass through the oropharyngeal space and re-enter the vocal cords [Figure and ].
We decided to remove ETT rather than cutting the tissues to free it, to avoid trauma to lingual nerve. We re-inserted another size 7 ETT with the aid of the GlideScope® camera. Positive EtCO2 and equal bilateral breath sounds was confirmed. Surgery was completed uneventfully; however, the surgeon stated multiple times that the patient's oral mucosa was very fragile and easily torn. The patient was easily extubated and transported to post anesthesia care unit (PACU). Both intubations were performed by the student registered nurse anesthetist (SRNA).
PACU staff was instructed to look for signs of lingual nerve injury (numbness in the tongue, loss of ability to taste, tingling sensation in the tongue, pain, burning, or electric shock sensations in the tongue, speech impairment and drooling).
The PACU stay was uneventful, the patient denied any of the above mentioned symptoms, and was discharged.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [157.5, 'cm']}",50.11819,47.61228,52.6241,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 157.5 cm, which is 157.5 cm * 0.393701 in/cm = 62.00791 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.00791 (in inches) - 60) = 50.11819 kg.
Hence, the patient's IBW is 50.11819 kg."
3515,10,Ideal Body Weight,physical,decimal,pmc-5366765-1,Extracted,"A 14-year-old boy was referred by his General Practitioner with history of abdominal pain and rash on his back for 12 months. The rash was treated with multiple topical agents including antifungal, antibiotic, and steroid ointments with no improvement. There was no history of loss of appetite, loose stools, diarrhoea, or bloating. He had no significant past medical history or medical problems within the family. He was weaned to solids without any difficulties and had no known food allergies.
On examination, he had a maculopapular and urticarial rash on his back and knees. The rest of his examination was normal.
Investigations including FBC, LFT, U&E, ESR, CRP, anti-tTG, IgA, IgG, and IgM all were normal, but anti-endomysial antibody was weakly positive.
Upper GI endoscopy showed normal oesophagus, mild antral erythema (negative CLO test), and normal mucosa in the duodenum. Partial villous atrophy with crypt lengthening and increasing intraepithelial lymphocytes was seen on histology. A diagnosis of seronegative CD was made. Quick mucosal lactase test was mildly suggestive of lactose intolerance.
The patient noticed a significant improvement in his rash within 12 days of starting gluten-free diet (GFD). He continued to improve on a GFD and when seen in the follow-up clinic a year later reported complete resolution of symptoms. His weight improved from 66.5 kg to 75 kg and height improved from 179.3 cm to 183.6 cm. Repeat investigations including anti-tTG antibody were normal. As there was improvement in his clinical symptoms, height, and weight, we did repeat endoscopy or do HLA-DQ2 and HLA-DQ8 investigations.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [183.6, 'cm']}",78.25205,74.33945,82.16465,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 183.6 cm, which is 183.6 cm * 0.393701 in/cm = 72.2835 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (72.2835 (in inches) - 60) = 78.25205 kg.
Hence, the patient's IBW is 78.25205 kg."
3516,10,Ideal Body Weight,physical,decimal,pmc-8718172-1,Extracted,"A 37-year-old woman had experienced galactorrhea, menstrual disorders, and headache for several years. In addition, she had undergone infertility treatment in the Department of Obstetrics and Gynecology since about 1 year before. It is well known that thyroid dysfunction could influence fertility, thyroid function was checked several times, thyroid ultrasonography was performed, and there was no abnormality in such examinations for a couple of years. However, hyperthyroidism was detected once, and the patient was referred to our institution. The data in our institution were as follows: FT3, 4.90 pg/mL; FT4, 2.06 ng/dL; TSH, 2.06 μIU/mL. Since FT3 and FT4 levels were high but TSH levels were not suppressed, she was suspected of having SITSH and was hospitalized in our institution for further examination.
On admission, his height, body weight, and body mass index were 167.3 cm, 63.4 kg, and 22.6 kg/m2, respectively. Blood pressure, heart rate, and body temperature were 120/68 mm Hg, 52 beats/min, and 36.2°C, respectively. The data on admission were as follows: FT3, 4.62 pg/mL; FT4, 1.86 ng/dL; TSH, 2.55 μIU/mL. Although both FT3 and FT4 levels were high, TSH levels were not suppressed, which was compatible with TSHoma. Thyroid autoimmune antibodies were all negative: antithyroid peroxidase antibody, 9.9 IU/mL; antithyroglobulin antibody, <10.0 IU/mL; thyrotropin receptor antibody, 1.0 IU/L; TSH antibody, 106%. PRL showed a normal upper limit (18.6 ng/mL), and LH and FSH were both lower than the reference range: LH, 1.8 mIU/mL; FSH, 2.8 mIU/mL. Growth hormone (GH) and insulin-like growth factor-1 levels were within normal ranges. Peripheral blood and electrolyte levels were within the normal range. Liver and renal function, diabetes, and lipid markers were all within normal ranges.
In addition, in brain contrast-enhanced magnetic resonance imaging (MRI), nodular lesions were detected in the pituitary gland with a diameter of approximately 10 mm (Fig. A). In the dynamic study, the nodule lesion was slightly contrasted, but the contrast effect was weaker than that of the adjacent pituitary gland (Fig. B). On thyroid ultrasonography, there was no abnormality: no swelling of the thyroid, no increase in blood flow, and no neoplastic lesion in the thyroid. In the thyrotropin-releasing hormone (TRH) load test with 0.5 mg of TRH, TSH did not increase and subsequently FT3 and FT4 levels did not increase, which was compatible with TSHoma (Fig. ). In contrast, PRL increased normally upon TRH stimulation. In the corticotrophin-releasing hormone load test with 100 μg of corticotrophin-releasing hormone, both adrenocorticotropic hormone and cortisol levels increased normally. In the luteinizing hormone-releasing hormone load test with 0.1 mg), both LH and FSH levels increased normally. In the growth hormone-releasing factor load test with 100 μg of growth hormone-releasing factor, the GH level increased normally. In octreotide load test with 100 μg of octreotide, TSH level was suppressed (Fig. ), and FT3 and FT4 levels were both suppressed 12 hours after octreotide load as follows: FT3, from 4.62 pg/mL to 3.74 pg/mL; FT4, from 1.65 ng/mL to 1.50 ng/mL.
In addition, it is important to perform a differential diagnosis of TSHoma and RTH in patients with SITSH. In the case of TSHoma, imaging is positive, and the TSH response is absent in the TRH load test. In this subject, in brain contrast-enhanced MRI, nodular lesions were clearly detected in the pituitary gland (Fig. ), and TSH levels were not increased at all in the TRH load test (Fig. ). In addition, while TSH secretion is usually suppressed in the octreotide load test in subjects with TSHoma, TSH secretion was clearly suppressed by octreotide in this subject. Furthermore, while subjects with RTH often have a family history, this subject did not have a family history. Based on these findings, we ruled out the possibility of RTH and finally diagnosed this subject as SITSH due to TSHoma.
After the final diagnosis, a Hardy operation was performed. The dissected pituitary adenoma was yellow in color, and its size was 10 mm × 10 mm × 12 mm. Hematoxylin and eosin staining of the resected pituitary adenoma revealed solid proliferation of chromophobe cells (Fig. A). In TSH staining, many TSH-producing cells were observed in the resected pituitary adenoma (Fig. B). These findings further confirmed the diagnosis of SITSH. About 2 months after the operation, TSH, FT3, and FT4 levels were decreased as follows: TSH, 0.47 μIU/mL; FT3, 2.64 pg/mL; FT4, 0.71 ng/dL. After the operation, she did not need any anterior pituitary hormone replacement, although slight pituitary hypothyroidism was transiently observed, as described above. Approximately 3 months after the operation, she became pregnant without any difficulty. She was 38 years old at that time, and therefore, she had some risk due to relatively late maternity. Nonetheless, she finally gave birth safely without any difficulty, and her baby's body weight was 3060 g. In addition, in follow-up brain contrast-enhanced MRI taken about 1 year later, there was no abnormality in the pituitary gland; there were no findings indicating the occurrence of TSHoma.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [167.3, 'cm']}",58.99221,56.0426,61.94182,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 167.3 cm, which is 167.3 cm * 0.393701 in/cm = 65.86618 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (65.86618 (in inches) - 60) = 58.99221 kg.
Hence, the patient's IBW is 58.99221 kg."
3517,10,Ideal Body Weight,physical,decimal,pmc-4352433-1,Extracted,"A 25-year-old female office worker visited the clinic of the Center for Kampo Medicine in Keio University Hospital. She suffered from severe menstrual pain since she was 20 years old and it turned to be worse when she started to work in the company. Also severe constipation started around that time. On the time of her visit, her bowel movement was once in 5 days. After she began to work, she was annoyed by acne and abdominal distension after meals. Physical examination revealed that she was 160 cm in height and 50 kg in weight; her body mass index was 19.5, blood pressure was 106/59 mmHg, and pulse was regular and at 63 per minute. Complexion and skin were normal. There were no abnormal findings on blood and urine analysis. Gynecological examination revealed no abnormal findings such as endometriosis. Tongue inspection revealed swelling of the sublingual vein. Abdominal strength was slightly strong; there were resistance in the hypochondrium and abdominal distention. We diagnosed the patient with excess heat, qi stagnation, and blood stasis pattern and prescribed 7.5 g of daisaikoto per day. Her constipation improved in 2 weeks. Twelve weeks later, she reported that her menstrual pain disappeared. Since then she has been free from a menstrual pain with daisaikoto.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3518,10,Ideal Body Weight,physical,decimal,usmle-9892,Extracted,"A 55-year-old woman seeks evaluation of difficult and incomplete voiding and spontaneous urine leakage that occurs continuously during the day and night. The symptoms are not associated with physical exertion. She denies any urethral or vaginal discharge. She is menopausal and does not take hormone replacement therapy. At 33 years of age, she had a right salpingectomy as treatment for an ectopic pregnancy. She has a 2-year history of a major depressive disorder and takes amitriptyline (100 mg before the bedtime). She was also diagnosed 5 years ago with arterial hypertension, which is controlled with enalapril (20 mg daily) and metoprolol (50 mg daily). The weight is 71 kg (156.5 lb) and the height is 155 cm (5 ft). The vital signs are as follows: blood pressure 135/80 mm Hg, heart rate 67/min, respiratory rate 13/min, and temperature 36.4℃ (97.5℉). The physical examination is significant for a palpable urinary bladder. The neurologic examination is within normal limits. The gynecologic examination shows grade 1 uterine prolapse.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3519,10,Ideal Body Weight,physical,decimal,pmc-7204778-1,Extracted,"A 55-year-old man with a previous surgical history of distal gastrectomy with antecolic Roux-en Y reconstruction performed 3 years previously for gastric cancer (tub2, T1, N0, M0, pStage IA) presented with a rapidly growing intraabdominal mass that had developed during the postoperative course. The patient had not undergone adjuvant chemotherapy and had no medical or surgical history other than that of gastric cancer.
On admission, his height was 167 cm, weight was 49 kg, blood pressure was 118/73 mm Hg, heart rate was 67 beats/min, and body temperature was 36.6°C. The abdomen was soft and flat with a midline incision scar. A mobile, elastic, hard mass was palpable on the left side of the abdomen. His complete blood count and serum chemistry results were normal, and all of the examined tumor markers (carbohydrate antigen 19-9, carcinoembryonic antigen, α-fetoprotein, neuron-specific enolase, cytokeratin 19 fragment, and soluble interleukin-2 receptor) were within their normal limits.
Abdominal contrast-enhanced computed tomography (CT) initially detected a newly appearing small mass measuring 14 mm, neighboring the Roux-en-Y limb anastomosis without invasion into the small bowel 22 months previously (although this was confirmed only via retrospective observation). The mass had increased in size from 33 mm (6 months before) to 82 mm at the time of the operation (Fig. ). On the preoperative CT, the tumor was 82 × 75 mm in size, and it appeared to originate from the mesentery of the small intestine. We determined the most likely differential diagnosis of gastrointestinal stromal tumor and lymph node recurrence of the gastric cancer, and DF was not included in the list. 18F-2-fluoro-2-deoxyglucose positron emission tomography (PET) revealed a heterogeneously enhanced uptake on the lesion (SUVmax = 4.40) in the lower abdomen. The mobility of the tumor from the previous CTs also supported the origin of the mesentery. Apart from this, there were no significant findings that indicated metastasis or any other lesions (Fig. ). Biopsy was considered because chemotherapy, not surgery, may be needed in case of recurrence of the gastric cancer. However, this strategy was abandoned owing to the lack of a suitable route for a percutaneous or endoscopy-assisted approach.
Overall, we suspected that a malignant lesion was located in the mesentery near the Roux-en-Y limb that was responsible for its rapid growth. There was no other lesion elsewhere; therefore, we decided to perform resection for both diagnosis and treatment.
Laparotomy showed that the tumor was located in the mesentery of the small intestine near the Roux-en-Y limb. The feeding vessels for the Roux-en-Y limb anastomotic site were partly involved by the tumor; therefore, the anastomotic site was resected en bloc with the tumor, and the whole Roux-en-Y limb was reconstructed with functional end-to-end anastomosis using a linear stapler. No intraperitoneal dissemination or distant metastasis was observed during the surgery.
Macroscopically, the resected specimen was a 10 × 9 × 8 cm-sized solid lesion with no necrosis or bleeding (Fig. ). No exposure to the mucosa of the adjacent small intestine was observed, indicating its origin in the mesentery. Histopathological findings revealed that the tumor was located in the mesentery of the small intestine, and spindle-shaped cells resembling fibroblasts or myofibroblasts proliferated sparsely with intervening collagen fibers. Invasive proliferation into the surrounding fat tissue was observed in the marginal area of the tumor (Fig. ). The immunohistochemistry results were negative for desmin, α-smooth muscle actin, CD34, and c-kit. Moreover, positivity for the nuclear accumulation of β-catenin was observed (Fig. ). In accordance with our findings, DF of the mesentery was diagnosed.
The postoperative course was uneventful, and the patient was discharged on postoperative day 13. At the time of writing of this report, the patient was free from recurrence with no adjuvant treatment and was being carefully followed up with CT.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [167.0, 'cm']}",63.22056,60.05953,66.38159,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 167.0 cm, which is 167.0 cm * 0.393701 in/cm = 65.74807 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.74807 (in inches) - 60) = 63.22056 kg.
Hence, the patient's IBW is 63.22056 kg."
3520,10,Ideal Body Weight,physical,decimal,pmc-6502161-1,Extracted,"A 27-year-old married man with TDT, while travelling abroad complained low back pain requiring a hospital treatment with subcutaneous morphine and blood transfusions (2 units of packed red blood cells) because of a severe anemia. After hospital discharge, the patient came back immediately home, but due to the back pain recurrence he was referred to our hospital. He did not have a history of a similar complaint in the past and no personal or family history of bleeding disorders. There was no history of fall or trauma, fever or abdominal pain, motor or sensory complaints. He referred an intact bowel and bladder functions.
The clinical examination, two days after the symptoms appearance, was remarkable only for positive straight leg raising test on right side and hepatosplenomegaly. He was discharged after pain management with a plan to do MRI of spine in our outpatient department. Due to worsening of his back pain, which radiated to right groin, and the “aspect” of right thigh, he returned to the hospital after a few hours. On admission, his weight was 56 kg, height 161 cm, vital signs were stable, but he was in severe pain, lying in bed with the right leg flexed. Physical examination revealed that he had tender fullness over the right iliac crest region compared to the left side. Tenderness was also noted on right upper gluteal area. Passive motion of the hip aggravated his pain, but there were no focal neurological deficits.
Initial laboratory tests showed were significant for white blood cells (WBC) count: 2.4x10^3/uL (reference range: 4-10^3/μL), platelets count (Plt): 110x10^3/uL (reference range: 150-400x10^3/μL), hemoglonin (Hb): 6.5 g/dL (reference range: 13-17 g/dL), International Normalised Ratio (INR): 1.5 (normal range for a healthy person 0.8-1.2), activated partial thromboplastin time (aPTT): 41 seconds (reference range: 9.4-12.5 sec), D Dimer: 0.98 mg/L fibrinogen-equivalent units (FEU) (reference range: 0-0.49 mg/L), fibrinogen: 5.3 g/L (reference range: 2-4.1g/L). Clotting factor assay showed a reduced level of factor VII: 25% (reference range: 50 to 150), and biochemistry was significant for indirect hyperbilirubinemia and mildly increase of aspartate aminotransferase (AST): 45 U/L (reference range: 0-34 U/L). No endocrine complications were documented.
He was regularly transfused with red blood cell concentrate and on treatment with deferasirox (35 mg/kg per day). His last serum ferritin level was 3.247 ng/mL (normal levels: 23-175 ng/mL) An extremely high liver iron content (LIC) measured, five months before, by FerriScan® () was found: 39.9 mg/g dry liver. Four classes of LIC have been reported in thalassemic patients: Class 1=normal LIC <3 mg Fe/g dry liver, Class 2=mild overload LIC 3-7 mg Fe/g dry liver, Class 3=moderate LIC overload 7-15 mg Fe/g dry liver, and Class 4=severe LIC overload ≥15 mg Fe/g dry liver ().
Magnetic resonance imaging (MRI) showed a hematoma in the right iliopsoas muscle extending to the upper thigh. The calculated size of the lesion in all imaging modalities was approximately 12x5x2.5 cm ().
He was managed conservatively with transfusion of red blood cell concentrate, analgesics, vitamin K, steroids, bed rest and physiotherapy. He showed a good response to treatment and was discharged home 11 days later. A new MRI, performed 7 months later, showed a complete resolution of the iliopsoashematoma ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [161.0, 'cm']}",57.78748,54.89811,60.67685,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 161.0 cm, which is 161.0 cm * 0.393701 in/cm = 63.38586 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (63.38586 (in inches) - 60) = 57.78748 kg.
Hence, the patient's IBW is 57.78748 kg."
3521,10,Ideal Body Weight,physical,decimal,pmc-8645136-1,Extracted,"A 14-year-old boy with no specific medical or family history was referred to our institute in order to identify the origin of his fever. 2 months before admission, he had a small amount of intermittent hematochezia (once or twice a day at most) attached to soft stools. Furthermore, he suffered from remittent fever of around 39 °C and malaise followed by diarrhea and appetite loss 3 weeks before admission. Thus, he visited his family physician and was referred to our institute for further investigation. However, he developed chronic chest pain before the outpatient follow-up (1 week before admission). Transthoracic echocardiography and thoracoabdominal contrast-enhanced CT showed a pericardial effusion. Because the pericardial effusion continued to increase, he was admitted to our institute for detailed examination and treatment of the underlying disease.
At the time of admission, his height and weight were 170 cm (70th percentile) and 47.2 kg (20th percentile, 0.8 kg less than 2 months before admission), respectively. Body temperature, blood pressure, heart rate, respiratory rate, and oxygen saturation on room air were 37.1 °C, 116/61 mmHg, 110 beats/minute, 14 breaths/minute, and 97%, respectively. On physical examination, he had a mildly pale complexion and eyelid conjunctiva, diminished heart sounds, anterior chest pain relieved by bending forward, and mild tenderness in the lower mid-abdomen. The patient’s laboratory findings are summarized in Table . No remarkable abnormalities were found on urinalysis. An electrocardiogram showed decreased T wave amplitude in V1 to V3, which may be a finding of low potentials due to a pericardial effusion and myocarditis. On chest X-ray, the cardiothoracic ratio increased from 41.0% to 55.0% in the week before admission (Fig. a). Transthoracic echocardiography showed an echo-free space of 30 mm from the apex to the pericardium on the left ventricular axial view, indicating a pericardial effusion (Fig. b). In addition, anomalous motion of the ventricular septum was also confirmed, and the diameter of the inferior vena cava was 22 mm, with no respiratory variability. After admission, a sudden drop of blood pressure to 85/70 mmHg with tachycardia (132 beats/minute) appeared on the second day. Emergent pericardiocentesis was performed to prevent hemodynamic collapse; 500 mL of bloody pericardial fluid were aspirated by the puncture (Fig. c). His blood pressure recovered rapidly to 115/65 mmHg. The heart rate also decreased to 80 beats/minute immediately after the puncture. Thus, after the procedure, he was finally diagnosed as having cardiac tamponade. The aspirated fluid was an exudative pericardial fluid, and no malignant cells were found on cytological examination. No mediastinal tumor was identified on chest contrast-enhanced MRI, but contrast delay along the pericardium was observed, which was consistent with the pericarditis (Fig. d). Whole-body gallium scintigraphy also showed no abnormal accumulation. After pericardiocentesis, the inflammatory response decreased mildly, but the hematochezia persisted. To clarify the etiology, esophagogastroduodenoscopy (EGD) and colonoscopy (CS) were performed. EGD showed no macroscopic or histological abnormalities. In contrast, CS showed multiple irregular-shaped aphthae on the contralateral side of the mesenteric attachments from the right transverse colon to the cecum (Fig. a). No abnormalities were observed on small intestinal capsule endoscopy. Mucosal biopsy at the ascending colon and cecum showed nonspecific inflammatory cell infiltration into the submucosa and some granulomatous findings with prominent neutrophilic infiltration adjacent to blood vessels (Fig. b). Head MRI showed nasal and sinus mucosal thickening and a cystic mass in the left sphenoid sinus (Additional file : Fig. S1). No abnormalities were found on renal biopsy. No genetic variants of monogenic inflammatory bowel diseases were detected on whole-exome sequencing of a peripheral blood specimen. GPA was diagnosed based on the American College of Rheumatology criteria, and the 2012 Revised International Chapel Hill Consensus Conference on the Nomenclature of Systemic Vasculitis [] and the Endorsed Consensus Criteria for the Classification of Childhood Vasculitides of the European League Against Rheumatism (EULAR)/Paediatric Rheumatology European Society (PRES) [], the EULAR/Paediatric Rheumatology International Trials Organisation (PRINTO)/PRES proposed validated classification criteria [], and the algorithm of the European Medicines Agency (EMEA) [].
After diagnosis, treatment with intravenous prednisolone (PSL) (40 mg/day) and azathioprine (AZA) (100 mg/day) was started on the 21st day of hospitalization, and negative fecal occult blood was confirmed on the 29th day. The patient was discharged on the 36th day, and PR3-ANCA converted to negative during outpatient treatment. However, the PR3-ANCA level increased again, the fecal occult blood test became positive, and micro occult blood and protein were found on urinalysis immediately after PSL tapering was completed. Oral PSL was resumed, and methotrexate (MTX) (12 mg/week) was started after the recurrence. Currently, he has no apparent clinical symptoms, and PR3-ANCA has remained around 3.0 IU/mL with the combination therapy of AZA and MTX.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3522,10,Ideal Body Weight,physical,decimal,pmc-8513168-1,Extracted,"A 67-year-old man with type 2 diabetes mellitus presented to our hospital with an elevated white blood cell (WBC) count (38,900/μL) and eosinophil count (13,600/μL). He had no allergies or showed signs of infection. Malignancy was suspected, and some tumor markers were examined on the same day, including carcinoembryonic antigen (CEA), carbohydrate antigen 19–9 (CA19–9), neuron-specific enolase (NSE), progastrin-releasing peptide (ProGRP), squamous cell carcinoma (SCC), cytokeratin fragment (CYFRA), sialyl Lewis X-i antigen (SLX), and soluble interleukin-2 receptor (sIL-2R). sIL-2R concentration was remarkably elevated at 3421 IU/mL. To identify the cause of these hematologic abnormalities, chest computed tomography (CT) was performed, which revealed small nodes on both sides of the lungs and enlargement of the left hilar and right subclavian lymph nodes. Lung cancer metastasis to the bone marrow was suspected; thus, bronchoscopic biopsy and bone marrow biopsy were performed.
Four weeks later, he noticed weakness on both sides of his arms. He could not walk and speak well on the next day. Subsequently, he was admitted to our hospital at 2 days after the appearance of the first symptoms. On admission, the patient was 167 cm tall, and his body weight was 53.3 kg. On examination, his blood pressure was 126/72 mmHg, his pulse was 79 beats per minute and regular, and his temperature was 36.9 °C. His consciousness level was E4V4M6 on the Glasgow Coma Scale. Impaired attention and visuospatial cognition, simultanagnosia, and oculomotor apraxia were observed []. He presented with dysarthria and mild limb weakness. Barré and Mingazzini signs were positive bilaterally. Deep tendon reflexes were accelerated on both sides of the upper and lower limbs, and Babinski’s sign was also positive. It was not possible to assess sensory, proprioceptive, joint, or vibration changes.
Peripheral blood examinations revealed leukocytosis with HE. His WBC count was elevated to 71,500/μL and eosinophil count was 36,465/μL, accounting for 51.0% of WBC. Finding for other inflammatory markers including anti-nuclear antibody, myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA), proteinase 3-ANCA (PR3-ANCA), anti-cardiolipin antibody, and lupus anticoagulant were negative. D-dimer level was 1.2 μg/mL. Antithrombin III activity, prothrombin time-international normalized ratio (PT-INR), activated partial thromboplastin time (APTT), and protein C and protein S activities were normal. Hemoglobin A1c (HbA1c) level was 8.4%. Findings related to tumor makers were as follows: the sIL-2R level was 4212 IU/mL and the levels of other tumor makers (NSE, CYFRA, SLX) were slightly elevated. Brain natriuretic peptide (BNP) level was slightly elevated at 47.5 pg/mL.
Magnetic resonance imaging (MRI) of the brain showed multiple acute small infarcts in the bilateral cortex, watershed area of the middle cerebral artery, and cerebellar hemispheres (Fig. a-d). Some of them showed hemorrhagic infarction. Magnetic resonance angiography (MRA) of the head and neck showed normal cerebral vasculature. Ultrasound examination of the carotid arteries indicated no stenosis or low echoic plaques. Holter electrocardiography did not detect any arrhythmia. Transthoracic echocardiography showed partial thickening of the left ventricular wall. The left ventricular ejection fraction was 68%, and no valvular abnormality was revealed.
On admission day, 2 days had already passed after the appearance of the first symptoms of infarction, and we could not carry out acute reperfusion therapy. Treatment was initiated with 50 mg/day of prednisolone for HE and 5000 units/day of unfractionated heparin for acute cerebral infarction (Fig. ). We gradually increased the heparin dose to 8000 units/day to avoid APTT overextension. His eosinophil count slightly decreased, and simultanagnosia and oculomotor apraxia disappeared. Follow-up MRI of the brain on day 15 of admission showed no increase in infarcts; however, microbleeds in the infarcts were increased (Fig. e). We changed heparin to aspirin in consideration of hemorrhage.
On day 22 of admission, the pre-admission bronchoscopic biopsies revealed eosinophilic infiltration of the bronchial epithelium and infiltration of cancer cells, eosinophils, and neutrophils into the bone marrow. Immunostaining of a bone marrow sample revealed the following pattern suggestive of lung adenocarcinoma: cytokeratin 7(+), cytokeratin 20(−), and thyroid transcription factor-1(+) (Fig. ). He was diagnosed with clinical stage IVb lung adenocarcinoma.
We considered that the cerebral infarctions were caused by HE induced by lung cancer metastasis to the bone marrow. As warfarin is not appropriate for drug interaction, we then continued treatment with aspirin. On day 30, chemotherapy with pemetrexed for adenocarcinoma was initiated. We subsequently discovered that the elevation in D-dimer level was associated with deep vein thrombosis; hence, we changed the antithrombotic drug to warfarin. Despite chemotherapy and steroid therapy, the number of eosinophils did not decrease. Therefore, we tapered and then stopped the use of prednisolone.
After the first round of chemotherapy, his WBC and eosinophil counts continued to increase, and his blood results indicated disseminated intravascular coagulation (DIC). His general condition deteriorated, and he died on day 57.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [167.0, 'cm']}",63.22056,60.05953,66.38159,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 167.0 cm, which is 167.0 cm * 0.393701 in/cm = 65.74807 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.74807 (in inches) - 60) = 63.22056 kg.
Hence, the patient's IBW is 63.22056 kg."
3523,10,Ideal Body Weight,physical,decimal,pmc-4107697-1,Extracted,"A 39 year old man was referred to Royan Institute cytogenetic laboratory suffering from infertility. He was born from a full term natural delivery with no apparent complication. The age of his mother at this pregnancy was 35 and his father was 40. The parents were unrelated. Family history of infertility was negative and his only brother fathered a child. On examination he was 180 cm, 82 kg. Each testis volume was 4 ml estimated by Prader’s orchidometer (normal range: 15-25 ml), with normal vas deferens. He had a history of right sided epididymo-orchitis. Stature growth was regular and puberty was normal without testosterone therapy. Motor and mental development of the patient was normal. There were no malformations, no gynecomastia, no diabetes and no reduced muscle strength. Olfaction was normal. The semen analysis showed total azoospermia with low volume (0.3 ml) and normal pH and fructose level. No spermatozoa were found in micro dissection TESE (MD-TESE) and the seminiferous tubules were hyalinized. Histology of testis biopsy specimen showed only Sertoli cells and moderate hyperplasia of the leydig cells. Endocrinological laboratory studies revealed elevated follicle stimulating hormone (FSH=43 mIU/ml, reference 0.9-8.9 mIU/ml) and luteinizing hormone (LH=14.3 mIU/ml, reference 0.8-10 mIU/ml) levels and low testosterone levels (1.4 ng/ml). The results were suggestive for hypergonadotropic hypogonadism and KS was the most probable diagnosis.
Chromosomal analysis was performed on phytohemagglutinin-stimulated peripheral lymphocyte cultures using standard cytogenetic methods. Two different cultures for the sample prepared and two different series of slides from each culture analyzed separately. Half of slides were investigated by GTG and the other half by FISH. 170 GTG banded metaphases from the patient were analyzed at the resolution of 550 bands.
The hybridization on metaphase chromosomes was performed according to standard cytogenetic protocols (). A triple-colour FISH with centromeric DNA probes for chromosomes X (CEP X SpectrumOrange) and telomeric DNA Probes for chromosomes Y telomer (Yq1.2-Satellite III SpectrumGreen, Direct Labeled Fluorescent DNA Probe Kit, Vysis, Abbott Molecular, USA) was used to determine the sex chromosome constitution of metaphase lymphocytes. Centromeric DNA probes for chromosomes 18 (CEP 18 SpectrumAqua) were used as control for binding efficiency (). 50 metaphase nuclei and 80 cells in interphase were scored by FISH and subsequent results are briefly given in table 1.
Accordingly, the karyotype of the case was ascertained as: 47,XXY[251]/46,XX[10]/45, X[10]/48,XXXY[7]/46,XY[22] according to The International System for Human Cytogenetic Nomenclature ISCN 2009 (). Molecular analysis showed no microdeletions in the Y chromosome.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [180.0, 'cm']}",74.99221,71.2426,78.74182,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 180.0 cm, which is 180.0 cm * 0.393701 in/cm = 70.86618 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.86618 (in inches) - 60) = 74.99221 kg.
Hence, the patient's IBW is 74.99221 kg."
3524,10,Ideal Body Weight,physical,decimal,pmc-5852298-1,Extracted,"A 62-year-old male was referred to the outpatient clinic of Kani Tono Hospital for a fever lasting seven days and suspected pneumonia. He had no medical, medication, or family history. The patient was a current cigarette smoker (40 cigarettes per day) and a habitual drinker consuming 42–84 g of ethanol per day. His occupation was a welder, presumably exposed to metallic dust. His vital signs at admission were as follows: body temperature, 37.8 °C; pulse rate, 120 bpm; blood pressure, 138/81 mmHg; and SpO2, 83% in room air. Physical examination showed a dry cough, dyspnea, tachypnea, and no pretibial edema. Bilateral wheezing was auscultated. Laboratory data showed a white blood cell count of 10,600 cells/μL (neutrophils, 86%; lymphocytes, 5%; monocytes, 10%; eosinophils, 0%; basophils, 0%); hemoglobin (Hb), 15.0 g/dL; HbA1c, 5.5%; platelets, 154,000/μL; and C-reactive protein, 22.39 mg/dL. Hepatic and renal functions were within normal limits. Tests were negative for human immunodeficiency virus, hepatitis B virus, and hepatitis C virus. Arterial blood gases were pH, 7.459; pO2, 53.4 mmHg; pCO2, 40.6 mmHg; HCO3-, 28.4 mEq/L; base excess, 4.6 mEq/L; lactate, 18.0 mg/dL; and blood glucose, 147 mg/dL. Chest radiography showed a slight infiltrative shadow (A). Thoracic computed tomography (CT) showed non-specific findings, such as thickened bronchial walls (B), slightly increased bronchial density, and mild emphysematous changes. The patient was immediately hospitalized (Day 0), suspected of an acute COPD exacerbation. Treatment started with the following drugs: 6-methylprednisolone, 40 mg ×2; ceftriaxone, 2 g; garenoxacin, 400 mg; and salmeterol xinafoate/fluticasone propionate.
On Day + 2, his respiratory status became severely dyspneic, and his arterial blood gases were pH, 7.25; pO2, 82.5 mmHg; pCO2, 78.0 mmHg; and HCO3-, 33.0 mEq/L. Noninvasive positive-pressure ventilation was performed, alternatively with an oxygen mask.
Invasive positive-pressure ventilation with tracheal intubation was started on Day + 3 due to exacerbated respiratory failure. However, effective oxygenation was not achieved because decreased pulmonary compliance and increased airway resistance made efficient ventilation difficult. Arterial blood gases were pH, 7.08; pO2, 70.9 mmHg; pCO2, 116 mmHg; and HCO3-, 32.7 mEq/L. The patient also developed heart and renal failure (BNP, 1543.5 pg/mL; BUN, 53.7 mg/dL; and creatinine, 2.92 mg/dL).
On Day + 4, a chest radiograph showed a clear infiltrative shadow (C). His platelet count was reduced to 88,000/μL, with D-dimer concentrations being elevated to 77.9 μg/mL. The overall data represented systemic inflammatory response syndrome with coagulative disorder. A filamentous fungus was isolated from the sputum collected on Day + 2. His serum (1,3)-β-D-glucan level was elevated to 530.7 pg/mL. Preemptive antifungal treatment was initiated at 70 mg of caspofungin acetate intravenously. However, therapeutic interventions did not improve the multiple organ failure, and the patient died on Day + 4. Three days later (Day + 7), the isolated fungus was identified as Aspergillus fumigatus based on colony morphology.
An autopsy was performed three hours after the patient's death (Day + 4). The body height was 160 cm, and the weight was 50 kg. The most remarkable findings were confined to the lungs. Grossly, both lungs were swollen and profusely consolidated. From the main bronchus to the peripheral branches, most bronchi were surrounded and occluded by necrotic ocher membranous lesions (D). A diffuse pulmonary hemorrhage was also observed. Histologically, the lung specimens revealed abundant Aspergillus proliferation in the bronchi, with severe necrosis and exudative inflammation (A). The microscopic bronchial lesions corresponded to the macroscopic ocher membranous lesions (D). Aspergillus also invaded the alveolar areas. These areas were severely damaged, showing neutrophil infiltration, hemorrhaging, and edema (B). Grocott's methenamine silver staining clearly showed invasive mycelial fungal growth (C) as well as conidial heads (D). Angioinvasion was also demonstrated, with the affected vessels being obliterated by thrombi (E). Based on the sputum culture and these histological findings, IPA was diagnosed. Apart from invasive aspergillosis, alveolar emphysematous changes were focal and mild (F). Iron deposition inside the alveolar macrophages (hemosiderin-laden macrophages) was remarkable (G), a finding likely associated with the patient's job as a welder. Systemic examination showed no disseminated infection elsewhere. Notably, no predisposing cavity was found that would provoke a fungal colonization. No hepatic or pancreatic lesions from alcohol consumption were observed. Passive congestion and hyperemia were observed in several organs, including the liver, kidneys, and alimentary tract.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [160.0, 'cm']}",56.88197,54.03787,59.72607,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.99216 (in inches) - 60) = 56.88197 kg.
Hence, the patient's IBW is 56.88197 kg."
3525,10,Ideal Body Weight,physical,decimal,pmc-7083393-1,Extracted,"A 54-year-old Caucasian woman presented with symptoms of chest tightness, palpitations, and non-sustained ventricular tachycardia (VT). Her past medical history was significant for supraventricular tachycardia; she took no prescription medications and lived in an area with high prevalence of tick-borne illnesses. Cardiovascular family history included heart failure (mother) and supraventricular tachycardia (daughter). Her physical examination was notable for clear lungs and no jugular venous distension, gallops, or murmurs. Vitals included a heart rate of 68 beats per minute, blood pressure of 100/60 mmHg, height of 64 inches, and weight of 62.5 kg. Her admission electrocardiogram showed biventricular bigeminy and Q waves in leads V1 and V2. Her labs were normal except for B-type natriuretic peptide of 237 pg/mL (reference range < 100 pg/mL) and troponin I 0.16 ng/mL (reference range < 0.08 ng/mL). Transthoracic echocardiogram demonstrated normal biventricular function, mild mitral regurgitation, mild pulmonary hypertension, and an estimated left ventricular ejection fraction (LVEF) of 60%. Coronary angiography revealed no coronary disease, and she was discharged on metoprolol, lisinopril, and mexiletine.
She was admitted three times the following year for VT with persistently elevated troponin levels (0.12–0.42 ng/mL). Her LVEF had declined to 30–35%, and a dual chamber implantable cardioverter-defibrillator was implanted. Cardiac magnetic resonance imaging found subepicardial hyper-enhancement along the mid-anterior wall of the left ventricle compatible with myocarditis and LVEF of 32.8% (Figure
). Her metoprolol was increased on discharge.
She was referred to an academic medical center for endomyocardial biopsy, which showed inflammatory findings thought to be most consistent with Lyme carditis, staining for amyloid was unrevealing (Figure
). Serologies for Lyme disease were negative. Treatment consisted of doxycycline, corticosteroid taper, and mycophenolate mofetil. A depiction of pharmacological therapy received during the patient's course is summarized in Figure . She had gradual improvement in LVEF that correlated with corticosteroid treatment and declined when corticosteroids were stopped. Despite treatment, her clinical status declined with recurrent heart failure admissions requiring inotropes, inability to tolerate evidence-based medical therapy, worsening LVEF, and recurrent VT, leading to consideration of advanced heart failure therapies.
Two years after initial presentation, a HeartMate II LVAD (Thoratec, Pleasanton, CA) was implanted as a bridge to transplant. Left ventricular apex core biopsy demonstrated a focal chronic lymphocytic infiltrate notable for multiple multinucleated cells and absence of granulomas, consistent with GCM (Figure ). Additionally, staining for mycobacteria, atypical mycobacteria, bacteria, and fungi was negative. After LVAD implantation, she restarted mycophenolate mofetil for approximately 1 year, transitioned to azathioprine for a few days, and then antimetabolites were withdrawn because of leukopenia. Time to transplant was prolonged because of the presence of high levels of preformed antibodies. She received antibody reduction therapy with rituximab and intravenous immunoglobulin 4 months following LVAD implant; plasma exchange was added 4 months later because of persistently high levels of preformed antibodies. During this time, she experienced an improvement in symptoms and left ventricular function; however, she was unable to tolerate a trial wean of LVAD support to 8400 rpm, with a VO2 max of 10 mL/kg/min and peak respiratory exchange ratio of 1.3. More aggressive immunosuppression regimens targeting GCM were ultimately not pursued because of infection risk.
A suitable donor with negative prospective crossmatch became available, and she underwent an OHT at age 60. Her induction immunosuppression included three doses of rabbit anti-thymocyte globulin, methylprednisolone 1 g followed by 250 mg every 8 h for six doses, and mycophenolate 1 g intraoperatively followed by 1 g twice/day. Maintenance immunosuppression included tacrolimus, prednisone, and mycophenolate. She is now 4 years post-transplant, doing well without cellular or antibody-mediated rejection or evidence of recurrent GCM.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [64.0, 'in']}",54.7,51.965,57.435,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 64.0 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.0 (in inches) - 60) = 54.7 kg.
Hence, the patient's IBW is 54.7 kg."
3526,10,Ideal Body Weight,physical,decimal,pmc-6069313-1,Extracted,"A 46-year-old woman (height – 160 cm, weight – 60 kg) underwent cytoreductive surgery for carcinoma of the left ovary under combined epidural and general anesthesia. Her past medical history was unremarkable, and her preoperative investigations including coagulation profile were within normal limits. Before induction of general anesthesia, an epidural catheter was inserted uneventfully at T7–T8 intervertebral level using 16G Tuohy needle. Epidural space was identified using loss of resistance to saline, with no blood seen through epidural needle and the catheter. Postoperative analgesia was provided with continuous epidural infusion of 0.2% ropivacaine along with 2 mcg/ml of fentanyl at the rate of 5 ml/h. Pneumatic calf pump was started preoperatively and continued in the postoperative period to prevent thromboembolism. On the 3rd postoperative day, epidural catheter was removed after confirming normal coagulation parameters. For deep vein thromboprophylaxis, a single dose of fractionated heparin (dalteparin 2500 U) was given subcutaneously 6 h after the removal of epidural catheter according to the American Society of Regional Anesthesia and Pain Medicine (ASRA) guidelines.
Six hours after the first dose of dalteparin, the patient complained of severe back pain along with loss of sensory and motor power in the lower limbs. Clinical examination revealed no sensations and muscle power of grade 0/5 in both the lower limbs.
With high index of suspicion of spinal/epidural hematoma causing spinal cord compression, the patient was started on intravenous methylprednisolone infusion, and further dosage of dalteparin sodium was withheld.
Within 2 h of onset of symptoms, an urgent magnetic resonance imaging (MRI) was obtained which revealed a localized epidural hematoma posteriorly from D6 to D8 level causing compression and significant anterior displacement of adjacent spinal cord [].
The patient was moved to the operating room directly from MRI suite for emergency laminectomy and decompression under general anesthesia. The hematoma was meticulously evacuated, and no active bleeding vessel could be identified [Figure and ].
She regained some sensory power in the lower limbs on the day of the spine surgery. On the 2nd postoperative day, some toe movement was seen. There was a gradual improvement in muscle power over the next few days, and on the 7th postoperative day, the patient had regained normal muscle power of both the lower limbs. Recovery was faster in the left lower limb as compared to right side.
Subsequent follow-up did not reveal any sensory-motor abnormality.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3527,10,Ideal Body Weight,physical,decimal,pmc-7831216-1,Extracted,"A 43-year-old man with a 20-year history of bipolar disorder attempted suicide by ingesting pills containing 20 g caffeine. He arrived at our hospital 100 min after ingestion. Vital signs included: respiratory rate, 30 breaths/min; SpO2, 97% (ambient air); heart rate, 130 b.p.m.; blood pressure, 126/69 mmHg; and Glasgow Coma Scale score, E4V5M6. The patient had 10 bouts of watery vomit. He was 176 cm tall and weighed 60 kg.
Premature ventricular contractions were observed on electrocardiography (Fig. ). Blood examination revealed: white blood cell count, 7500/μL; creatine phosphokinase, 66 IU/I; and potassium, 2.6 mEq/L. Arterial blood gas analysis revealed respiratory alkalosis and metabolic acidosis: pH 7.43; PCO2, 27.3 mmHg; PO2, 124 mmHg; HCO3, 17.7 nEq/L; and lactate, 6.5 mmol/L. He had ingested 333 mg/kg of caffeine, with blood levels showing 42 μg/mL (poisoning range ≥25 μg/mL) 2 h after ingestion. Blood theophylline levels, a metabolite of caffeine, were at or below measurement sensitivity (poisoning range ≥20 μg/mL). Although a normal blood pressure at arrival was maintained, a wide QRS complex and a pulse rate of 130 b.p.m. were observed.
At 50 min after arrival, a flexible double-lumen catheter was placed in the right internal jugular for emergency hemodialysis. Sixty minutes after arrival, when the arrhythmia occurred, a catheter sheath was placed in the right femoral vein and left femoral artery to enable rapid introduction of extracorporeal membrane oxygenation (ECMO). Sixty-five minutes after arrival, midazolam (10 mg), fentanyl (0.1 mg), and rocuronium (50 mg) were used to initiate tracheal intubation and artificial respiratory management. Eighty minutes after arrival, when he was placed in the left lateral decubitus position during endoscopy, he developed pulseless ventricular tachycardia. Eighty-two minutes after arrival, chest compressions and defibrillation yielded successful return of spontaneous circulation; however, he developed ventricular fibrillation. Eighty-five minutes after arrival, VA-ECMO was introduced from the sheath catheter site, ensuring a blood supply of 3.5 L/min at 2000 rpm. Because potassium levels were low, they were replenished, which eliminated premature ventricular contractions. One hundred minutes after arrival, hemodialysis was introduced at a flow rate of 100 mL/min from the flexible double-lumen catheter and a dialysate flow rate of 4000 mL/h. After hemodialysis, the patient’s tachycardia began to improve. Sixteen hours after arrival, the premature ventricular contractions decreased and hemodialysis was terminated. The premature ventricular contractions did not reappear after termination of dialysis, and his heart rate maintained a sinus rhythm at 90 b.p.m. Dialysis was terminated when the PaO2/FiO2 ratio was at 450 mmHg, and the patient was weaned off ECMO. On hospital day 2, ECMO was terminated when the patient had a heart rate of 70 b.p.m., blood pressure of 130/80 mmHg, respiration rate of 16 breaths/min, and electrocardiographic waveform with sinus rhythm, suggesting he had escaped the acute poisoning state (Fig. ). He also returned to a lucid state of consciousness. Extubation was carried out on hospital day 4, and the serum caffeine level was 5.5 μg/mL, with a serum theophylline level of 3.7 μg/mL (Fig. ). Rehabilitation was started on the day of extubation, and he was transferred to a psychiatric hospital on day 21.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [176.0, 'cm']}",71.37017,67.80166,74.93868,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 176.0 cm, which is 176.0 cm * 0.393701 in/cm = 69.29138 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.29138 (in inches) - 60) = 71.37017 kg.
Hence, the patient's IBW is 71.37017 kg."
3528,10,Ideal Body Weight,physical,decimal,usmle-1128,Extracted,"A 67-year-old woman comes to the physician with a 4-month history of chest pain that occurs on exertion. The pain is dull, and she experiences retrosternal pressure when she walks up the stairs to her apartment on the fifth floor. The pain disappears shortly after stopping for one minute. She has hypertension, for which she takes lisinopril and metoprolol daily. She does not smoke or drink alcohol. She is 158 cm (5 ft 2 in) tall and weighs 82 kg (180 lb); BMI is 33 kg/m2. Her pulse is 72/min and blood pressure is 140/85 mm Hg. Cardiac examination shows no murmurs, rubs, or gallops. Fasting lipid studies show:
Total cholesterol 196 mg/dL
LDL 110 mg/dL
HDL 50 mg/dL
A resting ECG shows no abnormalities. A week after uneventful initiation of aspirin, the patient is started on atorvastatin.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3529,10,Ideal Body Weight,physical,decimal,pmc-4384671-1,Extracted,"A 47-year-old woman was referred to our hospital due to watery diarrhea with weight loss. The patient had up to 20 episodes of watery diarrhea daily and a 15-kg weight loss over the previous 9 months. Thyroid function tests showed increased levels of triiodothyronine (221 ng/dL; normal range, 80 to 200 ng/dL) and free thyroxine (FT4; 3.51 ng/dL; normal range, 0.77 to 1.94 ng/dL) and decreased levels of thyroid stimulating hormone (TSH; 0.05 µIU/mL; normal range, 0.30 to 4.00 µIU/mL). Additionally, a thyroid autoantibody test showed increased levels of anti-thyroid peroxidase antibody (2,162 IU/mL; normal range, 0 to 8 IU/mL), anti-thyroglobulin antibody (166.4 IU/mL; normal range, 0 to 60 IU/mL), and TSH-binding inhibitory immunoglobulin (27.7%; normal range, 0% to 10%). Thyroid ultrasound revealed diffuse low echogenicity and increased blood flow on color Doppler.
Accordingly, she was diagnosed with Graves' disease and subsequently treated with methimazole. After 6 months of treatment, thyroid function tests showed normal levels of FT4 (1.3 ng/dL) and TSH (0.37 µIU/mL), but the patient still complained of persistent watery diarrhea and abdominal distension. A weight gain of 6 kg had been achieved in the 2 weeks following the initiation of treatment, but no further weight recovery was achieved.
She was admitted to the hospital to determine the cause of her persistent symptoms. Physical examination showed the patient had a height of 161 cm, weight of 60 kg, blood pressure of 124/67 mm Hg, pulse of 87 beats per minute, respiratory rate of 18 breaths per minute, and body temperature of 36.3℃. The patient had no abdominal pain, tenderness, or edema. Laboratory results were within normal limits. White blood cells (WBCs; 8,250/µL; normal range, 4,000 to 10,000/µL), hemoglobin (13.3 g/dL; normal range, 12 to 16 g/dL), platelet count (279,000/µL; normal range, 150,000 to 350,000/µL), sodium (139 mmol/L; normal range, 135 to 145 mmol/L), potassium (3.6 mmol/L; normal range, 3.5 to 5.0 mmol/L), total protein (6.6 g/dL; normal range, 5.8 to 8.0 g/dL), albumin (4.1 g/dL; normal range, 3.1 to 5.2 g/dL), cholesterol (126 mg/dL; normal range, <200 mg/dL), alkaline phosphatase (62 IU/L; normal range, 50 to 128 IU/L), aspartate aminotransferase (19 IU/L; normal range, <40 IU/L), and alanine transaminase (22 IU/L; normal range, <40 IU/L) were all normal. Stool lipid testing was found to be normal. No WBCs were observed in the stool examination, and no bacterial growth was identified in the stool culture. In addition, the patient showed negative results for detection of the antihuman immunodeficiency virus antibody and antinuclear antibody testing.
Abdominal computed tomography scan showed no ascites or enlarged lymph nodes, and no edema or masses were observed in the small intestine (). Esophagogastroduodenoscopy showed no abnormal findings in the duodenal bulb (). Colonoscopy showed no gross abnormal finding in the colonic mucosa. The patient also underwent 'random' biopsies. A random biopsy of the colon showed normal variation. A duodenal bulb biopsy showed no significant villous atrophy, but a slight increase in intraepithelial lymphocytes was seen ().
Based on the medical history of Graves' disease, persistent chronic diarrhea with weight loss, and increased intraepithelial lymphocytes of the patient, she was suspected to have celiac disease. Accordingly, the patient was placed on a gluten-free diet and subjected to serological and genetic tests.
As a result of HLA typing, HLA-DQA1*03 and *05 and HLA-DQB1*02:01 and *04:01 were detected in the patient. Thus, the patient had an HLA-DQ2 heterodimer (""DQ2.5"") comprising HLA-DQB1*02:01 and HLA DQA1*05. Megiorni and Pizzuti [] reported that DQ2.5 is a high-risk factor for celiac disease. Serological analysis showed that the patient did not have immunoglobulin A (IgA) anti-tissue transglutaminase (anti-tTG) or IgA endomysial antibodies.
Diarrhea was reduced from 20 times to 0 to 1 time per day starting from the second day of the gluten-free diet. At 4 weeks after initiating the gluten-free diet, the patient's weight had increased by 8 kg, reaching 68 kg, and her clinical symptoms had also improved. During a 6-month follow-up, diarrhea recurred only twice after consuming noodles containing gluten.
The patient is currently maintaining a gluten-free diet. Although serologic testing was negative, the patient was finally diagnosed with celiac disease after identifying the HLA-DQ2.5 genotype and the diagnosis of Graves' disease.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [161.0, 'cm']}",53.28748,50.62311,55.95185,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 161.0 cm, which is 161.0 cm * 0.393701 in/cm = 63.38586 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.38586 (in inches) - 60) = 53.28748 kg.
Hence, the patient's IBW is 53.28748 kg."
3530,10,Ideal Body Weight,physical,decimal,pmc-7337418-1,Extracted,"A 58-year-old Chinese female was admitted to our department of neurology with weakness of both arms and legs. Two months prior to admission, she had developed weakness in her bilateral limbs as well as pain in both shoulders. So, she went to a local hospital and reported that she felt the pain ease after receiving traditional Chinese medicine therapy. However, the weakness of her limbs gradually increased. So, she came to our hospital for further diagnosis and treatment. Her past medical history included well-controlled hypertension and diabetes mellitus. Furthermore, she had experienced pyrexia at times in recent years but without the detection of a raised temperature, and she did not seek diagnosis and treatment. She had no history of smoking, alcohol consumption, or recreational drug use. Her family history was unremarkable.
On admission, her height was 158 cm, body weight was 42 kg, body temperature was 38.9°C, pulse was regular at 122 beats/min, respiratory rate was 28 breaths/min, and blood pressure was 170/98 mm Hg. The physical examination revealed that multiple lymphadenopathies were present in the bilateral axillary and the right side of the middle neck triangle, hyperpigmentation in the abdomen, and bilateral pitting pedal edema. The neurological examination showed bilateral upper and lower limb muscle weakness. The upper and lower extremity strength scores, as determined by manual muscle testing, were 3/5 and 4/5, respectively. Tendon reflexes were absent in all extremities, and pathological reflexes were negative. The patient was lucid, and the neurological examination revealed no cranial nerve abnormalities.
Laboratory data on admission (Table ) revealed an elevated platelet count, but the coagulation profile was normal. The erythrocyte sedimentation rate was 41 mm/h (normal range 0 to 20 mm/h). The concentration of C-reactive protein was increased. The testing showed strongly raised creatine kinase (CK) activity (7845 U/L, normal range 40–200 U/L) and elevated liver enzymes in the serum. Blood tests showed a glucose level of 5.88 mmol/L and a glycosylated hemoglobin level of 7.1%. The renal function testing revealed that her creatinine level was normal, but Cystatin C was elevated, and her glomerular filtration rate was decreased. Meanwhile, her urine protein content was 133.35 mg/L (normal range 0 to 10 mg/L). Furthermore, her creatine kinase-MB, MB, and hs-TnT concentrations were significantly increased. Thyroid function tests revealed hypothyroidism. The thyroxin stimulating hormone level was 12.069 uIU/mL (normal range 0.35–4.94 uIU/mL), but the free-T3 and T4 concentrations were normal. The adrenocorticotropic hormone concentration was 3.24 pg/mL (normal range 4.7 to 48.8 pg/mL). The cortisol concentration was 1.1 ug/dL in 4pm (normal range 2.9 to 17.3 ug/dL). Human immunodeficiency virus, serology for hepatitis B and C, and tumor markers (cancer antigen 125, alphafetoprotein, careinoembryonic, carbohydrate antigen 199, cancer antigen 153, cancer antigen 242, prostate specific antigen and neuron specific enolase) were negative. Electrodiagnostic study showed that the motor conduction velocities, sensory nerve action potential, compound muscle action potential, and F wave latency were in the normal range in the bilateral median, ulnar, sural, and tibial nerves. Electromyography analysis showed there were mass abnormal spontaneous activities (fibrillation and positive sharp wave) in the left first dorsal interossei, biceps brachii, tibialis anterior, and the medial head of quadriceps femoris muscle, and myotonic potential in the left iliopsoas and tibialis anterior muscles. The neck triangle lymph node biopsy showed lymphadenosis, but the patient refused an immunohistochemical examination. On the thorax computed tomography (CT) scan, multiple enlarged axillary lymph nodes were observed (Fig. A). The flexor carpi radialis muscle biopsy showed many infiltrated lymphocytes, and the congo red staining test was negative. Combined with the symptoms, physical examination, and laboratory tests, we made a diagnosis of myositis. Hence, we treated the patient with methylprednisolone. However, she did not show a significant improvement, despite receiving standard therapy. Thus, immunoelectrophoresis was performed. Immunoelectrophoresis showed monoclonal IgA lambda serum. A bone marrow biopsy examination revealed that the plasma cell content was slightly elevated (0.84%). Furthermore, the concentrations of serum IgA and lambda free light chains were elevated. Serum IgG, IgM, and IgE levels and complements of C3, C4, and kappa free light chains were within the normal range. Furthermore, the VEGF concentration was slightly elevated. In addition, a X-ray of the skull revealed a small bone defect in the frontal lobe (Fig. B). Ultrasonography showed no cardiomegaly, hepatosplenomegaly, or pleuroperitoneal fluids. Based on the observed skin manifestations, lymphadenopathies, pedal edema, IgA-λ restricted paraproteinemia, plasma cell dyscrasia in bone marrow, elevation of VEGF, and other features, we made a diagnosis of atypical POEMS syndrome without polyneuropathy.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3531,10,Ideal Body Weight,physical,decimal,pmc-7148413-1,Extracted,"The patient is a 41-year-old male. His chief complaint is left flank pain. He has no medical history/family history.
The subject consulted a nearby doctor with left stomachache and fever as chief complaints in 1 month prior to the surgery. Diverticulitis of the descending colon splenic flexure was doubted in CT and the subject was hospitalized. A colonoscopy revealed an irregular flat elevated lesion on the splenic flexure. The subject was transferred to our hospital for examination and medical treatment.
The height is 175 cm, body weight 54.6 kg, pulse 66 beats/m, body temperature 36.3, and blood pressure 114/76 mmHg. The abdomen was slightly distended, and mild left stomachache was recognized. The stool frequency was 1 time/day.
In blood biochemistry examination, values were as high as 22.5 ng/ml in CEA and 81.0 U/ml in CA19-9 tumor markers.
Significant hyperplasia (4 cm) of the colon mucous membrane was observed on the descending colon splenic flexure and it was accompanied by elevation of surrounding adipose tissue density. The surrounding lymph nodes swelled up to around 5 mm. Since strong hyperplasia was seen in the mucous membrane, it was thought as reactive enlargement accompanied by inflammation. The finding that indicates distant metastasis was not seen in the liver and lung (Fig. ).
A semicircular, lateral spreading tumor of granular-type (i.e., an aggregate of IIa-like tumors) was observed in the descending colon splenic flexure (Fig. a).
Notable abnormality such as irregular ulcer and scar or bamboo joint-formed appearance was not recognized.
Biopsy was performed twice for the lateral spreading tumor of granular-type of descending colon. The tumor was diagnosed pathologically as a tubular adenoma without evidence of malignancy. However, we judged that the lesion in the descending colon was a cancer based on the elevated CEA level and CT findings. We also considered the possibility of coexistence of inflammatory lesion near the tumor because of an edematous change of the mucosa (Fig. b). Therefore, it was determined to place a covering stoma 20 cm proximal from the terminal ileum at the time of surgery.
D3 left hemicolectomy and loop type stoma construction were performed. No abnormality was confirmed in the small intestine such as thickness, fistula, mass, and adhesion to abdominal wall during the operation.
Gross examination confirmed that the main tumor was a laterally spreading tumor (granular-type) in the descending colon (Fig. a, b). No gross findings were recognized that supported Crohn’s disease, e.g., longitudinal ulcers, their scars, or cobblestone appearance. Histopathologically, the surface of the main tumor was composed of uniform proliferation of atypical glands (either tubular or villous in configuration) and containing both low- and high-grade areas (Fig. a, b). This lesion stained diffusely positive for p53 by immunohistochemistry (Fig. c). Therefore, we diagnosed these atypical glands in the surface area this as dysplasia, and this lesion continuously invaded the muscularis propria (Fig. d). In deeper areas of the main tumor, deposition of extracellular mucin was observed leading the diagnosis of mucinous adenocarcinoma (Fig. a). p53 was positive in 50% of tumor cells in mucinous carcinoma (Fig. b). The final diagnosis was mucinous adenocarcinoma associated with dysplasia, in the descending colon, type 5, 50 × 48 mm in size, pT4a (SE) pN2a (4/28), Ly1, V1, cM0, pStage IIIC (UICC TNM classification, 8th ed., and Japanese classification of colorectal carcinoma, 9th ed) []. Furthermore, another dysplasia, not continuous from the main tumor, was confirmed by multiple sampling analyses in the resected specimen approximately 5.2 × 1.8 cm in size (indicated by blue line in Figs. and ). This dysplasia was not associated with adenocarcinoma (i.e., completely confined in the mucosa). We further obtained the following findings that supported pre-existing transmural chronic inflammation (e.g., Crohn’s disease) as follows: (a) irregular thickening of the muscularis mucosae, (b) fibrosis in the submucosa and muscularis propria, and (c) sporadic formation of lymphoid aggregates in the submucosa and subserosa in the resected colon specimen (Fig. ). Taken together, the histopathological features of main tumor were consistent with colitis-associated cancer.
The ileus state was prolonged for over 40 days after the surgery. On day 55 endoscopies were performed to newly find orbicular ulcers in the terminal ileum (Fig. a, b). We excluded the possibility of tuberculosis or cytomegalovirus by an interferon-gamma release assay and serum antibody assay. Re-examination of endoscopy on day 77 revealed the development of longitudinal ulcers in the ileum (Fig. c). With a clinical diagnosis of Crohn’s disease, the patient received infliximab administration, and the lesions of small intestine ameliorated significantly on day 103. Furthermore, ileus was improved and therefore the subject was discharged on day 112 (Fig. d). Seventy-three days after the discharge, CEA suddenly was elevated and intestinal edema, and ascitic fluid appeared in abdominal contrast-enhanced CT. The subject was diagnosed as ileus attributable to peritoneal dissemination. Overall status gradually worsened and he passed away on day 207. The final cause of death was judged as peritoneal dissemination.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3532,10,Ideal Body Weight,physical,decimal,pmc-3409953-1,Extracted,"A 31-year-old, 54 kg, 155 cm, gravida-3, Para-1,37 weeks gestation, woman was admitted with complaint of tenderness at the site of previous cesarean section scar. She had an uneventful cesarean section under subarachnoid block 2½ years back and no other past medical illness. Her antenatal course was unremarkable. On examination, her blood pressure (BP) was 130/74 mmHg, pulse 94/minute and respiratory rate (RR) 18/minute. Ultrasonography revealed normally beating fetal heart at 140/minute. In view of the possible impending uterine rupture, the patient was scheduled for an urgent cesarean section.
In the operating room, standard monitoring was initiated and subarachnoid block was given in left lateral position with median approach at L2-3 interspace in the first attempt. Bupivacaine 7.5 mg (1.5 ml of 0.5% hyperbaric bupivacaine) with fentanyl 25mcg was injected after free flow of cerebro-spinal fluid. The patient was made supine, oxygen was supplemented by facemask and Ringer's solution was administered intravenously. Two minutes after spinal anesthesia, her pulse was 95/minute, BP 126/72mmHg and at 5 minutes, her pulse was 103/minute, BP 109/65mmHg, RR 20/min and peripheral oxygen saturation (SpO2) 99%. T4 level of sensory block was achieved and surgery was started. A healthy female baby was delivered after 5minutes with normal APGAR score. Three minutes after the delivery of the baby, the patient complained of weakness of voice and tingling sensation over the face, immediately followed by complete inability to speak. She was anxious but her vital signs were stable with SpO2 99%, pulse 104/minute, BP 110/64 mmHg and RR 16/minute. Sensory block was reassessed and found to be fixed at T4 level. She was conscious, alert, and able to follow commands. There was no difficulty in swallowing. The baby was shown to her and she was reassured. After 20 minutes, her aphonia resolved. The rest of the surgery was uneventful. Postoperatively, the patient was monitored in the recovery room and neurological examination revealed normal higher function, normal cranial nerve function with no sensory-motor abnormality. There was no history suggestive of preeclampsia or absence seizures. Magnetic Resonance Imaging (MRI) with diffuse weighed scan, duplex ultrasound for deep vein thrombosis, carotid artery Doppler, electroencephalography (EEG), and trans-thoracic echocardiography were all normal. Subsequent postpartum course was uneventful. She was followed up in neurology for three months without any complications.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3533,10,Ideal Body Weight,physical,decimal,pmc-4945533-1,Extracted,"A 70-year-old man visited our hospital complaining of chronic diarrhea for 3 months. He had increased bowel movements with excessive bowel sounds approximately half an hour after a meal, his stools were almost watery, and the frequency of his bowel movements was approximately 2−4 times per day. The diarrhea was not accompanied by abdominal pain before or after a bowel movement. The patient had lost 30 kg of weight (from 100 kg to 70 kg) in the 3 months since the diarrhea had begun. Before visiting our hospital, he had been admitted to two other hospitals, where he underwent esophagogastroduodenoscopy, colonoscopy, and an abdominopelvic CT scan, but none of the studies revealed the cause of his chronic diarrhea.
He was taking antihypertensives (amlodipine 5 mg/day, olmesartan 20 mg/day, and atenolol 50 mg/day) and an oral hypoglycemic drug (glimepiride 2 mg/day.) Twelve years previously, he had suffered from jaundice with intrahepatic stones and undergone removal of the stones via percutaneous transhepatic cholangioscopy three times. He had also undergone open cholecystectomy for empyema of the gallbladder 8 years previously. He had a 40-pack-year history of smoking but had stopped smoking 12 years previously.
He looked ill. His body height was 172 cm, and his weight was 71 kg (BMI 24 kg/m2). At the time of admission, his blood pressure, pulse rate, respiratory rate, and body temperature were 151/110 mmHg, 109 beats/min, 16 breaths/min, and 36.5℃, respectively. A peripheral blood test showed leukocyte, hemoglobin, and platelet levels of 8,500/mm3 (granulocytes, 63%; lymphocytes, 25%; and monocytes, 11%), 17.9 g/dL, and 123,000/mm3, respectively. A blood chemistry test revealed that levels of BUN/Cr, albumin, AST/ALT, ALP, amylase/lipase, and CRP were 12/0.99 mg/dL, 2.9 g/dL, 14/10 IU/L, 77 IU/L, 58/27 U/L, and 0.25 mg/dL, respectively. Electrolyte levels were within the normal ranges (sodium 135 mEq/L and potassium 4.1 mEq/L). Glycated hemoglobin level was 5.5%. A qualitative test of urine 5-hydroxyindoleacetic acid showed a negative result. The patient was in a euthyroid state (thyroid-stimulating hormone 3.6 µU/mL and free T4 1.1 ng/dL). The fecal occult blood test (immune latex agglutination method) result was negative. A routine stool examination showed no helminth ova, protozoa cysts, or trophozoites, and a stool Gram stain showed no leukocytes. There was no growth of Shigella, Salmonella, or Yersinia species on the stool culture. A Clostridium difficile toxin assay and culture showed a negative result.
Esophagogastroduodenoscopy did not detect any abnormal findings in the esophagus; however, multiple erosions and whitish scar changes were observed in the gastric body and antrum. Mucosal nodularity was observed in the second portion of the duodenum. Colonoscopy did not detect any abnormalities except one small polyp in the cecum and one in the rectum. Biopsy specimens were randomly obtained at each segment of the entire colon and the terminal ileum. A small bowel series showed no abnormal findings.
Histological examination of the stomach revealed a moderate mixed lymphoplasmacytic infiltration in the lamina propria. Duodenal biopsy showed chronic severe duodenitis with mucin depletion and flattening of the villi. Mild lymphocytic infiltrations were observed in the ileal and colonic biopsies of each segment of the entire colon.
The patient was treated empirically with antiparasitic drugs (400 mg of albendazole once and 1.8 g of praziquantel 3 times per day for 2 days) and antidiarrheal drugs (loperamide, which was initially started with a dose of 3 mg/day and later escalated to 9 mg/day; 1 g of a compound of bismuth, tannalbin, and kaolin 3 times per day; and 10 mg of codeine 3 times per day); however, the diarrhea continued. The patient received octreotide (0.05 mg subcutaneously 3 times per day), which was unable to relieve his symptom.
Because the cause of the diarrhea was still unclear after thorough evaluation, a second esophagogastroduodenoscopy was conducted. This time the endoscopy was advanced farther beyond the second portion of the duodenum, with the purpose of examining the proximal small bowel as far as possible. Mucosal changes indicative of metaplasia were detected from the second portion of the duodenum to the proximal jejunum. However, the most distal small bowel that could be observed during the endoscopy appeared normal. Biopsy specimens were randomly obtained from the duodenal bulb to the proximal jejunum (). Duodenal biopsy revealed blunting of the intestinal villi, detachment of surface epithelial cells, depletion of goblet cells, and moderate lymphoplasmacytic and mild eosinophilic infiltration in the lamina propria and crypts. Increased mast cell infiltrations into the lamina propria with more than 50 mast cells per high power field were observed by toluidine blue staining and CD117 (KIT) immunohistochemical staining (). Jejunal biopsies demonstrated similar histological features.
Treatment with hydroxyzine (10 mg per day), famotidine (20 mg per day), and ranitidine (300 mg per day) was started soon after confirmation of gastrointestinal mastocytosis. The patient returned to the outpatient clinic 2 weeks later, and his symptoms of chronic diarrhea were substantially improved. He took both H1 and H2 antagonists for a further 2 weeks, and his treatment was discontinued thereafter. There was no relapse of diarrhea up to his last visit to our hospital, which was 11 months after discontinuation of the medication.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [172.0, 'cm']}",67.74811,64.3607,71.13552,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 172.0 cm, which is 172.0 cm * 0.393701 in/cm = 67.71657 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.71657 (in inches) - 60) = 67.74811 kg.
Hence, the patient's IBW is 67.74811 kg."
3534,10,Ideal Body Weight,physical,decimal,pmc-6780877-1,Extracted,"The patient was a 23-year-old Italian male, professional cyclist, non-smoker, 190 cm tall and 82 kg, with a daily training load ranging from three to six hours, six days a week for an upcoming competition. The patient presented with no prior medical record but spontaneous and multidirectional multiple posterior dislocations of the right shoulder. In association with this complaint, the patient stated that he had widespread pain of the GHJ and paresthesias of the entire right hand, but predominantly on the palmar side of the fourth and fifth finger. Moreover, he complained about diffuse spasms (clonic manifestations) occurring around the shoulder, primarily of the pectoralis major and the biceps brachii muscles ().
After a fall during a cycling race, the athlete went to a medical clinic in March 2017 and was diagnosed with subsequent dislocations of the right shoulder. The fall occurred following contact with a teammate during an international championship while riding on a paved road. The patient was not able to describe the exact traumatic mechanism but remembers his attempt to place his hands toward the ground to avoid the collision. The diagnostic investigation at the time, a magnetic resonance image (MRI), signaled the presence of “intra-articular effusion with non-homogeneity of the antero-inferior portion of the glenoid rim, bone marrow edema on the anterior surface of the humeral head, and an extensive lesion of the subscapularis tendon” (). The anamnestic examination was highlighted by a numeric pain rating scale (NPRS) [] of 6/10 (while the patient was at rest), widespread tenderness on the entire joint complex, and positive clinical tests (posterior drawer test, sulcus sign, load and shift, and apprehension test). The patient did not report further trauma to the joint until May 2018, when, during normal work activities (while lifting a box onto a shelf that was above shoulder height), the patient experienced another posterior dislocation of his right shoulder. After this dislocation, the number of episodes of dislocation during limb movements in normal daily activities of living increased in frequency and intensity. Subsequently, spasms of the joint complex followed these episodes and became more frequent with multiple spontaneous and multidirectional dislocations of the shoulder ().
In June 2018, he returned to the clinic, complaining of a worsening of his clinical presentation and symptoms, characterized by an increase in spasmodic muscles surrounding his right shoulder, resulting in spontaneous multidirectional dislocations. The patient stated that these muscle spasms were associated with constant pain that worsened after the event and caused significant instability, weakness, and temporary tingling of the entire hand that was predominately located in the fourth and fifth finger. The spasms did not occur at night during sleep but appeared randomly and without warning throughout the day without apparent cause according to the patient. The patient also noted that the spasms were influenced by the patient’s mental state (with a reported increase of episodes and worsening following family disputes).
By analyzing the patient’s clinical history, family history, and the assessment scales, the PT identified various red and orange flags [] during the medical history and through analysis of the patient’s disability of the arm, shoulder, and hand (DASH) rating scale (depression, anxiety, and somatoform disorders). At the initial evaluation, the PT observed that the right shoulder was in an anterior and internally rotated position. The patient’s right scapula was also abducted and internally rotated. Muscular trophism was reduced in front of the contralateral side: Deltoid, biceps, and pectoral were hypotrophic. No differences in temperature, skin color, or swelling were appreciable and there were no scars present.
The PT had no opportunity to perform any clinical tests as the patient’s passive and active movements immediately set off multidirectional joint dislocations and any type of stimulation increased the spontaneous muscle spasms. Three assessment scales were used by the PT to frame pain presentation (NPRS), disability/psychosocial factors (DASH) [], and instability patterns (Western Ontario shoulder instability index (WOSI)) [].
The patient’s NPRS was 8/10. The DASH score was used to evaluate the disability/psychosocial factors: This scale evaluates the patient’s ability to perform a range of daily, work-related, and sports/recreational activities. The DASH reported a 74.6% disability for daily life activities (ADL) and a 100% disability for work/recreational activities.
The WOSI was used to evaluate the pathology-specific life quality for the patient with shoulder instability and the patient performed at 5.43%.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [190.0, 'cm']}",84.04734,79.84497,88.24971,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 190.0 cm, which is 190.0 cm * 0.393701 in/cm = 74.80319 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (74.80319 (in inches) - 60) = 84.04734 kg.
Hence, the patient's IBW is 84.04734 kg."
3535,10,Ideal Body Weight,physical,decimal,trec-ct-2021-71,Extracted,"The patient is a 34-year-old obese woman who comes to the clinic with weight concerns. She is 165 cm tall, and her weight is 113 kg (BMI: 41.5).  In the past, she unsuccessfully used  antiobesity agents and appetite suppressants. She is complaining of sleep apnea, PCO and dissatisfaction with her body shape. She is a high-school teacher. She is married for 5 years. She doesn't use any contraceptive methods for the past 4 months and she had no prior pregnancies. She rarely exercises and movement seems to be hard for her. She is not able to complete  the four-square step test in less than 15 seconds. She does not smoke or use any drugs. Her BP: 130/80, HR: 195/min and her BMI is: 41.54. Her lab results:
FBS: 98 mg/dl
TG: 150 mg/dl
Cholesterol: 180 mg/dl
LDL: 90 mg/dl
HDL: 35 mg/dl
She is considering a laparoscopic gastric bypass.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3536,10,Ideal Body Weight,physical,decimal,pmc-4127553-1,Extracted,"A thirty-seven-year-old Thai male was diagnosed with hemoglobin E/β-thalassemia (E/β-Thal) disease at four years of age. Splenectomy was done in December 2000 (23 years old) because of increasing blood transfusion requirement. However, 2 units of packed red blood cells transfusion were still required monthly to relieve anemic symptom. Pulmonary hypertension was diagnosed in February 2004. Hydroxyurea at 500 mg/d five days a week was prescribed in November 2007 to see if it could improve symptoms and transfusion requirement. Other medications were warfarin, aspirin, deferoxamine and folic acid. Baseline Hb was 7 g/dL.
In December 2007, acute massive hematochezia after naproxen usage in the preceding 2 weeks for plantar fasciitis necessitated hospital admission. Physical examination showed a markedly pale man with moderately icteric sclerae. Height and weight were 174 cm and 54 kg, respectively. The precordial area was mild to moderately active with increased P2. Liver edge was palpable 3 cm below the right costal margin. Prothrombin time international normalized ratio was 1.8. Blood transfusion followed by colonoscopy was prescribed. The latter showed multiple shallow ulcers at the cecum and normal-looking ileo-cecal (IC) valve. Histo-pathology of the biopsied specimen showed acute ulcers with chronic inflammation and severe tissue eosinophilia. Although the findings were non-specific, naproxen was discontinued. Periodic epigastric pain and mucous diarrhea persisted and were not alleviated by antacid or proton pump inhibitor. Meanwhile, hydroxyurea dosage was increased to 4.5 g/week due to a poor response.
Follow-up colonoscopy a year later showed an ulcerated IC valve with multiple small ulcers along the terminal ileum to the ascending colon. The differential diagnosis from endoscopic findings was infection, such as tuberculosis, cytomegalovirus, as well as non-infectious causes, such as Crohn’s disease and malignancy. Ischemic bowel disease was less likely because of his young age and no sharp demarcation of lesion according to the territorial vascular blood supply. Biopsies of the ulcers showed acute and chronic inflammation with tissue eosinophilia which was non-specific. There was no thrombus in the blood vessels. Special stain for acid fast bacilli (AFB) and Gomori methenamine silver (GMS) showed no organisms. Polymerase chain reaction for mycobacterium tuberculosis was negative. Thus, no specific treatment was given. Periodic epigastric pain and occasional mucous diarrhea persisted.
In December 2009, he presented with fever and mucous diarrhea. CT scan of the whole abdomen showed a circumferential thickened wall involving the ascending colon and the terminal ileum. Esophago-gastro-duodenoscopy revealed multiple erosions on the gastric mucosa, biopsy of which showed chronic gastritis. Colonoscopy revealed a markedly swollen and ulcerated IC valve and circumferentially thickened wall from the terminal ileum to the ascending colon. Biopsies of cecal ulcers showed acute ulcers with acute and chronic inflammatory cells infiltration to the muscularis mucosae. There was no feature of malignancy, vasculitis, viral inclusion or granuloma. GMS, Periodic Acid Schiff (PAS), and AFB stains were non-revealing. Various serologic tests for systemic vasculitis, such as antinuclear antibody, perinuclear and cytoplasmic antineutrophil cytoplasmic autoantibody were all negative. Empiric treatment with intravenous ceftriaxone was given.In February 2010, there was another episode of massive hematochezia, resulting in a partial right half colectomy. Multiple scattered ulcerative lesions involving the terminal ileum, the cecum and the ascending colon were found on gross examination (Figure ). The histo-pathologic findings were acute mucosal ulcers with granulation tissue and tissue eosinophilia. The submucosa was thickened and edematous. The acute and chronic inflammatory cells infiltrated through the submucosa to the inner muscular layer, not unlike the previous ones (Figure ). Leukocytoclastic vasculitis was not found. Special stains with GMS, PAS, and AFB were again non-revealing.
A month later, odynophagia was complained. Fiberoptic laryngoscopy showed a whitish ulcerative plaque at the right tonsillar fossa extending to the right posterior pharyngeal wall and the left tonsillar fossa. Punch biopsy was done. Symptoms got worse with lesions progressing to the hard palate, the pyriform sinus and the posterior pharyngeal wall. Histo-pathologic findings showed acute and chronic inflammatory changes with granulation tissue and tissue eosinophilia, not unlike those in the colon.
Hydroxyurea was discontinued in April 2010 because drug-induced ulceration was suspected. Odynophagia markedly improved. Two month-follow-up fiberoptic laryngoscopy showed clearing of all previous lesions. All GI symptoms disappeared without recurrence to date.
Ulcerative oral lesion is a rare adverse effect of hydroxyurea. All reported cases used hydroxyurea for chronic myeloproliferative neoplasm [-]. The lesions were confined to the lips, base of tongue and buccal mucosa, and were not related to myelosuppression or cumulative dose. They completely healed shortly after drug cessation. In some patients, the ulcers recurred after drug re-administration, reaffirming its causative role.
Our patient’s GI symptoms started about a month after having been on a low dose hydroxyurea for Hb F induction. A history of massive hematochezia following naproxen usage in the preceding 2 weeks led us to believe that naproxen was the cause. However, persistence of occasional mild epigastric pain together with a small amount of mucous diarrhea with and without blood despite naproxen cessation, and additional treatment with several proton pump inhibitors made it less likely. Due to a poor hematologic response, the hydroxyurea dose was increased. Abdominal symptoms remained the same despite the mildly progressive ulcerative lesions shown in the two consecutive annual colonoscopies. Shortly afterwards, a massive hematochezia developed, necessitating a partial right half colectomy. A more extensive investigation of the specimen for evidence of infectious causes, such as mycobacterium tuberculosis and cytomegalovirus, and for non-infectious causes, such as malignancy, inflammatory bowel disease and systemic vasculitis were non-revealing. Leukocytoclastic and hypersensitivity vasculitis were not observed in the ulcerative area. Thus, there was no change in the treatment plan.
Development of new painful oral ulcers, histo-pathologic findings of which were not unlike those in the colon led us to suspect that etiology of ulcers at these various sites was the same. Hydroxyurea was suspected because it can, on rare occasions, induce oral ulcers. After its cessation, odynophagia markedly improved in a month, and all GI symptoms disappeared in 2 months. Without recurrence up to now (4 years), the finding strongly suggested hydroxyurea as the culprit.
Hydroxyurea-related ulcers were previously reported to be confined to the oral area, the pathogenesis of which was unknown. Oral ulcers are not uncommon after methotrexate, also an anti-metabolite, and are related to the dose and severity of myelosuppression []. However, there was no myelosuppression in the reported cases of hydroxyurea-related oral ulcers. The dose of hydroxyurea used in our patient was relatively low, and there has never been myelosuppression. Thus, pathogenesis of these ulcers based on drug’s action on rapidly dividing cells is unlikely. Ours is the first report to show that these ulcers could also occur in the lower part of the GI tract. Its confinement to the ileum and the right-sided colon is intriguing and of unknown cause. Tuberculosis and amoebiasis also have a predilection for this region. The process of ulceration seemed to be very slowly progressive and reversible after drug cessation.
Hydroxyurea is more widely used in sickle cell than in β-thalassemia disease, and there never have been a report of ulcers such as those seen in our patient []. Taken together, these ulcers are likely to be idiosyncratic.
In contrast to hydroxyurea, non-steroidal anti-inflammatory drug-induced ulcers are typically confined to the stomach and small intestine []. Histo-pathologic findings of these ulcers, however, are not different, showing a non-specific infiltration by both eosinophils and neutrophils during the acute process. In addition to drug hypersensitivity, eosinophilic infiltration could also be due to allergy, vasculitis and parasitic infestation.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [174.0, 'cm']}",69.55913,66.08117,73.03709,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 174.0 cm, which is 174.0 cm * 0.393701 in/cm = 68.50397 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.50397 (in inches) - 60) = 69.55913 kg.
Hence, the patient's IBW is 69.55913 kg."
3537,10,Ideal Body Weight,physical,decimal,pmc-4030261-1,Extracted,"After taking written informed consent and informing the patient about possibility of reporting this case in a medical journal, a 45-year-old, 70 kg, 172 cm man with a history of episodic cluster headache was admitted to the hospital for pain management. He had periodic sharp excruciating pain on the left side of his face radiating from the back of his left eyeball. Lacrimation, conjunctival congestion, and nasal discharge were present on the left side. The present cluster was started one day ago. He experienced two severe episodes the day before; each lasted about 60 minutes with a six-hour pain relief between them. On the day of admission, he came with the same severe hemifacial pain initiated less than five minutes ago (he worked in the same hospital that researchers practiced). He was otherwise healthy and had no past medical history except some orthopaedic surgeries (due to an accident). He was not an alcohol or drug abuser. He had the same abrupt pain every three to six months that lasted about 15 days (the shortest and the longest clusters he remembered were five and 17 days, respectively). His symptoms started since five years ago and each year he experienced two to four clusters of headache on average, albeit he remembered a year with only a seven-day episode. The pain was not always completely improved with oral nonsteroidal anti-inflammatory drugs and very often, he was admitted to the hospital to receive oxygen therapy and intravenous painkillers. He mentioned that his first headache lasted six hours without any medication, as he was reluctant to receive any medication at first; however, he took painkillers for his following headaches. By taking medication, disabling episode of headaches lasted between 15 to 180 minutes; however, some mild to moderate pain remained for the same episode or following days of that cluster for which, he received trivial medication. He noted that he took just few hours sick leave and usually tolerated the pain. Once he received opioid (20 mg of intravenous meperidine) for his pain; however, it just added dizziness and nausea with no pain relief. He was reluctant to receive any prophylactic medication for his headaches. In his recent episode, he was admitted and hemodynamic and respiratory monitoring was utilized. Intravenous line was prepared and fluid was infused. He did not receive any supplemental oxygen. He received 20 mg of propofol (propofol 1% MCT/LCT, Fresenius, Germany) every four minutes () and simultaneous titrated dose of alfentanil (100 μg) every ten minutes. After the third injection of propofol and second prescription of alfentanil (about 15 minutes from the initiation of therapy), he reported acceptable pain relief with a mild remaining pain. He received a total dose of 120 mg of propofol (with the same protocol, however, as we encountered some drowsiness with no desaturation, we extended the interval for injection to every ten minutes and overall, it took about 50 minutes). Moreover, a total of 500 μg of alfentanil was infused (about 50 minutes). At this time he reported complete recovery with no remaining pain. He was just monitored and was discharged after two hours with no medication. He had no more episodes in the following days. In a four-month follow up, he did not experience any cluster headache.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [172.0, 'cm']}",67.74811,64.3607,71.13552,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 172.0 cm, which is 172.0 cm * 0.393701 in/cm = 67.71657 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.71657 (in inches) - 60) = 67.74811 kg.
Hence, the patient's IBW is 67.74811 kg."
3538,10,Ideal Body Weight,physical,decimal,pmc-4050942-1,Extracted,"A 55-year-old man weighing 50 kg and 160 cm tall, non-smoker, presented with cough with expectoration and shortness of breath on exertion since 3 years. He also gave a history of intermittent diarrhoea and flushing of the face and upper body since 3 months, precipitated by alcohol intake. He was a known hypertensive on tablet amlodipine 10 mg OD since 10 years.
Clinical examination revealed decreased air entry over left upper lung zone. Chest radiograph showed a mass in left suprahilar region. Computerised tomographic scan (CT scan) of the chest revealed a large, lobulated, heterogeneous enhancing mass lesion measuring 8.6 cm × 5.5 cm in left suprahilar region extending to left upper lobe bronchus [].
CT guided biopsy on histopathology showed a typical lung carcinoid. Blood chemistry, electrocardiogram (ECG) and echocardiogram were normal. His pulmonary function testing, arterial blood gas (ABG) analysis and breath holding time showed a predicted post-operative forced expiratory volume in 1 s of 54%, PaO2 of 93 mmHg, PaCO2 of 40 mmHg and breath holding time of 24 s. Urinary 5-hydroxy-3-indole acetic acid was 50 mg/day (n ≤ 10 mg/day). A diagnosis of left upper lobe bronchial carcinoid with carcinoid syndrome was made. Pre-operative preparation with subcutaneous (SC) octreotide 100 μg TDS relieved symptoms of flushing and diarrhoea. After 10 days, patient was scheduled for left upper lobectomy.
Premedication included tablet midazolam 7.5 mg and tablet ranitidine 150 mg at night and 1 h before surgery. On the morning of surgery, inj.octreotide 250 μg was given as an intravenous (IV) bolus followed by continuous infusion of 100 μg/h. An epidural catheter was sited at T7-T8 interspace and after test dose of 3 ml 2% lignocaine, 50 μg fentanyl in 6 ml saline was administered. Under local anaesthesia a radial artery catheter and right internal jugular line was inserted. Drugs for emergency use, octreotide, phenylephrine, glyceryl trinitrate, esmolol, corticosteroids and antihistaminics were kept handy. Anaesthesia was induced with fentanyl 100 μg, propofol 75 mg with preadministration of Inj. lignocaine 60 mg. Using vecuronium, Portex® right sided double lumen tube (DLT) 37 FG was inserted and position was confirmed by fibreoptic bronchoscope. Oxygen saturation (SpO2), end tidal CO2 (EtCO2), invasive blood pressure, ECG, central venous pressure, temperature and airway pressures were monitored throughout the procedure.
Anaesthesia was maintained with vecuronium and sevoflurane 1-1.2% in O2/N2O mixture. During surgical manipulation of tumour, there was sudden rise in peak airway pressure (P peak) from 20 to 35 cm H2O then to 42 cm of H2O and EtCO2, from 36 to 47 mmHg, then to 50 mmHg, accompanied by fall in SpO2 from 97% to 80%. On auscultation, there was marked reduction in breath sounds, with rhonchi. Flushing was observed all over the chest and face. Acute carcinoid induced bronchospasm was suspected. Surgical manipulation was stopped and N2O was discontinued. Octreotide 250 μg IV bolus was given and infusion rate was increased to 200 μg/h and inj. hydrocortisone 200 mg and chlorpheniramine 25 mg were administered IV.
Position of DLT was rechecked and ABG sample was taken. Clinical improvement was seen within 60 s of octreotide bolus and within 5 min respiratory parameters were normal. During this episode patient remained haemodynamically stable and decision was made to proceed with surgery.
Extubation was uneventful and post-operative analgesia was provided with bupivacaine and fentanyl. In the recovery room patient's SpO2 remained 97% on room air with no evidence of wheezing. Inj. octreotide infusion was tapered off over next 24 h. Histological examination of resected specimen confirmed diagnosis of carcinoid tumour.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [160.0, 'cm']}",56.88197,54.03787,59.72607,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.99216 (in inches) - 60) = 56.88197 kg.
Hence, the patient's IBW is 56.88197 kg."
3539,10,Ideal Body Weight,physical,decimal,pmc-6330755-1,Extracted,"A 69-year-old Japanese man (height, 158 cm; weight, 72 kg; body mass index, 28.8 kg/m2) was referred to our hospital because a right parotid gland tumor had rapidly enlarged and developed spontaneous pain 1 month previously. He had noticed the swelling on the buccal region 1 year previously. He had a medical history of hypertension and type 2 diabetes mellitus; he had also undergone surgical resection for gastric lipoma (15 years ago) and urothelial carcinoma (7 years ago). He was receiving oral medication for hypertension and type 2 diabetes mellitus. Medical follow-up revealed no recurrence of urothelial carcinoma. He was living with his wife and had been smoking cigarettes for 30 years, but quit 9 years ago. He had consumed one beer per week for over 40 years. His family and environmental history were unremarkable, and his employment history was not available. At admission, his blood pressure was 164/86 mmHg, but his other vital signs were normal: temperature, 36.4 °C; pulse, 80/minute; respiratory rate, 12/minute with O2 saturation of 100% at room air. The physical and neurological examinations were unremarkable except for tenderness in the region of his right parotid gland. The results of complete blood count, serological test, and dipstick urine test were within normal limits.
A computed tomographic examination showed a mass of 5-cm diameter located in the superficial lobe of his right parotid gland (Fig. a–b), and the mass had solid and cystic components based on contrast imaging (Fig. c). Serum levels of squamous cell carcinoma antigen and soluble interleukin-2 receptor were within reference limits. WT was clinically suspected based on the location in the tail of the right parotid gland, cystic morphology, gender, and age; however, a malignant salivary gland tumor could not be excluded. Superficial parotidectomy was performed for diagnosis and treatment. On gross examination, the formalin-fixed mass was solid, and the cut surface of the tumor had a grayish appearance (Fig. a). No fluid content was observed. A whole-mount preparation of the mass was performed. On histological examination, the mass showed typical focal features of WT, that is tubulocystic growth of bilayered, columnar, and oncocytic epithelium associated with abundant lymphoid stroma (Fig. b). In the other portion of the tumor, approximately 60% of it, there were eosinophilic materials suggesting coagulation necrosis of the tumor; the materials were surrounded by a non-oncocytic epithelium comprising non-keratinizing squamous cells and mucinous cells (Fig. c–h). The non-oncocytic epithelium was associated with a fibrous stroma or granulation tissue, but not with abundant lymphoid stroma (Fig. e). Granulomatous inflammation involving foreign body-type giant cells was also seen. The non-oncocytic epithelium showed neither distinct cellular atypia nor apparent invasive growth, but the fibrosis adjacent to the non-oncocytic epithelium showed a desmoplastic reaction. Thus, low-grade MEC could not be excluded. On immunohistochemical examination, the squamoid cells in the MEC-like lesions were positive for cytokeratin 5 (CK5) and p63, and mucinous cells were negative for these markers (Fig. h). The necrotic materials were diffusely positive for epithelial markers (AE1/AE3 and cytokeratin 7) and negative for CK5 and p63. The Ki-67 positive ratios in the WT and MEC-like components were similar; both components’ ratios were less than 5%. No diffuse immunoreactivity of p53 was observed. Results of FISH showed MAML2 gene rearrangements were not present in the typical portions of WT and the MEC-like lesion (Fig. i). Therefore, we diagnosed this tumor as a metaplastic or infarcted WT. Our patient was discharged without sequelae and was disease-free 8 months after the surgery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [158.0, 'cm']}",55.07095,52.3174,57.8245,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.20476 (in inches) - 60) = 55.07095 kg.
Hence, the patient's IBW is 55.07095 kg."
3540,10,Ideal Body Weight,physical,decimal,pmc-5502335-1,Extracted,"A 25-year-old woman with obesity (body mass index (BMI) 40.1 kg/m2, 158
cm, 100 kg) with a history of polycystic ovary syndrome, iodine allergy and gastritis
was admitted in 2005 to receive the LAGB procedure. The band was placed
laparoscopically via the pars flaccida technique. With an uneventful
post-operative course the patient was discharged on the third day. After several
months and numerous adjustments of the band the patient’s weight dropped to
only 95 kg. The patient reported occasional malaise, feverishness, and recurrent
upper respiratory tract infections. In 2008 she was readmitted to the surgery
department because of fever and signs of port site infection. The port was therefore
removed and the patient was discharged after a day. Occasional malaise and
feverishness appeared after a few months with unknown origin. In October 2010 a
gastroscopy did not reveal signs of a functioning band or its erosion. In January
2011 the patient was readmitted to another surgical department with a suspicion that
the band infection may be the cause of the patient’s recurring symptoms. A
laparoscopy with conversion to laparotomy was performed and the band was removed.
Bacterial culture revealed an E. coli band infection and proper
targeted antibiotics were administered. During the postoperative follow-up minimal
surgical wound infection was reported. On the 8th day the patient was
discharged. After 2 weeks the patient returned with hectic fever, elevated levels of
white blood cell counts (WBC) and C-reactive protein (CRP). An abdominal computed
tomography (CT) scan revealed peritoneal adhesions, abdominal and mediastinal
lymphadenopathy, and left pleural effusion. Despite the broad-spectrum antibiotics
(cilastatin and linezolid) administered, the patient’s condition did not
improve. A chest CT scan showed increased parenchymal density which may have
suggested pneumonia. Therefore the patient was referred to the pulmonology department
for further investigation. Elevated levels of Ca-125 antigen, CRP, WBC,
γ-glutamyltransferase (GGTP), D-dimer, procalcitonin, hypoalbuminemia and IgA
deficiency were found. Bone marrow biopsy revealed only reactive changes due to
infection. No parasite infection was confirmed. Broad-spectrum antibiotics and
antifungal agents were continued without improvement. Due to IgA deficiency
immunoglobulin therapy was administered. The patient was prepared for surgery because
of sudden abdominal pain and signs of septic shock. Urgent laparotomy revealed
massive peritoneal adhesions with moderate ascites, swabbed for culture. The parietal
and visceral peritoneum along with the greater omentum was covered in small nodules.
Liver, omental and peritoneal surgical biopsy was performed, suspecting malignant
neoplasm. A histopathological examination of the specimen ruled out cancer or
lymphoma, yet revealed chronic granulomatous inflammation. Ziehl-Neelsen stain was
negative. After the surgery the patient was transferred to the intensive care unit.
Bronchial lavage and peritoneal effusion were tested for Mycobacterium
tuberculosis DNA and it came out negative. Suspecting atypical
mycobacteriosis (yet with negative peritoneal effusion culture), ethambutol,
clarithromycin and amikacin were introduced along with antifungal (posaconazole) and
antiparasitic agents. Due to severe malnutrition, total parenteral nutrition was
introduced. The patient’s status stabilized along with CRP and WBC levels.
Persisting fever was lowered after administering corticosteroids. Enteral nutrition
was introduced with a good effect, allowing the patient’s discharge. The
postoperative specimen (omentum fragment) was tested further genetically, revealing
M. tuberculosis DNA. Corticosteroids were immediately
discontinued, and isoniazid, rifampicin, pyrazinamide and streptomycin were
administered for 4 months. After completion of the therapy an abdominal CT scan did
not show any pathological findings. The fever and malaise withdrew. Nowadays the
patient does not present any symptoms.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3541,10,Ideal Body Weight,physical,decimal,pmc-8637043-2,Extracted,"A 48-years-old, 140 kg, 164 cm, BMI 52.1 kg/m2, ASA III female. She was hospitalized for symptomatic angina. Owing to a gigantic appetite mainly on rice and pasta, her weight gradually increased in the past 20 years. Both her parents and sibling 3 were over obese. She had a history of hypertension (Bisoprolol 5 mg, Amlodipine 10 mg, and Olmesartan 40 mg), OSA, Diabetes, fatty liver and umbilical hernia, aortic stenosis and hypercholesterolemia. Preoperative airway assessment included a Mallampati class III, a 7.0 cm thyromental distance, a 5 cm interincisor distance and a 41 cm neck circumference. Physical examination showed nutritional obesity and mild cyanosis of the lips. Hematologic tests shows: WBC 10.93 × 109 /L, NEU% 0.798, CRP 11.7 mg/mL. CT showed fatty liver, umbilical hernia and dilatation of surrounding intestine. Admission diagnosis: Morbid obesity, Umbilical hernia, Hypertension, Fatty liver.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [164.0, 'cm']}",56.00401,53.20381,58.80421,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 164.0 cm, which is 164.0 cm * 0.393701 in/cm = 64.56696 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.56696 (in inches) - 60) = 56.00401 kg.
Hence, the patient's IBW is 56.00401 kg."
3542,10,Ideal Body Weight,physical,decimal,usmle-1336,Extracted,"A 62-year-old man is brought to the emergency department because of right-sided weakness and subjective decreased sensation that started 30 minutes ago. The patient reports that his symptoms started to ease 5 minutes after onset and have now completely resolved. He has hypertension, hyperlipidemia, and type 2 diabetes mellitus. He has smoked one pack of cigarettes daily for 40 years. His current medications include lisinopril, metformin, and sitagliptin. He is 183 cm (6 ft 0 in) tall and weighs 105 kg (220 lb); BMI is 32 kg/m2. He appears well. His temperature is 36.5°C (97.7°F), pulse is 80/min, and blood pressure is 150/88 mm Hg. Neurological examination shows no abnormalities. Cardiac examination shows regular rate and rhythm and a left-sided carotid bruit. Complete blood count, serum glucose, and electrolytes are within the reference ranges. An ECG shows sinus rhythm and left axis deviation. A CT scan of the head without contrast shows no abnormalities. Carotid doppler ultrasound shows 45% stenosis in the left carotid artery and 15% stenosis in the right.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [183.0, 'cm']}",77.70874,73.8233,81.59418,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 183.0 cm, which is 183.0 cm * 0.393701 in/cm = 72.04728 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (72.04728 (in inches) - 60) = 77.70874 kg.
Hence, the patient's IBW is 77.70874 kg."
3543,10,Ideal Body Weight,physical,decimal,pmc-2930169-1,Extracted,"In March 2007, a 65-year-old man with ADPKD, and consequently underwent hemodialysis since June 2001, was admitted to our hospital with symptoms of poor oral intake due to abdominal distention. His daily urine volume was approximately 300 mL and his abdomen was distended, with a maximum circumference of 105 cm. His weight and height were 63.8 kg and 170 cm, respectively. The laboratory findings were as follows: hemoglobin, 11.7 g/dL; albumin, 3.2 g/dL; BUN, 38 mg/dL; creatinine, 6.5 mg/dL; and total cholesterol, 206 mg/dL. A computed tomography (CT) of the abdomen revealed markedly enlarged polycystic kidneys bilaterally and multiple liver cysts. The renal volumes, appearing as an ellipsoid on CT images, were 3,309 mL and 3,173 mL on the right and left sides, respectively, according to the following formula: (π/6) × (length × width × depth).
Written informed consent was obtained from the patient. A TAE was performed in March 2007. This procedure was performed through the right femoral artery using the Seldinger technique, which involved the insertion of a Terumo guide wire (Radiofocus M; Terumo, Tokyo, Japan) and a 5-Fr Cobra catheter (Cook, Bloomington, IN) under local anesthesia. The arteriogram before the renal TAE showed bilateral narrowing (left > right), and stretched the renal arteries. Absolute ethanol was injected via the coaxial catheter (Progreat microcatheter system; Terumo, Tokyo, Japan) into the right renal artery. Seven mL of ethanol with 2 mL of Lipiodol was used to detect reflux of the radiolucent ethanol. After 5 minutes, the right renal artery was completely embolized. At this time, a renal TAE was performed on one side of the kidney only because the patient will only want to repeat the procedure on the contralateral kidney if the results of the first TAE are good. A second TAE of left renal artery was performed in March 2008. The procedure was the same as the previous TAE. At this time, we used a balloon catheter to prevent the reflux of the ethanol. After performing a selective renal arteriography, a 5-mm-diameter, 2-cm-long, 3-Fr balloon catheter (Savvy; Cordis Europe, Roden, The Netherlands) was positioned in the main renal artery. With the balloon inflated, 3 mL of ethanol was slowly injected for complete embolization ().
After the TAE, the patient experienced abdominal and lower back pain, which were ameliorated with opioids (pethidine - 25 mg three times a day for 2 days). The patient developed a fever the next day, which was controlled by a non-steroidal anti-inflammatory agent. He recovered and was discharged three days after the TAE. The poor oral intake due to abdominal distention was relieved one month after the TAE. Over the course of an 18 month follow-up period, the patient's general condition improved. His kidney size decreased bilaterally after the TAE (). The abdominal maximum circumference was reduced from 105 to 80 cm. The patient's dry weight decreased from 63 to 58 kg and hypertension did not develop. The daily 300 mL urine output did not change. The patient's serum hemoglobin and cholesterol levels did not change, but the albumin level increased slightly (). In summary, the patient experienced no recurrent symptoms or complications at 18 months after treatment.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3544,10,Ideal Body Weight,physical,decimal,pmc-4050074-1,Extracted,"In May 2013, a 32-year-old woman was referred to our hospital because of abnormal findings on a chest X-ray. She had been healthy until one month before, when a cough and intermittent chills developed. She was a current smoker but denied use of illicit drugs or other relevant medical history.
She had no familial history of TB and denied a contact with a person with TB infection. She acted with a touring company for five years. On examination, she appeared well. Her body weight was 69 kg, height 168.2 cm, temperature 36.2℃, blood pressure 123/80 mm Hg, pulse 78 beats per minute, and oxygen saturation 100% while breathing ambient air. Laboratory results were normal. A human immunodeficiency virus antibody test was negative.
A chest radiograph and computed tomography scan of the chest revealed uniform-sized small nodules randomly distributed throughout both lungs (). We performed bronchoalveolar lavage (BAL) and transbronchial lung biopsy at the anterior segment of the right upper lung.
The next day, the microbiological investigation of BAL fluid by TB polymerase chain reaction gave a positive result. We therefore diagnosed the patient with miliary TB and treated her with isoniazid, rifampicin, ethambutol, and pyrazinamide. She was discharged without complication. Two weeks after bronchoscopy, Mycobacterium tuberculosis was isolated from the liquid media of the BAL specimen. We then performed a reverse hybridization-based LPA and a solid-media drug sensitivity test (DST). The patient complained of myalgia and chills for two weeks.
One day later, the LPA revealed that the pathogen had mutations in the katG and rpoB genes (), so the patient was suspected to have miliary TB caused by MDR-TB pathogen. Her antituberculous treatment was changed to ethambutol, pyrazinamide, kanamycin, moxifloxacin, prothionamide, and cycloserine. A solid-media DST performed in the Korean Institute of TB using the absolute concentration method was consistent with MDR-TB eight weeks after the isolation of Mycobacterium tuberculosis from the BAL. The solid-media DST report was delayed because of contamination of the specimen. It showed the pathogen to be resistant to ethambutol and streptomycin in addition to isoniazid and rifampicin.
Finally, the patient was diagnosed with miliary TB caused by MDR-TB pathogen. Her antituberculous therapy has been maintained with the regimen described above with the exception of ethambutol. Three months after beginning treatment for miliary TB, the patient did not complain of any symptoms and the follow-up chest plain X-ray showed that the disease had partially resolved compared with the initial presentation ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [168.2, 'cm']}",59.80717,56.81681,62.79753,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 168.2 cm, which is 168.2 cm * 0.393701 in/cm = 66.22051 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.22051 (in inches) - 60) = 59.80717 kg.
Hence, the patient's IBW is 59.80717 kg."
3545,10,Ideal Body Weight,physical,decimal,pmc-6882602-1,Extracted,"A 24-year-old man with MFS-related cardiovascular complications was admitted to our Internal Medicine Department because of 3 consecutive episodes of acute decompensated HF with reduced ejection fraction (ADHFrEF) from 2014 through 2017. His remaining medical history includes arterial hypertension, dyslipidemia, hyperthyroidism, anaphylactic shock due to flecainide, and previous tabagic habit.
MFS diagnosis was made in 2010 when ascending aorta and aortic valve substitution with mechanical prosthesis were performed due to type A acute aortic dissection in presence of family history—mother, father, and 3 sons with MFS. During intraoperative period, inferior acute coronary syndrome occurred and was treated with coronary artery bypass graft surgery.
On May 2014, mechanical descending aorta and aortic arch prosthesis implantation were performed due to chronic dissecting aneurysm. Peri-aortic hematoma and medullary ischemia complicated surgery and caused lower limb paraplegia, dolorific and thermal hypoesthesia, and rectal incontinence. After 2 months, during his first admission for ADHFrEF, laboratory tests were notable for N-terminal pro-BNP (NT-proBNP) of 12,000 pg/mL and transthoracic echocardiogram showed normal prosthesis function, dilatation of all cardiac chambers (mainly the left ones) with moderate mitral and tricuspid insufficiency, left ventricular hypertrophy, inferior wall akinesis, septal dyskinesis, and hypokinesis of the remaining walls with severe left ventricular ejection fraction (LVEF) reduction −20%. He was treated with intravenous diuretics and internal cardiac defibrillator (St. Jude Ellipse DR, DDD mode) without cardiac resynchronization therapy (electrocardiogram criteria not met) and discharged on maximal medical therapy (furosemide, carvedilol, ramipril, spironolactone, digoxin, and amlodipine).
New episode of ADHFrEF occurred on august 2017. Notable admission laboratoristic values included NT-proBNP of 2719 pg/mL and midregional-proadrenomedullin (MR-proADM) of 1.61 nmol/L, whereas transthoracic and transesophageal echocardiogram showed an LVEF of 35%, normal prosthesis function, severe tricuspid regurgitation, and rupture of the anterior leaflet of the chordae tendineae with severe mitral regurgitation. Patients were treated yet with intravenous diuretics and digoxin and discharged on optimal medical therapy (furosemide, carvedilol, ramipril, spironolactone, digoxin, and amlodipine).
Lastly, he was readmitted to our Internal Medicine Department on November 2017 due to third episode of ADHFrEF and infected mediastinal fluid collection secondary to 1 month before severe valvular insufficiency surgical correction with mitral mechanical prosthesis implantation (31-mm ST Jude) and De Vega tricuspid annuloplasty.
Physical examination was notable for blood pressure 120/80 mm Hg, pulse 82 bpm, respiratory rate 26 apm, O2 saturation 87% on room air with orthopneic obligatory position, and Marfanoid habitus (weight 147 kg, height 2.2 m). Cardiopulmonary evaluation revealed metallic second heart sound, stony dull percussion with reduced tactile vocal fremitus and crackles at the basis of the lungs, widely diminished vesicular breath sounds, presence of abundant ascites, and leg swelling.
Notable laboratoristic values included NT-proBNP of 10,132 pg/mL and MR-proADM of 2.36 nmoL/mL.
Arterial blood gas analysis revealed severe hypoxemia with respiratory and metabolic alkalosis (pH 7.56, pO2 46 mm Hg, pCO2 24.8 mm Hg, HCO3− 21.9 mmol/L, alveolar-arterial gradient 31 mm Hg). Although electrocardiogram highlighted atrial fibrillation with ventricular rate of 80 bpm, left ventricular hypertrophy, and inferolateral subepicardial ischemia, transthoracic echocardiogram showed the same features as the previous except for LVEF of 30%, presence of mitral mechanical prosthesis, with paravalvular leak and mean gradient of 9 mm Hg, and mild tricuspid insufficiency (Fig. A and C).
Hilar congestion with cardiomegaly, right upper lobe pulmonary consolidation, and infected mediastinal fluid collection have been shown on chest x-ray and high-resolution computed tomography, respectively.
Patient was treated with intravenous furosemide 250 mg q.d., canrenone 100 mg q.d., piperacillin/tazobactam 4.5 g q6h, and teicoplanin 12 mg/kg b.i.d., then 12 mg/kg q.d. On day 9, once reaching hemodynamic stabilization, sacubitril/valsartan midrange dose of 49/51 mg b.i.d. has been added to carvedilol 3.125 mg b.i.d., spironolactone 100 mg q.d., furosemide 250 mg q.d., and digoxin 0.25 mg q.d.
On 1-month follow-up sacubitril/valsartan has been increased to 97/103 mg b.i.d. for patient's good clinical condition, allowing persistent and progressive clinical, laboratory (NT-proBNP reduction and MR-proADM increase), echocardiographic-LVEF increase (42% vs 30%), left ventricle end-systolic diameter, left ventricle end-diastolic diameter, left ventricular mass, and left ventricular mass index reduction, and quality of life improvement without new episodes of ADHFrEF until 9-month follow-up (Fig. B and D; Table ). Because of the lack of a specific dosage regimen for sacubitril/valsartan in MS-related cardiomyopathy, we used the recommended therapeutic scheme.[","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [2.2, 'm']}",111.21271,105.65207,116.77335,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 2.2 m, which is 2.2 m * 39.3701 in/m = 86.61422 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (86.61422 (in inches) - 60) = 111.21271 kg.
Hence, the patient's IBW is 111.21271 kg."
3546,10,Ideal Body Weight,physical,decimal,pmc-6261077-1,Extracted,"The patient was a 50-year-old male, 173 cm tall, and 85 kg in weight (body mass index (BMI): 27.7 kg/m2). He had a medical history of urinary tract cancer, type 2 diabetes mellitus, hypertension, and Hashimoto's disease. He underwent a robot-assisted radical cystectomy in lithotomy position. The total operation time was 419 min. The operative position was lithotomy position with his lower leg flexed and elevated by soft stirrups. Continuous compression devices on both calves were used for venous thrombosis prophylaxis throughout the procedure. No bleeding-promoting drug was used before and after the surgery.
Sixteen hours after the surgery, he complained of severe bilateral lower leg pain and swelling. Initial evaluation of lower extremities revealed foot drop, swelling and tightness of the anterolateral aspects, and stretch pain on passive ankle planter flexion. No remarkable finding was appreciated on the posterior aspects of his lower legs. Serum creatine kinase was elevated to at 28000 U/l. The compartment pressure was measured by an arterial line set with simple 18-gauge needle under the diastolic blood pressure of 98 mmHg. The measurement was performed at three places of each compartment, and the average value was recorded. The anterior and lateral compartment pressures in both legs had increased to 200 mmHg despite normal posterior compartment pressure (35 mmHg) or thigh compartment pressure (35 mmHg). Contrasting computed tomography (CT) showed swelling of the bilateral muscles in the anterior and lateral compartments without contrasting effect compared to the posterior compartments (). Based on these findings, WLCS localized in the anterior and lateral compartments was diagnosed.
An emergency fasciotomy was performed twenty hours after initial surgery. Anterior and lateral compartments were released with single incision (). Discoloration of the muscles improved within a few minutes after the fasciotomy (). Shoe-race procedure was added to prepare for secondary wound closure (). Symptoms such as unbearable pain or decreased sensation were drastically improved after the fasciotomy. The serum creatine kinase decreased and normalized eight days after the surgery. He recovered well without any motor and sensory dysfunction in both lower extremities. The fasciotomy wound was closed on the ninth postoperative day without additional stage procedure. Three months after the surgery, he had no neuromuscular dysfunction.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.0, 'cm']}",68.65362,65.22094,72.0863,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.0 cm, which is 173.0 cm * 0.393701 in/cm = 68.11027 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.11027 (in inches) - 60) = 68.65362 kg.
Hence, the patient's IBW is 68.65362 kg."
3547,10,Ideal Body Weight,physical,decimal,pmc-6232618-1,Extracted,"An 83-year-old man was admitted to our hospital for evaluation and management of a symptomatic liver mass. His medical history included diffuse large B-cell lymphoma, which was treated with rituximab + pirarubicin + cyclophosphamide + vincristine + prednisone therapy at 81 years old, and had bladder cancer (resected at 67 years) on follow-up. After resection of the bladder cancer, no recurrence was detected for 16 years. Liver dynamic computed tomography (CT) showed a low-density mass in the segment (S) 4 area, measured 40 mm in diameter. The density of the tumor was well enhanced in the arterial phase and washed-out in the portal phase. (a–d). The hepatobiliary phase of Gd-EOB-DTPA-MRI shows tumor nodules in the liver with low intensity (e). On positron emission tomography (PET)-CT, the maximum standard uptake value of the tumor in S4 of the liver was 3.2 (f). MRI and PET-CT confirmed a single liver tumor that was 40 mm in diameter and located in the S4 region. Liver metastasis of malignant lymphoma was suspected because of the patient’s medical history. Therefore, we performed a liver biopsy preoperatively. The patient was diagnosed with hepatocellular carcinoma (HCC) based on the biopsy results and imaging findings.
Upon presentation, the patient was afebrile, had no history of weight loss, and his appetite was good. His height was 166 cm, body weight 72 kg, and BMI 26.12. He has no drinking history. In a preoperative indocyanine green (ICG) test, the ICGR15 was 76.2%. The total bilirubin level was 1.1 mg/dL and the direct bilirubin level was 0.2 mg/dL. The serum albumin level was 4.7 g/dL and prothrombin activity was 96.3%. The Child–Pugh (CP) score was 5 points, which indicated a grade of A. The degree of liver damage was equivalent to A in accordance with the scoring system of the Liver Cancer Study Group of Japan. shows the patient’s laboratory data on admission. The hepatic uptake ratio of 99mTc-galactosyl human serum albumin (GSA) by liver scintigraphy (LHL15) was 0.931 and the heart uptake ratio (HH15) was 0.482. The maximal removal rate of 99mTc-GSA (GSA-Rmax) was 0.874 mg/min. GSA-Rmax in the predicted residual liver (GSA-RL) was greater than 0.765 mg/min, which was within the range considered safe for surgical procedures.
Despite this finding, Child–Pugh classification and 99mTc-GSA liver scintigraphy did not show any abnormal findings, and there was no background disease. Antibody against hepatitis C virus and hepatitis B virus surface antigen were negative. The serum anti-mitochondrial antibody and anti-nuclear antibody were negative. The serum tumor markers alpha-fetoprotein, carcinoembryonic antigen, and cancer antigen 19-9 were within the and normal range, but the protein level induced by vitamin K absence-II levels was increased (92 mg/dL). Therefore, we diagnosed constitutional ICG excretory defect with HCC and decided to perform radical surgery. Therefore, the patient underwent partial hepatectomy (S4). Pathologically, the tumor was diagnosed as moderately differentiated HCC (a). There was expansion and bleeding of perisinusoidal cells and an atrophic hepatic cord in the background of liver tissue. Because of previous chemotherapy, the diagnosis of sinusoidal obstruction syndrome (SOS) of the liver was established (b). After partial hepatectomy (S4), the postoperative course was uneventful and the patient was discharged on the 8th postoperative day. The patient remains in good general condition.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [166.0, 'cm']}",62.31505,59.1993,65.4308,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 166.0 cm, which is 166.0 cm * 0.393701 in/cm = 65.35437 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.35437 (in inches) - 60) = 62.31505 kg.
Hence, the patient's IBW is 62.31505 kg."
3548,10,Ideal Body Weight,physical,decimal,pmc-4421183-1,Extracted,"An 18-year-old woman had been well until 9 months previously. Then, she developed haemoptyses and haematuria. Haemoglobin was 9.4 g/dl, creatinine 2.3 mg/dl, anti-GBM antibodies 57 U/l (normal <10), while c-ANCA, p-ANCA, ANA and ds-DNA antibodies were negative. A renal biopsy was performed, and light microscopy revealed 10 glomeruli, with cellular and partly fibrinoid crescents in all glomeruli. Immunofluorescence showed linear deposition of IgG and C3 at the glomerular basement membrane. Treatment had been started with 100 mg prednisolone per day.
The patient was transferred to our hospital 3 weeks later, when her serum creatinine had risen to 527 μmol/l and urinary protein excretion was 9.17 g/24 h. Physical examination was normal except massive oedema of the legs. Weight was 71 kg, height 181 cm, blood pressure 120/80 mmHg and pulse rate 66/min.
Haemodialysis and daily plasmapheresis (each 4000 ml replaced by 30 g/l albumin) were started 3 days after admission. Additionally, the patient was treated with oral cyclophosphamide 200 mg/day adjusted to leukocyte counts. Prednisolone 100 mg/day was continued for 1 week and then tapered.
Because of the lack of clinical response to this therapy, a single dose of rituximab 1000 mg was administered intravenously on Day 9 after admission. Serum creatinine was 822 μmol/l on Day 14 after 1 week without dialysis. Anti-GBM antibodies could no longer be detected on Day 15 and later. Four weeks after administration of rituximab, CD19/20 cell expression monitored by flow cytometry was negative. In Week 4, plasmapheresis was performed again but renal function did not improve. Haemodialysis had to be resumed in Week 5, persumably because treatment was started in a very late stage of the disease.
In Week 6, the patient had a generalized seizure and had to be admitted to the intensive care unit. MRT of the brain showed enhanced subcortical and pontal signal intensity (Figure ). The neurological diagnosis was progressive leukoencephalopathy. Examination of the spinal liquor showed no cells and virological examination by PCR disclosed no polyoma virus replication in the liquor. The patient was treated with clobazam and lamotrigine. A second MRT of the brain was performed in Week 10 revealing improvement in the subcortical and pontal signal intensities.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [181.0, 'cm']}",71.39772,67.82783,74.96761,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 181.0 cm, which is 181.0 cm * 0.393701 in/cm = 71.25988 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (71.25988 (in inches) - 60) = 71.39772 kg.
Hence, the patient's IBW is 71.39772 kg."
3549,10,Ideal Body Weight,physical,decimal,pmc-6040299-2,Extracted,"A 39-year-old woman came to endocrinology clinic with a complaint of hirsutism started 4 years ago, alongside with oligomenorrhea followed by amenorrhea two years ago. There was no temporal baldness or deepening voice.
The patient was treated for a period of 3 months with combined oral contraceptive pills COCP and cyproterone acetate without improvement in symptoms, 6 months earlier to admission.
She was married, got 3 children and was nonsmoking or alcohol consuming. She was diagnosed 5 years ago with rheumatoid arthritis and treated for only one month with prednisolone and methotrexate.
On examination, she seemed well. The blood pressure was 120/80 mm Hg, the height 155 cm, the weight 65 kg, and the body mass index BMI 27.1 (overweight). The Ferriman-Gallwey score for hirsutism estimation was 16 (4 points for each chin, upper lip, low abdomen, and medial thigh), clitoromegaly (1 cm by 0.5 cm); she had no acanthosis nigricans or frontal baldness. Otherwise, she had normal findings.
Laboratory studies revealed a hemoglobin concentration of 10.3 g/dL, ferritin 10 ng/mL, serum sodium level of 138 mEq/L, and potassium level of 4.15 mEq/L. An automated chemistry panel showed normal findings except for fasting glucose 119 mg/dL. She started metformin therapy and ferrous replacement. Hormonal studies were as in .
Transvaginal ultrasonography showed that ovaries measured 3.3 by 2 cm and 3.2 by 2 cm for right and left ovary, respectively, without masses. CT scan for adrenals was within normal also and right ovary measured 3.8 by 2.3cm as shown in .
Since catheterization of the adrenal and ovarian veins was not available, the diagnostic and therapeutic options were explained to the patient and giving that she was not interested in future fertility, she underwent laparoscopic exploration for oophorectomy.
Pathologic report sowed 2.5 cm of Leydig cell tumor in the right ovary, while the left ovary was within normal as shown in (). Testosterone was normalized after surgery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3550,10,Ideal Body Weight,physical,decimal,pmc-4234795-1,Extracted,"This was a case of a 16-year-old female patient, with non-relevant family history, ASA-I with chronic rhino-sinusitis posted for functional endoscopic sinus surgery. At the pre-anesthetic clinic, the patient presented with a complaint of nasal blockade for 3 months without any fever.
General examination conducted by the anesthetist on duty showed strabismus of the left eye, rest other systemic examination was within the normal limits. No prior exposure to anesthesia was recorded. The patient gave a negative history of any drug use besides those employed for treatment of sinusitis. The body weight recorded was 50 kg and height corresponded to 155 cm and the body mass index was calculated to be 20.8 kg/m2. Blood investigations revealed hemoglobin of 10.4, total leucocyte count of 11,000 and platelets of 156,000. Random blood sugar was 86 mg/dl. Vital parameters as noted in the ward chart on the day of surgery were within the normal limits and a temperature of 36.8°C (axillary) was mentioned.
The patient was taken to the operating room, routine monitors in the form of non-invasive blood pressure (BP), SpO2 probe and three-lead electrocardiogram were applied. Vital parameters prior to induction were within normal limits.
Anesthesia was induced with intravenous midazolam 1 mg, fentanyl 100 μg, propofol 100 mg and vecuronium bromide 5 mg. Patient was mask ventilated by a mechanical ventilator to achieve normocarbia with O2 and N2O and isoflurane (0.9-1 MAC) for approximately 3 min. The trachea was then intubated using endotracheal tube no. 7 mm internal diameter. After confirming endotracheal placement, patient was mechanically ventilated with a tidal volume of 400 ml, respiratory rate 12/min maintaining ETCO2 32-35 mmHg and an esophageal temperature probe was inserted. The patient was maintained on O2, N2O and isoflurane (MAC 1).
Immediately following intubation, the ETCO2 rose up to 60 mmHg, heart rate 120/min, BP 130/90 mmHg, SpO2 100% and a temperature of 37.8°C were noted. The temperature within a few seconds rose to 38.2°C and within a minute it reached 38.9°C. Isoflurane was stopped and 100% oxygen administered. The surgery was halted and additional assistance was sought from the senior anesthetists in the operating theatre complex.
Intravenous paracetamol infusion and cold sponging were started simultaneously. The ventilator settings were also readjusted to facilitate normocarbia. The ETCO2 came down to 53 mmHg gradually, but the temperature still continued around 38.9°C. An arterial blood gas (ABG) sample was withdrawn, which showed respiratory acidosis with a pH of 7.30, pCO2 of 52 mmHg, bicarbonates of 24 mEq and pO2 of 100 mmHg and K+ of 5 mEq/L. Supportive management was aggressively continued and vital parameters were monitored continuously. The patient was intermittently given intravenous midazolam 1 mg and fentanyl 50 μg as bolus twice and N2O was continued to prevent awareness.
After 50 min, the temperature came down to 38.6°C and the ETCO2 normalized completely. In the next 20 min, there was a steady decline in the body temperature and it was recorded to be 38.2°C. The surgery was recommenced by employing intravenous propofol as an infusion in a manually controlled infusion pump while maintaining the patient on O2 and N2O along with intermittent boluses of intravenous fentanyl and vecuronium. The temperature showed a steady pattern of decline to 38°C and then to 37.8°C towards the end of the surgery. An ABG sample was re-sent which depicted a corrected pH of 7.35, pCO2 of 42 mmHg, bicarbonates of 22 mEq and pO2 of 100 mmHg.
At the end of the surgical procedure, the anesthesia was reversed and the patient was kept for further observation in the operating room for 15 min. The reversal was overall uneventful and the patient was shifted to the post anesthesia care unit where the vital parameters were found to be within normal limits and the axillary temperature was 37.7°C.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3551,10,Ideal Body Weight,physical,decimal,pmc-6528295-2,Extracted,"A 41-year-old female patient (height, 168 cm; weight, 72 kg; BMI, 25.5) had undergone right mastectomy for breast cancer (T2N2M0 stage 3) and immediate reconstruction surgery with an LD flap. After 4 years, the patient exhibited an acutely developed palpable mass at the back donor site and was examined at the surgery department in our center. Physical examination showed the development of a solid lesion that could not be aspirated. The patient did not have any specific triggering event or blunt trauma or any underlying diseases aside from uterine myoma and ovarian cyst. The patient was not under any medication. Chest CT confirmed the presence of an enlarged cystic mass (size 9 × 4 cm) in the right posterior chest wall, and surgical excision under general anesthesia was planned. During surgical excision, a capsule-enveloped hematoma was identified. A definitive diagnosis was made based on the results of pathological examination. Biopsy revealed no evidence of malignancy or benign cyst with fibrosis (Fig. ). There was no recurrence or complication for 3 years.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [168.0, 'cm']}",59.62607,56.64477,62.60737,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.14177 (in inches) - 60) = 59.62607 kg.
Hence, the patient's IBW is 59.62607 kg."
3552,10,Ideal Body Weight,physical,decimal,pmc-3710944-1,Extracted,"A 31-year-old man visited our clinic with chronic abdominal pain that persisted for approximately one year. He was 170 centimeters tall, and his body weight was 53 kilograms. He was a car mechanic, and had no specific medical history or trauma history. At first, the pain started after taking a late-night snack. It was described as being severe squeezing in nature, which located on the right side of the periumbilical area that had persisted all day long. He did not have history of any sports activities. The pain intensity in visual analogue scale (VAS) was about 60-70 of 100. He had been on medication for gastrointestinal tract with nonsteroidal anti inflammatory drugs (NSAIDs) at the other hospital for over two months. The medication had no effect at all. For further evaluation, abdominal ultrasonography, abdominal computed tomography (CT), contrast media study of small and large intestine, endoscopy, and colonoscopy were done. Laboratory tests and simple x-rays of chest, abdomen, and lumbar spine were also performed. The examinations showed no specific abnormal findings. The patient was examined in supine position, and the site of maximum tenderness was identified; then he was asked to fold his arms across the upper chest, and to sit half way up. He complained greater tenderness with continuous local palpation, which is called Carnett test positive. It implies that the pain originated from the abdominal wall []. For both diagnostic and therapeutic purpose, we decided to make an injection of local anesthetics at the area of rectus muscle where the entrapment of cutaneous nerve could occur. The patient was placed in supine position. We conducted Carnett test again to find the maximal tender point. The transducer (Linear probe 12-5 Hz, HDI 5000, Philips, USA) was positioned in the midline first, to get a short axis view (anatomic transverse view) so that the medial border of the rectus muscle and the linea alba are visulized. Then the transducer moved laterally to get a view of the lateral end of the rectus muscle and the linea semilunaris (). The abdominal cutaneous nerve generally exists between the rectus abdominis and linea semilunaris, approximately 0.5-1.0 cm medial to linea semilunaris. Using the transverse scan, 25G 38 mm needle (BD Precision Glide™ Needle, Becton Dickinson Medical, Singapore) was advanced with the short axis in plane technique to reach the target area (). We injected 10 ml of 1% of mepivacaine with 10 mg of triamcinolone. The pain intensity in VAS decreased to 30 of 100 with a single injection. With one week of interval, booster injection was done. After the second injection, the pain intensity in VAS decreased to 0-10 of 100. He remained symptom free for 10 months.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3553,10,Ideal Body Weight,physical,decimal,pmc-8133044-11,Extracted,"A 51-year-old man (weight, 93 kg; height, 177 cm; BMI, 30 kg/m2) was scheduled to undergo eye surgery. He had a K-score of 3. MO was 3 fingers wide. No remarkable risk factors were identified. Cormack grade was 2. BURP was performed, and intubation was completed. No other difficulties were observed. The IDS score was 2, and the duration was 61 s. In patients with a long epiglottis, the vocal cord can be difficult to expose, even with much lifting effort. For novices like me, it is important to cooperate with the assistant to perform BURP.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [177.0, 'cm']}",72.27568,68.6619,75.88946,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 177.0 cm, which is 177.0 cm * 0.393701 in/cm = 69.68508 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.68508 (in inches) - 60) = 72.27568 kg.
Hence, the patient's IBW is 72.27568 kg."
3554,10,Ideal Body Weight,physical,decimal,pmc-8314493-1,Extracted,"A 70-year-old Japanese man without any major family and psychosocial history was referred to our hospital to continue treatment for DME. At the patient’s former hospital, his major symptom was repeated visual disturbance of both eyes due to DME, and he received sub-Tenon’s triamcinolone acetonide injection and intravitreal anti-VEGF injection. Sub-Tenon’s triamcinolone acetonide injections were once in both eyes, and intravitreal anti-VEGF injections were 12 times in both eyes every 2–3 months (4 times with 0.5 mg ranibizumab and 7 times with 2 mg aflibercept in the right eye and once with aflibercept in the left eye) during the 2.5-year follow-up period. At the patient’s former hospital, the last anti-VEGF therapies were injected in the left eye in July 2016 and the right eye in December 2016.
At the patient’s first visit to our hospital in January 2017, his body height and weight was 160 cm and 52 kg [body mass index (BMI) 20.3], respectively. His HbA1c level was 6.3 %, and he has been suffering from diabetes mellitus for 10 years with only diet therapy. His blood pressure was 120/61 mmHg, and he had no hypertension. Although he had hyperlipidemia (total cholesterol 244 mg/dl, LDL cholesterol 148 mg/dl), he did not receive any pharmacological treatments for it. He has been treated with donepezil hydrochloride for mild cognitive impairment in the neurology department of Tokyo Takanawa Hospital. However, because he works regularly and can attend a hospital by himself, he has no hindrance to daily life. In addition, there was no issue on financial and language/cultural challenges. A dilated fundus examination showed mild nonproliferative diabetic retinopathy [], with several small hemorrhages without macular edema, and his best corrected visual acuity was 1.0 in both eyes. The central subfield macular thickness (CMT) on spectral-domain optical coherence tomography (SD-OCT) was 279/320 μm (right eye/left eye).
Five months later, he noticed blurred vision in both eyes (visual acuity was 0.8 in both eyes), and a fundus examination showed significant macular edema in both eyes (CMT, 404/478 μm). In June 2017, for the first time at our hospital, the patient received 2-mg intravitreal aflibercept injections in both eyes 1 week apart (6 June in the right eye and 13 June in the left eye). No laser therapy was applied. After short-term anti-VEGF therapies to both eyes, his systemic condition remained the same. The treatment was effective in both eyes, and 1 month later, his CMT recovered to 277/321 μm, and his blurred vision disappeared (visual acuity was 1.0 in right eye and 1.2 in left eye). Three months after the first treatment at our hospital (1 September 2017), significant macular edema relapsed in both eyes (CMT, 403/463 μm; Fig. ), visual acuity was 0.8 in right eye and 1.0 in left eye, and he desired continuous treatment for both eyes. In October 2017, he received intravitreal aflibercept injections in both eyes 1 week apart (3 October in the right eye and 10 October in the left eye). One month after treatment (10 November), his subjective complaint of blurred vision disappeared (0.8 in right eye and 1.2 in left eye), and the CMT decreased to 280/315 μm (Fig. ). During this period, his HbA1c levels were measured and kept at 6.5% (3 October, 10 October, and 10 November).
Upon initiating the intravitreal injection in the operating room, we measured his blood pressure as 141/69 mmHg (3 October) and 135/70 mmHg (10 October) without blood-pressure-lowering drugs (Fig. a). However, on 12 November, just 2 days after a follow-up visit to our hospital, he complained of a severe headache and walked to the emergency department at Tokyo Takanawa Hospital. He complained of a severe headache on the right back side of his head and visual disturbance of the left visual field with no other systemic neuropathological symptoms. He had no external injury presumed as trauma antecedent and no other apparent causes leading to cerebral hemorrhage. His blood pressure was elevated at 195/108 mmHg, and computed tomography (CT) of the brain revealed the presence of a high-density area (2.5 × 3.0 cm) in the right occipital lobe indicating a subcortical hemorrhage (Fig. a). The patient was treated with an intravenous injection of nicardipine hydrochloride to lower his systemic blood pressure to < 140 mmHg for 2 days. On 13 November, CT showed no enlargement of the high-density area (data not shown). On 15 November, 3 days after the stroke, magnetic resonance imaging (MRI) revealed a peripheral low-intensity zone in the same region (T2*-weighted MRI, Fig. b) and a low-intensity area (diffusion-weighted MRI, Fig. a) in the occipital lobe that was consistent with the CT results. Additionally, magnetic resonance (MR) angiography revealed no vascular anomalies or malformation (Fig. b), and T2*-weighted MRI revealed no cerebral microbleeds, thus ruling out cerebral amyloid angiopathy (Fig. b). He was therefore diagnosed with a hypertensive cerebral hemorrhage of the occipital lobe. On 14 November, 2 days after the stroke, the patient began oral treatment with 80 mg/day telmisartan, which was continued for 3 days. Starting 17 November, the telmisartan dose was reduced to 40 mg/day. During this period, his blood pressure was maintained at < 130/80 mmHg, and his symptoms of severe headache disappeared, and visual disturbance of the left visual field was alleviated. Ten days later, he was discharged from Tokyo Takanawa Hospital, and 20 days after discharge he visited our hospital to receive a follow-up ophthalmological examination. Two months after the stroke (5 January 2018), visual field tests with Goldmann perimetry at our hospital showed no apparent left homonymous hemianopsia (Fig. ). Follow-up CT (14 February 2018; Fig. c) and T2*-weighted MRI (24 July 2018; Fig. d) examinations revealed that the cerebral hemorrhage had been absorbed, and the lesion had decreased in size. One year after the cerebrovascular stroke, the telmisartan was discontinued because his blood pressure had stabilized to a normal level and remained around 110/60 mmHg.
The patient received no anti-VEGF therapy for 4 months prior to 3 October 2017 because his macular edema did not relapse. We happened to determine his plasma VEGF levels before and after the intravitreal anti-VEGF injections (October 2017) via specific enzyme-linked immunosorbent assay (SRL, Tokyo, Japan; Fig. b). The patient’s plasma VEGF level was 28 pg/ml on 3 October, just before the intravitreal injection of aflibercept in the right eye. However, the level rapidly decreased to below the detection limit (< 20 pg/ml) on 10 October, just before the injection in his left eye. Notably, the levels on 10 November (2 days before the cerebral hemorrhage) and 10 December were also below the detection limit. On 25 January 2018, we confirmed that his plasma VEGF level had recovered to 41 pg/ml. Thereafter, we continued to follow the patient for DME and diabetic retinopathy, and no cerebral hemorrhage recurred.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [160.0, 'cm']}",56.88197,54.03787,59.72607,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.99216 (in inches) - 60) = 56.88197 kg.
Hence, the patient's IBW is 56.88197 kg."
3555,10,Ideal Body Weight,physical,decimal,pmc-6287602-1,Extracted,"A 79-year-old man was admitted to the Department of Nephrology, Kansai Electric Power Hospital on January 14, 2014, for proteinuria. He had been followed up for hypertension and dyslipidemia in a local clinic since the age of 50. He had experienced several vascular events, such as total occlusion in the common iliac artery at the age of 63 and two histories of cerebral infarction at the ages of 70 and 77. He had 30 years of smoking history but no alcohol habit. He had no family history of kidney disease except for one cousin showing end-stage renal disease of unknown etiology. During his initial admission to our hospital, his urine protein level was 5.4 g/g Cr, and serum albumin was 3.2 g/dL; he was discharged because his condition was stable. Ten months later, edema of his lower limbs worsened, and renal biopsy was performed on his second admission.
On the second hospitalization, physical examination showed the following: height of 169 cm, weight of 70 kg, body mass index of 24.5, and blood pressure of 180/88 mmHg. Laboratory findings revealed a nephrotic range of urine protein, 9.15 g/g Cr accompanying microscopic hematuria of dysmorphic 10 – 19 RBC/HPF, and total serum protein and albumin of 4.8 and 1.8 g/dL, respectively. Serum creatinine was 0.95 mg/dL, AST was 29 IU/L, ALT was 14 IU/L, and ALP was 188 IU/L. Serological examination revealed serum IgG, IgA, and IgM of 875, 344, and 52 mg/dL, respectively. Antinuclear and antineutrophil cytoplasmic antibodies were negative.
Lipid analysis revealed elevated total cholesterol (259 mg/dL), triglyceride (376 mg/dL), and LDL cholesterol (167 mg/dL) levels, and a low HDL cholesterol level (45 mg/dL). The serum ApoE level was 13.6 mg/dL (normal range: 2.8 – 4.6 mg/dL). An oral glucose tolerance test showed no abnormality, and his hemoglobin A1c was 5.7%. Although hypertriglyceridemia was marked, systemic abnormalities characteristic of hyperlipidemia, such as corneal opacities, xanthoma, and Achilles tendon hypertrophy, were not found. Moreover, the patient had no family history of hyperlipidemia and diabetes mellitus.
Light microscopy (LM) revealed that the specimens contained 27 glomeruli, 8 of which showed global sclerosis (29.6%). Most glomeruli showed segmental sclerosis, infiltration of foam cells containing lipid deposits in capillary lumen (a). In periodic methenamine silver (PAM)-stained sections, spike formation and bubbling were detected on the glomerular basement membrane (GBM) (c, d). Mild to severe arteriosclerosis and arteriolosclerosis were also seen. Fibrosis was observed in ~ 20% of the whole interstitial area. Intriguingly, Sudan III staining was strongly positive not only in the mesangial and infiltrating foam cells but also in the focal capillary lumen in the glomerulus (b). Immunofluorescence (IF) studies demonstrated subtle granular staining for IgG along the capillary wall; however, C3 was not detected (data not shown). Electron microscopic (EM) findings analysis showed electron-dense deposits (EDDs) with a variety of densities and distributions. Highly-dense deposits accompanied by spike formation identical to MN were seen in the subepithelial area (a, b). In the subendothelial area, highly dense EDDs were detected but in higher magnification, and microbubbles were contained (a, b). Effacement of foot process was also accompanied with these depositions. In addition, EM findings demonstrated that the capillary lumina was filled with lipid deposits that did not show lamellar formation similar to “lipid thrombi” in LPG.
Plasma ApoE phenotypes were analyzed by isoelectric focusing in polyacrylamide gel electrophoresis and immunoblotting analysis as previously reported [, ]. The patient’s sample showed the position of ApoE2/2 (a, Lane 1).
The APOE genotype was determined by restriction fragment length polymorphism (RFLP) analysis as described previously [, ]. The PCR products were digested with the restriction enzyme HhaI. Genotype ε2/2 in the patient was identified by 91- and 83-bp fragments (b, Lane 1). The ApoE Toyonaka (Ser197Cys) as shown in d was also confirmed by RFLP analysis digested with SacI (c). Genomic DNA was amplified by polymerase chain reaction (PCR) using oligonucleotide primers, sense 5′-CGTGCGGGCCGCCACTGTGAGCT-3′ and antisense 5′-TCGCATGGCTGCAGGCTTCGGCGTTC-3′. The 335-bp fragment after cleavage by SacI suggested normal c.644C of ApoE in codon 197 (Lane 3). The 358- and 335-bp fragments after cleavage by SacI showed a heterozygous novel mutation of ApoE Toyonaka (Lane 2). Direct sequencing of APOE DNA was performed as described previously []. Based on the results, we identified a homozygous polymorphism at codon 158 (e2/2: c.526 C>T: Arg158Cys) (data not shown) and a heterozygous missense mutation (C to G) in exon 4 leading to an amino acid substitution Cys (TGC) for Ser (TCC) at codon 197 (c.644 C>G: p.S215C: Ser197Cys) (d). All these findings were the same as that of a previous case of ApoE2/2 and ApoE Toyonaka showing MN-like glomerular histology [6].
For hypertriglyceridemia, fibrate 400 mg/day was started. Obtaining the results of the IF and EM studies, which did not deny immune-related MN like lesions, PSL 10 mg/day and cyclosporine (CyA) 75 mg/day for NS were started. These treatments brought about a substantial improvement of hypertriglyceridemia and complete remission of NS by 300 days after admission. During maintenance therapy with oral PSL 5 mg and CyA 75 mg/day, he had cerebral infarction and aspiration pneumonia. After withdrawal of CyA, his NS relapsed with an increase of proteinuria more than 1 g/day.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [169.0, 'cm']}",65.03158,61.78,68.28316,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 169.0 cm, which is 169.0 cm * 0.393701 in/cm = 66.53547 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.53547 (in inches) - 60) = 65.03158 kg.
Hence, the patient's IBW is 65.03158 kg."
3556,10,Ideal Body Weight,physical,decimal,pmc-4452678-1,Extracted,"A 52-year old male patient, 177 cm in height and weighing 61 kg, was admitted to the hospital emergency room. He had experienced general weakness starting 10 days earlier and complained of right upper quadrant pain that had started 4-5 days before being admitted. The patient had been diagnosed with PC-type MCD five years earlier, which was confirmed by clinical findings; by computed tomography (CT) scans which had shown multiple lymph node enlargements in the neck, axillary, mediastinal, abdominal, and pelvic space; and by a right axillary lymph node biopsy under local anesthesia. After eight cycles of chemotherapy, the patient entered into complete remission, but there had been a loss to follow-up. Afterwards the patient had no history of taking any specific drugs, and he had a smoking history of 20 pack-years. A contrast-enhanced CT scan was obtained, which found acute calculous cholecystitis, lymphadenopathy with multiple enlarged nodes in the abdomen and pelvis, splenomegaly, bilateral pleural effusion, and small amounts of ascites in the cul-de-sac. The patient was scheduled for surgery, but during the preoperative evaluations, a blood test found anemia, thrombocytopenia, lymphopenia, and azotemia. The echocardiography showed findings of stress-induced cardiomyopathy (ejection fraction [EF] = 43%). Therefore, it was decided that the patient's underlying condition must be improved before having surgery. Accordingly, percutaneous transhepatic gallbladder drainage was first performed. A CT scan was also taken, which showed multiple lymph node enlargements which aroused suspicion of the recurrence of CD and prompted an evaluation. Serum immunofixation electrophoresis showed polyclonal hypergammaglobulinemia. In a bone marrow study, plasmacytosis was observed. Laboratory findings of reductions in his platelet count, hemoglobin (Hgb), lymphocyte, total cholesterol, and albumin and increases in his international normalized ratio (INR), blood urea nitrogen, creatinine, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and vascular endothelial growth factor (VEGF) were observed. These were findings that fit the clinical manifestations of a MCD patient, leading to the conclusion that CD had recurred. However, the serological test for human immunodeficiency virus (HIV) was negative. The patient was started on chemotherapy again. From day 7 after being admitted, pulmonary edema worsened due to the exacerbation of the stress-induced cardiomyopathy (EF = 25%), the patient complained of dyspnea, and oliguria occurred due to the worsening of the azotemia. As a result, after aggressive treatment including four days in the intensive care unit (ICU), the patient's clinical signs gradually improved. Twenty-three days after being admitted, the echocardiography showed normalization of the left ventricular systolic function (EF = 68%), as well as improvements in his pulmonary edema and azotemia. However, despite transfusions of leukocyte-poor and irradiated packed red blood cells (RBC) and platelets along with fresh frozen plasma (FFP), there was no significant improvement in the blood lab values, with Hgb at 3.8-11.6 g/dl, the platelet count at 31,000-132,000 /µl and INR remaining at 1.32-2.02. After one month of hospitalization, an elective laparoscopic cholecystectomy was planned for the patient.
An exhaustive preanesthetic evaluation was performed. Before surgery, a blood transfusion of packed 2 units of RBC, 8 units of platelets, and 4 units of FFP was given, which improved the blood lab values (Hgb 9.0 g/dl, platelet 78,000 /µl, INR 1.41). Although there were signs of mild dyspnea, there was no cough or sputum but there was abdominal distension found during a physical examination. A chest X-ray showed a waning pattern of ill-defined consolidation in both lungs. There were no rales or wheezing according to a chest auscultation. A pulmonary function test could not be performed because the patient was in a bed-ridden state. The electrocardiogram (ECG) findings were normal. A thoracic CT scan showed no findings of a mediastinal mass.
Without being premedicated, the patient was transferred to the operating room where ECG, a pulse oximetry monitor and bispectral index monitors were applied. After performing a modified Allen's test to assess the collateral blood flow to the hand, a 22 G catheter was inserted in the left radial artery for continual arterial pressure monitoring and arterial blood gas sampling. Moreover, for close fluid management and lessinvasive circulatory monitoring while the patient was under anesthesia, a catheter was connected to a FloTrac™/Vigileo™ monitor (Edwards Lifesciences, Irvine, CA, USA). Before preoxygenation, the patient's room air arterial blood gas analysis (ABGA) results were as follows: pH, 7.53; PaCO2, 27 mmHg; PaO2, 65 mmHg; HCO3-, 22.6 mEq/L; BE, -0.1 mEq/L; SaO2, 95 %; Hgb, 8.8 g/dl; and Hct, 26%. His electrolytes were in normal ranges. General anesthesia was induced with intravenous thiopental sodium (100 mg), 2% lidocaine (40 mg), etomidate (10 mg), cisatracurium (14 mg), and remifentanil (0.15 µg/kg/min), and a tracheal tube was inserted orotracheally. General anesthesia was maintained with sevoflurane (1.5-3 vol%), O2 (1.5 L/min), air (1.5 L/min), and remifentanil (0.05 µg/kg/min). For continuous central venous oxygen saturation (ScvO2) monitoring and for an aggressive administration of fluid, blood, and drugs in case of an emergency, a triple lumen PreSep™ central venous oximetry catheter (Edwards Lifesciences, Irvine, CA, USA) was inserted via his right internal jugular vein. A foley catheter was not inserted. Using a Vigileo™ monitor, cardiac output, stroke volume, stroke volume variation (SVV), systemic vascular resistance, and ScvO2 were continuously monitored during perioperative fluid and circulatory management. After starting the surgery, the Calot's triangle had severe inflammation and adhesion, making dissection impossible. Consequently, the surgery was switched to an open cholecystectomy. Perioperative drainage of the ascites was about 2 L. Cisatracurium of 2 mg and ephedrine of 5 mg were additionally administered intravenously. Vital signs monitored during the surgery were a BP of 105-150/50-85 mmHg, HR of 82-110 beats/min, and oxygen saturation of 100%. The parameters displayed on the Vigileo™ monitor all remained in their normal ranges without sudden changes. The bispectral index remained in the range of 32-39. The last measured ABGA results during surgery were as follows: pH, 7.39; PaCO2, 38 mmHg; PaO2, 141 mmHg; HCO3-, 23 mEq/L; BE, -2 mEq/L; SaO2, 99 %; Hgb, 7.8 g/dl; Hct, 23%; Na, 138 mmol/L; K 3.8 mmol/L; and Ca2+, 0.97 mmol/L. The surgery was uneventful, and the duration of the operation and anesthesia were 1.5 and 2.5 h. There was no significant blood loss, and infused crystalloid fluid amounted to 1,100 ml. Once anesthesia was terminated, the patient awakened smoothly and the tracheal tube was removed. The patient was transferred to the ICU for close monitoring. The patient's postoperative vital signs and laboratory findings were satisfactory, and the next day the patient was moved to the general ward. The patient was kept at the hospital for continuous chemotherapy for CD. Approximately one month after the surgery, the patient developed a cough and sputum. In an evaluation, fungal pneumonia was suspected and treatment was started. However, the patient's condition rapidly deteriorated. Despite aggressive treatment including ventilator care in the ICU, the patient expired three days into the treatment.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [177.0, 'cm']}",72.27568,68.6619,75.88946,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 177.0 cm, which is 177.0 cm * 0.393701 in/cm = 69.68508 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.68508 (in inches) - 60) = 72.27568 kg.
Hence, the patient's IBW is 72.27568 kg."
3557,10,Ideal Body Weight,physical,decimal,usmle-12112,Extracted,"A 65-year-old man presents to the diabetes clinic for a check-up. He has been successfully managing his diabetes through diet alone, and has not experienced any complications related to retinopathy, neuropathy, or nephropathy. He recently started a new exercise regimen and is eager to see whether his weight has declined since his last visit. The nurse measures his height to be 170 cm and his weight to be 165 lb (75 kg).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3558,10,Ideal Body Weight,physical,decimal,pmc-4471306-1,Extracted,"A 35-year-old man was admitted to emergency department with one-day history of hematemesis and melena after taking nonsteroidal anti-inflammatory drug. He had no medical illness. He denied smoking, alcohol consumption. The height and weight of patient were 178 cm and 68 kg, respectively (body mass index: 21 kg/cm2). On physical examination, blood pressure was 120/70 mmHg and pulse rate 86/min. There was a 2 cm mobile painless submucosal nodular lesion on the left neck. His abdomen was soft with no tenderness, rebound, mass lesion, or ascites. The patient was promptly given intravenous crystalloid and colloid fluid replacement; parenteral proton-pump inhibitor was administered. Initial laboratory values were as follows: leukocyte: 5800/mm3, hemoglobin: 14.8 g/dL, platelet: 347.000/mm3, prothrombin time: 12 sec, and INR: 1.05. Biochemical parameters were normal.
Upper gastrointestinal endoscopy revealed gastric and duodenal multiple submucosal mobile lesions with narrowing of antrum and constant deformation of duodenum. It was unable to proceed to the second part of duodenum with endoscope (). Colonoscopic examination was normal. Abdominal magnetic resonance imaging (MRI) showed that diffuse lipomatosis of abdominal cavity extending to the mediastinum () and obliteration at the distal part of stomach, bulb, and proximal duodenum due to submucosal lipomatous lesions with deplased small intestine loops to the right upper abdomen (). Laboratory investigation showed fasting glucose 68 mg/dL, fasting insulin 1.18 mg/dL, triglyceride 53 mg/dL, low density lipoprotein 62 mg/dL, and high density lipoprotein 47 mg/dL. His father similarly has mobile nontender lesions at neck and right upper extremity. However, submucosal lesions were not detected on UGIE examination. Abdominal MRI of his father showed similarly lipomatous tissue increase in abdominal cavity (). Endoscopic biopsy of submucosal polypoid lesion was diagnosed as lipoma and trucut biopsy of diffuse mass lesion filling abdominal cavity was consistent with fibroadipose tissue.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [178.0, 'cm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3559,10,Ideal Body Weight,physical,decimal,pmc-3350168-2,Extracted,"Patient 2 is a 15-year-old female who presented with a 2-month history of vomiting and weight loss. Laboratory evaluation prior to referral included normal H. pylori IgG and abdominal ultrasound. A large pyloric channel ulcer was seen on UGI. Weight was 53.8 kg (50% tile), height 160 cm (35% tile), and physical exam unremarkable.
She was treated for H. pylori. The EGD demonstrated a narrowed pyloric channel () and mucosal abnormalities. The pyloric channel was dilated with CRE Wire-guided 6-7-8 180 cm pyloric balloon dilator (Boston Scientific, Natick, MA). Biopsies showed normal histology of the esophagus and antrum and no tissue from the duodenal bulb. Repeat ultrasound revealed GOO caused by thickening of the pylorus channel length 3.2 cm, thickness 1.2 cm. Biopsies were negative for H. pylori, and serum gastrin and thyroid levels were normal. Over the next 6 weeks the patient had a total of 7 diltations, each resulting in transient improvement in symptoms. Surgical referral was made following the second dilatation, and following a failed seventh dilatation she underwent a Billroth I gastrectomy with preservation of the vagal nerve. Pathology of the stenosed area showed muscular hypertrophy with no identifiable etiology. Following surgery all symptoms of GOO resolved, and follow-up EGD 18 months after surgery showed no ulcer and no scaring.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3560,10,Ideal Body Weight,physical,decimal,pmc-8077912-1,Extracted,"A 53-year-old man with normal height (175 cm) and overweight (102 kg, body mass index = 33.3 kg/cm2) initially presented with low back pain and bilateral legs pain for 4 years and bilateral lower limps numbness for 2 years.
Four years ago, this patient gradually developed low back pain, radiating to hip and lateral side of both legs. The pain worsened after long time standing, walking and working and relieved when bending and crouching. Numerical rating scale (NRS, an 11-point scale where 0 = no pain and 10 = the worst pain) scored 4. The patient tried some unknown painkillers but they did not work. The intermittent pain lasted for years until 2 years ago when he started to have numbness of both lower limps, ranging from both sides of calfs to the dorsum of feet. Intermittent claudication occurs within 500 m’ walking. No cauda equina syndrome (CES) appeared. It should be noticed that this man gained 55 kg in weight during the past 20 years. Relevant history included hypertension for 10 years, smoking for 30 years and drinking for 30 years. In recent two weeks there was a fluctuation of blood sugar but no formal monitoring record was available. This patient had never received steroids medications.
A full endocrinologic workup was conducted in patient to rule out underlying endocrine abnormalities and type 2 diabetes mellitus was diagnosed. On physical exam, the patient showed 5/5 strength, normal muscle tone and intact superficial sensation in the upper and lower extremities bilaterally. Tendon reflexes of the right knee was absent and several myelopathic signs were recorded as follows: Chaddock sign ( +) on the left, Oppenheim sign ( +) on the left and Babinski sign suspected ( +) on both sides. CT scan indicated typical signs of LSS: intervertebral foraminal stenosis, ligamentum flavum hypertrophy, disc paracentral herniation and spinal stenosis from L2 to L5 (Fig. ), and MRI showed epidural abnormal fat deposition in the spinal canal from L2–L5 (Fig. ). According to a previous study of Borre et al., SEL could be graded on basis of the degree of epidural adipose tissue occupying the spinal canal (extradural fat [EF]-to spinal canal [SC] ratio); grade I, 41–50% of the canal; grade II, 51–74% of the canal; and grade III, > 75% of the canal []. This patient’s imaging revealed grade II (60% EF/SC ratio) lumbar epidural lipomatosis (Fig. d).
Based on the patient’s symptoms, history, physical examination and radiological imaging, a primary diagnosis of LSS and obesity-induced idiopathic SEL from L2–L5 was proposed. The compression of the cauda equina came from anterior protruding lumbar disc and posterior adipose tissue and ligamentum flavum, and pressure on nerve root is caused by intervertebral foraminal bony stenosis. Since refractory radiculopathic symptoms had appeared, indication of surgery was clear. Mimimally invasive surgery like endoscopic technique was insufficient to relieve bony stenosis, so extensive decompression was necessary. Internal fixation and bone graft fusion were adopted to maintain the stability of responsible vertebrae. Although the modified articular fusion had never been reported in such a rare disease, it was performed successfully in a large amount of obese patients with lumbar degenerative disease only. This was our first application of this modified surgical style on obesity SEL.
After a preoperative use of prophylactic antibiotics (cefuroxime 1.5 g, intravenous), the operation was performed under general anesthesia and in a prone position. Following careful stripping of the paraspinal muscles, spinous process, bilateral articular processes and roots of transverse processes were exposed. Afterwards, titanium polyaxial pedicle screws (6.5 mm in diameter, 50 mm long, Legacy, Medtronic, USA) were inserted bipedicularly from the L2 to L5 vertebrae. We chose used F4 reverse thread screws providing a tightening power in horizontal direction and minimizes the possibility of pulling out. This is quite important for such a patient with hight body weight. Then, pre-bended titanium rods were implanted and intraoperative fluoroscopy confirmed satisfactory position and length of screws. The resection range included spinous processes (L3, L4 and small portion of L2 and L5), 2/3 of the inferior L2 lamina, L3 and L4 lamina and 1/5 of upper L5 lamina, as well as the corresponding supraspinous ligament, interspinous ligament, ligamentum flavum and joint capsule. Then hyperplastic medial portion of facet joints, atrophic ligamentum flavum, stenosis of lumbar lateral recess and accumulation of epidural adipose tissue contributing to dural sac compression was visible (Fig. a). Decompression range of L2–L3 included medial 2/3 of the L2 bilateral inferior articular process, 1/3 of the medial side of bilateral superior articular processes of L5 and hyperplastic medial portion of L3 superior articular processes. Medial 2/3 of the bilateral L2 inferior articular process and 1/3 of the medial side of bilateral superior articular processes of L3 was carried out with a chisel and the lateral 2/3 portion was preserved for bone grafting. Management of L3–L4 and L4–L5 was the same as the above description. Following the decompression was resection of epidural adipose tissue with bipolar cautery (Fig. b).
Subsequently, inspection verified an adequate relaxation of nerve root and full decompression of dural sac. Removed tissue (Fig. c) had the appearance of normal adipose tissue. A round head grinding drill was then used to prepare the inter-articular space as grafting bed for autograft and allograft cancellous bone. After that, the surgery field was rinsed with saline before bone graft was pressed into the inter-articular space. Finally, a drainage tube was put in place and the wound was closed up. Intraoperative hemorrhage was 586 mL.
The patient showed full muscle strength and sensation once regained consciousness. Preoperative symptoms relieved obviously during the following days, and NRS scored 1. We removed the drainage tube and encouraged the patient to stand and walk on the third day after operation. Radiographs of lumbar spine were taken to verify the good location of screws and rods (Fig. ), and MRI confirmed complete decompression and elimination of excessive fat tissue (Fig. ). The patient was permitted to discharge with referral for outpatient rehabilitation. We also mobilized this patient to lose weight.
By now the man has come back for follow-up regularly and his low back and radiating leg pain has completely resolved, and NRS scored 0. X-Ray, CT and MRI at different follow-up time points showed persistent stability and graft and satisfactory fusion rate, and no evidence of reoccurred SEL was detected (Figs. and ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3561,10,Ideal Body Weight,physical,decimal,pmc-7482992-1,Extracted,"We present a case of a 36-year-old male wrestler, presented with pain in his chest and in his left leg for the past two days. He also complained of pain in the big toe. There is no history of palpitation, dyspnea, sweating, or cough. No fever or headache. There is no history of trauma of lower limbs or any neurological deficit. There is no urinary or bowel trouble. There is no history of vomiting, diarrhea, or pain in abdomen. The patient is a chronic cigarette smoker with a history of two packets of cigarettes per week for the past 20 years. There is no history of recreational drug use.
The patient had a history of recurrent deep vein thrombosis, pulmonary embolism (PE), obstructive sleep apnea, insulin-dependent type ll diabetes mellitus, and candidal balanitis. There is a history of multiple surgeries in the past. The patient had undergone left elbow surgery, left knee surgery, right ankle surgery, and foot surgery, due to injuries caused by his profession. The patient has mild pitting edema in both feet.
On examination, the patient is extremely obese with a weight of 456 lbs., a height of 188 cm, and a BMI of 63.53 kg/m2. His blood pressure is 99/56 mm of Hg, a temperature of 98.6 F, respiratory rate of 16 per minute, and oxygen saturation of 98%. The patient is fully conscious and well oriented. There is no anemia, cyanosis, or jaundice.
Doppler report of the lower limbs showed bilateral deep vein thrombosis (DVT) of popliteal veins and left common femoral vein, otherwise normal Doppler flow compressibility of profunda femoris and superficial femoral veins. Based on the clinical, laboratory, and the Doppler report, the patient was diagnosed with pulmonary embolism with bilateral DVT of popliteal veins and left common femoral vein (Table ).
Treatment
The patient was admitted to the inpatient unit. After consulting cardiologist, IV heparin was started right away for DVT with pulmonary embolism.
He was also prescribed supportive therapy for controlling blood glucose and obesity, in consultation with an endocrinologist and dietician. The patient was advised for lifestyle modifications such as losing weight and staying active, to manage DVT, obesity and co-morbidities.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [188.0, 'cm']}",82.23632,78.1245,86.34814,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 188.0 cm, which is 188.0 cm * 0.393701 in/cm = 74.01579 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (74.01579 (in inches) - 60) = 82.23632 kg.
Hence, the patient's IBW is 82.23632 kg."
3562,10,Ideal Body Weight,physical,decimal,pmc-7896647-1,Extracted,"A 39-year-old man who was 178 cm in height and 83 kg in weight came to our institute for consultation for rectal cancer resected more than 1 mo ago.
In February 2020, blood was found in his stool, and colonoscopy showed irregular protuberant lesions 7 cm above the anus. On April 3, 2020, he was pathologically diagnosed with moderately to poorly differentiated adenocarcinoma.
In December 2014, the patient was admitted to the First Affiliated Hospital of Nanjing Medical University for abdominal distention. On December 9, 2014, he was found to have mostly circular protuberant lesions in the gastric body and antrum by gastroscopy and then underwent distal gastrectomy and gastrojejunostomy. Histopathological examination of the surgical specimens revealed a 10 cm × 7 cm × 2 cm-sized mass, which invaded the entire layer of the gastric wall and reached the extracorporeal adipose fibrous connective tissue. This confirmed the diagnosis of stomach carcinoma with lymphoid stroma, diffuse type in the Lauren classification (Figure ). There was involvement of only one lymph node in the greater curvature with immunohistochemical staining including cytokeratin (CK)-L (++), Villin (+), P63 (-), P40 (-), CK5/6 (-), and EBV-encoded ribonucleic acid (RNA) (EBER) in situ hybridization (+) (Figure ). Adjuvant chemotherapy was administered after the operation. After two cycles of paclitaxel, cisplatin, and tegafur, the treatment regimen was changed to paclitaxel, oxaliplatin, and tegafur for four cycles because of Grade 4 myelosuppression.
On March 13, 2017, the patient had epistaxis, and he was diagnosed with poorly differentiated squamous cell carcinoma of the nasopharynx with pathology of nasal endoscopic biopsy (Figure ). Immunohistochemical findings were as follows: CK-pan (-), CK5/6 (-), P63 (-), Melan A (-), human melanoma black 45 (-), Ki67 (+), EBER (+) (Figure ), CK7 (-), CK8/18 (+), CK-L (+), and P40 (focal+).
On March 27, 2017, his nasopharyngeal biopsy specimen was pathologically consulted by the Cancer Hospital of Sun Yat Sen University and Fudan University Shanghai Cancer Center, and both institutions found that there was great similarity between the gastric and nasopharyngeal lesions in terms of hemoxylin & eosin morphology and immunohistochemistry (IHC). Both of them were likely to be primary tumors, but nasopharyngeal metastasis of gastric cancer could not be completely ruled out. The patient was concurrently treated with radical radiotherapy and cisplatin chemotherapy, followed by nimotuzumab for six cycles.
The patient had no history of diabetes mellitus, hypertension, or tobacco or alcohol abuse, and his family history was unremarkable.
The Eastern Cooperative Oncology Group score of the patient was 1, and no superficial lymph nodes could be palpated.
His serum tumor markers and other laboratory values were all within normal range.
The patient came to our hospital. Magnetic resonance imaging indicated a rectal malignant tumor approximately 58 mm away above the anus (Figure ). On April 13, 2020, whole-body positron emission topography/computed tomography with 18-fluorodeoxy-glucose (FDG) scanning revealed thickening of the mid-rectal wall with high FDG uptake, suggesting a malignant tumor (Figure ), and increased FDG uptake at the junction of rectum and colon, which was likely to be inflammatory. No abnormal FDG-uptake was observed in the rest.
On April 26, 2020, he underwent low anterior resection of the rectum and distal ileostomy. During the operation, the tumor was located 3 cm above the dentate line, with a size of 3 cm × 3 cm and no infiltration into the whole intestinal wall. Postoperative pathology revealed that the tumor was ulcerative, moderately to poorly differentiated adenocarcinoma (Figure ), a tumor size of 2.5 cm × 1.5 cm × 1 cm, infiltration into the superficial muscle layer, and T2N0, mesorectal fascia (-), and extramural venous invasion (-). IHC indicated the following tumor cells: Special AT-rich sequence-binding protein 2 (+), caudal-type homeobox 2-88 (+), CK20 (+), Villin (+), human MutL homolog 1 (+), human melanocyte stimulating hormone 2 (+), human melanocyte stimulating hormone 6 (+), PMS1 homolog 1 (+), CD44 (focal+), E-cadherin (+), hair and enhancer of split-1 (+), Ki-67 (80%+), CK7 (-), human epidermal growth factor receptor 2 (-), BRAF (-), 5-hydroxytryptamine receptor 2B (-), zinc finger E-box binding homeobox 1 (-), and EBER (-) (Figure ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [178.0, 'cm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3563,10,Ideal Body Weight,physical,decimal,pmc-7590699-1,Extracted,"A 62-year-old man presented to a nearby clinic with a chief complaint of abdominal fullness and abdominal pain. His medical history was not significant. He was on no medication. He was not allergic to any drug or food. Laboratory tests showed increased peripheral white blood cell count (17,900/µL) and eosinophil count (12,100/µL), measured by an automated hematology analyzer, Sysmex XN 2000 (Sysmex corporation, Hyogo, Japan). Abdominal computed tomography (CT) showed massive ascites and no other abnormalities (Fig. a).
He was referred to our hospital for further examination and treatment. His height was 173 cm, his weight was 105 kg, and his body mass index was 35 kg/m2. He had gained 15 kg in the last month. Physical examination showed abdominal distention and no abdominal tenderness. The white blood cell count was 19,400/µL, eosinophil count was 13,300/µL, and C-reactive protein was 0.70 mg/dL. The other data were normal: carcinoembryonic antigen 3 ng/mL, carbohydrate 19–9 6 U/mL, and serum IgE 112 IU/mL. His allergen-specific IgE tests were unremarkable. The interferon-gamma release assay was negative. Abdominal magnetic resonance imaging (MRI) showed massive ascites that had low and high signal intensities on T1-weighted and T2-weighted images, respectively. Abdominal paracentesis was performed, and the ascitic fluid was stained with Fluoocell WDF (Sysmex corporation, Hyogo, Japan), then analyzed by flow cytometry with the Sysmex XN 2000 []. The total number of nucleated cells in the ascites was 11,420/µL, and 69% of them were eosinophils. Its cytology also revealed the most nucleated cells had both of bilobed nuclei and cytoplasmic granules, with no evidence of malignancy (Additional file : Figure S1). Ascitic fluid culture was negative. Upper and lower GI endoscopies were performed on the suspicion of EGIDs. There was a Type II-like lesion in the descending colon that showed well-differentiated adenocarcinoma on pathological examination of a biopsy specimen (Fig. a). There were no other abnormal findings in the GI tract. The patient underwent exploratory laparoscopy to find the cause of the ascites, and massive brownish cloudy ascites with reddening or thickening of the mesentery and omentum was seen. The tumor was not exposed to the colonic serosa. There were no enlarged lymph nodes, no abnormal adhesions, and no metastases (Fig. c). Pathology of the mesentery and omentum showed infiltration of inflammatory cells, mainly eosinophils, with no malignancy (Additional file : Figure S2). Based on these findings, eosinophilic peritonitis associated with colon cancer was suspected.
After administration of systemic steroid therapy (prednisolone (PSL) 60 mg/day, 1 mg/kg/day), his blood eosinophil count and weight decreased immediately. The dose of PSL was then decreased biweekly. One and a half months after steroid administration, abdominal CT confirmed disappearance of ascites (Fig. b). Laparoscopic left hemicolectomy with regional lymph node dissection (D3) was performed. At laparoscopy, the inflammation of the mesentery and omentum was seen to be relieved, and there was no ascites (Fig. b, d). The patient’s postoperative course was uneventful, and he was discharged on the 5th postoperative day. According to the Union for International Cancer Control TNM classification 8th Edition, the pathological diagnosis was tubular adenocarcinoma, moderately differentiated, pT3 (SS), int, ly1, v1, PN1, EX0, pN0, sM0, pStage IIA. The pathological specimen also showed eosinophilic infiltration to various lesions, especially omentum, mesentery, and the submucosal layer of the descending colon. He was given adjuvant oral chemotherapy (uracil-tegafur with leucovorin) for six months because there was concern that the pathological ly1 and v1 could increase the risk for recurrence of the cancer [].
After the operation, the dose of PSL was again decreased monthly. He finally stopped taking PSL four months after it was started, and he remains asymptomatic without recurrent ascites at the present time (Fig. ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.0, 'cm']}",68.65362,65.22094,72.0863,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.0 cm, which is 173.0 cm * 0.393701 in/cm = 68.11027 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.11027 (in inches) - 60) = 68.65362 kg.
Hence, the patient's IBW is 68.65362 kg."
3564,10,Ideal Body Weight,physical,decimal,pmc-6967052-1,Extracted,"The patient was a 62-year-old man with a height of 167 cm and a body weight of 60 kg.
He has long shown cyanosis on his lips, and his mother had the same symptom.
The patient visited another hospital complaining of diarrhea, nausea, and dizziness, where a blood test revealed elevated liver enzymes (aspartate aminotransferase 122 IU/l, alanine aminotransferase 203 IU/l, lactate dehydrogenase 813 IU/l), total bilirubin (2.4 mg/dl), and C-reactive protein level (16.1 mg/dl), and an echocardiographic examination revealed cardiac tamponade; thus, he was referred to our hospital. Because an ascending aortic dissection (DeBakey II) was found by computed tomographic examination, the patient was advised to undergo emergency surgery on the same day of diagnosis.
He demonstrated cyanosis on his face and limbs, so even with oxygen inhalation, the percutaneous oxygen saturation (SpO2) was 75%. As the patient had cardiac tamponade, we suspected a decline in SpO2 due to heart failure. The arterial blood was venous blood-like blue-black blood. Transthoracic echocardiography revealed pericardial effusion, tricuspid regurgitation, and aortic regurgitation; however, neither ventricular collapse nor wall motion disorder was recognized, and the ejection fraction was 76%. Blood pressure was also maintained at 110–120/70–80 mmHg, and the heart rate was maintained at 70–80/min by using antihypertensive drugs, suggesting that the patient had a hemoglobin abnormality rather than a reduction in SpO2 due to heart failure. Therefore, the patient was suspected of having a hereditary disease. Subsequently, his case was referred to the hematology department; however, a definitive diagnosis could not be established. As the surgery had to be performed urgently, we investigated the cause of cyanosis after the surgery. Preoperative blood gas analysis and blood counts revealed the following results: PaO2 219 mmHg, SaO2 75%, Hb level 13.3 g/dl, hematocrit (Ht) 40.9%, white blood cell 11.30 × 103/μl, red blood cell 4.24 × 106/μl, and platelet 302 × 103/μl.
Anesthesia was induced with midazolam 5 mg, fentanyl 0.4 mg, and vecuronium 10 mg and maintained by the inhalation of 0.3%–0.5% isoflurane and 0.5–1.0 mg/kg/h propofol, as well as the adequate administration of vecuronium and fentanyl. After the induction of anesthesia, a pulmonary artery catheter was placed through the right internal jugular vein, and blood sampling from the pulmonary artery and radial artery was performed.
The SpO2 monitor showed a reading of 75%, and the blood gas analysis revealed the following results: PaO2 435 mmHg, SaO2 80.9%, Hb level 13.6 g/dl, and Ht 41.6% under the condition of FiO2 100%. The cardiac index was 2.3 L/min/m2, the mixed venous oxygen saturation (SvO2) was 61%, and the regional oxygen saturation (rSO2) of the forehead was 56%. When the surgery started, the pericardiotomy was opened, and after the release of cardiac tamponade, the cardiac index increased to 3.5 L/min/m2 and SvO2 increased to 68%. However, other values did not change. The intraoperative SvO2 maintained the latter half of the surgery was above 60%, and the intraoperative rSO2 of the forehead was maintained above 50%. Furthermore, the cardiac index was maintained above 3.0 L/min/m2. Additionally, there was no increase in lactate.
An ascending aortic replacement surgery was performed. Cardiopulmonary bypass (CPB) was initiated by right axillary artery blood flow after the superior and inferior vena cava were removed, and ascending aortic replacement surgery was performed under hypothermic circulation arrest with a bladder temperature of 22 °C. The anesthesia time was 375 min and the operation time was 340 min. After the patient was transferred to the postoperative intensive care unit, the divergence between PaO2 and SpO2 was confirmed; however, the circulation dynamics were stable and PaO2 was normal. The patient underwent tracheal extubation at 15 h postoperatively. He was moved to the general ward on the 3rd hospitalization day and was discharged without complications on the 32nd hospitalization day. During hospitalization, the patient was referred to the hematology department for a detailed examination and was diagnosed as having Hb Kansas through genetic analysis at 2 months after surgery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [167.0, 'cm']}",63.22056,60.05953,66.38159,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 167.0 cm, which is 167.0 cm * 0.393701 in/cm = 65.74807 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.74807 (in inches) - 60) = 63.22056 kg.
Hence, the patient's IBW is 63.22056 kg."
3565,10,Ideal Body Weight,physical,decimal,pmc-4066970-1,Extracted,"A 53-year-old, right-handed female (height 1.54 m; weight 48.2 kg) sustained a hemorrhagic right middle cerebral artery stroke 3 years earlier. The patient presented with left spastic hemiparesis involving, among others, the finger flexors. In addition, she exhibited weak voluntary finger and wrist extension. The patient underwent extensive physical and occupational therapy after the stroke and up to the time of presentation. A total of 50 units onabotulinum toxin A (BOTOX™, Allergan, Irvine, CA, USA) was administered to the left flexor digitorum superficialis (FDS) and flexor digitorum profundus, respectively. The injection was guided by percutaneous electrical stimulation of the motor points of these muscles.
After providing written consent, the subject attended three laboratory sessions before (Pre = Day 0), after (Post 1 = 10 days), and at the follow-up (Post 2 = 2.5 months) injection. Delays in grip initiation and release were assessed using electromyographic (EMG) signals in paretic and non-paretic sides, respectively. The Modified Ashworth Scale (MAS) was used to assess hypertonia. Bilateral grip strength was measured using a hand-held dynamometer (Lafayette Instruments, Lafayette, IN, USA), and the Functional Independence Measure (FIM) was used to evaluate clinical improvement.
During grip initiation and release tasks, the subject sat comfortably in a chair with a backrest to provide proper trunk support. The limb was supported and secured firmly on a customized apparatus on a desk and was placed with 45° shoulder abduction and flexion and a 90° elbow flexion. The wrist was placed and secured in a neutral position (with thumb pointing upward), and the hand was placed around a customized hand-held apparatus. The apparatus was fixed to the table and was adjusted to accommodate hand size, adjusting for comfort and a firm grip. First, the non-paretic hand was tested, followed by the impaired hand. In each 20-second trial, the subject was asked to relax the fingers for the first 10 seconds, maximally grip the apparatus and hold for 5 seconds, and then relax the hand for 10 seconds. Computer-generated audible tones cued the subject when to start and stop grip efforts. The subject was instructed to grip the apparatus as quickly as possible in response to the first tone (start), and then relax the hand as quickly as possible when the second tone (stop) was played. The patient practiced five trials prior to the grip initiation and release task, which allowed for familiarizing with the setting and task. After the practice sets, five trials for each side were performed.
Bipolar active surface electrodes (Delsys, Boston, MA, USA) were placed over the muscle bellies of FDS and extensor digitorum communis (EDC). The FDS muscle is the primary mover in power grip, and EDC muscle activity was recorded to monitor antagonist muscle activity. For consistency, electrode locations were recorded, and electrodes were placed at identical locations for all sessions. EMGs were recorded at 1 000 Hz using a Delsys amplifier and data acquisition system (National Instruments, Austin, TX, USA) controlled by custom LabView program (National Instruments). EMG signals were processed and analyzed offline using a custom Matlab program (The MathWorks, Natick, MA, USA). EMG signals were initially band-pass filtered (10-400 Hz), rectified, and then root-mean-square smoothed with a 40-ms time constant to create envelopes that clearly displayed aggregated muscle activity.
Delays in grip initiation and release were determined from the FDS EMG. The Teager-Kaiser energy operator was used to analyze surface EMG to improve the signal-to-noise ratio, as well as to optimize EMG onset/offset detection[]. The baseline FDS EMG was calculated as values for the EMG averaged across a 0.5-second window during the initial resting period of each trial. The FDS EMG onset time was identified when the EMG value increased more than the mean value plus 3 standard deviations of the baseline values. Grip initiation delay was calculated as the time difference between EMG onset and the “start” audible tone ().
The FDS EMG offset time was identified as the time when EMG values fell below the mean plus 3 standard deviations of the baseline values. The release delay was then calculated as the time difference between EMG offset and the “stop” audible tone ().
After BT injection to the finger flexor muscles (FDS and flexor digitorum profundus) of the paretic left hand, grip strength decreased at 10 days post-injection and returned to pre-injection levels at 2.5 months post-injection (Pre vs. Post 1 vs. Post 2: 2.3 vs. 1.0 vs. 2.2 kg), while grip strength of the non-paretic hand remained stable (Pre vs. Post 1 vs. Post 2: 22.7 vs. 20.4 vs. 22.2 kg). In parallel, the MAS scores of the affected finger flexors were as follows: Pre vs. Post 1 vs. Post 2: 2 vs. 0 vs. 1 for FDS; 2 vs. 0 vs. 1 for flexor digitorum profundus. FIM scores remained unchanged (FIM = 6 for Pre, Post 1, and Post 2), but the subject reported an improved overall ability for handling objects, as well as bimanual activities at home while performing activities of daily living in Post 1 and Post 2 measures.
Release delay time in the paretic hand resulted in dynamic changes (Pre: 2 223 ms; Post 1:1 024 ms; Post 2: 1 333 ms), without dramatic changes in grip initiation delay times in the paretic hand (Pre: 417 ms; Post 1: 439 ms; Post 2: 378 ms). It is noteworthy to mention that a decreased FDS release delay time was paralleled by shortened EDC and EDC EMGs (). In contrast, both grip initiation and release delay times in the non-impaired hand remained relatively stable in all measurements (Pre vs. Post 1 vs. Post 2: 468 ms vs. 404 ms vs. 371 ms for grip initiation delay; 725 ms vs. 740 ms vs. 691 ms for release delay).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.54, 'm']}",46.94889,44.60145,49.29633,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.54 m, which is 1.54 m * 39.3701 in/m = 60.62995 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.62995 (in inches) - 60) = 46.94889 kg.
Hence, the patient's IBW is 46.94889 kg."
3566,10,Ideal Body Weight,physical,decimal,pmc-8136201-1,Extracted,"A 71-year-old man (height, 163.4 cm; body weight, 71.2 kg; body mass index [BMI], 26.7 kg·m− 2) was scheduled for endoscopic submucosal dissection of early-stage gastric cancer. The patient had type 2 diabetes mellitus and had been on insulin therapy for 30 years. He had a history of total thyroidectomy 8 years ago and laparoscopic cholecystectomy 6 years ago. He was euthyroid (free T4, 1.24 ng·dl− 1; free T3, 2.06 pg·dl− 1; TSH, 0.586 μIU·ml− 1) with oral levothyroxine. Preoperative laboratory test results showed reduced estimated glomerular filtration rate (63.0 mL·min− 1), elevated hemoglobin A1c level (7.6%), and glucosuria (4+) due to sodium-glucose co-transporter-2 inhibitor use. Laboratory investigation results showed no other abnormalities.
In the operating room, routine monitoring including electrocardiography, noninvasive blood pressure measurement, and pulse oximetry was performed. After preoxygenation, general anesthesia was induced with 300 mg thiopental, 50 mg (0.7 mg·kg− 1) rocuronium, and 0.15 μg·kg− 1·min− 1 remifentanil. After tracheal intubation, the patient was mechanically ventilated to maintain an end-tidal carbon dioxide between 35 and 40 mmHg. Anesthesia was maintained with an end-tidal sevoflurane concentration of 1.2% and 0.1–0.15 μg·kg− 1·min− 1 remifentanil. Intraoperatively, the patient was administered 750 mL of crystalloids, and his urine output was 118 mL. The surgery was completed uneventfully and anesthesia was terminated in 71 min. No additional rocuronium was administered after anesthesia induction. Ninety-four minutes after rocuronium administration, neuromuscular monitoring (Intellivue NMT module®, Philips Japan, Tokyo) was applied and showed a TOF count of 0 and 20 twitches in response to PTC stimulation in the adductor pollicis muscle. The end-tidal sevoflurane concentration was 0.1%. Sugammadex (280 mg; 4 mg/kg) was administered, and four twitches in response to TOF stimulation appeared in 3 min. However, the twitches were still weak, and no spontaneous breathing or movement was observed. The TOF ratio was not measurable. Therefore, an additional dose of sugammadex (120 mg; 1.7 mg·kg− 1) was administered 5 min after the first dose. Five minutes after the second dose of sugammadex, the TOF ratio recovered to 92%, and 8 min after the second dose, it recovered to 107%. The patient opened his eyes; moved his neck, arms, and limbs; and regained consciousness. The trachea was extubated and the patient was transferred to the ward.
When we interviewed the patient at a postoperative follow-up, he told us he had felt “numbness” on awakening from anesthesia after the cholecystectomy he underwent 6 years ago and that the anesthesiologists “did something” to cure it. He and his family also had no history of neuromuscular disorders. He was discharged without complications on the fifth postoperative day.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [163.4, 'cm']}",59.9607,56.96267,62.95874,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 163.4 cm, which is 163.4 cm * 0.393701 in/cm = 64.33074 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.33074 (in inches) - 60) = 59.9607 kg.
Hence, the patient's IBW is 59.9607 kg."
3567,10,Ideal Body Weight,physical,decimal,pmc-6815596-1,Extracted,"An 82-year-old man was hospitalized because of fever, seizure, and consciousness disturbance. He had a history of gastrectomy for gastric ulcer when he was young. At age 74 years, he developed subarachnoid hemorrhage and secondary symptomatic epilepsy, and was treated with phenytoin, an AED. With progressive disuse syndrome after the brain event, he had been bedridden for the last 8 years under insufficient sunlight exposure. Two weeks before hospitalization, he suffered an acute seizure, followed by consciousness disturbance. Thereafter, food intake and oral dosing were insufficient. Three days before hospitalization, he developed a fever >38°C. Because of concurrent respiratory failure, he was transferred to our hospital for further treatment.
On admission, the patient showed impaired consciousness with closed eyes. Verbal response was incomprehensible, and the best motor response was a response to localized pain (Glasgow coma scale score: E1V2M5). His vital signs were: blood pressure, 84/52 mmHg; heart rate, 84 bpm; body temperature, 40.0°C; and arterial blood oxygen saturation measured by pulse oximetry of 94% with supplemental oxygen at 8 L/min. His height was 161 cm, his weight was 48.5 kg, and his body mass index was 18.7 kg/m2. He showed neither jolt accentuation of headache nor spastic rigidity. A coarse crackle was heard in his left lung. Importantly, Chvostek and Trousseau signs indicative of tetany were positive.
Laboratory data on admission are shown in . Briefly, the following results were obtained: white blood cell count (10 390/μL), serum albumin (3.1 g/dL), blood urea nitrogen (13.8 mg/dL), creatinine (0.44 mg/dL), estimated glomerular filtration rate (134.5 mL/min/1.73 m2), phosphate (1.6 mg/dL), Ca (3.7 mg/dL), ionized Ca (0.55 mmol/L), magnesium (2.97 mg/dL), intact PTH (386.8 pg/mL), and serum C-reactive protein (1.67 mg/dL). Although blood phenytoin concentration was low (<0.8 µg/mL), this value was plausible because phenytoin has a half-life of 20–30 h, and it was not being administered sufficiently at the time of hospitalization over the last few days. An electrocardiogram showed a sinus rate of 93 beats per minute with long QT interval (0.398 s) and corrected QT-T interval (0.398 second).
At the bottom of his left lung, a consolidation was visible that was suspected pneumonia, and interlobar pleural effusion was also identified on non-contrast-enhanced computed tomography (). Although acute-phase lesions such as bleeding were not observed, frontal lobe atrophy and ventricular enlargement were confirmed by head computed tomography (). Based on these results, he was diagnosed as having bacterial pneumonia and its related sepsis. Because the patient showed neither jolt accentuation of headache nor spastic rigidity, meningitis was ruled out as a cause of seizure.
At that point, several differential diagnoses were considered for the hypocalcemia. The serum Ca level corrected for serum albumin was 4.6 mg/dL, and ionized Ca was 0.55 mmol/L, indicating true hypocalcemia, not pseudo-hypocalcemia. CKD was also excluded as a possible cause based on his kidney function. There was also no evidence of severe hypomagnesemia to cause decreased secretion of PTH, although serum magnesium level was slightly low (1.6 mg/dL). In addition, serum intact PTH level on admission was very high. Accordingly, we considered that parathyroid gland was normally functioning because intact PTH appropriately increased in response to hypocalcemia. Bone formation was slightly increased in response to increased serum intact PTH, whereas bone resorption was decreased judging from the serum tartrate-resistant acid phosphatase-5b level. At that point, the differential diagnosis of hypocalcemia still included pancreatitis and sepsis. Pancreatitis was ruled out based on the normal serum amylase and lipase levels and absence of pancreas enlargement by imaging. Although the mechanism of hypocalcemia in septic patients is complex and not well understood, previous studies showed that kidneys are reported to increase urinary Ca excretion in sepsis []. However, fractional excretion of Ca was remarkably low (0.13%), indicating Ca resorption enhancement across renal tubules. Taken together, sepsis-related hypocalcemia was not regarded as the primary cause of the hypocalcemia in the present case.
Another potential mechanism for the severe hypocalcemia was decreased Ca absorption from the gastrointestinal tract. Because he had been in a nursing home, which was an environment with extremely low sunlight exposure, vitamin D3 generally produced in the skin was potentially lacking. Notably, he was on long-term treatment with phenytoin, which is shown to accelerate conversion of 25-hydroxyvitamin D to 24,25-dihydroxyvitamin D [, ]. The low level of 25-hydroxyvitamin D (5.4 ng/mL), which is an indicator of vitamin D status in the body, strongly indicated that he had been suffering from 25-hydroxyvitamin D deficiency, probably caused by combination of low sunlight exposure and long-term use of phenytoin.
The patient's clinical course is shown in . He received intravenous hydration for sepsis and antibiotics to target anaerobes (sulbactam + ampicillin 4.5 g/day) for possible aspiration pneumonia. He was treated with intravenous Ca gluconate (8.5% 10–20 mL, 3.9–7.8 mEq/day) and trans-gastric tube administration of Ca lactate/phosphate hydrate (3–6 g/day) and we discontinued phenytoin from the first hospital day. Administration of 0.25 µg/day of calcitriol by nasal gastric tube was performed between the first and second hospital days. From the third hospital day, we exchanged calcitriol with 0.75 µg/day of eldecalcitol, a VDRA often used for osteoporosis in Japan [], because eldecalcitol is shown to have a higher binding ability to vitamin D binding protein (DBP) than calcitriol: binding ability of eldecalcitol to DBP is 4.4 times higher than that of calcitriol []. Indeed, previous studies have shown that vitamin D analogues that have a higher affinity for DBP show a longer half-life. Although the mechanism remains unclear, vitamin D analogue that binds tightly to the DBP may be less catalyzed by the cellular 24-hydroxylase activity, which is expressed in the target cells of vitamin D []. After treatment with effective antibiotics, inflammatory markers decreased steadily, and oxygen support was discontinued. His consciousness recovered after improvements in the pneumonia and hypocalcemia. Glasgow coma scale score on the 8th hospital day was E4V4M6, and he was able to eat orally. Intravenous Ca gluconate was continued until his serum Ca level increased to within the reference range. While continuing intravenous Ca gluconate and oral administration of calcitriol and Ca supplement, we administered maxacalcitol ointment, another VDRA used for psoriasis. Maxacalcitol was applied to trunk and limbs twice daily with less than 10 g/day. The absorption rate, maximum drug concentration time, and biological half-life of maxacalcitol ointment are 83.1%, 3 h, and 2–4 h, respectively. An epileptic seizure occurred on the 15th hospital day when his serum Ca level was still below the lower reference limit. The seizure episode might also have been caused by his prolonged hypocalcemia or might have been related to his history of traumatic subarachnoid hemorrhage. Thereafter, oral administration of levetiracetam was started.
After those combined treatment, his serum corrected Ca level finally increased up to 8.2 mg/dL, and his serum phosphate level increased from 1.6 mg/dL to 3.1 mg/dL. After his serum Ca and phosphate levels were stabilized, he was discharged on the 24th hospital day. At 3 months after discharge, he was in the nursing home without relapse of hypocalcemia, followed by discontinuation of maxacalcitol ointment. With continuous eldecalcitol administration only, his serum Ca level remained stable after 5 months.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [161.0, 'cm']}",57.78748,54.89811,60.67685,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 161.0 cm, which is 161.0 cm * 0.393701 in/cm = 63.38586 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (63.38586 (in inches) - 60) = 57.78748 kg.
Hence, the patient's IBW is 57.78748 kg."
3568,10,Ideal Body Weight,physical,decimal,pmc-6132029-2,Extracted,"The patient was a 17-year-old Japanese girl (163 cm, 54 kg) with severe headache and vomiting that had continued for several months with no history of medication except for anti-pain drugs. Her lumbar CSF pressure was elevated to >50 cmH2O. An MR venogram showed severe stenosis at the right TS and occlusion of the left internal jugular vein (). An angiogram showed stenosis at the mid-portion of the right TS with an 11-mmHg pressure gradient across the stenosis (, ). We deployed a Precise Pro RX stent (10×40 mm; Cordis, Fremont, CA, USA), and it achieved complete dilatation without a pressure gradient (, ). All of the patient’s symptoms disappeared just after the operation. Her lumbar CSF pressure dropped to 13 cmH2O on discharge. The papilledema was almost eliminated. A follow-up angiogram taken 1 month later showed no restenosis ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [163.0, 'cm']}",55.0985,52.34358,57.85343,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 163.0 cm, which is 163.0 cm * 0.393701 in/cm = 64.17326 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.17326 (in inches) - 60) = 55.0985 kg.
Hence, the patient's IBW is 55.0985 kg."
3569,10,Ideal Body Weight,physical,decimal,pmc-3030052-1,Extracted,"A 44-year-old male, who was 175 cm tall and weighed 70 kg, was admitted to the emergency room after being hit hard on his abdomen by a rope. At first, the patient complained of pain in the abdomen and both lower limbs. There was no noteworthy record in his case history, and the preoperative blood test did not show notable findings except HBsAg positive. Electrocardiography manifested sinus tachycardia and premature ventricular contraction, but there were no notable findings in the biochemical test, urinalysis and the chest radiography. On the physical exam, pulse was not palpated in both insteps. Since computed tomography manifested the injury of superior mesenteric artery and vein in addition to small bowel laceration and the rupture of the descending colon, an emergency operation was performed.
Preanesthetic administration was not performed. Immediately before the operation, blood pressure was 80/57 mmHg and heart rate was 110 beat/min. Peripheral oxygen saturation was 98%. Electrocardiography manifested sinus tachycardia, and consciousness was clear. Anesthesia was performed through the intravenous injection of 14 mg of etomidate, 50 mg of rocuronium and 0.05 µg/kg/min, and endotracheal intubation was performed after a brief manual ventilation. Until the operation was completed, 2 L/min of oxygen, 2 L/min of air and 4 to 5 vol% of desflurane were administered. The electrocardiogram, blood pressure, heart rate, peripheral oxygen saturation, capnogram, body temperature and urine volume were checked during the operation. In order to monitor intraoperative conditions and supply infusion solutions invasively, a catheter was inserted into the radial artery and a central venous catheter was inserted into the right internal jugular vein. And anesthetic intensity was monitored on the basis of the bispectral index. The arterial blood gas analysis, performed before the operation, showed pH of 7.33, PaCO2 of 36 mmHg, PaO2 of 133 mmHg, base excess of -5.7 mEq/L, 99% SaO2, potassium of 3.2 mEq/L and calcium of 1.02 mEq/L at FiO2 of 0.21.
Vital signs did not change remarkably until the latter half of the operation, but the arterial blood gas analysis, performed 2 hours after anesthesia, showed pH of 7.39, PaCO2 of 36 mmHg, PaO2 of 240 mmHg, base excess of -3.2 mEq/L, 100% SaO2, potassium of 4.4 mEq/L and calcium of 0.97 mEq/L at FiO2 of 0.5. And the analysis, performed 3 hours later, showed pH of 7.26, PaCO2 of 43 mmHg, PaO2 of 256 mmHg, base excess of -7.4 mEq/L, 100% SaO2, potassium of 5.8 mEq/L and calcium of 0.97 mEq/L at FiO2 of 0.5. Notwithstanding that 6 units of regular insulin, 60 mEq of sodium bicarbonate and 600 mg of calcium chloride were intravenously injected during the operation, potassium increased continuously. And after the iliac artery, which sustained an ischemic injury in the process of the operation, was anastomosed and was reinfused, the electrocardiogram showed tall T waves and the arterial blood gas analysis showed pH of 7.26, PaCO2 of 49 mmHg, PaO2 of 251 mmHg, base excess of -5.3 mEq/L, 100% SaO2, potassium of 6 mEq/L and calcium of 0.85 mEq/L at FiO2 of 0.5 (). Hereat, it was regarded as an electrolyte disorder of emergency and thus 5 units of regular insulin and 200 ml of dextrose were intravenously injected 100 mEq of sodium bicarbonate along with the use of 100 mEq of sodium bicarbonate and the injection of 300 mg of 3% calcium chloride. And 30 minutes later the arterial blood gas analysis was performed, which showed that pH of 7.30, PaCO2 of 40 mmHg, PaO2 of 257 mmHg, base excess of -6.3 mEq/L, 100% SaO2, potassium of 7.7 mEq/L and calcium of 0.84 mEq/L at FiO2 of 0.5. Resultantly, potassium increased more and tall T waves were continuously observed on electrocardiography. At this, 10 units of regular insulin and 30 ml of 20% dextrose were intravenously injected simultaneously with the injection of 20 mg of furosemide. Just then the bispectral index, which was between 30 and 40 during the operation, indicated 65, hence 3 mg of midaxolam was intravenously injected. On this, hypotension suddenly occurred and lasted a while. To bring up blood pressure, ephedrine was intravenously injected three times, 5, 10 and 20 mg each. But blood pressure did not rise, and thus 5 µg/kg/min of dopamine was instilled.
After that, the abdominal and inguinal operation was finished and the region was disinfected. After the drape was pulled back, the patient manifested the compartment syndrome and thus fasciotomy was performed urgently. Hypotension and arrhythmia continued even while fasciotomy was being performed, whereupon norepinephrine was instilled. Then blood pressure was recovered by 110 to 120 and 70 to 80 mmHg.
It took 11 hours in all to finish the operation, and aortic tansection, small bowel laceration, the segmental rupture of the descending colon, the transverse rupture of the rectus muscle were diagnosed during the operation, for which aortobifemoral bypass, small bowel resection, descending colon resection and rectus muscle repair were performed. In the operating room, 8,000 ml of plasma, 1,300 ml of hartman solution, 9,800 ml of physiological saline, 1,500 ml of crystalloid solution, 9 units of packed red blood cells and 5 units of fresh frozen plasma were administered to the patient. They totaled 24,480 ml, and blood loss and urine volume were estimated at 5,000 ml and 3,350 ml each. After the operation was completed, the patient was transferred to the intensive care unit with a tube in his airway, to whom mechanical ventilation was applied at FiO2 0.8, PIP 20 cmH2O, respiratory rate of 20 breathe/min and PEEP 6 cmH2O.
Immediately after the patient was transferred to the intensive care unit, the potassium level increased by 8.8 mEq/L, and 30 minutes later ventricular tachycardia and fibrillation were observed on the electrocardiogram and systolic blood pressure dropped by 50 mmHg. After defibrillation was applied twice at 200 joule, sinus rhythm was recovered normally, whereat 1 g of calcium gluconate was administered and 10 units of regular insulin and 10 ml of 50% dextrose water were intravenously injected by mixture. And then kalimate enema was performed. The arterial blood gas analysis, performed after kalimate enema, showed pH of 7.30, PaCO2 of 38 mmHg, PaO2 of 404 mmHg, base excess of -8.4 mEq/L, 100% SaO2, potassium of 7.7 mEq/L and calcium of 0.98 mEq/L at FiO2 of 0.8. After that, urine became dark-brown and continuous renal replacement therapy was performed. During the operation the manifestation of rhabdomyolysis was observed and thus conservative treatment was performed, and after the operation, it was definitely diagnosed in view of the fact that the test blood showed blood urea nitrogen of 14.9 mg/dl, creatinine of 1.50 mg/dl, aspartate transaminase of 3,069 IU/L, alanine transaminase 0f 842 IU/L, lactate dehydrogenase of 14,202 IU/L, creatine phosphokinase of 354,000 IU/L and serum myoglobin of 18,869 ng/ml ().
Although infusion solutions were sufficiently supplied and dopamine and norepinephrine were used, blood pressure did not rise and also multiple organ failure took a turn for the worse in tandem with renal failure accompanied by oliguria. Eventually 5 days after the operation, the patient expired.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3570,10,Ideal Body Weight,physical,decimal,pmc-3927008-1,Extracted,"A 53-year old male (height 173.6 cm, weight 75.6 kg) was scheduled for emergency cadaveric donor liver transplantation due to hepatitis B virus-related liver cirrhosis and hepatocellular carcinoma. Microvascular angina was diagnosed 2 years earlier with atypical chest pain. Coronary angiography at that time showed no significant stenotic findings. The patient was diagnosed with atrial fibrillation at the same time, and he was started on nicorandile, molsidomine, isosorbide dinitrate, digoxin, furosemide, and spironolactone. An anticoagulant was excluded due to bleeding tendencies. Furthermore, the patient had liver cirrhosis-related diabetes mellitus, portal hypertensive gastropathy, and esophageal varix.
ECG was performed just before surgery and showed atrial fibrillation with a normal heart rate (). The calculated QTc interval was 455 ms. The patient had mild mitral regurgitation and tricuspid regurgitation, but no regional wall motion abnormality was seen on preoperative echocardiography. The calculated left ventricular ejection fraction was 68%, and the mean pulmonary arterial pressure was 24 mmHg. The PT INR was 1.38, total bilirubin was 2.2 mg/dl, platelet count was 48,000 /µl, and albumin was 2.5 g/dl. Other blood test findings were within normal limits.
Without preoperative medication, the patient entered the operating room and his vital signs were measured immediately. His blood pressure (BP) was 117/73 mmHg, heart rate (HR) was 80 beats/min, and his pulse oximetry oxygen saturation (SpO2) was 99%. After preoxygenation with a mask by applying 100% O2 at 6 L/min for a few minutes, palonsetron 0.075 mg, lidocaine 40 mg, and propofol 120 mg were administered intravenously. After the patient lost consciousness, manual assisted ventilation was performed with 100% O2 at 6 L/min and 5 vol% sevoflurane; in addition, rocuronium 50 mg was injected. With full relaxation, the patient's trachea was intubated using a cuffed 7.5 mm endotracheal tube without difficulty. The radial and femoral arteries were cannulated, followed by continuous arterial blood pressure monitoring. A central venous catheter (AVA HF; Edwards Lifesciences, Irvine, CA, USA) was placed at the right internal jugular vein with no resistance or difficulty. A pulmonary artery catheter (Swan-Ganz CCOmbo; Edwards Lifesciences, Irvine, CA, USA) was inserted and pulmonary artery pressure monitoring was started. By ECG, no clinically significant change occurred during insertion of the pulmonary artery catheter. The catheter's position was checked with a chest X-ray. Anesthesia was maintained with 0.7 L/min O2, 1.3 L/min air, and 1.5-4.0 vol% sevoflurane. Initial arterial blood gas analysis (ABGA) revealed normal electrolyte levels and adequate oxygenation. ECG showed atrial fibrillation, but no clinically significant abnormal change was observed.
At 50 minutes after the patient's arrival, the surgeon started to prepare for surgery. At that time, sudden-onset large QRS tachycardia () appeared, and the femoral and radial arterial waves became flat. The end tidal CO2 (ETCO2) pressure dropped rapidly, from 35 to 13 mmHg. Epinephrine 100 µg and calcium chloride 300 mg were administered twice. One of the surgeons started cardiac compression immediately, and mechanical ventilation was continued with 100% O2. Epinephrine 1 mg was injected intravenously. During CPR, defibrillation was performed four times using 150-200 J, and epinephrine 1 mg was administered intravenously every 3-5 minutes. Amiodarone 300 mg mixed with 100 ml of normal saline was administered. Additionally, magnesium sulfate 2 g and lidocaine 70 mg were injected intravenously. Calcium chloride, regular insulin, and sodium bicarbonate were also administered after checking ABGA (). During CPR, a bloody secretion started to come out of the endotracheal tube, and the peak inspiratory pressure increased. We repeatedly suctioned the endotracheal tube, and alveolar recruitment via manual bagging was attempted a few times.
After 30 minutes of CPR and the last defibrillation, large QRS tachycardia disappeared and ECG revealed a normal sinus rhythm. Simultaneously, the femoral and radial arterial waves recovered to normal wave forms. The patient's systolic BP was 80-85 mmHg, his HR was 40-45 beats/min, and ETCO2 was 17-19 mmHg. After the return of spontaneous circulation, we loaded 50 µg/kg milrinone intravenously and started continuous infusion of milrinone at 0.5 µg/kg/min and epinephrine at 0.1 µg/kg/min. Regular insulin, sodium bicarbonate, and vasopressin were also administered. The patient's temperature was 34.7℃, and both pupils were dilated without a light reflex.
A few minutes later, the patient's SpO2 increased to 100%, and ETCO2 increased to 28 mmHg. The patient's vital signs stabilized at a HR of 80-85 beats/min, systolic BP over 100 mmHg, and mean BP over 80 mmHg. Without proceeding with the operation, the patient was transferred to the intensive care unit (ICU). The total exposure time to anesthesia was about 110 minutes. 1 L of crystalloid and 400 ml of colloid were infused, and the patient's urine output was 30 ml during anesthesia. On arrival at the ICU, the patient's BP was 98/62/76 mmHg, his SpO2 was 100%, and ECG showed atrial fibrillation with a HR of 80 beats/min. The patient's pupil reflex returned to a normal response. Electrolytes and cardiac enzymes were evaluated. Neither hypokalemia nor hypocalcemia was detected, and all electrolyte values were within normal levels. The patient's CK was 106 IU/L, CK-MB was 2.6 ng/ml, and Troponin I was slightly elevated to 0.10 ng/ml. Bedside echocardiography revealed no regional wall motion abnormality or evidence of myocardial ischemia.
On the second day of ICU admission, pulse-less large QRS tachycardia appeared twice. Both events were terminated after applying defibrillation using 150 J and cardiac compression for 2 minutes. Metabolic acidosis, intravascular volume loss, and pulmonary edema were aggravated and the patient's BP and SpO2 continued to decrease. On the fourth day in the ICU, the patient expired. ECG showed a marked prolonged QTc interval (). Nevertheless, cardiac echocardiography performed on the day of the patient's expiry showed normal findings. No regional wall motion abnormality was observed, and the left ventricular wall thickness was normal with a calculated ejection fraction of 56%. The patient's systolic pulmonary arterial pressure was 33 mmHg.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.6, 'cm']}",69.19693,65.73708,72.65678,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.6 cm, which is 173.6 cm * 0.393701 in/cm = 68.34649 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.34649 (in inches) - 60) = 69.19693 kg.
Hence, the patient's IBW is 69.19693 kg."
3571,10,Ideal Body Weight,physical,decimal,pmc-8188103-1,Extracted,"A 39-year-old Ethiopian-American woman presented with a history of severe EDS since childhood. She recalled falling asleep in class, during conversations, and walking with her mother holding hands. She reported fragmented, unrefreshing sleep and occasional hallucinations on awakenings. Although a diagnosis of narcolepsy was not made in Ethiopia, where she spent her childhood, dextroamphetamine was prescribed. She relocated to the United States but interrupted her college education due to EDS, sleep fragmentation, and depression. She occasionally experienced loss of muscle control triggered by laughter, primarily in her hands, and experienced episodes of automatic behavior, mostly while driving. Daytime naps were refreshing. Her past medical history was significant for attention deficit disorder treated with dextroamphetamine 10mg, which partly improved her EDS. She denied head trauma, snoring, witnessed apneas, restless legs symptoms, or any other complaints. Family and social histories were unexceptional.
The patient appeared healthy with normal vitals and physical exam. She weighed 87.5kg, measured 157.5cm, and BMI was 35.3kg/m2. Laboratory analysis including urine toxicology and TSH were normal. She scored 24/24 on the Epworth Sleepiness Scale (ESS). An overnight PSG followed by Multiple Sleep Latency Test (MSLT) was conducted an American Academy of Sleep Medicine (AASM) accredited facility in Rockville, Maryland, United States. This demonstrated normal architecture without pathology (). The mean sleep latency (MSL) for five naps was 1.3 minutes with sleeponset rapid eye movement (REM) periods (SOREMPs) in all five nap periods (). HLA-typing and a CSF hypocretin level were not performed due to her classic presentation and reported cataplectic symptoms. She was diagnosed with N1. Dextroamphetamine was discontinued, and modafinil 200mg was prescribed (). She noted significant improvements in morning sleepiness but had residual afternoon sleepiness, which resolved with an additional modafinil 100mg. On followup, she reported significantly improved quality of life and daytime alertness.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [157.5, 'cm']}",50.11819,47.61228,52.6241,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 157.5 cm, which is 157.5 cm * 0.393701 in/cm = 62.00791 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.00791 (in inches) - 60) = 50.11819 kg.
Hence, the patient's IBW is 50.11819 kg."
3572,10,Ideal Body Weight,physical,decimal,pmc-7944535-1,Extracted,"We report the case of a 69-year-old woman who was diagnosed with type 2 diabetes when she was 65 years old, had had HBV infection for 10 years, and who presented with a blood glucose concentration of 21.3 mmol/L and decompensated liver cirrhosis. According to the patient, she had vomited ∼500 mL fresh blood twice a day 10 years previously. After treatment by esophageal and gastric fundic vascular ligation to provide hemostasis (details unknown), the patient’s hematemesis was significantly ameliorated. Hepatitis screening showed positivity for hepatitis B virus surface antigen (HBsAg), hepatitis B virus core antibody IgG (HBcAb IgG) and hepatitis B virus e antibody IgG (HBeAb IgG), but not for hepatitis B virus surface antibody (HBsAb) or hepatitis B virus e antigen IgG (HBeAg). The HBV DNA concentration was within the normal range, as were the circulating aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities and the total bilirubin concentration (21 IU/L, 29 IU/L, and 11 µmol/L, respectively). Elastography showed the presence of severe liver fibrosis, with a stiffness of 16.5 kPa. The patient had not undergone any antiviral therapy, but had taken some Chinese medicinal herbs 2 years after the onset of diabetes. Since then, she had been under the care of the Department of Endocrinology of Dongyang People’s Hospital.
After her first hospital stay, the patient weighed 56 kg, was 158 cm tall, and had a body mass index (BMI) of 22.4 kg/m2. She was administering 30 units daily of recombinant NovoRapid® 30Mix (BIAsp30). Lipoatrophy developed at the insulin injection site on the right side of her abdominal wall 1 year after the start of insulin therapy (), and during this period she was not admitted to hospital because of liver cirrhosis decompensation or other problems. Furthermore, after she started administering insulin on her left side, a second lesion developed there. She next started to rotate her injection sites, including both sides of her thighs (), buttocks (), and arms (), but lipoatrophic defects developed at all these injection sites, which were confirmed ultrasonographically (). The ultrasonographic examination showed that her skin was normal (), the underlying adipose tissue was dystrophic (), and the underlying muscle was normal (). The size of all the lesions increased steadily, and 1 year after starting insulin therapy, indentations of various sizes had developed. The dimensions of the smallest indentation were 0.4 cm × 1 cm (left arm) and those of the largest were 5 cm × 12 cm (thigh), with depths of 0.2 to 2 cm. The lipoatrophic lesions expanded around the insulin injection site. According to the patient, she had sought medical assistance in the city of Dongyang, and many attempts were made to ameliorate the lesions, mainly comprising changes in the injection site and insulin type, including a switch to Novolin 30R (an insulin mix consisting of 30% R/neutral insulin and 70% neutral protamine Hagedorn [NPH]). However, these measures failed to stop the development of lipoatrophic lesions or ameliorate the existing lesions. Four years after starting insulin therapy, when the patient was last examined, she had lost 2 kg of body mass, such that she weighed 54 kg and had a BMI of 21.6 kg/m2, with no ascites. Routine laboratory testing showed that her white blood cell count was within the normal range. Her circulating procalcitonin concentration was within the normal range (0.17 ng/mL), but those of interleukin-6 (IL-6) and C-reactive protein (CRP) were high (16.83 pg/mL and 8.13 ng/L, respectively).
She stopped injecting insulin for 6 months after visiting her physician, at the end of which she had a glycated hemoglobin (HbA1c) concentration of 8.3%, a fasting blood glucose concentration of 21.3 mmol/L and normal concentrations of relevant autoantibodies, including versus glutamic acid decarboxylase (GAD), islet cell cytoplasmic autoantibodies (ICAs), insulinoma-associated-2 autoantibodies (IA-2As), and insulin autoantibodies (IAAs).
At this time, the patient was instructed to stop her insulin injections and to start oral antidiabetic drugs (OADs; an alpha-glucosidase inhibitor [acarbose] and a sulfonylurea [glimepiride)). This treatment was successful because 1 month after discharge she had an HbA1c of 7.2% and there had been no deterioration in her liver indices. In addition, after 6 months of this regimen, there had been no deterioration of the lipoatrophy and no more new sites of lipoatrophy had developed.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3573,10,Ideal Body Weight,physical,decimal,pmc-4763651-1,Extracted,"We hereby report bleomyicn-induced lipodystrophy in 20-year-old female; weight 48 kg, height 1.65 m diagnosed with a case of germ cell carcinoma of the ovary (endodermal sinus tumor) reported in Adverse Drug Reaction Monitoring (Under PvPI) Centre vde no. 423/250211/ADRM.
Preoperative cancer marker levels were as follows: CA-125 = 26.6 U/ml; alpha fetoprotein = 3765 ng/ml; human chorionic gonadotropin <1 mIU/mL. Ultrasonography (USG) helped in establishing the diagnosis of an ovarian tumor/mass. Postoperative histopathological findings confirmed it as a case of germ cell carcinoma of the ovary (endodermal sinus tumor, also known as a yolk sac tumor).
Postoperatively, the patient was started with injections of bleomycin (30 mg/m2 D1, D8 and D15); injections of etposide (100 mg/m2 I.V. D1 and D5) and cisplatin (20 mg/m2 I.V. D1 and D5) combination in cyclic manner. The patient developed acquired partial lipodystrophy with subcutaneous fat loss limited to the trunk and left side of the back within 3 days of the first cycle [Figures –]. The patient had no history of smoking, alcohol consumption, any substance abuse, associated pathology, concurrent drug or vaccine intake.
There was no history of such an episode in the past. Clinical examination revealed no rheumatological, nephrological, neurological or liver problem present. Investigations revealed a normal chest skiagram. All basic investigations including complete blood count, hemoglobin, erythrocyte sedimentation rate, routine urine, stool examination, blood sugar, liver function test, renal function test, lipid profile, electrocardiogram, and USG were found to be normal. The HIV status of the patient was negative.
Since the adverse drug reaction (ADR) was not serious and had only cosmetic implications in the young woman, the patient was continued with the same drugs in cyclic manner and the cause of the ADR was most likely thought to be associated with bleomycin because of its known cutaneous toxicities.[]
Dechallenge of the bleomycin during chemotherapy recovery phase caused the ADR to ameliorate. Further rechallenge resulted in the reappearance of the ADR during next cycle. No treatment was given to the patient, and she is still on follow-up. Thus, the appearance of bleomycin-induced partial lipodystrophy could not be explained by a concurrent disease, other drug or chemicals. Dechallenge improved the condition and rechallenge resulted in reappearance of the ADR. On literature search there is no similar report of such ADR. However, skin toxicities are well-known with bleomycin.[]","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.65, 'm']}",56.90952,54.06404,59.755,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.65 m, which is 1.65 m * 39.3701 in/m = 64.96066 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96066 (in inches) - 60) = 56.90952 kg.
Hence, the patient's IBW is 56.90952 kg."
3574,10,Ideal Body Weight,physical,decimal,pmc-6547240-1,Extracted,"A 77-year-old man, who was 172 cm tall and weighed 70 kg, was scheduled for radical mastectomy and axillary clearance for breast cancer. He had a history of myocardial infarction one year previously, for which he had undergone insertion of multiple bare metal coronary artery stents. He had developed post-infarction dilated cardiomyopathy with a severe reduction in ejection fraction (30%), a marked increase in the left ventricular diastolic diameter (6.8 cm), and global left ventricular hypokinesia with apical akinesia. He also had moderate mitral and minimal tricuspid valve insufficiency. His preoperative chest radiograph revealed cardiomegaly. His past medical history also included hypertension, diagnosed forty years ago. He was also a current, light smoker (less than 10 cigarettes per day). At pre-anesthetic evaluation, he was on dual antiplatelet therapy with aspirin and clopidogrel and on valsartan for hypertension. After specialist consultation, we decided to continue preoperative medications.
We planned a regional anesthesia technique using a combination of ESP and SBP block to avoid the use of general anesthesia. This technique was explained to the patient, and a written informed consent was obtained for the procedure.
We used a high-frequency linear ultrasound transducer (M-Turbo, FUJIFILM SonoSite Europe, The Netherlands) and 22 G × 50 mm needles (SonoPlex STIM, Pajunk, Germany) for the procedure.
The ESP block was performed as described by Forero et al. [] with 20 ml of 0.5% ropivacaine. The patient was placed in the supine position with the ipsilateral arm abducted to perform the SBP block. The LTN was identified at the C7 level within the middle scalene muscle; 3 ml of 0.5% ropivacaine was injected to perform the block (). The TDN was identified in the infraclavicular region near the thoracodorsal artery and blocked with 3 ml of 0.5% ropivacaine (). The LPN and the MPN were blocked by injection of 10 ml of 0.5% ropivacaine between the pectoralis major and pectoralis minor muscles (). A total dose of 36 ml of 0.5% ropivacaine was used to perform the blocks.
An adequate level of anesthesia was ensured on assessment after 30 min by testing for pain sensation to pinprick (), followed by the commencement of the surgical procedure. During surgery, a score of 3–4 was achieved on the Observer’s Assessment of Alertness/Sedation scale with a bolus dose of propofol 40 mg followed by an infusion of 2 mg/kg/h. No intraoperative opioids were required, and the patient remained comfortable throughout the entire duration of surgery that lasted for about 100 min. Administration of 1 g acetaminophen every 8 h was performed for postoperative pain relief; no additional analgesics were required intraoperatively and for two postoperative days before discharge. Postoperative pain was assessed every 6 hours using the numerical rating scale (NRS). The patient reported a pain score of less than 3 on the NRS at each pain assessment. He was discharged on the second postoperative day without complications.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [172.0, 'cm']}",67.74811,64.3607,71.13552,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 172.0 cm, which is 172.0 cm * 0.393701 in/cm = 67.71657 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.71657 (in inches) - 60) = 67.74811 kg.
Hence, the patient's IBW is 67.74811 kg."
3575,10,Ideal Body Weight,physical,decimal,pmc-6739019-1,Extracted,"A 59-year-old Asian woman presenting with impaired consciousness and general malaise was brought to our hospital by her family. She had been diagnosed with anti-aminoacyl-tRNA synthetase antibody-positive interstitial pneumonia in February 2017 (13 months before admission) with the complaint of exertional dyspnea. She had never been diagnosed with diabetes; 13 months before admission, her glycosylated hemoglobin (HbA1c) level was 6.1%. On diagnosis of interstitial pneumonia, she started receiving 60 mg of methylprednisolone, followed by 40 mg of prednisolone (PSL) and 4.0 mg of TAC, which was considered effective and well-tolerated therapy for interstitial lung disease with anti-aminoacyl-tRNA synthetase antibody.[ The dosage of PSL was gradually decreased, and 5.0 mg of PSL and 4.0 mg of TAC had been continued to maintain the remission of interstitial pneumonia. She had no other specific medical history or any significant family history. Following were her vital signs on admission: blood pressure, 110/66 mmHg; respiratory rate, 18 breaths/min; pulse rate, 97 beats/min; and SpO2, 96% on room air. Her height was 159 cm and her weight was 90 kg; her body mass index (BMI) was 35.6 kg/m2. On physical examination, lungs were clear to auscultation and no significant abnormalities were observed, except slight dehydration of the tongue and axilla. Laboratory data revealed the following: extremely high plasma glucose levels, 989 mg/dL (54.9 mmol/L); presence of urinary ketone bodies; blood pH, 6.85; and bicarbonate level, 2.4 mmol/L; these findings met the diagnostic criteria for DKA proposed by the American Diabetes Association.[ Fasting serum C-peptide immunoreactivity (CPR) was 0.62 ng/mL and urinary CPR was 13.4 μg/d, indicating deterioration of endogenous insulin secretion. No islet-related autoantibodies were detected (Table ). Other laboratory data are shown in Table . Intravenous continuous insulin infusion and rapid saline infusion were administered; 2 days after admission, insulin administration was switched to multiple daily subcutaneous injections using insulin lispro and insulin glargine 300 mL/unit. The maximum amount of subcutaneous insulin administered was up to 0.9 unit/kg/d. Sixteen days after admission, 10 mg of empagliflozin was also administered for inducing weight reduction. She was discharged with a prescription of 25 units/d of total daily insulin and 10 mg of empagliflozin; the dosage of PSL and TAC were maintained at 5.0 and 4.0 mg, respectively. TAC was discontinued 4 weeks after the onset of DKA as good control of interstitial pneumonia was noted. She did not require insulin lispro and insulin glargine 300 mL/unit to maintain stable glycemic control 4 and 8 days after cessation of TAC, respectively. Finally, although empagliflozin administration was also stopped 16 weeks after TAC cessation, her blood glucose levels were under good control; her HbA1c level was 6.2%, even though PSL administration was continued. Notably, her fasting serum CPR level rapidly recovered to 4.15 ng/mL, which is within the normal range, 8 weeks after TAC cessation and was maintained at similar levels thereafter (Fig. ). Written informed consent was obtained from the patient for publication of this case report.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [159.0, 'cm']}",51.47646,48.90264,54.05028,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 159.0 cm, which is 159.0 cm * 0.393701 in/cm = 62.59846 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.59846 (in inches) - 60) = 51.47646 kg.
Hence, the patient's IBW is 51.47646 kg."
3576,10,Ideal Body Weight,physical,decimal,pmc-3668109-2,Extracted,"A 40-yr old man (body weight: 73 kg, height: 172 cm) was scheduled for living donor liver transplantation surgery due to acute liver failure. One week ago, he developed grade 1 hepatic encephalopathy. In the preoperative evaluation, electrocardiography and echocardiography were within normal range. Chest X-ray showed mild pleural effusion on both lungs. His laboratory examination showed Hb 9.9 g/dl, platelet count 107 × 109/L, prothrombin time 2.2 international normalized ratio, fibrinogen 82 mg/dl, antithrombin III 12%, sodium 135 mmol/L, potassium 3.0 mmol/L, creatinine 1.1 mg/dl, glucose 144 mg/dl, albumin 3.0 g/dl, total bilirubin 23.1 mg/dl, and ammonia 82 µmol/L. Her Child-Pugh and Model for End-Stage Liver Disease scores were 12 and 28, respectively.
Upon arrival at the operating room, his mental state was alert. His systolic/diastolic arterial blood pressure and heart rate were 132/68 mmHg and 98 beats/min, respectively. After establishing institutional standard monitoring, an ultrasound ONSD measurement was done by a physician well-trained in ocular ultrasonography. His ONSD just before anesthesia induction was 4.8 mm (). The bispectral index and suppression ratio were 98 and 0, respectively, and right and left regional cerebral oxygen saturations were 43 and 44%, respectively.
General anesthesia was induced and maintained by the standard protocol at our institute. His lungs were ventilated with a tidal volume of 8-10 ml/kg at a respiratory rate of 10 breaths/min (PaCO2, 35-40 mmHg). Intraoperative hemodynamics and laboratory data were shown . He experienced severe hypotension (systolic/diastolic arterial blood pressure: 62/48 mmHg) and bradycardia (56 beats/min) after graft reperfusion, and was treated with epinephrine (20 µg), after which systolic/diastolic arterial blood pressure (122/72 mmHg) and heart rate (92 beats/min) rapidly recovered to within the normal limit. His ONSD was dilated at 5.7 mm to 5 min after reperfusion (), and hyperventilation was performed with a tidal volume of 12 ml/kg at a respiratory rate of 13 breaths/min (PaCO2, 28 mmHg). His ONSD decreased to 5.1 mm at 30 min after reperfusion (), and ventilation was adjusted to maintain normocarbia until the end of surgery. He was moved to the surgical intensive care unit after surgery, and then transferred to a general ward without any complications on the seventh postoperative day.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [172.0, 'cm']}",67.74811,64.3607,71.13552,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 172.0 cm, which is 172.0 cm * 0.393701 in/cm = 67.71657 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.71657 (in inches) - 60) = 67.74811 kg.
Hence, the patient's IBW is 67.74811 kg."
3577,10,Ideal Body Weight,physical,decimal,usmle-276,Extracted,"A 43-year-old man is brought to the emergency department because of severe epigastric pain and vomiting for 6 hours. The pain radiates to his back and he describes it as 9 out of 10 in intensity. He has had 3–4 episodes of vomiting during this period. He admits to consuming over 13 alcoholic beverages the previous night. There is no personal or family history of serious illness and he takes no medications. He is 177 cm (5 ft 10 in) tall and weighs 55 kg (121 lb); BMI is 17.6 kg/m2. He appears uncomfortable. His temperature is 37.5°C (99.5°F), pulse is 97/min, and blood pressure is 128/78 mm Hg. Abdominal examination shows severe epigastric tenderness to palpation. Bowel sounds are hypoactive. The remainder of the physical examination shows no abnormalities.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [177.0, 'cm']}",72.27568,68.6619,75.88946,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 177.0 cm, which is 177.0 cm * 0.393701 in/cm = 69.68508 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.68508 (in inches) - 60) = 72.27568 kg.
Hence, the patient's IBW is 72.27568 kg."
3578,10,Ideal Body Weight,physical,decimal,pmc-4930821-1,Extracted,"The patient was an 80-year-old man who was referred to our division for the chief complaints of macroglossia and articulatory disorder. Oral findings showed painless tumors on the bilateral margins of the tongue and dysarthria/dysphasia (). His medical history included alcoholic liver injury, dyslipidemia, hypertension (HT), chronic gastritis, diabetes mellitus (DM), acute pancreatitis, glaucoma, and dementia. The patient was a heavy drinker. He had felt discomfort in the bilateral tongue margins for several decades but left it untreated. During an upper gastrointestinal endoscopy in the nursing home, tumors were found on the bilateral tongue margins and he was referred to our department. Findings at the first visit included a poor nutritional status (height: 160.0 cm, body weight: 52.7 kg, and BMI: 20.0 kg/m2). Extraoral findings showed facial symmetry and a good complexion. There were no significant findings in the cervical lymph nodes. Preoperative laboratory examination revealed high levels of TG (202 mg/dL), but TC and HDL and LDL-cholesterol were normal.
Multilocular tumors were found on the bilateral margins of the tongue, which formed macroglossia, and xanthic, elastic soft tumors were evident in the shallow submucosa. The surfaces of the tumors were smooth, and in particular, the left tongue margin was significantly elevated.
While there were no abnormalities in perception/taste, dysarthria was observed. MR images showed T2 hyperintensity and well-defined borders in the bilateral margins of the tongue and ill-defined trabecular structures like muscle bundles in the deep part of the tongue, which suggested that it might be symmetric lipomatosis (). The patient underwent bilateral partial glossectomy (tumor excision of the tongue) under general anesthesia. A spindle-shaped incision was made along the base of the tumors and the mucosa was detached along the tumor on the tongue margins (). The tumor margin was not clear in the deep portion and the tumor partially invaded into the muscle layer. Considering the potential for postoperative dysfunction, the muscle layer was also removed en bloc with the tumors (). While there were finely granular, lipoma-like lesions on the resected surface, conservative treatment was applied as resection of the abovementioned lesions might induce dysfunction. After confirming hemostasis, the incision was sutured and closed.
The resected specimens showed a relatively well-defined border in the mucosa but the encapsulation was not clear in the deep portion ().
The tumor consisted of proliferation of mature adipocytes, and there were no signs of encapsulation in the muscle layer or atypia, such as mitotic figures (Figures and ). Based on the abovementioned findings, the histopathological diagnosis showed lipomatosis. Therefore, clinically, the final diagnosis was SLT presenting as macroglossia.
At the present time, there has been no sign of postoperative dysfunction or complication, and the dysarthria and dysphasia have improved significantly. The patient's clinical course remains excellent ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [160.0, 'cm']}",56.88197,54.03787,59.72607,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.99216 (in inches) - 60) = 56.88197 kg.
Hence, the patient's IBW is 56.88197 kg."
3579,10,Ideal Body Weight,physical,decimal,pmc-7819202-1,Extracted,"Case 1 was a 20-year-old man with MMA. He was born via cesarean section because of placenta previa at gestational age of 37 weeks with birth weight of 2.7 kg. Due to positive family history (his brother had MMA), he underwent metabolic investigation. His metabolic evaluation revealed blood ammonia level of 400–500 mg/dL and elevated C3 carnitine level (48.8; reference range, < 4.1). The methylmalonic acid level in urine was 1617 µg/mg Cr, and elevation in plasma glycine (415 µmol/L) and alanine (978 µmol/L) levels were noted. Cobalamin (Cbl) incorporation study of 14C-propionate showed lack of response to Cbl (i.e. mut0) and slightly low response to adocobalamin (AdoCbl). Molecular investigations revealed a compound heterozygous c.1105C > T(p.R369C), p.G94Q mutation. He was fed with special formula (Propiomex), regular infant formula, low-protein food, and L-carnitine supplement (100 mg/kg/d). His developmental evaluation at 20 months of age showed a mild delay. Prior to 5 years of age, blood urea nitrogen (BUN) and creatinine were in the normal range (BUN 6.6–12.3 mg/dL /creatinine 0.7–0.8 mg/dL). However, after 5.5 years of age, his renal function slowly deteriorated, showing a BUN level of 16.2–29.2 and creatinine level of 0.81–1.02. He was hospitalized multiple times due to metabolic decompensations (acidosis, dehydration, and hyperammonemia) after trivial infections or skipping of the special formula. At 6 years of age, his eye sight deteriorated progressively and he became legally blind due to optic atrophy by 10 years of age. He received growth hormone treatment for metabolic induction to anabolism and improvement of his short stature. At 15 years of age, he experienced vomiting and abdominal pain due to pancreatitis. His metabolic status became unstable; he was hospitalized more than 7 times with pancreatitis (Table ). At this time, he began to experience hand tremors due to his metabolic condition. After recurrent pancreatitis at 19 years of age, he showed glucose intolerance. By the age of 20 years, he developed DM, requiring insulin injection. His most recent metabolic crisis was accompanied by severe metabolic acidosis (pH 6.8), liver dysfunction (aspartate aminotransferase (AST) 245 IU/L, alanine aminotransferase (ALT) 316 IU/L), hyperventilation, hemorrhagic gastritis, and left pleural effusion. His pancreatic amylase and lipase levels were > 4000 U/L. He was put on continuous renal replacement therapy for 3 days. During the metabolic crisis, he experienced seizures and hand tremors, although the results of brain magnetic resonance imaging (MRI) and electroencephalogram (EEG) were normal. The abdominal computed tomography (CT) showed necrotizing pancreatitis and follow-up ultrasound after 1 month of pancreatitis showed a pancreatic pseudocyst. His renal function progressively deteriorated, showing a BUN level of 40.1–60 mg/dL, Cr level of 2.04–2.81 mg/dL, and estimated glomerular filtration rate (eGFR) level of 43.7 mL/min/1.73 m2. His metabolic parameters were as follows: pH, 7.30–7.31; HCO3 level, 11.2–20.6; methylmalonic acid level, 1768–3861 µg/mg Cr; glycine level, 625–1187 µmol/L (normal range: 158–302 µmol/L); alanine level, 508–825 µmol/L (normal range: 185–537 µmol/L). His ferritin levels were 280–581.53 ng/mL (normal range: 50–200 ng/mL). His current weight is 46.1 kg and height is 164 cm. He has recovered completely from pancreatitis, and his glucose levels are being controlled using insulin (Table ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [164.0, 'cm']}",60.50401,57.47881,63.52921,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 164.0 cm, which is 164.0 cm * 0.393701 in/cm = 64.56696 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.56696 (in inches) - 60) = 60.50401 kg.
Hence, the patient's IBW is 60.50401 kg."
3580,10,Ideal Body Weight,physical,decimal,pmc-7724123-1,Extracted,"The patient was a 37-year-old man (148 kg, 183 cm, body mass index [BMI] 44.2 kg/m2) with a history of tracheostomy due to hypertensive intracranial hemorrhage that occurred 4 years ago. He was diagnosed with grade I tracheal stenosis above the tracheostomy site 2 years ago. Despite conservative treatment, dyspnea developed and the patient underwent endoscopic tracheal dilatation under general anesthesia. Baseline peripheral capillary O2 saturation (SpO2) was 94% and Cormack-Lehane grade was 3 at the time of intubation. Surgery was performed using the intermittent apnea technique with extubation, and a total of six apnea events occurred, with a mean duration of apnea was 147 s. The lowest SpO2 was 64%, and SpO2 recovered to 96–98% after manual ventilation via endotracheal tube. The patient had been treated conservatively after balloon dilatation with portable O2 at home. Dyspnea worsened again 1 year ago, despite O2 therapy, and serial fiberoptic steroid injections to the subglottic stenosis site were planned. In our hospital, fiberoptic steroid injections are usually performed according to the following steps. Topical anesthesia at nostrils is followed by sedation, applied by surgeon. The fiberscope is inserted through the nostril, and the glottis and lesion are sprayed with additional local anesthetics. Then, the lesion is injected with steroid. The otolaryngologist consulted us for safe sedation and monitoring due to the possibility of emergency caused by airway edema or airway obstruction. Considering the patient’s general condition, symptoms, and experience of previous surgery, we decided to perform the operation under general anesthesia with spontaneous breathing in preparation for airway manipulation, because general anesthesia using the intermittent apnea technique could limit the view of surgical field and damage the larynx and subglottic lesions.
On entering the operating room, the patient was placed in a 30° sitting position for the first steroid injection. Standard American Society of Anesthesiologists monitoring (non-invasive blood pressure [NIBP], electrocardiogram, and SpO2) and bispectral index (BIS) monitoring were applied. The baseline vital signs were as follows: BP, 105/52 mmHg; heart rate (HR), 66 beats per minute (beats/min); SpO2, 95%. Oxygenation was applied at 6 L/min O2 through a standard facial mask. End-tidal CO2 (EtCO2) was monitored continuously by capnography to confirm self-respiration. Dexmedetomidine was used for sedation. After delivering a loading dose of 1 μg/kg over 10 min, continuous infusion of 0.6 μg/kg/h was maintained. During infusion of the loading dose, the EtCO2 level decreased gradually until apnea was induced. An oral airway was inserted and the jaw-thrust maneuver was applied to maintain airway patency and support self-respiration. After confirming that the patient was unresponsive to verbal commands and tactile stimulus, the surgery was started while self-respiration was maintained. The surgeon requested lowering of the facial mask so that it would not interfere with the procedure and applied topical anesthesia by packing gauze soaked with Bosmin® (0.1% epinephrine) and Beracaine® (10% lidocaine) into both nostrils. The fiberscope was passed through the nostril to access the glottic and subglottic lesions, and additional 2% lidocaine was sprayed around glottis and lesions, and 3 ml of tamcetone® (Triamcinolone 40 mg/ml) was then injected. The procedure was interrupted by bag-valve-mask ventilation because SpO2 fell to 86%. After ventilator assistance for 117 s, SpO2 recovered to 96%. During surgery, HR remained within 20% of the baseline, but BP increased by more than 20% of the baseline. However, systolic BP remained below 160 mmHg, so no additional drug administration was necessary. The value of BIS was maintained between 55 and 80. The total surgery time was 20 min and the total anesthesia time was 40 min. The patient was discharged after 1 day of monitoring in the Intensive Care Unit (ICU), without dyspnea or complications.
Dyspnea improved noticeably, but on physical examination, grade II subglottic stenosis and stridor remained, thus necessitating a second steroid injection 1 month later. Based on our previous experience, we considered that there was a need to improve oxygenation during the procedure, so we decided to apply Optiflow®. In the same manner as in the first operation, the patient was placed in the 30° sitting position, and standard American Society of Anesthesiologists and BIS monitoring were applied. Baseline vital signs were as follows: BP, 102/58 mmHg; HR, 70 beats/min; and SpO2, 94%. O2 (100% warmed, humidified) was supplied through a nasal cannula at a rate of 30 L/min for preoxygenation. The patient tolerated this well, without any complaints. Dexmedetomidine was used for sedation at the same dose as before. Once the patient was unconscious, the O2 flow rate was raised to 70 L/min. EtCO2 was monitored by placing the EtCO2 sampling line at the nostril next to the Optiflow® nasal cannula; however, a low value was obtained, so we could only confirm self-respiration by monitoring the shape of the waveform (). Topical anesthesia was applied by packing gauze into both nostrils. This disturbed the O2 supply through the Optiflow® nasal cannula; therefore, we inserted an oral airway to maintain airway patency, and the Optiflow® nasal cannula was transferred to the opening of the oral airway. The EtCO2 line was also transferred to the opening of the oral airway, but it still showed a low value; thus, only the shape of waveform was monitored (). SpO2 was maintained at 98–100%, and no intervention, such as mask ventilation or jet ventilation, was required during surgery. Despite self-respiration, there was a drop in SpO2 to 86% () due to O2 leakage; the Optiflow® nasal cannula dislocated from the airway opening. After fixing the nasal cannula to the airway with plaster (), SpO2 immediately recovered to 99% and no additional desaturation events occurred. The vital signs were stable within 20% of baseline. Additional bolus of midazolam was injected to prevent the event of awareness because the value of BIS was maintained between 70 and 79 when the procedure was performed; 1mg for oral airway insertion, 2 mg for gauze packing into both nostrils. During the operation, the value of BIS was well maintained between 35 and 50, and spontaneous breathing was generally maintained well. The patient endured the surgical stimuli without coughing and movement throughout entire operation. The total operation time was 15 min and total anesthesia time was 40 min. The surgeon had prepared jet ventilation because of the experience during the previous surgery, but ultimately did not use it; thus, the surgeon was highly satisfied with THRIVE. After the surgery, the patient was transferred to the ICU. Arterial Blood Gas Analysis (aBGA) was performed after arrival in the ICU; partial pressure of O2, 94 mmHg; partial pressure of CO2 (PaCO2), 49 mmHg; pH, 7.30; bicarbonate, 21.3 mEq/L. The patient was discharged after 1 day of monitoring without complications.
This study was approved by the Institutional Review Board of Soonchunhyang University Bucheon Hospital (IRB No. 2020-02-026-001). And written informed consent, included the consent to publish images, was obtained from the patient in this study.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [183.0, 'cm']}",77.70874,73.8233,81.59418,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 183.0 cm, which is 183.0 cm * 0.393701 in/cm = 72.04728 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (72.04728 (in inches) - 60) = 77.70874 kg.
Hence, the patient's IBW is 77.70874 kg."
3581,10,Ideal Body Weight,physical,decimal,pmc-7476783-1,Extracted,"A 32-year-old man underwent primary THA for osteonecrosis of the femoral head. The patient was 1.72 m in height and 68 kg in weight (body mass index, 22.91 kg/m2). He had been under steroid therapy for 10 years because of dermatomyositis. This patient was informed that data from the case would be submitted for publication, and he gave his consent.
Staged THAs were performed with an interval of one month. The components used for the right hip were PLASMACUP SC® 56 mm (Aesculap, Tuttlingen, Germany), 3rd generation BIOLOX® forte liner (CeramTec), 3rd generation BIOLOX® forte 28 mm head with short neck, and BiCONTACT® (Aesculap) SD type stem of size 16. The components used for the left hip were PLASMACUP SC® 54 mm, BIOLOX® forte liner, BIOLOX® forte 28 mm head with medium neck, and BiCONTACT® SD type stem of size 17. There were no intra- or postoperative complications. On the right side, the inclination of the cup was 40.3° and the anteversion of the cup by the method of Bachhal et al. was 20.0°. On the left side, the inclination of the cup was 30.1° and the anteversion of the cup was 20.9°. The patient had been under annual routine follow-up with satisfactory clinical results. There was no overt negative symptoms, including squeaking.
At 14 years after surgery, the patient heard a pop in his right hip while pulling heavy luggage and visited the emergency room because of sustained pain and a clicking sound. Plain radiographs revealed a ceramic head fracture (). Revision surgery through trans-trochanteric approach was performed. During the revision surgery, ceramic liner fractures at multiple sites of its outer edge were identified in addition to the ceramic head fracture (). After meticulous removal of the fractured ceramic fragments, the remaining main body of the ceramic liner was extracted. After copious irrigation, a new ceramic liner and a 32 mm head with short neck were inserted. Both were made with the 4th generation alumina, BIOLOX® delta, and the head was coupled with a metal sleeve.
Postoperatively, the patient returned to normal activity after using crutches for eight weeks. At approximately 10 weeks after the operation, the patient experienced remarkable pain in his right hip immediately after falling resulting from a sudden forceful crush by a stranger while sitting in the squat position. The crushing force caused the right hip in the squatting position to be more flexed and abducted. He experienced persistent pain and crepitus in the right hip and visited the outpatient clinic at postoperative 12 weeks. Simple radiographs revealed multiple ceramic fragments presumed to be from the ceramic liner (). Re-revision surgery to exchange the ceramic head and liner with new ones was performed. During the operation, eight fractured segments and multiple smaller flakes of ceramic were identified originating from the edge of the ceramic liner. The fracture site occurred between 8 and 12 o'clock of the liner. When engaging in passive range of motion (ROM) of his right hip joint, impingement between the outer margin of the liner and the shoulder of the stem was observed. A notch on the shoulder-side of the stem was also observed (). All detected fragments were removed and the head and liner were exchanged after copious irrigation. The new head and liner were made of 4th generation BIOLOX® delta and a long neck head was used to prevent impingement between the stem shoulder and the liner. The patient is currently in satisfactory condition three years after re-revision surgery.
We retrospectively reviewed the patient's serial simple radiographs to detect signs of impingement between the ceramic liner and the stem shoulder. The notch on the medial side of the stem shoulder was continuously observed starting at 5 years after the initial operation ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.72, 'm']}",67.74811,64.3607,71.13552,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.72 m, which is 1.72 m * 39.3701 in/m = 67.71657 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.71657 (in inches) - 60) = 67.74811 kg.
Hence, the patient's IBW is 67.74811 kg."
3582,10,Ideal Body Weight,physical,decimal,pmc-4121497-1,Extracted,"A 41-year-old woman diagnosed with hepatitis B-related liver cirrhosis was scheduled for elective living-donor liver transplantation. The patient's height and weight were 157 cm and 58 kg, respectively. Her Child-Pugh classification grade was A with a model for end-stage liver disease (MELD) score of 8. She had no specific medical history. Her laboratory findings included hemoglobin 9.6 g/dl, platelet 47,000 /mm3, INR 1.19, albumin 3.7 g/dl, and total bilirubin 0.7 mg/dl. Her preoperative chest X-ray revealed no active lung lesion. The dynamic liver CT scan showed liver cirrhosis with portal hypertension. Esophagogastroduodenoscopy revealed esophageal varix which was treated by propranolol.
The patient did not take any premedication before surgery. Upon arrival in the operating room, routine monitoring including five-lead electrocardiogram, non-invasive blood pressure, and pulse oximetry was started. Her blood pressure was 115/75 mmHg, heart rate was 65 beats/min, and the oxygen saturation was 100%. Before induction of anesthesia, the right radial artery was cannulated to monitor continuous arterial pressure. The anesthesia was induced using thiopental 250 mg, fentanyl 100 µg, and midazolam 5 mg. Vecuronium 10 mg was injected for the ease of endotracheal intubation. The patient was aseptically prepared and draped for central venous catheterization. A 7.5- Fr pulmonary artery catheter (Swan Ganz CCOmbo V; Edwards Lifesciences, Irvine, CA) was inserted via a 9.0- Fr introducer (AVA HF; Edwards Lifesciences) through the right subclavian vein. The right subclavian vein was chosen because an 11.5 Fr. two-lumen central venous catheter (Mahurkar, Covidien, Mansfield, MA, USA) had been inserted in the right internal jugular vein (IJV) preoperatively for the purpose of therapeutic plasmapheresis owing to ABO incompatible transplantation. The tip of the PAC was ballooned and advanced through the introducer without resistance. While observing the waveforms of the PAC, the pressure wave on the monitor continuously showed a form of central venous pressure although the catheter was nearly 40 cm inside the vein. The catheter was pulled back outside the sheath for reinsertion. Further attempts were made, but the waveform did not change to a right ventricular pressure waveform. The vital signs were stable and no arrhythmia was present. Thus, to avoid any complications, an anteroposterior chest X-ray was taken when the catheter was about 40 cm inside the vein. The X-ray revealed that the PAC had erroneously advanced straight into the left brachiocephalic vein and turned to its opposite direction to slip into another vein that drains into the left brachiocephalic vein (). We were convinced that the catheter was not placed extravascularly and was therefore not resting on the mediastinum or in the pleural space, as confirmed by stable vital signs with freely regurgitating blood and intact lung parenchyma in the chest X-ray. Also, a venous anomaly such as bilateral superior vena cava was ruled out by a preoperative chest CT scan. We assumed that the catheter had most likely slipped through the left pericardiophrenic vein from the left brachiocephalic vein since the catheter follows the left heart border similarly to the route of this vein. We cautiously reviewed the chest CT once more with the radiologist and noticed that there were branches stemming out from the left brachiocephalic vein, which appeared to be the left pericardiophrenic vein (). The surgery was processed without the PAC insertion. Fortunately, the surgery was finished uneventfully and the patient had discharged from the hospital after 17 days.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [157.0, 'cm']}",49.66544,47.18217,52.14871,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 157.0 cm, which is 157.0 cm * 0.393701 in/cm = 61.81106 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.81106 (in inches) - 60) = 49.66544 kg.
Hence, the patient's IBW is 49.66544 kg."
3583,10,Ideal Body Weight,physical,decimal,pmc-3485494-1,Extracted,"Due to an uncertain raise in alcalic phosphatase and unspecific pain in the right upper abdomen a 28-year-old female patient (170 cm, 58 kg) underwent further diagnostic exploration. The abdominal ultrasound revealed a lesion of low echogenicity in the right upper abdominal quadrant with relation to the liver. A subsequent MRI scan showed an oval lesion at the right lower lobe of the liver measuring 5 × 9, 5 cm in craniocaudal extension. According to the imaging there were no signs of an infiltration of healthy liver tissue. Also, there were no signs of pathologically enlarged lymph nodes or ascitis. The preliminary diagnosis was a liver cell adenoma.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [170.0, 'cm']}",61.43709,58.36524,64.50894,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.92917 (in inches) - 60) = 61.43709 kg.
Hence, the patient's IBW is 61.43709 kg."
3584,10,Ideal Body Weight,physical,decimal,pmc-6051943-1,Extracted,"A 26-year-old man was admitted with known hypokalemia. He reported a 3-year history of nausea, vomiting, and diffuse muscle weakness. He complained of nausea and epigastric fullness in the absence of any identifiable organic gastrointestinal pathology, and his symptoms were known to subside after self-induced vomiting. Although he reported a normal appetite, he was known to vomit frequently, particularly after a large meal. He had been diagnosed with hypokalemia and had been treated with potassium supplements at a previous hospital. However, because of persistent nausea and vomiting, he was transferred to our hospital for evaluation of hypokalemia. His medical and family histories were unremarkable, and he did not report the use of medications such as diuretics and/or herbal medication. Physical examination upon admission showed he was 175 cm tall and weighed 44.5 kg, which indicated a weight loss from his previous weight of 58 kg over the previous 2 years. His body mass index was 14.53 kg/m2. Blood pressure was 100/60mmHg, pulse rate was 67/min, respiratory rate was 20/min, and his body temperature was 37.0℃.
Initial serum electrolyte testing showed the following: sodium 133 mEq/L, potassium 2.6 mEq/L, chloride 72 mEq/L, and total carbon dioxide 50mEq/L. Calcium/phosphorus were 11.2/4.1mg/dL, blood urea nitrogen/creatinine were 21.9/1.98mg/dL, the estimated glomerular filtration rate was 43.6mL/min/1.73m2, serum magnesium was 2.0mg/dL, blood glucose was 93mg/dL, and hemoglobin was 12.0 g/dL. Total cholesterol was 285mg/dL, serum protein/albumin were 8.1/5.3 g/dL. Thyroid and adrenal function tests, as well as serum renin and aldosterone levels were all within reference range. Arterial blood gas analysis showed pH 7.557, partial pressure of carbon dioxide was 65.8mmHg, and bicarbonate was 58.5 mEq/L. Urinary levels of sodium/potassium/chloride (Na/K/Cl) were 95/73.2/47mEq/L, respectively, his urinary creatinine measured 111.12mg/dL, and the trans-tubular potassium gradient was 17. Urinalysis showed the following findings: blood -, albumin ±, glucose -, and ketones -. Upper endoscopy and abdominal computed tomography showed no abnormalities. The SLC12A3 gene mutation test for Gitelman syndrome was observed to be negative. He was diagnosed with chloride-responsive metabolic alkalosis with kidney failure and treated with saline hydration, potassium supplementation, and spironolactone. Serum potassium increased to 3.0mEq/L; however, his nausea and vomiting persisted.
A renal biopsy was performed for the evaluation of renal dysfunction. Microscopically, interstitial mononuclear cell infiltration was identified. Renal tubular epithelial cells showed mild nuclear variation with conspicuous nucleoli and cytoplasmic vacuolization, indicating regenerative changes after acute tubular necrosis. Several foci of dystrophic calcification were identified among the tubular epithelial cells. A few shrunken glomeruli were observed suggesting ischemic damage; however, most glomeruli revealed no definitive abnormalities such as mesangial cell proliferation, segmental sclerosis, and/or deposition of immune complexes (). The patient showed an improvement in his gastrointestinal symptoms after treatment with mirtazapine. His serum potassium level increased to 3.5–4.4mEq/L and to date, he has been following-up at the outpatient clinic without any clinical signs and symptoms.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3585,10,Ideal Body Weight,physical,decimal,pmc-8289398-1,Extracted,"The author reports a case of bilateral DELC in a 23-year-old white female patient with PCOS. PCOS diagnosis was based on her menstrual irregularity and hirsutism since adolescence. She also had PCOS-associated metabolic disorders such as type 2 diabetes, nonalcoholic fatty liver disease, dyslipidemia, and hypothyroidism. She didn’t suffer from any cardiovascular diseases. In terms of lifestyle risk factors, the patient did not smoke tobacco or consume alcohol. Her activity levels were within the normal range. She also indicated that there was a strong family history of type 2 diabetes. Her medications included metformin, sodium-glucose co-transporter 2 (SGLT2) inhibitors, and levothyroxine.
The physical examination revealed that the patient had an android-type phenotype with centripetal fat distribution within the trunk and the face. However, she had no features suggestive of Cushing's syndrome. Bodyweight was 84 kilograms with height recorded as 162 centimeters; this gave the patient a BMI of 32.0 and a waist circumference of 92 centimeters. No acanthosis nigricans or striae were noted. Normal thyroid gland on palpation was also noted and the cardiovascular and pulmonary physical exams were unremarkable. An abdominal exam revealed a triangular male-pattern distribution of hair in the lower abdomen. It was also noted that the patient appeared to have bilateral symmetrical diagonal earlobe creases (Figure , point A) and localized areas of lateral facial fat corresponding to the buccal fat pad (BFP) of the sideburn regions of the cheeks (Figure , point B).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [162.0, 'cm']}",54.19299,51.48334,56.90264,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.77956 (in inches) - 60) = 54.19299 kg.
Hence, the patient's IBW is 54.19299 kg."
3586,10,Ideal Body Weight,physical,decimal,pmc-7675897-1,Extracted,"The participant, Ms X, was a 49-year-old South African citizen, with no known medical
history, who had been living and working in a Middle East country. In the latter
part of March 2020, most countries introduced COVID-19 lockdown measures, resulting
in the revoking of travel and working visas. The embassy arranged and funded an
evacuation flight for Ms X and other stranded South Africans in the region. After
return to South Africa, citizens were transported to a government site in
Johannesburg and underwent mandatory 14-day quarantine. Ms X was allocated a
4 × 4 m2 room with bed and amenities with meals and drinks provided.
Military and police personnel monitored the accommodation to ensure persons remained
confined to their rooms. Medical staff were on duty to monitor the general health
status of people. Extracted nasal and oropharyngeal samples for the detection of
COVID-19 were collected by on-call government laboratory staff. Individuals received
their test results from the in-house medical personnel. Given the rapid spread of
the virus and the urgent need and priority for screening in communities at the time,
the repatriated citizens could only be tested in the latter part of the quarantine
and, Ms X could only be tested on Day 14.
Ms X provided self-reported height (1.65 m) and weight (68 kg) on Day 1. A cloth
measuring tape was made available to measure waist and hip circumferences daily
using standard procedures. Circumferences were recorded by Ms X, and body mass index
(BMI) was calculated as kg/m2 and waist-to-height ratio (WHtR) was
calculated as waist (cm)/height (cm). Daily dietary intake and beverage consumption
was diarised and converted to macronutrients (calories, fats, carbohydrates, protein
and dietary fibre) using an online conversion application ().
The short-form health survey (SF-36) was completed online () to determine physical health
(physical function, role-physical, bodily pain and general health) and mental health
(vitality, role-emotional, social function and vitality). Scores ranged from 0 to
100 with higher scores indicating enhanced overall physical and mental health
(). Night-time sleep (hours/night)
and estimated sitting time per day were recorded by the study participant.
Ms X followed online curated moderate-to-vigorous home-based/indoor exercise videos
requiring no equipment with intermittent stepping during the 14-day quarantine
period. The type of exercises performed included continuous aerobic activity,
high-intensity interval training and resistance training using body weight. A
wireless heart rate (HR) monitor (MZ-3; Myzone Ltd, Isle of Man) was worn during
physical exercise and activity. Physiological measures, including peak and average
HR, calories expended and exercise intensity (%max) were monitored in real time on a
smartphone application and saved on a cloud-based facility (Myzone Ltd., Isle of
Man). The number of steps per day and duration spent stepping were recorded using
the iPhone Health application on the participant’s personal iPhone.
Ms X remained asymptomatic and tested negative for COVID-19 on Day 14. The
self-reported height (1.65 m) and weight (68 kg) did not change since Day 1. The BMI
was 25.0 kg/m2, classified as ‘overweight’ or BMI ⩾ 25 kg/m2, while waist circumference (82 cm) and hip circumference (102 cm) were
constant throughout the 14 days. The WHtR was 0.497, which is just below 0.5, the
cut-point for abdominal obesity.
The average resting HR was 63.8 b/min, ranging from 58 to 73 b/min, while average
night-time sleep was 8.4 h/night. Caloric intake fluctuated, with peaks in caloric
consumption on the second and fourth quarantine days that ranged from 1617 to
2854 kcal/day ().
Energy contribution from macronutrient intake during the 14-day period was provided
mostly by carbohydrates, contributing around 40%–54% to total dietary energy intake
on most days, followed by fats (25%–45% of energy) and proteins (15%–25% of energy).
Added sugars contributed 4.4%–12.5% of energy per day. The overall quality of life
outcomes were initially low and improved towards the end of the quarantine ().
Ms X did not participate in physical exercise or walking everyday (). Total sitting time
was an average of 516 min/day, ranging from 7 to 10 h/day. Time spent stepping
ranged from 20 to 49 min/day, spread over the course of each day. However, 10
exercise sessions were completed, with an average effort of 71.8 %Effort/session
(62–81 %Effort), average duration of 46.9 min/session (15–75 min/session) and
average caloric expenditure of 366 calories expended/session (79–591 calories
expended/session).
The total time spent in physical activity was 7.82 h over the 14-day period. Physical
exercise was completed at a moderate intensity using a mobile application which
provided real-time feedback.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.65, 'm']}",56.90952,54.06404,59.755,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.65 m, which is 1.65 m * 39.3701 in/m = 64.96066 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96066 (in inches) - 60) = 56.90952 kg.
Hence, the patient's IBW is 56.90952 kg."
3587,10,Ideal Body Weight,physical,decimal,pmc-4131310-1,Extracted,"A 56-year-old Saudi male was admitted to King Khalid University Hospital (KKUH) with the chief complaint of epigastric pain for 3 months associated with feeling of fullness, heartburn, and constipation. He had a past medical history of a surgical operation for renal stones and tympanoplasty, but with no significant family history. The vital signs recorded upon admission were as follows: Temperature 36.8°C, blood pressure 147/76 mmHg, pulse rate 72 beats/min, respiratory rate 20 breaths/min, and oxygen saturation 97%. His weight was 64 kg and height was 162 cm. Upon examination, the patient's abdomen was soft and lax with no tenderness, rigidity, or guarding noted.
Laboratory tests revealed an increase in white blood cells (WBC) and bilirubin with decreased red blood cells (RBC), hematocrit (HCT), and sodium level. Upper and lower endoscopic procedures were done, and colonoscopic findings were non-significant up to terminal ileum while gastroesophageal endoscopy showed a moderate hiatus hernia with peptic esophagitis Grade A and thickening of the mucosal folds at the pylorus. Ultrasound of the upper abdomen showed small cysts in both kidneys. Abdominal computerized tomography (CT) showed a small polypoidal lesion at the ileocecal valve []. The patient was later on discharged with home medication of Pantoprazole.
Laparoscopic right hemicolectomy was later performed. Histopathology of the resected specimen showed dilated lymphatic vessels consistent with a lymphangioma. Excess fat and congested blood vessels were also seen near the described lymphangioma. There was no evidence of malignancy and the excision appeared complete [Figures and ]. This finding confirms the lymphatic nature of the vessels shown in .
Patient was discharged without complications and he has been keeping well until this date.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [162.0, 'cm']}",58.69299,55.75834,61.62764,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (63.77956 (in inches) - 60) = 58.69299 kg.
Hence, the patient's IBW is 58.69299 kg."
3588,10,Ideal Body Weight,physical,decimal,pmc-4052474-1,Extracted,"A 25-year-old man presented with pain in both knees for four consecutive years and, since 3 months, bilateral groin pain and pain in the gluteal region, radiating to both knees.
The patient has been diagnosed with HHR as a child and has been on potassium phosphate and calcitriol tablets ever since. A typical bowing and anteromedial rotation of the tibia was corrected with tibial shaft osteotomies and Ilizarov fixators of both tibias about 10 years ago []. After these procedures, very slow healing of the bone with multiple revisions due to delayed union was observed.
The patient has had pain in both knees for four years, more in the right than in the left knee. Initially, at 6 years of follow-up, approximately 4 years ago, MRI of both knees and pelvic X-ray did not reveal any pathological changes other than a strong coxa vara malformation of both hips (). Pain was described by the patient as start-up pain that disappeared or bettered after walking with full weight bearing for a while. Since about 3 months, the pain began to concentrate on both hips radiating in both knees; the same start-up character of the pain was described. Upon questioning, the patient admitted that he has not been taking his medication regularly the last 6 months.
Clinical examination revealed a patient with athletic build, weighting 53 kg and measuring 155 cm. Hip range of motion was (right side/left side) flexion/extension 120/0/0 and 130/0/0, endo-/exorotation 20/0/5 and 20/0/30, and ab-/adduction 10/0/30 and 15/0/30. Trendelenburg's sign was positive on both sides. The patient complained of pain by abduction and exorotation. The Harris and Oxford hip scores were 86 and 43, respectively. Haematological and biochemical parameters were within normal range except for a low phosphate of 1.7 mg/dL (norm: 2.3–4.7) and low potassium of 3.1 mmol/L (norm: 3.5–5.1). Radiographs of hips and pelvis () revealed fractures in both femoral necks. An MRI of the pelvis showed an atrophic nonunion of both fractures ().
Treatment options were discussed with the patient and a conservative treatment was decided on. The patient was advised to participate in sports that did not involve shock loading of the hip joint, for example, swimming, cycling, and aquajogging. The patient was informed that a prosthetic replacement of the hip could become necessary by further increase of symptoms or necrosis of the femoral head.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [155.0, 'cm']}",52.35442,49.7367,54.97214,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (61.02366 (in inches) - 60) = 52.35442 kg.
Hence, the patient's IBW is 52.35442 kg."
3589,10,Ideal Body Weight,physical,decimal,pmc-7127884-1,Extracted,"A 14-year-old patient who had been raised as a male was brought to the pediatric endocrinology clinic for undescended testis and hypospadias. Although parental consanguinity was not reported to be present, the family history revealed that they were living in a village of only 500 inhabitants. The patient’s mother, who was first pregnancy and primigravida, had no symptoms during pregnancy of excessive androgen production, such as hair loss, virilisation, or acne. On physical examination, height, weight, and phallus were measured to be 154.9 cm [standard deviation score (SDS): -2.5], 57 kg (SDS: -0.6), and 2 cm respectively. Breast tissue and palpable gonads were not detected. Prader stage 3, two urogenital openings and stage 2 pubic pilosity were also noted. On laboratory examination, bone age was 11 years. Gonadotropin concentrations were: follicle stimulating hormone (FSH) 70 mIU/mL (1.5-12.8 mIU/L); luteinizing hormone (LH) 30 mIU/mL (0.1-12 mIU/mL); free testosterone 0.9 pg/mL (0.8-1.4 pg/mL); and estradiol 22.9 pg/mL (7-60 pg/mL). Adrenocorticotropic hormone (ACTH), cortisol and 17-hydroxyprogesterone (17-OHP) were all found to be in the normal range. Pelvic ultrasonography (USG) revealed 19x14 mm right ovary and 15x12 mm left ovary and an absence of uterus. Karyotype was 46,XX and no variants were found in the SRY gene on fluorescence in situ hybridization (FISH) analysis. On laparoscopic examination normal-looking bilateral ovaries and a small uterus were observed. The biopsy findings of the right gonad were consistent with ovarian tissue and ovarian follicle cysts were observed. Sequence analysis of the SOX9 gene revealed no mutation. Clinical and laboratory findings of the patient suggested aromatase deficiency and a novel homozygous nonsense p.R115X (c.343 C>T) pathogenic variant was found on Sanger sequencing of the CYP19A1 gene (). Both parents were heterozygous for the same mutation (, ). There were no unusual clinical findings in the parents. The mutation found in the cases was predicted to be pathogenic by in
silico analysis by Varsome program (https://varsome.com/).
The Institutional Council of Disorders of Sex Development decided that the case should be raised male on the ground of a more distinct male sexual identity. Salpingo-oophorectomy, hysterectomy and genitoplasty were performed. Intramuscular testosterone propionate and testosterone phenylpropionate treatments were administered with a 100 mg/month starting dose and gradually increased every six months. Oral estradiol hemihydrate treatment of 0.25 mg/day was initiated in the follow-up. At the age of 21, bilateral testicular prostheses were surgically implanted. During follow-up bone mineral densitometry showed early onset osteoporosis (L1-L4 bone mineral density Z score: -2,2) and oral calcium supplementation was given. Calcium, phosphorus, parathyroid hormone (PTH) and vitamin D concentrations were within normal limit. At the age of 22, weight, height, and phallus were measured to be 86.6 kg (SDS: 1.29), 173.5 cm (SDS: -0.43) and 7 cm respectively.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.5, 'cm']}",69.10638,65.65106,72.5617,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.5 cm, which is 173.5 cm * 0.393701 in/cm = 68.30712 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.30712 (in inches) - 60) = 69.10638 kg.
Hence, the patient's IBW is 69.10638 kg."
3590,10,Ideal Body Weight,physical,decimal,pmc-6721397-1,Extracted,"This case report was approved by the Institutional Review Board of Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation (IRB number: 08-CR-060).
A 31-year-old male presented with a productive cough and rhinorrhea for 4 days. He had no past medical history or medicine history. The symptoms were associated with intermittent high fever up to 39–40 °C and myalgia. He took symptomatic treatment but in vain. The patient went to a local medical doctor for treatment. While waiting outside the consulting room, syncope occurred twice and he contused the frontal area. There was no tonic or clonic seizure. Other symptoms, including skin rash, arthritis, or tendency for abnormal bleeding, were not found. Pneumonia-induced sepsis was suspected, and he was transferred to our emergency department. Upon admission, his temperature was 38.4 °C, blood pressure was 110/62 mmHg, heart rate was 129 beats/min, body weight was 90.6 kg, and height was 173 cm. Upon physical examination, his Glasgow Coma Score (GCS) score was E4V5M6 and bilateral pupil size was 2 mm with light reflex. There was no horizontal or vertical nystagmus. The neck was supple with no limited range of motion. The bilateral breath sound was clear without wheezing or crackle, and tachycardia was noted. There was no Babinski sign, decreased muscle power, or unsteady gait. The chest X-ray revealed no significant pulmonary nodules or pneumonia patch. An influenza A + B rapid screening test was performed, which showed negative results. A brain CT revealed a 13 mm lesion with hyperdensity in the left temporal region, with suspected intracerebral hemorrhage (). Laboratory evaluation of the patient revealed severe leukocytosis with blastemia ().
Results from the bone marrow biopsy report showed 90% cellularity. Blasts accounted for more than 90% of all nucleated cells. Hypercellular and monotonous bone marrow was noted with undifferentiated myeloblasts with prominent, convoluted nuclei, and agranular cytoplasm. There were significantly decreased erythroid and megakaryocyte lineages. The immunohistochemical profile was as follows: CD34(+), CD117(+), MPO(+), CD33(+), CD68(–), hemoglobin A(–), Factor VIII(–), CD19(–), CD3(–), TdT(–), and PAX5(–). The peroxidase and alpha naphthyl acetate esterase (ANAE) test was positive and chloroacetate esterase (CAE) test was negative. Acute myeloid leukemia was diagnosed. Broad-spectrum antibiotic and adequate hydration were administered. An antineoplastic agent, hydroxyurea (15 mg/kg/day), and emergency leukocytapheresis were used to control disease progression. Unfortunately, the patient became drowsy with asymmetric pupil size and no light reflex. The follow-up brain CT showed multifocal intracranial hemorrhage in the bilateral cerebral hemispheres with midline shift involving the brain stem (). Progressive hypotension was noted even using a vasopressor agent. Finally, the patient expired due to uncontrolled hemodynamic shock on the fourth day.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.0, 'cm']}",68.65362,65.22094,72.0863,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.0 cm, which is 173.0 cm * 0.393701 in/cm = 68.11027 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.11027 (in inches) - 60) = 68.65362 kg.
Hence, the patient's IBW is 68.65362 kg."
3591,10,Ideal Body Weight,physical,decimal,usmle-1623,Extracted,"A previously healthy 32-year-old man comes to the physician because of a 1-week history of upper back pain, dyspnea, and a sensation of pressure in his chest. He has had no shortness of breath, palpitations, fevers, or chills. He emigrated from Ecuador when he was 5 years old. He does not smoke or drink alcohol. He takes no medications. He is 194 cm (6 ft 4 in) tall and weighs 70.3 kg (155 lb); BMI is 19 kg/m2. His temperature is 37.2°C (99.0°F), pulse is 73/min, respirations are 15/min, and blood pressure is 152/86 mm Hg in the right arm and 130/72 mg Hg in the left arm. Pulmonary examination shows faint inspiratory wheezing bilaterally. A CT scan of the chest with contrast is shown.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [194.0, 'cm']}",87.66938,83.28591,92.05285,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 194.0 cm, which is 194.0 cm * 0.393701 in/cm = 76.37799 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (76.37799 (in inches) - 60) = 87.66938 kg.
Hence, the patient's IBW is 87.66938 kg."
3592,10,Ideal Body Weight,physical,decimal,pmc-3629350-1,Extracted,"A 48-year-old male patient (height 165 cm, weight 76 kg) visited our clinic with abdominal pain on the right upper abdomen. The patient had exploratory laparotomy for abdominal abscess 25 years ago, but there was no acute complication from the operation. However, the patient has felt localized pain and allodynia around the surgical scar since 4 years ago. The pain nature was continuous, throbbing, and pulsatile, and the pain was aggravated by overwork or alcohol consumption; relieved by compression of the scar. On rest, the pain was 4 out of 10 and when aggravated, went as high as 8 out of 10 on 11-points numeric rating scale. Whenever aggravated, the pain had radiated to his right upper arm once every 2-3 seconds. The nature and intensity of radiating pain was similar with the original pain. The pain has accompanied by heated sensation of the abdomen and right upper arm.
The patient had been taking aspirin and hypoglycemic medications for diabetes mellitus. However, his pain was regarded as different with diabetic truncal neuropathy that causes burning pain or dysthesias with multi-dermatomal distributions. Before visiting our clinic, he had taken CT scanning of abdomen twice and MRI of cervical spine and received conservative treatments, including oral analgesics (i.e. acetaminophen, tramadol, opioids), ketamine infusion therapy, intercostal nerve blocks, pulsed radiofrequency therapy of thoracic dorsal root ganglia in several other hospitals for 18 months. Abdominal CTs and cervical MRI did not show any abnormal conditions and his pain was not only alleviated temporarily, but he also suffered from drug adverse effects, including hepatitis and light-headedness.
Physical examination revealed 3 cm long surgical scar on the right upper abdomen and focal tenderness, allodynia and hyperesthesia around the scar. Contrastively, there were no abnormal findings in the right upper arm. Subsequently, gray-scale ultrasonography coupled with color Doppler flow imaging was performed to find any soft tissue lesion, such as inflammation and neuroma.
Color Doppler US showed a vascular mass with turbulent blood flow, which was a 0.62×0.27×0.69 cm sized mass in the subcutaneous layer of the mid-surgical scar (). The lesion was suspected to be a symptomatic pseudoaneurysm originating from an artery or possibly an arteriovenous fistula, while there was no demonstrable entering or exiting vessel. So, the patient was transferred to a vascular surgeon for treatment of it.
Sclerotherapy was decided for pseudoaneurysm under US guidance. Skin was punctured by medicut under US guidance and the mass was enhanced using contrast media under fluoroscopy (). A mixed material (glue:lipidol = 1:2) was used for embolization of pseudoaneurysm. The day after the procedure, US showed that a mixture of glue and lipidol had filled the pseudoaneurysm with posterior acoustic shadow. Patient was discharged with substantially diminished tenderness. Two weeks later, his symptoms, including referred pain to the right upper arm, were completely subsided without any medications.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3593,10,Ideal Body Weight,physical,decimal,pmc-8074472-1,Extracted,"On July 12, 2019, a 67-year-old male patient presented to the Affiliated Jinhua Hospital, Zhejiang University School of Medicine (Jinhua, China) because of occasional dull flank pain for 4 years and investigation of a mass on the right adrenal gland for 1 week.
The patient had suffered from pulmonary nodules for more than 10 years and regular reexamination of these nodules was performed every year.
The patient’s height and weight were 168 cm and 52.5 kg, respectively. There were no positive signs in the abdomen or a positive Murphy sign. He had no history of hypertension.
No abnormal hormone levels were detected during endocrinological examinations, and routine blood tests were within normal limits (plasma renin 7.70 pg/ml, plasma aldosterone 16.4 ng/dl, plasma adrenaline 32 pg/ml, plasma noradrenaline 730 pg/ml).
Preoperative computed tomography angiography + computed tomography urography (CTA + CTU) showed a mass with a heterogeneous shadow (9.5 × 6.3 cm) in the right adrenal gland (Fig. ). The mass was well-circumscribed, early peripheral enhancement was obvious in the arterial phase (Fig. ), with central progressive partial filling in the venous phase and in delayed imaging (Figs. , ).
The patient was diagnosed with an adrenal tumor preoperatively and pheochromocytoma was considered. However, he was subsequently diagnosed with an adrenal cavernous hemangioma.
Retroperitoneal laparoscopic adrenalectomy was performed following the oral administration of Phenoxybenzanine Hydrochloride 10 mg twice a day for one week. Blood volume was fully expanded by fluid infusion two days before surgery to reduce intraoperative blood pressure fluctuations. It took 145 min to complete the operation. Fluctuating or sometimes substantially elevated catecholamine levels in the blood of pheochromocytoma patients can trigger severe cardiovascular complications such as TTS, heart failure, cerebral haemorrhage and sudden cardiac arrest [] and secondary shock []; thus, perioperative monitoring is critical. In this case, the surgeon strictly followed the principle of “minimal touch” during the operation, and intraoperative anaesthetic monitoring showed that the tumour remained stable during intraoperative contact and tumour haemodynamics. Therefore, the patient was not transferred to the ICU for advanced monitoring, but to a general ward with continuous post-operative monitoring of vital signs for 24 h. After determining that their vital signs were stable, the patient was monitored regularly and discharged 6 days after surgery. The patient was discharged 6 d after surgery.
Histopathologic analysis of the surgical specimen showed an adrenal hemangioma with extensive internal hemorrhage and necrosis (Fig. ).
CT was repeated regularly after surgery. No recurrence, metastasis or other complications were observed after 1 year of follow-up.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.0, 'cm']}",64.12607,60.91977,67.33237,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg."
3594,10,Ideal Body Weight,physical,decimal,pmc-6755925-1,Extracted,"A 51-year-old gentleman, recently diagnosed to have type 2 diabetes mellitus and systemic hypertension, presented to the cardiology outpatient clinic on 28th July 2016 with history of pricking chest pain and shortness of breath for the past 7 years and recurrent attacks of syncope since the previous year. He weighed 49 kg and with a height of 157 cm; body mass index was 19.88 kg/m2. His blood pressure (BP) was 120/80 mmHg and pulse rate was 78/min and regular in rhythm. He was afebrile. Systemic examination was unremarkable.
Laboratory findings revealed hemoglobin of 15.1 g/dL, hematocrit of 47%, white blood cell count of 11,300/mm3 (differential count of neutrophils of 56%, lymphocytes 26%, eosinophils 11%, and monocytes of 7%), and platelet count of 293,000/mm3. Urine on routine examination showed a pH of 6.0, specific gravity of 1015, and was negative for albumin, glucose, red blood cells, and pus cells. Blood glucose fasting was 115 mg/dL and post-prandial was 219 mg/dL with an HbA1C of 7.1%. Blood urea was 27 mg/dL and creatinine was 1.0 mg/dL. Serum electrolytes were as follows: sodium 141 mEq/L, potassium 4.3 mEq/L, chloride 103 mEq/L, and bicarbonate 28 mEq/L. Serum cholesterol was 183 mg/dL, serum triglyceride 121 mg/dL, and serum uric acid 3.9 mg/dl. Two-dimensional (2D) echocardiogram showed normal left ventricular dimensions, no regional wall motion abnormality, and a left ventricular ejection fraction of 69%. Holter monitoring showed occasional supraventricular and ventricular premature complexes. On 2nd August, coronary angiography showed insignificant coronary artery disease with dominant right coronary system and he was discharged with medical advice.
On 3rd August, he attended emergency department with complaints of severe back pain, palpitation, and sweating. His back pain was sudden in onset, gradually progressive, throbbing type, rating 8/10 in pain scale, radiating to the left flank, aggravated by exertion, and partially relieved by rest. He had no other complaints. He was on metformin and calcium channel blocker. He looked anxious, agitated, and restless but was oriented and afebrile. His pulse rate was 112/min, respiratory rate was 28/min, and BP was 210/120 mmHg in the right upper limb and 210/100 mmHg over the left upper limb in supine position. There was no radio-femoral delay. Systemic examination was unremarkable except for a mild tenderness in the lumbar region.
On investigation, electrocardiography, chest X-ray, complete blood counts, liver function tests, 2D echocardiography, urine analysis, and toxicology screen were all within normal limits. Serum amylase and lipase were normal. Blood urea was 58 mg/dL and serum creatinine was 2 mg/dL. Venous blood gas (VBG) analysis showed a pH of 7.21, bicarbonate of 18 mmol/L, base excess of −9.4 mmol/L, and a lactate of 10.81 mmol/L. Serum electrolytes were sodium 138 mmol/L, potassium 3.8 mmol/L, and chloride 108 mmol/L, and anion gap was 12 mmol/L.
The following were considered in the differential diagnosis of this situation: (a) acute mesentric ischemia, (b) aortic dissection (c) hypertensive emergency, and (d) pancreatitis. Contrast-enhanced computed tomography abdomen showed a lesion in the left adrenal gland measuring about 3.5 × 3.2 cm with mild enhancement in the arterial phase, features consistent with pheochromocytoma [: Contrast enhanced CT scan of abdomen showing the mildly enhancing left adrenal mass]. No additional extra-adrenal tumors were seen. There was no evidence of mesenteric ischemia, aortic dissection, or pancreatitis. Upon further questioning his family members, it was known that he was unwell in the previous 6 months with on and off headache, palpitation, and anxiousness, which they attributed to the recently diagnosed diabetes mellitus.
His BP was managed with alpha adreno-receptor blocker and calcium channel blocker. Phenoxybenzamine was added at a dose of 10 mg twice a day and later increased to 20 mg three times daily. Persistent tachycardia and BP were stabilized with addition of beta blocker.
On 5th August 2016, the level of 24-h urine metanephrines was 14,536 mcg (reference range: less than 350 mcg/24 h) and nor-metanephrines was 7,607 mcg (reference range: less than 600 mcg/24 h).
Laparoscopic removal of pheochromocytoma was done under general anesthesia on 12th August 2016. After the surgery, there was a brief episode of hypoglycemia and hypotension, which was managed with 25% dextrose and normal saline, respectively. Azotemia resolved and blood gases were normalized. Pathological examination of the resected mass revealed a well-encapsulated tumor of size 5 cm × 4 cm × 3 cm, without hemorrhage. It showed polygonal and round cells with abundant cytoplasm and increased vasculature. There was no capsular or vascular invasion. Tumor cells were seen in the background of spindle cells with ganglion cells and Schwanian stroma. These features were reported as consistent with a CP–ganglioneuroma of the left adrenal gland []. Immunohistochemistry examination showed positivity for chromogranin, synaptophysin, and S-100 stains and negativity for calretinin in pheochromocytoma cells. Calretinin, chromogranin, synaptophysin, and S-100 stains were positive in the ganglioneuromatous component. Vimentin was positive and cytokeratin was negative. These staining characteristics confirmed the composite nature of the tumor.
At the time of discharge, his blood pressure and blood glucose were normal. Upon review on 28th February 2017, his BP was 130/80 mmHg without antihypertensive medicine. Blood glucose fasting was 90 mg/dL and post-prandial 66 mg/dL, with an HbA1C of 6.1% without any antidiabetic medicine. The levels of 24-h urinary metanephrines and normetanephrines were 62 and 604, mcg, respectively.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [157.0, 'cm']}",54.16544,51.45717,56.87371,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 157.0 cm, which is 157.0 cm * 0.393701 in/cm = 61.81106 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (61.81106 (in inches) - 60) = 54.16544 kg.
Hence, the patient's IBW is 54.16544 kg."
3595,10,Ideal Body Weight,physical,decimal,usmle-2957,Extracted,"A 58-year-old man comes to the physician because of a 4-day history of abdominal pain and vomiting. Initially, the vomitus was food that he had recently eaten, but it is now bilious. He has had similar complaints several times in the past 6 years. He has smoked 1 pack of cigarettes daily for the past 25 years and drinks 24 oz of alcohol daily. He is 160 cm (5 ft 3 in) tall and weighs 48 kg (105 lb); BMI is 19 kg/m2. His vital signs are within normal limits. Physical examination shows an epigastric mass. The remainder of the examination shows no abnormalities.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [160.0, 'cm']}",56.88197,54.03787,59.72607,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.99216 (in inches) - 60) = 56.88197 kg.
Hence, the patient's IBW is 56.88197 kg."
3596,10,Ideal Body Weight,physical,decimal,pmc-4216792-1,Extracted,"A 40-year-old woman (gravida 0, para 0, 153.8 cm, 66.9 kg) with placenta previa totalis and multiple myomas was admitted to our hospital at 36+6 weeks gestation for a cesarean delivery. She had no history of medical illness or trauma. Due to the possibility of massive bleeding during removal of the placenta, multidisciplinary management was considered. We discussed the delivery with the obstetrician and radiologist, and the decision was made to attempt preventive UAE before placental expulsion. Initially, the plan was to transfer the patient from the maternity ward on the 4th floor to the angiography room on the first basement level after fetal delivery, and, after finishing the intervention, to transfer her back to the operating theater. However, we strongly recommended intraoperative radiologic intervention to avoid both possible infection and difficult and unnecessary patient monitoring and management, as well as to reduce additional blood loss during transfer of the patient in such an emergent situation. In the end, we all agreed to perform the embolization intraoperatively immediately after delivery of the fetus and before removal of the placenta during cesarean delivery under spinal anesthesia. All equipment, including a C-arm fluoroscope for the interventional radiologist, was prepared in the operating room before the delivery. The patient's vital signs were stable on the day of operation. Preoperative blood pressure was 107/52 mmHg, heart rate was 80 beats/min, hemoglobin was 9.8 g/dl, and other laboratory findings were normal.
After arrival of the patient in the operating room, standard monitoring (electrocardiogram, pulse oximetry, and noninvasive blood pressure) was begun. Initial blood pressure was 100/49 mmHg, heart rate was 98 beats/min with normal sinus rhythm, SpO2 was 95% on room air, and 100% O2 was administered via face mask at a flow rate of 5 L/min. She had two 18-gauge intravenous lines in both arms, and an arterial catheter was placed in the right radial artery with a 20 G angiocatheter to monitor arterial blood pressure.
Under strict aseptic conditions, a combined spinal-epidural block was performed at the 2nd-3rd lumbar interspace in the right lateral position with a needle-through-needle technique using an 18 G Tuohy and 27 G pencil point spinal needle by the median approach without difficulty. After that, 8 mg of heavy bupivacaine and 20 µg of fentanyl was administered intrathecally. The epidural catheter tip was threaded 5 cm into the epidural space and 3 ml of 1% lidocaine with 1:200,000 epinephrine was then slowly administered into the epidural space. No changes were observed in cardiac rhythm, heart rate, or blood pressure. We subsequently assessed the extent of bilateral sensory blockade by observing the loss of cold sense to alcohol sponges and the loss of pain sense to pinpricks. At that time, the sensory level was located at T4. At 25 minutes after administration of the initial dose, block was established up to T1, and the obstetricians proceeded with the surgery. Before skin incision, 350 ml of crystalloid solution and 150 ml of colloid solution were infused.
At 9 minutes after skin incision, a 2.815 kg male baby (Apgar scores of 7 and 8 at 1 and 5 min, respectively) was delivered. At that time, the patient's blood pressure was 114/60 mmHg, heart rate was 79 beats/min, and SpO2 was 97%. The arterial blood gas analysis performed immediately before the embolization revealed the following: pH 7.35, PCO2 39 mmHg, PO2 81.5 mmHg, HCO3 - 21.2 mEq/L, SaO2 96.4%, Hct 24%.
At 25 minutes after skin incision, UAE of both arteries using gel foam particles was performed for 30 minutes without incident. During the embolization procedure, vital signs were as follows: blood pressure 110-115/48-55 mmHg, respiratory rate 18 breaths/min, heart rate 69-79 beats/min. Midazolam 3 mg was administered to reduce the patient's anxiety. After confirming successful complete embolization, placental expulsion was performed without complications. Three units of packed RBCs were transfused with a rapid blood infuser (Level-1®, Smiths Medical, Ashford, UK). The arterial blood gas analysis performed immediately after the placental expulsion and transfusion revealed the following: pH 7.33, PCO2 37.9 mmHg, PO2 149.7 mmHg, HCO3 - 19.5 mEq/L, Hb 7.1 g/dl, Hct 21%. Forty minutes after placental expulsion, 3 ml of 1% lidocaine with fentanyl 80 µg was administered via epidural catheter and midazolam 3 mg was intravenously injected. An additional forty minutes after that, 10 ml of 0.75% ropivacaine with fentanyl 50 µg was administered via epidural catheter. Two additional units of packed RBCs were also transfused.
The total operation time was 175 minutes, and anesthesia time was 225 minutes. Total infused amounts of crystalloid, colloid, and RBCs were 1,950 ml, 1,500 ml, and 5 U, respectively. Estimated blood loss and urine output were 2,500 ml and 300 ml. During the operation, the patient's hemodynamics were as follows: blood pressure 90-120/45-70 mmHg, heart rate 60-103 beats/min. The patient's postoperative pain was managed with an epidural patient-controlled analgesia device (0.15% ropivacaine 250 ml with fentanyl 1,500 µg, basal rate 4 ml, bolus 2 ml, and lockout time 30 min) for 3 days after the operation with numeric rating scale 3 points pain. She was discharged without complications on postoperative day 4.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.8, 'cm']}",46.76778,44.42939,49.10617,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.8 cm, which is 153.8 cm * 0.393701 in/cm = 60.55121 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.55121 (in inches) - 60) = 46.76778 kg.
Hence, the patient's IBW is 46.76778 kg."
3597,10,Ideal Body Weight,physical,decimal,pmc-4184321-1,Extracted,"A 19-year-old female, reported to the Department of Oral Medicine and Radiology, for complains of pain in mandibular anterior region for duration of 2 days. Patient was one of the two siblings of non consanguineous parents with no family history of orofacial or acral malformations. Detailed history revealed that the antenatal, neonatal and infancy had been uneventful. However, she was diagnosed as having atrial septal defect at the age of 7 years and had undergone surgical management for the same. Patient also reported history of menstrual irregularities (menarche achieved at the age of 16 years). She was moderately built, well nourished and appeared to have normal intelligence. Patient's height was 167 cm, within 75th percentile while weight (42 kgs) and head circumference (20 inches) were both below 3rd percentile. Routine general physical examination revealed broad halluces bilaterally exhibiting valgus deformity and dysmorphic nails []. In addition, duplication of 5th toe of right foot with syndactyly of the supernumerary digit with 5th toe was evident. There was flexion contraction of 4th and 5th toe of left foot and 4th toe of right foot. The upper limbs were essentially normal except for broadened right thumb and nail, and clinodactyly bilaterally []. No functional deficit in relation to hands or feet was noticed. On extra oral examination, acrocephalic skull, flattened frontal and occipital regions and low hairline was evident. The leptoprosopic flat face with mild maxillary hypoplasia and relative mandibular prognathism was exemplified by a prominent chin []. An increase in gonial angle was evident on profile view. Nose was long, thin, pointed with the nasofrontal angle flattened presenting as wide root of the nose. Thick eyebrows, prominent eyelashes, mild convergent strabismus and marginal hypertelorism were present. Intra-oral examination revealed high arched palate and generalized enamel hypoplasia []. Patient was currently undergoing orthodontic treatment for correction of crowding within the arches. Also anterior deep bite with 100% overlap of mandibular teeth was evident []. Patient gave previous history of endodontic treatment and apicoectomy of 31, 41 and at the time of presentation had pain in the same region along with vestibular obliteration and tenderness.
Orthopantomogram confirmed a cystic lesion in mandibular anterior region, increased gonial angles bilaterally and occlusal plane irregularities []. Further radiographic examination of craniofacial skeleton (P-A skull [] and Lateral skull radiographs [] revealed evidence of coronal sutural synostosis with prominent copper beaten appearance, flattened occiput and frontal bones, shallow orbits, gross prognathism with obtuse mandibular plane angle, maxillary sinus hyperpneumatization and falx calcification. Hand and wrist radiograph showed short and broad distal phalynx of right thumb, however all bones were otherwise normal. Radiograph of feet [] revealed duplication of distal phalynx of halluces and valgus deformity at distal interphalyngeal joint bilaterally. There was also evidence of partial duplication of 5th toe; Y-shaped proximal phalynx with one supernumerary phalynx in postaxial position exhibiting soft tissue syndactyly with 5th toe. Fourth and fifth digits of left foot were bent in clinically fixed flexion.
The diagnosis of Robinow-Sorauf syndrome was made based on clinical and imaging features. Surgical enucleation of radicular cyst and apicoectomy of mandibular anteriors was done following intentional root canal treatment of 32 and 42. Opinion regarding surgical correction of limb anomalies was sought. Patient is currently undergoing treatment for functional and esthetic corrections.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [167.0, 'cm']}",58.72056,55.78453,61.65659,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 167.0 cm, which is 167.0 cm * 0.393701 in/cm = 65.74807 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (65.74807 (in inches) - 60) = 58.72056 kg.
Hence, the patient's IBW is 58.72056 kg."
3598,10,Ideal Body Weight,physical,decimal,pmc-6624119-1,Extracted,"The patient is a 69-year-old, 55 kg, 153 cm female with metastatic appendiceal adenocarcinoma who presented with an enlarging abdomen consistent with loculated, mucinous ascites and omental thickening. The preoperative computerized tomography (CT) scan of the abdomen and pelvis showed a large cystic mass in the pelvis associated with a soft-tissue element of the mass. It extended into the retroperitoneum and encapsulated the right renal artery, impressing on the posterior wall of the inferior vena cava. A moderate to large hiatal hernia was also noted. CRS/HIPEC surgery was recommended.
Other significant past medical history included stable gastroesophageal reflux disease (GERD) and a history of left-sided breast cancer status post-mastectomy and vertical rectus abdominis musculocutaneous (VRAM) flap. During her preoperative workup, the patient endorsed increasing bilateral lower extremity edema, abdominal distension and bloating. An electrocardiogram (ECG) also revealed q waves in the anterolateral leads; as a result, she was referred for cardiac evaluation. An echocardiogram revealed an EF of 20-25% with diffuse global hypokinesis. A left heart catheterization revealed no obstructive disease. Therefore, she was diagnosed as having chronic heart failure with reduced ejection fraction due to non-ischemic cardiomyopathy. The etiology was presumed to be from previous chemotherapy for breast cancer. She was started preoperatively on lisinopril and furosemide which led to a notable improvement in symptoms including resolution of orthopnea and decreased lower extremity edema. Her preoperative hemoglobin was 10.3 grams per deciliter (g/dL) and sodium was 133 milliequivalents per liter (L). All other preoperative labs were generally unremarkable. She did not have an automated implantable cardioverter defibrillator (AICD) or history of noted arrhythmias.
On the day of surgery, we decided to forego epidural placement, which is standard, for this case because we wanted fewer confounders in the workup of any post-operative hypotension. After applying standard American Society of Anesthesiologists (ASA) monitors and giving 2 mg intravenous (IV) midazolam, a pre-induction arterial line was placed. The patient was then pre-oxygenated and induced with 100 mcg IV fentanyl, 60 mg 2% IV lidocaine, 14 mg IV etomidate, and 80 mg IV succinylcholine. A 16-gauge peripheral IV catheter was placed and additionally, an 8 French (Fr), double lumen, 16 cm central venous cannula was placed in the right internal jugular vein under ultrasound guidance. Both the arterial line and central line were connected to a FloTrac/Vigileo device (Edwards Lifesciences, Irvine, CA, USA) which then calculated cardiac index (CI), systemic vascular resistance (SVR), stroke volume variation (SVV), and CVP (Figure ).
We followed the trend of these numbers to guide fluid therapy. The initial values were CVP 17 mmHg, SVR 1500 dyn/s/cm5, CI 2.1, and SVV 3. A transesophageal echocardiography (TEE) probe was placed and connected to a Philips machine (Philips Professional Healthcare, Netherlands, Amsterdam). We performed a standard 28 view baseline exam (Figure ).
Findings included an ejection fraction (EF) of 25% and severe global hypokinesis as well as dilated left ventricle (LV) chamber, mild to moderate mitral regurgitation, no other significant valvular pathology, and normal right ventricle (RV) function (Figures -).
The patient also was found to have a baseline left mild to moderate pleural effusion (Figure ).
Premixed norepinephrine and epinephrine infusions were present in the room in case of any prolonged hypotension. Our plan was to be very judicious with fluids, making sure to keep our hands on the roller clamp any time medications were bolused, in order to immediately shut off the IV to avoid excessive crystalloid administration. We would preferentially use 5% albumin for volume if necessary and use SVV trend, CVP trend, UOP and TEE guidance during periods of hypotension, and periodically throughout the case to guide whether to administer colloid or vasopressor. Our vasopressor of choice to bolus was ephedrine due to inotropic qualities, and norepinephrine if we needed an infusion because of some Beta 1 activity providing inotropy without causing as much tachycardia and arrhythmia potential as other inotropes such as epinephrine and dobutamine. The patient’s baseline systolic blood pressure (SBP) was 114 mmHg; our goal was to stay within 20% which was an SBP > 90 mmHg. Our goal urine output was 0.5 mL/kg/hr which was about 30 mL/hr in this patient. We did not have a target amount of fluid replacement per hour and were rather going to give as little fluid as possible to maintain continued urine output and hemodynamic stability without high dose pressors. An SVV consistently greater than 13 along with hypotension was the threshold to give albumin or CVP continuing to trend down. We also looked at the trans-gastric short axis view of the left ventricle on TEE frequently to look for signs of the ventricular function worsening or improving with fluid or signs of the ventricle further dilating to signal possible fluid overload.
The surgeon commenced by making a large laparotomy incision and immediately drained 15 L of mucinous ascites from the patient’s very large, protuberant abdomen. He then performed cytoreductive surgery which included: appendectomy, splenectomy, bilateral removal of adnexal tumor, including ovary and tube, resection of umbilicus, resection of the falciform ligament with tumor and peritoneal resections of the right flank (20 cm), pelvis (10 cm), right upper quadrant (20 cm), and left upper quadrant (10 cm).
After draining the initial 15 L of ascites, the CVP dropped from 17 mmHg to 8 mmHg. We examined the LV on TEE and the contractility appeared to improve, going from EF 25% to about 30%. This also corresponded to improvement in CI from 2.1 to 2.5. The SVV stayed the same (around 3) as did the SBP, so therefore we did not bolus any additional fluid during this time. About two hours into the surgery, we began to very slowly infuse 5% albumin as SVV was slowly increasing up to 15, the UOP had slightly dropped, and we were giving frequent bolus doses of ephedrine and phenylephrine. The left ventricle (LV) chamber appeared less dilated than baseline indicating possible fluid responsiveness. As we infused about 750 mL of 5% albumin over the course of three hours and a small bolus dose of crystalloid, SVV trended down to below 13 and the LV did appear more distended with somewhat decreased LV function and dyskinetic movement (Figure ).
The CVP was unchanged over those few hours, but we decided based on the TEE that the patient was volume replete and we should stop our fluid infusion to avoid overload.
After about six hours, the patient’s incision was closed and the HIPEC portion commenced. Inflow and outflow cannulas were inserted into the abdominal wall and the circuit was run with inflow at 43 °C and the outflow of approximately 41 °C to instill mitomycin. The patient was manually agitated during the perfusion. During the HIPEC portion, the patient had relative hypotension and tachycardia due to hypermetabolism from hyperthermia. Due to the mechanical agitation of the patient, our Flotrac/Vigileo numbers were not accurate so we periodically examined the TEE to confirm the stability of cardiac function and chamber size. Afterward, the patient’s abdomen was irrigated and hemostasis and closure was achieved. We checked the arterial blood gas (ABG) at three points during the case. Hemoglobin on the ABGs trended from 8.8 g/dL to 8.2 g/dL mid-case to 6.9 g/dL by the end of the case. A complete blood count (CBC) was sent which showed a hemoglobin of 7.3 g/dL and we decided not to transfuse as the patient was hemodynamically stable without vasopressors and mildly fluid overloaded. The base balance on ABG went from 0.7 to 2 to -3.6 immediately prior to extubation at the end of case and bicarbonate went from 27 to 21 from the beginning to the end of the case. The patient was never significantly acidotic. Electrolytes were checked midway through the case and creatinine was 0.5. Total surgical time and total anesthesia time were 8 hours, 46 minutes and 9 hours, 15 minutes, respectively.
Regarding total fluid balance, the estimated blood loss was 150 mL and total urine output was 510 mL. We used a total of 1.7 L of crystalloid and 750 mL of 5% albumin. The hemodynamic parameters at the end of the case were a CVP of 6, SVV of 7, and TEE showed the LV function and chamber size was back to the patient’s beginning of surgery baseline. There were no new wall motion abnormalities and there was interval development of a small pericardial effusion without hemodynamic consequence to which we alerted the surgeon (Figure ).
The left pleural effusion was stable to slightly enlarged at the end of the case.
The patient was extubated at the end of the case and taken to the post-anesthesia care unit (PACU) with stable vital signs. Her post-operative course showed consistent improvement with each day, no requirement for supplemental oxygen, no signs or symptoms of gross fluid overload or heart failure, and excellent kidney function. Her prescription for lisinopril and furosemide was restarted post-operatively. The patient was discharged from the hospital to her home on post-operative day eight (POD) in stable and good condition.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.0, 'cm']}",46.04337,43.7412,48.34554,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.0 cm, which is 153.0 cm * 0.393701 in/cm = 60.23625 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.23625 (in inches) - 60) = 46.04337 kg.
Hence, the patient's IBW is 46.04337 kg."
3599,10,Ideal Body Weight,physical,decimal,pmc-5576131-1,Extracted,"A 30-year-old G4, P2 female, 160 cm tall, and weighing 68 kg, was admitted at 38 weeks of her third gestation for vaginal bleeding and hypogastralgia at her local hospital. Due to the combination of hypoxemia and abnormal electrocardiograph (ECG) findings, she was advised to transfer to our hospital; the patient did not receive prenatal obstetric care in our hospital. The admitting diagnosis was cardiac insufficiency, cyanotic CHD (dubious) and scarred uterus. The physical examination revealed blood pressure of 130/80 mmHg, a pulse of 90/min, a respiratory rate of 25/min, slightly cyanotic lips and the same on her cheeks, coarse breath sounds to auscultation in the lungs, and a regular heartbeat. A loud P2 and grade 3/6 systolic murmur was heard at the third and fourth ribs on the left edge of the sternum. The ECG showed sinus rhythm, complete right bundle branch block (CRBBB), first degree A-V block, inverted T wave, right ventricular hypertrophy, and severe cardiac clockwise rotation.
The obstetricians felt that the manifestations of cardiac insufficiency in the mother put her at high risk in a vaginal delivery. The fetus presented with abnormal heart rate variability, with no further evidence that the fetus was in a state of emergency. Considering that the mother had been in a condition of hypoxia, which would result in hypoxia in the baby, the obstetricians recommended emergency cesarean section for the benefit of both the mother and the baby.
The patient was transferred to the operating theater with a temperature of 36.8 °C, a heart rate of 92 beats/min, a respiratory rate of 23breaths/min, a blood pressure of 138/88 mmHg, and an oxygen saturation of 83-90% in air. With the administration of a fractional inspired concentration of oxygen (FiO2) of 0.5 to 0.6 via a Venturi mask, the patient’s oxygen saturation increased from 88 to 92%. Peripheral venous access was sited, and a 400-ml bolus of compound sodium chloride was commenced, after which a radial arterial line was placed under local anesthesia for beat-to-beat blood pressure monitoring.
Combined spinal-epidural anesthesia (single-shot spinal anesthesia) was administered in this case. The puncture point of spinal anesthesia was selected in the L2-3 interspace, and the procedure was performed using a needle-through-needle technique in the left lateral decubitus position. After cerebrospinal fluid (CSF) could be slowly aspirated through the needle, doses of 1.4 ml of 0.5% hyperbaric bupivacaine made up with 10% glucose for a hyperbaric solution that made it easy to adjust and control the anesthetic plane were injected into the subarachnoid space slowly towards the head, and an epidural catheter was inserted into the epidural space. The patient was then placed in the supine position with a left lateral tilt of at least 30 degrees; [] the patient’s abdomen could be raised softly if necessary to relieve vena caval compression. Within 20 min later of the anesthetic injection, we tested the block height every 1-2 min and adjusted the head-up or head-down tilt position to strictly control the blockade under the level of T6-8. Twenty minutes later, the level of spinal block was static at T8. One minute later, the patient was returned to the supine position, with a slight decrease arterial pressure to 122/82 mmHg and a heart rate of 97 beats/min. As small doses of metaraminol could resist the vasodilatation caused by anesthesia to maintain the afterload, 100 μg of metaraminol was administered, after which the patient’s arterial pressure increased to 130/84 mmHg, with a heart rate of 91 beats/min.
During the entire procedure, the key for safely administering anesthesia on such a patient was to keep her blood pressure stable and to carefully address the side effects of the changes in the hemodynamics []. Because the spinal anesthesia took action faster and due to the rapid sympathectomy in the intra-vertebral anesthesia, great care should be taken of the changes in arterial pressure and heart rate after puncture and injection.
A male baby was smoothly delivered 10 min after the surgery began; the baby had Apgar scores of 8 at 1 min and 9 at 5 min. In addition to the caution that must be paid due to the change in the patient’s venous return at the time of the delivery of the baby, some factors need to be given attention to avoid the occurrence of great amounts of intra-cardiac shunt changes and even heart failure. First, because the oppression of the inferior vena cava was relieved after childbirth, the lower limb venous blood flow increased rapidly, and the venous return increased in a short amount of time as a result. Abdominal sandbags were adopted to add pressure to reduce the returned blood volume. Further, the maternal “autologous blood transfusion effect” had to be considered: after the fetus was delivered, the myometrium contracted, and intrauterine blood flowed back to the blood vessels rapidly, thereby increasing the cardiac preload in a short amount of time. If the initial transfusion was too great, it could lead to heart failure. According to the patient’s fluctuations in blood pressure, a bolus of ephedrine 3 mg or metaraminol 100 μg was used to restore the blood pressure to 130 ~ 140/82 ~ 87 mmHg, with a heart rate of 90 ~ 98 beats/min and an SpO2 of 89 ~ 93% during the surgery. The goal was to balance the preload and afterload and to try to maintain the intra-cardiac shunt in the preoperative level of stability.
Uterine atony was noted by the surgeon after delivery of the placenta. Oxytocin is usually administered to increase the contractions so as to reduce bleeding; however, a rapid infusion of oxytocin could increase the patient’s heart rate, reduce the cardiac output and coronary blood flow, and break the balance of the intra-cardiac shunt, which could lead to cardiac insufficiency. Therefore, the application of oxytocin must begin with small doses, and the dosage should be adjusted over time. Thus, oxytocin (10 mIU/min) was intravenously infused, and the infusion was adjusted in accordance with the patient’s changes in heart rate and blood pressure. Continuous post-cesarean analgesia was provided through an epidural catheter. The patient was transferred to the intensive care unit (ICU) and was then sent to the ward in stable condition the following day.
We advised the patient to have an echocardiogram examination, which revealed CHD, a single atrium, and defects of the endocardial cushions (Fig. ). Thus, we made a complementary diagnosis of CHD: single atrium. The patient was in good condition at the 6-month follow-up.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3600,10,Ideal Body Weight,physical,decimal,pmc-8383548-1,Extracted,"A 33-year-old Japanese woman visited our hospital due to 1 week of continuous low-grade fever, low back pain, and numbness of the entire left lower limb. These symptoms occurred when she lifted a heavy suitcase. She had visited an orthopedic doctor and received a caudal block 4 days prior, followed by a high-grade fever and deteriorating low back pain starting 1 day prior. Her medical history included surgery to enlarge both breasts when she was 14 years old. She was not taking any medicines on a regular basis. She had a smoking history of five cigarettes a day starting at the age of 20, and no history of drinking alcohol. She underwent periodic medical exams, and the latest one, which had been 2 months before, appeared normal. The patient was employed at a film factory, as a product inspector, and had no food or drug allergies. She had no history of casual sex, intramuscular injections, or IV drug use.
She was 153 cm tall, and weighed 42 kg. Her vital signs were abnormal, with blood pressure of 104/85 mm Hg, a heart rate of 123 regular beats/min, a body temperature of 38.1 °C, oxygen saturation of 98% in ambient air, and a respiratory rate of 16/min; her Glasgow Coma Scale score was 15 (E4V5M6) points. She complained of percussion tenderness to the lower thoracic vertebra and the upper sacral bone. Her manual muscle testing score for the left lower limb was 4; on the other hand, nothing else abnormal, including skin or neurologic findings, was detected upon physical examination.
A routine laboratory examination of the patient revealed increased values of white blood cells, creatinine, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR), and decreased values of blood urea nitrogen and creatine kinase. On the other hand, other values were normal, including complete blood count (CBC), biochemistry, urine tests, and cerebrospinal fluid examination (). She also tested negative for rheumatoid factor, autoantibodies such as anti-nuclear antibodies, anti-neutrophil cytoplasmic antibodies, serologic test for hepatitis B and C, syphilis, HIV, thyroid hormone, soluble interleukin-2 receptor, flu test, and 2/2 sets of blood culture. Head and chest-abdomen computed tomography (CT) scans and transesophageal echocardiography revealed normal results. On the other hand, a complete spine magnetic resonance imaging (MRI) scan revealed a 0.5- mm-thick layer of spinal epidural fluid in the posterior epidural space in the whole thoracic and anterior epidural space from the L5 to S2 vertebral body level region, which compressed the epidural space (, and , respectively). These findings were revealed as low intensity in a T1-weighted image, and high intensity in a T2-weighted image. Other findings, such as discitis, were not confirmed.
At this point, we suspected a diagnosis of disseminated SEA, but the origin was still unknown. However, an orthopedic surgeon recommended against performing CT-guided percutaneous needle aspiration of the abscess, based on the locations of the lesions. The patient was hospitalized, and we started 13.5 mg/day of piperacillin-tazobactam, following which she gradually became symptom-free. However, on the 14th hospital day, she strongly requested that she be discharged from the hospital, so we changed her antibiotics to 500 mg/day of levofloxacin tablets, and continued treatment. During her return visit, 16 days after her discharge, she was well. We confirmed normal values of inflammation biomarkers, including WBC, CRP, and ESR, and in addition we also confirmed abscess improvements in both the thoracic and sacral regions through an MRI scan (, and , respectively). Based on these findings, we ended her treatment that day without treatment complications.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.0, 'cm']}",46.04337,43.7412,48.34554,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.0 cm, which is 153.0 cm * 0.393701 in/cm = 60.23625 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.23625 (in inches) - 60) = 46.04337 kg.
Hence, the patient's IBW is 46.04337 kg."
3601,10,Ideal Body Weight,physical,decimal,usmle-1111,Extracted,"A 35-year-old woman comes to the physician because of fatigue and a 9-kg (20-lb) weight gain over the past 12 months. She also has irregular menstrual cycles and difficulty sleeping. Menses occur at irregular 35- to 50-day intervals and last 3–7 days. Menarche was at age of 13 years and her last menstrual period was 4 weeks ago. She has 1-year history of hypertension treated with hydrochlorothiazide. She drinks a glass of wine daily. She is 163 cm (5 ft 4 in) tall and weighs 85 kg (187 lb); BMI is 32 kg/m2. Her temperature is 37°C (98.6°F), pulse is 82/min, respirations are 16/min, and blood pressure is 125/86 mm Hg. Examination shows acne on the face and hair on the chin and around the umbilicus. The face has a rounded shape and is reddened. There are several smaller bruises on both forearms.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [163.0, 'cm']}",55.0985,52.34358,57.85343,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 163.0 cm, which is 163.0 cm * 0.393701 in/cm = 64.17326 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.17326 (in inches) - 60) = 55.0985 kg.
Hence, the patient's IBW is 55.0985 kg."
3602,10,Ideal Body Weight,physical,decimal,pmc-7818608-2,Extracted,"A 78-year-old male patient who had undergone bilateral cemented THR in 2003 presented with sudden onset of left hip pain and inability to walk after a fall in the kitchen. He lived independently and was using a walking stick/mobility scooter to get around before this fall.
His medical history included a high BMI of 50 (ht, 170 cm; wt, 145 kg), type 2 diabetes mellitus, past cerebrovascular event, hypertension, and gastroesophageal reflux disease.
The radiographs revealed a fracture of the Exeter stem just below the trunnion ().
The implant used during his index procedure was Exeter V40 (44 offset no. 5) stem and a 28-mm/+4 mm head. The acetabular component was a cemented Opera cup (Smith and Nephew, Andover, MA) (53 mm OD, 28 mm ID). The acetabular cup had minimal wear and was found to be well-fixed intraoperatively. The stem was revised to a standard Exeter V40 (44 offset no. 3) stem using a cement in cement revision technique. His postoperative recovery was prolonged because of hospital-acquired pneumonia. At 6 months follow-up stage, he was ambulating with a single walking stick and progressing well ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3603,10,Ideal Body Weight,physical,decimal,pmc-4173574-1,Extracted,"A 30-year-old woman presented with the chief complaints of pain and swelling in the right elbow joint. There was no history of fall, fever, or weight loss. Patient was diagnosed as having pathological fracture of right radius. Patient gave history of breathlessness and was of New York Heart Association grade II. On general physical examination, patient weight was 55 kg, 160 cm in height, Polydactyl of all four limbs [], clinodactyly and loss of thenar prominence [] are noted. The airway assessment showed Mallampatti grade I, thyromental distance of 6 cm, and mouth opening of three fingers. Systemic examination showed fixed spilt second heart sound with grade two systolic murmur, regular good volume pulse. There was no organomegally, no raised jugular venous pressure, and no signs of congestive cardiac failure noted.
Preoperative hemogram, random blood sugar, electrolytes, renal function tests, and chest radiograph were normal. Electrocardiogram revealed right bundle branch block. The echocardiography showed large ostium primum ASD with left to right shunt, with cleft in anterior mitral leaflet, mild mitral regurgitation, moderate tricuspid regurgitation, moderate pulmonary artery hypertension, dilated right atrium, and ventricle with mild left ventricular dysfunction.
The patient received premedication of Tab. Diazepam 5 mg and Tab. Ranitidine 150 mg per oral night before surgery and on the day of surgery in the morning. Tab. amoxicillin 2 g orally 1 h prior to surgery was given to prevent infective endocarditis. Patient was kept nil per oral for 6 h before surgery and received intravenous (I.V.) fluids of 1 mL/kg/h.
On arrival to operating room blood pressure was 118/70 mm hg, heart rate 76/min, respiratory rate 14/min and oxygen saturation 96%. Electrocardiography monitoring was established, together with monitoring of noninvasive arterial pressure and pulse oximeter.
There are no data in the literature to suggest preferred anesthetic technique. Since the procedure was at the elbow region, the peripheral nerve block, that is, supraclavicular brachial plexus block was selected as it is much superior compared with general anesthesia in this case. Patient received Inj. Midazolam 2 mg and Inj. Fentanyl 55 mcg intravenously for procedural sedation. We identified the supraclavicular brachial plexus by peripheral nerve stimulator technique. A combination of inj. Lignocaine (2%) 5 mg/kg body weight and Inj. Bupivacaine (0.5%) 2 mg/kg body weight was injected after negative aspiration for blood. We did avoid combination of Ing Lignocaine with Adrenaline in view of possible new onset of arrhythmias. Successful block was achieved and procedure was uneventful. Patient received the inj. Diclofenac 75 mg I.V. infusion postoperatively after 4 h as the visual analogue score was 5. Patient was shifted to high dependency unit for monitoring 24 h and followed-up to note any complications related to nerve block.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3604,10,Ideal Body Weight,physical,decimal,pmc-5818840-1,Extracted,"A 43-year-old man (weight: 80 kg; height: 174 cm) with BD was referred to the Department of Orthopedic, Shohada Teaching Hospital, for repair of patella fracture and patella tendon tearing after falling. He was not a child of parents who have familial relations and he has a disabled brother who is still alive. The patient was diagnosed at the age of 17 years, when he could not do standard exercise due to leg weakness. The diagnosis was made by completing a muscle biopsy. He required a cane for walking or sometimes a wheelchair. He was a goldsmith, but can no longer work. The patient underwent a procedure for inserting a KÜNTSCHER intramedullary rod in the femur 7 years ago and fixation of femur fracture 4 years ago, and he also received 20 mg/day of prednisolone (at irregular intervals, based on the physician’s recommendation). The disease did not affect other members of his family. The myopathy affected him in his right side, making him unable to move his right thigh. The patient could walk for ~100–500 m, when he followed a good nutrition plan. Upon physical examination, he had hypoesthesia in the right foot and severe swelling in the right knee but was conscious and oriented. The patient had stable vital signs, and auscultation of the heart and lungs did not reveal any murmur or additional sounds. The laboratory test results were as follows: hemoglobin (Hb): 13.6 g/dL, hematocrit (Hct): 41.1%, white blood cells (WBC) count: 12.1/mm3, platelet count: 211,000/mm3, international normalized ratio (INR): 1, prothrombin time (PT): 13 seconds, partial thromboplastin time (PTT): 38 seconds, plasma blood urea nitrogen (BUN): 19.5 mg/dL and creatinine: 0.9 mg/dL, blood group: ARH+, potassium: 4 mg/dL and blood sugar: 71 mg/dL. Cardiologist and internist consultations revealed that he had no heart problems, and echocardiography was normal (ejection fraction [EF]: 60%, normal chamber size, absence of pulmonary hypertension, absence of pericardial effusion, left ventricular systolic diameter [LVSD]: 4.2 and right ventricular diastolic diameter [RVDD]: 2.2).
Electrocardiography was normal (sinus rhythm), and it was recommended that the procedure should be performed under general anesthesia.
On the day of the operation, the patient fasted for 8 hours and was hydrated with 400 mL ringer solution. Accordingly, in the operation room, the patient was monitored by routine standards (heart rate: 89 bpm, blood pressure: 133/86 mmHg, respiratory rate: 12/min, SpO2: 100% and body temperature: 37.3°C axillary). A total of 200 mg hydrocortisone was injected as the stress dose, and the total intravenous anesthesia (TIVA) technique was used. The patient was in the supine position and he was preoxygenated by 6 L/min O2 over 3 minutes via an anesthesia face mask. Induction of anesthesia was performed with 2 mg midazolam, 250 µg remifentanil and 60 mg lidocaine 2%. For maintenance of anesthesia, 200 mg of propofol was administered, and the patient was intubated with endotracheal tube (ETT) size 8; 3 L/min O2, 3 L/min N2O and 0.5% isoflurane were then discontinued. Furthermore, 75–100 µg/kg/min propofol and 0.05–2 µg/kg/min remifentanil were infused using a syringe pump until termination of the operation, which lasted 90 minutes. No muscle relaxant or nerve stimulator was used. End tidal carbon dioxide was measured by side stream capnography (30–35 mmHg). The patient was safely extubated after surgery and transferred to the post-anesthesia recovery unit. In Post Anesthesia Care Unit (PACU), the patient was routinely monitored for apnea symptoms. Urine was examined for rhabdomyolysis-induced myoglobinuria. The vital signs at this time were as follows: heart rate: 87 bpm, blood pressure: 108/74 mmHg, respiratory rate: 12/min, SpO2: 100% and body temperature: 37.5°C axillary. No adverse event was recorded during surgery and anesthesia. Antibiotics comprising of cefazolin 1 g intravenously every 6 hours and gentamicin 240 mg/stat (one dose) were administered over a 24-hour period. All laboratory tests were repeated and showed results were within normal range, and the patient was discharged after 72 hours of operation. The patient was called 3 months after surgery; he does not experience any new alteration in his general condition and continues to receive the same care that he did pre-surgery.
The authors obtained written informed consent for the publication of this case report.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [174.0, 'cm']}",69.55913,66.08117,73.03709,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 174.0 cm, which is 174.0 cm * 0.393701 in/cm = 68.50397 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.50397 (in inches) - 60) = 69.55913 kg.
Hence, the patient's IBW is 69.55913 kg."
3605,10,Ideal Body Weight,physical,decimal,pmc-8560865-3,Extracted,"A 37-year-old woman (G1P1; height, 158 cm; weight, 78 kg) without a significant medical history was referred to our hospital with a diagnosis of PPCM. Postpartum day 4, she developed dyspnea with lower leg edema, shock, and LVEF was 33% (INTERMAX profile 1). Medical treatment was started with inotropes and diuretics for heart failure. Subsequently, LVEF reduced to 20%, LVEDd was 69 mm, and mitral regurgitation worsened. IABP, VA-ECMO, and anti-prolactin therapy were started on postpartum day 7. However, congestion progressed with dilation of the left ventricle and left ventricular vent was inserted on postpartum day 11, which resulted in improvement of congestion. Postpartum day 19, VA-ECMO was stopped due to thrombus in its circulation, and at this time the LVEF was 35% and CO 4.76 L/min. Postpartum day 23, we had no choice but to removed IABP and continued medical treatment. However, the cardiac dysfunction could not be controlled and the patient needed IABP again, postpartum day 118. Postpartum day 129, the implantable LVAD was implanted and mitral valve replacement was performed. Postpartum day 386, LVEF recovered to 55% and CO 4.36 L/min, and the LVAD was withdrawn and the patient was discharged from the hospital.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3606,10,Ideal Body Weight,physical,decimal,pmc-4050940-1,Extracted,"A 29-year-old female (55 Kg and 160 cm), American Society of Anaesthesiologists (ASA) physical status I, presented for tubal reanastomosis surgery. Patient had undergone previous two normal vaginal deliveries uneventfully. Clinical examination was unremarkable and all the investigations were within normal limits, including ECG and chest X-ray (CXR). On the day of surgery, 18 G IV cannula was established on right forearm and preloading started with ringer lactate. ECG was showing normal sinus rhythm with heart rate of 88/min, non invasive blood pressure (NIBP) was 110/70 mm Hg and oxygen saturation (SpO2) was 99% on room air.
Patient was premedicated with Inj. midazolam 1 mg and Inj. ondansetron 4 mg intravenously. Subarachnoid block was given in right lateral position at L3-L4 interspace with 15 mg of hyperbaric Bupivacaine. After turning patient to supine position, monitor showed HR of 70/min with sinus rhythm and BP of 90/60 mmHg. Patient was supplemented with oxygen through Hudson's mask at 5 lit/min. Five minutes later, after checking adequate sensory level (T6), surgeon was asked to proceed. Within a minute, before surgeon could start surgery, patient developed seizure like activity. Monitor showed bradycardia (35/min). Inj. Atropine 0.6 mg was given intravenously but patient developed asystole. Cardiopulmonary resuscitation was started with chest compression and mask ventilation. Inj. Adrenaline 1 mg was given intravenously. After two minutes, return of spontaneous circulation (ROSC) was noticed. ECG showed sinus rhythm with HR of 101/min. Next moment, patient developed ventricular tachycardia with HR of 160/min with no palpable pulse. Patient was successfully defibrillated with 150J (biphasic). Rhythm reverted back to sinus with HR of 160/min with SpO2 of 100% and BP of 90/60 mmHg. Breathing was assisted as patient started breathing spontaneously. Within few minutes, patient started obeying verbal commands, was vocalizing and was able to lift both upper limbs. Sensory level at this time was T4. By that time, patient had received 1000 ml of IV crystalloids. Surgery was cancelled and patient was kept on table for observation. 12 lead electrocardiogram was done, which showed sinus tachycardia.
Over the period of next 2 hours, patient was given another 1000 ml of crystalloids, 500 ml of colloid and intermittent intravenous boluses of Inj. ephedrine (total 24 mg) to manage hypotension secondary to sympathetic blockade due to spinal anaesthesia. Mean arterial pressure was maintained around 60 mm Hg and 200 ml of urine output was recorded. Approximately two and half hours after ROSC, patient started desaturating with signs of pulmonary oedema, SpO2 dropping to 92% on Hudson's mask. RR became 30/min, and bilateral crepitations were heard on auscultation. Patient was given continuous positive airway pressure (CPAP) with 100% oxygen on mask in post anaesthesia care unit (PACU). Titrated doses of Inj. morphine (10 mg total) and Inj. frusemide were administered. Sensory blockade level was below L1. Patient developed hypotension with worsening respiratory distress and hypoxia. Blood gas analysis showed PO2 of 50 mmHg, PCO2-45 mmHg, pH-7.31 with normal serum electrolytes. BP dropped to 60/40 mm Hg, and HR was130/min with sinus rhythm, SpO2 was 72%. Dopamine infusion was started at 5 mcg/kg/min along with fluid support. Patient was intubated and ventilated with 100% Oxygen and IPPV and shifted to intensive care unit. Right internal jugular vein was cannulated with 7.5 F catheter and patient was started on noradrenaline 2 mcg/min. 2 D Echocardiography (ECHO) was done in view of persistent hypotension and unresponsive pulmonary oedema. It showed ejection fraction (EF) of 35% with global hypokinesis. Diagnosis of probable post cardiac arrest myocardial stunning was made. Cardiac support was continued with inj. noradrenaline with addition of inj. dobutamine. Subsequent ECHO, 2 days later showed EF of 43% with global hypokinesia. Over the period of next one week, patient improved clinically. Patient was weaned off from vasopressor support and extubated.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3607,10,Ideal Body Weight,physical,decimal,pmc-7233765-1,Extracted,"A Bulgarian boy, 17 years and 11 months old, referred to our Pediatric Endocrinology Unit for pubertal failure and hyposmia. His stature: 171.6 cm (-0.69 SDS), upper segment: 84.3 cm, lower segment: 87.3 cm and arm span 180 cm. His weight was 92 Kg (1.83 SDS) with BMI of 31.24 kg/m2 (2.22 SDS). Clinical evaluation revealed a high-pitched voice, gynecomastia, obesity and valgus knees. Penile length 3.2 cm, bilateral volume testes about 2 ml and pubic hair Tanner III stage. No evidence of dysmorphic features; he had a double upper urinary tracts. Hormonal basal study revealed low values of FSH (0.29 mUI/ml), LH (0.09 mUI/ml) and testosterone (0.2 ng/ml) for sex and chronological age. GnRH stimulation test elicited a prepubertal LH response with LH and FSH peaks of 1.18 mUI/mL and 2.43 mUI/mL respectively. The karyotype was 46, XY. Brain magnetic resonance imaging was normal. A subjective smell test confirmed hysposmia. According to this clinical and hormonal picture we hypothesized a Kallmann Syndrome and started gonadotropin therapy. After obtained an informed consent, we performed an extensive NGS mutational analysis by a specific platform including the following genes: CHD7, DUSP6, FEZF1, FGF17, FGF8, FGFR1, FLRT3, GnRH1/2, GnRHR, HS6ST1, IL17RD, ANOS1 (KAL1), KISS1, PROK2, PROKR2, SEMA3A, SEMA3E, SEMA7A, SOX2, SOX10, SPRY4, TAC3, TACR3, WDR11. The raw data for all of the above genes were then analyzed by filtering the sequence’s variants using a specific mutational reference panel for each gene (1000 Genes Project, Roche illumina data bank). The fgfr1 gene gave the highest score, and the final Sanger sequencing confirmed the presence of a c.1058 C>G transition in heterozygous state located on exon 8 leading to a Serine to Cystine change never previously described.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [171.6, 'cm']}",67.38591,64.01661,70.75521,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 171.6 cm, which is 171.6 cm * 0.393701 in/cm = 67.55909 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.55909 (in inches) - 60) = 67.38591 kg.
Hence, the patient's IBW is 67.38591 kg."
3608,10,Ideal Body Weight,physical,decimal,pmc-7488564-1,Extracted,"A 57-year-old Japanese man, height 170 cm, weight 75 kg, was carried to our hospital with sudden-onset chest/back pain. His only past medical history was untreated hypertension, and he had had no episode of blood coagulation abnormality. He was not taking any medication, and no significant family history was noted. When he arrived at our hospital, he was alert (Glasgow Coma Scale score 15), and he had no paralysis. Although his circulatory dynamics were almost stable, he was diagnosed with acute type A aortic dissection by contrast-enhanced computed tomography (CT). The aortic dissection extended to the abdominal aorta, left common iliac artery, and brachiocephalic artery; however, the persistence of perioperative malperfusion was not confirmed by CT. Thus, emergency aortic arch replacement surgery was scheduled. Before the surgery, there was no pericardial effusion and no major aortic valve regurgitation detected by transthoracic echocardiography, and the patient’s electrocardiogram revealed no abnormality. The results of arterial blood gas analysis were within the normal ranges, except for an increase in lactate of 4.60 mmol/L. Although the patient had no clinical bleeding tendency, a blood test prior to surgery showed coagulopathy: platelet count (PLT) 117 × 109/L, prothrombin time–international normalized ratio (PT-INR) 1.78, activated partial thromboplastin time (APTT) 69.7 seconds, fibrinogen < 50 mg/dl, and D-dimer 1560 μg/ml.
General anesthesia was induced with midazolam 5 mg, fentanyl 200 μg, and rocuronium 50 mg and maintained with sevoflurane 1.5% or midazolam (during cardiopulmonary bypass [CPB]), intermittent administration of fentanyl (total 600 μg), remifentanil 0.15–0.3 μg/kg/minute, and rocuronium. During the surgery, an electrocardiogram, left radial and left dorsal pedis arterial pressure, pulse oximetry, central venous pressure, regional cerebral oxygen saturation (rSO2) (INVOS 5100C; Medtronic, Boulder, CO, USA), bispectral index, and transesophageal echocardiography were monitored. Left and right rSO2 values before the induction of anesthesia were 74% and 75%, respectively.
A smaller-than-usual dose (8000 IU) of heparin was administered because activated clotting time (ACT) prior to heparin administration was extremely prolonged (> 999 seconds). ACT was assessed by using the HMS Plus system (Medtronic). Then, the left femoral artery, right subclavian artery, left femoral vein, and superior venae cavae were cannulated to establish CPB (MERA exceline CPB circuit; SENKO MEDICAL INSTRUMENT, Tokyo, Japan). There were no clinical signs of coagulopathy during opening of the chest or cannulation.
Following establishment of CPB, the patient was cooled to 25 °C tympanic temperature. Perfusion pressure was maintained at approximately 60 mmHg during CPB. Hemiarch replacement (replacement of the ascending aorta, proximal aortic arch, and right innominate artery) was performed by using the open distal anastomosis technique under circulatory arrest with brain protection by antegrade selective cerebral perfusion. The circulatory arrest time was 49 minutes. Moreover, aortic root replacement (Bentall procedure) was performed after reestablishing CPB via the graft anastomosed to the distal end. During the surgical procedure, the rSO2 value was maintained between 60% and 75%. ACT assessed every 30–60 minutes after the first heparin administration was unchanged, being > 999 seconds; therefore, additional heparin was not administered during surgery. There was no clinical problem during CPB.
After the CPB, 720 ml of fresh frozen plasma (FFP) and protamine sulfate 200 mg were administered, then ACT decreased to 159 seconds. Moreover, oozing persisted after first administration of FFP and protamine; thus, 1200 ml of FFP, 800 ml of platelet concentrates (PC), fibrinogen concentrate 3 g, and tranexamic acid 2 g were needed after the CPB for hemostasis, and ACT was 137 seconds at the end of surgery. The bilateral rSO2 gradually decreased from the end of CPB and was approximately 40% at the end of surgery. The CPB time was 492 minutes; the operative time was 667 minutes; the anesthesia time was 739 minutes; the intraoperative urine volume was 1185 ml; and the bleeding volume was approximately 5500 ml. After the surgery, the patient was transferred to the intensive care unit (ICU) with artificial respiration.
A blood test performed soon after the surgery showed the following values: PLT 123 × 109/L, PT-INR 1.52, APTT 38.3 seconds, fibrinogen 124 mg/dl, and D-dimer 116 μg/ml. After arrival in the ICU, bleeding from the drains in the pericardial cavity continued, and red blood cells and FFP were administered. On the first postoperative day (POD 1), dilation of the pupils and loss of light reflex were observed. A head CT indicated diffuse cerebral edema, and a diagnosis of global cerebral infarction was made. Although FFP and PC were administered on an as-needed basis from POD 1 to POD 7, ACT had been prolonged to approximately 150–200 seconds without using heparin. An additional blood coagulation test performed at POD 9 (Table ) indicated FXII deficiency (8.0%). At this point, global cerebral infarction was confirmed, and a poor prognosis was expected. Therefore, with written informed consent from the family of the patient, additional intervention for FXII deficiency was not performed. The patient died on POD 14.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3609,10,Ideal Body Weight,physical,decimal,pmc-3861361-1,Extracted,"The participant we describe here was a healthy 24-year-old woman (height 174 cm, weight 56 kg) with no history of drug allergy and alcohol use. Laboratory tests conducted during screening on July 17, 2009, found that she was negative for HIV, syphilis, and hepatitis B. Her hepatic enzymes and creatinine clearance were within normal limits.
After about 8 weeks of taking TDF-FTC, this participant complained of mild paresthesiae, numbness, and a tingling sensation in her upper limbs that was associated with pain and cold. The symptoms did not affect her daily activities, physical examination was normal, and she had not taken any medications that are known to cause peripheral neuropathy upon interaction with TDF-FTC. After an additional 4 days, she developed a disabling weakness of her upper limbs and bilateral weakness of power grip of grade 3–4 and fine tremors in her hands at rest and with activity. Neurological examinations found normal orientation in time and place as was her pupillary light reaction and fundoscopy. Muscle tone, reflexes, and somatic sensations were also normal, but there was a mild deviation of the mouth and the tongue to the left, on protrusion.
After trial closure, analysis of her plasma and intracellular drug levels at week 4 and 8 were consistent with moderate adherence to TDF-FTC., At week 10, TDF-FTC was temporarily withheld due to safety concerns and as per the study protocol. The participant was given oral Neurorubine® (Vitamins B1, B6, and B12; Mepha Ltd, Aesch, Switzerland) for 2 weeks. Within 2 weeks after stopping the study drug, she was free of all symptoms. At week 12, she was restarted on the study drug according to the protocol. However, 1 month after restarting the pill, the participant complained of other neurological symptoms of posture-dependent numbness of her upper limbs. The numbness occurred while bending down and resolved after assuming an upright posture. She did not experience the earlier disabling muscle weakness or tremors. Her neurological exam was normal, and she continued taking the study drug. Her drug levels at week 24 (analyzed on stored samples after study closure) were consistent with low adherence to TDF-FTC.
At week 25, the study team decided to withdraw the study drug until neurologic exploration was completed. At week 28, the participant reported having taken a traditional herbal medicine, orally as a single dose. The nature of the herbal medication could not be determined by the study team.
At week 29, the magnetic resonance imaging (MRI) of her brain and cervical spine was found to be normal. Blood tests (performed at that time) revealed her lactate dehydrogenase was elevated at 514 U/L (normal range: 230–460), but her aldolase and creatinine phosphokinase were normal. The neurologist – with extensive experience in the treatment of HIV-infected patients – who assessed the participant observed:
The clinical manifestation in this patient was not the usual peripheral neuropathy known in patients receiving TDF-FTC. A typical TDF-FTC-related neuropathy starts with feet and only later goes to upper extremities. The fact that the paresthesiae occurs when the patient bends forward (Lhermitte’s sign) suggests a possible lesion of the cervical spine, though MRI findings were normal.
In addition to the study drug, Neurorubine®, and the unknown herbal medication, the participant reported taking the following medications: 1) medroxyprogesterone acetate, from enrolment throughout the study period; 2) ibuprofen at week five for one day; 3) amoxicillin/clavulanic acid at week seven for 10 days; and 4) diclofenac at weeks 9 and 10 for 3 and 7 days respectively.
Overall, for safety concern, the participant was managed as if she was assigned the TDF-FTC arm. The clinical team decided not to un-blind the participant’s study group allocation, because this would not influence clinical case management. The participant’s postural numbness gradually improved and was completely resolved by her week 36 visit. The participant finished study follow-up on September 28, 2010. Her symptoms did not reoccur after she discontinued the study pill.
After trial closure, levels of vitamin B12 on her stored blood samples at weeks 4, 8, 12, and 16 all showed normal values: 625, 727, 744, and 791 ng/L respectively (normal range: 239–931 ng/L).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [174.0, 'cm']}",65.05913,61.80617,68.31209,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 174.0 cm, which is 174.0 cm * 0.393701 in/cm = 68.50397 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (68.50397 (in inches) - 60) = 65.05913 kg.
Hence, the patient's IBW is 65.05913 kg."
3610,10,Ideal Body Weight,physical,decimal,pmc-3581787-1,Extracted,"A 74 year-old female patient, 158 cm tall and weighing 62 kg, was diagnosed with a full thickness RC tear of her right shoulder. She was scheduled to undergo open RC repair. Her physical status was American Society of Anesthesiologists physical status II. Her prior medical history included hypertension, stable angina, and diabetes mellitus, which were well controlled with medication. Four years previously, the patient had experienced painless cramps in both hands and feet and excessive sweating without any palpitations, even during the winter season. Then, two years later she was diagnosed with Isaacs' syndrome through EMG. The nerve conduction study was unremarkable. Studies for serum anti-VGKC antibodies were not performed and antiacetylcholine-receptor antibodies produced negative results. The patient complained of gradual progressive painless flexion of her left ring and little fingers, which led to contractures (). The fingers could only be extended passively. No other neurologic abnormalities and sensory deficits were noted. A course of intravenous immunoglobulin was ineffective, and the patient was placed on a regimen of oral carbamazepine 200 mg and gabapentin 300 mg per day. She showed some improvement in symptoms without complete resolution.
Serum electrolytes including calcium, magnesium, sodium, and potassium ions were within the normal limits. Thyroid hormone levels, creatine kinase, and aldonase were also normal. Computerized tomographic scan of the thorax did not reveal thymoma. Pulmonary function tests showed a normal pattern. There was no family history of neuromuscular disease. The patient had undergone general anesthesia for spinal stenosis before her Isaacs' syndrome diagnosis in another hospital. Unfortunately, the details of the anesthetic agents used were unavailable.
Upon arrival in the operating room, the patient's blood pressure was 155/82 mmHg, heart rate was 51 beats/min, and oxygen saturation was 97%. She was premedicated with intravenous glycopyrrolate 0.2 mg before the surgery. Preoperative monitoring including ECG, pulse oximeter, capnogram, and direct arterial pressure monitoring via the left radial arterial cannula was performed. Bispectral index (BIS) and train-of-four (TOF) monitors were attached to the patient. Three minutes after preoxygenation, lidocaine 40 mg was administered prior to target controlled infusion (TCI) of propofol (target blood concentration 2.5 µg/ml) and remifentanil (target blood concentration 2.0 ng/ml). The patient rapidly fell into sleep with loss of eyelid reflex but abnormal muscle activity still persisted. When the numerical value of the BIS was 48, atracurium 30 mg (0.5 mg/kg) was administered. Ninety seconds later, the involuntary cramps were arrested and no response to TOF stimuli (2 Hz for 2 sec at 10-sec intervals) was observed. The patient was grade IIb on the modified Cormack and Lehane scoring system on laryngoscopy. Only the patient's glottis and vocal cords were visible. Nevertheless, endotracheal intubation was performed without complications. The patient was ventilated with a mixture of oxygen and air (FiO2 0.5). Warm forced air devices were used to maintain body temperature.
During anesthesia, the patient showed no specific abnormalities of her vital signs, and an open RC repair was smoothly performed in 90 minutes. At the end of the surgery, the propofol and remifentanil infusion was stopped and the patient resumed spontaneous breathing. On the nerve stimulator, the TOF ratio was kept above 0.90. After the patient had recovered spontaneous respiration to a sufficient extent, glycopyrrolate 0.4 mg and pyridostigmine 15 mg were intravenously injected to reverse the muscle relaxation. Extubation was performed at a final TOF ratio of 1. The time from the end of surgery to extubation was about 10 minutes. We then moved the patient to the intensive care unit for continuous hemodynamic monitoring. One day after the operation, the patient was transferred to the general ward, but she complained of difficult urination. Urologic evaluation revealed a flaccid-type neurogenic bladder, and a suprapubic catheter was placed for urination. There were no further complications, and on the 22nd day after the operation, the patient was discharged from the hospital.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3611,10,Ideal Body Weight,physical,decimal,pmc-7793217-1,Extracted,"A 31-year-old man with no past medical history presented to our institution with orthopnoea and systemic oedema. On admission, physical examination found a respiratory rate of 23 b.p.m., regular pulse rate of 45 b.p.m, and blood pressure of 140/95 mmHg. His body height was 173 cm and body weight was 136 kg (30 kg gained in 1 month). No abnormal heart or breath sounds were noted. His brain natriuretic peptide (BNP) level was elevated to 681 pg/mL. The electrocardiogram (ECG) showed complete atrioventricular block (CAVB) with atrial fibrillation (AF) (). The cardiothoracic ratio on chest X-ray was 74%, and echocardiography showed reduced LVEF of 40%. His father died of cardiovascular events at age 45 years, and his grandfather had undergone pacemaker implantation. Because of his family history, co-existence of AF and CAVB, and LV dysfunction, we suspected cardiomyopathy due to a lamin A/C (LMNA) gene mutation, and a genetic test subsequently confirmed this.
He underwent implantation of a dual-chamber CRT-defibrillator (CRT-D) for the following three reasons. (i) Optimized medical treatments including oral intake of enalapril maleate of 2.5 mg, bisoprolol of 1.25 mg, spironolactone of 50 mg, furosemide of 40 mg, and tolvaptan of 15 mg and intravenous infusion of dobutamine at 4 μg/min/kg neither reduced his body weight nor improved his HF symptoms. (ii) He was totally pacing-dependent due to CAVB. (iii) LVEF <50% may be a predictor of progression to end-stage HF or death among patients with lamin cardiomyopathy. Subsequently, the atrioventricular (AV) and interventricular (VV) delays were optimized by echocardiographic evaluation, and AF was converted to sinus rhythm by direct current cardioversion under oral intake of amiodarone of 200 mg daily, resulting in the improvement of New York Heart Association (NYHA) Class from IV to III. However, 12 months after the CRT implantation, AF recurred and persisted, and an echocardiogram showed a reduced LVEF of 19%. A 12-lead ECG showed a change in the paced QRS morphology () suggesting rapid progression of the disease. He had been inotrope dependent but decided against cardiac transplantation due to the expense. We offered the option of additional HBP and upgrade of CRT as a last resort for managing his end-stage HF, to which he consented. Although we performed mapping of the HB region with a decapolar catheter before placement of the HB lead (Model 3830: Medtronic, Minneapolis, MN, USA), a discrete HB potential could not be recorded, and the pacing threshold in most of the septal region was ≥5.0 V/2.0 ms, probably because of the advancement of septal fibrosis and myocardial degeneration in lamin cardiomyopathy, which did not allow evaluation of pacing output-dependent change of the QRS morphology. Furthermore, severe dilation of the right atrium (RA) and right ventricle (RV) made manipulation of the HB lead difficult (). After lead fixation, the HBP lead was connected to the atrial port because his AF had already become the permanent form of rhythm. Although the QRS duration did not shorten compared with that of BiVRVA+LV pacing (escape rhythm: 252, BiVRVA+LV: 220, and HBP: 213 ms, respectively) (), BiVHB+LV resulted in obvious narrowing of the QRS to 163 ms (). We also assessed ventricular dyssynchrony with speckle-tracking two-dimensional (2D) echocardiography (QLAB11; PHILIPS) and defined the standard deviation of the time to peak strain of six segments of the RV (RV-SD) on the apical four-chamber image and that for the LV (LV-SD) on the short-axis image at the papillary muscle level (). Although all pacing configurations caused worsening of RV-SD compared with the escape rhythm (possibly a junctional rhythm), the increase in the RV-SD was the mildest during BiVHB+LV compared with BVRVA+LV and HBP alone (escape rhythm, 63; BiVRVA+LV, 151; HBP alone, 126; and BiVHB+LV, 99 ms). Regarding LV synchrony, although neither BiVRVA+LV nor HBP alone improved LV-SD compared with the escape rhythm, BiVHB+LV did markedly improve it (escape rhythm, 54; BiVRVA+LV, 52; HBP alone, 40; and BiVHB+LV, 13 ms) (). Therefore, we programmed BiVHB+LV and DDD mode with a lower rate of 85 b.p.m., AV delay of 50 ms, and RV–LV delay of 20 ms with minimized RV pacing output to inactivate RVA pacing. This programming resulted in BiVHB+LV pacing with a VV delay (HB-LV delay) of 70 ms without RVA pacing. Additionally, ventricular arrhythmias were detected based on just their cycle length measured by single-chamber sensing without the sudden onset criterion because of the presence of CAVB and AF in this patient. Over the week following the pacing upgrade, his haemodynamics improved dramatically, and he was discharged and has remained free from HF (NYHA Class II) for more than 13 months.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.0, 'cm']}",68.65362,65.22094,72.0863,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.0 cm, which is 173.0 cm * 0.393701 in/cm = 68.11027 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.11027 (in inches) - 60) = 68.65362 kg.
Hence, the patient's IBW is 68.65362 kg."
3612,10,Ideal Body Weight,physical,decimal,pmc-8710137-1,Extracted,"A 42-year-old male, office employee, smoker, height 1.66 m, weight 66 kg, with no family history or antecedents of cardiovascular disease, who consulted at Instituto Cardiovascular de Rosario (ICR) for a condition characterized by progressive dyspnea lasting approximately two months, associated with episodes of mid-thoracic pain with radiation to the shoulders two hours long.
In the initial evaluation, signs and symptoms compatible with HF and holosystolic murmur in a polifocal bar were evidenced, with the presence of thrill and gallop rhythm. He was admitted and further evaluated by: (i) routine biochemistry examination within normal parameters except for an elevated N-terminal pro-brain natriuretic peptide (NT-ProBNP) of 5321 pg/ml. (ii) 12-lead electrocardiogram revealed sinus tachycardia of 130 beats per minute associated with signs of inferior-lateral myocardial fibrosis with compromised right leads. (iii) Chest X-ray, where signs of grade III venulo-capillary hypertension were observed. (iv) Color Doppler echocardiogram: systolic and diastolic diameter of the left ventricle 61/55 mm, respectively, impaired left ventricular ejection fraction (LVEF; 20%), abnormal segmental motility with apical akinesia in all its segments, inferior, septal, and anteromedial. Systolic displacement of the plane of the tricuspid annulus was 13 mm and grade II diastolic dysfunction. Pulmonary artery systolic pressure was 55 mmHg. At the junction of the middle and apical third of the interventricular septum, a continuity solution with a left to right flow of approximately 5.5 mm was observed (Table and Figure ).
The condition was interpreted as a mechanical complication of acute inferolateral myocardial infarction with a compromise of the right ventricle not reperfused because it was outside the therapeutic window associated with decompensated HF. He underwent aspirin 100 mg daily (8 hours), clopidogrel 75 mg daily (8 hours), bisoprolol 2.5 mg every 12 hours (8-20 hours), ivabradine 7.5 mg every 12 hours (8-20 hours), enalapril 5 mg every 12 hours (8-20 hours), eplerenone 50 mg per day (8 hours), furosemide 20 mg per day (8 hours), atorvastatin 80 mg per day (20 hours) with good clinical response.
Once his admission condition had stabilized, post-infarction risk stratification was continued by: (i) Cinecoronariography: the left main coronary artery did not present lesions, while angiographically significant stenotic lesions were evidenced (>60%) in the circumflex, anterior descending, and right coronary artery. (ii) Cardiac magnetic resonance imaging (MRI): severely increased ventricular volumes and severely depressed LVEF (28%). At the septoapical level, a 3.5 mm muscular interventricular communication was visualized. Absence of myocardial viability.
Due to the high risk of the patient due to severe ventricular dysfunction, interventricular defect, and HF, it was decided to implant a cardioverter-defibrillator as primary prevention of sudden death and to start the pre-cardiac transplant evaluation and subsequent inclusion on the waiting list on an elective basis. At the time of his discharge, outpatient CPR was indicated.
On January 31, 2020, the patient entered the CPR program. The sessions lasted 60 minutes, where the first 30 minutes were for aerobic training and the remaining 30 minutes for exercises for muscle strength, balance, coordination, and flexibility. ECG telemetric control and pulse oximetry were used to monitor the patient during the first sessions. The patient had a functional class III on the New York Heart Association (NYHA) scale at admission to the program. The first five weeks were for adaptation to training, where the intensity was lower than 4 (0-10) on the Borg scale.
The first cardiopulmonary exercise test (CPET) was performed on a treadmill on March 6, 2020. The protocol used was modified Bruce, where the intensity was increasing every three minutes. The reason for stopping the test was due to exhaustion and the request of the patient in stage 4 of Bruce protocol. At that time, the patient reached a VO2peak of 23.9 mL/kg/min, finding his anaerobic threshold at 100 beats per minute (bpm) and 70% of the VO2peak reached, and a maximum heart rate toward the end of the test of 124 bpm. Concerning the theoretical maximum heart rate (TMHR), it reached 70%, although the patient was on beta-blocker medication. The hemodynamic response of the patient during the test was normal, without presenting chest pain. The respiratory exchange ratio (RER) was 1.09 (Table ).
With these results, starting at week 5, the treadmill aerobic training was planned at an intensity of 80% with a variable continuous training method, where progressively, and depending on the patient's responses during the sessions, we modified the training protocol to perform four minutes at 80% interspersed by two minutes of recovery at 40%. Concerning the strength exercises, 4 or 5 exercises were performed per session, with an intensity measured by the Borg scale that should not be higher than level 5 when reaching the last repetitions of each series. As in aerobic training, depending on the patient's responses and adaptations, the number of series, number of repetitions, and complexity of the exercises progressed with the running of the sessions. The training protocol was carried out based on the recommendations of the American Association of Cardiovascular and Pulmonary Rehabilitation, the American Heart Association, and the American College of Cardiology guidelines [].
After 15 months within the CPR program and 122 sessions carried out, with a frequency of two-weekly sessions, a new follow-up CPET with the same protocol was carried out on May 14, 2021. It is essential to clarify that the patient was with the same medication as the baseline, although, at that time, he had NYHA functional class 0 and gained 3 kg. The test was stopped in stage 4 at the request of the patient. At the end of the test, the patient reached a VO2peak of 29.1 mL/kg/min, finding his anaerobic threshold at 125 bpm and 86% of VO2peak and a maximum heart rate of 136 bpm (82% of his TMHR). The RER was 1.09.
A second color Doppler echocardiogram was performed in May 2021, finding: left ventricular systolic and diastolic diameter of 54/41 mm, respectively, LVEF with moderate deterioration of 40%, abnormal segmental motility with apical, inferior and inferoseptal akinesia. Systolic displacement of the plane of the tricuspid annulus of 22 mm. Pulmonary artery systolic pressure of 40 mmHg. Interventricular communication of approximately 5.2 mm.
Due to the clinical improvements of the patient, the VO2peak value was reached during the second CPET and the absence of hospitalizations was associated with HF in this period, his cardiologist decided to exclude him from the national waiting list for a heart transplant and to continue within the CPR program, to maintain and/or improve his current physical condition.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.66, 'm']}",62.31505,59.1993,65.4308,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.66 m, which is 1.66 m * 39.3701 in/m = 65.35437 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.35437 (in inches) - 60) = 62.31505 kg.
Hence, the patient's IBW is 62.31505 kg."
3613,10,Ideal Body Weight,physical,decimal,pmc-8190499-1,Extracted,"Informed consent was obtained from the patient included in the study.
A 43-year-old female patient with pain in both thighs visited our clinic. She suffered from radiating pain in both legs in the area from the hip joint to the knee joint. She had been undergoing neuropsychiatric treatment for schizophrenia with persecutory delusions and auditory hallucinations. She had been taking medication to treat schizophrenia for 7 years, including ziprasidone, clonazepam, propranolol, and lorazepam. Her drug compliance was good, and she had been in a stable mood. She had no surgical history. She had a history of inadequate exercise and social alcohol use but did not smoke. She had never taken anti-resorptive drugs, had no history of steroids, and had no family history of fractures. She was obese with a height of 159 cm, weight 65 kg, and body mass index (BMI) of 25.71 kg/m2, but had no metabolic diseases and there was no evidence of cardiovascular disease. She suffered amenorrhea but not galactorrhea or breast tenderness.
The first X-ray taken after pain onset showed a slightly increased haziness compared to an X-ray taken three years prior, but there was no evidence of fracture and the patient was able to walk (). Thus, we recommended conservative treatment. One month later, she complained of further aggravated pain, so X-ray () and computed tomography (CT) scans were performed at that time. Both X-ray and CT scans showed a fracture in the right proximal femur, including a suspicious focal benign bone lesion in the subtrochanteric area. BMD and magnetic resonance imaging (MRI) were required as the patient was young, and the fracture lines were atypical. A sequence of MRI T2-weighted images showed a right proximal femur fracture with perilesional soft tissue injury, suspicious focal bone lesions in the bilateral subtrochanteric areas, and an incomplete left proximal femur fracture in the same subtrochanteric area (). BMD measurement showed osteoporosis, a femoral neck T-score of −2.6 with a Z-score of −1.6.
The patient had experienced no trauma that would explain the bilateral femur fractures at such a young age; therefore, bone scans were examined to identify other possible causes of fracture. A triple-phase bone scan using 25 mci of 99 mTc-DPD was done which indicated increased vascularity and bony uptake found only in the region of both femurs. A laboratory test was also conducted based on the patient's history having amenorrhea.
The test confirmed hyperprolactinemia. In women, the normal basal level of prolactin is 20 ng/mL whereas the patient's level was 246 ng/mL. We also checked the levels of other hormones, and results were as follows: basal LH, 6.30 mIU/mL; basal thyroid-stimulating hormone, 4.98 µlU/mL; basal FSH, 8.14 mIU/mL; basal cortisol, 6.75 µg/dL; basal adrenocorticotropic hormone, 22.10 pg/mL; estradiol, 43.109 pg/mL; testosterone, <0.137 ng/mL; and osteocalcin, 8.26 ng/mL. Other laboratory measurements and biomechanical tests were within the normal range.
Prolactin secretion in the pituitary is normally suppressed by dopamine. Drugs that block the effects of dopamine in the pituitary or deplete dopamine stores in the brain may cause the pituitary to secrete prolactin. The patient had been taking medication to treat schizophrenia for an extended period, thus, we concluded that hyperprolactinemia was likely caused by antipsychotic medications. Thereafter, the patient was prescribed aripiprazole, paliperidone, clonazepam, and alprazolam. Ziprasidone, etizolam, and lorazepam were discontinued under the advice of a psychiatrist.
An MRI of the pituitary is indicated for patients with hyperprolactinemia where the etiology is not clearly due to medication. We believed that there was another cause of hyperprolactinemia such as a pituitary prolactinoma. Thus, we checked the sella on MRI, which showed no evidence of a definite focal lesion in the pituitary gland ().
The patient was treated by close reduction and intramedullary nailing in the right femur and conservative treatment with teriparatide for the insufficiency fracture of the left femur (). The histopathological findings at the fracture site revealed some atypical hyaline cartilage, irregular woven bones, and fibrous tissue with granulation tissue formation (). After one month, the patient returned to her normal activities with a full range of motion in the hips. No perioperative complications occurred.
Seven months later, her basal prolactin level had decreased to 137 ng/mL and her estradiol levels increased to 95.00 pg/mL. Additionally, we confirmed bone union of the right femur fracture on X-ray, and an MRI was performed to evaluate the insufficiency fracture of the left femur. An MRI T2-weighted sequence of the pelvic area showed the incomplete fracture of the left proximal femur with healing of the perilesional soft tissue injury and disappearance of the signal change in the bone marrow and lesser trochanter of the proximal femur ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [159.0, 'cm']}",51.47646,48.90264,54.05028,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 159.0 cm, which is 159.0 cm * 0.393701 in/cm = 62.59846 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.59846 (in inches) - 60) = 51.47646 kg.
Hence, the patient's IBW is 51.47646 kg."
3614,10,Ideal Body Weight,physical,decimal,pmc-2892692-1,Extracted,"A 76-year-old man was scheduled for a three-vessel coronary artery grafting (CAG) using CPB.
His medical history included hypertension, a minor inferior myocardial infarction, amaurosis fugax, surgical resection of a vocal cord carcinoma, and an eyelid correction.
Physical examination showed a 70 kg, 1.69 m tall patient with a blood pressure of 170/70 mmHg and a pulse of 52. A bruit was heard over the heart, both carotid arteries and femoral arteries consistent with an aortic valve sclerosis. Cardiac ultrasound showed a hypokinetic inferior left ventricular wall, a good left and right ventricular function and an aortic valve sclerosis with minor aortic valve insufficiency. Coronary angiogram showed occlusion of the RCA, 90% occlusion of the LAD and 70% occlusion of the RCX. Patient took acetylsalicylic acid, chlortalidone, amlodipine, atorvastatin, metoprolol, isosorbide mononitrate, and isosorbide dinitrate. The patient was scheduled for a coronary bypass and premedicated with paracetamol 1000 mg and midazolam 7.5 mg, orally. Once in the operating theatre the patient was prepared for the operation with an 14 G IV infusion and a 20 G arterial cannula in the left radial artery as well as standard monitoring with a 5 lead ECG, pulsoximetry, and a noninvasive blood pressure band on the right arm. A BIS Quatro Sensor (XP) was placed and the monitor (Aspect Medical Systems, Inc. model A-2000 BIS Monitor) started. During this period the patient was alert and communicative. Without provocation, the patient suddenly complained of dizziness, stopped breathing, became unresponsive, and his eyes deviated upwards en laterally. The BIS monitor then gave its first reading of 60.
We initially ventilated the patient by mask and gave naloxone to rule out an accidental sufentanil bolus. Subsequently the patient was intubated without medication. We requested an emergency neurological consultation. During this period the blood pressure and pulse remained stable at around 170/85 with a pulse of 55.
Neurological examination showed a Glasgow Coma Score (GCS) of E-1, M-1, and V-T: eyes closed, no motor response to painful stimuli, and no sounds. He had pinpoint pupils and pupillary reactions showed minimal constriction to light. Corneal reflexes were present while oculocephalic reflexes were absent. Both eyes were deviated upwards and to the left. Tendon reflexes were increased on the left side, with bilateral extensor plantar responses.
We performed a CT-scan, which showed central and cortical atrophy with subthalamic and periventricular hypodensities consistent with older vascular damage. The CT-angiogram showed generalized atherosclerotic changes in all brachiocephalic vessels, especially in the common and internal carotid arteries and a slight stenosis of the origin of the left vertebral artery.
After the CT-scan, we restarted the BIS monitoring which still showed the BIS value at about 50 to 60. Eleven minutes after resuming BIS monitoring the patient opened his eyes, started breathing and responding to voice commands, and BIS values increased to around 80–85. The patient was extubated and wanted to know the result of the operation. On neurological examination, the patient was alert and responded adequately. There was a bilateral downbeat nystagmus in downgaze. Tendon reflexes remained increased on the left side, while both plantar responses were flexor. Based on the neurological examination, the transient nature of the neurological deficit, and the CT-scan, we concluded that the patient had suffered a transient ischemic attack of the brainstem.
During the whole event which lasted 102 minutes the patient had remained hemodynamically stable. He was transferred to the neurological intensive care where the rest of his stay remained unremarkable, and he recovered without any neurological deficit.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.69, 'm']}",65.03158,61.78,68.28316,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.69 m, which is 1.69 m * 39.3701 in/m = 66.53547 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.53547 (in inches) - 60) = 65.03158 kg.
Hence, the patient's IBW is 65.03158 kg."
3615,10,Ideal Body Weight,physical,decimal,pmc-3909042-1,Extracted,"29-years-old woman born to consanguineous parents (first degree cousins). She was born at term (39 weeks) but her weight and height at birth data are not available. Patient 1 was diagnosed with lipoatrophic diabetes, severe mixed dyslipidemia (total cholesterol = 960 mg/dl, triglycerides = 4,355 mg/dl) and fatty liver at 13-years-old. She has been treated with restriction of dietary fat and carbohydrates intake and various combinations of insulin sensitizers (rosiglitazone or metformin), DPP IV inhibitors (sitagliptin) and insulin, but glycemic and lipid control has been poor (). Before this current evaluation, no specific pharmacologic treatment was used for controlling her plasma lipids. She refers incidental appearance of yellowish maculo-papular cutaneous lesions mainly in her back and face after insulin supplementation. Because these complications she abandoned insulin therapy 4 years ago. The patient also complains of symmetric polyarthralgia of hands and knees and morning stiffness with no local inflammatory signs. Her menstrual cycles are irregular, with very long periods (years) of amenorrhea. Physical examination revealed normal height (1.6 m), low body weight (body mass index, BMI, 18.3 kg/m2), generalized and severe reduction of subcutaneous fat, acromegaloid features (prognathism and enlarged hands and feet), acanthosis nigricans on the neck and groins, sparse pink-yellowish small maculopapular skin lesions in the back, suggestive of eruptive xhantomas, and a small umbilical hernia. A firm nodular mass (3 cm diameter) on each calcaneus tendon was found. No visceromegaly was detected but a moderate intensity holosytolic murmur was present at mitral focus. She had advanced bilateral proliferative retinopathy, panphotocoagulation of both eyes and amaurosis of the left eye because of vitreous hemorrhage. No signs of arthritis were found. Biochemical analysis showed poorly controlled diabetes and severe mixed dyslipidemia (). Measured creatinine clearance and proteinuria were 89.7 ml/min/1.73 m2 and 2.79 g/24 hours, respectively (). Endocrine evaluation showed normal-low fasting insulin, normal thyroid function, reduced SHBG and normal testosterone (). Plasma leptin was severely reduced, adiponectin was undetectable but soluble leptin receptor was ∼2-fold increased relative to a group of control women (). Antibodies against plasma cyclic citrullinated peptides were negative and no signs of arthritis were detected by magnetic resonance imaging (MRI) analysis of her hands. MRI also revealed no abnormalities of intra-abdominal organs but incidental gallstones were observed data (not shown). A liver biopsy obtained during an elective cholecystectomy revealed no hepatic steatosis or any other histological abnormality. Body composition assessed by DEXA showed 12.3% of body fat and resting energy expenditure (REE) estimated by indirect calorimetry was 32.75 Kcal/Kg lean mass/day ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.6, 'm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.6 m, which is 1.6 m * 39.3701 in/m = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3616,10,Ideal Body Weight,physical,decimal,pmc-7660088-1,Extracted,"A 68-year-old deaf male patient (60 kg, 175 cm, BMI 19.6 kg/m2) with clinically manifest osteoporosis suffered a femoral neck fracture following a low-energy fall on his right hip. The initial treatment with uncemented THA was performed elsewhere (Versafit CC Trio cup with highly-crosslinked polyethylene liner, 32 mm CoCr head, Quadra-H stem; Medacta, Castel San Pietro, Switzerland), through a direct anterior approach on a traction hemi-table (). The stem was undersized by two sizes compared to preoperative templating and implanted in varus position in relation to the axis of the femoral diaphysis (A). The patient recovered from the operation without complications and was able to return to his partially institutionalised everyday life. A postoperative leg-length discrepancy, however, hampered ambulation, with recurrent tripping.
Approximately 14 months postoperatively, following another low-energy fall on his right hip, the patient suffered a multifragmentary periprosthetic fracture of the proximal femur with loosening of the stem (B). Corresponding to a periprosthetic fracture unified classification system (UCS) type B2 [], stem revision was indicated. Surgery was performed through a transfemoral approach to the hip, formally completing exposure through the fracture fragments [,]. This approach ensures good distal purchase of the uncemented, tapered, fluted, modular revision stem (Revitan straight, Zimmer Biomet, Winterthur, Switzerland) used []. The stem in situ was loose and could be retrieved without any instrumentation. Delamination of the HA coating from the stem had already been suspected on the preoperative conventional radiographies (C). Fragments from the bone at the implant interface could be chiselled off easily from the endostal surface of the medial cortex of the femur for further analysis before reaming for the new stem. The tissue samples were fixated and sent for further examination in a buffered formaldehyde solution (4%) (Formafix, Hittnau, Switzerland). Good osteointegration of the cup was confirmed, and it was therefore left in place, despite excessive anteversion of 28°, and measured in the plane of the lateral inclination [,]. However, to reduce the risk of dislocation, the liner was exchanged to accommodate a 36 mm head []. Internal fixation of the proximal femur was achieved with cerclage cables (Dall-Miles 2.0 mm; Stryker, Kalamazoo, MI, USA). As the femoral offset could not be reconstructed anatomically with the new stem, a certain degree of leg-lengthening had to be accepted, to avoid instability of the hip.
Microbiological samples and routine histopathological analysis showed no signs of infection. Postoperative recovery was uneventful. Follow-up more than two years postoperatively was uneventful, except that the leg length discrepancy had to be compensated with shoe sole raise on the contralateral side.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3617,10,Ideal Body Weight,physical,decimal,pmc-3872695-2,Extracted,"A 27 year old man became symptomatic following repeated falls on a slippery surface with chronic low backache and neck pain for one year. He also noticed bone pains and the severity progressed over six months to an extent that he had gross limitations of his daily activities, had to be bed bound and developed chronic insomnia. He didn’t have arthralgia, deformity of the joints/bones or systemic symptoms. He weighed 69 kgs for a height of 170 cm (he reported his height was 173 cm at the age of 18 years). He had tenderness at lower thoracic and lumbar spine. He had no deformity. His general and systemic examination was normal.
Investigations revealed a haemoglobin of 14.2 g/dL (14 ± 2.5), total leucocyte count 7,500/cu.mm (4,000-11,000), platelets 1,87,000/cu.mm (1,50,000-4,50,000), erythrocyte sedimentation rate 5mm fall at first hour (0-10), fasting blood glucose 97mg/dL (70-100), blood urea nitrogen 12 mg/dL (7-19), creatinine 0.8mg/dL (0.5-1.6), sodium 140 mEq/L (135-149), potassium 4.1mEq/L (3.5-5.0), bilirubin 0.9mg/dL (<1), aspartate trasaminase 85 U/L (<40), alanine trasaminase 78 U/L (<40), alkaline phosphatase 354 U/L (<250), protein 7.9 g/dL, albumin 4.2 g/dL, calcium 8.6 mg/dL (8.5-10.5), phosphorous 3.8 mg/dL (2.5-4.5), lactate dehydrogenase 811 U/L (230-460) and uric acid 7.2 mg/dL (2-6). CRP was 6mg/L (<6), HLA-B 27 was negative. X-ray of spine showed multiple lytic lesions with collapse of 8th dorsal vertebra and ill-defined radiolucencies in both pubic rami and ischium []. Computed tomography of spine showed extensive involvement of spine, sternum, pelvis, heads of humerus and femur []. MRI spine showed extensive marrow infiltration of spine and pelvic bone and collapse of C3, D1 and D8 vertebrae []. He was evaluated for multiple myeloma with serum electrophoresis which was negative for “M” band, light chain assay was negative and bone marrow aspiration was dry and bone marrow biopsy showed extensive fibrosis (?secondary). Bone scan showed increased uptake in involved areas []. FDG-PET confirmed increased metabolic activity in above area and was suggestive of malignancy with highest SUV of 7.6 in sacrum []. Parathormone (PTH) was 13 pg/mL (10-65), 25(OH) vitamin-D was 65 ng/mL (30-150) and endocrinal evaluations (thyroid, adrenal and pituitary function tests) were normal. Oncological markers including PSA, CEA and CA 19.9 were normal. BMD z-score at spine, hip and forearm were -2.6, -0.8 and 0.5 respectively. With the suspicion of lymphoma, infective etiology, or secondary a CT guided fine needle aspiration was done; but was inconclusive. To obtain tissue diagnosis an open biopsy of left sacral ala and a repeat bone marrow aspiration and biopsy from matched involved area from bone scan and CT scan at iliac spine was performed. Histopathology of bone biopsy was consistent with fibrous dysplasia []. Severity of fibrous dysplasia as interpreted by bone scan[] was 11%. He was started on intravenous zoledronic acid 4 mg quarterly, calcium and vitamin D supplements. Opioid analgesics were required to control his bone pain.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3618,10,Ideal Body Weight,physical,decimal,pmc-6967062-1,Extracted,"A 47-year-old man (body weight 62.1 kg and height 166.8 cm) was reported in our hospital with a past medical history of tongue cancer that was operable. The preoperative spirometry test, electrocardiography, and transthoracic echocardiogram were normal. He is a non-smoker with no history of cerebrovascular disease. In his thirties, he had undergone resection of the mandibular area with plate reconstruction for treatment of tongue cancer; however, the site became infected and the plate was removed 8 months before presentation. The patient returned for reoperation involving a free abdominal muscle flap with vascular anastomosis and partial mandibular resection with tracheostomy. After surgery, the patient was in the ICU for deep sedation and ventilator management for 48 h, until the vascular anastomosis stabilized. Initially, the iASV ventilator mode was selected to change only the percentage minute volume (%MV) automatically. On the postoperative day 3, the patient’s oxygenation worsened, and purulent sputum increased; fiberoptic suctioning of sputum was performed once along with sputum culturing. Although no significant organism was detected with sputum Gram staining, Klebsiella pneumoniae and Pseudomonas otitidis were detected in the sputum culture test. We therefore arrived at a diagnosis of VAP and changed the patient’s antibiotic from ampicillin/sulbactam 1.5 g per 6 h to meropenem 0.5 g per 8 h. At the time of entering the ICU, his PaO2/FiO2 ratio was 462, which indicated a good oxygenation capacity; this decreased to 171.5 at the time of VAP diagnosis. At the same time, the other patient entered the ICU with a severe respiratory emergency. We continued the iASV mode as we judged that the respiratory condition could be improved. PEEP and FiO2 were selected as additional automatic settings in iASV, %MV was automatically set, and the delta P (ΔP) approximating the driving pressure did not exceed 10 cm H2O. (Figs. and ).
Arterial blood gas (PaO2, PaCO2, and pH) was measured every 6 h to confirm that his respiratory condition was within the expected range.
Once the patient’s oxygenation capacity started improving, the INTELLiVENT®-ASV started to show a decline in FiO2, first until it reached 0.3, and then reduced PEEP from 14 to 5 cm H2O based on the lung protective ventilation strategy. Two days after changing the antibiotics to treat VAP, his WBC, CRP, and the sputum secretion from the lungs decreased, indicating resolution of VAP. Therefore, mechanical ventilation was successfully withdrawn. During this time, the ΔP obtained by subtracting PEEP from the inspiratory plateau pressure was kept below 10 cm H2O (Fig. ).
We used dexmedetomidine (0.2γ to 0.5γ) and propofol (1 mg/kg/h to 3 mg/kg/h) for sedation during his admission in ICU. We continued the same sedation dosage after VAP diagnosis, and after stopping ventilator usage, the propofol administration was also stopped. Dexmedetomidine was continued after extubation at night for the purpose of sleeping.
Two days after stopping ventilator usage, the patient’s respiratory condition was stable and he was transferred to the general ward.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [166.8, 'cm']}",63.03946,59.88749,66.19143,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 166.8 cm, which is 166.8 cm * 0.393701 in/cm = 65.66933 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.66933 (in inches) - 60) = 63.03946 kg.
Hence, the patient's IBW is 63.03946 kg."
3619,10,Ideal Body Weight,physical,decimal,pmc-3460156-1,Extracted,"A 42-year-old male (weight 71 kg; height 172 cm) was scheduled to undergo aortic-iliac-femoral bypass surgery for the treatment of arteriosclerosis obliterans (ASO). Other than smoking a pack of cigarettes per day for 20 years, the patient's past medical history revealed no unusual findings. There was no history of allergy, either for the patient himself or his family. There were no abnormalities in the preoperative physical examination, hematologic tests, simple X-ray test and ECG.
Thirty minutes before arriving in the operation room, 3 mg of midazolam and 0.2 mg of glycopyrrolate were administrated intramuscularly as premedication. Pre-anesthetic blood pressure (BP), heart rate (HR) and pulse oximeter oxygen saturation (SpO2) were 105/55 mmHg, 81 beats/min (bpm) and 99%, respectively. Endotracheal intubation was performed in the supine position, 1 minute after the IV administration of 12 ml 1% propofol (Pofol inj, Dongkook Co., Republic of Korea) and 50 mg rocuronium (Esmeron®, NV Organon, Netherlands). A mixture of sevoflurane air 2 L/min and O2 1 L/min was then delivered for maintenance of anesthesia under volume controlled ventilation, at which the peak inspiratory pressure (PIP) was 18 mmHg and the end tidal carbon dioxide concentrations (EtCO2) were between 35 and 40 mmHg. A radial artery catheter was inserted to continuously monitor the arterial BP. During the first 2 hours after the start of surgery, the vital signs were stable, but the urine output was not sufficient. Then, HES 130/0.4 (Voluven®, Fresenius Kabi, Bad Homburg, Germany) was administered through a peripheral i.v. line for volume therapy. About 5 minutes from the time when HES administration was started, erythema was observed in the face and neck, with normal body temperature. Within about 10 minutes of initiation of the HES infusion, and after approximately 200 ml were given, arterial BP suddenly dropped to 70/35 mmHg, and the HR was increased to 115 bpm. SpO2 was reduced to 92% with a high PIP (36 mmHg). Capnography showed an obstructive pattern and EtCO2 decreased abruptly from 35 mmHg to 22 mmHg. Assessment of the endotracheal tube, breathing circuit and anesthetic machine revealed no evidence of mechanical obstruction. On auscultation, mild wheezing was noted in both lung fields. All signs, including erythema, hypotension and bronchospasm, fulfilled the clinical criteria for diagnosing anaphylaxis. Because antibiotics or blood components were not used during the operation, rocuronium was injected before 70 minutes without any problem and the anaphylactic reaction occurred within minutes of HES exposure, HES was suspected as the culprit and its infusion was therefore discontinued. The patient's ventilation was switched to 100% O2 and multiple boluses of phenylephrine (cumulative dose 600 µg IV) and ephedrine (8 mg IV increments) were administered, in conjunction with isotonic crystalloid. Sevoflurane concentration was continuously maintained at 1 MAC during the event. The arterial blood gas analysis showed pH 7.31, PCO2 48 mmHg, PO2 82 mmHg, HCO3- 22.7 mmol/L and BE -3.6 mmol/L. Thus, diphenhydramine 50 mg IV and hydrocortisone 100 mg IV were administered. Fifteen minutes after the onset of hypotension, BP was restored with SpO2 of 97%, while PIP decreased gradually to 22 mmHg. Simultaneously, lung sounds recovered and the capnogram normalized with an EtCO2 of 37 mmHg. Surgery continued without unusual findings and ended 7 hours after the anaphylactic reaction. Facial erythema resolved spontaneously within 4 hours. On completion of surgery, the patient's trachea was extubated uneventfully. After being transported to the ICU, the patient's vital signs were stable and he did not complained of respiratory discomfort. However, he had mild pruritus on the trunk and diphenhydramine was administered for 3 days. He was discharged after 3 weeks of hospitalization.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [172.0, 'cm']}",67.74811,64.3607,71.13552,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 172.0 cm, which is 172.0 cm * 0.393701 in/cm = 67.71657 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.71657 (in inches) - 60) = 67.74811 kg.
Hence, the patient's IBW is 67.74811 kg."
3620,10,Ideal Body Weight,physical,decimal,pmc-8016778-1,Extracted,"A 68-year-old male with a height and weight of 174.5 cm and 43.6 kg, respectively, and a primary complaint of anemia was admitted to our facility. Abdominal examination revealed that the abdominal region was leveled and soft without any pressure or pain, and no palpable masses or superficial lymph nodes were observed. Hematological tests showed a hemoglobin (Hb) level of 11.8 g/dL, indicating anemia, and no abnormalities were indicated by CEA, CA19-9, and AFP tumor markers were observed. Esophagogastroduodenoscopy revealed a submucosal tumor-like mass with delle and bridging fold in the greater curvature of the lower stomach, and the tumor was suspected as the cause of anemia (Fig. ). Ultrasound endoscopy revealed a submucosal tumor (SMT) (with the fourth layer as the main locus) and a tumor (with the third layer as the main locus), with some areas of indistinct borders (Fig. b). Tissue biopsy of this tumor indicated group 5 tubular adenocarcinoma, and thoracoabdominal computed tomography (CT) showed a tumor with a mottled contrast stain in the stomach body and no regional lymph nodes or distant metastases (Fig. ). Based on the above findings, the patient was diagnosed with collision tumor of gastric cancer and SMT (GIST was highly suspected). Gastrectomy was performed via laparotomy, and the surgical findings were a diagnosis of H0P0CY0 according to the 3rd English edition of the latest edition of the Japanese classification of gastric carcinoma issued by the Japan Gastric Cancer Society []. Distal gastrectomy was performed with D2 lymph node dissection according to the Japanese Gastric Cancer Treatment Guidelines [].
The tumor was located in the greater curvature of the antrum of the stomach and measured 50 × 45 mm in size (Fig. a). On the cut surface, a nodular tumor was mainly observed in the submucosal layer, and the mucosal surface was ulcerated (Fig. b). A large part of the tumor was observed to be mixed and some of the cancer parts and GIST alone sites were observed. (Fig. c). The nodular tumor was characterized by the intermingled proliferation of carcinoma cells and spindle cells (Fig. d). The spindle cells formed a nodular tumor in the submucosal layer and the subserosal layer. Carcinoma cells invaded the nodular tumor of the spindle cells. Pathological examination revealed Ki67 positive cells comprised 2% of the GIST. The average mitotic count was ≤ 5 mitotic figures per 50 high power fields. GIST was classified as very low risk according to the guidelines for GIST risk stratification []. Tubular adenocarcinoma had reached the subserosa, and no lymph node metastases were observed. The pathological findings were a diagnosis of pT3N0M0 pStageIIA, according to the 3rd English edition of the latest edition of the Japanese classification of gastric carcinoma issued by the Japan Gastric Cancer Society []. Immunohistochemical staining demonstrated a positive reaction for cytokeratin (AE1/AE3) in the carcinoma cells (Fig. a). Further, the nuclei of adenocarcinoma cells were positive for TP53 (Fig. b). Although the spindle cells were negative for cytokeratin (AE1/AE3) and TP53, these cells were positive for c-kit (Fig. c), weakly positive for DOG-1, and negative for desmin and S-100. As a result, the tumor was diagnosed as a collision tumor of GIST and adenocarcinoma. Lymph node metastasis of GIST or adenocarcinoma was not observed, and the resected margins were negative for neoplastic cells. Histologically, the intratumoral GIST sections contained different KIT exon 17 mutations, and KIT exon 17 mutation corresponding to amino acid substitution Asp820Lys was observed. On the other hand, the adenocarcinoma section detected no KIT mutation.
No complications were observed postoperatively, and the patient was discharged from the hospital on postoperative day 14. No adjuvant therapy was required for GIST, as per the international guidelines for GIST risk stratification []. The patient was clinically and radiographically disease-free at 2.5 years after surgery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [174.5, 'cm']}",70.01189,66.5113,73.51248,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 174.5 cm, which is 174.5 cm * 0.393701 in/cm = 68.70082 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.70082 (in inches) - 60) = 70.01189 kg.
Hence, the patient's IBW is 70.01189 kg."
3621,10,Ideal Body Weight,physical,decimal,pmc-4608656-1,Extracted,"A 72-year-old Japanese male PD patient had experienced a slowly progressive gait disturbance and akinesia since 56 years of age. He was diagnosed with PD at 58 years. He had no history of any neurological disorders. His family history is unremarkable. During the next 15 years, he had been admitted to our hospital several times for drug control, and LD pharmacokinetics was checked twice when he was 68 years old. At the age of 71 years 10 months, although his parkinsonian features had not changed, he suddenly developed jaundice and he was diagnosed with cholangiocarcinoma. At this time, his Unified Parkinson's Disease Rating Scale (UPDRS) motor score (part III) was 28/108 [], and his daily antiparkinsonian treatment was 500 mg/50 mg of LD/carbidopa, 0.5 mg of cabergoline, and 2.5 mg of selegiline.
In the next month (at the age of 71 years 11 months), pancreaticoduodenectomy was performed. In this operation, subtotal removal of the stomach (3 cm from the pylorus side), total removal of the duodenum, and subtotal removal of the jejunum (20 cm from the ligament of Treitz on the distal side) was performed (fig. ). Reconstruction was made by end-to-end anastomosis of the pancreas to the bile duct to the jejunum (fig. ). There were no surgical complications in his post-operative course, and he recovered without any surgical problems. After 5 days, he could take the same oral antiparkinsonian agents as before the operation (500 mg/50 mg of LD/carbidopa, 0.5 mg of cabergoline, and 2.5 mg of selegiline); however, his Parkinsonian features were gradually remarkable within 2 weeks after the operation. The patient did not receive any agents as chemotherapy. He was then transferred to our ward for parkinsonian drug treatment.
At this time, his height, body weight, and body mass index were 158.0 cm, 61.0 kg, and 24.4, respectively. His neurological examination revealed marked masked face, dysarthria, and dysphagia. Mild tremor at rest in the left upper extremity, severe rigidity in the bilateral upper and lower extremity, and poor finger taps on the dominant left side were also observed. Gait was unable without assistance. His parkinsonian features were obviously getting worse, and UPDRS motor score (part III) was 68/108. Thus, we checked whether this worsening of parkinsonian features was due to a change in LD absorption in the gastrointestinal tract by checking his LD pharmacokinetics.
Written informed consent was obtained from this patient, and the approval of the Institutional Review Board was obtained for the examination of LD pharmacokinetics. To assess LD pharmacokinetics, he took a tablet containing 100 mg of LD and 10 mg of carbidopa at 9:00 a.m. following an overnight fast and a medication-free period of at least 18 h. Blood specimens were collected through an intravenous catheter at 0, 15, 30, 60, 120, and 180 min after LD administration, and plasma LD concentrations were measured by high-performance liquid chromatography with electrochemical detection. The procedure of measurement of blood LD concentration has been described in our previous report []. Peak drug concentration (Cmax), the time-to-peak drug concentration (Tmax), elimination halftime (T1/2), and area under the curve (AUC) were determined. Cmax and Tmax were observed values, T1/2 was determined by linear regression analysis, and AUC was estimated from the area under the time concentration line up to 3 h.
In his LD pharmacokinetics at the ages of 68 years 11 months (and 68 years 1 month), body weight was 64.2 (and 64.8) kg, AUC was 1,782.5 (and 1,825.0) mg·h/ml, Cmax was 1,500 (and 1,500) mg/ml, Tmax was 30 (and 30) min, and T1/2 was 48 (and 47) min. In the postoperative assessment (at the age of 72 years 4 months), AUC was 1,148.8 mg·h/ml, Cmax was 450 mg/ml, Tmax was 60 min, and T1/2 was >120 min (fig. ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [158.0, 'cm']}",55.07095,52.3174,57.8245,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.20476 (in inches) - 60) = 55.07095 kg.
Hence, the patient's IBW is 55.07095 kg."
3622,10,Ideal Body Weight,physical,decimal,pmc-4532024-1,Extracted,"A 40-year-old woman was admitted to the Chonnam University Hospital, with a three months history of severe generalized weakness and fatigue.
The first episode occurred three years ago and spontaneously remitted from it following bed rest, she denied ingestion of licorice, diuretics, laxative or any other medication, and she had no significant nausea, vomiting or diarrhea.
The patient appeared relatively well and had a height of 154 cm and a weight of 52 kg. The pulse rate was 98/min, the blood pressure 100/70 mmHg, and the respiration rate 18/min. The remainder of her physical examination was within normal limits.
Laboratory findings included persistent hypokalemic alkalosis with 2.4 mEq/L for serum potassium, 32.7 mEq/L for serum bicarbonate, 86.1 mmHg for PaO2, 48 mmHg for PaCO2 and 32 mmol/L for total CO2 content. The pH of plasma was 7.44 and that of urine 7.0. Electrocardiography revealed PR prolongation and T wave - flattening. Serum sodium averaged 139 mEq/L, chloride 85 mEq/L, total calcium 5.1 mEq/L, ionized calcium 2.0 mEq/L, inorganic phosphorus 4.7 mg/dl, magnesium 1.6 mEq/L, uric acid 13.4 mg/dl and serum osmolality 289 mosl/kg. The blood urea nitrogen was 44.0 mg/dl, serum creatinine 1.7 mg/dl and creatinine clearance 35 ml/min. There were no proteinuria, hematuria and abnormality of the urinary sediment. Pertinent studies of the blood and serum revealed a normal hemoglobin level, hematocrit value, white blood cell count, total protein, albumin, alkaline phosphatase and transaminase levels. Twenty four-hour urinary excretion of sodium was 183 mEq, potassium 67 mEq, chloride 247 mEq, calcium 120 mg, protein 150 mg, glucose 30 mg and urine amounts 2,300 cc. The urinary specific gravity was 1.010 and osmolality 310 mosm/kg. The plasma renin activity was 48.2 ng/ml/hr and aldosterone level 34.4 ng/dl. FENa was 2.6%, FECl, 5.7%, FEK 55%, and FEUric acid 8.2%. Thiazide and furosemide were not detected in her urine by high-performance liquid chromatography at the Department of Pharmacology, Chonnam University Medical School, Kwangju, Korea.
The renal biopsy was performed without difficulty. The biopsy specimen contained up to 8 glomeruli per section. Some glomeruli revealed focal and segmental glomerulosclerotic changes. Juxtaglomerular hyperplasia of varying degrees and multiple vacuolization of proximal tubule due to chronic hypokalemia were noted (, ). The tubules, interstitium and blood vessels were entirely normal with no scarring or atrophy. The constellation of hypokalemia, relative hypotension, increased renin activity, increased aldosterone level and juxtaglomerular hyperplasia substantiated the diagnosis of Bartter’s syndrome.
Following the renal biopsy, the patient had been treated with potassium chloride, 40 mEq twice a day, spironolactone, 50 mg three times a day, propranolol, 20 mg three times a day, enalapril, 2.5 mg a day and indomethacin, 25 mg three times a day. The administration of medications led to an increase in serum potassium to 3.5 to 4.5 mEg/L.
In association with this improvement in the serum potassium concentration, the patient’s muscle strength was rapidly recovered and the patient did well for the following two months ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [154.0, 'cm']}",46.94889,44.60145,49.29633,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 154.0 cm, which is 154.0 cm * 0.393701 in/cm = 60.62995 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.62995 (in inches) - 60) = 46.94889 kg.
Hence, the patient's IBW is 46.94889 kg."
3623,10,Ideal Body Weight,physical,decimal,usmle-563,Extracted,"A 22-year-old woman comes to the emergency department because of frontal throbbing headaches for 3 weeks. Yesterday, the patient had blurry vision in both eyes and a brief episode of double vision. She has been taking ibuprofen with only mild improvement of her symptoms. She has polycystic ovarian syndrome, type 2 diabetes mellitus, and facial acne. She has not had any trauma, weakness, or changes in sensation. Her current medications include metformin and vitamin A. She is 158 cm (5 ft 2 in) tall and weighs 89 kg (196 lbs); BMI is 36 kg/m2. Vital signs are within normal limits. Examination shows decreased peripheral vision. Fundoscopic examination of both eyes is shown. MRI of the brain shows an empty sella.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3624,10,Ideal Body Weight,physical,decimal,pmc-7852635-1,Extracted,"A 17-year-old female who was hospitalized in the Department of Psychiatry to treat a mental disorder suffered from rectal prolapse. She was referred to our surgical department because recurring rectal prolapse could worsen her psychiatric disorder.
The patient’s symptoms started approximately 3 mo before admission. She had repeated rectal prolapse due to chronic, frequent, and severe diarrhea from spice abuse, including taking 15 g of chili pepper at each meal, and a laxative addiction.
The patient was diagnosed with a mental disorder 1 year before admission. She was hospitalized in the Department of Psychiatry for the treatment of water intoxication 1 mo before being referred to our department.
Other history could cause rectal prolapse were excluded. Her family history has nothing notable.
The patient had anorexia, with a strong drive for thinness. Her height was 156.8 cm, her body weight was 40.0 kg, and her body mass index was 16.3 kg/m2. On physical examination, rectal prolapse measuring 10 cm from the anal verge was visible and easily reproducible. The anal sphincter tonus was normal and there was no evidence of a tumor on digital rectal examination or anoscopy, except for Goligher's grade I internal hemorrhoids. The mean maximum resting pressure and the voluntary anal constriction pressure were within normal limits on anorectal manometry.
No abnormalities were found in the patient's laboratory examinations.
Total colonoscopy revealed redness and erosion in the rectal mucosa related to rectal prolapse (Figure ). There was no evidence of other colonic pathologies. Abdominal computed tomography scans demonstrated that the peritoneal reflection lay below the lower sacrum, accompanied by a thickened rectal wall (Figure ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [156.8, 'cm']}",49.48434,47.01012,51.95856,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 156.8 cm, which is 156.8 cm * 0.393701 in/cm = 61.73232 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.73232 (in inches) - 60) = 49.48434 kg.
Hence, the patient's IBW is 49.48434 kg."
3625,10,Ideal Body Weight,physical,decimal,pmc-8077890-1,Extracted,"A 70-year-old man with a height of 161.0 cm, weight of 54.6 kg, and body mass index of 21.0 kg/m2 complained of difficulty in swallowing a meal and was referred from another hospital. He was diagnosed as having thoracic esophageal cancer (T3N1M0, Stage IIIA). We performed thoracoscopic esophagectomy in the prone position, two-fields lymphnode dissection, subtotal gastric tube reconstruction via the posterior mediastinal route, and jejunostomy after 2 courses of chemotherapy (bi-weekly DCF: docetaxel 35 mg/m2, cisplatin 40 mg/m2, fluorouracil 400 mg/m2) []. The thoracoscopic operation time was 299 min, and blood loss was 20 ml. During lymph node dissection around the right RLN, an unusual blood vessel was found running along the right subclavian artery (RSA). We assumed that the blood vessel was the RVA, which was very long at 7.02 cm (Fig. ). Because this anatomical abnormality was clarified, we could recognize that the right RLN coursed around the RVA and the RSA and thus was running in a larger arch than usual. As a result, lymph node dissection could be performed safely without damaging the RVA and the right RLN, and no metastasis was found in the excised station number of 106recR.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [161.0, 'cm']}",57.78748,54.89811,60.67685,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 161.0 cm, which is 161.0 cm * 0.393701 in/cm = 63.38586 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (63.38586 (in inches) - 60) = 57.78748 kg.
Hence, the patient's IBW is 57.78748 kg."
3626,10,Ideal Body Weight,physical,decimal,pmc-5100246-1,Extracted,"An 18-year-old woman first presented for medical attention due to primary amenorrhoea. She was then a tall, thin woman with female external genitalia and no vulval or inguinal masses, however breast development and secondary sexual hair were conspicuously absent. The karyotype was 46,XY leading to a presumptive diagnosis of CAIS. Because of the suspicion of cryptorchid, dysgenetic gonads with high malignant potential, the patient underwent open laparotomy revealing streak gonads which were removed, and an infantile uterus which was left in situ. Histopathology demonstrated bilateral gonadoblastoma, and dysgerminoma in the right gonad. She received abdominopelvic radiotherapy with no tumour recurrence. After gonadectomy, she was commenced on the oral contraceptive pill and later changed to lower dose hormone replacement therapy.
At age 46 years, the patient migrated to Australia and sought review at our institution. Her active medical issues included type 2 diabetes mellitus, dyslipidemia, obstructive defecation syndrome and colonic polyps. She had a tall, slim build with a body-mass index of 20.4 kg/m2 and her proportions were eunuchoid with height 181 cm, arm span 182 cm and lower segment length 102 cm. There was minimal pubic hair and no axillary hair, but breast development was now normal. She had female external genitalia and a retroverted uterus.
Results of hormonal studies and haematocrit were most consistent with hypogonadal female ranges (Table ). Dual-energy x-ray absorptiometry demonstrated mild osteopenia with T-scores of -1.1 at the hip and spine. Because of menorrhagia, she underwent transvaginal ultrasound which demonstrated a fibroid within an hypoplastic uterus (Fig. ). No renal tract anomalies were seen. After failed hysteroscopy and multiple alterations in hormone replacement, she was treated with transdermal oestradiol 25 mcg/hr and oral norethisterone 5 mg daily with cessation of menses at age 48 years.
It was now, in the patient’s fifth decade of life, that her original diagnosis of CAIS was questioned. Whilst the external female phenotype, XY karyotype and absence of secondary sexual hair were consistent with CAIS, the presence of streak gonads and functioning Müllerian structures along with the absence of spontaneous breast development favoured a diagnosis of CGD. Though Müllerian remnants have been observed in women with CAIS, there are no reports of the functioning uterine structures as found in our patient. We performed various genetic studies locally, beginning with a digital karyotype confirming the original 46,XY result. FISH demonstrated an intact SRY gene, excluding SRY deletion as the cause of the patient’s atypical DSD. Array comparative genomic hybridisation showed no copy number variation at an average effective resolution of 0.2 MB.
The major genetic possibilities at this stage were sequence variants and copy number variations in known CGD genes such as DHH, SRY, NR5A1 and NR0B1 []. In keeping with the patient’s original diagnosis overseas, synergistic mutations in AR and AMH or AMHR2 were considered possible, as this would theoretically result in an unvirilised XY female phenotype with intact Müllerian structures. Whole exome sequencing was contemplated as the next step in our genetic evaluation, however this was deemed less suitable due to the non-contiguous capture and amplification steps which may hinder identification of copy number variations which are a significant cause of CGD []. Single nucleotide polymorphism (SNP) array was an alternative as its utility has been established in DSD [], however the genetic resolution is low and does not allow for diagnosis of point mutations []. We instead opted for whole genome sequencing (WGS) in order to examine all susceptibility genes simultaneously and at high resolution. WGS was also favoured because of its capacity to detect copy number variations as the entire genome is contiguously analysed, allowing the detection of DNA breakpoints in cases of genetic deletions and duplications [].
WGS was performed using the Illumina HiSeq X Ten Sequencing system at the Garvan Institute of Medical Research (). Bioinformatic analysis was performed at the SA Pathology Molecular Genetics Laboratory with variant classification by the American College of Medical Genetics 5-tier system: benign, likely benign, uncertain significance, likely pathogenic, or pathogenic [].
Variants found on WGS were filtered based on mutational consequence (snpEff impact high or moderate) and phenotypic correlation. WGS revealed variants in eight genes associated with disorders of sexual development, namely: AKR1C4, DMRT1, MAP2K1, MAP3K1, NR0B1, NR5A1, POR and SRY. All but the NR0B1 and SRY variants were excluded based on variant population frequencies >1 % in the 1000 Genomes (1 K), Exome Sequencing Project (ESP) and Exome Aggregation Consortium (ExAC) databases. The NR0B1 variant was then excluded because of a population frequency >1 % amongst individuals in the ExAC database of the same ethnicity as the patient.
The remaining hemizygous missense variant in the SRY gene (NM_003140.2, p.Arg130Pro, c.389G > C) was confirmed to be present on Sanger sequencing of SRY. This variant has not been previously reported in the 1K, ESP, ExAC, or dbSNP databases, although there is an enrichment of pathogenic missense mutations at other locations of SRY reported in the ClinVar database (Fig. ). It is located at the 3’ end of the HMG box domain in a region required for nuclear localisation (UniProt Q05066) and it is predicted to be pathogenic by PolyPhen2 and MutationTaster, but not SIFT. It is moderately conserved (phyloP 3.43, CADD 10.44) and has a moderate Grantham difference of 103. Protein-DNA complex modelling demonstrated that substitution of arginine (Arg) to proline (Pro) causes steric hindrances to the native SRY protein structure which may affect DNA binding (Fig. and ).
The evidence collectively demonstrated this novel SRY variant to be likely pathogenic, which is consistent with a diagnosis of 46,XY DSD (OMIM 400044), and more specifically CGD, thus revising the patient’s diagnosis from CAIS to CGD 30 years after her original presentation. The patient’s Müllerian structures were now considered a consistent feature of her DSD, although the reason for the absence of secondary sexual hair remains unclear as we excluded a concomitant mutation in the AR gene on WGS.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [181.0, 'cm']}",71.39772,67.82783,74.96761,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 181.0 cm, which is 181.0 cm * 0.393701 in/cm = 71.25988 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (71.25988 (in inches) - 60) = 71.39772 kg.
Hence, the patient's IBW is 71.39772 kg."
3627,10,Ideal Body Weight,physical,decimal,pmc-4540992-1,Extracted,"A 27-year-old male patient was referred to the division of Pediatric Immunology at Hacettepe University for further evaluation of recurrent sinopulmonary infections, chronic diarrhea, and hypogammaglobulinemia. He had been followed up with the diagnosis of bronchiectasis () since the age of 7 years and undergone two separate pulmonary lobectomy surgeries at the ages of 15 and 18 years. On presentation, his chief complaints were diarrhea for 9 months and loss of weight (~10 Kg) within the past 6 months. The microbiological evaluation of stool was negative for a bacteria, parasite, or Cryptosporidium. He had been evaluated by a colonoscopy at outside hospital and this was reportedly normal. His physical examination revealed normal vital signs, body mass index of 14 (weight: 43 Kg, height: 175 cm), clubbing in both hands and feet, right sided rales on lung auscultation, perforated nasal septum and left tympanic membrane, and diffuse erythematous, squamous plaques on the trunk, hands, and behind the ears, compatible with psoriasis. The family history revealed consanguinity.
Laboratory tests on admission showed hypogammaglobulinemia (IgG, 290 mg/dL [n: 913–1884]; IgA, 75 mg/dL [n: 139–378]; IgM, 314 mg/dL [n: 88–322]; total IgE, 1.93 mg/dL), anemia, and elevated erythrocyte sedimentation rate (65 mm/hr [n: 0–20]), and CRP level (16.25 mg/dL [n: 0–0.8]). There was no lymphopenia (ALC: 2600) or neutropenia (ANC: 8500) in the complete blood count. Total protein and serum albumin were normal (6.5 and 4.3 g/dL, resp.). Urine analysis was negative for proteinuria. Flow cytometry of peripheral blood revealed CD3 of 90%, CD4 of 19%, CD8 of 60%, CD16 + 56 of 7%, CD19 of 0%, and CD20 of 0%. In order to rule out X-linked agammaglobulinemia, Bruton tyrosine kinase (BTK) mutation was tested and found to be negative. Pneumococcal antibody response was absent. The clinical findings and laboratory workup did not let us to classify as CVID or combined immunodeficiency (the molecular analysis did not result yet). He was evaluated under the CVID umbrella and was treated with intravenous immunoglobulin therapy (IVIg) with the dose of 400 mg/kg once every 21 days for hypogammaglobulinemia and daily trimethoprim-sulfamethoxazole prophylactically for CD4 + T cell lymphopenia (absolute count: 392/mm3). The patient initially responded to the treatment well with cessation of pneumonia episodes and requirement for hospitalizations. He gained 10 Kg during the first year of follow-up (from 43 to 53 Kg). Two years later, at the age of 29 years, his IgG levels started declining progressively to levels around 200–300 mg/dL despite regular IVIg infusions. His serum albumin level decreased to 3.2 g/dL (n: 3.4–4.8) and he was found to have massive proteinuria with 1726.4 mg/day protein loss on a 24-hour urine collection. Urinary ultrasonography demonstrated increased echogenicity of renal parenchyma (grade 1). Rectal and gingival biopsies were performed with the suspicion of amyloidosis; however, this was negative. A renal biopsy was performed and pathology analysis revealed focal segmental accumulation of AA type amyloidosis in glomeruli and focal accumulation in the interstitium and vessel walls accompanied by tubular atrophy and increased mononuclear cells in the interstitium (). Serum amyloid A (SAA) protein level was 330 mg/L (n: 0–10). Familial mediterranean fever was excluded with the absence of MEFV mutation. The patient was started on angiotensin receptor blocker and colchicine, since some previous reports showed decrease in proteinuria with colchicine treatment in patients with isolated renal amyloidosis [, ]. Three months/years later, the patient presented to our hospital with pneumonia leading to acute hypoxemic respiratory failure. He was treated with broad spectrum IV antibiotics, intubated and mechanically ventilated. Because of severe protein loss secondary to amyloidosis, his IVIg replacement dose was increased to 200 mg/kg twice monthly. His serum albumin levels progressively decreased to 1.3 g/dL despite all the aggressive measures and albumin infusions. The patient expired from sepsis and ARDS at the age of 33 years.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3628,10,Ideal Body Weight,physical,decimal,pmc-8536013-1,Extracted,"Our patient was a 32-year-old man, coming from a country with low availability of factor replacement therapy, height 185 cm, weight 90 kg, professional driver, with severe haemophilia A (F VIII < 1%). Family history positive for severe haemophilia A (his aunt was affected). The diagnosis of severe haemophilia A occurred in his hometown during childhood because he was involved in several atraumatic intra-articular haemorrhages in the elbows, ankles and knees.
In March 2017, after an accidental fall skiing, he reported a blunt trauma of the right iliac wing with development of blood collection in that site.
Pelvic X-rays and bone biopsy were performed at the local hospital and osteosarcoma was excluded. In July 2017 he went to another Haemophilia Centre for the appearance of swelling, fistulisation, leakage of serum blood material and functional limitation of the right hip. He also reported an evening fever of >39°. The physical examination also revealed severe atraumatic functional limitation of the left elbow and the right ankle. Laboratory tests performed showed F VIII <1%, F VIII inhibitors: 0 BU/mL. A pelvis CT was performed, showing the presence of an abscess and a fistula at the right iliac crest (). Staphylococcus aureus was isolated from the culture swab, therefore antibiotic therapy with Teicoplanin + Rifampicin was introduced but subsequently suspended for gastrointestinal intolerance. The patient started prophylaxis with pd-FVIII 30 IU/Kg three times a week. In June 2018, the patient was referred to our Clinic for right hip swelling, fistulisation, serum secretion, pain and functional limitation. Blood exams at the entrance showed Hb 8.6 g/dL, aPTT 40 s, F VIII 20.7% (range 70–120%), inhibitors F VIII 0 BU/mL, PCR 4.4 mg/dL (<0.5). A contrast medium pelvic CT scan demonstrated the presence, at the right iliac wing, of a large (10.1 × 14.2 × 10.7 cm) osteolytic lesion, inhomogeneous, septate and bounded by a peripheral wall of irregular thickness (6–7 mm). The lesion interrupted the cortical bone on both the posterior and anterior side of the iliac bone, also involving the sacroiliac joint plane and the sacral joint surface at S1-level. The lesion infiltrated both the gluteal muscle lodge posteriorly and the deep plane of the ileo-psoas muscle anteriorly. In addition, the presence of two subcutaneous fistulous communications was demonstrated, reaching the cutaneous plane respectively along the lateral side of the right flank and in the right paravertebral posterior lumbar region, at L5-level. Considering the patient’s medical history of haemophilia, a diagnosis of pseudotumour of the right iliac wing with an additional overlapping inflammatory-infectious complication was made.
Surgical treatment to remove the pseudotumour was proposed and accepted by the patient.
Pd-FVIII 20 IU/Kg were administered pre-operatively as a slow intravenous bolus every 12 h for seven days before surgery.
The day of the surgery, the patient underwent selective embolisation with Embosphere® 500–700 of the right superficial gluteal artery and the right lumbar artery ().
Just before the anaesthesia, pd-FVIII 50 IU/Kg was administered as a slow intravenous bolus. After that, 1 g of vancomycin was administered intravenously as intra-operative antibiotic prophylaxis. Under general anaesthesia, the patient has been placed in the lateral decubitus position. Support placed under the thorax allowed to put the patient’s pelvic area into a three-quarter anterior and posterior pelvic tilt during the intervention. Anterolateral and posterior access to the pelvis were used. The incision started along the contours of the iliac crest in a curvilinear manner and ends in the back with a vertical portion on the sacroiliac joint. The wing of the ilium and the sacrum are exposed, allowing for safety margins around the pseudotumour, which extend into the soft tissue. The iliac muscle was sectioned and detached from the endopelvic side of the ilium. The iliac vessels, ureter, lumbosacral trunk, sacral roots and sciatic nerve were identified and protected. On the exopelvic side, the gluteus muscles were moved as a unit with their fascia and skin, creating a lower myocutaneous flap.
After a layered dissection of the soft tissues, we reached the pseudotumour which appeared as a voluminous brownish-red mass with a pasty-like consistency; its capsule was emptied and removed. Subsequently, the right iliac crest was custom-fit by means of a pedicle-screw and rod system (PSRS), a metal bar and two fixing screws (one in correspondence with the acetabulum and the other on the sacro-iliac synchondrosis). Dead space between the implants and the remaining bone were therefore filled by antibiotic coated bone cement with the aid of two polyglycolic acid MESH in order to build up an artificial ilium-like bony mass, as well as graft compression.
Finally, two treble hooks were positioned for repositioning the pelvic muscles. One surgical drain was placed at the end of the surgery. Intraoperatively, a biopsy of the lesion demonstrated the presence of fibrin-haematic organised material with fragments of necro-inflammatory material and scattered microcalcifications. Swabs in fistulous passages were also performed and they showed that there was no superinfection. The patient was transfused intraoperatively with one unit of RBC
At the end of the surgical procedure, pd-FVIII 20 IU/Kg was administered as bolus, then pd-FVIII 20 IU/kg every 12 h on the first postoperative day; from the second post-operative day pd-FVIII 20 UI/Kg at 8 a.m. and 10 UI/Kg at 8 p.m., up to the 4th day postoperatively; from the fifth post-operative day pd-FVIII 30 IU/Kg at 8 a.m. and 10 IU/Kg at 8 p.m. for two weeks, with the aim of maintaining F VIII level > 50%. Every 48 h, before the administration of concentrate of FVIII, blood was taken to check Hb, PTT and FVIII. The variations of FVIII biological activity levels during the hospital stay are summarised in . Antibiotic intravenous post-operative prophylaxis with Vancomycin 500 mg every 12 h was continued until surgical drain removal. The surgical drain was kept for 24 h and then removed with a residual volume of 300 mL of serosanguinous liquid.
The patient was transfused with one RBC unit the day-4, the day-6 and the day-7 after surgery owing to post-operative anaemia. A 21-days hospital stay was necessary in order to achieve a good clinical condition.
In the immediate post-operative period, X-ray and CT of the pelvis showed emptying of the pseudotumour and correct positioning of screws and metal cerclage (). Physiotherapy was started during hospitalisation, from day-1 after surgery and continued during the hospital stay. The patient was discharged at home with the indications for the continuation of physiotherapy, with cautious and progressive recovery of total flexion of the trunk and right thigh. Walking was allowed with aids and load pain-compatible. The patient continued replacement therapy with recombinant F VIII and analgesic therapy with paracetamol. At discharge blood exams showed Hb 8.4 g/dL, aPTT 30.7 s, FVIII 96.5%, CRP 1.3 mg/dL, ESR 109 mm/h (<10). During the rehabilitation period the patient prophylaxis scheme was pd-FVIII 30 IU/Kg every other day. At the first outpatient visit, 8 days after discharge, the patient was in good general condition, he walked with aids, and the pain was well-controlled. The stitches were removed and medicated, no signs of inflammation were noted. Pelvis X-ray unchanged compared to the post-operative one. One month later the patient went to another emergency room for leakage of blood serum material from the surgical scar. A positive culture swab was found for MSSA. After two days, the patient was re-evaluated at our clinic, a wound dehiscence was observed, thus indication for wound revision was given. Five days later, the patient had a feverish episode (T 42 °C) with shaking chills and PCR increase. A broad-spectrum antibiotic therapy was begun and pd-FVIII 3000 IU at 8 and 1000 U at 20 was continued. Therefore, the patient was hospitalised at our Institution for wound surgical revision. Blood exams at the entrance showed Hb 10.6 g/dL, leukocytes 5.37 × 103/uL (4.00–10.00), CRP 0.97 mg/dL, ESR 85 mm/h. Preoperatively, pelvic CT was performed, and it showed a voluminous collection of infected blood fluids both on the pelvic side along the planes of the ileo-psoas muscle and on the buttock side. The fluid collection extended to the paravertebral musculature, the quadrate loin muscle, and the external oblique muscle superiorly and posteriorly. In the postero-superior site, the collection went beyond the muscle fascia and extended into the subcutaneous fat layer. Therefore, surgical toilet and abundant irrigation was performed. During the surgical procedure, swabs were carried out for culture tests, later found negative for infection. The patient was discharged with a recommendation to continue antibiotic therapy with Rifampicin and Levofloxacin for 5 days and to continue the factor VIII replacement therapy. In this second hospitalisation a 11-days hospital stay was necessary in order to achieve optimal medical condition.
Patients were followed at outpatient clinic, at 7, 14 and 21 days. He was always in good general condition with surgical wound healed without signs of inflammation. Right hip ROM was almost complete at one month with control X-ray () unchanged than the post-operative one. At the 6- and 12-month outpatient visit the patient was in good clinical conditions, he denied disorders or functional limitations in every-day life. Currently, the patient is checked with an X-ray every 6 months.
The patient continued prophylaxis with pd-FVIII 30 IU/Kg three times a week. No further bleeding manifestations occurred.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [185.0, 'cm']}",79.51979,75.5438,83.49578,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 185.0 cm, which is 185.0 cm * 0.393701 in/cm = 72.83469 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (72.83469 (in inches) - 60) = 79.51979 kg.
Hence, the patient's IBW is 79.51979 kg."
3629,10,Ideal Body Weight,physical,decimal,pmc-7441269-1,Extracted,"A 54-year-old Caucasian male was admitted to the Centre of Hepatology, Gastroenterology and Dietetics presenting with complaints in various organ systems. The patient was complaining of fatigue, weight loss (lost over 30 kg in 9 mo despite good appetite), frequent bowel movements (up to 3 times daily), dryness of the mouth along with changes of facial appearance due to bilateral salivary gland swelling, and difficulty urinating.
At the age of 36, the patient was diagnosed with autoimmune thyroiditis. It was managed with a low dose of prednisolone. The disease re-occurred as subacute thyroiditis several times within 15 years. This resulted in hypothyroidism, and 50 mcg of levothyroxine was added. The patient also had bronchial asthma, which was well controlled with bronchodilators on demand and currently in remission. Whereas the patient had a familial anamnesis of the thyroid disease, no additional testing for other possible reasons of thyroid disease was made at that time.
At the age of 52, the patient approached the ophthalmologist with a swollen right eye and visual impairment. The treatment with anti-inflammatory ointments, antibiotics and corticosteroid eye drops was initiated. However, the symptoms progressed, and the patient developed diplopia and strabismus, which did not respond to the vision correction with prism lenses. The neurologist then consulted the patient to differentiate possible mass of the sella turcica. Magnetic resonance imaging (MRI) of the head showed no pathology. Though the patient's symptoms further progressed and he developed the significant protrusion of both eyes, photophobia, eye-watering and impaired diplopia. At this point, the neurologist and ophthalmologist repeatedly consulted the patient. Negative antibodies against acetylcholine and neuromyography excluded myasthenia gravis. Ultrasound examination of the extracranial cerebrovascular system showed no sinus cavernosus pathology or carotid artery stenosis. Additionally, the inconsistent size heterogenic mass was spotted transorbitally on the left orbital cavity (Figure ).
The 1.5-T MRI scan of the orbital cavity pointed out the substantial enlargement in extraocular muscles (left lateral and inferior rectus muscles, right superior rectus muscle), sinusitis, and no signs of lacrimal glands pathology (Figure ). The symptoms were attributed to endocrine ophthalmopathy (Graves' disease), and the patient was referred to the tertiary Centre of endocrinology. At the time of admission, the patient’s laboratory tests showed normal levels of thyrotropin hormone (TTH) at 1.28 mU/L (normal range 0.4-4.0 mU/L), free thyroxine (FT4) 18.71 pmol/L (normal range 12–22 pmol/L) and anti-thyroid peroxidase (anti-TPO) antibodies at 0.6 kU/L (normal range < 5.61), also negative thyrotropin receptor antibodies (TRAb) at 5.1 U/L (negative when < 9). The patient then received twelve courses of weekly intravenous methylprednisolone (in total 4.5 g of methylprednisolone). Although the periorbital swelling decreased, diplopia, photophobia, and tearing remained. The patient then received a course of orbital radiotherapy for steroid-refractory endocrine ophthalmopathy. However, this treatment was also not sufficient enough. The patient was referred to otolaryngologist regarding the indications for the left orbital decompression due to aggressive exophthalmos. The surgical treatment was not indicated, though. The endocrinologists then doubted the diagnosis of Graves' disease and thought of idiopathic orbital inflammation, which can be treated with retrobulbar steroid injections. However, the patient refused this treatment after several injections and was out of reach for a year.
Two years later, the patient started complaining of abdominal pain, diarrhoea, severe weight loss (lost 20 kg per half-year), fatigue and urinary problems. Internal medicine doctor referred him to the gastroenterologist. Ultrasound of the abdomen showed hepatosteatosis, gastroscopy – erosive gastropathy, duodenal biopsy specimens revealed no signs of the celiac disease and colonoscopy indicated tubular adenoma. The patient had a urologist's consultation due to urinary hesitancy which was attributed to benign prostatic hyperplasia. At this period, the patient was also diagnosed with diabetes, which was managed with a strict diet and metformin.
As the patient developed vitiligo, muscular pain, sicca symptoms and severe fatigue, he was sent to the rheumatologist, and multiple blood tests were performed. Positive IgG, A, M antibodies against β-2 glycoprotein-1 and cardiolipin, positive antinuclear antibodies (ANA), negative anti-neutrophil antibodies (ANCA) and negative extractable nuclear antigens (ENA) (including anti-SSA, anti-SSB) were detected. Rheumatoid factor, complement C4 and C3c were within a normal range (Table ). These findings did not confirm any systemic rheumatological disease. However, elevated liver enzymes were noticed, and the patient was referred to the Centre of Hepatology, Gastroenterology and Dietetics for the liver biopsy.
The patient had had bronchial asthma since childhood, which was currently in remission. His mother underwent surgery on her thyroid gland in her youth, and his sister had second type diabetes. The patient was a non-smoker and denied alcohol consumption. He claimed to have no allergies to food or medicines.
Patient's symptoms started in his youth and had been continuously worsening and spreading to different organs throughout the years. The most recent deterioration started about 9 mo ago when he began losing weight, complaining of diarrhoea and severe fatigue, sicca symptoms. Several weeks before the hospitalization, he noticed continuously increasing masses on the neck, severe dryness of the mouth, difficulty swallowing and urinating.
At presentation, the patient was asthenic (height 188 cm, weight 68.3 kg, body mass index 19.32 kg/m2) and had vitiligo-like patches on the insides of his wrists and the lower left calf. We also noted large palpable hard masses in the projection of submandibular and parotid salivary glands bilaterally, diffuse I B stage goitre and the protrusion of the left eyeball.
Blood analysis was almost within the normal range (Table ). There were no elevated liver enzymes or signs of liver dysfunction, viral hepatitis markers were negative.
As there were no indications for liver biopsy, it was decided to perform abdominal MRI which displayed changes of pancreatic parenchyma, showing diffusely enlarged sausage-shaped pancreas with a peripancreatic rim of edematous tissue that is pathognomonic for AIP (Figure ). Severe weight loss with diarrhoea and diabetes indicated the endocrine and exocrine pancreatic insufficiency.
Combination of AIP, orbital myositis, salivary gland involvement, as well as the previous diagnosis of thyroiditis and uveitis, increased the suspicion of the IgG4-RD. Differential diagnosis was kept as possible Sjögren's syndrome (SS), lymphoma, and sarcoidosis. Consequently, we performed the ultrasound imaging of the neck. The thyroid was normal in size with several nodules on the right and left lobes (8 mm × 13 mm and 7 mm × 21 mm) (Figure ). There were several symmetrical rounded parenchymal masses (28 and 33 mm) in the area of submandibular glands (Figure ) and altered parotid gland tissue with indeterminate size masses observed bilaterally. It was decided to perform fine-needle aspiration from the palpable masses in the neck.
Histopathological examination of the salivary gland biopsy revealed signs of chronic lymphoepithelial sialadenitis: The infiltration of T and B lymphocytes, moderate plasma cell and eosinophil infiltration, acinar atrophy, moderate fibrosis. However, no clear histological and immunohistochemical evidence of IgG4-mediated chronic sclerotic sialoadenitis was found. There was no deposit of amyloid, no granuloma, any signs of mucosa-associated lymphoid tissue lymphoma or Langerhans histiocytosis. We also found elevated plasma IgG4 concentration at 6.87 g/L (normal range 0.08-1.40 g/L).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [188.0, 'cm']}",82.23632,78.1245,86.34814,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 188.0 cm, which is 188.0 cm * 0.393701 in/cm = 74.01579 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (74.01579 (in inches) - 60) = 82.23632 kg.
Hence, the patient's IBW is 82.23632 kg."
3630,10,Ideal Body Weight,physical,decimal,pmc-2082036-1,Extracted,"A 39-year old HIV seropositive woman, with a medical history of recurrent oral ulcerations, thoracic Herpes zoster, weight loss, caries, repeated pneumonia and three episodes of smear positive tuberculosis (1990, 2001 and 2003), presented in our clinic in May 2005 with chronic productive cough and intermittent hemoptysis. Her family history did not reveal any hereditary lung diseases. She had never smoked or used intravenous drugs. She received cotrimoxazole prophylaxis but had never had access to ART.
Clinical exam revealed a normal respiratory and cardiac rate, weight 47.3 kg and height 159 cm (body mass index; BMI: 18.7), pallor, lesions of an old zona eruption on the left shoulder, oral ulcerations and caries. Lung auscultation revealed discrete crepitations in both lung fields. The CD4+ T lymphocyte count was 329 cells/mm3.
A sputum specimen was negative for acid fast bacilli. Gram stain showed a large number of epithelial and polynuclear cells, gram negative bacilli and gram positive cocci. Sputum culture grew Klebsiella pneumoniae, sensitive to nalidixic acid, norfloxacin, ciprofloxacin, cefotaxime and gentamycin. Chest X-ray (Figure ) was compatible with surinfected dystrophic bullous emphysema and a small right-sided pleural effusion.
The patient was treated with seven days of clindamycin, followed by one week of amoxicillin/clavulanic acid, with good clinical response. ART (stavudine, lamivudine, nevirapine) was initiated, based on WHO stage III clinical disease. Because hemoptysis persisted and pulmonary infiltrates increased, treatment with fluconazole for presumptive fungal surinfection was started 2 weeks after initiation of ART with resolution of symptoms and signs.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [159.0, 'cm']}",51.47646,48.90264,54.05028,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 159.0 cm, which is 159.0 cm * 0.393701 in/cm = 62.59846 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.59846 (in inches) - 60) = 51.47646 kg.
Hence, the patient's IBW is 51.47646 kg."
3631,10,Ideal Body Weight,physical,decimal,pmc-7227336-1,Extracted,"A 36-year-old female patient of Tatarian origin was referred to the Endocrinology Research Centre, Moscow, with a diagnosis of type 1 diabetes mellitus complicated by diabetic foot syndrome. According to the medical documents, generalized lipoatrophy developed during the first months of life, and from the early childhood she suffered from an umbilical hernia, muscular hypotonia and delayed motor development (without mental retardation). Later moderate amyotrophy of the muscles of the shoulder girdle developed, with a lack of reflexes in the legs, muscle weakness and myalgia of lower extremities. Between the ages of 17 and 20 the patient underwent multiple surgeries for dolichosigmoid, perforation of diverticula and peritonitis, which resulted in local muscular weakness and malabsorption leading to generalized muscular weakness and dysphagia. At 19 years of age diabetes mellitus type 1 was diagnosed with normal body weight but for 2 years the patient was well compensated by a diet with fast carbohydrates restriction. At the age of 21, she started insulin therapy. A wound defect (trophic ulcer) in the area of the inner surface of the right thigh was diagnosed at the age of 35; after a few months, diabetic neuro-osteoarthropathy of the right foot was also diagnosed. For 3 months, the patient used a Total Contact Cast with positive effects. The patient had amenorrhea with 2 episodes of menorrhagia in her life between the ages of 18 and 19. Bilateral cataracts were first diagnosed at the age of 22, and were treated surgically 12 years later. Marked diffuse osteoporosis was diagnosed at the age of 28 by a multi-layer spiral CT (Computed Tomography) scan.
She had acromegaloid features, phlebomegaly and hypertrophy of the skeletal muscles in the upper and lower extremities, muscular hypotonia, generalized lipoatrophy, but no signs of hirsutism and clitoromegaly were found. Her height was 160 cm, weight 46.8 kg, BMI (Body mass index) 18.1 kg/m2.
Skin fold measurements, impedancemetry and “Total body” densitometry showed a significant decrease of subcutaneous fat tissue. The skin fold measurements were as following: supraclavicular skin fold, 4 mm; subscapular skin fold, 6 mm; triceps skin fold, 4 mm; anterior surface of the abdomen skin fold, 4 mm; hip skin fold, 6 mm; anterior surface of the thigh skin fold, 6 mm; posterior surface of the tibia skin fold, 3 mm. Impedancemetry showed 11.9% of body fat, and “Total body” densitometry demonstrated 7.8% of total fat (Fig. ). An abdominal ultrasound showed hepatosplenomegaly with severe hepatic steatosis. There was no cardiac pathology, except sinus tachycardia shown in the electrocardiogram. The densitometry showed severe osteoporosis of the lumbar spine (T-score L1-L4: − 5.6), osteoporosis of the proximal femur (T-score Neck: − 5.4). The laboratory data is presented in Table .
(Fig. ): a consanguineous marriage of grandparents (cousins) from the father’s side, type 2 diabetes (father and grandmother from the father’s side), breast cancer (father’s sister), acute myocardial infarction (2 father’s brothers), arterial hypertension (2 father’s brothers), bicornuate uterus and endometriosis (sister), Crohn’s disease (cousin from the father’s side), arterial hypertension and obesity (mother), death in early childhood from the unknown reason (mother’s brother and sister). The patient reported that the grandmother from the father’s side had a short stature.
The patient received insulin therapy (insulin glargine 20 U/day, insulin glulisine 40 U/day), nephroprotective therapy (enalapril 2.5 mg/day), bisoprolol 5 mg/day for tachycardia, antihyperuricemic therapy (allopurinol 150 mg/day), the native form of vitamin D, alfacalcidol and calcium for osteoporosis. The patient also receives symptomatic therapy for gastrointestinal pathology and nutritional therapy.
Based on typical clinical signs of generalized lipodystrophy (total lipoatrophy, muscular hypertrophy, phlebomegaly, acromegaloid features, hypertriglyceridemia, hepatosplenomegaly, steatohepatitis) and early onset of the disease, CGL was suspected. Taking into account muscular pathology, CGL type 4 appeared probable. Due to the variety of clinical features of different types of lipodystrophy syndromes and progeroid syndromes sequencing of 18 lipodystrophy candidate genes (AGPAT2, BSCL2, CAV1, CAVIN1, PSMB8, LMNA, PPARG, PLIN1, AKT2, CIDEC, LIPE, LMNB2, PIK3CA, PPP1R3A, POLD1, WRN, ZMPSTE24, BANF1) using a custom Ion Ampliseq panel and Personal Genome Machine (ThermoFisher Scientific, Waltham, MA, USA) semiconductor sequencer (Ion Torrent) was performed. A novel pathogenic homozygous variant c.631G < T: p.E211X was detected in the CAVIN1 gene (Fig. ), confirming the diagnosis of CGL type 4.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3632,10,Ideal Body Weight,physical,decimal,pmc-4518388-1,Extracted,"We present the case of a 44-year-old male with a fluctuating 10-year history of hemospermia. No lower urinary tract symptoms or sexual problems were reported. The genital examination and rectal digital exploration findings were normal. The patient reported no family history of collagen diseases and had no cardiac or vascular disorders. The blood pressure was within the normal range, and body weight was 75 kg with a height of 172 cm.
A fractionated culture of the ejaculate was performed, together with urine cytology, urine cultures for fungi, parasites and bacteria (including tuberculosis), biochemical testing, blood count, coagulation, and prostate-specific antigen (PSA) levels. All the parameters were within normal limits. The urine and semen cultures were negative.
Transrectal ultrasound (TUS) revealed a homogeneous prostate gland with a volume of 23 cm3. The seminal vesicles were normal in size and had no contents.
In view of the persistent symptoms, a pelvic magnetic resonance imaging (MRI) study was requested. The seminal vesicles were slightly distended, though the signal intensity was normal. On the other hand, dilatation of the venous plexuses was noted, resulting in a congestive appearance of the lesser pelvis, with significant dilatation of the iliac veins and inferior vena cava over its retroperitoneal abdominal trajectory. Considering the MRI findings, we decided to perform a computed tomography (CT) scan extending to the abdomen [Figures -].
The CT scan confirmed dilatation of the venous plexuses in the lesser pelvis, with nonpathological contrast uptake in the prostate and seminal vesicles. In addition, we observed symmetrical dilatation of the inferior cava vein, common, internal and external iliac veins, with no sacular venous aneurysms or associated obstructive disease, and the presence of varicosities in the pelvic venous plexuses. On the other hand, at renal sinus level, we observed a preaortic orthotopic left renal vein, with another vein in a retroaortic and prelumbar location, as a variant of normality [].
Based on the above findings, we referred the patient to the Unit of Vascular Surgery, where treatment with venoactive drugs (diosmin) and lifestyle adaptation measures were recommended reducing pelvic venous pressure by means of avoiding increase intraabdominal pressure (weight lifting) or prolonged standing time at work. The possibility of endovascular embolization/sclerosis in the case of worsening of the symptoms was considered.
Occasional hemospermia without anemia persists with no other associated symptoms.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [172.0, 'cm']}",67.74811,64.3607,71.13552,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 172.0 cm, which is 172.0 cm * 0.393701 in/cm = 67.71657 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.71657 (in inches) - 60) = 67.74811 kg.
Hence, the patient's IBW is 67.74811 kg."
3633,10,Ideal Body Weight,physical,decimal,pmc-7476613-1,Extracted,"A 29-year-old Chinese man who had no disease history expired suddenly and fell down from bed at home. As his death was sudden and unexpected, a forensic pathological team was commissioned to conduct a full postmortem examination in order to constitute a reportable death.
The decedent was a well-nourished adult male of appearance in keeping with his stated age, measuring 170 cm for a weight of 80 kg (body mass index = 27.7). In addition to peripheral subungual cyanosis, there was no evidence of other pathological findings.
Skeletal muscles of the body were almost replaced with adipose tissues, which could not be clearly discriminated (). The heart was enlarged and weighed 420 g (the normal weight for men is 300–350 g []). The surface of the heart was extensively covered with adipose tissue ((A)). A myocardial bridge was found in the intermediate portion of the left anterior descending artery. A focal atherosclerotic plaque with slight luminal stenosis was observed in the right main coronary artery. The left ventricle was dilated, the ventricular chamber diameter was 6.3 cm and scattered hyperplasia of adipose tissue could be seen beneath the endocardium of the left ventricle ((B)). The thickness of the left ventricle was 1.2 cm (normal thickness, 1.3–1.5 cm), while the thickness of the right ventricle was 0.1 cm (normal thickness, 0.3–0.5 cm). The cardiac muscle of the right ventricle was abundant with fatty tissues. The lungs were overweight (right: 550 g, left: 500 g), appearing pulmonary oedema. The weights of brain, liver and spleen were 1 430, 1 500 and 240 g, respectively. The weight of the kidneys was 150 g in each. The parenchyma of pancreas, thymus and thyroid gland showed a large content of adipose tissues on cross sections. The macroscopic examinations of other organs showed no obvious abnormalities.
A histopathological examination was carried out on the muscles, myocardium, brain, lungs, liver, kidneys, spleen, pancreas, thymus and thyroid gland using standard H&E staining. The veins in lungs and other organs appeared congested and dilated. There was no fat embolism and thrombi in the lungs. Significant histological findings were confined to the heart and the muscles of the body. It was found that most skeletal muscle fibres of quadriceps ((B)) and diaphragm ((C)) were replaced with adipose and fibrotic tissues. There were also evidences of marked variability in fibre size, focal fibre necrosis and invasion by monocytes compared with the normal control ((A)). Cardiac muscle exhibited variation in fibre size with a disarrayed appearance. The ventricular myocardium was infiltrated by diffused fatty foci. Degeneration of cardiac muscles and focal myocardial fibrosis were also observed ((D)).
Immunohistochemical staining of dystrophin was performed on the muscles and myocardium samples. Immunohistochemistry revealed total absence of dystrophin in the sarcolemma of quadriceps ((F)), diaphragm ((G)) and cardiac muscle ((H)) compared with the normal control ((E)).
Samples of heart blood, urine and gastric contents were submitted for screening analyses by gas chromatography and mass spectrometry. Common drugs of abuse and poisons were negative.
Post-mortem biochemical tests were performed on a sample of pericardial fluid with results as follows (standard levels are given in brackets): NT-proBNP 662.8 pg/mL (<115 pg/mL); CK-MB 4 234 ng/mL (340–2 420 ng/mL); cTnT 1 701 ng/mL (181–3 352 ng/mL). The creatine kinase (CK) of serum was 5 226 ng/mL (<250 ng/mL).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3634,10,Ideal Body Weight,physical,decimal,pmc-5602232-1,Extracted,"A 16-year-old Kannada-speaking Indian female presented with 3-week history of headache, and multiple episodes of vomiting. One day before her presentation to our hospital, she developed three episodes of generalized tonic–clonic seizures with preserved sensorium in between the attacks. She denied any double vision, facial weakness, tinnitus, speech, or swallowing difficulties. There was no history of fever, ear pain, or ear discharge. She was otherwise healthy without any prior medical or neurological illness. She was not on any long or short-term medications before her symptoms started. She was unmarried and had regular menstrual cycles. Her diet predominantly involved vegetarian menus, rich in carbohydrates, poor in protein, and dairy products.
On examination, her weight was 53 kg, height 160 cm, and body mass index = 20.7 kg/m2. She had knuckle hyperpigmentation with mild pallor. No organomegaly was detectable clinically. She was conscious oriented with normal higher mental functions and language assessment. Her vision for near and far objects was normal (6/6) without correction and so was her color vision in both eyes. Her visual fields by confrontation method were normal. Eye movements were normal and full range. Fundus examination showed swelling of her right optic nerve head with disc elevation, obliteration of the cup, blurring of the disc margins, and peripapillary halo with fundal hemorrhage with no major vessel obscurations on the right side (Frisen grade-2). The left eye fundus was normal [Figure and ]. The veins appeared congested in the right fundus, the left side being normal. Rest of the neurological examination was normal.
Her investigations included complete blood count, erythrocyte sedimentation rate, peripheral smear, liver/renal and thyroid functions tests, fasting glucose, lipid profile, antinuclear antibody, antiphospholipid antibody screening, serum homocysteine levels, Vitamin B12 levels, folate levels, and serum antibodies for human immunodeficiency virus by enzyme-linked Immunosorbent assay. She had dimorphic anemia (hemoglobin - 9.7 g/dl, normal 12–16 g/dl in females) with hypersegmented neutrophils, hyperhomocysteinemia (26 μmol/L, normal range 5–20 μmol/L), and low Vitamin B12 (<50 pg/ml, normal range-180–900 pg/ml) levels; other investigations were normal. Her brain imaging with computed tomographic scan (plain and contrast) (Philips Brilliance/Netherland/2010) showed hyperdense superior sagittal sinus with filling defect and similar findings in bilateral lateral sinuses [Figure and ] with the right temporal hypodensity suggestive of extensive CVT. Magnetic resonance imaging (MRI) with venography (Siemens 3 Tesla/Erlangen Germany/2014) also showed thrombosis of the superior sagittal sinus and bilateral lateral sinus with parenchymal lesion [Figure and ]; additionally, there was partial empty sella, prominence of perioptic spaces, tortuosity of the right optic nerve, and protrusion of the right papilla suggesting raised intracranial pressure [Figure , , , and ]. No obvious defect in the perioptic sheath was noted in the MRI. Protrusion of the right papilla was confirmed with orbital ultrasound B-scan (Philips/Netherland/2014). We did optic coherence tomography (OCT) both the eyes to detect any subclinical papilledema in the left eye. There was significant disc elevation in the right eye and normal disc in the left eye. Nerve fiber layer (NFL) thickness was increased on the right side being normal on the left [Figure –]. Intraocular pressure (IOP) was normal bilaterally (14 mm Hg). Her visual fields by perimetry showed mildly enlarged blind spot in the right eye whereas the left was normal. We did not perform cerebrospinal fluid examination as the patient had extensive sinus thrombosis with the right temporal parenchymal lesion and imaging showing futures of raised intracranial pressure. It would not have added to the management of our patient, and we were worried about the remote possibility of worsening of her clinical condition due to brain herniation. She was treated for cerebral CVT with unfractionated heparin 5000 units 6th hourly subcutaneously for 10 days followed by oral anticoagulation (acenocoumarol loading of 4 mg/day followed by maintenance dose of 1.5 mg/day once day),[] antiedema measures (mannitol 50 ml 6th hourly intravenously for 5 days and tapered gradually over next 3 days and oral glycerol 20 ml orally 4 times/day for 10 days), anticonvulsants (phenytoin sodium 200 mg/day in two divided doses), Vitamin B12 supplementation (1 mg intravenous injection for 7 days and 1mg intravenously once a week for 1 month followed by oral 1 mg/day tablets), pyridoxine (10 mg/day), and tablet folic acid 5 mg/day, iron supplementation (tablet ferrous sulfate 60 mg 3 times/day). Subsequently, maintenance doses of iron and vitamin supplementations were continued after 3 months. She is being followed up in the outpatient department monthly from the past 5 months. Her repeat eye examination showed resolved right optic fundus edema. We have planned to repeat her serum homocysteine and Vitamin B12 levels at 6 months and if they are normal, we will stop anticoagulation. She will continue to receive anticonvulsants for total duration of 1 year, followed by tapering and stopping if there is no seizure recurrence.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3635,10,Ideal Body Weight,physical,decimal,usmle-1339,Extracted,"A 36-year-old man is brought to the emergency department for right upper quadrant abdominal pain that began 3 days ago. The pain is nonradiating and has no alleviating or exacerbating factors. He denies any nausea or vomiting. He immigrated from Mexico 6 months ago and currently works at a pet shop. He has been healthy except for 1 week of bloody diarrhea 5 months ago. He is 182 cm (5 ft 11 in) tall and weighs 120 kg (264 lb); BMI is 36 kg/m2. His temperature is 101.8°F (38.8°C), pulse is 85/min, respirations are 14/min, and blood pressure is 120/75 mm Hg. Lungs are clear to auscultation. He has tenderness to palpation in the right upper quadrant. Laboratory studies show:
Hemoglobin 11.7 g/dL3
Leukocyte Count 14,000/mm
Segmented neutrophils 74%
Eosinophils 2%
Lymphocytes 17%
Monocytes 7%
Platelet count 140,000/mm3
Serum
Na+ 139 mEq/L
Cl- 101 mEq/L
K+ 4.4 mEq/L
HCO3- 25 mEq/L
Urea nitrogen 8 mg/dL
Creatinine 1.6 mg/dL
Total bilirubin 0.4 mg/dL
AST 76 U/L
ALT 80 U/L
Alkaline phosphatase 103 U/L
Ultrasonography of the abdomen shows a 4-cm round, hypoechoic lesion in the right lobe of the liver with low-level internal echoes.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [182.0, 'cm']}",76.80323,72.96307,80.64339,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 182.0 cm, which is 182.0 cm * 0.393701 in/cm = 71.65358 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (71.65358 (in inches) - 60) = 76.80323 kg.
Hence, the patient's IBW is 76.80323 kg."
3636,10,Ideal Body Weight,physical,decimal,pmc-3983425-1,Extracted,"An 18-year-old 170-cm-tall male weighing 51 kg was admitted via the emergency room complaining of palpitations, dyspnea, and cyanosis. The patient was born with complex congenital cardiac anomalies, consisting of a single ventricle (right ventricle type), a complete endocardial cushion defect, corrected transposition of the great arteries, right isomerism, and a supracardiac type total anomalous pulmonary venous return. The patient underwent correction of the total anomalous pulmonary venous return and bidirectional cavo-pulmonary shunt when he was 11 months old, and a Fontan procedure at age 3 years. The patient was taking aspirin (200 mg), digoxin (0.25 mg), enalapril (5 mg) and, atenolol (12.5 mg) daily. The initial vital signs were a systolic blood pressure (SBP) of 126 mmHg and heart rate (HR) of 116 beats/min. Arterial blood sampling was obtained on room air, and showed hypoxemia (PaO2 58 mmHg). The patient also had compensatory polycythemia (hemoglobin 15.8 g/dl) secondary to chronic hypoxemia. The last cardiac catheterization was performed when the patient was 12 years old, and it showed only mild atrio-ventricular valve regurgitation (AVVR). The mean pressure of the Fontan pathway was 13 mmHg. Laboratory testing revealed increased serum (3,533 pg/ml; normal < 1,050 pg/ml) and urine (768.2 µg/day; normal < 97 µg/day) norepinephrine and urine vanillylmandelic acid (8.8 mg/day; normal 2-7 mg/day) levels. Computed tomography showed a 4 cm mass in the left para-aortic area above the left kidney. With an impression of pheochromocytoma, the patient was scheduled for laparoscopic excision of the tumor. Phenoxybenzamine (10 mg) was administered daily for 2 weeks before the surgery. Preoperative electrocardiography showed supraventricular tachycardia and 24 h Holter monitoring showed no significant cardiac arrhythmia except intermittent junctional rhythm. Echocardiography revealed mild AVVR. The estimated ejection fraction of the ventricle was approximately 50% and the ventricular wall motion was normal. There was no obvious stenosis within the Fontan pathway or the scanned parts of pulmonary vessels.
After being administered intravenous midazolam (1.5 mg), the patient was brought to the operating room. The initial SBP and HR there were 144 mmHg and 94 beats/min, respectively. Anesthesia was induced with intravenous midazolam (2.5 mg), etomidate (10 mg), remifentanil (40 µg), and rocuronium (50 mg). The trachea was intubated and anesthesia was maintained with sevoflurane and 50% oxygen in 2 L/min fresh gas. In addition, intravenous remifentanil was infused continuously during the surgery. The right radial artery was cannulated for continuous arterial blood pressure monitoring. A central venous catheter was placed in the right internal jugular vein, and continuous central venous pressure (CVP) monitoring was started. The initial CVP was 15 mmHg. A transesophageal echocardiography (TEE) probe was inserted smoothly and the echocardiographic evaluation revealed normal ventricular function with mild AVVR. After achieving hemodynamic stability, a continuous infusion of milrinone (0.5 µg/kg/min) and magnesium sulfate (MgSO4) (1 g/h) was started after a 1-g loading dose of MgSO4 to prevent severe pulmonary hypertension and maintain a stable blood pressure during the surgery.
Surgery was started, and intra-abdominal CO2 insufflation was begun for the laparoscopic procedure. After insufflation, the CVP was increased to 28 mmHg and the SBP rose from 90 to 128 mmHg (). Simultaneously, the peak inspiratory pressure increased from 17 to 24 cmH2O. The arterial oxygen saturation decreased from 100 to 97%, and the arterial oxygen partial pressure dropped from 196 to 93 mmHg. The intra-abdominal pressure (IAP) was maintained between 13 and 15 mmHg. The inspired oxygen fraction was transiently set to 1.0, and an immediate TEE evaluation showed preserved ventricular contractility without aggravation of the mild AVVR. To prevent abrupt arterial hypertension, a continuous infusion of sodium nitroprusside (SNP) was started (0.5 µg/kg/min) and titrated up to 1.5 µg/kg/min. However, four further sudden increases in SBP over 160 mmHg, up to 194 mmHg, occurred during the dissection and approach to the tumor; these were controlled by intravenous bolus injections of SNP (30 or 40 µg) and remifentanil (40 or 50 µg). No significant cardiac arrhythmias were detected, except sinus tachycardia during the dissection.
Approximately 2 h after establishing pneumoperitoneum, the surgeon decided to convert from laparoscopic surgery to a laparotomy, suspecting aortic invasion of the tumor. After exsufflation, the CVP decreased from 18 to 10 mmHg and the SBP dropped from 120 to 70 mmHg. Subsequent TEE showed decreased ventricular volume with preserved contractility. After fluid resuscitation and continuous infusion of dopamine (5 µg/kg/min) and norepinephrine (0.02 µg/kg/min) for approximately 7 min, the SBP recovered and was maintained at 100-120 mmHg. Arterial blood gas analysis showed that the oxygen partial pressure had increased to 157 mmHg. Subsequently, there were several abrupt increases in SBP up to 190 mmHg until the tumor was excised; these were well controlled with bolus injections of SNP and remifentanil.
The tumor was removed approximately 260 min after beginning the surgery. After removing the tumor, the MgSO4 was discontinued and the milrinone was tapered (0.25 µg/kg/min). Continuous infusion of dopamine (5 µg/kg/min) and norepinephrine (0.04 µg/kg/min) was initiated. The infusion rates were tapered to 3 and 0.02 µg/kg/min, respectively, before the end of surgery. The duration of the surgery and anesthesia was 490 min. The patient was transferred to the surgical intensive care unit and extubated 12 h later. Intravenous patient-controlled analgesia with fentanyl was used to manage postoperative pain, which was relatively well controlled. All inotropics were discontinued on the third postoperative day. Subsequently, the patient was moved to a general ward and discharged uneventfully on the 13th postoperative day.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3637,10,Ideal Body Weight,physical,decimal,pmc-7193384-2,Extracted,"Patient 2 was a 58-year-old woman (height 1.53 m, weight 75 kg, BMI 32.0 kg m-2) with severe steroid-dependent allergic asthma who also failed to respond to omalizumab. Disease onset had occurred in early childhood; there had been no remission. The patient had mild bronchiectasis without chronic infection and had never smoked. IgE testing for Aspergillus fumigatus was negative on multiple occasions. The patient was on regular high-dose oral and inhaled corticosteroids plus LABA and had a history of multiple hospital admissions due to pulmonary exacerbations. In November 2015, bone marrow aspiration was performed, and the patient received a single dose of autologous BMMCs intravenously and was periodically followed for a year (Table ). Corticosteroids and LABA were continued. Whole-body 99mTc-BMMC scintigraphy performed 2 h after cell infusion demonstrated a normal biodistribution of labeled cells, with greater uptake in the liver, lungs, heart, blood pool, kidneys, and bladder (Fig. ). Thirty days after the procedure, asthma control was achieved, and the patient demonstrated better exercise tolerance as well as a reduction in corticosteroid requirements. During the following months, the patient had three pulmonary exacerbations, each requiring an increase in the dose of oral corticosteroids and prescription of antibiotics. No significant changes in ventilation or perfusion from baseline were observed on day 120 post-BMMC transplantation. Over the 1-year follow-up period, her asthma remained partially controlled. Lung function, 6MWD, and self-perceived QoL score improved slightly up to 30 days after BMMC transplantation (Table , Fig. ). On day 60, these parameters declined, which remained stable thereafter.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.53, 'm']}",46.04337,43.7412,48.34554,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.53 m, which is 1.53 m * 39.3701 in/m = 60.23625 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.23625 (in inches) - 60) = 46.04337 kg.
Hence, the patient's IBW is 46.04337 kg."
3638,10,Ideal Body Weight,physical,decimal,pmc-4041962-1,Extracted,"A 65-year-old man, who was 172 cm tall and weighed 76 kg, underwent arthroscopic rotator cuff repair for left shoulder rotator cuff tear. His medical history was significant for non-insulin dependent diabetes mellitus and stable angina, with medications to control those conditions (aspirin, oral hypoglycemic agent). Aspirin (100 mg/day) was discontinued 7 days before surgery. Results of all preoperative laboratory tests including electrocardiogram, chest X-ray, blood examination and urine examination were within normal limits. Preoperative prothrombin time and activated partial thromboplastin time were 13.4 and, 29.9, respectively. Platelet function tests were not performed.
Intraoperative monitorings included non invasive blood pressure, three lead electrocardiogram, and pulse oximetry. After arrival in the operating room, he patients vital signs were a blood pressure of 150/82 mmHg, a heart rate of 98 /min, a respiration rate of 20 /min and SpO2 of 99%. Infusion of remifentanil was started at the rate of 1 µg/kg/min. Lidocaine 80 mg and propofol 150 mg were then injected for induction of anesthesia. After loss of consciousness, rocuronium 60 mg was administered intravenously with mask ventilation and the patient was intubated endotracheally. During the surgery, the patient was maintained in a semi upright beach chair position. A blood pressure cuff was in place around the patient's right arm, and the mean blood pressure was maintained above 80 mmHg, considering the patient's position. Remifentanil was infused at the rate of 0.1-0.3 µg/kg/min to minimize hemodynamic changes, while at the same time anesthesia was maintained with sevoflurane and 40% oxygen. Arthroscopic irrigation was performed with 42,000 ml of saline and epinephrine 12 mg. At the end of the operation, pyridostigmine 15 mg and glycopyrrolate 0.4 mg were intravenously injected after the patient had recovered spontaneous breathing and the patient was then extubated. The total operation time was 3 hours, 50 minutes, and anesthesia time was 4 hours, 55 minutes. When the patient arrived at the post-anesthesia care unit, his vital signs were a blood pressure of 120/60 mmHg, a heart rate of 80 /min, a respiration rate of 15 /min and SpO2 of 100% with an oxygen mask at 5 L/min. The patient was at slightly sedated status in response to verbal commands. After 30 minutes, hemiplegia (motor grade I) and aphasia were observed. Immediately, after checking the blood sugar level (170 mg/dl), brain computed tomography (CT) was taken for differential diagnosis of acute cerebral infarction and acute cerebral hemorrhage. The result of the brain CT shows no intracranial hemorrhage (). Diffusion brain magnetic resonance imaging shows two focal hyper acute infarcts in the left anterior frontal lobe and basal ganglia, respectively (). Brain magnetic resonance angiography shows a significant narrowing at the left A1 and M1 segment occlusion of the left middle cerebral artery superior division (). At first, we considered administering intravenous rtPA, but decided to perform IAMT instead due to the risk of hemorrhage in the immediate postoperative period. The patient was sedated with midazolam due to confused mental status. Thrombus at A1 and the M1 branch of the middle cerebral artery were removed successfully (). The IAMT procedure took about 50 minutes, and it was begun 3 hours and 30 minutes after detection of AIS symptoms. Motor grade was changed from I to II shortly after the procedure was finished. The patient was observed in the intensive care unit for 7 days and showed improved mental status and motor function. Follow up brain CT and transthoracic echocardiography were done, and there were no significant findings. After one month, the patient was discharged without sequelae.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [172.0, 'cm']}",67.74811,64.3607,71.13552,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 172.0 cm, which is 172.0 cm * 0.393701 in/cm = 67.71657 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.71657 (in inches) - 60) = 67.74811 kg.
Hence, the patient's IBW is 67.74811 kg."
3639,10,Ideal Body Weight,physical,decimal,pmc-7739010-1,Extracted,"We present the case of a 12-year-old male who came to our emergency department complaining of progressive visual loss and intermittent frontal headache of moderate intensity, not accompanied by photophobia or ocular pain.
Symptoms started 2 weeks before, and had a progressively worsening course over the next days. Associated symptoms included apathy, accentuated in the last 3 days, nausea and 2 episodes of vomiting. He had no history of migraine headaches or any recent illness or fever. His medical records showed several episodes of recurrent laryngitis in the past.
The general examination was within normal limits, except for the blood pressure, which was 140/ 102+ mmHg. His weight was 81 kg, height 170 cm and BMI 28 kg/ m2.
On clinical examination, BCVA was 20/ 120 in the right eye and 20/ 200 in the left eye. The patient also presented a mild red-green color vision defect. Non-contact tonometry indicated an IOP value of 20 mmHg in both eyes. The patient had normal function of the cranial nerves III, V, VI and VII bilaterally.
Slit-lamp examination revealed a normal appearance of the anterior segment in both eyes. On fundus examination, an anomalous optic disc was noted with similar aspect in both eyes. Abnormal findings consisted of an elevated and highly hyperemic optic disc with blurred margins and filling the optic disc cup. Moreover, retinal and choroidal folds were present. Vascular changes included venous congestion of arcuate and peripapillary vessels, flame-shaped hemorrhages, cotton wool spots and hard exudates (). Macular examination showed no apparent changes.
An Optical Coherence Tomography was performed in order to assess the degree of severity of retinal damage. Macular examination revealed deformation of the foveal contour in both eyes and increased retinal thickness due to the accumulation of intraretinal fluid (). On tomographic examination of the optic nerve, changes included an artefactual increase of the thickness of the retinal nerve fiber layer (RNFL), a blurred margin of the papilla and a significant decrease of the topographic parameters of the excavation.
Humphrey Visual Field Analyzer perimetry was attempted and showed a mean deviation of -13.37 dB in the right eye with enlargement of the blind spot and a dense nasal field defect. In the left eye, the mean deviation was -16.81 dB and also showed an enlargement of the blind spot and a dense nasal field defect (). Also, both eyes presented unpatterned reduction of the light sensitivity.
An immunologic screening demonstrated negative anti-nuclear antibodies and anti-dsDNA in normal limits. A serologic infectious screening was performed and was negative for HIV infection, borreliosis, cat scratch disease, listeriosis and toxoplasmosis.
When he presented to our clinic, the patient had already undergone an MRI that showed mild ventriculomegaly with no apparent obstacle in the drainage of CSF.
We suspected the diagnoses of idiopathic intracranial hypertension and referred the patient to a pediatric neurologist for further workup and management.
In the first day of hospitalization in the pediatric neurology department, the patient developed diplopia due to abducens nerve palsy.
Cerebral angio MRI showed: mild internal tetraventricular hydrocephalus, periventricular white matter macrostructure alteration, a complete configuration of the circle of Wills without any cerebral arteriovenous malformation, a selar and orbital region with normal MRI signal; hypoplasia of the right transverse sinus.
The patient was put on a low-calorie diet. Mannitol 150 mg/ ml for 10 days was initiated, associated with Dexamethasone 8 mg/ 2 ml injection for 10 days, the latter being subsequently switched to Methylprednisolone 16 mg for 4 days.
The neurologist performed a lumbar puncture that showed an elevated opening pressure of 25 mmHg (34 cm H2O) and thus confirmed the diagnosis of intracranial hypertension. Subsequently, Acetazolamide 250 mg was added to the treatment in progressive highly dosage, from 250 mg/ day to 1000 mg/ day.
After 14 days of hospitalization, the patient was discharged with the following treatment: Methylprednisolone, Acetazolamide and proton-pump inhibitors.
We reevaluated the patient after his hospital discharge. BCVA was significantly improved, 20/ 20 in both eyes and normal ocular motility in both eyes with no diplopia.
Slit-lamp examination revealed a normal appearance of the anterior segment in both eyes. On fundus examination, we identified a significant reduction of the papillary edema, blurred margins of the optic disc but no elevation of the disc head and hard exudates in the foveolar and parafoveolar area. Also, the vascular configuration and calibre improved ().
An Optical Coherence Tomography was performed to assess the degree of severity of retinal damage. Macular examination showed no subretinal liquid, retinal thickness returned to normal values and hard exudates (hyperreflective dots) were present in the macular area (). On tomographic examination of the optic nerve, the average thickness of the retinal nerve fiber layer (RNFL) in both eyes was still above normal limits, with slightly blurring of the optic disc margins ().
On visual field examination, a significant improvement was noted: a mean deviation of -8.97 dB in the right eye with normal blind spot size and the persistence of a nasal defect. In the left eye, the mean deviation was -7.57 dB with some residual nasal and temporal defects ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3640,10,Ideal Body Weight,physical,decimal,pmc-4339194-2,Extracted,"The second case (GS0155) is a 27-year-old female. She had had some episodes of right hemiparesis and a bowel volvulus in pediatric age. She was studied in the Neurology Unit after an episode of right hemiparesis, paresthesia and a visual field deficit. Imaging studies did not show any significant alteration. Biochemical analysis showed calcium values in the lower limit of normality (8.5–9.3mg/dl) and elevated PTH (200–300pg/ml), so she was diagnosed of pseudohypoparathyroidism. She did not present any symptom of Albright’s hereditary osteodystrophy (height 1.65m; weight 68.5kg; BMI: 25.1). No other hormone deficit was detected (TSH, 3μU/ml). She referred regular periods. Calcium and vitamin D supplements (both cholecalciferol and calcifediol) were prescribed, although she is not properly following the treatment.
In the last visit, she referred paresthesia in upper extremities with no calcium supplementation for a month. She brought a report with analytical levels: Ca, 8.7mg/dl; P, 3.9mg/dl; Mg, 2.4mg/dl, TSH, 4.15μU/ml; PTH, 349pg/dl; 25(OH)D, 37.2 ng/ml; urine Ca, 76mg/day; CLcr, 177ml/min; Dual-energy X-ray absorptiometry (DXA) with a lumbar T score of -0.7 SD and a femoral T score of -0.3 SD. She is clinically stable, with no symptoms of latent tetany. Biochemical analysis were performed: Ca, 8.9mg/dl; P, 3.7mg/dl; HbA1c 5.4%, PTH, 417pg/dl; 25(OH)D, 44 ng/ml.
Her mother was diagnosed at age 48 years with a multinodular toxic goitre. She was treated with I131 that caused iatrogenic hypothyroidism, so she was prescribed levothyroxine 125μg/day. Her past clinical history showed symptoms of generalized anxiety, being followed in the Mental Health Unit. She does not present any characteristic phenotype, with a normal physic exploration (height 1.64m; weight 70kg; BMI: 26).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.65, 'm']}",56.90952,54.06404,59.755,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.65 m, which is 1.65 m * 39.3701 in/m = 64.96066 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96066 (in inches) - 60) = 56.90952 kg.
Hence, the patient's IBW is 56.90952 kg."
3641,10,Ideal Body Weight,physical,decimal,pmc-6304601-1,Extracted,"A 41-year-old woman, gravida 2, para 1, was diagnosed with esophageal cancer relapse at 16 weeks of gestation. At the age of 40, before this spontaneous conception, she underwent preoperative chemotherapy, minimally invasive esophagectomy, and postoperative chemotherapy for esophageal squamous cell cancer, cStageII, pStageIV. Since the postoperative chemotherapy, she had been amenorrhoeic. Ten months after the operation, contrast enhanced computed tomography (CT) of the neck, chest, and abdominal to pelvis region was performed to investigate recurrence or metastasis, and it showed a pregnant uterus. She visited our obstetric clinic and was confirmed to be at 8 weeks of gestation. Because the estimated fetal exposure dose of the CT examination was less than 8 mGy, she wished to continue the pregnancy. At 16 weeks of gestation, the scheduled gastrointestinal endoscopy and biopsy revealed relapse of esophageal cancer in the residual esophagus (). The fluorine-18 fluorodeoxyglucose (18F-FDG) uptake of the local recurrence in the residual esophagus was elevated according to positron emission tomography (PET)/CT, and no metastatic lesion was detected. A multidisciplinary treatment team consisting of medical oncologists, radiation oncologists, surgeons, and obstetricians recommended that the patient terminate the pregnancy and receive CRT, which was the standard treatment for localized recurrent disease [, ]. However, the patient and her husband strongly desired to continue the pregnancy.
To examine the safety and feasibility of radiotherapy for this patient, the fetal dose was estimated by a simulation study before CRT. We created the irradiation plan for the patient () and delivered doses to the phantom (). According to the radiation dosage measured by five dosimeters, which ranged from 0.052 to 0.176 mGy in one irradiation fraction (), the fetal dose was estimated as 1.56 to 5.28 mGy, even after 60 Gy in 30 fractions of radiotherapy. The anticancer drugs, which would be administered together with the radiation, were cisplatin (CDDP) and 5-fluorouracil (5-FU). Taking these results, we concluded that CRT during pregnancy in this case would be acceptable and, after receiving written informed consent, started the treatment at 19 weeks of gestation.
The CRT consisted of 50.4 Gy in 28 fractions of radiation and four courses of chemotherapy (CDDP 60 mg/m2 on day 1, 5-FU 750 mg/m2 on days 1 to 4). shows the course of treatment over time. As supportive therapy, palonosetron and dexamethasone were administered. To assess the actual fetal dose of radiotherapy, we put dosimeters on the patient's abdomen at every irradiation session. Dosimeters showed that the estimated fetal dose ranged from 0.08 to 0.34 mGy in one irradiation fraction. Consequently, the multidisciplinary team confirmed the safety and feasibility of radiotherapy for this pregnant patient and fetus and completed the planned radiotherapy. After chemoradiotherapy, at 27 weeks of gestation, the recurrent lesion was decreased in size. Furthermore, gastrointestinal endoscopy at 31 weeks did not detect the recurrent lesion after the third course of chemotherapy. During this treatment, the myelosuppression was mild; grade 2 anemia, grade 1 neutrophil count decreased, and grade 1 platelet count decreased, according to Common Terminology Criteria for Adverse Events (CTCAE) Version 5.0. The patient had also pharyngitis, anorexia, and vomiting. Regarding body habitus, her height was 162 cm, and her weight was 51 kg before the esophagectomy. Then she had lost 6 kg and her body mass index was 17.5 by the time she got pregnant. Her weight gain was only 3.9 kg during pregnancy because of impaired oral intake due to gastric tube reconstruction as well as adverse effect of CRT such as anorexia. The fetal estimated body weight fluctuated between the 10th and 20th percentile. Fetal well-being was monitored using ultrasound and nonstress fetal heart rate testing, and no abnormal findings were detected. At 38 weeks and 3 days of gestation, she underwent cesarean section (due to previous cesarean section) and gave birth to a female baby weighing 2,480 g. Apgar scores were 7 at 1 minute and 8 at 5 minutes, and the pH of umbilical artery blood was 7.327. The baby did not have any congenital anomalies, and the clinical course was uneventful. Twelve months have passed since the cesarean section, the patient has been free of disease, and the growth of the infant has been satisfactory.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [162.0, 'cm']}",54.19299,51.48334,56.90264,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.77956 (in inches) - 60) = 54.19299 kg.
Hence, the patient's IBW is 54.19299 kg."
3642,10,Ideal Body Weight,physical,decimal,pmc-8488087-1,Extracted,"A 15-year-old female was referred to the cardiology clinic with tachycardia, murmur and known hyperthyroidism. She had been suffering from fatigue, heat intolerance and nonspecific myalgias for six months, and subsequently developed shortness of breath on exertion. Her past medical history was unremarkable and there was no known family history of AF.
On initial visit, her weight was 53.9 kg (57.6th percentile, +0.19 SDs) and height was 158.8 cm (31.9th percentile, -0.47 SDs). Heart rate was 148 beats per minute and irregular, with a blood pressure of 138/72 mmHg. The precordium was hyperdynamic with normal first and second heart sounds, and a gallop rhythm. There was a grade II/VI systolic regurgitant murmur audible at the left lower sternal border and over the apex. Her thyroid was moderately enlarged with no palpable nodules. There was no peripheral edema or hepatosplenomegaly.
An electrocardiogram (ECG) showed AF with an average ventricular rate of 141 beats per minute, with irregular conduction and left ventricular hypertrophy (). Laboratory studies revealed a TSH of 0.01mU/L, free T4 of 75.4 pmol/L, free T3 of >30.8 pmol/L, thyroperoxidase antibodies of 114 IU/mL, and TSH receptor antibody of 25 U/L. She had a normal complete blood count, electrolytes and renal function (). An echocardiogram revealed an enlarged left atrium, left ventricle (>6cm), moderate mitral regurgitation and mild mitral valve prolapse with low normal cardiac function ().
The patient had a transesophageal echocardiogram that demonstrated no thrombus in the left atrium. She underwent synchronized cardioversion as daycare procedure, and successfully reverted to normal sinus rhythm at a rate of 90 beats per minute (). Warfarin was started post cardioversion and anticoagulation was discontinued after evidence of persistent sinus rhythm. Low dose aspirin was added as part of our institutional practice to use aspirin for patients with AF at low risk of an embolic event. Her medical management included methimazole at a dose of 0.5 mg/kg/day and bisoprolol 2.5mg once daily. A euthyroid state was achieved, and AF did not recur. She was seen in follow-up clinic in a week, a month, 6 months and 1 year period. She continued to be in sinus rhythm. Bisoprolol was discontinued 4 months after her initial presentation.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.8, 'cm']}",51.29536,48.73059,53.86013,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.8 cm, which is 158.8 cm * 0.393701 in/cm = 62.51972 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.51972 (in inches) - 60) = 51.29536 kg.
Hence, the patient's IBW is 51.29536 kg."
3643,10,Ideal Body Weight,physical,decimal,pmc-3591569-1,Extracted,"A 59-year-old, 74 kg, 165 cm, female was presented with a non-ST segment elevation myocardial infarction. Preoperative echocardiography findings included an ejection fraction (EF) of 50%, tight aortic valve stenosis, peak systolic gradient across the aortic valve of 45 mm Hg, trivial aortic regurgitation, no detected wall motions abnormalities, and normal right ventricular (RV) diameters. Cardiac catheterization showed two-vessel disease and fair left ventricular (LV) function. She was treated with clopidogrel, aspirin, captopril, bisoprolol, and intravenous infusions of heparin and nitroglycerin. She underwent an urgent bypass grafting for the left-anterior descending (LAD), diagonal and right coronary arteries (RCA), and prosthetic replacement of the aortic valve under the standardized target-controlled (TCI) propofol-sufentanil anesthesia and cisatracurium infusion.[] After heparinization, aortic cannulation was performed. It resulted in an abrupt decreases of RE and SE values from 49 and 46, respectively, to isoelectric silence. Transoesophageal echocardiogram (TOE) failed to detect aortic intraluminal thrombi and plaques. Target effect site concentrations (Ce) of propofol and sufentanil were lowered to 1 and 0.1 μg/mL, respectively, and continued till the end of surgery. Mild hypothermic cardiopulmonary bypass (CPB) was used. The cross-clamp time was 148 min and the CPB time was 289 min.
Isoelectric silence persisted till the end of reperfusion time. Then, gradual increases in RE and SE toward the low 30 s levels were noted and they persisted till the transfer of the patient to the intensive care unit (ICU).
The patient was subsequently successfully separated from CPB with intravenous epinephrine (7 μg/min). The cisatracurium, sufentanil, and propofol infusions were discontinued after surgical homeostasis, sternal closure, and skin closure, respectively.[]
Mean arterial and central venous blood pressures (MAP and CVP, respectively), arterial oxygen saturation (SaO2), normocapnia, and euglycemia were well maintained throughout the perioperative period. Rectal temperature >36°C was maintained before and after the CPB.
Postoperative ventilation was performed with synchronized intermittent mandatory (SIMV). Mediastinal bleeding of 750 mL during the first three postoperative hours was treated with transfusion of two U-packed red blood cells, five U platelets, and three U fresh frozen plasma. Unfortunately, the lady did not wake up even 8 h after the discontinuation of anesthetics. After that, she showed agitation and left-sided paresis. Brain CT showed a nonhemorrhagic right tempro-parietal infarction. Dexmedetomidine infusion was used to alleviate her agitation. Her consciousness was recovered and her trachea was extubated on the second postoperative day.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3644,10,Ideal Body Weight,physical,decimal,pmc-7673968-1,Extracted,"A 71-year-old man was admitted to our hospital with chief complaints of abdominal pain and vomiting.
A 71-year-old man was on treatment for chronic hepatitis B for 22 years when he was diagnosed with HCC. He was noted to have tumor nodules of size 20 mm in diameter, located in segment 8, on a follow-up abdominal computed tomography (CT) (Figure ) and had undergone partial liver resection 7 years previously. Based on the 8th Union for International Cancer Control classification of HCC, the tumor was classified as pT1N0M0 stage 1. Seven months after the first surgery, abdominal CT revealed recurrent HCC with nodules 10 mm in diameter, in segment 6 of the liver (Figure ). When laparotomy was performed, a peritoneal mass was found that was not apparent preoperatively; therefore, partial liver resection and peritoneal tumor resection were performed (Figure and ). The peritoneal tumor with peritoneal metastasis of HCC was diagnosed based on histopathological findings. Fourteen months after the first surgery, abdominal CT revealed a tumor nodule 32 mm in diameter in the pelvis, which was diagnosed as a peritoneal recurrence of HCC (Figure ). We determined that the recurrent tumor was solitary and decided to perform tumor resection. However, many small peritoneal nodules were found at the time of laparotomy, and radical resection was impossible (Figure ). Subsequently, the patient was followed up by the department of gastroenterology of our hospital, and 16 mo after the initial resection of HCC, administration of sorafenib of 400 mg/d was started. Since he developed a grade 2 hand-foot syndrome, the dosage was reduced to 200 mg/d. The administration was continued for 54 mo without any other major adverse events, and the disease was well controlled. Seventy months after the first surgery, he was admitted to our hospital with chief complaints of abdominal pain and vomiting.
The patient’s history was significant for extensive gastrectomy for duodenal ulcer at the age of 22 years. In addition, he had a history of hypertension since the age of 65, for which he was on treatment with amlodipine besilate (10 mg/d) and azilsartan (20 mg/d).
The patient’s social history consisted of a 40-pack year history and an alcohol intake of 350 mL beer per day. He had discontinued smoking and drinking alcohol 10 years previously. There was no history of cancer or liver disease in his family.
The height and weight of the patient at admission were 172 cm and 52 kg, respectively. There were no abnormalities in the vital signs. The abdomen was soft and slightly swollen. Tenderness was noted in the right lower abdomen.
No abnormal findings were found other than a high C-reactive protein level (4.95 mg/dL) in blood biochemical tests. Liver function tests revealed a class A Child-Pugh score.
Abdominal contrast-enhanced CT revealed a well-defined, rounded, enhancing endoluminal tumor in the small intestine, leading to intussusception and small bowel obstruction (Figure ). An ileus tube was inserted to decompress the small intestine.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [172.0, 'cm']}",67.74811,64.3607,71.13552,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 172.0 cm, which is 172.0 cm * 0.393701 in/cm = 67.71657 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.71657 (in inches) - 60) = 67.74811 kg.
Hence, the patient's IBW is 67.74811 kg."
3645,10,Ideal Body Weight,physical,decimal,pmc-5069927-1,Extracted,"A 39-year-old Japanese man visited our hospital with a 3-day history of mild headache, shoulder stiffness, and a feeling of dizziness. As the headache was only slight, he was able to remember what he was doing when the headache first developed. The patient was able to live a normal daily life prior to visiting our hospital with his symptoms. An initial examination on first presentation revealed that the patient was 170.0 cm in height, weighed 69.0 kg, and had a body mass index of 23.9. His blood pressure was 152/80 mmHg, with a regular pulse rate of 46 beats/min, and his body temperature was 35.9 °C. Physical examination revealed mild stiffness in the neck. No neurological findings were evident, and the patient’s laboratory data were normal. CT did not show any obvious abnormalities indicating hemorrhage or infraction. However, the Sylvian fissures were not clearly visible bilaterally due isoattenuating SAH in the Sylvian fissures (slightly hyperattenuating on the left) (Fig. ). Interestingly, the patient had visited our hospital 2 years ago complaining of occipital headache, nausea, and vomiting. At that time, CT was performed, which showed no abnormalities but provides useful normal comparison images (Fig. ). Another finding worth mentioning on Fig. was mild hydrocephalus - seen as enlargement of the third ventricle - again, in comparison to the previous CT (Fig. ). Consequently, he was diagnosed with a tension headache. Comparing the current CT images to those from his previous visit, we observed a clear difference in the sulcus in the cerebral cortex, which appeared to be narrower and was accompanied by cerebral edema. In addition, Fig. is at the level of the midbrain (mesencephalon) that traverses the infundibulum of third ventricle, interpeduncular cistern, there appears to be hyperattenuating blood in the medial portion of the left Sylvian fissure and extending into the anterior interhemispheric fissure, and shows mild dilation of the temporal horns of the lateral ventricles (looks like a moustache). In addition, the suprasellar cistern seem on this slice is filled with isoattenuating blood (evident in comparison with the normal Fig. ). In the center of the suprasellar cistern is cerebrospinal fluid (CSF) that is hypoattenuating in the dilated infundibulum of the third ventricle. These CT findings become clear in comparison to the previous CT (Fig. ). Thus, we suspected SAH, although the patient’s CT did not show obvious signs of SAH (Fig. ). Next, CT angiography (CTA) revealed an aneurysm between A1 and A2 of the left anterior cerebral artery (Fig. ). The patient received emergency neurosurgical clipping. He progressed after surgery without developing the initial complications and was discharged from our hospital without sequela.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3646,10,Ideal Body Weight,physical,decimal,usmle-6918,Extracted,"A 57-year-old man presents for a regular check-up. He does not have any complaints at the time of presentation. He has a history of several episodes of acute non-necrotizing pancreatitis with the last episode being 2 years ago. Also, he was diagnosed with hypertension 5 years ago. Currently, he takes aspirin, atorvastatin, enalapril, and indapamide. He plays tennis twice a week, does low impact cardio workouts 3 times a week, and follows a low-fat diet. He smokes half a pack of cigarettes per day and refuses to quit smoking. The patient’s blood pressure is 140/85 mm Hg, heart rate is 88/min, respiratory rate is 14/min, and temperature is 36.6°C (97.9°F). His height is 181 cm (5 ft 11 in), weight is 99 kg (218 lb), and BMI is 30.8 kg/m2. Physical examination reveals multiple xanthomas on the patient’s trunk, elbows, and knees. Heart sounds are diminished with fixed splitting of S2 and an increased aortic component. The rest of the examination is unremarkable.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [181.0, 'cm']}",75.89772,72.10283,79.69261,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 181.0 cm, which is 181.0 cm * 0.393701 in/cm = 71.25988 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (71.25988 (in inches) - 60) = 75.89772 kg.
Hence, the patient's IBW is 75.89772 kg."
3647,10,Ideal Body Weight,physical,decimal,pmc-4900239-1,Extracted,"A 17-year-old adolescent boy with Jeune syndrome underwent spinal correction. He was born abroad and immigrated to Japan when he was 5 months old. He survived infancy, although he was diagnosed with Jeune syndrome as the cause of thoracic deformity, renal dysfunction, and urinary tract abnormality at 11 months old at a university hospital. His renal condition became worse with age. He underwent a renal transplant to treat chronic renal failure at 10 years old. Although it was not clear when his spinal deformity was discovered, he had received no treatment until after he entered junior high school. He was treated with a brace at 14 years old. However, he disliked the brace and discontinued using it within a few months. His spinal deformity progressed and he was referred to our university hospital to treat scoliosis at the age of 16 years. He did not have any restriction of daily life at that time, but was worried about his trunk deformity.
He was 160 cm (−1.9 SD), 50 kg, and thus his body mass index (BMI) was 18.5 kg/m2. Physical findings were imbalance of his shoulder and waist lines, a prominent right scapula and rib hump, and left lumbar hump (Fig. ). He did not have obvious short stature or a small chest. We could not find any other abnormalities except for hypacusia. He had a scar in the center of his abdomen that was made when he received the renal transplant. The result of arterial blood gas analysis was almost normal and respiratory functional data showed moderately restrictive impairment of ventilation (vital capacity (VC) 2.25 L, %VC 54.4 %, and forced expiratory volume in 1 second (FEV1) 100 % predicted). A peripheral blood sample was obtained and all laboratory data were normal including renal function.
His total spine radiograph showed double major curves when we first saw him. The posterior–anterior total spine radiograph showed a coronal Cobb angle of 70° (T4–L2), 82° (T12–L3), and Risser grade V. A lateral total spine radiograph showed an 81° thoracolumbar kyphosis (T9–L3) and 10° thoracic lordosis (T5–L2) (Fig. ). We considered that he had indications for surgical treatment. We classified his spinal deformity as Lenke type 6C [] and planned the fusion area and surgical strategy. The risks and benefits of spinal correction were explained and informed consent was obtained from the patient and his family.
Sufficient attention was paid to avoid compressing his transplanted kidney, which was placed around the right lower abdomen and to maintain sufficient flow though the kidney when he was fixed in a prone position. The fusion area was from T4 to L4, using pedicle screws, hooks, and sublaminar wirings as anchors. Ponte osteotomy was added from T12 to L2 to correct the kyphotic deformity. Before wound closing, autogenous bone grafting was performed. There were no intraoperative complications associated with respiratory dysfunction or the transplanted kidney. Cobb angles were corrected by 49 % to 36° (T4–T12) and 42° (T12–L3), respectively. Thoracolumbar kyphosis was corrected by 63 % to 30° (T9–L3).
Our patient could be extubated immediately after wound closure and did not need to be treated at an intensive care unit (ICU). Oxygen supply was administered routinely for a single overnight period and respiratory dysfunction was not identified in the postoperative period. Sufficient perfusion ensured no circulatory failure of the transplanted kidney occurred. He was discharged 25 days postoperatively. His most recent radiographs at 2 years after surgery showed Cobb angles of 40° (T4–12), and 42° (T12–L3), and correction losses were 4° and 0° respectively. A lateral whole spine radiograph also showed thoracic lordosis was 5° and thoracolumbar kyphosis was 28° (Fig. ). A respiratory function test was performed at one year after surgery, showing VC 2.47 L, %VC 55.7 %, and FEV1 95.9 %. There were no other complications, including surgical site infection, within 2 years of surgery. The patient and his family were thoroughly satisfied with his treatment, including the surgery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [160.0, 'cm']}",56.88197,54.03787,59.72607,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.99216 (in inches) - 60) = 56.88197 kg.
Hence, the patient's IBW is 56.88197 kg."
3648,10,Ideal Body Weight,physical,decimal,pmc-8632216-1,Extracted,"A 52 year-old woman visited our hospital complaining of vertigo without neurological deficit. She had a height of 157cm and a weigh of 61kg. She did not have an abnormal appearance of the face or tongue. She was taking levothyroxine sodium 300 µg/2x and simvastatin 10 mg/2x for hypothyroidism and dyslipidemia. Laboratory analysis revealed a carcinoembyronic antigen, level of 73.4 ng/mL (normal: <5.0 ng/mL); a calcitonin level of 1074 pg/mL (normal: 15-86 pg/mL); an adrenaline level of 107 pg/mL (normal <120 pg/ml); noradrenalin, 1154 pg/mL (normal: 60-500 pg/mL); and a dopamine level of 36 pg/mL (normal: <30pg/mL). All other blood cell counts and serum biochemistry parameters were normal. Magnetic resonance angiography (MRA) revealed bilateral supraclinoid stenosis of the internal carotid artery and abnormal moyamoya-like vessels around the basal ganglion () but MRI FLAIR () and DWI () showed no specific ischemic or hemorrhagic lesions in the brain. SPECT showed no hypoperfusion or laterality (); using genomic DNA samples from the patients, we evaluated the polymorphism in c.14576G>A in the RNF213, a susceptibility gene for moyamoya disease, and the results showed a heterozygous variant of the RNF213.
The patient was diagnosed with stage T2N1M0 MTC at another hospital at age 23; the condition was managed surgically with total thyroidectomy and left central neck D2a dissection. At age 41, she was diagnosed with left-sided pheochromocytoma (PHEO) at our hospital, for which she underwent surgery. No postoperative recurrence of the left adrenal lesion was observed, and the right adrenal lesion was unchanged and showed 123I-MIBG accumulation. ()
Genetic testing, performed after she provided informed consent, revealed heterozygosity for a mutation at codon 634 in exon 11 (TGC-TTC mutation; p.Cys634Phe) of the RET gene. The patient’s mother underwent thyroid surgery and bilateral pheochromocytomas were observed. MEN2A patients are on the maternal side, but not on the paternal side. Moyamoya disease and stroke patients are neither on the paternal side nor the maternal side. The pedigree chart is shown in . There was a possibility that certain family members of the patient could not develop the moyamoya disease; however, this could not be confirmed because screening tests, such as MRA, were unavailable. On the basis of genetic analyses, imaging findings, and a history of clonal presence of multiple endocrine neoplasia type 2A (MEN2A; OMIM # 171400), MEN2A with moyamoya syndrome was diagnosed.
After 7 years, MRA revealed bilateral supraclinoid stenosis of the internal carotid artery as observed previously; however, right PCA blood flow decreased. () MRI FLAIR showed an increase in ischemic lesions in the bilateral hemiparesis. () MRI DWI showed new ischemic lesions in the right hemiparesis. () SPECT showed progressive hypoperfusion in the right hemiparesis (). Laboratory analysis revealed a carcinoembyronic antigen, level of 105.8 ng/mL (normal: <5.0 ng/mL); a calcitonin level of 440.7 pg/mL (normal: 15-86 pg/mL); an adrenaline level of 210 pg/mL (normal <120 pg/ml); noradrenalin, 1010 pg/mL (normal: 60-500 pg/mL); and a dopamine level of 18 pg/mL (normal: <30 pg/mL). All other blood cell counts and serum biochemistry parameters were normal. 123I-MIBG accumulation showed no changing compared to 7 years ago. () We planned STA-MCA bypass; however, it is pending because of the Corona virus disease 19 pandemic.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [157.0, 'cm']}",49.66544,47.18217,52.14871,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 157.0 cm, which is 157.0 cm * 0.393701 in/cm = 61.81106 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.81106 (in inches) - 60) = 49.66544 kg.
Hence, the patient's IBW is 49.66544 kg."
3649,10,Ideal Body Weight,physical,decimal,pmc-3598892-1,Extracted,"A 30 year old male patient having height of 180 cm and weight of 70 kg (Body Mass Index 21.6) presented to the emergency department of Civil Hospital Karachi with the complaint of a penetrating injury at the left side of upper torso. The patient was lying comfortably with no symptoms of respiratory distress or any obvious active bleeding. Vitally the patient was stable. There was slight blood staining of the upper garment with an obvious breach.
On examination a 1 cm × 1 cm entry wound at the left 3rd intercostal space in the mid clavicular line was identified. The chest and abdomen were otherwise unremarkable. Normal vesicular breathing was appreciated on chest auscultation. On palpation the abdomen was soft with no peritoneal signs.
Chest radiograph demonstrated clear lung fields with no indication of injury. The abdominal radiographs (Figures and ) displayed a bullet in the upper left quadrant of the abdomen lateral to spine. The radiographs were otherwise unremarkable for any other abnormality.
With this evidence of the bullets entry at 3rd intercostal space laterally to the mid clavicular line and its lodgment in the abdomen just lateral to the spine, the bullets trajectory was estimated to have encountered the left lung, left dome of the diaphragm, stomach, left lobe of the liver, splenic vessels, body of the pancreas and the left kidney. Despite this trajectory, the patient was clinically stable with no signs of either respiratory distress or any other visceral injury. An urgent CT scan was advised to identify any serious damage as was being predicted on the basis of the estimated trajectory.
The CT scan (Figure ) showed that the bullet was lying postero medially to the left kidney just lateral to the spine. All thoracic, intra peritoneal and retroperitoneal visceral structures were identified to be normal with no injury.
As the patient remained clinically and vitally stable with there being clear evidence of all visceral structures being unharmed from the bullet, the patient was admitted for nonoperative management and observation. Patients’ hemoglobin (Hb) concentration and other baseline investigations were performed on admission and subsequently after every 24 h. There was no drop in the Hb from the initial measurement of 12.5 mg/dl. Serial clinical examinations were performed that remained negative for any peritoneal signs, visceral damage or respiratory distress. The patient was therefore discharged after 48 h of observation.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [180.0, 'cm']}",74.99221,71.2426,78.74182,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 180.0 cm, which is 180.0 cm * 0.393701 in/cm = 70.86618 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.86618 (in inches) - 60) = 74.99221 kg.
Hence, the patient's IBW is 74.99221 kg."
3650,10,Ideal Body Weight,physical,decimal,pmc-4323070-1,Extracted,"A 15-year-old Chinese boy presented with a bilateral and symmetrical painful eruption on the upper abdomen of 7 days' duration. The eruption was preceded by a 2-day history of malaise and low grade fever. He did not have the varicella vaccine but had chickenpox at 3 years of age. His past health was otherwise unremarkable. In particular, he did not have recurrent or chronic infections. The patient did not have recent weight loss and was not on any medications. There was no history of recent travel. He did not have exposure to venereal or other infectious diseases. The family history was noncontributory.
Physical examination revealed multiple vesicles/bullae on an erythematous base, distributed bilaterally and symmetrically in a band-like distribution along T7, T8, and T9 dermatomes (). The rest of the physical examination was unremarkable. His weight was 76 kg (90th percentile) and height 178 cm (70th percentile). His vital signs were normal and he was not in distress. There was no lymphadenopathy in the axillary or groin area, no organomegaly, and no muscle wasting.
Laboratory investigations revealed hemoglobin of 12.8 g/dL and white blood cell count of 7.8 × 109/L with a normal differential count. His immunoglobulin levels were normal. The patient was treated with acyclovir 800 mg five times a day for 7 days. The blistering and discomfort resolved in 14 days, and the secondary dyspigmentation took 3 months to completely fade.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [178.0, 'cm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3651,10,Ideal Body Weight,physical,decimal,pmc-8601284-1,Extracted,"A 48-year-old woman visited the referral university hospital to jaundice and nausea. She was referred to the outpatient clinic of gastroenterology department in a tertiary hospital due to jaundice and increased levels of liver enzyme detected during blood test tracking after 5 weeks of pazopanib therapy.
The patient's medical history included end-stage renal disease on hemodialysis, liver cirrhosis with hepatitis B virus carrier. The patient underwent right nephrectomy for RCC 2 years ago. Newly onset liver and lung metastasis were detected 3 months ago by liver biopsy. The patient started taking immunotherapy agent (pazopanib) and prophylactic antiviral agent (tenofovir disoproxil fumarate) from 2 months ago. Pazopanib prescribe was started at half dose considering the patient's clinical history of liver cirrhosis. After administration at 400 mg per day, which is half the dose for 2 weeks, liver enzyme level was kept in the normal range and showed no change, so the dosage was increased to a fixed amount of 800 mg per day and dosing was maintained for an additional 2 weeks.
Before first visiting the outpatient clinic, the patient had symptoms of nausea with vomiting and jaundice for 2 weeks. The patient was suspected to progress acute hepatitis considering jaundice and increased liver enzyme. Elevated serum total bilirubin persisted 2 weeks after pazopanib discontinuation and she was hospitalized for further evaluation and treatment.
At the time of admission, she was 160.5 cm tall, weighed 61.1 kg, and had a body mass index (BMI) of 23.72. Blood pressure of the patient was normal with a systolic blood pressure of 123 mm Hg and a diastolic blood pressure of 74 mm Hg. Mild elevated body temperature (37.8 °C) and normal heart rate (95 bpm) with normal breathing rate (18 breaths per minute) was seen. The patient presented with nausea and jaundice. The patient had a soft abdomen on physical examination.
Liver-function test at baseline shows no abnormal findings measured before pazopanib treatment and 2 weeks after the start of treatment. However, blood tests measured 5 weeks after the start of treatment revealed abnormal findings in liver function. At the time 5 weeks after starting treatment of pazopanib, levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) were 306, 427, and 227 U/L, respectively. Prothrombin time-international normalized ratio value was in normal range (0.99). The total bilirubin level was 1.98 mg/dL (Fig. ). Alpha-fetoprotein (AFP) level was 6.1 ng/mL with in normal range. The blood test results related to hepatitis virus infection are as follows, hepatitis B surface antigen (positive); anti-HBs (negative); hepatitis B e antigen (negative); anti-HBe (positive); hepatitis B virus DNA (120 copies/mL); anti-hepatitis C virus (negative). Child-Pugh score and class were 5 points and class A. The model for end-stage liver disease (MELD) score was 20 points and estimated 3-month mortality was 19.6%.
Contrast-enhanced abdominal computed tomography (CT) revealed liver cirrhosis and there was no significant change of about 1.3 cm sized enhancing hepatic nodule on right lobe which is pathologically proven metastatic RCC. There was no obstructive lesion on biliary tract (Fig. ). Abdominal ultrasound also revealed no significant abnormality other than hepatic nodule and liver cirrhosis.
There was a clinical possibility of DILI caused by pazopanib, and the Roussel Uclaf Causality Assessment Method (RUCAM) score was used to evaluate the possibility of the disease. The patient was of the mixed type. Symptoms started appearing 5 weeks after administration (+2). Total bilirubin, AST, and ALT were normalized within 180 days of the cessation of drug administration (+2). There were no risk factors such as alcohol, pregnancy, and the elderly over 55 years of age (0). Although tenofovir was taken as a concomitant drug, the possibility of hepatotoxicity by the drug was low, and the time interval was not consistent with the onset of symptoms (0). There were no acute viral hepatitis, bile duct obstruction, alcoholism, or recent hypotension that could cause liver damage other than drugs (+2). Pazopanib, which was taken, is a drug with a warning of hepatotoxicity on the product according to previous studies (+2). The possibility of DILI can be known more clearly through re-administration of the drug, but re-administration was not performed in this patient (0). Taking these factors into consideration, the patient's RUCAM score was 8 points, and it was in the probable group corresponding to 6 to 8 points, so the possibility of DILI was high. At the beginning of the clinical course, it was unknown whether there will be any improvement after the cessation of drug administration, so even if this score factor (course-change after stopping drug) was excluded, the RUCAM score was already 6 points, indicating a high possibility of DILI, so treatment for pazopanib-induced DILI was initiated.
Finally, for confirmatory diagnosis, liver biopsy was performed to establish the cause of jaundice. Liver biopsy revealed hepatocyte swelling and degeneration with cholestasis in centrilobular area and the protal tract showed only sparse chronic inflammation. The final diagnosis was confirmed as acute cholestatic hepatitis consistent with toxic hepatitis (Fig. ). Therefore, the patient was diagnosed with severe DILI due to pazopanib.
The patient started to take prednisolone 40 mg daily for 1 week for empirical treatment of DILI. The dose of prednisolone was gradually reduced every 1 week and it was discontinued finally after 7 weeks of dosing. After discontinuation of pazopanib and taking empirical steroid treatment, the patient's AST and ALT levels were maintained within the normal range and total bilirubin level was decreased significantly from the peak level of 24.61 to 1.06 mg/dL on 12-weeks after pazopanib discontinuation (Fig. ). After discontinuation of pazopanib treatment, jaundice improved rapidly and the patient is currently being observed in the outpatient clinic.
The study protocol was approved by the Institutional Review Board of Soonchunhyang University Bucheon Hospital, and conformed to the ethical guidelines of the World Medical Association Declaration of Helsinki. Written informed consent was obtained because of the retrospective design.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.5, 'cm']}",52.83472,50.19298,55.47646,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.5 cm, which is 160.5 cm * 0.393701 in/cm = 63.18901 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.18901 (in inches) - 60) = 52.83472 kg.
Hence, the patient's IBW is 52.83472 kg."
3652,10,Ideal Body Weight,physical,decimal,pmc-7868318-1,Extracted,"A 27-year-old, non-smoking, 197 cm tall, 118 kg weight male patient presented himself at an external medical practice with symptoms including cough and right-sided, thoracic pain. His past medical history was uneventful. Next to signs of gigantism, the physical examination determined weak breath sounds of the right lung. Furthermore, the patient suffered from augmentation of the facial configurations, large extremities with oversized hands and feet, with no correlation to the height of his parents. Even though laboratory investigations showed normal results, growth hormone levels were found to be massively elevated: 27.6 µg/l (normal 0.1–4.1 µg/l).
A subsequent CT scan revealed a huge tumor in the right lower lobe accompanied with calcifications as well as moderate pleural effusion (Fig. ). The tumor seems to invade all 3 lobes of the right lung, the posterior wall of the right main bronchus, both the upper and lower lung veins, as well as the right main pulmonary artery after the origin of the upper arterial trunk (Fig. ). Body plethysmography showed FEV1 of 85% and VC of 90%. Bronchoscopic examination showed complete obstruction of the right intermediate bronchus; however, the endobronchial biopsy showed no diagnosis. Therefore, we decided to perform a surgical biopsy. The exploration showed a huge, solid tumor, mainly located within the lower lobe, but infiltrating the middle lobe as well as two more segments of the upper lobe. Further exploration showed adherence of the tumor on the posterior wall of the right main bronchus, obliteration of the right lower lung vein and near total obliteration of the middle and upper lung veins. A frozen section revealed a TPCT. In this situation, right pneumonectomy with systematic mediastinal lymph node dissection was performed though prolongation of the small incision to an antero-lateral thoracotomy. In fact, the tumor measured 20 × 13 cm in diameter (Fig. a). The histopathological work-up showed tumor invasion of all three lobes of the right lung and confirmed the invasion of the posterior wall of the right main bronchus, the lower, middle as well as the upper lung veins. There were thick adhesions not only in the fissure but also to the chest wall and the diaphragm. In the para vertebral region, local pleurectomy was done because of thick adhesions between the parietal pleura and the lower lobe. Systematic lymph node dissection was done with removal of the paratracheal lymph nodes, the infracarinal, the hilar as well as the paraoesophageal lymph nodes.
Histological specimen revealed typical carcinoid tumor with peripheral calcification indicating slow growing behavior (Fig. b). Fortunately, no hilar or mediastinal lymph node metastases were detected. Furthermore, the tissue was analyzed immunohistochemically revealing a positive reaction for AE1/AE3 and synaptophysin; however, low proliferation antigen (1% in the cell nucleus) Ki67 (MIB 1) was revealed. Further, mitosis activity was seen in 0–1/2 mm2 (Fig. ). Further testing determined negative reaction for chromogranin A. All these findings are characteristics for diagnosis of TPCT. According to WHO classifications in 1997, pathological tumor staging indicates in this case pT2, pN0, M0 (stage IB); whereas the WHO’s classification 2017 indicates pT4, pN0, M0 (stage IIIA).
The postoperative follow-up was uneventful. Growth hormone returned to normal levels (3.0 µg/l) within few days after surgery. The patient was discharged on the 11th postoperative day in an excellent physical condition. To date, the patient is recurrence-free and under follow-up (2- and 5- and 10-year follow-up was done performing CT scans).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [197.0, 'cm']}",90.38593,85.86663,94.90523,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 197.0 cm, which is 197.0 cm * 0.393701 in/cm = 77.5591 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (77.5591 (in inches) - 60) = 90.38593 kg.
Hence, the patient's IBW is 90.38593 kg."
3653,10,Ideal Body Weight,physical,decimal,pmc-3366317-1,Extracted,"A 48-year-old woman 155 cm tall weighing 30 kg, with cystic fibrosis had surgery planned for single lung transplantation. Twenty-years earlier, she was diagnosed with cystic fibrosis. She needed right lung transplantation because of progressive dyspnea and recurrent respiratory infection after left pneumonectomy, which was due to a huge aspergilloma in the upper lobe of the left lung 5 years before her visit to our hospital. There was nothing particular about her case except for her lung disease and her vital signs and laboratory workup were normal before surgery. In addition, arterial blood gas analysis (pH 7.35, PaCO2 51.8 mmHg, PaO2 74.6 mmHg, HCO3- 28 mEq/L, BE 1.3 mEq/L, SaO2 94.2%) showed mild respiratory acidosis. Results of the echocardiography before surgery showed a left ventricular ejection fraction of 69%, an enlargement of the right atrium and ventricle, a mild tricuspid regurgitation, severe pulmonary hypertension, and minimal pericardial effusion. The donor was a patient with traumatic SAH and SDH and was fit for donating a lung based of their medical history and laboratory workup.
The cystic fibrosis patient had an enlargement of the right thorax and a left mediastinal shift (organs such as trachea, heart, aorta, vena cava etc.) as a result of the past left pneumonectomy, and it caused an abnormal positioning, twisting, and narrowing of the subclavian vein and internal jugular vein; therefore, a 9 Fr. central vein catheter (advanced venous access, AVA high flow device, Edwards LifeSciences, USA) was inserted into the internal jugular vein under angiography in the angiography room because of difficulty in performing the catheter insertion and due to the risk of vascular perforation ().
The patient arrived at the operating room and was administered oxygen 5 L/min by nasal cannula. Additionally, noninvasive BP monitoring, electrocardiography, and pulse oxymetry was immediately done after arriving at the operating room, and a BIS monitor was attached and a monitor was connected to the right radial artery catheter and a femoral artery catheter. Before putting the patient under anesthesia, her measured vital signs were a BP of 115/78 mmHg, a HR of 85 beats/min, and a SaO2 of 95%. To induce anesthesia, 6 mg of etomidate and 5 mg of vecuronium were injected and an internal diameter 7.0mm tracheal tube was inserted after manual ventilation with 100% oxygen. The ventilator was set to a FiO2 of 0.5, a PEEP of 5 cmH2O, a RR of 10 breaths/min and a TV of 350 ml using the volume-controlled mode. After that, through the center vein catheter, which was inserted into the right internal jugular vein, a 7 Fr. pulmonary artery catheter (Swan-Ganz CCOmbo catheter, Edwards LifeSciences, USA) was inserted into the central pulmonary artery, and at that time, the pulmonary artery pressure was 61/26 mmHg. To maintain anesthesia, 3.5 µg/ml of propofol and 3.0 ng/ml of remifentanil with target-controlled infusion were consistently injected and the injection speed of these anesthetics was controlled according to the change in vital signs, and cell saver was used during the surgery.
After positioning the patient in the supine position with both arms elevated, the surgery started with a clamshell incision. First of all, before the pneumonectomy, by inserting a catheter into the aorta and the right atrium, cardiopulmonary bypass was done during surgery to not only prevent unstable vital signs due to severe pulmonary hypertension and profuse bleeding caused by severe adhesion of the right lung as a result of recurring infection but also to oxygenize the blood after the pneumonectomy. Before the cardiopulmonary bypass was started, 10,000 units of heparin were injected, and 3 minutes later, the activated coagulation time was 450-seconds. After starting the cardiopulmonary bypass, the ventilator was taken off and 1,000 mg of methylprednisolone were injected after the pneumonectomy. Thereafter, immediately, the bronchus, pulmonary artery, and vein of the transplanted lung were anastomosed to the patient. At some point, blood pressure dropped 80/45 mmHg because of bleeding or pressing of the intramediastinal structure, but it was relatively stable maintaining a blood pressure of more than 100/50 mmHg and SaO2 of 100%. The ischemic time of the right lung was 75-minutes.
Anastomosis of each organ was done well and reperfusion was attempted after pulmonary vein anastomosis. To reduce increased pulmonary artery pressure and prevent reperfusion injury, a weaning off of the cardiopulmonary bypass was attempted after setting the FiO2 to 0.4, the PEEP to 5 cmH2O, the RR to 14 breaths/min, the TV to 300 ml, and the nitric oxide (NO) to 20 ppm by the volume-controlled mode connected to a prepared NO ventilator. The results of the arterial blood gas analyses after connecting the NO ventilator were stable showing a pH of 7.48, a PaCO2 of 41 mmHg, a PaO2 of 449 mmHg, a HCO3- of 30.5 mEq/L, a BE of 6.4 mEq/L, and a SaO2 of 100%. The results of the arterial blood gas analyses after weaning off of the cardiopulmonary bypass was a pH of 7.42, a PaCO2 of 47 mmHg, a PaO2 of 89 mmHg, a HCO3- of 30.5 mEq/L, a BE of 5.2 mEq/L, and a SaO2 of 97%; therefore, a FiO2 of 1.0 was maintained. presents the results of the arterial blood gas analyses during the surgery.
The blood pressure decreased to 75/40 mmHg during the process of reducing the flow to gradually wean the patient off the cardiopulmonary bypass; thus, fluids were injected into her body, and 10 mcg/kg/min and 0.02 mcg/kg/min of dopamine and epinephrine, respectively, were consistently injected. After that, the surgery was completed with no complications and the patient was transferred to the SICU with manual ventilation. Total anesthesia time was 6 hours 45 minutes; the operation lasted 4 hours; cardiopulmonary bypass time was 2 hours 25 minutes. The volume of total bleeding was 3,000 ml; the amount of total fluid infused was 500 ml of crystralloid solution and 1,100 ml of colloid solution. Total transfusion was 10 units of irradiated WBC-depleted RBC, 7 units of FFP, 10 units of PC. Urine output was 1,600 ml.
2 days after the surgery, the patient received a tracheostomy to take her off the ventilator (). Six days after surgery, she was transported to the general ward and seemed to get better using a home ventilator. However, 42 days later, she died of inhalation pneumonia.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3654,10,Ideal Body Weight,physical,decimal,pmc-7676804-1,Extracted,"A 40-year-old male was brought by a friend to the emergency department (ED) for evaluation with a chief complaint of headache. The patient reported a headache that was diffuse, severe in intensity, throbbing in nature, and gradual in onset. The headache started when he lay down to sleep that evening. It was associated with nausea and numbness and tingling in his bilateral hands and feet. The headache was preceded by several hours of fatigue and generalized weakness. The patient drank six 12-ounce beers before going to bed. The friend at the bedside explained that he typically drank that amount, and expressed concern because the patient seemed much more intoxicated than he typically would be after drinking that amount.
The patient had a past medical history of depression and anxiety. He had a surgical history of an open reduction and internal fixation of a right calcaneal fracture 10 years prior. He took sertraline 100 milligrams (mg) daily, and had no drug allergies. He smoked one pack of cigarettes per day and was a daily drinker, but had not experienced alcohol withdrawal. He denied use of illicit drugs. Family history was notable for a cerebrovascular accident and myocardial infarction in his parents, and vertigo in a sibling. He worked as a contractor for a gas and electric company, and spent most of his day outside. He had no recent travel history. A review of systems revealed a one-week history of right ankle pain, swelling, and redness that the patient attributed to a “spider bite.”
The patient was alert, oriented, and uncomfortable but non-toxic appearing on the initial exam. His temperature was 36.8° Celsius (C), with a heart rate of 71 beats per minute, blood pressure (BP) of 139/83 millimeters (mm) of mercury, and an oxygen saturation of 98% on room air with a respiratory rate of 16 breaths per minute. He weighed 82.6 kilograms (kg), was 1.96 meters tall with a body mass index of 22.5 kg/m2. He appeared well developed and well nourished. His head was normocephalic and atraumatic. He had moist mucous membranes, without oral lesions, and with a normal oropharynx. Pupils were 2 mm, equal, and sluggishly reactive to light. His extraocular movements were normal. There was no scleral icterus or conjunctival pallor. Visual acuity was grossly normal. The neck was supple without cervical lymphadenopathy, meningismus, or midline or paraspinal cervical spine tenderness. Heart was regular rate and rhythm, without murmur, rubs, or gallops. Breath sounds were clear bilaterally without wheezing, rhonchi, or rales. Abdomen was soft and nontender, without rebound, guarding, or rigidity, and with normoactive bowel sounds. Extremities were warm and well perfused with good distal pulses.
There was a small area of blanching erythema and ecchymosis in the right lateral malleolar region. There was no increased warmth, edema, other evidence of trauma, or painful or limited range of motion of the ankle. Neurologic exam showed cranial nerves II–XII intact, 4/5 strength throughout the bilateral upper extremities, 5/5 strength throughout the bilateral lower extremities, with normal tone, and normal sensation throughout. Speech was clear and fluent, and mood and affect were appropriate. Skin was warm and dry. A papular rash was noted on his lower extremities (). It did not involve the palms or soles.
The patient’s initial laboratory testing results are shown in . His electrocardiogram showed a normal sinus rhythm, with normal axis, normal intervals, and no ST-segment elevation, depression, or T-wave inversions. Two hours after his initial evaluation, he began vomiting and complained of dysarthria, dysphagia, and vertigo. Tongue fasciculations were present. He received a dose of metoclopramide. Due to concern for an acute cerebral vascular accident, a computed tomography (CT) of the head, and a CT angiography of the head and neck were subsequently performed and showed no acute abnormality. Neurology was consulted, and a magnetic resonance imaging (MRI) of the brain without contrast was obtained per their recommendation. The MRI was markedly limited by motion artifact and was of poor diagnostic quality. As described by radiology, the image showed foci of increased fluid-attenuation inversion recovery (FLAIR) signal involving portions of the cortex of the frontal lobes bilaterally, deep periventricular white matter, left side of midbrain, throughout the pons, and in the deep left cerebellar hemisphere.
The patient was reassessed when he returned from MRI. His BP and heart rate were relatively unchanged, but he was febrile (38.4°C). The patient had become somnolent and he was no longer managing his oral secretions. It was determined that he was no longer adequately protecting his airway. He was intubated without complication, blood cultures were drawn, and he was started on empiric broad-spectrum intravenous (IV) antibiotics. A lumbar puncture was performed and cerebrospinal fluid (CSF) was obtained. The results are shown in . A diagnostic test was sent, which confirmed the diagnosis.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.96, 'm']}",89.48042,85.0064,93.95444,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.96 m, which is 1.96 m * 39.3701 in/m = 77.1654 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (77.1654 (in inches) - 60) = 89.48042 kg.
Hence, the patient's IBW is 89.48042 kg."
3655,10,Ideal Body Weight,physical,decimal,pmc-6358405-1,Extracted,"A 52-year-old male who was eventually diagnosed with a Wagner grade 4 diabetic foot ulcer combined with Budd-Chiari syndrome presented at the outpatient clinic of our hospital due to uncontrolled high body temperature, continued expansion of the right lower leg and a foot ulcer with increasing malodor. Random blood glucose test results, ultrasound imaging and magnetic resonance angiogram (MRA) confirmed this diagnosis. The man was diagnosed with type 2 diabetes in a rural community hospital four years previously. Four months ago, he developed a 1 cm × 2 cm ulcer on the lateral side of his right lower leg with a small amount of fluid exudate.
At the time of admission, the patient was in an acceptable condition, with a temperature of 38°C, a pulse of 88 beats / min, a respiration rate of 22 breaths / min, a blood pressure of 130 / 70 mmHg, a height of 1.75 m, a body weight of 60 kg, and a BMI of 19.5 kg / m2. Abdominal shifting dullness was positive, both lower extremities were swollen, and multiple fractures were visible on the wound surface on the medial and lateral sides of the right calf and right ankle. The dorsal right foot ulcer was visible and measured approximately 7 × 8 cm. All ulcers had a significant amount of yellow liquid exudate and odor (Fig. ). The random blood glucose test revealed that his glucose level was 20 mmol/L. The results of the computed tomography (CT) examination showed the followed: cirrhosis, splenomegaly, ascites, portal hypertension and collateral circulation. The MRA results showed the following:
inferior vena cava stenosis, indicating the possible need for embolization, and abdominal imaging changes in line with Budd-Chiari syndrome;
portal hypertension, ascites, splenomegaly, and intrahepatic and extrahepatic collateral circulation.
The ultrasound results showed the following:
the right and left hepatic veins were closed at the proximal end of the heart, and the middle hepatic vein was not apparent;
the intrahepatic traffic branch was formed;
there was diffuse damage to the liver parenchyma;
the portal vein was widened;
the umbilical vein was open;
the abdominal wall veins and gastric coronary veins were widened;
there was splenomegaly and splenic hilum varicose veins;
there was a tubular echo between the spleen and kidney, indicating the formation of traffic branches;
there was gallbladder edema;
there was diffuse injury to the kidneys;
there was abdominal effusion.
These findings conformed to the sonographic presentation of Budd-Chiari syndrome (intrahepatic type).
After admission, we established a treatment team consisting of multidisciplinary experts to develop treatment strategies to stabilize the patient's blood sugar, control the infection, and improve his microcirculation; we decided to apply this strategy throughout the treatment process. Figures and show the trends in the changes in C-reactive protein and 2-hour postprandial blood glucose levels throughout the treatment period. The treatment team then developed the following treatment plan:
interventional treatment of Budd-Chiari syndrome after the patient's general condition improved;
surgical debridement of large areas on the right lower extremity; and
amputation or skin grafting according to the wound condition after surgical debridement.
On the 6th day after admission, the patient underwent inferior vena cava angiography, hepatic venography, superior vena cava angiography, and inferior vena cava balloon dilatation under local anesthesia. During the operation, the hepatic vein was patent, the superior vena cava was unobstructed, the inferior vena cava below the hepatic vein plane was patent, the inferior vena cava above the hepatic vein plane was occluded, and the inferior vena cava was not developed below the opening, showing more collateral circulation. The thicker side branch had a diameter of approximately 10 mm. During the operation, it was difficult to pass the balloon through the occluded inferior vena cava segment. During this procedure, the surgeon used a 2.6-m Boston Amplatz hardened guide wire and delivered 10 × 40 mm and 16 × 40 mm balloons to the occluded inferior vena cava segment for balloon dilation. The procedure went well without complications. Postoperative angiography showed that the inferior vena cava was mostly unobstructed, with a stenosis of approximately 30%, and the collateral circulation had disappeared.
On the 9th day after admission, debridement was performed on the right lower leg and right foot of the patient under general anesthesia. During the operation, a large area of ulcerated skin was found on the right lower leg, and there was a substantial amount of exudate. On the dorsum of the right foot, a large area of necrotic skin was found on the leading edge of the right lower leg. The necrotic tissue spread to the proximal end along the tendon. Subcutaneous edema in the lower right limb was combined with an elevated skin temperature. The surgeon removed the previously confirmed necrotic tissue and preserved any tissue the necrotic status of which had not been verified (Fig. ). The wound was rinsed with saline and hydrogen peroxide after the surgery, sprayed with JEKSUNG (Changyi Pharmaceutical, China) and beifuxin (Zhuhai Yisheng Biological Pharmaceutical, China) on the surface, covered with Mepilex (Mölnlycke Health Care AB, Sweden), and then wrapped with sterile gauze.
On the 21st day after admission, debridement was again performed on the patient's right lower extremity under nerve block anesthesia. Then, a vacuum sealing drainage device was installed over the wound. During the surgery, we could see that there was some fresh granulation tissue covering the wound. The surgeon removed the remaining necrotic tissue, washed the wound with a normal saline and hydrogen peroxide, and then installed the vacuum sealing drainage device over the wound, using pressure dressings of sterile cotton pads and elastic bandages to cover the wound (Fig. ).
On the 32nd day after admission, under combined spinal and epidural anesthesia, the patient received skin grafts. We could see a substantial area covered with fresh granulation tissue above the wound (Fig. ). We saw skin defects in the foot dorsum and the anterior lateral of region the right lower leg; the extensor tendon of the foot was exposed. During the operation, we completely removed the clearly necrotic tissue, washed the wound with normal saline and hydrogen peroxide, excised free skin from the left thigh, and fixed it to the right lower extremity wound with interrupted sutures. Then, the wound surface was sprayed with JEKSUNG and beifuxin. The wound was covered with Mepilex and wrapped with sterile gauze.
On the 52nd day after admission, the attending physician confirmed that the skin had completely covered the wound, the postoperative recovery was excellent and the operation was successful. On the 56th day after admission, the wound had completely healed (Fig. ). The patient was discharged from the hospital after being examined by the attending physician.
During the entire treatment process from admission to discharge, we insisted on assessing the wound every day and changing the dressing based on that assessment. The specific steps involved in changing the dressing were as follows: the old dressing was removed, the wound was rinsed with saline and hydrogen peroxide, and the wound surface was sprayed with JEKSUNG and beifuxin. Then, the wound was covered with Mepilex and wrapped in sterile gauze.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.75, 'm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.75 m, which is 1.75 m * 39.3701 in/m = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3656,10,Ideal Body Weight,physical,decimal,pmc-6874974-1,Extracted,"Patient is a 38-year-old white male with a past medical history significant only for schizophrenia, currently on Abilify. He presented to the emergency department at the University of Toledo Medical Center with lower abdominal and back pain (Pain scale = 4/10) that had been intermittent for the past 2 weeks, with no particular inciting factor. On further questioning, he admits that a week earlier he fell and experienced sharp pain in his testicle. This pain was severe but subsequently subsided. Physical examination revealed height of 69 inches and weight of 220 pounds. His vital signs were within normal limits. The remaining physical examination was normal except for a firm enlarged left scrotum, which is nontender. Patient was given pain medications and imaging was ordered.
Bedside duplex ultrasound showed unremarkable right testis with good Doppler flow. However, the left testis had minimal to no blood flow and was extremely heterogeneous with small fluid collection, which was concerning for testicular torsion.
Testicular mass could not be excluded from the ultrasound study. Hence serum beta HCG, ALP, AFP were ordered, all of which were within normal range. In addition, CT of the chest, abdomen and pelvis with contrast showed left adrenal mass measuring a maximum of 1.9 cm, most likely a simple adenoma. There was no evidence of retroperitoneal or inguinal adenopathy. The left hemiscrotum showed enlarged contents with calcifications (). A diagnosis of testicular torsion was made and urgent scrotal exploration and hemiorchiectomy was performed. Postoperative course was uneventful and patient was discharged on Percocet, Colace, and Keflex. He was also advised to follow up with his doctor for the pathology results.
On gross examination, the testicle was enlarged (), measuring 7 × 5.4 × 5 cm, and the spermatic cord was 6.7 × 2.6 cm. Tunica vaginalis and albuginea showed no apparent gross invasion. The spermatic cord showed no gross abnormalities. Cut surface () showed a well-circumscribed variegated mass, measuring 7.0 × 5.2 × 4.8 cm. There were focal areas of calcifications and necrosis. In addition, there was a cystic structure (1.2 × 0.8 × 0.8 cm) filled with tan serous fluid.
Microscopic examination of the mass revealed predominantly overt malignant spindled cells displaying pleomorphism, hyperchromasia, and increased mitosis, with extensive necrosis in the background (). There were cells with abundant eosinophilic cytoplasm, some of which with striations, indicating rhabdomyoblastic differentiation (). Scrutinous searching further identified different benign tissues including cartilage, squamous epithelium, and rare bone, respiratory and glandular epithelium (). No other components of GCT or intratubular germ cell neoplasia were seen. The tumor was limited to the testis, and spermatic cord was not involved. However, extensive lymphovascular invasion was present. Immunohistochemistry revealed that the tumor cells were positive for desmin and vimentin (). The rhabdoid cells were positive for myogenin and focally weakly positive for MyoD (). A final diagnosis of teratoma with somatic-type malignancy: rhabdomyosarcoma was made.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [69.0, 'in']}",70.7,67.165,74.235,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 69.0 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.0 (in inches) - 60) = 70.7 kg.
Hence, the patient's IBW is 70.7 kg."
3657,10,Ideal Body Weight,physical,decimal,pmc-4435850-1,Extracted,"This is a case of a 50 years old female patient who is known to be hypertensive, dyslipidemic, obese (BMI: 31.88-Height: 168 cm Weight: 90 kg), and operated of sleeve gastrectomy in 2012.
On the morning of 13/02/2013, the patient noted a near syncope episode. She was transferred to the emergency department for a fever of 39.2°C, a microcytic anemia (Hb: 7 g/dl) with elevated inflammatory markers CRP 239 mg/l and ESR 90 mm and admitted for care and investigation.
Her physical exam showed lower limbs weakness at 4/5 proximally and distally (possible movement against gravity with moderate resistance). She was put on IV meropenem after blood and urine cultures were taken. The gram color was negative so were the cultures after 48 hours.
On the following morning she started complaining of paraparesia. Her physical examination showed a motor deficit of the lower limbs at 1/5 (visible contraction without any movement) with total anesthesia in all modalities (proprioceptive and thermo-algic). A D6 level was also noted.
An abdomino-pelvic computer tomography (CT) scan showed a complete thrombosis in the lower part of the mesenteric and the splenic veins extending to the portal bifurcation and the intrahepatic portal branches. It associated an important infiltration of the peritoneal and peri-pancreatic fat, and a mean abundance of free peri-hepatic, splenic and peri-pelvic ascites. There was a collection of 42 × 15 mm near the splenic hilum, containing a trace of contrast and a small two-fluid level. This collection seemed to communicate with the digestive tract at the gastro-esophago-jejunal anastomosis in its proximal part, suggestive of infected fistula (Figure ).
IV heparin was added to her medications.
An urgent brain and cervico-dorso-lombar MRI (magnetic resonance imaging) were performed and showed:Small brain abscesses formation Figure . An extensive transverse infectious myelitis Figure .
In front of these findings a lumbar puncture was performed revealing 430 WBC (92% neutrophils, 7% lymphocytes, and 1% mesothelial cells) 10 RBC with hypoglycorachia and hyperproteinorachia in favor of an inflammatory liquid with polymorphic predominance of polynucleated elements. The objective of this technique was to try to isolate a bacterium. The CSF culture returned sterile and PCR BK was negative.
An electromyogram was normal.
After this result vancomycin was added to the treatment regimen.
Clinical presentation, physical examination, and history are important diagnostic tools in assessing an acute myelopathy as the pattern of functional loss can help to determine the location of the lesion. When an acute myelopathy is suspected, a thorough neurological evaluation will help determine the region of the spinal cord affected and then the next diagnostic step is to evaluate for a compressive or structural etiology (Timothy W. []).
Magnetic resonance imaging (MRI) of the complete spinal axis is mandatory in any patient with myelopathic features to exclude structural lesions, particularly those amenable to emergent neurosurgical intervention [].
Once neuroimaging has excluded a compressive etiology, a lumbar puncture (LP) is indicated to determine if there are signs of inflammation within the cerebrospinal fluid (CSF). If the CSF is non-inflammatory, then vascular, toxic/metabolic, neurodegenerative, or neoplastic myelopathies become much more likely and the subsequent work-up should focus on these etiologies. If the CSF shows signs of inflammation (pleocytosis, elevated protein concentration, oligoclonal bands, or elevated IgG index), then the subsequent work-up should focus on demyelinating, infectious, or other inflammatory causes of an acute myelitis, as the differential diagnosis is broad [].
However, for elucidating the etiology of infectious myelitis, CSF studies are essential. CSF studies include cell count with differential protein and glucose concentrations. In addition, measurements of intrathecal immunoglobulin production with oligoclonal bands (OCBs) and an immunoglobulin G index or synthesis rate are very helpful when trying to determine the presence and etiology of myelitis.
An elevated protein concentration is the most common CSF abnormality in patients with spinal cord disease and is present in approximately 50% of patients with transverse myelitis []. A low CSF glucose concentration is defined as less than 60% of serum glucose and generally suggests fungal, bacterial, or mycobacterial infection, especially when associated with an elevated CSF white blood cell count. An isolated low CSF glucose concentration can occur in neurosarcoidosis, leptomeningeal carcinomatosis, subarachnoid hemorrhage, and even systemic lupus erythematosus (SLE) with CNS involvement []. The white blood cell differential can be very helpful as well. The presence of eosinophils can suggest parasitic or fungal infection, the presence of foreign material (such as surgical hardware following a spinal operation) or possibly neuromyelitis optica (NMO) (Timothy W. []).
The most frequent pathogens involved in transverse myelitis include Treponema palidum, Mycobacerium tuberculosis, Borrelia burgdorferi, Campylobacter jejuni, Acinetobacter baumanii, Coxiella burnetii, Bartonella henselae, Chlamydia psittaci, Leprospira, Chlamydia pneunoniae, Legionella pneumonia, Orientia tsutsugamushi (scrub typhus), Salmonella paratyphi B, Brucellosis melitensis, Group A and B streptococci [].
Intramedullary abscess may also complicate congenital dermal sinuses or bacterial endocarditis. So a cardiac echography should be performed to exclude endocarditis.
In our case, a PPD, HIV serology, wright and widal all returned negative. A cardiac echography was performed and ruled out any sign for endocarditis.
Successful treatment of infections of the nervous system depends on rapid and accurate diagnosis. The time course of symptom progression may suggest specific pathogens. In general, symptoms of less than 2 day’s duration bespeak bacterial processes. The clinical syndrome and associated extra neural infection sites favor certain organisms [].
Empiric corticosteroids may be of benefit in bacterial [] and in tuberculous meningitis []. For bacterial meningitis, the typical dosing is a four-day regimen of dexamethasone (0.6 mg/kg daily) started before or with the first dose of antibiotics [].
Our patient had developed an abdominal abscess with fistula. The bacteria implicated in her myelitis are probably an enterobacteriaceae or an enterococcus. The CSF culture was negative probably because we already initiated the meropenem before the lumbar puncture was performed.
A follow-up brain and cervico-dorsal MRI after 2 months of IV treatment (IV meropenem and vancomycine) showed: Figure .Net decrease of small contrast enhancing lesions scattered with persistence of nodular contrast right frontobasal, left upper front, in the region of the left and right thalamic lenticular ventricular junction, compared with small abscess formations in the process healing. We found a great reduction in the T2 signal abnormalities of the spinal, cervical, and thoracolumbar intramedullary spine signal. Virtual disappearance of intramedullary signal abnormality in the cervical spinal and back to a normal size.
1 year after the myelitis and physical rehabilitation, her physical exam shows motility at 3/5 (active movement against gravity) over both her lower limbs. The sensitivity over her lower limbs is recovering but poorly over the feet. Her sphincteral dysfunction is still persistent.
The differential diagnosis with the infectious myelitis is one caused by autoimmune disease. A thorough workup was conducted eliminating all autoimmune diseases. The antinuclear antibodies, antibodies to extractable nuclear antigen, rheumatoid factor, antiphospholipid antibodies, and anti-neutrophil cytoplasmic antibodies (ANCA) are all negative [].
CSF and blood angiotensin-converting enzyme levels are normal.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [168.0, 'cm']}",59.62607,56.64477,62.60737,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.14177 (in inches) - 60) = 59.62607 kg.
Hence, the patient's IBW is 59.62607 kg."
3658,10,Ideal Body Weight,physical,decimal,pmc-7195506-1,Extracted,"A 51-year-old man (height 168 cm; weight 57 kg) had severe mitral regurgitation due to posterior leaflet prolapse (P2) with exertional dyspnea. He had normal systolic function (ejection fraction 75%) with no past history. He was scheduled to undergo robot-assisted mitral valve repair.
General anesthesia was induced with 5 mg of midazolam, 50 mg of rocuronium, and 0.5 μg/kg/min of remifentanil intravenously. The trachea was intubated with a left-sided 37-French (Fr) double-lumen tube, followed by an insertion of a TEE probe CX-50 TEE machine (Philips Medical Systems Andover, MA). A central venous catheter and pulmonary artery catheter were placed in the left internal jugular vein, and a 16-Fr venous cannula was inserted through the right internal jugular vein for drainage of the superior vena cava, with the tip at the junction of the superior vena cava and innominate vein. Anesthesia was maintained with 1.5% of sevoflurane in oxygen, continuous infusions of 0.2‑0.4 μg/kg/min of remifentanil, and 4 mg/kg/h of propofol.
TEE showed posterior leaflet prolapse (P2) with a marked eccentric jet in the mid-esophageal long-axis view (Fig. ). After turning the probe clockwise from the mid-esophageal long-axis view, TEE showed a moderate central regurgitation jet (Fig. ). In the mid-esophageal commissure view, the “cobra head sign” indicating P2 prolapse (Fig. a) was noted. Moreover, a central regurgitation jet that was induced between the anterior leaflet (A3) and posterior leaflet (P3) was observed (Fig. b).
The three-dimensional (3-D) en face view showed a profound indentation, indicating that the cleft between P2 and P3 was noted at early diastole (Fig. ). TEE showed not only P2 prolapse but also a cleft between P2 and P3, and mitral regurgitation was caused by both etiologies.
After establishing cardiopulmonary bypass (CPB), an antegrade cardioplegia cannula was inserted into the ascending aorta and a flexible cross-clamp was subsequently applied.
For the mitral valve repair procedure, posterior leaflet resection was not performed; instead, neochordal reconstruction of P2 and P3 and ring annuloplasty were performed due to the risk of cleft dilation after resecting the posterior leaflet. After declamping of the aorta, a 3 μg/kg/min dopamine infusion was started. Weaning from CPB was very smooth. However, systolic anterior motion (SAM) occurred immediately after weaning from cardiopulmonary bypass. Dopamine was stopped to administrate. After volume loading and beta-blocker administration, SAM was improved. The hemodynamic status was stable. Subsequently, residual mitral regurgitation was not observed, and the postoperative course was uneventful.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.0, 'cm']}",64.12607,60.91977,67.33237,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg."
3659,10,Ideal Body Weight,physical,decimal,usmle-9441,Extracted,"A 36-year-old Asian G4P3 presents to her physician with a recently diagnosed pregnancy for a first prenatal visit. The estimated gestational age is 5 weeks. She had 2 vaginal deliveries and 1 medical abortion. Her children had birth weights of 4100 g and 4560 g. Her medical history is significant for gastroesophageal reflux disease, for which she takes pantoprazole. The pre-pregnancy weight is 78 kg (172 lb), and the weight at the time of presentation is 79 kg (174 lb). Her height is 157 cm (5 ft 1 in). Her vital signs are as follows: blood pressure 130/80 mm Hg, heart rate 75/min, respiratory rate 13/min, and temperature 36.7℃ (98℉). Her physical examination is unremarkable except for increased adiposity.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [157.0, 'cm']}",49.66544,47.18217,52.14871,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 157.0 cm, which is 157.0 cm * 0.393701 in/cm = 61.81106 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.81106 (in inches) - 60) = 49.66544 kg.
Hence, the patient's IBW is 49.66544 kg."
3660,10,Ideal Body Weight,physical,decimal,pmc-3253671-2,Extracted,26 year old female (upon admission). Diagnosed of Graves' disease at age 26 but presented with liver dysfunction with methimazole and mild neutropenia with propylthiouracil. Thyroid function was controlled with potassium iodide until surgery. She had a history of anorexia and bulimia since age 19. Her thyroid function and eating behavior were both stable at the time of surgery. There is no record of the use of SSRIs in the treatment of anorexia nervosa. Her height was 158.5 cm and her weight was 55.0 kg (BMI 21.9) at the time of surgery. Post operatively she was placed on 75 mcg of levothyroxine daily which maintained her thyroid function within normal levels. There was no relapse of her anorexia bulimia and her body weight increased slightly and gradually over the next seven years (to BMI 23.8).,"Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.5, 'cm']}",51.0237,48.47251,53.57489,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.5 cm, which is 158.5 cm * 0.393701 in/cm = 62.40161 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.40161 (in inches) - 60) = 51.0237 kg.
Hence, the patient's IBW is 51.0237 kg."
3661,10,Ideal Body Weight,physical,decimal,pmc-3689787-2,Extracted,"The patient is a 12-year-old boy born to non-consanguineous parents. No family history of congenital anomalies or mental retardation was reported. He has a healthy 4 year-old sister. The patient was born at full term after an uneventful pregnancy by spontaneous vaginal delivery. Exposure to drugs or infection during the pregnancy was denied. At birth, weight was 3.300 kg (25th–50th centile), length 54 cm (90–95th centile) and occipitofrontal circumference (OFC) 34 cm (10th–25th centile). Psychomotor development was normal. At the age of 12 years, weight was 30 kg (5th centile), height 165 cm (>97th centile) and OFC 53.7 cm (>50th centile). Marfanoid habitus, arachnodactyly of hands and feet with very long hallux bilaterally associated and mild syndactyly of 3rd, 4th and 5th fingers, and severe scoliosis were observed (). Echocardiography showed patent ductus arteriosus.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3662,10,Ideal Body Weight,physical,decimal,pmc-5156792-1,Extracted,"A 75-year-old man was hospitalized for mental confusion, muscular weakness, and severe hypokalaemia (2.5 mEq/L). The patient's medical history included hypertension and benign prostatic hyperplasia; he took ramipril 5 mg and dutasteride 0.5 mg daily. Few months before he had felt an increasing asthenia, he noted weight gain and the worsening of hypertension control and he experienced some episodes of low urinary tract infections. The laboratory tests evidenced the onset of diabetes (fasting glycaemia 160 mg/dL and HBA1C 50 mmol/L); prostate-specific antigen (PSA) was normal (2.39 μg/L). His wife reported that lastly he was physically exhausted and mentally confused. At physical examination the patient was 165 cm in height and he weighed 70 kgs (BMI 25.7); he showed slight round face and thin arms and legs; his arterial pressure was 160/105 mmHg. Digital evaluation revealed that the prostate was enlarged and firm in consistency. Laboratory tests () confirmed severe hypokalaemia (2.3 mmol/L) and documented high levels of midnight salivary cortisol (50.6 μg/L), elevated levels of plasma ACTH (155.4 ng/L), and plasma cortisol (398 μg/L). The overnight 8 mg dexamethasone suppression test did not properly suppress plasma cortisol (198 μg/L); high levels of plasma chromogranin A and calcitonin (272 ng/L) were also documented; PSA was confirmed to be normal (1.7 μg/L) ().
Magnetic Resonance Imaging (RMI) of the pituitary gland was normal; no nodules were found by thyroid ultrasonography. Total body computed tomography (TBCT) (Figures -) revealed a voluminous prostate gland (maximum diameter of 10 cm) heterogeneously enhancing the contrast medium. The tumour of the prostate had invaded the bladder; the rectum and multiple pathological retroperitoneal lymph nodes as well as bilateral enlarged adrenal glands were evident. A subsequent 68 Gallium DOTATATE PET/CT found a high uptake of the whole prostate (SUV max 12.7) and of the adjacent lymph nodes, confirming the presence of a neuroendocrine tumour in that site and excluding other distant metastases (). The patient underwent a transurethral prostate biopsy that showed a small cell prostate cancer focally positive for ACTH and calcitonin and negative for chromogranin A and PSA at immunocytochemistry (Figures and ). Continuous intravenous potassium infusion, potassium sparing drugs (Aldactone), and antihypertensive drugs were administered to the patient. Ketoconazole was also administered with an uptitrating dose of 400 mg/twice daily for 5 weeks and because of the poor control of cortisol secretion, octreotide 0.1 mg every 8 hours subcutaneously was added for further 13 days. Despite a reduction of plasma cortisol (195 mcg/L) after 6 weeks of treatment, no significant clinical benefit was achieved; in fact the patient continued rapidly to worsen becoming more asthenic and confused since he developed a glucocorticoid induced psychosis. The surgeon urologist excluded prostate resection and bilateral surrenectomy because they were considered too dangerous for the patient. The patient started a cycle of chemotherapy with epirubicin and carboplatin, but few weeks after the first cycle, febrile neutropenia, sepsis, and intestinal perforation occurred and the patient died.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3663,10,Ideal Body Weight,physical,decimal,pmc-3030045-1,Extracted,"A male patient (165 cm in height, 61 kg and 62-year-old) was transferred to our hospital because of the chief complaint of back pain. The back pain had developed approximately 2 months previously without specific trauma, and the area around the left buttock was most painful. The pain worsened while standing up and turning around, and it was improved while lying down. The pain score by the VNRS was 9-10/10 points. There were no findings of radicular pain, costovertebral tenderness or spinal tenderness, and the muscle strength of both low extremities was grade 5, which was normal. The patient was hospitalized for the evaluation of renal function and treatments because of the elevated CPR. The patient had been hospitalized at the A hospital for back pain 2 months previously and bulging discs (L3/4, L4/5) were detected by lumbar magnetic resonance imaging (). Hypoxia and fever had developed during the hospitalization; atypical pneumonia was suspected and he had received treatment. Nonetheless, the pain and other symptoms had not improved and so he was transferred to the B hospital. He was diagnosed with possible scrub typhus, doxycycline was prescribed and the fever subsided and he was discharged after one week.
At that hospital, he was diagnosed as suffering from chronic renal failure caused by glomerulonephritis. The back pain was diagnosed as L4-5 facet pain and so a lumbar median branch block was performed. After he initially improved 10-20% for 3 days, the back pain recurred and persisted until the time of transfer to our hospital. For his past medical history, he had undergone surgery for a ruptured infrarenal aorta aneurism 10 months previously. The vital signs of the patient at the time of transfer were a blood pressure of 115/90 mmHg, a pulse rate of 68 beats/min, a respiratory rate of 18 breaths/min and the body temperature was 36.4℃. The blood test of the patient showed that the number of leucocytes and the CRP level were normal, and the ESR was elevated to 49 mm/hr. First, a diagnostic epidural block was performed using a C letter type image intensifier (OEC® 9800 Plus, GE medical system, USA). Epidural block in the left L 4-5 interlaminar space was performed and 10cc of 0.125% ropivacaine and 20 mg tamceton were injected. The next day after the epidural block, the patient showed approximately 20% improvement for 1-2 hours. After this, the pain recurred and sitting was difficult and painful. Since the symptoms of the patient and the findings of the previously performed lumbar MRI did not concur, magnetic resonance imaging was performed again after 2 days. A paravertebral abscess and findings of infective spondylitis were detected on the lumbar magnetic resonance imaging (). An aspiration culture test was performed for the abscess and salmonella group D was cultured. The patient was finally diagnosed with salmonella spondylitis, and ceftriaxone was administered according to the results of the antibiotic sensitivity test. The symptoms of the patient and the results of the hs-CRP then showed a tendency to improve. During the administration of antibiotics, there was persistent deterioration of the kidney function and uremia symptoms developed, and so hemodialysis was performed. Despite the administration of appropriate antibiotics, the patient showed intermittent fever and a trend for increased pain. MRI follow-up was performed 4 weeks after the administration of antibiotics, and the abscess was shown to have increased in size. Even though we performed drainage, this failed because of septation of the abscess. The patient was then transferred to another hospital according to his wishes. Afterward, at that hospital, the patient was treated with a combination of ciprofloxacin and ceftriaxone without surgery for 4 weeks, and then he was again transferred to our hospital because it is located in his hometown. Thirteen weeks after the administration of antibiotics, his back pain was much improved (VNRS: 1/10) and he was able to walk. On the blood test, the hs-CRP level was 0.34 mg/dl. On the lumbar MRI, the abscess showed improvement and so the antibiotics were terminated. The patient is currently under follow-up observation at our outpatient clinic ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3664,10,Ideal Body Weight,physical,decimal,pmc-6392561-1,Extracted,"A 51-year-old woman visited our outpatient clinic because of latent tuberculosis infection detected by a screening examination performed by a healthcare worker. She had no relevant prior medical history. Laboratory findings were normal with a serum creatinine (Cr) level of 0.76 mg/dL (normal 0.6–1.5 mg/dL) and blood urea nitrogen (BUN) level of 12.8 mg/dL (normal 8–23 mg/dL). Antituberculosis treatment was started with isoniazid at 300 mg/d and rifampicin at 600 mg/d. During the 25-day antituberculosis therapy regimen, she complained of nausea, vomiting, general weakness, and edema. Serum Cr and BUN levels were 1.0 and 18 mg/dL, respectively. Rifampicin and isoniazid were discontinued. However, her symptoms progressed for 4 days and urinalysis revealed 4+ proteinuria (normal negative). She was admitted to the hospital for more detailed examinations.
On admission, her blood pressure was 110/80 mm Hg, body temperature was 36.5°C, height was 158 cm, and body weight was 68.6 kg. She had gained 8.6 kg in body weight over the preceding 1 month. The results of physical examination were unremarkable except for pitting edema on both lower extremities. Laboratory findings were as follows: white blood cell count 7490/mm3 (normal 4000–10,000/mm3) with 63.1% neutrophils and 1.4% eosinophils, hemoglobin 13.6 g/dL (normal 12–16 g/dL), platelet count in peripheral complete blood 295,000/mm3 (normal 140,000–440,000/mm3), BUN 45 mg/dL, serum Cr 1.72 mg/dL, total protein 3.67 g/dL (normal 6.5–8.2 g/dL), albumin 1.73 g/dL (normal 3.5–5.0 g/dL), total bilirubin 0.67 mg/dL (normal 0.1–1.2 mg/dL), aspartate transaminase 116 IU/L (normal 10–35 IU/L), alanine transaminase 94 IU/L (normal 0–40 IU/L), total cholesterol 453 mg/dL (normal 120–200 mg/dL), sodium (Na) 133 mEq/L (normal 135–145 mEq/L), potassium 5 mEq/L (normal 3.5–5.5 mEq/L), and chloride 103 mEq/L (normal 98–110 mEq/L). Urinalysis showed specific gravity >1.050 (normal 1.005–1.03), osmolality 687 mOsm/kg (normal 300–900 mOsm/kg), urine Na <10 mEq/L, and urinary Cr 267.34. The calculated fractional sodium excretion was 0.02%. The creatinine urine to plasma ratio was 155. Urinary sediment did not show either red blood cells or granular casts. A 24-h urine sample contained 12.2 g of protein. Serum and urine electrophoresis results showed no M-spike and nonselective proteinuria. The patient was negative for hepatitis B, hepatitis C, HIV, and syphilis serological markers. Rheumatoid factor, antinuclear antibody, antineutrophil cytoplasmic antibody, and antiglomerular basement membrane antibody tests were all negative. In addition, results for complement 3 (144.3 mg/dL, normal 90–180 mg/dL), complement 4 (32.4 mg/dL, normal 10–40 mg/dL), immunoglobulin G (551 mg/dL, normal 700–1600 mg/dL), immunoglobulin A (267 mg/dL, normal 70–400 mg/dL), and immunoglobulin M (111 mg/dL, normal 40–230 mg/dL) were negative. Chest X-ray revealed a small amount of bilateral pleural effusion (Fig. A). The patient was treated with torsemide at a dose of 50 mg/d for edema.
Renal biopsy was performed at 1 week after discontinuation of medication. However, she developed dyspnea and pulmonary edema on the day of the procedure (Fig. B). As we suspected nephrotic syndrome with acute nonoliguric renal failure, we performed dialysis and oral administration of prednisolone at 60 mg/d. Acute renal failure was confirmed with temporary loss of renal function that required dialysis, and with peaked serum Cr (2.68 mg/dL) that more than 3-fold increase in baseline Cr (0.76 mg/dL). Renal biopsy revealed nonsclerotic glomeruli with normocellularity and a mild focal tubular injury pattern on light microscopy (Fig. A and B). No deposition of immunoglobulins or complement components was observed in the glomeruli. Electron microscopy showed diffuse loss of the podocyte foot processes of glomerular epithelial cells, but the glomerular basement membrane showed normal thickness and architecture, consistent with MCD (Fig. A and B).
The diagnosis was confirmed to be MCD. Heavy proteinuria developed after using antituberculosis agents. We speculated that this was a case of antituberculosis medication-induced nephrotic syndrome and toxic hepatitis. Following discontinuation of rifampicin and isoniazid with the aid of prednisolone therapy, the patient's nausea, vomiting, and pulmonary edema improved after 1 week of steroid therapy, and dialysis was stopped. Her body weight recovered from 68.6 to 60.7 kg at 3 weeks after discontinuation of rifampicin and isoniazid, and she was then discharged. Proteinuria became negative and renal function tests showed normal results at 4 weeks (serum Cr, 0.86 mg/dL; BUN, 24.7 mg/dL). Furthermore, her albumin and cholesterol levels were 3.15 g/dL and 276 mg/dL, respectively, at 4 weeks after stopping the drugs. Prednisolone was then tapered and withdrawn 3 months after initiation. Recurrence of proteinuria was not observed during a 3-month follow-up. The patient's clinical course is summarized in Fig. .
Informed consents were obtained from the patient for the publication of clinical details and accompanying images. As this study is a clinical case report, no ethical committee approval was required for its conduction, which is in compliance with the institutional and national policies concerning research approvals.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3665,10,Ideal Body Weight,physical,decimal,pmc-5709897-1,Extracted,"A 15-year-old boy was referred to the neurodevelopmental clinic of our child and adolescent mental health services for a diagnostic assessment. He was assessed in the presence of his parents.
The primary concerns included difficulty in sustaining his concentration, organizing sequential tasks, completing tasks on schedule, being forgetful often, and easily distractible shifting to different tasks in quick succession. He was reported to be restless and fidgety in multiple settings including at school and home, with his difficulty being seated at his desk in classroom. He also encountered difficulties in waiting for his turn or in a queue and engaging in group activities. His symptoms were associated with significant impairment in his functioning at home and school. The rating scales from his parents as well as teachers (Conner's questionnaires) in addition to the school observation and occupational therapy group assessment reports supported the above findings. There were no pointers toward autistic traits or intellectual difficulties. Furthermore, there was no history suggestive of anxiety or mood symptoms.
He lives with his parents and two biological siblings. There is a family history of ADHD in one of his paternal cousin brothers (who has not been genetically tested). His antenatal history was uneventful. However, there were reported difficulties with sucking, feeding, and a low-pitched crying. He also appeared floppy though these difficulties eventually self-resolved. There were also delays in gross motor and language milestones, which he was eventually caught up with. There are no active physical health concerns currently. There is no history of seizure episodes.
During the assessment, he came across as a lively and boisterous boy who was warm and friendly. He made appropriate eye contact and expressed a range of facial emotions. However, he was constantly distracted by different environmental stimuli. He could not be engaged in a conversation on any specific topic beyond a few minutes since he kept losing thread of the conversation. There were no autistic traits elicited in history or during the interview.
On review of previous investigations, it was noted that genetic analysis fluorescent in situ hybridization technique was carried out, and it revealed chromosome 15 duplication (tested for the following constellation of clinical features: hypotonia, weak cry, and difficulties with sucking and feeding). No formal IQ testing has been carried out since he has been above average with his school lessons despite his attentional and behavioral difficulties, and there are no other pointers suggestive of intellectual or learning difficulties. Downslanting palpebral fissures were noted during the general examination. His height was measured to be 162.5 cm (14th centile) and he weighed 45.3 kg (8th centile) on the day of diagnostic assessment. His cardiovascular parameters (blood pressure and pulse rate) were within normal limits.
A diagnosis of ADHD and combined subtype was made based on the history, mental state examination, and other reports. His carers were psychoeducated regarding the disorder and different management options (pharmacological and nonpharmacological). Conners’ rating scale (parental version) was administered at baseline (t-score >70).[] The side effects of stimulant medication were discussed along with the potential benefits emphasizing that individuals with chromosomal mutations may tolerate stimulant medication differently. Taking this into account, it was decided to initiate him on 5 mg of methylphenidate, to be titrated upward gradually. It was also explained that we would be monitoring his growth at every visit (height and weight) along with his cardiovascular parameters (blood pressure and pulse rate). They were also provided self-help material on ADHD, and the parents were referred for parenting classes after their consent.
He was reviewed subsequently on multiple occasions. There was some initial increase in restlessness and agitation over the initial week. Fortunately, he later tolerated the medication reasonably well and no significant side effects were reported. The dose of methylphenidate was very gradually increased to 30 mg daily, and thereafter, he was shifted to longer acting preparation of methylphenidate, concerta-extended release 27 mg once daily to simplify the drug regimen. At a subsequent review 4 months from the index visit, Conners’ rating scale (parental version) was readministered (t-score <60) demonstrating a significant reduction in symptomatology.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [162.5, 'cm']}",59.14574,56.18845,62.10303,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 162.5 cm, which is 162.5 cm * 0.393701 in/cm = 63.97641 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (63.97641 (in inches) - 60) = 59.14574 kg.
Hence, the patient's IBW is 59.14574 kg."
3666,10,Ideal Body Weight,physical,decimal,pmc-8113941-1,Extracted,"A 59-year-old Asian woman (body weight: 57 kg, height: 153 cm, body mass index:
24.35 kg/m2, occupation: farmer) received TPI in the thoracolumbar
paraspinal muscles at a local medical center because of a 4-month history of
persistent middle back pain of a dull and achy nature. Her pain began spontaneously,
without any trauma history. She did not have any medical history such as
hypertension, diabetes, or neurological disorders. Prior to the TPI, she had not
exhibited any neurological symptoms. She had tenderness to palpation on both
thoracolumbar paraspinal muscles along with identifiable taut bands. A thoracolumbar
spine X-ray image revealed no specific abnormal findings. The physician, who had
25 years of training and experience, diagnosed the patient with myofascial pain syndrome. Her pain was not controlled by oral medication (meloxicam 7.5 mg). TPI was
performed using a blind technique without imaging guidance (ultrasound or
fluoroscopy) in the left thoracolumbar paraspinal muscles, with the patient in a
prone position. The patient had never received TPI prior to the injection. The
physician used a 24-gauge 60-mm spinal needle and 10 mL of 0.6% lidocaine (3 mL of
2% lidocaine and 7 mL of normal saline solution) as the injection solution. During
the procedure, the patient experienced an electric shock sensation throughout the
middle back and lower extremities. The physician stopped the procedure immediately,
and the solution was not infused.
Immediately after the TPI, the patient developed weakness and severe, sharp, and
lancinating pain in the left lower extremity. Three days after the TPI, she was
transferred to the rehabilitation department of our hospital, where she provided
written informed consent for participation in this report. The study was approved by
the institutional review board of Yeungnam University Hospital (2019-05-044).
On physical examination, the patient exhibited severe weakness in the lower left
extremity: her hip flexor and knee extensor manual muscle testing (MMT) scores were
grade 2, and her ankle dorsiflexor, long toe extensor, and ankle plantarflexor MMT
scores were grade 0. Furthermore, impaired light touch sensation was observed in the
L2 to S5 dermatomes on the left side, and she had impaired pain perception in
dermatomes L3 to S5 on the right side of the body. Based on the International
Standards for Neurological Classification of Spinal Cord Injury, her neurological level of injury was L1, and she was classified as grade D
according to the American Spinal Cord Injury Association Impairment Scale (AIS). She
was unable to walk and required a wheelchair to move around. Her tendon reflexes and
muscle tone were unaltered, and bladder and bowel symptoms were absent. The patient
complained of neuropathic pain (tingling, sharp, and lancinating; numeric rating
scale [NRS]: 7) in the left lower extremity. Thoracolumbar spine magnetic resonance
imaging (MRI) revealed a high-intensity T2 signal in the left T12 to L2 segments of
the spinal cord 3 days after TPI (). Electrophysiological recordings, which were performed 11 days
after TPI, showed no response in central motor conduction time (CMCT) in the left
tibialis anterior muscle, whereas the biceps brachii, adductor pollicis brevis, and
right tibialis anterior muscle CMCTs were within the normal range. The patient’s
compound motor action potentials and sensory nerve action potentials had normal
latencies and amplitudes during a nerve conduction test 11 days after TPI, and
electromyography revealed no active denervation potentials in the lumbar paraspinal
muscles or those of the bilateral lower extremities. Spine MRI revealed a
skin-to-epidural space depth of 4.6 cm.
The patient underwent comprehensive rehabilitative management, including
neuromuscular electrical simulation therapy for the knee extensors and ankle
dorsiflexors (20 minutes, twice per day, 7 days per week). In addition, movement
therapy was administered 6 days per week (Monday to Friday: 2.5 hours per day,
Saturday: 1 hour per day), primarily to improve motor function and postural control.
Seven months after the onset of SCI, the patient’s left hip flexor and knee extensor
motor functions had improved to MMT grade 3, and the left ankle plantarflexor muscle
function had improved to MMT grade 2. Conversely, motor functions in the left ankle
dorsiflexor and long toe extensor muscles had not improved (MMT grade: 0) (). The patient’s
pain perception remained impaired, but her ability to sense light touch in the left
lower extremity was nearly completely recovered. Additionally, her neuropathic pain
was reduced from an NRS score of 7 to an NRS score of 4 by treatment with 450 mg
pregabalin and 200 mg tapentadol, and she was able to walk independently using a
walker.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.0, 'cm']}",46.04337,43.7412,48.34554,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.0 cm, which is 153.0 cm * 0.393701 in/cm = 60.23625 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.23625 (in inches) - 60) = 46.04337 kg.
Hence, the patient's IBW is 46.04337 kg."
3667,10,Ideal Body Weight,physical,decimal,pmc-6616359-1,Extracted,"A 51-year-old man who worked at a building maintenance service was referred to our university hospital due to spontaneous bilateral groin pain that had continued for 1 month. The first doctor suspected an injury to the hip adductor muscle. The patient appeared to be a healthy middle-aged man. He was not an athlete and had no history of metabolic disease, diabetes, rheumatoid arthritis, impaired renal function, or use of corticosteroids. He smoked and drank heavily, averaging 30 cigarettes and 2000 mL of beer daily. He worked nights, and thus had inadequate sun exposure for more than 5 consecutive years. He reported no falls or other trauma. Physical examination revealed pain with hip movements. The patient was 166 cm tall, weighed 55 kg, and has a body mass index of 20.0 kg/m2. At presentation, physical examination revealed no hip deformities. The range of motion was 120° in flexion, 10° in extension, 30° in abduction, 20° in adduction, 40° in external rotation, and 10° in internal rotation in each hip. Neurovascular findings were normal for both lower extremities. Standard radiographic findings were normal except for mild pistol grip deformity in the right hip (). In the right hip, femoral neck-shaft angle was 128° and femoral neck anteversion was 10°; those values were 127° and 9°, respectively, in the left hip. Computed tomography multiplanar reconstruction showed a herniation pit indicating cam-type femoroacetabular impingement at the lateral femoral head-neck junction (A–C). Bone scintigraphy showed increased uptake in both femoral necks, indicating possible stress fractures (D). Findings from magnetic resonance imaging (MRI) of the pelvis indicated fracture on the compression side of the distal portion of each femoral neck (). His laboratory studies showed increased alkaline phosphatase (ALP) activity (511 U/L; reference range: 115–359 U/L), normocalcemia (9.2 mg/dL), and hypophosphatemia (2.1 mg/dL). The level of 25-hydroxy-vitamin D (25-OH D) was 7.5 ng/mL (<20 ng/mL is defined as deficiency), and parathyroid hormone (PTH) was 560 pg/mL (reference range: 160–520 pg/mL), indicating osteomalacia. Low bone mineral density (BMD) was noted on dual-energy X-ray absorptiometry DXA (lumbar: 0.805 g/cm2; T score, −1.7; Z score, −1.2; right hip total: 0.498 g/cm2; T score, −2.9; Z score, −2.6; left hip total: 0.490 g/cm2; T score, −2.9; Z score, −2.6).
We considered the patient’s past medical history, reviewed the risks and benefits of a surgical procedure [, , ], and decided to perform bilateral internal fixation with two 6.5-mm cannulated screws under general anesthesia (A–C). Because we wanted the patient to start walking with full weight-bearing as soon as possible after the surgery, we performed internal fixation on both the right hip (compression-sided fracture ≥50% of femoral neck width) and the left hip (compression-sided fracture <50% of femoral neck width). We received informed consent from the patient to perform hip arthroscopy on both hips to observe intra-articular pathology during the surgery and also to harvest bone marrow from iliac crest. Arthroscopic observation on the right hip showed typical pathological findings due to cam-type femoroacetabular impingement. The patient also had cleavage at the labro-cartilage junction and subsequent acetabular cartilage delamination classified as zone 2 grade 1 according to Konan’s classification [] (D). Histopathological examination showed the bone trabeculae to be relatively thin, considering the patient’s male gender and age (E). The undecalcified bone section showed an increase of unmineralized osteoid, suggesting the presence of osteomalacia (F). There were no postoperative complications. The patient was prohibited from weight bearing for 1 week following surgery, after which full weight bearing was encouraged with two crutches. At discharge, 1 month after the surgery, the patient was free of pain and was able to bear his full weight without crutches. He received weekly alendronate sodium hydrate and adequate activated vitamin D (eldecalcitol 0.75 μg/day). One year after fracture treatment, he had no complaints. Laboratory tests showed normal levels of calcium, inorganic phosphorus, PTH, and 25-hidroxyvitamin D level.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [166.0, 'cm']}",62.31505,59.1993,65.4308,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 166.0 cm, which is 166.0 cm * 0.393701 in/cm = 65.35437 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.35437 (in inches) - 60) = 62.31505 kg.
Hence, the patient's IBW is 62.31505 kg."
3668,10,Ideal Body Weight,physical,decimal,pmc-6487519-1,Extracted,"A 58-year-old Caucasian woman with hip osteoarthritis was examined by an anesthesiologist for a surgical procedure of total hip arthroplasty. She had a history of SCA, which started when she was 55-years old with motor dysfunction. Her clinical condition had slowly worsened with appearance of dysarthria, horizontal saccadic eye movements, and lower extremities hypertonia. An MRI of her brain showed olivopontocerebellar atrophy; a mild motor and sensory ataxic polyneuropathy was highlighted by electromyography. Recent neuropsychological examinations identified a dis-executive deficit. Her family history is negative for SCA and she denied any history of cardiovascular, respiratory, or gastrointestinal diseases. Prior to the diagnosis of SCA, she was in good health and did not regularly take drugs. She denied smoking tobacco or drinking alcohol. At the time of the examination, she was taking benzodiazepines (triazolam 0.25 mg once daily) for anxious depressive syndrome, baclofen 25 mg three times a day for spasticity, and anti-cyclooxygenase type 2 (COX-2) for pain treatment (etoricoxib 60 mg once daily). Preoperative blood tests, electrocardiogram, and thoracic X-ray were negative. On physical examination, it was possible to appreciate that she was tall, 168 cm, and weighed 63 kg. A cardiopulmonary examination was unremarkable. Her vital signs were normal with blood pressure of 135/90 mmHg and heart rate of 90 beats per minute. On neuropsychological examination, she presented a mild reduction in performance on the Rey–Osterrieth Complex Figure Test, a limited ability to inhibit cognitive interference (Stroop Test), inability during the Multiple Features Targets Cancellation task, and a Spatial Span Score lower than normal; these were proofs of her dis-executive deficit. After discussing the case with a neurologist, general anesthesia was planned. In fact, our patient’s anxiety and spasticity would have made regional anesthesia difficult to practice. Preoperatively, no medications were administered. General anesthesia was induced with propofol 2 mg/kg intravenously and fentanyl 2 mcg/kg intravenously. Tracheal intubation was facilitated with rocuronium 0.6 mg/kg intravenously. Anesthesia maintenance was performed with sevoflurane (in an oxygen/air mixture) and fentanyl. The minimum alveolar concentration of sevoflurane was set to achieve a Bi-spectral Index (BIS) value between 40 and 60. Mechanical ventilation was set with a tidal volume of 7 ml/kg, a positive end-expiratory pressure (PEEP) of 5 cmH2O, and an inspiration/expiration rate of 1:2. These parameters remained stable during the surgical procedure. The respiration rate was adjusted to obtain an end-tidal carbon dioxide (etCO2) between 38 and 45 mmHg. The surgery was uneventful with no significant blood loss and no transfusion was needed. The procedure lasted 2 hours. Upon awakening, she appeared calm and parameters were stable. In the post anesthesia care unit (PACU), she was warmed up and oxygen supplementation was administered. Thirty minutes after awakening, she developed an acute hyperactive delirium. She experienced episodes of confusion, logorrhea, and disorientation. She also exhibited reduced awareness of the environment and hallucinations with aggressive behavior. During this episode, her vital signs remained stable and her oxygen saturation was normal. An arterial blood test revealed no hypercapnia or hypoxia or electrolyte disorders. Haloperidol 5 mg was intravenously administered slowly over 5 minutes, but her behavior did not change. To avoid uncontrolled pain, a single shot fascia iliaca block was performed with 25 ml of ropivacaine 0.375% but she continued to have intermittent episodes of delirium. After 10 minutes, chlorpromazine 25 mg was infused intravenously. This drug seemed to have the same efficacy as haloperidol with a subsequent mild sedation. She was transferred to our intensive care unit (ICU) where chlorpromazine 25 mg was given again during the night for another crisis. She was discharged from ICU the next day under normal neurological conditions.
After 1 month, she was readmitted for the development of an acute periprosthetic hip infection sustained by Staphylococcus epidermidis and Staphylococcus haemolyticus without signs of systemic sepsis. On examination, her temperature was 36.7°C, blood pressure was 128/95 mmHg, and heart rate was 75 beats per minute. Only the wound swab was positive for infection; hemocultures and urine cultures were negative. Preoperative blood tests showed: hemoglobin 10.4 g/dL; platelets 233 × 109/L; neutrophils 4.26 × 10 9/L; erythrocyte sedimentation rate (ESR) 47 mm/hour, and C-reactive protein (CRP) 27.2 mg/L. Renal and hepatic function indices were within normal limits. Debridement, antibiotics, and implant retention (DAIR) was performed under general anesthesia with the same modalities []. During surgery and after taking new periprosthetic tissue for microbiological examination, teicoplanin was administered intravenously at a loading dose of 400 mg. For the second time, our patient developed POD treated with chlorpromazine 25 mg intravenously with immediate sedation. Within 24 hours, the delirium resolved with no consequences. During the following days, 200 mg of teicoplanin was administered daily and 1 gr of cefazolin every 12 hours intravenously until discharge.
One month after discharge, she returned for follow-up. She was taking her habitual medications and, at the time of the examination, she exhibited no evidence of new disorders or joint infection. She looked well and denied any symptoms of confusion, disorientation, or hallucinations. The hip infection healed without any complication. She was re-evaluated at 3 and 6 months after surgery. Her ESR, CRP, and other biochemical values were within normal limits and her neurological status was stable.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [168.0, 'cm']}",59.62607,56.64477,62.60737,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.14177 (in inches) - 60) = 59.62607 kg.
Hence, the patient's IBW is 59.62607 kg."
3669,10,Ideal Body Weight,physical,decimal,pmc-5005233-1,Extracted,"A 44-year-old Japanese man was referred to our hospital complaining of a large tumor that had been accidentally pointed out in a medical examination as being an esophageal submucosal tumor. Relevant family history brought to light that his father had been diagnosed as having MEN1. Our patient had undergone total parathyroidectomy and autologous transplantation for primary hyperparathyroidism at the age of 18. His height and weight were 187 cm and 120 kg, respectively, with a body mass index of 34 kg/m2 on admission. He also complained of sleep apnea and bilateral nipple discharge. He was not aware of the hypoglycemic symptoms before the admission, but he frequently encountered the symptoms under nutritional management after the admission. Laboratory data of blood chemistry were normal as well as the tumor markers, such as carcinoembryonic antigen and carbohydrate antigen 19-9, whereas neuron specific γ-enolase was high (19.1 ng/ml). Hormonal examinations revealed a hypoglycemia, a hyperinsulinemia (fasting serum glucose, insulin levels, and hemoglobin A1c, 76 mg/dl, 134.5 μU/ml, and 4.5 %, respectively), a hyperprolactinemia (serum prolactin level 871.2 ng/ml), and elevated urinary catecholamines. On an enhanced thin-slice abdominal computed tomography (CT), a large tumor was detected in the pancreatic tail, showing heterogeneous enhancement with partial calcification and cystic components. Its maximum diameter was about 18 cm (Fig., ). Other than a pancreatic tail tumor, six enhanced liver tumors, a right adrenal tumor (3.9 cm in diameter), and a left adrenal tumor (2.6 cm in diameter) were found (Fig. , ). The right adrenal tumor was heterogeneously enhanced. An endoscopic ultrasonography (EUS) revealed four tumors in the body and tail of the pancreas, except for the giant tumor, and abundant blood flow in all these tumors. Immunohistochemical examinations of a EUS-guided fine-needle aspiration biopsy showed that the giant pancreatic tumor and liver tumors were positive for chromogranin A, synaptophysin, and CD56; thus, the tumors were diagnosed as being a pancreatic neuroendocrine tumor (NET) and its liver metastases. They were NET G1 as the labeling index of Ki67 was 1.8 %. A calcium gluconate injection into the distal splenic artery during a selective intra-arterial calcium injection test resulted in a marked increase in serum insulin and C-peptide. Both 123I-metaiodobenzylguanidine scintigraphy and 131I-adosterol scintigraphy showed high radioactivity in the right adrenal tumor and no radioactivity in the left one. The left adrenal tumor was therefore diagnosed as having a non-functional adenoma. A magnetic resonance imaging (MRI) identified a heterogeneous pituitary adenoma, 3.1 cm in diameter.
His pedigree diagram is shown in Fig. . Five patients with MEN1, including our patient who has an MEN1 gene mutation, were identified within his family. Furthermore, the genetic examination revealed a deletion mutation (g.249_252delGTCT) at codons 83–84 in exon 2. He underwent distal pancreatectomy, splenectomy, cholecystectomy, right adrenalectomy, abdominal subcutaneous tumor excision, and cutaneous tumor biopsy for the purpose of tumor volume reduction. Six tumors in the resected pancreas were diagnosed as being pancreatic NETs. The giant tumor in the pancreatic tail was insulinoma, and NET G2 as the Ki67 labeling index was 4.2 % (Fig. ). Of the other five lesions, two tumors consisted of the insulin-positive tumor cells with less than 0.1 % of the Ki67 index, and three tumors consisted of the glucagon-positive tumor cells with less than 0.1 % of the Ki67 index. These tumors were diagnosed as being non-functional NET G1 because no symptom due to a glucagon excess was encountered. A non-functional adrenal cortical adenoma, measuring 1.3 cm in maximum diameter, and a pheochromocytoma, measuring 4.7 cm in maximum diameter, coexisted in the right adrenal gland (Fig. ). The abdominal subcutaneous tumor was found to be a neurofibroma, and the cutaneous tumor was a fibroma.
During the postoperative outpatient follow-up, he developed diabetes mellitus and required treatment with an oral antidiabetic drug. For the treatment of his pituitary prolactinoma, cabergoline was administered. Octreotide therapy for the multiple liver metastases of the NETs began 2 months after the operation. After the ninth administration of the octreotide, three new lesions were detected in the liver on a CT scan. His general condition was judged to be tolerable to undergo liver resection, and the radiological examinations showed that there was no recurrence except the liver. Complete surgical resection of liver metastases was therefore achieved by an extended right posterior segmentectomy with partial hepatectomy of S2, S3, and S8. Immunohistochemical examination revealed that liver metastases were derived from a glucagon-positive tumor of the pancreatic NET. The Ki67 labeling index of these lesions ranged from 1.5 to 5.4 %.
Nineteen months after the hepatectomy, a CT scan revealed a small nodule in the S4 of the liver. Twenty-three months after the hepatectomy, gadoxetic acid- or gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid-enhanced MRI demonstrated multiple liver tumors. We started everolimus therapy following a diagnosis of unresectable pancreatic NET recurrence. He is still alive after 4 years and 4 months after the initial surgery, although he is suffering from worsened diabetes mellitus, a pituitary prolactinoma that led to a hemorrhage into the pituitary tumor, and an increasing size of the left nonfunctional adrenal tumor.
MEN1 is an autosomal-dominant hereditary syndrome caused by germline mutations of the MENIN gene that predisposes the development of endocrine and non-endocrine tumors with variable penetrance [–, ]. The most frequent tumors in MEN1 patients arise in the parathyroid glands, the pancreas, and the pituitary gland [, , ]. The incidence of pancreatic NETs is reported to be from 50 to 70 %. Insulinoma is one of the pancreatic NETs arising in the setting of MEN1. In Japan, the mean tumor size of pancreatic NETs was reported to be 3.03 cm at the time of diagnosis [], whereas that of insulinoma was smaller than 2 cm in approximately 70 % of insulinoma patients, probably because insulinoma is a symptomatic disorder []. There are some previous reports on a giant insulinoma [–], and the insulinoma with a diameter of 18 cm in the present case is the second largest by referring to the previous reports. Moreover, only the present case did not complain of hypoglycemic symptoms, whereas all other patients with giant insulinoma presented such symptoms. The reasons why the present case showed no hypoglycemic symptoms were unclear; however, we can propose some hypotheses for this: pheochromocytoma might reduce hypoglycemia due to insulinoma; at the time of hypoglycemia, our patient overate unconsciously; and glucagon secreted from glucagon-positive tumor cells compensates hypoglycemia.
More than a half of the patients with a giant insulinoma reportedly had a liver metastasis at the time of diagnosis. Liver metastases of the present case were estimated to be derived from the glucagon-positive cells of the pancreatic NET. This was consistent with the consensus that non-functional tumor have a higher incidence of liver metastases than insulinoma []. On the other hand, the fact that the Ki67 labeling index of metastatic tumors was higher than that of the primary tumors suggested that highly proliferative components had more potential to form metastatic lesions.
An incidence of adrenal involvement in patients with MEN1 is about 20 % [], most of which lesions are derived from the adrenal cortex. Concomitant pheochromocytoma is rare [, ]. Corticomedullary mixed tumor is a single adrenal tumor mass composed of an intimately admixed population of both adrenal cortical cells and pheochromocytes []. However, in our case, adrenal cortical adenoma and pheochromocytoma separately coexisted in the same adrenal gland, which is extremely rare [–], and even more so in the setting of the MEN1.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [187.0, 'cm']}",81.33081,77.26427,85.39735,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 187.0 cm, which is 187.0 cm * 0.393701 in/cm = 73.62209 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (73.62209 (in inches) - 60) = 81.33081 kg.
Hence, the patient's IBW is 81.33081 kg."
3670,10,Ideal Body Weight,physical,decimal,pmc-6913300-1,Extracted,"A 45-year-old male patient was brought to the emergency department at 01 : 00 a.m. in unconscious status with multiple gunshot injuries. He weighed 70 kg and was 168 cm tall. The patient was paraplegic. One of the bullets entered from the left arm pit and left the body from the right scapula. There was another bullet entrance from the right upper abdominal quadrant. His relatives did not present any history of previous medical issues or regular use of medications. Chest roentgenogram and computerized tomography scans indicated hemopneumothorax in the left hemithorax with destruction of the upper lobe of the left lung. In addition, the vertebral corpuses of T4 and T5 were severely destructed. There were liver and spleen injuries with intra-abdominal fluid accumulation.
A chest tube was inserted emergently into the left hemithorax and revealed 650 ml hemorrhagic fluid drainage and resulted in expansion of the lung. He was intubated, and vertebral stabilization surgery, as well as laparotomy to treat hepatic and splenic lacerations was performed. The patient was followed at the intensive care unit, however could not be extubated. His status deteriorated on the third day (PaO2/FiO2 became 154). Endotracheal aspiration and wound cultures resulted negative. The appearance of the lungs worsened on chest roentgenograms, and we diagnosed him as ARDS according to the ARDS Berlin Criteria. Despite various mechanical ventilation and physiotherapy attempts, the status of the lungs did not improve and PaO2/FiO2 ratio became 53 and pulmonary compliance decreased to 18 ml/cmH2O. We decided to institute V-V ECMO with echocardiography guidance [], despite the risk of bleeding due to multiple penetrating injuries and recent surgical treatment. ECMO flow was adjusted to 2 lt/min at a rate of 9,000 rpm, mechanic ventilator FiO2 of 0.6, positive end-expiratory pressure (PEEP) of 12 cmH2O, tidal volume of 420 ml, peak inspirium pressure of (PIP) 24 mmH2O, and inspiration/expiration ratio of 1/1 which were adjusted according to the blood gas analysis. However, we needed to gradually increase the flow of ECMO to 6 lt/min due to worsening of oxygenation. V-V ECMO in conjunction with mechanic ventilation provided sufficient gas exchange ().
The patient developed septic cardiomyopathy which was confirmed with echocardiography indicating severely depressed myocardial functions (ejection fraction of 35%) on the postoperative 13th day, despite wide-spectrum antibiotherapy with vancomycin and meropenem. Although cultures were negative, white blood cell count increased to 19/uL, thrombocyte count decreased to 66/uL, CRP increased to 234 mg/L, procalcitonin increased to 8.5 ng/ml, and total bilirubin and direct bilirubin levels increased to 18 mg/dl and 16 mg/dl, respectively. His inotropic score gradually increased to 40 and we decided veno-arterio-venous (hybrid) ECMO with addition of V-A ECMO to the femoral artery and vein. The deterioration in patient's hemodynamics, echocardiography findings, and blood gas analysis are presented in .
His status gradually improved in time and he was weaned off V-A-V ECMO with rapid consecutive conversion to V-V ECMO for a few hours and then completely disconnected on the 20th day with decreased leucocyte count (9/uL), increased thrombocyte count (163/uL), decreased CRP (63), and decreased total bilirubin (3/uL) levels. His mechanical ventilation parameters were FiO2 0.5, P/F 262, PEEP 8 cmH2O, TV 450 ml, PIP 23 cmH2O, I/E 1/2, and compliance 37 ml/cmH2O which were confirmed with chest X-ray (). Two days after, he was in stable conditions, and percutaneous tracheostomy was performed. He was discharged from the intensive care unit and from the hospital on the 24th day and one week after, respectively.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.0, 'cm']}",64.12607,60.91977,67.33237,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg."
3671,10,Ideal Body Weight,physical,decimal,pmc-5647822-1,Extracted,"A 21-year-old man (ASA class I, weight 67 kg, height 171 cm) with a nasal bone and mandible fracture was scheduled for closed reduction of the nasal bone and open reduction with internal fixation of the right mandibular angle (). His past medical history was unremarkable; he had no history of previous surgeries. Preoperative evaluation including laboratory tests, electrocardiography, and chest radiography was normal. There were no specific findings upon airway examination, including mouth opening, thyromental distance, and Mallampati classification (grade II).
We discussed the anesthetic plan with the surgeon who suggested nasal intubation with an endotracheal tube (ETT) while performing the mandible surgery and oral intubation while performing the nasal bone surgery.
General anesthesia was induced using intravenous injection of 60 mg lidocaine, 100 µg fentanyl, 120 mg propofol, and 50 mg rocuronium, with standard monitoring and preoxygention. After the induction of anesthesia, 3 cotton swabs with water soluble jelly mixed with a 0.01% epinephrine solution were inserted into the right nostril. After mask ventilation for 3 minutes with 100% oxygen and 4 vol% sevoflurane, we removed the cotton swabs and inserted a lubricated 6.5-mm Polar™ Preformed Tracheal Tube (Smith Medical, Keene, NH, USA) under the guidance of an FOB (3.8 mm, Pentax, Japan). General anesthesia was maintained using 1.5-3 vol% sevoflurane; open reduction and internal fixation of the mandible was performed successfully; within an operating time of 1 hour and 45 minutes. We then tried to use an FOB to intubate the patient orally, but bleeding and secretions blocked the view of the FOB despite repeated suctioning. Subsequently, used a C-MAC® video laryngoscope (Karl Storz Endoscopy-America, CA, USA) to guide the route of FOB. The C-MAC® video laryngoscope showed a clear view of the glottis while the view of the FOB was blurred with secretion and blood. Using the C-MAC® video laryngoscope we successfully guided and inserted the FOB into the trachea without manipulating the nasal ETT (, ). After confirmation of the tracheal ring on the FOB view, we removed the nasal ETT and followed with the railroading of an oral ETT via the FOB (). After confirming the EtCO2 curve, mechanical ventilation was resumed. Closed reduction of the nasal bone was performed after the nasal to oral endotracheal tube exchange. Upon completion of the procedures, any residual muscle relaxation was reversed with atropine and neostigmine. The patient was successfully recovered without complications and was extubated. The postoperative period was uneventful.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [171.0, 'cm']}",66.8426,63.50047,70.18473,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 171.0 cm, which is 171.0 cm * 0.393701 in/cm = 67.32287 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.32287 (in inches) - 60) = 66.8426 kg.
Hence, the patient's IBW is 66.8426 kg."
3672,10,Ideal Body Weight,physical,decimal,pmc-2827123-1,Extracted,"In October 2001, a 33-year-old Caucasian female office employee visited our orthopedic outpatient clinic, with complaints of chronic pain in the left hip since 1997. Her medical history showed two episodes of pleuritis and infertility problems. The patient lived a healthy life; non-smoker and 2 units of alcohol per week. Her length was 1.68 m and her weight approximately 67 kg. In both episodes of pneumonia Ziehl-Nielsen staining showed no tubercles in pleural effusion.
In order to find an explanation for her infertility the patient had undergone a laparoscopy in 1999. Intra-abdominal granulomas, adhesions and signs of chronic peritonitis were found. Ziehl-Nielsen and periodic acid-schiff staining (PAS staining) of peritoneal effusion and granulomas did not show acid fast bacilli.
One year previously a clinical analysis of her hip complaints was performed on the rheumatology department of another hospital. There, the hip had been visualized by CT scan, MRI and skeletal scintigraphy, but no diagnosis had come up. Rheumatologic blood testing and Mycoplasma serology had been negative. Ziehl-Nielsen staining of pus aspired from the hip had been negative for acid fast bacilli, culture had been negative for Mycobacterium tuberculosis as had polymerase chain reaction.
When the patient first visited us, her walking distance was limited to thirty minutes with crutches. No other joints were affected. No fever, nocturnal sweating or weight loss was present. On physical examination, there were no symptoms of infection. All hip joint movements were limited and painful (flexion 80Â°; abduction 20Â°; adduction 10Â°; internal rotation 0Â°; external rotation 0Â°). Hematological blood testing revealed a total white blood count of 9.4/cu mm. and ESR of 30 mm in the first hour. Conventional hip radiography showed some osseous destruction of the joint with narrowing of the joint space, suggesting loss of articular cartilage (Figure and Figure ). A review of the earlier made MRI revealed osteonecrosis, destruction of the hip joint, periarticular oedema, and multiple fluid collections, and with these features and the abdominal granulomas in mind the suspicion of articular tuberculosis arose (Figure ). Additional chest radiography did not show any abnormalities. We decided to perform an open biopsy to obtain a diagnosis. At surgery, granulation tissue and destruction of the cartilage of the femoral head was seen, also suggesting articular tuberculosis. In comparison with the earlier made MRI, which showed some acetabular destruction, there was progressive destruction of the superior part of the acetabulum which had resulted in a large local osseous defect and superior migration and lateralization of the femur. Our goal was to fill the acetabular osseous defect by in situ ankylosis of the femoral head, instead of performing the classical Girdlestone resection arthroplasty. After soft tissue debridement, the left hip was immobilized in a hip-spica cast.
Ziehl-Nielsen staining of the debris was positive for acid-fast bacilli. A Mantoux-test was performed, which was strongly positive. The patient was treated with tuberculostatics (Isoniazid, Rifampicine, Ethambutol and Pyrazinamide) for 12 months. Filling of the acetabular defect resulting from ankylosis with the femoral head occurred approximately 4 months after initiation of chemotherapy and immobilisation (Figure ). After fusion, shortening of the left leg and an intentional flexion position of 20Â° were present. From then the patient was mobilized without crutches. In November 2003, two years after the index operation, a primary one-stage cementless total hip arthroplasty was performed (OsteonicsÂ© Total Hip System, Stryker USA). Histopathological examination of the retrieved bone and joint capsule showed no signs of tuberculosis. Therefore, postoperatively she did not receive any tuberculostatics. No peri or postoperative complications occurred.
At the latest follow up in March 2008, 52 months after total hip replacement, no signs of reactivation of the tuberculosis were present. The patient experienced no pain and had a normal range of motion. She did not suffer from any significant limitations in her daily activities, including sports and labour. The bone that formerly belonged to the femoral head, had fully integrated with the acetabulum. Radiological assessment of the left hip showed no signs of loosening (Figure ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.68, 'm']}",59.62607,56.64477,62.60737,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.68 m, which is 1.68 m * 39.3701 in/m = 66.14177 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.14177 (in inches) - 60) = 59.62607 kg.
Hence, the patient's IBW is 59.62607 kg."
3673,10,Ideal Body Weight,physical,decimal,pmc-4730928-1,Extracted,"A 22-year-old male, height 173 cm, presented with history suggestive of mania of 2 weeks duration. He had two prior episodes of mania that responded well to lithium, which he discontinued following remission of symptoms. His birth and developmental history was unremarkable and premorbidly he was well adjusted. There was no family history of any psychiatric illness. Physical and neurological examination was normal. Mental status showed features supportive of euphoric mania. Baseline investigations including blood count, thyroid profile, fasting and post prandial plasma glucose, lipid profile, liver and renal function test were normal. Considering past response, he was prescribed lithium carbonate 1,200 mg/day (with serum level of 1 meq/L) and quetiapine 400 mg/day with which there was complete resolution of manic symptoms over next two months. Thereafter, quetiapine was gradually tapered over next six months.
After nine months, he reported of weight gain of 12 kg from his baseline weight of 68 kg (body mass index [BMI] 22.72 kg/m2), while on maintenance dose of lithium 1,200 mg/day. He was suggested diet control and physical exercise (no formal program), and was maintaining well for next two years, after which he reported further weight gain of 13 kg (i.e., 93 kg, BMI 31.07 kg/m2, class I obesity). Investigations including blood sugar, lipid profile and thyroid functions were within normal range. Considering previous good response, lithium treatment was continued at the same dosage. He was started on metformin 500 mg daily which was increased to 500 mg twice daily for weight gain related to lithium. After six months, there was reduction of 8 kg (i.e., body weight of 85 kg), without any emergent adverse effect. The changes in body weight and BMI are summarized in . Fasting blood sugar was monitored during follow ups, which was within normal range.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.0, 'cm']}",68.65362,65.22094,72.0863,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.0 cm, which is 173.0 cm * 0.393701 in/cm = 68.11027 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.11027 (in inches) - 60) = 68.65362 kg.
Hence, the patient's IBW is 68.65362 kg."
3674,10,Ideal Body Weight,physical,decimal,pmc-6607871-1,Extracted,"A 36-year-old, gravida 5 para 2 parturient with a singleton pregnancy was scheduled for a cesearean delivery with possible hysterectomy at 34 3/7 weeks. She had been diagnosed with a complete placenta previa and focal accreta at 29 weeks gestation. She had three prior cesearean deliveries with the second one resulting in nonsurviving conjoined twins. She had been in the hospital for 2 weeks before her cesearean delivery due to a large volume bleed (estimated blood loss of 500 ml) that resulted in hypotension and required transfusion of 2 units of packed red blood cells (PRBC). She weighed 76 kg and was 157 cm tall. Her airway exam was Mallampati class II, with normal mouth opening, full range of motion of her neck and thyromental distance >6 cm. Admission hematocrit was 31.6 g/dL, platelet count was 139 × 109/L, and international normalized ratio (INR) was 1.1.
Intravenous (IV) access was obtained (2 × 16G peripheral IV cannulae). Combined spinal-epidural anesthesia was performed with a 17-G Touhy needle and Gertie Marx 26-gauge needle at the L3/4 interspace. The patient was given a spinal dose of 0.75% bupivacaine 12 mg, fentanyl 10 mcg, and preservative-free morphine 200 mcg intrathecally, and a Springwound 19-G epidural was inserted. The patient obtained a T4 sensory block to cold and sharp sensation bilaterally.
Cesarean delivery was performed through a midline skin incision followed by classical uterine incision with the neonatal Apgar scores were 2 and 8 at 1 and 5 min, respectively. Following delivery, general anesthesia was induced, and a supracervical hysterectomy was performed. There was significant bleeding from her sacral plexus, more specifically, the left ovarian vein. A general surgeon was consulted secondary to bleeding and increased hemodynamic instability.
A TEE probe was inserted during the hemorrhage resuscitation to help assess volume status and guide administration of blood, blood products, and fluid management. Soon after transthoracic echocardiography (TTE) insertion, an echodense freely-mobile mass consistent with a large clot swirling in the right atrium was observed. The clot then entered the right ventricle and exited through the outflow tract. Shortly afterward, the patient's end-tidal carbon dioxide suddenly declined, and she went into pulseless electrical activity requiring three rounds of cardiopulmonary resuscitation with chest compressions. She was given multiple doses of epinephrine, sodium bicarbonate, and calcium chloride as indicated. After return of spontaneous circulation, the TTE showed severe global hypokinesis of the right ventricle and left ventricle. Subsequent TEE examination several hours later showed the improved function of an now underfilled left ventricle, severe septal hypokinesis to akinesis with preserved right ventricle apical function consistent with McConnell's sign. Though poorly visualized, there was an echo density in the right pulmonary artery consistent with a large embolus.
The patient was started on inhaled nitric oxide at 15 ppm due to TEE signs showing increased right ventricular pressure, and an epinephrine infusion to maintain blood pressure was initiated. The patient continued to bleed from the surgical site as well as from a liver laceration sustained during the chest compressions, and a 10.5 L estimated blood loss was recorded during her surgery. Intraoperatively she received 48 units of PRBC's, 40 units of fresh frozen plasma, 13 units of platelets, 8 units of cryoprecipitate, 8 L of crystalloid, and 7 mg of factor VII. Hematological parameters after massive volume resuscitation were: hemoglobin 13.4 g/dL, platelet count 193 × 109/L, prothrombin time 13.8 sec, partial prothrombin time 37.1 sec, INR 1.1, and fibrinogen 263 mg/dL.
3 h after going to the intensive care unit she was brought back to the operating room for surgical exploration, abdominal washout, and re-packing. The partial pressure of oxygen in blood remained in the low 40's and epinephrine was required to keep her systolic blood pressure over 90 mmHg. An IABP was placed due to severe cardiac dysfunction, and resulted in a dramatic improvement of her hemodynamics and oxygenation. She was taken back to the intensive care unit on an IABP, inhaled nitric oxide and an epinephrine infusion. 3 days later her IABP was removed after she had stabilized hemodynamically. She continued to improve and was subsequently extubated on postoperative day 7. A bilateral upper extremity venous duplex showed evidence of occlusion in one of the two right brachial veins and noncompression of the cephalic veins bilaterally. She was started on therapeutic anticoagulation (heparin drip with goal of keeping partial thromboplastin time between 55 and 75 s). She required a cystotomy repair on day 30 and was discharged home 35 days after her cesarean hysterectomy without significant morbidity and intact neurological function.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [157.0, 'cm']}",49.66544,47.18217,52.14871,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 157.0 cm, which is 157.0 cm * 0.393701 in/cm = 61.81106 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.81106 (in inches) - 60) = 49.66544 kg.
Hence, the patient's IBW is 49.66544 kg."
3675,10,Ideal Body Weight,physical,decimal,usmle-3696,Extracted,A 21-year-old woman comes to the physician because of hair loss on her frontal scalp over the past year. Menses have occurred at irregular 40- to 60-day intervals since menarche at the age of 17 years. She has no history of serious illness and takes no medications. She is 162 cm (5 ft 3 in) tall and weighs 73 kg (158.7 lb); BMI is 28 kg/m2. Her pulse is 75/min and blood pressure 130/76 mm Hg. Physical examination shows scattered pustules on her face and patches of velvety hyperpigmentation on her axilla and groin. Her morning serum cortisol concentration is 18 μg/dL.,"Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [162.0, 'cm']}",54.19299,51.48334,56.90264,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.77956 (in inches) - 60) = 54.19299 kg.
Hence, the patient's IBW is 54.19299 kg."
3676,10,Ideal Body Weight,physical,decimal,pmc-4845710-1,Extracted,"A 24-year-old female patient complained of frequent yawning over the past month while
standing up at work. Her lips were occasionally cyanotic, as noticed by her mother.
The patient had undergone extracardiac TCPC at the age of 8 years due to a complex
of congenital cardiovascular malformations, including heterotaxy/asplenia/right
atrial isomerism, bilateral superior vena cava, common atrium, common
atrioventricular valve, double-inlet and double-outlet left ventricle,
dextro-transposition of the great arteries, supravalvular pulmonary stenosis, left
aortic arch, and total anomalous pulmonary venous connection.
During evaluation at the outpatient clinic, the patient presented orthodeoxia
detected by pulse oximetry, with an oxygen saturation (SpO2) of 96% in
the supine position and 88% in the upright position. Platypnea was not observed at
that time. With a diagnostic suspicion of secondary pulmonary arteriovenous
malformation (PAVM) following the TCPC, the patient was admitted for further
evaluation and treatment.
On admission, she weighed 63 kg and her height was 166 cm. Her blood pressure was
120/71 mmHg, pulse rate was 88 beats/min, and respiratory rate was 20 breaths/min.
Laboratory tests showed a hemoglobin level of 15.6 g/dL, and normal liver function
and blood coagulation tests. No information regarding the underlying cause of the
orthodeoxia could be obtained from plain chest radiograph and electrocardiogram
evaluations.
Cardiac catheterization, performed after the patient granted informed consent, showed
an SpO2 on the ascending aorta of 93%. Peak systolic pressure in the
inferior vena cava, TCPC conduit, left superior vena cava, and branch pulmonary
arteries were all 16 mmHg. Pulmonary capillary wedge pressure was 13 mmHg,
end-diastolic left ventricular pressure was 9 mmHg, and transpulmonary capillary
gradient was 7 mmHg. An angiography showed three anomalous systemic veins
corresponding to a VVM draining in sequence from the inferior vena cava, hepatic
vein, pulmonary veins, and pulmonary venous atrium (functional left atrium) ( and ). This VVM caused a right-to-left shunt, accounting for the oxygen
desaturation.
A percutaneous transvenous coil occlusion was performed uneventfully. After the
procedure, an angiography of the inferior vena cava showed complete occlusion of the
VVM ( and ). At a 12-month follow-up, the patient reported that the
yawning-orthodeoxia had disappeared, and a postural change test showed no oxygen
desaturation in the upright and supine positions, with SpO2 measurements
of ~92-96% (> 90%).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [166.0, 'cm']}",57.81505,54.9243,60.7058,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 166.0 cm, which is 166.0 cm * 0.393701 in/cm = 65.35437 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (65.35437 (in inches) - 60) = 57.81505 kg.
Hence, the patient's IBW is 57.81505 kg."
3677,10,Ideal Body Weight,physical,decimal,pmc-8005225-1,Extracted,"This case involves an unmarried 25-year-old phenotypic Japanese female, 154.1 cm in height and 48.5 kg in weight, and without a notable medical, family, or psychosocial history. She did not consume alcohol, tobacco, or any drugs. The patient was examined at the age of 18 at a gynecology clinic for primary amenorrhea where, given the patient’s active involvement in competitive track and field, she was diagnosed with athletic amenorrhea without further tests being conducted. Afterwards, the patient underwent no treatment and did not experience menstruation. Moreover, the patient had not engaged in sexual intercourse up to this point.
Upon examination by a local physician with the main complaint of abdominal distention, the patient was referred to our hospital with a suspected ovarian tumor, as a giant 17 cm tumor was found in the pelvis. The inspection of the external genitalia revealed clitoral hypertrophy and narrowing of the vaginal opening (Fig. ). Pelvic magnetic resonance imaging (MRI) revealed a tumorous lesion in the pelvis measuring 218 × 115 × 178 mm, containing a mixture of cystic and solid components. The uterus could not be found. The cystic components contained blood, and the solid portion had a contrast effect (Fig. ). Examination by 18F-fluorodeoxyglucose (FDG)-positron emission tomography/computed tomography revealed FDG accumulation in the tumor and in enlarged abdominal para-aortic lymph nodes. Blood tests revealed the following levels: white blood cells (WBC): 10.7/μL × 103; hemoglobin: 10.1 g/dL; platelets: 412/μL × 104; C-reactive protein (CRP): 18.1 mg/dL; total protein: 7.7 g/dL; albumin: 3.8 g/dL; urea nitrogen: 8 mg/dL; creatinine: 0.53 mg/dL; total bilirubin: 0.6 mg/dL; aspartate aminotransferase (AST): 30 IU/L; alanine aminotransferase (ALT): 8 IU/L; follicle-stimulating hormone (FSH): 52.4 mU/mL; luteinizing hormone (LH): 34.4 mU/mL; estradiol (E2): < 10 pg/mL; progesterone (P4): 0.66 ng/mL; and testosterone: 0.25 ng/mL. Serum alpha-fetoprotein (2.4 ng/mL) was within the normal range, but serum beta-human chorionic gonadotropin (5.86 ng/mL), lactate dehydrogenase (4574 µg/L), and CA125 (165 µg/mL) were elevated. Urinalysis was normal. As DSD was suspected because of the appearance of the pelvic tumor, chromosome testing was performed. The karyotype was found to exhibit 45,X/46,XY mosaicism, and the patient was diagnosed with MGD. Since the pelvic tumor was considered to be a gonadal tumor, a resulting complication of MGD, an exploratory laparotomy was performed in order to arrive at a definitive pathologic diagnosis of the tumor.
A physical examination revealed a patient who looked unwell, with blood pressure of 119/77 mmHg, heart rate of 117 beats per minute, and body temperature of 38.7 °C. Neurological examination was unremarkable and did not offer any substantial information. Surgical findings revealed marked adhesions between the tumor and the surrounding organs, making excision difficult. Therefore, only a biopsy of the tumor was performed (Fig. a, b). The final pathological diagnosis was “seminoma” (Fig. ). Consequently, the patient was diagnosed with clinical stage IIB testicular cancer (seminoma) with MGD.
Postoperative systemic chemotherapy was started promptly, consisting of bleomycin, etoposide, and cisplatin (BEP). At the time of the fourth course of BEP, tumor markers had normalized (Fig. ). Marked tumor reduction was confirmed with imaging, and subsequently the patient underwent interval debulking surgery. Surgery involved bilateral gonadectomy and resection of disseminated peritoneal lesions (Figs. a, b, ). Pathological examination of the excised specimens was consistent with necrosis of the seminoma due to the effect of chemotherapy. No viable tumor remains were found. No further chemotherapy was administered, and the initial course of treatment was completed. We notified the patient regarding MGD, and she decided her future sex as female. Therefore, we proposed some surgical options for clitoromegaly or vaginal stenosis. However, she did not wish to pursue those at that time.
Currently, 4 years and 11 months after the initial treatment, there has been no recurrence of the tumor. In addition, the patient has been on postoperative hormone replacement therapy in the form of an estradiol/norethindrone acetate patch and psychotherapy continuously.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [154.1, 'cm']}",47.03944,44.68747,49.39141,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 154.1 cm, which is 154.1 cm * 0.393701 in/cm = 60.66932 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.66932 (in inches) - 60) = 47.03944 kg.
Hence, the patient's IBW is 47.03944 kg."
3678,10,Ideal Body Weight,physical,decimal,pmc-2892671-1,Extracted,"A 48-year-old woman (weight: 108 kg, height-170 cm) was scheduled for a laparoscopic cholecystectomy because of cholelithiasis. At the preoperative assessment she reported postoperative apnoea following a Caldwell-Luc procedure at the ENT-OR in 1981. A prolonged effect of succinylcholine had been confirmed by a dibucaine number of 10, written on a crumpled warning card. The patient herself was absolutely clear about the condition of her butyrylcholinesterase deficiency. Her medical history showed an appendectomy, hypertension, and a trigeminal neuralgia due to repetitive sinus infections. Current medication was amitriptyline, gabapentin, diclofenac, omeprazole, metoprolol, and acetaminophen combined with codeine.
Induction of anaesthesia was carried out with fentanyl and propofol. To facilitate tracheal intubation 100 mg succinylcholine (0.9 mg/kg) had been administered unintentionally. Maintenance was performed with intermittent dosages of fentanyl, morphine and a continuous infusion of propofol. The surgical procedure lasted 90 minutes and was done uneventfully.
Monitoring of neuromuscular function was started using acceleromyography (TOF-Watch SX), by performing intermittently a “train-of-four”. Determination of the supramaximal stimulus could not be performed, as deep neuromuscular blockade was already induced. Anaesthesia, using propofol continuously in combination with intermittent doses of morphine, and neuromuscular monitoring were continued until recovery of the TOF-ratio above 90%; at this value it was assumed that the patient could breathe without help. Recovery of neuromuscular function took more than seven hours. The first twitch was seen 87 minutes after the administration of succinylcholine. The course was uneventful although the patient was emotional and anxious postoperatively we were able to regain her trust after several talks.
After informing this adverse event to the patient and her partner, she gave permission to take blood samples for quantitative and qualitative analysis and for molecular genetic investigation.
The plasma concentration of cholinesterase was 2520 U/l (ref: 4800–12000 U/l) and the dibucaine number was 8. These results are indicative for a homozygous atypical variant. Because of the very long clinical duration of action we did not limit molecular genetic investigations to known BCHE variants but decided to sequence both strands of the complete BCHE coding sequence. This identified a homozygous A- as well as a homozygous K-variant. The A-variant (209A > T, leading to Asp70Val) is most causative for the clinical feature and the K-variant (1615G > A, leading to Ala539Thr) contributed to the markedly prolonged muscle relaxation and the dibucaine number of 8. The clinical significance of the K-variant as a single mutation has been described by Gätke et al. [].","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [170.0, 'cm']}",61.43709,58.36524,64.50894,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.92917 (in inches) - 60) = 61.43709 kg.
Hence, the patient's IBW is 61.43709 kg."
3679,10,Ideal Body Weight,physical,decimal,pmc-6737443-1,Extracted,"A 19-year-old male presented with progressive bilateral breast enlargement for the past 4 years. He had no concomitant urologic or systemic complaints. History of the growth and development was normal with pubic hair being recorded at the age of 13 years. The patient described having erections but no experience of sexual activity. He is the second son of healthy parents and his elder brother is completely healthy. There is no history of sexual ambiguity in the extended family. Physical examination revealed an apparently healthy male weighing 58 kg and 163 cm tall. The amount of facial and axillary hair was normal. Bilateral gynecomastia without accompanying lymphadenopathy or nipple discharge was noted. Examination of genitalia revealed a small but well- developed male phallus with a normally positioned single orifice at the glans penis, consistent with Prader Stage V. There was no external vaginal opening. The patient did not state penile bleeding or any kind of penile discharge. No palpable gonads were present in both labioscrotal areas. However, in the left inguinal region, a mass that was likely to be a gonad was palpated.
Hormone testing revealed normal levels of total testosterone (322 ng/dl) and estradiol (28 pg/ml) for a male. Blood dehydroepiandrosterone and prolactin levels as well as thyroid function studies were normal. However, levels of luteinizing hormone (12.4 IU/L) and follicle-stimulating hormone (19.6 mIU/L) were elevated, consistent with primary testicular failure. The cytogenetic analysis of the karyotype was performed using peripheral blood, and the analysis showed the genotype 46, XX. No translocation of sex-determining region of the Y chromosome (SRY) gene was detected on the fluorescence in situ hybridization (FISH) study.
Transscrotal ultrasonography showed no gonads in the hemiscrota. There was a well-circumscribed, ovoid, heterogeneously hypoechoic lesion of 31 × 21 × 13 mm size in the left inguinal region. Multiple focal cystic areas were recorded throughout the lesion parenchyma. Abdominopelvic ultrasonography (US) depicted a small uterus, a vagina, a small prostate, and accompanying seminal vesicles. Subsequently, an abdominal magnetic resonance imaging (MRI) study was performed on a 1.5T unit. Sagittal T2-weighted imaging demonstrated a hypoplastic uterus, a normal-looking vagina, and a hypoplastic prostate. There was a well-circumscribed lesion in the left inguinal region showing a heterogeneous high signal, compatible with the left gonad. The penis was smaller than normal []. Sagittal T2-weighted images as well as the coronal short tau inversion recovery (STIR) and axial fat-suppressed T2-weighted images nicely delineated the left gonad containing a large number of high signal foci, consistent with cystic areas. Vas deferens was visible adjacent to the left gonad []. Coronal STIR and axial fat-suppressed T2-weighted sections through the prostate and seminal vesicles showed a small prostate and multiple disorganized tubular structures at both seminal vesicle locations []. The right gonad could not be detected in any imaging sequence.
Deep wedge biopsy of the left gonad was performed. Histological evaluation revealed an ovotestis with a distinct demarcation between ovarian and testicular tissues. The ovarian portion of the ovotestis showed normal ovarian tissue with primordial follicles and ovarian stroma. Seminiferous tubules and spermatogonia were found in the testicular portion. The number of seminiferous tubules was decreased, whereas interstitial tissue was increased. Exploratory laparoscopy revealed a streak right gonad in the abdomen. A gonadectomy was performed, and the gonadal histology revealed the presence of a dysgenetic streak gonad with fibrous tissue resembling ovarian stroma. Based on the specific histological findings as well as highly supportive imaging findings, the patient was diagnosed as having ovotesticular DSD.
After the diagnosis, partial left gonadectomy and uterocolpectomy were performed. Areas of focal hemorrhage of various ages along with follicles and ovarian stroma were recorded in the assessment of the resected ovarian portion of the gonad. Further, bilateral reduction mammoplasties were performed within a few months. In the 2nd year of patient follow-up, persistent testosterone deficiency developed, and the condition was controlled by androgen supplementation.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [163.0, 'cm']}",59.5985,56.61857,62.57843,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 163.0 cm, which is 163.0 cm * 0.393701 in/cm = 64.17326 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.17326 (in inches) - 60) = 59.5985 kg.
Hence, the patient's IBW is 59.5985 kg."
3680,10,Ideal Body Weight,physical,decimal,pmc-5842090-1,Extracted,"The patient's information released was permitted after discussion by the hospital ethics committee.
A 66-year-old woman with recurrent intermittent upper quadrant abdominal pain visited our hospital for further evaluation and treatment. Physical examination and initial vital signs were as follows: body temperature, 37.0℃; pulse rate, 66 beats/min; respiratory rate, 18 breaths/min; and blood pressure, 140/90 mmHg. Her height and body weight were 158 cm and 66 kg. She had a 10-year history of hypertension with good blood pressure control from oral Valsartan (40 mg/day). Her familial history was unremarkable. Laboratory examinations showed a low white blood cell count of 3,920/µL, a hemoglobin level of 11.8 g/L, and a platelet count of 124,000/µL. The liver function test results were as follows: serum aspartate transaminase: 14 U/L; alanine transaminase: 19 U/L; alkaline phosphatase: 88 IU/L; gamma-glutamyl transferase: 16 U/L; total bilirubin: 4.05 µmol/L; albumin, 35.7 g/L; and international normalized ratio: 0.93. CA 19-9 and α-FP were assayed for a malignancy workup, with results of 16.35 U/mL and 2.61 ng/mL, respectively. The results for viral markers including HBV surface antigen and anti-HCV were negative. Abdominal CT revealed an atrophic left lobar and dilated bile duct with the middle hepatic vein close to the cystic lesion (). Abdominal MRCP revealed irregular intrahepatic bile duct dilatation (IHBDD) of the left lobe with the left hepatic duct obstructed, while the common bile duct and right intrahepatic bile duct were normal (). However, we found that the irregular cystic dilatation of the bile duct was limited to the left liver and contained stones inside the cysts. No obvious abnormal dilated bile duct was found in the right liver. The common bile duct and the hepatic duct were normal, and no obvious dilatation was found. This patient was diagnosed with Caroli disease (type V). The surgical indication for the patient was explicit. However, the treatment prescription required consideration of the cystic wall being adjacent to the middle hepatic vein, the left hepatic atrophy and structure disorder, and the observation that the left hepatic vein was not visible. Although complete resection of the cysts may be a curative treatment for unilobar Caroli disease, this treatment was impossible for this patient due to the close adherence of the middle hepatic vein to the cystic wall. Therefore, we decided to perform laparoscopic left LR for the patient, while preserving a partial cystic wall close to the middle hepatic vein.
The standard laparoscopic equipment used to perform laparoscopic hepatectomy included a 30° 5-mm laparoscope, a hook dissector, 5-mm laparoscopic forceps, a 5-mm atraumatic grasper, a 10-mm GIA (Johnson & Johnson Medical, Shanghai, China), 5-mm harmonic (Johnson & Johnson Medical) and 10-mm locking pliers.
The conventional fully laparoscopic multiport approach was adopted. The patient was placed in a supine position, and the surgeon stood on the right side. Under general anesthesia, five 5- to 10-mm incisions were made in a “U” configuration. Division of the liver parenchyma was performed with Harmonic or Endo-GIA. Large pedicles were stapled or clipped.
Upon surgical exploration, the left lobe of the liver was found to be atrophied, and the right liver had developed compensatory hyperplasia with a red-brown and smooth surface. However, the left liver lobe was severely adherent. We gradually dissected the adhesion using harmonic pliers and exposed the atrophic left lobe (5 cm × 6 cm × 2 cm). The gallbladder was approximately 7 cm × 4 cm × 2 cm in size and was filled with bile and gallstones. Through intraoperative exploration, we confirmed the diagnosis of Caroli disease, limited to the left lobe of the liver. We obtained a biopsy from the edge of the lesion and performed a rapid intraoperative pathological examination to exclude malignant tumor. We then decided to perform a laparoscopic left liver and gallbladder resection. The difficulty was that the lesion was close to the middle hepatic vein. We opened the cysts and resected most of the lesion while retaining part of cystic wall close to the middle hepatic vein. After laparoscopic left half-liver and gallbladder resection, the liver lesion tissue and gallbladder were removed completely from the abdominal cavity. Histopathologic findings showed congenital dilatation of the intrahepatic bile ducts, confirming the preoperative diagnosis of Caroli disease (). Histopathology of the resected specimen revealed large, cystic dilations of the large intrahepatic bile ducts. This patient was seen regularly every 3 months at the outpatient department. There was no recurrence of abdominal pain, and no complications were discovered after 18 months of follow-up.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3681,10,Ideal Body Weight,physical,decimal,pmc-6329232-1,Extracted,"A 54-year-old man (174 cm, 72 kg) who had childhood asthma was scheduled for laparoscopic cholecystectomy. He had been treated for hypertension with a beta-adrenergic blocker (atenolol 100 mg/day) at an outside clinic from age 50 years, although he had no other cardiovascular disease. The preanesthetic interview revealed that he had experienced no symptoms of asthma nor use of medication for more than 40 years. His chest X-ray showed no abnormalities, and his preoperative PFT showed a percent vital capacity (%VC) of 89.4% and forced expiratory volume in one second (FEV1.0) of 84.6%, suggesting full resolution of his childhood asthma.
In the operating theater, after induction of anesthesia tracheal intubation was performed; anesthesia was maintained with desflurane at an end-tidal concentration of 3.0% supplemented by intermittent boluses of fentanyl and continuous remifentanil infusion (0.1–0.15 mcg/kg/min). His lungs were ventilated with a tidal volume of 500 mL and respiratory rate of 12/min with 35% oxygen (fresh gas flow, 3 L/min) under pressure control ventilation-volume guaranteed (PCV-VG®) mode with an Avance CS2 equipped with ecoFLOW® (GE Healthcare UK Ltd., Buckinghamshire, UK). His capnogram showed an airway obstructive pattern immediately after the initiation of mechanical ventilation []. His airway pressure during pneumoperitoneum was approximately 24–26 cm H2O. Because his blood pressure dropped to 83/54 mmHg in the middle of surgery, we administered 4 mg of ephedrine intravenously. His systolic blood pressure immediately increased to over 100 mmHg, and his airway pressure dropped to 19–21 cm H2O about 10 min after its administration. Furthermore, his obstructive capnogram reverted to normal about 20 min after ephedrine []. No other interventions were undertaken except for the administration of ephedrine. The pneumoperitoneum was maintained at 10 mmHg during laparoscopy. Neuromuscular block was reversed at the end of surgery with intravenous sugammadex 200 mg. His trachea was extubated without incident. His respiratory status on the ward was stable without wheezing and 99% SpO2 under O2 administered at 5 L/min through face mask.
On postoperative day 1, our interview revealed that in recent years, he had been wheezing slightly at the turn of the seasons. On postoperative day 3, he was diagnosed as having bronchial asthma by a respirologist because his exhaled nitric oxide was 47 ppb. After this diagnosis, we carefully rechecked his preoperative PFT results and found a low peak expiratory flow and sharp fall in the flow–volume loop []. The maximal expiratory flow rate at 25% of VC (V25) and V50 values on the flow–volume curve were 3.42 and 1.04 L/s, respectively, and both were quite below expectation (expected V25 and V50 in this patient were 5.23 and 2.20 L/s, respectively). Furthermore, the V50/V25 ratio of 3.29 was greater than 3.0. These results indicated small airway obstruction. Thereafter, his antihypertensive drug was changed from the beta-blocker atenolol to the calcium channel blocker amlodipine. Treatment for bronchial asthma by inhaled ciclesonide was also added.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [174.0, 'cm']}",69.55913,66.08117,73.03709,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 174.0 cm, which is 174.0 cm * 0.393701 in/cm = 68.50397 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.50397 (in inches) - 60) = 69.55913 kg.
Hence, the patient's IBW is 69.55913 kg."
3682,10,Ideal Body Weight,physical,decimal,pmc-4684581-2,Extracted,"A 31-year-old woman with failed back surgery syndrome following a right lumbar microdiscectomy. Her weight was 93.1 kg and height 165 cm (BMI, 34.2). In her pre-PMP assessment, she had moderate depression, moderate pain-related disability and average scores on pain distress and intensity. A percutaneous trial of spinal cord stimulation was judged positive and therefore the patient opted for permanent spinal cord stimulator insertion. An eight-electrode surgical lead was implanted with the IPG in the iliac fossa. Postoperatively there was good reduction in pain scores, analgesic usage and mobility; plain X-ray indicated satisfactory electrode placement.
Four weeks after insertion, symptoms recurred to preoperative levels. Interrogation of the system revealed high impedances suggestive of electrode failure. X-ray of the system indicated an abnormal twisting of the wiring between the implanted abdominal pulse generator and the spinal electrode. The subcutaneous pulse generator had undergone repeated rotation, twisting the connecting leads to the point of fracture (Fig. ).
Surgical revision of the system was performed. The X-ray findings were confirmed intraoperatively. The IPG had rotated on its axis many times (Fig. ). A new pulse generator was implanted in her right lumbar region above the iliac crest and belt line. Postoperatively, the patient reported restoration of good pain relief.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3683,10,Ideal Body Weight,physical,decimal,pmc-5628240-1,Extracted,"A 22-year-old woman (height 160 cm; weight 50 kg; BMI 19.5 kg/m2), gravida 1 para 0, at 16 weeks of gestation (WG) presented to the emergency department complaining of lack of ability to walk and severe weakness of the lower limbs. She had no history of symptoms similar to GS, and there was no family history of neuromuscular diseases. She previously had been in excellent health apart from mild hyperemesis gravidarum, which resolved spontaneously at approximately 10 WG without medication. She had no diarrhea and denied taking herbal medicine, diuretics, laxatives, or glucocorticoids prior to her illness.
The patient was in her usual state of health when 5 days back she noticed progressive fatigue and bilateral muscle cramping predominating in lower extremities. The patient noticed knee buckling with frequent falls. Rapidly, within that span, the muscle weakness worsened, and she was confined to bed and unable to mobilize her legs, when she decided to consult in the hospital.
Her vital signs on examination were heart rate 130/min, blood pressure 100/65 mmHg, respiratory rate 22/min, oxygen saturation 99% on room air, and temperature 37°C. The patient's review of systems was found negative for shortness of breath, cough, and swallowing difficulties. On neurological examination, the patient was alert and well-oriented. Her motor strength in upper limbs was 4/5. Hip flexors, quadriceps, and hamstrings were 1/5 bilaterally; dorsiflexors and plantar flexors were 0/5 bilaterally. Her cranial nerve examination was intact, and the sensation was diminished to touch and pinprick on lower extremities. Cranial and neck muscles were normal, but examination revealed deep tendon reflex to be absent on knees and ankles. The examination of other systems was unremarkable.
Table shows the initial laboratory data of the patient. Serum level of potassium was 2.2 mmol/L, serum magnesium 0.57 mmol/L, creatinine 68 μmol/L, and urea 2.8 mmol/L. Serum levels of sodium, total calcium, glucose, cortisol, thyroid, and liver function tests were found to be in normal range. Other blood investigations showed the following: hemoglobin 12.4 g/dL, white cell count 7.5 × 103/μL with a neutrophil count 5.9 × 103/μL, and C-reactive protein 5 mg/dL. Serum creatine phosphokinase level was 55 UI/L.
Her electrocardiogram (EKG) exhibited sinus tachycardia with inversion of T wave in leads D III, V1 to V4 suggesting hypokalemia.
She was assessed by a neurologist, and a diagnosis of Guillain–Barré Syndrome (GBS) was suspected. Her time nerve conduction studies (Table ) revealed increased distal motor and sensitive latencies and reduced conduction velocities predominating in low members suggestive of acute demyelinating polyradiculoneuropathy, in keeping with GBS. Her cerebrospinal fluid (CSF) analysis revealed normal white cell count, protein, and glucose levels. The infectious and autoimmune screen was nonrevealing, and a fetal ultrasound scan showed an ongoing pregnancy at the age of 16 weeks and 6 days.
She was then shifted to ICU, and the next day, a course of IV immunoglobulins (0.4 g/kg per day for 5 days) was started, but this therapy resulted in a very poor effect. She was also given a continuous potassium supplementation in form of potassium chloride infusion (130 mmol/day) and intravenous magnesium chloride (40 mmol/day) under cardiac monitoring. Her muscle weakness worsened over 5 days of the treatment and spread to the upper limbs, trunk, and neck muscles. There was no associated difficulty in breathing or swallowing at this time. Serial biochemical evaluations during her hospital stay revealed persistent hypokalemia and hypomagnesemia despite parenteral supplements (Fig. ). This was further investigated by urine analysis, which showed the potassium to be 51.5 mmol/L (normal range 16–83), chloride: 91 mmol/L (normal range 73–167), calcium: 29 mg/L (normal range 66–200 mg/L), and creatinine: 11.5 mmol/L (normal range 3.5–23). Arterial blood gas analysis was performed with the patient breathing room air, which showed metabolic alkalosis (pH 7.48, HCO3 37.3, PaCO2 43.5). She also had increased plasma renin activity (2.6 ng/mL/h; normal range 0.12–1.59) and serum plasma aldosterone (720 ng/dL; normal range 80–365). Under the presenting circumstances, a tubulopathy causing renal potassium loss was considered. Based on the findings of hypokalemic metabolic alkalosis without hypertension, severe hypomagnesemia, and hypocalciuria, a diagnosis of GS was suspected. This diagnosis was ascertained with the sequencing of the implicated gene, which confirmed GS as a heterozygous mutation in SLC12A3.
It was decided to reinforce ion supplementation, so potassium and magnesium supplements were increased to respectively 195 and 60 mmol/day.
On day 7 of her hospitalization, her condition deteriorated, and her tidal volume and minute volume decreased with swallowing difficulty. Oxygen saturation was 90% at 10 L/min delivered via a mask. To prevent hypoxemia and avoid emergency intubation, she was intubated and ventilated on controlled mandatory ventilation mode, and her vital parameters (electrocardiogram, invasive blood pressure, oxygen saturation, and temperature) were monitored. At this point, hypokalemia of 1.9 mmol/L was evident along with magnesium 0.43 mmol/L. Periodic fetal evaluation documented fetal well-being and normal size fetus with normal liquor and Doppler.
On day 8, the hemodynamic status worsened and the patient experienced prolonged hypotension and intermittent episodes of bradycardia, which occurred spontaneously, without relation to vagal maneuvers, such as endotracheal suctioning. She required vigorous volume replacement with normal saline and the use of vasopressor (Norepinephrine infusion) to maintain her mean arterial blood pressure up to 65 mmHg. EKG examination showed sinus bradycardia with the rate of 45 and prolonged QT interval. Echocardiographic and Doppler assessment failed to reveal any abnormalities in myocardial morphology or function.
On day 9, spontaneously fetal demise was observed, and the patient developed ventricular fibrillation (VF). She underwent electrical cardioversion (200 J biphasic), which restored sinus rhythm. Serum level of potassium was 1.5 mmol/L, and serum magnesium was 0.4 mmol/L. In view of the recent clinical deterioration, the use of a potassium-sparing diuretic or aldosterone antagonist was discussed, but this approach could result in hypovolemia and possibly worsen the hemodynamic status. Spironolactone was finally administered to this patient (100 mg/day). Subsequently, she continued to present repeated VF on the same day, which was complicated by a refractory cardiac arrest despite advanced cardiac life support.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3684,10,Ideal Body Weight,physical,decimal,pmc-4722418-1,Extracted,"A 31-year-old woman was diagnosed with hypertension by a private clinic in August 2013, based upon a systolic blood pressure of 160 mm Hg and she was prescribed antihypertensive drugs to treat the condition. Initial therapy consisted of hydrochlorothiazide 12.5 mg and losartan 50 mg daily. After 1 week, her blood pressure was still high, so the doctor changed her medication to amlodipine 5 mg, losartan 100 mg, and indapamide 2.5 mg per day. Five days after initiating this second regimen of drugs, she developed pretibial pitting edema, and thorough workup was done for the symptom. There were bilateral adrenal masses on abdominal-pelvic computed tomography (CT). Routine blood tests revealed the following: potassium 2.2 mmol/L, plasma renin activity (PRA) 0.12 ng/mL/hr, plasma aldosterone concentration (PAC) 16.76 ng/dL, and an aldosterone/renin ratio (PAC/PRA) >30, indicative of primary hyperaldosteronism.
Following her possible diagnosis of primary hyperaldosteronism, the patient was referred to our hospital for additional testing. At the time of admission, her blood pressure was 155/111 mm Hg, height was 164.5 cm, and weight was 63.5 kg (body mass index, 23.47 kg/m2). Pretibial pitting edemas were detected, but no physical signs of Cushing syndrome were observed.
A routine blood test at the time of admission showed the following: white blood cell 6,900/µL, hemoglobin 13.5 g/dL, platelet 351,000/µL, total protein 6.9 g/dL, albumin 4.1 g/dL, aspartate aminotransferase 76 U/L, alanine aminotransferase 126 U/L, blood urea nitrogen 7.3 mg/dL, creatinine 0.71 mg/dL, sodium 141 mmol/L, potassium 2.9 mmol/L, chloride 101 mmol/L, total cholesterol 210 mg/dL, triglyceride 104 mg/dL, high density lipoprotein 50 mg/dL, low density lipoprotein 141 mg/dL, and hemoglobin A1c 5.9%. Biochemical evaluation of pheochromocytoma showed no excessive catecholamine production. The transtubular potassium concentration gradient was 12.64%, suggesting the possibility of hyperaldosteronism or hypercortisolism. PAC and PRA were 24.4 ng/dL and 0.76 ng/mL/hr, respectively, and the PAC/PRA ratio was 32.11 (). After correcting for hypokalemia, a saline loading test was performed, which revealed no suppression of the aldosterone level after saline administration, consistent with a diagnosis of hyperaldosteronism (the basal PAC 24.4 ng/dL increased to 27.3 ng/dL after a 2 L saline infusion). Dexamethasone suppression tests (DSTs) resulted in no suppression of cortisol levels (). Adrenal CT demonstrated two bilateral adrenal masses in each of the adrenal glands, including a 1.6-cm mass on the right and a 2-cm mass on the left adrenal gland (). An adrenal cortical scan using iodine-131-6β-iodomethyl-19-norcholesterol (NP-59) showed focally increased radioactive uptakes in the bilateral adrenal gland areas, with a substantially higher uptake on the left side ().
Bilateral adrenal venous sampling (AVS) with adrenocorticotropic hormone (ACTH) stimulation () revealed inadequate right adrenal venous blood sampling (right adrenal vein cortisol level/peripheral blood cortisol level [CRt/CP] <10), whereas the cortisol concentration in the left adrenal venous blood showed successful sampling on the left side. One explanation for this difference may be that the low level of CRt was the result of suppressed cortisol secretion due to excessive cortisol secretion from the left adrenal mass. The left adrenal vein aldosterone/cortisol (ALt/CLt) ratio was lower than that of peripheral blood, implying the possibility of suppressed aldosterone secretion from this side caused by a contralateral adrenal mass which might secrete excessive aldosterone []. Four days after the first AVS, a second AVS was performed using low-dose DST but without ACTH infusion (). This time, we also measured the epinephrine levels in the both adrenal veins and peripheral blood; a large peripheral-to-adrenal gradient of epinephrine assured successful catheterization on both sides []. CLt/CP testing confirmed that the left adrenal mass was a cortisol-secreting adenoma [].
Even though those two AVS results appeared to provide clear evidence of the lateralization of functioning adrenal masses, such an independent functioning of bilateral masses was highly suspicious. We therefore concluded that sequential adrenalectomies, rather than concurrent operations, would be beneficial for making a definitive diagnosis. Moreover, the patient agreed to do sequential operations. The first procedure was a laparoscopic partial adrenalectomy of the right adrenal gland to remove the putative aldosterone-producing mass, with the goal of controlling hypertension and hypokalemia. A firm, 1.5-cm ovoid, well-circumscribed, bright yellow tumor mass lacking necrosis or hemorrhage was arising from the cortex of the adrenal gland in the pathologic specimen. Within 24 hours after surgery, the patient's blood pressure had fallen to 110/80 mm Hg without antihypertensive medication, serum potassium normalized at 4.5 mmol/L, and PAC decreased to 3 ng/dL. These large postoperative changes strongly suggested that the right adrenal adenoma was producing excessive aldosterone. By day 3, an overnight DST continued to show no cortisol suppression, indicating persistent secretion of corticosteroid from the left adrenal mass. To limit the likelihood of subclinical Cushing syndrome progressing to overt Cushing syndrome, we opted to completely remove the left adrenal gland as a means of controlling hypercortisolism. The excised portion of the adrenal mass contained an encapsulated brown solid mass.
The patient began taking prednisolone 10 mg once a day for steroid replacement 1 day after the second surgery. By 2 months she had lost 5 kg of body weight. At that time, a rapid ACTH test revealed adrenal insufficiency (). At 16 months after surgery, the patient has gradually reduced her prednisolone intake to 5 mg every other day. Her blood pressure and serum potassium levels have remained within normal ranges, without the need for additional antihypertensive medications or potassium supplements.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [164.5, 'cm']}",56.45676,53.63392,59.2796,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 164.5 cm, which is 164.5 cm * 0.393701 in/cm = 64.76381 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.76381 (in inches) - 60) = 56.45676 kg.
Hence, the patient's IBW is 56.45676 kg."
3685,10,Ideal Body Weight,physical,decimal,pmc-6565551-1,Extracted,"The index patient was a 34-year old female referred to the bariatric clinic by the general practitioner on her own request to treat her morbid obesity. She was born with a normal birth weight but large head circumference for which she never had a diagnostic analysis. At the age of five, her body weight was already significantly higher compared to her peers. No specific life events could explain her obesity. Cognitive development was normal and she followed normal education. She underwent treatment for recurrent nasal polyps. Her mother also had a large head size and suffered from morbid obesity as well. She was diagnosed with thyroid cancer and died from a pulmonary embolism after placement of an Adjustable Gastric Band. A maternal aunt was diagnosed with breast cancer before the age of 50 and the maternal grandmother died from breast cancer at young age. The younger sister of the index patient was overweight and was reported to also have a large head size (Figure ).
Since childhood, the index patient followed several different coaching programs to change her eating behavior and exercise pattern to induce weight loss. She lost weight several times but was never able to maintain her weight loss. At the time of the intake procedure at the bariatric clinic, her height was 1.69 m (SD −0.2) and weight 164 kg (SD +6.8), resulting in a Body Mass Index (BMI) of 57.6 kg/m2 and a predominant abdominal obesity. Head size was not measured at that time since this is not part of bariatric screening procedures. Biochemical analysis of the blood revealed no abnormalities, and excluded endocrine hormonal disorders such as hypothyroidism. The fasting glucose level was 5.9 mM.
The combination of early onset morbid obesity resulted in suspicion of a genetic cause of her obesity. She was offered diagnostic genetic analysis of 52 obesity–associated genes to identify a possible underlying genetic obesity cause.
The patient was eligible for bariatric surgery and underwent a sleeve gastrectomy without complications (performed in 2014 using a standardized fashion). At 1, 2 and 3 years after surgery, she achieved a percentage Total Body Weight Loss of 39.4, 48.8 and 44.9, respectively. This resulted in a current BMI of 30.1 kg/m2. This was within the range of the results which were observed in a control group of 18 female patients, with a negative obesity genetic test result. These female patients were matched for age and BMI and achieved a percentage Total Body Weight Loss (TBWL) of 30.3 after 1 year, 31 after 2 years and 30 after 3 years of follow-up.
A few months after surgery, the result of the obesity gene panel analysis was returned and showed heterozygosity for a known pathogenic mutation in the PTEN gene (): c.202T>C p.(Tyr68His). This mutation has been described previously in patients with PTEN Hamartoma Tumor Syndrome (PTEN HTS) (Marsh et al., ). No other pathogenic mutations were shown in the remaining 50 obesity–associated genes (Table ). At the genetic clinic, a head circumference of 63 cm (+5SD) and pedigree analysis (family history of multiple tumors) further supported the molecular diagnosis of PTEN HTS.
According to the PTEN HTS guidelines, patients with pathogenic PTEN mutations are advised to visit the outpatient clinic for familial tumors, for lifelong surveillance of tumors that are associated with the PTEN mutations (Dutch Guidelines, ; Eng, ). Our patient underwent additional biochemical laboratory- and ultrasound screening to exclude thyroid gland carcinoma. Besides a few benign nodules on the ultrasound, no abnormalities could be determined. A yearly follow-up ultrasound of her thyroid gland and yearly serum thyroid stimulating hormone analysis was advised. Screening for breast, endometrium and colorectal cancer, also revealed no anomalies.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.69, 'm']}",60.53158,57.505,63.55816,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.69 m, which is 1.69 m * 39.3701 in/m = 66.53547 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.53547 (in inches) - 60) = 60.53158 kg.
Hence, the patient's IBW is 60.53158 kg."
3686,10,Ideal Body Weight,physical,decimal,pmc-4752942-1,Extracted,"A 64-year-old Japanese man without any symptoms had a medical checkup, and abdominal ultrasonography revealed a mass of the right upper abdomen with acoustic shadow. He had hypertension and underwent appendectomy for appendicitis by McBurney’s incision at 13 years old. He was 162 cm tall and weighted 70 kg (body mass index, 26.8). His blood pressure, pulse, oxygen saturation, and body temperature were 146/76 mmHg, 66 beats/min, 97 %, and 36.2 °C, respectively. His abdomen was flat and soft without any palpable masses. Laboratory examinations revealed no remarkable abnormalities of complete blood count, inflammation, liver function, renal function, electrolytes, or coagulation system. Plain computed tomography showed a mass with extremely high densities; it was 6.5 cm in the longest diameter and located next to the undersurface of the right hepatic lobe and the right kidney (Fig. , ). Contrast enhanced computed tomography did not reveal any other lesions in the chest and abdomen. Magnetic resonance imaging showed low signal intensities on both T1- and T2-weighted images (Fig. , ). We considered that the lesion mainly consisted of calcification and diagnosed large peritoneal pearl body or sponge-induced granuloma due to the past appendectomy. Malignant fibrous histiocytoma, dedifferentiated liposarcoma, or extraskeletal osteosarcoma were considered as differential diagnoses although they were atypical or rare according to the imaging findings. We informed the patient about a low possibility of malignancy of the lesion and he wished observation. Two years after, the patient hoped surgical excision although the lesion showed a stable imaging in computed tomography (Fig. ).
We performed laparoscopic resection of the mass. We broke up adhesions between the omentum and the right upper abdominal wall and found a white and hard mass in the retroperitoneum over the adhesions (Fig. ). It was excised from the retroperitoneum using ultrasonically activated scalpel. Operative duration was 115 min and intraoperative hemorrhage was little. On gross examination, the excised specimen entirely looked like calcification (Fig. ). Division surface of the specimen mainly presented calcification and partially red soft tissues (Fig. ). Microscopically, small quantities of densely proliferated spindle cells were scattered in major quantities of hyalinizing collagen fiber (Fig. ). The spindle cells showed low cytological atypia and no mitosis. Immunohistochemistry showed positive staining of CD34 and vimentin and negative staining of Bcl-2, SMA, A-100, or p53 (Fig. –). Immunoreaction for Ki-67 was detected in fewer than 1 % of the neoplastic cells (Fig. ). The surgical margin was free from the tumor cells. We diagnosed morphologically and immunologically benign SFT in the retroperitoneum. The patient recovered without any postoperative complications, discharged 9 days after the surgery, and had no recurrence 1 year after the surgery.
SFT which is currently known as an uncommon soft tissue neoplasm was first reported as a kind of pleural neoplasms in 1931 [] and was originally an exclusive diagnosis of pleural neoplasms []. Recent electron microscopic and immunohistochemical studies revealed that SFT derives from fibroblastic or myofibroblastic cells under the mesothelium [, ]. Thoracic SFT has an age-standardized incidence rate of 1.4 per million, typically occurs in the sixth and seventh decade, and affects both genders equally [, ]. Eighty percent of SFT occurs in the thoracic cavity while 20 % of that is found in extrathoracic regions including the retroperitoneum [, ]. Retroperitoneal SFT as in the present case is considered to be comparatively rare.
SFT can cause local pressure syndrome [] and some reports described that SFT presented hypoglycemia due to the insulin-like growth factor II secretion from the tumor [, ]. In imaging studies, SFT typically presents well-defined and lobulated mass with well-enhancement []. Wignall et al. investigated characteristics of radiologic findings in 34 SFTs and revealed that 62 % of them had the lobulated contours, 9 % had the local invasions, 79 % had heterogenous enhancement patterns, and 65 % had strong contrast enhancement []. On magnetic resonance imaging, SFT typically exhibits hypo- or isointensity in T1-weighted image and heterogeneous hyperintensity in T2-weighted image [], the differential diagnoses of SFT in the retroperitoneum include liposarcoma, leiomyosarcoma, lymphoma, schwannoma, neurofibroma, leiomyoma, myolipoma, angiomyolipoma, sympathetic paraganglioma, desmoid tumor, and epithelioid sarcoma []. In the present case, SFT was incidentally detected without any symptoms, imaging inspection provided extremely atypical findings as any retroperitoneal neoplasms including SFT, and thus a precise preoperative diagnosis was difficult. Non-neoplastic lesions such as peritoneal pearl body or foreign body granuloma due to retained surgical sponge in the past appendectomy were exclusively considered, but the imaging findings were not typical of them as well as of neoplastic disease []. Fine needle aspiration or biopsy might be difficult due to its marked calcification.
Microscopically, SFT shows multiplying spindle cells in the patternless appearance and the hemangiopericytoma-like appearance with prominent vascularity []. England et al. described high cellularity, high mitotic activity (more than 4 mitoses per 10 high-power field), pleomorphism, necrosis, and hemorrhagic changes as the criteria for morphological malignancy of SFT []. Those malignant features are observed in about 10 % of SFTs []. In immunohistochemistry, CD34 and Bcl-2 are especially useful for differentiating SFT from the other spindle cell neoplasia [, ]. Immunoreactivity for CD34 was observed in 98 % and that for Bcl-2 was confirmed in 90 % of SFTs []. Other immunological targets such as CD99, desmin, SMA, c-kit, S-100, EMA, CK, CD31, and inhibin are also used for specific diagnosis of SFT []. In the present case, the marked calcification was extremely unusual but the scattered tumor cells provided typical structures of SFT with positive immunostaining of CD34 and were considered to be morphologically benign.
The problem regarding malignancy of SFT is discrepancies of morphological malignancy and clinical malignancy [, , ]. The discrepancy may be partially due to malignant transformation with dedifferentiation of the tumor cells [, ]. Therefore, we should not trust morphological findings but immunohistochemistry for some relevant proteins may provide indications of SFT’s clinical malignancy. Takizawa et al. reported that patients with positive immunostaining of both CD34 and Bcl-2 had no recurrence []. Loss of immunoreactivity for CD34 and Bcl-2 was observed in the component with malignant transformation [, ]. Immunoreaction for p53 was not observed in benign SFT but much confirmed in morphologically and clinically malignant SFT []. The present case morphologically yielded typical benign features without immunoreactivity for p53 but can potentially cause a recurrence and should be carefully followed up.
Almost all patients with SFT underwent surgical excision. Many surgical doctors recommend complete surgical excision to obtain clear margins with careful long-term follow-up [, , , ]. There have been few reports concerning chemotherapy for SFT and thus its efficacy is not evident. Baldi et al. used anthracycline and ifosfamide for a patient with recurrent SFT and got partial response; cisplatin and gemcitabine, progressive disease []. We performed microscopically complete resection of the tumor and consider follow-up without adjuvant chemotherapy as reasonable.
SFT in the retroperitoneum is rare, and 31 cases have been reported including this case for the last 15 years [, , , , –, –] (Table ). The English language literature was extracted from PubMed from 2000 to 2015 using the following Medical Subject Heading terms: “solitary fibrous tumor” and “retroperitoneum”. Age of onset ranged from 17 to 83 and its median was 56. Male to female ratio of the patients was 16:15. Ten patients (38 %) complained of local pressure symptoms in 26 patients with description of any symptoms; 9 patients (35 %), palpable mass; 7 patients (27 %), asymptomatic. Location of the tumor varied all over the retroperitoneal cavity. Size of the tumor ranged from 3.1 to 36 cm and its median was 11.5 cm. No cases were preoperatively diagnosed as SFT. Surgical excision was performed in all cases. Morphologically, 16 cases (62 %) presented benign features while 10 cases (38 %) exhibited malignant findings. Positive immunostaining for CD34, Bcl-2, and p53 was observed at 28 (97 %), 14 (74 %), and 2 (22 %) in described 29, 19, and 9 cases, respectively. Clinical outcomes varied; 21 (78 %) patients remained disease-free after the surgery, 4 patients (15 %) had local recurrence or distant metastasis after the operation, and 3 patients of them died of the disease. One case was diagnosed morphologically benign but suffered distant metastasis 13 years after the surgery and died. The only case of negative immunostaining for CD34 died of the disease. One of the 2 cases in which p53 was immunohistologically positive was dead of the disease. These results indicate that retroperitoneal SFT is quite difficult to diagnose and can be clinically malignant although morphological examinations yield benign findings and negative immunostaining of CD34 or positive immunostaining of p53 can be signs of clinical malignancy.
The present case showed prominent calcification in preoperative imaging and the excised mass mostly consisted of calcification with scattered tumor cells. Calcification is not rare for various neoplastic or non-neoplastic lesions in the retroperitoneum such as lipoma, liposarcoma, schwannoma, germ cell tumors, lymphoma after chemotherapy or radiotheraphy, and peritoneal pearl body [, ]. Nakashima et al. suggested that the absence of calcification can predict malignancy of primary retroperitoneal tumor []. In SFT, calcification was reported to be observed in 3 of 34 cases (8.8 %) [] and regarded as an indicator of malignancy []. However, those kinds of calcification are tiny, scattered, or partial in the lesion. There has been no report of integrally calcified SFT like the present case. The reason why SFT coexisted with such significant calcification is not apparent but the fact is very interesting for considering carcinogenesis or nature of SFT.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [162.0, 'cm']}",58.69299,55.75834,61.62764,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (63.77956 (in inches) - 60) = 58.69299 kg.
Hence, the patient's IBW is 58.69299 kg."
3687,10,Ideal Body Weight,physical,decimal,pmc-3030039-1,Extracted,"We report a case of a 70-year-old male patient with a height of 170 cm and a weight of 66 kg taking allopurinol 100 mg three times a day after being diagnosed gout 20 years ago. Four years ago, he underwent total parotidectomy under general anesthesia for adenocarcinoma of the right parotid gland and received radiation therapy. During the tracing survey of his adenocarcinoma of the right parotid gland, a 1.5 × 1 cm solitary pulmonary nodule in his right upper lobe was detected from positron emission tomography performed 8 months ago, and the size was gradually increasing. A right upper lobectomy was planned depending on the results of the biopsy and frozen section with VATs.
Vital signs at the time of hospitalization were within normal range, and there was no special opinion about the patient except the increased level of creatinine at 2.11 mg/dl from the preoperative evaluation. For premedication, 0.2 mg of glycopyrrolate was injected intramuscularly 30 minutes before the surgery. Vital signs at the time of arrival at the operation room were blood pressure at 178/110 mmHg, heart rate at 77 beats/min, and body temperature at 35.9℃. For the induction of anesthesia, while 300 mcg/hr of remifentanil was infused, 2 mg/kg of propofol and 0.6 mg/kg of rocuronium were also injected. Then a left 37 French Robertshaw double lumen endobronchial tube (Broncho-Cath Left, Mallinckrodt Medical, Ireland) was intubated with a stylet. After the tip of the tube passed the vocal cords, the stylet was removed; and after the tracheal cuff passed the vocal cords, the tube was advanced by rotating it at a 90 degree angle counterclockwise. When the tube was inserted at a depth of 29 cm to lips, resistance was felt. The resistance indicated that the tube is at the left mainstem bronchus, so that the tracheal cuff and the bronchial cuff were inflated with 6 ml and 2 ml of air, respectively. After making a judgment that the location of tube is appropriate by auscultation without using bronchoscope, the bronchial cuff was deflated in order to prevent bronchial injury from postural changes. After that, it was confirmed that there was no problem with the location of the tube by auscultation after the posture of the patient was changed to the left lateral decubitus position and the bronchial cuff was inflated with 2ml of air. Anesthesia was maintained with isoflurane 1.2 vol%-oxygen 2 L/min-air 2 L/min and remifentanil 250 mcg/hr were continuously infused intravenously. The results of the arterial blood gas analysis (ABGA) right after the anesthesia induction was pH 7.34, PaCO241 mmHg, and PaO2 279 mmHg (FiO2 0.5) during bilateral lung ventilation; the results from ABGA one hour after the beginning of the operation was pH 7.33, PaCO2 41 mmHg, PaO2 236 mmHg (FiO2 0.5).
After 170 minutes from the beginning of VATs operation, the airway pressure suddenly increased to 40 cmH2O and the capnogram was not detected. At that moment, the patient's muscle relaxation was enough and self-respiration was not detected. Immediately, manual ventilation was performed but upon the auscultation, ventilation was not detected. The depth of the tube was 26 cm to lips, shifted a bit from the beginning, so after removing all air in the cuff, the tube was advanced again to the depth of 29 cm while the tracheal cuff was inflated by 6 ml of air. Until then, the saturation of pulse oximeter was maintained at 99%. Due to no ventilation, it was decided to check the location of the tube with a bronchoscope after identifying ventilation first. As the result of auscultation during the manual ventilation, breathing sounds from both sides of the chest were detected and the expansion of lungs could be seen by thoracoscope. After expanding the bronchial cuff with 2 ml of air, breathing sounds from both sides of the chest were still detected. The left one-lung ventilation was attempted by clamping the tracheal tube with forceps, but while the expansion of the right lung was detected on the screen with the thoracoscope, breathing sounds from the left side were not detected. After removing the forceps from the tracheal tube and clamping the bronchial tube with the forceps, the left one-lung ventilation was detected. It was concluded that the tube is located at the right side of the bronchus, so we monitored by inserting a fiberoptic bronchoscope into the tracheal tube. It was detected that the tube is located in the right bronchus, so after removing the air of all cuff, the tube was pulled off up to the depth of 24 cm. Although the tube was advanced through the use of the bronchoscope, the tube kept falling into the right bronchus. We made two more attempts but the results were the same. Therefore we put the bronchoscope into the left mainstem bronchus through the bronchial tube. The tube was advanced using the bronchoscope as a guide-wire to the depth of 29 cm. Although there was a sense of resistance at 27 cm, we considered that it was from the friction caused by the bronchoscope. As a result of monitoring the tracheal tube with the bronchoscope, the tube located in the left mainstem bronchus was detected to be at the proper depth. After that, the left one-lung ventilation developed normally.
The operation was performed again, and when sampling the lymph nodes of the subcarinal region after finishing right upper lobectomy, an air bubble coming from the direction of the left mainstem bronchus was detected. When dissecting tissue to the direction of the air bubble, the amount of air leakage increased. Then the appropriate lung ventilation was not performed and the saturation of pulse oximeter was decreased to 89%. We transited to the bilateral lung ventilation immediately, and after starting the manual ventilation by inhaling 100% oxygen, the saturation was maintained at 99%. After removing all the air inside the cuff and pulling the tube out by 6 cm, the tracheal cuff was inflated by 6 ml of air. The carinal region and the left and the right bronchus were examined with a fiberoptic bronchoscope, and the linear rupture in the traveling direction from the left mainstem bronchus was detected. As the result of monitoring from immediate thoracotomy, the rupture with the length of 1.5 cm was detected from the posteromedial surface of the left mainstem bronchus just below carina (). The simple primary suture was done on the rupture region with vicryl, and there was no more air leakage after finishing the repair ().
After finishing the operation, the tube was extubated in the operation room, and the patient was monitored for a day in the intensive care unit. On the next day, the patient was moved to general ward. From the bronchoscope examination conducted 7 days after the operation, a linear laceration from the upper left mainstem was detected, indicating that the patient was recovering well (). Nine days after the operation, the patient left the hospital after making a full recovery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3688,10,Ideal Body Weight,physical,decimal,pmc-4340458-1,Extracted,"An 18-year-old young woman presented to our clinic for primary amenorrhea and dyspareunia. She developed clinical signs of puberty at 12 years old (thelarche -11 years old, pubarche - 12 years old) and she became sexually active at 14 years. She had two previous surgical interventions, an appendectomy and an exploratory laparotomy. The physical exam noted an average stature and body mass index (165cm in height, 66 kilos in weight), normal developed breast (Tanner 5) (Fig .a) and normal body hair distribution, including arm span, pubic and axillary hair (Fig .b.c). The clinic examination revealed normal clitoris, labia major and minor, and a short (2 cm) vagina, that ended in a blind pouch (Fig .d).
The US exam (Voluson Pro 730 GE Medical Systems, Zipf, Austria machine, equipped with 4-8-MHz and 5-9 MHz curvilinear transducers) found an ectopic right solitary kidney (with mild pyelectasis), located in the right low quadrant of the abdomen, and failed to identify the uterus and ovaries using both transabdominal and transvaginal approach (Fig .a.b).
Due to the discordance between the clinical and laboratory findings (normal complete sexualisation, normal hormones) and ultrasound features (absent ovaries) we considered these findings incomplete. Thus, we performed MRI, which revealed normal liver, pancreas, confirmed the right solitary ectopic kidney and the absence of uterus, but failed to visualize any tubal remnants and the ovaries.
Blood routine and renal function were in normal limits. Hormone profile included measurement of follicular stimulating hormone (4.3mUI/ml), estradiol (840pmol/l) and testosterone (1.59 nmol/l), which were all normal, indicating normal function of the hypothalamic-pituitary-ovarian axis.
Classic G banding is the elective genetic method used to differentiate the Mayer- Rokitansy-Kuster-Hauser syndrome from other genital tract development defects such as Turner syndrome (45, 0X) and androgen insensitivity syndrome (46, XY). The karyotype was normal (46, XX).
The cardiologic exam (ECG and echocardiogram) showed normal heart functionality with no evidence of morphological anomalies and the chest X-ray was also normal. Intravenous pyelography showed left renal agenesis, right hypertrophic kidney in ectopic ilio-pelvic position, with normal secretion and excretion function and normal urinary bladder (Fig .c).
After counselling, informed consent for laparoscopic exploration was obtained, in order to locate and describe the internal genitals. Laparoscopy confirmed normal urinary bladder, absent uterus (Fig .a), left renal agenesis and a right ectopic kidney (Fig .b). Both ovaries were found in an ectopic high position, in the right and left superior quadrants, with adjacent small fallopian tubes. The right ovary had a normal aspect (Fig .d) and the left ovary presented a haemorrhagic cyst that was removed (Fig .c). Complete inspection of the peritoneal cavity showed a congestive cecal appendix, also removed. After acknowledging the topography of the ovaries, we were able to identify them on later US scans (Fig .d). There were no postoperative complications and the patient was discharged after 3 days. Before discharge, another ultrasonographic evaluation was performed and revealed both high positioned ectopic ovaries. Further psychological support was provided and corrective dilatory surgery of the vagina was recommended.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3689,10,Ideal Body Weight,physical,decimal,pmc-6967071-1,Extracted,"A 77-year-old man, 55 kg in weight and 165 cm in height, was scheduled to undergo m-ECT, due to a decreasing efficacy of drug treatment for depression over 9 years.
Seven years earlier, coronary computed tomography (CT) showed two CAAs with diameters of 7 × 8 mm and 6 × 11 mm at the distal first diagonal branch of the left coronary artery and right ventricular fistula formation (Fig. ). The diameter of CAAs had no changes during the follow-up observation for 7 years. In adenosine myocardial load scintigraphy as a preoperative examination, neither myocardial ischemia nor infarction was detected. We surmised that the infarct range of the heart would be limited even if a thrombus was formed because the CAAs were located at the distal side of the left first diagonal branch. For that reason, we decided to prioritize m-ECT for depression rather than treatment for the CAAs.
Upon entering the operation room for the first m-ECT, the patient exhibited noninvasive blood pressure (NIBP) of 124/79 mmHg, and the BP on the ClearSight™ system was 132/74 mmHg (Fig. a). For setting the ClearSight™ system, we measured NIBP five times and confirmed that there was not much difference between NIBP and BP on the ClearSight™ system, and blood pressure was measured by this system throughout the procedure. General anesthesia was induced with propofol 1 mg kg-1, and after he lost consciousness, rocuronium 0.35 mg kg-1 was administered. Nine minutes after rocuronium administration, the psychiatrist performed electrical stimulation. As soon as the seizure started, HR increased from 83 beats min-1 to 102 beats min-1, and BP increased from 101/59 mmHg to 143/85 mmHg. The seizure duration was 51 s on the electroencephalogram. When the seizure stopped, the BP rapidly decreased to 120/75 mmHg without the use of any antihypertensive agent. After completing the seizure, sugammadex sodium 2 mg kg-1 was administered. When the patient regained consciousness, the BP was 112/71 mmHg. Neither asynergy nor pericardial effusion was detected by transthoracic echocardiography.
At the second m-ECT performed 4 days after the first procedure, when entering the operation room, NIBP was 144/111 mmHg, and the BP was 152/89 mmHg (Fig. b). General anesthesia was performed by referring to the first m-ECT. As soon as the seizure began after electrical stimulation, the BP increased from 155/93 mmHg to 186/105 mmHg. Therefore, nicardipine 0.01 mg kg-1 was administered, and BP decreased to 155/89 mmHg immediately. After completing the seizure, the BP was 164/92 mmHg. The seizure duration was 50 s on the electroencephalogram. We confirmed that there was no asynergy or pericardial effusion in the transthoracic echocardiography when he regained consciousness.
Both m-ECTs increased HR and BP. However, no decrease in HR or BP due to parasympathetic nervous stimulation or asystole was recognized. With reference to the first and second m-ECTs, we administered nicardipine hydrochloride prophylactically prior to the start of electrical stimulation every time after the third procedure. We performed a total of 10 m-ECTs, and the maximum NIBP in the all m-ECT procedures was 171/99 mmHg.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3690,10,Ideal Body Weight,physical,decimal,usmle-1535,Extracted,"A 26-year-old medical student comes to the physician for a chest x-ray to rule out active pulmonary tuberculosis. He needs a medical and radiological report before starting a medical internship in South Africa. He has no history of serious illness and does not complain of any symptoms. He has smoked 1 pack of cigarettes daily for the past 6 years. He does not drink alcohol. He is 190 cm (6 ft 3 in) tall and weighs 75 kg (165 lbs); BMI is 20.8 kg/m2. His temperature is 37°C (98.6°F), pulse is 80/min, respirations are 18/min, and blood pressure is 128/89 mm Hg. The lungs are clear to auscultation. Cardiac examination shows no abnormalities. The x-ray of the chest shows a small pneumothorax (rim of < 2 cm) between the upper left lung margin and the chest wall.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [190.0, 'cm']}",84.04734,79.84497,88.24971,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 190.0 cm, which is 190.0 cm * 0.393701 in/cm = 74.80319 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (74.80319 (in inches) - 60) = 84.04734 kg.
Hence, the patient's IBW is 84.04734 kg."
3691,10,Ideal Body Weight,physical,decimal,pmc-4346461-1,Extracted,"The first donor was a 28-year-old man who came to donate to his brother who had hepatitis C-related liver cirrhosis. His blood group was A+. He had a weight of 66 kg, height of 182 cm (BMI of 20 kg/m2), no previous medical conditions, normal physical examination, no laboratory abnormalities, and took no medications ()
The patient donated a right lobe liver graft without the middle hepatic vein weighing 850 g. The pre-operative total liver volume measured by CT volumetry was estimated at 1400 g, which left the donor with a residual left lobe of 550 g (39%). The estimated blood loss was 250 mL; no blood transfusion was needed. The operative time was 8 hrs 45 min, which was longer than our average 6 hrs 30 min, due to a delay in the recipient hepatectomy ().
Adequate hydration of the donor was ensured with fluid balances of +1500 mL/24 hrs, +1350 mL/24 hrs, +95 mL/24 hrs, and +2591 mL/24 hrs in the first four days, followed by a net balance of around 0 mL/24 hrs on the subsequent days. The central venous pressure (CVP) was kept above 5 mm Hg; the urine output was satisfactory.
On the fourth post-operative day, thrombosis of the portal vein was detected by routine duplex ultrasonography and confirmed by CT (). The liver enzymes were not elevated but the lactate was mildly high. Surgical exploration was done. Intra-operative ultrasonography (IOUS) was done using a sterilized T-shaped linear probe with a central frequency of 7.5–10 MHz, which showed the presence of clots. A small transverse 3-mm venotomy was done in the main portal vein, 1 cm proximal to the bifurcation on the accessible right aspect of the vein, since the common bile duct and the left hepatic artery are anterior to the vein. The clot was fresh and soft, so a size 7 Fogarty balloon catheter allowed extraction of the liquefied clots, which was aided by digital milking of the loose thrombus out of the vein. The Fogarty catheter was passed several times until no more thrombus was obtained. When the catheter was passed proximally an atraumatic vascular clamp was placed distal to the venotomy so the clots were directed out of the vein instead of into the liver, and when the Fogarty was passed into the liver a clamp was placed proximal to the venotomy. The usual practice is to deflate the balloon when it approaches the venotomy to avoid tearing the venotomy and to milk the remaining thrombus digitally. This was followed by a gush of blood from the proximal inflow as well as the distal back bleeding from the liver. The venotomy was oversewn with 5-0 interrupted polypropylene.
At this point the IOUS showed restoration of flow to the liver. However, there were two problems: The first was stenosis at the origin of the left portal vein and acute angle between the main and left portal vein from torsion of the remaining left lobe. The second was a remaining thrombus at the confluence of the superior mesenteric vein and splenic vein (). The first step was to correct the stenosis by placing a venous patch from great saphenous vein. A small double angled partial side occluding atraumatic vascular clamp (Satiniski) was placed on the oversewn right portal vein stump. This allowed the liver to be perfused while placing the patch. The 5-0 continuous polypropylene sutures from the initial right donor hepatectomy surgery was cut and the currently opened right portal vein ostium was closed with an elliptical patch using a valveless reversed saphenous vein segment (). After removal of the clamp, the angle between the main and left portal vein was less acute and of a larger diameter. The falciform ligament was reattached to avoid kinks. Attention was then directed to extracting the residual thrombus, making sure the catheter was passing into both superior mesenteric vein and splenic vein under ultrasonography guidance. We used a size 16 French Foley catheter for the thrombectomy via the initial 3-mm venotomy and inflated it with 3 mL of saline to avoid rupture the vein from over inflation (), using the same thrombectomy principles mentioned above. Heparin infusion was started intra-operatively and continued post-operatively to maintain a PTT 70–90 sec. Seven units (250 mL) of packed red cells were given. Four units were given intra-operatively to replace the 1000 mL bleeding and three units were administered over 24 hrs to replace the continuous oozing from the incision.
On the fifth post-operative day re-thrombosis of the portal vein was detected again. The enzymes were declining. A second surgical exploration was done. IOUS showed diffused partial thrombosis of the segmental branches of the left portal vein. Portal vein thrombectomy was done again via the same venotomy. However, we used a smaller Fogarty catheter (size 4 and 3) into the liver. IOUS showed restoration of blood flow. However, a residual thrombus in the splenic vein was detected. Therefore, we decided to insert a thrombolysis catheter into the inferior mesenteric vein. We used a Fountain® Infusion System (Merit Medical Systems, Inc) catheter size 4 French, 90 cm long, with a 20-cm side holes segment inserted over a 0.035” soft wire. Under ultrasonography guidance the catheter tip was advanced to the main portal vein while the side holes segment was centered in the thrombus. The other end of the catheter was brought out of the abdominal wall (). Streptokinase bolus of 250,000 units was given over 30 min via the inferior mesenteric vein catheter, after which the IOUS demonstrated a patent portal vein and its segmental branches. Streptokinase infusion was continued at a rate of 100,000 U/hr for 24 hrs via the inferior mesenteric vein catheter. The patient continued on heparin infusion as well and a target activated clotting time of 200–300 was achieved. Four units of packed red cells were given over the following 48 hrs to replace the oozing.
On the seventh post-operative day, the inferior mesenteric vein catheter was removed after confirmation of the patency of portal vein and intrahepatic branches by duplex sonography. Warfarin was started and titrated to a target INR of 2–3 and continued for six months. The patient recovered gradually, and was discharged on post-operative day nine in stable condition with no complaints or laboratory abnormalities.
During the follow-up visits, the laboratory values were normal and duplex sonography showed patent main and left portal vein with minimal partial chronic occlusion of the intrahepatic segment 2 portal vein. The patient remained asymptomatic after two years of follow up.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [182.0, 'cm']}",76.80323,72.96307,80.64339,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 182.0 cm, which is 182.0 cm * 0.393701 in/cm = 71.65358 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (71.65358 (in inches) - 60) = 76.80323 kg.
Hence, the patient's IBW is 76.80323 kg."
3692,10,Ideal Body Weight,physical,decimal,pmc-4916829-1,Extracted,"A 51-year-old man (height 168 cm, weight 79 kg) presented with right vestibular schwannoma and an underlying bronchiectasis of the right lung. He had presented with the symptoms of progressive loss of hearing and imbalance while walking.
He gave a history of a cough with expectoration and recurrent lung infections since childhood and was evaluated for tuberculosis and found to be negative. During this admission, he had a cough but he could not bring out the sputum. Since there were no signs of active lung infection, we did not perform a bronchoscopy to evaluate cause for bronchiectasis. He is a hypertensive for 20 years on treatment with amlodipine 5 mg once daily. On examination, he had extensive crepitation over the right hemithorax, and tracheal shift to the right. His magnetic resonance imaging brain (T2-weighted image), showed a large vestibular schwannoma (5.2 cm × 4.3 cm × 3.5 cm in size) with obstructive hydrocephalus []. His chest X-ray findings showed right-sided bronchiectasis and fibrosis with the gross mediastinal shift []. Spirometry revealed a moderate obstructive pulmonary disease. Preoperative arterial blood gas analysis (ABG) on room air showed compensated respiratory acidosis with the pH of 7.43, PaO2 of 74 mmHg and partial pressure of arterial carbon dioxide (PaCO2) of 48 mmHg with HCO3 of 31 mmHg. An echocardiogram revealed left ventricular (LV) hypertrophy with normal LV systolic function, and there was no pulmonary hypertension.
In view of severe bronchiectasis and long duration surgery in the left lateral position (diseased side of the lung being up), decided to isolate the right lung using right-sided double lumen tube (RDLT). In this case, we chose to put a RDLT because of the following reasons.
The angle between bronchus and trachea was obliterated because of lung fibrosis with the mediastinal shift. Right bronchus was almost in a straight line with the trachea []. Hence, placement of RDLT will be easy when compared to the left. With a left DLT, secretion from the right lung can get accumulated above the left bronchial cuff. The presence of low pressure cuff cannot provide a tight seal against spillage. Hence, we felt that presence of RDLT will give better protection than the left DLT.
In the operating theater, standard monitors including electrocardiogram, pulse oximetry, and noninvasive blood pressure were connected. His room air saturation was 94%. Modified rapid sequence induction was done using 2 μg/kg of fentanyl and 2 mg/kg of propofol, and was then paralyzed with 1.0 mg/kg of rocuronium and intubated with 39F RDLT. Mallinckdrodt™ the tube position was confirmed by fiber-optic bronchoscopy (FOB). Both the lungs were suctioned separately before placing the patient in the left lateral position. After positioning, the head was fixed using Mayfield head clamp, repeat FOB was done to confirm the lung isolation. Copious thick purulent secretion was suctioned out from the right lung. To assess the contribution of the right lung on CO2 elimination split lung ventilation was performed by ventilating only diseased lung (right side). There was a significant ETCO2 value noted (20 mmHg) while ventilating the right lung, we have decided ventilate both lungs. The patient was ventilated with pressure controlled ventilation using lung protective ventilation strategies. The end-tidal CO2 was maintained between 35 and 37 mm of Hg.
Intraoperatively, anesthesia was maintained using air, oxygen (FiO20.6) and isoflurane, and vecuronium infusion. Intermittent bolus doses of fentanyl and intravenous paracetamol were given for analgesia. Serial ABG's were taken to ensure the adequacy of ventilation. PaCO2 was maintained between 40 and 45 mmHg (baseline value was 49 mmHg). Vitals were stable throughout the surgery. Brain relaxation was reported adequate during the surgery.
The surgery lasted for 6 h. At the end of surgery, bilateral endobronchial suctioning was done in the lateral position. An intravenous lignocaine (1.5 mg/kg) was given to prevent coughing before placing the patient in supine oblique (left side up). Residual neuromuscular blockade was reversed with neostigmine (0.05 mg/kg) and glycopyrrolate (0.01 mg/kg). The trachea was extubated when the patient was fully awake. The patient was shifted to the Neurosurgical Intensive Care Unit (NICU) in the right lateral position. His postoperative chest X-ray showed clear lung field on the left side []. He was monitored in NICU for 2 days and shifted to ward. Later, he was discharged from the hospital in a good clinical state.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.0, 'cm']}",64.12607,60.91977,67.33237,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg."
3693,10,Ideal Body Weight,physical,decimal,pmc-5528908-1,Extracted,"A 17-year-old Thai female with human immunodeficiency virus type 1 (HIV-1) infection who had received TIV for 2012-2013 in August 2013 presented at the Bamrasnaradura Infectious Diseases Institute (BIDI) complaining of 2 days of fever, malaise, headache, cough, and sore throat in April 2014. She had been diagnosed with HIV infection confirmed by machine-based assay (ArchiTECT, Abbott, chemiluminescent test), particle agglutination test (Serodia HIV, Fujirebio), and immunochromatography test (Allere Determine or TriLine) at BIDI. Approximately 13 years prior to presentation, she received zidovudine (AZT) plus didanosine (ddI) from 2001 to 2005; AZT, ddI, and efavirenz (EFV) from 2005 to 2007; and has been receiving EFV plus lopinavir/ritonavir in combination (LPV/r) from 2007 to present. Before TIV was given in 2013, she had a CD4 count of 922 cell/µL (31%), plasma HIV-1 RNA <40 copies/mL by quantitative real-time polymerase chain reaction (RT-PCR), a body weight of 85.7 kg, and a height of 165 cm. She received TIV 2011-2012 on August 1, 2012, and TIV 2012-2013 on August 28, 2013. TIV in 2012-2013 included the A/California/7/2009 (H1N1)-derived strain using NYMC X-179A, the A/Victoria/361/2011 (H3N2)-like strain using IVR-65, and the B/Wisconsin/1/2010-like strain using NYMC BX-39 derived from the B/Hubei-Wujiagang/158/2009 strains. At presentation of influenza-like illness symptoms, the physical examination was unremarkable except for a body temperature 38.5°C and body mass index of 31.48 kg/m2. Because of a positive rapid influenza test (Quidel QuickVue Influenza A+B test), the patient was given oseltamivir for 5 days and the clinical symptoms resolved The positive rapid influenza test result was from the BIDI, Nonthaburi, Thailand, with a confirmatory PCR result from the Siriraj Influenza Cooperative Research Center, Department of Microbiology, Faculty of Medicine, Siriraj Hospital, Bangkok, Thailand. The specimen was identified by the amino acid sequence of full hemagglutinin (HA) gene to evaluate the match between the influenza infection and TIV strains.
To perform nucleotide sequencing, total RNA was extracted using a QIAamp viral RNA mini kit (Qiagen) from direct nasal swab specimens of a vaccinated person who had developed a PCR-confirmed influenza illness from the 2009 pandemic virus. The RNA sample was amplified for the complete influenza HA gene, and the amplified product was subjected to nucleotide sequencing. The sequence was edited, aligned, and translated into an amino acid sequence by BioEdit program (version 7.1.11; available at ). The sequence was submitted to the GenBank database with the accession number of KU144591.
shows the percentage of identity match of amino acid sequences of the full HA gene. The specimen of the present case matches TIV strains CA 07 vaccine strain, H1N1 A/Nonthaburi/102/2009, and H1N1 A/Thailand/104/2009 by 97%, 98%, and 98%, respectively. The matches of the specimen for H1N1 2014 isolates are 99% to 100%.
To perform phylogenetic analysis, the HA amino acid sequence of virus from the case was analyzed for its correlation with the sequences from A/California/07/2009 (H1N1) vaccine strain, 2 Thai virus isolates obtained from the first epidemic wave (A/Nonthaburi/102/2009 and A/Thailand/104/2009), and 2 more virus isolates from 2014 (A/Thailand/NMA_1/2014 and A/Thailand/BKK_1/2014) See . The results demonstrate a closer relationship between the causative virus and the circulating strains rather than the vaccine strain closely related to the Thai viruses from the first epidemic wave.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3694,10,Ideal Body Weight,physical,decimal,pmc-7725579-1,Extracted,"A 68-year-old male patient presented for the removal of an intramedullary nail (IMN) from his right femur and possible total knee arthroplasty (TKA) for his dislocated right knee following a traumatic event. His past medical history is significant for hypertension, hyperlipidemia, hyperkalemia, benign prostatic hyperplasia with urinary hesitancy, atrial fibrillation, a crush injury that caused a closed fracture of multiple ribs on the right side and the pelvis, and tobacco use. The patient's surgical history includes a colonoscopy and multiple orthopedic surgeries. His previous surgeries did not have any history of abnormal urine output or sodium levels. The patient denied complaints of frequent urination; however, his history included a complaint of urinary hesitancy. His medications included aspirin, atorvastatin, celecoxib, and oxycodone, and a medication allergy to losartan. Preoperative laboratory tests indicated slightly low sodium levels and slightly elevated glucose levels, but a well-functioning renal system. On physical exam, height was 1.753 m and weight 116.9 kg (body mass index of 38.14).
On the day of surgery, the anesthesia team planned for spinal block (hyperbaric bupivacaine, 2 mL of 0.75%) and monitored anesthesia care (MAC) with a propofol infusion. The patient was given 2 mg of midazolam preoperatively. Supplemental oxygenation was provided and standard American Society of Anesthesiologists (ASA) monitors were utilized for continuous monitoring. Total volume of 1500 mL of Lactated Ringer's (LR) premix infusion was given intraoperatively. The surgery lasted a total of 5 hours and 32 minutes and the patients urine output for the duration of the operation totaled 1240 mL, 975 mL of which were excreted within a two-hour span and hour and a half following the delivery of the boli of dexmedetomidine (12 mcg, 12 mcg, and 16 mcg) ().
The postoperative period was uncomplicated, the patient maintained normal sodium levels and normal electrolytes despite frequent monitoring in the immediate period after surgery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.753, 'm']}",70.73632,67.1995,74.27314,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.753 m, which is 1.753 m * 39.3701 in/m = 69.01579 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.01579 (in inches) - 60) = 70.73632 kg.
Hence, the patient's IBW is 70.73632 kg."
3695,10,Ideal Body Weight,physical,decimal,pmc-8443410-1,Extracted,"A 66-year-old man (body height, 168 cm; body weight, 88.5 kg) experienced dyspnea, a sensation of chest tightness, and back pain for a few days before he was brought to our hospital on an emergency basis. His symptoms became aggravated suddenly as he was about to get off a taxi on his way home from work. He presented with a history of close contact with a coworker with COVID-19 and was waiting for instructions from a public health center.
In the ambulance, the following conditions were documented: Glasgow Coma Scale score, E4V5M6; heart rate, 80/min and irregular; blood pressure, 100/60 mmHg; body temperature, 38.4ºC; oxygen saturation, 98% (O2 delivered with reservoir mask at a rate of 15 L/min). On admission, his white blood cell count was 22,300/µL; hemoglobin, 14.7 g/dL; platelet count, 35 × 104/µL; creatinine level, 2.23 mg/dL; creatine kinase level, 2582 IU/L; creatine kinase myocardial band level, 164 ng/mL; low-density lipoprotein cholesterol level, 97 mg/dL; high-density-lipoprotein cholesterol level, 19 mg/dL; triglyceride level, 173 mg/dL; hemoglobin A1c level, 7.9%; C-reactive protein level, 13.8 mg/dL; troponin T level, 9.640 ng/mL; N-terminal pro-brain natriuretic peptide level, 11753 pg/mL; procalcitonin level, 0.62 ng/mL; d-dimer level, 16.34 µg/mL; and soluble fibrin level, 113.1 µg/mL. An electrocardiogram showed atrial fibrillation; ST-elevation in II, III, aVF, and V2–V6 leads; and ST depression in aVR leads (Figure ). Echocardiography revealed severe hypokinesis extending from the anterior wall to the apex and the inferior wall in left ventricle, with an approximate ejection fraction of 20%. We diagnosed STEMI and decided to perform emergency coronary angiography (CAG). A chest radiograph showed infiltrative shadows in both lungs and tracheal intubation was performed in the emergency outpatient unit (Figure ). Continuous infusion of noradrenaline (0.1 μg/kg/min) was started because his systolic blood pressure dropped below 80 mmHg. After heparin (5,000 U) was administered intravenously, the patient was transferred to the cardiac catheterization room.
CAG was performed by cardiologists, emergency physicians, clinical engineers, nurses, and radiological technologists who donned appropriate personal protective equipment before entering the room. CAG revealed total occlusion of the middle of the right coronary artery (RCA) and left anterior descending artery (LAD; Figure ). After a loading dose of dual antiplatelet therapy (aspirin, 162 mg; clopidogrel, 300 mg), an intra-aortic balloon pump catheter was inserted, and a 7-Fr guiding catheter was inserted into the left coronary artery. We removed white material, which did not at a first glance appear to be a typical thrombus, with an aspiration catheter, but blood flow did not improve. The onset-to-device time and door-to-device time were 116 and 84 minutes, respectively. Subsequent intravascular ultrasonography (IVUS) revealed several structures, which were thought to be thrombi; therefore, we performed plain old balloon angioplasty (Figure ). After the balloon was expanded, blood flow improved slightly in the LAD but not distally. Next, we placed an everolimus-eluting stent (4.0 × 38 mm) in the middle of the LAD, but peripheral blood flow was still not observed. Repeated IVUS revealed severe stenosis caused by plaque with thrombi. An additional balloon was inflated at the distal site, and a cutting balloon was also used. Another everolimus-eluting stent (2.25 × 38 mm) was placed at the distal site, but no blood flow improvements were seen angiographically.
We moved a double-lumen catheter to the distal LAD and performed CAG from the distal LAD, which revealed retrograde blood flow up to the middle of the LAD and collateral circulation from the septal branch to the RCA. Repeated IVUS examination revealed thrombi and plaque at the distal end of the stent and no intrastent blood flow (Figure ). Then, we tried to perform PCI for the total occlusion of RCA, but it was unsuccessful. At this point, 7 hours passed since the patient entered the cardiac catheterization room, and so we finished the procedure. The levels of activated clotting time during PCI were maintained at 280–310 seconds. After PCI, pathological examination proved the aspirated white material was white thrombi. Chest computed tomography performed after PCI showed ground-glass opacities distributed unevenly in both the lungs, as well as left-sided pleural effusion (Figure ). After the patient was transferred to the intensive care unit, he showed pulseless electrical activity, and cardiopulmonary resuscitation (CPR) was initiated. Return of spontaneous circulation was achieved with 1 mg of epinephrine and one cycle of CPR. Veno-arterial extracorporeal membrane oxygenation was considered, but his family decided against it. The blood pressure was maintained through the continuous administration of noradrenaline, dobutamine, and adrenaline. His nasopharyngeal swab was tested with polymerase chain reaction for SARS-CoV-2, and COVID-19-related pneumonia was diagnosed. Remdesivir treatment was initiated at a dose of 200 mg/day on the 5th day of hospitalization and continued at 100 mg/day. Because of the possibility of concomitant bacterial pneumonia, ampicillin sodium/sulbactam sodium (9 g/day) was also administered. However, the patient's oxygenation level worsened, and he died on the 7th day. It was difficult to confirm a main cause of death because we were not permitted to dissect patients due to COVID-19. We assumed that he had died from both cardiogenic shock due to myocardial infarction and septic shock due to covid-19 infection.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.0, 'cm']}",64.12607,60.91977,67.33237,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg."
3696,10,Ideal Body Weight,physical,decimal,pmc-4331399-2,Extracted,"Case 2: A 47-year-old female diagnosed with type 2 diabetes 2 years before, and treatment started immediately thereafter. However, after a year, she stopped taking medications on her own decision. She presented to emergency department of our hospital with a fever of 38°C and bilateral lower leg pain for three days. She was hospitalized with a diagnosis of lower right leg cellulitis, and we began cefazolin administration at 3 g/day. On admission, her diabetic control was poor (HbA1c, 11.5%, postprandial blood glucose, 268 mg/dL); in addition, her body temperature was 39.2°C, pulse rate 106 beats/min, blood pressure 137/71 mmHg, height 166 cm, and body weight 61 kg. Routine laboratory testing showed an elevated leukocyte count of 13.8 × 103 cells/μL and a C-reactive protein level of 4.49 mg/dL. Serological tests for syphilis and HIV were negative. Soon after starting antibiotic treatment, her fever subsided. Five days later, redness and swelling disappeared; therefore, we changed treatment to cefdinir at 900 mg/day. She was discharged on day 8. The following day, we confirmed H. cinaedi from the blood culture taken on day 1; nevertheless, we decided to adopt a wait-and-see approach because no exacerbation of disease was observed since her initial admission.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [166.0, 'cm']}",57.81505,54.9243,60.7058,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 166.0 cm, which is 166.0 cm * 0.393701 in/cm = 65.35437 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (65.35437 (in inches) - 60) = 57.81505 kg.
Hence, the patient's IBW is 57.81505 kg."
3697,10,Ideal Body Weight,physical,decimal,pmc-5023828-1,Extracted,"In the past year, a 57-year-old Caucasian female (61 kg, 166 cm) felt gradually empty, exhausted, tired, and lethargic. In addition, she perceived constipation and cold intolerance, which was accompanied by a decline of appetite, concentration, and productivity. She attributed her complaints to the growing level of distress at her work as a teacher and preferred to watch and wait without consulting a physician. Apart from that, her medical, addiction, and familial history were unremarkable. In the last four weeks, she developed a state of apathy and mutism combined with fluctuating confusion, amnesia, disorganization, and incontinence, which led to hospital treatment that was initiated by her husband. Upon emergency admission, a hypoactive delirium and severe hypothyroidism were diagnosed (). Physical and neurologic examination showed signs of hypothyroidism (shortness of breath, bradycardia, hypothermia, swollen limbs, dry skin, delayed relaxation of tendon reflexes, and myalgia) []. Transabdominal echocardiography found pericardial effusion []. Routine lab checks revealed further signs of hypothyroidism, such AST- and CK-elevations and hypercholesterinemia () []. Alcohol intoxication and hyperammonemia were excluded. Moreover, macrocytic anemia was found together with slight hyperhomocysteinemia (12.4 μmol/L, reference level <9 μmol/L), but without laboratory vitamin B deficiency (normal serum levels of vitamins B1, B6, B9, and B12, methylmalonic acid, and holotranscobalamin). Vitamin D was found to be slightly reduced and substituted then. The EEG was slightly slowed (). The brain MR imaging showed a few unspecific T2-hyperintense areas in the white matter (WMH) of both temporal lobes, which could be compatible with severe hypothyroidism, vasculitis, or autoimmune encephalopathy. In the serum, elevated TPO-Abs () were found which pointed to Hashimoto thyroiditis [, , ] being responsible for the hypothyroidism. This was underlined by an atrophic thyroid gland in ultrasound. Regarding the remaining serum antithyroid autoantibodies, TSH-receptor autoantibodies (TR-Abs, ) were also elevated and thyroglobulin autoantibodies were normal. Later on, elevated autoantibodies against parietal cells (PC-Abs, ) and intrinsic factor (11.43 U/mL, normal <1.5 U/mL) were found, which most likely corresponded to a helicobacter pylorus-negative lymphocytic gastroduodenitis in histopathology (up to 80 intraepithelial lymphocytes per 100 epithelial nuclei, T-lymphocytes) and macrocytic anemia. The lymphocyte typing of the blood found increased T-helper-lymphocytes (1350/μL, normal 645–1289/μL), cytotoxic T-lymphocytes within its normal range, and no evidence of a cellular immune deficiency as being measured in the last asymptomatic month (). Helicobacter pylori antibodies were negative. There were no clinical or immunologic signs of Addison's disease, diabetes mellitus, vitiligo, alopecia, or celiac disease. Thus, outside the CNS, the autoimmune disease appeared to be limited to a gastroduodenal-thyroidal syndrome, classified as autoimmune polyendocrine syndrome type 3B []. Other forms of limbic encephalopathies that could have been associated with antibodies against intracellular, synaptic, or other cell surface antigenic targets [], neoplasm, connective tissue, or vasculitis diseases [, ] were excluded.
In the CSF, TPO-Abs (33.8 IU/mL, normal: 0–8 IU/mL) [] were detected, while TR-Abs and thyroglobulin antibodies were not investigated. Moreover, CSF protein (43.7 mg/dL, normal 15–35 mg/dL), S-100 protein (3200 pg/mL, normal <2700 pg/mL), and neuronal specific α-enolase (NSE, 16.9 μg/L, normal <13 μg/L) were elevated. Pleocytosis or oligoclonal bands were missing. Also, neurodegeneration markers (beta-amyloid, tau-, and phospho-tau protein), angiotensin converting enzyme (ACE), lysozyme, titers of immunoglobulins (IgM, IgA, and IgG), IgM-, IgA-, and IgG-indices, antibody index for either herpes simplex virus, varicella zoster virus, cytomegalovirus, measles virus, rubella virus, or Borrelia burgdorferi, and 14-3-3 protein were unremarkable in the CSF.
Ophthalmological, angiological, and nephrological examinations were unremarkable, too. Subsequent electrocardiograms, abdominal ultrasound, chest X-ray, and the remaining serum routine lab including ferritin and transferrin were normal as well as immunoglobulins including subclasses, carbohydrate deficient transferrin, parathyroid hormone, lysozyme, ACE, carbohydrate deficient transferrin, gastrin, and serum autoantibodies against thyroglobulin and the amino terminal of α-enolase (NAE). Virus hepatitis, HIV, herpes, syphilis, Lyme disease, and M. Whipple were excluded. Drug urine screen was negative.
Regarding the increasing somnolence and falling heart rate (down to 40 bpm) and body temperature (down to 33.8°C) the critical care management included an accelerated thyroid hormone replacement therapy (THRT) with L-thyroxine (IV, 250 μg/day in the first 5 days) and IV glucocorticoids (125 mg/day IV methylprednisolone) to prevent the progression of the hypoactive delirium to myxedema coma []. In the next few days, the critical condition improved. Hypothermia and bradycardia resolved within 36 hours and thyroid-stimulating hormone (TSH) started to fall. Simultaneously, the delirium turned into a mixed state (), requiring low doses of haloperidol (up to 10 mg/day) and clonazepam (up to 1 mg/day) to cope with arising visual or auditory hallucinations and agitation.
When the results of elevated serum TPO-Abs came in, the IV glucocorticoid treatment was enhanced to 250 mg/day IV methylprednisolone assuming that the delirium was based on HE [, ]. Thereafter, the mixed delirium (fluctuating vigilance, disorientation, disorganization, starring, memory impairment, irritability, hallucinations, and delusion of reference) turned to a hyperactive state with striking manic features (euphoria, grandiosity, racing thoughts, sleeplessness, and risky and reckless behavior). Meanwhile, the patient's physical condition had been stabilized and she was voluntarily transferred from the critical care unit to the psychiatric ward. Assuming that the glucocorticoids had evoked the mania, the prednisolone dose was reduced to 25 mg/day which was followed by a worsening of both delirium and mania (). A subsequent pulse therapy of 1000 mg/day IV methylprednisolone over 3 days was associated with a prompt resolution of the delirium and improvement of the mania (). As the mania did not completely resolve along with oral prednisolone (100 mg/day), the treatment was augmented with quetiapine (up to 300 mg/day). The patient became euthymic within the next 3 weeks and could be transferred to an outpatient treatment (). Quetiapine and prednisolone were tapered within the subsequent 4 and 24 weeks, respectively, without changing the normal mental and physical health condition under THRT alone, which is still continuing up until now, 3 years later (). No further medications were required. Vitamin D supplementation was stopped after 6 months and the 25-OH-vitamin D-levels were normal in the controls carried out every six months.
Serum antithyroid autoantibody titers respond to the glucocorticoid treatment without a timely correlation with the patient's mental status (). TR-Abs sustainably normalized while TPO-Abs gradually increased after glucocorticoid taper, however, without a worsening of her normal mental status (). Simultaneously, the THRT could be reduced (). Macrocytic anemia resolved although the PC-Ab titers increased progressively () and antibodies against the intrinsic factor were found. Vitamin B levels, holotranscobalamin, and homocysteine were controlled every six months and remained normal. Brain MR imaging and EEG normalized under the combined glucocorticoid and thyroid hormone treatment, which corresponded to the resolution of delirious mania (). Furthermore, brain MR imaging and EEG were normal in the controls carried out 12 and 30 months after termination of the glucocorticoid treatment.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [166.0, 'cm']}",57.81505,54.9243,60.7058,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 166.0 cm, which is 166.0 cm * 0.393701 in/cm = 65.35437 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (65.35437 (in inches) - 60) = 57.81505 kg.
Hence, the patient's IBW is 57.81505 kg."
3698,10,Ideal Body Weight,physical,decimal,pmc-6099020-1,Extracted,"The patient is 84-year-old Caucasian woman, height 160 cm, weight 50 kg, who was referred for impaired consciousness. Her previous history was noteworthy for dementia, aphonia, hypothyroidism, strumectomy, hysterectomy, arterial hypertension, paroxysmal atrial fibrillation, lung emphysema, and diabetes. Clinical neurologic examination revealed sopor, positive frontal signs, rigor, cogwheel-rigidity bilaterally, exaggerated tendon reflexes, and diffuse wasting on the upper limbs, and reduced tendon reflexes, positive pyramidal signs, diffuse wasting, and calf fasciculations on the lower limbs. Cerebral CT showed diffuse atrophy, basal ganglia calcification, and leucencephalopathy. Cerebral MRI revealed multiple, spot-like, embolic, ischemic lesions, some microbleeds, diffuse cerebral atrophy, and leucencephalopathy. Electroencephalography was abnormal revealing a discontinuous, nonconvulsive epileptic state. Blood tests showed anemia, hyponatriemia, transient hypokaliemia, and a HbA1c of 6.4% (n, <6.0%). Resting serum lactate was increased to 2.4 mmol/L (n, <2.0 mmol/L). A previous lactate stress test was highly abnormal. Routine ECG showed an AV-block III without indication of implantation of a pacemaker. Repeated X-ray of the lung revealed ARE of 46 mm. ARE was confirmed by CT-angiography of the aorta. Magnetic resonance imaging angiography was scheduled, but the patient received a DNR order and died during the further course before the investigation and work-up for MID could have been carried out. Based upon the history, the clinical examination, the instrumental investigations, and the MIMODS score (n = 43) (see Appendix ), MIMODS was diagnosed.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3699,10,Ideal Body Weight,physical,decimal,pmc-7196934-1,Extracted,"A 45-year old male bus driver represented to our clinic with a one-week history of persistent left shoulder pain, which had now spread to his left upper back. He also felt feverish and had reduced appetite. He first saw a colleague four days prior with just left shoulder pain. Shoulder examination then revealed a normal-looking joint with no redness, swelling or tenderness. There was a slight pain on abduction and external rotation. There were post-inflammatory depigmented scars seen on the upper back area which were not hot or tender. He was treated symptomatically with simple analgesics and advised to return if the symptoms persisted or increased.
On the latest presentation, his left shoulder pain was dull in nature and was rated at 5 over 10 in severity. He had no associated numbness or pins and needle around the area of concern. Mefenamic acid tablets provided some relief. He had been working continuously for the preceding week. However, he could not recall any history of heavy lifting, trauma, cuts or bites to the area. There was no constitutional symptom, abdominal pain, nausea or vomiting.
He was on metformin and gliclazide for type 2 diabetes mellitus, perindopril and amlodipine for hypertension, and simvastatin for dyslipidemia. The most recent glycated hemoglobinA1c (HbA1c) level from two months ago was 8.1%.
Clinically, he was alert, oriented and non-toxic looking. His temperature was 37.6°C, oxygen saturation was 98% on air, blood pressure was 122/72 mmHg, and pulse rate was 90 beats per minute. His height and weight were 173 cm and 115.8 kg respectively making his body mass index (BMI) 39 kg/m². Capillary blood glucose was 17.2 mmol/L.
Upon removing his shirt for full shoulder examination, a purplish swelling located on the midline to the left upper back was noticed. It was warm, firm and mildly tender on palpation. There was a punctum seen (). Examination of the left shoulder revealed a normal-looking joint, which was not red, hot or tender on palpation. However, its range of movements were slightly limited secondary to pain from his upper back.
Given his history of poor glycemic control and mild fever, initial blood tests were sent urgently. These showed a white cell count (WCC) of 35.00 (normal 4.00-10.00 x10³/uL), erythrocyte sedimentation rate (ESR) of 97 mm/hr, C-reactive protein (CRP) of 382.3 mg/L, sodium of 130 (normal 136-145 mmol/L) and venous blood pH 7.44.
The provisional diagnosis of an upper back carbuncle, on a background of poorly controlled diabetes was made. His case was discussed with the general surgeon on duty who agreed to admit the patient for further management. He was commenced on intravenous ampicillin and sulbactam 3g QID, intravenous fluid and adequate analgesia. Intravenous insulin infusion was initiated to control his blood glucose level.
Ultrasonographic evaluation at the area of concern showed a collection at the subcutaneous tissue, however the depth and extent of it could not be determined due to its large size and the presence of acoustic shadowing from the air within the collection. A contrast-enhanced CT thorax was obtained for further evaluation. This showed features suspicious for necrotizing fasciitis due to presence of extensive soft tissue gas within the fascial layer at the region of the upper back, with associated non-enhanced fascial thickening, fat stranding and overlying skin thickening ().
Incision and drainage with wound debridement was performed by the surgical team. Intraoperatively, necrotizing fasciitis of the left upper back extending to the midline was confirmed along with an infected sebaceous cyst measuring 2x2 cm.
Postoperatively, the patient’s antibiotics was escalated to intravenous meropenem 1g TDS along with optimal analgesia. Tissue, pus and blood culture sent subsequently showed no growth. Acid fast bacilli were also not seen on the sent tissue specimen. The patient had no postoperative complications, had good wound healing and was fit for discharge a week after his surgery. His gliclazide was substituted with dapagliflozin, and he was commenced on a basal-bolus insulin regimen. He will continue to see an endocrinologist for his diabetic care. At the time of writing, he remained well and continued to attend his wound care appointments. His latest HbA1c had decreased to 6.8%.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.0, 'cm']}",68.65362,65.22094,72.0863,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.0 cm, which is 173.0 cm * 0.393701 in/cm = 68.11027 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.11027 (in inches) - 60) = 68.65362 kg.
Hence, the patient's IBW is 68.65362 kg."
3700,10,Ideal Body Weight,physical,decimal,pmc-2533299-1,Extracted,"A 29-year-old healthy gravida two, para one with previous caesarean section underwent a lower segment caesarean section at 36 weeks for premature labor under general anaesthesia.
Patient history details were as follows: Occupation: housewife; Ethnicity: Greek; Weight: 87 Kgr; Height: 167 cm; Medical history: one previous caesarean section, otherwise unremarkable; Family history: unremarkable; Patient habits and medication: non-smoker, no alcohol consuption, vitamin supplement during pregnancy.
Delivery of the fetus was uneventful. After the baby was born, an intravenous bolus of 10 i.u of oxytocin was administered. Uterine contraction was noted and gentle cord traction was applied in order to remove the placenta. With slight cord traction, complete inversion of the uterus, through the uterine incision occurred with the placenta remaining firmly attached to the uterine fundus (Fig. ). The inverted uterus was exteriorized at once and the placenta was manually removed. Several attempts for uterine reversion were done unsuccessfully for less than five minutes. Eventually, sevoflurane anesthesia was deepened from 1% to 5% and reversion of the uterus was finally achieved by gradually rolling the lowermost part of the posterior edge over the uterine fundus, thereby reverting that part that inverted last. The uterus was repositioned intraabdominally and an infusion of 20 i.u oxytocin plus 0.2 mg methylergometrine in 1000 ml Ringer's Lactated set maintained the uterine contractions. Sevoflurane progressively was reduced to the initial concentration. Uterine closure was followed by closure of the abdominal cavity. No significant changes in the haemodynamic status of the patient were noted during the operation. Blood loss was estimated at 1500 ml and two units of whole blood were transfused. After the end of cesarean section, 0.8 mg of misoprostol was given per rectum. The postoperative period was uneventful and the patient was discharged from the hospital on the 4th postoperative day.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [167.0, 'cm']}",58.72056,55.78453,61.65659,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 167.0 cm, which is 167.0 cm * 0.393701 in/cm = 65.74807 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (65.74807 (in inches) - 60) = 58.72056 kg.
Hence, the patient's IBW is 58.72056 kg."
3701,10,Ideal Body Weight,physical,decimal,pmc-4028563-1,Extracted,"A 45-year-old man (51.5 kg, 161 cm) with idiopathic pulmonary fibrosis had undergone a double lung transplantation 4 months earlier. His antirejection protocol included tacrolimus 1.25 mg/day, prednisolone 7.5 mg/day, and mycophenolate mofetil 500 mg bid. Three months following transplantation, he was diagnosed with steroid-induced diabetes mellitus and cholecystitis. One month later, the patient was admitted to the emergency room for abdominal pain. Abdominal X-rays and computed tomography showed a small bowel perforation requiring an emergency operation. Pulmonary function tests showed moderately restrictive disease; his functional vital capacity (FVC) was 44%, his forced expiratory volume in one second (FEV1.0) was 46%, and his FEV1.0/FVC ratio was 89. Before anesthesia, he gargled his mouth and throat with povidone-iodine. General anesthesia was induced using etomidate 10 mg and succinylcholine 75 mg, and rapid sequence intubation was performed with an 8.0 mm internal diameter single lumen tube. Anesthesia was maintained with propofol, remifentanil and rocuronium. Propofol and remifentanil were administered using a target-controlled infusion (TCI) device (Orchestra®, Fresenius Vial, Brezins, France), which calculates infusion rate according to the patient's body weight and height and measures the plasma concentration of drug, to maintain the effective site concentrations of propofol and remifentanil at 1-1.2 µg/ml and 7-10 ng/ml, respectively; and rocuronium was continuously infused at 20 mg/hr. The ventilator was set to pressure control mode with a peak inspiratory pressure (PIP) between 16-18 cmH2O and a respiratory rate of 12 breaths per minute to protect the transplanted lung. A tidal volume of approximately 300 ml was achieved, with a positive end-expiratory pressure (PEEP) of 5 cmH2O. Direct intraarterial pressure with stroke volume variation was monitored, as well as pulse oximetry, temperature, end-tidal carbon dioxide tension, and non-invasive blood pressure. A central venous catheter was placed in the right jugular vein, with initial central venous pressure of 15 mmHg. Intraoperative arterial blood gas analysis (ABGA) indicated pH 7.37, PaCO2 34 mmHg, PaO2 274 mmHg, HCO3- 19.7 mEq/L, and 100% O2 saturation (SaO2) with 0.5 fraction of inspired oxygen (FiO2). The surgical finding was duodenal ulcer perforation and primary closure was performed. The total operating time was 2 hours and 35 minutes. The total amounts of intraoperative fluids were 400 ml of plasmalyte and 500 ml of 6% hydroxyethyl starch in saline. Urine output during the surgery was 130 ml and estimated blood loss was less than 100 ml. Norepinephrine 0.5 µg/kg/min was infused intraoperatively to maintain his mean arterial pressure above 60 mmHg. Central venous pressure was 15 mmHg at the end of the surgery and did not change during the operation, and stroke volume variation was maintained between 10 and 16%. The patient's trachea was extubated at the end of the surgery with a tidal volume greater than 300 ml, during spontaneous ventilation, and when fully awake. However, the patient required re-intubation in the intensive care unit 1 hour later due to respiratory failure. His SaO2 fell down below 70% despite ambu-bagging with 15 L/min of O2, with ABGA showing a pH of 7.03 and a PaCO2 of 73 mmHg. He was maintained on mechanical ventilation in pressure control mode and PEEP for 7 hours and changed to T-piece at dawn, with ABGA showing pH 7.36, PaCO2 36 mmHg, PaO2 163 mmHg, HCO3- 20 mEq/L, SaO2 99%, and FiO2 0.5. He was extubated on the morning of postoperative day 1. After extubation, the patient complained of dyspnea and a high-pitched stridor was heard. Dexamethasone 10 mg was injected intravenously and his respiration was maintained with nasal prong O2 2 L without difficulty. The patient's immunocompressive protocol was maintained throughout the perioperative period. However, fever was observed and the patient was diagnosed with aspergillus pneumonia on postoperative day 8. The pneumonia was treated with intravenous voriconazole and the patient was discharged on postoperative day 23 with oral voriconazole ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [161.0, 'cm']}",57.78748,54.89811,60.67685,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 161.0 cm, which is 161.0 cm * 0.393701 in/cm = 63.38586 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (63.38586 (in inches) - 60) = 57.78748 kg.
Hence, the patient's IBW is 57.78748 kg."
3702,10,Ideal Body Weight,physical,decimal,pmc-3350097-1,Extracted,"A 41-year-old woman (height 1.66 m; weight 62 kg) with SMA type IV was scheduled for mammectomy. The diagnosis of SMA type IV was based on clinical progressive symptoms of limb muscular weakness that began eight years ago. She has been on wheelchair since five years ago. At present, she even could not lift her arms up but had no difficulty in swallowing or breathing. She had a family history of SMA, her mother (died at 50 years old) and uncle both had the same disease. She had resection of right breast fibroadenoma under local anesthesia 6 years ago and right oophorocystectomy under epidural anesthesia 12 years ago. Physical examination revealed that she had a hoarse throat, normal gape degree, proximal muscular atrophy of the limb, muscular strength 2–4 degrees (with 4 degrees in the upper limb and 2 degrees in the lower limb), decreases of tendon reflex in extremities, no pyramidal tract signs, and paraesthesia. Chest X-ray showed increases in lung markings. ECG was normal. The laboratory examinations were normal except serum creatinine 31.00 μmol/L (normal value is 44–133 μmol/L). Bronchofiberscopy showed limitation of vocal fold abduction. A size 6 cm × 6 cm lump (benign fiber-epithelial tumor confirmed by a biopsy pathological examination) was found in her right breast, and at her request, her admission was scheduled to remove her right breast in fear of malignancy in the future.
On the operating day, no premedication was given to the patient. Electrocardiogram, cuffed blood pressure, and SpO2 were monitored. External jugular vein was inserted with an 18 ga catheter due to collapse of extremity veins. Anesthesia was induced with remifentanil (target-controlled infusion at plasma concentration of 3 ng/mL) and propofol (target-controlled infusion at plasma concentration of 3 μg/mL) and a size 4 laryngeal mask airway (LMA) was tried to but failed. Then rocuronium 30 mg was given to facilitate the endotracheal intubation. The patient was intubated with an insertion of a size 7 endotracheal tube. Anesthesia was maintained with intravenous remifentanil (target-controlled infusion at plasma level of 2-3 ng/mL), propofol (target-controlled infusion at plasma level of 3-4 μg/mL), and 50% nitrous oxide balanced with oxygen. The hemodynamic parameters were stable during the one-hour surgery. Morphine 3 mg was given intravenously 30 minutes before the end of operation. The patient woke up quickly after cessation of anesthesia and could raise her head. Antagonists of muscle relaxant (neostigmine 2 mg plus atropine 1 mg) were given. She was extubated and transferred to the surgical intensive care unit (SICU), where she recovered uneventfully. She returned to the general ward on the following day and was discharged from hospital 5 days after operation.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.66, 'm']}",57.81505,54.9243,60.7058,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.66 m, which is 1.66 m * 39.3701 in/m = 65.35437 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (65.35437 (in inches) - 60) = 57.81505 kg.
Hence, the patient's IBW is 57.81505 kg."
3703,10,Ideal Body Weight,physical,decimal,pmc-7235834-1,Extracted,"A 57-year-old woman with a history of aquaporin-4 (AQP4) antibody-positive optic neuritis presented with progressive visual impairment of the left eye over two days and was admitted for further evaluation and treatment. The patient had been diagnosed with anti-AQP4 antibody-positive optic neuritis two years earlier due to visual impairment of the right eye. However, no medical treatment had been initiated at that time due to the patient’s refusal. On watchful waiting, her visual symptoms had not deteriorated notably until her admission here. Her medical history also included hypertension and diabetes mellitus diagnosed at 47 years of age. The patient had developed diabetic polyneuropathy and proliferative diabetic retinopathy for which pan-retinal photocoagulation was given, but nephropathy had not emerged as a complication. Glycated hemoglobin on admission was 8.0%; at this time, medication consisted of 36 units of insulin glargine U-300 once-daily, anagliptin 200 mg/day, and metformin 500 mg/day. Hypertension was treated with telmisartan monotherapy at 40 mg/day alone and was satisfactorily controlled. The patient drank alcohol only socially and never smoked.
On physical examination, the patient’s body mass index was 20.9 kg/m2 (height 153 cm, weight 49.0 kg), body temperature was 36.1 °C, blood pressure was 107/55 mmHg, and pulse was regular at 86 beats/min. While Goldman perimeter testing revealed a newly developed central visual field defect in the left eye, the status of the diabetic retinopathy was not markedly changed. A bilaterally weakened Achilles tendon reflex and impaired vibration sensation over the medial malleolus was observed. Laboratory parameters on admission () showed unremarkable electrolytes, preserved estimated glomerular filtration rate, and normo-albuminuria.
The clinical course of hospitalization is shown in . From the fourth hospital day, the patient received pulsed intravenous methylprednisolone 1000 mg/day for three consecutive days, followed by oral prednisolone 30 mg/day. Additionally, low-dose trimethoprim–sulfamethoxazole prophylaxis (160 mg and 800 mg daily) was concomitantly administered. Subsequently, the serum sodium level steadily decreased, and the potassium level was slightly elevated despite normal renal function. A second course of pulsed methylprednisolone was given on days 13–15. Telmisartan was stopped on day 16, but electrolyte abnormalities did not improve. Therefore, on day 21, arterial blood gas analysis, urinalysis, and hormonal status tests were carried out in addition to routine examinations and body weight measurements (). Hypotonic hyponatremia with high urinary sodium excretion and mild hyperkalemia with low urinary potassium excretion were observed. While primary respiratory alkalosis was present, decreased bicarbonate levels greater than compensatory changes and negative base excess indicated the co-existence of primary metabolic acidosis. Based on the above findings and on the normal serum anion gap, the patient was diagnosed as having hyperkalemic RTA. After the discontinuation of trimethoprim–sulfamethoxazole, electrolytes and acid–base imbalances swiftly resolved. Visual impairment also improved and did not recur during prednisolone tapering, and the patient could be discharged on hospitalization day 29.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.0, 'cm']}",46.04337,43.7412,48.34554,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.0 cm, which is 153.0 cm * 0.393701 in/cm = 60.23625 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.23625 (in inches) - 60) = 46.04337 kg.
Hence, the patient's IBW is 46.04337 kg."
3704,10,Ideal Body Weight,physical,decimal,pmc-6635262-2,Extracted,"A male patient, 77 years old, 55.7 kg and 157.3 cm in height, had been diagnosed with chronic obstructive pulmonary disease, and was scheduled for the bronchoscopic volume reduction surgery upon exacerbation of his symptoms of dyspnea and cough with sputum. The pulmonary function test showed severe obstructive lung defect (FVC 73, FEV1 38, FEV1/FVC ratio 34). Written informed consent was obtained from the patient for the publication of this case report and accompanying images.
He arrived at the operation room wearing a nasal prong with the oxygen flow at 5 L/min. The vital signs were monitored: blood pressure of 140/80 mm Hg, heart rate of 90 and SpO2 of 92%. The initial ABGA showed pH 7.49, PCO2 38 mm Hg, PaO2 68 mm Hg, HCO3 29 mmol/L, BE 5.4 mmol/L, and SaO2 95%. Preoxygenation was performed with HFNC (Fisher&Paykel Optiflow ThriveTM) for 3 minutes before anesthetic medications; the oxygen flow was set at 50 L/min and the FiO2 at 1.0. After preoxygenation, SpO2 reached 100%, and the ABGA after HFNC showed pH 7.49, PCO2 39 mm Hg, PaO2 343 mm Hg, HCO3 29.7 mmol/L, BE 5.9 mmol/L, and SaO2 100%. While maintaining the HFNC, the rigid bronchoscope was then inserted after the administration of propofol 2 to 5 μg/mL, remifentanil 1 to 5 ng/mL and rocuronium 50 mg.
SpO2 remained at 100% until the rigid bronchoscope was completely inserted and the ABGA performed at the point showed pH 7.36, PCO2 59 mm Hg, PaO2 209 mm Hg, HCO3 33.3 mmol/L, BE 6.2 mmol/L, and SaO2 100%. The total apneic time measured was 3 minutes 10 seconds. Mechanical ventilation combined with assisted ventilation was maintained during the surgery. The rigid bronchoscope was removed after the volume reduction surgery (Fig. ). The procedural time was 1 hour 20 minutes and the anesthetic time was 1 hour 35 minutes. HFNC was applied in the recovery room with the oxygen flow of 20 L/min. However, the patient complained of dyspnea in the recovery room, with decrease of SpO2 from 90% to 85%. Endotracheal intubation was performed with 8.0 ID and the patient was sent to the intensive care unit with an Ambu- bag streamed with the oxygen flow of 5 L/min.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [157.3, 'cm']}",54.43709,51.71524,57.15894,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 157.3 cm, which is 157.3 cm * 0.393701 in/cm = 61.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (61.92917 (in inches) - 60) = 54.43709 kg.
Hence, the patient's IBW is 54.43709 kg."
3705,10,Ideal Body Weight,physical,decimal,pmc-3506861-1,Extracted,"A 40-year-old woman (height 157.8 cm, weight 46.8 kg) was scheduled for a laparoscopic low anterior resection (LAR) and hepatic tumorectomy due to colorectal cancer with liver metastasis. The patient had a history of paroxysmal supraventricular tachycardia which was controlled by medication with verapamil 180 mg daily. A week before the surgery, she had undergone a radiofrequency catheter ablation for paroxysmal supraventricular tachycardia. A follow-up electrocardiography (ECG) showed normal sinus rhythm, and transthoracic echocardiography showed normal chamber size, normal left ventricular wall thickness, and normal left ventricular ejection fraction without regional wall motion abnormalities. Laboratory studies were unremarkable.
The patient received glycopyrrolate 0.2 mg intramuscularly as premedication 30 minutes before surgery. Monitoring included non-invasive blood pressure determination, ECG (lead II), pulse oximetry, and end-tidal CO2 concentration (ETCO2) measurements. Vital signs included a blood pressure (BP) of 125/80 mmHg, a heart rate (HR) of 82 beats/min with regular sinus rhythm, and peripheral oxygen saturation (SpO2) of 98%. Anesthesia was induced using mask administration of 100% O2. 2% lidocaine 30 mg, propofol 100 mg and rocuronium 40 mg were administered intravenously, and the trachea was intubated using a 7.0 mm cuffed endotracheal tube. Anesthesia was maintained using 2 L/min O2, 2 L/min nitrous oxide (N2O), and 1.5-2.0 vol% sevoflurane. Ventilation was mechanically performed with a tidal volume of 500 ml and a rate of 10 breaths/min. The right radial artery was cannulated for continuous monitoring and a central venous catheter was placed in the right internal jugular vein to be prepared for massive bleeding.
The operative technique involved intraperitoneal insufflation of CO2 via a Veress needle inserted through a small infraumbilical incision. Pneumoperitoneum was maintained with a variable-flow insufflator at a pressure of 15 mmHg throughout surgery. ETCO2 was kept within the range of 30-35 mmHg with a respiratory rate of 15 breaths/min, a tidal volume of 450 ml, and an inspiration: expiration ratio of 1 : 1.5. The patient was placed in the Trendelenburg position during the LAR. Vital signs were stable, and the duration of the operation was 190 minutes.
After the LAR, hepatic tumorectomy was performed in the reverse Trendelenburg and left lateral position. Twenty minutes after changing the position, ETCO2 increased to 48 mmHg. Assuming CO2 absorption, ventilation was converted to a rate of 18 breaths/min and a tidal volume of 400 ml. Peak airway pressure did not exceed 25 mmHg. Ten minutes after changing the ventilator settings, ETCO2 decreased to 32 mmHg and the vital signs were stable.
Fifty minutes later, the right hepatic vein was accidentally disrupted during liver dissection. Laparoscopic ligation was impossible because the hepatic vein was not compressed. An emergent laparotomy to control bleeding was immediately performed in the neutral position. A few minutes later, systolic arterial pressure decreased from 110 to 62 mmHg. We accelerated the infusion rate of Hartmann's solution, and 10 mg ephedrine was administered intravenously. However, the vital signs deteriorated. Arterial blood gas analysis showed pH 6.994, PaCO2 106 mmHg, PaO2 259 mmHg, HCO3- 24.4 mEq/L, SaO2 98.3% (FiO2: 0.5), hemoglobin 9.4 g/dL and hematocrit 29%. The waveform of the capnogram suddenly decreased, and progressive arterial desaturation developed. This was followed by bradycardia (HR = 30-40 beats/min) and the pulsatile activity disappeared from the arterial line. External cardiac massage, epinephrine (two doses of 1 mg) and atropine (one dose of 0.5 mg) were given. At the same time, ventilation with 100% O2 was begun and the patient was moved to the Trendelenburg position because pulmonary gas embolism was strongly suspected. Two minutes after initiation of cardiac massage, a cardiac rhythm reappeared and a pulsatile arterial waveform was displayed dramatically. A TEE was performed, and it showed air bubbles in the right pulmonary artery on a mid-esophageal ascending aortic short axis view (). At that time, we decreased the infusion of intravenous solution in order to avoid the formation of an echocardiographic contrast caused by rapid intravenous infusion. However, a mid-esophageal four chamber view showed no residual presence of air bubbles, a normal right ventricle without septal shift, and non-compression of the left ventricle. Fifteen minutes after cardiopulmonary resuscitation, arterial blood gas analysis showed pH 7.280, PaCO2 34 mmHg, PaO2 499 mmHg, HCO3- 15.4 mEq/L, SaO2 99.2% (FiO2: 1.0), hemoglobin 6.9 g/dl and hematocrit 22%. The patient received 2 units of packed red blood cells.
The operation was completed using an open approach without any additional major problems. The patient was transferred to the intensive care unit and recovered consciousness 20 minutes later. She was extubated 2 hours later and experienced no cardiopulmonary or neurological sequelae.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [157.8, 'cm']}",50.38985,47.87036,52.90934,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 157.8 cm, which is 157.8 cm * 0.393701 in/cm = 62.12602 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.12602 (in inches) - 60) = 50.38985 kg.
Hence, the patient's IBW is 50.38985 kg."
3706,10,Ideal Body Weight,physical,decimal,pmc-3916142-1,Extracted,"A 25-y old male () was referred with dry skin, lentigines, cutaneous warts and dysmorphic features. He was conceived by healthy, non-consanguineous Caucasian parents and born after an uneventful pregnancy. At the age of three, he was diagnosed with strabismus and hypermetropia and since 12 y of age he used hearing aids because of sensorineural hearing loss. Since early childhood the patient suffered from very dry skin and became easily sunburned despite preventive measures although he never developed blisters. From early puberty he gradually developed many freckles, sparse, thin hair, photophobia and growth retardation ().
He had an older brother who died at age 26 due to ruptured appendicitis and salmonella sepsis. The deceased brother had a similar phenotype with short stature, ichthyosis, hypogonadism, epilepsy, mild mental retardation and diabetes mellitus. A second brother and a sister displayed none of these traits and were considered healthy. The patient’s height was 165 cm (healthy siblings had a height between 180 and 200 cm). Medical history, clinical examination and laboratory and imaging test revealed diseases in many organs.
He had dry, parchment-like skin with ichthyosiform scaling mainly on the back and scattered, but pronounced, lentiginous pigmentation (). Viral warts were seen on his hands, knees and feet. He had sparse, brittle and unruly hair and koilonychia with distal nail splitting (). Hair microscopy showed some variation in the calibre of the hair shafts with few trichorrhexis nodosa-like defects. Some hairs had focal ribboning/undulation and irregular contours. No “tiger-tail pattern” was observed using polarizing light microscopy. Cystine content in hair was only slightly decreased to 8.2 mol% (normal values 10.0−10.5 mol%, analysis performed by Dr Josef Föhles, Aachen, who provided reference values). At the age of 28, basal cell carcinoma was diagnosed on his shoulder.
Eye examination revealed photophobia and severely decreased visual acuity (1/60 on the right eye and 12/60 on the left eye) (). He had esotropia but no nystagmus. He had bilateral microphthalmos with an axial length of 18.39 mm on the right eye and 18.53 mm on the left eye, but normal corneal size (12 mm on both eyes). He had hypopigmentation of the iris with transillumination. Corneas were normal with the exception of limbal vascularization. Before cataract surgery he had an excessive hyperopia +13 D on both eyes. He had bilateral cataract with punctate lens opacities. Ophthalmoscopy revealed hypopigmentation of the retina, tortuosity of the vessels and macular lesions with pigment epithelial derangement and atrophy, retinal fibrosis and macular folds on both eyes. Earlier performed visual evoked potential (VEP) was normal and electroretinography did not show any signs of tapetoretinal degeneration.
He had a high-pitched voice, micropenis (2 cm) and cryptorchidism with high levels of plasma luteinizing- and follicle stimulating hormones and very low plasma testosterone. Pubic and axillary hairs were absent. Type 2 diabetes was diagnosed at the age of 26 and required insulin treatment. The pituitary-adrenal axis and thyroid function were normal.
Neurologic examination showed progressive ataxia and a broad-gauged gait. Varying imaging studies showed thickened theca cranii and a dysmorphic sella turcica as the only clear-cut abnormal findings and EEG was normal. Multiple CT scans as well as an MRI of the cerebrum were normal at around age 27.
Between ages 25 to 31, he developed progressive renal disease with an increase in P-creatinine from 114 to 252 µmol/l, persistent albuminuria around 1.0 g/l and intermittent hematuria. Renal biopsy revealed partial atrophy and sclerosis with scattered hyaline tubular casts but immunoflourescent evaluations were all negative. Electron microscopy showed expanded mesangium and unevenly thickened glomerular basement membranes with varying density but without deposits. The renal disease was complicated by nephrogenic anemia, renal osteodystrophy and arterial hypertension. MCV was low, but within normal range and HBa2 was not tested. Due to hypercholesterolemia treatment with Simvastatin was initiated but had to be discontinued due to acute renal failure caused by rhabdomyolysis. Kidney function was restored after three weeks on dialysis.
Mitochondrial function was normal when respiratory enzymes were measured in a liver biopsy. Plasma concentrations of amino acids were normal except for a slight elevation of P-cysteine. A biopsy from striated muscles did not reveal any primary muscular disorder.
Due to recalcitrant viral warts and frequent pneumonias, a lymphocyte-subpopulation evaluation was conducted showing normal fractions and concentrations of T-, B- and NK-cells. CD4+ count was slightly below normal levels and CD4+/CD8+ levels inversed T- and B- memory cell levels were unexpected high, mimicking levels of a much older person. It was concluded that the patient was slightly immunodeficient.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3707,10,Ideal Body Weight,physical,decimal,pmc-7452794-1,Extracted,"The case was a 42-year-old male patient who had suffered of acute-on-chronic liver failure because of hepatitis B virus-associated liver cirrhosis and alcoholic liver disease. This patient was referred to our center for LT. SI totalis was identified at the pretransplant computed tomography scan (), but detailed studies on vascular anatomy were not done because of severe renal dysfunction. The model for end-stage liver disease (MELD) score was 41 at admission, so he was enrolled in the waiting list with Korean Network for Organ Sharing (KONOS) old status 2A, which provided priority allocation. His height and body weight were 178 cm and 95 kg, respectively.
Considering the recipient status of SI, we waited for a deceased donor with a small body size. After eight days of waiting, a whole-liver graft of a 69-year-old female donor was allocated for this patient. Her height and body weight were 159 cm and 58 kg, respectively. The donor-recipient body weight ratio was 0.61. The graft weight was 1360 g, so the graft-recipient body weight ratio was 1.43. After laparotomy, the recipient’s native liver was removed according to the standard procedures of deceased-donor liver transplantation (DDLT). We performed veno-venous bypass using a centrifugal biopump with inflow from the portal vein and left iliac vein. At this stage, the whole-liver graft was temporarily placed within the upper abdominal cavity to assess its proper location and orientation. Since the upper abdominal cavity was large enough to accommodate the whole-liver graft in the orthodox position, we decided to perform a large cavocaval anastomosis using a modified piggyback technique (). After clamping of the suprahepatic and retrohepatic inferior vena cava (IVC), the orifices of the right, middle and left hepatic vein trunks were opened altogether to make a large single orifice. In addition, we made a 5-cm-long longitudinal incision at the ventral surface of the retrohepatic IVC to enlarge the anastomotic vein orifice further. The corners of the recipient and graft IVC orifices were tagged with 4-0 Prolene sutures, and then a 4-cm-long longitudinal incision was also made at the dorsal surface of the graft IVC. These triangular-shaped orifices at the recipient and graft IVCs were matched and sutured with 4-0 Prolene. Thereafter, we packed a large bulk of surgical gauzes at the left subphrenic space to support the liver graft. The portal vein was anastomosed under this orientation with gauze packing. We performed hepatic artery reconstruction using branch patches and duct-to-duct biliary anastomosis with insertion of a rubber T-tube (). In order to maintain the orientation of the outflow and inflow vessels of the liver graft in the designed position, we placed a large tissue expander at the left subphrenic space for mechanical support of the liver graft.
The graft function was recovered uneventfully with no surgical complications (), but hospitalization was prolonged because of poor general condition and pneumonia. The water within the tissue expander was gradually removed, and the expander was removed at 46 days after transplantation. This patient was finally discharged 63 days after the DDLT.
At 30 months after DDLT, the liver function deteriorated progressively (). Initial liver biopsies suggested acute cellular rejection. Subsequent repeated liver biopsies revealed severe cholestasis, mild portal inflammation with bile duct atrophy and loss, and perisinusoidal fibrosis, strongly suggesting chronic rejection. At 34 months after first DDLT, his liver function deteriorated with MELD score of 28 and KONOS old status 2B. After some waiting period, he was finally allocated for whole-liver graft for retransplantation. The donor was a 43-year-old male with height of 174 cm and body weight of 73 kg. The graft weighed 1760 g, and the recipient’s body weight was 83 kg at that time, thus GRWR was 2.12. After laparotomy, the recipient’s first liver graft was removed according to the standard procedures of DDLT. We also performed veno-venous bypass using a centrifugal biopump. When the second whole-liver graft was temporarily placed within the upper abdominal cavity, we found that the right upper abdominal cavity was too small to accommodate the whole-liver graft in the orthodox position. Since the spleen was definitely enlarged, we performed splenectomy to make room to accommodate the bulky right liver of the whole-liver graft. The surgical techniques used for the first DDLT were used again in the second DDLT operation, including large cavocaval anastomosis using a modified piggyback technique, end-to-end portal vein and hepatic artery reconstruction, and duct-to-duct biliary reconstruction. A tissue expander was not necessary in this operation because the left subphrenic space was already shrunken. The recovery of the graft function was delayed because of the extrinsic compression of the liver graft, although there were no surgical complications (). Hospitalization was very prolonged because of very poor general condition and repeated lung problems. This patient was finally discharged 254 days after the second DDLT.
During follow-up at the outpatient clinic, renal function deteriorated progressively, and hemodialysis started at 5 years after the second DDLT. After hemodialysis for 8 months, he underwent living-donor kidney transplantation from his wife. Currently, he is doing well at 10 years after the first DDLT ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [178.0, 'cm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3708,10,Ideal Body Weight,physical,decimal,pmc-8720780-1,Extracted,"The patient was a formerly healthy 17-year-old young male (weight: 74.5 kg; height: 185 cm. brachial systolic/diastolic blood pressure: 129/78) with no family history of inflammatory joint- or connective tissue diseases. Further, the patient did not suffer from any cardiovascular diseases. After a week of sickness due to a gastrointestinal infection the patient developed ReA in both of his knee joints as well as the left hip joint, hence resulting in hip- and knee joint pain as well as joint swelling, ultimately reducing his physical activity level and quality of life. The ReA of hip joint as well as the knee joints was successfully treated with arthrocentesis, with full recovery in knee joint mobility and only small reduction in hip flexion and hip internal rotation as compared with the right hip joint. At the physical examination at the hospital, the range of motion was not quantified, but only compared between each limb. Thirty-six months after the first ReA, the patient suffered a relapse in his right knee. Similar to the episode, he suffered from knee joint pain and knee joint swelling which resulted in a reduced physical activity-level as well as a reduced quality of life. Treatment with non-steroid anti-inflammatory drugs (NSAID) did not reduce symptoms and a new arthrocentesis and aorticosteroid injection only reduced the knee swelling temporary. After 3 months without improvements, the patient was offered 12 weeks of BFR-RT to (i) improve his functional capacity, (ii) reduce swelling of the knee joint, and (iii) reduce knee symptoms (). The patient accepted to engage in the study and signed a written informed consent in accordance with the Helsinki Declaration. According to Danish law, case studies do not require formal ethical approval.
The BFR-RT was performed at home every second day for 12 weeks, and consisted of squat and lunges (). The load in each exercise was the body weight. A conically shaped pneumatic cuff (Occlude APS, size: Large, width = 11.7 cm) was placed around the proximal part of the right thigh (). Each exercise was performed in 4 sets with 30 repetitions (reps) in round one and 15 reps in round two, three, and four. Each set was interspaced with 30 sec rest and each exercise was separated by a 5-min rest pause. A physiotherapist supervised the exercises during the first week of exercise (). The patient was instructed to apply the cuff correctly, to inflate/deflate the cuff, and check that the inflation was kept constant during the entire duration of each exercise. Also, the patient was carefully instructed in how to perform the exercises correctly. The cuff pressure was an absolute pressure and not determined based on the total limb occlusion pressure. As we decided to maintain a preset repetition scheme (30-15-15-15) and use body weight as load, we decided to gradually increase the cuff pressure with 10 mmHg from week 1 to week 6 (110–150 mmHg). For safety reasons the cuff pressure was kept constant from week 6 to week 12. Immediately after the last set of each exercise, the cuff was deflated.
One physiotherapist collected outcome measures at baseline and after 3, 6, 9, and 12 weeks of BFR-RT and included unilateral 30-Sec chair-stand test (u30-sec CST) (Thongchoomsin et al., ; Waldhelm et al., ) and low-thigh circumference with tape measure (Jakobsen et al., ) proximal to the upper edge of the patella in standing position. Also, the patient completed the Knee Injury and Osteoarthritis Outcome Score (KOOS) (Roos and Lohmander, ) and the Forgotten Knee Joint Score (FJS) (Behrend et al., ).
The u30-sec CST is a functional test used to assess lower limb strength (Waldhelm et al., ). Before testing, the physiotherapist demonstrated the movement after which the participant performed two practice repetitions to demonstrate the understanding of the test. From sitting on a 45 cm high chair, the patient performed as many single-leg sit to stands with full hip- and knee extension as possible in 30 Sec with the arms crossed in front of the chest. The patient descended until the buttock made contact with the chair. The patient was allowed to reverse the downward-movement as soon as he felt the chair. Thus, he did not have to bear weight through his buttock. Only repetitions correctly performed repetitions (i.e., as described above) were counted. (Waldhelm et al., ).
Low-thigh circumference was measured with the patient laying prone on an examination table. To measure low-thigh circumference, a tape measure was placed around the proximal border of the patella while the patient lay relaxed without contraction his knee extensor muscles. A reduction in circumference from baseline to follow-up would represent less joint swelling. Assessing low-thigh circumference with a tape measure has previously been demonstrated to be reliable and reproducible in patients suffering from osteoarthritis (Silva et al., ).
The KOOS-questionnaire was completed by the patient prior to the functional tests on each testing day. The patient completed the questionnaire in quiet and undisturbed environment with the possibility to ask the physiotherapist in charge of testing whenever he had questions. The KOOS is a patient-administered knee specific questionnaire comprising five subscales: Pain; Symptoms; Activities of daily living; Sport & Recreation; and Knee-Related Quality of Life. All questions are related to the patients' experiences the last seven days. Each item is scored from 0 to 4 (Roos and Lohmander, ). The raw score for each of the five subscales is the total sum of the associated item scores. Scores are transformed to a 0 to 100 scale. The scores of the five subscales are expressed as a composite outcome profile, higher scores indicate fewer problems, and a 10-point change in a subscale score is considered to represent a clinically meaningful change (Nilsdotter et al., ; Lyman et al., ).
The FJS consists of 12 questions with a five-point Likert response format from 0-4 point (Behrend et al., ). The FJS was completed prior to functional performance tests and after completing the KOOS questionnaire on each testing day. As with the KOOS questionnaire, the patient completed the questionnaire in an undisturbed and quiet environment with the possibility to ask the physiotherapist in charge of testing whenever he had questions. The score is transformed into a 0 to 100-point scale with high scores indicating good outcomes (i.e., being less aware of the knee during every day activities) (Behrend et al., , ).
The numeric rating scale for pain (NRS) was used to quantify the level of pain prior to each testing session (Hawker et al., ). Thus, prior to completing the KOOS questionnaire, the patient reported the level of pain experienced in each knee while sitting relaxed in a chair with ~90 degree knee flexion on a scale from 0 to 10, where 0 represented no pain at all, and 10 represented the worst imaginable pain (Hawker et al., ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [185.0, 'cm']}",79.51979,75.5438,83.49578,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 185.0 cm, which is 185.0 cm * 0.393701 in/cm = 72.83469 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (72.83469 (in inches) - 60) = 79.51979 kg.
Hence, the patient's IBW is 79.51979 kg."
3709,10,Ideal Body Weight,physical,decimal,pmc-4409735-1,Extracted,"A 47-year-old woman was transported to our hospital because of the sudden onset of severe pain in her left lower back. She was alert and conscious, with a blood pressure of 165/95 mmHg, pulse of 77 beats/minute, and oxygen saturation of 95%. She appeared to be in distress and complained of sharp spontaneous pain in her left lower back. She was 162.0 cm tall and weighed 84.5 kg. There were no physical features suggestive of Cushing’s syndrome. The patient had been healthy with no particular past medical history or familial disease. Her white blood cell count was 11,800/μL and her hemoglobin level was 8.8 g/dL. Other than these findings, biochemical tests and urinalysis on admission demonstrated no particular abnormalities (Table ). Emergency contrast-enhanced computed tomography (CT) of the abdomen revealed a tumor-like soft mass accompanied by massive bleeding in the retroperitoneum on the upper pole of the left kidney, in addition to vascular leakage from the middle suprarenal artery (Figure a, b). Immediately after obtaining the results of the CT scan, transcatheter embolization therapy of the left middle adrenal artery was performed based on a diagnosis of acute adrenal hemorrhage, possibly from a ruptured adrenal tumor (Figure a, b). The patient’s condition subsequently stabilized and a detailed investigation of the cause of the adrenal hemorrhage was initiated. Magnetic resonance imaging (MRI) revealed a hematoma expanded within the Gerota’s fascia, and a round tumor was detected in addition to the hematoma, with a rich vasculature and possible necrotic area (Figure a, b). No liver nodules or swelling of the retroperitoneal lymph nodes suggestive of metastasis were observed. Endocrine function of the adrenal gland appeared normal. The above findings indicated a ruptured non-functional adrenocortical tumor. Imaging confirmed the absence of metastatic lesions, and the tumor was removed by elective laparotomy surgery 2 months later. Regarding the surgical findings, no hemorrhage or abnormal adhesion was observed in the abdominal cavity. A soft elastic tumor measuring 10 cm was palpable in the retroperitoneum at the inferior border of the pancreatic body. Although it adhered closely to the surrounding retroperitoneal fatty tissue, the tumor was removed en bloc by partially excising Gerota’s fascia, without leaving any remnants. No invasion into the surrounding organs, lymph node metastasis, or liver metastasis was observed. The operative time was 229 min, and the surgical blood loss was approximately 500 mL. The patient recovered uneventfully. The tumor measured 13.5 × 8.6 × 4.2 cm and weighed 380 g. The cut surface indicated a yellowish solid tumor, with areas of bleeding accompanied by necrosis in a branched pattern (Figure a, b). The normal adrenal gland could not be identified visually. Histopathological examination revealed proliferated tumor cells with an atypical morphology, with an eosinophilic or clear cytoplasm and large nucleus containing a distinct nucleolus (Figure a, b). Nuclear atypia and abundant nuclear mitotic images were observed (≥11 per 50 high-power fields (HPF)). A wide focus of necrosis was also noted, although there was no apparent invasion outside the capsule. The final diagnosis was a ruptured, non-functioning left adrenocortical carcinoma, pT2N0M0, stage II. Mitotane administration for 2 years was planned as adjuvant therapy. The patient was alive at 6 months after surgery, with no serious adverse events or relapse.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [162.0, 'cm']}",54.19299,51.48334,56.90264,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.77956 (in inches) - 60) = 54.19299 kg.
Hence, the patient's IBW is 54.19299 kg."
3710,10,Ideal Body Weight,physical,decimal,usmle-1222,Extracted,"A 32-year-old man comes to the physician because of a progressive development of tender breast tissue over the past 18 months. He used to ride his bicycle for exercise 4 times a week but stopped after he had an accident and injured his left testicle 3 months ago. He has gained 5 kg (11 lb) during this period. For the last 10 years, he drinks one to two beers daily and sometimes more on weekends. He occasionally takes pantoprazole for heartburn. He is 171 cm (5 ft 7 in) tall and weighs 87 kg (192 lb); BMI is 30 kg/m2. Vital signs are within normal limits. Examination shows bilaterally symmetrical, mildly tender gynecomastia. A nontender 1.5-cm mass is palpated in the left testis; transillumination test is negative. The remainder of the examination shows no abnormalities.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [171.0, 'cm']}",66.8426,63.50047,70.18473,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 171.0 cm, which is 171.0 cm * 0.393701 in/cm = 67.32287 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.32287 (in inches) - 60) = 66.8426 kg.
Hence, the patient's IBW is 66.8426 kg."
3711,10,Ideal Body Weight,physical,decimal,pmc-5984920-1,Extracted,"A 45-year-old Caucasian woman presented with abdominal pain, nausea, and vomiting for 17 h. At 22 h prior to admission, she went out to dinner and drank one glass of wine. A few hours after the meal, she developed epigastric and left upper quadrant abdominal pain that was moderate, persistent, cramping, and aching; the pain radiated to her left middle back and arm without exacerbating or alleviating factors. The pain was associated with nausea, vomiting, and she could not tolerate any oral intake. She felt thirsty and had polyuria and positional lightheadedness. She reported no fever, chills, chest pain, cough, sputum production, dysuria, hematuria, diarrhea, hematochezia, and melena.
On further questioning, the patient shared that she had a history of gestational glucose intolerance 6 years ago, and has had occasional impaired fasting glucose of 81–107 mg/dL for the past 6 years. She began following an American Diabetes Association (ADA) diet 2 years ago and lost 25 lb. Additionally, she had a past medical history of supraventricular tachycardia, irritable bowel syndrome, social alcohol use, cholecystectomy, and thyroid papillary adenocarcinoma status post partial thyroidectomy complicated by postsurgical hypothyroidism. Home medications included metoprolol tartrate, levothyroxine, and meloxicam. The patient reported no family history of diabetes.
Temperature 97.7 °F, pulse 130 bpm, respiratory rate 28 bpm, BP 134/71 mmHg, weight 87 kg, height 1.68 m, BMI 31 kg/m2, SpO2 99% on room air.
The patient was in moderate distress. There was no acanthosis nigricans. Cardiovascular system revealed tachycardia. A pulmonary exam revealed tachypnea, accessory muscle usage with moderate respiratory distress. Abdominal exam revealed central obesity, normoactive bowel sounds, left upper quadrant and epigastric tenderness to palpation, no rigidity or guarding. No costovertebral angle tenderness.
CBC: WBC 25.9 × 109/L, hemoglobin 14.7 g/dL, hematocrit 45.8%, platelet 386 × 109/L, MCV 100.2 µm3. BMP: sodium 135 mmol/L, potassium 7.4 mmol/L, chloride 89 mmol/L, bicarbonate 5 mmol/L, BUN 37 mg/dL, creatinine 1.27 mg/dL, glucose 931 mg/dL, eGFR 46 mL/min.
Liver chemistry: Total bilirubin 0.2 mg/dL, AST 23 U/L, ALT 54 U/L, ALP 138 U/L, total protein 7.5 g/dL, albumin 4.5 g/dL. Calcium 8.7 mg/dL, phosphate 1.4 mg/dL, magnesium 2.1 mg/dL. VBG: pH 6.92. Repeated ABG 2 h later: pH 7.21, pCO2 16 mmHg, pO2 129 mmHg, HCO3− 6.4 mmol/L, SaO2 98% on 2 L/min oxygen by nasal cannula. Beta-hydroxybutyrate 28 mmol/L, lactic acid 4.0 mmol/L. Urinalysis showed urine ketones 80 mg/dL, leukocyte esterase negative, urine culture no growth. HbA1c 6.4%. Lipid profile: triglycerides 89 mg/dL, total cholesterol 144 mg/dL, LDL 91 mg/dL, HDL 35 mg/dL. TSH 3.12 mIU/mL, free T4 1.26 ng/dL. Troponin I < 0.01 ng/mL.
Ultrasonography of the abdomen revealed mild hepatic steatosis, incidental mild to moderate right-sided hydronephrosis, status post cholecystectomy. ECG on admission: sinus rhythm, HR 126 bpm, peaked T waves at lead V2–V6 consistent with hyperkalemia, no ischemic changes.
All procedures performed in this study were in compliance with the ethical standards of the institutional and/or national research committee and with the 1964 Declaration of Helsinki and its later amendments or comparable ethical standards. Informed consent was obtained from the individual participant for being included in the study.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.68, 'm']}",59.62607,56.64477,62.60737,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.68 m, which is 1.68 m * 39.3701 in/m = 66.14177 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.14177 (in inches) - 60) = 59.62607 kg.
Hence, the patient's IBW is 59.62607 kg."
3712,10,Ideal Body Weight,physical,decimal,pmc-8179055-1,Extracted,"A 78-year-old woman, who had a history of hypertension and diabetes mellitus and no history of surgery, was admitted to the ED of Erzurum Regional Education and Research Hospital, Erzurum, Turkey, in December 2020 with acute cough and shortness of breath for three days. The patient had no history of anticoagulant therapy use. On evaluation, the patient’s vital findings were as follows: blood pressure, 103/52 mmHg; pulse rate, 108 beats/ min (bpm); oxygen saturation on room air, 88%‒90%; respiratory rate, 24 times/min; and fever, 37.0°C. Auscultation of the lungs revealed only wheezing. An abdominal physical examination was benign. The patient's weight was 107 kg, and her height was 160 mm (BMI of the patient = 41.79).
The patient’s levels of C-reactive protein (CRP) (63 mg/L), lactate dehydrogenase (320 U/L), and D-dimer (995 ng/mL) were elevated. The results of other laboratory tests were unremarkable. The patient’s hemoglobin level was 13.4 g/dL. On CT scan, the pulmonary findings were consistent with COVID-19 pneumonia (Figure ). Therefore, the patient was admitted for follow-up, and treatment was begun using favipiravir 200 mg tablets (four tablets per day), moxifloxacin 400 mg tablets (one tablet per day), and piperacillin-tazobactam 4.5 g IV (four vials per day). In addition, enoxaparin sodium (40 mg / 0.4 mL subcutaneously every 12 h) was started as prophylactic dose based on BMI of the patient.
On the ninth day of the patient’s follow-up, her hemoglobin levels decreased to 7.3 g/dL. At that point, her blood pressure was 84/52 mmHg, and her heart rate was 120 bpm. An abdominal exam revealed a mass in the left lower quadrant. CT scan of the abdomen and pelvis showed a left inferior RSH approximately 9 cm wide (Figure ).
Anticoagulation therapy was stopped. Vital signs monitoring and fluid replacement were begun. The goal was to maintain hemoglobin value above 7 g/dL. As the hemoglobin value of the patient fell below 7 g/dL twice, four units of erythrocyte suspension (ES) was administered to the patient. Abdominal examination was performed daily. One week after the diagnosis of RSH, a CT of the abdomen and pelvis was performed. The scan showed no significant increase in the size of the hematoma. On the 18th day after admission, the patient was discharged because her hemoglobin value, which was 10.2 g/dL at that point, had not decreased, her vital signs were stable, and her treatment for COVID-19 was completed. From the moment of diagnosis to discharge, the patient required no interventional or surgical procedures.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'm']}",14395.6968,13675.91196,15115.48164,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 m, which is 160.0 m * 39.3701 in/m = 6299.216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (6299.216 (in inches) - 60) = 14395.6968 kg.
Hence, the patient's IBW is 14395.6968 kg."
3713,10,Ideal Body Weight,physical,decimal,usmle-10701,Extracted,"A 46-year-old male presents in consultation for weight loss surgery. He is 6’0” and weighs 300 pounds. He has tried multiple dietary and exercise regimens but has been unsuccessful in losing weight. The surgeon suggests a sleeve gastrectomy, a procedure that reduces the size of the stomach removing a large portion of the stomach along the middle part of the greater curvature. The surgeon anticipates having to ligate a portion of the arterial supply to this part of the stomach in order to complete the resection.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [6.0, 'ft']}",77.6,73.72,81.48,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 6.0 ft, which is 6.0 ft * 12 in/ft = 72.0 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (72.0 (in inches) - 60) = 77.6 kg.
Hence, the patient's IBW is 77.6 kg."
3714,10,Ideal Body Weight,physical,decimal,pmc-6937415-1,Extracted,"We report a 15-year-old girl who presented with recurrent headaches, arterial hypertension, and a systolic murmur.
Echocardiographic examination in a medical practice had revealed a potential coarctation of the aorta.
The patient had no history of serious illness.
There were no medically relevant aspects from the patient’s personal history. Other than arterial hypertension and coronary artery disease in the patient’s grandfather, there was no known cardiac disease within the family.
The patient presented in good general condition. Body weight was 61 kg and height were 172 cm. Her blood pressure in the right arm with 144/86 [MAP (mean arterial pressure) 110 mmHg] was significantly higher than that in the left arm [118/82 (MAP 96) mmHg] and of the right leg [118/72 (MAP 91) mmHg]. We consistently felt an unequal pulse between the right and left radial arteries (right stronger than left). A 2/6 systolic murmur was identified ventrally in the second and third left intercostal space, and, less prominently, dorsally between the shoulder blades. All other aspects of the physical examination were normal.
No laboratory examinations were done in the diagnostic work-up.
Echocardiography and cardiac MRI revealed a hypoplastic native aortic arch with a bi-carotid trunk and a segment just proximal of the left subclavian artery which was stenosed by 75% ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [172.0, 'cm']}",63.24811,60.0857,66.41052,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 172.0 cm, which is 172.0 cm * 0.393701 in/cm = 67.71657 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (67.71657 (in inches) - 60) = 63.24811 kg.
Hence, the patient's IBW is 63.24811 kg."
3715,10,Ideal Body Weight,physical,decimal,pmc-4851159-1,Extracted,"A 27 years old woman was referred to our hospital, with recurrent episodes of profuse
vomiting and upper abdominal pain associated with loss of appetite and dyspepsia since
two years. She had no other comorbidities. Had been treated at another hospital with
proton pump inhibitors, analgesics and intravenous fluids. She had a history of chronic
anorexia and progressive loss of weight along with recurrent episodes of vomiting and
upper abdominal pain. Clinical examination revealed dehydration, asthenicity (body mass
index 19,5 kg/m2, weight: 50 kg, length:160 cm), abdominal distension,
epigastric tenderness. Laboratory investigations showed a total white cell count of 9
500 mm and hypokalaemia (serum potassium: 3
mEq/l). Plain radiograph of the abdomen revealed gastric dilation. Ultrasonography was
unremarkable. Upper gastrointestinal endoscopy showed dilated stomach and duodenum.
Contrast-enhanced computerized tomography scan revealed grossly
distended stomach and duodenum proximal to the third part of the duodenum at the level
of the origin of superior mesenteric artery with abrupt narrowing at this level,
suggestive of Wilkie's syndrome. While, normally, the angle between the SMA and the
aorta is 22° to 60°, in this case, the aortomesenteric angle was 13,5°(). In this case, conservative management was
inefficient, so surgical treatment aiming to bypass the obstruction by an anastomosis
between the jejunum and the proximal duodenum (duodenojejunostomy) was successful.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3716,10,Ideal Body Weight,physical,decimal,pmc-2672139-1,Extracted,"A 29-yr-old woman presented with colicky lower abdominal pain. Her abdominal pain had developed 3 yr before intermittently, but it had worsened over the past 6 months. She was unable to sleep well due to her abdominal pain, which aggravated after eating meals. She also experienced episodes of abdominal distension, constipation, and urinary frequency or urgency. Other symptoms, as well as her past medical history and family history, were otherwise unremarkable.
The patient had a height of 164 cm and weight of 59.6 kg, for a body mass index of 22.2. Physical examination revealed a slightly distended abdomen, but the remainder of the examination was unremarkable. Routine blood tests, including renal function and urine analysis, were normal.
Computed tomography (CT) of the abdomen and pelvis revealed a homogenous fatty mass in the lower abdominal cavity (). The entire small bowel loop was displaced upward by the mass, and one segment of the ileal loop was slightly straightened by entrapment of the bowel. Small bowel series revealed ileal loop entrapped in fatty tissue and associated ileal diverticula ().
Laparoscopic surgical resection was recommended because of her symptoms. The laparoscopic surgery showed an encapsulated, yellowish mass originating from the ileal mesentery in the lower abdominal cavity. The mass extended to the antimesenteric border of the small bowel and was free of any adhesions or signs of necrosis. Some segment of the ileum appeared to be ""stretched"" over the fatty mesenteric mass with edema, however, its luminal patency was preserved in spite of luminal narrowing by compression. Lymphadenopathy or fluid collection was not observed. Surgical removal of the fatty mass and the affected ileal loop was performed without difficulty under a laparoscopic magnified view. The resected mesenteric mass was a soft, yellow mass and 19×10×5.1 cm in size (). Microscopically, the mass was characterized by homogenous mature adipose tissue without cellular atypia, which was compatible with the diagnosis of a mesenteric lipoma (). Any evidence of necrosis or malignancy was not observed.
She had no postoperative complications and was free of any signs of disease recurrence 15 months after the operation.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [164.0, 'cm']}",56.00401,53.20381,58.80421,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 164.0 cm, which is 164.0 cm * 0.393701 in/cm = 64.56696 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.56696 (in inches) - 60) = 56.00401 kg.
Hence, the patient's IBW is 56.00401 kg."
3717,10,Ideal Body Weight,physical,decimal,pmc-6347737-1,Extracted,"A 47-year-old man (height of 175.8 cm and weight of 74.8 kg) complained of a tingling sensation in his leg. He had a history of hypertension and asthma in the previous two years, and history of sinus surgery for sinusitis in the previous one year. Ten days before admission, the patient had a tingling sensation in his left leg, from the posterior thigh to the foot. His spinal radiography findings were unspecified. Therefore, the patient was suspected as having a disc herniation, and observation was decided while continuing the medical treatment. Four days before admission, the patient had a tingling sensation that progressed in both legs. The symptoms did not improve, and motor weakness progressed below the ankle. In the physical examination at admission, motor power was grade 5 in the hip flexor and knee extensor in both lower extremities. However, it was grade 0 in the ankle dorsiflexor, and first toe extensor and flexor, and grades 4 and 0 in the ankle plantar flexor on the right and left sides, respectively. Sensory loss was not found in the L1 - L4 dermatomes, yet was 50% on the right side and 0% on the left side for the L5 and S1 dermatomes. He also had a heating sensation in his left foot and no knee-jerk reaction. He showed a weight loss of 6 kg during the last month, and the signal intensity of the bone marrow on L-spine magnetic resonance imaging (MRI) was diffusively reduced to be less than or equal to the disc. These findings indicated a hematologic disease and the possibility of malignancy with little preserved fat marrow. Abdominal and pelvic computed tomography (CT) revealed diffuse wall thickening of the gallbladder with some irregularity. However, the bone marrow biopsy slides showed a generally hyper-cellular (50% to 60%) marrow for the patient’s age, with small hypo-cellular regions (0% to 20%). On aspirate smears, the eosinophil counts were markedly increased, with expanded eosinophil myelocytes and metamyelocytes. The results of the pulmonary function tests showed an obstructive pattern, such as a forced vital capacity of 54%, a forced expiratory volume in one second of 46%, and forced expiratory flow between 25% and 70% of 33% of the predicted values. The findings from a nerve conduction study suggested multiple mono-neuropathies. In addition, his laboratory findings showed peripheral eosinophilia and positivity for myeloperoxidase anti-neutrophil cytoplasmic autoantibody (MPO-ANCA; ). Therefore, CSS was strongly suspected, and steroid and cyclophosphamide therapies were started after nerve biopsy under spinal anesthesia. At that time, the symptoms were progressing to the left wrist drop and both legs. However, nerve biopsy results were consistent with demyelinating peripheral neuropathy. The patient underwent cholecystectomy under general anesthesia to exclude gallbladder cancer, suspected on the basis of CT findings, and pathological confirmation was possible with a gallbladder specimen ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.8, 'cm']}",71.18907,67.62962,74.74852,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.8 cm, which is 175.8 cm * 0.393701 in/cm = 69.21264 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.21264 (in inches) - 60) = 71.18907 kg.
Hence, the patient's IBW is 71.18907 kg."
3718,10,Ideal Body Weight,physical,decimal,pmc-5337861-1,Extracted,"Our patient is a 58-year-old Caucasian man weighing 92.9 kg, 175 cm tall, with a history of type 1 DM who presented for repair of a hip labral tear. His past medical history was significant for obstructive sleep apnea (OSA), gastroesophageal reflux disease, bicuspid aortic valve, bipolar disorder, obsessive-compulsive disorder, and cataracts. His only prior anesthetic exposure was for cataract surgery and he had no complications. However, the patient's daughter, who also had DM, experienced severe respiratory depression following general anesthesia, requiring intensive care unit (ICU) admission postoperatively. Primary considerations in relation to anesthesia include the disease's association with cardiomyopathy and cardiac conduction abnormalities, sensitivity to respiratory depression and ventilatory weakness, prolonged gastric emptying, and myoclonus triggered by stimuli such as hypothermia and specific medications.
Following the application of standard ASA monitors, a combined spinal and epidural anesthetic technique was performed successfully. Fifteen mg of isobaric bupivacaine was injected into the subarachnoid space at the L4-L5 interspace and an epidural catheter was inserted immediately. The spinal level was tested and found to be at a T10 dermatomal level. External pacer/defibrillator pads were applied and an arterial line was used for continuous blood pressure monitoring and to facilitate arterial blood gas measurements in the event of pulmonary compromise. A thermometer was placed in the patient's axilla for continuous monitoring. The operating room's ambient temperature was increased, a forced-air warming blanket was applied to the patient, and a fluid warmer was connected to his intravenous line. Intraoperatively, the patient received small (0.5 to 1 mg) boluses of midazolam titrated for a Richmond Agitation-Sedation Scale (RASS) of −3. For the 3 hour and 43 minute procedure, the patient received a total of 10 mg of midazolam and 50 mcg of fentanyl. Forty-five minutes into the surgical procedure the surgeon requested further relaxation of the patient's hip muscles and the epidural catheter was subsequently bolused with 5 mL of 2% lidocaine. Two hours into the procedure, another 5 mL of 2% lidocaine was bolused into the epidural. No complications were noted in the intraoperative period. The patient was transported to the postanesthesia care unit (PACU) with continuous SpO2, ECG, and blood pressure monitoring. A written consent was obtained from the patient for this case report.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3719,10,Ideal Body Weight,physical,decimal,pmc-8690463-1,Extracted,"Our patient was a 70-year-old Asian woman who visited the hospital with a complaint of epigastric pain. She had no notable family history and no history of smoking or drinking. She underwent upper endoscopy, and was diagnosed with gastric cancer; therefore, she was referred for surgery.
The patient was 153 cm tall, weighed 44 kg, and had a body mass index (BMI) of 18.8 kg/m2. Her abdomen was flat and soft, and Virchow’s lymph nodes were not palpable. The patient’s hemoglobin concentration was 6.1 g/dL, blood urea nitrogen concentration was 25.8 mg/dL, carcinoembryonic antigen (CEA) was 0.9 ng/mL, and carbohydrate antigen (CA)19-9 was 9.6 U/mL. Upper endoscopy showed a type 3 tumor on the lesser curvature side of the gastric angle (Fig. ), and biopsy revealed a group 5, well-differentiated adenocarcinoma. Computed tomography (CT) of the chest and abdomen showed wall thickening with contrast enhancement on the lesser curvature side of the angular incisure, part of which was in contact with the pancreas. Gastric cancer may have invaded the pancreas because the fat at the border with the pancreas had disappeared. In addition, the lymph nodes on the lesser curvature and the liver hilum were slightly swollen (Fig a and b). A positron emission tomography (PET) scan showed accumulation only in tumors (SUV max 8.0), but not in lymph nodes or other organs. Based on these findings, the preoperative pathological diagnosis was T4b N1 M0 stage IIIb, and surgery was indicated.
Intraoperative findings showed no ascites or peritoneal dissemination. However, because gastric cancer had invaded the pancreas, total gastrectomy, splenectomy, and resection of the pancreatic tail were performed. The postoperative course was uneventful, and the patient was discharged 18 days after surgery.
Postoperative pathological examination revealed small disseminated nodules in the resected specimen. The final diagnosis was T4bN3aM1, stage IV, according to the 8th Union for International Cancer Control (UICC) TNM classification []. Immunohistochemically, the tumor was negative for human epidermal growth factor receptor 2 (HER2). Therefore, we started combination therapy with S-1 and cisplatin as first-line chemotherapy. S-1 was administered orally at a dose of 40 mg twice daily for the first 3 weeks in a 5-week cycle, with an intravenous dose of 60 mg/m2 cisplatin on the seventh day of each cycle. The therapeutic effect was judged according to the RECIST guidelines, version 1.1; adverse events were recorded in accordance with CTCAE criteria, version 4.0 [, ]; and no recurrence was observed during the first 6 months of treatment. However, owing to a grade 3 loss of appetite, the patient experienced marked weight loss to 37 kg; therefore, cisplatin administration was discontinued after seven courses, and therapy was changed to S-1 monotherapy. After the change, her condition stabilized, but a CT scan 3 years after surgery showed a 20 mm nodule on the stump of the resected pancreas (Fig. a and b). The CEA concentration was 3.6 ng/mL and the CA19-9 concentration was 10.8 U/mL, which were within the normal ranges; however, positron emission tomography-CT (PET-CT) showed contrast accumulation at the pancreatic stump (Fig. ). Therefore, we diagnosed recurrence owing to dissemination. Because it was a treatment for local recurrence, radiation therapy was administered for the nodule, and chemotherapy with docetaxel was started at the patient’s request. She received docetaxel 60 mg/m2 intravenously on the first day of the 21-day cycle. Although side effects such as malaise were observed, the nodule tended to shrink with continued administration. However, after 14 courses of systemic treatment (4 years after surgery), abdominal CT showed new peritoneal dissemination and lymphadenopathy. The largest disseminated nodule was a 13 mm contrast-enhanced nodule around the superior mesenteric artery that increased in size over time (Fig. a and b). The CEA concentration increased to 11.4 ng/mL and the CA19-9 concentration increased to 10.8 U/mL. PET-CT showed accumulation in the pancreatic stump and in the periaortic lymph nodes. Accumulation was also seen in part of the abdominal wall (Fig. ). With dissemination, the patient’s symptoms progressed, and she was diagnosed with lymph node recurrence and peritoneal dissemination; therapy was changed to intravenous nivolumab 3 mg/kg every 2 weeks. Owing to a subsequent change in the dosage standard, the dose was increased to 240 mg. After starting immunotherapy, CT scans were done every 3–4 months. Nodules or lymph node swelling were not identified on CT 54 courses after beginning nivolumab (Fig. ). Currently, approximately 3.5 years have passed since beginning nivolumab, and the CEA concentration has normalized to 3.7 ng/mL and CA19-9 to 11.1 U/mL. The most recent CT showed no progression of symptoms; therefore, a complete clinical response was achieved. In addition, the patient developed no side effects during the course of treatment, including immune-responsive adverse events. As a result, her body weight improved significantly to 49 kg, she returned to work, which she could not do previously owing to the side effects of treatment, and her quality of life (QOL) improved. The patient is currently receiving nivolumab, and there is no evidence of recurrence approximately 3 years after starting this therapy (7 years after surgery) (Fig. ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.0, 'cm']}",46.04337,43.7412,48.34554,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.0 cm, which is 153.0 cm * 0.393701 in/cm = 60.23625 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.23625 (in inches) - 60) = 46.04337 kg.
Hence, the patient's IBW is 46.04337 kg."
3720,10,Ideal Body Weight,physical,decimal,pmc-4251529-1,Extracted,"A 47-year-old Hispanic male presented with lower back pain, and lethargy. The symptoms started approximately 1 week before presentation. The patient denied having any upper respiratory symptoms, rash, or joint pain. The patient also denied having any gross hematuria, foamy urine, or any other urinary symptoms. The patient’s history included GPA, diagnosed by a renal biopsy 2 years ago, diabetes mellitus, hypertension, hyperlipidemia, and diverticulosis requiring colostomy.
His medication at the time included simvastatin, lisinopril, azathioprine, and insulin. His azathioprine was reduced from 200 mg/day to 100 mg/day 6 months before presentation. He had recently lost his job and insurance, and denied smoking, alcohol use, or any substance abuse. On physical examination, he was afebrile. His blood pressure was 99/51 mmHg, pulse was 74 beats/minute, and respiration rate 18 breaths/minute, height was 165 cm, and weight was 97 kg. He was in no apparent distress. The patient’s lungs were clear, heart sounds were regular without any murmur, rub, or gallop, the abdomen was soft, and no edema or skin rash was present.
Laboratory data revealed the patient’s blood urea nitrogen (BUN) to be 73 mg/dL and serum creatinine (Scr) 5.2 mg/dL with otherwise normal electrolytes, hemoglobin 12.7 mg/dL, platelets 257,000/mm3, albumin 3.5 mg/dL, and normal liver enzymes. Two years prior to current presentation his Scr level was 1.5 mg/dl. Urinalysis showed large protein, large blood, many dysmorphic red blood cells and red blood cell casts. The urine protein to creatinine ratio was 2.03 mg/mg. Renal sonogram revealed kidney sizes of 11.3 cm and 10.6 cm on right and left kidneys, respectively, without any evidence of obstruction and an unremarkable bladder with no significant postvoid residual volume.
The patient was started on high dose pulse methylprednisolone intravenously (1 g/day for 3 days), and his azathioprine dose was increased to 200 mg/day. His serology showed normal complement titers, negative hepatitis profile, and mildly elevated rheumatoid factor at 24 IU/ml (normal <14). ANCA serology showed proteinase-3 (PR3) antibody (anti-PR3, cytoplasmic c-ANCA) reactive at low levels −4.1 (<1.0 reported as negative) and negative myeloperoxidase (MPO) antibody (anti-MPO, perinuclear p-ANCA). Anti-GBM titers were negative.
Based on clinical presentation and the patient’s past medical history, it was presumed that the most likely cause of worsening renal function was a relapse of GPA. However, very low levels of anti-PR3 antibodies, and the questionable duration of the progression of the patient’s renal disease prompted the nephrology team to proceed with a repeat kidney biopsy.
The kidney biopsy showed focal segmental necrotizing and crescentic glomerulonephritis, with weak linear staining of IgG, which was not seen on previous biopsy. Out of 19 glomeruli examined, nine showed complete or near complete global sclerosis. Crescents were seen in eleven of 19 glomeruli. The other biopsy findings included moderate tubular atrophy, moderate interstitial fibrosis with inflammation, and moderate arteriosclerosis ( and ). The pathologist reported findings suggestive of moderate disease activity and moderate chronicity. Although the biopsy indicated some evidence of chronic disease, there was still significant active disease that should be treated. Provided that the disease process responded to the treatment, there was a possibility of at least partial recovery of renal function.
The biopsy findings presented a treatment dilemma. The patient had a history of GPA and initially presented with PICGN and crescentic glomerulonephritis with negative IF findings 2 years previously (). At that time, he was treated with pulse methylprednisolone followed by 6 months of oral prednisone and cyclophosphamide, which successfully induced remission. His renal function had improved; Scr decreased from 3.1 mg/dL to 1.5 mg/dL and proteinuria decreased from 2.3 g/day to <500 mg/day. He was then switched to maintenance immunosuppression with azathioprine. At the time of his initial presentation, his anti-PR3 level was >100 U/ml. After initial induction therapy, anti-PR3 level was reduced below assay limits and remained negative during follow up.
This patient was treated with pulse dose of intravenous methyl prednisolone 1 g/day for 3 days followed by maintenance oral prednisone at 1 mg/kg/day. He was also treated with monthly intravenous cyclophosphamide (15 mg/kg). Three months later, the patient had partially responded with proteinuria decreasing to 800 mg/day and Cr stabilizing to 2.8 mg/dL.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3721,10,Ideal Body Weight,physical,decimal,pmc-7788116-1,Extracted,"A 36-year-old Japanese female was referred to our hospital with morbid obesity and T1DM. She was diagnosed with T1DM at the age of 6 years, thereafter, treatment with multiple daily insulin was started. By the age of 20 years, she had a body weight of 70 kg, increasing to > 100 kg at the age of 34 years. Her required daily dose of insulin increased as a function of her body weight. At her initial assessment, she required 45 units of insulin aspart and 30 units of insulin glargine per day. Although a temporary weight loss and reduction in daily insulin dose was achieved with an in-hospital treatment, her weight rebounded shortly after discharge and the patient experienced difficulty in controlling her body weight. The patient expressed her intention for surgical treatment for weight loss, and she was referred to our department.
At the time of admission, her height was 159 cm and her weight 106.7 kg, BMI of 42.2 kg/m2. Blood analyses indicated HbA1c of 9.0%, and blood C-peptide levels were undetectable (< 0.01 ng/mL), suggesting her insulin secretion capacity was completely depleted. With medication, her blood lipid levels were within normal range. On computed tomography (CT) examination, the calculated visceral fat area was 162.6 cm2, with a subcutaneous fat area of 527.9 cm2, measured at level of the umbilicus (Fig. a, b). Upper gastrointestinal endoscopy revealed no abnormalities in the esophagus, stomach, or duodenum.
To prevent complications associated with rapid postoperative blood glucose improvement, she was admitted to our hospital 2 weeks before operation for strict glycemic control, dietary restrictions, and exercise therapy. As a result, preoperative HbA1c was reduced to 7.8% and body weight was reduced to 101.1 kg.
We performed a laparoscopic sleeve gastrectomy (LSG) [], using five ports,, as shown in Fig. a. The blood vessel along the wall of the greater curvature of the stomach was first dissected. We then inserted a 36 Fr (12 mm) bougie into the stomach and resected the greater curvature of the stomach, from a point, on the oral side, 4 cm from the pylorus to the His angle, using a linear stapler. The staple line was reinforced with continuous seromuscular sutures using non-absorbable stitches (Fig. b, c).
After the operation, a unit of insulin aspart was mixed with 5 g of glucose contained in the infusion solution and sliding scale insulin was added as needed. From postoperative day 2, insulin glargine was administered. Sliding scale insulin was added depending on fasting blood sugar level and oral intake and her daily insulin dose was determined accordingly.
There were no postoperative complications, including severe hypoglycemic episodes. One year after the procedure, her body weight had decreased to 81.0 kg, with a BMI of 32.2 kg/m2, with this decrease being mainly due to a decrease in the body fat mass. Her HbA1c level improved to 7.7%, and her daily required insulin dose had been reduced to 24 units (10 units of insulin aspart and 14 units of insulin glargine per day: Fig. a–d). On abdominal CT images, the visceral fat area, measured at level of the umbilicus, was 44.8 cm2, with a subcutaneous fat area of 408.8 cm2 (Fig. c, d). Therefore, there was a marked decrease in both visceral and subcutaneous fat.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [159.0, 'cm']}",51.47646,48.90264,54.05028,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 159.0 cm, which is 159.0 cm * 0.393701 in/cm = 62.59846 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.59846 (in inches) - 60) = 51.47646 kg.
Hence, the patient's IBW is 51.47646 kg."
3722,10,Ideal Body Weight,physical,decimal,usmle-1002,Extracted,"A 42-year-old woman comes to the physician for a routine health maintenance examination. She has generalized fatigue and has had difficulties doing her household duties for the past 3 months. She has eczema and gastroesophageal reflux disease. She has a history of using intravenous methamphetamine in her youth but has not used illicit drugs in 23 years. Her medications include topical clobetasol and pantoprazole. She is 160 cm (5 ft 3 in) tall and weighs 105 kg (231 lb); BMI is 42 kg/m2. Her temperature is 37°C (98.6°F), pulse is 95/min, and blood pressure is 145/90 mm Hg. The lungs are clear to auscultation. Cardiac examination shows no abnormalities. Pelvic examination shows a normal vagina and cervix. Laboratory studies show:
Hemoglobin 13.1 g/dL
Leukocyte count 7,800/mm3
Platelet count 312,000/mm3
Serum
Na+ 141 mEq/L
K+ 4.6 mEq/L
Cl- 98 mEq/L
Urea nitrogen 12 mg/dL
Fasting glucose 110 mg/dL
Creatinine 0.8 mg/dL
Total cholesterol 269 mg/dL
HDL-cholesterol 55 mg/dL
LDL-cholesterol 160 mg/dL
Triglycerides 320 mg/dL
Urinalysis is within normal limits. An x-ray of the chest shows no abnormalities. She has not lost any weight over the past year despite following supervised weight loss programs, including various diets and exercise regimens.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3723,10,Ideal Body Weight,physical,decimal,pmc-6993917-1,Extracted,"A 77-year-old white Spanish woman referred to our outpatient clinic with hypertension and albuminuria with a normal glomerular filtration rate (GFR). In addition, she had a history of PXE since 1997, progressive visual deficiency, chronic left lower extremity oedema and an ischaemic stroke 4 years previously. She had primary hyperparathyroidism as a recent diagnostic. None of the patient’s first-degree relatives had a history of PXE.
The physical examination showed a weight of 61 kg; a height of 1.71 m; BMI of 20.8 kg/m2; blood pressure at 160/90 mmHg. Multiple, discrete, symmetrical, small yellow plaques as leathery skin were present bilaterally in the axillae, inguinal region and the neck. Angioid streaks were seen in the fundus. Asymmetric left lower extremity oedema was observed.
Laboratory findings were significant for an elevated parathyroid hormone level (170 pg/ml, reference range: 10–65 pg/ml); low serum phosphorus (2.3 mg/dl, reference range: 2.7–4.5 mg/dl); hypercalcaemia (11.6 mg/dl, reference range: 8.5–10.5 mg/dl) with a calcium-phosphorous product of 26.6 mg/dl; calciuria 376 mg/24h and albuminuria 132 mg/g. The remainder of the blood test results were normal (Hb 13.7 g/dl; Hto 43%; fasting glucose 99 mg/dl; uric acid 4.0 mg/dl; total cholesterol 200 mg/dl; TG 100 mg/dl; creatinine 0.6 mg/dl; eGFR <90 ml/min; K 4.7 meq/l; Na 131 meq/l; Cl 107 meq/l; calcitriol 46 pg/ml.
Imaging tests showed kidney ultrasound imaging with a slight increase in the echogenicity of the renal parenchyma () and normal BMD ().
The patient was taking: losartan 50 mg BID, acetylsalicylic acid 100 mg OD, simvastatin 20 mg OD, omeprazole 20 mg OD, pregabalin 25 mg OD.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.71, 'm']}",62.3426,59.22547,65.45973,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.71 m, which is 1.71 m * 39.3701 in/m = 67.32287 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (67.32287 (in inches) - 60) = 62.3426 kg.
Hence, the patient's IBW is 62.3426 kg."
3724,10,Ideal Body Weight,physical,decimal,pmc-7546790-1,Extracted,"A 27-year-old man was admitted to the cardiology department with symptoms of biventricular heart failure (NYHA class III), excessive sweating, and pain in the postoperative wound area at the site of thrombectomy 6 months prior to hospitalization.
His family history was unremarkable. Parents were not consanguineous. The father died at the age of 35, in a traumatic accident, and to the best of the patient’s knowledge, had no cardiac complaints. At the time of the first hospitalization, the mother was 56 years old and had no complaints. The proband had a sister who died at 15 days of age due to a congenital heart disease (transposition of the great arteries). No other relative was diagnosed with cardiomyopathy of other cardiac disease before 50 years of age. External risk factors: smoking average of three cigarettes/day for 7 years. No alcohol abuse or other toxic factors were mentioned.
Personal medical history with main milestones and medications taken (when possible) was reconstructed from the available medical records ().
The patient had an average height (174 cm) and weight of 79 kg for his age, BMI 26.1 kg/m2, and normal arterial blood pressure (120/80 mmHg). Edema of the leg and slight serous discharge from the wound in the right groin area were found on the initial physical examination.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [174.0, 'cm']}",69.55913,66.08117,73.03709,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 174.0 cm, which is 174.0 cm * 0.393701 in/cm = 68.50397 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.50397 (in inches) - 60) = 69.55913 kg.
Hence, the patient's IBW is 69.55913 kg."
3725,10,Ideal Body Weight,physical,decimal,pmc-4410173-1,Extracted,"We present a case of a 30-year-old woman with JPD. Her parents, grandparents, and two siblings had no history of any bone disease. They had normal alkaline phosphatase (ALP) level and had no known clinical bone abnormalities. However, we were unable to submit them to genetic testing. When the patient was 11 years old, she had a non-traumatic fracture on the left tibia. At that time, the serum ALP activity was elevated to 414 U/L. The bowing deformities of her lower extremities were noted and the diagnosis of JPD was made. Her bone age was normal. She received calcitonin therapy for six months and according her mother she tolerated the injections without apparent side effects and seemed to have less pain in her lower limbs. After this, she had no clinical progression for nineteen years.
In May 2011, she was referred to the National Institute of Rheumatology and Physiotherapy suffering from fatigue and bone pain in her lower extremities. Physical examination showed normal vital signs, weight of 47 kg, and height of 156 cm. She had marked scoliosis of the lumbar spine and the lower limbs showed anterior bowing of both femora and tibias (). She had no difficulties in hearing and no eye or neurological problems. The study was approved by the National Institute of Rheumatology and Physiotherapy Committee of Research Ethics, and the patient gave written informed consent.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [156.0, 'cm']}",48.75993,46.32193,51.19793,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 156.0 cm, which is 156.0 cm * 0.393701 in/cm = 61.41736 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.41736 (in inches) - 60) = 48.75993 kg.
Hence, the patient's IBW is 48.75993 kg."
3726,10,Ideal Body Weight,physical,decimal,pmc-3281774-1,Extracted,"In January 2008, a 61-year-old man with a history notable for diabetes mellitus (DM), autonomic neuropathy, diffuse brain atrophy, optic nerve atrophy (OA), and profound amnesia was referred to us to establish neurologic care. The patient carried a diagnosis of multiple system atrophy- cerebellar type (MSAc), principally because of severe cerebellar and brainstem atrophy on MRI.
The patient's early history was remarkable only for childhood bedwetting and urinary urgency as a young adult. He was otherwise well during this time and was a talented athlete who completed college and practiced as an accountant. In his early 20s, he developed bladder dysfunction of unclear etiology requiring intermittent straight catheterization, as well as erectile dysfunction.
At age 33, he was diagnosed with DM, presumed to be type 1, and began treatment with insulin therapy. Although there is no biochemical data available from the time of his original diagnosis, recent testing demonstrated a random C-peptide level of 0.6 ng/mL (reference range 0.9 to 4.3 ng/mL) at a time when his blood glucose was 83 mg/dL. He takes an average of 24 units of insulin per day, and has had good glycemic control with hemoglobin A1c measurements ranging between 6.5 and 7.2% over the last several years. He has had no evidence of retinopathy, or other microvascular or macrovascular complications. He had polyuria and polydipsia at the time of his initial DM diagnosis, but these symptoms resolved once he initiated insulin therapy.
The patient began dressing in strange colors in his 30s, and color blindness was ultimately diagnosed in his 40s. At age 53, the patient presented for a routine screening ophthalmology exam and was discovered to have bilateral OA with preserved vision. Brain MRI at that time revealed severe atrophy of the cerebellar hemispheres and vermis, pons, and middle cerebellar peduncles as well as moderate cerebral atrophy; a more recent study at age 61 showed these findings as well as more severe cerebral atrophy (Figure ). Despite these radiographic findings, the patient and his wife reported no gait instability or upper extremity incoordination.
During his late 50s, the patient's neurologic status deteriorated. Formal neuropsychological evaluation revealed profound anterograde amnesia, with additional impairments in cognitive flexibility, executive function, naming, and high order visual processing skills. Attention span, mental tracking, verbal abstract reasoning, complex auditory instructions, and visual spatial functions were preserved. From a psychiatric perspective, he developed symptoms of depression, which responded to treatment with sertraline.
In parallel with the decline in his memory, the patient also developed progressive autonomic neuropathy, with gastroparesis and severe postural hypotension. The autonomic dysfunction exceeded what might be expected from his diabetes mellitus, given his good glycemic control and the absence of other diabetic complications. His bladder dysfunction worsened and he required suprapubic catheter placement at the age of 61. Due to his multiple functional deficits, the patient became unable to work and is now completely reliant upon his wife for care.
Regarding his family history, the patient was born to Ashkenazi Jewish parents and there was no parental consanguinity. His mother died from melanoma, and his father died from multiple strokes and a myocardial infarction. He has two adult daughters, one of whom has attention deficit hyperactivity disorder (ADHD) and Tourette syndrome, while the other suffers from chronic urinary tract infections. His maternal grandmother had type 2 DM, and a maternal first cousin had type 1 DM. No other close relatives have suffered from endocrine, psychiatric, or neurologic disease.
On physical examination, he appeared generally medically well. He weighed 79 kilograms and was 178 cm tall, yielding a body mass index of 25. Postural hypotension was evident with systolic blood pressure falling from 150 to 95 after one minute of standing, though asymptomatic. Funduscopic examination revealed optic atrophy bilaterally with no sign of diabetic retinopathy. Visual acuity was 20/40 in each eye. Pupil responses to light and accommodation were normal. Eye movements were normal with the exception of saccadic intrusion into horizontal smooth pursuit. Clinical examination revealed high tone hearing loss bilaterally. Audiometry demonstrated moderate sensorineural hearing loss in the high frequencies on the left, and mild sensorineural hearing loss in the mid-frequencies on the right sloping to a severe loss in the high frequencies (Figure ). Word recognition was excellent in both ears; 98% on the right and 96% on the left. Muscle tone in the extremities was normal, bulk was intact, and strength was full. There was no evidence of dysmetria with finger-to-nose and heel-to-shin testing, and gait was slow but stable. His affect was flat and he was passive throughout the interview, speaking only when spoken to. He was not oriented to time or place. He could repeat four words, but could not learn them despite multiple attempts. He was unable to provide information concerning major current political or national news. He could, however, recall sizable fragments of remote memory from his college years.
The absence of the cerebellar motor syndrome and the presence of a profound amnestic syndrome on examination called the patient's diagnosis of MSAc into question [], and we undertook re-evaluation of his case to explore alternate diagnoses. His laboratory work-up revealed an undetectable thiamine level, a surprising finding given his normal diet and the absence of alcohol abuse. We ascribed his amnestic disorder to presumed long-standing thiamine deficiency, but repletion produced minimal clinical impact. The involvement of multiple systems suggested the possibility of a mitochondrial disorder. Genetic testing for OPA1, MELAS, MERFF, LHON and NARP were negative, however analysis of mitochondrial DNA (mtDNA) from a muscle biopsy sample by both Southern blotting and PCR analysis revealed multiple heteroplasmic deletions. Biochemical testing revealed a minor defect in complex I of the electron transport chain. COX and SDH staining of the muscle biopsy specimen were unremarkable, and the mitochondria appeared grossly normal on electron microscopic examination. Occasional central vacuoles and tubular aggregates were seen in the myocytes, which were felt to be consistent with a mild non-specific myopathy.
Given the diagnostic uncertainty and concern for a mitochondrial disorder, the patient was enrolled in the mitochondrial disease registry at Massachusetts General Hospital. As part of this program, a sample of the patient's DNA from whole blood underwent targeted exome (""MitoExome"") sequencing. Mitochondrial DNA and the exons of 1,600 nuclear genes either encoding mitochondrial proteins or implicated in Mendelian disorders with multi-system phenotypes were targeted using hybrid selection []. Amplified targets were sequenced on the Illumina GAIIx platform. Rare, protein-modifying variants found to be homozygous or potentially compound heterozygous were prioritized (Figure ), revealing an X-linked functional polymorphism c.937G > T (p.D313Y) in GLA that is not considered pathogenic [] and a homozygous c.1672C > T (p.R558C) missense mutation in exon 8 of WFS1 that has previously been reported in a patient with Wolfram syndrome []. No heteroplasmic mtDNA deletions were detected in whole blood. The patient's WFS1 mutation was verified through Sanger sequencing in a CLIA-certified laboratory, though not without complications; the initial report came back negative and only after requested follow-up was the homozygous mutation detected, thereby confirming the diagnosis of Wolfram syndrome.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [178.0, 'cm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3727,10,Ideal Body Weight,physical,decimal,pmc-7726678-2,Extracted,"A 31-year-old man with acute on chronic liver failure secondary to alcohol was emergently admitted to our hospital for evaluation as a candidate for LDLT. On admission, his model for end-stage liver disease score was 22, and his mother, aged 52 years, was the living donor candidate. Her height and body weight were 156 cm and 51 kg, respectively, and the recipient's height and body weight were 157 cm and 52 kg, respectively. Multidetector row CT was used for preoperative dynamic CT. Figure shows a simulation of the donor hepatectomy, which was performed using the SYNAPSE VINCENT three-dimensional CT software (Fujifilm). The predicted right- and left-lobe volume was 635 and 379 mL, respectively. The right-lobe graft was sufficiently large for the recipient, with a graft–recipient weight ratio of 1.22%, while the left-lobe graft was small, with a ratio of 0.72%. Three-dimensional CT angiography revealed that the anterior and posterior arteries originated separately from the proper hepatic artery (Figure ). It was impossible to procure the right-lobe graft with single right hepatic artery because the anterior and posterior hepatic arteries encircled the common hepatic duct. Moreover, because the anterior artery travelled a deep roundabout route toward the infundibulum of the gall bladder and there was a severe adhesion around the anterior artery, we could not separate the anterior hepatic artery from the cystic artery (Figure ). Even if we could have separated the anterior artery from the cystic artery, we considered that the graft artery of the anterior artery was redundant and inappropriate for the reconstruction. Therefore, we planned to divide the anterior artery and to anastomose each anterior artery stump to avoid redundancy, using the surgical microscope, during back-table angioplasty (Figure , ). Figure shows the microsurgical angioplasty of the anterior artery and the anastomosis of the recipient's left hepatic artery. It took 9 minutes for ex vivo- and 35 minutes for ex vivo hepatic artery reconstruction. Total arterial reconstruction time was 44 minutes. Flow in the reconstructed artery was 56 mL/min, and the flow shapes in the anterior and posterior artery were confirmed as good using Doppler ultrasonography.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [157.0, 'cm']}",54.16544,51.45717,56.87371,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 157.0 cm, which is 157.0 cm * 0.393701 in/cm = 61.81106 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (61.81106 (in inches) - 60) = 54.16544 kg.
Hence, the patient's IBW is 54.16544 kg."
3728,10,Ideal Body Weight,physical,decimal,pmc-3985564-2,Extracted,"Patient B: 73-year-old male, 94 kg, 183 cm (BMI = 28 kg/m2) underwent knee replacement surgery under regional anesthesia. Past medical history was negative for OSA, or any other chronic respiratory conditions. Before the procedure, the patient received a single injection femoral nerve block and spinal anesthesia. Pre-operatively, 50 μg of fentanyl and 1 mg midazolam were administered intravenously. Intra-operatively, the patient received intravenously an additional 125 μg fentanyl, 135 mg propofol, and 1.5 mg midazolam. RVM data were collected for 558 minutes (111 minutes pre-op, 115 minutes during surgery, and 332 minutes in the PACU). Vital sign and oxygen saturation measurements were also obtained. The patient entered the PACU on 6 L/min of O2 via face mask but was switched to room air after 15 minutes. One hundred and seventy five minutes after arrival in the PACU, the patient received 2 mg of morphine intravenously.
Based on the BSA formula, his predicted MV was 8.7 L/min, consistent with his MV measured prior to surgery (8.4 ± 0.2 L/min, mean ± SEM). He had no episodes of apnea noted in the 111 minutes of RVM recording before surgery. Post-operatively, he had 88 apneic events occurring over 5.5 hours in the PACU (RDI = 16 events/hour). He had two distinct time periods where repetitive apneas occurred: one prior to the administration of 2 mg morphine and one after the morphine was administered (). During apneic breathing episodes his MV was reduced to 4.5 L/min, 54% of his pre-operative MV (). Similar to patient A, recovery breaths were not large enough to compensate for the apnea and return MV to baseline levels () (MV = 4.7 L/min, 56% of pre-op). Prior to opioid dosing, 18 apneic events occur over 1.5 hours (RDI = 12 events/hour) with an average length of 14 ± 4 sec. After administration of a single small dose of opioid, the apneic events became more frequent and longer in duration and snoring was observed. Seventy events occurred in the 1.4 hours post-opioid (RDI = 50 events/hour) with an average apnea length of 18 ± 5 seconds.
Similar to patient A, the pre-operative RVM measured MV ranged from 2.6 to 17.7 L/min with an average of 8.4 L/min () (left). Over 70% of pre-operative MV measurements were above 80% and 98% were above 40% of this patient’s predicted MV () (right). Post-operatively, the average MV was decreased from preoperative levels to7.4 L/min before the opioid was given and dropped further to an average of 6.3 L/min after the opioid was given, where MV fell to as low as 1.0 L/min during periods containing apneic episodes. Postoperatively in the 175 minutes before the opioid was given in the PACU, 51% of the time patient B’s MV was below 80% predicted and 4% of the time below 40% predicted MV. In the 157 minutes after opioid administration prior to leaving the PACU, 63% of the time his MV was below 80% predicted and 13% of the time was below 40% predicted. Thirteen percent of the time his MV was below 40% of predicted, post-opioid, compared to 4% of the time pre-opioid and less than 2% of the time pre-operatively. The cumulative distribution of MV values for patient B during pre-op, post-op pre-opioid and post-op post-opioid periods are shown in , right. Pulse oximetry data were recorded during the PACU stay, but the oxygen saturation never fell below 95% and there were no indications that apneic breathing had occurred.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [183.0, 'cm']}",77.70874,73.8233,81.59418,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 183.0 cm, which is 183.0 cm * 0.393701 in/cm = 72.04728 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (72.04728 (in inches) - 60) = 77.70874 kg.
Hence, the patient's IBW is 77.70874 kg."
3729,10,Ideal Body Weight,physical,decimal,pmc-8522227-1,Extracted,"A 27-years-old female patient presenting with recurrent coughing and hemoptysis for more than 10 years first came to our hospital in January 2019. According to the medical history information provided, the patient was previously diagnosed as pneumonia and treated symptomatically in local clinical institution. The symptoms of patient were once relieved after the treatment, but recurred frequently. The patient has no family history of primary lung malignancy and genetic disease, 155 cm in height and 42 kg in weight with a lean body shape, symmetrical thorax without deformity. The trachea of the patient deviated to the right slightly, no obvious rhonchi and moist rale as well as wheezing rale were heard. The heart rhythm was regular, the auscultation area of heart sound apparently deviated to the right thorax, and no obvious abnormality was found in abdominal physical examination.
A chest radiograph and computed tomography were performed for the patient showed a giant abnormal space-occupying lesion in the hilum of right lung. The tumor was closely related to the right pulmonary artery and bronchus (Fig. a, b). The right lung was atelectasis and some of the left lung as well as heart were obviously deviated to the right thoracic cavity. A Chest MRI showed a mass abnormal signal tumor in the region of right hilum about 10.0 × 4.5 cm in size. The T1WI was isointense, while T2WI and DWI were both hyperintense. A 3D reconstruction of the hilar structures have shown a complete anatomical disorganization of right pulmonary artery and vein (Fig. c). A neoplasm with smooth surface was observed in the right main bronchus by bronchoscopy examination. However, a biopsy was not performed concerning that existing hemoptysis might be aggravated (Fig. d). Pulmonary function showed a severe obstructive mixed ventilation dysfunction. The forced expiratory volume in 1 s (FEV1) was 1.36 L, accounting for 45% of the predicted value, Maximal voluntary ventilation (MVV) was 27.63L, accounting for 43% of the predicted value. The renal function, electrolyte, coagulation function, arterial blood gas analysis were all normal. Due to long-term persistent hemoptysis, the patient’s blood routine examination showed moderate anemia with hemoglobin 69 g/L. Biochemical examination showed moderate malnutrition, with prealbumin only 85 g/L, albumin 31 g/L. The patient’s tumor markers showed CA125 434.77 µ/ml, CEA 12.43 ng/ml, CA724 233.3 μ/ml, while CA242, CA199, AFP, SCCA, NSE were all normal. No sign of abnormality or metastasis was found in enhanced MRI of brain and bone scan. No abnormal or enlarged lymph nodes were observed in neck and supraclavicular region by ultrasound examination.
We diagnosed the patient with a large tumor in the right lung and firstly considered a special type of malignancy. Because of concerning about a high potential bleeding risk due to the rich supply of tumor and in view of personal willingness of the patient, a preoperative CT-guided percutaneous aspiration biopsy of the tumor was not performed preoperatively. After discussion with a multidisciplinary team which included thoracic surgeons, radiologists, and respiratory physicians, we decided to perform a surgical treatment for the patient.
A thoracotomy was performed under general anesthesia with left lung ventilation. The patient was in left 90°lateral position, a 20 cm long posterolateral incision at the 5th intercostal space was made overlying the right chest wall. Surgical exploration revealed a complete atelectasis of the right lung with obvious consolidation in lung tissue. The lingual segment and anterior segment of left upper lobe herniated into right upper thoracic cavity while the heart of patient also apparently deviated into right lower thoracic cavity. The lymph nodes of each group in mediastinum were checked in the operation and no significantly enlarged lymph nodes were observed. Because of the large size and invasion of the tumor, a right pneumonectomy with mediastinal lymph nodes dissection was initially considered before surgery. The right main bronchus was significantly thicker than normal and the outer diameter of the right main bronchus was 2.4 cm. The bronchial arteries around the bronchus were extremely twisted and dilated. The upper lobe of the right lung was completely consolidated into a mass, the middle and lower lobes of the right lung were atelectatic. Subsequently, we performed a right pneumonectomy for this patient. After confirming the malignacy of the tumor in the right lung and a negative surgical margin by intraoperative frozen section examination, a systematic hilar and mediastinal lymph node dissection was performed.
We checked the surgical specimens and found that the tumor originated from the right main bronchus, about 1 cm away from the tracheal carina, grew distally along the lumen of the bronchus and completely blocked the lumen (Fig. a, b). The tumor was about 8.6 × 4.5 × 4.4 cm in size (Fig. c) and pathological diagnosis showed a malignant tumor orignated from right main bronchus. The cellular morphology of tumor under optical microscope demonstrated that the tumor cells were diffusely arranged and showed large polygonal cells with eosinophilic, granular cytoplasm as well as round, eccentric nuclei. No metastasis of mediastinal lymph node was found. Immunohistochemistry of the tumor showed AE1/AE3 (+), Ki-67 (2% +),α1-ACT (+), AB-PAS (+), CK7 (+), Calponin (±), Vimentin (+), CK19 (+). While CD56, S-100, P63, TTF-1, CDX2, CK5/6, SYN, Dog-1, SOX-10 were all negative (Fig. ). Combining the microscopic morphology of the tumor cells and the results of immunohistochemical staining, we concluded that this was a case of primary lung AciCC.
The patient recovered well through the operation, only a slight chest tightness appeared in the first few days after the operation, which was quickly relieved after adjustment of drainage. We removed the drainage on the 8th day after surgery and the patient discharged on the 10th day postoperatively. The patient was examined every 3 months during the first year after surgery. Enhanced CT of the chest and abdomen, ultrasound of the superficial lymph nodes, as well as routine blood test, liver function, kidney function, and tumor markers were performed each time. Examinations began semiannually in the second year after surgery, and the contents of the examinations were the same as in the previous year.
At present, the patient has been followed up for 24 months with no evidence of recurrence and metastasis.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3730,10,Ideal Body Weight,physical,decimal,pmc-5005623-1,Extracted,"Patient A, a 54-year-old woman (weight 79 kg, height 177 cm, body mass index [BMI] 25.2 kg/m2) had been using the phytotherapeutic product MenoCool® (two times daily; morning one tablet, evening 0.5 tablet per oral administration) for the indication hot flushes and vaginal dryness due to the menopause. She had bought the product online through the manufacturer’s website (). The patient had not previously used the suspected drug. At that time, she had not menstruated for 2 years but had experienced hot flushes for approximately 4 years. The patient had never had an abnormal cervix smear, except a Pap III result 20 years previously. However, a repeated smear test showed no abnormalities. She had no medical history of vaginal bleeding, endometrial hyperplasia, endometrial polyps, or uterine leiomyomas. Her concomitant medication consisted of fexofenadine 120 mg once daily and mometasone 50 μg/dosage nasal inhalation spray, both since 2005. The patient started using MenoCool® in April 2014. After using MenoCool® for 2 months, the patient started to experience abdominal cramps and vaginal hemorrhage. These complaints were diagnosed by a gynecologist as related to a high proliferation of the endometrium. The patient was hospitalized for a day and underwent a curettage. After the curettage, the patient went for a follow-up appointment to her gynecologist and a significant increase in the endometrium was found again. The patient was treated with a course of norethisterone. Norethisterone has been effective in the treatment of dysfunctional uterine bleeding in patients with a proliferative or hyperplastic endometrium [] and, as expected, the patient had a heavy withdrawal bleeding following withdrawal of norethisterone that lasted for several days. The following control appointment showed proliferation of the endometrium again but still within the normal range; this time no action was deemed necessary. According to the patient, the gynecologist in the hospital had no explanation for the rapid and extreme growth of the endometrium. The patient ceased the use of the phytotherapeutic product in September 2014 and had fully recovered by the time follow-up information was received by the pharmacovigilance center in February 2015. After a consultation in a women’s health clinic, the patient was told by another gynecologist that she should not use drugs against hot flushes containing phytoestrogens to prevent a repeat of her complaints. Her endometrium was diagnosed at this clinic as thick but within the normal range, and there has been no hyperplasia of the endometrium or vaginal bleeding since.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [177.0, 'cm']}",67.77568,64.3869,71.16446,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 177.0 cm, which is 177.0 cm * 0.393701 in/cm = 69.68508 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (69.68508 (in inches) - 60) = 67.77568 kg.
Hence, the patient's IBW is 67.77568 kg."
3731,10,Ideal Body Weight,physical,decimal,pmc-7843668-1,Extracted,"A 55-year-old, 168-cm, 88.3-kg male with a body mass index (BMI) of 31.3 kg/m2 was scheduled to undergo RARC for bladder cancer. He had diabetes mellitus and a history of smoking.
After placement of a lower thoracic epidural catheter, general anesthesia was induced. Anesthesia was maintained with combined general and epidural anesthesia. The FloTracTM system (Edwards Lifesciences, Irvine, CA, USA) was used to achieve adequate fluid management. The patient was placed in the lithotomy position with stirrups (Levitator®, Mizuho Medical, Tokyo, Japan), after elastic stockings (ES; Comprinet Pro® Size 3, Terumo, Tokyo, Japan) and intermittent pneumatic compression (IPC) devices (Flowtron Excel®, Muranaka, Osaka, Japan) were applied to prevent deep vein thrombosis (DVT). Intraoperatively, phenylephrine was infused at 0.5–1 mg/h to maintain mean blood pressure (BP) above 60 mmHg. Heart rate was kept stable between 50 and 90 beats/min and SpO2 was maintained at 98% or more.
RARC was performed using the da Vinci Xi surgical system® (Intuitive Surgical Inc., Sunnyvale, CA, USA). Total cystectomy, extended pelvic lymph node dissection, and intracorporeal urinary diversion with an ileal conduit were performed uneventfully. However, the surgical duration was prolonged as long as 481 min due to expansion of lymph node dissection. Total blood loss, including urine volume, and total infusion volume were 300 ml and 5560 ml, respectively. The patient remained in the lithotomy position for 515 min, during which he remained in an extreme 25-degree Trendelenburg position for 201 min. He was extubated immediately after the surgery and was transferred to the intensive care unit.
At 3 h postoperatively, he complained of paresthesia and pain over the right calf. The epidural infusion was discontinued because the paresthesia might result from the effect of epidural analgesia. However, the paresthesia and pain were exacerbated 1 h after suspension of the epidural infusion. Urgent blood examinations revealed an elevated level of creatine kinase (CK) (15,800 U/l). Computed tomography (CT) revealed swelling of the right calf (Fig. a). He was diagnosed with WLCS and transferred back to the operating theater for urgent fasciotomy at 7 h postoperatively.
Compartment pressures of the right calf measured under general anesthesia with a needle manometer (TraWave®, Edwards Lifesciences, Irvine, CA, USA) were high at 38, 19, and 14 mmHg in the anterior, lateral, and posterior compartments, respectively. Fasciotomies performed on both sides of the calf reduced compartment pressures to 18, 14, and 12 mmHg, respectively (Fig. b). Subsequent hematological examinations indicated a return of CK to a normal level (218 U/l) by postoperative day 15.
After the fasciotomy, he required debridement procedures twice due to local infection, followed by a skin graft to compensate for the skin defect 43 days after RARC. He was finally discharged from hospital 78 days after RARC without any neuromuscular disorders and in an ambulatory condition.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.0, 'cm']}",64.12607,60.91977,67.33237,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg."
3732,10,Ideal Body Weight,physical,decimal,pmc-3655504-1,Extracted,"A 77-year-old woman with a history of interstitial pneumonia and uveitis visited our institution complaining of general fatigue. Chest radiography revealed a mass in the upper lung fields (), and she was thus admitted for further examinations.
Her blood pressure was 130/71 mmHg, heart rate was 106 beats/min, body temperature was 36.8°C, and O2 saturation was 96% in room air. She had a history of smoking 15 cigarettes per day for 55 years but no history of alcohol consumption. On initial clinical examination, her weight was of 50.8 kg, height was 158 cm, body mass index was 20.3 kg/m2, and BSA was 150 m2. Mild anemia was revealed in the palpebral conjunctiva. No abnormal murmur could be heard on auscultation although dry rales were heard in both lungs.
Laboratory test results demonstrated a markedly elevated white blood cell count (266 × 102/μL; normal: 39–94 × 102/μL) with 81% neutrophils, mild anemia (red blood cell count: 322 × 104/μL; normal: 367–479 × 104/μL; hemoglobin: 9.8 mg/dL; normal: 11.5–14.9 mg/dL), elevated platelet count (56.9 × 104/μL; normal: 13–33 × 104/μL), mild renal dysfunction (serum creatinine: 0.96 mg/dL; normal: 0.47–0.79 mg/dL; serum urea nitrogen: 23.4 mg/dL; normal: 7–20 mg/dL), mild hyponatremia (133 mEq/mL; normal: 137–146 mEq/mL), mild hypercalcium (11.4 mg/mL; normal: 8.4–10 mg/dL), and markedly elevated C-reactive protein level (14.0 mg/dL; normal: 0–0.3 mg/dL). The tumor marker squamous cell carcinoma antigen was also elevated (5.5 ng/mL; normal: 0–1.5 ng/mL).
Chest computed tomography (CT) revealed interstitial shadows in both lungs. Chest CT also showed a 5.2 cm irregular mass with cavity and speculated margin in the right S3 as well as a 7.6 cm irregular mass with cavity and air bronchogram sign, which were adjacent to the pleural walls (Figures and ). A few nodules were found in the right lung. Left hilar and subcarinal lymph nodes were swollen. The pathological findings for an endoscopic biopsy specimen revealed squamous cell carcinoma (Figures and ). Abdominal CT and brain magnetic imaging showed no lesion suggestive of metastasis. Radiographic findings confirmed T4N3M0 lung cancer of stage IIIB.
After admission (), high-grade fever developed and laboratory tests revealed sustained elevated white blood cell counts and C-reactive protein level. Therefore, the cooccurrence of a respiratory tract infection was suspected. The administration of antibiotics was initiated (sulbactam/ampicillin at 3.0 g/day for 6 days, and, subsequently, pazufloxacin at 1000 mg/day for 4 days). However, the elevated inflammatory marker levels and high-grade fever were not resolved. After administering nonsteroidal anti-inflammatory drugs (loxoprofen sodium hydrate at 180 mg/day), her temperature returned to normal.
The cause of fever and elevated inflammatory reaction levels was suspected as cytokine production by tumor cells. Therefore, serum G-CSF and IL-6 levels were measured, which showed that both serum G-CSF (117 pg/mL; normal: <57.5 pg/mL) and IL-6 (83.5 pg/mL; normal: <2.41 pg/mL) levels were high. Immunohistochemical examination of biopsy specimens showed positive staining with anti-G-CSF monoclonal and anti-IL-6 monoclonal antibodies (Figures and ). Therefore, diagnosis of G-CSF- and IL-6-producing tumor was established.
Although surgical treatment was considered, it was not indicated because her respiratory function was poor because of interstitial pneumonia. Chemotherapy was recommended, but she declined. Therefore, she was administered best supportive therapy. She was discharged 19 days after her admission, after which she visited our institution regularly. However, she was transferred by ambulance because of dyspnea, and she died of hypoxemia due to interstitial pneumonia exacerbation two months after diagnosis of lung cancer.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3733,10,Ideal Body Weight,physical,decimal,pmc-7391090-1,Extracted,"A 75-year-old Japanese male with end-stage renal disease due to antineutrophil cytoplasmic antigen (ANCA)-associated vasculitis had been receiving continuous ambulatory peritoneal dialysis (CAPD) for 9 years. He also had an implanted defibrillator (cardio-resynchronized therapy with defibrillator) to treat chronic heart failure resulting from a myocardial infarction. He had a poor appetite and general malaise without abdominal pain or fever. These symptoms gradually worsened, and he was hospitalized. At the time of admission, his blood pressure was 94/52 mmHg, his height was 165 cm, and his weight was 53 kg. At auscultation, no gallop rhythm was heard, and his extremities were not edematous. The laboratory parameters at the time of admission were as follows: white blood cells, 8080/μL; hemoglobin, 13.5 g/dL; platelets, 121 × 103/μL; total protein, 5.2 g/dL; albumin, 1.8 g/dL; lactate dehydrogenase, 309 U/L; glutamate oxaloacetate transaminase, 25 U/L; glutamate pyruvate transaminase, 19 U/L; blood urea nitrogen, 28 mg/dL; creatinine, 4.97 mg/dL; sodium, 125 mmol/L; potassium, 2.7 mmol/L; chlorine, 91 mmol/L; calcium, 6.8 mg/dL; phosphorus, 4.1 mg/dL; C-reactive protein, 0.092 mg/dL; procalcitonin, 0.21 ng/mL; BNP, 319 pg/mL; intact parathyroid hormone, 149 pg/mL; and β2-microglobulin, 23.4 μg/mL. Chest X-ray revealed bilateral free air in the abdomen (). Subsequent computed tomography of the abdomen revealed marked PP (Figures and ).
Peritonitis due to perforation of the digestive tract was suspected, but the possibility of perforation was considered very low because of the absence of abdominal pain, fever, and turbidity of dialysis drainage. Insufficient priming (air removal) at the time of peritoneal dialysis bag replacement was suspected, and the patient was instructed on how to perform sufficient priming. As a result, the free air in his abdominal cavity gradually disappeared ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3734,10,Ideal Body Weight,physical,decimal,pmc-5813332-1,Extracted,"A 34-year-old woman (height = 160 cm; weight = 50 kg) was scheduled for emergency surgery due to an open fracture of her left tibia and closed fracture of her right femur, which were sustained during a traffic accident. She had no past medical history. There were no other organ injuries, including those of the neck, face, thorax, or abdomen. The results from an ECG and chest radiograph revealed no acute or pathologic lesions.
After obtaining informed consent for surgery and anesthesia, the patient entered the operating room and routine monitoring, including capnography, a 3-lead ECG, non-invasive blood pressure monitoring, mechanosensor-neuromuscular transmission (M-NMT) module, and Entropy module on Datex-Ohmeda, was performed. Her initial blood pressure (BP) was 120/70 mmHg, heart rate (HR) was 93 beats/min, and her pulse oximetry oxygen saturation (SpO2) was 99%. After preoxygenation with 100% O2 at 8 L/min delivered through a mask for a few minutes, a remifentanil infusion (0.02 mcg/kg/min) was started and 80 mg of propofol was administered intravenously. After LOC, supramaximal stimulation using NMT was checked; thereafter, 35 mg of rocuronium was injected. Tracheal intubation using a cuffed 7.0-mm endotracheal tube was performed without difficulty. Anesthesia was maintained with 1.5 L/min of O2, 1.5 L/min of medical air, 1.0 to 2.0 vol% of sevoflurane, and a 0.02 - 0.10 mcg/kg/min remifentanil infusion. Thirty minutes after intubation, surgical drapes and other preparations were completed and an incision was performed. Her vital signs and other monitored parameters were within a 20% range of the preoperative levels.
However, 45 min after intubation, the response entropy (RE) abruptly increased up to 100 and the state entropy (SE) to 91. NMT was exhibited in 4 of the counts with a 46% train of four (TOF) ratio, even though capnography showed no sign of spontaneous breathing. There were no significant changes in her vital signs. Even though 3 vol% of sevoflurane was temporarily administered, the entropy did not change. Because there was no other evidence of ROC, we applied additional EEG monitoring and used the Root with SedLine monitor (Fig. ) and confirmed a PSI of 50% and EMG of 23% (Fig. ). We assumed that the elevated EMG activity might cause an unusual elevation in the readings from the Entropy monitor. Thereafter, 10 mg of rocuronium was injected. After a few tens of seconds, TOF of NMT and RE/SE values on the Entropy monitor decreased gradually and simultaneously. When the NMT count reached 2 (2 mins after rocuronium injection), 59% of RE, 58% of SE, 40% of PSI, and 0% of EMG were assessed. Coincidently, the surgeon started to hammer on the nail in the patient’s tibia. He hammered regularly using the continuously repeated “hit - hit - pause” method. The “pause” step occurred at approximately 1.8 Hz of frequency. Within a minute, 3 TOF counts of NMT, 94% of RE, 79% of SE, 47% of PSI, and 0% of EMG were assessed (Fig. ). However, after a few minutes, the value of entropy decreased by less than 60. Twenty minutes later, the TOF count reached 4 and RE/SE values on the Entropy monitor increased to above 90 again while the PSI values were maintained below 50. Therefore, we discontinued monitoring with Entropy.
No other specific events occurred during the remaining intraoperative period. The patient did not complain of recall in the postoperative period. Upon discharge from the PACU, the last memories the patient had prior to sleep were the events of the surgical time-out just after entering the operating room. The first memory the patient had after awakening was the instruction from the medical staff to open her eyes in the recovery room. The patient did not dream during surgery. Mild surgical pain and dry mouth were the only discomforts the patient complained of in the recovery room.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3735,10,Ideal Body Weight,physical,decimal,pmc-3629342-1,Extracted,"A 42-year-old male patient (height 170 cm, weight 63.7 kg) visited our pain clinic with complaint of severe right groin pain. Two years earlier, the patient had been diagnosed with bilateral cam type FAI and underwent arthroscopic surgery in the right hip after hip magnetic resonance imaging which showed fibrocystic change of the right femur and superior labral tear and minimal joint effusion on both hips. The recurrent pain began about 1 year prior to his visit and walking was impossible. The degree of pain was 10/10 on the visual analogue score system (VAS, ranging from 0 = no pain to 10 = absolutely intolerable pain) and the Oxford hip score (OHS, function of hip joint, excellent = below 19, good function = 19-26, fair = 27-33, poor = 33 or more) was 47/60. During the physical examination, the straight leg raising test (SLR) was right 45° and left 80°. The FABER test and anterior impingement test (flexion and internal rotation of knee) were all positive at the right hip. The frog lateral view of the X-ray showed left superior labral calcification and an osteophyte at the right femur neck. In addition, the head-neck offset of the left femur was decreased (). The alpha angle in the translateral view was 78.2° (). The ultrasonographic finding showed mild effusion and capsular thickness. The patient had no previous past medical history and took tramadol 200 mg, NSAIDS 200 mg and gabapentin 600 mg per day. We decided to perform IA steroid injection under C-arm guidance. Written informed consent was received after sufficient explanation about the procedure and related complications. With the patient in the supine position, C-arm fluoroscopy was focused on the hip joint in the anterolateral view. After insertion of a 22 gauge spinal needle, 0.75% ropivacaine 5 ml and triamcinolone 40 mg injection was achieved in the right hip joint (). The patient visited our clinic again checking his VAS, OHS and satisfaction scores (5-point Likert scale; 5 = very satisfied, 4 = somewhat satisfied, 3 = neither satisfied nor dissatisfied, 2 = somewhat dissatisfied, 1 = very dissatisfied) at 2, 4, 8 and 12 weeks after injection (). The patient took NSAIDS 200 mg intermittently during the 12 weeks. Although moderate right hip pain remained, the patient could walk and return to work.
A 59-year-old female patient (height 161 cm, weight 59 kg) visited our pain clinic with left hip joint pain. The patient had been taking medications for rheumatoid arthritis. The patient had been diagnosed with pincer type FAI about two years prior to her visit. The hip AP (anteroposterior) view of the X-ray showed suspicious FAI, with labral calcification and excessive coverage by the superior margin of both acetabula (). The pain site was in the lateral and subgluteal area of only the left hip joint. The degree of pain was 7/10 on the VAS and the OHS was 26/60. During the physical examination, the SLR was right 90° and left 90°. FABER test was positive on the left side. However, the anterior impingement test was negative for both hips. No abnormality was found in the ultrasonographic image. We decided to perform ultrasound guided IA steroid injection. Written informed consent was received after sufficient explanation of the procedure and related complications. With the patient in the supine position, the hip was internally rotated about 15-20°. An ultrasound convex probe (2-5 MHz, MicroMAXXTM, Sonosite, USA) was aligned with the long axis of the femoral neck, including the acetabulum and the femoral head. A 22 gauge spinal needle was then advanced under direct ultrasonographic guidance into the anterior synovial recess at the junction of the femoral head and neck (). Injection of 0.75% ropivacaine 5 ml and triamcinolone 40 mg in the left hip joint was performed. The patient visited our clinic again checking her VAS, OHS and satisfaction scores at 2, 4, 8 and 12 weeks after injection (). The patient took her previous medications for rheumatoid arthritis during the 12 weeks and additional analgesics were not prescribed. Three months after the injection, the pain in the trochanteric area was partially reduced.
A 50-year-old male patient (height 175 cm, weight 73 kg) visited our pain clinic with complaint of pain in both hip joints. The pain had been ongoing for one year prior to his visit. The patient had been prescribed NSAIDS and muscle relaxants at a local pain clinic whenever he felt pain. The pain in the right anterior groin area was more severe than that of the left side. Because of the hip pain, the patient could not sit crossed-legged on the floor. The degree of pain was 3/10 on the VAS scale and the OHS was 21/60. During the physical examination, the SLR was right 90° and left 90°. The FABER test and anterior impingement test were positive on both sides. The frog lateral view of the X-ray showed the possibility of mixed type FAI of the right hip (). The head-neck offset of the right femur was decreased and there was excessive coverage by the superior margin of the right acetabulum. The alpha angle in the translateral view was 75.3°. No abnormality was found in the ultrasound image. We performed C-arm fluoroscopy guided injection of 0.75% ropivacaine 5 ml and triamcinolone 40 mg in the right hip joint just like case 1. His symptom was much improved after the injection. The patient visited our clinic again checking his VAS, OHS and satisfaction scores at 2, 4, 8 and 12 weeks after injection (). The patient took NSAIDS 200 mg during the first month after injection and thereafter, was discontinued. The patient could sit crossed-legged on the floor 2 weeks after the injection although mild right hip pain remained.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3736,10,Ideal Body Weight,physical,decimal,pmc-6896632-1,Extracted,"A 72-year-old male, 70 kg and 167 cm height, who underwent L2–L5 decompression and transforaminal interbody fusion presented with chief complaints of pain in the lower back and bilateral lower limbs for the past 1 month. During preoperative anesthesia workup, it was found that patient was on irregular medications for hypertension. The preoperative blood investigations were within normal limits, and electrocardiography showed normal sinus rhythm. As a part of the protocol in our hospital, echocardiography was done and there was no regional wall motion abnormality seen and ejection fraction was 55%. Premedication was given to the patient, and antihypertensives were continued as per schedule. Standard general anesthesia was given. Routine monitors (electrocardiogram, noninvasive blood pressure, pulse oximetry, and capnography) were attached, and intravenous glycopyrrolate 0.2 mg was given. Induction of anesthesia was done using titrated doses of propofol, and muscle relaxation achieved using rocuronium 50 mg. Intravenous morphine 7 mg was used to provide analgesia. Intubation response was prevented using fentanyl 100 mcg. The maintenance of anesthesia was carried out using oxygen/air mixture and sevoflurane along with intermittent boluses of atracurium. Volume control mode of ventilation was used intraoperatively, and a target end-tidal carbon dioxide of 32–35 mmHg was kept. Vascular cannulation in the left radial artery was performed for continuous blood pressure monitoring. In addition to the routine monitors, temperature and urine output were monitored. In order to facilitate surgery, after induction of anesthesia patient was made to lie in the prone position. Postprone positioning, all pressure points including eye pressure were checked, the neck was kept in the neutral position, vitals were stable, and surgery was started. During the middle of surgery when transforaminal dilatation near the lumbar vertebra (L3) was being performed, there was a sudden onset of bradycardia (heart rate (HR) dropped to 38 beats per min) with a simultaneous fall in arterial blood pressure (72/34 mmHg), with no change in end-tidal carbon dioxide levels and oxygen saturation []. The surgeon was informed about the event, and the surgical stimulus was released immediately. Within few minutes following the release of surgical stimulus, HR and arterial blood pressure came to baseline. There was a recurrence of similar episodes twice during the surgery which again responded to the removal of surgical stimulus. Towards the end of surgery, the patient's trachea was extubated in the supine position after reversal of neuromuscular blockade once the patient became fully awake, conscious, and was following commands. Furthermore, the patient's stay in the postoperative anesthesia care unit was uneventful and there was no neurological deficit. Consequently, the patient was shifted to the ward for further management.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [167.0, 'cm']}",63.22056,60.05953,66.38159,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 167.0 cm, which is 167.0 cm * 0.393701 in/cm = 65.74807 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.74807 (in inches) - 60) = 63.22056 kg.
Hence, the patient's IBW is 63.22056 kg."
3737,10,Ideal Body Weight,physical,decimal,pmc-2827053-1,Extracted,"A 36-year-old, previously healthy Hispanic female with no significant past medical history and no prior history of hypertension presented to the emergency room with sharp retrosternal chest pain radiating to the back. She was 165 centimeter tall and weighed 70 kilogram. She was a housewife and mother of two living children. She smoked one pack of cigarettes a day for more than ten years. For 3 months prior to presentation, she had been taking 18-20 tablets of caffeine-based weight loss pills daily, which was higher than the recommended daily dose. Each tablet contains 60-100 mg of caffeine and she was taking 1080 mg to 2000 mg of caffeine daily. She denied the use of other medications, stimulants, herbal, alcohol and illicit drugs. She said that she had lost approximately 20-25 kilograms in last 3 months. No family history of hypertension, diabetes or coronary artery disease. She denied palpitation, chest pain, insomnia, headache, abdominal pain or increase in urination.
On presentation, her blood pressure was found to be 220/110 mm Hg in right arm and 230/118 mm Hg in left arm. Her initial work-up included an electrocardiogram which showed T-wave inversion in leads III, aVF and V6. A complete blood count showed hemoglobin 12.9 g/dl (normal: 12.0-16.0 g/dl), white blood cell count 15.1 k/ul (normal: 4.0-11.0 k/ul) and platelet count 231 k/ul (normal: 150-450 k/ul). Serum basic metabolic panel showed sodium 132 mmol/L (normal: 135-145 mmol/L), potassium 3.3 mmol/L (normal: 3.5-5.3 mmol/L), chloride 103 mmol/L (normal: 95/105 mmol/L), bicarbonate 23 mmol/L (normal: 22-31 mmol/L), creatinine 1.3 mg/dl (normal: 0.6-1.3 mg/dl), calcium 8.3 mg/dl (normal: 8.6-10.3 mg/dl), and anion gap 6 mmol/L (normal: 7-17 mmol/L). Liver function test showed normal aspartate transaminase (15 U/L; normal: 0-55 U/L), alanine transaminase (23 U/L; normal: <45 U/L), alkaline phosphatase (55 U/L; normal: 34-104 U/L) and albumin (3.5 g/dl,normal:3.0-5.1 g/dl). Urinalysis showed only elevated specific gravity of 1.031(normal: 1.005-1.03). There were no crystals, protein and glucose in the urinalysis. Troponin I level was less than 0.030 ng/ml (normal: 0.0-0.049 ng/ml). Urine and serum toxicology screens were negative for cocaine, amphetamine, marijuana, benzodiazepines, barbiturates and phencyclidine. A chest X-ray did not show any infiltrate, consolidation, effusion or mediastinal widening. A computed tomography aortogram showed aortic dissection involving the posterior aspect of the arch extending into the common iliac arteries and right proximal external iliac artery. The dissection extended into the left subclavian and axillary arteries. There was narrowing of the origin of the right renal artery due to dissection (Stanford type B dissection) (Figure ,Figure , & Figure .)
She was started on intravenous esmolol and nitroprusside for blood pressure control and was admitted to the medical intensive care unit. During hospitalization, her blood pressure remained well controlled with amlodipine. All other investigations for a secondary cause of hypertension were negative.Patient was discharged home and upon follow-up 2 week later, her blood pressure remained well controlled with low dose amlodipine.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3738,10,Ideal Body Weight,physical,decimal,pmc-2259372-1,Extracted,"A 19-year-old Russian woman (height, 1.69 m; weight, 54 kg) with non-specific upper abdominal pain presented to a local hospital for evaluation. She complained of recurrent pain for weeks. Clinical examination revealed neither jaundice nor a palpable abdominal mass. The clinical laboratory data were normal.
Ultrasonography revealed a hypoechogenic, nearly spheric, homogenous formation with a smooth contour in direct contact with the underside of the liver and without any intermediate layer. The finding was most compatible with a large hepatic cyst. Computer tomography showed a clearly limited, hypodense, homogenous structure with a transverse diameter of 11 cm in the immediate vicinity of the liver, anterior to the right kidney, and posterior to the gall bladder (Fig. , upper panel). Cystic echinococcosis was excluded serologically. The documented adjacent lower computer tomography-slice depicted a similar hypodense structure, which was nearly circular and only 3 cm in diameter. The larger structure was interpreted as a congenital hepatic cyst due to the direct contact to segment 5 of the liver. The smaller structure was judged as an independent hepatic cyst because it resembled the large cyst, except for its smaller size (Fig. , lower panel). Further diagnostic procedures were not performed because the computer tomography was considered sufficient.
Because of the recurrent pain, a laparoscopic fenestration of the large cyst was recommended and this was performed at a primary care hospital. During the procedure, the cyst was approached via the inferior border. The cyst was in direct contact with the underside of segment 5, and the surgeon had no doubt about the liver as the origin of the cyst. A second cyst could not be identified.
A puncture was performed, which resulted in the evacuation of more than 100 ml of bile. Then, the cyst was opened by a 4 × 3 cm incision. Laparoscopic evaluation of the inner cyst revealed two bile ducts and, under the assumption of eroded bile ducts, clips were attached to effect closure. After fenestration, a drain was placed into the abdomen.
The drainage was consistent with a biliary leakage on the second postoperative day. Bilirubin increased to 6.21 mg/dl and the patient developed jaundice. An endoscopic retrograde cholangiography showed a massive dilatation of the distal common bile duct. The injected radiopaque material leaked into the abdomen. The intrahepatic bile system could not be detected. A stent from the duodenum into the dilated bile duct was inserted.
Due to these ambiguous findings, the patient was transferred to our university hospital on the third postoperative day. Computer tomography showed incipient pancreatitis. After re-evaluation of the original computer tomography, a large choledochal cyst involving the distal part of the common bile duct was recognized. The patient underwent repeat surgery on the fourth day after the original surgery, and a large choledochal cyst, Todani type 1A, with a diameter of 8–10 cm was found (Fig. ). The distal end of the stent was palpable in the duodenum, whereas the other end was visible in the fenestrated cyst (Fig. ). After further exploration of the choledochal cyst, the clips became visible in the cyst (Fig. ). However, these clips had not closed the suspected fistular ducts, but had occluded the right and left hepatic ducts (Fig. ). The clips were removed. The cyst was completely excised and the distal common bile duct was closed (Fig. ). A hepatojejunostomy was performed by a Roux-en-Y loop as the curative therapy.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.69, 'm']}",60.53158,57.505,63.55816,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.69 m, which is 1.69 m * 39.3701 in/m = 66.53547 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.53547 (in inches) - 60) = 60.53158 kg.
Hence, the patient's IBW is 60.53158 kg."
3739,10,Ideal Body Weight,physical,decimal,pmc-8093371-1,Extracted,"A 27-year-old man presented with adenoid hyperplasia and bilateral palatal tonsillar hyperplasia. Bilateral tonsillectomy was performed for adenoid hyperplasia. Abdominal ultrasonography (AUS) and enhanced computed tomography (CT) performed as part of the preoperative examination revealed the presence of a 15-cm tumor in the spleen. The patient was obese (height, 164.8 cm; weight, 128.8 kg; body mass index, 47.4 kg/m2) and did not have tuberous sclerosis (TS). His laboratory findings were within the normal range (white blood cell count, 8800/µL; red blood cell count, 433 × 104/µL; hemoglobin, 12.7 g/dL; platelet count, 17.4 × 104/µL; glycated hemoglobin, 6.3%; and C-reactive protein, 0.32 mg/dL).
AUS showed a solid tumor of approximately 14 cm in the spleen, and the tumor was found to be in contact with the pancreatic tail, left kidney, and stomach. The edges were smooth; the inside was uneven with mixed high- and low-echoic masses (Fig. ). Enhanced CT revealed a solid tumor of approximately 14 cm with a clear border on the ventral side of the spleen, which was continuous with the spleen. The inside mainly contained fat components around the blood vessels, and the solid part was imaged incrementally. The splenic artery supplied blood to the tumor. A dilated blood vessel, thought to be a vein draining into the splenic vein, was found on the caudal side of the tumor. Only hemangioma was seen in the liver, and no other findings were noted in the pancreas, liver, or kidney (Fig. ). Magnetic resonance imaging (MRI) could not be performed because of the patient’s claustrophobia.
The tumor was primarily located in the spleen and could not be adequately diagnosed. However, it was large, and the possibilities of rupture and malignancy could not be ruled out. Hence, we opted for a surgical resection.
Partial resection of the spleen was performed. The abdomen was opened using an upper abdominal L-shaped incision. A giant tumor of approximately 13 cm with a smooth surface was observed in the upper left quadrant of the abdomen (Fig. a). The tumor was confirmed to be continuous with the upper spleen, and there was no invasion of the other organs. The vein draining the tumor encircling the left kidney was ligated and dissected. ECHELON FLEX® 60 powered stapler (Ethicon Inc., Somerville, NJ, USA) was used to perform a partial resection of the spleen, including the tumor (Fig. b, c). Since we managed to preserve the splenic arteries and veins, no vascular treatment was performed at the splenic hilum. Before splitting the splenic parenchyma, it was pressed and thinned with the operator's finger for 5 min and then dissected using an automatic suturing device once. The operative time was 173 min. The volume of blood loss was 300 mL. The postoperative course was good, with no effect on the platelets, and the patient was discharged on the 7th postoperative day.
The excised specimen was a smooth, extremely soft tumor measuring 123 × 120 × 82 mm. The cleaved surface of the tumor was reddish brown, and a distressing yellow color was observed (Fig. d). Pathological examination indicated mature adipocyte proliferation and increased number of blood vessels of various sizes. Additionally, spindle-shaped cell proliferation foci were found between the adipocytes and the surrounding blood vessels. Profuse leakage of erythrocytes from the blood vessels, hemosiderin deposition, and small round cell infiltration were also observed (Fig. a, b). Immunostaining exposed that the spindle-shaped cells were weakly positive for smooth muscle antibody (SMA), and were identified as smooth muscle cells (Fig. c). The adipocytes and spindle cells were negative for HMB 45, Melan A, MDM, and CDK4. However, some parts of the cells were positive for estrogen and progesterone receptors. Vascular endothelial cells were positive for CD31 and CD34 and negative for CD8. Based on the above-mentioned findings, the tumor was diagnosed as primary angiomyolipoma of the spleen.
Four years postoperatively, the patient has not faced any hematological problems, including those involving the platelets, and no new tumors have been identified in the spleen or other organs.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [164.8, 'cm']}",61.22842,58.167,64.28984,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 164.8 cm, which is 164.8 cm * 0.393701 in/cm = 64.88192 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.88192 (in inches) - 60) = 61.22842 kg.
Hence, the patient's IBW is 61.22842 kg."
3740,10,Ideal Body Weight,physical,decimal,pmc-7680296-1,Extracted,"A 77-year-old woman visited a local clinic because of persistent cough for the past 6 months. A tracheal tumor was suspected on imaging and she was referred to us for further evaluation and treatment. Her medical history included hypertension and atrial fibrillation, for which she was treated with medications. Her height was 156 cm and weight was 56 kg. Respiratory noise was audible on respiration. There was no enlargement of surface lymph nodes. Additionally, there were no abnormalities in blood biochemistry and tumor marker levels were normal. Radiography showed a mass in the trachea. Computed tomography (CT) and magnetic resonance imaging (MRI) findings revealed a 1.5 cm large border and a smooth surface nodule shadow on the posterior wall of the thoracic trachea approximately 5 cm below the glottis. Mass formation with a major axis of 1.0 cm in diameter extending from the trachea to the esophagus was observed. Based on MRI findings, the border with the surrounding organs was clear and it was diagnosed as primary tracheal tumor invasion (Fig. a, b) Furthermore, bronchoscopy showed a smooth-surfaced submucosal tumor with abundant neovessels, which accounted for 80% of the cross-sectional area of the trachea (Fig. ). Biopsy was not performed, because there was a strong possibility of airway obstruction due to bleeding. Fluorodeoxyglucose-positron emission tomography (FDG-PET) showed accumulation with a maximum standardized uptake value of 2.9 for the lesion and the possibility of malignancy could not be excluded (Fig. ). The patient was not in a state of respiratory distress and tumor resection using a bronchoscope was at risk of bleeding, we decided to remove the tumor by tracheal sleeve resection, because the patient had symptoms and was at risk of airway obstruction. Regarding anesthesia, the percutaneous cardiopulmonary support (PCPS) was put on standby in consideration of the possibility of suffocation due to intubation difficulties and bleeding during intubation. There were no problems during anesthesia except for the operation of the intubation tube. Surgery was performed via median sternotomy. The thymus and surrounding structures were separated to expose the trachea, and then five tracheal rings, including the tumor, were removed by sleeve resection. Separation from the esophagus was relatively easy. After resection of the trachea, the airway was secured by intubation. End-to-end anastomosis of the trachea was performed using 3-0 monofilament synthetic absorbable suture material. A continuous suture was initiated in the membranous portion. The orally inserted tracheal tube was then advanced to the distal portion to secure the airway and interrupted suture of the portion of the tracheal cartilage was performed. The anastomosis site was covered with the thymus (Fig. ). Five tracheal rings were excised for excision of one or more tracheal rings above and below the tumor. Based on the results of intraoperative pathology, it was judged that there was no tendency for tumor infiltration and additional resection was not performed. The postoperative course was favorable. There has been no recurrence for 2 years after surgery. The resected specimen showed a white–pink tumor (maximum diameter of 23 mm) protruding into the tracheal lumen and the membranous portion (Fig. ). Pathological examination showed a mass of hyperplastic atypical cells with spindle-shaped nuclei arranged in bundles running in various directions in the submucosa. On immunostaining, the tumor was positive for vimentin, CD34, and Bcl-2, and negative for α-smooth muscle actin (α-SMA). Based on these findings, the tumor was diagnosed as an SFT (Fig. , ). There were no malignant findings and the resected stump was negative. The postoperative course was favorable and there has been no evidence of recurrence for 2 years after the surgery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [156.0, 'cm']}",48.75993,46.32193,51.19793,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 156.0 cm, which is 156.0 cm * 0.393701 in/cm = 61.41736 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.41736 (in inches) - 60) = 48.75993 kg.
Hence, the patient's IBW is 48.75993 kg."
3741,10,Ideal Body Weight,physical,decimal,pmc-3770039-1,Extracted,"A 47-year-old man was admitted to the Department of Plastic Surgery, Kobe University Hospital, for treatment of a chronic ulcer on his left heel. The size of the ulcer was 4 × 3 cm, and the calcaneal cortex was partially exposed (). There was no improvement in the ulceration following curettage and repeated local treatments for three months. Magnetic resonance imaging was performed. T1-weighted sagittal imaging showed diffuse low signal intensity in posterior calcaneus. T2-weighted sagittal imaging showed diffuse high signal intensity in the same region (Figures and ). Based on these findings, osteomyelitis of the calcaneus was diagnosed, and the patient was referred to our department.
General physical examination on admission showed that the patient was 165 cm in height and 54 kg in weight. His extremities were thin. Atrophied skin and decreased subcutaneous fat and muscle were observed in the periphery of the extremities. His external genitalia appeared atrophied. His hair was generally scarce and markedly gray. His face looked aged and had a “bird-like” appearance (). His voice was high-pitched and hoarse. When he was 32 years old, he underwent surgery for cataracts in both eyes.
His family history revealed that his parents were cousins, but there were no symptoms of note in his siblings, and no other family members had Werner's syndrome.
Surgical treatment was considered because the ulcer did not respond to conservative treatment. Under general anesthesia, the ulcer was debrided and osteomyelitis was performed followed by a curettage of the dome form as fully as possible. We drilled the calcaneus in order to improve the recipient ground circulation (). The drilling was performed manually with 1.5 mm diameter Kirschner wire (K-wire) at a number of center points, and with 1.0 mm in diameter K-wire at multiple periphery points. Five days after operation bleeding, of the calcaneus stopped and under local anesthetic the calcaneus was covered by an ultra-thin split thickness skin graft with the left thigh skin as the donor site (). One month later, the lesion was healed. One year postoperatively, there has been no recurrence of the ulcer or the osteomyelitis (Figures , , and ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3742,10,Ideal Body Weight,physical,decimal,pmc-3389323-1,Extracted,"A 34-year-old male patient was admitted for an occipital headache that had started 1 month prior to his visit. He had no history of head trauma, injury to the spine or dura puncture. The headache was postural in nature because the headache occurred when he stood up or sat, and it subsided when he lay down. The character of the headache was a dull, continuous pain in the occipital area with some radiating pain to the parietal and frontal areas. Visual analog scale (VAS) score was 8-9 points and dizziness was accompanied when standing or sitting. However, when he lay down, the VAS score decreased to 1-2 points. Physical and neurological examinations were performed on the day of admission and no abnormal findings were observed. Brain magnetic resonance imaging showed no abnormal findings and laboratory data on the patient were also within normal limits. Radionuclide cisternography was checked and it showed possible cerebrospinal fluid leakage at the cervicothoracic junction level () and the patient was diagnosed with spontaneous intracranial hypotension. Conservative management was administered including hydration, bed rest, and NSAIDs. Yet, the symptom persisted and the patient was referred to the pain clinic for an epidural blood patch. The patient was 175.2 cm high and his body weight was 77 kg. His occupation was aquaculture, breeding abalone. The patient was not obese, but he had a relatively well-developed musculature. Upon entering the operation room, the patient was placed in the prone position on the C-arm table. Both arms of the patient were placed over his head. The lower cervical area and the upper thoracic area were prepared and the skin was anesthetized with a local anesthetic agent. A modified 18G Tuohy needle was inserted at the C7-T1 intervertebral space and it was advanced at the anteroposterior (AP) view. For further advancement and visual identification of the epidural space, the C-arm was rotated to the lateral plane. The patient had very well developed shoulder muscles; therefore, the true lateral view image of the C7 and T1 vertebrae was difficult to obtain due to the superimposition of the shoulder muscles and bones (). The optimal oblique view provided an increasingly more distinct image of the cervicothoracic junction and the needle was further advanced accompanied by the LOR technique and the imaging of the intermittent AP plane view (). To obtain sufficient visualization, the C-arm unit was rotated in the AP/lateral plane until a perpendicular view of the target level lamina was achieved. The laminar was visualized as an enface image of a hollow tube (). A hollow tube means the cross-sectional view of the target laminar as the perpendicular view of the target level when the target laminar is parallel with X-ray beam. The angle of the oblique position of the C-arm unit was calculated in reference to the cervical CT findings (). As the needle entered the interlaminar opening, radiocontrast dye was administered. The AP view along with the oblique view was acquired to confirm the positioning of the needle tip in the epidural space () and then 8ml of autologous blood was injected. On rounds the next day, the patient reported a pain score of 1/10 on the VAS. He was discharged 3 days after the procedure without any remaining symptoms.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.2, 'cm']}",70.64577,67.11348,74.17806,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.2 cm, which is 175.2 cm * 0.393701 in/cm = 68.97642 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.97642 (in inches) - 60) = 70.64577 kg.
Hence, the patient's IBW is 70.64577 kg."
3743,10,Ideal Body Weight,physical,decimal,pmc-3384799-1,Extracted,"A 29-year-old woman (height, 164 cm; weight, 85 kg; gravid 2; parity 0) underwent cesarean delivery at 23 weeks' gestation. She had a history of antiphospholipid syndrome diagnosed by her rheumatologist 11 years ago. She experienced deep vein thrombosis with antiphospholipid antibodies and was lupus anticoagulant positive in that time. She was taking Astrix (100 mg/day). Six days before operation, she was admitted due to persistant epigastric pain. Blood pressure was 120/80 mm Hg, heart rate was 72 beats/min and body temperature was 36.8℃. Blood laboratory data were as follows: serum aspartate aminotransaminase (AST) 549 IU/L, serum alanine aminotransaminase (ALT) 489 IU/L, serum lactate dehydrogenase (LDH) 790 IU/L, blood urea nitrogen (BUN) 17.5 mg/dl, creatinine 0.5 mg/dl, hematocrit 29.7%, platelet count 54 × 103/ml, prothrombin time (PT) 12 sec and activated partial thromboplastin time (aPTT) 82.4 sec. A urine specimen demonstrated proteinuria (1+). Transabdominal ultrasound showed weak portal vein flow (main, 18.4 cm/sec; right, 30 cm/sec; left, 29 cm/sec) with a small amount of ascites. The obstetrician suggested autoimmune hepatitis or portal vein thrombosis was complicating antiphospholipid syndrome rather than HELLP syndrome because of the early gestational period and normal blood pressure. Repeated daily blood chemistries revealed an aPTT of 41-60 sec and therefore 1,000 unit/hour of heparin was initiated to reach the target aPTT of 80-100 seconds and 40 mg of prednisolone was added as treatment. For evaluating autoimmune hepatitis, auto-antibodies were checked. Anti-cardiolipin antibodies were examined by enzyme linked immunosorbent assay (ELISA). The IgG (51.8 GPL units/ml) was positive and IgM (2.76 MPL units/ml) was negative. A lupus anticoagulant test was also positive (control ratio of 2.67). Other laboratory investigations were unremarkable. On the morning of the operation, she had abrupt vomiting with generalized tonic-clonic seizures with eyeball deviations of 30-40 sec; she recovered spontaneously. One hour after the 1st seizure attack, she had another seizure attack with high blood pressure (200/100 mmHg); hydralazine and diazepam was given. The laboratory findings revealed AST/ALT 1,459/1,108 IU/L, LDH 1,424 IU/L, hematocrit 30%, platelet count 43 × 103/ml, aPTT 87.6 sec and urine protein (4+).
An emergency cesarean delivery was scheduled, she was not premedicated and upon arrival to the operating room, standard monitoring devices were applied. Vital signs were blood pressure 190/120 mmHg, heart rate 110 beats/min and pulse oxymetry revealed 99% oxygen saturation before anesthetic induction. The patient already received heparin and therefore, the patient did not wear a compression stocking as this could increase arterial blood pressure with increased venous return. Anesthesia was induced with 300 mg of pentothal sodium and 50 mg of rocuronium. Tracheal intubation was performed using a single lumen internal diameter (ID) 6.5 mm tube in one attempt without difficulty. Anesthesia was maintained with sevoflurane (1-2%) within BIS between 30-60. Systolic blood pressure was maintained about 140-160 mmHg using intravenous nicardipine (100-300 ug bolus) and body temperature was maintained about 36.8-37.3℃. A cesarean delivery was performed by a Pfannenstiel incision and a 470 gram live-born male infant was delivered (APGAR score; at 1 min, 3 and at 5 min, 7). Intravenous magnesium sulfate (170 mg/hour) and alfentanyl (1,000 ug) were given to the patient. The cesarean delivery proceeded without an event. The patient received fentanyl (1,000 ug) in 100 ml of normal saline for 48 h using patient controlled intravenous analgesia. At the end of surgery, all anesthetic agents were discontinued and the residual neuromuscular blockade was reversed with pyridostigmine and glycopyrrolate. Estimated blood loss was 500 ml and she was not transfused with blood components. The tracheal tube was removed when the patient responded to verbal commands and showed sufficient spontaneous respiration and neuromuscular function. There were no signs of uterine atony or bleeding. Pathologic observation of the placenta revealed mulifocal infarction involving up to 40% of the placenta. The patient remained in the post-anesthetic care unit for 1 hour event free and was then transferred to the intensive care unit. Intravenous magnesium sulfate used for 24 hours and she was transferred to the general ward at postoperative day 1. She had an uneventful recovery with improved liver function and platelet counts () and was discharged on postoperative day 8.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [164.0, 'cm']}",56.00401,53.20381,58.80421,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 164.0 cm, which is 164.0 cm * 0.393701 in/cm = 64.56696 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.56696 (in inches) - 60) = 56.00401 kg.
Hence, the patient's IBW is 56.00401 kg."
3744,10,Ideal Body Weight,physical,decimal,pmc-6215971-1,Extracted,"A 43-year-old man with pituitary gigantism from the age of 16 secondary to a GH-functional PA. He underwent microsurgical trans sphenoidal surgery for resection of a PA in 1990 and adjuvant radiotherapy given in 2011 (radiotherapy scheme, original radiology and pathology unavailable). In 2016, almost 27 years after the initial surgery, he presented progressive decrease in vision on the left eye for six months. He also complained of excessive perspiration and sweating and had a past history of carpal tunnel syndrome. He was found to have gigantism features as extreme physical size (2.07 mts height) and pigmentation around eyes, neck and flexures.
In ophtalmologic examination, a left ptosis with both exophthalmos and upward/inward limitation on left eye movements was achieved, and in the Goldmann’s test perimeter an ipsilateral amaurosis and right hemianopia (Octopus 900 Haag Streit Inc., Bern, Switzerland) ().
Random serum GH level was 0.071 ng/ml (0.003–0.97 ng/mL) with a normal GH concentration during the Oral Glucose Tolerance Test (OGTT) with a GH-nadir of 0.13 ng/ml (the gold standard for diagnosis is that GH excess fails to suppress serum GH level to less than 1 ng/ml after OGTT). The Insulin-like Growth Factor-1 (IGF-1) 84.3 ng/ml (64–210 ng/mL); the rest of hormones are listed and shown in .
On brain Magnetic Resonance-Imaging (MRI) (Siemens 3.0 T magnetic resonance scanner and a 32-channel head coil) revealed a large policystic selar lesion with extensive osteophytic reaction and invasion of the ipsilateral orbital apex associated with fibrous dysplasia (see A and B) with a T2-weighted hypointense and enhancing selar mass lesion with Calcium intensity on the Gradient echo sequences (GRE) (C). Also the skull CT-scan (Siemens SOMATOM Sensation 64-slices) revealed an osteolytic lesion on the right orbital apex with thickness of the diploe (E) and pituitary gland with a calcified rim around the tumor (D, F and G). There was no personal or family history of prior endocrine disease.
A second surgical resection was performed in 2016 by a left orbitozygomatic approach for tumor removal with no acute complications (A–C). Three days after the resection, the patient presented sudden unresponsiveness with an asymmetrically larger left pupil and rostrocaudal deterioration due to an ischemic stroke on left Anterior Cerebral Artery (ACA) and Middle Cerebral Artery (MCA), performing an urgent ipsilateral decompressive craniectomy. Unfortunately after surgery the patient continued unresponsive, leading to his death.
After the informant consent was obtained, brain autopsy was performed. Neuropathologic examination of the pituitary lesion removed in 2016 (first neuropathology report was unavailable) was characterized macroscopically by a 40 × 40 mm mass with grayish outer surface and inner yellowish-irregular zones thickened by “sand-like” calcifications (A and B). Histologically micro-hemorrhage with ossification areas within a thick pseudocapsule and multiple calcifications with a diffuse desmoplastic stromal component even within blood vessels were observed (C and D). Immunohistochemistry stains were positive for Growth Hormone and osteoconine (F–G). Brain autopsy showed perivascular granular-dystrophic calcifications in thalamus, hypothalamus and basal ganglia (D, H–J).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [2.07, 'm']}",99.44105,94.469,104.4131,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 2.07 m, which is 2.07 m * 39.3701 in/m = 81.49611 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (81.49611 (in inches) - 60) = 99.44105 kg.
Hence, the patient's IBW is 99.44105 kg."
3745,10,Ideal Body Weight,physical,decimal,pmc-3546190-1,Extracted,"A 77-year-old female patient with the main complaint of gait disturbance was transferred to the Department of Rehabilitation Medicine. The patient had been diagnosed with colorectal cancer 6 years ago and received right Hemicolectomy and Total Hip Replacement Arthroplasty due to the metastasis of cancer to her right hip joint, two days before. In an ultrasonography on her leg veins, as an examination carried out two days before the surgery, a blood clot on the posterior tibial vein and thromboembolism on the right upper lobe, in addition to mesenchyma on the left inferior lobe from a chest CT were observed. As such, an anticoagulation treatment of thrombotic lesion was started on the next day from the surgery. The patient, on the day of the transfer to the Department of Rehabilitation Medicine, was taking oxcodone (20 mg/day), atorvastatin (20 mg/day), gabapentin (900 mg/day), levosulpiride (25 mg/day), and cetamadol (R) (325 mg/37.5 mg), three times a day. Her weight was 57.6 kg and her height was 160 cm. There was no special opinion on the basic blood chemistry and electrolyte, and on the first blood coagulation test, PT was 14.2 seconds and INR was 1.10, which were normal.
As an anticoagulation treatment, the administration of warfarin started using enoxaparin (60 mg/day). The initial dose of warfarin was 8 mg after dinner on the first day, and PT next morning was 15.8 seconds and INR was measured 1.26. In the evening on the same day, 8 mg was administered again, and PT on the following morning was 62.6 seconds and INR was 7.33. In addition, the value of the coagulation remarkably increased. Thus, the authors, first considered the possibility of overdose of warfarin and an interaction with other drugs. The administration of cetamadol and warfarin was stopped, and Vitamin K 10 mg IV was administered to prevent copious bleeding, and then stopped the rehabilitation and radiation treatments. On the following morning, PT was reduced to 23.0 seconds and INR to 2.03, so warfarin was administered again for two days (2 mg/day), and the next morning's PT remarkably increased to 69.1 seconds and INR to 8.31. Again, Vitamin K 10 mg IV was administered, and the administration of warfarin was stopped. Four days after, INR was maintained at more than 4.0 and on the fifth day, PT was reduced to 20.8 and INR to 1.79. As a result, it turned out to be CYP2C9*1/*3 genotype, in which the heterozygous A1075C (Ile359Leu) polymorphism was found on the result of a CYP2C9 genotype analysis, in which a Polymerase Chain Reaction (PCR) and Direct Sequencing method were carried out, and an intermediate metabolizer with deteriorated activation of enzyme compared to that of a wild type person. It was found that VKORC1 genotype as 1173TT (homozygous) had a genetically high warfarin sensitivity. Thus, the authors started to find the maintained dose of warfarin of about 0.5-1 mg/day again, and with the dose of 0.5 mg/day, for the patient's value of coagulation, PT and INR was maintained at 21 seconds and about 1.9, respectively, and two weeks later, the radiation treatment was terminated. Consequently, the patient was discharged from the hospital with the proper function of independent walking, using a rolling walker.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3746,10,Ideal Body Weight,physical,decimal,pmc-3193693-1,Extracted,"A 24-year-old unmarried nulliparous woman, of weight 54 kg and height 170 cm, reported pain and pressure symptoms in the lower abdomen for 8 months. The pain, increasingly progressive for 4 months, was continuous, moderate to severe in intensity and increased after defaecation, especially during menstruation. Her pain was associated with urinary frequency and urgency. The colour Doppler ultrasound showed a unilocular cyst, measuring 9.9 × 9.2 cm in size, and computer tomography showed a large unilocular cyst in the left ovary, measuring 10.1 × 9.5 × 7.2 cm in size, with minimal solid tissue []. Preoperative CA-125 levels were in normal limits (24 ng/ml). Right ovary and the uterus were normal.
The bowels were prepared with oral polyethylene glycol (Peglec) a day before the surgery. The patient was administered general anaesthesia and positioned in Trendelenberg position with left side up. The umbilicus was everted and a midline vertical 2.5-cm incision was made inside the umbilicus. After retracting the edges of the incision, a 2.5-cm plane was created in the subcutaneous plane around the incision. One 10-mm port and two 5-mm ports were inserted as shown in [Figures and ]. A 10-mm, 30° telescope was inserted through the 10-mm port and other instruments were inserted through the 5-mm ports. Peritoneal and pelvic cavity inspection revealed a large left ovarian cyst occupying the whole of pelvic cavity []. Aspiration of the cyst produced 175 ml of chocolate-coloured dense fluid. A 2-0 silk suture on a straight 45-mm needle was inserted through the abdominal wall in the right iliac fossa. The needle was grasped through a needle holder inside the abdominal cavity and passed through the right edge of the collapsed cyst []. Similarly, a suture was taken through the left edge of the cyst from the left iliac fossa. On tightening both the sutures, the cyst was suspended from the abdominal wall []. A harmonic scalpel and a grasper were inserted through the 5-mm ports. The cyst wall was cut with harmonic scalpel (Ethicon Endo-surgery, Cincinnati, OH, USA) on coagulation mode, first vertically and then around the base of the cyst. The epithelial lining in the residual cyst was removed or electrocauterised with a monopolar cautery hook. The abdominal and the pelvic cavity were then washed with copious amount of saline and perfect haemostasis was assured. The excised cyst wall (in two pieces) was suspended from the abdominal wall from their respective sutures. After a complete visual inspection of the right ovary, uterus, pelvic and abdominal contents, the cyst wall pieces were removed through the 10-mm port. The sheath between the 10-mm port and one of the 5-mm ports was cut to enlarge the sheath incision to facilitate the cyst wall removal. The sheath was closed with 2-0 vicryl (Polyglactin) and the same suture was taken through the subcutaneous edge of both the skin incisions to facilitate the inversion of umbilicus. The final wound in the skin was 2.5 cm and was closed with 3-0 nylon suture. The cosmesis of the final wound was excellent [].
The patient recovered well in the postoperative period. The patient was started orally after 6 hours, ambulated after 10 hours and was discharged after 24 hours.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [170.0, 'cm']}",61.43709,58.36524,64.50894,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.92917 (in inches) - 60) = 61.43709 kg.
Hence, the patient's IBW is 61.43709 kg."
3747,10,Ideal Body Weight,physical,decimal,pmc-8383591-1,Extracted,"A 78-year-old woman was admitted to Matsushita Memorial Hospital for the treatment of atrioventricular block. The patient was in a normal state of health until 2 weeks before presentation, when dyspnea on effort developed. A diagnosis of 2:1 atrioventricular block was made at another facility and she was referred to this hospital. Her previous medical history included hypertension and operation for a tumor of the parotid gland. Her medications were azilsartan at a dose of 20 mg daily and herbal medicine, Shakuyaku-Kanzo-To, at a dose of 2.5 g daily. The patient occasionally drank, did not smoke or use illicit drugs, and had no known allergies. There was no family history of cardiovascular disease.
She was alert and did not seem sick, but looked lean with a height of 153.2 cm and weight of 41.2 kg (body mass index: 17.6 kg/m2). On examination, the blood pressure was 132/71 mm Hg, pulse was 49 beats per minute and regular, body temperature was 36.2 °C, and oxygen saturation was 98% while breathing ambient air. The jugular venous pressure was not high, but the third heart sound was audible at the apex with a grade 2 systolic ejection murmur. No pulmonary rales were heard and there was no edema in the legs.
Electrocardiography demonstrated bradycardia with a heart rate of 45 beats per minute, a normal axis, atrioventricular block with 2:1 conduction, and left ventricular high voltage. Chest radiography revealed cardiomegaly with a cardiothoracic ratio of 58% without pleural effusion or pulmonary congestion. The complete blood cell counts were normal, as were the levels of renal and liver function tests, electrolyte balance, and thyroid function test. The level of brain natriuretic peptide was 36.9 pg/mL (reference value ≤ 18.4). No remarkable findings were demonstrated on echocardiography; no Chiari network was detected.
Dual-chamber pacemaker implantation was scheduled after obtaining informed consent from the patient. A 6.0-Fr guiding catheter was inserted via the left subclavian vein using the Seldinger technique, and was advanced close to the interventricular septum from the right ventricle. A 4.1-Fr ventricular lead (SelectSecure MRI SureScan 3830, Medtronic, Minneapolis, MN, USA) was screwed into the right ventricular side of the interventricular septum. A tined J-shaped 5.3-Fr atrial lead (CapSure Sense MRI SureScan 4574, Medtronic, Minneapolis, MN, USA) was placed at the right atrial appendage. During removal of the guiding catheter of the ventricular lead, the tined atrial lead became dislodged to a lower position and entrapped.
A removal procedure was performed by pulling the lead and using a gooseneck snare with the support of an 8.0-Fr catheter, without success. Given the contrast images via the 8.0-Fr catheter (), the dislodged atrial lead was likely to be entrapped by the tricuspid valve, but echocardiography was not informative regarding the entrapment site due to insufficient image quality. A Chiari network as well as Thebesian and Eustachian valves was also considered as a possible cause of the entrapment because echocardiography did not show an increase in tricuspid regurgitation by pulling the entrapped lead.
Following multiple unsuccessful attempts to withdraw the lead for 3 h, surgical removal was decided to be performed. The patient was transferred to another hospital and the atrial lead was surgically removed with a thoracotomy and right atriotomy. The lead was reported to be strictly entangled within the fibrous threads of the Chiari network and resection was required to remove the lead from the network. The patient underwent pacemaker implantation with epicardial electrodes. The clinical course was complicated by wound infection, which was treated with antibiotics and debridement. She was discharged to home and had been scheduled to visit Matsushita Memorial Hospital for a pacemaker check at regular intervals.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.2, 'cm']}",46.22448,43.91326,48.5357,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.2 cm, which is 153.2 cm * 0.393701 in/cm = 60.31499 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.31499 (in inches) - 60) = 46.22448 kg.
Hence, the patient's IBW is 46.22448 kg."
3748,10,Ideal Body Weight,physical,decimal,pmc-7584932-1,Extracted,"A 34-year-old nulliparous woman (gravida 1, para 0) of 158 cm height and 53 kg weight had no allergies and no family history of the disease. She had been suffering from recurrent oral and genital ulcers that were not properly treated for 10 years. Moreover, she had a history of early miscarriage and had been suffering from infertility for two years after that unfavorable event. For this reason, the patient visited the Infertility Center and later consulted the Department of Maternal-Fetal Biology. Moreover, the genital ulcers and the stomatitis got worse. Her physical examination revealed a 5 mm aphthous ulcer on the left side of the tongue. In addition, a genital ulcer was identified on the inside of the left labia minora (Figures and ). The patient's diagnosis was an incomplete-type BD, with the main symptoms being recurrent genital and oral ulcerations (herpetiform) and skin lesions. Furthermore, no arthritis, gastrointestinal, vascular, or ocular lesions were observed. Laboratory analyses revealed that total protein (TP) [8.2 g/dL (normal range, 6.5–8.2)], C-reactive protein (CRP) [0.44 mg/dL (normal range, 0.00–0.30)], immunoglobulin G (IgG) levels [2266 mg/dL (normal range, 870–1700)], white blood cell count (WBC) [9300/μL (normal range, 4000–9000)], and 50% hemolytic complement activity (CH50) [57.3 U/mL (normal range, 30–45)] were higher than the normal levels, while iron (Fe) levels [29 μg/dL (normal range, 48–154)] were lower than normal. The percentages of Th1 (interferon (IFN)γ+/IL-4-/CD4+) cells, Th2 (IFN-γ-/IL-4+/CD4+) cells, and activated natural killer (NK) cells were 10.1%, 4.2%, and 56% (normal range, 18–40), respectively. Other laboratory findings related to miscarriage, such as antiphospholipid syndrome (anti-CL IgM Ab, anti-PE IgG Ab, and anti-PE IgM Ab), autoimmune disease (ANA and anti-DNA Ab), and disorders of blood coagulation (protein S activity, protein C activity, and factor XII activity), were all negative.
All the general fertility tests, including the husband's semen analysis, performed at the Department of Reproductive Medicine indicated no apparent abnormalities. Therefore, we performed AIH through ovulation induction with clomiphene citrate for treating unexplained infertility. After the failure of first AIH, the patient was treated with 10 mg/day prednisolone (PSL) for 4 weeks, which improved the genital ulcer, chronic inflammation (TP, platelet (PLT), CRP, CH50, Fe, and IgG), and immune status (Th2 and NK activity) (, Figures and ). Pregnancy was established at the second AIH attempt after PSL administration. PSL was maintained at 8 mg/day during the course of the pregnancy, and no mucosal lesions were observed. At 38 weeks and 4 days of gestation, a healthy baby boy weighing 3090 g was vaginally delivered.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3749,10,Ideal Body Weight,physical,decimal,usmle-639,Extracted,"A 42-year-old woman is brought to the emergency department because of intermittent sharp right upper quadrant abdominal pain and nausea for the past 10 hours. She vomited three times. There is no associated fever, chills, diarrhea, or urinary symptoms. She has two children who both attend high school. She appears uncomfortable. She is 165 cm (5 ft 5 in) tall and weighs 86 kg (190 lb); BMI is 32 kg/m2. Her temperature is 37°C (98.6°F), pulse is 100/min, and blood pressure is 140/90 mm Hg. She has mild scleral icterus. The abdomen is soft and nondistended, with tenderness to palpation of the right upper quadrant without guarding or rebound. Bowel sounds are normal.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3750,10,Ideal Body Weight,physical,decimal,pmc-6612968-1,Extracted,"A 28-year-old woman (1.65 m, 85 kg, BMI 31.2) was referred to our department five days postpartum with a bilateral femoral neck fracture.
During the last two months before the delivery of her first child (begin with the sixth month of gestation), she had complained about increasing weakness and pain in both hips and thighs. In the last two weeks of her pregnancy (begin of the 35th week of gestation), she had to walk on crutches, as she was unable to bear her full weight due to the severe pain in her hips. During this time she took paracetamol daily. Her treating gynaecologist did not initiate any clarification of the symptoms by radiologic imaging methods in this period. Considering her severe pain, it was decided to deliver the child per elective caesarean section (37th +4 week of gestation). Three days postpartum, after being released from the hospital, she had an epileptic seizure and fell. She was admitted to a neurological department of another hospital. During her two-day stay in this department, the woman complained of severe pains in both hips. X-rays and a computer tomography (CT) of the pelvis were performed, revealing bilateral femoral neck fractures. Following this diagnosis, the patient was referred to our department for further treatment.
Regarding her past medical history, she had childhood migraine and epilepsy. She suffered from her first epileptic seizure at the age of 15. She was treated with valproate over 11 years and remained seizure-free during that time. Her treating neurologist stopped the medication two years prior to her pregnancy. The patient did not have any other comorbidities. Particularly, she did not report on any past history of fractures, irregular menstruation, or family history of osteoporosis.
At presentation in our department, the clinical examination showed massively reduced hip movement on both sides because of severe pain. Serum laboratory examination was normal.
Based on the age of the patient, the limited bone quality, the age of the fractures, and their displacement (Figures and ), it was decided to perform a bilateral hip joint replacement with the use of short-stemmed prostheses (). There were no intra- or postoperative complications. Both femoral heads were sent for further histopathological examination. The results of both femoral heads revealed fracture areas with hemorrhagia, proliferation of fibroblasts in the marrow cavities, and formation of focal woven bone as a sign of the bone remodelling, being indicative for a TOH. Postoperatively, the patient was mobilized on crutches under full weight bearing of the operated extremities. After consultation with our Department of Neurology, the patient restarted her valproate medication. Due to this medication, the patient was advised not to breastfeed her child. Since the TOH is regarded to be a self-limiting disorder, no specific osteoporotic treatment was applied. The further course was uneventful, and the patient was dismissed after two weeks.
At 1-year follow-up, the patient is free of any complaints and has no limitation in the range of motion of both hips (extension/flexion 0°-0°-100°, abduction 50°).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.65, 'm']}",56.90952,54.06404,59.755,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.65 m, which is 1.65 m * 39.3701 in/m = 64.96066 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96066 (in inches) - 60) = 56.90952 kg.
Hence, the patient's IBW is 56.90952 kg."
3751,10,Ideal Body Weight,physical,decimal,pmc-6186811-1,Extracted,"In June 2016, a 34-year-old woman from Hunan Province in South China came to our hospital presenting with apparent weakness of the whole body, muscular atrophy, facial diplegia, hypophonia, dysphagia, and intermittent fasciculations of facial muscles starting in 2007 when she delivered her first child. The patient’s symptoms gradually deteriorated and worsened after her second child was born in 2011. She was diagnosed in local hospitals with gastritis at that stage. In 2012, she developed dysphagia and dysarthria. She had electromyography (EMG) in 2013, and the result showed extensive neurogenic damage, supported by reduced amplitude on musculus facialis, all limb muscles, and the sternocleidomastoid muscle. Two other hospitals diagnosed her with motor neuron disease (MND). She refused to use Riluzole, the first-line drug for amyotrophic lateral sclerosis (ALS), so no specific treatment was taken. She came to our hospital with respiratory distress, accompanied with symptoms of pneumonia such as cough and expectoration. She did not complain of visual or hearing impairment. She was a pharmacist and denied any poisonous substance exposure. Her father and mother had a first-degree consanguineous marriage. No other member in her family presented with any similar disorder.
On physical examination, her higher mental function was found to be unaffected. Her height was 157 cm, and weight was 27 kg, with a body mass index of 10.95 kg/m2. She had facial diplegia (Figure ) with incomplete eyelid closure, and Bell sign was positive on the right side. Her muscles of mastication had decreased power and salivation was obvious. Sluggish palatal and gag reflexes, and fasciculation and atrophy of the tongue (Figure ) were observed. Fasciculation of the facial muscles was detected. She had generalized and symmetrical muscular atrophy, involving the face, trunk, and limbs (Figures ). She had an exhausted look with bulbar palsy and severe dyspnea. Muscle strength in the upper and lower limbs was assessed at United Kingdom Medical Research Council (MRC) grade IV. Bilateral Rossolimo sign was positive, and Babinsiki sign was positive on the right side. Tendon reflexes in the arms and legs were feeble. No sensory abnormality was detected. Coordinative movements including finger–nose incoordination, alternating movement, heel knee incoordination, and Romberg sign were normal. Meningeal irritation sign was absent.
After admission, the following tests were normal or negative: serum creatinine kinase, copper, mercury, anti-neutrophil cytoplasmic antibody, anti-nuclear antibodies, thyroid hormones and antibodies, HIV antibody, tumor markers, and electrocardiogram. Paraneoplastic antibodies including Hu, Yo, Ri, CV2, Ma2, Amphiphysin, TR, ANNA-3, PCA-2, and GAD were negative. Genetic studies for whole exome sequencing were negative, including SOD1, ALS2, SETX, C9orf72, and FUS.
Results of the following serum tests were abnormal (normal reference range in brackets): creatine 27 μmol/L (31.8–91.0 μmol/L), prealbumin 83 mg/L (200–400 mg/L), uric acid 74 μmol/L (90–420 μmol/L), low density lipoprotein 1.93 mmol/L (2.07–3.10 μmol/L), apolipoprotein B 0.52 g/L (0.6–1.1 g/L), cysteine protease inhibitor 0.39 mg/L (0.55–1.55 mg/L), β2 microglobulin 0.72 mg/L (1.00–3.00 mg/L), serum iron 2.1 μmol/L (11.0–27.0 μmol/L), and zinc 9.64 μmol/L (11.1–19.4 μmol/L). Superoxide dismutase (SOD) 121 U/ml (129–216 U/ml), vitamin B12 184 pg/ml (200–900 pg/ml), and vitamin B2 189.7 μg/L (>200 μg/L).
Her blood white cell count was 10.8 × 10E9/L, neutrophil rate 87.4% (40–75%). Arterial blood gas analysis showed her oxygen was 72 mmHg and carbon dioxide 57 mmHg, and lactic acid 0.8 mmol/L, while the pH was normal. Sputum smear found gram positive cocci and Candida albicans, but sputum cultures for bacteria and fungus were negative. Abdomen ultrasound revealed hepatic microhemangioma.
Chest CT showed bilateral pneumonia. Mild reduction in low frequencies (125, 250, and 500 Hz) in the left ear was detected by pure tone audiometry. EMG showed denervation in the muscles of the right paravertebral T10 and lower limbs, and chronic reinnervation in the upper and lower limbs. The patient refused EMG of the sternocleidomastoid muscle. Brain MRI demonstrated atrophy of cerebellum, with anterior lobe involved more severely (Figure ).
Our patient was characterized with progressive general muscle weakness and atrophy, involving the limbs, trunk, and muscles of cranial nerves (cranial nerve VII, X, and XI). Clinical signs and symptoms and EMG suggested damage to the pyramidal tract, anterior horn cells, and bulbar nuclei. Her history and laboratory findings excluded intoxication, metabolism disorders, vascular diseases, trauma, tumors, and autoimmune diseases. The consanguineous parents suggested that it might be an inherited disorder, though exome investigations were normal. Her condition was special in the involvement of the facial nerve, which is rare in MND. After analysis, her clinical manifestations indicated MMND. So, the final diagnosis of MMND, with complications of pneumonia, respiratory failure (type 2), and malnutrition, was made. We treated her with intravenous immunoglobulin (IVIG) (0.4 g/kg once daily for 5 days) and other symptomatic treatment (e.g., oxygen inhalation, intravenous levofloxacin, and nutritional support). Her symptoms of cough and expectoration relieved a little, but her other symptoms did not improve. She refused ventilatory support by continuous positive airway pressure. She was discharged after the pneumonia was controlled, but intermittently needed treatment for pneumonia and respiratory failure. Her condition deteriorated and she died of respiratory tract obstruction caused by sputum in March 2017. We got her husband’s inform consent for reporting this case.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [157.0, 'cm']}",49.66544,47.18217,52.14871,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 157.0 cm, which is 157.0 cm * 0.393701 in/cm = 61.81106 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.81106 (in inches) - 60) = 49.66544 kg.
Hence, the patient's IBW is 49.66544 kg."
3752,10,Ideal Body Weight,physical,decimal,pmc-3569886-1,Extracted,"A 33-year-old woman affected by hypergonadotropic hypogonadism (FSH 71.38 mIU/L; LH 35.50 mIU/L; estradiol <7 pg/mL) had been treated with estroprogestinic therapy “Triminulet” for nine years. Treatment was then suspended to allow a reevaluation of ovarian functionality. Upon drug withdrawal the patient presented secondary amenorrhea and was referred to our unit for an indepth diagnostic evaluation. A written informed consent was obtained.
Medical history revealed that the patient was born with normal delivery, bottle-fed, and showed standard psychosomatic development, menarche at age of 13 and oligomenorrhea since then up until estroprogestinic therapy was established. Pelvic US demonstrated a normally placed and normally developed uterus with a slightly dishomogeneous structure. The ovaries were not visible.
The patient was also affected by autoimmune thyroiditis, treated with levotiroxin. Ten years earlier (2002) the patient received a diagnosis of lactotrophic microadenoma (PRL 125 ng/dL); brain MRI “dubious small area of enhancement in the lower right paramedian pituitary” and was treated with different dosages of cabergoline. This treatment was suspended in august 2010. In 2011 a brain MRI was substantially unmodified compared with with the previous one. In addition the patient reported myopia and arthralgia since she was 15 years old Family history showed familiarity for thyroid, neurological cardiovascular diseases (see pedigree: ).
Physical examination: height 158 cm (3°–25°p), weight 64 Kg (50°p), BMI 25,63 Kg/m2, waist circumference 92 cm, cranic, and upper and lower limb measurements between 50° and 75° percentile. No alterations detected in fingers and toes. Apparently a normal development was observed for secondary sex characteristics. Facial features revealed no dysmorphisms, moreover neither mental impairment or cognitive deficit was evident. Vital signs were normal.
A blood sample was drawn in Sodium (Na) heparin coated tube (vacutainer) for mononuclear cells culture and GTG karyotyping. High-definition GTG banding analysis of 100 metaphases (Leica CW4000 software) demonstrated a 45,X (41%)/46,X,rea(X) (59%) mosaicism ().
CBG staining of a new lymphocyte preparation demonstrated the presence of two centromeres in the X rearranged population [46,X,rea(X)] (). Finally FISH analysis (kit ToTelVysion (TM) Multicolor DNA probe mixtures (Vysis)), confirmed the presence of two X centomeres in rearranged X chromosomes with 2 Xp extremities and no Xq extremity. In the rearranged X chromosome the Xq extremity was substituted by Xp and pericentrometric Xq region. After FISH analysis the subpopulation previously indicated as 46,X,rea(X) was then redefined as 46,X,idic(X)(q24) ().
The final definition of the karyotype as released to the is mos 46,X,idic(X)(q24)?[59]/45,X [41], compatible with a “Turner like” condition that can account for the clinical and endocrinological condition of the patient.
After a written informed consent was obtained from first degree relatives of our patient (parents and sister), a GTG karyotype analysis extended to family members demonstrated that the phenotype observed in our patient was the result of a de novo alteration.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3753,10,Ideal Body Weight,physical,decimal,usmle-1085,Extracted,"A 15-year-old girl comes to the physician because she has not had menstrual bleeding for the past 3 months. Menses had previously occurred at irregular 15–45 day intervals with moderate to heavy flow. Menarche was at the age of 14 years. She started having sexual intercourse with her boyfriend about 3 months ago. Six months ago she had a manic episode, which was treated with risperidone. Her mother has PCOS and her father has diabetes mellitus. She is very conscious of her weight and appearance. She is 171 cm (5 ft 6 in) tall and weighs 79 kg (174 lb); BMI is 27.02 kg/m2. Her temperature is 37°C (98.6°F), pulse is 60/min, and blood pressure is 116/70 mm Hg. The abdomen is soft and nontender. Pelvic examination shows a normal vagina and cervix. Serum hormone studies show:
Prolactin 16 ng/mL
Thyroid-stimulating hormone 3.8 μU/mL
Follicle-stimulating hormone 6 mIU/mL
Luteinizing hormone 5.1 mIU/mL
Progesterone 0.8 ng/mL (follicular N <3; luteal N >3–5)
Testosterone 2.2 nmol/L (N <3.5)
A urine pregnancy test is negative.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [171.0, 'cm']}",62.3426,59.22547,65.45973,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 171.0 cm, which is 171.0 cm * 0.393701 in/cm = 67.32287 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (67.32287 (in inches) - 60) = 62.3426 kg.
Hence, the patient's IBW is 62.3426 kg."
3754,10,Ideal Body Weight,physical,decimal,usmle-8551,Extracted,"A 26-year-old primigravida presents to her physician’s office at 35 weeks gestation with new onset lower leg edema. The course of her pregnancy was uneventful up to the time of presentation and she has been compliant with the recommended  prenatal care. She reports a 4 pack-year history of smoking prior to her pregnancy. She also used oral contraceptives for birth control before considering the pregnancy. Prior to pregnancy, she weighed 52 kg (114.6 lb). She gained 11 kg (24.3 lb) during the pregnancy thus far, and  2 kg (4.4 lb) during the last 2 weeks. Her height is 169 cm (5 ft 7 in). She has a family history of hypertension in her mother (diagnosed at 46 years of age) and aunt (diagnosed at 51 years of age). The blood pressure is 145/90 mm Hg, the heart rate is 91/min, the respiratory rate is 15/min, and the temperature is 36.6℃ (97.9℉). The blood pressure is unchanged 15 minutes and 4 hours after the initial measurement. The fetal heart rate is 144/min. The examination is remarkable for 2+ pitting lower leg edema. The neurologic examination shows no focality. A urine dipstick test shows 2+ proteinuria.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [169.0, 'cm']}",60.53158,57.505,63.55816,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 169.0 cm, which is 169.0 cm * 0.393701 in/cm = 66.53547 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.53547 (in inches) - 60) = 60.53158 kg.
Hence, the patient's IBW is 60.53158 kg."
3755,10,Ideal Body Weight,physical,decimal,pmc-4008446-1,Extracted,"A 48-year-old male finished Triple-Ironman distance in 41 hours and 18 minutes (11.4 km swimming, 540 km cycling, and 126 km running). At the time of the examinations, he had been practising his current diet of raw vegan diet for 6 years. Prior to this, the vegan athlete had been living as a vegan for 3 years and as a vegetarian for the previous 13 years.
All last competitions were performed only based on a raw diet. At the time of both examinations, the vegan athlete was 48 years of age and 1.80 metres in height. In the sporting season he was 79.7 kg in weight, with a body fat index of 12.9%; in the off-season he weighed 80.3 kg with a body fat index of 16.3%. Clinical examination showed a regular heart rhythm at 60 beats/min. Blood pressure was 115/70. The heart sounds were normal.
Prior to the spiroergometry, echocardiography was performed based on ASA criteria (1).
For comparison purposes, we refer to the values for 10 Ironman triathletes of similar age living on a mixed diet.
The results of the spiroergometry are shown in , those of echocardiography are in , and blood analysis findings are presented in . The athletes of the control group were aged 47.4 ± 5.2, weighed 76.2 ± 8.9 kg (with 13.4 ± 2.0% body fat), and were 1.816 metres ±6.6 cm in height. In the active phase the vegan athlete was training on average 18 hours per week, consisting of 2 hours of swimming, 11 hours of cycling, and 5 hours running. This involved covering distances of 5 km (swimming), 330 km (cycling) and 50 km (running). The athletes of the control group were training for a total of 15.9 ± 2.1 hours weekly, involving 2.5 ± 0.7 hours and 5.6 ± 1.5 km swimming, 8.6 ± 1.5 hours and 215.5 ± 53.0 km cycling, and 4.9 ± 0.7 hours and 55.2 ± 6.5 km running.
In terms of performance diagnostics, the vegan athlete showed comparable VO2max, VO2 at VAT, and %VO2max at VAT values as compared with the control group (statements regarding significant differences are not possible). VO2 and %VO2max at RCP were somewhat higher for the vegan athlete. The maximum ergometric performance is higher for the vegan athlete in absolute terms but not relative to the body weight. At RCP the ergometric performance of the vegan athlete is somewhat higher than that of the control group. The vegan athlete had lower pulse rates at rest, at VAT, at RCP, and at the endurance limit. In comparison with the off-season, in the active season the vegan athlete had a higher maximum ergometric performance, VO2, and %VO2max, as well as cardiac frequency at RCP.
In morphological terms, the vegan athlete showed a greater left ventricular end diastolic diameter, with consecutively higher end diastolic volume and stroke volume. The systolic and diastolic functions seem to be similar for the vegan athlete and the control group.
Besides a mild thrombopenia, slightly higher CK-NAC levels in the active season and a slight drop of free testosterone (in both examinations) all remaining values were within normal ranges.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.8, 'm']}",74.99221,71.2426,78.74182,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.8 m, which is 1.8 m * 39.3701 in/m = 70.86618 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.86618 (in inches) - 60) = 74.99221 kg.
Hence, the patient's IBW is 74.99221 kg."
3756,10,Ideal Body Weight,physical,decimal,pmc-4748504-1,Extracted,"A 30-year-old Caucasian male, philosophy graduate, came to our Department of Internal Medicine, referring a history of prolonged fatigue for more than 10 consecutive months, being more evident as the day progressed, and did not improve with bed rest and worsened with physical and mental effort, significantly interfering with daily activities and work. He also reported that was accompanied by unrefreshing sleep, impairment in short-term memory and concentration, together with headache behind the eyes and in the back of the head and postexertional malaise that lasted more than 24 hours.
These symptoms began approximately 6 months after the diagnosis of infective endocarditis of the native valve with negative blood cultures, treated successfully with antibiotics, replacement of the aortic valve, and oral anticoagulation.
The patient also complained of other medical conditions, such as dry eye sensation, slow digestion with postprandial fullness, and Raynaud’s phenomenon in the coldest winter months. He knew it from his youth but could not specify the age of onset.
Family history included the following: mother with mild hypertension; angina pectoris, hypertension, and dyslipidemia in the father; 2 sisters and 2 nephews apparently healthy.
Physical examination revealed only a systolic murmur II/VI from the prosthetic valve in aortic area and no other abnormalities.
Routine hematological and biochemical parameters in blood and urine showed no abnormalities, except international normalized ratio 2.8. Other tests performed were iron homeostasis, basal and 2-hour plasma glucose test, thyroid function, creatine kinase, basal cortisol, 25(OH)D, folic acid, B12, B6 serum level, cell-mediated and humoral immunity, C-reactive protein, angiotensin-converting enzyme levels, serum protein electrophoresis, antinuclear antibody (ANA), anti-Ro (SSA) and anti-La (SSB), anti-endomysial, anti-neutrophil cytoplasmic antibodies, as well as cryoglobulins, and all were negative. Serologic tests for Borrelia burgdorferi, Brucella, Chlamydia pneumoniae, Bartonella henselae and B quintana, Coxiella burnetii, Helicobacter, HBsAg, anti–hepatitis C virus, anti-cytomegalovirus IgG and IgM antibodies, and Epstein–Barr virus (EB V) IgM antibodies were negative. Only EBV IgG was positive.
Doppler echocardiographic evaluation of the function of the aortic valve prosthesis and the heart was normal, as well as electrocardiogram. Tear breakup time and Schirmer test were equivocal. Upper gastrointestinal endoscopy was normal.
Therefore, the patient appeared to meet the CDC-1994/Fukuda criteria for CFS, and the diagnosis of CFS was made. He was treated for 1 year with cognitive behavioral therapy, graded exercise therapy, and antidepressants, finding very slight improvement, and the headache did not respond to triptans or ergot alkaloids and responded only partially to nonsteroidal anti-inflammatory drugs.
As recommended, patients with ME/CFS require a regular reassessment and follow-up of symptoms (annually) to reconfirm or change the diagnosis. Therefore, we followed the patient for several years paying attention to the emergence of new symptoms and signs.
During follow-up, at the end of the second year, the patient reported feeling more tired, lack of energy, exhausted, with heaviness in the arms and legs, muscle pain, and proximal muscle weakness became more evident throughout the day, and even more after exercise often accompanied by muscle cramps. About 6 months later, the patient began to feel tingling in the feet, and then in the hands and sometimes burning sensation, along with a sense of restless legs. In the middle of the third year, these symptoms were more evident and the patient also complained of dry eyes, dry mouth, orthostatic intolerance, intestinal motility disorder with very annoying abdominal bloating, and with persistence of slow digestion with postprandial fullness.
The headache was now more accurately described as unilateral paroxysmal pain in the back of the head characterized by the sensation of pain as stabbing or electric shock that radiates to the area of the occipital and parietal scalp, and sometimes on the front and periorbital area. When the pain was strong, it was associated with pain behind the eye on the affected side. The pain was reproduced locally by manually compressing the greater occipital nerve. Given the characteristics of this headache, with a frequency of about once every 2 weeks, our diagnosis was occipital neuralgia. Furthermore, triptans and ergot alkaloids therapies were unsuccessful.
On examination, the patient weighed 75 kg and measured 168 cm of height. Body mass index was 26.6 kg/m2. At rest the blood pressure was 115/70 mm Hg, the pulse 83 beats per minute, and the respiratory rate 18 breaths per minute. Systolic murmur of aortic prosthetic valve had not changed. Arterial pulses were normal. Muscle strength in the arms was 4/5 proximal, 4−/5 proximal legs, and distal 5/5 both (according to MRC scale). Sensory examination showed a slight decrease in sensitivity to light touch and pinprick symmetric distribution within a distal-to-proximal gradient in the upper and lower extremities. Deep tendon reflexes, vibration, and proprioception were preserved. Romberg sign was absent, and the gait was normal.
The laboratory tests were repeated, and the results were unchanged.
Head-up tilt-table testing was positive for postural hypotension. Cranial and cervical spine magnetic resonance imaging and thorax and abdominal computed tomography scans were normal. Electromyography and nerve conduction studies were carried out in the upper and lower extremities and were normal. Tear breakup time and Schirmer test were positive.
After these results, we considered the possibility of mitochondrial myopathy in this patient. After obtaining informed consent, a histochemical analysis of a deltoid muscle biopsy revealed 3% ragged-blue fibers with the succinate dehydrogenase (SDH) stain.
In addition, a lip biopsy was also performed and was normal, dismissing Sjögren’s syndrome.
Spectrophotometric enzyme analysis of a fresh muscle extract showed a severe deficiency of activity in complex I (nicotinamide adenine dinucleotide: ubiquinone oxidoreductase) and IV (cytochrome c oxidase) below 42% and 70% of the minimum reference of control value normalized to citrate synthase activity, respectively. Thus, he was diagnosed of definite respiratory chain disorder because of fulfillment of 2 major criteria. All these findings were consistent with a primary mitochondrial myopathy.
Mitochondrial genome sequencing in blood sample was performed using the Sanger method, which revealed several mtDNA variants (A750G, T1189C, and A1438G) (Sistemas Genómicos, Valencia, Spain).
Therefore, the final diagnosis was adult-onset mitochondrial myopathy, with clinical manifestation of peripheral sensory neuropathy, autonomic symptoms, and occipital neuralgia.
Subsequently, we conducted a clinical study of the family, and the results are shown in . We can observe that all adults have muscle symptoms, sensory peripheral neuropathy, restless legs, occipital neuralgia, and autonomic manifestations—dry eyes, mouth, Raynaud phenomenon, postural hypotension, gastrointestinal dysmotility. shows the diagram of the family pedigree.
In our patient, treatment started on a regimen of a combination of riboflavin (100 mg 3 times per day) and thiamine (300 mg/day). During the first month of treatment, the patient started a marked and sustained improvement, which continues (5 years later) in the tiredness, impairment in short-term memory and concentration, muscle weakness, cramping in muscles after exercise, and the patient can now perform exercise, such as bicycling.
However, peripheral sensory neuropathy improved slightly with the vitamin regimen, but a manifest and sustained improvement was achieved together with the occipital neuralgia, when added pregabalin therapy at doses of 50 mg at night. Replacement therapy with tears and saliva provided a clear and sustained improvement of dry eyes and dry mouth.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.0, 'cm']}",64.12607,60.91977,67.33237,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg."
3757,10,Ideal Body Weight,physical,decimal,pmc-7716334-1,Extracted,"A 67-year-old Chinese man was referred to our hospital with diarrhea for more than 5 mo and for management of early colon cancer discovered by colonoscopy in another hospital.
The patient visited a hospital for the first time due to diarrhea of yellow watery stool 8-9 times per day on December 20, 2018. Colonoscopy suggested colon polyps with a pathology of tubular adenoma. No significant improvement was observed in the symptoms after antidiarrheal treatment. The patient underwent colonoscopy in another hospital again, which revealed multiple polyps in the liver curvature of the colon, cecum, and descending colon on April 23, 2019. The biopsy pathology of the polyp (liver curvature) in our hospital’s consultation indicated villous adenoma, and some glands showed moderate-to-severe dysplasia with focal early carcinogenesis, roughly showing in situ adenocarcinoma changes. Therefore, the patient was admitted to our hospital for evaluation and treatment of early colon cancer.
The patient underwent right lung nodule resection 1 year prior and lumbar disc herniation surgery 28 years ago. He had no history of other diseases or allergic drugs. He had a smoking history of 30 years and had quit smoking for 8 years. His younger brother died of lung cancer. The patient had no familial history of genetic diseases.
The patient’s personal and family history was unremarkable.
On physical examination upon admission, the patient’s height and weight were 160 cm and 55 kg, respectively, and he had a blood pressure of 96/58 mmHg and pulse rate of 80 beats/min. There were no other pathognomonic signs during physical examination, except for enhanced bowel sounds at 8 beats/min.
After admission, the patient underwent thorough evaluations including routine blood tests, routine urine tests, routine fecal tests, occult blood tests, blood biochemistry, infection indices, and serum tumor markers. He had hypoproteinemia and hypokalemia with serum albumin and potassium levels of 29.61 g/L and 3.37 mmol/L, respectively. The C-reactive protein level was 7.79 mg/L. His erythrocyte sedimentation rate and white blood cell count were normal. He had a slightly elevated carcinoembryonic antigen level of 5.11 ng/mL. The levels of IgG antibodies to Epstein-Barr virus capsid and nuclear antigen were more than 50.00 and 7.42 AU/mL, respectively. The antinuclear antibody was positive, with a titer of 1:3200. Immunoglobulin E significantly increased with a value of 265.30 IU/mL. The fecal occult blood test results were negative, and stool flora analysis was normal. No other significant abnormal laboratory results were recorded in this patient.
Chest computed tomography (CT) showed a clear lung field (Figure and ). We observed a liver cyst and part of the small intestine that was slightly dilated on abdominal CT (Figure and ). Chest CT on April 14, 2020 revealed new nodules in the lower lobe of both lungs. However, multiple masses in both lungs had progressed more than before excluding tumorous lesions on chest CT on May 31, 2020 (Figure and ). Abdominal CT revealed multiple nodules in the right lobe of the liver and multiple soft tissue nodules in the abdominal cavity with a greater possibility of tumor and ascites, and the colorectal wall was slightly thickened (Figure and ).
Colonoscopy in our hospital revealed a hemispherical polyp with a diameter of approximately 5 mm in the liver curve and a long-pedicle polyp in the descending colon, with a lobular pattern of 10 mm in diameter at the tip. At the same time, it was found that the terminal ileum, ileocecal valve, and entire colonic mucosa were slightly swollen, with pit patterns of types I-II, which were finely grained (Figure ).
In addition, gastroscopy showed swelling of the whole gastric mucosa and flaky erosions in the gastric angle and antrum with fine granular mucosa. The mucosa of the descending duodenum was also swollen in the form of fine granules (Figure ).
After admission, we performed endoscopic mucosal resection to remove the two polyps located in the liver curve of the colon and descending colon, respectively. Simultaneously, the entire colonic mucosa was swollen and finely granular. Routine hematoxylin and eosin staining revealed tubular adenoma with diffuse proliferation of atypical lymphocytes in the mucosal layer in the polyp of the liver curve.
The polyp of the descending colon was diagnosed as villous adenoma with focal carcinoma–adenocarcinoma (moderately differentiated) limited to the mucosal layer. However, the high-magnification view showed that diffusely proliferated atypical lymphocytes infiltrated mainly in the mucosal epithelium and lamina propria, partially invading the submucosa. The lymphocytes had a relatively simple morphology and medium-sized cell bodies containing few cytoplasm and large oval or irregular nuclei with some visible nucleoli (Figure ). Additionally, immuno-histochemical staining was positive for CD3, CD7, CD8, CD43, and Bcl-2 but negative for CD20, CD4, and CD56, and the Ki-67 index was approximately 80%. In situ hybridization, Epstein-Barr virus-encoded RNA, and IGH, IGK, and IGL rearrangement were negative.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [160.0, 'cm']}",56.88197,54.03787,59.72607,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.99216 (in inches) - 60) = 56.88197 kg.
Hence, the patient's IBW is 56.88197 kg."
3758,10,Ideal Body Weight,physical,decimal,usmle-333,Extracted,"A 52-year-old man comes to the physician because his skin has been progressively yellowing for the past 4 weeks. He also reports low appetite and difficulty fitting into his pants because of his swollen legs over the past several months. There is no personal or family history of serious illness. He does not smoke and drinks 1 to 2 beers on special occasions. He used to be sexually active with multiple female partners but has lost interest in sexual intercourse recently. He is 178 cm (5 ft 10 in) tall and weighs 68 kg (150 lb); his BMI is 22 kg/m2. Vital signs are within normal limits. Physical examination shows yellowing of the skin and sclera as well as erythema of the palms. There is bilateral enlargement of breast tissue. Cardiopulmonary examinations show no abnormalities. The abdomen is distended. The liver is palpated 2 to 3 cm below the right costal margin. On percussion of the left abdomen, a thrill can be felt on the right side. Hepatojugular reflux is absent. There is bilateral edema below the knees.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [178.0, 'cm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3759,10,Ideal Body Weight,physical,decimal,pmc-7995720-1,Extracted,"An 18-year-old Persian man (60 kg, 180 cm) with a case of Marfan syndrome (MFS) identified from family history and genetic assessment was referred to our center. He presented mainly with right thoracic scoliosis of 70° and excessive joint laxity, without any previous disease history (Fig. ). Scoliosis of 70° and the deteriorating condition of our patient led to the decision to perform surgery. In April 2016, a right thoracotomy for anterior spinal fusion (ASF) was performed from the sixth rib under general anesthesia in the left lateral decubitus position. After 3 days, posterior spinal fusion and instrumentation (PSF) was done successfully. He was discharged with a total contact body brace. On the 2 months postoperative visit, he complained of weakness of the right upper limb during overhead activities. On physical examination, the right upper limb was intact for both sensory and motor innervation, but the right scapula was winged and he was not able to flex his arm forward over 60° (Fig. ). Electromyography (EMG) and nerve conduction velocity (NCV) confirmed long thoracic nerve injury. A conservative treatment, physiotherapy, was provided for 3 months. Ultimately, the patient recovered completely in the last follow-up visit 6 months after the surgery. Electromyography and nerve conduction velocity revealed a return to normal position. However, scapula is more prominent than normal due to the hyperlaxity of MFS (Fig. ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [180.0, 'cm']}",74.99221,71.2426,78.74182,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 180.0 cm, which is 180.0 cm * 0.393701 in/cm = 70.86618 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.86618 (in inches) - 60) = 74.99221 kg.
Hence, the patient's IBW is 74.99221 kg."
3760,10,Ideal Body Weight,physical,decimal,pmc-4454702-1,Extracted,"The patient was a 48-year-old woman, measuring 58 kg in weight and 155 cm in height, with a body mass index (BMI) of 24 kg/m2. She underwent a revisional THA for aseptic loosening, 9 years after which a stem fracture occurred. The case history was complex. First, she received a compression hip screw (CHS) for an intertrochanteric fracture suffered in a traffic accident at the age of 20, which was soon followed by a bipolar hemiarthroplasty (BHR) procedure because of failure of the CHS. Thereafter, aseptic loosening of the BHR was noted and she underwent conversion from BHR to a cementless THA (Zimmer, Warsaw, IN, USA) at the age of 26 (Figures and ). At 39 years of age, a revisional THA (Trilogy cup, versis beaded full coat plus stem, 26 mm cobalt-chrome inner head, Zimmer) was performed because of aseptic loosening of the previous THA (Figures and ). This cobalt-chrome alloy stem was extensively porous-coated, with a diameter of 12 mm and length of 200 mm. During the operation, a strut allograft bone graft was required because of a comminuted fracture in the proximal portion of the femur that occurred during extraction of the stem, even though an extended trochanteric osteotomy (ETO) was performed. After the operation, the comminuted fragments and strut allograft were gradually absorbed. Additionally, a late acute homogeneous infection occurred 7 years after the revisional THA. The infection completely resolved following two operations for debridement and application of antibiotics-loaded cement beads, and the prosthesis was preserved. Thereafter, posterior dislocations occurred several times, the final one 7 months before the stem fracture.
Two years later after the infection was finally healed, the stem was suddenly fractured while the patient was walking with a single axillary crutch (). She underwent a re-revisional THA with a Delta-lock system (Nakashima Medical, Okayama, Japan) without a change of cup (). The section pictures of retrieved implant revealed a clear step in the medial side, suggesting that medial side was lastly fractured (Figures and ). The new titanium-6 aluminum-4 vanadium alloy stem diameter was 14 mm and the length was 280 mm, fixed with six screws.
Immediately after the revisional THA was performed, stem bending was 0° (), which gradually progressed (). The degree of stem bending immediately after the first dislocation was 1.9°. After the final dislocation, the degree of bending (5.3°) was more pronounced than before (Figures and ). The bending angle immediately before stem fracture was 5.2°. No bending was seen on lateral views obtained by radiography at any time. A scanning electron microscope (SEM) examination showed striation in the medial and lateral sections. SEM-energy dispersive X-ray spectroscopy (SEM-EDX) revealed that there was much higher oxygen at the medial and lateral sections as compared with the central section, suspecting that there had been in vivo corrosion before sudden implant fracture ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3761,10,Ideal Body Weight,physical,decimal,pmc-5647822-2,Extracted,"A 69-year-old man (ASA class II, weight 79 kg, height 168 cm) with a fracture of the right side mandibular angle was scheduled for emergency open reduction with internal fixation (). The patient had a history of diabetes and hypertension and was on medications. The patient had no history of prior surgery. Preoperative evaluations including laboratory tests, electrocardiography, and chest radiography was normal. The patient was transferred to the operating room with endotracheal intubation because of an unstable airway caused by sublingual and submandibular swelling. The surgeon, however, opted for nasal intubation of the ETT during the mandibular surgery.
General anesthesia was induced with sevoflurane and intravenous injection of 60 mg rocuronium, with a standard monitoring. After the induction of anesthesia, we tried direct laryngoscopy with a conventional Macintosh blade and FOB to change the tube but failed because of massive airway edema and bleeding. The tube exchange procedure was then postponed and the surgical procedure was performed under oral intubation. The open reduction and internal fixation of the mandible was performed successfully within an operating time of 2 hours and 15 minutes. The surgeon again opted for a change to nasal intubation for arch bar wiring. An attempt to intubate the patient via the nasal route using FOB, was made. We inserted a 6.5-mm Polar™ Preformed Tracheal Tube via left nostril and tried to intubate the trachea under the guidance of the FOB. However, bleeding and secretions blocked the FOB view despite repeated suctioning as in the first trial. Next, we attempted to use a C-MAC® video laryngoscope which showed a clear view of the glottis; the FOB view was blurred with secretions and blood. Using a C-MAC® video laryngoscope we guided the FOB into the trachea. After confirmation of the tracheal ring on the FOB view, we removed the oral ETT and followed with the railroading of the nasal ETT via the FOB. After confirming the EtCO2 curve, mechanical ventilation was resumed. After the arch bar wiring of the maxilla and mandible, the patient was transferred to the intensive care unit. The postoperative period was uneventful.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.0, 'cm']}",64.12607,60.91977,67.33237,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg."
3762,10,Ideal Body Weight,physical,decimal,pmc-5597541-1,Extracted,"A 49-year-old female (154.6 cm, 50.8 kg) presented with a mass on her left breast that was identified by the ultrasound imaging, and mammography (). The patient was diagnosed with invasive ductal carcinoma by core biopsy. She had no medical history and was scheduled to undergo breast conserving surgery (BCS) at 2 weeks after the completion of neoadjuvant chemotherapy. Because the patient was reluctant to go under the GA, the Pecs I and II block with MAC was prepared.
The left infraclavicular and axillary regions were cleaned with potadine, the ultrasound probe was placed obliquely between the third and fourth ribs under the lateral one third of the clavicle. After recognition of the appropriate anatomical structures, the skin puncture point was infiltrated with 1% lidocaine. The block was performed using a medial in-plane approach with a 22-G Tuohy needle ().
For Pecs I block, the needle was advanced to the tissue plane between the pectoralis major muscle and pectoralis minor muscle at the vicinity of the pectoral branch of the acromiothoracic artery and 10 mL of 0.25% levobupivacaine was injected. For Pecs II block, 20 mL was deposited at the level of the third rib above the serratus anterior muscle with intent to spread the local anesthetics over the axilla. The overall procedure of Pecs block took about 15 minutes, and the onset time of analgesia was an average of 3 minutes after completion of the procedure. However, sufficient analgesia for surgical procedure was obtained after 15 minutes from that time. We confirmed the anesthetic area over T2–T6 of dermatomes by a pinprick test. Subsequently, dexmedetomidine was infused with a loading dose of 1 mcg/kg for 10 minutes, followed by a maintenance dose of 0.2–0.7 mcg/kg/h with titration, for targeting Ramsay sedation scale of 3, responding to verbal commands. The sentinel node was identified intra-operatively and dissected; then the 10 × 10 × 6-cm mass, 5 cm lateral to the nipple was excised. After the sentinel lymph node was confirmed as metastasis on frozen biopsy, the incision for axillary dissection was extended from the border of the pectoralis major muscle to the border of the latissimus dorsi muscle along the naturally occurring skin lines. Dissection along the anterior serratus muscle was carefully conducted, taking care to preserve the integrity of the long thoracic nerve. The neuromuscular bundle, comprising the subscapular vessels, the thoracodorsal vessels and nerves, was identified and dissected from the axillary contents, while being preserved intact, adjacent to the latissimus dorsi muscle. The entire adipose tissue with the axillary lymph nodes was removed by en bloc resection. Closed suction drain was inserted at the axillary site and the operation was completed. The total operating time was approximately 3 hours 30 minutes. In the post anesthesia care unit (PACU), vital signs were stable, and visual analogue scale (VAS) score for pain was 1. Also, postoperative nausea and vomiting (PONV) were absent. The analgesic effect of Pecs block lasted about 8 hours; and analgesics were not required for 1 day.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [154.6, 'cm']}",47.49219,45.11758,49.8668,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 154.6 cm, which is 154.6 cm * 0.393701 in/cm = 60.86617 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.86617 (in inches) - 60) = 47.49219 kg.
Hence, the patient's IBW is 47.49219 kg."
3763,10,Ideal Body Weight,physical,decimal,pmc-5538031-1,Extracted,"A 54 year old asymptomatic female patient was seen by her family physician in Marcaibo, Venezuela, for her annual health exam in January 2014 in a primary care center. She had no complaints, except for recent unintended weight gain. Her past medical and surgical history are notable for a left breast lumpectomy (1973), a salpingectomy (1994), a hysterectomy without oophorectomy for NIC III (2005), and a left unilateral oophorectomy for ovarian torsion (2007). The patient used no medications and has no known allergies, and denied tobacco, alcohol, or drug use. The patient is monogamous and happily married. Her family history is notable for a sister who died of Hodgkin Lymphoma.
On physical exam, the patient was afebrile with normal vital signs. Her weight was 92.5 kg, 1.74 meters tall, with a BMI of 30.6. She appeared well hydrated with moist mucous membranes. She had an unremarkable exam - no findings of violaceous striae, acanthosis, acrochordons, or signs of virilization.
Laboratory results showed a normal complete blood count, mixed dyslipidemia, fasting blood glucose levels >125 mg/dl (normal range, 70–100 mg/dl) on more than two occasions, and HOMA1-IR index >2.5 (normal index, ≤ 2.5) (
); meeting the diagnostic criteria for type 2 diabetes mellitus (DM2) and metabolic syndrome. Initial recommendations were lifestyle changes, including 30 minutes walks five days a week, and a nutritionist consult. Additionally, pharmacotherapy, sitagliptin/metformin (Janumet
®, 50/1000mg) 1 tab daily, ezetimibe/simvastatin (Vytorin
®,10/40 mg) 1 tab daily, gemfibrozil (Lipontal
®, 900 mg) 1 tab daily, and orlistat (Xerogras
®, 120 mg) 1 cap daily, was initiated.
Simultaneously, a right upper quadrant ultrasound was ordered showing slight hepatic steatosis, as well as a round space occupying lesion with well-defined hyperechoic borders measuring 5.6×7.3cm in segment V of the right lobe suggestive of a hemangioma. Of note, a bilateral non-obstructive nephrolithiasis was observed (
). Due to these findings, the patient was referred to a local hospital diagnostic center for imaging studies, a triphasic hepatic MRI was performed as part of an additional workup. This identified a 7.0×6.0cm right adrenal space occupying lesion suggestive of a large adrenal adenoma (
). A hormone profile was performed with normal results - classifying this mass as a non-functional adenoma. Lack of reagents in local laboratories caused that the patients moved to Avila Clinic in Caracas (Capital of Venezuela) (
). The work up was completed with a serologic evaluation to rule out fungal infection with negative results for mycoplasma IgM (0.15; normal range: 0.00 – 0.90).
In April 2014, a right subcostal adrenalectomy was performed in at a level three hospital so as to ensure the presence of an intensive care unit due to the potential bleeding risk. The pathology report described a 4×7×6cm adrenal mass with a grey-yellow surface covered partially with a thick grey capsule with brown areas with a hemorrhagic and yellow adipose center. The microscopic evaluation showed an external layer of clear cortical cells of the adrenal granulosa; a center made of mature adipocytes and all three hematopoietic cell lines without calcifications or fibrosis. The final diagnosis was determined to be an adrenal myelolipoma (
).
The patient experienced no post-surgical complications. She has subsequently completed regular physical activity and continues with the same treatment at the same dosage. Standard laboratory checks at three months showed notable improvement in all parameters.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.74, 'm']}",65.05913,61.80617,68.31209,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.74 m, which is 1.74 m * 39.3701 in/m = 68.50397 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (68.50397 (in inches) - 60) = 65.05913 kg.
Hence, the patient's IBW is 65.05913 kg."
3764,10,Ideal Body Weight,physical,decimal,pmc-6805429-5,Extracted,"At the time of assessment, patient 7 was an 18-year-old Asian female, the first-born child of non-consanguineous Hmong parents, who subsequently had four additional healthy, developmentally normal children. She was born at full term after an uneventful pregnancy. At birth, her weight was 3.062 kg (35th centile), her length was 48.3 cm (32nd centile), and her head circumference was not available. Her early motor development was normal. She had delayed speech with first words at 18 months, followed by additional developmental delays and eventual development of cognitive impairment. At 3 years, she was diagnosed with PDD-NOS, due to loss of social and behavioral skills starting around 2 years of age, sensitivity to loud sounds, impaired coordination, and difficulties with balance.
She had a history of behavioral aggression throughout her schooling, particularly with regard to ownership and sharing, which intensified between 16 and 17 years of age, associated with diagnoses of obsessive-compulsive disorder and anxiety. She had one acute out-of-character behavioral episode, characterized by disinhibited behavior and unusual delusions, without hallucinations, lasting a few days at age 17, for which brain MRI, 24-h continuous EEG, and subsequent neurological evaluation were negative. She has never had any observed seizures.
In an assessment at 18 years, she was noted to need substantial help with self-care activities and could not understand or follow instructions. Her interactions and behaviors were immature, characterized as a 4-year-old level by her school evaluations. She had short stature and obesity (weight 88.2 kg, > 98th centile; height 153.0 cm, 6th centile; BMI 37.7 kg/m2, 98th centile) with macrocephaly (head circumference 58 cm; > 98th centile) (Table ). She had a history of continuously gorging or binge eating to the point of vomiting, requiring her parents to restrict her food intake.
She was mildly dysmorphic, with sparse lateral eyebrows, telecanthus, left preauricular pit, prominent cupid bow configuration of the upper lip, and slack facial expression. She had numerous self-inflicted, skin-picking lesions on her arms, in various stages of healing, and one hyperplastic keloidal scar elsewhere. Her speech was fluent but very simple, with sound substitution errors very typical of a young child. There was periodic echolalia, in addition to outbursts of out-of-context speech, without regard to interrupting other speakers. Negative genetic testing included Prader-Willi/Angelman syndrome methylation and MLPA, fragile X, and CNV analysis via SNP microarray. However, areas of homozygosity were identified across multiple chromosomes, with an overall percentage of autosomal/genomic homozygosity of 2.5%. No candidate recessive genes were identified within the homozygous regions. As no specific disease could be suspected on the basis of the clinical presentation, family trio sequencing of GeneDx’s Autism/ID Xpanded Panel with 2308 genes was performed, using oral rinse samples from her and both parents. This patient was identified through GeneMatcher [].","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.0, 'cm']}",46.04337,43.7412,48.34554,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.0 cm, which is 153.0 cm * 0.393701 in/cm = 60.23625 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.23625 (in inches) - 60) = 46.04337 kg.
Hence, the patient's IBW is 46.04337 kg."
3765,10,Ideal Body Weight,physical,decimal,pmc-3049978-1,Extracted,"A 60-year-old woman (height, 162 cm; weight, 61 kg) visited pain clinic with tactile allodynia and electric shock-like pain in the left dorsal scapular area around the T3 dermatome, which had been diagnosed as PHN about 1 month previously and attack of the herpes zoster was 1 year ago. The 100-mm visual analogue scale (VAS) of allodynia and electric shock-like pain was rated between 70 and 80 mm on a scale from 0 (no pain) to 100 (worst pain imaginable). The interlaminar epidural block was performed at the T3-4 space by the paramedian approach with 5 ml of 0.2% ropivacaine and 20 mg of triamcinolone acetate. Pregabalin and morphine at doses of 150 mg and 10 mg, respectively, twice a day, amitriptyline at a dose of 10 mg before sleep and topical lidocaine patches were prescribed. Dosages of all drugs were adjusted depending on the side effects during the follow-up period. Epidural blocks were repeated twice with a 1-week interval and the continuous intravenous infusion of ketamine (60 mg) was performed over a period of 1 hour twice a week under careful monitoring. The dose of ketamine was increased gradually up to 120 mg. After 1 month elapsed, electric shock-like pain was reduced to a VAS score of 30/100, but allodynia was not diminished (VAS score of 70/100).
After 4 months elapsed, we decided to administer magnesium sulfate via the intravenous route. And it was done with continuous intravenous infusion of 1,000 mg of magnesium sulfate in 50 ml of normal saline for 1 hour. Before and after infusion, the serum magnesium levels were checked. After magnesium therapy, she felt very good about her pain and the VAS of allodynia was reduced to 40-50. At 1-week follow-up, she was very satisfied with the treatment and reported the reduction of allodynia on the dorsal scapular area of up to 50% (VAS 25-30/100). However, the serum magnesium level had increased above normal range (2.3 mEq/L to 2.9 mEq/L) after infusion. Although it was below the serum level reveals of the adverse effect, we decided to stop intravenous infusion of magnesium sulfate. For more accurate and safe delivery of magnesium to the target site, we applied magnesium using the transforaminal epidural injection technique.
With the patient's informed consent, left T3 TFEMI was performed under fluoroscopy guidance. The patient was placed in the prone position and draped in the sterile manner. A 22-gauge, 3.5-inch spinal needle was advanced into the left. T3 nerve root foramen under fluoroscopic guidance. The final needle placement was confirmed on posterior-anterior and lateral fluoroscopic images. Identification of the T3 nerve root sheath and epidural space was performed using contrast media (). Then, 100 mg of magnesium sulphate and 1 ml of 0.2% ropivacaine (total volume, 2 ml) was carefully injected. TFEMI was repeated twice with a 1-week interval (total of three times) and the degree of pain decreased gradually during the follow-up period.
One week after the last procedure, the VAS score of allodynia decreased to 15/100 and all medications except pregabalin were discontinued. The VAS was 10/100 throughout 1-month follow-up, and pregabalin had also been tapered. The patient remained free of symptoms at 6-month follow-up.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [162.0, 'cm']}",54.19299,51.48334,56.90264,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.77956 (in inches) - 60) = 54.19299 kg.
Hence, the patient's IBW is 54.19299 kg."
3766,10,Ideal Body Weight,physical,decimal,pmc-3948444-1,Extracted,"A 54-year-old male, 165.8 cm in height, weighing 55.6 kg was scheduled for PPPD and video-assisted thoracic surgery (VATS) due to a previously diagnosed duodenal cancer and a 1.1 cm-sized mass on the right apex of the lung, suspected to be a duodenal cancer metastasis. He had no other underlying disease but had a known large epiglottic cyst, which resulted in intubation failure and the cessation of surgery at a previous hospital. Laryngoscopic examination revealed a bulge arising from the center of the epiglottis and stretching to the glottis. It covered most of the epiglottis and occupied most of the pharyngeal space (). Despite the large size (> 2 cm) of this epiglottic cyst, the patient did not complain of any laryngeal symptoms such as dyspnea, dysphagia, hoarseness, and sleep apnea. A preoperative evaluation by an otolaryngologist concluded that the patient be kept under close observation as he did not show any symptoms. Preoperative airway assessment demonstrated excellent mouth opening and that the jaw could be thrust forward, corresponding to a class 1 Mallampati score. His temporomandibular joint activity, neck movement and thyromental distance were also normal.
The patient was informed at the preoperative visit about the likelihood of a difficult intubation, the procedures involved with an awake intubation, and the necessity for his cooperation with this procedure. In the operation room, we decided to perform an awake orotracheal intubation using CVS loaded with a left 37 Fr DLT (). The patient was premedicated intravenously with 0.2 mg glycopyrrolate, and 50 µg fentanyl. A superior laryngeal nerve block with 2 ml of 2% lidocaine was performed bilaterally and 10% lidocaine spray was applied to the oropharyngeal mucosal surface with direct laryngoscopic exploration. Preoxygenation was performed using a closed facemask with 100% oxygen delivery at 8 L/min over 10 minutes. The CVS loaded with a lubricated 37 Fr DLT was smoothly inserted into the posterior pharynx. After identifying the epiglottis and glottis opening, the distal tip of the CVS was carefully advanced below the mass to the glottis aperture (). The DLT was further advanced until the tracheal cuff passed through the vocal cord. After endotracheal intubation was confirmed by auscultation of the bilateral breath sound and end-tidal CO2 detection, the patient was given propofol 140 mg and vecuronium bromide 10 mg intravenously.
The time taken to complete awake intubation was less than 1 minute. Spontaneous breathing was maintained and no desaturation occurred during the entire procedure. General anesthesia was maintained with a 2-3 vol% of sevoflurane with 50% oxygen and medical air mixture. After the position change for VATS, the final position of the DLT was confirmed by flexible fiberoptic bronchoscopy (FOB) (Olympus LF-DP; Olympus optical Inc., Tokyo, Japan). At the completion of VATS, the patient's position was changed to supine and the PPPD preceded without an endotracheal tube change. Although the DLT is a larger tube with the potential to cause more airway trauma or edema postoperatively, we decided not to change the tube because this would have caused an even higher risk to the patient from possible cyst damage or intubation failure.
After these surgical procedures were completed, the patient was fully awakened and extubated. The patient was then transferred to the general ward via a recovery room with no respiratory or hemodynamic complications.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.8, 'cm']}",62.13395,59.02725,65.24065,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.8 cm, which is 165.8 cm * 0.393701 in/cm = 65.27563 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.27563 (in inches) - 60) = 62.13395 kg.
Hence, the patient's IBW is 62.13395 kg."
3767,10,Ideal Body Weight,physical,decimal,pmc-3795405-3,Extracted,"A 72-year-old woman, 155.0 cm tall and weighing 57.0 kg with no history of OA visited our hospital. Bilateral hip joint pain started about 5 years ago; since then, bilateral joint pain has improved and worsened repeatedly. She first visited our hospital about 6 months ago and complained of continuous right hip joint pain (P4). Her left hip joint pain has improved (P1). Plain radiographs showed bilateral hip OA of KL grading III (Fig. ). MRI analysis showed no signal changes in the left hip joint, and bone cysts and local signal changes in her right femoral head (Fig. , ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3768,10,Ideal Body Weight,physical,decimal,pmc-3176407-1,Extracted,"A 20-year-old female college-level soccer player presented to the senior author’s clinic due to symptoms of left knee instability. Her height was 177.8 cm, and her weight was 70.3 kg. Her past surgical history was remarkable for contralateral (right) knee ACL double-bundle reconstruction performed approximately 2 years prior to this visit. Two months ago, the patient suffered a non-contact cutting injury to her left knee (valgus and internal rotation of the tibia) during a game. She heard a pop in the left knee, immediately felt pain, and was unable to continue playing. She had a positive Lachman test and positive pivot shift test. Interestingly, 1 month before her injury, she had been involved in a clinical research program comparing the MRI studies of reconstructed and normal anterior cruciate ligaments. Thus, we were able to obtain a pre-injury 3T MRI of the left knee joint. On the MRI image, we found an abnormal band originating from the medial meniscus, coursing in the front of the ACL (Fig. ). Post-injury MRI revealed increased signal and complete loss of continuity of the ACL fibers. The corresponding sagittal MRI slice showed a slackened low-signal band which we suspected as an AIMM.
During the arthroscopic examination, a white-colored, round band could be seen running from the medial meniscus to the torn ACL remnant (Fig. a). The distal end of this structure fanned out in the shape of a “hockey stick blade.” The proximal end of the abnormal band was directed toward the femoral ACL insertion site and attached on the bony surface adjacent to the remnant ACL tissue on the ACL insertion site. Next, careful examination was performed to determine the tear pattern of the meniscus. The medial meniscus that was attached to the abnormal band was torn along the inner meniscus from the anterior insertion site on the tibial plateau to the anteromedial corner of the medial meniscus (Fig. b). The torn inner meniscus was still attached to the outer meniscus, similar to a posterior-based flap tear.
After inspection, the abnormal band and torn meniscus were excised using a basket forcep. Abrasion was performed by a motorized shaver. Finally, the planned double-bundle ACL reconstruction was performed [].","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [177.8, 'cm']}",68.50009,65.07509,71.92509,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 177.8 cm, which is 177.8 cm * 0.393701 in/cm = 70.00004 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (70.00004 (in inches) - 60) = 68.50009 kg.
Hence, the patient's IBW is 68.50009 kg."
3769,10,Ideal Body Weight,physical,decimal,pmc-6158874-1,Extracted,"The patient was a 79-year-old man with chief complaints of exertional dyspnea, leg edema, and weight loss. On transthoracic echocardiography (TTE), a 25 × 40 mm mobile pedunculated mass continuous with the right ventricular heart muscle was detected in the right atrium and the patient was admitted to our department for close examination and treatment. At admission, his height was 162.0 cm, body weight was 61.1 kg, body temperature was 36.3 °C, pulse was 62 beats/min, blood pressure was 112/59 mmHg, and SpO2 was 100% (room air). Pulmonary sounds were clear with no crackles, and heart sounds were regular with no murmur. Leg edema was present.
Plain chest radiography revealed a cardiothoracic ratio of 49% with no cardiac dilation. Electrocardiography revealed a sinus rhythm with a heart rate of 71 beats/min with nonspecific ST-T segment changes. Blood chemistry revealed the following: white blood cell (WBC) count of 51.9 × 104/μL, hemoglobin (Hb) of 14.9 g/dL, platelet (Plt) count of 16.3 × 104/μL, creatine kinase (CK) of 81 U/L, creatine kinase-MB (CKMB) of 8 ng/mL, lactate dehydrogenase (LDH) of 161 U/L, C-reactive protein (CRP) of 0.10 mg/dL, carcinoembryonic antigen (CEA) of 0.7 ng/mL, prostate-specific antigen (PSA) of 1.2 ng/mL, squamous cell carcinoma (SCC) antigen of 1.2 ng/mL, and soluble IL-2 receptor: 633 U/mL. Inflammatory parameters were within the normal range and the soluble IL-2 receptor level was slightly elevated, but the levels of other tumor markers were within their normal ranges. A coronary computed tomography (CT) scan showed no significant stenosis. It was deemed very difficult to completely excise, so we decided on partial tumor resection with MICS to reduce the risk of tumor embolism and to obtain an accurate pathology diagnosis. Therefore, we did not perform CAG. If we had performed a CAG, we may have seen arteries feeding the tumor.
TTE showed a 40 × 30-mm mobile pedunculated tumor in the right atrium that was continuous with the right ventricular heart muscle (Fig. ). Transesophageal echocardiography (TEE) showed a solid septated tumor with an irregular surface invading the free wall of the right atrium and surrounding the annulus of the anterior cusp and right and left coronary cusps of the aortic valve (Fig. ). Contrast-enhanced CT showed invasion based on soft tissue intensity near the tricuspid valve above the anterior right ventricle in the region between the aorta and pulmonary artery and around the pulmonary artery (Fig. , ). Cardiac magnetic resonance imaging (MRI) showed a thickened anterior wall near the tricuspid valve and a mass protruding into the lumen and expanding into the region between the aorta and the pulmonary artery (Fig. , ); in addition to the patient’s advanced age, these features made it difficult to perform extended cardiac surgery. On fluorodeoxyglucose positron emission tomography (F-18 FDG-PET), there was abnormal accumulation in the right atrium surrounding the aortic root (Fig. ).
Surgery was performed to prevent tumor embolism-induced sudden death and to obtain a pathological diagnosis. Anticoagulation was not performed preoperatively because it was unlikely that the tumor was a thrombus. A double-lumen tube was inserted during surgery and a Swan-Ganz catheter and 14-Fr cannula were inserted through the right internal jugular vein after draping. In a supine position with 30° elevation of the right side, a 4-cm skin incision was made in the fourth intercostal region at the medial aspect of the nipple. Meanwhile, the femoral artery (FA) and femoral vein (FV) were exposed. A pericardiotomy was performed 2 cm anterior to the phrenic nerve and the pericardium was elevated. After systemic heparinization, an 18-Fr blood supply tube was inserted through the right FA, and a 25-Fr cannula was inserted through the right FV to establish a cardiopulmonary bypass (CPB). The superior vena cava was blocked with a bulldog clamp and the heart rate was controlled at 40–50 bpm with a β-blocker. An oblique incision was made in the right atrium with the heart beating, and the lumen was observed. The tumor adhered to the anterior surface of the right atrium but not to the annular region and had marked mobility. The tumor was grasped with an Endocatch and the pedicle of 1-cm width was transected using electric cautery (Fig. ). The lack of any residual right atrial tumor or shunt was confirmed and the right atrium was closed in a double suture pattern; the patient was then weaned from CPB. The pericardium was closed as far as possible, the wound was closed by the standard method, and surgery was completed. The operative time was 1 h 56 min, and the duration of CPB was 38 min (Additional file ).
Intraoperative macroscopic findings revealed a tumor with a smooth, greyish-white surface (Fig. ). A blackish-brown region suggestive of hemorrhage was present inside and on pathological examination (Fig. ), a diffuse proliferation of round cells with a high nuclear-to-cytoplasmic (N/C) ratio were observed on hematoxylin and eosin staining. The tumor cells were mainly medium- and small-sized cells that contained nuclei with a shallow cut that were the same size or slightly smaller than the nuclei of vascular endothelial cells; large cells were also present. Broken nuclear products and histiocytes phagocytosing these products were also observed. Upon immunohistological staining, the tumor cells were CD79α-positive and CD3-negative. B-cell-derived cells were overwhelmingly predominant, which suggested that the lesion was a B-cell-derived tumor. Epithelial membrane antigen (EMA) immunostaining was negative. Based on these findings, the patient was diagnosed with diffuse large B-cell lymphoma (DLBCL).
Extubation was performed 6 h after surgery and the patient was transferred to a general ward 2 days after surgery. The disappearance of the tumor from the annular region was confirmed on TTE 5 days after surgery and the patient was discharged when he was able to independently walk 6 days after surgery. After observation at an outpatient clinic, rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) therapy was initiated 37 days after surgery. After 8 cycles were administered in total, an FDG-PET scan performed 456 days after surgery showed no abnormal accumulation (Fig. ), indicating CR.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [162.0, 'cm']}",58.69299,55.75834,61.62764,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (63.77956 (in inches) - 60) = 58.69299 kg.
Hence, the patient's IBW is 58.69299 kg."
3770,10,Ideal Body Weight,physical,decimal,pmc-8473927-1,Extracted,"A 30-year-old Chinese woman was evaluated for gradually enlarging localized plates over the scalp hairline, which later coalesced into large plaques that were present over the past 11 years. New lesions had progressively appeared on the bilateral temporalis over the last 5 years, and these lesions increased and merged into plate-like plaques. She is 160 cm tall and weighs 70 kg. No history of previous traumatic or inflammatory processes was determined. Family history denied a history of skin and subcutaneous ossification.
On dermatological examination, three hard, painless, and free movable irregular pinked plaques were located in the forehead region, in the left temple region and in the right temple region. These lesions were approximately 9.5 cm x 9 cm, 7.5 cm x 5 cm and 7 cm x 7 cm in size (). There was a surrounding pink-red nodule. She had no features of acromegaly or myxedema, and her toes and long bones are of normal thickness. Serum calcium and phosphate, renal function, parathyroid hormone, and vitamin D levels were in the normal range. Skin biopsy showed lamellar bone tissue distributed in the dermis. Osteocytes were in the bone tissue, and osteoblasts were seen around the bone tissue (). The pathological diagnosis was osteoma cutis. Owing to the paucity of associated findings, a diagnosis of acquired plate-like osteoma cutis was made.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3771,10,Ideal Body Weight,physical,decimal,pmc-6389502-1,Extracted,"The patient was a 34-year-old Japanese man, whose family history included a father with hypertension, and a mother that suffered a subarachnoid hemorrhage, but which did not include either a consanguineous marriage or any incidence of renal cysts. At the age of 31, the patient presented with mild albuminuria, and a serum creatinine (Cr) level of 2.98 mg/dL. At the age of 34, the patient was admitted to hospital with a creatinine level of 8.2 mg/dL.
Upon admission, the patient's height, weight, and blood pressure were 179 cm, 58 kg, and 126/80 mm Hg, respectively. The patient exhibited anemia (Hb 8.2 g/dL), azotemia (Cr 8.38 mg/dL), hyperphosphatemia, metabolic acidosis, and secondary hyperparathyroidism; thus, he was diagnosed with ESRD. An abdominal ultrasonography revealed that, although the size of both kidneys appeared to be normal, the patient's renal parenchyma showed increased brightness. We performed a percutaneous renal biopsy; histologically, six of 16 glomeruli displayed global sclerosis, along with mild cellular infiltration, conspicuous interstitial fibrosis, renal tubular atrophy, and cystoid irregular dilation (Figure ), suggesting an NPHP diagnosis. We performed targeted sequencing using a next-generation sequencer, with the approval by the research ethics committee of Tokyo Medical and Dental University in accordance with the Declaration of Helsinki and the patient's written informed consent. A homozygous full gene deletion of NPHP1 (NM_000272.3:g110879716-110962709) was resultantly identified, as well as heterozygous substitutions in PKD1 (NM_0001009944.2:c.6395T>G(p.Phe2132Cys)) (Figure ), BBS1 (NM_024649.4:c.908T>C(p.Val303Ala)), and INPP5E (NM_019892.4:c.1652C>T(p.Thr551Met)).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [179.0, 'cm']}",74.0867,70.38236,77.79103,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 179.0 cm, which is 179.0 cm * 0.393701 in/cm = 70.47248 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.47248 (in inches) - 60) = 74.0867 kg.
Hence, the patient's IBW is 74.0867 kg."
3772,10,Ideal Body Weight,physical,decimal,pmc-6862922-1,Extracted,"A 21-year-old man (height, 158 cm; weight, 40 kg) was scheduled for wedge resection with video-assisted thoracoscopic surgery for treatment of pneumothorax. The patient had visited our hospital because of sudden chest discomfort the day before admission. He had been diagnosed with CMTD 14 years previously. Surgical treatment of scoliosis had been performed 6 years previously, and chest tube insertion for treatment of right pneumothorax had been performed 3 years previously. The patient had also undergone surgery for CMTD-related bilateral foot deformities and arm dislocation. He reported that the surgery and anesthesia were uneventful at that time. Although the operations for the scoliosis, foot deformities, and arm dislocation had been conducted under general anesthesia, no other information was available because the operation had been performed in another hospital. The patient had muscle weakness in both upper extremities (manual muscle testing grade 2−), and only smartphone manipulation was possible using finger movements. Atrophy and deformation of both feet were noted (), and the patient was unable to stand up on his own. His condition was so severe that even using a wheelchair was not possible. Neck movements were normal, and physical examination showed atrophy of the peroneal muscles of both lower extremities (manual muscle testing grade 1) with normal sensory function. The tendon reflexes were decreased in the knees and ankles. Additionally, atrophy was present in the upper extremities.
The patient’s mouth opening width was normal, thyromandibular length was >5 cm, Mallampati classification was class II, and American Society of Anesthesiology physical status was grade III. Preoperative laboratory studies showed no abnormal findings. Chest radiographs showed right chest tube insertion for treatment of right pneumothorax accompanied by fixation of the thoracolumbar spine with scoliosis (, ). Electrocardiography (ECG) revealed signs of left anterior fascicular block, and the patient’s vital signs were as follows: blood pressure (BP), 120/60 mmHg; heart rate (HR), 64 beats/minute; body temperature (BT), 36.6°C; oxygen saturation, 100%; and respiratory rate (RR), 20 breaths/minute.
Premedication was not given because the patient had CMTD with pneumothorax. The patient was transferred to the operating room and underwent noninvasive BP, ECG, pulse oximetry, and bispectral index monitoring. Additionally, a neuromuscular monitoring (NMT) module (IntelliVue NMT module, Model 865383; Philips, Amsterdam, Netherlands) was set up. Before induction, the patient’s vital signs were as follows: BP, 116/63 mmHg; HR, 84 beats/minute; BT, 36.4°C; oxygen saturation, 100%; and RR, 12 breaths/minute.
Anesthesia was induced with 2% propofol (Fresofol 2%; Fresenius Kabi, Bad Homburg, Germany) and remifentanil (Ultiva; GlaxoSmithKline, Brentford, UK) administered at an effect-site concentration of 2.5 μg/mL and 2 ng/mL, respectively, using a target-controlled infusion pump (Orchestra Base Primea; Fresenius Vial, Brezins, France) under 100% oxygen inhalation (6 L/min). A neuromuscular block was achieved using intravenous injection of 15 mg of rocuronium. However, as the patient’s respiration continued, 5 mg of rocuronium was administered again after 2 minutes.
A 35-Fr left-sided double-lumen tube was inserted without difficulty. Anesthesia was maintained with 2% propofol at 1.5 to 2.5 μg/mL and remifentanil at 1 to 2 ng/mL (effect-site concentration) using a target-controlled infusion pump for TIVA, with 1 L/minute of oxygen and 2 L/minute of air.
For one-lung ventilation, the pressure-controlled ventilation–volume guaranteed mode was used with a tidal volume of 250 mL, RR of 14 breaths/minute, and peak airway pressure of 25 cmH2O. The patient was switched to the left lateral decubitus position for the video-assisted thoracoscopic surgery. However, the patient’s muscle relaxation was insufficient, and there was a collision between the ventilator and self-respiration. Therefore, 5 mg of rocuronium was administered again.
No adverse events occurred during the surgery, and 0.4 mg of glycopyrrolate and 15 mg of pyridostigmine were administered to reverse the neuromuscular block. The endotracheal double-lumen tube was removed after confirming that the patient had recovered spontaneous breathing and consciousness.
The total duration of anesthesia was 55 minutes, and that of the surgery was 25 minutes. The patient was transferred to the post-anesthesia care unit, and his vital signs were as follows: BP, 112/78 mmHg; HR, 68 beats/minute; BT, 36.5°C; oxygen saturation, 100%; and RR, 24 breaths/minute. After the patient was monitored for about 1 hour in the post-anesthesia care unit, he was transferred to the ward.
No abnormalities were found on the postoperative laboratory studies, chest radiographs or ECG or with the patient’s movement and respiration. The patient was discharged on postoperative day 3.
This study was approved by the institutional review board of Eulji University Medical Center and was performed in compliance with the EQUATOR Network guidelines. Written informed consent for publication was obtained from the patient and his parents.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [158.0, 'cm']}",55.07095,52.3174,57.8245,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.20476 (in inches) - 60) = 55.07095 kg.
Hence, the patient's IBW is 55.07095 kg."
3773,10,Ideal Body Weight,physical,decimal,pmc-5564066-1,Extracted,"A 25-year-old female patient (weight: 52 kg and height: 162 cm) with dentofacial anomalies having both anterior edge to edge bite relationship and facial asymmetry was scheduled to have Le Fort I osteotomy and bilateral sagittal split osteotomy (BSSRO) surgery under general anesthesia. The patient was also diagnosed with factor XI deficiency with an increased activated partial thromboplastin time (aPTT) of 87.5 seconds (normal: 26-35.3 seconds), and a factor XI activity of 5% (normal: 60-150%). Other laboratory values, including prothrombin time and international normalized ratio (PT INR) (1.06, normal: 0.8-1.2), and PT % (91.0%, normal: 80-120%) were within normal limits. The hemoglobin (Hb), hematocrit (Hct) and platelet counts were 12.8 g/dl (normal: 12-16 g/dl), 37.6 (normal: 36-48%), and 194,000/mm3, respectively. A chest radiograph, electrocardiogram (ECG), and other laboratory findings were unremarkable. The decision was made to operate on the patient using both the SpHb and rotation thromboelastometry for effective perioperative management.
During surgery, the patient's ECG, noninvasive blood pressure, percutaneous oxygen saturation, temperature, and arterial line were actively monitored. Intravenous thiopental 175.0 mg was used to induce anesthesia. The patient was intubated nasally after the administration of cisatracurium 12.0 mg. Anesthesia was maintained with 5-6% desflurane, 50% nitrous oxide and oxygen. The patient's vital signs were stable throughout the procedure (). The surgery time was total 250 minutes and the anesthesia time was 300 minutes. There was a total of 560 ml blood loss, and 500 ml of urine output. The patient's Hb levels were continuously checked through the SpHb values (). Four units of fresh frozen plasma (FFP) and two autologous units of blood (360 ml) were used during surgery based upon the continuously monitored blood levels of Hb. At the end of surgery, the patient's Hb was 8.1 g/dl and Hct was 27%. The patient was extubated with the removal of the endotracheal tube when she resumed spontaneous breathing but before she recovered consciousness. The patient was transferred to the recovery room. The ROTEM™ analysis showed normal variables in the extrinsically activated test (EXTEM) and intrinsically activated test (INTEM) ().
After surgery but before the patient's discharge, her bleeding tendency was investigated using coagulation tests including aPTT. Seven days after surgery, aPTT was slightly elevated at 48.4 seconds. The patient was discharged without any complications.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [162.0, 'cm']}",54.19299,51.48334,56.90264,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.77956 (in inches) - 60) = 54.19299 kg.
Hence, the patient's IBW is 54.19299 kg."
3774,10,Ideal Body Weight,physical,decimal,pmc-3071489-1,Extracted,"A 53-year-old female patient, 161 cm and 46 kg was diagnosed with mechanical ileus and admitted for adhesiolysis. She underwent total gastrectomy for cancer of stomach 2 months ago and had received adjuvant chemotherapy three weeks ago; 2nd time with S-1 (TS-1®, Jeil Pharmaceutical Co., Ltd, Seoul, Korea) 60 mg bid, for 14 days plus cisplatin (Cispuran®, Dong-A Pharmaceutical Co., Ltd, Seoul, Korea) 60 mg/m2 on day 1. There was no previous history of cardiopulmonary disease, allergies, tuberculosis exposure, or smoking.
On her visit to emergency room, vital signs of the patient were as follows: body temperature, 37.2℃; heart rate, 106 beats/minute with a regular rhythm; SpO2, 100% (on room air); and blood pressure, 116/86 mmHg. Physical examination revealed distended and diminished bowel sounds. Laboratory findings on ER were: white blood cell (WBC) count, 3.3 × 103/mm3; hemoglobin (Hb), 12.8 g/dl; platelet count, 184 × 103/mm3; C-reactive proteins (CRP), 0.56 mg/dl; PT (INR), 1.05 (normal, 0.8-1.3); and activated PTT, 20.9 sec (normal, 25.0-35.0). A preoperative chest X-ray, pulmonary function test and electrocardiogram were within the normal range. She was premedicated by oral midazolam (3.75 mg).
After the patient was taken to the operating room, she was on ECG standard leads II, noninvasive monitors for blood pressure, heart rate, arterial oxygen saturation, capnogram, and bispectral index. The patient underwent 3 minutes of denitrogenation with 100% oxygen through a facemask following which 2% propofol and remifentanil with the Master target controlled infusion was given (Orchestra® Base Primea; Fresenius-MCM GmbH, Germany) after administration of lidocaine (40 mg). After confirming loss of consciousness, rocuronium (0.5 mg/kg) was administered. Endotracheal intubation was then performed without any complications. After verifying that patient continued to have clear breath sounds in both lung fields, the tube was fixed at a depth of 20 cm at the level of incisor teeth. The ETCO2 was monitored by capnogram and maintained at 35-40 mmHg.
During the operation, 700 ml of Hartmann solution was administered. After discontinuing the anesthetics, she began to respirate spontaneously. A mixture of glycopyrrolate (0.4 mg) and pyridostigmine (15 mg) were administered for muscle recovery and the endotracheal tube was carefully extubated. She was awake fully and had no complaints of any discomfort or respiratory disturbance except for the surgical site pain, and she was therefore transported to the post anesthetic care unit. Oxygen at 5 L/min was administered through a Venturi mask when the pulse oximetry indicated a SpO2 of 97%.
Fifteen minutes after extubation, the pulse oximeter indicated SpO2 of 70%. A sudden onset of dyspnea and hemoptysis developed. The patient was promptly intubated and approximately 50 ml of fresh blood was suctioned through the endotracheal tube. A bronchoscopy was immediately performed to determine the cause of hemoptysis and hypoxia. The apparent bleeding was localized to originate from right upper lobe in the beginning, but the bleeding continued to become bilaterally with no identifiable bleeding focus (). The chest radiograph revealed bilateral diffuse alveolar infiltrates (). Arterial blood gas analysis after endotracheal intubation and mechanical ventilator applied were: arterial oxygen tension (PaO2), 55 mmHg; arterial carbon dioxide tension (PaCO2), 47 mmHg; pH, 7.31; Hb, 10.5 g/dl.
The patient was transferred to the intensive care unit (ICU) due to her unstable vital signs. The vital signs measured upon arrival showed a blood pressure of 80/50 mmHg, heart rate of 162/min and SpO2 of 90% and Swan-Ganz catheter was inserted. The blood test results revealed the following: Hb, 8.7 g/dl; hematocrit, 26%; platelet count, 57,000/mm3; WBC count, 900/mm3; absolute neutrophil, 640/mm3. The PT was 19.8 sec and the activated PTT was 37.1 sec. The vasopressor drugs such as dopamine, norepinephrine and vasopressin were infused to stabilize the blood pressure and hydrocortisone (300 mg) was injected. Five units of packed RBCs, 6 units of fresh frozen plasmas and 10 units of platelets were transfused for 7 hours. A bronchoscope was performed again at the ICU by pulmonologist after the vital signs were stable. The bronchoscopy revealed presence of alveolar hemorrhage in both lungs and no focal bleeding sources again. Urinary analysis with microscope and serologic laboratory were checked.
Five days after the intubation, the patient sufficiently recovered and subsequently mechanical ventilation was discontinued. On the postoperative day 6, there was no evidence of alveolar hemorrhage by bronchoalveolar lavage (BAL). Bilateral infiltration resolved and confirmed by high resolution computed tomography (HRCT) scan images (). The patient became symptom-free and was discharged from the hospital 20 days after the surgery. S-1 was excluded from the chemotherapy regimen in this patient and no recurrences of symptoms were observed after discharge.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [161.0, 'cm']}",53.28748,50.62311,55.95185,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 161.0 cm, which is 161.0 cm * 0.393701 in/cm = 63.38586 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.38586 (in inches) - 60) = 53.28748 kg.
Hence, the patient's IBW is 53.28748 kg."
3775,10,Ideal Body Weight,physical,decimal,pmc-3315621-1,Extracted,"A 14-year-old girl was admitted to the hospital after becoming acutely drowsy and suffering three generalized, tonic-clonic seizures, each episode lasting more than 10 minutes. Three days before admission, she had a fever of up to 38℃, muscle weakness, polyarthralgia, and an erythematous papular skin rash on both hands. Her history and family history included no psychiatric diseases, seizures, or other medical problems. She was an above-average eighth-grade student. Her initial vital signs were stable, with a body temperature of 36.5℃, heart rate of 92 beats per minute, respiratory rate of 24 breaths per minute, and blood pressure 91/50 mmHg. She was 163.5 cm tall (75 to 90th percentile) and weighed 59.2 kg (75 to 90th percentile), for a body mass index of 22.1 kg/m2. On physical examination, her heart, lungs, liver, and abdomen were normal and she had no palpable goiter. A formal neurological examination did not reveal any focal abnormal findings. The initial laboratory findings were as follows: white blood cell count 8,000/mm3, hemoglobin 13.7 g/dL, platelet count 221,000/mm3, and C-reactive protein 0.09 mg/dL. Routine biochemical analyses of serum, blood gases, electrolytes, blood ammonia, and lactate were within normal limits. The cerebrospinal fluid (CSF) analysis showed normal pressure and a normal cell count and protein and glucose levels. Cultures of blood and CSF were sterile. Serum and CSF examination for herpes, zoster, enterovirus 71, influenza, Ebstein-Barr virus, and mycoplasma were negative. Brain magnetic resonance imaging (MRI) was normal. Electroencephalography (EEG) showed generalized slow waves with diffuse cortical dysfunction, without any epileptiform discharges. In the acute stage, the seizures did not respond to conventional antiepileptic drugs, including valproic acid (20 mg/kg/day), phenytoin (5 mg/kg/day), and topiramate (100 mg). On the 4th day, she reported visual hallucinations before the onset of seizures; these consisted of a blue circle and unknown men wearing blue shirts in one event and unknown men wearing red shirts in another. She also showed personality changes, mood swings between depressive and maniac states, difficulty with concentration, insomnia, and agitation. The etiology of the acute encephalopathy (i.e., the mental changes, seizures, and psychosis) was not clear. Therefore, we checked her autoimmune status. The serum anti-nuclear antibodies, rheumatic factor, and anti-DNA screening were negative. TFTs were normal (TSH, 4.78 µIU/mL, free T4, 1.33 ng/dL, and T3, 89 ng/dL), but the anti-thyroid antibodies were elevated: the thyroperoxidase antibody titer was 280 IU/mL (normal<100) and the antithyroglobulin antibody was 138 IU/mL (normal<100). Given the indications for Hashimoto's encephalopathy, she was subsequently started on intravenous methylprednisolone therapy, beginning at 1 g intravenously per day for 3 days, followed by prednisone 60 mg orally per day. The patient's clinical improvement was impressive and her neuropsychiatric symptoms resolved. On the 14th day, she was discharged. On follow-up as an outpatient, she had been symptom free for 1 month and her anti-thyroid antibodies level was normal. However, the seizures recurred while tapering the steroid.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [163.5, 'cm']}",55.55125,52.77369,58.32881,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 163.5 cm, which is 163.5 cm * 0.393701 in/cm = 64.37011 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.37011 (in inches) - 60) = 55.55125 kg.
Hence, the patient's IBW is 55.55125 kg."
3776,10,Ideal Body Weight,physical,decimal,pmc-7516164-1,Extracted,"Patient 1 was a 37-years-old single female (height, 155 cm; weight, 49.1 kg; blood pressure, 108/48 mmHg) with chief complaints of cold sensitivity, tinnitus, dizziness, headache, and irregular menstruation. The patient had no noteworthy family medical history or genetic information. She had no yellowing of the conjunctiva bulbi; no conjunctival anemia; no cervical, thoracic, or abdominal abnormalities; and no edema on the anterior tibia. Considering that the patient was somewhat ectomorphic and tended to experience worsening of symptoms during menstruation, tokishakuyakusan extract granules (5.0 g/day), which are effective for treating cold sensitivity and headaches, were prescribed (). After taking tokishakuyakusan extract granules, symptoms including cold sensitivity, tinnitus, dizziness, and headache were alleviated; however, her menstrual cycle had remained irregular. Three years after the initiation of the Kampo treatment she had no menstruation for more than 2 months, so Kampo treatment was started anew for the irregular menstruation.
Subjective symptoms included cold sensitivity of the lower body, tinnitus, and lower back pain, in addition to irregular menstruation; thus, the prescription was changed from tokishakuyakusan extract granules to HJG extract granules (5.0 g/day). Two months later, she reported no menstruation despite continuous administration of HJG extract granules.
The patient's chief complaint was irregular menstruation with subjective symptoms including cold sensitivity of the lower body and lower back pain. In addition, she was somewhat thin and had weakness of the lower abdominal region. Thus, treatment with HJG was expected to be effective for this patient, and as a result, treatment was changed to HJG pills (40 pills/day) instead of simply increasing the dose of HJG extract granules.
One month after the administration of HJG pills, the patient had menstruation for 5 days. She continued taking the medication and menstruated again, but her cycle was abnormally long at around 40 days. Hence, the dose of HJG pills was increased from 40 to 60 pills/day. Since then, her menstrual cycle has become ~30 days.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3777,10,Ideal Body Weight,physical,decimal,pmc-3118944-1,Extracted,"33 years old male patient was referred to Department of Otolaryngology, Medical University of Warsaw, due to isolated longstanding hoarseness. At first visit weight was 98.5 kg, and height: 186 cm. The patient had no medical history (diagnoses or operations), was non-smoker and was not under any treatment.
In May 2005, the patient underwent a direct laryngoscopy. During the procedure, samples of the tumor located in right side of glottis were collected for pathologic examination. Due to indistinct result of the first histo-pathological examination, the direct laryngoscopy was repeated in June 2005 at the Department of Otolaryngology of the Medical University of Warsaw, where the tumor was subsequently resected and examined by a pathologist. A second histopathological examination revealed fragments of edematous mucous membrane partially covered with columnar epithelium, nondysplastic and paraepidermal in majority. In the stroma, active granulation was identified. Moreover numerous ""bizarre"" pleomorphic stromal cells and proliferating epithelial cells were identified. Due to the lack of correlation between the result of the pathological examination and the clinical manifestation, the slides were sent to The Maria Sklodowska-Curie Memorial Cancer Centre and the Institute of Oncology in Warsaw for revision and additional specification. This consultation revealed rhabdomyosarcoma embryonale. For treatment planning in August 2005, computed tomography (CT) examination of the larynx was performed with contiguous 2.7 mm thick slices and showed a poorly delineated tumor located on the right side of the larynx, invading the vocal fold and the ventricular fold, contracting the pyriform recess and constricting the glottis. Contrast enhancement in the tumor was observed in the CT scans (Figure ).
Due to the rarity of this type of tumor in laryngeal localization two cycles of VAC1 induction chemotherapy were administered (VAC1-vincristine, D-aktynomycine and cyclophosphamide: 1.5 MG/M2 IV day 1, 0.3 MG/M2 IV days 1-5, 150 MG/M2 IV days 1-5; every 28 days). The first chemotherapy cycle began on September 8th 2005. It was followed by chemo-radiotherapy in November and December 2005. Radiotherapy was administered in fractions of 200 cGy and total dose of 7000 cGy over 6 weeks. In parallel two cycles of maintenance VAC1 chemotherapy were given. CT was performed on the February 1st 2006 and revealed no tumor regression according to RECIST criteria. In accordance to CT scan no significant clinical response was observed. Subsequently on February 3rd 2006 vertical hemilaryngectomy was performed. Postoperative histopathological examination confirmed rhabdomyosarcoma located in the right side of the larynx. All examined margins were negative for cancer cells. The patient was discharged from the hospital with tracheostomy and nasogastric tube.
First cycle of adjuvant chemotherapy was administered on April 21st 2006. Chemotherapy was continued until August 24th 2006. In total the patient received twelve cycles of VAC1, with 50% dose reduction after V cycle due to neutropenic fever in November 2005. The patient had the nasogastric tube removed in May 2006 and was decaniulated in October 2006. Following the surgery, the patient was monitored by a laryngologist and oncologist and underwent regular fiberoptic examinations of the larynx and direct laryngoscopy in case of unclear fiberoptic examination results. Follow-up CTs were performed in October 2006, June 2007, November 2007, June 2008 and March 2009, and did not reveal any tumor recurrence (Figure ). Due to persistent swelling in the region of the arytenoid cartilage, a PET examination was performed on February 1st 2007. This examination did not reveal any focal lesions suggesting metastases. On March 2007, a check-up direct laryngoscopy with deep tissue biopsy was performed. The histopathological examination was negative. The patient remains under strict laryngological and oncological monitoring and no symptoms or signs of disease recurrence have been noticed. On June 24th 2010 patient had a follow-up PET-CT scan, which revealed normal glucose metabolism in the postoperative site (Figure ). No metastases or local recurrence were found until now (May 2011).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [186.0, 'cm']}",80.4253,76.40403,84.44656,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 186.0 cm, which is 186.0 cm * 0.393701 in/cm = 73.22839 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (73.22839 (in inches) - 60) = 80.4253 kg.
Hence, the patient's IBW is 80.4253 kg."
3778,10,Ideal Body Weight,physical,decimal,pmc-5732123-1,Extracted,"Our patient was a 54-year-old man who was originally diagnosed with a gastric SMT in 2008. He underwent an annual follow-up by upper GI endoscopy at another hospital but was referred to our hospital for further examination and treatment in September 2016, during which his main clinical symptoms were epigastric soreness, general malaise, and melena. He had an unremarkable family history.
On admission, he measured 161.6 cm tall and weighed 58 kg and his pulse was 115 beats/min, and blood pressure was 69/43 mmHg. There were no significant findings on abdominal examination, but laboratory analysis revealed a hemoglobin level of 5.6 g/dl. Other hematological and biochemical parameters were within normal limits. Chest X-ray, electrocardiography, and echocardiography results were normal. On admission, because he had advanced anemia and low blood pressure, he received blood transfusion (480 ml). On upper GI endoscopy, an SMT was identified with an associated ulcer on the anterior wall of the lower body of the stomach (Fig. ). There was an extrinsically compressing mass on the anterior wall of the greater curvature and the posterior wall of the stomach (Fig. ). However, no active bleeding from the SMT or ulcer was observed.
We diagnosed lipoma without malignancy based on the biopsy of the SMT and ulcer. Endoscopic ultrasound (EUS) confirmed a high-echoic submucosal lesion in the antral wall that extended to the stomach body (Fig. ), and computed tomography (CT) and magnetic resonance imaging confirmed a fat-containing mass spanning entire gastric walls of the stomach antrum and body, but excluding the lesser curvature, with a mass protruding on the anterior wall of the greater curvature (Figs. and ). CT images revealed no metastasis to lymph nodes or to other organs, and the serum tumor markers CEA and CA19-9 were within the normal limits.
Based on our findings, we suspected a giant gastric lipoma and proceeded to perform a standard total gastrectomy. We considered the execution of resection of the stomach, but we decided to perform total gastrectomy because the range of the tumor was unclear and the risk of recurrence could not be determined. The specimen was opened along the greater curvature, revealing a mucosal surface that was smooth and diffusely elevated by the submucosal mass, but with no involvement of the lesser curvature (Fig. ). There was a compressing lesion associated with an ulcer on the anterior wall of the lower body. The gross pathology was of a yellowish adipose tissue with no fibrous capsules.
Gastric lipomatosis was confirmed by a histological examination of the resected specimen. Microscopy revealed adipocyte proliferation without nuclear atypia and mature adipocytes replacing the submucosal and muscle layers of the stomach. Lipomatosis was present only in the fundic gland zone, and there was no intestinal metaplasia or atrophic gastritis. Multiple hyperplastic polyps were observed on the mucosa overlying the area of diffuse lipomatosis. Immunostaining was negative for MDM2, CDK4, and p16. Moreover, there was no evidence of malignancy in the fatty lesion.
The patient recovered well following surgery and was discharged on the postoperative day 14. At the latest follow-up, he was continuing to do well and showed no evidence of recurrence in other organs.
Gastric lipomas are characterized by smooth, sharply marginated, and oval or spherical submucosal masses comprising well-differentiated adipose tissues surrounded by a fibrous capsule [–]. In contrast, gastric lipomatosis is characterized by multiple gastric lipomas or diffuse infiltration of mature adipose tissues into the gastric submucosal or subserosal layers. GI lipomas are extremely common benign colonic tumors, whereas gastric lipomatosis is particularly rare [, –].
Approximately, 90–95% of lipomas are submucosal, and the rest are subserosal []. Most gastric lipomas are small (4–9 cm) and asymptomatic, occur on the posterior wall of the antrum, and are incidentally detected on radiographic or endoscopic examination of the upper GI tract. Smaller lesions are rarely symptomatic, but large tumors can present with symptoms of gastric ulcer, including epigastric pain, nausea, vomiting, and upper GI tract bleeding. Indeed, the most frequent clinical manifestation is GI bleeding, which is due to the ulceration of the overlying mucosa in 50% of the patients [, ]. When a large lipoma is present, venous stasis is probably the single most important factor underlying mucosal ulceration, which may lead to acute, and sometimes severe, upper GI hemorrhage. Several authors have reported anemia as the primary indicator of large gastric lipomas [–]. In the present case, we suspect that a part of the tumor rapidly increased in size and led to the collapse of the mucosal surface with subsequent ulceration and bleeding.
CT is an excellent diagnostic tool because it allows the diagnosis of lipoma based on tumor fat density, precluding the need for an endoscopic biopsy. Indeed, a homogeneous mass with a fat density ranging between − 70 and − 120 Hounsfield units is considered pathognomonic of gastric lipoma []. Histologically, GI tract lipomas typically have well-differentiated adipose tissue structures. If a large submucosal tumor is detected on an endoscopic or upper GI examination, then a CT scan can be used to confirm the diagnosis and to inform therapy decisions. However, EUS is the most useful diagnostic tool for assessing neoplasia originating from the submucosa. In the present case, EUS showed a submucosal hyperechoic and homogeneous mass and diagnosed lipoma.
Although conservative treatment is preferred for asymptomatic solitary lipomas, surgical intervention should be considered for symptomatic lipomas associated with ulcers or non-fatty elements. Endoscopic polypectomy is an option for submucosal lesions that are smaller than 3 cm, but larger broad-based tumors have a higher risk of perforation using this approach. In our case, we decided to treat the patient by total gastrectomy for three main reasons: first, a large and symptomatic lipoma was present at surgery; second, although biopsy suggested lipoma, we could not completely exclude malignancy; and third, anastomotic leakage and tumor recurrence were possible if partial resection was performed.
Eight reports of gastric lipomatosis exist in the literature, of which five describe a detailed pathology (Table ) [, , , –]. According to these reports, lipomatosis in the upper stomach can occur with multiple organ involvement or with multiple types of lipomatosis. However, no tumor has been reported in any other organ when lipomatosis occurs in the lower stomach. Most previous cases have reported multiple lipomas, and this is only the second case of gastric lipomatosis presenting as a diffuse lipoma []. In our case and in that by Jeong et al. [], the cases not only had similar specimens and histological findings but were also diagnosed as diffuse-type lipomatosis. In our case, it was noteworthy that the lipomatosis was present only in the fundic gland zone, without intestinal metaplasia or atrophic gastritis. Furthermore, multiple hyperplastic polyps were observed on the mucosa overlying the diffuse lipomatosis. We hypothesize that a relationship exists between hyperplastic polyposis and lipomatosis in some cases.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [161.6, 'cm']}",58.33078,55.41424,61.24732,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 161.6 cm, which is 161.6 cm * 0.393701 in/cm = 63.62208 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (63.62208 (in inches) - 60) = 58.33078 kg.
Hence, the patient's IBW is 58.33078 kg."
3779,10,Ideal Body Weight,physical,decimal,pmc-7328960-1,Extracted,"A 33-year-old Chinese male was referred for infertility consultation in our center after ten years’ primary infertility. His height was 182 cm and weight was 77 kg. The development/growth of penis was normal. And the left and right testicular volume is about 12 mL separately. Moreover, no other physical abnormalities were observed. A series of routine examinations were conducted. Semen analysis and levels of sex hormones were listed in Table . The male was finally diagnosed as severe oligozoospermia according to the semen routine examination.[ Our study protocol was approved by the Ethics Committee of the First Hospital of Jilin University (No.2016–430), and the informed written consents were obtained from the patient and his family members for publication of this case report and accompanying images.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [182.0, 'cm']}",76.80323,72.96307,80.64339,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 182.0 cm, which is 182.0 cm * 0.393701 in/cm = 71.65358 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (71.65358 (in inches) - 60) = 76.80323 kg.
Hence, the patient's IBW is 76.80323 kg."
3780,10,Ideal Body Weight,physical,decimal,pmc-7511777-1,Extracted,"An 83-year-old male was hospitalized five months after being recovered from pneumonia. His blood eosinophil level was ~10 × 103/μL. He was admitted to Showa General Hospital after presenting with hypoxaemia and multiple erythematous lesions. Physical examination during his initial visit revealed that he was 165.0 cm and 60.7 kg with a body temperature of 38.6°C and had a blood pressure of 138/84 mmHg, radial pulse rate of 106/min, respiratory rate of 28/min, and peripheral capillary oxygen saturation (SpO2) of 75% (room air)–92% (6 L/min oxygen). There were multiple erythematous lesions throughout his whole body. Fine crackles were heard in both his lungs upon auscultation. Laboratory work-up revealed leucocytosis with 21.8 × 103/μL, 48.0% eosinophils, and C-reactive protein levels of 12.88 mg/dL. Chest radiographs showed consolidation mainly in the left lung and right upper lung (Fig. ). Computed tomography showed a mixed pattern of air-space consolidation, air bronchogram, and ground-glass opacities (Fig. ). Skin biopsy revealed significant infiltration of eosinophils around the blood vessels in the dermis. His peripheral blood was negative for FIP1L1-PDGFRA with normal levels of serum immunoglobulin (Ig) E and Ig antinuclear antibodies. He was negative for MPO-ANCA and PR3-ANCA. He did not have sinus disease or nasal polyps. He was negative for HIV five years ago. Other possible causes of hypereosinophilia, such as parasite infection and drugs, were not detected. He was diagnosed with I-HES based on Chusid's criteria.
Figure shows the clinical course of the patient. He was commenced on prednisolone 40 mg/day with a plan to wean this over time after pulse steroid therapy for three days. His blood eosinophil count decreased, thereby improving the state of disease. He was prescribed a daily dose of 30 mg of prednisolone and discharged (Fig. ). Mepolizumab was added when the prednisolone dose was 25 mg/day. Unfortunately, at a prednisolone dose of 5 mg/day, there was evidence of disease progression. He was readmitted for hypoxaemia, SpO2 of 90% (room air), and multiple erythematous lesions. Chest radiographs and computed tomography showed ground-glass opacities and pleural effusion in both lungs (Fig. ). We diagnosed recurrence and the dose of prednisolone was increased to 40 mg/day, thereby improving the disease. The patient was switched to benralizumab. His blood eosinophil count was almost 0/μL and the disease has been in remission for about two years (Fig. ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3781,10,Ideal Body Weight,physical,decimal,pmc-3784233-1,Extracted,"A 72-year old man was referred to our outpatient clinic suspected of suffering from uveitis in his left eye. He initially presented 2 years ago with acute angle-closure glaucoma in his right eye that was treated with lowering the intra ocular pressure by local beta blockers and local prostaglandins followed by neodymium: YAG laser peripheral iridotomies in both eyes. Intraocular pressure values were 36 mmHg in the right eye and 18 mmHg in the left eye on admission and lowered to 16 mmHg in the right eye and 12 mmHg in his left eye before performing the iridotomies. After that, the IOP was within normal limits for 2 years, and there is no documentation of recurrent iritis in either eye in this period of time.
The patient had chronic renal failure, cardiac arrhythmia, and arterial hypertension.
On examination at referral, best-corrected visual acuity was 6/10 in his right eye and 6/12 in his left eye. Refraction was −2.5 spherical in the right eye and −3.25 spherical in the left eye. The intraocular pressure was 8 mmHg in his right eye and 26 mmHg in his left eye. He had bilateral neodymium: YAG laser peripheral iridectomies. Both eyes had a shallow anterior chamber. In the left eye, the lens was located slightly forward causing a pupillary block, and the anterior chamber angle was very narrow on indentation gonioscopy (). C/D ratio was 0.3 in the right eye and 0.4 in the left eye. Retina was normal in both eyes. Full-threshold visual fields were normal in both eyes. The sagittal lens diameter was 5.35 mm in the right eye and 5.70 mm in the left eye (the mean sagittal lenticular diameter in a young adult's eye is 3.7 mm ± 0.26 SD and in spherophakia 4.5 to 4.9 mm) [].
Ultrasonographic A-scan biometry recorded axial length of 22.2 mm in the right eye and 22.15 mm in the left eye. Ultrasound biomicroscopy with a 50 mHz probe showed a spherophakia lens in both eyes and pupillary block in the left eye due to forward subluxation of the lens (). On the basis of these findings, a diagnosis of spherophakia in both eyes was made. In light of the diagnosis of spherophakia the patients' medical history and examination were reviewed. The patient had no history of cardiovascular diseases or skeletal problems and had high intellect. The patient's height was 173 cm with normal skeletal proportions. There were no features of Marfan's syndrome, the Weill-Marchesani syndrome, or homocystinuria.
Chronic pupil block was believed to be responsible for the uncontrolled glaucoma in the left eye. At this stage, we performed lens extraction in the left eye by phacoemulsification, and we implanted a foldable 3-piece acrylic intraocular lens. The postoperative course was routine. The intraocular pressure was controlled with no antiglaucoma drugs, the anterior chamber depth was normal, and the final uncorrected visual acuity was 6/9.
The patient had the same surgical procedure in his right eye with an excellent outcome.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.0, 'cm']}",68.65362,65.22094,72.0863,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.0 cm, which is 173.0 cm * 0.393701 in/cm = 68.11027 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.11027 (in inches) - 60) = 68.65362 kg.
Hence, the patient's IBW is 68.65362 kg."
3782,10,Ideal Body Weight,physical,decimal,pmc-4031929-1,Extracted,"A 56-year-old Han Chinese woman (153cm, 39kg) with severe mitral valve stenosis and moderate mitral valve regurgitation was scheduled to undergo an MVR. She had a four-year history of mitral valve disease. She also had progressive dyspnea on exertion and moderate cardiac dysfunction classified as New York Heart Association class II or III. She was receiving vigorous diuretic and digoxin therapy.
An indirect (Seldinger) technique was used to achieve central catheterization through her right internal jugular vein (Arrow® central venous catheter, 7Fr, 20cm, 0.32 inches, two lumen; Arrow International, Asheboro, NC, USA). No arrhythmia was observed on the monitor while the J wire was advanced. After blood aspiration, the catheter was fixed at the 15cm mark. Her central venous pressure ranged between 7 and 13mmHg throughout the operation and she was transferred to our intensive care unit immediately after surgery.
A control anteroposterior chest radiograph of our patient was obtained on the second day after her operation. This graph revealed that the catheter tip was fixed at the superior vena cava (SVC)-right atrial (RA) junction which caused no attention (Figure ). Because our patient was unstable, the catheter was not removed and fluid replacement was performed via the CVC. Seven days later, replacement of the catheter was planned for clinically suspected catheter-related sepsis. There was obvious resistance while removing the catheter. Despite gentle traction and clavicular maneuvering, the catheter could not be removed. Additional posteroanterior and lateral chest radiographs were obtained, which showed that the catheter tip was still located in its previous position, the SVC-RA junction.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.0, 'cm']}",46.04337,43.7412,48.34554,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.0 cm, which is 153.0 cm * 0.393701 in/cm = 60.23625 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.23625 (in inches) - 60) = 46.04337 kg.
Hence, the patient's IBW is 46.04337 kg."
3783,10,Ideal Body Weight,physical,decimal,pmc-4421183-2,Extracted,"A 20-year-old man who had experienced fatigue for over 2 months was admitted to our hospital with serum creatinine of 3.4 mg/dl and macrohaematuria. Physical examination was normal, weight 88 kg, height 178 cm, heart rate 80 beats/min and blood pressure 124/75 mmHg.
The results of laboratory tests were as follows: haemoglobin 7.8 g/dl, creatinine 370 μmol/l, anti-GBM antibodies 94 kU/l (normal <10), while c-ANCA, p-ANCA, ANA and ds-DNA antibodies were normal. Urine examination showed many red cells with acanthocytes and proteinuria of 1.89 g/g creatinine.
A renal biopsy was performed, and light microscopy showed 8 glomeruli with cellular partly fibrinoid crescents in all of them. Immunofluorescence showed linear deposition of IgG and C3 at the glomerular basement membrane.
Treatment was started with 1000 mg prednisolone intravenously for 3 days and oral cyclophosphamide 200 mg/day. Prednisolone 100 mg/day was given orally for three weeks and then slowly tapered. Sporadic haemodialysis and daily plasmapheresis were started on Day 5.
Because of rising creatinine (654 μmol/l), rituximab 1000 mg was administered once intravenously after 2 weeks (Figure ). Plasmapheresis was ceased in order to prevent inadvertent elimination of rituximab. Four weeks after administration of rituximab, CD19/20 cell cytometry was negative. Since renal function deteriorated, accompanied by oliguria, plasmapheresis was resumed three times a week for 7 weeks. On this therapy, renal function slowly improved. Anti-GBM antibodies could no longer be detected after Week 12 (Figure ). Renal function recovered and serum creatinine decreased to 300 μmol/l. It was finally possible to discharge the patient from hospital without dialysis after 3 months.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [178.0, 'cm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3784,10,Ideal Body Weight,physical,decimal,usmle-712,Extracted,"A 37-year-old woman comes to the physician because of a 2-week history of generalized fatigue and malaise. During this period, she has had a non-productive cough with a low-grade fever. Over the past 6 months, she has had a 13-kg (28.6-lb) weight loss and intermittent episodes of watery diarrhea. She has generalized anxiety disorder and hypothyroidism. She has a severe allergy to sulfa drugs. She is sexually active with 3 male partners and uses condoms inconsistently. She has smoked one pack of cigarettes daily for 20 years and drinks 2–3 beers daily. She does not use illicit drugs. Current medications include paroxetine, levothyroxine, and an etonogestrel implant. She is 162.5 cm (5 ft 4 in) tall and weighs 50.3 kg (110.2 lbs); BMI is 19 kg/m2. She appears pale. Her temperature is 38.7°C (101.6°F), pulse is 110/min, and blood pressure is 100/75 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 94%. Examination of the lungs shows bilateral crackles and rhonchi. She has white plaques on the lateral aspect of the tongue that cannot be scraped off. A chest x-ray shows symmetrical, diffuse interstitial infiltrates.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [162.5, 'cm']}",54.64574,51.91345,57.37803,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 162.5 cm, which is 162.5 cm * 0.393701 in/cm = 63.97641 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.97641 (in inches) - 60) = 54.64574 kg.
Hence, the patient's IBW is 54.64574 kg."
3785,10,Ideal Body Weight,physical,decimal,pmc-2861069-1,Extracted,"Our first patient was a 43-year-old Hispanic Mexican man with a carbohydrate-based diet. He had smoked one or two cigarettes per day from 18 to 40 years of age. He had been consuming almost 250 mL of red wine per day since he was 20 years old. He also occasionally consumed one bottle of beer. Five years prior to the study, he was diagnosed with hypercholesterolemia and hypothyroidism for which he remained under treatment with levothyroxine 100 μg daily. He was also diagnosed with chronic renal failure eight months prior to the study. His nephrologists did not suggest any specific medical treatment for this condition.
He was diagnosed with NAFLD after he presented with asthenia, fatigue, nausea without vomiting and hypochondrial pain. He was noted to have both elevated cholesterol and TAG levels. An ultrasound examination revealed a ""brilliant liver"", which is congruent with a diagnosis of fatty liver disease.
His physical examination revealed the following: 1.72 m height, 77 kg weight, body mass index (BMI) of 26 kg/m2, blood pressure of 120/90 mmHg, respiratory rate of 21 breaths per minute and a body temperature of 36.5°C. His head and neck were without alterations. His heart had normal sounds and adequate rhythm and frequency. His pulmonary area had adequate ventilation. An exploration of his abdomen showed no clinical signs of significance and his hip-to-waist ratio was 0.75. His genitalia also had no alteration. His musculoskeletal system was found to be normal.
He was then started on a treatment of a low-caloric diet, daily exercise (30-minute walk) and ingestion of Spirulina maxima. Adverse side-effects included flatulence, meteorism and abdominal pain of moderate intensity without irradiation.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.72, 'm']}",67.74811,64.3607,71.13552,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.72 m, which is 1.72 m * 39.3701 in/m = 67.71657 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.71657 (in inches) - 60) = 67.74811 kg.
Hence, the patient's IBW is 67.74811 kg."
3786,10,Ideal Body Weight,physical,decimal,pmc-4336266-1,Extracted,"A 28-year-old Nepali male was referred to our hospital with suspected gastroenteritis. He had a 3-week history of high fever (around 38°C-39°C), appetite loss, and general fatigue. He had visited a nearby hospital, where he was found, on abdominal CT, to have ascites and duodenal swelling without free air. On admission to our hospital, he complained of general fatigue and slight abdominal pain but was not experiencing diarrhea. He had been in Japan for 4 years and had not been back to Nepal for the last 2 years. He was living with four other Nepali males who were not experiencing similar physical problems. He denied being males who sex with males. He was a Hindu and ate Japanese food bought in a nearby supermarket. He had no remarkable past medical history and was not taking any medications. He works so hard on a supermarket in Japan and he could not sleep well. He also feels loss of appetite. He had been repeated low-grade fever around 37°C and general fatigue before coming to our hospital.
In general, the patient did not look sick. His height was 170 cm, weight was 46.5 kg, and BMI was 16.1. His blood pressure was 90/64, pulse rate 109/min, and body temperature 36.2°C. His eyes were not anemic or icteric, and chest sounds were clear. His abdomen was soft and flat, although there was slight tenderness in the left lower quadrant.
Laboratory data on admission showed a slightly elevated white blood cell count of 7,600/μl (neutrophil 5,920/μl, lymphocyte 880/μl, monocyte 790/μl, eosinophil 0/μl, and basophil 10/μl) and highly elevated CRP (13.9 mg/dl). His albumin was low at 3.0 g/dl. A chest radiograph was clear, and there were no signs of pneumonia. An abdominal computed tomography (CT) scan on admission showed ascites with swollen intestines but no free air (Figure ).
We hospitalized the patient for observation. His temperature rose to 40°C, and laboratory data on day 2 showed highly elevated inflammatory markers. Microbiological studies including sputum, urine, and blood cultures were all negative. He was constipated until day 3. His stool on day 3 looked normal; it was not watery and contained no blood. Stool microscopy revealed numerous strongylid larvae (Figure ). We diagnosed a Strongyloides hyperinfection. Serum human T-cell leukemia virus type 1 (HTLV-1) and human immunodeficiency virus (HIV) tests were negative, and CD4 counts were not decreased. We prescribed 12 mg of ivermectin. Although his general condition improved within 24 h after treatment in that he was eating well and had no diarrhea or abdominal pain, his temperature continued to exceed 39°C. The course of his inflammatory laboratory data and temperature are shown in Figure . On day 7, his stool sample was negative for strongylid larvae. An abdominal CT scan on day 6 revealed massive ascites, but the culture of the ascites on day 9 was negative for strongylid larvae. He did not complain of dyspnea throughout his hospitalization. A second 12-mg dose of ivermectin was administered on day 17.
After the second dose of ivermectin, the patient still had a low-grade fever of 37°C-38°C. His laboratory data were within the normal limit except for relatively low albumin (2.6 g/dl) and still low lymphocyte count (470/μl). He looks lethargy. We thought this is due to long-term hospitalization; thus, we transferred him to another hospital for further rehabilitation. However, he returned to our hospital 4 days later for pleural effusion of unknown etiology. He had massive pleural effusion in his left chest, and his ascites had not diminished. Thoracentesis was performed on admission, and the pleural fluid was positive for adenosine deaminase (ADA) as 128 IU/l. Ascites were also positive for ADS as 156.6 IU/l. QuantiFERON was positive, and mycobacterial culture of gastric secretions revealed Mycobacterium tuberculosis. Sputum culture and Gaffky staining were negative. Repeated stool microscopy was negative for Strongyloides. The patient transferred to another hospital for tuberculosis treatment.
We encountered a case of Strongyloides hyperinfection, which is rarely seen in Japan. This patient also developed a tuberculosis infection after successful treatment of his strongyloidiasis. Although the relationship between these two infections is not apparent, there may be an association because of the unique characteristics of these infections.
Strongyloidiasis is endemic in tropical and subtropical regions. In Japan, the Okinawa prefecture, which is in the southern islands, is the only endemic region []. Because our patient had never been to the Okinawa prefecture, we believe he became infected in Nepal. Strongyloides can cause acute, chronic, hyper, and disseminated infection. Strongyloides hyperinfection occurs due to the unique life cycle of the Strongyloides stercoralis. Their eggs are embedded in the intestinal mucosal epithelium, and non-infectious rhabditiform larvae hatch into the intestinal lumen. The rhabditiform larvae become free-living adults when secreted in feces into the soil. They can develop to infectious filariform larvae, at which point they can penetrate human skin and invade the intestine via the bloodstream []. Strongyloides hyperinfection is an accelerated autoinfection in which increasing numbers of infectious filariform larvae are produced. Such hyperinfections can occur when the host becomes immunosuppressed, such as with steroid use or HTLV-1 infection []. These infections can occur even 57 years after chronic infection []. In chronic infection, more than 50% of patients are asymptomatic []. Our patient had no symptoms and had not been to an endemic area for 2 years; therefore, we believe this patient had been chronically infected since he was in Nepal and became hyperinfected in Japan. Although this patient does not have history of steroid use or HTLV-1 infection. The patient had worked so hard that he could not eat well. Malnutrition induced decreased number of lymphocyte and subsequently hyperinfected with Strongyloides.
Tuberculosis is a re-emerging infection in Japan and is endemic in Nepal. It is an infection that can be re-activated when the host becomes immunosuppressed. There is one previous report in the literature of a co-infection with strongyloidiasis and tuberculosis []. The authors concluded that their patient developed tuberculosis because of Strongyloides hyperinfection. However, the possibility that the patient developed strongyloidiasis hyperinfection during the course of the tuberculosis infection is not discussed. Similarly, in our patient, it is not clear whether the strongyloidiasis stimulated the tuberculosis re-activation or vice versa. However, it is clear that both Strongyloides infection and tuberculosis infection are associated with impaired cellular immunity [].
Our patient’s lymphocyte count was low, indicating that he was at risk of infection with both strongyloidiasis and tuberculosis. We estimated that malnutrition due to poor diet caused decreased lymphocyte. The decreased lymphocyte caused Strongyloides hyperinfection and tuberculosis. We believe Strongyloides hyperinfection occurred earlier and subsequently tuberculosis, because there were no signs and symptoms of tuberculosis infection on admission. Regardless, patients with either strongyloidiasis or tuberculosis should be examined carefully for other infections, particularly when the patient has impaired cellular immunity.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3787,10,Ideal Body Weight,physical,decimal,pmc-6996394-1,Extracted,"A 69-year-old male presented to the hospital with a one-month history of fever and cough. Four months before admission, he had completed concurrent chemoradiotherapy for stage IIIB (cT4N2M0) squamous cell carcinoma of the lung (Fig. A). Regimen of chemotherapy consisted of carboplatin AUC2 and paclitaxel 40 mg/m2 on day 1 and repeated every week. He received six cycles of chemotherapy and a total of 60 Gy radiation with three-dimensional conformal radiation therapy. No complications were encountered during chemoradiotherapy including neutropenia. After chemoradiotherapy, the inside of the tumour was necrotic and became a cavity (Fig. B). Two months before admission, he developed radiation pneumonitis and was receiving oral prednisolone. Bronchoscopy performed before the initiation of prednisolone did not reveal any pathogens. At first, he was administered prednisolone 20 mg/day and reduced amount of prednisolone every two weeks. He smoked for 49 pack-years before diagnosis of lung cancer, and his medical history included chronic obstructive pulmonary disease (COPD), which was treated with tiotropium bromide hydrate 3.124 μg/olodaterol hydrochloride inhaler 2.736 μg. He neither had pets nor a hot tub and was unemployed. Before admission, the patient's symptoms did not improve despite oral levofloxacin 500 mg/day administered for two weeks; he was on oral prednisolone (5 mg/day).
On examination, he was 157.8 cm in height and weighed 48.5 kg. He was ill-appearing and febrile with a temperature of 38.2°C. His other vital signs were as follows: blood pressure, 90/63 mmHg; pulse, 103/min; and respiratory rate, 20/min with 93% O2 saturation on room air. Breath sounds were reduced on the left side. The laboratory results on admission were as follows: white blood cells, 5800/mm3 with 85.2% neutrophils and 7.7% lymphocytes; haemoglobin, 9.3 g/dL; albumin, 2.8 g/dL; and C-reactive protein, 14.4 mg/dL. β-D-glucan, a fungal cell wall constituent, level was normal (<11.0 pg/mL). The serum galactomannan antigen was negative, whereas the immunoglobulin G antibody against Aspergillus was positive. Chest X-ray and computed tomography images showed a cavity with surrounding consolidation with a thick wall (Fig. C). Bronchoscopy was performed on the first day of admission for bronchoalveolar lavage; biopsy was not performed due to the concern regarding bleeding. Initially, intravenous tazobactam/piperacillin 13.5 mg/day was administered; however, following the detection of fungi by staining of the bronchoalveolar lavage fluid in the absence of malignant cells (Fig. ), micafungin (150 mg/day) was started on the fourth day for the presumptive diagnosis of SIPA. As the patient's condition worsened over time, the micafungin dose was increased to 300 mg/day on the fifth day. His condition did not improve (Fig. D), and the antifungal agent was changed to liposomal amphotericin B (L-AMB) at 150 mg/day on the ninth day. However, fever and cough did not improve, and intravenous voriconazole (540 mg/day as the loading dose followed by 360 mg/day as the maintenance dose) was added on the 15th day. Aspergillus fumigatus was detected later in culture, and definitive diagnosis of SIPA was made. The patient recovered gradually. L-AMB was used for 38 days, and voriconazole was changed from intravenous to oral use (300 mg/day) on day 40 after admission; he was discharged on day 51 after admission. The trough concentrations of voriconazole were 1.39 and 3.57 mg/mL on days 23 and 47, respectively.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [157.8, 'cm']}",54.88985,52.14536,57.63434,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 157.8 cm, which is 157.8 cm * 0.393701 in/cm = 62.12602 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.12602 (in inches) - 60) = 54.88985 kg.
Hence, the patient's IBW is 54.88985 kg."
3788,10,Ideal Body Weight,physical,decimal,pmc-6716019-1,Extracted,"A 47-year-old man with suspected myocarditis, due to nivolumab therapy was admitted to our hospital. He complained of diplopia 8-months prior to admission and was diagnosed with ethmoid sinus cancer (T4bN2bM0) at the referral hospital. The biopsy specimen showed positive staining for insulinoma-associated protein 1 (INSM1) or neural cell adhesion molecule 1 (CD56), but negative staining for nuclear protein in testis or synaptophysin, indicating neuroendocrine carcinoma. Systemic chemotherapy (cisplatin and irinotecan) and radiotherapy were administered. However, 18F-fluorodeoxyglucose-positron emission tomography scan suggested multiple bone metastases (). Nivolumab (3 mg/m2) was started and administered every 2 weeks. Although the fourth administration was scheduled, nivolumab was discontinued because of elevation in the levels of total CK (946 U/L; reference range, 30–200 U/L), CK-MB (484 IU/L; reference range, 0 to 12 IU/L), and cardiac troponin-T (1.25 ng/mL; reference range, <1 ng/mL) in the serum, which was evident at 16 days since the third nivolumab administration. The patient received methyl-prednisolone (1,000 mg/day) for 3 days, after which it tapered to 500 mg/day for 3 days, 250 mg/day for 3 days, and 125 mg/day for 3 days at the referral hospital. Thereafter, he developed lower back pain but no chest discomfort or palpitation.
On examination, his temperature was 36.9°C, the blood pressure was 130/82 mmHg, the heart rate was 90 beats/min, and the respiratory rate was 17 breaths/min. His weight was 67 kg, height was 169.3 cm, and body mass index was 23.4. Heart sounds were normal, and murmurs were inaudible. Chest radiographs revealed a 49% cardio-thoracic ratio, and hilum in the left lung showed a swollen lesion (). The twelve-leads-electrocardiogram showed a normal sinus rhythm, normal axis deviation, and no change in the ST-T segments (). The transthoracic echocardiogram showed a 63% ejection fraction without regional wall motion abnormality in the left ventricle, and the thickness of the intraventricular septal wall and left ventricular posterior wall at diastole were 10 and 11 mm, respectively. The global longitudinal strain was −19.3%. Cardiac magnetic resonance imaging showed normal systolic contractility () and minimal myocardial edema and inflammation (). Blood test findings showed an increased number of white- blood cells (18,800 /mm3; reference range, 3,300–8,600 /mm3: neutrophils, 90.3 %; reference range, 37–72 %, eosinophils, 0.1 %; reference range, 0.6–8.3%), but a decrease in the platelet cell count (70,000/mm3; reference range, 158,000–348,000/mm3). The levels of lactate dehydrogenase (8,695 U/L; reference range, 124–222 U/L), aspartate aminotransferase (157 U/L; reference range, 13–30 U/L), total CK (3,385 U/L; reference range, 59–248 U/L), MB isoenzyme (1,221 U/L; reference range, <12 U/L), and cardiac troponin-T (3.30 ng/mL; reference range, <0.1 ng/mL) were markedly elevated. Electrophoretic findings did not show the presence of the macro CK isoenzyme (CK-BB, 2%; CK-MB, 33%; CK-MM, 65%). The C-reactive protein level was 0.50 mg/dL (reference range, 0–0.14 mg/dL). The brain natriuretic peptide level was normal (<5.8 pg/mL; reference range, <18.4 pg/mL). We continued to administer 125 mg/day of methyl-prednisolone, and we added 5 g/day of γ-globulin for 7 days, but the patient persistently showed elevated levels of total CK and cardiac troponin-T within 1 month (). The twelve-leads-electrocardiogram was repeated 7 times after nivolumab administration, but it did not show any changes in the ST-T segments or arrhythmias. In fact, the echocardiogram was performed 5 times after nivolumab administration, and showed a normal range of left ventricular ejection fraction (58~63%) in the clinical course, despite elevated serum cardiac troponin-T and CK-MB isoenzyme levels. This finding raised the concern of whether cardiac troponin-T and CK-MB isoenzymes were released from the damaged myocardium into the blood because of nivolumab. Blood clots in the bone marrow aspirates obtained from the left side of the pelvis exhibited consistent immunohistological features of the primary lesion, which showed positive staining for INSM1 and CD56 (). These clots also showed positive staining for cardiac troponin-T () and CK-MB () in the cytoplasm and nucleoplasm of metastatic neoplastic cells. These molecules were also scattered in the primary lesion of the ethmoid sinus (). The patient died from progressive disease at 10 months after the initial presentation, and postmortem autopsy was not performed.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [169.3, 'cm']}",65.30323,62.03807,68.56839,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 169.3 cm, which is 169.3 cm * 0.393701 in/cm = 66.65358 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.65358 (in inches) - 60) = 65.30323 kg.
Hence, the patient's IBW is 65.30323 kg."
3789,10,Ideal Body Weight,physical,decimal,usmle-209,Extracted,"A 28-year-old woman comes to the physician with a history of bright red blood in her stools for 3 days. She has defecated once per day. She does not have fever, pain on defecation, or abdominal pain. She was treated for a urinary tract infection with levofloxacin around 3 months ago. Menses occur at regular intervals of 28–30 days and lasts 3–4 days. Her father died of colon cancer 4 years ago. Her only medication is an iron supplement. She is 162 cm (5 ft 4 in) tall and weighs 101.2 kg (223 lbs); BMI is 38.3 kg/m2. Her temperature is 36.5°C (97.7°F), pulse is 89/min, and blood pressure is 130/80 mm Hg. Rectal examination shows anal skin tags. Anoscopy shows multiple enlarged bluish veins above the dentate line at 7 and 11 o'clock positions. When asked to exhale through a closed nostril a mass prolapses but spontaneously reduces when breathing normally.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [162.0, 'cm']}",54.19299,51.48334,56.90264,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.77956 (in inches) - 60) = 54.19299 kg.
Hence, the patient's IBW is 54.19299 kg."
3790,10,Ideal Body Weight,physical,decimal,pmc-2923787-1,Extracted,"A 43-yr-old female visited a nearby hospital because of abnormal shadows including multiple nodules and reticular shadows on chest radiography found at an annual medical checkup in 2005. A bronchoscopic examination was performed. They were unable to obtain a biopsy specimen from one of the nodules in S10 of the left lung because the patient had a strong bleeding tendency. She was referred to this hospital for further examination on June 30, 2005.
On admission, her height was 157.5 cm and weight, 50.3 kg. Her consciousness was clear. The conjunctivas were anemic and not jaundiced. Her heart sounds were normal. Fine crackles were audible in the right lower lung field. The abdomen was not distended. Her inguinal lymph nodes were palpable and no other superficial lymph nodes were palpable. She was experiencing slight polyarthralgia, however, radiography films showed no joint anomalies.
The laboratory data were: erythrocyte sedimentation rate, 119 mm/1 hr; white cell count, 8,900/µL; hemoglobin, 8.4 g/dL; platelet count, 39.4×104/µL; serum aspartate aminotransferase, 22 IU/L; alanine aminotransferase, 22; total protein, 9.7 g/dL; albumin 2.6; creatinine, 0.48; PT, 13.1 sec (INR 1.45); aPTT, 39.6 (control, 10.4); fibrinogen, 750 mg/dL; KL-6, 277 U/mL (reference range <500); C-reactive protein, 11.7 mg/dL (<0.3); serum immunoglobulin (Ig)G, 4,570 (870-1740); IgA, 491(110-400), IgM, 706 (35-220), CH50, 52.3 U/mL (30-50), soluble IL-2 receptor, 1,400; serum IL-6, 6.8 pg/mL (<4); rheumatoid factor (RF), 1,330 IU/mL (<20). Autoantibodies, including antinuclear antibody, anti-ds-DNA, anti-Sm, anti-RNP, cytoplasmic antineutrophil cytoplasmic antibody (ANCA), and myeloperoxidase-ANCA were all negative. M-protein was not noted in serum immunoelectrophoresis. Bone marrow aspiration showed hyperplasia with no abnormal morphology on smear specimens.
Chest radiographys showed multiple nodules and reticular shadows mainly in the lower lung field. Chest CT scan disclosed a slight enlargement of the mediastinal lymph nodes, centrilobular nodules, thin-walled cysts, the thickening of the bronchovascular bundles, and ground-grass opacities, all of these findings were compatible with those of lymphocytic interstitial pneumonia (LIP; ) (, ). 67Gallium citrate scintigraphy did not reveal any evident accumulation.
A lung surgeon and a thoracic physician declined to perform a lung biopsy because of her bleeding tendency (bleeding time: 6 min 30 sec) and poor general condition. A biopsy of an inguinal lymph node was obtained for making a definite diagnosis (). She was diagnosed with MCD and undifferentiated arthritis based on the characteristic pathology of the specimen of the inguinal lymph node, CT findings of the bilateral lung lesions and laboratory data.
She was initially administered intravenous corticosteroid (methylprednisolone, 500 mg/day, 3 consecutive days) followed by oral corticosteroid (methylprednisolone, 16 mg/day), and, 375 mg/m2 rituximab every week for 4 weeks. The polyarthralgia instantly disappeared; however, none of the other clinical and laboratory parameters were fully resolved. Therefore the therapeutic regimen was changed to tocilizumab (8 mg/kg, every 2 weeks), oral corticosteroid (methylprednisolone, 16 mg/day) on October 25, 2005. The patient requested that the interval between tocilizumab to be increased to more than every two weeks. The dose of corticosteroid in combination with tocilizumab should be kept as low as possible to avoid various side effects, such as osteoporosis, hyperglycemia, and hypertension. It is indicated for the treatment of rheumatoid arthritis in Japan. The addition of tacrolimus to the regimen was considered to fulfill such requirements. Both the possible merits and demerits of the drug were explained to the patient and her oral consent was obtained. Tacrolimus (3 mg/day) was introduced on November 10, 2005. Laboratory findings, including anemia, hypergammaglobulinemia, and an increase in acute phase proteins responded to this regimen (). The enlargement of mediastinal lymph nodes and abnormal shadows were also partially alleviated (). The intervals of the tocilizumab-administration sessions were extended from every 2 weeks to every 3 weeks from January 2006. Oral corticosteroid was gradually tapered from 16 mg/day finally to 4 mg/day. The dose of tacrolimus has been unchanged. The disease activity has been totally suppressed for 36 months by this maintenance regimen.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [157.5, 'cm']}",50.11819,47.61228,52.6241,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 157.5 cm, which is 157.5 cm * 0.393701 in/cm = 62.00791 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.00791 (in inches) - 60) = 50.11819 kg.
Hence, the patient's IBW is 50.11819 kg."
3791,10,Ideal Body Weight,physical,decimal,pmc-4808533-1,Extracted,"A 72-year-old Japanese man had a history of proximal gastrectomy for early gastric cancer located in the upper third of the stomach in 2007. Our usual treatment strategy for early gastric cancer in the upper third of the stomach at this time was open proximal gastrectomy reconstructing by jejunal interposition with a 10 cm single loop. In this patient, interposed jejunum was approached via the retrocolic route. Lymphadenectomy was D1 (station numbers 1, 2, 3a, 4sa, 4sb, and 7) according to the Japanese Gastric Cancer Association (JGCA) guidelines for initial proximal gastrectomy []. Upon physical examination, he was found to be 165 cm in height and weighed 55 kg. There was an upper middle operative scar, 17 cm in length, in his abdomen. All of the laboratory data were within the normal range and the tumor markers CEA and CA 19-9 were 7.4 ng/mL and 9.7 U/mL, respectively. Upper gastrointestinal fiberscopy for annual follow-up revealed a type 0-IIc-shaped tumor with ulcer scar, 4.0 cm in size, located in the gastric remnant near the jejunogastrostomy (). Biopsy specimen showed well-differentiated adenocarcinoma. A clinical diagnosis of early gastric cancer according to the Japanese Classification of Gastric Carcinoma [], T1b(SM)N0M0, Stage IA, following the proximal gastrectomy was made. A laparoscopic approach was selected for remnant gastrectomy because of the cancer's early stage.
Surgery was carried out with five ports by the pneumoperitoneal method using our usual laparoscopic technique (). The lateral segment of the liver was retracted using a Nathanson Liver Retractor (Cook Surgical, Bloomington, Indianapolis, USA). At initial laparoscopy, there was a little adhesion in the median abdominal incision. At first, adhesion was removed as much as possible and omentum was dissected to open the bursa. The tightest adhesion in this operation was that between the lateral segment of the liver and the dissected lesser curvature of the remnant stomach. The right gastroepiploic artery and vein were clipped and divided, and station number 6 lymph nodes were completely removed (). After dividing the right gastric artery (station number 5), the duodenum was transected using a linear stapler (GIA™ Tri-Staple™ 60 mm, purple 60 mm, Covidien, Tokyo, Japan). The suprapancreatic lymph nodes (station numbers 8a, 9, and 11p) could be easily dissected en bloc because these regions were not dissected at initial proximal gastrectomy (). After gastrectomy, the reconstructed jejunum was resected. The mesentery of the interposed jejunum was transected using a vessel sealing system (LigaSure™ Blunt Tip 5 mm–37 mm, Covidien) (). After the abdominal esophagus had been scarified circumferentially, the esophagus was transected using a linear stapler on the proximal side of the anastomosis of the esophagojejunostomy at initial proximal gastrectomy (). The remnant stomach and interposed jejunum were successfully reduced back into the peritoneal cavity through the umbilical port-side. A minilaparotomy incision of about 5 cm was made in the umbilical port site, for an Alexis® Wound Retractor S (Applied Medical Resources Co., Tokyo, Japan). Reconstruction using the Roux-en-Y method via the antecolic route was performed. At first, jejunojejunostomy was carried out by side-to-side anastomosis using a linear stapler extracorporeally (). Next, esophagojejunostomy was performed by an end-to-side anastomosis using a circular stapler (DST Series™ EEA™ Staplers, 25 mm, Covidien) (Figures and ). Total operative time was 395 min and blood loss was 40 mL.
The postoperative course was uneventful and the patient was discharged on the 10th postoperative day. The resected stomach contained a superficial depressed-type tumor, 37 × 17 mm in size (, black arrowhead). Histological examination revealed well-differentiated adenocarcinoma to the depth of the mucosa, with no lymph node metastasis, which was pathologically classified as Stage IA.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3792,10,Ideal Body Weight,physical,decimal,pmc-8102796-1,Extracted,"A 31-year old woman with documented AKU was reviewed in 2014 in the NAC. Apart from urine turning dark she has not had any renal stones, fracture, or ruptures of Achilles tendon, muscle or any other ligaments or tendons. She had pain in the hips, knees and lower back intermittently, without affecting her activity. Previous medical history included recovered childhood asthma, visual disturbance during migraines, panic attacks and acid reflux. She consumed unrestricted dietary protein, 8 and 16 units of alcohol per week, and had briefly smoked between 2007 and 2010. Her menstrual periods were regular with menarche at 12 years. She was born of a non-consanguineous union, with neither parent having AKU or arthritis. Her family included a sister aged 39 years, a son of 4 years and a daughter of 3 months. She had never received any previous treatment for AKU. She was 1.68 m tall, weighing 58.6 kg with a BMI of 21 kg/m2. Blood pressure was 110/80 mmHg with a pulse rate of 80 per minute. Mild pigmentation was found in her ears. The rest of the general and systems examinations were all within normal limits. The 12-lead surface ECG demonstrated sinus rhythm with a normal axis. Her transthoracic echocardiogram demonstrated a LA of 31.9 ml. The mitral valve leaflets were slightly thickened but opened well with trace regurgitation. The aortic valve was normal. Whole body F18PETCT showed mildly increased tracer uptake in the right patella and in the inferior tibiofibular regions bilaterally consistent with early arthropathy. Volumetric CT bone densitometry showed T score −0.36; Z score −0.32 at L1–3 vertebra, T-score of −1.27 at neck of femur (Z score −1.25), and a T score −1.47 for total hip (Z score −1.46), consistent with normal BMD in L1–3 vertebra and osteopaenia in hip. MRI of right knee was normal except for mild chronic quadriceps insertional tendinosis. MRI of spine showed early degenerative disc disease at L5/S1 with disc dehydration, focal postero-central annular bulging and an associated annular fissure. Ultrasound of abdomen and pelvis was normal except for a 2 mm gall bladder polyp on the posterior wall. ESR and FBC were normal except for mild neutropenia 1.6 × 109/l (ref range 2.0–7.5). Biochemistry electrolyte and organ profiles were all normal; urine urea and creatinine were measured, the latter using Jaffe reaction in order to overcome the HGA-interference in the analyses [].
During monitoring in the NAC, she showed further symptoms of GORD and anxiety in 2016, with increase in F18PETCT uptake in both femoral condyles and right foot (in addition to both ankles). At the 2017 annual, she raised the issue of having a further pregnancy and its effect on her health; as very little was known about pregnancy in AKU, she consented to collect random urine at regular intervals during her pregnancy, which could be used to characterise changes in AKU metabolism, nutrition and tissue remodelling. At her 2018 visit, she had her third child delivered by Caesarian section 11 weeks previously, and both mother and daughter were doing well. During the pregnancy she experienced discomfort in knees, hips and lower back. The review in 2019 revealed deterioration in osteopenia, and she was asked to begin calcium 500 mg daily and 20,000 units cholecalciferol monthly; she reported pain in hips, knees, and the thoracic spine at this time. Her review in 2020 revealed peripheral sensory neuropathy. Her F18PETCT scan had been stable since 2017. Assessments carried out at her annual NAC visits allowed a validated semiquantitative composite score to be derived for ochronosis and overall AKU disease, termed ochronosis and AKUSSI scores respectively. At each NAC visit she also completed Bath indices questionnaires to assess the axial spondylosis in AKU, and clinical gait analysis. A dietician discussed and assessed dietetic and nutritional aspects of her condition. At annual NAC visits circulating c-terminal telopeptide-1 (CTX-1) and procollagen-1-N-terminal telopeptide (P1NP) were measured as indicators of bone resorption and formation; serum samples were unavailable during pregnancy.
Eight random urine samples were collected by the patient during her pregnancy in 2017, at 8, 12, 16, 20, 24, 28, 32 and 36 weeks, once her pregnant state was confirmed. Metabolic analyses such as HGA, tyrosine (TYR) and phenylalanine were carried out in house both during her annual NAC visits and the random urine samples during pregnancy, as previously described [,]. Urine connective tissue markers were analysed and included, c-terminal telopeptide-1 (uCTX-I; marker of bone resorption), αc-terminal telopeptide-1 (uαCTX-I; marker of subchondral and young bone remodelling), c-terminal telopeptide-II (uCTX-II; a cartilage marker), and C3M (a metabolite of collagen III produced by action of matrix metalloproteinases). Urine urea and creatinine were measured on all samples, the latter using Jaffe reaction.
The body weight and BMI showed the expected minor variations over time and were largely stable. The data elicited from the Bath indices and KOOS questionnaires were mostly unchanged during the annual visits. Likewise, the number of steps (cadence), stride length and speed during formal gait analysis were stable throughout. There was an increase in ochronosis and AKUSSI scores over the six years of follow-up, especially starting around the time of the pregnancy. (See .)
The serum CTX-I and P1NP during annual visits remained stable throughout, suggesting stable coupled bone turnover. Urea and creatinine in random urine show the expected variations due to visit-to-visit differences in osmolality due to hydration. Increasing serum urea, as well as increasing urea/creatinine ratios suggest progressively increasing protein intake, especially starting around 2017. The increasing sHGA since 2018, is consistent with increased protein consumption. Similarly, urine HGA (uHGA)/urine creatinine (uCR), and urine tyrosine (uTYR)/uCR increased from 2017/2018, also supporting increased protein consumption.
All urine tissue degradation markers showed a biphasic response, an early and a late response consistent with significant remodelling of bone (uCTX-1), subchondral bone (uαCTX-1), cartilage (uCTX-II) and other tissues including heart and uterus (C3M). Early peak was higher than the late peak for uCTX-1, uαCTX-1 and uC3M, whereas uCTX-II late peak was higher. Relative to each other, urine bone markers change more than cartilage early in pregnancy. Similarly, relative changes in uC3M, which includes interstitial membranes (including synovial membrane), heart and uterus are earlier than bone and cartilage. It appears that generalised bone changes and subchondral changes parallel each other during pregnancy in urine. All these tissue markers returned to pre-peak values at delivery, unlike the metabolic/nutritional ratios which remained increased at delivery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.68, 'm']}",59.62607,56.64477,62.60737,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.68 m, which is 1.68 m * 39.3701 in/m = 66.14177 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.14177 (in inches) - 60) = 59.62607 kg.
Hence, the patient's IBW is 59.62607 kg."
3793,10,Ideal Body Weight,physical,decimal,pmc-3971556-1,Extracted,"A 30-year-old man consulted for limping. In the past three years, the patient had been having trouble walking, could not squat down, or go up and down stairs. The patient's history included a knee injury at the age of 5 in a road accident. He did remember neither precise diagnosis nor functional or surgical previous treatment. There were no scars on the knee. The patient was 1.76 m tall and weighed 68 kg with varus knee morphology and no leg-length discrepancy. Placing weight on one foot resulted in lateral patellar dislocation, and squatting was impossible. The patella was mobile, but systematically dislocated laterally at 30° of flexion ().
The rest of the clinical examination, in particular the neurological, muscular, and tendon results were normal. X-ray confirmed genu varum, showing a patellar tilt angle of 30°. The trochlear morphology (groove and depth) was normal as well as the height of the patella with Caton-Deschamps index equal to 1 []. There was no patellar dysplasia, but the trochlea was slightly flattened (Figures and ).
The medial border of the patella was calcified. There was no associated leg dysplasia. CT scans of leg rotation showed physiological tibial torsion and femoral anteversion. Femoral anteversion measured on CT scan between the femoral neck angle and the biepicondylar axis was symmetrical, 12° on the right and 13° on the left. The preoperative Kujala et al. score [] was 41%. The preoperative Lysholm score was 6%. The subjective IKDC score was 10% for pain, 17% for symptoms, and 17% for recreational and sports activities, or a global IKDC of 14.7%. The diagnosis of habitual posttraumatic patellofemoral dislocation was made. The indication for reconstruction of the stabilizing ligament of the patella was based on the significant functional incapacitation and the lack of appropriate conservative treatment.
An open surgery procedure was performed. First lateral retinacular release of the patella was performed. Then the ipsilateral gracilis tendon was harvested at its distal insertion with a tendon stripper. The graft was 12 cm long. Two holes were drilled into the patellar bone by a medial parapatellar approach. After pulling a suture through the holes the femoral attachment point was found and with the help of a temporary pin in the medial epicondyle, favorable anisometry could be obtained (the graft relaxed as the knee was flexed) and a Corkscrew suture anchor (Arthrex, Naples, FL, USA) was put in place. After confirming patellar centering during 4 to 6 flexion-extension cycles, the suture anchor was secured in its final position. The graft was placed into the drill holes then secured to the suture anchor and doubled back on itself as described by Thaunat and Erasmus [, ]. The vastus medialis (vastus internus) was then placed below and outside the patella and secured with “U-” stitches to provide overlapping reinforcement. The postoperative course was simple with a brace to walk for 45 days and immediate rehabilitation at between 0 and 80° of flexion.
At 4 months of follow-up, the patient was able to work normally as construction worker in public works. At the final 50-month clinical follow-up, the operated knee was stable and there was no pain. There was no recurrent dislocation or apprehension. There was full range of motion (Figures and ).
Postoperative X-rays show the patella recentered at 60°. The patient was very satisfied with the results.
Results of knee function were excellent on functional scales for patellar instability with significant improvement of all clinical scores. The Kujala score was 83/100 points and the Lysholm score 90/100. The global IKDC score was 90.8%. The items for pain, symptoms, and leisure and sports activities were scored 93.3%, 90%, and 90%, respectively.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.76, 'm']}",71.37017,67.80166,74.93868,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.76 m, which is 1.76 m * 39.3701 in/m = 69.29138 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.29138 (in inches) - 60) = 71.37017 kg.
Hence, the patient's IBW is 71.37017 kg."
3794,10,Ideal Body Weight,physical,decimal,pmc-6971432-1,Extracted,"A 15-year-old boy presented at our hospital emergency department with sudden-onset epigastric and left-sided abdominal pain that had developed while playing handball. He had experienced no recent trauma or infections. He had no history of surgeries and an unremarkable family medical history.
Physical examination revealed a height of 165 cm and weight of 58 kg. His body temperature was 37.2°C, blood pressure 159/101 mmHg, heart rate 86 b.p.m. and stable, and respiratory rate 24 breaths/min. Thoracic findings were normal. The patient’s abdomen was flat and soft, with tenderness in the left lower abdomen. The mass was not palpable, and the patient reported subjective colic extending from the left abdomen throughout the body, causing a bruise-like sensation.
At admission, laboratory assessment results, including the complete blood count, were normal, except for the leucocyte count, which was 8,330/µL (neutrophils, 80%; lymphocytes, 24.0%; basophils, 0.1%).
Abdominal ultrasonography revealed a thin-walled multilocular cyst with no internal protrusions and no blood flow (Fig. ). Abdominal computed tomography (CT) revealed a cystic shadow, 58 mm in diameter, within the spleen. The cyst had a septate internal structure. A small volume of ascitic fluid was observed in the pelvic region. No evidence of malignancy was observed (Fig. ). Abdominal T2-weighted magnetic resonance imaging revealed a high-signal cystic mass with a clear internal structure, suggestive of a clear cystic tumor (Fig. ). Diagnostic imaging showed no cystic lesion rupture.
Pathological examination was not undertaken as no biopsy or surgery was carried out, which made diagnosis difficult. Splenic lymphangioma was strongly suspected; however, the patient continued to have left upper abdominal pain and tenderness in the same region. His respiratory rate increased to 24 breaths/min, and he was slightly febrile (37.8°C). Considering the elevated leucocyte count and neutrophilia, splenic abscess could not be eliminated as a possible cause. Fosfomycin at 2 g/day was initiated as empirical antibiotic therapy. We had also considered the possibility of a hydatid cyst. However, we did not observe an increase in the basophil numbers of the leucocyte count, and hydatid cysts are very rare in Japan. Hence, it was difficult for us to consider this to be a hydatid cyst. We also suspected infective endocarditis to exclude the possibility of hematogenous spread to the spleen; however, echocardiography revealed normal results. Furthermore, fasting therapy was initiated as soon as possible following admission to reduce the chances of an infection if surgery was planned.
The patient’s abdominal pain improved on day 2 of hospital stay, his respiratory rate decreased to approximately 16 breaths/min and body temperature decreased to 36.6°C. The pelvic region ascitic fluid volume had decreased according to follow-up CT examination. On day 3 of hospital stay, the patient no longer experienced any abdominal pain and all his vital signs had stabilized. The differential white blood count was 4,550/µL, with 52% neutrophils. On examination, signs of infection were found to have improved. No bacteria were detected in the two sets of blood samples collected at the time of admission, and the data did not meet the modified Duke criteria for infective endocarditis. The antibiotic therapy course was completed on day 7 of the hospital stay, and the patient was discharged on day 8.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3795,10,Ideal Body Weight,physical,decimal,pmc-4989811-1,Extracted,"A 54-year-old woman (height, 169 cm and weight, 74 kg) underwent elective surgery for a left posterior parietal meningioma. Her medical history consisted of arterial hypertension well controlled by nebivolol therapy (10 mg/day) that was not interrupted before surgery. The patient was free of visual complaints before surgery. The pre-operative anaesthesia evaluation found her to be in excellent condition. The patient was accepted in the American Society of Anesthesiologists’ physical status 1 with a Lee's cardiac risk index of 1. Pre-operative laboratory investigations were within normal limits. Pre-operative arterial blood pressure was 160/80 mm Hg. Haemoglobin concentration at the beginning of surgery, however, was 11.2 g/dL and haematocrit 35%. She was induced with controlled administration of propofol and sevoflurane. Cisatracurium was used to achieve orotracheal intubation with the help of a No. 8 endotracheal tube. Anaesthesia was maintained with propofol target-controlled infusion (target: 4-6 μg/ml) and continuous infusion of remifentanil (0.5-1 μg/kg/min). Central venous pressure (CVP) and arterial pressure were monitored after cannulation. She was then positioned for surgery in the prone position, with a mild inclination of the table towards a reverse Trendelenburg position. Her head was maintained in a Mayfield frame, with a mild flexion. There was no external compression of the ocular globes. During anaesthesia, end tidal CO2 was continuously kept in the range of 30 mm Hg and oxygen saturation always above 95%. The patient received 200 ml mannitol 15% for brain relaxation 1 h after the beginning of surgery. Her systolic and mean blood pressure was maintained in the range of 80-100 mm Hg and around 60 mm Hg, respectively, throughout the surgery []. Total duration of anaesthesia was 7 h and the patient remained in prone position for 6 h. Total blood loss was around 50 ml. Total fluid infused was 2000 ml crystalloids and intraoperative urine output was 700 ml. There was no use of vasopressors at any point. Extubation was performed 49 min after the surgery. The patient did not receive neuromuscular reversal agents. At the end of surgery, the haemoglobin concentration was 11.7 g/dL and the haematocrit was 36%. The patient was then transferred to Intensive Care Unit (ICU) for further management. On admission, her CVP was 8 mm Hg, systolic arterial pressure 135 mm Hg and mean pressure 85 mm Hg, and these values were maintained during the whole ICU stay. Fluid balance over the first 24 h was slightly negative (−300 mL). After recovery from anaesthesia in ICU, the patient began complaining of a significant decrease in visual acuity without any ocular pain. She was unable to count fingers at a distance of 2 m. The ophthalmological examination was otherwise unremarkable, except for a sluggish pupillary light reflex. There was no evidence of papilloedema on fundoscopy. Intraocular pressure was within normal range. The post-operative brain computed tomography ruled out ischaemic or haemorrhagic complications. The patient was assessed with VEPs on the 1st post-operative day. The examination consisted of flash VEPs (fVEPs) (day 1) and monocular pattern reversal VEPs (pVEPs) (day 1 and 5). The fVEPs were elicited by light-emitting diode goggles (monocular stimulation; red light; flash duration: 1000 μsec; rate: 1.7 Hz; analysis time 500 ms) and recorded at left and right occipital location (O1 and O2). The pVEPS were obtained on day 1 and day 5 by reversal of a black-and-white checkerboard (monocular stimulation, using 3 check sizes, respectively, of 1΀, 30’ and 15’ of arc, at a rate of 1.7 Hz). The pVEPs were recorded at the medial occipital location (Oz) referred to the central medial location (Cz). The fVEPs remained normal at day 1 and were not retested (data not shown). In contrast, the latency of the pVEPs showed significant slowing in both eyes, irrespective of the check size, with a typical paramacular profile (positivity-negativity-positivity) [ above panel]. This alteration in the structure of the VEPs suggested that all nervous fibres in the optic nerve were not affected to the same extent. The latency and structure of pVEPs were normalised by day 5 [, lower panel].
Starting from post-operative day 2, the patient made a complete recovery of visual acuity. This was confirmed by ophthalmological examination at discharge.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [169.0, 'cm']}",60.53158,57.505,63.55816,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 169.0 cm, which is 169.0 cm * 0.393701 in/cm = 66.53547 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.53547 (in inches) - 60) = 60.53158 kg.
Hence, the patient's IBW is 60.53158 kg."
3796,10,Ideal Body Weight,physical,decimal,pmc-8605164-1,Extracted,"Mr. MT, 32-year-old has been married to his cousin for 11 years and has 5 children. He had no somatic or psychiatric history. The patient has a secondary school level and works as a builder. He has no history of past or present substance use a side of smoking weaned for 4 years.
He was referred to the psychiatric examination at Mannouba's Razi Hospital, Tunisia, after seeing urologists, neurologists, and general practitioners. Indeed, a few minutes (10–15 mn) after each ejaculation, he felt intense fatigue, exhausted and severe muscle, bone and joint pain that persisted for a few days (3–7 days). He also reported the straights of sneezing with eye redness and sensations of itching throughout the body as well as intense impaired concentration.
The patient also reported temporary dental pain that accompanied disappeared spontaneously later.
The symptoms have been reported in all ejaculations, independently with the sexual activity “nocturnal emission, masturbation or vaginal ejaculation.”
The protests began with puberty at the age of 14 years old “his first masturbation.” The symptoms increased in severity and duration with age: at first, they lasted 3 days, which drove the patient to take days off but in the last 2 years these symptoms last for 7 days causing financial difficulties.
The evolution of these symptoms was complicated by a sexual avoidance behavior in spite of a preserved sexual desire and rigid erections. The frequency of the sexual intercourse went from 2 per week to 1 per month. Since 2 years, secondary premature ejaculation has been installed.
On examination, the patient was in good general health, well constructed, and had complete secondary sexual characteristics. His weight was 97 kg, his height was 180 cm, and his blood pressure was 120/80 mm/Hg.
Clinical examination, particularly neurological and urological, was strictly normal. No abnormalities were detected in further investigations: The results of laboratory tests routine (CBC, renal function, blood glucose) and the hormone levels (FT4, TSH, prolactin, cortisol, Testostérone, DHEA) were normal (Table ).
In order to investigate the immunoallergic origin of the POIS, the skin prick test was performed on extremely diluted sperm: The sperm freshly emitted from the patient was diluted to a concentration of 1: 40,000, then injected intracutaneously into the palmar surface of the left forearm, and compared to a cutaneous reaction to placebo with 0.9% intracutaneous saline. This test came back positive (Figure ).
This case report was revised to comply with recommendations of the Case Report guidelines, and an informed consent publication was obtained from the patient.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [180.0, 'cm']}",74.99221,71.2426,78.74182,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 180.0 cm, which is 180.0 cm * 0.393701 in/cm = 70.86618 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.86618 (in inches) - 60) = 74.99221 kg.
Hence, the patient's IBW is 74.99221 kg."
3797,10,Ideal Body Weight,physical,decimal,pmc-6277870-6,Extracted,"A 22-year-old white female patient complained of dizziness, nausea, and vertigo for the last 4 years; she was diagnosed with labyrinthitis. Treatment with flunarizine was initiated and the condition partially improved, except nausea that progressively worsened. She also presented galactorrhea and amenorrhea for the past 4 years. Menarche occurred at age 15 and menstrual cycles remained irregular for 6 months; since then, she presented with amenorrhea. Regarding her family history, she reported having a fourth cousin with a pituitary tumor (case 3 of the present study). She had a height of 1.59 m, a weight of 60 kg, and a BMI of 23.8 kg/m2. She had a blood pressure of 120/70 mmHg, and galactorrhea was observed.
The initial hormonal assessment showed a prolactin concentration of 430 ng/mL, FSH of 4.1 mIU/mL, and LH of 2.2 mIU/mL. Treatment with 2.5 mg bromocriptine per day was started. Prolactin concentration in response to treatment with bromocriptine is shown in Figure . The concentration of prolactin 6 months after starting the treatment was 354 ng/mL. The dose of bromocriptine was increased every 6 months at subsequent visits to 5.0, 10, and 12.5 mg per day. However, after 28 months of follow-up, the concentration of prolactin was 155 ng/mL and, therefore, the patient was diagnosed as having resistance to bromocriptine. This was replaced by 1.0 mg per week of cabergoline. After 4 months on 1.0 mg per week of cabergoline, the concentration of prolactin was 126 ng/mL, and she reported a menstrual cycle which lasted 3 days. At the time, surgery was indicated, but the patient preferred to maintain the drug treatment and continued the treatment with 1.0 mg per week of cabergoline. After 15 months of using cabergoline and 43 weeks after starting the treatment, the concentration of prolactin was 103 ng/mL, and the patient reported regular menstrual cycles, improved libido, and the disappearance of galactorrhea. Since then, the dose of cabergoline has been gradually increased to the maximum dose of 3.0 mg per week, 6 years after starting the use of this agonist. The patient had a collateral effect with increasing dose to 3.5 mg per week: nausea and vomiting. The patient continued using 3.0 mg for 4 years, and the concentration of prolactin was 34.17 ng/mL. The dose of cabergoline was reduced to 1.0 mg per week, but the concentration of prolactin increased to 67 ng/dL. Increasing the dose to 1.5 mg for 1 year decreased the concentration of prolactin to 18.7 ng/mL. At that time, the dose was decreased to 0.5 mg per week and the final assessment, after 2 years, showed a prolactin concentration of 24.6 ng/mL. This corresponds to 16 years from the start of the treatment with dopamine agonists and 14 years of using cabergoline.
The first assessment of the sella turcica was performed by computed tomography with contrast. A heterogeneous mass was observed in the pituitary region, predominantly on the left, which widened the sella turcica and destroyed the adjacent bone structures, superficially invading the suprasellar cistern and inferiorly the sphenoid sinus. There was no compression of the optic chiasm. The mean size of the lesion was 2.8 × 3.0 × 3.0 cm. Six months after starting the treatment with 2.5 mg per day of bromocriptine, MRI of the sella turcica showed an expansive lesion of 20 × 15 × 12 mm in the left half of the anterior pituitary with invasion of the cavernous sinus, enveloping the left carotid artery and widening the sella floor on that side. The pituitary stalk was diverted to the right.
After 4 months on 1.0 mg per week of cabergoline, MRI of the sella turcica showed an expansive lesion of 12 × 10 × 8 mm, compromising the left half of the anterior pituitary with lateral expansion to the corresponding cavernous sinus. A discrete deviation of the pituitary stalk to the right was observed, without an existing suprasellar component. At the time, surgery was indicated, but the patient preferred to maintain the drug treatment and continued treatment with 1.0 mg per week of cabergoline. After 28 months of treatment with cabergoline, MRI of the sella turcica showed a nodular lesion of 0.4 cm in the left half of the anterior pituitary. She used 3.0 mg per week of cabergoline until completing 116 months of treatment, and the MRI performed on that occasion showed an increase in the size of the sella turcica, which was filled by cerebrospinal fluid with a small volume of pituitary glandular tissue on the floor, featuring a partially empty sella.
The images described above were not presented.
Assessments of thyroid function showed TSH ranging from 1.46 to 3.89 mIU/mL and FT4 ranging from 0.56 to 0.94 mIU/mL, consistent with the diagnosis of secondary hypothyroidism. The patient uses 50 μg per day of levothyroxine.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.59, 'm']}",51.47646,48.90264,54.05028,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.59 m, which is 1.59 m * 39.3701 in/m = 62.59846 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.59846 (in inches) - 60) = 51.47646 kg.
Hence, the patient's IBW is 51.47646 kg."
3798,10,Ideal Body Weight,physical,decimal,pmc-3866344-1,Extracted,"A 31-year-old pregnant woman (59 kg/170 cm, 34w+5, G4P2A1L2) was admitted for Caesarean section. The patient had no problems until fetal bowel obstruction was diagnosed by routine obstetrical ultrasonography taken 10 days earlier ().
General anesthesia was induced with 250 mg of thiopental sodium and 75 mg of succinylcholine. Ten minutes after skin incision, a 2.66 kg, 46 cm of male baby was born with an Apgar score of 7 at 1 min and 9 at 5 min. The newborn cried relatively well despite the moderately distended abdomen, so routine care was given, which included transfer to the neonatal intensive care unit (NICU).
Peripheral oxygen saturation (SpO2) of the baby was maintained at 96-97% with 2 L/min of oxygen in the hood and first urine was passed at 4 h of age. However, abdominal distention was sustained and nothing was aspirated through the positioned oro-gastric tube. An infantogram, bowel sonography, and barium enema were performed. Distended small bowel loops up to 3 cm and microcolon were seen and no more contrast was passed proximal to terminal ileum, which suggested ileal atresia ().
Emergency surgery was performed at 10 h of age. Under standard monitoring including electrocardiography (ECG), non-invasive blood pressure (NIBP), end-tidal CO2 (ETCO2), and SpO2 (dual monitor at right arm and left foot), the patient was intubated with a 3.5 Fr cuffed endotracheal tube. Two 24 gauge intravenous (IV) lines were started on the left arm and right leg, a 6 Fr feeding tube was inserted for gastric decompression, and a Foley catheter was inserted for hourly urine count. To minimize heat loss, the room temperature was increased, the patient was hatted, a warm air mattress and warmed IV fluids were used, and body temperature was monitored. The anesthesia was maintained with sevoflurane, FiO2 of 0.3-0.4 with air, pressure control mode of 18 mmHg, and a respiratory rate (RR) of 20 breaths/min. BP was maintained at 50-80/30-45 mmHg, heart rate (HR) at 140-160 beats/min, ETCO2 at 32-40 mmHg, and SpO2 98-100%. There were severe adhesions on the entire abdomen such that the anatomy was not easily distinguishable. After massive adhesiolysis, segmental resection of injured bowel and anastomosis were performed. Moderate amount of reactive fluid was seen and moderate bleeding was ongoing. At 90 min of the surgery, HR abruptly rose to 170 beats/min. Arterial blood gas analysis was taken, which showed pH 7.34, PaCO2 38 mmHg, PaO2 191 mmHg, HCO3 20.5 mM/L, Na 134 mEq/L, K 4.2 mEq/L, Hb 10.2 g/dl, and blood sugar 118 mg/dl. Packed red blood cells 30 ml were transfused and no other intraoperative symptoms were found. Total time taken for surgery was 2 h 45 min and for anesthesia, 3 h 20 min. Total fluid administered was SD 1 : 3 solution 20 ml, lactated Ringer's solution 50 ml, and normal saline 10 ml.
After the surgery, the patient was extubated and SpO2 was maintained over 97% without supplemental oxygen. Urine output was 1 ml/h and 1.5 ml/h, respectively, during the first 2 h of surgery, however, no further urine was observed during last hour of surgery. However, 7 ml of urine was formed after 2 h of surgery without fluid loading and no further oliguria was seen. Hb after transfusion was 13.6 g/dl and hemodynamic parameters were stable thereafter. Breast feeding was started 5 days after the surgery and the baby was discharged at postoperative day 24.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [170.0, 'cm']}",61.43709,58.36524,64.50894,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.92917 (in inches) - 60) = 61.43709 kg.
Hence, the patient's IBW is 61.43709 kg."
3799,10,Ideal Body Weight,physical,decimal,pmc-5240319-1,Extracted,"In 2005, an otherwise healthy 55 year-old female patient, with a primary diagnosis of hip osteoarthritis and otherwise unremarkable history, underwent bilateral staged THA at another institution. A cementless system with a ceramic-on-ceramic articulation was used on both occasions (R3 acetabulum, Synergy femoral stem; Smith & Nephew, Memphis, TN, USA). Commencing early postoperatively, the patient had recurrent dislocation of her right arthroplasty () as often as 3-4 times a year, which she managed to reduce on her own. Six years postoperatively, the patient sustained a fracture of the right ceramic head (). The acetabular prosthesis was exchanged with a tantalum shell and an ultra-high molecular weight polyethylene liner. The existing stem was well fixed and therefore was left in situ. The fractured ceramic head was exchanged with one made of cobalt-chromium alloy (Continuum acetabulum, Versys head; Zimmer, Warsaw, IN, USA) ().
In the following months, the patient gradually developed severe activity related right hip pain. Six months post-revision, the patient developed erythema nodosum of the left leg and bilateral chorioretinitis and papilledema. A chest computed tomography (CT) revealed diffuse radiopaque nodules in both lungs and enlargement of the right hilum (). Biopsy of the right lung showed fibrosis and extensive inflammation with multiple non-necrotizing granulomata, consisting of histiocytes, multinucleated giant cells, and lymphocytes (). Special stains for mycobacteria and fungi were negative and no atypical cells were found. A diagnosis of sarcoidosis was made. The patient received corticosteroids and azathioprine for six months, which led to clinical and radiological improvement. Between 2013 and 2015, echocardiograms and chest magnetic resonance imaging showed severe cardiomyopathy with the ejection fraction decreasing from 70% to 35% and evidence of non-ischemic type fibrosis of the lower and posterior ventricular wall, as well as moderate dilation of the left ventricle.
The patient sought advice from our team in February 2015. Physical examination revealed a 76 kg, 159 cm tall woman, with a severely antalgic gait and painful, decreased range of motion of the right hip. Radiographic imaging showed severe osteolysis of the proximal femur (). A CT of pelvis revealed an iliac pseudotumor (). The presence of a pseudotumor, extensive osteolysis, and the history of a fractured ceramic implant exchanged with a metal alloy head and a polyethylene liner, aroused suspicion for metallosis. A hip aspiration produced black fluid with high concentrations of chromium and cobalt, 25,400 µg/L and 26,500 µg/L respectively (). Whole blood chromium and cobalt concentrations were also significantly elevated, 31.8 µg/L and 22.2 µg/L respectively.
It was therefore decided to proceed with a second revision operation. Intraoperatively, gross local metallosis was found and large volumes of black fluid poured out from a trochanteric pseudotumor. There was extensive osteolysis of the proximal femur but the stem remained fixed (). Multiple ceramic fragments were still present in the periprosthetic tissues. Ceramic debris was also embedded in the articular surface of the polyethylene liner (). The metallic head was distorted due to massive wear (). The Morse taper of the stem was also damaged, allowing free rotation of the prosthetic head ().
Meticulous soft tissue debridement was carried out. The acetabular shell, which remained well fixed, was left in place but the worn polyethylene liner was removed. The femoral stem was exchanged with a long revision implant (Wagner SL revision uncemented stem; Zimmer GmbH, Winterthur, Switzerland). To prevent recurrence of the problem, a ceramic-on-ceramic articulation was inserted (Biolox Delta; Zimmer GmbH) ().
Recovery was uneventful. At three months, blood chromium and cobalt levels had returned to normal, 1.17 µg/L and 0.19 µg/L respectively. One year later, the patient was able to mobilize painlessly, using one crutch. She had no respiratory symptoms and her pulmonary function tests were normal. Her heart function had stabilized to an ejection fraction of 50%.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [159.0, 'cm']}",51.47646,48.90264,54.05028,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 159.0 cm, which is 159.0 cm * 0.393701 in/cm = 62.59846 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.59846 (in inches) - 60) = 51.47646 kg.
Hence, the patient's IBW is 51.47646 kg."
3800,10,Ideal Body Weight,physical,decimal,pmc-6537418-1,Extracted,"A 21-year-old Caucasian male was admitted to a hospital (collaborating institution) in Southern Germany in late summer with newly manifested jaundice as well as a seven-day-history of myalgia, retro-orbital headaches, fatigue, recurrent fever, and nausea. Since the beginning of his illness, myalgia — especially in the calf region — intensified, causing the patient an increasing difficulty in walking. He reported an episode of gum bleeding after cleaning his teeth. There was no history of traveling abroad in the last months and no recent contact with animals. Two weeks prior to the onset of his symptoms the patient sustained a minor knee injury resulting in a skin abrasion while bathing in the river Isar close to Munich, Germany.
The patient works as a computer scientist and has no relevant medical history. Weight and height upon admission were recorded to be 90 kg and 189 cm, respectively (BMI = 25.2 kg/m2). Alcohol, nicotine, or drug anamnesis was negative. No medication or allergies were reported.
On examination, the patient appeared tired, but he displayed no neurological abnormalities. Body temperature was 36.8 °C, pulse 90 bpm, blood pressure 114/75 mmHg, respiratory rate 16 bpm, and oxygen saturation 99% while breathing ambient air. The lungs and heart auscultation was unremarkable, the abdomen was soft and non-tender. The skin and scleral inspection revealed jaundice and a slight gum bleeding was observed during the examination of the oral cavity. Upon pressure, tenderness in the thighs and calves was reported.
Abdominal ultrasound upon admission to the hospital revealed hepatosplenomegaly and no signs of intra- or extrahepatic cholestasis. White-cell count was 9.9 G/L (87% neutrophils and 3.5% lymphocytes), platelet count 39 G/L, and hemoglobin 13.3 g/dl. Serum sodium level was 123 mmol/l, potassium 3.15 mmol/l, and creatinine 2.8 mg/dl (248 μmol/l) with glomerular filtration rate of 31 ml/min/1.73m2. C-reactive protein was 15.4 mg/dl, procalcitonin 2.86 ng/ml, and interleukin-6 was 66.4 pg/ml. Aspartate aminotransferase was 92 U/L, alanine aminotransferase 65 U/l, total bilirubin 17.3 mg/dl (with direct bilirubin reaching 14.7 mg/dl), gamma-glutamyltransferase 47 U/l and alkaline phosphatase 108 U/l. Creatine kinase was 1197 U/l, prothrombin time international normalized ratio 1.2, and partial-thromboplastin time 33 s. Urinalysis revealed a pH of 8, 3+ protein (6.3 g protein/12 h), 5–10 leukocytes per high power field, and 0–2 erythrocytes per high power field. An overview of laboratory test results with the corresponding reference ranges is shown in Table .
On day 1 upon admission an empiric intravenous antimicrobial regime with doxycycline (100 mg every 24 h) and ceftriaxone (2 g every 24 h) was initiated while a selection of tests in search for microbial and viral agents was pending. The patient received intravenous fluid and electrolyte replacement. Within 48 h upon admission, hypokalemia (2.32 mmol/l) and hyponatremia (113 mmol/l) worsened significantly without signs of acid-base dysregulation in blood gas analysis. Creatinine increased to 4.37 mg/dl (386 μmol/l), and a polyuria with up to 7.2 L urine output /24 h was documented. The patient was transferred to the intensive care unit (ICU) at the initial collaborating institution and — approximately 48 h later — transferred to the ICU at our university hospital. Starting from day 4 since the initial admission creatinine levels started to decrease, polyuria was in regress and potassium and sodium levels normalized. In addition, platelet count improved and C-reactive protein decreased. The patient remained afebrile. Despite the gradually improving general condition of the patient, serum bilirubin levels were constantly rising starting from day 1 since admission, reaching its maximum on day 4 (54 mg/dl total bilirubin, 39 mg/dl direct bilirubin). Aspartate and alanine aminotransferases, alkaline phosphatase and gamma-glutamyltransferase remained normal or mildly elevated (Table ).
Urine and blood cultures revealed no growth. Screening tests for hepatotropic viruses (hepatitis A, B, C, and E) as well as HIV, Epstein-Barr virus, and cytomegalovirus were negative. Elevated IgG antibodies to herpes simplex virus (HSV 1 and 2) were detected while IgM antibodies remained within the normal range, suggesting an earlier or latent infection with HSV virus. Quantitative serology assays for hantavirus, Chlamydia, Brucella, and Rickettsia (rickettsii/conorii) showed no evidence for infection with these pathogens. Urine test for Legionella antigen was negative. Within normal range were: antinuclear antibodies (ANA), antimitochondrial antibodies (AMA), anti-liver/kidney microsomal antibodies type 1 (anti-LKM-1), anti-soluble liver antigen antibody/liver-pancreas (a-SLA/LP), anti-liver membrane antibodies (LMA), anti-liver specific protein antibodies (LSP), and perinuclear- and cytoplasmic-antineutrophil cytoplasmic antibodies (p-ANCA and c-ANCA) whereby autoimmune hepatitis could be ruled out. Normal levels of serum copper (110 μg/dl, reference range: 70–140 μg/dl) as well as serum ceruloplasmin (0.44 g/l, reference range: 0.2–0.6 g/l) allowed to dismiss Wilson’s disease from diagnostic consideration.
The presumptive diagnosis of icteric leptospirosis was strengthened by detection of antileptospiral IgM antibodies with the use of ELISA in the acute phase serum specimen (38 U/ml, reference range: < 15 U/ml, SERION ELISA classic Leptospira IgG/IgM, Virion Serion, Würzburg, Germany) and confirmed by an accredited PCR method using proprietary primers at the Institute for Medical Microbiology and Hygiene at the University of Regensburg, Germany. The therapy with doxycycline was discontinued (total duration of 3 days) and the regime with ceftriaxone carried on as a targeted monotherapy (total duration of 12 days).
The patient was discharged home after a total of 12 days of hospitalization (3 days at the ICU). The general condition upon discharge was reported as good; fatigue was declining and the remaining symptoms, with the exception of jaundice (total bilirubin 6.2 mg/dl), subsided.
Throughout hospitalization and a 3-month follow-up period, indocyanine green plasma disappearance rates were recorded multiple times. For each measurement, 25 mg of the ICG dye were dissolved in 5 ml of distilled water, and a dose of 22.5 mg (0.25 mg/kg body weight) was injected intravenously. ICG-PDR was determined via non-invasive, transcutaneous pulse dye densitometry with the use of the LiMON device (Pulsion Medical Systems SE, Feldkirchen, Germany). Initial concentration at time “0” was set to be 100% and plasma disappearance rate was calculated as percentage change over time (%/min) []. Normal values for ICG-PDR are considered to be 18–25%/min [, ]. The measured ICG-PDR values, total bilirubin and alanine aminotransferase serum levels are displayed in Fig. .
Initially severely reduced ICG-PDR (2%/min on day 5 upon initial admission) gradually improved within several days to reach almost normal level on day 10 upon initial admission to hospital (17.4%/min). Approximately 7 weeks after initial hospitalization, ICG-PDR was recorded to be within normal range (23.7%/min) and reached 33.4%/min on day 85. While ICG-PDR values rapidly normalized in parallel with clinical improvement, serum bilirubin levels were slowly decreasing (44.4 mg/dl on day 5 and 9.0 mg/dl on day 10 upon hospitalization), and it was only until 7 weeks upon admission that they reached normal levels (Fig. ). Mild elevation of serum alanine aminotransferase was at its peak of 124 U/l on day 12 upon hospitalization (Table ) and reached close to normal levels by week 7 upon admission (Fig. and Additional file ). Within the 3-month follow-up period, fatigue resolved and the patient reported no remaining symptoms.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [189.0, 'cm']}",83.14183,78.98474,87.29892,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 189.0 cm, which is 189.0 cm * 0.393701 in/cm = 74.40949 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (74.40949 (in inches) - 60) = 83.14183 kg.
Hence, the patient's IBW is 83.14183 kg."
3801,10,Ideal Body Weight,physical,decimal,pmc-4005209-1,Extracted,"A 53-year-old man, nonalcoholic, nonsmoker, presented with complaints of persistent vomiting, burning micturation, increased frequency of urine since last 10 days, and pain and swelling in both feet and ankle since 15 days. There was history of similar pain in leg which started at the age of 17 years and later occurred frequently at varied intervals. There was history of loss of all hair from the body at the age of 17 year. He had been treated for left ureteric stone a year back and his family including his mother, two younger brothers, and one of his sons had renal stones. His son also lost his hair all over the body at the age of 10 years. On examination his pulse was 122 beats per min, blood pressure (BP) 70 mmHg systolic, respiratory rate (RR) 26/min, and he was afebrile. His anthropometric measurements were: Waist circumference 106 cm, height 170 cm, and weight 85 kg. He had bilateral tender swelling involving both feet and ankle. There were no hair on his body [] and multiple skin tags around neck, axilla were found [Figures and ]. Systemic examination including cardiovascular, respiratory, and per abdomen were unremarkable. A probable diagnosis of alopecia universalis with urinary tract infection with systemic inflammatory response syndrome (SIRS) was made and patient was investigated. The investigations revealed: Hemoglobin (Hb) 12.2 g%, erythrocyte sedimentation rate (ESR) 74 mm in 1st h, total leukocyte count (TLC) 7,800/mm3, blood urea 125 mg/dl (17-43), serum creatinine 2.27 mg/dl (0.67-1.17), serum uric acid 21.7 mg/dl, total bilirubin 0.5 mg/dl, direct 0.2 mg/dl, total serum protein 6.0 mg/dl, albumin 3.9 mg/dl, serum glutamic-oxaloacetic transaminase (SGOT) 18 U/l, serum glutamic-pyruvic transaminase (SGPT) 15 U/l, alkaline phosphatase (ALP) 174 U/l, sodium 140 mEq/l, potassium 2.97 mEq/l, chloride 88 mEq/L, calcium 9.6 mg/dl, phosphorus 4.6 mg/dl, vitamin D 53.94 nmol/l, serum total cholesterol 287 mg/dl, triglyceride 404 mg/dl, high density lipoprotein (HDL) 36 mg/dl, low density lipoprotein (LDL) 170.2 mg/dl, very low density lipoprotein (VLDL) 80 mg/dl, prostate specific antigen (PSA) 1.04 ng/ml (<4), blood sugar (fasting (F)) 108 mg/dl, and HbA1c 5.7%. Urine examination showed presence of albumin, pus cells 20-25/high power field (HPF), red blood cell (RBC) 2-4/HPF, and no growth in urine culture. The 24 h urine protein was in nephrotic range with 7.07 g excretion/day. Thyroid stimulating hormone (TSH) was 14.51 μIU/ml (0.35-5.50), triiodothyronine (T3) 0.8 ng/dl (2-4.4), thyroxine (T4) 0.01 pg/dl (0.6-2.2), and C-reactive protein (CRP) was positive. Other investigation including arterial blood gas (ABG), human immunodeficiency virus (HIV), hepatitis C virus (HCV), hepatitis B surface anitgen (HBsAg), complement levels (C3, C4), antinuclear antibody (ANA), rheumatoid arthritis factor (RA), and anti-thyroid peroxidase (TPO) antibodies were not significant. Computed tomography (CT) scan of abdomen showed multiple crystals in both kidneys. Patient was treated with intravenous crystalloids, antiemetic (ondansetron/promethazine), antibiotic (levofloxacin), oral hypouricemic drug (fabuxostat), rozuvastatin, thyroxin, and tramadol. Patient started improving gradually and his uric acid level decreased from 21.7 to 10.4 mg/dl over a period of 2 weeks.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3802,10,Ideal Body Weight,physical,decimal,pmc-5292792-1,Extracted,"A 45-year-old Japanese man was referred to our hospital in March 2007 because of thyrotoxicosis. His family history was unremarkable, but he had a medical history of thyrotoxicosis that was treated with oral MMI at a local hospital from 23 to 43 years of age, at which time he discontinued the therapy based on his own judgment. He had smoked 20 cigarettes per day since he was 20-years old, had taken no medication (except for MMI), would drink a glass of beer on a social basis, and ingested an adequate amount of iodine with the traditional Japanese diet. He visited his primary care doctor for the first time in the previous 2 years because of months of fatigue, palpitations, and finger tremors and was diagnosed with thyrotoxicosis. He was subsequently referred to our hospital.
A physical examination revealed that he was 161 cm tall, weighed 51 kg, had a body temperature of 36.8 °C, and had a blood pressure of 143/75 mmHg. He did not exhibit exophthalmos or skin eruption but presented with a soft and mild goiter without pain, moist skin, and bilateral finger tremors. In addition, thrill and vascular bruit were audible on his goiter. No heart murmurs, chest rales, or peripheral edema were detected, and an electrocardiogram revealed sinus tachycardia with a heart rate of 108 beats per minute. His laboratory data revealed a normal complete blood count, high serum alkaline phosphatase level, and severe hyperthyroidism: free triiodothyronine (FT3) >25.0 pg/mL and free thyroxine (FT4) 7.90 ng/dL (Table ). His TSAb test (Yamasa Corporation; Chiba, Japan) was negative, but his second-generation TBII (Yamasa Corporation), thyroid peroxidase antibody (TPOAb)-radioimmunoassay (RIA; Cosmic Corporation; Tokyo, Japan), and thyroglobulin antibody (TgAb)-RIA (Cosmic Corporation) tests were positive. Thyroid ultrasonography showed a diffusely enlarged thyroid gland in the absence of a tumor lesion, and color flow Doppler detected increased blood flow. Thus, he was considered to have Graves’ hyperthyroidism, and he began treatment with oral MMI (30 mg/day). In addition, he was instructed to discontinue smoking cigarettes.
After 3 months of treatment with oral MMI, his serum thyroid hormone levels decreased to almost within the normal range, and he experienced improvements in his palpitations, sweating, and finger tremors and gained 4 kg of body weight during this period. In December 2007, he had a normal serum FT3 level (2.24 pg/mL) with a detectable TSH level, and his second-generation TBII titer had normalized (Fig. ); thus, his dose of MMI was titrated to <10 mg/day. However, he exhibited persistent hyperthyroidism and continued oral MMI treatment at 10 to 15 mg/day.
He discontinued the oral MMI treatment of his own accord in April 2012 and then revisited our hospital in June 2012 due to fatigue and palpitations. Laboratory findings revealed hyperthyroidism (FT3 6.98 pg/mL, FT4 2.59 ng/dL; Fig. ). He resumed medication with oral MMI (15 mg/day); his thyrotoxicosis symptoms had resolved and his serum FT3 and FT4 levels had normalized within 3 months.
A detailed examination of his unresolved thyrotoxicosis was performed in July 2013. At this time, he presented with a soft goiter with audible bruit but did not exhibit exophthalmos or skin eruption. A blood chemistry analysis showed slightly high serum levels of FT3 (5.45 pg/mL) and FT4 (2.21 ng/dL) under treatment with oral MMI (10 mg/day). He tested negative on TSAb (107%) and first-generation (3%; reference range –10 to +10%; Cosmic Corporation), second-generation (<1.0 IU/L), and third-generation (0.9 IU/L; reference range <2.0 IU/L; Roche Diagnostics K.K.; Tokyo, Japan) TBII assays. He showed positive test results on a TPOAb-electrochemiluminescence immunoassay (ECLIA; TPOAb titer 218 IU/mL, reference range <16.0 IU/mL; Roche Diagnostics K.K.) and a TgAb-ECLIA (TgAb titer 740 IU/mL, reference range <28.0 IU/mL; Roche Diagnostics K.K.). A thyroid ultrasonography showed heterogeneous and reduced echogenicity in a diffusely enlarged thyroid gland without a mass lesion, and color flow Doppler detected increased blood flow (Fig. ). Technetium-99 m thyroid scintigraphy showed diffuse and elevated uptake (Fig. ). These findings indicated persistent Graves’ hyperthyroidism []. Human leukocyte antigen (HLA) typing revealed the presence of A*24:02:01/31:01:02, B*40:02:01/51:01:01, and C*03:04:01/14:02:01 class I genes and DRB1*04:10:01/12:01:01, DQB1*03:03:02/04:02:01, DQA1*03:02/03:03, and DPB1*05:01:01/(−) class II genes.
In terms of the long-term management of his hyperthyroidism, he was informed of various treatment options, such as radioiodine therapy and thyroidectomy, but he expressed his hope to continue with the anti-thyroid medication. Because the MMI treatment had previously appeared to effectively control his hyperthyroidism with no obvious side effects, he continued oral MMI treatment at 15 mg/day (Fig. ). Accordingly, his peripheral thyroid hormone levels were maintained within approximately normal reference ranges during the course of the MMI treatment.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [161.0, 'cm']}",57.78748,54.89811,60.67685,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 161.0 cm, which is 161.0 cm * 0.393701 in/cm = 63.38586 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (63.38586 (in inches) - 60) = 57.78748 kg.
Hence, the patient's IBW is 57.78748 kg."
3803,10,Ideal Body Weight,physical,decimal,pmc-7726185-1,Extracted,"Case1: A 39-year-old woman was admitted to our hospital with a history of headache dating back 3 months. The headaches were occasionally associated with transient binocular visual obscurations. As time went by, the headaches increased in intensity and transient right monocular visual loss lasting for several seconds appeared. She was non-obese with a weight of 55 kg and height of 155 meters (BMI 22.9), without history of menstrual irregularity, and had received no drugs. Neurological examination revealed nothing except for papilla edema found by ophthalmoscopic examinations of the fundus. Visual field examinations revealed a larger blind spot in both eyes. Visual acuity was normal. Fluorescein angiography confirmed papilla edema with dilatation of the optic disc capillaries. A lumbar puncture revealed a recumbent opening pressure of 330 mmH2O and the components of cerebrospinal fluid were normal, including cell count and protein and glucose levels. No pathogenic organisms were found in the cerebrospinal fluid. Other laboratory studies, including blood cell counts, erythrocyte sedimentation rate, blood electrolytes, blood glucose, immunoglobulins and complement, serum creatine levels, cholesterol, triglyceride, liver function, C reactive protein, anti-cardiolipid antibody, anti-nuclear antibody, thyroid function, hormone level of parathyroid, and estradiol, were normal. No abnormalities were seen on transcranial doppler. Magnetic resonance imaging (MRI) of the brain and the veins only demonstrated partial empty sella and excluded the stenosis or occlusion of the veins in the brain. As we could not identify any causes, idiopathic intracranial hypertension was proposed. After glycerol were taken, her headaches subsided, but papilledema still existed.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'm']}",13942.94065,13245.79362,14640.08768,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 m, which is 155.0 m * 39.3701 in/m = 6102.3655 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (6102.3655 (in inches) - 60) = 13942.94065 kg.
Hence, the patient's IBW is 13942.94065 kg."
3804,10,Ideal Body Weight,physical,decimal,pmc-4192804-1,Extracted,"A 49-year-old man visited our hospital for polydipsia (8 to 9 L/day) and polyuria that started one month prior. He had no remarkable family history. Two years prior, the patient had experienced right chest pain and osteolytic lesions of the right 6th and 7th ribs were detected on X-ray. He was diagnosed with LCH after surgical excision of the rib mass in our hospital. At that time, subsequent bone scan and brain computed tomography (CT) revealed an osteolytic lesion in the occipital skull without involvement of brain parenchyma. The skull lesion was carefully followed up with skull X-ray, but the patient was lost to follow-up after 1 year.
On physical examination, the patient appeared well. Blood pressure was 130/90 mm Hg, pulse rate was 72 beats per minute, respiratory rate was 20 breathes per minute, and body temperature was 36.2℃. His height and weight were 164 cm and 70 kg, respectively. His tongue was not dry and skin turgor was normal without evidence of dehydration. Inspection and palpation of the chest revealed no masses, lung sounds were clear at auscultation, and no lymph nodes were palpable in the neck or limbs. Neurologic examination revealed normal motor and sensory functions, symmetric reflexes, and no evidence of clonus, fasciculations, or ataxia. The results of other physical examinations were unremarkable.
Blood cell count, urinalysis, serum chemistry, and electrolytes were within normal range. Basal anterior pituitary hormones were also normal. Serum osmolality at admission was 295 mOsm/kg and urine osmolality was 75 mOsm/kg. For differential diagnosis of polydipsia, the water deprivation test was performed. After 8 hours of water deprivation, serum osmolality reached 303 mOsm/kg and urine osmolality was stable with variation of less than 30 mOsm/kg, ranging from 99 to 118 mOsm/kg. We injected five units of vasopressin subcutaneously and urine osmolality was followed serially. After vasopressin injection, urine osmolality markedly increased to 562 mOsm/kg (more than 50% from baseline) after 1 hour and we reached a diagnosis of central DI ().
Magnetic resonance imaging (MRI) of the pituitary gland revealed a solid mass involving the infundibulum (6 mm) and the posterior lobe of the pituitary gland with loss of bright spot on T1 weighted imaging (). We further performed the combined pituitary stimulation test and anterior pituitary function was normal.
Chest X-ray showed cavitary lesions in the right upper lobe and reticular opacities in right lower lobe (). CT of the chest with contrast enhancement demonstrated multiple patchy infiltrations in both lung fields with ground glass opacity and air bronchogram (). Chest CT also revealed new osteolytic bone lesions in the right 9th rib and left 10th rib, which were visualized as hot uptake on bone scan.
We concluded that LCH had spread to the pituitary gland, lung and bone and we planned treatment with inhaled desmopressin and systemic chemotherapy. The patient received intranasal desmopressin 10 µg twice daily and urine volume decreased to 1.5 to 2 L per day. He was treated with 6-week induction chemotherapy with prednisolone (40 mg/m2/day for 6 weeks) and vinblastine (weekly 6 mg/m2 intravenous bolus injection), followed by maintenance chemotherapy with 6-mercaptopurine (50 mg/m2 per day), vinblastine (6 mg/m2 intravenous bolus injection every 3 weeks), and prednisolone (40 mg/m2/day for first 5 days every 3 weeks) for 12 months.
Two months later, follow-up sella MRI demonstrated disappearance of the mass in the infundibulum of the pituitary gland (). During maintenance chemotherapy, chest CT with contrast enhancement revealed complete disappearance of the lung lesions 11 months after the start of chemotherapy (). Six years after chemotherapy, the patient has shown no evidence of recurrence at regular follow-up examinations and polyuria is well controlled with intranasal desmopressin.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [164.0, 'cm']}",60.50401,57.47881,63.52921,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 164.0 cm, which is 164.0 cm * 0.393701 in/cm = 64.56696 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.56696 (in inches) - 60) = 60.50401 kg.
Hence, the patient's IBW is 60.50401 kg."
3805,10,Ideal Body Weight,physical,decimal,pmc-7533046-1,Extracted,"A 57-year-old male (height 166 cm, weight 92 kg, body mass index 33.4 kg/m2) received total aortic arch replacement for acute type A aortic dissection. His past medical histories included right nephrectomy for right kidney cancer and hypertension. The aortic replacement was performed under general anesthesia, which was induced with propofol (target-controlled infusion [TCI] 6.0 μg/mL), fentanyl 0.5 mg, and rocuronium 100 mg. Thereafter, a cuffed tracheal tube with an inner diameter of 8.0 mm was orally intubated and fixed at 22 cm at the corner of the mouth. There were no particular problems, including tooth damage during tracheal intubation. Anesthesia was maintained with propofol (TCI 2.0–2.2 μg/mL, total 4860 mg), remifentanil, fentanyl (total 2.5 mg), and rocuronium. The operative time was 532 min, and the anesthesia time was 638 min.
After the surgery, the patient was transferred to the intensive care unit (ICU) with artificial respiration, and dexmedetomidine 0.43 μg/kg/h and fentanyl 30 μg/h were administered for sedation and analgesia. On the first postoperative day (POD 1), an extreme elevation of creatine kinase (CK, 3,730 U/L) and a 39 °C fever of uncertain etiology were observed. We suspected propofol infusion syndrome (PRIS), malignant hyperthermia (MH), neuroleptic malignant syndrome, drug-induced rhabdomyolysis, and/or serotonin syndrome; therefore, we ceased administration of any potentially related drugs (propofol, piperacillin/tazobactam, fentanyl) and started administration of midazolam and dexmedetomidine instead. Although the CK value peaked at 45,288 U/L on POD 7 after gradual increase from POD 1, it was decreased after POD 8 due to the dantrolene 40 mg administrated on POD 7. In addition, a decrease in renal function (estimated glomerular filtration rate: 17.6 mL/min/1.73 m2) was observed postoperatively; thus, continuous hemodiafiltration (CHDF) was performed from POD 2. Moreover, mechanical ventilation had been continued because of poor oxygenation due to pneumonia since surgery. We did not perform tracheostomy because of the high possibility of mediastinitis due to the protruding sternal wires and possible difficulty of hemostasis by anticoagulants for CHDF, in spite of long-term mechanical ventilation.
A chest X-ray on POD 34 revealed an abnormal shadow near the larynx (Fig. ). Review of previous X-ray showed the same shadow in the hypopharynx on POD 19, although it was not identified immediately after arrival in the ICU. A loss of a front tooth was found on POD 22; however, a foreign substance was not confirmed in the oral cavity or on the abdominal X-ray, and the patient was placed under observation. A simple computed tomography (CT) scan on POD 34 showed a shadow with metal artifacts, indicating a crown bridge, outside of the tracheal tube, inside the trachea, and just under the glottis (Fig. ). Upper esophageal gastrointestinal endoscopy performed on POD 34 also revealed tooth fragments in the stomach. The pharynx and larynx were examined at bedside using McGRATHTMMAC video laryngoscope (Medtronic, MN, USA); however, no foreign matter was found. Observation from the inside of the tracheal tube using the bronchial fiber revealed a foreign body in the trachea just below the glottis, outside (ventral side) the tracheal tube. We therefore considered that the removal of the foreign body in a well-equipped environment would be more suitable than in the ICU and that the foreign body would not cause airway obstruction immediately.
Removal of the airway foreign body was performed in the operating room on POD 35. Preoperative ventilator settings were pressure support (PS) mode, an inspiratory oxygen concentration of 60%, a PS of 8 cmH2O, a positive end expiratory pressure of 5 cmH2O, and an arterial oxygen partial pressure of 274 mmHg. His consciousness level was E4VtM5 on the Glasgow Coma Scale. The CHDF and administration of heparin were interrupted 90 min before entering the operating room. For the procedure, three anesthesiologists, one thoracic surgeon (bronchoscopy operator), one cardiac surgeon (attending physician), and three nurses were convened, and a difficult airway management (DAM) cart was prepared in the operating room.
The patient entered the operating room while maintaining spontaneous breathing. After administration of atropine 0.5 mg, continuous administration of dexmedetomidine 0.22–0.89 μg/kg/h was started under standard monitoring as well as neuromuscular monitoring. In addition, ketamine 10 mg was administered seven times in total while observing the capnogram and the patient’s condition. Then, his respiratory rate became 12 breath/min, and he was sedated (Richmond Agitation-Sedation Scale score of − 2 to − 3). A total of 5 mL of 4% lidocaine was sprayed into the pharynx and larynx for local anesthesia via a Jackson’s spray. With the trachea intubated, the larynx was visualized using a blade size 4 of McGRATHTMMAC, and a bronchial fiber (OLYMPUS BF TYPE 1T260, tip outer diameter 5.9 mm, Olympus Corporation, Tokyo, Japan) was inserted into the oral cavity to observe the larynx. No foreign body was confirmed in the pharynx and larynx; however, when the bronchial fiber was inserted into the glottis from the gap between the glottis and the cuff of the tracheal tube, a part of the foreign body appeared and disappeared between the arytenoid cartilage and the vocal cord according to the patient’s breathing (Fig. a). Although we could not confirm the whole image of the foreign body, we were able to confirm that it was mobile. At this point, hiccups, cough, and/or gag reflex occurred and it became difficult to secure a field of view with the fiber. We judged that the foreign body could be removed via an oral approach using the bronchial fiber while maintaining intubation. Thus, rocuronium was administered to eliminate spontaneous breathing and body movement, and mechanical ventilation was started. After that, grasping forceps were inserted via the bronchial fiber, and the foreign body was pulled up to the pharynx. Then, it was removed using Magill forceps (Fig. b, c). Following the administration of sugammadex 200 mg, the patient’s respiratory condition returned to the preoperative level, and he was returned to the ICU. The surgery time was 35 min, the anesthesia time was 51 min, the lowest percutaneous oxygen saturation during the procedure was 93%, and there was no bleeding associated with the removal procedure.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [166.0, 'cm']}",62.31505,59.1993,65.4308,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 166.0 cm, which is 166.0 cm * 0.393701 in/cm = 65.35437 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.35437 (in inches) - 60) = 62.31505 kg.
Hence, the patient's IBW is 62.31505 kg."
3806,10,Ideal Body Weight,physical,decimal,pmc-6094035-1,Extracted,"A 78-year-old woman complaining of shortness of breath visited our hospital. Her dyspnea had worsened considerably during one week. Four days prior to her visit, she was diagnosed with bronchitis at a local clinic, and an antitussive and expectorant were prescribed; however, dyspnea and edema of the lower extremities developed. Investigation of the patient’s history revealed that she had been taking medication for the treatment of hypertension and hyperlipidemia since she was 50 years old, and, at 70 years of age, she had experienced a dorsal compression fracture because of osteoporosis. Her body temperature was 36.9°C, her pulse was regular, her heart rate was 100 beats/min, and her blood pressure was 163/83 mmHg. Physical examination revealed edema of both feet. She was 153 cm tall and weighed 63 kg. Abnormal laboratory findings included high levels of D-dimer (8.04 µg/mL; normal range, <1.00 µg/mL) and brain natriuretic peptide (BNP, 542.5 pg/mL; normal range, <18.4 pg/mL). A chest X-ray image revealed cardiomegaly and bilateral lung congestion (cardiothoracic ratio 54%; normal range: <50%). Electrocardiography revealed normal sinus rhythm, with a negative T-wave at leads V1–V4. Echocardiography revealed hyperkinetic movement, with moderate tricuspid regurgitation, without the collapse of the inferior vena cava (IVC). Enhanced computed tomography (CT) indicated an AVF associated with a left iliac pseudoaneurysm (). In addition, left hydronephrosis, uterine myoma, pulmonary artery thromboembolism of the right lower lobe branch, pleural effusion, and pulmonary congestion with right predominance were detected. We diagnosed dyspnea and edema of the lower extremities as acute right congestion heart failure with an AVF related to the left common iliac pseudoaneurysm.
The patient was treated with intravenous diuretics, and further examinations (magnetic resonance imaging and vascular ultrasound) were conducted. However, a final diagnosis was not obtained, and we selected urgent abdominal surgery for AVF treatment.
Urgent surgery was performed through median laparotomy, following urethroscopy performed by a urologist. The findings indicated only pressure from outside the urinary tract, without a tumor in the left ureter. A ureteral stent was deployed in the left ureter for marking during surgery. After laparotomy, severe adhesion around the left iliac pseudoaneurysm was noted. We initially taped the terminal abdominal aorta and right common iliac artery using the tape. We could not tape the left common iliac artery. Further, we attempted to tape the IVC. But we had to abandon taping the IVC because we were afraid of the possibility of injury due to severe dilatation of the IVC. We subsequently cut open the sigmoid mesocolon and secured the peripheral sides of the left internal and external iliac arteries. We judged that only digital compression would help to control bleeding from the AVF. Following heparin injection, we clamped the terminal abdominal aorta, right common iliac artery, and left internal and external arteries. On opening the wall of the pseudoaneurysm, a large amount of venous blood flowed, and shock was noted. During massive blood transfusion, we continued digital compression. We finally achieved complete hemostasis with various medical styptics. The AVF site had multiple fistulae of the venous wall. We submitted a specimen of the arterial wall for histological examination. Finally, we performed bypass from the right common femoral artery to the left common femoral artery, by using an 8-mm ringed prosthesis (FUSION Vascular Graft, Maquet, Germany) following the achievement of a stump for each artery (proximal sites of the left common iliac artery, external iliac artery, and internal iliac artery). After protamine administration, hemostasis was reviewed. After washing the area with a lot of warm saline, we closed the abdominal wall. The operation time was 636 min, and the amount of blood loss was 5,471 mL despite several blood transfusions being administered. The patient was extubated in the operating room. Her postoperative course was uneventful. Pathology examination of the surgical specimen revealed leiomyosarcoma; however, the patient did not seek active treatment. Histological examination of the resected aorta revealed colonization by spindle-shaped cells, with nuclei of various sizes, and accompanying acidophils (). Immunohistology findings were as follows: smooth muscle actin (+), CD34 (−), c-kit (−), S-100 (−), and a MIB-1 index of more than 80% (). The final diagnosis made by a pathologist was of primary leiomyosarcoma of the left iliac artery. Enhanced CT revealed no bleeding sites and indicated patency of the anti-anatomical bypass graft (). On postoperative day 21, the patient was discharged, because she stubbornly refused further active treatment and expected palliative treatment; as a result, we expected her prognosis to be very poor.
The patient lived well for three months after discharge. However, 3 months later, enhanced CT revealed tumor recurrence. Furthermore, 4 months later, CT revealed not only a large tumor but also multiple pulmonary metastases (). She died 8 months after the vascular surgery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.0, 'cm']}",46.04337,43.7412,48.34554,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.0 cm, which is 153.0 cm * 0.393701 in/cm = 60.23625 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.23625 (in inches) - 60) = 46.04337 kg.
Hence, the patient's IBW is 46.04337 kg."
3807,10,Ideal Body Weight,physical,decimal,pmc-3272533-1,Extracted,"A 73-year-old female patient (Height: 160 cm, weight: 58 kg) was diagnosed with degenerative osteoarthritis and admitted for bilateral total knee arthroplasty replacement. The patient was previously diagnosed and medicated for hypertension for 5 years, and diagnosed with suspected angina 5 months prior to the surgery receiving aspirin but was discontinued 7 days prior to the surgery. Blood and biochemistry tests done prior to the surgery were within normal limits. The chest radiography examination showed no special findings except cardiomegaly, bronchiectasis or nonspecific fibrosis in right lower lung zone. Upon electrocardiogram examination and echocardiography, a normal sinus rhythm of 66 beats per minute (bpm) along with a nonspecific T wave abnormality and about 57% ejection fraction without abnormalities of regional wall motion, thrombi, and vegetation and normal left atrium and ventricle size, normal valve function were revealed.
To perform the surgery under combined spinal epidural anesthesia (CSE), 8 mg of 0.5% heavy marcaine (Marcaine, Astrazeneca, Sweden) was injected into the subarachnoid space using a needle through the needle technique, and 3 ml of a test dose using 0.375% of levobupivacaine containing epinephrine (1 : 200,000) was given following insertion of an epidural catheter. Surgery began after sensory blocked level reached the T10 dermatome and maintained with intermittent injections of 0.5% levobupivacaine. The patient was monitored using routine methods [EKG with ST depression, pulse oximeter (SpO2), noninvasive blood pressure, arterial blood pressure, urine output (UO), and BIS]. 5 L/min of 100% oxygen was administered via facemask and monitored SpO2 was 98 to 100%, and intermittent midazolam was given for sedation with a BIS level of 65 to 80.
The patient remained hemodynamically stable [Blood pressure (BP); 130-150/70-85 mmHg, heart rate (HR); 65-85 bpm, respiration rate (RR); 15-18/min, SpO2; 100%] through the intraoperative period immediately before tourniquet release of the second knee arthroplasty, and UO was 900 ml during the 5 hours procedure. The estimated blood loss was 400 ml, and intraoperative fluid replacement consisted of 1,600 ml of crystalloid and 500 ml of hetastarch solution. Immediately after tourniquet release of the second knee arthroplasty, the patient was transfused with PRBC. Twenty-five minutes after tourniquet release and initiation of PRBC transfusion, the patient's blood pressure and SpO2 decreased to 87/46 mmHg and 90-95%, respectively, with tachypnea and cyanosis so normal saline and a second packed RBC transfusion were rapidly replaced along with a 5 mg injection of ephedrine. Her arterial blood gas analysis (ABGA) showed a pH of 7.32, a PaCO2 of 43 mmHg, a PaO2 of 73 mmHg, and oxygen saturation (SaO2) at 93%. At the end of the operation (about 30 minutes after transfusion), sudden paroxysmal atrial fibrillation developed with systolic BP dropping below 70 mm Hg, and a SpO2 of 80% and her mental state changed to drowsy with intact light, eyerish, and gag reflex upon her neurological examination. Respiration and reviving the patient to a conscious state was encouraged, but consciousness continually diminished. Since the oxygen saturation was reduced to 80% with rigidity of temporomandible joint, etomidate and midazolam were injected, and positive pressure ventilation was performed using a ventilator after endotracheal intubation. The patient's SpO2 increased to 95-98%, but pulmonary edema was suspected because a rale was heard by auscultation from both lungs in addition to the secretion of a frothy sputum. Suddenly, ventricular tachycardia occurred and the HR dropped to less than 30 bpm; therefore, cardiopulmonary resuscitation was done. After epinephrine was injected three times and cardioversions with 200 J biphasic waveform shocks, the patient's rhythm returned to a normal state, and thus, a joint diagnosis was done by the Cardiology and Neurology Departments. There was no specific abnormal findings neurologically, and her transthoracic echocardiography in the OR did not show any fine emboli or embolic mass or pulmonary hypertension or ventricular dysfunction, but did show a decrease in volume and a hyperdynamic status of the heart. Upon portable Chest X-ray examination, it showed bilateral pulmonary infiltrates (). The patient was given 20 mg of furosemide and 500 mg of methylprednisolone IV with inotrophic support (dopamine: 5-15 µg/kg/min, Dobutamine: 5-15 µg/kg/min) and manually assisted ventilation for pulmonary edema and 60° semifowel's position, and yet, her condition of respiratory insufficiency with frothy secretions did not improve over time. She was transferred to ICU for further management by department of cardiogy 1 hour after an advent event. The femoral vein was catheterized, and we continued to focus on treatment for her pulmonary edema, which consisted of medical treatment with furosemide, dopamine: (10-20 µg/kg/min), dobutamine (10-20 µg/kg/min), norepinephrine (> 20 µg/kg/min), and volume maintenance using packed RBCs and least crystalloid fluid therapy, but copious pinkish frothy secretions began to flow out from her tracheal tube, and her vital signs and SpO2 were aggravated with anuria and DIC. At this time, her ABGA showed a pH of 7.25, a PaCO2 of 43.8mmHg, a PaO2 of 59.7 mmHg, and a SaO2 of 87.7%. Despite her mechanical ventilatory support (FIO2 of 1.0 with PEEP 10-15 cmH2O) and inotropic treatment, her SpO2 was still low (70-90%), and her blood pressure (60-90/40-50 mmHg) was unstable and decreased gradually. ABGA, cardiac enzymes including N-terminal probrain natriuretic peptide BNP (NT-proBNP) and Troponin T, and other blood chemistry tests were done (). EKG and TTE also were done reevaluate and determine the origin of the pulmonary edema. Her cardiac enzymes including Troponin T were slightly increased though her NT-proBNP level was within normal limits, her transthoracic echocardiography in the ICU did not show any signs of heart failure but did show a hyperdynamic and more hypovolemic heart. Although she was again given a total of 7 units of packed RBC for volume maintenance and 2 units of FFP for correction of a coagulation abnormality 3 hours after the initial adverse event during the ICU stay, her HR began to decrease to < 40 bpm. She died 1 hour later despite attempts at cardiopulmonary resuscitation.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3808,10,Ideal Body Weight,physical,decimal,pmc-6745402-1,Extracted,"The 68-year-old male received left upper pneumonectomy for lung cancer with lymph node dissection (ND2a-1, pT2bN0M0, Stage2A) 1 year ago. The lung cancer consisted of moderately differentiated squamous cell carcinoma with keratinization and intercellular bridge. Immunohistochemistry showed positive for cytokeratin 7 (CK7), and negative for cytokeratin 20 (CK20) and caudal-related homeobox 2 (CDX2).
Five months after the surgery for lung cancer, he developed dyspnea, and fecal occult blood test was positive. Colonoscopy revealed a hemorrhagic ulcerated lesion with marginal elevation in the transverse colon (Figure A). Chemotherapy for the recurrence of lung cancer was required; however, surgical intervention for progression of anemia due to the advanced tumor in the transverse colon was considered before initiating chemotherapy.
He had a medical history of old myocardial infarction (18 years prior; postpercutaneous cardiac intervention, and long-term use of antithrombotics (including ticlopidine hydrochloride and dabigatran etexilate), diabetes mellitus, hypertension, and dyslipidemia. He had no family history regarding malignancy. On admission, his height was 182 cm, and weight was 81 kg. Blood pressure was 112/66, heart rate was 82 beats per minute, body temperature was 36.6°C, and oxygen saturation was 96% on room air, Glasgow Coma Scale was 15 points, and performance status was 2. The abdomen was soft and flat without any palpable mass.
Laboratory evaluation showed anemia (hemoglobin 9.7 g/dL), extremely low albumin (1.9 g/dL) and choline esterase (107 U/L), suggesting poor nutrition. Renal function was slightly lowered (blood urea nitrogen 14.1 mg/dL, creatinine 1.13 mg/dL), and there were high inflammatory markers (WBC 9300/mm3, C-reactive protein 10.27 mg/dL). Electrolytes were normal, and tumor markers (squamous cell carcinoma antigen, neuron-specific enolase, sialyl Lewis Xi antigen, progastrin releasing peptide, carcinoembryonic antigen, and carbohydrate antigen 19-9) were within normal limits except for slight elevation of soluble cytokeratin 19 fragment of 12.1 ng/mL (range 0-2.8 ng/mL). Electrocardiogram showed incomplete right bundle branch block and old myocardial infarction. Echocardiogram showed sustained systolic function of ejection fraction (56.9%) and asynergy with dyskinesis around the apex of the heart, akinesis and thinning of the anterior wall. The lateral deformity was observed by contrast enema using gastrografin, suggesting advanced tumor (Figure B).
Biopsy of the tumor in the transverse colon showed cancer cells in a small gland formation proliferating mainly in the submucosal layer. Immunohistochemistry was positive for CK7, and negative for CK20, CDX2, and thyroid transcription factor-1 (TTF-1), which was incompatible with primary colon cancer, leading to the preoperative diagnosis of lung cancer metastatic to the colon.
Chest CT showed multiple dilated lymph nodes in the left lung hilum and mediastinum (Figure A). Left pleural effusion and irregular thickening of the left pleura were also observed, suggesting left pleural dissemination. Abdominal CT showed thickened left side transverse colon with several nearby dilated lymph nodes (Figure B). No ascites and peritoneal dissemination were observed. Fluorodeoxyglucose positron emission tomography showed enhanced uptake in the mediastinum, left lung hilum, and the sites of thickened pleura. The tumor in the transverse colon showed limited uptake with SUVmax of 11.76. In summary, preoperative diagnosis of lung cancer metastatic to the colon was determined.
Differential diagnosis included primary colon cancer; however, past medical history, regional relapse in the left lung hilum and mediastinum, and left pleural effusion suggested lung cancer metastatic to colon.
On admission, patient was given 13.5 g piperacillin/tazobactam and 1500 mg metronidazole to decrease inflammation. A chest tube was inserted into the left pleural space to control left pleural effusion. Anemia was treated with transfusion. Antithrombotics were discontinued, and heparin replacement was initiated. After the systemic condition improved, laparoscopic resection was successfully performed. Operation time was 102 minutes, and blood loss was 5 mL.
The resected specimen was a well-circumscribed tumor measuring 6.5 × 5.5 cm in the transverse colon (Figure A and B), and histopathological finding was carcinoma without any specific differentiation (Figure A). The tumor was exposed onto the serosa, and intense lymphatic invasion was observed. Immunohistochemistry was positive for keratin AE1/AE3 and CK7, and negative for CK20, p40, and CDX2, resembling the tissue of the previously resected lung cancer (Figure B). The final diagnosis of lung cancer metastatic to the colon was confirmed.
Postoperative course was uneventful, and no gastrointestinal bleeding or progression of anemia was observed, even after he was restarted on antithrombotics. The patient was discharged on the thirteenth postoperative day. He died from systemic deterioration on the 40-second postoperative day.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [182.0, 'cm']}",76.80323,72.96307,80.64339,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 182.0 cm, which is 182.0 cm * 0.393701 in/cm = 71.65358 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (71.65358 (in inches) - 60) = 76.80323 kg.
Hence, the patient's IBW is 76.80323 kg."
3809,10,Ideal Body Weight,physical,decimal,pmc-7020965-2,Extracted,"Patient E.P.N, male, 29 years old, professional soccer athlete, without risk factors for early CAD, without previous use of anabolic, ergogenic, illicit or anorectic drugs. Negative family history for coronary heart disease, cardiomyopathy or thrombotic disease. He sought medical attention because of insidious retrosternal chest fatigue and discomfort evolving for a month, with strong intensity and short duration, related to intense physical efforts (soccer training) and relieved at rest.
He denied irradiation or associated symptoms, but presented progressive symptom worsening. The patient, who initially only had indefinite tiredness at the end of the match, ended up developing burning chest pain early in the training.
Upon physical examination, the patient was well overall, eupneic at ambient air, normal color, acyanotic, feverless and anicteric.
The patient weighed 79 kg; 1.79 m tall; with a heart rate of 60bpm; and blood pressure (BP) at 120/80 mmHg.
Chest examination showed an apical thrust and normal heart and lung sounds.
Pulses were symmetrical with normal amplitudes and there was no peripheral edema. Laboratory tests within normal limits.
Resting ECG evidenced ARV with anterior septum T-wave inversion ().
Following the investigation, he underwent ergospirometric testing that showed no arrhythmias or electrocardiographic changes for myocardial ischemia, but there were symptoms of mild typical chest pain during the examination and abnormal findings concerning oxygen consumption (VO2) - 48.3mL/kg/min (the reference standard was 48.9); and the oxygen pulse was 21.1 ml 02/bpm (the reference standard was 19.9), with a plateau curve at the peak effort reached.
He then underwent transesophageal echocardiography, which showed normal wall thickness and dimensions, no septal defects and normal LV systo diastolic function, despite anteroapical hypokinesia.
The patient remained with anginal pain when an anatomical evaluation with CT angiography was necessary and showed proximal obstruction in the ADA which presented normal distal flow due to the receipt of collateral circulation in the right circumflex and coronary arteries.
The examination disregarded coronary atherosclerosis ( and ). Thrombophilias, rheumatological, inflammatory and connective tissue diseases were also investigated; with negative results.
Due to the obstruction of the ADA, we investigated the repercussion of this lesion on ventricular function by myocardial scintigraphy, which showed transient hypocaptation in the anterior, apical and septal walls with great extent, reaching 28% of the LV.
Once the lesion was evidenced and its relevant repercussion was demonstrated, the patient was submitted to CATE, confirming the previous findings, in which the ADA TCA was performed with a pharmacological stent (Promus 4.0 × 2.8 mm), although the patient was aware of the possibility of distal embolization, resulting in a final TIMI 3 flow.
After the procedure, the patient remained asymptomatic receiving daily ASA, prasugrel and continued cardiac rehabilitation.
A control scintigraphy, after three months of CATE, demonstrated total reversal of myocardial ischemia.
Currently, the patient remains asymptomatic, performing outpatient follow-up, and practicing intense physical activity.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.79, 'm']}",74.0867,70.38236,77.79103,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.79 m, which is 1.79 m * 39.3701 in/m = 70.47248 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.47248 (in inches) - 60) = 74.0867 kg.
Hence, the patient's IBW is 74.0867 kg."
3810,10,Ideal Body Weight,physical,decimal,usmle-1639,Extracted,"A 16-year-old girl is brought to the physician because of a 6-month history of menstrual cramps, heavy menstrual flow, and fatigue; she has gained 5 kg (11 lb) during this period. Menses occur at regular 30-day intervals and last 8 to 10 days; during her period she uses 7 tampons a day and is unable to participate in any physical activities because of cramping. Previously, since menarche at the age of 11 years, menses had lasted 4 to 5 days with moderate flow. Her last menstrual period was 3 weeks ago. She has limited scleroderma with episodic pallor of the fingertips. She takes no medications. She is 160 cm (5 ft 3 in) tall and weighs 77 kg (170 lb); BMI is 30 kg/m2. Her temperature is 36.5°C (97.7°F), pulse is 56/min, respirations are 16/min, and blood pressure is 100/65 mm Hg. Physical examination shows a puffy face with telangiectasias and thinning of the eyebrows. Deep tendon reflexes are 1+ bilaterally with delayed relaxation. Pelvic examination shows a normal appearing vagina, cervix, uterus, and adnexa.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3811,10,Ideal Body Weight,physical,decimal,pmc-4119244-1,Extracted,"A 79-year-old male with height of 167.5 cm and preoperative body weight of 52.8 kg underwent removal of a pancreatic tumor. Total intravenous anesthesia with propofol and remifentanil combined with continuous epidural block using 6 ml/h of 1.0 % carbocaine was given to the patient. Approximately 2 h before completion of the surgical procedure, MAP started to gradually decrease and reached 61 mmHg at 20:00, and the carbocaine infusion was switched to 0.2 % ropivacaine infusion (5 ml/h). The lowest MAP of 55 mmHg was recorded at 20:09, and MAP gradually increased thereafter. While CCO decreased from 6.5 to 5.2 L/min (Fig. , Interval A: 20:15–20:45), SVR increased from 640 to 1,100 dyne s cm−5. esCCO decreased from 8.3 to 6.8 L/min, and the amplitude of the SpO2 pulse wave also decreased.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [167.5, 'cm']}",63.67332,60.48965,66.85699,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 167.5 cm, which is 167.5 cm * 0.393701 in/cm = 65.94492 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.94492 (in inches) - 60) = 63.67332 kg.
Hence, the patient's IBW is 63.67332 kg."
3812,10,Ideal Body Weight,physical,decimal,pmc-3606595-1,Extracted,"Patient A is a 23-year-old married female with one child. After her husband had an affair with a thinner woman, she decided to lose weight. Subsequent to this, she began to experience nausea and palpitations on eating. Before these symptoms developed, she weighed approximately 50 kg, with a body mass index (BMI) of 20.6. Within 5 months, she weighed 41 kg and was amenorrheic. Her eating patterns were severely restricted to one meal between morning and noon per day.
She presented at our clinic complaining of noncausal nausea and weight loss. At her first visit, she measured 158-cm tall and weighed 41.3 kg, with a BMI of 16.5. At this point, she had already lost 8 kg and had not had menses for almost 4 months. Although she admitted that she had lost weight, she felt that she still looked the same and expressed a desire to reduce her weight further to 30 kg. She also complained about a fear of gaining weight. She was diagnosed in accordance with DSM-IV-TR as having AN of restricted type (ANR).
She was prescribed 1 mg of ethyl lofrazepate to combat her anxiety attacks and palpitations. While this symptom showed small improvement, she maintained her fear of weight gain and eating patterns and showed further weight loss from 41.3 to 40 kg (BMI 16.4). At a weight of 40.0 kg, her EDE-Q subscales of restricting/eating concern/weight concern/shape concern and global scores were 4.6/1.6/3.6/4.88 and 3.67, respectively. She was started on tandospirone because of its fewer side effects on the digestive system relative to SSRIs and its antianxiety effects. Patient A was scheduled for two weekly visits to our clinic to monitor side effects, although no specific psychological treatment was provided. At these visits and in the absence of side effects, tandospirone was initiated at 20 mg and escalated by 20 mg every 2 weeks until it reached 60 mg. It was recommended that she take tandospirone twice daily (when prescribed 20 and 40 mg) or three times daily (when prescribed 60 mg). From the onset of treatment, our patient’s dietary intake gradually increased, and she began to gain weight. In addition, she no longer complained about feelings of fear and guilt. Four weeks into therapy, her weight had increased to 43 kg (BMI 17.7), and her EDE-Q scores reduced, with the subscale scores of restricting/eating concern/weight concern/shape concern and global score being 3.4/0.6/1.2/4.0 and 2.3, respectively. After approximately 20 weeks, her menses resumed. At the 6-month point, she was still adhering to her treatment regime, her EDE-Q diagnostic score was 6, and the subscales restricting/eating concern/weight concern/shape concern and global score were 1.2/0/2.0/3.0 and 1.55, respectively. Also, she had gained weight to reach 45.0 kg with a BMI of 18.5.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3813,10,Ideal Body Weight,physical,decimal,usmle-1419,Extracted,"A 24-year-old woman is brought to the physician for the evaluation of fatigue for the past 6 months. During this period, she has had recurrent episodes of constipation and diarrhea. She also reports frequent nausea and palpitations. She works as a nurse at a local hospital. She has tried cognitive behavioral therapy, but her symptoms have not improved. Her mother has hypothyroidism. The patient is 170 cm (5 ft 7 in) tall and weighs 62 kg (137 lb); BMI is 21.5 kg/m2. She appears pale. Vital signs are within normal limits. Examination shows calluses on the knuckles and bilateral parotid gland enlargement. Oropharyngeal examination shows eroded dental enamel and decalcified teeth. The remainder of the examination shows no abnormalities.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [170.0, 'cm']}",61.43709,58.36524,64.50894,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.92917 (in inches) - 60) = 61.43709 kg.
Hence, the patient's IBW is 61.43709 kg."
3814,10,Ideal Body Weight,physical,decimal,usmle-1158,Extracted,"A 63-year-old man comes to the physician because of shortness of breath and swollen extremities for 2 weeks. He has had excessive night sweats and a 4-kg (8.8-lb) weight loss over the last 8 weeks. He had an anterior myocardial infarction 3 years ago. He has type 2 diabetes mellitus and hypertension. He immigrated from Indonesia 4 months ago. He works in a shipyard. He has smoked one pack of cigarettes daily for 48 years. Current medications include insulin, aspirin, simvastatin, metoprolol, and ramipril. He is 160 cm (5 ft 3 in) tall and weighs 46.7 kg (103 lb); BMI is 18.2 kg/m2. His temperature is 38.0°C (100.4°F), pulse is 104/min, respirations are 20/min, and blood pressure is 135/95 mm Hg. Examination shows generalized pitting edema. There is jugular venous distention, hepatomegaly, and a paradoxical increase in jugular venous pressure on inspiration. Chest x-ray shows bilateral pleural effusion, patchy infiltrates in the right middle lobe, and pericardial thickening and calcifications.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [160.0, 'cm']}",56.88197,54.03787,59.72607,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.99216 (in inches) - 60) = 56.88197 kg.
Hence, the patient's IBW is 56.88197 kg."
3815,10,Ideal Body Weight,physical,decimal,pmc-4499709-1,Extracted,"A 51-year-old male patient had been suffering from a massive lymphedema of the lower extremities also including the scrotum for almost 20 years. Despite consequent lymph drainage up to four times per week, the patient showed progressive symptoms with suddenly occurring diarrhoea, a massive impairment of physical capabilities and a severe reduction in the quality of life. The patient's weight was consistent with 110 kg at a height of 184 cm [body mass index (BMI): 32.5 kg/m²]. Pulmonary, cardiac and hepatological diagnostics showed no underlying disease. Gastroscopy and colonoscopy gave no pathological findings. The only exceptional result was a protein deficiency with a chronic lowered total serum protein (47 g/l; normal range 64–84 g/l). Gel serum electrophoresis showed a general protein deficiency.
Since conservative treatment with lymph drainage showed no improvement of the patient's symptoms, further diagnostic steps including a push–pull enteroscopy revealed the PIL of the jejunum to an extent of about 50 cm (). Subsequent capsule endoscopy confirmed the limited involvement of the proximal to mid jejunum.
Due to the extensive impairment of the patient and the therapy-refractory course, the indication to exploratory laparoscopy with segmental intestinal resection was given.
During the laparoscopic operation, an extensive part of the small intestine appeared macroscopically clearly altered (). Thus, the laparoscopic-assisted resection of the conspicuous intestine (95 cm) with end-to-side anastomosis was performed.
Histopathological analysis confirmed the PIL with dilated submucosal and subserosal lymphatic vessels (Fig. a and b).
The patient was discharged on the seventh postoperative day. During an outpatient visit after 2 weeks, a slight improvement of the total serum protein to 52 g/l was obtained.
An outpatient follow-up after 6 months showed a reduction in the patient's weight from 110 to 105 kg (BMI: 31 kg/m²), and the frequency of lymph drainage had been reduced to twice per week. Physical capabilities improved, and diarrhoea has not occurred since 4 weeks after the operation. Total serum protein level was at the lower end of the normal range (63 g/l) with an otherwise normal serum electrophoresis.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [184.0, 'cm']}",78.61425,74.68354,82.54496,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 184.0 cm, which is 184.0 cm * 0.393701 in/cm = 72.44098 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (72.44098 (in inches) - 60) = 78.61425 kg.
Hence, the patient's IBW is 78.61425 kg."
3816,10,Ideal Body Weight,physical,decimal,pmc-6362890-1,Extracted,"A 70-year-old man underwent a colonoscopy after having episodes of bright red stool per rectum and diarrhea. A lower rectal cancer was diagnosed based on a histology obtained through a biopsy of the rectal lesions (Rb, T2N0M0 cStageI (UICC Classification, 7th ed)). The past medical history was notable for hypertension untreated and smoking 50 pack year. His height was 173 cm, and weight was 73 kg with body mass index of 24.4. The creatinine clearance was 87 ml/min. Although the preoperative history talking failed to recognize the symptoms of intermittent claudication and sensory impairment of his lower extremities, a preoperative contrast enhanced computed tomography (CT) scan demonstrated a significant stenosis in bilateral external iliac artery due to arteriosclerosis obliterans (ASO) (Fig. ) and occlusions of bilateral internal iliac artery. There was no coagulation abnormality in his blood test or atrial fibrillation on an electrocardiogram.
He underwent an elective laparoscopic abdominoperineal resection with a lithotomy position. There was no vascular injury or compression with laparoscopic forceps as far as we were able to recognize retrospectively based on the laparoscopic video and the memory. The duration of surgery was 4 hours and 48 minutes. Blood loss was estimated 100 ml, the urine volume was only 50 ml during the operation. In-out balance during operation divided body weight and time of operation was 6.38 ml/kg/h. The patient reported a severe pain in the left leg, when he woke up post-operatively. The left leg was pale and cold, associating sensory abnormality and motor dysfunction; left pedal and popliteal pulses were absent. A CT scan revealed the contrast interruption of left common iliac artery (CIA) over 11.5 cm and suspected to be due to an arterial thrombosis (Fig. ). Under the local anesthetic technique, the left femoral artery was exposed and performed thrombectomy with a 5Fr Fogarty catheter. After a new clot was removed, aortography revealed persistent stenosis in left iliac artery. Consequently, a Percutaneous transluminal angioplasty (PTA) with stent (Express LD 8 × 37 mm) was added (Fig. ) via left femoral artery. Blood perfusion in his left leg improved markedly immediately post PTA. The patient was transferred to the intensive care unit for two days due to the complications with a rhabdomyolysis (creatinine phosphokinase up to 23 598 IU/l). The patient started walking 5 days post-surgery, however, the patient was left with the numbness in his left lower leg. A heparinization had been commenced on the postoperative day 1, then this was switched to the cilostazol prior to the discharge for home. We note that the patient continued reporting the left lower leg numbness even one year past the surgery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.0, 'cm']}",68.65362,65.22094,72.0863,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.0 cm, which is 173.0 cm * 0.393701 in/cm = 68.11027 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.11027 (in inches) - 60) = 68.65362 kg.
Hence, the patient's IBW is 68.65362 kg."
3817,10,Ideal Body Weight,physical,decimal,pmc-4548424-1,Extracted,"A 72-year-old gentleman weighing 68 kg and 160 cm tall and hypertensive on treatment for past 10 years with metoprolol-XL-50 mg and amlodipine 5 mg was operated for anterolisthesis of disc at L4-L5 level with canal stenosis. He had previously undergone an uneventful surgery for right rotator cuff repair under general anesthesia 6 years ago. Present preanesthetic check-up was normal with heart rate (HR) of 62/min, blood pressure (BP) of 110/74 mmHg, normal electrocardiogram (ECG), and heart sounds on auscultation. His effort tolerance was only limited by pain in lower limbs. On the day of surgery, he received his regular antihypertensives. The preoperative cardiac assessment on the table was uneventful. Preinduction vitals were stable with HR of 58/min and BP of 122/78. Premedication included glycopyrrolate 0.2 mg, fentanyl 100 μg, and ondansetron 8 mg. Anesthesia was induced with propofol 2 mg/kg intravenous (IV) and after confirming ventilation, vecuronium 0.1 mg/kg was given IV. Anesthesia was maintained with oxygen in nitrous oxide, supplemented with isoflurane, vecuronium and propofol infusion, and morphine. The blood loss was approximately 100 ml and 1.5 L crystalloid was infused. Intraoperative period of 4 h in the prone position was uneventful except for a drop in BP at induction to 80/54 mmHg, which was managed with a bolus of 250 ml crystalloid. He was extubated and vitals in the recovery room before shifting to Intensive Care Unit (ICU) were stable for HR of 64/min and BP of 108/54 mmHg.
An hour after receiving the patient in ICU, his BP dropped to 82/48 mmHg with no change in HR or consciousness. Fluid boluses of 250 ml ringer lactate in two aliquots were administered without benefit. ECG was normal with a sinus rhythm and nonspecific t wave inversion in lead III. Arterial blood gas (ABG) on room air showed normal oxygenation with metabolic acidosis with elevated strong ion difference (pH - 7.268, PaO2 -112, PaCO2 -40, bicarbonate - 19.3 with BE - 5.6, and lactate - 1.9). Ultrasonography (USG) revealed completely collapsed inferior vena cava (IVC) which was treated with 2 L of crystalloid administered cautiously over 1 h without any significant improvement. The patient remained conscious and could move his lower limbs well ruling out any spinal shock. Vasoactive drugs (adrenaline, dopamine, and noradrenaline) were serially added and escalated to maximum (20 mcg/min) without any remarkable change in BP. The HR increased from 60 to 100/min. Gradually he began manifesting signs of hypoperfusion in multiple organs. His urine output reduced, and he developed hypothermia. Cardiac evaluation by a senior cardiologist with bedside ECHO and enzymes ruled out any cardiac pathology. Serial ABGs revealed worsening lactic acidosis and deteriorating oxygenation though mentation remained intact. After administration of 6 L of crystalloids, bedside USG revealed an adequately filled IVC without any signs of fluid overload in the lungs. Having ruled out cardiac pathology and hypovolemia as the cause of hypotension with worsening organ perfusion the possibility of BB and CCB toxicity was considered. As glucagon was not available in the institution, we started an infusion of insulin in dextrose at 0.15 U/kg/h (25% dextrose with 15 units of insulin at 60 ml/h) (glucose-insulin-potassium therapy) along with calcium infusion at 0.5 g/h and potassium at 30 mEq over 3 h.
Glucose and potassium values were monitored every hour, and the infusion was adjusted accordingly. Within an hour of treatment with this regime BP improved to 100/60 mmHg. The inotropes could be tapered and stopped within 2 h, urine output improved and euthermia was attained.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [160.0, 'cm']}",56.88197,54.03787,59.72607,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.99216 (in inches) - 60) = 56.88197 kg.
Hence, the patient's IBW is 56.88197 kg."
3818,10,Ideal Body Weight,physical,decimal,pmc-4983355-1,Extracted,"The patient is a 47-year-old, HIV-negative, Caucasian male, height 180 cm, weight 81 kg, with a history of nondifferentiated schizophrenia since the age of 26 y. Shortly after onset of psychosis he developed fever and severe headache which resolved spontaneously without therapy or residual deficits. Although he did not undergo CSF investigations, meningitis was retrospectively suspected. Exacerbations of psychosis required recurrent admissions to psychiatric departments at ages 26 y, 28 y, 29 y, 31 y, and 34 y and were successfully treated with neuroleptics. During the first psychotic episode he developed severe pneumonia. Temporarily he was also taking cannabinoids. Additionally, he suffered from chronic alcohol disease since the age of 33 y. His father had a history of questionable Guillain-Barre syndrome (GBS) with complete remission and prostate cancer but no cardiac compromise and no psychiatric disorder.
At the age of 47 y he was hospitalised because of extensive leg edema, weight gain, and resting dyspnoea. X-ray of the lungs showed an enlarged heart and pulmonary congestion grade I. Blood pressure was 110/80 mmHg. Transthoracic echocardiography showed an enlarged left ventricle with an ejection fraction (EF) of 15–20% and surprisingly LVHT in the apical segment (). Additionally, the left atrium was enlarged, the right ventricular cavities were mildly enlarged, and there were secondary pulmonary hypertension (55 mmHg) and a small pericardial effusion. Cardiac MRI revealed an enlarged left ventricle, with increased myocardial mass and markedly reduced systolic function and severe diffuse hypokinesia (). There was no late enhancement but bilateral enlargement of both atria and a small pericardial effusion. LVHT was confirmed by cardiac MRI (). Since coronary angiography was normal, dCMP was diagnosed. ECG showed signs of left ventricular hypertrophy. Blood tests revealed hyperbilirubinemia, hypocalcemia, and occasional hyperCKemia with values up to 236 U/L (n <190 U/L). NT-proBNP values were elevated to 2871 ng/L (n <84 ng/L). Intravenous diuretic therapy led to a weight loss of 19 kg. A therapy with candesartan and nebivolol was started. Because of severely reduced systolic function and the increased risk of sudden death, a wearable cardioverter (LifeVest®) was recommended but refused by the patient. Since clozapine has an arrhythmogenic effect [, ] and a potential to induce cardiomyopathy [] or myocarditis [], psychiatrists recommended switching to aripiprazole which the patient refused. Two months after discharge, the patient was in NYHA stage I of heart failure and echocardiography showed only a slight improvement in systolic function with an EF of 30%. He was taking candesartan (20 mg/d), nebivolol (2.5 mg/d), and spironolactone (25 mg/d). Because of low systolic blood pressure, the neurohumoral therapy could not be uptitrated into the target dose so far. He continued refusing a LifeVest or an implantable cardioverter/defibrillator. His last psychiatric medication included clozapine 6.25 mg/d. Clinical neurologic examination was normal and the patient refused work-up for hyperCKemia.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [180.0, 'cm']}",74.99221,71.2426,78.74182,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 180.0 cm, which is 180.0 cm * 0.393701 in/cm = 70.86618 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.86618 (in inches) - 60) = 74.99221 kg.
Hence, the patient's IBW is 74.99221 kg."
3819,10,Ideal Body Weight,physical,decimal,pmc-3205363-1,Extracted,"Our patient was a 27-year-old man who was diagnosed with adult-onset type II citrullinemia (CTLN2) at age 24. The patient's height was 178 cm with a body weight of 60 kg. The patient had been treated with a low protein diet and oral administration of lactulose. Intermittent lactulose enemas were provided for intermittent alteration of consciousness. Recently, the patient has had more frequent alterations of his mental status with irritability and altered consciousness. Even though oral administration of L-arginine, Kanamycin and intravenous hyperalimentation with branched chain amino acids was started, his plasma levels of ammonia and citrulline were highly elevated, up to 844 µg/dL (normal range, 19 to 87 µg/dL) and 682 µmol/L (normal range, 12 to 55 µmol/L), respectively. Despite the conservative medical treatment including alternative pathway medication, intermittent continuous renal replacement therapy and hemodialysis, his condition failed to improve. Therefore, living donor liver transplantation was planned using a right lobe graft from his 25-year-old sister. However, the estimated volume of the donor's right lobe was 800 mL compared to 180 mL of the left and in addition there was a type III portal vein anomaly. We eventually decided to perform an APOLT using the extended left lobe of the liver from the donor. The patient underwent APOLT in February of 2008. The actual graft volume was 200 g and the graft-to-recipient weight ratio (GRWR) was only 0.33%. The patient's extended left lobe (including caudate lobe) was resected and the extended left lobe graft (including middle and left hepatic vein) was transplanted orthotopically. The left and middle hepatic vein trunk of the extended left lobe graft was anastomosed to the left and middle hepatic vein trunk of the recipient in end-to-end fashion with interposition venoplasty using the recipient's greater saphenous vein as a patch. The left portal vein of the graft was anastomosed to that of the recipient in end-to-end fashion. Considering that the graft was too small, the recipient's right portal vein was narrowed by surgical clipping, instead of total diversion, for prevention of the development of portal venous hypertension. The left hepatic artery of the graft was anastomosed to that of the recipients in end-to-end fashion. Intraoperative Doppler ultrasonography demonstrated that portal and arterial blood flow were well maintained in both the native liver and the graft. Biliary drainage was accomplished by a Roux-en-Y hepaticojejunostomy. On postoperative day 7, abdominal computed tomography demonstrated orthotopically transplanted small left lobe graft with well-enhanced pattern (). The post-operative course was uneventful and the patient was discharged without any problems. The plasma concentrations of ammonia were at the upper limits of normal, so only a low protein diet (50 g/day) was supplied without any specific medication. On post-operative day 33, the patient reported a sudden severe visual disturbance and the plasma levels of ammonia were noted to have increased up to 209 µg/dL. The estimated computed tomography volume of the graft was decreased to 190 mL and a left portal vein stenosis was suspected. Direct portography was performed and a severe left portal vein stenosis was confirmed. Immediate coil embolization of 8th segmental branch of right anterior portal vein and self-expandable stent placement for left portal vein was performed in order to increase the portal flow to the graft (). On post stent insertion day 7, the calculated computed tomography volume of the graft was increased to 250 mL (). The plasma level of ammonia was within normal range. By the thirtieth postoperative month, the patient had no signs of rejection or vascular problems.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [178.0, 'cm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3820,10,Ideal Body Weight,physical,decimal,pmc-4173442-1,Extracted,"A 45-year-old male patient Asian origin (—Kerala, India) was admitted with pain in abdomen, nausea, and vomiting with fever since 2 days. Clinical symptoms, signs, and investigations were suggestive of acute appendicitis. Patient was scheduled for an emergency appendicectomy. His weight and height were 70 kg and 173.5 cm, respectively with BMI 23.25. On medical history he had chest pain and for the same was admitted to Hamad general Hospital 1 year back. There was no history of chest pain after that episode, syncope, palpitations in the past. He was investigated with normal blood investigations during that time. But on ECG there was RBBB with ST elevation (coved) in lead V1–V3. Holtermonitorings were done suggestive of atrial premature contractions. On the stress test, as per Bruce protocol, it was negative with the target rate, no ECG abnormality. So cardiologist suggested that baseline ECG suggestive of Brugada syndrome. He was having past history of productive cough, which was diagnosed as asthmatic bronchitis 3 weeks back. He received antibiotics and salbutamol inhaler (as and when required- last used 3 weeks back). There was family history of father's sudden death, but details are not available. No past surgical or allergic history. On general and airway examination was normal except fever. Systemic examination was normal except abdominal tenderness. Chest X-ray was normal. ECG findings same as before RBBB with ST elevation (coved) in lead V1–V3 with QTc 420 msec.
Looking at clinical examination, investigations and as per surgical indication, general anesthesia with avoidance of sodium channel blocker medications was planned. Detail explanation given to patient and consent was taken. Routine monitorings were used. Defibrillator was kept ready. Atropine as per routine was kept ready for abolish any vagal effect. As any vagal stimulation in this type of cases, this leads to dysrrthymias.
General anesthesia was induced with propofol 2.5 mg/ kg and neuromuscular blockade provided through atracurium 0.5 mg/kg. Analgesia was supplemented with fentanyl 2 mcg/kg and patient maintained on sevoflurane with air for controlled ventilation. Paracetamol 1 gm intravenous was given. Spontaneous extubation was carried out with smooth emergence and breathing spontaneously, obeying commands, and satisfactory muscle power. Neostigmine was avoided due to its ability to produce dysrthymia in these cases. Postoperative analgesia provided with morphine in titrated doses. Postoperative care was given in the postanaesthesia care unit. No untoward events (no bradycardia or ventricular fibrillation) occurred during the anesthesia. Total surgery and anaesthesia times were 45 and 65 min, respectively. Invasive monitorings were avoided due to short surgical procedure without much haemodynamic instability. Patient was discharged following an uneventful hospital stay.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.5, 'cm']}",69.10638,65.65106,72.5617,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.5 cm, which is 173.5 cm * 0.393701 in/cm = 68.30712 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.30712 (in inches) - 60) = 69.10638 kg.
Hence, the patient's IBW is 69.10638 kg."
3821,10,Ideal Body Weight,physical,decimal,pmc-7992980-1,Extracted,"A 48-year-old Japanese woman was admitted to hospital because of a two-month history of NS. Seven years before admission, she had been diagnosed with pSS from keratoconjunctivitis sicca, elevated serum anti-Ro/SSA antibody titer and lymphoplasmacytic cell infiltration around salivary ducts of the small salivary glands. At no time had she developed any extra-glandular manifestations. Although anti-nuclear antibodies were positive with a speckled pattern, no signs/symptoms satisfied the classification criteria of systemic lupus erythematous. Although a persistently elevated serum IgA level (400–500 mg/dL) was noted, she had no history of macrohematuria accompanied by upper-airway infection. In addition, there was no evidence of hypocomplementemia, cryoglobulinemia or M-protein. She had no pertinent family history, medication use, smoking or alcohol consumption habit, or occupational history.
Two months before admission, she noticed gradually appearing symmetric pedal edema. Urinalysis revealed 6.7 g/day urinary protein but no glomerular hematuria or cellular casts. On admission, her general appearance and vital signs were stable. She had no fever or malaise, and a good appetite. Her height was 152.6 cm, and weight was 45.9 kg, representing a gain of 5 kg from baseline. Physical examination showed no significant findings except for pitting edema in the bilateral lower limbs. Blood tests showed hypoalbuminemia (2.2 mg/dL) with normal kidney function (serum creatinine 0.64 mg/dL). No electrolyte imbalance was noted.
Renal biopsy showed 11 glomeruli, one of which showed global sclerosis. In the other glomeruli, diffuse bubbling appearance in the glomerular basement membrane (GBM) and slight mesangial proliferation were confirmed (Fig. a). There were no crescents, endocapillary proliferation, double contour of GBM, interstitial nephritis or vasculitis. Immunofluorescence (IF) revealed granular IgA and C3 deposition in GBM (Fig. b and c) but was negative for IgG. Light chain staining indicated no monoclonality. Anti-human Gd-IgA1 antibody (KM55) (Immuno-Biological Laboratories, Cat. No.:10777) staining was significantly positive in GBM with a granular pattern (Fig. d). In electron microscopy, a few electron dense deposits located in the subepithelial area, and more so in intra-membranous and paramesangial lesions accompanied diffuse GBM thickening (Fig. e and f). Diffuse podocyte foot process effacement was also observed. Screening for secondary MN showed no evidence of neoplasms or infection of hepatitis B virus, hepatitis C virus or human immunodeficiency virus. Additional serum analysis confirmed an elevated Gd-IgA1 level (13.5 μg/mL), comparable to that seen in IgAN, [] and qualitative enzyme-linked immunosorbent assay (ProGen Biologics, Cat. No.:IC-003) of IgA-containing circulating immune complex (IgA-CIC) was positive. Thus, we diagnosed GN induced by IC composed of Gd-IgA1. Furthermore, retrospectively performed immunofluorescence of the small salivary gland evaluated at the diagnosis of pSS showed positive Gd-IgA1 staining of infiltrating lymphoplasmacytic cells (Fig. ). Therefore, we concluded that Gd-IgA1 produced by over-activated B cells in pSS formed circulating IC and GN.
NS deteriorated rapidly, with the urinary protein elevated to 12 g/day by the 10th day after admission which resulted in nephrotic crisis requiring hemodialysis for 1 week (Fig. ). Induction therapy with high dose prednisolone (PSL) (1 mg/kg/day) and 1 g/day of mycophenolate mofetil (MMF) were administered on the 17th day, after which the amount of urinary protein reduced dramatically. NS remitted on the 24th day and she recovered baseline renal function by discharge. Five months after discharge, the remission was maintained with 1 g/day of MMF and PSL tapered to 9 mg/day. Moreover, in the 6th month after induction therapy, the serum Gd-IgA1 level decreased to the normal range (3.8 μg/mL), [] and serum IgA-CIC disappeared.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [152.6, 'cm']}",45.68117,43.39711,47.96523,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 152.6 cm, which is 152.6 cm * 0.393701 in/cm = 60.07877 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.07877 (in inches) - 60) = 45.68117 kg.
Hence, the patient's IBW is 45.68117 kg."
3822,10,Ideal Body Weight,physical,decimal,pmc-3316462-1,Extracted,"A 15 7/12 years old female patient was admitted with complaints of fatigue and abdominal pain. She was diagnosed as type 1 diabetes mellitus two years ago and had never experienced an attack of DKA at the time of diagnosis or at follow-up. In the past 24 hours, she had complained of abdominal pain, was not able to eat, and had poor appetite. Her glycemic control showed mild hypoglycemia (61 mg/dL, 3.4 mmol/L) in the morning of admission. Due to poor appetite and hypoglycemia, the patient omitted her insulin dose at lunch time; the same evening, she felt worse and was brought to our emergency department by her parents. On physical examination, she was alert, dehydrated, had deep sighing respirations and smell of ketones. Her height was 168 cm (+1.02 SDS), weight 68 kg (+1.66 SDS), body mass index 24.1 kg/m2 (+1.08 SDS); respiratory rate was 38/min, pulse 80/min. She had normal body temperature (36.4°C, axillary) and normal blood pressure (110/80 mmHg). Blood glucose was 414 mg/dL (23 mmol/L), capillary pH was 6.99 and bicarbonate 5.0 mmol/L. Base excess was -25.2 mmol/L and anion gap was 29.8 mmol/L. Blood urea, liver enzymes and electrolytes were within normal limits (). After the initial saline bolus of 400mL/m2 over the first hour, insulin infusion was started at a rate of 0.05 U/kg/h in an infusion fluid containing 2 parts saline:1 part 5% dextrose, with added potassium.
At the 6th hour of treatment, the patient became agitated and tried to get up and walk. She could not be appeased and attacked the staff. She ripped off her infusion sets three times in 30 minutes. With a suspicion of brain edema, her head was elevated, fluid infusion was restricted by 1/3 and mannitol infusion was started. A cerebral computed tomography was performed immediately and showed no brain edema or hemorrhage. She had high blood pressure (180/100 mmHg) but no bradycardia. In the mean time, the patient was very agitated and we had to strap her to the bed as she injured two nurses. The acidosis could not be corrected because the insulin and fluid therapy was interrupted. At the eighth hour, her Glasgow Coma Scale was 9. In consultation with an anesthesiologist, 1 mg of midazolam was given for sedation, thus, we were able to start an iv line. At the 10th hour, to correct the acidosis, bicarbonate infusion was initiated with insulin 0.1 u/kg/h though her bicarbonate level was 7 mmol/L. Mannitol infusion was stopped since there was no improvement in consciousness. At the 12th hour, despite the improvement in acidosis, delirium still persisted. A brain magnetic resonance imaging (MRI) performed at this time was reported as normal. Substance abuse and drug intoxication were suspected. The patient’s blood pressure decreased to 130/90 mmHg, but tachypnea persisted. She was screaming, making incomprehensible sounds and was responding to painful stimuli. We continued with the same fluid infusion, but the rate of insulin was increased stepwise to 1.7 u/kg/h as serum glucose level did not decrease. At the 16th hour, the blood gas analyses showed a worsening (). This change was attributed to cessation of insulin and fluid infusion during the MRI. Therefore, the HCO3 infusion was repeated.
At the 18th hour of treatment, the patient developed a high fever. Serum C-reactive protein level was high (7.2 mg/dL; N: 0-0.8 mg/dL). Samples for blood and urine cultures were taken and iv ceftriaxone was started. Lumbar puncture was considered but postponed due to the instability of the patient. Retinal examination was normal. At this time, her agitated state disappeared and the patient began to sleep. At the 24th hour, acidosis had resolved completely, but she was still unconscious with little response to verbal stimuli. The patient had vulvovaginitis and treatment with fluconazole was started. In the following hours, consciousness improved slowly. At the 30th hour of treatment, she could open her eyes in response to calling her name. Finally, at the 36th hour, the patient was able to obey commands and sit up. The fluid and insulin infusions were stopped and subcutaneous insulin was started. The patient could not remember the delirium episode and no neurological sequelae were observed. She was discharged after a few days with complete recovery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [168.0, 'cm']}",59.62607,56.64477,62.60737,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.14177 (in inches) - 60) = 59.62607 kg.
Hence, the patient's IBW is 59.62607 kg."
3823,10,Ideal Body Weight,physical,decimal,usmle-11461,Extracted,"A 17-year-old male college athlete visits your clinic for a physical exam prior to starting his first season with the basketball team. He reports that he has no complaints when working out and admits that he is happy about recently surpassing the 7-foot mark. He has extremely long limbs and has grown at a rate of around 3 inches every year since hitting puberty. Although vitals are normal, eye exam shows an unusually placed lens (Figure A) and auscultation at the apex reveals a mid-systolic click.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [7.0, 'ft']}",105.2,99.94,110.46,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 7.0 ft, which is 7.0 ft * 12 in/ft = 84.0 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (84.0 (in inches) - 60) = 105.2 kg.
Hence, the patient's IBW is 105.2 kg."
3824,10,Ideal Body Weight,physical,decimal,pmc-2843710-1,Extracted,"In November 1999, a 63-year-old Caucasian woman from Italy (weight = 100 kg, height = 1.60 m, body mass index = 39) with a history of symptomatic left knee osteoarthritis underwent a TKA in another hospital. The implant used was a NexGen PS knee prosthesis (Zimmer, Warsaw, Indiana, USA) with a tibial component size of 4, a femoral component size of D, and a polyethylene insert 10 mm in thickness. No problem was reported during the follow-up examination, and the patient was able to perform normal life activities for the next nine years.
In March 2008, while rising from a chair, she felt a sudden pain and instability in her left knee. After this acute event she was unable to bear weight on her left knee, and was thus forced to use crutches. On physical examination she presented a mild effusion of the knee, a flexion of 90°, and knee hyperextension. The joint presented signs of both anteroposterior and varus to valgus instability. X-ray examinations showing the anteroposterior view of the knee did not indicate any remarkable alteration in polyethylene wear, while the lateral view showed a hyperextension of the tibia with a posterior subluxation of the femur (Figure ). The hypothesis of post breakage was thus made.
Our patient underwent diagnostic knee arthroscopy and was scheduled to have her polyethylene insert changed. The procedure granted a clear view of the polyethylene and the broken post in articulation. However, actual findings showed that the polyethylene had no relevant wear areas or alterations. Based on these findings, we performed an anterior approach with medial parapatellar arthrotomy. During surgery, samples of the periprosthetic tissue were taken in order to obtain a histological evaluation. These specimens were treated with haematoxylin-eosin and von Kossa staining, and were then studied under light microscopy using polarized light in order to detect the typical birefringence of the polyethylene debris.
The total knee components appeared to be well fixed intraoperatively. The polyethylene insert was substituted with a 12-mm CD LPS Flex articular surface (Zimmer, Warsaw, Indiana, USA). The stability in full extension, mid-flexion, and full flexion of the knee was tested intraoperatively, and appeared to be good. The patient had no postoperative complications and recovered well.
The polyethylene insert and the broken post were both prepared for scanning electron microscopy (SEM) evaluation (Figure ).
At six months follow-up the patient had recovered complete function of her left knee. She was free from pain and could walk normally without any support (Figure ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.6, 'm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.6 m, which is 1.6 m * 39.3701 in/m = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3825,10,Ideal Body Weight,physical,decimal,pmc-6379869-1,Extracted,"A 41-year-old woman with refractory hypothyroidism was referred to our hospital. She was diagnosed with Graves' disease with thyrotoxicosis at the age of 36 years (thyroid weight: 51.1 g, TSH: <0.001 μU/mL (reference range; 0.4 to 4.0), FT3: 21.85 pg/mL (reference range; 2.36 to 5.00). FT4: 4.00 ng/dL (reference range; 0.88 to 1.67), TSH receptor antibody (TRAb) 22.7 IU/L (reference range; < 2.0)). Neither methimazole, iodine potassium, nor three times of 131I ablation therapy ameliorated thyrotoxicosis. At the age of 39 years, she underwent total thyroidectomy, and oral LT4 replacement was initiated after surgery. Although the dose of LT4 was increased to 650 μg/day (11.8 μg/kg/day), with 150 μg/day of liothyronine (LT3) also being administered, severe hypothyroidism persisted.
She had general fatigue, mild diarrhea, anasarca, hair loss, peripheral coldness, and dry skin. She was hospitalized for further examination to exclude malabsorption.
She was 161.6 cm in height and 55 kg in weight and had a body temperature of 36.3°C. Physical examinations showed a blood pressure of 101/67 mmHg with a heart rate of 56 beats/min, and laboratory findings revealed anemia, mild renal dysfunction, and hypercholesterolemia. Her serum TSH levels were extremely high as 146.8 μIU/mL and FT3 and FT4 levels were undetectable (). Glucose tolerance (fasting plasma glucose of 71 mg/dL and HbA1c of 5.4%) and adrenal and pituitary hormone levels were within normal ranges. Autoimmune antibodies other than thyroid peroxidase antibody (TPOAb) were all negative (). Ultrasonic cardiography showed pericardial effusion with normal cardiac output, and electrocardiography revealed a very low voltage and mild bradycardia (data not shown). She was not receiving any concomitant medication that may have interfered with the absorption or metabolism of LT4 []. Her serum albumin levels were within normal range, suggesting no evidence of malabsorption (). Moreover, anemia and hypocalcemia prior to admission to our hospital were successfully treated by the administration of iron and calcium, respectively. Helicobacter pylori and other gastrointestinal tract infections were negative. A stool examination was normal. Upper and lower gastrointestinal endoscopies were performed and were also normal. Duodenal biopsy was performed and did not show pathological abnormalities consistent with malabsorptive disorder. After her admission to our hospital, the patient was handed LT4 tablets by nurses every morning; however, her intake was not confirmed.
Since the additional rectal administration of LT4 suppository preparation (100 μg/day) did not ameliorate hypothyroidism, we attempted its intravenous administration to treat refractory hypothyroidism under the permission and approval of the Ethical Committee of Tokyo Medical and Dental University Hospital and written informed consent was obtained from the patient and her father. An intravenous LT4 formula was dispensed in the Department of Pharmacy of the Tokyo Medical and Dental University hospital, following a previously reported prescription []. In brief, LT4 sodium salt pentahydrate (Sigma-Aldrich T2501, #6106-07-6) was dissolved by 0.1 N NaOH solution and diluted to a concentration of 200 μg/2 mL by saline. A total of 300 μg of LT4 was then diluted in 50 mL of saline and administered to the patient by intravenous drip infusion in 15 min. Since the patient had suffered from severe hypothyroidism for a long time, we did not really know whether her adrenal function was potentially normal or not. Therefore, prior to the intravenous administration of LT4, we administered 100 mg/day of hydrocortisone (HDC) in an intravenous drip to avoid relative adrenal insufficiency caused by rapid increases in thyroid hormone levels. Six days after the daily intravenous administration HDC, her thyroid hormone levels markedly improved. Therefore, we tapered oral administration of LT4 to 200 μg/day and intravenously a bolus of LT4 was administered (100 μg/day). Following the intravenous administration of a single bolus of LT4 (100 μg/day), her serum FT4 levels were rapidly and markedly increased in 1 hour (). At the time of discharge, we decided to administer 200 μg/day of LT4 orally without the intravenous administration. Since we had already administered 100 mg/day of HDC in an intravenous drip for 10 days, we tapered oral administration of HDC to 20 mg/day upon the discharge. However, 7 days after her discharge, her thyroid hormone levels markedly decreased under the prescription. Thus, in the outpatient clinic, we administered 300 μg of LT4 by intravenous bolus injection weekly for several weeks. Then, we examined the time course of serum FT4, FT3 and TSH levels for optimization (). Serum FT4 and FT3 levels increased within 3 days of the administration and deceased thereafter (Figures and ). Within seven days following the bolus intravenous administration, serum FT4 and FT3 levels remained mostly within normal range. Serum TSH levels increased again 14 days after the intravenous administration of a bolus of LT4 (300 μg) in accordance with the decreases observed in serum FT4 and FT3 levels (). Based on these results, we selected the weekly intravenous administration of LT4 (300 μg). Since then, her serum FT4 and FT3 levels had been maintained as low-normal with the weekly intravenous administration of LT4 for 14 months, whereas serum TSH levels had vary (). At the time of the intravenous bolus administration of high dose LT4 (300 μg) in the outpatient clinic, since HDC administration was already started, we decided to administer 20 mg/day of PSL orally instead of increasing the dose of HDC to avoid relative adrenal insufficiency. However, no symptom of adrenal insufficiency was found and her plasma ACTH and serum potassium levels decreased, possibly due to the administration of PSL. Therefore, we tapered the dose of PSL to 10 mg/day in a month after the onset of the weekly intravenous administration of LT4 (300 μg). Thereafter, we carefully tapered the daily doses of PSL by 1 mg per month to avoid steroid withdrawal syndrome and subsequently withdrew PSL administration ().
Twelve months after weekly intravenous administration of LT4 (300 μg), her hemoglobin levels increased, while serum creatinine, low-dense lipoprotein cholesterol, creatine kinase, and prolactin levels decreased to the normal range. No liver dysfunction or cardiovascular events were detected (). Under oral administration of 200 μg/day of LT4, we attempted the intravenous administration of LT4 (300 μg) once in two weeks, which resulted in the relapse of severe hypothyroidism, suggesting the pseudomalabsorption of LT4 due to poor compliance (). We then attempted the single oral bolus administration (1400 μg) under direct observation instead of the weekly intravenous administration of LT4 [, ]. The dose of LT4 selected was 7-fold the usual daily dose, which was 200 μg/day [, ]. Following the oral administration of a single bolus of LT4, her serum FT4 levels rapidly elevated within 2 hours (0.52 to 4.56 ng/dL) as shown in . Her serum FT4, FT3, and TSH levels were maintained within normal range for 15 days after the single bolus oral administration, and hypothyroidism relapsed thereafter (). Based on the results, we employed 700 μg of LT4 for a weekly oral administration protocol, which was 100 μg of LT4 daily, because when we administered 1400 μg of LT4, her FT4 levels after 2 hours were extremely high, which were clearly harmful and had remained elevated for more than one week. Under the weekly oral administration of 700 μg of LT4, her serum FT4 and FT3 levels were elevated for 2 hours (FT4: 0.96 to 1.36 ng/dL, FT3: 1.41 to 1.56 pg/mL), and TSH levels decreased (52.8 to 48.6 μIU/mL) without liver dysfunction or electrocardiogram abnormalities (). Her serum FT4 and FT3 levels were maintained within normal ranges for 8 days after the single bolus oral administration, which demonstrates the relevance of the weekly oral administration of 700 μg of LT4 ().
Six months after the weekly oral administration of LT4, her renal and liver dysfunction and lipid profile improved (). We concluded that she developed severe hypothyroidism due to poor compliance to the daily oral LT4 replacement, even though she denied the poor compliance. Shi is currently being followed up at the psychiatric clinic. To date, her euthyroid status is maintained under the weekly oral administration of LT4 (700 μg) for two years.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [161.6, 'cm']}",53.83078,51.13924,56.52232,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 161.6 cm, which is 161.6 cm * 0.393701 in/cm = 63.62208 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.62208 (in inches) - 60) = 53.83078 kg.
Hence, the patient's IBW is 53.83078 kg."
3826,10,Ideal Body Weight,physical,decimal,pmc-4705745-1,Extracted,"A 48-year-old man was first seen by a rheumatologist in the beginning of 2011 because of progressing weakness, 10 kg weight loss during the recent year, diminishing height and muscular and bone pain in arms, lower back and chest which severely limited his movements. The patient felt unhealthy since 2009; however, his life history had no recorded health-related problems except for rib fracture during a car accident in his childhood and many years of smoking. His family history revealed that his father died of pancreatic cancer, his brother died of oncohematology condition and his mother lives with oncohematological disease. At the time of investigation, he was 180 cm tall (being 184 cm when healthy) and weighted 73 kg (BMI = 22.5 kg/m2). Physical examination revealed scoliosis and kyphosis of the spine, overall weakness, weakness in muscles and pain in both arms when palpating. The laboratory investigations showed no inflammation, and the only abnormality in serological readings was elevated alkaline phosphatase—248 U/l (normal values, 40–150) due to its bone-specific fraction comprising 80.5 % (Table ). The radiology of the spine revealed compressive fracture in Th11–Th12, which was confirmed by the following computed tomography (CT) scan and magnetic resonance imaging (MRI) readings as well. Bone mineral density was 0.840 g/cm2 indicating osteopenia. Because of the family history, the patient underwent urological examination and ultrasound of the thyroid gland, liver, spleen and prostate. His lung CT scan was inconspicuous with small atelectasis in lower segments. He was also referred to a haematologist and endocrinologist, but after examination, both myeloma and parathyroid disease were excluded, although autoimmune thyroiditis due to raised autoantibodies against thyroid tissue was diagnosed. No treatment except for painkillers was prescribed.
With continuing weight and height loss together with bone and muscle pain, the patient was hospitalised at the Department of Rheumatology for thorough examination in November 2011. The alkaline phosphatase remained elevated and hypophosphatemia 0.48 mmol/l (normal values, 0.87–1.45) was documented for the first time. The 24-h urine sample phosphaturia showed normal phosphate clearance 26.5 mmol/24 h (normal values, 12.9–42.0 mmol/24 h) and subsequent phosphate readings in urine were within normal values as well. Vitamin D levels, calcium and ionised calcium readings were found within the normal values: vitamin D being 78.4 nmol/l (normal values, 75–100); calcium 2.25 mmol/l (normal values, 2.15–2.50); and ionised calcium 1.12 mmol/l (normal values, 1.05–1.30); nevertheless, he used periodically prescribed bone mineral supplements from the beginning of disease. The radiology of spine showed a new compressive fracture in the level Th7–Th8 in addition to the old fracture, which was later confirmed by CT scan. Whole body bone scintigraphy with 99mTc-MDP 550 MBq showed increased focal uptake of a radiotracer in the left shoulder and in the ribs on both sides due to osteoblastic process and reduced uptake in right femoral on SPEC/CT sclerotic bone lesion without tumour at that time or Morbus Paget specificity (Fig. ). At that time, undifferentiated bone structural changes (M85.9) were diagnosed because of compressive fractures in spine, increased bone specific fraction of alkaline phosphatase and no evidence found for oncologic disease.
In February 2012, the avascular necrosis of both femur heads with osteosclerotic locus in the right femur of unknown origin was found by MRI. During routine follow-up in 2013, additional compressions were found in spine CT, now overtaking the segment from T5 to T12. The bone density continued to diminish up to 0.76 g/cm2 in the hip and spine, and alkaline phosphatase readings remained elevated. The antiosteoporotic treatment was started at that time with ac. zolendronicum (5 mg/100 ml) administered intravenously and repeated after a year of interval but with no clinical or laboratory improvement. It was discontinued and switched to oral bisphosphonate. Natrium risedronate was initially prescribed in dosage of 35 mg once per week and subsequently increased to 35 mg per day but was discontinued in the fall 2014 because of no effect.
During the time period of almost 4 years, the clinical condition continued to worsen with a loss of height for 15 cm and weight for 20 kg from year 2011 now standing for 165 cm height and 53 kg weight (BMI = 23.1 kg/m2), permanent pain in chest and hips, progressing breathing discomfort, muscular weakness, inability to bend below knees and posture change (Fig. , photo taken in October 2014). Taking in account hypophosphatemia, elevated alkaline phosphatase from the beginning of disease, compressive fractures and avascular necrosis in femur heads, the differential diagnosis was broadened to acquired Fanconi’s syndrome, X-chromosome-linked hypophosphataemia and phosphaturic tumour-induced osteomalacia. To rule out Fanconi’s syndrome, the heavy metals analysis for copper, lead, cadmium and mercury were ordered and were found to be in normal ranges: copper 15.7 μmol/l (n, 11–22), lead 9.60 μg/l (n, 0–90), cadmium 0.8 μg/l (n, 0–1.7) and mercury <1.0 μg/l (n, 0–5). Because of disease manifestation in adulthood, no analysis for FGF gene mutation was requested. FGF-23 readings were found increased fivefold and being 589 U/l (normal values, 26–110 U/l). The whole body scintigraphy with somatostatin analogues 99mTc-tekrotyd 605 MBq revealed intensive uptake of radiotracer in the right femoral head, and SPECT/CT demonstrated uptake in sclerotic bone lesion in the right femoral head—tumour intensively expressing somatostatin receptors (Fig. ). For possible multicentre tumour localization, the whole body CT was ordered. CT indicated deformations in skeletal bones, ribbons, thoracic vertebrae and pelvic bone due to osteomalacia or stress fractures, and no signs of healing were observed. CT also showed compressive fractures in Th3–Th11 with pathologic kyphosis, stress fractures in both femoral heads and osteosclerotic tumour in right femur head (Fig. ). No deformations were found in soft tissues, parenchymal organs, lungs or lymph nodes.
With strong prediction of phosphaturic mesenchymal tumour-induced osteomalacia, a tumour-removal surgery was performed, and subsequently, removal of the head and the neck of the right femur was required following total hip arthroplasty in October 2014. Surgical specimen was presented by femur proximal head. Examination revealed ill-defined intramedullary grey tumour, approximately 2 cm in diameter. Bone tissue was soft, macroscopically intact by tumour and showed a broad band of cartilage under articular surface. Histologic examination of the specimen revealed a hypercellular tumour composed of spindle-shaped cells in fibromyxoid matrix, with a hemangiopericytoma-like pattern. Tumour cells had clear to eosinophilic cytoplasm; nuclei were oval or elongated, of monomorphic appearance and with no signs of atypia. Mitotic figures were rare. Surrounding bone trabeculae were irregular in size and shape with wide osteoid seams and foci of hyaline cartilage, showing enchondral ossification. The tumour cells were strongly and diffusely positive with vimentin but exhibited no reactivity with PanCK, SMA, CD34, CD10 and D2-40 (Fig. ).
The post operation period went without clinical complications and after 3 months the levels of phosphorus, alkaline phosphatase and FGF-23 were measured. Alkaline phosphatase remained elevated 316 IU/l (40–150) with bone fraction now standing at 57.7 % and FGF-23 returned to normal values 104 IU/l (26–110 IU/l). Three months after surgical procedure, the body pain almost disappeared and the weight increased up to 62 kg and height up to 166 cm (BMI = 22.5 kg/m2). The alkaline phosphatase returned to normal values 6 months after tumour extirpation and remained within normal values after 1 year of follow-up (Table ). The phosphorus level increased remarkably up to 1.51 mmol/l (normal range, 0.87–1.45) after 3 months and normalised within 1 year. We have to admit that measuring 24-h urinary phosphate was not a proper phosphate balance measure throughout the disease course. Without applying more sophisticated methods, e.g. percent tubular reabsorption of phosphate (%TRP) or tubular maximum for phosphate corrected for glomerular filtration rate (TmP/GFR) as it is recommended [], significant loss of phosphate was probably missed from the beginning of disease. Conventional radiography of the spine after 1 year showed permanent and nonreversible spine deformation due to the old compressions from Th3 to Th11 with no evidence of new compression fractures (Fig. ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [166.0, 'cm']}",62.31505,59.1993,65.4308,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 166.0 cm, which is 166.0 cm * 0.393701 in/cm = 65.35437 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.35437 (in inches) - 60) = 62.31505 kg.
Hence, the patient's IBW is 62.31505 kg."
3827,10,Ideal Body Weight,physical,decimal,pmc-2923800-1,Extracted,"A 38-yr-old Korean woman visited a private clinic for the evaluation of anterior neck swelling. The initial laboratory examination revealed an elevated levels of serum thyroid hormone without accompanying TSH suppression (free T4 2.67 ng/dL [range, 0.64-1.72] and TSH 1.82 µIU/mL [range, 0.4-4.5]). She had no signs or symptoms of typical thyrotoxicosis except diffuse goiter and mild palpitations. However, due to findings of elevated serum thyroid hormone levels and goiter, she was diagnosed with Graves' disease, and prophylthiouracil (PTU) was prescribed. After three months of PTU (100 mg three times daily), she complained of generalized weakness, a weight gain of about 3 kg, and generalized edema. Consequently, she was referred to our hospital.
When first seen at our hospital on December 9, 2008, her height and weight were 162 cm and 49 kg, respectively, with a blood pressure of 97/68 mmHg and a pulse rate of 96 beats/min. Her thyroid gland was symmetrically enlarged, and exophthalmos and myxedematous skin lesions were absent. Past medical history was significant for goiter first detected at age 13. At that time, the physician recommended regular checks for thyroid function because of elevated levels of thyroid hormones, but she was lost to follow-up. Her family history included one sister who had a diffuse goiter and a thyroid nodule.
The laboratory examination revealed an elevated level of TSH despite an elevated levels of thyroid hormone [total T3 181 ng/dL (range, 76-190), free T4 2.50 ng/dL and TSH 10.23 µIU/mL]. Thyroid autoantibodies against thyroperoxidase, thyroglobulin, and TSH-receptor were all negative. Thyroid ultrasonography (USG) revealed several micro-nodules in both lobes. USG-guided fine-needle aspiration was performed for the nodule which showed suspicious features of malignancy in the right thyroid lobe (), and the cytologic diagnosis was papillary thyroid carcinoma. A 99m technetium thyroid scan showed diffuse enlargement of the thyroid gland with increased uptake (10.1%) (). PTU was discontinued due to TSH elevation and the occurrence of hypothyroid symptoms. After PTU was stopped for one month, hypothyroid symptoms disappeared and thyroid function tests (TFTs) revealed elevated thyroid hormone levels [free T4 2.20 ng/dL and total T3 141 ng/dL] and a nearly normal level of TSH (5.60 µIU/mL).
The differential diagnosis at this point was between RTH and a TSH-secreting pituitary adenoma based on the TFTs findings. TSH-secreting pituitary adenoma was ruled out because the patient had no clinical features of thyrotoxicosis, a negative MRI of the pituitary gland, a normal level of the α-subunit of TSH (0.36 mIU/mL, range, 0-0.9), and an exaggerated response of TSH to a thyrotropin-releasing hormone (TRH) stimulation test ().
Accordingly, genomic DNA was isolated from the peripheral blood leukocytes of the patient with a G-DEX™ Ilb Genomic DNA Extraction Kit (Intron Biotechnology, Seongnam, Korea). PCR amplification was conducted on seven coding exons (from exon 4 to 10) of the TRβ gene. The sequences were analyzed using the computational software ABI 3730 XL (Applied Biosystems, Foster City, USA). A point mutation was detected in exon 9 of the TRβ gene that caused the substitution of threonine (ACG) for methionine (ATG) at codon 310 (M310T). This mutation has not yet been reported in Korea. The patient's sister had normal TFTs and no mutation by DNA sequencing analysis ().
Ultimately, the patient was diagnosed with RTH and papillary thyroid carcinoma. She underwent a total thyroidectomy and the pathologic diagnosis was two micropapillary thyroid carcinomas in both lobes (0.4 cm in the right and 0.2 cm in the left lobe). After surgery, she received levothyroxine (L-T4) at 150 µg/day). After three months of L-T4 therapy, her TSH level was still elevated (TSH 45.1 µIU/mL) and she complained about symptoms of hypothyroidism; therefore, we increased the dose of L-T4 to 200 µg/day. After two months, her TSH level decreased to 15.5 µIU/mL, and most of her hypothyroid symptoms disappeared. Ultimately the dose of L-T4 was increased to 250 µg/day titrated to achived a TSH level comparable to the preoperative value.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [162.0, 'cm']}",54.19299,51.48334,56.90264,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.77956 (in inches) - 60) = 54.19299 kg.
Hence, the patient's IBW is 54.19299 kg."
3828,10,Ideal Body Weight,physical,decimal,pmc-2565670-1,Extracted,"A 19-year-old Caucasian Greek male was operated for an asymptomatic left Bochdalek hernia. The patient was a student without a history of smoke, alcohol, or medications. He was a 187 cm height and 72-kgr weight male without significant medical and family history. Chest radiography (Figure ) that was performed for his pre-employment check up showed the possible intrathoracic presence of abdominal content and the patient was referred for Thoracic CT scan that confirmed the diagnosis of Bochdalek hernia (Figure ).
We performed a left thoracotomy and the thoracic cavity was entered in the bed of the 5th rib. The abdominal content was easily reduced from the chest back in the abdominal cavity and the diaphragm was closed with silk interrupted sutures. The patient was easily weaned and transferred to the ward. Five hours later the patient was symptomatic for abdominal heaviness, dyspnoea, chest pain and vomiting. His heart pulse was 155/min and arterial blood pressure 75/45 mm Hg. The patient was in profound respiratory distress. We transferred the patient to the operating room again and a midline abdominal incision was done. The abdominal route was preferred due to awareness of the syndrome. Small bowel loops were heavily ischemic. The abdomen remained open with proper dressing for 2 days. The patient remained in the ICU for six months. Nine months later in good condition he was discharged from the hospital. During this period he was subjected three times in partial enterectomies, four times in plastic reconstructions of the abdominal wall, and a cholocystectomy. The patient received a total of 196 units of blood during these months. Two years later the patient is in excellent condition. His case is a classic example of devastating complications even after simple thoracic operations.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [187.0, 'cm']}",81.33081,77.26427,85.39735,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 187.0 cm, which is 187.0 cm * 0.393701 in/cm = 73.62209 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (73.62209 (in inches) - 60) = 81.33081 kg.
Hence, the patient's IBW is 81.33081 kg."
3829,10,Ideal Body Weight,physical,decimal,pmc-6040299-1,Extracted,"A 60-year-old woman came to the endocrinology clinic with a complaint of rapidly progressive signs and symptoms of hyperandrogenism over 6 months. She mentioned hirsutism noticed especially in the face and chin, hair loss that took a male-pattern baldness in all over the head, deepening voice, and increased libido.
She had no galactorrhea, muscle weakness, hyperpigmentation, bruising, weight loss, or anorexia.
She was married, housewife, and smoker (5 pack-years), got 6 children, did not consume alcohol; she had regular menses since puberty until she had amenorrhea 22 years ago after hysterectomy (because of leiomyoma). She was diagnosed with hypothyroidism 15 years ago treated with L-Thyroxine (700 μg∖weekly) and osteoporosis 7 years ago treated with Calcium supplements + alendronate 70 mg weekly. She denied the use of any drugs that may cause hyperandrogenism.
On examination, the patient seemed well. The blood pressure was 120/80 mm Hg, the pulse 83 beats per minute, the height 154 cm, the weight 72 kg, and the body mass index (BMI; the weight in kilograms divided by the square of the height in meters) 30.2 (obesity class I). The Ferriman-Gallwey score for hirsutism estimation was 6 (4 in the chin, 2 in upper lip); she had acanthosis nigricans, frontal baldness, and clitoromegaly (2 cm by 3 cm) as shown in (). Except for a cesarean scar in the abdomen, the rest of examination was unremarkable.
Laboratory studies revealed a hemoglobin concentration of 15 g/dL, serum sodium level of 141 mEq/L, and potassium level of 4.5 mEq/L. An automated chemistry panel showed normal findings. Hormonal studies were as in .
Transvaginal ultrasonography showed that uterine and left ovary was removed, right ovary measured 2.1 cm by 2 cm by 4.5 cm with a volume of 7.8 cm3. Abdominal computed tomography (CT) showed bilateral adrenal nodular hyperplasia as in (). All adrenal function tests (hypo- and hypersecretion) were proved to be normal: 24-hour urine normetanephrine 47.3 μ/24hours (up to 600), metanephrine 107 μ/24hours (up to 350), 8 A.M cortisol 13.02 μg/dL, adrenocorticotrophic hormone ACTH 19.69 pg/mL (7-63), and 11 P.M cortisol 1.66 μg/dL
In order to distinguish ACTH-dependent hyperandrogenism from other causes of hyperandrogenism, a 48-h low-dose (2mg) dexamethasone-suppression test was carried out [], without a decrease in testosterone value (10.94 ng/mL) though enough cortisol suppression at the end of the test 0.58 μg/dL.
In such cases the catheterization of the adrenal and ovarian veins may be useful in identifying the source of hyperandrogenism but it was not available at our center. Since the lack of dexamethasone-induced inhibition of testosterone was suggestive of an ACTH-independent etiology mainly ovarian, and the patient was postmenopausal, the decision of laparoscopic oophorectomy was made. The pathology report confirmed the diagnosis of 2.8 cm Leydig cell tumor (). Testosterone was performed 72-hour postsurgery and it was 0.03 ng/mL. 17 hydroxy-progesterone and testosterone were performed 1 month later and they were in normal limits.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [154.0, 'cm']}",46.94889,44.60145,49.29633,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 154.0 cm, which is 154.0 cm * 0.393701 in/cm = 60.62995 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.62995 (in inches) - 60) = 46.94889 kg.
Hence, the patient's IBW is 46.94889 kg."
3830,10,Ideal Body Weight,physical,decimal,pmc-6939787-1,Extracted,"A 43-year-old female patient with no cardiovascular risk factors, weight 57 kg, height 170 cm, presented to our hospital with constrictive chest pain at rest radiating to both arms for 20 min disappearing spontaneously. Admitted to the coronary care unit for monitoring, clinical examination was normal, blood samples found elevated ultrasensitive troponin at 236 for a normal <14 pg/mL. She was not pregnant. The electrocardiogram recorded sinus rhythm at 63/min with negative T waves at V1 and V2 leads. The echocardiography showed a moderate left ventricle dysfunction (left ventricular ejection fraction 45%) with severe apical and anterior wall hypokinesia.
The patient was referred to our Cath lab after receiving Aspirin 250 mg IV, oral Ticagrelor 180 mg, and Fondaparinux 2.5 mg subcutaneous. Coronary angiography showed a long (22 mm) moderate smooth stenosis (50%) of the proximal left anterior descending artery (LAD) (). Optical coherence tomography (OCT) analysis highlighted an intramural coronary haematoma starting at the ostium of the artery to its middle part without a dissection plane visualized ().
The patient was admitted to our intensive cardiac care unit for monitoring. She has been treated with aspirin 75 mg, bisoprolol 2.5 mg, and atorvastatin 80 mg orally. She was asymptomatic with no signs of haemodynamic instability and normal clinical examination. Five days later, she presented several recurrences of chest pain with good response to nitroglycerine administration associated to an increased level of troponin; average blood pressure was 125/85 mmHg. The angiogram control revealed a significant worsening of the stenosis with an extension of the wall haematoma towards the middle part of the LAD () with normal run flow (TIMI 3).
After heart-team discussion, a conservative strategy was decided upon with hospital monitoring and medical treatment with aspirin, beta-blockers, and nitrates. Chest pain totally disappeared without recurrences. Angiogram control at 2 weeks () showed an extension of the haematoma to the distal LAD.
In the following days, the patient remained totally asymptomatic and was then discharged with the same treatment. Strict rest was also suggested.
The patient has been consulting in our centre once a week for 3 months.
After 3 months, she was totally asymptomatic. Cardiac magnetic resonance imaging showed limited apical myocardial late gadolinium enhancement with normal left ventricle ejection fraction. Coronary angiogram showed a quite normal appearance of the LAD (). Optical coherence tomography control showed a significant regression of the LAD wall haematoma with dispersed, vanishing haematoma remnants ().
At 1 year, she remained asymptomatic and her echocardiography showed persistent limited apical akinesia with normal left ventricular function.
An angio computed tomography (CT) scan revealed diffuse atheromatous infiltration of both carotid and vertebral arteries. An aortic and renal artery CT scan did not find any sign for fibromuscular dysplasia.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [170.0, 'cm']}",61.43709,58.36524,64.50894,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.92917 (in inches) - 60) = 61.43709 kg.
Hence, the patient's IBW is 61.43709 kg."
3831,10,Ideal Body Weight,physical,decimal,pmc-7405338-1,Extracted,"A 44-year-old woman with 5-year history of Basedow’s disease had a total thyroidectomy. She had no past and family history and had no drug allergy. She was diagnosed as Basedow’s disease at 39 years old and after then she started taking 30 mg of thiamazole (MMI). In physical examination, she had no remarkable symptom such as palpitation, general fatigue and insomnia and did not have a goiter. Her height and body weight were 158.0 cm and 63.6 kg. Her vital signs were: heart rate 112 beats/min, blood pressure 132/86 mmHg. Laboratory data were as follows: white blood cell count, 4580 /μL (neutrophil 57.7%); red blood cell count, 476 × 104 /μL; hemoglobin, 12.7 g/dL; platelet, 26.5 × 104 /μL; Na, 142 mmol/L; K, 5.2 mmol/L. Renal and liver function was within normal range (creatinine (CRE), 0.38 mg/dL; blood urea nitrogen (BUN), asparate aminotransferase (AST), 25 U/L; alanine transaminase (ALT), 26 U/L; alkaline phosphatase (ALP), 231 U/L; γ-glutamyltranspeptidase (γ-GTP), 17 U/L; lactate dehydrogenase (LDH), 174 U/L). Thyroid-associated data were as follows: thyroid-stimulating hormone (TSH), < 0.010 μIU/mL; free triiodothyronine (FT3), 19.05 pg/mL; free thyroxine (FT4) 4.88 ng/dL; TRAb, 10.6 IU/L (electro chemiluminescence immunoassay (ECLIA), SRL Inc., Tokyo); TPOAb, 216.9 IU/mL (ECLIA, SRL Inc., Tokyo); TgAb antibody, 428.9 IU/mL (ECLIA, SRL Inc., Tokyo). Ultrasound examination revealed that the thyroid gland was hypervascular although it was not enlarged (Fig. ). Based on such findings, we finally diagnosed her as Basedow’s disease. Two weeks after starting MMI therapy, she had liver dysfunction (AST, 420 U/L; ALT, 368 U/L; ALP, 565 U/L; γ-GTP, 178 U/L; LDH, 337 U/L), and we changed the treatment of MMI to 300 mg of propylthiouracil (PTU) although her thyroid hormone levels were decreased (TSH, < 0.010 μIU/mL; FT3, 7.2 4 pg/mL; F T4 1.97 ng/dL). After then, her liver function was improved, and we tapered PTU. About 2 years later, her thyroid hormone levels were within normal range with 50 mg of PTU every other day, and her TRAb became negative. After then, we stopped PTU therapy.
About 1.5 years later, she had low grade fever and palpitation and visited our office again. Her body weight was 70.9 kg. Her vital signs were: heart rate 116 beats/min, blood pressure 140/98 mmHg. Laboratory data were as follows: white blood cell count, 3710 /μL (neutrophil 58.3%); red blood cell count, 535 × 104 /μL; hemoglobin, 12.2 g/dL; platelet, 22.4 × 104 /μL; Na, 142 mmol/L; K, 4.2 mmol/L. Renal and liver function was within normal range (CRE, 0.52 mg/dL; BUN 9 mg/dL; AST, 25 U/L; ALT, 17 U/L; ALP, 218 U/L; γ-GTP, 19 U/L; LDH, 206 U/L). Thyroid-associated data were as follows: TSH, < 0.010 μIU/mL; FT3, 5.22 pg/mL; FT4, 1.85 ng/dL; TRAb, 4.6 IU/L; TPOAb, 147.4 IU/mL; TgAb, 591.2 IU/mL. Ultrasound examination revealed that the thyroid gland was not hypervascular compared to that at the onset of Basedow’s disease (Fig. ). Based on such findings, we finally diagnosed her as the relapse of Basedow’s disease. We started again 300 mg of PTU and tapered PTU dose. About 4 months later, her thyroid hormone levels became within normal range by taking 50 mg of PTU every other day. During the PTU therapy, her WBC levels were slightly lower and CRP levels were slightly higher, although she had no symptom in the whole body including in skin. We checked various autoimmune antibodies. Anti-double stranded DNA IgG antibody, anti-SS-A/Ro antibody and anti-SS-B/La antibody were all negative. However, anti-nuclear antibody (ANA), myeloperoxidase-anti-neutrophil cytoplasmic antibody (MPO-ANCA) and proteinase3-anti-neutrophil cytoplasmic antibody (PR3-ANCA) were all positive (ANA, 37.8 (+); MPO-ANCA, 35.0 U/mL; PR3-ANCA, 36.9 U/mL).
We performed a total thyroidectomy. Table shows laboratory data before a total thyroidectomy in this subject taking 50 mg of PTU every other day. In general, the thyroid gland in subjects with Basedow’s disease shows diffuse goiter due to chronic stimulation. However, her thyroid was flat and atrophic although diffuse hyperplasia of the thyroid gland was observed in histopathological macroscopic findings (Fig. ). Furthermore, hyperplasia of the thyroid gland was shown in part and hyperplastic thyroid follicles with papillary infoldings was observed in histopathological microscopic examination. Tall follicular cells with papillae usually lacked fibrovascular cores and peripheral scalloping was present (Fig. ). On the other hand, a part of the thyroid area showed a dense lymphoplasmacytic infiltrate, accompanied by follicles containing germinal centers. In addition, a destroyed pattern of lymphoid follicle was observed (Fig. ).
One year later, thyroid-associated autoimmune antibodies were all decreased (TRAb, 2.2 IU/L; TSAb, 130% (enzyme immunoassay, SRL Inc., Tokyo); TPOAb, 98. 3 IU/mL; TgAb, 151.0 IU/mL), and 2 years later thyroid-associated autoimmune antibodies were further improved (TRAb, 1.1 IU/L; TSAb, 90%; TPOAb, 24.0 IU/mL; TgAb, 12.8 IU/mL). White blood cell count became within normal range (about 5000–7000 /μL (neutrophil 58–68%) and CRP level became almost normal (0.15–0.20 mg/dL).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3832,10,Ideal Body Weight,physical,decimal,usmle-524,Extracted,"A 45-year-old man comes to the physician because of a 3-week history of progressive diarrhea and a 2.2-kg (5-lb) weight loss. During the past week, he has had six small bloody stools daily. He is employed as a sales manager and regularly flies to South America. He has HIV, gastroesophageal reflux disease, and hypertension. Current medications include chlorthalidone, omeprazole, emtricitabine, tenofovir, and efavirenz. He reports taking efavirenz irregularly. He is 175 cm (5 ft 9 in) tall and weighs 64 kg (143 lb); BMI is 22 kg/m2. His temperature is 38.1°C (100.6°F), pulse is 91/min, and blood pressure is 116/69 mm Hg. The abdomen is scaphoid. Bowel sounds are normal. His CD4+ T-lymphocyte count is 44/mm3 (N ≥ 500), leukocyte count is 6,000/mm3, and erythrocyte sedimentation rate is 12 mm/h. Colonoscopy shows areas of inflammation scattered throughout the colon with friability, granularity, and shallow linear ulcerations. The intervening mucosa between areas of inflammation appears normal. A biopsy specimen is shown.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3833,10,Ideal Body Weight,physical,decimal,pmc-5154314-1,Extracted,"A 37-year-old woman presented an asymptomatic and voluminous ovarian cyst, detected during a routine ultrasound scan, one month before presentation. The personal history included menarche at 14 years old, regular periods and 2 pregnancies completed by cesarean. She denied having experienced weight loss, fever, chills, night sweats, urinary tract symptoms, or other gastrointestinal complaints.
The clinical examination revealed a good physical appearance, weight of 55 kg and height of 160 cm. During a deep abdominal palpation, a voluminous adnexal mass with the upper pole corresponding to the umbilical scar was revealed. On pelvic exam, a smooth, round, rubbery mass, non-adherent to the surrounding tissues and no vaginal bleeding was found. Laboratory tests and tumor markers were within normal limits. Transvaginal ultrasound 2D and color Doppler revealed a cystic adnexal mass with 10 cm transonic, smooth, homogeneous content and avascular walls with no internal papillary projections, delimitated from the ovarian capsule by a “hyperechoic line” sign, being easier to establish the paraovarian origin by mobilizing the adnexa; a normal uterus and normal bilateral ovaries were described ().
The laparoscopic diagnostic and curative surgery (laparoscopic cystectomy) was indicated. The cyst had no attachments to the abdominal wall, intestine, or mesentery and it was successfully removed during the procedure (). The uterus, both ovaries and fallopian tubes were normal. Patient recovery was quick and uneventful.
Microscopically, the paraovarian cyst wall was lined with the mesonephric epithelium, containing fibrous connective tissue with vascular structures and glandular epithelium, columnar and cuboidal at the periphery (, ). There was no evidence of malignancy, borderline epithelium, vascular malformation or other neoplasm. No ovarian stroma was found in any of the sections.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3834,10,Ideal Body Weight,physical,decimal,pmc-6337715-2,Extracted,"This patient was an otherwise healthy 17-years-old male. He was 1.70 m tall and weighed 59 kg. He was in high school. For 1 year, he had suffered from excessive sleepiness characterized by multiple irresistible naps even when ambulating, episodes of sudden muscular weakness triggered by laughing, and visual hallucinations while falling asleep. The patient and his parents reportedly did not seek medical attention. His Epworth Sleepiness Scale was 15. His HAMA was 6 and HAMD was 4. Physical examination, regular laboratory examination, and brain magnetic resonance imaging results were normal. A polysomnographic examination showed that his sleep efficiency was 82.3%. NREM1 was 17%, NREM2 was 43%, NREM3 was 9.5%, REM was 24.5%, AHI was 1.5/h, PLMDI was 12.1/h, and RSWA was not observed. His MSLT showed a mean MSLT sleep latency of 2.6 min, fewer than 8 min, and the presence of 4 REM sleep-onset periods while napping (Figure ).
Cerebral autoregulation before treatment markedly decreased compared to the normal level (phase difference, 24 degrees in the left and 25 degrees in the right). The patient was diagnosed with narcolepsy type 1 and administered fluoxetine treatment (20 mg/d once a day in the morning). After 1 month of treatment, his clinical symptoms were relieved, and his Epworth sleep scale was 9. His cerebral autoregulation had the tendency to rise (phase difference, 45 degrees in the left and 40 degrees in the right). At the end of a 6-months follow-up period, his cataplexy symptoms occurred occasionally, and his Epworth sleep scale was 11. Simultaneously, the phase difference was 46 degrees in the left and 42 degrees in the right. The patient received venlafaxine (75 mg/d once a day in the morning) during the following month. His clinical symptoms were relieved, and his Epworth sleep scale was 10. His cerebral autoregulation improved clearly (74 degrees in the left and 68 degrees in the right, Figure ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.7, 'm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.7 m, which is 1.7 m * 39.3701 in/m = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3835,10,Ideal Body Weight,physical,decimal,pmc-4495851-1,Extracted,"A 77-year-old woman underwent an annual medical checkup and was diagnosed with a cystic tumor in the pancreas by computed tomography (CT) of the abdomen. The patient was referred to our hospital for further examination. Her medical history included a radical parotidectomy for a parotid gland tumor and a total knee replacement for the right leg. In addition, she was receiving treatment for hypertension and osteoporosis. On admission, she had no clinical symptoms. Her height was 154 cm and her body weight was 61 kg. There was no superficial lymphadenopathy or palpable mass in the abdomen. Her serum amylase level was 211 U/L (normal range; 30–120 U/L), and other biochemical data, including tumor marker levels, fasting plasma glucose, and hemoglobin A1c, were within normal ranges. An upper gastrointestinal endoscopy showed esophageal hiatal hernia and short-segment Barrett’s esophagus. Colonoscopy showed diverticula in the sigmoid colon. Contrast-enhanced abdominal CT scanning demonstrated a cystic tumor in the head of the pancreas measuring 40 mm in diameter with slightly enhancing mural nodules within the cyst (Fig. ). Magnetic resonance cholangiopancreatography (MRCP) revealed a cystic tumor in the head of the pancreas along with a normal, non-dilated dorsal pancreatic duct throughout the pancreas (Fig. ). The presence of a connection between the cystic lesion and the main pancreatic duct was unclear. Endoscopic retrograde pancreatography (ERP) via the major duodenal papilla showed a cystic tumor and a slightly dilated main pancreatic duct, but the main pancreatic duct was abruptly interrupted at the head of the pancreas (Fig. ). The major duodenal papilla was enlarged and the orifice was filled with abundant mucin (Fig. ). The minor duodenal papilla was normal in size and ERP via the minor papilla was not possible. The diagnosis based on pancreatic juice cytology was “highly suspicious for adenocarcinoma,” suggestive of an intraductal papillary mucinous carcinoma (IPMC) arising in the ventral pancreas of pancreas divisum. The patient underwent a pylorus-preserving pancreaticoduodenectomy (PPPD) with regional lymphadenectomy. The postoperative course was uneventful, except for a Grade A pancreatic fistula (staged according to the International Study Group on Pancreatic Fistula clinical criteria []), and the patient was discharged on postoperative day 29.
A pancreatography via the major and minor duodenal papillae on the surgical specimen revealed no connection between the ventral and dorsal pancreatic duct systems (Fig. ). Macroscopically, a multilocular cystic tumor, 40 × 35 × 25 mm in size, with abundant accumulation of mucin was identified in the ventral pancreas. Microscopically, the tumor was composed of atypical epithelial cells showing nuclear enlargement, clear nucleoli, and disordered polarity (Fig. ). They formed prominent papillary structures. The Mib-1 index was up to 80 %. The tumor cells slightly progressed into the main pancreatic duct. Finally, the tumor was determined to be a mixed type IPMC (well-differentiated adenocarcinoma) with partial microinvasion. The pancreas bearing the tumor was drained by the pancreatic duct, which opened into the major papilla, suggesting that it was the ventral pancreas. The region surrounding the IPMC was mainly composed of fibrous tissue, which was clearly distinguished from the normal pancreas (Fig. ). The normal pancreas was relatively rich in adipose tissue and the islets of Langerhans were typically oval in shape, features consistent with the dorsal pancreas. Furthermore, the pancreatic duct in the region of the normal pancreas was linked to the minor papilla, also suggesting a dorsal pancreas origin.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [154.0, 'cm']}",46.94889,44.60145,49.29633,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 154.0 cm, which is 154.0 cm * 0.393701 in/cm = 60.62995 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.62995 (in inches) - 60) = 46.94889 kg.
Hence, the patient's IBW is 46.94889 kg."
3836,10,Ideal Body Weight,physical,decimal,pmc-2804009-1,Extracted,"The long-term treatment period of a Finnish, ethnically Caucasian, 21-year-old high school graduate and shop assistant, started when she was admitted to the acute ward of the local psychiatric hospital in August 2007 with a diagnosis of anorexia nervosa according to the criteria of the ICD-10. Her eating disorder had started in 2001, when she was 13 and began to exercise and avoid fattening food. Her weight dropped from 78 kg to 49 kg (her height is 178 cm) in a few months. At that time her parents were having severe marital problems. However, the parents did not separate or divorce. At the same time Ms. P.M. had started high school in a boarding school about 50 km away from her home, which was an exceptional choice as boarding schools are a rarity in Finland.
During the first months of her eating disorder she had psychiatric outpatient treatment, but in summer 2002 her condition deteriorated as she started bulimic behaviour and vomiting, and also had symptoms of depression (depressive mood, loss of pleasure, low energy, insomnia). In September 2003 she was admitted to the Department of Adolescence Psychiatry, Tampere University Hospital and hospitalized for two months. During her hospital treatment she had no psychotropic medication. Her relationship to her parents was found to be exceptionally close and she had only one friend of her own age. There were many unsolved family problems but abuse was not among them. However, the eating disorder had brought the parents closer to each other, which pleased the patient.
The patient subsequently resumed psychiatric outpatient treatment until spring 2005. The outpatient treatment consisted of visits to a psychologist with CBT training once a week, psychotropic medication (fluoxetine 40-60 mg/day), and nutritional advising. She was able to complete her high school studies with good grades in May 2005. She then got a job as a shop assistant. She moved away from her parents' home with her only (female) friend as a room-mate. She also began occasionally dating a boyfriend of her own age and the relationship was a good one. In summer 2007 her room-mate moved to another town to work. Soon after that the patient's eating disorder became more severe and she had amenorrhoea. She also began to mutilate herself with a knife and to drink quite a lot of alcohol (cider). She was admitted to the acute ward of the local psychiatric hospital in August 2007. At that time her weight was 56.2 kg and Body Mass Index (BMI) 17.7. The patient's hospital treatment was then two months. After that there was an outpatient period of seven weeks, a new hospital treatment of one month, and again an outpatient treatment of six weeks. Poor compliance was the biggest problem in this outpatient treatment.
Since the beginning of April 2008 she has been almost continuously hospitalised for more than a year (there was a short period of outpatient treatment in August 2008). She began her psychiatric inpatient treatment again in the local hospital. At the beginning of summer 2008 her weight was 40.0 kg and BMI 12.6. At that time she was admitted for two weeks for rapid nasogastric refeeding on the medical ward of the local hospital. Her weight rose to 49.6 kg in only two weeks, making her mood more and more anxious. Thereafter she was admitted to the psychiatric ward of the University Hospital, again for four days on the medical ward of the University Hospital, and then back to the psychiatric ward. Besides anorexia nervosa (F50.0), major depressive disorder (MDD; F32.2) was also diagnosed according to the criteria of the ICD-10. Her symptoms of depression were: lowering of mood, reduction of energy, decrease in activity, reduced capacity for enjoyment and interest, hopelessness, appetite diminished, feelings of worthlessness, agitation and suicidal acts. She had delusional thoughts about her body shape and weight. She totally refused to eat and regarded even water as a fattening foodstuff. She tried to vomit aggressively and exercise physically all the time. Mechanical restraints, nasogastric refeeding, and constant observation 24 hours a day were provided. She nevertheless managed to abuse herself by hysterical cutting and vomiting. At that time her medication included fluoxetine (60 mg/day) and olanzapine (30 mg/day) and also lorazepam (2 mg/day) before main meals. Later on fluoxetine was supplied in a combination of venlafaxine (150 mg/day) and mirtazapine (60 mg/day). Because the symptoms of MDD were not relieved with AD treatment, ECT was used. ECT was administered three times a week. Anaesthesia was induced with methohexital and muscle relaxation with succinylcholine. Physiological monitoring included pulse oximetry, blood pressure, ECG, four channel EEG and EMG. She had ten bifrontotemporal ECT sessions in July 2008. The psychotropic medication was continued during the ECT treatment. There were no anaesthetic complications. The respective Beck Depression Inventory (BDI) [] scores were 52 and 35 before and after the ECT treatment, meaning that her depression was not totally relieved. Clinically, the patient was satisfied with the outcome of the ECT, her behaviour continued to be self-destructive but her mood was better, she was more active, no longer hopeless, no longer delusional, and her appetite was no longer impaired. BMI had risen only slightly from 15.0 to 15.3. She continued exercising but the vomiting had diminished.
In August 2008 she first spent three weeks on the psychiatric ward of the local hospital and then returned to the psychiatric ward of the University Hospital with BMI only 13.8. She had started to exercise aggressively again. At the beginning of September 2008 her BMI was only 12.2. Two short treatment periods of nasogastric refeeding on the medical ward were initiated. She then requested a new series of ECT. Before the ECT her BDI was 35, her Montgomery-Åsberg Depression Rating Scale (MADRS) [], score 28 and BMI 14.2. After 12 bifrontotemporal ECT treatments BMI had risen slightly to 14.6, her mood was slightly better according to MADRS (scoring 24) and she began to smile, but she was acting out (lying and stealing) and the self-rated BDI was higher than it was before the ECT: 43. Vomiting and exercising had diminished quite a lot. In October 2008 she was transferred to a psychiatric ward specialized in treating refractory patients. At that time a decision was taken on mECT: bifrontotemporal ECT once a week or once in two weeks. The medication was again supplied: quetiapine (600-800 mg/day) was used instead of olanzapine and fluoxetine (60-70 mg/day) instead of other ADs. She had creative art therapy and physiotherapy in order to improve her body image of which physiotherapy was of some help by teaching the patient to relax. In December 2008 she was allowed to spend some days at (her parents') home. By the end of 2008 BMI was16.4 and she had no symptoms of depression. During the first weeks of 2009 mECT was only given once in 4 weeks. Very soon she became anxious again and started exercising, stealing sweets, binge eating, vomiting with the help of various hoses, and evacuating her rectum. Her mood became low and she was tired and hopeless. In the middle of February 2009 the frequency of mECT was then temporarily increased to twice a week for two months. Her mood improved and she was active and optimistic. Her weight remained at 50-51 kg (BMI about 16) until the beginning of April. The most aggressive exercising and vomiting faded away. Then quetiapine was changed to aripiprazole (20-30 mg/day), and at the same time the frequency of mECT was changed to once in 2 weeks. A new type of therapy was also initiated: the patient was given more responsibility for her own behaviour and the use of strict weight limits in order to obtain new benefits was abandoned. Her mood remained in balance and the acting out behaviour (stealing, lying, hysterical cutting) declined, but her weight dropped rapidly from 51 kg to 46 kg (BMI 14.5) in only eight weeks.
Ms. P.M. underwent a series of 10 ECT in the summer, a series of 12 ECT in the autumn, and a total of 23 mECTs during the winter and spring 2008-9. In order to control for possible side-effects of the mECT, a magnetic resonance image (MRI) of her head was taken and a psychologist's assessment was conducted in May 2009. The MRI was normal. Maintenance ECT was discontinued in order to get a psychologist's assessment of memory functions during a four-week time free of ECT. Soon depressive symptoms again became prominent: low mood, reduction in energy, difficulties in concentrating, but no hopelessness or suicidality. BMI remained low at 14.5. However, according to the psychologist's assessment in May 2009, the patient's cognitive capacity had been impaired during the last 21 months. A shorter psychological assessment had been conducted in August 2007 and at that time the patient's cognitive skills were clearly better (IQ was 116 in August 2007 and 102 in May 2009). Moreover, her memory functions three weeks after the latest ECT yielded a very uneven memory profile, indicating difficulties in verbal memory (word lists) possibly due to fluctuating attention. The psychologist's assessment even suggested that the patient's semantic memory might have deteriorated. As we did not want to expose her to possible difficulties with memory the idea of more mECT was abandoned.
She has now been 10 weeks without mECT. Her regular medication has been aripiprazole 30 mg/day, fluoxetine 60 mg/day and lorazepam 1 mg twice a day before main meals. At first her mood became depressive, but after 5-6 weeks she was no longer depressive but only feeling down once in a while. Her BMI has slightly risen from 14.8 to 15.3.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [178.0, 'cm']}",68.68119,65.24713,72.11525,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (70.07878 (in inches) - 60) = 68.68119 kg.
Hence, the patient's IBW is 68.68119 kg."
3837,10,Ideal Body Weight,physical,decimal,pmc-7422010-1,Extracted,"A 19-year-old male presented to the emergency room as a level 1 trauma with a self-inflicted GSW to the abdomen. The patient was attempting to put his 380 caliber handgun on safety when it discharged. On physical exam, the patient's abdomen was rigid and tender with a presumed entry point in the periumbilical area () and a presumed exit point in the left posterior superior buttock (). No other injuries were present. The patient's measurements included a height of 165 cm and a weight of 60.1 kg (BMI 22.1). The vital signs upon arrival were BP 132/66 mmHg, pulse 106 bpm, and GCS 15/15. The patient's blood pressure decreased slightly to 101/45 mmHg; however, this corrected with intravenous (IV) fluids.
Computed tomography (CT) was performed and showed a mild amount of free fluid and air in the abdomen and pelvis (). There was no evidence of great vessel injury. Given the known trajectory of the bullet and lack of severity in the CT findings, diagnostic laparoscopy was pursued with readiness to convert to laparotomy if necessary.
An initial periumbilical incision was made, and the abdomen was entered through a 5 mm port utilizing the Optiview technique. Pneumoperitoneum was obtained to 15 mmHg. Upon laparoscopic entrance, a small amount of blood and stool was noted in the left lower quadrant (). Additional ports were placed in the left lower quadrant (5 mm port) and right upper quadrant (11 mm port), both using the same optical trocar insertion method. Initial inspection of the sigmoid colon revealed a perforation with minimal contamination from stool spillage (). This was cleared and washed out followed by intracorporeal repair using 2-0 V-Loc™ suture in a running fashion done in 2 layers (). A second sigmoid perforation was found in the 4-5 cm distal to the first perforation as was repaired in a similar fashion (Figures and ). The sigmoid was followed systematically to the pelvis, and a rectal wall laceration was noted (). It was found to penetrate the serosa and muscle layer but lack mucosal involvement. This was again repaired using 2-0 V-Loc™ suture in 2 layers (). After advancing down the rectum, a laceration was noted in the peritoneum over where the bladder was located (). Of note, preoperative urinary catheterization yielded hematuria and this laparoscopic finding confirmed bladder injury. The on-call urologist was contacted intraoperatively, and it was agreed upon for the primary surgeon to repair it in 2 layers with 2-0 V-Loc™ sutures and leave a Foley in place for 2 weeks postoperatively (Figures and ). The colon was then systematically examined proximally including the rest of the sigmoid, descending colon, transverse colon, ascending colon, and cecum with no additional injuries noted. The ileocecal valve was identified; the small bowel was then run from the terminal ileum proximally. Another perforation was found approximately midsmall bowel with an enterotomy measuring less than 1 cm in size (). This was closed in 2 layers using 2-0 V-Loc™ suture (). The rest of the small bowel was run up to the ligament of Treitz with no additional injuries found. Of note, all the mesentery was examined while running the bowels with no significant injuries noted. All solid organs were intact on inspection. After abdominal and pelvic washout was performed, a size 19 French Blake drain was placed in the pelvis exiting through the left lower quadrant port site.
The GSW to the abdominal wall itself was examined. The bullet trajectory was angled in such a way that when it penetrated the skin, there was about a 5 cm difference from the presumed skin entry point and peritoneum entry point. Given this tangential path, the wound was not closed due to a low risk of herniation. The tract was thoroughly irrigated. Port sites were closed and dressings were placed. The patient tolerated the procedure well and was transferred to the postanesthesia care unit following extubation.
Postoperatively, the patient was placed in the surgical intensive care unit. There he progressed well and remained NPO with a NG tube in place. A urologist recommended the Foley catheter remains in place for 7 to 10 days with a cystogram done prior to removal. The patient was started on ertapenem upon his arrival and remained on IV antibiotics throughout his admission. Repeat CT with oral, rectal, and IV contrast on POD 5 was negative for any occult injury or contrast leak. Following this, the patient was started on a clear liquid diet with progression to full liquids. The patient was tolerating this well and was having normal bowel movements. He was advanced to a soft diet the following day. The patient's drain remained serosanguineous in nature and was able to be removed. The patient was discharged home on POD 6 with a Foley catheter in place, which was removed by a urologist 5 days later.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3838,10,Ideal Body Weight,physical,decimal,pmc-7220192-1,Extracted,"An 18-year-old man was admitted to our hospital for a 1-year history of chronic inflammatory skin lesions in both inferomedial gluteal areas. Although he had recurrent episodes of painful abscess and spontaneous pus-like discharge without any symptom of systemic inflammation, he took only anti-inflammatory drugs and dressed himself without visiting the hospital. He was a non-smoker and his body mass index was 18.17 kg/m2 (weight 55 kg, height 174 cm). He had no other pertinent medical history and no family history of HS. Physical examination revealed multiple sinuses with broad surrounding scars without active inflammation in both inferomedial gluteal areas. Laboratory tests of inflammatory markers including white blood cell count, C-reactive protein, and erythrocyte sedimentation rate were within normal range. We diagnosed his lesions as HS and planned surgical management.
We opted for a complete resection of all affected lesions and flap coverage (Fig. A). The operation was performed with the patient in the prone position under general anesthesia. We performed wide excision of the affected lesions and debridement of surrounding unhealthy tissues using the Versajet II hydrosurgery system (Smith and Nephew, St. Petersburg, 98 FL). The final post-debridement defects were 6 × 10 cm on the right side and 5 × 9 cm on the left side; the defects were very close to the anus medially (Fig. B). We symmetrically designed a 9 × 15 cm–sized KF (right side) and an 8 × 12 cm–sized KF (left side) based on the hot spots of the interior gluteal artery and internal pudendal artery perforators (Fig. C). At this time, we designed the long axis of each flap to be parallel to RSTLs in order to minimize wound tension and scar formation[ and the width of each flap was designed to be larger than the vertical width of the defect. Once the skin incision was made along the flap design, the dissection proceeded from the subcutaneous layer to the deep fascia. The fibrous subcutaneous septa and deep fascia were released using a monopolar device until the flaps could be moved freely from the surrounding tissues. After creating the island-shaped flap structure, the margin of the flaps was undermined minimally to preserve the integrity of the perforators (Fig. D). The procedure of insetting the flaps was first performed at its central portion on the side of the defect, and then on both ends, which were aligned in a V-Y apposition. Thus, both tension-free insetting of the flaps and primary closure of the donor sites were achieved (Fig. A and B). Mild compressive dressings were made with a foam material.
The total operative time was 185 minutes and the total flap elevation time was 39 minutes. The flaps completely survived without postoperative complications, such as hematoma, seroma, infection, or wound dehiscence. The patient was satisfied with the final outcome after 6 months of follow-up. The final scars were well hidden by the underpants and were tolerable without scar contracture, especially in the perianal area (Fig. C and D).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [174.0, 'cm']}",69.55913,66.08117,73.03709,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 174.0 cm, which is 174.0 cm * 0.393701 in/cm = 68.50397 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.50397 (in inches) - 60) = 69.55913 kg.
Hence, the patient's IBW is 69.55913 kg."
3839,10,Ideal Body Weight,physical,decimal,pmc-7220338-1,Extracted,"A 40-year-old Asian male patient was referred to our hospital by his primary doctor due to warmth, pain, edema, and swelling in the left leg. He had experienced similar symptoms intermittently over the last 2 years, which were initially managed with non-steroidal anti-inflammatory drugs. (NSAIDs) The symptoms were accompanied by a rash, which was seen not only in the lower extremity but also around the neck and eyelids, with repeated appearances and disappearances. The patient also complained of recurrent oral ulcers. He was also sometimes aware of atypical chest pain during the 2-year period. He was suspected of having venous thrombosis by venous ultrasound at a dermatology clinic 2 months before the referral, but no evidence of venous thrombosis was found and no further treatment out with NSAIDs was required. His medical history was a surgery for the rupture of median nerve 9 years ago. He had a continuous smoking habit of 20 cigarettes a day for 20 years and had taken a small amount of alcohol every weekend. His family history was unremarkable. He had worked in the transportation industry for 20 years. His medication profile for the pain and edema of the left leg included celecoxib 200 mg twice a day and azosemide 30 mg once a day. Examination findings upon admission were as follows; his height and weight were 1.72 m and 66.0 kg, respectively (body mass index [BMI], 22.3 kg/m2), swelling and tenderness on his left leg and the left thigh circumference was greater than the right (42.0 vs 38.0 cm), blood pressure was 139/87 mmHg, pulse 97 bpm (regular), and a respiratory rate of 18/minute with an oxygen saturation of 97% on room air, and body temperature was 36.6°C. Furthermore, the patient had neither anemia nor jaundice, while bulbar conjunctiva was congested. On the ophthalmologist's examination, no uveitis or fundus abnormalities suggestive of BD were found. He presented with a 2-mm aphthous ulcer on the right side of the tongue. Dermatological status showed pustules, which were localized to hair follicles on the back of the thigh and fingers, blisters of the foot, left abdominal crust formation after drainage, pigmentation of the thigh, and a painful rash with infiltrative erythema on his left lower extremity. Heart sounds were normal, and no murmurs were detected. The lung fields were clear to auscultation and the abdomen was soft with normal bowel sounds. The patient was awake, alert, and oriented. His neurological examination on admission did not find any motor or sensory deficits and the cranial nerves were normal. Orthopedic physical examination showed no local inflammatory findings including an abnormal increase in synovial fluid in his knee joint.
Laboratory tests revealed an increased white blood cells 9500/μL (normal range, 4000–9000/μL), erythrocyte sedimentation rate 18 mm/first hour (<10 mm/first hour), C-reactive protein 1.33 mg/dL (0.00–0.47 mg/dL), D-dimer, 1.7 μg/mL (<1.0 μg/mL), and fibrinogen 407 mg/dL (150–400 mg/dL). Thrombophilia investigation did not show any abnormalities, and anti-nuclear antibody, anti-DNA antibody, anti-cardiolipin IgG antibody, and myeloperoxidase and proteinase 3 anti-neutrophil cytoplasmic antibody tests were all negative. The human leukocyte antigen (HLA)-51 serologic test was also negative. The patient's laboratory data, including the above-mentioned parameters, are shown in Table . A bacterial culture obtained from a pustule on the back of the left thigh was negative. A skin biopsy from the left low extremity revealed lobular and septal panniculitis with variable numbers of perivascular neutrophils and lymphocytes, as well as variable numbers of necrotic adipocytes (Fig. ). An electrocardiogram showed a normal sinus rhythm and findings on the chest radiograph were unremarkable. Transthoracic echocardiography revealed a left ventricular ejection fraction of about 60% with normal sized right-sided cardiac structures. Contrast computed tomography (CT) disclosed a thrombus from the left femoral vein to the left popliteal vein, vein wall thickening, dilatation of the entire veins, and associated inflammatory stranding of the perivascular fat (Fig. ). Venous Doppler ultrasonography revealed that a part of the thrombus was organized, without a blood flow signal (Fig. ). On dynamic contrast thorax CT, several clots were detected in the bilateral lower lobe branch (Fig. ). Neither aneurysm formation nor irregular contours were seen in the pulmonary arteries. The diagnosis of PAT was also confirmed by 99mTc-macroaggregated albumin scintigraphy which was presented with perfusion defects in the inferior lobe of the bilateral lung.
On the day of admission, the patient was therapeutically anticoagulated with continuous intravenous administration of heparin sodium (18 units/kg/h), an unfractionated heparin. Initial treatment with heparin for 6 days was effective for swelling in the lower extremity, while it did not relieve the leg pain. Left thigh circumference reduced to 39.0 cm. His D-dimer level was slightly reduced to 1.4 μg/mL. Contrast CT demonstrated the reduction of clots in pulmonary arteries, but it showed no sign of improvement of the thrombus in his lower extremity. Heparin sodium therapy was switched to direct oral anticoagulant (DOAC, Edoxaban; 60 mg per day) on the seventh day of admission. At the same time, colchicine therapy for suspected BD was added to his drug regimen at a dose of 1.5 mg per day, and he was discharged on the tenth day of admission. One week after discharge, the symptoms associated oral ulcers and DVT had improved gradually. Furthermore, because cutaneous lesions, such as chronic pustules and blisters, had greatly diminished, colchicine was reduced to 1.0 mg per day in consideration of a side effect of diarrhea. Approximately 1 month after treatment with edoxaban and colchicine, the follow-up contrast CT confirmed the complete resolution of thrombus in the pulmonary arteries and almost disappearance, except for residual microthrombi, in his left popliteal vein (Fig. ). During this period, significant improvement of the laboratory parameters of this patient was obtained as follows: white blood cells 6200/μL, erythrocyte sedimentation rate 2 mm/first hour, C-reactive protein 0.10 mg/dL, D-dimer, <0.1 μg/mL and fibrinogen 186 mg/dL. Three months after the start of oral medication, edoxaban treatment was discontinued, and only colchicine was subsequently prescribed as maintenance therapy. Colchicine, which was continued at 1.0 mg per day until that time, was to be gradually increased to 1.5 mg per day due to the instability of skin findings such as new several pustules on the right leg and the back of the right hand and new red papules on the right popliteal fossa. Infiltrative erythema was also newly identified in the right forearm, which was suggestive of superficial thrombophlebitis. Clinical and laboratory examinations revealed no signs of recurrence of DVT during the 6-month follow-up after discharge.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.72, 'm']}",67.74811,64.3607,71.13552,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.72 m, which is 1.72 m * 39.3701 in/m = 67.71657 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.71657 (in inches) - 60) = 67.74811 kg.
Hence, the patient's IBW is 67.74811 kg."
3840,10,Ideal Body Weight,physical,decimal,pmc-5507570-1,Extracted,"A 64-year-old man sought medical care complaining of weakness, a weight loss of 10 kg, and back pain for the last 2 months that had worsened during the last 2 weeks. His medical history comprised hypertension and type 2 diabetes mellitus, which was regularly controlled with hydrochlorothiazide, losartan, and metformin. He smoked 80 packs/year of tobacco. He denied abdominal pain, nausea, vomiting, gastrointestinal bleeding, or intestinal habit changes. The initial physical examination showed a well-looking patient, though markedly emaciated. His weight was 68.3 kg, height 1.79 m (body mass index was 23.6), pulse 104 beats/min, and blood pressure 102/64 mmHg. No peripheral lymphadenomegaly was palpable. A mild systolic cardiac murmur was audible in the aortic area, and the abdomen was plain, flaccid, and free of ascites and visceromegaly. The remaining examination was normal. The laboratory tests showed bicytopenia represented by erythrocytes of 1,300,000/mm3 (reference range [RR]: 4,500,000-5,900,000/mm3), hemoglobin of 3.9 g/dL (RR: 12.3-15.3 g/dL), hematocrit of 13.3% (RR: 36.0-45.0%), mean corpuscular volume of 102.3 fL (RR: 80-100 fL), red cell distribution width of 23.2% (RR: <14.9%) and reticulocytes of 78,000/mm3 (RR: 16,400-95,000/mm3). The peripheral blood smear revealed the presence of 18% of orthochromatic erythroblasts per 100 leukocytes. The platelet count was initially 80,000/mm3, then 18,000/mm3 in a second measurement (RR: 150,000-400,000/mm3). Leukocytes of 14,100/mm3 (RR: 4,500-11,000/mm3) showed a marked shift to the left (neutrophils of 82%, promyelocytes 1%, myelocytes 2%, metamyelocytes 3%, bands 5%, segmented 71%, lymphocytes 15%, and monocytes 3%). Lactic dehydrogenase determination was 809 U/L (RR: <250 U/L). Renal function tests, electrolytes, liver enzymes, bilirubins, clotting tests, vitamin B12, and folic acid determinations were normal. Even though blood transfusions were carried out, the hemoglobin level returned to a very low titer over the following 2 days. Therefore, the patient was hospitalized with the working diagnoses of occult bleeding, myelodysplastic syndrome, or hemolysis.
The abdominal computed tomography (CT) showed lymphadenomegaly in the periaortic, interaortocaval portocaval, and in the lesser gastric curvature topographies.
Because of the hematological features, which were consistent with leukoerythroblastosis, a bone marrow biopsy was performed. After a suspicious episode of melena, an upper digestive endoscopy was undertaken, which revealed a protruding infiltrative and ulcerated lesion located in the cardia extending to the distal third of the esophagus. The gastric chamber was full of clots due to diffuse tumoral bleeding that hampered the evaluation of the tumor size (). Biopsies were performed, followed by adrenalin and ethamolin infiltration in an attempt to control the bleeding sites. The histological report of the gastric biopsies revealed signet ring cell adenocarcinoma with mucinous areas (). The bone marrow was so extensively infiltrated by the neoplasia that the hematopoietic elements were scarcely represented (1% of the sample). The immunohistochemical profile of the bone marrow biopsy revealed positivity for CK7, CK20, and CDX-2, and negativity for TTF-1 and PSA, which was consistent with the gastrointestinal primary site of the neoplastic cells ().
The treatment consisted on hemostatic radiotherapy and chemotherapy for metastatic gastric cancer. Modified FLOX (oxaliplatin, 5-fluorouracil, and leucovorin) was administered. The outcome was unfavorable and the patient died on the 15th day of the first chemotherapy cycle.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.79, 'm']}",74.0867,70.38236,77.79103,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.79 m, which is 1.79 m * 39.3701 in/m = 70.47248 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.47248 (in inches) - 60) = 74.0867 kg.
Hence, the patient's IBW is 74.0867 kg."
3841,10,Ideal Body Weight,physical,decimal,pmc-5640928-1,Extracted,"A 28-year-old pregnant woman (height 167 cm, weight prior to pregnancy 97 kg) and her 31-year-old partner, both healthy, non-consanguineous, and with uneventful family history, presented at our genetic department. During ultrasound examination in the 17 + 0 week of gestation in our center, the fetus showed intrauterine growth retardation, left diaphragmatic hernia with parts of stomach and bowel localized in the chest, dextrocardia, a short nasal bone, and single umbilical artery. These findings were confirmed at the 18 + 1 week when the pregnancy was terminated. The pregnancy was conceived spontaneously.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [167.0, 'cm']}",58.72056,55.78453,61.65659,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 167.0 cm, which is 167.0 cm * 0.393701 in/cm = 65.74807 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (65.74807 (in inches) - 60) = 58.72056 kg.
Hence, the patient's IBW is 58.72056 kg."
3842,10,Ideal Body Weight,physical,decimal,pmc-7826241-1,Extracted,"A 28-year-old man (height 194 cm, PBW 88 kg) with no previous medical conditions was involved in a single-vehicle collision resulting in ejection from the vehicle. His initial Glasgow coma scale (GCS) score was 12 when the paramedics arrived, which later deteriorated to 3 upon arrival to the emergency department at a tertiary care trauma centre. On physical examination, he had reduced air entry to the right chest with bruising, subcutaneous emphysema, and significant hypoxemia on a nonrebreather mask. On point-of-care ultrasound, the absence of lung sliding was identified over the right chest. Due to significant hypoxemia, he was intubated. A chest tube was inserted into the right pleural space, and a second chest tube was inserted on the right due to an ongoing air leak.
Hypoxemia persisted with a large air leak on the right and substantial difficulties with mechanical ventilation with low return in VT. A significant bronchopleural fistula or tracheobronchial injury was suspected. Following selective isolation of the right lung with a double-lumen endotracheal tube, the patient's condition stabilized enough to perform a computed tomography (CT) scan. The CT scan confirmed the presence of a large right-sided pneumothorax, extensive pneumomediastinum, right-sided pulmonary contusions, subcutaneous emphysema, and numerous bilateral rib fractures. Other injuries included a stable T4 and an unstable T5 vertebral body fracture, a small 6 mm right subdural hemorrhage, and a left adrenal gland injury. Postadmission, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) testing was also performed and was negative. His clinical parameters and ventilator settings over the course of his intensive care unit (ICU) stay are summarized in .
The patient was taken to the operating room and diagnosed with a ruptured right main bronchus after an intraoperative bronchoscopy. A right posterior lateral thoracotomy was performed with an initial attempt to repair this injury, but due to ongoing patient instability, a right sleeve pneumonectomy was performed. At the end of the case, the double-lumen endotracheal tube was changed to a single lumen tube, and the patient was transferred to the ICU. A follow-up CT scan of the head demonstrated reduction in the size of the subdural hemorrhage to 3 mm, and follow-up chest radiographs demonstrated evolving atelectasis and opacification in the left lower lobe ().
On postoperative day (POD) #3, he had T2-T7 posterior instrumentation and fusion. Liberation from the ventilator was attempted; however, the patient could not wean due to secretions and mucous plugging requiring bronchoscopy and tracheobronchial toileting. He was subsequently diagnosed with a Haemophilus influenzae ventilator-associated pneumonia (VAP) and started on ceftriaxone on POD #4. By POD #8, the patient had developed worsening left-sided opacities and was eventually diagnosed with ARDS, using the Berlin definition with the exception of bilateral opacities on chest imaging due to the absence of one lung () []. A further sputum culture and sensitivity was performed and was positive for Gardnerella vaginalis. Subsequently, his antibiotics were changed to piperacillin-tazobactam and moxifloxacin.
He progressed to having worsening hypoxemia and hypercapnia. As a result, he was sedated to a Richmond Agitation-Sedation Scale (RASS) score of -4 to -5. By POD #11, his PaO2/FiO2 (P/F) ratio had remained in the low 100 s despite sedation, with evidence of patient-ventilator asynchrony. To minimize further VILI, the patient was started on neuromuscular blockade, an adult esophageal balloon (CooperSurgical, Connecticut, United States) was inserted, and prone positioning was initiated. A negative fluid balance was attained with furosemide. After prone positioning and optimization of positive end-expiratory pressure (PEEP), his condition stabilized. His airway driving pressure (ΔP) was maintained below 14 cm H2O, and esophageal balloon monitoring was used to maintain end-inspiratory transpulmonary pressure (PL) less than 15 cm H2O and end-expiratory PL between 0 and 5 cm H2O.
The patient further improved and had a tracheostomy on POD #18. He was liberated from the ventilator by POD #25 and decannulated on POD #32. On POD #35, he was discharged home. One month later, he was reviewed in the trauma clinic and he was doing well with ambulation. He had no respiratory concerns and was working on improving muscle strength.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [194.0, 'cm']}",87.66938,83.28591,92.05285,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 194.0 cm, which is 194.0 cm * 0.393701 in/cm = 76.37799 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (76.37799 (in inches) - 60) = 87.66938 kg.
Hence, the patient's IBW is 87.66938 kg."
3843,10,Ideal Body Weight,physical,decimal,pmc-6732835-1,Extracted,"An 18-year-old Caucasian man presented in January 2019 to our Emergency Department (ED) for evaluation of sudden-onset right-sided chest pain while sleeping. He reported waking up with acute right-sided pleuritic chest pain underneath his ribs with radiation to his right scapula, which was made worse with inspiration and movement. He denied classic triggers, including excessive coughing, recent respiratory tract infection, or trauma prior to the onset of pain. However, he reported multiple episodes of vaping daily and rare intermittent marijuana use, but denied cigarette smoking or use of smokeless tobacco. He had no past medical or surgical history, history of vision changes, heart problems, or joint laxity. In addition, there was no family history of Marfan syndrome or lung disease. He reported no current medications, cigarette smoking, or alcohol consumption.
A physical examination revealed a height and weight of 54.9 kg and 180 cm, respectively with decreased breath sounds over his right lung. His calculated BMI had an underweight BMI of 16.9 kg/m2. His vital signals were notable for a temperature of 36.4 °C, heart rate of 64, blood pressure of 112/59 mmHg, respiratory rate of 19, and oxygen saturation of 95%. A neurological examination revealed he was alert and oriented to person, place, and time, and he moved all extremities equally. The remainder of the neurologic examination was non-focal. Laboratory examinations were all normal (Table ).
A chest X-ray (CXR) obtained in our ED demonstrated a large right-sided pneumothorax with evidence of tension (Fig. a). A chest tube was placed to suction with improvement in symptoms and our patient was admitted to the medicine service for further management. During admission, he received a lidocaine patch every 24 hours, acetaminophen (650 mg) every 6 hours, and ketorolac tromethamine (15 mg) every 6 hours, as needed. His pneumothorax resolved within the next few days and the chest tube was removed in a stepwise fashion. His presentation at the time was attributed to his body habitus. He was encouraged to quit vaping. He was scheduled for a follow-up CXR 2 weeks after discharge.
One week after discharge, he presented again to our ED for sudden-onset right-sided pleuritic chest pain and shortness of breath. Upon being admitted for recurrent spontaneous pneumothoraces, he reported daily vaping after discharge, but no fever, chills, hemoptysis, cough, upper respiratory infection (URI) symptoms, trauma, or recent airplane travel. At this time, he described a 1.5-year history of vaping with multiple devices. In addition, he again described occasional marijuana use, although marijuana had not been used between episodes of pneumothoraces.
On physical examination, his vital signs were within normal limits. His pupils were equal and reactive to light, without evidence of lens subluxation. His vital signals were notable for a temperature of 37.2 °C, heart rate of 63 beats/minute, blood pressure of 118/56 mmHg, respiratory rate of 18, and oxygen saturation of 97%. A neurological examination revealed him to be alert and oriented to person, place, and time, and moving all extremities equally. The remainder of the neurologic examination was non-focal. Laboratory examinations were all normal (Table ). He had normal heart sounds without murmurs, rubs, or gallops. A lung examination was notable for decreased breath sounds over the right posterior chest.
A CXR revealed the presence of a large recurrent right-sided spontaneous pneumothorax without evidence of significant mediastinal shift (Fig. b). A follow-up chest computed tomography (CT) study without contrast after chest tube placement was notable for a small right residual pneumothorax with residual subsegmental atelectasis in his right lung and small right apical blebs (Fig. ). The spontaneous pneumothorax was recategorized as secondary after noting apical blebs. He was treated with a pigtail chest tube after the initial CXR determined the presence of the spontaneous pneumothorax. His chest tube was removed when imaging confirmed durable resolution of the pneumothorax. His lungs were clear to auscultation bilaterally with symmetric breath sounds. During this second admittance, our patient was treated with lidocaine patch every 24 hours, acetaminophen (650 mg) every 6 hours as needed, and ibuprofen (600 mg) every 6 hours, as needed. A follow-up CXR 2 weeks after removal of the chest tubes confirmed resolution of the pneumothorax (Fig. c). At his follow-up appointment, he reported that he had quit using all e-cigarette products. A physical examination at this follow-up observed a temperature of 37.28 ºC, heart rate 79, blood pressure 110/72, respiratory rate of 20, and oxygen saturation of 96% on room air. On physical examination, he was in no acute distress with lungs clear to auscultation bilaterally and good excursion. No rales, wheezes, or rhonchi were noted on examination. In alignment with British Thoracic Society (BTS) guidelines [], he was offered chemical pleurodesis and/or surgical options; however, he declined the procedure. Written informed consent was provided by our patient for the publication of this case report.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [180.0, 'cm']}",74.99221,71.2426,78.74182,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 180.0 cm, which is 180.0 cm * 0.393701 in/cm = 70.86618 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.86618 (in inches) - 60) = 74.99221 kg.
Hence, the patient's IBW is 74.99221 kg."
3844,10,Ideal Body Weight,physical,decimal,pmc-3106390-1,Extracted,"A 62-year-old male (height 170cms, weight 45 kgs, Body Mass Index 15.5) was posted for elective oesophageal resection and reconstruction for carcinoma of the middle third of oesophagus. Patient was a chronic smoker and chronic alcoholic. He had a history of breathlessness at ordinary physical activity. Chest X-ray showed emphysematous lung fields []. In pulmonary function tests, there was severe obstructive airway disease pattern with observed FEV1 (Forced Expiratory Volume) being 30% only []. On examination neck flexion (10°) and extension (30°) were restricted []; mouth opening was three fingers with modified Mallampati Grade III. In the operating room, thoracic epidural via midline approach was planned before induction. Patient was placed in sitting position and under all aseptic precautions local anaesthesia (2 ml of 2% lignocaine) was infiltrated in thoracic T6-T7 intervertebral space. An 18-gauge epidural needle was inserted at an angulation of 40° with skin and epidural space was located in first attempt at 5 cm by loss of resistance to air technique. Epidural catheter was threaded very smoothly and then fixed at 9 cms at skin entry point. Epidural catheter was advanced 4 cms into the epidural space and was flushed with saline to check for its patency. Because of paucity of time both epidural test dose and analgesia was given after induction to this patient. There was no respiratory distress during and immediately after the procedure. Prior to induction, check laryngoscopy was done after nebulisation with lignocaine. It revealed Cormacke Lehane (IIA). While keeping the difficult airway cart ready, anaesthesia was induced with propofol 80 mg, fentanyl 50μg and vecuronium 5mg intravenously. After 3 min of intermittent positive pressure ventilation, intubation was done with 37 French left-sided double lumen tube. Anaesthesia was maintained with isoflurane 1 volume% in oxygen, vecuronium for muscle relaxation and fentanyl intravenously for analgesia. Epidural test dose of 3 ml of 1.5% lignocaine with 1:200,000 epinephrine was negative for intravascular or intrathecal injection.
Intraoperatively, epidural dose of bupivacaine 0.125% failed to cause decrease in heart rate and change in blood pressure. After 4 hours of laparotomy, thoracotomy was done on the right side. Repeated aspiration from epidural catheter during thoracotomy expressed frank blood, which continued even when catheter was withdrawn by 1 cm []. Epidural test dose was again repeated but it failed to show any changes in heart rate and electrocardiography. It was then suspected that epidural catheter might be misplaced and surgeons were asked to explore the epidural catheter, which was found lying in the right pleural cavity []. The epidural catheter was flushed with normal saline and removed very slowly. The tip of removed catheter was intact and the rest of the surgery was uneventful. Patient was transferred to intensive care unit for post-operative care and cardiopulmonary monitoring. He was discharged after 12 days from the Intensive Care Unit.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3845,10,Ideal Body Weight,physical,decimal,pmc-3977455-1,Extracted,"A 41-year-old nulliparous female (1.73 m/67 kg) with PD had been treated with enzyme therapy for 18 months at time of presentation. Before starting enzyme therapy there was a marked deterioration in muscle function, which manifested as a limb girdle weakness and a decrease in respiratory function, for which she needed nocturnal mechanical ventilation. After starting enzyme replacement therapy, there was a significant improvement in muscle strength.
As her pregnancy progressed, she noticed a marked deterioration in her effort tolerance. She needed more sleep, her walking distance decreased, and she felt short of breath. At 20 weeks pregnancy, her lung function tests showed a functional vital capacity of 1.6 l (40% of normal predicted value) sitting and FVC of 1.1 l (26%) supine. These results were similar to her lung function results prior to her pregnancy and were therefore related to the increased metabolic and respiratory demands of pregnancy rather than deterioration in her muscle function.
Following a multidisciplinary discussion, it was decided to do a caesarean section at 38 weeks of gestation, under combined spinal-epidural anaesthesia (CSE). In the normal healthy population, there is an increased risk of pelvic floor problems (including faecal and urinary incontinence) with a vaginal delivery. The recently reported incidence of previously unrecognised and underreported gastrointestinal symptoms including malabsorption and diarrhoea in patients with PD was a reason to avoid a vaginal delivery [, ]. Furthermore, there may be glycogen storage in the uterus as well, with unknown consequences during vaginal delivery.
The patient received our routine antacid prophylaxis, for example, oral ranitidine, sodium citrate, and metoclopramide. Monitoring was done by pulse oximeter, ECG, and automatic noninvasive blood pressure, set to record every 2.5 minutes. Combined spinal-epidural anaesthesia (CSE) at the L3-4 interspace was performed with the patient being in the sitting position. 1.6 mL bupi 0.5%/sufentanil (6.4 mg hyperbaric bupivacaine and 1.6 mcg sufentanyl) was injected intrathecally. Voluven coload of 500 mL and a phenylephrine infusion at 0.1 mcg/kg/min were commenced. The patient was placed supine in left lateral tilt position. She put on her own CPAP mask to assist her own ventilation. Throughout the operation her oxygen saturation remained above 95%. An adequate sensory block was reached 13 minutes after spinal injection. The phenylephrine infusion was increased to 0.24 mcg/kg/min to maintain baseline mean BP (80 mmHg). A live male infant was delivered 10 minutes after incision. Oxytocin 5 IU was titrated slowly intravenously (iv) followed by an infusion of 2.5 IU/hour of syntocinon for 4 hours. Routine antibiotic prophylaxis of 1 gram cefazolin was also administered intravenously. Estimated blood loss was 300 mL. Postoperative analgesia included regular oral paracetamol (four times a day) and a continuous infusion of ropivacaine 0.2% + sufentanil 0.5 mcg·mL−1 6.0 mL per hour via the epidural catheter. She was monitored on the high-care unit before returning to the obstetric ward. The patient was discharged with her healthy baby boy four days postpartum.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.73, 'm']}",64.15362,60.94594,67.3613,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.73 m, which is 1.73 m * 39.3701 in/m = 68.11027 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (68.11027 (in inches) - 60) = 64.15362 kg.
Hence, the patient's IBW is 64.15362 kg."
3846,10,Ideal Body Weight,physical,decimal,pmc-4442265-1,Extracted,"A 15-year-old girl presented with primary amenorrhea. She attained thelarche at 10 years of age and pubarche at 11 years of age. She had a history of cyclic pelvic pain since the age of 12. Her past medical history was remarkable for a ventricular septal defect as an infant which was subsequently repaired. She also had left renal agenesis which was diagnosed over a decade later. Multiple surgical procedures were performed for correction of severe scoliosis in her lumbar spine with placement of screws and rods. She had no family history of cardiac or genitourinary disease.
Physical examination revealed normal build with a height of 162 centimeters (cm). Her weight was 75 kilograms with a body mass index (BMI) of 28.6 kg/m2. She had normal development of secondary sexual characteristics, categorized as Tanner stage 5. Pelvic examination was limited since she was virginal.
On laboratory analysis of her blood, the complete blood count and biochemistry were within the normal range. Endocrinological laboratory values were also within normal limits and consistent with her age, including thyroid stimulating hormone of 3.0 uU/mL, testosterone of 11 ng/dL, and hemoglobin A1C of 5.3%. A pelvic transvaginal sonogram suggested that the uterus was distended with fluid. Magnetic resonance imaging (MRI) showed a 12 × 7 cm fluid collection in the uterus and an obstruction likely at the level of the vagina which was concerning for imperforate hymen or a transverse vaginal septum. The MRI also showed marked underdevelopment of the right side of the uterus (). No other Müllerian anomalies were identified.
The patient was diagnosed with multiple Müllerian anomalies as the cause of her primary amenorrhea. Surgical intervention was suggested to the patient and her family. Exam under anesthesia revealed a 3 cm blind ending vagina and a 7 × 7 cm pelvic mass. She subsequently underwent diagnostic laparoscopy () and vaginoscopy (). Intraoperatively she was found to have a distended left unicornuate uterus with a right uterine horn with associated fallopian tube on the right side. Bilateral ovaries and fallopian tubes were present. Extensive hemosiderin deposits were identified in the pelvic cavity. On local genital examination, a 1 cm thick complete TVS was identified at the junction of the upper one-third and the lower two-thirds of the vagina. This TVS was diagnosed under ultrasound (US) guidance. The septum was grasped with Allis tissue holding forceps and a stab incision was made. The hematocolpos was drained, and her cervix was subsequently visualized. The vaginal septum was then excised circumferentially. The vaginal epithelium was then approximated with polyglactin 910 throughout its circumference using simple end-to-end anastomosis. A sponge vaginal mold coated with estrogen cream was then placed in vagina to prevent stricture formation.
She was discharged home on postoperative day one. The vaginal mold was removed on the day of discharge and the patient was advised to apply estrogen cream in the vagina locally. As our patient was not sexually active, she was instructed to manually dilate the vagina everyday with the placement of dilators. She was given 10 mg of norethindrone daily for 4 weeks to prevent her menstrual cycle and allow adequate healing of her surgical site. After withdrawal of norethindrone, she had a normal menstrual period.
Two months later at a follow-up visit she presented with pelvic discomfort and dark brown discharge from her vagina. Clinical examination revealed a stricture at the surgical site resulting in stenosis of the vagina. This stricture was then dilated under anesthesia. The margins of the stricture were surgically resected and the vaginal epithelium was approximated. She was discharged home on postoperative day two. She was again extensively counseled regarding the use of manual vaginal dilation methods in order to prevent recurrent stenosis.
However, she was unable to perform manual vaginal dilatation at home due to vaginal spasms and apprehension. She presented again a month later with vaginal stenosis. The stenosed vaginal edges were again excised and reapproximated and a plastic vaginal stent was placed in the vaginal canal to maintain patency. This stent was then removed after two months and she was again educated about the dilatation methods, but she still presented with restenosis three weeks later. The stenosed margins were resected again and the patient was then evaluated every day in the clinic where she demonstrated vaginal dilatation in the presence of a clinician. After 3 months, the patient was able to perform vaginal dilatation successfully without any apprehension and the vaginal patency was maintained without any recurrent stricture formation. She was also instructed to place a vaginal mold nightly for the next six months. Subsequent evaluation at 4 and 6 months from the last surgery demonstrated a patent vaginal canal with adequate vaginal length of 8 cm. She was then experiencing normal menstrual cycles.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [162.0, 'cm']}",54.19299,51.48334,56.90264,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.77956 (in inches) - 60) = 54.19299 kg.
Hence, the patient's IBW is 54.19299 kg."
3847,10,Ideal Body Weight,physical,decimal,pmc-5346126-1,Extracted,"A 24-year-old Turkish woman with known non-transfusion dependent thalassemia was admitted to a specialized trauma center due to an undisplaced low-traumatic fracture of the inferior pubic ramus on the right side. The trauma was sustained when the patient was walking downstairs. First treatment involved an analgesic therapy, anticoagulation therapy and early mobilization with progress in weight-bearing strength.
To better understand the cause of the fracture the patient was admitted to a specialized bone center. The patient’s
medical history revealed no signs of secondary osteoporosis or endocrinological disorders. The family anamneses further
revealed beta thalassemia of both the patient’s mother and her grandmother with no fractures in their respective medical histories. Sex hormones as well as gonadotropin levels were clarified before admission to the bone center and were within normal range. She neither had received any chelation therapy nor any hormone supplementation. The patient had no births and her menstrual cycle was normal and regular. The hemoglobin electrophoreses test as well as genetic testing for thalassemia was conducted. The results showed that the patient is heterozygous for both beta thalassemia and alpha thalassemia (‑α3.7/aa deletion mutation).
On clinical examination, a reduced BMI of 15.2 kg/m2 (weight 42 kg; height 166 cm) was observed. Due to a transient depressive period the patient lost 6 kg (from BMI 17.4 to 15.2 kg/m2) and regained weight again after several months. Psychiatric and dietetic examinations investigating a possible eating disorder did not show any indications of diseases such as anorexia and bulimia. Furthermore, the investigations demonstrated a well-balanced and calcium-rich dietary behavior.
Laboratory investigations (fasting, before 10 am) demonstrated high levels of erythrocytes and iron with reduced values of hemoglobin, MCV, MCH, MCHC and 25-hydroxyvitamin D. Serum values reflecting bone metabolism including procollagen aminoterminal propeptide type I (PINP, osteoblast activity), calcium, phosphate, intact parathyroid hormone (iPTH), type-1 collagen crosslinked C‑telopeptide (CTX, osteoclast activity) levels were all in normal range (Table ).
A dual-energy x‑ray absorptiometry (DXA) bone densitometry revealed a Z‑score of less than −2 reflecting a diminished age-adjusted BMD (see Table ). High-resolution peripheral quantitative computed tomography (HR-pQCT, Scanco, Bruettisellen, Switzerland) was performed according to the manufacturer’s recommendations on calibration and scanning procedures. With an in vivo resolution of 82 μm, HR-pQCT was used to noninvasively assess volumetric bone mineral density and bone microarchitecture at the distal tibia and ultradistal radius. At the tibia (Fig. ) normal cortical vBMD but very low total vBMD and trabecular vBMD were observed. The trabecular bone volume (BV/TV), number of trabeculae (Tb.N) and the trabecular thickness (Tb.Th) were also decreased. In addition, a high level of inhomogeneity of trabeculae was shown by this measurement. Additionally, the cortical thickness was decreased (Table ).
At the radius (Fig. ) as a non-weight-bearing bone site, similar alterations in trabecular bone were observed. In contrast the cortical vBMD was slightly increased and cortical thickness as well as total vBMD were within normal range (Table ).
Due to 25-hydroxyvitamin D insufficiency and the deterioration of bone microarchitecture in conjunction with a fragility fracture, a supplementation with cholecalciferol and calcium as well as a primary osteoanabolic treatment with teriparatide was initiated. After 9 months of osteoanabolic therapy a combination with denosumab as an antiresorptive treatment is planned. Close follow-up and aftercare programs were arranged on the patient’s behalf. The patient was informed that data concerning the case would be submitted for publication and she provided written consent.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [166.0, 'cm']}",57.81505,54.9243,60.7058,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 166.0 cm, which is 166.0 cm * 0.393701 in/cm = 65.35437 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (65.35437 (in inches) - 60) = 57.81505 kg.
Hence, the patient's IBW is 57.81505 kg."
3848,10,Ideal Body Weight,physical,decimal,pmc-7931020-4,Extracted,"A 77-year-old Caucasian male patient (body mass: 77 kg; height: 178 cm; BMI: 24.3 kg/m2) presented with a grade 2 [] open fracture of the femur (AO 33 C1) and a closed tibial and fibular fracture (AO 43 A3) following a bicycle accident (collision against a truck). He was treated with an ORIF and plate osteosynthesis of the femur (less invasive stabilization system (LISS) plate, DePuy Synthes, USA) as well as ORIF and plate osteosynthesis of the tibia (distal tibia LCP plate, DePuy Synthes, USA) and fibula (1/3 tubular plate, DePuy Synthes, USA). Eighteen months later an atrophic nonunion was diagnosed and revision surgery of both femur (LISS pate) and tibia (distal tibia LCP plate) was performed. This procedure included decortication, re-osteosynthesis, and application of autologous cancellous bone from the iliac crest. Intraoperative samples showed no sign of infection. The fracture of the femur showed normal healing. Once again, the tibial fracture showed no healing tendency and the diagnosis of an atrophic nonunion (a) was made 11 months after the revision surgery operation and 29 months after the initial injury. The patient was referred for further osteological treatment of the tibia. Biomechanical analysis showed a correct anatomical reduction and therefore the decision against further operations was made. Calcium and vitamin D supplementation was initiated and a teriparatide treatment was conducted over a period of 21 months. CTX increased by 83% after the teriparatide therapy. The fracture gap showed gradual callus build-up on the serial x rays (b,c). A radiological and clinical union was achieved 4 years after the initial injury (d).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [178.0, 'cm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3849,10,Ideal Body Weight,physical,decimal,pmc-2988177-1,Extracted,"A 16-year-old man presented to the ED with the sensation of a foreign object in his throat 30 minutes after swallowing a peach seed by mistake at dinner. He complained of odynophagia and neck discomfort. He denied neck trauma or any activity that may result in a Valsalva maneuver such as coughing, retching or vomiting; and the use of any medications or illicit drug. He did not have remarkable medical history, especially any pulmonary diseases, as asthma. He was a non-smoker and healthy high-school student.
On physical examination, his blood pressure was 110/80mmHg, with pulse rate 82 beats/min. respiratory rate 18 breaths/min, and body temperature of 36.0’C. His height was 175 cm, weight 80 kg. There was no crepitus on neck. There was no foreign body or abnormal finding in the oropharynx. Laryngopharygoscopy did not reveal mucosal lesions or signs of submucosal swelling, and did not reveal any foreign body in the airway above the vocal cords. The heart sounds were normal. The trachea was in central position, and chest percussion was and breath sounds were all normal.
The patient had a normal ECG. Chest X-ray did not show subcutaneous emphysema and active lesions in the lungs. Blood tests revealed no abnormalities. However, lateral neck X-ray revealed emphysema in prevertebral space, C-spine []. A subsquent CT of the neck and chest revealed emphysema of both neck retropharyngeal area with pneumomediastinum []. There was no evidence of foreign body or pneumothorax or esophageal rupture. Esophagogram demonstrated a good passage of barium in esophagus without obstruction or leakage.
The patient was admitted and treated conservatively. The patient’s progress was uneventful and after two days he was discharged.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3850,10,Ideal Body Weight,physical,decimal,pmc-3259138-1,Extracted,"A 37-year-old male patient 163 cm tall weighing 45.6 kg visited the hospital with paraplegia, voiding difficulty, hypesthesia below L1, and pain with a visual analogue scale (VAS) score 8/10 as post lumbar surgery syndrome, which occurred after receiving surgery for congenital scoliosis. Twenty-four months prior to his visit, he had received treatment from an another hospital, which included caudal epidural block and epidural adhesiolysis, and medication including transdermal fentanyl patch (Durogesic D-trans®, Janssen Korea Ltd., Seoul, Korea) 37 mcg/h, oxycodone hydrochloride (Oxycontin CR®, Mundipharma Korea Ltd., Seoul, Korea) 40 mg/d, Ultracet® (Janssen Korea Ltd., Seoul, Korea) 4 tablets/d, and pregabalin (Lyrica®, Pfizer Korea Inc., Seoul, Korea) 600 mg/d was prescribed; however, there was no improvement in his pain. Hence, 20 months before visiting our hospital, the patient had an ITDAS (SynchroMed® II, Medtronic Inc., Minneapolis, MN, USA) inserted with the catheter tip positioned at the L1 body height. After the procedure, the ITDAS was refilled with 18 ml of morphine sulfate (Highmol® 10 mg/ml, BCWorld Pharm. Co., Korea) every three months, and the injected quantity was maintained between 0.95-1.7 mg/d, and the pain was controlled with a VAS score of 3-4/10.
Fifteen months after inserting the ITDAS, the remaining medication was removed to refill the device; however, 17 ml of morphine sulfate was left in the device, which should have been 5.6 ml had the injections been normal. Other than increased pain with a VAS score of 8/10, there were no neurological abnormalities that had newly occurred, and the test program within the instrument was functioning normally without any failures. The patient had undergone surgery in the left elbow joint two months prior; thus, a temporary software problem due to the monopolar electrocautery during the surgery was believed to be the cause of the problem. After disposing the remaining medication, another 18 ml of morphine sulfate was refilled, and the program was reset. At that time, the patient's pain had not controlled; therefore, oxycodone hydrochloride (IRcodon®, Mundipharma Korea Ltd., Seoul, Korea) 30 mg/d was taken by the patient whenever there was pain. A transdermal fentanyl patch (Durogesic D-trans®, Janssen Korea Ltd., Seoul, Korea) 25 mcg/h was additionally prescribed.
Three months later, when the patient visited the hospital to refill the device, the 18 ml of morphine sulfate were still in the device, and the test program in the instrument was functioning normally. To examine whether the instrument was operating properly, priming bolus mode was initiated, and 15 minutes later, the movement of the rotor was confirmed under the fluoroscope, which confirmed it was operating normally (). Therefore, it seemed that there could be a catheter obstruction rather than problems with the instrument itself; therefore, it was decided to aspirate some of the cerebrospinal fluid from the catheter's access port. The total volume of the catheter was calculated as 0.132 ml; thus, a 1 ml needle was used. The needle was inserted into the access port and aspiration was attempted, but the authors were unable to aspirate any of the cerebrospinal fluid. An emergency kit was prepared and 0.05 ml of normal saline was injected into the catheter's access port; however, it was unable to enter the port. Another attempt was made with 0.05 ml, but there was strong pressure and the normal saline did not go in at all. Catheter kinking or blockage by a mass was suspected; therefore, the decision was made to extract the catheter for confirmation. The catheter and instrument were extracted, and it was confirmed that the catheter's side hole was blocked by a tissue mass, and it was also observed that the catheter's lumen was blocked (). We had planned to exchange the catheter, but the patient and his wife were worried about repeated occurrences of the catheter being blocked. They wanted to remove the ITDAS; therefore, the ITDAS was completely removed. At present, the pain is maintained at a VAS score of 6/10 with a transdermal fentanyl patch (Durogesic D-trans®, Janssen Korea Ltd., Seoul, Korea) 50 mcg/h, pregabalin (Lyrica®, Pfizer Korea Inc., Seoul, Korea) 600 mg/d, tramadol hydrochloride 100 mg/d (Tramaconti®, Whanin Pharm co., Seoul, Korea), and oxycodone hydrochloride (Oxycontin CR®, Mundipharma Korea Ltd., Seoul, Korea) 40 mg/d.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [163.0, 'cm']}",59.5985,56.61857,62.57843,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 163.0 cm, which is 163.0 cm * 0.393701 in/cm = 64.17326 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.17326 (in inches) - 60) = 59.5985 kg.
Hence, the patient's IBW is 59.5985 kg."
3851,10,Ideal Body Weight,physical,decimal,pmc-2542401-1,Extracted,"A 39-year-old man was admitted in October 2006 with a 2-week history of sharp, non-radiating pain of the right shoulder blade with associated dyspnea upon exertion and 5 kg loss of weight. He denied fever, chills, night sweats or cough. His symptoms did not interfere with his occupation as a gardener. Vitals demonstrated a normotensive, afebrile 155 cm, 100 kg man with an oxygen saturation of 96% on room air.
Physical examination was normal with the exception of decreased breath sounds half way up the right lung field along with dullness to percussion and without tactile fremitus. A chest radiograph showed a moderately sized, right pleural effusion (Figure ). The right thoracentesis fluid analysis showed a slightly cloudy and yellow fluid. Cell count results were 1,164 nucleated cells, 12% polymorphonuclear leukocytes, 80% lymphocytes, 7% monocytes, 1% eosinophils, glucose 123 mg/dl, lactate dehydrogenase (LDH) 103 units/l, and protein 5.3 g/dl (pleural to serum protein ratio, 0.8; pleural to serum LDH ratio, 0.7). Bacterial Gram stain and culture, acid-fast bacilli smears, fungal culture and cytology were all negative. Histopathological evaluation of the pleural biopsy noted granulomatous inflammation and fungal elements consistent with coccidioides (Figure ). Cultures for tuberculosis remained negative even after 7 weeks. Purified protein-derivative skin test to the right forearm produced a 0 mm induration. Tests for human immunodeficiency virus were negative by both enzyme-linked immunosorbent assay and Western blot. Serum coccidioidomycosis complement fixation was normal (< 1:2). A post-thoracentesis chest radiograph did not reveal any evidence of parenchymal infiltrate. After several weeks of fluconazole therapy, the patient improved clinically, and follow-up chest radiograph showed near-complete resolution of the pleural effusion.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [155.0, 'cm']}",52.35442,49.7367,54.97214,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (61.02366 (in inches) - 60) = 52.35442 kg.
Hence, the patient's IBW is 52.35442 kg."
3852,10,Ideal Body Weight,physical,decimal,pmc-2803961-1,Extracted,"Mrs. S., a 46-year-old woman from Azerbaijan who had lived in Germany for the past eight years, had always been healthy and had never been under the care of a general practitioner. In November she visited a general practitioner complaining of right upper abdominal pain with no radiation. The pain, which was described as pressing in character, had been present for about three months and was intermittent. There was no nausea, vomiting, weight loss, melaena, change in bowel habit, urinary symptoms, or fever. The patient denied alcohol abuse and said that she was a nonsmoker and took no regular medication.
Blood pressure 140/80 mmHg, weight 75 kg, height 170 cm. Heart and lungs normal to percussion and auscultation. No lymph node enlargement. Abdomen slightly obese and soft. Tenderness present in the right upper abdomen. Bowel sounds normal. Renal angles clear. The clinical findings did not indicate a need for immediate hospital admission. On the basis of the history and the findings at the initial consultation, a series of laboratory tests and an ultrasound scan of the abdomen were ordered.
Relevant abnormal laboratory test results: C-reactive protein 108 mg/l (normal range < 5 mg/l), erythrocyte sedimentation rate 91 mm after two hours (normal range < 20 mm). The following values were within normal limits: blood count, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltransferase, alkaline phosphatase, creatinine, bilirubin, serum electrolytes. Sonography showed an irregularly echogenic, partially calcified septate cystic structure in segment VIII of the liver (Fig. ). No other abnormalities were apparent. In view of the sonographic findings, the radiologist arranged for the immediate performance of a contrast-enhanced computed tomographic scan of the abdomen. This showed a circumscribed rounded lesion measuring 5.8 × 4.7 × 5 cm in hepatic segment VIII (Fig. ). The lesion showed a thick rim of calcification and a suggestion of fine septa with no affinity for contrast medium. The liver was otherwise homogeneous and of normal appearance. The other parenchymal abdominal organs appeared normal and there were no enlarged lymph nodes.
Additional laboratory tests showed an antibody titre of 1:512 for E. granulosus and the presence of anti-E. multilocularis IgG. A western blot analysis was positive for Echinococcus granulosus and negative for Echinococcus multilocularis. After being informed about possible treatment options, the patient was referred to the university hospital. There she underwent hepatic segmental resection and cholecystectomy. Histological preparation of the material removed at operation showed caseating necrosis with a moderately severe, partly giant-cell, inflammatory reaction at the margin of an echinococcal cyst. There was no evidence of malignancy. The histological appearance was consistent with Echinococcus granulosus infection. Moderately severe chronic cholecystitis with moderate fibrosis of the gallbladder wall and cholecystolithiasis were also present. The skin sutures were removed on the tenth postoperative day. As a result of wound dehiscence, the wound healed partly by second intention. The patient was free of symptoms. Follow-up treatment with Eskazole® 400 mg (active ingredient: albendazole) b.i.d. was given. The patient's subsequent progress was without complication.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [170.0, 'cm']}",61.43709,58.36524,64.50894,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.92917 (in inches) - 60) = 61.43709 kg.
Hence, the patient's IBW is 61.43709 kg."
3853,10,Ideal Body Weight,physical,decimal,pmc-5434261-1,Extracted,"A 66-year-old man was transferred to our hospital because of confusion, severe general fatigue, and dyspnea of 1-week duration. The patient had chronic kidney disease related to diabetic nephropathy. Although we strongly recommended initiation of chronic HD, the patient refused the treatment.
The patient had a 15-year history of type 2 diabetes mellitus with triopathy. Other medical history included hypertension of unknown duration that was being treated with amlodipine besylate, losartan, and carvedilol. There was no prior history of seizures, neurological symptoms, loss of vision or other underlying illnesses, or use of any other drugs. Upon arrival at our outpatient department, the patient had severe dyspnea.
On admission (day 0), the patient had mild confusion and anasarca. His height was 168 cm; body weight, 74 kg; blood pressure, 124/43 mmHg; and body temperature, 35.7°C. Urinalysis showed 1+ proteinuria and 2+ occult blood, − glucose, and − ketone and urinary sediment revealed 1–4 erythrocytes, 1–4 leukocytes, 1–4 squamous cells, and 0-1 transitional cells per HPF, but no casts. Blood tests showed low hemoglobin (4.6 g/dL), white blood cell count of 5240/µL (82.3% neutrophils, 12.8% lymphocytes, 1.1% eosinophils, 3.6% monocytes, and 0.2% basophils), and thrombocytopenia (platelet count 84 × 103/µL). Blood chemistry showed blood urea nitrogen (BUN) of 222 mg/dL; serum creatinine, 25.4 mg/dL; total protein, 5.7 g/dL; albumin, 3.3 g/dL; lactate dehydrogenase, 403 IU/L; aspartate aminotransferase, 46 IU/L; alanine aminotransferase, 44 IU/L; serum sodium, 139 mmol/L; and serum potassium, 6.1 mmol/L, glucose 97 mg/dL. Serological tests showed C-reactive protein of 0.2 mg/dL. Coagulation parameters were normal. Chest X-ray showed congestion of the lung fields. The patient had pulmonary edema and uremic symptoms (vomiting and consciousness disorder). We performed brain MRI and electroencephalogram (EEG) to evaluate cerebral function.
T2-weighted fluid attenuated inversion recovery (FLAIR) MRI showed several old, small brain infarcts (Figures and ). Diffusion-weighted MR imaging (DWI) did not show increased apparent diffusion coefficient (ADC), which would be suggestive of vasogenic edema. EEG showed frequent slow waves, consistent with metabolic encephalopathy ().
The patient was placed on short-duration HD (2 hours) with smaller surface area (cellulose triacetate; membrane area: 0.7 m2) and low blood flow (100 mL/min) to avoid DDS (). His consciousness gradually improved and he did not develop symptoms of DDS.
On day 15, we repeated MRI and EEG. T2-weighted FLAIR MRI showed increased signal intensities bilaterally in the cortical and subcortical areas of the occipital lobe (Figures and ). DWI demonstrated no hyperintense signal alterations in these regions. He had no cerebral infarcts, but the ADC was elevated in bilateral occipital lesions (Figures and ). Thus, although the patient did not have clinical symptoms of DDS, we diagnosed that he had asymptomatic brain edema. EEG on day 15 had been compared with the findings on admission; namely, the slow waves on EEG had decreased, consistent with improving uremic encephalopathy. The patient underwent vascular access surgery for HD and continued maintenance HD. On day 29, a third MRI was performed and showed return to findings on admission ().
The patient was discharged on regular intermittent HD without any neurological deficits. No further neurological disturbances were noted during 1-year follow-up.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.0, 'cm']}",64.12607,60.91977,67.33237,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg."
3854,10,Ideal Body Weight,physical,decimal,pmc-3328672-2,Extracted,"Case 2 was a 53-year-old woman (height 159 cm, weight 56.6 kg). She was diagnosed with CHC at 39 years of age, but had not taken any medication because of low serum ALT levels. Symptoms of dry eye and mouth appeared in January 2008, and she was diagnosed with Sjögren’s syndrome and mixed connective tissue disease based on the symptoms and serological tests, by a specialist in collagen diseases. Her hepatic function worsened after oral administration of pilocarpine hydrochloride, therefore, she was referred to our department.
She had a history of transfusion of blood coagulation factors during childbirth. Laboratory tests showed that theALT level was 128 IU/L, IgG level was 1933 mg/dL, ANA titer was 1:1280, LKM-1 was negative, HLA typing showed DR9 and DR15, HCV genotype was 1b and viral load was 3.3 log IU/mL (Table ). Histological findings of a liver biopsy specimen showed moderate infiltration of lymphocytes and plasma cells in portal areas, interface hepatitis and rosette formation, which are typical AIH characteristics (Fig. ). Although the score according to the simplified criteria of AIH (IAIHG 2008) [] was 6 points, which means ‘probable’ for AIH, we judged that her hepatic disorder was mainly caused by AIH, similar to Case 1.
After starting oral administration of 40 mg PSL (0.7 mg/kg) in February 2009, her ALT and IgG levels immediately decreased and became normalized. Serum HCV load increased to 5.6 log IU/mL during PSL administration. After PSL administration for 13 weeks, with a gradual decrease in dose, a weekly subcutaneous injection of 80 μg PEG-IFN-alpha-2b and daily oral 600 mg RBV were started in combination with 20 mg/day PSL. HCV RNA disappeared from her serum at week 8 of PEG-IFN plus RBV therapy, and an SVR was achieved by continuing the treatment for 48 weeks. After the end of the PEG-IFN plus RBV therapy, PSL dose was gradually decreased and daily administration of 5 mg has continued to date. Consequently, her ALT and IgG levels have remained within the normal range (Fig. ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [159.0, 'cm']}",51.47646,48.90264,54.05028,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 159.0 cm, which is 159.0 cm * 0.393701 in/cm = 62.59846 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.59846 (in inches) - 60) = 51.47646 kg.
Hence, the patient's IBW is 51.47646 kg."
3855,10,Ideal Body Weight,physical,decimal,pmc-5813716-1,Extracted,"We have obtained a written informed consent for publication of this case report from the patient.
A 36-year-old parturient (170 cm, 74.8 kg, gravida 1, para 1) with a suspicion of placenta accreta at 34 weeks gestation was admitted into our university hospital. She did not have any abnormal medical history. On the 3rd day after admission, tocolytic therapy against frequent uterine contractions started with intravenous infusion of ritodrine at 50 μg/min. On the 5th day, its infusion dose reduced to 35 μg/min because of her palpitation with tachycardia (HR 120 bpm). On the 6th day, the serum potassium level was 4.1 mmol/L. On the 7th day, as spontaneous amniorrhexis occurred, emergency cesarean section was scheduled, and the ritodrine infusion was discontinued (1 h before cesarean section).
We chose general anesthesia for the emergency cesarean section as massive bleeding due to placenta accreta was anticipated. Anesthesia was induced with intravenous propofol (150 mg) and suxamethonium (50 mg) followed by tracheal intubation uncomplicatedly, and then maintained with propofol (6 mg/kg/h) till delivery. The baby was delivered 6 min after induction of anesthesia. Then, fentanyl and ketamine were additionally given to deepen anesthesia. Rocuronium was also given to maintain muscle relaxation. After the manual removal of the placenta from the uterus, the bleeding was massive and uncontrollable (2200 g in about 20 min). We rapidly transfused colloidal solution against hypotension (63/35 mmHg), and blood pressure increased to 90/50 mmHg within 10 min. We also established an arterial line to left radial artery to maintain blood pressure. Arterial blood gas analyses revealed hyperkalemia (5.8 mmol/L), anemia (Hb 5.0 g/dL), and mild metabolic acidosis (pH 7.33, base excess (BE) −4.5 mEq/L, lactate 1.7 mmol/L). We started blood transfusion with potassium removal filter (potassium adsorption filter (KPF-4), Kawasumi, Tokyo). One hour later, hemostasis was still difficult, and the biochemical date showed further hyperkalemia (6.1 mmol/L) without any electrocardiographic changes and development of metabolic acidosis (pH 7.33, BE –5.2 mEq/L, lactate 1.0 mmol/L). To treat hyperkalemia, glucose insulin therapy started with intravenous furosemide (10 mg). Because of insufficient hemostasis, gynecologists decided to induce the Bakri balloon tamponade for the treatment of postpartum hemorrhage. At the induction of the Bakri balloon, the hematological data were improved (Hb 6.1 g/dL). In addition, plasma potassium level also reduced to 5.5 mmol/L. Thus, the operation was terminated (1 h 54 min) with a total blood loss of 4000 g and urine output of 400 mL. Crystalloid (800 mL), colloid (HES 130/0.4) (1500 mL), 5% albumin (500 mL), and packed red blood cell (6 units) were totally transfused during operation. She postoperatively moved to the intensive care unit under propofol sedation with tracheal intubation. The trachea was extubated after confirming stable hemodynamics and oxygenation. However, as the bleeding still continued, radiologists finally performed bilateral internal iliac artery embolization for full hemostasis. The postoperative course was uneventful and plasma potassium level was 3.3 mmol/L in the next morning. She was discharged from the hospital on foot without any sequelas on the 13th postoperative day.
Ritodrine is a β2-mimetic and commonly used for management of preterm labor. The common side effect of ritodrine is hypokalemia as β2-adrenoceptor stimulation in pancreatic islets by ritodrine promotes insulin secretion to increase uptake of extracellular potassium []. However, in the present case, hyperkalemia occurred 1 h after cessation of ritodrine. Vanishing β2-stimulation following cessation of ritodrine conversely increases efflux of potassium from the cells to increase plasma potassium levels. Indeed, there are several similar case reports revealing hyperkalemia following cessation of ritodrine in parturients [–]. In addition, in the present case, surgical stress with massive bleeding could reduce insulin secretion and induce insulin resistance by increases in catecholamine and cortisol release. As a result, efflux of potassium from the cell was promoted to enhance hyperkalemia.
In the present case, hyperkalemia became rapidly apparent even 1 h after cessation of ritodrine infusion. It has been reported that plasma ritodrine concentration rapidly declines following termination of its infusion with a distribution half-time of 5.9 ± 6.0 min and a disposition half-time of 156 ± 51 min []. Thus, we have to monitor plasma potassium levels around 3 h after cessation of ritodrine. Indeed, Kotani and colleagues [] reported that maximal hyperkalemia was observed 90–150 min after its cessation in six patients.
Unexpected hyperkalemia following intravenous suxamethonium has also been reported in parturients treated with magnesium and ritodrine under prolonged immobilization []. As suxamethonium was used to facilitate tracheal intubation in the present case, it might reinforce ritodrine-induced rebound hyperkalemia. Although plasma potassium levels may increase up to 1.0 mmol/L within 2–5 min following intravenous suxamethonium and the level quickly returns to a baseline value in healthy persons [], hyperkalemia was detected even 1 h after iv suxamethonium. Therefore, iv suxamethonium may not be the main cause of hyperkalemia in the present case.
The following causes of perioperative hyperkalemia should also be considered: rhabdomyolysis from malpositioning, tissue ischemia, metabolic and respiratory acidosis, and blood transfusion []. In the present case, as positioning was carefully done to avoid peripheral nerve injury, rhabdomyolysis could be excluded from the cause. Although the lowest blood pressure was 63/35 mmHg, blood pressure increased to 90/50 mmHg by rapid blood and colloid transfusion. In addition, intraoperative plasma lactate level was also within normal (<2 mmol/L) during surgery. Thus, tissue ischemia could also be excluded. As arterial blood gas analysis revealed mild metabolic acidosis (BE, –4.5 and –5.2 mEq/L), it might cause an increase in plasma potassium level. However, a parturient generally show low arterial CO2 with a parallel reduction in plasma HCO3
− because of hyperventilation induced by effects of progesterone on the respiratory center []. Particularly in labor, BE and HCO3
− decrease to −4.8 and 20.3 mEq/L []. Therefore, slight low BE in the present case would be acceptable and would not cause hyperkalemia.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [170.0, 'cm']}",61.43709,58.36524,64.50894,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.92917 (in inches) - 60) = 61.43709 kg.
Hence, the patient's IBW is 61.43709 kg."
3856,10,Ideal Body Weight,physical,decimal,usmle-1298,Extracted,"A 53-year-old woman is brought to the emergency department because of an episode of lightheadedness and left arm weakness for the last hour. Her symptoms were preceded by tremors, palpitations, and diaphoresis. During the past 3 months, she has had increased appetite and has gained 6.8 kg (15 lbs). She has hypertension, hyperlipidemia, anxiety disorder, and gastroesophageal reflux. She works as a nurse in an ICU and has been under more stress than usual. She does not smoke. She drinks 5 glasses of wine every week. Current medications include enalapril, atorvastatin, fluoxetine, and omeprazole. She is 168 cm (5 ft 6 in) tall and weighs 100 kg (220 lb); BMI is 36 kg/m2. Her temperature is 37°C (98.8°F), pulse is 78/min, and blood pressure is 130/80 mm Hg. Cardiopulmonary examination shows no abnormalities. The abdomen is soft and nontender. Fasting serum studies show:
Na+ 140 mEq/L
K+ 3.5 mEq/L
HCO3- 22 mEq/L
Creatinine 0.8 mg/dL
Glucose 37 mg/dL
Insulin 280 μU/mL (N=11–240)
Thyroid-stimulating hormone 2.8 μU/mL
C-peptide 4.9 ng/mL (N=0.8–3.1)
Urine screen for sulfonylurea is negative.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [168.0, 'cm']}",59.62607,56.64477,62.60737,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.14177 (in inches) - 60) = 59.62607 kg.
Hence, the patient's IBW is 59.62607 kg."
3857,10,Ideal Body Weight,physical,decimal,pmc-4958681-1,Extracted,"A 40-year-old para 1 woman without significant medical history was transferred to Chonnam National University Hospital. She had bilateral ovarian tumors detected by pelvic ultrasonography at a local gynecologic clinic for the evaluation of dysmenorrhea and hypermenorrhea. A pelvic ultrasonography revealed a 6.4×5.8×5.3-cm3 mass with irregular margin in the right ovary and a 6.3×5.2×4.2-cm3 multi-septated cystic mass in the left ovary. There was no obvious ascite in the abdominal cavity. Pulsed Doppler examination revealed low-resistant blood flow (resistance index 0.24). On physical examination, severe adhesion between these tumors and the cul-de-sac was noted. The patient's preoperative CA 125 level was 97.3 U/mL and other tumor markers (CA 19-9, CA 72-4, and CEA) were within normal ranges. Pelvic magnetic resonance imaging showed a 6.0×4.8×5.3-cm3 ill-defined, heterogenous signal intensity mass, including mixed cystic and solid portions in the right ovary. This mass was considered as a malignancy (i.e., clear cell carcinoma) likely arising from underlying endometriosis. Between the posterior portion of the right ovarian tumor and the cul-de-sac, there was a 5.5×5.0-cm2 enhanced solid mass with an irregular margin invading into the rectal serosa (). Additionally, there was a 7.2×5.9×6.1-cm3 multi-septated cystic mass in the left ovary () that was considered as a benign mucinous cystadenoma. Positron emission tomography-computed tomography revealed a high probability of ovarian malignancy involving both ovaries and possibly peritoneal carcinomatosis. The patient's preoperative body mass index was 30.84 kg/m2 (height 158-cm, weight 77 kg).
The patient underwent total abdominal hysterectomy, bilateral salpingo-oophorectomy, both pelvic lymph nodes dissection, omentectomy, and appendectomy through median incision at supine position. We performed operation for the basis of epithelial ovarian malignancy. A small number of ascites (500 mL) was present and peritoneal cytology was done. The right ovarian tumor measured at approximately 5.0×5.0-cm2 contained a 2.0×3.0-cm2 solid mass and chocolate-colored fluid. This mass was fixed in the cul-de-sac. It was hard indurated because of cancer infiltration. The left ovary mass measured at roughly 5.0×6.0-cm2 was an inflammatory cyst containing yellowish fluid. Multiple seeding lesions were found at rectal serosa, posterior uterine serosa, and appendix. Multiple whitish nodular lesions of up to 3.0×3.0-cm2 were detected at the omentum. These suspicious lesions were biopsied. No intrauterine tumor was found (). Intra-operative frozen biopsy analysis of the right ovarian tumor showed ESS with endometriosis because proliferative stromal cells with scant nuclear pleomorphism and mitosis were seen. Postoperative course was complicated by a disrupted vaginal stump. There was no other complication.
Final pathology was consistent with bilateral ovarian ESS arising from foci of endometriosis and involving the uterine serosa, rectal serosa, parametrium, peritoneum, omentum, and appendix (International Federation of Gynecology and Obstetrics [FIGO] stage IIIC). No evidence of tumor was found in the corpus of the uterus or the uterine cavity. Both pelvic lymph nodes were negative for tumor cells. The result of peritoneal cytology was negative for malignant cells. The mitotic activity in the spindle cells in the cellular area was limited to a maximum of two figures per 10 high-power fields. Stromal tissues had the characteristic tongue-like growth pattern (). Immunohistochemical staining revealed that neoplastic cells were immunopositive to antibodies specific for cluster of differentiation 10 (CD 10) (), Ki 67 (Ki index 3% to 5%) (), and progesterone receptor (). However, these neoplastic cells were immunonegative to estrogen receptor, desmin, alpha inhibin, calretinin, and actin.
The patient's CA 125 level was decreased from 97.3 U/mL before surgery to 38.8 U/mL after surgery. Adjuvant hormonal therapy was started one month after the operation in an effort to suppress the growth of any microscopic tumors. The patient had been taking oral megestrol acetate (Megesia, Dalimpharm, Seoul, Korea) at 160 mg daily for one month. She complained about weight gain. Therefore, the patient had been taking oral medroxyprogesterone acetate (Farlutal, Pfizer, New York, NY, USA) at 500 mg daily for four months. Six months after the beginning of treatment, her CA 125 level was decreased to 22.7 U/mL. Subsequent Positron emission tomography-computed tomography revealed no evidence of recurrence or metastases. However, she had complaints of generalized edema. Therefore, we decreased her drug dosages. She was taking oral medroxyprogesterone acetate (Provera, Pfizer) at 200 mg daily for three months. Three months later, she refused further hormonal therapy because of lasting side effects. At that time, an abdominopelvic computed tomography showed no evidence of recurrence. Therefore, we stopped the hormonal therapy and planned regular checkups with pelvic examination, tumor markers, and imaging studies. To date, she has shown no signs of recurrence.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3858,10,Ideal Body Weight,physical,decimal,usmle-1396,Extracted,"A 55-year-old nulligravid woman comes to the physician because of a 3-day history of heavy vaginal bleeding, requiring more than 5 pads per day. Menopause occurred 1 year ago. She attained menarche at 10 years of age. She has a history of hypothyroidism and type 2 diabetes mellitus. She has smoked 1 pack of cigarettes daily for 20 years but quit 5 years ago. Current medications include levothyroxine and metformin. She is 165 cm (5 ft 5 in) tall and weighs 86 kg (190 lb); BMI is 32 kg/m2. Physical examination shows mild vaginal atrophy and a normal cervix. The uterus and adnexa are nontender to palpation. Transvaginal ultrasonography shows an endometrial thickness of 6 mm. Endometrial biopsy shows non-invasive proliferation of endometrial glands with no nuclear or cytological atypia.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3859,10,Ideal Body Weight,physical,decimal,pmc-5402786-1,Extracted,"A 27-yr-old Iranian man was presented to the Rasuol-Akram Hospital Dermatology Day-Clinic, Tehran, Iran with a 3-yr history of progressive, asymptomatic and fusiform symmetrical swellings, localized to the medial and lateral aspects of several fingers of the left hand. The patient did not have any similar familial history. Furthermore, no history of significant trauma and pain or arthritic symptoms was present. The subject also had relatively long fingers in both hands (right handed, height: 175 cm, weight: 70 kg, hand span: 188 cm and index finger: 105 mm).
Physical examination revealed doughy fusiform swellings, limited to the medial and lateral sides of the PIP joints of the second through to the fifth fingers of the left hand (). These changes were extended to the metacarpophalangeal (MCP) joints of the second and third fingers of the same hand. These lesions were firm plaques, and overlying skin was lichenified, dry and mildly scaly. The swellings did not cause any range of motion reduction. The patient had no evidence of joint warmth or synovitis. The first and the fifth finger were spared. The X-rays of the affected hand revealed only soft tissue swelling without bone or articular abnormalities or space loss. His left-hand span was broader and his left fingers were longer than right ones, and had borderline joint laxity but without any remarkable signs of Ehlers Danlos. Routine laboratory screening, were normal.
An incisional biopsy was taken through the lichenified skin overlying the left second PIP joint, and stained with hematoxylin and eosin, which revealed marked compact orthokeratosis hyperkeratosis, prominent granular cell layer, mild acanthosis of the epidermis, and thickened, tortuous, haphazardly oriented collagen bundles in the reticular dermis. Normal fibroblasts were evident. No inflammatory infiltrate was present (). Ehlers Danlos syndrome was ruled out by negative skin biopsy, absence of neurological symptoms and Brighton criteria. Based on the clinical and histologic findings, a diagnosis of PDD was made.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3860,10,Ideal Body Weight,physical,decimal,pmc-5879769-1,Extracted,"A 51-year-old male taxi driver was admitted to Fukuoka City hospital with high fever (40 °C) and a shaking chill despite his use of over-the-counter antipyretics. He was transferred to the emergency department about 14 h after the symptoms onset. His medical history included bronchial asthma, pneumonia, and a surgical procedure for the resection of bilateral orbital tumors at 40 years of age. The patient had neither a history of contact with sick persons nor of any travel abroad. His body height was 160 cm and his body weight was 52 kg.
At the time of admission, his vital signs were as follows: blood pressure, 108/74 mmHg; heart rate, 90 beats/min; respiratory rate, 40 breaths/min; body temperature, 40.1 °C; and Glasgow Coma Scale, E4V4M6 (total 14/15). Upon physical examination, a swelling of the bilateral eyelids (Fig. ) and petechiae were detected on the conjunctiva. Some dental caries, purpura and petechiae were noted on the limbs (Fig. ), and 1–2 cm sized swollen lymph nodes noted at submandibular and inguinal areas were remarkable. Neck stiffness was not detected. Laboratory data on admission revealed high inflammation (white blood cell 13,500 μL, and c-reactive protein 12.29 mg/dL), normocytic anemia (Hemoglobin 8.7 g/dL), high protein and low albumin levels (total protein 12.3 g/dL and albumin 2 g/dL), renal failure (serum creatinine 4.52 mg/dL), hyperkalemia (6.12 mEq/L), proteinuria and hematuria (Table ). Computed tomography showed enlargement of the liver and bilateral kidneys (Fig. ) in addition to swelling of the cervical, supraclavicular, axillary, mediastinal, and celiac lymphadenopathy.
Severe infectious disease was suspected, and we started ceftriaxone 1 g intravenously every 12 h after drawing a blood culture. However, purpura spread rapidly and the progression of drowsiness and fever was sustained on the 2nd hospital day. We performed a lumbar puncture and the turbid spinal fluid analysis revealed meningeal inflammation (white blood cell count, 2370 /fields; protein, 293 mg/dL; and glucose, 16 mg/dL), which was compatible with bacterial meningitis (Fig. ). Gram-staining of the spinal fluid showed gram-negative diplococci. The blood culture also became positive for gram-negative diplococci. We strongly suspected that the septic status of the patient’s meningitis and bacteremia was due to N. meningitidis. We increased the dose of ceftriaxone to 2 g intravenously every 12 h. The patient’s general status and consciousness then improved and his fever subsided. On the 5th hospital day, the patient’s fever (38 °C) re-appeared with hypotension, hyponatremia and eosinophilia, which led to a suspicion of relative adrenal insufficiency due to meningococcemia. We started a daily intravenous administration of 300 mg hydrocortisone on the 7th hospital day, and tapered the regimen to a daily oral administration of hydrocortisone on the 11th hospital day. Ceftriaxone was stopped on the 12th hospital day. No recurrence of infection was observed and he was discharged on the 25th hospital day. The clinical course is summarized in Fig. .
We investigated the patient’s co-morbidities and performed microbiological analysis of the strain. His past surgical history (bilateral orbital tumors), his symptoms (swelling lachrymal glands and lymph nodes), the elevated levels of IgG4 (3200 mg/dL) and immunoglobulin E (304 IU/ml), and hypocomplementemia (C3 37 mg/dL, C4 7 mg/dL, and CH50 < 12.0 U/ml) were the characteristics of Mikulicz’s disease included in IgG4-related disease. Furthermore, a biopsy of the patient’s lymph nodes confirmed the presence of IgG4-related disease (IgG4/IgG index 100%). We prescribed oral prednisolone 30 mg a day on the 19th hospital day. In addition, the strain of N. meningitidis was identified as non-typable. The sequence type (ST) was identified as ST-11448, which belongs to ST-23 (ST-23 complex), the most common ST in Japan []. Moreover, we also analyzed the N. meningitidis strain according to PorA and FetA typing, which has a higher resolution power than that of ST, and identified that the PorA VR1, PorA VR2 and FetA were 5, 2–82, and F4–1, respectively. These results suggested that this N. meningitidis strain was a non-capsulated derivative of the domestic ST-23 strain. (See ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [160.0, 'cm']}",56.88197,54.03787,59.72607,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.99216 (in inches) - 60) = 56.88197 kg.
Hence, the patient's IBW is 56.88197 kg."
3861,10,Ideal Body Weight,physical,decimal,pmc-4056715-1,Extracted,"Thirty-six year-old male patient reported the presence of desquamative and pruritic
hypertrophic lesions on the trunk and back for the last 14 years. He related several
treatments with topical medications, without satisfactory results. The patient
denied comorbidities and was not using any medication at that moment. Dermatological
examination showed macules and papules with a velvety and scaly surface, converging
centrally and with a peripheral reticulate pattern (). The patient presented axillary, cervical and pubic
hyperpigmentation. Weight: 98 kg. Height: 1.78 m. BMI: 30.9 (obesity class I).
Dermoscopy evidenced a brownish pigmentation of poorly defined borders, covered with
white scales and a pattern of ""sulci and gyri"" (). Direct mycological examination of the lesion was negative and
culture did not show fungi growth. Lesion biopsy on the dorsal area demonstrated
mild parakeratosis, compact hyperkeratosis, hyperpigmentation of the basal layer,
papillomatosis and superficial perivascular mononuclear infiltrate and ). PAS staining was negative. Diagnosis of confluent and reticulated
papillomatosis of Gougerot and Carteaud was established and weight loss was
initially suggested. The patient returned after 45 days presenting a significant
reduction in the number of lesions ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.78, 'm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.78 m, which is 1.78 m * 39.3701 in/m = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3862,10,Ideal Body Weight,physical,decimal,pmc-7479551-1,Extracted,"A 63-year-old woman presented with right upper quadrant abdominal discomfort.
The patient’s symptoms developed insidiously over 3 d. She did not show any symptoms related to portal hypertension.
Two weeks ago, she presented to our hospital with proteinuria of approximately 1350 mg/d and hematuria and was diagnosed with IgAN. Light microscopic findings of kidney biopsy showed a moderate increase in mesangial matrix and mesangial cellularity (Figure ) with focal severe tubular atrophy and interstitial infiltration of mononuclear cells. Out of 37 glomeruli, 2 glomeruli (5%) showed global sclerosis. Immunofluorescence microscopy showed predominant mesangial IgA staining (Figure ) and C3 staining (Figure ). Electron microscopy revealed mesangial electron-dense deposits and focal effacement of the epithelial cell foot processes (Figure ). Laboratory findings were as follows: aspartate aminotransferase (AST), 20 IU/L; alanine aminotransferase (ALT), 8 IU/L; and serum creatinine, 1.21 mg/dL. She was not taking any other medications except an angiotensin II receptor blocker.
On admission, she had a height of 155.5 cm, a weight of 53.7 kg, a blood pressure of 120/70 mmHg, a regular heart rate of 64 bpm, and a temperature of 36.1 °C. The patient had mild right upper quadrant pain and tenderness and icteric sclera. She denied taking any new medication or alcohol consumption.
Laboratory findings were as follows: white blood cell count, 4090/µL; hemoglobin, 10.6 g/dL; platelet count, 99 × 10³/µL; AST, 771 IU/L; ALT, 488 IU/L; alkaline phosphatase, 92 IU/L; total bilirubin, 3.04 mg/dL; direct bilirubin, 1.86 mg/dL; total protein, 6.89 g/dL; albumin, 3.13 g/dL; and prothrombin international normalized ratio, 1.57. Serum creatinine and estimated glomerular filtration rate were 1.26 mg/dL and 45.6 mL/min per 1.73 m², respectively, similar to the values 2 wk prior. She was negative for anti-hepatitis B surface antigen, anti-hepatitis B core antibody, anti-hepatitis C virus antibody and anti-hepatitis A virus IgM. The results of immunological studies and serum iron and copper studies are shown in Tables and .
A contrast-enhanced computed tomography (CT) scan of the abdomen revealed a distal common bile duct (CBD) stone with mild upstream bile duct dilatation and an intrahepatic portosystemic shunt in the left lobe of the liver. There was not any evidence of chronic liver injury or portal hypertension such as esophageal varix, splenomegaly and ascites. Endoscopic retrograde cholangiopancreatography showed CBD stone without bile duct narrowing.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.5, 'cm']}",48.30717,45.89181,50.72253,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.5 cm, which is 155.5 cm * 0.393701 in/cm = 61.22051 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.22051 (in inches) - 60) = 48.30717 kg.
Hence, the patient's IBW is 48.30717 kg."
3863,10,Ideal Body Weight,physical,decimal,usmle-9171,Extracted,"A 66-year-old woman presents with urinary incontinence, difficulty urinating, incomplete voiding, and dull pain in the suprapubic region. She reports that she has not urinated for the past 2 days and that the urine leakage occurs during both day and night and is not associated with physical exertion. The medical history is significant for arterial hypertension and poorly controlled type 2 diabetes mellitus for 8 years, and depression for 3 years. She is prescribed amlodipine, valsartan, atorvastatin, metformin, and amitriptyline. Her weight is 75 kg (165 lb) and her height is 166 cm (5 ft 40 in). Her vital signs are as follows: blood pressure, 120/80 mm Hg; heart rate, 91/min; respiratory rate, 13/min; and temperature, 36.4℃ (97.5℉). The physical examination reveals lower abdominal tenderness with a distended urinary bladder that is palpated in the suprapubic region. The neurological examination shows decreased Achilles reflexes bilaterally, and diminished fine touch and vibratory sensation. On gynecologic examination, the cervix was normally positioned, mobile, and without any visible lesions. Bulging of the posterior vaginal wall was noted. The adnexa were not palpable. An ultrasound examination showed an overdistended urinary bladder with no structural abnormalities.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [166.0, 'cm']}",57.81505,54.9243,60.7058,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 166.0 cm, which is 166.0 cm * 0.393701 in/cm = 65.35437 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (65.35437 (in inches) - 60) = 57.81505 kg.
Hence, the patient's IBW is 57.81505 kg."
3864,10,Ideal Body Weight,physical,decimal,pmc-5621081-1,Extracted,"A 40-year-old woman presented to the emergency department with severe epigastric pain and nausea. She had been trying to get pregnant with assisted reproductive technology for 2 years due to unexplained infertility. Previously, she received 2 cycles of intrauterine insemination and 6 cycles of in vitro fertilization-embryo transfer (IVF-ET), which all failed. She underwent cryo-thawed ET a week ago, and she had been on estradiol valerate (Progynova®; Bayer-Shering Pharma, Berlin, Germany) 2 mg per os every 8 hours for 24 days, vaginal progesterone 90 mg (Crinone® gel 8%; Merck Serono SA, Geneva, Switzerland) every 12 hours for 10 days, and enoxaparin sodium (Clexane®; Sanofi-Aventis, Paris, France) 40 mg subcutaneous injection once a day for 7 days before presenting. She had taken estrogens in previous IVF-ET cycles, but denied any severe abdominal pain like this time. She had 3-year history of diabetes mellitus, which was under control with insulin injection. Hemoglobin A1c concentration was 6.8% and the serum cholesterol levels were within normal range on blood test which was performed 1 month before the symptom. She denied smoking and drinking and she did not have familial hypercholesterolemia.
On physical examination, her blood pressure was 145/87 mmHg, pulse rate was 65/min and body temperature was 37.5℃. Abdominal examination revealed that the abdomen was distended with whole abdomen tenderness and bowel sound was hypoactive. Her weight and height were 77.25 kg/156.2 cm, and body mass index was 29.91 kg/m2.
Blood tests revealed elevated levels of amylase (416 U/L), lipase (790 U/L), white blood cell count (12.24×103/uL), lactate dehydrogenase (442 IU/L), total cholesterol (723 mg/dL), triglycerides (4,051 mg/dL) and C-reactive protein (5.54 ng/mL). Serum blood urea nitrogen, creatinine, alkaline phosphatase, alanine aminotransferase, and bilirubin level were within reference range.
An abdominal computed tomographic (CT) scan was performed showing mild swelling of pancreas head with peripancreatic infiltration, the presence of peripancreatic fluid and fluid in the upper mesentery which was categorized into grade D of Balthazar CT grade ().
The patient was managed with supportive therapy including intravenous hydration, antibiotics, and analgesics. As her abdominal pain still remained and fever sustained at fourth hospital day, follow-up abdominal CT scan was performed and the result revealed increased peripancreatic fluid collection (). We changed antibiotics from third generation cephalosporin to ertapenem and clinical condition improved. She was discharged on the 10th hospital day. Follow-up CT scan performed 2 months after discharge showed much decreased peripancreatic fluid collection (). Fortunately, she became pregnant naturally after the treatment of pancreatitis and has been maintaining her pregnancy for about 36 weeks without complication.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [156.2, 'cm']}",48.94103,46.49398,51.38808,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 156.2 cm, which is 156.2 cm * 0.393701 in/cm = 61.4961 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.4961 (in inches) - 60) = 48.94103 kg.
Hence, the patient's IBW is 48.94103 kg."
3865,10,Ideal Body Weight,physical,decimal,pmc-8457346-1,Extracted,"Mr. Y, a 60-year-old household appliance dealer, weighing 65 kg, and 165 cm tall, came to the ER with dizziness, nausea, vomiting, and abdominal pain for 5 days. The patient was previously managed in private hospital for a week where a diagnosis of GIT disorder was made. Before coming to Special Hospital for Infection Universitas Airlangga (Rumah Sakit Khusus Infeksi/RSKI, Universitas Airlangga), this patient experienced complaints of shortness of breath, but there was no cough and febrile. Due to the suspicion of COVID-19, PCR for SARS COV-2 was requested, and the result was positive. Patient was, however, referred to RSKI hospital due to lack of bed-space in the diagnosing hospital where he was immediately admitted into the ICU and was managed for 14 days, followed by low care for 7 days.
Therapy in the previous hospital: potassium tablet 2 times daily (3 days), antacid syrup 3 times daily at 15ml (for 3 days), salt capsules 2 x 500 mg (for 3 days), hydroxy-chloroquine, 2 x 200 mg (for 4 days), liver supplement (contain lecithin, silymarin, schizandra, and vitamin E) 2 times daily (for 1 day), hyoscine butylbromide, 3 times daily if needed, intravenous (iv) vitamin C,1000 mg once daily (for 4 days), corticosteroid once daily at 5 mg (for 4 days), acetylcysteine 1 x 5000 mg (for 4 days), proton pump inhibitors, 2 x 40 mg (1 day), midazolam 2 mg/hr (1 day), antiviral 500/24 hour (1 day), AseringR Infusion 500ml/24 hour (1 day), Clinimix15ER 500ml/24 hour (7 days), plasma convalescent 2 x 200 ml.
Therapy while in RSKI: including antivirals (75 mg two times daily for 7 days), chloroquine 300 mg two times daily for 5 days, probiotics lactobacillus strain three times daily, multivitamin once daily, Curcuma three times daily, heparin 500 IU/hour for eight days, corticosteroid for extra two days, and N-acetyl cysteine, 5000 mg once daily.
Patient was intubated on arrival at the RSKI hospital and mechanically ventilated in the ICU for 15 days. He was extubated with the PaO2/FiO2 ratio 353, as shown in . Enteral nutrition was provided with the concept of start low, go slow, 30 Cal/kg body weight/24 hours, divided into 6 times of administration through a nasogastric tube. The nutritional composition consists of 70% carbohydrates, 30% fat of the total calories needed. Protein was given 0.8 grams/kg body weight/day outside of calculating the total calorie requirement.
Sugar containing fruit juice was also provided but the sugar contained therein was not included in calculating the total calorie requirement. The fruit juice was given based on fiber requirements and possible antioxidant content.
The fluid balance was adjusted with a maximum deficit target of 1000 ml/day regarding fluid requirements. All fluids that enter the patient’s body were counted, either intravenously or through a nasogastric tube. Likewise, the discharge fluid, urine, and gastric retention were calculated through the nasogastric tube.
Laboratory tests () and chest X-rays () were carried out every 3 days, as shown in . The antibiotic, tigecycline 50 mg iv was given twice a day to treat Acinetobacter baumanii detected on day 8 at RSKI. Acinetobacter baumanii infection is known from an increase in leukocytes, evidence of sputum culture, and clinical patients with febrile condition.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3866,10,Ideal Body Weight,physical,decimal,pmc-2926431-1,Extracted,"A 26-year-old woman at 41 weeks of gestation with a known history of vasovagal syncope was scheduled to undergo an emergency cesarean section due to fetal distress. She weighed 92 kg and was 165 cm tall. Two years earlier, she visited the hospital with complaints of frequent abdominal discomfort, cold extremities, cold sweating, and a brief loss of consciousness. Such symptoms began 4-5 years earlier. They lasted for 5-10 minutes and resolved spontaneously. She experienced episodes of syncope that was induced by many conditions. She was diagnosed with vasovagal syncope by a cardiologist and neurologist through a careful history and physical examination, echocardiography, treadmill test, Holter monitoring and positive tilt table test, and a β-blocker was prescribed (atenolol 25 mg/d). She stopped medication herself after a few days. The other pre-anesthetic assessment was unremarkable, with no medical problems except dizziness and healthy pregnancy. Initially, she planned a normal vaginal delivery under epidural analgesia. With the patient in the left lateral decubitus position and using an aseptic technique, a lumbar epidural catheter was inserted at the L3-4 interspace with rapid fluid administration and tested with 1% lidocaine 3 ml. She did not show any changes in vital signs, and was observed without a further epidural injection until a cervical dilatation of 5-6 cm.
She complained dizziness twice, which was resolved with bed rest and atenolol medication. During non-invasive fetal monitoring, the fetus showed variable heart rate deceleration and an emergency cesarean section was decided. No premedication was prescribed. She had a heart rate of 60-115 beats/min and an arterial pressure of 90-110/60-90 mmHg at the delivery unit. When the patient arrived in the anesthetic room, monitoring of the ECG, oxygen saturation and arterial pressure was started, showing a heart rate of 75 beats/min and an arterial pressure 120/80 mmHg. Because epidural catheter was already inserted, it was decided to proceed with the operation under epidural anesthesia. After placing the patient in the supine position with a left lateral tilt, a 20-gauge catheter was inserted at left radial artery after modified Allen's test for direct arterial pressure monitoring. A 16-gauge peripheral line was inserted and Hartmann's solution 600 ml was administered. Oxygen was administered via a face mask. After a negative aspiration test, 2% lidocaine 20 ml plus fentanyl 100 µg was injected through the epidural catheter. Ten minutes after the epidural injection, she had a heart rate and arterial pressure of 74 beats/min and 89/54 mmHg, respectively. Accordingly, ephedrine 5 mg was injected with rapid fluid administration. The anesthetic level was T5 to light touch with an alcohol sponge at 15 minutes after the epidural injection, and a cesarean section proceeded rapidly without complications. A male infant was delivered with a 1 and 5 minutes Apgar score of 7 and 9. The baby was ventilated manually with a bag and a mask due to cyanosis, and transferred to the neonatal ICU. He weighed 3,510 g and showed mild cardiomegaly and a ductal aneurysm on the echocardiographic examination. Over a 2-day admission, the baby showed a normal muscle tone and respiratory pattern. After delivery 10 units oxytocin was infused with fluids. The decrease in heart rate and blood pressure to 50 beats/min and 76/40 mmHg, respectively, was treated with rapid fluids administration, intravenous glycopyrrolate 0.2 mg and ephedrine 5 mg intravenously three times. She complained of dizziness that disappeared after normalizing the blood pressure. The total operation time was 80 minutes and 1,900 ml of Hartmann's solution was infused. Epidural PCA with 0.15% ropivacaine plus fentanyl was connected for postoperative pain control. The patient did not show any changes in their vital signs or syncopal attack at recovery room over a 60 minutes observation period and was transferred to the general ward.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3867,10,Ideal Body Weight,physical,decimal,pmc-3350152-1,Extracted,"A 38-year-old primigravida (height, 155 cm; weight, 76 kg) presented for elective induction of labour at 40+3 weeks of gestation with oedema of both legs lasting the last 2 weeks. She had no significant past medical history except for chronic hepatitis B. No coronary risk factors were reported. On admission, her blood pressure was 150/90 mmHg and urinary protein level was as high as 500 mg/dL. Her blood tests revealed haemoglobin 11.9 g/dL, platelets count 106 × 109/L, prothrombin time 11.0 s (normal range 9.8–13 s), international normalized ratio of 1.11, and activated partial thromboplastin time 47.7 s (normal range 26.5–41 s). Severe preeclampsia was diagnosed and MgSO4 4 g i.v. plus 10 g intramuscularly was given initially as a loading dose, followed by 1 g/h as infusion for seizure prophylaxis.
After 6 h in hospital, labour was induced with insertion of extraovular catheter through the cervical canal of the uterus and spontaneous uterine contraction began 5 hours thereafter. When the cervix was 2.5 cm dilated, an infusion of oxytocin was started to augment labour and the membranes were ruptured 3 hours thereafter. Throughout the labour course including 4 h of active, her arterial pressure was stable in the range of 140–160 mmHg systolic, 90–100 mmHg diastolic. She declined epidural labour analgesia because of possible aggravation of the backache she had had.
Twenty-one hours after labour onset, when the cervix was 10 cm dilated, the foetal vertex did not descend past 1 station (arrest disorder) and the foetus developed deceleration (90 beats/min). The patient became dyspneic and diaphoretic and complained of sudden onset of severe left-sided chest pain. Her blood pressure was 160/90 mmHg. On electrocardiogram (ECG), a sinus tachycardia (100 beats/min) was noted with no ST-segment changes. She had been tolerating oral fluids but had taken nothing by mouth for more than seven hours. The decision was made to perform category-1 caesarean delivery. The potential risks and benefits of general, spinal, or epidural anaesthesia were explained to the patient, who accepted the anaesthetist's inclination towards general anaesthesia.
The patient received 30 mL of 0.3 M sodium citrate before induction of anaesthesia. Upon arrival in the operating theatre, the patient was positioned supine with left lateral tilt and routine monitoring devices including continuous EKG, noninvasive blood pressure, temperature, and pulse oximetry were applied. A 20-gauge catheter was placed into a radial artery and connected to a pressure transducer to measure blood pressure. Initial recordings showed a heart rate of 103 beats/min, blood pressure 170/110 mmHg, respiratory rate 25 breaths/min, and peripheral oxygen saturation (SpO2) 96% on air. After preoxygenation, a rapid sequence technique with remifentanil 1 μg/kg, thiopentone 300 mg, and suxamethonium 75 mg was employed and cricoid pressure was applied. After endotracheal intubation, anaesthesia was maintained with 1.2% sevoflurane (end-tidal) and 50% nitrous oxide in oxygen, with vecuronium 6 mg for neuromuscular block. A female infant weighing 4000 g was born through a low transverse uterine incision with Apgar scores of 5 and 7 at one and five minutes, respectively, and the baby was transferred to the neonatal ICU for observation. After cord clamping, an oxytocin infusion of 40 units in 500 mL of normal saline was commenced at 125 mL/h. In addition, i.v. 0.15 mg/kg morphine, cefazolin 1 g, and midazolam 3 mg were given while nitrous oxide was increased to 70% and end-tidal sevoflurane concentration was reduced to 0.8%. Approximately 5 min after delivery, the uterus was found to be atonic and bleeding diffusely. The oxytocin infusion rate was increased to 240 mL/h after an i.v. bolus of carbetocin 100 μg with continuous bimanual compression of the uterus. The fluid infusion rates were increased by pressurizing the infusion bags. Additional peripheral venous and central (left subclavian vein) venous assess was established with initial central venous pressure (CVP) value of 5.5 cm H2O. As the bleeding continued, bimanual uterine compression was combined with i.v. ergometrine 250 μg and blood transfusion. Nevertheless, the uterus was still atonic with blood spurting from the lax uterus. There were no vaginal or cervical lacerations. The patient lost more than 2500 mL within 30 min and rapidly became haemodynamically unstable. Additional oxytocics including intramyometrial carboprost (1 mg in divided doses), and repeated doses of i.v. oxytocin 5 units with warmed fluids and blood products were given. However, this was inadequate to address the clinical situation and finally, decision was made to proceed to hysterectomy.
During the surgery, the systolic blood pressure was decreased to 70–90 mmHg and the pulse was tachycardic at 122–130 beats/min, despite the massive intravenous fluids and blood products combined with inotropic support (dopamine at 2 to 5 μg/kg/min). Her SpO2 remained between 92% and 98% at FiO2 0.5 during the operation. On physical examination, rales were detected in both lungs and diuresis was started with furosemide. Her haematocrit level dropped below 15%. A total of 6700 mL crystalloid, 2,000 mL colloid, 9 units packed red blood cells, 3 units fresh frozen plasma, and 8 units cryoprecipitate were administered during the 4.5 h surgical procedure. Intraoperative blood loss was estimated to be 5,800 mL and urine output was about 260 mL in the operating theatre. Arterial blood gas analysis on an FiO2 of 0.5 revealed a pH of 7.25, PaO2 11.89 kPa (89 mmHg), PaCO2 5.60 kPa (42 mmHg), HCO3 18.4 mmol/L, and base excess −8.8 mmol/L at the end of operation (an acute onset of hypoxemia with a ratio of arterial PaO2 to FiO2 of <200). Tentative diagnosis of pulmonary oedema related to fluid overload was made.
On completion of the procedure, the patient was transferred intubated and sedated to the intensive care unit (ICU) for further management. Initial recordings on arrival in the ICU were heart rate 132 beats/min, blood pressure 125/76 mmHg, and CVP 18.5 cm H2O with dopamine infusion at 5 μg/kg/min. Because of the tachycardia dopamine was switched to dobutamine (3–5 μg/kg/min) which was continued until the weaning of inotropic support. The patient was mechanically ventilated with a tidal volume of 8 mL/kg at an assisted control rate of 12 breaths/min and a 10 cm H2O positive end-expiratory pressure with supportive care for pulmonary oedema, including oxygen, furosemide (20 mg q 4 hour), and fluid restriction. A chest X-ray taken immediately after ICU admission showed extensive bilateral pulmonary infiltrates in both hilar areas and pleural effusion in both lungs with normal lung volume and normal heart size. On the postoperative day 2, the patient became haemodynamically stable and was weaned off inotropic support. On the day of admission, urine output was about 80 mL/h but her renal function continued to deteriorate, and oliguria (creatinine 369.6 μmol/L) set in by day 4. Continuous renal replacement therapy (CRRT) was initiated to treat the acute pulmonary oedema as well as acute renal failure. Over the next 3 days, renal function gradually improved, and CRRT was discontinued on the third day, and the patient was weaned off the ventilator on the next day. However, she was still tachypneic (22–30 breaths/min) with peripheral oxygen saturation of 94–98% on 5 L/min of oxygen via nasal prongs over the following 4 days. Therefore, a cardiac workup was initiated, and an initial transthoracic echocardiogram (TTE) on the 12th day revealed severe left ventricular (LV) systolic dysfunction and ejection fraction of 23.5% with extensive akinesia of the LV base extending to the midcavity of the heart, together with preserved apical function (Figures and ). ECG on the same day revealed nonspecific ST-T wave changes with normal sinus rhythm, and peak troponin I was slightly raised to 0.88 ng/mL (reference range, 0–0.1 ng/mL) with normal creatine kinase-MB fraction level 2.2 U/L (reference range, 2.3–9.5 U/L) and proBNP level >35000 pg/mL. Based on the patient's history of chest discomfort when she was in active labour along with absence of cardiovascular risk factors, mild cardiac enzyme elevation, and the characteristic TTE findings, she was diagnosed with inverted TTC. She was started on heparin, a ß-adrenergic blocker, and an angiotensin-converting enzyme inhibitor, after which her clinical condition improved steadily. On the 14th day, the followup TTE showed slight improvement in LV function with an ejection fraction of 29.4%. On the 28th day, TTE showed a return to near normal LV function (ejection fraction 54.6%) with resolution of the basal wall motion abnormalities (Figures and ). The following hospital course was uneventful. She was discharged home 38 days after surgery. The patient remained asymptomatic at the 5-month followup with complete recovery of LV systolic function on TTE (ejection fraction 65.0%).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3868,10,Ideal Body Weight,physical,decimal,pmc-8551419-1,Extracted,"A healthy and active 44-year-old male patient (height 1.90 m; weight 95.0 kg; body mass index 26.3) presented at our emergency department with pain in the left groin or hip. A sudden “crack” had occurred during a low-speed pivoting movement while working as a kitchen chef and left him unable to bear weight. Exactly 6 years earlier, the patient had been treated for a 4-week-old fracture of the left hip with hybrid THA (Tritanium solid back size-52 cup; Exeter 44-3 stem; 32 + 0 LFIT head); the stem was cemented at that time because of the superior survival of cemented stems after femoral neck fractures []. The obtained radiographs showed a fracture of the Exeter stem at the neck (), and after discussion and consent, the patient was scheduled for revision arthroplasty. After the revision surgery, the patient was satisfied with no pain or functional limitations up to his latest follow-up at 2 years postoperatively. Informed written consent was obtained from the patient to publish his personal and clinical details. Approval for the study by the local institutional review board was not required because it was a case report.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.9, 'm']}",84.04734,79.84497,88.24971,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.9 m, which is 1.9 m * 39.3701 in/m = 74.80319 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (74.80319 (in inches) - 60) = 84.04734 kg.
Hence, the patient's IBW is 84.04734 kg."
3869,10,Ideal Body Weight,physical,decimal,pmc-7863479-1,Extracted,"A 49-year-old Japanese man visited our department in November 2017 with chief complaints of indolent right scrotum enlargement and a right inguinal mass. History showed that the patient visited our department of gastroenterology with chief complaints of blackish feces and ill complexion in February 1997. Gastrointestinal fiberscopy was used to treat duodenal ulcer bleeding. Computed tomography (CT) showed a right retroperitoneal tumor, which was removed in the same month.
Histopathological examination showed a teratoma and yolk sac tumor (Fig. ). He was diagnosed with primary retroperitoneal EGCT and underwent three courses of chemotherapy (bleomycin/etoposide/cisplatin; BEP) starting in May 1997. He was closely followed using procedures including periodic imaging, tumor markers determination, and self-palpation.
He was followed up on an outpatient basis 5 years after treatment and was subsequently lost to follow-up. In August 1999, he underwent surgery of the right hydrocele. At that time, perioperative findings were unremarkable, indicating no clear tumor in either testicle.
At the first visit, his height was found to be 163 cm, and weight was 58.5 kg.
Blood pressure was 128/78 mmHg, heart rate was regular at 62 beats per minute, and body temperature was 36.4 °C.
He had no history of smoking or drinking, and there was nothing remarkable in the family history.
On physical examination, the right testicle was found to be elastic, hard, and enlarged to the size of 40 × 40 mm. A 45 × 40 mm sized induration was palpable in the right inguinal area and was adequately mobile. Neurological examination showed no abnormal findings. Blood biochemistry examination, urinalysis, and tumor markers (alpha-fetoprotein [AFP], human chorionic gonadotropin [HCG], and lactate dehydrogenase [LDH]) showed no abnormal findings.
Ultrasound findings showed a mosaic shadow inside the right testicle, with no abnormal findings in the left testicle.
During other diagnostic imaging procedures, enlargements of the right external iliac lymph node (24 × 14 mm) and right inguinal lymph node (43 × 29 mm) and a 31 × 22 mm mass with uneven contents were found in the right testicle (Fig. ). There was no evidence of any distant metastasis.
For the right testicular tumor, the patient underwent high orchiectomy and resection of the right inguinal lymph nodes in November 2017. The testicular tumor was 40 × 40 × 30 mm in size and weighed 34 g. The lymph node was 40 × 40 × 30 mm in size and weighed 21 g. The cut surfaces of both specimens were yellowish and solid, and the testicular tumor was localized in the testicle (Fig. ).
Histopathological findings showed irregular cobblestone proliferations of germ cell-like atypical cells with clear nucleoli and massive necrotic changes that partially resulted from self-destruction. The tumor did not extend into the tunica albuginea, and no vascular infiltration was found. Spermatic cord stumps were negative. Tumor diagnosis was a classical seminoma with no other elements. Lymph node metastases were also diagnosed as a result of the seminoma (Fig. ).
Based on the above findings, this seminoma was diagnosed as pT1, pN2, M0, S0, and TNM stage IIB [].
The patient received postoperative chemotherapy with one course of BEP therapy and three courses of etoposide and cisplatin (EP) therapy at the Japan Community Health care Organization Kani Tono Hospital starting in January 2018.
Post-chemotherapy CT confirmed a complete clinical response (cCR) at the right external iliac lymph node, and this response continued 12 months later (Fig. ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [163.0, 'cm']}",59.5985,56.61857,62.57843,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 163.0 cm, which is 163.0 cm * 0.393701 in/cm = 64.17326 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.17326 (in inches) - 60) = 59.5985 kg.
Hence, the patient's IBW is 59.5985 kg."
3870,10,Ideal Body Weight,physical,decimal,pmc-2995984-1,Extracted,"Three month before hospitalization, a 29 year-old woman sought medical help for obesity. She was otherwise healthy and did not smoke cigarettes. There was no family history of pulmonary hypertension. She had not been pregnant and did not take any other medications including oral contraceptives and herbal medications at the time of symptom onset. She weighted 73 kg and was 1.60 m (65 in.) tall. Her body-mass index (the weight in kilograms divided by the square of the height in meters) was 28. Oral medication therapy with phentermine HCl (adipex®) at a dose of 37.5 mg taken every morning was prescribed. The medication continued for 35 days, during which the patient lost 13 kg. After two months since the start of the prescription, the patient began to feel tachycardia and she was admitted for shortness of breath. Laboratory investigation did not show abnormal findings. Chest radiographs showed mild prominence of the right ventricular outflow tract. Right ventricular hypertrophy was shown in electrocardiography () while echocardiography showed moderate pulmonary hypertension (right ventricular pressure: 63 mmHg) with tricuspid regurgitation and D-shaped left ventricle (LV) (). There was no pericardial effusion. Cardiac catheterization showed moderate pulmonary hypertension and elevated pulmonary vascular resistance. The right ventricular pressure was 70/29 mmHg; the pulmonary-artery pressure was 69/26 mmHg, with a mean of 42 mmHg while resting; the pulmonary-capillary wedge pressure was 7 to 11 mmHg. A heart MRI showed no visible intracardiac shunt or pulmonary thromboembolism. Other studies were performed to rule out various causes of pulmonary hypertension. Liver-function studies showed a mild elevation of alanine aminotransferase. Abdominal ultrasonography revealed no liver abnormalities. Tests for anti-centromere antibodies and anti-HIV Ag were negative.
Bosentan 125 mg was prescribed with diuretics. Radical anticoagulation therapy was administered. The patient was discharged after three days and followed-up with subjective symptom improvement.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.6, 'm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.6 m, which is 1.6 m * 39.3701 in/m = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3871,10,Ideal Body Weight,physical,decimal,pmc-7440271-1,Extracted,"A 52-year-old male presented to the emergency department with diffuse, nonradiating abdominal pain of three-day duration. In addition, there were about four episodes of nonbloody and nonbilious emesis daily. The patient also reported 10-15 bowel movements consisting of clear water daily. The patient denied any alleviating or exacerbating factors.
His past medical history was significant for medullary thyroid cancer secondary to multiple endocrine neoplasia type 2A diagnosed in 1994. His disease was complicated by recurrence in 1998, 2005 and finally in 2018 for which he received palliative chemotherapy with carboplatinum/VP-16, which showed improvement in his left cervical lymphadenopathy. His last positron emission tomography (PET) scan in 2019 revealed clinical stable disease with a favorable prognosis. Notably in 2012, he was complaining of chronic diarrhea which was successfully controlled with prescribed octreotide and promethazine. In 2018, the biopsy of the recurrent cancer revealed small cell variant medullary thyroid carcinoma (MTC).
He had no known allergies and did not smoke or drink alcohol. His home medications included codeine 30 mg for diarrhea, hydrocodone 5 mg/acetaminophen 325 mg for pain, promethazine 25 mg for nausea and vomiting, synthroid 0.112 mg and lanreotide 120 mg subcutaneous once every four weeks with the most recent dose due just prior to admission. Lanreotide was used in place of octreotide due to policy changes at the Veterans Affairs.
On examination, his weight was 63.14 kg and his height was 170.2 cm, giving him a body mass index of 21.8 kg/m2. Blood pressure was 131/91 mmHg, pulse was 116 bpm, oxygen saturation was 99% on room air, respiratory rate was 20 breaths per minute and temperature was afebrile at 36.6 degrees Celsius. He was alert and oriented but was in discomfort and exhibited multiple episodes of retching in the examination encounter. His abdomen was soft but diffusely tender. However, there was no rebound tenderness or rigidity.
Laboratory investigations revealed a mildly elevated white blood count of 14,000 cells/mcL. The hemoglobin was 11.6 g/dL on admission; however, it gradually declined to plateau around 8 g/dL after an admission period of four weeks with daily blood draws. Comprehensive metabolic panel was unremarkable with a normal lipase level 20 U/L. He had chronic gastrointestinal blood loss with a mean corpuscular volume of 76.2 fL. Prior colonoscopy a year ago had only shown a rectal ulcer.
Imaging of the abdomen suggested colitis and revealed changes in liver nodules that had been detected six months earlier (Figure ). Some of these nodules were larger, while some had gotten smaller. The liver function tests were unremarkable. He was admitted for intractable nausea and vomiting. He was given synthroid 0.224 mg daily. Phenergan, zofran and a clear liquid diet were given. He continued to have symptoms. Gastroenterology, surgery and psychiatry observed the patient, and all recommended conservative therapy. When there was no improvement within a week gastroenterology performed an esophagogastroduodenoscopy, which revealed antral erosions, gastric inlet pouch and an irregular Z-line. The patient would improve enough to tolerate clear liquids only to have the progress lost by returning abdominal pain, nausea and vomiting. This cycle occurred for approximately three weeks.
The abdominal pain was finally resolved after a subcutaneous nerve block was attempted; however, the nausea, vomiting and diarrhea persisted. Oncology was consulted and did not believe that the patient’s symptoms were due to progression of MTC. Various medications such as scopolamine, metoclopramide, marinol, dexamethasone and withholding of pain medications were tried with variable results. A nasogastric tube was attempted and then a transpyloric tube feed was started with fluctuating results. Oncology was consulted again and recommended to switch lantreotide to octreotide and to give supratherapeutic intramuscular levothyroxine to depress the TSH. After implementation of this plan, the nausea and vomiting rapidly improved. The patient was finally able to tolerate a consistent carbohydrate diet. His symptoms did not relapse after the implementation of this plan. Repeat abdominal imaging was unchanged from initial scans (Figure ).
After discharge, a specific set of labs were ordered prior to the patient’s outpatient oncology appointment. A complete metabolic panel, TSH and serum calcitonin were redrawn. During his hospital stay, the TSH was 6.658 uIU/mL and the calcitonin was 64,059 pg/mL. He was discharged with synthroid 0.112 mg tablets oral twice daily, octreotide depot 30 mg every three weeks and a dexamethasone taper. Repeat measurements two weeks after discharge showed TSH equal to 1.058 uIU/mL and calcitonin now down to 37,213 pg/mL (normal 0.0-8.4 pg/mL).
Two weeks after discharge, the patient reported continued cessation of symptoms. He was on schedule with his medications. His abdomen was soft and nontender.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.2, 'cm']}",66.11819,62.81228,69.4241,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.2 cm, which is 170.2 cm * 0.393701 in/cm = 67.00791 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.00791 (in inches) - 60) = 66.11819 kg.
Hence, the patient's IBW is 66.11819 kg."
3872,10,Ideal Body Weight,physical,decimal,pmc-7879298-1,Extracted,"An 81-year-old man presented with left groin pain for 1 month, and he was previously diagnosed with incarcerated left groin hernia 1 month back at another hospital. The hernia was repaired using ProLoopTM (L) Mesh Plug. He was referred to our institution due to left femoral swelling and pain lasting for 9 h. He was 155 cm tall and weighed 50 kg (body mass index of 20.8). Physical examination revealed left femoral tenderness below the surgical scar (Fig. ). However, the patient did not complain of abdominal pain and rebound tenderness. The femoral hernia cannot be repaired. The laboratory examination findings were normal. Abdominal radiography revealed no gas fluid and signs of small bowel dilatation. Abdominal computed tomography scan showed a small round mass compressing the left femoral vein and small bowel obstruction (Fig. ). Based on these findings, a preoperative diagnosis of incarcerated femoral hernia was made, and emergency surgery was performed.
Laparoscopic small bowel resection and femoral ring repair were conducted under general anesthesia. The patient was in supine position, and the three-port method was used. Three operation ports were established, which were as follows: a 12-mm umbilical camera port and 5-mm working ports in the lower right and left flank area. We found that the small bowel was incarcerated into the left femoral ring. However, there was no recurrence of left groin hernia (Fig. ). The left inguinal ligament was amputated, thereby loosening the formal ring. A hernia was found, and a surface area of 4 cm in the small bowel was dark red (Fig. ). To reduce the risk of infection, small bowel resection was performed after closing the femoral ring. The diameter of the femoral ring was 1 cm, and it was washed and closed with a one-needle suture (Fig. ). The umbilical port was extended by 3 cm, and the small bowel was resected via a functional end-to-end anastomosis. The patient had an uneventful postoperative course and was discharged 8 days after the surgery. There was no recurrence of femoral hernia after 1 year.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [155.0, 'cm']}",52.35442,49.7367,54.97214,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (61.02366 (in inches) - 60) = 52.35442 kg.
Hence, the patient's IBW is 52.35442 kg."
3873,10,Ideal Body Weight,physical,decimal,pmc-5348075-1,Extracted,"A 12-year-old Caucasian male patient presented with a diagnosis of unspecified DM. At the age of 8, it was incidentally discovered that the patient had fasting hyperglycemia (7.7 mmol/L) without clinical symptoms. The oral glucose tolerance test (OGTT) showed glucose levels at baseline and 120 min of 6.6 and 12.1 mmol/L, respectively. Other findings included the absence of glycosuria and glycated hemoglobin (HbA1c) level of 6.4%. The patient was diagnosed with DM type 1 (DM1) and prescribed Actrapid HM (3 U/day; NovoNordisk A/S, Bagsværd, Denmark) and Protaphane HM (2 U/day; NovoNordisk A/S). The daily glucose levels were 4.0−8.6 mmol/L and his HbA1c levels ranged between 6.6%–7.7% for 4 years.
At the time of admission (12-years-old), the body mass index and height both expressed with standard deviation (SD) were 17.3±0.21 kg/m2 and 148.6±0.28 cm, respectively. No signs of acanthosis were observed. The daily insulin dose was 5 U (0.13 U/kg), blood glucose fluctuated from 4.1 to 8.2 mmol/L, and glycated hemoglobin was 7.0%. There were no signs of dyslipidemia. The OGTT demonstrated impaired glucose tolerance (6.5 mmol/L at baseline, 8.9 mmol/L on 120 min), pronounced hyperinsulinemia (immunoreactive insulin [IRI] from 321.3 mU/L up to 442.1 mU/L), and IR (Caro index 0.02 [normal >0.2], homeostasis model assessment [HOMA] 92.82 [normal <3.4]).
Glutamic acid decarboxylase, islet cell, insulin, and tyrosine phosphatase antibodies were negative. Typing for HLA-protective haplotypes revealed the presence of DM1 protective haplotypes DRB1*1313, DQA1*0103, and DQB1*0602-8. The patient had no family history of glucose metabolism disorders ().
Considering the mild course of the disease during the previous 4 years, despite pronounced IR, the GCK nucleotide sequence was analyzed using polymerase chain reaction followed by direct sequencing. A heterozygous mutation (p.E256K) was identified in GCK (MIM #138079, reference sequence NM_000162.3). After the genetic testing, insulin therapy was cancelled and metformin (1,000 mg/day) was prescribed.
The patient’s parents also had molecular genetic testing done. The nucleotide sequence of exon 7 of GCK (Gene ID 2645) was analyzed using polymerase chain reaction followed by direct sequencing. There were no mutations in the nucleotide sequence of exon 7. Because of ethical considerations, genetic paternity test was not performed.
A year later, patient parameters were assessed: 1) height (SD), 155.4 cm (0.05); 2) body weight, 44 kg; 3) body mass index (SD), 18.22 kg/m2 (0.0); and 4) Tanner development, stage 4. The blood glucose ranged from 6.4 to 10.1 mmol/L. HbA1c level was 6.9%. According to his OGTT results, there was deterioration of glucose metabolism (glycemia after 2 h was 15.4 mmol/L), hyperinsulinemia increased (up to 508.9 mU/L) and IR (HOMA index 114.26, Matsuda index 0.15) (). During a mixed-meal glucose tolerance test, the glycemic rate was high. However, daily fluctuations of the blood glucose were between 6.4 and 10.1 mmol/L, which corresponded with an HbA1c of <7%.
A hyperinsulinemic euglycemic clamp test, the gold standard for the study of IR, was performed for the patient.
The rate of insulin infusion in this patient was 1.0 mU/kg/min, and the M-index (glucose disposal rate) was 2.85 mg/kg/min. For adults, a normal M-index is >6.0 mg/kg/min, and a value <2 mg/kg/min indicates a moderate IR. There is no established normal range for adolescents. Even taking into account the physiological IR of adolescence, we considered these results to confirm IR in our patient. A hyperinsulinemic–euglycemic clamp test confirmed the presence of IR in this patient.
Owing to the increased IR, metformin dose was increased to 1,700 mg/day. After 6 months from increasing the dose, the glycemic profile showed no significant improvement of glycemic control. The HbA1c level was 6.6% and an OGTT demonstrated increased glycemia and IRI after 60 and 120 min without significant changes in IR (HOMA index was 112.86, Matsuda index 0.12) ().
The following genes were analyzed on an Ion Torrent sequencing system with a custom DM-HI (monogenic forms of diabetes, hyperinsulinism) AmpliSeq panel: GCG, GLUD1, WFS1, HNF1A, GCK, INS, HNF1B, ABCC8, HNF4A, RFX6, PTF1A, NEUROD1, AKT2, ZFP57, INSR, EIF2AK3, PPARG, PAX4, PDX1, GLIS3, KCNJ11, SLC16A1, FOXP3, BLK, CEL, KLF11, SCHAD and GCGR (total coverage 96.5%). The analysis showed the presence of the same p.E256K mutation in GCK gene. Thus, the diagnosis of MODY2 can be confirmed by performing molecular genetic testing twice. There were no mutations in other tested genes, including INSR and PPARG. We did not test for mutations in other genes such as those responsible for lipodystrophy-associated insulin resistant diabetes mellitus, including gene LMNA, because there were no clinical signs of lipodystrophy.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [155.4, 'cm']}",52.71662,50.08079,55.35245,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 155.4 cm, which is 155.4 cm * 0.393701 in/cm = 61.18114 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (61.18114 (in inches) - 60) = 52.71662 kg.
Hence, the patient's IBW is 52.71662 kg."
3874,10,Ideal Body Weight,physical,decimal,pmc-3348632-1,Extracted,"A 38-year-old woman with a childhood history of atopic dermatitis and allergic rhinitis came to our outpatient clinic because of polyarthralgia and swelling of her fingers. Five days prior to her visit, she had upper respiratory symptoms and a low grade fever (). Oral administration of 400 mg acetaminophen relieved those symptoms. Then, however, she developed a butterfly-shaped erythema on her face and swelling of her fingers. Three days later, although the facial erythema had improved, she developed joint pain in her fingers, wrists, shoulders, and knees, for which acetaminophen did not work. On physical examination, the patient looked tired. Her body temperature was 36.7°C, blood pressure was 94/50 mmHg, and pulse rate was 61 beats/min. She weighed 48 kg and was 153 cm tall. She had no rash except for a malar erythema that was faint at that time. All her fingers were swollen, but her wrist, shoulder, and knee joints were not. Both her legs had pretibial pitting edema. Laboratory data showed mild hypoproteinemia (serum protein 6.4 g/dL) and slightly decreased peripheral white blood cell count (4,100/μL). However, other hematologic parameters were relatively normal (hemoglobin 11.2 g/dL, hematocrit 35.2%, reticulocyte 1.4%, and platelet count 230,000/μL). Liver enzymes and C-reactive protein levels were not elevated. Regardless of hypocomplementemia (C3 72 mg/dL, C4 9 mg/dL, and CH50 18.6 U/mL), the tests for serum antinuclear antibodies and rheumatoid factor were negative. Althoughthe IgG antibody was not examined, a positive result for HPV-B19 IgM antibody (index 7.97) indicated a recent infection of the virus []. Since microbiological tests for other viruses, such as measles and rubella, were negative, a diagnosis of HPV-B19 infection was finally made. Because her symptoms deteriorated despite the use of acetaminophen, oral administration of loxoprofen (180 mg/day) was alternatively started immediately after the diagnosis (). The symptoms, including facial erythema, polyarthralgia, and the swelling of her fingers, rapidly disappeared within 12 hours after the initiation of the drug. No recurrence of the symptoms or signs was noted afterwards, indicating the complete remission of the disease.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.0, 'cm']}",46.04337,43.7412,48.34554,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.0 cm, which is 153.0 cm * 0.393701 in/cm = 60.23625 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.23625 (in inches) - 60) = 46.04337 kg.
Hence, the patient's IBW is 46.04337 kg."
3875,10,Ideal Body Weight,physical,decimal,pmc-4897797-1,Extracted,"We present a report of a 42-year-old woman of African descent who presented to our fertility clinic with a 10-year history of primary subfertility and amenorrhea of 6 years duration. She was a nurse in a medical ward and had no prior history of TB. She was separated from her husband and intended to use donated sperm for her assisted conception treatment. The timeline of interventions is summarized in Table below.
The initial evaluation for subfertility (in a different institution) included a diagnostic laparoscopy performed 8 years prior. The laparoscopy had revealed dense pelvic adhesions (“a frozen pelvis”), and an impression of tubal factor subfertility was made. It appears that there was no deliberate attempt to make a definitive diagnosis as to the cause of the tubal disease as no tissue samples or swabs were assessed. She had undergone a pelvic ultrasound scan which was reported as normal and had had a negative pap smear. There were neither further details of this prior evaluation nor a detailed summary from her previous gynecologist.
She neither had a history of pelvic pain nor a history suggestive of previous sexually transmitted infections. She did not report any symptoms suggestive of TB, notably fever, night sweats, or weight loss. She weighed 84 kg, was 1.58 meters tall with a body mass index (BMI) of 33. Her blood pressure was 140/90 mmHg and her clinical examination was essentially normal. She had no lymphadenopathy, acne, or hirsutism. Her gonadal hormone profile presented in Table was in keeping with PCOS.
The initial high estradiol (E2) levels and the biochemical evidence of PCOS prompted the use of an exogenous progestogen to initiate endometrial shedding prior to baseline ultrasound scan in preparation for an in vitro fertilization (IVF) cycle. She received medroxyprogesterone (Provera) 10 mg orally once a day for 5 days but had no withdrawal bleed. Two weeks after administration of medroxyprogesterone, she still reported no withdrawal bleed. A subsequent pelvic ultrasound scan showed normal uterine morphology. Her endometrial thickness was 3 mm with a small amount of endometrial fluid with no focal endometrial pathology demonstrable on ultrasound. Her ovaries had a polycystic appearance with multiple small peripheral follicles. A simple cyst of 4 cm in size was visualized in her right ovary. The ultrasound findings further supported the diagnosis of PCOS.
Endometrial assessment by hysteroscopy was undertaken in view of the presence of endometrial fluid and the negative progesterone challenge test. Hysteroscopy revealed an atrophic endometrium interspersed with areas of thickened endometrium, with no synechiae, and bilaterally obliterated and poorly visualized tubal ostia. Directed endometrial biopsies were taken. Histology showed endometrial tissue with a normal gland to stromal ratio. Numerous granulomas, with epithelioid histiocytes, plasma cells and Langhans giant cells were visualized in the stroma with some areas of necrosis. A Ziehl–Neelsen stain was negative. A conclusion of granulomatous endometritis possibly TB endometritis was made.
Following the diagnosis of TB, further investigations were carried out. A chest X-ray was normal and an HIV test was negative. Her liver function tests, creatinine, and full blood count were all normal. She was referred to a physician for TB treatment and plans for assisted reproductive technology (ART) were deferred. Treatment for TB endometritis was started by use of a 6-month regimen of antitubercular therapy. An initial 2-month intensive phase of four drugs (rifampicin 600 mg once daily, isoniazid 300 mg once daily, pyrazinamide 2000 mg once daily, and ethambutol 1600 mg once daily) was followed by a 4-month course of two drugs (rifampicin 600 mg once daily, isoniazid 300 mg once daily). In addition, a daily dose of pyridoxine 25 mg was administered throughout the 6 months. Antihypertensive treatment was initiated in the second month of antitubercular treatment. She was evaluated after a week of initiation of TB therapy and thereafter every month by the physician. She was compliant on all her medications and experienced no adverse effects. She reported no menses despite completing the TB treatment. The supervising TB physician did not consider it clinically relevant to re-biopsy after a full course of TB therapy.
She maintained her desire for conception and revisited the fertility clinic. A follow-up ultrasound scan showed less evident endometrial fluid compared to the initial pelvic ultrasound scan with an endometrial thickness of 3.7 mm. Her ovaries were still polycystic but the 4 cm right ovarian cyst was no longer present. A decision on a second trial of endometrial stimulation/shedding was made. She received one cycle of low-dose combined oral contraceptive pills but reported no menses. There was no change in endometrial findings on follow-up scan.
A conclusion of endometrial scarring post-endometrial TB was made. Further attempts at endometrial stimulation were discouraged in view of her very high endogenous E2 and complete failure of response to exogenous steroids. The options of surrogacy or adoption were discussed while further ART interventions were discouraged due to the endometrial damage.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.58, 'm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.58 m, which is 1.58 m * 39.3701 in/m = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3876,10,Ideal Body Weight,physical,decimal,pmc-7387025-1,Extracted,"The 12-year-old boy was admitted to emergency department of Changsha Central Hospital at 17:45 on January 8, 2018, due to hemiplegia of left limbs for 3 hours without physical collision and trauma. Besides the symptom of hemiplegia, he also had urinary incontinence and unclear speech. He was diagnosed with AIS in a local hospital after performing a magnetic resonance imaging (MRI) examination (Fig. ) and magnetic resonance angiography (MRA) examination (Fig. ). Cerebral infarction in the right parietal, temporal, insular, and frontal lobes was revealed by the MRI test. The MRA test detected occlusions in right internal carotid artery, A1 segment of right anterior cerebral artery, right middle cerebral artery, and distal branch. For further treatment, he was admitted to our hospital. The patient reported no history of coagulation disorders, cardiovascular disease, special medication, or any other systemic immune disorder, nor was there any recent history of trauma. On admission, the boy was not mentally oriented. His weight was 65 kg and height 168 cm, with 36.3°C body temperature, 82 beats per minute pulse rate, 22 per minute breathing rate, and 119/62 mm Hg blood pressure. The physical examination revealed normal heartbeat and no crackles in the lungs. Neurological examination showed Glasgow Scale of 14, equal and reactive pupils, and unclear speech. In addition, both eyes gazed to the right side. He showed flattened left nasolabial fold, and left deviation of the protruded tongue. The muscle tension of left limbs increased while the muscle strength of left upper limb and left lower limb were grade 1 and grade 2, respectively. He could not perform the left finger-nose test and the heel-knee-tibia test and his left pathological reflex was positive with 12 points of National Institute of Health Stroke Scale. Laboratory findings demonstrated that a white blood cell count of 12,770/mm3, with 84.5% neutrophils as well as hemoglobin concentration of 12.6 g/dL and a platelet count of 297,000/mm3. There was no abnormality in liver and kidney function test. D-dimer was 0.10 μg/mL, and C-reactive protein was 3.03 mg/L. Triglyceride was 1 mmol/L and low-density lipoprotein was 2.29 mmol/L. Tests of anti-Sjogren's syndrome B, anti-Sjogren's syndrome A, anti-Jo1, antinuclear antibody, antihistone antibody (AHA) and anti-SM measured by enzyme-linked immunosorbent assay were negative. After admission, emergency cerebral angiography and mechanical thrombectomy were performed under local anesthesia. Cerebral angiography revealed that occlusion in the end segment of right internal carotid artery and normal blood flow of left anterior communicating artery. The operation of mechanical thrombectomy was performed successfully. For antiplatelet aggregation, tirofiban was given continuously intravenously (0.15 μg/kg/min body weight). After 24 hours, oral clopidogrel was prescribed (75 mg once per day) and atorvastatin (20 mg once per day) were also administered for him. And after 48 hours, tirofiban was discontinued while clopidogrel (75 mg once per day) and atorvastatin (20 mg once per day) were continuously given. On January 9, 2018, computed tomography angiography (Fig. ) illuminated that the blood flow of right internal carotid artery was restored, and the right middle cerebral artery and the anterior cerebral artery were demonstrated normally. At the same time, further examinations were arranged for the young patient. Laboratory examinations including thyroid function, antineutrophil antibody, biomarkers of lupus, and tumor revealed no abnormality. Dynamic electrocardiogram showed sinus arrhythmia. There was no abnormality in Doppler echocardiography. Ultrasonography of carotid artery, abdomen, and veins of both lower extremities were also normal.
Around 2 weeks after admission, the patient was transferred to the rehabilitation department for further treatment. After being with active rehabilitation training for several months, physical examination for him revealed that muscle strength of left limbs were both grade 3, and clear speech. On May 5, 2018, he was discharged from hospital and prescribed with clopidogrel (75 mg once per day) and atorvastatin (20 mg once per day). The patient was followed up for a year. On June 20, 2018, the patient came to hospital for a checkup and the results showed a significant improvement in his physical conditions. Muscle strength of left limbs both increased to grade 4 and muscle tension also improved. He could walk by himself without any assistance and had Modified Rankin Scale (MRS) of 2. In June 2019, he recovered well except feeling a bit pain of left lower limb when walking, with final MRS of 1.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.0, 'cm']}",64.12607,60.91977,67.33237,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg."
3877,10,Ideal Body Weight,physical,decimal,usmle-520,Extracted,"A 66-year old man comes to the physician because of fatigue for 6 months. He says that he wakes up every morning feeling tired. Most days of the week he feels sleepy during the day and often takes an afternoon nap for an hour. His wife says he snores in the middle of the night. He has a history of heart failure and atrial fibrillation. His medications include aspirin, atorvastatin, lisinopril, metoprolol, and warfarin. He drinks 1–2 glasses of wine daily with dinner; he does not smoke. He is 175 cm (5 ft 9 in) tall and weighs 96 kg (212 lb); BMI is 31.3 kg/m2. His blood pressure is 142/88 mm Hg, pulse is 98/min, and respirations are 22/min. Examination of the oral cavity shows a low-lying palate. Cardiac examination shows an irregularly irregular rhythm and no murmurs. The remainder of the examination shows no abnormalities.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3878,10,Ideal Body Weight,physical,decimal,pmc-7370489-1,Extracted,"We report the case of a 30-year-old nulliparous black woman with a history of primary mesenteric cystic lymphangioma requiring multiple bowel resections in childhood. This history was responsible for chronic malabsorption resulting from short bowel syndrome, for which our patient received long-term monthly supplemental parenteral nutrition. She weighed 41 kg for 1.57 m at the beginning of pregnancy (a body mass index [BMI] of 16.6).
Her first trimester of pregnancy followed a normal course and combined aneuploidy screening did not identify increased risk (combined risk 1/10,000). A control ultrasound at 22 WG showed a eutrophic female fetus with no observable morphological abnormalities (particularly of the urinary tract and abdomen) or excess amniotic fluid.
At 26 WG, our patient presented with mild to moderate bowel occlusion on computed tomography (CT) scan. Medical treatment involving nasogastric intubation and parenteral nutrition supplementation provided rapid though transient clinical improvement. After multidisciplinary consultation, it was decided to maintain exclusive parenteral nutrition until the end of the pregnancy due to signs of recurrent occlusion at 28 WG.
At 29 WG, our patient was hospitalized for bilateral lumbar pain. A renal ultrasound revealed dilatation of the bilateral pyelocaliceal cavities (27 mm on the right, 30 mm on the left) attributed to compression by the gravid uterus. Given the persistent pain and a slight rise in serum creatinine (63 to 84 micromol/L), an internal ureteral bypass with double J stents was rapidly performed. The procedure proved to be difficult due to ureteral siphons hindering the insertion of the stents and resulted in accidental bilateral ureteral perforation. Postoperative pain required the use of level III analgesics: oral morphine: immediate release oxycodone 5 mg 4 times a day and nefopam 120 mg continuous intravenous daily.
At 29 weeks and 4 days gestation, our patient was transferred to an ICU near the level 3 maternity ward. A CT scan revealed significant uroperitoneum and bilateral pleural effusion. Worsening of respiratory manifestations and onset of acute renal impairment (serum creatinine 180 micromol/L, potassium 5.2 mmol/L) required thoracic drainage (1900 mL) and bilateral nephrostomies. Our patient’s nephrological and respiratory condition rapidly improved.
During her ICU stay, our patient presented painful uterine contractions, for which she received tocolytic treatment with atosiban. For the persistent low back pain, morphine was continued intravenously at a mean dose of 50 mg of oxynorm per day (patient-controlled analgesia). Antenatal corticosteroid therapy was given. The fetal heart rate (FHR) was normal.
On ultrasound, the fetus was eutrophic (estimated fetal weight [EFW]: 1250 g at 29 weeks and 3 days), in cephalic presentation, with a moderate excess of amniotic fluid (cisterna magna 112 mm) and increased bladder volume. At 29 weeks and 5 days gestation, 5 days after parenteral introduction of high-dose opioids, fetal megacystis increased (50 mm × 52 mm) and was associated with pyelocaliceal dilatation (Fig. ).
Three days later, an ultrasound revealed voluminous fetal ascites and a small bladder with thickened walls (3 mm) (Fig. ). The fetal kidneys were morphologically normal. No anasarca or sign of fetal anemia (normal middle cerebral artery peak systolic velocity) was evident and the amniotic fluid index was normal. Possible spontaneous bladder rupture with urinary peritonitis was suggested. In the absence of a clear cause, the morphine derivatives administered to the mother, for 8 days (from 29 to 30 + 1 WG), were suggested as a contributing factor to the fetal megacystis.
After multidisciplinary discussion (pediatric surgeon, pediatric nephrologist, and obstetrician), anticipatory management was decided. Urgent extraction or draining of antenatal ascites were not performed because fetal hemodynamics were satisfactory. Our patient was closely monitored with three fetal heart rate (FHR) recordings per day and two ultrasounds per week. The maternal and fetal condition remained stable for 9 days (from 30 weeks and 1 day to 31 weeks and 3 days) and the fetal bladder remained unchanged throughout the monitoring.
At 31 weeks and 4 days gestation, our patient went into labor spontaneously and received epidural anesthesia. Labor was rapid and marked by moderate FHR abnormalities. Our patient gave birth vaginally to a girl weighing 1700 g, presenting moderate ischemic anoxia with Apgar scores at 1/1/10 and umbilical cord pH 7.19 (artery) and 7.27 (vein). Neonatal intensive care included mask ventilation followed by orotracheal intubation and external cardiac massage. Paracentesis of ascites (300 mL citrinic fluid) was carried out at 8 minutes. The infant was then transferred to the ICU. Her respiratory state required tracheal instillation of surfactant with a favorable respiratory outcome. Her hemodynamic condition was stable. No definite neonatal infection was identified, and intravenous antibiotic treatment was maintained for 8 days with cefotaxim based on the notion of peripheral ampicillin-resistant Escherichia coli carriage. Enteral feeding was initiated on the first day with the mother’s milk and then with specific infant formula for preterm neonates, followed by central line parenteral nutrition for 15 days. Transfontanellar cranial ultrasounds showed a grade 1 intraventricular hemorrhage with no parenchymal lesion.
Ascites drained at birth showed a biochemical profile similar to plasma, in favor of uroperitoneum. No metabolic disorder was found except for a plasma creatinine level at 79 μl/L on day 1 which quickly normalized within the first week of life. A urinary catheter was inserted following delivery. The abdominal ultrasounds performed on day 1 and day 6 were normal with a normal bladder wall. Cystography was normal on day 9 and the bladder catheter was removed. Ascites did not recur. The infant’s course was favorable without complications during hospitalization.
Regular pediatric monitoring was performed after discharge and showed a strictly normal outcome at last follow-up at 2 years of age (adjusted). The mother has been regularly monitored and has presented no complication. From a medical standpoint, a new pregnancy is not recommended.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.57, 'm']}",49.66544,47.18217,52.14871,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.57 m, which is 1.57 m * 39.3701 in/m = 61.81106 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.81106 (in inches) - 60) = 49.66544 kg.
Hence, the patient's IBW is 49.66544 kg."
3879,10,Ideal Body Weight,physical,decimal,pmc-4745965-1,Extracted,"The patient is a 28-year-old man, 175 cm and 82 kg (BMI 26.6) with no past medical history, who tore his left anterior cruciate ligament (ACL) while playing basketball. There were no other associated injuries. When he presented to the orthopedic surgeon he only complained of 2/10 pain on the numeric rating scale (NRS) and instability in his left knee. He denied taking routine daily medications, allergies to medications, illicit drug use, or contributory family history. One month after injury he presented for left knee arthroscopy with ACL reconstruction with hamstring autograft.
Prior to surgery the patient underwent ultrasound guided left sciatic and left femoral nerve blocks. For sedation he received midazolam 2 milligrams intravenously (IV), in divided doses prior to the needle placement. The sciatic nerve block was completed using real time ultrasound with direct visualization of the needle by an anesthesiology resident who was supervised by a skilled regional anesthesiologist. The block was performed immediately distal to the bifurcation of the sciatic nerve into its tibial and common peroneal branches. A Pajunk needle, 21-gauge, length 4-inch (10 centimeters), was used and the needle tip was placed between the tibial and common peroneal nerves. The injectate consisted of 25 milliliters of 0.5% ropivacaine, which was injected in incremental doses with frequent negative aspirations. Perineural, circumferential spread of local anesthetic around the tibial and common peroneal nerves was noted. No paresthesias were noted at the time of injection. The femoral nerve block was completed using a Pajunk needle, 21-gauge, length 2-inch (5 centimeters), using real time ultrasound with direct visualization of the needle. The needle tip was placed underneath the femoral nerve, immediately superficial to the iliopsoas muscle. The injectate consisted of 22 milliliters of 0.5% ropivacaine, which was injected incrementally with frequent negative aspirations. Perineural injection of local anesthetic was noted as the femoral nerve was lifted off the surface of the iliopsoas muscle. No paresthesias were noted at the time of injection. Both nerve blocks provided expected dermatomal sensory anesthesia prior to induction of general anesthesia. No additives such as epinephrine, clonidine, or dexamethasone were added to the ropivacaine injectate.
General anesthesia was induced and maintained with propofol, and a laryngeal mask airway was used. The surgery was uneventful with a total surgical time of approximately 1 hour and 15 minutes. Controlled hypotension [] with intermittent doses of IV labetalol was used to lower the mean arterial pressure (MAP) in order to mitigate blood loss. No tourniquet was used. Blood loss was noted to be minimal and the patient received 600 milliliters of IV Lactated Ringer's solution. The patient's mean arterial pressure remained consistently between 70 and 80 mmHg for the entire case. He was discharged home the same day. He returned to the orthopedic surgeon for a postoperative visit on postoperative day (POD) 8 and noted good pain control taking only scheduled ibuprofen 400 milligrams by mouth every four hours with an average of 10 mg of hydrocodone (with 325 mg of acetaminophen) by mouth daily. On POD 34, he attended his next follow-up visit with his orthopedic surgeon at which time he noted numbness and pain (NRS 4/10) located across the top and lateral aspects of his left foot in the distribution of the common peroneal (superficial and deep) and the lateral sural cutaneous nerves. He noted that the pain was present immediately after surgery and it progressively worsened over the prior two weeks. He described the pain as burning with intermittent electrical shock sensations and noted no other specific inciting factors. He was diagnosed with an acute post-op neuropathy and prescribed gabapentin 300 milligrams by mouth three times daily. At this time there were no noted motor or sensory deficits on physical exam.
On POD 40, the patient was again seen in the orthopedic clinic for followup due to worsening pain (NRS 7–10/10) that was now impacting his ability to sleep. The pain was now worsened by wearing socks or the brushing of his bed sheets against his left foot. The orthopedic surgeon consulted a pain medicine physician, who recommended he uptitrate his gabapentin to 600 milligrams by mouth three times daily. Additionally, a lidocaine 5% patch was prescribed. Ibuprofen 400 milligrams by mouth every 8 hours was resumed. Two days later he called the orthopedic clinic to say that the lidocaine patch did not work. At this point, amitriptyline 25 milligrams by mouth daily was prescribed and a referral placed for patient to be formally evaluated at the pain management clinic.
He visited the pain management clinic on POD 52. By this time he was taking gabapentin 900 milligrams by mouth three times daily and amitriptyline 25 milligrams at bedtime. The neuropathic pain questionnaire (NPQ) [, ] was performed. He noted periods of electrical shock sensations followed by numbness in addition to burning and pinprick sensations in the distribution of the sural and superficial peroneal nerves. The pain improved with cold compress and was worsened by wearing a sock or having anything lightly touching his foot. Brush evoked allodynia was noted on physical exam. Patient was very anxious and deferred pinprick exam. Titration schedules were given to the patient to increase these medications further as pain dictated. An electromyography and nerve conduction study had been completed on POD 45 which revealed a left sciatic mononeuropathy with mild to moderate axon loss in addition to a left femoral neuropathy with mild motor axon loss. A magnetic resonance neurogram (MRN) was ordered at this visit, which showed nonspecific long segmental thickening and increased T2 signal involving the left femoral nerve and extra pelvic left sciatic nerve, which corresponded to the areas where the peripheral nerve blocks were performed. At the time of this visit he did not fit Budapest criteria [] for a diagnosis of complex regional pain syndrome.
One month later at the pain clinic follow-up visit he noted no benefit with gabapentin despite uptitration to 1200 milligrams by mouth three times daily. He had stopped the amitriptyline due to paradoxical insomnia. He had begun a trial of topiramate starting at 25 milligrams by mouth daily. At this visit it was recommended that he cross-titrate off gabapentin onto pregabalin and that he replace daily ibuprofen with celecoxib. Over the next weeks, he decreased his gabapentin and eventually was transitioned to pregabalin 150 milligrams by mouth twice daily alongside celecoxib 100 milligrams by mouth twice daily. Topiramate had not provided additional relief with intolerable neurologic side effects (dizziness, fatigue, and impaired cognition) and thus was discontinued.
Approximately three months after surgery the patient noted that his pain started to subside. The severe burning sensation in the distribution of the left lateral sural cutaneous nerve and the common peroneal nerves was replaced by pruritis. By four months after surgery his nerve pain was much improved with only occasional bouts of provoked pain, including prolonged periods of sitting and attempts at return to basketball. Rest consistently relieved these flares. He continued to take pregabalin 150 milligrams by mouth twice daily and celecoxib 100 milligrams by mouth twice daily. By six months post-op he was 95% pain-free and was able to wean off pregabalin completely. At last pain clinic visit, he was advised to wean off celecoxib 100 milligrams by mouth as pain allowed and to return to clinic on an as-needed basis. No further followup was needed.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3880,10,Ideal Body Weight,physical,decimal,pmc-4523672-1,Extracted,"A 26-year-old female patient was referred to our clinic with a 3 yr history of amenorrhea. Medical history showed a diagnosis of β-thalassemia major since the age of one and treatment with regular blood transfusions (once a month until the age of seven, thereafter twice a month) to maintain adequate levels of hemoglobin. She had also undergone splenectomy due to hypersplenism and massive splenomegaly at eight years old. She received iron chelation therapy with deferasirox (500 mg t.i.d.) for the last 6 years, having had irregular desferroxamine treatment before this. Her menarche was at the age of 13 years. She had a regular menstrual cycle over the next 10 years. There were no other possible causes of functional hypothalamic amenorrhea such as weight loss, eating disorders, excessive exercise, and psychosocial stress. Her blood pressure was 110/65 mmHg, she was 168 cm tall, and she weighed 53 kg. Stages of female breast and pubic hair development, according to Marshall and Tanner, were stages B-4 and P-5, respectively. There were no pathological findings except for skin hyperpigmentation on physical examination. The patient had low LH and FSH levels in association with the low estradiol levels. A bolus of 100 g synthetic LHRH was administered intravenously, and serum samples for gonadotropin measurements were drawn 0, 30, 60, 90, and 120 minutes after LHRH injection. Even after stimulation with LHRH, pituitary response was subnormal, consistent with hypogonadotropic hypogonadism. Peak levels of growth hormone and cortisol with insulin tolerance test were 11.6 ng/mL and 26.3 μg/dL, respectively. Her serum ferritin was 887 ng/mL (normal range 4.6–204) and transferrin saturation was 66.4%. Other laboratory test results were normal except for the anemia and thrombocytosis (). Abdominal magnetic resonance imaging was unremarkable except for asplenia. Magnetic resonance imaging (MRI) showed decreased signal intensity of the pituitary gland on T2-weighted images (). With these findings, the patient was accepted as isolated gonadotropin deficiency resulting from iron deposition in the pituitary gland. Additionally, bone densitometry (BMD) showed osteopenia, with a Z score of −1.8 in the femur and −2.1 in the spine. Combined estrogen/progesterone replacement therapy and calcium/vitamin D supplementation therapy were then prescribed for hypogonadism and osteopenia.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [168.0, 'cm']}",59.62607,56.64477,62.60737,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.14177 (in inches) - 60) = 59.62607 kg.
Hence, the patient's IBW is 59.62607 kg."
3881,10,Ideal Body Weight,physical,decimal,pmc-7803851-1,Extracted,"A 53-year-old Nigerian male with hepatitis C virus (HCV) infection treated with peginterferon alfa-2a and ribavirin, to which he showed a null response, presented to our hospital. Three months after the initial visit, multiple hepatocellular carcinomas (HCCs) were detected in segments 7 and 8 of the liver according to the Brisbane 2000 Nomenclature of Liver Anatomy and Resections [], and radiofrequency ablation (RFA) was performed for each HCC. Seventeen months after RFA, a recurrence of HCC was detected in segment 4 (the medial section) by follow-up computed tomography (CT), and the patient was referred to our department.
Physical examination showed that the patient was an 87.9 kg, 168.5 cm male in good condition. The patient received medical treatment for diabetes mellitus and hypertension. He had neither a history of transfusion nor a history of SCT. The laboratory test results showed moderate liver damage, as shown in Table . Microscopic examination of peripheral blood erythrocytes did not show any morphological abnormalities.
Contrast-enhanced CT showed a 4.0 × 3.4 × 3.2 cm tumor in segment 4 adjacent to the left branch of the portal vein and the middle hepatic vein (Fig. ). An irregular liver surface; the hypertrophy of segments 1, 2 and 3; and splenomegaly all suggested the presence of cirrhosis. The normal liver parenchyma of the medial section accounted for 10% of the total liver volume according to CT volumetry.
With the diagnosis of solitary HCC in segment 4, left medial sectionectomy was conducted. Hepatic resection was performed with intraoperative ultrasonography (IOUS) guidance with Pringle’s maneuver (hepatic inflow occlusion time 15–30 min and reperfusion time 5 min; the total blood flow occlusion time was 165 min). Multiple IOUS examinations and inspections of the liver surface revealed no hepatic blood flow impairment during surgery (Fig. ). At the end of the operation, laboratory data showed no conspicuous abnormalities, with total bilirubin (T-Bil) 1.6 mg/dL, aspartate aminotransferase (AST) 316 IU/L, alanine aminotransferase (ALT) 323 IU/L, hemoglobin (Hb) 11.6 g/dL, and prothrombin time (PT)% 52.5%. A drain was inserted along the resected plane of the liver. The operation time was 305 min, and the estimated blood loss was 714 mL. No blood transfusion was performed.
However, the laboratory tests on postoperative day (POD) 1 revealed severe liver damage and acidosis: T-Bil 2.8 mg/dL, AST 9250 IU/L, ALT 6120 IU/L, PT% 20.9%, blood pH 7.29, lactate 6.6 mmol/L, and base excess − 5.4 mmol/L. Figure shows the trends of postoperative laboratory data. The bedside US did not indicate an impairment of hepatic blood perfusion. The drain output was 460 mL/15 h, with serosanguineous appearance. Because his vital signs were stable and it was difficult to identify a cause of the acute severe liver damage, we selected conservative management while performing fresh frozen plasma transfusion. The values of AST and ALT declined gradually, but the level of T-Bil continued to increase, and renal and respiratory dysfunction emerged and subsequently deteriorated; therefore, we initiated continuous hemodiafiltration and plasma exchange under mechanical ventilation. Contrast-enhanced CT showed a slightly heterogeneous enhancement of the liver parenchyma without apparent major vessel occlusion on POD 13 (Fig. a), and diffuse cerebral infarction on POD 16 (Fig. b).
Although clinico-radiological examinations could not identify the cause of acute liver damage, the pathological examination of the resected specimen revealed that the intrahepatic peripheral blood vessels were occluded by sickled erythrocytes (Fig. ). Morphological abnormalities were not found by microscopic examination of the peripheral blood erythrocytes after surgery, but we requested an analysis of the patient’s hemoglobin by high-performance liquid chromatography (HPLC) with a suspicion of hemoglobinopathy. HPLC demonstrated an abnormal sharp peak indicating the presence of abnormal hemoglobin, which accounted for 34.4% of total hemoglobin (Fig. ). These findings strongly suggested the presence of HbS. Despite intensive treatments, he died of multiple organ failure on POD 20. Autopsy was rejected by his bereaved family for religious reasons.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.5, 'cm']}",64.57883,61.34989,67.80777,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.5 cm, which is 168.5 cm * 0.393701 in/cm = 66.33862 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.33862 (in inches) - 60) = 64.57883 kg.
Hence, the patient's IBW is 64.57883 kg."
3882,10,Ideal Body Weight,physical,decimal,pmc-5818770-1,Extracted,"A 41-year-old man (height 171.5 cm, body weight 67 kg) was transferred to the regional medical center due to right hemiplegia and aphagia. Cerebral magnetic resonance imaging revealed cerebral infarction caused by occlusion of the left middle cerebral artery, while cerebral magnetic resonance angiography showed the development of a network of abnormal collateral vessels. Hence, the patient was diagnosed with MMD.
Before cerebral revascularization surgery, severe MR (III/IV) due to the prolapse of the P2 leaflet in the mitral valve was indicated by transthoracic echocardiography. Cardiac catheterization indicated elevated pulmonary arterial pressure (PAP) (systolic/diastolic/mean: 86/33/60 mmHg) and pulmonary capillary wedge pressure (32 mmHg) at the systemic arterial pressure of 120/83/102 mmHg. Hence, the patient was admitted to our university center for the surgical treatment of MR.
Preoperative single-photon emission computed tomography revealed reduced cerebral blood flow in the left cerebral hemisphere (especially in the external left frontal cortex; Fig. ). Neurosurgeons at our center judged that the patient did not have an indication for cerebral revascularization surgery, which is used to prevent ischemic complications during the perioperative period of mitral valve plasty. This was because his left frontal lobe showed extensive cerebral infarction and no cerebral infarction symptoms were observed in the right cerebral hemisphere. Therefore, mitral valve plasty without cerebral revascularization was chosen.
In the operation room, the patient’s monitoring of electrocardiogram, oxygen saturation, systemic arterial pressure via right radial artery catheter, bispectral index, and regional cerebral oxygen saturation (rSO2) at the right and left forehead (INVOS™ 5100C, Somanetics, USA) was initiated before the administration of general anesthesia. The rSO2 values for the left and right forehead were 72 and 81 %, respectively.
General anesthesia was induced by intravenous administration of 3 mg of midazolam, 0.4 mg of fentanyl, and 50 mg of rocuronium. After tracheal intubation, a transesophageal echocardiography (TEE) probe was inserted. Then, a central venous catheter and right heart catheter were inserted via the right internal jugular vein, and central venous pressure, PAP, cardiac output, and mixed venous oxygen saturation were measured. The nasopharyngeal temperature and urinary bladder temperature were also measured.
Before CPB, general anesthesia was maintained by inhalation of sevoflurane (1–1.5 % of end-tidal concentration). The patient’s PaCO2 was maintained between 38 and 42 mmHg. Intra-aortic balloon pumping (IABP) was placed at the start of surgery and the augmented pressure was maintained. The mean arterial pressure was constantly above 70 mmHg. Before CPB, rSO2 values were almost above 80 % on both sides (Fig. ).
During CPB, administration of sevoflurane via the oxygenator was also continued because of its cerebrovascular dilatation activity and potential preconditioning effect against focal cerebral ischemia. PaCO2 was maintained between 45 and 50 mmHg, and alpha-stat management of pH was performed. Hypothermia was induced; the temperature at the bottom of the nasopharyngeal temprature was 28 °C. We used pulsatile perfusion assist to maintain cerebral circulation during CPB with IABP. A decrease in rSO2 was observed 162 min after the initiation of CPB. Our perfusionist increased the CPB pump flow from 2.2 L/min/m2 to 2.8 L/min/m2 in order to increase cerebral blood flow. Moreover, the concentration of sevoflurane was increased to 2 %. Yet, rSO2 desaturation (15 % reduction from baseline) was not improved. We decided to increase the depth-of-anesthesia with another dose of midazolam. After administration of 3 mg of midazolam, the rSO2 values increased from 67 to 73 % on the right side and from 71 to 74 % on the left side. During CPB, the lowest values (and variation) of rSO2 in the left and right forehead were 71 % (−2 %) and 67 % (−17 %), respectively. Mitral valve plasty was performed as planned.
At the weaning from the CPB, the disappearance of MR was confirmed by TEE; the weaning was not difficult. Pulmonary hypertension also improved (PAP was 26/12 mmHg, while systemic arterial pressure was 105/56 mmHg). After CPB, inhalation of sevoflurane (1–1.5 % of end-tidal concentration) was also continued. The rSO2 values were almost above 75 % on both sides and not below the awake rSO2 values (Fig. ). CPB and aortic cross-clamping lasted 352 min and 289 min, respectively. On the completion of the surgery, the IABP was discontinued and sevoflurane administration was stopped. The patient was transferred to the intensive care unit with ventilator support under propofol sedation.
On the 1st postoperative day (POD), the patient was weaned from the ventilator, and the patient did not complain about any new neurological deficits. We monitored the rSO2 of his forehead until the 2nd POD and no significant decrease (−20 %) of the rSO2 values was confirmed. The postoperative course was uneventful. On the 15th POD, single-photon emission computed tomography revealed that the low cerebral blood flow lesions had not changed (Fig. ), and the patient was discharged from our hospital on the 16th POD.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [171.5, 'cm']}",67.29536,63.93059,70.66013,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 171.5 cm, which is 171.5 cm * 0.393701 in/cm = 67.51972 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.51972 (in inches) - 60) = 67.29536 kg.
Hence, the patient's IBW is 67.29536 kg."
3883,10,Ideal Body Weight,physical,decimal,pmc-7476800-1,Extracted,"A 65-year-old man was referred to the hospital in 5th July 2019 because of refractory edema in both legs.
The patient had a history of CKD stage 3a, a hypotrophic left kidney, and hypertension. He had been prescribed amlodipine 2.5 mg for hypertensive medication. He also underwent radical prostatectomy for prostate cancer two years earlier. He underwent pelvic MRI using gadoterate meglumine (15 mL), immediately after iodide contrast-enhanced chest and abdomen computed tomography (CT) for cancer surveillance. Thirty days before CT scan, his creatinine level was 1.28 mg/dL and his estimated glomerular filtration rate (eGFR) was 58 mL/min/1.73 m2. After 185 days, he visited a local clinic because of edematous changes in both lower extremities. CT angiography of the lower extremities was performed; no stenosis or occlusion of vessels was observed. Although diuretics were administered for 2 weeks, the edema worsened and was accompanied by pruritus and pain (). Eventually, he was referred to our hospital for further evaluation.
Upon admission, his body temperature was 36.8°C and his blood pressure was 110/60 mmHg. His height was 161.3 cm, weight was 53.2 kg and body mass index was 20.4 kg/m2. Physical examination revealed grade 2+ pretibial pitting edema with redness, mild heat, and tenderness in both lower extremities. Both inguinal lymph nodes were not enlarged.
Initial laboratory findings at admission (about 210 days after MRI scan) were as follows: white blood cell count, 6,200 /μL (neutrophil 66%, lymphocyte 22%, monocyte 10.3%, eosinophil 0.5%); hemoglobin, 10.7 g/dL; platelet, 253,000 /μL; blood urea nitrogen, 41 mg/dL; serum creatinine, 2.07 mg/dL; eGFR, 32 mL/min/1.73 m2; serum sodium, 134 mmol/L; potassium, 3.4 mmol/L; chloride, 102 mmol/L; total CO2, 20 mmol/L; calcium, 9.3 mg/dL; phosphate, 1.5 mg/dL; total protein, 6.9 g/dL; albumin, 4.0 g/dL; aspartate transaminase, 43 U/L; alanine aminotransferase, 15 U/L; and C-reactive protein, 0.96 mg/dL. Routine urine analysis revealed a pH of 6.0 and trace proteins. Red and white blood cells were absent in the urine. The spot urine protein/creatinine ratio was 209 mg/g and the spot urine albumin/creatinine ratio was 60 mg/g. Thyroid function tests were normal: thyroid stimulating hormone, 2.47 μIU/mL and free T4, 0.98 ng/dL. Fractional excretion of Na 0.1% and Fractional excretion of urea on admission was 17.6%, which suggested the patient was prerenal AKI.
Chest radiography and echocardiogram findings were normal. During doppler sonography of both lower extremities, the venous velocity was normal and there was no evidence of thrombosis. None of the aforementioned findings were suggestive of refractory edema.
Fluid therapy was administered to treat the AKI, which was probably caused by the diuretics he was given during his two-week stay in the local clinic. Subsequently, his renal function improved: serum creatinine, 1.18 mg/dL; and eGFR, 63.9 mL/min/1.73 m2. Since the redness and tenderness of both legs were suggestive of cellulitis-associated edema, intravenous cefazolin was administered for two weeks. However, the lesion gradually spread from his ankle to his thigh and changed into fibrotic induration. Contracture of the ankle and knee joints also occurred ().
To detect diffuse or localized systemic sclerosis, antinuclear antibody, anti-Scl 70 antibody, and anti-centromere antibody tests were performed, but the results were all negative. Also, eosinophilia and paraproteinemia was not seen, which is commonly accompanied in scleromyxedema or eosinophilic fasciitis. Although approximately 50 weeks had passed since he was exposed to the gadolinium, the characteristic clinical features led to the suspicion of NSF. A biopsy of the right anterior tibial skin lesion was performed to examine tissue for disease. This revealed unique features of the NSF such as dermal thickening with collagen fibers extending into the subcutaneous septa and a large number of spindle-shaped fibrocytes (). Neither eosinophilic tissue infiltration nor fat necrosis with calcification of adipocytes was found.
Systemic methylprednisolone (20 mg/day) was administered for two weeks to treat the NSF. Additionally, UV-A1 topical phototherapy of 1.5 joule (J)/cm2 was administered to the lower leg lesion twice a week. The patient underwent intensive physical therapy including stretching, pneumatic compression, and Transcutaneous Electric Nerve Stimulation . We administered MTX 15 mg weekly while reducing the methylprednisolone dose weekly by half until a dose of 2 mg/day was administered. Simultaneously, the UV-A1 intensity was gradually increased to 3.0 J/cm2. After 6 months of treatment, the reddish edema improved and the skin induration decreased. Although the contracture of the ankles was still present (), there was no further disease progression. Currently, the patient receives MTX (10 mg) weekly and methylprednisolone (2 mg) daily.
Informed consent for publication of clinical data was submitted by the patient and the images are published with the consent of the patient.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [161.3, 'cm']}",58.05913,55.15617,60.96209,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 161.3 cm, which is 161.3 cm * 0.393701 in/cm = 63.50397 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (63.50397 (in inches) - 60) = 58.05913 kg.
Hence, the patient's IBW is 58.05913 kg."
3884,10,Ideal Body Weight,physical,decimal,pmc-4879802-1,Extracted,"A full term female neonate born out of a nonconsanguineous marriage by cesarean section (indication-previous cesarean section with polyhydramnios) to a 25-year-old (weight – 58 Kg, height – 155 cm) booked G3P1L1A1 with unremarkable antenatal history. There is no significant history of drug intake. Family history revealed that the father has radial ray deformity of left upper limb without any cardiac anomaly.
Physical examination revealed an active baby weighing 2790 g and length of 49 cm, heart rate of 146/min, blood pressure of 70/30 mm of Hg, respiratory rate of 40/min, and systemic oxygen saturation of right upper limb being 83% in room air and that of right lower limb being 74% in room air []. On musculoskeletal examination, left upper limb shortening was noticed with absent radius bone, radial flexion deformity of the wrist and also absent thumb []. Triphalangeal thumb was seen in the right upper limb []. No obvious deformities were noticed elsewhere. On cardio-vascular system examination, the pansystolic murmur of grade III at the mitral and left parasternal area was heard. Per abdominal and respiratory system examination was within normal limits.
On further investigation, chest X-ray showed normal thoracic situs with cardiomegaly, plain radiograph of both upper limbs revealed absent radius on left side with absent carpal bones and absent first metacarpal bone and phalanges (thumb), right side showing absent carpal bones and triphalangeal thumb []. No obvious bony deformities elsewhere were noted.
The baby developed cyanosis couple of hours after delivery, following which an ECG was done which was normal and a 2D echocardiography was done which revealed severe aortic atresia with hypoplastic arch, large perimembranous VSD and ASD as well []. These findings were confirmed by coronary angiography. The neonate was referred to a cardiac center for further management, however due to lack of resources the baby died on day 4 of life.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3885,10,Ideal Body Weight,physical,decimal,pmc-3982982-1,Extracted,"A 53-year-old married man (weight: 85 kg, height: 187 cm, body mass index: 24 kg/m2) presented with a history of nasal obstruction for two years. Otorhinolaryngologists planned a septoplasty operation under general anesthesia for him. He had not had any prior operation under general anesthesia, so he did not have any history of difficult intubation, and he did not have any chronic systemic disease. The patient was evaluated for obstructive sleep apnea syndrome (OSAS) with a comprehensive questionnaire on his sleeping habits and medical history; no complaints or predictors pertaining to OSAS were identified.
The patient’s preoperative airway assessment was normal, Mallampati class was II, thyromental distance was 7 cm, inter-incisor gap was 5 cm, and head extension was >35°. His physical examination was characterized by lack of secondary sexual characteristics and presence of fine facial wrinkles. Although, as previously indicated, the patient was married, he had had no children. He had consulted urologists, and primary infertility and erectile dysfunction had been diagnosed. His hormone profile was: testosterone 0.3 ng/mL (reference range 1.75–7.81), free testosterone 0.91 (reference range 4.5–42.0), prolactin 1.31 ng/mL (reference range 2.64–26.72), luteinizing hormone (LH) 0.33 mIU/mL (reference range 1.24–103.03). His thyroid hormone levels were normal. No other pathological finding was obtained as the result of magnetic resonance imaging of the pituitary gland. Thus, the patients was diagnosed with primary hypogonadotropic hypogonadism.
He was admitted to the operating theater, and following the induction of anesthesia with a dose of 5 mg/kg intravenous thiopental, bag-mask ventilation was barely sustained. Fentanyl (1–2 μgr/kg) and, as a muscle relaxant, rocuronium (0.6 mg/kg) were administered. While the patient’s head was in the sniffing position, direct laryngoscopy and intubation of the trachea were attempted three times with different sizes of Macintosh and Miller blades by an assistant professor of anesthesiology with 5 years’ experience. However, unfortunately, the intubation failed. The lungs were then ventilated with 100% oxygen via a face mask in order to avoid desaturation. Glottic visualization was assessed with Cook’s modification of the Cormack–Lehane classification; a grade of 3A (with direct laryngoscopy, only the epiglottis can be visualized; the epiglottis can be lifted using an introducer or bougie) was assigned. The patient was subsequently successfully intubated with a gum-elastic bougie.
After the operation, the patient was extubated successfully without any complication and then examined by otorhinolaryngologists via fexible laryngoscopy. The epiglottis was found to be in a slightly lower than normal position ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [187.0, 'cm']}",81.33081,77.26427,85.39735,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 187.0 cm, which is 187.0 cm * 0.393701 in/cm = 73.62209 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (73.62209 (in inches) - 60) = 81.33081 kg.
Hence, the patient's IBW is 81.33081 kg."
3886,10,Ideal Body Weight,physical,decimal,pmc-8651153-1,Extracted,"We discuss a 45-year-old Saudi woman with no known chronic conditions. She came to the emergency department at King Khalid Hospital in Hail, Saudi Arabia (SA), complaining of progressive fatigue and dizziness for two months. Her fatigue was exacerbated by minimal physical activity and associated with palpitations and dyspnea. She also had a history of appetite decline and weight loss for six months. She denied any recent traumas, bleeding, fever, or night sweats. She denied any history of abdominal or pelvic pain. Apart from that, her past medical and surgical history was unremarkable, and she had no previous admissions or similar complaints. She was not on any medications. There was no history of similar conditions in the family. Regarding the patient's gynecological history, she stated that her menstrual periods had changed in the last two years. They became abnormally long, lasting for more than a week most of the time, with heavy fresh blood flow and intense menstrual pain. She had to change her pads more frequently than usual, but the frequency of her cycles was regular. Regarding her obstetric history, the patient had four normal pregnancies, with full-term deliveries by cesarean section, without complications.
On clinical examination, she was conscious, alert, and oriented to time, place, and person. She showed no signs of dyspnea and was able to speak comfortably in full sentences. The patient had notably pale skin and conjunctivas. Her extremities were cold, but no nail changes were detected. Her vitals: temperature 36.9°C, blood pressure 96/50 mmHg, a pulse of 98 beats per minute, oxygen saturation (SpO2) 99 percent with room air, and a respiratory rate of 21 breaths per minute, with a weight of 50.7 kg, and a height of 155 cm. The abdominal examination revealed a soft and lax abdomen with no organomegaly or palpable masses. Both the cardiovascular and neurological examinations yielded normal findings. For the musculoskeletal and neurological examinations, the patient was ambulatory, with bilateral, active, full-range motion in both upper and lower limbs, along with normal sensation. The patient was offered a pelvic examination, but she refused.
For initial assessment, a complete blood count (CBC) was done and revealed a severely low hemoglobin level of 3.0 g/dL. The result was verified after CBC repetition. A pregnancy test was ordered, which was negative. The patient was admitted under medical care. Table summarizes CBC laboratory results ordered upon her arrival. Hematocrit was 12.0%, and hemoglobin was severely low at 3.0 g/dL. Her results for mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC) were 59.1 fL, 14.8 pg, and 25.0 g/dL, respectively. The red cell count was 2.03 x1012/L, with a red cell distribution width (RDW) of 19.5%. These findings, with the peripheral blood smear, were consistent with microcytic hypochromic anemia.
Table shows chemistry lab results. The serum ferritin level was extremely low, at 1.93 ng/mL. Further investigations, including coagulation profile, liver function test (LFT), fecal occult blood test, and chest X-ray, were all unremarkable.
We performed a transvaginal ultrasound (Figure ), revealing heterogeneous well-defined uterine lesions. The patient was eventually diagnosed with intramural uterine fibroids, complicated with life-threatening IDA.
During her two-day hospital stay, she was given four units of packed red blood cells. She received a total of 1,000 mg ferrous sulfate intravenous therapy, beginning during her hospital stay and continuing in the clinic after discharge. Before that, her hemoglobin level reached 9.1 g/dL. When she returned for a follow-up visit after one week, she felt much better, and her symptoms had resolved. She was referred to the gynecological department for definitive management, given oral iron supplements, multivitamins, and long-term follow-up. After partial correction of the anemia, the patient was admitted under gynecological care, with a total hysterectomy done.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3887,10,Ideal Body Weight,physical,decimal,pmc-4855041-1,Extracted,"The 27-year-old Korean woman with no underlying disease or medical history volunteered in this research to improve obesity. She visited outpatient department of family medicine on October 1, 2013. According to anthropometric measurements, she was 1.73 meters tall with body mass index (BMI) of 23.2 kg/m2 with weight of 69.5 kilograms. The WHO Regional Office for the Asia Pacific Region recommends defines obesity by a BMI ≥ 25 kg/m2 and overweight by BMI above 23 kg/m2 and below 25 in Asians. The Korean Society for the Study of Obesity also adopted the WHO-recommended definition to study the cutoff of BMI for obesity-related disease []. Now, Korean government organizations officially use this definition when defining and implementing health policies regarding obesity in Korea.
After verifying obesity test results, she was explained about the research in detail and asked to compose a meal record for three days prior to the test. The result from the hospital's dietician showed the causes of overweight are frequent drinking and meat consumption at late evening hours.
To determine the diet responsible for the weight loss, change in the intakes of total calorie, carbohydrate, and fat (especially animal fat) were analyzed based on the diet history of the case. The result showed that overall intakes of total calories, carbohydrate, and protein were evenly decreased after the diet intervention, and the reduction in large amount of animal fat was observed by cutting down the consumption of fish and meat.
She regularly participated in hazardous drinking twice a week. The amount of alcohol she consumes at once is approximately total of 95 grams; from 30 grams in 4.5 glasses of Soju and 65 grams in 9 cups of beer. Blood and urine tests were performed to determine whether comorbid conditions associated with drinking habit. The results confirmed normal except for mild anemia (Hemoglobin, Hb 11.6g/dL) and mild increases in aspartate aminotransferase (AST; 58IU/L).
In detail, frequent intake of carbohydrate= and excessive consumption of fish, meat, bread, ice cream, etc. at late evening hours was noticed. However, after the diet intervention, she put efforts to reduce food intake and select vegetable side dishes and fruit as a replacement for snacks, thus, average consumption of calories, carbohydrates, protein, and animal fat decreased ().
Additionally, decrease in frequency of food intake with high in sodium such as soup or stew was observed. Changed behavior in alcohol consumption cannot be determined by the short study period; however, a consultation confirmed that she managed to reduce her alcohol intake by approximately 50 percent.
For 47 days, she was administered an improved diet with breakfast and dinner with less meat and reduction of alcohol consumption and frequency by 50% and once a week, respectively. At the second follow-up, her weight has reduced to 66.5 kilograms. Compared to the initial weight at the first visit, she lost 3 kilograms.
The request on case's fecal sample analysis was submitted to Chunlab, Inc. prior to participating in diet improvement research. After the 47 days of research, the case's fecal sample was again collected on November 19, 2013 to compare the distribution of intestinal micro flora with the first sample. The Seoul National University-Boramae Hospital Institutional Review Board approved this study.
Bacterial DNA was extracted from the fecal samples of subjects before and after the treatment using a FastDNA SPIN extraction kit (MP Biomedicals, Santa Ana, CA, USA). Gut microbiota were compared before and after the treatment using the high-throughput sequencing technique. Obtained sequences from the pyrosequencer were analyzed according to previous descriptions []. The shift of gut microbiota was clearly observed after the diet correction. The compositions of phyla and genera were compared between before and after the diet correction. Firmicutes was predominant phylum (75.7% of total microbiota) before the diet correction, whereas Firmicutes (47.3%) and Bacteroidetes (47.7%) were dominant phyla after the diet correction. In sample collected before the diet correction, genera of Faecalibacterium (14.9% of total microbiota), Roseburia (14.8%), Blautia (9.5%) and Lactobacillus (9.1%) within Firmicutes, and Prevotella (15.0%) within Bacteroidetes were dominant members of gut microbiota. After the diet correction, the relative abundance of Prevotella (42.1% of total microbiota) and Megasphaera (10.7%) within Firmicutes was observed, while those of Faecalibacterium (8.6%), Roseburia (1.2%), Blautia (3.0%), and Lactobacillus (1.7%) were decreased. The proportion of Bacteroides (4.4%) within Bacteroidetes was also increased after sample ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.73, 'm']}",64.15362,60.94594,67.3613,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.73 m, which is 1.73 m * 39.3701 in/m = 68.11027 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (68.11027 (in inches) - 60) = 64.15362 kg.
Hence, the patient's IBW is 64.15362 kg."
3888,10,Ideal Body Weight,physical,decimal,pmc-4823414-1,Extracted,"A 31-year-old male patient (height 173 cm, weight 70 kg) with no medical history of particular significance had been receiving treatment at a dermatology clinic for ten years for erythematous patches accompanied by non-painful itching in both nasal alar creases, both perioral areas, and both posterior auricular folds (). A topical steroid treatment was chosen, as he had tested negative on the KOH test. The steroid treatment alleviated the symptoms but could not eliminate them completely. It was notable that even on the steroid treatment, skin lesions appeared when he consumed alcohol or was dehydrated. The patient was on the topical steroid treatment when he visited our hospital, and erythematous patches were visible in the nasal alar creases and perioral areas. As a previous study had reported a case of acne vulgaris treatment with SGB [], and the mechanisms of acne vulgaris and seborrheic dermatitis are presumed to be similar, we determined to use SGBs on this patient. An anterior blind approach was selected. The patient was positioned with the anterior spine extended, so that the transverse process of the C6 vertebra (Chassaignac's tubercle) could be easily detected. A needle was vertically inserted at the anterior tubercle and was placed on the transverse process. Five ml of 1% mepivacaine were injected after fixing the needle in position and confirming that there were no abnormal sensations in the upper limb or blood aspiration []. The same procedure was performed daily, on one side each day. After administration of the injection on one side, ipsilateral ptosis and nasal obstruction occurred but faded about two hours later. The skin lesions disappeared within three days, after which the patient wished to stop the treatment for personal reasons. However, the patient revisited the hospital two months later due to a relapse. During the follow-up, the patient noted that there had been no symptoms up to one week before the revisit. We initiated the same treatment procedure and the patient's skin lesions disappeared after five trials (). Fifty more trials were performed, and the patient has not seen a relapse of the symptoms or side effects since.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.0, 'cm']}",68.65362,65.22094,72.0863,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.0 cm, which is 173.0 cm * 0.393701 in/cm = 68.11027 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.11027 (in inches) - 60) = 68.65362 kg.
Hence, the patient's IBW is 68.65362 kg."
3889,10,Ideal Body Weight,physical,decimal,pmc-4644167-4,Extracted,"A 50-year-old female weighing 60 kg and 1.60 m height (BMI 23.4). Clinical evaluation confirmed osteoarthritis of the right knee. Pretreatment KOOS subscale scores of Pain 64; Symptoms 21; ADL 81; Function in Sport/Rec 10, and knee-related QOL 25 were reported (). Initial functional assessment by the SCT and GUG test confirmed an RPE of 8 of 5, respectively for the right knee. The patient was given a single dose of SVF (6.0×107) cells and 3 mL of PRP to the right knee following extraction from the patient’s own lipoaspirate. The patient received further injections of PRP into the knee at the 2nd, 3rd, and 4th month. Three months posttreatment the patient began an exercise program consisting of water- and land-based exercises. KOOS scores improved to normal (100) in all five subscales (). Measures of functional assessments using the SCT and GUG test indicated a normal exertion score of 0, ( and , respectively).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.6, 'm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.6 m, which is 1.6 m * 39.3701 in/m = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3890,10,Ideal Body Weight,physical,decimal,pmc-6984193-5,Extracted,"A 13-year-old boy was presented to our hospital with complaints of dizziness and upper abdominal pain. On admission, the BH and BW were 153 cm and 38.3 kg, respectively. Blood testing revealed anemia (hemoglobin 9.2 g/dL), and the FOBT was positive (). Since melena was observed on hospitalization, we performed a US, which revealed a mass-like region surrounded by a blood vessel () that appeared to be connected to the duodenum. The HH sign was not observed. No remarkable findings were found in the CT image. In the endoscopy, the ulcer was identified at a site between the anterior and posterior bulb. A US performed 20 days after treatment revealed that the mass-like lesion disappeared.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [153.0, 'cm']}",50.54337,48.0162,53.07054,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 153.0 cm, which is 153.0 cm * 0.393701 in/cm = 60.23625 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (60.23625 (in inches) - 60) = 50.54337 kg.
Hence, the patient's IBW is 50.54337 kg."
3891,10,Ideal Body Weight,physical,decimal,pmc-5385993-1,Extracted,"A 14-year-old girl was admitted to our emergency department with a four-day history
of generalized myalgia, muscular weakness and dark urine. On the day of admission,
she noted much-reduced diuresis and had difficulty walking. During the previous
days, the patient had been participating in a dance festival in hot conditions.
There was no past history of muscle cramps or hospital admissions due to
rhabdomyolysis. She was the only child of non-consanguineous parents.
At presentation, she was dehydrated. Her blood pressure was 120/60 (90th
percentile). Her muscle strengths in the proximal and distal muscles of the upper
and lower extremities were 4/5. Deep tendon reflexes were normal, and there was no
neurologic deficit. The remainder of her physical examination was normal. Her weight
was 57kg, and her height was 165cm.
The laboratory evaluation revealed ARF with a blood urea nitrogen of 263mg/dL (range
19.3 - 44.9mg/dL), a blood creatinine of 9.59mg/dL (range 0.60 - 1.30mg/dL) and a
glomerular filtration rate calculated according to the original Schwartz formula of
11.6mL/min/1.73m2. The blood gases showed metabolic acidosis (pH
7.30; HCO3 17.7mmol/L; base excess - 7.9; lactate 1.4mmol/L). Blood
biochemistries were as follows: sodium 129mmol/L (range 136 - 145mmol/L), potassium
6.12 (range 3.4 - 5.1mmol/L), ionized calcium 1.03mmol/L (range 1.13 - 1.32mmol/L),
phosphorus 9.3mg/dL (3.1 - 5.5mg/dL), magnesium 1.8mg/dL (range 1.6 - 2.3mg/dL),
myoglobin 28173mg/dL (range 9 - 82mg/dL), creatine kinase > 400,000UI/L (range 28
- 142UI/L), aspartate aminotransferase 3266UI/L (range 0 - 26), alanine
aminotransferase 1310UI/L (range 19 - 44UI/L).
Because of massive rhabdomyolysis, the patient was admitted to our pediatric
intensive care unit and was given intravenous fluid combined with diuretic therapy
to reverse ARF, glucose and insulin therapy to correct hyperkalemia and calcium
gluconate to prevent cardiac arrhythmias secondary to ion changes. During the first
hours of admission, she presented anuria that was unresponsive to medical therapy.
After eight hours of receiving supportive therapy, she was started on continuous
veno-venous hemodiafiltration (Gambro Prismaflex® System, Lisbon;
Portugal).
A hemodialysis catheter (12F; triple lumen) was inserted in the right femoral vein.
Hemodiafltration was performed using the hemofilter ST 60, and heparin was the
anticoagulant chosen. The following initial settings were used: blood-pump
150mL/min, dialysate (Prismasol 4®) 1000mL/hr, pre-filter
replacement solution (Prismasol 4®) 500mL/hr, post-filter
replacement solution (Prismasol 4®) 500mL/hr and fluid removal
50mL/hr. During the first two days of therapy, the main problem with
hemodiafiltration was easy coagulability of the hemofilter due to high levels of
myoglobin in circulation. To overcome this problem, higher pre-dilution flow rates
were used (maximum 1500mL/h). After 48 hours, she had asymptomatic hypophosphatemia
of 2.7mg/dL that was corrected after adding phosphorous to the replacement
solutions. On day 5, intermittent hemodialysis was started, and three sessions on
alternate days were performed. A calcium antagonist was prescribed on day six due to
worsening hypertension.
Signs and symptoms were controlled with medical treatment and renal replacement
therapy. Creatinine kinase and myoglobin returned to normal values in two weeks. Her
diuresis started to recover after the second day of therapy. At discharge, her renal
function was recovering, and she had a glomerular filtration rate of
88.9mL/min/1.73m2.
Regarding the investigation of the underlying insult, an acylcarnitine analysis by
tandem mass spectrometry of the patient's dried blood spot revealed a deficiency of
very long-chain acyl-CoA dehydrogenase (VLCAD). A genetic study revealed the
following mutations in compound heterozygosity of the VLCAD gene: p.P65Tfs*7 (c.
187_192insA) and p.R336H (c.1097G > A).
Frequent meals with carbohydrate-rich intake before exercise and restriction of
long-chain fatty acids intake along with medium-chain fatty acid supplementation
were recommended to prevent further attacks.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3892,10,Ideal Body Weight,physical,decimal,pmc-6477550-1,Extracted,"A 16-year-old female adolescent was referred to our hospital with severe hypertension (systolic pressure 178 mmHg), which was first detected 7 months prior to presentation during a routine annual physical examination. She complained of intermittent headache for about 1 year, and her previous blood pressure, measured 1 month prior to her detection of hypertension, had been normal. She showed mild hypokalemia (3.4 mmol/L) in a routine blood test, and an additional workup considering secondary hypertension was planned. Despite taking amlodipine (0.1 mg/kg twice a day), her blood pressure remained uncontrolled.
Upon admission to our hospital, her systolic and diastolic blood pressures were 155 mmHg (>99th percentile) and 111 mmHg (>99th percentile) respectively. She was 162.8 cm tall (50th–75th percentile) and weighed 55 kg (50th–75th percentile). Physical examination including ophthalmological examination revealed no abnormality other than hypertension, and her family history was negative for hypertension or renal diseases. Laboratory examination revealed normal levels of hemoglobin (14.4 g/dL), serum creatinine (0.57 mg/dL), serum total cholesterol (144 mg/dL), and normal urinalysis. Serum sodium, potassium, chloride, and total carbon dioxide levels were 134 mmol/L, 3.4 mmol/L, 102 mmol/L, and 27 mmol/L, respectively. Plasma renin activity was 9.83 ng/mL/hr (normal, 0.5–3.3 ng/mL/hr), and serum aldosterone level was 77.3 ng/dL (normal, 4–48 ng/dL). Urinary levels of vanillylmandelic acid, epinephrine, norepinephrine, dopamine, metanephrine, and normetanephrine were normal, and plasma levels of epinephrine, norepinephrine, and dopamine were also normal. Chest radiography, electrocardiography, and echocardiography showed normal findings. Renal Doppler ultrasonography revealed an avascular bilobed cyst in the lower pole of the right kidney (). Abdominal computed tomography (CT) angiography showed bilaterally normal renal arteries and an eccentric soft tissue component at the peripheral aspect of the cystic lesion (). The mass remained unenhanced during the arterial phase, and its margin was indistinguishable from the surrounding tissue (). During the delayed phase, its eccentric capsule showed enhancement, and an intact mass could be observed (), consistent with CT findings of JGC tumors.
A right partial nephrectomy was performed, and a clear resection margin was identified. The well-encapsulated mass measured 2.5 cm ×2.2 cm×2.0 cm in size with a partially cystic-appearing cut surface. Microscopic examination revealed sheets of polygonal tumor cells with amphophilic cytoplasm. Immunohistochemical examination showed that the tumor cells stained positive for CD34 and focally positive for CD117 (C-Kit) and smooth muscle actin. ()
Postoperatively, her blood pressure returned to normal (105/63 mmHg) without using any antihypertensive medication. On the 3rd postoperative day, the plasma renin activity (0.52 ng/mL/hr), serum aldosterone (3.9 ng/dL), and serum potassium (3.6 mmol/L) levels returned to normal. Her blood pressure and laboratory findings remained within the reference range over the next 3 years postoperatively until her last follow-up.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [162.8, 'cm']}",54.9174,52.17153,57.66327,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 162.8 cm, which is 162.8 cm * 0.393701 in/cm = 64.09452 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.09452 (in inches) - 60) = 54.9174 kg.
Hence, the patient's IBW is 54.9174 kg."
3893,10,Ideal Body Weight,physical,decimal,pmc-8489098-1,Extracted,"We saw a 59-year-old White female patient with a history of sarcoidosis at the outpatient department in early September 2012. On first sight, the left side of her face was significantly swollen, and she had pain in the preauricular area. The condition had started a few days earlier with swelling of the lips and progressed to left-sided facial edema and unilateral painful preauricular mass.
C-reactive protein was elevated at 54 mg/l (normal concentration up to 5mg/l). Transaminases, cholestasis and retention parameters, urinalysis, and microbiological findings were unremarkable. At this time, the patient was treated with 1 mg tacrolimus 1-0-0, 20 mg leflunomide 1-0-0, and 7.5 mg prednisolone.
For clarification, an inpatient admission to our tertiary center was arranged.
During the clinical examination, we saw a patient in moderate general condition and obese nutritional status with a body weight of 104.7 kg and a height of 168 cm. The patient did not show temperature elevation. Blood pressure was normal at 120/80 mmHg, and pulse rate was 80 beats/minute. On oral examination, the patient showed tender firm swelling of lips, erythematous and swollen gingiva of the upper and anterior teeth, and fissured tongue. In addition, there was generalized gingivitis, and the left side of the face was also markedly swollen and red. Furthermore, there was left-sided fascial paresis. There was no evidence of mouth sores, and odontogenic infections were ruled out. The eyes did not show any pathology. The heart rhythm was regular, the heart sounds S1/S2 were pure, and there were no heart murmurs. Examination of the lungs was without pathological findings. Pressure pain in the area of the abdomen could not be triggered, there was no organomegaly, and bowel sounds were unremarkable. Peripheral edema was absent on both sides, and no calf pressure pain could be induced. The joints were unremarkable. The neurological examination was regular except the facial palsy.
Magnetic resonance imaging of the neck on admission showed an enlargement of the left parotid gland with enhancement of contrast medium susceptive of abscess formation. Furthermore, on magnetic resonance imaging, there was a suspicion of a necrotic melting in the left parotid gland, which was displayed with a total extension of approximately 4–5 cm in the three spatial directions. The meltings are displayed with different signal strengths T2-hyperintense and T1-hypointense, and showed both marginal and septal internal contrast enhancement at this time. The findings further included the ramus mandibulae from the dorsal side and extended medially to the pterygoid muscles and laterally to the masseter muscle. The masseter muscle partially showed adjacent contrast enhancement with suspected inflammatory co-reaction. The angle of the jaw showed only small lymph nodes on both sides (Fig. ).
After surgical excision of the abscess formation and systemic antibiotic therapy, the patient developed soft-tissue ulceration in pre- and retroauricular area (Fig. b). A few days later, a left-sided peripheral facial palsy developed (Fig. a). The peripheral left facial palsy was due to swelling and inflammation from parotitis and developed independently of surgery.
No bacteria could be isolated from several wound swabs. Immunoglobulin M (IgM) antibody titer and polymerase chain reaction (PCR) for herpes simplex virus were negative. In addition, a PCR for atypical mycobacteria was done, and again the test was negative. IgM antibody titer and PCR for herpes simplex virus were negative.
Histopathological examinations of the parotid gland revealed necrotizing tissue but also epithelioid granulomas. Malignancy could be excluded.
At that point, a systemic corticosteroid therapy with methylprednisolone 500 mg daily for 3 days was given with no significant improvement of the soft-tissue ulcerations. Therefore, a parotidectomy was performed. Microbiological examinations on bronchoalveolar fluid were negative for pathogenic species. Serological tests such as tuberculosis were also negative. The patient did not report intestinal problems at any time that would have suggested Crohn’s disease. Hence, a colonoscopy did not seem to be justified.
This condition appeared under an immunosuppressive therapy with leflunomide 20 mg once a day in combination with 1 mg tacrolimus daily starting due to pulmonary sarcoidosis, diagnosed 2 years earlier.
The patient was known to have autoimmune thyroid disease with hypothyroidism prior to the diagnosis of sarcoidosis. In addition, the patient had a history of kidney stone disease and had undergone surgery on the menisci of both knee joints. The patient has an allergy to amoxicillin, and did not have any pregnancies. She has never smoked or had significant alcohol consumption. There was no history of tuberculosis. The patient worked as a commercial employee and was continuously working in the office and not exposed to any noxae.
In October 2009, the patient had a severe feeling of illness with a body weight loss of 15 kg, bloody sputum, and a marked tendency to sweat. Bronchoscopy initially revealed chronic florid inflammation with epitheloid-cell-containing granulomas. Despite slightly elevated antineutrophil cytoplasmic antibody (c-ANCA), there was no evidence of granulomatosis with polyangiitis. Malignancy could also be excluded. From December 2009, the patient was treated with glucocorticoids, and as there was only partial remission in January 2010, the patient was treated with azathioprine for 4 months. Since there was insufficient improvement while taking azathioprine, therapy was switched to methotrexate in May 2010. Methotrexate was then used for a total of 11 months. With disease activity not adequately controlled, methotrexate was discontinued in February 2011, and oral cyclophosphamide was started after four courses of cyclophosphamide pulse therapy. After oral cyclophosphamide therapy, the patient was switched to tacrolimus and leflunomide in September 2011. Recurrent gingivitis occurred from summer 2012 onward. Beside recurrent gingivitis, the patient had orofacial edema and lip swelling as well as a fissured tongue in the past. The final diagnosis based on clinical and histopathological findings was MRS in the context of sarcoidosis.
After treatment with systemic steroids, the labial and facial swelling improved. However, the preauricular ulcerations did not respond to this treatment. At that point of time, the medication with clofazimine 100 mg per day was initiated, which was well tolerated. After 4 weeks of therapy, the tissue ulceration resolved gradually, so that 150 mg of clofazimine three times a week was given for 15 weeks (Fig. ). After that, clofazimine treatment could be stopped. During 7 years of follow-up, there was no recurrence (Fig. a, b).
During the course of the 4-month successful therapy with 150 mg clofazimine 1-0-0, the underlying disease was treated with rituximab. Initially, induction therapy was given with 4 × 375 mg at weekly intervals followed by B-cell and immunoglobulin-controlled therapy. Starting from June 2013, rituximab has been given in combination with 15 mg methotrexate once per week.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [168.0, 'cm']}",59.62607,56.64477,62.60737,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.14177 (in inches) - 60) = 59.62607 kg.
Hence, the patient's IBW is 59.62607 kg."
3894,10,Ideal Body Weight,physical,decimal,pmc-3659367-1,Extracted,"A 22-year old female (height 158 cm, weight 43 kg, BMI 17.22) presented with a 1.5 year history of dysphagia in the retrosternal area. Initially, her dysphagia could be alleviated within 1–3 min by drinking warm water. Six months before hospital admission (Renmin Hospital of Wuhan University), her dysphagia became more frequent (once every 2–3 weeks), lasting for up to 10 min and could not be relieved by drinking warm water. The retrosternal chest pressure was relieved by regurgitation. These episodes were associated with hypersalivation and profuse sweating. Heartburn and retrosternal chest pain were frequent. Three weeks prior to hospitalization, she was unable to tolerate any solid food orally.
Physical examination showed no focal abnormality. Complete blood count, liver biochemistry, electrolytes and creatinine were normal. An upper gastrointestinal barium swallow study showed typical features of achalasia, demonstrating the bird's beak sign, no barium passed into the stomach during the investigation. Endoscopy, performed after two days of fasting, showed no mucosal abnormality although there was an increased resistance passing the endoscope through the LES.
Esophageal manometry using a 8-channel water perfused system with a Dent sleeve for LES pressure, showed high LES pressure and regular spontaneous rhythmic non-propagating contractions in the esophageal body at a frequency of 7/min, with an amplitude between 48 and 51 mm Hg (Figures , ). An initial dry swallow did not affect the contractile activity but two subsequent dry swallows decreased amplitude and frequency (Figure ). Subsequent wet swallows, using 20 ml of warm water, increased the frequency to 8/min and also increased the amplitude (Figure ). Drotaverine hydrochloride (40 mg intramuscular) was given to reduce the LES pressure; this markedly reduced the contraction frequency from 7 to 3/min without a significant effect on the amplitude; a subsequent wet swallow increased the frequency to 9/min and also increased the contraction amplitude (Figure ). Significant swallow-induced LES relaxation was still present.
Pneumatic balloon dilatation of the LES was performed uneventfully. The balloon was 35 mm in diameter, 80 mm in length, obtained from EndoFlex Germany. A small amount of blood was seen on the balloon after the dilation procedure. Omeprazole 40 mg iv daily was administered for 3 days. Thereafter the diet was advanced gradually as tolerated. By day 5, liquid meals passed down the stomach without pain. The patient was discharged 7 days after the dilatation. At the 23-month follow up visit, she reported a normal eating habit without any gastrointestinal symptoms.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3895,10,Ideal Body Weight,physical,decimal,pmc-7954628-1,Extracted,"A 33-year-old G4P3 woman at 24 weeks and 1 day of gestation presented for prenatal repair of fetal myelomeningocele. The fetal abnormality was discovered during routine prenatal ultrasound exam and confirmed with magnetic resonance imaging (MRI) scan. Past medical history was significant for postpartum preeclampsia, mild intermittent asthma, depression, and chronic hypertension. After extensive counseling with various fetus medicine specialists including the fetal surgery team on the risks and benefits of in-utero surgery, the patient decided to proceed with prenatal surgery. Physical exam and blood tests were within normal limits on the day of surgery. The patient's weight was 90.7 kg, height was 172.7 cm, and the estimated fetal weight was 0.630 kg.
Standard monitoring devices were used. A lumbar epidural catheter was placed uneventfully, followed by induction of general anesthesia and uncomplicated intubation of the trachea. A radial arterial catheter was then placed in the left arm. General anesthesia was maintained with sevoflurane 3.3–4% end-tidal concentration. Muscle relaxation was maintained with rocuronium. A loading dose of 6 g of magnesium sulfate (2 g prior to uterine incision and 4 g before uterine closure) followed by a continuous infusion (1 g/hr) was given to suppress uterine contractions. Hypotensive events were treated by a continuous infusion of phenylephrine at a rate of 20–40 mcg/min. Fetal anesthesia was reinforced with intramuscular injection of fentanyl 10 mcg and vecuronium 0.1 mg. The myelomeningocele defect was repaired in 69 minutes ().
The fetal heart rate was monitored via ultrasound and was stable throughout the entire surgery. The uterine tone, which was assessed manually by an experienced Maternal-Fetal Medicine (MFM) specialist, was low during the uterine exposure. An epidural infusion consisting of bupivacaine and hydromorphone solution was initiated at the end of the operation. The patient received 900 ml of crystalloid solution, urine output was 300 ml, and the estimated blood loss was 50 ml. Muscle relaxation was reversed with sugammadex. The patient awoke from anesthesia, was extubated, and was transferred to the postanesthesia care unit (PACU). The surgical duration was 143 minutes, and no procedural complications were reported.
Upon arrival in the PACU, oxygen was given via nasal cannula and pain was well controlled with epidural analgesia. A continuous infusion of phenylephrine was initiated to minimize hypotension. The fetal heart rate and uterine contractions were monitored with cardiotocography. Thirty minutes after admission to the PACU, a significant increase in the frequency of uterine contractions required an additional dose of 2 g of intravenous magnesium sulfate. The frequency of uterine contractions did not change, and the patient complained of shortness of breath in spite of the administration of continuing oxygenation. Oxygen saturation decreased from 100% to 94%, and pulmonary auscultation revealed coarse breath sounds with rales suggesting the onset of pulmonary edema. The nasal cannula was replaced by face mask (10 L/min), magnesium sulfate was discontinued, and 20 mg of furosemide was given.
Nitroglycerine and epinephrine infusions were started (at 1 mcg/kg/min and 0.05 mcg/kg/min, respectively) with the dual goal of slowing uterine contractions and to treat the pulmonary edema. Within the next hour oxygen saturation normalized, urine output increased to 200 ml, uterine contractions became sparse, and shortness of breath disappeared. The epinephrine infusion was discontinued. The nitroglycerine infusion was slowly decreased from 0.5 mcg/kg/min to 0.3 mcg/kg/min with oxygen delivery decreased to 2 L/min. The patient was comfortable, and vital signs were stable. Uterine contractility was controlled, nitroglycerine infusion was discontinued, and the patient was discharged to the maternal unit.
The patient experienced an uncomplicated caesarean section at 36 weeks of gestation. Physical examination of the newborn revealed evidence of wound healing of the skin with the allograft patch. The newborn was able to move his lower extremities without limitations, and a computed tomography of the head revealed resolution of the cerebellar tonsillar descent and stable ventricular size. No neurological sequelae were present.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [172.7, 'cm']}",63.88197,60.68787,67.07607,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 172.7 cm, which is 172.7 cm * 0.393701 in/cm = 67.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (67.99216 (in inches) - 60) = 63.88197 kg.
Hence, the patient's IBW is 63.88197 kg."
3896,10,Ideal Body Weight,physical,decimal,pmc-7359153-3,Extracted,"Severe vasogenic hypertension with severely impaired cardiac function.
A 33-year-old obese mother (162 cm, 95.5 kg, BSA 2.14 m2) with 3 prior pregnancy’s complicated by moderate hypertension, presented at 32 weeks gestational age with severe hypertension, BP 165/95 (MAP = 118) and increasing oedema and leg pitting. The patient was scheduled for a therapeutic induction at 32 weeks gestational age.
Caesarean section delivered small for dates baby, 1550 g at 32 weeks gestational age with an Apgar score at 1 min of 9, at 5 min 7, and at 10 min 9, followed by a 3-day ICU stay.
Summary—Severe vasogenic hypertension, with a severely elevated SVR (2332 v normal 1100 dyne s cm−5). Additionally, there was severe impairment of the SV (46 v normal 79 ml), CO (4 v 6.9 L/min), SMII (1.1 v 2.0 W/m2) and, importantly, DO2 was approximately 60% of normal (594 v 900 ml/m2) (Fig. ).
Physiologically guided therapy would have targeted reducing the SVR with a vasodilator, and an inotrope to stimulate the LV function.
Outcome—The baby, after Caesarean birth, had a depressed 5 point APGAR score, which recovered over the first hour, while the mother required 3 days of ICU care. It is probable that this significant haemodynamic dysfunction would have been expressed in the first trimester and would have been detected by haemodynamic monitoring. This may have led to improved physiologically targeted management and a more stable haemodynamic course through pregnancy and improved outcome.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [162.0, 'cm']}",54.19299,51.48334,56.90264,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.77956 (in inches) - 60) = 54.19299 kg.
Hence, the patient's IBW is 54.19299 kg."
3897,10,Ideal Body Weight,physical,decimal,pmc-6176126-1,Extracted,"A 41-year-old woman was referred to our hospital because of an abnormal shadow on a chest roentgenogram during a medical check-up. She had no complaints. She was a non-smoker and not obese (42 kg, 158 cm tall). Although she had not undergone abdominal or thoracic surgery, she had a history of hyperprolactinemia at the age of 24 years, for which she received hormonal therapy with dopamine agonist for 3 years. Physical findings and laboratory tests were normal except for the prolactin concentration (42.3 ng/mL; reference range: 6.1–30.5 ng/mL). Chest computed tomography showed a 3-cm-diameter cystic tumor in front of the Th10 vertebra (Fig. A and B). Chest T2-weighted magnetic resonance images showed a tumor with homogenous high-intensity signals equal to water, and T1-weighted images showed a hypointense lesion (Fig. ). The patient underwent two-port thoracoscopic tumor resection. The cyst wall was thin and lucent. There was no adhesion or direct communication between the tumor and the spinal cord, tracheobronchial system, esophagus or surrounding tissue.
Histologic examination of the specimen revealed a thin-walled cyst lined by ciliated or non-ciliated columnar epithelium with scant connective tissue and bundles of smooth muscle fibers in the wall. The lesion resembled a paraovarian/tubal cyst. There was no evidence of malignancy (Fig. A and B). Immunohistochemical staining revealed a positive reaction of the lining cells to paired box gene 8 (PAX8), estrogen receptor (ER), progesterone receptor (PgR) and CK7, and a negative reaction thyroid transcription factor 1 (TTF-1), CK20, calretinin and D2-40. Lining fibers under the cyst wall were positive for α-smooth muscle actin (αSMA) but negative for CD10 (Fig. ). The pathological diagnosis was a mediastinal Müllerian cyst. The postsurgical course was uneventful, and the patient was discharged from the hospital on postoperative Day 4.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3898,10,Ideal Body Weight,physical,decimal,pmc-5428599-1,Extracted,"A 27-year-old primigravida (weight 50 kg, height 158 cm) was referred to our hospital on August 2010 with a 37-week gestation due to shortness of breath after a 3-day history of sore throat. She was asymptomatic before 36 weeks’ gestation. The patient complained of a sore throat and cough that started 3 days before admission, followed 1 day later by fever, dizziness, breathlessness, and palpitation on exertion. She reported no medical history except for a fully-recovered acute nephritis 15 years ago. On physical examination, the patient appeared acutely ill, and vital signs were temperature 37.8°C, heart rate 94 beats/min, respiratory rate 28 breathes/min, blood pressure 107/70 mm Hg, and oxygen saturation by pulse oximetry 98% on room air. Auscultation revealed a loud P2 and a grade 4/6 systolic murmur over the precordial region, best heard in the pulmonary area. Breath sounds were low in both lungs, without rales or rhonchi. Her functional status of New York Heart Association (NYHA) was class II–III.
Laboratory tests on the admission day were normal. Transthoracic color Doppler echocardiography revealed an 8 mm × 9 mm aneurysm in the right coronary sinus of Valsalva, protruding into the right ventricular outflow tract (RVOT), with a 4 mm-wide perforation. A high pressure left-to-right jet started from a laceration of aneurysm, the peak flow velocity (PFV) is 5.8 m/s and pressure gradient (PG) is 136 mm Hg. A mild tricuspid regurgitation was present. A 3 mm intracristal ventricular septal defect (VSD) was also present on echocardiography. The left atrium (37 mm) and left ventricle (55 mm) were enlarged. Of note, the size of right atrium (45 mm) and right ventricular (51 mm) were also enlarged. In addition, there was evidence of mild pulmonary hypertension, with an estimated pulmonary artery systolic pressure of 42 mm Hg and an estimated left ventricular ejection fraction of 69% at rest. The functional capacity of patient could not be determined due to bed rest requirement.
The patient asked for cesarean delivery without maternal or fetal indication. Four days after admission, the patient received cesarean delivery under epidural anesthesia.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [158.0, 'cm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3899,10,Ideal Body Weight,physical,decimal,pmc-7598812-1,Extracted,"A 74-year-old male (weight: 66 kg, height: 168 cm) with a 2-year history of left TN was receiving regular carbamazepine (200 mg bid) treatment. However, his symptoms aggravated over the past year. The patient found it difficult to tolerate the side effects of larger doses of carbamazepine (dizziness) and came to seek PBC treatment. The patient had a history of hypertension, and blood pressure was controlled around 140/90 mm Hg under medication. Preoperative electrocardiogram (ECG), chest X-ray, and related laboratory examinations showed no abnormalities. A head magnetic resonance imaging (MRI) showed bilateral trigeminal vascular compression with a more obvious compression on the left side.
After the patient entered the operating room, 12-ECG, SpO2, bispectral index (BIS), and continuous arterial pressure monitoring (Mindray T9, China) were performed. Anesthesia was induced by intravenous injection of midazolam (4 mg), propofol (50 mg), sufentanil (25 μg), and vecuronium bromide (8 mg), with mechanical ventilation after intubation. Anesthesia was maintained by continuous infusion with propofol and remifentanil, maintaining the BIS between 40 and 50. All vital signs were stable after anesthesia.
At the beginning of the operation, 0.5 mg atropine was administered. Sudden sinus arrest (lasting 5 seconds) occurred during puncture; the operation was stopped immediately, and HR quickly returned to normal. C-arm fluoroscopy showed the puncture needle entering the foramen ovale (Fig. ). Due to safety considerations, we administered 0.5 mg atropine again. However, when we reoperated the puncture needle, bradycardia occurred (HR change: 80 to 47 bpm). The HR returned to normal after immediate cessation, while bradycardia recurred (HR changes: 89 to 43 bpm, 74 to 31 bpm) as soon as the puncture needle moved slightly (Fig. ).
For the safety of the patient, we requested assistance from the superior doctor. After the arrival of the professor, 2% lidocaine (1 mL) was injected into the puncture site through the puncture needle. After 3 minutes, we started the operation again. However, transient sinus arrest reappeared (lasting 4 seconds), and the operation was suspended again. The was no improvement after another 2 minutes of waiting, and bradycardia occurred again (HR change: 77 to 49 bpm) (Fig. ). Thus, we decided to try one last time before canceling the operation. Isoproterenol (1 mg + 25 mL normal saline) was continuously pumped to the patient, and the speed was dynamically adjusted to maintain the HR at approximately 90 bpm. Norepinephrine (2 mg) was administered when the blood pressure was below 90/60 mm Hg. We continued the operation again after stabilizing the HR, with only a slight decrease in HR (HR change: 89 to 72 bpm) (Fig. ), and we completed the operation. All medications were discontinued upon cessation of the balloon compression. Intraoperative blood pressure was stable, and mean arterial pressure fluctuated between 60 and 102 mm Hg.
The patient recovered quickly after the operation and was clearly conscious with facial numbness (an indicator of the effectiveness of the operation). No complaints of discomfort were reported after the operation. The postoperative ECG was normal, and the patient was discharged satisfactorily. During follow-up period, the patient showed significant pain relief and no discomfort.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.0, 'cm']}",64.12607,60.91977,67.33237,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg."
3900,10,Ideal Body Weight,physical,decimal,pmc-6478612-1,Extracted,"Abdominal pain and fullness.
The patient was a 52-year-old Asian woman, who was diagnosed with liver dysfunction during a medical examination in her twenties. A diagnosis of autoimmune hepatitis was made at 40 years of age. When the patient was 46 years old, the patient developed ascites, which improved with oral steroids. However, with disease progression, she developed decompensated cirrhosis at 51 years old that was resistant to medical management. She was then referred to our department.
There was no other significant medical history.
The patient was a nonsmoker and had stopped drinking socially 5 years prior. Her occupation was a housewife. There was no relevant family history.
According to the Eastern Cooperative Oncology Group Performance Status, her performance status was 2. At the physical examination, the patient’s height was 155 cm, her weight was 47 kg, and her vitals were stable; yellowish bulbar conjunctivae, ascites, and bilateral pedal edema were observed.
The Child-Pugh score was 11 points in class C, and the Model for end stage liver disease score was 11 points. The serologic tests for CMV showed that the patient was IgG positive (+), IgM negative (-), and AG negative, which is indicative of past CMV infection. A PCR test for CMV was not performed routinely before transplantation at our facility and was not performed in this case.
Abdominal computed tomography (CT) revealed liver cirrhosis with ascites before LDLT.
A blood-type compatible LDLT was performed using a left lobe graft, with the patient’s second son as the donor (20 years old, CMV IgG+/IgM-, which is indicative of past CMV infection). The graft-to-recipient weight ratio was 0.73, the operation duration was 849 min, and the bleeding volume was 822 mL. At our facility, in accordance with the protocol of CMV monitoring and treatment after a liver transplantation, CMV-AG is tested twice a week, but a CMV-PCR test is not performed routinely. In addition, prophylactic ganciclovir (GCV) is not administered, but GCV is initiated when the patient becomes CMV-AG positive or in the case of a seropositive donor.
Initially, cyclophosphamide (CyA), prednisolone (PSL) and mizoribine (MIZ) were used as the postoperative immunosuppressants, in accordance with the protocol of our facility[,], however, for this patient, MIZ was replaced by mycophenolate mofetil (MMF) due to pancytopenia, and CyA was replaced by tacrolimus (FK) due to renal failure. As the patient had jaundice and persistently elevated aspartate transaminase and alanine transaminase levels, a liver biopsy was performed on the 10th day after transplantation. The histopathological examination was negative for both acute cellular rejection (ACR) and CMV hepatitis, so her condition was suspected to be drug-induced or caused by cholestasis.
Starting on the 12th day after transplantation, the patient’s anemia worsened, and she required frequent packed red blood cell transfusions. Further investigations confirmed thrombocytopenia, jaundice, and renal failure. We suspected thrombotic microangiopathy (TMA), even though the peripheral smear was negative for fragmented red blood cells, and a fresh frozen plasma transfusion and FK dose reduction were carried out. The CMV-AG remained negative, and there were no clinical findings that were characteristic of a CMV infection, but prophylactic GCV administration was initiated. Thereafter, the thrombocytopenia gradually improved. On the 20th day after transplantation, the patient reported abdominal pain and black-colored stools, so upper gastrointestinal endoscopy was performed, which showed multiple gastric ulcers (Figure ). A biopsy tissue sample, taken from an ulcer, showed large cells with intranuclear inclusions with hematoxylin and eosin (HE) staining (Figure ), and CMV-positive cells were observed through immunostaining (Figure ). Once the diagnosis of CMV gastroenteritis was confirmed, GCV, which had already been initiated, was continued, and the dosage of all 3 immunosuppressants, FK, PSL, and MMF, was reduced.
On the 26th day after transplantation, the patient had frequent, watery diarrhea, for which a lower gastrointestinal endoscopy was performed, and a deep ulcer was observed in the transverse colon (Figure ). The biopsy tissue diagnosis of the ulcerative lesion revealed large cells with intranuclear inclusions with HE-staining (Figure ) and CMV-positive cells with immunostaining (Figure ). On the 28th day after transplantation, we noted the findings of abdominal pain, fever and an increased inflammatory response. A plain abdominal CT scan revealed intraperitoneal free air adjacent to the transverse colon (Figure ) and hemorrhagic ascites in the pelvis (Figure ).
The patient was diagnosed with gastrointestinal perforation, and an emergency surgery was performed. When the abdomen was incised, contaminated ascites were not observed. In the transverse colon, an impending perforation with a thinned serous membrane was confirmed.
The rejection activity index score of the liver tissues collected during the surgery was found to be P2, B1, and V1 during the histopathologic examination, indicating ACR.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3901,10,Ideal Body Weight,physical,decimal,usmle-3602,Extracted,"A 21-year-old woman comes to the physician for a routine physical examination. She feels well. She is 163 cm (5 ft 4 in) tall and weighs 54 kg (120 lb); BMI is 20.3 kg/m2. Physical examination shows no abnormalities. Her fasting serum glucose concentration is 132 mg/dL. Serum insulin concentration 30 minutes after oral glucose administration is 20 mIU/L (N: 30–230). Her hemoglobin A1C concentration is 7.1%. After a thorough workup, the physician concludes that the patient has a chronic condition that can likely be managed with diet only and that she is not at a significantly increased risk of micro- or macrovascular complications.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [163.0, 'cm']}",55.0985,52.34358,57.85343,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 163.0 cm, which is 163.0 cm * 0.393701 in/cm = 64.17326 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.17326 (in inches) - 60) = 55.0985 kg.
Hence, the patient's IBW is 55.0985 kg."
3902,10,Ideal Body Weight,physical,decimal,pmc-6393920-1,Extracted,"A 66-year-old Japanese man, 177 cm tall and weighing 66 kg (body mass index of 21.1), had been treated for hypertension for more than seven years. He had yearly medical evaluations but was never diagnosed with diabetes (postprandial glucose and hemoglobin A1c [HbA1c] levels in March 2017: 141 mg/dL and 5.4%, respectively). However, results of an annual medical check-up in March 2018 showed remarkable elevation of postprandial glucose and HbA1c levels (265 mg/dL and 11.4%, respectively). The following month (April), he reported symptoms of thirst and polyuria. His postprandial glucose and HbA1c levels on that day were 529 mg/dL and 13.1%, respectively. A high glycoalbumin level (43.2%) also suggested acute glucose elevation (). The patient's anti-glutamic acid decarboxylase antibody test was negative; however, because his postprandial C-peptide level was low (1.15 ng/mL), the patient's pancreas presumably had reduced insulin-secreting capacity. We noted that the patient's daily life had not changed in years; and he had no diabetic complications such as retinopathy, nephropathy, or neuropathy.
To identify the cause of hyperglycemia, we performed several imaging studies. Abdominal computed tomography, magnetic resonance imaging, and magnetic resonance cholangiopancreatography (MRCP) revealed diffuse swelling that extended from the pancreatic body to tail (Figures –). In addition, MRCP showed narrowing of the associated main pancreatic duct (). The patient did not complain of any digestive symptoms such as upper abdominal pain; however, based on the imaging scans and elevation of serum immunoglobulin G4 (IgG4) levels (141.0 mg/dL), we diagnosed him with type 1 AIP.
To control diabetes, the patient began self-administering insulin injections: insulin aspart (Novo Nordisk) three times per day before each meal and insulin degludec (Novo Nordisk) before going to bed. Because tight adjustment of insulin dosage is required for achieving good glycemic control, the patient received a flash glucose monitoring system (Freestyle Libre™; Abbott Diabetes Care, Witney, UK) [] upon initiation of insulin. He initially had considerable ketosis (), but, soon after, the levels of total ketone bodies, acetoacetate, and β-hydroxybutyrate declined to the normal range (36 μmol/L, 12 μmol/L, and 24 μmol/L, respectively). By the end of April, the patient's total insulin dosage was 36 units/day (). In May, prednisolone (35 mg/day) was initiated for the treatment of AIP. At that time, 42 units/day of insulin was not sufficient to control glucose elevation (); the patient required a maximum of 52 units/day (). One month later, IgG4 levels declined to 54.3 mg/dL. The dosage of prednisolone, which was being tapered by 5 mg/day every 2 weeks, was 20~25 mg/day; and the total dosage of insulin was also lower than that of the previous month. However, 42 units/day of insulin was required to maintain glycemic control (). In addition, the combination of high-dose insulin and prednisolone caused our patient to gain 3.6 kg weight from the start of prednisolone initiation.
To improve glycemic control, empagliflozin was added to insulin therapy. Because we expected empagliflozin to lower blood glucose levels, we reduced the dosage of insulin to 29 units/day beforehand. Nevertheless, the patient experienced hypoglycemia 1 hour after breakfast and 1 hour after dinner on the day of empagliflozin initiation (). By the end of June, 20 days after the addition of empagliflozin, the patient had lost 1.2 kg and his total insulin dosage had declined to 20 units/day (). In July, the prednisolone dosage was reduced to 10 mg/day. Because the patient had achieved good glycemic control (postprandial glucose, HbA1c, and glycoalbumin levels: 159 mg/dL, 6.9%, and 14.3%, respectively), the total dosage of insulin was further reduced and then eventually discontinued (). Thereafter, he maintained good glycemic control (postprandial glucose and HbA1c levels: 130–180mg/dL and 5.4–5.8%, respectively) despite receiving only empagliflozin for diabetes (). However, his postprandial C-peptide level remained low (1.84 ng/mL), revealing that although the insulin-secreting capacity of his pancreas had slightly recovered, it remained insufficient.
In October, the patient's prednisolone dosage was 4 mg/day. His follow-up magnetic resonance imaging and MRCP showed that both the diffuse swelling of the pancreatic tail and narrowing of the associated main pancreatic duct had been ameliorated (Figures and ). To date, the patient's AIP is well controlled and has not relapsed.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [177.0, 'cm']}",72.27568,68.6619,75.88946,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 177.0 cm, which is 177.0 cm * 0.393701 in/cm = 69.68508 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.68508 (in inches) - 60) = 72.27568 kg.
Hence, the patient's IBW is 72.27568 kg."
3903,10,Ideal Body Weight,physical,decimal,pmc-5256956-1,Extracted,"A 22-year-old woman was seen for pain in her right shoulder. Plain radiographs of the proximal humerus revealed a poorly defined, irregular osteolytic lesion (Fig. A). T1-weighted magnetic resonance imaging showed a lesion with low-signal intensity, and T2-weighted imaging showed heterogeneous low- to high-signal intensity (Fig. B). Ewing sarcoma was diagnosed from an open biopsy specimen.
The patient's height was 156 cm and weight was 45 kg. She did not have a history of smoking or drinking alcohol. Results of laboratory testing were unremarkable, except for a slightly elevated serum C-reactive protein level (0.83 mg/mL).
The patient underwent preoperative chemotherapy with vincristine, doxorubicin, cyclophosphamide, ifosfamide, and etoposide, followed by resection of the lesion that included surrounding normal tissue, and joint replacement (Fig. C). She then underwent chemotherapy consisting of total doses as follows: doxorubicin 375 mg/m2, cyclophosphamide 10,800 mg/m2, vincristine 1.8 mg/body, ifosfamide 72,000 mg/m2, and etoposide 4000 mg/m2. She maintained her weight, and her serum albumin level remained within the normal range throughout her treatment.
Routine computed tomography (CT) at the completion of chemotherapy detected a 5-mm nodule in the patient's right upper pulmonary lobe (Fig. D), which had not been seen on the CT examination performed at the beginning of chemotherapy. In order to exclude multiple pulmonary metastases, a repeat CT examination performed 6 weeks after the completion of chemotherapy revealed only the solitary nodule.
Because Ewing sarcoma is frequently metastatic to the lung, the patient underwent resection of the solitary lung nodule based on a probable diagnosis of metastatic tumour. Examination of the resected lesion revealed pulmonary cryptococcosis due to Cryptococcus neoformans (Fig. ). Lumbar puncture ruled out infection of the central nervous system. The patient was administered oral fluconazole (100 mg daily) for 18 weeks. No recurrence was seen during a 2-year follow-up period.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [156.0, 'cm']}",48.75993,46.32193,51.19793,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 156.0 cm, which is 156.0 cm * 0.393701 in/cm = 61.41736 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.41736 (in inches) - 60) = 48.75993 kg.
Hence, the patient's IBW is 48.75993 kg."
3904,10,Ideal Body Weight,physical,decimal,pmc-4280482-1,Extracted,"An 81-year-old male patient of 166 cm and 65 kg was scheduled for a laparoscopic cholecystectomy. The induction of the anesthesia was done with midazolam 1.5 mg, propofol 50 mg, remifentanil 60 µg, and rocuronium 50 mg. The anesthesia was maintained with O2 1.5 L/min, air 2.5 L/min, sevoflurane 1.5-2.0 vol% and remifentanil 0.05-0.2 µg/kg/min. The patient was mechanically ventilated with a tidal volume (TV) of 500 ml and a respiratory rate (RR) of 10 rates/min. The end tidal CO2 partial pressure (ETCO2) was 32 mmHg, and the peak airway pressure was 12 cmH2O. During the operation, the monitoring of the patient included an electrocardiography, a noninvasive and invasive blood pressure (Philips IntelliVue MP40), a pulse oxymetry, and a bispectral index.
The laparoscopic cholecystectomy was initiated from a transperitoneal approach. A skin incision was made under the umbilicus to insert a Veress needle and CO2 was then insufflated to create a pneumoperitoneum with an intra-abdominal pressure of 14 mmHg. During the pneumoperitoneum, the fraction of inspired oxygen (FIO2) was 0.5, the TV was adjusted to 450 ml, and the RR was adjusted to maintain the ETCO2 at 30-35 mmHg. The patient was placed in the reverse Trendelenburg position with left tilting. Fifty minutes into the surgery, when the surgeon controlled the bleeding in the dissected area, the systolic blood pressure (SBP) decreased rapidly from 130 to 70 mmHg, the heart rate (HR) increased from 90 to 140 beats/min and the ETCO2 dropped from 35 to 13 mmHg, although the peripheral O2 saturation (SpO2) was maintained at 100%. Despite a prompt injection of phenylephrine 100 µg, the SBP further dropped under 50 mmHg. Subsequently, the arterial pulse wave disappeared (the SpO2 was not checked), and the cardiac rhythm was converted from sinus tachycardia to ventricular fibrillation. We asked the surgeon to stop the operation and the CO2 insufflation, and immediately initiated chest compression. At the same time, 100% O2 was supplied, and epinephrine 1 mg was injected twice intravenously. Then, defibrillation was performed using a biphasic defibrillator (150 J), and amiodarone 300 mg was injected intravenously. The cardiac rhythm reverted to a sinus rhythm, and the BP and HR were recovered at 120/80 mmHg and 140 beats/min respectively following the cardioversion. The arterial blood gas analysis (ABGA) at that time showed pH 7.06, arterial O2 partial pressure (PaO2) 222 mmHg, arterial CO2 partial pressure (PaCO2) 71 mmHg, base excess -10.2 mmol/L, and arterial O2 saturation (SaO2) 100%. It took less than 15 minutes to achieve full recovery of the vital signs. Although the blood pressure was incidentally decreased, the SBP was maintained above 100 mmHg with a rapid intravenous fluid infusion of plasmalyte (1 L for 20 minutes) and a dopamine 10 µg/kg/min and phenylephrine 0.8 µg/kg/min infusion.
Considering the possibility of a middle hepatic vein injury during the gallbladder dissection and intra-operative monitoring review of the patient, we assumed a CO2 gas embolism as the underlying condition. TEE monitoring was initiated and it revealed diffuse gas bubbles in the cardiac chamber in the midesophageal right ventricle inflow-outflow view (). The midesophageal 5 chamber view provided a closer look at the gas bubbles in the left atrium, the left ventricle, and the aorta (). To prevent a cerebral embolism, we left the patient in the Trendelenburg position and aspirated the blood through a central venous catheter in the right internal jugular vein which had been inserted during the CPR. Although some gas bubbles remained in the cardiac chamber, the vital sign was stable, at SpO2 100% and ETCO2 32 to 38 mmHg. The operation was resumed with open surgery for the repair of the injured vessels and the patient was maintained in the Trendelenburg position to limit the risk of a cerebral embolism. Thirty minutes after the operation was resumed, the ABGA read pH 7.35, PaO2 204 mmHg, PaCO2 42 mmHg, base excess -2.4 mmol/L, and SaO2 100%. At the same time, the amount of gas bubbles on the TEE had declined gradually, and almost no gas bubble remained in the cardiac chamber (). One hour later, the full surgical procedure was completed. After extubation, the patient could breathe spontaneously (100% O2) without any problem. However, he was eventually transported to the intensive care unit owing to disorientation as to his name and place. Although this was fully recovered within one hour, weaknesses of his left arm and leg (3/5 strength grade) appeared on his physical examination. The computed tomography, 3D angiography, and magnetic resonance image showed only a chronic cerebral cortical atrophy and chronic microvascular encephalopathy, without any acute lesion. On postoperative day (POD) 2, the patient's muscular strength had improved to 4/5 and was completely recovered as 5/5 by POD 3. The patient was transported to a ward on POD 5 and he was discharged on POD 10 without any complications or sequelae.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [166.0, 'cm']}",62.31505,59.1993,65.4308,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 166.0 cm, which is 166.0 cm * 0.393701 in/cm = 65.35437 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.35437 (in inches) - 60) = 62.31505 kg.
Hence, the patient's IBW is 62.31505 kg."
3905,10,Ideal Body Weight,physical,decimal,pmc-8405533-1,Extracted,"The patient is a 57-year-old man (height, 173.5 cm; weight, 61.7 kg), and the remaining teeth in his lower jaw were 1, 2, and 3 on the right side and 1, 4, and 5 on the left side. The patient had chronic apical periodontitis and severe periodontal disease. There was teeth movement, and it was difficult to preserve them. We planned to extract these teeth and place six implants (Figure ).
A physician had suspected the presence of VWD when the patient was aged 21 years, but no detailed testing or treatment was performed. The family history was not relevant, and the patient was on no current medications.
In terms of preoperative chest findings, the chest X-ray was normal (Figure ) with a normal cardiothoracic ratio of 42%, and there were no particular issues. Blood test results are shown in Table . The platelet count, a hemostatic factor, was 360,000/µl, the activated partial thromboplastin time was 35.4 s, and the prothrombin time was 11.7 s; all were within normal limits. However, coagulation factor VIII was 49%, VWF activity was 24%, and VWF antigen was 26% indicating that the coagulation factor was lower than normal. Based on detailed testing carried out by our hospital's hematology department, the patient was diagnosed with Type 1 VWD, in which there is a quantitative decrease in the VWF.
There was nothing of particular note in terms of family history. Implants in the upper jaw had already been placed at a different hospital, and there had been some difficulty stopping the bleeding when the teeth were extracted. In this case, after consulting with the hematology department, we decided that surgery would be possible by transfusing heat-treated factor VIII concentrate (Confact F®), which contains VWF. This transfusion was done to prevent abnormal bleeding during surgery. Furthermore, considering the risk of bleeding due to fluctuations in hemodynamics, with the patient's consent, we planned to carry out tooth extraction and implant placement under local anesthesia with intravenous sedation.
One hour before entering the operating room, 1500 units of Confact F® were transfused. In terms of transfusion volume, although we planned to carry out implant placement, it was determined that the amount of bleeding would not differ greatly from that of tooth extraction alone, so we used 25 IU/kg, basing our calculations on those published in the New England Journal of Medicine (Table ). Immediately before surgery, we took another blood sample. We confirmed that VWF activity was 127% and that coagulation factor VIII had increased to 104%. We then proceeded with the surgery. Considering that fluctuations in hemodynamics during surgery promote bleeding, intravenous sedation was performed to stabilize circulation. Oxygen (2 L/min) was administered transnasally, and cefmetazole sodium (1 g) was administered preoperatively to prevent infection. During the operation, we used midazolam iv and propofol (1% Diprivan Injection kit®) target-controlled infusion for continuous intravenous sedation. Also, 2% Xylocaine Dental® with epinephrine 1:80,000 was used for local anesthesia. The operation time was 3 h and 37 min, the anesthesia time was 4 h and 16 min, and blood loss was 405 ml. Although it was a little difficult to stop bleeding during the operation, we completed the procedure with no major problems. No postoperative complications, such as bleeding, were observed, and the prognosis was favorable. One week after the operation, evaluation of the coagulation factor VIII and VWF activity revealed that they had decreased to 48% and 23%, respectively, which were close to their preoperative values (Table ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.5, 'cm']}",69.10638,65.65106,72.5617,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.5 cm, which is 173.5 cm * 0.393701 in/cm = 68.30712 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.30712 (in inches) - 60) = 69.10638 kg.
Hence, the patient's IBW is 69.10638 kg."
3906,10,Ideal Body Weight,physical,decimal,pmc-3110300-1,Extracted,"A 73-year-old man (168 cm, 59 kg) presented at our institution complaining of neck stiffness and dysphagia that had been slowly increasing over the last 2 years. He had been diagnosed with atrial fibrillation and stable angina, and undertook percutaneous coronary intervention (PCI) 6 months prior to the surgery. He had undergone anticoagulation therapy, which was changed to heparin 3 days before surgery. On physical examination, the patient was alert and afebrile; and his vital signs were stable. Oral examination was unremarkable. Blood chemistry revealed no remarkable findings. Heparin was discontinued at preoperative midnight. Lateral radiography of the cervical spine demonstrated extensive osteophyte formation from C2 to C4 (). A preoperative neck computed tomography (CT) revealed slight narrowing of the airway at the level of epiglottis, a finding compatible with Forestier's disease. General anesthesia was induced with thiopental sodium 250 mg and rocuronium 50 mg and endotracheal tube was inserted with lightwand without difficulty. The intraoperative findings using an anterolateral transverse approach included a hard bony mass at the level of C2-4 and compression of the esophagus and trachea. Decompression of the osteophyte was performed with a drill for 135 minutes. The patient was transferred to the postanesthetic care unit (PACU) following the operation. In the PACU the endotracheal tube was removed after full assessment of consciousness and muscle power. The patient was transferred to the general ward and had no complaints until 6 hour after the completion of surgery. At that time, patient complained of dyspnea and sudden respiratory compromise and cardiac arrest were developed. Emergent endotracheal tube insertion was attemped but the hypopharyngeal structure could not be identified because of severe laryngeal edema. Emergency tracheostomy was done with an ID 7.0 tube. With the impression of postoperative bleeding, emergent surgery was arranged. However, there was no bleeding at the operative site. Instead, the connective tissue and mucosa were severely edematous. Lateral radiography of the cervical spine demonstrated extensive soft tissue edema and airway narrowing (). There was no evidence of remaining osteophyte. The patient's brain was damaged and discharged with serious neurologic sequelae.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.0, 'cm']}",64.12607,60.91977,67.33237,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg."
3907,10,Ideal Body Weight,physical,decimal,pmc-2924339-1,Extracted,"55-year-old man (height 1,78 m; weight 70 kg) with severe heart failure - NYHA class III/IV was admitted to cardiology department for evaluation for surgery of incompetent mitral and tricuspid valves. Transthoracic echocardiogram confirmed diagnosis of severe mitral and tricuspid incompetence, dilated left ventricle, poor contractility (EF - 40%), pulmonary hypertension (PASP 90 mmHg).
On physical examination right lower abdomen mass was found and CT scan revealed large (12 cm × 11 cm × 7 cm) right kidney tumor with extension to infradiaphragmatic juxtahepatic part of inferior vena cava (caval thrombus 9 cm × 5 cm) (See Figures,,). 
Several options of treatment were considered but during discussion with cardiac surgeons and urologists one stage operation was decided and carefully planed.
In preoperative period patient received hypotensive drugs (furosemide 0,04 g, spironolactone 0,025 g), beta-blocker (metoprolol 0,05 g), antyarrhytmic drug (amiodarone 0,2 g), anticoagulant (enoxaparin 0,06 g), potassium and magnesium.
Cardiac part of operation was performed first. Chest was open through median sternotomy and cardiopulmonary bypass (CPB) was established by cannulation of both venae cavae and ascending aorta. After clumping the aorta heart was stopped by cold blood cardioplegia, and both valves were repaired - dilated mitral annulus with C-G Future Band (Medtronic Inc.USA) and tricuspid annulus with De Vega plasty. After aortic clump was removed heart rhytm was restored with DC shock. CPB was discontinued without problems, patient was decannulated, heparin reversed with protamine. Transoesophageal echocardiogram confirmed good result of valves repair. The extracorporeal circulation time was 72 minutes, the aorta was clumped for 49 minutes.
The second part of the operation was carried out just after the patient was hemodynamically stable. Urologists performed right radical nephrectomy through laparotomy. Accurate localization of the thrombus was assessed intraoperatively and a decision not to use cardiopulmonary bypass for thrombectomy was made. The kidney, the adrenal gland and the thrombus were removed intact (Figure ).
The operation took 4 hours 25 minutes. Blood loss was 600 ml. 5 units of fresh frozen plasma (5 × 220 ml), 2 units of red blood cells (2 × 500 ml) and 1 unit of platelets were administered. There were no complications. Macroscopic evaluation of the specimen showed 10 × 10 × 9 cm renal mass and 6 × 3 × 4 cm neoplasmatic thrombus. Microscopic examination revealed clear cell carcinoma of the kidney at the stage G1 pT3bN0M0, not infiltrating renal capsule (Figure). 10 lymphatic nodules were negative.
In postoperative echocardiography there were no signs of mitral either tricuspid incompetence or pericardial effusion. Electrocardiogram demonstrated regular sinus rhythm. In peri- and postoperative period patient received antibiotic prophylaxis (ceftriaxone 2,0 g) , hypotensive drugs (furosemide 0,04 g, enalapril 0,05 g), beta-blocker (metoprolol 0,05 g), antyarrhytmic (amiodarone 0,2 g), anticoagulant (enoxaparin 0,06 g), acetylsalicylic acid (0,075 g), omeprazole (0,02 g), potassium and magnesium. 6 days after surgery oral anticoagulant therapy was started with acenocoumarol (0,002 g).
9 days after the operation the patient was transferred from cardiosurgical department to urologic centre. 4 days later he was discharged in good condition. 12-month follow-up showed that the patient remains without any complaints. Computed tomography demonstrated no signs of reccurrence.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.78, 'm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.78 m, which is 1.78 m * 39.3701 in/m = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3908,10,Ideal Body Weight,physical,decimal,pmc-6188736-1,Extracted,"The patient was a 60-year-old man who was diagnosed with alcoholic liver cirrhosis and type 2 diabetes when he was 50 years old. His drinking history was 540–720 mL Japanese sake per day for 35 years, and his smoking history was 30 cigarettes per day for 30 years. His ascites increased in 2008 when he was 57 years old, and he repeatedly exhibited symptoms of hepatic encephalopathy. Due to the liver cirrhosis symptoms, the patient was treated with several medications including furosemide, spironolactone, lactulose, and total amino acid preparation. To prevent the complications of liver cirrhosis, coil embolization to a portal venous shunt was performed twice. The patient was admitted to our hospital in June 2012 because of slowly progressive renal impairment and nephrotic syndrome.
Upon admission, the patient's height and weight were 166 cm and 64 kg, respectively. His body temperature was 36.7°C and his blood pressure was 150/60 mmHg. His consciousness was clear. His abdomen was slightly expanded but exhibited no tenderness. The liver and spleen were not palpable. No rash or purpura was noted on the skin. Diabetic and/or hypertensive changes were not observed in the ocular fundus.
The laboratory findings on admission were hemoglobin level of 9.4 g/dL (normal range 13.5–17.6 g/dL), platelet count of 11x104/μL (normal range, 13.1–36.2x104/μL), prothrombin time measurement of 68% (normal range, 70–130%), total bilirubin level of 0.9 mg/dL (normal range, 0.3–1.2 mg/dL), NH3 level of 85 mg/dL (normal range, 30–80 mg/dL), blood urea nitrogen level of 41 mg/dL (normal range, 8–20 mg/dL), serum creatinine concentration of 1.77 mg/dL (normal range, 0.5–1.1 mg/dL), serum total protein level of 5.7 g/dL (normal range, 6.7–8.3 g/dL), serum albumin level of 2.1 g/dL (normal range, 3.5–5.2 g/dL), total cholesterol of 188 mg/dL (normal range, 120–219 mg/dL), and HbA1c of 5.8% (normal range, 4.3–5.8%). The serum levels of IgG were 1558 mg/dL (normal range, 870–1700 mg/dL), of IgA were 481 mg/dL (normal range, 110–410 mg/dL), of IgA1 were 398 mg/dL (normal range, 50–314 mg/dL), of IgA2 were 83 mg/dL (normal range, 10–156 mg/dL), and of IgM were 219 mg/dL (normal range, 35–220 mg/dL). The serum levels of free κ and λ light chains were 149.0 mg/L (normal range, 3.3–19.4 mg/L) and 106.0 mg/L (normal range, 5.7–26.3 mg/L). The serum free light chain ratio was within normal range. The serum level of complement factor C3 was 79 mg/dL (normal range, 65–135 mg/dL), of C4 was 17 mg/dL (normal range, 13–35 mg/dL), and of CH50 was 41.1 U/mL (normal range, 30–50 U/mL). All of the other serology findings including anti-nuclear antibody, hepatitis B virus surface antigen, hepatitis C virus antibody, anti-neutrophil cytoplasmic antibody, and anti-glomerular basement membrane antibody were negative. There was no M-spike on serum and urine protein electrophoresis. A serum test for a cryoglobulin precipitation was negative.
The urinary sediments showed many red blood cells in high power fields together with granular casts and dysmorphic red blood cells. The urinary protein excretion was 4.7 g/day. The 24-hour creatinine clearance was 45 mL/min. Computed tomography revealed liver deformity with moderate accumulation of ascites. The kidneys were normal in size and there were no signs of urinary tract obstruction.
The renal biopsy specimens contained a total 28 glomeruli, 12 of which were globally sclerotic. The degree of interstitial fibrosis/tubular atrophy was 50–60% of the total biopsy specimen identified. Moderate fibrous intimal hyperplasia was observed in the arcuate artery. Diffuse segmental double-contours of the glomerular basement membrane and mesangial cell hypercellularity were identified in nonsclerotic glomeruli, exhibiting a membranoproliferative glomerulonephritis-like pattern (). Some glomeruli showed moderate-to-severe endocapillary hypercellularity, accompanied by fibrocellular crescents (). Fluorescent immunostaining showed granular staining of IgA and C3, but not of IgG, IgM, or C1q, on glomerular capillaries and some mesangial areas (Figures –). Among the IgA subtypes, staining of IgA1 (GenWay Biotech, San Diego, CA, USA) was observed, but staining of IgA2 (GenWay Biotech) was not identified (Figures and ). With light chain immunostaining, only κ (SouthernBiotech, Birmingham, AL, USA) was identified and no λ staining (SouthernBiotech) was seen (Figures and ). On electron microscopy, the glomerular capillary walls showed double contours. Electron-dense deposits were found in the paramesangium and around the subendothelial space of the glomeruli (). No organized structure deposits were identified (). Based on these findings, this case was histologically diagnosed as diffuse membranoproliferative glomerulonephritis with monoclonal IgA1-κ deposits.
Because this case was accompanied by moderately advanced decompensated liver cirrhosis, there was a concern that the patient may have serious side effects due to aggressive treatment such as the administration of corticosteroids. Thus, supportive treatment based on medications such as RAS inhibitors/diuretics, in addition to dietary therapy including salt restriction/branched-chain amino acid administration, was selected. Although these treatments led to a modest decrease in the urinary protein excretion, the patient's renal dysfunction slowly progressed and finally resulted in end-stage renal failure and initiation of dialysis therapy.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [166.0, 'cm']}",62.31505,59.1993,65.4308,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 166.0 cm, which is 166.0 cm * 0.393701 in/cm = 65.35437 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.35437 (in inches) - 60) = 62.31505 kg.
Hence, the patient's IBW is 62.31505 kg."
3909,10,Ideal Body Weight,physical,decimal,pmc-3848677-1,Extracted,"The 39-year old, 68 kg and 165 cm patient, mother of a 20 year old son, was referred to our institution during the 33rd week of pregnancy. One year before, she had experienced multiple transitory ischemic attacks, she was in NYHA (New York Heart Association) class IV and IVNC was diagnosed based on echocardiography. Besides warfarin, which during pregnancy was switched to low molecular weight heparin, pharmacological therapy with an angiotensin converting enzyme inhibitor had been established. Although severe ventricular arrhythmias had been diagnosed, the patient refused implantation of an internal defibrillator. The transthoracic echocardiography (TTE) at admission showed the typical picture of IVNC: a massively dilated left ventricle (end-diastolic diameter of 80 mm - normal value <50mm), a mitral valve regurgitation grade I, a severely impaired left ventricular ejection fraction (LVEF) of 25% (normal value>55%) and a semi-systemic systolic pulmonary artery pressure (PAP) of approximately 60 mmHg. Due to the inherent risk of cardiac decompensation in the late pregnancy, the patient was admitted to our heart centre one week later and elective caesarean section scheduled for the 35th week of gestation. Due to the risk of sudden life-threatening decompensation during surgery, it was planned to perform the operation under general anaesthesia and “stand by” of veno-arterial extracorporeal membrane oxygenation (ECMO) for extracorporeal life support. On the day before surgery, TTE revealed further decrease of the LVEF to 20%, increase of the mitral valve regurgitation to grade II and increase of the systolic PAP to 2/3rds of the systemic value of approximately 80 mmHg.
The patient received 150 mg of ranitidine 12 and 2 hours before the operation. After having arrived in the anaesthesia induction room in nearly sitting position, 30 ml of sodium citrate (0.3 molar) was administered orally. Standard monitoring with electrocardiogram and pulsoxymetry was established. In addition, paddle leads for external defibrillation were placed. Thereafter, an arterial line was placed into the left radial artery; a 4 lumen central venous catheter and a 9 gauge introducer were placed into the right jugular internal vein in local anaesthesia. A pulmonary artery (PA) catheter with atrial and ventricular pacing option (Baxter International, Illinois, USA) was inserted into the introducer and placed into the PA.
At this time the heart rate was 110/min with multiple polytopic ventricular extra-systolic (VES) beats. In the nearly sitting position, the arterial blood pressure was 110/70/90 mmHg and the PAP 75/30/50 mmHg with a pulmonary capillary wedge pressure of 30 mmHg. Pharmacologic therapy with a continuous infusion of dobutamine 3 µg/kg/min and milrinone 0.25/kg/min was started. Additionally, two 6 French introducer catheters were placed under local anaesthesia into the right femoral artery and right femoral vein. These catheters were inserted to facilitate quick percutaneous access to the vessels for emergency installation of ECMO for extracorporeal life support in case of acute cardiac decompensation.
After these preparations, the patient was transferred into the operating room and preparations for surgery were performed.
After pre-oxygenation, anaesthesia was induced with 5 mg of rocoronium, 15 mg of etomidate, 35 mg of S ketamine and 100 mg of succinylcholine and a rapid sequence intubation was performed. Three minutes later, a healthy 2800 g child was delivered by classic longitudinal caesarean section (APGAR values of 9-10-10). Thereafter, anaesthesia was continued with a bolus of 30 mcg of sufentanil and 35 mg of rocoronium and a continuous infusion of remifentanil (2 µg/kg/min) and propofol (0.1 mg/kg/min) without using Target Controlled Infusion (TCI). Additionally, 1 g of paracetamol and 1 g of novamin-sulfate and 4 mg of ondansetron were infused. At the end of the procedure residual muscle relaxation was antagonized with 300 mg of sugammadex.
During the entire period of anesthesia, hemodynamics remained completely stable, the PAP decreased to 1/3rd systemic values of 50/30/20 mmHg while, however, polytopic VES were still observed. The completely awake and orientated patient was extubated on the surgical room. The patient was transferred to the intensive care unit (ICU) and she remained here for 5 days. Therapy with milrinone and dobutamine was continued during ICU stay. The patient was discharged uneventfully from hospital 14 days after surgery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3910,10,Ideal Body Weight,physical,decimal,pmc-4411460-1,Extracted,"A 21-year-old female presented with a migraine. For about 3 years, she at times experienced being likely to faint upon standing and dimmed vision. However, she did not show neurological dysfunction; therefore, cerebral infarction was not suspected. When she was working in standing position for a long time in the middle of the night, she started experiencing dimmed vision, labile vertigo, and hindrance in the ability to stand at her workplace. Such episodes were associated with a following numbness and weakness in the lower extremities on the left half of her body. The estimated time from the onset of symptoms to hospital presentation was about 6 h. This consequently caused the delay between neurologic symptoms onset and diagnostic of stroke in the patient. She was hospitalized in Jichi Medical University Hospital (Shimotuke, Japan) on the morning of the same day. Upon examination, her level of consciousness was alert, and she had a body weight of 47 kg, height of 160 cm, body mass index of 18, blood pressure of 84/64 mmHg, and pulse rate of 84 beats/min. A “gallop” sound was heard along with her heart sound, but her pulmonary sound was normal, and there was no pedal edema. Neurological examination revealed muscle weakness of the left upper and lower limbs (manual muscle testing; MMT 4: holds test position against slight to moderate pressure), a decrease of superficial sensation and dysesthesia of the left half of the body, and ataxia of the left upper limb. The National Institutes of Health Stroke Scale (NIHSS) score was 4. Increasing scores indicate a more severe stroke and have been shown to correlate with the size of the infarction on both CT and MRI evaluation. Many guidelines and protocols warn that administering tPA in patients with a high NIHSS score (>22) is associated with increased risk of hemorrhagic conversion. Laboratory findings showed no abnormalities except for a slight increase in C-reactive protein (1.61 mg/dL). Her electrocardiogram showed a normal sinus rhythm. Multiple hyperintense areas in the left basal ganglia, corona radiata, and cortex of the temporal lobe were found by brain diffusion-weighted magnetic resonance imaging (MRI), indicating acute cerebral infarction (). Therefore, we diagnosed the patient with cerebral embolisms. MR angiography did not reveal cervical angiostenosis () or intracranial aneurysm (). Transthoracic 2D-echocardiography revealed a giant left atrial tumor of the diameter 7 × 4 cm attached to the atrial septum causing mitral valve prolapse that moved during diastole and occluded the mitral orifice ().
Therefore, we diagnosed the patient with cerebral embolisms due to left atrial myxoma. The reason to not select tPA as the emergency treatment was that the estimated time from the onset of symptoms to hospital presentation was too long for patients with cerebral embolism to treat by tPA. To prevent recurrence, she underwent the resection of the myxoma with cardiopulmonary bypass and the reconstruction of the atrial septum using a bovine pericardial patch 1 day after her stroke. Gross examination showed a 7 × 6 × 4 cm brown, gray, and whitish myxoid mass (). Pathology confirmed atrial myxoma. The patient uneventfully recovered from cardiac surgery, and her postoperative general and neurological symptoms improved. Thirteen days after admission, her NIHSS score improved to 0 and she was discharged from our hospital.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3911,10,Ideal Body Weight,physical,decimal,pmc-7106884-4,Extracted,"Patient 4 is a 61-year-old female whose cause of the liver disease was primary biliary cirrhosis complicated by ascites not requiring paracentesis and esophageal varices, with a preoperative MELD of 26. Her medical history also included diffuse alveolar lung disorder and fibromyalgia. She received a deceased donor orthotopic liver transplant with a graft volume of 1909 cm3 (as estimated by donor preoperative CT volumetry) using the piggyback technique of veno-venous bypass with a choledocho-choledochostomy and portal vein eversion thrombectomy. Her height was 154.9 cm, and her weight was 56.5 kg, while her donor's height and weight were 157.5 cm and 63.3 kg, respectively, giving a donor-weight-to-recipient-weight ratio of 1.12. Due to concerns of compartment syndrome because of large graft size, a bridging mesh was utilized to achieve a tension-free fascial closure. Her postoperative course was complicated by possible acute rejection evidenced by elevated alkaline phosphatase, which responded to 3 days of stress-dose steroids. She was discharged on postoperative day 8. She is currently 8 months postoperatively and doing well with good graft function.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [154.9, 'cm']}",47.76384,45.37565,50.15203,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 154.9 cm, which is 154.9 cm * 0.393701 in/cm = 60.98428 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.98428 (in inches) - 60) = 47.76384 kg.
Hence, the patient's IBW is 47.76384 kg."
3912,10,Ideal Body Weight,physical,decimal,pmc-7784716-1,Extracted,"The index patient is a 55-year-old Caucasian male, height 160cm, weight 72kg, with a multisystem MID diagnosed upon clinical presentation, immune-histo-chemical, and biochemical investigations of a muscle biopsy at age 34. His history was noteworthy for mental retardation, epilepsy since age 12, cataract surgery, hypoacusis, vitamin D deficiency, hypertrophic cardiomyopathy (hCMP), left ventricular hypertrabeculation (LVHT)/noncompaction (Figure ), QT-prolongation (Figure ), left anterior hemiblock (LAH), anemia, cholecystolithiasis, sleep disorder, hepatopathy, hyperlipidemia, benzodiazepine misuse, myopathy, prostate hyperplasia, right total hip endoprosthesis, and iron deficiency (Table ). Since at least age 47 camptocormia became apparent. At age 48 he experienced a deep venous thrombosis after left tibial fracture. At age 51 he had undergone surgery for right-sided scrotal hernia. Seizures were well controlled with a seizure frequency of about two generalised tonic-clonic seizures per year and several focal seizures.
Clinical neurologic exam revealed short stature, hypertelorism, myopia, bilateral ptosis (left > right), signe des cils bilaterally, bulb protrusion bilaterally, upslanting palpebral fissures, positional nystagmus when looking in any direction, cognitive impairment, hypoacusis, a barrel thorax, gibbus, camptocormia, generally reduced tendon reflexes on the upper and lower limbs, diffuse wasting, dysdiadochokinesia, mild postural tremor, mild weakness for foot extension bilaterally (M5-), ataxia of the lower limbs, genu valga, outwardly rotated feet, and flexion contractures of the knees with right-sided predominance.
Creatine-kinase (CK) was repeatedly elevated. Serum lactate was elevated to 2.5 mmol/l (n, <2.2 mmol/l). The lactate stress test was abnormal. Nerve conduction studies were indicative of axonal polyneuropathy. MRI of the lumbar spine revealed a wedge vortex L3, vertebral stenosis L2/3, and lumbar osteochondrosis. Muscle biopsy from the right gastrocnemius muscle revealed subsarcolemmal accumulation of mitochondria, ragged red fibers, tubular-shaped mitochondria, and bizarre cristae proliferation. Biochemical investigations of the muscle homogenate revealed a combined complex-I and complex-IV defect. His last medication included lamotrigine 400 mg/d, levetiracetam 1000 mg/d, lacosamide 250 mg/d, and vitamin D.
The 78-year-old mother of the index patient had a history of arterial hypertension, diabetes, hyperlipidemia, polyarthralgias due to polyarthrosis, deep venous thrombosis, recurrent leg edema, phlebitis, hyperuricemia, and listhesis L3/4. She had surgery of the right shoulder after a trauma, cataract surgery bilaterally, surgery for carpal tunnel syndrome bilaterally, and veins tripping four times. She refrained from being investigated neurologically during years despite frequently accompanying her son to his regular neurological visits. At the age of 74 she sought neurological advice for the first time after nerve conduction studies, carried out for sensory disturbances of the feet, had revealed sensori-motor polyneuropathy.
Clinical exam of the mother revealed short stature (164 cm), alopecia, madarosis, dysarthria, diffuse weakness of the left upper limb, hypoesthesia of the left upper limb, reduced triceps tendon reflexes bilaterally, dysdiadochokinesia, dysmetria bilaterally, reduced tendon reflexes on the lower limbs, and discrete wasting of the thighs. The hemoglobin A1c (HbA1c) value was 7.3 % (n, 4-6%). Triglycerides were 313 mg/dL (n, <150 mg/dL). Serum iron was elevated to 187mg/dl (n, 27-145 mg/dl), the CK was 224 U/L (n, <170 U/L). There was mild lactic acidosis. Cerebral MRI showed gliotic spots bilaterally including the basal ganglia and diffuse atrophy. Nerve conduction studies revealed a sensori-motor polyneuropathy. Her last medication included simvastatin, enalapril, acetyl-salicylic acid, vitamins, and antidiabetics. She refused to undergo muscle biopsy. Phenotypic features the index patient and his mother had in common included cerebral atrophy, myopathy, neuropathy, cataract, hyperlipidemia, short stature, disturbed iron metabolism, and deep venous thrombosis (Table ). Other family members had anginal chest pain (brother, father, mother), subarachnoidal bleeding (father), and cholecystolithiasis (grandmother from the mother's side).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [160.0, 'cm']}",56.88197,54.03787,59.72607,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.99216 (in inches) - 60) = 56.88197 kg.
Hence, the patient's IBW is 56.88197 kg."
3913,10,Ideal Body Weight,physical,decimal,pmc-7136759-1,Extracted,"A 31-year-old Saudi male patient presented to a restorative clinic at the College of Dentistry, King Saud University, Saudi Arabia. The patient was seeking permanent restoration of an endodontically treated tooth on the left side of his lower jaw which had undergone significant decay many years prior.
The dental history of the patient included extraction of a mandibular left molar, multiple restorations, and a root canal treatment. The patient stated that he underwent a surgical procedure to the gingiva to help his anterior permanent teeth erupt during childhood. Medical history revealed no significant reports. The family history for the patient also revealed no evidence of any medical condition.
Height and weight recorded for the patient were 185 cm and 114 kg, respectively. A head and neck extraoral examination revealed a mandibular protrusion leading to a straight facial profile () and tight lips upon closure with a thick lower lip. An intraoral examination showed racial melanin pigmentation, especially on attached gingiva, with anterior and bilateral cross bites (Figures and ). Generalized gingivitis with bad oral hygiene and heavy plaque accumulation were observed in the crowded anterior segments. Areas of deep pockets and bleeding were also noted. Tooth #32 presented hypomineralization, while a very deep vault in the hard palate and bony enlargement of the posterior areas of the maxillary arch were also observed (). Crowded teeth characterize both of the patient's arches since the patient has a full set of teeth and narrow upper and lower arches.
A panoramic view of the patient's teeth show long roots (radiculomegaly) for most of the teeth, especially for the molar teeth (). Periapical radiographs also show unusually long roots (). Cone beam computed tomography (CBCT) software was used to measure the length of the patient's entire set of teeth. Measurements were made from the apex to the tip of the cusps in a slice orientation manner ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [185.0, 'cm']}",79.51979,75.5438,83.49578,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 185.0 cm, which is 185.0 cm * 0.393701 in/cm = 72.83469 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (72.83469 (in inches) - 60) = 79.51979 kg.
Hence, the patient's IBW is 79.51979 kg."
3914,10,Ideal Body Weight,physical,decimal,pmc-5738009-1,Extracted,"A 65-year-old married woman visited our emergency room of Obstetrics and Gynecology Department, Soonchunhyang University Cheonan Hospital, due to a chief complaint of lower left abdominal pain which started 3 days before her visit and aggravated on the day of visit. Her obstetric history was the patient has had 2 term births, 0 preterm births, 2 abortions, 2 living children and had menopause 10 years ago. At the time of visit, her systemic condition was favorable. Her height was 162 cm and weight was 61 kg. Vital signs were normal with a blood pressure of 110/60 mm Hg, pulse rate of 60 beats/min, body temperature of 36.0°C, respiratory rate of 19 breaths/min, and no apparent specific signs. There was slight abdominal distension, but no tenderness or rebound tenderness on abdominal palpation. In pelvic examination, no vaginal bleeding or discharge was noted.
In radiologic assessment, transvaginal and abdominal ultrasound showed a normal uterus and a 13 × 9 cm sized multicystic tumor with irregular surface of the left ovary (Fig. A). Abdominal and pelvic computed tomography scans revealed a 16 × 9 × 14 cm sized multiseptated cystic mass with large enhancing solid portion in the left ovary, and malignancy was suspected (Fig. B). In addition, there was a finding of mild dilation of the right distal ureter caused by the compression of the left ovarian mass, and there were no findings of ascites, pleural effusion, and lymph node enlargement. Test results were normal in peripheral blood smear, blood coagulation, liver function, renal function, urinalysis, and C-reactive protein, and her chest x-ray and electrocardiogram were normal. The test for serum tumor markers revealed normal levels of cancer antigen 125 (CA-125) at 8.69 IU/mL (range 0–35 IU/mL) and carbohydrate antigen 19–9 at 3.29 U/mL (range 0–34 U/mL). The patient underwent exploratory laparotomy with a suspicion of borderline or malignancy of an adnexal mass. A white-gray 17 × 9 cm sized cystic tumor was detected in the left adnexa, having a torsion of 720° in a counterclockwise direction or no necrosis (Fig. ). Uterus, right ovary, large intestine, bladder, small intestine, and liver were normal in inspection and palpation of abdominal organs. There were no presentations of ascites or nodules within the peritoneal cavity. We carried out laparotomy because there was the possibility of ovarian malignancy, but torsion of the left ovary was observed. So, we decided to conduct frozen biopsy of left ovary for confirming malignancy before performing staging surgery. Salpingo-oophorectomy on the left side was performed after washing cytology from the peritoneal cavity, and the result of an emergent frozen section biopsy confirmed a borderline Brenner tumor associated with a benign mucinous tumor. Subsequently, total hysterectomy and right salpingo-oophorectomy were performed. The operation was completed without additional procedures such as pelvic lymph node dissection.
Gross pathologic findings revealed that the left ovary showed a well-demarcated oval mass composed of both solid and cystic components, measuring 17.0 × 16.0 × 8.5 cm in dimensions. The cystic area showed multilocular appearance and it contained mucin materials. On microscopic examination, the cyst wall was lined by a single layer of benign mucinous cells, which was consistent with benign mucinous cystadenoma. The solid area displayed round to oval tumor cell nests within fibrous stroma and the tumor cells had fine chromatin pattern, obvious nucleoli, and longitudinal grooving with no cytologic atypia or mitotic activity. Histologic features of solid area were benign Brenner tumor (Fig. ). Therefore, we diagnosed this ovarian tumor as benign mixed Brenner-mucinous tumor.
The patient was discharged in good condition on the 15th postoperative day without specific complications.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [162.0, 'cm']}",54.19299,51.48334,56.90264,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.77956 (in inches) - 60) = 54.19299 kg.
Hence, the patient's IBW is 54.19299 kg."
3915,10,Ideal Body Weight,physical,decimal,pmc-5564172-1,Extracted,"A 47-year-old male patient weighing 70 kg with a height of 173 cm was scheduled for enucleation of a dentigenous cyst of the mandibular bone (). The patient's medical and surgical history was unremarkable, with an American Society of Anesthesiologists (ASA) physical status of I. His laboratory findings were routine and his Mallampati classification score was class 2. His neck mobility and mouth opening were also unremarkable. He had a roughly 3 × 3 cm sized elevation in the left submandibular area; however, this was not taken seriously. He denied symptoms related to obstructive sleep apnea, dysphagia, and respiratory difficulty.
After applying standard monitoring, anesthesia was induced with intravenous fentanyl (100 µg), lidocaine (60 mg), propofol (120 mg), and rocuronium (50 mg). After mask ventilation, a lubricated right angle endotracheal tube was inserted via the right nostril and direct laryngoscopy was attempted, which showed a severely distorted glottis (). We then tried direct laryngoscopy with a C-MAC® videolaryngoscope (KARL STORZ Endoscopy-America, Inc., El Segundo, CA, USA), but we could only see the tip of the epiglottis without the vocal cords and a severely distorted larynx. Next, we tried to guide a fiberoptic bronchoscopy tube under the aid of the C-MAC® videolaryngoscope, but this was not effective because of the distortion of the glottis as well as bleeding from the oral cavity and epistaxis. We then attempted retrograde wire intubation with the guide wire of a central venous catheter set. We punctured the cricothyroid membrane with an 18 G intravenous needle and inserted an 18 G Teflon catheter after confirming the aspiration of air. We inserted the guide wire via the catheter under the aid of video laryngoscopy and were able to guide the wire to the right nostril. Then, we intubated using a 6.5 mm internal diameter right angle endotracheal tube over the guide wire. However, the length of the right angle endotracheal tube was too long and we could not grab the tip of the guide wire at the end of the tube. Thus, we had to guide the tube with the guide wire and fiberoptic bronchoscope until we could see the vocal cords with the fiberoptic bronchoscope at the tip of the endotracheal tube in order to insert the tube successfully. After confirming the proper position of the endotracheal tube with fiberoptic bronchoscopy, the guide wire was removed. Anesthesia was maintained with oxygen, medical air, sevoflurane, and intermittent boluses of rocuronium. After surgery, the patient recovered uneventfully.
On the first postoperative day, magnetic resonance imaging of the head and neck area showed a mass of about 6 × 4 × 8.6 cm in size in the left prestyloid parapharyngeal space (). One month later, the patient was scheduled for tumor excision under general anesthesia. We planned awake fiberoptic bronchoscopy with guided intubation. The patient was premedicated with an intravenous injection of 0.2 mg glycopyrrolate 10 minutes before anesthetic induction. Before the intubation procedure, the patient was mildly sedated with an intravenous infusion of dexmedetomidine. After topical anesthesia with 4% lidocaine spray, nasal packing was performed with a cotton swab soaked with 4% lidocaine and 1:10,000 phenylephrine solution. Superior laryngeal nerve block was performed with a 2% lidocaine injection and translaryngeal anesthesia was administered with 4 ml of 4% lidocaine injection through the cricothyroid membrane. Awake fiberoptic bronchoscopy was performed and a 6.5-mm internal diameter reinforced endotracheal tube was successfully intubated without specific event. After intubation, general anesthesia was induced with an intravenous injection of propofol (120 mg) and rocuronium (50 mg) and continued with 7 vol% of desflurane. Surgery time was about 2 hours and the patient recovered from general anesthesia and was extubated uneventfully. The tumor was diagnosed as a schwannoma. The patient was discharged on the fourth postoperative day without any complications.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.0, 'cm']}",68.65362,65.22094,72.0863,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.0 cm, which is 173.0 cm * 0.393701 in/cm = 68.11027 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.11027 (in inches) - 60) = 68.65362 kg.
Hence, the patient's IBW is 68.65362 kg."
3916,10,Ideal Body Weight,physical,decimal,usmle-2390,Extracted,A 71-year-old man with type 2 diabetes mellitus comes to the physician because of a 9-month history of pain and stiffness in the right knee. He reports that the stiffness lasts approximately 10 minutes after waking up and that the pain is worse in the evening. There is no history of trauma. He is 175 cm (5 ft 9 in) tall and weighs 102 kg (225 lb); BMI is 33 kg/m2. Examination of the right knee shows tenderness in the anteromedial joint line and crepitus during knee movement. Laboratory studies show an erythrocyte sedimentation rate of 15 mm/h and a serum uric acid concentration of 6.9 mg/dL.,"Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3917,10,Ideal Body Weight,physical,decimal,pmc-6206937-1,Extracted,"A 69 year-old Caucasian male Army veteran was referred to a chiropractor at a Veterans Affairs Medical Center. He presented with left shoulder pain in the setting of a full thickness supraspinatus tear. A thorough history of his neck was gathered as it related to the left shoulder pain. His cervical spine was “stiff” most mornings, which abated with movement and activity. The patient had limited cervical range of motion in all planes and noted episodic neck pain secondary to injuries he sustained from multiple fragment wounds to left side of his neck in 1969.
A review of the final field hospital narrative at the time of initial trauma revealed the multiple frag wounds to the neck, shoulder and scrotum. These injuries subsequently resulted in a trachea-esophageal cutaneous fistula with left cervico-mediastinal abscess and cervical VO. During hospitalization, cervical plain films were reported on which described “prominent demineralization of the bones of the cervical spine with decrease in disk spaces C2 through C6. More demineralization anteriorly with apparent destruction of the anterior aspect of vertebral bodies with resultant reversal of normal lordotic curve. Neural foramina appear intact.” There was no mention of zygapophyseal joint fusion in the original radiographic reports following injury. He was hospitalized for 17 months following the gunshot wound with multiple surgeries to debride the region and reconstruct the left cervical musculature as well as antibiotic therapy. Cervical plain films at time of discharge described “bony healing and fusion of the mid-cervical spine with fusion of 2nd through 5th cervical bodes and calcification of the anterior ligament, C5-C6, C6-C7”. Again there was no remark of zygapophyseal joint fusion after treatment for the initial injuries and subsequent infection.
In office, he endorsed occasional axial neck pain and occipital headache that occurred 1 time per week. Neck Disability Index (NDI) score was 2 out of 50 (4%) []. Pertinent details from the review of systems revealed type 2 diabetes mellitus, carpal tunnel syndrome, hypothyroidism, and irritable bowel syndrome. His medications included tramadol and butalbital, both taken as needed. He used a Thera Cane for self-management of myofascial pain. Despite this history, the patient worked full time from his 20s and was planning to retire at the age of 70.
Physical exam findings revealed a man of anticipated age who was oriented to person, place and time. He weighed 82 kg (181.2 lbs) and measured 177 cm (70 in.). Neurologic examination of the upper and lower extremity dermatomes revealed no deficits. Romberg test was negative and failed to elicit body sway or sense of loss of balance. Biceps, triceps and brachioradialis deep tendon reflexes were 2+ when elicited bilaterally. The plantar response was down going and symmetric. Finger to nose movements were without dysmetria or tremor. Cervical rotation was found to be severely limited in both directions. Global restriction of the cervical spine was noted when assessing joint play, with no isolated segmental motion.
Radiographs of the cervical spine on file demonstrate osseous ankylosis from C2/C3 to C7/T1 with obliteration of the intervertebral discs and accompanying endplates from C2/C3 to C5/C6. (Figs. , , , , ) The C6/C7 and C7/T1 intervertebral discs and accompanying endplates are visualized, though the levels are ankylosed. The facet joints from C2-C6 are ankylosed as well. There is a mild kyphotic alignment of the cervical spine. Metallic fragments are seen in the soft tissues of the neck and upper thorax consistent with the stated history. Provided the history of osteomyelitis secondary to the treatment of the wound and multiple surgeries, the most likely diagnosis is post-infectious ankylosis from C2-T1. The initial field narrative did describe spondylodiscitis with observation of fusion of multiple segments of the cervical spine upon discharge 17 months later. No clear infection of the facet joint was described at the time. Traditional spondylodiscitis is observed to be contained to the anterior column of the spine, primarily the vertebral endplate and adjacent intervertebral disc. However, it has been reported, when infection involves a vertebral body, that it may extend into the pedicles and articular processes which may result in adjacent septic facet arthritis [].
No manual care to the cervical spine occurred following the evaluation as the patient had no complaint in addition to the NDI score of 4%. There was no indication for additional imaging or further work-up regarding the cervical spine. The patient reported complete functional independence in all activities of daily living with reasonable expectation of associated stiffness and limited cervical range of motion. Following the evaluation, the extent of care included education to the patient. Further work-up for the left shoulder and referral to physical therapy resolved left shoulder pain.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [177.0, 'cm']}",72.27568,68.6619,75.88946,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 177.0 cm, which is 177.0 cm * 0.393701 in/cm = 69.68508 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.68508 (in inches) - 60) = 72.27568 kg.
Hence, the patient's IBW is 72.27568 kg."
3918,10,Ideal Body Weight,physical,decimal,pmc-5914225-1,Extracted,"A 46-year-old female, known the case of nonimmune, chronic hemolytic anemia, stable for 10 years with Vitamin B12 and Folic acid supplements. She had admitted with the history of severe abdominal pain, fever, and dyspnea for 3 months. She was initially diagnosed with myeloproliferative neoplasm and was started on tablet thalidomide (50 mg/day) and prednisolone (25 mg/day) for the same for 3 weeks. Since she needed frequent transfusions (>12 in 3 weeks with Heinz body positive), she was planned for splenectomy. She was diagnosed incidentally to have a bulla involving the right upper lobe communicating into right subsegmental bronchi. Although the bulla was large enough to occupy the whole right upper lobe, it was decided not to intervene as it was noninfectious, causing no obstructive signs or symptoms to the patient, and there was no history of spontaneous pneumothorax or recurrent respiratory tract infection in the past. The potential problems of the bulla and its associated complications were discussed with the patient.
On examination, she was 47 kg, and the height was 161 cm, and she was icteric. Systemic examination revealed the absence of breath sounds in the right infraclavicular and infra-axillary area and had hepatosplenomegaly. Other systemic examinations including airway examination were within normal limits. Laboratory investigation revealed severe anemia with a hemoglobin of 4.8 g/dL. Liver function test was normal except for the total bilirubin of 9.3 with the direct bilirubin of 0.9. Renal function and the coagulation workup were within normal limit. Chest X-ray showed a giant bulla over the right upper lobe []. Computed tomography-thorax revealed 9 cm × 9 cm, thin-walled right upper lobe bulla communicating into right upper lobe subsegmental bronchi, with segmental atelectasis of inferior lingula [Figure and ]. Spirometry revealed moderate obstructive ventilatory defect with no significant reversibility. She was transfused with two units of packed red cell during the preoperative period and taken up for surgery.
Since she had planned for splenectomy, the need for general anaesthesia with IPPV necessitates us to isolate the right upper lobe subsegmental bronchus for segregating the bulla. She was premedicated with 5 mg of diazepam and 20 mg of omeprazole 90 min before surgery. After bringing her to odds ratio, standard monitoring such as electrocardiogram, pulse oximetry, and noninvasive arterial blood pressure were established. ETCO2 and the nasopharyngeal temperature monitoring were done after induction.
An 18-G peripheral intravenous (IV) cannula was started. Since she was on prednisolone during the preoperative period (can cause hypothalamic-pituitary axis suppression), 100 mg of hydrocortisone was given to prevent stress-induced perioperative adrenocortical insufficiency. Then, she was preoxygenated with 6 L/min of 100% oxygen for 10 min. Anesthesia induction was carried out with fentanyl 100 mcg, propofol 120 mg, and succinylcholine 100 mg. After 60 s of apneic oxygenation, a 35 F left-sided double-lumen tube (DLT) (Mallinckrodt™, USA) was introduced, and its position was confirmed by 2.5 mm fiberoptic bronchoscope (FOB) (Karl Storz, Germany). Then, the anesthesia circuit was connected to the bronchial lumen to ventilate only the left lung. While the ventilation was continued through the left lung, a FOB was introduced through the tracheal lumen of DLT then into the right ULB and into the subsegmental bronchus to study anatomy.
Under FOB (2.5 mm) guidance, a seven size Arndt blocker (65 cm) was passed into the RUL bronchus, and then, into the subsegmental bronchus which was communicating to the bulla. To achieve this, Arndt blocker adopter was connected to the tracheal lumen of Left DLT, the Arndt blocker was passed through the blocker port (side port), and its wire loop was kept such a way to receive the fiberoptic scope which was passed through the FOB port. Once the FOB was snared into the wire loop, both were advanced simultaneously into the RUL subsegmental bronchus. After reaching the subsegmental bronchus, the snare was loosened, and the FOB was slowly pulled out into right upper lobe bronchus. Then, the final position of Arndt blocker position was adjusted and confirmed once again with FOB and was inflated with 1 ml of air. There was no desaturation noted during the insertion of Arndt blocker. Before moving onto two lung ventilation, the position of Arndt blocker was confirmed once again using the FOB, and then, the two-lung ventilation was resumed. The patient got ventilated with pressure controlled ventilation keeping the peak inspiratory pressure <15 cm of H2O. Respiratory rate was adjusted to maintain the ETCO2 between 33 and 35 mmHg. The surgery lasted for 2 h with minimal blood loss of 200 ml. Adequacy of muscle relaxation was monitored, using a neuromuscular monitoring device. TOF count was maintained between 1 and 2 during surgery to avoid coughing and bucking on the tube which can lead to rupture of the bulla. The patient's hemodynamics and body temperature were maintained within the normal limits. At the end of surgery, the muscle relaxation was reversed with neostigmine 2.5 mg and glycopyrrolate 0.4 mg. Once the patient was breathing spontaneously with adequate tidal volume, Arndt blocker was deflated and taken out. The DLT was removed when the patient was fully awake. IV Xylocaine (1.5 mg/kg) was given to facilitate smooth extubation without coughing. Postoperative pain was managed using IV morphine using the patient-controlled analgesia technique. The postoperative chest X-ray showed intact bulla []. Her postoperative course was uneventful, and she got discharged from the hospital on the 10th postoperative day.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [161.0, 'cm']}",53.28748,50.62311,55.95185,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 161.0 cm, which is 161.0 cm * 0.393701 in/cm = 63.38586 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.38586 (in inches) - 60) = 53.28748 kg.
Hence, the patient's IBW is 53.28748 kg."
3919,10,Ideal Body Weight,physical,decimal,pmc-2892589-1,Extracted,"A 51-year-old female patient, 52 kg in weight and 155 cm in height, visited to receive total hip arthroplasty due to osteoarthritis caused by acetabular dysplasia in her left hip joint. There were no special findings in her personal medical history, including a recent physical examination, chest X-ray, electrocardiogram and blood test before surgery.
Before the operation, 20 mg of famotidine and 0.2 mg of glycopyrrolate were administered intramuscularly. Due to a spinal block, 10 mg of 0.5% bupivacaine was injected into the subarachnoid space and a lack of sensation in the 9th thoracic vertebrae was confirmed. For sedation during surgery, 1.0 mg of midazolam was injected and 5 L/min of oxygen was administered through a face mask. The patient was placed under anesthesia for approximately two hours. The amount of blood loss, fluid administered during surgery and urine output was 400 ml, 2,100 ml and 950 ml, respectively. Arterial blood gas analysis immediately before completion of the surgery revealed the following: pH 7.386, PaCO2 42.5 mmHg, PaO2 164.7 mmHg, HCO3 24.6 mM/L, SaO2 99.8%, and Hb 10.1 g/dl.
When the patient arrived in the recovery room, her blood pressure, heart rate and pulse oximetry was 110/60 mmHg, 65 beats/min, and 99%, respectively. The patient was covered with a warm blanket because she complained of being cold and shivered. After approximately three hours, a blood test, a chemical test and coagulation were performed because she complained of dizziness and showed slight cyanosis in her lips. At this time, her blood pressure, heart rate and pulse oximetry was 90/50 mmHg, 70-95 beats/min and 98%, respectively. The test results showed 7.9 g/dl of hemoglobin and 24.3% of hematocrit, due to suspected hypovolemia.
A decision was made to provide a central venous catheter to secure the routes for fluids and monitor the cardiovascular status. In addition an attempt was made to insert 7 Fr (Two-lumen central venous subclavian catheter set with blue flex tip, Arrow, USA) to the left, because a large assortment of wires for monitors, fluids and racks were dangling and attached to the patient. The bed was inclined slightly to hold the patient in the Trendelenburg position. Her left arm was in complete internal rotation and her neck was turned to the right. Lidocaine was administered at 2-3 cm downward from themidpoint of the left central clavicle for local anesthesia and the skin was punctured using an 18 G, 6.35 cm needle. The needle was inserted along the back of the clavicle to proceed toward the sternal notch parallel to the clavicle. A J-inducing wire was inserted after venipuncture and the needle was removed. Space for the catheter was expanded using an expander and after inserting the central venous catheter, it was confirmed that blood had been absorbed at the two catheters without resistance. They were fixed at an approximately 15 cm length from the skin. At this time, the patient's blood pressure, heart rate and pulse oximetry was 110/60 mmHg, 78-100 beats/min and 99%, respectively. 500 ml of packed red blood cells was injected through a central venous catheter.
The emergency blood test found that approximately 50 ml of blood had drained into the Hemovac, which was much lower than that drained extracoporeally. Therefore, a decision was made to use computed tomography (CT) on the next morning to locate the bleeding, considering that 50 ml of blood had drained into the Hemovac, which was too little. Iopromide, a contrast medium, was injected at a rate of 2 ml/s to a total dose of 120 ml through a central venous catheter of the left subclavian vein for CT of the abdomen and pelvis.
Immediately after CT, the patient complained of heaviness in her chest and 5 L/min of oxygen was administered through a face mask. At that time, her blood pressure and heart rate was 110/66 mmHg and 70 beats/min, respectively. The results of her arterial blood gas analysis were as follows: pH 7.406, PaCO2 36.8 mmHg, PaO2 109.6 mmHg, HCO3-11.5 mM/L and SaO 299.3%. There were no outstanding symptoms evident after the electrocardiogram, an echo cardiogram and a cardiac enzyme test, and no signs of an allergic reaction that could occur after using the contrast medium. However, after a chest X-ray, the tip of the central venous catheter was placed at the brachiocephalic vein () and a hydrothorax on the left was observed by abdominal CT.
At the department of radiology, the site of a hydrothorax was detected using a sono guide and a Chiba needle was inserted between the 8th and 9th rib to drain approximately 100 ml of pleural effusion. An 8.5 F pig tail catheter was inserted using a hair wire. A slightly transparent fluid was absorbed through the piercing needle, which was checked by X-ray and established to be contrast medium. A contrast medium was injected slowly through the catheter to eliminate the possibility that it originated from the central venous catheter, which is a possible reason for it permeating through the chest cavity. It was confirmed that the contrast medium flowed inside the vein through the catheter and blood was sucked in slowly into the catheter without resistance. Although the central venous catheter was needed, a hair wire carefully was inserted to recheck the site of the catheter within the vein while double checking it with a sono guide and chest X-ray. It was replaced with another catheter and fixed 20 cm of its length away from the skin. Again we checked to see if blood was sucked into the catheter without resistance as well as its place using chest X-ray ().
The patient did not complain of dyspnea or any other symptoms and approximately 20 ml of extracoporeal drainage was obtained with a pig tail catheter inserted in her chest cavity. The patient was observed after the surgery using a chest X-ray and her vital signs were monitored carefully to guard against anaphylaxis by the contrast medium or cardiopulmonary side-effects.
Observations of her condition by chest X-ray showed that the hydrothorax had disappeared with no side-effects or cardiopulmonary symptoms. After seven days, the catheter was removed and the patient was moved to the general ward. Finally, she was discharged without a permanent lesion after 14 days.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3920,10,Ideal Body Weight,physical,decimal,usmle-2194,Extracted,"A 48-year-old woman comes to the physician because of recurrent right upper abdominal pain for 3 weeks. The pain usually occurs after meals and tends to radiate to the right shoulder. She reports that she otherwise feels well. She has more energy since she started an intermittent fasting diet and has rapidly lost 9.0 kg (20 lbs). She is 160 cm (5 ft 3 in) tall and weighs 100 kg (220 lb); BMI is 39.1 kg/m2. Physical examination shows a nontender abdomen. Abdominal ultrasonography shows several small stones in the gallbladder without calcification. When discussing treatment options, she states that she does not wish to undergo surgery and asks about other possibilities.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3921,10,Ideal Body Weight,physical,decimal,pmc-5448039-1,Extracted,"A 16-year-old adolescent male presented with multiple linear striae affecting both axillae and proximal arms. The striae were first noted a year ago. For the past two years, he indulged in heavy weight-lifting in a fitness center. He spent at least one hour per day in heavy weight-lifting, several days per week. The patient had quite a rapid growth spurt over the past few years. He grew 10 to 12 cm and gained 5 to 6 kg per year in the past two years. The patient noted that the deltoid areas became larger with the growth spurt and weight-lifting. He was in good health and was not on any medications. There was no family history of similar skin lesions.
On examination, he was alert and not in distress. His height was 165 cm and weight 57 kg with a body mass index (BMI) of 20.9 kg/m2. His heart rate was 70 beats per minute and blood pressure 105/75 mm Hg. Multiple violaceous, atrophic, vertical linear striae were noted affecting the axillae and proximal arms (). There were no striae elsewhere on the body. His pubic hair was of adult quality but did not spread to the junction of the medial thigh with perineum (Tanner stage 4). Hair was noted in both axillae. The long axis of the testes measured 4 cm. The penile length was 5.5 cm when flaccid. Acne vulgaris was noted on his face and forehead. All other physical findings were normal.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3922,10,Ideal Body Weight,physical,decimal,pmc-5331980-1,Extracted,"A 31-year-old pregnant woman, gravida 2, para 1, in the 11th week of gestation was referred to our nephrology clinic for evaluation of hypokalemia detected incidentally during a routine health exam. She complained of chronic fatigue and recurrent numbness of both her hands. She had no relevant medical history, and denied laxative or diuretic abuse. There was no history of renal disease in her family.
On examination, she was thin (height 160 cm, weight 40 kg) with blood pressure of 90/60 mmHg without significant postural drop and no evidence of dehydration or fluid overload.
Biochemical investigation revealed hypokalemia with metabolic alkalosis, hypocalciuria, increased plasma re-nin activity and aldosterone (serum K, 2.57 mmol/L; total CO2, 32.3 mmol/L; random urine calcium/creatinine (Cr), 0.00016 mg/mg Cr; plasma renin activity, 10.83 ng/mL/hr; aldosterone, 24.9 ng/dL; respectively). The patient’s transtubular potassium gradient (TTKG) was elevated despite hypokalemia (TTKG, 8.25). Serum magnesium level was within normal range (2.11 mg/dL) (). Neither proteinuria (33 mg/gCr) nor hematuria was detected. These findings suggested Gitelman syndrome, with the exception of the normal magnesium level. The diagnosis was confirmed when a mutation c.2716C>T (p.Pro906Ser) (heterozygote) in the SLC12A3 gene was found on genetic analysis (). Oral potassium supplementation was started, and the patient underwent routine examination during her pregnancy (). Spironolactone was not given because of the possible antiandrogenic effects on the male fetus.
When the patient was at 33 weeks’ gestation, she visited the emergency department with a tingling sensation and tetany in both the upper and lower extremities. Her blood pressure was 120/80 mmHg, within normal range, but higher than her usual blood pressure (90/60 mmHg). Her Cr level was elevated (2.03 mg/dL) and renal protein excretion was slightly increased (0.2 g/gCr). Additional laboratory results were compatible with HELLP (hemolysis, elevated liver enzyme, low platelet) syndrome, including decreased haptoglobin (8 mg/dL) and increased plasma hemoglobin (12.5 g/dL) levels, increased lactic acid dehydrogenase (969 IU/L) levels, schistocytes on peripheral blood smears, elevated liver enzymes (aspartate aminotransferase, 210 IU/L; alanine transaminase, 108 IU/L), and decreased platelet counts (101,000/mm3). Fractional excretion of sodium was 0.72% and serum uric acid was 23.86 mg/dL.
The patient had abnormal uterine contractions resulting in spontaneous vaginal delivery of a male infant weighing 1,630 g (50% for his gestational age). His Apgar score was 4 in the first minute and 5 after five minutes, and he was admitted to the neonatal intensive care unit. Hyperbilirubinemia (peak total bilirubin 9.87 mg/dL, indirect bilirubin 1.03 mg/dL) was detected, but his electrolytes were normal other than mild hyponatremia (sodium, 126.7 mmol/L; potassium, 3.01 mmol/L; chloride, 88.8 mmol/L). Postpartum, the patient suffered from disseminated intravascular coagulation (platelets, 89,000/μL; prothrombin time, 9.9 sec; activated partial thromboplastin time, 32.4 sec; D-dimer, 2.60 μg/mL; fibrin degradation products 8.1 μg/mL; and antithrombin III, 22%). The patient and neonate recovered slowly during the following weeks (). The patient was discharged on daily oral potassium and spironolactone (). Outpatient follow-up after five months revealed patient blood pressure of 90/60 mmHg and serum potassium and magnesium levels of 3.03 mmol/L and 2.17 mg/dL, respectively.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3923,10,Ideal Body Weight,physical,decimal,pmc-4660710-1,Extracted,"A 16-year-old with male habitus presented with complains of cyclic hematuria. The episodes of hematuria occurred monthly for a duration of 3–4 days since 6 months, which were always preceded by lower abdominal cramps. There was no antenatal hormonal or drug exposure, no history of precocious neonatal death in the family, ambiguous genitalia, genetic syndromes or any known endocrinopathy.
On physical examination, the patient was a thin built male with height 154 cm, weight 56 kg, normal intellectual function, and bilateral gynecomastia (Tanner stage 3). Facial hair was absent, and axillary hair growth was sparse. External genitalia examination revealed pubic hair of feminine distribution type (Tanner stage 3), penile length of 4 cm with normally located external meatus, and unilateral left cryptorchidism without a detectable hernia. The right side testis was of normal size and consistency normally located in the hemiscrotum. Digital rectal examination revealed smooth cystic swelling above small size prostate over the left half. The rest of the systemic examination was unremarkable [Figure –].
On ultrasonography, a cystic area of 42 mm × 32 mm was seen behind the left posterior half of urinary bladder with mild left sided hydroureteronephrosis. Magnetic resonance imaging findings were also consistent with ultrasonography report with no evidence of left side testis in the abdomen. The right side gonad was confirmed to be testis by radio imaging [Figure and ].
Hormonal findings of the patient are depicted in . The patient was subjected to chromosomal analysis (GTG banding with 500 band resolution) which revealed 46, XX/47, XXY mosaicism of female karyotype and KS. Specimen studied was whole blood, and 50 cells were counted and analyzed. Of 50, 40 cells showed mosaicism 46, XX, and the remaining 10 cells showed 47, XXY [Figure and ].
Subsequently, patient underwent cystoscopy during episode of hematuria, which revealed smooth walled bladder with a large bulge over the left half due to which left ureteric orifice was displaced superiorly and medially, and small size prostate with prominent verumontanum. Abdominal exploration through midline revealed a cystic swelling through which remnant of the uterus was attached to the prostatic urethra in the midline with single fallopian tube and ovary. [] These structures were excised in view of patient reared as male.
The histopathological report confirmed the excised structures to be ovary with cystic follicles, a uterus with endometrium in the proliferative phase and fallopian tube. Cystic swelling showed a few glandular structures with stratified squamous epithelium in cyst wall suggestive of the cervix [Figure –].","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [154.0, 'cm']}",51.44889,48.87645,54.02133,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 154.0 cm, which is 154.0 cm * 0.393701 in/cm = 60.62995 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (60.62995 (in inches) - 60) = 51.44889 kg.
Hence, the patient's IBW is 51.44889 kg."
3924,10,Ideal Body Weight,physical,decimal,usmle-8717,Extracted,"A 45-year-old man presents to the physician with complaints of burning pain in both feet and lower legs for 3 months. He reports that the pain is especially severe at night. He has a history of diabetes mellitus for the past 5 years, and he frequently skips his oral antidiabetic medications. His temperature is 36.9°C (98.4°F), heart rate is 80/min, respiratory rate is 15/min, and blood pressure is 120/80 mm Hg. His weight is 70 kg (154.3 lb) and height is 165 cm (approx. 5 ft 5 in). The neurologic examination reveals loss of sensations of pain and temperature over the dorsal and ventral sides of the feet and over the distal one-third of both legs. Proprioception is normal; knee jerks and ankle reflexes are also normal. The tone and strength in all muscles are normal. The hemoglobin A1C is 7.8%.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3925,10,Ideal Body Weight,physical,decimal,pmc-6311974-1,Extracted,"A 38-year-old man presented to an emergency department with progressive weakness and decreased urine output after having vomited up to 20 times per day over a period of 7 days. The patient was referred to our intensive care unit. Before medical consultation, he was healthy, and no other symptoms were reported. Diarrhea, fever, chills, or abdominal pain was absent.
Clinical examination revealed a patient of normal weight (height: 180 cm, weight: 70 kg). Blood pressure and heart rate were elevated (150/80 mmHg, 105/min); the respiratory rate was normal (13/min), but oxygen saturation was low (89%). During blood pressure measurement, a positive Trousseau sign was noted. The mucous membranes were dry, and the physical examination was otherwise unremarkable.
Arterial blood gas analysis revealed a metabolic alkalosis with partial respiratory compensation (pH: 7.71 [7.35–7.45], base excess: 40.5 mmol/l [-2-3 mmol/l], pCO2: 56.1 mmHg [32–45 mmHg], pO2: 43.5 mmHg [83–108 mmHg], bicarbonate: 72.2 mmol/l [21–26 mmol/l], lactate: 2.8 mmol/l [0.5–1.6 mmol/l], chloride: 52 mmol/l [98–106 mmol/l], sodium: 130 mmol/l [136–146 mmol/l], potassium: 2.4 mmol/l [3.5–5.1 mmol/l], ionized calcium: 0.77 mmol/l [1.15–1.29 mmol/l] and glucose: 165 mg/dl [70–105 mg/dl]).
Ultrasound revealed a distended and full stomach; the inferior vena cava was collapsing on inspiration. Otherwise, the ultrasound was unremarkable. The electrocardiography [] showed a prolonged QT interval (QTc 547 ms).
Laboratory tests were consistent with acute kidney injury (creatinine: 5.2 mg/dl, urea: 176 mg/dl); liver function tests, coagulation tests, albumin, lipase, procalcitonin, total calcium, hemoglobin, and thyroid-stimulating hormone were normal. Leukocytes were minimally elevated (11500/μl).
We suspected a prerenal acute kidney injury and a hypochloremic metabolic alkalosis due to gastric losses of HCl and fluids. Initial management consisted of oxygen therapy to correct hypoxemia and intravenous fluid therapy with normal saline and potassium chloride. Initially, a balanced crystalloid solution was infused, and later normal saline with KCl (40 mmol/l) was used because of the higher chloride content. Metoclopramide was administered to promote gastric emptying. To prevent further gastric losses of HCl, a proton-pump inhibitor was given. The patient was put on nihil per os for 24 h.
After 24 h, a total of 4.5 l of crystalloid fluid was infused. There was no further vomiting. A repeated bedside ultrasound revealed an empty stomach. The pH was corrected to 7.49, bicarbonate was reduced to 48.6 mmol/l, base excess was 23.4, chloride was 69 mmol/l, and potassium was still low at 2.8 mmol/l. There was hypoventilation with a pCO2 of 68.4 mmHg. We noted onset of diuresis. After 72 h of fluid therapy, the acid-base and electrolyte status was normal. Creatinine had decreased to 3.5 mg/dl. Small meals were tolerated.
Since there was no evidence of an infectious etiology for the excessive vomiting and the ultrasound had shown a distended stomach, an upper gastrointestinal endoscopy was performed []. A significant stenosis of the duodenum was diagnosed. Although there was no ulcer visible, an occult ulcer was deemed to be possible. A portal hypertensive gastropathy was diagnosed while esophageal varices were absent. Helicobacter pylori testing was positive, so an eradication therapy was initiated. A repeated endoscopy confirmed the stenosis, but again, no ulcer was seen. Since a focused abdominal ultrasound did not reveal the reason for the stenosis, a magnetic resonance imaging scan was performed to rule out malignancy such as pancreatic or gallbladder cancer or a thrombosis of the mesenteric vein. There was no evidence of malignancy or cirrhosis. An endosonography was done without evidence of malignancy or mesenteric vein thrombosis. At that point, the stenosis had partly resolved, and endoscopic passage was possible. We concluded that the temporary duodenal stenosis was caused most likely by portal hypertension of unknown etiology, and our differential diagnosis included idiopathic noncirrhotic portal hypertension after exclusion of cirrhosis and portal vein obstruction.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [180.0, 'cm']}",74.99221,71.2426,78.74182,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 180.0 cm, which is 180.0 cm * 0.393701 in/cm = 70.86618 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.86618 (in inches) - 60) = 74.99221 kg.
Hence, the patient's IBW is 74.99221 kg."
3926,10,Ideal Body Weight,physical,decimal,pmc-6167670-1,Extracted,"A 61-year-old Japanese male visited our clinic with a pretibial edema which had already persisted for a few days. He did not show any symptoms suggestive of viral infection and did not have any chronic illness and allergic disease. He had a history of nephrotic syndrome that initially developed when he was 5 years old. His nephrotic syndrome was corticosteroid dependent, i.e., his urinary protein level rapidly reduced with corticosteroids, but relapses were common after the reduction or discontinuation of corticosteroids. He had not experienced a relapse since he was 9 years old. He could recall undergoing a renal biopsy but not its outcomes. Although his medical records were not available, we assumed that he had MCNS. He was not treated with immunosuppressive agents at that time because they were not available in Japan.
Physical examination revealed a pitting edema of his lower extremities (Fig. ). His blood pressure was 176/100 mm Hg, his height was 169.8 cm, and his weight was 72.0 kg. The laboratory test results were as follows: hemoglobin, 14.9 g/dL; red blood cell count, 518 × 104/mm3; white blood cell count, 7,990/mm3; platelet count, 28.9 × 104/mm3; total protein, 5.5 g/dL; serum albumin, 2.7 g/dL; Na, 139 mEq/L; K, 4.2 mEq/L; Cl, 104 mEq/L; serum creatinine, 0.92 mg/dL; eGFR, 65.3 mL/min/1.73m2; AST, 23 IU/L; ALT, 21 IU/L; cholesterol, 318 mg/dL; triglyceride, 219 mg/dL; blood glucose, 94 mg/dL; and HbA1c 5.4%. Urinalysis showed urinary protein 3+, negative glucose, and 5–9/HPF red blood cells in the sediment. The amount of urinary protein was 13.3 g/g creatinine.
The patient was diagnosed with relapsed MCNS and was treated with 40 mg of prednisolone, 40 mg of furosemide, 75 mg of spironolactone, and 20 mg of azilsartan daily. In 1 week, his pretibial edema and urinary protein level reduced, and his blood pressure became normal. In 3 weeks, his serum total protein level was 6.1 g/dL and his serum albumin level was 3.6 g/dL. Subsequently, furosemide and spironolactone were discontinued, and the dose of prednisolone was reduced. After 6 months, prednisolone was discontinued; no relapse has been noticed till now.
A renal biopsy was not performed because the proteinuria quickly responded to the corticosteroids, which is a characteristic of MCNS and is unusual in other causes of glomerulonephritis.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [169.8, 'cm']}",65.75599,62.46819,69.04379,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 169.8 cm, which is 169.8 cm * 0.393701 in/cm = 66.85043 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.85043 (in inches) - 60) = 65.75599 kg.
Hence, the patient's IBW is 65.75599 kg."
3927,10,Ideal Body Weight,physical,decimal,pmc-4464031-1,Extracted,"In January 2013, a 65-year-old Japanese woman was admitted to our hospital for the evaluation of renal dysfunction. In 2005, when she was 56 years old, SS was diagnosed because of a positive Schirmer/Rose Bengal test and the detection of anti-SS-A antibody at a titer of 1:16. A limited form of SSc was also diagnosed at that time because of a thickening of the finger skin, Raynaud phenomenon, and positivity for anti-centromere antibody (titer of 1:167). Thereafter, she was followed up without any medication. In April 2012, serum creatinine was 1.0 mg/dl and urinalysis was normal.
On admission, the patient was 155 cm tall and weighed 48.2 kg, with a blood pressure of 139/70 mm Hg and a temperature of 36.5°C. Her serum creatinine was 1.6 mg/dl, proteinuria was 1.6 g daily, and the urine sediment contained 20–29 erythrocytes/high-power field. ANCA was measured by enzyme-linked immunosorbent assay. It was positive for myeloperoxidase (MPO) at 130 enzyme-linked immunosorbent assay units (EU)/ml (normal <10 EU/ml), but was negative for anti-proteinase-3 and anti-glomerular basement membrane (GBM) antibodies. Antinuclear antibody was positive at a titer of 1:1280, anti-centromere antibody was positive at a titer of 167.0 U/ml (normal; <10.0), anti-SS-A antibody at a titer of 1:16, and anti-SS-B antibody was positive at a titer of 1:8. However, double-stranded-DNA, Smith, U1-nuclear ribonucleoprotein (RNP), RNA-polymerase III, rheumatoid factor, cyclic citrullinated peptide, and scleroderma (Scl)-70 antibodies were all negative.
Interstitial lung disease was noted by CT, but there was no neurological or skin involvement.
A light microscopic examination of a renal biopsy specimen containing 23 glomeruli revealed a global or segmental sclerosis in 5 glomeruli and necrotizing glomerulonephritis with fibrin deposition in 2 glomeruli (fig. ), but definite crescent formation was not noted. Focal interstitial lymphoplasmacytic infiltration was also seen (fig. ). There was no edematous narrowing or obliteration of renal interlobular arteries and arterioles. Immunofluorescence microscopy did not demonstrate any deposits of immunoglobulin or complement, and there were no electron-dense deposits on electron microscopy. ANCA-related necrotizing glomerulonephritis and focal interstitial nephritis were diagnosed, and tubulointerstitial nephritis was considered to have a close association with SS. However, SSc-related small arterial lesions were not noted.
Her treatment was initiated with intravenous methylprednisolone pulse therapy (1,000 mg/day for 3 days), followed by prednisolone (PSL) at 40 mg/day. The MPO-ANCA titer became normal within 6 months of starting treatment, and PSL was gradually tapered to 10 mg daily. Proteinuria decreased to 0.3 g daily, but serum creatinine remained at 1.6 mg/dl. One year after starting treatment, PSL was tapered to 5 mg daily and azathioprine was added at 50 mg daily. Urinalysis remained almost normal.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3928,10,Ideal Body Weight,physical,decimal,pmc-4173451-1,Extracted,"A 65-year-old male patient, known hypertensive on regular medication, weighing 96 kg, height 167 cm, body mass index (BMI) 34.5 kg/m2, with no other known comorbidities was admitted with complaints of swelling, approximately 10 × 8 cm size over the lower abdomen, which was diagnosed as umbilical hernia. The patient was posted for umbilical hernia repair. The patient was evaluated the day prior to surgery and written and informed consent for anaesthesia was taken after explaining the various anaesthetic options and their perioperative implications. Preanaesthetic evaluation revealed his vitals: The heart rate of 90/min and blood pressure in the left arm supine position was 160/94 mmHg. The patient was a known hypertensive for 10 years on regular medication with a calcium channel blocker. Airway examination revealed modified mallampati class of four. Thoracic and lumbar intervertebral spaces were not felt due to subcutaneous fat. Preoperatively, complete blood picture, coagulation profile, serum electrolytes, and renal parameters were within normal limits. Electrocardiogram (ECG) showed left ventricular hypertrophy, but echocardiography was normal other than the same finding.
The patient was asked to continue his antihypertensive medication with tablet amlodipine 10 mg as scheduled. Antiaspiration prophylaxis was achieved with tablet ranitidine 150 mg and tablet metoclopramide 10 mg the night and 3 h prior to surgery. After assuring adequate nil per oral, the patient was shifted to the operation theatre. We had planned for epidural analgesia with general anaesthesia. Our preinduction monitors included five electrode ECG, noninvasive blood pressure, pulse oximetry, and capnography. Baseline vitals were recorded, heart rate of 90/min, blood pressure of 154/88 mmHg in the left arm supine position, and room air saturation was 98%. Using aseptic precautions, intravenous cannulation was done in the nondominant hand with 18 gauge cannula. An attempt was made to position the patient for epidural both in lateral decubitus and later in the sitting position, but could not be optimally attained due to his truncal obesity. Moreover, we could not appreciate the intervertebral spaces and spinous processes in either thoracic or lumbar region, so epidural plan was unsuccessful. The patient was explained about this eventuality. We planned for ultrasound-guided TAP block postinduction, for which written consent was taken. Since we expected this to be a difficult airway and the procedure was expected to last about 30-40 min as discussed with surgeons, we planned for general anaesthesia with ProSeal laryngeal mask airway (PLMA) on spontaneous/assisted ventilation without paralysis and USG-guided TAP block. The difficult airway cart was checked and kept ready in the operating room. After 5 min of preoxygenation in propped up position, anaesthesia was induced with 100 μg fentanyl and titrated dose of 250 mg propofol iv, till loss of verbal response. The anaesthetic plane was deepened with 2% isoflurane in 100% oxygen, size five ProSeal laryngeal mask airway was inserted, and position was confirmed after getting a capnograph trace and equal chest expansion bilaterally. Ryles tube was inserted and stomach was deflated. As patient was having inadequate spontaneous tidal volumes (200-300 mL), was put on synchronised Intermittent mandatory ventilation (SIMV) with mandatory rate of 12 breaths/min, tidal volume 600 mL, and a positive end expiratory pressure of 5 cm H2O using the DatexOhmedaAespire machine. Anaesthesia was maintained on oxygen and nitous oxide (O2: N2O; 50:50) and 1.5% isoflurane. The TAP block was given bilaterally under ultrasound guidance, 15 mL of 0.5% bupivacaine was diluted with 15 mL normal saline (total volume 30 mL) was injected on each side, after placing the ultrasound probe transversely between the costal margin and iliac crest on the lateral abdominal wall, with the needle tip between the internal oblique and transversus abdominis. The pain relief was adequate as evidenced by the absence of tachycardia with skin incision and no supplemention was required with opioids or an anaesthetic throughout the procedure. The surgery was uneventful. Stomach was deflated again and antiemetic was given. PLMA was removed after patient was fully awake and breathing adequately. Intraoperatively, patient's hemodynamics were stable. Postoperatively, we monitored the pain scores using visual analogue scale (VAS) for next 24 every hour we monitored the VAS score and patient's comfort was ensured. During the first 14 h postoperatively, VAS was 1-2 and patient was not supplemented with any other analgesic. During the next 10 h, the effects of TAP block gradually weaned off and in the 15th hour postoperatively, when the VAS was 4-5, the patient required additional analgesia in the form of 1 g (100 mL) of paracetamol intravenously over 15 min. At the end of 24 h postoperatively, the VAS was 4 and additional dose of paracetamol 1 g intravenously was given and shifted to ward. Thus, the requirement of opoids analgesics postoperatively.
Thus, the requirement of opoids analgesics reduced postoperatively by using the TAP block.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [167.0, 'cm']}",63.22056,60.05953,66.38159,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 167.0 cm, which is 167.0 cm * 0.393701 in/cm = 65.74807 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.74807 (in inches) - 60) = 63.22056 kg.
Hence, the patient's IBW is 63.22056 kg."
3929,10,Ideal Body Weight,physical,decimal,pmc-2813128-1,Extracted,"A 34-year-old man was admitted for evaluation of worsening pedal edema. He was apparently healthy until four years back, when he developed edema of both feet and nonpruritic macular skin rash involving both lower limbs. Subsequently, he was detected to have hypertension, proteinuria and mild renal failure (6 months ago). He had no history of arthralgia, Raynaud's phenomenon, paraesthesia or gastrointestinal hemorrhage.
Six weeks prior to admission in our centre, he developed weakness of left upper and lower limbs with slurring of speech and was hospitalized elsewhere. A computerized tomographic scan of head had revealed an infarct in the right middle cerebral artery territory and he was treated with aspirin, statins, and antihypertensives. He made a complete recovery but was detected to have renal failure and was referred to us for further evaluation.
He weighed 74 kg and had a height of 174 cm. He had pallor and bilateral pitting pedal edema. There was no skin rash or lymphadenopathy. Blood pressure was 140/90 mmHg. Examination of cardiovascular system, respiratory system, and abdomen was normal. There were no neurological deficits.
Investigations revealed hemoglobin of 8.79 gm/dL, platelet count of 112000/mm3, total WBC count of 7960/mm3 - with a normal differential count, ESR of 40 mm at end of first hour. Urinalysis showed protein ++++, 6-8 RBCs/HPF; and 24 hour urine protein was 4420 mg. Blood urea was 72 mg/dL and serum creatinine was 3.1 mg/dL with normal serum levels of electrolytes. Liver function tests, PT and aPTT were normal. Serum albumin was 3.6 gm%, serum globulin 3.8 g/dL and serum cholesterol 240 mg/dL. Serum protein electrophoresis was normal. Blood and urine cultures were sterile. HBsAg, antihepatitis C virus (HCV) and HIV antibodies were negative VDRL, cANCA, pANCA, antiphospholipid antibodies, ANA, antids DNA were negative. Serum homocysteine [12 µmol/L] was normal and serum complement levels were reduced (C3:70 mg/dL, C4:18 mg/dL). Serum cryoglobulin assay was positive. On PAGE electrophoresis, the mobility was suggestive of mixed cryoglobulins. HCV RNA was negative in serum [polymerase chain reaction (PCR)]. Qualitative analysis for HCV RNA [by reverse transcriptase-PCR (RT-PCR)] in the cryoprecipitate was negative []. Doppler study of extra cranial carotid and vertebral vessels was normal. Ultra sonogram of abdomen, ECG, and echocardiogram were normal. Bone marrow examination was normal. X-rays of chest, skull spine, and pelvis were normal. Kidney biopsy showed lobular accentuation of glomeruli with mesangial proliferation, mild endocapillary proliferation, and double contour of glomerular basement membrane on light microscopy. Intracapillary eosinophilic PAS positive hyaline deposits were noted []. Interstitium showed mononuclear infiltrates. Immunofluorescence showed mesangial and capillary granular positivity for C3 IgG and IgM.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [174.0, 'cm']}",69.55913,66.08117,73.03709,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 174.0 cm, which is 174.0 cm * 0.393701 in/cm = 68.50397 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.50397 (in inches) - 60) = 69.55913 kg.
Hence, the patient's IBW is 69.55913 kg."
3930,10,Ideal Body Weight,physical,decimal,pmc-7567531-1,Extracted,"A 48-year-old man (80 kg, 177 cm, and ASA PS-IV) was scheduled for emergent below-knee amputation after he was found to have left lower limb diabetic foot ulcer associated with whole foot gangrene and osteomyelitis. His medical history was significant for uncontrolled type II DM and New York Heart Association class IV stage C CHF secondary to ischemic 4-chamber DCM. Electrocardiography analysis showed sinus tachycardia, left axis deviation, left ventricular hypertrophy, and inferior myocardial infarction. Bedside examination of transthoracic echocardiography prior to surgery estimated left ventricular EF of 27% and noted minimal tricuspid regurgitation. Posteroanterior chest radiography revealed cardiomegaly with signs of left chamber enlargement and grade-2 pulmonary edema. Bilateral lower limb arterial duplex ultrasonography was suggestive of peripheral arterial disease with mild atherosclerotic changes. Other organ function and biochemical disturbances included mild hypokalemia, hypernatremia, hyperchloremia, hyperglycemia, and leukocytosis (). His medications on admission included NPH insulin, aspirin, atorvastatin, furosemide, and metoprolol. We estimated his subjective metabolic equivalent of tasks ≤4, revised cardiac risk index (Lee criteria) of >11%, and glomerular filtration rate of 21,518 mL/min/1.73m2.
At admission to the operation theatre, he was diaphoretic with cold and clammy hands and feet. After informed consent, he was taken to the operating room where standard monitors were placed, and supplemental oxygen was administered via nasal cannula. A urinary catheter was placed to monitor urine output. The patient was then placed in a sitting position for spinal anesthetic administration.
The spinal block was performed by a consultant anesthetist between the level of L3 and L4 interspace using the midline approach. The skin was anesthetized with 3 mL of lidocaine 2%, and a 24-G Quincke spinal needle was used to administer a mixture of heavy bupivacaine 7.5 mg in 1.5 mL volume (BUPICAN™ HEAVY, 20mg/4mL ampule, Baxter Pharmaceuticals, India), dexmedetomidine 4 μg in 1 mL volume (Precedex™, 400 μg/100 mL vial, Hospira, USA), and fentanyl 25 μg in 0.5 mL volume (Fentanyl®, 100 μg/2 mL ampule, Janssen-Cilag Pharmaceutica, Germany). Phenylephrine, 50 µg, was administered intravenously, just before the subarachnoid block, as prophylaxis to postspinal hypotension. Immediately after the intrathecal injection, the patient was placed in the lateral position for 15 minutes, with the operative side down and the head 15°up. Then, he was turned supine and properly positioned for surgery. The sensory assessment revealed a loss of pinprick sensation to the level of T11 dermatomes and extending to both posteriorly and anteriorly.
Heart rate, oxygen saturation, and blood pressure were recorded before spinal anesthesia (baseline: mean blood pressure, MAP 87 mmHg; heart rate, HR 92 bpm; and SpO2 at room air, 90%), just after spinal anesthesia, and then every 5 minutes till the end of surgery. Hemodynamic stability was maintained throughout surgery (ie, MAP, 75–92 mmHg; HR, 80–100 bpm; and average hourly urine output, 50 mL). His SpO2 and skin temperature were maintained between 95% and 99%, and 36.0–36.8 °C, respectively. The rapid blood sugar test result at admission to operation theatre was 235 mg/dL. Intravenous regular insulin infusion (1unit/hour) was administered over an hour of the procedure, and the serum glycemic level was kept below 180 mg/dL. The surgical procedure was done by an orthopedic surgeon with 6 years of experience and lasted 80 minutes without any apparent complications. He received a total of 950 mL crystalloid and 350 mL packed red blood cells (PRBCs). The total estimated blood loss (EBL) was 350 mL, and the urine output was 150 mL. The patient was transferred to the postanesthesia care unit for further monitoring and then transported to the medical ward. He did not experience any side effects of perioperative therapy, including nausea, vomiting, pruritus, hypotension, or postdural puncture headache during his postoperative course. Postoperative laboratory exam on day one revealed hemoglobin, 12.1 g/dL; hematocrit, 35%; platelet, 185 ×103 cells/µL; white blood cells, 15.6 ×103 cells/L; creatinine, 0.97 mg/dL; blood urea nitrogen, 42 mg/dL; K+, 3.7 mmol/L; Na+, 160 mmol/L; and Cl−, 112.8 mmol/dL. He was discharged home on postoperative day 8 after the medical conditions were optimized.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [177.0, 'cm']}",72.27568,68.6619,75.88946,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 177.0 cm, which is 177.0 cm * 0.393701 in/cm = 69.68508 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.68508 (in inches) - 60) = 72.27568 kg.
Hence, the patient's IBW is 72.27568 kg."
3931,10,Ideal Body Weight,physical,decimal,pmc-3330246-1,Extracted,"A 43-year-old woman, divorced with no children, on leave from her work as a pharmacist, had a longstanding history of severe and refractory AN, binge-eating/purging type. She was first hospitalized at 15 years of age with restricted eating and extreme weight loss (height, 157 cm, weight, 31.7 kg; BMI, 12.9) and diagnosed with AN. She began to engage in binge-eating episodes shortly thereafter, and added self-induced vomiting and some compensatory exercise at age 20. Her first episode of depression developed at the same age. The frequency and severity of depressive episodes, binge-eating and self-induced vomiting increased steadily over the next 20 years.
There was a marked increase in illness severity in 2007, when her husband of 8 years ended their relationship. For approximately 4 years thereafter, she engaged in one to two binge-eating episodes per day, each lasting at least 5 h, followed immediately by purging by vomiting. By 2010, she was engaging in binge-eating and purging almost to the exclusion of all other activities including socializing, paying bills, or doing errands. She reported that she would often remain awake throughout the night to continue these behaviors, and at times would have insufficient time to shower or dress in the morning due to the duration and intensity of the episodes. Her weight gradually increased into the normal range as a consequence of the severity of her bulimic behavior, so that her diagnosis shifted to BN. As of June of 2010, she was obliged to give up her work as a pharmacist due to the severity of her illness.
There was no history of hypomania or mania, panic disorder, obsessions or compulsions, delusions or hallucinations, or self-harm behavior, either past or present. She had never engaged in any substance use aside from one to two alcoholic drinks per month. Her past medical history was remarkable for osteopenia and poor dentition secondary to purging. Although there were no family members with any formal psychiatric diagnosis, her mother and sister were reported to have symptoms of MDD, and a maternal aunt was reported to have symptoms of AN. She did have a history of paternal physical abuse in childhood.
From age 30, she had had unsuccessful trials of multiple SSRIs, trazodone, and desipramine, with add-on treatment using risperidone, quetiapine, methylphenidate, and modafinil. She had also unsuccessfully pursued several courses of intensive treatment for eating disorders, including four admissions to inpatient programs, six admissions to day hospital programs, and participation in mindfulness-based stress reduction, cognitive behavioral therapy, occupational therapy through a community outreach program, group therapy, and intensive treatment for her trauma history. In June 2010, she had attempted a day program at the Toronto General Hospital but was unable to significantly modify her eating behavior and was obliged to withdraw. In October 2010, at a weight of 47 kg (BMI, 18.9), she entered a 6-week inpatient treatment and was able to normalize her eating in this setting. However, she suffered a complete relapse 4 days after discharge to outpatient treatment, returning to twice-daily 5 h binge-eating episodes followed by purging, to the exclusion of most other activities. These episodes continued uninterrupted for the next 5 months until the beginning of her rTMS treatment.
In April, 2011, she was referred for rTMS to address her refractory depression, rather than her disordered eating. At her intake assessment, she reported a current episode of depression beginning in 2009, with daily symptoms of low mood, partial anhedonia, loneliness, highly impaired concentration and decision-making abilities, social withdrawal, decreased energy and motivation, and persistent thoughts of hopelessness and self-criticism about her inability to follow through with plans. She had thoughts that life was no longer worth living, but no specific suicidal intent or plan. She reported her depressive symptoms as moderately improved on a regimen of venlafaxine XR 300 mg once daily and desvenlafaxine 50 mg once daily, which she had been taking for the last 3 months. Her baseline pre-treatment scores were 26 on the 17-item Hamilton Depression Rating Scale (HamD17) and 28 on the Beck Depression Inventory-II (BDI-II) self-report, suggesting a moderate to severe level of depressive symptoms.
In addition, she reported symptoms of disordered eating with twice-daily 5 h binges followed by purging for the last 5 months. She had a distortion of body image, describing her own appearance as “too old” and “funny-looking.” Her menses had been present over the past year. At this time her weight was 50 kg (BMI, 20.3). She reported her current major stressors as being primarily around loneliness, separation from her husband, difficulty following through on her plans, and difficulty managing her eating and purging behavior.
Following assessment, she was accepted for treatment and underwent a preliminary MRI, followed by 20 sessions of neuronavigated rTMS, one session per weekday, over 4 weeks. Neuronavigation employed the Visor 2.0 frameless stereotaxic system (Advanced Neuro Technologies, Madison, WI, USA) to position the coil at the scalp point at minimum distance from the coordinate (x 0, y + 28, z + 45) in standard space (Talairach and Tournoux, ), corresponding to DMPFC. Stimulation employed a MagPro R30 rTMS device connected to the fluid-cooled Cool-DB80 coil (MagVenture, Farum, Denmark), which has windings angled at 120° rather than 180° to achieve greater depths of stimulation.
Each treatment session involved stimulation of right then left DMPFC with 60 trains of 10 Hz stimulation at 120% of resting motor threshold in 5 s trains with a 10-s inter-train interval, for a total of 3000 pulses to each hemisphere, as per a previously published protocol (Hadley et al., ). Prior to the first session, motor thresholds for flexion of the contralateral hallux were determined for each hemisphere using previously published methods (Schutter and van Honk, ; Hayward et al., ). The primary motor cortical region for the lower extremity lies on the medial wall at depths comparable to the DMPFC. Preferential stimulation of each hemisphere was achieved by orienting the coil at 90° to midline, so that the direction of current flow at the coil intersection was aimed toward the hemisphere to be stimulated. As in the previous reports, this technique produced asymmetric motor activation of the contralateral lower extremity during motor threshold determination. The same approach was used for stimulation of left and right DMPFC during treatment.
The patient tolerated the treatment well. The only adverse effects were headache and localized scalp discomfort around the site of stimulation during the first 10 sessions, and mild pre-syncopal episodes on the first and second sessions. On both occasions, she was able to recover with a brief period of rest and complete the session.
Her depression symptoms remitted over the course of treatment on both self- and clinician-rated measures, accompanied by marked and rapid improvement in daily psychosocial functioning. Her baseline BDI-II score, monitored daily, dropped from 28 at baseline to 7 after 11 sessions, and remained in this range thereafter. On the HamD17, monitored weekly, her score dropped from 26 at baseline to 0 by the end of treatment.
The more striking and unexpected outcome was that, after the second session of treatment, both the binge-eating and the purging behaviors stopped abruptly (Figure ). As previously noted, the patient had been referred for rTMS for depression and there was no prior expectation of improvements in her disordered eating. For this reason, standardized measures of eating disorder severity using standard scales are not available. However, even using the coarse measure of daily binge incidence, the degree of improvement was pronounced. Using a daily log, she reported complete remission throughout the remainder of the first week of treatment. During sessions 6–10, she reported a single binge-purge episode per day. These resolved once again by the session 11 of treatment, and did not recur thereafter. Subjectively, she reported that she found herself better able to apply strategies she had learned in therapy to redirect her thoughts and behavior away from binge-eating and purging. Specifically, she reported a reduction in her sense of urgency or impulsiveness when she had the urge to binge or purge, and an enhanced ability to make other choices and follow through on planned alternative behavior. As she continued to be successful in resisting these impulses, a sense of optimism and positive self-esteem developed, and her mood then began to improve.
Full remission of both depression and disordered eating was maintained for a period of 64 days after the last session of treatment. On days 65, 70, and 71 post-treatment, she had a single episode of binge-eating and purging. She had reported the emergence of a significant psychosocial stressor (contact with her former spouse) immediately prior to this recurrence, and requested a repeat course of rTMS to avoid relapse. A second 20-session course of rTMS was initiated on day 82 post-treatment, by which time her BDI-II had increased to 20 and her HamD17 had increased to 11. After 5 sessions of treatment these had decreased to 7 and 7, respectively. Binge-eating and purging once again resolved completely after the first session of rTMS. She remained in remission from both depression and disordered eating throughout the rest of the course of treatment.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [157.0, 'cm']}",49.66544,47.18217,52.14871,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 157.0 cm, which is 157.0 cm * 0.393701 in/cm = 61.81106 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.81106 (in inches) - 60) = 49.66544 kg.
Hence, the patient's IBW is 49.66544 kg."
3932,10,Ideal Body Weight,physical,decimal,pmc-6241716-1,Extracted,"Written informed consent has been provided and signed by the patient to have the case details and any accompanying images published.
A 23-year-old man presented with a diagnosis of DEB and secondary pyoderma. His family history was unremarkable.
Review of medical history revealed that vesicles first started to appear on the patient’s feet when he was beginning to walk at 11 months of age. Later, at the age of 20 months, the vesicles spread to the hands, and subsequently, lesions have always been associated with injury. As his growth progressed, skin lesions continuously progressed and occupied a large area of skin. Permanent formation of vesicles on the skin was noted, with nonhealing erosive surfaces with a bright red base at the age of 4 years. By the age of 8 years, bullous and erosive lesions were localized to the skin of the abdomen, back, and upper and lower extremities. On erosion sites, scar tissue had formed. At the same age, he had also developed contractures and pseudosyndactyly of the toes and hands.
Later in his life, periodic exacerbations of the disease occurred approximately every 2 months leading to the formation of new vesicles with purulent exudate and erosions, sometimes accompanied by fever up to 39°C. During exacerbations, the patient was given oral antibiotics, immunoglobulin, antihistamines, and topical agents that are mentioned in more detail below. The effect of treatment was insignificant. In addition, in the last 5 years, the patient experienced an increased frequency of allergic reactions, particularly to food, which were accompanied by pronounced redness and pruritus. More recently from 2016 to 2017, the patient used bandages comprising coarse nonwoven material impregnated with anhydrous ointment and silicone bandages. Zinc-containing creams and pastes were applied during dressing changes. As a result of this treatment, the patient noted a decrease in purulent exudate from the lesions and scar tissue formation.
In November 2012, the patient was examined at The Epidermolysis Bullosa Center Freiburg. Histological examination of skin biopsy showed no signs of squamous cell carcinoma, and X-ray contrast study of the esophagus revealed second-degree stenosis of the upper esophagus. Indirect immunofluorescence (IF) using antibodies to numerous proteins of the skin (desmoplakin, placefiles-1, citace-5, cytokeratin-14, plectin, integrin-α6, integrin-β4, collagen type XVII/BP 180, silvery-nu-332, collagen type IV, collagen type VII, and kind-Lin-1) showed decreased expression of collagen type VII on the surface of the vesicle. Based on these data, the diagnosis of recessive DEB was established. The acute generalized form was unlikely in this case because of the presence of a distinct residual glow of collagen type VII in biopsy material of the skin.
To clarify the subgroup of recessive EB, molecular genetic analysis of mutations in COL7A1 was suggested, but the patient declined.
On admission, the patient complained of rashes on the skin of the trunk and upper and lower extremities, accompanied by difficulty in swallowing, intense itching, and pain, which were aggravated by movements. Examination of the skin revealed that 70% of the body surface was covered with lesions. Rashes were localized to the skin of the trunk and upper and lower limbs. The scalp and face were free of lesions. The patient’s height and weight were 166 cm and 39.7 kg, respectively.
There were multiple erosions, which were bright red and irregular in shape, on the skin of the upper extremities, mainly in the shoulders, armpits, projection of the clavicle, and elbow and wrist joints. The surface of the erosions was marked by multiple-layered dirty yellow crust that secreted purulent discharge when pressed. The skin of the trunk, back, shoulder girdle, buttocks, inguinal areas, thighs, and knee joints showed extensive lesions of bright erythema, with erosive defect areas of atrophy of the skin, and multiple yellow crusts. He had pronounced flexion contractures of his hand joints with minimal finger range of motion. Although there existed finger deformities on the left hand, range of motion was preserved (–).
In the ankle and dorsum of the feet, there were minor red-colored erosions of irregular shape, with clear boundaries and multiple brownish-yellow laminated crusts on the surface. Areas of skin atrophy and scarring were noted on the periphery of the lesions.
In addition, there were contractures and pseudosyndactyly in the first and second digits of the left foot, the first, second, and third digits of the right foot, and dislocation of the fifth digit of the left foot. Nail plates on the fingers and toes were absent. During the inspection of the oral cavity, absence of eight teeth, as well as limitation of language skills, was noted.
Positive biochemical analysis results: potassium 5.7 mmol/L (normal: 3.5–5.5 mmol/L), chloride 112 mmol/L (normal: 99–109 mmol/L), phosphorus 1.64 mmol/L (normal: 0.81–1.45 mmol/L), iron 5.5 mmol/L (normal: 9.0– 30.4 mmol/L), transferrin 1.81 g/L (normal: 2.0–3.6 g/L), % saturation of iron 12.03% (normal: 20–55%), amylase 18.2 μ/L (normal: 30–118 μ/L), and IgA 3.59 g/L, IgM 1.27 g/L, and IgG 27.42 g/L (normal: 28–365 ng/mL);
Immunological study results: total IgE (ELISA) 371.76 IU/mL (normal: 0–100 IU/mL);
Immunological study results: antistreptolysin 0–232 IU/mL (normal: 0–125 IU/mL), C-reactive protein 11.40 mg/dL (normal: 0–0.8 mg/dL), and rheumatoid factor 25.30 IU/mL (normal: 0–20 IU/mL);
Ultrasonography of the abdominal cavity: echographic signs of a slight increase in the right lobe of the liver and inflection of the gallbladder;
Osteodensitometry results: bone density 0.503 g/cm2, which is found in 41% of the healthy people in this age group;
Age determination by roentgenogram of the hand bones: bone age was 17 years, which is a younger number than chronological age of 23 years (flexion contracture of fingers, severe osteopenia); and
Biopsy examination result: subepidermal blisters with variable inflammation; superficial dermis was fibrotic (collagen type IV positive, granular staining within basal and lower suprabasal keratinocytes; absent or markedly reduced staining along the dermoepidermal junction) ( and ).
During admission, the patient received the following treatments:
Actovegin 5 mL (200 mg:1 mL) intravenous infusion daily; Rifampicin 400 mg one tablet two times/day for a total of 14 days; Venofer 10 mL infusion three times/week after dilution of the drug with 0.9% NaCl solution in a ratio of 1:20 intravenously; Albumin 100 mL 5% intravenous infusion with the aim of maintaining the plasma albumin level of 3–4 mg/dL; Vitamin B12 1 mL+0.9% NaCl 10 mL/jet once a week for 3 weeks; Folic acid one tablet three times a day for 6 days; Chlorpheniramine one tablet three times a day PRN; Metoclopramide 10 mg three times a day PRN.
The overall management included antibiotic rifampicin to fight the existing infections and prevent secondary skin infections from developing, venofer iron sucrose to replenish the iron stores and treat anemia, albumin to treat hypoalbuminemia, and antihypoxic effect with actovegin which normalizes pH, promotes blood circulation, intensifies energy-intensive processes of regeneration and repair, and improves tropism of tissues. In addition, the patient was supplemented with vitamin B12 and folic acid due to their deficiencies and was given antihistamine and antipruritic as per the need to control pruritus and nausea as a side effect of treatment.
Local treatment included dioxomethyltetrahydropyrimidine and collagen sponge (Meturacol), spray dexpanthenol, algipor, octenidine dihydrochloride and phenoxyethanol antiseptic spray (Octenisept), betamethasone + gentamicin + clotrimazole ointment (Triderm), and hydrocortisone + natamycin + neomycin ointment (Pimafucort). Wound care was done daily using nonadhesive silicone dressings, which absorb exudate without causing detachment of the epidermis and shedding, and coarse atraumatic dressings saturated with anhydrous ointment. Before bandaging, erosive surfaces were treated with the abovementioned antiseptic preparations, aerosols, antibiotic ointments, glucocorticosteroids, agents stimulating tissue regeneration, azulene cream, and Unna zinc paste.
To stimulate epithelialization of erosions in the complex treatment of the patient, we included low-level laser therapy in order to provide trophic and regenerative action.
Given this complex treatment regimen, the patient’s skin in the trunk and lower extremities showed improvement with a decrease in the area of erosions, accompanied by a decrease in pain and itching of the lesions. The patient was discharged with the following recommendations in addition to close follow-up with the dermatologist ( and ): vitamin A and E; Aevit one capsule two times/day for 1 month; Ascorbic acid (vitamin C); Ascorutin one capsule two times a day for 1 month; Actovegin 200 mg one tablet three times a day for 6 weeks; Methyluracil 0.5 g one tablet three times a day for 1 month; Likopid one tablet sublingually for 10 days; Folic acid one tablet three times a day for 2 months; Human immunoglobulin 3 mL intramuscularly two times per week; Aktinolizat immunostimulant 3 mL intramuscularly two times a week; Local: collagen sponge: metrical and algipore.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [166.0, 'cm']}",62.31505,59.1993,65.4308,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 166.0 cm, which is 166.0 cm * 0.393701 in/cm = 65.35437 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.35437 (in inches) - 60) = 62.31505 kg.
Hence, the patient's IBW is 62.31505 kg."
3933,10,Ideal Body Weight,physical,decimal,pmc-4027082-1,Extracted,"A 13-year-old boy presented with sudden palsy of the left side of the face. Prednisolone (60 mg/day) and acyclovir (800 mg/day) were prescribed, however, the patient's facial palsy did not improve completely as we expected it was Bell palsy. He appeared lethargic and pale, and his parents suspected he had gained weight over the past two years. They also suspected his chronic fatigue was due to the weight gain.
The patient had no history of a viral infection, exposure to high levels of iodide or any medication. He was born at term weighing 3,500 g by spontaneous vaginal delivery without complication, and is the first child of unrelated parents. He also had no family history of any autoimmune or thyroid disease. His father's height was 176 cm. Mother's height was 155 cm, The mid parental height was 172 cm. His blood pressure was 100/60 mmHg, and ha had pulse rate of 70 beats/min.
Upon physical examination, he was found to be myxedematous with coarse facial features including dry and thickened skin. However, no goiter was found. His weight, height, and body mass index (BMI) were 68.5 kg (90-95 percentile), 155 cm (50th percentile), and 28.5 kg/m2 (>97th percentile), respectively. Pubertal development was also noted (penis, Tanner stage 2-3; pubic hair, Tanner stage 1; testis, 6-8 mL). Ophthalmological examinations, including a visual field test, revealed no abnormal findings.
Laboratory data revealed normocytic normochromic anemia (hemoglobin, 10.3 g/dL), and increased aspartate transaminase (68 IU/L), and alanine transaminase (139 IU/L), hypercholesteremia (total cholesterol, 378 mg/dL), hypertriglycemia (409 mg/dL), and increased creatine kinase (912.2 IU/L) levels (). Endocrinological testing showed severe primary hypothyroidism, elevated thyroid stimulating hormone level (TSH>100 µIU/mL) (normal range, 0.5 to 4.8 µIU/mL), decreased total thyroxine level (1.04 µg/dL) (4.5 to 12.0 µg/dL), decreased total triiodothyronine level (0.31 ng/mL) (1.19 to 2.18 ng/mL) and decreased free thyroxine level (0.07 ng/dL) (0.8 to 2.3 ng/dL), In addition, elevated levels of serum antithyroid peroxidase antibodies (1,933.39 IU/mL) (<10 IU/mL), antithyroglobulin antibodes (848.16 IU/mL) (<100 IU/mL), and TSH receptor antibodies (immunoassay>40 IU/L) (0.3 to 1.22 IU/L) were found. The results of the bioassay were negative for TSH receptor stimulating antibodies ().
Additional results of the laboratory analysis are as follows: prolactin, 29.04 ng/mL (3 to 18 ng/mL); morning serum cortisol, 6.69 µg/dL (3 to 21 µg/dL); adrenocorticotropic hormone, 20.31 pg/mL (10 to 60 pg/mL); growth hormone, 0.08 ng/mL (0.07 to 5.68 ng/mL); insulin like growth factor-I (IGF-I), 105.0 ng/mL (145.2 to 647.8 ng/mL); IGF binding protein-3 (IGFBP-3), 3,270 ng/mL (2,200 to 4,490 ng/mL); luteinizing hormone, 1.32 mIU/mL (0.2 to 4.9 mIU/mL); follicle stimulating hormone, 4.29 mIU/mL (1.8 to 3.2 mIU/mL); and testosterone, 0.2 ng/mL (0.18 to 1.5 ng/mL) (). According to the Greulich-Pyle method, bone age was 12.5 years (chronological age, 13 years). Thyroid sonography revealed a heterogenous internal structure; neither the size nor the vascularity of the bilateral gland was increased (). Thyroid scintigraphy with 99mTc revealed a substantially decreased uptake in both lobes (). Magnetic resonance images displayed an enlarged pituitary gland, with upward convexity, measuring 13.0 mm in height and a transverse diameter of 8 mm ().
After L-thyroxin treatment was initiated, the symptoms of facial palsy and the patient's clinical condition improved (, ). After 3 months, the second magnetic resonance images revealed a regression of the pituitary hyperplasia and a smaller pituitary gland than that from the first round of images. This condition was described as reactive hyperplasia caused by primary hypothyroidism. After 8 months, follow-up thyroid sonography revealed that the parenchymal echogenicity was coarse, and had decreased in size. However, changes to the size or echogenicity of the thyroid gland were not significant.
After 1 year, the patient's height was 166.2 cm (50-75th percentile), which is an 11 cm gain in height and his weight was 66 kg (75-90th percentile). His BMI also improved to 23.9 kg/m2 (75-85th percentile). Bone age was 14.5 years with the chronological age of 14 years. He was performing well academically.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [166.2, 'cm']}",62.49615,59.37134,65.62096,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 166.2 cm, which is 166.2 cm * 0.393701 in/cm = 65.43311 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.43311 (in inches) - 60) = 62.49615 kg.
Hence, the patient's IBW is 62.49615 kg."
3934,10,Ideal Body Weight,physical,decimal,pmc-4574176-1,Extracted,"The patient, a 13-year old boy, was the first and only child of unrelated healthy Caucasian parents. He was born by cesarean section after a full term pregnancy. Birth weight was 2,800 g (10th percentile), length 50 cm (50th percentile) and head circumference (HC) 35.5 cm (50th percentile). Neonatal and infancy periods were uneventful; nevertheless his motor development was delayed as he did not sit independently until the age of 15 months or walk unaided until the age of 22 months.
At the age of 5, language delay was observed and laboratory investigation was performed, including audiogram, biochemical and thyroid tests, which proved normal. He received speech therapy for a two-year period and his language difficulties resolved. He attended mainstream primary school with extra educational support and finished this level at the age of 12 years. At the age of 13 years he was referred for full developmental assessment because he was experiencing severe learning difficulties in secondary school. Upon physical examination, he was characterized as quite a sociable child, with mild dysmorphic facial features such as almond shaped eyes, hypertelorism, anteverted nostrils, and gothic palate. His weight at the time was 49 kg (40th percentile), height 160 cm (60th percentile) and HC 54 cm (25th percentile). Upon neurological examination, he showed mild motor delay with severe clumsiness but without focal neurological signs. Ophthalmologic examination was normal. Heart auscultation revealed a mild systolic murmur.
Upon developmental evaluation, he was found to function at the mental level of a 10-year old. His cognitive abilities, according to the Wechsler Intelligence Scale for Children test (WISC III), were assessed as borderline, as his full-scale score was 75 with verbal score 75 and performance score 80.
Extensive laboratory investigation followed, including brain magnetic resonance imaging (MRI), electroencephalogram, kidney-liver- spleen ultrasound, bone age, biochemical tests, blood and urine amino acids, organic acids, very low fatty acids, thyroid function, ACTH, FSH, LH, DHEA-S, prolactin, estradiol e2, progesterone, testosterone, 17a-OH progesterone and IGF-1, all proved normal. Heart ultrasound showed mild mitral valve prolapsed.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [160.0, 'cm']}",56.88197,54.03787,59.72607,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.99216 (in inches) - 60) = 56.88197 kg.
Hence, the patient's IBW is 56.88197 kg."
3935,10,Ideal Body Weight,physical,decimal,pmc-6502766-1,Extracted,"A 43-year-old male patient (ASA class I, weight 65 kg, height 173 cm) with right-side ankle fracture was scheduled for closed reduction and internal fixation. The medical history was unremarkable, with no history of surgery. Preoperative evaluations including laboratory tests, electrocardiography, and chest radiography revealed normal results. The patient denied the presence of any loose teeth or presence of dental prosthesis on questioning.
After the institution of standard monitors and pre-oxygenation, general anesthesia was induced with intravenous injection of 60 mg lidocaine, 100 µg fentanyl, 100 mg propofol, and 40 mg rocuronium. Following mask ventilation for 3 min with 100% oxygen and 7 vol% desflurane, the patient was intubated with conventional direct laryngoscopy, and a bite-block was used to protect the endotracheal tube. The induced general anesthesia was maintained with 7–8 vol% desflurane, and the surgery was performed successfully in an operating time of 2 h 45 min. Residual muscle relaxation was reversed with atropine and neostigmine after procedure completion. The patient successfully recovered without any complications and was extubated. No dental damage was noticed when the oral secretions were cleared with a suction apparatus, before and after extubation. The patient was transferred to the post-anesthesia care unit (PACU), and the patient complained of chest discomfort 20 min later and could not feel his upper incisors. An oral examination revealed that the upper incisors were missing, and we assumed that the patient had lost the dental bridge. Chest radiography was performed immediately, and a radiopaque shadow of the dental bridge in the esophagus was observed (). The patient was transferred to the endoscopy room to remove the foreign object. During the pre-procedure check in the endoscopy room, the nurse again asked the patient whether he had any other dental prostheses, and he said that he had removed his dentures before the esophagoscopy. The impacted dental bridge was successfully removed using esophago-gastroscopy, without any complications (). The patient was discharged 6 days after surgery with no complications.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.0, 'cm']}",68.65362,65.22094,72.0863,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.0 cm, which is 173.0 cm * 0.393701 in/cm = 68.11027 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.11027 (in inches) - 60) = 68.65362 kg.
Hence, the patient's IBW is 68.65362 kg."
3936,10,Ideal Body Weight,physical,decimal,pmc-6967327-1,Extracted,"Written informed consent was obtained from the patient for the publication of this case report.
An otherwise healthy 63-year-old man (166.7 cm/54 kg) with left inguinal hernia was planned to undergo an ambulatory open herniorrhaphy. General anesthesia combined with local infiltration was planned, according to the rule of the hospital for ambulatory herniorrhaphy.
Premedication was not given. Standard monitors were attached to the patient on entering the operating room. Anesthesia was induced with 140 mg of propofol, and 50 mcg of fentanyl after the venous access was established. The airway was secured with supraglottic airway after muscle relaxation had been acquired with 0.9 mg/kg of rocuronium. Anesthesia was maintained with 5% desflurane, and mechanical ventilation by pressure control was maintained throughout the surgery. The local anesthetic mixture was made from 10 mL of 0.75% ropivacaine and 10 mL of 1% lidocaine with adrenaline 1:200,000. The surgeon administered 5 mL of the mixture into the subcutaneous tissue before the incision, 3 mL between Camper’s fascia and Scarpa’s fascia, and 2 mL into the inguinal canal. The rest of the mixture (10 mL) was administered with intense pressure between the internal oblique and transversus abdominis muscles at the end of the surgery before skin closure. Another 50 mcg of fentanyl was administered intraoperatively, and 0.5 mg of droperidol was administered before emergence. Surgery was performed with only slight changes in heart rate and blood pressure. The muscle relaxation was reversed with 200 mg of Sugammadex at the end of the surgery. The patient was extubated after stable spontaneous respiration, and good emergence was confirmed. The patient seemed to be able to perform the adduction and abduction of his shoulders, and the extension and flexion of his elbows, hips, knees, and ankles at this point. The duration of the surgery was 45 mins, and anesthetic time was 70 mins. The patient was transferred to the postanesthetic care unit without trouble.
The patient condition was observed 1 h after the transfer. The mental status was alert with E4V5M6 at Glasgow coma scale. He experienced no postoperative nausea and vomiting. There was a slight dull pain around the surgical wound, which soon resolved after 1000 mg of rescue acetaminophen. He was able to drink clear water without nausea or aspiration. Although the patient was able to walk to the restroom with the drip stand and void without trouble, he complained of discomfort in his left thigh. The physical examination revealed that we had not recognized that he could adduct his left hip joint poorly with grade 1 at the manual muscle test (MMT) without any apparent sensory deficit in the left leg. His leg flexion, knee extension, and the sensation of the lateral and medial thigh were normally maintained. Three hours after the surgery, the adduction of the hip recovered to MMT 3. However, the patient could not perform ipsilateral leg flexion nor knee extension against moderate pressure (MMT 4), and there was slight hypoesthesia in the lateral thigh. Seven hours after the surgery, both the muscle weakness and hypoesthesia completely resolved. The patient had not experienced any pain after the first rescue. The patient strongly wished to discharge from the hospital and discharged without trouble.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [166.7, 'cm']}",62.94891,59.80146,66.09636,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 166.7 cm, which is 166.7 cm * 0.393701 in/cm = 65.62996 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.62996 (in inches) - 60) = 62.94891 kg.
Hence, the patient's IBW is 62.94891 kg."
3937,10,Ideal Body Weight,physical,decimal,pmc-4090998-1,Extracted,"Fifty-nine-year-old female presented to our hospital for arthroscopic repair of rotator cuff tear of right shoulder caused by a fall. She was a known case of PD since last 20 years with the history of slowing of movements, stiffness, speech disturbance, and tremors controlled only after the implantation of DBS 8 years back. She gave the past history of snoring, mild gastro-oesophageal reflux, depression, laparoscopic cholecystectomy, and three surgeries related to DBS. Her medical therapy included tablet L-dopa plus carbidopa, bromocriptine, clonazepam, escitalopram, and trihexyphenidyl. Patient weighed 80 kg, 155 cm tall (body mass index 32 kg/m2) with a mouth opening of 4.5 cm, removable complete artificial denture, Mallampati grade 3, limited neck extension, and a thyromental distance of 6.2 cm. Her pulse rate was 96/min, noninvasive blood pressure (NIBP) 135/84 mmHg, breath holding time 20s, and chest auscultation was normal. Examination of central nervous system revealed cog-wheel rigidity, short shuffling gait, and mild tremors. Haematological and Biochemical investigations, electrocardiogram, and echocardiogram were within normal limits. Chest radiograph showed IPG with leads of DBS on the left side, which was otherwise normal []. She was assessed by a neurologist, DBS was interrogated, a procedure where battery life and device settings are evaluated and manipulated noninvasively. DBS status was acceptable. She was taken up for shoulder arthroscopy with informed high risk consent in view of long standing PD and DBS, kept nil per oral after midnight, and advised to continue all her medications till the morning of surgery along with tablet ranitidine 150 mg. Operation room (OR) and drugs were prepared; difficult airway cart was kept ready. After placing standard monitors we gave iv midazolam 1 mg and oxygen by facemask. Right-sided brachial plexus block by the interscalene approach using a peripheral nerve stimulator (PNS) was given using 21G, 50 mm insulated PNS needle with 25 ml of 0.25% bupivacaine after eliciting contraction of muscles at and below shoulder at a current of 0.4 ma. After observing for 10 min, she was placed in ramp position; general anaesthesia was induced with iv fentanyl 100 μg, propofol 100 mg, vecuronium 8 mg and trachea was intubated. Patient's neck circumference was measured. DBS was turned off by a trained personnel. Patient was placed in left lateral position taking care to pad all the pressure points including DBS skin site, eye, and breast care. Anaesthesia was maintained with nitrous oxide (50%) and isoflurane (0.6-0.8%) in oxygen, iv fentanyl and vecuronium. Her baseline heart rate was 80 beats per minute (bpm) and remained between 68-80 bpm throughout the procedure. Baseline BP was 140/80 mm Hg, SBP was maintained between 110-140 mm Hg, DBP was maintained between 66-84 mm Hg intraoperatively. Thirty minutes after the onset of surgical procedure, patient's BP rose to 190/90 mm Hg which was controlled with nitroglycerine infusion (0.7-1 μg/kg/min) after ensuring adequate analgesia and muscle relaxation. Postinduction iv dexamethasone 8 mg for prophylaxis of PONV and diclofenac sodium 75 mg was administered towards the end of surgery. Blood loss was minimal. Surgeons used 26 1 (litres) of normal saline for irrigation of shoulder joint using arthroscopic infusion pump at a pressure of 70 mm Hg. Arthroscopic repair and subacromial decompression lasted 1.5 h. Before closure of arthroscopic ports, fluid was vented out. After turning the patient supine, neck circumference was measured and was same as preoperatively. DBS was turned on by the trained personnel, reprogrammed to its original setting was functional. At return of spontaneous respiratory efforts, neuromuscular blockade was reversed and trachea was extubated. Patient was conscious, haemodynamically stable and followed verbal commands with a visual analog score of 4 for pain. Postoperative analgesia was provided with intravenous paracetamol infusion 1 gm. Antiparkinsonian medications were resumed 4 h after surgery. Patient had an uneventful hospital stay and was discharged on the fifth day postoperatively.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3938,10,Ideal Body Weight,physical,decimal,pmc-4607013-1,Extracted,"This is a 28-year-old woman, who got the clinical diagnosis of Noonan syndrome (NS) at the age of 4 years because of growth retardation, cardiomyopathy and facial features. She is the only child of non-related parents. The father (Case 2) has facial features of NS, but few additional clinical symptoms. She was born to a mother with diabetes during pregnancy with a birth weight of 4.7 kg (+3 SDS), a length of 52 cm (+1 SDS) and a head circumference of +2 SDS. She also had a large left ventricle, and a systolic murmur, but this disappeared at the age of six years. Postnatally, her growth decelerated and she had feeding difficulties. At 6.5 years of age, her height was 104 cm (−2 SDS) and her weight 18.5 kg (−2 SDS). She had low endogenous growth hormone (GH) secretion defined as “partial GH deficiency”, and started GH therapy within a formal clinical trial (NovoNordisk) from 6.5 years of age. She was treated with GH (dose of 66 μg/kg/day) and responded exceptionally well and treatment was discontinued after two years. However, at 10 years of age, she had her first pubertal signs and GH-treatment was started again using a standard dose of 33 μg/kg/day. At 12.3 years of age, she had menarche. The GH-treatment continued until final height (FH) was reached at the age of 14 years. Her FH is 164.5 cm (−0.45 SDS) and weight of 60 kg (+0.3 SDS). Her psychomotor development is normal, but she has slight problems of attention deficit. She attended regular school and works as an assistant nurse. At the age of 24 years, she has the following features of NS (Fig. ): a large skull (62 cm) with a broad forehead, hypertelorism, down slanted palpebral fissures, bilateral ptosis (especially of her left eye), short and broad neck with a low hairline, and low-set ears with broad helices. Her hair is normal. She has two large Café-au-lait spots on her back and >50 freckles (lentigines) all over her body, especially on her back (Fig. ) and arms (Fig. ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [164.5, 'cm']}",56.45676,53.63392,59.2796,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 164.5 cm, which is 164.5 cm * 0.393701 in/cm = 64.76381 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.76381 (in inches) - 60) = 56.45676 kg.
Hence, the patient's IBW is 56.45676 kg."
3939,10,Ideal Body Weight,physical,decimal,pmc-5674842-1,Extracted,"A 30-year-old pregnant Japanese woman was diagnosed with GDM at 23 weeks and 3 days of gestation during her first pregnancy, based on the results of a 75-g oral glucose tolerance test (OGTT). Her blood glucose levels before the test, after 60 min, and after 120 min were 81 mg/dL, 151 mg/dL, and 180 mg/dL, respectively. She was not obese before the pregnancy, had a height of 163 cm, a body weight of 54 kg, a body mass index (BMI) of 20.3 kg/m2 and had no family history of diabetes. She received dietary counselling, began SMBG (ONETOUCH UltraVue™ Johnson & Johnson, New Brunswick, NJ), and successfully achieved good glycemic control until the day of her delivery (a healthy boy with a birth weight of 3164 g). At 3 months after the delivery, she completed a follow-up 75-g OGTT, and the blood glucose levels before the test, after 30 min, after 60 min, and after 120 min were 82 mg/dL, 146 mg/dL, 102 mg/dL, and 189 mg/dL, respectively. Her plasma insulin levels before the test and after 30 min were 2.20 μU/mL and 33.2 μU/ml, respectively. Therefore, she was diagnosed with IGT based on these results, an insulinogenic index of 0.48, and a homeostatic model assessment of insulin resistance (HOMA-IR) result of 0.44. Thereafter, her HbA1c level was regularly monitored and ranged from 5.4% to 5.7%.
At the age of 33 years, the patient became pregnant with twins. At approximately 5 weeks of gestation, her SMBG began showing high postprandial glucose levels (up to 140–180 mg/dL), and she began self-administered insulin injections using insulin aspart (Novo Nordisk) three times per day before each meal. The doses of these insulin injections increased with gestational age, and reached 20–22 units before each meal. At 31 weeks and 3 days of gestation, the patient was urgently admitted to our hospital due to premature labor contractions. We initiated a continuous intravenous infusion (500 mL/day of 5% glucose solution containing 50 mg of ritodrine) that was continued until the day of her delivery. The patient experienced adverse effects from the ritodrine, required complete bed rest, and her glucose levels kept increasing (2200 kcal/day in 3 meals). Even with 25 units of injected insulin before each meal, her postprandial glucose levels increased to 211 mg/dL at 2 h after lunch, and she occasionally experienced hypoglycemia (59 mg/dL at 3 h after lunch or 50 mg/dL at approximately 10 PM). Thus, to reduce the fluctuations in her glucose levels, her food intake (2200 kcal/day with 59% carbohydrates, 15% protein, and 26% fat) was separated into 5 meals: first breakfast at 8 AM, second breakfast at 10 AM, first lunch at noon, second lunch at 3 PM, and dinner at 6 PM. The patient also received 1 cup of yoghurt immediately before going to sleep (Fig. ). However, the patient subsequently experienced abdominal distension and difficulty eating, and we reduced her intake to 1960 kcal/day (Fig. ).
Based on the increased meal frequency, the patient required more frequent SMBG and insulin injections, which she found to be painful and depressing. Thus, we introduced the FGM system, which does not require finger punctures, to reduce her physical and emotional burden. During the first few days after its introduction, the FGM system exhibited discrepancies with the results from the conventional SMBG method, especially when her glucose levels were <70 mg/dL or >180 mg/dL. Therefore, she measured her glucose levels using both methods when her glucose levels were abnormally high or low. The patient also experienced difficulty consuming the second breakfast because of the short interval between the first and second breakfasts. Thus, her intake was revised to 1960 kcal/day (53% carbohydrates, 21% protein, and 26% fat) in 4 meals: breakfast at 8 AM, first lunch at noon, second lunch at 3 PM, and dinner at 6 PM. The re-distributed meals and flash glucose monitoring system allowed the patient to achieve good glycemic control, and the doses of the injected insulin decreased to 35 units (Fig. ) and then to 18 units (Fig. ). Her HbA1c level was maintained, ranging from 5.1% to 5.2% (these values were considered as a reference due to her anemia), and her glycoalbumin levels ranged from 10.6% to 11.6% during pregnancy. She gained 10.5 kg during her pregnancy and subsequently delivered twins via Caesarean procedure (2280 g and 2778 g) at 37 weeks and 1 day of gestation, without any adverse events or hypoglycemia. After the delivery, the patient stopped all insulin injections and had glucose levels of 70–140 mg/dL throughout the day with a normal puerperium diet (2200 kcal/day in 3 meals) (Fig. ). The patient and her twins were discharged in healthy states at 7 days after the delivery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [163.0, 'cm']}",55.0985,52.34358,57.85343,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 163.0 cm, which is 163.0 cm * 0.393701 in/cm = 64.17326 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.17326 (in inches) - 60) = 55.0985 kg.
Hence, the patient's IBW is 55.0985 kg."
3940,10,Ideal Body Weight,physical,decimal,pmc-2585581-1,Extracted,"A 50 year old South Indian woman presented to the outpatient department of our tertiary care hospital with complaints of productive cough with hemoptysis for the past 2 months. She was a house wife and was from a low socio economic class. She was diagnosed to have pulmonary tuberculosis 2 years ago and was started on anti-tuberculous therapy consisting of Isoniazid (300 mg), Rifampicin (600 mg), Ethambutol (1200 mg), and Pyrazinamide (1500 mg). But within just 3 weeks she had discontinued treatment on her own. She suffered from diabetes mellitus with peripheral neuropathy for the past 8 years and was taking oral hypoglycemic agents for the same. There was no history of hypothyroidism, coronary artery disease, hepatic disease or renal disease. No history of relevant family diagnosis of parents, siblings, or children was elicited. She is not a known smoker or alcoholic. She is married and currently postmenopausal for past 5 years. She weighed 53 kgs and was 156 cms tall with a body mass index was 22 kg/m2. General physical examination was unremarkable. Respiratory system exam revealed bronchial breath sounds in the right infraclavicular area. Admission baseline investigations showed anemia. Renal and liver functions were within normal limits (Table ). Computed tomogram of the thorax revealed a thick walled cavity in the right lung upper lobe with an indwelling aspergilloma (Figure ). 3 sputum samples were tested positive for acid fast bacilli by Ziehl Neelsen's staining technique. Conventional method of culture on Lowenstein Jensen's medium yielded growth of M. tuberculosis in 6 weeks time. The anti-tuberculosis drug susceptibility performed by resistance ratio method using Lowenstein Jensen's medium showed resistance to Isoniazid, Rifampicin but sensitive to Ethambutol, Pyrazinamide and Streptomycin in their critical concentrations of 2 ug, 50 ug and 4 ug respectively as given by Lee and Heifet.8. Consequently in view of hemoptysis and presence of an aspergilloma a right upper lobectomy was performed (after anemia correction with 3 units of packed red cell transfusion). Biopsy of the resected specimen showed caseous necrosis and granuloma formation (Figure ) and septate fungal elements suggestive of Aspergillus species (Figure ). A fungal culture of the resected specimen in Sabouraud's dextrose agar grew 'dirty green colonies', with lactophenol cotton blue slide mount showed fungal elements characteristic of Aspergillus fumigatus. 2 Blood culture inoculated in Sabouraud's dextrose agar also grew Aspergillus fumigatus. In view of invasive Aspergillosis patient was given an oral loading dose of Voriconazole 400 mg 12th hourly for 2 doses which was followed by an oral maintenance dose of 200 mg 12th hourly was continued for 6 weeks. Initially before AFB culture reports were ready, the patient was initiated empirically on a daily dose of Isoniazid (300 mg), Ethambutol (1200 mg), Pyrazinamide (1500 mg) and Streptomycin 1 g. Rifampicin due to its interactions with Voriconazole was not included in the treatment regimen []. After culture demonstrated MDR-TB, Isoniazid was stopped and oral Levofloxacin 750 mg once a day and Ethionamide 250 mg 12th hourly were included as per WHO protocol for MDR-TB []. Hemoptysis completely resolved after lobectomy. Within a week of initiating Voriconazole blood became sterile for fungal elements. After 3 weeks sputum became negative for acid fast bacilli. Currently patient is in the 4th month of treatment and is doing well.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [156.0, 'cm']}",48.75993,46.32193,51.19793,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 156.0 cm, which is 156.0 cm * 0.393701 in/cm = 61.41736 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.41736 (in inches) - 60) = 48.75993 kg.
Hence, the patient's IBW is 48.75993 kg."
3941,10,Ideal Body Weight,physical,decimal,usmle-1547,Extracted,"A 20-year-old man comes to the emergency room because of palpitations and mild dyspnea for the last 2 hours. He has had similar episodes in the past that resolved within 20 minutes, but they have been worsening since he started training for his first marathon 1 month ago. Ten years ago, he was treated for streptococcal pharyngitis with a 10-day course of penicillin. His maternal uncle passed away unexpectedly from a heart condition at age 40. He is 180 cm (5 ft 11 in) tall and weighs 85 kg (187 lb); BMI is 26.2 kg/m2. His temperature is 36.5°C (97.7°F), pulse is 70/min, respirations are 18/min, and blood pressure is 132/60 mm Hg. On examination, there is a decrescendo early diastolic murmur heard best along the left sternal border. His head slightly bobs about every second. The remainder of the examination shows no abnormalities.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [180.0, 'cm']}",74.99221,71.2426,78.74182,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 180.0 cm, which is 180.0 cm * 0.393701 in/cm = 70.86618 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.86618 (in inches) - 60) = 74.99221 kg.
Hence, the patient's IBW is 74.99221 kg."
3942,10,Ideal Body Weight,physical,decimal,usmle-1965,Extracted,A 45-year-old woman comes to the physician for the evaluation of persistent headaches for the last 2 months. The symptoms started insidiously. Menses had previously occurred at regular 28-day intervals with moderate flow. Her last menstrual period was 12 weeks ago. She is sexually active with her husband but reports decreased interest in sexual intercourse over the past few months. The patient does not smoke or drink alcohol. She is 168 cm (5 ft 6 in) tall and weighs 68 kg (150 lb); BMI is 24 kg/m2. She appears uncomfortable. Vital signs are within normal limits. A urine pregnancy test is negative. A pelvic ultrasound shows atrophic endometrium. A cranial MRI with contrast shows a 2-cm intrasellar mass. A hormone assay is performed and is positive.,"Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [168.0, 'cm']}",59.62607,56.64477,62.60737,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.14177 (in inches) - 60) = 59.62607 kg.
Hence, the patient's IBW is 59.62607 kg."
3943,10,Ideal Body Weight,physical,decimal,pmc-4976162-1,Extracted,"Patient's written consent was obtained and any information, including illustrations, was anonymized as far as possible.
A 32-year-old male patient having 180 cm height and 75 kg weight (BMI 23.1) presented to the Emergency Department (ED) of General Hospital of Filiates complaining from a gunshot penetrating injury at left lower anterior abdominal wall.
The patients vital signs were BP 120/80 mm, Hg HR 80/min, and Glasgow Coma Scale (GCS) 15/15. On clinical examination 1 cm diameter entry wound was revealed at the left lower abdominal wall. There was no exit wound. On palpation the abdomen was soft with mild tenderness. The Complete Blood Count (CBC) and urinalysis were normal. Abdominal X-rays showed the bullet in the pelvic cavity (Figures and ). Chest X-ray did not show free air under the diaphragm. After these examinations, abdominal CT scan was scheduled to identify any serious damage. The CT scan identified the bullet lying in the peritoneal-pelvic cavity and intraperitoneal and retroperitoneal visceral structures were identified to be normal with no injury ().
After conservative treatment and vital signs follow-up for the first 24 hours and series of clinical examinations, an EL was scheduled. EL identified the bullet in the peritoneal cavity, with no other damages. Finally, the bullet was removed laparoscopically (). The patient remained for 24 hours in the surgical department and was discharged from hospital in good conditions.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [180.0, 'cm']}",74.99221,71.2426,78.74182,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 180.0 cm, which is 180.0 cm * 0.393701 in/cm = 70.86618 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.86618 (in inches) - 60) = 74.99221 kg.
Hence, the patient's IBW is 74.99221 kg."
3944,10,Ideal Body Weight,physical,decimal,pmc-7478461-1,Extracted,"An 18-year-old male patient was admitted to the emergency department after he fell to the ground while climbing a 2-m fence. The weight and height of the patient was 101 kg and 1.76 m, respectively, and his body mass index (BMI) was 32.6 kg/m2. This patient was clear minded by presentation. He was unable to bear weight on his right ankle, which was in a severely malformed and swollen condition, but there appeared to be no open wound on the skin. The patient complained of pain and swelling and was unable to perform active ankle movements. Meanwhile, passive ankle movements were limited and painful. No other discomfort or past medical history was declared. A normal finding was obtained on neurovascular examination. A direct radiographic examination of the ankle showed a displaced lateral malleolar fracture with the talus wedged into the distal tibiofibular joint (Fig. A-B). An immediate manual reduction followed by fixation with plaster was performed by orthopedists (Fig. C-D). To further understand the pattern of injury, a computerized tomography (CT) examination with 3D reconstruction was performed, which demonstrated distal fibular fracture and widening of the distal tibiofibular syndesmosis (Fig. E-H). Magnetic resonance imaging (MRI) revealed rupture of the superior and deep deltoid ligament and the anterior-inferior tibiofibular ligament (AITFL) (Fig. J-L). Based on the radiological outcomes, the fracture-dislocation classification was considered as 44C1.1 (AO/OTA classification) and pronation-external rotation (Lauge-Hansen classification). Due to the extreme ankle instability caused by bone and ligament injury, surgical intervention was recommended and performed after 7 days until swelling in the foot and ankle had adequately dissipated, as indicated by a positive wrinkle test.
For the surgery, the patient was placed in a supine position under spinal anesthesia and tourniquet control. First, a curved 6 cm incision was made just below the medial malleolus and extended distally to expose the ruptured deltoid ligament and its individual components. Two suture anchors were placed at the insertion point of the deep component of the deltoid ligament of the talus, and 1 suture anchor was placed into the tip of anterior colliculus of the medial malleolus in preparation for deltoid ligament reconstruction. After that, an incision of approximately 10 cm was made on the lateral side of the fibula. Soft tissue was incised by sharp dissection to expose the broken site of the fractured fibula. Reduction of the fibula was conducted to recover the length, followed by applying a screw vertical to the fracture line for stabilization. Then, a 3.5 mm locking compression plate (LCP) was placed for neutralization. A large reduction clamp was maintained at the space of the syndesmosis and medial malleolus while the ankle joint was held in a neutral position. The mortise width and distal tibial-fibular space were restored and confirmed under C-arm fluoroscopy, and a 3.5 mm syndesmotic screw was applied. Finally, we repaired the deltoid ligaments with sutures (Fig. A-B).
Plaster was not applied after surgery. We applied early functional exercise, to include passive motion of the ankle and mobilization of the toes and knee joint 2 days postoperatively. Weight bearing was avoided. However, a radiographic examination 1 week after surgery showed that the distal tibiofibular syndesmosis was slightly wider than on intraoperative fluoroscopy, as the syndesmotic screw has a tendency to loosen (Fig. C-P). Therefore, a re-operation was conducted to deal with the syndesmosis. Using the same lateral approach as the first operation, a Weber forceps was used to reduce the gap between the tibia and fibula. Then, 2 more syndesmotic screws were inserted outside of the plate. The former syndesmotic screw was substituted with a longer one. Stability of the distal tibiofibular syndesmosis was confirmed by the “HOOK” test (Fig. ).
Early passive motion of the ankle was continuously performed by a physical therapist. The radiographic examination and CT after the second operation showed a well reduced and aligned distal tibiofibular syndesmosis. Twelve weeks postoperatively, 2 syndesmotic screws were removed, and partial weightbearing was allowed with the assist of single crutch; 16 weeks postoperatively, the last syndesmotic screw was removed. Full weight bearing was allowed immediately. At 1 year after surgery, the patient was called back to the hospital for a radiographic and clinical examination. Radiographs and CT showed union of the fibular fracture; however, the syndesmotic space was slightly increased compared to the contralateral side (Fig. ). Fortunately, the patient was free of pain and returned to his previous level of daily activity; the range of motion of the injured ankle was nearly parallel with the contralateral side (Fig. ). According to American Orthopedic Foot and Ankle Society Score (AOFAS),[ the score was 90. This study was approved by the ethics committee of Nanjing first hospital. Signed written informed consents were obtained from the patient.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.76, 'm']}",71.37017,67.80166,74.93868,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.76 m, which is 1.76 m * 39.3701 in/m = 69.29138 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (69.29138 (in inches) - 60) = 71.37017 kg.
Hence, the patient's IBW is 71.37017 kg."
3945,10,Ideal Body Weight,physical,decimal,pmc-4823490-1,Extracted,"A 13-year-old girl with a past medical history of CF was admitted to our clinic for annual review.
She was diagnosed with CF at the age of 7 months, due to failure to thrive, with sweat test (Cl−: 114 mEq/L) and molecular testing (genotype: ΔF508del/ΔF508del).
The girl was not colonized with Pseudomonas; spirometry was within normal limits (FVC: 102% predicted and FEV1: 99% predicted). Her weight has been stable over the years in the 10th centile (41 kgr at the age of 13) with her height in the 25th (153 cm). She was on pancreatic enzymes and A, D, E, and K vitamins, due to pancreatic insufficiency.
At the age of 11 years, during her annual review, abdominal ultrasound had revealed hyperechoic pancreas with multiple cysts along the peripancreatic duct with an average diameter of 3 cm per cyst. Further imaging with MRI confirmed the ultrasound findings. MRI findings revealed complete replacement of the pancreatic tissue by multiple cystic lesions of various sizes, with thin and smooth walls. The cystic lesions showed high signal intensity on T2-weighted images and low signal intensity on T1-weighted images and ranged in diameter (max 4.6 cm (). The largest cyst that appeared homogenous on the initial exam presented a fluid-fluid level on the first MRI follow-up two years later. Initial MRI findings revealed one cyst anterior to the right kidney, but MRI follow-up after two years showed that a new cyst anterior to the previously described cyst had been formed. In comparison, the diameter of a cyst at the tail of the pancreas had increased from 2.5 cm to 3.1 cm whereas the diameter of a cyst at the splenic hilum had decreased from 2.2 cm to 1.7 cm (). On the first follow-up MRI, some cysts demonstrated fluid-fluid levels due to hemorrhage (). T2-weighted MR image—HASTE (Half-Fourier Acquisition Single-Shot Turbo Spin Echo) sequence—demonstrated complete replacement of the pancreas by multiple cysts of variable size with thin and smooth walls. No communication of cysts with pancreatic ducts was found (). Oral Glucose Tolerance Test (OGTT) was normal.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.0, 'cm']}",46.04337,43.7412,48.34554,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.0 cm, which is 153.0 cm * 0.393701 in/cm = 60.23625 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.23625 (in inches) - 60) = 46.04337 kg.
Hence, the patient's IBW is 46.04337 kg."
3946,10,Ideal Body Weight,physical,decimal,pmc-6389057-1,Extracted,"A 47-year-old male with a body weight of 84 kg and height of 1.65 m living in underprivileged part of Islamabad has a history of generalized pain, fatigue, and fever. He was diagnosed with chronic HCV (3a genotype) infection in 2003. The patient’s medical history was not significant except for dental surgery and few surgical stitches. He remained treatment naïve for 5 years. In 2007, he received the first IFN (100 mg/week) plus RBV (400 mg/day) combination therapy and was on this treatment for 6 months. However, SVR was not achieved. He remained without treatment for the next 2 years (2008–2009). In 2010, he again underwent the same combination therapy. After 6 months of treatment, he, remained positive for HCV RNA. These treatments were not only expensive but also resulted in adverse effects, including stomach burning, loss of appetite, nausea, fever, fatigue, and anxiety.
In 2011, Patient was advised to undergo PEG-IFN plus RBV combination therapy. However, he remained a non-responder. After one and a half year, in 2013, patient received the same (PEG-IFN plus RBV) combination therapy for 6 months. Yet patient’s serum was still positive for HCV RNA. Eventually, in 2015, he underwent SOF (400 mg/day) plus RBV combination therapy for 6 months. Still SVR was not achieved and surprisingly a high viral load of 5.2 × 105 IU/ml was reported by real-time polymerase chain reaction (PCR) diagnosis. An ultrasound revealed that his liver was of normal shape, size, and echotexture; he had a mildly fatty liver with no fibrosis or lesion.
The patient’s diagnostic and treatment history are summarized in Tables and , respectively. Viral genotype remained undetermined/untypable for the years 2012, 2014, and early 2016 (Table ) following 6 months of combination therapy (Table ), perhaps due to the detection method’s incapability or the detection limit as it was performed on conventional PCR-based method followed by detection on the agarose gel. In late 2016, the viral load was found to be 5.2 × 105 IU/ml and the patient was found positive for genotype 3a (Table ).
After partial genome sequencing of NS5B, BLAST analysis showed 93% similarity to the already existing NS5B nucleotide sequences in the GenBank database (Fig. ). This shows virus (accession number KY971494; variant ‘Pk1-RV’) is of genotype 3a. Analysis further confirmed that the variant (Pk1-RV) is distinct from HCV genotypes 3 k, 3b, 1a, and 1b (Fig. ).
Taking into account the medical history of the patient, we performed restriction fragment length polymorphism (RFLP) for interleukin 28B (IL28B) at rs8099917 and rs12979860. The present study showed polymorphism cytosine and thymine (CT) and guanine and thymine (GT) at (rs12978960, (rs8099917) respectively, as in (Fig. ). Same polymorphism was reported by Yang et al. who has linked it with successful treatment outcome (SVR) [].","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.65, 'm']}",61.40952,58.33904,64.48,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.65 m, which is 1.65 m * 39.3701 in/m = 64.96066 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96066 (in inches) - 60) = 61.40952 kg.
Hence, the patient's IBW is 61.40952 kg."
3947,10,Ideal Body Weight,physical,decimal,pmc-3420708-1,Extracted,"A 29-year-old primigravida (G1P0A0) African American woman presented during her 18th week of gestation with a one-day history of nausea and vomiting. She had experienced an unremarkable pregnancy up until this time. She denied any history of abdominal pain, dysuria, constipation, polydipsia, polyuria, weight loss, anorexia, or muscle weakness during her pregnancy. She had no history of calcium disorders, kidney stones, fractures, osteoporosis or endocrinopathies. Family history was negative for calcium disorders, kidney stones, fractures, osteoporosis, endocrinopathies or parathyroid disorders. She was taking prenatal multivitamins as prescribed. She was not taking thiazide diuretics, antacids, or lithium which could influence her calcium status.
On physical examination, she was well nourished and in no distress. Her blood pressure was 110/68 mmHg, heart rate 60/min and regular, respiratory rate 18/minute, and weighed 295 pounds (134 kg) with a height of 62 inches (157.5 cm). Examination of her neck revealed a 30 gm goiter without any nodules or bruits. There were no palpable neck masses, jaw abnormalities, or cervical or supraclavicular lymphadenopathy. On abdominal examination, there was evidence of a palpable uterus up to 2 cm below the umbilicus, consistent with an 18-week gestation. There was no edema of her extremities. She had no kyphosis or bone tenderness. The remainder of the systemic examination was unremarkable.
Initial laboratory evaluation revealed severe hypercalcemia with a calcium level 13.9 mg/dL (reference range 8.5–10.3), albumin 3.3 g/dL (3.2–5.5), and a phosphorous level 2 mg/dL (2.4–4.1). She had normal renal function with a low potassium level 3.0 mmol/L (3.5–5.0), related to emesis. Her 1,25-dihydroxycholecalciferol level was 94.3 ng/mL (reference range 15.9–55.6), 25-hydroxyvitamin D level 40 ng/mL (8.9–46.7), and parathyroid-hormone-related peptide (PTHrp) was <0.3 pmol/L (0.0–1.5). EKG showed right bundle branch block with a normal QT interval. An endocrine consult was ordered in view of her significant hypercalcemia. On further workup, she was found to have an elevated PTH level 261.8 pg/mL (16–48 pg/mL) and a urinary calcium level 479 mg/24 hr (reference range 100–300 mg/24 h) confirming a diagnosis of primary hyperparathyroidism and ruling out familial hypocalciuric hypercalcemia. Laboratory workup was inconsistent with vitamin D intoxication, milk alkali syndrome, or malignancy. She was biochemically euthyroid.
Ultrasonography of her neck revealed a hypoechoic nodule suggestive for an enlarged right inferior parathyroid gland measuring 1.9 × 0.4 × 1 cm. It was seen just deep to the inferior aspect of the right lobe of the thyroid gland (). An obstetrical ultrasound confirmed a live single intrauterine gestation consistent with 18-week of gestation.
She was initially managed with conservative measures namely, a eucalcemic diet and aggressive hydration with minimal improvement in her clinical or biochemical status. Due to her persistent symptomatic hypercalcemia despite conservative measures, the decision was made to perform an elective parathyroidectomy of the enlarged parathyroid gland. She underwent a minimally invasive right inferior parathyroidectomy at 18-week gestation. There was a marked drop in the intraoperative PTH levels from 203 pg/mL initially to 28.5 pg/mL at 10 minutes after the removal of the enlarged parathyroid gland, confirming a successful operation. Postoperative calcium and PTH levels were 9.4 mg/dL and 28.5 pg/mL, respectively. Pathological evaluation of the resected mass demonstrated a parathyroid gland weighing 700 mgs. Histopathologic examination of the parathyroid gland was consistent with a parathyroid adenoma (). The patient was discharged home on postoperative day number one with a normal calcium level. The remainder of her pregnancy was uncomplicated until week 37 of her gestation.
At 37-week gestation, induction of labor was necessary due to preeclampsia. Her corrected calcium level at that time was 10.3 mg/dL. The patient delivered a healthy baby girl weighing 5 pounds and 11 ounces (2.27 kg) with APGAR scores at both 1 and 5 minutes of 9/10. The baby was normocalcemic with a calcium level of 8.8 mg/dL and a PTH level of 109 pg/mL on day 2. The mother and baby were discharged home on the third day after delivery.
The patient remained normocalcemic 1 year post-op with a parathyroid level of 54 pg/mL.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [157.5, 'cm']}",50.11819,47.61228,52.6241,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 157.5 cm, which is 157.5 cm * 0.393701 in/cm = 62.00791 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.00791 (in inches) - 60) = 50.11819 kg.
Hence, the patient's IBW is 50.11819 kg."
3948,10,Ideal Body Weight,physical,decimal,pmc-6661044-2,Extracted,"A 73-year-old woman (height 155 cm, weight 49 kg) had right renal arterial embolism, chronic kidney disease, and pleurisy in her past history.
Preoperatively, her upper arm blood pressure exhibited no laterality (HR 76/min, BP right 120/80 mmHg, BP left 123/75 mmHg).
Preoperative enhanced computed tomography (CT) imaging revealed a thoracic aortic aneurysm with a maximum diameter of 52 × 50 mm, but the left AAO was not obvious because the left innominate vein’s enhancement concealed LSAO findings.
We planned zone 2 thoracic endovascular aneurysm repair (TEVAR) for thoracic aortic aneurysm and embolization of the left subclavian artery via the left brachial artery, but we failed to pass through the left subclavian artery because of AAO, and therefore, we simply covered the orifice of the left subclavian artery using a stent graft without embolization. No endoleak was observed postoperatively.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3949,10,Ideal Body Weight,physical,decimal,pmc-8191267-1,Extracted,"A 68-year-old woman (165 cm; 64 kg) with no known allergies to medication and a past history significant for arterial hypertension, chronic bronchitis, ischemic heart disease (stent in the circumflex artery in 2017) and obstructive HOCM was scheduled to undergo an elective extended transaortic septal myectomy. Her usual treatment consisted of bisoprolol, torasemide, disopyramide, pantoprazol, acetylsalicylic acid and bronchodilators. She was referred to our hospital from another center following a diagnosis of HOCM manifesting clinically as intense dyspnea on exertion, occasional dizziness and episodes of chest pain extending to the left arm.
Preoperative ECG showed sinus rhythm (56 bpm), left ventricular hypertrophy (LVH) and repolarization abnormalities, while a cardiac MRI scan revealed a maximum left ventricular thickness of 19 mm. TTE showed findings suggestive of HOCM involving the anterior ventricular septum, with a maximal wall thickness of 20 mm, peak LVOT gradient of 144 mmHg, grade-2 diastolic dysfunction, normal systolic function, systolic anterior motion (SAM) with moderate mitral insufficiency (MI), biatrial enlargement and mild pulmonary hypertension.
Upon entry to the operating room, the patient was monitored for the following: arterial blood pressure by invasive monitoring through the left radial artery, ECG with ST-segment analysis, oxygen saturation through pulse oximetry, capnography, Bispectral Index (BIS™) monitoring to measure the hypnotic effects of anesthesia, Near-infrared spectroscopy (INVOS™ 5100C Cerebral/Somatic Oximeter, Covidien®), body temperature using an esophageal thermometer, central venous pressure and hourly urine output. When the patient arrived in the operating room, her arterial pressure was 145/69 mmHg and she had a heart rate of 72 bpm and oxygen saturation of 96%.
She was then given intravenous midazolam (2 mg), propofol (60 mg), fentanyl (150 μg) and rocuronium (50 mg). The trachea was intubated with 7.5 cuffed tube. Intraoperative TEE revealed severe hypertrophy (20 mm) of the intermuscular septum and LVOT obstruction with SAM associated with the mitral valve [] as well as a peak gradient between the left ventricle (LV) and the aorta (Ao) of 100 mmHg. Following the sternotomy, another measurement was taken from the surgical field using two catheters placed directly in the LV and the Ao respectively, revealing a gradient of 116 mmHg. Anesthesia was maintained with sevoflurane, fentanyl and rocuronium. As the patient displayed a tendency toward hypotension, she required single-dose boluses of phenylephrine and continuous perfusion of noradrenaline at a rate of 0.04 mcg/kg/min to achieve an average arterial pressure of >60 mmHg until cardiopulmonary bypass was performed. An extended transaortic septal myectomy was conducted without incident. When CPB was discontinued, the patient presented ventricular fibrillation, which resolved with amiodarone (300 mg) and 3 automated internal defibrillator shocks of 10 J. At this time, the patient entered sinus rhythm at 40 bpm and atrial and ventricular pacemaker electrodes were placed at a rate of 80 bpm. Postoperative TEE evidenced resolution of hypertrophy in the LVOT [], an LV-Ao gradient of 8 mmHg, mild MI, absence of iatrogenic ventricular septal defects and normal biventricular function. LV-Ao gradient measurement from the surgical field was 7 mmHg [], which closely resembled the value obtained using TEE and thereby confirmed that the intervention had been done successfully. Given the absence of complications associated with the surgical procedure CPB was terminated and the patient was shifted to the intensive care unit with stable hemodynamics. The traquea was extubated after 6 h and shifted to hospitalization ward after 24 h.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3950,10,Ideal Body Weight,physical,decimal,pmc-6820436-1,Extracted,"Chest computed tomography revealed a cavity in the upper right lung in a 40-year-old man. A diagnosis of pulmonary Mycobacterium avium complex infection was made with the help of bronchoalveolar lavage culture. The patient was prescribed ethambutol, rifampicin, and isoniazid for 1 year, and a combination of four antituberculous drugs: rifampicin, ethambutol, clarithromycin, and levofloxacin, for the subsequent year, which eventually proved to be ineffective. The patient's height was 180 cm, weight was 60 kg, and body mass index was 18.5 kg/m2. The patient complained of general malaise and anorexia. Subsequently, 7.5 g/day NYT extract (Kracie Co., Ltd, Tokyo, Japan), which is a Kampo preparation used for the treatment of general fatigue and loss of appetite, was administered.[] Reports indicate that this medication is effective for treating infections caused by Mycobacterium fortuitum,[] when administered in combination with antituberculous drugs. Six months after treatment with NYT, the patient's body mass index increased to 22 kg/m2, and a subsequent chest computed tomography scan revealed significant reduction in the size of the lung cavity. The patient discontinued the use of the antituberculosis drugs and the disease did not recur [Figure , ]. The patient continued taking NYT for one and a half years without adverse effects and discontinued it subsequently. No lung cavities have been observed in the patient since treatment with a combination of NYT and antituberculosis drugs.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [180.0, 'cm']}",74.99221,71.2426,78.74182,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 180.0 cm, which is 180.0 cm * 0.393701 in/cm = 70.86618 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.86618 (in inches) - 60) = 74.99221 kg.
Hence, the patient's IBW is 74.99221 kg."
3951,10,Ideal Body Weight,physical,decimal,pmc-7463145-1,Extracted,"A boy named D, 15 years old, with a diagnosis of LMA, 5th day of care. At the time of assessment, the main complaint was that of fever for two days. The parents said the peak of body temperature was 38.4°C. Presence of bruises in the right knee and both hands of the child. Hemoglobin (Hb) value: 6.9 gr/dL, platelets: 5000/mm3, hematocrit (Ht): 19.2%, leukocytes: 2740/mm3, ANC: 81/mm3, BP: 107/85 mmHg, HR: 115 x/minute, RR: 20 x/minute, body temperature: 38.0°C, SpO2 98%, BW: 55, 6 kg, BH: 165 cm. There were complaints of nausea. The child had good nutritional status and his hydration status was adequate, with a positive fluid balance and no signs of overload. The child’s rest and sleep statuses were adequate.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3952,10,Ideal Body Weight,physical,decimal,pmc-6521524-1,Extracted,"A 62-year-old Japanese male with a horseshoe kidney was referred to our hospital for further examination of left hydronephrosis. The patient was obese with a body mass index of 32.0 kg/m2 (height 170 cm, body weight 92 kg) and had undergone medical treatment for hypertension. Laboratory examination results showed mild renal dysfunction with a serum creatinine level of 1.21 mg/dL and estimate glomerular filtration rate of 48.2 mL/minute. Computed tomography (CT) revealed a left lower ureteral mass near the ureteral orifice, resulting in renal hydronephrosis (Figures and ). Furthermore, three-dimensional (3-D) CT imaging showed a normal renal vascular system, while an aberrant renal artery located just below the root of the inferior mesenteric artery (IMA) was found to supply the bilateral sides of the lower part of the horseshoe kidney (). In addition, urine cytology findings were positive for malignancy. Based on these findings, we diagnosed a left lower ureteral tumor associated with a horseshoe kidney.
In June 2017, laparoscopic left nephroureterectomy and bladder resection procedures were performed with 5 laparoscopic ports, with the port schema shown in . Using an intraperitoneal approach, we cut the peritoneum and dislocated the intestine to approach the renal helium. After visualizing the left renal vascular system, the main renal artery supplying the left side of the upper part of the horseshoe kidney and left branch of the aberrant renal artery passing under the IMA were ligated by use of a Hem-o-lok® polymer clip and divided, after which the left renal vein was ligated and divided in the same manner (). Next, we were able to observe the renal isthmus using an NIRF system (da Vinci Xi FireFlyTM®) at 1 minute after intravenous administration of 1 mL of ICG (Diagnogreen 0.25%; Daiichi Pharmaceutical, Tokyo, Japan). Strong ICG fluorescence was observed in the dominant region of the right part of the kidney, while no fluorescence was noted in the left kidney region (). These findings indicated that blood supply to the left side of the kidney was completely blocked, which was more apparent as compared to white light images (). Subsequently, the heminephrectomy was started under the assistance of NIRF imaging using cold scissors. During excision, visualization with white light and the NIRF was switched at the discretion of the operator in order to confirm the plane of excision between the right and left parts of the kidney (Figures and ). Adequate hemostasis from the resected area could be obtained by electrocautery bipolar coagulation and use of a TacoSil® tissue sealing sheet, with no suturing required (Figures and ). Following completion of the laparoscopic heminephrectomy, the patient was placed in a supine position and partial resection of the bladder was performed. The total operation time was 5 hours 21 minutes and blood loss was 410 mL (obtained in urine from the bladder). A histopathological examination revealed an invasive urothelial carcinoma (grade 2>1, INFβ, pT2a, ly0, v0, u-lt0, RM0). There were no perioperative complications and the patient was discharged 9 days after surgery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3953,10,Ideal Body Weight,physical,decimal,pmc-2892593-1,Extracted,"A 70-year-old man (155 cm and 52.7 kg) presented with progressive dysphagia underwent an endoscopic examination and was diagnosed with esophageal cancer. He did not have a prior medical history of diabetes or hypertension but he had undergone esophageal stent insertion one month earlier due to an esophageal stricture caused by lye ingestion.
Preoperative thoracic epidural catheter insertion was performed for patient controlled analgesia during the postoperative period. Informed consent for the epidural catheter was obtained from the patient after explaining the insertion, objective, and complications. With the patient in the prone position, a pillow was inserted under the chest to maintain the thoracic kyphosis, such as lateral decubitus or sitting position. 10% povidone-iodine (PVP-I, Betadine) and 75% alcohol were used to sterilize the area of interest. The left 10 thoracic pedicle was identified for skin insertion using a C-arm and 1% lidocaine was infiltrated subcutaneously. A 17 G Tuohy needle was inserted via the paramedian approach at the T7-T8 vertebral interlaminar space. Although there was some difficulty in inserting the catheter into the epidural space, after several attempts, the epidural space was confirmed using the loss of resistance technique and a lateral view of the C-arm using contrast. A 19 G epidural catheter (FlexTip Plus®, Arrow, USA) was inserted and advanced 3 cm into the epidural space, i.e. 10 cm from skin, and the tip of catheter was then located at the upper end plate of the T7 vertebra and fixed with a catheter fixator (Statlock®, Bard, USA). There was no significant resistance in the insertion of the epidural catheter and there was no cerebrospinal fluid or blood in the aspiration. An epidural test dose of 3 ml of 1.5% lidocaine with 1 : 200,000 epinephrine indicated a decrease in sensation between the T4-T8 sensory dermatome in the sensory test using alcohol and there were no significant changes in his vital signs and power of the upper and lower extremities.
The patient underwent an Ivor-Lewis operation according to the schedule and pain control with less than 2 on the visual analogue scale. Three days after surgery, thoracic surgeon attempted to remove the epidural catheter. The patient was placed in the sitting position but removal was difficult. During the removal procedure, the patient did not complain of pain. The thoracic surgeon attempted to remove the catheter by grasping the proximal portion of the catheter in contact with the skin using Kelly. At that time, the epidural catheter broke and the coil remained in the body. The remaining catheter was confirmed to be in the epidural space from a thoracic x-ray (). Because the epidural catheter could be a cause of infection in the epidural space, foreign body removal was scheduled under general anesthesia. The site of the remnant epidural catheter was confirmed using C-arm and the skin was cut from the site of catheter insertion to 7 cm cephalad. The surgeons gently removed the epidural catheter after exposing the interlaminar space between T7 and T8 by dissecting through the layers of subcutaneous tissue and paraspinal muscles. After surgery, the patient was discharged without significant neurological complications.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [155.0, 'cm']}",52.35442,49.7367,54.97214,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (61.02366 (in inches) - 60) = 52.35442 kg.
Hence, the patient's IBW is 52.35442 kg."
3954,10,Ideal Body Weight,physical,decimal,pmc-5696664-1,Extracted,"A 17-year-old female was admitted to bilateral blurring of vision, neck pain, and headache; she had experienced these symptoms for 5 days. She had neither a remarkable medical history nor infectious symptoms. She had been vaccinated for Bacillus Calmette–Guérin in infancy. Initial vital signs were within normal limits: body temperature 36.4°C, heart rate, 80 beats/min; blood pressure, 100/60 mmHg; and respiratory rate, 20/min. Her weight and height were 56 kg (percentile 50%) and 155 cm (percentile 10%), respectively. On physical examination, optic neuritis was diagnosed with pallor optical disc, although the cranial nerves, muscles power, and deep tendon reflexes were all normal. The result of other system examinations was unremarkable, except right cervical lymphadenopathy (2 cm × 2 cm). Her primary laboratory data were as follows: white blood cell counts, 9.700/mm3, neutrophils, 65%; lymphocytes, 25%; monocyte, 10%; hemoglobin 9.7 g/dL; platelets, 242.000/mm3; erythrocyte sedimentation rate, 50 mm/h; C-reactive protein, 12 mg/dL; urea, 43 mg/dL; and creatinine, 1.54 mg/dL. All other measures were within normal limits. MRI of the spine showed an intramedullary lesion that was isointense on the T1-weighted and hyperintense on the T2-weighted images, extending from the brainstem to the full lumbar spine []. Vertebrae, intervertebral discs, and brain MRI were normal. The MRI images were consistent with a diagnosis of holocord LETM. Lumbar puncture showed normal intracranial pressure (160 mmH2O). Cerebrospinal fluid (CSF) analysis revealed 11 cells/mm3 with lymphocyte, and elevated protein (148 mg/dL) and normal glucose (59 mg/dL) levels. CSF polymerase chain reaction (PCR) for MTB, herpes simplex virus, Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, and Enterovirus, acid-fast bacillus (AFB) stain, and an agglutination test for brucella were all negative. Serology results for Lyme and brucella in the blood were negative. CSF NMO antibodies and oligoclonal bands were negative. Serum viral serology was unremarkable, and an ELISA for human immunodeficiency virus was negative.
On follow-up, blood pressure was found to have remained high (220/110 mmHg), and urea and creatinine levels had progressively increased (132 mg/dL and 3 mg/dL, respectively). The markers for autoimmune and connective tissue disorders (i.e., antinuclear antibodies, anti-dsDNA, C3, C4, Coombs, anticardiolipin antibody, thyroid-stimulating hormone, and free T4) were all negative, and echocardiography and urine calcium testing were within normal limits. Sarcoidosis was ruled out by the laboratory tests. Chronic renal failure was diagnosed, but hypertension could not be controlled, despite aggressive medical therapy. The result of tuberculin skin testing (TST) was positive (23 mm), but the chest X-ray was normal. AFB and MTB-PCR on three consequtive sputum samples were negative. The results of the patient's immunological screening tests were normal. On follow-up, the patient had transient left upper limb muscle weakness (muscle power grade 4/5). Pulse steroid therapy was initiated. Computed tomography of the chest revealed a calcified lymph node (3 cm × 1.5 cm) in the right paratracheal region. On abdominal MRI, a few nodular lesions were detected on the left liver lobe. On the histopathological evaluation of the cervical lymph node and liver, necrotizing granulomatous inflammation with positive AFB was detected. The clinical and imaging findings supported a diagnosis of disseminated tuberculous with holocord LETM. Four antituberculous drugs (isoniazid, rifampin, pyrazinamide, and ethambutol) were administered with corticosteroid therapy (2 mg/kg/day). The patient received prednisone for the first 8 weeks. All sputum, tissue, and CSF cultures remained negative for MTB. After 16 weeks of treatment, her complaints disappeared, and the results of control spinal MR were completely normal []. At the end of the one year, antituberculosis therapy was stopped without any sequelae.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3955,10,Ideal Body Weight,physical,decimal,pmc-7339471-1,Extracted,"A 71-year-old male patient was admitted into our hospital with chronic right flank pain. The abnormal computed tomography (CT) image presentation of right renal mass, revealed by occasional health examination, accompanied with the complaint of intermittent nausea. Besides, his past medical history also included diabetes mellitus (type 2) for 10 years and significant hypertension for 12 years, ranging from 140–160/90–95 mmHg, fluctuated periodically. Regular combined subcutaneous injection of short-acting insulin and insulin glargine was recorded for the treatment of diabetes mellitus, and the patient claimed that the serum glucose level was controlled satisfactorily all the time. As for hypertension, nifedipine sustained-release tablets were prescribed as the oral therapy by the physician, but the patient admitted that he failed to follow the long-term regular medication.
The patient’s height was 171.0 cm, and the body weight was 65.0 kg. The BMI was 22.23 kg/m2. The laboratory tests presented the elevated level of white blood cell (WBC) count (29.9 × 109/L). The red blood cell (RBC) count and other vital parameters were all within the reference range.
As for the medical image examinations, the routine chest X-ray image did not reveal the abnormal findings. The strong and heterogeneous enhancement pattern from the dual-source 64-slice enhanced CT-scanned films including arterial phase, venous phase, and excretory phase indicated the radiologic diagnosis of right malignant renal tumor with the size of 13.0 × 10.0 × 8.0 cm (Fig. ) [].
In order to facilitate the surgical orientation and improve the manipulating accuracy, the data from CT images was extracted, and the three-dimensional digital model (3D-DM) was reconstructed. The copied information was analyzed and reconstructed into the 3D-DM by using a postprocessing software named three-dimensional medical image reconstructing and guiding system (3D-MIRGS, China). The retroperitoneal space along with critical anatomic structures including renal tumor, the relevant vasculature, the kidney, and the renal collecting system on the affected side were reconstructed and marked by using different colors simultaneously (Fig. ).
The retrolaparoscopic RN was performed under the assisted navigation of 3D-DM at the Department of Urology. The right kidney along with the right adrenal gland was dissected and excised completely. The hemostasis was achieved carefully.
The operative time was 1 h and 30 min, with no intraoperative complications happened. The estimated blood loss was about 20 mL. The size of resected tumor was 10.0 × 8.0 × 6.0 cm. The final pathological diagnosis was hybrid (clear cell and papillary type) renal cell carcinoma (nuclear grading III) (Fig. ). WBC count fell back to the level of 10.6 × 109/L at the first day postoperatively, which further dropped down to 7.3 × 109/L 2 days later. The recovery course was uneventful, and the patient was discharged after 7 days postoperatively.
Ten days after the patient was discharged, he was readmitted with the chief complaint of high fever with severe right flank pain. CT scanning revealed that right retroperitoneal hematoma (Fig. ) and the blood routine showed the dramatic elevation of WBC count (96.3 × 109/L). At the same time, the body temperature was high (37.9 to 40.5 °C). ALR was established. He was treated with systemic antibiotics and the temperature decreased, but the WBC count still remained on high level. After the consultation of multi-disciplinary team and department discussion, we decided to perform the percutaneous puncturing and drainage for him after a 5-day systemic antibiotic therapy. Even though there was bloody drainage fluid with the amount of about 300 mL each day, the patient’s condition still exacerbated rapidly and the CT scanning result showed no significant shrinkage for the retroperitoneal hematoma (Fig. ). Five days after the drainage, the patient’s symptom of right flank swelling and pain still aggravated significantly. In spite of the immediate reoperation of hematoma evacuation, the patient died of multiple organ failure 10 days after the reoperation eventually. The day before his clinical death, the rechecked CT scanning images showed the rapid retroperitoneal cavity metastasis with obvious sign of puncturing track implantation (Fig. ). From the admission to clinical death, the trend of WBC counts can be seen in Fig. .
The final pathological result of reoperation showed the necrotic and hematoma tissue blended with RCC tumor cells (nuclear grading IV) (Fig. ). Furthermore, the immunohistochemical staining from the specimens of two operations was performed to evaluate the expressions of 4 markers. Primary antibodies used in the study included paired box 8 (Pax8) (Santa Cruz Biotechnology sc-514352, Dallas, TX, USA), carbonic anhydrase 9 (CA9) (Santa Cruz Biotechnology sc-365900, Dallas, TX, USA), cytokeratin 7 (CK7) (Santa Cruz Biotechnology sc-23876, Dallas, TX, USA), and α-methylacyl-coenzyme A racemase (AMACAR) (Santa Cruz Biotechnology sc-515623, Dallas, TX, USA). UltraView™ DAB detection kit was purchased from Ventana (Arizona, America). All immunohistochemistry assays were performed on the Roche BenchMark XT fully automatic IHC/ISH instrument by optimized protocols. The results of immunohistochemical staining from the specimens of two operations all indicated that the tumor cells were immunopositive for Pax8 and CA9, but negative for CK7 and AMACAR (Fig. ).
After the death of the patient, we retrieved part of the surgical specimens from two operations he underwent and delivered them to a biochemical company (Life Healthcare, China) which provides the service of genetic testing. Both of the postoperative tissue-originated comprehensive genomic profiling by using the specimens from the RN and reoperation respectively indicated significant mutations of several genes (Fig. and the detailed data of comprehensive genomic profiling is shown in Supplemental. ). There are 7 genes’ mutation abundance that showed a statistical difference between two operations’ specimens, featuring the most dramatic elevated mutation of phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) and epidermal growth factor receptor (EGFR) (Table and Fig. ).
Given some cases of G-CSF-producing RCC with leukemoid reactions have been reported previously [, ], the IHC for assessment of G-CSF expression in the renal tumor and in the specimen from the reoperation were performed on formalin-fixed paraffin-embedded tissue blocks. The blocks were sectioned into 4 μm and pretreated using PT Link (Dako, Glostrup, Denmark) with EnVisionTM FLEX Target Retrieval Solution High pH (Dako) containing Tris/EDTA buffer at pH 9.5. All washing was performed with EnVision FLEX Wash Buffer pH 7.75 (Dako). Staining was performed according to the manufacturer’s protocol (Dako). The samples were incubated with the primary mouse monoclonal anti-G-CSF antibody (Santa Cruz Biotechnology sc-53292, Dallas, TX, USA) at dilution 1:50 for 30 min. The secondary antibody incubation time was 15 min. All detection reagents were from the EnVision FLEX series by Dako (secondary antibodies, EnVision FLEX HRP, and EnVision FLEX Substrate Buffer). The slides were counterstained with hematoxylin (EnVision FLEX Hematoxylin) and dehydrated. Both of the staining outcomes revealed the positive expression of G-CSF (Fig. ).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [171.0, 'cm']}",66.8426,63.50047,70.18473,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 171.0 cm, which is 171.0 cm * 0.393701 in/cm = 67.32287 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (67.32287 (in inches) - 60) = 66.8426 kg.
Hence, the patient's IBW is 66.8426 kg."
3956,10,Ideal Body Weight,physical,decimal,pmc-7234858-1,Extracted,"On April 6, 2018, a 49-year-old Korean man with end stage renal disease (ESRD) was transferred to our hospital for kidney transplantation. He visited emergency room at local hospital due to nausea and vomiting one month ago. Laboratory findings revealed renal failure (blood urea nitrogen 137 mg/dL, serum creatinine 20.5 mg/dL) and anemia (hemoglobin 9.1 g/dL) and metabolic acidosis on arterial blood gas analysis (pH 7.3, bicarbonate 16.4 mEq/L). Routine urinalysis revealed no proteinuria or hematuria. Complement levels were normal range and autoantibodies (Antinuclear antibody and antineutrophil cytoplasmic antibody) were negative. Chest PA showed no cardiomegaly or pulmonary edema, and Kidney-Ureter-Bladder radiography (KUB) was non-specific. Kidney ultrasonography revealed diffusely increased echogenicity and kidney size was smaller than normal (8.2 × 5.0 cm). The abdominal computed tomography showed no evidence of stone in both kidneys ().
Due to uremic symptoms, emergency hemodialysis was started and the kidney biopsy was performed to identify the cause of ESRD. The kidney biopsy showed foci of tubular damage with deposition of translucent crystals of different shapes which are predominantly intraluminal, and confirmed these crystals as calcium oxalate crystals using polarized light (). Final report of pathology was chronic tubulointerstitial nephritis with oxalate crystal deposits and a change of ESRD.
He was an office worker. He received regular national health examination including renal function and urinalysis, and both results were normal until two years before admission. His height and body weight were 167 cm and 70 kg. Body mass index was 25 kg/m2. Review of medical history revealed no history of kidney stone, diabetes, hypertension and operation. He had no medical family history. From the drug history, he had taken Chaga mushroom powder for 5 years due to atopic dermatitis. Initially, he had taken 3 g daily for 4 years following company's recommendation and 9 g of powder for another year because his symptom did not improve.
Based on pathologic finding (oxalate nephropathy) and drug history (long-term exposure to Chaga mushroom), we suspected the association between Chaga mushroom and oxalate nephropathy in our case. Thus, we requested oxalate content of remained Chaga mushroom to researcher/clinical pharmacology division of Catholic Medical center clinical research coordinating center of Korea. Measurement of oxalate was performed by high performance liquid chromatography (HPLC), and analysis revealed extremely high content of oxalate in Chaga mushroom powder (0.14 g of oxalate per 1 g of Chaga mushroom powder).
We finally diagnosed this case as Chaga mushroom-induced oxalate nephropathy with kidney biopsy findings, drug history and high content of oxalate. Clinical course of our case was unfavorable. Renal function has not recovered and he is on maintenance hemodialysis for 18 months.
This study was approved by the Institutional Review Board (IRB) of the Catholic University of Korea (IRB No. 2019-3713-0001) and an informed consent was received from the patient and a caregiver. The images are published under agreement of the patient.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [167.0, 'cm']}",63.22056,60.05953,66.38159,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 167.0 cm, which is 167.0 cm * 0.393701 in/cm = 65.74807 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.74807 (in inches) - 60) = 63.22056 kg.
Hence, the patient's IBW is 63.22056 kg."
3957,10,Ideal Body Weight,physical,decimal,usmle-1082,Extracted,"A 15-year-old boy is brought to the physician by his mother because of a 2-month history of pain in his left hip. The pain started suddenly and has worsened over the past 2 weeks. The pain radiates down the thigh and is aggravated by movement. He had a fall while cycling around a month ago. He had a urinary tract infection 3 months ago that resolved with trimethoprim/sulfamethoxazole. There is no family history of serious illness. His immunizations are up-to-date. He is 165 cm (5 ft 5 in) tall and weighs 85 kg (187 lb); BMI is 31.2 kg/m2. His temperature is 37.5°C (99.5°F), pulse is 65/min, and blood pressure is 104/70 mm Hg. Examination shows an antalgic gait. The left groin is tender to palpation and internal rotation is limited due to pain. Flexing the hip causes external rotation and abduction. His leukocyte count is 9,800/mm3 and erythrocyte sedimentation rate is 12 mm/h. An x-ray of the pelvis is shown.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3958,10,Ideal Body Weight,physical,decimal,usmle-2472,Extracted,"A 16-year-old girl is brought to the physician because she has not attained menarche. There is no personal or family history of serious illness. She is 165 cm (5 ft 5 in) tall and weighs 60 kg (132 lb); BMI is 22 kg/m2. Breast development is Tanner stage 4, and pubic hair development is Tanner stage 1. Pelvic examination shows a blind vaginal pouch.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3959,10,Ideal Body Weight,physical,decimal,pmc-8317470-1,Extracted,"A 15-year-old male patient presented to the clinic reporting exertion palpitations and feeling hot, with no other complaints. The patient had no growth chart until he came to our hospital. The patient did not gain weight as well as his monozygotic twin brother ().
A physical examination revealed the following: pulse, 120 beats per minute; blood pressure, 140/80 mmHg; weight, 50 kg; height, 173 cm; body mass index (BMI) 16.7 kg/m2; and BMI percentile according to age, 6.1. No abnormalities in the heart, lung, abdomen, or nerve were detected. However, he presented signs of hand tremor at rest, and an enlarged thyroid gland was detected with a firm density. No eye abnormalities due to hyperthyroidism and no signs of acromegaly, gynecomastia, or galactorrhea were detected. He had normal secondary sexual characteristics, with his genitalia and pubic hair (Tanner stage 3). The patient had no history of prior thyroid disease. The monozygotic twin brother presented no clinical symptoms of hyperthyroidism, with a normal thyroid function test.
The test results revealed secondary hyperthyroidism, with elevated FT3 levels at 23.08 pmol/L, FT4 levels of 86.32 pmol/L, and TSH levels of 8.25 mUI/L. Investigations of other hormones, including cortisol, adrenocorticotropic hormone (ACTH), testosterone, luteinizing hormone (LH), insulin-like growth factor-1 (IGF-1), and prolactin, showed normal results ().
Thyroid ultrasound revealed that the thyroid gland was heterogeneous, without increased vascularity. Magnetic resonance imaging (MRI) of the pituitary showed a pituitary lesion with mild hyperintensity on the T2-weighted image (), which was less enhancing than the surrounding pituitary parenchyma () and measured 5 × 6 × 7 mm in size. This lesion was suspected to be a pituitary microadenoma.
The patient could not afford the cost of somatostatin analog; therefore, thyroid hormone levels were normalized by methimazole (20 mg per day) and propranolol (10 mg three times per day) before performing an endoscopic transsphenoidal resection of the pituitary tumor. When the patient was admitted to the hospital for surgery, he received a short-term treatment with sandostatin (0.1 mg three times a day), propylthiouracil (PTU), and propranolol. Because the patient was treated with oral methimazole 20 mg per day for 5 months and still had high serum FT4 before surgery, we switched to PTU to prevent thyroid storm during surgery. Postoperative pathology results revealed an adenoma of the pituitary gland ().
After surgery, the doses of PTU and propranolol were gradually reduced. Two weeks following the operation, the patient was stabilized, PTU and propranolol were discontinued, and he was discharged from the hospital. Serum TSH and FT4 levels were evaluated and showed a decreasing tendency after treatment ().
After discharge, the patient presented no clinical symptoms of hyperthyroidism. His weight was 50 kg before surgery and, 2 years later, it was 60 kg (gain 10 kg in 2 years); his height was 173 cm before surgery and later, his height was 175 cm. Hormonal testing after discharge was performed after 2 months, 6 months, and 18 months, and serum TSH, FT4, ACTH, and cortisol levels were detected in the normal range. MRI of the pituitary gland after 1 () and 2 years () showed the complete removal of the tumor, with no recurrence.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.0, 'cm']}",68.65362,65.22094,72.0863,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.0 cm, which is 173.0 cm * 0.393701 in/cm = 68.11027 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.11027 (in inches) - 60) = 68.65362 kg.
Hence, the patient's IBW is 68.65362 kg."
3960,10,Ideal Body Weight,physical,decimal,pmc-6044176-2,Extracted,"A 22-year-old male weighing 60 kg and height of 162 cm, ASA I patient with alleged history of penetrating injury was posted for VATS after 1 week of conservative management as there was persistent pneumothorax. Blood investigations were in normal limits. General anesthesia was induced with IV fentanyl 150 mcg, propofol 120 mg and rocuronium 40 mg. A 39 Fr left-sided DLT was inserted, and the depth of insertion was confirmed with fiber-optic bronchoscope. Anesthesia was maintained with O2, air, and isoflurane. The patient was positioned right lateral and all the pressure points were well padded. After painting and draping, one-lung ventilation was initiated. Two 10 mm ports and one 5 mm port were put and surgery started. However, due to suspected iatrogenic injury to the left lower lobe, the surgery was converted to open posterolateral thoracotomy. Further, intraoperative analgesia was maintained with intermittent fentanyl boluses. Thorough adhesiolysis, repair of lacerated lung and pleural toileting were done. Two chest drains were put and chest wall was closed. In view of open thoracotomy, we planned for continuous ESP block for postoperative analgesia. Maintaining the lateral position T2 to T7 area was cleaned and draped. At T3–4 level, a low-frequency (2–5 Hz) probe was placed longitudinally 3 cm away from the midline, and 18 G Tuohy needle was introduced in plane to the probe craniocaudally []. A volume of 20 ml of 0.375% ropivacaine was deposited, following which the multiport catheter was threaded 4 cm beyond the tip []. The entry point was then secured by Tegaderm []. The patient was then made supine, reversed of muscle relaxation, and extubated when awake. The NRS on awakening was found to be 2/10 at rest and 3/10 on deep breathing. The patient was then shifted to HDU for further observation. 0.2% ropivacaine continuous infusion was started at 6 ml/h through the catheter for 48 h. IV paracetamol 1 g was administered 6 hourly and IV diclofenac 75 mg was administered 12 hourly. The NRS score was assessed as in the previous case. The maximum NRS score reported was 4 in the first 12 h. Next day in the morning round, the patient had pain during physiotherapy session and specifically at intercostal chest drain insertion site. The NRS score was 4/10 at rest and 6/10 during physiotherapy. A volume of 5 ml bolus of 0.2% ropivacaine was administered through the catheter along with IV fentanyl 30 mcg. Pain was relieved after 15 min and he could complete the session. On day 2, the maximum NRS score was 3/10 during physiotherapy. The catheter was removed, and for rest of the hospital stay, he received tablet paracetamol 1 g orally 8 hourly and tablet diclofenac 75 mg 12 hourly. The patient was discharged home on day 5 and his pain score was 1/10 at rest and 2/10 on coughing at that time.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [162.0, 'cm']}",58.69299,55.75834,61.62764,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (63.77956 (in inches) - 60) = 58.69299 kg.
Hence, the patient's IBW is 58.69299 kg."
3961,10,Ideal Body Weight,physical,decimal,pmc-4737662-1,Extracted,"A 24-year-old Korean male visited the emergency room (ER) of our hospital on April 1, 2015 with pain in both flanks. The initial impression was ureter stone due to his symptom; thus, a computerized tomography (CT) of his abdomen was performed. Abdomen CT showed a decreased enhancement of both kidneys but no evidence of urolithiasis. After ruling out urolithiasis, the patient was admitted for diagnostic evaluation. Upon history taking, he stated that he had suffered from urolithiasis 4 years prior, and had passed the stone spontaneously. He also stated that his mother had a history of AKI, and both his aunt and uncle, had a history of urolithiasis. Despite the patient's mother's AKI history, no other specific medical history was noted with familial history taking (). His blood pressure was 130/70mmHg, and his weight and height were 78 kg and 170 cm, respectively. The patient showed pain in both flanks. Laboratory tests on admission revealed the following results: Cr, 1.6mg/dL; blood urea nitrogen (BUN), 17mg/dL; C-reactive protein, 1.40 mg/dL; white blood cell count, 11,380/µL; potassium, 4.0 mmol/L; lactate dehydrogenase, 494 U/L (normal range: 263-450 U/L), creatine kinase, 86 U/L (normal range; 60- 220 U/L); total CO2, 24.8mmol/L; and a low uric acid level of 0.5mg/dL. The urinalysis revealed a specific gravity of 1.012, a pH of 5.0, and 0-1 red blood cells/µL. No glycosuria, aminoaciduria was found. The 24-hour urinary protein was 17mg. The following parameters were within normal limits or negative: serum immunoglobulin; serum complement; antinuclear antibody; perinuclear/ cytosolic-antineutrophil cytoplasmic antibody; and HIV, HBsAg, and hepatitis C antibodies. Fractional excretion of uric acid (FeUA) was 23.95%. Abdominal ultrasonography was unremarkable. After conventional causes of Cr elevation were ruled out, the patient's history was taken again, during which he stated that he had been swimming prior to the flank pain event. The patient was suspected to have familial renal hypouricemia based on, the exclusion of other causes of hypouricemia, familial histories of AKI and urolithiasis, and decreased renal enhancement on abdominal CT (). Thus, the patient was also suspected to be in an EIAKI state. Therefore, genetic analysis for SLC22A12 mutations was conducted. The patient was discharged 6 days after admission. During the outpatient follow up, the patient was stable and the Cr level was maintained at <1.0mg/dL.
AKI recurred 10 weeks after the first episode. On June 17, 2015, the patient was admitted to our hospital via the ER due to pain in both flanks that occurred following swimming. The physical examination did not reveal abnormalities. The patient's blood pressure was 120/80 mmHg, his 24-hour urine protein excretion was 718mg. In addition, serum Cr was 2.2mg/dL, BUN was 21mg/dL, and uric acid was 2.4mg/dL. The renal ultrasound showed increased echogenicity of both kidneys, but structural abnormalities were not observed. We again performed a FeUA and the result was 14.61%. The history of flank pain after swimming may indicate recurrent EIAKI. Hydration and symptomatic treatment were performed during the admission. The symptoms of the patient resolved upon treatment and the serum Cr level decreased gradually. The patient was discharged on day 9 of hospitalization. Anaerobic exertion was prohibited including swimming. At the time of the 1-month follow up, the patient had a normal serum Cr level of 1.0mg/dL, but his hypouricemia (uric acid, 0.7mg/dL) remained. No further episode of EIAKI was noted.
Sequence analysis of the SLC22A12 gene was performed on the patient and his mother due to the suspicion of EIAKI associated with familial renal hypouricemia. T he sequence analysis of SLC22A12 revealed a mutation of c.774 G>A (p.[Trp258Ter]:[Trp258Ter]), or homozygous W258X, which causes renal hypouricemia. The patient's mother exhibited a heterozygous mutation of W258X, making her a carrier of renal hypouricemia; her results were consistent with autosomal recessive inheritance of the disease (). We also proposed another molecular biologic analysis to the patient's father, but the father refused further genotyping since he had normal uric acid level and the cost.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3962,10,Ideal Body Weight,physical,decimal,pmc-6343319-1,Extracted,"A 67-year-old postmenopausal woman with hirsutism of increased hair around the upper lip and armpit and clitoromegaly for five months was referred to the endocrinology clinic of our hospital. She had normal physiological development during her infancy and childhood, and also has a normal sexual life with no other medical history. Her menarche was at 18 years old, and her menopause at age of 56. She had a normal menstrual history before menopause and had no postmenopausal bleeding. She had two healthy children and no miscarriages. She denied taking estrogen, progesterone or health care products. There are no similar patients in her family.
On physical examination, she was 153 cm tall and weighed 53 kg with body mass index of 22.6 kg/m2. Increased hair was observed in her upper lip and armpit (Ferriman- Gallwey score of 8), and a physical examination of genital revealed clitoromegaly. There was no acne, deepening of the voice or other virilization signs. Findings on examination of the head and neck, breasts and abdomen were unremarkable. She had no signs of Cushing syndrome, or acanthosis nigricans syndrome.
The hormonal test showed high total testosterone levels (714.8 ng/dL, reference value 14–56). Serum DHEAS (145.8 ng/mL, reference value 25.9–460.2), androstenedione (2.4 ng/mL, reference value 0.3–3.3) and 17-hydroxyprogesterone (1.7 nmol/l, reference value 0–11.5) levels were within normal range. The serum values of follicle-stimulating hormone, luteinizing hormone, and prolactin were also within the normal range for the menopause. The levels of anti-mullerian hormone, human chorionic gonadotropin (hCG), thyroid- stimulating hormone (TSH), plasma renin activity and aldosterone, adrenocorticotropic hormone (ACTH), serum cortisol, 24-h urinary free cortisol, and 1 mg dexamethasone suppression test were in normal range. The ovarian tumor markers (Ca 125, CEA, Ca 199) were in normal reference range. The repeated samples confirmed that her high testosterone levels were within the tumor range. We excluded overt Cushing Syndrome on the basis of normal cortisol suppression after 1 mg dexamethasone and normal urinary free cortisol levels, as recently proposed by Ceccato F []. Then a middle dosage dexamethasone test (0.75 mg, 4 times a day for 5 consecutive days) without testosterone inhibition strongly suggested the potential androgen-producing tumor, further examinations were needed to distinguish ovarian or adrenal origin of hyperandrogenemia.
Initially, the lack of co-secretion of DHEAS and androstenedione indicated that her elevated testosterone might be of ovarian origin. However, pelvic ultrasound disclosed that there was no ovarian mass, while adrenal ultrasound showed a hypoechoic nodule in the left adrenal gland. Further pelvic magnetic resonance image (MRI) showed submucous myoma of uterus, but no abnormal of ovarian, and adrenal CT scan was also performed and a left adrenal mass of about 1.5 cm in diameter was revealed (Fig. a and b). PET-CT confirmed a round nodule in the external branch of the left adrenal gland with slight increase in FDG metabolism (the SUV max of the nodule was 2.56), considering the possibility of benign adenoma. No ovarian abnormalities or other ectopic tumors were found by PET-CT.
Based on the clinical characteristics, hormone detection and imaging appearances of the case, pure testosterone-secreting adrenal tumor was suspected. Subsequently, the patient underwent a laparoscopic resection of left adrenal tumor. Histological examination (Fig. a) and immunohistochemistry also confirmed the diagnosis of benign adrenocortical adenoma with immunohistochemistry positive for inhibin α, melan A, β-captenin (Fig. b-d), SYN (focal), Ki-67 (< 3%), and negative for chromogranin (CgA), cytokeratin (CK), S-100, P53. The level of testosterone decreased to 15.8 ng/dl on the 3rd day after operation, and the symptoms of virilization were alleviated during the follow-up, which further confirms the adrenal etiology of the testosterone production.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.0, 'cm']}",46.04337,43.7412,48.34554,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.0 cm, which is 153.0 cm * 0.393701 in/cm = 60.23625 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.23625 (in inches) - 60) = 46.04337 kg.
Hence, the patient's IBW is 46.04337 kg."
3963,10,Ideal Body Weight,physical,decimal,usmle-3210,Extracted,"A 42-year-old woman with hypertension comes to the physician because of a 2-month history of persistent reddening of her face, daytime fatigue, and difficulty concentrating. She has fallen asleep multiple times during important meetings. Her only medication is lisinopril. She is 170 cm (5 ft 7 in) tall and weighs 88 kg (194 lb); BMI is 30 kg/m2. Her blood pressure is 145/85 mm Hg. Physical examination shows erythema of the face that is especially pronounced around the cheeks, nose, and ears. Serum glucose concentration is 120 mg/dL.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [170.0, 'cm']}",61.43709,58.36524,64.50894,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.92917 (in inches) - 60) = 61.43709 kg.
Hence, the patient's IBW is 61.43709 kg."
3964,10,Ideal Body Weight,physical,decimal,pmc-5628239-1,Extracted,"A 45-year-old male presented at the emergency department complaining of sudden chest pain and dyspnea. He was transported and admitted to our hospital after 26 min of symptom onset. He had hypertension, dyslipidemia, diabetes mellitus, sleep apnea syndrome, and obesity as his medical history. He had no allergies and had no familial history of coronary artery disease. His Glasgow coma scale was 15 (E4V5M6), and his other vital signs on admission were as follows: blood pressure: 160/113 mmHg; heart rate: 74 beats/min; body temperature: 36.1°C (96.98°F); and pulse oximetry oxygen saturation (SpO2): 98% on room air. He was 173 cm tall and weighed 105 kg (body mass index was 35.1). A chest examination revealed normal heart and breath sounds. No leg edema was observed. Additional physical examinations revealed no abnormalities. Immediately after admission, electrocardiography (ECG) findings revealed normal sinus rhythm with narrow QRS duration, ST-segment elevation in lead aVR, and ST-segment depression in leads I, II, III, aVL, aVF, and V4-6 (Fig. ). Echocardiography also revealed broad anterolateral akinesis without aortic regurgitation, pericardial effusion, or definite aortic flap. The diameter of the aortic root was 45 mm (Fig. ). As his chest pain had frequent improvements and exacerbations in a short period, we suspected not only the presence of acute coronary syndrome (ACS) of the culprit lesion with LMT, but also Stanford type-A AAD involving LMT compression. As plain computed tomography (CT) imaging demonstrated no definitive signs of AAD with 42 mm in the shortest transverse diameter of the aortic root (Fig. ), he underwent emergency coronary angiography (CAG) soon after the plain CT scan. Because there was no information about his renal function at the time pending the outcome of the blood test on admission and we were concerned about the possibility of the presence of ACS of the culprit lesion with LMT, he did not undergo contrast-enhanced CT scan before CAG. Following some difficulties in manipulating the catheters, CAG revealed 75% stenosis of the LMT ostium (Fig. A). Intravascular ultrasound imaging (IVUS) revealed compression of the LMT ostium from the outside of the true lumen (Fig. ). The vessel size of the LMT ostium was 4.9 mm × 4.7 mm by IVUS, and the lumen size of the LMT ostium was changed from 3.9 mm × 3.5 mm to 1.6 mm × 3.4 mm by IVUS according to LMT compression from the outside of the true lumen. As the patient was in shock state with respiratory failure requiring inotropic agents and intubation at the catheterization laboratory, a bare-metal stent (3.5 mm × 9 mm) was implanted into the LMT ostium, 2–3 mm in the aorta, as a bridge to surgery with low pressure (nine atmosphere) so that a surgeon could pull out the stent during surgery (Fig. B). Antiplatelet agents were not administered in order to help minimize perioperative bleeding complications. A total 5000-U amount of heparin was given during percutaneous coronary intervention (PCI). His hemodynamics were stabilized, and echocardiography revealed normal left ventricular function after PCI. Left ventriculography revealed compression of the true lumen of the ascending aorta from the false lumen of the ascending aorta during heart beats (Fig. C). Then, after PCI, he underwent contrast-enhanced CT imaging, which indicated Stanford type-A AAD (Fig. ). He was safely transferred to another hospital to undergo surgery after three hours of stenting. He underwent hemiarch replacement with coronary artery bypass grafting (saphenous vein graft [SVG] to left anterior descending artery, and SVG to left circumflex artery). During the surgery, the stent was pulled out from the LMT ostium. He was discharged from the hospital to home on day 27.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [173.0, 'cm']}",68.65362,65.22094,72.0863,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 173.0 cm, which is 173.0 cm * 0.393701 in/cm = 68.11027 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.11027 (in inches) - 60) = 68.65362 kg.
Hence, the patient's IBW is 68.65362 kg."
3965,10,Ideal Body Weight,physical,decimal,pmc-4857343-1,Extracted,"The patient was a 29-year-old female athlete (height = 170 cm; weight = 60 kg). Exercise intensity before the injury included 16 h/week of volleyball training and another 6 h/week of kite surfing (Tegner score 9). Injury occurred during an indoor volleyball game, in which the patient landed poorly. The injury was an acute indirect injury to the knee (Video 1). The protocol was approved by the Institutional Helsinki Committee (Trial registration number NCT00767780). Written informed consent was obtained from the patient for publication of this case report and any accompanying images.
Immediately after injury, the patient experienced pain, swelling and difficulty bearing weight. She arrived at the emergency room after the injury, where the physician on staff noted pain, swelling and effusion of the knee. A radiograph ruled out a fracture. A joint aspiration suggested an acute ACL tear. The patient was discharged with instructions for physical therapy and a follow-up after a week. At follow-up, the patient underwent a magnetic resonance imaging (MRI) analysis, which showed a complete ACL rupture, lateral bone bruising and minor medial and lateral meniscal tears to her left knee. A total of 2 days after injury, the subject arrived at the AposTherapy center and underwent a gait analysis. Following the gait analysis, the all phases of step-cycle (Apos) system was calibrated. Treatment was then initiated, which included carrying out her daily routine with the biomechanical device. In all, 10 days post-injury, the patient started traditional physiotherapy in addition to AposTherapy for 6 months. The subject underwent follow-up gait analyses at weeks 1, 2, 4, 8, 12 and 26.
AposTherapy uses a biomechanical device () comprising four modular elements attached to foot-worn platforms (Apos system, Apos Medical and Sports Technologies Ltd., Herzliya, Israel). The modules are two convex-shaped biomechanical elements attached to each foot. One is located under the hindfoot region, and the other is located under the forefoot region. The elements are attached to the subject’s foot via a platform in the form of a shoe. The platform is equipped with a specially designed sole that consists of two mounting rails that enable flexible positioning of each element under each region. Each element can be individually calibrated to induce specific biomechanical challenges in multiple planes.
Gait analysis was carried out using a computerized mat (GaitMat™ system; E.Q. Inc. Chalfont, PA, USA). During each gait analysis, the subject was required to walk barefoot at a self-selected speed for 3 m before and after the end of a walkway mat to allow sufficient acceleration and deceleration space outside the measurement area. Each gait test included four walks, and the average value of the four walks was calculated for each parameter. The following spatiotemporal parameters were evaluated in each gait test: velocity (cm/s), step length (SL) (cm), single limb support (SLS) (%gait cycle), base of support (BOS) (cm) and temporal distance (T-D) symmetry. T-D symmetry was calculated for SLS and SL (see ).
At the end of the study, the patient was asked to fill out the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) and the Short Form 36 (SF-36) to evaluate the severity of pain and the levels of function and quality of life.
A physical examination of the patient at 3 weeks post-injury showed that the knee was swollen with minimal to moderate effusion. A range of motion exam showed full extension and painful flexion to 100°. Anteroposterior (AP) stability was examined via the Lachman maneuver, anterior drawer test and pivot shift test. All tests were positive and confirmed the findings of the MRI exam of an ACL rupture. Over the rest of the study, the swelling and effusion reduced significantly. At 3 months post-injury, the subject first returned to beach volleyball, and by 6 months, she returned to her previous level of activity (Video 1).
Gait measurements at baseline and at each follow-up are presented in . All gait parameters and T-D symmetry steadily improved from baseline to week 4, after which, they remained stable for the rest of the treatment period. Compared to baseline, velocity steadily increased by 244% of its original value (); SL gradually increased by 66% and 90% in the involved and uninvolved limb, respectively (); SLS increased by 43% for the involved limb and decreased by 24% for the uninvolved limb () and BOS decreased by 46% and 32% in the involved and uninvolved limb, respectively (). T-D symmetry for SL improved from a value of 12.2% at baseline to −1.4% at the end of the study period. T-D symmetry for SLS improved from a value of −62.1% at baseline to 0.0% at the end of the study period ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [170.0, 'cm']}",61.43709,58.36524,64.50894,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.92917 (in inches) - 60) = 61.43709 kg.
Hence, the patient's IBW is 61.43709 kg."
3966,10,Ideal Body Weight,physical,decimal,pmc-6661044-1,Extracted,"A 76-year-old woman (height 156 cm, weight 47 kg) had previously undergone intestinal resection procedures because of superior mesenteric artery occlusion and carotid artery stenting for bilateral internal carotid artery stenosis. As a result, she had a past medical history of old cerebral infarction.
We planned endovascular aneurysm repair (EVAR) for para-renal abdominal aortic aneurysm using the snorkel technique for the renal artery, but we failed to pass through the left subclavian artery when approaching from the left brachial artery because of AAO.
Before the operation, her pulse was palpable and there was no difference between the left and right upper extremity. Her upper arm blood pressure at that time exhibited no laterality (HR 87/min, BP right 149/90 mmHg, BP left 148/84 mmHg).
Preoperative enhanced computed tomography (CT) imaging revealed a para-renal abdominal aortic aneurysm with a maximum diameter of 58 × 63 mm. The axillary artery was densely calcified, but the AAO was not obvious since the contrast medium was injected from the left upper extremity during preoperative enhanced CT, and this caused severe halation at the axillar/subclavian vein, which made visualization of the adjacent left subclavian artery difficult or impossible.
We planned EVAR for her para-renal abdominal aortic aneurysm using the snorkel technique in the renal arteries. We attempted cannulation of the renal artery approaching from the left brachial artery, but failed to pass through the left subclavian artery because of AAO. Therefore, we decided to compromise the EVAR by landing the proximal stent in the short neck without the snorkel technique. Since the completion angiogram showed the absence of endoleak and complete exclusion of the aneurysm, we did not access the right upper extremity to perform the originally planned snorkel technique.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [156.0, 'cm']}",48.75993,46.32193,51.19793,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 156.0 cm, which is 156.0 cm * 0.393701 in/cm = 61.41736 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.41736 (in inches) - 60) = 48.75993 kg.
Hence, the patient's IBW is 48.75993 kg."
3967,10,Ideal Body Weight,physical,decimal,pmc-7713822-1,Extracted,"The present case report was published with the prior consent of the patient’s guardians.
A 23-year-old, 168 cm tall female patient, weighing 42 kg, visited the emergency room with a chief complaint of abdominal pain. The abdominal pain, accompanied by nausea and vomiting, kept increasing gradually for eight hours. The patient was diagnosed with major depression and bulimia nervosa nine years ago. The patient also had a history of frequent vomiting after episodes of binge eating, along with numerous suicide attempts. Ten hours before reporting to the hospital, the patient ate a very large quantity food, equivalent to approximately ten portions; however, the quantity of the vomit was much less, relative to the amount of food taken. The physical examination revealed abdominal pain and distension in the entire region, along with tenderness, but no rebound tenderness. Subsequent abdominal computed tomography (CT) revealed clear gastric distension. The results of various blood tests were normal. In the joint general surgery consultation that followed, it was decided that an immediate surgical treatment was not necessary; hence, the need for continuous observation of the condition was explained, and a gastroenterological or psychiatric hospitalization was advised, but both the patient and her guardians declined hospitalization. Afterward, they were warned of the possible complications, such as electrolyte imbalance, aspiration pneumonia, gastrointestinal perforation, ischemic changes, due to the pressure applied by gastrointestinal distension, and the possibility of death, in case the condition worsened. The self-discharge form was signed, and they returned home.
Seven hours after returning home, the patient re-visited the emergency room due to persistent abdominal pain, and mental confusion. At the time of the visit, the patient was unconscious. On physical examination, a more severe abdominal distension, and signs of abdominal rigidity were observed. Both legs of the patient had turned pale in color. No auscultation sounds were heard over the abdomen, and the dorsalis pedis pulse was not felt on either foot. Shock was suspected due to a 60/40 mmHg blood pressure, 160 beats/min heart rate, 22 times/minute aspiration rate, and 36.4℃ temperature. Other findings included pH 7.076, PaCO2 22.3 mmHg, PaO2 122 mmHg, HCO3- 6.3 mM/L, base excess (BE) 23.7 mM/L, and lactic acid 11.1 mM/L, which were measured in the arterial blood gas analysis and, thus, metabolic acidosis was confirmed. The electrolyte levels Na+ 157 mM/L, K+ 6.2 mM/L, and Cl- 130 mM/L, indicated that the electrolyte imbalance was severe (). In addition, the patient was in a severe hypoglycemic state with a blood sugar level of 15 mg/dl; because of an elevated creatinine level of 2.84 mg/dl, acute renal failure was suspected. First, to treat the metabolic acidosis, sodium bicarbonate was set at 80 mEq/h. In the abdominal X-ray, the gastrointestinal tract (GIT) was seen to be filled with a large amount of food but without any bowel gas (). Abdominal CT revealed a very large dilation of the stomach, esophagus, and the second part of the duodenum; it was suspected that the distended organs were pressing against the descending aorta, and the right kidney was pressed upwards (). One hour after the emergency room re-visit, the patient's mental state became lethargic—communication became impossible and spontaneous respiration decreased; as SpO2 was measured to be 88%, endotracheal intubation was performed. A Foley catheter was then inserted, but no urine was drained; an emergency hemodialysis was prepared, and for enough fluid supply, a central venous catheter was inserted into the right jugular vein. For continuous monitoring of changes in the vital signs, a conduit was placed in the right radial artery. An attempt was made to insert a nasogastric tube to relieve gastrointestinal pressure, but the food was not drained due to a blockage near the esophagus, which made further insertion impossible. An abdominal CT performed for follow-up observation revealed that the abdomen was still filled with food, and the nasogastric tube was twisted at the end of the esophagus (). It was also suspected that insertion was not possible due to gastroesophageal junction deviation or esophageal stenosis; however, no such sign was seen.
There was no decompression through the nasogastric tube, and as time passed, the mental state of the patient changed into a state of confusion. The patient’s vital signs became increasingly unstable. Since the symptoms and follow-up blood test results exacerbated, instead of performing a percutaneous drainage, it was decided to attempt a surgical decompression; subsequently, the patient was transferred to the operation room six hours after the re-visit. In the emergency room, a total of 3,170 ml of crystalloid fluid, in which a 5% glucose solution was included, was administered. Urine volume was not measured.
After reaching the operation room, the patient’s blood pressure was 70/46 mmHg and the heart rate was 128 beats/min. First, in order to improve the vital signs, crystalloid fluid was administered at the highest speed via the right arm’s peripheral venous catheter and via the central venous catheter of the right internal jugular vein. The instillation of norepinephrine was initiated with sustained dosing at an additional rate of 0.2 μg/kg/min, and continuous infusion of vasopressin at 4–8 unit/h was also initiated. Subsequently, general anesthesia was induced using sevoflurane 1–2 vol% and rocuronium 50 mg. In the arterial blood gas analysis conducted after entering the operating room, pH 7.45, PaCO2 20.8 mmHg, PaO2 335 mmHg, Na+ 161 mM/L, K+ 3.8 mM/L, glucose 205 mg/dl, lactate 13 mM/L, hemoglobin 6.8 g/dl, and HCO3- 14.4 mM/L were measured (). Four units of erythrocytes were prescribed to correct the reduced hemoglobin, and 20 mg of furosemide was injected due to a continuous lack of urination. Furthermore, for rapid transfusion, the rapid infusion system (RIS) was connected to the central venous catheter of the right internal jugular vein, and the transfusion of four erythrocyte units was initiated.
The operating surgeon planned and performed a gastrotomy, after making a skin incision of approximately 10 cm and within 20 min of beginning the surgery. The food and 5,000 ml of body fluid present in the stomach were drained via suction. Thirty minutes after the operation, blood pressure was maintained low at 60/40 mmHg and almost all food was drained; as a large amount of continuous gastric bleeding occurred after decompression, a total of 6,000 ml was drained into the suction bottle. In the follow-up arterial blood gas analysis, results showed: pH 6.75, PaCO2 46 mmHg, and lactate 20 mM/L. Acidosis had worsened, the blood sugar level had significantly increased to 469 mg/dl, electrolyte imbalance had exacerbated with K+ 7.5 mM/L, and hemoglobin had fallen to 4.3 g/dl, suggesting a large amount of bleeding. To correct this, 60 mEq of sodium bicarbonate, and two units of insulin were administered. Further, 1.2 g of calcium chloride was administered to treat hyperkalemia. Moreover, additional 20 μg of epinephrine was injected to correct persistent hypotension.
Bleeding in the stomach continued, and despite initiating erythrocyte transfusion via RIS, hemoglobin level decreased. As a result, a large amount of internal bleeding was suspected, and additional eight units of erythrocytes, and eight units of fresh frozen plasma were prescribed. The operating surgeon tried to determine the cause and area of bleeding, but as the surgical incision was only 10 cm, abdominal organs other than the stomach could not be identified with the naked eye. To reduce bleeding, the operating surgeon considered performing a total gastrectomy or extending the abdominal incision to confirm the bleeding areas from, other organs but concluded that the bleeding was due to ischemia-reperfusion injury after surgical decompression, and DIC. Since the patient’s vital signs steadily worsened, it was decided that the abdomen be closed urgently, and the patient moved to the intensive care unit (ICU).
One hour after the start of the operation, suturing after gastrectomy was completed. When the closing of the abdomen started, non-invasive blood pressure was not measured, and flat waveforms were observed in the catheter of the right radial artery. There was no pulse detected via palpation, and after confirming pulseless electrical activity through the observation of electrocardiogram, an additional 1 mg of epinephrine was injected, and cardiopulmonary resuscitation (CPR) was initiated.
A total of 3 mg of epinephrine was injected, with cardiac rhythm monitoring at 2 min intervals; afterward, 2 units of vasopressin were injected at 2 min intervals, totaling an injection of 4 units of vasopressin. After completing the abdominal closure while performing CPR, the patient was transferred to the intensive care unit, and no urine output was seen until the patient left the operation room.
The operation was conducted for 1 h 20 min, and the anesthesia time was 1 h 50 min. During the operation, a total of 800 ml, four erythrocyte units, were transfused, and 6,200 ml of crystalloid fluid were administered. A total of 6,000 ml was drained into the suction bottle—5,000 ml of food and body fluid through the suction unit via gastrectomy, and 1000 ml due to bleeding that had occurred after decompression from the start of the operation until finish; however, as mentioned earlier, the incision area was small, and bleeding occurring from other abdominal organs could not be confirmed, making it difficult to estimate the exact estimated blood loss. Additionally, prescribed erythrocytes and fresh frozen plasma were transfused through the RIS as the patient left the operation room.
After entering the ICU, CPR was stopped due to a return of spontaneous circulation, but the existing usage of epinephrine, norepinephrine, and vasopressin was preserved, and transfusion continued. However, blood pressure was still not measured, an additional 1,000 ml of bleeding was confirmed through the nasogastric tube, and bleeding from the closed abdominal area continued. Subsequently, as 3.5 g/dl hemoglobin was measured in the follow-up test, transfusion continued, and a 113.1-second prothrombin time, 180-s activated partial thromboplastin time, and platelet count of 22,000/μl were found, confirming that the patient was in a state of DIC. Despite continuous drug administration and transfusion, the hemoglobin level decreased to 1.8 g/dl, and after three hours in the ICU, the heartbeat disappeared, and the patient was declared dead.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [168.0, 'cm']}",59.62607,56.64477,62.60737,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.14177 (in inches) - 60) = 59.62607 kg.
Hence, the patient's IBW is 59.62607 kg."
3968,10,Ideal Body Weight,physical,decimal,pmc-3866704-2,Extracted,"A 67-year-old woman, 166 cm tall and weighing 57 kg, visited our hospital very recently. Her pain in the right hip joint started during gait without any episode. Plain radiographs showed a KL grading of 0 in the right hip (KL grading 0, Fig. ). ROM in the right hip joint was full. A week after the onset of pain, hip MRI revealed femoral-lateral local bone alterations in the right hip joint (Fig. , ). More joint space narrowing was seen in the right hip on a plain radiograph (KL grading I, Fig. ). Her right hip pain is currently much reduced.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [166.0, 'cm']}",57.81505,54.9243,60.7058,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 166.0 cm, which is 166.0 cm * 0.393701 in/cm = 65.35437 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (65.35437 (in inches) - 60) = 57.81505 kg.
Hence, the patient's IBW is 57.81505 kg."
3969,10,Ideal Body Weight,physical,decimal,usmle-1427,Extracted,"A 44-year-old woman comes to the emergency department because of a 10-hour history of severe nausea and abdominal pain that began 30 minutes after eating dinner. The pain primarily is in her right upper quadrant and occasionally radiates to her back. She has a history of type 2 diabetes mellitus and hypercholesterolemia. Current medications include metformin and atorvastatin. She is 163 cm (5 ft 4 in) tall and weighs 91 kg (200 lb); BMI is 34 kg/m2. Her temperature is 38.8°C (101.8°F), pulse is 100/min, respirations are 14/min, and blood pressure is 150/76 mm Hg. Abdominal examination shows right upper quadrant tenderness with guarding. A bedside ultrasound shows a gall bladder wall measuring 6 mm, pericholecystic fluid, sloughing of the intraluminal membrane, and a 2 x 2-cm stone at the neck of the gallbladder. The common bile duct appears unremarkable. Laboratory studies show leukocytosis and normal liver function tests. Intravenous fluids are started, and she is given ketorolac for pain control.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [163.0, 'cm']}",55.0985,52.34358,57.85343,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 163.0 cm, which is 163.0 cm * 0.393701 in/cm = 64.17326 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.17326 (in inches) - 60) = 55.0985 kg.
Hence, the patient's IBW is 55.0985 kg."
3970,10,Ideal Body Weight,physical,decimal,pmc-2728610-2,Extracted,"A previously healthy 68-year-old man, father of one child, presented in 1994 with fatigue and nausea. For many years he had suffered arthralgic pain and had been treated with antiflogistics. The last months he had experienced problems with nocturia and impotence. He was referred to ultrasonography of the abdomen, on which a tumor in the right adrenal was detected. An adrenal CT scan showed a 4 × 4 × 2.5 cm tumor in the right adrenal with high fat content, which was radiologically considered to be a myelolipoma. The left adrenal was evaluated as normal.
Further clinical investigation showed height 165 cm, blood pressure 140/80 mmHg, and normal male genitalia with testicular tenderness bilaterally. Biochemical investigation showed high basal level of 17-OH-progesterone, which was suppressible with dexamethasone, and an impaired cortisol response to ACTH stimulation (). Adrenal iodomethyl-19-norcholesterol scintigraphy showed high uptake in the right adrenal, which however was suppressed by dexamethasone; uptake was normal or low in the left adrenal. DNA sequencing of CYP21 revealed compound heterozygozity for the I172N mutation (c. 515T > A) and the I2 splice mutation (g.655A/C > G, I172N/I2splice).
The myelolipoma was not removed and the tumor size did not increase during a four-year observation period. The patient was started on treatment with 5 mg prednisolone daily for one year, later cortisone acetate 12.5 mg twice a day whereupon his condition improved. The patient died suddenly, 73 years old, in his home; the cause of death remains unknown.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3971,10,Ideal Body Weight,physical,decimal,pmc-3804680-1,Extracted,"A 53-year-old male cadaver was donated to our laboratory. He was 175 cm tall and weighed 80 kg. The cause of death was acute myocardial infarction. There was no evidence of trauma or surgery. During an autopsy, the authors observed morphological features and distribution of the tumors and took photographs. The histological samples were obtained and analysed by hematoxylin-eosin stain and immunohistochemistry and then consulted with pathologist on the microscopic findings of the tumors.
After the opening of the anterior abdominal wall and peritoneum, a large number of round and various-sized tumors (0.5~2.4 cm in diameter) were exposed on the greater omentum (). The superior part of the greater omentum was stuck in the right iliac fossa and adhered to adjacent peritoneal surfaces. The authors examined the intestinal loop following the removal of the greater omentum, and then the first primary mass was detected on the ileum at 90 cm proximal to the ileocecal junction. The mass was 6.1×3.4×4.0 cm sized. It was firm and adhered to adjacent parietal peritoneum and the greater omentum. A cutting plane of the mass was bright brown coloured and the cavity of the central necrosis was open to the lumen of the intestine (). The second primary mass was detected at the middle of the small intestinal loop and 3.7×4.2×3.2 cm sized (). It was adhered to adjacent small bowel and its cutting plane was bright brown coloured. The small foci of the central necrosis and a pattern of swirl were also observed on cutting planes. Moreover, a lot of mesenteric and iliac lymph nodes were enlarged.
The tumor mass lied within the tunica muscularis of the intestinal wall and there was no evidence of mucosal invasion. The tumor cells were spindle-shaped and densely packed in swirling pattern. The cytoplasm of the cells were eosinophilic and the nucleus did not show distinct mitotic figure. Lymphatic spread was confirmed by identification of the subcapsular lymphatic sinus within the pathologic samples obtained from the greater omentum, mesentery, and posterior abdominal wall (). The CD117 antigen was negative and the CD34 was partially positive in immunohistochemical assay (). The desmin and the S-100 protein were not detected. Consequently, the authors diagnosed this tumor as the GIST with lymph node metastasis on the basis of the diagnostic guide of Hirota and Isozaki.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3972,10,Ideal Body Weight,physical,decimal,pmc-7565434-1,Extracted,"Male newborn from a controlled pregnancy without incidents. Eutocic vaginal delivery. Expulsion of meconium before 24 hours of life. Gestational age: 41 weeks. Birth weight: 4.830 g. Breastfeeding. Family history: healthy 21-year-old mother and 23-year-old father. He had no siblings. There was no consanguineous relationship between the parents or family history of interest.
On the NBS, he presented with an acylcarnitine profile compatible with carnitine transporter deficiency, with low levels of carnitine (C0), acetylcarnitine (C2), propionylcarnitine (C3), palmitoylcarnitine (C16), and stearoylcarnitine (C18), as shown in . Given the possibility that this metabolic disorder was of maternal origin, we performed a maternal screening for acylcarnitines on a DBS. The results of this test confirmed greatly decreased levels of C0, but also revealed elevated levels of glutarylcarnitine (C5DC), which made us suspect a maternal glutaric aciduria type 1 (GA-1) with a secondary carnitine deficiency (). When reviewing the newborn DBS results, it was striking that he had some slightly elevated ratios despite having normal levels of C5DC: C5DC/C8 6.72 (NV: <5.0) and C5DC/C16 0.14 (NV: <0.12).
On the maternal anamnesis, it was verified that her psychomotor development had been normal. The mother had completed compulsory secondary education and was currently working in the hotel/restaurant sector. During pregnancy, she had developed subclinical hypothyroidism and after delivery, she had anemia that required oral iron supplementation. She did not report any symptoms except asthenia. She had no exercise intolerance. She also had no headaches, tremor, or any other neurological symptoms.
The examination did not reveal macrocephaly. Her weight was 67 kg and height was 167 cm. Plasma C5DC was elevated (1.98 µmol/L; NV: 0.01–0.33) as well as urinary glutaric acid (1701 mmol/mol crea; NV: 1–4) and 3-OH-glutaric acid (106 mmol/mol crea; NV: 0–7). Plasma-free carnitine levels were considerably decreased (1.79 µmol/L; NV: 21–64). This biochemical study confirmed that she was a high excretory GA-1 patient.
The molecular study of the GCDH gene revealed the existence of two heterozygous variants: a pathogenic variant c.1204C>T (p.Arg402Trp) and a probable pathogenic variant c.853-26_854del (p.?). The c.1204C>T variant is one of the most frequent changes identified in patients of European origin with GA-1. The variant affects a conserved amino acid arginine and it is well-known that its replacement with tryptophan has deleterious consequences for structure and protein function. The c.853-26_854del mutation involves the deletion of 28 nucleotides from intron 8 and affects the canonical splice site -2 of exon 9 of the GCDH transcripts described in the RefSeq database. This variant has not been previously described in the healthy control population or in the literature associated with GA-1.
A brain magnetic resonance imaging (MRI) scan was recommended (which was not performed because she became pregnant again) as well as a dietary record to assess protein intake and oral carnitine supplementation (50 mg/kg/day). She is currently nearing the end of her pregnancy and is clinically well.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [167.0, 'cm']}",63.22056,60.05953,66.38159,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 167.0 cm, which is 167.0 cm * 0.393701 in/cm = 65.74807 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.74807 (in inches) - 60) = 63.22056 kg.
Hence, the patient's IBW is 63.22056 kg."
3973,10,Ideal Body Weight,physical,decimal,pmc-7513492-1,Extracted,"A 23-year-old male presented to our cardiovascular department with progressive exertional chest distress and fatigue for over one year. One month before the admission, the patient experienced novo occasional precordial pain in addition to the presenting symptoms. On admission, physical examinations revealed heart rate of 96 beats/minute with a sinus rhythm, blood pressure of 130/55 mmHg, high myopia, 190.5 cm of height and a diastolic murmur at the aortic valve area. Laboratory examinations for systemic vasculitis and infectious diseases were unremarkable. Transthoracic echocardiography (TTE) demonstrated a giant aortic root aneurysm, an enlarged left ventricle (LV; 99 mm in end-diastolic dimension) and severe aortic regurgitation combined with extremely poor ejection fraction (EF; 18%). No mitral regurgitation or tricuspid regurgitation were observed. Enhanced thoracic CT scan performed with a 16-detector row confirmed the extensive dilated aortic root aneurysm, bulging against the sternum (Fig. a and b, asterisks; 125.1 mm in short-axis), while the morphology of the distal of ascending aorta and descending aorta were normal (30 mm in short-axis). Three-dimensional enhanced CT scan revealed that the aortic root aneurysm is like a “bulging balloon” (Fig. c, asterisk). According to the patient’s self-statement, both of his grandpa and father died from aortic dissection caused by MFS, and he was identified with FBN1 mutations when he was a child. Unfortunately, the patient was lost to follow up owing to his poor compliance. Taken together, this patient was diagnosed with MFS based on the Revised Ghent Criteria [].
The cardiac dysfunction of this patient was improved after receiving cardiotonic and diuretic therapy. After multidisciplinary discussion, surgical intervention, instead of continuously medical therapy, was accepted as reasonable and life-saving, in consideration of the risk of rupture/dissection of the aortic root aneurysm and deteriorating cardiac function. The specific surgical approaches should be decided based on the intraoperative exploration results. Elective femoral arteriovenous cardiopulmonary bypass was performed to avoid unexpected rupture of the giant aneurysm during median sternotomy. Following pericardiotomy, the aneurysm almost completely filled the pericardial cavity and compressed the right atrial and the pulmonary artery (Fig. a, asterisk). After clamping the aorta and opening the aneurysm sac, we observed a tricuspid aortic valve with multiple fenestrations occurring towards the commissures, a torn leaflet and a dilated aortic annulus which was measured over 38 mm. Further exploration verified the morphology of mitral valve was normal. Considering the patient’s poor cardiac function with bad aortic valvular condition and he may not be able to tolerate time-consuming procedures, we decided to perform Bentall procedure with a 28-mm conduit composite a 25-mm mechanical aortic valve (Fig. b). Postoperative three-dimensional enhanced CT scan revealed a normal sized reconstructed aortic root (Fig. c) and pre-discharge TEE examination confirmed the patient’s EF was improved to 40% and the LV end-diastolic dimension was reduced to 59 mm. The patient received anticoagulation therapy and he was discharged uneventfully 7 days later. Regular follow up was required to reduce the risk of anticoagulation-related complications. Moreover, enhanced thoracic CT scan and echocardiography examination were required at least once per year to monitor the morphology of valved conduit and the cardiac function and valvular condition of this patient.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [190.5, 'cm']}",84.50009,80.27509,88.72509,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 190.5 cm, which is 190.5 cm * 0.393701 in/cm = 75.00004 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (75.00004 (in inches) - 60) = 84.50009 kg.
Hence, the patient's IBW is 84.50009 kg."
3974,10,Ideal Body Weight,physical,decimal,pmc-7561635-1,Extracted,"A 44-year-old woman (height 155 cm, body weight 65 kg) was diagnosed with right breast carcinoma and was scheduled to undergo right MRM surgery under general anesthesia and right SAP block. The patient had ASA physical status II, and preoperative examinations were unremarkable. The procedure was performed after informed consent for the SAP block was obtained. The procedure was performed under ultrasonography (USG) guidance using a 38-mm 6 MHz linear transducer and a 22G 100-mm regional block needle. The patient was in the left lateral decubitus position. Aseptic and antiseptic techniques were done around the area of mid-axillary line. Scans were performed while moving the transducer laterally and distally until the 4th and 5th ribs were visualized. The transducer was then rotated into the coronal plane and tilted posteriorly until the serratus anterior muscle and latissimus dorsi muscle were identified. After local infiltration with 1% lidocaine 2 ml and confirming no intravascular injection by aspiration, 0.25% bupivacaine 30 ml was injected on the fascia between the serratus anterior muscle and latissimus dorsi muscle (Fig. ). For general anesthesia, patients were induced using 1% propofol 2 mg/kg with titration, isoflurane 1.5–2.0 vol%, and atracurium 0.1 mg/kg. The patient was intubated using direct laryngoscopy with endotracheal tube (ETT) no. 7. Ringer lactate was used as the maintenance liquid. The duration of the surgery was 120 min. Intravenous ketorolac 30 mg/8 h and oral paracetamol 500 mg/8 h were given as postoperative analgesia for 48 h. Intravenous tramadol 100 mg/8 h was also given for 24 h. The patient was monitored for 2 h postoperatively in recovery room, then for 24 h postoperatively in medical ward. Postoperative NRS is demonstrated on Fig. . The patient does not report any nausea/vomiting or breakthrough pain during monitoring period.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
3975,10,Ideal Body Weight,physical,decimal,usmle-1318,Extracted,"A 58-year-old man comes to the physician for recurrent heartburn for 12 years. He has also developed a cough for a year, which is worse at night. He has smoked a pack of cigarettes daily for 30 years. His only medication is an over-the-counter antacid. He has not seen a physician for 8 years. He is 175 cm (5 ft 9 in) tall and weighs 95 kg (209 lb); BMI is 31 kg/m2. Vital signs are within normal limits. There is no lymphadenopathy. The abdomen is soft and nontender. The remainder of the examination shows no abnormalities. A complete blood count is within the reference range. An upper endoscopy shows columnar epithelium 2 cm from the gastroesophageal junction. Biopsies from the columnar epithelium show low-grade dysplasia and intestinal metaplasia.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3976,10,Ideal Body Weight,physical,decimal,usmle-1544,Extracted,"A 48-year-old man with HIV comes to the physician because of skin lesions over his face and neck for 2 weeks. They are not itchy or painful. He does not have fever or a sore throat. He was treated for candidal esophagitis 3 months ago. He is sexually active with his wife, who knows of his condition, and uses condoms consistently. He is currently receiving triple antiretroviral therapy with lamivudine, abacavir, and efavirenz. He is 175 cm (5 ft 9 in) tall and weighs 58 kg (128 lb); BMI is 18.8 kg/m2. Examination shows multiple skin colored papules over his face and neck with a dimpled center. Cervical lymphadenopathy is present. The remainder of the examination is unremarkable. His hemoglobin concentration is 12.1 g/dL, leukocyte count is 4,900/mm3, and platelet count is 143,000/mm3; serum studies and urinalysis show no abnormalities. CD4+ T-lymphocyte count is 312/mm3 (normal ≥ 500).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
3977,10,Ideal Body Weight,physical,decimal,pmc-4982782-1,Extracted,"A 76-year-old Caucasian woman sought medical care complaining of the presence of scattered nodules all over her body surface. She referred the onset of the appearance of a few dispersed lesions on the neck 18 months before. Since then, new lesions had appeared in the inframammary region, abdomen, and back, which centrifugally spread to the lower and upper limbs, and finally to the face involving the nose and ears. The patient was reluctant to seek medical care until the lesions began to appear in exposed areas, especially on her face. During this period, she maintained in good health.
She had recently used a corticoid cream over her face with subjective improvement. She denied fever, weight loss, or any other complaint except for hopelessness caused by her appearance. Her medical history included the diagnosis of hypertension and the regular use of valsartan, levanlodipine, clopidogrel, and simvastatin; she also had a myocardial infarction 10 years ago, which had been treated with an angioplasty. The physical examination showed an apparently depressed patient, weighing 78 kg, with a height of 1.58 m, and normal vital signs. The skin examination revealed multiple reddish or brown dome-shaped, non-pruriginous, painless papules of varying sizes (1-5 mm) of firm consistency that eventually ulcerated (). The remaining examination was normal.
The laboratory work-up, which included a total blood cell count and erythrocyte sedimentation rate, electrolytes, renal function tests, calcium, hepatic enzymes, uric acid, thyroid function, protein electrophoresis, β2 microglobulin, and immunoglobulin dosage, was within the normal range. Serology for HIV1 and HIV2, hepatitis B, hepatitis C, syphilis, antinuclear antibody, and anti-DNA were negative. A bone radiological inventory ruled out any lesion. A thoracic tomography disclosed signs consistent with pulmonary emphysema. The positron emission tomography-computed tomography scans showed multiple hypermetabolic cutaneous lesions, but no other suspicious lesions were described. The magnetic resonance imaging showed no evidence of central nervous system disease. Therefore, she was deemed free of internal disease.
The patient was submitted to a skin biopsy, which revealed a dense superficial dermal infiltrate composed of histiocytoid cells with oval-shaped nuclei sometimes presenting longitudinal chromatin grooves. Sparse multinucleated cells and plasma cells were also present. Small lymphocytes surrounded groups of histiocytes. The epidermis showed spongiosis, lymphocytes exocytosis, and a focally ulcerated area (). Immunostains were focally positive for S100 () and CD68 (); diffusely positive for CD1a () and were negative for CD207 (langerin) (). The Ki67 labeling index was about 60% (). Based on these findings, the diagnosis was concluded as an indeterminate dendritic cell tumor; also called indeterminate cell (IC) histiocytosis. The BRAF V600 mutation was negative in the neoplastic cells (sequencing analysis of BRAF gene mutations technique).
With the diagnosis of IC histiocytosis of exclusive cutaneous involvement (single multifocal system), corticosteroid (prednisone 0.5 mg/kg/day) was started but the patient’s blood pressure increased. Muscular pain and headache ensued and another treatment modality needed to be scheduled. Taking into account the patient’s intolerance to the intermediate steroids dose, age, and comorbidities, a reasonable option was local therapy, so the patient was treated with narrowband ultraviolet B (UVB) phototherapy three times a week for 2 months. The lesions started effacing after the first month of the phototherapy and completely subsided on the third month leaving local hyperpigmentation. The patient is now at the sixth month of follow-up and is completely symptomless (); she did not report any adverse reactions.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.58, 'm']}",50.57095,48.0424,53.0995,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.58 m, which is 1.58 m * 39.3701 in/m = 62.20476 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.20476 (in inches) - 60) = 50.57095 kg.
Hence, the patient's IBW is 50.57095 kg."
3978,10,Ideal Body Weight,physical,decimal,pmc-6723553-1,Extracted,"A gentleman, 76 years old, was scheduled for catheter ablation of atrial fibrillation (AF) and atypical left atrial flutter in the context of symptomatic left ventricular dysfunction. He reported fatigue and exertional dyspnea, and presented persistent AF on EKG. He had a weight of 68 kg, and a height of 170 cm (BMI = 23 kg/m2), with high estimated thromboembolic risk (CHA2DS2VASc = 4). He was previously prescribed with anticoagulation (Dabigatran 110 mg bid), beta-blocker (bisoprolol 5 mg od), ACE-inhibitor (ramipril 5 mg od), diuretic (furosemide 50 mg) therapy. A 2D-echocardiogram documented left ventricle dilation (LVEDD (end diastolic diameter): 61 mm) with systolic dysfunction (EF (ejection fraction): 38%). A 2D-transesophageal echocardiogram (TEE) showed absence of images referable to atrial and auricular thrombosis. Single-lobe left appendage displayed reduced function with velocity peaks of 25 cm/sec. The left atrial area was 28 cm2. No relevant atherosclerotic plaques were found in the thoracic aorta. Written informed consent was obtained and the patient underwent radiofrequency electrical pulmonary veins isolation plus roof and mitral isthmus ablation lines during systemic intraprocedural heparinization (activation clotting time (ACT)-target: 300–350 s). Electrical cardioversion was also performed due to presence of persistent AF. The total procedural time was 180 min. Dabigatran was temporarily interrupted for 36 h across the procedure and the patient was discharged the next day. After one week he was admitted to the emergency department for sudden dyspnea, being hospitalized for acute heart failure. At admission the EKG showed sinus tachycardia, while chest X-ray depicted bilateral alveolar edema. During hospitalization, after achieving hemodynamic stabilization, the patient suffered aphasia and space-time disorientation with near loss of consciousness. The Angio-CT (computational tomography) showed hypodense lesions in the left cortico-subcortical temporo-occipital area and in the left cerebellar hemisphere as showed in . Carotid and vertebral arteries were free from hemodynamic atherosclerotic plaques. Symptoms completely disappeared after two days and at the 24 h CT scan control, the lesions were stable, in the absence of hemorrhagic transformation. After a few days, the patient complained left limb pain and an acute distal embolism was diagnosed. A new transthoracic echocardiogram revealed a further deterioration of left ventricular ejection fraction (EF: 30%) with no evidence of intraventricular thrombosis and a clearly discernable interatrial septal defect with left-to-right shunt, this was likely attributable to the trans-septal puncture performed during the ablation (). Ultrasonography of the groin region documented in situ not compressible left femoral vein thrombosis (). Non fractioned heparin infusion was administered with complete resolution of both the arterial embolic occlusion and venous thrombosis. After a few days, oral anticoagulation with apixaban was initiated and the patient was discharged. At the six months follow-up, he presented with mild cognitive impairment, which persisted overtime till the last visit.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
3979,10,Ideal Body Weight,physical,decimal,pmc-7489619-2,Extracted,"A 50-year-old woman (weight = 51.6 kg, height = 155.7 cm, body mass index = 21.3 kg/m2) with ovary cancer was scheduled for elective debulking surgery. The patient presented no medical history. No abnormalities were noted on physical examination. After induction of general anesthesia, CVC insertion was planned to prepare for massive bleeding. The patient was placed in the Trendelenberg position. US short-axis images were used to assess the patency of the right IJV and surrounding structures before needle insertion. The needle was advanced in the short-axis view of real-time US using the one-handed technique. After confirming that the blood was aspirated, the guidewire was inserted using the Seldinger maneuver without US guidance. US was used to monitor the location of the guidewire in the IJV lumen, and a 3-lumen CVC was inserted up to 15 cm without any problems. All 3 lumens showed blood aspiration before connecting the fluid lines. The proximal lumen was connected to the pressure kit transducer for central venous pressure (CVP) monitoring, and CVP waveform appeared to be slightly overdamping. After zeroing, the CVP value was within 10 to 15 mmHg. However, a typical waveform was still not detected. Other intravenous fluids connecting to CVC were infused properly.
The operation lasted over 2 hours, and self-respiration continued to recover excessively, even though 0.5 mg/kg neuromuscular blocking agent was infused through the CVC line. Because there were no abnormal findings on the anesthetic machine or other monitors, CVC malposition was suspected and we checked CVC lumens. Clear fluid was aspirated through the distal lumen of CVC instead of blood, and the other 2 lumens were not aspirated.
US revealed malpositioned CVC penetrating IJV (Fig. ). We could not detect CVC tip. A thoracic surgeon suspected that CVC was entering the interpleural space. All fluid volumes injected through CVC were almost aspirated, and CVC was then removed under the attendance of a thoracic surgeon. Chest radiography performed immediately after hemostasis showed haziness in the entire right lung (Fig. ). Consistently, arterial blood gas analysis showed normal results. After accessing the additional peripheral 18 G intravenous line, the operation was completed after nearly 6 hours. The patient was extubated without any difficulty and transferred to the ward after sufficient observation in the postanesthetic care unit. The patient was discharged 1 week later without any complications.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.7, 'cm']}",48.48828,46.06387,50.91269,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.7 cm, which is 155.7 cm * 0.393701 in/cm = 61.29925 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.29925 (in inches) - 60) = 48.48828 kg.
Hence, the patient's IBW is 48.48828 kg."
3980,10,Ideal Body Weight,physical,decimal,pmc-8196242-1,Extracted,"A 76-year-old man was admitted to our hospital because of congestive heart failure. He had a history of CKD, for which he had undergone treatment for more than seven years. Furthermore, the patient also had hypertension for 26 years, but his blood pressure was poorly controlled. He had a history of heart failure caused by CKD and was treated with diuretics. The patient had already consulted with his home doctor about the preparation for HD a month before the current admission. He also experienced dyspnea and palpitations for a couple of days. On admission, the patient had a good appetite and was completely alert, with no neurological symptoms. His height was 168.5 cm, and his body weight was 83.9 kg (his average body weight was 80.0 kg). The patient’s blood pressure was 140/113 mmHg, body temperature was 36.2⁰C, and pulse rate was 107 bpm. His respiratory rate was 20 breaths/min with a SpO2 of 99%, and he felt dyspnea while talking. He did not have any peripheral edema, while the heart and respiratory sounds were normal. The results of the laboratory tests were as follows (Table ): white-cell count: 11,200/µL, hemoglobin level: 11.8 g/dL, platelet count: 200,000/µL, urea nitrogen level: 83.2 mg/dL, creatinine level: 5.11 mg/dL, and uric acid concentration: 7.0 mg/dL. He had a severe chronic renal failure that might have been caused by nephrosclerosis due to a long history of poorly controlled hypertension. The patient did not undergo renal biopsy because his kidney had already atrophied, but no physical findings or laboratory data indicated any other renal disease. Moreover, laboratory data and the clinical course also revealed that he had anemia from chronic kidney disease and chronic liver dysfunction induced by alcohol.
Chest radiograph showed a cardiothoracic ratio of 57.7%, and costophrenic angles were bilaterally dull. An electrocardiogram revealed atrial fibrillation, which had never been detected before. It also revealed an ejection fraction of 66% with no wall motion disorder or severe valvular disease. The left ventricle and atrium were dilated, as well as the inferior vena cava without respiratory changes. On day one, he was treated with intravenous furosemide and oral tolvaptan for volume overload, as well as oral warfarin for atrial fibrillation. The patient showed a quick response to diuretics, with a decrease in body weight to 80.0 kg and resolution of dyspnea on day three. However, on day 10, he complained of malaise and presyncope while standing. On day 12, laboratory tests revealed an acute drop in hemoglobin, a coagulation disorder, and a worsened renal function (Table ).
Vitamin K was administered for increased international normalized ratio (INR) using warfarin, and red blood cells were transfused. Upper gastrointestinal endoscopy revealed active bleeding from a gastric ulcer, which was successfully stopped. Unfortunately, the bleeding led to renal dysfunction, profound urea nitrogen accumulation, and a rapidly deteriorating consciousness (Glasgow Coma Scale {GCS} E3V4M6). Therefore, an urgent HD was initiated on day 13.
A right internal jugular vein triple-lumen catheter was placed for HD without any complications. We planned the slow and gentle dialysis prescription such that there was the least reduction of plasma urea. We used a cellulose triacetate membrane with a relatively small surface area of 1.3 m2. The dialysate flow rate was maintained at 500 mL/min, with a blood flow rate of 120 mL/min. We originally aimed to conduct a short-duration HD; however, the procedure continued for four hours to accommodate red blood cell transfusion. The patient was drowsy (GCS: E3V4M6) even before HD. Three hours after the induction of the procedure, the patient gradually became unresponsive, and he experienced tremors in his mouth and extremities. Approximately four hours after the start of HD, he developed sudden generalized tonic convulsions. We immediately administered diazepam 5 mg intravenously to stop his seizures and stopped the dialysis. The patient subsequently went into a coma (GCS: E1V1M3). Head computed tomography (CT) scans showed a mild edematous change of brain, and laboratory tests revealed a rapid decrease of urea nitrogen (Table ). We also performed a lumbar puncture, but unfortunately, the cerebrospinal fluid could not be obtained as he had a spinal deformity. As we could not detect any other causes for the adverse symptoms, he was diagnosed with DDS and admitted to the intensive care unit. Levetiracetam (500 mg) was administered intravenously every 12 hours, and no seizures were observed again. Furthermore, glycerol (200 mL) was administered every 12 hours to avoid worsening of DDS. On day 14, we tried to perform the HD procedure again, but tremors were again seen in his extremities 20 minutes after starting the procedure. Accordingly, we stopped, after which his tremors resolved almost spontaneously. The patient then underwent continuous hemodiafiltration (CHDF) on day 15. A smaller polymethyl methacrylate membrane was selected (1.3 m2). The blood flow rate was maintained at 100 mL/min, the dialysate flow rate at 500 mL/h, and the filtration flow rate at 500 mL/h. As shown in Figure , plasma urea concentrations slowly decreased following the procedure. The patient's consciousness gradually improved, and he was fully alert. However, severe aspiration pneumonia occurred, necessitating intubation and mechanical ventilation (continuous positive airway pressure (CPAP); positive end-expiratory pressure (PEEP): 9mmHg; FiO2: 0.7) on day 18. He was successfully treated with antibiotics, extubated on day 23, and moved to the general ward on day 25.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.5, 'cm']}",64.57883,61.34989,67.80777,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.5 cm, which is 168.5 cm * 0.393701 in/cm = 66.33862 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.33862 (in inches) - 60) = 64.57883 kg.
Hence, the patient's IBW is 64.57883 kg."
3981,10,Ideal Body Weight,physical,decimal,pmc-8009549-1,Extracted,"In 2018, a 63-year-old male (height 1.81 m, weight 63.5 kg) was admitted to our hospital with a recent history of diffuse abdominal pain associated with change in bowel habits (4 bowel movements/day without mucus and blood) and severe weight loss (about 25 kg in the last two years). In anamnesis, he reported only classic infectious diseases of childhood. He did not refer previous surgery or familiar history of gastrointestinal diseases and cancer. Physical exam revealed a palpable abdominal mass in mesogastrium. Laboratory findings were normal in absence of anemia or leukocytosis. No serological inflammatory status was observed. Ileocolonoscopy was normal. Ultrasound (US) showed a well-defined hyperechoic mass (measuring 41 x 110 mm) in the root of the small bowel mesentery with reactive sub-centimetric node in the context of the thickened mesenteric fat (shown in ). On the basis of clinical and ultrasonographical signs, the diagnosis of “sclerosing mesenteritis” was made. After the exclusion of a possible associated immuno-mediated disorders by serology, a whole-body computed tomography (CT) scan was performed to rule out the occurrence of a concomitant neoplasia. The CT confirmed the US diagnosis of sclerosing mesenteritis by highlighting the presence of a “misty mesentery”, characterized by the increase of mesenteric fat density associated with enlarged inflammatory nodes. Finally, the patient underwent a US-guided biopsy of mesentery with a histology indicative for SM (shown in ). After a brief course of steroids (prednisone 50 mg), we decided to maintain treatment with tamoxifen 20 mg/daily associated with aspirin 100 mg/daily, in order to prevent a potential vascular complication, such as mesenteric ischemia. At US-based 6-months and 12-months follow-up visits, we recorded an improvement of US picture associated with weight gain (about 10 kg) and a stable remission of diarrhea and abdominal pain. After 2 years of follow-up, the patient is healthy and continues to report for US-based follow-ups. No additional CT scans were needed.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.81, 'm']}",75.89772,72.10283,79.69261,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.81 m, which is 1.81 m * 39.3701 in/m = 71.25988 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (71.25988 (in inches) - 60) = 75.89772 kg.
Hence, the patient's IBW is 75.89772 kg."
3982,10,Ideal Body Weight,physical,decimal,pmc-8556027-1,Extracted,"A 25-year-old woman developed lower back pain after her first delivery. As time progressed, her lower back pain worsened. She was previously diagnosed with lower back sprain at another medical center and treated with physical modalities and analgesic myorelaxants. However, these treatments failed to provide pain relief. The patient was admitted to our medical center because of severe back pain after collapsing to the ground a month after delivery. She was unable to ambulate or transfer because of severe back pain, and also experienced difficulties with her daily activities. Due to her severe pain, the patient was unable to hold or breastfeed her baby so she used a breast pump for lactation. The patient reported that she had been completely healthy before pregnancy. She had no diseases that could cause osteoporosis and did not use any medications. She was a nonsmoker and had no family history of osteoporosis or thyroid disease. She weighed in at 47 kg with a height of 163 cm. Informed written consent was obtained from the patient for publication of this case report.
On physical examination, tenderness was observed in the thoracolumbar vertebrae and spasm of the vertebral muscles. Although her spinal range of motion was limited, there were no abnormal neurological symptoms or signs on physical examination. The pain was localized to the back. There was no numbness or weakness.
A bone scan showed multiple compressions of the lumbar spine, consistent with the lumbar magnetic resonance image (Fig. ). Bone mineral density showed that the t score of the L1–4 spine was −3.5 and the z score −2.5 (Fig. A). Both the t score and the z score of the femur neck were −2.6 (Fig. B). In the thyroid scan, decreased trapping was observed in both thyroids (Fig. ). On thyroid ultrasonography, no abnormal nodules were detected.
The laboratory findings showed a total calcium level of 10.4 mg/dL (normal range: 8.1–10.4), plasma 25-OH Vit D level of 9.2 ng/mL (normal range: 4.8–52.8), intact parathyroid hormone (PTH) level of 31.1 pg/mL (normal range: 14.0–72.0), PTH-related peptide level of 1.1 pmol/L (normal range: 0–1.1), adrenocorticotropic hormone level of 19.7 pg/mL (normal range: 5.0–60.0), cortisol level of 7.31 μg/dL (normal range: 3.09–16.66), and erythrocyte sedimentation rate of 11 mm/hr (normal range: 0–25). However, there were increases in the alkaline phosphatase level at 4.7 mg/dL (normal range: 2.7–4.7), T3 level at 253 ng/dL (normal range: 65–150), free T4 level at 2.94 ng/dL (normal range: 0.78–1.54), thyroid microsomal Ab level at 1300 U/mL (normal range: 0.0–60.0), prolactin level at 90.20 ng/mL (normal range: 4.79–23.30 ng/mL), and estrogen level of 265 pg/mL (normal range: 61–437 pg/mL). In addition, the TSH level at 0.04 μIU/mL (normal range: 0.35–5.50) and progesterone level at 0.4 μg/mL were decreased.
The patient was advised to immediately discontinue lactation. In addition, a thoracolumbosacral orthosis was prescribed. A bisphosphate intravenous injection of 3 mg/3 months, elementary calcium at 1000 mg/day, and calcitriol at 0.5 μg/day were commenced. For pain management, analgesics and physical modalities were recommended. The patient underwent a lumbar facet block. An exercise program including back muscle strengthening, range of motion, and relaxation exercises, as well as weight-bearing exercises, was started. A month after rehabilitative management, her pain improved (visual analog scale score improved from 6 to 2). She was able to walk independently indoors. At the 3-month follow-up, she had only L4–5 focal area back pain, felt better, and was comfortable performing daily activities. There was no new vertebral fracture or progressive collapse of pre-existing vertebrae. She received antiosteoporosis treatment (ibandronate intravenous injection 3 mg/3 months, elementary calcium 1000 mg/day, calcitriol 0.5 μg/day) during the rehabilitation process. About 5 years later, the following measurements were found to be within normal range: total calcium level of 9.6 mg/dL (normal range: 8.1–10.4), intact PTH level of 30.4 pg/mL (normal range: 14.0–72.0), plasma 25-OH Vit D level of 12.1 ng/mL (normal range: 4.8–52.8), alkaline phosphatase level at 3.2 mg/dL (normal range: 2.7–4.7), T3 level at 119 ng/dL (normal range: 65–150), free T4 level at 1.47 ng/dL (normal range: 0.78–1.54), and TSH level at 1.05 μIU/mL (normal range: 0.35–5.50). Finally, the BMD score improved. It showed that the t score of the L1–4 spine was −1.9 and the Z-score was −1.8 (Fig. A). The t score and the z score of the femur neck were both −2.2 (Fig. B).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [163.0, 'cm']}",55.0985,52.34358,57.85343,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 163.0 cm, which is 163.0 cm * 0.393701 in/cm = 64.17326 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.17326 (in inches) - 60) = 55.0985 kg.
Hence, the patient's IBW is 55.0985 kg."
3983,10,Ideal Body Weight,physical,decimal,pmc-3640171-1,Extracted,"An 80-year-old woman (weight, 53 kg; height, 154 cm) was scheduled for TKRA of the left knee due to degenerative joint disease. She was diagnosed with hypertension 1 year ago but did not receive any medication. Preoperative blood and coagulation tests were normal. She had not undergone any previous operations. At admission, her vital signs were stable. Preoperative electrocardiography (ECG) showed normal sinus rhythm and a complete right bundle branch block (). A chest X-ray showed a hypertensive heart contour. We did not perform an echocardiogram, because it was obtained at another hospital, and cardiac function was normal except for the hypertension.
The patient was premedicated with glycopyrrolate 0.2 mg intramuscularly 30 min before anesthesia. Upon arrival in the operating room, standard ECG, pulse oximeter, noninvasive blood pressure, and bispectral index monitoring (Model A-2000; Aspect Medical Systems, Newton, MA, USA) were applied. Her vital signs were pulse rate, 76 beats/min (bpm); oxygen saturation, 97%; and blood pressure, 177/83 mmHg. Anesthesia was induced with 40 mg lidocaine and 60 mg propofol. Rocuronium was given at a dose of 0.6 mg/kg to facilitate endotracheal intubation after loss of consciousness. After a few minutes, the ECG showed a complete AV block and ventricular rhythm of about 40 bpm (). Despite the administration of 0.5 mg atropine, the arrhythmia persisted (blood pressure, 90/40 mmHg; pulse rate, 30-49 bpm). At that time, her trachea was intubated with a 7.0-sized endotracheal tube under direct laryngoscopy, and a radial arterial line was placed for continuous arterial pressure monitoring and blood gas analysis. A central venous catheter was also inserted via the right internal jugular vein catheter. About 10 minutes after the propofol injection, her blood pressure was 145/55 mmHg, and her pulse rate was 66 bpm. The ECG showed a sinus rhythm. The operation was delayed, and she was transferred to the intensive care unit until fully awake for close observation and further evaluation.
We assessed the patient's creatine kinase-MB, troponin T, and myoglobin, and all values were normal. An echocardiography taken the next day exhibited a left ventricular ejection fraction of 63%, which was suggestive of an indeterminate left ventricular filling pattern due to complete AV block. In addition, a 24-h ECG Holter monitor showed AV dissociation. Three-dimensional (3D) computed tomography of the heart revealed that the proximal and middle parts of the left anterior descending artery were narrowed by 50%. She also had a focal aortic valve and mitral annular calcification.
We had planned to perform the surgery again. She received a temporary pace maker (VDD mode) with the minimum rate was set to 60 bpm. She was taken to the operating room, where her blood pressure was 180/95 mmHg and pulse rate was 72 bpm. A 22-gauge catheter was placed in the left radial artery for blood pressure monitoring. A central venous catheter was already inserted via the right internal jugular vein. The patient was placed in the right lateral decubitus position, and spinal anesthesia was performed at the L4/L5 interspinous space with 0.5% hyperbaric bupivacaine 8 mg. The sensory level reached the 10th thoracic segment. The surgeon then began the operation with an initial blood pressure of 170/80 mmHg and a heart rate of 90 bpm. The operation lasted about 2 h. She asked for sedation and we administered midazolam 3 mg intravenously. However, because adequate sedation was not achieved, she received a continuous infusion (50 µg/kg/min). A few minutes after the propofol infusion, the ECG showed a complete AV block with a ventricular rhythm of about 40 bpm. The complete AV block disappeared soon after the propofol infusion was stopped. During the remainder of the surgery, her vital signs were stable. At the end of the operation, she had a blood pressure of 150/55 mmHg, a pulse rate of 55 bpm, and oxygen saturation of 96%.
A permanent pacemaker (DDDR mode) on postoperative day 2 was inserted (). On postoperative day 27, she remained hemodynamically stable and was discharged from the hospital uneventfully.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [154.0, 'cm']}",46.94889,44.60145,49.29633,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 154.0 cm, which is 154.0 cm * 0.393701 in/cm = 60.62995 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.62995 (in inches) - 60) = 46.94889 kg.
Hence, the patient's IBW is 46.94889 kg."
3984,10,Ideal Body Weight,physical,decimal,pmc-6414314-1,Extracted,"A 22-year-old male patient visited the renal department of Chonnam National University Hospital for evaluation of an abnormal computed tomography (CT) finding. His height was 179 cm, body weight was 58 kg, and body mass index was 18 kg/m2. There was no history of any underlying disease and, at the time, he was not taking any medication. His family history was non-specific. Initial laboratory findings were all within normal range. Laboratory investigations showed leukocyte count, 9,500 cells/mL; hemoglobin, 13.0 g/dL; platelet count, 340,000 cells/mL; blood urea nitrogen level, 16.1 mg/dL; creatinine, 0.75 mg/dL; estimated glomerular filtration rate, 130.2 mL/min/1.73 m2 (which was calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula: mL/min/1.73 m2=141 × minimum(creatinine/k, 1)α × maximum (creatinine/k, 1)−1.209 × 0.993age × 1.018 (if female) × 1.159 (if black), where κ is 0.7 for women and 0.9 for men, and α is −0.329 for women and −0.411 for men; sodium level, 138 mEq/L; potassium level, 4.0 mEq/L; chloride level, 114 mEq/L; magnesium level, 2.0 mg/dL; total calcium level, 8.4 mg/dL; and serum osmolality, 290 mOsmol/kg. Urine analysis showed the following values: urine osmolality, 312 mOsmol/kg; random urine sodium, 120 mEq/L; random urine potassium, 30.4 mEq/L; random urine chloride, 61 mEq/L; and urinary pH, 7.0. Urine analysis did not show any proteinuria, hematuria, or glucosuria. Contrast-enhanced CT of the abdomen () was performed. Over 20 cysts were detected in both kidneys and in the liver. The right kidney size was 171.30mm (length) × 120.29 mm(width) × 65.80 mm(depth), and the left kidney size was 163.42 mm(length) × 101.88 mm(width) × 79.86mm(depth).
Genetic analysis was performed using Sanger's method. Direct sequencing revealed that the 22nd intron had translocated from G to A, which was previously reported as a pathogenic variant, but the change in amino acid was unknown ().
An angiotensin-converting enzyme inhibitor treatment was started and a follow-up CT was performed after 2 years (). The volume of each kidney was as follows: right kidney volume, 828 mL; left kidney volume, 791 mL; total kidney volume (TKV), 1,620 mL; and height-adjusted total kidney volume (HtTKV), 905 mL/m. The CT showed that the growth rate of the HtTKV was 7.33% per year.
From May 2017, tolvaptan therapy was initiated at a dose of 60 mg per day, with morning and afternoon doses at 45 mg and 15mg, respectively. Monthly checks of the body weight, blood pressure, and laboratory tests including complete blood count, renal function test, electrolyte text, liver function test, random urine electrolytes, and osmolality were performed. Further clinical course was uneventful and the electrolyte levels remained unremarkable. The patient did not report any specific side effects of the tolvaptan therapy, except polyuria and polydipsia. The liver enzyme profile and serum sodium level and osmolality remained within normal range. The serum creatinine was 0.97 mg/dL after 1 year of the tolvaptan therapy (). The urine osmolality decreased to less than 300 mOsmol/kg and urine sodium was less than 100 mOsmol/kg.
Another follow-up abdominal CT was performed 11 months after commencement of tolvaptan therapy (). The size of each kidney was as follows: right kidney volume, 837 mL; left kidney volume, 792 mL; TKV, 1,629 mL; and HtTKV, 910 mL/m. The growth rate of HtTKV decreased from 7.33% to 0.66%(). Till the foreseeable future, the plan is to maintain the current tolvaptan therapy with its same dosage, unless a specific problem occurs.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [179.0, 'cm']}",74.0867,70.38236,77.79103,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 179.0 cm, which is 179.0 cm * 0.393701 in/cm = 70.47248 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.47248 (in inches) - 60) = 74.0867 kg.
Hence, the patient's IBW is 74.0867 kg."
3985,10,Ideal Body Weight,physical,decimal,pmc-5944540-1,Extracted,"A 33-year-old woman, G0P0, who complained of atypical vaginal bleeding and abdominal pain during a period of 4 months was referred from a local clinic. The patient was 165 cm in height, weighed 100 kg, and had a body mass index of 36.7 kg/m2. Her past medical history included schizophrenia treated with risperidone and an appendectomy at the age of 8. An endometrial biopsy revealed differentiated endometrioid carcinoma with trophoblastic components. Then, she was referred to our hospital. Physical examination revealed the presence of a solid mass measuring 8 cm in the left ovary and anther tumor mass in the uterus. Transvaginal ultrasonography showed a mixed echogenic mass in the left ovarian, size 138 x 90 x 65 mm; a mass invading the uterine, size 64 x 54 x 53 mm. Magnetic resonance imaging (MRI) of the pelvic revealed an ill-defined large heterogeneous soft tissue masses in the uterus and left adnexa area. Preoperative chest computed tomographic (CT) scan was negative. Because of the histologic and imaging results, both of the serum β-hCG and AFP were tested and found to be elevated (β-hCG: 238,418.35 U/L, normal value ≤ 4 U/L; AFP: 800.10 ng/mL, normal value ≤ 7 ng/mL). Other markers including carbohydrate antigen (CA)-125 and neuron-specific enolase (NSE) were within the normal range. She underwent abdominal surgical treatment, and the left ovary and fallopian tube were removed and sent for intraoperative consultation. On frozen section, a poorly differentiated ovarian malignant tumor was diagnosed. Then, total hysterectomy with contralateral salpongo-oophorectomy, total omentectomy, and systemic pelvic lymphadenectomy was performed.
Gross morphologically, the uterus measured 16 x 10 x 5 cm. Two protruding masses were found in the endometrial cavity. Both of the 2 polypoid masses (size 6 x 5 x 5 cm and 2 x 1 x 1 cm, respectively) were infiltrating into the myometrium. And the smaller one was extending from the fundus to the cervix. The left ovarian tumor (12 x 10 x 6 cm) was involved with large necrosis and hemorrhages.
Microscopically, both of the 2 masses in the uterus were composed predominately of intermediated-sized, poorly differentiated cells without obvious nested or trabecular patterns. The tumors had deeply (> 50%) infiltrated the myometrium and showed extensive necrosis (Fig. A). In addition, multinucleated choriocarcinoma-like cells were identified in the area of confluent necrosis. Involvement of undifferentiated carcinoma (UC) components was also identified in the left ovary (Fig. B). However, fewer syncytiotrophoblasts were presented in ovarian lesion than that in the uterine lesion. Lymphovasular invasion was found. The tumor was diagnosed as DEAC metastatic to the left ovary. According to the International Federation of Gynecology and Obstetric (FIGO) system, the case was considered FIGO stage IIIA. A panel of immunohistochemical (ICH) analysis was performed to confirm the histologic diagnosis (Fig. A–D). The results of ICH analysis are summarized in Table .[ In the uterus, focal positivity for cytokeratine (CK7), epithelia membrane antigen (EMA), and vimentin was detected in the UC components suggesting epithelia neoplasms. Markers such as β-hCG, human placental lactogen (HPL), and alkaline placental phosphatase (PLAP) were positive in the multinucleated choriocarcinoma-like cells. PAX8, estrogen receptor (ER), and progesterone receptor (PR) staining were absent in UC components. And, AFP and CD30 status were both negative.
Both the serum β-hCG and AFP were dramatically decreased postoperatively (Fig. ). Unfortunately, 3 weeks postoperatively, nodules were identified in the lungs by chest CT, with associated elevations in her serum β-hCG. No adjuvant chemotherapy was given since the patient declined. She was dead of extensive disease approximately 5 months after her primary surgery.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [165.0, 'cm']}",56.90954,54.06406,59.75502,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.96067 (in inches) - 60) = 56.90954 kg.
Hence, the patient's IBW is 56.90954 kg."
3986,10,Ideal Body Weight,physical,decimal,pmc-6402535-1,Extracted,"A 51-year-old female (weight: 73.5 kg; height: 160 cm) with ARDS secondary to aspiration pneumonia was placed on VV ECMO using a single 27 Fr Avalon cannula to the right internal jugular vein. Her peak airway pressure was 46 cm H2O, even with low tidal volume (200 ml) ventilation, and eventually, she was unable to ventilate safely due to decompensated compliance. HFOV with a frequency of 300 bpm and 5 Hz was introduced on ECMO Day #16 to decrease the risk of volutrauma while also preventing atelectasis from hypoventilation. Her mean airway pressure (mPaw) became 29.3 cm H2O with HFOV, which comparatively had been 16 cm H2O on the conventional ventilator. At the time of transition to HFOV, her settings were: ECMO flow 4.56 L/min, Sweep 6 L/min, FiO2 70%, with ventilator FiO2 50%. Approximately two hours later, the patient desaturated requiring FiO2 100% on both the ECMO and HFOV to maintain an O2 saturation (SaO2) of 85%, although the ECMO flow was maintained at 4.5 L/min. These same settings were continued before a flash of bright red, oxygenated blood was noted flowing into the venous return lumen of the Avalon cannula which synchronized with each beat of the oscillator (Video ).
The correct placement of the Avalon catheter and endotracheal tube were confirmed by chest x-ray, and an echocardiogram further confirmed the cannula position (the tip in the inferior vena cava and the access lumen facing the tricuspid valve), as well as ruled out a patent foramen ovale or an atrial septal defect. Inter-atrial shunting within the Avalon cannula was diagnosed, and the ECMO flow was increased above 5.5 L/min to overcome the additional resistance. This provided a resolution of the retrograde shunt. Despite all efforts, this patient, unfortunately, expired due to multi-organ failure. Her family elected to withdraw care after a total of 20 days on ECMO and four days on HFOV.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
3987,10,Ideal Body Weight,physical,decimal,pmc-3314839-1,Extracted,"A 39-year-old male patient reported to the dental institute with the complaint of pus discharge from right lower posterior region of the jaw since one month ago. The patient noticed decayed teeth in the same region, which was not associated with pain. He had visited a private dental clinic, where decayed tooth had been extracted and medications had been given for about 5 days.
On general physical examination, the patient was well built, 182 cm tall with normal gait and satisfactory vital signs. The extraoral examination revealed hypertelorism, strabismus, and a cystic swelling on the left eyelid as well as his neck (). Intraoral examination revealed missing teeth of the right mandibular first and second molars and pus discharge from the same region. No other skeletal abnormalities were detected.
Panoramic radiograph revealed well defined multiple unilocular radiolucencies with sclerotic borders in the mandibular body, ramus, and symphysis areas. The unilocular radiolucencies varied in diameter from minimum 3 cm to around 7 cm in diameter. The largest one was located in the body of the mandible on the right side extending superiorly from the edentulous area to the lower border of the mandible inferiorly. Three smaller radiolucencies measuring around 3 cm in size were located in the posterior part of the right mandibular body and ramus as well in the left symphysis region. A smaller radiolucency measuring around 1 cm in size was observed in the periapical region of the right maxillary third molar. There was no radiographic evidence of tooth displacement and root resorption (). Cross sectional mandibular occlusal radiograph revealed a radiolucent area with minimum cortical plate expansion (). The findings of panoramic radiograph raised the possibility of Gorlin-Goltz syndrome and further investigations were carried out. Chest radiograph revealed the bifid fourth and eighth rib on the right side ().
CT images showed hypodense areas in relation to the right mandibular body separated by a hyperdense septae. Minor breach in the cortical integrity was observed in the lingual aspect of the ramus region. A single lytic lesion was observed in relation to symphysis region. The lesion involved the right half of maxilla including maxillary sinus. Mucosal thickening in the right maxillary sinus was also observed (). Calcification of falx cerebri and tentorium cerebella was also observed (). Incisional biopsy of the lesion through intraoral approach revealed the following histopathological features: parakeratinized, corrugated, 6-10 layers thick epithelium with palisaded, polarized basal cell layer. The connective tissue showed daughter cysts suggestive of keratocystic odontogenic tumor ().
Owing to the familial tendency of this diagnosed condition, the family members were subjected to thorough clinical and radiological examination. The patient's 8-year-old daughter showed a clinical feature of hypertelorism (). Her panoramic radiograph revealed well defined, unilocular radiolucency measuring approximately 2.5 cm in diameter with sclerotic border in her mandibular symphysis region. The radiolucent area extended superiorly from the root apices of the mandibular anterior teeth to the lower border of the mandible inferiorly enclosing the left canine and premolar tooth buds ().
Histopathological evaluation of the specimen obtained after intraoral biopsy procedure revealed histopathological features similar to that of her father (). No other family members were affected by this condition (). A diagnosis of Gorlin-Goltz Syndrome was made on the basis of clinical, imaging, and histological findings. The father and daughter were advised surgical removal of the keratocystic odontogenic tumor. Unfortunately due to certain logistical and financial reasons, the patients could not keep up with appointments.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [182.0, 'cm']}",76.80323,72.96307,80.64339,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 182.0 cm, which is 182.0 cm * 0.393701 in/cm = 71.65358 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (71.65358 (in inches) - 60) = 76.80323 kg.
Hence, the patient's IBW is 76.80323 kg."
3988,10,Ideal Body Weight,physical,decimal,pmc-8159308-1,Extracted,"A 16-year-old female (169cm, 70kg, BMI 24.5) with TCS status post genial tubercle advancement, mandibular reconstruction with graft, and LeFort I osteotomy and craniotomy, presented for removal of left maxillary bone plate and screws and implantation of customized right and left malar implants. Patient’s previous anesthesia record revealed that she had adequate mask ventilation with an oral airway, chin and jaw lift and that she was intubated electively with a nasal fiberoptic scope and extubated in the operating room the following day. Patient’s exam revealed Mallampati IV, short thyromental distance (3cm), small chin, limited mouth opening (2cm), and large tongue relative to oral cavity (Figure ). General anesthesia with an elective asleep fiberoptic intubation was performed. After induction, mask ventilation was feasible with jaw and chin lift and the patient was intubated with 6.5 oral endotracheal tube with cuff via fiberoptic bronchoscope with one attempt.
The surgery was uneventful. During the operation, the patient received 100mcg of fentanyl at the induction and 0.5mg hydromorphone at the incision for pain control. Since incision, no more opioid was given to avoid the risk of respiratory depression at extubation. Prior to extubation, the surgeon inserted an orogastric tube to suction any bloody secretion to prevent the risk of aspiration. At the end of the 3.5-hour procedure, the neuromuscular blockade was reversed with neostigmine and glycopyrrolate with a Train-of-Four of four twitches and no fade. The patient was breathing spontaneously, following simple commands and opening her eyes. The decision was made to extubate her in the operating room. Soon after extubation, silent chest movement was observed with no end-tidal carbon dioxide (ETCO2) and oxygen saturation (SpO­2) deteriorated rapidly. An oral airway was inserted, and positive pressure bag-mask ventilation was initiated. The patient continued to have no ETCO2, then two nasal airways were inserted in the patient’s bilateral nostrils with chin lift, jaw lift by using a two-person ventilation technique, and 110mg of propofol was administered intravenously. At the same time, the emergent surgical airway was called to be ready in a case of an impossible re-intubation if laryngospasm persisted. Laryngospasm improved after propofol bolus as ETCO­­2 returned and SpO2 improved significantly to 100% within two minutes. The patient’s respiratory status eventually stabilized with oxygen saturation of 97%, breathing on her own with both oral and nasal airway adjuncts without jaw lift or chin lift support.
At the time patient was transferred to post-anesthesia recovery unit, she developed hypoxemia with oxygen saturation in the low 80s despite her good respiratory effort. The patient was awake, alert and sitting in bed. Non-rebreather mask with high flow supplemental oxygen was initiated. Physical exam revealed that her lungs were clear to auscultation bilaterally without wheezes or crackles. No pink frothy secretion was seen when the patient was asked to take deep breaths and cough. Bedside chest radiograph revealed bilateral pulmonary opacities and gastric distension (Figure ), leading to the diagnosis of NPPE in the setting of her negative cardiac history. The gastric distension was likely from insufflation of the stomach secondary to the attempted positive pressure ventilation via face mask. The patient then received diuretics and was admitted to the intensive care unit for airway monitoring and management of pulmonary edema. On post-operative day 1, the patient improved clinically. Repeat chest radiograph showed improved pulmonary opacities bilaterally with residual atelectasis and improved gastric distension (Figure ). The patient was discharged home the following day.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [169.0, 'cm']}",60.53158,57.505,63.55816,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 169.0 cm, which is 169.0 cm * 0.393701 in/cm = 66.53547 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.53547 (in inches) - 60) = 60.53158 kg.
Hence, the patient's IBW is 60.53158 kg."
3989,10,Ideal Body Weight,physical,decimal,pmc-5885367-1,Extracted,"A 41-year-old Japanese man with depression complained of nighttime eating. The patient could not remember these events the next morning. He has been obese for 20 years. He had no history of sleep apnea, restless leg syndrome, somnambulism, or eating disorders and no symptoms similar to binge eating or night eating. He had no family history of any sleep-related disorders. He had developed depression and insomnia because of stress after 5 months on a new job, and he visited our clinic 2 months later. He was not receiving any medication and did not take herbal medicine or supplements. He did not have suicidal thoughts or self-harm behavior. During his first visit, a physical examination revealed that his height was 167 cm, body weight was 90 kg, and body mass index (BMI) was 32.2 kg/m2. His laboratory test results revealed slight liver damage and hyperlipidemia, with a serum alanine aminotransferase level of 52 U/L (normal range, 10–42 U/L), aspartate aminotransferase level of 35 U/L (normal range, 13–30 U/L), and triglyceride level of 277 mg/dl (normal range, 40–150 mg/dl). His Self-Rating Depression Scale score was 62 (normal range, 27–47; range of values, 20–80) [].
The patient was diagnosed with depression and obesity. Along with supportive psychotherapy, he began sertraline treatment prior to sleep; his dose was titrated up to 100 mg (Japanese full dose) over 4 weeks. In addition, he received the sleep inducers zolpidem and flunitrazepam, and the anxiolytic clotiazepam. His depressive mood slightly improved, but it continued for an additional 4 months despite resolution of insomnia. Subsequently, 3 mg of aripiprazole was added as an adjunctive therapy. His depressive mood immediately improved, and his appetite increased. The patient reported enjoying driving and cleaning up his room, but felt fatigued the next morning. Three weeks after the initiation of aripiprazole treatment, the patient’s mother found that the patient woke up and ate food from the refrigerator during the night. The patient did not respond to the mother during this episode. The patient did not remember this event, felt full, and wondered why the bags of food were empty the next morning. He did not consume any improper substances such as raw, frozen, or spoiled food. This episode lasted for 2 days. During the 3 weeks after aripiprazole treatment, the patient gained 5 kg. The patient acknowledged that he remembered urinating at night only once before starting aripiprazole. Re-examination of laboratory results revealed that the patient’s serum glucose, cortisol, and thyroid hormone levels were normal. He was advised to reduce his aripiprazole and zolpidem doses. However, he continued to use the same zolpidem dose because his insomnia returned after a dose reduction.
After aripiprazole was reduced to 1.5 mg, the patient’s nocturnal eating episodes rapidly and completely disappeared. However, amnesia of nocturnal urination occurred three times during the next 6 months. This amnesia of nocturnal urination disappeared after zolpidem was replaced with triazolam. The patient’s depressive mood continued to improve, and his body weight remained at 94 kg (Fig. ). He did not exhibit any psychotic features during his entire treatment.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [167.0, 'cm']}",63.22056,60.05953,66.38159,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 167.0 cm, which is 167.0 cm * 0.393701 in/cm = 65.74807 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.74807 (in inches) - 60) = 63.22056 kg.
Hence, the patient's IBW is 63.22056 kg."
3990,10,Ideal Body Weight,physical,decimal,pmc-2827126-1,Extracted,"The patient was a 26-year-old Caucasian Greek male (178 cm, 75 kgs) was admitted to the Cardiology Department for the evaluation of a retrosternal constant pain of 3 hours duration. The pain started abruptly without any preceding symptoms. The pain was excruciating retrosternal pain and radiating to his right arm with a 8/10 intensity. The examination of the patient was unremarkable and his medical, surgical and family history was negative. The patient had no clinical features of Marfan syndrome. His biochemical values were normal.
On examination, the patient was now in moderate pain (4-5/10) but he was very anxious and worried because he had never experienced this type of pain. He actually was in active duty in the army until recently (15 days before) and he was extremely active to all the exercises he had to perform. He never had any form of disease or hospitalization. His pulse was 100/min and his blood pressure was 130/65 mmHg. No murmurs or extra sounds were audible on cardiac examination. Chest x-ray was essentially normal (Figure ). ECG was on sinus rhythm without any abnormalities. Cardiac ultrasound set the question of aortic dilatation with the possible presence of hematoma in the aortic wall or a small intimal flap in the proximal ascending aorta. Although there was an intact aortic and mitral valve function. No pericardial effusion was noted. A chest computerized tomography showed the presence of an ascending aortic aneurysm at 6 cm and a circumferential aortic tear with the possible presence of an intimal tear in the ascending aorta as well (Figure ).
The patient was emergently operated. We performed ascending aortic replacement under the support of cardiopulmonary bypass and moderate hypothermia. Intraoperatively a complete circumferential aortic tear was noted just above the sinotubular junction. The entry and exit point of the dissection were confined in the ascending aorta. Ascending aorta was replaced with a 26 Dacron graft. The patient recovered well and discharged on seventh postoperative day. Pathology revealed no specific findings in the resected aortic segment. A three years follow up showed that the patient was negative and in excellent clinical condition.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [178.0, 'cm']}",73.18119,69.52213,76.84025,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 178.0 cm, which is 178.0 cm * 0.393701 in/cm = 70.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.07878 (in inches) - 60) = 73.18119 kg.
Hence, the patient's IBW is 73.18119 kg."
3991,10,Ideal Body Weight,physical,decimal,usmle-1498,Extracted,"A 56-year-old woman, gravida 3, para 3, comes to the physician because her left breast has become larger, hot, and itchy over the past 2 months. The patient felt a small lump in her left breast 1 year ago but did not seek medical attention at that time. She has hypertension and hyperlipidemia. Menarche was at the age of 11 years and menopause at the age of 46 years. Her mother died of breast cancer at the age of 45 years. The patient does not smoke or drink alcohol. Current medications include labetalol, simvastatin, and daily low-dose aspirin. She is 170 cm (5 ft 7 in) tall and weighs 78 kg (172 lb); BMI is 27 kg/m2. Her temperature is 37.7°C (99.9°F), pulse is 78/min, and blood pressure is 138/88 mm Hg. Examination shows large dense breasts. There is widespread erythema and edematous skin plaques over a breast mass in the left breast. The left breast is tender to touch and left-sided axillary lymphadenopathy is noted.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [170.0, 'cm']}",61.43709,58.36524,64.50894,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.92917 (in inches) - 60) = 61.43709 kg.
Hence, the patient's IBW is 61.43709 kg."
3992,10,Ideal Body Weight,physical,decimal,pmc-2572044-2,Extracted,"45 year old female active smoker who weighted 62 kg, ht 171 cm, with a 45 pack year smoking history underwent excisional biopsy and sentinel node dissection for a T1bN0 left breast cancer. Her only medical history was discomfort in her neck and back which was felt to be due to her work, which requires heavy lifting. A Mammosite partial breast irradiation catheter was inserted. The patient underwent evaluation by a radiation oncologist, who deemed the minimum cavity surface to skin distance to be 5 mm, as well as the conformation of the balloon within the cavity to be satisfactory for radiation delivery. The patient continued to smoke after surgery despite being instructed to stop. One month after surgery the wound had redness. It was unclear if this was radiation effect, infection, or both. The patient was treated with antibiotics. The redness resolved, but a 1 × 1 cm area of skin developed obvious necrosis with clear yellow drainage, requiring debridement. The wound is now healing by secondary intention.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [171.0, 'cm']}",62.3426,59.22547,65.45973,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 171.0 cm, which is 171.0 cm * 0.393701 in/cm = 67.32287 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (67.32287 (in inches) - 60) = 62.3426 kg.
Hence, the patient's IBW is 62.3426 kg."
3993,10,Ideal Body Weight,physical,decimal,pmc-3512220-1,Extracted,"The proband is a 30-year-old woman. She was born after an uneventful pregnancy at full term. Her parents were nonconsanguineous. SD was diagnosed at 3 years of age on the basis of clinical symptoms and increased level of free sialic acid in the urine.
The patient's development during the first year of life was relatively normal, but crawling was unstable and muscular hypotonia and nystagmus were noticed. The patient spoke her first words at 1 year of age and her first sentences at 2 years of age. She learned to walk by 1.5 years of age, but her gait and balance were abnormal. At 3 years of age, her cognitive development was assessed as normal, except for mild slowness and clumsiness when performing fine motor skills. The followup evaluations showed mild delays in motor tasks, eye-hand coordination, and concentration. Her verbal development was slightly delayed, and verbal dyspraxia was reported. At 6 years of age, the developmental delay was approximately 2 years.
Inattentiveness, hyperactivity, and problems with sleep were reported during childhood. The patient also had problems with balance and body awareness. Ataxic symptoms were prominent in childhood, but improved during the teenage years.
During her school years, the neurocognitive development fluctuated notably. Verbal performance was consistently better than visual performance or fine motor skills. Intellectual disability was considered to be mild.
At the age of 12 years, the patient's verbal skills, as assessed using the Wechsler Intelligence Scale for Children-R test [], were at the level of a 7 year old, and her performance skills varied between those typical of a child of 5 years 6 months and 6 years 6 months of age. Two years later, her verbal skills had improved. At 14 years of age, no progression was noted in the neurocognitive deficits. The developmental age of the patient varied between 4 and 8 years, and her verbal skills were notably better than her motor and visual abilities.
At the age of 30 years, the proband was living alone with support. She was a social person, keen on the arts and team sports. She was 157 cm in height and weighed 56 kg. She was taking no medications. On examination, auscultation of the heart and lungs was unremarkable, her blood pressure was 114/74 mmHg, and the electrocardiogram was normal. Her facial features were slightly coarse. The proband could walk without aid, but both legs were in a pes planus position. When walking, she had some athetotic movements in her upper extremities. Muscle strength and skin sensation were normal, tendon reflexes were symmetrical and normal, and the plantar responses were in flexion. Both Achilles tendons were slightly shortened and there was mild spasticity in both legs. Neurological examination revealed only mild ataxia. There was mild instability in the Romberg test and the patient was unable to stand with her eyes closed. There was no ataxia or dysmetria shown by coordination tests, but her hand movements were clumsy. She suffered from marked myopia and used six dioptre corrective lenses. Clear outward strabismus was seen in her right eye. However, the eye movements were normal and nystagmus was not detected. The neurological condition of the patient had not deteriorated during the previous 10 years.
There had been no deterioration of the patient's motor skills in adulthood. Her skills had improved with respect to balance, coordination of body movements, and reciprocal motor actions, as well as processing the sequences of movements. The speed of motor actions had become slightly slower during the last few years.
The electroencephalogram (EEG) was normal at 3 years of age, but showed mild generalized background abnormality with occasional spikes and sharp waves at the left temporo-parieto-central region at 5 years of age. Quantitative EEG was normal at 15 years of age. There was no history of epileptic seizures, but symptoms that resembled the startle reflex were noticed in response to sudden noises.
The methods that were used for neuropsychological evaluation of the patient are presented in . Her developmental age, as assessed by Wechsler Intelligence Scale for Children-III [] at the age of 30 years, was 7 years 9 months for the verbal scale and 5 years 4 months for the perceptual scale. Her neurocognitive performance was remarkably better than those of other patients with the conventional type of SD and the SallaFIN mutation []. Other patients with SD (n = 37) have been evaluated using the Bayley Scales of Infant Development-II [], because the tasks that are used in the Wechsler children's tests were too demanding.
There was a slowing in visuomotor speed as well as eye-hand coordination during the followup of our patient after her teenage years. Visual reasoning and spatial orientation were mildly delayed, and the visuoconstructive skills were diminished. However, verbal skills had improved. Repetition of nonsense words and oromotor sequences were difficult for the proband because of verbal and oral dyspraxia, but the proband was able to learn and repeat long, logical stories. She had difficulties with time orientation.
Motor problems were evident but the symptoms had not progressed during the followup. The proband was able to walk on the toes and sides of the feet, but the forward tandem walk was insecure, and motor persistence and motor coordination were clumsy. Static cerebellar tests were performed quite well, with only slight problems with balance. Two of the dynamic cerebellar tests—finger-to-thumb tapping and toe tapping—were performed slowly but correctly. Visuomotor deficits were evident, but the proband managed the test of basic functional mobility quite well.
Brain imaging performed at 15 years of age showed dysmyelination. The corpus callosum was hypoplastic, but the cerebellum, pons, and the proximal part of the cervical cord were normal. There was no enlargement of the ventricles or signs of cortical atrophy. The MRI findings at 30 years of age were mild ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [157.0, 'cm']}",49.66544,47.18217,52.14871,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 157.0 cm, which is 157.0 cm * 0.393701 in/cm = 61.81106 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.81106 (in inches) - 60) = 49.66544 kg.
Hence, the patient's IBW is 49.66544 kg."
3994,10,Ideal Body Weight,physical,decimal,pmc-3983424-1,Extracted,"A 56-year-old male, 168 cm tall and weighing 71 kg, with a traumatic right rotator cuff injury, was scheduled for arthroscopic reconstruction surgery under general anesthesia. This patient had a history of diabetes mellitus and was taking oral hypoglycemic agents and insulin. For several years, he experienced recurrent episodes of severe left ocular pain and increased IOP, which later resolved. On close ophthalmic examination, he was diagnosed with Posner-Schlossman syndrome. There was mild epithelial edema of the cornea with a few keratic precipitates, and his cup/disc ratio was 0.5 with no visual field change. During the acute crisis period, the measured IOP in his left eye was above 30 mmHg and the IOP in his right eye was 13 mmHg. His symptoms were relieved after applying eye drops containing dorzolamide, a carbonic anhydrase inhibitor, and prednisolone acetate, but frequently recurred. Three weeks before his scheduled surgery, the IOP in his left eye rose again and he became extremely anxious about the operation. After consultation with an ophthalmologist, we decided to measure the patient's IOP intraoperatively using portable tonometry, and obtained informed consent from the patient for this perioperative risk.
Preoperative laboratory findings, including hemoglobin concentration, liver function and coagulation tests, and arterial blood gas analysis, were normal, as were chest X-rays. The patient had a left axis deviation and an incomplete right fascicular block on electrocardiography and a mild restrictive pattern on pulmonary function test without any significant symptoms. In the morning of the day of surgery, the patient received 7.5 mg of midazolam per os. Before entering the operating room, his vital signs were stable, with a blood pressure of 133/75 mmHg, a heart rate of 82 beats per min, and an oxygen saturation of 99%. Two drops of 0.5% proparacaine hydrochloride were applied to each eye, and IOP was measured by portable tonometry (Tono-Pen Avia, Ametek, NY, USA) (). Initially, IOP was 19 mmHg in his left eye and 16 mmHg in his right eye. A 20-gauge catheter was inserted into his left radial artery to monitor continuous arterial pressure. Anesthesia was induced with propofol 100 mg, lidocaine 75 mg, rocuronium 50 mg, and a supplemental dose of fentanyl 100 µg, and ventilation was controlled to maintain end tidal carbon dioxide at 35 ± 5 mmHg. Anesthesia was maintained with 2-2.5% sevoflurane in an oxygen-air mixture (FiO2 0.5). Immediately after tracheal intubation, IOP increased to 23 mmHg in his left eye and 21 mmHg in his right eye, but decreased within 5 min to 14 mmHg and 12 mmHg, respectively. Initial arterial blood gas analysis showed an Hct of 39%, a pH of 7.48, a PaCO2 of 34 mmHg, and a PaO2 of 240 mmHg. After changing the patient's position to left lateral decubitus, the IOP was 15 mmHg in his left eye and 14 mmHg in his right side, but increased to 20 mmHg and 14 mmHg, respectively, after skin incision and arthroscopic insertion. The concentration of inhaled sevoflurane was adjusted in response to instantaneous IOP variation, and the occurrence of IOP surge was closely monitored. During the 210 min operation, the patient's vital signs remained stable and no adverse event occurred. Serial measurements by portable tonometry showed that his IOP remained within an acceptable range throughout the entire perioperative period (). The patient's postoperative course was uneventful.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [168.0, 'cm']}",64.12607,60.91977,67.33237,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.14177 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.14177 (in inches) - 60) = 64.12607 kg.
Hence, the patient's IBW is 64.12607 kg."
3995,10,Ideal Body Weight,physical,decimal,pmc-6726413-1,Extracted,"A 58-year-old female (height 170 cm, body weight 65 kg, body surface area 1.7 cm2) presented to the outside hospital’s emergency department complaining of shortness of breath and “hot flashes”. Her past medical history was significant for a pituitary adenoma, which had been resected two years prior. Electrocardiogram (EKG) on presentation showed sinus bradycardia (55 beats per min) with frequent premature ventricular ectopy and prolonged QT intervals (550 msec). Echocardiogram revealed a dilated left ventricle with an ejection fraction 10% with right ventricular dysfunction. She underwent cardiac catheterization and no significant coronary disease was identified. Cardiac index was measured at 1.2 L/min/kg and, as a result, she was placed on norepinephrine and dobutamine infusions for hemodynamic support. During catheterization, the patient acutely decompensated, developing hypoxia and mental status change. Arterial blood gas drawn at the outside hospital recorded a PaO2 of 37 mmHg with O2 saturation 69% on a non-rebreathing facemask. She required emergent intubation and was admitted to the cardiac care unit (CCU) at the outside institution for further management. While in the CCU, she continued to develop unstable ventricular tachycardia refractory to medical management, including the administration of multiple anti-arrhythmic medications and defibrillation. She was hypotensive with a mean arterial pressure of 55 mmHg, requiring high dose of norepinephrine (0.6 mic/kg/min) and dobutamine (10 mic/kg/min). She was also hypoxic requiring 100% FiO2 to maintain appropriate oxygen saturation. Due to hemodynamic instability, she was placed on VA-ECMO via bilateral groin access and transferred to our institution for further management.
Repeated echo at our institution showed cardiac standstill (Video ).
A routine admission laboratory panel revealed hypocalcemia, elevated lactate, hyperglycemia with a normal renal and hepatic functions (Table ). Shortly after admission, she was noted to be producing large amounts of urine. Her urine output was measured at 8 liters over the first 12 hours at our institution. Initially, VA-ECMO flow was restricted to 2-2.4 L/min, most likely due to hypovolemia. Aggressive fluid replacement therapy was initiated and ECMO flow improved to 4.5 L/min. A subsequent endocrine panel was abnormal (Table ).
Endocrine and nephrology were consulted to assist with the diagnosis and treatment plan. Based on the history of pituitary resection, as well as the discovery that the patient was noncompliant with her medications for approximately six months prior to presentation, it was believed her numerous endocrine abnormalities and cardiogenic shock were secondary to acute panhypopituitarism. Initial treatment included intravenous fluid replacement for central diabetes insipidus, intravenous levothyroxine for hypothyroidism (50 mcg daily), corticosteroids for adrenal insufficiency (100 mg every eight hours), and calcium replacement (1000 mg three times a day). As her fluid balance normalized, her lactic acidosis eventually resolved.
After three days of ECMO support and medical treatment, a repeat transthoracic echocardiogram (TTE) confirmed improving left and right ventricular function. An ECMO weaning trial with decreased ECMO flow was conducted on ECMO day 4 and she was decannulated from ECMO support on ECMO day 5. Inotropic support was not required after post-decannulation. Echocardiography after ECMO removal showed a left ventricular ejection fraction of 45% and normal right ventricular function (Video ).
After being successfully weaned from ECMO therapy, the patient was transitioned to oral prednisone (5 mg daily) for adrenal insufficiency, oral levothyroxine (100 mcg daily) for hypothyroidism, and intravenous calcitriol (1 mcg daily) and oral calcium carbonate (1,000 mg three times daily) for hypocalcemia. She was extubated and liberated from mechanical ventilation on post-decannulation day 3. She was then transferred back to the referral facility on post-decannulation day 7 and eventually discharged to a rehabilitation facility and home without recurrence of heart failure symptoms.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [170.0, 'cm']}",61.43709,58.36524,64.50894,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (66.92917 (in inches) - 60) = 61.43709 kg.
Hence, the patient's IBW is 61.43709 kg."
3996,10,Ideal Body Weight,physical,decimal,pmc-6357658-2,Extracted,"The patient was a 28-year-old female, physician by profession, recreational runner, physically active non-smoker who complained of 2-week deep left groin pain during usual exercise of 60 minutes running 2–3 times per week. She had no allergies to medications. She did not drink or smoke and denied any drug use. She did not report specific history of previous trauma, also in her right hip. She had no past medical history except for polycystic ovary syndrome (POS).
As her symptoms did not abate taking NSAIDs regularly, she came to our outpatient department. At the time of presentation, her height was 164 cm and her weight 57 kg (BMI 21.2 Kg/m2). Clinical examination revealed no deformities or shortening either lower limb, and excellent capillary refill and good pulses. No neurological deficit was identified. Her left hip ROM was complete, comparable with the contralateral and with no pain limitations. However, the symptoms started and increased with load. The iliopsoas test and those for labral pathology were negative. The contralateral hip did not present any pathology. Tumor markers, a urine calcium level test and all blood tests prescribed resulted normal. As vitamin D was just at the normal limit (), Cholecalcipherol 50.000 U.I./month was suggested. Imaging studies were performed including first pelvis and x-rays of the hips (antero-posterior and lateral views), which did not show any alteration (). The MRI of her pelvis was performed 6 days later (), identifying a left femoral neck stress fracture on the medial side without cortical bone involvement and with surrounding edema of the spongy bone. Following Fuellerton and Snowdy, the injury was classified as a Type II, compression-side, incomplete, FNSF with a good prognosis. On the basis of clinical signs and radiographic results, the patient was treated conservatively and advised to rest, use walking aids to avoid full weight-bearing on her left lower limb. Unfortunately, when at 2-month-follow-up assisted loading by crutches was permitted, the pain increased suddenly. Immediate hip-x-rays were performed with a suspect of a Type II, compression-side, complete FNSF, which was radiologically confirmed as a superior neck margin fracture with cortical bone involvement. Hence, surgical treatment was proposed, and the patient underwent an internal fixation procedure on her proximal left femur using a DHS® DePuy-Synthes plate. After surgery, she was discharged with assisted loading by elbow crutches. After 30 days, she was able to walk with complete load, without aids and pain, starting stationary cycling and swimming. Finally, the patient was followed at 3, 6 and 12 months following the injury, being clinically, metabolically and radiographically assessed. At 6-month follow-up, the blood level of vitamin D and PTH were improved (), and at the last follow-up, the plain x-rays () and MRI showed evidence of a healed stress fracture without signs of AVN ().","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [164.0, 'cm']}",56.00401,53.20381,58.80421,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 164.0 cm, which is 164.0 cm * 0.393701 in/cm = 64.56696 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (64.56696 (in inches) - 60) = 56.00401 kg.
Hence, the patient's IBW is 56.00401 kg."
3997,10,Ideal Body Weight,physical,decimal,pmc-3927006-1,Extracted,"A 70-year-old male patient underwent a Bentall operation due to annulo-aortic ectasia, which was combined with severe aortic valvular insufficiency. The patient's height and weight were 165 cm and 50.9 kg, respectively and he had no co-morbid diseases except for hypertension, which was treated with a calcium channel blocker and an angiotensin converting enzyme inhibitor. The patient had a normal sinus rhythm, and the preoperative transthoracic echocardiography (TTE) revealed a left ventricular ejection fraction of 58% with no other intracardiac pathologies. Coronary angiography also revealed normal coronary arteries. After anesthetic induction, the patient's hemodynamic variables were as follows; systemic blood pressure 113/38 mmHg, heart rate 83 beats/min, central venous pressure 9 mmHg, and pulmonary arterial pressure 33/15 mmHg. A Bentall procedure was uneventfully performed and the patient was weaned off from cardiopulmonary bypass (CPB) without difficulty. The total aorta cross clamp time was 95 minutes and the total CPB time was 115 minutes. Before leaving the operating room, there was no evidence of fluid collection in the pericardial and pleural space in the transesophageal echocardiography (TEE), with the estimated left ventricular ejection fraction being 50%. Receiving norepinephrine 0.08 µg/kg/min, milrinone 0.25 µg/kg/min, and vasopressin 0.8 IU/hr, the hemodynamic parameters were as follows: heart rate of 80 beats/min, blood pressure of 87/48 mmHg, CVP of 10 mmHg, pulmonary arterial pressure of 24/15 mmHg, cardiac index of 3.4 L/min/m2, mixed venous oxygen saturation of 90%, right ventricular ejection fraction of 39%, and right ventricular end diastolic volume index of 141 mm/m2. The patient was transported to the intensive care unit (ICU) without any further events. In the ICU, as in the operating room, the patient's lungs were ventilated with a tidal volume of 500 ml at a rate of 12 breaths/min, with a fraction of inspired oxygen of 40% medical air, along with 5 cmH2O of positive end-expiratory pressure. The corresponding peak airway pressure and plateau airway pressure were 19 cmH2O and 17 cmH2O, respectively. The arterial blood gas analysis revealed pH 7.419, PaO2 123.8 mmHg, and PaCO2 34.7 mmHg. Over a period of 30 minutes in the ICU, the CVP increased from 10 to 23 mmHg, and the pulmonary artery diastolic pressure increased from 14 to 17 mmHg. The blood pressure was 90/49 mmHg, and the cardiac index was maintained at 2.7 L/m/m2 without increasing doses of norepinephrine, milrinone, and vasopressin. The electrocardiogram (ECG) revealed nonspecific ST wave changes without any changes in the height of the QRS waves, and the chest X-ray showed partial atelectasis of the right lung and moderate cardiomegaly. The patient's respiratory mechanics and follow-up arterial blood gas analysis showed no significant changes. His hemoglobin was 8.7 g/dl which is near the former value measured in the operating room of 9.0 g/dl. The platelet count was 82 × 109/L and the International Normalized Ratio of the prothrombin time was slightly elevated at 1.54. During the first 15 minutes after the surgery, 100 ml of blood were drained from his mediastinal and chest drains. Because, there was no further chest tube drainage, 100 ml of 6% hydroxyethyl starch 130/0.4 solution was infused without any transfusions.
A TEE examination was immediately performed to confirm the cause of the CVP elevation, which revealed minimal pericardial fluid collection and preserved biventricular function in the midesophageal four-chamber view and the transgastric short axis view. The midesophageal bicaval view showed the right atrium (RA) being pushed anteriorly and laterally by a large mass measuring 6.06 cm × 8.78 cm (). The mass contained echogenic materials with some echo-free areas, which is consistent with hematoma, and as a result the SVC was almost completely obliterated by it. In the midesophageal aortic valve long axis view, the hematoma occupied the transverse sinus as well (). The patient was immediately transferred to the operating room for re-exploration. A loculated hematoma around the valved graft was found to compress the entire SVC and extended to the RA. After evacuation of the hematoma, the CVP decreased immediately from 23 to 11 mmHg. The cardiac index and the blood pressure remained stable despite the discontinuation of the vasopressor and inotropic agents. However, the patient's postoperative course deteriorated, with the development of acute renal failure and adult respiratory distress syndrome, which resulted in the prolongation of ICU stay. The patient was then transferred to the general ward at postoperative day (POD) 52 for rehabilitation, and discharged at POD 109.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
3998,10,Ideal Body Weight,physical,decimal,pmc-5058839-1,Extracted,"A 62-year-old man presented to his local hospital after 1 month of mucous and bloody stool and 2 weeks of worsening abdominal pain. He had leukocytosis (1.4 × 104/μL), thrombocytopenia (6.4 × 104/μL), and elevated blood urea nitrogen (BUN; 71 mg/dL) and serum creatinine (2.56 mg/dL) levels. The patient was admitted with a suspicion of sepsis secondary to intraabdominal infection, and broad-spectrum antimicrobial therapy was initiated. However, his condition deteriorated, and after 7 days, he was transferred to the intensive care unit (ICU) at Chiba University Hospital.
On admission to the ICU, the 165.3 cm tall patient weighing 99.3 kg was fully conscious (Glasgow Coma Scale E4V5M6), but he had a tendency to somnolence. His blood pressure was 154/103 mm Hg, heart rate 115/minutes, respiratory rate 30/minutes, body temperature 37.9 °C, and SpO2 96% on room air. The conjunctiva and skin were icteric. The chest was clear to auscultation. There was abdominal distention with mild hypogastric tenderness but no sign of peritoneal irritation. There was pitting edema in the upper and lower extremities. The white blood cell count was 1.2 × 104/μL, C-reactive protein level was 23.9 mg/dL, and procalcitonin level was 8.92 ng/mL, which were consistent with a diagnosis of bacterial infection. The platelet count had dropped to 3.8 × 104/μL, and the prothrombin time was 41% with a fibrin degradation product level of 53.1 μg/mL, indicative of coagulopathy. The lactate dehydrogenase level was 392 IU/L, aspartate transaminase and alanine transaminase levels were 50 and 17 IU/L, respectively, and also total and direct bilirubin levels were 6.2 and 4.6 mg/dL, respectively; however, other indicators of hemolysis, including anemia and schistocytosis, were absent. The BUN had increased to 92 mg/dL and the creatinine level was stable at 2.09 mg/dL. The CH50 level was 40.6 U/mL (normal range: 30–50 U/mL), the C3 level was 85 mg/dL (normal range: 65–135 mg/dL), and the C4 level was 23 mg/dL (normal range: 13–35 mg/dL).
The patient's clinical course is summarized in the Fig. . Since a stool culture test on ICU admission identified Enterococcus species and Corynebacterium striatum, a diagnosis of severe sepsis derived from bacterial enteritis was established and wide-spectrum antimicrobial therapy was initiated. Continuous hemodiafiltration was initiated on ICU day 3 but oliguria progressed to anuria, thrombocytopenia persisted, and laboratory values did not improve. Blood, urine, and spinal fluid cultures taken on admission to the ICU were all negative, which eliminated the possibility of additional foci of infection. Two polyps (one each in the sigmoid colon and the rectum) were discovered on lower gastrointestinal endoscopy, which were diagnosed at histopathology as early-stage nonhemorrhagic adenocarcinoma. The polyps did not appear to be the cause of the bloody stool. Additional laboratory evaluations were negative for other hematological disorders or connective tissue diseases. On ICU day 9, schistocytosis (0.5%) was noted on the peripheral blood smear, and a diagnosis of TMA was established. The Hct level also had dropped to 23.5% on the same day and the declining trend continued, therefore red blood cell transfusion was performed days later when he complained dyspnea. Plasma exchange (PE) therapy was initiated on ICU day 11. The patient had only a slight remission of thrombocytopenia after a total of 8 PE sessions (2.1 × 104/μL before the 1st PE and 5.9 × 104/μL after the 8th PE), but there was no notable clinical improvement and the anuria persisted (Fig. ). The level of ADAMTS13 activity in a plasma sample collected from the patient prior to initiation of PE was 25.1%, and the sample was negative for ADAMTS13 inhibitor. These findings eliminated the possibility of TTP. Furthermore, the stool was negative for Shiga toxin-producing-strains of Escherichia coli, and the serum titer for anti-Shiga-toxin antibody was also negative, eliminating the possibility of HUS. Although we considered TMA secondary to colorectal cancer in the differential diagnosis, the endoscopic findings of intramucosal carcinoma and negativity for tumor markers eliminated this possibility. Careful consideration of other possible causes, previous history, and drug history failed to identify an extrinsic etiology of TMA in this patient, and we ultimately suspected aHUS as the cause. Accordingly, intravenous eculizumab treatment (900 mg, once a week) was initiated on ICU day 26. An increase in urine output was observed on the next day, and renal support was successfully discontinued on the same day. And also marked recovery of the platelet count was obtained in combination with the effectiveness of supportive therapy including PE. Biweekly eculizumab infusion was repeated 4 times and then discontinued.
After approval by the institutional review boards of Chiba University, the University of Tokyo, and National Cerebral and Cardiovascular Center, an anticomplement factor H (CFH) antibody assay and an analysis of complement factor H-related (CFHR) genes were performed using a blood sample collected from the patient prior to initiation of PE. Also written informed consent was obtained from the patient before the assays. The anti-CFH antibody level was 6.16 AU/mL, which indicated negativity for anti-CFH antibody. We performed the multiplex ligation-dependent probe amplification (MLPA) analysis to screen the copy numbers of CFHR1/3 on chromosome 1q32 using a commercially available kit (MLPA kit P236-A2; MRC-Holland, The Netherlands),[ and found that CFHR1/3 did not show gene deletions. However, moderate hemolysis was induced in concomitant hemolytic assays using sheep red blood cells (RBCs), and analysis for mutations potentially associated with aHUS identified a nonsynonymous mutation (p.Ala311Val) in the gene encoding membrane cofactor protein (MCP). All screened genes are presented in the Table .
The patient was discharged from the ICU on day 37 and was discharged to home on day 58. He was followed up regularly as an outpatient and was receiving 40 mg/day of prednisolone. At approximately 1 year after discharge, the patient remained in stable condition without relapse or resumption of eculizumab therapy.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.3, 'cm']}",61.68119,58.59713,64.76525,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.3 cm, which is 165.3 cm * 0.393701 in/cm = 65.07878 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.07878 (in inches) - 60) = 61.68119 kg.
Hence, the patient's IBW is 61.68119 kg."
3999,10,Ideal Body Weight,physical,decimal,pmc-5187906-1,Extracted,"A then 28-year-old Caucasian woman presented with right-sided hemihypesthesia and weakness of the right leg in March 2013. Magnetic resonance imaging showed multiple contrast-enhancing cranial and spinal lesions indicating high disease activity. Diagnosis of RRMS was made based on the revised McDonald criteria 2010 [] supported by cerebrospinal fluid results and exclusionary laboratory tests. Prior to diagnosis, she suffered from weakness of her right leg for several weeks in 2010 and 2012. Moreover, in December 2012, she had blurred vision in the right eye for a few weeks. The only concomitant diseases were type I DM since the age of 18, treated with both long- and rapid-acting insulin (insulin glargine and aspart), and arterial hypertension, treated with enalapril 2.5 mg once daily. The patient was obese with a weight of 80 kg, height of 153 cm, and a BMI of 34.2 kg/m2. HBA1c values (December 2012: 9.4%, April 2013: 9.1%, July 2013: 9.8%, December 2013: 10.1%), cholesterol (December 2012: 212 mg/dL, April 2013: 301 mg/dL, July 2013: 299 mg/dL, December 2013: 210 mg/dL), as well as triglyceride levels (December 2012: 261 mg/dL, April 2013: 373 mg/dL, July 2013: 446 mg/dL, December 2013: 318 mg/dL) were markedly increased.
Intravenous steroid treatments (1 g methylprednisolone daily over five days) in March and April 2013 were considered insufficiently effective because of persisting paresis of the right leg. In May 2013, plasmapheresis was initiated and led to a slow but complete resolution of the paresis resulting in an expanded disability status scale score of 2.0 due to mild coordination deficits, reflex inequalities, absent cutaneous reflexes, and urinary urgency.
Because of the high disease activity, fingolimod was started at the end of July 2013. An ophthalmic examination before initiating fingolimod therapy was not performed. Four weeks later she complained about a progressive decrease in vision in her left eye. Best corrected visual acuity was 20/20 in her right and 20/25 in her left eye. Funduscopic examinations revealed a mild non-proliferative diabetic retinopathy in both eyes (see A,B). Spectral domain optical coherence tomography (OCT) showed cystoid ME in the left eye with a central foveal thickness of 264 μm in the right and 463 μm in the left eye (; 27 August 2013). Fingolimod was discontinued immediately. Two weeks later, ME was detected in both eyes, the central foveal thickness on OCT increased to 642 μm in the right and to 709 μm in the left eye and, after another week, slightly decreased to 618 μm and 648 μm in the right and left eye, respectively (; 9 and 16 September 2013). Fluorescein angiography documented diffuse cystoid ME in both eyes, affecting the left eye more significantly (G,H). Since the patient’s visual acuity rapidly deteriorated to 20/160 in both eyes, a volume of 0.05 mL ranibizumab (0.5 mg; Lucentis®) was injected into each vitreous cavity of both eyes on 16 September 2013 using a 30-gauge needle after topical anesthesia. Already after one week following administration of ranibizumab, a rapid and sustained remission of the bilateral ME was attained (; 24 September 2013). Despite this improvement, intravitreal injection of ranibizumab into both eyes was repeated on 16 October 2013 because of bilateral central and nasal scotoma as assessed by Amsler grid testing. Best corrected visual acuity increased to 20/63 in both eyes, while treatment did not lead to any change of the scotoma. In a follow-up examination on 16 August 2015, best corrected visual acuity was 20/20 in both eyes, scotoma had significantly regressed and OCT examination did not reveal any ME (foveal thickness of 196 und 197 μm in the right and left eye, respectively).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [153.0, 'cm']}",46.04337,43.7412,48.34554,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 153.0 cm, which is 153.0 cm * 0.393701 in/cm = 60.23625 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.23625 (in inches) - 60) = 46.04337 kg.
Hence, the patient's IBW is 46.04337 kg."
4000,10,Ideal Body Weight,physical,decimal,pmc-2740165-1,Extracted,"A 36-year-old Indian man was hospitalized 72 hours after forceful vomiting followed by the onset of chest pain, dyspnoea and fever. The patient had no previous medical history and no family history of relevance. He worked as construction worker. He was non-smoker and consumed an average of 40 unit of alcohol per week. His height was 170 cm and his weight was 64 kg. Initial chest radiography showed left-sided hydropneumothorax with mediastinal emphysema. Computed tomography of the chest with contrast showed spontaneous esophageal perforation (Boerhaave’s syndrome) in the left lower third of thoracic esophagus. Patient underwent emergency direct surgical repair with pleural flap reinforcement (first operation). Subsequently he developed an esophageal leak with mediastinitis and empyema, followed by a septic shock. Esophagectomy with cervical esophagostomy, gastrostomy and feeding jejunostomy was done (second operation) with a preparation for esophageal reconstruction at a later stage. Six weeks later, a retrosternal gastric transposition with CEGA was performed using circular stapler (third operation). Transmediastinal gastric transposition was found to be difficult because of the two previous surgeries and inflammatory process. Five days later, the patient developed discharge from the neck incision which required bedside drainage and packing. Contrast study revealed a major disruption of the cervical anastomosis ().
Patient underwent exploration which revealed a necrosis of the gastric tip, resulting in complete anastomotic disruption. Complete median sternotomy was done with extra care not to injure the retrosternal gastric conduit, followed with tedious blunt dissection of the stomach that was firmly adherent to the sternum anteriorly and mediastinum posteriorly. Finally, it was freed with maximum possible mobilization, in order to gain a sufficient length. After generous excision of the necrotic gastric tip and the edge of cervical esophagus, a new CEGA was performed, using manual anastomosis with interrupted 4-0 vicryl (forth operation). Patient made steady postoperative recovery with no signs of sterna infection or mediastinal collection. On the 10th postoperative day esophagogram with gastrograffin showed a patent and competent anastomosis (). Patient was discharged in a stable condition and remained well six months later.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [170.0, 'cm']}",65.93709,62.64024,69.23394,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 170.0 cm, which is 170.0 cm * 0.393701 in/cm = 66.92917 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.92917 (in inches) - 60) = 65.93709 kg.
Hence, the patient's IBW is 65.93709 kg."
4001,10,Ideal Body Weight,physical,decimal,pmc-6385396-1,Extracted,"A 73-year-old Japanese man with a 2-month history of dysphasia and heartburn first presented to his local doctor and was later admitted to our hospital. He had difficulties in swallowing and eating; did not have melena, epigastralgia, or hematemesis; and had a history of hypertension and no known allergies. At the time of admission, he was taking at lansoprazole 15 mg/day and olmesartan medoxomil 10 mg/day. He did not drink alcohol but used to smoke 30 cigarettes per day for 45 years. His environmental and employment histories were unremarkable. His family history was remarkable for colon cancer in his father and lung cancer in his brother. On admission, his height was 161 cm, body weight was 56.5 kg, blood pressure was 126/62 mm Hg, pulse was 70 beats per minute, temperature was 36.9 °C, and oxygen saturation was 98% while he was breathing ambient air. His conjunctiva was not icteric but slightly anemic. On chest examination, his heart rhythm was regular with no murmur, and his lungs were clear to auscultation. His abdomen was soft, not distended, and not tender. A soft and movable mass was palpable around the epigastrium. The legs and feet showed no edema. Laboratory tests showed a creatinine level of 0.89 mg/dl, blood urea nitrogen level of 12.6 mg/dl, total bilirubin level of 0.3 mg/dl, aspartate transaminase level of 17 IU/L, and alanine transaminase level of 19 IU/L. The patient’s white blood cell count was 8930 per cubic milliliter, hemoglobin was 9.2 g/dl, and platelet count was 438,000 per cubic milliliter. An esophagogastric fiber (EGF) showed type 3 gastric carcinoma in the antrum. The tumor caused pyloric stenosis and invasion to the duodenum, so the patient was admitted to the hospital (Fig. a–c). Staging laparoscopy was performed to assess the extent of tumor spread, and laparoscopic bypass was performed. Staging laparoscopy revealed peritoneal dissemination, and peritoneal lavage cytology revealed tumor cells in the abdominal cavity. We diagnosed L, type 3, circ, cT4a(SE), cNx, pP1, pCY1, M0, stage IV (the Japanese classification of gastric carcinoma). The patient was initially treated with docetaxel 40 mg/m2 on day 1, cisplatin (CDDP) 60 mg/m2 on day 1, and TS-1 120 mg/day on days 1–14, followed by a 2-week recovery period (DCS regimen). Dexamethasone 9.9 mg and palonosetron 0.75 mg were administered on day 1, and dexamethasone 6.6 mg was administered on days 2 and 3 as premedication. The patient had grade 3 diarrhea (according to Common Terminology Criteria for Adverse Events criteria) after one course (Fig. a, b). Then TS-1 was reduced (100 mg). After two courses of the DCS regimen, EGF and computed tomography (CT) showed that the tumor had shrunk (Fig. c–e), and then staging laparoscopy was performed to evaluate a response. Peritoneal dissemination disappeared, and peritoneal lavage cytology revealed no tumor cells in the abdominal cavity. Then salvage operation, laparoscopic distal gastrectomy with D1+ dissection, was performed. Pathological findings were ypT2(MP), ypN2(3/15), ypP0, ypCY0, M0, ystage II (Fig. ). TS-1100 mg/day on days 1–14, every 3 weeks was started as adjuvant chemotherapy. After 15 months, CT revealed multiple peritoneal nodules (Fig. a). They were highly suspected as a recurrence. Paclitaxel 80 mg/m2 on days 1, 8, and 15 was started as a second regimen. Dexamethasone 6.6 mg, famotidine 20 mg, and granisetron 3 mg were administered on days 1, 8, and 15 as premedication. This regimen achieved partial response (Fig. b), but its efficacy did not last. After 3 months, CT revealed progressive disease (Fig. c). The original gastric carcinoma was HER2-positive (Fig. ). The patient’s Eastern Cooperative Oncology Group performance status was 2; his body weight was 50.7 kg; and he complained of appetite loss. We concluded that the patient could not tolerate doublet therapy. Therefore, TS-1100 mg on days 1–14 with Herceptin 6 mg/kg (Roche/Genentech, South San Francisco, CA, USA) on day 1 every 3 weeks was introduced. This regimen was substantially effective and achieved CR after 9 months based on CT findings (Fig. d, e). The patient had no adverse effects while receiving this regimen (Fig. a, b). Since then, the patient has been treated with only Herceptin 6 mg/kg every 3 weeks without any side effects, and no radiological findings of recurrence had yet occurred for 6 years, 7 months after surgery (Fig. f).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [161.0, 'cm']}",57.78748,54.89811,60.67685,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 161.0 cm, which is 161.0 cm * 0.393701 in/cm = 63.38586 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (63.38586 (in inches) - 60) = 57.78748 kg.
Hence, the patient's IBW is 57.78748 kg."
4002,10,Ideal Body Weight,physical,decimal,pmc-7017661-1,Extracted,"A 59-year-old female of height 156 cm with carcinoma of lung left lower lobe was posted for left lower lobectomy. Her preoperative assessment revealed adequate cardiopulmonary reserve and had predicted postoperative Forced Expiratory Volume (FEV1) of 58%. Anaesthetic plan included thoracic epidural analgesia and general anaesthesia. During intubation there was difficulty in negotiation of tracheal cuff of 35- French left sided double lumen tube (DLT) through the glottis. Hence a 7-French bronchial blocker (Arndt- Cook® Medical) was chosen for lung isolation. A 7.5 mm endotracheal tube was placed through which bronchial blocker was placed in left main bronchus guided by a fibreootic bronchoscope (FOB). Position of the bronchial blocker and isolation of left lung was ensured by FOB in right-lateral position. After docking of the Robotic da Vinci Xi® surgical system, capnothorax was created in left pleural cavity with pressure of 8 mmHg. Commencement of dissection of left lower bronchus resulted in sudden increase in EtCO2 with intermittent normal range of EtCO2. Patient's heart rate, saturation (SpO2), blood pressure, temperature, and airway pressure were stable throughout the procedure. Arterial blood gas revealed partial pressure of CO2 (PaCO2) of 45 mmHg. Suspecting increased systemic absorption of CO2 from capnothorax, respiratory rate was increased to increase minute-ventilation [tidal volume-300 ml, respiratory rate – 18.min-1, positive end-expiratory pressure (PEEP) 4 cm H2O]. Few minutes later, EtCO2 continued to rise up to 114 mmHg [] with PaCO2 of 42 mmHg. At this point, the left lung remained collapsed and bronchial cuff position was confirmed by FOB. On inspection, open left lower lobe bronchus communicating with capnothorax was suspected to be the cause for negative arteriolar to EtCO2 gradient []. The surgeon was notified regarding the same and the capnothorax pressure was reduced to 5 mmHg (6.5 cmH2O). PEEP was increased to 8 cmH2O thereby reversing the pressure gradient across the open bronchus and proximal bronchial cuff. These manoeuvres led to the reduction in efflux of capnothorax CO2 into the airway which was reflected in EtCO2. Thoracoscopic lobectomy was continued and rest of the procedure was uneventful.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [156.0, 'cm']}",48.75993,46.32193,51.19793,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 156.0 cm, which is 156.0 cm * 0.393701 in/cm = 61.41736 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.41736 (in inches) - 60) = 48.75993 kg.
Hence, the patient's IBW is 48.75993 kg."
4003,10,Ideal Body Weight,physical,decimal,usmle-539,Extracted,"A 68-year-old man comes to the physician because of fatigue and muscle cramps for the past 4 weeks. He has also noticed several episodes of tingling in both hands. He has not had fever or nausea. He has had a chronic cough for 10 years. He has chronic bronchitis, hypertension, and osteoarthritis of both knees. His father died from lung cancer. Current medications include salbutamol, ibuprofen, and ramipril. He has smoked 1 pack of cigarettes daily for 45 years. He is 175 cm (5 ft 9 in) tall and weighs 68 kg (163 lb); BMI is 22 kg/m2. His temperature is 36.7°C (98°F), pulse is 60/min, and blood pressure is 115/76 mm Hg. While measuring the patient's blood pressure, the physician observes carpopedal spasm. Cardiopulmonary examination shows no abnormalities. His hematocrit is 41%, leukocyte count is 5,800/mm3, and platelet count is 195,000/mm3. Serum alkaline phosphatase activity is 55 U/L. An ECG shows sinus rhythm with a prolonged QT interval.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [175.0, 'cm']}",70.46466,66.94143,73.98789,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.89768 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (68.89768 (in inches) - 60) = 70.46466 kg.
Hence, the patient's IBW is 70.46466 kg."
4004,10,Ideal Body Weight,physical,decimal,pmc-3830326-1,Extracted,"A 15-year-old male presented with macromastia. He had delayed puberty.
Wt - 62.7 kg; Ht - 155 cm; Sexual Maturation Rate (SMR) - G1P1, testes - 3 ml, stretched penile length (SPL) - 5 cm.
LH - 6.3 IU/L, follicle-stimulating hormone (FSH) - 2.9 IU/L, prolactin (PRL) - 5.1 ng/ml, normal thyroid-stimulating hormone (TSH) and T4.
Testosterone (T) - 43.8 ng/dl and estradiol (E2) - 9.79 pg/ml. T/E2 = 4.4:1. He was prescribed letrozole 2.5 mg - 3 times/week.
After 6 months of AI therapy:
Wt - 68.8 kg; Ht - 158.5 cm; SMR - G3P3, testes 10 ml, SPL - 6 cm. There was insignificant change in breast enlargement.
T - 331.62 ng/dl; E2-8.05 pg/ml. T/E2 = 41.2.
There was 650% increase in T and 17.9% decrease in E2.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [158.5, 'cm']}",55.5237,52.74751,58.29989,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 158.5 cm, which is 158.5 cm * 0.393701 in/cm = 62.40161 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (62.40161 (in inches) - 60) = 55.5237 kg.
Hence, the patient's IBW is 55.5237 kg."
4005,10,Ideal Body Weight,physical,decimal,pmc-3965284-1,Extracted,"We present the case of a 23-year-old female who was diagnosed with GSD type Ia shortly after birth. She was hospitalized for the first time at the age of 6 months for hypoglycaemia and metabolic acidosis that occurred during a respiratory infection. She had a doll-like facial appearance, hepatomegaly and kidney enlargement. She had been repeatedly hospitalized for episodes of enormous hypoglycaemia during infancy and adolescence. The patient was treated out of hospital with frequent meals rich in carbohydrates during the day and every 2–3 h during the night and as a result she developed obesity. Besides nutritional therapy, she was also treated with allopurinol for hyperuricaemia. She came to our clinic at the age of 22 years for the diagnostic evaluation of arterial hypertension and dyslipidaemia. Her weight was initially 80 kg, height was 157 cm and BMI was 32.5. The levels of uric acid were 425 nmol/l, LDL 3 mmol/l, HDL 0.8 mmol/l, cholesterol 5.2 mmol/l and TG 2 mmol/l. Her in-office blood pressure measurement repeatedly showed raised values (160/90 mmHg in average). We carried out a 24-h ambulatory blood pressure monitoring, which revealed normal daily and average 24-h values of both systolic and diastolic pressure, but also the non-dipping pattern of systolic pressure during the night (a, b and c). The latter can be attributed to excessive nocturnal eating and consequently disturbed sleeping pattern.
The patient used to control glycaemia with self-measurements, mostly in preprandial periods, and results were recorded in a blood glucose diary. The self-measurements were made only during the daytime and revealed no abnormal excursions of glucose levels in either direction.
It has been shown previously that glucose levels obtained by continuous subcutaneous glucose monitoring (CGM) correspond to those obtained by venous blood sampling or self-measurements 
. To evaluate the actual prevalence of eventual hypoglycaemic episodes, we proposed CGM during a 72-h period.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [157.0, 'cm']}",49.66544,47.18217,52.14871,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 157.0 cm, which is 157.0 cm * 0.393701 in/cm = 61.81106 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.81106 (in inches) - 60) = 49.66544 kg.
Hence, the patient's IBW is 49.66544 kg."
4006,10,Ideal Body Weight,physical,decimal,pmc-2596111-1,Extracted,"The case was a 58 year old Caucasian Greek female (weight 78 kgr, height 162 cm) without a significant past occupational, medical and family history. She had 2 vaginal deliveries 30 and 28 years before. The patient had no history of smoke or alcohol use. The patient was presented with an asymptomatic mass in a chest x ray that was performed for a routine check up. A CT scan (Figure ) confirmed the presence of a mass at the right posterior mediastinum that was not accessible for FNA (fine needle aspiration) biopsy. She had no fever or secondary symptoms of malignancy. Abdominal and brain CT (Computerized Tomography) scan was negative. Barium swallow examination of the esophagus was negative for pathology. The patient was subjected to right posterolateral thoracotomy with radical excision of the mass. The lung was easily freed and the mass was completely excised encapsulated in a clear 'plan de cleavage'
Pathology examination of the specimen showed Castleman's disease.(hyaline vascular pattern). According to the patterns of the disease there was no need for additional treatment. The hyaline vascular subtype was characterized by multiple germinal centers surrounded by circumferential arranged layers (onion skin) of small lymphocytes interconnected by a prominent vascular stroma with occasional plasma cells.
Follow up of the patient for the last 8 years has showed that she is free of the disease.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [162.0, 'cm']}",54.19299,51.48334,56.90264,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 162.0 cm, which is 162.0 cm * 0.393701 in/cm = 63.77956 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (63.77956 (in inches) - 60) = 54.19299 kg.
Hence, the patient's IBW is 54.19299 kg."
4007,10,Ideal Body Weight,physical,decimal,pmc-7078131-1,Extracted,"A 40-year-old man was admitted to our department for glycemic control. He had a 6-year history of poorly controlled diabetes. He was of tall stature (height 188.4 cm, bodyweight 97.5 kg), and his testes were bilaterally small. We found decreased serum total testosterone (0.76 ng/mL), elevated gonadotropin (luteinizing hormone [LH] 27.8 mIU/mL, follicle-stimulating hormone 22.9 mIU/mL) and low human chorionic gonadotropin-stimulated total testosterone level (0.76 ng/mL). KS was suspected, and G-band karyotyping showed 47, XXY. Testosterone enanthate was initiated, and diabetes was well controlled with insulin degludec and dulaglutide.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [188.4, 'cm']}",82.59852,78.46859,86.72845,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 188.4 cm, which is 188.4 cm * 0.393701 in/cm = 74.17327 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (74.17327 (in inches) - 60) = 82.59852 kg.
Hence, the patient's IBW is 82.59852 kg."
4008,10,Ideal Body Weight,physical,decimal,pmc-4307179-1,Extracted,"A 70-year-old Caucasian man (weight: 75kg; height: 165cm) with T2DM, hypertension and prostatic hypertrophy was referred to our unit for CRC treatment. His usual medications included metformin (3000mg/day), irbesartan/hydrochlorothiazide 150mg/12.5mg/day and tamsulosin (0.4mg/day).
Ten weeks after receiving pre-operative chemoradiotherapy, the patient underwent a low anterior rectal resection with a diverting ileostomy. Metformin treatment was suspended 3 days before the operation.
The patient’s post-operative course was uneventful. His renal function was normal; his blood glucose was between 150mg/dl and 200mg/dl after a meal; and his stoma output was approximately 600ml/day.
Metformin therapy was resumed 5 days after surgery, when the patient returned to a normal diet. He was discharged to home in good condition on the ninth post-operative day.
Two weeks later, he returned to our department because of nausea, vomiting and diffuse abdominal pain. In the preceding days, he had noticed an increased stoma output that required him to empty the stoma bag four or five times per day. He also referred to being anuric for the preceding 24 hours.
During his examination, the patient appeared dehydrated and had tachypnea and a reduced level of consciousness. His blood pressure was 90/60mmHg, and his pulse rate was 90/min. His laboratory tests showed acute kidney injury (AKI) (creatinine, 8.94mg/dl; blood urea nitrogen, 324mg/dl) with severe lactic acidosis (pH, 6.99; partial pressure of carbon dioxide, 12mmHg; base excess, -26.9 mM).
Aggressive hydration with crystalloids and intravenous bicarbonate infusion was initiated. The patient’s internal jugular vein was cannulated, and he was promptly transferred to the hemodialysis unit. Hemodialysis was performed for 6 hours and repeated 12 hours later for 3 hours using bicarbonate-buffered dialysate. His chemical profile and clinical condition then improved dramatically. His acidosis resolved over the course of 24 hours; his spontaneous diuresis resumed after 48 hours; and his renal function recovered. The patient was discharged 8 days after admission with a serum creatinine level of 2.5mg/dl and a blood urea nitrogen concentration of 50mg/dl. His ileostomy was closed about 1 month later, and he did not experience any further similar episodes. At a follow-up examination almost 1 year later, he was well and disease-free.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [165.0, 'cm']}",61.40954,58.33906,64.48002,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.96067 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (64.96067 (in inches) - 60) = 61.40954 kg.
Hence, the patient's IBW is 61.40954 kg."
4009,10,Ideal Body Weight,physical,decimal,pmc-7784182-2,Extracted,"A 26-year-old married female presented with a chief complaint of menorrhagia for the last 3 months with intermittent abdominal pain for the last month. She had been bleeding heavily for the last 12 days, along with the passage of clots. Over the last 3 months, her cycle interval had increased from 45 to 60 days and bleeding had increased in duration and amount. Her menarche was at a normal age of 11 years followed by regular cycles until the last 3 months. There was history of weight gain and malaise for last 2-3 yrs. Her physical examination revealed weight 75 kg, height 156 cm and BMI 30.8. She had an apathetic expression. Her pulse was 64 bpm and BP 124/92 mm Hg. Her IQ was normal. She was pale with periorbital puffiness, dry skin and swelling over hands and feet and delayed reflexes. The thyroid gland was not enlarged and there was no galactorrhea. On abdominal examination, an abdominopelvic mass reaching upto the umbilicus was felt, which was cystic, non-tender and mobile. Her laboratory tests revealed mild anemia with a dimorphic picture on peripheral blood film. Ultrasound of the abdomen and pelvis showed bilateral enlarged multicystic ovaries. The uterus was normal with endometrial thickness of 6.4 mm. Her TSH 124.6 IU/L (0.2–4.6 IU/L), total T4=1.2 μg/dl (5–12.5 μg/dL), T3=12.5 ng/dL (60–180 ng/dL)]. Ultrasound of the thyroid showed small thyroid lobes with heterogenous coarsened echo pattern suggestive of chronic thyroiditis. Antithyroid peroxidase was positive 1300 U/ml (positive >50). Patient was started on 50 ug of thyroxine and gradually increased to 125 ug. The acute bleeding episode was controlled with oral progesterone and hemostatic drugs. She was started on oral iron supplemenation and calcium. By 6 weeks, both the ovarian cysts had resolved completely. At the 3rd month follow up, the patient was euthyroid with TSH level of 3.67 μIU/ml along with normal menstrual cycles and weighed 64 kg.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [156.0, 'cm']}",48.75993,46.32193,51.19793,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 156.0 cm, which is 156.0 cm * 0.393701 in/cm = 61.41736 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.41736 (in inches) - 60) = 48.75993 kg.
Hence, the patient's IBW is 48.75993 kg."
4010,10,Ideal Body Weight,physical,decimal,pmc-8614210-1,Extracted,"A 42-year-old woman reported to the outpatient department of National Institute of Ayurveda Jaipur on April 14, 2015, for complaints of tingling sensation in fingers of the right hand and around neck region, numbness in right upper limb, and right lower limb for few seconds. She had feeling of general fatigue, occasional headache and dizziness when she changed the position of her head. She experienced instant chest pain on the right side which was not related with any activities or time of the day.
The patient had been experiencing these complaints for 16 months. She had consulted rheumatology department of an allopathic hospital and a year ago before coming to Ayurveda hospital. Magnetic resonance imaging angiography indicated TA. An absence of arm pulse bilaterally was noticed during first pregnancy in year 2000 following which the blood pressure was monitored in the lower extremities. Transient cyanosis in hands was noticed during the first pregnancy just before delivery. In 2004, she had right thoracic herpes zoster which resolved completely. The patient had also suffered from longitudinal extensive transverse myelitis (LETM) in 2014 from which she completely recovered clinically. She was on prednisolone 60 mg for a day and mycophenolate mofetil 1000 mg twice a day since August 23, 2014 for TA but had stopped the treatment from last 3 months due to increased weight and abnormal liver profile. She was admitted in the inpatient department of Panchakarma department of National Institute of Ayurveda on April 14, 2015, for the administration of Panchakarma procedures.
On physical examination, patient was anxious, body weight was 79 kg, height was 155.7 cm and body temperature was 37.5°C. Patient had Vata Pitta pre dominance Prakriti with Madhyama Sara (medium strength), Madhyam Samhanana (medium built), Sama Pramana (proportionate body), Madhyama Satmya (medium homologation), Madhayam Satva (medium mental strength), Madhyam Vyayamshakti (medium capability to carry on physical activities), Madhyama Ahara Shakti (medium food intake capacity) and Uttama Jaranashakti (optimum digestive power).
On neurological examination, higher mental function-attention, memory, calculation abstract thought, spatial perception, visual and body perception, and speech were normal. On cranial nerve examination, Grade I nystagmus to left gaze was found. Visual acuity was normal. Slit-lamp examination of the eye and audiometric results were normal. On motor examination, bulk, tone, power and coordination of upper limbs and lower limbs were normal. Joint position sense and vibration sensation was normal.
On cardiovascular examination, pulse in both upper arms was absent. In the neck region, right carotid pulse was forceful and left carotid pulse was not palpable. Pulse in lower extremities was normal. No bruits on the carotid and renal artery were found. Blood pressure could not be measured from the upper limbs. BP was 120/76 mmHg measured from the lower limbs. Auscultation of the chest showed no heart murmur or crackles. Pulse of the right brachial and radial arteries was palpable but feeble. Pulse of the left brachial and radial arteries was not palpable. Pulse rate and respiratory rate was 60/min and 18/min, respectively. Skin, cardiorespiratory, musculoskeletal, and genitourinary system examination was normal.
A detail of the case study and follow-up is given in .
Patient was a known case of TA. CTA of the brain and neck revealed-severe stenosis (approx. 90%–95%) of right subclavian artery, complete block of left subclavian artery and proximal left vertebral artery with normal CTA of brain that is a suggestive of TA []. TA was graded as Type I, on the basis of angiographic findings and in group I, on the basis of Ishikawa clinical classification. These grading denoted the better prognosis of the case.
Atherosclerosis, giant cell arteritis, polyarteritis nodosa, infectious aortitis, secondary vasculitides and developmental abnormalities (coarctation of the aorta and marfan syndrome) are the differential diagnoses of TA. Atherosclerotic plaques are commonly found in patients aged 45 years and above and also not usually associated with long segment luminal stenosis. Giant cell arteritis mostly affects patients older than 50 years. Branches of the external and internal carotid arteries are most frequently affected in giant cell arteritis. Polyarteritis nodosa commonly affects 30–50 years old, predominantly males, renal arteries, gastrointestinal arteries as the primary sites diseased and multiple small aneurysms in the involved artery. Development abnormalities are not associated with stenotic lesions in large vessels. Varicella zoster virus (VZV) culture and deoxyribonucleic acid (VZV), serology triple and oligoclonal bands test were negative for the case so infectious aortitis (tuberculosis, syphilis, Staphylococcus aureus and Salmonella, treponema, cyto-megalo virus or herpes virus) is unlikely. Test for antinuclear antibody was negative and no lupus was found, so secondary vasculitides (systemic lupus erythmatosus and sarcoidosis) were ruled out. Antiaquaporin-4 (NMO-IGG) antibodies were seropositive as the patient was suffering from longitudinally extensive transverse myelitis (LETM) in past. Hence, TA was the diagnosis for the patient []. Any disease can be considered as Vata Vikara (diseases by Vata Dosha) if it have the symptoms of Shosha (atrophy/weight loss), Shoola (pain), Supti (paresthesia, tingling sensation), Sankocha (concentric wall thickening/contracture), Stambhana (stenosis/stiffness), and Khanjata (limping).[] All these symptoms remain present in TA, hence, it can be considered as Vata Vikara. More specifically, TA can be correlated with Siragata-Vata, a disease of Vata Vyadhi spectrum. Manda Sharira Ruja (mild body pain) Shopha (inflammation) and Shosha (atrophy/loss of weight), Spandana (fasciculation) in the body, Supta Sira (absence of pulsation in the blood vessels/arteries), Tanavyo Sira (spasm of vessels leading to reduction of lumen/thinning of vessels/stenosis) and Mahat Sira (dilatation of vessels/aneurysm) are the manifestation of the Siragata-Vata.[] Aneurysms, segmental narrowing, and variations in the calibre of arteries and stenosis/occlusions are the manifestation of vasculitis[] and these are also the manifestation of Siragata Vata. TA is also described as pulse less disease and having stenosis of the large vessels as cardinal feature. These symptoms are described as Supta Sira and Tanavyo Sira in Siragata-Vata disease. Hence, Siragata-Vata was considered as the Ayurvedic diagnosis for this case of TA.
There is no specific treatment advised for Siragata-Vata in classical texts. Hence, general line of treatment of Vata Vikara viz. Snehana (oleation), Swedana (sudation) Niruha Basti (enema mainly with decoction), Anuvasana Basti (enema with medicated oil), and Nasya Karma (nasal therapy) was adopted for the patient.[] According to Ayurveda, Siragata-Vata is a disease of Madhyama Roga Marga (disease pathway related to vascular system and other vital organs); hence, Basti Karma was also adopted for treatment. Castor oil in the dose of 20 ml with milk was given for first three consecutive nights for Koshtha Shuddhi (evacuation of the bowel). Shastikshali Pinda Swedana was done for 16 days starting from the 1st day. From 4th day, Erandamuladi Niruha Basti[] alternated with Anuvasana Basti of Ashwagandha Taila[] was given for 16 days. After the completion of Basti procedure, Shirovirechana (nasal therapy for purification), a form of Nasya Karma with Triphaladi Taila (oil) in a dose of 06 drops (0.4 ml)/nostril was done on alternate days for 7 days []. Ayurvedic oral medicines such as Yogaraja Guggulu-1 g (500mgx2tab), Shiva Gutika-500 mg, Dashamula Kvatha-40 ml, Narsinha Churna-3 g, Brihadvatachinamani Rasa 125 mg twice a day were prescribed to the patient []. These oral medicines except Brihadvatachinamani Rasa were prescribed up to 30 January 2016. Brihadvatachinamani Rasa was prescribed initially only for 1 month. Same Panchakarma procedure was repeated after 6 months from November 17, 2015 to December16, 2015. Chyavanaprasha Avaleha in the dose of 10 g with milk was advised twice a day after meals from February 2016 to June 2018.
Patient’s condition was assessed on Indian ITAS-2010, which is validated in Indian patients for disease activity of TA.[] Features of domains – systemic, abdomen, cardiovascular system, genitourinary, renal (systolic and diastolic hypertension), and nervous system are comprises in ITAS2010 and are scored if new or worse over the past 3 months. Weightage are given for diastolic hypertension, bruits, new pulse loss, pulse inequality, stroke, carotidynia and claudication. A maximum score of 51 is possible in this scoring and score of 4 or more is considered active. Score was 17 at the time of admission and it changed to 05 after completion of Panchakarma procedures []. After 1 month of treatment, BP was measurable from both upper limbs, but pulse in the left upper limb and left carotid artery was weak. Unequal BP in both upper limbs was noted. BP in the right hand was 120/76 mmHg and in the left hand was 110/68 mmHg. MRA which was done on June 25, 2015 showed that the TA was stable and there was no new lesion []. ITAS-2010 score was 03 after 06 months. MRA done on November 2015 and CT angiograph done on January 29, 2016 and July 1, 2016 revealed no new lesion for TA in the case [Figures and ]. ITAS-2010 score was 4 on June 13, 2018. Follow-up of the patient was scheduled annually since June 2018. The patient was assessed on June 21, 2019 and her condition was stable and there was no relapse of any manifestation at that time.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.7, 'cm']}",48.48828,46.06387,50.91269,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.7 cm, which is 155.7 cm * 0.393701 in/cm = 61.29925 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.29925 (in inches) - 60) = 48.48828 kg.
Hence, the patient's IBW is 48.48828 kg."
4011,10,Ideal Body Weight,physical,decimal,pmc-6849168-1,Extracted,"In August 2018, a 58-year-old man [height: 169 cm, body weight: 56 kg, and body mass index (BMI): 19.6 kg/m2] was admitted to our emergency department with upper abdominal pain, hyperglycaemia and metabolic acidosis. He had lived with type 2 diabetes for 16 years and had no history of any allergy, hypertension, hyperlipidaemia or renal diseases. Five months prior to admission, he initiated subcutaneous insulin administration (SIA) with the biphasic insulin analogue aspart after failure of sitagliptin and metformin therapies (HbA1c: 8.07% [65 mmol/mol]). Glycaemic control did not improve (HbA1c: 10.2% [88 mmol/mol]; total daily insulin dose was 20 UI), and aspart administration caused mild allergic symptoms. Aspart was then substituted by biphasic human insulin in which the total daily insulin dose increased up to 37 units. However, 5 months after the initiation of these regimens, he developed a pruritic wheal, especially distinct at the injection site (Fig. a). Pruritic wheals appeared within 10 min of injection and lasted over 24 h. The levels of fasting blood glucose and HbA1c deteriorated to 8.6 mmol/litre and 11.2% (99 mmol/mol), respectively. An allergy to insulin was then suspected. A skin prick test was carried out with different types of insulin [insulin aspart (NovoRapid®), recombinant human insulin (Actrapid® and Insulatard®), insulin glargine (Lantus Solostar®), and insulin lispro (Humalog®, Humalog mix®)] in which the test was positive for all of these types. Two days before admission, he stopped SIA because of an allergic reaction and was treated with anti-allergic drugs.
One day later, he experienced weakness and upper abdominal pain. On admission, clinical examination revealed a dehydrated patient with a heart rate (HR) of 130 beats/minute, a temperature of 37 °C and a systolic/diastolic blood pressure (BP) of 150/90 mmHg. He was tachypnoeic and dyspnoeic with a respiratory rate (RR) of 28 breaths/minute. He had hot and dry skin without pruritic wheals, isochoric pupils, and had no focal neurological deficit. He had normal breath sounds and a soft and non-tender abdomen. Electrocardiogram showed sinus tachycardia at a rate of 130 beats/minute. Echocardiography revealed normal chamber size and systolic function, without valvular lesions. Laboratory tests revealed high anion gap metabolic acidosis with an arterial blood pH of 6.984, bicarbonate of 2.5 mmol/litre and a serum anion gap (AG) of 26.4 mmol/litre. The arterial PO2 and PCO2 levels were 164.3 mmHg and 10.5 mmHg, respectively. Serum glucose was 20.79 mmol/litre, serum lactate was 1.5 mmol/litre, and urinary ketone was 11.44 mmol/litre. Serum potassium, sodium and chloride levels were 5.7 mmol/litre, 137.4 mmol/litre and 114.2 mmol/litre, respectively. Liver and renal function tests were normal, and there was a slightly elevated white blood cell count of 14.1 × 109/l. He was admitted to our emergency ICU with a diagnosis of severe DKA in a patient with type 2 diabetes with an insulin allergy. Intravenous (IV) fluids, bicarbonate and potassium replacement and intermittent haemodialysis (IHD) were initiated. During the first 12 h, he received an initial 1 litre IV bolus of normal saline (0.9% NaCl) in the first hour, followed by a rate of 250 mL/hour, with 26 mmol of potassium chloride added per litre of normal saline. He also received 500 mL of sodium bicarbonate 1.4% solution over 2 h and then repeated as needed. However, his tachypnoea (35 breaths/minute) and metabolic acidosis persisted (arterial blood pH of 7.192, bicarbonate of 4.0 mmol/litre, PO2 of 156.1 mmHg, PCO2 of 10.3 mmHg, AG of 24.69 mmol/litre), prompting the initiation of CVVHDF using the Prismaflex® system (Gambro Lundia AB, Sweden) at the following settings: blood flow, 160 mL/minute; replacement volume, 1200 mL/hour; and dialysate, 1200 mL/hour. After 24 h of fluid resuscitation (6500 mL), he was haemodynamically stable and had 3500 mL of urinary output. However, he developed a decreased level of consciousness, agitation, and fatigue of his respiratory muscles. He was intubated for airway protection and was mechanically ventilated for respiratory support. Furthermore, hypotension (HR and BP were 120 beats/minute and 80/40 mmHg, respectively) occurred after intubation. A bolus of normal saline (1000 mL) was provided, and norepinephrine was administered at a rate of 0.3 μg/kg/minute. Haemodynamic stability was recovered after 1 h, with a HR of 110 beats/minute, BP of 120/60 mmHg, and measured CVP value of 8 cmH2O. Arterial blood gases revealed a worsening metabolic acidosis with an arterial blood pH of 7.022, bicarbonate of 2.5 mmol/litre and a serum AG of 25.75 mmol/litre. Renal function declined with a serum creatinine level of 198 μmol/litre. Serum glucose, potassium, sodium and chloride levels were 23.32 mmol/litre, 4.35 mmol/litre, 140.5 mmol/litre and 116.6 mmol/litre, respectively. CVVHDF and IV fluids and potassium replacement were continued. Although haemodynamic and respiratory stabilities were maintained, metabolic acidosis persisted. Further skin prick testing with different types of insulin [insulin aspart (NovoRapid®), recombinant human insulin (Actrapid®, Insulatard®, Mixtard®, Humulin R®, and Humulin N®), and insulin glargine (Lantus®)] only showed positivity to two (aspart, human) of these types. However, the intradermal test with these types was positive (the time of testing as shown in Additional file ). A 40 mg dose of methylprednisolone sodium succinate and 10 mg of diphenhydramine were given in the event of the possible occurrence of a severe allergic reaction, and continuous IV infusion of recombinant human insulin was initiated at a rate of 0.1 units/kg/hour. Approximately 60 min after continuous IV infusion of insulin, he developed hypotension without any signs or symptoms of allergic reactions of the skin and mucosa, and the HR was 115 beats/minute and BP was 80/40 mmHg. Infusion of insulin was temporarily stopped followed by intravenous epinephrine administration at a starting rate of 0.15 μg/kg/minute in addition to an IV bolus of 1000 mL of normal saline. He regained haemodynamic stability after 30 min, including a HR of 110 beats/minute and a BP of 120/70 mmHg, and did not require any additional administration of epinephrine after 5 h. Continuous IV infusion of recombinant human insulin at a rate of 0.1 units/kg/hour continued without any events such as signs or symptoms of allergic reactions and hypotension.
On day 5 of follow-up, ketonaemia, metabolic acidosis (arterial blood pH of 7.465, bicarbonate of 18.4 mmol/litre and AG of 12.73 mmol/litre), and renal dysfunction (serum creatinine of 108 μmol/litre) had almost resolved, and CVVHDF was withdrawn. He did not require vasoconstrictors. Continuous IV infusion of recombinant human insulin continued and was adjusted according to blood glucose levels measured with a portable blood glucose meter. He was extubated on day 7 and transitioned from continuous IV insulin infusion to subcutaneous insulin (combined regular human insulin with insulin glargine) administration on day 14. He was discharged on day 21 with SIA (combined regular human insulin with insulin glargine) in combination with an oral antidiabetic drug (sitagliptin and metformin). Three months later, glycaemic control was gradually restored (HbA1c: 8.3% [67 mmol/mol]; total daily insulin dose was up to 44 UI); he still appeared to have mild allergic symptoms, such as local erythaema and swelling, especially distinct at the injection site of insulin glargine (Fig. b).","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [169.0, 'cm']}",65.03158,61.78,68.28316,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 169.0 cm, which is 169.0 cm * 0.393701 in/cm = 66.53547 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (66.53547 (in inches) - 60) = 65.03158 kg.
Hence, the patient's IBW is 65.03158 kg."
4012,10,Ideal Body Weight,physical,decimal,pmc-4697967-1,Extracted,"A 43-year-old man was referred in March 2008 with an 8-month history of progressive headache, loss of peripheral vision, and hyposexuality. He did not have polyuria, polydipsia, or any symptoms of hypercortisolism, hypermetabolism, or acromegaly. He was 1.66 m tall and weighed 76 kg (body mass index [BMI] of 27.6 kg/m2). Endocrine investigations were suggestive of hypotestosteronism, but plasma cortisol, prolactin, growth hormone, and thyroid hormone concentrations were normal (Table ). Computed tomography (CT) showed enlargement of the sella turcica containing a well-defined 15 × 15 × 21-mm mass compressing the optic chiasm, infiltrating the right side of the cavernous sinus and extending around the right internal carotid artery (Figure A). The patient underwent transsphenoidal surgery, and the mass was partially resected. Conventional histopathological examination of the excised tissue showed tumor cells consistent with a pituitary chromophobic adenoma (Figure A-C), and stained negative for ACTH (Figure B) and other pituitary hormones (growth hormone, prolactin, luteinizing hormone, follicle stimulating hormone, and thyroid-stimulating hormone). The Ki-67 proliferative index was 3% (Figure C). Postoperative endocrine studies reported blood concentrations of total triiodothyronine of 0.84 nmol/L (normal range 1.18–2.23 nmol/L), total thyroxine of 70.22 nmol/L (normal range 57.92–154.44 nmol/L), thyroid-stimulating hormone of 0.292 μIU/mL (normal range 0.47–4.64 μIU/mL), and cortisol of 580.46 ng/mL (normal range 30.0–230.0 ng/mL). The latter was higher than the physiological upper limit, which was considered to be the result of surgical trauma and stress, and hydrocortisone therapy. Replacement therapy with prednisone 7.5 mg once daily and levothyroxine 50 μg once daily was begun postoperatively. Postoperative endocrine studies 3 months later found that the serum cortisol concentration was 5.60 μg/dL (normal range 5.0–25.0 μg/dL) at 8 am, the dose of prednisone decreased to 5 mg qd.
Six months later, in September 2008, the patient presented with a 2-month history of headaches and progressive visual impairment. Follow-up magnetic resonance imaging showed substantial growth of the residual tumor into a mass measuring 25 × 15 × 20 mm. Although the patient reported no symptoms of hypercortisolism, preoperative endocrine studies revealed hypothyroidism, hypercortisolemia, and hypotestosteronism (Table ). The levothyroxine dose was increased to 100 μg once daily, prednisone was maintained 5 mg once daily. A second transsphenoidal partial excision of the tumor was performed, and histopathologic analysis of the tissue revealed megakaryocytes and sporadic ACTH-positive cells with a Ki-67 proliferative index of 1.5%. There was no immunohistochemical evidence of other pituitary hormones, suggestive of a pituitary adenoma.
In June 2009 (15 months after the first surgery), the patient presented again with a 2-month history of headache and blurred vision. Imaging suggested a further recurrence of the adenoma. After the second partial resection, the patient checked his plasma cortisol regularly, and the prednisone dose was adjusted according to the cortisol levels and electrolyte concentration. And the prednisone dose was maintained 5 mg once daily. Preoperative endocrine testing suggested persistent central hypothyroidism, and the levothyroxine replacement dose was increased to 125 μg once daily (Table ). The size and location of the tumor necessitated a subfrontal craniotomy, during which a nearly complete resection of the 15 × 15 × 20 mm tumor was achieved. Postoperative histopathologic examination yielded evidence of an actively growing pituitary adenoma, with a Ki-67 proliferative index of 1.5%. There was no evidence of staining for any of the adenohypophyseal hormones.
The number and frequency of recurrences called into question the benign nature of the tumor. Three months following the craniotomy, Gamma Knife radiotherapy was administered at a peripheral dose of 14 Gy, equating to a central dose of 31 Gy.
In December 2011, the patient developed bilateral hip pain and was diagnosed with femoral head necrosis, for which he was treated with traditional Chinese medicine. Endocrine investigations showed the level of plasma cortisol was 39.40 μg/L (normal range 67–226 μg/L) at 8 am, and the prednisone dose was decreased 2.5 mg once daily. In January 2013, he developed repeated episodes of lower limb edema, facial edema, and chemosis, and developed a round face, but did not seek treatment. In May 2013, the patient was admitted to his local hospital with an intracranial pyogenic infection. At that time he was noted to have hypocortisolemia and loss of circadian rhythms. The infection resolved with treatment, and the patient was advised to discontinue prednisone.
In October 2014, the patient complained of worsening and repeated lower limb edema, facial edema, and chemosis. He was noted to have rapidly developed cushingoid facies, a buffalo hump, supraclavicular fat pads, central obesity, hypertension, hypokalemia, and osteoporosis. His BMI had increased substantially to 32.3 kg/m2. It was at this stage that the patient was referred to our hospital and came under our care. Further endocrine testing found elevated concentrations of ACTH and cortisol with loss of circadian rhythms, and substantially elevated 24-hour urinary-free cortisol (Table ). A high-dose (8 mg) dexamethasone suppression test only slightly decreased serum cortisol concentration, from 2441.6 μg/24 h to 1524.64 μg/24 h. An overnight low-dose (1 mg) dexamethasone suppression test resulted in more than 50% suppression of cortisol concentration, which fell from 2441.6 μg/24 h to 780.08 μg/24 h. These equivocal results prompted a decision to perform inferior petrosal sinus sampling (IPSS) with administration of desmopressin acetate (DDAVP). The right inferior petrosal venous ACTH concentration increased following intravenous DDAVP administration, with a more than 3-fold increase in the ratio of the right inferior petrosal to peripheral concentration (Table ). CT of the adrenals showed bilateral hyperplasia (Figure A), and a head CT scan revealed a space-occupying lesion in the sellar region, suggesting another recurrence of the pituitary adenoma (Figure B). Together, these findings provided unequivocal evidence of CD.
The patient was transferred to the neurosurgery department for another transsphenoidal resection of the pituitary adenoma. The histopathological examination was consistent with a pituitary adenoma (Figure D-F), but immunohistochemical staining for ACTH was positive (Figure E), and the Ki-67 proliferative index was 2% (Figure F). The postoperative course was uneventful, and the patient's fatigue and edema resolved. The concentrations of cortisol and ACTH remained elevated, with loss of circadian rhythms 7 days after surgery. Postoperative endocrine studies 3 months later found that the serum cortisol concentration was 90.0 ng/mL at 8 am, 58.2 ng/mL at 4 pm, and 75.1 ng/mL at midnight (normal range 50–250 ng/mL). The serum ACTH concentration was 124 pg/mL at 8 am, 102 pg/mL at 4 pm, and 109 pg/mL at midnight (normal range 0–46 pg/mL), and that the 24-hour urine-free cortisol remained elevated. A repeat abdominal CT scan showed that both adrenal glands were markedly smaller, close to the normal size (Figure B). Gamma Knife radiotherapy was recommended to control tumor growth and hypersecretion of ACTH.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [1.66, 'm']}",62.31505,59.1993,65.4308,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 1.66 m, which is 1.66 m * 39.3701 in/m = 65.35437 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.35437 (in inches) - 60) = 62.31505 kg.
Hence, the patient's IBW is 62.31505 kg."
4013,10,Ideal Body Weight,physical,decimal,pmc-6967287-1,Extracted,"A 60-year-old woman (height 154 cm, weight 35 kg) was transported to our hospital by ambulance with chest pain and dyspnea. After evaluation, she was diagnosed with left pneumothorax (Fig. ). She had a history of muscular dystrophy, dilated cardiomyopathy, and atrial fibrillation. She had been receiving ASV therapy for 2 years because of type 2 respiratory failure. Before admission, she was classified as Hugh-Jones level 5 with the oxygen flow rate, IPAP, and EPAP set to 1 L/min, 7–16 cm H2O, and 4 cm H2O, respectively. Prehospital respiratory function test and transthoracic echocardiography results are presented in Table . Despite chest tube drainage and pleurodesis, the air leak persisted. Thus, VATS bullectomy was scheduled. It was thought that the operation would not take much time because of the substernal location of the bulla suspected as the cause of the pneumothorax. Moreover, she had severe respiratory dysfunction and refused tracheal intubation due to the risk of tracheal intubation, and she also considered that initiation of mechanical ventilation would make it difficult to wean from mechanical ventilation. Therefore, VATS without tracheal intubation was chosen.
Standard monitoring included electrocardiogram, arterial blood pressure, and pulse oximetry. She was kept on ASV performed with a full face mask in the operating room. The settings were oxygen flow rate, 4 L/min; IPAP, 7–16 cm H2O; and EPAP, 4 cm H2O. After peripheral arterial cannulation, an epidural catheter was placed at the thoracic 5–6 level, and 3 ml of 0.5% ropivacaine were injected through the epidural catheter following 2 ml of 1% mepivacaine as a test dose. Then, an infusion of 1 μg/kg/h dexmedetomidine was started. Before she was turned to the right lateral position, it was confirmed that the extent of epidural anesthesia was from thoracic 2 to 8. Local anesthesia was not performed. A 5-cm skin incision was made in the third intercostal space. When surgical pneumothorax was created by incision of the pleura, her respiratory status remained stable. In addition, lung collapse was obtained with ease at operation while she was on ASV, a form of NPPV. In the middle of the operation, the dosage of dexmedetomidine was reduced to 0.6 μg/kg/h to maintain the Richmond Agitation-Sedation Scale around − 2. The leaking bulla was easily identified, and bullectomy was performed. After a negative air leak test, a chest tube was inserted. The operation time was 56 min, and the anesthesia time was 116 min. During surgery, although her arterial blood gas analysis showed respiratory acidosis (Table ), oxygen saturation was maintained higher than 90%. In addition, she continued spontaneous breathing and did not complain of pain or discomfort. She was transferred to the intensive care unit (ICU) with ASV. The chest tube was removed on postoperative day (POD) 1, and she was transferred out of the ICU on POD 2. She was discharged on POD 12 with no respiratory complications.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [154.0, 'cm']}",46.94889,44.60145,49.29633,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 154.0 cm, which is 154.0 cm * 0.393701 in/cm = 60.62995 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (60.62995 (in inches) - 60) = 46.94889 kg.
Hence, the patient's IBW is 46.94889 kg."
4014,10,Ideal Body Weight,physical,decimal,pmc-6865051-1,Extracted,"A 71-year-old woman was evaluated in the Internal Medicine Department for a 15 kg-weight loss during the preceding 14 months and a 20-day history of watery diarrhea. Laboratory studies, including blood tests and urinalysis, carried out a few days before presentation were normal. Moreover, computed tomography (CT) of the abdomen as well as upper and lower gastrointestinal endoscopy performed seven months and one year before presentation, respectively were unremarkable. The patient had a medical history of hypertension for the last 5 years and depression since the age of 25.
Her medication included olmesartan 40 mg and amlodipine 5 mg which were stable for the past 5 years, whereas there was a recent modification in her antidepressant medication (venlafaxine 75 mg was replaced by amitriptyline 50 mg, duloxetine 40 mg and clorazepate 15 mg) about 15 days before presentation. However, there was no change in her symptoms with this treatment modification. She denied using tobacco, alcohol or illicit drugs. Her father died at 67 from lung cancer and her sister at 47 from breast cancer; the rest family history was insignificant.
At presentation the temperature was 36°C, the blood pressure was 143/82 mmHg, the heart rate was 69 beats per minute, the respiratory rate was 16 breaths per minute and the oxygen saturation was 98%, while the patient was breathing ambient air. Her height was 1.60 m and her weight was 43 kg (body mass index 17 kg/m2). Bilateral pitting edema was detected on her lower extremities, while the remainder physical findings were unremarkable. The electrocardiogram was normal. Laboratory (Table ) and imaging studies were obtained.
The laboratory exams were significant for International Normalized Ratio (INR) prolongation, which was corrected with vitamin K administration, hypoalbuminemia without albuminuria and hypokalemia. Stool was negative for clostridium difficile, parasites or other enteropathogens. Chest radiograph and CT of brain, chest and abdomen were normal. The remainder thorough investigation for underlying infections, endocrinopathies, immunological diseases and malignancy was negative. Upper endoscopy demonstrated an edematous, reddish duodenal mucosa with reduced mucosal folds. Duodenal biopsies demonstrated the increased presence of inflammatory cells and crypt cell proliferation with substantial villous atrophy. Lower endoscopy was insignificant. Tissue transglutaminase antibodies (IgA) and deaminated gliadin peptide antibodies (IgA and IgG) were negative, while a gluten-free diet was found to be ineffective.
Taking into account the aforementioned examinations and by excluding almost with certainty celiac disease and neoplasia, we considered the possibility of olmesartan-induced enteropathy and discontinued olmesartan. Ten days after drug removal diarrhea resolved completely. Few months later, complete recovery of weight was observed along with normalization of laboratory tests (Table ). The patient denied a new upper endoscopy to confirm resolution of the lesions. As all symptoms disappeared and the patient returned to her usual condition after olmesartan withdrawal, we decided not to re-introduce the drug; in fact, we substituted olmesartan with a blood pressure lowering drug from another class.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [1.6, 'm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 1.6 m, which is 1.6 m * 39.3701 in/m = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
4015,10,Ideal Body Weight,physical,decimal,pmc-4370314-1,Extracted,"A 65-year-old Japanese man was diagnosed with HIV infection in October 2005. There were no comorbidities, including hypertension, diabetes mellitus and dyslipidemia. cART, comprising lamivudine, abacavir and atazanavir/ritonavir (300 mg of atazanavir boosted by 100 mg of ritonavir), was started to treat his low CD4+ T-cell count (205 cells/μL) and high HIV-RNA (230 000 copies/mL) in June 2006. Soon after the initiation of cART, both proteinuria and hematuria emerged (1+ and 1+ on dipstick test, respectively) and his renal function started to decline slowly, yet there were no crystalline precipitates in the urine. Serum creatinine (Cr) increased from 0.6 to 1.0 mg/dL in June 2009, and to 1.4 mg/dL in February 2012, with persistent proteinuria (1+) and occult hematuria (2+) on a dipstick test. As serum Cr increased to 1.7 mg/dL, he was admitted to the Department of Nephrology in April 2012. The cART regimen remained unchanged, since the control of HIV infection was good at the time.
On admission, his blood pressure was 102/78 mmHg and pulse rate 98 beats per minute. His height was 154 cm and his weight was 35.4 kg (body mass index, 14.9 kg/m2). There were no particular abnormalities on physical examination. The blood data were as follows: white blood cell count 6400/μL; red blood cell count 387 × 104/μL; hemoglobin 12.5 g/dL; platelet count 27.0 × 104/μL; serum urea nitrogen 21 mg/dL; serum Cr 1.7 mg/dL; serum sodium 139 mEq/L; serum potassium 4.5 mEq/L; serum chloride 103 mEq/L and serum C-reactive protein 0.49 mg/dL. Urine dipstick test showed pH 6.0, proteinuria (1+), and occult blood (3+). The urinary concentrations of biomarkers for tubular damage, which was corrected for urinary Cr concentrations, were as follows: N-acetyl-β-d-glucosaminidase (NAG), 12.0 IU/gCr (normal level of NAG concentration, 0.0–7.0 IU/L) and β2M, 391 μg/gCr (normal level of β2M concentration, 27–265 μg/L), respectively. The daily amount of urinary protein was 250 mg. Urinary sediments included 50–99 red blood cells/high power field (HPF), 20–29 white blood cells/HPF and small amounts of crystalline precipitation (no detail for its shape). Infrared spectroscopic analysis was implemented to test whether the urinary crystalline precipitation included atazanavir crystals. In brief, the patient's urine was stored for 24 h, and some of the urine was centrifuged for 2 min at 2000 rpm. The supernatant was used for infrared spectroscopic analysis, and the spectrum of the infrared absorbance was compared with that of the standard for atazanavir analysis (Santa Cruz Biotechnology, Inc., Dallas, TX, USA). This analysis strongly indicated that the urinary crystalline precipitation of the patient included atazanavir crystals (Figure ). The first renal biopsy was performed in May 2012. The kidney tissue contained eight glomeruli, one of which (12.5%) was globally sclerotic. The remaining glomeruli showed no convincing histological changes indicating renal failure. In contrast, interstitial nephritis, accompanied by diffuse inflammatory infiltrates consisting of lymphocytes and plasma cells, was noted (Figure A). Moreover, needle-shaped crystalline precipitation, likely in the epithelia of the tubule, surrounded by multinuclear giant cells, was very characteristic (Figure B). Immunohistochemistry was negative. Electron microscopy showed no electron-dense deposits in the glomeruli; however, crystalline precipitation was confirmed within the tubular epithelial cells (Figure C). In June 2012, atazanavir was replaced by raltegravir, but renal function did not improve. From November 2012, 6 months after the first renal biopsy, oral prednisolone was started at the initial dose of 0.75 mg/kg daily for 4 weeks, and was slowly decreased in the subsequent 5 months. However, serum Cr remained constant at 1.5 mg/dL. In August 2013 (1 year and 3 months after the first renal biopsy), a second renal biopsy contained 28 glomeruli, 5 of which (17.9%) were globally sclerotic. The remaining 23 glomeruli had unremarkable changes. Needle-shaped crystals surrounded by lymphocytes and multinuclear giant cells in the tubulointerstitial compartment were completely removed. Sclerotic findings of glomeruli and intrarenal arterioles including interlobular arteries were more prominent than those observed in the first renal biopsy. Additionally, tubular atrophy and interstitial-fibrosis developed further, although the severe interstitial inflammation was almost cured (Figure D). Immunohistochemistry and electron microscopy showed no characteristic findings.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [154.0, 'cm']}",51.44889,48.87645,54.02133,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 154.0 cm, which is 154.0 cm * 0.393701 in/cm = 60.62995 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (60.62995 (in inches) - 60) = 51.44889 kg.
Hence, the patient's IBW is 51.44889 kg."
4016,10,Ideal Body Weight,physical,decimal,pmc-7780453-1,Extracted,"A 36-year-old man (weight 81 kg, height 180 cm) symptomatic for fatigue and dyspnoea on mild exertion (New York Heart Association Class III) with past medical history of two aortic valve replacements (AVR) was referred to our institution because of a relapse of Staphylococcus warneri prosthetic valve endocarditis (PVE). He underwent the first AVR 2 years earlier for a steno-insufficient bicuspid aortic valve. After 8 months a redo AVR with annular reconstruction was needed due to PVE; S. warneri was isolated from the explanted valve. At time of referral the patient had completed the antibiotic therapy, the blood cultures were negative and the laboratory findings were within normal ranges. No risk factors for recurrent infections were identified. On physical examination, the main finding was a holodiastolic murmur over the aortic valve area. The transthoracic echocardiogram showed a peri-prosthetic leak that determined a severe aortic insufficiency, good left ventricle’s (LV) contractility, and ejection fraction (EF = 60%). The transoesophageal echocardiography (TOE) and electrocardiogram (ECG)-gated computed tomography scan demonstrated a pseudoaneurysm at the level of the LV outflow tract (LVOT) extending towards the mitro-aortic intervalvular fibrosa (Video 1). Pre-operative coronary angiography (CA) showed normal coronary arteries ().
A modified-Bentall technique with a composite mechanical valve conduit (St. Jude Medical Masters HP valved graft with Gelweave Valsalva conduit) was carried out. After transecting the ascending aorta, two buttons of aortic wall including the coronary ostia were isolated and mobilized. By implanting the valved conduit, the pseudoaneurysm was excluded and the LVOT was reconstructed. Then, the ostia were sutured to two corresponding openings in the Dacron graft with a continuous suture of 6-0 Prolene without using any foreign material and without the addition of glue. By using the Valsalva graft, tension-free anastomoses of the buttons were expected. No macroscopic technical problems were encountered.
At the time of weaning off cardiopulmonary bypass (CPB) the LV showed signs of failure. Intraoperative TOE evaluation in the transgastric short-axis view revealed a marked hypokinesis of the entire anterolateral wall and septum from the basal segments to the apex. Transoesophageal echocardiography findings in addition to the concomitant anterolateral ST-segment elevation on the 12-lead ECG suggested an acute impairment in blood supply thorough the proximal left coronary system. The origin of both coronary arteries was identified on TOE; kinking was excluded and Doppler evaluation showed the presence of blood flow through the ostia. The haemodynamic instability and difficulty in CPB weaning prompted an early strategy to re-establish coronary perfusion to the left coronary system. Surgical revascularization was performed with a saphenous vein graft anastomosed to the mid-left anterior descending (LAD) artery and reimplanted on the aortic Dacron conduit. The second attempt of weaning from CPB was successful with normal ECG tracing and good whole myocardial contractility. The patient was admitted to the intensive care unit with stable haemodynamic. A control CA was performed after 48 h. The angiography showed a significant stenosis of the left main stem (LMS) due to a recently developed lesion consistent with haematoma of the coronary wall. The saphenous vein graft to mid-LAD anastomosis was patent and effectively supported the coronary flow downstream the lesion (). No percutaneous coronary interventions (PCI) were performed for the lesion. Hospital monitoring, medical treatment (aspirin 100 mg/day and warfarin with a target international normalized ratio range 2.0–3.0 due to the mechanical aortic valve), and angiographic follow-up were planned.
The post-operative course was further complicated by hospital-acquired pneumonia successfully treated with IV antibiotics. The patient presented neither symptoms nor signs of angina and was discharged home on Day 28. At discharge the echocardiogram showed a good functioning prosthesis, mildly decreased LVEF (56%). The control CA was repeated after 6 months. It clearly revealed the resolution of the haematoma, a recovered LMS and LAD artery, while the vein graft was occluded (). The patient has been followed at outpatient clinic uneventfully for 1 year.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [180.0, 'cm']}",74.99221,71.2426,78.74182,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 180.0 cm, which is 180.0 cm * 0.393701 in/cm = 70.86618 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (70.86618 (in inches) - 60) = 74.99221 kg.
Hence, the patient's IBW is 74.99221 kg."
4017,10,Ideal Body Weight,physical,decimal,pmc-8044273-1,Extracted,"The patient was a 57-year-old woman (height, 155 cm; weight, 36.1 kg; body mass index, 15.0) with biopsy-proven adenocarcinoma of the transverse colon, referred to our department for treatment. She was not in distress (performance status, 0; American Society of Anesthesiologists score, 1). Her past medical history included psoriasis and urolithiasis. Family history, lifestyle, and medication use were non-contributory.
Preoperative blood tests revealed the following: white blood cells (WBC), 6720 cells/μl; hemoglobin, 13.9 g/dl; platelet count, 212 × 103 cells/μl; C-reactive protein, 0.01 mg/dl; albumin, 4.2 g/dl; carcinoembryonic antigen (CEA), 2.5 ng/ml; and Carbohydrate antigen19-9(CA19-9), 18.7 U/ml. Tests assessing physiologic functions were not abnormal. Lower gastrointestinal endoscopy exposed a 30-mm lesion of transverse colon that likely invaded submucosa (Paris Classification, 0-Is + IIc). Computed tomography (CT) imaging also disclosed mural thickening and contrast effect at mid-transverse colon, but there were no signs of metastasis. Based on the Japanese Classification of Colorectal, Appendiceal, and Anal Carcinoma (9th edition), the preoperative diagnosis was Stage I (cT1b, N0, M0) cancer of transverse colon. We then chose the Senhance system for transverse colon resection.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [155.0, 'cm']}",47.85442,45.4617,50.24714,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.02366 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.02366 (in inches) - 60) = 47.85442 kg.
Hence, the patient's IBW is 47.85442 kg."
4018,10,Ideal Body Weight,physical,decimal,pmc-8557451-1,Extracted,"A 65-year-old Caucasian female (height, 156 cm; weight, 123 kg; body mass index [BMI], 50.5) presented for elective laparoscopic cholecystectomy for recurrent biliary colic. There were almost 2 years between her initial ambulatory evaluation and the index operation, prolonged by the COVID-19 pandemic.
Apart from severe obesity, her medical history included obstructive sleep apnea (with home continuous positive airway pressure therapy, CPAP), type 2 diabetes, hypertension, dyslipidemia and reflux. She had no prior history of abdominal surgeries, smoking or alcohol. Pre-operative stress test, almost 4 years prior, was normal. Family history was non-contributory.
On the day of the operation, pre-operative vital signs were as follows: blood pressure, 145/82; heart rate, 86; SpO2, 96% on room air. The patient received general anesthetic per standard protocol. In preparation for Veress needle insufflation, a small skin incision was made at Palmer’s point, below the costal margin in the left upper quadrant. The needle was inserted deeply at 90°, with no flash of gas or blood. Saline drop did drip through. CO2 insufflation was initiated at 2 L/min, and pressures were noted to be higher than expected. Almost immediately, SpO2 dropped from 97% to 67%. Insufflation tubing was detached, and the Veress needle was removed. Oxygen saturations remained low, mean arterial pressure dropped to <50, end title CO2 (ETCO2) dropped to 8. Cardiac monitoring showed sinus tachycardia with ST segment elevation. Epinephrine was required for cardiac support.
Initial differential diagnosis included possible Veress misplacement into the thoracic cavity, resulting in pneumothorax. However, immediate decompression of the left chest cavity with a 14-gauge catheter, followed by finger thoracostomy and chest tube placement, did not demonstrate any gas or blood. Cardiac anesthesia performed transesophageal echocardiogram (TEE), and copious gas was seen in the right atrium and ventricle, associated right ventricular dysfunction, and estimated low cardiac output. A right intrajugular catheter was inserted, but unable to aspirate any gas. In the subsequent 20 min, with ongoing bag-ventilation, saturations improved to 97%. Epinephrine was weaned and ST elevation resolved. Repeat TEE showed dissolution of gas in cardiac chambers, normalization of biventricular function, no pericardial effusion and no clot.
The planned cholecystectomy was not re-attempted, and the patient remained intubated. She underwent emergent infused CT chest and abdomen to rule out other injuries (). It showed severe fatty infiltration of the liver, with tracking of gas into the liver parenchyma. No other abnormalities were noted. It was evident that the needle had entered the liver, leading to a gas embolus. Uninfused CT brain and CT angiography later that day were unremarkable with no evidence of infarction and no abnormalities noted within cranial circulation.
The patient was extubated on post-operative day (POD) 1. On awakening, she had left arm paresis. She was unable to flex her left shoulder or elbow but did have a weak grip strength. Right arm, and bilateral leg had preserved motor function. By the end of the day POD 1, she was able to hold both arms overhead, but still had left sided weakness and poor coordination. By POD 2, she was noted to have full range of motion, still with slight weakness on left. MRI Brain on POD 3 showed ‘subtle diffusion restriction of the cortex of the right precentral gyrus consistent with right MCA acute non-hemorrhagic infarction.’ A formal transthoracic echocardiogram confirmed a patent foramen ovale.
Full arm strength returned by POD 3. The patient continued to improve and was discharged on POD 5. Written consent was completed by the patient for publication of her case.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [156.0, 'cm']}",48.75993,46.32193,51.19793,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 156.0 cm, which is 156.0 cm * 0.393701 in/cm = 61.41736 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (61.41736 (in inches) - 60) = 48.75993 kg.
Hence, the patient's IBW is 48.75993 kg."
4019,10,Ideal Body Weight,physical,decimal,pmc-4166389-2,Extracted,"A 50-year-old man (height, 167 cm; weight, 65 kg) was diagnosed with esophageal achalasia due to swallowing difficulty for several years. He was scheduled for peroral endoscopic myotomy (POEM), which is a technique that was developed in the context of transesophageal NOTES as an endoscopic alternative to laparoscopic esophageal myotomy. The patient had no relevant medical history, and preoperative examination did not reveal any specific conditions. He was premedicated using 1 mg of butorphanol and 0.2 mg of glycopyrrolate intramuscularly before surgery.
In the operating room, routine monitoring was conducted using ECG (lead II), pulse oximetry, ETCO2 measurements and noninvasive BP monitoring. The patient's vital signs were as follows: BP, 110/69 mmHg; heart rate (HR), 65 beats/min; and peripheral oxygen saturation (SpO2), 100%. General anesthesia was induced using 120 mg of propofol, 50 mg of rocuronium, and 100 µg of fentanyl, and nasotracheal intubation was performed using a nasal RAETM tracheal tube with a 7.5 mm ID. For the same reason as in case 1, tracheal intubation was performed through the nose. Anesthesia was maintained using O2 at 2 L/min, N2O at 2 L/min, and 1.5-2.5 vol% of sevoflurane. Volume controlled ventilation was performed using a tidal volume of 600 ml and at a rate of 10 breaths/min.
The patient was placed in the left lateral decubitus position, and the endoscopic operator stood on the left side of the patient. CO2 gas was provided for insufflation during the procedure, using a CO2 insufflator and a standard insufflating tube. Endoscopic CO2 insufflation was controlled with a gas feed of 1.2 L/min. The operation comprised the following steps: (1) creation of the mucosal entry and submucosal tunnel, (2) endoscopic myotomy, and (3) closure of the mucosal entry. First, the endoscopic operator administrated a submucosal injection (0.9% normal saline with indigo carmine dye) at the level of the midesophagus in order to ensure a safe mucosal incision. The mucosal incision was then made on the mucosal surface using an electric knife, and the endoscope was inserted into the submucosal space. The submucosal tunnel was then extended 2 cm below the gastroesophageal junction via the endoscopic submucosal dissection technique. Next, the endoscope was withdrawn to the mucosal incision and a circular muscle myotomy was performed. After completion of the myotomy, the mucosal entry site was closed using several hemostatic clips.
For this patient in particular, the surgical duration was relatively long as the achalasia lesion was large.
During surgery, ETCO2 was maintained at 30-34 mmHg and PIP at 13-15 mmHg. The patient's abdomen was not covered using surgical drapes to ensure visibility so that severe pneumoperitoneum could be recognized immediately (). The patient was hemodynamically stable throughout the entire surgery. The time required for the operation and anesthesia were 120 min and 160 min, respectively. The patient was transferred to the general ward after surgery, and a postoperative chest radiograph showed no pneumomediastinum.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Male', 'height': [167.0, 'cm']}",63.22056,60.05953,66.38159,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Male.
The patient's height is 167.0 cm, which is 167.0 cm * 0.393701 in/cm = 65.74807 in. 
Plugging in the values for the IBW formula for males gives us 50 kg + 2.3 kg * (65.74807 (in inches) - 60) = 63.22056 kg.
Hence, the patient's IBW is 63.22056 kg."
4020,10,Ideal Body Weight,physical,decimal,pmc-3348632-2,Extracted,"A 36-year-old woman with a past history of allergic rhinitis came to our outpatient clinic because of polyarthralgia and swelling of her fingers. Ten days prior to her visit, she had a low grade fever () when her 9-year-old son was diagnosed as having erythema infectiosum because of his slapped cheek rash. Seven days later, she developed a butterfly-shaped erythema transiently on her face that disappeared the next day. Then, she developed swelling of her fingers and joint pain in her shoulders, ankles, and knees. Since oral administration of acetaminophen did not relieve her symptoms, she came to our clinic. On physical examination, the patient looked tired. Her body temperature was 37.0°C, blood pressure was 110/72 mmHg, and pulse rate was 66 beats/min. She weighed 52 kg and was 160 cm tall. At that time, she presented no malar erythema and no rash in her body. Although all her fingers were swollen, the swelling of her shoulder, ankle, and knee joints was not obvious. Laboratory data showed normal hematologic parameters (white blood cell count 6,300/μL, hemoglobin 12.6 g/dL, hematocrit 37.6%, and platelet count 264,000/μL). Liver enzymes and C-reactive protein levels were not elevated. Due to a positive result for HPV-B19 IgM antibody in the serum (index 8.20) and the preceding infection of her son, a diagnosis of HPV-B19 infection was made. Oral administration of loxoprofen (180 mg/day) was immediately started after the diagnosis (). Her deteriorating symptoms, including polyarthralgia and the swelling of her fingers, quickly disappeared within 12 hours after the initiation of the drug.","Using the Ideal Body Weight Formula, what is the patient's ideal body weight in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'sex': 'Female', 'height': [160.0, 'cm']}",52.38197,49.76287,55.00107,"For males, the ideal body weight (IBW) is calculated as follows: IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
For females, the ideal body weight (IBW) is calculated as follows: 45.5 kg + 2.3 kg * (height (in inches) - 60)
The patient's gender is Female.
The patient's height is 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.99216 in. 
Plugging in the values for the IBW formula for females gives us 45.5 kg + 2.3 kg * (62.99216 (in inches) - 60) = 52.38197 kg.
Hence, the patient's IBW is 52.38197 kg."
4021,11,QTc Bazett Calculator,physical,decimal,22,Template,A patient has a heart rate of 49 bpm and a QT interval of 257 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [49, 'beats per minute'], 'QT Interval': [257, 'msec']}",232.24988,220.63739,243.86237,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 49 beats per minute.
The QT interval is 257 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/49 = 1.22449.
Hence, plugging in these values, we will get 257/√(1.22449) = 232.24988.
The patient's corrected QT interval (QTc) is 232.24988 msec."
4022,11,QTc Bazett Calculator,physical,decimal,23,Template,A patient has a heart rate of 102 bpm and a QT interval of 337 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [102, 'beats per minute'], 'QT Interval': [337, 'msec']}",439.39248,417.42286,461.3621,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 102 beats per minute.
The QT interval is 337 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/102 = 0.58824.
Hence, plugging in these values, we will get 337/√(0.58824) = 439.39248.
The patient's corrected QT interval (QTc) is 439.39248 msec."
4023,11,QTc Bazett Calculator,physical,decimal,24,Template,A patient has a heart rate of 139 bpm and a QT interval of 401 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [139, 'beats per minute'], 'QT Interval': [401, 'msec']}",610.34937,579.8319,640.86684,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 139 beats per minute.
The QT interval is 401 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/139 = 0.43165.
Hence, plugging in these values, we will get 401/√(0.43165) = 610.34937.
The patient's corrected QT interval (QTc) is 610.34937 msec."
4024,11,QTc Bazett Calculator,physical,decimal,25,Template,A patient has a heart rate of 159 bpm and a QT interval of 350 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [159, 'beats per minute'], 'QT Interval': [350, 'msec']}",569.75758,541.2697,598.24546,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 159 beats per minute.
The QT interval is 350 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/159 = 0.37736.
Hence, plugging in these values, we will get 350/√(0.37736) = 569.75758.
The patient's corrected QT interval (QTc) is 569.75758 msec."
4025,11,QTc Bazett Calculator,physical,decimal,26,Template,A patient has a heart rate of 112 bpm and a QT interval of 294 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [112, 'beats per minute'], 'QT Interval': [294, 'msec']}",401.68208,381.59798,421.76618,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 112 beats per minute.
The QT interval is 294 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/112 = 0.53571.
Hence, plugging in these values, we will get 294/√(0.53571) = 401.68208.
The patient's corrected QT interval (QTc) is 401.68208 msec."
4026,11,QTc Bazett Calculator,physical,decimal,27,Template,A patient has a heart rate of 135 bpm and a QT interval of 221 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [135, 'beats per minute'], 'QT Interval': [221, 'msec']}",331.50166,314.92658,348.07674,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 135 beats per minute.
The QT interval is 221 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/135 = 0.44444.
Hence, plugging in these values, we will get 221/√(0.44444) = 331.50166.
The patient's corrected QT interval (QTc) is 331.50166 msec."
4027,11,QTc Bazett Calculator,physical,decimal,28,Template,A patient has a heart rate of 164 bpm and a QT interval of 420 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [164, 'beats per minute'], 'QT Interval': [420, 'msec']}",694.38089,659.66185,729.09993,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 164 beats per minute.
The QT interval is 420 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/164 = 0.36585.
Hence, plugging in these values, we will get 420/√(0.36585) = 694.38089.
The patient's corrected QT interval (QTc) is 694.38089 msec."
4028,11,QTc Bazett Calculator,physical,decimal,29,Template,A patient has a heart rate of 115 bpm and a QT interval of 477 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [115, 'beats per minute'], 'QT Interval': [477, 'msec']}",660.37605,627.35725,693.39485,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 115 beats per minute.
The QT interval is 477 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/115 = 0.52174.
Hence, plugging in these values, we will get 477/√(0.52174) = 660.37605.
The patient's corrected QT interval (QTc) is 660.37605 msec."
4029,11,QTc Bazett Calculator,physical,decimal,30,Template,A patient has a heart rate of 71 bpm and a QT interval of 230 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [71, 'beats per minute'], 'QT Interval': [230, 'msec']}",250.19665,237.68682,262.70648,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 71 beats per minute.
The QT interval is 230 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/71 = 0.84507.
Hence, plugging in these values, we will get 230/√(0.84507) = 250.19665.
The patient's corrected QT interval (QTc) is 250.19665 msec."
4030,11,QTc Bazett Calculator,physical,decimal,31,Template,A patient has a heart rate of 115 bpm and a QT interval of 456 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [115, 'beats per minute'], 'QT Interval': [456, 'msec']}",631.30289,599.73775,662.86803,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 115 beats per minute.
The QT interval is 456 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/115 = 0.52174.
Hence, plugging in these values, we will get 456/√(0.52174) = 631.30289.
The patient's corrected QT interval (QTc) is 631.30289 msec."
4031,11,QTc Bazett Calculator,physical,decimal,32,Template,A patient has a heart rate of 128 bpm and a QT interval of 330 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [128, 'beats per minute'], 'QT Interval': [330, 'msec']}",481.99585,457.89606,506.09564,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 128 beats per minute.
The QT interval is 330 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/128 = 0.46875.
Hence, plugging in these values, we will get 330/√(0.46875) = 481.99585.
The patient's corrected QT interval (QTc) is 481.99585 msec."
4032,11,QTc Bazett Calculator,physical,decimal,33,Template,A patient has a heart rate of 109 bpm and a QT interval of 269 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [109, 'beats per minute'], 'QT Interval': [269, 'msec']}",362.56794,344.43954,380.69634,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 109 beats per minute.
The QT interval is 269 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/109 = 0.55046.
Hence, plugging in these values, we will get 269/√(0.55046) = 362.56794.
The patient's corrected QT interval (QTc) is 362.56794 msec."
4033,11,QTc Bazett Calculator,physical,decimal,34,Template,A patient has a heart rate of 123 bpm and a QT interval of 417 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [123, 'beats per minute'], 'QT Interval': [417, 'msec']}",597.05612,567.20331,626.90893,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 123 beats per minute.
The QT interval is 417 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/123 = 0.4878.
Hence, plugging in these values, we will get 417/√(0.4878) = 597.05612.
The patient's corrected QT interval (QTc) is 597.05612 msec."
4034,11,QTc Bazett Calculator,physical,decimal,35,Template,A patient has a heart rate of 90 bpm and a QT interval of 315 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [90, 'beats per minute'], 'QT Interval': [315, 'msec']}",385.79367,366.50399,405.08335,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 90 beats per minute.
The QT interval is 315 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/90 = 0.66667.
Hence, plugging in these values, we will get 315/√(0.66667) = 385.79367.
The patient's corrected QT interval (QTc) is 385.79367 msec."
4035,11,QTc Bazett Calculator,physical,decimal,36,Template,A patient has a heart rate of 176 bpm and a QT interval of 496 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [176, 'beats per minute'], 'QT Interval': [496, 'msec']}",849.49692,807.02207,891.97177,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 176 beats per minute.
The QT interval is 496 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/176 = 0.34091.
Hence, plugging in these values, we will get 496/√(0.34091) = 849.49692.
The patient's corrected QT interval (QTc) is 849.49692 msec."
4036,11,QTc Bazett Calculator,physical,decimal,37,Template,A patient has a heart rate of 90 bpm and a QT interval of 436 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [90, 'beats per minute'], 'QT Interval': [436, 'msec']}",533.98743,507.28806,560.6868,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 90 beats per minute.
The QT interval is 436 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/90 = 0.66667.
Hence, plugging in these values, we will get 436/√(0.66667) = 533.98743.
The patient's corrected QT interval (QTc) is 533.98743 msec."
4037,11,QTc Bazett Calculator,physical,decimal,38,Template,A patient has a heart rate of 158 bpm and a QT interval of 470 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [158, 'beats per minute'], 'QT Interval': [470, 'msec']}",762.69161,724.55703,800.82619,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 158 beats per minute.
The QT interval is 470 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/158 = 0.37975.
Hence, plugging in these values, we will get 470/√(0.37975) = 762.69161.
The patient's corrected QT interval (QTc) is 762.69161 msec."
4038,11,QTc Bazett Calculator,physical,decimal,39,Template,A patient has a heart rate of 74 bpm and a QT interval of 365 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [74, 'beats per minute'], 'QT Interval': [365, 'msec']}",405.35293,385.08528,425.62058,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 74 beats per minute.
The QT interval is 365 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/74 = 0.81081.
Hence, plugging in these values, we will get 365/√(0.81081) = 405.35293.
The patient's corrected QT interval (QTc) is 405.35293 msec."
4039,11,QTc Bazett Calculator,physical,decimal,40,Template,A patient has a heart rate of 128 bpm and a QT interval of 260 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [128, 'beats per minute'], 'QT Interval': [260, 'msec']}",379.75431,360.76659,398.74203,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 128 beats per minute.
The QT interval is 260 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/128 = 0.46875.
Hence, plugging in these values, we will get 260/√(0.46875) = 379.75431.
The patient's corrected QT interval (QTc) is 379.75431 msec."
4040,11,QTc Bazett Calculator,physical,decimal,41,Template,A patient has a heart rate of 124 bpm and a QT interval of 412 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [124, 'beats per minute'], 'QT Interval': [412, 'msec']}",592.28791,562.67351,621.90231,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 124 beats per minute.
The QT interval is 412 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/124 = 0.48387.
Hence, plugging in these values, we will get 412/√(0.48387) = 592.28791.
The patient's corrected QT interval (QTc) is 592.28791 msec."
4041,11,QTc Bazett Calculator,physical,decimal,42,Template,A patient has a heart rate of 65 bpm and a QT interval of 430 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [65, 'beats per minute'], 'QT Interval': [430, 'msec']}",447.55744,425.17957,469.93531,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 65 beats per minute.
The QT interval is 430 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/65 = 0.92308.
Hence, plugging in these values, we will get 430/√(0.92308) = 447.55744.
The patient's corrected QT interval (QTc) is 447.55744 msec."
4042,11,QTc Bazett Calculator,physical,decimal,43,Template,A patient has a heart rate of 78 bpm and a QT interval of 227 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [78, 'beats per minute'], 'QT Interval': [227, 'msec']}",258.81995,245.87895,271.76095,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 78 beats per minute.
The QT interval is 227 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/78 = 0.76923.
Hence, plugging in these values, we will get 227/√(0.76923) = 258.81995.
The patient's corrected QT interval (QTc) is 258.81995 msec."
4043,11,QTc Bazett Calculator,physical,decimal,44,Template,A patient has a heart rate of 136 bpm and a QT interval of 497 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [136, 'beats per minute'], 'QT Interval': [497, 'msec']}",748.25302,710.84037,785.66567,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 136 beats per minute.
The QT interval is 497 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/136 = 0.44118.
Hence, plugging in these values, we will get 497/√(0.44118) = 748.25302.
The patient's corrected QT interval (QTc) is 748.25302 msec."
4044,11,QTc Bazett Calculator,physical,decimal,45,Template,A patient has a heart rate of 97 bpm and a QT interval of 476 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [97, 'beats per minute'], 'QT Interval': [476, 'msec']}",605.22385,574.96266,635.48504,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 97 beats per minute.
The QT interval is 476 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/97 = 0.61856.
Hence, plugging in these values, we will get 476/√(0.61856) = 605.22385.
The patient's corrected QT interval (QTc) is 605.22385 msec."
4045,11,QTc Bazett Calculator,physical,decimal,46,Template,A patient has a heart rate of 178 bpm and a QT interval of 449 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [178, 'beats per minute'], 'QT Interval': [449, 'msec']}",773.35669,734.68886,812.02452,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 178 beats per minute.
The QT interval is 449 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/178 = 0.33708.
Hence, plugging in these values, we will get 449/√(0.33708) = 773.35669.
The patient's corrected QT interval (QTc) is 773.35669 msec."
4046,11,QTc Bazett Calculator,physical,decimal,47,Template,A patient has a heart rate of 62 bpm and a QT interval of 347 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [62, 'beats per minute'], 'QT Interval': [347, 'msec']}",352.73628,335.09947,370.37309,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 62 beats per minute.
The QT interval is 347 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/62 = 0.96774.
Hence, plugging in these values, we will get 347/√(0.96774) = 352.73628.
The patient's corrected QT interval (QTc) is 352.73628 msec."
4047,11,QTc Bazett Calculator,physical,decimal,48,Template,A patient has a heart rate of 105 bpm and a QT interval of 328 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [105, 'beats per minute'], 'QT Interval': [328, 'msec']}",433.90267,412.20754,455.5978,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 105 beats per minute.
The QT interval is 328 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/105 = 0.57143.
Hence, plugging in these values, we will get 328/√(0.57143) = 433.90267.
The patient's corrected QT interval (QTc) is 433.90267 msec."
4048,11,QTc Bazett Calculator,physical,decimal,49,Template,A patient has a heart rate of 168 bpm and a QT interval of 303 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [168, 'beats per minute'], 'QT Interval': [303, 'msec']}",507.018,481.6671,532.3689,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 168 beats per minute.
The QT interval is 303 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/168 = 0.35714.
Hence, plugging in these values, we will get 303/√(0.35714) = 507.018.
The patient's corrected QT interval (QTc) is 507.018 msec."
4049,11,QTc Bazett Calculator,physical,decimal,50,Template,A patient has a heart rate of 134 bpm and a QT interval of 326 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [134, 'beats per minute'], 'QT Interval': [326, 'msec']}",487.18617,462.82686,511.54548,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 134 beats per minute.
The QT interval is 326 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/134 = 0.44776.
Hence, plugging in these values, we will get 326/√(0.44776) = 487.18617.
The patient's corrected QT interval (QTc) is 487.18617 msec."
4050,11,QTc Bazett Calculator,physical,decimal,51,Template,A patient has a heart rate of 57 bpm and a QT interval of 227 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [57, 'beats per minute'], 'QT Interval': [227, 'msec']}",221.2524,210.18978,232.31502,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 57 beats per minute.
The QT interval is 227 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/57 = 1.05263.
Hence, plugging in these values, we will get 227/√(1.05263) = 221.2524.
The patient's corrected QT interval (QTc) is 221.2524 msec."
4051,11,QTc Bazett Calculator,physical,decimal,52,Template,A patient has a heart rate of 59 bpm and a QT interval of 378 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [59, 'beats per minute'], 'QT Interval': [378, 'msec']}",374.83661,356.09478,393.57844,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 59 beats per minute.
The QT interval is 378 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/59 = 1.01695.
Hence, plugging in these values, we will get 378/√(1.01695) = 374.83661.
The patient's corrected QT interval (QTc) is 374.83661 msec."
4052,11,QTc Bazett Calculator,physical,decimal,53,Template,A patient has a heart rate of 123 bpm and a QT interval of 380 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [123, 'beats per minute'], 'QT Interval': [380, 'msec']}",544.07992,516.87592,571.28392,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 123 beats per minute.
The QT interval is 380 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/123 = 0.4878.
Hence, plugging in these values, we will get 380/√(0.4878) = 544.07992.
The patient's corrected QT interval (QTc) is 544.07992 msec."
4053,11,QTc Bazett Calculator,physical,decimal,54,Template,A patient has a heart rate of 134 bpm and a QT interval of 230 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [134, 'beats per minute'], 'QT Interval': [230, 'msec']}",343.72031,326.53429,360.90633,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 134 beats per minute.
The QT interval is 230 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/134 = 0.44776.
Hence, plugging in these values, we will get 230/√(0.44776) = 343.72031.
The patient's corrected QT interval (QTc) is 343.72031 msec."
4054,11,QTc Bazett Calculator,physical,decimal,55,Template,A patient has a heart rate of 106 bpm and a QT interval of 325 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [106, 'beats per minute'], 'QT Interval': [325, 'msec']}",431.97618,410.37737,453.57499,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 106 beats per minute.
The QT interval is 325 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/106 = 0.56604.
Hence, plugging in these values, we will get 325/√(0.56604) = 431.97618.
The patient's corrected QT interval (QTc) is 431.97618 msec."
4055,11,QTc Bazett Calculator,physical,decimal,56,Template,A patient has a heart rate of 162 bpm and a QT interval of 227 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [162, 'beats per minute'], 'QT Interval': [227, 'msec']}",372.99925,354.34929,391.64921,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 162 beats per minute.
The QT interval is 227 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/162 = 0.37037.
Hence, plugging in these values, we will get 227/√(0.37037) = 372.99925.
The patient's corrected QT interval (QTc) is 372.99925 msec."
4056,11,QTc Bazett Calculator,physical,decimal,57,Template,A patient has a heart rate of 83 bpm and a QT interval of 218 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [83, 'beats per minute'], 'QT Interval': [218, 'msec']}",256.4014,243.58133,269.22147,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 83 beats per minute.
The QT interval is 218 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/83 = 0.72289.
Hence, plugging in these values, we will get 218/√(0.72289) = 256.4014.
The patient's corrected QT interval (QTc) is 256.4014 msec."
4057,11,QTc Bazett Calculator,physical,decimal,58,Template,A patient has a heart rate of 55 bpm and a QT interval of 394 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [55, 'beats per minute'], 'QT Interval': [394, 'msec']}",377.22612,358.36481,396.08743,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 55 beats per minute.
The QT interval is 394 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/55 = 1.09091.
Hence, plugging in these values, we will get 394/√(1.09091) = 377.22612.
The patient's corrected QT interval (QTc) is 377.22612 msec."
4058,11,QTc Bazett Calculator,physical,decimal,59,Template,A patient has a heart rate of 145 bpm and a QT interval of 353 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [145, 'beats per minute'], 'QT Interval': [353, 'msec']}",548.76286,521.32472,576.201,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 145 beats per minute.
The QT interval is 353 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/145 = 0.41379.
Hence, plugging in these values, we will get 353/√(0.41379) = 548.76286.
The patient's corrected QT interval (QTc) is 548.76286 msec."
4059,11,QTc Bazett Calculator,physical,decimal,60,Template,A patient has a heart rate of 165 bpm and a QT interval of 474 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [165, 'beats per minute'], 'QT Interval': [474, 'msec']}",786.03615,746.73434,825.33796,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 165 beats per minute.
The QT interval is 474 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/165 = 0.36364.
Hence, plugging in these values, we will get 474/√(0.36364) = 786.03615.
The patient's corrected QT interval (QTc) is 786.03615 msec."
4060,11,QTc Bazett Calculator,physical,decimal,61,Template,A patient has a heart rate of 112 bpm and a QT interval of 300 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [112, 'beats per minute'], 'QT Interval': [300, 'msec']}",409.87967,389.38569,430.37365,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 112 beats per minute.
The QT interval is 300 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/112 = 0.53571.
Hence, plugging in these values, we will get 300/√(0.53571) = 409.87967.
The patient's corrected QT interval (QTc) is 409.87967 msec."
4061,11,QTc Bazett Calculator,physical,decimal,62,Template,A patient has a heart rate of 114 bpm and a QT interval of 482 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [114, 'beats per minute'], 'QT Interval': [482, 'msec']}",664.38849,631.16907,697.60791,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 114 beats per minute.
The QT interval is 482 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/114 = 0.52632.
Hence, plugging in these values, we will get 482/√(0.52632) = 664.38849.
The patient's corrected QT interval (QTc) is 664.38849 msec."
4062,11,QTc Bazett Calculator,physical,decimal,63,Template,A patient has a heart rate of 114 bpm and a QT interval of 399 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [114, 'beats per minute'], 'QT Interval': [399, 'msec']}",549.98135,522.48228,577.48042,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 114 beats per minute.
The QT interval is 399 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/114 = 0.52632.
Hence, plugging in these values, we will get 399/√(0.52632) = 549.98135.
The patient's corrected QT interval (QTc) is 549.98135 msec."
4063,11,QTc Bazett Calculator,physical,decimal,64,Template,A patient has a heart rate of 91 bpm and a QT interval of 399 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [91, 'beats per minute'], 'QT Interval': [399, 'msec']}",491.3808,466.81176,515.94984,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 91 beats per minute.
The QT interval is 399 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/91 = 0.65934.
Hence, plugging in these values, we will get 399/√(0.65934) = 491.3808.
The patient's corrected QT interval (QTc) is 491.3808 msec."
4064,11,QTc Bazett Calculator,physical,decimal,65,Template,A patient has a heart rate of 107 bpm and a QT interval of 411 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [107, 'beats per minute'], 'QT Interval': [411, 'msec']}",548.85444,521.41172,576.29716,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 107 beats per minute.
The QT interval is 411 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/107 = 0.56075.
Hence, plugging in these values, we will get 411/√(0.56075) = 548.85444.
The patient's corrected QT interval (QTc) is 548.85444 msec."
4065,11,QTc Bazett Calculator,physical,decimal,66,Template,A patient has a heart rate of 59 bpm and a QT interval of 397 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [59, 'beats per minute'], 'QT Interval': [397, 'msec']}",393.6776,373.99372,413.36148,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 59 beats per minute.
The QT interval is 397 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/59 = 1.01695.
Hence, plugging in these values, we will get 397/√(1.01695) = 393.6776.
The patient's corrected QT interval (QTc) is 393.6776 msec."
4066,11,QTc Bazett Calculator,physical,decimal,67,Template,A patient has a heart rate of 121 bpm and a QT interval of 424 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [121, 'beats per minute'], 'QT Interval': [424, 'msec']}",602.11846,572.01254,632.22438,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 121 beats per minute.
The QT interval is 424 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/121 = 0.49587.
Hence, plugging in these values, we will get 424/√(0.49587) = 602.11846.
The patient's corrected QT interval (QTc) is 602.11846 msec."
4067,11,QTc Bazett Calculator,physical,decimal,68,Template,A patient has a heart rate of 69 bpm and a QT interval of 307 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [69, 'beats per minute'], 'QT Interval': [307, 'msec']}",329.21992,312.75892,345.68092,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 69 beats per minute.
The QT interval is 307 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/69 = 0.86957.
Hence, plugging in these values, we will get 307/√(0.86957) = 329.21992.
The patient's corrected QT interval (QTc) is 329.21992 msec."
4068,11,QTc Bazett Calculator,physical,decimal,69,Template,A patient has a heart rate of 91 bpm and a QT interval of 205 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [91, 'beats per minute'], 'QT Interval': [205, 'msec']}",252.46382,239.84063,265.08701,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 91 beats per minute.
The QT interval is 205 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/91 = 0.65934.
Hence, plugging in these values, we will get 205/√(0.65934) = 252.46382.
The patient's corrected QT interval (QTc) is 252.46382 msec."
4069,11,QTc Bazett Calculator,physical,decimal,70,Template,A patient has a heart rate of 63 bpm and a QT interval of 349 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [63, 'beats per minute'], 'QT Interval': [349, 'msec']}",357.61876,339.73782,375.4997,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 63 beats per minute.
The QT interval is 349 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/63 = 0.95238.
Hence, plugging in these values, we will get 349/√(0.95238) = 357.61876.
The patient's corrected QT interval (QTc) is 357.61876 msec."
4070,11,QTc Bazett Calculator,physical,decimal,71,Template,A patient has a heart rate of 171 bpm and a QT interval of 485 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [171, 'beats per minute'], 'QT Interval': [485, 'msec']}",818.77096,777.83241,859.70951,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 171 beats per minute.
The QT interval is 485 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/171 = 0.35088.
Hence, plugging in these values, we will get 485/√(0.35088) = 818.77096.
The patient's corrected QT interval (QTc) is 818.77096 msec."
4071,11,QTc Bazett Calculator,physical,decimal,72,Template,A patient has a heart rate of 148 bpm and a QT interval of 212 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [148, 'beats per minute'], 'QT Interval': [212, 'msec']}",332.95737,316.3095,349.60524,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 148 beats per minute.
The QT interval is 212 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/148 = 0.40541.
Hence, plugging in these values, we will get 212/√(0.40541) = 332.95737.
The patient's corrected QT interval (QTc) is 332.95737 msec."
4072,11,QTc Bazett Calculator,physical,decimal,73,Template,A patient has a heart rate of 85 bpm and a QT interval of 413 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [85, 'beats per minute'], 'QT Interval': [413, 'msec']}",491.56914,466.99068,516.1476,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 85 beats per minute.
The QT interval is 413 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/85 = 0.70588.
Hence, plugging in these values, we will get 413/√(0.70588) = 491.56914.
The patient's corrected QT interval (QTc) is 491.56914 msec."
4073,11,QTc Bazett Calculator,physical,decimal,74,Template,A patient has a heart rate of 90 bpm and a QT interval of 246 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [90, 'beats per minute'], 'QT Interval': [246, 'msec']}",301.28649,286.22217,316.35081,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 90 beats per minute.
The QT interval is 246 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/90 = 0.66667.
Hence, plugging in these values, we will get 246/√(0.66667) = 301.28649.
The patient's corrected QT interval (QTc) is 301.28649 msec."
4074,11,QTc Bazett Calculator,physical,decimal,75,Template,A patient has a heart rate of 93 bpm and a QT interval of 497 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [93, 'beats per minute'], 'QT Interval': [497, 'msec']}",618.76063,587.8226,649.69866,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 93 beats per minute.
The QT interval is 497 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/93 = 0.64516.
Hence, plugging in these values, we will get 497/√(0.64516) = 618.76063.
The patient's corrected QT interval (QTc) is 618.76063 msec."
4075,11,QTc Bazett Calculator,physical,decimal,76,Template,A patient has a heart rate of 127 bpm and a QT interval of 479 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [127, 'beats per minute'], 'QT Interval': [479, 'msec']}",696.88671,662.04237,731.73105,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 127 beats per minute.
The QT interval is 479 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/127 = 0.47244.
Hence, plugging in these values, we will get 479/√(0.47244) = 696.88671.
The patient's corrected QT interval (QTc) is 696.88671 msec."
4076,11,QTc Bazett Calculator,physical,decimal,77,Template,A patient has a heart rate of 58 bpm and a QT interval of 307 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [58, 'beats per minute'], 'QT Interval': [307, 'msec']}",301.84037,286.74835,316.93239,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 58 beats per minute.
The QT interval is 307 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/58 = 1.03448.
Hence, plugging in these values, we will get 307/√(1.03448) = 301.84037.
The patient's corrected QT interval (QTc) is 301.84037 msec."
4077,11,QTc Bazett Calculator,physical,decimal,78,Template,A patient has a heart rate of 169 bpm and a QT interval of 280 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [169, 'beats per minute'], 'QT Interval': [280, 'msec']}",469.92171,446.42562,493.4178,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 169 beats per minute.
The QT interval is 280 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/169 = 0.35503.
Hence, plugging in these values, we will get 280/√(0.35503) = 469.92171.
The patient's corrected QT interval (QTc) is 469.92171 msec."
4078,11,QTc Bazett Calculator,physical,decimal,79,Template,A patient has a heart rate of 123 bpm and a QT interval of 411 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [123, 'beats per minute'], 'QT Interval': [411, 'msec']}",588.46539,559.04212,617.88866,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 123 beats per minute.
The QT interval is 411 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/123 = 0.4878.
Hence, plugging in these values, we will get 411/√(0.4878) = 588.46539.
The patient's corrected QT interval (QTc) is 588.46539 msec."
4079,11,QTc Bazett Calculator,physical,decimal,80,Template,A patient has a heart rate of 115 bpm and a QT interval of 474 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [115, 'beats per minute'], 'QT Interval': [474, 'msec']}",656.22274,623.4116,689.03388,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 115 beats per minute.
The QT interval is 474 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/115 = 0.52174.
Hence, plugging in these values, we will get 474/√(0.52174) = 656.22274.
The patient's corrected QT interval (QTc) is 656.22274 msec."
4080,11,QTc Bazett Calculator,physical,decimal,81,Template,A patient has a heart rate of 97 bpm and a QT interval of 329 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [97, 'beats per minute'], 'QT Interval': [329, 'msec']}",418.31649,397.40067,439.23231,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 97 beats per minute.
The QT interval is 329 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/97 = 0.61856.
Hence, plugging in these values, we will get 329/√(0.61856) = 418.31649.
The patient's corrected QT interval (QTc) is 418.31649 msec."
4081,11,QTc Bazett Calculator,physical,decimal,82,Template,A patient has a heart rate of 57 bpm and a QT interval of 322 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [57, 'beats per minute'], 'QT Interval': [322, 'msec']}",313.84701,298.15466,329.53936,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 57 beats per minute.
The QT interval is 322 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/57 = 1.05263.
Hence, plugging in these values, we will get 322/√(1.05263) = 313.84701.
The patient's corrected QT interval (QTc) is 313.84701 msec."
4082,11,QTc Bazett Calculator,physical,decimal,83,Template,A patient has a heart rate of 142 bpm and a QT interval of 311 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [142, 'beats per minute'], 'QT Interval': [311, 'msec']}",478.43889,454.51695,502.36083,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 142 beats per minute.
The QT interval is 311 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/142 = 0.42254.
Hence, plugging in these values, we will get 311/√(0.42254) = 478.43889.
The patient's corrected QT interval (QTc) is 478.43889 msec."
4083,11,QTc Bazett Calculator,physical,decimal,84,Template,A patient has a heart rate of 163 bpm and a QT interval of 356 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [163, 'beats per minute'], 'QT Interval': [356, 'msec']}",586.7689,557.43046,616.10735,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 163 beats per minute.
The QT interval is 356 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/163 = 0.3681.
Hence, plugging in these values, we will get 356/√(0.3681) = 586.7689.
The patient's corrected QT interval (QTc) is 586.7689 msec."
4084,11,QTc Bazett Calculator,physical,decimal,85,Template,A patient has a heart rate of 72 bpm and a QT interval of 207 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [72, 'beats per minute'], 'QT Interval': [207, 'msec']}",226.75759,215.41971,238.09547,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 72 beats per minute.
The QT interval is 207 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/72 = 0.83333.
Hence, plugging in these values, we will get 207/√(0.83333) = 226.75759.
The patient's corrected QT interval (QTc) is 226.75759 msec."
4085,11,QTc Bazett Calculator,physical,decimal,86,Template,A patient has a heart rate of 169 bpm and a QT interval of 300 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [169, 'beats per minute'], 'QT Interval': [300, 'msec']}",503.48754,478.31316,528.66192,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 169 beats per minute.
The QT interval is 300 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/169 = 0.35503.
Hence, plugging in these values, we will get 300/√(0.35503) = 503.48754.
The patient's corrected QT interval (QTc) is 503.48754 msec."
4086,11,QTc Bazett Calculator,physical,decimal,87,Template,A patient has a heart rate of 50 bpm and a QT interval of 331 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [50, 'beats per minute'], 'QT Interval': [331, 'msec']}",302.16028,287.05227,317.26829,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 50 beats per minute.
The QT interval is 331 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/50 = 1.2.
Hence, plugging in these values, we will get 331/√(1.2) = 302.16028.
The patient's corrected QT interval (QTc) is 302.16028 msec."
4087,11,QTc Bazett Calculator,physical,decimal,88,Template,A patient has a heart rate of 148 bpm and a QT interval of 412 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [148, 'beats per minute'], 'QT Interval': [412, 'msec']}",647.0681,614.71469,679.42151,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 148 beats per minute.
The QT interval is 412 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/148 = 0.40541.
Hence, plugging in these values, we will get 412/√(0.40541) = 647.0681.
The patient's corrected QT interval (QTc) is 647.0681 msec."
4088,11,QTc Bazett Calculator,physical,decimal,89,Template,A patient has a heart rate of 107 bpm and a QT interval of 349 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [107, 'beats per minute'], 'QT Interval': [349, 'msec']}",466.05888,442.75594,489.36182,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 107 beats per minute.
The QT interval is 349 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/107 = 0.56075.
Hence, plugging in these values, we will get 349/√(0.56075) = 466.05888.
The patient's corrected QT interval (QTc) is 466.05888 msec."
4089,11,QTc Bazett Calculator,physical,decimal,90,Template,A patient has a heart rate of 80 bpm and a QT interval of 379 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [80, 'beats per minute'], 'QT Interval': [379, 'msec']}",437.6315,415.74993,459.51308,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 80 beats per minute.
The QT interval is 379 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/80 = 0.75.
Hence, plugging in these values, we will get 379/√(0.75) = 437.6315.
The patient's corrected QT interval (QTc) is 437.6315 msec."
4090,11,QTc Bazett Calculator,physical,decimal,91,Template,A patient has a heart rate of 160 bpm and a QT interval of 439 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [160, 'beats per minute'], 'QT Interval': [439, 'msec']}",716.884,681.0398,752.7282,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 160 beats per minute.
The QT interval is 439 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/160 = 0.375.
Hence, plugging in these values, we will get 439/√(0.375) = 716.884.
The patient's corrected QT interval (QTc) is 716.884 msec."
4091,11,QTc Bazett Calculator,physical,decimal,92,Template,A patient has a heart rate of 144 bpm and a QT interval of 282 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [144, 'beats per minute'], 'QT Interval': [282, 'msec']}",436.87077,415.02723,458.71431,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 144 beats per minute.
The QT interval is 282 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/144 = 0.41667.
Hence, plugging in these values, we will get 282/√(0.41667) = 436.87077.
The patient's corrected QT interval (QTc) is 436.87077 msec."
4092,11,QTc Bazett Calculator,physical,decimal,93,Template,A patient has a heart rate of 81 bpm and a QT interval of 283 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [81, 'beats per minute'], 'QT Interval': [283, 'msec']}",328.81645,312.37563,345.25727,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 81 beats per minute.
The QT interval is 283 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/81 = 0.74074.
Hence, plugging in these values, we will get 283/√(0.74074) = 328.81645.
The patient's corrected QT interval (QTc) is 328.81645 msec."
4093,11,QTc Bazett Calculator,physical,decimal,94,Template,A patient has a heart rate of 169 bpm and a QT interval of 317 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [169, 'beats per minute'], 'QT Interval': [317, 'msec']}",532.0185,505.41757,558.61943,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 169 beats per minute.
The QT interval is 317 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/169 = 0.35503.
Hence, plugging in these values, we will get 317/√(0.35503) = 532.0185.
The patient's corrected QT interval (QTc) is 532.0185 msec."
4094,11,QTc Bazett Calculator,physical,decimal,95,Template,A patient has a heart rate of 47 bpm and a QT interval of 453 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [47, 'beats per minute'], 'QT Interval': [453, 'msec']}",400.93206,380.88546,420.97866,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 47 beats per minute.
The QT interval is 453 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/47 = 1.2766.
Hence, plugging in these values, we will get 453/√(1.2766) = 400.93206.
The patient's corrected QT interval (QTc) is 400.93206 msec."
4095,11,QTc Bazett Calculator,physical,decimal,96,Template,A patient has a heart rate of 59 bpm and a QT interval of 422 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [59, 'beats per minute'], 'QT Interval': [422, 'msec']}",418.46838,397.54496,439.3918,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 59 beats per minute.
The QT interval is 422 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/59 = 1.01695.
Hence, plugging in these values, we will get 422/√(1.01695) = 418.46838.
The patient's corrected QT interval (QTc) is 418.46838 msec."
4096,11,QTc Bazett Calculator,physical,decimal,97,Template,A patient has a heart rate of 72 bpm and a QT interval of 358 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [72, 'beats per minute'], 'QT Interval': [358, 'msec']}",392.17014,372.56163,411.77865,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 72 beats per minute.
The QT interval is 358 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/72 = 0.83333.
Hence, plugging in these values, we will get 358/√(0.83333) = 392.17014.
The patient's corrected QT interval (QTc) is 392.17014 msec."
4097,11,QTc Bazett Calculator,physical,decimal,98,Template,A patient has a heart rate of 108 bpm and a QT interval of 205 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [108, 'beats per minute'], 'QT Interval': [205, 'msec']}",275.03526,261.2835,288.78702,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 108 beats per minute.
The QT interval is 205 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/108 = 0.55556.
Hence, plugging in these values, we will get 205/√(0.55556) = 275.03526.
The patient's corrected QT interval (QTc) is 275.03526 msec."
4098,11,QTc Bazett Calculator,physical,decimal,99,Template,A patient has a heart rate of 101 bpm and a QT interval of 200 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [101, 'beats per minute'], 'QT Interval': [200, 'msec']}",259.48654,246.51221,272.46087,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 101 beats per minute.
The QT interval is 200 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/101 = 0.59406.
Hence, plugging in these values, we will get 200/√(0.59406) = 259.48654.
The patient's corrected QT interval (QTc) is 259.48654 msec."
4099,11,QTc Bazett Calculator,physical,decimal,100,Template,A patient has a heart rate of 107 bpm and a QT interval of 287 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [107, 'beats per minute'], 'QT Interval': [287, 'msec']}",383.26332,364.10015,402.42649,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 107 beats per minute.
The QT interval is 287 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/107 = 0.56075.
Hence, plugging in these values, we will get 287/√(0.56075) = 383.26332.
The patient's corrected QT interval (QTc) is 383.26332 msec."
4100,11,QTc Bazett Calculator,physical,decimal,101,Template,Patient has a heart rate of 111 bpm and a QT interval of 330 msec.,"Using the Bazett Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [111, 'beats per minute'], 'QT Interval': [330, 'msec']}",448.84875,426.40631,471.29119,"The corrected QT interval using the Bazett formula is computed as  QTc = QT interval / √ (RR interval), where the QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 111 beats per minute.
The QT interval is 330 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/111 = 0.54054.
Hence, plugging in these values, we will get 330/√(0.54054) = 448.84875.
The patient's corrected QT interval (QTc) is 448.84875 msec."
4101,18,HEART Score for Major Cardiac Events,risk,integer,usmle-9855,Extracted,"A 25-year-old woman presents to the emergency department with palpitations, sweating, and blurry vision after playing volleyball on the beach. She denies chest pain and shortness of breath. She states that these episodes occur often, but resolve after eating a meal or drinking a sugary soda. Past medical history is unremarkable, and she takes no medications. Temperature is 37°C (98.6°F), blood pressure is 135/80 mm Hg, pulse is 102/min, and respirations are 18/min. Fingerstick blood glucose level is 42 g/dL. ECG reveals sinus tachycardia. Urinalysis and toxicology are noncontributory. Appropriate medical therapy is administered and she is discharged with an appointment for a fasting blood draw within the week.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [25, 'years'], 'Hypertension history': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 25 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4102,18,HEART Score for Major Cardiac Events,risk,integer,pmc-3017924-1,Extracted,"A 57-year-old lady presented with exertional dyspnea and NYHA class II angina since last 3 years which had aggravated in last 6 months. She had been previously diagnosed with hypertension and hypercholesterolemia and was put on medical treatment.
Physical examination was unremarkable except a soft (grade II/VI) continuous murmur that was heard most clearly over the pulmonary area. An electrocardiogram was normal without any evidence of ischemia, and echocardiogram showed mild dilatation of the left atrium and left ventricle. Coronary angiography demonstrated multiple coronary artery to pulmonary artery fistulae originating from the left anterior descending (LAD) and right coronary arteries (RCA). There were no flow-limiting lesions in the coronary arteries. There was TIMI III flow in coronary vessels distal to the origin of the fistulae [Figures and ]. After a thorough discussion during the weekly catheterization meeting, it was decided to close the fistulae surgically in order to alleviate symptoms. Issues that prompted against transcatheter intervention were acute angle of origin of the fistula arising from LAD and the excessive tortuosity that would make transcatheter coil embolization of the coronary fistula extremely cumbersome and complex. Intra-operatively, the coronary fistulae were confirmed to be originating from the RCA and the LAD and terminating into pulmonary artery with an intervening “fistula lake.” The “lake” next to the LAD was identified, and the vessels feeding this lake were occluded with surgical clips as were the vessels coming from RCA. The aneurysmal sac was further obliterated using a larger surgical clip. Post-operative coronary angiogram showed no evidence of residual fistulae [Figures and ]. The patient made an uneventful recovery and at 1-month follow-up, she was symptom free.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [57, 'years'], 'Hypertension history': True, 'Suspicion History': 'Moderately suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': True, 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 57 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 1 + 1 = 2.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4103,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8464441-1,Extracted,"Our patient was a 60-year-old Caucasian male who presented in September 2019 with syncope associated with hypotension.
The patient had no previous symptoms and syncope was indeed the first clinical manifestation.
The patient had no history of previous disease and he was not taking any medications.
The only red flags were the known congenital bicuspid aortic valve and family history of congestive heart failure (sister).
When he came to the emergency department, he presented hypotensive, with tachyarrhythmic peripheral pulse. A paroxysmal atrial fibrillation (AF) episode was diagnosed, which regressed after a few hours.
Routine laboratory tests (complete blood count, kidney function, electrolytes, liver and heart enzymes) were all in the normal ranges.
Transthoracic echocardiography showed no pathological findings.
The 24-h electrocardiogram Holter monitoring recorded frequent episodes of high-grade atrioventricular block with no further AF episodes. Upon suspicion of an ischemic aetiology, he was admitted to the cardiology unit and underwent coronarography, which indicated intermediate stenosis (50%) in the left anterior descending artery. This stenosis was not considered hemodynamically significant. Thus, the decision was to implant a dual chamber anti-bradycardia pacemaker. Given the single and short AF episode and the CHA2DS2-VASc score of 0, no anticoagulation treatment was initiated. In December 2019, he underwent a scintigraphy stress–rest test, during which he presented loss of consciousness due to the onset of sustained ventricular tachycardia (VT) (Figure ), which was successfully treated with cardiopulmonary resuscitation manoeuvres and lidocaine infusion. The arrhythmia was considered to be of ischaemic origin. Therefore, the patient underwent percutaneous transluminal coronary angioplasty with drug-eluting stent (DES) implantation at the known coronary stenosis. During and after hospitalization, numerous non-sustained VTs were recorded, for which he was given amiodarone, with clinical benefit. After a few weeks, a treadmill stress test was also performed under antiarrhythmic therapy, which was negative for both myocardial ischemia and VTs. During the follow-up examinations, considering the patient’s clinical picture, encompassing VT, atrioventricular block, family history, and echocardiographic findings showing accentuated right ventricular apex trabeculation, the treating cardiologist decided to reassess the clinical case. He recommended that the patient undergo cardiac magnetic resonance and molecular analysis performed with a panel of 128 genes known to be associated with cardiomyopathies and channelopathies. Both tests were performed in February 2020 (6 wk after DES implantation, as indicated in the manufacturer’s data sheet). The former showed a left ventricular ejection fraction (LVEF) of 50% without any areas of late enhancement or myocardial fibrosis (Figure ).
The results of the genetic testing took 3 mo to be validated, during which outpatient appointments with patients were suddenly stopped due to the severe acute respiratory syndrome coronavirus 2-related pandemic. Considering the need to supervise the patient during this time for the possible onset of life-threatening ventricular tachyarrhythmia (LTVT) and AF, without the possibility of a periodic in person interrogation of the PM arrhythmias registry, as was usually done, it was decided to give the patient a remote monitoring device (Medtronic Carelink Network®). The device was configurated to transmit the data it recorded, automatically every week. At the same time, both LTVT and AF were set up as “care alerts”, which meant that an automatic alert would have been sent immediately after identification, , as long as the potential LTVT or AF onset would have required a prompt and potentially lifesaving intervention, either the upgrading the PM to an implantable cardioverter defibrillator (ICD) or the initiation of a life-long anticoagulant therapy, respectively. Fortunately, no arrhythmias were detected during that time.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [60, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': True, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 60 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: family with cvd. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4104,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7873793-1,Extracted,"A 22-year-old woman from sub-Saharan Africa presented to our emergency department after 1 week of dyspnoea, leg swelling, and haemoptysis. Haemoptysis had started as blood-streaked sputum 3–4 weeks before, gradually increasing to multiple daily blood clot expectorations within 2 weeks.
In her past medical history, we highlight a triple valve replacement for rheumatic heart disease at age 16 (19-mm CarboMedics mechanical aortic valve prosthesis; 27-mm CarboMedics mechanical mitral valve prosthesis; 27-mm Magna biological tricuspid valve prosthesis). Her medical history also comprised a right middle cerebral artery stroke at age 17, conditioning left hemiplegia and aphasia at presentation with subsequent full recovery. In addition, she was known for chronic haemolytic anaemia and thalassaemia trait. The patient denied any allergy, and her family history was unremarkable. She was taking vitamin K antagonists for anticoagulation.
Upon presentation, the patient was apyretic and her blood pressure was 120/70 mmHg. She was comfortable at rest, New York Heart Association (NYHA) class III. Heart rate was 110 b.p.m. and oxygen saturation was 99% on room air. Her physical examination was characterized by prosthetic heart sounds with a 4/6 systolic murmur, diminished breath sounds in lung bases, mild hepatomegaly, moderate bilateral ankle oedema, and mild jugular venous distention.
Electrocardiogram on presentation showed sinus tachycardia at 105 b.p.m. with first-degree atrioventricular block. Arterial blood gas test showed compensated respiratory alkalosis. Lab tests showed mild microcytic anaemia (haemoglobin 11.8 g/dL, reference interval (RI) 12.5–14.0 g/dL) and an International Normalized Ratio of 4.13 (RI 0.80–1.16). Renal function and electrolytes were between normal ranges, while mild liver enzyme alterations were recorded (total bilirubin 3.8 mg/dL, RI 0.20–0.90 mg/dL). Brain natriuretic peptide was 401 pg/mL (RI 10–100 pg/mL). C-reactive protein and procalcitonine were both negative. Chest X-ray showed an enlarged heart with minimal bilateral pleural effusion.
The patient was hospitalized for heart failure and haemoptysis. Daily treatment with intravenous furosemide 40 mg and bisoprolol 1.25 mg was started. Haemoptysis was treated with inhaled tranexamic acid 500 mg twice a day and iced saline lavages. Warfarin was stopped; enoxaparin 6000 IU twice a day was started. Airway bleeding rapidly improved.
Chest computed tomography (CT) scans excluded pneumonia, bronchiectasis, and neoplasms. Pulmonary tuberculosis was ruled out with a negative sputum smear examination and negative molecular tests for Mycobacterium tuberculosis. Echocardiogram during sinus tachycardia showed normally functioning prosthetic aortic and mitral valves, a hyperdynamic left ventricular wall motion with above-normal ejection fraction. Right ventricular longitudinal function was preserved and the biological tricuspid prosthesis showed an increased transvalvular gradient (mean gradient 13 mmHg, ) and a mild-to-moderate regurgitation; pulmonary artery systolic pressure could not be estimated. Inferior vena cava (IVC) was dilated (22 mm) with reduced collapsibility. No echocardiographic finding was suspicious for infective endocarditis. Contrast chest CT scan excluded pulmonary embolism, arteriovenous malformations, and additional scans excluded possible mechanical valve obstruction, such as pannus or thrombi. It also revealed marked systemic venous hypertension, manifesting as dilation of venae cavae, suprahepatic veins, cardiac veins, and of the coronary sinus (). It showed also veno-venous shunts, as well as mild ascites and hepatomegaly. Right heart catheterization confirmed increased right heart pressures, severe bioprosthetic tricuspid valve stenosis (mean gradient 9 mmHg), elevated venous pressure in venae cavae, and a mean right atrial pressure of 22 mmHg (). The increase in venous pressures due to tricuspid stenosis caused veno-venous shunts, resulting in augmented venous pressure in the azygos vein and in the bronchial circulation, eventually leading to haemoptysis.
Severe symptomatic tricuspid stenosis was referred for surgery. Due to the high operative mortality and morbidity of redo tricuspid valve surgery, pre-operative evaluation was challenging. Eventually, due to the patient’s age and the possible long-term need for reoperation, we opted for a percutaneous approach. The patient underwent transfemoral tricuspid valve-in-valve replacement, using an Edward Sapien 3 (29 mm) bioprosthesis (). Early post-procedural echocardiogram showed a normally functioning bioprosthetic tricuspid valve, no paravalvular leakage, a mean transvalvular gradient of 4–5 mmHg (), and a slight reduction in IVC diameter (19 mm).
The patient was discharged asymptomatic in NYHA class I. Discharge medications included bisoprolol 1.25 mg, lansoprazole 30 mg, and warfarin. Complete resolution of airway bleeding was recorded. During a follow-up visit at 6 months, the patient denied any airway bleeding but complained of occasional palpitation. Echocardiogram at 6 months showed normally functioning tricuspid valve-in-valve bioprosthesis, mean transvalvular gradient 5 mmHg, no paravalvular leak; IVC diameter 12 mm.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [22, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': True, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 22 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4105,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5686933-1,Extracted,"A 31-year-old male patient presented to the emergency department with sudden onset of palpitations of 2 h duration. He has no history of chest pain, shortness of breath, or syncopal attack. He had experienced one similar episode 18 months previously that had responded to medical treatment in another hospital. No old medical report was available, and he could not recall what drugs he had been given. There was no significant past medical, family, or surgical history and he was not on any regular medication. He did not smoke and denied any use of alcohol or illicit drug.
Physical examination revealed blood pressure (BP) of 107/72 mm Hg and heart rate of 225 beats/min. On cardiac examination, S1 and S2 were normal, no murmurs, or additional sounds. The chest was clear on auscultation. ECG revealed a narrow complex tachycardia, RBBB, and LAD [].
Intravenous adenosine, amiodarone and beta blocker wee tried but failed to terminate the arrhythmia. Cardiology consultation was sought and a diagnosis of fascicular tachycardia was suspected based on ECG findings of narrow complex tachycardia, RBBB and LAD. Additional doses of intravenous verapamil were given which slowed down the heart rate to 170 beats/min. The ECG revealed tachyarrhythmias with AV dissociation which suppots that the origin of tachyarrhythmia was from the left ventricle []. After 12 hours, patient developed shortness of breath and dizziness associated with hypotension with BP 81/50 mmHg. An electrical cardioversion was attempted but failed to terminate the arrhythmia.
Subsequently, patient was admitted to the coronary care unit where serial ECGs were done. Laboratory tests revealed normal hemoglobin, liver function tests, renal function tests, serum electrolytes, and thyroid-stimulating hormone.
Initial transthoracic echocardiography during tachycardia revealed moderate global hypokinesia with left ventricular ejection fraction (LVEF) of 45%; other structures were normal. After obtaining informed consent, an electrophysiological study was performed. The electroanatomical bipolar voltage map did not show any area of the ventricular scar. The mechanism of the tachycardia was confirmed as reentry arising from the basal and mid septum. Multiple ablations were performed to the basal and mid septum, guided by Purkinje and P2 potential. The arrhythmia was terminated after ablation, and no arrhythmias could be induced after Isoprenaline administration. The final ECG showed sinus rhythm [].
After 24 hours, transthoracic echocardiography was repeated showing normal structures with normal LVEF of 60%. The patient was discharged from the cardiac department after 48 hours with cardiology follow up.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [31, 'years'], 'Hypertension history': False, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 31 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4106,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8515633-1,Extracted,"A 43-year-old nonalcoholic male, on treatment for type 2 diabetes for more than 6 years with oral hypoglycemic drugs, presented with worsening of glycemic control, weight loss (5 kg), and fatigability. However, due to these symptoms, he stopped all his medications about 6 months ago. The patient's body mass index was 19.5 kg/m2 with HbA1c ~ 12. Other investigations done showed that hemoglobin level, total leukocyte count, lipid profile, and renal function test were within normal limits except for mild elevation of liver function test (total bilirubin – 1.7; direct – 0.7; indirect – 1.0, and serum glutamic oxaloacetic transaminase – 54).
Since he was found to be a lean diabetic with no family history of type 2 DM, C-peptide level along with other routine investigations was done. Serum C-peptide at fasting (using chemiluminescence Immunoassay method) was 0.37 ng/ml (normal value: 0.8–3.5 ng/ml), so a possibility of autoimmune DM was thought and anti-insulin and anti-islet cell antibodies were tested which turned out to be negative. No excessive insulin resistance was noted as evidenced by HOMA-IR of 0.4. Further evaluation of pancreatic function revealed normal amylase and lipase levels. Deranged liver function prompted us to do an ultrasound abdomen to rule out the possibility of hepatic or gallbladder pathologies [].
Surprisingly, ultrasound showed atrophic pancreas, multiple tiny hyperechogenic foci with postacoustic shadowing noted in the head and body of the pancreas (suggestive of calcifications). The main pancreatic duct appeared dilated with an intraductal calculus seen []. No peripancreatic fat stranding or fluid collection was seen. Computed tomography (CT) confirmed chronic calcific pancreatitis [Figures and ].
The expensiveness of fecal elastase for evaluation of the exocrine function of the pancreas precluded the patient from doing it. However, indirect tests of pancreatic functions showed low Vitamin D level (25-hydroxycholecalciferol), i.e., 10.1 ng/ml (normal: 30–100), slightly increased prothrombin time (an indirect measure of Vitamin K) ~14.5 s (normal 10–14), and marginally lower spectrum of triglyceride to high-density lipoprotein ratio ~ 1.1, indicating fat malabsorption.
There was an ambiguity in classifying him as type I or II, as his anti-insulin and anti-islet cell autoantibodies were negative and he also did not have evidence of insulin resistance. Identification of CP by ultrasound made the diagnosis of pancreatogenic DM-type 3c possible. Henceforth, the management protocol was modified with addition of insulin, withdrawing oral hypoglycemic agents. He was also started on a modified low carbohydrate diet with Vitamin D and omega-3 supplements. The patient's glycemic control improved (HbA1c ~ 6) and weight increased by 5 kg within the next 4 months. Further follow-up after 2 months showed sustained glycemic control and weight gain.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [43, 'years'], 'Diabetes mellitus': True, 'obesity': False, 'hypercholesterolemia': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Hypertension history': False, 'Initial troponin': 'less than or equal to normal limit'}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 43 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: diabetes mellitus. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4107,18,HEART Score for Major Cardiac Events,risk,integer,usmle-10048,Extracted,"A 43-year-old Caucasian woman is admitted to the hospital with acute onset right upper quadrant (RUQ) pain. The pain started 6 hours ago after the patient had a large meal at a birthday party and has progressively worsened. She recalls having similar pain before but not so intense. No significant past medical history. Current medications are only oral contraceptive. Vitals are blood pressure 140/80 mm Hg, heart rate 79/min, respiratory rate 14/min, and temperature 37.6℃ (99.7℉). The patient’s BMI is 36.3 kg/m2. On exam, the patient appears slightly jaundiced. Her cardiac and respiratory examinations are within normal limits. Abdominal palpation reveals tenderness to palpation in the RUQ with no rebound or guarding, and there is an inspiratory arrest on deep palpation in this region. The remainder of the examination is within normal limits.
Laboratory tests are significant for the following:
RBC count 4.1 million/mm3
Hb 13.4 mg/dL
Leukocyte count 11,200/mm3
ESR 22 mm/hr
Platelet count 230,000/mm3
Total bilirubin 2 mg/dL
Direct bilirubin 1.1 mg/dL
ALT 20 IU/L
AST 18 IU/L
Amylase 33 IU/L
Ultrasound of the abdomen shows the following result (see image):
The common bile duct (CBD) (not shown in the image) is not dilated.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [43, 'years'], 'Hypertension history': True, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'obesity': True, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'Initial troponin': 'less than or equal to normal limit'}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 43 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: hypertension, obesity. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4108,18,HEART Score for Major Cardiac Events,risk,integer,usmle-9228,Extracted,"A 26-year-old pregnant woman (gravida 2, para 1) presents on her 25th week of pregnancy. Currently, she has no complaints. Her previous pregnancy was unremarkable. No abnormalities were detected on the previous ultrasound (US) examination at week 13 of pregnancy. She had normal results on the triple test. She is human immunodeficiency virus (HIV), hepatitis B virus (HBV), and hepatitis C virus (HCV)-negative. Her blood type is III(B) Rh+, and her partner has blood type I(0) Rh-. She and her husband are both of Sardinian descent, do not consume alcohol, and do not smoke. Her cousin had a child who died soon after the birth, but she doesn't know the reason. She does not report a history of any genetic conditions in her family, although notes that her grandfather “was always yellowish-pale, fatigued easily, and had problems with his gallbladder”. Below are her and her partner’s complete blood count and electrophoresis results.
Complete blood count
  Patient Her husband
Erythrocytes 3.3 million/mm3 4.2 million/mm3
Hb 11.9 g/dL 13.3 g/dL
MCV 71 fL 77 fL
Reticulocyte count 0.005 0.008
Leukocyte count 7,500/mm3 6,300/mm3
Platelet count 190,000/mm3 256,000/mm3
Electrophoresis
HbA1 95% 98%
HbA2 3% 2%
HbS 0% 0%
HbH 2% 0%
The patient undergoes ultrasound examination which reveals ascites, liver enlargement, and pleural effusion in the fetus. Further evaluation with Doppler ultrasound shows elevated peak systolic velocity of the fetal middle cerebral artery.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'parent or sibling with Cardiovascular disease before age 65': False, 'Hypertension history': False, 'smoking': False, 'Diabetes mellitus': False, 'age': [26, 'years'], 'atherosclerotic disease': False, 'obesity': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 26 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4109,18,HEART Score for Major Cardiac Events,risk,integer,pmc-3178521-1,Extracted,"A 61-year-old Caucasian woman, previously in good health, presented with a three-day history of feeling generally unwell with dizziness, vomiting, abdominal, left lower chest pain and shoulder pain. She denied any sore throat, feeling feverish or other symptoms suggestive of an influenza-like illness. There was no cough or sputum production. There was nothing in the history to suggest a recent viral or other infective process including human immunodeficiency virus or acquired immune deficiency state and no history of any trauma or injury. She had no significant previous medical or surgical history and was not taking any medications. There was no background or family history of cancer, hematologic or clotting disorders. She was a smoker of approximately 40 pack years and had unlimited exercise tolerance. She worked as a nurse and there was no history of previous exposure to asbestos or other occupational hazards.
On examination she was ill-looking, conscious and orientated with a blood pressure 89/49 mmHg, heart rate of 72 beats per minute, saturations 97% on a non-rebreather mask and temperature of 36.9°C. The admission examination revealed normal cardiac examination and bibasal inspiratory crepitations with left upper quadrant and epigastric tenderness on abdominal examination.
Her blood work-up on admission showed a hemoglobin level of 11.4 g/L, white cell count of 19 × 109/L with neutrophils of 17 × 109/L and a C-reactive protein of 7 mg/L. Urea and electrolytes, liver function and coagulation tests were in the normal range. A blood film examination did not reveal any atypical lymphocytes or other abnormalities. A posteroanterior and lateral chest radiograph was performed (Figure ).
Hemodynamic stability was achieved following rehydration with intravenous fluids. However, eight hours after admission she developed an acute abdomen with clinical signs of shock. Her blood pressure was 88/52 mmHg and heart rate 105 beats per minute. Further to that her oxygen saturations were 91% on a non-rebreather mask with a Glasgow coma scale of 14/15 (E = 4, V = 4, M = 6). Inspection revealed skin and conjunctival pallor. Clinical examination revealed new abdominal signs of generalized abdominal tenderness with guarding, rigidity and absent bowel sounds, consistent with an acute abdomen. A repeat test showed her hemoglobin level had dropped to 5.0 g/L.
She was stabilized with multiple blood transfusions and underwent an urgent computer tomography scan of her thorax and abdomen, which showed an 8.5 × 3.6 cm left hilar mass with extensive mediastinal adenopathy, bibasal small effusions and consolidation, and a large splenic hematoma of 15 × 12 cm with high attenuation suggestive of active bleeding (Figure , Figure and ). There was a lytic area affecting her T9 vertebra, which likely represented metastases rather than wedge fracture, but there were no abnormalities or neoplastic disease affecting the intra-abdominal organs.
Pneumococcal and meningococcal vaccines were administered and our patient was then promptly taken to theater for laparotomy. On examination of her internal organs at laparotomy, other than hemorrhage and rupture of her spleen, there was no other gross abnormality and no evidence of disease in her other intra-abdominal organs. She spent two days being ventilated in our intensive care unit and subsequently made a full recovery from the surgery. She was commenced on life-long penicillin V and was subsequently discharged home a week after admission, fully mobile and independent in terms of her activities of daily living.
Her splenic histology was negative for hematologic or other malignancy and no other pathology was identified. She then underwent a bronchoscopy; transbronchial needle aspiration revealed numerous malignant nodes consistent with non-small cell carcinoma. Histology of bronchial biopsies confirmed invasive adenocarcinoma. This was consistent with likely stage IV in view of the likely bone metastases found on CT. She was referred to the local oncologist and her case was discussed at the lung cancer multidisciplinary team meeting. In view of the diagnosis and staging, a palliative treatment pathway was agreed from the outset and our patient received palliative chemotherapy. She died five months after her presentation.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [61, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': True, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 61 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4110,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8607133-1,Extracted,"A 59-year-old male with past medical history of hypothyroidism, atrial fibrillation and atopic rhinitis presents to our tertiary care center for follow-up CT chest for incidentally detected pulmonary cysts on CT Chest Abdomen and Pelvis as part of a trauma workup. He was afebrile and had stable vitals. No history of smoking, dyspnea, chest pain, cough, fatigue or fever.
CT Chest (, , ) was performed which demonstrated multiple thin elliptical well-defined para-mediastinal air-filled cysts without internal structure, in a basilar distribution with preserved lung volume and no evidence of interstitial lung disease. The distribution pattern was concerning for cystic lung disease associated with Birt-Hogg-Dubé syndrome. The patient had no personal or family history of thyroid cancer, renal cancer or spontaneous pneumothorax.
He subsequently underwent genetic testing. Analysis of 106 gene revealed a pathogenic variant in the FLCN gene, FLCN c.1285dup (p.His429Profs*27) heterozygous, confirming the diagnosis of Birt-Hogg-Dubé syndrome.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [59, 'years'], 'Hypertension history': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 59 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4111,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8369973-1,Extracted,"A 50-year-old Hispanic male presented with moderate chest pain and discomfort that began the night prior to admission. On presentation, the patient was noted to have a fever of 39.5°C and found to be tremulous with marked altered mental status. Shortly after admission, the patient reportedly suffered multiple witnessed generalized tonic-clonic seizures for which he was emergently treated with lorazepam. The rest of the history could not be obtained from the patient due to his somnolent status. The family was therefore called at the patient’s bedside. They reported that the patient has a history of heavy alcohol consumption and was complaining of chest pain prior to presentation. They denied any history of seizures or patient noting any weakness or numbness prior to arriving to the hospital. Given the patient’s history of alcohol withdrawal, persistent fever and deteriorating clinical condition, the patient was taken to medical ICU for treatment of alcohol withdrawal. The patient did not have any other known chronic medical conditions. Initial complete blood count showed leukocytosis of 19.63 with bandemia and metabolic profile showed lactic acidosis. Initial electrocardiogram evaluation demonstrated sinus tachycardia with an unremarkable cardiac physical examination. Initial chest X-ray was unremarkable and non-enhanced CT of the head did not show any acute intracranial abnormalities. Ultrasound of the liver showed findings of hepatic steatosis, with patient having negative results for hepatitis panel, human immunodeficiency virus (HIV) and anti-nuclear antibody (ANA). The patient met systemic inflammatory response syndrome (SIRS) criteria with a heart rate of 108 beats per minute, fever of 39.5°C and leukocytosis of 19.63 for which reason two sets of blood cultures from different sites were collected for microbiological analysis and the patient was started on empiric piperacillin-tazobactam within hours of admission. Soon after initiating treatment for sepsis and alcohol withdrawal, patient’s altered mental status resolved, and his condition began to improve. Subsequent neurological exams done on the patient were all unremarkable with no signs of focal neurological deficits. Blood cultures subsequently grew multiple gram-negative rod species, later confirmed as various Salmonella spp. on two out of two plates at 12 and 24 hours, respectively. Antibody analyses revealed the following serotypes: Salmonella H, type-a, Salmonella H, type-b, Salmonella H, type-d, and Salmonella O, type-Vi. These findings prompted a transthoracic echocardiogram study which was unremarkable which led to a subsequent transesophageal echocardiogram (TEE). The TEE ultimately revealed a small 2.5 mm x 2.7 mm echo dense vegetation or mass observed on the aortic valve (Figure ).
Given the patient’s aortic native valve endocarditis and gram-negative non-HACEK etiology per the IDSA/AHA guidelines, the patient as started on dual therapy, which based on susceptibility resulted in a regimen of cefepime and levofloxacin. As per the ACC/AHA guidelines, the patient did not meet the criteria for surgical considerations. The patient did not meet the criteria of complicated IE, which included findings such as heart failure, intra-cardiac abscess or fistula, native valve S. aureus IE, or systemic embolization. Hence cardio-thoracic surgery input was not sought and prolonged antibiotic therapy was recommended []. After multiple negative blood cultures at 48 hours, along with clinical stabilization at the hospital the patient was discharged on oral levofloxacin 750 mg and IV cefepime 2 g twice daily for six weeks. At his six-week follow-up, the patient was asymptomatic, with negative blood culture and unremarkable labs at the end of therapy.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [50, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Moderately suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': True, 'atherosclerotic disease': False, 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 50 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 1 + 1 = 2.
The following risk factor(s) are present based on the patient's note: smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4112,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8257461-1,Extracted,"A 28-year-old Hispanic female with no comorbidities presented with sudden-onset, sharp chest pain, and shortness of breath for one day. She denied any cough, fever, chills, hemoptysis, calf swelling, or leg pain. She reported that she underwent liposuction at a local clinic two weeks prior to the onset of symptoms. She reported no family history of bleeding, clotting, or rheumatologic disorders, no drug allergies, and toxic habits. She had one healthy baby delivered vaginally five years ago. She was never on oral contraceptive medications.
On presentation, her pulse rate was 116 beats per minute and oxygen saturation was 98% on room air. Her body mass index (BMI) was 29. On examination, her breath sounds were decreased bilaterally due to pain. Her right lower extremity was swollen compared to the left lower extremity. Her neurological examination was normal and no skin rashes were noted. Her electrocardiogram revealed Q waves in lead III and S wave in lead I, in the setting of sinus tachycardia. Her laboratory tests showed a prothrombin time of 11.2 seconds, activated partial thromboplastin time of 51.9 seconds, D-dimer of 424 ng/mL, troponin T <12 ng/L, and pro-brain natriuretic peptide of 91 pg/mL. The Wells score was calculated to be 6. Doppler venous ultrasonography did not reveal any deep venous thrombus. Computerized tomography (CT) imaging of the chest revealed partially occlusive pulmonary emboli within the segmental and subsegmental branches of the right anterior lung basal arteries. This has been shown in Figure .
The CT scan also showed focal airspace opacities within the anterior basal segment of the right lower lobe, suggestive of a pulmonary infarct. This has been shown in Figure .
She was started on a heparin drip, which was later bridged to apixaban. She improved symptomatically and her heart rate normalized. Hypercoagulable workup has been presented in Table .
She was discharged on a three-month supply of apixaban and was advised to follow up in the hematology and rheumatology clinics for repeat testing as per current guidelines. However, the patient was lost to follow-up.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [28, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Diabetes mellitus': False, 'obesity': True, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 28 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: obesity. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4113,18,HEART Score for Major Cardiac Events,risk,integer,usmle-5839,Extracted,"A 55-year-old man presents to his primary care physician for trouble swallowing. The patient claims that he used to struggle when eating food if he did not chew it thoroughly, but now he occasionally struggles with liquids as well. He also complains of a retrosternal burning sensation whenever he eats. He also claims that he feels his throat burns when he lays down or goes to bed. Otherwise, the patient has no other complaints. The patient has a past medical history of obesity, diabetes, constipation, and anxiety. His current medications include insulin, metformin, and lisinopril. On review of systems, the patient endorses a 5 pound weight loss recently. The patient has a 22 pack-year smoking history and drinks alcohol with dinner. His temperature is 99.5°F (37.5°C), blood pressure is 177/98 mmHg, pulse is 90/min, respirations are 17/min, and oxygen saturation is 98% on room air. On physical exam, you note an overweight man in no current distress. Abdominal exam is within normal limits.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'Hypertension history': True, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': True, 'obesity': True, 'smoking': True, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 55 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, obesity, smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 4 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 1 + 2 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4114,18,HEART Score for Major Cardiac Events,risk,integer,pmc-3410002-1,Extracted,"A 50-year-old female presented with history of sudden onset weakness of right upper and lower limb for 1 day with deviation of angle of mouth to the left side. There was no history of headache, vomiting, seizures, or previous history of stroke or transient ischemic attacks. Also there was no history of chest pain, palpitations, or any cardiac disease. She is not a diabetic or hypertensive and there was no other comorbid illness. Her general examination revealed a pulse rate of 180/ min, regular, low volume, and blood pressure of 130/80 mmHg. The central nervous system examination showed normal higher mental functions, right upper motor neuron facial nerve palsy, and muscle power of 3/5 in upper limbs, 2/5 in lower in lower limbs with right extensor plantar response. The examination of other systems was normal. The laboratory investigations revealed normal liver and renal function tests. The serum calcium, magnesium, and potassium levels were normal. The serum troponin T and creatine phosphokinase levels were normal. The CT brain revealed left middle cerebral artery territory infarct measuring around 2×3 cm.
Our patient presented to the emergency medical services department within 8 h of acute stroke. Her ECG showed regular narrow QRS complex long RP tachycardia at a rate of 186 beats per minute (bpm) with inverted p waves in lead III []. She had a normal study on echocardiography without structural changes or thrombus. On intravenous injection of 6 mg of adenosine, the patient transiently developed complete atrioventricular block but the atrial rate was persisting at the same 186 bpm with regular p waves separated by isoelectric baseline [] which reverted back to AT within a minute []. A diagnosis of atrial tachycardia was made and she was started on verapamil 40 mg three times daily orally. Following one dose of verapamil she developed sinus bradycardia (50 bpm). So verapamil was withheld and she was monitored in intensive care unit. In the following 1 week, she did not had any other episode of arrhythmia. Considering her elderly age, she was advised to undergo electrophysiological study to know whether she has any substrate for inducible arrhythmia but she did not consent for that. The ECG took before discharge showed normal sinus rhythm (64 bpm), with occasional premature atrial complex. One month later, she came for follow up and she did not report any palpitation and her ECG was in normal sinus rhythm with rate of 68 bpm.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [50, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 50 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4115,18,HEART Score for Major Cardiac Events,risk,integer,pmc-3318852-1,Extracted,"A 65-years-old male patient presented to emergency department with complaints of progressive dyspnea, dysuria, and change in mental status in last six hours. The patient had a history of hypertension, type-2 diabetes mellitus, coronary artery disease, hypertriglyceridemia, peripheral vascular disease, chronic pancreatitis, gastroesophageal reflux disease, chronic back pain and depression. Surgical history included left popliteal-femoral bypass and coronary artery stenting. He had 25-pack-years history of smoking, but denied significant alcohol or illicit drug use. His customary medications were lantus insulin, glimeperide, verapamil, losartan, aspirin, rosuvastatin, fenofibrate, cilostazole, esomeprazole, dicyclomine, eszopiclone, venlafaxine, alprazolam, testosterone lotion, and hydrocodone-acetaminophen.
On physical examination, he was alert but not oriented, and in severe respiratory distress. Blood pressure (BP) was 160/94 mmHg in right arm, pulse rate was 140 per minute, respiratory rate was 30 breaths per minute, and temperature was 38.4oC. The Oxygen saturation via pulse oximeter was 86% while the patient was breathing 100% O2 by non-rebreather mask. There was decreased air movement at both lung bases, and consolidation at right lung base. Cardiac examination showed no abnormalities except tachycardia. The remainder of the examination was unremarkable.
The initial labs and arterial blood gas (ABG) analysis are shown in and . Serum lactate at the beginning was elevated at 4.1 mmol/L (normal: 0.5-1 mmol/L). Initial electrocardiogram showed sinus tachycardia with rate of 144 beats per minute. A chest radiograph showed increased interstitial markings and right lower lobe infiltrates (). Urine analysis study revealed presence of urinary tract infection and results are shown in . He was immediately started on fluid replacement, intravenous (IV) antibiotics which included levofloxacin, piperacillin/tazobactam and vancomycin, and high flow oxygen, and was transferred to medical intensive care unit (ICU) for further care.
Later on, patient went into severe respiratory distress, and endotrachial intubation was performed. Soon after intubation, patient went into pulseless electrical activity, and a code blue was called. Cardio-pulmonary resuscitation was performed as per standard protocol for 15 minutes, and patient came back to sinus rhythm. After the code, patient was hypotensive and required three vasopressors including epinephrine, norepinephrine and dopamine to maintain systolic BP more than 90. Oxygen saturation was 90% on 100% FiO2. After one hour, patient again went into cardiac asystole, then ventricular fibrillation, and then pulseless electrical activity. Successful resuscitation was done for 15 minutes. After this second code, the systolic BP was in 80s, and IV phenylephrine was added. Hear rate was 146 beats per minute, and oxygen saturation 88% on 100% FiO2. The laboratory results showed lactate level of 12.1 mmol/L; transaminase in 1000's and blood urea nitrogen and creatinine of 53 mg/dl and 4.9 mg/dl respectively. Serum troponin level was 2.92 ng/ml (normal ≤ 0.04 ng/ml). Arterial blood gas (ABG) revealed worsening metabolic acidosis.
An emergent two-dimensional echocardiogram was obtained and revealed normal left and right ventricular function. His left ventricular ejection fraction was found to be 50%, and there was no pericardial effusion, or right ventricular strain. Patient was started on IV hydrocortisone, and anidulafungin was added to cover for fungal pathogens. A decision was also made to start patient on activated protein C infusion considering high risk of death. In addition, bicarbonate drip was also started.
Twelve hours after his admission to this hospital, patient started showing signs of anoxic brain injury. At that time, he was on maximum doses of five vasopressors, but was still hypotensive and tachycardic. The oxygen saturation decreased to 88% on 100% of FiO2. ABG at that time is shown in . Family meeting was called, and they requested for withdrawal of care. Thirty minutes later, care was withdrawn and patient expired within 10 minutes of extubation and stopping IV medications. Family refused autopsy. The next day, two out of four blood cultures were positive for Escherichia coli.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [65, 'years'], 'Hypertension history': True, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': True, 'Diabetes mellitus': True, 'smoking': True, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Suspicion History': 'Slightly suspicious', 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",6,6,6,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 65 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 0 + 2 = 2.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, smoking, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: obesity, family with cvd. The following risk factor(s) are missing from the patient's data: obesity, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 4 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 2 + 2 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 4 + 2 = 6.
Based on the patient's data, the HEART Score is 6."
4116,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5358128-1,Extracted,"An eighty-one-year-old woman without significant cardiovascular risk factors presented to the emergency department with chief compliant of acute onset of severe pressure-like, left-sided chest pain as she was walking back from church in the afternoon. It was associated with nausea but no vomiting, shortness of breath, diaphoresis, or palpitations. Prior to the onset of these symptoms she had been in her usual state of health and denied any cardiac complaints.
Her past medical history was significant for asthma, arthritis, and immune thrombocytopenic purpura (ITP) diagnosed one year ago by bone marrow biopsy with baseline platelet level 50,000 per µl requiring no treatment. She reported allergic reaction to aspirin which caused respiratory impairment and never underwent desensitization.
Upon arrival in the Emergency department chest pain had resolved. She was 5 feet 1 inch and 188 lbs; initial vital signs were blood pressure of 149/79 mmHg and heart rate of 88 bpm. The physical exam including cardiac exam was unremarkable. The electrocardiogram (ECG) () revealed sinus rhythm with premature atrial and ventricular contractions, ST Elevation and Q waves in II, III, and aVF and tall R wave in V2 consistent with infero-post wall MI, STEMI. Laboratory results were significant for platelet count of 34,000 per µl, decreasing from baseline 50K (without any prior history of bleeding), and cardiac enzymes were as follows: Troponin I initial 0.3929 ng/ml and peaked at 10.9 ng/ml; Creatine Kinase (CPK) 666 U/L and peaked at 800 U/L with CK-MB and CK Index of 54.5 ng/ml and 7.9 respectively. The remainder of laboratory results, including coagulation profile, was normal at this time. The patient received Plavix 600 mg PO, Metoprolol 25 mg orally. An unfractionated heparin was used, with a loading dose of 5,100 international units (IU) intravenously then a continuous intravenous infusion of 13 U/hr with baseline PTT of 33.7 seconds, and transdermal nitroglycerin patch was placed during the emergency department course. Subsequent ECGs () showed formation of Q waves and normalization of the ST-T changes, decision was made to medically treat the patient for the STEMI and plan for cardiac angiography since the patient was chest pain free.
The patient later underwent diagnostic coronary angiography via radial approach which revealed a 90% occlusion of the mid right coronary artery (RCA) with a TIMI 1 antegrade flow as well as thrombus formation (). It also revealed a 70% stenosis in the mid left circumflex (LCx) with an aneurysmal segment, a 75% stenosis in the proximal left anterior descending (LAD), a 70% stenosis in the diagonal (D2) ostium, and non-obstructive disease in the left main. The radial artery approach was uneventful, with the patient having a small proximal hematoma (1 cm x 2 cm approximately) that resolved with pressure dressing and warm compresses within the next 48 hours. Because the patient was stable and had history of aspirin allergy, she underwent aspirin desensitization while being on medical treatment pending staged percuteous coronary intervention (PCI) and stenting to the mid RCA lesion via femoral artery access. Later, the patient underwent successful desensitization of the aspirin and was started on a daily dose of 81 mg of aspirin. Repeat coronary angiography by femoral approach was performed for the PCI and bare metal stent was implanted in the mid RCA without any complications. The procedure was successfully concluded and final flow was TIMI 3 (). Her platelet level post-procedure upon discharge was 32,000 per µl and had ranged from 20K to 30K. The patient continued to tolerate aspirin 81 mg PO daily and Clopidogrel 75 mg PO daily three months post-procedure with stable platelet count.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [81, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'obesity': True, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False}",7,7,7,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 81 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 2 + 2 = 4.
The following risk factor(s) are present based on the patient's note: obesity, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 4 + 1 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 5 + 2 = 7.
Based on the patient's data, the HEART Score is 7."
4117,18,HEART Score for Major Cardiac Events,risk,integer,usmle-8096,Extracted,"A 45-year-old man presents to the physician with a complaint of recurrent chest pain for the last 2 weeks. He mentions that the pain is not present at rest, but when he walks for some distance, he feels pain like a pressure over the retrosternal region. The pain disappears within a few minutes of stopping the physical activity. He is an otherwise healthy man with no known medical disorder. He does not smoke or have any known dependence. There is no family history of ischemic heart disease or vascular disorder. On physical examination, his vital signs, including blood pressure, are normal. The diagnosis of coronary artery disease due to atherosclerosis is made.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'years'], 'Hypertension history': False, 'Suspicion History': 'Moderately suspicious', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 45 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 1 + 1 = 2.
The following risk factor(s) are present based on the patient's note: atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4118,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7966959-1,Extracted,"The proband was a 33-years-old male (FM 1), who was diagnosed with acute ST-elevated MI 5 months ago. Emergency coronary angiography showed that 60 to 80% obstruction of left anterior descending artery (LAD) and 50% stenosis of left circumflex artery (LCX) (). The patient was presented to our hospital due to chest pain and fatigue during physical exercise recurrently. Electrocardiogram and laboratory cardiac enzyme test were all normal. The myocardial perfusion tomographic imaging (adenosine) revealed transverse, coronal, and sagittal planes showing areas of reduced radioactivity distribution in the basement of the posterior lateral wall of the left ventricle. His hyperlipidemia was first diagnosed at age 28, he had taken atorvastatin (10 mg, q.d.) irregularly since then for 4 years, and the LDL-C level ranged between 2.6 to 3.8 mmol/L. Unexpectedly, his LDL-C level rose to 6.18 mmol/L 1 month before MI owing to drug withdrawal ().
His mother experienced lethal MI at the age 50. She was also diagnosed with type 2 diabetes mellitus (T2DM) and hypertension. His several maternal aunties had hyperlipidemia and one of them was died of MI at the age 41. His father had T2DM at age 50. His sister was diagnosed of hypertension, T2DM, and hyperlipidemia at age of 29.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [33, 'years'], 'Suspicion History': 'Highly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': True, 'parent or sibling with Cardiovascular disease before age 65': True, 'atherosclerotic disease': True, 'Initial troponin': 'less than or equal to normal limit', 'Hypertension history': False, 'Diabetes mellitus': False, 'obesity': False, 'smoking': False}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 33 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: family with cvd, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4119,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7269878-1,Extracted,"A 42-year-old woman with an unremarkable medical history was admitted with recent onset of dyspnea on exertion. Physical examination, electrocardiography, chest radiography, and blood tests revealed no abnormalities. Transthoracic echocardiography revealed a cyst-like structure attached to the interatrial septum, protruding into the right atrium. This mass measured 2.9 × 2.2 cm and showed well-defined margins (). Computed tomography (CT) revealed a well-defined, homogeneous hypodense mass in the low interatrial septum (). CT angiography revealed no feeding vessels from the coronary arteries.
Surgical excision of the cystic tumor was planned, and the patient underwent standard median sternotomy and cannulation of the ascending aorta and the superior and inferior vena cava. Cardiac arrest was induced with cold blood cardioplegia. The right atrium was opened and a 2.5 cm round cyst with a smooth surface was identified in the fossa ovalis (). The mass was completely excised from the interatrial septum and the resultant atrial septal defect after cyst resection was repaired using an autologous pericardial patch. Weaning from extracorporeal circulation was uneventful. The cyst contained whitish-yellow colored mucous fluid. The patient’s postoperative course was uneventful, and she was discharged on the 10th postoperative day. The patient is asymptomatic without any evidence of recurrence over 2-year’s follow-up.
Histopathological examination of the resected cyst showed that it was lined with pseudostratified ciliated columnar epithelium, and the findings were consistent with a bronchogenic cyst without any evidence of malignancy ().",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [42, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 42 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4120,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6926137-1,Extracted,"A 58-year-old female presented with chronic history of exertional shortness of breath for 2 years. The patient had negative past medical and surgical histories, and the family history was positive for hypertension and diabetes mellitus.
The drug history, family for any genetic disorders, and psychosocial history were non relevant.
Clinical findings: The patient had normal general clinical examination with normal vital signs. Auscultation of the chest revealed a diastolic mummer.
Diagnostic assessment: Echocardiography showed mitral valve stenosis. Coronary angiography showed normal coronaries, but abnormal course of right coronary artery.
Patient started on medical therapy for 3 months for symptomatic mitral valve stenosis, but her symptoms continues. The echocardiography was repeated which detected an abnormal lesion in the right ventricle, further assessment was suggested. Computerized tomography scan of the chest was done and a big complicated hydatid cyst arising from the wall of the right ventricle was discovered. .
Decision of surgery done, and the plan of surgery was to do median sternotomy, excision of the hydatid cyst, and repair of mitral stenosis by commissurotomy. Isolation of the hydatid cyst from the surgical field was done using surgical sponges soaked with chlorhexidine solution. The cyst was involving the muscular layer of the right ventricle, excision of the cyst was done and cavity of hydatid cyst was marsipulized and patient weaned from cardiopulmonary bypass. , .
The operation was performed by two cardiac surgeons who are specialized in the field of cardiac and vascular surgery.
Postoperative echocardiography showed normal right ventricular function, mild valve mitral stenosis. Patient put on three cycles of albendazole for three months.
No specific post intervention considerations were undertaken, but the patient was informed about the importance of regular visits and follow-up.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [58, 'years'], 'Hypertension history': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 58 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4121,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5727695-1,Extracted,"An 83-year-old woman with diabetes mellitus type 2, essential hypertension, and hyperlipidemia came to the emergency department with history of 3 days of progressive cough and shortness of breath and 1 day of pressure-like chest pain and anxiety. She did not have a history of smoking. Initial physical examination revealed a patient in severe respiratory distress. Oxygen saturation (O2Sat) was 94% with a nonrebreather mask at 80% FIO2 and cardiovascular examination revealed a soft 2/6 holosystolic murmur located in the left sternal border, without gallops. Diffused rales were auscultated in both lung fields. The rest of examination and vital signs were unremarkable.
ABG analysis showed acute respiratory alkalosis with moderate hypoxemia and laboratory panels including complete blood count, electrolytes, and troponins were within normal limits. Electrocardiogram (ECG) was normal; chest X-ray and chest computed tomography angiography exhibited diffuse interstitial ground-glass opacities bilaterally suggestive of pulmonary edema and no filling defects ruling out pulmonary embolism. The patient was transferred to the Intensive Care Unit for close monitoring and treated with bilevel positive airway pressure and intravenous diuretics demonstrating a slight clinical improvement; however, hypoxemia persisted and orthodeoxia was identified. O2Sat decreased significantly from 91% in decubitus to 86% when adopting a sitting position.
Echocardiography (TTE) showed ejection fraction 50–55% with RVSP 63 and a slightly positive agitated saline contrast test (ASCT) consistent with an interatrial shunting. Transesophageal echocardiography (TEE) was performed showing a positive interatrial communication; nevertheless, images were inconclusive to further evaluate and to determine the precise location of this interatrial defect due to suboptimal echocardiographic images. Cardiac magnetic resonance was not definitive for the presence of an atrial septal defect. Coronary computed tomography angiography was recommended and exhibited mild nonobstructive coronary atherosclerosis and nonspecific pulmonary vascular congestion with no evidence of atrial septal defect or an unroofed coronary sinus.
Decision was made to clarify the diagnosis with a right heart catheterization and intracardiac echocardiography, which revealed an intact interatrial septum with an evident PFO. An absent “step up” in saturation ruled out a left-to-right shunt. A TTE with ASCT was repeated and performed in reversed Trendelenburg position demonstrating a strongly and obvious right-to-left shunt through a PFO (). The defect was emergently closed using an 18 mm Amplatzer Cribriform Septal Occluder (). The patient expressed sudden severe chest pain after the procedure. ECG exhibited ST-segment elevation in leads II, III, and aVF, followed by a significant decrease in the mean arterial pressure. Bedsides ultrasonography showed proper device position and no cardiac tamponade was noted. Intra-aortic balloon pump was inserted for hemodynamic support and vasopressors were started. A right coronary artery air embolism was suspected; therefore a coronary angiogram was performed and showed no abnormalities. Left ventricular angiogram and aortogram were within normal parameters.
The patient stabilized with resolution of chest pain and normalization of the ECG changes and became normotensive. A TTE was repeated showing normal left ventricle function, no evidence of pericardial effusion, and no wall motion abnormalities. The patient remained hemodynamically stable, vasopressors were weaned off, and the intra-aortic balloon pump was removed. The patient experienced a positive outcome with complete resolution of respiratory failure with low requirements of oxygen therapy. The patient was discharged to home saturating 98% on room air.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [83, 'years'], 'Hypertension history': True, 'Suspicion History': 'Moderately suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': True, 'Diabetes mellitus': True, 'smoking': False, 'atherosclerotic disease': True, 'Initial troponin': 'less than or equal to normal limit', 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 83 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 1 + 2 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 3 + 2 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 5.
Based on the patient's data, the HEART Score is 5."
4122,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6861042-1,Extracted,"A 25-year-old female with no past medical or surgical history presented to the emergency department with a complaint of intermittent epigastric and abdominal pulsation sensation that she had been experiencing for the prior year. An abdominal aorta ultrasound showed no evidence of aneurysm or dissection, but a 3.9-centimeter, echogenic tubular structure was found in the distal abdominal aorta consistent with a retained catheter fragment ( and ). The patient reported that she was born premature at seven months at an outside hospital. Given her history and the ultrasound findings, there was high suspicion for a retained fragment of an umbilical catheter in her aorta. Vascular surgery was consulted. The patient was seen in clinic but was later lost to follow-up before further imaging and treatment.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [25, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 25 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4123,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4421607-1,Extracted,"A previously healthy 54-year-old white man, with no family history of kidney disease, came to our attention with a 4-h history of excruciating chest pain, irradiated to both upper limbs and, later, to the thighs, associated with tremor; pain had begun 2 h after consuming a meal, shared with other family members, which included roasted quails which had been shot in a rural area the end of September, (2 months earlier) and stored in a deep freezer; he was not taking any medications and denied having had fever, traumas or having done strenuous exercise, but admitted being a heavy smoker (∼25 cigarettes/day). His past medical history included only a diagnosis of borderline hypertension, made 1 year earlier, treated with a low-sodium diet alone. On admission, physical exam was unrevealing, except for proximal muscle tenderness on palpation; his blood pressure was 210/130 mmHg, oxygen saturation 97% in ambient air and his body temperature was 36.6°C. An electrocardiogram showed sinus tachycardia with no other abnormalities; in order to rule out aortic dissection, a computed tomography scan of the thorax and abdomen was performed, which showed mild chronic lung disease, cysts of the liver and both kidneys and no evidence of aortic dissection. Lab testing on admission demonstrated signs of severe rhabdomyolysis, with preserved renal function. displays the time course of muscle enzyme levels, serum creatinine and other relevant parameters. A toxicology screen for substances of abuse was negative on admission. HIV, as well as B and C hepatitis markers were negative. The patient’s urine (pH 6.5) was reddish brown and tested strongly positive (+++) at the benzidine test; mild proteinuria (2+ dipstick) was also present, whereas the urine sediment was unremarkable. The patient was immediately hydrated intravenously (3500 mL normal saline/24 h); his symptoms subsided within 24 h, the urine cleared after 48 h and he was dismissed on the fourth day, after an uneventful hospital course. The patient was again seen 1 week later, and all lab tests (including renal function and muscle enzymes) had returned to normal.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'Hypertension history': True, 'smoking': True, 'Suspicion History': 'Highly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'obesity': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit'}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 54 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 3 + 1 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 4.
Based on the patient's data, the HEART Score is 4."
4124,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8080730-1,Extracted,"A 46-year-old woman with a family history of ADPKD presented to our emergency department with acute chest pain.
Her chest pain lasted for 1 day and radiated to the back of her left shoulder.
Her ADPKD had affected kidney function (eGFR: 15.98 mL/min/1.73 m2), and she exhibited extrarenal features of polycystic liver as shown in Figure .
She had no cardiovascular risk factors except a long history of hypertension and emotional stress. Blood pressure at admission was 142/70 mmHg.
Auscultation revealed that the heart sounds were normal, without rales in the lungs.
At the emergency department, her troponin I was 0.268 ng/mL and the peak value during hospitalization was 1.928 ng/mL. Hematological examination found no signs of inflammation and anemia. The low-density lipoprotein cholesterol was 3.32 mmol/L, High density lipoprotein cholesterol cholesterol was 1.10 mmol/L, total cholesterol was 4.07 mmol/L, triglyceride was 0.82 mmol/L, and body mass index was 21.87 kg/m2.
Her initial electrocardiogram in the emergency room was normal without any changes in ST segment and T wave (Figure ). Transthoracic echocardiography revealed mild dilation of the left atrium (left atrium inner diameter 42 mm), normal left ventricular ejection fraction (62%), and mild mitral regurgitation.
After three days of antiplatelet therapy, we performed coronary angiography which found no obvious characteristics of coronary dissection (Figure and ). Given the particularity of the patient, IVUS examination was performed at the same time to further examine the condition of her coronary artery. Interestingly, obvious IMH formation from the distal to proximal was found in the left circumflex (Figure ). IVUS was also performed on the left anterior descending artery, and found only a few atherosclerotic plaques (Figure ).",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'parent or sibling with Cardiovascular disease before age 65': True, 'Suspicion History': 'Moderately suspicious', 'Hypertension history': True, 'smoking': False, 'Diabetes mellitus': False, 'age': [46, 'years'], 'Electrocardiogram Test': 'Normal', 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'hypercholesterolemia': True, 'obesity': False, 'Transient Ischemic Attacks History': False}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 46 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 1 + 1 = 2.
The following risk factor(s) are present based on the patient's note: hypertension, family with cvd. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4125,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8069519-1,Extracted,"Sudden onset chest pain.
A previously healthy 33-year-old Hispanic female with no significant medical history presented to the emergency room with sudden onset of chest pain while she was cooking dinner. The pain originated in the neck area on the left side and mid-back region, radiated to the anterior chest, was 10/10 intensity, pressure-like, lasted for 15 min, and resolved with aspirin. Chest pain was associated with nausea, vomiting, diaphoresis, shortness of breath, and lightheadedness. A month ago, she delivered her third child by normal vaginal delivery at 37 wk of gestation. The review of systems was otherwise unremarkable.
The patient had no prior history of coronary artery disease, aortic dissection, or pulmonary embolism.
She had no significant social history including smoking, alcohol or recreational substance use. She denied use of any over the counter medicines and denied use of any hormonal contraceptives before. Her only medications included prenatal vitamins and iron supplements. There was no history of sudden cardiac death or early myocardial infarction in the family.
Her physical examination was unremarkable. Blood pressure was 104/56 mmHg and heart rate was 82 beats per minute. Equal intensity pulses were palpable in both arms. There were no cardiac murmurs, jugular venous distension, crackles on auscultatory lung areas, and pedal edema.
Laboratory markers showed low hemoglobin of 11.6 g/dL (normal 12-15.5 g/dL) , white blood cell count of 6 × 109 cells/L, creatinine of 0.6 mg/dL, ESR of 16 mm/h (normal range, 0-20 mm/h) and CRP of 2.7 mg/L (normal range, 0-10 mg/L). Serial Troponins (Troponin T) were abnormal and trended up from 0.01 ng/mL and peaked at 15.5 ng/mL.
Her initial electrocardiogram (EKG) was normal. Subsequent EKGs showed dynamic T wave inversions. Chest radiography did not reveal mediastinal widening or any fractures and dislocations. Transthoracic echocardiogram revealed 48% LVEF, moderate-sized apical wall motion abnormality with akinesia of the anteroseptal segments.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [33, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Highly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'greater than three times normal limit', 'hypercholesterolemia': False, 'obesity': False}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 33 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 2.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 2 + 2 = 4.
Based on the patient's data, the HEART Score is 4."
4126,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4994762-1,Extracted,"A 77-year-old retired army service man with past history of hypercholesterolaemia and previous tuberculosis presented to the Emergency Department having briefly lost consciousness. On recovering, he was aware of a chest discomfort with radiation to the back and neck. He was an ex-smoker. Initial assessment revealed an irregular pulse with a rate between 30 and 50 bpm and a blood pressure of 103/56 mmHg. Cardiac examination was unremarkable with no murmurs heard and the jugular venous pressure was not raised. Auscultation of the chest was also unremarkable. He had different blood pressures between left (103/56 mmHg) and right arms (76/59 mmHg). His ECG revealed atrial fibrillation, a new finding, partial right bundle branch block and left axis deviation but no other ischaemic changes. A CT aortogram excluded aortic dissection and pulmonary embolus. Blood tests revealed an initial troponin T of 96 ng/l (normal < 14), which subsequently rose to 1088 ng/l. He was treated as an acute coronary syndrome. Echocardiography revealed mild left ventricular impairment with lateral wall hypokinesis and no evidence of intra-cardiac thrombus. Whilst on the ward he complained of intermittent chest discomfort and we proceeded to coronary angiography 48 h after admission, which revealed an unobstructed left main stem and minor irregularities within the left anterior descending artery. The right coronary artery was co-dominant and unobstructed. However, the left circumflex (LCx) artery was co-dominant and there was a large area of solid thrombus covering a 2 cm stretch of the artery. Given the history of atrial fibrillation we felt that this most likely represented an embolic occlusion. A guide wire was placed across the occlusion and the thrombus was aspirated successfully with an aspiration catheter. A significant amount of red thrombus was obtained. Subsequent angiographic images of the LCx revealed a completely smooth normal looking artery without any area of stenosis or irregularity. The patient remained well following his procedure and was discharged on apixaban 5 mg twice daily, atorvastatin 80 mg daily, bisporolol 2.5 mg daily, clopidogrel 75 mg daily and ramipril 1.25 mg daily.
There was no evidence of an atrial septal defect or suspicion of a patent foramen ovale on the trans-thoracic echocardiogram thus making the diagnosis of an embolic coronary embolus secondary to atrial fibrillation and possibly thrombus in the left atrial appendage the most likely cause of his myocardial infarction.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [77, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': True, 'smoking': True, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",8,8,8,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 77 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 2 + 2 = 4.
The following risk factor(s) are present based on the patient's note: hypertension, smoking, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 4 + 2 = 6.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 6 + 2 = 8.
Based on the patient's data, the HEART Score is 8."
4127,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8349522-1,Extracted,"A 60-year-old male non-smoker, non-diabetic, and normotensive patient was referred to our center with a history of retrosternal chest pain and dyspnea [New York Heart Association (NYHA) class IV] for two days. The patient had a history of exertional dyspnea and angina (NYHA class II) for the past year, but he was neither on any sort of medication and nor had consulted any physician for the same. The patient denied any past history of fever, joint pain, limb claudication, trauma to the chest. He was a farmer by occupation, and prior to this visit, there was no history of any medication or procedure done on him. On physical examination, his blood pressure was 100/70 mmHg, pulse was 100/minute, and regular in rhythm. The rest of the cardiovascular examination was unremarkable. An electrocardiogram at admission showed sinus rhythm with ST elevation in inferior leads (lead III/aVF) along with reciprocal ST depression in lead I, aVL, and V5-V6 (Figure ). The cardiac biomarkers were significantly elevated. Initial imaging with chest X-ray revealed cardiomegaly with enlarged right heart border (Figure ), and 2D-echocardiogram demonstrated inferior wall hypokinesia with mildly reduced left ventricular systolic fraction and a well-circumscribed cystic mass adjacent to the right ventricle (Figures , ). The routine biochemistry findings are provided in Table .
Angiogram of the left coronary system (Figures -; Videos , ) showed significant left main stenosis with a GCA arising from proximal LAD (Figures -) with Thrombolysis in Myocardial Infarction (TIMI) grade II flow distal to the aneurysm. Diffuse significant lesions in the proximal left circumflex artery and its major branches were also observed.
The ostium of RCA could not be engaged selectively despite several attempts, and a nonselective angiogram revealed occlusion of RCA from the ostium with mild disease in the conal branch of RCA arising from a separate ostium (Figure , Video ).
Subsequently, contrast-enhanced CT (CECT) of the thorax and coronary CT revealed a partially thrombosed giant aneurysm (80 x 60 mm) arising from the proximal RCA (Figure ), compressing the proximal segment of RCA against the aortic wall and causing occlusion from the ostium and a giant saccular coronary aneurysm (30 x 30 mm) arising from the proximal segment of LAD. No other abnormality was noted in the aorta and other major vessels, nor any signs of vasculitis were detected.
The patient was counseled on the need for surgical intervention for his treatment, but he opted for medical management only. He was treated with guideline-directed medical therapy including anticoagulation and was discharged in a hemodynamically stable condition. The follow-up data was not available at the time of writing this case report.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [60, 'years'], 'Hypertension history': False, 'Suspicion History': 'Moderately suspicious', 'Diabetes mellitus': False, 'smoking': False, 'Initial troponin': 'greater than three times normal limit', 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 60 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 1 + 1 = 2.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 2.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 2 + 2 = 4.
Based on the patient's data, the HEART Score is 4."
4128,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6984153-1,Extracted,"A 4-year-old male was brought to the outpatient clinic complaining of vision loss. The mother noticed clumsiness, constant eye rubbing, head tilting and covering one eye, holding things close to his face, and occasional ocular pain. He was diagnosed at birth with 47, XYY syndrome by clinical findings and karyotyping. Other comorbidities were asthma diagnosed at 2 years, under control, the rest was unremarkable. There was no family history suggestive of any genetic diseases. On exam, macroscopically there were no conjunctival injection or epiphora; the ocular range of movements was normal. The pupils were round and reactive with normal reflexes. Right-eye refraction was −6.00 −1.00 × 30°, and left-eye was −5.00 −1.50 × 20°. We did not perform visual acuity and peripheral vision exams due to an underaged uncooperative patient. Under anesthesia, we observed a translucent right cornea with a horizontal diameter of 12.5 mm, a well-formed narrow anterior chamber (depth 1.04 mm), closed iridocorneal angle in 360°, round translucent crystallin protruding anteriorly, and intraocular pressure of 26 mm Hg (Fig. , ). Left eye examination evidenced a corneal horizontal diameter of 11.5 mm with an open iridocorneal angle in all four quadrants. Additionally, multiple iridian processes with a posterior embryotoxon in the temporal sector were present. The intraocular pressure on tonometry was 14 mm Hg. Fundoscopic examination revealed an excavated papilla of 90% OD and 40% OS with no other retinal or macular changes. Based on these findings, we diagnosed right microspherophakia with phacomorphic glaucoma. We performed phacoemulsification and aspiration of the lens with posterior capsulotomy and anterior vitrectomy. An intraocular lens (IOL) was implanted in the capsular bag. Despite a successful IOL position, the patient continued with increased right intraocular pressure postoperatively. Three weeks later, we decided to place an Ahmed valve implant for intraocular pressure control. During follow-up, the right intraocular pressure remained within normal limits. No additional intraocular pressure-lowering drugs were required as an adjuvant.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'parent or sibling with Cardiovascular disease before age 65': False, 'Hypertension history': False, 'smoking': False, 'Diabetes mellitus': False, 'age': [4, 'years'], 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 4 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4129,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6432745-1,Extracted,"A 73-year-old Caucasian woman with a past medical history (PMHx) of esophageal dysmotility, gastroesophageal reflux disease (GERD), lymphocytic colitis, chronic obstructive pulmonary disease (COPD), essential hypertension (HTN), hyperlipidemia (HLD), neuropathy, and depression presented with substernal pleuritic chest pain and lightheadedness that began 2 hours after an uncomplicated outpatient upper and lower endoscopy. She did not have any known allergies. Her family history was significant for myocardial infarction (MI) in her father and cerebrovascular accident in her mother. She was married with two children, retired, previously worked for an advertising agency, and resided in New York City. She smoked one pack of cigarettes per day for 30 years and quit in 2001. She drank two alcoholic drinks per night. Medications taken prior to admission, during hospitalization, and after discharge included a 10 mg oxybutynin extended-release oral tablet once daily for urinary symptoms, a 40 mg omeprazole oral tablet once daily for GERD, a 10 mg amlodipine oral tablet once daily for HTN, a 300 mg bupropion extended-release oral tablet once daily for depression, a 20 mg escitalopram oral tablet once daily for depression, a 100 mg topiramate oral tablet once daily for neuropathy, a 50 mg tramadol oral tablet as needed every 4 hours for pain, and a 135 mg fenofibric acid delayed-release oral tablet once daily for HLD. Prior to presentation, the patient had undergone three endoscopies, after which her postprocedure course was uncomplicated. Upper and/or lower endoscopies were done on March 11, 2013, May 29, 2014, and December 3, 2015, for epigastric abdominal pain, periumbilical abdominal pain, and chronic diarrhea, respectively.
Biopsies were taken throughout the esophagus, stomach, duodenum, jejunum, ileum, and colon. The upper endoscopy and lower endoscopy took 5 and 25 minutes to complete, respectively.
In the emergency room, her vital signs were as follows: afebrile (36.8 °C), heart rate of 101 beats/min, blood pressure of 116/59 mmHg, respiratory rate of 16 breaths/min, and oxygen saturation of 93% on room air. She was a well-appearing woman, alert, and in no acute distress. She was well hydrated and well nourished. Her skin color, texture, and turgor were all normal without any suspicious rashes or lesions. Her head was normocephalic and atraumatic without any masses, lesions, or tenderness. Her eye examination included anicteric sclera with pupils that were equally round and reactive to light and with intact extraocular movements. Her ear, nose, and throat examination were all normal. Her neck was supple without any adenopathy. Her thyroid was of normal size and symmetric without any bruits. Her lungs were clear to auscultation without any wheezing, rhonchi, or rales. Her heart sounds included a regular rhythm and rate without murmurs, rubs, or gallops. Her abdominal examination revealed a soft, nontender abdomen, normoactive bowel sounds, and was nonsignificant for masses or organomegaly. Her extremities did not show any deformities, edema, skin discoloration, clubbing, or cyanosis and had good capillary refill. No joint swelling, deformity, or tenderness was observed. Her peripheral pulses were normal. The patient was alert and oriented to person, place, and time. Her speech was fluent with appropriate repetition and comprehension. Cranial nerves II–XII were intact without any deficits. Her gait was normal and steady. Her sensation (light touch, pinprick, position sense, and vibration sense) was grossly intact. Her reflexes were 2+ and symmetric at the biceps, triceps, knees, and ankles. She had no pronator drift of outstretched arms; her muscle bulk and tone were normal; and she had full strength bilaterally.
Initial laboratory studies revealed a hemoglobin level of 11.5 g/dl (normal range for females, 12.0 to 15.0 g/dl), which was the patient’s baseline hemoglobin; a troponin I level of 8 ng/ml (normal range, 0 to 0.4 ng/ml); and a B-type natriuretic peptide level of 2900 pg/ml (normal range, up to 100 mg/L). Other laboratory findings, including electrolytes, liver function tests, renal function tests, complete blood count, serology, and urinalysis, were all within normal limits.
An initial ECG was notable for T-wave inversions in the anterolateral leads and submillimeter ST elevations in the V4–V6 precordial leads, concerning for ACS (Fig. ). A bedside transthoracic echocardiogram (TTE) revealed apical hypokinesis (Fig. ), and computed tomography of the chest, abdomen, and pelvis did not reveal pulmonary emboli or acute abdominal processes. Left heart catheterization demonstrated nonobstructive CAD with a left ventriculogram of 45% and diffuse wall hypokinesis, consistent with a diagnosis of takotsubo cardiomyopathy, thought to be precipitated by the patient’s recent upper and lower endoscopic procedures (Fig. a and b). The patient’s angina resolved after the procedure, and repeat ECG revealed less marked ST depressions and resolved ST elevations (Fig. ). She was discharged home on hospital day 7. She did not require any further intervention or medical management.
The patient did well after discharge. After nine months post-discharge, she was admitted for worsening lower extremity edema. The TTE at the time was significant for a high left ventricular outflow tract (LVOT) gradient (peak LVOT gradients of 42 mmHg at rest and 122 mm Hg with Valsalva maneuver). Her ejection fraction (normal range, 55–70%) at the time was 81%, and pertinent results of TTE included fibrocalcific changes of the aortic valve with mildly reduced opening; moderate mitral annular calcification; systolic anterior motion of the anterior mitral valve leaflet; and normal functioning of the left atrium, right ventricle, tricuspid valve, and pulmonic valve. She was discharged with instructions on avoiding diuresis and beginning initiation of metoprolol (6.25 mg every 6 hours) for negative inotropy and to decrease systolic anterior motion.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [73, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': True, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': True, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'obesity': False}",8,8,8,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 73 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 2 + 2 = 4.
The following risk factor(s) are present based on the patient's note: hypertension, family with cvd, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 4 + 2 = 6.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 6 + 2 = 8.
Based on the patient's data, the HEART Score is 8."
4130,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7410440-1,Extracted,"A 60-year-old male patient was admitted with myalgia and fatigue for 2 days. The patient had no fever, cough, sore throat, chest tightness, and shortness of breath.
The patient had no previous history of chronic diseases such as kidney disease, hypertension, and an endocrine disorder; muscle diseases such as muscular dystrophy and neuromuscular disorders; or a statin class of drug use that could lead to muscle breakdown. There was no trauma and no history of medication. The patient reported no alcohol intake and smoking.
Blood pressure was 120/70 mmHg, respiratory rate 18/minutes, heart rate 93/minutes, temperature 36.7°C, and arterial oxygen saturation 98% in room air. The patient was conscious and had a clear mind. He was in a regular heart rhythm without any obvious murmur. There were obvious moist crackles during auscultation of inferior lobes in the lung.
Routine blood test results were as follows: white blood cells, 2.91 × 109/L; neutrophils, 55.7%; lymphocytes, 30.2%; total number of lymphocytes, 0.88 × 109/L; C-reactive protein (CRP), 35.1 mg/L; potassium, 4.3 mmol/L; sodium, 138 mmol/L; urea, 21 mg/dL; D-dimer, 210 ng/mL; alanine aminotransferase (ALT), 52 U/L; aspartate aminotransferase (AST), 117 U/L; lactate dehydrogenase (LDH), 575 U/L; ferritin, 428 ng/mL; international normalized ratio, 1.07; prothrombin time, 11 minutes; total bilirubin, 0.5 mg/dL; and direct bilirubin, 0.2 mg/dL. Cardiac acute damage marker values such as creatine kinase myocardial band (CK-MB: 3.80 U/L) and troponin (13.6 pg/mL) were among normal reference values at the time of hospital admission.
The patient’s baseline serum creatinine (Cr) level was 0.91 mg/dL and baseline serum CK level was 4,267 U/L. Changes in CK, CRP, AST, ALT, LDH, ferritin, and D-dimer during the patient’s hospitalization are presented in .
Blood tests for rapid detection of influenza A, influenza B, respiratory syncytial virus, adenovirus, hepatitis A, and hepatitis B were all negative. Electrocardiogram was normal; no significant cardiac arrhythmia was detected.
The patient, who was admitted with frequent complaints of myalgia and fatigue, was diagnosed in the emergency department. Considering the clinical features, physical examination, and chest radiography, the patient was hospitalized with the diagnosis of suspected viral infection. However, considering COVID-19 infection to the epidemic area, atypical pneumonia virus infection had to be ruled out. On the same day, a chest computerized tomography (CT) scan was performed, and small ground-glass nodules were seen, suggesting viral pneumonia scattered across the two lungs (). Two days later, a real-time reverse transcription–PCR (RT-PCR) analysis of the patient’s throat swab sample indicated SARS-CoV-2 infection.
We hospitalized the male patient diagnosed with COVID-19. When we evaluated according to the WHO classification, we found that our patient had severe pneumonia. During hospitalization, hydroxychloroquine (first day 2 × 400 mg loading + 4 days 2 × 200 mg maintenance), oseltamivir (2 × 75 mg, 5 days), and azithromycin (first day 1 × 500 mg loading + 4 days 1 × 250 mg) therapy were used as recommended in the COVID-19 guidelines. The patient was quickly treated with a combination of IV fluids and sodium bicarbonate for alkalization. After five days of treatment, the patient’s clinical condition deteriorated, and the patient’s respiratory rate was 30 breaths/min; severe respiratory distress developed, and SpO2 was ≤ 93% on room air. Favipiravir (first day 2 × 1,600 mg loading + 4 days 2 × 600 mg) antiviral treatment was added to the treatment of the patient, who was thought to develop severe pneumonia. The length of hospital stay of our patient was 10 days between April 9, 2020 and April 19, 2020. After 11 days of treatment, the patient’s symptoms improved significantly, and he recovered with a negative RT-PCR test.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [60, 'years'], 'Hypertension history': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'Initial troponin': 'less than or equal to normal limit', 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 60 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4131,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6488346-1,Extracted,"A 45-year-old male with a history of a Wolff-Parkinson-White pattern was admitted to the hospital with complaints of a sudden onset of chest heaviness radiating to left arm, along with profuse sweating, for two hours. His family history was unremarkable. He denied smoking, alcohol, cocaine, and tobacco use. Physical examination revealed a blood pressure of 160/100 mmHg and a regular pulse rate of 100/min. The remainder of the physical examination was unremarkable. EKG on arrival revealed sinus rhythm with a right bundle branch block (RBBB), normal axis, and ST-segment elevation of 2 mm in leads V3-V5 with reciprocal changes in leads I and aVL. A short PR interval with delta waves was also observed in the EKG (Figure ). In light of the patient's symptoms and EKG findings, a diagnosis of acute myocardial infarction (AMI) with a WPW pattern was made. Immediate therapy, including aspirin, clopidogrel, metoprolol, nitroglycerine, and heparin, was administered, and the patient was rushed for an emergent coronary angiogram.
A coronary angiogram revealed a nondominant right coronary artery (RCA), a non-obstructive left circumflex (LCX) artery, and a severe lesion in the mid-segment of the left anterior descending (LAD) artery (Figure ). Primary percutaneous coronary intervention (PPCI) to the LAD was performed, and a drug-eluting stent (DES) was deployed (Figure ). During the procedure, the patient developed narrow complex regular tachycardia with poor hemodynamics, so synchronized electrical cardioversion was performed with 100 joules. Post-percutaneous coronary intervention (PCI), thrombolysis in myocardial infarction (TIMI)-3 flow was achieved successfully (Figure ). Complete resolution of the patient's symptoms and EKG changes were reported after the angioplasty (Figure ).
The laboratory evaluation, including a complete blood count (CBC), serum creatinine (Cr), glycated hemoglobin (HbA1c), and posterior-anterior chest X-ray, was within normal limits pre- and post-procedure. Cardiac troponin-I levels came back elevated with a serially rising trend (0.3 ng/ml, 28 ng/ml, 37ng/ml). The echocardiogram revealed moderate left ventricular systolic dysfunction with apical and septal akinesia and an ejection fraction (EF) of 35% with Grade I left ventricular (LV) diastolic dysfunction. The rest of the hospital course was unremarkable, and the patient was discharged home in stable condition. Follow-up echocardiogram at six weeks revealed improvement in the LV systolic function (left ventricular ejection fraction (LVEF) was 45% with apical akinesia). The patient was followed up for two years after the event, and at the last recent follow-up, there were no reported symptoms or events.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False}",6,6,6,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 45 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 3 + 1 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 4 + 2 = 6.
Based on the patient's data, the HEART Score is 6."
4132,18,HEART Score for Major Cardiac Events,risk,integer,usmle-401,Extracted,"A 62-year-old man comes to the physician because of a persistent cough for the past 2 weeks. During this time, he has also had occasional discomfort in his chest. Three weeks ago, he had a sore throat, headache, and a low-grade fever, which were treated with acetaminophen and rest. He has a history of hypertension and hyperlipidemia. His father died of myocardial infarction at the age of 57 years. He has smoked a pack of cigarettes daily for the past 40 years. Current medications include enalapril and atorvastatin. His temperature is 37°C (98.6°F), pulse is 70/min, and blood pressure is 145/90 mm Hg. Physical examination shows no abnormalities. An x-ray of the chest is shown.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'parent or sibling with Cardiovascular disease before age 65': True, 'Suspicion History': 'Moderately suspicious', 'Hypertension history': True, 'smoking': True, 'age': [62, 'years'], 'atherosclerotic disease': True, 'hypercholesterolemia': True, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 62 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 1 + 1 = 2.
The following risk factor(s) are present based on the patient's note: hypertension, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 4 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 2 + 2 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 4.
Based on the patient's data, the HEART Score is 4."
4133,18,HEART Score for Major Cardiac Events,risk,integer,pmc-3891065-1,Extracted,"A 37-year-old woman was transferred to our emergency room with the history of syncope. Three days previously, she experienced chest discomfort, dyspnea, palpitations and a low grade fever, but had no relevant past medical history or co-morbidity. At presentation her blood pressure was 80/50 mmHg, pulse rate 76/min, respiratory rate 36/min and body temperature 37.5℃. The physical examination was remarkable for: dyspnea, orthopnea, absence of normal heart sounds, and jugular vein dilatation; Additional tests revealed: low voltage ECG, sinus tachycardia and a large cardiac shadow on X-ray. Laboratory findings showed a pH of 7.37, PaCO2 18.8 mmHg, PaO2 88.5 mmHg, HCO3- 10.8 mmol/L on ABGA, hemoglobin 9.2 g/dL, white blood cell of 12900/µL, and platelet 476000/µL on CBC. ANA, rheumatoid factor, and VDRL were all negative and non- reactive. The patient had a suspected cardiac tamponade therefore a transthoracic echocardiography (TTE) was performed immediately and revealed moderate pericardial effusion and a hypokinetic LV at the anterior, anterolateral and apex portions of the heart (). Pericardiectomy with a window formation was performed to remove the effusion and hematoma. The drained fluid had a white blood cell 225 (PML 100%), red blood cell 90,000/µL LDH 1064U/L, and glucose 190 mg/dL; there were no organism on gram stain and culture. A class I cytology, indicating acute and chronic inflammation was revealed. On postoperative day 3, fever, dyspnea, oliguria and mental status changes developed and the patient deteriorated rapidly. A follow-up evaluation showed the serum hemoglobin to be 6.9 g/dL, white blood cell 14900/µL, platelets 18000/µL and AST, ALT and CPK of 272, 151, and 247 U/L, respectively. Blood urea nitrogen was 40.6 mg/dL, creatinine 4.9 mg/dL, LDH 2279 U/L, PT 11.6 seconds and aPTT of 32 seconds.
A chest X-ray revealed a ground glass appearance in both lungs. The brain MRI was reported as normal. A peripheral blood smear was remarkable for schistocytosis, anisocytosis, normoblasts and a thrombocytopenia, suggestive of microangiopathic hemolytic anemia (). All of these findings were compatible with the diagnosis of thrombotic thrombocytopenic purpura (TTP). Treatment with methylprednisolone pulse therapy was started (1 g/day for 3 days). Investigation for the etiology of TTP revealed that the patient had suffered from severe recurrent oral and genital ulcers. The ulcers were reported to be as frequent as 3 to 4 per month and were exacerbated by menstruation after the age of 20. The patient also reported taking medications intermittently for painful skin indurations and eruptions as well as arthralgia. Considering the clinical symptoms in total the diagnosis, of Behcet's disease complicated by TTP and hemorrhagic pericarditis, was made. Treatment with methylprednisolone pulse therapy resulted in a dramatic response with improvements of the CBC, LFT, azotemia, and improved mental status. The patient went on to fully recover and returned to normal activities of daily living within a few days. Follow-up evaluation with TTE after complete recovery showed a normal right and left ventricular heart function and a minimal pericardial effusion. After discharge, the patient continued taking medication including colchicine 1.2 mg/day and prednisolone 5 mg/day. The patient continued to be followed.
Six months after discharge, the patient required readmission to the hospital. She presented with a sudden onset left leg swelling and pain that was diagnosed as a left proximal femoral vein thrombosis by duplex scan. There were no associated signs or symptoms such as dyspnea or fever. A venogram demonstrated that a filling defect obstructed the left proximal femoral vein. the patient was treated with catheter directed thrombolysis using urokinase, thrombectomy and venoplasty and then started on combination anticoagulation therapy (). Six months after maintenance therapy with coumadin, colchicines, and sulfasalazine was started, a homogenous soft tissue mass was found, incidentally, on routine laboratory and radiologic follow up. The soft tissue density was attached to the left perihilar area by the pulmonary conus (). The laboratory tests showed a hemoglobin of 11.1 g/dL, platelet 324000/µL, WBC 6000/µL, ESR 39 mm/H, CRP 1.59 mg/dL, albumin 4.5 g/dL, LDH 503 U/L, BUN 11.8 mg/dL, creatinine 1.0 mg/dL, PT 29.7 second, INR 2.95.
Chest CT angiography and cardiac MRI revealed a 5x5cm sized round aneurysmal sac between the left atrium and left ventricle adjacent to the proximal pulmonary artery, but no definite stalk from the origin could be found (). A doppler echocardiography demonstrated holosystolic ejection flow from the surface of the left ventricle (). Despite the fact that the origin of aneurysmal stalk could not be identified, the pressure gradient calculated by the color doppler flow from the aneurysmal stalk to lumen was about 9 mmHg. The dilated vascular sac appeared to be a pseudo aneurysm with a coronary artery origin. A Tc99m sestamibi scan was performed to investigate the possibility of myocardial ischemia. The scan revealed a reversible perfusion defect on the antero-septal wall (). Subsequent coronary angiography allowed us to confirm the diagnosis of a pseudo aneurysm from the mid-left anterior descending artery (LAD), which interrupted distal flow by creating indentations and diffuse stenotic lesions along the whole length of the right coronary artery (RCA). In addition, a well developed collateral circulation was observed from the LAD and the left circumflex artery (LCX). An emergency operation was planned for aneurysmal resection and coronary artery bypass grafting (CABG). However, because of the size and thus the risk of rupture, we opted instead for balloon angioplasty with a U-pass and graft stent. Implantation proceeded using a Graftmaster 3.0×19 mm at the mid LAD the origin of pseudo aneurysm (). Because of the compromised distal flow of the RCA, the LAD would be of no advantage to the outcome of the CABG. If packed completely, it was expected that the aneurysmal sac would not grow any more and would regress by resorption and fibrosis. The administration of high dose glucocorticoid therapy (prednisolone 1 mg/kg/day) with azathioprine (150 mg/day) in addition to the mechanical intervention were both highly effective management as demonstrated by a follow-up TTE and coronary angiography which showed no further diversion of flow from the LAD and regression of the aneurysmal size to 3.9×3.8 cm from 5×5 cm Initially. and a preserved heart function (LVEF 60%) (). Six months after discharge, the patient was asymptomatic and only a vestige of the aneurysm was evident by routine chest X-ray ().",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [37, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Highly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 37 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4134,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7426987-2,Extracted,"A 36-year-old Caucasian gentleman with no past medical history presented to the ED for management of nephrolithiasis. Upon arrival, the patient was given ketorolac and Hyoscyamine immediately after which he developed chest pressure, severe shortness of breath with desaturation to 83% on RA, hypertensive emergency with BP of 188/122, sinus tachycardia with HR as high as 130 bpm. At this time, CT chest with contrast was performed which showed left ventricular dilatation and bilateral airspace disease representing pulmonary edema. EKG revealed diffuse ST-T wave elevations, which prompted troponins that were peaked at 2.16. A follow-up echocardiogram as seen in and revealed diffuse hypokinesis, RVSP of 45 mmHg and LVEF of 35%. The patient was taken for cardiac catheterization and was found to have no coronary artery disease, however, did have ballooning of the basal myocardium with a hyperdynamic apex; findings consistent with reverse Takotsubo cardiomyopathy. This case illustrates one of the rare cases of reverse Takotsubo cardiomyopathy in the setting of anticholinergic toxicity. Hyoscyamine, which is used as an antispasmodic commonly, results in anticholinergic side effects on the cardiovascular system causing tachycardia which in this case resulted in reverse Takotsubo cardiomyopathy. Clinicians should remain cognizant of the effect of anticholinergic medications, particularly the cardiovascular system as it may result in the aforementioned findings.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [36, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'Initial troponin': 'greater than three times normal limit', 'Diabetes mellitus': False, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 36 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 3 + 2 = 5.
Based on the patient's data, the HEART Score is 5."
4135,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7485917-1,Extracted,"A 47-year-old Caucasian female presented to the emergency department for worsening shortness of breath. She described a three-month history of dyspnea on exertion, difficulty with deep breathing, dry cough, and right-sided pleuritic chest pain. Symptoms gradually worsened until three days prior to presentation when she started having symptoms at rest. Pertinent negative findings included no fevers, chills, upper respiratory symptoms, hemoptysis, orthopnea, swelling, additional chest pain, or weight changes. Her past medical history was significant for menorrhagia and uterine ablation 15 years ago. Family history was notable for a brother and mother with multiple sclerosis and a father who passed away from gastric cancer. She denied smoking, alcohol use, recreational drug use, sick contacts, or recent travel. Vital signs were remarkable for tachycardia with a rate of 114 beats per minute, tachypnea of 22 breaths per minute and hypoxia of 87% oxygen saturation on room air that improved to 92% on 2 liters of supplemental oxygen. Pertinent physical exam findings included decreased breath sounds on the right lower lung fields and dullness to percussion over the same area.
On laboratory testing alkaline phosphatase was elevated at 217 U/L, beta-hCG was elevated at 1,364 MIU/mL, arterial blood gas on 2 liters of oxygen showed no further hypoxemia, troponin levels were negative times two, and brain natriuretic peptide, basic chemistry panel, and complete blood counts were unremarkable. A chest X-ray showed a large right pleural effusion and suggested possible underlying atelectasis or infiltrate (Figure ). Electrocardiogram showed non-specific ST segment changes and sinus tachycardia. Further workup included cancer antigen 125 (CA-125) elevated at 55.6 with follicle-stimulating hormone, and thyroid stimulating hormone levels within the normal limits. Novel coronavirus 2019, influenza nasal swabs, urine legionella and Streptococcus pneumoniae antigen testing were all negative. She was started on diuretic therapy and underwent thoracentesis with indwelling catheter drainage. A hemorrhagic exudative effusion was drained concerning for underlying malignancy. While awaiting pathology report the patient’s hCG remained elevated but consistent.
Further imaging included a transvaginal ultrasound with no reported acute abnormalities. A computed tomography (CT) angiogram of the chest showed a soft tissue mass in the anterior medial right lung base/right middle lobe contacting the anterior mediastinum and anterior pleura measuring 5.0 x 4.8 cm (Figure ). No pneumothorax or evidence of pulmonary embolism were identified. An abdominal and pelvis CT noted no acute abnormalities. Thoracentesis returned positive for cytokeratin-7, placental alkaline phosphatase, pankeratin, and GATA 3 consistent with malignant cells and favoring a germ cell tumor. A fiberoptic bronchoscopy did not identify any endobronchial lesions and washings were negative for malignancy. Subsequently a CT-guided biopsy of the aforementioned mediastinal mass was performed. In addition to the above stains, inhibin was weakly positive and both hCG and CD-10 were positive. Given the entire clinical scenario a diagnosis of primary choriocarcinoma was made. The patient’s breathing improved after pleural fluid drainage and she was discharged to follow up with a positron emission tomography (PET) scan and Oncologist as an outpatient.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [47, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 47 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4136,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5965406-1,Extracted,"The patient is a 38-year-old male with a history of coronary artery disease, hypertension and morbid obesity status post gastric bypass who presented to the ED with a chief complaint of chest pain. He stated that the pain began insidiously approximately five hours before he presented to the ED. He characterized the pain as a “pricking” sensation in his right anterior chest that radiated to his right scapula. He rated the pain as a 3–4 severity on a 10-point pain scale. He stated that the pain was continuous and currently present. The pain was unrelated to exertion. He denied any associated symptoms including fever, chills, cough, dyspnea, dizziness, diaphoresis, nausea, vomiting and diarrhea.
The patient had a past medical history significant for obesity, hypertension, hyperlipidemia, gastroesophageal reflux disease, deep venous thrombosis (DVT) and two prior ischemic strokes. Previous work-up of his prior cerebrovascular accidents revealed a patent foramen ovale, believed to be the underlying etiology. He denied congestive heart failure and prior myocardial infarction. Surgical history included gastric bypass three years earlier at which point an IVC filter had been placed. The IVC filter was never removed. However, after the procedure, a trans-esophageal and trans-thoracic echocardiogram, chest radiograph (CXR), magnetic resonance imaging/angiography of the abdomen and pelvis, and ultrasound of the aorta, IVC, and iliac vessels were all negative for the IVC filter. Per the medical record, it was concluded that the filter never deployed because it could not be located with the above imaging.
On initial presentation, the patient was conversational and in no acute distress. Physical exam revealed a well appearing, obese male who appeared his stated age with normal vital signs. A nine-system exam was unremarkable. The lungs were clear to auscultation bilaterally. The cardiac exam demonstrated regular rate and rhythm with no audible murmur, rub, or gallop. He was not diaphoretic, his jugular veins were flat and he had equal pulses without edema in his lower extremities. The chest, flank and back were not tender to palpation.
The patient declined pain medications. A chest pain work-up was done, which included a CXR, complete blood count, basic metabolic panel, troponin and an electrocardiogram (EKG).
Portable CXR showed stable cardiomegaly, interpreted by radiology to be consistent with prior radiographs. His EKG was normal without evidence of ST segment changes or T wave abnormalities. Bedside troponin was 0.00. Given that the patient had significant risk factors, we decided to perform a computed tomography triple rule-out (CT TRO) study of the chest to rule out pulmonary embolism (PE), aortic disease and to assess for coronary artery disease. The CT showed no evidence of significant coronary artery disease, pulmonary embolus, or acute aortic injury; however, it did demonstrate an IVC filter lodged in the right ventricle, seemingly adherent to the moderator band and right ventricular trabeculation. The patient’s CT was reconstructed to create the image below () in which the IVC filter is clearly seen lodged in the right ventricle.
The patient was subsequently admitted into the cardiology service and multiple consultations were obtained. Interventional radiology and interventional cardiology did not believe they could safely extract the filter percutaneously due to concerns that they would injure the tricuspid valve. Cardiothoracic (CT) surgery recommended that the device be extracted via an open procedure that included sternotomy, cardiopulmonary bypass, and a brief period of cardioplegic arrest. The patient requested a second opinion from a CT surgery consultant who also recommended that the filter be removed. The patient had not yet made a decision and was subsequently discharged home on warfarin while considering his options.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [38, 'years'], 'Hypertension history': True, 'Suspicion History': 'Slightly suspicious', 'atherosclerotic disease': False, 'Electrocardiogram Test': 'Normal', 'obesity': True, 'Initial troponin': 'less than or equal to normal limit', 'Transient Ischemic Attacks History': True, 'hypercholesterolemia': True, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 38 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: hypertension, obesity. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4137,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7453687-1,Extracted,"A 51- year old male, with no prior medical history, no medication, non-smoker and without risk factors for venous thrombo-embolism arrived at the end of April to the emergency department with exercise induced dyspnea during 4–5 weeks and for the last 48 h dyspnea also at rest. Prior to the onset of symptoms, he had lived socially isolated with his wife from mid-March, approximately 40 days, both working from home and with their two children home from school. He described a short period in the beginning of March, 7 weeks before hospitalization, when he felt difficulties taking deep breaths for a couple of days but no other symptoms like cough, fever or feeling of malaise. Following that episode he experienced a gradually increased fatigue on his regular run and in the beginning of April he had to start walking when running uphill. During the last 5 weeks before hospitalization his wife and daughter had noticed signs of heavy breathing when he walked up the stairs.
Physical examination was normal, examination of the heart and lungs revealed no discrepancies, no swollen legs or other signs of cardiac decompensation. The bodyweight of the patient was 90 kg and his height was 1.88 m, body mass index (BMI) was 25,5 kg/m2. He had normal temperature and a regular heart rate of 80 beats/min. He had a blood pressure of 180/65 mmHg and an oxygen saturation of 93% breathing ambient air. High sensitivity Troponin T was markedly elevated, 1200 (reference < 15 mg/L) and also B-type natriuretic peptide was increased, 737 (reference < 125 ng/L). He had a slightly increased C-reactive protein of 15 (reference < 5 mg/L) and modest leukocytosis 11,7 (normal range 3,5–8,8 × 109/L). ECG showed incomplete right-sided branch block. Computerized Tomography Angiography (CTA) of the chest was performed as pulmonary embolism was suspected. The CTA revealed widespread bilateral segmental pulmonary embolism (Fig. ) and an additional area of consolidation in the right upper lobe consistent with infarction. Additional findings of ground glass opacities that could match Covid-19 were also found (Fig. ). The patient tested negative for SARS -CoV-2 (polymerase chain reaction SARS -CoV-2, GeneXpert, Cepheid, Sunnyvale, CA, United States) at two consecutive nasopharynx tests. No antibody test was performed. The patient was given oxygen and subcutaneous low molecular weight heparin (LWMH), tinzaparin 18,000 units daily during 2 days of hospitalization and was discharged with apixaban 5 mg, twice daily, with a treatment recommendation for 6 months.
Echocardiography revealed dilated right chamber, midventricular diameter of 5 cm and left septum deviation, light to moderate insufficiency of the tricuspid valve with a velocity max of 4,2 m/s. Vena cava inferior showed normal width and breathing variation. Severe pulmonary hypertension with a systolic pulmonary pressure of approximately 75–80 mmHg (normal upper limit 35 mmHg) was present. No significant amount of pericardial fluid was present.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [51, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': False, 'obesity': True, 'smoking': False, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 51 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: obesity. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 2 + 2 = 4.
Based on the patient's data, the HEART Score is 4."
4138,18,HEART Score for Major Cardiac Events,risk,integer,pmc-2728612-1,Extracted,"A 73-year-old man was admitted with severe chest pain at rest for 3 hours. He had previous three myocardial infarctions with the last one occurring 14 years before this admission. At that time, he underwent coronary artery bypass grafting (CABG) with LIMA to left anterior descending artery and two saphenous vein grafts to the right coronary and first obtuse marginal arteries. Following surgery, his chest pain resolved, but he had frequent admissions with chest pain over the last four years which was misdiagnosed as coronary artery spasm. In addition, his past medical history included congestive heart failure and cardiac arrest twelve years ago. His coronary risk factors were hypertension, hypercholesterolemia, family history of ischaemic heart disease, and a 45 pack-year history of cigarette smoking.
His physical examination revealed a blood pressure of 124/63 mmHg in the right arm and 83/50 mmHg in the left, a regular pulse of 84 beats/minute, and respiratory rate of 18 breaths/minute. He had normal heart sounds and the lung fields were clear. The vascular examination revealed easily palpable right upper extremity and bilateral lower extremity pulses. Left upper extremity pulses were present but diminished. Carotid arteries were palpable with no audible bruits. No abdominal masses were palpated.
A 12-lead electrocardiogram demonstrated ischaemic changes in lateral leads and a chest x-ray showed cardiomegaly. Cardiac enzymes revealed troponin of 0.05 μg/L. On diagnostic coronary angiography, there was 50% stenosis in left main stem and 50% stenosis in left anterior descending artery in mid-segment with good run off. Failure to pass the catheter through the left subclavian artery indicated possible stenosis raising suspicion of CSSS.
CT Angiogram confirmed a 2 cm stenosis at the origin of left subclavian artery (). Stenting of left subclavian artery was considered hazardous due to the risk of occlusion of the adjacent vertebral artery. The patient was referred to undergo left common carotid to subclavian artery bypass. After exploration, the left subclavian artery was found to have significant atherosclerosis. Therefore, an infraclavicular incision was utilised for access to the left axillary artery. A 6 mm ringed Vascutek PTFE graft (Sulzer Vascutek Ltd.; Renfrewshire, Scotland, UK) was used to construct a bypass between the left common carotid artery and the left axillary artery tunnelled beneath the clavicle. Carotid shunt was not used while systemic heparin (5000 units) was administered during the operation. Postoperatively, a good graft pulse was felt in addition to easily palpable left upper extremity pulses. The patient made an uneventful recovery, the angina pain disappeared and he was discharged 4 days following the operation. Two months later, he reported improvement in symptoms and his blood pressure was equal in both arms. Control CT angiogram nine months later revealed an intact PTFE graft between carotid and axillary artery.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [73, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': True, 'smoking': True, 'parent or sibling with Cardiovascular disease before age 65': True, 'atherosclerotic disease': True, 'Initial troponin': 'less than or equal to normal limit', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'obesity': False}",6,6,6,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 73 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 2 + 2 = 4.
The following risk factor(s) are present based on the patient's note: hypertension, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 4 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 4 + 2 = 6.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 6.
Based on the patient's data, the HEART Score is 6."
4139,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8150416-1,Extracted,"A 62-year-old woman was admitted to the emergency department of our hospital complaining of a 24-hour history of a sensation of laryngeal obstruction. The patient did not have any chest pain, shortness of breath, sore throat, nausea, vomiting, heartburn, diaphoresis, fevers, or chills. She could not recall an obvious cause of her upper airways problem. She did not drink or alcohol or smoke cigarettes. Physical examination on presentation showed: body mass index (BMI), 25-kg/m2; temperature, 35.9°C; respiration rate (RR), 16 breaths/min; oxygen saturation, 98%; blood pressure (BP), 117/80 mmHg; pulse rate (PR), 73 beats/min. A cardiovascular examination showed normal rate and rhythm with no murmurs or friction rub. A laryngopharyngeal examination was unremarkable with no evidence of discharge, hyperaemia or swelling and vocal cord function appeared normal. The patient’s medical history was insignificant apart from a left nodular goitre excision she had undergone two years previously. A routine electrocardiogram (ECG) showed sinus rhythm and a chest computed tomography (CT) scan showed a small inflammatory lesion in the lower lobe of the right lung and confirmed the absence of an intra/extra-thoracic goitre. Her troponin I levels were <0.025 ng/ml (normal range <0.1 ng/ml) and her blood lipids were within normal range (triglycerides, 1.16 mmol/l [normal 0.00–1.70 mmol/l]; total cholesterol, 5.40 mmol/l [normal 3.00–5.70 mmol/l]; low density lipoprotein, 2.39 mmol/l [normal 1.89–3.37 mmol/L]). Therefore, because the patient exhibited no risk factors or evidence of ACS, a presumptive diagnosis of laryngopharyngitis was made and she was discharged from hospital with symptom-alleviating medication.
The patient returned to the emergency department 24 hours later. Her main complaint was that of a continuous sensation of laryngeal obstruction with accompanying mild fatigue. She reported that she had no chest pain or shortness of breath. Her vital signs were: BP, 104/77 mmHg, PR, 80 beats/min; RR, 15 breaths/min; oxygen saturation, 97%. A routine 12-lead ECG showed an anterior wall MI with ST segment elevation in leads V1-V4 (). Bedside ECG showed a dramatically decreased ejection fraction of 35% with wall motion abnormalities. Laboratory data showed elevated levels of: troponin I, 13.2 ng/ml; B-type natriuretic peptide, 259 pg/ml (normal ≤100 pg/ml); D- Dimer, >3680 ng/ml (normal 0–243 ng/ml); creatine kinase, 2043 U/l (normal <140 U/l). On the basis of elevated troponin levels combined with ECG changes, her diagnosis was amended to acute anterior wall MI. After a MI protocol was initiated, a cardiology consultation was requested. However, after 10 minutes, her BP fell progressively to a minimum of 60/40 mmHg and she became unconscious. Ventricular fibrillation (VF) was detected in the ECG monitor and so cardiopulmonary resuscitation with advanced life support was initiated immediately. In spite of high doses of catecholamines and unsynchronous direct current defibrillation, her haemodynamics deteriorated dramatically. Refractory VF occurred repeatedly and her cardiac rhythm and function could not be restored. Her family consented to an autopsy that showed total occlusion of the left anterior descending artery with thrombus below the proximal segment and 80% stenosis of the left circumflex artery middle part. Definitive histology using haematoxylin and eosin (H&E) staining confirmed anterior wall myocardial necrosis ( and ), which was consistent with our diagnosis of acute anterior wall MI.
Written informed consent for the publication of this report was obtained from the patient’s husband and the study was reviewed and approved by the local ethics committee of Ningbo First Hospital. This report adheres to CARE guidelines.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [62, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'Diabetes mellitus': False, 'obesity': False, 'smoking': False, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 62 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 1.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 1 + 2 = 3.
Based on the patient's data, the HEART Score is 3."
4140,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8276621-3,Extracted,"A 34-year-old male patient without cardiovascular risk factors presented at the ED with
acute tearing chest pain after exercise radiating to the interscapular region. Patient ECG
showed sinus rhythm with symmetric T waves in leads V1 through V4 and hs-cTn T was
30.5 ng/L (3–14 ng/L normal value). Clinical suspicion was aortic dissection and patient
was referred for non-ECG-gated contrast-enhanced CTA of the thoracic aortic. Normal aorta
was shown and a transmural apical and anteroseptal MCTP defect was demonstrated using the
late-phase contrast imaging started 60 s after the end of the arterial phase. In
consequence, invasive coronary angiogram was indicated showing a total occlusion of the
mid LAD which was stented. Resting cMRI, obtained before hospital discharge, demonstrated
a non-transmural apical and anteroseptal infarct that correlates with MCTP imaging
().",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [34, 'years'], 'Suspicion History': 'Highly suspicious', 'Hypertension history': False, 'smoking': False, 'Diabetes mellitus': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 34 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 3 + 2 = 5.
Based on the patient's data, the HEART Score is 5."
4141,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7354665-1,Extracted,"A 49-year-old woman without significant cardiovascular risk factors was transferred to our hospital with a 1-hour history of sudden-onset chest pain. She had taken no medication and experienced no physical or emotional stress preceding the chest pain. On arrival, physical examination revealed stable vital signs with no abnormal findings. Electrocardiography revealed no clear findings of ischemic ST-T changes or prior Q-wave myocardial infarction, but laboratory testing showed elevated cardiac enzymes such as troponin T (0.855 ng/mL) as well as creatine phosphokinase (565 U/L) and its MB isozyme (66 U/L). Bedside transthoracic echocardiography revealed impaired contractility in the focal apical segment of the left ventricle, but there was no clear finding of basal hypercontractility or an apical ballooning sign suggestive of stress-induced cardiomyopathy. Overall, the estimated ejection fraction of the left ventricle was broadly preserved (60%). The patient was diagnosed with non-ST-elevation acute myocardial infarction. Because her condition was stable without chest pain on arrival, we initially administered conservative medical therapy including aspirin, prasugrel, nicorandil, perindopril, pitavastatin, and bisoprolol.
Three days later, we electively performed coronary angiography via the right radial artery using a 6 Fr sheath to determine the etiology of the myocardial injury. Coronary angiography showed no significant atherosclerotic stenosis in the right coronary artery and LCX, but a dissection was found from the midportion of the LMT to the proximal site of the LAD, suggestive of type 1 SCAD (, Video) []. Because the coronary blood flow of the LAD was impaired from thrombolysis in myocardial infarction (TIMI) flow grade III to I after contrast injection () and the patient had chest pain with ST elevation, we decided to perform urgent PCI. The first wire (SION Blue; Asahi Intecc Co., Ltd., Nagoya, Japan) was initially introduced into the distal LAD, but IVUS imaging revealed that the guide wire had passed through the true lumen of the left coronary artery ostium, false lumen at the ostium of the LCX, and true lumen of the distal LAD (true-false-true) (). In addition, the true lumen of the proximal LAD was compressed by the false lumen (), and no significant atherosclerosis was observed within the vessel on IVUS. We then inserted the second guide wire (SION Blue; Asahi Intecc Co., Ltd.) into the LCX (), and IVUS imaging confirmed that it had been placed in the true lumen from the LMT to LCX (). Next, we inserted the third guide wire (SION Blue; Asahi Intecc Co., Ltd.) from the true lumen of the LCX to the compressed true lumen of the LAD using a double-lumen catheter (Crusade Type R; Kaneka Corporation, Tokyo, Japan) by referring to the IVUS findings of the dissected segment (Video). We initially inserted the third guide wire into the true lumen of the obtuse marginal branch using a double-lumen catheter that was placed in the true lumen of the LCX (). We then pulled the wire back and controlled it toward the true lumen of the LAD, which was located under the first guide wire from the right anterior oblique and caudal view (Figures and ). The IVUS-guided rewiring technique was successful, and the subsequent IVUS imaging confirmed that the third guide wire had passed entirely through the true lumen from the LMT to LAD (, Video). After the successful rewiring from the true lumen of the LMT to distal LAD, we removed the first wire () and deployed a drug-eluting stent (Resolute Onyx, 3.5 × 30 mm; Medtronic plc, Fridley, MN, USA) from the LMT to LAD (Figures , , and ). Because the blood flow of the LCX was preserved after stenting, we did not perform rewiring of the side branch and final kissing balloon inflation. Final coronary angiography showed acceptable results and TIMI grade III flow in both the LAD and LCX ().
The postprocedural course was uneventful, and no major adverse cardiovascular events were observed. The peak levels of creatine phosphokinase and its MB isozyme were 1155 and 142 U/L, respectively. Follow-up coronary computed tomography (CT) angiography was performed 12 months after the procedure and showed acceptable results with no clear findings of in-stent restenosis or incomplete stent apposition (Figures and ). The patients' clinical course was uneventful during an 18-month follow-up.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [49, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'between the normal limit or up to three times the normal limit', 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'obesity': False}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 49 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 3.
The value of 'initial troponin' in the patient's note is determined to be 'between the normal limit or up to three times the normal limit'. Based on the HEART Score criteria, 1 point is added for 'initial troponin', increasing the current total to 3 + 1 = 4.
Based on the patient's data, the HEART Score is 4."
4142,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6415980-1,Extracted,"A 66-year-old male with a past medical history significant for hypertension, hyperlipidemia, ischemic stroke, coronary artery disease, and asthma was admitted for cardiac catheterization for worsening angina. He had symptoms of crescendo angina with New York Heart Association (NYHA) class IV symptoms and was referred by his primary cardiologist for coronary angiography with the intent to pursue revascularization as warranted. He had established coronary artery disease in 2012, with pharmacological myocardial perfusion imaging demonstrating inferior infarct and peri-infarct ischemia with an overall preserved systolic function for which medical treatment was pursued. In 2014, he reportedly underwent coronary angiography, which demonstrated a chronic total occlusion of the right coronary artery with grade III collaterals to the right coronary system and moderate non-obstructive disease of the left circumflex artery. In the interim, he ceased tobacco smoking and received guideline-directed medical therapy. He was doing well with optimal medical therapy, which included aspirin and clopidogrel, until three weeks prior to this presentation when he noted the onset of recurrent angina. Angina initially occurred with mild exertion, subsequently progressed to angina at rest, and he was admitted to hospital with unstable crescendo angina.
On admission, his vital signs were stable. His physical exam was unremarkable. A 12-lead electrocardiogram (EKG) demonstrated inferior Q waves and left ventricular hypertrophy without acute ST-T abnormalities (Figure ). Cardiac biomarkers were normal (peak creatinine phosphokinase-MB (CK MB) fraction and troponin T were 9.9 ng/mL (normal range 0.0-10.4) and less than 0.03 ng/mL (<0.03 negative), respectively. Coronary angiography revealed multi-vessel coronary artery disease with a likely culprit lesion involving the proximal left circumflex artery (Videos -). He underwent successful drug-eluting stent (DES) deployment to the proximal left circumflex artery (Video ). PCI was uneventful and guideline-directed medical therapy was continued. Despite long-term adherence to clopidogrel, platelet reaction unit (PRU) was 235. Due to a high on treatment PRU, with levels greater than 208 associated with an increased risk of stent thrombosis [-], a decision was made to transition to ticagrelor. He received a single 180 mg loading dose of ticagrelor. Four hours after receiving ticagrelor, he complained of shortness of breath, throat pain, neck discomfort, and swelling of the tongue. His vital signs remained stable, and he did not exhibit any skin eruption. He demonstrated mild swelling of the tongue and significant swelling of his throat and uvula. No wheezing was noted on exam. He received supplemental oxygen and otolaryngology (ENT) consultation was sought. He was treated with dexamethasone, as well as H1 and H2 histamine blockers. After the first dose of treatment, his symptoms improved. He was closely monitored. The following morning, ENT performed flexible fiberoptic laryngoscopy, which revealed a mild edematous pharyngeal area. Based on the clinical scenario, a provisional diagnosis of ticagrelor-induced angioedema was entertained. He did not have any history of allergy to any medications, contrast medium, or heparin. The decision was made to discontinue ticagrelor. His symptoms improved over the next few days with a tapering dose of steroids and antihistamines. The final decision was made to double the dose of clopidogrel and the patient was discharged with 150 mg of clopidogrel and 81 mg of aspirin daily. He has not had any ischemic symptoms or coronary events over a six-month period of follow-up.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [66, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': True, 'smoking': False, 'atherosclerotic disease': True, 'Initial troponin': 'less than or equal to normal limit', 'Transient Ischemic Attacks History': True, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 66 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 2 + 2 = 4.
The following risk factor(s) are present based on the patient's note: hypertension, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 4 + 1 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 5.
Based on the patient's data, the HEART Score is 5."
4143,18,HEART Score for Major Cardiac Events,risk,integer,usmle-6404,Extracted,"A 50-year-old man visits his physician after 20 years of not seeking any medical care. He is concerned about his health after a colleague recently had a heart attack. The patient has no active complaints and says he feels healthy; however, he does not exercise regularly and lives a sedentary lifestyle. He is employed as an administrative position at a local college, and is seated at a desk most of the day. His father had a heart attack at age 54 and his mother is still alive with no health concerns. He does not smoke, only drinks socially, and does not use drugs. Today, his blood pressure is 130/90 mm Hg, pulse is 84/min, and respiratory rate is 14/min. Physical examination reveals an obese male with no significant findings.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [50, 'years'], 'Hypertension history': True, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': True, 'Diabetes mellitus': False, 'obesity': True, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': True, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 50 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: hypertension, obesity, family with cvd. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, smoking, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, smoking, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 1 + 2 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4144,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7505637-1,Extracted,"A 54-year-old male with a medical history of hypertension and transient ischemic attack, presented to the emergency department (ED) for evaluation of dyspnea on exertion. The patient reported that his dyspnea started one week prior to ED visit. He also endorsed orthopnea and intermittent chest pain. He also endorsed mild orthopnea and lightheadedness, though he denied any syncopal event. Vital signs were found within normal limits on arrival. He clinically appeared to be volume overloaded which improved quickly with IV furosemide. The physical examination also revealed a loud 3/6 systolic harsh murmur appreciated on the apex with radiation to the axillae. Laboratory testing was notable for an elevated troponin I of 0.10 ng/ml with a flat trend, elevated BNP of 301 pg/mL, lactate of 0.9 mmol/L, potassium of 3.8 mEq/L, sodium of 130 mEq/L, and magnesium of 2.1 mg/dl. The electrocardiogram showed sinus tachycardia with no ischemic changes and otherwise unremarkable. He underwent a 2D echocardiogram (Figure ) with a subsequent transesophageal echocardiogram (TEE) with 3D image acquisition which was significant for hyper-dynamic LV function and evidence of isolated flailed P3 scallop of the MV leaflet resulting in a severe eccentric, anteriorly directed MR jet (Figure ). The MV leaflets did not appear thickened and there was no evidence of mitral or aortic stenosis. Cardiac catheterization showed multivessel disease (Figures and 4) for which the patient underwent coronary artery bypass grafting and MV repair.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'Hypertension history': True, 'Transient Ischemic Attacks History': True, 'Suspicion History': 'Moderately suspicious', 'Electrocardiogram Test': 'Normal', 'atherosclerotic disease': True, 'Initial troponin': 'less than or equal to normal limit', 'hypercholesterolemia': False, 'Diabetes mellitus': False, 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 54 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 1 + 1 = 2.
The following risk factor(s) are present based on the patient's note: hypertension, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4145,18,HEART Score for Major Cardiac Events,risk,integer,trec-cds-2014-1,Extracted,"A 58-year-old African-American woman presents to the ER with episodic pressing/burning anterior chest pain that began two days earlier for the first time in her life. The pain started while she was walking, radiates to the back, and is accompanied by nausea, diaphoresis and mild dyspnea, but is not increased on inspiration. The latest episode of pain ended half an hour prior to her arrival. She is known to have hypertension and obesity. She denies smoking, diabetes, hypercholesterolemia, or a family history of heart disease. She currently takes no medications. Physical examination is normal. The EKG shows nonspecific changes.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [58, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': False, 'Diabetes mellitus': False, 'obesity': True, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Electrocardiogram Test': 'Normal', 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit'}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 58 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, obesity. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 3 + 1 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 4.
Based on the patient's data, the HEART Score is 4."
4146,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7645603-1,Extracted,"A 26-year old previously healthy, not obese female presented with severe, holocranial throbbing headache with nausea, dizziness, and significant visual blurring on the second day past flu-like symptoms due to SARS-CoV-2 infection. Ophthalmological examination revealed bilateral optic disc oedema. Optical coherence tomography was suggestive of optic disc oedema (). No focal deficit, ataxia, or pupil light response abnormalities were found on the neurological examination. Brain and orbital MRI were normal except for discrete white matter lesions in the pons and the cerebral hemispheres suggestive of small vessel disease best observed on T2/FLAIR sequences. Brain venous MRI found no evidence of cerebral venous thrombosis. On the eighth day, she underwent lumbar puncture. CSF analysis revealed an opening pressure of 350 mmH2O, 2 cells/mm3, 15 mg/dL of protein level, and 58 mg/dL of glucose. RT-PCR for SARS-CoV-2 was negative in the CSF. Due to the pontine lesion, extensive laboratory exams were required to exclude demyelinating disease. CSF oligoclonal bands were not present, and serum anti-NMO (CBA method) was negative. No other causes of intracranial hypertension were found. The patient was treated with acetazolamide 500 mg bid and had partial improvement of symptoms to date.
The clinical and laboratory characteristics of this clinical series are presented in . In this study, 56 consecutive COVID-19 patients underwent lumbar puncture for different neurological conditions during the SARS-CoV-2 infection, and 13 of these (23.2%) had a new, persistent headache that prompted a CSF analysis. The most frequent complaint in these patients was a throbbing, holocranial, or bilateral intense daily headache. In four patients, there was a previous history of migraine without aura. However, the current headache was different, with more intense and more persistent pain than usual for them. Other relevant neurological complaints in these patients were peripheral facial palsy in one and blurred vision in three, with documented papilledema in two; all other patients had normal fundoscopy.
The opening CSF pressure of one of these patients with papilledema was 210 mmH2O, below the level required for the diagnosis of pseudotumor cerebri syndrome (PTCS), according to a revised diagnostic criteria (). All patients had normal cell counts and glucose and protein levels on the CSF analysis. Besides, RT-qPCR for SARS-CoV-2 in CSF was negative in all patients. Median values for cell counts, glucose, and protein were of 1.6/mm3 (1-4/mm3), 55.6 mg/dL (38–71mg/dL), and 29.6 mg/dL (15–45mg/dL), respectively. CSF opening pressure ranged from 150 to 600 mmH2O (median of 270 mmH2O). In 12 patients, the opening pressure was ≥200 mmH2O (median of 251 mmH2O) and in six of these ≥250 mmH2O (median of 355 mmH2O). No other causes for intracranial hypertension, such as obesity, venous thrombosis, or drugs, were identified in these patients. All patients were submitted to brain MRI and only in one patient were abnormalities typically seen in intracranial hypertension detected (see ).
To date, nine out of 13 patients were pain-free 8 days after the headache onset on average (3–15 days), and five had a partial recovery, with mild headache (follow-up of 66 days to date).
Other neurological conditions that prompted lumbar puncture were meningoencephalitis/encephalopathy in 35 patients, Guillain-Barré syndrome in four, Miller-Fisher syndrome in two, and acute myelitis in two individuals. Median CSF opening pressure in this group was of 200 mmH2O (150–400).",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [26, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'obesity': False, 'smoking': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 26 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4147,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7236309-1,Extracted,"A 60-year-old female patient was hospitalized for swelling and pain in the left lower extremity for 5 days. It was reported that, 5 days ago, the patient experienced swelling of thigh, which gradually spread to the lower leg, and increased local skin tension and temperature. The patient had no fever, shortness of breath, chest pain, cough, expectoration, hemoptysis, amaurosis, or syncope; no special relevant medical, family, psycho-social past histories, and no history of chronic lower limb symptoms, even during her previous pregnancy. Deep vein ultrasound of the lower extremity at local hospital reported thrombosis of left common femoral vein, superficial femoral vein, deep femoral vein, popliteal vein, anterior tibial vein, posterior tibial vein, and intermuscular vein for the first time. She had no history of surgery or catheterization. On physical examination, her heart rate was 88 bpm, and blood pressure was 130/74 mmHg. Examination of the left lower limb revealed swelling and edema with moderate tenderness and pain, while the right lower limb was normal. Blood tests revealed normal blood routine and normal liver and kidney functions. Computed tomography angiography (CTA) indicated compression of LCIV by RCIA, narrowed LCIV lumen, thrombi formed from the femoral vein to left external iliac vein, and collateral circulation formed between bilateral external iliac vein (Fig. ). She was diagnosed with DVT along with MTS.
The patient underwent IVC angiography, filter placement, left iliac vein plasty, and stent implantation under local anesthesia. The right femoral vein was punctured successfully with Seldinger technique [] and then placed into the catheter sheath. Contrast agent was passed smoothly through IVC without filling defect (Fig. a). The sheath of the filter was transported, and a Cordis Optease filter was placed in the IVC at second lumbar vertebrae (Fig. b), followed by puncturing of the left femoral vein. The catheter sheath was then inserted; angiography revealed severe stenosis of the left external iliac vein and the common iliac vein, and the pelvic collateral compensation was seen through contralateral reflux (Fig. c). A 14 mm - 60 mm balloon was inserted into the IVC through a narrow segment of left external iliac vein and common iliac vein (Fig. d). Then, an E-lunimexx 14 mm - 60 mm self-expanding stent was inserted (Fig. e). The stent was in good position, and the expansion remained satisfactory (Fig. f). The contrast medium was passed through smoothly, and the original stenosis was relieved. At the end of the operation, the sheath of the bilateral inguinal area was removed, and the wound was dressed with a bandage. The patient returned to the ward safely and tolerated well, and was discharged 5 days after the surgery. The patient was prescribed with oral rivaroxaban and aspirin. After 28 days of the surgery, she came back to the hospital for the removal of IVC filter. This procedure was successful. The DVTs were ablated after 4 months of anticoagulation therapy.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [60, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 60 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4148,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7788985-1,Extracted,"A 23-year-old African-American man with past medical history of G6PD-deficiency and obesity presented with dyspnea and pleuritic chest pain that improved upon leaning forward and scant hemoptysis of two weeks duration. He was notably hypertensive to the 220/110 s mmHg and tachycardic to the 120 s, but had a preserved respiratory rate and oxygen saturation. Physical exam was remarkable for bilateral diffuse wheezing throughout all lung fields. Other parts of the exam including cardiovascular, nasopharynx, skin and musculoskeletal systems were unremarkable. Additional pertinent history was remarkable only for marijuana smoking. Electrocardiogram was unremarkable except for left atrial enlargement. Chest X-ray revealed bilateral pulmonary infiltrates, cardiomegaly, and mediastinal enlargement suggestive of bulky hilar adenopathy. Computed tomography (CT) scan of the chest with contrast was performed which was negative for pulmonary embolism, but revealed bilateral centrilobular opacities, hilar/mediastinal lymphadenopathy, and a trivial pericardial effusion (Fig. a). Initial laboratory diagnostics were significant for acute kidney injury with a serum creatinine of 2.03 (mg/dL), trace proteinuria, troponin elevation to 0.232 (ng/mL), and a D-Dimer of 1.3 (mcg/mL). Complete blood count revealed no leukocytosis, but concomitant eosinophilia, with no evidence of anemia. The patient was subsequently admitted to the medicine wards and a therapeutic regimen of antihypertensive agents as well as intravenous ceftriaxone and azithromycin for presumed community acquired pneumonia was initiated.
Additional diagnostic evaluation demonstrated marked elevation of CRP (80 mg/L) and ESR (67 mm/hr). Pheochromocytoma screening with serum catecholamines and metanephrines was negative. An echocardiogram revealed an ejection fraction of 40%, moderate concentric left ventricular hypertrophy, and trivial pericardial effusion without evidence of tamponade or pulmonary artery hypertension. Despite continuation of antibiotics for pneumonia and adjunctive heart failure management, the patient’s clinical status failed to improve. In the setting of an unremarkable infectious workup and concern for an autoimmune etiology, the patient was started on oral prednisone 60 mg daily. The patient remained symptomatic, experiencing episodic chest pain and shortness of breath, with blood pressure lability. Repeat chest X-ray showed worsening bilateral infiltrates. Subsequently, ANA resulted weakly positive (1:160) with a homogenous pattern and rheumatoid factor (RF) returned negative.
On the fifth day of admission, antibiotics were discontinued in light of negative cultures and lack of significant clinical improvement. The patient’s blood pressure was noted to be slightly improved with addition of prednisone however remained poorly controlled on multiple medications (Fig. ). Autoimmune panel including ANCA (MPO/p-ANCA, and PR3/c-ANCA), anti-double-stranded DNA antibody, anti-Smith antibody, C3 and C4 complements, anti-histone antibody, as well as other autoimmune related factors and infectious serologies returned negative or within normal limits (Table ). Renal ultrasound and renal artery duplex were performed which did not reveal any evidence of hydronephrosis or renal artery stenosis, respectively. A repeat high-resolution chest CT scan was obtained, both in supine and prone positions, to help differentiate early interstitial lung disease from intra-alveolar processes, which showed persistent intra-alveolar opacities without any change on prone position (Fig. b). Over the course of the following days, the patient reported improvement in his symptomatology and his blood pressure improved, therefore he was taken off prednisone on the sixth day. Pulmonary function testing was performed in the setting of bilateral hilar adenopathy and fixed infiltrates, which revealed a mixed obstructive and restrictive pattern. He eventually underwent lung biopsy by video-assisted thoracoscopic surgery (VATS) with right medial lobe wedge resection and was subsequently discharged with instructions to follow up with rheumatology for planned initiation of rituximab. The histopathological results of his lung biopsy demonstrated extensive intra-alveolar hemorrhage with linear polymorphonuclear (PMN) cell collections in alveolar septa and capillaritis without any evidence of granulomatous changes, indicative of microscopic polyangiitis (Fig. ). Immunohistochemistry on lung biopsy samples was not performed and renal biopsy was deferred to outpatient rheumatology.
Unfortunately, the patient was lost to follow up, failing to attend any of the scheduled appointments. He was subsequently readmitted six months later with similar symptoms, and once again found to be in hypertensive emergency, complicated by acute decompensated heart failure. Repeat echocardiogram revealed a further decline in his ejection fraction to 25% and a trivial pericardial effusion. Rheumatology was consulted and recommended pulse steroid therapy with methylprednisolone 250 mg four times a day for three days, which led to significant improvement in symptoms and blood pressure. Repeat ANCA and autoimmune serological workup remained negative. Following initiation of pulse steroid therapy, he underwent renal biopsy. The biopsy contained forty glomeruli, six of which were globally sclerotic. One glomerulus had segmental sclerosis. There were changes suggestive of microangiopathic injury in some arteries and glomeruli, such as bloodless glomeruli and mild intimal myxoid changes in arteries, with associated acute tubular injury. Focal tubular atrophy and interstitial fibrosis were estimated to involve approximately 10% of the cortex. No evidence of crescents or granulomatous changes were observed. Immunofluorescence was unremarkable, with only non-specific linear glomerular and tubular basement membrane staining for IgG, kappa, lambda, and albumin, indicative of pauci-immunity. Electron microscopy demonstrated segmental effacement of podocyte foot processes (40%) with vacuolation and microvillous transformation of the podocyte cytoplasm, ischemic-type capillary wall wrinkling, and subendothelial electron lucent widening (Fig. ). He was subsequently discharged on a steroid taper with plans for outpatient rituximab. Despite extensive education about his condition he was once again lost to follow up and missed appropriate treatment.
Over the course of the next year, he was readmitted on multiple occasions and eventually progressed to dialysis-dependent end-stage renal disease. His two most recent admissions were characterized by pancreatitis with pancreatic pseudoaneurysm complicated by retroperitoneal hematoma and cardiac tamponade, respectively. With respect to his pancreatitis, he presented in the context of acute onset abdominal pain with associated nausea and vomiting. Laboratory diagnostics demonstrated an elevated lipase (3400), normal triglycerides, and a negative IgG4 serology. Abdominal CT was significant for peripancreatic fat stranding and inflammatory changes without evidence of gallstones or biliary ductal dilation. He denied recent alcohol use. Pancreatitis course was further complicated by retroperitoneal hematoma, which was found to be secondary to a 7 mm pancreatic pseudoaneurysm rupture, as revealed on repeat abdominal CT angiography (Fig. ). He was managed conservatively and subsequently discharged. One month later he presented with dyspnea, chest pain and nausea, and was found to have large pericardial effusion with an acute decrease in ejection fraction to 10% (Fig. ). He underwent pericardiocentesis with removal of one liter of serosanguineous fluid. Fluid analysis was indicative of hemorrhagic etiology and negative for malignancy. On review of most recent outpatient records, the patient has been maintained on high-dose suppressive steroid therapy with plans for initiation of Rituximab or Cyclophosphamide.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [23, 'years'], 'Hypertension history': True, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': False, 'obesity': True, 'smoking': True, 'Initial troponin': 'between the normal limit or up to three times the normal limit', 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 23 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: hypertension, obesity, smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 0 + 2 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'between the normal limit or up to three times the normal limit'. Based on the HEART Score criteria, 1 point is added for 'initial troponin', increasing the current total to 2 + 1 = 3.
Based on the patient's data, the HEART Score is 3."
4149,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6460839-1,Extracted,"A 64 year-old Caucasian female former smoker (4 pack-year) originally presented to the emergency department with painless jaundice. Physical exam revealed an afebrile female with scleral icterus and jaundice. Her abdomen was soft, non-tender, and non-distended in all quadrants with normal bowel sounds and no organomegaly. CT imaging demonstrated a large (10 cm) retroperitoneal mass, necessitating biliary stenting. Fine needle aspiration of the mass revealed a CD10+clonal B cell population by flow cytometry, consistent with presumptive B cell lymphoma. During the staging workup for the lymphoma, right-sided cervical level IIA and III lymphadenopathy was found incidentally during a routine dental check-up, which was initially thought to be of the same disease process. She had no supraclavicular or axillary lymphadenopathy. CT demonstrated right level II/III LN and possible right base of tongue (BOT) mass. Flexible laryngoscopy revealed an exophytic mass involving the right BOT that extended to the right glosso-tonsillar sulcus and beyond the midline measuring approximately 3 cm (Fig. ). Excisional biopsy of two right cervical lymph nodes unexpectedly demonstrated squamous cell cancer (SCC) that was positive for p16 and HPV. Subsequently, positron emission tomography/computed tomography (PET/CT) demonstrated an FDG-avid right BOT mass (2.3 × 0.9 cm) with right-sided level IIA, IIB and III lymphadenopathy (all < 3 cm), consistent with biopsy-proven HPV-associated SCC (Fig. ). There was also an intensely FDG-avid retroperitoneal mass (8.2 × 13.4 × 10.7 cm) along with left mesenteric, left periaortic, and left retroperitoneal lymph nodes (Fig. ). Laparoscopic biopsy of gastroepiploic, mesenteric, and gastrocolic lymph nodes confirmed follicular lymphoma. Pathology showed relatively low number of centroblasts (fewer than 15 per high power field) compatible with low grade follicular lymphoma (WHO grade 1–2) with significantly elevated Ki-67 proliferation index (~ 80%) suggesting clinical behavior similar to WHO grade 3 follicular lymphoma. Omentum and liver were not involved. Therefore, a diagnosis of synchronous stage IV T2N2bM0 HPV+ SCC of right BOT and stage IIAX follicular lymphoma was made. At the time, she was relatively asymptomatic from the BOT cancer. She denied dysphagia, odynophagia, trismus, otalgia, or speech or voice change. She also denied night sweats, fevers, significant weight loss, or infectious symptoms. Videofluoroscopic swallow study evaluation was normal. ECOG performance status was 1. After stenting, the patient’s bilirubin normalized and she was asymptomatic. Her case was discussed at multidisciplinary case conferences, and the initial plan was to treat the BOT cancer first due to its likely curability and shorter treatment course.
One month later, however, the patient was admitted to the hospital because of worsening abdominal pain. Given concern for lymphoma becoming increasingly symptomatic, R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy was initiated. She tolerated therapy well and had resolution of abdominal pain. After completion of 3 cycles of R-CHOP, PET/CT scan demonstrated interval markedly decreased size and uptake of the retroperitoneal mass, as well as interval resolution of the FDG-avid BOT lesion, and most of the FDG-avid cervical lymph nodes (Figs. and ). She had no symptoms referable to lymphoma at this time. Nasopharyngolaryngoscopy also revealed no residual fullness in the area of the right BOT (Fig. ). After completion of another 3 cycles of R-CHOP (in total 6 cycles), PET/CT scan demonstrated sustained metabolic resolution of the abdominal mass. However, FDG-avid right BOT lesion as well as right cervical level II and III nodes had become slightly more prominent compared to the end of cycle 3. The decision was made to start 7-week concurrent chemoradiation with weekly cisplatin 40 mg/m2 for the SCC. Unfortunately, she was found to be neutropenic and cisplatin was switched to cetuximab. At the end of the first cetuximab infusion, she developed a Grade 3 infusion reaction with rigors and chest pain and was diagnosed with NSTEMI. An attempt to re-initiate cisplatin treatment after ANC normalized was unsuccessful as patient experienced fever and altered mental status necessitating hospital admission. She had received a total of one dose of cetuximab and two doses of cisplatin before the decision was made to proceed with radiation therapy (RT) without further chemotherapy. In total, the patient received 6996 cGy, 212 cGy per day in 33 fractions with coverage of the oropharynx and bilateral neck using tomotherapy-based image-guided intensity-modulated radiation therapy. Despite experiencing significant anterior mouth sores from cetuximab early in treatment, as well as significant oropharynx mucositis late in treatment, she was ultimately able to complete RT without an enteral feeding tube. At 3-month follow-up, she had no clinical or radiographic evidence of disease on exam or PET/CT scan. At the time of this manuscript submission, 3 years after completion of the radiation therapy, she remained in remission for both cancers.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [64, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 64 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4150,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7598218-1,Extracted,"A 30-year-old male patient presented to the outpatient clinic with a three-day history of lower abdominal pain. The pain was localized to the left lower quadrant, aching, intermittent, non-radiating, with an intensity of 7/10. The pain was aggravated by movement, partially relieved by acetaminophen, and had gradually worsened over three days. He denied a history of fever, loss of appetite, vomiting, constipation, diarrhea, tenesmus, blood in the stools, dysuria, and increased urinary frequency. There was no history of recent travel or contact with sick persons. He was not on any regular medications, and his past medical history was unremarkable. Past surgical history was significant for laparoscopic cholecystectomy at 25 years of age.
On examination, the patient was afebrile and hemodynamically stable. His temperature was 35.5℃, heart rate was 60 beats/min, blood pressure was 120/88 mm Hg, and his respiratory rate was 16 breaths/min. The abdomen was soft and non-distended with audible bowel sounds. Palpation revealed tenderness in the left iliac fossa with mild voluntary guarding. No rebound tenderness or rigidity was noted. The liver and spleen were not palpable. The remaining systemic exam was unremarkable. A provisional diagnosis of acute diverticulitis was made based on the clinical presentation.
Lab investigations, including complete blood count, electrolytes, amylase, lipase, urinalysis, liver, and renal function tests, were within normal limits. A non-contrast CT of the abdomen and pelvis was ordered, which revealed a fat-containing nodule adjacent to the descending colon with surrounding inflammatory stranding, which was suggestive of acute epiploic appendagitis (Figure ). The patient was discharged home in stable condition with ibuprofen for pain control. At a follow-up on day 5, the patient reported complete resolution of his pain with no recurrence.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [30, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 30 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4151,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7072715-2,Extracted,"Patient 2 is a 45-year-old man treated with high insulin doses (100 UI/day) for diabetes mellitus diagnosed at 34, complicated with non-proliferative retinopathy and microalbuminuria. He also suffered from hypertriglyceridemia (from 5.46 mmol/L to 13.45 mmol/L) despite high doses of statins (Rosuvastatin 10 mg/day). Leptin was measured at 8.49 ng/mL (reference 3.3–8.7). He had a family history of diabetes mellitus (A). His mother was diabetic and died of a myocardial infarction at 44 and his father died of a brain hemorrhage at 72. On his mother’s side, diabetes mellitus was described for his grandparents and three uncles.
A physical examination revealed a BMI = 26.5 kg/m², WC = 107 cm with no lipodystrophy (B). The patient complained of occasional muscular cramps. The percentage of fat mass was 31.1% with DEXA (C). The mean subcutaneous adipocyte diameter was 109.9 ± 24.3 µm (D). Abdominal CT scan revealed the presence of superficial (103 cm2) and deep (224 cm2) subcutaneous adipose tissue with excessive visceral fat accumulation (167 cm2) (E). The anti -glutamic acid decarboxylase (GAD) and anti-tyrosine phosphatase-like insulinoma antigen 2 IA-2 antibodies and Maturity Onset Diabetes of the Young (MODY) testing were negatives. An abdominal echocardiography revealed liver steatosis and hepatomegaly (right hepatic arrow at 20 cm). A myocardial evaluation showed no cardiac or coronary artery disease. The exercise stress testing was normal.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'years'], 'Diabetes mellitus': True, 'hypercholesterolemia': True, 'obesity': True, 'Electrocardiogram Test': 'Normal', 'parent or sibling with Cardiovascular disease before age 65': True, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'Hypertension history': False, 'smoking': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 45 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: diabetes mellitus, obesity, family with cvd. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, smoking, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, smoking, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 1 + 2 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4152,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7402536-1,Extracted,"A 23-year-old male was brought to the emergency room (ER) for evaluation after a syncopal episode. The episode was without involuntary shaking, tongue biting, and bowel or bladder incontinence. He had no similar episodes in the past. He reported no significant past medical history. However, he reported cough, sore throat, subjective fever, and chills one week before the presentation. Family history was significant for hereditary spherocytosis in his mother and younger brother. He had a blood pressure of 117/66 mmHg, a heart rate of 98/min, and a temperature of 98.7°F. Upon physical exam, he had a bruise on the left side of his face from the fall, and enlarged tonsils with grayish exudates. There was no rash, lymphadenopathy, or hepatosplenomegaly. Labs showed hemoglobin and hematocrit of 5.0 g/dL and 13.6%, respectively. One week prior, they were 11.8 g/dL and 33.4%. His white blood cell (WBC) count was 8.7 K/µL, and the platelet count was 146 K/µL. His lactate dehydrogenase (LDH) was elevated to 368 U/L, total bilirubin to 2.2 with indirect bilirubin of 2.0, a reticulocyte number of <10 K/µL, and a haptoglobin of <7.75 mg/dL. He had a B12 of 474 pg/mL and serum folate of 13.6 ng/mL. Iron panel showed a low serum iron 284 µg/dL, normal total iron binding capacity (TIBC) 320 µg/dL, high iron saturation 89%, and normal serum ferritin 122.6 ng/mL. The peripheral blood smear showed spherocyte (Figure ). Chest x-ray showed small left lower lobe pneumonia.
Ultrasound revealed moderate splenomegaly (measuring 17.5 cm x 6 cm x 5 cm), and coarse echotexture of the hepatic parenchyma secondary to fatty infiltration (Figure ). CT of the head was normal, and a CT of the maxillary sinuses showed mild sinusitis in the maxillary sinuses. The patient was transfused four units of blood and was given IV antibiotics. He was later found to be positive for parvovirus DNA by PCR and Epstein-Barr virus (EBV) IgG and IgM. An osmotic fragility test was positive, confirming the diagnosis of hereditary spherocytosis. He tested negative for cold agglutinin, direct antiglobulin, serum protein electrophoresis, and urine hemosiderin. The patient’s condition improved over time with supportive care and close monitoring. On follow-up, his hemoglobin improved to 10 g/dL, hematocrit to 33.6%, reticulocyte count increased to 261.9 K/µL, LDH 158 U/L, and a haptoglobin <7.75 mg/dL.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [23, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 23 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4153,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4446062-1,Extracted,"This is a 53 year-old African American male, with no significant past medical history who presented with a one-day history of right arm swelling. He woke up with a swollen arm and dull, aching pain in the right upper extremity. Our patient, a retired office manager, reported exercising daily over the prior week with a new “vibrating device” (Figure ). Patient denies any past interventions to the right upper extremity.
Patient denied: known malignancy, personal or family history of DVT, trauma, intravenous therapy, and drug abuse. Physical examination was unremarkable except for extensive right upper extremity swelling.
See Additional file .
Laboratory testing revealed CBC, CMP, PT/INR and aPTT all within normal limits.
A venous doppler study revealed an occlusive thrombus in the right axillary, proximal brachial and basilic veins. Access via a forearm vein was achieved and venography confirmed extensive occlusion of the right axillary, proximal brachial and basilic veins (Figure ).
An infusion catheter was positioned to allow tPA infusion of the thrombus throughout its entire length over the ensuing 24 hours. The following day, a venogram revealed the presence of a small residual thrombus and a 50% stricture in the right axillary vein (Figure ). Mechanical thrombectomy using an angiojet device, followed by balloon angioplasty and deployment of a 12 × 6 mm stent resolved the residual thrombosis and stenosis. Completion angiography showed complete resolution of the stricture and thrombus (Figure ).
The patient was discharged the following day on warfarin and aspirin. There were no adverse or unanticipated events.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [53, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'hypercholesterolemia': False, 'obesity': False}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 53 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4154,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4222711-1,Extracted,"A healthy 21-year-old male African American college football player, with a body mass index (BMI) of 39 and no additional risk factors for coronary artery disease, was admitted to the emergency department. The patient was complaining of a single episode of unrelenting sharp chest pain immediately after he had finished powerlifting 400 lbs in a bench press lift. The chest pain was largely typical: substernal, associated with shortness of breath, exertional, constant, and not musculoskeletal in nature.
The patient reported no known drug allergies and took no medications or supplements. He had no chronic medical problems and both parents were alive without chronic medical problems. There was no history of deep venous thrombosis (DVT), pulmonary embolism, or coronary heart disease in the family. A review of systems was only positive for the above. His vital statistics on admission were within normal limits. The physical exam was largely benign.
Imaging results obtained included chest radiography that only showed cardiomegaly, consistent with an athletic heart. An electrocardiogram showed a sinus rhythm with a right bundle branch block (RBBB) (). A urine toxicity screen was negative for cocaine and central nervous system stimulants. The lipid profile was within normal limits. At the emergency room, blood tests showed elevated serum levels of cardiac enzymes, with troponin at a level of 0.53, which peaked at 10.43 the next day (). Non-ST elevation myocardial infarction was diagnosed and the patient received medical treatment as per acute coronary syndrome protocol, which includes aspirin, a statin, a high intensity intravenous heparin protocol, an angiotensin converting enzyme (ACE) inhibitor, and a beta blocker.
Transthoracic echocardiography (TTE) was performed in the emergency room and was unremarkable. A computerized tomography (CT) angiogram of the chest was negative for aortic dissection. A transesophageal echocardiogram (TEE) showed a very minor patent foramen ovale (PFO) only with a Valsalva maneuver and was not apparent on a Doppler view (). During the Valsalva maneuver, a single bubble became apparent (). There was no aortic dissection. A coronary angiography showed a thrombus in the proximal to mid left anterior descending artery (LAD) in otherwise normal coronary arteries (). Intravascular ultrasound showed evidence of thrombotic material in the mid LAD in addition to mild plaque disease, and no evidence of dissection in the left main, proximal, or mid LAD (). The patient received Integrilin® after coronary angiography. One week after the onset of chest pain, another coronary angiography showed resolution of the LAD thrombus (). The patient was then discharged with aspirin (81 mg daily), clopidogrel (75 mg daily), and atorvastatin (80 mg daily), with advice to avoid strenuous activities such as heavy weight lifting. The patient received six sessions in the cardiopulmonary rehabilitation program before volitional discontinuation.
Five months later, the patient had another episode of chest pain after heavy weight lifting. This episode was similar to the last, but had less intense, substernal nonradiating pressure without shortness of breath or lightheadedness. Pain was relieved with aspirin, nitroglycerin, and morphine. His vital statistics on admission this time showed some stage II hypertension.
He admitted not taking his medication for several days to a week before this episode of chest pain. The physical exam was again benign. Cardiac enzymes were elevated, with electrocardiography showing marked sinus bradycardia with PAC and existing T wave inversions in the inferior leads ( and ). The patient had a coronary angiography on the day of symptom onset. A thrombus was again found in the mid LAD, but was longer than the thrombus found 5 months previously. It was thought that this site had provided a nidus for thrombus formation via recurrent plaque rupture and previous vessel injury. Hence, a bare metal stent was placed on this occasion, as the patient had a previous thrombus that had recurred at the same location. The rest of the coronary arteries were normal by angiography. Due to the PFO, a hypercoagulable workup was performed. A lower extremity ultrasound did not show any DVT. Results of laboratory studies showed elevated factor VIII activity at 205% (). A decision to put the patient on anticoagulation therapy was made in light of the likely arterial embolus versus paradoxical embolism. He was discharged home with aspirin (81 mg daily), prasugrel (10 mg daily), atorvastatin (80 mg daily), and warfarin (5 mg daily with enoxaparin bridging). The ACE inhibitor was temporarily held because of mild acute kidney injury that was more likely a falsely elevated creatinine secondary to increased muscle mass. A beta blocker was stopped secondary to bradycardia.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [21, 'years'], 'Hypertension history': True, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': False, 'Diabetes mellitus': False, 'obesity': True, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal'}",6,6,6,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 21 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: hypertension, obesity, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 2 + 2 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 4 + 2 = 6.
Based on the patient's data, the HEART Score is 6."
4155,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5810438-1,Extracted,"A 62-year-old woman presented with exertional chest pain. She visited our hospital because her symptoms were gradually intensifying for several years. Her only risk factor for heart disease was hypertension; she had no history of smoking, and she did not have dyslipidemia. Electrocardiography did not show any ischemic changes. On echocardiography, left ventricular function was preserved and neither hypokinesia nor valvular heart disease was observed. Further evaluation of coronary artery disease was considered necessary; therefore, she underwent a detailed examination using coronary computed tomography (CT) (Fig. ), which revealed an LMT occlusion. Coronary angiography also revealed that the LMT was occluded at the origin. The entire left coronary artery was visualized through collateral circulation in right coronary angiography (Fig. ). Based on blood test findings and aortic CT results, arteritis and autoimmune disease were ruled out.
We performed off-pump CABG to treat this patient. We anastomosed the left internal thoracic artery to the left anterior descending coronary artery and the right internal thoracic artery to the left marginal artery. The patient’s hemodynamics were stable during and after the operation. The patient’s postoperative progress was smooth; her ventilator was removed the day after the operation, she began walking independently on Day 3 post-operation, and she was discharged on Day 8 post-operation. Graft patency was confirmed with coronary CT on Day 7 post-operation (Fig. ). She goes well without any symptoms during 3-years follow up.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [62, 'years'], 'Hypertension history': True, 'Suspicion History': 'Moderately suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'smoking': False, 'atherosclerotic disease': True, 'Diabetes mellitus': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 62 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 1 + 1 = 2.
The following risk factor(s) are present based on the patient's note: hypertension, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4156,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5642777-1,Extracted,"A 24-year-old Nepalese male patient who worked as a shepherd in a suburban farm in Doha, Qatar, and with no significant past medical history, presented to the emergency room with a sudden onset of nausea, vomitting, dizziness and profuse sweating around 30 minutes after a scorpion sting to the right big toe. The patient described the scorpion as “yellowish-white color”. Upon arrival to the emergency room, the patient was still having severe pain localized at the site of sting.
A physical examination revealed a young male patient who was conscious, oriented but anxious. He looked sick, sweaty, pale and dyspnic. He was hypotensive with a blood pressure of 75 mmHg systolic and 55 mmHg diastolic, and tachycardiac with regular heart beats of 125 beat per minute. He had raised jugular venous pressure, bilateral diffuse lung fields crepitations up to the mid-zones, normal first and second heart sounds and summation gallop. No focal neurological deficits.
By this time patient had received the scorpion anti-venom (1 vial intravenous), IV hydrocortisone 200 mg, and 2000 ml of normal saline over 4 hrs. The IV fluids were stopped when the patient developed signs of pulmonary edema.
ECG showed sinus tachycardia with diffuse ST segment depression (). Cardiac markers came positive (Troponin T: 0.26–1.3 ng/ml, CK-MB: 52 ng/ml) and pro BNP was elevated (4216 pg/ml). Chest radiography showed moderately severe lung congestion (). Urgent echocardiography revealed moderate to severe left ventricular global hypokinesia and impaired systolic function (ejection fraction of 35%) with mild mitral regurgitation and normal study otherwise. Patient was admitted to CCU with an admission diagnosis of toxic myocarditis and cardiogenic shock.
The patient was intubated, mechanically ventilated and maintained on titratable doses of both inotropic agents noradrenaline and dopamine, and maintenance doses of IV hydrocortisone and antibiotics (piperacillin plus tazobactam). Right heart catheterization suggested a picture of cardiogenic shock with cardiac output of 1.88 l/min (normal: 4.5–7 l/min), cardiac index of 1.34 l/min/m2 (normal: 2.5–4.2 l/min/m2), systemic vascular resistence of 3150 d s/cm5 (normal: 800–1200 d s/cm5), and pulmonary capillary wedge pressure of 32 mmHg (normal: 6–12 mmHg) ().
Next day, the patient was febrile with a temprature of 39°C. He developed short runs of ventricular tachycardia () which spontaneously resolved. Two days after admission, his ECG showed sinus rhythm with resolution of the ST segment changes and prolongation of QT interval, corrected QT interval was 503 ms (), while the QT interval was partially normalized five days after admission with a corrected QT interval of 471 ms (). Prazocin (1mg orally twice daily) was then started after hemodynamic stabilization and withdrawal of inotropic agents. Cardiac MRI with gadolinium contrast was arranged, and revealed global LV hypokinesia and systolic dysfunction with global myocardial edema suggestive of diffuse myocarditis; no evidence of myocardial scar by delayed gadolinum enhancement views ( and ).
After one week of CCU course, patient was off-sedation, fully conscious, afebrile wih stable hemodynamics. He was maintaining good oxygen saturation on 40% FiO2, with clear lung fields. He was then successfully extubated.
Two days later, echocardiography revealed significant improvement with normal LV systolic function (EF: 55%). Coronary angiography was normal for both left and right coronary arteries ( and ). Patient was discharged home in a stable condition, on proton pump inhibitor (Rabiprazole 20mg once/day) and a plan for outpatient follow up.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [24, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'Initial troponin': 'between the normal limit or up to three times the normal limit', 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 24 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'between the normal limit or up to three times the normal limit'. Based on the HEART Score criteria, 1 point is added for 'initial troponin', increasing the current total to 0 + 1 = 1.
Based on the patient's data, the HEART Score is 1."
4157,18,HEART Score for Major Cardiac Events,risk,integer,usmle-11977,Extracted,"A 28-year-old female comes to the physician’s office with a complaint of episodic chest pain. She describes the pain as squeezing and tightness in her chest. This pain has been happening every few days for 3 months. She says there is no association of the pain with food or exercise. She is able to climb up to her fourth floor apartment daily without issue. Her only past medical history is migraines for which she takes appropriate medication. Here temperature is 98.6°F (37°C), blood pressure is 120/68 mmHg, pulse is 60/min, respirations are 16/min, and oxygen saturation is 98% on room air. She has no known family history. The patient is not in pain on presentation and EKG in the office is normal. 24-hour ECG monitoring shows transient ST elevations during the episodes of pain that resolve completely.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'parent or sibling with Cardiovascular disease before age 65': False, 'Suspicion History': 'Slightly suspicious', 'Hypertension history': False, 'smoking': False, 'Diabetes mellitus': False, 'age': [28, 'years'], 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 28 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4158,18,HEART Score for Major Cardiac Events,risk,integer,pmc-3420509-1,Extracted,"A 52-year-old Thai man presented with acute chest tightness and palpitation while rubber farming for 1 week. He had a history of hypertension and heavy smoking for 10 years. He was admitted at a local hospital, and the results of the complete blood count and lipid profile showed within normal limits. His electrocardiogram showed a normal sinus rhythm with Wolff-Parkinson-White syndrome, and his clinical signs did not improve, so he was referred to our hospital. His clinical condition was suspected to be due to coronary arterial disease by a cardiologist. However, his exercise stress test was inconclusive, so he was further investigated by CTCA.
The 64-slice CTCA findings showed no calcified coronary artery walls, and the calcium score was zero. A completely absent LCx was observed, which was associated with multiple enlarged diagonal branches of the left anterior descending artery (LAD) to supply the lateral wall of the left ventricle (). Also seen was the superdominant RCA with its posterolateral branch continuing into the territory of the LCx (Figures and ). No significant stenosis was detected. The patient was treated with antiarrhythmic drug (amlodipine 2.5 mg/day) and scheduled for follow-up visits at his district hospital.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [52, 'years'], 'Hypertension history': True, 'smoking': True, 'Electrocardiogram Test': 'Normal', 'Suspicion History': 'Moderately suspicious', 'atherosclerotic disease': False, 'hypercholesterolemia': False, 'Diabetes mellitus': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 52 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 1 + 1 = 2.
The following risk factor(s) are present based on the patient's note: hypertension, smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4159,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7188002-1,Extracted,"A 61-year-old woman presented to a local hospital with typical chest pain lasting for approximately 1 h. The patient history was significant for coronary angiography performed three years prior to this presentation due to typical angina pectoris induced by exercise, revealing normal coronary arteries. On this presentation, serum troponin level was high and her electrocardiogram revealed 0,5-1 mm ST segment depression in precordial derivations (Figure ). The patient was referred to our hospital for invasive management of myocardial infarction.
Except for hypertension treated with irbesartan/hydrochlorothiazide and metoprolol, the patient had no other risk factors for coronary artery disease (CAD). She denied substance abuse, including cocaine abuse. No structural heart disease was detected by transthoracic echocardiography. Early invasive management was planned, therefore coronary angiography was performed. Left coronary angiography, performed with a 6 French Judkins diagnostic catheter, revealed a severe tubular stenosis in circumflex (Cx) artery, evident on various left and right anterior oblique projections. No other lesions (including atherosclerotic plaques) were observed in the left coronary system. On right coronary angiography, performed with a 6F right Judkins diagnostic catheter, diffuse spasm of RCA was observed, most prominent in the distal vessel. A second right coronary angiography, performed 30 s following a 200 peg nitroglycerin intracoronary bolus, revealed complete resolution of spasm (Figure ). Having suspected spasm as etiology of the severe lesion in Cx, angiography was repeated, revealing complete resolution (Figure ). The patient did not report any symptoms throughout the procedure. Resolution of the RCA and Cx stenosis with nitroglycerin suggested CIV in both territories. Furthermore, concentric lesions with otherwise angiographically normal vessels along with morphology of both stenoses were more compatible with arterial vasospasm rather than an atherosclerotic plaque. Beta blocker therapy was discontinued and the patient was discharged on oral diltiazem. On follow-up, she remained symptom-free with medical treatment.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [61, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': False, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'greater than three times normal limit', 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'obesity': False}",6,6,6,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 61 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 3 + 1 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 4 + 2 = 6.
Based on the patient's data, the HEART Score is 6."
4160,18,HEART Score for Major Cardiac Events,risk,integer,usmle-6215,Extracted,"A 30-year-old man is brought into the emergency room for complaints of acute onset chest pain and shortness of breath. He has a history of mental retardation and lives at home with his adoptive parents. His parents inform you that he has not seen a doctor since he was adopted as child and that he currently takes no medications. The patient’s temperature is 99.1°F (37.3°C),pulse is 108/min, blood pressure is 125/70 mmHg, respirations are 25/min, and oxygen saturation is 92% on 2L nasal canula. Physical exam is notable for a tall, thin individual with high-arched feet and mild pectus excavatum. There is mild asymmetry in the lower extremities with discomfort to dorsiflexion of the larger leg. Lung auscultation reveals no abnormalities.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [30, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'obesity': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit'}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 30 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4161,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5965180-1,Extracted,"A 37-year-old male with no significant past medical history presented to the ED with a chief complaint of heart palpitations. He appeared well and was hemodynamically stable. His electrocardiogram (ECG) showed AF with RVR at a rate of 129 beats per minute. Lab work, including a complete blood count and comprehensive metabolic panel were unremarkable, and his troponin was negative. He had a normal echocardiogram and received 30 mg of intravenous diltiazem over a four-hour period in the ED after which time he remained in AF with a heart rate in the 80s.
Our virtual hospital service, the Center for Remote Medical Management (CRMM), was consulted and the patient’s care was transferred to two CRMM remote physicians (an internist and a cardiologist). He was given aspirin and 150 milligrams of oral diltiazem prior to leaving the hospital. We then used a COTLT device to manage his care from home.
The device includes technology in which a 12-lead ECG heart monitor tracks real-time telemetry data sent over 3G/4G/WIFI to be monitored remotely. In the event of an emergency, the patient’s location can be pinpointed using geolocation, so that emergency services may be notified. This also allows for activation of the local catheterization lab, if necessary and available.
The patient applied the device, established a continuous connection with CRMM and was transported to his home. At home the patient had 49 episodes of AF with RVR (HR > 100 bpm), many of which were in close proximity to one another, for which the CRMM cardiologist was consulted and who directed the patient to take oral diltiazem. The shows real-time monitoring and interpretation of one episode of home AF with RVR managed remotely by the cardiologist. All episodes of AF with RVR were rate controlled with oral diltiazem. Emergency response was never initiated. The patient was consented in writing prior to transfer of care to CRMM and is also registered with the Western Institutional Review Board.
Early the following morning while the patient was sleeping, he spontaneously converted to sinus rhythm as captured on remote telemetry. After sustained normal sinus rhythm a video cardiology consult was performed, for which non-emergent stress test and repeat echo were ordered. Given spontaneous cardioversion, lack of symptoms and lack of risk factors, the remote telemetry was discontinued and he was discharged from CRMM.
Follow-up at seven days revealed maintained sinus rhythm. The platform provided a reliable alternative to inpatient admission, with decreased cost, increased patient satisfaction, decreased exposure to nosocomial infections, and anticipated equivalent outcome of diagnostic results",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [37, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 37 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4162,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8292945-1,Extracted,"We present a 53-year-old female with a past medical history significant for right breast cancer, status-post lumpectomy followed by completion of six rounds of chemotherapy (Taxotere [Sanofi-Aventis, France], Herceptin [Genentech, USA], and carboplatin) and 36 rounds of radiation six years prior and currently in remission, hypertension, and bilateral lower extremity varicose veins, status-post phlebectomy 14 years prior complicated by a post-operative right lower extremity deep vein thrombosis treated successfully with three months of Coumadin (Bristol Myers Squibb, USA). She presented to the hospital with complaints of sudden onset sharp, constant, and non-radiating substernal chest pain while eating dinner with her husband at home. Her symptoms were not associated with nausea, diaphoresis, haemoptysis, palpitations, or syncope. She denied any symptoms suggestive of acid reflux; however, she did endorse shortness of breath and dyspnoea on exertion. There were no provoking factors. She denied any recent history of recent immobilization, trauma, calf/leg pain or swelling, long car rides, or air travel. There was no surgical history of prior lobectomies, lung transplants, or atrial fibrillation ablations. Her family history is negative for blood dyscrasias or blood clots and her social history is negative for tobacco or illicit drug use. She has no active cancer disease.
Her initial investigations in the emergency department demonstrated completely unremarkable parameters in regards to her complete blood count, complete metabolic panel, prothrombin time, troponin-I, d-dimer, and electrocardiogram. Her physical examination was unrevealing. The chest radiograph did not demonstrate evidence of acute disease. A computed tomography (CT) pulmonary angiogram was performed which did not demonstrate evidence of pulmonary arterial embolism; however, there was evidence of significant thrombosis of a right lower lobe segmental pulmonary vein without an obvious visualizable aetiology (Fig. ). Her transthoracic echocardiogram demonstrated normal left ventricular systolic function without evidence of right heart strain or elevated right ventricular systolic pressure. There was no evidence of mitral stenosis and no presence intra-atrial or ventricular thrombus formation. A hypercoagulable workup, consisting of anti-cardiolipin IgG/M, lupus anticoagulant, and proteins C and S, was performed and found to be negative. No identifiable source was determined to be the underlying culprit; therefore, her pulmonary vein thrombus was determined to be idiopathic in nature.
The rest of her hospital course was unremarkable after the initiation of intravenous therapeutic anticoagulation via unfractionated heparin. She was discharged home with instructions to continue apixaban for three months followed by re-evaluation in the outpatient setting. During her follow-up visit in our outpatient pulmonary clinic, she was found to be in good health with complete resolution of all prior presenting symptoms and normoxic on ambient air. A follow-up CT scan was offered to evaluate for resolution of the thrombus; however, due to the risk of further radiation, the patient declined.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [53, 'years'], 'Hypertension history': True, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 53 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4163,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7026587-1,Extracted,"A 64-year-old man with a history of hypertension, diabetes mellitus, and coronary artery disease with multiple percutaneous coronary interventions (PCI) of the left anterior descending artery and left circumflex arteries, most recently 2 weeks prior, presented to the emergency room with chest pain. On the day of admission, he noted the sudden onset of precordial chest pain associated with dyspnoea while ambulating consistent with his prior angina. This pain was initially relieved by nitroglycerine spray, but due to continued pain he presented to the emergency room. On arrival, his vital signs were notable for heart rate of 75 beats per minute, blood pressure of 167/72 mmHg, respiratory rate of 20 breaths per minute, and oxygen saturation of 98% on ambient air. His body mass index was 35 kg/m2. Physical examination was notable for regular rate and rhythm, clear lung sounds, and a jugular venous pressure of 9 cmH2O. Serial cardiac enzymes were normal (troponin T 0.02 ng/mL, normal 0–0.03 ng/mL), and an electrocardiogram showed sinus rhythm with right bundle branch block and lateral t-wave inversions, unchanged compared to prior. His medication list prior to hospitalization included aspirin 81 mg daily, clopidogrel 75 mg daily, atorvastatin 40 mg daily, metoprolol tartrate 25 mg twice daily, amlodipine 10 mg daily, ranolazine 500 mg twice daily, and furosemide 20 mg daily. A TTE was performed for further evaluation of his chest pain and to assess for regional wall motion abnormalities. The study showed a homogenous echo-dense, intracardiac mass present within or attached to the interatrial septum () measuring 4 cm × 4 cm. The mass was noted within the superior aspect of the interatrial septum and extended superiorly and posterior to the aortic root. Movement of the mass was synchronous with the atrial walls (). The right and left atrial and left ventricular size were normal with normal left ventricular wall thickness and function. Pulmonary artery pressure was unable to be measured due to the absence of tricuspid regurgitation. Although images from a prior TTE were not available, a report of a TTE performed 1 year prior made no mention of an interatrial mass.
The differential diagnosis for this mass includes an atrial myxoma, iatrogenic haematoma, invasive or metastatic tumour, lipoma, liposarcoma, and LHIAS. While the most common cause of interatrial septal thickening is LHIAS, an extensive differential diagnosis was considered because of the absence of the typical symmetrical ‘dumbbell’ shape. In the setting of a clinical history of severe chest pain after a PCI, we were concerned about a complication of the procedure including vascular trauma and haematoma. To further localize the mass and evaluate for tumour and iatrogenic haematoma, a CT angiogram of the chest was performed. There was no evidence of aortic dissection or haematoma and no extension of the mass outside of the cardiac structures. The homogenous mass seen on echocardiogram was similar in radiodensity to extracardiac and pericardial fat with Hounsfield units (HU) within the fat range (−64 HU). The mass extended from the interatrial septum to the posterior left and right atria and spared the fossa ovalis suggestive of LHIAS (, , ). Contrast imaging using CT demonstrated no enhancement to suggest vascularity to the mass and a normal pericardium.
Although the attenuation on CT was similar to fat, the mass was not completely visualized. For further evaluation of the mass and chest pain, the patient was referred for CMR imaging without the stress protocol. Cardiac magnetic resonance imaging was performed on a 1.5-T scanner and confirmed LHIAS by homogenous signal that was nulled on fat suppression images (, , Video S1). Although T1 weighted spin echo with and without fat suppression is more widely used in this situation, we used gradient echo technique here due to the benefit of shorter imaging times.
Cardiac magnetic resonance and TTE demonstrated normal ventricular function. Ultimately, the patient’s chest pain was determined to be of non-cardiac origin and he was discharged from the hospital in stable condition with recommendations for repeat imaging with TTE and/or CMR every 6 months to 1 year to monitor for interval progression.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [64, 'years'], 'Hypertension history': True, 'Diabetes mellitus': True, 'atherosclerotic disease': True, 'obesity': True, 'Initial troponin': 'less than or equal to normal limit', 'Suspicion History': 'Highly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 64 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, obesity, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: smoking, family with cvd. The following risk factor(s) are missing from the patient's data: smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 4 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 3 + 2 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 5.
Based on the patient's data, the HEART Score is 5."
4164,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6389040-5,Extracted,"A 45 year-old male developed flushing and urticaria 15 minutes after eating pineapple, then he felt precordial squeezing pain radiating to the left shoulder, lasting for several minutes, accompanied by palpitation and excessive sweating. He is a smoker with no other cardiac risk factors and no history of CVD, he was allergic to pineapple before but only manifested as slight itching and skin rashes which spontaneously disappeared in hours. Before this onset, he had been working day and night for 1 month with doubled tabacco smoking, though he did not smoke after eating pineapple. The patient was sent to the emergency room, on arriving, his symptoms had been relieved by sublingual nitroglycerin, his blood pressure was 120/70mmHg, pulse rate was 80 beat per minute, and ECG revealed no abnormalities while the symptom had relieved. 24h Holter (Figs. , and ) revealed ST segment elevation for 2~3 mm in leads II, III, aVF, V5, V6 at 13:40-13:42 (when he felt malaise, chest pain and palpitation at rest) and 20:20-20:22 (when he was driving, he felt chest pain and left arm numb), as well as ventricular bigeminy and nonsustained ventricular tachycardia at 13:20 and 13:42. He was admitted to cardiology department, blood test showed normal troponin I level and elevated eosinophil of 7.6% on the first day of admission. Coronary angiography showed subocclusion in the proximal segment of LCX with TIMI grade 3 flow, which was relieved by 3 times of 200μg intracoronary nitroglycerin. He was diagnosed as coronary vasospasm on the basis of anaphylaxis to pineapple, and received anti-vasospasm therapy of mononitrate and nifedipine as well as antiallergic agent, the eosinophil rate declined to 6.1% on the 7thday, chest pain didn’t relapse during hospitalization. After 12 months of mononitrate and nifedipine medication, anti-vasospasm therapy was discontinued. During 3 years follow-up, he kept free of cardiac events.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'smoking': True, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'atherosclerotic disease': False}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 45 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 3 + 1 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 4.
Based on the patient's data, the HEART Score is 4."
4165,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5099078-1,Extracted,"A 22-year-old female patient with a history of depression presented to the emergency department with a one-week history of epigastric abdominal pain, abdominal distention, constipation, and bloating. She denied recent fever, chills, night sweats, weight loss, sick contacts, and recent travel. Home medication included only fluoxetine. She had no history of allergies, asthma, arterial or venous thromboembolism. A review of systems was negative for cardiac, neurologic or renal involvement. A physical examination revealed moderate abdominal distension and tenderness. The initial abdominopelvic computed tomography (CT) scan showed small intestinal mucosal thickening suggestive of enteritis with a moderate amount of free pelvic fluid. Symptomatic treatment was initiated and the patient was discharged home. Due to worsening abdominal pain and distention, she was readmitted two weeks later. The laboratory investigation was significant for leukocytosis of 18.9 k/µL with peripheral blood eosinophilia of 8.8 k/µL (47%). The liver profile and total protein counts were within normal limits. A repeat CT scan showed extensive abdominal and pelvic ascites, dilated jejunal loops and mucosal thickening, with a few slightly prominent mesenteric lymph nodes, and mild bilateral pleural effusions (Figure ). No air-fluid levels or other signs of small bowel obstruction were noted. An ultrasound guided abdominal paracentesis demonstrated a low serum to ascites albumin gradient of 0.3 g/dL (albumin 2.8 g/dL, simultaneous serum albumin 3.1 g/dL), with significantly elevated white blood cells (WBCs) (6900/mm3) and > 90% eosinophils. Evaluation for underlying infectious causes, including stool cultures, Giardia, Strongyloides, Entamoeba histolytica, human immunodeficiency virus (HIV), Toxocara, and Cryptosporidium were negative. The antineutrophil cytoplasmic antibodies (ANCA) testing was negative, while immunoglobulin E (IgE) was normal at 18 IU/mL and tryptase was 11.5 ng/mL.
Given the radiographic suspicion of an inflammatory process involving the jejunum, she subsequently underwent push enteroscopy that revealed gastric antral erythema, edematous mucosa of the duodenal bulb, and scattered jejunal erythema and edema (Figure ). The histology showed extensive eosinophilic involvement reaching the deep lamina propria of the jejunum, duodenum, stomach and esophagus, reaching up to 74 eosinophils/high-power field, consistent with EGE (Figure ).
The diagnosis was made after other causes of eosinophilia and eosinophilic gastrointestinal infiltration was excluded. Parasitic infection was excluded based on the stool studies and serologic testing. Gastrointestinal malignancy and inflammatory bowel disease were ruled out based on endoscopy and biopsy results. Hypereosinophilic syndrome was unlikely given a lack of other organ involvement. Polyarteritis nodosa was ruled out with biopsy results negative for perivascular eosinophilia. Eosinophilic granulomatosis with polyangiitis is very unlikely given a negative ANCA and the absence of a history of asthma.
She was started on oral prednisone 40 mg tapered over six weeks and an empiric six-food elimination diet (fish, milk products, nuts, shellfish, soy products, and wheat). A two-week follow-up showed major improvement of her abdominal pain, ascites, and eosinophilia (eosinophilic count of 0.29 k/µL five days after treatment). A long-term follow-up nine months after presentation continued to show complete resolution of her symptoms and eosinophilia while the patient continued to follow the six-food elimination diet.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [22, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 22 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4166,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8186915-1,Extracted,"A 53-year-old male presented to our hospital with substernal, non-radiating, squeezing chest pain that started 18 hours prior to his presentation. It was associated with dyspnoea, palpitations, and diaphoresis. He was haemodynamically stable, and physical exam was unrevealing. He had no medical problems except active smoking history since he was a teenager. He had no history of premature coronary artery disease in his family. Electrocardiogram showed sinus rhythm with ventricular rate of 64 beats per minute and no evidence of ST elevations (). Troponin-I peaked at 18.6 ng/mL (normal < 0.04 ng/mL). Global Registry of Acute Coronary Events score was consistent with low mortality risk. Myocardial infarction was the working diagnosis based on the clinical symptoms. Myocarditis or pulmonary embolism could be in the differential diagnoses.
Patient was started on appropriate medical management for presumed ACS, including a dual antiplatelet regimen and heparin drip. Coronary angiogram (A,B) was performed the next day and revealed angiographically normal coronary arteries except two small filling defects noted in the distal first obtuse marginal branch of the left circumflex artery. Optical coherence tomography (OCT) imaging (; ) confirmed the presence of red organized thrombus in the coronary lumen, with no evidence of plaque rupture. Aspiration thrombectomy was not done due to limited thrombus burden. Transthoracic echocardiogram showed severely dilated LV (LV end-diastolic dimension of 7.3 cm) with severely reduced systolic function at 15%. There were prominent trabeculations of LV suggestive of non-compaction. The right ventricle was normal in size and function. Contrast and agitated saline demonstrated no evidence of interatrial shunt. Cardiac magnetic resonance imaging (MRI) ( and ) was performed for further evaluation of the cardiomyopathy, which confirmed the diagnosis of LV non-compaction cardiomyopathy with a ratio of non-compacted to normal myocardium of 4.5:1 in the lateral wall. It also revealed a dilated LV (indexed LV end-diastolic volume of 191 mL/m2) with a severely reduced systolic function (LV ejection fraction 21%). There was severe global hypokinesis with akinesis of the mid-lateral wall. Early gadolinium enhancement imaging with a long inversion time showed no intracardiac thrombus. Late gadolinium enhancement (LGE) imaging demonstrated transmural infarction of the mid-lateral wall, as well as mid-myocardial LGE of the mid to distal septum, a pattern associated with non-ischaemic cardiomyopathy (). The right ventricle showed no findings of non-compaction and was normal in size and shape with mildly reduced ejection fraction at 47%. Atrial fibrillation and paradoxical thrombus were considered as a source of the thrombus; however, they were very unlikely given the absence of arrhythmias on telemetry monitoring and absence of shunts on agitated saline echocardiography study.
Given the MRI findings and intracoronary imaging in the absence of any overt source of thromboembolism, it was presumed that the thrombus likely originated from the non-compacted LV myocardium resulting in CE and subsequently type 2 MI. Due to the underlying pathophysiology of MI, antiplatelet drugs were discontinued. Given the low calculated 10-year atherosclerotic cardiovascular disease risk, no statin was prescribed. The patient was discharged home on warfarin with low-molecular-weight heparin bridging. Medical therapy was initiated for the new diagnosis of non-compaction cardiomyopathy, including metoprolol, lisinopril, and spironolactone. The patient was closely followed as an outpatient after his initial presentation. Follow-up echocardiographic imaging at 3 months after initial presentation showed persistently reduced LV ejection fraction at 20–25% despite guideline directed medical therapy. Consequently, the patient was referred to electrophysiology for consideration of implantable cardioverter-defibrillator. On annual follow-up, the patient remained asymptomatic.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [53, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': True, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'hypercholesterolemia': False, 'obesity': False}",6,6,6,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 53 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: smoking, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 3 + 1 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 4 + 2 = 6.
Based on the patient's data, the HEART Score is 6."
4167,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5353565-1,Extracted,"A 37-year-old woman was referred to our emergency department of our hospital. She dropped during the second prostration in prayer and decreased her mental state, with no prior history of syncope, shortness of breath, or chest pain. She had no significant past medical history, but she had a positive family history of early cardiovascular disease. At presentation, the patient was afebrile and had normal vital signs (heart rate 80 bpm, blood pressure 110/70 mmHg, oxygen saturation 97% while breathing room air) and jugular venous pressure (JVP) was normal.
A 12-lead electrocardiogram revealed normal sinus rhythm with nonspecific minor ST-T abnormalities. On cardiac examination, S1 was accentuated and S2 was normal. There was an early diastolic sound that was compatible with a tumor plop.
A transthoracic echocardiogram (TTE) was performed which showed the presence of a pediculated mass in the left atrium, with an appearance suggestive of atrial myxoma, that was prolapsed through the mitral valve towards the left ventricle by changing patient's position [Figure –].
The patient was referred for urgent surgery. The intraoperative findings included a mass, and histopathology confirmed an atrial myxoma. She recovered without major complication and was discharged. At 2-year follow-up, she remains with excellent cardiac function.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'parent or sibling with Cardiovascular disease before age 65': True, 'Suspicion History': 'Slightly suspicious', 'Hypertension history': False, 'smoking': False, 'Diabetes mellitus': False, 'age': [37, 'years'], 'Electrocardiogram Test': 'Normal', 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 37 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: family with cvd. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4168,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6390538-1,Extracted,"A 25- year-old Sri- Lankan female presented with progressively worsening shortness of breath, orthopnoea and dry cough for three days. Her symptoms were not associated with chest pain, fever, oedema or wheezing. At the onset she noted shortness of breath on mild exertion which progressed to shortness of breath even at rest by third day. The patient reported a good urine output throughout. She was asymptomatic prior to the onset of this illness excepting a mild iron deficiency anaemia for which she was on oral iron treatment and dysmenorrhoea attributed to an ovarian cyst. The patient had undergone an appendicectomy eight months prior to the presentation for appendicitis associated with round worm infestation.
Examination revealed dyspnoea at rest, elevated jugular venous pulse, tachycardia with a heart rate of 120/min, blood pressure of 100/70 mmHg on both arms. There was an early diastolic murmur over left sternal edge associated with a thrill and bilateral lower lung field crackles. Rest of the examination was normal. Her estimated body surface area was 1.24m2 with a body weight of 40 kg and height of 140 cm.
Investigations revealed white cell count of 7.1 × 109/l (4–11 × 109/l), platelet count of 435 × 109/l (150–400 × 109/l),haemoglobin of 10.9 g/dl (11.5–15.5 g/dl) with mean corpuscular volume of 78 fl (80-96 fl). C- reactive protein was 18 mg/l (< 6 mg/l) and Erythrocyte sedimentation rate (ESR) was 114 mm/1st hour (< 20 mm/1st hour). Renal and liver functions, urinalysis, blood sugar and coagulation profile were in normal range. Electrocardiogram revealed sinus tachycardia with no ischaemic changes. Troponin I was negative. Chest radiograph had findings consistent with pulmonary oedema. Repeated blood cultures were negative. Transthoracic echocardiogram demonstrated ejection fraction > 60%, severe aortic regurgitation with dilated aortic root when adjusted for her body surface area(annulus 21 mm, sinus 34 mm). Aortic valve leaflets were morphologically normal. There was no left ventricular hypertrophy, regional wall motion abnormalities or vegetations. Other cardiac valves were normal. All four cardiac chambers were of normal size. Transoesophageal echocardiogram confirmed the absence of vegetations.
She was started on supportive management for acute pulmonary oedema and treatment was initiated as for infective endocarditis empirically. Though she was referred to cardiac surgery team urgent surgical interventions were not performed since she improved with medical management. After completion of four weeks empiric antibiotics her echocardiographic changes and ESR remained unchanged. However, heart failure improved with medical management with complete resolution of orthopnoea and dyspnea being limited to moderate exertion. Intravenous antibiotics were omitted in the absence of convincing evidence of endocarditis.
Further evaluation was performed in view of persistently high ESR and aortic regurgitation with no definitive cause. Chronic infections such as tuberculosis, vasculitic conditions such as Takayasu arteritis were considered. Further questioning did not reveal constitutional symptoms, contact with tuberculosis, arm claudication, headache or any neurological symptoms. Examination did not reveal any lymphadenopathy, hepatosplenomegaly, cutaneous or joint involvement, fundoscopic abnormalities, pulse deficit or vascular bruits. Rheumatoid factor, serum cryoglobulins, anti nuclear antibodies and complement levels were normal. Peripheral blood smear revealed rouleaux formation with evidence of mild iron deficiency anaemia. Serum protein electrophoresis and serum Lactate dehydrogenase were normal. Human Immunodeficiency Virus antibodies and Serology for syphilis were negative. Mantoux test and induced sputum for acid fast bacilli were negative. Ultrasound abdomen, Contrast enhanced Computed tomography (CT) of the chest, abdomen and pelvis as well as CT aortogram with arch vessels were normal except mild aortic root dilatation. Bone marrow biopsy revealed reactive marrow with no other abnormalities while bone marrow culture for bacteria, fungi, mycobacteria, brucella and leishmania were negative. Colonoscopy and biopsy did not reveal any abnormality.
The patient was followed up for one year with detailed clinical assessment and continuation of medical management of heart failure. She did not develop any new symptoms and her exertional dyspnoea remained static. Her ESR remained above 100 mm/1st hour. Clinical examination about one year after initial presentation revealed a reduced pulse volume of left upper limb with a blood pressure difference (right- 100/70 mmHg, left- 70/40 mmHg). There was a left subclavian bruit as well. But, patient did not have any constitutional symptoms or any symptoms of left upper limb ischaemia. Digital subtraction angiography at that point revealed significant stenosis at first part of left subclavian artery and at the origin of left vertebral artery (Fig. ). Based on the new findings she was diagnosed to have Takayasu arteritis and was started on prednisolone 1 mg/kg body weight daily with plan for follow up at cardiology and rheumatology units. Six weeks after initiation of glucocorticoids patient remained clinically well and ESR decreased to 25 mm/1st hour. Glucocorticoid dose was slowly tapered. Decision on aortic valve replacement was decided to be made few months later after resolution of active inflammation and repeat cardiac assessment. Ravascularisation for arterial stenosis was not offered in the absence of symptoms of upper limb or cerebral ischaemia. Sequence of events from her presentation to the diagnosis is given in a timeline in Table .",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [25, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'Diabetes mellitus': False, 'obesity': False, 'smoking': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'parent or sibling with Cardiovascular disease before age 65': False}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 25 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4169,18,HEART Score for Major Cardiac Events,risk,integer,usmle-12327,Extracted,"A 57-year-old male presents to his primary care physician with upper abdominal pain. He reports a 3-month history of mild epigastric pain that improves with meals. He has lost 15 pounds since his symptoms started. His past medical history is notable for gynecomastia in the setting of a prolactinoma for which he underwent surgical resection over 10 years prior. He has a 15-pack-year smoking history, a history of heroin abuse, and is on methadone. His family history is notable for parathyroid adenoma in his father. His temperature is 98.8°F (37.1°C), blood pressure is 125/80 mmHg, pulse is 78/min, and respirations are 18/min.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [57, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Diabetes mellitus': False, 'smoking': True, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 57 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4170,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7153810-1,Extracted,"The index patient is a 36-year-old Caucasian male who underwent a screening transthoracic echocardiogram (TTE) at age 31 years after his older brother had a sudden cardiac death. The patient has a past medical history of mild hypertension successfully treated with clonidine, nicotine dependence, and post-traumatic stress disorder. Social history is significant for a 27-pack-year smoking history and rare alcohol use. Family history is significant for an older brother with Wolff-Parkinson-White (WPW) syndrome and sudden cardiac death at age 33 years. Autopsy showed evidence of hypertrophic cardiomyopathy (HCM) of unknown etiology. Family history is also significant for multiple maternal relatives with premature coronary artery disease and myocardial infarction.
The index patient’s initial TTE at age 31 years showed preserved left ventricular ejection fraction (LVEF), normal diastolic function, no valvulopathy, and no left ventricular hypertrophy (LVH) with a septum measurement of 8.1 mm and a posterior wall measurement 10.3 mm in diastole. The patient was referred to cardiology outpatient clinic for further evaluation due to increased risk for cardiac pathology because of his family history. On presentation, he did not exhibit any signs or symptoms of active cardiac disease. He denied chest pain, palpitations, dyspnea, orthopnea, lightheadedness, dizziness, and syncopal or presyncopal episodes.
Vital signs showed temperature 99.2°F, pulse 70 beats per minute (bpm), respiratory rate 18 breaths per minute, and blood pressure 106/70 mmHg. On physical examination, he had a normal heart rate and regular rhythm, normal heart sounds, no murmurs, no evidence of jugular venous distention, and no lower extremity edema. There were no signs of neurological or dermatological disease. A complete metabolic panel and complete blood count were within normal limits. Observation and routine surveillance was recommended.
The patient had another TTE at age 33 years which showed mild LVH as his interventricular septum measured 12 mm and the posterior wall measured 13 mm in diastole. There was a normal resting left ventricular outflow tract (LVOT) gradient, but there was chordal systolic anterior motion (SAM). End diastolic dysfunction was not present at that time. More recently, at age 36 years during routine cardiology follow-up, the patient’s review of systems was now positive for rare episodes of orthostatic dizziness and progressive dyspnea with moderate exertion. The patient had a repeat TTE at that time which showed evidence of progressive, now moderate LVH. In diastole, the septum measured 17 mm which was increased from 12 mm on previous imaging and the posterior wall measured 16 mm which was increased from 13 mm on previous imaging (Figure ). There was chordal SAM. Grade II diastolic dysfunction was present with preserved LVEF of 65%.
Further diagnostic testing included an electrocardiogram (EKG) which showed normal sinus rhythm but no unusual voltage for LVH. Echocardiogram exercise stress test did not show evidence of ischemia or malignant arrhythmias with maximal stress. LVOT gradient of 33 mmHg was noted in the recovery phase with a heart rate of 106 bpm. No symptoms of chest pain or angina were noted. Duke protocol risk stratification was low. Cardiac monitoring for two weeks showed a predominant underlying sinus rhythm. No significant non-sustained ventricular tachycardia (VT) or sustained VT was noted.
With the diagnosis of HCM along with the history of sudden cardiac death of his first-degree relative, he was referred for genetic counseling at the Genetic-Arrhythmia Clinic for further evaluation. Cardiac MRI showed HCM with a maximum interventricular septal dimension of 18 mm (Figure ) and a posterior wall dimension of 17 mm. There was no evidence of LVOT obstruction. There was a hyperdynamic left ventricular (LV) function with an ejection fraction of 64% and a normal right ventricle size, wall thickness, and systolic function. His genetic testing demonstrated a variant of unknown significance (VUS) for the GLA gene (c.574 A>T). Further measurement of α-Gal A leukocyte activity showed low levels of 1.5 nmol/h/mg (lab reference range ≥ 23.1 nmol/h/mg), which was diagnostic for FD. The patient was subsequently initiated on beta-blocker therapy with plan for serial cardiac MRI to monitor for progression of LVH. After genetic counseling and discussion regarding the initiation of enzyme replacement therapy (ERT), the patient opted to be monitored for further progression and/or symptoms prior to initiation due to potential adverse events of initiating therapy.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [36, 'years'], 'Hypertension history': True, 'smoking': True, 'parent or sibling with Cardiovascular disease before age 65': True, 'Diabetes mellitus': False, 'Electrocardiogram Test': 'Normal', 'Initial troponin': 'less than or equal to normal limit', 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'atherosclerotic disease': False}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 36 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: hypertension, smoking, family with cvd. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 0 + 2 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4171,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6894017-1,Extracted,"A 36 year-old woman with no significant past medical history complained of crushing chest pain followed by collapse while deboarding a cruise ship. She received immediate cardiopulmonary resuscitation (CPR) at the scene and was found to be in ventricular fibrillation. Heart rhythm was recovered after defibrillation. However, she sustained a second episode of ventricular fibrillation requiring CPR for 15 minutes. She was successfully defibrillated with resumption of sinus rhythm and normal blood pressure.
The patient was air-lifted to our hospital, where her electrocardiogram showed sinus rhythm with no ST elevation. Transthoracic echocardiogram showed ejection fraction of 35 to 40%, with severe apical-septal hypokinesis and moderate to severe anterior wall hypokinesis. She underwent emergent cardiac catheterization, which showed SCAD involving the left anterior descending (LAD) coronary artery ().
There were considerable multidisciplinary discussions with cardiologists, surgeons and interventionists as to the best approach to treat this patient. Several factors were considered: her young age, complexity of the LAD dissection, the risk of percutaneous coronary intervention (PCI) if acute occlusion occurred during insertion of the stent, and stent stenosis in this young patient. Due to her previous two episodes of ventricular fibrillation, and the nature of the dissection of the LAD, it was decided to proceed with emergent off-pump coronary artery bypass graft. The left internal mammary artery (LIMA) was anastomosed to the LAD, and high diastolic flow, via flowmeter, was confirmed at the time of chest closure ().
A 12-lead electrocardiogram performed on post-op day one showed normal sinus rhythm. The patient made an uneventful recovery and was discharged on post-op day four wearing a cardioverter defibrillator LifeVest (ZOLL, Pittsburgh, PA), until evaluation by an electrophysiologist at her one month follow up. At follow up, there were no indications for insertion of an automated implantable cardioverter defibrillator, as she had no arrhythmias and normal left ventricular function, and the LifeVest (ZOLL, Pittsburgh, PA) was discontinued.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [36, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Highly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 36 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4172,18,HEART Score for Major Cardiac Events,risk,integer,pmc-2599899-1,Extracted,"A 67- year old German female with a history of hypertension and Crohn's disease was admitted to our emergency department with chest pain. One year ago the patient was admitted with the same symptoms. A Takotsubo Cardiomyopathy was diagnosed and typical apical ballooning (akinesia of apical left ventricular segments and hyperkinesis of basal segments; Figure ) was seen in the left ventricular angiogram. On admission she did not report about an obvious emotional stress situation (like news of an unexpected death of a relative or news of a catastrophic medical diagnosis) preceding chest pain. She was under chronic therapy with betablockers (Metoprolol 47,5 mg/od), ACE-inhibitors (Ramipril 2,5 mg/od) and aspirin (100 mg/od). Initially she had a pulse rate of 60 beats/min and a blood pressure of 120/80 mmHg. Her physical examination was essentially normal. Laboratory testing revealed elevated levels of Troponin T (0.13 ng/ml, [<0.03 ng/ml]) and creatinine kinase (208 U/l, [<145 U/l]]. Catecholamine plasma levels were not elevated.
The initial electrocardiogram showed sinus rhythm and T-inversions in the leads I, II, aVL, V1 and V2.
An acute Non ST-elevation infarction was suspected based on the clinical presentation including chest pain, electrocardiographic changes and elevated myocardial markers. The patient received aspirin, clopidogrel und unfractionated heparin. Recent angiogram showed an isolated midventricular ballooning (akinesia anterolateral and diaphragmal; Figure ) and an ejection fraction of 48 %. In both cases the coronary angiography showed a mild coronary artery disease with a 50 % stenosis in the left anterior descending. Contrast enhanced cardiac magnetic resonance imaging excluded myocardial necrosis as well as ischemia in the anterior wall.
Within one week wall motion abnormalities and ejection fraction fully recovered.
Her recovery was uneventful and she was doing well at discharge. She was discharged with a chronic medication including betablockers (Metoprolol 47,5 mg/td), ACE-inhibitors (Ramipril 2,5 mg/td), aspirin (100 mg/od) and statins (Simvastatin 40 mg/od).",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [67, 'years'], 'Hypertension history': True, 'Suspicion History': 'Moderately suspicious', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'Electrocardiogram Test': 'Normal', 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",6,6,6,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 67 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 1 + 2 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 3 + 1 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 4 + 2 = 6.
Based on the patient's data, the HEART Score is 6."
4173,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7568822-1,Extracted,"A 27-year-old man (75 kg) presented to our emergency department and was monitored by a cardiologist. Dissection occurred following weightlifting across his chest and shoulders. He described multiple episodes of faintness over the preceding hours. These were associated with sweating, dyspnea, and temporal right eye vision deficit. The first episode began during heavy weight lifting (180 kg) and lasted 10 minutes before resolving with rest and drinking fluids. The second episode began while lifting weights again, which was more intense in severity and lasted for 20 minutes. The third fainting episode occurred when he left the gym, whereby he fell over the floor outside the club. The patient was a coach and a professional bodybuilder. During the first lifting, he remembered weight training heavier than his normal regimen involving squatting with weights of around 140 kg in the supine position across the anterior chest wall. He initially denied taking illicit drugs but, upon insistence, he confessed that he took intramuscular 250 mg testosterone twice per week and human growth hormone 20 mg/day for two years. In the emergency room, the patient’s vital signs were a blood pressure of 90/60 mmHg, heart rate of 120 beats/min, respiratory rate of 26 breaths/min, and temperature of 36 oC. Blood chemistry revealed increased levels of cardiac troponin (up to 7.6 ng/mL) and creatine kinase (CK) (up to 597 IU/L). Transthoracic echocardiography (TTE) revealed ascending aorta dissection with severe aortic regurgitation. The patient underwent emergency cardiac surgery.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [27, 'years'], 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'obesity': False, 'smoking': False, 'atherosclerotic disease': False, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'Hypertension history': False, 'hypercholesterolemia': False, 'parent or sibling with Cardiovascular disease before age 65': False}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 27 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 2.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 2 + 2 = 4.
Based on the patient's data, the HEART Score is 4."
4174,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6657459-1,Extracted,"A 26-year-old male with the complaints of near-syncope attacks and worsening dyspnea on exertion for 2 years was admitted to our hospital. His past medical history was unremarkable. Physical examination was normal except for a harsh systolic murmur best audible at the lower left sternal border. Transthoracic echocardiogram (TTE) revealed a large mass with lobular contours in the RV that occupied almost the whole RV [ and ]. The mass was protruding into the pulmonary artery and produced right ventricular outflow obstruction with a maximal peak gradient of 30 mmHg [ and ]. A few days after the diagnosis, surgical intervention was made using median sternotomy and cardiopulmonary bypass. After a longitudinal right atriotomy, the mass with the base deeply embedded within the trabeculae carneae was resected as much as possible through the tricuspid valve. On gross examination, the mass had a gelatinous consistency with hemorrhagic areas []. The De Vega annuloplasty technique was used to repair tricuspid valve regurgitation before closure of the right atriotomy. Microscopically, the mass consisted of areas of stellate cells scattered in a myxoid stroma []. A definitive diagnosis of right ventricular myxoma was made. Control TTE before discharge revealed normal functioning tricuspid valves with a minimal degree of tricuspid regurgitation. The postoperative course was uneventful, and the patient was discharged on day 17.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [26, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'smoking': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 26 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4175,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7042141-1,Extracted,"A 54-year-old woman presented with a 2-year history of progressive dyspnoea on exertion. At the time of presentation, she had intermittent (angina) chest pain, pedal oedema, and dyspnoea at minimal exertion. For the last 2 months, she had anorexia and weight loss (4 kg in 1 month). There were no documented episodes of fever. Her past medical history was significant for hypothyroidism, well-controlled on levothyroxine supplementation.
On evaluation, the patient was normotensive, pulse regular, and afebrile. Systemic examination was unremarkable except for mild bilateral pedal oedema. Electrocardiogram showed normal sinus rhythm and was otherwise unremarkable. Her erythrocyte sedimentation rate (ESR) was 56 and C-reactive protein (CRP) 22.4 mg/L; normal <7.5 mg/L. Her N-terminal prohormone of brain natriuretic peptide level was 74.6 pg/mL. HIV antibodies were negative by enzyme-linked immunosorbent assay. Two-dimensional echocardiography (Figure ) revealed mild pericardial effusion with pericardial thickness of 0.58 cm. Inferior vena cava was dilated (2.12 cm with no respiratory variation) and significant trans-mitral and trans tricuspid respiratory flow variation suggestive of effusive constrictive pericarditis. Though annulus reversus could not be documented (e’l = 8.70 cm/s and e’s = 7.72 cm/s), e’l and e’s were almost equal and e’l was reduced. E/e’ were 8.48 for septal and 7.53 for lateral annulus. Contrast-enhanced tomography of thorax (Figure ) revealed mild pericardial effusion with thickened pericardium [along right ventricular (RV) free wall 6.9 mm and along left ventricular (LV) free wall 7.5 mm] with biatrial enlargement; it also revealed few homogenous subcentimetric prevascular, pre-, and para- tracheal lymph nodes without any necrosis. There was left-sided pleural effusion along with atelectatic bands in bilateral lung bases, left lingula, and bilateral upper lobes and traction bronchiectasis along medial segment of right middle lobe. Overall the computed tomography (CT) images were suggestive of chronic infective aetiology.
Cardiac catheterization revealed equalization of diastolic pressures with significant respiratory variation in LV and RV pressures. Coronary angiography revealed normal epicardial coronaries. These findings strongly suggested a constrictive physiology.
As tuberculosis is the commonest aetiology of constrictive pericarditis in the Indian subcontinent, and as there was evidence of lung involvement, the patient was started on ATT (isoniazid + rifampicin + pyrazinamide + ethambutol for 2 months followed by isoniazid and rifampicin for 4 months). The patient improved over the next 4 months, there was return of appetite with weight gain; and the repeat echocardiography (Figure ) was normal with no features of either constriction or effusion. Repeat ESR was 31 and CRP came down to 8 mg/L. Repeat CT also revealed normalization of pericardial thickening and enhancement when compared with the earlier. It also revealed clearance of pleural effusion, lymphadenopathy, and lung findings when compared with the earlier CT. To evaluate the symptoms and to document the functional capacity of the patient, treadmill test was done which was normal with good functional capacity.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'Hypertension history': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'obesity': True, 'smoking': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'parent or sibling with Cardiovascular disease before age 65': False}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 54 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: obesity. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4176,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7567320-1,Extracted,"A 19-year-old girl with a remote history of bipolar disorder and a five-year history of multiple hospitalizations for hypokalemic paralysis was brought to the emergency room for sudden-onset bilateral thigh cramping progressing to the shoulder and biceps after awakening from a nap. The patient reported that her symptoms were similar to her previous episodes and were exacerbated by her menses, which she had recently completed four days prior to symptom onset. A review of systems did not reveal syncope, gastrointestinal disturbances, urinary symptoms, joint pain, rashes, diuretic/laxative abuse, or suicidal or homicidal ideation. There was no family history of autoimmune diseases. She endorsed smoking cannabis occasionally and denied tobacco or alcohol use. Aside from her potassium chloride and sodium bicarbonate regimen, the patient was not on any psychotropic or other medications.
Except for bradycardia (heart rate of 50 bpm), her vital signs were within normal limits and physical examination was unremarkable. Results of initial lab tests showed sodium of 143 mmol/L, potassium of 2.1 mmol/L, chloride of 110 mmol/L, and bicarbonate of 17 mmol/L. Venous blood gas pH was 7.21. Urine sodium was 74 mmol/L, urine potassium was 18.4 mmol/L, and urine chloride was 68 mmol/L. Urinalysis showed a urinary pH of 7.0 without blood or protein (Table ). The renal sonogram did not show nephrolithiasis. Electrocardiogram showed sinus bradycardia, delayed intraventricular conduction, and U waves. With a positive urine anion gap of 24 and hyperchloremic non-anion gap metabolic acidosis, she was diagnosed with distal RTA. She was promptly hydrated with intravenous normal saline and was given potassium chloride and sodium bicarbonate, which corrected both her hypokalemia and hyperchloremic non-anion gap metabolic acidosis. She was later discharged on oral potassium chloride and sodium bicarbonate.
Over the next few months, the patient had several similar presentations at hospitals for upper and lower extremity weakness and paralysis secondary to hypokalemia. Initially, exposure to synthetic cannabinoids was believed to have induced the patient’s severe hypokalemia and acid-base disturbances in the absence of known nephrotoxic drug exposure and autoimmune history. Additionally, suspicion of disordered eating/exercise or diuretic/laxative abuse as a contributor to her metabolic derangements was low based on patient report and chart review. On further probing, she admitted to infrequent, intermittent dry mouth and dry eyes with a sand-like sensation associated with ocular pruritus for several months, but denied any history of eye inflammation, use of artificial teardrops, or increased occurrence of cavities.
Her autoimmune panel was positive for antinuclear antibodies (ANA) (1:2560) and anti-Ro/SSA antibody (SSA-52: 261 AU/mL and SSA-60: 130 AU/mL) and negative for anti-double-stranded DNA (dsDNA), anti-Smith, anti-La/SSB, and anti-U1-ribonucleoprotein (RNP) antibodies (Table ). Diagnostic tests for SCN4A deletion/duplication, urine organic acids, plasma amino acids, carnitine (total and free), acylcarnitine, and urine porphyrins were all within normal reference values. Given the patient did not have other derangements of urine and serum electrolytes, other causes of renal tubulopathies, such as Bartter, Gitelman, and Fanconi syndromes were subsequently ruled out. Based on sicca symptoms and positive anti-Ro/SSA antibodies, a presumptive diagnosis of Sjögren’s syndrome was made. She was advised to follow up with nephrology and rheumatology in the outpatient setting; however, the patient never attended her appointments.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [19, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 19 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4177,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4489815-1,Extracted,"A 33-year old African–American female presented to the emergency room with a 2-day history of progressively worsening nausea, vomiting, and severe abdominal pain. The patient denied any cardiovascular, respiratory, or urinary symptoms nor had she been around any sick contacts. The patient denied any abdominal surgeries or prior history of gallstones, dyslipidemia or pancreatitis. She denied any alcohol, cigarette use, or illicit drug use. She had a history of diabetes mellitus, hypertension and hypothyroidism; however, there was no family history of autoimmune conditions or AP. Her home medications included long-term metformin and levothyroxine. In addition, the patient recently began canagliflozin therapy 2 weeks prior to her admission.
In the emergency department, she was found to be hypotensive with a blood pressure of 79/36, heart rate of 118 bpm, and a respiratory rate of 27. Her temperature was 40.3 degrees Celsius. Serum chemistries revealed leukocytosis with a white blood cell count of 23.6×103/mm3, creatinine of 3.19 mg/dL, calcium of 9.3 mg/dL, amylase 535 IU/L, and lipase 373 IU/L. HbA1c was recorded as 13.5% and her triglyceride level was within normal limits. Additionally, she displayed an elevated anion gap of 19 and acidosis with a pH of 6.89 with blood glucose level of 563 mg/dL and positive urine ketones (beta-hydroxybutyrate: 2.90). Subsequent arterial blood gas revealed PCO2 of 48.8 and FiO2 of 100. Maximum blood alcohol was negative. She was initially diagnosed with diabetic ketoacidosis (DKA) and given several liters of normal saline followed by a bicarbonate and insulin drip. Urine and blood cultures were drawn and she was started on broad-spectrum antibiotics for her fever and leukocytosis. A computerized tomography (CT) scan of the abdomen was obtained due to the elevated pancreatic enzymes and it showed evidence of AP with peripancreatic inflammation and ascites (). Chest X-ray additionally revealed bilateral pleural effusions. Echocardiogram though was unremarkable.
Despite aggressive fluid resuscitation, the patient became progressively more hypotensive and became unresponsive. She was started on a norepinephrine drip, intubated and admitted to the intensive care unit. Her renal function deteriorated with decreased urine output and increasing serum creatinine reaching 4.26 (pre-morbid creatinine: 1.0) with persistent acidemia requiring continuous renal replacement therapy. In the intensive care unit, an APACHE (Acute Physiology and Chronic Health Evaluation) II score was calculated for the patient and revealed an estimated mortality rate of 97.2%.
Despite the poor prognosis the patient’s condition remarkably improved and vasopressors were discontinued and she was successfully extubated after 4 days. The source of leukocytosis was indeterminate as cultures of blood, urine, and mini bronchoalveolar lavage were all negative. After excluding all other causes for her symptoms and given the chronology of her presentation, it was determined that canagliflozin was likely the source of her illness. Canagliflozin was discontinued and the patient has remained stable since discharge.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'parent or sibling with Cardiovascular disease before age 65': False, 'Hypertension history': True, 'smoking': False, 'Diabetes mellitus': True, 'age': [33, 'years'], 'Electrocardiogram Test': 'Normal', 'atherosclerotic disease': False, 'hypercholesterolemia': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 33 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4178,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8180216-1,Extracted,"In May 2020, a 54-year-old woman was hospitalized with a chief complaint of exertional chest pain for more than 10 years.
Chest pain was located in the upper part of the sternum, lasted for approximately a few seconds, and could be relieved after rest. The symptoms worsened 6 mo prior, with chest pain occurring after mild activity and more frequently than before.
The patient had a history of hypertension for more than 5 years and took drugs regularly to control her blood pressure, and her blood pressure was acceptable.
The patient had no significant prior personal or family history.
The patient’s blood pressure was 159/104 mmHg on admission, and the remainder of the physical examination showed no obvious abnormalities.
The low-density lipoprotein cholesterol was 4.18 mmol/L (normal reference range: 1.10-3.50 mmol/L), cardiac biomarkers such as troponin and N-terminal pro-brain natriuretic peptide were normal, and the other blood tests were also approximately normal.
Electrocardiogram showed abnormal Q waves in leads II, III, aVF, V5-V6, and V7-V9 and slight elevation of the ST segment in leads II, III, aVF, and V1-V4. There were no remarkable findings on ultrasonic cardiogram.
Subsequent coronary angiography (CAG) revealed a normal right coronary artery and circumflex artery without any anomalies or sign of atherosclerosis. In the proximal to middle part of the left anterior descending artery (LAD), there was a near 25 mm long tumor-like aneurysm. The diameter of this aneurysm varied with the cardiac cycle. During cardiac systole, the aneurism was compressed by approximately 70% (Figure and ). There was no obvious sign of atherosclerosis within other segments of LAD. Following intravascular ultrasound (IVUS) examination showed that the maximum diameter of the CAA during systole was 7.7 mm, the minimum diameter during systole was 4.02 mm, and the muscle bridge was clearly visible above the coronary artery (Figure and ).",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': True, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'obesity': False}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 54 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 3 + 1 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 4.
Based on the patient's data, the HEART Score is 4."
4179,18,HEART Score for Major Cardiac Events,risk,integer,usmle-1047,Extracted,"A 58-year-old woman comes to the physician because of intermittent painful retrosternal dullness for 4 weeks. The pain is recurrent and occurs when she exerts herself or when she is outside during cold weather. She also experiences shortness of breath and palpitations during these episodes. The symptoms resolve spontaneously when she stops or sits down for a while. Over the past few days, the episodes have increased in frequency. She has hypertension, type 2 diabetes mellitus, and osteoarthritis. Her left leg was amputated below the knee after a motorcycle accident 25 years ago. She is currently waiting for a new prosthesis and walks with crutches. Current medications include captopril, glyburide, and ibuprofen. She does not smoke or drink alcohol. Her pulse is 88/min, respirations are 20/min, and blood pressure is 144/90 mm Hg. Cardiac examination shows no abnormalities. An x-ray of the chest shows no abnormalities. An ECG shows a normal sinus rhythm without any signs of ischemia. Serum cardiac markers are within the reference range.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [58, 'years'], 'Hypertension history': True, 'Suspicion History': 'Moderately suspicious', 'Diabetes mellitus': True, 'smoking': False, 'Electrocardiogram Test': 'Normal', 'Initial troponin': 'less than or equal to normal limit', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 58 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 1 + 1 = 2.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4180,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7182159-1,Extracted,"A 44-year-old female with no significant past medical history was admitted for atypical chest pain, described as a precordial non-exertional pressure sensation. The review of systems was largely negative. Vital signs were significant for mild tachycardia. Physical exam was significant for the presence of S3 and S4. The admission laboratory evaluation, as shown in Table , was only significant for chronic anemia, elevated N-terminal pro-brain natriuretic peptide (NT-BNP), and mildly elevated lactate dehydrogenase (LDH).
Computed tomography (CT) angiography (Figure ) was negative for pulmonary embolism but incidentally revealed a moderate pericardial effusion with two mediastinal masses along the left cardiophrenic angle and within the superior pericardial recess. Additional infiltration was found along the left aspect of the pericardium, left ventricular myocardium, left hemithorax pleura, and the lateral left wall of the main pulmonary artery with an endoluminal component partially obstructing the lumen.
Echocardiogram (Figure ) confirmed severe left ventricle (LV) hypertrophy, mostly affecting the lateral wall, apex, and interventricular septum with impaired LV diastolic filling.
In order to establish a tissue diagnosis, a CT-guided biopsy was performed by interventional radiology. Pathology revealed the tumor was positive for multiple myeloma oncogene 1 (MUM1) and lambda light chain, consistent with plasma cell neoplasm (Figure ).
Flow cytometry demonstrated cytoplasmic lambda-restricted monoclonal plasma cells that were CD138-, CD38+, CD19-, CD20-, CD56-, CD117-, and CD45-. Serum immunoglobulin quantification (Table ) revealed elevated immunoglobulin G (IgG) and beta2 microglobulin. Serum protein electrophoresis and immunofixation were significant for monoclonal M protein and elevated IgG alpha 1 (Table ). In the myeloma workup, the complete bone survey was negative for lytic bone lesions while bone marrow biopsy and flow cytometry revealed no monoclonal plasma cells. Furthermore, positron emission tomography/computed tomography (PET/CT) (Figure ) confirmed the intrathoracic hypermetabolic lesion without metastasis or bony involvement.
Based on the above findings, SEP was diagnosed due to the absence of plasma cell monoclonality or myeloma defining features. Immunoglobulin-producing plasma cell tumors are known to cause amyloid deposition in various organs including the heart [,]. In order to rule out cardiac amyloidosis, a cardiac MRI was ordered and demonstrated the mass infiltrated and replaced most of the anterior, anteroseptal, and anterolateral wall of the LV, resulting in myocardial stiffening with limited radial contraction at the level of the infiltration. Moreover, there was encasement, extrinsic compression, and moderate narrowing of the pulmonary trunk, right pulmonary artery, aortic arch, and right brachiocephalic artery. The pulmonary trunk was directly invaded by a 1.98 cm mobile endoluminal thrombus.
Upon reviewing the patient’s previous medical record, it was found that the patient was admitted 11 years ago for a two-week history of epigastric discomfort, bilateral lower extremity edema, and a 40-pound unintentional weight loss. CT chest demonstrated an approximately 7 cm mass abutting the left ventricle, laterally extending to the left lung, and multiple mediastinal lymph nodes and nodularity throughout the pericardium. Fine needle aspiration (FNA) revealed a monotonous plasma cell population that was CD138+ with restricted monoclonal lambda light chain expression. Cardiothoracic surgery was consulted for an anterior mediastinotomy. Direct cardiac structures invasion was visualized intraoperatively. Pathology confirmed a neoplastic infiltration of the epicardium and pericardium. A bone survey revealed several lucent lesions in the frontal calvarium. Serum immunoglobulin G (IgG) was elevated at 2,090 ng/dL. Despite negative bone marrow biopsy, the patient was diagnosed with MM (biopsy confirmed extramedullary plasmacytoma and bony lesions). She was treated with Revlimid and zoledronic acid for a short period of time. Despite the treatment, the mediastinal mass continued to grow. Hence, the regimen was subsequently switched to cyclophosphamide, bortezomib, and dexamethasone for a total of six cycles. Follow-up PET/CT demonstrated significant improvement of the mediastinal mass and osseous lesions. Then, autologous stem cell transplantation was performed following intravenous melphalan. The patient remained in remission for 11 years, evident by multiple negative surveillance CT scans and bone marrow biopsies, before this relapse.
The possibility of radiation therapy was evaluated after the diagnosis of relapsing cardiac SEP. The risk of cardiotoxicity was deemed too high. Hence, the patient was started on chemotherapy, entailing carfilzomib, cyclophosphamide, and dexamethasone. She was discharged after one cycle and has been following with oncology as an outpatient for continued treatment. The patient responded favorably, as demonstrated by the shrinking mass and normalized serum IgG four months post-discharge. She remained largely asymptomatic after seven months.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [44, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 44 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4181,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4295136-1,Extracted,"An 85-year-old Caucasian female presented to the emergency room (ER) with a three-day history of right lower quadrant and periumbilical abdominal pain. Her primary care physician had prescribed oral levofloxacin 750 mg once daily for seven days, for a presumptive diagnosis of diverticulitis. Since antibiotic did not seem to bring about a change in her clinical status, the patient decided to seek help at the ER. She was known to have diverticulosis, several past episodes of left sided diverticulitis, hypertension, hyperlipidemia, hypothyroidism, esophageal reflux, a hiatal hernia, and chronic obstructive pulmonary disease (COPD). Surgery for the recurrent diverticulitis was not done because of the old age of the patient who preferred to use antibiotics and be on follow-up. On chart review, there was a mention of supraventricular tachycardia but the patient had no recall of its nature and records were not available. She had had a cholecystectomy in 1991 and prior colonoscopies which had revealed extensive diverticulosis throughout her descending and sigmoid colon. Her medication list included omeprazole, levothyroxine, and vitamin D. Of note is the fact that she was not on medications for hypertension, hyperlipidemia, and COPD. She had no known allergies. She had 50 pack-year smoking history but quit 10 years ago. Family history was notable for coronary artery disease in her father who died of an acute myocardial infarction.
On exam, her vital signs were found to be normal. The only significant finding was periumbilical and right lower quadrant abdominal tenderness, without rebound, guarding, or rigidity of the abdomen. Initial testing showed mild leukocytosis with all other laboratories including hemoglobin, platelet count, renal, and kidney chemistries being within the reference ranges. Lipid panel was as follows: total cholesterol 212 mg/dL, triglycerides 167 mg/dL, LDL cholesterol 151 mg/dL, and HDL cholesterol 43 mg/dL. Patient was on diet modification for hyperlipidemia and refused any medications for that. An obstructive series ruled out intestinal obstruction. CRP was not measured as the CT scan results were satisfactory to the managing team. A computed tomographic (CT) scan () of the abdomen with contrast showed diverticulosis coli without surrounding inflammation. Wedge-shaped hypodense lesions were incidentally identified on the upper and mid poles of the right kidney as well as the upper pole of the left kidney. This necessitated a renal protocol CT scan () with and without intravenous contrast, only to confirm multiple infarcts in the right kidney with small ischemic foci in the left kidney. An admission electrocardiogram (EKG) accidentally revealed new onset atrial fibrillation with controlled ventricular response.
Heart rate was still well controlled at 80s and patient was started on oral bisoprolol and apixiban. An echocardiogram was performed and showed ejection fraction of 58.9% with left atrium diameter 2.7 cm. There was moderate to severe tricuspid regurgitation with elevated right ventricular systolic pressures. The patient was discharged to home on apixiban and bisoprolol with marked clinical improvement. Follow-up labs after 3 months were normal showing stable normal kidney function tests. Patient remained in atrial fibrillation with ventricular rate controlled on discharge.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [85, 'years'], 'Hypertension history': True, 'hypercholesterolemia': True, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': True, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 85 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 0 + 2 = 2.
The following risk factor(s) are present based on the patient's note: hypertension, family with cvd. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4182,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8613055-1,Extracted,"A 42-year-old male patient presented to the emergency department with severe retrosternal chest pain radiating to the left arm for two hours. The pain was associated with sweating and vomiting. Patient was a febrile with no cough, no dyspnea and no other cardiac symptoms. The patient is smoker (I pack/day for 20 years), no hypertension, or diabetes mellitus. He has a past history of right nephrectomy due to renal stones.
On examination the patient was conscious, oriented with heart rates of 80 beats/minute, respiratory rate of 17 cycle/minute, and blood pressure= 118/80 mmHg. Normal oxygen saturation (SpO2= 100%), normal jugular venous pressure and no carotid bruits. Chest: normal vesicular breathing. Heart: normal first and second sounds with no additional sounds. Abdomen: soft, no organomegaly, no bruit at renal artery site auscultation. Lower limbs were intact with normal pulse and no edema.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [42, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'smoking': True, 'Diabetes mellitus': False, 'Electrocardiogram Test': 'Normal', 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 42 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4183,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6641677-1,Extracted,"A 28-year old Korean woman presented to the emergency department after a witnessed syncopal episode on July 2017. She had epigastric discomfort and experienced dyspnea on exertion upon climbing stairs 2 days before admission. On the day of admission, she had transiently lost consciousness while complaining of dizziness. Her previous medical history was unremarkable. History of smoking tobacco, alcohol, or drug abuse was denied. Upon further inquiry, she admitted to having taken oral contraceptive pills for 5 days before going on a trip.
On admission, she was alert and oriented but lethargic with initial blood pressure of 78/38 mm Hg, a pulse rate of 116/minutes, and oxygen saturation 76% while breathing ambient air. Cardiac examination showed regular tachycardia with accentuated S2 sound and wheezing, crackles were present in the lower lung field. Abdominal findings were unremarkable. There was no leg edema. Her electrocardiogram revealed sinus tachycardia, normal axis, and normal intervals. Arterial blood gas analysis results were as follows: pH 7.46, pCO2 31.2 mm Hg, pO2 39.4 mm Hg, and bicarbonate 21.9 mmol/L. D-dimer was elevated to 10.1 μg/ml (reference range < 0.5 μg/ml). The complete blood count, electrolyte, glucose, prothrombin time, activated partial thromboplastin time, renal-, and liver-function tests were within normal range. A contrast-enhanced computed tomography (CT) scan was performed. There was near total occlusion of both main pulmonary arteries and upper, middle, and lower lobar pulmonary arteries that were consistent with acute pulmonary thromboembolism and deep vein thrombosis was seen at the left popliteal vein (Fig. ). Echocardiography showed dilated right ventricle with dysfunction, D-shaped left ventricle and inferior vena cava dilatation without plethora.
The patient was transferred to the intensive care unit (ICU) for close monitoring. She was hemodynamically stabilized after aggressive fluid resuscitation without need for thrombolysis or embolectomy, and supplemental oxygen was discontinued after several days. Anticoagulation treatment with low-molecular weight heparin was initiated and she was successfully discharged on hospital day 5 after switching to a direct oral anticoagulant (DOAC), rivaroxaban 15 mg every 12 hours.
Thrombophilia study for the patient showed the following results: PC 103 IU/dl (reference range 70–130 IU/dl), PS 75 IU/dl (reference range 70–130 IU/dl), and AT III 95% (reference range 80–120%), all levels within normal range. Lupus anticoagulant, anticardiolipin antibodies, and prothrombin G20210A gene mutation were negative. Homocysteine level was 6.59 μmol/L (reference range 4–15 μmol/L) and factor VIII level 164% (reference range 52–192%) were within normal range. Multiplex PCR was carried out using SNaPshot system to screen for FVL. Screening for FVL showed heterozygous mutation (1691G > A), confirming the diagnosis for massive VTE due to FVL mutation. The patient's family was counselled, and further investigations were done for the patient's father, mother, and brother. The patient's mother was found to have FVL mutation, but other family members were found to be normal (Fig. ).
Rivaroxaban was tapered down to a dose of 20 mg once daily after an initial 21-day course of higher dose therapy. Follow-up chest CT at 6 months of anticoagulation therapy showed no evidence of remnant pulmonary thromboembolism. After 12 months of anticoagulation therapy, rivaroxaban was discontinued. The patient is under close surveillance and has not had a subsequent thromboembolic event after discontinuation of rivaroxaban.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [28, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Moderately suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': True, 'hypercholesterolemia': False, 'obesity': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit'}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 28 years old. The patient's age is less than 45 years and so keep the current total at 1.
The following risk factor(s) are present based on the patient's note: family with cvd. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4184,18,HEART Score for Major Cardiac Events,risk,integer,trec-ct-2022-5,Extracted,"A 23-year-old man comes to the emergency department following an episode of syncope.  He was working out when he felt dizzy and passed out without head injury.  He has had 3 other episodes of light-headedness over the last year, all happening during physical activity. He never had this experience while resting. He has no other medical conditions.  The patient does not use tobacco, alcohol, or illicit drugs.  His father died suddenly at age 35.  Vital signs are within normal limits.  On physical examination, the patient has a harsh systolic murmur.  The lungs are clear with no peripheral edema. Echocardiography shows asymmetric interventricular septal hypertrophy.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'parent or sibling with Cardiovascular disease before age 65': True, 'Suspicion History': 'Slightly suspicious', 'Hypertension history': False, 'smoking': False, 'Diabetes mellitus': False, 'age': [23, 'years'], 'atherosclerotic disease': False, 'obesity': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'Initial troponin': 'less than or equal to normal limit'}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 23 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: family with cvd. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4185,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5864775-1,Extracted,"A 64-year-old female patient was admitted to our clinic with dyspnea. She had a 4-year history of dyspnea and visited medical centers with no satisfaction. Her past history included right nephrectomy due to renal calculi 33 years ago.
On admission, she presented with tachypnea, normal blood pressure, and no fever. Her low oxygen saturation increased to 95% with oxygen supply. She had sinus rhythm with 90 bpm and no pathologic signs. Jugular distention was noticed. Fine rales were heard in the basal area of the lungs. Ascites and hepatomegaly with a lower board 2 cm below the costa were noted. Lower extremities showed edema. Interestingly, a murmur was heard in the right periumbilical region of the abdomen. The murmur was high-pitched and continuous with no change in position. Chest X-ray showed blunted costophrenic sinuses. No infective or tumoral infiltration was seen. Echocardiographic findings were normal. Abdominal Doppler ultrasonography showed a communication between the right renal artery and the inferior vena cava (IVC). Computed tomography showed a dilated (11 mm) right renal artery with a fistula draining into the IVC (). After stabilization of heart failure symptoms with diuretics, peripheral angiography confirmed a renal AVF (, ). According to the anatomical compatibility of the right renal artery and after consultation with the vascular surgery department, percutaneous closure with Amplatzer vascular plug (AVP) II was decided as the next step. AVP II of 12×9 mm in dimension was delivered percutaneously via the transfemoral approach and implanted into the proximal region of the right renal artery. Selective right renal artery angiography showed occlusion of the flow through the renal artery and IVC (, ). Heart failure signs and symptoms dramatically resolved and the patient was discharged healthy.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [64, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 64 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4186,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7415096-1,Extracted,"A 50-year-old man presented to the emergency department (ED) at SUNY Downstate Medical Center with complaint of intermittent epigastric pain that began a few days prior. The patient was slightly confused at time of presentation but was able to provide some history. Collateral history was collected from his daughter who lives with the patient and was also present at time of the patient's presentation to the ED. The patient reported that his epigastric pain was nonradiating, associated with nausea along with multiple episodes of nonbilious, nonbloody emesis. The patient also reported subjective fevers, chills, and cough for one week. He denied any flank pain, changes in bowel habits, appetite, or amount of oral intake. He also denied any changes in his weight. His daughter, however, noted that over the past week, she observed a decrease in the patient's appetite and oral intake. Patient's medical history was significant for hypertension, for which he did not take any medication, and hepatitis B (Hep B), for which he was hospitalized in 1983. He was unable to recall the cause of the hepatitis. He denied any history of tobacco, alcohol, illicit drug, or recent NSAID use. He does not take any prescribed or over-the-counter medications. His family history was unremarkable.
A thorough occupational history collected later in the course of hospitalization revealed that the patient has worked in the aviation industry as an aircraft refueler at a local airport, where he refuels up to nine aircrafts per day for the past three and half years. At work, the patient reports wearing a uniform and “long medical gloves,” which he described as being approximately five times the thickness of standard hospital gloves. He also stated that he wears a respirator mask about 60% of the time during refueling. The patient reported direct skin contact with jet fuel when it spills onto his arms at least three times per day on average, despite wearing a uniform and gloves. He mentioned one instance, where he was completely covered in jet fuel. He also noted that he could often smell fuel on his hands for several days after a spill. At time of admission, the patient was oliguric and in acute renal failure (ARF) as his serum chemistry showed a strikingly elevated blood urea nitrogen (BUN) and creatinine that were each about 20 times over the normal limits. He was normotensive, and his physical exam was only revealing of dry mucous membranes, clear lungs, and a cardiac exam that was within normal limits. He had no edema of his lower extremities bilaterally. The cause of his ARF was unknown at this time.
The patient's hospital course included extensive medical and diagnostic testing to investigate the etiology of his acute renal failure. His baseline renal function was unknown. The patient's initial serum chemistry showed a BUN level of 215 mg/dL and creatinine level of 20.41 mg/dL with an estimated glomerular filtration rate (eGFR) of 3 mL/min/1.73 m2. Electrolytes showed slight hyponatremia with a serum sodium level of 126 mmol/L, normal serum potassium level of 4.6 mmol/L, blood glucose level of 130 mg/dL, normal magnesium level of 2.3 mg/dL, modest hyperphosphatemia level of 5.3 mg/dL, calcium level of 9.1 mg/dL, and a mild metabolic acidosis with a serum bicarbonate level of 17 mmol/L. The patient was seen by the Nephrology consultation service who recommended continuing aggressive intravenous fluid (IVF) hydration and strict urine output monitoring and deferred on initiating renal replacement therapy at the time. The patient had placement of an indwelling Foley catheter for strict urine output measurement. His urinalysis was mainly unrevealing showing no glucosuria, no proteinuria, 11 white blood cells, 6 red blood cells per high-power field, and a specific gravity of 1.010. His calculated fractional extraction of sodium (FeNa) was 6% indicating an intrinsic renal or postobstructive cause. As we continued aggressive IVF hydration, patient's urine output improved and so did his mental status. He became more awake and alert and was able to provide better history. Other workups during hospital course included a negative HIV and negative hepatitis C serology. He had a known history of hepatitis B, and his serology demonstrated prior exposure with developed immunity (positive Hep B core antibody, positive Hep B surface antibody, and a negative Hep B surface antigen). The patient also had normal C3 and C4 levels. C-ANCA and P-ANCA testings were also negative. The creatinine phosphokinase (CPK) level was only modestly elevated to 493 u/L, which is insufficient to explain the degree of renal impairment in the patient. As we continued aggressive hydration, his renal function continued to improve with a quicker fall in the serum creatinine compared to the BUN. Other laboratory testings included an elevated iPTH level of 275.4 pg/mL. The patient also underwent a computed tomography (CAT) scan of the abdomen and pelvis without intravenous contrast that showed no acute pathology in the abdomen, and a renal ultrasound did not show any evidence of obstruction bilaterally but, however, did report mildly echogenic kidneys consistent with medical renal disease. After 11 days of hospitalization, the patient had fully returned to his baseline mental status and was stable for discharge to home. His chemistry on the final day of hospitalization showed a BUN level of 39, serum creatinine level of 1.8 mg/dL, and serum bicarbonate level of 23 mmol/L.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [50, 'years'], 'Hypertension history': True, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'greater than three times normal limit', 'hypercholesterolemia': False, 'atherosclerotic disease': False}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 50 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 2 + 2 = 4.
Based on the patient's data, the HEART Score is 4."
4187,18,HEART Score for Major Cardiac Events,risk,integer,usmle-2267,Extracted,"A 26-year-old man comes to the physician because of a 1-week history of left-sided chest pain. The pain is worse when he takes deep breaths. Over the past 6 weeks, he had been training daily for an upcoming hockey tournament. He does not smoke cigarettes or drink alcohol but has used cocaine once. His temperature is 37.1°C (98.7°F), pulse is 75/min, and blood pressure is 128/85 mm Hg. Physical examination shows tenderness to palpation of the left chest. An x-ray of the chest is shown.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [26, 'years'], 'Hypertension history': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 26 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4188,18,HEART Score for Major Cardiac Events,risk,integer,pmc-2546413-1,Extracted,"A 56-year-old Caucasian man with type 2 diabetes mellitus, hypothyroidism, idiopathic thrombocytopenic purpura status post splenectomy in 1979, and remote testicular cancer status post orchiectomy and radiation therapy in the 1970s was admitted with 2 days of progressive fatigue, exertional dyspnea, low back pain and cranberry-colored urine. He had been started on metformin 500 mg twice a day 4 days previously for type 2 diabetes but called in to his physician the following day with complaints of ""palpitation, heavy breathing, and tossing and turning last night"" after taking the metformin, which he declined to continue. Two days before admission he was seen at an outside emergency room with hematuria and anemia; he was diagnosed with a urinary tract infection and started on oral ciprofloxacin. His other medications were pantoprazole, levothyroxine and glyburide. On the day of admission, vital signs were temperature 37.1°C, pulse rate of 133 per minute, respiration rate of 32 breaths per minute, blood pressure of 155/84 and pulse oxygen 94% on 6 liters O2. Physical examination was significant for respiratory distress, scleral icterus and generalized jaundice. There was no jugular venous distention and no enlarged thyroid gland or lymphadenopathy. His lungs were clear, heart sounds were distant, his abdomen was soft without masses or enlargement of organs, he had no rashes and no peripheral edema. Mild lumbar and thoracic spinous tenderness was noted; neurological examination revealed mild lethargy but otherwise normal mental status, with no focal findings. Laboratory studies (Table ) were significant for hemoglobin of 6.6 g/dl, which had dropped from 14.7 g/dl 4 days before, total bilirubin 6.6 mg/dl (direct 2.7 mg/dl), reticulocyte count 3.51%, lactate dehydrogenase 4829 U/l, and haptoglobin less than 6 mg/dl, all consistent with severe hemolysis. The direct antiglobulin (Coombs) test (DAT) was positive for anti-IgG and negative for anti-C3. The peripheral blood smear on admission significantly showed no schistocytes; 4% immature granulocytes and 4% nucleated red blood cells (RBCs) were noted. Other significant findings included marked leukocytosis to 46.1 K/cmm, acute renal failure, elevation of troponin-I and marked transaminase elevations (aspartate aminotransferase (AST) 1711, alanine aminotransferase (ALT) 806) with normal international normalized ratio and alkaline phosphatase. Blood and urine cultures showed no growth. Despite treatment with corticosteroids and transfusion of packed RBCs, the patient became increasingly dyspneic and agitated, complained of abdominal pain and developed hypotension followed by cardiorespiratory arrest approximately 8 hours after admission. Over the next 4 hours he was treated following the advanced cardiac life support protocol for recurrent bouts of pulseless electrical activity and asystole, with worsening hyperkalemia and metabolic acidosis. Despite transfusion, hemoglobin was noted to have declined to 3.3 g/dl. The patient died approximately 12 hours after admission.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [56, 'years'], 'Hypertension history': True, 'Diabetes mellitus': True, 'Suspicion History': 'Moderately suspicious', 'atherosclerotic disease': False, 'Initial troponin': 'greater than three times normal limit', 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 56 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 1 + 1 = 2.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 3 + 2 = 5.
Based on the patient's data, the HEART Score is 5."
4189,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6666888-1,Extracted,"A 67-year-old previously healthy female with a known diagnosis of POAG for five years presented to the clinic with a new onset of loss of consciousness which had started two weeks ago. She was doing perfectly fine when she experienced her first episode of loss of consciousness (LOC) which occurred all of a sudden causing her head to drop on to the table, followed by three more episodes before she finally presented to the clinic. She had these episodes after eating food. These syncopal events did not progress up the course of her illness. The episodes were brief, ranging from a few seconds to a few minutes. She did not experience any aura, lightheadedness, narrowing of the vision, diaphoresis, and shortness of breath, palpitation or a funny chest sensation before passing out. There were no shaky movements and she would regain complete consciousness after the episodes resolved. She denied tongue biting, frothing from the mouth, or urinary or fecal incontinence. She was started two months ago on timolol ocular preparation of 0.5% at night time daily, which she used to take 15-30 min before dinner. She denied any history of skipping meals, nausea, vomiting, alteration of bowel habits, or alcohol intake. No headache, weakness, numbness, or tingling were reported. She had a past surgical history of laparoscopic cholecystectomy that was done 10 years back. She had no significant past medical, psychiatric, or family history of a similar illness.
On admission, she was fully responsive, alert, and oriented with normal effect. The patient was afebrile with a pulse of 67 beats per minute (BPM), blood pressure (BP) of 123/67 mmHg, and respiratory rate of 13/min. Her abdomen was nondistended, nontender with normoactive bowel sounds and no organomegaly. The neurological exam for bulk, tone, power, and reflexes was insignificant for any finding. Sensations and joint position sense were intact. Cerebellar signs of co-ordination and cranial nerves two till 12 were intact and with no observed nystagmus or visible tremors. The cardiovascular exam was normal with regular rate and rhythm and no added sounds or murmurs. The pulmonary exam was normal with bilateral audible breath sounds clear to auscultation with no added wheeze. The patient had no lymphadenopathy, edema, conjunctival pallor, jaundice, rashes, or tightening of the skin.
Orthostatic vitals were also obtained in both the supine and standing position but revealed no significant difference in the blood pressure reading.
The complete blood count (CBC) showed a total leukocyte count (TLC) of 3.78 x 109/L with neutrophils being 89% and lymphocytes being 6%. Platelets were 430 x 109/L. Erythrocyte sedimentation rate and C-reactive protein levels were within normal limits. The coagulation profile was normal as well. The electrolyte panel indicated normal potassium, calcium, and sodium levels. The serum and urine osmolality was normal as well.
The glycosylated hemoglobin (HbA1c) level was 4.6% with a random blood sugar level of 89 mg/dL (normal: 79-160 mg/dL). Her blood sugar did not drop during or after the consumption of the meal. Serum insulin levels and C-peptide levels were investigated to check for the remote possibility of insulinoma but turned out to be normal as well. Ultrasound abdomen exhibited biliary duct dilatation of 7 mm, which was consistent with post-cholecystectomy status. The pancreas could not be visualized and hence endoscopic ultrasound (EUS) was done to check for any echogenic change in the pancreas but turned out to be negative. CT scan of the abdomen was also done but returned negative. A gastric emptying study was also done to look for any delays in emptying and concomitant blood sugar levels were also drafted but they were insignificant for suspected dumping syndrome.
She had head-drops after having meals which drifted our diagnosis towards more central causes as of epilepsy or a space-occupying lesion in the brain. In order to be certain, electroencephalography was done which returned to normal. MRI of the brain was also conducted but showed no growth or changes in intensity.
Finally, to exclude cardiac causes of syncope, electrocardiography, and echocardiography were done which also failed to indicate a cause. Holter monitoring was advised which turned out to be the only pertinent study showing bradyarrhythmia especially post-meal that is within 30 min of timolol maleate 0.5% drop application. Her heart rate went to 46 bpm, but she remained hemodynamically stable throughout the course with mean BP being 108/76 mmHg. Surprisingly, she did not show any palpitations.
Her regimen for POAG was then changed from timolol 0.5% to latanoprost 0.005% ophthalmic solution, a prostaglandin F2 analog, which not only aided in lowering the intraocular pressure (IOP) but also halted the syncopal head-drops that the patient was experiencing. On her six months follow up visit, the patient happily concluded that her syncopal episodes had completely resolved.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [67, 'years'], 'Hypertension history': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 67 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 0 + 2 = 2.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4190,18,HEART Score for Major Cardiac Events,risk,integer,pmc-2871533-1,Extracted,"A 59-year-old man with a history of type 2 diabetes mellitus, hypertension, and dyslipidemia was referred to cardiology clinic for evaluation of atypical chest pain. The patient denied any family history of coronary artery disease and had a history of 60 pack years of smoking. Physical examination was normal as was the 12-lead electrocardiogram. He had a recent workup, including transthoracic echocardiography that showed a left ventricular ejection fraction of 60%, stage II diastolic dysfunction and mild biatrial enlargement, and a radionuclear myocardial perfusion imaging stress test that showed no evidence of inducible ischemia or previous myocardial infarction. Patient underwent cardiac catheterization for definite evaluation of coronary artery disease. Selective right coronary angiography with a 6 F right coronary Judkins 4 catheter revealed a common blood vessel from which the right coronary artery (RCA) and the LMCA were arising. The RCA followed its normal course around the atrioventricular groove and the LMCA traveled to the left side of the heart and divided at the level of the interventricular septum giving off a long LADCA and the LCXCA (). Selective left coronary angiography with a 6F left Judkins 3.5 catheter revealed a second short hypoplastic LADCA that ended at the distal end of the proximal third of the interventricular sulcus without giving any branches of significant size (). An aortogram was done to demonstrate the origins of the coronary blood vessels. Four coronary arteries were identified, one arising from the left coronary sinus and the other three originating from a main blood vessel from the right sinus of Valsalva. Left ventriculography showed normal chamber size and wall motion. There was significant calcification of the proximal segments of the RCA, LMCA, the longer LADCA, and the LCXCA without significant diameter stenoses. A coronary computed tomography angiography (CTA) was ordered to further delineate the course of the longer LADCA. Images were acquired with prospective gating on a 64-Multislice detector computed tomography scanner (Somatom Definition, Siemens, Forchheim, Germany) in the craniocaudal direction during suspended respiration at 0.75 mm slice thickness and reconstruction interval, 0.33 second gantry rotation speed, tube voltage 120 kVp, and a peak tube current of 390 mA. Cumulative dose-length product was 651 mGy × cm. Iso-osmolar nonionic contrast material (Omnipaque, GE Healthcare, Princeton, NJ) was used. Premedication with nitroglycerin 0.6 mg SL was administered. No beta blocker was given since heart rate was <70 per minute. CTA demonstrated the LMCA traveling to the left side of the heart behind the right ventricular outflow tract and through the interventricular septum (Figures and ). No angiographically significant stenoses or high-degree calcifications were noted.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [59, 'years'], 'Hypertension history': True, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': True, 'smoking': True, 'Electrocardiogram Test': 'Normal', 'atherosclerotic disease': False, 'hypercholesterolemia': True, 'parent or sibling with Cardiovascular disease before age 65': False, 'Transient Ischemic Attacks History': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 59 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 1 + 2 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4191,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6054366-1,Extracted,"An otherwise healthy 25-year-old man presented to the emergency department with a substernal chest pain for an hour accompanied by shortness of breath, nausea, and vomiting. The chest pain was sudden in onset, 8/10 in intensity, and radiating to his right arm. The chest pain was slightly relieved on lying flat and aggravated by walking. He had no associated symptoms such as fever, cough, runny nose, or rash. He did not have any antecedent infection.
Patient’s past medical, surgical and family history was unremarkable, and he had no modifiable or non-modifiable cardiovascular risk factors. He had no known allergic reaction to food or drugs. He was a nonsmoker and did not use any illicit drugs. A comprehensive history revealed a daily intake of seven to nine cans of caffeinated energy drinks for the past week. The patient reported significant improvement in his chest pain after receiving sublingual nitroglycerin and diamorphine intravenously.
His vital signs on examination were (1) Temperature: afebrile, (2) Blood Pressure: 155/95 mmHg in his right arm and 150/90 mm Hg in his left arm, (3) Respiratory Rate: 25 breaths/min, d-Heart Rate: 110 beats/min. Pulse oximetry showed 98% oxygen saturation on room air. Cardiac examination revealed S4 on auscultation of the chest. On palpation of the chest, there was no point tenderness. Rest of the systemic examination was unremarkable.
The initial electrocardiogram (EKG) on admission (Figure 1) showed sinus rhythm with ST depression in precordial leads V2-V6. Chest X-ray was insignificant with no signs of pulmonary congestion. Laboratory findings were as follow: (1) an elevated level, 32.22 µg/ml, of 12-h troponin I (normal range <0.07); confirming definite acute coronary syndrome. (2) d-Dimers were 380 ng/ml (normal range <500). (3) Thrombophilia and drug screen were negative. After appropriate initial resuscitation for the coronary syndrome, the patient was transferred to the catheterization laboratory for the percutaneous coronary intervention.
Coronary angiography showed normal coronary arteries. Transthoracic echocardiography (TTE) showed ejection fraction of 60% with left ventricular diameters within normal limits. The patient was discharged after five-day observation period and was counseled to limit/stop the ingestion of energy drinks. He was discharged with aspirin, spironolactone, perindopril, and atenolol.
On the post-hospital follow-up visit, the patient had completely stopped consuming energy drinks and was symptom-free. TEE at this visit revealed ejection fraction of 62% with preserved global left ventricular function.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [25, 'years'], 'Hypertension history': True, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'greater than three times normal limit', 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 25 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 1 + 2 = 3.
Based on the patient's data, the HEART Score is 3."
4192,18,HEART Score for Major Cardiac Events,risk,integer,pmc-3286501-2,Extracted,"A 78-year-old female patient, temporarily admitted to the recovery department after ECT, developed atrial fibrillation and chest pain. Her medical history showed hypertension, severe depression and paroxysmal atrial fibrillation. Her ECG 3 months before ECT was completely normal. Immediately after ECT her blood pressure was 230/140 mmHg, but later decreased to 110/45 mmHg. Examination of heart and lungs revealed no abnormalities. The ECG showed atrial fibrillation with a ventricular rate of 140 beats/min and new negative T waves in leads I, II, aVL and V2-6. The second ECG showed sinus rhythm and persisting negative T-waves (Fig. ). Troponin T level was 0.02 μg/l (normal) and no other laboratory abnormalities were found. A differential diagnosis was made and the following possible causes were taken into account: post ECT, post tachycardia due to atrial fibrillation, severe hypertension or myocardial ischaemia. Since the patient reported to have had previous anginal complaints, coronary angiography was performed. In the left anterior descending artery two significant stenoses were identified in the proximal and the mid section, respectively. Furthermore, a stenosis was found in the right coronary artery. Due to her psychiatric condition, PCI was not performed and she was treated with anti-anginal medication and warfarin.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [78, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': True, 'Initial troponin': 'less than or equal to normal limit', 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 78 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 2 + 2 = 4.
The following risk factor(s) are present based on the patient's note: hypertension, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 4 + 1 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 5.
Based on the patient's data, the HEART Score is 5."
4193,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5637702-1,Extracted,"A 35-year-old, healthy male presented with acute onset of severe left-sided chest pain, which started while he was exercising at the gym. This episode was associated with diaphoresis and nausea. He denied any personal history of similar complaints or known medical problems. He also denied a family history of sudden death or congenital heart disease. The pain was significantly relieved with aspirin, nitroglycerin and morphine. Vital signs were stable and physical exam was benign including cardiac exam. The initial electrocardiogram (EKG) was not significant; however, a repeat EKG about 4-hours later showed significant ST segment elevations in the inferior leads (). Initial troponin was 0.04 ng/ml, which jumped to 97 ng/ml in about six hours. Emergent coronary angiogram was performed and revealed total occlusion at the ostium of the right posterolateral artery (RPLA) and mid-to-distal portion of right posterior descending artery (RPDA), with largely patent left coronary circulation. Diffuse ectasia of right coronary artery (RCA) and left anterior descending artery (LAD) was also discovered during angiography (, ). The obstruction at the ostium of RPLA was successfully treated with primary percutaneous transluminal coronary angioplasty (PTCA) and placement of two drug-eluting stents (2.5 × 12 mm and 2.5 × 16 mm Promus Premier DES). The procedure was uneventful with complete chest pain resolution shortly after. Transthoracic echocardiogram showed left ventricular ejection fraction of 60–65% with inferior wall hypokinesis. The patient was discharged with dual anti-platelet therapy (aspirin and prasugrel), atorvastatin, carvedilol, and lisinopril. Follow-up at one month showed no cardiac events.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [35, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': True, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'obesity': False, 'atherosclerotic disease': False}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 35 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 2.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 2 + 2 = 4.
Based on the patient's data, the HEART Score is 4."
4194,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4268617-1,Extracted,"A 45-year-old male with no history of ischemic heart disease presented to the emergency department 45 min after the onset of retro-sternal chest pain which radiated to the left arm and accompanied with cold sweating. His past medical history was only indicative of cocaine and tobacco abuse for several years. Initial physical examination demonstrated a blood pressure of 145/90 mmHg, heart rate of 94/min, respiratory rate of 18/min, oral temperature of 37.4°C and oxygen saturation 95% while he was breathing ambient air. Heart and lung examinations were unremarkable.
On admission, the electrocardiography revealed sinus rhythm and elevated ST segment in V1-V4 leads and depressed ST segment in II, III, AVF, V5 and V6 leads, well-suited with the diagnosis of acute antroseptal myocardial infarction. Bed-side echocardiography showed ejection fraction of about 35% and antroseptal akinesia.
The patient was immediately transferred to the intensive care unit for cardiac monitoring and thrombolytic therapy. Pain was alleviated with nitroglycerine and morphine. An intravenous infusion of 1.5 million units of streptokinase over 50 min, followed by heparin at 900 U/h and one 325 mg tablet of aspirin and one 75 mg tablet of clopidogrel were administered.
Results of laboratory evaluation included normal levels of electrolytes and glucose. The blood urea nitrogen level was 16 mg/dl and the creatinine level was 1.3 mg/dl. The alanine aminotransferase level was 64 U/l (reference range: 8-40), the aspartate aminotransferase level 180 U/l (reference range: 8-30), the alkaline phosphatase level 130 U/l (reference range: 35-125), total bilirubin level 0.8 mg/dl (reference range: 0.2-1.2 mg/dl), the albumin level 4.4/dl (reference range: 3.7-5.5), and the total protein level 7.3 g/dl (reference range: 6.0-8.0). The white blood cell count was 11,000/mm3, the hematocrit was 45.9% and the platelet count was 218,000/mm3. Also, creatinine kinase myocardial bound/creatinine kinase equal to 597/8932 U/l and elevated troponin-I level equal to 29 ng/ml were recognized.
After 8 hours of admission, the patient gradually developed shortness of breath, hypoxemia and fever (38.5°C) and after 3 h later, cough and hemoptysis developed. Bed-side chest X-ray showed bilateral basal alveolar infiltrates. Finally, endotracheal intubation and mechanical ventilation was necessitated when hypoxemia (SaO2= 78%) and symptoms of respiratory distress were present with a respiratory rate of 40/min. Laboratory tests showed a fall in the hemoglobin level from 15.8 to 12 g/dl within 20 h, and to 9 g/dl within 48 h; so two units of packed cell were administered. Activated partial thromboplastin time was 99 s. In addition, he received four units of fresh frozen plasma and eight units of cryoglobulin with the purpose of pulmonary hemorrhage control. There was no sign of hematuria or melena. The lab tests of admission time showed normal coagulation, liver and kidney functions tests. No other bleeding site was discovered.
On the next day, the patient remained febrile (39.0°C) with constant and moderate hemoptysis. Due to the increased blood urea nitrogen and creatinine during the 72 h after admission, bed-side hemodialysis according to the nephrology consult was done for him with the impression of acute renal failure. Bronchoscopy on the 3rd day showed no lesion in the bronchial tree and broncho-alveolar lavage was positive for hemosiderin laden macrophages (90%) and negative for acid fast bacillus. Computerized tomography of the chest on the 3rd day revealed diffuse alveolar infiltrates []. The results of anti-glomerular basement membrane antibody, antinuclear antibodies, anti-double-stranded deoxyribonucleic acid antibody, peripheral antineutrophil cytoplasmic antibodies (p-ANCA), and cytoplasmic ANCA were all negative.
The patient was intubated for 9 days with no significant improvement in his condition and in the 10th hospital day his blood pressure was not detected and cardiac rhythm became asystole; in spite of cardiopulmonary resuscitation for 60 min he remained pulseless and eventually expired.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'smoking': True, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",7,7,7,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 45 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, smoking, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 3 + 2 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 5 + 2 = 7.
Based on the patient's data, the HEART Score is 7."
4195,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5902109-1,Extracted,"A 22-year-old African American male presented to the ER with acute onset of “pressure-like” substernal, nonradiating chest pain. His symptoms started while playing basketball. The pain was associated with shortness of breath and nausea. He had no significant past medical history or family history of coronary artery disease or sudden deaths. He denied excessive caffeine use, smoking, or alcohol intake. There was no reported use of any illicit drugs such as cocaine or amphetamines and was physically very active. Vital signs on admission included blood pressure of 138/89 mmHg, heart rate of 94/min, and respiratory rate of 22 breaths/min. His BMI was 28. Physical examination was unremarkable with no chest tenderness on palpation and no jugular venous distention. Heart sounds were normal with no murmurs or additional sounds. The electrocardiogram showed ST-segment elevation myocardial infarction (STEMI) in leads II, III, aVF, and V4–V6 (). On subsequent EKGs, the patient had new ST-segment elevations in anterolateral leads with dynamic changes. Laboratory studies were pertinent for a troponin-I level of 0.83 ng/ml. The patient was given aspirin and ticagrelor loading doses, metoprolol succinate 25 mg, intravenous morphine, intravenous heparin drip, and sublingual nitroglycerin which did not relieve his chest pain.
The patient was taken for emergent cardiac angiography within 60 minutes of presentation and revealed acute dissection with thrombosis of the distal left main coronary artery (LCA) leading into the proximal left anterior descending artery (LAD) (Figures and ). An EBU 3.5 guide catheter was advanced over the wire with repeat injection of the left main performed revealing persistence of acute occlusion. Repeat angiography after balloon inflation revealed significant improvement in flow from TIMI 2 to TIMI 4. An extending thrombus was noted in the distal LAD which was suctioned out. Following this, a bare metal stent was inserted in the distal LCA ostial and the proximal LAD (Figures and ).
After catheterization, the patient was pain-free and hemodynamically stable. He was on epitifibatide infusion for a total of 18 hours. Other medications including carvedilol, lisinopril, aspirin, ticagrelor, and atorvastatin were initiated. The patient's peak troponin went up to 48.56 ng/ml in less than 24 hrs of initial laboratory studies and subsequently was trending down. Additional laboratory studies including hemoglobin A1c and lipid profile were normal. He was also worked up for thrombotic conditions which might lead to arterial thrombi such as homocystinemia and antiphospholipid antibody syndrome both of which were negative. Transthoracic echocardiography performed revealed preserved left ventricular systolic function normal with ejection fraction estimated to be 0.50 to 0.54%. There was no patent foramen ovale that might have led to paradoxical embolus. A urine and serum toxicology screen was also done on the patient who came back as negative for cocaine or methamphetamine.
After the procedure, the patient was further questioned to elicit any history that might shine light to the etiology of his STEMI. He admitted to the use of two different weight-loss products (Performix™ stim-free; Performix SST) for the past 1 year, taking one capsule up to three times a day as indicated on the product label. However, he took Performix SST for the first time on the afternoon of presentation, drinking 3 scoops mixed with water, approximately 2 hours before started playing basketball. On reviewing, the contents of the supplement, it was noted to contain synephrine, an epinephrine analogue. Other contents of the mixture consisted of anhydrous caffeine, sensoril ashwagandha extract, bitter orange extract, n-methyltyramine, hordenine, tyramine, octopamine, huperzine A, yohimbine HCL, mucuna pruriens, and Bioperine. The patient was advised to avoid the use of the supplements. He was discharged home from the hospital with outpatient cardiology follow-up and advice to be maintained on dual antiplatelet therapy for at least one year.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [22, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'obesity': True, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'Electrocardiogram Test': 'Normal'}",6,6,6,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 22 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: hypertension, obesity, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 2 + 2 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 4 + 2 = 6.
Based on the patient's data, the HEART Score is 6."
4196,18,HEART Score for Major Cardiac Events,risk,integer,pmc-3848848-1,Extracted,"A 21-year-old Japanese woman who had no specific medical history consulted a primary care clinic. Although she had been aware of the edema of her lower extremities for 2 weeks, her chief complaints were palpitations and chest pain, which had started the day before. An electrocardiogram (ECG) and chest radiograph did not reveal any specific abnormality. The next day she consulted another physician but her etiology was still not clear. She was referred to the emergency division in a municipal hospital 2 days later. Arterial blood gas analysis did not reveal hypoxemia. However, computed tomography (CT) revealed thrombi in her bilateral pulmonary arteries and left iliac vein, and a laboratory examination revealed NS. She was admitted and anticoagulant therapy was initiated immediately. The next day she was referred to a nephrologist at our university hospital.
She had no family history of thromboembolism; she is a nonsmoker and not obese. She has never taken a contraceptive pill. On admission, her physical characteristics were: weight 53kg; height 166cm; body mass index 19.2kg/m2; blood pressure 110/62mmHg; pulse rate 120 beats/minute; respiratory rate 20 breaths/minute and saturation of peripheral oxygen (pulse oximetry) 97% (room air). Her physical examination was normal except for the edema of the lower extremities. The laboratory investigation data were as follows: leukocyte 9660 cells/μL; hemoglobin 14.8g/dL; platelets 329,000/μL; hematocrit 42.2%; blood urea nitrogen 19mg/dL; serum creatinine 1.26mg/dL; serum albumin 1.7g/dL; total protein 4.3g/dL; total cholesterol 497mg/dL; triglyceride 187mg/dL; the levels of serum complement C3 were 116mg/dL and C4 34mg/dL. Serum antinuclear antibody was negative. The coagulation profile revealed the following: prothrombin time 15.2 seconds; activated partial thromboplastin time (APTT) 84.5 seconds; D-dimer 6.9μg/mL (normal: 0 to 0.4μg/mL); fibrinogen 832mg/mL (normal: 150 to 410mg/mL); fibrin-fibrinogen degradation product 10.5μg/dL (normal: 0 to 5μg/dL); antithrombin III 70% (normal: 80% to 120%); protein C 29% (normal: 70% to 140%); and protein S 66% (normal: 65% to 135%). Urinary protein excretion was 14g/g creatinine, and microhematuria was absent. In addition, arterial blood gas analysis revealed the following: pH 7.46, carbon dioxide 35.5mmHg, partial pressure of oxygen 88.6mmHg, and bicarbonate 26.0mEq/L (room air). Her chest radiograph and ECG were normal. A CT angiogram revealed thrombi of her bilateral pulmonary arteries and left common iliac vein (Figure ). Presumably, the pulmonary thrombosis originated from the thrombi of the left iliac vein.
Treatment of thrombosis was initiated with intravenous administration of heparin and urokinase. First, 18IU/kg of heparin per hour was initiated while adjusting the dose to maintain APTT between 60 and 85 seconds, thereafter, urokinase was infused at 10,000U/hour for 24 hours. Oral warfarin administration was also started, aiming at a prothrombin time-international normalized ratio of between 1.5 and 2.5, and heparin infusion was gradually decreased. An inferior vena cava (IVC) filter was placed percutaneously to avoid further development of pulmonary thrombosis by the left common iliac vein thrombi. Furthermore, corticosteroid therapy was initiated with prednisolone at a dose of 0.8mg/kg per day. Contrast-enhanced CT performed on day 14 revealed a reduction of the pulmonary thrombi and capture of the thrombi in the inferior vena cava (IVC) filter (Figure ). The patient’s proteinuria resolved after 3 weeks of treatment. The prompt and complete response to the corticosteroid therapy suggested that minimal change disease was the etiology of NS and pulmonary artery thrombosis.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [21, 'years'], 'Hypertension history': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': True, 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'Diabetes mellitus': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 21 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4197,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8060147-1,Extracted,"A 42-year-old Caucasian woman with a recent diagnosis of anorectal cancer presented to tertiary care hospital with chest pain, shortness of breath, and palpitations. She started having intermittent chest pain and heaviness three days prior to presentation. Her chest pain was typical for stable angina, i.e., localized to the central chest, worsened with activity, and improved with rest. Her review of systems was significant for cough productive of orange-colored sputum, palpitations, lightheadedness, fatigue, blurred vision, oral sores, and hallucinations. She denied fevers, chills, orthopnea, paroxysmal nocturnal dyspnea, or lower extremity edema. She was started on 5-FU chemotherapy five days ago for her cancer and denied any anginal symptoms prior to chemotherapy. Her oncological history was significant for biopsy and imaging proven stage IIa squamous cell carcinoma of the anus. She underwent radiotherapy a week prior to admission and was started on five days of continuous 5-FU infusion. The patient had a remote history of smoking one pack per day, but otherwise she had no history of diabetes or hypertension, or a family history of accelerated CAD.
On presentation, the patient’s vital signs were notable for temperature of 36.4°C, blood pressure of 104/83 mm Hg, heart rate of 133 beats per minute, respiratory rate of 27 per minute, and oxygen saturation of 94% on 3 liters of oxygen via nasal cannula. Physical examination revealed dry oral mucosa with supple neck, no jugular venous distention, and carotid bruit. Cardiovascular examination revealed tachycardic rate with regular rhythm and no murmurs, rubs, or gallops. Pulmonary examination was significant for crackles from the bases to the mid-lung fields bilaterally. Extremities showed no clubbing, cyanosis, and edema, and pedal pulses were symmetrically intact.
Investigations
Laboratory investigations at the time of presentation are illustrated in Table .
Electrocardiogram (EKG) on presentation showed normal sinus rhythm with a regular rate of 136 beats/minute and ST changes including ST elevation in anterior leads and ST depression in inferolateral leads (Figure ).
Infectious workup showed negative respiratory infectious disease panel, no growth for five days on blood cultures, and normal flora on respiratory culture. Computed tomographic (CT) angiography of the chest showed no pulmonary embolism but revealed bilateral pleural effusions and diffuse bilateral ground-glass opacities, raising suspicion for pneumonia. Transthoracic echocardiogram (TTE) showed severely reduced LV systolic function with an estimated ejection fraction of 17%. It also showed severe global hypokinesis with apical akinesis and matted thrombus at the apex. The patient subsequently underwent a left heart catheterization (LHC), which showed 20% occlusion of the left anterior descending (LAD) artery, and other vessels were free of any occlusive disease (Figures , ).
Differential diagnosis
The patient’s anginal symptoms were highly suspicious for acute coronary syndrome (ACS). This was supported by the EKG and cardiac biomarker findings. Diffuse ST-segment changes in the EKG suggested involvement of multiple coronary arteries. Since TTE findings were indicative of TCM, LHC was performed, which ruled out ACS. Other causes of chest pain, such as pulmonary embolism and aortic dissection, were ruled out with CT angiography of the chest. CT angiography initially showed concerns for pneumonia with lung infiltrates, but as culture data and laboratory findings resulted, her empiric antibiotics were discontinued. Acute pericarditis was ruled out based on the history of non-positional nature of the chest pain and no echocardiographic evidence of pericardial effusion. Multiple triggers were considered for TCM, but it was concluded that her condition is secondary to 5-FU because clinical manifestation of TCM started at the end of 5-FU chemotherapy and resolved completely with supportive care and discontinuation of medication.
Treatment
The patient received aspirin 325 mg, clopidogrel 75 mg, and high-dose statin at the time of admission. She was started on heparin infusion, scheduled intravenous furosemide for cardiogenic pulmonary edema, and nitroglycerin infusion due to persistent angina. Uridine triacetate 10 mg for 20 doses was started as an antidote per oncology recommendations because of concerns for 5-FU induced cardiotoxicity. After ACS was ruled out with LHC, heparin infusion was stopped and was transitioned to apixaban for LV thrombus.
At the time of admission, the patient also received azithromycin and ceftriaxone empirically for community-acquired pneumonia, but these were discontinued after respiratory and bacterial cultures came back negative, and procalcitonin was reported normal. She was discharged home on uridine triacetate 10 milligram (mg), aspirin 81 mg, apixaban 5 mg, lisinopril 2.5 mg, metoprolol 25 mg twice daily, and furosemide 40 mg twice daily.
Outcome and follow-up
She was closely followed as an outpatient in the heart failure clinic. Scheduled furosemide was switched to as needed after improvement in heart failure symptoms. Lisinopril was slowly titrated up to 10 mg per day. TTE was repeated after six weeks of hospital discharge, which showed resolution of heart failure with ejection fraction of 70% and complete resolution of LV thrombus. Aspirin and apixaban were continued for a total of three months. Metoprolol was progressively lowered in dosage and eventually discontinued.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [42, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'smoking': True, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 42 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4198,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4912657-1,Extracted,"A 55-year-old Southeast Asian male patient, chronic smoker with smoking index of 350, without any significant previous medical history, presented to us with a complaint of sudden onset swelling of face, neck, and anterior part of the chest since 18 days. The swelling was associated with shortness of breath and headache. However, the patient denied any history of cough, haemoptysis, chest pain, or wheeze. There was no history of fever, loss of weight or anorexia, although the patient mentioned about easy fatigability for the similar duration. He was a non-alcoholic and denied any use of illicit drugs. On clinical examination, the patient was found to be afebrile, tachypneic and non-pulsatile venous engorgement was seen over the neck and anterior chest wall with direction of blood flow from above downward. Dilated and tortuous veins were also noted over upper extremities and abdomen ().
Bilateral conjunctiva was suffused, but no icterus, clubbing, oedema or cyanosis was detected. There was palpable right supraclavicular small but firm lymph node along with bilateral significant axillary lymphadenopathy. The patient was hospitalized with a provisional diagnosis of SVC syndrome and was kept at head end elevated position with oxygen supplementation.
However, unlike to the majority of the cases of SVC syndrome, the chest X-ray (posteroanterior view) did not show any obvious mass lesion, mediastinal widening, or hilar enlargement, which resulted in a diagnostic dilemma regarding aetiology of the current case. Only emphysematous bullous lesion was noted in the right upper lung zone ().
Routine blood investigations, including complete blood count, plasma glucose, serum electrolytes, renal and liver function test were all within normal range except for mild anaemia (haemoglobin 12.3 gm/dl). HIV status was negative. A contrast enhanced computed tomography (CT) of the thorax and neck was done which showed the presence of a small, moderately enhancing nodular lesion (21×20 mm) with spiculated margin in the apical segment of right upper lobe along with surrounding emphysematous bullae ().
Multiple marginally enlarged lymph nodes were noted at pretracheal, right paratracheal, subcarinal region and at aortopulmonary window; but once again, the aetiology of SVC syndrome remained undiagnosed as no lymph node or mass was found to compress SVC. An additional small well-defined heterogeneously enhancing nodule (26×33 mm) was detected in right lobe of thyroid.
Subsequently, Doppler ultrasonography (USG) of neck was advised to find the cause of SVC syndrome, which revealed intraluminal thrombus in the right internal jugular, right subclavian and visualised extent of right brachiocephalic vein with no significant flow ()
Superior most part of the right internal jugular vein and right axillary veins were patent showing normal colour uptake. Right external jugular vein was found to be prominent with significant collateralization. Few discrete bilateral cervical lymph nodes with preserved morphology were also detected on USG of neck.
Next, a CT guided trucut biopsy was done from the right upper lobe pulmonary nodule and the histopathological examination confirmed presence of a non-small cell lung cancer (NSCLC) of adenocarcinoma type. Thyroid nodules were also evaluated which showed normal thyroid profile and only nodular hyperplasia in a background of nodular goitre on USG guided fine needle aspiration from the right thyroid lobe nodule.
On review of the history, patient stressed on the mode of onset of the symptoms which was acute in nature, but denied any previous history of venous thrombosis or any drug intake which increases blood coagulability. There was no history of prolonged immobilization or any cardiac procedure or central venous cannulation. Clinical examination did not reveal any feature of deep vein thrombosis (DVT) as well.
Later on, a battery of tests was done to exclude other causes of hypercoagulability of blood. Bleeding time, clotting time, prothrombin time, activated partial thromboplastin time (aPTT) and international normalized ratio (INR) were all normal. Antiphospholipid antibody IgG and IgM were found to be negative by ELISA method. Other coagulation studies, like factor V Leiden mutation, prothrombin gene mutation, protein C and protein S level did not detect any prior prothrombotic state. Transthoracic 2D echocardiography was normal except for grade I diastolic dysfunction. Other investigations like fibreoptic bronchoscopy and bronchoalveolar lavage were inconclusive. Sputum examination for acid-fast bacilli and malignant cell yielded negative results. Thereby, the patient was finally diagnosed to have SVC syndrome due to thrombosis as a paraneoplastic syndrome in bronchogenic carcinoma.
After consultation with cardiothoracic surgeon and oncologist, the patient was put on systemic corticosteroid, low molecular weight heparin (LMWH) and was subsequently taken up for concurrent chemoradiotherapy. Curative surgery for bronchogenic carcinoma was not considered as excision biopsy from right supraclavicular lymph node showed metastatic deposit (T1bN3M0, stage IIIb). Although only partial improvement was seen initially with the above-mentioned conservative management, stenting of SVC could not be considered due to financial constraint. Currently, he is being treated for bronchogenic carcinoma with chemoradiation under the department of oncology and is on long-term LMWH treatment.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'Hypertension history': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': True, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 55 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4199,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4557151-1,Extracted,"A 22-year-old nonalcoholic male with 6 days history of intermittent fever with chills presented with 2 days history of upper abdomen pain radiating to back, reduced by sitting. The pain was associated with vomiting. His pulse rate was 134/min regular and of feeble volume, and blood pressure (BP) was 80/60 mmHg. The respiratory rate was 24 breaths/min and temperature was 36.7°C by axilla. The abdomen was distended with the presence of shifting dullness. Upper abdomen was tender. Heart sounds were feeble. There was reduced air entry bilaterally. His consciousness was intact and had no neurological deficit. There was reduced urine output. The patient had no history of similar episodes of abdominal pain in the past. There was no significant medical or surgical history in the past.
The investigations revealed hemoglobin 12.7 g/dL, (12–16), total leukocyte count 14,190/mm3 (4000–11,000) with differential leukocyte count of neutrophils 73%, lymphocytes 20%, and eosinophils 1%, and platelet count 159,000/mm3. Blood urea was 190 mg/dL (14–40), serum creatinine 4.27 mg/dL (0.5–1.2), serum Na+ 142 mEq/L (135–145), K+ 4.5 mEq/L (3.5–5.0), serum Ca2+ 8.8 mg/dL (8.5–10.2), and blood glucose 110 mg/dL (70–110). Serum bilirubin was 2.94 mg/dL (0.3–1.3) with direct 1.02 mg/dL (0.1–0.4), serum glutamic pyruvic transaminase 54 U/L (8–40 U/L) and serum glutamic oxaloacetic transaminase 99 U/L (10–38), alkaline phosphatase 125 U/L (13–100), and serum albumin 3.7 g/dL (3.5–5.5). The serum amylase was 1882 U/L (10–200), S. lipase 210 U/L (10–140), and serum lactate dehydrogenase (LDH) 478 U/L. The coagulation profile showed bleeding time 1 min 30 s, clotting time 3 min, prothrombin time 13 s (control 13) INR 1, and activated partial thromboplastin time was 34.6 s (control 32.2). The lipid profile showed S. cholesterol 121 mg/dL, S. triglyceride 197 mg/dL, S. low-density lipoprotein 49 mg/dL, S. high-density lipoprotein 36 mg/dL. C-reactive protein level was 170 mg/dL (0–6).
The peripheral blood film showed ring form of trophozoite of P. vivax []. The antigen testing including parasite LDH tested positive for P. vivax and negative for P. falciparum. The chest X-ray PA view and two-dimensional echocardiogram were normal. Ultrasonography of abdomen showed bulky pancreas, moderate ascites, and edematous both kidneys. There was no gallstone. A non contrast computerised tomography scan of the abdomen revealed finding suggestive of acute pancreatitis [Figure and ]. Ascitic fluid examination was hemorrhagic and had protein 3.0 g/dL, sugar 110 g/dL, white blood cell 2200 mm3 with 83% neutrophils, 11% lymphocyte, 6% monocyte, and numerous red blood cell (RBC). The ascitic fluid amylase was 550 U/L. A diagnosis of P. vivax infection, acute pancreatitis, acute renal failure, and shock was made. The patient was put on intravenous chloroquine, inotropic support, and antibiotics. The BP normalized after 2 days of treatment. He tested negative for P. vivax after 3 days of treatment. After normalization of BP, he was put on hemodialysis. He improved over a period of next 4 weeks and was discharged. At the time of discharge, his blood urea was 56 mg/dL, S. creatinine 1.1 mg/dL, C-reactive protein was 4 mg/dL. Other investigations had normalized.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [22, 'years'], 'Hypertension history': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 22 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4200,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5871219-1,Extracted,"A 74-year-old woman was assessed in the outpatient cardiology clinic for an incidental finding of PAA on computed tomography (CT) of the chest. Past medical history was only significant for minimal past smoking and mild chronic obstructive pulmonary disease (COPD) with FEV1 of 87% predicted. Four months before her presentation, she had received antibiotics for a presumed respiratory tract infection with productive cough and an episode of scant hemoptysis. A chest X-ray done as part of an infectious work-up incidentally showed abnormal contour of the pulmonary artery. This was further characterized on a chest CT where an aneurysmal dilatation of the main pulmonary artery up to 5.7 cm was identified ().
Clinically, she was asymptomatic with no chest pain or dyspnea. She had intermittent productive cough but no history of hemoptysis except the streaks of blood-tinged sputum during her recent respiratory infection. She had no systemic symptoms including fever, weight loss, or any clinical features of vasculitis. Her physical exam was unremarkable. Blood pressure was within normal range with no differential in extremities. There were no vascular bruits or pulse differential.
Laboratory investigations showed normal inflammatory markers with C-reactive protein 1.3 mg/L (normal <3 mg/L) and erythrocyte sedimentation rate of 14 mm/h (normal <20 mm/h). Complete blood cell count, renal function, and liver enzymes were normal. Autoimmune investigations were also unremarkable with negative antinuclear, extractable nuclear antigen, and anti-neutrophil cytoplasmic antibodies. The remainder of her rheumatologic work-up including rheumatoid factor, anti-cyclic citrullinated peptide, and immunoglobulin G (IgG) subclasses were negative. Infectious work-up did not reveal any Hepatitis B and C, syphilis, or HIV.
Transthoracic echocardiography demonstrated enlargement of the PA at 32 mm () with normal cardiac chambers sizes and preserved biventricular function. The maximum diameter of the aneurysm was not within the field of the echocardiogram. The pulmonary valve was structurally normal with no significant stenosis or regurgitation. The right ventricular systolic pressure was normal. Right and left heart catheterization provided direct confirmation of an aneurysm in the proximal main PA (). There was no evidence of left-to-right shunting and no obstructive coronary disease. The pulmonary arterial pressures and hemodynamics were within the normal ranges. A repeat non-contrast CT of the chest showed an increase in dilatation of the PAA to 6.4 cm (from 5.7 cm) in a six-month interval.
The large size of the PAA and its rapid progression prompted a surgical assessment with resection of the PAA. Intraoperatively, the PAA was found to involve the main PA and its bifurcation. After the PAA resection, the PA bifurcation was reconstructed with an 18-mm Dacron and the main pulmonary trunk was replaced with homograft PA. The histopathology from the resected PAA showed extensive granulomatous vasculitis with numerous multinucleated giant cells and prominent lymphocytic infiltration (). Microbiology staining including special stains for fungus, acid-fast bacilli, and spirochetes as well as immunohistochemistry for IgG4 were negative. There was no evidence of fibrinoid deposition arguing against ANCA-associated vasculitis. A temporal artery biopsy and CT angiography of the abdomen and pelvis were completed to assess for involvement of other arteries. Both studies were normal.
In view of the histopathological findings from the main PA resection, a final diagnosis of isolated large-vessel vasculitis was made. We believe that her clinical picture presents a rare case of isolated PA vasculitis leading to aneurysmal dilation of the main pulmonary trunk. Extensive cardiac, rheumatologic, and infectious work-up failed to show any systemic features of vasculitis or other disorders that may trigger secondary vasculitis. Given the absence of symptoms, normal inflammatory markers, and isolated vessel involvement treated with surgical resection, conservative management with serial monitoring was pursued. Follow-up chest CT showed intact surgical anastomosis with main PA diameter of 32 mm. The patient continues to do well one year after her PAA resection and is followed annually with repeat imaging and echocardiogram.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [74, 'years'], 'Hypertension history': False, 'smoking': True, 'Diabetes mellitus': False, 'Electrocardiogram Test': 'Normal', 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 74 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 0 + 2 = 2.
The following risk factor(s) are present based on the patient's note: smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4201,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5903413-1,Extracted,"A 61-year-old male with a history of hypertension, hyperlipidemia, active smoking and coronary artery bypass grafting (CABG) 10 years prior was admitted to the hospital with substernal chest pain. In the past, his left heart catheterization had revealed multi-vessel coronary artery disease for which revascularization was accomplished via a left internal mammary graft to the LAD artery (LIMA to LAD), saphenous vein graft to the obtuse marginal (SVG to OM), and saphenous vein graft to the right coronary artery (SVG to RCA). He had not experienced angina since the CABG until now. Upon presentation for the current admission, his vital signs were significant for an elevated blood pressure to 203/91, but no signs of cardiac decompensation. Laboratory findings were significant for a troponin I that peaked at 29.6 (NG/ML). His electrocardiogram demonstrated sinus rhythm with left ventricular hypertrophy and a marked repolarization abnormality (Fig. ). Based on these findings, he was treated as a non-ST segment elevation myocardial infarction with Aspirin (325 mg), Lisinopril (10 mg), Carvedilol (6.25 mg twice a day), Simvastatin (80 mg), Clopidogrel (600 mg) and intravenous unfractionated Heparin. He was then taken to the catheterization lab the next morning. Coronary angiography revealed an ostial 70% stenosis in the LIMA and a chronic total occlusion of the LAD after the anastomosis which reconstituted via septal collaterals (Fig. ). The rest of his native coronary arteries and grafts were reported as the following: the left main was occluded, the RCA was small caliber with diffuse significant luminal narrowing, the SVG to Ramus and OM was patent, there was retrograde filling of distal LCx and the SVG to RCA was occluded. There was no deep engagement of the catheter during the index coronary angiography. Intravascular ultrasound (IVUS) exam of the ostium of LIMA revealed a bulky plaque in the ostium with minimal diameter of 1mm. A DES was then deployed in the ostium of LIMA (Fig. ) and post-dilated successfully (Fig. ). Final angiogram showed no edge dissection, distal embolization or perforation. The rest of his hospital course was uneventful and he was discharged without any complications. Upon follow up 4 months after discharge, the patient was reported to be free of angina and doing well from the cardiac standpoint.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [61, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': True, 'smoking': True, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",7,7,7,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 61 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, smoking, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 3 + 2 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 5 + 2 = 7.
Based on the patient's data, the HEART Score is 7."
4202,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8629686-1,Extracted,"A 76-year-old female presented for an elective cholecystectomy after being evaluated for cholelithiasis with pericholecystic fluid that was identified in ultrasound. She was diagnosed with chronic cholecystitis. The patient complained of some food intolerances and minimal tenderness of the RUQ abdomen. The patient has a history of hypertension, type 2 diabetes, osteopenia, obesity, diverticulosis, hyperparathyroidism, osteoarthritis (OA) of knees, and hyperlipidemia. The patient's family history consists of hypertension (HTN), diabetes mellitus (DM), cerebral vascular accident (CVA), in the patient’s mother. Surgical history is comprised of parathyroidectomy, pericardial window, colonoscopy with polypectomy, and left total knee arthroplasty.
A laparoscopic cholecystectomy was initially the plan of choice. During dissection of the gallbladder, significant scarring was noted and a structure entering the gallbladder anterior to the cystic duct was observed, which was carefully dissected and a ductotomy was performed. Intraoperative cholangiogram through the duct showed proximal CBD filling defect with extravasation of dye. Due to a possible CBD ductotomy, the procedure was converted to open. The ductotomy was within the CBD which was further explored and flushed and did not show any evidence of stones within the duct but did show amounts of biliary sludge and sediment. A t-tube was inserted into the ductotomy and intraoperative t-tube cholangiogram revealed the ductotomy within the CBD and dye extravasating into the gallbladder itself (Figure ). After the cystic duct was visualized and clipped, the gallbladder was dissected from the liver bed and opened to further visualize the CBD communication with the gallbladder. The t-tube was seen passing through the infundibulum of the gallbladder with clear visualization of a long fistula tract between the CBD and gallbladder itself. The remainder of the gallbladder was closed over a Blake drain and a Jackson-Pratt (JP) drain was inserted in the infrahepatic space.
Postoperative management consisted of strict ins and outs of drains and assessing the patient’s clinical examinations and labs. The patient was discharged postoperative delirium (POD) 7 when she was tolerating a regular diet, with decreased bilious output, and liver function tests were normalized. At one-month outpatient follow-up, the patient had 200-300cc per day drainage from the t-tube and about 50cc drainage each from the other two drains. At this time, the patient had a CT abdomen taken and showed no evidence of biloma or biliary dilatation. Both the JP and Blake drains were removed at this time. At the two-month postoperative, the t-tube had less than 5 cc output in the t-tube study performed at this time showed contrast into the duodenum (Figure ). The t-tube was then clamped and removed three months postoperatively. The patient’s drain and incision sites were well healed and closed at the three-month postoperative visit.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [76, 'years'], 'Hypertension history': True, 'Diabetes mellitus': True, 'obesity': True, 'hypercholesterolemia': True, 'parent or sibling with Cardiovascular disease before age 65': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'smoking': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit'}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 76 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 0 + 2 = 2.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, obesity. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 2 + 2 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 4.
Based on the patient's data, the HEART Score is 4."
4203,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5489329-1,Extracted,"Female patient, 52 years old, presenting atypical chest pain, witha 26.5 body mass
index, diabetic, hypertensive, dyslipidemic, usingASA, ARBS, Insulin, Metformin. She
was forwarded to the nuclear medicine sector with a Myocardial Scintigraphy request
for ischemia survey.
The patient was invited to participate in the research project, approved by the
ethics committee no. 392,966, which aims to compare the perfusion findings of the
nuclear medicine exam to those from the angiotomography of the coronary arteriesat
rest and under stress. The patient performed a specific myocardial scintigraphy
procedure () on a 1-collimator Gamma
Camera device (Millennium MPR, GE) and acomputed tomography scan of 64 detectors
(Brilliance, Philips), to evaluate the calcium score, myocardial perfusion at rest
and under stress associated with coronary anatomical evaluation. The stress
acquisition was conducted following dipyridamole infusion at a dose of 0.56 mg/kg,
in 4 minutes. On the sixth minute, 25 mCi of 2-methoxyl-isobuthyl-isonitrile-99 m Tc
(sestamibi-99mTc) was administered. In the same minute, the perfusion images under
pharmacological stress by angiotomography () were acquired, with infusion of iodinated contrast at a 70 ml dose
under a 5 ml per second flow rate. The myocardial perfusion scintigraphy images,
stress stage, were acquired 30 to 90 minutes after the administration of the
radiopharmaceutical.
The stress scintigraphic images demonstrated reversible perfusion defectswithin the
territory of the anterior descending artery. Theperfusion computerized tomography
confirmed the presence of perfusion defects and did not evidence a presence of
atherosclerotic lesion in coronary arteries. A significant myocardial bridge
constricting the anterior descending artery was diagnosed by the angiotomography of
coronary arteries (), configuring the
most probable mechanism for the observed perfusion defects.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [52, 'years'], 'Hypertension history': True, 'Diabetes mellitus': True, 'hypercholesterolemia': True, 'obesity': True, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 52 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, obesity. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 1 + 2 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4204,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4443876-1,Extracted,"A 64-year-old man, a 30-year-long cigarette smoker (30 pieces per day), was admitted with syncope twice on one day to our hospital emergency department in Oct 17, 2013. The patient has two years of high blood pressure history while without any medicine treatment. He had no diabetes mellitus history. In the past two months, he felt chest discomfort sometimes. In the morning of Oct 14, 2013, he suddenly lost consciousness with incontinence while walking in the park. He felt pericardium discomfort before losing consciousness. After regaining consciousness several minutes later, he felt dyspnoeic and sweaty. In the afternoon, syncope occurred again while he was watching TV. His electrocardiogram showed a slight sinus bradycardia of 47 bpm. 24-hour Holter indicated the average heart rate was 66 bpm, the slowest heart rate 47 bpm, the fastest heart rate 129 bpm, and the longest R-R interval 1.6 second. Cranial CT produced no unusual findings (). Moderate ST-segment depression was determined in lead II and aVF on treadmill exercise ECG. Ultrasound cardiography (UCG) indicated normal function with the left ventricular ejection fraction 69.4%. No unusual finding was found in chest X-ray. Blood myocardial enzyme, renal function, electrolytes, and D-dimer values were all within normal ranges.
Five days later, the patient had coronary angiography examination. Coronary angiography revealed 80% stenosis of proximal segment and 85% stenosis of distal segment in left anterior descending (LAD) coronary artery, 90% stenosis of middle and distal segment in left circumflex (LCX) coronary artery, 50% stenosis of proximal segment, and 80% stenosis of middle segment in right coronary artery (RCA). The patient refused to have coronary artery bypass grafting surgery. So we decided to perform percutaneous coronary intervention (PCI). After balloon predilatation, 3.0 × 24 mm EXCEL rapamycin-eluting stent (Jiwei, Shandong, China) was implanted in RCA. A 2.5 × 14 mm EXCEL rapamycin-eluting stent and a 3.0 × 21 mm Partner sirolimus-eluting stent (Raisedragon, Peking, China) were implanted in distal and proximal segment of LAD, respectively. The further PCI was scheduled one week later for LCX. Unexpectedly, syncope occurred again. On the afternoon while sitting 2 days later, symptoms of dyspnea and palpation accompanied with hypotension occurred. Electrocardiogram monitor indicated that the heart rate was serious sinus bradycardia of nearly 30 bmp. Blood pressure was below 80/40 mmHg. The symptom disappeared after atropine and dopamine were infused. Consider the patient is a 64-year-old person with 30-year-long cigarettes intake history. We put a serum marker screen. Unexpectedly serum tumor marker results indicated that carbohydrate antigen 19-9, carbohydrate antigen 72-4, and alpha fetoprotein are all within normal ranges whereas cytokeratin-19-fragment (CYFRA21-1) and neuron-specific enolase (NSE) values elevated slightly (CYFRA21-1 3.75 ng/mL, normal <3.3 ng/mL; NSE 16.62 ng/mL, normal <16.3 ng/mL).
Examination of enhanced chest CT led to suspicion of central lung cancer (). PET-CT confirmed the leaf of central type lung cancer (4.2 × 3.7 × 2.6 cm) of left lung with multiple lymph node metastasis and the tumor infiltration of adjacent thoracic aorta and left pulmonary artery and vein. No brain metastasis or heart metastasis was found on PET-CT examination. Immunohistochemical examination of the specimens collected with bronchoscopy revealed the following: CKpan(+), CKL(+), Syn(+), CgA(+), CD50(+), CD30(−), CK20(−), CK7(−), CK5/6(−), P63(−), and Ki-67(+).
The diagnosis of small cell bronchogenic carcinoma was made; this tumor was clinically staged at T4N2M0 IIIB. Chemotherapy was promptly initiated with use of combination of carboplatin and topotecan. Shortly after the first chemotherapeutic infusion, the patient reported feeling much better. At follow-up a year later, enhanced CT scan showed that the tumour volume decreased and the patient did not experience syncope anymore.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [64, 'years'], 'Suspicion History': 'Moderately suspicious', 'Hypertension history': True, 'smoking': True, 'Diabetes mellitus': False, 'atherosclerotic disease': True, 'Initial troponin': 'less than or equal to normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 64 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 1 + 1 = 2.
The following risk factor(s) are present based on the patient's note: hypertension, smoking, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 2 + 2 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 4.
Based on the patient's data, the HEART Score is 4."
4205,18,HEART Score for Major Cardiac Events,risk,integer,pmc-3391847-1,Extracted,"A 49-year-old male, parachute instructor by profession, presented to the ED with complaint of non-radiating substernal chest pain following chute deployment. During the episode, he noted associated headache, diaphoresis, and palpitations, which subsequently spontaneously resolved after landing. The parachute jump was described as standard: there was no unusually traumatic parachute opening or landing. The patient denied significant environmental conditions, such as a high altitude jump or extreme cold exposure. There was no change in intensity, location, or character of his pain during the remainder of his parachute ride to landing. There was no change in pain with position, movement, or deep inspiration. He subsequently had two hours of continuous chest pain prior to arrival.
His pain was described as dull, non-radiating, and rated 7/10 improving to a 5-6/10. No prior history of similar chest pain, associated shortness of breath, nausea, change in sensation, or weakness was reported. He was a non-smoker and denied personal cardiac or pulmonary disease history. The patient did admit to a history of gastroesophageal reflux and was intermittently compliant with his prescribed ranitidine. His family history was unremarkable for coronary disease, sudden, or early death.
The patient arrived to the medical center via his private vehicle. Upon presentation, the glasgow coma scale (GCS) was 15 with pulse of 80, blood pressure (BP) of 132/87, respirations of 16, temperature of 100.5 degrees Fahrenheit, and room air saturation of 96%. His physical exam was unremarkable on presentation. The ED management included sublingual nitroglycerine, which resolved his chest pain after one dose, followed by nitroglycerine paste and aspirin. Initial troponin was 0.01. Remainder of laboratory evaluation was unremarkable. Dynamic electrocardiogram (ECG) changes were noted and Cardiology consultation was made. [] Differential diagnosis included a traumatic aortic dissection, so a cardiac gated computed tomography (CT) was obtained that did not demonstrate this etiology as a source for his chest pain. However, an incidental retroperitoneal mass below the level of the left kidney was discovered, which appeared to be highly vascular, with central necrosis, and had at least one feeding artery coming directly off of the aorta []. A rising second troponin was noted in the ED at 0.08. He was started on low weight molecular heparin with clopidogril and admitted for further observation to the cardiac intensive care unit with a planned diagnostic cardiac catheterization. The catheterization showed no angiographic evidence of coronary artery disease (CAD) and normal left ventricular function. Over the course of the hospitalization the patient's BP was intermittently hypertensive without report of associated chest pain. A neuroendocrine work-up for the para-aortic mass demonstrated a normal catecholamine metabolites, normetanephrine (329 mcg/24 hours [reference range: 88-649 mcg/24 hours]) and metenephrine (164 mcg/24 hours [reference range: 58-203 mcg/24 hours]) on 24-hour urine. His troponin peaked at 0.31.
The patient was discharged home with atenolol and atorvastatin after a four-day hospitalization. He underwent laparoscopic retroperitoneal mass excision one month after presentation. Intravenous fluids, phentolamine, and metoprolol were utilized for presurgical treatment in this patient. Induction of anesthesia was done with fentanyl, lidocaine, propofol, and rocuronium. The anesthesia maintenance agent was isoflurane. No adverse complications such as hypertensive episodes or bleeding were reported. He returned to his profession as a full-time parachute instructor three months later and subsequently discontinued antihypertensive medications.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [49, 'years'], 'Hypertension history': True, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 49 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4206,18,HEART Score for Major Cardiac Events,risk,integer,usmle-9895,Extracted,"A 52-year-old man presents to the emergency department with sudden-onset dyspnea, tachycardia, tachypnea, and chest pain. He works as a long-haul truck driver, and he informs you that he recently returned to the west coast from a trip to Tennessee. His medical history is significant for gout, hypertension, hypercholesterolemia, diabetes mellitus type 2, and mild intellectual disability. He currently smokes 2 packs of cigarettes/day, drinks a 6-pack of beer/day, and he endorses a past history of injection drug use but currently denies any illicit drug use. The vital signs include: temperature 36.7°C (98.0°F), blood pressure 126/74 mm Hg, heart rate 87/min, and respiratory rate 23/min. His physical examination shows minimal bibasilar rales, but otherwise clear lungs on auscultation, grade 2/6 holosystolic murmur, and a benign abdominal physical examination. A computed tomography angiography (CTA) demonstrates a segmental pulmonary embolism (PE).",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [52, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': True, 'Diabetes mellitus': True, 'smoking': True, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit'}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 52 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 3 + 2 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 5.
Based on the patient's data, the HEART Score is 5."
4207,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6458957-1,Extracted,"A 67-year-old man, who was suffering from long-lasting (>2 hours) severe chest pain, was admitted in our hospital. He was an ex-smoker (between the ages of 20 and 25 years) and had been treated for hypertension and hyperlipidemia. He was diagnosed with ITP 6 months before admission and maintained his platelet count between 10.0 × 109/L and 15.0 × 109/L by receiving prednisolone (10 mg daily) and eltrombopag (50 mg daily). He was immediately relieved of chest pain after admission, and there was no significant finding on a 12-lead electrocardiogram except a left axis deviation (). However, a cardiac catheterization was performed urgently due to the significant increase of serum myocardial enzymes (troponin-I 1.56 ng/mL, creatine kinase (CK) 233 IU/L, and CK-muscle/brain 20 IU/L). Although coronary angiography (CAG) revealed no artery occlusion (), left ventriculography showed mild hypokinesis in the posterior wall, and cardiac magnetic resonance imaging exhibited a delayed gadolinium enhancement in the posterior wall area (), suggesting myocardial infarction in the territory of the left circumflex coronary artery (LCX).
Because the patient persistently complained of chest pain even after discharge, the second CAG was performed 3 months after the discharge. CAG revealed de novo stenosis in the obtuse marginal branches (#12: 75% with haziness, ), and adenosine stress myocardial perfusion scintigraphy (Tc-99m tetrofosmin) showed myocardial ischemia in the posterior wall area (), where the tracer uptake was reduced at stress and restored at rest. Thus, the first PCI was planned for #12, and a dual antiplatelet therapy (aspirin 100 mg daily and clopidogrel 75 mg daily) was started more than 1 month before the procedure, where his platelet was kept at 27.4 × 109/L by eltrombopag (50 mg daily). The first PCI toward #12 was successfully performed by implantation of a zotarolimus-eluting stent (3.0 × 12 mm) and CAG revealed no residual stenosis (). However, the patient complained of severe chest pain with significant ST depression after returning to his hospital room (3 hours after the PCI). The emergent CAG demonstrated a stent thrombosis at the proximal edge of the stent (). Although the intravascular ultrasound imaging exhibited neither the underexpansion of the prior-implanted stent nor the coronary artery dissection around the stent, it showed new lining thrombus (white arrows) at the proximal edge of the stent (). An additional drug-eluting stent (3.0 × 12 mm, everolimus-eluting stent) was implanted at the proximal edge of the prior stent lesion of #12 (, second PCI) under the support of an intra-aortic balloon pumping. To avoid further stent thrombosis, the antiplatelet agent was changed from clopidogrel (75 mg daily) to prasugrel (3.75 mg daily). However, CAG, performed 3 days after the second PCI, revealed a massive thrombus with 75% stenosis in #12 (). Urokinase (UK 240.000 U) was selectively injected into the LCX, instead of balloon inflation for the third PCI, because recurrent coronary thrombosis was occurring at the area of the dual stent implantation. CAG after the UK injection revealed the residual stenosis (50%) in #12. The follow-up CAG, which was performed 14 days after the third PCI, again revealed the recurrence of stent thrombosis with 75% stenosis in #12 (). Subsequently, a coronary thrombus aspiration was performed as the fourth PCI. The final CAG after coronary thrombus aspiration exhibited 50% residual stenosis. Since his platelet maintained at >39.3 × 109/L by eltrombopag during all PCIs, the association between a recurrence of coronary thrombosis and inappropriate platelet increase induced by eltrombopag was suspected. Thus, we transiently ceased eltrombopag, and his platelet promptly decreased to 8.0 × 109/L after 7 days of cessations. CAG, after the cessation of eltrombopag, showed 50% of residual stenosis with thrombus; hence, we did not perform further PCI to #12 (). In addition, after he received a splenectomy to cease eltrombopag, he has not complained of any chest pain, and CAG after splenectomy revealed no thrombus in #12.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [67, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': True, 'smoking': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",7,7,7,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 67 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 2 + 2 = 4.
The following risk factor(s) are present based on the patient's note: hypertension, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 4 + 1 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 5 + 2 = 7.
Based on the patient's data, the HEART Score is 7."
4208,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8494381-1,Extracted,"A 77-year-old man with a history of long-standing rheumatoid arthritis with possible lung involvement, chronic obstructive pulmonary disease, asbestos-related pleuropulmonary disease, traumatic hydropneumothorax, controlled type-1 diabetes mellitus, and coronary artery bypass grafting (25 years ago), presented with two days of purulent drainage from his distal sternum. He reported having had a persistent dry cough and left-sided chest pain for over a year. Multiple computed tomograms (CTs) of the chest had shown stable left-sided pulmonary nodules with fibrotic changes and a post-traumatic hydropneumothorax. His pulmonary signs/symptoms and imaging findings had been attributed to rheumatoid lung disease and remote trauma. The patient had received rituximab for the past eight months but had previously also been treated with etanercept, methotrexate, leflunomide, and intermittent courses of corticosteroids. He denied fever, weight loss, or joint pain. The patient lived in Minnesota during the summer and Arizona during the winter. He denied any other travel, exposure to mold or dust, or pet ownership.
On presentation, vital signs were normal. The only notable physical findings were a fluctuant swelling over the distal sternum, with a small sinus tract that drained copious amounts of cloudy brown fluid, and faint pre-sternal erythema. His white blood cell count was 7,300 cells/µL, alkaline phosphatase level 296 IU/L, C-reactive protein level 98 mg/L, and erythrocyte sedimentation rate >130 mm/h. A chest CT showed new bony destruction of the left sixth rib, with an adjacent parasternal fluid collection, but otherwise stable left-sided pleuropulmonary changes (Figure ).
The patient received vancomycin and piperacillin/tazobactam, and the following day underwent surgical debridement. Histopathological examination of the rib cartilage showed septate fungal hyphae with acute-angle branching consistent with Aspergillus spp. (Figure ), and culture of the tissue yielded A. fumigatus (Figure ).
The antibiotics and immunosuppressive therapy for rheumatoid arthritis were stopped, and the patient received oral voriconazole and underwent aggressive debridement of bone and soft tissues. After four months of voriconazole therapy, the sternal wound was healing, and repeat chest CT showed stable pulmonary and bone changes. Unfortunately, shortly thereafter, the patient died of unknown causes.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [77, 'years'], 'Hypertension history': True, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': True, 'atherosclerotic disease': True, 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 77 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 0 + 2 = 2.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 2 + 2 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 4.
Based on the patient's data, the HEART Score is 4."
4209,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7954261-1,Extracted,"A 37-year-old Caucasian male presented to the Emergency Department with chest pain. He described awaking with central chest tightness radiating to both arms lasting 20 min. The chest pain was associated with diaphoresis and resolved spontaneously. He smoked 10–15 cigarettes a day and had previously used anabolic steroids some 10–12 years ago, although denied any current drug use. His past medical history included a respiratory arrest following anaphylaxis to NSAIDs, asthma, and pulmonary sarcoidosis.
On examination, his body habitus was of muscular build; cardiac auscultation revealed no murmurs and there were no signs of heart failure. Serial ECGs during his hospital admission showed normal sinus rhythm with no dynamic or ischaemic changes (). Full blood count and renal function were normal. High-sensitivity troponin-I was positive at 63 ng/L (99th percentile upper reference limit, <15 ng/L) with a repeat value of 45 ng/L approximately three and a half hours later. Serum cholesterol levels were elevated with a total cholesterol of 5.4 mmol/L, LDL 3.1 mmol/L, and triglycerides 2.9 mmol/L. He was treated as an ACS with dual anti-platelets, statin, and B-blocker therapy.
Echocardiogram showed normal biventricular function with no obvious regional wall motion abnormalities (Videos 1–3). Coronary angiography was performed approximately 24 h following admission to the hospital, during which time the patient remained free of chest pain. Severe stenoses were observed at the ostium of a diagonal branch of the left anterior descending artery (LAD), proximal diagonal vessel, proximal intermediate artery, non-dominant circumflex (LCx), distal right coronary artery, and posterior descending artery (). There was also a moderate lesion in the mid-LAD at the bifurcation with the diagonal vessel (, Videos S1 and S2). No ischaemic ECG changes were seen during coronary angiography.
Angiographic appearances were atypical of coronary plaque and computed tomography coronary angiography (CTCA) was performed to exclude a differential diagnosis of spontaneous coronary artery dissection (SCAD). This demonstrated normal coronary arteries () and repeat invasive coronary angiography confirmed resolution of the severe coronary vasospasm seen previously (, Videos S3 and S4). Cold pressor testing during coronary angiography was unsuccessful in reproducing vasospasm.
A drug screen was not performed at this stage as the patient had denied the recent use of illicit drugs and more than 48 h had passed from the time of presentation to the CT findings. Anti-platelet and statin treatment were discontinued; he was commenced on Amlodipine 5 mg daily and received smoking cessation advice prior to discharge from the hospital. At cardiology clinic follow-up, 7 months later, he has experienced no further episodes of cardiac chest pain.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [37, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Highly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': True, 'Diabetes mellitus': False, 'obesity': False, 'smoking': True, 'atherosclerotic disease': False, 'Initial troponin': 'greater than three times normal limit', 'parent or sibling with Cardiovascular disease before age 65': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 37 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 3 + 2 = 5.
Based on the patient's data, the HEART Score is 5."
4210,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6682247-1,Extracted,"A 23-year-old African-American female presented to our ED with one day of sharp, midline chest pain that radiated to her jaw and left arm. She reported mild associated shortness of breath but no exertional symptoms. The review of systems was otherwise unremarkable. Her past medical history was significant for adrenal insufficiency on daily hydrocortisone, hypothyroidism, and two prior episodes of pericardial effusion with previous drainage procedures. Vital signs included a blood pressure of 129/96 mmHg, heart rate 99 beats per minute, and oxygen saturation 100% on room air. The patient was afebrile. Initial laboratory workup was unremarkable with a negative troponin. Due to the patient’s history of pericardial effusions, a formal transthoracic echocardiogram was performed, which demonstrated normal systolic function with an ejection fraction of 50–55% and no evidence of a pericardial effusion (). The patient was then discharged home.
The following day, the patient presented to our ED with similar symptoms, including chest pain and shortness of breath. Upon evaluation, her vital signs demonstrated severe hypotension with a blood pressure of 71/52 mmHg, heart rate 121 beats per minute, respiratory rate 16 breaths per minute, oxygen saturation 100% on room air, and temperature 36.8°C. Her exam was now significant for depressed mental status and lethargy. A point-of-care cardiac ultrasound was performed, which demonstrated a large amount of pericardial fluid and right ventricular collapse. Immediate transthoracic echocardiogram confirmed these findings ( and ).
Interventional cardiology and cardiovascular surgery were consulted, and a decision was made to take the patient to the operating room emergent pericardiectomy. In the operating room, approximately 300 mL of turbid, yellow fluid was evacuated from the underlying pericardium. A 24 French Blake drain was placed in the pericardium and the patient was admitted to the intensive care unit.
With the patient’s previous pericardial effusion, past laboratory workup demonstrated high titers for coxsackie B virus. Upon this admission, a viral panel was negative, including hepatitis B panel, influenza, respiratory syncytial virus, corona virus, metapneumovirus, parainfluenza virus types 1,3, and 4, Epstein-Barr virus, cytomegalovirus, human immunodeficiency virus, coxsackie, influenza A, myocoplasma pneumonia, Chlamydia pneumoniae, buccal virus, and rhinovirus. Rheumatologic workup was also negative, including antinuclear antibody, anti-double stranded deoxyribonucleic acid, antimicrosomal antibody, anticentromere antibody, Sjogren’s syndrome A and B, Smith antibody, celiac screen, anti-Jo 1 antibody, and anti-SCL–70 antibody (anti-topoisomerase I). Further testing for anti-21 alpha hydroxylase and anti-TPO antibodies were also negative.
Pericardial fluid analysis demonstrated predominantly acute inflammatory cells without any evidence of malignancy. Pericardial biopsy results were unrevealing. Repeat echocardiogram demonstrated normal left ventricular ejection fraction of 50–55% and no significant pericardial effusion. The patient was discharged 10 days following initial presentation and has not had any subsequent episodes of cardiac tamponade or pericardial effusions diagnosed at our institution.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [23, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'hypercholesterolemia': False, 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 23 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4211,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4554224-1,Extracted,"A 44-year-old man was referred to the cardiology department because of an incomplete right bundle branch block (IRBBB) detected in the electrocardiogram (EKG). No epsilon or negative T waves were found on the EKG (). He had no history of familiar sudden cardiac death and he did not have any previous disease despite he was a carrier of C-hepatitis virus. No medication was needed for the treatment of that virus because transaminase enzymes in blood analysis were in normal range and abdominal echography showed normal liver morphology. He was only taking sertraline and bromazepam because of depressive syndrome. He remained completely asymptomatic, in NYHA functional class I/IV, and his physical examination did not show any abnormal finding. In order to begin the study of the IRBBB we first performed an echocardiogram in which a severe right ventricle (RV) dilatation () and a moderate tricuspid regurgitation (TR) appeared. Left ventricle ejection fraction (LVEF) was preserved (55%) and mitral and aortic valves were normal, in function and morphology. The estimated systolic pulmonary pressure was normal and there was not any indirect sign of pulmonary hypertension. To better characterize the findings in the RV, a magnetic resonance (MR) was performed. It showed a diastolic diameter of the RV of 55 mm () and confirmed the functional cause of the TR (ring dilatation). There were not any dyskinesia or akinesia areas (Supplementary Videos 1 and 2, www.jocmr.org) or pathologic gadolinium enhancement, and RV ejection fraction was 57%. Abnormal venous drainage was also excluded with the MR. The transesophageal echocardiography did not find any interatrial () or interventricular septal defects. Holter monitoring did not find any arrhythmic event. Hemodynamic study showed normal pulmonary pressures (systolic pulmonary artery pressure/mean pulmonary artery pressure/diastolic pulmonary artery pressure of 24/14/7 mm Hg respectively) and normal pulmonary wedge pressure (12 mm Hg) which led us to exclude pulmonary hypertension as the cause of the RV dilatation. Cardiac ischemic disease was excluded by performing a coronary angiography. No atherosclerosis plaques in the coronary arteries were found. Pulmonary functions tests (forced expiratory volume in 1 s (FEV1): 117%; FEV1/forced vital capacity (FVC): 84%), diffusion capacity (DLCO: 115%), artery gasometry and polysomnographic study were also normal. We lastly performed a pulmonary angiography, in which a chronic thromboembolic pulmonary disease was also excluded. We decided not to start any medication due to the lack of symptoms of the patient and we also decided to keep a watchful waiting attitude. The patient was catalogued as an isolated form of right ventricular dilated cardiomyopathy due to the finding of an RV dilatation, without any potential cause for it. After 2 years of follow-up, the patient remains asymptomatic and the RV persists dilated.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [44, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 44 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4212,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7548916-1,Extracted,"A 73-year-old woman with a history of hypothyroidism and hypertension visited another hospital because of a several-day history of nausea and vomiting and abdominal distension for several months. She had no family history of malignancy or neurological disease.
Arterial blood gas analysis showed lactic acidosis with increased anion gap (pH 7.248, base excess −10.6 mEq/L, lactate level 7.30 mmol/L). Her blood glucose level was 78 mg/dL. Abdominal CT imaging revealed peritoneal thickening and a small amount of ascites (Fig. ).
She was referred to us for suspected peritoneal cancer or peritoneal dissemination of cancer of unknown primary site. On admission, she was afebrile, with a heart rate of 100 beats/min, blood pressure of 173/90 mm Hg, respiratory rate of 20 breaths/min, and oxygen saturation at 98% on room air.
On physical examination, cardiac and pulmonary auscultation revealed normal findings. There was mild tenderness on abdominal examination, but no splenomegaly. The superficial lymph nodes were not palpable. After admission, esophagogastroduodenoscopy revealed a submucosal tumor-like mass with ulceration localized in the anterior wall of the gastric antrum and the greater curvature, and a few small flat elevated lesions with an apical depression in the gastric body. Biopsy was performed at the periphery of the ulcer and small flat elevated lesions. Histologically, the H&E sections of the biopsy specimens showed atypical large lymphocytic infiltrates with an irregular nucleus. Immunohistochemical studies showed that the atypical large cells were positive for CD20, CD79a, and BCL-6 and negative for CD3, CD10, and MUM1 (Fig. ); therefore, we diagnosed the patient as having DLBCL.
Exploratory laparoscopy revealed disseminated nodules in the inferior abdominal omentum, mesenteric fatty tissue, and intestinal serosa, as well as pale bloody ascites. A disseminated nodule from the omentum was excised and submitted for pathological examination. The pathological results showed the same findings as did gastric biopsy, and the patient was diagnosed as having gastric DLBCL with peritoneal dissemination.
Blood test results after admission showed hypoglycemia with a blood glucose level of 50–70 mg/dL; lactic acidosis with pH 7.166; lactic acid 12.7 mmol/L; and base excess −21.0 mEq/L. Despite continuous intravenous glucose and sodium bicarbonate administration, the hypoglycemia and lactic acidosis aggravated. The patient's consciousness was clear at the time of admission, but gradually deteriorated with respiratory failure.
At that time, we considered the Warburg effect as the cause of lactic acidosis and hypoglycemia associated with malignant lymphoma. We considered that the prompt introduction of treatment for gastric DLBCL was necessary because the Warburg effect has a poor prognosis [, ]. Thus, on day 16 since admission, CHOP chemotherapy (cyclophosphamide, doxorubicin hydrochloride, vincristine, prednisolone) without rituximab was initiated with a 50% dose reduction in light of the patient's poor condition. After the treatment start, the acidosis, hypoglycemia, and impaired consciousness improved promptly.
Lactic acidosis resolved on day 22 from admission (Fig. ). Thereafter, both the lactic acid and blood glucose levels remained within normal ranges.
On day 30, the patient developed weakness of the bilateral lower and upper extremities. She was diagnosed with Guillain-Barré syndrome and received intravenous immunoglobulin and steroid pulse treatment. The symptoms improved with the treatment and rehabilitation.
After the first course of chemotherapy, immunohistochemical examination revealed CD20 positivity; hence, a second course of R-CHOP (rituximab, cyclophosphamide, doxorubicin hydrochloride, vincristine, prednisolone) chemotherapy at 100% dose was initiated on day 39. On day 46, CT showed that the peritoneal thickening and ascites had almost disappeared. By day 107, the patient underwent five courses of chemotherapy. Although a total of eight courses were planned, subsequent chemotherapy was postponed as the patient developed pneumocystis pneumonia, cytomegalovirus infection, and candidemia after the fifth course. At day 226, the patient remains hospitalized and will resume chemotherapy after the infection is under control.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [73, 'years'], 'Hypertension history': True, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 73 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 0 + 2 = 2.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4213,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7454494-1,Extracted,"A 38-year-old mestizo Colombian woman without previous history of cardiovascular disease or any other medical history presented to the emergency room. The patient was not taking any medicine prior to her arrival. She had been having palpitations for 3 days that started suddenly, associated with general malaise, without dyspnoea, chest pain, or respiratory symptoms. The patient reported having recently arrived from Spain, 5 days before presenting herself to the hospital. Upon arrival, the patient’s cardiovascular examination revealed her to be tachycardic without audible heart murmurs or an elevated jugular venous pressure. The respiratory examination revealed soft inspiratory crackles bibasally. Her vital signs included a heart rate of 137 b.p.m., blood pressure of 98/54 mmHg (cardiogenic index >1.1 stage B cardiogenic shock), pulse oximetry of 95% SaO2, and body temperature of 36.5°C. The electrocardiogram showed a diffuse and concave elevation of the ST-segment, with PR segment depression and Spodick’s sign ().
The initial chest X-ray showed reticular interstitial opacities (), and computed tomography (CT) of the chest showed compromise of the lung parenchyma, and mixed opacities, mainly alveolar and ground-glass of peripheral and basal predominance, a classic pattern of pulmonary involvement in COVID-19 (). The biomarkers of myocardial injury were significantly elevated (). The transthoracic echocardiogram revealed a left ventricle with global hypokinesia, with severely reduced systolic function, an ejection fraction of 30%, without valvular heart disease, and mild pericardial effusion (2 mm). Nasopharyngeal and oropharyngeal swabs were taken in order to identify microorganisms causing the infection in the respiratory tract (14 viral and 4 bacterial); the swabs were negative, and nucleic acid amplification by PCR was positive for SARS-CoV-2.
Finally, it was concluded that the patient should be diagnosed with fulminant myocarditis with stage B cardiogenic shock and COVID-19 pneumonia. Treatment in the intensive care unit (ICU) consisted of oxygen therapy without mechanical ventilation, methylprednisolone (200 mg/day), and intravenous human immunoglobulin (IVIG; 20 g/day) for 4 days, hydroxychloroquine (800 mg on day 1, then 400 mg/day) and azithromycin (500 mg/day), both during 5 days without a QTc greater than 450 ms, and lopinavir/ritonavir (800/200 mg/day, 10 days). The initial support was performed with norepinephrine and subsequently inotropic support with dobutamine and levosimendan, in addition to intravenous furosemide, without the need for circulatory assistance devices. The patient showed a sustained clinical, haemodynamic, and respiratory improvement (). After 16 days of hospital stay (10 days in the ICU), the patient was discharged with heart failure management which included bisoprolol 5 mg/day, spironolactone 25 mg/day, and enalapril 10 mg b.i.d. Before discharge, cardiac magnetic resonance imaging (MRI) was performed (), which showed inflammatory manifestations, with the recovery of the ejection fraction. The performance of a myocardial biopsy after the clinical improvement was considered, but the patient did not consent to the procedure.
The medical control performed after 2 weeks showed that the patient had no new symptoms and transthoracic echocardiography was normal.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [38, 'years'], 'Hypertension history': False, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'greater than three times normal limit', 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 38 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 0 + 2 = 2.
Based on the patient's data, the HEART Score is 2."
4214,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7927542-1,Extracted,"A 28-year old man, with no known previous medical history, was admitted to the emergency department with a 6-day history of pleuritic chest pain and gradual-onset shortness of breath. The patient also noted going through upper respiratory tract infection symptoms (fever, malaise and rhinorrhea) a couple of days before the onset of above-mentioned symptoms which had got better gradually without seeking medical advice. Moreover, he reported new onset anosmia from one week before admission. The patient’s history of smoking was remarkable in his record.
Upon admission, his blood pressure was measured at 95/60 mmHg and he had tachycardia with heart rate of 125 beats per minute.
He was afebrile (temperature: 36.8 degree centigrade) and in respiratory distress with oxygen saturation of 85% in room air.
On physical examination heart sounds were determined to be muffled, no gallop or heart murmurs were detected and only tachycardia was noticed. The Jugular Venous Pressure (JVP) was also prominent (10 cm H2o) and lung auscultation revealed normal vesicular breath sounds.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [28, 'years'], 'Hypertension history': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': True, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 28 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4215,18,HEART Score for Major Cardiac Events,risk,integer,usmle-11554,Extracted,"A 31-year-old woman visits her primary care physician with the complaint that over the past 6 months she has “felt out of breath and dizzy while walking, even after short distances.” She reports no other medical problems and denies taking any medications, vitamins, supplements, recreational drugs, alcohol or tobacco. Her BMI is 24kg/m2. On physical examination, the patient has a loud second heart sound over the left upper sternal border, increased jugular venous pressure, and a palpable right ventricular impulse.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [31, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'Diabetes mellitus': False, 'obesity': False, 'smoking': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 31 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4216,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6693794-1,Extracted,"A 71-year-old man presented to ED with a chief complaint of left-sided numbness. Approximately five hours prior to arrival, the patient developed sudden onset of left-sided perioral, thumb, and thenar numbness. Past medical history was significant for coronary artery disease, type 2 diabetes, chronic kidney disease, hypertension, and clear cell renal cell carcinoma status post nephrectomy (10 years prior). The patient had taken two tablets of baby aspirin prior to arrival. He denied having any deficits prior to onset of symptoms, and denied any changes in vision, speech difficulties, weakness, ataxia, chest pain, palpitations, or shortness of breath. Vitals were notable for hypertension with systolic blood pressures ranging from 150s to 190s. Symptoms resolved spontaneously about 30 min after arrival to the ED and on examination the patient was found to have no residual neurological deficits. The patient denied secondary causes for perioral numbness including hypocalcemia, thyroid dysfunction, history of seizures, and/or migraines. Due to complaint of lateralized paresthesias and multiple risk factors for stroke, workup for a potential transient ischemic attack was begun.
Laboratory workup was significant for serum creatinine of 1.28 mg/dL and glucose of 213 mg/dL, otherwise basic metabolic panel (BMP) was normal. Thyroid stimulating hormone (TSH), complete blood count (CBC), and coagulation screen were unremarkable. Lipid panel was remarkable for cholesterol of 199 mg/dL, low density lipoprotein (LDL) of 98 mg/dL, triglyceride of 259 mg/dL, and high density lipoprotein (HDL) of 49 mg/dL. Glycated hemoglobin was 7.0%. Initial imaging was done with noncontrast CT of the head which showed age-appropriate involutional changes without acute intracranial hemorrhage (Figure ).
Computed tomography angiography (CTA) of the head and neck was unremarkable. Transthoracic echocardiogram (TTE) did neither reveal a patent foramen ovale nor thrombi. Electrocardiogram (ECG) was unchanged from prior and revealed normal sinus rhythm.
Follow up imaging was done with MRI of the brain which showed an acute lacunar infarct of the right thalamus and other chronic changes (Figures -).
The patient was diagnosed with an acute right thalamic infarct with findings consistent with COS. He was not a candidate for thrombolytic therapy with intravenous alteplase. He was started on high-intensity statin therapy, and dual antiplatelet therapy (DAPT) with aspirin and clopidogrel for 30 days, with plans to continue clopidogrel monotherapy thereafter. His antihypertensive medication regimen was also optimized, and he was advised to quit smoking.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [71, 'years'], 'Hypertension history': True, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': True, 'Diabetes mellitus': True, 'smoking': True, 'atherosclerotic disease': True, 'Transient Ischemic Attacks History': True, 'Suspicion History': 'Slightly suspicious', 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 71 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 0 + 2 = 2.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, smoking, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: obesity, family with cvd. The following risk factor(s) are missing from the patient's data: obesity, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 4 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 2 + 2 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 4.
Based on the patient's data, the HEART Score is 4."
4217,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4369977-1,Extracted,"A 55-year-old right-handed male presented to the emergency department after a syncopal episode. He was teaching a karate class when a coworker saw him fall to the ground. He spontaneously regained consciousness after a few seconds but was confused for ∼15–20 min. He had no recollection of the event, and was hemodynamically stable and neurologically intact. He denied illicit drug use. Vitals, physical examination and laboratory studies were within normal limits. ECG showed normal sinus rhythm with normal PR and QT intervals and no ST-T wave changes. He was on no AV blocking agents. Head CT showed no intracranial bleed or mass lesion.
He had a history of five similar episodes in the past. During the last episode, he had been noted to have sinus arrest on telemetry and underwent single atrial lead pacemaker placement. The pacemaker was programmed to AAI mode. AV conduction was tested and was normal. Coronary angiogram showed no evidence of coronary artery disease. EEG had been minimally abnormal with left temporal theta slowing, suggestive of an area of neurophysiologic dysfunction, but no epileptiform activity was noted. He had no history of febrile seizures, central nervous system infection or cranial trauma.
The patient was admitted for further work up. Continuous EEG monitoring was ordered to evaluate for seizure activity. At ∼7 min and 36 s, the patient started to have recurrent automatisms and became unresponsive, with the EEG showing complex partial seizure activity emanating from the left anterior temporal region with continued post-ictal right temporal delta slowing. The seizure lasted ∼1 min. The simultaneous ECG lead demonstrated heart rate slowing toward the end of the seizure episode, with the rhythm changing from sinus to atrially paced at 60 beats min−1 with 1:1 conduction, to atrially paced with 2:1 AV block, followed by complete heart block for 4 s, followed by resumption of the baseline atrially paced rhythm with 1:1 conduction (Fig. ).
Cardiac electrophysiology recommended treating the seizure episodes before considering upgrade of the pacemaker to a dual-chamber device. The patient was started and subsequently discharged on levetiracetam. More than 15 months later, he has had no seizures or syncopal events.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 55 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4218,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8020123-1,Extracted,"The patient was a 58-year-old non-smoking male Ohio native with hyperlipidemia, environmental allergies and no other known medical problems who presented to the emergency department within hours of his return from a ski trip to Breckenridge, Colorado (altitude 2926 m) complaining of dyspnea, orthopnea, dizziness, chest tightness and weakness in the pre-Covid-19 era. He developed mild dyspnea within 48 hours of arrival to Colorado but returned to Ohio after five days with increasing dyspnea that did not improve with descent. His initial evaluation revealed a pale mildly diaphoretic adult in severe respiratory distress who was able to speak in short sentences. His initial vital signs were blood pressure 189/101mmHG, temperature 37°C, respirations of 40 breaths per minute, and pulse rate of 112 beats per minute. Physical exam was significant for normal cardiac exam except tachycardia, increased work of breathing, conversational dyspnea, bibasilar rales, normal heart sounds, 2+ distal pulses without peripheral edema and mildly diaphoretic cool skin. Oxygen saturation on room air was 72% and chest X-ray demonstrated pulmonary edema without cardiomegaly (). Electrocardiogram revealed sinus tachycardia of 104 beats per minute with minimal flattening of the T-waves in V5 and V6. Lab work revealed an elevated white blood cell count of 21.6 Reference Interval (RI) (4.5–11.5E9/L), a normal hemoglobin of 13.7 RI (12.5–16.5g/dl) and an elevated brain natriuretic peptide level of 1031 RI (0–125pg/dl), three serial troponin levels were less than 0.01 RI (0.00–0.03ng/mL). D-dimer level was not obtained due to the pulmonary infiltrates and a basic metabolic panel was normal, as was a viral respiratory film array panel, and two sets of blood cultures. A trans-thoracic echocardiogram revealed normal valvular function and an ejection fraction of 65% with normal diastolic function. The echocardiogram did not include a pulmonary ultrasound and B-lines were not assessed. Pulmonary consultation noted rapid resolution of the pulmonary infiltrates as well as hypoxia with the emergency department treatment and a decision not to perform bronchoscopy was made. In the emergency department, nitroglycerine 0.4mg sublingually, extended-release nifedipine 30 mg orally, and dexamethasone 10mg intravenously were administered. A brief emergency department literature review led to this therapeutic regimen. Due to persistent dyspnea despite resolving hypoxia, he was placed on bilevel positive airway pressure (BIPAP) at 15/5 cmH2O with further improvement in his dyspnea. Due to the local lack of familiarity with HAPE, he was admitted to the intensive care unit where the BIPAP was continued until he could be weaned to room air and was subsequently discharged on no medications. He was counseled against further trips to high altitude without acclimatization.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [58, 'years'], 'Hypertension history': True, 'Suspicion History': 'Moderately suspicious', 'hypercholesterolemia': True, 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 58 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 1 + 1 = 2.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4219,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5398907-1,Extracted,"A 62-year-old Afro-Caribbean male was diagnosed with congestive heart failure with left ventricular ejection fraction (LVEF) 35% two years ago at his home country and presented with progressing shortness of breath, paroxysmal nocturnal dyspnea, orthopnea. Other comorbidities included well-controlled type two diabetes mellitus and hypothyroidism. His home medications included furosemide, metformin, and levothyroxine. He has two family members who passed away from unknown heart disease after their 50s. Vital signs were significant for chronic borderline hypotension. Examination showed elevated jugular venous pressure, decreased breath sounds at the left base, and S3 heart sound. The electrocardiogram (EKG) showed low QRS voltage, but no ischemic changes [Figure ].
Troponins were equivocal. The N-terminal pro-B-type natriuretic peptide (NT-proBNP) was elevated. Chest X-ray showed a moderate left pleural effusion with basilar atelectasis and mild pulmonary edema. Transthoracic echocardiography (TTE) revealed global hypokinesis with LVEF 16% and severe concentric biventricular hypertrophy [Figure ].
The patient was started on IV diuretics, dobutamine drip and had left-sided therapeutic thoracentesis with symptomatic improvement. Cardiac magnetic resonance imaging (MRI) with late gadolinium enhancement revealed diffusely enlarged concentrically thickened ventricles with increased myocardial signal suggestive of amyloid deposition by appearance [Figure ].
Left and right heart catheterization showed single-vessel coronary artery disases (CAD) isolated to the first obtuse marginal artery. Serum and urine immunofixations were negative. Right ventricular endomyocardial biopsy was obtained with amyloid subtype staining indicating ATTR [Figures -].
Further genetic sequencing analysis showed pathogenic Val122Ile mutation and confirmed familial ATTR cardiomyopathy. The patient developed several runs of asymptomatic non-sustained ventricular tachycardia during the hospital stay. Due to high risk for deadly arrhythmias, the patient underwent single-chamber automatic implantable cardioverter-defibrillator (AICD) placement. He was started on warfarin for long-term anticoagulation due to nearly immobile atriums and ventricles. He was evaluated for heart and liver transplants. The liver transplant was postponed due to his heart condition, and ideally, should be pursued after the heart transplant in order to preserve the transplant heart from amyloid deposition. Due to severe hypertrophy with significantly decreased chamber size, left ventricular assisted device was not feasible. Eventually, he was deemed not to be a candidate for the heart transplant due to increased pulmonary vascular resistance. He is currently on palliative care.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [62, 'years'], 'Hypertension history': True, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': True, 'parent or sibling with Cardiovascular disease before age 65': True, 'atherosclerotic disease': True, 'Initial troponin': 'less than or equal to normal limit', 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'smoking': False}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 62 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, family with cvd, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: obesity, smoking. The following risk factor(s) are missing from the patient's data: obesity, smoking. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 4 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 1 + 2 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4220,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7559682-1,Extracted,"A 58-year old man was hospitalized to the Federal Center for Cardiovascular Surgery of the Russian Ministry of Health (Chelyabinsk) complaining of dyspnea, general weakness, dizziness during physical exertion, and fatigue.
Over the past five years, the patient experienced rare heart palpitations that have occurred and stopped on their own after a few minutes. Six months before hospitalization, shortness of breath, weakness, and post-exertion dizziness appeared. Heart rate increased to 120 per minute. The electrocardiogram taken in an outpatient clinic revealed an irregular form of atypical atrial flutter. Based on the results of echocardiography, an aneurysm of the left atrium was suspected. Warfarin was prescribed. The maintenance dose was 2.5 mg daily.
The patient had a free previous medical history.
On the patient’s visit to the Center for Cardiovascular Surgery, his vital signs were within normal limits.
The Quick prothrombin activity was 27.9% (reference values were 70%-120%), INR was 2.52, and the prothrombin time was 45.6 s due to warfarin treatment. Other laboratory parameters of blood and urine analyses, blood biochemistry, and arterial blood gas were within normal limits.
A free-breathing real-time cine magnetic resonance imaging (MRI) with electrocardiograph synchronization did not reveal any defects in the leaves of the pericardium and extrapericardial protrusions of the heart cavities. A giant aneurysm of the left atrial appendage (123 mm × 90 mm × 70 mm in size) had uneven and clear contours, thin walls, and turbulent blood flow in the cavity. The aneurysm had a wide communication with the cavity of the left atrium. The neck of the aneurysm was 51 mm × 55 mm in size. The cavity of the aneurysm had no pathological formations, there were no blood clots. The aneurysmically dilated left atrial appendage was adjacent to the trunk and left branch of the pulmonary artery, to the upper and lower left pulmonary veins, and to the left atrioventricular sulcus. The lower contour of the aneurysm reached the diaphragmatic surface of the pericardium. The left atrium was of normal size (Figure ). Preoperative coronary angiography showed the absence of coronary artery stenosis.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [58, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'hypercholesterolemia': False, 'obesity': False, 'smoking': False}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 58 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4221,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5458028-1,Extracted,"A 58-year-old male with dyslipidemia, an eight-year history of T2DM, a family history, his mother, of T2DM, with no known micro- or macrovascular complications, was admitted to the emergency department for malaise, epigastric pain, polyuria, and progressive dyspnea which had begun 10 h ago. He had experienced a 2-kg weight loss over the last few days. His usual medications included aspirin 100 mg q24 h, atorvastatin 40 mg q24 h, and metformin 850 mg q8 h, which had been switched to dapagliflozin 20 days before, due to poor glycemic control, with HbA1c 12% (108 mmol/mol). His vital signs included a heart rate of 122 bpm, respiratory rate 33 rpm, blood pressure 142/70 mmHg, temperature 36.1°C, and body mass index 22.5 kg/m2. On physical examination, somnolence, dry skin and mucous membranes, a Kussmaul breathing pattern, and a capillary refill of 3 sec were observed. Blood tests revealed hemoglobin 17.1 g/dL (13.5–18), leukocytes 19.5 × 103 (4–10 × 103), platelets 296 × 103 (150–450 × 103), glucose 248 mg/dL (60–100), creatinine 0.97 mg/dL (0.67–1.17), sodium 136 mmol/L (135–145), potassium 4.7 mmol/L (3.5–5.5), chloride 101 mmol/L (95–112), phosphate 4.9 mg/dL (2.5–4.5), amylase 70 U/L (10–115), lipase 28 U/L (1–67), pH 6.95 (7.35–7.45), pCO2 23 mmHg (35–45), HCO3 5 mmol/L (22–26), lactate 1.8 mmol/L (0–1.5), urine ketone bodies >150 mg/dL (0–0), CK 112 U/L (1–190), CK-MB 7.3 ng/mL (0.1–5), and troponin I 0.07 ng/mL (0.001–0.05). The electrocardiogram (EKG) showed sinus rhythm with right bundle branch block, and nonspecific repolarization abnormalities. Because of the right bundle branch block was not previously known, a new troponin test was performed six hours later with a peak value of 4.28 ng/mL. Treatment with crystalloids, continuous infusion of intravenous insulin, and administration of potassium and sodium bicarbonate were begun in the emergency room (ER). Due to a poor response over the first two hours, with the persistence of lactic acidosis, the patient was transferred to the intensive care unit (ICU), where more aggressive rehydration with crystalloids was started, without further modifications of the original therapeutic plan.
Two days later, the patient was discharged from the ICU to the endocrinology ward. Because of his coronary risk factors and the elevated troponin on admission, a coronary angiography was performed, showing triple-vessel disease. Successful bypass surgery without extracorporeal circulation was performed a few days later, with internal mammary artery grafts to the anterior descendent and marginal obtuse arteries and a saphenous vein graft to the right coronary artery. He was discharged 3 days later on Lantus™ Sanofi-aventis S.p.a Valcanello,03012 Anagni (FR), Italia (insulin glargine) 20 IU and Insulina Novorapid™: Novo Nordisk A/S. Hallas Allé, DK-4400. Kalundborg, Dinamarca (insulin aspart) 6-4-4-0 IU subcutaneous insulin, aspirin, clopidogrel, enalapril, bisoprolol, atorvastatin, and furosemide. The oral antidiabetic treatment with dapagliflozin was not restarted. During follow-up by endocrinology, C-peptide, anti-GAD, and IA-2 antibodies were required due to normal BMI and lack of family history suggested T1DM or a latent autoimmune diabetes of adults (LADA) rather than T2DM as etiology of his diabetes. C-peptide was 1 mg/dL (0.9–7.1) with glycemia 214 mg/dL (60–100), anti-GAD <5 U/mL (0–12.5), and anti-IA-2 <7.5 U/mL (0–7.5).",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [58, 'years'], 'hypercholesterolemia': True, 'Diabetes mellitus': True, 'Suspicion History': 'Highly suspicious', 'obesity': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'parent or sibling with Cardiovascular disease before age 65': True, 'Electrocardiogram Test': 'Normal', 'Hypertension history': False, 'smoking': False}",7,7,7,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 58 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: diabetes mellitus, family with cvd, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, obesity, smoking. The following risk factor(s) are missing from the patient's data: hypertension, obesity, smoking. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 3 + 2 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 5 + 2 = 7.
Based on the patient's data, the HEART Score is 7."
4222,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4532120-1,Extracted,"A 31-year-old Korean male patient was transferred to our hospital from a local hospital because of persistent melena of undetermined origin. Four months ago, the patient visited the hospital with complaints of chest tightness and productive cough. An X-ray film of the chest at that time showed a patch infiltration in the right lower lung field. Studies of the sputum for acid fast bacilli were negative but anti-tuberculosis medications were started under the impression of pulmonary tuberculosis. Three months later, he was admitted to the same hospital because of melena and underwent extensive work-ups including gastroscopic examination, barium studies of the colon and small bowels, and a gastric mucosa scan for Meckel’s diverticulum, but no bleeding focus was found. During the stay in that hospital, the melena improved spontaneously and he was discharged. He did fairly well until 10 days prior to this admission when recurrent melena developed. Additional studies including 99mTC-sulfur colloid scintigraphy were carried out, but no bleeding focus was found.
On admission, the patient appeared pale and acutely ill. The blood pressure was 130/70 mm/Hg, pulse rate 120/min, respiratory rate 20/min, and the temperature 36.5°C. The heart sound was normal without murmur. Breathing sound was decreased at the right lower lung field. No lymphadenopathy was found in the neck or axilla. No palpable abdominal mass was felt. Rectal examination revealed internal hemorrhoid and hematochezia.
The hemoglobin was 4.6 g/dl and the hematocrit was 14%. The white blood cell count was 6300/mm3 and the platelet 203,000/mm3. The urea nitrogen was 22.4 mg/dl, the creatinine 1.5 mg/dl, the protein 2.5 g/dl (the albumin 1.3 g/dl and the globulin 1.2 g/dl), the bilirubin 0.4 mg/dl, the alkaline phosphatase 53 IU, the aspartate aminotransferase (AST) 10 IU, and the alanine aminotransferase (ALT) 10 IU. The serum sodium was 127 mEq/L and the potassium 4.1 mEq/L. Chest X-ray film revealed an ill defined dense infiltrate with air bronchogram in the right lower lung field (). Mesenteric arteriography was performed but could not find any bleeding focus. Because of severe hematochezia, the flexible sigmoidoscopy was not available. The hemorrhoid with massive bleeding was found by anoscopy. An emergency hemorrhoidectomy was carried out on the second hospital day. However, a large amount of hematochezia persisted even after the operation and signs of serious disseminated intravascular coagulopathy (DIC) follwed. On the 10th hospital day while the DIC improved, the patient complained of abdominal distension and pain. Ascites was suspected.
An abdominal paracentesis revealed intraabdominal bleeding. An emergency exploratory laparotomy was perfomed. On operation, multiple polypoid masses of various sizes were palpated intraluminally in the jejunum from 10 cm below the Treitz ligament to the 120 cm distally. A large perforation of the jejunum (8 cm in diameter) probably caused by necrosis of the bowel wall was found on the antemesenteric border of the jejunum 20–25 cm below the Treitz ligament. Multiple mass lesions including hematomes were also found in the mesenteric root of the small intestine. Small bowel resection and end-to-end anastomosis were performed. On section, 36 polypoid masses were scattered grossly along the full length of the resected jejunum. The largest mass was 5.0×8.0×4.0 cm in size and composed of brownish homogeneous materials. Similar materials were filled in the mesenteric arteries and veins ().
Mlicroscopically, numerous hemosiderin pigments were scattered throughout the fields. The cells in the polypoid mass lesion were consistent with large round cells of undetermined origin. Each cell had a round nucleus containing prominent nucleoli. The cytoplasm was homogenous and clear (). The immunohistochemical study for S-100 protein was negative. Electron microscopically, obvious desmosomes were identified as convincing evidence of carcinoma (). Bronchoscopic examination, which was done on the 10th postoperative day, revealed an obstructing round mass at the entrance of the right main bronchus (). Histologically, this lesion was diagnosed as large cell carcinoma of the lung ().
On the 27th postoperative day, massive amounts of hematemesis and hematochezia developed again. The patient died on the 31st postoperative day due to hypovolemic shock.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [31, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 31 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4223,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8683674-1,Extracted,"A 57-years-old man with a history of smoking interrupted 6 months prior, and no other significant past medical history, was admitted in the emergency department for acute epigastralgia and vomiting. On arrival, he was alert and oriented with a blood pressure of 130/90 mmHg, a heart rate of 85/minute, and a respiratory rate of 19 breaths/minute. Cardiovascular examination was unremarkable. His blood glucose was 260 mg/dl without acetonuria. His electrocardiogram revealed normal sinus rhythm with ST segment depression in lateral, inferior, and posterior leads. His cardiac enzymes were elevated (First Troponin I at 755 ng/L, the second at 1600 ng/l), serum creatinine and electrolyte levels were normal. Echocardiography demonstrated an akinesia of the lateral wall with a left ventricular ejection fraction of 50%. The patient was admitted to the intensive care unit and prepared for cardiac catheterization. He received 300 mg of aspirin, 600 mg of clopidogrel and full dose 6000 UI of enoxaparine subcutaneously, with a slight regression of the pain. An electrocardiogram performed 6 h after his admission showed an ST elevation in the lateral and posterior leads (). Urgent coronary angiography revealed a concomitant occlusion of the mid LAD and the proximal Left circumflex artery with a collateral flow from the RCA (). We proceeded with primary per cutaneous intervention of the circumflex occlusion that was crossed by a floppy guidewire and predilated with a 2 × 15 mm balloon, then we deployed a 2,75 × 38 mm drug eluting stent (DES). Afterward, we proceeded to the PCI of the LAD using the same procedure to deploy a 2,75/28 mm DES. The angiographic result showed Thrombolysis In Myocardial Infarction III flow in both arteries (). Unfortunately, IVUS was not available. Aside from an inaugural diabetes mellitus (an incidental finding during this case presentation), there was no clinical or biological feature suggestive of an underlining condition predisposing to multiple thrombosis. The clinical course was uneventful and the patient was discharged well on day 4.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [57, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': True, 'smoking': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",7,7,7,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 57 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 3 + 2 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 5 + 2 = 7.
Based on the patient's data, the HEART Score is 7."
4224,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7411456-1,Extracted,"A 42-year-old Norwegian woman presented in November 2006 with a low-grade fever and severe left-sided chest wall pain that was felt to be pericardial in nature. She was otherwise in good health apart from Raynaud's phenomenon and seronegative Sjögren's syndrome. Her erythrocyte sedimentation rate and C-reactive protein were slightly elevated and her enterovirus antibody titer was positive at 128 (normal, <20). She was diagnosed with viral pericarditis.
One month later, she developed generalized body pain that was accompanied by fasciculations, painful cramps, burning sensations, and hyperalgesia that was so severe that she could not wear a watch, bra, or tight-fitting clothes. She reported painful swallowing and marked skin discoloration was noted on the extensor surfaces of the knees and elbows. There was no joint swelling. She then developed proximal muscle weakness in the thighs and became bed-bound. Blood tests for antinuclear antibody (ANA) and its subgroups were negative. The erythrocyte sedimentation rate and C-reactive protein and creatine kinase levels were normal. No muscle biopsy, neuroimmunology blood tests, or neurophysiological evaluation were performed at that time. She was treated with prednisone 40 mg and weaned over approximately 6 months but without significant benefit. The diagnosis was an immunological reaction with muscle involvement triggered by a viral infection.
The patient slowly improved over a period of 3 years. However, in the autumn of 2009, she started to develop further symptoms, including weight loss, anxiety, difficulty lifting her arms, and inability to drive a car. In the spring of 2010, she developed a tonic-dystonic posture and had difficulty relaxing her shoulders. She also developed severe insomnia and facial flushing with rosacea. Her insomnia was treated with a benzodiazepine that triggered a psychotic reaction during which she became manic, could not sleep, was prone to frequent bouts of singing, and was easily distracted. Eventually, this led to a psychiatric hospitalization during which she was diagnosed to have a somatoform disorder.
The psychotic reaction lasted for 6 weeks and was followed by a severe somatic exacerbation. During the course of a week, she developed torticollis-like head movements, myoclonic-like jerks in her right arm and leg, fluctuating flexion contractures in her elbows, dyspnea caused by both episodes of laryngospasm and chest muscle stiffness, and purplish skin discoloration on her hands and feet. During the subsequent weeks, she developed total body stiffness, palmar flexion contractures of her wrists and fingers, and ankles and toes that were fixed in plantar flexion. She was admitted to the neurology department but underwent limited testing. Needle electromyography (EMG) was essentially normal. Nerve conduction studies indicated F-wave hyperexcitability in the tibial nerve (see ) but were misinterpreted as normal. Repetitive nerve stimulation was not performed to look for afterdischarges. However, she did have positive ANA and ribonucleoprotein results with nonspecific inflammation and some atrophy in a biopsy from the right deltoid muscle. Unfortunately, she was suspected of malingering and her symptoms were considered to be psychogenic. Therefore, she was again diagnosed to have a somatoform disorder.
Over the next couple of years, she was essentially bed-bound because of her generalized muscle stiffness and contractures. Her symptoms gradually resolved spontaneously, and by 2014, she could walk 3-4 km. However, excessive physical activity at this time triggered a new relapse, which resulted in debilitating disease and the patient becoming bedridden again for about a year.
Her VGKC antibody titer was first measured (by radioimmunoassay, Euroimmun AG, Lübeck, Germany) in May 2015 and found to be positive at 100 pmol/l. She continued to have positive ANA and ribonucleoprotein tests. She was positive for SS-B at this time but later became negative. Other investigations included a comprehensive paraneoplastic evaluation and tests for antiglutamate, anti-GABA, glycine receptor antibodies, Caspr2, and LGI1, all of which were negative. An MRI scan of the brain and an analysis of cerebrospinal fluid were normal. In December 2015, she was readmitted to the neurology department as an inpatient because of her ongoing symptoms. She was presumed to have an autoimmune disorder and started on intravenous immunoglobulin (IVIg) 2 g/kg administered at a daily dosage of 30 g for 5 days, for a total dose of 150 g. She responded well to this treatment, which was repeated at the same dosage in March 2016 and June 2016.
In July 2016, she was referred to a well-regarded clinic in the US where nerve conduction studies confirmed normal sensory and motor conduction responses. Needle EMG showed slightly larger motor units in the distal muscles, which raised the question of motor involvement, but no neuromyotonia, cramps, fasciculations, or myokymic discharges were seen. An autonomic reflex screen was normal, including the Quantitative Sudomotor Axon Reflex Test. The Thermoregulatory Sweat Test revealed sweating abnormalities with hypohidrosis in the areas of worst pain, specifically the lateral aspects of the legs, thighs, and arms, consistent with small fiber neuropathy (see ). Laboratory investigations with markers for diffuse autoimmunity revealed a ribonucleoprotein level of >8, which was positive. On paraneoplastic peri-inflammatory evaluation, her anti-VGKC value was 0.01 nmol/l, which was within the normal range. This was 4 weeks after treatment with 150 g of IVIg and likely reflected the good response to treatment. LGI1 and Caspr2 were negative and there was mild immunofluorescent cerebellar staining. The diagnosis was immunotherapy-responsive VGKC-associated autoimmunity with multiple immune-inflammatory markers.
Further ancillary tests were performed. Serum tested weakly positive for staining live-cell hippocampal neurons in one test at the Nuffield Department of Clinical Neurosciences (Oxford, UK). Immunohistochemistry of brain tissue showed fine granular to smooth fluorescence of the hippocampus and the molecular layer on rat cerebellum 1 : 100 and monkey cerebellum 1 : 32 (Euroimmun AG). Antibodies to subunits of the VGKC channel itself (anti-KCNA 1, 2, and 6) were negative, as was contactin 2 (Euroimmun AG). Paranodal/nodal testing with Caspr1, contactin 1, neurofascin 155, and neurofascin 186 was also negative (Euroimmun AG). Excitability tests using the QTRAC threshold-tracking software were normal. However, needle EMG revealed abnormal spontaneous activity in the form of fibrillation potentials, complex repetitive discharges, and myotonic discharges in the abductor pollicis brevis and extensor digitorum brevis muscles ().
Treatment with IVIg was continued after she was correctly diagnosed in 2016. At first, 30 g of IVIg was administered every fourth week (0. 1 g/kg/week). However, her VGKC titer increased again from 10 pmol/l to 98 pmol/l. Therefore, the doses of IVIg were increased to 60–90 g every fourth week (0.2–0.3 g/kg/week). Serial anti-VGKC titers were ≤100 pmol/l but were never again found to be as low as 10 pmol/l. IVIg has been continued in this patient and she now seems to be dependent on this immunotherapy. Although she is still symptomatic, her autoimmune disease is now considered to be in remission. Her functioning and quality of life have improved markedly, given the previous severity of her symptoms and the lengthy course of the illness. She has much less pain and stiffness and a higher exercise tolerance, which has allowed her to resume her daily activities, including ambulation and part-time work. Her response to treatment is very similar to that in another report on a patient who developed VGKC autoimmunity (negative for both Caspr2 and LGI1) after exposure to aerosolized porcine neural tissue [].",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [42, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 42 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4225,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7087456-1,Extracted,"A 31-year-old male patient without any history of chronic diseases, thyroid pathologies or previous neck surgery, was admitted to the ear-nose-throat outpatient clinic with the complaints of neck pain, dysphagia, swelling and redness on midline neck region, fever, and palpitations that started 10 days ago. He had tremor on hands and was generally agitated. The patient had no history of neck trauma and his medical history and family history were uneventful. Blood pressure was 120×70mmHg, axillary temperature 38.5°C, pulse rate 120/minute, respiratory rate 16/minute, and oxygen saturation was 99%. Otolaryngology examination revealed swelling, redness, and tenderness of approximately 7cm, especially in the area corresponding to the thyroid region (). In his systemic examination, breath sounds were normal, tachycardia was present, but no pathological sounds or murmurs were detected. In the endoscopic examination, the patient’s nasopharynx, oropharynx, and larynx examinations were normal and there was no fistula in the pyriform sinuses. The other otolaryngology examinations were normal. The patient presented with tremor on the hands and was agitated. Sinus tachycardia was present in the electrocardiogram. In laboratory examinations white blood cell count was 13,200 (75% neutrophil); hemoglobin 15.2g/dL; erythrocyte sedimentation rate (ESR) 54mm/hour; C-reactive protein (CRP) 152mg/L; and liver function tests were minimally elevated. With the suspicion of thyroid diseases, thyroid function tests were analyzed and thyroid-stimulating hormone (TSH) was 0.01µIU/mL (0.38µIU/mL to 5.33µIU/mL), free T4 was 4.9ng/dL (0.58ng/dL to 1.6ng/dL), free T3 was 13.27pg/mL (2.66pg/mL to 4.37pg/mL). These tests showed the patient had thyrotoxicosis.
Anti-thyroglobuline and anti-thyroperoxidase antibodies were negative. Immunoglobulin values were normal. Neck and thyroid ultrasound showed a heterogeneous lesion of 33×34×66mm in left thyroid lobe, formed by septated cystic components, and no robust thyroid parenchyma was seen in the left lobe. In the left anterior neck region, there were compartments with cystic echogenicity on the skin, subcutaneous tissue and thyroid region, while the right thyroid gland parenchyma was normal (). The patient was hospitalized.
Neck computed tomography with no contrast enhancement revealed a heterogeneous, hypodense lesion, containing some areas of necrotic-liquid density, 65×60×65mm in size, located on the left lobe, along the isthmus level and extending from the midline to the right lobe (). Due to the presence of multiple small areas with several septations, only 2mL of purulent fluid could be aspirated in FNAB, and the material was sent for culture antibiogram.
Empirically, treatment was initiated with ampicillin/sulbactam (1,500mg, four times a day, intravenous; Sulcid, İbrahim Etem-Menarini, Istanbul, Turkey) and ornidazole (500mg, twice a day, intravenous; Orniject, Tüm Ekip İlaç, Istanbul, Turkey) for infection. Propranolol hydrochloride (20mg, twice a day, PO; Dideral, Sanofi, Istanbul, Turkey) was started for patient’s agitation, tremor and palpitations. Methylprednisolone (40mg a day, intravenous; Prednol-L, Mustafa Nevzat Pharmaceuticals, Istanbul, Turkey) was started for inflammation of thyroid gland and dexketoprofen trometamol (100mg a day, intravenous; Arveles, İbrahim Etem – Menarini Group, Istanbul, Turkey) for pain and inflammation. Methimazole (5mg, three times a day, PO; Thyromazol, Abdi İbrahim İlaç, Istanbul, Turkey) was prescribed for thyrotoxicosis, as an antithyroid drug.
In culture antibiogram showed Eikenella corrodens, susceptible to ampicillin. Ornidazole was discontinued and the treatment was continued with ampicillin/sulbactam. On the 5th day of the treatment, TSH was 0.003µIU/mL, freeT4 3.61ng/dL, freeT3 4.32pg/mL, ESR 35mm/hour, and CRP was 8mg/L. Ampicillin-sulbactam treatment was continued for 14 days, then TSH was 0.01µIU/mL, freeT4 1.14ng/dL, freeT3 2.90pg/mL, ESR 8mm/hour, and CRP was 6mg/L. These findings showed that the patient’s infection was regressing and thyrotoxicosis was getting better.
The patient was discharged 17 days after hospitalization, since he had a complete regression of agitation, tremor, palpitations and painful redness on the neck. Thyroid function tests, ESR and CRP levels were normal at the first month after treatment. The patient was followed as euthyroid in the first year after treatment.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [31, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 31 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4226,18,HEART Score for Major Cardiac Events,risk,integer,pmc-2790183-1,Extracted,"This is the case of 61-year-old African-American woman with a history of depression and anxiety who presented to the emergency room in May 2008 with an acute episode of left-sided chest pain/pressure with associated shortness of breath, diaphoresis, and an impending sense of doom lasting 2-3 minutes. There was no identifiable precipitant to this event.
She was admitted and placed on a cardiac telemetry monitoring. In the hospital, she was free of chest pain. The electrocardiogram, telemetry, and serial cardiac enzymes did not reveal myocardial infarction or any acute cardiac event. There was no family history of coronary artery disease. Medical history included hypertension, obesity, sleep apnea, and a history of smoking (quit 10 years prior) and alcohol abuse (from age 40 to 51). During hospitalization, the patient voiced concern that her chest pain may have been related to a recent recurrence of depressive symptoms. She recalled having similar chest pain 10 years ago. At that time, she had had cardiac testing including angiography, which was normal, and the pain was diagnosed as panic attacks. At that time (10 years ago) some relief was provided by diazepam and sertraline. As a young adult, the patient described low-level depression with suicidal ideation. Her other past psychiatric medications included fluoxetine, buspirone, trazodone, and risperidone. Her family psychiatric history included a father with depression, a brother with alcohol abuse, and one son with depression, alcohol abuse, and completed suicide (7 years ago). At the time of hospitalization, the patient was divorced with one living son. At discharge, she was scheduled for an outpatient stress test.
Six days after hospitalization, she was seen in the medical clinic. She was free of chest pain but reported depression with decreased energy, lethargy, and decreased interest in activities. Therapy was started with 25 mg of sertraline for 2 weeks, which was titrated up to 50 mg at week 3. A referral was made to the psychiatry department.
One month after being started on sertraline (early June), she was seen in psychiatry clinic. At that time, she was tolerating 50 mg of sertraline but without much benefit. She described depression with anergia and a lower level of anxiety than she had previously in psychiatric care years ago. She also reported 2 episodes of chest pain with tremor and sensation of heart racing in the past month. Laboratory analyses were ordered to rule out organic fatigue, and a referral was made to a sleep clinic as she had been diagnosed with sleep apnea 8 years before by a polysomnogram (PSG) test, but failed to follow up. Bupropion (Bupropion SR, 100 mg) was added to sertraline to address her depression with anergia, and alprazolam was given for anxiety as needed. Two and a half weeks after being started on bupropion the patient was still complaining of depression and fatigue, and bupropion was increased to 150 mg.
Three weeks after the bupropion dose change, the PSG results came back revealing sleep apnea, and the patient was placed on continuous positive airway pressure (CPAP) therapy. A week after PSG results were received, during her sleep clinic appointment, the patient experienced substernal chest pain with pressure radiating down her left arm. The physician from the sleep clinic made a referral to cardiology, as she had failed a previous appointment for cardiology and a stress test. In a psychiatric follow-up (one week after her sleep clinic appointment), she was feeling much better, including improved mood and less fatigue and anxiety.
One week later, the patient was seen in the cardiology outpatient clinic describing a 3-month history of frequent (10 or 15) episodes of severe midsternal chest pain lasting 5 to 10 minutes that was associated with left arm weakness. The symptoms were neither exercise-induced nor predictable. The symptoms were extremely anxiety-provoking but she reported no associated diaphoresis or shortness of breath. The electrocardiogram revealed sinus rhythm and left ventricular hypertrophy. The cholesterol panel was unremarkable. Due to worrisome clinical presentation, coronary angiography was performed. The coronary arteries were angiographically normal. There were no wall motion abnormalities, and the ejection fraction was normal. The patient was discharged with a cardiac event monitor. Within 5 days the patient experienced two recurrences of her symptoms. The event monitor revealed ST elevations that were associated with anxiety-provoking chest pain (). There were no significant changes in heart rate and no arrhythmias were recorded. The patient was diagnosed with vasospastic (Printzmetal's or variant) angina and started on amlodipine (2.5 mg daily) and isosorbide mononitrate (30 mg daily).
In a subsequent psychiatric follow-up, the patient was free of chest pain and panic attacks. Bupropion was tapered off, and sertraline was increased to 75 mg daily because it was feared that bupropion could contribute to or worsen her coronary vasospasm.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [61, 'years'], 'Hypertension history': True, 'smoking': False, 'hypercholesterolemia': False, 'obesity': True, 'atherosclerotic disease': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Suspicion History': 'Moderately suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 61 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 1 + 1 = 2.
The following risk factor(s) are present based on the patient's note: hypertension, obesity. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4227,18,HEART Score for Major Cardiac Events,risk,integer,usmle-7966,Extracted,"A 25-year-old man presents to the emergency department complaining of palpitations, lightheadedness, and sweating. He just started working at an investment firm and has been working long hours to make a good impression. Today, he had a dozen cups of espresso to keep himself awake and working. He has never had such an episode before. His past medical history is unremarkable. His pulse is 150/min, blood pressure is 134/88 mm Hg, respirations are 12/min, and temperature is 36.7°C (98.0°F). ECG shows supraventricular tachycardia with sinus rhythm.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [25, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 25 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4228,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7457112-1,Extracted,"A 66-year-old male had chest squeezing at rest for more than 30 years.
Thirty years ago, the patient had chest squeezing at rest which occurred most often from midnight to early morning lasting from 5 to 15 min, and was not usually induced by exercise in the daytime. Over the preceding 13 years, he had undergone coronary angiography 4 times and percutaneous transluminal coronary angioplasty procedures twice at other hospitals without a diagnosis of coronary artery spasm. In July 2006, 70% stenosis was found in the ostial left anterior descending artery and 90% stenosis was found in the mid left circumflex. The left circumflex was dilated by balloon without a stent as the left circumflex was small according to the previous angiography report. The patient was given various medications, such as beta blocker, aspirin, angiotensin-converting-enzyme inhibitor, clopidogrel, and statin, but his chest symptoms were not relieved. Due to repeated similar complaints, angiography was performed again without percutaneous transluminal coronary angioplasty in November 2014 and August 2015. In August 2017, an electrocardiography was performed during a chest squeezing episode in the early morning at 6:08 in a hospital and ST-segment elevations in II, III, aVF and V2-V5 leads were observed. Subsequently, ST-segment depression in II, III and aVF, and ST-segment elevation in V2-V5 leads became apparent. The symptoms and ST-segment elevation or depression disappeared 3 min and 25 s after sublingual administration of nitroglycerin (Figure ). However, the doctors did not realize that the symptoms were caused by coronary artery spasm. Coronary angiography was performed and showed severe stenosis in the proximal left circumflex which was dilated by balloon again without a stent. However, his chest symptoms occurred approximately 5 times/mo. The patient presented to the emergency room of our hospital with frequent chest squeezing episodes in March 2019.
The patient had a history of hypertension for 10 years.
The patient had a history of cigarette smoking for more than 40 years.
No family history of inherited diseases, autoimmune diseases or coronary heart disease was recorded.
Vital signs were stable and physical examination was unremarkable.
No elevation in high sensitivity troponin T was detected and the rest of his laboratory examinations were also completely normal.
Electrocardiography was performed during a chest pain episode and ST-segment elevations in I, aVL and V2-V3 leads were recorded which spontaneously resolved, accompanied by pain relief (Figure ). Neither chest X-ray nor echocardiography showed any specific changes.
In order to evaluate the condition of the coronary artery, coronary angiography and IVUS were performed. An injection of acetylcholine into the coronary artery was administered to induce spasm. Coronary angiography was performed via right radial access. Intravenous injection of diltiazem and intracoronary injection of nitroglycerin were administered to prevent coronary artery spasm induced by the catheter or guidewire.
An initial coronary angiography showed mild atherosclerotic changes from the proximal to the mid segment in the right coronary artery. There were no obvious atherosclerotic changes in the left main trunk, left anterior descending coronary artery and left circumflex (Figure ).
After intracoronary injection of 200 μg of nitroglycerin, each segment was examined using a mechanical IVUS system. During IVUS checking of the right coronary artery and left anterior descending coronary artery, the patient felt chest squeezing without the use of acetylcholine or ergonovine. Coronary angiography showed that a local coronary spasm occurred at the distal segment of the right coronary artery and a diffuse coronary spasm occurred at the proximal-distal segment of the left anterior descending coronary artery (Figure ). Following an intracoronary injection of nitroglycerin (right coronary artery with 400 μg nitroglycerin and left coronary artery with 1000 μg nitroglycerin), the patient’s chest symptoms and coronary spasm were relieved (Figure ).
IVUS images showed that the right coronary artery and left anterior descending coronary artery demonstrated increased media thickness (Figure ).",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [66, 'years'], 'Suspicion History': 'Highly suspicious', 'Hypertension history': True, 'smoking': True, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'Initial troponin': 'less than or equal to normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'Diabetes mellitus': False, 'obesity': False}",6,6,6,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 66 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 2 + 2 = 4.
The following risk factor(s) are present based on the patient's note: hypertension, smoking, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 4 + 2 = 6.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 6.
Based on the patient's data, the HEART Score is 6."
4229,18,HEART Score for Major Cardiac Events,risk,integer,usmle-159,Extracted,"A 60-year-old man comes to the physician for a routine health maintenance examination. He feels well. Five years ago, he underwent a colonoscopy, which was unremarkable. He has no history of serious illness except for an episode of poststreptococcal glomerulonephritis at the age of 10 years. His father died of bladder carcinoma at the age of 55 years. The patient works at a rubber factory. He has smoked one pack of cigarettes daily for the past 25 years. He drinks 1–2 cans of beer per day. He takes no medications. He has never received any pneumococcal vaccination. His temperature is 37°C (98.6°F), pulse is 70/min, and blood pressure is 120/80 mm Hg. Digital rectal examination shows mild symmetrical enlargement of the prostate with no masses.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [60, 'years'], 'Hypertension history': True, 'smoking': True, 'Diabetes mellitus': False, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 60 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: hypertension, smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4230,18,HEART Score for Major Cardiac Events,risk,integer,pmc-3914134-1,Extracted,"A 30-year-old male patient presented to the emergency room with the chief complaint of a dull pain in the left lower lateral abdomen. The onset of pain had been approximately 2-3 days before presentation. He did not have a remarkable past history. He complained of frequency but denied recent trauma or any problems moving his bowels. Although he had visited the outpatient department 2 days before coming to the ED, he was discharged because of normal urine examination and intravenous pyelography results. Because of discomfort with frequency, he visited the ED for medical attention. In the ED, the urine analysis was redone. Similarly, urinalysis did not detect red blood cells in the urine. Serum electrolytes, blood urea nitrogen, creatinine levels, and white blood cell count were normal. Kidney sonography did not show obvious hydronephrosis. Although he did not complain of dysuria, he did mention increased micturation frequency. He did not seem anxious or hypochondriatic, and he went to the toilet several times during observation.
The MEAD device was then used to record the data in the ED. The meridian electrical conductance was low (14.9 μA; normal range, 30–64 μA). The index of sympathovagal balance was high (3.75; normal range, 1.0–1.5). The ratio of electrical conductance of the left side to the right side bladder meridian was obviously abnormal (L/R: 2.09) (). A urologist was consulted at this time. Unenhanced helical computed tomography (CT) was performed and depicted a tiny calculus at the left ureterovesical junction (). The patient was admitted to the urological service and started on an aggressive hydration regimen in an attempt to “flush” the stone. One day later, with his pain worsening, he was taken to the operating room to perform ureteroscopy. A ureteral stone (about 4 mm) was removed, and the patient's pain was relieved (meridian electrical conductance: 14.6 μA; index of sympathovagal balance: 3.31; ratio of electrical conductance of left to right side bladder meridian: 3.26). The subsequent hospital course was uncomplicated. The patient was discharged the following day and instructed to follow up as an outpatient. At the same time, he was encouraged to drink sufficient amounts of fluid to prevent the recurrence of ureteral calculi. The follow-up measurements of the meridian parameters (meridian electrical conductance: 47.8 μA; index of sympathovagal balance: 2.0; ratio of electrical conductance of left to right side bladder meridian: 1.19) returned to normal 1 month after treatment.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [30, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 30 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4231,18,HEART Score for Major Cardiac Events,risk,integer,usmle-4620,Extracted,"A 36-year-old man presents to the emergency room with subacute worsening of chronic chest pain and shortness of breath with exertion. The patient is generally healthy, lifts weights regularly, and does not smoke. His temperature is 97.8°F (36.6°C), blood pressure is 122/83 mm Hg, pulse is 80/min, respirations are 13/min, and oxygen saturation is 98% on room air. Cardiac auscultation reveals a crescendo-decrescendo murmur heard right of the upper sternal border with radiation into the carotids. An ECG shows left axis deviation and meets criteria for left ventricular hypertrophy. An initial troponin is < 0.01 ng/mL.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [36, 'years'], 'Hypertension history': False, 'Suspicion History': 'Moderately suspicious', 'Diabetes mellitus': False, 'obesity': False, 'smoking': False, 'Initial troponin': 'less than or equal to normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 36 years old. The patient's age is less than 45 years and so keep the current total at 1.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4232,18,HEART Score for Major Cardiac Events,risk,integer,usmle-1738,Extracted,"Two days after an uncomplicated laparoscopic abdominal hernia repair, a 46-year-old man is evaluated for palpitations. He has a history of hypertension, type 2 diabetes mellitus, and a ventricular septal defect that closed spontaneously as a child. His father has coronary artery disease. Prior to admission, his only medications were hydrochlorothiazide and metformin. He currently also takes hydromorphone/acetaminophen for mild postoperative pain. He is 180 cm (5 ft 11 in) tall and weighs 100 kg (220 lb); BMI is 30.7 kg/m2. His temperature is 37.0°C (99°F), blood pressure is 139/85 mmHg, pulse is 75/min and irregular, and respirations are 14/min. Cardiopulmonary examination shows a normal S1 and S2 without murmurs and clear lung fields. The abdominal incisions are clean, dry, and intact. There is mild tenderness to palpation over the lower quadrants. An electrocardiogram is obtained and shown below.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'parent or sibling with Cardiovascular disease before age 65': True, 'Hypertension history': True, 'Diabetes mellitus': True, 'age': [46, 'years'], 'Electrocardiogram Test': 'Normal', 'atherosclerotic disease': False, 'obesity': True, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'smoking': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 46 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, obesity, family with cvd. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: smoking, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: smoking, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 4 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 1 + 2 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4233,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5075289-2,Extracted,"Patient 2 is a 62-year-old male smoker with hyperlipidaemia and positive family history for premature coronary artery disease who originally presented with a non-ST-elevation myocardial infarction (NSTEMI) for which he had three DES implanted in the left anterior descending artery (LAD). He represented with anterior STEMI due to ST 795 days after his index admission while on aspirin 75 mg daily. He was treated with intravascular ultrasound guided POBA. Platelet function testing using sTEG demonstrated an inadequate response to P2Y12 receptor inhibitors. Initial response to aspirin 75 mg daily appeared adequate (%CI 61); however response to clopidogrel 75 mg daily was suboptimal (%CI 21) after 36 days of treatment. As a result, the patient was commenced on prasugrel 10 mg daily with no initial loading. Testing, after 70 days of treatment, again revealed hyporesponsiveness (%CI 17). Finally, ticagrelor 90 mg bd was introduced, with no initial loading, with similar effect (%CI −21) after 263 days of treatment (). Ultimately, he was maintained on ticagrelor 90 mg twice daily for life and has suffered no further ST or ischaemic events to date.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [62, 'years'], 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': True, 'smoking': True, 'parent or sibling with Cardiovascular disease before age 65': True, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'Hypertension history': False, 'Diabetes mellitus': False, 'obesity': False}",7,7,7,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 62 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 3 + 2 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 5 + 2 = 7.
Based on the patient's data, the HEART Score is 7."
4234,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8634395-1,Extracted,"A 41-year-old man was admitted to our hospital because of 11 days of sudden discomfort and pain in the chest. Approximately 3 months previously, the patient experienced chest tightness and discomfort, lasting for approximately 5 min, during exercise, excitement, and emotional upset. These symptoms were relieved with rest. He also experienced fatigue and coldness. Eleven days before admission, he had sudden onset of chest tightness and crushing pain, which persisted without relief and did not radiate to the surrounding areas. On admission, the patient showed a dull facial expression and minimal attentiveness and concentration, and his skin was rough. A physical examination showed that his vital signs were stable. His blood pressure was 120/70 mmHg, heart rate was 85 beats/min with regular rhythm, and no pathological murmurs or pericardial friction rubs were heard over each valve area after auscultation. No obvious abnormal signs were observed in the lungs or abdomen, and there was no pitting edema in the bilateral lower extremities. He denied a previous history of hypertension or diabetes. An electrocardiogram performed on admission showed sinus rhythm, complete right bundle branch block, pathological Q waves in leads V1–V3, and T wave changes in some leads (). Color Doppler echocardiography revealed abnormal echoes in the mid and apical segments of the left ventricular anterior wall and segmental wall motion abnormalities, which were consistent with ultrasound features of coronary heart disease. The apex of the left ventricle was dilated at the right ventricular apex. The ventricular wall was thin and the thinnest area was 17 mm. The ventricular wall bulged outwards and downwards and it showed paradoxical movements. Mural thrombus was not observed, and a left ventricular apical aneurysm had formed. The left ventricular ejection fraction was 36%. Echocardiography showed left ventricular systolic and diastolic dysfunction (). Thyroid function tests showed the following: triiodothyronine (T3) level, 0.504 nmol/L; free triiodothyronine (FT3) level, 1.66 pmol/L; thyroxine (T4) level, 12.35 nmol/L; free thyroxine (FT4) level, 1.91 pmol/L; thyrotropin (TSH) level, 168.531 mIU/L; antithyroglobulin antibody (TgAb) level, 69.9I U/ml; thyroid peroxidase antibody (TPOAb) level, 486.9 IU/ml; total cholesterol (TC) level, 6.08 mmol/L; triglycerides (TG) level, 5.87 mmol/L; high-density lipoprotein cholesterol (LDLC) level, 0.97 mmol/L; low-density lipoprotein cholesterol (LDLC) level, 4.36 mmol/L; apolipoprotein A (apoA) level, 1.08 g/L; apolipoprotein B (apoB) level, 2.53 g/L; prothrombin time (PT), 14.9 s; international normalized ratio (INR), 1.14; activated partial thromboplastin time (aPTT), 57.8 s; thrombin time (TT), 111.2 s; fibrinogen (FIB) level, 3.23 g/L; aspartate aminotransferase (AST) level, 110 U/L; lactate dehydrogenase (LDH) level, 251 U/L; creatine kinase (CK) level, 169 U/L; creatine kinase-MB (CKMB) level, 10 U/L; hydroxybutyrate hydrogenase (HBD) level, 128 U/L; and troponin T level, 12.3 pg/ml. Ultrasound of the thyroid showed Hashimoto's thyroiditis. Coronary angiography showed that there was no obvious stenosis in the left main coronary artery. Additionally, 40–50% stenosis was found in the proximal LAD, plaques and MB were observed in the distal LAD, and forward flow was TIMI grade 3. There was no obvious stenosis in the left circumflex coronary artery or right coronary artery, and forward flow was TIMI grade 3 (). Left ventricular angiography, which was performed using a pigtail catheter, showed formation of ventricular aneurysm ().
The abovementioned findings suggested the diagnosis of coronary atherosclerotic heart disease, old myocardial infarction, and ventricular aneurysm formation. Acute myocardial infarction was excluded. On the basis of our findings of thyroid function tests showing decreased T3, FT3, T4, and FT4 levels and increased TSH and TPOAb levels, hyperthyroidism was excluded, and the diagnosis of hypothyroidism and Hashimoto's thyroiditis was made.
A total of 75 mg of clopidogrel with 100 mg of Bayaspirin was administered orally once daily to inhibit aggregation of platelets. Additionally, 20 mg of atorvastatin calcium tablets were administered orally once daily for lowering lipid and stabilizing plaques. Furthermore, a 23.7-mg metoprolol succinate extended-release tablet was administered orally once daily to slow down heart rate. The patient also received thyroid hormone replacement therapy (levothyroxine). The starting dose of levothyroxine was 12.5 μg/day with a progressive increase of 25 μg/day every 2 weeks. He was also treated with conservative medical therapy for ventricular aneurysm.
After 8 days of treatment, the chest tightness and pain of the patient were relieved, and he was then discharged. The patient was advised to follow a low-sodium, low-fat diet; take medications as prescribed; and exercise appropriately. He was not advised to consume foods containing iodine. He was asked to return to the clinic regularly every month to test thyroid function and to have echocardiography and thyroid ultrasound performed. The dose of levothyroxine was adjusted to 50 μg/day. Additionally, oral administration of clopidogrel (75 mg/day), Bayaspirin (100 mg/day), atorvastatin calcium tablets (20 mg/day), and metoprolol succinate extended-release tablets (23.75 mg/day) was continued. After 6 months of follow-up, thyroid function returned to normal. There was no complaint of chest tightness, fatigue, or coldness, and his skin was smooth and thin. He provided correct answers to asked questions, he had high attentiveness and concentration, and his condition further improved (). The patient refused to receive further cardiac surgery for left ventricular aneurysm.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [41, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': True, 'Diabetes mellitus': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 41 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 3 + 2 = 5.
Based on the patient's data, the HEART Score is 5."
4235,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5292180-1,Extracted,"A 38-year-old man with no significant past medical history was admitted to the emergency department presenting with sudden onset of discontinuous severe abdominal pain that was focused in the right quadrants and radiated to the right iliac fossa and to the back. The patient did not report any relief with common analgesic drugs (paracetamol, 1000 mg). Blood pressure and heart rate were within normal limits, 130/85 mm/Hg and 90 bpm, respectively. ECG showed normal sinus rhythm and no cardiac abnormalities. Physical examination found deep tenderness at McBurney's point and abdominal rebound tenderness, while there was not tenderness when eliciting the costovertebral angle. Laboratory tests revealed leukocytosis (12.000/μL) and high levels of LDH (651 U/L), whereas kidney function tests and urine analysis did not show any significant alterations. Clinical and biological findings were initially suggestive for appendicitis and according to our internal guidelines an Ultrasound (US) was made to confirm the diagnostic hypothesis. The US examination was performed at first with a high-frequency probe (10–15 MHz) to evaluate the appendix and the surrounding area; however, no ultrasonographic abnormalities suggestive for appendicitis were detected. The US study was completed with a convex probe (5–7 MHz) to exclude other possible causes of abdominal pain and it showed, at the level of the middle-upper pole of the right kidney, a wedge-shaped hypoechoic area (), which did not show any vascular signal at color and power-Doppler study, unlike the adjacent parenchyma. In addition, there was a triple renal artery with lack of perfusion of the median branch (). The described hypoechoic area appeared clearly demarcated and suggestive for acute renal infarction. However, further diagnostic images were needed. A contrast-enhanced computed tomography (CT) was performed and showed a cuneiform low attenuation area of 5 cm in diameter at the middle-upper pole of the kidney (). Moreover, there was a triple right renal artery, with an incomplete filling defect due to a thrombosis involving the median artery from the origin up to its most peripheral ramifications (). This abnormality was likely related to the described hypovascular area of the renal parenchyma, with normal enhancement in the medium-caudal portion of the kidney (). Beside continuous intravenous hydration, anticoagulation with enoxaparin was started immediately after the contrast-enhanced CT. Because of lack of identifiable causes, clotting studies including INR, antithrombin III, C3c, C4, and anticardiolipin antibodies were sent and came back negative. Thus, without other possible risk factors of thromboembolic disease, the patient was diagnosed with idiopathic acute renal infarction. Having had the patient's symptoms improved he was discharged home on warfarin. At one-year follow-up he had no clinical and US recurrence.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [38, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 38 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4236,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7373792-1,Extracted,"The proband (II-2), a 54-year-old lady, came to the hospital due to recurrent chest pain in last 2 years. Coronary angiography indicated approximately 60–80% stenosis of the anterior descending coronary artery (), ECG testing also suggested the patient suffered from CHD (). However, the lipid testing described the level of LDL-c (3.94 mmol/L; control: <3.12 mmol/L) and a distinctly reduced levels of HDL-c (0.41 mmol/L; control: 0.9–2.19 mmol/L) of the proband (). This discovery attracted our interest because most patients with ASCVD commonly presented high levels of LDL-c, TC, and TG (). We then investigated the family history of the proband (II-2), which indicated that her young sister (II-4) has been diagnosed as the occlusion of left iliac artery and her father (I-1) was died from myocardial infarction at 60-year-old. Lipid testing further described that both her son (III-1) and her young sister (II-4) showed an overt reduced levels of HDL-c and normal levels of LDL-c, TC, and TG (). And his young sister (II-4) also suffered from arterial plaque in the left lower limb. The blood pressure of the proband was 80–120 mmHg and the fasting blood-glucose was 5.2 mmol/L. The proband (II-2) accepted the treatment of percutaneous coronary intervention, the proband did not complain any uncomfortable after treatment. And breathing sound of the lungs was clearly, the heart rate was normal (), and the insertion site recovered well. The II-4 is accepting recovery treatment by exercise and diet control.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'Suspicion History': 'Moderately suspicious', 'Hypertension history': False, 'Diabetes mellitus': False, 'Electrocardiogram Test': 'Normal', 'atherosclerotic disease': True, 'hypercholesterolemia': True, 'parent or sibling with Cardiovascular disease before age 65': True, 'obesity': False, 'smoking': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 54 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 1 + 1 = 2.
The following risk factor(s) are present based on the patient's note: family with cvd, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4237,18,HEART Score for Major Cardiac Events,risk,integer,pmc-3813461-1,Extracted,"A 31-year-old male, airline pilot, with no clinical history or cardiovascular risk factors, was admitted to the emergency room with 12 h history of retrosternal chest pain radiating to the jaw and upper extremities, during a trans-Atlantic flight, which did not improve with analgesia. Because of persistent pain, he came to our hospital. Upon arrival to the emergency room, his vital signs were stable and he had a normal physical examination but complained of precordial pain. The cardiac enzymes were elevated and the EKG detected S-T changes consistent with MI (Fig. ). A multidetector CT coronary angiography was performed showing left main trunk dissection with 50% stenosis (Fig. ).
The patient underwent emergent coronary revascularization with saphenous vein grafts to the first obtuse marginal and the left anterior descending artery (LAD). His postoperative course was uneventful and the patient was discharged home 7 days later. Control CT coronary angiography was performed 2 months later revealing patent aorto-coronary grafts (Fig. ).",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [31, 'years'], 'Suspicion History': 'Highly suspicious', 'Hypertension history': False, 'Diabetes mellitus': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'hypercholesterolemia': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'obesity': False, 'smoking': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 31 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 3 + 2 = 5.
Based on the patient's data, the HEART Score is 5."
4238,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8581035-2,Extracted,"MR is a 48-year old, obese (BMI 34.94 kg/cm2) man, former smoker of 10 pack-year. He suffers from arterial hypertension, has a family history of dilated cardiomyopathy and sudden cardiac death, and is on chronic therapy with thiazide, angiotensin II receptor blocker and statin. In November 2020, he reported fever, cough, weakness, diarrhea, and dyspnea. A nasopharyngeal swab for SARS-CoV-2 tested positive. The patient was started on oral prednisone 25 mg and LMWH 6,000 UI daily. Few days after symptom onset, he entered the ED for worsening dyspnea. ABG showed hypocapnic hypoxemia and high-flow oxygen therapy and CPAP cycles were started. The patient was hospitalized and i.v., dexamethasone was initiated. Due to persistent reduced PaO2/FiO2, the patient was transferred to ICU where initial CPAP and prono-supination cycles were soon followed by OTI and mechanical ventilation. Prophylactic antibiotic therapy was administered. Despite therapy, the patient did not show any improvement in the lung function. Chest CT scan showed extensive lung parenchymal alterations with widespread consolidations and signs of initial evolution toward lung fibrosis. The patient was transferred to our third-level hospital to start ECMO support. He was treated with i.v. steroid therapy, anticoagulant therapy (bivalirudin, antithrombin III), and prophylactic i.v. antibiotics. The patient was progressively weaned from ventilator support and finally extubated on December 28. He continued ECMO support and NIV cycles alternated with high-flow O2 therapy. As lung function did not improve since extubation, nintedanib was started through compassionate use after obtaining the signature of the informed consent, at the dosage of 150 mg orally twice a day. Eleven days after the introduction of nintedanib, it was possible to discontinue ECMO support due to progressively improved lung function up to PaO2/FiO2 ratio normalization. The CRP levels decreased concertedly (). The patient was discharged from ICU and transferred to the Rehabilitation Unit. A chest CT scan performed 40 days after nintedanib introduction showed a consistent reduction in consolidating areas, despite the persistence of GGO and peripheral interstitial thickening. At hospital discharge (day 60), the patient was eupneic on room air at rest and necessitated oxygen support with NC at 4 L/min during exercise. A 6MWT on NC at 3 L/min uncovered exertional desaturation (the lowest value of SpO2: 78%) and nocturnal oximetry showed episodes of hypopnea necessitating CPAP during sleep. Nintedanib treatment was discontinued after 71 days. A third chest CT scan performed 1 month after nintedanib withdrawal revealed a further reduction of lung alterations, albeit with persisting diffuse GGO. At follow-up evaluation (37 days after nintedanib withdrawal), SpO2 at rest was 96% on room air and RR 21 breaths/min. At 6MWT performed with NC at 3 L/min, the patient reached 88% of the predicted distance, with a nadir level of SpO2 of 92%. At the following evaluation (81 days after nintedanib suspension), SpO2 at rest was 100% on room air ().",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [48, 'years'], 'Hypertension history': True, 'smoking': False, 'Diabetes mellitus': False, 'obesity': True, 'atherosclerotic disease': False, 'parent or sibling with Cardiovascular disease before age 65': True, 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': True, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 48 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: hypertension, obesity, family with cvd. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, smoking, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, smoking, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 1 + 2 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4239,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5863286-1,Extracted,"A 69-year-old Afro-American man was admitted in the emergency department of a public institution in Port of Spain, Trinidad, in February 2015 with EKG findings consistent of an acute coronary syndrome: an inferior wall ST elevation myocardial infarction (inferior STEMI). The symptoms of chest pain initiated 5 hours before admission, he was in Killip-Kimball class I, and he received thrombolytic therapy with Tenecteplase, with clinical, ECG, and biomarkers criteria of successful reperfusion and good clinical in-hospital outcome; primary PCI was not performed because there was not a catheterization laboratory available in that public hospital.
The patient's prior history is that he smokes 10 to 15 cigarettes a day for the last 15 years and had no previous heart disease, hypertension, diabetes, and dyslipidemia nor family history of early coronary artery disease. He was discharged with medical treatment since he had an uncomplicated inferior myocardial infarction (MI) that was stratified for noninvasive evaluation, but due to the presence of postmyocardial infarction effort angina 5 days after discharge, he was admitted to Caribbean Heart Care Medcorp (CHCM) at St. Clair Medical Centre Hospital for diagnostic catheterization. The EKG revealed sinus rhythm with an inverted p wave in DI, aVL, and aVR, with right axis deviation, positive QRS complex in aVR, and poor progression of r waves in precordial leads and signs consistent of a prior inferior MI with q waves at DII, DIII, and aVF. The TIMI risk score was 2 (8% risk of event at 30 days). The EKG findings made us suspicious of a malposition syndrome ().
The physical exam with right-sided heart sounds, including a 4th heart sound and a right-sided apex with a palpable liver in the left side, and the radiogram findings with right-sided cardiac apex and gastric chamber confirmed our suspicion of situs inversus totalis, which was an incidental diagnosis.
Coronary angiography was performed via femoral access using the standard Judkins technique [] with 6 French catheters (Judkins left: JL 4.0 and Judkins right: JR 3.5), which showed right-sided aortic arch and mirror image of coronary circulation. Horizontal axis mirror-image inversion of the angiographic views was used. A two-vessel coronary artery disease was diagnosed. There were a significant 70% stenosis at the proximal segment of the left anterior descending artery (LAD) and a right coronary artery (RCA) 90% stenosis in the distal segment.
On May 25, 2015, percutaneous coronary intervention (PCI) was performed with an extra-backup support EBU 3.5, 6 French guiding catheter with the standard Judkins technique, using inverted horizontal axis angiographic views of the left coronary artery, to mimic a left anterior oblique (LAO) with a cranial view for the left anterior descending artery (LAD), an inverted view; that is, to the other side, a right anterior oblique (RAO) view was used, to proceed with a direct stenting of the proximal segment stenosis of the LAD, implanting a 2.5 × 16 mm drug-eluting (everolimus) stent (Promus Premier, Boston Scientific) successfully (Figures and ). Then, we proceeded to treat the right coronary artery 90% distal segment stenosis; for this, we used a right Judkins 3.5, 6F guiding catheter with horizontal mirror imaging, using a RAO view to mimic the LAO view; the anatomical right coronary artery was engaged easily using an opposite maneuver to the usual, with the tip of the catheter pointing leftward and rotated counterclockwise (instead of rotating clockwise), and then, we passed a Whisper 0.014 angioplasty guidewire and crossed the distal stenosis; predilatation was done with a 1.5 × 10 mm balloon (Apex, Boston Scientific), and then, a 2.5 × 12 mm zotarolimus-eluting stent (Resolute Integrity, Medtronic) was successfully implanted, obtaining excellent angiographic results and final TIMI grade 3 flow (Figures and ).
The patient had an excellent in-hospital follow-up, without any symptoms and complications; there was no rise in cardiac biomarkers and was discharged after 48 hrs. With life style modification and receiving coated aspirin 81 mg/d, clopidogrel 75 mg/d, and atorvastatin 80 mg/d, a 3-month follow-up showed no recurrent ischemia, and a treadmill stress test (positioning electrodes to the right side) was performed which was negative.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [69, 'years'], 'Suspicion History': 'Highly suspicious', 'Hypertension history': False, 'smoking': True, 'Diabetes mellitus': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'hypercholesterolemia': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 69 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 2 + 2 = 4.
The following risk factor(s) are present based on the patient's note: smoking, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 4 + 1 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 5.
Based on the patient's data, the HEART Score is 5."
4240,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6011436-1,Extracted,"A 32-year-old woman with no significant medical and family history presented to the local emergency department (ED) referring malaise, anxiety, dizziness and nausea. Symptoms like chest pain, syncope, palpitations or fever were denied.
The initial physical examination at triage revealed a Glasgow Coma Scale (GCS) of 15, a respiratory rate of 19 breaths/min, 100% oxygen saturation on room air, blood pressure of 112/70 mm Hg, pulse of 80 beats/min and had a normal tympanic temperature. Also, the blood sugar was 147 mg/dL.
After observation, the patient had an episode of presyncope followed by agitation and vomiting. At this point, the patient was pale and sweaty with a GCS of 11 (eye opening: 4; verbal response: 2; motor response: 5), blood pressure of 115/75 mm Hg, tachycardia (160 beats/min) and 99% oxygen saturation on room air. Her pupils were equally round and reactive to light, and no muscle weakness or sensory deficits were found.
The ECG showed a polymorphic broad QRS tachycardia and the arterial blood gas revealed metabolic acidaemia with severe hypokalemia. The dysrhythmia was successfully treated with 5 mg of propranolol intravenous in total. Acid–base and hydroelectrolytic disorders were also corrected.
After stabilisation, the patient informed the ED’s physician that when she was preparing the preworkout supplement, used the same dosage of the proteic supplement for anhydrous caffeine, instead of 1 dose of 300 mg (6 mg/kg) of anhydrous caffeine, the patient consumed a total of 5000 mg (89 mg/kg), 30 min before going to the ED. The patient switched the dose dispensers shown in .
The patient’s body weight was 56 kg. The patient also indicated that she occasionally drinks one espresso (60 mg of caffeine) and has never used alcohol or any recreational drugs.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [32, 'years'], 'Hypertension history': False, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': True, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit'}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 32 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: diabetes mellitus. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4241,18,HEART Score for Major Cardiac Events,risk,integer,usmle-600,Extracted,"A 65-year-old man is brought to the emergency department 30 minutes after the onset of acute chest pain. He has hypertension and asthma. Current medications include atorvastatin, lisinopril, and an albuterol inhaler. He appears pale and diaphoretic. His pulse is 114/min and blood pressure is 130/88 mm Hg. An ECG shows ST-segment depressions in leads II, III, and aVF. Laboratory studies show an increased serum troponin T concentration. The patient is treated for acute coronary syndrome and undergoes percutaneous transluminal coronary angioplasty. At the time of discharge, echocardiography shows a left ventricular ejection fraction of 58%.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [65, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': True, 'Electrocardiogram Test': 'Normal', 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False}",7,7,7,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 65 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 2 + 2 = 4.
The following risk factor(s) are present based on the patient's note: hypertension, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 4 + 1 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 5 + 2 = 7.
Based on the patient's data, the HEART Score is 7."
4242,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7218459-1,Extracted,"A 30-year-old female primary school teacher of African descent was referred to Jakaya Kikwete Cardiac Institute from a northern zone referral hospital (540 km away) for etiological determination of chest pain and expert management. She has never smoked cigarettes or used illicit drugs and denied a family history of heart disease. Her medical history was only significant for menorrhagia. She presented to us with a 7-day history of ongoing sharp central chest pain that was radiating to the neck and jaws and relieved temporarily by morphine. The pain woke the patient from sleep and was accompanied by shortness of breath, diaphoresis, and nausea without emesis. She was hospitalized at the upcountry hospital for the initial 3 days of chest pain and was prescribed acetylsalicylic acid 75 mg od (once a day), clopidogrel 75 mg od, atorvastatin 40 mg nocte (every night), and syrup morphine PRN (as needed). Cardiac biomarkers and echocardiography (ECHO) were unremarkable, but her initial ECG (done 7 days prior) showed a strain pattern ().
She had stable vitals (blood pressure 133/74 mm Hg, pulse rate 75 beats/min, respiratory rate 19 breaths/min, temperature 36.8°C, and body mass index 22 kg/m2), and her systemic examination was unremarkable. Nonetheless, a 12-lead ECG done at our center revealed deeply inverted T-waves on leads V2 through V4 (). A 2-dimensional ECHO showed anterior wall hypokinesia with preserved left ventricular (LV) systolic functions (ejection fraction 62%). Evaluation of valves and pericardium was unremarkable. Hematologic and biochemical tests were evident for a microcytic hypochromic anemia (hemoglobin 6.5 g/dL, mean corpuscular volume 73.2 fL, mean cell hemoglobin 21 fL, red cell distribution width 17.6%) otherwise normal. Cardiac biomarkers (troponin I and CK-MB) remained within acceptable limits. Furthermore, sickling test, glucose-6-phosphate-dehydrogenase deficiency, thrombophilia, and autoimmune (rheumatoid factor, antineutrophil cytoplasmic antibody, and antinuclear antibody) screenings revealed negative findings. Based on our extensive history, physical examination, and ECG features, we came up with a diagnosis of type B Wellens syndrome with impending anterior wall MI. Isosorbide mononitrate 10 mg bd (twice a day) and bisoprolol 5 mg od were added to the ongoing regime of acetylsalicylic acid, clopidogrel, and atorvastatin.
Due to the ongoing chest pain and pathognomonic ECG features, the patient was counseled and consented for an elective cardiac catheterization (on the 11th day since onset of chest pain), which revealed a nonthrombogenic severe subocclusive (>95%) mid-LAD stenosis with a TIMI I flow (). The left main, circumflex, and right coronary arteries were unremarkable. Subsequently, angioplasty was performed successfully with a resolute integrity stent, and TIMI III flow was achieved (). She was also transfused 3 units of packed red blood cells during hospitalization, and her control hemoglobin was 11.3 g/dL. During a brief coronary care unit stay, there was neither recurrence of chest pain nor hemodynamic instability; hence, the patient was transferred to the general cardiac ward in a fairly stable clinical state and was discharged after 13 days of hospitalization. Four weeks postdischarge, she was reviewed at our outpatient department, and although she was asymptomatic with an improved effort tolerance, a detailed ECHO revealed dyskinesia of the anterolateral wall with no evidence of LV aneurysm. Moreover, her ECG during follow-up was unremarkable (). A magnetic resonance imaging for myocardial perfusion test was ordered but was not done due to patient’s financial constraints.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [30, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'atherosclerotic disease': False}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 30 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4243,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7809680-1,Extracted,"A 71-year-old man came to the hospital in November 2019 with a palpable left inguinoscrotal mass and symptoms of intermittent left quadrant abdominal pain for more than 6 mo.
The patient had received total gastrectomy and chemotherapy in December 2016 for pT4aN2 gastric cancer. The histopathology disclosed mixed poorly differentiated adenocarcinoma with signet ring cell components. Chemotherapy regimens against the primary gastric cancer was oral TS-1 20 mg (gimeracil + oteracil + tegafur) from February 2017 to June 2018.
The patient had been in good health.
The patient denied any positive personal or family history.
The physical examination revealed a palpable, left inguinoscrotal mass with induration at the spermatic cord and epididymis. An abdominal examination showed no palpable mass nor tenderness.
Tumor biomarkers were: AFP, 2.5 ng/mL; prostate-specific antigen, 1.11 ng/mL; LDH 265 U/L; βHCG < 1 mIU/mL; CEA 3.95 ng/mL; and CA19-9, 16.6 U/mL.
Renal and testicular echography showed left hydronephrosis and a left peritesticular soft tissue lesion with blood flow. CT revealed a left scrotal mass (Figure ) and left mild hydronephrosis (Figure ). Left retrograde pyelography revealed multiple stenosis and narrowing points causing left hydronephrosis and hydroureter (Figure ).
Diagnostic ureteroscopy showed left lower ureter segmental narrowing without an intraluminal lesion. Scrotal exploration and biopsy of the indurated spermatic cord and epididymis disclosed metastatic poorly differentiated adenocarcinoma (Figure ). An immunohistochemical study showed nests of poorly differentiated adenocarcinoma diffusely and strongly positive for homeobox protein CDX2 (Figure ). The features of the tumor were consistent with metastatic adenocarcinoma of the primary gastric cancer.
Positron emission tomography with 2-deoxy-2-[fluorine-18]-fluoro-D-glucose integrated with computed tomography (18F-FDG PET/CT) from skull vertex to upper thighs was performed at 60 min after injection of 18F-FDG. The examination revealed a gastric stump recurrence, positive celiac lymph nodes, and distant metastases to the spine, ribs, sternum, pelvic bones, bilateral scapulae, pelvic cavity, left spermatic cord, and epididymis (Figure ).",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [71, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 71 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 0 + 2 = 2.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4244,18,HEART Score for Major Cardiac Events,risk,integer,pmc-3166914-1,Extracted,"A 59-year-old caucasian man was found by his wife collapsed in the bathroom after sexual intercourse. On arrival the rescue team found an unconscious patient with ventricular fibrillation. After single defibrillation and 15 minutes of cardiopulmonary resuscitation spontaneous circulation was restored. His wife reported that the patient has ingested Sildenafil (50 mg) 30 minutes before the cardiac arrest for the first time. Except from a vascular-type erectile dysfunction he had no previous medical history and no familial history of cardiovascular disease or sudden death. The patient did not take a regular medication. After admission in our hospital a 12-lead electrocardiogram showed no signs of significant repolarization abnormalities. There were increases in cardiac enzymes with a troponin I (TNI) of 5.57 ng/ml (reference range < 0.05 ng/ml), a creatinine-kinase (CK) of 3285 U/l (reference range < 180 U/l), a creatine kinase MB (CKMB) of 124 U/l (reference range < 12 U/l) and a CRP of 2.2 mg/dl (reference range < 0.5 mg/dl). 12 hours later TNI and CKMB had decreased to 2.34 U/l and 87 U/l and at 24 hours they had further decreased to 2.09 U/l and 78 U/l, respectively. Echocardiogram showed impaired left ventricular function, ejection fraction was 46 percent. A coronary arteriography (Figure ) and an angiographic CT scan (Figure ) were performed. The coronary arteriography revealed an atypical origin of the left coronary artery from the right aortic sinus as well as a distal stenosis of the right coronary artery. Coronary anomaly was confirmed by the angiographic CT scan which showed the interarterial course of the left coronary artery between the pulmonary trunk and the aorta. Due to these findings he was transferred to the cardiac surgery department and coronary artery bypass surgery was performed with the left mammary artery supplying the left anterior descending artery and two venous grafts supplying the ramus circumflexus and right coronary artery. A proximal ligation of the left anterior descending artery was not performed. After 6 months ventricular function had recovered, echocardiography showed an ejection fraction of 54 percent.
CAAs are a group of congenital disorders which rarely present with symptoms such as angina pectoris, dyspnoe or cardiac arrhythmias. Also in our patient the cardiac arrest was the first event and no other symptoms in the past have been observed. Before the event occurred the patient had ingested Sildenafil (50 mg), an oral phosphodiesterase type 5 (PDE5) inhibitor used for the treatment of erectile dysfunction. It has been demonstrated in several studies that the use of sildenafil is not associated with an increased risk for cardiovascular events in a cardiovascular healthy population []. However, Patients with known coronary artery disease using PDE5 inhinbitors are at risk of developing myocardial infarction after receiving sildenafil in combination with nitrates or calcium antagonists due to prolonged and exaggerated vasodilatation and hypotension []. In the present case, the combination of sildenafil-triggered vasodilatation and exercise maybe caused a coronary steal phenomenon following ischemia with lethal arrhythmias. Patients with coronary anomalies usually become symptomatic in their childhood or adolescence. The relatively late age of our patient might indicate that sildenafil as a trigger was necessary to induce a perfusion deficit. Another pathogenetic link in exercise related death in patients with CAAs is suggested to be the compression of the intraarterial coronary artery leading to ischemia in these patients []. Due to the high risk of sudden cardiac death in patients with an interarterial course of the aberrant coronary artery reinsertation of the coronary ostia is recommended. In case of additional coronary stenoses bypass surgery should be performed.
In patients with an extraarterial course of the aberrant coronary artery an increased risk of sudden cardiac death could not be observed, coronary interventions are not indicated.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [59, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Highly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'hypercholesterolemia': False, 'obesity': False, 'smoking': False}",6,6,6,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 59 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 3 + 1 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 4 + 2 = 6.
Based on the patient's data, the HEART Score is 6."
4245,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6939822-1,Extracted,"A 44-year-old woman was referred by her gastrointestinal surgeon to the emergency room (ER) because of multiple episodes of chest pain. She was, like her mother, known with ADPKD as well as polycystic liver disease, without (intracranial) aneurysms. Two months earlier, a liver transplantation had been performed because of dyspnoea caused by the liver cysts. She was under treatment with antirejection medication (tacrolimus, mycophenolate mofetil, and steroids that were tapered recently). She did not smoke and there were no other cardiovascular risk factors but stress. The chest pain started during sleep, radiated to the left arm and subsided spontaneously after 5 min. The electrocardiogram (ECG) in the ER showed a normal sinus rhythm without ST segment or T-wave abnormalities. Patient was afebrile, with a blood pressure of 137/74 mmHg and a regular pulse of 77 b.p.m. On auscultation heart sounds were normal and lungs were clear. There was no peripheral oedema and peripheral pulsations were normal. Chest X-ray was normal. Blood samples showed a chronic but stable kidney disease (eGFR 36 mL/min/1.73 m2), absence of inflammation or anaemia. High-sensitive troponin T-level was significantly elevated (53 pg/mL) but showed no significant evolution after 3 h. A transthoracic echocardiogram (TTE) demonstrated a non-dilated ventricle (end-diastolic diameter 41 mm) with mild septal hypertrophy (14 mm), normal regional contractility, a preserved left ventricular (LV) systolic function and absence of significant valvulopathy. A coronary angiography was performed and showed diffuse narrowing of the distal left anterior descending artery (LAD) with ‘stick insect’ aspect, compatible with a SCAD Type 2 with preserved distal flow (). The patient was admitted to the intensive cardiac care unit for further observation and treatment. Dual antiplatelet therapy (DAPT) with clopidogrel and aspirin was started, as well as pravastatin and a low dose of bisoprolol. During the following days, the troponin level steadily rose with stable kidney function. Three days later, chest pain redeveloped for which IV nitrates were associated but these were quickly interrupted because of headache. The ECG was progressively abnormal with diffuse biphasic T waves in the anterior leads (V2–5). A repeat TTE now showed apicoseptal hypokinesia. A new coronary angiography showed a more proximal and prominent dissection of the mid and distal LAD (75–95% stenosis), with preserved distal flow (). Transdermal nitrates were associated after which the pain subsided. Clopidogrel was interrupted because of the progression under DAPT and a small dose of angiotensin-converting-enzyme (ACE)-inhibition was initiated because of the depressed LV function. Prolonged monitoring revealed a single episode of non-sustained ventricular tachycardia. The patient remained asymptomatic and the rest of the stay was uneventful. She was discharged after 10 days and was still doing well at follow-up after 1 month with cardiac enzymes that returned to baseline levels. Cardiac rehabilitation, including psychological support, was initiated.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [44, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': True, 'Initial troponin': 'greater than three times normal limit', 'hypercholesterolemia': False, 'obesity': False, 'atherosclerotic disease': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 44 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: family with cvd. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 3 + 2 = 5.
Based on the patient's data, the HEART Score is 5."
4246,18,HEART Score for Major Cardiac Events,risk,integer,usmle-10067,Extracted,"A 57-year-old man is brought to the emergency department after having chest pain for the last hour. He rates his pain as 8/10, dull in character, and says it is associated with sweating and shortness of breath. He has a history of diabetes and hypercholesterolemia. His current medication list includes amlodipine, aspirin, atorvastatin, insulin, and esomeprazole. He has smoked 2 packs of cigarettes per day for the past 25 years. His blood pressure is 98/66 mm Hg, pulse is 110/min, oxygen saturation is 94% on room air, and BMI is 31.8 kg/m2. His lungs are clear to auscultation. An electrocardiogram (ECG) is shown below. The patient is given 325 mg of oral aspirin and sublingual nitroglycerin.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [57, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': True, 'hypercholesterolemia': True, 'smoking': True, 'obesity': True, 'Electrocardiogram Test': 'Normal', 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit'}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 57 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, obesity, smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 4 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 3 + 2 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 5.
Based on the patient's data, the HEART Score is 5."
4247,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5516357-1,Extracted,"A 70-year-old Asian man with ESRD due to nephrosclerosis complained of chest discomfort during exercise and was referred to our hospital. He had been receiving hemodialysis for 20 years, and had a past medical history of hypertension, hyperuricemia, and reflux esophagitis. He had no history of thromboembolism or endocarditis. He smokes one pack of cigarettes per day, and drinks socially.
He had no significant social and environmental history. His medication list included amlodipine, allopurinol, ferric citrate hydrate, and lansoprazole. He had no family history of cardiovascular diseases.
He was afebrile, with a blood pressure of 114/50 mmHg and a regular pulse rate of 61 beats per minute. His oxygen saturation was 96% on ambient air. There was no evidence of lung rales, cardiac murmur, and abdominal tenderness. His neurological examinations were unremarkable. Blood investigations showed: hemoglobin 14.0 mg/dl, white blood cells 4700/mm3, and platelets 134,000/mm3. His liver and renal function tests revealed total bilirubin 0.4 mg/dl, aspartate aminotransferase 24 IU/l, alanine aminotransferase 34 IU/l, blood urea nitrogen 54.2 mg/dl, and serum creatinine 11.1 mg/dL. His C-reactive protein was 0.16 mg/dl. His serum electrolyte tests were within normal limits, including calcium and inorganic phosphorus. In addition, his brain natriuretic peptide was raised at 605.1 pg/dl. His blood cultures were negative.
A chest X-ray showed mild cardiomegaly without pulmonary congestion (Fig. ). An electrocardiogram suggested left ventricular hypertrophy with nonspecific ST-T wave changes (Fig. ). A transthoracic echocardiogram revealed MAC and a highly mobile mass (8 × 6 mm) attached to the ventricular side of the posterior mitral valve leaflet (Fig. ). The echogenicity of the mass was similar to MAC. The mitral valve was mildly thickened with mild mitral stenosis. Left ventricular systolic function was normal. Cardiac computed tomography demonstrated a calcified cardiac mass in the mitral annulus with heavy MAC (Fig. ). As the mass was highly mobile, suggesting a high risk of embolization, he underwent surgical resection of the mass. Intraoperative findings demonstrated a severely calcified mitral annulus and attachment of the calcific mass to the P2 segment of the mitral valve. Surgical resection was performed successfully.
Macroscopic findings of the resected mass showed a yellowish colored and partially calcified mass (7 mm in diameter; Fig. ). A histopathological examination revealed multiple nodular amorphous calcifications and fibrous connective tissue. There were no identifiable myxoma or malignancy cells (Fig. ). Consequently, the diagnosis of CAT was confirmed. He recovered uneventfully and was discharged without any complications.
No evidence of tumor recurrence was detected after the surgery, and he is doing well after 6 months of follow-up.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [70, 'years'], 'Hypertension history': True, 'Suspicion History': 'Moderately suspicious', 'smoking': True, 'Diabetes mellitus': False, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 70 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 1 + 2 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 3 + 1 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 4.
Based on the patient's data, the HEART Score is 4."
4248,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4323914-1,Extracted,"A 54-year-old man was detected to have hyperlipidemia and was prescribed atorvastatin 20 mg and a multivitamin capsule 1 month prior to initial consultation and and received no other drug. He was detected to have diabetes mellitus 6 months ago, but received no medication. He felt unwell after taking atorvastatin and on evaluation had normal renal function (blood urea: 38 mg/dl, serum creatinine [SCr]: 1.1 mg/dl). Since he continued to feel tired, he had a review 3 weeks later and was detected to have azotemia (blood urea: 54 mg/dl, SCr: 1.9 mg/dl) and was referred to our unit. He complained of tiredness, but did not have fever, skin rash, muscle weakness or tenderness. Blood pressure was 105/80 mm Hg and pulse rate was 75/min. Clinical examination was unremarkable. Urine examination showed no albuminuria and no sediment on microscopy. Serum creatine kinase (CK) was normal (70 U/L). He denied taking any other drug, including indigenous or over the counter medications, other than atorvastatin and multivitamin capsule. He was thought to have AKI due to atorvastatin and it was discontinued. After 1 week SCr rose to 2.4 mg/dl and he underwent renal biopsy, which showed nine glomeruli, of which one showed periglomerular fibrosis. Moderate interstitial round cell infiltrates [] were seen along with few eosinophils. Mild hyaline arteriosclerosis was seen. Immunoflurescence study showed minimal mesangial deposits of immunoglobulin M and was negative for other immunoglobulins and C3. The renal biopsy was consistent with acute interstitial nephritis.
He was started on oral prednisolone 1 mg/kg/day for 2 weeks and then slowly tapered the dose over 2 months and stopped. The response to corticosteroid was good and SCr improved to 1.3 mg/dl at the end of 2 months []. He was advised not to take statins in the future.
He was admitted 6 months after the initial presentation with acute myocardial infarction (AMI) and underwent primary percutaneous transluminal coronary angioplasty (PTCA) and stenting. He was given atorvastatin 40 mg post PTCA, but was replaced with rosuvastatin 10 mg after 2 days in view of previous allergic interstitial nephritis attributed to atorvastatin. He was explained about the possible cross reactivity with atorvastatin and SCr was monitored on weekly basis. SCr was 1.4 mg/dl at the initiation of rosuvastatin therapy and gradually increased to a peak of 1.8 mg/dl at 4 weeks []. Serum CK was normal (55 U/L) and there was no evidence of any other etiologic factor to account for AKI during this period. After much deliberation, rosuvastatin was stopped and he was followed closely. The renal biopsy was not repeated since antiplatelet drugs could not be stopped so early after PTCA and steroid were not given in view of possible worsening of dyslipidemia and hyperglycemia. SCr returned to baseline value spontaneously over next 2 months and remained stable over next 12 months.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': True, 'Diabetes mellitus': True, 'atherosclerotic disease': True, 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 54 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: diabetes mellitus, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 3 + 1 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 4.
Based on the patient's data, the HEART Score is 4."
4249,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4357046-1,Extracted,"A 33-year-old Somalian man initially presented with loss of neurological function of the left arm, hazy vision, and headache. A few weeks prior to this episode he had had an episode during which he experienced chest pain, nausea, and vomiting. Our patient does not drink alcohol. He smokes tobacco and chews two bundles of khat a week for more than 10 years. No other risk factors for atherosclerosis at young age were present. The blood levels of cholesterol and triglycerides were within normal range. Family history was negative for inherited thrombophilia. His ECG on admission showed a Q wave in V1 and V2 and 2 mm ST-elevations in V1, V2, and V3 and a terminal negative T wave in I, aVL, V2, V3, and V4, consistent with a recent, evolving anterior infarction (). On admission the highly sensitive troponin T was 18 ng/L (normal value < 14 ng/L). The transthoracic echocardiogram showed a poor left ventricular function with akinesia of the anterior wall and left ventricular dilatation. No thrombus was seen.
The noncontrast enhanced CT of the brain showed ischemia in the right middle cerebral artery vascular territory. The CTA of the carotids showed no stenosis or venous thrombosis.
An MRI of the brain was performed to rule out vasculitis or other vascular malformations. The MRI showed recent ischemia in the vascular territory of the posterior division of the right middle cerebral artery (Figures –).
Coronary angiography showed a 70% stenosis with haziness of the proximal left anterior descending artery (LAD) (), which disappeared after intracoronary nitroglycerine injection (). The other coronary arteries were normal.
MRI of the heart showed a poor left ventricular function, with a calculated ejection fraction of 29%. The left ventricle was dilated, with an end diastolic left ventricular diameter of 63 mm (normal value < 55 mm). There was thinning of the myocardium in the apex and the midcavitary anteroseptal, anterior, and anterolateral segments. There was hypo- to akinesia of these areas with subendocardial and transmural delayed enhancement (Figures and ) in these regions. No thrombi were seen. The signs on the MRI are consistent with infarction in the vascular territory of the LAD.
Screening for thrombophilia (lupus anticoagulants, cardiolipin antibodies, factor V Leiden, and antithrombin III deficiency) was negative. A presumptive diagnosis was made of khat induced coronary spasm with myocardial infarction and khat induced cerebral infarction. Due to hypotension treatment with calcium blocking agents was not possible. He was advised to refrain from khat use. Furthermore he underwent a percutaneous coronary intervention of the proximal LAD with stent placement to prevent stenosis in case of possible future coronary spasm. His left ventricular function remained poor, which was a reason for ICD implantation for primary prevention. During admission all neurological complaints resolved.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [33, 'years'], 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': False, 'smoking': True, 'atherosclerotic disease': True, 'Initial troponin': 'between the normal limit or up to three times the normal limit', 'Electrocardiogram Test': 'Normal', 'Hypertension history': False, 'Diabetes mellitus': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 33 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: smoking, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'between the normal limit or up to three times the normal limit'. Based on the HEART Score criteria, 1 point is added for 'initial troponin', increasing the current total to 3 + 1 = 4.
Based on the patient's data, the HEART Score is 4."
4250,18,HEART Score for Major Cardiac Events,risk,integer,usmle-6100,Extracted,"A 33-year-old female with no significant medical history presents to the emergency department complaining of shortness of breath and palpitations. The patient was in her usual state of health until 30 minutes ago when she bent over to lift her son and she suddenly felt like “my heart began to beat out of my chest.” She denies losing consciousness or any prior episodes of palpitations or syncope. She takes a daily multivitamin and oral contraceptive pill. On presentation to the ED her temperature is 98.6°F (37°C), blood pressure is 124/86 mmHg, pulse is 160/min, and respirations are 16/min. Physical exam is unremarkable. Her EKG is shown in Figure A. Carotid sinus massage and Valsalva maneuvers are attempted with no improvement in symptoms.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'parent or sibling with Cardiovascular disease before age 65': False, 'Hypertension history': False, 'smoking': False, 'Diabetes mellitus': False, 'age': [33, 'years'], 'Electrocardiogram Test': 'Normal', 'atherosclerotic disease': False, 'hypercholesterolemia': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 33 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4251,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5596476-1,Extracted,"A 41-year old male patient with an oligosymptomatic wide complex tachycardia was referred to the emergency department. The tachycardia was terminated by a 360 J DC-shock after unsuccessful administration of adenosine prehospitally. ECG documentation of the tachycardia was not available. The patient had no history of relevant comorbidities. Physical exam was unremarkable, the patient did not take any medication. Similar episodes with palpitations over several minutes and one syncope in the past were reported. Initial 12-lead ECG showed a shortened PR interval with prominent delta waves in I, II, aVL, V4-V6 and R/S transition at V4/V5 suggesting a right midseptal pathway (Fig. ). Diagnosis of WPW syndrome was established. Non-invasive cardiologic work-up did not show significant pathologies.
AVRT was suspected as the underlying mechanism of arrhythmia. Due to recurrent symptomatic paroxysmal tachycardias an electrophysiological study (EPS) was scheduled. An accessory pathway with bidirectional conduction in right-midseptal location was diagnosed and successfully ablated. After ablation no tachycardia could be induced by atrial and ventricular stimulation at rest and following isoprenaline infusion. The patient was discharged the next day.
Five months later the patient was admitted to the emergency department complaining about palpitations and dyspnea since the evening before. ECG showed a wide complex tachycardia (168 beats per minute (bpm); QRS duration 130 ms) with right bundle branch block (RBBB) morphology, left axis deviation and AV (atrioventricular) dissociation (Fig. ). Diagnosis of an ILVT was made. Following administration of Verapamil (cumulative: 240 mg p.o. and 40 mg i.v.) tachycardia slowed down and converted into sinus rhythm. After hospital admission the patient remained in sinus rhythm on Verapamil (120 mg sustained release b.i.d.) and was discharged 1 day later. EPS and ablation of ILVT was recommended. At scheduled ablation the patient presented the ECG of the index-tachycardia, which was terminated by DC-shock. This ECG showed the ILVT rather than the initially suspected AVRT.
In the EPS ILVT of the common type was induced by atrial burst-stimulation and radiofrequency ablation of the ILVT was performed. The patient showed normal AV conduction without signs of pre-excitation. Figure displayed ECG after ablation of WPW syndrome and ILVT. There were no palpitations or symptoms during a follow up of 18 months.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [41, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'Diabetes mellitus': False, 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 41 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4252,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5288504-1,Extracted,"A 27-year-old man with no previous medical history presented to the emergency department with 1 hour of acute onset of left-sided chest pain, shortness of breath, and diaphoresis. He reported active tobacco smoking but denied other drug use. He used nonsteroidal anti-inflammatory medications for back pain. There was a family history of coronary artery disease in an uncle who underwent coronary revascularization. He had also recently been using energy drinks (Rockstar, Rockstar, Inc., Las Vegas, NV), sometimes 4-5 beverages in a 12-hour period, in order to stay awake during his evening work shift in a warehouse. He denied any previous episodes of chest pain, exertional symptoms, previous thromboembolic disease, nausea or vomiting, or syncope. On examination, his blood pressure was elevated at 155/100, pulse was 74 beats per minute, respiratory rate was 18 breaths per minute, and oxygen saturation was 100% on 2 liters of supplemental oxygen. His cardiac examination was normal, including a normal first and second heart sound and no appreciable murmur or pericardial friction rub. His laboratory values were notable for hemoglobin of 15.4 g/dL, white blood cell count of 5.8, platelet count 254,000, normal blood chemistry, and an elevated troponin T of 0.41 (normal reference range < 0.01 ng/mL) and CK-MB of 123.4 (normal reference range < 7.8 ng/mL). His electrocardiogram demonstrated ST-segment elevations in leads V2–V6, I, and aVL along with reciprocal changes in leads III and aVF, concerning for an acute anterior ST-segment elevation myocardial infarction (STEMI) (). He was treated with sublingual nitroglycerin, unfractionated heparin, and aspirin in the emergency department which improved but did not completely alleviate his symptoms and brought urgently to the cardiac catheterization laboratory. Coronary angiography was performed from a radial approach and symptom relief was documented after intra-arterial injection of a radial antispasmodic cocktail (i.e., 200 mcg nitroglycerin, 2.5 mg verapamil, and 5,000 units of heparin). Coronary angiography showed normal coronary arteries with TIMI III flow without any angiographic evidence of stenosis, dissection, embolism, or plaque rupture (). A repeat electrocardiogram after his coronary angiogram demonstrated normalization of his ST-segment abnormalities (). An echocardiogram was performed and demonstrated significant akinesis of the left ventricular apex (Figures and ), findings that were confirmed with abnormal longitudinal strain in the apical segments (). Cardiac magnetic resonance imaging (cMRI) also documented akinesis in the left ventricular apex, similar to the wall motion abnormalities present on echocardiography. In addition, cMRI confirmed areas of abnormal delayed gadolinium enhancement in both a patchy and full-thickness configuration along the mid and distal anterior wall and the mid septum (Figures and ). A formal toxicology examination was not requested given that the patient rapidly recovered after his initial presentation. The absence of the toxicology leaves the question as to whether other potential substances could have been associated with the acute cardiac presentation. A urine drug screen at the time of admission was negative for cocaine, amphetamines, and barbiturates. The patient was treated with long acting nitrates and calcium channel blocker, though he continued to have occasional episodes of chest discomfort. Given the concern of recurrent spasm and given that the presumed etiology of his ST-elevation myocardial infarction was coronary vasospasm, he was referred for repeat coronary angiography, including a functional protocol to test the response of the coronary endothelium and the coronary microcirculation. His coronary angiogram was normal, with no evidence of atherosclerosis or vasospasm. Intracoronary adenosine was administered at a dose of 60 mcg and coronary flow reserve (CFR) was normal at 3.0 using intracoronary Doppler study in the left anterior descending (LAD) artery. These findings suggested normal microcirculatory function. Subsequently, increasing concentrations of intracoronary acetylcholine were administered with no significant change in the Doppler-derived average peak velocity, CFR, symptoms, angiographic appearance of the LAD, or electrocardiographic parameters, all consistent with normal endothelial function. Based on these results, he was not felt to have any functional coronary or endothelial abnormalities. He was advised to abstain from any further use of energy drinks.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'parent or sibling with Cardiovascular disease before age 65': False, 'Suspicion History': 'Slightly suspicious', 'Hypertension history': True, 'smoking': True, 'Diabetes mellitus': False, 'age': [27, 'years'], 'atherosclerotic disease': False, 'Initial troponin': 'between the normal limit or up to three times the normal limit', 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 27 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: hypertension, smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'between the normal limit or up to three times the normal limit'. Based on the HEART Score criteria, 1 point is added for 'initial troponin', increasing the current total to 1 + 1 = 2.
Based on the patient's data, the HEART Score is 2."
4253,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4058489-1,Extracted,"A 43 year old man without cardiovascular risk factors, other chronic diseases, and history of trauma had a history of 20 days of progressive dyspnea on exertion after two episodes of flu-like symptoms, such as fever and chill. He was hospitalized in another center for more evaluation and was discharged with diagnosis of idiopathic moderate pericardial effusion due to viral infection on ibuprofen. He came to our center after 2 days because of exacerbated dyspnea, NYHA III–IV, orthopnea, and palpitation. Physical examinations showed heart rate = 114 bpm, blood pressure = 110 / 60 mmHg, distended jugular veins, and holodiastolic murmur along the left parasternal line without thrill. In addition, the electrocardiogram showed sinus tachycardia, left axis deviation, right bundle branch block, and Q wave in III and aVF leads. Besides, normal lung vascularity and cardiomegaly (round shaped heart) were observed in the chest X-ray. In the first lab data, WBC count (12510 / µL), Hgb (8.9 g / dL), ESR (60 mm / hr), and CRP (0.94 mg / L) were abnormal.
Moreover, Transthorcic Echocardiography (TTE) in the emergency department documented mild left ventricular enlargement with normal ejection fraction (55%), normal right ventricle size, mild right ventricular dysfunction, mild mitral regurgitation, moderate to severe aortic regurgitation, mild tricuspid regurgitation, severe pericardial effusion in favor of tamponade, and normal ascending aorta and aortic arch without visible dissecting flap in the aorta. Therefore, the patient was referred to the operating room for emergent pericardiocentesis. While operation, the surgeon was encountered with hemopericardium and pericardium was full of blood and fresh clots. Thus, he was suspected of accompanied missed aortic dissection with hemopericardium. After some clot removal, the patient was admitted in the ICU for ruling out the aortic dissection.
After few hours, multislice (256 slices) CT angiography was performed, but aortic dissection or intra mural hematoma was not seen, and ascending, arch, and descending parts of the aorta and coronary arteries were normal. The only abnormal finding was severe pericardial effusion and dilated deformed RCS (). Because of high suspicion of the cardiac surgeon to pathology of the aorta, TTE and Transesophageal Echocardiography (TEE) were repeated. Echocardiography findings showed a localized dissection in the right aortic sinus, resulting in false lumen, from which the right coronary artery seemed to originate. The findings also revealed ruptured right coronary-nonocoronary commissure and that the false lumen had perforated to the left ventricular outflow tract with 7mm orifice. This rupture had, in turn, resulted in severe eccentric aortic regurgitation and mild to moderate central aortic regurgitation. Severely thickened, concentrated, and semiliquid pericardial effusion was also visible ().
After echocardiography, the patient was prepared for aortic repair surgery. The procedure was done via median sternotomy with cardiopulmonary bypass. The aorta was cross clamped. A classic windsock tract was seen arising from the RCS protruding into the pericardial sac. However, the other sinuses were normal. The RCS was ruptured into the pericardial space. Additionally, the base of the right coronary cusp avulsed from aortic annulus and the cusp was flittering in the aortic root. The orifice of the right coronary artery was not compromised. Pericardial sac was full of fresh clot. The opening of the aneurysm (2 * 4 mm) was resected by a small windsock and was closed using a pericardial patch from the aortic side and a 0.6 mm Gortex patch from outside. Moreover, the aortic valve was replaced by a mechanical aortic valve because of repair impossibility. Cardiopulmonary bypass time was 130 min and aortic clamping time lasted for 93 min. Sternum was closed immediately after the surgery and the patient had a normal recovery.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [43, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 43 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4254,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8491024-1,Extracted,"A 54-year-old male patient without relevant medical history was referred to the emergency department (ED) due to dyspnoea with an oxygen saturation of 85%, tachypnoea, and tachycardia. He reported a general fatigue, increased stress at work as a salesman, a single episode of angina, and a flight journey of 1.25 h 7 days prior to admission. The electrocardiogram (ECG) showed new T-wave inversions in the anterior leads (V1–V5). Laboratory analysis indicated global respiratory insufficiency, troponinemia (high sensitive troponin T of 77.3 ng/L, cut-off <14.0 ng/L), elevation of the N-terminal fragment of pro-brain natriuretic peptide (NT-proBNP), and D-Dimer. Consecutive thoracic computer tomography (CT) revealed the presence of subsegmental PE, but no pathological masses. Aetiological clarification revealed multiple DVT and elevated factor VIII in thrombophilia screening.
For cardiac assessment and additional clarification of newly observed T negativities, TTE showed a left ventricular ejection fraction of 50%, with hypokinesia, but no signs of intraventricular masses. Coronary angiography showed normal coronary arteries.
To clarify ECG and laboratory abnormalities and considering also inflammatory causes and myocarditis as aetiology, we conducted a CMR, which did not show any Gadolinium enhancement nor oedema or other abnormalities in the myocardium. As an incidental finding, a partially fixed and partially floating mass measuring 32 mm × 11 mm () at the lateral wall of the right ventricle was detected. It showed hyperintense characteristics in T1w and T2w compared to the myocardium, absent mass perfusion at first-pass perfusion and no uptake of contrast with homogeneous signal suppression within the mass at EGE and LGE (), thus, according to the criteria of standardized CMR tissue characterization, indicating thrombotic nature of the mass., Hyperintense appearance of this thrombus in T1w and T2w sequences indicated its recent character.
Considering the stable cardiopulmonary condition and morphology of the thrombus, we waived surgical embolectomy, thrombolysis or percutaneous retrieval, and continued anticoagulation instead. Follow-up CMR after 3 months showed complete resolution of the thrombus.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 54 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 3.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 3 + 2 = 5.
Based on the patient's data, the HEART Score is 5."
4255,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7085172-1,Extracted,"A 49 year-old Caucasian woman with psoriasis, psoriatic arthritis, multivessel coronary artery disease, hypertension, subclinical hypothyroidism, and diabetes mellitus presented with bilateral lower extremity weakness and severe anemia. Regarding her history of psoriasis, she initially developed diffuse psoriatic plaques and axial psoriatic arthritis at age 19. Her first severe psoriasis flare occurred at age 29. Chart review did not reveal recorded Psoriasis Area and Severity Index (PASI) scores but there was documentation of erythema and pustular psoriasis measured over 70% of her body surface area with elevated white blood cell count. Despite treatment with prednisone and acitretin, after 1 year she developed severe cutaneous flares of pustular psoriasis measuring up to 90% of total body surface area with spared regions in her legs, necessitating multiple hospitalizations. Her treatment was escalated to Geockerman therapy, methotrexate, and topical steroids, in addition to prednisone and acitretin. In subsequent years, her chronic psoriatic skin manifestations involved roughly 30% of her total body surface area, meeting criteria for severe psoriasis, and these skin manifestations were managed primarily with topical steroids. Plain films ultimately revealed active inflammatory spondylitis. Despite recommendations to start disease modifying therapy, the patient declined further treatment.
Six years prior to the most recent presentation, the patient was diagnosed with metabolic syndrome. Risk factors measured at the time of diagnosis included a peak hemoglobin A1c level of 11.6%, body mass index of 36, triglycerides of 310, high density lipoprotein (HDL) of 34, and systolic blood pressures routinely measured between 140 and 160. For her modifiable risk factors of diabetes, dyslipidemia, and hypertension, she was prescribed insulin, statins, and antihypertensive agents, respectively. Her family history was notable for ischemic stroke in her mother though of unknown etiology and age. There were no known inflammatory disorders in the family. Three months prior to the most recent presentation, the patient was hospitalized for a non-ST elevation myocardial infarction (NSTEMI). Cardiac catheterization revealed severe right coronary artery (RCA) disease and in-stent thrombosis of a pre-existing stent within the left circumflex artery placed 6 years prior. She underwent re-stenting for her left circumflex artery and RCA and was subsequently treated with a dual antiplatelet therapy regimen with aspirin and clopidogrel.
Subsequently, she presented with subacute bilateral lower extremity weakness and confusion. Her brain MRI revealed acute bilateral watershed infarcts, in addition to subacute left parietal and frontal gyrus infarcts. CT angiography of the head and neck revealed diffuse atherosclerotic plaques in the aortic arch and carotid bulbs, occlusion of the left internal carotid artery (ICA), and narrowing of the bilateral M1 segments of the middle cerebral artery (MCA). (Fig. a-c). There was reconstitution of flow in the left cavernous and supraclinoid segments of the ICA via an intact Circle of Willis. In addition to the bilateral MCA narrowing, there was mild narrowing of the right carotid artery and a single diminutive A1 segment which perfused bilateral anterior cerebral arteries (ACA) vessels.
There were no known preceding hemodynamic changes or systemic illnesses. Possible etiologies of her multifocal infarcts included severe atherosclerosis and related artery-artery thromboembolic events, cardioembolic events, hypercoagulable state, infection, or vasculitis. Cardiac rhythm telemetry did not reveal atrial fibrillation. Transthoracic echocardiogram revealed normal left ventricular function, normal left and right atrial size, no thrombus, and no intra- or extra-cardiac shunt. Subsequent transesophageal echocardiogram (TEE) again did not reveal thrombus or valvular lesions. The TEE also demonstrated atheromatous plaque in the proximal descending aorta greater than 4 mm in thickness. Laboratory studies included hemoglobin (Hg) of 4.2 g/dL, an elevated erythrocyte sedimentation rate > 100 mm/hr. (normal 0–15 mm/hr) and lipoprotein (a) 133 nmol/L (normal < 75 nmol/L) but were otherwise unrevealing (Table ). The cerebral spinal fluid (CSF) did not have infectious or inflammatory properties. Workup of anemia was consistent with alpha thalassemia and severe iron deficiency, also supported by peripheral blood smear.
Despite aggressive medical management, the patient clinically deteriorated. Repeat imaging revealed marked interval infarct progression involving multiple vascular territories (Fig. d). She underwent a left-sided decompressive hemicraniectomy as a life sustaining maneuver, and concomitant brain biopsy did not demonstrate evidence of vasculitis or infection. Clinical course was further complicated by sepsis, renal failure, and an acute generalized exanthematous pustulosis drug reaction to iodine contrast. In accordance with the patient’s prior wishes, she was transitioned to comfort-focused care and her family agreed to an autopsy.
The autopsy revealed eccentric, firm, yellow plaques involving all proximal intracranial vessels, consistent with severe atherosclerosis. There was an occlusive thrombus of the right ACA as well as diffuse arteriolar microthrombi. Elements of acute and chronic ischemic changes were seen on histology, including extensive ischemic neuronal necrosis. Diffuse, severe atherosclerosis was determined to be the cause of fatal burden of ischemic stroke (Fig. ).",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [49, 'years'], 'Hypertension history': True, 'Diabetes mellitus': True, 'obesity': True, 'smoking': False, 'atherosclerotic disease': True, 'Suspicion History': 'Highly suspicious', 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 49 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, obesity, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: smoking, family with cvd. The following risk factor(s) are missing from the patient's data: smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 4 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 3 + 2 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 5.
Based on the patient's data, the HEART Score is 5."
4256,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8263221-1,Extracted,"The patient was a 37-year-old woman, G2P1, with an unremarkable family history. She had been diagnosed with bronchial asthma by her family doctor at the age of 33 years. The use of steroid inhalation therapy did not appear to impact her condition []. Her previous pregnancy had resulted in an emergency cesarean delivery at 33 weeks of gestation due to severe hypertensive disorders of pregnancy (HDP) and fetal growth restriction (FGR). She became pregnant for the second time and was referred to our hospital owing to her previous birth history. Her estimated due date was confirmed from the CRL value during the first trimester. Her pregnancy was uneventful; however, she developed fever and cough at 26 weeks of gestation and was subsequently diagnosed with sinusitis due to deteriorated bronchial asthma. She was admitted to the hospital under the care of the respiratory team and was administered ceftriaxone. However, despite administration of antibiotics, the wet cough associated with asthma persisted. She suffered from pneumonia at 28 weeks of gestation, and atelectasis was detected in the left lower lobe using a chest radiograph. Although her symptoms began to improve, bronchoscopy was performed at 34 weeks of gestation due to recurrent pneumonia. Bronchoscopy showed a tumor with a smooth surface measuring approximately 1.5 cm in the left main lung bronchus. The tumor obstructed nearly 100% of the trachea () []. Further enlargement of the mass would have led to complete tracheal obstruction, suggesting a risk of sudden left lung atelectasis and maternal hypoxia; therefore, early medical intervention was necessary. Additionally, her blood pressure was elevated at 32 weeks of gestation and fetal growth was restricted at -2.0 SD of normal fetal growth, so that she was diagnosed with preeclampsia (PE-EO). Following counseling with the patient, her family, and respiratory medicine doctors, a bronchoscopic tumor resection was planned following the delivery of the baby. A cesarean section was performed at 34 weeks of gestation due to previous cesarean delivery. She delivered a female infant weighing 1322 g, with Apgar score of 8 and 9 points at 1 minute and 9 points at 5 minutes, respectively. The pH of umbilical artery blood gas was 7.321. A chest CT taken after delivery revealed a bronchial tumor in the left main bronchus without invasion to surrounding organs (), and the patient underwent rigid endoscopic bronchial tumor resection 7 days after the cesarean section () []. The histological type could not be identified at this point, and left lung atelectasis developed due to postoperative inflammatory changes. CT examination 4 weeks after the endoscopic resection confirmed relapse of bronchial tumor. Owing to obstruction by the recurrent bronchial tumor and to rule out the possibility of malignancy, left main lung bronchial resection and bronchoplasty were performed 6 weeks after the endoscopic resection. The pathological diagnosis of the resected specimen was a low-grade mucoepidermoid carcinoma (). No postoperative adjuvant treatment was needed, and her postoperative course was uneventful. There was no recurrence evident 18 months later.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [37, 'years'], 'Hypertension history': True, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 37 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4257,18,HEART Score for Major Cardiac Events,risk,integer,usmle-6420,Extracted,"A 35-year-old man presents to the physician’s clinic due to episodic chest pain over the last couple of months. He is currently pain-free. His chest pain occurs soon after he starts to exercise, and it is rapidly relieved by rest. He recently started training for a marathon after a decade of a fairly sedentary lifestyle. He was a competitive runner during his college years, but he has only had occasional exercise since then. He is concerned that he might be developing some heart disease. He has no prior medical issues and takes no medications. The family history is significant for hypertension and myocardial infarction in his father. His vital signs include: pulse 74/min, respirations 10/min, and blood pressure 120/74 mm Hg. The ECG test is normal. The physician orders an exercise tolerance test that has to be stopped after 5 minutes due to the onset of chest pain.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [35, 'years'], 'Hypertension history': False, 'Suspicion History': 'Moderately suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': True, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 35 years old. The patient's age is less than 45 years and so keep the current total at 1.
The following risk factor(s) are present based on the patient's note: family with cvd. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4258,18,HEART Score for Major Cardiac Events,risk,integer,pmc-2572041-1,Extracted,"A 71 year-old woman with a history of depression, refractory to medical management, presented with a major depressive episode for electroconvulsive therapy (ECT).
She had an uneventful ECT series four years prior, consisting of approximately 10 sessions. Her past medical history was significant only for hypertension. Her medications included daily quetiapine 300 mg, nortriptyline 25 mg, metoprolol succinate 100 mg, amlodipine 5 mg, and ativan 0.5 mg. She was also taking a four-day course of cefuroxime for a urinary tract infection. She had no allergies, and no family history of heart disease. Her electrocardiogram one day prior to ECT revealed normal sinus rhythm, at 97 beats per minute, with no ST or T abnormalities, or Q waves.
Anesthesia was induced with 50 mg of methohexitol, and 50 mg of succinylcholine. After unilateral ECT was delivered to the right side of the head, a generalized seizure was initiated. The patient remained hemodynamically stable, resumed spontaneous respirations, and emerged rapidly.
Three to four hours following the procedure she complained of chest pain. Her ECG revealed T wave flattening in AVL, and poor precordial R wave progression. A troponin level performed at that time was 3.28 ng/mL. Cardiac catheterization revealed non-obstructive coronary artery disease. Echocardiography demonstrated LV dysfunction with an ejection fraction of 20%, and a large apical aneurysm. A follow up echocardiogram one day later revealed improved LV function, and an EF of 45%. The troponin levels decreased over seven days to 0.18 ng/mL. Based on these results, the consulting cardiologist diagnosed Takotsubo cardiomyopathy. Subsequently, this patient's blood pressure regimen was modified with the addition of an angiotensin converting enzyme inhibitor. Follow-up echocardiography four months later revealed normal ejection fraction. Since that episode, the patient has had nineteen uneventful follow-up ECT treatments. These follow-up ECT treatments were performed with the addition of nicardipine, esmolol, and/or labetolol for blood pressure management, and cardioprotection.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [71, 'years'], 'Hypertension history': True, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'greater than three times normal limit', 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 71 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 0 + 2 = 2.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 3 + 2 = 5.
Based on the patient's data, the HEART Score is 5."
4259,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7219983-1,Extracted,"A 55-year-old man presented to the emergency department (ED) of an urban, academic, medical center with intermittent palpitations (fast beats accompanied by a “pounding” sensation in the chest) for the prior month. Palpitations were most noticeable at night but had become more severe and constant over the preceding three days. He also reported shortness of breath while supine in bed and lightheadedness with exertion. The patient is an avid hiker, so he only presented once his dyspnea prevented him from completing a typical family hike. He denied any chest pain, fevers, weight loss, syncope, leg swelling, cough, nausea, vomiting, or rashes.
The patient was diagnosed with type 1 diabetes mellitus when he was 30 and has a history of hypertension. He was taking insulin glargine nightly with sliding-scale insulin aspart during meals and had recently switched from ramipril to losartan 50 milligrams (mg) daily due to nocturnal cough. He denied any drug, alcohol, or tobacco use. His father died suddenly at age 42 due to a heart attack. He denied any allergies.
The patient’s vital signs on presentation were as follows: temperature 97.2 degrees Fahrenheit; blood pressure 131/83 millimeters of mercury (mm Hg); pulse 55 beats per minute, respiratory rate 18 breaths per minute; and oxygen saturation 99% on room air, with a body mass index of 28.6 kilograms per meters squared. Physical exam revealed a well-developed and well-nourished male patient in no acute distress. His head was normocephalic and atraumatic. His eye exam was normal with pupils that were equal, round, and reactive to light. No scleral icterus was seen. His neck was supple and had normal range of motion. There was no jugular venous distension seen. The patient’s cardiac exam was notable for a bradycardic and irregularly irregular heartbeat without a murmur. His lungs were clear to auscultation bilaterally, and no wheezes or rales were heard. The patient’s abdomen was soft, non-tender, and non-distended. His extremities were warm and well perfused, and without edema. The patient’s cranial nerves II–XII were intact, and gait and strength assessments were unremarkable. No pronator drift was seen. Skin was normal in appearance, without any lesions or rashes. The patient demonstrated a normal mood and affect throughout the history and exam.
A chest radiograph (CXR) and electrocardiogram (ECG) were obtained ( and , respectively). Laboratory studies () were notable for a white blood cell count of 6.2 thousand per microliter, hemoglobin of 15.1 grams per deciliter, platelets of 190,000 per microliter, glucose 250 milligrams per deciliter, negative troponin, B-type natriuretic peptide (BNP) of 502 picograms per deciliter, a thyroid stimulating hormone level of 1.2 milli-international units per liter with free thyroxine of 1.4 nanomoles per liter, and a Borrelia Burgdorferi IgM/IgG (immunoglobulin) titer of 0.28, negative antinuclear antibody test. (The latter test resulted after the patient was admitted.) While in the ED the patient experienced an acute episode of palpitations. His rhythm, as recorded by telemetry, is shown in . An echocardiograph was performed, which showed severe global hypokinesis with a left ventricular ejection fraction (LVEF) of 15%, mild dilation, biatrial enlargement, and no pericardial effusion.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'Hypertension history': True, 'Suspicion History': 'Slightly suspicious', 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': True, 'Diabetes mellitus': True, 'Initial troponin': 'less than or equal to normal limit', 'obesity': True, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'atherosclerotic disease': False}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 55 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, obesity, family with cvd. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: smoking, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: smoking, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 4 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 1 + 2 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4260,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6993381-1,Extracted,"A 69-year-old Caucasian man came to A&E complaining of episodes of lightheadedness. He described a sensation beginning in his feet, spreading upwards, and then becoming lightheaded, hot, and clammy. Each episode lasted for a few minutes. The episodes occurred randomly in the past year, were not provoked by any stimuli, and there were no focalized neurological symptoms.
In general, he had felt unwell for the past year, feeling tired and weak, had reduced appetite, but no weight loss.
He had a past medical history of hypertension treated with ramipril. He was previously investigated for ischemic heart disease with exercise tolerance test that was negative for ischemic changes and 90% predicted heart rate was achieved. His echocardiogram showed good global systolic and diastolic function. He was previously investigated for syncope with a 7-day electrocardiogram (ECG) tape recording, which showed sinus rhythm with 12 episodes of bradycardia in 24 hours, the longest for 27 beats, lowest rate 23 beats per minute (bpm), ventricular ectopic beats, and pauses in cardiac activity < 2.5 seconds (at random times), and no ischemic changes. The pauses occurred at random times and were not related to any physical activity or time of day. This was not investigated further.
He does not smoke tobacco; he is a social drinker. He is a retired engineer and lives with his wife in a house, completely independent in his daily activities.
On examination, his temperature was 36.9, blood pressure 170/100 mmHg, oxygen saturation 98% on room air, and respiratory rate 12. His heart rate was 54. CNS, peripheral nervous system, chest, heart, and abdominal examinations were normal. There was no chest pain.
Metabolic, infectious, cardiac, and CNS causes for syncope were considered for the differential diagnosis. His blood tests were normal (Table ), venous blood test was normal (not shown), and lying and standing blood pressures were 170/100 and 160/100, respectively. His heart rate was 54 bpm without orthostatic changes. Urine analysis and chest X-ray were normal, ruling out significant infection.
Heart block, ectopic beats, and arrhythmias were investigated by ECG, which showed sinus bradycardia of 54 bpm with occasional premature ventricular complexes and no features of acute ischemic event (Fig. ).
Cranial causes for syncope include epilepsy, cerebrovascular accident (CVA), transient ischemic attack (TIA), space-occupying lesion, raised intracranial pressure, and trauma.
A computed tomography (CT) head scan showed a hyperdense lesion 2.8 × 1.8 cm in left basal ganglia region, causing localized mass effect with minimal effacement of left sylvian fissure (Fig. ). Our patient was admitted for further investigations. Based on CT findings, magnetic resonance imaging (MRI) was requested, which showed diffuse high signal and mild degree of enhancement in medial portion of left temporal lobe extending into globus pallidus and thalamus corresponding to CT appearance. These appearances were most consistent with infiltrating glioma (Fig. ). A CT scan of his chest/abdomen/pelvis was then requested to assess for other cancer lesions. It demonstrated multinodular goiter, but otherwise no obvious primary or metastatic disease.
He had a primary tumor biopsy which showed anaplastic astrocytoma: isocitrate dehydrogenase (IDH) wild type, grade III, IDH r132h negative. He was discussed with a multidisciplinary team (MDT) and was treated with 8 mg dexamethasone and radiotherapy. His ECG improved showing 74 bpm sinus rhythm with first degree AV block. He is currently asymptomatic and has no syncopal episodes.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [69, 'years'], 'Hypertension history': True, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'smoking': False, 'atherosclerotic disease': False, 'hypercholesterolemia': False, 'Diabetes mellitus': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 69 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 0 + 2 = 2.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4261,18,HEART Score for Major Cardiac Events,risk,integer,pmc-2983030-1,Extracted,"A 30-year-old female patient presented to the emergency department with dyspnea on exertion and severe left anterior chest pain that had begun about 30 minutes prior to arrival, and which increased in intensity over time. She reported a history of exertional chest pain that had begun 10 days prior to her presentation. Previous studies, including electrocardiography (ECG), cardiac biomarkers, echocardiography, and an exercise treadmill test had shown no abnormalities. Her chest pain had been slightly alleviated by sublingual nitroglycerine. The patient had no smoking history and had no cardiovascular risk factors such as hypertension, dyslipidemia, or diabetes mellitus. The patient had been diagnosed with ET 6 months previously at a workplace health screening, and was being treated with 100 mg aspirin, 500 mg hydroxyurea twice a day, and 1 mg anagrelide three times daily. Her ET was relatively well controlled without any other complications, and her platelet counts had been within the normal range. Initial vital signs were stable, with a blood pressure of 110/80 mmHg, a heart rate of 78 beats/min, and a respiratory rate of 18 breaths/min. S1 and S2 were normal and S4 was faintly audible at the apex. An ECG showed T-wave inversions in leads I, aVL, and in V2 through V5, which were consistent with myocardial ischemia (). Neither cardiomegaly nor pulmonary congestion was noted on a chest X-ray. The MB fraction of creatinine phosphokinase (CK-MB) was 8.5 ng/mL and cardiac troponin I was 3.08 ng/mL (upper normal limit, 0.07 ng/mL). B-type natriuretic peptide (100 pg/mL) was also slightly elevated. A complete blood count showed the following: a leukocyte count of 3.70×103/µL, hemoglobin of 10.5 g/dL, and a platelet count of 388×103/µL. Low density lipoprotein (LDL) cholesterol level was 54 mg/dL. An echocardiograph revealed hypokinesis in the anteroseptal wall and a left ventricular ejection fraction of 55%. These results were compatible with an acute, non-ST-elevation MI. Immediately, the patient was treated with anti-platelet therapy (300 mg aspirin and 600 mg clopidogrel). In addition, according to the early invasive strategy, coronary angiography was performed, which revealed significant segmental stenosis (90%) of the mid left anterior descending artery (LAD) (). The segmental lesion in the mid LAD did not respond to intracoronary nitroglycerin injection, which excluded coronary spasms as the causative factor (). An intravascular ultrasound (IVUS) scan showed a focal soft plaque with a ruptured cap and thrombus formation (). Percutaneous coronary angioplasty and stenting (Promus, 3.5×18 mm) were performed successfully. After coronary angioplasty, the chest pain and T-wave inversions on ECG disappeared. Anagrelide was discontinued, anti-platelet and anti-anginal agents were added to the treatment, and the patient was discharged without further cardiac symptoms.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [30, 'years'], 'Suspicion History': 'Slightly suspicious', 'Hypertension history': False, 'smoking': False, 'Diabetes mellitus': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'hypercholesterolemia': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 30 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 1 + 2 = 3.
Based on the patient's data, the HEART Score is 3."
4262,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8260191-1,Extracted,"A 49-year-old Hispanic female with past medical history of asthma presented to the Emergency Department (ED) with a chief complaint of progressively worsening dyspnea over the past one week. The patient endorsed no alleviation with a rescue albuterol inhaler. She was a non-smoker with occasional alcohol use and no recreational drug use. Family history was significant for hypertension and hyperlipidemia. Her initial vital signs were as follows: heart rate 82/min, blood pressure 135/84 mmHg, 96% on room air, and afebrile. Physical examination was significant for diffuse inspiratory and expiratory wheezing. Cardiovascular examination revealed S1/S2 heart sounds with no murmur gallop or rub. The patient had no jugular vein distention (JVD), peripheral pulses were intact and no cyanosis, clubbing or edema was noted. Initial imaging including a chest X-ray and CT angiogram chest was negative for acute abnormality.
In the emergency department, the patient received nebulization with albuterol and intravenous steroids resulting in alleviation of symptoms. The patient was admitted to the medical floor for further management of acute asthma exacerbation. Over the course of hospitalization, patient’s breathing gradually worsened to the point of requiring non-invasive positive pressure ventilation with bi-level positive airway pressure (BIPAP) as the arterial blood gas revealed acute respiratory acidosis.
The patient was adequately treated with BIPAP resulting in normalization of her arterial blood gases (ABGs) as well as her clinical respiratory status, but her Troponin I continued to trend up to 0.48 ng/ml two hours after her admission, then 2.22 ng/ml eight hours after admission and finally 4.08 ng/ml 11 hours after her admission. An urgent transthoracic echocardiogram (Figure ) was performed, which revealed: ejection fraction in the range of 40-45%, severe posterior wall and anteroseptal hypokinesis with normal apical function. Cardiology was consulted and patient was taken for an emergent left heart catheterization. The coronary angiography (Figure ) revealed patent coronary arteries with ejection fraction in the range of 40-45% and proximal anterior and inferior hypokinesis consistent with rTTC.
Over the course of her hospitalization, her respiratory symptoms improved, she no longer required BIPAP and was stable for discharge three days after her admission. The patient was discharged with instructions to follow up outpatient with cardiology and pulmonology and was given prescriptions for inhaled corticosteroids as well as short-term systemic corticosteroids.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [49, 'years'], 'Hypertension history': True, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': True, 'Diabetes mellitus': False, 'smoking': False, 'Initial troponin': 'greater than three times normal limit', 'Suspicion History': 'Slightly suspicious', 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 49 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 2 + 2 = 4.
Based on the patient's data, the HEART Score is 4."
4263,18,HEART Score for Major Cardiac Events,risk,integer,pmc-3705791-1,Extracted,"A 61-year-old female presents with a non-ST elevation myocardial infarction (NSTEMI) in the setting of previous percutaneous coronary intervention (PCI) to the right coronary artery (RCA) with a bare metal stent (BMS) in 2004 on a background of treated hypertension and hypercholesterolemia and smoking. Her regular medications were aspirin 81 mg OD, metoprolol 25 mg BID, ramipril 5 mg OD and atorvastatin 40 mg OD. Since admission, she had ongoing chest pain. Her ECG had lateral ST-T changes and the peak cTnI was 3.0 ng/mL. She was brought emergently to the cardiac catheterization laboratory. The procedure was completed via right transradial catheterization. Coronary angiography showed diffusely diseased left anterior descending coronary artery (LAD) with a 70% stenosis in the mid third with an occluded first obtuse marginal coronary artery (OM1) with TIMI 0 flow (). The RCA was anterior in origin and nonselective coronary injection showed a patent stent (). The OM1 was considered to be the culprit vessel and attempted to cross with Pilot 50 wire (Guidant Corp., Indianapolis, IN, USA). The wire crossed the proximal subsection of the left circumflex (LCX) with support (Abbott TREK 2.0 mm × 15 mm coronary dilatation catheter) (). There was a resultant type B coronary dissection of the mid subsection of the proximal LCX. A Wizdom Supersoft wire (Cordis Corp., Miami, FL, USA) was used to cross the dissection plane as a “parallel wire technique” to deal with the wire-induced dissection []. The proximal LCX was predilated with the 2.0 mm × 15 mm coronary dilation catheter to seal the proximal LCX dissection plane. Once flow was reestablished, the Pilot 50 wire and the 2.0 mm × 15 mm coronary dilation catheter were removed. The Wizdom Supersoft wire was used to advance down the OM1. A secondary type B coronary dissection was noted in the mid subsection of the mid third of the OM1 (). The proximal LCX dissection plane appeared to have reduced flow and the dissection plane was again sealed with multiple balloon inflations. The patient remained pain-free with stable hemodynamics. The proximal LCX dissection plane appeared stable with TIMI 3 flow. Given the stable situation, the decision was made to stop. IV Eptifibatide infusion was started to stabilize the dissection plane with a plan to reattempt the CTO in 72 hours (). The second procedure was also completed successfully via right transradial catheterization. Selective left coronary angiography showed a coronary artery (LCX) to coronary sinus fistula (). The proximal LCX and the mid OM1 dissection planes appeared stable. As the patient remained pain-free and hemodynamically stable for 72 hours, the decision to manage medically with repeat noninvasive testing in 6–8 weeks was made. If there was evidence of reversible ischemia in the LCX territory (coronary steal syndrome), the decision would be to close the coronary AV fistula. Stress echocardiogram in 8 weeks showed no evidence of reversible ischemia in the LCX territory. The patient was advised to stay compliant with her current medications, continue dual antiplatelet therapy for a year, and make strong efforts to quit smoking.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [61, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': True, 'smoking': True, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",7,7,7,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 61 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, smoking, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 3 + 2 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 5 + 2 = 7.
Based on the patient's data, the HEART Score is 7."
4264,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7358831-1,Extracted,"The patient was a 55-year-old male farmer who was previously healthy. At 15:50 on April 29, 2018, the patient came to the Emergency Department (ED) of our hospital due to sudden pain in the precordial area for 6 hr. At 15:52, blood sample was collected for an emergency cardiac troponin I (cTnI) test（Beckman ASSECC2）, and at 17:02, the laboratory result showed cTnI level of 0.06 ng/ml (normal reference value of 0.033 ng/ml). The level of cTnI reached 79.27 ng/ml on April 30 and 7.52 ng/ml on May 3. The initial ECG was performed at 16:08 and showed an acute extensive anterior wall myocardial infarction (Figure ). The patient was given a loading dose of aspirin and clopidogrel (300 mg and 300 mg) for antiplatelet treatment, and morphinye for analgesia. 8 min after the first ECG, the second ECG revealed De Winter syndrome (Figure ). Emergency coronary angiography demonstrated 90% stenosis in the proximal and middle segments of LAD; and 70% stenosis in the distal segment of the left circumflex artery (LCA) (Figure ). Percutaneous coronary intervention (PCI) of LAD was performed after consultation with family members.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False}",6,6,6,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 55 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 3 + 1 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 4 + 2 = 6.
Based on the patient's data, the HEART Score is 6."
4265,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7837248-1,Extracted,"A 61-year-old South Asian female with past medical history of hypertension, hyperlipidaemia, diabetes mellitus complicated by neuropathy, and gastroesophageal reflux disease presented to the emergency department for atypical angina associated with palpitations, dizziness, decreased exercise tolerance, and dyspnoea on exertion. On examination she was overweight, breathing comfortably on room air at rest, cardiac exam was normal, and there was no jugular venous distension. Given her risk factors, the patient was considered to have intermediate pretest probability for coronary artery disease. She was admitted as an inpatient and an acute coronary syndrome was excluded by serial negative cardiac enzymes and normal electrocardiogram (ECG). She was therefore referred for dobutamine stress echocardiography.
Rest ECG demonstrated normal sinus rhythm (). Baseline heart rate (HR) 65 b.p.m., systolic blood pressure (SBP) 120 mmHg, diastolic blood pressure (DBP) 80 mmHg, asymptomatic (). Baseline echocardiogram demonstrated normal cardiac wall motion, normal left ventricular size and systolic function, and an estimated ejection fraction of 65%. Dobutamine infusion was begun at 10 μg/kg/min, with increase in HR to 93 b.p.m. accompanied by SBP 137, DBP 73 without electrocardiographic changes. Dobutamine infusion rate was increased to 20 μg/kg/min with reproduction of chest pain. Shortly after the start of 20 μg/kg/min infusion, ECG demonstrated asystole with a 5.1-s sinus arrest (). Examination was terminated. Following resolution of the sinus arrest, the patient developed brief sinus bradycardia followed by resumption of normal sinus rhythm (). Throughout the exam, maximal heart rate achieved was 114 b.p.m. (72% of maximal predicted HR). At peak stress, there remained no regional wall motion abnormalities, and there was a reduction in left ventricular rate an augmentation in left ventricular function. The stress echocardiogram was non-diagnostic, though diagnostic sensitivity was limited by suboptimal stress.
Patient was subsequently referred for coronary angiography, which was normal (). An electrophysiology study was performed during the patient’s inpatient stay. The result was also normal, with mildly prolonged SnRT and normal atrioventricular nodal function. She then had a loop recorder implanted to record any further arrhythmia events 1 day after the asystole event. Patient was discharged without symptoms or sequelae. There was no follow-up as of 1 year after device placement, and remote monitoring did not reveal any events as of the last transmission 4 months after device placement.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [61, 'years'], 'Hypertension history': True, 'hypercholesterolemia': True, 'Diabetes mellitus': True, 'obesity': True, 'Electrocardiogram Test': 'Normal', 'Suspicion History': 'Moderately suspicious', 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 61 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 1 + 1 = 2.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, obesity. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 2 + 2 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 4.
Based on the patient's data, the HEART Score is 4."
4266,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7800327-1,Extracted,"This case report describes a 52-year-old Cuban female with a past medical history significant for bipolar disorder, borderline personality disorder, PTSD, alcohol use disorder in full sustained remission, migraines, RA, fibromyalgia, obstructive sleep apnea, severe obesity, fatty liver, hypothyroidism, hypertriglyceridemia, acne, allergic rhinitis, and herpes simplex. The patient was previously stable on DVP delayed-release (DR) 500 mg every morning and 1500 mg every evening (19.5 mg/kg/day). Her most proximal valproic acid trough concentration was 99.8 mcg/mL 6 weeks prior to rifampin initiation. Refill history using proportion of days covered indicated at least 80% medication adherence throughout DVP therapy—above the threshold at which most medications are expected to achieve the most clinical benefit. The patient was also prescribed gabapentin 900 mg 3 times daily, acyclovir 400 mg twice daily, levothyroxine 25 mcg daily, 2 fluticasone nasal sprays in each nostril daily, loratadine 10 mg every morning, montelukast 10 mg daily, albuterol inhaler 1 to 2 puffs every 4 to 6 hours as needed, and potassium chloride 10 mEq/d. Rifampin 600 mg daily × 4 months was started by an infectious disease physician to treat latent TB infection, an incidental finding during workup for etanercept initiation for RA treatment.
Recognizing the rifampin-DVP interaction and general timeline for enzyme induction (eg, 1 to 4 weeks after initiation),, close monitoring occurred during this period. Telephone follow-up was scheduled weekly for 6 weeks after starting rifampin to assess psychiatric stability. Valproic acid steady-state trough concentrations were scheduled at 2, 4, and 6 weeks to provide objective data to supplement subjective assessments. Proactive DVP regimen adjustments were not planned given the limited information around the clinical significance of this drug-drug interaction. Any DVP dose or frequency adjustments that occurred were promptly in response to subjective reports of hypomanic symptoms, such as pressured speech, decreased need for sleep, impulsive spending, psychosis, increased irritability, distractibility, and flight of ideas, and not primarily in response to reduced valproic acid steady-state trough concentrations. See the for timing of dose adjustments and total daily dose prescribed. The patient first reported symptoms within 2 weeks after starting rifampin. Approximately 6 weeks after rifampin initiation, DVP frequency of administration was adjusted from 2 to 3 times daily while maintaining the same total daily dose to provide more frequent DVP DR dosing in the presence of a potent inducer expected to significantly increase DVP clearance. Additional medication exposures during this time included etanercept initiation for RA, a 10-day benzonatate course for upper respiratory infection–associated cough, and a short course of ziprasidone 40 mg daily during weeks 12 to 14, none of which were expected to significantly interact with DVP. Ziprasidone was added because of continued symptoms despite an ∼50% increase of DVP dose. However, the patient refused to continue ziprasidone, so DVP dose adjustments continued as clinically indicated. Ultimately, the patient no longer reported hypomanic symptoms 4 days after increasing DVP DR to 1000 mg every morning, 1000 mg every afternoon, and 1500 mg nightly.
Recognizing the potential for DVP side effects or toxicities to occur as rifampin induction effects dissipate over 1 to 4 weeks, the treatment team planned a gradual dose reduction after her rifampin course was completed: a decrease in DVP DR by 500 mg/d every week until the pre-rifampin DVP regimen was reached. Additionally, weekly valproic acid steady-state trough concentrations (), ALT, and CBC were ordered to monitor for DVP-related toxicities. Facility protocol is to check ALT first and then complete additional tests if indicated. ALT and CBC labs were within normal limits throughout DVP and rifampin therapy; therefore, further liver panel tests were not ordered. All valproic acid steady-state trough concentrations were <100 mcg/mL. A drug interaction probability scale calculation was performed and resulted in a score of 5, indicating a probable drug-drug interaction.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [52, 'years'], 'Hypertension history': True, 'smoking': False, 'Diabetes mellitus': False, 'obesity': True, 'atherosclerotic disease': False, 'hypercholesterolemia': True, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 52 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: hypertension, obesity. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4267,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4925396-1,Extracted,"A 22-year-old otherwise healthy man presented to the clinic complaining of recurrent episodes of ""heart racing"". Physical examination was unremarkable. Prior laboratory testing was not significant for anemia, infection, thyroid or adrenal disease, vitamin deficiencies or electrolyte derangements. He underwent serial electrocardiograms and holter monitoring and had no detection of cardiac arrhythmias. A transthoracic echocardiogram revealed a preserved left ventricular ejection fraction of 55%, normal left ventricle size and thickness, normal diastolic filling and an unusual incidental finding of a unileaflet mitral valve. The anterior mitral valve leaflet was markedly elongated, mildly thickened, and occupied the entire closure line of the mitral annulus with no contribution of the hypoplastic posterior leaflet. The coaption zone was intact with no MR (, , and , and ). As to his palpitations, he was diagnosed with an underlying anxiety disorder and successfully treated with anxiolytic therapy. Follow up was arranged yearly for his abnormal mitral valve.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [22, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 22 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4268,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5282642-1,Extracted,"We report the case of a 32-year-old Indian woman admitted to our institute with angina on exertion. This symptom first appeared 2 years prior to her presentation, with gradual onset and progressive worsening from class I to class III associated with multiple episodes of pre-syncope. She had no history of diabetic mellitus, arterial hypertension, palpitation, or syncope and no family history of similar complaints or sudden death. On physical examination, our patient appeared generally well. Her blood pressure and pulse rate were 128/84 mmHg and 57 beats per minute, respectively.
Electrocardiography revealed a sinus rhythm and left ventricular hypertrophy by Sokolow–Lyon criteria, with secondary ST depression and biphasic T-waves in leads I, aVL, and V4–V6. A chest X-ray was normal. A Holter study was not suggestive of any significant arrhythmias or pause as a plausible cause of the pre-syncope. Her biochemical blood parameters were also within normal ranges. Echocardiography revealed HOCM (Fig. ) with systolic anterior movement. Pulsed wave Doppler showed a dagger-shaped spectral profile with a peak sub-aortic velocity of 287 cm/s and a maximum pressure gradient of 33 mmHg (Fig. ), with mild eccentric mitral regurgitation. After an initial evaluation, our patient underwent cardiac catheterization to exclude concomitant coronary artery disease and to rule out other coexisting congenital coronary anomalies. Coronary angiography showed no significant stenosis due to coronary artery disease. However, angiography revealed multiple coronary microfistulas originating from both her left coronary artery system (Fig. , Additional file 1) and her right coronary artery (Fig. , Additional file 2). Our patient also underwent a cardiac catheterization study with oximetry analysis to confirm that the microfistulas originated from her left anterior descending coronary artery (LAD), left circumflex artery (LCX), and right coronary artery (RCA). The rapid filling of her pulmonary artery after dye was injected into her left coronary artery during the catheterization study demonstrated that the microfistulas were all draining into her right ventricle (RV) (Fig. , Additional file 3). Further confirmation came from an oxygen step up of 15 % (from 65 % to 80 %) from her right atrium (RA) to her RV during oximetry analysis.
Our patient was discharged 5 days after the completion of her clinical investigation on medical therapy including metoprolol and nicorandil. At a follow-up 1 month later, her angina grade had decreased from class III to class II.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [32, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'smoking': False, 'Initial troponin': 'less than or equal to normal limit'}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 32 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4269,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4163392-1,Extracted,"A 24-year-old female presented to our ED with a six-hour duration history midsternal chest pain of pleuritic quality (rated as 8 out of 10 on a pain scale) radiating to her neck and jaw. The chest pain was continuous after its onset, not related to rest or exertion with no reported alleviating or aggravating factors. The patient denied any history chest trauma. Family history was negative for premature cardiovascular disease or early death.
Review of systems was otherwise negative for cough, sweating, nausea, vomiting, abdominal pain, and diarrhea. The patient was a never smoker, drank alcohol socially, and did not use any recreational drugs. The patient had a history of bronchial asthma which was well controlled. The patient used albuterol as needed and did not report using oral contraceptive pills or other medications. The patient did not report any previous surgeries, immobilization, long distance travel, and personal or family history of blood clots or cancer.
Blood pressure was 133/56 mm Hg, heart rate was 70, respiratory rate was 18, oxygen saturation was 100% on room air, and temperature was 97.6 F (36.4 C). On a physical examination, the patient was in moderate distress due to chest pain, with no jugular venous distention, normal pulmonary examination with good bilateral breath sounds, minimally reproducible chest pain on palpation, and normal heart rate and normal heart sounds with no murmurs, rubs, or gallops and equal bilateral pulses. Abdominal and neurological examination was unremarkable. There was no extremity swelling or erythema. However, pectus excavatum or “sunken chest” was noted by a physical examination.
12-lead EKG was done which showed normal sinus rhythm, normal axis, normal rate, normal intervals, and no evidence of T wave and ST segment abnormalities on 2 separate occasions 3 hours apart. CXR did not show pneumothorax, pneumonia, esophageal rupture, or perforation and was read as normal. Troponin was negative. The patient was deemed to be a low pretest probability for PE according to the Wells score and D-dimer was ordered [, ]. D-dimer was found to be elevated at 3041 ng/mL (normal range <500 ng/mL). Computed tomography (CT) of the chest with intravenous (IV) contrast was ordered. CT chest with IV contrast showed type A Stanford dissection involving the ascending aorta involving the aortic arch and great vessels (please see ) []. The patient was immediately transferred to a tertiary center for emergent aneurysm repair surgery. The patient surgery and inpatient stay were uneventful with return to a baseline functional level.
Our patient was tested positive for type IV Ehlers-Danlos syndrome. Ehlers-Danlos type IV syndrome is a genetic disease (typically autosomal-dominant one) with predisposition rupture of vasculature, intestine, and uterus []. Given the fact that there was no family history of Ehlers-Danlos syndrome in the family, it is possible that this could represent a de novo mutation [].",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'parent or sibling with Cardiovascular disease before age 65': False, 'Suspicion History': 'Slightly suspicious', 'Hypertension history': True, 'smoking': False, 'Diabetes mellitus': False, 'age': [24, 'years'], 'Electrocardiogram Test': 'Normal', 'Initial troponin': 'less than or equal to normal limit', 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'obesity': False, 'atherosclerotic disease': False}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 24 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4270,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4606557-1,Extracted,"A 53-year old female presented to the Emergency Department for cough, nausea, vomiting and “feeling sick for 3 weeks.” She reported an allergy to penicillin but no other significant past medical history. On initial assessment, patient was afebrile, tachycardic (125 beats/minute), tachypneic (22 breaths/minute), with blood pressure of 109/74 mmHg, and oxygen saturation of 72 % on room air. Physical exam showed no other abnormalities.
Initial laboratories showed leukocytosis (WBC 22,000 k/mcgl), hyperglycemia (glucose 796 mg/dl), hyponatremia (Na 120 mEq/L; corrected 131 mEq/L), a hemoglobin A1c of 17.2 %, and an elevated troponin T (0.19 ng/mL) and BNP (2137 pg/mL). Measured osmolarity was 349 mOsm/L with only small ketones in the blood and an arterial lactate of 5.62 mmol/L. Arterial blood gas suggested metabolic acidosis (pH = 7.264 | PCO2 = 25.9 mmHg | Bicarbonate = 13 mmol/L). Calculated anion gap was 30 mEq/l. Chest X-ray showed bilateral reticular opacities without cardiomegaly (Fig. ). The patient was also found to have an abnormal thyroid hormone profile suggesting NTIS: TSH 1.35 mcgUI/mL (nr: 0.27–4.20), free T4 0.88 ng/dL (nr: 0.93–1.70), free T3 0.95 pg/ml (nr:2.30–4.20), mixed hyperlipidemia, mild elevation of lipase and amylase, and transaminitis.
Intravenous fluids, insulin and levofloxacin were started; the patient’s clinical condition improved in 24 hours, although she continued to complain of shortness of breath and remained hypotensive. Blood and urine cultures were ultimately negative. Initial EKG changes suggested previous myocardial infarction (Fig. ). A transthoracic echocardiogram demonstrated a severely depressed LV systolic function (ejection fraction = 26 %), grade 2 diastolic dysfunction, and multiple regional wall motion abnormalities (Fig. -). However, on Day 4 after admission, a Myoview stress test showed no stress-induced ischemia, normal LV function, no regional wall motion abnormalities, and an estimated ejection fraction of 50 %. A repeat transthoracic echocardiogram performed on Day 7 demonstrated an ejection fraction of 50–55 % (Fig. -3d). A follow-up EKG on Day 4 showed no significant changes (Fig. ).
On 6-month follow-up, the patient’s A1c remained elevated but the NTIS and cardiomyopathy had resolved. Her HgA1c was 9.4 %, TSH 1.86 mcgUI/mL (nr: 0.27–4.20), free T4 1.01 ng/dl (nr: 0.93–1.70), free T3 2.89 pg/ml (nr:2.30–4.20). BNP was 42 pg/ml (normal).",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [53, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': True, 'Diabetes mellitus': True, 'smoking': False, 'atherosclerotic disease': True, 'Initial troponin': 'less than or equal to normal limit', 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 53 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: diabetes mellitus, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4271,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4644054-1,Extracted,"A 49-year-old Caucasian female presented to a community ED by EMS after having abrupt onset chest pain following ingestion of sumitriptan for migraine. She reportedly took sumitriptan orally approximately 60 minutes prior to treat the typical symptoms of her migraine, which she has had intermittently for years. She had taken sumitriptan multiple times in the past without incident. Shortly after taking her medication she had an acute onset of sub-sternal chest pressure, which radiated to her jaw. This pain started at rest and had never occurred before.
She had a past medical history of migraine and depression, for which she took sumitriptan and desvenlafaxine, respectively. Desvenlafaxine is a serotonin–norepinephrine reuptake inhibitor (SNRI) that she has been taking for years. Her last dose of sumitriptan prior to the incident was several weeks before. She had no history of coronary artery disease (CAD), diabetes mellitus, pulmonary disorders, tobacco abuse, cocaine use, or any recent illness or injury. She did not take exogenous estrogen nor had any family history of heart disease.
She called EMS after having 30 minutes of constant chest pain that radiated to her jaw. She was assessed by the local EMS crew and was given 324mg aspirin PO and 0.4mg nitroglycerine sublingually. Her initial EMS 12-lead electrocardiogram (ECG) showed ST elevations in I, aVL, V1, and V2. She also had ST depressions in II, III, aVF, and V3–V6 (). The ECG was transmitted electronically to the ED. The emergency physician interpreted the ECG as a likely anterior myocardial infarction with reciprocal changes in the inferior and lateral leads. The cardiac catheterization lab was activated and the cardiologist on call contacted.
During patient transport, her pain gradually improved after administration of the nitroglycerine and a second ECG was electronically transmitted () which showed some improvement in the ischemic changes. Once she arrived to the ED, her chest pain had nearly resolved, she had stable vitals and her arrival ED ECG showed resolution of ischemic changes (). Cardiac enzymes showed an initial troponin of 0.05ng/mL. Urine drug screen was negative, confirming that no recreational drug use, to include cocaine, was used. Cardiology was present in the ED and elected to take the patient for emergent coronary angiography.
Coronary angiography demonstrated severe constriction of the left anterior descending artery responsive to intracoronary nitroglycerin. There were no lesions suggesting CAD. The left ventricular systolic function was normal with an ejection fraction of 60%. She was diagnosed with severe spasms of the left anterior descending artery leading to myocardial infarction. The patient was transferred to a step-down bed and discharged from the hospital the next morning. The patient’s cardiologist advised her to avoid all anti-migraine medication and to use sublingual nitroglycerin tablets as directed to prevent further angina.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [49, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 49 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 3.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 3.
Based on the patient's data, the HEART Score is 3."
4272,18,HEART Score for Major Cardiac Events,risk,integer,pmc-2615063-1,Extracted,"A 22-yr-old male, farmer by occupation was referred to our tertiary cardiac care institute for management of abnormal ECG changes mimicking acute coronary syndrome. He had sustained accidental electric burn injury (240V) while carrying out some work at home 2 hours prior to admission. He was thrown to the ground following an electrocution and was found to have brief period of loss of consciousness for few seconds with spontaneous recovery. He was immediately attended at a local hospital where ECG changes were noticed and referred to our institution for opinion and further management. He had no prior history of cardiac illness. There was no history of chest pain, palpitation or neurological deficits. There was no history suggestive of sudden or premature cardiac death in his family. He was not on any medications.
On physical examination, patient was conscious alert and had deep electric burn entry wound over the dorsum of left hand and an exit wound over the left ankle. The arterial blood pressure and heart rate were 120/80 mmHg and 78 beats per minute, respectively. Cardiovascular assessment was normal. Other systemic examinations were normal. Surface electrocardiogram done immediately following injury demonstrated a sinus rhythm with RBBB with coved ST segment elevation with negative T wave in V1 mimicking type 1 Brugada pattern and saddle back ST segment with upright T wave in V2 mimicking type 2 Brugada pattern with early repolarisation (). QTc was normal. Echocardiographic assessment revealed a normal left ventricular size and function, and no valvular pathology. Routine laboratory tests, including blood urea, serum creatinine, serum electrolytes and cardiac biomarkers were normal. Repeat ECG at 2 hours showed disappearance of above mentioned Brugada type pattern with persistent early repolarisation. Patient was observed in the ICU for rhythm disturbances for 24 hours. Repeat ECG after 24 hours was normal pattern. Since patient had no family history of sudden cardiac death and family members showing normal ECG and clear precipitating event that can result in above mentioned ECG changes he was not subjected for further investigations like induction with class I antiarrhythmics or electrophysiological studies.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [22, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'hypercholesterolemia': False, 'obesity': False}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 22 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4273,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7891237-1,Extracted,"A 23-year-old woman presented to the emergency department with sudden onset of non-pleuritic chest pain that radiated to her arms. She was diaphoretic. The patient had no family history of heart disease. She did not smoke or use alcohol or illicit drugs. She had been shopping in a local store when the pain suddenly started. The patient was haemodynamically stable, and there were no pertinent cardiovascular findings on physical examination.
In the emergency department, her electrocardiogram showed sinus bradycardia (, ) with no significant changes concerning for ischaemia. Initial serum troponin I was 1.2 ng/mL (reference range 0–0.04 ng/mL). The patient was admitted, and serial troponins were performed. Her troponin peaked at 16 ng/mL. She was started on a heparin drip. A transthoracic echocardiogram (TTE) showed apical dyskinesia (Video 1) with hyperdynamic motion of the spared myocardium resulting in a preserved ejection fraction of 65% and reduced apical strain (). Coronary angiography revealed triple vessel coronary ectasia with significant thrombus burden in the occluded left anterior descending artery (LAD) ( and Video 2).
Aspiration thrombectomy or intracoronary thrombolysis was contemplated, but, because she was haemodynamically stable and there were no signs of worsening ischaemia, conservative management was recommended. The patient was bridged to warfarin, in addition to dual antiplatelet therapy with aspirin and ticagrelor. Low-dose metoprolol was started. The patient had low blood pressures throughout the admission so we deferred initiation of an angiotensin-converting enzyme inhibitor; she was intolerant to statin therapy due to myalgias. She was discharged on the above regimen. Prior to discharge, the patient was able to return to her baseline activities of daily living with no chest pain or dyspnoea on exertion. It was decided to monitor her closely and follow-up in an outpatient setting to pursue further imaging. Given her age, Kawasaki disease was thought to be the likely aetiology of her CAE.
One month after discharge, the patient underwent computed tomography (CT) angiography of the coronary arteries, which confirmed prior findings of multiple coronary artery ectatic changes. The largest diameters noted were 10 mm in the mid-LAD (), 9 mm in the proximal LAD, 6.5 mm in the left marginal branch (), and 7.5 mm in the right coronary artery (). Previously identified coronary thrombi resolved as well. Three-dimensional reconstruction of the coronary vessels was done (). Repeat TTE continued to show a preserved ejection fraction of 65%, as well as resolved apical dyskinesia and improved apical strain ( and Video 3).
Soon after, she reported that, contrary to medical advice, she was pregnant. Warfarin was stopped owing to the teratogenicity of the drug, and she was continued on aspirin, metoprolol, and ticagrelor. As there are no standard guidelines, we decided to de-escalate to dual antiplatelet therapy rather than reintroduce triple therapy with a new agent. Throughout her 37-week pregnancy, the patient did not have any reoccurrence of chest pain, dyspnoea, or palpitations. At 21 weeks of gestation, the patient had a TTE that continued to show a stable ejection fraction and strain pattern. The patient stayed on dual antiplatelet therapy until 5 days before delivery. She delivered a healthy child at 37 weeks via vaginal delivery under epidural anaesthesia with no complications. Two days post-delivery the patient had an echocardiogram that continued to show resolved strain pattern (, ) and left ventricular function. Further coronary imaging will be pursued in the future.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [23, 'years'], 'Hypertension history': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'greater than three times normal limit', 'hypercholesterolemia': False, 'obesity': False, 'atherosclerotic disease': False}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 23 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 0 + 2 = 2.
Based on the patient's data, the HEART Score is 2."
4274,18,HEART Score for Major Cardiac Events,risk,integer,usmle-8831,Extracted,"A 23-year-old man presents to the emergency department presenting with sudden-onset dyspnea and left-sided chest pain over the last hour. This event started when he was in class sitting for an exam. He reports that the pain is worse with inspiration and does not radiate. He says he has anxiety and takes alprazolam as needed. He smokes half a pack of cigarettes a day and drinks alcohol socially. The temperature is 36.7°C (98.0°F), the blood pressure is 130/80 mm Hg, the pulse is 82/min, and the respiratory rate is 14/min. Pulse oximetry shows 97% on room air. The patient’s weight is 63.5 kg (140 lb), height is 185 cm (6 ft 1 in), and he has a BMI of 18.5 kg/m2. A chest X-ray is taken (see exhibit). After an hour of supplemental oxygen, rest, and careful monitoring his dyspnea improves and chest pain resolves without medication.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [23, 'years'], 'Hypertension history': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'Diabetes mellitus': False, 'obesity': False, 'smoking': True, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 23 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are present based on the patient's note: smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 0 + 1 = 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4275,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8371657-1,Extracted,"The 43-year-old female patient has no special history, and she has an annual check-up of computerized tomography to detect the mass in the right middle mediastinum, so the patient is admitted to the hospital. On-board examination, the patient was awake with good overall condition and has no abnormalities of the cardiovascular system and thoracic system during clinical examination. The manifestation on thoracic X-ray: right pulmonary hilum has an even, well-defined border (). Chest computerized tomography image showed a mass in the middle mediastinum with the size of 23 × 22.3 mm located between the right pulmonary artery and the pericardium with uniform margins and clear boundaries and did not invade the surrounding organization. A modest amount of contrast was absorbed after injection (). Echocardiography and respiratory function measurements were normal. Biochemical blood tests and complete blood count were in normal range. The preoperative diagnosis indicated that the tumor is located in the middle mediastinum with suspected mediastinal lymphadenopathy. The patient underwent uniportal video-assisted thoracoscopic surgery for tumor resection.
Operative procedure. We made a 3 cm skin incision on the VI intercostal space in the right anteriolateral side. The intraoperative examination found that the tumor of the right diaphragmatic nerve was about 2 × 3 cm in size () with clear tumor boundary to surrounding organs (including pericardium, pulmonary artery, and lung parenchyma), proving the noninvasiveness. We conducted a segmentation of the right phrenic nerve to remove the tumor and release the length of the phrenic nerve associated with reconnecting the right phrenic nerve with a prolene 8/0 through endoscopy (). The removed specimen was pale yellow with superficial hemorrhage (). Postoperatively, the patient was discharged after 4 days of treatment with a clinical condition of no difficulty breathing and no chest pain, and postoperative X-ray showed no abnormality; the right diaphragm was unchanged (). CT scanner result 1 month after discharge showed no abnormal images compared to the preoperative results ().",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [43, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 43 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4276,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4352363-1,Extracted,"In February 2011, this 26-year-old Ethiopian male awoke in the morning with bilateral paralysis of his extremities. When he presented to the emergency department 4 h later he exhibited partial recovery. He had no associated swallowing or breathing difficulty, weakness of the facial muscles, sphincter disturbances, pain, sensory symptoms, or change in mental state. Two months earlier, he had undergone a similar episode, beginning after midnight, which resolved spontaneously within 3 h. He had been experiencing heart palpitations for several months, along with heat intolerance and failure to gain weight despite a good appetite. He had no other known prior medical or surgical illnesses. He denied alcohol abuse or illicit drug use and was not on any medications. No similar weakness or other remarkable diseases in the family was reported.
At presentation, his blood pressure was 120/80 mmHg and his heart rate was 114 beats/min. He had no thyromegaly, and his skin was warm and dry. He was fully oriented and cooperative. No gross cranial nerve deficits were noted. He demonstrated flaccid symmetrical proximal and distal weakness of the arms and legs (power: legs 3/5, arms 4/5). Knee and ankle deep tendon reflexes were depressed bilaterally (grade 1/4). Sensation was intact.
Blood tests showed serum K+, 2.7 mmol/L (normal range: 3.6–5.5); Mg2+, 1.8 mg/dL (normal range: 1.9–2.5); and creatine kinase-total, 223 IU/L (normal range: 38–174). Serum phosphate was not determined, but results of the remainder of the electrolyte panel, complete blood count, and blood chemistry were normal. Thyroid-stimulating hormone (TSH) was less than 0.0005 IU/mL (normal range: 0.27–4.2), free triiodothyronine (T3) was 17.72 pg/dL (normal range: 2.02–4.43), and free thyroxine (T4) was 5.33 ng/dL (normal range: 0.93–1.71). The ECG showed sinus tachycardia at 120 beats/min, U waves fused with P waves, and inferior T-wave inversions (Fig.). Results of an electromyography and a nerve conduction study conducted the following day were within normal limits. Because of logistical constraints, a thyroid radioiodine uptake scan could not be done until ≈6 weeks later, during which time the patient had been receiving antithyroid medication. The results were reported normal.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [26, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 26 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4277,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6713366-1,Extracted,"A 29-year-old woman was admitted with a 2-week history of progressive paroxysmal
palpitations accompanied by persistent chest tightness and dyspnea. She had no other
medical history. During her 3 years of marriage, she had encountered difficulty
achieving pregnancy naturally. When admitted, she was in the 11th week of
gestation following in vitro fertilization. Physical examination revealed a pulse of
167 beats per minute (bpm), regular heart rhythm, clear heart sounds with no
pathological murmur and no lower limb edema. Auxiliary examinations included a
12-lead electrocardiogram (ECG) which showed AT at 150 bpm with a negative
P-wave in leads I, aVL and aVR, as well as a positive
P-wave in leads II, III, aVF and V1 (), and an echocardiogram which revealed
an LA of 42mm (anteroposterior diameter), left ventricular end-diastolic dimension
(LVEDD) of 55mm and left ventricular ejection fraction (LVEF) of 48%. She was found
to be euthyroid and her N-terminal pro-brain natriuretic peptide level was 4285
pg/ml. The patient was diagnosed with atrial tachyarrhythmia. An esophageal lead was
applied to confirm the diagnosis, but rapid pacing failed to terminate it. Rest ECG
showed a rate of 110 to 120 bpm. Slight movement, such as eating or going to the
toilet, caused her heart rate to exceed 150 bpm. Intravenous administration of
propafenone transiently converted the tachycardia to sinus rhythm but could not
sustain. Other medications such as metoprolol could not adequately control the heart
rate either.
Ablation was performed under local anesthesia, Multichannel EP recorder (EP
MedSystems, USA) and three-dimensional (3D) electroanatomic mapping system
(CartoSound, Biosense Webster, CA, USA). The patient still exhibited tachycardia
while undergoing the procedure. The right femoral vein was cannulated using an
8French (F) sheath, through which a saline infusion ablation catheter (ThermoCool
Electrophysiology Catheter, Biosense Webster, CA, USA) was introduced into the right
atrium (RA). A detailed electro-anatomic map of the RA and coronary sinus (CS) were
created using fast anatomical mapping (FAM). Then the right internal jugular vein
was cannulated using a 6F sheath through which a decapolar EP catheter (Rithm ID,
Synaptic Medical, CN) was introduced into the CS under the guidance of the
electro-anatomic map. The intracardiac electrogram showed a cycle length of 330-370
msec and CS activation order of CS1,2 earlier than CS9,10
(), which confirmed the AT
originating from the LA. Then the right femoral vein was cannulated using a 10F
sheath and an 8.5F long sheath, through which an EP catheter (SoundStar, Biosense
Webster, CA, USA) was introduced and a transseptal needle (St. Jude Medical, USA)
was applied to perform transseptal puncture under CartoSound guidance. Four thousand
units of unfractionated heparin were administered intravenously with access to LA to
maintain an active clotting time of approximately 350 seconds. The ablation catheter
and a circular decapolar catheter (Lasso, Biosense Webster, CA, USA) were introduced
into the LA via the transseptal site. A detailed electro-anatomic map of LA was
created and clearly demonstrated focal activation originating from the very distal
LAA (). There was no evidence of
macro-reentry. Radiofrequency (RF) ablation was performed using 20 watts, titrating
up to 25 watts, for approximately 16 times (power control mode, 40℃, 30cc/min). Each
time, ablation energy was delivered for 6-10 seconds. Ablation at this site
terminated the tachycardia with no recurrence noted during a 30-minute observation
period. No tachycardia was induced by programmed stimulation and rapid atrial
pacing. The procedure lasted for 2.5 hours with no fluoroscopy and without
complications.
At the 1-month follow-up visit, the ECG showed normal sinus rhythm and the
echocardiogram showed LA of 30 mm, LV of 48 mm, LVEF of 52%. Three months after the
procedure, a 24-hour Holter exam revealed sinus rhythm with 7987 atrial premature
beats and 903 episodes of paroxysmal AT (8.1% of the day). And the patient
complained of occasional palpitations. Six months later, a 24-hour Holter exam
conducted showed sinus rhythm with 37 atrial premature beats and 5 episodes of
paroxysmal AT (0.06% of the day). A healthy baby boy was eventually delivered by
Cesarean section. No palpitations were reported thereafter.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [29, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 29 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4278,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5358296-1,Extracted,"A 69 year old Hispanic female with past medical history of hyperthyroidism (Graves' Disease), heart failure with ejection fraction 45%, was presented to the emergency department with intermittent chest pain and palpitations. Chest pain was substernal, dull aching type, 5/10 in intensity and non-radiating.
Vital signs were stable with a blood pressure of 126/70 mmHg, pulse rate of 135 bpm, respiratory rate of 16 breaths per minute and temperature of 36.7 °C. On physical exam, pupils were equal, reactive to light and accommodation and notable for arcus senilis. There was no JVD present. Lungs were clear to auscultation bilaterally with no wheezing. Cardiovascular exam was notable for a grade 3/6, holosystolic murmur at the apex and irregularly irregular rhythm. Abdomen was soft, non-tender, non-distended with normal bowel sounds in all four quadrants. Pulses were intact bilaterally in upper and lower extremities with no edema.
Laboratory findings were as follows: WBC 7.5 K/ul, Hb 12.1 g/dl, Hct 36.8 %, Platelets 212 K/ul. Electrolyte panel findings were as follows: Na 143 mmol/L, K 4.0 mmol/L, bicarbonate 20 mmol/L, chloride 113 mmol/L, BUN 21 mg/dl, Cr 0.8 mg/dl, Glucose: 96 mg/dl. Other labs included: TSH 1.86 MIU/ml, Digoxin level < 0.1 ng/ml.
EKG showed atrial fibrillation with Rapid Ventricular Response at 135 bpm ().
Transthoracic Echocardiogram (TTE) showed EF 45%, severe mitral regurgitation and a large mass in the left atrium, attached to interatrial septum, filling the whole chamber with slight protrusion into the anterior mitral valve leaflet and left ventricle during diastole (). It measured 16 cm2. Mitral valve diastolic velocity was increased to 2.5 m/s.
A diagnosis of left atrial myxoma was made and the case was referred to another hospital for surgical intervention. Patient was promptly transferred the next day and underwent resection of the left atrium myxoma and left atrial wall with pericardial reconstruction, mitral valve repair with # 24 Medtronic CG Future annuloplasty ring, left-sided modified MAZE RF atrial fibrillation ablation and amputation of left atrial appendage.
Post-operatively EKG showed Normal Sinus Rhythm at 80 bpm TTE showed no intracardiac mass and a normal left ventricle ejection fraction of 60%. Patient was started on anticoagulation and is being monitored in the outpatient clinic.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [69, 'years'], 'Hypertension history': False, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 69 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 0 + 2 = 2.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4279,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7885139-1,Extracted,"A 31-year-old male of Indian descent, with no known comorbidities except for a history of borderline obesity in the past presented with shortness of breath and chest discomfort post SARS-CoV-2 infection. He had tested positive for SARS-CoV-2 infection about 3 weeks prior to this (mid-June 2020) presentation. He had returned to work following 2 weeks of isolation, but had difficulty coping due to exertional dyspnoea. Pulse oximetry demonstrated oxygen desaturation to 85%, particularly whilst wearing an N95 mask. His blood pressure (122/76 mmHg) and heart rate (76 beats/min) remained normal. There were no clinically relevant findings other than a body mass index of 25.3 kg/m2. He had poor effort tolerance on a 6-min walk test, managing a distance of only 120 m.
The following differential diagnoses were considered: pneumonia, pulmonary embolism, myocardial infarction and myocarditis. Chest X-ray and 12-lead electrocardiogram (ECG) were normal ( and ). Laboratory investigations showed a white blood cell count of 4.80x 109/l (normal 3.92–10.4) with a normal differential count, C-reactive protein 5 mg/l (normal < 10 mg/l), ferritin 267 μg/l (normal 30–400 ug/l), D-dimer < 0.10 mg/l (0.0–0.25 mg/l) and NT-proBNP of 143 ng/l (normal < 300 ng/l). However, his high sensitivity Troponin T level was elevated at 319 ng/l (normal < 14 ng/l) and showed a steady rise to 490 ng/l. His transthoracic echocardiogram (TTE) revealed preserved left ventricular (LV) and right ventricular (RV) contractility and no regional wall motion abnormality or myocardial hypertrophy. There was no pericardial effusion. The pulmonary arteries were of normal size. Computed tomography (CT) of the chest was normal (). The coronary arteries were normal. Based on the clinical findings, rising troponin-T levels, and new T wave inversion in lead III on a repeat 12-lead ECG, a diagnosis of likely COVID-19-related viral myocarditis was made. Treatment with colchicine 0.5 mg twice daily and prednisone 40 mg once daily were initiated whilst awaiting a CMR scan.
The CMR scan confirmed normal LV and RV function and wall thickness with an LV ejection fraction of 65%, RV ejection fraction of 56% and wall thickness at end-diastole of 7 mm. There was delayed late gadolinium enhancement (LGE) within the mid-wall as well as the epicardial regions involving the LV basal inferolateral wall, mid-anterolateral and mid- inferolateral wall (). T2 short tau inversion recovery (STIR) black blood imaging showed high signal intensity within the LV anterolateral, inferolateral wall at the base and mid-ventricle level (). On non-contrast T1 mapping, there was prolongation of T1 time at the mid-ventricle segment 5 (1212 ± 141 ms) and segment 6 (1113 ± 93.8 milliseconds) (). The aforementioned findings were compatible with Lake Louise criteria for diagnosis of focal viral myocarditis [].
There was significant improvement in the patient’s symptoms; his 6-min walk test improved to 417 m and cardiac biomarkers returned to normal (hs-Troponin T 10 ng/l) after 1 week of medical therapy (). The treatment was continued for further 1 week. He has subsequently returned to work and is doing well.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [31, 'years'], 'Suspicion History': 'Highly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'obesity': True, 'atherosclerotic disease': False, 'Initial troponin': 'greater than three times normal limit', 'Hypertension history': False, 'hypercholesterolemia': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 31 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: obesity. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 3 + 2 = 5.
Based on the patient's data, the HEART Score is 5."
4280,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6555498-1,Extracted,"A 39-year-old White female presented to the hospital with a three-day history of epigastric pain. She described her pain as a burning pain that started at rest and was radiating to her neck. Her pain was associated with shortness of breath, and she denied any episodes of nausea, vomiting, cough, fevers, chills, or sweating. She recently had a twin pregnancy and gave birth at about 32 weeks of gestation via caesarian section, but lost both her children after birth. This event had been very emotionally taxing on her for the past three months.
Her past medical history was only remarkable for gestational diabetes during her last pregnancy. She typically smoked one pack per day of cigarettes for the last 20 years. Recently, she increased her smoking to two packs per day for the past few months. She denied any use of alcohol or recreational drugs. She also denied any other cardiac risk factors, significant family history of cardiac disease, sudden cardiac death, or connective tissue disease. She had no allergies and was not taking any medications.
On examination, she was afebrile with a temperature of 36.9°C, heart rate of 82 beats/min, a blood pressure of 165/110, respiratory rate of 18 breaths/minute, and oxygen saturation of 99% on room air. Her head and neck examination were unremarkable with no jugular venous distention. On auscultation, there was good air entry bilaterally and normal heart sounds with no murmurs, rubs, or gallops. There was no edema on examination of the lower extremities.
An initial electrocardiogram (EKG) was obtained as can be seen in Figure .
Her EKG showed sinus rhythm with sinus arrhythmia and anterolateral T wave inversions concerning for anterior ischemia. Cardiac biomarkers included a creatine kinase level of 261 U/L (normal range, 33-211 U/L), a creatine kinase-MB fraction of 13 U/L (normal, <10 U/L), and a troponin I level of 5.22 ng/mL (normal, <0.01 ng/mL). She was transferred from an urgent care facility after aspirin and ticagrelor loading for percutaneous coronary intervention. Her peak troponin I was 5.4. Angiography revealed spontaneous coronary artery dissection (SCAD) of the distal left anterior descending (LAD) artery without any other atherosclerotic disease (Figures -). The other coronary arteries were normal. Catheterization also revealed a mildly reduced left ventricular ejection fraction of 45% and akinetic apical segments of the left ventricle.
She was started on medical management for SCAD, which included low dose aspirin, metoprolol, and captopril. Dual antiplatelet therapy and heparin were not given because of the risk for increased bleeding and no clear evidence of benefit. She was admitted to the cardiac critical care unit for observation and remained hemodynamically stable during her stay. Echocardiography done after one day confirmed wall motion abnormalities of the left ventricular apex with an estimated low normal left ventricular ejection fraction of 50%-55% (Figure ). Laboratory workup for possible connective tissue disorders or vasculitis was done as underlying coronary vasculitis may increase the risk for spontaneous dissection and it was negative for rheumatoid factor, anti-CCP and ANA and only positive for atypical perinuclear anti-neutrophil cytoplasmic antibodies (P-ANCA). She was discharged two days after the presentation on medical therapy. The patient was doing well on the subsequent follow-up visit.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [39, 'years'], 'Hypertension history': True, 'Suspicion History': 'Moderately suspicious', 'hypercholesterolemia': False, 'Diabetes mellitus': True, 'smoking': True, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'obesity': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 39 years old. The patient's age is less than 45 years and so keep the current total at 1.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 1 + 2 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 3 + 2 = 5.
Based on the patient's data, the HEART Score is 5."
4281,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4107425-1,Extracted,"A 43-year-old Caucasian man with history of premature ventricular contractions (PVCs) and mild-moderate left ventricular (LV) systolic dysfunction with normal LV dimensions on echocardiogram performed at an outside institution was admitted from the clinic after a second opinion with a chief complaint of increasing palpitations over a period of 2 months. The patient did not smoke, denied chest discomfort, shortness of breath with daily activities, paroxysmal nocturnal dyspnea, and orthopnea. There was no history of hypertension, dyslipidemia, coronary artery disease (CAD), and no family history of premature CAD or stroke. The patient also did not have a recent history of severe illness, respiratory or otherwise, or travel outside of the United States.
On physical examination, the patient appeared physically fit in no apparent distress. The vital signs were temperature 97.8 F, blood pressure 137/71 mmHg, heart rate 45 beats/min (bpm), respiratory rate 18 breathes/minute, and oxygen saturation 100% on room air. There was no jugular venous distention and no carotid bruits. Lungs were clear to auscultation. Palpation of the heart was unremarkable. The heart rate was regular with an occasional premature beat. The first and second heart sounds were normal, and no murmurs, rubs, or gallops were appreciated. The abdomen was soft, nontender, nondistended, with no hepatosplenomegaly. There was no peripheral clubbing, cyanosis, or edema. No skin lesions were noted.
Laboratories were notable only for hyperlipidemia (Table ); cardiac troponin T, creatine kinase (CK), CK-myocardial band, and brain natriuretic peptide were all within normal limits. The 12-lead electrocardiogram (ECG) demonstrated a junctional rhythm with frequent PVCs and a right bundle branch morphology (Fig. ). Repeat echocardiography was notable for mild-moderate dilation of the left ventricle, with overall mild-moderate reduction of LV systolic function with an ejection fraction (EF) of 40%. The basal-to-mid inferoposterior wall was akinetic, and the inferior wall and apex were severely hypokinetic. The LV wall thickness was normal and the right ventricular (RV) size and function, atria, pericardium, and pleura were each normal. A standard Bruce Protocol exercise stress test was carried out to assess for potential underlying etiology that led to the patient’s ECG findings with exercise []. The patient exercised for 15 min and 15 s, achieving a maximum heart rate of 160 bpm (90% of the maximum predicted for the patient’s age) and blood pressure of 166/70 mmHg. No ischemic symptoms or ST-segment changes were noted. There were multiple PVCs present during exercise with triplets and three 5-beat runs of nonsustained ventricular tachycardia (VT) during the recovery period.
A diagnostic right and left heart catheterization with coronary angiography was performed. The filling pressures (mmHg) were as follows: right atrium 10/9, right ventricle 28/4, pulmonary artery 26/10, pulmonary capillary wedge pressure 14 with ventricular waves to 18, LV end diastolic pressure 12, aorta 126/76 with no gradient on pull-back across the aortic valve. The wave forms were not suggestive of a restrictive pattern. Coronary angiography revealed no significant CAD (Fig. ).",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [43, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': True, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': False, 'obesity': False}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 43 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4282,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7319821-1,Extracted,"A 72-year-old man with exertional chest pain lasting 5 months was referred to our hospital. He had hypertension and hyperlipidaemia without prior cardiovascular history. A stress test with single-photon emission computed tomography 2 months before the catheterization showed a small sized anteroseptal wall ischaemia. An echocardiography 1 month before the catheterization showed normal left ventricular systolic function. Given his persistent symptom despite the medication of aspirin and calcium channel blocker, he underwent coronary angiography. Coronary angiography showed a systolic compression at the mid-left anterior descending artery (LAD) without any other significant stenosis (). Optical coherence tomography (OCT) corresponding to the angiographic squeezing showed an MB defined as a homogeneous intermediate intensity band (similar to the intensity of media of which major composition is smooth muscle cell) above the epicardial artery (i.e. perivascular side); the minimal lumen area measured 2.15 mm2 (). The depth and length of the intramyocardial tract of the LAD were 0.39 mm and 16.8 mm, respectively, indicating the superficial type., Full-cycle ratio, defined as the lowest ratio of distal coronary pressure (P) to aortic pressure (P) during the entire cardiac cycle, was measured with a dobutamine challenge with a pressure sensor located distal to the MB. The full-cycle ratio at rest and then inotropic stimulation by intravenous dobutamine of 5, 10, and 20 µg/kg/min were 0.89, 0.90, 0.86, and 0.73, respectively (). Compared with the waveform of atherosclerotic stenosis, which typically shows the lowest ratio in late diastole, the lowest ratio in this case was observed in early diastole. Chest discomfort was induced by dobutamine of 10 µg/kg/min and increased along with heart rate as the dosage of dobutamine increased. With dobutamine of 20 µg/kg/min, full-cycle ratio pullback showed a significant pressure step-up at the site of MB (). The cut-off value of full-cycle ratio to correlate with ischaemia at rest has been reported to be 0.89. Because dobutamine incudes hyperaemia, the value of 0.73 (<0.80) at 20 µg/kg/min of dobutamine was considered significant ischaemia. Metoprolol succinate dosage was increased from 50 mg/day to 100 mg/day and has not been further increased because of a bradycardia. The patient has been free from chest pain for 7 months after the discharge.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [72, 'years'], 'Hypertension history': True, 'Suspicion History': 'Moderately suspicious', 'hypercholesterolemia': True, 'Transient Ischemic Attacks History': False, 'Diabetes mellitus': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Electrocardiogram Test': 'Normal', 'obesity': False, 'smoking': False, 'Initial troponin': 'less than or equal to normal limit'}",4,4,4,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Moderately suspicious'. Based on the HEART Score criteria, 1 point is added for 'history', increasing the current total to 0 + 1 = 1.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 1.
The patient is 72 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 1 + 2 = 3.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 3 + 1 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 4.
Based on the patient's data, the HEART Score is 4."
4283,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4096671-1,Extracted,"A 51-year-old man presented to the outpatient department because of dyspnea with strenuous aerobic exercise. As an amateur rollerblader, he has rollerbladed twice a week for the past 5 years. About 9 months ago, dyspnea occurred abruptly during rollerblading at full speed for over ten minutes. At that time, he felt like collapsing but his symptom improved completely within 3 minutes after stopping the exercise. He had no history of known airway or cardiovascular disease.
At rest, he was asymptomatic and physical examination revealed clear lung sound and normal heart sounds without murmurs. Electrocardiography, chest radiography, and blood tests were normal. Oxygen saturation was 99 at room air and pulmonary function test was also normal at rest. A transthoracic echocardiogram revealed normal cardiac structure and function. After a baseline echocardiogram, agitated saline contrast echocardiography was performed to evaluate intra- or extracardiac shunt as a cause of the dyspnea. Only a few air bubbles appeared in the left heart after 9 cardiac cycles from the onset of right heart opacification (). To assess for the presence of intrapulmonary (IP) shunt, such as pulmonary arteriovenous malformation (AVM), computed tomography of the chest () and pulmonary angiography () were performed and they showed no significant abnormality. Since the patient complained of dyspnea during strenuous exercise, a cardiopulmonary treadmill exercise test (Quark b2, COSMED, Rome, Italy) with arterial blood gas analysis (ABGA) was performed. While increasing the exercise intensity, the patient suddenly complained of dyspnea at 205 watts of exercise and the values obtained from cardiopulmonary exercise test and ABGA at that time were as follows (). We confirmed the presence of severe exercise-induced arterial hypoxemia and an excessive alveolar-arterial oxygen tension difference (A-aDO2) widening in this patient. Bilateral breathing sounds were normal in auscultation during the dyspneic episode.
When an exercise echocardiography was done within one minute after stopping the exercise, there was no evidence of exercise-induced deterioration of cardiac function. However, the agitated saline contrast echocardiography revealed that large amount of microbubbles appeared in the left atrium and leaded to complete left heart opacification after > 5 cardiac cycles from the onset of right heart opacification (), suggesting the presence of exercise-induced IP shunts. The patient's dyspnea and hypoxemia in pulse oxymetry were completely normalized within one minute of rest. He has been limiting strenuous exercise for one year and remains free of symptoms.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [51, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'hypercholesterolemia': False, 'obesity': False}",1,1,1,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 51 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 1.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 1.
Based on the patient's data, the HEART Score is 1."
4284,18,HEART Score for Major Cardiac Events,risk,integer,pmc-2769286-1,Extracted,"A 55-year-old white British man very fit and well, presented with complaints of central chest tightness. It was non-radiating and lasted about 30 minutes. He usually walks two miles and does frequent cycling and swimming. He has not had chest pain previously and has always been in excellent health. He had a day case surgery for nasal polyp removal one week previously. He did not have any medical problems in the past and was not on any medications. He was a non-smoker. On examination all observations were normal and systematic examination was normal. All blood tests were normal. Electrocardiogram (ECG) and chest X-ray were normal. The Troponin-T test later came back raised at 0.14 micrograms per litre. A diagnosis of NSTEMI (non-ST elevated myocardial infarction) was made and he was started on appropriate treatment. The next day he had an in-patient coronary angiogram, which was normal (). The cardiologist concluded that a diagnosis of myocardial infarction was unlikely in his case, all treatment was stopped and the patient was allowed to go home with no further follow-up.
Four weeks later the patient again presented, this time with a history of left-sided chest pain. He described a sharp stabbing pain initially in the left rib cage and then in both sides later. Pain was made worse on inspiration, not related to posture or exertion and was only partially relieved with analgesics. He felt short of breath on walking which was unusual for a man of his fitness. On examination his observations were all normal. Systemic examination was normal. ECG and chest X-ray were normal. Arterial blood gases (ABG) showed- pH of 7.45, pCO2 of 4.3, PaO2 of 10.4, bicarbonate of 26 and saturation of 96%. Initially it was thought by the attending physician that the pain may be musculoskeletal. A diagnosis of pulmonary embolism (PE) was considered very unlikely in his case as he had no risk factors and was very fit, but in view of a slightly low PaO2 (though pCO2 was not low as would be expected in PE) for his level of fitness it was decided to do a CT pulmonary angiogram (CTPA) the next day. A troponin level on this occasion was normal but D-dimer came back as positive. No prediction score like Wells or Geneva was used at time of admission to determine the probability of PE. It is likely that even any such score had been used it would have shown a low probability given the absence of any risk factors for thromboembolism. To our surprise the CTPA showed bilateral pulmonary emboli in both the main pulmonary arteries and the segmental branches ( and ). The patient was started on warfarin following initial low molecular weight heparin. Once the INR was therapeutic, the patient was allowed to go home and was advised to continue on warfarin for 6 months.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'Hypertension history': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': False, 'Initial troponin': 'greater than three times normal limit', 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 55 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 1.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 1 + 2 = 3.
Based on the patient's data, the HEART Score is 3."
4285,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4214496-1,Extracted,"A 52-year-old male was hospitalized with intermittent pain in the right abdomen that had persisted for one week. The medical history revealed hypertension, but no history of trauma and radiation exposure or a family history of genetic diseases. Physical examination showed a large, hard, immobile mass with a smooth surface, ~6×6 cm in size. Laboratory tests revealed a small increase in the serum creatinine level to 120 μmol/l (normal range, 40–110 μmol/l), while the remaining results, including that for alkaline phosphatase (ALP), were normal. An abdominal computed tomography (CT) scan () showed a large, dense mass, with calcification, located below the right kidney, an oppressed upper ureter and thickening of the renal fascia. An exploratory laparotomy discovered a stiff calcified immobile retroperitoneal mass of 5×6 cm, with a wide base below the right kidney. The mass could not be completely resected of its attachment to the surrounding organs. Pathology revealed that the tumor was composed of spindle- and polygonal-shaped tumor cells, with a banded or irregular osteoid matrix. The tumor cells exhibited varying degrees of atypia and visible mitotic figures (). From these results, a diagnosis of extraskeletal osteosarcoma was formed. Immunohistochemistry showed the positive expression of vimentin and S-100, whereas examination of cytokeratin, cluster of differentiation (CD)117, CD34, epithelial membrane antigen, melanoma, B-cell lymphoma-2 and CD99 staining was negative.
Two months after the surgery, CT imaging () revealed a retroperitoneal ESOS near the right upper ureter, with a large amount of calcification. The imaging also revealed multiple metastases of the hepatic capsular, renal fascia and peritoneum. After four months, the patient underwent a second exploratory laparotomy due to tumor relapse. The surgery demonstrated that the retroperitoneal mass of ~10×10 cm in size was closely adhered to the right kidney, ileocecum and the posterior abdominal wall. There was significant chondroid tissue present on the omental tumors, which were 0.5×1.5 cm in size. Only the omental metastases were cut, and cytoreductive surgery was not viable due to the multiple metastases of the abdominal cavity and the severe adhesion with the retroperitoneal tissue. Pathological examination showed that the tumor tissue was predominantly composed of spindle-shaped cells and differentiated immature bone tissue. The cells showed mild-moderate atypia and were ordered in a storiform arrangement, with visible mitotic figures. From these results, a diagnosis of an omental osteosarcoma was formed.
The patient was administered two courses of chemotherapy, where each cycle lasted 28 days. During each cycle Endostar (15 mg/day for the first 14 days), cisplatin (100 mg/m2 on the first day) and epirubicin (25 mg/m2 for the first three days) were administered intravenously, but this had minimal efficacy. Five months after the second surgery, the patient experienced vomiting and an incomplete intestinal obstruction was suspected. The patient therefore underwent a third exploratory laparotomy. The surgery revealed a 25×30-cm right retroperitoneal mass oppressing the descending section of the duodenum and surrounded the descending colon, and a 1.1×1.2-cm implantation metastasis nodule in the outer membrane of the gastric body anterior wall (). The liver and spleen exhibited no metastatic nodules. A gastrojejunostomy and ileocolonic anastomosis were performed, and the pathology () revealed components of an osteosarcoma in the outer stomach wall, in accordance with a gastric wall osteosarcoma metastasis. The serum ALP level gradually increased to 199 U/l (normal range, 40–130 U/l). The patient eventually succumbed to retroperitoneal ESOS one year after the first surgery.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [52, 'years'], 'Hypertension history': True, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'smoking': False, 'Initial troponin': 'less than or equal to normal limit'}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 52 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4286,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5033796-1,Extracted,"A 21-year-old man presented to an accident and emergency department on a Sunday morning. Starting the evening before, he had acute chest pain that persisted till the morning. Apart from smoking (1.5 pack-years), no other cardiovascular risk factors could be detected. Known comorbidities were bronchial asthma, coeliac disease, depression and ADHD. ADHD was diagnosed 6 years before. His current medication was citalopram 10 mg (Cipramil® 10 mg), a selective serotonin reuptake inhibitor (SSRI), once daily, for about 2 years (noncontinuous) and methylphenidate 20 mg (Ritalin® Adult 20 mg) once daily. He had just recently started therapy with methylphenidate (3 days ago). Methylphenidate was started because of progressive problems regarding attention deficits. There was no ADHD-specific medication in the past (just behaviour therapy) and there was no specific medication for his bronchial asthma or the coeliac disease. Excepting his new medication, no other medically relevant events during the last weeks (infections etc.) were reported. Ritalin® Adult has been labelled for use in adult ADHD patients in Germany since 2014.
In the accident and emergency department, a clinical examination, an electrocardiogram (ECG) and a blood sample were performed. The results of the physical examination were without pathological findings, the vital signs were normal (blood pressure 117/63 mmHg, heart rate 53/min, temperature 36.9 °C). The ECG showed ST elevations in II, III, aVF, (0.1 mV) and V4–6 (0.2 mV) (Fig. ). The troponin rapid test was positive. Therefore, the patient was immediately transferred to our accident and emergency department because of the diagnosed ST elevation myocardial infarction (STEMI). The ECG results were confirmed in the blood sample, where highly elevated troponin and creatine kinase (CK) could be detected (troponin 990 pg/mL; CK 1068 U/L [CK-MB 89 U/L]). At the first contact hospital the patient was given morphine 2.5 mg, acetylsalicylic acid 500 mg and heparin 5000 IU, intravenously. Afterwards, the chest pain decreased rapidly. Before performing the coronary angiography in our department, 60 mg prasugrel (Efient®) was given orally as a starting dose. Percutaneous coronary angiography was immediately performed. Apart from signs of a coronary vasospasm in segment 1 of the right coronary artery (RCA) (Fig. ), the coronary arteries were normal. Regular conditions regarding supply area of coronary arteries could be detected. An acetylcholine spasm provocation test was not performed. After the coronary angiography, the patient was monitored in our Intermediate Care Unit. In the orienting echocardiography, a mildly reduced left ventricular ejection fraction (EF 49 %) could be seen.
During the next 4 days in the Intermediate Care Unit, the patient remained stable and asymptomatic. A daily oral dose of acetylsalicylic acid 100 mg (ASS 100 mg Hexal®) was given. CK elevated to 1800 U/L (CK-MB 98 U/L) on the second day of observation and then decreased successively to normal values. Troponin fluctuated around 900 pg/mL for the following 5 days, and then decreased too. The ECG normalised within the first 48 hours after onset of chest pain (Fig. ).
The urine toxicological testing was positive for tetrahydrocannabinol (THC). The patient admitted that he consumed cannabis 2 days before his admission to hospital. THC had been sporadically consumed by the patient in the past.
Because of the diagnostic results, the initial differential diagnosis was myocarditis. A myocardial biopsy was performed. The histological analysis of the myocardial tissue demonstrated no active acute myocarditis. Only a moderate atrophy of cardiomyocytes indirectly indicated a prolonged or already past myocardial impairment process and was therefore compatible to a status after myocarditis. Only a low viral load (106 viral copies/μg, Erythrovirus genotype 1, 40 mRNA copies) was found. The cardiac MRI showed no signs of acute myocarditis. The echocardiographic examination before discharge showed a return to a normal left ventricular function (EF 66 %).
Consequently, acute myocarditis as the reason for the patients’ symptoms and our diagnostic findings was not reasonable. We suggested that the STEMI was induced by a coronary vasospasm because of methylphenidate, as we could see in our performed coronary angiography. The medication with methylphenidate was stopped. In a telephone follow-up 1 week after discharge from hospital, the patient still had no more symptoms.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [21, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'smoking': True, 'atherosclerotic disease': False, 'Initial troponin': 'greater than three times normal limit', 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 21 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 3 + 2 = 5.
Based on the patient's data, the HEART Score is 5."
4287,18,HEART Score for Major Cardiac Events,risk,integer,pmc-8688793-1,Extracted,"A 54-year-old male patient with a height and weight of 180 cm and 78 kg, respectively, presented to our hospital with a 2-month history of non-productive cough and progressive exertional dyspnea. The patient was a smoker (30 pack-years) without any other relevant medical history. Preoperative electrocardiography (ECG) and transthoracic echocardiography did not reveal any abnormalities. Chest radiography showed ill-defined bilateral opacities in the lower lung zones, and chest computed tomography showed extensive patchy ground-glass opacities in both lower lobes (). The left lung had more severe ill-defined opacities than the right lung. Preoperative pulmonary function testing results showed one-second forced expiratory volume (FEV1) of 3.23 L (80% of predicted), forced vital capacity (FVC) of 4.11 L (78% of predicted), FEV1/FVC ratio of 79%, total lung capacity (TLC) of 5.40 L (75% of predicted), and carbon monoxide diffusion capacity (DLCO) of 49%. The patient exhibited a mild restrictive physiological pattern with decreased TLC and DLCO. Cytological examination of the bronchoalveolar lavage fluid was suggestive of PAP, and pulmonologists planned for a WLL as first-line treatment.
Upon entering the operating room with a nasal cannula with 4 L/min O2, the patient was subjected to standard monitoring practices such as ECG, noninvasive blood pressure, bispectral index, and pulse oximetry. Before induction of anesthesia, all necessary equipment was checked and included 30 L of normal saline, a Y-piece connector, an irrigation set with clamps, a plastic container, and a rapid infusion system (RIS). Initial vital signs were stable at a blood pressure of 130/90 mmHg, heart rate of 90 beats/min, respiratory rate of 16 breaths/min, and temperature of 36.2°C. Initial arterial blood gas analysis (ABGA) showed a pH of 7.42, arterial partial pressure of carbon dioxide of 34 mmHg, arterial partial pressure of oxygen of 54 mmHg, bicarbonate concentration of 22.1 mmol/L, and arterial oxygen saturation of 88% on room air. The alveolar-arterial oxygen difference was 53 mmHg, suggesting gas exchange issues. After preoxygenation, the anesthesiologist intravenously administered 1% propofol (2 mg/kg) and rocuronium (0.6 mg/kg). Total intravenous anesthesia with propofol and remifentanil was maintained throughout the procedure. A 37-French (Fr) left-sided double-lumen endotracheal tube (DLT) was used for one-lung ventilation (OLV). We confirmed proper tube placement by auscultation of lung sounds and fiber-optic bronchoscopy. Because the left lung was more affected, a right-sided OLV was performed. A manual leak test was performed by immersing the non-ventilated left lung tube in saline while ventilating the right lung. Radial arterial and jugular venous catheters were used to continuously assess arterial blood gas and hemodynamic status during the perioperative period. The mechanical ventilation parameter setting was as follows: tidal volume was 6 mL kg−1 during two-lung ventilation (TLV), 4 mL/kg−1 during OLV, with 5 cmH2O positive end-expiratory pressure (PEEP) maintained throughout. Initially, WLL was started in the supine position. A Y-piece connected to the non-ventilated lung tube served as a link between the DLT and RIS. The warmed normal saline was then instilled into the left lung through the left tracheal lumen using the RIS at a rate of <125 mL/min with a 30° head-up tilt (reverse Trendelenburg) position to facilitate the instillation (). While draining the lavage fluid, the patient was placed in the head-down tilt (Trendelenburg) position (), and the pulmonologist performed the process of chest percussion [].
LUS was performed using a Versana Balance echograph and a 2–5 MHz convex array probe (GE Healthcare, Chicago, IL, USA). The patient was scanned in the supine position by a single anesthesiologist (JO). Three regions (phrenic point, upper and lower BLUE points) were identified bilaterally in each hemithorax according to the bedside LUS in emergency (BLUE) protocol () []. Images were obtained at four intervals: (1) baseline (before anesthetic induction), (2) end lavage (after the introduction of the last bolus of normal saline into the non-ventilated lung), (3) reventilation (after reinflation of the non-ventilated lung), and (4) pre-extubation (immediately before extubation). Six points were explored, and ABGA was performed in each of the four steps. Each finding was classified into three patterns according to previously reported LUS semiotics () []. The lavage procedure was terminated when a tissue pattern (No. 3 in ) appeared in all areas of the non-ventilated lung or three or more B-lines (No. 2 in ) appeared in the ventilated lung without waiting for the fluid to overflow into the endotracheal tube. At the same time, serial ABGAs were performed to monitor hypoxemia, hypercapnia, acidosis, and electrolyte imbalance (). At the 9th cycle, an imbalance of more than 100 mL between infusion and drained volumes, as well as an increased number of B-lines of the ventilated lung, was observed compared to the previous cycle (II in ). We managed with an adequate PEEP of 7 cmH2O and negative water balance using intravenous diuretics (0.5 mg/kg intravenous furosemide). The procedure was then terminated. Subsequently, TLV was initiated. Several B-lines were observed in the lavaged lung, whereas the ventilated lung showed a regular pattern with a marked decrease (III in ). The total normal saline administered was 9.8 L, and 8.9 L saline was retrieved from the left lung. Intraoperative fluid management was performed with intermittent confirmation of the volume status by qualitative methods such as visual estimation using transthoracic echocardiography because of its technical complexity and time-consuming nature. The total volume of intravenously infused crystalloid solution administered to the patient during the WLL procedure was 1,850 mL, and the total urine output during the procedure was 450 mL. The DLT was exchanged for a 7.0 mm single lumen, and the patient was transferred to the intensive care unit. The next day, the patient was extubated. Manual chest physiotherapy was continued postoperatively. The symptoms improved clinically with a saturation of ≥94% on room air (), and he was discharged 1 week after the procedure.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'Hypertension history': False, 'Electrocardiogram Test': 'Normal', 'Diabetes mellitus': False, 'obesity': False, 'smoking': True, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'hypercholesterolemia': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 54 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: smoking. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4288,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7918336-1,Extracted,"A 38-year-old, right-handed lady developed chest pain and acute pulmonary edema 4 hours following explantation of stereoelectroencephalogram (sEEG) electrodes. She had poorly controlled, post-traumatic right temporal lobe epilepsy but no additional past medical history or risk factors for cardiovascular disease. MRI brain demonstrated multiple areas of gliosis, particularly laterally and anteromedially in the right temporal lobe, the right, and to a lesser degree, left orbitofrontal cortex, with focal white matter loss in the corpus callosum. Video-telemetry was consistent with focal-onset, nondominant mesial temporal or orbitofrontal lobe seizures; semiology consisted of right upper limb and oral motor automatisms preceded by prolonged aura, including olfactory and autonomic features. Generalized convulsive seizures were not observed during this period of recording. Robotic sEEG (Renishaw Neuromate) was undertaken to further localize seizure onset; 13 electrodes were implanted in the right hemisphere in a frontotemporal distribution and 1 in the left orbitofrontal region (Figure ). Routine postinsertion CT demonstrated a small parenchymal hematoma related to the right posterior temporal electrode ((electrode F); entry via middle temporal gyrus, deep contacts in the fusiform gyrus) which was asymptomatic. Over 9 days, a total of 14 stereotyped seizures were recorded (Figure ); all initiated from the right mesial temporal structures starting in the amygdala with rapid spread to the hippocampus and right temporal pole. Apparently uneventful explantation occurred at day 10 on the ward. This was several hours after the last recorded seizure, and prophylactic enoxaparin had been withheld for 48 hours.
Four hours postexplantation during which time seizures did not occur, the patient experienced severe central chest pain at rest with radiation to the neck and associated dyspnea, diaphoresis, and nausea. Pain responded to glyceryl trinitrate and morphine. She denied headache. Oxygen (O2) saturations were 73% on air, improving to 98% with 3 L O2. There was hemodynamic instability, sinus tachycardia (rate 125/min) and episodic hypotension (minimum systolic 70 mmHg). Cardiorespiratory examination was consistent with pulmonary edema secondary to acute left ventricular (LV) failure, and there were no focal neurological findings or seizures. Electrocardiogram demonstrated new-onset anterolateral T-wave inversion with reciprocal changes in leads II, III, and aVF (Figure A,B). Chest X-ray findings confirmed pulmonary edema (Figure ). Intravenous frusemide was administered, and, given concern regarding the possibility of non-ST elevation myocardial infarction (NSTEMI), dual antiplatelet therapy was commenced.
Clinical improvement with resolution of chest pain and dyspnea occurred over 24 hours. Troponin level rose from 13 to 33 ng/L. ECG changes resolved, and the coronary angiogram was normal. Antiplatelet therapy was discontinued at 48 hours. Transthoracic echocardiogram revealed evidence of moderate LV systolic dysfunction (estimated ejection fraction 40%–45%) and hypokinesis of the cardiac apex as well as the anterior and anteroseptum. The right temporal lobe hematoma was again noted on MRI brain at 2 days postexplantation along with right frontal pole edema (Figure ) but there was no extension of the hematoma when compared with the initial postexplantation CT scan. TTE demonstrated improvement in LV systolic function at 4 weeks and near normal function at 6 months.
Following initial concern regarding the possibility of NSTEMI, the diagnosis was revised to takotsubo stress cardiomyopathy (TTS). TTS, also known as “stress-induced cardiomyopathy” and “broken heart syndrome,” is characterized by LV dysfunction with regional wall abnormalities including apical ballooning and focal wall-motion abnormalities; the end-systole radiological appearance of the left ventricle is said to resemble a Japanese octopus trap (“takotsubo”). TTS occurs more often in postmenopausal females and at times of emotional and physical stress. The pathogenesis remains uncertain although sympathetic stimulation is key and a link between the insular cortex and central autonomic network recognized. Acute neurological diseases including subarachnoid hemorrhage, stroke, and seizures are well-recognized precipitants for TTS, and an association between TTS and sudden unexplained death in epilepsy (SUDEP) has been proposed. TTS has not previously been recorded in the context of sEEG.
Level C evidence for treatment of TTS is available, and management is generally based on guidelines for treatment of acute coronary artery syndrome with particular consideration given to beta-blockers in view of association with elevated catecholamine levels, diuretics for pulmonary edema, and nitroglycerin in LV failure.
Intracranial hemorrhage (ICH) is well recognized to be a precipitant for TTS, and ICH has been reported to occur in approximately 1% patients undergoing sEEG. The presence of temporal lobe hemorrhage could therefore have been a trigger for TTS. Takosubo syndrome has also been reported several days after convulsive and nonconvulsive seizures, so seizure activity may also have been a contributory factor. While we cannot categorically state that explantation induced TTS in our patient, we consider the timing suggestive although the association has not, to the best of our knowledge, been reported previously. Furthermore, the multiple potential triggers may have contributed to the presentation.
Given the potential for overlapping risk factors of seizures and ICH, this case highlights the importance of awareness of TTS in the context of an epilepsy surgery program. We advise early involvement of cardiologists in the care of patients suspected of having TTS and, if clinically safe to do so, prompt neuroimaging to exclude ICH.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [38, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Initial troponin': 'between the normal limit or up to three times the normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False}",3,3,3,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 38 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 2.
The value of 'initial troponin' in the patient's note is determined to be 'between the normal limit or up to three times the normal limit'. Based on the HEART Score criteria, 1 point is added for 'initial troponin', increasing the current total to 2 + 1 = 3.
Based on the patient's data, the HEART Score is 3."
4289,18,HEART Score for Major Cardiac Events,risk,integer,pmc-4974773-1,Extracted,"A 41-year-old man, unemployed, brown, parent of two school-age children, with no prior comorbidities, and presenting with dyspnoea, fever, and oedema was admitted to the cardiac emergency service. The patient had undergone no related interventions in the past and had no cardiac risks based on his family history.
He had fever and dry cough, which aggravated into progressive respiratory distress, lower limb oedema, and orthopnoea 30 days prior to hospitalisation. Physical examination revealed fever (38 °C), pallor (++/4+), dyspnoea, tachycardia [heart rate (HR) = 136 bpm], cardiac gallop rhythm (presence of S3), mitral systolic murmur as well as absent breath sounds at the lung base, and crackles and rales up to the middle third of both the lungs. Additionally, he experienced hepatomegaly, splenomegaly, painless oedema, positive pitting oedema (++++/4+) of the lower limbs, bruises, and petechiae (Fig. ).
The electrocardiogram revealed sinus tachycardia, first-degree right bundle branch block, and ventricular and left atrial overload as well as diffuse and nonspecific disturbances of ventricular repolarization (Fig. ). The chest radiographs revealed bilateral pleural effusion in the lung base and an enlarged cardiac silhouette (Fig. ). A transthoracic echocardiogram revealed 35 % ejection fraction (EF) of the left ventricle (LV) and an increase in the left cavity (70 mm LV). Coronary angiography revealed no obstructive atherosclerosis lesions in the coronary artery.
Serological tests were conducted for HIV-1 and HIV-2, hepatitis B and C, CMV, and Chagas disease. The serological tests results were negative for all the viruses except CMV, which included positive results for IgM (1.54 UI/mL) and IgG (2.5 UI/mL) by using ELISA.
Laboratory-based tests conducted upon admission revealed the following: haemoglobin level, 9.15 g/dL; leukocyte number, 8400/mm3; segmented neutrophil fraction, 77.5 %; platelet number, 289,000/mm3; unchanged coagulation; erythrocyte sedimentation rate, 120 mm/h; and C-reactive protein (CRP) level, 96 mg/dL. Troponin I level increased but the creatinine kinase-MB level did not increase (3.12 and 2.1 ng/mL, respectively). The renal scores and ionogram values were within the reference values. In addition, the patient showed significantly increased levels of canalicular liver enzymes [alkaline phosphatase (ALP) and gamma glutamyl transferase (GGT)] during hospitalisation.
The patient was diagnosed with cardiac insufficiency due to CMV myocarditis. He was administered 250 mg of ganciclovir IV twice a day for 10 days and received supportive medication that included oral administration of 0.25 mg of digoxin once a day, 50 mg of losartan twice a day, 25 mg of carvedilol twice a day, 40 mg of furosemide twice a day, and 25 mg of spironolactone once a day. After receiving the anti-viral medication, the patient’s liver enzyme levels decreased, as revealed by laboratory-based tests (Fig. ); in addition, the hepatosplenomegaly improved. Abdominal CT was performed following the drug therapy, and normal liver characteristics were revealed with no biliary tract dilatation. The ecchymotic spots and petechiae that were observed upon admission and that had emerged during the course of infection were also treated.
The patient showed improvement in clinical and laboratory-based tests and was discharged in functional class I (New York Heart Association) after 14 days of hospitalisation. The serological tests confirmed CMV infection (IgM, 0.9 UI/mL and IgG, 10.1 UI/mL). One month after discharge, routine echocardiography revealed a 75 % EF of the LV and almost normal values for the diameter of the left chambers. The cardiac enzyme levels were normal.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [41, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'hypercholesterolemia': False, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'obesity': False, 'Initial troponin': 'less than or equal to normal limit'}",0,0,0,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 41 years old. The patient's age is less than 45 years and so keep the current total at 0.
The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 0 risk factors are present and so 0 points are added for the risk factors criteria, keeping the current total at 0.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 0.
Based on the patient's data, the HEART Score is 0."
4290,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6904778-1,Extracted,"The case is of a 71-year-old man with a history of coronary artery disease status
post coronary artery bypass grafting, hypertension, and type 2 diabetes mellitus,
who initially was evaluated in the outpatient gastroenterology clinic for
progressively chest pain, regurgitation, and mild odynophagia. His symptoms had
developed over the course of several months and were initially felt to be due to
uncontrolled, severe gastroesophageal reflux. Esophagogastroduodenoscopy (EGD) was
performed, and it revealed severe esophagitis (). Multiple biopsies taken of the
affected areas remarked only upon sloughed esophageal mucosa. Outpatient treatment
with a twice-daily, high-dose oral proton pump inhibitor for 2 months improved most
symptoms. Repeat EGD, 2 months later, demonstrated a benign, distal esophageal
stricture that was dilated with good endoscopic and symptomatic effect. Over the
next year, his symptoms gradually returned. He regurgitated almost all solid foods
and also had new, intractable nausea culminating in 2 weeks of anorexia with
associated 10-pound weight loss. He was then admitted to the hospital for further
evaluation and management.
On admission, vital signs were normal, and though no major abnormality was noted on
physical examination, he was observed coughing up blood-streaked phlegm, small blood
clots, and what appeared to be fragments of mucosal tissue. Laboratory studies,
including basic metabolic panel and liver function studies, were otherwise within
normal limits. Computed tomography scan of his chest showed marked thickening of the
distal esophagus. EGD was performed the following day and revealed severe,
circumferential esophagitis with deep, serpiginous ulcerations and mucosal sloughing
( and ), most consistent with EDS.
Multiple biopsies were taken and showed parakeratosis and minimal inflammation. A
thorough skin examination after the procedure was repeated and did not reveal any
skin or mucosal blistering or lesions. Direct and indirect immunofluorescence
microscopy of the biopsies were negative and no specific immune deposits were
present. Infectious etiologies were appropriately ruled out. Further laboratory
studies were notable for elevated erythrocyte sedimentation rate (68 mm/h, normal =
0-10 mm/h) and C-reactive peptide (4.5 mg/dL, normal <0.3 mg/dL), normal
immunoglobulin G-4 (53.8 mg/dL, normal = 4-86 mg/dL), and serum protein
electrophoresis. Given the severity of his symptoms, nonresponse to standard
therapies, and no evidence of active infection, he was started on high-dose
corticosteroids (intravenous methylprednisolone 125 mg daily for 3 days followed by
oral prednisone 40 mg daily for 1 week). He was discharged on prednisone 10 mg daily
and omeprazole 40 mg twice daily. His dysphagia and odynophagia subsequently
resolved. EGD, 1 month later, demonstrated persistent, but overall much improved
esophagitis, without mucosal sloughing or stricture ().",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [71, 'years'], 'Hypertension history': True, 'Diabetes mellitus': True, 'atherosclerotic disease': True, 'Suspicion History': 'Highly suspicious', 'Electrocardiogram Test': 'Normal', 'Initial troponin': 'less than or equal to normal limit', 'hypercholesterolemia': False, 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False}",6,6,6,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 71 years old. The patient's age is greater than 65 years and so we increment the current total by 2, making the current total 2 + 2 = 4.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 4 + 2 = 6.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 6.
Based on the patient's data, the HEART Score is 6."
4291,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6884731-1,Extracted,"A 43-year-old non-athlete man patient was referred to Cardiac Emergency Unit due to an intermittent typical chest pain from 2 days before. The chest pain severity was grade III according to Canadian Cardiovascular Society Angina Grading Scale. The “at-rest” chest pain was started 40 minutes prior to admission, and continued without any other symptoms as shortness of breath or dyspnea. The patient had no cardiovascular risk factor, and was not on any medication.
Laboratory tests showed elevated and raising troponin I (TPI) levels (TPI of 40.2 ng/l at admission time and 1524 ng/l 3 hours later, normal range: ≤ 19 ng/l). Furthermore, the laboratory results revealed dyslipidemia [triglyceride: 72 mg/dl, cholesterol: 222 mg/dl, high-density lipoprotein (HDL) cholesterol: 47 mg/dl and low-density lipoprotein (LDL) cholesterol: 151 mg/dl]. The first ECG showed pre-excitation WPW as well as de Winter pattern ().
According to patient’s symptoms and suggestive ECG for probable LAD occlusion, emergent angiography was scheduled. The coronary angiography revealed sever LAD occlusion (). Diagonal, left circumflex and left main arteries were normal, left and right coronary artery had significant lesion at mid part. The patient was symptom free after successful ballooning.
The ballooning was performed by use of guiding catheter Judkins left 6-3.5, and workhouse Guidwire Runthrough Hypercoated was used to pass the lesion. Then semicopliant balloon used for dottering and pre-dilatation of the lesion. After this step, the Resulut Onyx stent 3*32 mm was deployed, and post-dilatation by non-compliant balloon (Apollo 3*20 mm) was done. The post-percutaneous angiography ECG indicated the absence of de Winter pattern (). The patient was discharged healthy and aspirin, clopidogrel, atorvastatin, carvedilol, spironolactone, and captopril were prescribed. The patient remained asymptomatic in 1-year follow-up period.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [43, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': True, 'Diabetes mellitus': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'obesity': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 43 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 3 + 2 = 5.
Based on the patient's data, the HEART Score is 5."
4292,18,HEART Score for Major Cardiac Events,risk,integer,usmle-6153,Extracted,"A 56-year-old man presents to the emergency department with increasing shortness of breath and mild chest discomfort. One week ago he developed cold-like symptoms, including a mild fever, headache, and occasional night sweats. He noticed that he required 2 additional pillows in order to sleep comfortably. Approximately 1-2 nights ago, he was severely short of breath, causing him to awaken from sleep which frightened him. He reports gaining approximately 6 pounds over the course of the week without any significant alteration to his diet. He says that he feels short of breath after climbing 1 flight of stairs or walking less than 1 block. Previously, he was able to climb 4 flights of stairs and walk 6-7 blocks with mild shortness of breath. Medical history is significant for coronary artery disease (requiring a left anterior descending artery stent 5 years ago and dual antiplatelet therapy), heart failure with reduced ejection fraction, hypertension, hyperlipidemia, and type II diabetes. He drinks 2 alcoholic beverages daily and has smoked 1 pack of cigarettes daily for the past 35 years. His temperature is 98.6°F (37°C), blood pressure is 145/90 mmHg, pulse is 102/min, and respirations are 20/min. On physical exam, the patient has a positive hepatojugular reflex, a third heart sound, crackles in the lung bases, and pitting edema up to the mid-thigh bilaterally.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [56, 'years'], 'Suspicion History': 'Highly suspicious', 'Hypertension history': True, 'smoking': True, 'Diabetes mellitus': True, 'atherosclerotic disease': True, 'hypercholesterolemia': True, 'Electrocardiogram Test': 'Normal', 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 56 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, smoking, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: obesity, family with cvd. The following risk factor(s) are missing from the patient's data: obesity, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 4 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 3 + 2 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 5.
Based on the patient's data, the HEART Score is 5."
4293,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6376548-1,Extracted,"A 59-year-old diabetic and hypertensive male patient presented to our department with acute onset chest pain radiating to the left arm. His blood pressure was 110/70 mmHg, pulse rate was 68 beats/min, the respiratory rate was 16 breaths/min, and oxygen saturation was 99% on room air. His 12-lead electrocardiography revealed QS complexes in the inferior leads (). Two-dimensional echocardiography showed the absence of regional wall abnormality of the left ventricle and normal valvular function. His high-sensitivity troponin T (Elecsys Assay, Roche diagnostics, MA) level was 5.16 ng/mL (N < 0.014 ng/mL). The patient had undergone CABG 7 years back in another hospital for stable angina. One arterial graft, that is, LIMA to left anterior descending (LAD) artery and two venous grafts, one each to the first obtuse marginal (OM1) and the posterior descending artery (PDA) were implanted at that time. His previous left ventricular ejection fraction was also normal. He was doing well on guideline-directed medical therapy since then. He was compliant to drugs. His blood sugar levels were under control with oral hypoglycemic agents. His estimated glomerular filtration rate (eGFR) by the Modification of Diet in Renal Disease (MDRD) equation was 65.87 mL/min/1.73 m2. Other hematological and biochemical parameters were within normal range.
He was taken upon coronary angiogram with an intention to revascularize. His native coronary angiogram revealed severe triple vessel disease with total occlusion of the right coronary artery in mid part ( and ). To our surprise, both venous grafts were patent ( and ). To our dismay, LIMA graft to LAD graft was 100% occluded proximal to distal anastomotic site ( and ). Therefore, we considered LIMA graft as the culprit lesion and decided to intervene. However, the patient refused any intervention and opted for medical therapy. During his hospital stay, he demonstrated hemodynamic stability and pain-free status for the next 72 hours. He was discharged on dual antiplatelet (aspirin plus ticagrelor) regimen supplemented by other drugs for secondary prevention after myocardial infarction as directed by the guidelines. At first and second follow ups at 15 days and 1 month thereafter, he was symptomatic free on optimal medical therapy.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [59, 'years'], 'Hypertension history': True, 'Diabetes mellitus': True, 'Suspicion History': 'Highly suspicious', 'Electrocardiogram Test': 'Normal', 'Initial troponin': 'greater than three times normal limit', 'atherosclerotic disease': True, 'hypercholesterolemia': False, 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False}",7,7,7,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 59 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, diabetes mellitus, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 3 risk factors are present and so 2 points are added as 3 or more risk factors are present, making the current total 3 + 2 = 5.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 5 + 2 = 7.
Based on the patient's data, the HEART Score is 7."
4294,18,HEART Score for Major Cardiac Events,risk,integer,pmc-5350291-1,Extracted,"A 54-year-old Caucasian female with a medical history significant for hypertension, hyperlipidemia, cervical disc disease, and depression was admitted for routine cervical spine surgery. She has never smoked and does not drink alcohol. Her medications included lisinopril 10 mg, atorvastatin 40 mg, citalopram 20 mg, and furosemide 20 mg. She has severe degenerative disk disease at C4–C7, with herniated nucleus pulposus. The patient was admitted to hospital for an elective cervical disk arthroplasty with diskectomy at C4 to C7 and fusion at C5–C7.
The patient failed weaning off the ventilator on multiple attempts postoperatively. There were no observed symptoms of an allergic reaction. Her vital signs and laboratory tests were unremarkable. CT scan of the neck showed extensive edema at the level of the arytenoids, but no retropharyngeal hematoma or abscess were noted (). A bronchoscopy confirmed arytenoid edema.
Dexamethasone 8 mg was given every 6 hours for 4 days to reduce the edema without successful resolution. On review of her medications, it was found that the patient was on lisinopril following the procedure for the treatment of hypertension. It was subsequently discontinued. The following day, the patient was weaned and successfully extubated.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'Hypertension history': True, 'hypercholesterolemia': True, 'smoking': False, 'Diabetes mellitus': False, 'atherosclerotic disease': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Electrocardiogram Test': 'Normal', 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False, 'Initial troponin': 'less than or equal to normal limit'}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 54 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: hypertension. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4295,18,HEART Score for Major Cardiac Events,risk,integer,pmc-6098913-1,Extracted,"A 46-year-old male presented to the emergency department (ED) after three syncopal episodes. In the preceding three days, the patient experienced the onset of cough, congestion, and generalized malaise. His son had similar symptoms. On the morning of his arrival to the ED, the patient experienced lightheadedness while he was in the bathroom getting ready for work. He lost consciousness and reported waking up against the sink. Twenty minutes later, while sitting on his bed, he experienced another syncopal episode and fell against his dresser. He tried to get up, but again lost consciousness. It was at this time that he called 911 and the patient was brought to the ED. None of the episodes were associated with chest pain, palpitations, shortness of breath, vertigo symptoms, or headaches.
The patient's past medical history was notable for obstructive sleep apnea. He had myringotomy tubes as a child but no other surgeries. He occasionally smoked cigars and drank alcohol socially and had no history of drug use or abuse. He reported that his grandfather had coronary artery disease (CAD). There was no family history of cardiac conduction abnormalities. The patient was allergic to penicillin, latex, and shellfish. He did not take any prescribed or over-the-counter medications.
Vital signs on arrival were blood pressure of 126/70 mm Hg, heart rate of 82 beats per minute, respiratory rate of 16 breaths per minute, and temperature of 99.2 degrees F orally with oxygen saturation of 96% on room air.
The patient was awake and alert in no apparent distress. His head was normocephalic and atraumatic. Neck was supple and the posterior elements did not have any tenderness or step-offs. There were no carotid bruits. The heart exam revealed a normal rate with no murmurs, rubs, or gallops. There was no displacement of point of maximal intensity. The lungs were clear to auscultation bilaterally. Abdomen exam was unremarkable. The extremities had no edema. His skin was warm, dry, without any obvious rashes. The neurological examination was unremarkable.
Diagnostic studies showed serum glucose of 178 mg/dl. Tests of sodium, potassium, BUN, creatinine, TSH, calcium, and magnesium were within normal limits. Cardiac biomarkers were negative. The white blood cell, hemoglobin, hematocrit, and platelet counts were within normal limits.
The chest X-ray did not reveal any evidence of effusions or infiltrates. An influenza swab was influenza B positive. The patient had not received influenza vaccine for the year. A dose of Tamiflu (oseltamivir) was initiated.
While in the ED, the patient had a witnessed syncopal event. Telemetry tracings at the time of the episode was reviewed and showed bradycardia and 6-second sinus arrests [].
A 12-lead electrocardiograph (ECG) was obtained and showed junctional bradycardia with a rate of 39 [].
The cardiology team evaluated the patient in the ED. A 2D echo showed borderline concentric left ventricular hypertrophy and trace tricuspid regurgitation but preserved left and right ventricular systolic function with ejection fraction estimated to be approximately 60-65%. Given the patient's multiple episodes of syncope, telemetry data, and his ECG findings, a permanent pacemaker was recommended.
The patient was taken to the OR and a permanent pacemaker was successfully implanted. The patient was monitored in the Intensive Care Unit (ICU) postoperatively. A repeat ECG on post-op day number one showed normal sinus rhythm with rate of about 75 beats per minute and no ischemic changes []. Telemetry monitoring did not show any additional bradycardic episodes or sinus blocks. Lyme IgG and IgM testing was negative. The rest of his hospitalization was unremarkable and patient was discharged to home with an outpatient cardiology follow up one week from discharge.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [46, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Slightly suspicious', 'Diabetes mellitus': False, 'smoking': True, 'parent or sibling with Cardiovascular disease before age 65': True, 'atherosclerotic disease': False, 'Initial troponin': 'less than or equal to normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False}",2,2,2,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Slightly suspicious'. Based on the HEART Score criteria, 0 points are added for 'history', keeping the current total at 0.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 0.
The patient is 46 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 0 + 1 = 1.
The following risk factor(s) are present based on the patient's note: smoking, family with cvd. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, atherosclerotic disease. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, atherosclerotic disease. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 1 + 1 = 2.
The value of 'initial troponin' in the patient's note is determined to be 'less than or equal to normal limit'. Based on the HEART Score criteria, 0 points are added for 'initial troponin', keeping the current total at 2.
Based on the patient's data, the HEART Score is 2."
4296,18,HEART Score for Major Cardiac Events,risk,integer,pmc-3127305-1,Extracted,"A 57-year-old female was admitted to our coronary care unit with the complaints of severe chest pain radiating to left arm and diaphoresis. She was a known hypertensive and on oral metoprolol 100 mg/day for the last 7 years. On examination she was found to be tachypnoeic; with a pulse rate 110/minute, regular, normal volume; and blood pressure 165/95 mmHg. Examination of other systems revealed no abnormalities. The biochemical parameters were within normal limits. Troponin-T value was strongly positive. After initial stabilization, she underwent coronary angiography and detected to have triple vessel disease with >80% blockade of all the major coronary vessels. Surgical correction was planned a week later.
She was premedicated with diazepam 10 mg night before, 5 mg in the morning PO and morphine sulfate 0.2 mg/kg, and phenergan 25 mg IM 1 hour before surgery. Metoprolol 50 mg PO was continued till the morning of surgery. The anesthesia induction and maintenance regime included thiopentone sodium, midazolam, fentanyl, rocuronium, and pancuronium. Coronary artery bypass grafting was done under moderate hypothermia and cold blood cardioplegia. The patient was weaned off successfully from cardiopulmonary bypass under the cover of nitroglycerine infusion and shifted to postoperative cardiac surgical intensive care unit. The trachea was extubated 6 hours after surgery. She was found to be comfortable, breathing normally, with blood pressure of 118/68 mmHg, pulse rate 67/minute, and SaO2 97% in room air. Two hours later she was found to be agitated, had a sudden rise in blood pressure to 200/100 mmHg and diaphoresis. As the last dose of fentanyl was administered 3 hours before extubation, pain was considered the cause and she was administered 1 μ/kg body weight fentanyl to get a quick relief from symptoms. However, instead of relief, she developed myoclonus, headache, nausea, and vomiting. An infusion of nitroglycerine 1 μg/kg/min was started to reduce the blood pressure. A possibility of neurological complication related to cardiopulmonary bypass was thought and an emergency CT scan of the head was performed which revealed no abnormality. The family was informed of the condition and possibility of an adverse outcome. Her husband revealed that she was under fluoxetine 60 mg/day therapy since the last 18 weeks. The possibility of serotonin syndrome was considered. Diazepam 5 mg was administered IV and cyproheptadine 20 mg PO to reduce the symptoms. The improvement in symptoms was noticed within 4 hours and complete resolution was achieved after 30 hours. Fluoxetine therapy was resumed after 36 hours in a reduced dose of 40 mg/day after a psychiatric consultation. The balance postoperative course was uneventful and she was discharged from hospital on 8th postoperative day.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [57, 'years'], 'Hypertension history': True, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'smoking': False, 'parent or sibling with Cardiovascular disease before age 65': False}",6,6,6,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 57 years old. The patient's age is between 45 and 65 years and so we increment the current total by 1, making the current total 2 + 1 = 3.
The following risk factor(s) are present based on the patient's note: hypertension, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 3 + 1 = 4.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 4 + 2 = 6.
Based on the patient's data, the HEART Score is 6."
4297,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7212751-1,Extracted,"A 40-year-old male called the emergency medical services immediately after experiencing an unrelenting headache, nausea, and chest pain, that evolved shortly after consuming rhino and completing intercourse. He denied having a medical history, experiencing anginal symptoms in the past and denied using any medications, including herbal supplements. He denied a tobacco or alcohol history but endorsed to using alprazolam and various sexual enhancers for years. He stated that he began using sildenafil years prior despite not displaying any signs or symptoms of sexual dysfunction and using it solely for recreational purposes. Eventually, he switched to tadalafil when the effects began wearing off. On the insistence of his friends and looking for cost-effective methods, he switched to rhino in 2016, stating that the potency was producing satisfying results with lower costs compared to PDE5i. He would acquire rhino for $8 from multiple gas stations and endorsed being a chronic user of rhino, usually consuming one 950 mg pill before the intended use, but this particular time he took three pills. During his years of sexual enhancer use, he did endorse to frequently experiencing similar headaches in the past after use, although it was never to this degree, nor was it ever un-interrupting. A pre-hospital electrocardiograph (ECG) revealed an inferior ST-segment elevation myocardial infarction (STEMI) and complete heart block manifested by bradycardia (Figure ).
His vitals while at the emergency department were blood pressure of 111/63 mm Hg, heart rate of 48 beats per minute, respiratory rate of 22, oxygen saturation of 99% on room air, and Glasgow Coma Scale of 15. On physical examination, he was diaphoretic with cold extremities and had precordial chest pain and brisk pulses throughout. A repeat ECG in the emergency department reported similar findings of inferior ST-segment elevations in leads II, III, aVF, V5, and V6 and ST-segment depressions in leads I, aVL, and V2 while high-sensitivity troponin I was 163.41 ng/mL. Notable labs was a white blood cell count of 14.3 K/UL without left shift, total cholesterol 184 mg/dL, triglycerides 283 mg/dL, high density lipoprotein (HDL) 26 mg/dL, low density lipoprotein (LDL) 101 mg/dL, mild transaminitis with aspartate aminotransferase at 307 U/L, and alanine aminotransferase at 117 U/L. Urine toxicology screen came back positive for benzodiazepines. As per protocol, the cardiac catheterization lab was activated, and the patient received fentanyl 50 mcg and a loading dose of aspirin 325 mg before the procedure. Coronary angiography revealed 100% occlusion with thrombolysis in myocardial infarction (TIMI) grade flow of 0 (Figure ). He underwent percutaneous coronary intervention (PCI) with a drug-eluting stent (DES). Post dilation demonstrated 0% stenosis with a TIMI grade flow of 3 (Figure ). He was simultaneously transvenously paced after demonstrating complete heart block morphology. After the procedure, he was started on dual antiplatelet therapy with aspirin 81 mg and ticagrelor 90 mg twice daily and was given analgesia. His sheath was removed shortly after and he recovered without any complication. An ECG completed post procedure revealed disappearance of ST changes and the presence of a Q wave consistent with a previous MI (Figure ). A reconstructed diagram of the coronaries can be seen below (Figure ).",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [40, 'years'], 'Hypertension history': False, 'Suspicion History': 'Highly suspicious', 'hypercholesterolemia': True, 'Diabetes mellitus': False, 'smoking': False, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Transient Ischemic Attacks History': False, 'Electrocardiogram Test': 'Normal', 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 40 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, smoking, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, smoking, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 1 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 3 + 2 = 5.
Based on the patient's data, the HEART Score is 5."
4298,18,HEART Score for Major Cardiac Events,risk,integer,pmc-7026880-1,Extracted,"A healthy 41-year-old male with no past medical history apart from alcoholism and smoking presented with chest pain after a high-speed motor vehicle accident and steering wheel trauma to the chest. On admission, his vitals were stable and physical examination was unremarkable. EKG showed ST elevations in leads II, III and aVF consistent with inferior wall MI and troponin was elevated at 5.38 ng/ml (Figure ).
Before any other diagnostic tests could be performed, the patient developed severe substernal chest pain and soon became confused. EKG showed a complete heart block causing hemodynamic instability that required immediate transcutaneous pacing. An urgent bedside echocardiogram showed right ventricular akinesia with no evidence of pericardial effusion or other structural injuries to the heart. The patient was urgently taken to the cardiac catheterization laboratory. Coronary angiography revealed a long intimal flap in the RCA resulting in a 99% stenosis of the vessel, without resolution on intracoronary nitroglycerin administration (Figure ). The remaining coronaries were normal.
He underwent percutaneous coronary intervention, with the subsequent deployment of four drug-eluting stents with improvement from initial 99% stenosis (TIMI 1flow) to final 0% stenosis with TIMI 3 flow (Figure ). Further imaging showed no evidence of other forms of blunt trauma injury like a cardiac contusion, hemopericardium, hemothorax or pneumothorax. The patient was monitored in the cardiac ICU and once medically stable, was discharged on dual antiplatelet therapy and a beta-blocker.",What is the patient's score of the HEART Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [41, 'years'], 'Hypertension history': False, 'Transient Ischemic Attacks History': False, 'Suspicion History': 'Highly suspicious', 'Diabetes mellitus': False, 'smoking': True, 'atherosclerotic disease': True, 'Initial troponin': 'greater than three times normal limit', 'Electrocardiogram Test': 'Normal', 'hypercholesterolemia': False, 'obesity': False, 'parent or sibling with Cardiovascular disease before age 65': False}",5,5,5,"The HEART Score for risk stratification in patients with chest pain is shown below:

1. History: Slightly suspicious = 0 points, Moderately suspicious = +1 point, Highly suspicious = +2 points
2. EKG: Normal = 0 points, Non-specific repolarization disturbance = +1 point, Significant ST deviation = +2 points
3. Age: <45 years = 0 points, 45-64 years = +1 point, ≥65 years = +2 points
4. Risk factors (HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m²), smoking (current or cessation within 3 months), positive family history of cardiovascular disease before age 65, atherosclerotic disease such as prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease): No known risk factors = 0 points, 1-2 risk factors = +1 point, ≥3 risk factors or history of atherosclerotic disease = +2 points
5. Initial troponin level: ≤normal limit = 0 points, 1-3x normal limit = +1 point, >3x normal limit = +2 points

The total score is calculated by summing the points for each criterion.
    
The current HEART Score is 0.
The value of 'history' in the patient's note is determined to be 'Highly suspicious'. Based on the HEART Score criteria, 2 points are added for 'history', increasing the current total to 0 + 2 = 2.
The value of 'electrocardiogram' in the patient's note is determined to be 'Normal'. Based on the HEART Score criteria, 0 points are added for 'electrocardiogram', keeping the current total at 2.
The patient is 41 years old. The patient's age is less than 45 years and so keep the current total at 2.
The following risk factor(s) are present based on the patient's note: smoking, atherosclerotic disease. The following risk factor(s) are mentioned in the patient's note, but these risk factors are noted to be absent from the patient: hypertension, diabetes mellitus, obesity, family with cvd. The following risk factor(s) are missing from the patient's data: hypertension, diabetes mellitus, obesity, family with cvd. We will assume that these are all absent from the patient. Based on the HEART Score risk factors criteria, 2 risk factors are present and so 1 point is added for the risk factors criteria, making the current total, 2 + 1 = 3.
The value of 'initial troponin' in the patient's note is determined to be 'greater than three times normal limit'. Based on the HEART Score criteria, 2 points are added for 'initial troponin', increasing the current total to 3 + 2 = 5.
Based on the patient's data, the HEART Score is 5."
4299,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-3994266-1,Extracted,"A 17-year-old girl visited Chungbuk National University Hospital, presenting with fever and abdominal pain that had developed 7 days previously. She had undergone an operation for gastroschisis repair at birth. At the time of admission, her vital signs were as follows: blood pressure, 120/80 mm Hg; pulse rate, 70 beats per minute; respiration rate, 18 breaths per minute; and body temperature, 37.5℃. She appeared emaciated and acutely ill. Her body mass index was 18.1 (height, 151 cm; and weight, 41.3 kg). A physical examination revealed icteric sclera, a very thin abdominal cavity, and a longitudinal surgical scar at the midline. Tenderness was noted in the upper abdominal area, and normal bowel sounds were heard. There was no particular finding in the limb or neurological examinations. Laboratory analysis revealed a white blood cell count of 27,000 cells/mm3; hemoglobin level, 12.3 g/dL; platelet count, 277,000 cells/mm3; aspartate aminotransferase level, 108 IU/L; alanine aminotransferase level, 144 IU/L; alkaline phosphatase level, 476 IU/L; total protein level, 6.5 g/dL; albumin level, 3.7 g/dL; total bilirubin level, 14.1 mg/dL; direct bilirubin level, 9.2 mg/dL; amylase level, 592 U/L; lipase level, 825 U/L; blood urea nitrogen level, 5.0 mg/dL; and creatinine level, 0.5 mg/dL. These data were compatible with diagnoses of acute cholangitis and acute biliary pancreatitis. An abdominal computed tomography scan revealed a round calcifying lesion near the pancreas (), and the absence of the retroperitoneal duodenum and the anterior position of the spleen with respect to the left kidney. The anterior and left-sided position of the superior mesenteric vein compared with that of the superior mesenteric artery was observed in the abdominal computed tomography scan (). The coronal view revealed the distorted architecture of the liver and a high-attenuation lesion at the extrahepatic bile duct (). Results of a barium examination revealed a right-sided duodenojejunal flexure and malpositioning of the bowel, with the small bowel on the right side and the colon on the left side (). Intestinal malrotation could be diagnosed based on these findings. ERCP was performed by using a lateral-view endoscope in the usual way. After approaching the ampulla, the endoscope was pushed against the duodenal wall to maintain the papilla in the correct position, and a selective bile duct cannulation confirmed the presence of a 12-mm round stone in the common bile duct. With a guidewire-assisted technique, the single dark brown stone was removed by using a Dormia basket after the endoscopic sphincterotomy (). The procedure lasted for 15 minutes. A cholangiogram obtained through an endoscopic nasobiliary drainage tube revealed a distorted biliary system, which was characterized with diffuse dilatation of the intrahepatic and extrahepatic biliary trees, downward-positioned gallbladder and a right intrahepatic biliary tree, and a horizontally located common bile duct. The abnormal orientation of the duodenum suggested intestinal malrotation (). Clinical symptoms and liver function tests normalized after the ERCP procedure. The patient has been monitored for 3 years and is in a normal state.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [17, 'years'], 'Alanine aminotransferase': [144.0, 'U/L'], 'Aspartate aminotransferase': [108.0, 'U/L'], 'Platelet count': [277000.0, 'µL']}",0.55235,0.52473,0.57997,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 108.0 U/L.
The patient's concentration of ALT is 144.0 U/L.
The patient's concentration of platelets is 277000.0 count/µL. To convert 277000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 277000.0 platelets count/µL * 1000000.0 µL/L = 277000000000.0 platelets count/L. This means that there are 277000000000.0/(10^9) = 277.0 billion platelet counts per liter.
Plugging these values into the formula, we get (17 * 108.0)/(277.0 * sqrt(144.0)) = 0.55235.Hence, the Fibrosis-4 score is 0.55235."
4300,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-7557520-1,Extracted,"A 43-year-old female with a past medical history of insulin-dependent diabetes mellitus, hypertension, and hyperlipidemia presented to the hospital with progressive shortness of breath, polyuria, dysuria, and polydipsia. The patient was diagnosed with COVID-19 by polymerase chain reaction (PCR) five days before coming to the hospital. Physical examination revealed hypoxia with decreased lung sounds and negative abdominal findings. Her labs on initial presentation revealed white blood count 21.2x109/L (normal range = 4.5 to 11.0 x 10^9/L), hemoglobin 15.1 gm/dl (normal range = 12 to 15.5 gm/dl), prothrombin time 12 seconds (normal range = 11 to 12.5 seconds), international normalized ratio (INR) 1.2 (normal range = < 1.1), fibrinogen 620 mg/dl (normal range = 200 to 400 mg/dL), D-dimer 2.03 mcg/mL fibrinogen equivalent units (FEU) (normal range < 0.5 mcg/mL FEU), blood glucose 430 mg/dl (normal range < 140 mg/dL) with an elevated anion gap, lactate 3.4 mmol/L (normal range = 0.5 to 1 mmol/L), and normal total bilirubin/liver enzymes.
CT chest revealed extensive consolidative airspace opacities with ground glass opacities while the CT abdomen was normal (Figure ). She was admitted to the intensive care unit (ICU) for diabetic ketoacidosis and progressive respiratory failure requiring endotracheal intubation on day 2 of hospitalization. Her pulmonary condition was further complicated by pulmonary edema likely related to cytokine release syndrome. She was initially treated with hydroxychloroquine and as her inflammatory markers continued to rise, she was administered tocilizumab on the day of intubation. Two days after the tocilizumab, the patient also received COVID-19 convalescent plasma. Her ICU course was further prolonged by superimposed bacterial infections including methicillin-sensitive Staphylococcus aureus pneumonia, treated with vancomycin, aztreonam, and meropenem, as well as fungal urinary tract infection, treated with fluconazole. She was successfully extubated eleven days later and was transitioned to the step-down unit.
On day 15 of admission, the patient developed severe right upper quadrant pain and back pain.Her complete blood count revealed hemoglobin of 6.1 gm/dl (normal range = 12 to 15.5 gm/dl), platelet count of 217,000/microliter of blood (normal range = 150,000 to 400,00/microliter of blood). The coagulation panel showed a prothrombin time of 13 seconds (normal range = 11 to 12.5 seconds) and an INR of 1.3 (normal < 1.1). Comprehensive metabolic panel revealed a sudden increase in liver enzymes with aspartate aminotransferase (AST) of 1111U/L (normal range = 5 to 40 U/L), alanine aminotransferase (ALT) of 1020 U/L (normal range = 19 to 25 U/L), and alkaline phosphatase (ALP) of 203 IU/L (normal range = 44 to 147 IU/L) with normal total bilirubin (normal range = 0.1 to 1. 2 mg/dL). CT abdomen without contrast revealed a heterogeneous attenuation pattern area in the right hepatic lobe (Figure ). A follow-up ultrasound abdomen with Doppler confirmed patent vasculature. We obtained a three-phase liver CT with contrast which showed large areas of heterogeneous hypodensity and heterogenous enhancement most consistent with intraparenchymal hemorrhage (Figure ). At this point, the patient's hemoglobin had also dropped by 2 gm/dl but fecal occult blood was negative, ruling out any gastrointestinal lumen bleeding. The patient was transfused with two units of packed red blood cells and her prophylactic anticoagulation was held.
While admitted, the patient’s AST peaked at 2177 U/L, ALT peaked at 1881 U/L and ALP peaked at 369 U/L. After discussing with the gastroenterology team, we started her on a trial of N-acetylcysteine (NAC) for her acute liver injury. Labs after a 21-hour infusion of NAC revealed a drastic and rapid improvement of her transaminitis. CT abdomen was repeated the next day which showed stabilization in the heterogeneous area in the right hepatic lobe. The patient continued to improve from the cardiorespiratory and gastrointestinal point of view and was discharged to an acute care rehab facility with normalized liver enzymes.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [43, 'years'], 'Alanine aminotransferase': [1020.0, 'U/L'], 'Aspartate aminotransferase': [1111.0, 'U/L'], 'Platelet count': [217000.0, 'µL']}",6.89323,6.54857,7.23789,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 1111.0 U/L.
The patient's concentration of ALT is 1020.0 U/L.
The patient's concentration of platelets is 217000.0 count/µL. To convert 217000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 217000.0 platelets count/µL * 1000000.0 µL/L = 217000000000.0 platelets count/L. This means that there are 217000000000.0/(10^9) = 217.0 billion platelet counts per liter.
Plugging these values into the formula, we get (43 * 1111.0)/(217.0 * sqrt(1020.0)) = 6.89323.Hence, the Fibrosis-4 score is 6.89323."
4301,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-7357018-1,Extracted,"A 54-year-old male presented to the emergency department for shortness of breath. His past medical history was remarkable for severe emphysema/chronic obstructive pulmonary disease, asbestos exposure, and erosive RA with positive rheumatoid factor (RF) and anti-CCP antibody. He was diagnosed with RA more than 20 years ago but has only been on steroids in the past, more so for his lung problems. He had never been on DMARDs (Disease Modifying Anti-Rheumatic Drugs) treatment and never followed with a rheumatologist. His medications included Spiriva inhaler, Ventolin inhaler, and prednisone 15 mg daily. Social history was remarkable for smoking 40 years of 1.5 PPD and quit 5 months before the presentation. Family history was remarkable for RA in his mother and aunt. He admitted shortness of breath, fever, night sweat, and unintentional weight loss about 30 lbs over the past few months. Physical examination was significant for bilateral lungs wheezing on auscultation, bilateral swan neck deformity of digits, and Z deformity of bilateral thumbs. Joints range of motion was intact with no RA nodule or active synovitis. Laboratory findings were as follows: white blood cells 710/µL with 76% lymphocytes, 6.0% neutrophils, 16% monocytes, 1.0% eosinophils, and 1.0% basophils; hemoglobin 10.6 g/dL; platelet 160 000/µL; total bilirubin 0.9 mg/dL; alkaline phosphatase 68 U/L; alanine aminotransferase 18 U/L; aspartate aminotransferase 16 U/L; and serum albumin of 2.4 g/dL. C-reactive protein 3.4 mg/dL, antinuclear antibodies (ANA) was positive, RF was 3810.0 IU/mL, and anti-CCP antibody was 250 U/mL. Serum SSB/SSA, dsDNA, C3, and C4 were within the normal limit. Chest X ray showed pulmonary emphysema, bibasilar subsegmental scarring, and pleural effusion. Bilateral hand X-ray showed carpal periarticular osteopenia, carpal bone erosions, and swan-neck deformity of the bilateral fifth digits. A computed tomography scan of the abdomen revealed mild splenomegaly (14 cm). Hematology/oncology was consulted. Peripheral blood smear revealed numerous large granular lymphocytes. Bone marrow biopsy and aspiration were reported as insufficient for diagnosis. Immunophenotyping of bone marrow revealed an increased number of T-cell lymphocytes about 91% of cells analyzed with marked aberrant loss of CD5 and moderate loss of CD7. CD4:CD8 ratio was markedly decreased (0.23) with an abnormal increase in CD8 cells. NK cells were within normal limits. Approximately 40% of the T-cell lymphocytes express a marker profile consistent with T-LGL cell lineage (positive for CD3, CD57, and CD8; negative for CD25). Clonal rearrangement of the T-cell receptor gamma (TCRG) and beta (TCRB) genes detected by polymerase chain reaction consistent with the presence of a clonal T-cell population. These results were consistent with T-LGL. The patient was diagnosed with T-LGL and started on Cytoxan 100 mg PO (per os) daily. Methotrexate was avoided due to severe lung disease. In 1-year follow-up, leukocyte count was 7860/µL with neutrophils of 74%.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'Alanine aminotransferase': [18.0, 'U/L'], 'Aspartate aminotransferase': [16.0, 'U/L'], 'Platelet count': [160000.0, 'µL']}",1.27279,1.20915,1.33643,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 16.0 U/L.
The patient's concentration of ALT is 18.0 U/L.
The patient's concentration of platelets is 160000.0 count/µL. To convert 160000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 160000.0 platelets count/µL * 1000000.0 µL/L = 160000000000.0 platelets count/L. This means that there are 160000000000.0/(10^9) = 160.0 billion platelet counts per liter.
Plugging these values into the formula, we get (54 * 16.0)/(160.0 * sqrt(18.0)) = 1.27279.Hence, the Fibrosis-4 score is 1.27279."
4302,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4421225-1,Extracted,"A 35-year-old female with ESRD was admitted to our hospital 2 years ago. She had a history of aplastic anaemia since she was 11 years old and was complicated by chronic hepatitis C probably due to frequent blood transfusion. She underwent peripheral blood stem cell transplantation at the age of 32. Her renal function deteriorated rapidly after the treatment. She started PD with the regimen of a single 6-h dwell of 2 L glucose dialysate. Considering that her genotype of HCV was 2a, which is known to be more susceptible to IFN therapy than genotype 1, and that she was a candidate for cadaveric kidney transplant, we decided to treat her with PEG-IFN alpha-2a (Pegasys&#61650, Hoffmann-LaRoche, Basel, Switzerland) monotherapy 1 year after the beginning of PD.
Laboratory results before introduction of PEG-IFN were as follows: white blood cell count, 7000/μL; neutrophil count, 56%; haemoglobin, 9.9 g/dL; platelet count, 261 000/μL; serum albumin, 3.9 g/dL; aspartate transferase, 13 IU/L; alanine transferase, 16 IU/L and HCV-RNA, 3600 KIU/ml. Because IFN may adversely affect residual renal function, we adopted a dose escalation strategy in order to minimize the total dose of PEG-IFN. Thus, the treatment was initiated at a dose of 30 μg subcutaneously once a week for the first 6 weeks, being escalated to a maximum dose of 90 μg over the next 4 weeks and continued for subsequent 38 weeks. The plasma HCV-RNA levels decreased to be undetectable at the 17th week and constantly negative thereafter. During the PEG-IFN therapy, flu-like symptoms and progression of anaemia were observed, which were treated by a transient cessation of PEG-IFN therapy for a couple of weeks and an increase in the dose of erythropoietin, respectively. The residual renal function remained stable during the course of 48 weeks (renal Kt/V; from 1.28 to 1.26). Six months after the end of the treatment, sustained virological response (SVR) was achieved.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [35, 'years'], 'Alanine aminotransferase': [16.0, 'U/L'], 'Aspartate aminotransferase': [13.0, 'U/L'], 'Platelet count': [261000.0, 'µL']}",0.43582,0.41403,0.45761,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 13.0 U/L.
The patient's concentration of ALT is 16.0 U/L.
The patient's concentration of platelets is 261000.0 count/µL. To convert 261000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 261000.0 platelets count/µL * 1000000.0 µL/L = 261000000000.0 platelets count/L. This means that there are 261000000000.0/(10^9) = 261.0 billion platelet counts per liter.
Plugging these values into the formula, we get (35 * 13.0)/(261.0 * sqrt(16.0)) = 0.43582.Hence, the Fibrosis-4 score is 0.43582."
4303,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-8383690-1,Extracted,"A 52-year-old woman with a known liver cyst and gall stone disease presented with 1 week of right upper quadrant (RUQ) pain, nausea without vomiting, anorexia, jaundice and itching. She presented similarly 6 years before. At that time, computed tomography (CT) scan was suspicious for hydatid cyst, and local hospital echinococcal antibodies were positive. However, sent-out repeat tests were negative. The patient denied contact with animals but did have multiple visits to Jerusalem. Given low epidemiology in the United States, negative repeat tests and low suspicion, the patient was scheduled to undergo hepatic cyst resection for diagnosis, but she was lost to follow-up. On this admission, the patient was afebrile and had scleral icterus with mildly jaundiced skin. Laboratory results revealed eosinophilia (white blood cell count of 7,200/µL with absolute eosinophil count of 710/µL, Hb of 14 g/dL and platelet count of 299,000/µL) with biliary pattern liver function tests that showed alkaline phosphatase (ALP) of 367 U/L with total bilirubin of 3.5 mg/dL and direct bilirubin of 3.0 mg/dL with elevated transaminases (aspartate transaminase (AST) 136 U/L and alanine aminotransferase (ALT) 244 U/L). This time, echinococcal antibodies were positive for both local and sent-out ones. Ultrasound showed cholelithiasis without evidence of cholecystitis and calcified right hepatic cystic lesion. CT scan demonstrated large hepatic hypodense lesion with thick calcified rim (). Magnetic resonance cholangiopancreatography (MRCP) showed hepatic cyst along with dilated central bile ducts and abrupt narrowing at the biliary confluence (). The endoscopic retrograde cholangiopancreatography (ERCP) revealed mild stenosis in the upper third of the common bile duct (CBD) from external compression, and the copious mucus obtained through balloon sweeps showed scolices. Based on the presentation and workup, the patient was diagnosed with HLD concerning for cystobiliary fistula and was started on albendazole. The patient was scheduled for cholecystectomy and surgical cyst removal. Since the cyst was densely adherent to the right hepatic vein and inferior vena cava, radical resection was impractical. Therefore, she underwent partial cystectomy, cystobiliary fistula repair and omentoplasty. Subsequent intraoperative cholangiogram showed no leak (). However, 2 weeks after the surgery, the patient developed a refractory biliary leak for which aggressive endotherapy, necrosectomy procedures and cystobiliary fistula embolization failed (). The case was further complicated by hepatic abscess and colonic fistula that required multiple admissions and variable antibiotic courses, and for which the patient is planned to undergo percutaneous closure. Probable next step, per multidisciplinary team discussions, is right hepatectomy with or without Roux-en-Y hepaticojejunostomy, and right hemicolectomy with diverting loop ileostomy.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [52, 'years'], 'Alanine aminotransferase': [244.0, 'U/L'], 'Aspartate aminotransferase': [136.0, 'U/L'], 'Platelet count': [299000.0, 'µL']}",1.51418,1.43847,1.58989,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 136.0 U/L.
The patient's concentration of ALT is 244.0 U/L.
The patient's concentration of platelets is 299000.0 count/µL. To convert 299000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 299000.0 platelets count/µL * 1000000.0 µL/L = 299000000000.0 platelets count/L. This means that there are 299000000000.0/(10^9) = 299.0 billion platelet counts per liter.
Plugging these values into the formula, we get (52 * 136.0)/(299.0 * sqrt(244.0)) = 1.51418.Hence, the Fibrosis-4 score is 1.51418."
4304,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-3342553-1,Extracted,"A 59-yr-old man presented to the emergency department complaining of continuous epigastric and right upper quadrant pain for the previous 3 weeks on 23th March, 2009. He had no history of hypertension or diabetes. He had smoked one pack of cigarettes every day for 40 yr and was a social drinker. He did not have any changes in bowel habit or hematochezia. The patient had undergone a gastrofiberoscopy and colonoscopy 20 days earlier in a local clinic. Endoscopic findings had revealed chronic gastritis and a polyp in the colon. Fatty liver had also been reported on the abdominal ultrasonography.
The patient had the persistent abdominal pain worsened during the last 3 days. He had focal rigidity and tenderness in the right upper quadrant of his abdomen. His initial vital signs were: blood pressure 110/60 mmHg, pulse rate 88/min, respiratory rate 20/min, and temperature 36.3℃. Six hours after presentation, he complained of chills with a high body temperature of 38.0℃. The complete blood count showed a white blood cell count of 16,800/µL, hemoglobin concentration of 14.1 g/dL, and platelet count of 350,000/µL. Blood chemistry data revealed severe increases in C-reactive protein (346 mg/L) and erythrocyte sedimentation rate (55 mm/hr), with mildly elevated levels of aspartate aminotransferase and alanine aminotransferase (127 and 175 IU/L). Bilirubin, albumin, and other blood component chemistries were all within the normal range.
Plain radiographs of the chest and abdomen were unremarkable. Pre-contrast and contrast enhanced computed tomography (CT) showed an approximately 6.0 cm, ill-defined heterogeneous enhancing hypodense mass lesion in the gastrocolic ligament (). The mass extended to its peripheries, with ill-defined infiltration of the surrounding omentum. Radiologists called for further workup to differentiate among metastatic mass, primary omental tumor, and omental infarction.
Viral and tumor markers, including carcinoembryonic antigens, alpha-fetoproteins, CA 19-9, and CA 125, were within normal ranges. Gastroduodenoscopy and colonoscopy showed simple chronic gastritis. Abdominal ultrasonography displayed an ill-defined, heterogeneous echogenic mass between the stomach and transverse colon (). Further imaging with positron emission tomography CT revealed a large intense hypermetabolic mass in the gastrocolic ligaments without evidence of metastasis. An exploratory laparotomy was consequently performed under the impression of necrotic tumorous lesion.
The operative field revealed a 4-cm crab leg embedded within the approximately 6-cm abscess in the perforated antrum of the stomach (). Streptococcus sp. was cultured from the abscess. The patient underwent antrectomy, vagotomy, and transverse colon wedge resection. A detailed history taken after surgery uncovered the Kanjang-gaejang ingestion three weeks before, one day prior to the onset of abdominal pain. Twenty days after admission, the patient was discharged from the hospital with no complications.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [59, 'years'], 'Alanine aminotransferase': [175.0, 'U/L'], 'Aspartate aminotransferase': [127.0, 'U/L'], 'Platelet count': [350000.0, 'µL']}",1.61834,1.53742,1.69926,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 127.0 U/L.
The patient's concentration of ALT is 175.0 U/L.
The patient's concentration of platelets is 350000.0 count/µL. To convert 350000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 350000.0 platelets count/µL * 1000000.0 µL/L = 350000000000.0 platelets count/L. This means that there are 350000000000.0/(10^9) = 350.0 billion platelet counts per liter.
Plugging these values into the formula, we get (59 * 127.0)/(350.0 * sqrt(175.0)) = 1.61834.Hence, the Fibrosis-4 score is 1.61834."
4305,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4379202-1,Extracted,"A 90-year-old male who presented with symptoms of general weakness and poor oral intake visited the emergency department of our hospital. He was diagnosed with hepatitis C-related liver cirrhosis and hepatocellular carcinoma (HCC) in our hospital. Abdominal computed tomography had been performed about one month previously and had revealed multiple viable HCCs in both lobes of the liver. Their largest diameter was 10.7 cm (). The patient's HCC was classified as stage B according to the Barcelona Clinic Cancer staging classification. He had undergone radio frequency thermal ablation (RFTA) once and TACE six times in our hospital. Two days ago he visited our outpatient clinic with symptoms such as general weakness, nausea, and vomiting. Because the symptoms had suggested adrenal insufficiency, he had been empirically administered prednisolone 10mg per day by the oral route for two days. ACTH stimulation test couldn't be performed at our outpatient clinic and the patient refused the test. Else he had been taking furosemide 20 mg, aldactone 50 mg a day. Before taking prednisolone, serum creatinine was 1.12 mg/dL, estimated glomerular filtration rate (eGFR) was 65 mL/min/1.73 m2, and his renal function had been well preserved considering his age.
The patient's vital signs were within normal limits at our emergency department. On physical examination, the abdomen was distended, without tenderness or rebound tenderness. A complete blood cell count showed mild leukocytosis with mild anemia: leukocytes, 14.4 × 103/µL; hemoglobin, 10.8 g/dL; and platelets, 180 × 103/µL. The following additional laboratory values were found: serum sodium, 145 mEq/L; potassium, 5.4 mEq/L; chloride 110 mEg/L; bicarbonate 24.0 mEq/L; total protein, 7.1 g/dL; albumin, 3.0 g/dL calcium, 8.7 mg/dL; inorganic phosphorus, 5.8 mg/dL. In addition, serum urea nitrogen level was 100.5 mg/dL, creatinine level was 3.00 mg/dL, eGFR was 21 mL/min/1.73 m2. AST was 310 U/L, ALT was 171 U/L, total bilirubin was 5.24 mg/dl, prothrombin time was 12.5 sec, α-fetoprotein (AFP) was 647.4 ng/mL. His Child-Turcotte-Pugh score was 9. Chest radiography revealed only an old tuberculosis lesion in the right upper lung zone. His electrocardiogram was normal. Because he had acute kidney damage, and adequate hydration could not correct it, hepatorenal syndrome was suspected. He was treated by intravenous hydration at first, and was also administered terlipressin and albumin.
Though serum uric acid was 8.0 mg/dL about 6 months ago, the following day, serum uric acid increased to 18.3 mg/dL. Serum sodium was 146 mEq/L, potassium was 5.4 mEq/L, inorganic phosphorus was 6.2 mg/dL, calcium was 8.7 mg/dL, serum urea nitrogen level was 104.6 mg/dL, creatinine level was 2.90 mg/dL, and eGFR was 22 mL/min/1.73 m2. Though oliguria was not present, his urine output was lower than a day earlier. Hydration and treatment for hepatorenal syndrome were maintained.
In next day, he had severe metabolic acidosis and acute kidney injury. Multiple organ failure progressed steadily, and he expired three days after admission.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [90, 'years'], 'Aspartate aminotransferase': [310.0, 'U/L'], 'Alanine aminotransferase': [171.0, 'U/L'], 'Platelet count': [180000.0, 'µL']}",11.85315,11.26049,12.44581,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 310.0 U/L.
The patient's concentration of ALT is 171.0 U/L.
The patient's concentration of platelets is 180000.0 count/µL. To convert 180000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 180000.0 platelets count/µL * 1000000.0 µL/L = 180000000000.0 platelets count/L. This means that there are 180000000000.0/(10^9) = 180.0 billion platelet counts per liter.
Plugging these values into the formula, we get (90 * 310.0)/(180.0 * sqrt(171.0)) = 11.85315.Hence, the Fibrosis-4 score is 11.85315."
4306,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4397463-1,Extracted,"A 65-year-old woman was admitted to the hospital for evaluation of multiple lung nodules. The patient had been living in an urban area of Korea. She denied any previous overseas travel history. The patient was seronegative for hepatitis B surface antigen, and for antibodies to hepatitis C, and HIV. She was diagnosed with autoimmune hemolytic anemia 2 years before the admission, and had been receiving corticosteroid monotherapy of 20 mg/day prednisolone. The patient was admitted because a chest X-ray showed new nodular opacities in both lungs, compared with a chest X-ray taken 6 months ago (). She did not report cough, dyspnea, hemoptysis, or pleuritic chest pain. She denied fever, night sweats, anorexia, or weight loss. Body temperature was 36.8℃, respiratory rate was 18/min, and blood pressure was 120/80 mm Hg. The chest was clear to auscultation. The laboratory results were as follows: hemoglobin, 11.7 g/dL; white blood cell count, 6230/uL (88.4% neutrophils, 5.9% lymphocytes); platelet count, 152000/µL; erythrocyte sedimentation rate, 12 mm/hr; C-reactive protein, 11.94 mg/dL; blood urea nitrogen, 23 mg/dL; creatinine, 0.87 mg/dL; aspartate aminotransferase, 15 IU/L; alanine aminotransferase, 19 IU/L; total bilirubin, 0.61 mg/dL; and reticulocyte count, 4.39%. Blood and sputum cultures were negative for any pyogenic bacteria. Sputum was negative for acid-fast bacilli by smear. A computed tomography (CT) scan of the chest showed multiple ill-defined consolidations and cavitations in all lobes of both lungs with the absence of mediastinal lymphadenopathy (). The patient underwent a CT-guided lung biopsy. A histopathology study revealed many oval shaped, budding yeast-form fungal micro-organisms in the cytoplasm of CD68(+) alveolar macrophages (), which was clearly identified by Periodic acid-Schiff and Gomori Methenamine Silver stains. The patient was diagnosed with chronic cavitary pulmonary histoplasmosis. Therapy was initiated with 200 mg itraconazole orally three times per day for 3 days and maintained with 200 mg orally twice per day for 12 months. She was well following treatment, and the follow-up chest X-ray taken 1 year later revealed complete resolution ().",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [65, 'years'], 'Alanine aminotransferase': [19.0, 'U/L'], 'Aspartate aminotransferase': [15.0, 'U/L'], 'Platelet count': [152000.0, 'µL']}",1.47158,1.398,1.54516,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 15.0 U/L.
The patient's concentration of ALT is 19.0 U/L.
The patient's concentration of platelets is 152000.0 count/µL. To convert 152000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 152000.0 platelets count/µL * 1000000.0 µL/L = 152000000000.0 platelets count/L. This means that there are 152000000000.0/(10^9) = 152.0 billion platelet counts per liter.
Plugging these values into the formula, we get (65 * 15.0)/(152.0 * sqrt(19.0)) = 1.47158.Hence, the Fibrosis-4 score is 1.47158."
4307,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4847331-1,Extracted,"A 16-year-old female patient presented with a history of fever, joint pains, amenorrhea and generalized body swelling since 6 months. Fever was of high grade, intermittent in nature, associated with erythematous rashes which were localized to the upper trunk and back. Joint pains mainly involved the elbow and knee joints, and were associated with redness and swelling restricting movement. There was a history of recurrent oral ulcers, decreased appetite and significant weight loss. There was no history of urinary disturbances, bleeding tendencies, abdominal distension, altered bowel habits, altered mentation, photosensitivity or bluish discoloration of skin/mucous membranes. There was no past history of delayed developmental milestones, blood transfusions, diabetes, or thy. There was no family thyroid disease or any other chronic illness. No family member suffered from a similar disease.
On general examination, the patient was febrile with an oral temperature of 39.6°C. Vitals were within normal limits. Pallor, pedal edema and facial puffiness were evident. There were enlarged, non-tender, mobile lymph nodes present in the cervical region. Erythematous, non-tender, non-blanchable rashes were present over the chest and upper back (). Per abdomen examination revealed hepatosplenomegaly. Cardiovascular, respiratory and central nervous system examination was essentially normal. On musculoskeletal examination, the patient had tenderness over bilateral hip joints, knee joints and small joints of hands (proximal interphalangeal joints and metacarpophalangeal joints) associated with swelling and redness.
On the day of patient admission the laboratory investigations revealed some abnormalities including anemia with hemoglobin of 7.9 g/dl, leukopenia with a leukocyte count of 3000/mm3, and platelet count of 150 × 103/µl. Renal function parameters were normal with blood urea of 18 mg/dl (10–50), serum creatinine 0.6 mg/dl (0.7–1.3), serum uric acid 5.1 mg/dl (4–7), serum calcium 7.9 mg/dl (8.5–10.5) and serum phosphate 3.4 mg/dl (2.5–4.5). Random blood sugar of the patient was 93 mg/dl. Liver function tests were slightly deranged, with serum alanine aminotransferase (ALT) of 60 U/l (up to 40), serum aspartate aminotransferase (AST) 79 U/l (up to 40), serum alkaline phosphatase (AP) 243 U/l (30–117), total serum bilirubin 0.8 mg/dl (0.2–0.8) and serum total protein 6 g/dl. The lipid profile was within the normal range. Anemia work-up showed MCV (mean corpuscular volume) of 125.4 fl/cell, MCH (mean corpuscular hemoglobin) 37.3 pg/cell, and MCHC (mean corpuscular hemoglobin concentration) 30.1 g/dl, revealing a macrocytic picture. The corrected reticulocyte count was 0.16% and the serum ferritin level was 1144.6 µg/l.
Direct and indirect Coombs’ tests were negative, and hemoglobin electrophoresis was normal. Erythrocyte sedimentation rate (ESR) was raised with a value of 140 mm/1st hour. The serum fibrinogen level was 280 mg/dl. Additional investigations included raised C-reactive protein (CRP; 100 mg/dl), negative antinuclear antibodies (ANA), negative rheumatoid factor (RF) and negative anti-dsDNA. Anti-SS-A/Ro antibodies, anti-SS-B/La antibodies and HLA-B27 were negative. To rule out infectious causes of fever a series of tests was performed: the malaria card test, Widal test, serology for Leptospira, Leishmania and scrub typhus, blood and urine cultures, Mantoux test, HIV antibodies, Hbs-antigen and anti-HCV antibodies. We also performed a heterophile test for Epstein-Barr virus infection and excluded presence of antibodies in IgM/IgG class to parvovirus B19 and autoantibodies for cytomegalovirus. None of the performed tests confirmed viral or bacterial infection.
Eye examination was normal. Ultrasonography of the abdomen showed hepatosplenomegaly and presence of free fluid. Echocardiography was normal. Lymph node biopsy showed diffuse follicular hyperplasia which suggested a chronic inflammatory state. Bone marrow aspiration revealed megaloblastic erythropoiesis. Minor salivary gland biopsy was undertaken to exclude Sjögren's syndrome, but there were no typical inflammatory infiltrates. Radiological investigations included X-ray of chest, hands and knees and magnetic resonance imaging (MRI) of the sacroiliac spine, which were normal (, ).
In view of the patient being a 16-year-old female with a history of fever, polyarthritis and rash, examination revealing hepatosplenomegaly and lymphadenopathy, and investigations showing high ESR and ferritin values, with absence of ANA and RF, a possible diagnosis of systemic onset juvenile idiopathic arthritis was established.
As the patient had moderate to high grade fever, generalized edema, swollen and tender joints, and poor general condition, a possible association of JIA with MAS was suspected. The presence of ferritin > 684 ng/ml, platelet count of ≤ 181 × 109/l, AST level 79 U/l and serum fibrinogen level of 280 mg/dl satisfied the 2016 criteria for classification of MAS in sJIA, and hence the diagnosis was made.
During the course of hospital stay, the patient received anti-inflammatory therapy, blood transfusions, glucocorticoids and methotrexate. The patient recovered dramatically within a span of two weeks.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [16, 'years'], 'Alanine aminotransferase': [60.0, 'U/L'], 'Aspartate aminotransferase': [79.0, 'U/L'], 'Platelet count': [150000.0, 'µL']}",1.08788,1.03349,1.14227,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 79.0 U/L.
The patient's concentration of ALT is 60.0 U/L.
The patient's concentration of platelets is 150000.0 count/µL. To convert 150000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 150000.0 platelets count/µL * 1000000.0 µL/L = 150000000000.0 platelets count/L. This means that there are 150000000000.0/(10^9) = 150.0 billion platelet counts per liter.
Plugging these values into the formula, we get (16 * 79.0)/(150.0 * sqrt(60.0)) = 1.08788.Hence, the Fibrosis-4 score is 1.08788."
4308,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-7703462-1,Extracted,"A 64-year-old white male retired military intelligence officer had a 6-year history of cirrhosis associated with hepatitis B virus (HBV) infection when he was admitted to a referral hospital for liver transplant evaluation. His HBV infection was thought most likely contracted in 13 years of military service in the Orient in the era of the cold war between capitalist and communist countries. The patient had no history of alcohol use, smoking or transfusions. The patient had a son, age 40, who had chronic hepatitis with negative serology for viral etiologies; the son had hyperpigmented skin and may have had elevated serum iron (according to family), but not diabetes mellitus. The patient had diabetes mellitus diagnosed 18 months ago and treated with oral hypoglycemic agents until 6 months ago when insulin therapy became necessary. He had an esophageal variceal hemorrhage 6 years ago treated with sclerotherapy and a splenocaval shunt. He had been experiencing increasing lethargy, confusion and easy bruising, starting 6 months ago. The patient developed jaundice, fatigue, poor oral intake, weakness, lethargy and mildly slurred speech, despite treatment with lactulose, spironolactone and omeprazole.
On admission, the patient was lethargic, with mildly slurred speech. His skin was markedly jaundiced. His temperature was 36.4o C, pulse 82/minute, blood pressure 110/60 mm Hg and respirations 16/minute. His chest was clear with no cardiac abnormalities noted. He had 2+ leg edema. Electrocardiogram (ECG) showed sinus rhythm and nonspecific T-wave changes. Chest radiograph showed moderate cardiomegaly and no pulmonary abnormalities. The patient’s bilirubin was 15 mg/dL (reference range [RR]: 0.3-1.5 mg/dL), alanine aminotransferase (ALT) 119 U/L (RR: <40 U/L), aspartate aminotransferase (AST) 222 U/L (RR: <40 U/L), gamma-glutamyl-transferase (GGT) 53 U/L (RR: <30 U/L), albumin 1.8 g/dL (RR: 3.5-5 g/dL), ammonia 74 umol/L (RR: 10-47 umol/L), blood urea nitrogen (BUN) 16 mg/dL (RR: 9-20 mg/dL), creatinine 1.0 mg/dL (RR: 0.8-1.5 mg/dL), glucose 361 mg/dL (RR: 70-110 mg/dL), hemoglobin (Hgb) 11.1 g/dL (RR: 12.9-16.9 g/dL), mean corpuscular volume (MCV) 102.4 fL (RR: 80-100 fL), white blood cell (WBC) count 15,500/mm3 (RR: 4,000-10,000/mm3) (80% segmented neutrophils, 3% bands, 9% lymphocytes, 7% monocytes, 1% atypical lymphocytes), platelet count 102,000/mm3 (RR: 140,000-440,000/mm3), prothrombin time (PT) 21 seconds (RR: 10.5-13 seconds) and partial thromboplastin time (PTT) 48.4 seconds (RR: 25-33 seconds).
The results of blood testing more specifically for liver transplant evaluation returned later, showing: hepatitis B surface antigen (HBsAg) positive, anti-HBsAg antibodies negative, anti-hepatitis B core antibodies positive, HBV e antigen negative, anti-hepatitis A virus antibodies positive (IgM negative), anti-human immunodeficiency virus (HIV) antibodies negative, anti-cytomegalovirus (CMV) antibodies >120 U/L (IgM negative), antinuclear antibodies positive at a titer of 1:40 (speckled pattern), carcinoembryonic antigen (CEA) 14.8 ng/mL (RR: <5 ng/mL), zinc 0.16 mcg/mL (RR: 0.55-1.5 mcg/mL), iron 106 mcg/dL (RR: 65-165 mcg/dL), iron binding capacity 107 mcg/dL (RR: 250-420 mcg/dL) and ferritin 4392 ng/mL (RR: 10-282 ng/mL).
The patient was treated with lactulose, neomycin, spironolactone, omeprazole and insulin. On hospital day 2, his WBC count was 19,800/mm3, glucose 338 mg/dL and ammonia 78 umol/L. Pulmonary function testing showed a forced expiratory volume in one second (FEV1) of 2.34 L (88% of predicted), forced vital capacity (FVC) of 2.69 L (71% of predicted) and diffusing capacity of 19.9 mL/min/mm Hg (92% of predicted). Urine culture yielded Enterococcus faecalis, 50,000 colonies/mL. The patient remained afebrile, but that evening, he had increased lethargy and encephalopathy. His ammonia level rose acutely to 197 umol/L. His lactulose and neomycin were increased.
On day 3, the patient’s ammonia was 45 umol/L; he had brief episodes of atrial tachycardia. ECG showed sinus rhythm and nonspecific T-wave changes. Chest x-ray showed mild bilateral interstitial pulmonary edema and a left pleural effusion. Echocardiogram showed normal left ventricular size and function, but mild mitral regurgitation. Over the next 3 days, the patient was afebrile and hemodynamically stable but had increasing jaundice. On day 6, he complained of dyspnea on exertion as well as feeling tired, weak and sleepy. He was afebrile. His WBC count rose to 31,900/mm3 (90% segmented neutrophils, 5% lymphocytes, 5% monocytes).
On day 8, the patient was lethargic and slightly confused. His ammonia was 60 umol/L, bilirubin 25.5 mg/dL, albumin 2.2 g/dL, ALT 109 U/L, BUN 26 mg/dL and creatinine 2.5 mg/dL. He was given prednisone and zinc. Over the next 3 days, the patient was afebrile and hemodynamically stable but had increasing bilirubin, BUN and creatinine. He developed fine bibasilar pulmonary crackles with moderate pulmonary edema, along with left pleural effusion and cardiomegaly on chest x-ray, which was treated with furosemide. On day 12, the patient’s mental status had slowly deteriorated. His ammonia was 31 umol/L, bilirubin 37.5 mg/dL, ALT 71 U/L, GGT 55 U/L, BUN 60 mg/dL, creatinine 4.9 mg/dL and chest x-ray unchanged. Adenosine thallium cardiac scan showed fixed defects in anterior and lateral left ventricle. He was given bumetanide and metolazone. At 15:00, his blood pressure fell to 82/48 mm Hg, with heart rate 60/minute and respirations 16/minute. At 16:15, he developed sinus bradycardia (rate 50/minute). At 16:20, arterial blood showed pH 7.37, PCO2 29 mm Hg and PO2 32 mm Hg (on room air). With 100% oxygen via facemask, his PO2 improved to 63 mm Hg, with PCO2 35 mm Hg and pH 7.35. His blood pressure increased to 113/48 mm Hg at 20:00.
On day 13 at 00:05, chest radiograph showed decreased pulmonary edema. At 01:15, he was afebrile, but his blood pressure decreased to 89/43 mm Hg and an infusion of dopamine was initiated. At 03:00, emergency hemodialysis was started. At 03:20, the patient’s WBC count was 57,500/mm3, Hgb 10.1 g/dL, platelets 94,000/mm3, PT 20 seconds, sodium 132 mEq/L (RR: 136-145 mEq/L), potassium 3.6 mEq/L (RR: 3.5-5.1 mEq/L), chloride 97 mEq/L (RR: 95-110 mEq/L), bicarbonate 26 mEq/L (RR: 21-31 mEq/L), calcium 10.6 mg/dL (RR: 8.5-10.5 mg/dL), phosphorus 4.1 mg/dL (RR: 2.5-4.5 mg/dL), glucose 115 mg/dL, BUN 40 mg/dL, creatinine 3.7 mg/dL, ammonia 45 umol/L, ALT 121 U/L, AST 469 U/L, GGT 62 U/L and bilirubin 42 mg/dL. At 05:15, he developed labored breathing, with arterial pH 7.36, PCO2 36 mm Hg and PO2 38 mm Hg on 100% oxygen via facemask. Manual ventilation was started. He developed bradycardia with blood pressure 70/30 mm Hg. The patient then suffered a cardiopulmonary arrest and could not be resuscitated. The patient had been afebrile, with no antibiotic therapy except oral neomycin, throughout his hospitalization.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [64, 'years'], 'Alanine aminotransferase': [119.0, 'U/L'], 'Aspartate aminotransferase': [222.0, 'U/L'], 'Platelet count': [102000.0, 'µL']}",12.76907,12.13062,13.40752,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 222.0 U/L.
The patient's concentration of ALT is 119.0 U/L.
The patient's concentration of platelets is 102000.0 count/µL. To convert 102000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 102000.0 platelets count/µL * 1000000.0 µL/L = 102000000000.0 platelets count/L. This means that there are 102000000000.0/(10^9) = 102.0 billion platelet counts per liter.
Plugging these values into the formula, we get (64 * 222.0)/(102.0 * sqrt(119.0)) = 12.76907.Hence, the Fibrosis-4 score is 12.76907."
4309,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-8083905-1,Extracted,"A 73-year-old male with a medical history of hypertension, coronary artery disease, and chronic alcohol use presented to the emergency department (ED) with fever, melena, and intermittent episodes of confusion. The patient was admitted to the hospital seven weeks prior to this admission for an elective laparoscopic cholecystectomy. His course was complicated by a right hepatic artery injury treated with ligation and clipping, with subsequent development of multiple hepatic abscesses, Escherichia coli, Bacteroides fragilis, Enterococcus faecium bacteremia, and a bile leak. The bile leak required treatment with endoscopic retrograde pancreatography (ERCP) with sphincterotomy and a common bile duct (CBD) stent placement. The patient was discharged to rehab with a Jackson Pratt (JP) drain (Cardinal Health, Dublin, Ohio) in place. He was continued on daptomycin and ertapenem for four weeks for hepatic abscesses per the infectious disease specialist. The patient returned to the hospital for recurrent fevers and melena. History was limited due to acute delirium but right upper quadrant abdominal pain was noted. He denied bright red blood per rectum, hematemesis, nausea, vomiting, or nonsteroidal anti-inflammatory drug (NSAID) use. His JP drain had a recorded output of approximately 30-40 cc/day.
The patient was febrile with a temperature of 101.7 Fahrenheit within a few hours of admission. Other vital signs were significant for sinus tachycardia, with 110 beats per minute, and tachypnea, with 22 breaths per minute. Blood pressure and oxygen saturation were at 154/65 and 100% on room air, respectively. The physical exam was notable for confusion, abdominal tenderness to palpation that was worse in the right upper quadrant, and the JP drain in the right upper quadrant. Laboratory findings on admission were significant for leukocytosis, with a white blood cell (WBC) count of up to 13,200/mm3. His hemoglobin and hematocrit were noted to be at 6.2 gm/dL and 19%, respectively, which was decreased from the hemoglobin of 10.3 gm/dL on the day of his last discharge. Platelets on admission were within normal limits at 213,000/mm3. His comprehensive metabolic panel from admission revealed transaminitis, with an elevated aspartate aminotransferase of 149 U/L, alanine aminotransferase of 134 U/L, and alkaline phosphatase at 51 0U/L. There was no significant elevation of total bilirubin. The patient's prothrombin time was elevated to 16.1 seconds, and the international normalized ratio INR was 1.41 on admission.
On day one, the patient became hemodynamically unstable, with worsening mentation, tachycardia, and tachypnea, requiring a transfer to the intensive care unit. Surgery and gastrointestinal medicine were consulted for evaluation. The patient underwent imaging with computed tomography (CT) of the abdomen and pelvis, which revealed persistent postsurgical changes of cholecystectomy and an unchanged common bile duct stent. A right-sided abdominal drain was noted to be in the right upper quadrant. Multilobulated, predominantly hypoattenuating masses were noted throughout the liver, with persistent hyperdensity, more centrally suggestive of combined multifocal hepatic abscess and central hemorrhage, also reported. He was transfused with 2 units of packed red blood cells (RBCs) and resuscitated with intravenous (IV) lactated ringer fluids. Blood cultures were obtained, and the patient was started on broad-spectrum antibiotics.
He was taken for an esophagoduodenoscopy (EGD) to assess for causes of upper gastrointestinal bleeding (UGIB). This did not show any evidence of active bleeding or hemobilia at the previous sphincterotomy site; however, the patient had significant melena noted at the end of the exam and was emergently taken for further evaluation with computed tomographic angiography (CTA). CTA revealed transient hyperdensity within the right lobe of the liver, adjacent to the right portal vein, suspicious for a hepatic artery injury/pseudoaneurysm as seen in Figure .
Figure shows CTA findings of the clipped right hepatic artery from the patient's initial surgery.
He was then taken for visceral angiography by interventional radiography (IR), which confirmed a previous iatrogenic hepatic artery ligation and showed an arterial enhancing structure within the central aspect of the liver consistent with a hepatic artery pseudoaneurysm, as seen in Figure and Figure .
The patient’s pseudoaneurysm was not amenable to catheter-directed embolization, as there was no direct feeding arterial structure identified. He was subsequently taken to the operating room for a right hepatectomy. Post right hepatectomy, the patient remained tenuous and began to decline quickly after developing acute oliguric renal failure, which required continuous renal replacement therapy (CRRT) and resistant hypoglycemia. Additionally, worsening shock required pressure and, ultimately, disseminated intravascular coagulopathy (DIC). Due to the patient’s acute decompensation and prolonged hospital course, his wife elected to move toward comfort care and withdrawal of aggressive measures.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [73, 'years'], 'Alanine aminotransferase': [134.0, 'U/L'], 'Aspartate aminotransferase': [149.0, 'U/L'], 'Platelet count': [213000.0, 'µL']}",4.41141,4.19084,4.63198,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 149.0 U/L.
The patient's concentration of ALT is 134.0 U/L.
The patient's concentration of platelets is 213000.0 count/µL. To convert 213000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 213000.0 platelets count/µL * 1000000.0 µL/L = 213000000000.0 platelets count/L. This means that there are 213000000000.0/(10^9) = 213.0 billion platelet counts per liter.
Plugging these values into the formula, we get (73 * 149.0)/(213.0 * sqrt(134.0)) = 4.41141.Hence, the Fibrosis-4 score is 4.41141."
4310,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-3915077-1,Extracted,"A 30-year-old female with acute hepatitis was referred to our hospital in 1995. She had been asymptomatic until the disease onset. She had no history of significant medical condition, blood transfusion, or daily intake of medicine and did not consume alcohol. Her serum alanine aminotransferase (ALT) level had fluctuated from 300 to 1116 IU/L for 3 months before admission. On admission, laboratory examinations revealed total bilirubin 2.5 mg/dL, aspartate transaminase (AST) 842 IU/L, ALT 956 IU/L, alkaline phosphatase 153 IU/L, γ-glutamyl transpeptidase 68 IU/L, γ-globulin 2.3 g/dL, and immunoglobulin G 2,710 mg/dL. Hepatitis B virus surface antigen and hepatitis C virus antibody were negative, antinuclear antibody was weakly positive (1:40, homogeneous), anti-smooth muscle antibody was positive (1:320), and anti-mitochondrial antibody was negative. Human leukocyte antigen was positive for DR-4. Histological analysis of the liver revealed marked interface hepatitis with rosette formation in the parenchyma. On the basis of these findings, she was diagnosed with autoimmune hepatitis and started on prednisolone (30 mg/day). Her serum ALT level gradually declined. Her prednisolone dose was tapered to 10–15 mg/day, which was administered with ursodeoxycholic acid (UDCA; 600 mg/day) to maintain her ALT level <40 IU/L. Since 2002, she had been treated by a doctor at home, and the aforementioned regimen was continued. In 2008, she developed steroid-induced cataract and was referred to our hospital to consult about treatment options for autoimmune hepatitis. At the time of referral, she was 150 cm in height and weighed 43.5 kg (body mass index 19.3 kg/m2), and she was being administered 12.5 mg/day of prednisolone and 600 mg/day of UDCA, and her serum AST and ALT levels were 23 and 34 IU/L, respectively. We added azathioprine (100 mg/day) to this regimen and gradually tapered the prednisolone dose to 10 mg/day; her ALT level was maintained between 22 and 40 IU/L with occasional mild flare-ups. In May 2012, she complained shortness of breath and easy fatigability and significant pallor was noted on physical examination. A hemogram revealed hemoglobin 6.4 g/dL, mean red cell volume 117.3 fL, reticulocyte count 0.6 %, white blood cell count 2,600 cells/μL, and platelet count 207,000 cells/μL. Laboratory serum analyses revealed total protein 6.0 g/dL, albumin 3.7 g/dL, AST 32 IU/L, ALT 42 IU/L, lactic acid dehydrogenase 221 IU/L, and normal bilirubin and alkaline phosphatase levels. Her serum iron level was 214 μg/dL, erythropoietin level was 3,750 mIU (normal 9.1–32.8 mIU), and vitamin B12 and folic acid levels were 307 pg/mL (normal 233–914 pg/mL) and 3.3 ng/mL (normal 3.6–12.9 ng/mL), respectively. She showed no symptoms of recent infection, such as fever or myalgia, and gastrointestinal endoscopy showed no evidence of hemorrhagic lesions. She was initially suspected of having azathioprine-induced anemia; therefore, azathioprine was discontinued. A red cell transfusion was performed, which increased her hemoglobin level to 8.3 g/dL; however, after 4 weeks, her hemoglobin levels decreased to 6.1 g/dL (Fig. ). Another transfusion was performed; however, severe anemia kept recurring and repeat transfusions were required. Her reticulocyte count was consistently low (0.2–0.6 %) except just after transfusion. In July 2012, bone marrow aspiration was performed, which revealed hypocellular bone marrow with an absence of erythroblasts. Giant proerythroblast was not observed and her serum was negative for immunoglobulin (Ig)M antibody to parvovirus B19, although viral DNA was not examined. Therefore, she was diagnosed with acquired PRCA on the basis of these findings, and CsA was administered on September 2012 at an initial dose of 6 mg/kg/day (250 mg/day). After 7 weeks, her hemoglobin level and reticulocyte count both showed considerable improvement (12.4 g/dL and 2.4 %, respectively). The CsA dose was gradually reduced and maintained at 1.6 mg/kg/day (70 mg/day) since April 2013, without relapse of anemia. Her cyclosporine trough blood level has ranged from 69 to 88 ng/mL. In October 2012, UDCA was discontinued and the prednisolone dose was tapered to 9 mg/day; prednisolone has been maintained at 8 mg/day since January 2013. The mild fluctuations in serum AST and ALT levels noted after azathioprine discontinuation ceased after initiating CsA therapy. Her AST and ALT levels have remained <20 IU/L for 8 months since the initiation of therapy.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [30, 'years'], 'Alanine aminotransferase': [956.0, 'U/L'], 'Aspartate aminotransferase': [842.0, 'U/L'], 'Platelet count': [207000.0, 'µL']}",3.9467,3.74936,4.14403,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 842.0 U/L.
The patient's concentration of ALT is 956.0 U/L.
The patient's concentration of platelets is 207000.0 count/µL. To convert 207000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 207000.0 platelets count/µL * 1000000.0 µL/L = 207000000000.0 platelets count/L. This means that there are 207000000000.0/(10^9) = 207.0 billion platelet counts per liter.
Plugging these values into the formula, we get (30 * 842.0)/(207.0 * sqrt(956.0)) = 3.9467.Hence, the Fibrosis-4 score is 3.9467."
4311,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-2934912-1,Extracted,"A 27-year-old woman was referred to the emergency department with complaints of icterus, nocturnal fever, arthralgia, and abdominal pain. The patient had been well until two weeks earlier, when symptoms developed. She was a farmer in a village and owned a lot of sheep. There were no allergies and no history of recent use of drugs but she was consuming a large amount of nonpasteurized traditional cheese.
On physical examination, the patient was nonedematous. Her temperature was 38.5°C, with a blood pressure of 70/45 mm Hg, a pulse rate of 70 beats per minute, and respirations of 18 per minute. The oxygen saturation was 96 percent while she was breathing room air.
The liver edge was palpable 5 cm below the costovertebral margin. Her right upper quadrant of abdomen was diffusely tender to palpation. Additionally, there was marginal splenomegaly. The heart sounds and the results of the remainder of the examination were normal.
Laboratory studies performed at admission revealed a WBC count of 5400 cells/mm³, a hemoglobin level of 10.6 g/dL, a platelet count of 216.000 platelets/mm³, an aspartate aminotransferase level of 224 U/L, an alanine aminostransferase of 159 U/L, an alkaline phosphatase level of 2340 U/L, a gamma glutamyl transferase level of 597 U/L, a direct bilirubin level of 3.1 mg/dL, an albumin level of 3.3 g/dL, a globulin level of 4.3 g/dL and a uric acid level of 1.4 g/dL. Serum pituitary, thyroid, and adrenal function tests were in normal ranges.
Her other laboratory parameters included erythrocyte sedimentation rate 47 mm/hr, C-Reactive Protein level 26 U/L, serum sodium level 124 mmol/L, potassium 4.4 mmol/L, chloride 95 mmol/L, and plasma osmolality 262 mmol/kg/H2O. Urine biochemistry showed osmolality 274 mmol/kg/H2O and urinary sodium 64 mmol/L. Serologic tests for Epstein-Barr virus, cytomegalovirus, and hepatitis viruses were negative. Electrocardiographic examination showed minimal ST-T elevations.
Ultrasonography and Computed Tomography scan (CT scan) of the abdomen showed a small pericardial effusion with mild splenomegaly and hepatomegaly (Figures and ). However, there was no evidence of biliary dilatation or cholecystitis. CT scan of thorax and brain revealed no abnormality. Echocardiography detected mild pericardial effusion without cardiac dysfunction.
At the next day, serum agglutination test for Brucella was positive and its titer was 1/1240. The diagnosis of SIADH in association with cholestatic hepatitis and pericardial effusion due to Brucellosis was made. After intramuscular streptomycin (1000 mg/day for 20 days) with oral Doxycycline (100 mg twice daily for 6 weeks), the patient's symptoms, cholestasis, pericardial effusion, and hyponatremia resolved dramatically.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [27, 'years'], 'Alanine aminotransferase': [159.0, 'U/L'], 'Aspartate aminotransferase': [224.0, 'U/L'], 'Platelet count': [216000.0, 'µL']}",2.22054,2.10951,2.33157,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 224.0 U/L.
The patient's concentration of ALT is 159.0 U/L.
The patient's concentration of platelets is 216000.0 count/µL. To convert 216000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 216000.0 platelets count/µL * 1000000.0 µL/L = 216000000000.0 platelets count/L. This means that there are 216000000000.0/(10^9) = 216.0 billion platelet counts per liter.
Plugging these values into the formula, we get (27 * 224.0)/(216.0 * sqrt(159.0)) = 2.22054.Hence, the Fibrosis-4 score is 2.22054."
4312,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-3304659-1,Extracted,"A 68-year-old man was referred for evaluation of a hepatic mass. He had history of hepatitis B virus carrier for 20 years and liver cirrhosis for 3 years. He has been taking an angiotensin receptor blocker and digoxin due to hypertension and heart failure. He has suffered from repeated episodes of epistaxis from his teens and gastrointestinal bleeding from his mid-thirties. All of his five children also had the history of recurrent epistaxis. Also his sister was suffering from the sequelae of cerebrovascular accident. On physical examination, several telangiectatic macular lesions were found on his arms and trunk (). The laboratory work-up at first visit revealed the following: WBC, 4.6×103/mm3; platelet, 172×103/mm3; hemoglobin, 12.6 g/dL; aspartate aminotransferase (AST), 42 IU/L; alanine aminotranferase (ALT), 20 IU/L; hepatitis B virus surface antigen, positive; hepatitis B surface antibody, negative; anti-hepatitis C virus antibody, negative; and alpha-fetoprotein (AFP), 345 ng/mL (normal, 0-20). Other laboratory results including bleeding time, coagulation time, prothrombin time and activated partial thromboplastin time were normal. Gastroduodenal endoscopy disclosed a telangiectasia at the lesser curvature in mid-body of the stomach (). Liver dynamic CT (LDCT) revealed multiple HCCs in the right lobe of liver and there was no evidence of distant metastasis or vascular invasion. The HCC lesions showed heterogenous wash-out compared to well enhancing round homogenous AVMs in delayed phase of LDCT ().
Liver transplantation was recommended, however, the patient refused it due to economic problem. TACE was performed in three consecutive sessions, but lipiodol uptake in the tumor mass was very poor at every session. HCC progressed after each TACE session. Fever developed up to 38℃, and AST and/or ALT increased more than two times of baseline following the first two TACE sessions.
Because of unusual TACE effect, we reviewed all the radiologic images of the patient and found an enlarged tortuous hepatic artery, multiple arteriovenous malformations, and early visualization of hepatic veins in LDCT () and hepatic angiography (). Based on these findings and positive family history, he was diagnosed as Osler-Weber-Rendu disease and genetic tests for the ENG and ACVRL1 were performed. Patient's genomic DNA was isolated from peripheral blood using the QuickGene DNA blood kit (Fujifilm, Tokyo, Japan) and BigDye Terminatore V3.1 Cycle Sequencing Ready reaction kit (Applied Biosystems, Foster city, CA, USA). Fourteen and ten exons and their intronic flanking sequences of the ENG and ACVRL1, respectively, were amplified by polymerase chain reaction with appropriate primers ( and ). The molecular genetic analysis for the whole exons with their flanking sequences of the ENG was negative. However, the patient harbors a deletion mutation, c.145del (p.Ala49ProfsX5), in the ACVRL, the diagnosis of HHT type 2 with hepatic involvement was confirmed by the results of genetic study. He is waiting for deceased donor liver transplantation for the treatment of HCC.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [68, 'years'], 'Alanine aminotransferase': [20.0, 'U/L'], 'Aspartate aminotransferase': [42.0, 'U/L'], 'Platelet count': [172000.0, 'µL']}",3.71291,3.52726,3.89856,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 42.0 U/L.
The patient's concentration of ALT is 20.0 U/L.
The patient's concentration of platelets is 172000.0 count/µL. To convert 172000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 172000.0 platelets count/µL * 1000000.0 µL/L = 172000000000.0 platelets count/L. This means that there are 172000000000.0/(10^9) = 172.0 billion platelet counts per liter.
Plugging these values into the formula, we get (68 * 42.0)/(172.0 * sqrt(20.0)) = 3.71291.Hence, the Fibrosis-4 score is 3.71291."
4313,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4722098-1,Extracted,"A 60-year-old woman was hospitalized for a week-long history of progressive dyspnea and general weakness. She had a medical history of diabetes mellitus and hypertension. She had ingested approximate 14 g/day of alcohol for 20 years. She was acutely ill-looking and had an alert mental status. Upon admission, her vital signs included a blood pressure of 132/80 mmHg, pulse of 76/min, respiratory rate of 20/min, and body temperature of 36.8°C. Decreased breathing sounds and dullness to percussion were evident over the lower one-third of the right hemithorax. No friction rub was auscultated. Heart sounds were regular and there was no murmur. The liver and spleen were not palpated. Palmar erythema, vascular spider, and peripheral edema were absent.
Initial laboratory data revealed albumin 3.2 g/dL, total protein 6.4 g/dL, lactate dehydrogenase (LDH) of 229 IU/L, aspartate transaminase/alanine aminotransferase of 33/24 IU/L, alkaline phosphatase of 801 IU/L, total bilirubin of 0.6 mg/dL, blood urea nitrogen/creatinine of 12.5/0.89 mg/dL, white blood cell (WBC) count of 3430/mm3, hematocrit of 38.4%, platelet count of 150,000/mm3, prothrombin time (international normalized ratio) of 1.08, C-reactive protein of 0.07 mg/dL, and blood analysis of N-terminal-pro-brain natriuretic peptide of 257 ng/mL. Urinalysis revealed no proteinuria. Hepatitis B surface antigen and hepatitis C antibody were not detected.
Chest X-ray showed a significant right-sided pleural effusion. A thoracentesis was performed and 1500 mL of the pleural effusion was drained. The pleural fluid was yellowish, and an analysis revealed a pH of 7.3, glucose of 212 mg/dL, LDH of 105 IU/L, protein of 3.0 g/dL, red blood cell count of 330/mm3, WBC count of 1/mm3, adenosine deaminase of 11.9 IU/L, and carcinoembryonic antigen of 2.5 mg/mL. Pleural fluid was transudate. Culture for bacteria as well as an acid-fast bacillus smear and culture were negative. No malignant cells were observed.
A chest computed tomography scan revealed no parenchymal lung disease or pleural thickening. On abdominal ultrasonography, the liver size and contour were within the normal range without evidence of ascites, but the liver parenchymal echogenicity was slightly increased, which was suggestive of fatty liver. We also performed an esophagogastroduodenoscopy, which revealed gastric erosion but no esophageal varices. Echocardiography revealed no evidence of cardiac disease.
We repeated the thoracentesis every 3 days for 2 weeks and empirically prescribed diuretics. The collected fluids were also transudate, but the right-sided pleural effusion was not improved.
Although laboratory findings and abdominal ultrasonography did not show the evidence of liver cirrhosis, due to her alcoholic history, we performed an examination using a transient elastography, which can measure liver stiffness. The transient elastography result was 35.3 Kpa, which was suggestive of liver cirrhosis. Accordingly, we suspected a hepatic hydrothorax in the absence of ascites. A radioisotope 99mTc-sulfur colloid injected in peritoneal cavity resulted in a positive uptake of radioactivity within the right pleural cavity (Fig. 
). This finding suggested that the pleural effusion originated in the peritoneal cavity and that there was a diaphragmatic defect.
We diagnosed the patient as having hepatic hydrothorax without ascites, which was the first sign of alcoholic liver cirrhosis. Once the patient was started on a strict low salt diet and a water restriction with diuretics, the pleural effusion slowly regressed. After 2 months of treatment, the hydrothorax was resolved.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [60, 'years'], 'Alanine aminotransferase': [24.0, 'U/L'], 'Aspartate aminotransferase': [33.0, 'U/L'], 'Platelet count': [150000.0, 'µL']}",2.69444,2.55972,2.82916,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 33.0 U/L.
The patient's concentration of ALT is 24.0 U/L.
The patient's concentration of platelets is 150000.0 count/µL. To convert 150000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 150000.0 platelets count/µL * 1000000.0 µL/L = 150000000000.0 platelets count/L. This means that there are 150000000000.0/(10^9) = 150.0 billion platelet counts per liter.
Plugging these values into the formula, we get (60 * 33.0)/(150.0 * sqrt(24.0)) = 2.69444.Hence, the Fibrosis-4 score is 2.69444."
4314,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-7486015-1,Extracted,"A 50-year-old female with past medical history of hypertension, autosomal dominant polycystic kidney disease and end-stage renal disease (on hemodialysis) underwent a renal transplant from a living unrelated donor in June 2016.
She received the influenza vaccine in November 2017 at the outpatient transplant nephrology clinic. She presented to her next appointment eight days later with complaints of fevers with chills, night sweats, lethargy, headaches, myalgias, nausea, anorexia, left-sided pleuritic chest pain and multiple episodes of watery, non-bloody diarrhea. She was directed to the emergency department for further evaluation.
She denied sick contacts, recent travel, medication changes or medication non-compliance. At the time of admission, she was on prednisone 5 mg PO (oral) QD, mycophenolate mofetil (MMF) 360 mg PO QID, tacrolimus 0.5 mg PO BID.
Her vitals on admission were significant for temperature 101.7 F, heart rate 100/minute, blood pressure 118/79 mm Hg, respirations 18/minute and oxygen saturation 98% on room air. Physical exam revealed no acute abnormalities.
Admission labs were significant for white blood cell (WBC) 2,070/mm3 [normal range (N): 3,800-10,500/mm3], absolute neutrophil count (ANC) 1,865/mm3 [N: 1,800-7,400/mm3], lymphocyte count 500/mm3 [N: 1,000-3,300/mm3], platelets 108,000/mm3 [N: 150,000-400,00/mm3], aspartate transaminase (AST) 81 U/l [N: 10-40 U/l], alanine transaminase (ALT) 87 U/l [N: 10-45 U/l], alkaline phosphatase (ALP) 137 U/l [N: 40-120 U/l] and normal renal function. Electrocardiogram revealed sinus rhythm with no acute changes. Chest radiography and computed tomography (CT) ruled out the presence of pneumonia. Abdominal ultrasound showed polycystic liver and kidneys, contracted gallbladder with negative sonographic Murphy’s sign. CT of the abdomen and pelvis confirmed polycystic liver and kidneys, as well as mural thickening of ascending colon with mild surrounding inflammatory changes (suggestive of colitis) (Figures , ).
Urinalysis was not suggestive of infection. Respiratory viral panel multiplex test was negative. Clostridium difficile toxin test was negative. Stool cultures were negative. Stool microscopy was negative for ova and parasites. Urine cultures revealed Escherichia coli (10,000-49,000 CFU/ml) combined with normal urogenital flora. Blood cultures revealed no growth. Testing for acute hepatitis A, B and C viruses was negative. Epstein-Barr virus serology revealed prior infection. BK virus DNA, Parvovirus B19 DNA and adenovirus DNA were not detected by specific polymerase chain reaction (PCR) tests.
Infectious diseases service was consulted. Given the presence of leukopenia, thrombocytopenia, transaminitis and multi-systemic symptoms, there was concern for an ongoing viral process. She was started on valganciclovir 900 mg PO BID for presumed CMV disease, with intravenous fluid support. The E. coli in the urine was thought to be a colonization and she was successfully monitored off antibiotics.
She continued to have persistent fevers and diarrhea, with worsening leukopenia (lowest WBC count 1700/mm3 with lowest ANC 800/mm3), thrombocytopenia (nadir 86,000/mm3) and liver function abnormalities (AST 139 U/l, ALT 135 U/l, ALP 167 U/l). Given the persistent symptoms and worsening laboratory parameters, MMF was discontinued. Serum CMV PCR testing revealed 154,697 IU/ml (5.19 log10 IU/ml) [lower limit of assay detection 60 IU/ml (1.78 log10 IU/ml)]. Gastroenterology service was consulted for worsening liver function abnormalities and they attributed the clinical picture to systemic CMV infection.
She had clinical improvement, with improving CMV PCR tests [504 IU/ml (2.70 log10 IU/ml)] after 12 days of antiviral therapy. She was discharged on the twelfth day of hospital stay, with recovery of WBC count to 5,600/mm3 and platelets 147,000/mm3.
She was followed up by in the outpatient transplant nephrology and infectious diseases clinics. CMV PCR was negative 60 days after initiation of antiviral therapy and she was restarted on a lower dose of MMF. After the second negative CMV PCR a week later, MMF dose was increased and valganciclovir was decreased to prophylactic dosing. She received valganciclovir for a total of 87 days.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [50, 'years'], 'Alanine aminotransferase': [87.0, 'U/L'], 'Aspartate aminotransferase': [81.0, 'U/L'], 'Platelet count': [108000.0, 'µL']}",4.02042,3.8194,4.22144,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 81.0 U/L.
The patient's concentration of ALT is 87.0 U/L.
The patient's concentration of platelets is 108000.0 count/µL. To convert 108000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 108000.0 platelets count/µL * 1000000.0 µL/L = 108000000000.0 platelets count/L. This means that there are 108000000000.0/(10^9) = 108.0 billion platelet counts per liter.
Plugging these values into the formula, we get (50 * 81.0)/(108.0 * sqrt(87.0)) = 4.02042.Hence, the Fibrosis-4 score is 4.02042."
4315,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-6547267-1,Extracted,"We report the case of a 58-year-old female with a personal history of diabetes mellitus diagnosed 8 years prior, treated with metformin and glibenclamide, a surgical history of two cesarean sections, without complications, and a family history of diabetes mellitus, arterial hypertension, and cholangiocarcinoma. She was referred to our hospital in November 2015 presenting nausea, vomiting, black stools, and diffuse and sporadic epigastric pain; she also lost 4 kg in 4 months, from 65 to 61 kg, which means a total of 7% weight loss, and showed signs of digestive tract bleeding and anemic syndrome. Serological studies, prior to hospital arrival, showed hemoglobin of 8.4 g/dL.
Initial laboratory results included leukocytes 8,260 μ/L, hemoglobin 10.56 g/dL, platelets 222,000 μ/L, gamma glutamyl transpeptidase 22 μ/L, lactate dehydrogenase 207 μ/L, alkaline phosphatase 71 μ/L, AST 15 μ/L, ALT 13 μ/L, prothrombin time 6.7 s, serum albumin 3.5 g/dL, glucose 185 mg/dL, urea 26.9 mg/dL, creatinine 0.5 mg/dL, and serum carcinoembryonic antigen was elevated to 114.56 UI.
The approach protocol started with panendoscopy, showing body and fundus gastropathy and presence of Helicobacter pylori. Four months later, a colonoscopy was performed which revealed a right colonic tumor.
An abdominal CT scan followed, which revealed the following: liver with hypodense tumor, with regular edges, in segment V, 24 × 22 × 16 mm, and longitudinal thickening of 82 mm with a reduction of 100% of the intestinal lumen (Fig. ). PET CT showed a nodular lesion of 25 × 21 mm in segment V with maximum SUV of 17.1, a poorly defined lesion in segment VI of 11 mm in diameter, and maximum SUV of 6; ascending colon of 45 cm3 with maximum SUV of 51.4 (Fig. ).
An open surgical procedure was performed in May 2016 with right hemicolectomy with ileorectal mechanical anastomosis and hepatic bisegmentectomy V and VI (Fig. ). The duration of the surgical procedure was 4 h, with a 6 h anesthetic time, and total estimated bleeding was 900 mL. The oral feeding started 24 h after the procedure, presenting intestinal gas release at 24 h and evacuations at 48 h. Total intrahospital stay was 5 days, presenting right axillary vein thrombosis due to placement of central venous catheter guided by interventional radiology.
The histological diagnosis was moderately differentiated adenocarcinoma, intestinal type, with cecum, ascending colon, and appendicular involvement; free surgical margins (R0), nodules 2/11; hepatic lesions with neoplastic cells (Fig. ).
The postoperative stay was uneventful while the patient received chemotherapy with capecitabine and oxaliplatin. The patient showed carcinoembryonic antigen 3.93 UI without tumor activity by CT. ECOG was 0 and IK was 1000 during the follow-up time of 9 months.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [58, 'years'], 'Aspartate aminotransferase': [15.0, 'U/L'], 'Alanine aminotransferase': [13.0, 'U/L'], 'Platelet count': [222000.0, 'µL']}",1.08691,1.03256,1.14126,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 15.0 U/L.
The patient's concentration of ALT is 13.0 U/L.
The patient's concentration of platelets is 222000.0 count/µL. To convert 222000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 222000.0 platelets count/µL * 1000000.0 µL/L = 222000000000.0 platelets count/L. This means that there are 222000000000.0/(10^9) = 222.0 billion platelet counts per liter.
Plugging these values into the formula, we get (58 * 15.0)/(222.0 * sqrt(13.0)) = 1.08691.Hence, the Fibrosis-4 score is 1.08691."
4316,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-8122135-1,Extracted,"A 20-year-old nonalcoholic, nonsmoker Nepalese man with no significant past medical history presented to the outpatient department with melena for 10 days. This was associated with fatigue and generalized weakness of the body. He denied any abdominal pain, nausea, vomiting, or recent weight loss. He also gave a history of low-grade fever with an evening rise of temperature for the same duration. It was not associated with chest pain, cough, hemoptysis, runny nose, watery eyes, or sore throat. He had no history of similar illness in the past or any recent sick contacts. His family history was unremarkable.
Vitals on presentation revealed blood pressure 100/70 mm Hg, pulse 120/min, respiratory rate 24/min, and temperature 100.5°F. On physical examination, he was pale and icteric. There were no edema, ecchymosis, or any palpable lymph nodes. Chest auscultation revealed diminished breath sounds over the right infrascapular region. The rest of the systemic examination was normal.
Blood investigations showed hemoglobin (Hb) 5.3 g/dL and white blood cells (WBC) 5400/mm3 with neutrophils 79% and lymphocytes 18%, and platelets 319 000/mm3. His renal function tests showed urea 4.5 mmol/L and creatinine 95 μmol/L. Liver function test (LFT) showed total bilirubin 66 μmol/L, direct bilirubin 7 μmol/L, alanine aminotransferase (ALT) 23 U/L, aspartate aminotransferase (AST) 38 U/L, and alkaline phosphatase (ALP) 161 U/L. His lactate dehydrogenase (LDH) was elevated to 1450 U/L. Direct Coombs test was positive for antibodies against red blood cells.
Serologies were negative for human immunodeficiency virus (HIV), hepatitis B virus, and hepatitis C virus. Serological evaluation for antinuclear antibody (ANA), antidouble-stranded deoxyribonucleic acid antibody (ds-DNA), and anti–smooth muscle antibody (ASMA) were negative. Immunoglobulin levels were normal. A presumptive diagnosis of autoimmune hemolytic anemia was made, and the patient was started on oral prednisone 60 mg daily.
Due to the presenting complaint of melena, upper gastrointestinal endoscopy was done, which revealed a peptic ulcer in the first part of the duodenum. A tissue sample was taken during endoscopy, which did not reveal Helicobacter pylori. He was treated with proton pump inhibitors for his peptic ulcer disease.
Meanwhile, a chest X-ray showed right-sided pleural effusion (Figure ). The pleural fluid analysis showed an exudative pleural effusion with lymphocyte predominance, lymphocyte to neutrophil ratio of 4, and high adenosine deaminase activity (89 units/L). Computed tomography scan (CT) of the chest with and without contrast showed multiple centriacinar nodules giving tree in bud appearance, fibrotic changes in the right upper lobe, and moderate right-sided pleural effusion suggestive of tubercular pathology. Acid-fast bacilli (AFB) was not visualized in the microscopic analysis of the sputum. However, due to high clinical suspicion, corroborative pleural fluid analysis and chest imaging findings, he was started on antitubercular treatment with isoniazid, rifampin, pyrazinamide, and ethambutol.
Follow-up laboratories showed Hb stable at 5-7 g/dL. Platelet count decreased to 127 000/mm3 at the time of discharge (Figure ). Following discharge on antitubercular medications and prednisone, he was lost to follow up.
The patient presented to our clinic after 3 months following an exacerbation of his symptoms after the inadvertent stopping of his prednisone. He presented with increased fatigue, generalized weakness, and jaundice. He had no preceding upper respiratory tract symptoms. Blood investigation this time showed Hb: 4 g/dL, WBC: 6500/mm3, and platelets: 10 000/mm3. LFT showed total bilirubin: 48.05 μmol/L and direct bilirubin: 13.51 μmol/L. LDH was elevated to 851 U/L.
The development of thrombocytopenia in a patient with pre-existing autoimmune hemolytic anemia led us to consider the possibility of Evans syndrome as the cause of bicytopenia. He was started on intravenous methylprednisolone 1 g once daily for 3 days, followed by oral prednisone 60 mg daily. However, there was no improvement in his Hb or platelet count. We considered other immunosuppressive therapies like intravenous immunoglobulin, rituximab, and cyclosporine as possible treatment options, but we faced two challenges with their use: fear of reactivation of TB and the prohibitive cost. Eventually, we decided to start him on cyclosporine, given its affordable cost despite the risk of reactivation of TB. He was discharged on oral cyclosporine 10 mg daily for a month. Unfortunately, he was again lost to follow up.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [20, 'years'], 'Alanine aminotransferase': [23.0, 'U/L'], 'Aspartate aminotransferase': [38.0, 'U/L'], 'Platelet count': [319000.0, 'µL']}",0.49677,0.47193,0.52161,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 38.0 U/L.
The patient's concentration of ALT is 23.0 U/L.
The patient's concentration of platelets is 319000.0 count/µL. To convert 319000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 319000.0 platelets count/µL * 1000000.0 µL/L = 319000000000.0 platelets count/L. This means that there are 319000000000.0/(10^9) = 319.0 billion platelet counts per liter.
Plugging these values into the formula, we get (20 * 38.0)/(319.0 * sqrt(23.0)) = 0.49677.Hence, the Fibrosis-4 score is 0.49677."
4317,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-8085791-1,Extracted,"A 32-year-old male with a history of polysubstance abuse presented to the emergency department (ED) with complaints of bilateral feet numbness. The patient stated that he had consumed alcohol the evening prior to the presentation, and upon awakening the next morning, he had been unable to bear weight on lower extremities. He admitted to decreased sensation bilaterally, which extended from the foot to the ankle, more pronounced on the right side. Furthermore, the patient had a 7/10 dull pain sensation radiating from the lower back to bilateral lower extremities as well as generalized body aches. It was the progressive worsening of his symptoms that had prompted his hospital visit. He denied any other aggravating factors.
In the ED, the patient's vital signs were found to be remarkable for a temperature of 97.1 °F, respiratory rate of 19 breaths per minute, heart rate of 124 beats per minute, and blood pressure of 146/27 mmHg. The patient denied any history of diabetes, kidney disease, or back pain. He had smoked half pack of cigarettes a day for ""a few years"", drank a pint of vodka three to four times a week, and used cocaine as well as marijuana daily for ""numerous"" years. He reported that he had used cocaine and marijuana a ""few"" days prior to the presentation. The patient's physical examination was significant for a decreased dull and sharp sensation of bilateral feet with intact sensation above the ankle as well as 1/5 muscle strength of bilateral legs and feet. The muscle strength was 4/5 in bilateral thighs as well as upper extremities.
An alcohol level screening was done in the ED, which revealed a level of less than 10 mg/dl. Urine drug screen was positive for cocaine, cannabinoids, and opiates. Lactic acid was elevated at 4.2. Urinalysis revealed a specific gravity greater than 1.030 with large bilirubin, proteinuria, and hematuria. Urine microscopy revealed red blood cells of 4-6 high power field (HPF).
Initial complete blood count revealed a WBC of 20.9 K/UL with 83.2% absolute neutrophils, and hemoglobin and hematocrit level of 21.7 gm/dl and 64.1%, respectively, with a platelet count of 344 K. The patient’s complete metabolic panel was significant for elevated liver enzymes - aspartate aminotransferase (AST): 3,334 U/L (normal range: 15-41 U/L), alanine aminotransferase (ALT): 850 U/L (normal range: 17-63 U/L), alkaline phosphatase (ALP): 151 U/L (normal range: 38-126 U/L); there was renal insufficiency with a creatinine level of 4.16 mg/dl (normal range: 0.7-1.2 mg/dl), urine nitrogen of 32 mg/dl (normal range: 8-20 mg/dl), and potassium of 7.4 mmol/l (normal range: 3.6-5.1 mmol/L) with high anion gap of 21. An arterial blood gas revealed PH of 7.23, PCO2 of 32 mmHg, HCO3 of 14.9 mmol/L, signifying metabolic acidosis with adequate respiratory compensation. CPK levels were markedly elevated at 100,809 U/L. Initial ECG revealed sinus tachycardia with peaked T wave as seen in Figure .
The patient received 2 grams of calcium gluconate infusion for cardiac membrane stabilization. He also received insulin and Kayexalate, which corrected his hyperkalemia. The patient was started on IV fluid (IVF) hydration with strict urine output monitoring. Initial MRI without contrast of spine was performed and was only remarkable for mild spondylosis without spondylolisthesis in the L4-L5 region. Neurology was consulted for a more thorough neurological examination, and the patient was transferred to the intensive care unit (ICU) for close monitoring and management.
In the ICU, the patient’s symptoms started to worsen and he reported progression of the numbness up to the knee in both lower limbs. He also complained of worsening pain and weakness in the right lower extremity. During the ICU stay, the right thigh became more swollen compared to the left. Urgent CT scan of the right lower extremity revealed right leg edema without focal tissue or osseous abnormality, as seen in Video .
Doppler ultrasound showed normal arterial flow and no evidence of deep vein thrombosis. The patient started experiencing new-onset right lower extremity weakness. Dorsal pedis and tibial pedis pulses were present bilaterally. At this juncture, there were concerns for acute compartment syndrome. The patient was placed on neurovascular checks every hour. Intracompartmental pressures were measured frequently, which remained low. Also, surgery was consulted for possible fasciotomy.
Despite aggressive IVF hydration, the patient’s CPK levels continued to rise. CPK levels peaked at 237,025U/L, even though his hemoconcentration had resolved. Creatinine levels continued to increase, and the patient became anuric and IVF hydration was discontinued. Vascular surgery and nephrology were consulted for emergent Uldall catheter placement and urgent hemodialysis, respectively.
Following repeat sessions of hemodialysis, the patient's renal function improved and CPK levels declined. His lower extremity weakness also started to improve. There was a significant improvement in his left lower extremity numbness. The right leg swelling resolved; however, there was only a mild improvement of motor and sensory loss. The patient continued to undergo physical therapy during his hospitalization. He was subsequently discharged to subacute rehabilitation. The patient was advised to continue with outpatient hemodialysis till full recovery of his renal function was achieved. He was also recommended to follow up with neurology as an outpatient.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [32, 'years'], 'Alanine aminotransferase': [850.0, 'U/L'], 'Aspartate aminotransferase': [3334.0, 'U/L'], 'Platelet count': [344000.0, 'µL']}",10.6377,10.10581,11.16959,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 3334.0 U/L.
The patient's concentration of ALT is 850.0 U/L.
The patient's concentration of platelets is 344000.0 count/µL. To convert 344000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 344000.0 platelets count/µL * 1000000.0 µL/L = 344000000000.0 platelets count/L. This means that there are 344000000000.0/(10^9) = 344.0 billion platelet counts per liter.
Plugging these values into the formula, we get (32 * 3334.0)/(344.0 * sqrt(850.0)) = 10.6377.Hence, the Fibrosis-4 score is 10.6377."
4318,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-8143661-1,Extracted,"Ultrasonographic examination of an asymptomatic 62-year-old woman with chronic HCV genotype 1b infection revealed a hypoechogenic lesion in liver segment III. Active chronic liver disease was diagnosed 12 years previously based on liver biopsy that revealed a grade of 8 and stage 3 according to the Ishak staging system. Results of laboratory investigations were as follows: HCV RNA, 2530000 IU/ml; normal lactate dehydrogenase level (270 U/l [normal, 240–450 U/l]); haemoglobin, 12.9 g/dl; platelet count, 175.000/mm3; white blood cell count, 4900/mm2; aspartate aminotransferase, 40 U/l; alanine aminotransferase, 65 U/l; albumin, 4.1 g/dl and total bilirubin 1.0 mg/dl. Total body computed tomography (CT) with intravenous contrast revealed several nodular liver lesions with early arterial phase enhancement and slow washout with uncertain diagnosis. Magnetic resonance imaging (MRI) demonstrated hyperintensity on post-contrast T1-weighted images of the lesions and isointensity in the T2 phase (). Positron emission tomography-CT (PET-CT) using 18F-fluorodeoxyglucose demonstrated only intense fluorodeoxyglucose uptake in different areas of the liver as a unique localization of the neoplasm. A liver biopsy was prompted by the uncertain behavior of the liver lesions. Microscopic examination of the liver biopsy revealed infiltration of typical centrocyte-like lymphoid cells and lymphoepithelial lesions in these small- to medium-size lymphocytes (). Immunohistochemistry findings were positive for CD20, CD79a and BCL-2, and negative for CD3, CD5, CD10, CD43 and cyclin D1 (). A diagnosis of stage IV liver MZL was made. Bone marrow biopsy did not reveal infiltration of lymphocytes. After haematology consultation, it was decided to administer antiviral therapy with sofosbuvir (NS5B inhibitor) associated with simeprevir (a protease inhibitor) for a duration of 12 weeks. Three months after the conclusion of antiviral treatment, HCV RNA was negative, thus confirming the eradication of HCV infection. MRI performed 6 and 12 months after antiviral therapy demonstrated complete resolution of the liver lesions (). Currently, no liver lesions are apparent on MRI after 3 years of follow-up.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [62, 'years'], 'Alanine aminotransferase': [65.0, 'U/L'], 'Aspartate aminotransferase': [40.0, 'U/L'], 'Platelet count': [175000.0, 'µL']}",1.75775,1.66986,1.84564,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 40.0 U/L.
The patient's concentration of ALT is 65.0 U/L.
The patient's concentration of platelets is 175000.0 count/µL. To convert 175000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 175000.0 platelets count/µL * 1000000.0 µL/L = 175000000000.0 platelets count/L. This means that there are 175000000000.0/(10^9) = 175.0 billion platelet counts per liter.
Plugging these values into the formula, we get (62 * 40.0)/(175.0 * sqrt(65.0)) = 1.75775.Hence, the Fibrosis-4 score is 1.75775."
4319,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4276122-1,Extracted,"A 42-year-old man was referred to our hospital for treatment after intentionally ingesting fertilizer containing 100% sodium silicate. He had ingested about 50 mL of fertilizer 2 days prior to admission. On presentation, he complained of a sore throat and epigastric pain. The patient had a medical history of unmedicated chronic hepatitis B and had worked in a car-manufacturing factory for 10 years. He had a 20 pack-year smoking history. On admission, his blood pressure was 130/78 mmHg, pulse rate was 98 beats per minute, respiratory rate was 22 breaths per minute, and body temperature was 38.3°C. He had mild painful oral erosion and his lungs sounded clear to auscultation. Laboratory results from another hospital immediately after the ingestion had revealed the following findings: serum creatinine (Cr), 1.1 mg/dL; white blood cell (WBC) count, 113,600 cells/μL; the arterial blood gas analysis (ABGA) results were as follows: pH, 7.340; PCO2, 40.3 mmHg; PO2, 96.8 mmHg; HCO3, 21.2 mm/L; and O2 saturation, 96.8% on room air. On admission to our hospital, laboratory findings were as follows: hemoglobin, 16.3 g/dL; WBC count, 23,290 cells/μL; platelet count, 167,000 cells/μL; blood urea nitrogen (BUN), 48 mg/dL; serum Cr, 5.06 mg/dL; total bilirubin, 1.7 mg/dL; aspartate aminotransferase, 68 U/L; alanine aminotransferase, 43 U/L; and glucose, 140 mg/dL. ABGA results were as follows: pH, 7.415; PCO2, 36.6 mmHg; PO2, 73 mmHg; HCO3, 25.5 mm/L; and O2 saturation, 95% on room air. Urinary analysis revealed a pH of 6.0, specific gravity of 1.010, 2+ protein, 2+ glucose, trace occult blood, and no WBCs, with proteinuria at 550 mg/day. Antinuclear antibody (ANA) titers were below 1 : 40 (nuclear pattern) and results for other serologic markers were nonspecific. Abdominal sonography revealed increased kidney size with increased parenchymal echogenicity.
Despite continuous fluid therapy, the patient's levels of BUN and Cr increased gradually, and thus renal biopsy was performed on day 3 of admission. The kidney biopsy showed acute tubular necrosis without infiltration of inflammatory cells. Although the histologic findings were not diffuse, definite features of tubular damage were noted. Necrotic sloughing of tubular cells was found, with mitotic figures present in regenerating tubular cells. Necrotic cellular casts were also noted in the tubular lumina (). Ultrastructural examination revealed electron-dense deposits in subendothelium of glomerular capillaries. And focal effacement and fusion of foot processes of podocytes were noted (). Tubular cells contained electron-dense lysosomes in the cytoplasm and lumina ().
The development of acute respiratory distress syndrome was observed on day 4: arterial PaO2/FiO2 < 100 mmHg. Corticosteroid therapy for acute lung injury was administered for 28 days, beginning on day 5 (1 mg/kg/day of intravenous methylprednisolone for 2 weeks, followed by a 2-week taper). Hemodialysis was provided 5 times from day 5 to day 10 for the treatment of hyperkalemia and oliguria. After the termination of hemodialysis, the patient's renal function recovered completely. During the administration of corticosteroid therapy, pulmonary fibrosis was observed on chest computed tomography. On day 16, bilateral spontaneous pneumothorax, pneumomediastinum, and subcutaneous emphysema occurred. Although bilateral closed tube thoracotomy and a lung protective ventilation strategy were applied, the pneumothorax and pulmonary fibrosis progressed gradually. The patient died of complicated lung fibrosis and persistent pneumothorax/pneumomediastinum on day 40 of hospitalization.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [42, 'years'], 'Alanine aminotransferase': [43.0, 'U/L'], 'Aspartate aminotransferase': [68.0, 'U/L'], 'Platelet count': [167000.0, 'µL']}",2.608,2.4776,2.7384,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 68.0 U/L.
The patient's concentration of ALT is 43.0 U/L.
The patient's concentration of platelets is 167000.0 count/µL. To convert 167000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 167000.0 platelets count/µL * 1000000.0 µL/L = 167000000000.0 platelets count/L. This means that there are 167000000000.0/(10^9) = 167.0 billion platelet counts per liter.
Plugging these values into the formula, we get (42 * 68.0)/(167.0 * sqrt(43.0)) = 2.608.Hence, the Fibrosis-4 score is 2.608."
4320,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-6126084-1,Extracted,"An 81-year-old male presented to the clinic with yellowish discoloration of skin and urine for 2 weeks. He denied any fever, abdominal pain, nausea, vomiting, melena, hematochezia, or acholic stools. Past medical history was significant for hypertension, hyperlipidemia, diabetes mellitus type II, coronary artery disease, and chronic kidney disease stage IV. He reported recent loss of appetite but denied any significant weight changes. Ultrasound ordered by primary care physician showed intra- and extra-hepatic biliary dilation with distension of gall bladder without cholelithiasis. He was sent to the emergency department (ED) for further evaluation.
On examination, blood pressure was 133/60 mmHg, heart rate was 75 beats per minute, respiratory rate was 23 breaths per minute, temperature was 97.7°F, and oxygen saturation was 98% in room air. He had mild icteric sclera, and chronic venous stasis changes in bilateral lower extremities were noted. Bowel sounds were normal, and no hepatosplenomegaly or abdominal tenderness was noted on exam.
Laboratory investigations showed a hemoglobin count of 11 g/dl, white blood cell count of (WBC) 3800 cell/mm3, and platelet count of 214,000/mm3. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were elevated at 326 and 321 IU/L, respectively. Total bilirubin was 3.1 mg/dl with direct bilirubin of 1.8 mg/dl. Alkaline phosphatase (ALP) was 1,219 IU/L with lipase 250 IU/L. Renal function tests were at baseline at 1.72 mg/dl (baseline 1.7–1.9 mg/dl). Recent upper and lower endoscopy (1 month earlier) did not show significant abnormalities, except for mild antral gastropathy. A computed tomography (CT) scan of abdomen and pelvis revealed stable pelvic adenopathy with largest lymph node measuring 4.4 × 1.7 cm (which was noted on the earlier CT scan as well). The pancreatic tissue and abdominal vessels appeared normal. With concern for underlying malignancy, a lymph node biopsy was performed. Endoscopic retrograde of cholangiopancreatography revealed distal common bile duct stricture of 3 cm without obstruction, for which a biliary stent was placed. No pancreatic lesions were observed, and biliary brushings were negative for malignancy.
The patient returned to the ED two months later; this time with a fever (102°F), nausea, and right upper quadrant pain for 2 days. Complete blood counts revealed elevated white cell count of 18,700/mm3. AST, ALT, and bilirubin levels were within normal limits, and ALP was elevated at 127 IU/L. The CT scan of abdomen revealed intrahepatic biliary ductal dilatation and gall bladder wall thickening with pericholecystic inflammatory stranding with normal pancreas (). He was started on broad-spectrum antibiotics with piperacillin-tazobactam. Urgent surgical decompression with percutaneous drain placement was performed for stent blockage (with re-stent placement) and bile duct stricture from unknown etiology.
Meanwhile, histopathology from the earlier right iliac lymph node biopsy revealed sinus histiocytic aggregates interlaced with lymphocytes and plasma cells (), majority of cellular constituents being plasma cells, characterized by oval cellular contours and eccentrically located nuclei (); this was confirmed by diffuse immunoreactivity for CD138 (). Chromogenic in situ hybridization for kappa light chain () and lambda light chain () showed a mixture of kappa and lambda-bearing cells (approximate kappa to lambda ratio of 3 : 1); this finding suggested that the plasma cells were reactive in nature, arguing against the possibility of a plasma cell neoplasm. In situ hybridization for EBV-encoded RNA (EBER) was interpreted as negative.
As there was no evidence to suggest a lymphoma or a plasma cell neoplasm, a diagnosis of IgG-related disease was considered. Additional immunohistochemistry showed that the plasma cells present expressed predominantly IgG (); of these, the majority (over 60%) were reactive for IgG4 (). Serum protein electrophoresis and immunofixation showed polyclonal increase in IgG with no monoclonal proteins. Serum immunoglobulin (Ig) G levels were high (3390 mg/dl) with normal IgA and IgM. IgG subclasses were also high with IgG1 of 1800, IgG2 975, IgG3 324, and IgG4 729 mg/dl.
A diagnosis of IgG4-related sclerosing cholangitis was made, and he was started on prednisone 40 mg daily for 6 weeks. A follow-up CT scan of abdomen after a month revealed significant reduction in the size of his pelvic lymph nodes with largest lymph node measuring 1.8 × 0.7 cm (). Endoscopic retrograde cholangiography (ERC) performed revealed resolution of stricture (). The biliary stent was removed following resolution of the stricture. He remains on prednisone 20 mg daily with close rheumatology follow-up. Rituximab therapy is being considered as a steroid-sparing agent.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [81, 'years'], 'Alanine aminotransferase': [326.0, 'U/L'], 'Aspartate aminotransferase': [321.0, 'U/L'], 'Platelet count': [214000.0, 'µL']}",6.72926,6.3928,7.06572,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 321.0 U/L.
The patient's concentration of ALT is 326.0 U/L.
The patient's concentration of platelets is 214000.0 count/µL. To convert 214000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 214000.0 platelets count/µL * 1000000.0 µL/L = 214000000000.0 platelets count/L. This means that there are 214000000000.0/(10^9) = 214.0 billion platelet counts per liter.
Plugging these values into the formula, we get (81 * 321.0)/(214.0 * sqrt(326.0)) = 6.72926.Hence, the Fibrosis-4 score is 6.72926."
4321,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-3961391-1,Extracted,"A 64-year-old male patient was admitted to the Division of Hematology and Oncology, Department of Medicine, Dankook University Hospital (Cheonan, Korea) for treatment of progressive dyspnea and cough. The patient had undergone right lobectomy of the liver due to HCC at Severance Hospital (Seoul, Korea) on October 23, 2006. At that time, the surgical specimen was confirmed to be HCC, Edmondson grade II. After 14 months, a chest computed tomography (CT) scan revealed multiple lung metastases and left adrenal gland metastasis. The level of serum protein induced by vitamin K absence or antagonist II (PIVKA II) was elevated abnormally (207 mAU/ml). Diagnosed with recurrent HCC with multiple lung metastases and adrenal metastasis, the patient received palliative chemotherapy with 5-fluorouracil, adriamycin and carboplatin. Following two cycles of first-line chemotherapy, the disease progressed. The patient was administered two more cycles of second-line chemotherapy with 5-fluorouracil, etoposide and carboplatin, and three cycles of third-line chemotherapy with oral capecitabine. However, the disease demonstrated no objective response and further progressed. The patient and physician agreed to discontinue cytotoxic chemotherapy, and the patient was transferred to Dankook University Hospital for paliative care on February 19, 2009.
The patient was a chronic hepatitis B virus carrier and an older brother had hepatitis B viral liver cirrhosis. Initial laboratory data from our hospital was as follows: White blood cell count, 4,970 cells/μl; hemoglobin level, 17.2 g/dl; platelet count, 16.4×104 platelets/μl; aspartate aminotransferase : alanine aminotransferase level, 32:41 IU/l; total bilirubin level, 0.97 mg/dl; gamma guanosine triphosphate level, 17 IU/l; alkaline phosphatase level, 89 IU/l; protein : albumin level, 8.4:4.3 g/dl; prothrombin time (international normalized ratio), 13.2 sec (1.14); α-fetoprotein (AFP) level, 16.55 ng/ml (normal range, 0–15 ng/ml); and PIVKA II level, 12,900 mAU/ml (normal range, 0–40 mAU/ml). Hepatitis B virus DNA polymerase chain reaction test results were positive. At the time of admission, a chest radiograph of the patient revealed miliary nodules in the entirety of the lungs. CT scan of the chest and abdominopelvis indicated miliary metastases throughout the lungs, bilateral adrenal metastases and metastatic abdominal lymph nodes (). The patient was observed at regular three-monthly follow-ups. After the first three months, the patient continued to exhibit cough and dyspnea, and there was no definitive interval change of the multiple lung metastases on the chest radiograph. At the second visit on September 14, 2009, the general condition of the patient had improved, and the cough and dyspnea had stopped. A chest radiograph revealed that all metastatic nodules had disappeared (). Serum AFP level had decreased to 1.5 ng/ml. Spontaneous tumor regression of HCC was observed, and whole-body positron emission tomography-CT scan in December, 2009 revealed that all metastatic nodules in the lung, as well as the metastatic lesions of the two adrenal glands and lymph nodes, had disappeared. The patient had taken an alternative herbal medicine for approximately one week, on the recommendation of his family. The herbal medicine was Dendropanax morbifera Leveille, which is a subtropical, broad-leaved evergreen tree belonging to the family Araliaceae ().
Follow-up CT scans revealed no recurrent lesions, and follow-up chest radiograph also indicated no metastatic lesions. Serum AFP and PIVKA II levels were within the normal range (). The patient is alive without any symptoms or signs as of May 2013.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [64, 'years'], 'Alanine aminotransferase': [41.0, 'U/L'], 'Aspartate aminotransferase': [32.0, 'U/L'], 'Platelet count': [164000.0, 'µL']}",1.95027,1.85276,2.04778,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 32.0 U/L.
The patient's concentration of ALT is 41.0 U/L.
The patient's concentration of platelets is 164000.0 count/µL. To convert 164000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 164000.0 platelets count/µL * 1000000.0 µL/L = 164000000000.0 platelets count/L. This means that there are 164000000000.0/(10^9) = 164.0 billion platelet counts per liter.
Plugging these values into the formula, we get (64 * 32.0)/(164.0 * sqrt(41.0)) = 1.95027.Hence, the Fibrosis-4 score is 1.95027."
4322,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-7331852-1,Extracted,"A 65-year-old female with history of chronic alcohol use was hospitalized for sudden onset of hematemesis. She also reported few days of nausea and vomiting associated with worsening ascites. She denied any significant past medical history except for a ruptured ovarian cyst at age of 30 years that required emergent surgery. Patient had a long history of alcohol use (two glasses of vodka daily) for over 10 years. Physical exam showed scleral icterus, there was mild abdominal distention with epigastric tenderness, no hepatosplenomegaly was noted. No signs of encephalopathy or asterixis were seen. Blood test showed hemoglobin 10.4 × 10 g/dL, white blood cell count of 7.7 × 103 cells/µL and platelet count of 190 × 103 cells/µL. Her prothrombin time and international normalized ratio (INR) were elevated at 1.4 and 14.3 s, respectively. Liver function test showed aspartate transaminase 140 U/L, alanine transaminase 29 U/L, alkaline phosphatase 332 U/L, total bilirubin 9.6 mg/dL (direct 7.4 mg/dL, indirect 2.2 mg/dL). Few hours after admission, she developed an episode of hematemesis with drop in hemoglobin to 7.7 g/dL. Emergent endoscopy showed a non-bleeding 2 cm prepyloric gastric antral ulcer (). Biopsy of the ulcer base was negative for malignancy or H. pylori.
Follow-up endoscopy at an interval of 6 weeks showed a healing prepyloric antral ulcer with mild portal hypertensive gastropathy (). Patient had a repeat endoscopy at 4 months for persistent nausea and vomiting which again showed a healing antral ulcer. She continued to drink alcohol and was intermittently followed by her the primary care physician. She also reported daily NSAID use for abdominal pain and nausea. She had multiple emergency department (ED) visits for the same complaints and underwent repeat endoscopy which showed a duodenal ulcer (). She was managed with pantoprazole twice daily and was advised to avoid NSAIDs and alcohol. She also underwent extensive workup for recurrent nausea and vomiting which were all unremarkable. Systemic disorders including but not limited to neurological cause, adrenal, parathyroid and diabetes were also ruled out.
She again presented to the ED for worsening nausea and vomiting associated with upper abdominal pain. Endoscopy, now 7 years from the discovery of the initial lesion, showed a GDF. The prepyloric antral ulcer had fistulized into the duodenal bulb creating the appearance of a double pylorus (). Biopsy of the ulcer base was again negative for malignancy or H. pylori. H. pylori stool antigen and serum H. pylori antibody test were also negative. She was discharged on oral proton pump inhibitor and has been followed up with gastroenterology for management of Laennec’s cirrhosis. With more frequent outpatient follow up, alcohol abstinence and use of acid-suppression medication, she had gradual improvement in her symptoms in about 1 - 2 months.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [65, 'years'], 'Alanine aminotransferase': [29.0, 'U/L'], 'Aspartate aminotransferase': [140.0, 'U/L'], 'Platelet count': [190000.0, 'µL']}",8.89383,8.44914,9.33852,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 140.0 U/L.
The patient's concentration of ALT is 29.0 U/L.
The patient's concentration of platelets is 190000.0 count/µL. To convert 190000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 190000.0 platelets count/µL * 1000000.0 µL/L = 190000000000.0 platelets count/L. This means that there are 190000000000.0/(10^9) = 190.0 billion platelet counts per liter.
Plugging these values into the formula, we get (65 * 140.0)/(190.0 * sqrt(29.0)) = 8.89383.Hence, the Fibrosis-4 score is 8.89383."
4323,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-6176381-1,Extracted,"A 61-year-old male was admitted to general hospital in Tangerang, due to progression of fatigue since a week before. The patient had history of essential thrombocythemia (ET) and hemolytic anemia since 12 and 7 years ago consecutively. The ET was diagnosed based on bone marrow biopsy done that showed proliferation of megakaryocytes, not meeting other myelodysplastic syndrome. He was treated with hydroxyurea for 5 years and then substituted with azathioprine due to possible of hydroxyurea-induced hemolytic anemia. The patient was diagnosed of hemolytic anemia as the immunoglobulin G (IgG) on Coombs test was positive. Approximately 3 years ago, the patient experienced abdominal enlargement with tenderness on the upper left quadrant of the abdomen. Noncontrast abdominal computed tomography (CT) scan examination was done and the results showed hepatic cirrhosis, splenomegaly, portal hypertension and ascites. He had history of packed red cell transfusion due to anemia 7 years ago. A year before admission, he experienced mutiple episodes of hematemesis and melena that caused anemia and series of packed red cell transfusion. He underwent esophagogastroduodenoscopy (EGD), which showed rupture of esophageal varives, which was then ligated ( and 2).
At admission, the patient was compos mentis with vital signs blood pressure of 100/60 mmHg, pulse rate of 96 beats perminute, respiratory rate of 17 times perminute, and temperature 36°C. His body weight was 58 kg, height 173 cm, BMI of 19.3. His skin was icteric, with icteric sclera and pale conjunctiva. In the abdomen, there was schuffner 3 splenomegaly with ascites and no palpated liver.
Laboratory results 3 months before admission showed decrease cholinesterase of 3135 U/L, normal albumin of 3.79 mg/dL, decreased globulin of 1.61 mg/dL, increased total/direct and indirect bilirubin of 6.36 mg/dL, 2.86 mg/dL and 4.1 mg/dL, increased alkaline phosphatase of 245 U/L and normal gamma glutamyl transferase of 174 U/L. Upon admission, laboratory results showed microcytic hypochromic anaemia with hemoglobin level of 6.3 g/dL, increased leucocyte of 29,420/μL, normal platelet of 402,000/μL. Aspartate and alanine aminotransferase were in normal range (9 U/L and 26 U/L), the total, direct and indirect bilirubin was 2.84 mg/dL, 1.06 mg/dL and 1.78 mg/dL. There were an increase in prothrombin and activated parsial thromboplastin time of 12.1 and 46.7 seconds, and in D-Dimer of 3.57. Viral hepatitis B and C examination were negative. Stool examination showed positive occult blood. This patient was treated with methylprednisolone 16 mg O.D., azathioprine 50 mg B.I.D, propranolol 10 mg T.I.D, spironolactone 100 mg and furosemide 40 mg O.D.. The patient was discharged with resolution of his fatigue.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [61, 'years'], 'Alanine aminotransferase': [26.0, 'U/L'], 'Aspartate aminotransferase': [9.0, 'U/L'], 'Platelet count': [402000.0, 'µL']}",0.26783,0.25444,0.28122,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 9.0 U/L.
The patient's concentration of ALT is 26.0 U/L.
The patient's concentration of platelets is 402000.0 count/µL. To convert 402000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 402000.0 platelets count/µL * 1000000.0 µL/L = 402000000000.0 platelets count/L. This means that there are 402000000000.0/(10^9) = 402.0 billion platelet counts per liter.
Plugging these values into the formula, we get (61 * 9.0)/(402.0 * sqrt(26.0)) = 0.26783.Hence, the Fibrosis-4 score is 0.26783."
4324,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-6822057-1,Extracted,"A 60-year-old Japanese man was admitted to Honjo Daiichi Hospital due to proteinuria and edema. He had been diagnosed with type 2 diabetes. On admission, his blood pressure was 136/83 mmHg. A physical examination showed bilateral pretibial edema. No abnormal signs were observed in the lungs, heart, or abdomen.
Urinalysis showed heavy proteinuria (5.1 g/g creatinine) without hematuria. His leukocyte count, hemoglobin level, and platelet count were 5,900/µL, 14.7 g/dL, and 191,000/µL, respectively. Serum total protein was 5.2 g/dL, albumin 2.4 g/dL, blood urea nitrogen 8.4 mg/dL, creatinine 0.79 mg/dL, alanine aminotransferase 16 U/L, aspartate aminotransferase 11 U/L, lactate dehydrogenase 206 U/L, total cholesterol 261 mg/dL, IgG 572 mg/dL, IgA 345 mg/dL, IgM 93 mg/dL, C3 80 mg/dL (normal range: 65 – 135 mg/dL), and C4 12 mg/dL (normal range: 13 – 35 mg/dL). Tests for anti-nuclear antibodies, cryoglobulin, hepatitis B virus antigen, and anti-hepatitis C antibodies were all negative. Monoclonal proteins were not detected in the serum or urine. Circulating IgA-class anti-PLA2R antibodies were not determined by our in-house ELISA [] using peroxidase-conjugated anti-human IgA as a secondary antibody.
Due to the presence of NS, a renal biopsy was performed. Light microscopy showed global scleroses in 2 of 20 glomeruli. The functioning glomeruli showed no mesangial proliferation and no bubbling/spike appearance along the glomerular capillary walls (). In the tubulointerstitium, mild lymphocyte infiltration, tubular atrophy, and interstitial fibrosis were observed. There was moderate arteriolar hyalinosis. Immunofluorescence microscopy showed 2+ granular staining for IgA- and IgA1-heavy chains (b, c), 2+ granular staining for κ- and λ-light chains (f, g), and trace granular staining for C3 (h) along the glomerular capillary walls, but no significant staining for IgG-, IgA2-, IgM-heavy chains, or C1q (a, d, e, i). An immunofluorescence study using anti-PLA2R antibodies (Sigma-Aldrich, St. Louis, MO, USA) showed negative glomerular staining. Electron microscopy revealed extensive foot process effacement of the podocytes, which contained large amounts of dense materials mainly in the area covering the surface of the glomerular basement membrane, but not in the mesangial area (a). Small amounts of electron-dense deposits were observed beneath the cytoplasm of the podocytes containing the dense materials (b). From the above-mentioned pathological findings, the diagnosis of early stage MN with solitary polyclonal IgA deposition was made.
He was treated with low-dose prednisolone (PSL) (10 mg/day for 8 weeks) in consideration of his history of type 2 diabetes. Thereafter, partial effects on proteinuria were observed, and PSL doses were gradually tapered. At the 3-year follow-up he was well. His urinary protein was 2.1 g/g creatinine, serum total protein 5.8 g/dL, albumin 3.5 g/dL, and creatinine 0.87 mg/dL.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [60, 'years'], 'Alanine aminotransferase': [16.0, 'U/L'], 'Aspartate aminotransferase': [11.0, 'U/L'], 'Platelet count': [191000.0, 'µL']}",0.86387,0.82068,0.90706,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 11.0 U/L.
The patient's concentration of ALT is 16.0 U/L.
The patient's concentration of platelets is 191000.0 count/µL. To convert 191000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 191000.0 platelets count/µL * 1000000.0 µL/L = 191000000000.0 platelets count/L. This means that there are 191000000000.0/(10^9) = 191.0 billion platelet counts per liter.
Plugging these values into the formula, we get (60 * 11.0)/(191.0 * sqrt(16.0)) = 0.86387.Hence, the Fibrosis-4 score is 0.86387."
4325,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-7269883-1,Extracted,"A 69-year-old man presented with general malaise, anorexia, and a history of daily alcohol consumption;he was admitted to Hanawa Kousei Hospital. There was no pertinent history pertaining to medical treatment, family, medication, blood transfusion, or allergy. He had been drinking approximately 900 mL of sake daily for the past 49 years, and had a 29 pack-year smoking history. He had bowel movements once or twice daily with no history of habitual laxative use or enemas. On physical examination, he was lucid, had a heart rate of 84/min, blood pressure of 138/66 mm Hg, and a temperature of 36.9°C;there was jaundice and hepatomegaly. Laboratory findings included white blood cells 9,100/μL, red blood cells 366×10
4/μL, hemoglobin 12.9 g/dL, platelets 15.1×10
4/μL, total protein 5.4 g/dL, albumin 2.3 g/dL, total bilirubin 5.85 mg/dL, direct bilirubin 4.02 mg/dL, aspartate aminotransferase 185 U/L, alanine aminotransferase 182 U/L, lactate dehydrogenase 526 U/L, alkaline phosphatase 1,312 U/L, gamma glutamyl transpeptidase 1.782 U/L, amylase 42 U/L, blood urea nitrogen 29.4 mg/dL, serum creatinine 1.54 mg/dL, C-reactive protein 6.31 mg/dL, carcinoembryonic antigen (CEA) 9.7 ng/mL, carbohydrate antigen 19-9 (CA19-9) 54 U/mL, and soluble interleukin-2 receptor 510 U/mL. Hepatitis virus markers and autoantibodies were negative. Urine was positive for ketone bodies. A non-contrast CT confirmed hepatomegaly, with no evidence of bile duct obstruction or malignant tumor (). In addition, CT showed localized colonic wall-thickening at the splenic flexure (). We diagnosed the patient as having acute alcoholic hepatitis in light of his drinking history. He had avoided medical checkups previously; on the other hand, he had no other conditions, such as hypertension, diabetes mellitus, hyperlipidemia, or hyperuricemia, after admission. His clinical symptoms, jaundice, and liver dysfunction rapidly improved with fluid replacement and rest. Non-contrast CT on admission showed colonic wall-thickening at the splenic flexure, and a blood test showed a slight increase in CEA. Since the patient had not previously undergone CS, it was performed to rule out colon cancer on the seventh hospital day. The colonic splenic flexure showed redness over two-thirds of its circumference and an ulcerative, slightly constricted lesion approximately 5 cm in length (). Differential diagnosis included IC, colon cancer, malignant lymphoma, infectious enteritis, and inflammatory bowel disease, but the histopathological findings on biopsy showed only nonspecific inflammatory changes. On the 12th hospital day, contrast-enhanced CT of the abdomen revealed a thickened colonic splenic flexure wall. There was no enhancement of the intestinal wall (). Although calcification of the aorta was observed, there was no evidence of calcification or occlusion in the superior mesenteric artery, inferior mesenteric artery, superior mesenteric vein, inferior mesenteric vein, branches, or portal vein. The patient had constipation after initiation of conservative treatment, and malignancy could not be ruled out from the findings of contrast-enhanced CT. On day 30 after starting treatment, a second CS revealed complete circumferential stenosis of the colonic splenic flexure with difficulty in passing the scope through the proximal side (). With gastrografin contrast radiography through CS, full-circumference stenosis to approximately 3 cm was recognized (). Stricture-type IC was suspected based on the first endoscopy and rapid course of circumferential stenosis. Histopathological findings on biopsy showed erosion of the mucosa, edema of the stroma, and infiltration of inflammatory cells, confirming the diagnosis of IC (). Surgery was also considered, but the patient had only mild symptoms of constipation, which were judged not to be indicative of complete intestinal obstruction. Therefore, conservative treatment with oral laxatives and intestinal motion regulators was performed. CEA decreased to 6.0 ng/mL on the 56th hospital day. CS showed scarring and healing of the lesion on the 105th hospital day (), and histopathological findings on biopsy showed no evidence of malignancy.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [69, 'years'], 'Alanine aminotransferase': [182.0, 'U/L'], 'Aspartate aminotransferase': [185.0, 'U/L'], 'Platelet count': [151000.0, 'µL']}",6.26626,5.95295,6.57957,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 185.0 U/L.
The patient's concentration of ALT is 182.0 U/L.
The patient's concentration of platelets is 151000.0 count/µL. To convert 151000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 151000.0 platelets count/µL * 1000000.0 µL/L = 151000000000.0 platelets count/L. This means that there are 151000000000.0/(10^9) = 151.0 billion platelet counts per liter.
Plugging these values into the formula, we get (69 * 185.0)/(151.0 * sqrt(182.0)) = 6.26626.Hence, the Fibrosis-4 score is 6.26626."
4326,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-6919534-1,Extracted,"A 38-year-old Taiwanese man having a history of alcoholic liver cirrhosis, without regular medical follow-up, was admitted to the hospital. Right flank pain had occurred 10 days before this admission, and treatment was then prescribed for a muscle strain at a rural hospital. The pain, which radiated to the right upper abdomen, was accompanied with a fever, which developed for 3 days. The patient was then referred to our hospital for further analysis and management. Upon arrival to our hospital, his vital signs included a respiratory rate of 18 breaths/min, a heart rate of 122 beats/min, blood pressure of 120/72 mm Hg, and a body temperature of 39.5°C. A physical examination revealed mild pale conjunctiva, rapid regular heart beats, tenderness, and rebounding pain over the right upper quadrant of the abdomen, and also a knocking tenderness over the right flank region. Laboratory tests uncovered a white blood cell count (WBC) of 31,700/mm3, with segmented neutrophils at 96.6%, hemoglobin at 10.8 g/dL, platelet counts of 407 × 103/mm3, blood urea nitrogen at 50 mg/dL, creatinine at 2.7 mg/dL, lactate at 16.3 mg/dL, albumin at 2.3 g/dL, glutamic-oxaloacetic transaminase at 122 U/L, glutamic-pyruvic transaminase at 49 U/L, lactate dehydrogenase at 486 U/L, alkaline phosphatase at 432 U/L, C-reactive protein at 40.4 mg/dL, blood glucose at 106 mg/dL, along with other test result levels which were unremarkable. A CT scan demonstrated fluid accumulation at the right subphrenic and retroperitoneal spaces, multiple cystic lesions within the right kidney, along with an irregular surface of the kidney adjacent to retroperitoneal fluid (Fig. ). Purulent fluid was aspirated from the right subphrenic space for analysis, with the results indicating there was a WBC of 78,750/mm3, with an 85% level of segmented neutrophils. Percutaneous catheters were implanted for drainage of the right subphrenic and retroperitoneal abscesses using ceftriaxone at 2000 mg once daily. Six days later, an uncontrolled sepsis persisted due to the patient's failure to respond to medical treatment. Subsequently, a nephrectomy for the renal abscess was carried out involving debridement of the retroperitoneal abscess. Anaerobic cultures of the right subphrenic and retroperitoneal abscess grew both A israelii and Bacteroides fragilis. Aerobic cultures of the ascites and abscess uncovered no traces of bacteria. An anaerobic culture of the nephrectomy specimen yielded A israelii. Anaerobic, aerobic bacterial, and fungal cultures of the patient's blood and urine proved to be negative. Acid fast stain and cultures for tuberculosis were not found in either the urine or nephrectomy specimen. The pathologic results revealed multiple renal abscesses involving actinomycosis with the characteristics of sulfur granules (Fig. ). A full course of antibiotics with intravenous penicillin G (3 million units every 4 hours) was prescribed for 2 weeks, followed by oral penicillin V given at a dose of 2 grams per day for 6 months at our out-patient facility.
Written informed consent was obtained from the patient for publication of this case report and all accompanying images. Ethical approval was not required, but the patient's informed consent and agreement of images for publication were completed.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [38, 'years'], 'Alanine aminotransferase': [49.0, 'U/L'], 'Aspartate aminotransferase': [122.0, 'U/L'], 'Platelet count': [407000.0, 'µL']}",1.62724,1.54588,1.7086,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 122.0 U/L.
The patient's concentration of ALT is 49.0 U/L.
The patient's concentration of platelets is 407000.0 count/µL. To convert 407000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 407000.0 platelets count/µL * 1000000.0 µL/L = 407000000000.0 platelets count/L. This means that there are 407000000000.0/(10^9) = 407.0 billion platelet counts per liter.
Plugging these values into the formula, we get (38 * 122.0)/(407.0 * sqrt(49.0)) = 1.62724.Hence, the Fibrosis-4 score is 1.62724."
4327,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-7900318-1,Extracted,"A 66-year-old woman presented with acute back pain after having lunch and she was transported by ambulance. Her body temperature was 35.9 °C, heart rate was 80 bpm, blood pressure was 101/65 mmHg, and consciousness was clear. On abdominal examination, she had upper quadrant spontaneous pain and moderate tenderness, but no guarding or rebound pain. She had a duodenal ulcer several years ago. She was taking 10 mg of steroids per day for rheumatoid arthritis.
The admission laboratory data included the following: white blood cell count, 18.2 × 103/μl, hemoglobin, 10.7 g/dl, hematocrit, 32.4%, platelets, 22.6 × 104/μl, C-reactive protein, 3.32 mg/dl, aspartate aminotransferase, 25 IU/l, alanine aminotransferase, 49 IU/l, and serum amylase, 43 IU/l. Contrast-enhanced computed tomography (CT) demonstrated a retroperitoneal hematoma at the ventral side of the left kidney, extravasation of contrast agent from a branch of the SMA, and ascites in the pelvis (Fig. a–c). Utilizing detailed three-dimensional CT (3DCT), we confirmed the extravasation of contrast agent from a branch of the SMA (Fig. a and b).
We diagnosed her with a ruptured artery aneurysm of the TPA originating from the SMA. We conferred with our IVR team on treatment strategy for the ruptured aneurysm. In addition, we finally selected operation since the branch of the SMA to the aneurysm was too thin and complex to conduct IVR. In addition, the patient went into shock in the emergency room. For these reasons, we immediately performed emergency surgery. When we opened the abdomen, we found hematoma in the omental bursa. We opened the omental bursa and removed the transverse mesocolon from the lower edge of the pancreas. There was massive hematoma behind the pancreas. After removing the hematoma, we found that a branch of the SMA was bleeding. This branch was the TPA and it had a hemorrhagic aneurysm of approximately 5 mm (Fig. ). We ligated and resected the aneurysm, and the surgery was finished. The patient was hospitalized in the intensive care unit for 3 days. Although she had pancreatitis, the postoperative course was relatively smooth and she was discharged home 30 days after surgery.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [66, 'years'], 'Alanine aminotransferase': [49.0, 'U/L'], 'Aspartate aminotransferase': [25.0, 'U/L'], 'Platelet count': [226000.0, 'µL']}",1.04298,0.99083,1.09513,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 25.0 U/L.
The patient's concentration of ALT is 49.0 U/L.
The patient's concentration of platelets is 226000.0 count/µL. To convert 226000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 226000.0 platelets count/µL * 1000000.0 µL/L = 226000000000.0 platelets count/L. This means that there are 226000000000.0/(10^9) = 226.0 billion platelet counts per liter.
Plugging these values into the formula, we get (66 * 25.0)/(226.0 * sqrt(49.0)) = 1.04298.Hence, the Fibrosis-4 score is 1.04298."
4328,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4386617-1,Extracted,"A 41-year-old female (human leucocyte antigen (HLA)-A1, -A11, -B7, -B35, -Cw4, -Cw7, -DR1 and -DR14) received CMV mismatched (D+/R−) bilateral sequential LTx in June 2012 for cystic fibrosis. Immunosuppression was tacrolimus, prednisolone and azathioprine. CMV prophylaxis was CMV hyperimmune globulin and ganciclovir, followed by continuous valganciclovir 450 mg twice daily. The patient had mild renal impairment (estimated glomerular filtration rate of 46 ml min−1). Three months post transplant, she developed an asymptomatic increase in blood CMV PCR (DNAemia: 2769 DNA copies ml−1; ), new onset pancytopaenia (haemoglobin 97 g l−1, white cell count 3.64 × 109 l−1, platelets 140 × 109 l−1) and liver dysfunction (gamma glutamyl transferase (GGT) 175, alkaline phosphatase (ALP) 134, alanine aminotransferase (ALT) 79 and aspartate aminotransferase (AST) 69 U l−1) consistent with hepatitis. Despite intravenous ganciclovir and CMV hyperimmune globulin, the blood CMV PCR continued to rise. CMV PCR was also detected in bronchoalveolar lavage (BAL) fluid during bronchoscopy. Foscarnet was commenced. Leukopenia was minimised by cessation of azathioprine and trimethoprim/sulfamethoxazole. Tacrolimus was changed to everolimus and leflunomide added. CMV PCR peaked at 344 386 DNA copies ml−1 on day 18 post ganciclovir commencement (). CMV gene results confirmed UL97 gene mutation L595S conferring ganciclovir resistance. Foscarnet was continued. Resolution of the pancytopaenia and hepatic dysfunction occurred, while CMV PCR fluctuated and gradually reduced to undetectable levels after 6 weeks of continuous treatment with foscarnet and reduced immunosuppression. Surveillance transbronchial biopsies showed mild (A2) acute cellular rejection, treated with methylprednisolone and oral steroids and fortnightly IVIg. After 2 weeks of undetectable CMV PCR levels, foscarnet was ceased. Two weeks later, the patient had another asymptomatic rise in CMV PCR (2059 DNA copies ml−1) requiring a further 2 weeks of foscarnet, which reduced the CMV PCR back to undetectable (). The patient continued IVIg fortnightly until T-cell therapy was commenced 5 months after the initial presentation.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [41, 'years'], 'Alanine aminotransferase': [79.0, 'U/L'], 'Aspartate aminotransferase': [69.0, 'U/L'], 'Platelet count': [140000000.0, 'L']}",2273.48119,2159.80713,2387.15525,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 69.0 U/L.
The patient's concentration of ALT is 79.0 U/L.
The patient's concentration of platelets is 140000000.0 count/L. This means that there are 140000000.0/(10^9) = 0.14 billion platelet counts per liter.
Plugging these values into the formula, we get (41 * 69.0)/(0.14 * sqrt(79.0)) = 2273.48119.Hence, the Fibrosis-4 score is 2273.48119."
4329,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-2740308-1,Extracted,"A 78-year-old Indian, non-smoker man, presented to out patient department with progressively increasing generalized weakness for two months. He gave history (on leading question) of weight loss (about 2 kg) during this period. There was no history of fever, cough, expectoration, hemoptysis or chest pain. Patient denied any history of joint pain, skin rash, photosensitivity, Raynaud's phenomenon or oral ulcers. There was no history high risk sexual behavior, intravenous drug abuse or blood transfusion. Patient had history of type-2 diabetes mellitus since last 10 years and was taking oral hypoglycemic agents (Metformin SR 850 mg twice daily and Glimiperide 2 mg once a day) with good control of blood sugars. He was also suffering from coronary artery disease for which he was taking his medications (Aspirin 75 mg once a day, Metoprolol SR 25 mg twice daily and Atorvastatin 10 mg once a day at night). There was no history of tuberculosis in the past. Family history was non contributory. Physical examination revealed well built and nourished elderly. He was afebrile with oral temperature of 98.2°F. His pulse was 82/minute and blood pressure was 126/72 mm of Hg. There was no pallor, icterus, peripheral lymphadenopathy, clubbing or bony tenderness. Chest examination revealed reduced expansion in infrascapular region on the right side with dull percussion note and reduced breath sounds in the same region. There was no hepatosplenomegaly. Examination of cardiovascular and nervous system did not reveal any abnormality.
Blood investigations revealed hemoglobin of 13.5 gm/dl, total leukocyte count 5,400/µl with differential counts showing mild eosinophilia (neutrophil 56%, lymphocyte 32%, monocyte 05%, and eosinophils 07%), platelets were 2,24,000/µl and ESR was 110 mm in 1st hour. Serum biochemistry including calcium (10 mg/dl), uric acid (4.0 mg/dl), sodium (141 mg/dl) and potassium (5.0 mg/dl) were normal. Liver function tests showed raised total protein (8.4 gm/dl) and reversed albumin (3.5 gm/dl) and globulins (4.9 gm/dl) ratio. Total bilirubin (0.4 mg/dl), alanine aminotransferase (39 U/L; reference value 30-65 U/L), aspartate aminotransferase (26 U/L; reference value 15-37 U/L) and alkaline phosphatase (51 U/L; reference value 50-136 U/L) were normal. Fasting blood sugar was 107 mg/dl. Renal functions tests showed normal blood urea (12 mg/dl) and creatinine (0.9 mg/dl). Lipid profile was also within normal limits. Patient tested for HIV infection by ELISA was negative.
Chest radiograph () showed mass lesion in right lower zone and multiple nodules in bilateral lung fields. For further characterization, CT of chest was done. It revealed a large mass with sharp margins in right lower lobe and multiple nodules in both lungs. Multiple nodules of varying sizes were seen in left upper lobe, lingula and apical segment of left lower lobe (, ). It also revealed mild right sided pleural effusion. On the basis of radiological findings, metastatic lung disease from extra thoracic origin, carcinoma lung with metastases were considered as differentials diagnoses. Patient was evaluated for extrathoracic primary site of malignancy. Stool samples for occult blood were negative for three times. Urine did not show any evidence of hematuria. Prostate specific antigen levels were normal. Urine examination was negative for Bence-Jones proteins. Serum electrophoresis revealed M-band and ß-2 microglobulins were raised (1952 µg/l; reference value 510-1470 µg/l) but other tests including bone marrow aspirate and biopsy did not reveal any evidence of plasma cell dyscrasia. Serum LDH was normal.
For the histological diagnosis, CT guided biopsy from the right lung mass was done. Histopathological examination () showed fibrocollagenous tissue infiltrated by monomorphic round cells with scanty cytoplasm, high nucleo-cytoplasmic ratio, large vesicular nucleus and prominent nucleoli in some of the cells. Frequent mitotic activity and apoptotic bodies were noted. Immunohistochemistry showed the cells to be positive for leukocyte common antigen (LCA) and CD20 (B-cell marker) while being negative for CD3 (T-cell marker), cytokeratin and neuroendocrine markers. Stains for acid fast bacilli and fungus were negative. Thus, a final pathological diagnosis of diffuse large cell B-cell lymphoma was rendered. Patient was evaluated for involvement of other sites by lymphoma. Contrast enhanced CT of abdomen did not revealed any mass lesion. Patient was referred to medical oncology for chemotherapy. However, family declined any treatment. Patient last seen a week back was stable.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [78, 'years'], 'Alanine aminotransferase': [39.0, 'U/L'], 'Aspartate aminotransferase': [26.0, 'U/L'], 'Platelet count': [224000.0, 'µL']}",1.44973,1.37724,1.52222,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 26.0 U/L.
The patient's concentration of ALT is 39.0 U/L.
The patient's concentration of platelets is 224000.0 count/µL. To convert 224000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 224000.0 platelets count/µL * 1000000.0 µL/L = 224000000000.0 platelets count/L. This means that there are 224000000000.0/(10^9) = 224.0 billion platelet counts per liter.
Plugging these values into the formula, we get (78 * 26.0)/(224.0 * sqrt(39.0)) = 1.44973.Hence, the Fibrosis-4 score is 1.44973."
4330,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-7797408-1,Extracted,"A 55-year-old woman presented with a past medical history of smoking until five years ago (60 pack/year), arterial hypertension, chronic obstructive pulmonary disease with no supplementary oxygen use, and chronic hepatitis B infection with no history suggestive of cirrhosis. Her chief complaint was one year of abdominal discomfort associated with an epigastric mass and weight loss of 30 kg. Simple and contrasted abdominal computed tomography (CT) showed hepatomegaly with focal lesions, the largest being 15 cm in segment VIII, and satellite lesions of up to 5.5 cm in segment VII and 3.5 cm in segment III, with similar morphologic characteristics. Abdominal magnetic resonance imaging (MRI) showed a liver with no signs of chronic disease, and an infiltrative dominant lesion of 11 x 8 cm in segments IV and V, associated with smaller lesions in both lobules of 1.6 cm in segment III, and 0.9 cm in segments VII and VIII (Figure ). Subsequently, the patient presented aggressiveness and disorientation, where hypoglycemia was documented (33 mg/dL) and treated with dextrose 10% with complete symptom resolution.
Physical examination revealed cachectic facies, and an abdominal mass of approximately 13 cm located in epigastrium and right hypochondrium, associated with hepatomegaly. Initial laboratory were: white blood count of 9900/uL, neutrophils 8000/uL, lymphocytes 1700/uL, monocytes 300/uL, red blood cells 5,540,000/uL, hemoglobin 16.6 g/dL, hematocrit 49.6%, mean corpuscular volume 89.6 fL, platelet count 357,000/uL, international normalised ratio (INR) 1.05 (normal range (NR) 0.8-1.4), partial thromboplastin time 33 seconds (NR 25-35), serum potassium 3.3 mmol/L, chloride 104 mmol/L (NR 98-107), sodium 141 mmol/L (NR 136-145), total bilirubin 1.01 mg/dL (NR 0.2-0.9), direct bilirubin 0.48 mg/dL (NR 0-0.3), alkaline phosphatase 404 U/L (NR 38-110), gamma-glutamyl transferase (GGT) 1017.6 U/L (NR 10-38), lactic dehydrogenase (LDH) 293 U/L (NR 120-246), alanine transaminase (ALT) 124 U/L (NR 9-52), aspartate transaminase (AST) 226 U/L (NR 14-36), serum creatinine 0.22 mg/dL (NR 0.5-0.8), serum alpha fetoprotein (AFP) 23184.1 ng/mL (NR 0.8-1), carcinoembryonic antigen 0 ng/mL, CA 19-9 antigen 26.86 U/mL (NR 0-37), cortisol 8.9 ug/dL (NR 5.27-22.45), blood ketones 1.0 mg/dL (NR < 3.5), serum glucose 17 mg/dL (NR 74-106), baseline insulin 0.40 uU/mL (NR 2.6-24.9), IGF-I < 15 ng/mL (NR 45-210), C peptide 0.0407 ng/mL (NR 1.1-4.4), IgM antibodies against hepatitis B core antigen non-reactive, antibodies against hepatitis B surface antigen < 3.10 mUI/mL (NR 0-10), antibodies against hepatitis C non-reactive, hepatitis B surface antigen (HBsAg) > 1000 (NR 0-1). Given our patient’s profile, a “big” IGF-II measurement was attempted, but the assay is not available in Colombia. Therefore, hypoglycemia due to tumor consumption vs paraneoplastic hypoglycemia due to “big”-IGF II production were the suspected diagnoses. The patient required treatment with 50% dextrose in continuous infusion to achieve normal blood glucose and to remain symptom free.
A positron emission tomography (PET/CT) with fluorine-18-fluorodeoxyglucose (18-FDG) was performed (Figure ), where multiple hypermetabolic hepatic masses were observed, in both hepatic lobules; the high uptake index suggested an elevated glucose consumption tumor. Liver biopsy confirmed the diagnosis of trabecular and fibrolamellar hepatocarcinoma (Figure ). Given the size and presence of metastatic disease, the patient was not a candidate for surgical treatment; transarterial chemoembolization (TACE) was done twice with partial improvement, but the dextrose infusion could not be stopped. A glucagon therapeutic test was performed, with inadequate response. Thereafter, an OctreoScan was performed (Figure ) to determine if the patient could benefit from somatostatin analogs, but uptake was observed in a pulmonary metastasis only, reducing success probability with such therapy. Finally, despite different interventions, hypoglycemia control could not be achieved and, consequently, parenteral nutrition with a high dextrose load was started to continue ambulatory palliative care.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'Alanine aminotransferase': [124.0, 'U/L'], 'Aspartate aminotransferase': [226.0, 'U/L'], 'Platelet count': [357000.0, 'µL']}",3.12674,2.9704,3.28308,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 226.0 U/L.
The patient's concentration of ALT is 124.0 U/L.
The patient's concentration of platelets is 357000.0 count/µL. To convert 357000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 357000.0 platelets count/µL * 1000000.0 µL/L = 357000000000.0 platelets count/L. This means that there are 357000000000.0/(10^9) = 357.0 billion platelet counts per liter.
Plugging these values into the formula, we get (55 * 226.0)/(357.0 * sqrt(124.0)) = 3.12674.Hence, the Fibrosis-4 score is 3.12674."
4331,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-8285274-1,Extracted,"A 79-year-old woman with prior cerebral infarction in the left basal ganglia presented with headache and dizziness. Magnetic resonance imaging revealed an unruptured aneurysm on the right superior cerebellar artery (SCA). She had been taking an aspirin (100 mg/d) and atorvastatin (40 mg/d) since the occurrence of cerebral infarction, amlodipine (5 mg/d) and telmisartan (40 mg/d) for hypertension, and metformin (1700 mg/d) for type 2 diabetes mellitus. Her hypertension was uncontrolled before cerebral infarction, but it became controlled after taking the medication for hypertension. The patient never smoked and had no history of autoimmune diseases or allergic reactions.
Cerebral angiography revealed a small SCA aneurysm with a broad neck, with a maximum diameter of 2.62 mm and a neck diameter of 2.73 mm. In addition, there was narrowing of both anterior cerebral arteries (ACA), which could lead to extensive cerebral infarction. Because the unruptured SCA aneurysm was small and unlikely to rupture, it was determined to be followed with periodic brain imaging. A dual antiplatelet regimen of aspirin (100 mg/d) and clopidogrel (75 mg/d) was used because of severe stenosis of the ACA.
Two weeks later, the patient was admitted to the hospital due to dyspnea that started 3 days prior. She complained of anorexia, nausea, dyspnea on exertion, and chest pain. There was no complaint of cough, sputum, rhinorrhea, or chills. On admission, she was hypoxemic (room air pulse oximetry, 91%), and chest radiography revealed features of multifocal consolidation and reticulonodular opacities in both lungs ( and ). The patient presented the following vital signs: blood pressure, 136/66 mmHg; heart rate, 78 beats/min; respiratory rate, 20 breaths/min; and body temperature, 36.7 °C. The results of arterial blood gas analysis were the following: pH, 7.422; PaCO2, 38.3 mmHg; PaO2, 57 mmHg; SaO2, 88.1% (2 L/min of oxygen with a nasal prong). Laboratory test results were: hemoglobin, 11.5 g/dL; white blood cell count, 7410 cells/μL (neutrophils, 65.1%; lymphocytes, 24.3%; monocytes, 9.0%; eosinophils, 0.9%; and basophils, 0.7%); platelet count, 327,000 cells/μL; and C-reactive protein, 1.6mg/dL. The following serum biochemistry results were within normal limits: aspartate aminotransferase, 19 IU/L; alanine aminotransferase, 5 IU/L; total bilirubin, 0.7 mg/dL; alkaline phosphatase, 59 IU/L; total protein, 7.0 g/dL; albumin, 3.5 g/dL; blood urea nitrogen, 7 mg/dL; and creatinine, 0.57 mg/dL. Forced expiratory volume in one second and forced vital capacity were 1.02 L (predicted, 75%) and 1.07 L (predicted, 52%), respectively, and carbon monoxide diffusion capacity was 2.6 mL/mmHg/min (predicted, 19%). Congestive heart failure was excluded because of normal ultrasound cardiography results and a normal level of serum brain natriuretic peptide.
Empirical antibiotics (piperacillin/tazobactam 4.5 g every 6 hours plus levofloxacin 75 mg every 24 hours) were administered because bacterial pneumonia was not ruled out based on chest radiography findings. Enhanced chest computed tomography (CT) revealed symmetric peribronchial ground-glass opacity (GGO), reticulation, and consolidation in both lungs ( and ).
The patient had fever (37.8 °C) on the second day of hospitalization. In addition, oxygen saturation could not be maintained at 5 L/min via nasal prong, and oxygen was administered via a high-flow nasal cannula (30 L/min; FiO2, 35%). On day 4, bronchoalveolar lavage (BAL) was performed to rule out diffuse alveolar hemorrhage and atypical pneumonia. Bacterial polymerase chain reaction (PCR), viral PCR, Cytomegalovirus PCR, Pneumocystis jirovecii PCR, fungal culture, and acid-fast bacilli smear were performed in BAL samples. BAL samples revealed a clear color fluid, and no microorganisms were detected from any of the examinations. Nonetheless, patient’s clinical symptoms continued to deteriorate.
One day 5, and clopidogrel-associated ILD was suspected after ruling out all other possible causes of her symptoms. We changed dual antiplatelet regimen of aspirin and clopidogrel to aspirin and initiated intravenous treatment with 1 mg/kg/day of methylprednisolone. Clinical signs and chest X-ray improved after clopidogrel withdrawal and steroid treatment (). The patient was discharged with oral prednisolone (25 mg/day) on day 21 of hospitalization. The steroid dose was tapered over 6 months in the outpatient setting. A follow-up chest radiograph at 6 months after discontinuation of steroid treatment showed no recurrence, and the patient’s health status was good ().",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [79, 'years'], 'Alanine aminotransferase': [5.0, 'U/L'], 'Aspartate aminotransferase': [19.0, 'U/L'], 'Platelet count': [327000.0, 'µL']}",2.05281,1.95017,2.15545,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 19.0 U/L.
The patient's concentration of ALT is 5.0 U/L.
The patient's concentration of platelets is 327000.0 count/µL. To convert 327000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 327000.0 platelets count/µL * 1000000.0 µL/L = 327000000000.0 platelets count/L. This means that there are 327000000000.0/(10^9) = 327.0 billion platelet counts per liter.
Plugging these values into the formula, we get (79 * 19.0)/(327.0 * sqrt(5.0)) = 2.05281.Hence, the Fibrosis-4 score is 2.05281."
4332,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-5083268-1,Extracted,"A 46-year-old man presented with cramping abdominal pain and borborygmi, which aggravated with food and water intake. Over the previous 12 months, he had lost 6 kg of body weight. He reported two similar episodes of abdominal pain during the previous 14 months. The previous two episodes were conservatively managed with Levin tube drainage with nil per os, and the symptoms improved thereafter. He was diagnosed with LC associated with chronic hepatitis B 18 years ago. Additionally, 15 years ago, he started taking oral propranolol (40 mg/day) for the prophylaxis of gastroesophageal variceal bleeding. Further, 14 months earlier, he was diagnosed with end-stage renal disease due to uncontrolled hypertension and started to undergo hemodialysis. He had no history of spontaneous bacterial peritonitis (SBP), abdominal surgery, or CAPD. At the time of presentation, the patient was taking propranolol, nifedipine, valsartan, pantoprazole, oral iron, calcium carbonate, and multivitamins.
On physical examination, the patient was afebrile and hemodynamically stable. The abdomen was distended with increased bowel sounds. Percussion of the abdomen resulted in audible tympanic sounds. Shifting dullness was present and splenomegaly was detected. Laboratory findings were as follows: white blood cell count, 5,100/mm3; hemoglobin, 9.6 g/dL; platelet count, 107×103/mm3; blood urea nitrogen, 54 mg/dL; creatinine, 7.9 mg/dL; albumin, 2.6 g/dL; aspartate transaminase, 21 IU/L; alanine transaminase, 10 IU/L; alkaline phosphatase, 45 IU/L; CRP, 3.67 mg/dL; and prothrombin time, 64.3% (1.27 INR). Diagnostic paracentesis showed no evidence of SBP. Plain abdominal radiography showed small bowel dilatation with air-fluid levels on the right side of the abdomen (). Abdominal CT showed large amounts of ascites and ileal loops encapsulated by soft tissue with dilatation of the proximal small bowel on the right side of the abdomen (). Barium follow-through showed conglomerated distal ileal loops with a cauliflower-like appearance. Palpation did not separate these conglomerated bowel loops, but allowed passage of contrast medium (). On the basis of these findings, the patient was diagnosed with partial small bowel obstruction due to SEP. As his symptoms were recurrent and did not improve with conservative management, exploratory laparotomy was performed, which showed a thick, fibrous, and white capsule encapsulating the ileal loop (). The capsule was dissected and excised, releasing a 1.5-m section of the small bowel (). Histopathological examination of the capsule revealed a dense fibrous wall without epithelial lining (). The postoperative period was uneventful, and symptoms improved after the procedure. Propranolol was stopped after surgery. The patient has been receiving conservative management for LC and hemodialysis for 58 months after the surgery, without recurrence of bowel obstruction.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [46, 'years'], 'Aspartate aminotransferase': [21.0, 'U/L'], 'Alanine aminotransferase': [10.0, 'U/L'], 'Platelet count': [107000.0, 'µL']}",2.85492,2.71217,2.99767,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 21.0 U/L.
The patient's concentration of ALT is 10.0 U/L.
The patient's concentration of platelets is 107000.0 count/µL. To convert 107000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 107000.0 platelets count/µL * 1000000.0 µL/L = 107000000000.0 platelets count/L. This means that there are 107000000000.0/(10^9) = 107.0 billion platelet counts per liter.
Plugging these values into the formula, we get (46 * 21.0)/(107.0 * sqrt(10.0)) = 2.85492.Hence, the Fibrosis-4 score is 2.85492."
4333,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-7443662-1,Extracted,"A 43-year-old woman presented to the outpatient clinic with the chief complaint of insidious-onset, persistent, moderately severe, and poorly localized abdominal pain for more than a month. She also mentioned the rapid onset of yellowish skin color, tea-colored urine, and swelling in bilateral legs 1 week prior to admission. She had a history of chronic hepatitis B infection and did not follow up regularly. The physical examination at admission revealed acute ill-looking appearance as well as icteric sclera, skin, and mucus membrane. Abdominal examination showed palpable liver and spleen contour with shifting dullness while no muscle guarding or rebounding pain was found upon palpation. The rest of the physical examination was unremarkable.
Laboratory examination revealed a total leukocyte count of 9,060 cells/μL, hemoglobin concentration of 12.1 g/dL, and platelet count of 243,000/μL. Her ALT was 127 U/L, AST 268 U/L, ALP 468 U/L, serum total bilirubin 2.9 mg/dL (direct fraction 1.1 mg/dL), albumin 3.2 g/dL, creatinine 76.9 µmol/L, lactate dehydrogenase 537 U/L, alpha-fetoprotein 317,333 IU/mL, INR 1.26, and activated partial thromboplastin time of 26.2 s on initial presentation. In addition, serum markers were positive for hepatitis B surface antigen and hepatitis B envelope antigen while hepatitis B virus DNA was 1.67 × 106 IU/mL. Abdominal sonography showed multiple hepatic masses over bilateral lobes, hepatosplenomegaly, and massive ascites indicating hepatic malignancy and liver cirrhosis. Triple-phase CT of the abdomen revealed infiltrative HCC bilaterally with lymphadenopathy over the retroperitoneum, main portal vein thrombosis, and bone metastasis at the third lumbar spine (Fig. ). According to the Barcelona Clinic Liver Cancer (BCLC) classification the patient was diagnosed with advanced-stage HCC and received entecavir upon admission. Due to the rapid progression of tumor burden we administered nivolumab 200 mg (2.1 mg/day) intravenously on the 8th day of hospitalization and prescribed sorafenib 200 mg daily as combination therapy from the 9th day of hospitalization. On the 15th day sorafenib was discontinued due to deterioration of serum total bilirubin to 5.8 mg/dL, and on the 18th day her ALT was 1,303 U/L, AST 6,220 U/L, ALP 752 U/L, serum total bilirubin 16.9 mg/dL, INR 1.88, ammonia 54 µmol/L, creatinine 236 µmol/L, potassium 6.1 mmol/L, phosphate 7.4 mmol/L, calcium 2.1 mmol/L, and uric acid 1,118.2 µmol/L. Decompensated hepatic failure associated with TLS was diagnosed according to clinical and laboratory criteria defined by Cairo et al. []. After establishing TLS, we prescribed 1.5 mg of rasburicase twice daily from the 18th day, and the patient was admitted to the intensive care unit with vigorous hydration to maintain urine output. We also corrected electrolyte abnormalities and monitored vital signs closely. However, acute kidney injury with anuria developed along with hepatic encephalopathy despite intensive care, and the patient expired on the 21st day of hospitalization.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [43, 'years'], 'Alanine aminotransferase': [127.0, 'U/L'], 'Aspartate aminotransferase': [268.0, 'U/L'], 'Platelet count': [243000.0, 'µL']}",4.20819,3.99778,4.4186,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 268.0 U/L.
The patient's concentration of ALT is 127.0 U/L.
The patient's concentration of platelets is 243000.0 count/µL. To convert 243000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 243000.0 platelets count/µL * 1000000.0 µL/L = 243000000000.0 platelets count/L. This means that there are 243000000000.0/(10^9) = 243.0 billion platelet counts per liter.
Plugging these values into the formula, we get (43 * 268.0)/(243.0 * sqrt(127.0)) = 4.20819.Hence, the Fibrosis-4 score is 4.20819."
4334,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4825159-1,Extracted,"A 48-year-old man visited outpatient clinic with abdominal discomfort. He was a hepatitis B surface antigen (HBsAg) carrier for long time. The physical examination showed shifting dullness and pitting edema. Laboratory findings were as follows: white blood cell count of 5,100/µL (N:4,000-10,000), hemoglobin of 15.3 g/dL (N: 13-17), platelet count of 1.79×105/µL (N:150,000-450,000), creatinine of 1.2 mg/dL (0.9-1.3), aspartate aminotransferase level of 442 IU/L (N:8-38), alanine aminotransferase (ALT) level of 414 IU/L (N:4-44), total bilirubin of 1.7 mg/dL (N:0.2-1.2), albumin of 3.3 g/dL (N:3.8-5.3), and prothrombin time of 1.1 international normalization ratio (INR) (N:0.88-1.2). HBsAg and hepatitis B e antigen (HBeAg) were positive. Anti-HBs and anti-HCV were negative. Serum level of HBV DNA was 3.87×105 IU/mL. Ultrasonography showed coarse echogenicity in liver parenchyma, nodularities in liver surface, and moderate amount of ascites, which were suggestive of liver cirrhosis (). The size of spleen was 10cm in long axis. Esophagogastroduodenoscopic examination showed straight and slightly enlarged tortuous varices in distal esophagus (, , ), designated as F1 or F2 according to the general rules for recording endoscopic findings of esophagogastric varices [].
Entecavir of 0.5 mg/day orally per day was initiated on April 12, 2010. Spironolactone was also started at this time and continued until ascites and pitting edema resolved. Routine laboratory tests, including liver function tests and HBV DNA level were performed every 1-3 months. HBeAg, anti-HBe, AFP, and abdominal ultrasonography were performed every 6 months. Alanine aminotransferase (ALT) were normalized after 3 months of entecavir therapy. Undetectable HBV DNA (< 20 IU/mL) was achieved after 6 months of entevavir therapy. Serum ALT showed persistent normal value and HBV DNA was undetectable until the last follow up (November 18, 2014).
Follow-up endoscopy, performed on February 9, 2012 and November 28, 2014, showed minimal esophageal varices () and complete regression of esophageal varices (, ), respectively.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [48, 'years'], 'Alanine aminotransferase': [414.0, 'U/L'], 'Aspartate aminotransferase': [442.0, 'U/L'], 'Platelet count': [179000.0, 'µL']}",5.82519,5.53393,6.11645,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 442.0 U/L.
The patient's concentration of ALT is 414.0 U/L.
The patient's concentration of platelets is 179000.0 count/µL. To convert 179000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 179000.0 platelets count/µL * 1000000.0 µL/L = 179000000000.0 platelets count/L. This means that there are 179000000000.0/(10^9) = 179.0 billion platelet counts per liter.
Plugging these values into the formula, we get (48 * 442.0)/(179.0 * sqrt(414.0)) = 5.82519.Hence, the Fibrosis-4 score is 5.82519."
4335,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-8051530-1,Extracted,"A 63-year-old African American male with past medical history of congestive heart failure, pulmonary sarcoidosis, non-alcoholic liver cirrhosis, chronic kidney disease, and hypertension presented with complains of shortness of breath and bilateral lower extremity swelling. He denied abdominal pain, upper respiratory tract symptoms, fever, chills, and rigor. He also denied recent exposure to pets and animals including dogs. Initial vital signs were stable. He was afebrile, normotensive, and saturated at 100% on room air. Physical examination was significant for a markedly distended abdomen, which was soft and non-tender to light and deep palpation. Jugular venous distension was evident with extensive bilateral lower extremity edema with scrotal edema. There was no jaundice on examination. Chest X-ray was unremarkable with no infiltrates and consolidations. Initial laboratory investigation revealed a white count of 4.2 cells/mm3 (4.4-11.0 cells/mm3), hemoglobin of 10.7 g/dL (13.5-17.5 g/dL), platelet of 188 cells/mm3 (150-450 cells/mm3), lactic acid of 2.3 mmol/L (0.0-2.0 mmol/L), creatinine of 1.7 mg/dL (0.6-1.2 mg/dL), B-type natriuretic peptide of 823.71 pg/mL (0.0-100.0 pg/mL), protein of 8.2 g/dL (6.4-8.4 g/dL), and albumin of 2.6 g/L (3.5-4.5 g/L). Liver function tests were mildly elevated with an aspartate aminotransferase of 43 U/L (10-36 U/L), alanine aminotransferase of 20 U/L (9-46 U/L), and alkaline phosphatase of 134 U/L (40-115 U/L). Total bilirubin was within normal limit. Coagulation profile showed slightly prolonged international normalized ratio of 1.46.
He was admitted and managed for decompensated liver cirrhosis with diuresis to relieve the edema. He had undergone similar admissions in the past and also had multiple paracentesis done, the most recent was a month earlier, for symptomatic relief. A large-volume paracentesis was done during this hospitalization with the removal of 10 L of peritoneal fluid. Following paracentesis, he became hypotensive despite resuscitative efforts with appropriate albumin. Peritoneal fluid analysis revealed a white blood cell count of 72/mm3, 49% lymphocyte differential, 44% neutrophil differential, protein of 2.6 g/dL, lactate dehydrogenase of 91 U/L, and glucose of 113 mg/dL. This analysis was consistent with a diagnosis of portal hypertension likely as a result of his liver cirrhosis, and spontaneous bacterial peritonitis was unlikely. No organism was isolated from peritoneal fluid cultures and gram stain showed no organism.
In the setting of his persistent hypotension, sepsis was considered, blood cultures were drawn, and meropenem was empirically started. Ultrasound of the abdomen was done to look for a source and showed moderate ascites with a contracted gallbladder with no evidence of cholecystitis (Figure ).
Computed tomography of the abdomen was also done which showed cirrhosis and cholelithiasis with no evidence of intra-abdominal abscess (Figure ).
A hepatobiliary iminodiacetic acid scan was done which revealed no biliary obstruction but delayed visualization of the gallbladder. Surgery was consulted and in the absence of clinical signs of cholecystitis with his multiple comorbidities, elective cholecystectomy was postponed, and ongoing antibiotic management was advised. B. bronchiseptica was isolated from blood cultures (Table ).
Echocardiogram was performed and did not show any vegetations (Figure ).
Meropenem was stopped and based on a review of the available literature, we decided to start the patient on doxycycline for the bacteremia. Blood pressure stabilized after 48 hours and repeat blood cultures were negative. The patient tolerated doxycycline and was discharged with a seven-day course of oral doxycycline.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [63, 'years'], 'Alanine aminotransferase': [20.0, 'U/L'], 'Aspartate aminotransferase': [43.0, 'U/L'], 'Platelet count': [188000.0, 'µL']}",3.22208,3.06098,3.38318,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 43.0 U/L.
The patient's concentration of ALT is 20.0 U/L.
The patient's concentration of platelets is 188000.0 count/µL. To convert 188000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 188000.0 platelets count/µL * 1000000.0 µL/L = 188000000000.0 platelets count/L. This means that there are 188000000000.0/(10^9) = 188.0 billion platelet counts per liter.
Plugging these values into the formula, we get (63 * 43.0)/(188.0 * sqrt(20.0)) = 3.22208.Hence, the Fibrosis-4 score is 3.22208."
4336,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-3751378-1,Extracted,"A 64-year-old Jewish male of Indian origin was hospitalized in our department, with a 5-day history of fever (39°C), cough, and fatigue. He denied abdominal pain, vomiting, diarrhea, or other symptoms.
His medical history was significant for alcoholic cirrhosis with portal hypertension, splenomegaly, hypersplenism, and ascites. Furthermore, he had diabetes mellitus type 2 (hemoglobin A1c of 7%) and hypertension for years.
His medications included propranolol, lactulose, Aldospirone, omeprazole, and metformin.
On physical examination the patient was alert without encephalopathy or jaundice. The following characteristics of chronic liver disease were present: spider angiomas on his chest, hepatomegaly, splenomegaly, ascites, caput medusa, and pedal edema. His abdomen was swollen with tenderness in the right upper quadrant.
Laboratory tests showed a total bilirubin level of 1.76 mg/dL (normal range, 0.21–1 mg/dL); alanine aminotransferase level of 20 U/L (normal values, <40 U/L); aspartate aminotransferase level of 24 U/L (normal values, <40 U/L); alkaline phosphatase level of 147 U/L (normal range, 30–150 U/L); γ-glutamyl transpeptidase level of 73 U/L (normal range, 5–60 U/L); albumin level of 1.3 g/dL; prothrombin time of 15 seconds (international normalized ratio, 1.4); creatinine 2.7 mg/dL. His Model for End-Stage Liver Disease score on admission was 22. Complete blood count showed leukocytosis, 14,000 cells/μL, with 85% neutrophils, hemoglobin 7.1 g/dL, and platelets 100,000 cells/μL.
Chest X-ray showed mild right pleural effusion with no pulmonary infiltrates, and his abdominal ultrasonograph showed moderate ascites and hepatosplenomegaly. Blood, urine, and pleural fluid cultures were negative.
Abdominal paracentesis was done and revealed 134,800 leukocytes/mm3 (100% neutrophils), a serum-ascites albumin gradient of 1.4; levels of lactate dehydrogenase, amylase, and triglycerides were not elevated, and the level of glucose was within normal limits. The unusually high peritoneal fluid leukocyte count raised the suspicion of secondary peritonitis.
The patient underwent computed tomography of the abdomen with oral contrast, and no evidence of perforation or abdominal abscess was found.
A peritoneal fluid culture was positive for H. influenzae, and the patient was treated with ceftriaxone. Abdominal paracentesis was repeated 48 hours after beginning antibiotic treatment and showed a significant decrease of leukocyte count to 3,000/mm3. After hospitalization for 2 weeks the patient improved significantly; his fever resolved, and the patient felt better and was discharged. Three days later, the patient readmitted with septic shock due to Escherichia coli and methicillin-resistant Staphylococcus aureus. Unfortunately, despite antibiotic therapy, the patient died.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [64, 'years'], 'Alanine aminotransferase': [20.0, 'U/L'], 'Aspartate aminotransferase': [24.0, 'U/L'], 'Platelet count': [100000.0, 'µL']}",3.4346,3.26287,3.60633,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 24.0 U/L.
The patient's concentration of ALT is 20.0 U/L.
The patient's concentration of platelets is 100000.0 count/µL. To convert 100000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 100000.0 platelets count/µL * 1000000.0 µL/L = 100000000000.0 platelets count/L. This means that there are 100000000000.0/(10^9) = 100.0 billion platelet counts per liter.
Plugging these values into the formula, we get (64 * 24.0)/(100.0 * sqrt(20.0)) = 3.4346.Hence, the Fibrosis-4 score is 3.4346."
4337,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-7346448-1,Extracted,"A 42-year-old, previously healthy Sri Lankan man presented with low-grade fever, upper respiratory symptoms, and fatigue of 1-week duration. Investigations revealed elevated liver enzymes: aspartate aminotransferase (AST) 117 U/L and alanine aminotransferase (ALT) 186 U/L. There was no history of jaundice, pruritus, or alcohol use. An ultrasound scan of his abdomen showed grade 1 fatty liver with no liver parenchymal changes. Viral screening for hepatitis A, B, and C were negative. Serum ferritin was 1292 μg/L. Full blood count was normal, including hemoglobin (Hb) 147 g/L, white blood cells (WBC) 6.5 × 109/L, and platelets 213 × 109/L; C-reactive protein (CRP) was 4.8 mg/dL, total bilirubin was 15.9 μmol/L, total protein was 74 g/L, and albumin was 44 g/L, which were all normal. Serum ferritin repeated in a month, after complete resolution of the illness, was 1103 ng/mL, with a transferrin saturation of 75%, and liver enzymes remained moderately elevated (AST 83.4 U/L, ALT 155 U/L). There was no consanguinity in his parents and no family history of HH. Investigation in regards to inherited iron loading conditions were considered after excluding secondary causes of iron overload. Genetic testing for p.H63D and p.C282Y mutations in the HFE gene by DNA extraction, allele-specific polymerase chain reaction (PCR), and agarose gel electrophoresis showed that he was homozygous for the H63D mutation. A liver biopsy showed increased hepatocellular iron content and features of steatohepatitis. Investigations to assess complications of iron overload, including fasting blood sugar, electrocardiography, and two-dimensional echocardiography, were normal. He was started on venesections. Following two venesections done 2 weeks apart, his liver enzymes started to decline slowly (AST 76 U/L, ALT 151 U/L), serum ferritin came down to 200 μg/L, and transferrin saturation to 26%.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [42, 'years'], 'Alanine aminotransferase': [186.0, 'U/L'], 'Aspartate aminotransferase': [117.0, 'U/L'], 'Platelet count': [213000000.0, 'L']}",1691.60545,1607.02518,1776.18572,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 117.0 U/L.
The patient's concentration of ALT is 186.0 U/L.
The patient's concentration of platelets is 213000000.0 count/L. This means that there are 213000000.0/(10^9) = 0.213 billion platelet counts per liter.
Plugging these values into the formula, we get (42 * 117.0)/(0.213 * sqrt(186.0)) = 1691.60545.Hence, the Fibrosis-4 score is 1691.60545."
4338,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4753743-1,Extracted,"A 51-year-old female was diagnosed to have essential hypertension since 12 years and CKD since last 4 years. She progressed to end-stage renal disease 2 years back and was initiated on maintenance hemodialysis. For initial 1-year, she was on twice-weekly hemodialysis, which was subsequently increased to thrice weekly. She presented to us with complaints of progressive painless abdominal distension of 8-month duration along with anorexia and weight loss. There was no history of abdominal pain, altered bowel habits, pedal edema, fever, jaundice and no history to suggest hypothyroidism or connective tissue disease. There was no history of diabetes mellitus, jaundice, abdominal surgery and anti-tubercular treatment in past. Her medication included prazosin 10 mg/day, amlodipine 10 mg/day, calcium carbonate 1500 mg/day, twice weekly subcutaneous erythropoietin, oral iron and multivitamin. On examination, she had normal sensorium with blood pressure of 180/120 mm of Hg, pulse rate - 110/min, respiratory rate - 20/min, was afebrile and pale. Her abdomen was symmetrically distended with fluid thrill. There were no visible veins; hernial sites were normal with no cutaneous stigmata of chronic liver disease. Patient had hemoglobin of 7.7 g/dl, total leukocyte count (TLC) of 10400/mm3, with normal differential, platelet count 2.50 lakh/mm3, mean corpuscular volume 90.8 fl, mean corpuscular hemoglobin 30.1 pg/cell, mean corpuscular hemoglobin concentration 33.2 g/dl, normal coagulogram, urea 197 mg/dl, creatinine 9.4 mg/dl, sodium 144 mEq/L, potassium 6.1 mEq/L, chloride 110 mEq/L, aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase were 27, 15 and 254 IU/L respectively, bilirubin 0.8 mg/dl, total protein and albumin 6.5 and 2.7 g/dl, calcium 9.7 mg/dl, phosphorous 9.3 mg/dl, and intact parathyroid hormone 346.8 pg/mL. The serology was negative for hepatitis B, hepatitis C and human immunodeficiency virus. On tapping, the ascitic fluid was hemorrhagic and showed TLC of 70/mm3 with 70% polymorphonuclear cells, protein was 3.8 g/dl, sugar 83 mg/dl, with adenosine deaminase of 32 IU/L, and serum ascites albumin gradient of 0.8. The Ziehl–Neelsen stain and Gram-stain were negative, as was the culture for Mycobacterium tuberculosis, and pyogenic organisms. The TB polymerase chain reaction and ascitic fluid for malignant cytology were also negative. Other cancer markers such as cancer antigen (CA) 125, CA 19–9, and carcinoembryonic antigen were also normal. Her electrocardiogram revealed left ventricular hypertrophy with strain pattern, while echocardiography revealed mild mitral regurgitation, left ventricular ejection fraction of 45–50% with no evidence of systolic or diastolic dysfunction. An ultrasound abdomen performed showed gross ascites, bilateral contracted kidneys and cholelithiasis while other abdominal organs were normal. Subsequently, a contrast-enhanced computed tomography (CECT) abdomen was performed which revealed gross ascites with peritoneal enhancement and hyper-densities within fluid, in addition to the finding of contracted kidneys and cholelithiasis []. Suspecting inadequate dialysis, the patient was subjected to daily dialysis. However, there was no improvement in her ascites, and it required repeated therapeutic aspiration. To ascertain the cause of refractory ascites, the patient was subjected to exploratory laparotomy, which showed hemorrhagic ascitic fluid, thickened peritoneum and dense adhesions in-between the bowel loops and bowel loops with the abdominal wall. Keeping the possibility of cocoon abdomen, an intra-operative peritoneal biopsy was taken, which showed hyalinized fibrocollagenous tissue devoid of any lining epithelium with fibrin deposition and inflammatory cell infiltrate. There was no evidence of granulomatous inflammation or malignancy in biopsy specimen []. A diagnosis of cocoon abdomen secondary to uremia was made, and the patient was managed with daily intensive hemodialysis. Over next 1-month, there was gradual improvement in her symptoms along with decrease in ascites.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [51, 'years'], 'Alanine aminotransferase': [15.0, 'U/L'], 'Aspartate aminotransferase': [27.0, 'U/L'], 'Platelet count': [250000.0, 'µL']}",1.42216,1.35105,1.49327,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 27.0 U/L.
The patient's concentration of ALT is 15.0 U/L.
The patient's concentration of platelets is 250000.0 count/µL. To convert 250000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 250000.0 platelets count/µL * 1000000.0 µL/L = 250000000000.0 platelets count/L. This means that there are 250000000000.0/(10^9) = 250.0 billion platelet counts per liter.
Plugging these values into the formula, we get (51 * 27.0)/(250.0 * sqrt(15.0)) = 1.42216.Hence, the Fibrosis-4 score is 1.42216."
4339,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-2640350-1,Extracted,"A 47 year old male with a past history of asymptomatic chronic Hepatitis C diagnosed 4 years ago, on no home medications, came to the hospital with chief complaints of right upper quadrant abdominal pain and vomiting for one day. His vital signs on admission were stable. On physical examination the abdomen was tender to palpation in right upper quadrant with no palpable organomegaly. He had no stigmata of end stage liver disease. Laboratory data at the time of admission showed WBC 14.5 th/mm3 (normal 4 – 11 th/mm3), Hemoglobin 16 g/dl (normal 14 – 18 gm/dl), Platelets 190 th/mm3 (normal 130 – 400 th/mm3), Total bilirubin 0.7 mg/dl (normal 0.0 – 1 mg/dl), INR 1.4, total protein 5.3 gm/dl (normal 6.3 – 8.2 gm/dl), Albumin 2.6 gm/dl (normal 3.4 – 5 gm/dl), AST 28 U/l (normal 15 – 37 U/l), ALT 52 U/l (normal 30 – 65 U/l), Alkaline phosphatase 99 U/l (normal 50 – 136 U/l) and a Lipase level of 174 U/l (normal 114 – 286 U/l). An ultrasound of the abdomen done at the time of admission showed a stone in the gall bladder neck with pericholecystic fluid consistent with our clinical diagnosis of acute cholecystitis. The patient was admitted to the hospital, started on Morphine, Cefoxitin and Famotidine and subsequently underwent laparoscopic cholecystectomy the next day. Fentanyl, propofol and vecuronium were used for anesthesia. His hospital course was uneventful until the third day when he started complaining of some abdominal pain with a change in urine color. A complete metabolic panel was obtained on the patient at this time which now showed AST 8466 U/l, ALT 4755 U/l, Total bilirubin 2.5 mg/dl, INR 2.4 with a normal alkaline phosphatase. The sudden elevation in liver enzymes within a couple of days of hospitalization made us think of a possible medication induced adverse reaction. The patient's medications at that time were cefoxitin, morphine and famotidine. Famotidine was discontinued at this time and serial measurements of liver enzymes were done. The liver enzymes started improving from the next day and were back to normal within the next 7 days. (Figure ) No further investigations were done on the patient as the temporal association of the administration of famotidine and elevation in liver enzymes combined with the response demonstrated after discontinuation of famotidine was very significant in this case.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [47, 'years'], 'Alanine aminotransferase': [4755.0, 'U/L'], 'Aspartate aminotransferase': [8466.0, 'U/L'], 'Platelet count': [190000.0, 'µL']}",30.37017,28.85166,31.88868,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 8466.0 U/L.
The patient's concentration of ALT is 4755.0 U/L.
The patient's concentration of platelets is 190000.0 count/µL. To convert 190000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 190000.0 platelets count/µL * 1000000.0 µL/L = 190000000000.0 platelets count/L. This means that there are 190000000000.0/(10^9) = 190.0 billion platelet counts per liter.
Plugging these values into the formula, we get (47 * 8466.0)/(190.0 * sqrt(4755.0)) = 30.37017.Hence, the Fibrosis-4 score is 30.37017."
4340,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4594969-2,Extracted,"50-year-old male patient. The patient had been receiving antiviral treatment for 13 years with a diagnosis of chronic hepatitis B and he was under control. Five years ago, a mass with a diameter of 2 cm was found in the eighth segment of the liver. The patient was operated and his pathology was reported as HCC. The patient who developed abdominal pain in his follow-ups was hospitalized. The patient had no peculiarity in his anamnesis and family history. He had been using tenofovir 245 mg/day and had been smoking for 10 package/years. His physical examination was normal. His laboratory findings were as follows: Glucose: 86 mg/dl, Creatinine: 0.9 mg/dl, AST: 92 U/L, ALT: 89 U/L, ALP: 139 U/L, GGT: 386 U/L, LDH:162 U/L, Total bilirubin: 6.3 mg/dl, Conjugated bilirubin: 6.0 mg/dl, Albumin:3.2 g/dl, Wbc: 5060 mm3, Hct: 38.4%, Platelet:109.000 mm3, Prothrombrin time: 14 sec, AFP:4.1 ng/mL and HbsAg: positive, HBV DNA: negative. His abdominal tomography (AT) showed a solid mass with a regular contour in the left lobe of the liver next to the lateral segment anterior. The mass had extrahepatic location, it had a size of 80x52 mm, it had a heterogeneous inner structure, it had intense contrast at arterial phase but it did not have typical wash-out. AT angiography showed thrombus at the portal vein left branch. The patient underwent EUS and biopsy was taken from the mass on the left lobe of the liver with 22 G needle and FNA biopsy was taken from the thrombus on the portal vein with 25G needle. The biopsy results of both the mass in the liver and the thrombus were HCC. The patient underwent radiofrequency embolisation and he was taken under control.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [50, 'years'], 'Alanine aminotransferase': [89.0, 'U/L'], 'Aspartate aminotransferase': [92.0, 'U/L'], 'Platelet count': [109000.0, 'µL']}",4.47339,4.24972,4.69706,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 92.0 U/L.
The patient's concentration of ALT is 89.0 U/L.
The patient's concentration of platelets is 109000.0 count/µL. To convert 109000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 109000.0 platelets count/µL * 1000000.0 µL/L = 109000000000.0 platelets count/L. This means that there are 109000000000.0/(10^9) = 109.0 billion platelet counts per liter.
Plugging these values into the formula, we get (50 * 92.0)/(109.0 * sqrt(89.0)) = 4.47339.Hence, the Fibrosis-4 score is 4.47339."
4341,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-5838453-1,Extracted,"A 37-year-old male with a past medical history of Epstein-Barr Virus (EBV) infection was admitted for jaundice and right upper quadrant abdominal pain. He reported having worsening symptoms for one month duration. The patient was a non-smoker and non-alcohol drinker. Review of systems was positive for decreased appetite and weight loss of 10 lbs. over the past two months. His family history was unknown. Physical examination was significant for mild scleral icterus and abdominal distension. Heart rate was 92/min, blood pressure was 107/67 mm Hg, respiratory rate was 20/min, oxygen saturation was 94% on room air, and temperature was 98.1 °F. Laboratory results were within normal limits with a white blood cell count (WBC) of 11.4/μL, hemoglobin of 12.2 g/dL, hematocrit of 37%, and platelet count of 291 k/cmm. Total bilirubin was 5.7 mg/dL, alkaline phosphatase (ALP) was 1005 U/L, LDH was 830 U/L, albumin was 3.2 g/dL, aspartate aminotransferase (AST) was 257 U/L and alanine aminotransferase (ALT) was 239 U/L. EBV serology was negative for IgM, and positive for IgG and EBV nuclear antigen, consistent with prior infection.
Abdominal magnetic resonance imaging (MRI) showed mild intrahepatic ductal dilatation, peripheral areas of arterial enhancement in liver felt to be related to vascular shunting, periportal edema, a cut off in the course of the biliary tree at the bifurcation, a simple liver cyst, and enlarged left retroperitoneal nodes. Upper endoscopy showed gastropathy in the gastric fundus and body. Endoscopic ultrasound was unremarkable. Following a liver biopsy, histopathology showed several large dense clusters of atypical T-lymphocytes, which appeared to be centered in the portal areas. The atypical lymphocytes were medium to large in size and were CD2+, CD3+, CD4+, CD5+, CD7-, CD8-, CD56-, CD57-, CD30+, by immunohistochemistry (Figure ).
The proliferation index was approximately 70% by labeling for ki67/mib1. Labeling for CD68 was seen in Kupffer cells, and in a few scattered histiocytes only. There were rare, scattered, unremarkable small B-lymphocytes (CD20+, CD79a+). Stains for CD138, kappa, lambda, were noncontributory. The above histological profile was consistent with hepatic peripheral T-cell lymphoma. The patient was subsequently transferred to a tertiary care center for further management where he had a bone marrow biopsy which was negative for malignancy, further supporting hepatic origin.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [37, 'years'], 'Aspartate aminotransferase': [257.0, 'U/L'], 'Alanine aminotransferase': [239.0, 'U/L'], 'Platelet count': [291000.0, 'µL']}",2.1137,2.00801,2.21939,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 257.0 U/L.
The patient's concentration of ALT is 239.0 U/L.
The patient's concentration of platelets is 291000.0 count/µL. To convert 291000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 291000.0 platelets count/µL * 1000000.0 µL/L = 291000000000.0 platelets count/L. This means that there are 291000000000.0/(10^9) = 291.0 billion platelet counts per liter.
Plugging these values into the formula, we get (37 * 257.0)/(291.0 * sqrt(239.0)) = 2.1137.Hence, the Fibrosis-4 score is 2.1137."
4342,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-6408836-1,Extracted,"An 84-year-old Caucasian man with a distant past history of Billroth II gastrectomy for peptic ulcer disease and cholecystectomy for cholelithiasis was admitted to hospital for investigation of painless jaundice following referral from his general practitioner (GP).
He had a 1-month history of anorexia, weight loss, malaise, and painless progressive jaundice. An examination revealed normal vital signs, icterus without stigmata of chronic liver disease, and a soft abdomen with no organomegaly. Biochemistry demonstrated: microcytic anemia with hemoglobin of 108 g/L, mean corpuscular volume 72 fL, and ferritin 4557 μg/L; obstructive cholestasis with bilirubin of 164 umol/L, alkaline phosphatase (ALP) 2167 units/L, gamma-glutamyl transferase (GGT) 857 units/L, aspartate transaminase (AST) 225 units/L, and alanine transaminase (ALT) 301 units/L; modestly raised inflammatory markers with white cell count (WCC) of 12.77 × 109/L and C-reactive protein (CRP) 80 mg/L; and hypoalbuminemia (24 g/L) with a normal international normalized ratio (INR) of 1.2 and platelet count of 294 × 109/L. Cancer antigen 19-9 (CA 19-9) was raised at 132 kU/L.
His common bile duct, liver parenchyma, pancreas, and portal vein were of normal appearance on abdominal ultrasonography, with a subsequent MRCP showing no dilatation of the biliary tree and no evidence of any intraductal, pancreatic, or hepatic lesions. The MRCP did, however, exhibit dilatation of the afferent duodenal limb being 4.8 cm in maximal width (Fig. ) and a single enlarged portal hilar lymph node measuring 13 mm in its short axis. Given the discordant lack of biliary dilatation on imaging, a liver biopsy was performed.
Histopathology demonstrated edematous portal tracts with inflammation within the portal tracts including neutrophils, which were not seen within the lumen of the ductal epithelial cells (Figs. and ). Furthermore, lobular bile accumulation was present as was ductular proliferation at the edge of the portal tracts, highlighted by cytokeratin immunoperoxidase (Fig. ). Focal steatosis was present with no distinct zonal pattern but with a tendency to be periportal. A suspicion of cholangitis was raised and treated with appropriate antibiotics, but with no clinical improvement. The histopathology and clinical picture taken together was felt to be most in keeping with acute large bile duct obstruction. A full hepatic biochemical screen investigating for infective and autoimmune causes was unremarkable.
A gastroscopy was subsequently performed to investigate the enteric abnormalities noted on MRCP, revealing a markedly deformed remnant stomach with a mass lesion at the gastroenteric anastomosis suspicious for malignancy (Fig. ). The afferent limb was stenosed and unable to be intubated preventing visualization of the major duodenal papilla. Biopsies of the mass lesion confirmed moderately differentiated gastric adenocarcinoma.
The biliary obstruction was managed by endoscopic wire-guided stent insertion through the obstructing tumor into the afferent duodenal limb (Fig. ) with subsequent resolution of jaundice (bilirubin 16 umol/L) and significant improvement in liver enzymes (ALP 424 units/L, GGT 346 units/L, ALT 33 units/L). As our patient was not a candidate for surgical intervention or chemotherapy due to locoregional disease extent and frailty, he was eventually discharged home with palliative support following a period of in-patient rehabilitation.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [84, 'years'], 'Alanine aminotransferase': [301.0, 'U/L'], 'Aspartate aminotransferase': [225.0, 'U/L'], 'Platelet count': [294000000.0, 'L']}",3705.36697,3520.09862,3890.63532,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 225.0 U/L.
The patient's concentration of ALT is 301.0 U/L.
The patient's concentration of platelets is 294000000.0 count/L. This means that there are 294000000.0/(10^9) = 0.294 billion platelet counts per liter.
Plugging these values into the formula, we get (84 * 225.0)/(0.294 * sqrt(301.0)) = 3705.36697.Hence, the Fibrosis-4 score is 3705.36697."
4343,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-3477656-1,Extracted,"A 58-year-old white man was referred to the outpatient nephrology office by his gastroenterologist because of microscopic hematuria and proteinuria in the setting of an evolving purpuric rash. The rash had progressed proximally from both feet to his thighs, upper extremities and abdomen over the past two weeks. He complained of nausea, and vomiting for one day but denied hematemesis, melanotic stools, or arthralgia. His significant comorbidities included hypertension, untreated hepatitis C, and alcohol abuse. He took no medications.
On physical examination blood pressure was 105/62 mmHg, pulse was 84 beats/minute and regular, and temperature 37.7°C. The skin showed nontender, palpable purpuric lesions involving both upper and lower extremities and the abdominal wall. Lungs were clear to auscultation and the cardiovascular exam was unremarkable. On abdominal examination no organomegaly was appreciated. There was no pedal edema.
Laboratory tests revealed a white blood cell count of 13.1 × 10³/mcL, hemoglobin 14.7 g/dL, hematocrit 42.9%, and platelet count of 234 × 10³/mcL. Serum chemistry showed sodium 136 mEq/L, potassium 4.2 mEq/L, chloride 101 mEq/L, bicarbonate 24 mEq/L, blood urea nitrogen (BUN) 34 mg/dL and serum creatinine 2.0 mg/dL. Liver function tests revealed a total bilirubin of 1.3 mg/dL, direct bilirubin 0.5 mg/dL, ALT 75 units/L, AST 93 units/L, alkaline phosphatase 75 units/L, total protein 7.6 g/dL and albumin 3.7 g/dL. Hepatitis B core antibody, hepatitis B surface antibody and hepatitis C antibody were all positive. Urinalysis demonstrated trace hematuria and proteinuria. He was sent to the emergency room for further evaluation.
On admission the patient was started on intravenous fluids and additional tests were obtained. Antinuclear antibody (ANA) and serum complements (C3 and C4) were normal and antineutrophil cytoplasmic antibody (ANCA) and cryoglobulins were negative. The serum creatinine improved to 0.75 mg/dL on hydration alone. Two days later he complained of diffuse abdominal pain and dark stool followed by hematochezia. He remained afebrile with a blood pressure of 120/50 mmHg. On physical examination he had significant right upper abdominal quadrant and epigastric tenderness. Esophagogastroduodenoscopy (EGD) was performed that failed to reveal a lesion that could account for his symptoms. A biopsy of the stomach mucosa demonstrated mild chronic inflammation. Computerized tomography (CT) scan of the abdomen was next performed and showed marked thickening of the terminal ileum (). Abdominal pain intensified, and the patient became tachycardic and tachypneic with a leukocytosis of 23 × 10³/mcL, with deteriorating renal function (BUN 54 mg/dL, serum creatinine of 2.0 mg/dL) and evolving acidosis (bicarbonate 17 mEq/L). An emergency exploratory laparotomy was performed which revealed gangrenous bowel from the beginning of the ileum to the transverse colon. Small bowel resection (90 cm of ileum) and right hemicolectomy (including appendix which was involved) with end jejunostomy were performed.
Histopathologic examination of the resected intestinal tissue demonstrated an extensive necrotizing vasculitis with IgA deposition characteristic of HSP (). Of particular note was the very widespread (perhaps 50%) involvement of medium sized vessels, particularly arteries, with extensive necrosis and secondary ischemic injury to the intestines. Small arteries, arterioles, and venules were also involved. Heavy granular IgA deposition was seen with no staining for IgG or IgM. Lesser amounts of C3 paralleled the IgA deposition.
Intravenous methylprednisolone 1 g daily for three days was administered and then 30 mg every 12 hours. Postoperatively he continued to have an elevated white blood cell count and persistent fever, but his renal function improved. A repeat CT scan of the abdomen revealed persistent small bowel wall thickening. A second exploratory laparotomy was performed, but no additional ischemic bowel was identified. The patient was continued on broad-spectrum antibiotics and maintained on a ventilator due to respiratory failure. Eight days after the second laparotomy he developed severe lactic acidosis, right upper abdominal quadrant tenderness jaundice and worsening renal function. Ultrasound of the right upper quadrant showed findings compatible with portal vein thrombosis and cholelithiasis. Repeat CT scan of the abdomen showed increased ascites with intraperitoneal hemorrhage. Hemodialysis was initiated due to worsening oliguric acute kidney injury. His condition continued to deteriorate, and he died one day later, a total of 27 days after admission.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [58, 'years'], 'Alanine aminotransferase': [75.0, 'U/L'], 'Aspartate aminotransferase': [93.0, 'U/L'], 'Platelet count': [234000.0, 'µL']}",2.66173,2.52864,2.79482,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 93.0 U/L.
The patient's concentration of ALT is 75.0 U/L.
The patient's concentration of platelets is 234000.0 count/µL. To convert 234000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 234000.0 platelets count/µL * 1000000.0 µL/L = 234000000000.0 platelets count/L. This means that there are 234000000000.0/(10^9) = 234.0 billion platelet counts per liter.
Plugging these values into the formula, we get (58 * 93.0)/(234.0 * sqrt(75.0)) = 2.66173.Hence, the Fibrosis-4 score is 2.66173."
4344,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-8708605-1,Extracted,"A 45-year-old female patient with past history of hypertension for 2 years presented to our emergency room with the chief complaint of dyspnea on exertion and low-grade fever for 2 weeks. She also mentioned insidious onset of muscle soreness of the anterior thighs for one month, which was followed by the appearance of itchy rashes over the knuckles of both hands and the sun-exposed area of the anterior chest. She was first diagnosed with community-acquired pneumonia a week before coming to our emergency room, but empirical antibiotics had failed to improve her symptoms. Physical examination at admission revealed a temperature of 38.1 °C, a pulse rate of 104 beats per minute, a respiratory rate of 21 breaths per minute, pulse oximeter Sp02 88% under ambient air, inspiratory rales over bilateral lower lung, Gottron papules at bilateral PIP and MCP joints with ulceration over the right MCP3 joint, V sign with cutaneous ulceration, periungual erythema, and normal muscle power.
Laboratory examination revealed a total leukocyte count of 4640/μL, hemoglobin concentration of 10.9 g/dL, and platelet count of 262,000/μL. Her ALT was 100 U/L, AST was 125 U/L, serum total bilirubin was 0.5 mg/dL, lactate dehydrogenase was 422 U/L, creatine kinase (CK) was 264 U/L, creatinine was 0.52 mg/dL, and thyroid function test was normal. In addition, autoimmune tests showed anti-nuclear antibody 1:80 (equivocal), negative anti-SSA/SSB, negative anti-Jo-1, and a strongly positive anti-MDA5 detected by a commercial line-blot immunoassay kit (EUROIMMUN-DL 1530-1601-4 G). Nerve conduction velocity and electromyography disclosed mild myopathic changes indicated by BSAPPs over bilateral iliopsoas muscles and deltoid muscles. Chest X-ray showed increased interstitial infiltration over bilateral lower lung fields. High-resolution computed tomography (HRCT) showed subpleural consolidation with interstitial thickening of bilateral lungs with lower lung predominance (). Anti-MDA5-associated DM with ILD was diagnosed.
We started the treatment with an equivalent dosage of 0.4 mg/kg/day oral prednisone, with intravenous rituximab at a dose of 1000 mg and tacrolimus at a dose of 0.5 mg/day. Fever subsided following the treatment, and her cutaneous lesions and dyspnea improved one week later. However, skin rashes recurred at week 4 and dyspnea on exertion also worsened. Laboratory examination during readmission revealed elevated liver enzymes (ALT 233 U/L, AST 248 U/L) and lower CK levels (93 U/L) (a). Progression of interstitial lung disease was evident on HRCT, which showed increased peribronchial and subpleural consolidation with ground glass opacities in bilateral lungs (a). A multidisciplinary team comprising a rheumatologist, a pulmonologist, and a radiologist was created as the disease progressed rapidly, and a diagnosis of organizing pneumonia related to anti-MDA5-positive RP-ILD was reached by the team. Due to RP-ILD, corticosteroid was titrated from 0.4 mg/kg/day to 0.8 mg/kg/day, and the second dose of rituximab was given 3 weeks after the first dose. Additionally, we shifted tacrolimus to tofacitinib with a dosage of 5 mg twice daily. At the same time, the anti-fibrotic agent pirfenidone was started with a dosage of 600 mg per day in combination with the immunosuppressive agents due to unsatisfactory treatment response. Respiratory condition and rashes improved slowly, and the patient still depended on home oxygen therapy upon discharge. The dosage of pirfenidone was titrated to 1200 mg per day as the patient could tolerate it well. It was not until week 20 that the patient was able to do without oxygen therapy, and repeated HRCT showed regressive changes of the organizing pneumonia with partial resolution of subpleural consolidative patches (c). The corticosteroid was successfully tapered from 0.8 mg/kg/day to 0.1 mg/kg/day. The residual subpleural interstitial thickening and ground glass opacities on HRCT showed substantial improvement and near-complete resolution of pulmonary infiltrates at week 42 (d).
Lung function testing, including forced vital capacity and diffusing capacity of carbon monoxide, was not tolerable due to dyspnea initially until week 20 post-therapy, and it revealed restrictive lung disease with moderately impaired gas exchange. Both forced vital capacity and diffusing capacity of carbon monoxide also improved markedly under serial follow-up in concordance with the findings on HRCT (b). The titer of anti-MDA5 declined at week 42 and turned negative at week 76 (c). The clinical symptoms and muscle enzymes of the patient remained stable throughout the follow-up of 76 weeks.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'years'], 'Alanine aminotransferase': [233.0, 'U/L'], 'Aspartate aminotransferase': [248.0, 'U/L'], 'Platelet count': [262000.0, 'µL']}",2.79052,2.65099,2.93005,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 248.0 U/L.
The patient's concentration of ALT is 233.0 U/L.
The patient's concentration of platelets is 262000.0 count/µL. To convert 262000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 262000.0 platelets count/µL * 1000000.0 µL/L = 262000000000.0 platelets count/L. This means that there are 262000000000.0/(10^9) = 262.0 billion platelet counts per liter.
Plugging these values into the formula, we get (45 * 248.0)/(262.0 * sqrt(233.0)) = 2.79052.Hence, the Fibrosis-4 score is 2.79052."
4345,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-3784272-1,Extracted,"A 39-year-old Caucasian woman presented with palpitations and a two-week history of progressive fatigue, shortness of breath, and abdominal pain with distension. Her past medical history was significant for hypothyroidism on thyroid replacement therapy and amenorrhea since the age of 20 that had not been evaluated. Family history was pertinent for a first cousin who had died suddenly of “cardiac arrest” at 20 years old. Her mother and father were both in good health. There was no family history of iron overload or liver disease. The patient was an unmarried teacher. She had never smoked, rarely drank alcohol, and had no history of illicit drug use. Her physical exam showed mild jaundice and an irregular cardiac rhythm. The abdomen was diffusely tender with hepatomegaly, no splenomegaly or evident ascites. An electrocardiogram showed atrial fibrillation with rapid ventricular response, and an echocardiogram showed globally decreased left ventricular systolic function with an estimated ejection fraction of 26%.
The patient was admitted to the cardiovascular intensive care unit where management of heart failure was initiated, her heart rate was controlled, and she was started on anticoagulation. Hematologic findings included a hemoglobin concentration of 13 g/dL, platelet count of 100 K/mm3, and leucocyte count of 9.7 K/mm3. Blood chemistries revealed the following results: total bilirubin 2.6 mg/dL, direct bilirubin 1.1 mg/dL, aspartate aminotransferase 1476 U/L, alanine aminotransferase 702 U/L, alkaline phosphatase 139 U/L, gamma-glutamyl transpeptidase 52, albumin 4.1 g/dL, and lactate dehydrogenase 968 U/L. Review of the peripheral blood smear showed no evidence of hemolysis. Coagulation studies showed a prothrombin time of 20 sec and an international normalized ratio (INR) of 2.1. Other relevant tests included thyroid-stimulating hormone 40 uIU/mL (normal 0.27–4.2), free thyroxine 1.05 ng/dL (normal 0.93–1.7), thyroid peroxidase autoantibody (anti-TPO) 1586 IU/mL (normal < 2), follicle-stimulating hormone 0.3 mIU/mL (normal 3.5–12.5 mIU/mL), and luteinizing hormone 0.1 mIU/mL (normal 2.4–12.6 mIU/mL). Abdominal ultrasound showed an enlarged liver with diffusely increased echogenicity, minimal ascites and a normal-sized spleen. Doppler findings were consistent with congestive heart failure.
Testing for viral hepatitis and autoimmune serologies was negative. Alpha 1-antitrypsin and ceruloplasmin levels were normal. However, iron studies were markedly abnormal with a transferrin saturation of 100% and ferritin of 116,070 ng/mL (normal 22–322 ng/mL). Transjugular liver biopsy showed cirrhosis with 4+ iron deposition in hepatocytes and in biliary epithelium, as well as focal centrilobular necrosis, likely due to congestion (). HFE genotyping by the amplification refractory mutation system was negative for both C282Y and H63D mutations. JH was suspected and further testing was performed on a research basis. Amplification of the HFE2 gene by polymerase chain reaction with genotyping by direct sequencing disclosed that the patient was homozygous for the HFE2 Gly320Val mutation ().
Once her heart rate and congestive heart failure were controlled, she began weekly phlebotomies. Erythropoietin was administered because of concomitant anemia, but she did not undergo chelation. One month after her presentation, except for persistent fatigue, her symptoms had resolved. The ferritin level had decreased to 7400 ng/mL. Unfortunately, two months later, after 8 phlebotomies, she was hospitalized for severe shortness of breath and hypotension. An echocardiogram showed worsening left ventricular function with ejection fraction of 10%. She was intubated and treated with vasopressors and an intra-aortic balloon pump to maintain her blood pressure. Antiarrhythmic medications were given for recurrent nonsustained ventricular tachycardia. Despite the aggressive medical management, she developed multiorgan failure and died five days after admission. The family declined an autopsy. As part of family screening, her mother had iron studies done, which were normal. Her father and half-brother declined screening with iron studies.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [39, 'years'], 'Aspartate aminotransferase': [1476.0, 'U/L'], 'Alanine aminotransferase': [702.0, 'U/L'], 'Platelet count': [100000.0, 'µL']}",21.72613,20.63982,22.81244,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 1476.0 U/L.
The patient's concentration of ALT is 702.0 U/L.
The patient's concentration of platelets is 100000.0 count/µL. To convert 100000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 100000.0 platelets count/µL * 1000000.0 µL/L = 100000000000.0 platelets count/L. This means that there are 100000000000.0/(10^9) = 100.0 billion platelet counts per liter.
Plugging these values into the formula, we get (39 * 1476.0)/(100.0 * sqrt(702.0)) = 21.72613.Hence, the Fibrosis-4 score is 21.72613."
4346,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4345234-1,Extracted,"A 63-year-old woman with a history of mixed connective tissue disease (MCTD), interstitial lung disease, severe pulmonary hypertension, and paroxysmal atrial fibrillation was admitted for a one-day history of jaundice and a two-week history of malaise and confusion. The patient's MCTD had historically been controlled with azathioprine and prednisone. Six weeks prior to presentation, the patient's rheumatologist increased the dosage of prednisone from 2 mg daily to 40 mg daily due to worsening myositis. One month after the increase in steroid dose, the patient noticed worsening pedal edema and the development of large bullae in the bilateral lower extremities that subsequently ruptured and left behind ulcers. Two weeks later, the patient's family noticed increasing confusion along with somnolence and brought the patient to the emergency department for evaluation.
On admission, temperature was 36.7°C (98.0 F), blood pressure 124/98 mmHg, and regular pulse of 69 beats per minute. Respiratory rate was 22 breaths per minute, and oxygen saturation was 97% on room air. Pertinent physical exam findings include marked scleral icterus, jaundice, diffuse abdominal tenderness, a nonverbal state, and two symmetric well-circumscribed oval shallow ulcerations on bilateral lower medial legs (). Laboratory findings were significant for a white blood cell (WBC) count of 900 per cubic millimeter (82% N, 13.8% L, 1.0% M, 1.3% E, and 1.9% B, ANC 700 per cubic mm), hemoglobin of 12.8 g/dL, and platelet count of 155,000 per cubic millimeter. Aspartate transaminase (AST) and alanine aminotransferase (ALT) were 83 and 144 units per liter, respectively. Total serum bilirubin count was elevated at 24.2 mg/dL. International normalization ratio (INR) was 8.8 on chronic warfarin therapy, which the patient was taking due to atrial fibrillation. Serum ammonia was 42 μg/dL. Urinalysis showed mild proteinuria and 11–25 leukocytes per high power field. Blood culture was positive for aerobic gram negative rods on two sequential tubes. Abdominal ultrasound showed cholelithiasis without biliary dilation. Computed tomography of the abdomen showed a small enhancing lesion in the medial segment of the left hepatic lobe.
Initially, the patient was diagnosed with septicemia, cholestatic jaundice, hepatic encephalopathy, and neutropenia. She was treated with ceftazidime, ciprofloxacin, and lactulose. Warfarin was not resumed. Azathioprine was stopped due to concern of causing bone marrow suppression and contributing to hepatic toxicity. Prednisone dose was tapered off. Other causes of liver injury were investigated, with hepatitis A IgM, hepatitis B surface antigen, hepatitis B and C polymerase chain reaction (PCR), anti-mitochondrial antibody, and anti-smooth muscle antibody all returning negative.
In the subsequent hospital days, the patient's liver markers remained stably elevated. Her mental status gradually worsened, with unresponsive episodes at times. She later developed worsening right heart failure with systemic congestion. Brain magnetic resonance imaging and electroencephalography were performed, which did not explain the etiology of encephalopathy. The gram negative rod was eventually speciated as extended-spectrum-beta-lactamase (ESBL) Escherichia coli, so the antibiotic regimen was switched to meropenem.
On hospital day six, WBC count was 600 per cubic millimeter and platelet count was 90,000 per cubic millimeter. Total serum bilirubin was 25.7 mg/dL. Cytomegalovirus (CMV) DNA PCR of serum returned with 173,953 copies. CMV serum IgM avidity index (AI) was elevated at 2 (lab threshold of 1.1 AI for positive antibody) and IgG level was elevated at an AI of 36.3 (lab threshold of 1.1 AI for positive antibody). There were no prior levels for comparison. The patient was started on IV ganciclovir at 5 mg/kg every 12 hours. Subsequently, the patient had rapid and marked improvement in laboratory markers and mentation. Two days after initiating ganciclovir, she was able to speak a few words and follow basic commands. Leg ulcerations improved rapidly and significantly (). Total serum bilirubin count decreased to 17.2 mg/dL after four days of treatment. WBC count recovered to 2,000 per cubic millimeter and platelets to 221,000 per cubic millimeter after six days of therapy.
Shave biopsy of the left lower leg legion was performed on hospital day five, prior to initiation of IV ganciclovir. The formalin-fixed, paraffin-embedded tissue samples were cut into 3 to 4 μm thick sections and the slides were then subjected to heat-induced epitope retrieval methods. Immunohistochemistry was performed with an automated immunohistochemistry staining system (Ventana BenchMark ULTRA). A polymer-based method using the ULTRAVIEW Universal DAB detection kit (Ventana) with a commercially purchased primary antibody against cytomegalovirus (Clones DDG9 and CCH2) was used. Appropriate positive and negative controls were used. Using this protocol, histopathology showed scattered endothelial cells with eosinophilic cytoplasmic inclusions and a characteristic halo surrounding the nuclear inclusion (). Immunohistochemistry was positive for CMV inclusions (). Staining was negative for bacterial and fungal elements. No perivascular infiltration of leukocytes was seen. No other causative etiology of ulceration was seen on pathology. Subsequent ophthalmologic evaluation was negative for retinal involvement due to CMV.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [63, 'years'], 'Alanine aminotransferase': [144.0, 'U/L'], 'Aspartate aminotransferase': [83.0, 'U/L'], 'Platelet count': [155000.0, 'µL']}",2.81129,2.67073,2.95185,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 83.0 U/L.
The patient's concentration of ALT is 144.0 U/L.
The patient's concentration of platelets is 155000.0 count/µL. To convert 155000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 155000.0 platelets count/µL * 1000000.0 µL/L = 155000000000.0 platelets count/L. This means that there are 155000000000.0/(10^9) = 155.0 billion platelet counts per liter.
Plugging these values into the formula, we get (63 * 83.0)/(155.0 * sqrt(144.0)) = 2.81129.Hence, the Fibrosis-4 score is 2.81129."
4347,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-6022254-1,Extracted,"A 57-year-old Thai man from Sa Kaeo, a province in the Eastern region of Thailand referred to a University Teaching Hospital in Bangkok due to swelling and pain at the left side of the neck for one month. One week prior he was admitted to the local hospital due to low-grade fever, difficulty swallowing and hoarseness. He received intravenous ceftriaxone and clindamycin for presumptive diagnosis of deep neck infection. He had history of hypertension treated with amlodipine 10 mg and enalapril 10 mg daily. He had habits of heavy alcohol drinking for 40 years, and smoking. He works at the department of fisheries. He swam, cleaned fish pond and mowed the lawn. Upon admission (day 0), the patient's body weight was 52 kg, body mass index was 19.7 kg/m2. His vital signs were as follows: body temperature, 38.7 °C; blood pressure, 170/100 mmHg, pulse rate, 100 beats/min; respiratory rate, 24 breaths/min. On physical examination, mild pale conjuctivae, anicteric sclerae. The neck exam revealed pulsatile left neck mass size 5 × 5 cm in diameters, mild tender on palpation, no sign of inflammation. No limitation of neck movement. Oropharyngeal exam revealed bulging of left posterior pharyngeal wall and tonsil enlargement causing the narrowing of upper airway. Thyroid gland was not enlarged. Other exams included neurological exam were normal. Skin exam revealed multiple ill-defined scaly mild erythematous patches on both legs and dystrophic nails. Initial laboratory results showed anemia with hemoglobin concentration of 9.6 g/L and Hematocrit of 28%, MCV of 75 fl, white blood cell count of 6800 cells/mm3 with 80% neutrophil 7.7% lymphocytes, platelet count of 574,000 cells/mm3. Hemoglobin typing was normal (HbF 0.2% HbA2 2.9% HbA 85.9%; HbA2A). Liver function test showed AST 87 U/L, ALT 97 U/L, ALP 127 U/L, GGT 936 U/L, TB 0.3 mg/dl, DB 0.1 mg/dl, TP 81.2 g/L, Alb 28.7 g/L. Fasting glucose of 95 mg/dL, HbA1C of 4.74%, BUN 14 mg/dL, Cr 1.05 mg/dL, Anti-HIV test was negative. Viral hepatitis profile were negative. His chest X-ray was normal. He was diagnosed with anemia of chronic disease, alcoholic hepatitis, and xerotic eczema. Computer tomography of the neck showed a concealed ruptured of left external carotid artery 0.9 × 1.9 cm in size with surrounding hematoma (3.6 × 3.6 ×5.8 cm) at medial aspect of an aneurysm resulted in narrowing of the upper airway (A, B). Urgent surgical exploration on day 0 revealed severe adhesion around pseudoaneurysm (size 5 × 6 cm) confined around common carotid artery, carotid bifurcation, extended to the angle of mandible. The diameter of pseudoaneurysm neck was one cm, located at medial wall of common carotid artery just distal to carotid bifurcation. External carotid artery was obliterated. Angiogram and balloon occlusion was performed at the left common carotid artery. External carotid artery and internal carotid artery were ligated at the arterial stump just beneath the angle of mandible. Pseudoaneurysm was resected and internal content show pus and clot. Surgical margins were not free in gross section. The pus was sent for bacterial culture. Blood agar plate revealed rare growth of whitish colony, direct exam from the colony revealed broad rare septate fungal hyphae. Infectious disease was consulted on day 5 of admission. Serum antibodies to pythium antigen using an in-house rapid immunochromatographic test were positive on day 5. Sabouraud's glucose agar (SGA) grew fungal colony which identified as P. insidiosum by the induction of motile zoospore and confirmed by fungal broad-range 18S rDNA gene polymerase chain reaction. Pathology of carotid artery revealed acute suppurative inflammation () with branching broad rare septate hyphae demonstrated by Gomori Methanamine Silver stain and Periodic acid-Shiff stain (A) Immunohistochemistry stain for P. insidiosum was positive (B). Medical therapy with oral itraconazole 200 mg oral twice daily combined with terbinafine 250 mg oral twice daily were started on day 5. Adjunctive immunotherapy with subcutaneous injection of PIA vaccine 500 microliter (4 mg/ml) was given on day 6 and 18 of admission. Day 5, Computer tomography of the aorta shows atherosclerotic change without aneurysm or dissection. Postoperatively, physical exams revealed narrowing of upper airway, hypoglossal nerve palsy on the left side without motor deficit. Neurology was consulted on day 6. He was diagnosed with hypoglossal nerve palsy secondary to compression of carotid artery aneurysm. On Day 6, MRI and MRA of the brain revealed pseudoaneurysm of carotid artery at left carotid-parapharyngeal spaces (2.8 × 2.0 × 3.1 cm) associated with extensive inflammation of the surrounding soft tissue resulting in mild narrowing of upper airway. Left common carotid artery was occluded along the origin to the cavernous part of left internal carotid artery with the evidence of wall enhancement. Multifocal cerebritis consistent with cerebral septic emboli and leptomeningeal enhancement at the left cerebral hemisphere (). The patient underwent second exploration of the left neck on day 9 aiming to remove the residual infected necrotic tissue. Operative findings revealed pus with necrotic soft tissue extended to parapharyngeal space, however artery cannot be defined. The radical neck dissection could not be performed due to the morbidity outweigh the possibility of the cure. Tissue specimen revealed identical findings with the first operation. On day 6, the dosage of terbinafine was increased to 250 mg three times daily, itraconazole was continued. The patient and family decided for palliative care, no aggressive treatment. He was discharged on day 19 of hospitalization. On day 29 after discharge, upon an outpatient visit, his family mentioned that he developed progressive right hemiparesis over the two days after discharge. Physical exams revealed healed surgical wound of the left neck, narrowing of upper airway, neurological exams revealed global aphasia, right facial palsy (upper motor neuron), motor power grade I on the right side. His family denied further investigation. He continued to take combination of oral terbinafine, itraconazole and PIA vaccine. On day 49, upon an outpatient visit, he had flaccid hemiparesis on the right side without other deficit. He received fourth dose of PIA vaccine and continued oral itraconazole and terbinafine. On day 82, he expired at a local hospital due to complication of diseases.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [57, 'years'], 'Alanine aminotransferase': [97.0, 'U/L'], 'Aspartate aminotransferase': [87.0, 'U/L'], 'Platelet count': [574000.0, 'µL']}",0.8772,0.83334,0.92106,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 87.0 U/L.
The patient's concentration of ALT is 97.0 U/L.
The patient's concentration of platelets is 574000.0 count/µL. To convert 574000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 574000.0 platelets count/µL * 1000000.0 µL/L = 574000000000.0 platelets count/L. This means that there are 574000000000.0/(10^9) = 574.0 billion platelet counts per liter.
Plugging these values into the formula, we get (57 * 87.0)/(574.0 * sqrt(97.0)) = 0.8772.Hence, the Fibrosis-4 score is 0.8772."
4348,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4208425-1,Extracted,"This is a 27-year-old female patient, who came to A&E with 9-day history of epigastric pain, nausea, anorexia, and generalized fatigue. The pain increased over the last 5 days with the radiation to right hypochondriac area and to the upper back and increased after meal with yellowish discoloration of sclera and dark color urine; history of occasional attacks of vomiting, no history of fever, and no past medical illnesses were reported, her husband has chronic HBV infection recently diagnosed but not on treatment (planned to start treatment within next few weeks). Upon physical examination her sclera is icteric; abdominal examination revealed epigastric and right hypochondriac area tenderness, liver palpable two fingers below costal margin. Blood investigations showed normal complete blood count, normal electrolytes, normal urea, and creatinine.
Alanine aminotransferase (ALT) 2488 u/L (norml 0–31) and aspartate aminotransferase (AST) 1590 u/L (normal 0–30), total bilirubin 63 umol/L and direct bilirubin 52 umol/L, alkaline phosphatase (ALP) 152 u/L, and amylase and lipase are normal; total protein 70 g/L and albumin is 41 gm/L, her prothrombin time (PT) is 18.8 second, INR is 1.7, partial thromboplastin time (PTT) is 25.6 second, WBC is 6300, Hb is 12.9 gm/dL, platelets are 172,000, ESR is 42, CRP is 65, hepatitis B surface Ag is positive, hepatitis B core antibody IgM is positive, hepatitis B e antigen and antibody are positive, and hepatitis A IgM and hepatitis C virus antibody are negative.
Abdominal ultrasound () on admission revealed mild hepatosplenomegaly, and gall bladder showed diffuse thickening and stratification of wall (11.7 mm), no calculi/pericholecystic fluid, normal CBD (4.8 mm), and free fluid along subhepatic region as well as right iliac region.
The patient was treated with supportive therapy of intravenous (I.V.) fluid, I.V. metoclopramide, and I.V. ranitidin with low fat and high carbohydrate diet.
During the followup, her symptoms of abdominal pain and nausea improved gradually, while vomiting and jaundice have settled completely by day 5 and her investigations showed the following: ALT 595 u/L (normal 0–31), AST 77 u/L (normal 0–30), ALP 118 u/L, total bilirubin 22 umol/L, PT 13.4 second, INR 1.1, and PTT 28 second; HBV DNA viral load was done later with lower limit of detection.
Abdominal U/S was repeated on day 5 of admission () and revealed normal size gallbladder with no calculi and wall thickness about 2.8–3 mm, bulky fatty liver.
The patient was discharged with good general condition and a medical clinic appointment for followup was given.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [27, 'years'], 'Alanine aminotransferase': [2488.0, 'U/L'], 'Aspartate aminotransferase': [1590.0, 'U/L'], 'Platelet count': [172000.0, 'µL']}",5.00388,4.75369,5.25407,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 1590.0 U/L.
The patient's concentration of ALT is 2488.0 U/L.
The patient's concentration of platelets is 172000.0 count/µL. To convert 172000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 172000.0 platelets count/µL * 1000000.0 µL/L = 172000000000.0 platelets count/L. This means that there are 172000000000.0/(10^9) = 172.0 billion platelet counts per liter.
Plugging these values into the formula, we get (27 * 1590.0)/(172.0 * sqrt(2488.0)) = 5.00388.Hence, the Fibrosis-4 score is 5.00388."
4349,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-3953743-2,Extracted,"A 61-year-old woman with CHC genotype 1, biopsy-proven cirrhosis, and previous nonresponse to three courses of interferon-based therapy was started on telaprevir-based therapy. Cirrhosis was well compensated, without evidence of ascites or hepatic encephalopathy. Upper endoscopy was negative for esophageal varices. Laboratory evaluation revealed albumin 2.7 g/dL, AST 132 U/L, ALT 81 U/L, alkaline phosphatase 394 U/L, total bilirubin 0.8 mg/dL, hemoglobin 13.3 g/dL, platelet count 156,000/μL, and HCV viral load 71,600 IU/mL.
After initiation of telaprevir-based therapy, the patient achieved rapid virologic response. Side effects of therapy included anemia, requiring ribavirin dose reduction and erythropoietin therapy. Treatment was noteworthy for stable hypoalbuminemia, with albumin level 2.1 g/dL without edema or ascites. She completed 12 weeks of telaprevir-based therapy, but therapy was discontinued at treatment week 31 due to a severe facial rash requiring systemic steroids for 2 days. HCV viral load remained undetectable from treatment week four until the end of therapy. Laboratory evaluation at the end of therapy revealed albumin 2.1 g/dL, AST 64 U/L, ALT 32 U/L, alkaline phosphatase 347 U/L, total bilirubin 1.3 mg/dL, hemoglobin 10.8 g/dL, and platelet count 80,000/μL. Weight at the end of therapy was 122 lb.
The patient presented 1 month later with 8 lb weight gain (weight 130 lb) over 2 weeks, new ankle edema, and abdominal distention. Abdominal ultrasound showed moderate ascites. HCV viral load was undetectable, albumin 2.9 g/dL, AST 71 U/L, ALT 37 U/L, alkaline phosphatase 309 U/L, total bilirubin 1.5 mg/dL, BUN 13 mg/dL, and creatinine 0.7 mg/dL. The patient refused diagnostic paracentesis. An echocardiogram was obtained, which revealed normal left and right ventricular function, with no sign of pulmonary hypertension. Sodium-restricted diet and diuretics (spironolactone 50 mg, furosemide 20 mg daily) were started, with prompt resolution of edema and ascites. Three months after the end of therapy, HCV viral load was 203 IU/mL, and on repeat 69,900 IU/mL, confirming relapse. Albumin level was 2.6 g/dL, AST 91 U/L, ALT 55 U/L, alkaline phosphatase 348 U/L, total bilirubin 1.1 mg/dL, BUN 12 mg/dL, creatinine 0.6 mg/dL, hemoglobin 13.5 g/dL and platelet count 140,000/μL. Diuretics were tapered, then discontinued at posttreatment week 20 with continued control of ascites. Albumin level remained stable at 2.6 g/dL.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [61, 'years'], 'Alanine aminotransferase': [81.0, 'U/L'], 'Aspartate aminotransferase': [132.0, 'U/L'], 'Platelet count': [156000.0, 'µL']}",5.73504,5.44829,6.02179,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 132.0 U/L.
The patient's concentration of ALT is 81.0 U/L.
The patient's concentration of platelets is 156000.0 count/µL. To convert 156000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 156000.0 platelets count/µL * 1000000.0 µL/L = 156000000000.0 platelets count/L. This means that there are 156000000000.0/(10^9) = 156.0 billion platelet counts per liter.
Plugging these values into the formula, we get (61 * 132.0)/(156.0 * sqrt(81.0)) = 5.73504.Hence, the Fibrosis-4 score is 5.73504."
4350,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-3970313-1,Extracted,"A 71-year-old male was admitted due to headache, dizziness, and nausea for three days. He was healthy, except that he had been diagnosed with hypertension two years before. His past medical history was unremarkable. His social history included intermittent alcohol consumption without smoking. The initial vital signs revealed blood pressure of 120/80 mmHg, heart rate of 76 beats per minute, respiration rate of 18 breaths per minute and body temperature of 36.9℃. He was alert upon admission. Physical examination revealed clear lung sound without rale or wheezing. The heart beat was regular without any murmur. There was no tenderness or rebound tenderness in the abdomen. Findings from other physical and neurological examinations were normal. There were no other symptoms such as fever, neck stiffness, photophobia, papilledema or other abnormalities. The initial peripheral blood count showed a white blood cell count of 11,200/mm3 (neutrophils 64.6%, lymphocytes 24.5%, monocytes 6.8%), hemoglobin level of 13.0 g/dL, platelet count of 211,000/mm3, erythrocyte sedimentation rate of 38 mm/hr, and C-reactive protein level of 1.11 mg/dL. Blood chemistry showed a total protein level of 7.6 g/dL, albumin level of 4.3 g/dL, total bilirubin level of 0.9 mg/dL, aspartate aminotransferase/alanine aminotransferase 27/16 IU/L, alkaline phosphatase 77 IU/L, BUN/Cr 9.2/0.8 mg/dL, Na/K 136/3.8 mEq/L, and Ca/P 9.0/4.7 mg/dL. Result of urinalysis was normal. Human immunodeficiency virus (HIV) antibody, hepatitis B surface antigen and hepatitis C antibody were all negative. Chest and abdomen radiographs were normal. Brain CT scan and magnetic resonance (MR) imaging showed multiple rim enhancing lesions with surrounding edema, which was presumed to be a brain abscess ().
After admission, the patient underwent a craniotomy with stereotactic aspiration of the abscess. During the operation, yellowish and turbid pus was aspirated and a cerebral abscess was diagnosed. Empirical parenteral antibiotics were started with ceftriaxone 2 g bid and metronidazole 500 mg tid. Gram stain of the pus showed beaded branching gram-positive bacilli. Urease test, esculin hydrolysis test, citrate test, and modified acid-fast stain using 1% acid alcohol were all positive and the bacteria grew at 42℃. Nocardia species were suggested by colonial morphology, Gram-stain, and modified acid fast bacillus (AFB) stain (). By manual, culture was identified as Nocardia species. For the accurate identification of Nocardia species, 16S ribosomal RNA (rRNA) gene-based polymerase chain reaction (PCR) and sequencing was carried out. Primers of 27F (5'-AGA GTT TGA TCM TGG CTC AG-3') and 1492R (5'-TAC GGY TAC CTT GTT ACG ACT T-3') were used for 16S rRNA gene amplification. Size of 1466 bp 16S rRNA gene amplification sequencing was carried out by Solgent (Solgent Co, Daejeon, Korea) company which uses Big Dye Terminator Cycle Sequencing Kit and ABI PRISM 3730 DNA analyzer (PE Applied Biosystem, Foster, CA, USA). It showed 100% concordance to N. farcinica (GenBank accession number: KC478309) by BLAST Similarity Searching in GenBank. The organism was susceptible to amikacin, imipenem, trimethoprim-sulfamethoxazole (TMP-SMX), ciprofloxacin, and resistant to erythromycin, kanamycin, ampicillin, gentamicin. After identifying the result of pus culture, the antibiotic regimen was changed to TMP-SMX (15 mg/kg of the TMP component per day) and imipenem 500 mg qid. Due to the persistence of the patient's symptoms, re-imaging was performed two weeks later. On day 24 of admission, the patient underwent a repeated craniotomy with stereotactic aspiration of the abscess because the abscess and surrounding edema have increased than before. Ciprofloxacin (400 mg every 12 h, intravenous) was added to the TMP-SMX treatment and changed from imipenem to meropenem. After performance of repeated surgery and administration of additional antibiotics, we observed improvement of the patient's symptoms. Contrast-enhanced brain CT scan performed three weeks after reoperation, showed substantial resolution of the brain lesion. Meropenem and ciprofloxacin were continued for six weeks. On hospital day 67, he was discharged to go home to complete four months of oral TMP-SMX therapy. On three-month follow-up brain CT after discharge, resolution of the brain abscess was confirmed.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [71, 'years'], 'Alanine aminotransferase': [16.0, 'U/L'], 'Aspartate aminotransferase': [27.0, 'U/L'], 'Platelet count': [211000.0, 'µL']}",2.27133,2.15776,2.3849,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 27.0 U/L.
The patient's concentration of ALT is 16.0 U/L.
The patient's concentration of platelets is 211000.0 count/µL. To convert 211000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 211000.0 platelets count/µL * 1000000.0 µL/L = 211000000000.0 platelets count/L. This means that there are 211000000000.0/(10^9) = 211.0 billion platelet counts per liter.
Plugging these values into the formula, we get (71 * 27.0)/(211.0 * sqrt(16.0)) = 2.27133.Hence, the Fibrosis-4 score is 2.27133."
4351,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-6280163-1,Extracted,"A 49-year-old female was referred for further evaluation of hepatomegaly, abdominal pain, and thrombocytopenia. On interview, she endorsed a several year history of right upper quadrant abdominal pain and very mild dyspnea with exertion. She reported that the abdominal discomfort was worse in a sitting position. At the time of initial evaluation she was feeling well with no symptoms of jaundice, pruritus, abdominal pain, nausea, vomiting, edema, or ascites. She also reported no constitutional symptoms.
Past medical history was notable for a 10-year history of mild thrombocytopenia (platelet count 90000-130000) of unclear etiology with negative laboratory workup. Past surgical history was remarkable for an enlarged and nodular appearing liver observed during laparoscopic cholecystectomy performed one year prior due to the same symptoms. The patient has been followed by a hematologist as an outpatient, and a recent liver spleen single photon emission computed tomography scan had confirmed hepatomegaly without splenomegaly. Abdominal ultrasound characterized the liver as 18.1 cm in size with no evidence of cirrhosis or portal hypertension. Patent vasculature was reported throughout with normal hepatopedal flow. The patient had also previously undergone a computer tomography-guided liver biopsy, which showed mild perivascular and pericellular fibrosis but no evidence of advanced fibrosis or cirrhosis.
Physical examination revealed hepatomegaly 4 cm below the costal margin but was otherwise unremarkable. Initial labs included a complete blood count (white count: 4.6, hemoglobin: 13.5, platelets: 112000), comprehensive metabolic panel (sodium: 141, potassium: 3.8, urea nitrogen: 11, creatinine: 0.8, alkaline phosphatase: 51, total protein: 7.3, aspartate aminotransferase: 30, and alanine aminotransferase: 29), and coagulation panel (international normalized ratio: 1.0). Additional workup revealed a ferritin of 28. Antimitochondrial antibody and actin IgG were negative. Ceruloplasmin level was 32. Patient also tested positive for antinuclear antibody titer (1:80, diffuse pattern) and epstein-barr virus IgG. An elevated transient elastography score of 9.6 was also noted.
Due to concern for early cirrhosis in the setting of thrombocytopenia and an elevated transient elastography score, the patient was advised to pursue a healthy lifestyle and abstain from alcohol. A magnetic resonance venography of the abdomen showed no evidence of thrombosis or obstruction.
At this point in time the patient reported worsening, intermittent, epigastric abdominal discomfort that radiated to the right upper quadrant of her abdomen, often waking her up at night and only improved with standing upright or walking. She occasionally felt nauseous but otherwise reported no jaundice, pruritus, edema, ascites, chest pain, or dyspnea. Physical examination showed a positive hepatojugular reflux, consistent with hepatic congestion. The patient was evaluated by a cardiologist, and a transthoracic echocardiogram showed pericardial thickening but no evidence of constrictive pericarditis or systolic or diastolic dysfunction.
The patient then underwent a transjugular liver biopsy with intravenous ultrasound and pressure measurements, which showed an elevated central venous pressure at 13-15 mmHg, wedged right hepatic vein pressure with occlusion balloon measuring 16-17 mmHg, and a dilated IVC of 3 cm cephalad to the patent veins prior to reentry into the right atrium. Significant respiratory variation involving near-collapse of the retrohepatic IVC at end-expiration was noted. There was question of intraluminal narrowing of the retrohepatic IVC down to approximately 10-15 mm, which had significantly improved upon Valsalva maneuver. Right heart catheterization showed hepatic congestion with normal intracardiac and pulmonary artery pressures.
A multidisciplinary conference among the hepatology, vascular surgery, and cardiology services was held. It was suspected that the diaphragm, via the diaphragmatic hiatus through which the IVC was passing, was causing extrinsic compression of the vessel, thereby eliciting symptoms of epigastric and right upper quadrant pain. Repeat transient elastography was still elevated and the patient underwent an exploratory laparotomy with IVC venolysis and division of the diaphragmatic constriction. After the above intervention, resolution of previously identified constriction was noted via repeat venogram (Figures and ) and intravascular ultrasound.
Intraoperative liver biopsy revealed sinusoidal congestion with dilatation in the perivenular areas, features consistent with extrahepatic venous outflow obstruction. The patient recovered remarkably well from the laparotomy. The available pre- and post-venolysis labs are presented in Table . At her four week postoperative follow up visit, she reported resolution of her abdominal discomfort and complete ability to perform her activities of daily living without the use of any pain medications. Unfortunately, follow-up liver enzymes were unable to be obtained due to losing her health insurance.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [49, 'years'], 'Alanine aminotransferase': [29.0, 'U/L'], 'Aspartate aminotransferase': [30.0, 'U/L'], 'Platelet count': [112000.0, 'µL']}",2.43725,2.31539,2.55911,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 30.0 U/L.
The patient's concentration of ALT is 29.0 U/L.
The patient's concentration of platelets is 112000.0 count/µL. To convert 112000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 112000.0 platelets count/µL * 1000000.0 µL/L = 112000000000.0 platelets count/L. This means that there are 112000000000.0/(10^9) = 112.0 billion platelet counts per liter.
Plugging these values into the formula, we get (49 * 30.0)/(112.0 * sqrt(29.0)) = 2.43725.Hence, the Fibrosis-4 score is 2.43725."
4352,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-5139723-1,Extracted,"A 53 years old female was brought to emergency department with abdominal pain and altered mental status (AMS). Her medical history was significant for chronic alcoholism, tobacco abuse and hepatitis C. Her blood pressure upon presentation was 101/64 mmHg, pulse 109 beats/min, respirations 22breaths/min, oxygen saturation of 97% on 4 liters oxygen per minute and she was afebrile. On examination she had generalized yellow discoloration of the body. Abdominal examination was significant for right upper quadrant tenderness, hepatosplenomegaly and absence of bowel sounds. The rest of the examination was unremarkable.
Her initial laboratory showed Hb 14.5 g/dl, WBC 10.2 thousand/mm3, platelets 106,000 thousand/mm3, Na 116 meq/L, K 2.9 meq/L, BUN 13 mg/dl, Cr 2.7 mg/dl, CK-MB 18 ng/ml and troponin 0.08 ng/ml, ammonia 168 umol/L, bilirubin 29.2 mg/dl with direct bilirubin of 18.5 mg/dl, albumin 2.8 g/dl, INR 2.34, alkaline phosphatase 270 IU/L, ALT 172 IU/L, AST 679 IU/L and lactate of 10.5 mmol/L. Abdominal ultrasound showed an enlarged liver with distended gall bladder. She was admitted to Intensive Care Unit (ICU) because of AMS. The patient started having coffee ground emesis within an hour of admission to the ICU. A nasogastric tube was placed which recovered 600 ml of coffee ground aspirate. She gradually became hypotensive and was subsequently started on pressors.
The patient underwent an emergent esophagogastroduodenoscopy which revealed severe reflux esophagitis without active bleeding in the distal esophagus and no varices. The duodenum was erythematous and eccymotic, consistent with ischemia. General surgery was consulted and patient underwent an exploratory laparotomy which revealed dark brown serosa of jejunum 3 cm distal to the ligament of Treitz extending distally to approximately 180 cm sparing the ileum (). The infracted bowel was resected. Liver was found to be massively enlarged with multiple small nodules grossly suspected of cirrhosis and a needle biopsy was done. The colon was normal on visual inspection. Her abdomen was left open as her intestine was in discontinuity as well as for a possible second look in 24 - 48 hours.
Postoperatively the patient was continued on multiple pressors as she was still profoundly hypotensive. As her condition continued to decline and showed no signs of improvement on mechanical ventilation, support was withdrawn according to her wishes.
Pathology of the specimen showed an extensive full thickness ischemic necrosis of the intestine without any significant evidence of atherosclerosis or thrombus in the vessels, consistent with NOMI. The liver biopsy confirmed cirrhosis with macrovesicular steatosis and necrosis ().",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [53, 'years'], 'Alanine aminotransferase': [172.0, 'U/L'], 'Aspartate aminotransferase': [679.0, 'U/L'], 'Platelet count': [106000.0, 'µL']}",25.88663,24.5923,27.18096,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 679.0 U/L.
The patient's concentration of ALT is 172.0 U/L.
The patient's concentration of platelets is 106000.0 count/µL. To convert 106000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 106000.0 platelets count/µL * 1000000.0 µL/L = 106000000000.0 platelets count/L. This means that there are 106000000000.0/(10^9) = 106.0 billion platelet counts per liter.
Plugging these values into the formula, we get (53 * 679.0)/(106.0 * sqrt(172.0)) = 25.88663.Hence, the Fibrosis-4 score is 25.88663."
4353,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-6952481-1,Extracted,"A 50-year-old man with loss of appetite and abdominal pain came to our hospital. His medical history included alcoholic liver cirrhosis (Child-Pugh score was B), and he had undergone proximal gastrectomy with double-tract reconstruction for esophagogastric junctional cancer 3 months before. On admission, he complained of severe abdominal distension and rebound tenderness. Laboratory examination showed white blood cells of 2800/μL; hemoglobin, 9.5 g/dL; platelet count, 180,000/μL; total-bilirubin, 2.5 mg/dL; and C-reactive protein, 0.93 mg/dL. Contrast-enhanced CT scan revealed free air with edematous wall thickening around of gastro-jejunal anastomosis. Gastrointestinal perforation was suspected and emergency surgery was performed. Intraoperatively, much ascites was stored in the peritoneal cavity, and 5 mm perforation was observed at gastro-jejunal anastomosis. There was no additional perforation (e.g., esophagojejunal anastomosis or jejunal-jejunal anastomosis), and no findings could be detected suggesting exacerbation of portal hypertension (e.g., dilation of the mesenteric vein, new formation of collateral circulation, or enlargement of splenomegaly). We performed suture closure, omentum covering, and wash drainage.
Abdominal symptoms and inflammatory response improved postoperative. However, on POD 3, he complained a large amount of tarry stool. Laboratory examination showed rapid progression of anemia and increased blood urea nitrogen (BUN)/creatinine ratio; hemoglobin, 6.8 g/dL; platelet count, 320,000/μL; asparate aminotransferase (AST), 136 U/L; alanine aminotransferase (ALT), 55 U/L; total bilirubin, 2.2 mg/dL; BUN, 20 mg/dL; and creatinine, 0.50 mg/dL. Emergency upper gastrointestinal endoscopy revealed an exposed blood vessel with eruptive bleeding at the just anal side of esophago-jejunum anastomosis (Fig. a). We attempted endoscopic clipping. However, the procedure was unsuccessful because the mucosa was fragile and easily lacerated. In the meanwhile, the patient became severe hemorrhagic shock and hemostasis was obtained (Fig. b).
On POD 20, a contrast-enhanced CT scan was taken again because anemia continued to progress gradually despite fasting or RBC transfusion. The results revealed the dilatation of the jejunal vein flowing into the ascending jejunal limb (Fig. ). Based on this finding, the patient was diagnosed with esophagojejunal varices rupture, and we tried PTO for hemostasis. The portal and superior mesenteric veins were catheterized with the percutaneous transhepatic approach. Contrast agent injection into the jejunal branch demonstrated retrograde flow to the azygos vein through esophagojejunal varices (Fig. a, b). The microcatheter was inserted into the variceal blood supply branch, and 50% glucose solution was injected to reduce blood flow. Then, we injected 10 mL of 5% ethanolamine oleate with iopamidol (5% EOI). After obliteration therapy, the superior mesenteric venogram showed complete occlusion of the variceal supply branch (Fig. c).
There were no complications during or after the operation, and the subsequent course showed no further bleeding. The patient discharged 14 days after the operation.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [50, 'years'], 'Aspartate aminotransferase': [136.0, 'U/L'], 'Alanine aminotransferase': [55.0, 'U/L'], 'Platelet count': [320000.0, 'µL']}",2.86535,2.72208,3.00862,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 136.0 U/L.
The patient's concentration of ALT is 55.0 U/L.
The patient's concentration of platelets is 320000.0 count/µL. To convert 320000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 320000.0 platelets count/µL * 1000000.0 µL/L = 320000000000.0 platelets count/L. This means that there are 320000000000.0/(10^9) = 320.0 billion platelet counts per liter.
Plugging these values into the formula, we get (50 * 136.0)/(320.0 * sqrt(55.0)) = 2.86535.Hence, the Fibrosis-4 score is 2.86535."
4354,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-6860775-1,Extracted,"A 70-year-old woman with loss of appetite and weight loss of 10 kg over a three-month period consulted her family doctor. There was no pancreatic cancer patient in her family. A subsequent computed tomography (CT) scan showed a mass in the pancreas and she was referred to our hospital for further examinations. Laboratory results at admission were as follows: leukocyte count, 7.12 × 103/µL; platelet count, 300 × 103/L; total bilirubin, 1.3 mg/dL; aspartate aminotransferase, 19 U/L; alanine aminotransferase, 19 U/L; alkaline phosphatase, 216 U/L; amylase, 65 U/L; CEA, 171.9 ng/mL; CA19-9, 16 U/mL; DUPAN-2, <25 U/mL; and Span-1, 6 U/mL. Dynamic enhanced CT revealed a low density tumor measuring 4 cm in diameter in the body of the pancreas, with a poor contrast effect and an unclear outline (Figure ).
The main pancreatic duct was dilated on both the head and caudal side of the tumor. T2-weighted magnetic resonance imaging (MRI) showed the mass as a high intensity area (Figure ).
The internal echo of the tumor shown by endoscopic ultrasonography was a mosaic pattern (Figure ), while endoscopic retrograde cholangiopancreatography (ERCP) indicated that the main pancreatic duct was continuous with the lumen of the tumor, with disruption and dilatation observed (Figure ).
A cytological examination of pancreatic juice obtained from the patient during ERCP showed the tumor to be class IV. Differential diagnoses considered included invasive ductal carcinoma derived from an IPMN, mucinous carcinoma, anaplastic carcinoma, and mucinous cyst carcinoma. Neither distant nor lymph node metastasis was observed. We performed a pancreatic tail splenectomy as a curative resection procedure.
Macroscopic findings of the resected specimen showed a tumor 10 cm in size in the body of the pancreas and protruding to the ventral side. On the cleaved surface, tumor lesions with mucus in the lumen were recognized, and occupied most of the body tail (Figure ).
Histologically, the tumor was divided into invasive and non-invasive parts. Most of the macroscopic mass corresponded to the invasive part, in which tumor cells with mucous and nuclear atypia showed increasing invasion of the constructing duct structures and mucus stored in the tumor duct (Figure ).
Furthermore, numerous signet ring cells were seen suspended in mucus (Figure ).
On the other hand, in the non-invasive part, papillary epithelium of the main pancreatic duct had spread to both the head and caudal side of the tumor, and was continuous with the main lesion (Figure ).
Pathological features of mucinous cyst neoplasm such as ovarian-type stroma were not observed. Results of hematoxylin eosin staining of the resected tumor excluded a mucinous cyst carcinoma, and the diagnosis was IPMN-derived invasive cancer or mucinous carcinoma. To distinguish between those, immunostaining for MUC1, MUC2, and MUC5AC was performed. The invasive part was positive for all three types of mucin, while the non-invasive part was positive for only MUC2 and MUC5AC, which supported IPMN-derived invasive cancer (Figure ).
Additionally, we examined for GNAS and K-RAS mutations in the tumor. The main lesion was scraped to obtain a representative section, which was embedded in paraffin, with DNA isolated using a Takara DEXPAT kit (Takara Bio). PCR amplification of the GNAS gene exon 8 and K-RAS gene exon 2 regions was performed using the isolated DNA. The forward and reverse primers used for the GNAS gene were 5’-TTATTACTGTTTCGGTTGGC-3’ and 5’-TCAAGAAACCATGATCTCTG-3’, respectively, and those for the K-RAS gene were 5’-CATGTTCTAATATAGTCACATTTTC-3’ and 5’-ATCGTCAAGGCACTCTTGCC -3’, respectively []. Amplifications were performed by initial denaturation at 94°C for 1 minute, followed by 30 cycles of denaturation at 98°C for 10 seconds, annealing at 61°C for 15 seconds, and extension at 68°C for 30 seconds using Takara Gflex polymerase (Takara Bio). The PCR products thus obtained were then purified using an Illustra ExoProStar kit (GE Healthcare), and sequenced by use of a Big Dye cyclic sequencing kit and ABI 310 sequencer (Applied Biosystems, Forster City, CA). Sequencing analysis was successfully performed. Neither the GNAS mutation c602G>A nor K-RAS mutation c35G>A was observed (Figure ).",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [70, 'years'], 'Alanine aminotransferase': [19.0, 'U/L'], 'Aspartate aminotransferase': [19.0, 'U/L'], 'Platelet count': [300000.0, 'µL']}",1.01708,0.96623,1.06793,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 19.0 U/L.
The patient's concentration of ALT is 19.0 U/L.
The patient's concentration of platelets is 300000.0 count/µL. To convert 300000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 300000.0 platelets count/µL * 1000000.0 µL/L = 300000000000.0 platelets count/L. This means that there are 300000000000.0/(10^9) = 300.0 billion platelet counts per liter.
Plugging these values into the formula, we get (70 * 19.0)/(300.0 * sqrt(19.0)) = 1.01708.Hence, the Fibrosis-4 score is 1.01708."
4355,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-8674478-1,Extracted,"A 66-year-old female was diagnosed with CHB in Nanjing Jiangbei Hospital on 17 September
2019. Diagnosis results on hepatitis B surface antigen (HBsAg), hepatitis B e antigen
(HBeAg), and hepatitis B core antibody (anti-HBc) were positive, while antibodies to
hepatitis A, hepatitis C, hepatitis D, and hepatitis E were negative. There was no evidence
of infection with cytomegalovirus, HIV virus, herpes simplex virus, or Epstein–Barr virus.
In addition, the results were also negative for serologic markers of autoimmune diseases
(antinuclear antibody (ANA), antinuclear ribonucleoprotein (anti-nRNP), anti-Smith antibody
(anti-Sm), anti-Sjogren’s syndrome antigen A antibody (anti-SSA), anti-Ro-52 antibody
(RO-52), anti-Sjogren’s syndrome antigen B antibody (anti-SSB), anti-scleroderma-70 antibody
(anti-ScL-70), anti-histidyl-transfer RNA synthetase antibody (anti-JO-1), centromere
protein B (CB), antidouble-stranded DNA antibody (anti-dsDNA), (NUC), (HI),
anti-ribosomal P-protein antibody (RIB), anti-PM/Scl antibody (PM-Scl), proliferating cell
nuclear antigen (PCNA), anti-mitochondrial antibody (AMA), anti-liver and kidney microsomal
antibody (LKM), anti-liver cytosol antigen type 1 antibody (LC-1), and soluble liver antigen
(SLA) were all negative). Meanwhile, alanine aminotransferase (ALT): 41 IU/L and aspartate
aminotransferase (AST): 41 IU/L. HBV-DNA in serum was 6.14 × 106 IU/ml, and the
platelet count was 111*109/L. An abdominal magnetic resonance imaging (MRI) scan
showed signs of fatty liver. The patient started taking ETV 0.5 mg/day after being diagnosed
with CHB. She did not experience any discomfort during the treatment.
Till December 13, she found herself prone to gum bleeding and skin ecchymosis without nasal
hemorrhage or sclera bleeding, She denied epistaxis, melena, hematochezia, hematuria, or
other bleeding manifestations, and without other chronic or neoplastic disease. Results of
blood examination showed that platelet count dropped to 3*109/L, while white
blood cell (WBC) and hemoglobin (HGB) remained normal. HBV-DNA in serum was raised to
4.42 E+02 IU/ml with ALT: 52 U/L, AST: 54 U/L, IgA: 2.15 g/L, IgG: 17.90 g/L, and IgM
1.54 g/L. On physical examination, her temperature was 36.9°C; blood pressure, 116/77 mmHg;
pulse, 67 beats/min; and respiratory rate, 18 beats/min. She looked tired but had no pallor,
icterus, or generalized lymphadenopathy. The anterior nares were clear without epistaxis.
The mucous membrane was moist, and the oral mucosa of the oropharynx has many scabs and
dried blood. Auscultation of chest revealed that S1 and S2 were normal, without fricative,
murmur, gallop, or blister, and the patient had normal breath sounds. Her abdomen was soft
without tenderness, hepatosplenomegaly, or ascites. The skin was warm and dry, with several
ecchymoses on the chest and back.
She immediately underwent bone marrow aspiration. The bone marrow examination revealed that
the hyperplasia was significantly active, granulocytic and erythroid hyperplasia were
active, megakaryocytes were common, and platelets were rare. Immunotype lymphocytes occupy
about 12% of nucleus cells, and the proportion is reduced. Among them, precursor
B-lymphocytes account for 0.5% of lymphocytes, which increases, but there is no obvious
light-chain restriction. The cells in the primitive area occupy about 1% of the nuclear
cells and are scattered. Monocytes occupy about 4% of the nucleus cells and have a mature
phenotype. Granulocytes accounted for about 68% of nuclear cells, and no significant
abnormalities were observed (). Peripheral blood flow cytometry showed a significant increase in
B-lymphocytes (29.20%) (). All performance was in accordance with thrombocytopenia.
Platelet count may be decreased by the factor of aplastic anemia, leukemia, cancer, severe
infections, immune abnormalities, drugs, vaccines, and so on. Since the patient had no history of other
medications or infections while taking ETV, and no other causes of thrombocytopenia were
identified. The patient was diagnosed with entecavir-associated thrombocytopenia.
ETV medication was replaced by tenofovir (TDF) immediately. Since the patient was in urgent
condition, frequent platelets transfusions and thrombopoietin were applied for several days,
and daily prednisone of 50 mg was concomitantly taken. Platelet count increased after 10
days, and her symptoms of bleeding faded away gradually. The platelet count reached
297*109/L after 18 days ().",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [66, 'years'], 'Alanine aminotransferase': [52.0, 'U/L'], 'Aspartate aminotransferase': [54.0, 'U/L'], 'Platelet count': [297000000.0, 'L']}",1664.10059,1580.89556,1747.30562,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 54.0 U/L.
The patient's concentration of ALT is 52.0 U/L.
The patient's concentration of platelets is 297000000.0 count/L. This means that there are 297000000.0/(10^9) = 0.297 billion platelet counts per liter.
Plugging these values into the formula, we get (66 * 54.0)/(0.297 * sqrt(52.0)) = 1664.10059.Hence, the Fibrosis-4 score is 1664.10059."
4356,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-5152786-1,Extracted,"A 30-year-old man presented with a 3-month history of nausea, bloating, dizziness, dyspnea on exertion, and self-limiting episodes of melena. His past medical history included obesity, hypertension, diabetes mellitus, hypercholesterolemia, and metabolic syndrome. He was initially seen at a primary clinic. A subepithelial duodenal lesion was detected on esophagogastroduodenoscopy, and this was diagnosed as a lipoma on endoscopic ultrasonography. He was managed conservatively, and received two 8-unit blood transfusions for his iron deficiency anemia. Subsequent abdominal ultrasound and colonoscopy findings were normal. However, the patient did not improve over the next 3 months and complained of persistent dizziness and nausea.
He was then referred to our hospital for further investigation. On questioning, he denied weight loss or the use of nonsteroidal anti-inflammatory drugs. His height and weight were 180.9 cm and 145.8 kg, and he had a body mass index of 44.5 kg/m2. Physical examination did not reveal any abdominal tenderness, rebound tenderness, or palpable masses. His complete blood count was white blood cells 9,770/μL, hemoglobin 9.7 g/dL, hematocrit 31.6% (mean corpuscular volume 71.8 fL, mean corpuscular hemoglobin 22 pg), and platelets 281,000/μL. Serum total bilirubin was 1.2 mg/dL, serum aspartate aminotransferase was 37 IU/L, and serum alanine transaminase was 67 IU/L. Abdominal computed tomography showed a large polypoid mass in the duodenum (). It was a hypodense tubular intraluminal mass measuring about 9.3×2 cm in the first and second parts of the duodenum. Esophagogastroduodenoscopy showed a large pedunculated and eroded mass with a thick stalk arising from the duodenal bulb. The tumor was located on the anterior surface of the duodenal bulb and had a wide base, causing near-total obstruction (-). The tip of the tumor also was covered with exposed vessels and hematin, but was not actively bleeding (). Endoscopic polypectomy was performed. However, the lesion was too large to fit into the conventional snare. We grasped a portion of the mass and pulled it up into the stomach with the snare, and then performed two partial snare polypectomies (). Next, we performed endoscopic submucosal dissection on the bulb of the duodenum after the duodenal U-turn (, ). Hemoclips were applied to prevent bleeding and perforation. The gross endoscopic resection specimen showed a large duodenal lesion measuring 9.3×2 cm (). Histology confirmed a Brunner’s gland hamartoma (, ).
The patient did not experience any serious complications from this procedure. He was started on proton pump inhibitor therapy and discharged after 7 days. His dizziness and melena resolved after the endoscopic procedure, and his anemia resolved after 1 month. At 4 months after discharge, his complete blood count had normalized. At 6 months, a repeat esophagogastroduodenoscopy did not find any evidence of recurrence or tumor remnants ().",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [30, 'years'], 'Alanine aminotransferase': [67.0, 'U/L'], 'Aspartate aminotransferase': [37.0, 'U/L'], 'Platelet count': [281000.0, 'µL']}",0.48259,0.45846,0.50672,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 37.0 U/L.
The patient's concentration of ALT is 67.0 U/L.
The patient's concentration of platelets is 281000.0 count/µL. To convert 281000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 281000.0 platelets count/µL * 1000000.0 µL/L = 281000000000.0 platelets count/L. This means that there are 281000000000.0/(10^9) = 281.0 billion platelet counts per liter.
Plugging these values into the formula, we get (30 * 37.0)/(281.0 * sqrt(67.0)) = 0.48259.Hence, the Fibrosis-4 score is 0.48259."
4357,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4238166-1,Extracted,"A 70-year-old woman, with a history of alcoholic cirrhosis was admitted to our hospital because a liver mass had been discovered by ultrasonography scan. Her Eastern Cooperative Oncology Group (ECOG) performance score was 1. Physical examination showed no palpable mass, abdominal distension, or weight loss. Laboratory details showed white blood cell 5,980/μL; red blood cell 4,24 × 106/μL; haemoglobin 10,8 g/dL; hematocrit 35%; platelet 137,000/μL; INR 1,11; urea nitrogen 26 mg/dL; creatinine 0,73 mg/dL; total protein 7,8 g/dL; albumin 3,5 g/dL; aspartate aminotransferase (AST) 55 U/L; alanine aminotransferase (ALT) 42 U/L; alkaline phosphatase (ALP) 500 U/L; gamma-glutamyl transpeptidase (GGT) 264 U/L; cholinesterase 5238 U/L; total bilirubin 0,64 mg/dL; alpha-fetoprotein (-FP) 319 ng/mL. Gastroscopy showed esophageal varices grade F1-F2. Her Child-Pugh score was A, and Meld score was 7. Both contrast-enhanced ultrasonography (CEUS) and CT scan revealed an 8 × 5 × 7 cm sized arterial enhancing and delayed washout mass extended to the VII and VIII hepatic segments associated with underlying cirrhosis and without portal invasion, ascites, and splenomegaly. Tumor stage was Barcelona Clinic Liver Cancer (1) stage C.
According to the practice guidelines of the American Association for the Study of Liver Disease (AASLD), transarterial chemoembolization (TACE) with epirubicin-lipiodol was performed. Thirty days after TACE, a noncontrast-enhanced CT showed no tumor shrinkage and a slight accumulation of lipiodol (pattern type IV). These data [] evidenced an unsatisfactory response to TACE procedure. A hypofractionated stereotactic radiotherapy (HSRT) was performed. Patient was immobilized using the Elekta Stereotactic Body Frame which uses a rigid frame and a vacuum pillow and an abdominal compression device to reduce respiratory target motion. Treatment planning contrast-enhanced CT (3 mm slice thickness) was obtained to identify target volume visualization. According to our internal protocol based on the recent literature data (5), HSRT was delivered in 5 fractions for a total of 40 Gy on alternate days, and dose was prescribed to the 97% isodose line (). As constrains for normal tissues, 33% and 50% of the whole liver volume received a total dose less than 21 Gy and 15 Gy, respectively; the percentage of each kidney volume to receive a total dose of 15 Gy was less than 35%, while the maximum total dose did not exceed 27 Gy for the spinal cord and stomach/small intestine and 30 Gy for heart.
Planning was conducted on the Pinnacle 3D 8.0 m Version Planning System (Philips Healthcare, Best, Netherlands). The patient had no discomfort after the procedure, and no acute toxicity was reported.
At 1, 2, and 3 months after HSRT, ALP, GGT, and a-FP decreased, respectively, to 411→ 400→361 U/L, 199→156→118 U/L, and 107,6→ 38→19,8 ng/mL; a further reduction of a-FP value at 7,4 ng/mL was observed within 6 months (). CEUS at 1 and 2 months showed 3 large necrotic areas inside an unchanged size tumour mass. CT scan showed a 90% objective tumour response and a complete remission at 3 and 6 months after treatment, respectively ().
Twenty-four months following HSRT, patient showed a multifocal intrahepatic dissemination without evidence of “in-field” local recurrence; therefore a systemic therapy with sorafenib was planned.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [70, 'years'], 'Alanine aminotransferase': [42.0, 'U/L'], 'Aspartate aminotransferase': [55.0, 'U/L'], 'Platelet count': [137000.0, 'µL']}",4.33626,4.11945,4.55307,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 55.0 U/L.
The patient's concentration of ALT is 42.0 U/L.
The patient's concentration of platelets is 137000.0 count/µL. To convert 137000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 137000.0 platelets count/µL * 1000000.0 µL/L = 137000000000.0 platelets count/L. This means that there are 137000000000.0/(10^9) = 137.0 billion platelet counts per liter.
Plugging these values into the formula, we get (70 * 55.0)/(137.0 * sqrt(42.0)) = 4.33626.Hence, the Fibrosis-4 score is 4.33626."
4358,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-6478490-1,Extracted,"A 30-year-old male with no comorbidities presented to the emergency room in February 2018 with complaints of headache, fatigue, dry cough, and abdominal pain that started three days prior to admission. Apart from occasional alcohol consumption, his past medical history was unremarkable with no history of surgery or trauma.
On presentation, vitals were within normal limits with the exception of a temperature of 102 °F and his physical exam results were as follows: he appeared to be in moderate distress. Skin was jaundice; his abdominal exam was notable for diffuse abdominal tenderness with hepatosplenomegaly. Lower extremities revealed traced edema. Initial laboratory studies revealed a white blood count of 4.4 K/uL with lymphocytic predominance, hemoglobin of 16 g/dL, platelets 150 K/uL, aspartate aminotransferase (AST) 116 U/L, alanine aminotransferase (ALT) 119 U/L, and creatinine level of 1.1 mg/dL. Hepatitis and human immunodeficiency virus (HIV) panels were negative. Herpes simplex virus (HSV) and cytomegalovirus (CMV) were negative. A presumptive diagnosis of infectious mononucleosis was made and confirmed by serological and polymerase chain reaction (PCR). The EBV viral capsid antigen IgM antibody was >160 (normal <0.9); viral capsid antigen IgG antibody was negative, EBV early antigen IgG was 1.54 (normal <0.9), and the EBV nuclear antigen IgG was negative.
On day three of admission, acute worsening of abdominal pain with shortness of breath complicated the hospital course. Repeat labs were white blood corpuscle (WBC) count of 17.1 K/uL with lymphocytic predominance, hemoglobin 7.8 g/dL, platelets 667 K/uL, AST 332 U/L, and ALT 146 U/L. A computed tomography (CT) was performed, which revealed a wedge infarct of the spleen (Figure ). APAs were sent at that time and were positive. He was transferred to the intensive care unit and started on bilevel positive airway pressure (BiPAP) and continuous renal replacement therapy (CRRT) due to anuria. His clinical status improved with supportive therapy; a repeat CT scan showed improvement of splenic infarcts and he was discharged 27 days later. Repeat APA testing six weeks later was negative.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [30, 'years'], 'Alanine aminotransferase': [119.0, 'U/L'], 'Aspartate aminotransferase': [116.0, 'U/L'], 'Platelet count': [150000.0, 'µL']}",2.12674,2.0204,2.23308,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 116.0 U/L.
The patient's concentration of ALT is 119.0 U/L.
The patient's concentration of platelets is 150000.0 count/µL. To convert 150000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 150000.0 platelets count/µL * 1000000.0 µL/L = 150000000000.0 platelets count/L. This means that there are 150000000000.0/(10^9) = 150.0 billion platelet counts per liter.
Plugging these values into the formula, we get (30 * 116.0)/(150.0 * sqrt(119.0)) = 2.12674.Hence, the Fibrosis-4 score is 2.12674."
4359,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-5566969-1,Extracted,"A 52-year-old Hispanic male patient presented with right upper quadrant abdominal pain and weight loss of 25 pounds in 2 months. On admission, the patient's vital signs showed a blood pressure of 140/95 mm Hg, pulse of 97 bpm, respiratory rate of 18 per min, and an oxygen saturation of 94% on room air. Patient was alert and oriented to time, person, and place, and the rest of the physical examination was significant for icteric sclera and moderately distended abdomen with right upper quadrant tenderness. There was no jugular venous distention, significant cardiac murmurs, or lower extremity edema. Laboratory workup showed deranged liver function tests (AST 413 U/L, ALT 146 U/L, ALP 1,256 U/L, total bilirubin 3.77 mg/dL, direct bilirubin 2.651 mg/dL, albumin 2.7 g/dL), INR of 1.23, WBC 11 k/μL, hemoglobin of 12.9 g/dL, Hct 39.5%, and platelet count of 233 k/μL. Basic metabolic profile showed sodium level (Na) of 140 mmol/L, potassium (K) 4.00 mmol/L, bicarb (HCO3) 25 mmol/L, BUN 13 mg/dL, and creatinine level of 0.7 mg/dL. Hepatitis panel was positive for chronic hepatitis B infection. Alpha-fetoprotein was 5,287 mg/mL.
Chest X-ray showed multiple nodules of various sizes in both lung fields without effusion (Fig. ). Electrocardiogram was unremarkable. Computed tomography of the abdomen and pelvis revealed diffused heterogeneous lesions throughout the liver, moderate ascites, and gallbladder wall thickening. Computed tomography of the chest with contrast showed innumerable bilateral pulmonary nodules consistent with metastasis (Fig. ).
Magnetic resonance imaging of the abdomen showed multiple heterogeneously T2 hyperintense, centrally necrotic round hepatic masses with internal neovascularity and avid peripheral enhancement. These included a 9.4 × 11.2 × 11.2 cm left hepatic lobe mass with invasion into the middle and left hepatic veins as well as into the inferior vena cava and right atrium. There was also invasion of the left portal vein and distal right portal vein. A 9.0 × 9.2 × 5.3 cm right hepatic lobe mass centered on segment 7, a 6.8 × 5.7 × 6.3 cm right hepatic lobe mass centered on segment 5, and a 4.0 × 3.5 × 6.7 cm contour-deforming mass within the anterior left hepatic lobe with foci of internal steatosis consistent with fatty metamorphosis were observed (Fig. ). Multiple additional smaller masses were scattered throughout the liver. The liver had a nodular, lobulated contour. Magnetic resonance cholangiopancreatography showed multiple centrally necrotic round hepatic masses with internal neovascularity, avid peripheral enhancement, fatty metamorphosis, and invasion of portal veins, hepatic veins, inferior vena cava, and right atrium. Ultrasound of the liver showed portal vein thrombosis.
A routine echocardiography showed a huge homogeneous mass occupying the entire right atrium and prolapsing across the tricuspid valve into the right ventricle, with a normal left and right ventricular systolic function (Fig. ).
Patient was started on 60 mg of Lovenox every 12 h because a possibility of superimposed intracardiac tumor thrombus could not be excluded. On day 2 of the hospital stay, patient was found to be hypoxic and was started on 3 L of O2 per nasal cannula, with subsequent clinical improvement. Pulmonary embolism was ruled out. On day 12 of the hospital stay, patient developed altered mental status, with low blood pressure, tachycardia, tachypnea, and worsening hypoxia. Patient was afebrile, with no signs of heart failure at that time, and the patient's chest X-ray did not show any new infiltrates suggestive of pneumonia or pleural effusion. Patient was intubated; however, unfortunately he died on the 18th day of hospital stay.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [52, 'years'], 'Alanine aminotransferase': [146.0, 'U/L'], 'Aspartate aminotransferase': [413.0, 'U/L'], 'Platelet count': [233000.0, 'µL']}",7.62818,7.24677,8.00959,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 413.0 U/L.
The patient's concentration of ALT is 146.0 U/L.
The patient's concentration of platelets is 233000.0 count/µL. To convert 233000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 233000.0 platelets count/µL * 1000000.0 µL/L = 233000000000.0 platelets count/L. This means that there are 233000000000.0/(10^9) = 233.0 billion platelet counts per liter.
Plugging these values into the formula, we get (52 * 413.0)/(233.0 * sqrt(146.0)) = 7.62818.Hence, the Fibrosis-4 score is 7.62818."
4360,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-5265797-1,Extracted,"A 45-year-old male patient visited the emergency room (ER) because of lower chest discomfort starting 6 hours earlier. He also complained of thirst and limb numbness. His medical history included diabetes mellitus, bronchial asthma, and unstable angina for 4 years, 2 years, and 1 year, respectively. He had been taking aspirin (100 mg/d), clopidogrel (75 mg/d), atorvastatin (10 mg/d), and candesartan (8 mg/d) for 1 year without changes. He took those medicines on the morning of his admission. He regularly used a Symbicort Turbuhaler® (AstraZeneca Korea, Seoul, Republic of Korea) (160/4.5 μg) for asthma management. One month before the present admission, he discontinued the oral hypoglycemic agents prescribed by his primary physician. He denied recent alcohol consumption and had quit smoking 1 year earlier. Except for these symptoms, he initially had no complaints, such as muscular pain, fever, upper respiratory symptoms, or signs, on visiting the ER. He had no history of excessive physical activity or recent trauma.
On initial physical examination in the ER, his vital signs were as follows: blood pressure, 100/60 mm Hg; heart rate, 71 beats/min; respiratory rate, 20 times/min; and body temperature, 36.6 °C. On chest auscultation, no abnormal sounds, such as rales or wheezing, were audible, and his heartbeat was regular without murmur. His general skin turgor was decreased, and his tongue was dry. His conjunctivae were not anemic and sclerae were not icteric. There were no palpable lymph nodes in the head or neck area. Organomegaly was not seen in the abdomen. No pretibial pitting edema, muscular swelling, or skin color changes were detected on either lower extremity. There was no tenderness in the upper or lower extremities. His muscle power was within normal limits.
Compared with a previous ECG, the rhythm and voltage were unchanged. His initial troponin-I was less than 0.1 ng/mL, creatinine kinase (CK) was 144 U/L (0–190 U/L), lactate dehydrogenase (LDH) was 220 U/L (135–225 U/L), and CK-MB, subunit of CK, was 3.5 ng/mL. Other initial laboratory data were hematocrit 45% (39%–52%), hemoglobin 14.5 g/dL (13–17 g/dL), white blood cell count 11,280/mm3 (4000–10,000/mm3, neutrophils: 68.2%, lymphoid cells: 25.6%, and monocytes: 4.5%), and platelet count 256,000/mm3 (130,000–400,000/mm3). Liver function tests were as follows: alkaline phosphatase 84 IU/L (35–130 IU/L), aspartate aminotransferase (AST) 21 IU/L (0–37 IU/L), alanine aminotransferase (ALT) 42 IU/L (0–41 IU/L), and glucose 696 mg/dL. Hemoglobin A1c (HbA1c) was 9.3% (4.2%–5.9%). Blood urea nitrogen (BUN) and creatinine were 19.9 mg/dL (6.0–20.0 mg/dL) and 1.11 mg/dL (0.6–1.2 mg/dL), respectively. Electrolyte results were sodium 123 mmol/L (135–145 mmol/L), potassium 4.7 mmol/L (3.3–5.1 mmol/L), and chloride 80 mmol/L (98–110 mmol/L). Serum osmolality was 296 mOsm/kg. Urinalysis with micro revealed no protein or blood on a dipstick and red blood cell 1 to 4/high-power field.
Continuous intravenous insulin and hydration with normal saline were started. In addition, 40 mg of esomeprazole was infused intravenously under a suspicion of GERD. Glucose levels, measured by a blood sugar meter, decreased to 240 mg/dL and chest discomfort improved 6 hours after this management. In the mean time, there were no other oral, intramuscular, and intravenous drug therapies except for oral lactulose for his constipation. He felt mild discomfort in the right buttock at that time but did not complain to the medical team. However, he complained of severe right buttock pain 12 hours after the esomeprazole infusion. Tender muscle swelling of 8 cm in diameter was seen in the right buttock area and a reddish skin color change was noted (Fig. ). Serum CK and LDH levels increased to 40,533 and 1326 U/L, respectively, and AST and ALT levels also increased to 320 and 83 IU/L, respectively. BUN and creatinine levels were 23.9 and 1.49 mg/dL, respectively. We started vigorous hydration through isotonic saline infusion and urine alkalinization by intravenous bicarbonate infusion. Another 40 mg of esomeprazole was administered because we did not regard esomeprazole as the causative agent of the rhabdomyolysis at that time. Serum CK, LDH, AST, and ALT levels were 84,226, 1943, 603, and 171 IU/L, respectively, 24 hours later. On the third day in hospital, he was admitted to the nephrology ward. Esomeprazole was ended, and hydration and alkalinization were continued. Serum CK and LDH levels decreased gradually (Fig. A and B), and his muscular symptoms and swelling in the buttock area improved gradually. A bone scan using 20 mCi of 99mTc-hydroxymethylene diphosphonate was performed on the seventh day in hospital and revealed multiple and diffuse uptake in the soft tissues of the right buttock and both lower legs (Fig. ). His clinical manifestations and laboratory findings improved, so he was discharged on the 12th day. We added oral hypoglycemic agents, linagliptin 5 mg and metformin 500 mg, to his previous drugs (aspirin, clopidogrel, candesartan, and atorvastatin). He is being followed in our outpatient department with no recurrence of rhabdomyolysis at 6 months.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'years'], 'Alanine aminotransferase': [42.0, 'U/L'], 'Aspartate aminotransferase': [21.0, 'U/L'], 'Platelet count': [256000.0, 'µL']}",0.5696,0.54112,0.59808,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 21.0 U/L.
The patient's concentration of ALT is 42.0 U/L.
The patient's concentration of platelets is 256000.0 count/µL. To convert 256000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 256000.0 platelets count/µL * 1000000.0 µL/L = 256000000000.0 platelets count/L. This means that there are 256000000000.0/(10^9) = 256.0 billion platelet counts per liter.
Plugging these values into the formula, we get (45 * 21.0)/(256.0 * sqrt(42.0)) = 0.5696.Hence, the Fibrosis-4 score is 0.5696."
4361,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-5400514-1,Extracted,"A 47-year-old male presented with diarrhea and a worsening abdominal distention for three months. The physical examination was remarkable for muscle wasting and ascites. Laboratory analysis showed hemoglobin 7.2 g/dl, hematocrit 22.7%, mean corpuscular volume (MCV) 77.3 fl, platelets 172 thousand/mm3, serum albumin 1.9 g/dl, total protein 4.1 g/dl, bilirubin 0.3 mg/dl, alanine transaminase (ALT) 23 IU/L, aspartate aminotransferase (AST) 28 IU/L, international normalized ratio (INR) 1.2, iron 23 mcg/dl, and ferritin 24 ng/ml. Stool analysis was negative for blood, clostridium difficile, ova, and parasites. Urine analysis was negative for protein. Hepatitis viral serologies, immunoGlobulins A anti-tissue transglutaminase antibody (IgA-anti-tTG), antinuclear antibody (ANA), anti-mitochondrial antibody (AMA), and anti-smooth muscle antibodies (AMSA) were all negative. Alpha-1 antitrypsin and ceruloplasmin levels were normal. Ascitic fluid was clear with albumin 1.1 g/dl, protein 2.9 g/dl, and white blood cell (WBC) 63/mm3 with two percent granulocytes and 17% lymphocytes. Ascitic fluid was negative for any malignant cells. Serum-to-ascites albumin gradient was < 1.1 g/dl; therefore, ascites was less likely to be present due to portal hypertension. Echocardiography (ECG) showed ejection fraction of 60-65% with a pulmonary artery systolic pressure of 42 mmHg. Right heart catheterization showed mild pulmonary hypertension. The severity of ascites could not be explained by mild pulmonary hypertension. Upper gastrointestinal (GI) endoscopy and colonoscopy were normal. Therefore, no biopsies were performed. He had recurrent ascites that was managed periodically with therapeutic paracentesis and diuretics. After eight weeks, the patient became severely malnourished and he was started on total parenteral nutrition. As recurrent ascites could not be explained by mild pulmonary hypertension, a liver biopsy was performed. The liver biopsy was normal. Enteroscopy showed the erythematous, edematous duodenum and jejunum (Figure ).
The duodenal bulb was erythematous, which was normal in the initial upper GI endoscopy. Biopsy samples from the inflamed mucosa showed abundant periodic acid-Schiff stain (PAS) positive macrophages consistent with Whipple’s disease (Figure ).
The patient was started on intravenous (IV) ceftriaxone. During the hospital course, the patient’s diarrhea improved on ceftriaxone and he was discharged on a one-year course of co-trimoxazole.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [47, 'years'], 'Alanine aminotransferase': [23.0, 'U/L'], 'Aspartate aminotransferase': [28.0, 'U/L'], 'Platelet count': [172000.0, 'µL']}",1.59538,1.51561,1.67515,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 28.0 U/L.
The patient's concentration of ALT is 23.0 U/L.
The patient's concentration of platelets is 172000.0 count/µL. To convert 172000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 172000.0 platelets count/µL * 1000000.0 µL/L = 172000000000.0 platelets count/L. This means that there are 172000000000.0/(10^9) = 172.0 billion platelet counts per liter.
Plugging these values into the formula, we get (47 * 28.0)/(172.0 * sqrt(23.0)) = 1.59538.Hence, the Fibrosis-4 score is 1.59538."
4362,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-3214852-1,Extracted,"A 36-year-old male was admitted with a 3-day history of fever, jaundice, and vomiting. His medical history was unremarkable. On admission, he was alert and oriented. His vital signs were as follows: blood pressure, 120/90 mmHg; heart rate, 88 beats/min; respiratory rate, 18/min; and body temperature, 37.1℃. He had obvious jaundice and icteric sclera. The conjunctiva was not anemic. The liver and spleen were not palpable. His hemoglobin concentration was 17.1 g/dL, his red cell count was 5.74×106/µL, his white blood cell count was 5,000/µL, and his platelet count was 114,000/µL. Blood chemistry analyses revealed a total bilirubin level of 3.8 mg/dL; direct bilirubin, 2.39 mg/dL; AST, 7736 IU/L; ALT, 3558 IU/L; LDH, 14,407 IU/L; albumin, 3.8 g/dL; prothrombin time, 18.6 s (10.1-12.4 s); BUN, 50.9 mg/dL; and Cr, 5.7 mg/dL.
The test for hepatitis A virus IgM antigen was positive. Tests for hepatitis B surface antigen, and IgM anti-hepatitis B core, and anti-hepatitis C virus antibody were all negative. Tests for human immunodeficiency virus antibody and Epstein-Barr virus VCA IgM antibody were negative and parvovirus was undetectable by polymerase chain reaction. Tests for anti-nuclear antibody and rheumatoid arthritis factor were negative. C3 was 86.6 mg/dL, C4 was 53 mg/dL, IgG was 746 mg/dL, IgA was 442 mg/dL, and IgM was 469 mg/dL. Direct Coombs' test was positive and haptoglobin decreased to 3.5 mg/dL. The results of a chest X-ray, abdominal ultrasonography, and duodenoscopy were unremarkable.
He received hemodialysis treatment owing to acute renal failure three times a week from day 2. On day 4, he was diagnosed with hepatitis A and treated with fluid therapy. On admission, there was no sign of anemia, but his hemoglobin level had gradually decreased. No sign of gastrointestinal bleeding was observed. On day 23, his hemoglobin level had dropped to 4.8 g/dL and his reticulocyte count had significantly decreased to 0.13%. The peripheral blood smear showed microcytic, normochromic anemia with anisopoikilocytosis. A total of 6 U of red cells were administered for 3 days. Bone marrow biopsy and aspiration were performed on day 25. The bone marrow biopsy showed 50% cellularity and the myeloid:erythroid ratio was 16.1:1. Marked hypoplastic erythropoiesis was observed (). A paucity of erythroid precursors was noted, although granulopoiesis was normal in number and maturation. Megakaryocytes were normally observed (). Differential erythroid cell counts of aspirates were as follows: pronormoblast, 1.4%; basophilic normoblast, 2.4%; polychromatic normoblast, 0.0%; and orthochromatic normoblast, 0.0%.
As a result of these findings, he was diagnosed with pure red cell aplasia associated with acute hepatitis A. He began treatment with intravenous methylprednisolone (1 mg/kg/day) daily at day 29. After the steroid therapy, his hemoglobin level and renal function began to improve steadily. Hemodialysis was stopped on day 34, and the hemoglobin level had increased to 8.3 g/dL on discharge. Methylprednisolone was tapered by 10 mg every week until discharge. One month after discharge, the prednisolone dose was tapered to 10 mg in the outpatient clinic. On day 48 after discharge, prednisolone treatment was stopped, because the hemoglobin level had improved to 13.9 g/dL and the Cr level had decreased to 1.3 mg/dL ().",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [36, 'years'], 'Aspartate aminotransferase': [7736.0, 'U/L'], 'Alanine aminotransferase': [3558.0, 'U/L'], 'Platelet count': [114000.0, 'µL']}",40.9554,38.90763,43.00317,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 7736.0 U/L.
The patient's concentration of ALT is 3558.0 U/L.
The patient's concentration of platelets is 114000.0 count/µL. To convert 114000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 114000.0 platelets count/µL * 1000000.0 µL/L = 114000000000.0 platelets count/L. This means that there are 114000000000.0/(10^9) = 114.0 billion platelet counts per liter.
Plugging these values into the formula, we get (36 * 7736.0)/(114.0 * sqrt(3558.0)) = 40.9554.Hence, the Fibrosis-4 score is 40.9554."
4363,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-2580005-1,Extracted,"A 47-yr-old male patient came to our emergency center due to fever, chill, myalgia, nausea, vomiting and skin rash on both forearms for 6 hr after antiparasitic drug ingestion 2 days before. He received medication for common cold at local clinic for 2 days but showed no improvement of the symptoms. There was no history of specific medication. He was a social alcohol drinker and had a previous history of admission due to unknown origin hepatitis 3 yr before at our hospital, which the patient correlated with albendazole ingestion. The initial vital signs were blood pressure 150/70 mmHg, heart rate 72/min, respiratory rate 20/min and body temperature 38.3℃. He had no recent history compatible with acute hypotension or having underlying heart disease. In the physical examination liver was not palpable, liver percussion span was normal and there was no remarkable finding except icteric sclerae. In laboratorial analysis WBC was 6,790/µL (eosinophil 8.2%), hemoglobin 15.7 g/dL, and platelet 147,000/µL showing mild increase of eosinophil count. Prothrombin time 17.4 sec (INR 1.44), AST 5,402 IU/L, ALT 4,622 IU/L, alkaline phosphatase 40 IU/L, total bilirubin 2.8 mg/dL, r-GTP 101 IU/L, LDH 8,799 IU/L, total protein 6.9 g/dL, albumin 4.0 g/dL, serum glucose 115 mg/dL, and BUN/Cr, 19/1.1 mg/dL. IgM anti-HAV, HBsAg, IgM anti-HBc and anti-HCV Antibodies were negatives. Anti-CMV, anti-EBV, and anti-HSV were also negatives. Antinuclear antibody was weakly positive with homogeneous pattern and anti-mitochondrial antibody, anti-smooth muscle antibody were negative. The level of copper (urine) was 48.40 g/day, ceruloplasmin 26.1 mg/dL, IgG 1,313.2 mg/dL, and IgM 56.2 mg/dL showing normal values. Liver sonography showed no significant abnormality except increased liver echogenicity. Sonography-guided liver biopsy showed periportal invasion of inflammatory cells, cytotoxic necrosis and different sizes of steatosis (, ). We suspected drug-induced hepatitis due to albendazole. And after a new interrogation of his past medical history, we knew that he had a previous history of albendazole ingestion before hospital admission due to unknown origin toxic hepatitis 3 yr previously. We diagnosed the patient as toxic acute hepatitis due to the Council for International Organizations of Medical Sciences (CIOMS) score of 9 and performed conservative medical treatment. The patient showed rapid improvement of liver function test with AST 35 IU/L, ALT 301 IU/L, alkaline phosphatase 45 IU/L and total bilirubin 0.8 mg/dL on 8th day of admission. The patient was discharged and on follow-up at the outpatient department without significant symptoms.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [47, 'years'], 'Alanine aminotransferase': [4622.0, 'U/L'], 'Aspartate aminotransferase': [5402.0, 'U/L'], 'Platelet count': [147000.0, 'µL']}",25.40505,24.1348,26.6753,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 5402.0 U/L.
The patient's concentration of ALT is 4622.0 U/L.
The patient's concentration of platelets is 147000.0 count/µL. To convert 147000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 147000.0 platelets count/µL * 1000000.0 µL/L = 147000000000.0 platelets count/L. This means that there are 147000000000.0/(10^9) = 147.0 billion platelet counts per liter.
Plugging these values into the formula, we get (47 * 5402.0)/(147.0 * sqrt(4622.0)) = 25.40505.Hence, the Fibrosis-4 score is 25.40505."
4364,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-6855017-1,Extracted,"A 78-year old Caucasian female with a history of well-controlled type 2 diabetes mellitus, and essential hypertension reported the presence of jaundice and acholic stools for one week. She denied any fever, abdominal pain, pruritus or changes in her bowel habits. She denied any consumption of alcohol as well as the use of any analgesics or antibiotics. She also denied any history of travel outside Michigan, United States of America. Her medications included aspirin (81 mg), citalopram, losartan, metformin, and oxybutynin, all of which she has taken for at least one year. She also took simvastatin for 2 years with no adverse effects but had replaced it a month prior to her presentation with a once daily over the counter curcumin supplement without seeking medical advice.
On physical examination, her blood pressure was 126/65 mmHg, her heart rate 66 beats/min, and her temperature 36.6°C. She appeared in no acute distress and was jaundiced. No hepatosplenomegaly, ascites, asterixis, encephalopathy, or other stigmata of chronic liver disease were noted on physical examination.
Her laboratory results showed a white blood cell count of 5,300 cells/mm3 with a normal differential, hemoglobin of 12.6 g/dl, platelet count of 282,000 cells/mm3, blood urea nitrogen of 11 mg/dl, creatinine of 0.59 mg/dl, alkaline phosphatase (ALP) of 171 U/L (lab normal: 33–120 U/L), aspartate aminotransferase (AST) of 581 U/L (lab normal: 0–34 U/L), alanine aminotransferase (ALT) of 609 U/L (lab normal: 9–47 U/L), total bilirubin of 12.8 mg/dl, direct bilirubin of 7.4 mg/dl, international normalized ratio (INR) of 1.1, serum albumin of 4.5 g/dl, and thyroid stimulating hormone (TSH) level of 1.99 mU/L. Liver chemistries from 5-years ago were normal (ALP: 101 U/L, AST 13 U/L, ALT 19 U/L, total bilirubin 0.3 mg/dl). Her R-factor was calculated at 15 consistent with a hepatocellular pattern of liver injury. Hepatitis A, B, C, and cytomegalovirus serologies were negative. Epstein-Barr virus and herpes simplex virus-1 serologies indicated previous exposures. Hepatitis E testing was not obtained given the patient had no exposure to jaundiced individuals, no recent travel history, and lived in a nonendemic country. Serum IgG level was 951 mg/dl (lab normal: 550–1650 mg/dl) with normal subclass levels. Antinuclear antibody (ANA) titers were 1 : 320 with a speckled pattern, and anti-smooth muscle antibody (ASMA) titers were 1 : 20. Anti-LKM (liver-kidney-microsomal) and antimitochondrial antibodies (AMA) were negative. Ferritin level was 689 ng/ml with a transferrin saturation of 32%. An abdominal ultrasound demonstrated a normal hepatic echotexture and incidental cholelithiasis. A magnetic resonance cholangiopancreaticogram (MRCP) revealed no additional findings.
A liver biopsy was planned if no improvement in the patient's liver chemistries was noted. Her liver function tests on day 7 of her admission showed an improvement of >40% in her ALT and AST, and so a biopsy was deferred. The curcumin supplement was discontinued on admission to the hospital, and the remainder of her medications continued except for simvastatin which wasn't restarted. A follow-up visit 42 days from the initial presentation showed complete resolution of her jaundice, and repeat labs showed normalization of her liver enzymes. The patient was instructed to avoid the curcumin supplement and no re-challenge was performed. No immunosuppressive treatments were initiated at any point during her management. The curcumin supplement the patient was taking was reviewed, and the label reported the following ingredients; 500 mg of curcumin; bovine gelatin; less than 2% of silica; and vegetable magnesium stearate. Follow-up liver enzymes two months and at 18 months from presentation remained normal. A trend of the patient's liver chemistries was summarized in Figures and .",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [78, 'years'], 'Alanine aminotransferase': [609.0, 'U/L'], 'Aspartate aminotransferase': [581.0, 'U/L'], 'Platelet count': [282000.0, 'µL']}",6.51198,6.18638,6.83758,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 581.0 U/L.
The patient's concentration of ALT is 609.0 U/L.
The patient's concentration of platelets is 282000.0 count/µL. To convert 282000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 282000.0 platelets count/µL * 1000000.0 µL/L = 282000000000.0 platelets count/L. This means that there are 282000000000.0/(10^9) = 282.0 billion platelet counts per liter.
Plugging these values into the formula, we get (78 * 581.0)/(282.0 * sqrt(609.0)) = 6.51198.Hence, the Fibrosis-4 score is 6.51198."
4365,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-2816294-1,Extracted,"A 55-yr-old man was admitted to our hospital because of oliguria and progressive proximal muscle weakness of the lower limbs. Two weeks earlier, prior to admission into the hospital, he felt fine. He began experiencing chill, malaise and myalgia. The patient complained of right upper quadrant abdominal pain. Past medical history was not contributory. The patient denied ethanol ingestion and recent use of drugs. He also denied any traumatic injury. On physical examination, he looked acutely ill. Temperature was 36.7℃, respiration rate 24/min, and blood pressure 110/70 mmHg. Auscultation of the heart and both lungs were normal. The abdomen was soft. The edge of the liver descended 3 cm below the right costal margin. Proximal muscle weakness was marked and muscle power was grade 3 for the lower limbs and grade 4 for the upper limbs. The laboratory investigations were as follows: WBC count 12,700/µL (segmented neutrophil 81%), hemoglobin 13.9 g/dL, platelet 189,000/µL, total protein 6.8 g/dL, albumin 3.0 g/dL, AST 1,074 U/L, ALT 764 U/L, alkaline phosphatase 82 IU/L, GGT 38 U/L, total bilirubin 1.0 mg/dL, international normalized ratio for prothrombin 1.6, BUN 99 mg/dL, creatinine 9.1 mg/dL, calcium 6 mg/dL, phosphorus 7.6 mg/dL, ionized calcium 0.7 mmol/L (normal 1.05-1.35 mmol/L), intact parathyroid hormone 201.87 pg/mL (normal 12-72 pg/mL). erythrocyte sedimentation rate 55 mm/hr, C-reactive protein 200 mg/dL, creatine kinase 40,000 U/L, LDH 3,286 U/L, serum aldolase 66 sigma U/mL, serum myoglobin 1,140 ng/mL, and urine myoglobin 948 ng/mL. Urinalysis revealed 10-20 RBC per high power field. Urine myoglobin was positive and urine hemoglobin was negative. Tests for anti-HBs, anti-HCV, anti-HAV, anti-HIV, rheumatoid factor, anti-nuclear antibody, anti-dsDNA antibody, anti-neutrophil cytoplasmic antibody, anti-Jo-1 antibody were all negative. Serum levels of complements and alpha-fetoprotein were normal. Hypercalcemia appeared on day 14 and lasted for 28 days. The serum level of intact PTH measured on the 37th hospital day was 5.81 pg/mL. A chest radiograph showed bilateral pleural effusion. Computed tomography of the abdomen demonstrated a 6 cm sized-exophytic bulging mass in the hepatic angle. Two smaller satellite nodules near the main hepatic mass and several enlarged intraperitoneal lymph nodes were also detected. A radionuclear bone scan image showed increased uptake of radioisotope in the most of the skeletal muscles including the both lower limbs, indicative of inflammatory myopathy or rhabdomyolysis. Fat suppressed T2-weighted MR imaging of the thigh showed high signal intensity and gadolinium enhancement along the whole length of vastus muscle group, biceps femoralis and adductor longus. Needle electromyography showed spontaneous activity of fibrillations, sharp positive waves, polyphasic motor unit potentials of low amplitude, and short duration in all muscle fibers during voluntary contraction. The muscle biopsy was obtained from the left thigh and showed extensive myofiber necrosis with heavy infiltration of macrophages within necrotic fibers, multifocal calcifications in myofibers, and multifocal lymphocytic infiltrations in endomysium (). The emergent hemodialysis was initiated with a tentative diagnosis of ARF. After 15 days with hemodialytic support, his renal function was gradually restored to allow withdrawal of dialysis. The liver biopsy was performed on the 20th day of hospitalization under ultrasonographic guidance. Immunohistochemical stain of biopsied tissue showed positive for AFP and negative for CEA, and poorly differentiated HCC was diagnosed (). Under the diagnosis of PM, our patient was put on methylprednisolone (1 mg/kg/day) concurrently with hemodialysis. Treatment was switched to oral prednisolone and persisted for following 5 weeks. However, muscle power did not improve significantly. Chemotherapy for HCC was considered, but the patient had an episode of hemorrhagic shock from a sudden rupture of hepatic mass on the 44th day of hospitalization. He progressively deteriorated and remained in an unstable condition until he passed away on the 54th day.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'Alanine aminotransferase': [764.0, 'U/L'], 'Aspartate aminotransferase': [1074.0, 'U/L'], 'Platelet count': [189000.0, 'µL']}",11.30729,10.74193,11.87265,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 1074.0 U/L.
The patient's concentration of ALT is 764.0 U/L.
The patient's concentration of platelets is 189000.0 count/µL. To convert 189000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 189000.0 platelets count/µL * 1000000.0 µL/L = 189000000000.0 platelets count/L. This means that there are 189000000000.0/(10^9) = 189.0 billion platelet counts per liter.
Plugging these values into the formula, we get (55 * 1074.0)/(189.0 * sqrt(764.0)) = 11.30729.Hence, the Fibrosis-4 score is 11.30729."
4366,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-2729907-1,Extracted,"A 23-yr-old woman with type 2 DM and Graves' disease has revisited to the Department of Emergency of Gyeongsang National University Hospital due to nausea, generalized weakness, polyuria and weight loss of 5 kg for 7 days in October 2003 since she was discharged from our hospital three weeks before. She was previously diagnosed as type 2 DM in 1996, and recently started insulin treatment to improve glycemic control due to persistently elevated HbA1c irrespective of oral administration of hypoglycemic agents. Three years before, she had taken propylthiouracil for hyperthyroid Graves' disease for 2 yr. In May 2003, she was diagnosed as relapse of hyperthyroidism at a local clinic and referred to our hospital for management of thyrotoxicosis refractory to usual dosage of propylthiouracil, 300 mg/day and proliferative diabetic retinopathy and nephropathy. She had 7.9 mM/L fasting blood glucose, 1.07 nM/L C-peptide (reference range [RR], 0.1-0.83), 222 mM/L fructosamine (RR, 205-285), 8.3% HbA1c (RR, 4.5-5.6) and 0.01 mU/L TSH and 2.02 pM/L free T3 on thryoid function tests. At that time, Her weight was 54 kg and height was 147 cm (body mass index, 25.0 kg/m2). Her thyroid had the volume of about 40 g and it looked diffusely enlarged and rubbery consistency on palpation. The technetium-99m (Tc-99m) thyroid scan revealed marginally increased and somewhat irregular uptake (3.8%). As from hospitalization, the patient had oral administration of relatively high dose of methimazole (60 mg daily), propranolol (160 mg daily) and 12 drops of Lugol's solution (three times a day) for 14 days, and consecutively lithium carbonate (900 mg daily) for 14 days because of persisting tachycardia (>110/ min), dyspnea on exertion and still high concentration of free T3 (4.44 pM/L). She was discharged with receiving methimazole (60 mg daily) and beta-blocker ().
She had no family history of thyroid disease, but both parents have been suffering from type 2 DM. She denied ingestion of any drugs including alcohol or excessive consumption of fizzy drinks these days. She also has been adhering to administration of antithyroid drug, beta-blocker and insulin (0.5 units/kg/day) since being discharged. On physical examination, the patient had 143/89 mmHg blood pressure, 36.8℃ body temperature, 22/min respiration rate, and 121/min pulse rate. She looked acutely ill, and had slightly tremulous, warmhands, and decreased skin turgor and dried tongue. She was 48 kg weight and body mass index 22.2 kg/m2. Exophthalmos was not present. The abdomen was soft and flat, and liver and spleen were not palpable.
On admission, her laboratory findings were as follows; hemoglobin 12.3 g/dL, WBC 8.65×109/L (segmented neutrophil 58%, lymphocyte 29%), platelet 398×109/L, total protein 65 g/L, albumin 32 g/L, ALP 3.47 ukat/L, AST 0.42 ukat/L, ALT 0.6 ukat/L, BUN 9.2 mM/L and creatinine 88.7 µM/L. Levels of blood glucose (32.7 mM/L) and fructosamine (396 mM/L) were elevated. Her serum electrolytes and blood gas parameters were as follows: sodium 144.1 mM/L, potassium 5.4 mM/L, chloride 102 mM/L, calcium 2.5 mM/L, phosphorus 1.0 mM/L, pH 7.32, pCO2 35 mmHg, pO2 98 mmHg, and bicarbonate 16 mM/L. The fasting serum C-peptide was 0.44 nM/L. Serum anion gap was 20.9 and osmolarity was calculated as 321 mosm/kg. Amylase and lipase levels were normal and anti-GAD antibody was negative. Thyroid function tests revealed that the patient had more aggravated hyperthyroid state; 0.01 mU/L TSH, 2.78 pM/L free T3 and 45.38 pM/L free T4 (RR, 11.41-23.08) than when she was hospitalized two weeks before (0.12 mU/L TSH, 1.41 pM/L free T3 and 30.26 pM/L free T4). TSH-receptor antibody level was 26.3 IU/L (RR, <1) and antimicrosomal antibody was 29.3 U/mL (RR, <60). The Tc-99m scan showed still enlarged thyroid with more increased uptake 6.5% than previous uptake scan (3.8%) performed taking propylthiouracil two months before. Based on above results, the patient was diagnosed as HHS accompanying mild ketosis on type 2 DM and aggravated Graves' hyperthyroidism. We treated her with intravenous insulin injection and large volume of intravenous fluid administration. And also, she took high dose of methimazole (90 mg daily, six times a day) and beta-blockers. On the second day, nausea and generalized weakness have been improved.
At two months after acute presentation, we measured levels of C-peptide after 75 g glucose loading; 0 min (0.12 nM/L), 30 min (0.74 nM/L), 60 min (1.02 nM/L), 90 min (1.49 nM/L) and 120 min (1.32 nML). Throughout follow-ups for 2 months, she took insulin (0.9 units/kg/day), metformin (1,500 mg daily) and methimazole (45 mg daily). The mean fasting capillary blood glucose level on self monitoring was rather elevated than the target, but free T3 level became normalized ().",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [23, 'years'], 'Aspartate aminotransferase': [0.42, 'U/L'], 'Alanine aminotransferase': [0.6, 'U/L'], 'Platelet count': [398000000.0, 'L']}",31.33419,29.76748,32.9009,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 0.42 U/L.
The patient's concentration of ALT is 0.6 U/L.
The patient's concentration of platelets is 398000000.0 count/L. This means that there are 398000000.0/(10^9) = 0.398 billion platelet counts per liter.
Plugging these values into the formula, we get (23 * 0.42)/(0.398 * sqrt(0.6)) = 31.33419.Hence, the Fibrosis-4 score is 31.33419."
4367,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4217349-1,Extracted,"A 31-year-old African-American man underwent orthotopic liver transplantation 10 years ago for primary sclerosing cholangitis (PSC). He had moderate acute cellular rejection five months after the transplant but had no history of any transplant-related infections. He presented to the emergency department with a one-week history of lower abdominal pain and dysuria. His past medical history was pertinent for ulcerative colitis and type 2 diabetes mellitus. He had been hospitalized multiple times in the past year for abdominal pain. Extensive investigation had shown partial small bowel obstruction caused by intussusception that was treated conservatively, in addition to chronic elevation of total bilirubin, alkaline phosphatase, and transaminases attributed to possible recurrence of PSC in the hepatic graft. At the time of suspicion of possible PSC recurrence, his prednisone dosage had been increased and later tapered when liver function studies improved. He had last been admitted to the hospital 2 weeks earlier for diarrhea and fever, diagnosed with Clostridium difficile infection (CDI), and discharged 10 days prior with oral vancomycin. At the time of current presentation, his immunosuppression regimen included tacrolimus 1 mg twice daily, mycophenolate mofetil 500 mg twice daily, and prednisone 5 mg daily. He reported temporal insertion of indwelling urinary catheters during some of his previous hospital admissions for management of small bowel obstruction. Otherwise, he denied any intravenous (IV) drug use, history of urethral instrumentation, or chronic indwelling urinary catheters. His vital signs on admission revealed blood pressure 134/68 mmHg, heart rate 80 beats per minute, 20 respirations per minute, and temperature 98.5°F. On physical exam, his abdomen was soft with mild tenderness to palpation in the left lower quadrant. Rectal exam revealed a normal-sized, painless prostate with fluctuation at the right base. Laboratory investigation showed white blood cell count of 22,600/μL (94% neutrophils, 2% lymphocytes, 1% bands), hemoglobin 12.3 g/dL, and platelet count 309,000/μL. Biochemistry tests revealed creatinine 1.2 mg/dL, alanine aminotransferase 199 U/L, aspartate aminotransferase 157 U/L, alkaline phosphatase 719 U/L, and total bilirubin 18.3 mg/dL (direct bilirubin 15.6 mg/dL), which were unchanged compared to previous laboratory results. Human immunodeficiency virus (HIV) antibody was negative. Urinalysis showed 11–20 white blood cells/high power field (HPF), 0–2 red blood cells/HPF, few bacteria, and no casts. Contrast-enhanced computed tomography (CT) of the abdomen and pelvis revealed multiple stable areas of intussusception and a 3.0 cm × 1.9 cm prostatic abscess (Figures and ). We empirically treated for infection with IV ceftriaxone and vancomycin. MRSA was isolated from both urine (<10,000 CFU/mL) and 2 sets of blood cultures (aerobic and anaerobic bottles) obtained upon admission. Cultures were sensitive to daptomycin, clindamycin, gentamycin, rifampin, tetracycline, levofloxacin, trimethoprim-sulfamethoxazole, and vancomycin (MIC < 0.5). Both transthoracic and transesophageal echocardiography were negative for vegetations. Based on his recent hospitalizations, he was diagnosed with health-care associated MRSA bacteremia. Detailed review of his hospital records revealed that colonization with MRSA had been detected 2 weeks prior in a nasal swab sample and treated accordingly with topical chlorhexidine and mupirocin. A final diagnosis of MRSA prostatic abscess with bacteremia was made. Due to his immunosuppression and bacteremia, it was decided that he was not a candidate for oral antibiotics. IV vancomycin was continued while ceftriaxone was stopped. We opted for conservative management in this case, which showed rapid improvement of symptoms and inflammatory response. Therefore, abscess aspiration was not deemed necessary. We also continued oral vancomycin to complete 14 days of treatment for CDI. The same dosage of immunosuppressant medications was continued, with the exception of tacrolimus, which was held due to acute kidney injury. Leukocytosis resolved at day 3 while symptoms started to improve at day 5. Repeat blood cultures at day 4 were negative. Urine cultures failed to grow any organism at day 11 of active therapy. His creatinine rose to 1.6 mg/dL and IV vancomycin was switched to daptomycin on day 12 of treatment. He was discharged from the hospital at day 22, with instructions to continue daptomycin for a total of 6 weeks of antibiotics. During a follow-up clinic appointment at 8 weeks after completion of antibiotics, his symptoms were resolved, cultures were negative, and repeat CT of the abdomen and pelvis showed complete resolution of the prostatic abscess (Figures and ).",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [31, 'years'], 'Alanine aminotransferase': [199.0, 'U/L'], 'Aspartate aminotransferase': [157.0, 'U/L'], 'Platelet count': [309000.0, 'µL']}",1.11655,1.06072,1.17238,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 157.0 U/L.
The patient's concentration of ALT is 199.0 U/L.
The patient's concentration of platelets is 309000.0 count/µL. To convert 309000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 309000.0 platelets count/µL * 1000000.0 µL/L = 309000000000.0 platelets count/L. This means that there are 309000000000.0/(10^9) = 309.0 billion platelet counts per liter.
Plugging these values into the formula, we get (31 * 157.0)/(309.0 * sqrt(199.0)) = 1.11655.Hence, the Fibrosis-4 score is 1.11655."
4368,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-3540342-1,Extracted,"A 36-year-old woman presented at our institution (Gachon University Gil Hospital) with erythematous confluent maculopatches on her face, trunk, and palms; jaundice; fatigue; pruritus; and aggravation of skin lesions over the previous week. She had been previously diagnosed as having erythema multiforme 2 weeks earlier at a private dermatology clinic and had also been administered dapsone with oral antihistamines (mequitazine and cetirizine) and topical corticosteroid for 8 months.
On admission, her vital signs were a blood pressure of 110/70 mm Hg, heart rate of 78 beats/min, respiratory rate of 18 breaths/min, and body temperature of 38.8℃. She reported no night sweats, loss of weight, or arthralgia. A physical examination conducted at presentation revealed bilateral, multiple enlarged lymph nodes on both sides of the neck with splenomegaly. All of the nodes were non-tender, firm, and measured 0.5 cm to 1.0 cm in diameter. Laboratory tests results were as follows: Hb 11.2 g/dL, white blood cell 13,070/mm3 (segmented neutrophils 24%, lymphocytes 66.3%, and eosinophils 0.1%), platelets 245,000/mm3, total bilirubin 5.4 mg/dL, direct bilirubin 3.8 mg/dL, aspartate aminotransferase/alanine aminotransferase (AST/ALT) 233/366 U/L, lactate dehydrogenase 1,610 IU/L (normal range, 200 to 485 IU/L), and an international normalized ratio of 1.25. She was negative for hepatitis B surface antigen, anti-hepatitis C virus Ab, and anti-human immunodeficiency Ab, but positive for hepatitis B surface antibody; and positive for anti-nuclear Ab, but negative for rheumatoid factor, anti-neutrophil cytoplasmic Ab, anti-Ro (SS-A, B) Ab, and anti-smith Ab. Serology tests showed no evidence of active Epstein-Barr virus (EBV) infection and no bacterial growth was found during a blood culture study. There was no hypergammaglobulinemia.
An excisional biopsy of a 1.0 cm cervical node showed diffuse polymorphic lymphoid hyperplasia with effacement of the normal architecture and abundant high endothelial venules; the cellular infiltrate was polymorphic, with abundant transformed lymphocytes and plasma cells (). Sinuses were frequently recognizable, but reactive germinal centers were not found.
Immunohistochemically, the majority of infiltrating atypical lymphocytes were CD3+ T-cells (), and some activated large cells were reactive for CD30 (). Follicular dendritic cell meshworks expressing CD21 were expanded (), and infiltrating atypical T-cells were negative for CD10, BCL-6, and EBV by in situ hybridization. For a definitive diagnosis, a molecular study on the rearrangement of the T-cell receptor (TCR)-gamma gene was performed and showed polyclonality (). An IgH gene rearrangement study also showed polyclonality.
An abdomino-pelvic computed tomography (CT) scan revealed splenomegaly (14 cm), an enlarged portocaval lymph node (1.7 cm), and gallbladder wall edema (). No evidence of lymphomatous involvement was found by chest CT or a bone marrow trephine biopsy.
Because aggravation of the skin eruption persisted and the liver function test remained abnormal, the possibility of DHS (exfoliative dermatitis, acute hepatitis, and multiple lymphadenopathy) was raised. The findings of a transjugular liver biopsy were compatible with drug-induced hepatitis manifesting as granulomatous inflammation (). No evidence of lymphomatous hepatic involvement was found. In view of her skin lesions, medication history, and age, we concluded that the cervical lymphadenopathy was actually pseudolymphoma. Accordingly, low dose prednisolone (30 mg/day) per os was started after transjugular liver biopsy to relieve the dapsone-induced skin lesions and hepatitis. Gradually, the skin lesions improved and the cervical lymph node enlargement regressed. Her total bilirubin, AST, and ALT values also normalized after 3 weeks of prednisolone, which was then tapered over a month. Follow-up CT scans conducted 3 and 6 months after presentation showed that the size of the cervical lymph nodes and spleen had normalized, and produced no other findings suggestive of lymphoma progression ().",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [36, 'years'], 'Aspartate aminotransferase': [233.0, 'U/L'], 'Alanine aminotransferase': [366.0, 'U/L'], 'Platelet count': [245000.0, 'µL']}",1.78958,1.7001,1.87906,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 233.0 U/L.
The patient's concentration of ALT is 366.0 U/L.
The patient's concentration of platelets is 245000.0 count/µL. To convert 245000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 245000.0 platelets count/µL * 1000000.0 µL/L = 245000000000.0 platelets count/L. This means that there are 245000000000.0/(10^9) = 245.0 billion platelet counts per liter.
Plugging these values into the formula, we get (36 * 233.0)/(245.0 * sqrt(366.0)) = 1.78958.Hence, the Fibrosis-4 score is 1.78958."
4369,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-7417490-1,Extracted,"A 71 year old man with a medical history of alcohol abuse, diabetes mellitus, essential hypertension, and depression was admitted to the intensive care unit suffering from dyspnea, productive cough, hematemesis, and black colored stools. Physical examination revealed the patient in poor general condition; hypotensive with blood pressure 87/50 mm Hg, pulse 106 b.p.m, a temperature of 37.8 C and saturating 100% on 3 liters of oxygen. Laboratory tests showed hemoglobin 7.9 gram/deciliter (g/dl), leukocytes 7.9 kilo/microliter (k/uL), platelets 155 k/uL , sodium 129 mg/dL , potassium 3.4 millimole/liter (mmol/L) , BUN 22 mg/dL, creatinine 0.96 mg/dL, glucose 150 mg/dl, anion gap 25 mmol/L, lactic acid 5.3, ALT 44 units/liter (U/L), AST 74 U/L, total bilirubin 2.25 mg/dL, international normal ratio (INR) 1.6 and urine ketones negligible.
Blood pressure responded to intravenous (IV) hydration 30ml/kg. The patient was started on IV Rocephin,and azithromycin for pneumonia based on symptoms and chest XR showing right lower lung infiltrates. The patient has suspected bleeding from esophageal varices, an indication of heavy alcohol abuse. He was started on proton pump inhibitors and an octreotide drip was administered.
Esophagogastroduodenoscopy (EGD) revealed circumferential, diffuse, friable mucosa extending from the proximal esophagus to the distal esophagus with sharp demarcation at the esophagogastric junction (GEJ) ().
There were areas of black appearing esophageal mucosa in the distal esophagus. The gastric exam showed mild areas of erythema in the body but no Wischnewsky lesions, in other words gastric mucosal petechial hemorrhages. The duodenum revealed an area of semi-lunar ulceration in the bulb and several areas of ulceration/semi-circumferential with a black eschar-like appearance at the ulcerative base in the second and third part of the duodenum ().
Proton pump inhibitors continued, while octreotide drip was discontinued. Abdominal and pelvic CT with contrast was unremarkable for any thrombosis. It showed hepatic steatosis. The patient continued to improve on symptomatic management. One week later, a repeat EGD showed improving esophagitis and duodenum ulcers. Black discoloration of esophagus and duodenum was resolved. The patient continued to improve and was discharged.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [71, 'years'], 'Alanine aminotransferase': [44.0, 'U/L'], 'Aspartate aminotransferase': [74.0, 'U/L'], 'Platelet count': [155000.0, 'µL']}",5.11013,4.85462,5.36564,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 74.0 U/L.
The patient's concentration of ALT is 44.0 U/L.
The patient's concentration of platelets is 155000.0 count/µL. To convert 155000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 155000.0 platelets count/µL * 1000000.0 µL/L = 155000000000.0 platelets count/L. This means that there are 155000000000.0/(10^9) = 155.0 billion platelet counts per liter.
Plugging these values into the formula, we get (71 * 74.0)/(155.0 * sqrt(44.0)) = 5.11013.Hence, the Fibrosis-4 score is 5.11013."
4370,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4025146-1,Extracted,"A 50-year-old Japanese woman was referred to Chiba University Hospital in April 2012 because of jaundice and abnormal liver tests. She took several drugs for her depression and hypertension and drank alcohol (∼90 g daily). One year before admission, she had had a history of DILI by mianserin for her depression. Her height and body weight were 152 cm and 55 kg, respectively. She did not have hepatic encephalopathy. Laboratory findings were as follows: white blood cell count 7,100/μl (eosinophils 0.8%), platelets 155,000/μl, prothrombin time 18% (INR 2.36), total protein 5.3 g/dl, total bilirubin 21.9 mg/dl (direct bilirubin 15.0 mg/dl), alkaline phosphatase 313 IU/l, aspartate aminotransferase (AST) 314 IU/l, alanine aminotransferase (ALT) 112 IU/l, and γ-glutamyl transpeptidase 190 IU/l. Serum immunoglobulin G of 1,695 mg/dl and immunoglobulin M of 116 mg/dl were normal, but antinuclear antibody (ANA) was not positive (×80). Virus serology was negative for hepatitis A, B, C and E viruses, cytomegalovirus and Epstein-Barr virus acute infection. Computed tomography and abdominal ultrasound findings showed a non-atrophic liver with slightly ascites. We suspected a diagnosis of DILI or AIH, although her AIH score was underscored [, ], and administered corticosteroids. She was given bed rest and peripheral parenteral nutrition.
After 2 weeks, AST (73 IU/l), ALT (136 IU/l), total bilirubin (3.4 mg/dl) and prothrombin time (92%) were improved and liver biopsy was performed to diagnose her disease (fig. ). Hepatic architecture was preserved without cirrhosis, and inflammation of the periportal area was obvious with centrilobular necrosis. There were mononuclear cells in the portal area, but marked plasma cell infiltration was not observed. This observation might have been affected by the corticosteroid therapies. We diagnosed her as acute exacerbation of chronic hepatitis of unknown etiology. After ∼1 month, she was discharged (AST 22 IU/l, ALT 56 IU/l, total bilirubin 1.8 mg/dl and prothrombin time 98%). Two months later, her liver test had suddenly deteriorated (AST 76 IU/l, ALT 249 IU/l and γ-glutamyl transpeptidase 1,262 IU/l). At the same time, we became aware of her alcohol consumption and she was diagnosed with alcohol dependence by a psychiatrist.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [50, 'years'], 'Aspartate aminotransferase': [314.0, 'U/L'], 'Alanine aminotransferase': [112.0, 'U/L'], 'Platelet count': [155000.0, 'µL']}",9.57104,9.09249,10.04959,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 314.0 U/L.
The patient's concentration of ALT is 112.0 U/L.
The patient's concentration of platelets is 155000.0 count/µL. To convert 155000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 155000.0 platelets count/µL * 1000000.0 µL/L = 155000000000.0 platelets count/L. This means that there are 155000000000.0/(10^9) = 155.0 billion platelet counts per liter.
Plugging these values into the formula, we get (50 * 314.0)/(155.0 * sqrt(112.0)) = 9.57104.Hence, the Fibrosis-4 score is 9.57104."
4371,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-5305665-1,Extracted,"A 35-year-old Asian man was referred to Good Gang-An Hospital mainly because of intermittent pruritus and fatigue that lasted for two months. The patient was suspected to be in the window period of hepatitis B based on the detection of IgM anti-HBc antibody (+) with increased aspartate transaminase (AST) and alanine transaminase (ALT) levels in his blood about a month ago. He had been drinking approximately a bottle of beer once a month but does not smoke. His family history was not significant. At the time of his visit to this hospital, his blood pressure was 120/80 mm Hg; pulse rate, 76/min; respiration rate, 20/min; and temperature, 36.5℃. Moreover, the patient was conscious and had no specific symptom but fatigue. His breath sound was normal during chest auscultation; neither whole body jaundice nor icteric sclera was observed. No tactile mass was noted in the abdominal region; neither abdominal pain nor abdominal fluid was found. The peripheral blood test showed that his hemoglobin was 14.6 g/dL (reference range, 11–16 g/dL); white blood cell count, 4,880 cells/mcL (reference range, 3,600–9,500 cells/mcL); and platelet, 181,000 cells/mcL (reference range, 150,000–450,000 cells/mcL). The biochemical test revealed the following: total protein, 9.2 g/dL (reference range, 6.4–8.3 g/dL); albumin, 4.4 g/dL (reference range, 3.8–5.3 g/dL); AST, 107 IU/L (reference range, 8–38 IU/L); ALT, 104 IU/L (reference range, 5–43 IU/L); alkaline phosphatase (ALP), 1,431 IU/L (reference range, 35–105 IU/L); gamma-glutamyl transpeptidase (GGT), 813 IU/L (reference range, 15–75 IU/L); total bilirubin, 0.4 mg/dL (reference range, 0.2–1.2 mg/dL); direct bilirubin, 0.1 mg/dL (reference range, 0–0.4 mg/dL); blood urea nitrogen, 13.9 mg/dL (reference range, 7–20 mg/dL); creatinine, 1.0 mg/dL (reference range, 0.7–1.3 mg/dL); and lactate dehydrogenase, 518 IU/L (reference range, 263–450 IU/L). The immunoserological test found hepatitis B surface (HBs) antigen/antibody (−/−), hepatitis B e (HBe) antigen/antibody (−/−), hepatitis C virus antibody (−), anti-hepatitis A virus (HAV) IgM (−), anti-HAV IgG (−), IgM anti-HBc antibody (+), and hepatitis B virus (HBV) DNA quantification (−) (). He was diagnosed with PBC because of his increased ALP and GGT levels in the blood test and increased IgM/IgG (518/1,740 mg/dL) in the additional blood test; he was also both AMA and antinuclear antibody (ANA) positive. Nothing significant was noted on his chest and simple abdominal X-ray. Moreover, no abnormal findings were observed; however, an approximately 2 cm hepatic cyst was found through abdominal computed tomography (). The development of the disease and screen associated autoimmune hepatitis was assessed. Liver biopsy found intrahepatic bile duct injury and epithelial cell infiltration in the lymphocytes, both of which characterize PBC, but did not indicate severe fibrosis or any condition that suggested autoimmune hepatitis (). Based on AMA and ANA (+) and the blood test results, which suggested a cholestatic disease, he was diagnosed with PBC. The patient was administered with a high dose of ursodesoxycholic acid (UDCA, 900 mg/d) for three months. After the treatment, both fatigue and pruritus decreased, and the AST, ALT, ALP, and GGT were 34, 18, 350, and 107 IU/L, respectively. Six months later, the patient exhibited lower ALP and GGT levels and negative IgM anti-HBc antibody in the follow-up test ().",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [35, 'years'], 'Alanine aminotransferase': [104.0, 'U/L'], 'Aspartate aminotransferase': [107.0, 'U/L'], 'Platelet count': [181000.0, 'µL']}",2.02888,1.92744,2.13032,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 107.0 U/L.
The patient's concentration of ALT is 104.0 U/L.
The patient's concentration of platelets is 181000.0 count/µL. To convert 181000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 181000.0 platelets count/µL * 1000000.0 µL/L = 181000000000.0 platelets count/L. This means that there are 181000000000.0/(10^9) = 181.0 billion platelet counts per liter.
Plugging these values into the formula, we get (35 * 107.0)/(181.0 * sqrt(104.0)) = 2.02888.Hence, the Fibrosis-4 score is 2.02888."
4372,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4408944-1,Extracted,"A 65-year-old man presented at our hospital complaining of intermittent fever and chills for 14 days. He denied any recent foreign travel, and had no other constitutional or abdominal symptoms, but reported anorexia and generalized fatigue for 1 month. He had a continuous history of alcohol consumption of 150–180 g (alcohol conversion) daily for 40 years. He denied any history of systemic diseases including diabetes mellitus, hypertension, and cirrhosis. He had no history of non-recent travel, exposure to animals, or invasive medical procedures. Physical examination showed remarkable generalized muscle wasting of the whole body, and mild right upper quadrant and epigastric tenderness. His body temperature was 40°C. Pulmonary, cardiac and abdominal examinations revealed no abnormalities. An electrocardiogram was normal. The hematological tests showed white blood cell count of 14.13/μL (normal range 3.30–9.00), hemoglobin 14.5 g/dL (normal range 11.5–15.0), and platelet count 20.7×104/μL (normal range 14–34). Prothrombin time (international normalized ratio) was 12.1 s (93%) (normal range 9.5–12.0 s). Biochemical tests revealed total bilirubin of 1.6 mg/dL (normal range 0.2–1.0), direct bilirubin 0.3 mg/dL (normal range 0.0–0.2), aspartate aminotransferase 65 IU/L (normal range 10–35), alanine aminotransferase 77 IU/L (normal range 5–40), alkaline phosphatase 597 IU/L (normal range 115–359), γ-guanosine triphosphate 367 IU/L (normal range <80), and C-reactive protein 25.16 mg/dL (normal value <0.5). Tests for hepatitis B virus (HBV), hepatitis C virus (HCV) and human immunodeficiency virus (HIV) were negative. Blood culture yielded S. choleraesuis. A chest X-ray showed an elevated right hemidiaphragm. Abdominal ultrasonography findings showed multiple low density lesions with sizes ranging 2.3–4.1 cm in the right and left lobes of the liver.
Computed tomography (CT) scan of the abdomen revealed multiple masses in various segments (mainly segments IV, VI, VII and VIII) of the right hepatic lobe, and segment II of left hepatic lobe. The masses ranged in size from 1 cm to 3 cm, and were hypodense with irregular margins, strongly suggestive of liver abscesses (). Moreover, CT imaging showed a thick, hyper-enhanced wall and adjacent fat stranding in the appendix (). Antibiotic treatment with cefoperazone was initiated, but was switched to meropenem on the patient’s fourth day in hospital when his fever did not subside. In addition, ultrasound-guided percutaneous catheter drainage (PCD) was performed for rapidly expanding hepatic abscesses measuring over 4 cm. Two 8 Fr pigtail catheters placed in segments VI and VIII yielded thick tenacious pus (). Diagnostic aspiration of the lesion yielded 50 mL of purulent material, which grew S. choleraesuis [O7:c:1,5; H2S(−), invA (+), stn (+)], Streptococcus milleri, Enterobacteriaceae, and Bacteroides. Auto-drainage from each catheter yielded approximately 20 mL per day. The cavity was washed with sterile saline solution injected gently to avoid pressure. On the patient’s fourteenth day in hospital, drainage fluid decreased suddenly, but body temperature remained elevated. Epigastric tenderness aggravated and bowel sounds decreased. The abdomen was soft, and no muscle guarding and rebound tenderness were found. An abdominal CT scan showed further spread of abscesses in segments II, IV, VI, VII and VIII of the liver and in the subphrenic space (). Since fever did not resolve, transcatheter regional hepatic arterial infusion of antibiotics was performed. Because of peritonitis, abdominal CT was performed and revealed air-containing abscesses in the right and left subphrenic regions. Then, right pleural effusion and empyema () with clinical features of respiratory failure appeared after the twentieth day. His clinical condition decompensated quickly thereafter, requiring endotracheal intubation and mechanical ventilation on the patient’s twenty-fifth day in hospital. Due to incomplete drainage by catheters, CT guided percutaneous needle aspiration of other abscesses was performed. Antibiotic treatment with meropenem was continued, and a few blood transfusions were performed. The patient was clinically improved, but abscesses persisted despite adequate catheter placement. The 8 Fr PCD catheters were exchanged to 12 Fr or 14 Fr large-bored catheters and placed into the abscess cavity. An additional 8 Fr pigtail catheter was placed into segmental VII on the patient’s thirtieth day in hospital (). A colobiliary fistula with a liver abscess was detected by PCD catheter (). Surprisingly, on the patient’s thirtieth day in hospital, an intraperitoneal abscess was noted and 30 mL of turbid pus was aspirated from the peritoneal cavity (). Thereafter his clinical condition and laboratory data improved gradually. We removed PCD from segment II. However, CT scans showed gradual enlargement of abscesses in segments II, VII and VIII of the liver () on days 40–50. PCD catheters were reinserted into segments II and VII, and the catheter in segment VIII was exchanged. Upon aspiration of the lesions, purulent material yielded Enterococcus faecium from segment II in the left hepatic lobe. The E. faecium isolate was resistant to β-lactams and carbapenem. The oxazolidinone derivative linezolid was administered. Moreover, Stenotrophomonas maltophilia and Candida albicans were detected from cloudy materials aspirated from lesions in segments II and VII on the patient’s ninetieth day in hospital. Trimethoprim-sulfamethoxazole (TMT-SMXD) and fosfluconazole (INN) were administered. Abdominal CT repeated on the patient’s one-hundredth day in hospital showed resolution of the previously described masses () and the patient’s clinical condition improved gradually ().",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [65, 'years'], 'Alanine aminotransferase': [77.0, 'U/L'], 'Aspartate aminotransferase': [65.0, 'U/L'], 'Platelet count': [207000.0, 'µL']}",2.32601,2.20971,2.44231,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 65.0 U/L.
The patient's concentration of ALT is 77.0 U/L.
The patient's concentration of platelets is 207000.0 count/µL. To convert 207000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 207000.0 platelets count/µL * 1000000.0 µL/L = 207000000000.0 platelets count/L. This means that there are 207000000000.0/(10^9) = 207.0 billion platelet counts per liter.
Plugging these values into the formula, we get (65 * 65.0)/(207.0 * sqrt(77.0)) = 2.32601.Hence, the Fibrosis-4 score is 2.32601."
4373,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,usmle-1232,Extracted,"A 73-year-old man comes in to the emergency department because of nausea and severe pain in his upper abdomen and right shoulder blade for the past day. He was able to eat a little for breakfast but vomited up the meal a couple of hours later. He has type 2 diabetes mellitus treated with metformin. He has smoked half a pack of cigarettes daily for 40 years and drinks 4 beers every week. He appears acutely distressed. His temperature is 38.8°C (102°F), pulse is 124/min, and blood pressure is 92/68 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 95%. The abdomen is soft and there is tenderness to palpation of the right upper quadrant with soft crepitus. The remainder of the examination shows no abnormalities. Laboratory studies show:
Hemoglobin 14.3 g/dL
Leukocyte count 18,100/mm3
Platelet count 216,000/mm3
Serum
Aspartate aminotransferase (AST, SGOT) 41 U/L
Alanine aminotransferase (ALT, SGPT) 19 U/L
Alkaline phosphatase 110 U/L
Total bilirubin 0.9 mg/dL
Direct bilirubin 0.2 mg/dL
Albumin 4.1 g/dL
Ultrasonography of the right upper quadrant shows a gallbladder with an air-filled, thickened wall and no stones in the lumen.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [73, 'years'], 'Alanine aminotransferase': [19.0, 'U/L'], 'Aspartate aminotransferase': [41.0, 'U/L'], 'Platelet count': [216000.0, 'µL']}",3.17889,3.01995,3.33783,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 41.0 U/L.
The patient's concentration of ALT is 19.0 U/L.
The patient's concentration of platelets is 216000.0 count/µL. To convert 216000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 216000.0 platelets count/µL * 1000000.0 µL/L = 216000000000.0 platelets count/L. This means that there are 216000000000.0/(10^9) = 216.0 billion platelet counts per liter.
Plugging these values into the formula, we get (73 * 41.0)/(216.0 * sqrt(19.0)) = 3.17889.Hence, the Fibrosis-4 score is 3.17889."
4374,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-3878461-1,Extracted,"A 50-year-old male patient previously diagnosed with acute myelomonocytic (M4) leukemia in July 2009 was given 2 courses of doxorubicin and cytarabine as induction chemotherapy. After complete remission was achieved, high-dose cytarabine was given as a consolidation regimen. The patient had 1 mismatched donor and underwent allo-HSCT. The conditioning regimen was busulfan + cyclophosphamide. The laboratory findings were as follows: HBsAg: (–); anti-HDV: (–); anti-HCV: (–); anti-HEV: (–); anti-HBs: 96 mIU mL–1; anti-HBe: (–); ant-HBc Ig M: (–); anti-CMV Ig M: (–); anti-EBV Ig M: (–); anti-ParvoV IgM: (–); anti-HIV: (–). Clostridium difficile toxin A was negative and genetic analysis for inv (16) was negative. Complete blood count analysis was as follows: Hb: 14.6 dL–1 (13-17 g dL–1); WBC: 8790 µL–1 (4-10×103 μL–1); platelet count: 271,000 µL–1 (150-400×103 μL–1). Biochemical findings were as follows: glucose: 69 mg dL–1 (74-106 mg dL–1); BUN: 20 mg dL–1 (7.9-21 mg dL–1); creatinine: 0.87 mg L–1 (0.66-1.09 mg L–1); Ca: 10.3 mg dL–1 (8.8-10.6 mg dL–1); ALT: 20 u L–1 (0-35 u L–1); AST: 30 u L–1 (0-31 u L–1); ALP: 83 u L–1 (30-120 u L–1); GGT: 25 (0-38); albumin: 4.9 d L–1 (3.5-5.2 g dL–1); direct/indirect bilirubin: 1.01/0.19 mg dL–1 (0.3-1.2/0-0.2 mg dL: –1); LDH: 230 u L–1 (100-245 u L–1). Prothrombin and activated partial thromboplastin time was 12 and 40.8 s–1 (12-18 and 26-44 s–1), respectively.
During the pre-transplant period the patient’s complete blood count (CBC), liver and renal function tests, coagulation tests, and other parameters were normal. No genetic aberrations or mutations were observed. Following administration of the conditioning regimen (busulphan + cyclophosphamide), the patient underwent allo-HSCT in January 2010. On the first d of transplantation teicoplanin (400 mg d–1 for the first 3 d, and then 400 mg d–1) and caspofungin (first dose 1×70 mg d–1, followed by 1×50 mg d–1) were given intravenously due to white plaques and oropharyngeal candidiasis in the patient’s mouth, and perianal erythema. On the second d of transplantation, imipenem (4×500 mg d–1) was added to the treatment due to neutropenic fever.
On the 14th d of the transplantation watery diarrhea occurred, along with abdominal discomfort, nausea, and fatigue. Stool examination showed no findings of bleeding, but a rare pathogen E. intestinalis was detected via immunofluorescence antibody (IFA) assay (), which was performed according to the manufacturer’s instructions, as follows: stool sample was diluted with PBS and filtrated through a 50-μm filter; 2 μL of the fecal sample suspension was placed on 18-well slides and dried for 1 h; the slides were fixed with methanol dipped subsequently in acetone for 10 min at –20 °C; 20 μL of the monoclonal antibodies was added to the slides and incubated for 30 min at room temperature in a humid atmosphere; the slides were washed in PBS 3 times; 20 μL of conjugate was added to the slides and incubated for 30 min at room temperature in the dark; cover slips were mounted on glass slides with 3 drops of anti-fading fluorescence mounting medium and viewed with a fluorescence microscope equipped with the 450-nm fluorescein filter.
Immediately after the diagnosis was confirmed, albendazole treatment was started at a dose of 2×400 mg d–1. On the fifth d of albendazole treatment (18th day of treatment) LFT results began to deteriorate. First, teicoplanin was discontinued on the 18th day of transplantation, and imipenem together with caspofungin was initiated on the 19th d. As the LFT results continued to deteriorate, albendazole was discontinued on the seventh d of albendazole treatment (). The patient was thought to have toxic hepatitis and percutaneous liver biopsy was performed for differential diagnosis. During the pre-transplant period the patient did not have liver function abnormality and abdominal ultrasonography showed no pathological findings, such as hepatosteatosis or cholestatic disorder.
After the biopsy was performed on the 22nd day of transplantation, histopathological analysis of the specimen confirmed the diagnosis of toxic hepatitis. Stool examination was repeated 8 d after the diagnosis and was negative. As the patient’s diarrhea resolved, the medications used to treat diarrhea were withdrawn. LFT results began to decrease immediately after the discontinuation of albendazole treatment. On the 13th d of albendazole treatment, all LFT values returned to normal (). The patient was discharged on d 34 of treatment.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [50, 'years'], 'Alanine aminotransferase': [20.0, 'U/L'], 'Aspartate aminotransferase': [30.0, 'U/L'], 'Platelet count': [271000.0, 'µL']}",1.23768,1.1758,1.29956,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 30.0 U/L.
The patient's concentration of ALT is 20.0 U/L.
The patient's concentration of platelets is 271000.0 count/µL. To convert 271000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 271000.0 platelets count/µL * 1000000.0 µL/L = 271000000000.0 platelets count/L. This means that there are 271000000000.0/(10^9) = 271.0 billion platelet counts per liter.
Plugging these values into the formula, we get (50 * 30.0)/(271.0 * sqrt(20.0)) = 1.23768.Hence, the Fibrosis-4 score is 1.23768."
4375,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-5122834-1,Extracted,"A 63-year-old female with past medical history of diabetes mellitus and hypertension presented to emergency department for abdominal distention for 2 weeks associated with poor appetite and weight loss. She denied current fever, chills, rigors, night sweat, cough, abdominal pain, leg edema, facial swelling, bowel problems, headache, vomiting, nausea, dizziness, blurry vision, chest pain, palpitations, paroxysmal nocturnal dyspnea, orthopnea, or similar illness in the past. The patient does not have any family history of rheumatologic diseases, and she denied any rash, joint pain, morning stiffness, and muscle weakness. She is a nonsmoker. She lives in central Africa and travelled to the United States to visit her daughter.
Initial vital signs included temperature 97°F (36.1°C), pulse rate 103 beats/minute, respiratory rate 18 breaths/minute, blood pressure 137/97 mm Hg, and oxygen saturation 96% on room air. Physical examination showed markedly distended abdomen, soft, nontender without palpable mass. There was fluid thrill with shifting dullness. Bowel sounds were normoactive. Respiratory exam was unremarkable except for mildly reduced air entry in lung bases.
Laboratory tests showed white blood cells 6.4 × 109/L, hemoglobin 11 g/dL, platelet counts 367 000/µL, bilirubin 0.5 mg/dL, aspartate transaminase 36 IU/L, alanine transaminase 22 IU/L, alkaline phosphatase 67 IU/L, and albumin 2.9 g/dL. Tumor marker α-fetoprotein level, carcinoembryonic antigen, cancer antigen 19-9, coagulation profile, lipase, hepatitis A, B, and C panels, B-type natriuretic peptide, antinuclear antibody, kidney function tests, and thyroid function tests were within normal limits. Blood test revealed CA 125 antigen level 390.9 (normal = 0-38 U/mL) and rheumatoid factor level 41.6 IU/mL (normal = 0-13.9 IU/mL). Anti–cyclic citrullinated proteins test was not done. Purified protein derivative test was positive with 20 mm; however, 3 sets of sputum for acid-fast bacilli were negative.
Chest X-ray showed atelectasis in lung bases. Abdomen ultrasound computed tomography scan of abdomen and pelvic with intravenous contrast showed large amount of ascites without masses. Transvaginal ultrasound revealed large pelvic ascites and nonvisualization of both ovaries. Diagnostic and therapeutic paracentesis showed yellow, cloudy fluid, white blood cells 910 cells/µL, neutrophils 13 cells/µL, lymphocytes 89 cells/µL, red blood cells 395 cells/µL, total protein 6.1 g/dL, and albumin 2.5 g/dL. Serum-ascites albumin gradient was 0.4.
The patient underwent peritoneal laparoscopy, which showed straw colored ascitic fluid with whitish tuberculous peritoneal nodules (-). Four liters of fluid was drained. Both ovaries were not enlarged and looked grossly normal. Biopsy of peritoneum revealed multiple nonnecrotizing and necrotizing granulomas with Langham type of giant cell and acid-fast bacilli seen on special stain, consistent with mycobacterial infection and negative for malignant cells.
The patient was started on anti-TB drugs (rifampin, isoniazid, pyrazinamide, and ethambutol) with resolution of ascites 2 weeks later.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [63, 'years'], 'Alanine aminotransferase': [22.0, 'U/L'], 'Aspartate aminotransferase': [36.0, 'U/L'], 'Platelet count': [367000.0, 'µL']}",1.31755,1.25167,1.38343,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 36.0 U/L.
The patient's concentration of ALT is 22.0 U/L.
The patient's concentration of platelets is 367000.0 count/µL. To convert 367000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 367000.0 platelets count/µL * 1000000.0 µL/L = 367000000000.0 platelets count/L. This means that there are 367000000000.0/(10^9) = 367.0 billion platelet counts per liter.
Plugging these values into the formula, we get (63 * 36.0)/(367.0 * sqrt(22.0)) = 1.31755.Hence, the Fibrosis-4 score is 1.31755."
4376,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-5045328-1,Extracted,"A 20-year-old male presented to our institution with a seven-month history of progressively
worsening jaundice. The patient denied abdominal pain, nausea, and vomiting. His past
medical history was unremarkable with no preexisting gastrointestinal or liver illnesses. He
had not recently taken any medication. The patient was a nonsmoker, nonalcoholic, and he did
not have a history of illicit substance use. The physical exam was unremarkable other than a
malnourished physique with a BMI of 18.6 (normal, 18.5–24.9).
The initial laboratory studies revealed alanine transaminase 1204 IU/L (normal, 10–40
IU/L), aspartate transaminase 721 IU/L (normal, 5–40 IU/L), serum alkaline phosphatase 153
IU/L (normal, 32–92 IU/L), total bilirubin 9.7 mg/dL (normal, 0.3–1.2 mg/dL), and
international normalized ratio (INR) 1.24 (normal, 0.8–1.2). The complete blood count was as
follows: WBC 25,200/mm3, hemoglobin 12.6 g/dL, platelets 499,000/mm3, eosinophils
67%, absolute total eosinophils 16,884/mm3. The serum IgG level was 1620 mg/dL
(normal, 700–1600 mg/dL). The patient had no evidence of allergic or hypersensitivity
conditions or connective tissue diseases based on bronchoscopy, pulmonary function tests,
and serologic tests. A transthoracic echocardiogram was unremarkable. A bone marrow biopsy
for neoplastic or primary bone marrow disorders showed marked eosinophilia, but no other
abnormalities.
A workup for infectious causes demonstrated negative results for viral markers (hepatitis
A, B, C, E, adenovirus, cytomegalovirus, and human immunodeficiency virus), serum antibodies
to helminth (worm) parasites, autoimmune antibodies (antinuclear, anti-dsDNA, and
anti-neutrophilic cytoplasmic antibodies), tumor markers (alpha-fetoprotein, carbohydrate
antigen 19-9, and carcinoembryonic antigen), and rheumatoid factor. No pathogens were
detected in a microbiological blood culture, and the stool examinations for parasites and
protozoa were negative. The flow cytometry was normal.
A computed tomography scan of the abdomen demonstrated a thick-walled gallbladder with a
rim of pericholecystic fluid present in the gallbladder fossa with a normal-appearing liver
(Figure ).
Furthermore, the colon showed a loss of normal mucosal pattern with no visible
haustrations. The rectum had a normal wall thickness, and the perirectal fat planes appeared
to be preserved (Figure ).
A flexible sigmoidoscopy exam was performed to assess colonic tissues following radiologic
manifestations. It revealed mild inflammatory changes, multiple mucosal erosions, and patchy
erythema (Figure ).
In addition to the other findings on colonoscopy, the loss of vascularity was evident.
These findings were consistent with mildly-active chronic colitis (Figure ).
The colonic biopsy was not obtained due to friability of mucosa and the potential risk of
perforation.
On day 4 of admission, a repeat blood workup showed a white cell count of
23,700/mm3 with eosinophils 67% and an absolute total eosinophil count of
15,879/mm3. The liver function tests were markedly elevated. On hospital day 5,
a liver biopsy was pursued to investigate the possibility of autoimmune hepatitis based on
the laboratory abnormalities. The histopathologic analysis of the liver specimen revealed
chronic active hepatitis with significant eosinophilic infiltration in the portal triad, but
no interface activity or rosette formation was evident. The surrounding periportal
hepatocytes showed mild steatosis (Figure ).
On high power view of the liver biopsy, infiltrating eosinophils were found with mild
cholestasis presenting as intrahepatocytic bile pigment (Figure ).
Based on the calculator from the International Autoimmune Hepatitis Group, the patient’s
clinical picture was not consistent with a definitive diagnosis of autoimmune hepatitis.
Given the significant presence of eosinophils, the patient most likely had chronic hepatitis
secondary to HES.
Eventually, the patient was diagnosed with idiopathic HES based on the persistent elevation
in eosinophil count for more than six months, an otherwise negative workup as described
above, and evidence of end-organ involvement of the liver, gallbladder, and colon. The
patient was initiated on prednisone 60 mg/day. He showed a dramatic response to the
prednisone therapy with normalization of eosinophil count within three weeks. The liver
enzymes normalized after six weeks of therapy. Subsequently, the prednisone dose was
gradually tapered. Since then, the patient has been disease free and continues to do well on
regular follow-ups with serum troponin level measurements every three to six months and
echocardiography and pulmonary function tests every six to 12 months.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [20, 'years'], 'Alanine aminotransferase': [1204.0, 'U/L'], 'Aspartate aminotransferase': [721.0, 'U/L'], 'Platelet count': [499000.0, 'µL']}",0.83282,0.79118,0.87446,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 721.0 U/L.
The patient's concentration of ALT is 1204.0 U/L.
The patient's concentration of platelets is 499000.0 count/µL. To convert 499000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 499000.0 platelets count/µL * 1000000.0 µL/L = 499000000000.0 platelets count/L. This means that there are 499000000000.0/(10^9) = 499.0 billion platelet counts per liter.
Plugging these values into the formula, we get (20 * 721.0)/(499.0 * sqrt(1204.0)) = 0.83282.Hence, the Fibrosis-4 score is 0.83282."
4377,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-8192200-1,Extracted,"A 55-year-old African American male with a medical history of hypertension, hyperlipidemia, chronic hepatitis B, and well-controlled HIV on ART presented to the hospital with a one-week history of fatigue, fever, myalgias, shortness of breath, and dark-colored urine. He denied any history of alcohol, illicit drug use, or family history of liver disease.
On physical exam, he had scleral icterus and mild lower abdominal pain without guarding, rebound, or rigidity. He was alert and oriented without focal deficit or asterixis. He had no ascites. Vital signs were within normal limits. Lab work was significant for creatinine at 6.38 mg/dL (0.7–1.3), BUN 48 mg/dL (7–18), total bilirubin 51.8 mg/dL (0.2–1), direct bilirubin 40.4 mg/dL (≤0.2), lactate dehydrogenase 2678 unit/L (87–241), haptoglobin <7.7 mg/dL, alkaline phosphatase 195 unit/L, AST 216 unit/L (15–37), ALT 6,244 unit/L (16–61), lactic acid 5.5 mmol/L (0.4–2), WBC 16.6 thou/mcL (4.2–10.2), hemoglobin 7.5 g/dL (12.8–16.4), platelet 344 × 103/microL (150–400), and INR 1.6 (0.8–1). His model for end-stage liver disease (MELD) score was 40. Urine drug screen, acetaminophen, and alcohol level were negative. Serologic studies for Treponema pallidum, cytomegalovirus, Epstein–Barr virus, herpes simplex virus, and parvovirus were negative. Influenza and COVID-19 PCR were negative. The hepatitis panel was positive for hepatitis A IgM, hepatitis A total antibody, and hepatitis B core IgG antibody. Hepatitis C antibody, hepatitis E IgG/IgM, and HBV DNA were negative. His autoimmune markers including antinuclear antibody, antismooth muscle antibody, antimitochondrial antibody, and myeloperoxidase autoantibody were negative. Serum ceruloplasmin was also negative. Erythrocyte G6 PD level was normal due to acute hemolysis. A computed tomography (CT) scan of the abdomen and pelvis showed normal appearing liver with nondilated bile ducts and patent hepatic vasculature. A transthoracic echocardiogram (TTE) showed LVEF 60–65% with normal wall motion, no diastolic dysfunction, valvular disease, or thrombus.
The patient was treated empirically with antibiotics and intravenous fluids. Patient continued to be oliguric and hemodialysis was initiated. Peripheral smear showed fragmented erythrocytes, spherocytes, bite cells, and target cells indicative of hemolysis. Fibrinogen was normal, and Coomb's test was negative. Liver biopsy showed cholestatic hepatitis with areas of resolving necrosis (). Renal biopsy showed acute tubular injury with bilirubin and hemoglobin casts (). The patient was initially listed for transplant but clinically improved with supportive measures alone. Over the next few weeks, patient's liver functions test and hemolysis labs steadily improved (Figures and ). He was discharged to a rehab facility and has since followed up in our clinic. His most recent liver function tests, 3 months after hospitalization, are normal. Erythrocyte G6PD is 3.3 U/g Hb, confirming the diagnosis of G6PD deficiency. His renal function also improved, and he is no longer on dialysis.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'Alanine aminotransferase': [6244.0, 'U/L'], 'Aspartate aminotransferase': [216.0, 'U/L'], 'Platelet count': [344000.0, 'µL']}",0.43705,0.4152,0.4589,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 216.0 U/L.
The patient's concentration of ALT is 6244.0 U/L.
The patient's concentration of platelets is 344000.0 count/µL. To convert 344000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 344000.0 platelets count/µL * 1000000.0 µL/L = 344000000000.0 platelets count/L. This means that there are 344000000000.0/(10^9) = 344.0 billion platelet counts per liter.
Plugging these values into the formula, we get (55 * 216.0)/(344.0 * sqrt(6244.0)) = 0.43705.Hence, the Fibrosis-4 score is 0.43705."
4378,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-3683444-1,Extracted,"A 63-year-old male with history of untreated Chronic hepatitis C and alcohol abuse was admitted to the Internal Medicine Department with 4-day history of nausea, diffuse abdominal pain, and jaundice. On physical exam he was jaundiced with scleral icterus. The abdomen was diffusely tender with guarding. Laboratory data revealed total bilirubin 16.9 mg/dL (normal: <1.0), Alkaline phosphatase 243 IU/L, aspartate transaminase (AST) 97 IU/L (normal: <35), alanine transaminase (ALT) 69 IU/L (normal: <35), alpha fetal protein: 3.0 IU/mL, lactate dehydrogenase (LDH) 267 IU/L, albumin 2.7 g/dL (normal: 3.2–4.6), total protein 5.7 g/dL (normal: 6.4–8.3), blood urea nitrogen (BUN) 14 mg/dL (normal: 8–23), creatinine 0.85 mg/dL (normal: 0.80–1.30). CBC showed white cell count (WBC): 6.3 K/μL (normal: 5–10.2), hemoglobin 13.7 g/dL (normal: 13.5–17.5), and platelet 117 K/μL (normal: 150–450). Liver ultrasound showed a mass-like structure around gallbladder fossa, and common bile duct (CBD) diameter was 6 mm. Computed tomography (CT) of the abdomen and pelvis showed a large irregular mass at the porta hepatis. Magnetic resonance cholangiopancreatography (MRCP) revealed 5.5 × 5.4 × 4.9 cm mass and biliary ductal dilatation from extrinsic compression (). Pathology of fine needle biopsy of mass () showed diffuse large B cell lymphoma, positive for CD20, BCL2, BCL6, CD79a, and PAX5 and negative for CD3, CD5, CD10, CD23, CD138, cyclin D1, CK7, CK20, and p63. Positron emission tomography (PET) scan showed multiple liver lesions and right lower lung nodule, without involvement of mediastinal lymph nodes or peritoneum. Bone marrow biopsy was negative for lymphoma. Endoscopic retrograde cholangiography (ERC) was performed for biliary decompression but CBD could not be cannulated, and limited cholangiogram showed distal CBD stricture. Percutaneous transhepatic cholangiography (PTC) was performed with successful internal and external biliary drain placement (). His ECOG (Eastern Cooperative Oncology Group) score was 3 and chemotherapy was planned. After few days he was readmitted with acute renal failure (BUN/Cr: 100/4.1), WBC 25.1 K/μL, total bilirubin 6.4 mg/dL, intractable nausea and vomiting, and hypotension with multiorgan failure. He was found to be in septic shock. The patient died even before starting chemotherapy.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [63, 'years'], 'Alanine aminotransferase': [69.0, 'U/L'], 'Aspartate aminotransferase': [97.0, 'U/L'], 'Platelet count': [117000.0, 'µL']}",6.28785,5.97346,6.60224,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 97.0 U/L.
The patient's concentration of ALT is 69.0 U/L.
The patient's concentration of platelets is 117000.0 count/µL. To convert 117000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 117000.0 platelets count/µL * 1000000.0 µL/L = 117000000000.0 platelets count/L. This means that there are 117000000000.0/(10^9) = 117.0 billion platelet counts per liter.
Plugging these values into the formula, we get (63 * 97.0)/(117.0 * sqrt(69.0)) = 6.28785.Hence, the Fibrosis-4 score is 6.28785."
4379,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-5729656-1,Extracted,"A 65-year-old Korean man had been diagnosed with pulmonary tuberculosis (TB) 40 years earlier. Four years before he presented to our clinic, he was told that he had TB-destroyed lung and a fungus ball. The patient visited our hospital on June 14, 2014 with dyspnea, blood-tinged sputum, and weight loss, which developed 2 months earlier. He denied experiencing fever, chills, or night sweats. He denied any history of overseas travel.
His initial blood pressure was 99/65 mmHg, respiratory rate was 16/min, and body temperature was 36.8°C. His chest was clear to auscultation. The laboratory results were as follows: hemoglobin, 11.3 g/dL; white blood cell count, 6,050/µL (64.7% neutrophils, 16.0% lymphocytes); platelet count, 291,000/µL; C-reactive protein, 5.56 mg/dL; blood urea nitrogen, 18 mg/dL; creatinine, 1.20 mg/dL; aspartate aminotransferase, 18 IU/L; alanine aminotransferase, 15 IU/L; and total bilirubin, 0.4 mg/dL.
Blood and sputum cultures were negative for any pyogenic bacteria. Sputum was negative for acid-fast bacilli (AFB) by smear. A computed tomography (CT) scan of the chest showed numerous clumps of tiny nodules in both lungs, which were aggravated by the combination of bronchiectasis and cavitary lesions in both upper lobes and a fungus ball in the left upper lobe (). No enlarged mediastinal or hilar lymph nodes were found. He had experienced a progressive decline in lung function and had recently developed recurrent pneumothorax.
Serological and antigen tests for any fungus were negative. Culture studies of bronchial alveolar lavage fluid (BALF) were negative for any fungus. Antigens for histoplasmosis in the BALF were not investigated.
The patient underwent a VATS-based lung biopsy. The biopsy showed necrotizing granuloma and peribronchial lymphocytic infiltrations, and Gomori methenamine silver (GMS) staining revealed a fungal organism. AFB staining results were negative. The tissues contained multiple small (< 5 µm) yeast-like fungi. Considering the size and characteristics of the lesion, we suspected that these organisms were Histoplasma spp. (), and tissue culture confirmed Histoplasma capsulatum. The patient was diagnosed with pulmonary histoplasmosis. Therapy was initiated with 200 mg itraconazole orally once per day for 12 months. He adhered to the treatment, and the symptoms disappeared 1 week after the treatment started. After 4 months, low-dose chest CT showed improvement of the ground glass opacity and size of the lung lesion () although cystic lesions were increased. At the end of treatment, plain chest X-ray showed that the ground glass opacity lesion has almost disappeared ().",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [65, 'years'], 'Alanine aminotransferase': [15.0, 'U/L'], 'Aspartate aminotransferase': [18.0, 'U/L'], 'Platelet count': [291000.0, 'µL']}",1.03812,0.98621,1.09003,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 18.0 U/L.
The patient's concentration of ALT is 15.0 U/L.
The patient's concentration of platelets is 291000.0 count/µL. To convert 291000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 291000.0 platelets count/µL * 1000000.0 µL/L = 291000000000.0 platelets count/L. This means that there are 291000000000.0/(10^9) = 291.0 billion platelet counts per liter.
Plugging these values into the formula, we get (65 * 18.0)/(291.0 * sqrt(15.0)) = 1.03812.Hence, the Fibrosis-4 score is 1.03812."
4380,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-4020534-1,Extracted,"A 45-year-old African American male with a past medical history of hypertension, HCV infection, and polysubstance abuse was admitted with epigastric and right upper quadrant abdominal pain, pruritus, and itching for two days. Symptoms are associated with nonbilious vomiting, fatigue, and a 9 kg unintentional weight loss over three months. He denied any history of Hepatitis B in the past. Ten months before, he had a similar complaint where evaluation at an outside facility showed a hepatic mass. A liver biopsy at that time showed acute inflammation suggestive of an abscess with extensive chronic inflammation and fibrosis adjacent to the necrosis, moderate to severe acute and chronic periportal inflammation with portal lymphoid aggregates. Cultures from the biopsy were negative for any organisms but the patient was treated with an empiric course of vancomycin and piperacillin/tazobactam for four weeks. His social history was significant for cigarette smoking, alcohol, and intravenous illicit drug use of heroin and cocaine. The family history was significant for a brother with gastric lymphoma, now in remission. Physical exam was significant for skin excoriations, scleral icterus without any lymphadenopathy, hepatomegaly, and tenderness along the epigastrium and right upper quadrant areas.
Initial laboratory values showed a hemoglobin of 13.0 gm/dL, hematocrit of 37.7%, white blood cell count of 4.4 × 103, and platelet count of 240 × 103. His metabolic panel showed normal renal function tests with a calcium of 9.4 mg/dL. His comprehensive metabolic panel revealed a total bilirubin of 6.1 mg/dL, direct bilirubin of 4.1 mg/dL, aspartate aminotransferase (AST) of 150 U/L, alanine aminotransferase (ALT) of 142 U/L, alkaline phosphatase (ALP) of 282 IU/L, gamma-glutamyl transferase (GGT) of 385 IU/L, total protein of 7.4 g/dL, and albumin of 3.6 g/dL. His prothrombin time was 13.7 seconds with an International Normal Ratio (INR) of 1.04. Amylase and lipase levels were within normal limits. Hepatitis B panel showed immunity to Hepatitis B. His HCV RNA viral load was 422131 IU/mL (5.63 log). HCV genotype is 1b. HIV by ELISA was negative. His alpha-fetoprotein levels (AFP) were 2.2 ng/mL. Blood cultures were negative. Triphasic computed tomography (CT) of the abdomen and pelvis with contrast showed multiple masses in the liver (largest being 8.8 cm) without any cholelithiasis or extrahepatic bile duct dilatation (). There was no significant enhancement of the hepatic lesions on arterial phase, while on portal venous phase the lesions showed slight enhancement. The spleen, pancreas, gallbladder, kidneys, and adrenals appeared within normal limits. Over his hospital course, his bilirubin levels increased to 23.3 mg/dL on eleventh day along with aspartate transaminase (AST) of 277 U/L, alanine aminotransferase (ALT) of 197 U/L, and alkaline phosphatase (ALP) of 199 IU/L (). In spite of high bilirubin levels, the patient maintained normal coagulation parameters and showed no evidence of hepatic encephalopathy. CT chest with contrast was within normal limits. Meanwhile, both upper endoscopy and colonoscopy were negative for occult malignancy. The biopsy of the liver mass done under fluoroscopic guidance was consistent with diffuse large B cell lymphoma (DLBCL). By immunohistochemistry, the cells were positive for CD 20, CD 10, and BCL-6. The Ki-67 proliferative index was 100% (). FISH for c-myc rearrangement was negative. Bone marrow biopsy was negative for lymphoma.
With stage IVB DLBCL and elevated bilirubin levels, there was a concern for giving full dose chemotherapy, since the liver metabolizes most of the chemotherapy agents. A decision was made to do local irradiation to the liver and reevaluate his bilirubin level to determine if chemotherapy could be administered. The patient's liver received a total dose of 6 Gy in 4 fractions of 1.5 Gy each using a 2-field 3D conformal technique with 10 MV photon beam therapy on days 1, 2, 9, and 12. Initial staging positron emission tomography- (PET-) CT showed decreased metabolic activity compared with normal adjacent liver parenchyma, suggesting a positive response to treatment and no extranodal disease. Meanwhile, total bilirubin levels fell to 3.4 mg/dL () and allowed the first dose of R-CHOP (rituximab combined with cyclophosphamide, adriamycin, vincristine, and prednisone) chemotherapy to be administered at a 50% dose reduction. The patient subsequently received six cycles of R-CHOP. After completion, beside neutropenia, no other significant adverse effects were noted. Restaging PET-CT showed no hypermetabolic activity in the liver.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'years'], 'Alanine aminotransferase': [142.0, 'U/L'], 'Aspartate aminotransferase': [150.0, 'U/L'], 'Platelet count': [240000.0, 'µL']}",2.3602,2.24219,2.47821,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 150.0 U/L.
The patient's concentration of ALT is 142.0 U/L.
The patient's concentration of platelets is 240000.0 count/µL. To convert 240000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 240000.0 platelets count/µL * 1000000.0 µL/L = 240000000000.0 platelets count/L. This means that there are 240000000000.0/(10^9) = 240.0 billion platelet counts per liter.
Plugging these values into the formula, we get (45 * 150.0)/(240.0 * sqrt(142.0)) = 2.3602.Hence, the Fibrosis-4 score is 2.3602."
4381,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-5298492-1,Extracted,"An 82-year-old male presented with progressive weakness, early satiety, and failure to thrive. He experienced an 80-pound unintentional weight loss in the past 3.5 years, with 34 pounds in the past 8 months. His last colonoscopy 2 years ago showed small tubular adenomas. Physical examination was unremarkable except for cachexia and pallor. Baseline labs were as follows: white blood cell count 4600/µL, hemoglobin 8.5 g/dL, hematocrit 25%, mean corpuscular volume 95.8 fL, platelet count 169 000/µL, blood urea nitrogen 41 mg/dL, creatinine 1.8 mg/dL, total bilirubin 0.24 mg/dL, aspartate transaminase 10 U/L, alanine transaminase 16 U/L, alkaline phosphatase 114 U/L, albumin 3.6 g/dL, total protein 5.8 g/dL, lactate dehydrogenase 118 U/L, iron 92 µg/dL, ferritin 87 ng/mL, iron saturation 35%, positive stool occult blood, folate 8.7 ng/mL, and vitamin B12 490 pg/mL. A chest computed tomography (CT) was unremarkable. An abdominal CT showed mild fat stranding as well as minimal fluid surrounding the ascending colon without any evidence of intraabdominal lymphadenopathy. He underwent an esophagogastroduodenoscopy (EGD) to investigate the cause for significant weight loss and early satiety. EGD demonstrated multiple ulcerated gastric lesions in the fundus and body (). The antrum was characterized by mild erythematous gastropathy. Additionally, no sites of active bleeding were found. The ulcerated lesions and the uninvolved antrum/incisura were biopsied. Histopathology revealed ulcerated mucosa with atypical lymphoid infiltrations, characterized by large lymphocytes with irregular nuclei, distinct nucleoli, vesicular chromatin, and evident mitoses and apoptosis (). Immunohistochemistry was positive for cluster of differentiation (CD) 45, CD20, paired box 5 (PAX-5; ), and B-cell lymphoma 6 (BCL-6) and negative for cytokeratin and melanoma associated antigen (mutated) 1 (MUM-1). Ki-67 showed a high proliferative index (80%). The gastric biopsies from the nonulcerated mucosa in the antrum/incisura demonstrated inflammatory cells consistent with gastritis, and immunohistochemistry was negative for Helicobacter pylori. The findings are consistent with DLBCL, stage 1E. Gastrectomy was not pursued due to his frailty and advanced age. He was initiated on abbreviated chemotherapy with subsequent involved field radiation. An attenuated immunochemotherapy regimen (R-miniCHOP; rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) was started. He tolerated chemotherapy but presented with coffee-ground emesis, after completing 3 cycles of chemotherapy. EGD noted a bleeding ulcer, which was treated endoscopically. There was notable improvement in DLBCL-related ulcers compared to previous EGD ( and ). He had no recurrent bleeding and subsequently underwent involved field radiation.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [82, 'years'], 'Alanine aminotransferase': [16.0, 'U/L'], 'Aspartate aminotransferase': [10.0, 'U/L'], 'Platelet count': [169000.0, 'µL']}",1.21302,1.15237,1.27367,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 10.0 U/L.
The patient's concentration of ALT is 16.0 U/L.
The patient's concentration of platelets is 169000.0 count/µL. To convert 169000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 169000.0 platelets count/µL * 1000000.0 µL/L = 169000000000.0 platelets count/L. This means that there are 169000000000.0/(10^9) = 169.0 billion platelet counts per liter.
Plugging these values into the formula, we get (82 * 10.0)/(169.0 * sqrt(16.0)) = 1.21302.Hence, the Fibrosis-4 score is 1.21302."
4382,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-7001129-1,Extracted,"An 80-year-old Caucasian man presented to the emergency department (ED) with one-week history of ankle swelling and abdominal pain. Per family members, the patient was confused, having memory loss, increased urinary frequency, cough, mild dyspnea and generalized weakness. He had a prior history of hypertension, dyslipidemia, chronic kidney disease stage III, benign prostatic hyperplasia, transitional cell carcinoma of the urinary bladder for which he underwent transurethral resection of bladder tumor. His prescription medications included tamsulosin, benazepril, simvastatin and a multivitamin. He denied any intake of calcium supplements, antacids or vitamin D. He was a former alcoholic (quit 10 years ago) and an ex-smoker (quit 15 years ago) and denied any illicit drug use. He was recently discharged from the hospital a week ago when he was admitted for acute kidney injury, secondary to dehydration.
All his initial vital signs in the emergency department were within normal limits and physical examination was unremarkable with the exception of 2+ pitting pedal edema bilaterally up to mid-shins. Serum chemistries showed a white blood cell count (WBC) 15,600/mm3 (normal: 4,000-11,000), neutrophil count 12,900/mm3 (normal: 1500-8,000), monocytes 1300/mm3 (normal: 200-1000), hemoglobin 17.4 g/dl (normal: 13.5-17.0), red blood cell 5.78 million/mm3 (normal: 4.3-6.0), platelets 145,000/mm3 (normal: 150,000-450,000), blood urea nitrogen 31 mg/dl (normal: 7-20), creatinine 1.76 mg/dl (normal: 0.6-1.2), calcium 12.2 mg/dl (normal: 8.5-10.2), albumin 3.1 g/dl (normal: 3.5-5.5), total bilirubin 1.5 mg/dl (normal: 0.1-1.2), aspartate aminotransferase (AST) 73 IU/L (normal: <40), alanine aminotransferase (ALT) 33 IU/L (normal: <56), alkaline phosphatase (ALP) 218 IU/L (normal: 44-147), NT-proBNP 638 pg/ml (normal: <450) and serum procalcitonin 35.6 ng/ml (normal: <0.5).
Chest radiograph done in emergency department showed bilateral infrahilar and basilar subsegmental atelectasis though early infiltrate versus aspiration could not be ruled out. Ventilation-perfusion nuclear medicine scan showed low probability of pulmonary embolism. The patient was empirically started on piperacillin-tazobactam by ED physician for possible healthcare-associated pneumonia and admitted to the hospital for further care.
Suspecting the possibility of congestive heart failure, the admitting physician started patient on intravenous furosemide, ordered an echocardiogram and added intravenous vancomycin for empiric coverage as well. Echocardiogram showed a normal ejection fraction of 60% with no valvular abnormalities. Nephrology service was consulted by the admitting physician for management of hypercalcemia. Nephrologist ordered studies to evaluate the cause of hypercalcemia, discontinued furosemide and gave calcitonin to treat hypercalcemia. Investigative workup for hypercalcemia revealed parathyroid hormone level < 6 pg/ml (normal: 15-65), 25-hydroxy vitamin D 45 ng/ml (normal: 30-100), 1, 25-dihydroxy vitamin D 17 pg/ml (normal: 18-72), angiotensin converting enzyme level 11 U/L (normal: 9-67), 24-hour urinary calcium excretion 153 mg/dl (normal: 50-300), normal IgA, IgG, IgM levels, serum protein electrophoresis showed hypoalbuminemia without any evidence of monoclonal protein, serum and urine immunofixation was negative. Ordered serum parathyroid hormone-related peptide (PTHrP) revealed elevated levels of 62 pg/ml (normal: 14-27 pg/ml). As hypercalcemia did not respond to calcitonin, the patient was given intravenous pamidronate (twice). As his leukocytosis continued to worsen (19,100/mm3) along with procalcitonin (38.15 ng/ml) despite being on broad-spectrum antibiotics for one-week, infectious diseases service was consulted and leukemia/lymphoma flow cytometry panel, peripheral blood smear was ordered to evaluate for hematologic malignancy. Infectious disease physician discontinued vancomycin and ordered Indium-111 labeled whole body WBC scan which showed no abnormal areas of increased tracer uptake to suggest a focus of infection. Leukemia/lymphoma flow cytometry was negative for any specific phenotypic abnormality. Peripheral blood smear showed presence of neutrophilia without any evidence of malignant leukocytes.
Meanwhile, the patient went in to acute hypoxic respiratory distress with wheezing and so pulmonary service was consulted which transferred the patient to ICU, started him on intravenous methylprednisolone and initiated non-invasive positive pressure ventilation (bi-level positive airway pressure - BiPAP). As PTHrP had come back elevated, the patient underwent a CT scan of chest, abdomen and pelvis, which showed a hypodense mass in the right posterior lobe of liver measuring 9.3 cm x 8.3 cm in size with presence of moderate abdominal and severe pelvic ascites (Figure ). The patient underwent paracentesis with removal of 2.6 L of straw-colored fluid. Ascitic fluid did not show any malignant cells or evidence of spontaneous bacterial peritonitis. Ultrasound of the liver showed a 10.9-cm mass in the right lobe of liver along with portal vein occlusion. Hematology and oncology service was then consulted. Oncologist did not recommend anticoagulation for portal vein occlusion and ordered tumor markers evaluation which showed alpha-fetoprotein 14.7 ng/ml (normal: <8.7), CA 19-9 2907 U/ml (normal: < 35), carcinoembryonic antigen (CEA) 5.2 ng/ml (normal: <3.4). A possibility of hepatocellular carcinoma was discussed with the patient and he was scheduled to undergo CT-guided liver biopsy. Broad spectrum antibiotics were discontinued after 10 days of administration as they neither lowered procalcitonin nor WBC count. Blood, urine and other body fluid cultures remained negative during the entire hospital stay. Either partly because of being on intravenous steroids and/or due to underlying disease process, patient’s WBC count peaked at 40,100/mm3 during this hospital stay. Though he presented with polycythemia, his peak hemoglobin and hematocrit during admission was 19.7 g/dl and 57%. Serum erythropoietin level was found to be elevated 21.4 mIU/ml (normal: 2.6-18.5).
Patient’s liver profile worsened during his ICU stay with serum bilirubin escalating up to 12 mg/dl, ALP 470 IU/L, AST 429 IU/L, ALT 362 IU/L, international normalized ratio (INR) 2.8, albumin 1.8. MRI liver/magnetic resonance cholangiopancreatography (MRCP) abdomen was ordered which did not show any evidence of biliary obstruction. Viral hepatitis panel came back negative as well. Liver biopsy revealed moderately differentiated ductal adenocarcinoma of hepatobiliary origin reported as primary intrahepatic cholangiocarcinoma under current clinical settings (Figure ). Immunohistochemical stains revealed CK Oscar(+), CK7(+) (Figure ), CK20(-) (Figure ), Villin(+) (Figure ), CDX2(-) (Figure ), TTF-1(-), Napsin A(-), PSA(-) and NKX3.1(-).
Oncology service recommended no chemotherapy at the moment as the patient was thought to be too frail. Three weeks after his admission to the hospital, his blood pressure dropped in ICU requiring initiation of norepinephrine infusion. A temporary hemodialysis catheter was inserted and sustained-low efficiency dialysis (SLED) was initiated as well. Given his dismal prognosis in the setting of malignancy and multi-organ failure, a detailed discussion was held with the patient and his family members when it was decided to proceed with comfort care options and hospice. The patient was discharged to hospice the following day.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [80, 'years'], 'Alanine aminotransferase': [362.0, 'U/L'], 'Aspartate aminotransferase': [429.0, 'U/L'], 'Platelet count': [145000.0, 'µL']}",12.44013,11.81812,13.06214,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 429.0 U/L.
The patient's concentration of ALT is 362.0 U/L.
The patient's concentration of platelets is 145000.0 count/µL. To convert 145000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 145000.0 platelets count/µL * 1000000.0 µL/L = 145000000000.0 platelets count/L. This means that there are 145000000000.0/(10^9) = 145.0 billion platelet counts per liter.
Plugging these values into the formula, we get (80 * 429.0)/(145.0 * sqrt(362.0)) = 12.44013.Hence, the Fibrosis-4 score is 12.44013."
4383,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-2693865-1,Extracted,"A 39-yr-old female presented with recurrent oro-genital ulcers, erythema nodosum, and arthralgia. She was diagnosed as having Behcet's disease. She had taken the maintenance therapy with colchicines. Two years later, she was admitted to our hospital because of oral and genital ulcer, lower abdominal pain, and frequent diarrhea for 15 days. She had suffered from intermittent hematochezia and cramping abdominal pain for the previous two years. Further history taking revealed she had a post-traumatic epilepsy by traffic accident 13 yr before and had taken anti-epilepsy drugs, carbamazepine and sodium valproate.
On admission, her blood pressure was 90/60 mmHg, her pulse rate was 70/min, body temperature was 36.5℃, and respiration rate was 20/min. Her abdominal pain was located in the bilateral lower quadrants without rebound tenderness. She felt cramping pain intermittently. She appeared chronically ill and reported that her stools were maroon, followed by mucoid. On examination of external genitalia, a linear to ovoid shaped ulcerating wound was observed ().
Laboratory values showed a white blood cell count of 8,600/µL, hemoglobin of 9.1 g/dL, and a platelet count of 172,000/µL. Her liver function test showed aspartate transaminase of 13 IU/L, alanine transaminase of 6 IU/L, albumin of 2.3 g/dL, alkaline phosphatase of 357 U/L, and total bilirubin of 0.2 mg/dL. The other laboratory findings showed fast blood sugar of 119 mg/dL, blood urea nitrogen of 5.2 mg/dL, creatinine of 0.8 mg/dL, sodium of 136 mEq/L, and potassium of 3.3 mEq/L.
An esophagogastroduodenoscopy (EGD) was performed to rule out the presence of a massively bleeding upper gastrointestinal lesion. The EGD was normal. Colonoscopic examination revealed grossly normal-appearing mucosa in the rectum and the sigmoid colon. However, descending, transverse, and ascending colon, including the cecum, showed multiple longitudinal ulcers and inflammatory pseudopolyps with a cobblestone appearance. The ileocecal valve and terminal ileum were preserved from the inflammation. A suspicious fistular opening just above the anus was observed (). Microscopically, specimens from ulcers of the colon showed shallow ulcerations with inflammatory infiltration consisting of lymphocytes and plasma cells. There were no granulmas ().
Further studies during her hospitalization showed that the patient was negative for HIV. She was negative for antinulear antibody and HLA-B51. Under sterile condition, intradermal injection of the skin with a 20-guage needle was done. Within 48 hr, an erythematous papule developed. The pathergy test was positive. Histological examination of the perineal lesion revealed chronic ulcer with acute and chronic inflammatory cell infiltration and increased small blood vessels (). On ophthalmologic examination, there was no ocular manifestation of Behcet's disease.
Total parenteral nutrition with nothing per oral and intravenous administration of methylprednisolone, 62.5 mg were started. In addition, metronidazole was injected for anal fistula. After 1 week, the patient responded well clinically and was tolerable with diet. Treatment with prednisone, 40 mg and 5-aminosalicylate (mesalazine), 4.0 g by mouth was started. The abdominal symptoms and vulva ulcer improved gradually, and she was discharged 2 months after admission. The dose of prednisone was tapered and discontinued. One year later, she was doing well without recurrence of symptoms.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [39, 'years'], 'Aspartate aminotransferase': [13.0, 'U/L'], 'Alanine aminotransferase': [6.0, 'U/L'], 'Platelet count': [172000.0, 'µL']}",1.20338,1.14321,1.26355,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 13.0 U/L.
The patient's concentration of ALT is 6.0 U/L.
The patient's concentration of platelets is 172000.0 count/µL. To convert 172000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 172000.0 platelets count/µL * 1000000.0 µL/L = 172000000000.0 platelets count/L. This means that there are 172000000000.0/(10^9) = 172.0 billion platelet counts per liter.
Plugging these values into the formula, we get (39 * 13.0)/(172.0 * sqrt(6.0)) = 1.20338.Hence, the Fibrosis-4 score is 1.20338."
4384,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-7682974-1,Extracted,"A 30-year-old woman and known case of liver transplantation due to decompensated cirrhosis secondary to autoimmune hepatitis from 5 years ago was admitted to the emergency room of Taleghani Hospital, a teaching referral hospital in Tehran, Iran, with fever, chills, watery (non bloody) diarrhea, nausea, vomiting, abdominal pain, and loss of appetite. She had experienced an episode of rejection 2 years after her liver transplant manifested by an elevation in liver enzymes up to 3 times the upper limit of normal and a total bilirubin increase. Fortunately, abnormal liver function tests completely responded to the typical pulse regimen of methylprednisolone. After that, she underwent an inevitable splenectomy because of severe pancytopenia, multiple tortuous venous collaterals and multiple hypodense parenchymal infarcts in the spleen attributed to huge splenomegaly and hypersplenism. At the time of admission, physical examination revealed her vital signs to be body temperature: 39oC, heart rate: 110 beats per minute, respiratory rate: 21 times per minute, and blood pressure: 120/75 mmHg. Her cardiac and chest examination were unremarkable. Her chest spiral CT scan showed no specific abnormality ().
The patient’s abdomen was soft, but a generalized abdominal tenderness was remarkable in her physical examination. Her liver function profile showed aspartate aminotransferase (AST): 18 IU/l, alanine aminotransferase (ALT): 15 IU/l, alkaline phosphatase (ALP): 254 IU/l, total bilirubin: 0.4 mg/dl, direct bilirubin: 0.2 mg/dl, albumin: 3.8 gr/dl. Her coagulopathy parameters were PT=13 seconds, INR=1, and PTT=32 seconds. Stool exam was non inflammatory without WBC or RBC and no evidence of parasitic infection. Urine, blood, and stool cultures were all negative. Complete blood counts (CBC) were as follows: white blood cells (WBC)=10100 cells per cubic millimeter, hemoglobin (Hb)=10.1 gr/dl, mean corpuscular volume (MCV)=79.6 fl, platelet (Plt)=310000 per microliter. C-reactive protein (CRP) was 18 mg/l and erythrocyte sedimentation rate (ESR) was measured 22 mm/hr. Kidney function tests were BUN=23 mg/dl, and creatinine=2.1 mg/dl at the time of admission and 1.4 mg/dl at the time of discharge, natrium=139 meq/l and Kalium=4.2 meq/l. Trough level of tacrolimus was 8.7 ng/ml, which is within accepted range. CMV PCR and toxin A&B stool assays for clostridium difficile were negative. The patient previously took cellcept 1500 mg per day in divided doses, prograf (tacrolimus) 4 mg per day in divided doses, prednisolone 10 mg per day, aspirin 80 mg daily, levothyroxine 200 microgram daily, calcium-vitamin D supplement, folic acid 1 mg per day, and ferrous sulfate 60 mg daily. Initially, the patient was asked to discontinue cellcept because of an increased risk of developing severe sepsis in such circumstances. Hydration and empiric antibiotic therapy were started. Nephrology consult was requested because of a rise in serum BUN and creatinine level probably due to prerenal azotemia. Ultrasonography revealed a decrease in kidney size and an increase in corticomedullary differentiation, indicating an episode of acute kidney injury in addition to a preexisting chronic kidney disease. Moreover, ultrasonography findings revealed a normal orthotopic liver in size and contour. Normal intra and extra biliary ducts were detected. Color Doppler ultrasound demonstrated normal flow, size and patency of orthotopic vessels including portal vein, superior mesenteric vein, inferior venacava, and splenic vein before and at anastomosis sites.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [30, 'years'], 'Aspartate aminotransferase': [18.0, 'U/L'], 'Alanine aminotransferase': [15.0, 'U/L'], 'Platelet count': [310000.0, 'µL']}",0.44977,0.42728,0.47226,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 18.0 U/L.
The patient's concentration of ALT is 15.0 U/L.
The patient's concentration of platelets is 310000.0 count/µL. To convert 310000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 310000.0 platelets count/µL * 1000000.0 µL/L = 310000000000.0 platelets count/L. This means that there are 310000000000.0/(10^9) = 310.0 billion platelet counts per liter.
Plugging these values into the formula, we get (30 * 18.0)/(310.0 * sqrt(15.0)) = 0.44977.Hence, the Fibrosis-4 score is 0.44977."
4385,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-2803926-1,Extracted,"A 72-years-old Caucasian Greek male patient presented with epigastric pain of low intensity, jaundice and loss of appetite for the past 30 days. The patient was a heavy smoker (50 cig/day) and consumed alcohol (wine) occasionally, in small quantities. Physical examination revealed a distressed male patient with a body temperature of 37°C, blood pressure of 130/85 mmHg and pulse rate about 85/min. Painless jaundice was the presenting symptom and Courvoisier sign was present. The patient had no sings of ascites, or gastrointestinal obstruction. Hematocrit was 31%, white blood cells 10630/μL with neutrophil prevalence 77% and platelets 341.000/μL. Biochemical profile showed Tbil: 7.50 mg/dl, Dbil: 5.50 mg/dl, SGOT: 109 U/L, SGPT: 145 U/L, γGT: 517 U/L, ALP: 467 U/L, LDH: 503 U/L, CA125: 244, 50 U/L, CA19.9: 51.30 U/L. The patient was receiving digoxin and warfarin for chronic atrial fibrillation. Thin section computer tomography showed dilatation of the gallbladder and intra/extrahepatic biliary tree, while a 5 cm mass of the uncinate process of the pancreas was identified to invade the intrapancreatic portion of the bile duct, as well as the 2nd and 3rd portion of the duodenum (Figure ). There was no extrapancreatic disease, no extension to the superior mesenteric artery and celiac axis. The superior mesenteric-portal confluence was patent. The decision for surgical intervention was taken, and a pylorus preserving pancreaticoduodenectomy was performed after exploratory laparoscopy. The patient had an uneventful postoperative course and discharged on the 11th day.
Histological evaluation of the pancreatic tumor showed an adenosquamous carcinoma which was extensively infiltrative with perineural invasion, involvement of peripancreatic lymph nodes and all the thickness of the duodenum wall. The tumor elicited an intense desmoplastic stromal reaction and areas of necrosis (Figure ). Focal areas of high grade pancreatic intraepithelial neoplasia were seen. The tumor exhibited a biphasic malignant growth identified as, well to moderate differentiated adenocarcinoma and well to poorly differentiated squamous cell carcinoma (Figure ). The adenocarcinoma component contained ductal or glandular structures with focal intracellular or extracellular mucin (Figure ). Squamous differentiation was characterized by irregular and infiltrative nests or sheets of polygonal cells with distinct cellular borders, intercellular bridges, eosiniphilic cytoplasm and varying degrees of keratinization (Figure ). These two different patterns could be seen separated topographically within the substance of the tumor or intimately admixed. Six of the 15 resected lymph nodes were positive for metastatic tumor which was composed of squamous carcinoma only (Figure ).
The immunohistochemical study showed that the tumor cells were positive for cytokeratin AE1 and AE2. Cam 5.2 and Ker 7 were reactive predominantly in the adenocarcinoma component and in few squamous cells (Figure ). Immunoreactivity for CK 5/6 was restricted to the squamous component, while the glandular component was negative (Figure ). A few number of tumor cells were immunoreactive with CEA and Ca 19-9. All tumor cells were negative for Ker 20, chromogranin and synaptophysin.
The patient received adjuvant therapy (5-FU in combination with radiation). He received 40 Gy in two 20 - Gy courses and 500 mg per m2 5-FU by intravenous bolus delivered daily for the initial 3 days of each radiation course and then weekly. The patient 24 months postoperatively, remains disease free.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [72, 'years'], 'Aspartate aminotransferase': [109.0, 'U/L'], 'Alanine aminotransferase': [145.0, 'U/L'], 'Platelet count': [341000.0, 'µL']}",1.91126,1.8157,2.00682,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 109.0 U/L.
The patient's concentration of ALT is 145.0 U/L.
The patient's concentration of platelets is 341000.0 count/µL. To convert 341000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 341000.0 platelets count/µL * 1000000.0 µL/L = 341000000000.0 platelets count/L. This means that there are 341000000000.0/(10^9) = 341.0 billion platelet counts per liter.
Plugging these values into the formula, we get (72 * 109.0)/(341.0 * sqrt(145.0)) = 1.91126.Hence, the Fibrosis-4 score is 1.91126."
4386,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-5141538-1,Extracted,"A 66-year-old male with past medical history of chronic alcoholic and chronic hepatitis C (not sure if it was treated or not) was brought in by Emergency Medical Service (EMS) because of drowsiness and fatigue for 1 day. He denied any history of trauma.
Vital signs were pulse rate of 123 beats/minute, respiratory rate of 23 breaths/minute, and blood pressure of 82/55 mmHg. Physical examination revealed drowsy and pale patient that responded only to painful stimuli. Abdomen examination showed distended, tense abdomen with hypoactive bowel sounds. No organomegaly was found on palpation. Cardiovascular and chest examinations were within normal limits. No external bleeding source was identified.
laboratory tests showed white blood cells of 17.4 × 109/L, hemoglobin of 5 g/dL, hematocrit of 15%, platelet counts of 120,000/μL, mean corpuscular volume of 90.2 fL, absolute reticulocyte count of 63 K./μL (normal = 24–84 K./μL), haptoglobin of 68 mg/dL, bilirubin of 1.5 mg/dL, aspartate transaminase (AST) of 50 IU/L, alanine transaminase (ALT) of 103 IU/L and alkaline phosphatase of 90 IU/L, ammonia of 34 μmol/L, and tumor marker alpha fetoprotein level of 2556 ng/mL (normal = 0–8.3). Serum electrolytes, coagulation profile, amylase, and lipase were within normal limits. Baseline hemoglobin was 14.7 g/dL and hematocrit was 44% in 2011. Occult blood was negative.
Chest X-ray was unremarkable. Abdominal ultrasound revealed free peritoneal fluid and computed tomography (CT) scan of head showed no acute hemorrhage or infarct. CT scan of abdomen and pelvic revealed hemoperitoneum in the abdomen and pelvis and heterogeneous mass-like density abutting the gallbladder and lower right hepatic lobe (Figures , , and ).",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [66, 'years'], 'Aspartate aminotransferase': [50.0, 'U/L'], 'Alanine aminotransferase': [103.0, 'U/L'], 'Platelet count': [120000.0, 'µL']}",2.70966,2.57418,2.84514,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 50.0 U/L.
The patient's concentration of ALT is 103.0 U/L.
The patient's concentration of platelets is 120000.0 count/µL. To convert 120000.0 count/µL of platelets to L, multiply by the conversion factor 1000000.0 µL/L which will give 120000.0 platelets count/µL * 1000000.0 µL/L = 120000000000.0 platelets count/L. This means that there are 120000000000.0/(10^9) = 120.0 billion platelet counts per liter.
Plugging these values into the formula, we get (66 * 50.0)/(120.0 * sqrt(103.0)) = 2.70966.Hence, the Fibrosis-4 score is 2.70966."
4387,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-3705134-1,Extracted,"A 72-year-old man having recurrent lymph node metastases from gastric cancer was admitted to Saiseikai Sendai Hospital to receive chemotherapy for gastric cancer. He had a history of distal gastrectomy plus right hepatic lobectomy for advanced gastric cancer with liver metastases (). As paraaortic lymph node metastases had re-grown despite 17 courses of combination chemotherapy of paclitaxel (Bristol-Myers Squibb, NY, US) and S-1 (Taiho Pharmaceutical CO., LTD, Tokyo, Japan), the chemotherapy regime was changed to drip infusion of docetaxel (Sanofi-aventis, Paris, France). He showed no definite adverse effects at the first administration of docetaxel in short term hospitalization. This was the second treatment of docetaxel. On admission, he looked well-being and blood chemistry data showed no inflammatory disease. Before chemotherapy, abdominal CT showed neither metastasis nor abscesses in the liver. A total of 95 mg of docetaxel was infused intravenously. Before docetaxel administration, 8 mg of methyl predonine was routinely pretreated. One day after chemotherapy, the patient presented with a high-grade fever up to 39℃ and low blood pressure (80/55 mmHg). At that time, laboratory findings revealed a white blood cell count of 13,550/L, a red blood cell count of 2,420,000/L, a blood platelet count of 109,000/L, aspartate aminotransferase of 1,112 IU/L, alanine aminotransferase of 774 IU/L, and CRP of 4.6 mg/dl. Since he was diagnosed with septicemia unknown etiology, continuous dopamine infusion and broad-band antibiotics were started. The next day, blood chemistry examination revealed serious liver and renal dysfunction. Although sepsis was strongly suspected from leucocytosis and the high value of C-reactive protein, the origin of sepsis could not be identified. Despite intensive care including hemodialysis and respiratory support, the patient died 5 days against strong medical care after docetaxel administration. Blood bacterial culture revealed strongly positive E. coli. An autopsy was performed to check the cause of rapid multiple organ failure. There was no evidence of myelo-suppression by sequential chemotherapy from the result of bone marrow histology. Residual lymph node metastases from gastric cancer were histologically confirmed. Multiple occult liver abscesses which could not identified macroscopically were diagnosed by the histological examine (). They consisted of gram-negative rods and fungi (). Therefore, we concluded that fatal E. coli septicemia had been induced from multiple occult liver abscesses as a result of immuno compromised host induced by anticancer drug treatment.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [72, 'years'], 'Alanine aminotransferase': [774.0, 'U/L'], 'Platelet count': [109000.0, 'L'], 'Aspartate aminotransferase': [1112.0, 'U/L']}",26402211.48,25082100.91,27722322.05,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 1112.0 U/L.
The patient's concentration of ALT is 774.0 U/L.
The patient's concentration of platelets is 109000.0 count/L. This means that there are 109000.0/(10^9) = 0.000109 billion platelet counts per liter.
Plugging these values into the formula, we get (72 * 1112.0)/(0.000109 * sqrt(774.0)) = 26402211.47939.Hence, the Fibrosis-4 score is 26402211.47939."
4388,19,Fibrosis-4 (FIB-4) Index for Liver Fibrosis,lab test,decimal,pmc-5937617-1,Extracted,"An 83-year-old Caucasian male with past medical history of hypertension, diabetes, and coronary artery disease presented to the emergency department with extreme fatigue, weakness, and disorientation. He reported a history of 10–15-pound weight loss over the previous month. Physical exam did not yield any focal signs. Laboratory evaluation revealed pancytopenia (Hgb 9.6 g/dL, WBC 3.0 bil/L, and platelets 169 bil/L) and increased liver function enzymes (AST 311 U/L, ALT 62 U/L, and ALP 237 U/L). The patient was admitted for generalized weakness and fatigue.
An unenhanced CT scan of the abdomen and pelvis obtained in the emergency department showed a nondistended gallbladder with diffuse wall thickening (). A small calcified gallstone was identified in the neck of the gallbladder. Neither a soft tissue mass nor lymphadenopathy was present. Although acute cholecystitis was not a leading differential diagnosis based on the clinical presentation, HIDA scan was recommended based on the unexpected CT findings.
The patient developed worsening alteration of mental status, metabolic acidosis, further increase in liver function tests, and pancytopenia. D-dimer was elevated (1830 ng/mL). There was initially clinical concern for pulmonary embolism versus disseminated intravascular coagulation. Nuclear medicine testing with ventilation-perfusion (VQ) scan was performed and low probability for pulmonary embolism was found. Coagulation testing remained stable.
The HIDA scan revealed cystic duct patency (). Subsequently, a targeted sonographic examination of the right upper quadrant was performed to further characterize the nonspecific findings on the CT scan. This revealed diffuse gallbladder wall thickening measuring up to 8 mm. The gallbladder wall had a striated appearance with a central hypoechoic stripe surrounded by an echogenic band on either side (). The sonographic Murphy's sign was negative. The gallbladder was decompressed and contained a few small stones. An MRI of the abdomen with contrast showed diffusely thickened gallbladder wall measuring up to 12 mm with intramural increased signal intensity on T2 weighted images. Contrast enhanced T1 weighted sequences showed no abnormal enhancement or nodularity of the gallbladder wall. The gallbladder did contain a few small stones, but there was no luminal distention, pericholecystic fluid, or lymphadenopathy (). Clinical concern further developed for septicemia with the gallbladder as the primary site of origin given the imaging findings. The patient underwent laparoscopic cholecystectomy.
Pathologic evaluation of the surgical specimen revealed findings of intravascular large B-cell lymphoma (IVLBCL), a rare variant of extranodal diffuse large B-cell lymphoma. Histologic evaluation with hematoxylin and eosin stain demonstrated diffuse gallbladder wall thickening with lymphatic ectasia (). Several blood vessels in the subserosal fat showed infiltration with large, atypical lymphomatous cells. The mucosa was uninvolved. These features explained all the imaging findings well in this particular case.
Flow cytometry of the peripheral blood revealed a small population of aberrant B-cells which correlate to the pathologic gallbladder wall findings. Subsequent bone marrow core biopsy and aspiration were performed. Pathologic evaluation demonstrated slight hypercellularity of the marrow and 10–15% involvement by diffuse large B-cell lymphoma. Immunohistochemical stain of bone marrow core biopsy sample was positive for CD79a, confirming B-cell origin.
Postoperatively, the patient's condition continued to deteriorate requiring respiratory support in the intensive care unit. He developed severe metabolic acidosis and hemodynamic instability. Given the patient's poor functional status and concomitant diagnosis of IVLBCL, the decision to withdraw supportive care was made by his family. The patient expired 7 days after initial presentation.",What is the patient's score of the Fibrosis 4 Index? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [83, 'years'], 'Aspartate aminotransferase': [311.0, 'U/L'], 'Alanine aminotransferase': [62.0, 'U/L'], 'Platelet count': [169000000000.0, 'L']}",19.39795,18.42805,20.36785,"The formula for computing Fibrosis-4 is Fib-4 = (Age * AST) / (Platelet count (in billions) * √ALT), where platelet count is the number of billions per L, and the units for AST and ALT are both U/L.
The patient's concentration of AST is 311.0 U/L.
The patient's concentration of ALT is 62.0 U/L.
The patient's concentration of platelets is 169000000000.0 count/L. This means that there are 169000000000.0/(10^9) = 169.0 billion platelet counts per liter.
Plugging these values into the formula, we get (83 * 311.0)/(169.0 * sqrt(62.0)) = 19.39795.Hence, the Fibrosis-4 score is 19.39795."
4389,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-5503,Extracted,"A 48-year-old nurse presents with left-sided chest pain and nonproductive cough. He thinks both the chest pain and the cough began about two months ago. He recently joined a meditation group and found that the deep breathing exercises exacerbate his chest pain. The patient denies headaches, fever, or chills. He reports a 3 lb weight loss over the last two weeks, which he attributes to a change in his diet that he and his wife recently started. The patient drinks a glass or two of whiskey on the weekends and is a non-smoker. The patient’s medical history is significant for type II diabetes and Hodgkin lymphoma. He was treated with chemotherapy and radiation 25 years ago without complications. His current medications include metformin and glyburide. His HbA1c is 7.5%. His temperature is 99°F (37.2°C), blood pressure is 121/82 mmHg, pulse is 86/min, respirations are 12/min, and oxygen saturation is 95% on room air. Physical exam is notable for coarse rhonchi in the left lung. There is no appreciable lymphadenopathy. A chest radiograph is performed, which is shown in Figure A.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [48, 'years'], 'Exudate or swelling on tonsils': False, 'Tender/swollen anterior cervical lymph nodes': False, 'Temperature': [99.0, 'degrees fahrenheit'], 'Cough Absent': False}",-1,-1,-1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 48 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 99.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 67.0 = 37.22222 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at -1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at -1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at -1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at -1.
Hence, the Centor score for the patient is -1."
4390,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-8306,Extracted,"A 12-year-old girl brought to the clinic by her mother has a 3-day history of fever and sore throat and hematuria since this morning. The patient’s mother says she had a fever up to 39.5℃ (103.1℉) for the last 3 days and a severe sore throat, which has improved slightly. The mother states that she noticed her daughter had red urine today. The patient’s temperature is 39.3℃ (102.8℉), pulse is 89/min, respiratory rate is 25/min, and blood pressure is 109/69 mm Hg. On physical examination, her pharynx is erythematous. There is significant swelling of the tonsils bilaterally, and there is a white exudate covering them. Ophthalmologic examination reveals evidence of conjunctivitis bilaterally. Otoscopic examination is significant for gray-white tympanic membranes bilaterally. The remainder of the exam is unremarkable.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [12, 'years'], 'Exudate or swelling on tonsils': True, 'Temperature': [39.3, 'degrees celsius'], 'Cough Absent': False, 'Tender/swollen anterior cervical lymph nodes': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 12 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 39.3 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
Hence, the Centor score for the patient is 3."
4391,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-2628029-1,Extracted,"A 67-year-old man was referred for biopsy of a known retroperitoneal mass in April 2006 after suddenly developing gross hematuria two months earlier. The patient was diagnosed with Hashimoto's thyroiditis at a hospital three years previous on the basis of profound hypothyroidism, markedly increased levels of autoimmune antibody (thyroglobulin antibody 1,587.2 U/mL, normal values: 0 - 60 U/mL; microsomal antibody > 3,000 U/mL, normal values: 0 - 60 U/mL), and a diffuse hypoechogenic ultrasonographic pattern. Upon referral in April of 2006, he had been taking levothyroxine to control his Hashimoto's. Computed tomography (CT) scan of the abdomen and pelvis at a previous hospital revealed a retroperitoneal soft tissue mass extending from the lower pole of the kidney to the iliac chains, inducing bilateral ureteral obstruction. The CT did not demonstrate soft tissue between the aorta and vertebra or lymphadenopathy, excluding malignancy. A right percutaneous nephrostomy was also performed at the previous hospital in order to decompress hydronephrosis due to the retroperitoneal mass.
On admission, the patient's blood pressure was 140/100 mmHg and body temperature was 36.5℃. The lungs were clear to auscultation, heart sounds were within normal limits, and the abdomen was soft with no masses or tenderness. There was no lower extremity edema observed and the thyroid gland was not enlarged. Results of the complete blood count, electrolytes, creatinine, urea nitrogen, protein, albumin, bilirubin, β2-microglobulin and lactate dehydrogenase (LDH) were within normal ranges. Upon immunological testing, immunoglobulin G, C3 and C4 levels remained within normal ranges. No cytoplasmic antineutrophil cytoplasmic antibody or cryoglobulin was detected, and antinuclear antibodies and anti-DNA antibodies were negative. The patient showed signs of hypothyroidism with an elevated thyroid stimulating hormone (TSH) (69.56 µIU/mL, normal values: 0.4 - 3.1 µIU/mL) and reduced free T4 (0.83 ng/dL, normal values: 0.73 - 1.95 ng/dL). Upon autoantibody screening, the thyroglobulin (1,368.7 U/mL, normal values: 0 - 60 U/mL) and microsomal antibodies were elevated (> 3,000 U/mL, normal values: 0 - 60 U/mL) despite good medication compliance. After initiating an increased dose of levothyroxine (0.2 mg), laparoscopic biopsy of the retroperitoneal mass was performed.
Microscopically, the mass was ill-defined and composed predominantly of chronic inflammation and fibrosis. The inflammatory cells were mainly lymphocytes and plasma cells with the occasional formation of lymphoid follicles (). Based on pathologic diagnosis, the patient was started on deflazacort 72 mg daily. The patient was discharged after 13 days of hospitalization and continued to receive steroid therapy at the outpatient clinic. Normal thyroid function was achieved after two months of steroid treatment; therefore levothyroxine therapy was withdrawn. Steroids were tapered to 6 mg after two months, which is the patient's current dose. The patient experienced no side effects during steroid treatment. Abdominal ultrasound demonstrated marked reduction of the retroperitoneal mass and no sign of hydronephrotic change in either kidney. Moreover, an abdominal-pelvic CT scan performed nine months after steroid treatment showed reduced mass lesion in the retroperitoneal space with resolved right side hydronephrosis ().",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [67, 'years'], 'Exudate or swelling on tonsils': False, 'Temperature': [36.5, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Cough Absent': False}",-1,-1,-1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 67 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 36.5 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at -1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at -1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at -1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at -1.
Hence, the Centor score for the patient is -1."
4392,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-7300,Extracted,"A 5-year-old boy presents to your office with his mother. The boy has been complaining of a sore throat and headache for the past 2 days. His mother states that he had a fever of 39.3°C (102.7°F) and had difficulty eating. On examination, the patient has cervical lymphadenopathy and erythematous tonsils with exudates. A streptococcal rapid antigen detection test is negative.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [5, 'years'], 'Temperature': [39.3, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True, 'Cough Absent': False}",4,4,4,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 5 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 39.3 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 3 + 1 = 4.
Hence, the Centor score for the patient is 4."
4393,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-6762,Extracted,"A 15-year-old girl presents to her primary care physician with her parents. She is complaining of fever and a sore throat for the past 4 days. She was born at 39 weeks gestation via spontaneous vaginal delivery and is up to date on all vaccines and is meeting all developmental milestones. Her boyfriend at school has the same symptoms including fever and sore throat. Today, her heart rate is 90/min, respiratory rate is 17/min, blood pressure is 110/65 mm Hg, and temperature is 38.2°C (100.8°F). Examination revealed cervical lymphadenopathy and mild hepatosplenomegaly. Oral exam reveals focal tonsillar exudate. A monospot test is positive.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [15, 'years'], 'Exudate or swelling on tonsils': True, 'Temperature': [38.2, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Cough Absent': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 15 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 38.2 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 1 + 1 = 2.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
Hence, the Centor score for the patient is 3."
4394,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-560,Extracted,"A previously healthy 11-year-old boy is brought to the emergency department because of a 3-day history of fever, cough, and a runny nose. During this period, he has also had pink, itchy eyes. The patient emigrated from Syria 2 weeks ago. His parents died 6 months ago. He has not yet received any routine childhood vaccinations. He lives at a foster home with ten other refugees; two have similar symptoms. He appears anxious and is sweating. His temperature is 39.2°C (102.5°F), pulse is 100/min, respirations are 20/min, and blood pressure is 125/75 mm Hg. Examination shows conjunctivitis of both eyes. There are multiple bluish-gray lesions on an erythematous background on the buccal mucosa and the soft palate.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [11, 'years'], 'Temperature': [39.2, 'degrees celsius'], 'Cough Absent': False, 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",2,2,2,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 11 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 39.2 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
Hence, the Centor score for the patient is 2."
4395,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-4716281-1,Extracted,"In March 2015, a 45-year-old Korean woman presented to our emergency department (ED) with shortness of breath and an episode of seizure. Five hours before arriving in the ED, she developed a tonic-clonic seizure for 30 seconds and a high temperature of 40℃. The patient had preceding upper respiratory infection 4 days before coming to the ED. She also complained of severe coughing productive of blood-tinged sputum, and generalized myalgias. Her past medical history was unremarkable except for recurrent (one or two per year) epileptic seizures with oral phenytoin maintenance for 25 years. She had no known allergies. She did not receive the seasonal influenza vaccine.
On physical examination, the patient's blood pressure was 91/59 mmHg, and she had tachycardia (114/min), tachypnea (32/min), and a temperature of 37.9℃. She looked acutely ill, but was mentally alert. Examination of her lungs revealed coarse crackles throughout bilaterally. Other findings were unremarkable. A chest radiograph showed cardiomegaly and bilateral patchy consolidations. An electrocardiogram revealed low QRS voltage in the precordial leads (the entire QRS-complex amplitude was <8 mm). Arterial blood gas analysis revealed pH of 7.38, carbon dioxide tension of 27.7 mmHg, partial pressure of oxygen of 59.8 mmHg, bicarbonate level of 16.7 mmol/L, base excess of 6.4 mmol/L, and oxygen saturation level of 90.7%. The patient was given supplemental oxygen via nasal cannula (2 L/min).
Initial laboratory findings revealed a hemoglobin level of 10.0 g/dL, white blood cell count of 18.8 × 103/mm3 (neutrophils, 85.6%), platelet count of 504 × 103/mm3, blood urea nitrogen level of 14.9 mg/dL, creatinine level of 0.6 mg/dL, and C-reactive protein level of 4.92 mg/L (normal range, 0.0-5.0 mg/L). An influenza rapid antigen test on the patient's nasopharyngeal swab sample, which was promptly performed because of residual seasonal influenza activity in the community, was positive for influenza A virus. She was immediately given a single dose (300 mg) of IV peramivir, and levofloxacin, 500 mg/day.
The patient's dyspnea worsened, however, and she became hypotensive (blood pressure, 86/53 mmHg). She was managed with increased oxygen supply (4 L/min), furosemide, and norepinephrine (0.125 µg/kg/min). Additional blood tests revealed the following component levels: troponin I, 1.36 ng/mL (normal range, 0.0-0.16 ng/mL); creatine kinase-MB (CKMB), 49.27 ng/mL (normal range, 0.0-3.61 ng/mL); creatine phosphokinase (CPK), 1,585 IU/L (normal range, 38-185 IU/L); lactate dehydrogenase, 937 IU/L (normal range, 238-422 IU/L); N-terminal pro b-type natriuretic peptide, 162.8 pg/mL (normal range, 0-125 pg/mL), and myoglobin, 138.8 ng/mL (normal range, 25-58 ng/mL). Serology for hepatitis B virus, hepatitis C virus and HIV were all negative.
A chest computed tomography scan demonstrated multifocal patch consolidations in both lungs, with ground-glass opacities, suggestive of pulmonary edema or atypical pneumonia. Transthoracic echocardiogram showed a depressed left ventricular (LV) ejection fraction of 30%, LV enlargement, diffuse hypokinesia with sparing LV apex, and decreased right ventricular apical wall motion, which was compatible with acute myocarditis ().
The patient was clinically diagnosed with influenza A-associated fulminant myocarditis, resulting in pulmonary edema and cardiogenic shock, and admitted to the intensive care unit. On day 2 of hospitalization, her hemodynamic state had stabilized and she no longer required norepinephrine to maintain blood pressure within a normal range. A follow-up transthoracic echocardiogram taken on day 3 showed improved ventricular systolic function, with LV ejection fraction at 55% to 60%. Laboratory tests on day 4 revealed a troponin I level of 0.168 ng/mL, CK-MB level of 41.31 ng/mL, and CPK level of 1,459 IU/L. On day 5 of her hospitalization, the patient's dyspnea had improved and supplemental oxygen was stopped. On day 6, she was transferred to a general ward. A follow-up chest computed tomography scan demonstrated improved status of pulmonary edema, with residual, mild bilateral pleural effusion. The patient was discharged with recovery on day 9 after admission. Although her muscle enzyme levels still remained elevated 16 days after discharge (CK-MB, 42.63 ng/mL; CPK, 1,340 IU/L), she had been asymptomatic and carefully observed in the outpatient clinic ().
Monitoring of real-time reverse transcription-polymerase chain reaction assays (Real-Q Flu A, B Detection Kit; BioSewoom Inc., Seoul, Korea) using the patient's nasopharyngeal aspirates showed positivity for both influenza A (threshold cycle value, 27.23) and subtype hH3N2 (threshold cycle value, 27.39) on day 2 (), but became negative by day 4 of the patient's hospitalization.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'years'], 'Temperature': [37.9, 'degrees celsius'], 'Cough Absent': False, 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",-1,-1,-1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 45 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 37.9 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at -1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at -1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at -1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at -1.
Hence, the Centor score for the patient is -1."
4396,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-7168152-1,Extracted,"A 22-month-old African-American girl was transferred from an outside hospital to the intensive care unit for further evaluation and the management of uncontrolled severe hypertension. She had a three-day history of fever, cough, rhinorrhea, shortness of breath, dizziness and vomiting. She was born at term with a weight of 2.8 kg and had an unremarkable perinatal course. She had no known genetic syndromes. Besides a history of difficulty gaining weight with a current weight of 10.7 kg (seventh percentile) and a height of the 25th centile, she had no other known medical problems in the past. There was no history of urinary tract infections or blood in urine. She did not have headaches, seizures or fainting episodes. Immunizations were up-to-date. Prior blood pressure (BP) measurements were unknown because they were never obtained. There were no other past hospitalizations. She had not been taking any medications. Family history was unremarkable for kidney disease, hypertension, dialysis or transplantation.
Upon physical examination, her vital signs were as follows: a temperature of 36.9 °C (98 °F), a respiratory rate of 16 per minute, a heart rate of 145 beats per minute, an oxygen saturation of 100% on room air, and an elevated BP of 200/120 mm Hg (manual, right upper extremity, proper size cuff; 95th percentile value for her age, gender and height 104/62 mm Hg). The examination showed a thin-appearing toddler who was not in obvious distress. The rest of the examination was negative except for tachycardia and a grade II/VI systolic murmur at the apex. A renal bruit was not heard upon auscultation. There was no skin rash or edema. The neurologic examination was normal.
The nasal swab for a respiratory viral panel test was positive for parainfluenza 3. Besides mild nasal congestion, she had no cough, difficulty breathing, or wheezing, and she remained stable in room air. She remained afebrile throughout the hospital admission. Her throat culture was negative for beta-hemolytic streptococcus. Her blood culture showed no growth. Her chest x-ray showed mild cardiomegaly but no focal airspace disease, pneumothorax or pleural effusion. Her electrocardiogram showed supraventricular tachycardia. Her echocardiogram revealed a dilated left ventricle with severe concentric left ventricular (LV) hypertrophy, with an LV mass index of 187 gm/m2.7 and a mildly depressed LV systolic function with an ejection fraction of 50%. There was a thrombus in the apex of the LV. The serum brain natriuretic peptide and troponin I levels were 1565 pg/mL (normal: <100 pg/mL) and 242 pg/mL (normal: <15 pg/mL), respectively. For possible viral-induced cardiomyopathy, she was started on intravenous immunoglobulin and methylprednisolone. For hypertension, she was started on nicardipine infusion, along with nitroprusside with a goal BP reduction of 30% over 24 hours. Milrinone was added for depressed LV systolic function. She remained on the maximum nicardipine infusion rate for several days due to persistent hypertension, with systolic BPs of 140–150 mm Hg. Heparin was transitioned to enoxaparin and aspirin, with the resolution of the cardiac thrombus by day three. A non-contrast computed tomography (CT) scan of head showed no mass, acute intracranial hemorrhage, cytotoxic edema, midline shift, or signs of herniation. Her urine output was normal.
A renal function test showed an initial serum sodium level of 131 meq/L with a nadir of 121 meq/L at day three of admission, a serum chloride level of 97 meq/L (nadir 84 meq/L at day three), a serum potassium level of 3.2 meq/L, a blood urea nitrogen level of 25 mg/dL, and a serum creatinine level of 0.5 mg/dL. Her fasting blood glucose level was 90 mg/dL. Her urine sodium level was 89 mmol/L with a fractional excretion of sodium of 1.5%. Her serum albumin level was between 2.1 and 2.5 gm/dL, and her random urine protein to creatinine ratio was 4.6 (normal: <0.2). There was no microscopic hematuria. Her urine culture showed no growth. Her blood counts and serum complements were both normal. Her sickle cell screen was negative. A renal sonogram showed a small right kidney of 6 cm in length (36th centile) and a left kidney of 7.7 cm in length (96th centile), with good blood flow in both kidneys. Her serum aldosterone and plasma renin activity at the time of admission were both elevated at 106 ng/dL (normal: <16 ng/dL, supine, quantitative chemiluminescent immunoassay) and >150 ng/mL/h, respectively (normal: 1.7–11.2 ng/mL/h, supine, quantitative enzyme-linked immunosorbent assay; both ARUP laboratories, Salt Lake City, UT, USA).
A work-up for possible catecholamine-secreting tumors due to severe hypertension included the evaluation of urine and serum catecholamines. Her 24-hour urine normetanephrine, metanephrine, vanillylmandelic acid, and homovanillic acid levels were 1525 µg/g of creatinine (normal: 0–1300 µg/g of creatinine), 433 µg/g of creatinine (normal: 0–530 µg/g of creatinine), 10 mg/g of creatinine (normal: <16 mg/g of creatinine), and 12 mg/g of creatinine (normal: <25 mg/g of creatinine), respectively. Her serum fractionated catecholamines showed the following: an epinephrine level of 152 pg/mL (normal: 36–640 pg/mL) and a norepinephrine level of 1964 pg/mL (normal: 68–1810 pg/ml), respectively. Given a less than two-fold increase from normal range of serum norepinephrine, the suspicion of the presence of a neuroendocrine tumor was low.
A diuretic nuclear renogram showed asymmetrical renal function with decreased blood flow and function in the small right kidney relative to the left. Her differential function was 70% in the left and 30% in the right. There was a normal uptake of the technetium-99 m MAG3 (mercaptoacetyltriglycine) with prompt excretion from the left kidney. Her right kidney had little delayed uptake with prompt excretion ( and , ). A duplex sonogram of her RA showed focal elevation in velocity in the proximal right main RA (peak systolic velocity (PSV): 405 cm/second) with a decreased velocity in the mid and distal RAs (PSV: 117 and 110 cm/sec, respectively). The renal aortic ratio (RAR, the ratio of renal to aortic PSV) was elevated at 3.2. Additionally, distinct “tardus-parvus” (tardus-slow and late, parvus-small and little) waveforms were seen at the right hilar and interlobar arteries. This combination of an elevated PSV at the proximal right main RA along with an elevated RAR (usual cut-off 3) and abnormal waveforms was highly suggestive of proximal right main RAS. Velocities in the left main RA were normal with no differences at various segments of the main artery. A CT angiogram (CTA) of the RAs showed a small right kidney of 6 cm in length with a decreased enhancement of the superior pole of the right kidney. The origin of the right main RA was diminutive compared to the left. There was a homogenous enhancement of the left kidney with a normal appearing left RA. Hypertension at that time was well controlled with amlodipine, clonidine, furosemide, spironolactone and labetalol. Nicardipine infusion was discontinued at day seven of admission.
A few days later, she underwent a digital subtraction angiogram (DSA), which showed a beaded appearance of the right proximal main RA, which caused a focal stenosis with post-stenotic dilatation ( and ). The pressure gradient across the stenotic lesion was 40 mm Hg. There was normal renal parenchymal perfusion. The left RA demonstrated a normal appearance of the main and branch arteries with normal renal parenchymal perfusion and no evidence of stenosis and irregularity. A diagnosis of right RA stenosis, most likely due to focal FMD, was made. In conjunction with vascular surgery and intervention radiology, it was collectively decided not to pursue the intervention of the stenotic lesion due to the risk of complication, specifically the injury or dissection of the right RA, especially because her BPs were relatively controlled on five antihypertensive agents. Subsequent to the angiogram, enalapril was added once bilateral RA stenosis was excluded for optimal BP control. A CTA of the head and neck vessels to look for evidence of FMD in the head and neck showed a normal vasculature of the vessels. Baby aspirin was started to prevent thromboembolic events.
Though fever, parainfluenza virus infection, and LV thrombus could have partly contributed to the elevated BPs initially, these signs and symptoms had resolved at the time of or soon after admission. Additionally, the finding of a discrete anatomic lesion in the right RA that is known to cause hypertension suggests that the right RA FMD indeed was the most probable cause of the severe, long-standing hypertension, as suggested by the severe concentric LV hypertrophy. At the time of discharge two weeks later, her BPs were relatively optimal (105–110 mm Hg SBPs) on enalapril, amlodipine and labetalol. Subsequent monthly clinic follow-up visits seven months later have shown stable SBPs with no clinical symptoms of hypertension. Her renal function has remained stable with normal serum electrolytes without hyponatremia and hypokalemia. Her proteinuria has resolved. A follow-up echocardiogram showed normal LV systolic function and stable but persistent LV hypertrophy with no reappearance of the thrombus that was seen in the first echocardiogram. For now, we plan to closely follow-her BPs, along with a follow-up diuretic renogram and a DSA in a few months, with a tentative plan for either continued medical treatment or surgical intervention (angioplasty with or without stent and surgical revascularization or right nephrectomy) based on the clinical course.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [22, 'months'], 'Exudate or swelling on tonsils': False, 'Temperature': [36.9, 'degrees celsius'], 'Cough Absent': False, 'Tender/swollen anterior cervical lymph nodes': False}",0,0,0,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
This means that the patient is 1 year and 10 oldThe patient's temperature is 36.9 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 0.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 0.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
Hence, the Centor score for the patient is 0."
4397,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-11684,Extracted,"A 16-year-old male presents to his pediatrician with a sore throat. He reports a severely painful throat preceded by several days of malaise and fatigue. He has a history of seasonal allergies and asthma. The patient is a high school student and is on the school wrestling team. He takes cetirizine and albuterol. His temperature is 100.9°F (38.3°C), blood pressure is 100/70 mmHg, pulse is 100/min, and respirations are 20/min. Physical examination reveals splenomegaly and posterior cervical lymphadenopathy.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [16, 'years'], 'Temperature': [100.9, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': True, 'Cough Absent': False, 'Exudate or swelling on tonsils': False}",2,2,2,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 16 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 100.9 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 68.9 = 38.27778 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 1 + 1 = 2.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
Hence, the Centor score for the patient is 2."
4398,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-4262,Extracted,"A 5-year-old male presents to the pediatrician with a 10-day history of cough that is worse at night. The patient has a history of mild intermittent asthma and has been using his albuterol inhaler without relief. He has also been complaining of headache and sore throat, and his mother has noticed worsening rhinorrhea. The patient’s past medical history is otherwise unremarkable, and he has no known drug allergies. In the office, his temperature is 101.8°F (38.8°C), blood pressure is 88/65 mmHg, pulse is 132/min, and respirations are 16/min. The patient has purulent mucus draining from the nares, and his face is tender to palpation over the maxillary sinuses. His pharynx is erythematous with symmetric swelling of the tonsils.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [5, 'years'], 'Temperature': [101.8, 'degrees fahrenheit'], 'Exudate or swelling on tonsils': True, 'Cough Absent': False, 'Tender/swollen anterior cervical lymph nodes': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 5 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 101.8 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 69.8 = 38.77778 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
Hence, the Centor score for the patient is 3."
4399,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-8103,Extracted,"A 17-year-old boy is admitted to the emergency department with a history of fatigue, fever of 40.0°C (104.0°F), sore throat, and enlarged cervical lymph nodes. On physical examination, his spleen and liver are not palpable. A complete blood count is remarkable for atypical reactive T cells. An examination of his tonsils is shown in the image below.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [17, 'years'], 'Temperature': [40.0, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Cough Absent': False, 'Exudate or swelling on tonsils': False}",2,2,2,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 17 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 40.0 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 1 + 1 = 2.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
Hence, the Centor score for the patient is 2."
4400,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-9299,Extracted,"An otherwise healthy 27-year-old man presents to the Emergency Department with dark urine and left flank pain. He has had a fever, sore throat, and malaise for the last 2 days. Vital signs reveal a temperature of 38.1°C (100.5°F), blood pressure of 120/82 mm Hg, and a pulse of 95/min. His family history is noncontributory. Physical examination reveals enlarged tonsils with tender anterior cervical lymphadenopathy. Urinalysis shows pink urine with 20–25 red cells/high power field and 2+ protein.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [27, 'years'], 'Exudate or swelling on tonsils': True, 'Temperature': [38.1, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Cough Absent': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 27 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 38.1 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 1 + 1 = 2.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
Hence, the Centor score for the patient is 3."
4401,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-4538967-1,Extracted,"A 41-year-old female presenting with complaints of fever, chills, and symptoms of an upper respiratory tract infection including sore throat and difficulty swallowing for three days arrived at our emergency department in December 2014. The patient did not have vomiting, diarrhea, chest distress, abdominal pain, rash, jaundice, cough, or expectoration. The patient had no history of smoking or alcohol intake, hypertension, diabetes, kidney disease or other chronic diseases, tuberculosis, hepatitis, typhoid fever, or other infectious diseases. In addition, there was no history of trauma, surgery or history of medicine, or food allergies. One month previously, the patient had been diagnosed with hyperthyroidism and prescribed methimazole (10 mg BID) and propranolol (20 mg BID) at a local hospital. The patient discontinued the medicine after taking this treatment for ten days and three weeks prior to admission, since she thought that she may be pregnant because of a delayed menstrual cycle.
The patient's initial assessment in the emergency department revealed a temperature of 39.9°C, heart rate of 129 beats/min, and blood pressure of 174/76 mmHg. The patient had pharyngeal congestion, bilateral tonsil enlargement, and visible purulent secretions on bilateral tonsils. The patient had a mild hand tremor; however, there was no rash or jaundice. There were normal S1 and S2 sounds in cardiac examination. The patient's abdomen was normal, and no peripheral edema or lymphadenopathy was observed. There was bilateral grade 2 thyroid enlargement. There was no evidence of ophthalmopathy. The results of a neurologic and rheumatic examination were unremarkable.
The laboratory findings before antithyroid treatment were as follows: white blood cell count (WBC) and absolute neutrophil count were normal at 5200/μL (reference range, 3500 to 10500/μL) and 2300x/μL (reference range, 1500 to 8000/μL), respectively, with free T3, 16.8 pg/mL (reference range, 1.71–3.71 pg/mL), free T4 3.9 ng/dL (reference range, 0.7–1.48 ng/dL), and thyroid-stimulating hormone (TSH) 0.0001 μIU/mL (reference range, 0.35–4.94 μIU/mL) in thyroid function tests.
The results from peripheral-blood count tests showed an absolute neutrophil count of zero and a WBC count of 400/μL at admission. Hemoglobin concentration and platelet count were normal at 13.6 g/dL (reference range, 11.5–16.5 g/dL) and 165 × 103/μL (reference range, 100–400 × 103/μL), respectively. C-reactive protein level was markedly elevated at 155 mg/L (reference range, 0–5 mg/L). Erythrocyte sedimentation rate was 18 mm/h (reference range, 0–10 mm/h). Thyroid function tests were as follows: free T3, 3.63 pg/mL (reference range, 1.71–3.71 pg/mL), free T4 2.2 ng/dL (reference range, 0.7–1.48 ng/dL), and TSH, 0.0001 μIU/mL (reference range, 0.35–4.94 μIU/mL). The pregnancy test was negative. Results from the electrocardiogram showed sinus tachycardia. Chest radiography divulged no infiltration. An abdominal ultrasonography was unremarkable. A peripheral-blood smear was normal except for agranulocytosis. There were no pathological findings except for borderline anti-nuclear antibody (ANA) positivity in rheumatic, viral, and bacterial serological tests (). Based on these results, the patient was diagnosed with ATD-induced agranulocytosis, acute tonsillitis, and hyperthyroidism.
On admission to our hospital, the patient was given intravenous antibiotics (amikacin and imipenem) to control infection and propranolol to hinder T4 transformation into T3 and to prevent excitatory effects on the heart. Methimazole was not restarted because of the neutropenia. After three days the neutrophil count increased to 600/μL, after six days the neutrophil count increased to 700/μL, and after seven days the neutrophil count increased to 2600/μL. After 10 days of treatment, a blood culture yielded no microbes, the neutrophil count was increased to 2900/μL, and the patient's symptoms were generally improved; the patient no longer had fever or throat symptoms. With clinical improvement of her symptoms and recovered neutropenia, antibiotherapy was discontinued.
Results from the thyroid ultrasonography showed bilateral parenchymal heterogeneity, increment blood supply, and a 16 mm solitary nodule in the right thyroid lobe. On thyroid scintigraphy, there was diffusely increased radioiodine uptake in the thyroid gland and a hypoactive nodule in the right lobe. Fine needle aspiration biopsy performed at two different times on the nodule was insufficient. The option of surgical treatment was agreed upon because possible thyroid malignancy could not be ruled out due to inadequate biopsy results. In January 2015, she received a bilateral total thyroidectomy for surgical treatment after obtaining euthyroidism with combination therapy including lugol solution, corticosteroid, cholestyramine, and propranolol. The results of surgical histopathology were consistent with a benign nodular hyperplasia. The patient was followed with levothyroxine replacement treatment and the absolute neutrophil count remained within the reference range at 1600 to 3600/μL.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [41, 'years'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': True, 'Temperature': [39.9, 'degrees celsius'], 'Cough Absent': True}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 41 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 39.9 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 1 + 1 = 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
Hence, the Centor score for the patient is 3."
4402,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-6552945-1,Extracted,"Our patient is a 2-year-old male who presented with a 1-day fever (Temperature: 103.6°F), cough, congestion, and inadequate oral intake. The patient's history was obtained from the patient's mother. She denied any signs of vomiting, abdominal pain, diarrhea, respiratory distress, ear pain, or a sore throat. Additionally, the patient showed signs of dehydration. Upon an initial examination, he was agitated but consolable. An examination of his ears revealed no external deformities; his canals were patent and without inflammation, and his tympanic membranes were intact, gray, translucent, and mobile. His nose showed no external deformities, and the nares were patent. His nasal turbinates were erythematous, but no inflammation was exhibited. His oral structures were normal for a child of his age, and the mucous membranes were moist and pink, without any lesions or exudates. His teeth did not have any dental caries. His neck was supple, and no cervical lymphadenopathy was present. The rest of his physical examination also revealed negative findings. The patient's fever and irritability warranted initial laboratory tests, including a rapid influenza test, a complete blood cell count (CBC), a C-reactive protein (CRP) test, and a blood culture. Abnormal values included leukocytosis that exhibited a left shift (26 500 cells/µL) and an elevated CRP (24.7 mg/L).
Due to his elevated CBC and CRP, the patient was called back into the office for a re-evaluation the next day. His physical examination revealed new findings of erythematous tonsils with a midline uvula, as well as left and right posterior cervical nodes. The tenderness of the nodes was difficult to decipher because the patient was irritable throughout the examination. The hydration status of the patient had improved from the previous night. The rest of his physical examination revealed similar findings as the previous day. A urinalysis was obtained via catheterization and revealed negative results. Since his elevated WBC count raised concerns of the possibility of a bacterial infection, an intramuscular ceftriaxone injection was given. The patient was sent home with instructions to the parents to report any changes in his symptoms or any reactions to the antibiotics. Subsequent tests for CBC and CRP, which were obtained on the 4th day of the patient's symptoms, were still elevated, although the levels had improved (20 000 cells/µL and 14.6 mg/L, respectively). The patient initially responded well to the antibiotics; however, his fever returned, with a temperature of 103.8°F. He was seen again in the office on the 6th day of his symptoms. At this point, he presented with a new finding of left neck swelling. He had cervical asymmetry, and his left tonsil was deviated toward the midline, due to soft tissue swelling.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [2, 'years'], 'Temperature': [103.6, 'degrees fahrenheit'], 'Exudate or swelling on tonsils': True, 'Tender/swollen anterior cervical lymph nodes': True, 'Cough Absent': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 2 years old. The patient's temperature is 103.6 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 71.6 = 39.77778 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 1 + 1 = 2.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
Hence, the Centor score for the patient is 3."
4403,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-7377013-1,Extracted,"The patient is a 35-year-old lady presented to the primary care physician with the chief complaint of cough. Her past medical history is significant for a possible tuberculosis infection 15 years ago. She was in direct contact with another patient who was positive for tuberculosis at a gathering event and later completed a six-month course of anti-tuberculosis regimen prescribed by her primary care physician. She otherwise remained to be asymptomatic and healthy. Her nonproductive cough began three weeks ago. She denied fever, chest pain, dyspnea, night sweats, and weight loss but did complain of sore throat and occasional chills. She lived at home with her family and reported to have sick contact with her kids as they were suffering from an upper respiratory infection. She decided to present to the office for further evaluation due to concerns about possible tuberculosis reactivation.
Her initial vital signs on presentation were as follows: blood pressure 116/59 mmHg, heart rate 81 beats per minute, temperature 97.8°F, body mass index 20.97. Physical examination was completely benign. There was a low clinical suspicion of active tuberculosis given her overall clinical impression. She was recommended to follow up in the clinic in a few weeks after obtaining a two-view chest x-ray (CXR), sputum acid-fast bacillus (AFB) smear, and culture. The patient was followed up via telemedicine over the next few weeks. She continued to have a mild cough with a low clinical suspicion for tuberculosis. The AFB smear and culture could not have been completed due to a lack of sputum samples. CXR revealed small rim calcified lesions in the right mid and upper lung zones suggestive of a benign etiology without findings of active or latent tuberculosis infection (Figure ). The patient was recommended to schedule a follow-up appointment in six months while maintaining a close observation of her symptoms.
Six months later, her cough reoccurred after an initial improvement over the past few months. The cough was accompanied by occasional sputum. She denied fever, chills, night sweat, sore throat, chest pain, dyspnea, or weight loss. She had been in close contact with people who were diagnosed with an upper respiratory infection. She was recommended to undergo a pulmonary function test (PFT) as well as a chest CT for further evaluation. She was prescribed dextromethorphan for symptomatic relief, educated on the symptoms of active tuberculosis, and instructed to give frequent updates of her symptoms. CT with intravenous contrast revealed a high right paratracheal and medial right apical heterogeneous soft tissue with central areas of calcification (Figure ). She agreed to opt for a routine endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) to rule out malignancy.
Bronchoscopy inspection revealed unremarkable trachea, left upper lobe, left lingula, left lower lobe, right middle lobe, and right lower lobe; but interestingly, no right upper lobe was observed. Furthermore, EBUS-TBNA showed a right paratracheal mass without surrounding lymphadenopathies that was biopsied and sent to pathology for analysis. The presumptive diagnosis for the right paratracheal mass was likely due to a nondeveloped right upper lung with associated scarring and atelectasis. The pathology report later confirmed the finding as there was no indication of malignancy or fungal infection.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [35, 'years'], 'Cough Absent': False, 'Temperature': [97.8, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",0,0,0,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 35 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 97.8 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 65.8 = 36.55556 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 0.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 0.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
Hence, the Centor score for the patient is 0."
4404,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-8478693-1,Extracted,"An 18-year-old female with a history of RT presented with a two-day history of bilateral tonsillar swelling, with accompanying sore throat, difficulty swallowing, pharyngeal exudates, and a hot potato voice, features common to tonsillitis (Figure ).
Surgical history included only a breast abscess drainage. Two weeks prior, she was found to have bilateral tonsillitis, successfully treated with a 10-day course of amoxicillin before arrival to the ED.
On clinical examination, her vitals were slightly abnormal, with a fever of 100.7°F, a corresponding pulse of 104 beats per minute, and an elevated blood pressure at 135/70 mmHg. Neck examination revealed lymphadenopathy. Ears, nose, and throat examination revealed pharyngeal erythema, bilateral tonsillar erythema, bilateral tonsillar exudate, bilateral tonsillar swelling, and a left peritonsillar abscess (Figure ).
The patient had an elevated white blood cell count in response to the tonsillar infection (Table ). Head and neck computed tomography scans revealed moderate heterogeneous prominence of the bilateral palatine tonsils with a small tonsillar abscess (15 mm hypodensity on the left) (Figure ).
Also noted is an esophageal diverticulum (3.5 cm) and moderate somewhat symmetric bilateral neck lymphadenopathy particular to the submandibular regions with tonsillar abscess (Figure ).
The patient was admitted to the hospital, seen by otorhinolaryngology, and treated with amoxicillin-clavulanate. Her symptoms subsided over a few days and the patient was discharged home.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [18, 'years'], 'Temperature': [100.7, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True, 'Cough Absent': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 18 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 100.7 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 68.7 = 38.16667 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 1 + 1 = 2.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
Hence, the Centor score for the patient is 3."
4405,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-1376,Extracted,A 4-year-old boy is brought to the physician by his father because of a 3-day history of generalized rash. The rash is not pruritic. He has no cough. He has had a fever and a sore throat for 4 days. He was born at term and has been healthy except for an episode of tonsillitis 6 months ago treated with erythromycin. His immunizations are up-to-date. His temperature is 38.5°C (101.3°F). Examination shows cervical lymphadenopathy. The tongue is bright red. There is tonsillar erythema without any exudate. A photograph of the rash is shown.,What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [4, 'years'], 'Cough Absent': True, 'Temperature': [38.5, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': False}",4,4,4,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 4 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 38.5 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 2 + 1 = 3.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 3 + 1 = 4.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 4.
Hence, the Centor score for the patient is 4."
4406,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-8648291-1,Extracted,"A 75-year-old Caucasian female with a past medical history of polymyositis on a maintenance dose of prednisone of 10 mg daily, diabetes mellitus, status post right nephrectomy presented to the ED with complaints of generalized weakness and drowsiness. At baseline, the patient was minimally mobile due to active polymyositis. The patient was less responsive and confused with episodes of falling from her bedside commode. She denied having a cough, chest pain, shortness of breath, abdominal pain, nausea, vomiting, or diarrhea. In the last week, she had close contact with her grandchildren, who experienced a flu-like illness without rash treated with an antibiotic.
On physical examination, her vitals were significant for elevated blood pressure of 174/82 mmHg, the temperature of 37.1 °C (98.7 °F), respiratory rate of 16 breaths per minute. Bilateral lower extremity swelling was present. On neurological exam, she was alert but not oriented on the place and time. Her Glasgow Coma Score (GCS) was 13. The patient showed decreased consciousness level, slowly followed commands, and slurred speech. Her reflexes were diminished: 2/4 in the bilateral biceps, triceps, brachioradialis, patellae, and Achilles. The rest of the exams were unremarkable without any focal neurological signs. Laboratory tests as noted in Table . The hepatitis panel was negative, and blood cultures showed no growth at 120 hours.
Computed tomography (CT) brain without contrast showed scattered white matter hypodensities, which were nonspecific but compatible with chronic microvascular ischemic disease.
Further ischemic workup was deferred due to acute kidney injury in the setting of chronic kidney disease (CKD) stage 4. The patient had minimal responsiveness with a loop diuretic, and therefore she was started on hemodialysis for better volume management. MRI brain without contrast showed 14 mm high T2/fluid-attenuated inversion recovery (FLAIR) signal intensity focus in the left temporal lobe, suspicious for primary versus metastatic neoplasm (Figure ). The neurologist was consulted and recommended a follow-up assessment with a gadolinium-enhanced MRI of the brain.
CT chest/abdomen/pelvis with intravenous (IV) contrast did not find any malignancy or metastatic disease. Given the cortical location of intracranial lesions, she was started prophylactically on levetiracetam 250 mg daily. Electroencephalograms (EEG) showed generalized slowing and triphasic waves. MRI with contrast was deferred due to worsening kidney. With her history of chronic steroid therapy, a lumbar puncture (LP) was considered and showed protein 75 mg/dL (15-60 mg/dL), glucose 55 mg/dL (50-80 mg/dL), WBC 22/mm3 (0-8/mm3), 7RBC/mm3 (<1RBC/mm3), with a pleocytosis of lymphocytic predominance. Meningitis/encephalitis polymerase chain reaction (PCR) panel detected HHV-6. The patient was started on acyclovir 530 mg IV, and the infectious disease was consulted. Afterward, the patient was started on ganciclovir 75 mg IV as an induction dose for 14 days as ganciclovir has been shown in studies to be active against HHV6. Serologic testing also revealed a positive IgG 1:40 (reference <1:10) but negative IgM. Serum HHV-6 viral load was undetectable.
Repeat MRI brain without contrast after 14 days of treatment with ganciclovir showed chronic microvascular-type ischemic disease and some T2 shine through in the left frontal area (Figure ). The location of abnormality seen in the left temporal region in the subcortical white matter was less prominent. By this time, there was a significant improvement in her mental status. She was not placed on prophylaxis because there was no clear indication due to her marked symptomatic improvement and resolution of the area of abnormality in the left temporal region on the MRI. The patient has been discharged with her home regimen of prednisone 10 mg for polymyositis. Post-discharge at three-week outpatient follow-up, she was doing well without evidence of any further neurologic deterioration.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [75, 'years'], 'Cough Absent': True, 'Temperature': [37.1, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",0,0,0,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 75 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 37.1 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at -1.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score -1 + 1 = 0.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
Hence, the Centor score for the patient is 0."
4407,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-5689425-1,Extracted,"A previously healthy 23-year-old Japanese woman presented to the Internal Medicine Department in our hospital after 5 days of fever, sore throat, aphthous stomatitis, and enlargement of the bilateral cervical lymph nodes with tenderness. She experienced similar symptoms 1, 2, and 9 months ago, and in each case, these symptoms lasted for approximately 5 days regardless of therapy with nonsteroidal anti-inflammatory drugs or antibiotics. There was no remarkable family history except for her mother's neuromyelitis optica. Her menstrual period was regular. She had taken no drugs except for multi-ingredient cold medication prescribed by a local clinic. She had never traveled abroad.
On admission, her body temperature was 37.7°C, and her other vital signs were within the normal ranges. On physical examination, aphthous stomatitis, enlargement of the bilateral submandibular lymph nodes with tenderness, pharyngeal erythema, and enlarged palatine tonsils with white exudates were observed (Figure ).
Laboratory investigations revealed slightly elevated serum transaminase (aspartate aminotransferase level, 112 IU/L and alanine aminotransferase level, 92 IU/L) and immunoglobulin D (29.1 mg/dL) levels. Bacterial cultures from a throat swab and blood sample showed no growth. Anti-Epstein-Barr virus capsid antigen immunoglobulin G and M titer were order of 160 and under the order of 10. Epstein-Barr virus nuclear antigen was not investigated. Computed tomography revealed enlargement of the bilateral submandibular lymph nodes with no evidence of other abnormal findings. Transthoracic echocardiogram revealed no vegetations. The patient refused to undergo genetic examination.
The patient was diagnosed with PFAPA syndrome based on two clinical diagnostic criteria. She satisfied five of six items in Padeh's diagnosis criteria: monthly cyclic fever in any age group, possible aphthous stomatitis, cervical lymphadenitis, exudative tonsillitis with negative throat culture, completely asymptomatic during intervals, and rapid response to glucocorticoid. She also fulfilled four of five items in Thomas’ criteria: regularly recurring fever under 5 years old; presence of at least one of these symptoms, aphthous stomatitis, cervical adenitis, or pharyngitis, without upper respiratory infection; exclusion of cyclic neutropenia; completely asymptomatic during intervals; normal growth and development. Her diagnosis was confirmed with no evidence of other possible febrile diseases.
After admission, her symptoms recovered within a few days without any treatment. We prescribed cimetidine 800 mg per day to prevent recurrence. Although the aphthous stomatitis and enlarged cervical lymph node appeared a few days per month, none of the other symptoms were observed again. Moreover, the aphthous stomatitis has also stopped occurring 5 months after starting cimetidine therapy (Figure ).",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [23, 'years'], 'Cough Absent': True, 'Temperature': [37.7, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 23 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 37.7 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 0.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 0 + 1 = 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 1 + 1 = 2.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
Hence, the Centor score for the patient is 3."
4408,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-8819,Extracted,"A 16-year-old girl presents with a sore throat. The patient says symptoms onset acutely 3 days ago and have progressively worsened. She denies any history of cough, nasal congestion or rhinorrhea. No significant past medical history or current medications. The vital signs include: temperature 37.7°C (99.9°F), blood pressure 110/70 mm Hg, pulse 74/min, respiratory rate 20/min, and oxygen saturation 99% on room air. Physical examination is significant for anterior cervical lymphadenopathy. There is edema of the oropharynx and tonsillar swelling but no tonsillar exudate.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [16, 'years'], 'Cough Absent': True, 'Temperature': [99.9, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': False}",2,2,2,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 16 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 99.9 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 67.9 = 37.72222 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 0.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 0 + 1 = 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 1 + 1 = 2.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
Hence, the Centor score for the patient is 2."
4409,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-6692547-1,Extracted,"On January 31, 2018, a usually healthy, 9-year old, non-Hispanic white female was screened for ORCHARDS eligibility (Figure ). She was a vaccinated (quadrivalent inactivated influenza vaccine on October 9, 2017) 4th-grade student who lived with both parents and two younger siblings. All family members had received the 2017/2018 influenza vaccine. A home visit was conducted 25 hours after symptom onset. Her moderate ILI was characterized by fever (measured temperature = 37.2°C after antipyretic), chills, cough, sore throat, rhinorrhea, nasal congestion, headache, malaise, myalgia, anorexia, and sneezing. There was no recent travel, exposure to farm animals, or identified sick contact preceding onset. Nasal and oropharyngeal specimens were collected. Although the RIDT result was negative, rRT-PCR was positive for influenza A (H3N2) (cycle threshold value [Ct] = 31.48) and RPP was positive for coronavirus HKU1. At follow-up, she reported 2 days of absenteeism and continued cough, rhinorrhea, sore throat, myalgia, and headache. There had been no medical follow-up or antiviral treatment. The rRT-PCR result from the subject's day 7 swab was negative for influenza. No other family members reported illness on day 0, but one sibling developed mild respiratory illness on day 6. All family members tested negative for influenza by rRT-PCR on day 0 and day 7.
On March 9, 2018, 37 days after the initial encounter, the subject was again screened due to a new ILI episode. A home visit was conducted 49 hours after symptom onset. Now 10 years old, the subject complained of significant symptoms including fever (measured temperature = 37.6°C after antipyretic), chills, cough, wheezing, nasal congestion, headache, malaise, myalgia, anorexia, burning eyes, and dizziness. Again, there was no recent travel, exposure to farm animals, or identified sick contact preceding onset. The subject's RIDT result was positive for influenza A, and rRT-PCR results confirmed the presence of influenza A (H3N2) (Ct = 26.48). At follow-up, she reported 2 days of absenteeism and continued fever, chills, cough, rhinorrhea, malaise, myalgia, headache, and anorexia. There had been no medical follow-up or antiviral treatment. The rRT-PCR results from the subject's day 7 swab continued to show influenza A (H3N2) (Ct = 33.30). No other family members reported illness on day 0 or day 7. All family members tested negative for influenza by rRT-PCR on day 0 and day 7.
The subject's initial specimen from each episode, collected on January 31 and March 9, 2018, was prepared for full genomic sequencing at the WSLH. Both A (H3N2) strains were of the hemagglutinin gene clade 3C2.a2. After WSLH performed a consensus sequence comparison between the two viruses collected from the subject, three single nucleotide polymorphisms (SNPs) were identified within the coding region of the HA protein. Only one SNP was non-synonymous and resulted in an isoleucine to leucine change at position 67 (in HA1). This particular polymorphism was near 100% frequency in the sequence reads and was four amino acids away from an established antibody epitope site (Site E). Both sequences (first isolate ORCH00001 and second isolate ORCH00002) were submitted to the GenBank® genetic sequence database and given accession numbers (MK262897 and MK262898, respectively).",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [10, 'years'], 'Cough Absent': False, 'Temperature': [37.6, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 10 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 37.6 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
Hence, the Centor score for the patient is 1."
4410,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-5219707-1,Extracted,"A 16 year old female Muslim from the Extreme North of Cameroon with no significant past history was treated for severe malaria using intravenous quinine. Due to refractory nausea and vomiting she was also put on intravenous metoclopramide, 10 mg three times a day. A few minutes after administration of the second dose of metoclopramide, she complained of pain and stiffness of the neck and an inability to keep her tongue in her mouth. On examination, she was conscious and anxious with a blood pressure of 124/78 mmHg, pulse rate of 90 beats/minute, respiratory rate of 20 breaths/minute and temperature of 37.3 °C. Her neck was slightly arched backwards and her tongue was hanging out. There was no accumulation of saliva in her mouth and she could swallow, but with difficulty. There were no signs of respiratory distress. The rest of her examination was unremarkable. A diagnosis of metoclopramide induced acute dystonic reaction was made. She was administered 8 mg of oral chlorpheniramine. Her dystonic symptoms subsided 4 h later, as did the nausea and vomiting. She continued her antimalarial treatment and the metoclopramide was discontinued. She did not have any further dystonic symptoms. She was discharged 2 days later and was advised to avoid taking metoclopramide. Follow-up visit 2 weeks later was unremarkable.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [16, 'years'], 'Temperature': [37.3, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False, 'Cough Absent': False}",0,0,0,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 16 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 37.3 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 0.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 0.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
Hence, the Centor score for the patient is 0."
4411,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-2583042-1,Extracted,"Subject 1 (S1), a 54-year old Chinese man, was well until 19 August 2006 when he developed sudden onset of high fever with chills and rigor. This was associated with cough, sore-throat and headache. There was no associated dyspnoea, tachypnoea, haemoptysis or chest pain on coughing. Besides the severe frontal throbbing headache, he had generalized body aches, myalgia and severe malaise. On the following day, he developed nausea, vomiting and diarrhoea. The vomitus consisted of food taken and was not bile-stained. The stool was described as watery without excessive mucous and it was non-malenic. The gastrointestinal symptom was associated with abdominal pain and loss of appetite. His illness was not relieved with self-medication of antipyretics. On review, there was no associated giddiness, blurring of vision, photophobia, skin bleeding or arthritis.
He sought medical treatment at the government health clinic in Kampar on 21 August 2006. At the outpatient clinic, he was noted to be febrile (an axillary temperature of 40.1 degree Celsius), ill-looking with a generalized body erythema that blanched on pressure and was more prominent over the face and upper trunk. He had mild conjunctivitis but there was no jaundice. His tonsils were enlarged and injected but there was no white exudate noted over the tonsils. He was not in any respiratory distress and his lungs were clear with good air entry on auscultation. Other systemic examination was essentially normal and there was no significant lymphadenopathy noted. A provisional diagnosis of influenza-like illness was made at which he was given a higher dose of anti-pyretic. His illness was noted to resolve on 23 August 2006 although he still appeared weak and lethargic.
Venous blood samples were taken from the patient for full blood count analysis, and the results are shown in . These results indicated that his white blood cell and platelet counts were within normal limits although there was a relative lymphopenia in the blood sample taken at first examination.
His throat swab was taken on August 21 for virus isolation as described below.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'Cough Absent': False, 'Temperature': [40.1, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",0,0,0,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 54 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 40.1 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score -1 + 1 = 0.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 0.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
Hence, the Centor score for the patient is 0."
4412,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-7219986-1,Extracted,"A 55-year-old woman presented to the emergency department (ED) with the chief complaint of headache for three days, associated with nausea, vomiting, and visual changes. The headache was described as being sudden in onset, constant, bilateral, retro-orbital, and throbbing. The pain was a six out of ten in intensity. The pain was not alleviated with over the counter acetaminophen use. She was not able to describe any alleviating or exacerbating factors. The visual changes were described by the patient as “blurry vision” and “double vision” affecting her left eye greater than her right. She reported photophobia and difficulty keeping the left eye open. The patient described this difficulty of keeping the eye open as a weakness and not secondary to pain. She had approximately five episodes of non-bloody and non-bilious vomiting over the past three days and reported inability to tolerate her home medications. She also reported a sore throat and cough productive of yellow sputum for the previous two to three days, but denied fever, chills, chest pain, hemoptysis, or dyspnea.
Her past medical history included essential hypertension, hyperlipidemia, and a remote history of uterine fibroids associated with iron deficiency anemia. Prescribed medications included losartan 25 milligrams (mg) and hydrochlorothiazide 12.5 mg. She had no known drug allergies, did not smoke, drink alcohol, or use illicit drugs. She was unemployed and lived alone. The patient was post-menopausal and was pregnant three times-two of which were normal spontaneous deliveries with two living children and one prior abortion.
Vital signs were: temperature 98.8° Fahrenheit, heart rate 84 beats per minute, blood pressure 135/74 millimeters of mercury, respiratory rate of 18 breaths per minute and room air oxygen saturation 97%. Her body mass index was 42 (normal 18.5–24.9). Complete physical examination was unremarkable except her left eye’s lateral gaze was restricted by approximately 25%. Her visual acuity was 20/25 and 20/30, right and left eyes, respectively. Initial laboratory testing were resulted ( and ). An electrocardiogram was performed ().",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'Cough Absent': False, 'Temperature': [98.8, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",-1,-1,-1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 55 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 98.8 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 66.8 = 37.11111 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at -1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at -1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at -1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at -1.
Hence, the Centor score for the patient is -1."
4413,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-9657,Extracted,"A 34-year-old gravida-1 at 8 weeks gestation seeks evaluation for a fever and sore throat for 3 days. She also reports generalized body pain and fatigue over this period. She was diagnosed with Graves’ disease 6 months ago. Before conception, methimazole was switched to propylthiouracil. She appears ill. The vital signs include: axillary temperature 38.0℃ (100.4℉), pulse 88/min, respiratory rate 12/min, and blood pressure 120/80 mm Hg. A 1 × 1 cm ulcer is seen on the side of the tongue. The ulcer is tender with surrounding erythema. Examination of the neck, lungs, heart, and abdomen shows no abnormalities.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [34, 'years'], 'Temperature': [100.4, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': False, 'Cough Absent': False, 'Exudate or swelling on tonsils': False}",0,0,0,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 34 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 100.4 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 68.4 = 38.0 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 0.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 0.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
Hence, the Centor score for the patient is 0."
4414,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-1001,Extracted,"A 16-year-old boy comes to the physician with a 4-day history of sore throat and mild fever. He is on the varsity soccer team at his high school, but has been unable to go to practice for the last few days because he has been very tired and is easily exhausted. He has no history of serious illness and takes no medications. His mother has type 2 diabetes mellitus. He appears weak and lethargic. His temperature is 38.7°C (101.7°F), pulse is 84/min, and blood pressure is 116/78 mm Hg. Examination shows enlarged, erythematous, and exudative tonsils; posterior cervical lymphadenopathy is present. Abdominal examination shows no abnormalities. His hemoglobin concentration is 14.5 g/dL and leukocyte count is 11,200/mm3 with 48% lymphocytes. A heterophile antibody test is positive.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [16, 'years'], 'Temperature': [38.7, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True, 'Cough Absent': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 16 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 38.7 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 1 + 1 = 2.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
Hence, the Centor score for the patient is 3."
4415,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-12,Extracted,"A 4-year old boy is brought to the emergency department with fever, painful swallowing, headache, and neck spasm that began shortly after waking up. He has had a sore throat over the last week that acutely worsened this morning. He has no history of serious illness and takes no medications. He lives at home with his mother. His older brother has asthma. His immunizations are up-to-date. He appears acutely ill. His temperature is 38.4°C (101.2°F), pulse is 95/min, respirations are 33/min, and blood pressure is 93/60 mm Hg. Examination shows drooling. The neck is stiff and extension is limited. Respirations appear labored with accessory muscle use. Inspiratory stridor is heard on auscultation of the chest. Cardiac examination shows no abnormalities. Oropharyngeal examination shows a bulge in the posterior pharyngeal wall. Intravenous access is obtained and laboratory studies are ordered.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [4, 'years'], 'Temperature': [38.4, 'degrees celsius'], 'Exudate or swelling on tonsils': True, 'Cough Absent': False, 'Tender/swollen anterior cervical lymph nodes': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 4 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 38.4 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
Hence, the Centor score for the patient is 3."
4416,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-1536,Extracted,"A 7-year-old boy is brought to the physician with a 2-day history of fever, chills, malaise, and a sore throat. He has otherwise been healthy and development is normal for his age. He takes no medications. His immunizations are up-to-date. His temperature is 38.4°C (101.4°F), pulse is 84/min, respirations are 16/min, and blood pressure is 121/71 mm Hg. Pulse oximetry shows an oxygen saturation of 100% on room air. Examination shows discrete 1–2-mm papulovesicular lesions on the posterior oropharynx and general erythema of the tonsils bilaterally.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [7, 'years'], 'Temperature': [38.4, 'degrees celsius'], 'Exudate or swelling on tonsils': True, 'Cough Absent': False, 'Tender/swollen anterior cervical lymph nodes': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 7 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 38.4 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
Hence, the Centor score for the patient is 3."
4417,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-2649860-1,Extracted,"A 45-year-old male patient, who used to work in the livestock industry, was hospitalized with symptoms of fever, chills, sweating, headache, intermittent myalgia and a past month weight loss of 10 kg. He had taken cold medicine, which included acetaminophen, mucolytics and antihistamines, for 2 weeks. He had no past medical history of rheumatic fever or any other heart diseases. His cattle's brucellosis tests from six months ago were all negative; in addition, he stated that he had never ingested any dairy products from his cattle.
His physical examination showed a body temperature of 38.8℃, blood pressure of 102/80mmHg, and a heart rate of 90 beats/minute. A diastolic murmur of grade 2 was auscultated at Erb's point. Laboratory studies were as follows: hemoglobin 12.6 g/dL, hematocrit 35.65%, leukocyte 5,580/mm3 (granulocyte 51.4%, lymphocyte 40.6%, monocyte 5.5%), platelet 218,000/mm3, erythrocyte sedimentation rate (ESR) 29 mm/hour, C-reactive protein (CRP) 4.31 mg/mL, aspartate aminotransferase (AST) 56 IU/L, alanine aminotransferase (ALT) 52 IU/L, gamma guanosine triphosphate (γ-GTP) 72 IU/L. All other lab values were normal. Chest X-ray did not show any cardiomegaly or enhanced opacity of pulmonary vasculature. Electrocardiography appeared normal without atrial enlargement, ventricular hypertrophy, ST-T change, or dysrhythmia. Abdominal computed tomography (CT) scan revealed a 15.6 cm splenomegaly with a partial wedge shaped splenic abscess (). Transthoracic echocardiography (TTE) showed normal left ventricular systolic function. Mild aortic and tricuspid valve regurgitation was present. TTE also revealed an oscillating vegetation on the noncoronary cusp (3 × 5 mm) and right coronary cusp (2 × 4 mm) (). The other echocardiographic parameters were as follows: left ventricular end diastolic dimension (LVEDD), 57 mm, left ventricular end systolic dimension (LVESD), 33 mm, left ventricular ejection fraction (LVEF), 72%, dimension of aortic root, 37 mm, dimension of left atrium, 38 mm, pulmonary artery systolic pressure (PASP), 31 mmHg, left ventricular septal thickness in diastole (LVSTd), 13 mm, and left ventricular posterior wall thickness in diastole (LVPWTd), 13 mm. Serum antibody test using standard tube agglutination (STA) upon admission had a positive result as the Brucella serologic titer was over by 1 : 160 dilution (200 IU). Anti-brucella IgG and IgM antibodies by ELISA (PanBio #BAB01M, G, Australia) were also positive (IgM 48, IgG 31). A blood culture test with trypticase soy agar (TSA, containing 5% sheep blood) and BACTEC culture (PEDS plus media) were used to isolate and identify the bacteria causing his symptoms. The genus-specific bcsp31 (223 bp), omp36 (195 bp), and 16s rRNA (905 bp) polymerase chain reaction (PCR) identified all the isolates as Brucella species (). Brucella abortus bv 1 strain was identified by a species-specific associative memory organization system (AMOS)-PCR ().
Gentamycin (160 mg/day, intravenous [IV]), rifampicin (600 mg/day, per os [po]) and doxycycline (200 mg/day, po) were administered. Clinical symptoms started improving beginning the fourth day of treatment and he was discharged on the 16th day. He was followed up in the outpatient department and was given further antibiotic treatment of trimethoprim/sulfamethoxazole (320 mg/1600 mg/day, po), rifampicin (600 mg/day, po) and doxycycline (200mg/day, po). After one month of treatment, ESR and CRP were 9 mm/hour and 0.09 mg/mL respectively. Two months later, follow-up transesophageal echocardiography (TEE) showed no change in the size of the vegetation on the noncoronary cusp, while that on the right coronary cusp completely disappeared. Seven months later, follow up TEE showed complete resolution of the remaining vegetation. The patient completed the 12 months long drug regimen. Therapy side effects of neutropenia, hepatitis, or skin eruption were not observed. Twelve months later, we followed up with an abdominal CT scan, serological assay, and blood culture. Abdominal CT scan showed a normalized spleen size of about 11 cm compared to the previous splenomegaly size of 15 cm. The partial splenic abscess changed into cortical dimpling with segmental shrinkage without any additional abscess formation (). Follow-up serum antibody test results were STA 1:20 (24 IU); ELISA tests were IgM < 11 and IgG 19 and blood culture tests showed no organisms. The patient has been followed up with control visits and has shown no sign of a recurrence.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'years'], 'Cough Absent': True, 'Temperature': [38.8, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 45 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 38.8 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score -1 + 1 = 0.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 0 + 1 = 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
Hence, the Centor score for the patient is 1."
4418,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-7479573-1,Extracted,"A 5-year-old boy was admitted to our hospital due to recurrent cough and fever that had persisted for more than a month.
The patient’s symptoms started over a month ago with recurrent cough and fever, which had worsened over the previous week.
The patient had a history of multiple respiratory infections and sinusitis episodes since the age of 1 year, but no peripheral lymphadenopathy, tonsil enlargement, or hepatosplenomegaly were observed.
The boy was the first child of Han Chinese nonconsanguineous parents. He was born full term with a birth weight of 4000 g and a length of 50 cm. There was no family history of immunodeficiency or recurrent infections.
The patient’s temperature was 36.6°C, heart rate was 90 bpm, respiratory rate was 25 breaths per minute, blood pressure was 121/60 mmHg and oxygen saturation in room air was 97%. His mind was clear, he had shortness of breath, middle trachea, hyperemia of the pharynx, no obvious enlargement of the tonsils, thick breath sounds in both lungs, obvious moist rale, homogeneous rhythm, no obvious pathological Mur, soft abdomen, normal bowel sound, no obvious abnormalities during nervous system examination.
The patient’s routine blood results were as follows: White blood cell count, 21.5 × 109/L (4.0-12.0 × 109/L); neutrophils, 67.9% (50%-70%); lymphocytes, 18.1% (20%-40%); hemoglobin, 131 g/L (120-140 g/L); platelet count, 401 × 109/L (100-300 × 109/L); and high-sensitivity C-reactive protein, 112.7 mg/dL (0–8 mg/dL). Agammaglobulinemia was characterized as follows: IgG, 20.0 mg/dL (800-1800 mg/dL); IgG subtype 1, 0.26 g/L (3.62-12.28 g/L); IgG subtype 2, 0.10 g/L (0.57-2.9 g/L); IgG subtype 3, 0.009 g/L (0.129-0.789 g/L); IgG subtype 4, 0.003 g/L (0.013-1.446 g/L); IgA, 90.0 mg/dL (90-450 mg/dL); and IgM, 18.0 mg/dL (60-280 mg/dL) (determined by enzyme-linked immunosorbent assay kits from Shanghai Langton Biotechnology Co., Ltd.). Complement C4 and C3 levels were found to be 18.0 mg/dL (7-149 mg/dL) and 106.0 mg/dL (58-160 mg/dL), respectively. CD3+, CD4+, and CD8+ T lymphocytes were 74.6% (50%-84.0%), 47.3% (27.0%-51.0%), and 24.9% (15.0%-44.0%), respectively.
A chest spiral computed tomography scan revealed a bilateral lung infection.
Due to the patient’s history of repeated respiratory tract infections, his very low serum IgG levels (< 2.5 g/L), and general agammaglobulinemia, he was treated with Ig infusions every four weeks. This treatment markedly reduced the patient’s respiratory infection incidence.
Genetic analysis: Genomic deoxyribonucleic acid (DNA) was extracted from peripheral blood samples obtained from the proband and his parents. Sequence variants detected in BTK were described according to the National Center of Biotechnology Information entry NM_000061.2. An analysis of pathogenicity and mutation conservation was performed with the bioinformatics Mutation Taster () and University of California Santa Cruz Genome Browser () programs.
Molecular modeling: The three-dimensional structure of the mutation was generated in the Swiss-Model program ().
BTK expression: The wild-type (WT) full-length human BTK messenger ribonucleic acid (mRNA) (NM_000061.2), which includes NheI and BamH1 restriction enzyme sites, was synthesized (Tsingke, China), and cloned into the plasmid vector pEGFP-N1. The mutation 902-904delAAG was introduced into the BTK sequence via two polymerase chain reaction (PCR) rounds with mutagenic primers. The two PCR products were connected by homologous recombination[] with a TreliefTM SoSoo cloning kit (Tsingke, China). The connection product was transformed into Escherichia coli DH5α. Positive clones were selected, and the full-length mutant cDNA was sequenced to confirm the site-directed mutation.
For transient transfection, HEK-293T cells were cultured in 24-well plates to 70%-80% confluence and transfected with 500 ng of pEGFP-N1 containing no insert, pEGFP-N1-WT-BTK (WT), or pEGFP-N1-Mutation-BTK (Mut) with Lipofectamine™ 3000 transfection reagent (Thermo Fisher Scientific). Cells were collected 24 h later.
Quantitative real-time PCR: Cells were collected from 24-well plates and total RNA preparations were obtained with a MiniBEST Universal RNA Extraction Kit (Takara). cDNA was produced with a Primescript RT reagent kit with gDNA Eraser, applied prior to reverse transcription to remove genomic DNA (Takara, AK3920). Glyceraldehyde 3-phosphate dehydrogenase gene fragment was used as an internal reference, and quantitative PCR was performed with a real-time fluorescence quantitative PCR instrument (BIO-RAD CFX Connect). The forward and reverse primers used for the PCR amplification were 5’ GAA AGG TTC CCT TAT CCC TTC C 3’ and 5’ GAA TCC ACC GCT TCC TTA GTT 3’, respectively.
Western blotting: Cell protein was extracted with a whole cell extraction kit (Abcam), and 10-μg protein aliquots were subjected to 12% sodium dodecyl sulfate polyacrylamide gel electrophoresis. Protein bands were electro transferred onto a polyvinylidene difluoride membrane and detected with monoclonal anti-BTK antibody (Abcam) and horseradish peroxidase-conjugated goat anti-rabbit secondary antibody. Immunoreactive bands were visualized with enhanced chemiluminescence reagent (Super Signal, Pierce) and observed with a gel imaging system.
Genetic diagnosis and protein structure modeling: Genetic analysis revealed that the proband had a de novo hemizygous deletion in BTK: c.902_c.904delAAG/p.E301del. No BTK variants were detected in the proband’s parents’ genomes (Figure ). Bioinformatics analysis in Mutation Taster indicated that BTK c.902_c.904delAAG /p.E301del would be highly pathogenic. Furthermore, sequence alignment revealed that the E301 residue lost in this deletion is conserved across diverse vertebrates (e.g. Homo sapiens, Pan troglodytes, Macaca mulatta, Felis catus, Mus musculus, Gallus gallus, and Xenopus tropicalis), a finding consistent with it being functionally important (Figure ). The deletion did not produce a frameshift. However, three-dimensional structural modeling indicated that the deletion altered the Src homology (SH) 2 domain of the mutant BTK protein relative to WT BTK (Figure ).
Reduction in steady-state levels of BTK: Quantitative PCR results revealed similar BTK mRNA levels between WT and mutant cDNAs, indicating that the mutation was not disruptive to transcription (Figure ). Western blotting revealed plentiful overexpression of WT BTK (75.8% ± 2.98%) and markedly reduced overexpression of the BTK c.902_c.904delAAG/p.E301del deletion mutant (9.49% ± 1.58%, P < 0.01) (Figure ). Hence, mutant BTK protein levels were depressed despite the deletion mutation not being disruptive to transcription, providing evidence of a posttranslational loss.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [5, 'years'], 'Cough Absent': False, 'Temperature': [36.6, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 5 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 36.6 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
Hence, the Centor score for the patient is 1."
4419,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-8371619-1,Extracted,"We present an 11-year-old female with complex medical history consisting of developmental delay, septo-optic dysplasia, central DI, panhypopituitarism including central adrenal insufficiency, hypothyroidism, and epilepsy. Her weight at presentation was 49.5 kg. She presented to the emergency department (ED) of a tertiary care academic medical center with impending respiratory failure (approximately two months after the first confirmed case of SARS-CoV-2 within the United States). She became ill eight days before presenting to the ED with fever. At that time, she was taken to a local urgent care facility where she was diagnosed with an acute otitis media. She was started on PO amoxicillin for an anticipated 10-day course of therapy. She was also given stress-dosed hydrocortisone (30 mg PO, twice daily) given her underlying panhypopituitarism. During the subsequent days, there was no reported change in oral intake or urine output (UOP). Her fevers initially improved; however, they never fully resolved. Three days prior to presentation, the patient experienced increased frequency and temperature of fevers. She again presented to a local urgent care facility where a nasopharyngeal swab was positive for the SARS-CoV-2 virus (via the PCR test). Within a few days, she developed a persistent, nonproductive cough, increased work of breathing, and shortness of breath, prompting the evaluation in the ED. Initial vital signs were remarkable for rectal temperature of 40.8°C, heart rate of 163 beats per minute, respiratory rate of 34 breaths per minute, and oxygen saturation of 89%. Physical exam revealed an alert female in a moderate amount of respiratory distress as evidenced by tachypnea and intermittent grunting. Dry oral mucosa was noted indicating a mild amount of dehydration. The remainder of the physical exam was unremarkable. Laboratory results were remarkable for hyperosmolar hypernatremia (serum sodium of 156 mmol/L and serum osmolality of 321 mOsm), mild hyperglycemia (serum glucose of 146 mg/dL), and elevated ESR (21 mm/hr), CRP (2.3 mg/dL), and procalcitonin (6.9 ng/dL). Her respiratory distress acutely worsened within hours of her ED arrival, and she was intubated for acute hypoxic and hypercarbic respiratory failure (immediate postintubation arterial blood gas with pH 7.20, PCO2 78, PO2 132, HCO3 30, and BD 1.7).
The patient was admitted to the pediatric intensive care unit (PICU). She was transitioned from her home regimen of subcutaneous desmopressin to a 0.5 mU/kg/hr Vasopressin infusion. Review of her baseline condition revealed that her DI was well controlled on her home regimen. She was continued on stress-dosed steroids (methylprednisolone 20 mg q6h IV). The patient had acute lung injury (SaO2/FiO2 = 120). Mechanical ventilator settings were adjusted to minimize ventilator-induced lung injury. Arterial and central venous lines were placed to promote more accurate determination of oxygenation (PaO2/FiO2 ratios) and venous monitoring. She was started on ceftriaxone, azithromycin, and hydroxychloroquine in addition to receiving one dose of tocilizumab. Ceftriaxone was used to treat presumed bacterial superinfection based on the severity of the patient's clinical status. At the time of the patient's presentation, our institutional protocol for the treatment of severe COVID-19 infection was based on current literature suggesting that the combination of azithromycin and hydroxychloroquine may achieve antiviral and anti-inflammatory effects against SARS-CoV-2 []. Additionally, at this time, tocilizumab was suggested to have beneficial effects against “cytokine storming” in SARS-CoV-2 patients []. The patient had hypotension that was unresponsive to fluid resuscitation. An epinephrine infusion was started to maintain adequate blood pressures. Given the patient's underlying conditions and critical state, chemistry panels were drawn every six hours on day one of admission. These panels quickly revealed a steady worsening of hypernatremia to a maximum value of 171 mmol/L associated with increasingly abundant UOP of more than 4 L on the first day of hospitalization (Figures and ). These changes occurred despite a maximum Vasopressin infusion rate of 8 mU/kg/hr along with appropriate, simultaneous adjustments in both the sodium concentration and rate of administered IV fluids.
By the second day of hospitalization, a net positive fluid balance of 2.8 L was noted and severe hypernatremia persisted (serum sodium of 160 mmol/L). Her moderate ARDS continued (PaO2/FiO2 = 132) []. When the hypernatremia persisted into the third day of hospitalization, a trial of Furosemide (10 mg IV) in addition to decreasing the Vasopressin dose from 8 mU/kg/hr to 6 mU/kg/hr was attempted. After five doses of IV Furosemide over a 48-hour period along with reduction in the Vasopressin dose, successful diuresis along with resolution of hypernatremia was achieved (net balanced fluid balance of -497 mL and reduction in serum sodium to 138 mmol/L, respectively) (Figures and ). Her ARDS gradually improved. The patient was extubated on hospital day 10. She remained hospitalized in the PICU for a total of 29 days during which time she was weaned from supplemental oxygen and was gradually weaned from sedative medications. She had normal serum sodium levels and UOP throughout the remainder of her PICU stay. She was discharged to her home with an outpatient subspecialist follow-up.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [11, 'years'], 'Cough Absent': False, 'Temperature': [40.8, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",2,2,2,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 11 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 40.8 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
Hence, the Centor score for the patient is 2."
4420,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-2031,Extracted,"A 7-year-old girl is brought to the emergency department with a 10-day history of fever and sore throat that acutely worsened over the past 2 days. Her sore throat is worse on the right side. She has difficulty swallowing and opening her mouth due to pain. She has also noticed a change in the quality of her voice over the last day. Her temperature is 38.2°C (100.8°F), pulse is 86/min, respirations are 18/min, and blood pressure is 110/75 mm Hg . Examination shows cervical lymphadenopathy. Oropharyngeal examination shows erythematous tonsils and swelling of the right tonsillar pillar. The uvula is deviated to the left.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [7, 'years'], 'Temperature': [38.2, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True, 'Cough Absent': False}",4,4,4,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 7 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 38.2 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 3 + 1 = 4.
Hence, the Centor score for the patient is 4."
4421,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-7508641-1,Extracted,"A previously healthy 69-year-old woman was admitted to Wuhan Huoshenshan Hospital with a 20-day history of anorexia and fatigue, as well as a 7-day history of fever. Her highest temperature was 38.5 °C, accompanied by progressing fatigue and anorexia after exposure at a bank in Wuhan 1 month prior. After that, she was admitted to a local hospital and was administered a medical history of Lianhuaqingwen capsule and arbidol, with a subsequent improvement of her respiratory symptoms.
On admission, her temperature had returned to normal and the SARS-CoV-2 test of her throat swab was negative. In contrast, she presented with nausea, anorexia and loose stool, with an intermittent dry cough during the preceding 3 weeks. A routine stool check demonstrated a loose sample with positive occult blood. Routine blood, chemistry and coagulation tests showed no abnormalities. The pertinent laboratory results are summarized in Table . The lymphocyte subset percentages are summarized in Table .
The initial treatment was supportive and most of her symptoms improved, including cough and shortness of breath; however, after an 18-day hospitalization, she presented recurrent gastrointestinal complaints of anorexia and mild diarrhea. On hospital day (HD) 21, HD25 and HD29, the SARS-CoV-2 RNA tests of her throat swabs were positive, after two consecutively negative results on HD16 and HD19.
On HD30, approximately 400 mL of CP was administered to the patient. No adverse reaction occurred after CP infusion. On HD31, SARS-CoV-2 RNA tests were negative on her throat and anal swabs, whereas SARS-CoV-2 RNA remained detectable in her nasal swab. On HD33, the patient’s condition was much improved, with subsiding anorexia and nausea. On HD35, the SARS-CoV-2 RNA test of her nasal swab returned negative, which was consistent with her throat swab. On HD36, the patient recovered from both respiratory and gastrointestinal symptoms except for mild diarrhea. She showed complete recovery on HD38 and was discharged on HD39 (Fig. ). SARS-CoV-2 RNA remained negative at her follow-up visits on quarantine day (QD) 6 and QD10.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [69, 'years'], 'Cough Absent': True, 'Temperature': [38.5, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 69 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 38.5 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score -1 + 1 = 0.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 0 + 1 = 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
Hence, the Centor score for the patient is 1."
4422,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-5879030-1,Extracted,"A 21-year-old male with CF (homozygous for F508del mutation) was admitted to the Respiratory Medicine ward for 18 days with type 1 respiratory failure (arterial blood gas: pH 7.41, PaCO2 43, PaO2 54, HCO3 26, BE 2) following a routine outpatient appointment at the CF centre. The patient had transitioned from the paediatric centre three years prior and had minimal contact with the adult CF or CHD service during this period. At presentation, his predicted forced expiratory volume in 1 s (ppFEV1) was 31% (previously 76%). Oxygen saturations (SpO2) were 81% on room air (RA) (previously 92%), temperature was 37.6°C, heart rate (HR) was 100 bpm, and blood pressure (BP) 130/80 mmHg. He had no dyspnoea at rest or with mild exertion. C-reactive protein was 29 mg/L. Chest radiography (CXR) showed bilateral patchy consolidation (Fig. ). Blood sugar levels on presentation ranged between 11 and 18 mmol/L but remained between 5 and 14 mmol/L after day 3 of admission.
Past medical history included complex CHD (functionally univentricular heart (FUVH): TAt, right ventricular hypoplasia, ASD, VSD, and severe pulmonary stenosis) for which he had undergone a two-staged surgical and then a Fontan procedure (Total CavoPulmonary Connection with Extracardiac Conduit (ECC) aged 1, 2, and 8 years old, respectively). He had diabetes mellitus, liver cirrhosis, portal hypertension, oesophageal varices, splenomegaly, anaemia, osteopenia, vitamin deficiency, and substance abuse.
During the admission, he received intravenous antibiotics, and intensive medical and allied health input, including physiotherapy for airway clearance and exercise training. An Aerobika® (Trudell Medical International, London, Ontario, Canada) combined with saline or hypertonic saline was used for airway clearance, with low expiratory resistance used and HR and BP monitored carefully during initial sessions. Supplementary oxygen was provided to maintain SpO2 above 92%. After consultation with the adult congenital cardiologist, physiotherapists were advised to allow desaturation during exercise training and use patient-reported dyspnoea when determining exercise intensity. The patient performed a 6-min walk test (6MWT) on day 9 (8 L/min supplemental oxygen) and day 16 (on RA) (Table ). Despite a clinically significant worsening in SpO2 during the second 6MWT, the 6MWT distance (6MWD) improved, and dyspnoea (Borg scale) remained unchanged. At discharge, the patient had a ppFEV1 of 42% and SpO2 of 84% (RA), which improved to a ppFEV1 of 51% and SpO2 was 88% 9 months post-discharge.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [21, 'years'], 'Cough Absent': True, 'Temperature': [37.6, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 21 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 37.6 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 0.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 0 + 1 = 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
Hence, the Centor score for the patient is 1."
4423,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-3749082-1,Extracted,"A 3-year-old female patient presented with a 5-day history of fever, sore throat, and cough, but no rash. Past medical history was unremarkable, as was family history. Immunizations were up to date for age. On admission to the ward, her vital signs were: temperature 39.5°C; pulse 130 beats per minute; blood pressure 100/70 mmHg, respiratory rate 50 per minute; oxygen saturation 90% on oxygen 2/L per minute via nasal cannula; weight 13.8 kg (50th percentile); and length 94 cm (48th percentile). Her skin had normal texture, with no rashes, hypopigmentation, or hyperpigmentation, her capillary refill was around 3 seconds, and the oral mucosa was mildly dry. The patient had decreased air entry and coarse crackles in the right lower and middle zones of the lung. The throat was erythematous and there was no cervical lymphadenopathy. The rest of the physical examination was unremarkable.
Initial laboratory results were: white blood cells 24,000/μL (neutrophils 60.2%, lymphocytes 35.4%, monocytes 4.3%, basophils 0.1%), hemoglobin 10.3 g/dL, and platelets 206,000/μL. C-reactive protein was 100 mg/L, erythrocyte sedimentation rate was 65 mm/hour, albumin was 18 g/L, creatinine was 66 μmol/L, aspartate aminotransferase was 100 U/L, and alanine aminotransferase was 60 U/L. Serum glucose, blood urea nitrogen, calcium, sodium, chloride, and potassium were normal. Venous blood gas was pH 7.2, pCO2 44 mmHg, pO2 29 mmHg, and HCO3 17 meq/L, with a base excess of 11. Anteroposterior chest radiographs showed a right middle and lower lobar consolidation with moderate pleural effusion.
The patient was started on intravenous normal saline 20 mL/kg due to dehydration. She was then transferred to the pediatric intensive care unit due to increased oxygen requirement. A chest tube was inserted and 200 mL of pus was drained. The pleural fluid culture yielded GAS. The patient was started on intravenous cefuroxime and clindamycin. Nasopharyngeal and throat swabs, blood culture, and a Mantoux skin test were all negative.
On the eighth hospital day, there was no clinical response to antibiotics, and fever persisted, with new onset of abdominal pain, diarrhea, and slight tachycardia at a heart rate of 150 beats per minute.
A repeat blood count showed a significant white cell count of 30,000/μL, hemoglobin 7.7 g/dL, platelets 600,000/μL, aspartate aminotransferase 180 U/L, alanine aminotransferase 120 U/L, and albumin 18 g/L, with a rise in erythrocyte sedimentation rate and C-reactive protein.
The differential diagnosis included bacterial resistance to antibiotics, nonbacterial etiologies such as a virus or aspiration of a foreign body, bronchiolitis obliterans, hypersensitivity pneumonitis, atypical Kawasaki disease, eosinophilic pneumonia, Wegener’s granulomatosis, pulmonary sequestration, and cystic adenomatoid malformation.
Since atypical Kawasaki disease was in the differential diagnosis, an echocardiogram was ordered which showed a prominent of left anterior descending artery (0.26 cm, z-score 3.2) and left main coronary artery (0.35 cm, z-score 3.2), with no vegetations or pericardial effusion. Our team decided to give one dose of intravenous immunoglobulin 2 g/kg, and high-dose aspirin (80 mg/kg/day) was started. The fever resolved in 24 hours and the patient’s general condition improved, but desquamation developed on the hands and feet. The diagnosis of atypical Kawasaki disease was confirmed.
The patient was discharged home in a stable condition on oral antibiotics for 2 weeks and on an antiplatelet dose of aspirin. She was seen in the outpatient clinic in good condition, and a repeat echocardiogram at 6 weeks was normal.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [3, 'years'], 'Cough Absent': False, 'Temperature': [39.5, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",2,2,2,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 3 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 39.5 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
Hence, the Centor score for the patient is 2."
4424,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-7401,Extracted,"A 28-year-old man presents to the office complaining of a sore throat, difficulty swallowing, and difficulty opening his mouth for the past 5 days. He states that he had symptoms like this before and ""was given some antibiotics that made him feel better"". He is up to date on his immunizations. On examination, his temperature is 39.5°C (103.2°F) and he has bilateral cervical lymphadenopathy. An oropharyngeal exam is difficult, because the patient finds it painful to fully open his mouth. However, you are able to view an erythematous pharynx as well as a large, unilateral lesion superior to the left tonsil. A rapid antigen detection test is negative.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [28, 'years'], 'Temperature': [39.5, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True, 'Cough Absent': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 28 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 39.5 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 1 + 1 = 2.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
Hence, the Centor score for the patient is 3."
4425,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-1375,Extracted,"A 17-year-old boy comes to the physician because of body aches and sore throat for 1 week. He has no history of serious illness and takes no medications. He lives with his parents; they recently adopted a cat from an animal shelter. He is sexually active with one female partner, and they use condoms consistently. His temperature is 38.7°C (101.7°F), pulse is 99/min, and blood pressure is 110/72 mm Hg. Examination shows bilateral posterior cervical lymphadenopathy. The pharynx is red and swollen. Laboratory studies show:
Hemoglobin 15 g/dL
Leukocyte count 11,500/mm3
Segmented neutrophils 48%
Band forms 2%
Basophils 0.5%
Eosinophils 1%
Lymphocytes 45%
Monocytes 3.5%
When the patient's serum is added to a sample of horse erythrocytes, the cells aggregate together.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [17, 'years'], 'Cough Absent': True, 'Temperature': [101.7, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True}",4,4,4,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 17 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 101.7 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 69.7 = 38.72222 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 1 + 1 = 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 3 + 1 = 4.
Hence, the Centor score for the patient is 4."
4426,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-9179,Extracted,"A 6-year-old girl is brought to the clinic by her mother with fever, sore throat, and a rash. The patient’s mother says that her symptoms started 3 days ago with a high-grade fever, sore throat, vomiting, and malaise. Twenty-four hours later, she says a rash appeared on the patient’s neck and, over the next 24 hours, spread to the trunk and extremities. The patient’s mother mentions she had a bad sore throat about a week ago but denies any chills, seizures, or sick contacts. The patient has no significant past medical history and takes no current medications. Her birth was uncomplicated, and she has been meeting all developmental milestones. The patient’s vital signs include: pulse 90/min, respiratory rate 20/min, temperature 39.0℃ (102.2℉), and blood pressure 90/50 mm Hg. On physical examination, the patient has a whole-body, erythematous punctate, maculopapular rash, as shown in the exhibit (see image). Oropharyngeal examination shows circumoral pallor and a red tongue. The remainder of the examination is unremarkable.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [6, 'years'], 'Temperature': [39.0, 'degrees celsius'], 'Cough Absent': True, 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 6 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 39.0 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 2 + 1 = 3.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 3.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 3.
Hence, the Centor score for the patient is 3."
4427,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-6971214-1,Extracted,"A 52-year-old man was diagnosed with carcinoma on his EGJ following complaints of appetite loss. A histopathological examination of a biopsy specimen revealed adenosquamous carcinoma at a previous hospital. He was then referred to our hospital.
He had undergone appendectomy due to appendicitis at 13 years of age. He was an ex-smoker and drank 360 ml of distilled spirits every day. His height and weight were 178.1 cm and 51.9 kg, respectively. His body temperature was elevated to 38.5 °C. A hematologic examination showed inflammatory reaction (white blood cell 12430/μL, neutrophil cell 86%, and C-reactive protein 4.80 mg/dL), mild renal disorder (blood urea nitrogen 26.8 mg/dL and creatinine 1.07 mg/dL), and alkaline phosphatase elevation (361 U/L). All tumor markers (carcinoembryonic antigen, squamous cell carcinoma antigen, alpha-fetoprotein, and carbohydrate antigen 19-9) were within the respective normal ranges. Bacterial cultivation of the blood, sputum, and urine showed no obvious infectious findings.
Esophagogastroduodenoscopy showed a 150-mm (100 mm esophageal side and 50 mm gastric side) type 1 tumor on his EGJ that was obstructing the passage of food (Fig. ). The epicenter of the tumor appeared to be on the esophagus. A histopathological examination of a biopsy specimen revealed well-differentiated tubular adenocarcinoma at the gastric side; however, only necrotic tissue was observed at the esophageal side. Endoscopically, there was no evidence of Barrett’s esophagus.
Contrast-enhanced computed tomography did not reveal any invasion of the adjacent structures; however, five swollen regional lymph nodes were detected. 18F-Fluorodeoxyglucose positron emission tomography with computed tomography did not reveal distant metastases. We clinically diagnosed his tumor as advanced esophageal cancer, Lt Ae G, type 1, 150 mm, well-differentiated tubular adenocarcinoma, cT3 N2 M0, cStage IIIB according to the Union for International Cancer Control TNM classification of malignant tumors, seventh edition (UICC-TNM 7th).
We performed video-assisted thoracic subtotal esophagectomy, open total gastrectomy, two-field plus left cervical paraesophageal lymphadenectomy, subcutaneous reconstruction using a free jejunal graft, and jejunostomy. The operation time was 8 h and 35 min, and the estimated blood loss was 64 mL. He experienced postoperative complications of grade IIIb anastomotic leakage, grade II pneumonitis, and grade I left recurrent laryngeal nerve paralysis according to the Clavien–Dindo classification [], all of which improved with treatment, and he was discharged on post-operative day 24.
Macroscopically, the lesion consisted of two components: a 7.5-cm type 2 tumor and a 9-cm type 1 tumor at the proximal end of the type 2 tumor (Fig. a). The type 2 tumor showed a white-gray cut surface, while the type 1 tumor showed the same white-gray cut surface with necrosis and hemorrhaging (Fig. b). Whether the epicenter of the lesion was at the gastric side or esophageal side was unclear, as most of the EGJ had been replaced by the tumor. Microscopically, the type 2 tumor was predominantly solid or cribriform proliferation of tumor cells with clear cytoplasm, which was moderately differentiated adenocarcinoma with enteroblastic-like differentiation (Fig. b, Fig. a). The tumor cells of the adenocarcinoma component had periodic acid-Schiff (PAS)-positive globules and were positive for sal-like protein 4 (SALL 4) and negative for α-fetoprotein (AFP) or human epidermal growth factor receptor type 2 (HER2) (Fig. b–e). The reasons why enteroblastic-like differentiation was considered to have occurred were as follows: the tumor cells had clear cytoplasm, while they were also PAS-positive and SALL 4-positive. The type 1 tumors consisted of adenocarcinoma, like the type 2 tumor, which was positive for SALL 4, and spindle cells (sarcomatous component) growing mainly in the submucosal layer (Fig. b, Fig. a, b). There was no obvious SCC component in the type 1 tumor. Part of the sarcomatous component showed cartilage differentiation (Fig. c). The type 2 and type 1 lesions were continuous lesions, and there were smooth transitional features between the two lesions. The epicenter of the tumor was at the EGJ. The deepest invasive site was associated with the type 2 tumor, which showed invasion to the subserosa. The horizontal and vertical margins were negative for tumor cells. Histologically, there was no evidence of Barrett’s esophagus in the resected specimen. We observed all resected esophagus specimens with a cutting width of approximately 10 mm. The adenocarcinoma component was present in 10 of 27 resected lymph nodes. The tumor was finally diagnosed as carcinosarcoma of the EGJ with a carcinomatous component of adenocarcinoma, Siewert type II, type 1 + 2, 110 mm, pT3 N3 M0, pStage IIIC according to UICC-TNM 7th.
The patient underwent adjuvant systemic chemotherapy with S-1 for gastric adenocarcinoma but developed para-aortic lymph node metastases 5 months after surgery.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [52, 'years'], 'Temperature': [38.5, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Cough Absent': False, 'Exudate or swelling on tonsils': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 52 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 38.5 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score -1 + 1 = 0.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 0.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 0 + 1 = 1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
Hence, the Centor score for the patient is 1."
4428,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-12811,Extracted,"A 24-year-old college student presents to student health with 2 days of developing a sore throat, runny nose, and a cough that started today. He states that he has been getting mild fevers which began yesterday. On exam, his temperature is 102.0°F (38.9°C), blood pressure is 135/76 mmHg, pulse is 95/min, and respirations are 12/min. His physician recommends over-the-counter cold medications and reassures him that his symptoms are due to a viral infection that is self-limited.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [24, 'years'], 'Cough Absent': False, 'Temperature': [102.0, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 24 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 102.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 70.0 = 38.88889 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
Hence, the Centor score for the patient is 1."
4429,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-8333,Extracted,"A 4-year-old boy is brought to the pediatrician in the month of January with a one-week history of a cough and somnolence. He developed a fever and cough and stated that his legs hurt ‘really bad’ 3–4 days prior to his symptoms. He has asthma but no other significant past medical history. He takes albuterol and his mom administered acetaminophen because he was feeling ‘hot’. The blood pressure is 92/66 mm Hg, the heart rate is 118/min, the respiratory rate is 40/min, and the temperature is 39.2°C (102.6°F). On physical examination, the visualization of the pharynx shows mild erythema without purulence. Auscultation of the lungs reveals crackles over the right lung base. The rapid strep test is negative. A chest X-ray shows homogenous opacity in the lower lobe of the right lung.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [4, 'years'], 'Cough Absent': False, 'Temperature': [39.2, 'degrees celsius'], 'Exudate or swelling on tonsils': False, 'Tender/swollen anterior cervical lymph nodes': False}",2,2,2,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 4 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 39.2 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
Hence, the Centor score for the patient is 2."
4430,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-8710360-1,Extracted,"A 55-year-old Caucasian male with significant past medical history of hypertension, hyperlipidemia, patent foramen ovale, heart failure with preserved ejection fraction, impaired glucose tolerance, and obesity, presented to the emergency department on account of sudden onset generalized maculopapular rash involving his face, extremities, and trunk, with associated fever and chills. He was hospitalized 1 month earlier and managed for methicillin-sensitive Staphylococcus aureus (MSSA) bacteremia and thoracic vertebrae (T11–T12) discitis. During his recent hospitalization, he presented with mid-back pain, fever, and chills. His blood cultures revealed growth of MSSA that was pansensitive to oxacillin, cefazolin, ampicillin/sulbactam, clindamycin, daptomycin, ciprofloxacin, tetracycline, trimethoprim/sulfa, and vancomycin. Magnetic resonance imaging (MRI) of the thoracolumbar spine revealed T11–T12 discitis with no evidence of epidural collection or abscess (Fig. ). Transthoracic and transesophageal echocardiogram revealed his underlying patent foramen ovale, with no evidence of endocarditis or valvular vegetations. He was reviewed by the infectious disease specialist and managed with intravenous oxacillin 2 g administered every 4 hours during his hospitalization. He had resolution of his fever with intermittent mid-back pain. Repeat blood cultures showed no organism growth. He was discharged on intravenous oxacillin 2 g 4 hourly based on a scheduled 6-week course to be administered via a peripherally inserted central catheter (PICC) line.
The patient remained apparently well until 3 weeks after the start of antibiotic therapy, when he developed sudden onset generalized skin rash with associated pruritus, fever, and chills. He had no recent travel or contact with anyone who had a similar rash. He was sexually active in a monogamous heterosexual relationship. He had no associated symptoms of runny nose, sore throat, cough, shortness of breath, joint pain, or myalgia. He had intermittent back pain on account of thoracic discitis, with no localized swelling or limited mobility of his spine. He was up to date on his vaccinations. His home medications included lisinopril, probiotics, ibuprofen, and a remaining 3-week course of oxacillin. He had no known drug allergies. He had no known history of direct exposure to environmental pollutants. He had 30 pack year history of smoking cigarettes. He quit smoking 15 years prior to the current hospitalization. He consumed two standard drinks of alcohol per week. He had no history of recreational drug use. He worked as a truck driver transporting gasoline and diesel, and used personal protective equipment including respirator masks and gloves. He had significant history of asthma in his brother. No other known history of hypersensitivity in his family.
Due to the sudden and unexpected onset of generalized rash, he was apprehensive and immediately set up a telehealth visit with his infectious diseases specialist who recommended the use of over-the-counter oral diphenhydramine. However, with the onset of fever and persistence of his rash, he was advised to discontinue the use of oxacillin and present to the emergency department. On arrival, he was alert, oriented to person, place, and time, and not in acute distress. He had unstable vital signs including fever at 101.2 °F, elevated blood pressure 152/87 mmHg, tachycardia with heart rate 136 beats per minute, respiratory rate 18 breaths per minute, and pulse oximetry 96% on room air. He had generalized blanchable maculopapular and morbilliform rash involving the face, trunk, upper and lower extremities, and sparing the palms, soles, and oral mucosa (Fig. ). He had palpable nontender lymph nodes in the cervical and inguinal regions bilaterally. His conjunctiva was not pale and sclera anicteric. He had clear vesicular breath sounds bilaterally. He had rapid and regular heart rate, normal rhythm, and normal heart sounds with no murmurs. His abdomen was obese, nontender, no palpable masses or hepatosplenomegaly, with the presence of normoactive bowel sounds. His neurological examination revealed normal cranial nerves II–XII with no neurologic deficits, 5/5 motor strength in his upper and lower extremities, normal deep tendon reflexes, strength, and sensation bilaterally. No swelling or tenderness on his spine. He had a normal gait and balance, with no evidence of cerebellar dysfunction. Hematologic lab values revealed white blood cell count 4.6 × 1000/µL (reference range 4–11 × 1000/µL), atypical lymphocytosis 0.5 × 1000/µL; 13% (reference range 0–4.5 × 1000/µL; 0–7%), eosinophilia 0.6 × 1000/µL (reference range 0–0.4 × 1000/µL), neutrophilic bandemia 18% [reference range 0–8%]. He had elevated transaminases including aspartate transaminase (AST) 101 U/L (reference range 0–55 U/L), alanine transaminase (ALT) 115 U/L (reference range 0–44 U/L), and alkaline phosphatase (ALP) 216 U/L (reference range 25–150 U/L). Inflammatory markers were elevated, including erythrocyte sedimentation rate (ESR) 31 20 mm/hour (reference < 20 mm/hour) and C-reactive protein (CRP) 34.5 mg/dL (reference < 8 mg/dL). He was further evaluated to rule out other potential infectious etiology, which were unrevealing as urine, blood, and PICC line catheter tip cultures showed no growth of organisms. Blood culture samples for aerobic and anerobic bacteria were obtained by venipuncture using two sets of sterile blood culture bottles and cultured in BacT-ALERT. No organism growth was seen in the blood cultures after 5 days of incubation. No fungal organisms were detected. Tests for herpes simplex virus (HSV) I and II immunoglobulin (IgM) antibody, infectious mononucleosis, rubeola IgM, urine legionella antigen, hepatitis A, B, and C panel, and CMV DNA polymerase chain reaction and IgM antibody were all negative, as well as human immunodeficiency virus (HIV) 1 and 2 antigen/antibody fourth generation test, which was nonreactive, and corona virus 2019 (COVID-19) SARS-CoV-2 was undetected (Table ).
He was managed as a case of DRESS syndrome with intravenous fluids (2 L of 0.9% normal saline), intravenous diphenhydramine HCL 25 mg 8 hourly as needed for itching (three doses), acetaminophen 650 mg 8 hourly via oral route as needed for fever (three doses), and topical application of calamine lotion three times daily. For deep venous thrombosis prophylaxis, he received subcutaneous heparin sodium 5000 units every 8 hours (four doses), for prevention of stress ulcers he received pantoprazole 40 mg (two doses), and two doses of Lactobacillus acidophilus tablet. His home medication of lisinopril 10 mg daily for hypertension was withheld for concerns for potential acute kidney injury. On the second day of hospitalization, there was resolution of his fever. However, his generalized rash persisted, alongside elevated transaminases, and abnormal cell count. He remained hemodynamically stable and did not develop any new symptoms. To complete his course of antibiotic therapy for MSSA bacteremia, he was switched to an alternative therapy with cefazolin 2 g every 8 hours for 6 weeks. He received four doses of cefazolin prior to hospital discharge and was closely monitored to ensure that he had no reaction to cefazolin. The choice of cefazolin was based on the considerable severity of his thoracic discitis and the intention to appropriately manage him with the most sensitive antibiotic available. The possibility of cross reaction with cefazolin was considered less likely and he was closely monitored for any adverse reaction with weekly follow-up assessments in the outpatient setting. He tolerated the cefazolin without any untoward reaction and successfully completed his course of treatment.
Within a week of follow-up with the infectious disease specialist, he had notable clinical improvement with resolution of his rash and normalization of his liver enzymes. However, he had persisting mild anemia (hemoglobin 12.5 g/dL), eosinophilia (eosinophils 890 cells/µL), and elevated inflammatory markers including ESR (36 mm/hour) and CRP (17.3 mg/dL). In the subsequent week of follow-up, there was no recurrence of his rash, his liver enzymes were not elevated, he had improving anemia with hemoglobin at 13.1 g/dL, and resolving inflammatory markers with ESR at 29 mm/hour and CRP within normal limits. No new medication was initiated during outpatient follow-up with the infectious disease specialist. Upon resolution of his symptoms and completion of his antibiotic therapy, he reported improvement in his quality of life and intention to return to work. He was medically cleared and deemed fit to work. The patient was counseled by the infectious disease specialist on potential triggers of DRESS syndrome and avoiding future occurrence.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'Cough Absent': True, 'Temperature': [101.2, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': False}",2,2,2,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 55 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 101.2 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 69.2 = 38.44444 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score -1 + 1 = 0.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 0 + 1 = 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 1 + 1 = 2.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
Hence, the Centor score for the patient is 2."
4431,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-7501657-1,Extracted,"A 72-year-old man with chronic kidney disease stage 5 dialysis (CKDG5D) secondary to hypertension and diabetes was hospitalised in April 2020, reporting abdominal pain and fever after noticing cloudy PD effluent 3 days before hospitalisation.
The initial physical examination showed that the patient’s general condition was reduced and that he was obese (body mass index [BMI], 34.5). He had a fever of 38.5 °C. His blood pressure was 116/74 mmHg, his heart rate was 80 beats per minute, his respiratory rate was 14 breaths per minute, and his oxygen saturation was 96% without supplementation. He reported no vomiting, nausea, or diarrhoea. There were no signs of meningeal irritation. Examination showed strong, diffuse abdominal tenderness with maximal pain in the right lower abdomen. The PD catheter exit site was clean and dry, and there was no tunnel tenderness.
The patient’s medical history included type 2 diabetes (first diagnosed in 2012, insulin-dependent since 2018), hypertension, severe coronary heart disease requiring multiple revascularizing procedures (including bypass surgery), and persistent atrial fibrillation necessitating implantation of a cardiac pacemaker and a left atrial appendage (LAA) occluder. The patient had required continuous ambulatory peritoneal dialysis (CAPD) since June 2018 and had not experienced any previous dialysis-related infections or other complications.
During the course of this infection, an outpatient analysis of the PD effluent found a leukocyte count of 11,000/nL. At the time of hospital admission, the first PD effluent was cloudy, with a leukocyte count of 7060/nL. Initial blood tests found elevated levels of indicators of inflammation: C-reactive protein (CRP), 17.5 mg/dL (normal, < 0.5 mg/dL); procalcitonin (PCT), 3.22 ng/mL (normal, < 0.5 ng/mL). Blood gas analysis found a serum lactate level of 2.4 mmol/L (normal, < 1.2 mmol/L) but no acidosis or electrolyte disorders. The urine test strip results were negative for leukocytes and nitrites.
Initially, we intensified dialysate exchanges till PD effluent was clear and the patient’s abdominal pain decreased followed by an increased number of daily dialysate exchanges for the first 3 days of treatment. From the fourth day of treatment on, the patient was placed on a continuous cyclic peritoneal dialysis (CCPD) regimen.
After obtaining blood, urine, and PD effluent samples for microbiological analysis, we initiated antibiotic therapy because analysis of ambulatory PD effluent detected L. monocytogenes. In the first 24 h of hospital stay the patient showed fever up to 39 °C and hypotension associated with reduced vigilance. Therefore, a septic course of disease in terms of a meningitis could not be ruled out. On the basis of the results of resistance testing, we treated the patient with ampicillin administered intravenously at a dosage of 6 g twice daily according to German meningitis guideline [].
We also treated the patient empirically with intraperitoneal cefazolin and ceftazidime because we could not rule out infection with a different or an additional bacterium at the time of admission.
Microbiological cultures of the PD effluent samples obtained on the first day of hospitalisation detected L. monocytogenes. The German Consultant Laboratory for Listeria confirmed the identification and classified the bacterium as a member of serotype IIa. Additional microbiological analysis confirmed the presence of L. monocytogenes in the PD effluent. Because no other pathogen was detected in the PD effluent, intraperitoneal antibiotic treatment with cefazolin/ceftazidime was discontinued after the administration of a single dose on the first day of treatment. No bacterial growth was detected in cultures of blood or urine samples. Cultures of consecutive samples of PD effluent obtained on the next day and on ten other days during the hospital stay did not grow bacteria.
During intravenous antibiotic treatment, the leucocyte count in the PD effluent decreased continually to 315/nL, but on the fifth day of treatment the leukocyte count increased to 3778/nL. The CCPD regimen had not changed, and the CRP and PCT levels had decreased continually. There were no further episodes of fever. To rule out underdosing of ampicillin, we determined the serum ampicillin level and its association with the minimal inhibitory concentration (MIC) of the Listeria isolate, which was determined to be 0.5 mg/L and was interpreted as “susceptible” according to the clinical breakpoints provided by the European Committee on Antimicrobial Susceptibility Testing (EUCAST) []. With expert consent, we determined to establish a therapeutic range of serum ampicillin levels of at least four times the MIC []. The first test of the serum ampicillin level (after 5 days of intravenous ampicillin administration with the last dose given 7 h before sample taking) found a concentration of 149 mg/L. We collected further samples at two and 4 h after the next dose of intravenous antibiotic, and tests showed sufficient serum ampicillin levels of 235 mg/L at 2 h and 95.5 mg/dL at 4 h. Therefore, we continued the previous intravenous antibiotic treatment.
At day seven the leukocyte count in the PD effluent had increased to 5182/nL; therefore, escalation of antibiotic therapy became crucial. The recent International Society for Peritoneal Dialysis (ISPD) Guideline does not provide any recommendations for monotherapy with intraperitoneal ampicillin by intermittent application (with one exchange daily) []. Also, the adequate duration of therapy has not yet been established. We decided that, in addition to continuing intravenous administration of ampicillin, we would add a dose of 4 g ampicillin to a 2-L bag of Extraneal dialysate (Baxter International, Deerfield, IL, USA). The bag was shaken to ensure adequate mixing of the drug in the dialysate. The antibiotic-containing dialysate was drawn into the peritoneal cavity and allowed to dwell for 12 h.
With this combination of intravenous and intraperitoneal antibiotic therapy, the leukocyte count in the PD effluent finally declined permanently. We continued drug monitoring and detected sufficient serum ampicillin levels even when the drug was administered intraperitoneally only at a dosage of 4 g daily. The leukocyte count stayed low. Detailed information about antibiotic therapy and serum ampicillin levels can be found in the figure and the table (Table and Fig. ).
After the PD leukocyte count had been lower than 100/nL for 7 days, we discontinued antibiotic therapy on day 21 and discharged the patient from the hospital. A more detailed anamnesis led us to suspect that the Listeria infection was caused by consumption of a creamed cheese. This cheese was analysed by the local health authority, but no Listeria could be detected. Moreover, the bacterium was not detectable in stool samples obtained during inpatient treatment. Therefore, the origin of the infection remained unclear. Outpatient examination 3 days after hospital discharge found that the patient was fit and well. There were no signs of a relapse of infection. The patient is under regular outpatient supervision. Within 3 months there was no recurrence of infection.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [72, 'years'], 'Cough Absent': True, 'Temperature': [38.5, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 72 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 38.5 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score -1 + 1 = 0.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 0 + 1 = 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
Hence, the Centor score for the patient is 1."
4432,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-2171,Extracted,A 27-year-old woman comes to the physician because of a 3-day history of a sore throat and fever. Her temperature is 38.5°C (101.3°F). Examination shows edematous oropharyngeal mucosa and enlarged tonsils with purulent exudate. There is tender cervical lymphadenopathy.,What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [27, 'years'], 'Cough Absent': False, 'Temperature': [38.5, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 27 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 38.5 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 1 + 1 = 2.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
Hence, the Centor score for the patient is 3."
4433,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-6068367-1,Extracted,"A 50-yr-old man in the north of China went to Uganda to search for a work on Jul 14, 2016, and returned home on Jul 25. No obvious cause of fever with a temperature of 38.5 °C and occasional cough were found on Jul 30. After intravenous cephalosporin medication in local clinic for 3 d since the night of July 30, his body temperature dropped to normal. The patient became partially unconscious at 18:00 on Aug 2, and was sent to the Second Hospital of Changli County firstly, and then transferred to our hospital due to dangerous condition. Upon admission, the patient was found to have body temperature of 38.5 °C, unconsciousness, irritability, BP of 137/93 mm Hg and heart rate of 122 times/min with the consideration of febrile diseases. After being given intravenous cefoperazone sulbactam symptomatic treatment in the fever clinic, his status showed no improvement and the patient was transferred to intensive care unit for further treatment at 10:30 on Aug 3.
In IUC, physical examination gave the following results as blurred consciousness, irritability, high blood pressure, skin and sclera yellow dye, but few of other positive changes. The patient was treated with sedative, acid suppression, liver protection, clearing mind and anti-infection of meropenem. Considering the falciparum malaria with the warning of local CDC, the patient was transferred to the Third Hospital of Qinhuangdao (the infectious diseases hospital of Qinhuangdao) for continued treatment at 17:00. Considering the patient with cerebral falciparum malaria associated with liver and myocardial damage, more tests were performed and results indicated a lung infection and metabolic acidosis.
The patient was given sodium bicarbonate intravenous drip to correct acidosis, magnesium isoglycyrrhizinate, and reduced glutathione to protect liver, pantoprazole intravenous drip to protect the gastric mucosa, meropenem to anti-infection, diazepam and cockstailytic for sedation treatment, artemether and dihydroartemisinin-piperaquine tablets for anti-malaria treatment. Unfortunately, the patient’s status showed no improvement till 00:20 on Aug 4, and was transferred to ICU of Beijing Ditan Hospital for further treatment at 04:47 on Aug 4. After antimalarial therapy with intramuscular artemether, anti-infection treatment with intravenous cefmetazole and other symptomatic treatment, the disease did not relieve and acidosis became heavier; the patient had already in a deep coma at 15:00 on Aug 5, and then died of septic shock at 20:40.
The study was approved by the hospital.
Blood sample showed hemoglobin of 127 g/l, red blood cell count of 4.29×1012/l, total white blood cell count of 6.71×109/l, 85.5% neutrophil and platelet count of 14×109/l; his liver function test showed hyperbilirubinaemia of 247.68 μmol/l and transaminitis with serum ALT 84.4 U/l, AST 113.4 U/l, LDH 492 U/l, total bile acid 32.46 μmol/l, rglutamyltranspeptidase 431.2 U/l, blood ammonia 35.8 μmol/l and the total protein 62.3 g/l; his serum D- dimmer, fibrinogen and procalcitonin raised to 13.72 μg/ml, 5.38 g/l and 6.23 ng/ml, respectively; bicarbonate was 16.7 mmol/l and plasma protamine paracoagulation was weakly-positive; urine analysis revealed elevated bilirubin, protein, occult blood and ketone.
Red blood cell (RBC) morphology was normal and about 40% of them contained 1–2 mainly or occasionally 3 early trophozoites of Plasmodium falciparum. The early trophozoites were annular and some were located on the edge of RBC, the ring was slender and it accounted for 1/4–1/5 of the diameter of RBC, the ring contained 1–2 nucleuses, which was dark purple, dense, round or oval. Big trophozoite was visible and occasionally schizonts in the smear. The malaria pigment phagocytosed by neutrophils or mononuclear cells was visible occasionally; it showed granular clumps of dark brown or yellowish brown. Finally, infection by P. falciparum was identified. Blood smear examination was performed again at the Third Hospital of Qinhuangdao after 4 h interval, the result showed that approximately 70% of RBC containing early trophozoites, in which three parasites were easy to be seen and 7 rings occasionally, furthermore mixed metabolites of Plasmodium were visible easily ().
Take the patient’s blood samples from our hospital and the Third Hospital of Qinhuang-dao to analyze the RET scatter plots respectively, the results showed RET increased and the percentage of RET to RBC were 5.8% and 9.3% respectively ().
In the Qinhuangdao CDC, the serological detection result supported the mixed infection of P. falciparum by the colloidal gold method. In the Hebei Provincial CDC, dengue real-time polymerase chain reaction (RT-PCR) was positive, serum IgM was positive but IgG against the virus was negative by ELISA.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [50, 'years'], 'Cough Absent': True, 'Temperature': [38.5, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 50 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 38.5 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score -1 + 1 = 0.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 0 + 1 = 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
Hence, the Centor score for the patient is 1."
4434,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-7859,Extracted,"A 6-year-old boy presents with fever, sore throat, hoarseness, and neck enlargement. The symptoms started 3 days ago and progressed gradually with an elevated temperature and swollen lymph nodes. His family immigrated recently from Honduras. He was born via spontaneous vaginal delivery at 39 weeks after an uneventful gestational period and he is now on a catch-up vaccination schedule. He lives with several family members, including his parents, in a small apartment. No one in the apartment smokes tobacco. On presentation, the patient’s blood pressure is 110/75 mm Hg, heart rate is 103/min, respiratory rate is 20/min, and temperature is 39.4°C (102.9°F). On physical examination, the child is acrocyanotic and somnolent. There is widespread cervical edema and enlargement of the cervical lymph nodes. The tonsils are covered with a gray, thick membrane which spreads beyond the tonsillar bed and reveals bleeding, erythematous mucosa with gentle scraping. The lungs are clear to auscultation.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [6, 'years'], 'Cough Absent': False, 'Temperature': [39.4, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True}",4,4,4,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 6 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 39.4 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 3 + 1 = 4.
Hence, the Centor score for the patient is 4."
4435,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-6743,Extracted,"An 11-year-old boy presents with a sore throat, fever, chills, and difficulty swallowing for the past 3 days. The patient’s mother says that last night he was short of breath and had a headache. Past medical history is unremarkable. The patient has not been vaccinated as his mother thinks it is ""unnecessary"". His temperature is 38.3°C (101.0°F), blood pressure is 120/70 mm Hg, pulse is 110/min, and respiratory rate is 18/min. On physical examination, the patient is ill-appearing and dehydrated. A grayish-white membrane and pharyngeal erythema are present in the oropharynx. Significant cervical lymphadenopathy is also present. A throat swab is taken and gram staining shows gram-positive club-shaped bacilli along with few neutrophils.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [11, 'years'], 'Temperature': [38.3, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True, 'Cough Absent': False}",4,4,4,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 11 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 38.3 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 3 + 1 = 4.
Hence, the Centor score for the patient is 4."
4436,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-565,Extracted,"A 7-year-old boy is brought to the physician because of a 4-day history of fever, headache, earache, and sore throat that is worse when swallowing. He has not had a runny nose or cough. He had a similar problem 1 year ago for which he was prescribed amoxicillin, but after developing a skin rash and facial swelling he was switched to a different medication. His immunizations are up-to-date. He is at the 75th percentile for height and the 50th percentile for weight. His temperature is 38.9°C (102°F), pulse is 136/min, and respirations are 28/min. Examination of the oral cavity reveals a coated tongue, red uvula, and enlarged right tonsil covered by a whitish membrane. The deep cervical lymph nodes are enlarged and tender. A throat swab is taken for culture.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [7, 'years'], 'Cough Absent': True, 'Temperature': [38.9, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True}",5,5,5,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 7 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 38.9 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 2 + 1 = 3.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 3 + 1 = 4.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 4 + 1 = 5.
Hence, the Centor score for the patient is 5."
4437,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-2737790-1,Extracted,"A 54-year-old, Greek woman was admitted to our Internal Medicine Department with a high-spiking fever accompanied by rigor. She also complained of myalgias and sore throat. The symptoms started 3 days earlier. A few hours before admission, a severe headache started and led her to seek medical advice.
Her medical history was not significant. She did not report any visits to the dentist or any dental-related disease in the recent past. She had not undergone any invasive endoscopic procedure, nor had she exhibited any symptomatology in the weeks before her admission. She was not immunocompromised and did not regularly take any medications. On clinical examination, her temperature was 39.50C, and her blood pressure normal. There were no clinical indications of active pulmonary or cardiac involvement, and a brief neurological examination detected no abnormalities. Nuchal rigidity was absent. A laboratory examination revealed anemia (hemoglobin 11 g/dL), and increased erythrocyte sedimentation rate (72 mm/hour) and C-reactive protein (321 mg/L). During paraclinical work-up, the patient developed multiple purpural lesions on her legs. There was no nail hemorrhage or petechial lesions on her soles or palms on clinical examination.
Multiple cultures were drawn and a brain computed tomography (CT) scan was performed. Its findings were further assessed by magnetic resonance imaging (MRI), which revealed (Figure ) multiple cerebellar, white matter, and sub-grey matter, low-signal T1-weighted and high-signal T2-weighted lesions. Some of these lesions exhibited no-signal T2-weighted areas, consistent with a hemorrhage.
Immediately following the MRI results, and upon strong suspicion of endocarditis leading to cerebral embolization, transesophageal echocardiography was performed, revealing two 20 mm mitral valve vegetations.
The patient was started on ceftriaxone, 2 g intravenously b.i.d. and vancomycin, 500 mg intravenously q.i.d., and mitral valve replacement surgery was performed later that day, embolization being an indication for valve replacement in infective endocarditis in the case of large vegetations such as the ones present in this patient []. Following valve replacement, antibiotic therapy was continued.
Four days after the valve replacement, blood cultures were positive for H. parainfluenzae. Throat swab specimens were cultured after the initiation of antimicrobial therapy and were negative as expected. The strain was susceptible to a variety of antibacterials, including amoxicillin-clavulanate. A decision was made to continue on ceftriaxone though, while vancomycin was discontinued. Ceftriaxone was administered, uneventfully, for six more weeks, together with gradual initiation of warfarin therapy.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'Cough Absent': True, 'Temperature': [39.5, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 54 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 39.5 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score -1 + 1 = 0.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 0 + 1 = 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
Hence, the Centor score for the patient is 1."
4438,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-5411,Extracted,"A 24-year-old man with no significant past medical history presents to urgent care with a cough and fatigue. The patient states his symptoms have persisted for the past 48 hours and have made work difficult for him. He has been taking an antibiotic he had left over from a previous infection but states it did not improve his symptoms. His temperature is 101°F (38.3°C), blood pressure is 127/68 mmHg, pulse is 110/min, respirations are 17/min, and oxygen saturation is 97% on room air. A chest radiograph is perfomed as seen in Figure A. Physical exam is notable for obesity, gynecomastia, and the finding in Figure B as well as some erythema of the posterior oropharynx.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [24, 'years'], 'Cough Absent': False, 'Temperature': [101.0, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 24 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 101.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 69.0 = 38.33333 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
Hence, the Centor score for the patient is 1."
4439,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-3424642-1,Extracted,"A 52-year-old woman was admitted to our hospital with chronic cough, exertional dyspnea, and edema of lower extremities in November 2010. Dermatomyositis sine myositis was diagnosed for her with typical Gottron's sign, heliotrope rash, episodes of mechanic's hand, and nail fold capillary changes without muscle weakness about 6 years ago. At that time, serologic tests such as ANA and anti-dsDNA were negative, and C3, C4, and CH50 levels were normal. Her ischemic ulcers on hand knuckles showed infiltrations of lymphoplasma cells without evidence of overt vasculitis on biopsy specimens in favor of nonspecific connective tissue diseases.
In April 2004, She developed fever, cough, diarrhea, and vomiting, while she had been treated with prednisolone and azathioprine. After a course of antibiotic therapy and due to cytopenia, azathioprine switched to cyclosporine. Six years later, the patient had several hospital admissions because of dry cough, exertional dyspnea, and fever. Initially, computed tomography (CT) of the chest and echocardiography were normal. However, later pulmonary function tests revealed restrictive pattern and high-resolution CT scan of the lungs showed fibrosis of anterior segment of the right upper lobe. She developed diabetes mellitus and hypertension 3 years ago.
The patient was taking prednisolone, cyclosporine, hy droxychloroquine, amlodipine, triamterene, hydrochlorothiazide, aspirin, and glybenclamide, without kidney involvement over the past 6 years. She never used any immunosuppressive drugs before the diagnosis of dermatomyositis sine myositis.
On last admission, body temperature of 37°C and blood pressure of 160/85 mmHg were recorded. Physical exam revealed heliotrope rash in upper eyelids, coarse crackles over the base of the right lung, and pitting edema of lower extremities. Laboratory findings were as follows: mild anemia Hemoglobin 11.1 g/dL (12–16 g/dL), White blood cell 7900 cells/mm3 (3500–10500 cells/mm3), blood urea nitrogen 28 mg/dL (7–20 mg/dL), creatinine 1 mg/dL (0.5–0.9 mg/dL), 24-hours creatinine clearance 83 cc/min, triglyceride 325 mg/dL (30–200 mg/dL), total cholesterol 340 mg/dL (<200 mg/dL), high-density lipoprotein 68 mg/dL (40–60 mg/dL), low-density lipoprotein 207 mg/dL (<130 mg/dL), and abnormal urinalysis with 2+ proteinuria; urinary protein excretion level was 2.2 g/day. The serum creatine kinase (CK), lactate dehydrogenase (LDH), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were 34 IU/L (39–238 IU/L), 579 IU/L (100–500 IU/L), 23 IU/L (7–41 IU/L), and 16 IU/L (12–38 IU/L), respectively. Erythrocyte sedimentation rate (ESR) was substantially elevated 75 mm/hour and C-reactive protein was 2+ positive. Anti-dsDNA, p-ANCA, and c-ANCA were negative. Complement levels (C3, C4, and CH50) were within normal range. Serologic tests for hepatitis B and C were negative. Later assays showed positive fluorescent ANA result with homogeneous pattern. But anti-Jo1 test was not available in our center at the time of primary investigations.
A percutaneous renal biopsy was performed. Microscopic examination revealed diffuse enlargement of glomeruli with thickening of the capillary walls, thickened mesangial matrix, mesangial cells proliferation causing lobulation of the tufts, and scattered infiltration of neutrophils (). The capillary wall had tram-track appearance in silver staining (). The interstitium had no significant pathological changes. Immunofluorescence showed granular pattern of C3 and IgG deposition along the capillary walls and mesangial matrix. Based on biopsy results, diagnosis of membranoproliferative glomerulonephritis was made.
On last admission, the patient was treated with 500 mg intravenous methylprednisolone and 1000 mg cyclophosphamide for 3 subsequent months. She started to get 2000 mg mycophenolate mofetil and 30 mg prednisolone daily. After 10 months of beginning treatment, 24-hour protein excretion was decreased to less than 150 mg/day.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [52, 'years'], 'Cough Absent': False, 'Temperature': [37.0, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",-1,-1,-1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 52 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 37.0 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at -1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at -1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at -1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at -1.
Hence, the Centor score for the patient is -1."
4440,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-5847404-1,Extracted,"A 77-year-old male with no significant past medical history presented to our medical center's Emergency Department with symptoms of bright red blood per rectum. Two years prior, the patient had undergone a TRUS-guided prostate biopsy at an outside hospital for an elevated PSA of 7 ng/mL (normal <4 ng/mL) and was found to have a Gleason score of 6. The patient elected to pursue surveillance, and in the following year, his PSA was 5 ng/mL. One month prior to presentation at our facility, the PSA was 6 ng/mL. Four days prior to presentation, the patient had undergone a repeat TRUS-guided prostate biopsy in the other hospital's urological procedure room. No immediate complications were encountered, so the patient was sent home. Several hours later, he developed lightheadedness and bright red blood per rectum. Upon returning to the outside hospital, he developed syncope and was taken to their Emergency Department, where he had ongoing bright red blood per rectum. The hemoglobin was found to have decreased from a preprocedural level of 12.9 g/dL (normal, 13.5??7.5 g/dL) to 9.7 g/dL. Computed tomography (CT) angiography of the abdomen and pelvis showed active bleeding in the rectum. The patient was observed, and his bleeding appeared to self-resolve. He was not given blood products and was discharged on the next day, 3 days prior to his presentation at our medical center.
On the evening of the fourth day postprocedure, the patient again developed lightheadedness and bright red blood per rectum. He was brought to our Emergency Department for further evaluation. He had not taken any medications. His temperature was 36.3℃, his heart rate 110 per minute, his blood pressure 109/62 mmHg, and his oxygen saturation was 96% on room air. On physical examination, he appeared diaphoretic and pale; no abdominal tenderness was found. Laboratory studies revealed a hemoglobin level of 7.7 g/dL. The platelets, prothrombin time (PT), and partial thromboplastin time were within their normal ranges. CT angiography of the abdomen and pelvis showed active bleeding in the anterior rectum. Over the next 12 hours, the patient had eight episodes of large-volume bright red blood per rectum and clots. He received seven units of blood and 2 units of fresh frozen plasma. Although the patient was alert and oriented at the time of presentation, he subsequently developed syncope with poor arousability and was intubated in our intensive care unit for airway protection. A 500-mL tap water enema was administered, and he underwent flexible sigmoidoscopy.
On sigmoidoscopy, bright red blood and clots were noted from the rectum to 15 cm of intubation, where normal mucosa was visualized. On the anterior aspect of the rectum, at 1 to 2 cm from the dentate line, an approximately 3-mm ulcerated lesion was noted overlying a raised lesion that was pulsatile (). Six mililiters of 0.0001% epinephrine solution was injected circumferentially around this lesion, with immediate brisk bleeding noted at the injection sites. Although clipping and/or cautery were initially considered for hemostasis, on retroflexion, the lesion was apparently contiguous with what appeared to be a large internal hemorrhoid (). As such, band ligation (Speedband Superview Super 7, Boston Scientific, Marlborough, MA, USA) was performed using a single band around the site of the ulcerated lesion, with successful hemostasis being achieved (). After the procedure, the patient had no further signs of bleeding and showed stable hemoglobin levels on serial testing. He was successfully extubated within 24 hours and was discharged 5 days later.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [77, 'years'], 'Temperature': [36.3, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False, 'Cough Absent': False}",-1,-1,-1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 77 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 36.3 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at -1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at -1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at -1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at -1.
Hence, the Centor score for the patient is -1."
4441,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-8610458-1,Extracted,"We present the case of a 40-year-old male with no significant past medical history, aside from a penicillin allergy, who presented to the emergency department (ED) with a chief complaint of severe right elbow pain, swelling, and limited passive and active range of motion for one day. He reported a prodromal flu-like syndrome of subjective fever, chills, and myalgias with associated right-arm soreness for two days prior to symptom onset. The patient stated that his right elbow started to swell and he progressively experienced increased pain over the following day. He attempted to use heating pads and ice without symptomatic relief. On further history, he reported recent unprotected sex with a new sexual partner in addition to right knee and hip pain without a history of trauma. At the time of his presentation, he denied any penile discharge, burning during urination, or pain in other joints.
On physical exam, the patient was in moderate distress due to pain. His right elbow was erythematous, edematous, warm, and tender to palpation. Passive and active range of motion were limited and worsened pain. Mild effusion was noted on palpation of the joint. He was initially afebrile with a temperature of 99.9°F, mildly tachycardic to 110 beats per minute, normotensive, and had 100% oxygen saturation. Labs were remarkable for an elevated erythrocyte sedimentation rate of 68 millimeters per hour (mm/hr) (reference range: 0–30 mm/hr), borderline leukocytosis of 10.7*103 cells per milliliter (mL) (4.0–11.0*103 cells/mL), mild hyponatremia, and mild hypokalemia. Complete blood count, creatinine kinase, and lactic acid were within normal limits. Blood cultures were obtained for Gram stain and culture.
Right elbow radiograph revealed joint effusion without evidence of fracture or soft tissue swelling (). Arthrocentesis from the right elbow was performed with 18 mL of aspirate. Synovial fluid analysis revealed cloudy fluid with small clots, a SF WBC count of 22,000 cells per cubic millimeter /(mm3) (reference range: 0–200 cells/mm3), 90% segmented neutrophils, and 66,500 red blood cells. Synovial fluid was cultured and sent for Gram staining. Intravenous (IV) ketorolac and morphine were given for pain control, and the patient was empirically started on IV clindamycin for suspected skin and soft tissue infection. While he was in the ED, there was suspicion for an inflammatory process of the joint with an overlying soft tissue infection. However, due to the risk of SA, he was admitted to the floor for further workup and evaluation.
On the floor, antibiotics were switched to aztreonam and vancomycin by the primary team due to suspicion of SA. Rapid human immunodeficiency virus (HIV)-1/2 antibody/antigen and gonorrhea-chlamydia tests were ordered. Orthopedic and infectious disease teams were consulted for further management and recommendations. Further laboratory testing revealed HIV 1/2 antibody positive, absolute cluster of differentiation (CD4) count of 82 cells/mm3 (reference range: 518–1,472 cells/mm3), CD4:CD8 of 0.2 (0.9–5.0), and positive blood cultures for H. influenzae. Upon blood culture results, the infectious disease team switched antibiotics to ceftriaxone and vancomycin to cover for H influenzae bacteremia. Due to the low CD4 count of 82 cells/mm3, trimethoprim-sulfamethoxazole was started for Pneumocystis jirovecii pneumonia (PJP) prophylaxis. The patient underwent right elbow arthrotomy, irrigation, and excisional debridement of the synovium and subcutaneous tissue. Postoperatively, he experienced intermittent fevers that responded to acetaminophen and improved over a few days.
During his hospital course, the patient experienced polyarticular joint pain in his right knee and hip with swelling and difficulty weight bearing. This development was concerning for spread of H influenzae to the right hip and/or knee. Magnetic resonance imaging (MRI) of the right hip revealed trace effusion with edema within and surrounding the inferior segment of the visualized right iliopsoas muscle. This MRI finding was concerning for myositis secondary to H influenzae bacteremia. The patient then underwent aspiration of the right knee, which revealed no organisms and a SF WBC count of 3057 cells/mm3. Aspiration of the right hip also revealed an unremarkable SF analysis. Given systemic symptoms, echocardiogram was performed to rule out endocarditis and was negative for vegetations. As pain, swelling, and fever improved, a peripherally inserted central catheter (PICC) line was placed for outpatient IV antibiotics.
After eight days of in-patient evaluation and treatment, the patient’s clinical status and acute febrile illness had improved significantly. Per infectious disease final recommendations, the patient was discharged with a PICC line to receive IV ceftriaxone 2 grams daily for four weeks. He was also instructed to continue trimethoprim-sulfamethoxazole for PJP prophylaxis and to follow up with infectious disease as an outpatient to begin anti-retroviral therapy.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [40, 'years'], 'Cough Absent': True, 'Temperature': [99.9, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 40 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 99.9 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 67.9 = 37.72222 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 0.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 0 + 1 = 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
Hence, the Centor score for the patient is 1."
4442,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-5111284-1,Extracted,"Twenty-eight years old, Female.
At 15:40 on January 16, 2016, the patient visited emergency department and was presented with dyspnea accompanied by visual disturbance.
She had a 3 months history of common cold like symptoms including cough, headache and fatigue. Her Symptoms did not differed depending on the times, day-and-night and working or not. On January 15, she worked as night shift from 21:00 to 9:00. She felt nausea and vomited once on duty. She visited a local hospital and received a blood test during on duty at 22:00. However she heard that she doesn’t have any clinical problems. She came back to work and continued to work. In the morning of January 16, she had dimmed vision shortly before she was dismissed from the work. However she thought that the symptom was caused by fatigue and just went to home. She went to sleep when she arrived home. When she waked up after 5 h, she had difficulty to breathe and chest tightness. Dyspnea was aggravated gradually. At the same time, the appearance of black curtain over the upper and lower side of visual field occurred.
No specific past medical history.
No specific hobby history, no specific drug history, the married state.
One pack × 9 years = 9 pack-years.
Soju, 2 bottles per week.
According to the interview with her and her husband, she had worked in a semi-conductor factory which was located in Bucheon for 8 years. She quitted the job and rested for 6 months. She started working at a small factory which manufactured cell phone parts in Bucheon since September, 2015. She worked to find defected goods placing her own face toward the machine closely. She used air-gun to remove remaining solvent on aluminum plate without proper personal protectors like mask and gloves. She has worked as a shiftwork employee who inspects the finished products.
No specific family history.
In emergency room, initial vital signs were as follows: blood pressure 144/80 mmHg, pulse 78 beats/min, respiration 28 breaths/min, body temperature 36.1 °C, and saturation of O2 100%. Upon auscultation, clear breathing sound without rale and wheezing was heard in both lung fields. Regular heart beat without murmur was heard.
Her electrocardiogram indicated normal sinus rhythm. She received arterial blood gas analysis (ABGA) and pulmonary embolism computed tomography (CT) to evaluate the cause of dyspnea. The initial ABGA (pH 7.131, pCO2 10.3, pO2 132, Base excess -26, Bicarbonate 3.5) and serum electrolyte results (Na+ 138, K+ 4.7, Cl− 106, tCO2 6 mEq/L, anion gap 26) supported that she had increased anion-gap metabolic acidosis with respiratory compensation. In addition, pulmonary embolism CT was negative.
She was immediately treated with sodium bicarbonate. Despite the continuous bicarbonate infusion, metabolic acidosis as well as her physical status was not improved. Rather, her mental status worsened to drowsiness with decreased respiration. Emergency intubation was performed immediately and she was put on a ventilator (Pressure regulated volume control (PRVC) mode: tidal volume 380 ml, respiration 8 breaths/min, fraction of inspired O2 40%, positive end-expiratory pressure 5cmH2O).
Brain magnetic resonance image (MRI) was taken to confirm a problem about respiratory control center. MRI results did not indicate respiratory control center problem. However it showed diffuse restriction in bilateral putamina, bilateral anterior insular cortices, and bilateral medial frontal cortices. It needed to rule out subtle diffusion restriction in bilateral precentral cortices. It also showed peripheral rim enhancement in bilateral putaminal lesions (Fig. , , ). Thereafter, she was admitted in intensive care unit (ICU) under the nephrology department.
On January 17, she still had drowsy mental status and was assisted by mechanical ventilator to breath. Arterial blood gas analysis identified that she still had increased anion-gap metabolic acidosis (pH 7.220, pCO2 16.0, pO2 149, Base excess -20.2, Bicarbonate 6.3, Na+ 143, K+ 3.4, Cl− 113, tCO2 6 mEq/L, anion gap 24). On January 17–18, she received hemodialysis treatment once a day. This hemodialysis allowed her to recover from drowsy mental status as well as metabolic acidosis (pH 7.484, pCO2 32.5, pO2 93.8, Base excess 1.6, Bicarbonate 24.1).
On January 18, the nephrologist requested a consultation with a specialist of occupational and environmental medicine, because he heard from her family that the patient used to smell of liquor after work. The specialist of occupational and environmental medicine interviewed her about her occupational history including information of working process. She did not know that what kinds of materials she used in the factory. However, the specialist of occupational and environmental medicine suspected that this case was a work-related disease and recommended that her urinary and blood samples need to be collected to analyze exposure materials. Her blood and urinary samples were collected on January 19.
On January 19, 2016, she was transferred to general ward. She complained that she had blurred vision and failure to distinguish objects and person. Moreover, she showed binocular pupil dilatation. On January 20, 2016, she was transferred to ophthalmologist who performs a special ophthalmologic test following visual acuity test, visual field test, color vision test, fundus examination and optical coherence tomography (OCT). Her visual acuity was as follows: right (finger count 20 cm), left (finger count 30 cm). Both pupils were slightly dilated with light reflex. Isihara color vision test results were as follows: right (0/24), left (2/24). Moreover, OCT indicated that both optic nerves were edematous. She was diagnosed with toxic optic neuropathy by ophthalmologist and treated with steroid.
On January 21, 2016, the neurologist had an exam about her brain function and confirmed that she spoke abnormally quiet and acted too slow. Specific tests including mini mental state examination (MMSE), electroencephalography (EEG) and nerve conduction velocity (NCV) were taken to confirm neurologic problems. Her MMSE score was in the normal range (28/30). EEG showed diffuse symmetric theta to delta slow activities in the bilateral hemispheres, suggesting moderate to severe diffuse cerebral dysfunction, which is compatible with toxic or metabolic encephalopathy. NCV revealed no specific abnormality. She was diagnosed with toxic encephalopathy by neurologist and treated with choline alfoscerate. On January 25, 2016, she discharged to home with near complete nephrologic recovery. However other conditions such as ophthalmologic and neurologic dysfunction were not fully recovered until March 31, 2016.
Her urinary sample was analyzed to detect a concentration of methyl alcohol after the inspection of her factory confirmed that she had been exposed to 99.9% methyl alcohol in the workplace. Her urinary methyl alcohol concentration was detected as 7.632 mg/L (Biological Exposure Indices (BEI) is 15 mg/L of methyl alcohol in urine at end of shift) although 3 days had passed since she stopped work and she was treated hemodialysis twice.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [28, 'years'], 'Cough Absent': True, 'Temperature': [36.1, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 28 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 36.1 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 0.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 0 + 1 = 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
Hence, the Centor score for the patient is 1."
4443,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-8670145-1,Extracted,"A two and a half years old male with fever was admitted to our hospital on August 2019. He had been diagnosed as pineoblastoma 7 months ago and underwent surgical resection and chemotherapy. He received a ventriculo-peritoneal shunt for obstructive hydrocephalus 4 months ago. He presented with fever (up to 40.4 °C), chills and nausea 2 days before hospital admission. Physical examination did not reveal any significant findings except pharyngeal hyperemia and swollen tonsils. His breath and heart sounds were normal. No redness or swelling occurred at the peripherally inserted central catheter (PICC) site, which had been in indwelled for 6 months, and the catheter was flushed. Computed tomography, urine examination and cerebrospinal fluid were normal. His white blood cell count and C-reaction protein concentration were 17.6 × 109/L (96.3% neutrophils) and 130.5 mg/L (Fig. ). Three sets of blood cultures were collected from peripheral venipuncture at the beginning of the febrile period, then he was treated with cefoperazone/sulbactam. Two of the blood cultures were positive and the pathogens were identified as Stenotrophomonas maltophilia by MALDI-TOF MS (bioMérieux, Marcy-l’Étoile, France). Susceptibility testing showed the organism was susceptible to sulfamethoxazole-trimethoprim, minocycline, ceftazidime, levofloxacin, chloramphenicol, and ticarcillin/clavulanate. The antibiotic treatment was changed to the combination of cefoperazone/sulbactam and sulfamethoxazole–trimethoprim. Then the boy remitted and the body temperature dropped to normal range within 3 days since the treatment was adjusted. The white blood cell counts also returned to normal level and repeated blood cultures (collected from peripheral vein) were negative. However, on the 13th day, his temperature increased again with the highest point of 39.1 °C, and blood specimens were collected from two peripheral veinpuncture sites (left hand and right foot). After 12 h of incubation, gram-negative bacilli were detected from one blood culture, which was collected from right foot. Two types of colonies grew in the blood agar after cultivation, which were identified as S. maltophilia and O. intermedium (strain 045999) by MALDI-TOF MS with 99.9% confidence; however, the Vitek II automated system (bioMérieux) failed to identify strain 045999. Genomic DNA of strain 045999 was prepared using the QIAamp DNA mini kit (Qiagen; Hilden, Germany) and were subjected to whole genome sequencing using the HiSeq X10 Sequencer (Illumina; San Diego, CA, USA). For the whole genome sequence of strain 045999, 5,619,077 reads and 1.69 GB bases were generated (coverage, 400), which were assembled into a 4.9 Mb draft genome contains 82 contigs ≥ 200 bp in length (N50, 454,256 bp) with a 57.71 mol% GC content. ANI between strain 045999 and the type strain LMG 3301T of O. intermedium (ACQA00000000) was determined using the JSpecies []. The ANI value was 97.57%, which was above the cutoff (≥ 95–96% ANI) defining the boundaries of bacterial species [], confirming that the identification was precise. The same organisms were isolated from the other blood culture collected from left hand after 4 days incubation. Antimicrobial susceptibility testing was performed using broth microdilution with the Vitek II automated system (bioMérieux) and interpreted according to the guidelines for other non-Enterobacterales in CLSI M100 (2019). The strain 045999 was susceptible to sulfamethoxazole–trimethoprim, minocycline, tigecycline, cefepime, levofloxacin, meropenem, imipenem (Table ). The strain 045999 formed beige, translucent, shiny and mucoid colonies on blood agar within 24 h of incubation at 35 °C and gram-staining indicated gram-negative, rod-shaped bacteria without spores. The antimicrobial susceptibility of the S. maltophilia was consistent with previous results. According to the results of susceptibility test, the S. maltophilia was susceptible to levofloxacin and ceftazidime, and strain 045999 was also susceptible to sulfamethoxazole–trimethoprim and levofloxacin. Therefore, cefoperazone/sulbactam was replaced with levofloxacin and ceftazidime, and sulfamethoxazole–trimethoprim was continued as before. One week after the treatment, blood cultures were obtained from both peripheral venipuncture and PICC. The blood culture obtained from PICC was positive with the growth of S. maltophilia and O. intermedium whereas the blood obtained from peripheral venipuncture was negative. Meanwhile, the PICC was removed and the culture was negative. Therefore, the therapy mentioned above was continued for 10 days, and the patient discharged after recovery.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [5, 'years'], 'Cough Absent': True, 'Temperature': [40.4, 'degrees celsius'], 'Exudate or swelling on tonsils': True, 'Tender/swollen anterior cervical lymph nodes': False}",4,4,4,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 5 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 40.4 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 2 + 1 = 3.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 3.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 3 + 1 = 4.
Hence, the Centor score for the patient is 4."
4444,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-4546785-1,Extracted,"An eight years old girl has presented to pediatric emergency with a recent history of febrile odynophagie subsequently complicated by a torticollis that has settled 5days after. Clinical examination has found a febrile child at 39°C and a bulging anterior pillar of the right tonsil without rash or conjunctival hyperemia. CT scan was performed and has revealed right peritonsillar and parapharyngeal abscess (). At laboratory tests we found a white blood cell count (WBC) of 14000/mm3 and C - reactive protein (CRP) of 102mg / l. The child underwent a trans-oral drainage of the abscess under general anesthesia and airway protection. The bacteriological sampling objectified mixed unspecific flora sensitive to amoxicillin-clavulanic acid with no evidence of mycobacterium tuberculosis. Antibiotherapy was prescribed based on amoxicilline- clavulanic acid (80mg/kg a day) and aminoglycoside (3mg/kg a day for 5 days). The child was apyretic 48 hours after, and C- reactive protein 72 hours later was at 45 mg/l. Cervical spine traction was not necessary since the torticollis has been resolved after 5 days.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [8, 'years'], 'Temperature': [39.0, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': True, 'Cough Absent': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 8 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 39.0 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
Hence, the Centor score for the patient is 3."
4445,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-1208,Extracted,"A 15-month-old girl is brought to the physician because of a 2-day history of low-grade fever and a painful lesion on her right index finger. She was born at term and has been healthy except for a rash on her upper lip 2 weeks ago, which resolved without treatment. She lives at home with her parents, her 5-year-old brother, and two cats. Her temperature is 38.5°C (101.3°F), pulse is 110/min, respirations are 30/min, and blood pressure is 100/70 mm Hg. A photograph of the right index finger is shown. Physical examination shows tender left epitrochlear lymphadenopathy.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [15, 'months'], 'Temperature': [38.5, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False, 'Cough Absent': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
This means that the patient is 1 year and 3 oldThe patient's temperature is 38.5 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
Hence, the Centor score for the patient is 1."
4446,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-5061,Extracted,"A 22-year-old female college student presents to student health with a chief complaint of fatigue. She states that she has been excessively tired since returning from a hiking trip with her sorority to celebrate their victory over a rival college in a rugby tournament. The patient's past medical history includes depression, anxiety, two prior suicide attempts, and three bouts of an ""STD"" that was treated with ceftriaxone and doxycycline. She has no known drug allergies and is currently taking fluoxetine daily and ibuprofen as needed. On physical exam, she is a young and fatigued woman in no acute distress. Examination of the oropharynx reveals tonsillar exudates and cervical lymphadenopathy. Her temperature is 101 °F, her pulse is 100/minute, and respirations are 17/minute. She is prescribed antibiotics and sent home. She returns one day later stating she feels slightly better after taking a day off from school. On exam you note the findings in Figure A. Her vitals and the remainder of her physical exam are similar to her first visit.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [22, 'years'], 'Temperature': [101.0, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True, 'Cough Absent': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 22 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 101.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 69.0 = 38.33333 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 1 + 1 = 2.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
Hence, the Centor score for the patient is 3."
4447,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-5781,Extracted,"An 11-year-old boy presents to his pediatrician with his mother for a sore throat. His symptoms began approximately a few days ago after attending a birthday party with his friends. His symptoms are accompanied by nausea, vomiting, and a mild headache. He also has mild discomfort in his throat when eating food or drinking water. The patient denies rhinorrhea, conjunctivitis, cough, myalgias, or a rash. His mother said his temperature last night was 101°F (38.3°C). On physical exam, the patient has tender and enlarged anterior cervical lymph nodes. Upon oral inspection, there is pharyngeal inflammation and exudates with petechial lesions on the soft palate.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [11, 'years'], 'Cough Absent': True, 'Temperature': [101.0, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True}",5,5,5,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 11 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 101.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 69.0 = 38.33333 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 2 + 1 = 3.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 3 + 1 = 4.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 4 + 1 = 5.
Hence, the Centor score for the patient is 5."
4448,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-977,Extracted,"A 62-year old female comes to the physician because of vaginal spotting and urinary urgency for the past 4 days. She has had no fever, abdominal pain, or diarrhea. Menopause occurred at 52 years of age. Her last Pap smear 1 year ago was normal. She has hypertension, hypercholesterolemia, and diabetes. Medications include atorvastatin, hydrochlorothiazide, metformin, and aspirin. She is sexually active with her husband. Her temperature is 37°C (98.6°F), pulse is 95/min, respirations are 12/min, and blood pressure is 155/65 mm Hg. Pelvic exam demonstrates a 4 x 3 cm firm, immobile erythematous mass on the right inner vaginal wall.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [62, 'years'], 'Cough Absent': True, 'Temperature': [37.0, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",0,0,0,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 62 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 37.0 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at -1.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score -1 + 1 = 0.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
Hence, the Centor score for the patient is 0."
4449,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-3974040-1,Extracted,"The index case, 36 year old man, lived with his wife, two daughters and his son. He presented to a clinic with fever (37.8°C) and cough on April 16. He felt well after taking compound paracetamol tablets (II), Ibuprofen Tablets and Radix Isatidis on April 17. On April 18, he continued fever and developed pneumonia and was admitted to Zaozhuang City Hospital on April 21. Due to progressive respiratory distress and suspicion of impending acute respiratory distress syndrome, he was transferred to intensive care unit on the day of admission. Bilateral ground-glass opacities and pulmonary lesions were observed on chest radiography (Figure ). The index patient recovered and was discharged on May 16. The positive throat-swab collected on April 21 was confirmed by Chinese Center for disease Control and Prevention on April 23 and virus was A/Shandong/01/2013(H7N9) (SD/01). The antibody titers was 1:80 for the serum sample collected on May 21st compared with 1:5 on April 24 by the micro-neutralization assay [].
The second case was the index patient’s 4 years old son. He began to have fever (37.8°C) and cough on April 14. He was given domiciliary care before April 18. From April 18 to 20, he was treated for common cold at the clinic with his father and recovered. On 21st April, when the index case was hospitalized, the boy separated with him and was under medical observation till April 27 when the fever (38.3°C) and cough started again. After taking antipyretic granules and cephalosporin on the morning, the temperature decreased to 37°C in the afternoon. On 28th morning, he was hospitalized with fever (37.2°C) and was treated with oseltamivir (5 mg). Initial testing identified leucopenia and multiple patchy shadows in the lungs bilaterally. He was discharged on May 6. The throat swab collected on April 23 was negative for H7N9. On April 27, PCR test from throat swabs was H7N9 positive and virus was A/Shandong/0068A/2013(H7N9) (SD/0068A). The antibody titers was 1:20 for the serum sample collected on May 21st compared with 1:5 on April 24 and May 1st.
Table summarized the demographic and clinical characteristics of the two cases.
The index case lived in rural–urban fringe zone in Zaozhuang City. There were several living chicken in the cage and vegetable gardens fertilized with fences in the living community away 10 meters from their apartment. And there were two living poultry slaughter sites in the Mazhuang Farm Market located 500 and 1000 meters from the residential district (Figure ).Interviews with the family members, other close contacts and the first case after recovery constructed the timeline of the two cases onset of ill and treatment (Figure ). From April 6 to 16, the index case always stayed at home except taking his two daughters to school on the morning and picking them up after school every day by car with his wife and his son, while they passed the poultry slaughter sites in the Mazhuang Farm Market. Two days before the onset of illness, the index case had visited a village with several large poultry farms in the other city, but he didn’t enter the poultry farms. At the same time, his son didn’t go to the kindergarten and stayed at home since April because he always got sick and had a cold on April 14.
Furthermore, the index case was not in charge of purchase the foodstuff and his family members didn’t buy poultry from the two living slaughter sites in the Mazhuang Farm market and the other markets. None of the members of his family raised poultry or other animals, none brought live poultry to their home, none had direct contact with sick or dead poultry, and none played with the living chicken in the living community.
After the index case fell ill, his family, including his son had prolonged, close, unprotected contact with him, including eating together. Furthermore his son was the nearest to him when they ate, watched TV and slept till April 20. His son also accompanied the index case while seeking medical care from April 18 to 20. After the index case hospitalization, his son was under the medical observation till April 27 in his apartment and didn’t go out.
11 close contacts of the two H7N9 cases were identified and followed up daily for 7 days. Of these, seven were family members or relatives, two were health care workers and two were index case’s friends. All the throat swabs collected on April 23 were negative for H7N9 virus. Four close contacts of the second case were the same as those of index case, all being family members (the index case’s wife, his two daughters and mother in law), whose specimens collected on April 28 were negative for H7N9. No micro-neutralization antibodies against A (H7N9) virus were detected from paired serum samples of all close contacts. To trance the infectious source, 96 environment samples were collected and only one chopping block swab from Jinniu living poultry market located 10 kilometers away from the living community was positive for H7N9 by rRT-PCR and virus was A/environment/Shandong/01/2013(H7N9) (Ev/SD/01),while the samples from the surrounding areas of the living community including the slaughter sites were negative.
Complete genomic sequencing of SD/01, SD/0068A and Ev/SD/01 were analyzed. The homologous analysis showed that they were 97.92% to 100% identical in all eight gene segments and the two human A (H7N9) viruses were 100% identical in HA, PB1, PA, NS and M genes (Table ). There are only four amino acid substitutions between the two human A (H7N9) viruses, two in the PB2 (E341K and R427Q substitutions), one in NA (L399S substitution) and one in NP (M191V substitution), respectively. The full-length gene sequence number in GISAID are EPI 1447715–1447721 and 1447618 [SD/01], EPI 1457428–1457435 [SD/0068A], EPI1447645-651 and 1447628 [Ev/SD/01].",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [36, 'years'], 'Cough Absent': False, 'Temperature': [37.8, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",0,0,0,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 36 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 37.8 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 0.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 0.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
Hence, the Centor score for the patient is 0."
4450,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-13,Extracted,"An 8-year-old boy is brought to the physician because of a 7-day history of a progressively worsening cough. The cough occurs in spells and consists of around 5–10 coughs in succession. After each spell he takes a deep, noisy breath. He has vomited occasionally following a bout of coughing. He had a runny nose for a week before the cough started. His immunization records are unavailable. He lives in an apartment with his father, mother, and his 2-week-old sister. The mother was given a Tdap vaccination 11 years ago. The father's vaccination records are unavailable. His temperature is 37.8°C (100.0°F). Examination shows no abnormalities. His leukocyte count is 42,000/mm3. Throat swab culture and PCR results are pending.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [8, 'years'], 'Cough Absent': False, 'Temperature': [37.8, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 8 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 37.8 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
Hence, the Centor score for the patient is 1."
4451,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-7704157-1,Extracted,"An eight-year-old boy with no co-morbid illnesses presented with a history of sore throat and swelling of the neck for the past three days. He had been under treatment elsewhere with amoxicillin-clavulanate for presumed bacterial tonsillitis and had been on the antibiotic since the onset of symptoms. His medical history was remarkable for his partially immunized status with missed booster doses of the diphtheria-pertussis-tetanus (DPT) vaccine. On clinical examination, he was febrile with a temperature of 100 F. Examination of the throat showed enlarged tonsils with evidence of a greyish membrane, and neck examination showed cervical lymphadenopathy (Figure ). Abdominal examination revealed hepatosplenomegaly. Workup showed a total leukocyte count of 27,690 (4000-11,000/uL) with 66% lymphocytes and atypical lymphocytes on the peripheral blood smear. His C-reactive protein (CRP) was 12 (<10 mg/dl), erythrocyte sedimentation rate (ESR) was 16 (0-15 mm/h), aspartate aminotransferase (AST) was 415 (0-35 u/L) and alanine aminotransferase (ALT) was 293 (0-35 u/L).
A throat swab was obtained for culture & sensitivity, and testing for diphtheria. Given his partial immunization status and the clinical picture, he was started on anti-diphtheritic serum (80,000 units) along with parenteral crystalline penicillin and oral Clindamycin. Two days later, he developed blood-stained nasal discharge along with hoarseness of voice and stridor. A lateral radiograph of the neck was normal. A mono spot was positive. An EBV panel consisting of IgM EBV-viral capsid antigen (VCA), IgG-VCA, IgG-early antigen, and nuclear antigen was sent on day five of illness, and IgG early antigen and IgM-VCA came positive. EBV quantitative polymerize chain reaction (PCR) was sent on the same day, which showed significant copies (36,275 copies/ml) confirming primary EBV infection.
His throat swab inoculated on sheep blood, MacConkey, and Tellurite blood agar cultures, but all were sterile. A repeat sample for inoculation on Loeffler's agar could only be collected 36 hours after starting crystalline penicillin and this too was sterile, and an Elek test could not be performed. However, PCR was positive for a toxigenic strain of Corynebacterium diphtheriae, confirming the diagnosis of diphtheria.
By day seven of illness, he improved clinically with a decrease in soft tissue swelling, reduction in hoarseness, and disappearance of stridor. However, he continued to spike a fever. In view of the persisting fever spikes despite appropriate antibiotics, the possibility of an abscess or suppurative cervical lymphadenitis was considered. CT scan of the neck was done and it showed considerable enlargement of the tonsils, adenoids, edema of the posterior glottis, and cervical lymphadenopathy (Figures , ). The antibiotics were continued and the fever spikes resolved on day 10 of the illness.
He developed a rash suggestive of IMN on day 10 of the illness (eight days after receiving amoxicillin-clavulanic acid) which started as an erythematous maculopapular over the face, spreading to the trunk and extremities including palms and soles. This rash resolved in the next three days. He made an uneventful recovery and was closely monitored for features of myocarditis in the second week of illness and neuropathy in the later weeks. Contact tracing for diptheria was carried out, but no probable or possible sources were found. All immediate contacts were initiated on chemoprophylaxis and given a dose of the tetanus-diphtheria (Td) vaccine. On follow up, the boy was vaccinated with a booster dose of the Tdap vaccine.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [8, 'years'], 'Cough Absent': True, 'Temperature': [100.0, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True}",4,4,4,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 8 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 100.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 68.0 = 37.77778 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 1.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 1 + 1 = 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 3 + 1 = 4.
Hence, the Centor score for the patient is 4."
4452,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-7234,Extracted,"A 6-year-old boy presents with high fever, sore throat, and cough for the past day. The patient’s mother also says he is complaining of generalized muscle aches and chills. Past medical history is significant for childhood asthma, managed with inhaled mometasone furoate. The patient’s temperature is 39.1°C (102.3°F), pulse is 120/min, and respiratory rate is 20/min. On physical examination, his oropharynx is erythematous with mild swelling of the pharyngeal tonsils. Chest auscultation reveals crepitus over the lung bases bilaterally. There are no signs of respiratory distress. Rapid diagnostic testing for influenza B infection in this patient is positive.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [6, 'years'], 'Cough Absent': False, 'Temperature': [39.1, 'degrees celsius'], 'Exudate or swelling on tonsils': True, 'Tender/swollen anterior cervical lymph nodes': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 6 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 39.1 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
Hence, the Centor score for the patient is 3."
4453,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-5528908-1,Extracted,"A 17-year-old Thai female with human immunodeficiency virus type 1 (HIV-1) infection who had received TIV for 2012-2013 in August 2013 presented at the Bamrasnaradura Infectious Diseases Institute (BIDI) complaining of 2 days of fever, malaise, headache, cough, and sore throat in April 2014. She had been diagnosed with HIV infection confirmed by machine-based assay (ArchiTECT, Abbott, chemiluminescent test), particle agglutination test (Serodia HIV, Fujirebio), and immunochromatography test (Allere Determine or TriLine) at BIDI. Approximately 13 years prior to presentation, she received zidovudine (AZT) plus didanosine (ddI) from 2001 to 2005; AZT, ddI, and efavirenz (EFV) from 2005 to 2007; and has been receiving EFV plus lopinavir/ritonavir in combination (LPV/r) from 2007 to present. Before TIV was given in 2013, she had a CD4 count of 922 cell/µL (31%), plasma HIV-1 RNA <40 copies/mL by quantitative real-time polymerase chain reaction (RT-PCR), a body weight of 85.7 kg, and a height of 165 cm. She received TIV 2011-2012 on August 1, 2012, and TIV 2012-2013 on August 28, 2013. TIV in 2012-2013 included the A/California/7/2009 (H1N1)-derived strain using NYMC X-179A, the A/Victoria/361/2011 (H3N2)-like strain using IVR-65, and the B/Wisconsin/1/2010-like strain using NYMC BX-39 derived from the B/Hubei-Wujiagang/158/2009 strains. At presentation of influenza-like illness symptoms, the physical examination was unremarkable except for a body temperature 38.5°C and body mass index of 31.48 kg/m2. Because of a positive rapid influenza test (Quidel QuickVue Influenza A+B test), the patient was given oseltamivir for 5 days and the clinical symptoms resolved The positive rapid influenza test result was from the BIDI, Nonthaburi, Thailand, with a confirmatory PCR result from the Siriraj Influenza Cooperative Research Center, Department of Microbiology, Faculty of Medicine, Siriraj Hospital, Bangkok, Thailand. The specimen was identified by the amino acid sequence of full hemagglutinin (HA) gene to evaluate the match between the influenza infection and TIV strains.
To perform nucleotide sequencing, total RNA was extracted using a QIAamp viral RNA mini kit (Qiagen) from direct nasal swab specimens of a vaccinated person who had developed a PCR-confirmed influenza illness from the 2009 pandemic virus. The RNA sample was amplified for the complete influenza HA gene, and the amplified product was subjected to nucleotide sequencing. The sequence was edited, aligned, and translated into an amino acid sequence by BioEdit program (version 7.1.11; available at ). The sequence was submitted to the GenBank database with the accession number of KU144591.
shows the percentage of identity match of amino acid sequences of the full HA gene. The specimen of the present case matches TIV strains CA 07 vaccine strain, H1N1 A/Nonthaburi/102/2009, and H1N1 A/Thailand/104/2009 by 97%, 98%, and 98%, respectively. The matches of the specimen for H1N1 2014 isolates are 99% to 100%.
To perform phylogenetic analysis, the HA amino acid sequence of virus from the case was analyzed for its correlation with the sequences from A/California/07/2009 (H1N1) vaccine strain, 2 Thai virus isolates obtained from the first epidemic wave (A/Nonthaburi/102/2009 and A/Thailand/104/2009), and 2 more virus isolates from 2014 (A/Thailand/NMA_1/2014 and A/Thailand/BKK_1/2014) See . The results demonstrate a closer relationship between the causative virus and the circulating strains rather than the vaccine strain closely related to the Thai viruses from the first epidemic wave.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [17, 'years'], 'Cough Absent': True, 'Temperature': [38.5, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",2,2,2,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 17 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 38.5 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 1 + 1 = 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
Hence, the Centor score for the patient is 2."
4454,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-7374812-1,Extracted,"Index case: A 48-year-old UK born male was referred to a Scottish hospital on 31 October 2019 by his family doctor with a 10-day history of sore throat and dysphagia. He had returned from a holiday in Tunisia on 18 October 2019. He had previously presented to his family doctor on two occasions following the onset of symptoms. He had completed his childhood vaccinations (including diphtheria toxoid), and had a diphtheria toxoid booster 15 years previously.
On examination in the hospital, his heart rate was 98 bpm and the temperature was 37.8 °C. He had a thick white pseudomembrane extending over both pharyngeal pillars and a swollen uvula with patchy exudate. Initial blood tests showed a white cell count of 11.2 × 109/l (normal range: 4–11) and C-reactive protein (CRP) of 344 mg/l (normal range: 0–5). Throat and nasopharyngeal swabs were taken. The local Health Protection Team and Public Health England (PHE) were informed, and based on epidemiological and clinical evidence the case was classed as a possible case of diphtheria. He was started on 1.2 g benzylpenicillin IV four times daily, 500 mg clarithromycin IV twice daily and 500 mg metronidazole IV three times daily. He was placed in isolation within 2 h of admission with droplet precautions.
Small numbers of C. diphtheriae were isolated from his throat swab on 3 November 2019. The National Reference Laboratory confirmed the identification of C. diphtheriae and the presence of the diphtheria toxin gene by real-time PCR []. The expression of diphtheria toxin was confirmed using the modified Elek immunoprecipitation test [].
He improved with treatment and his pseudomembrane had largely disappeared by 8 November 2019 (Image 1). Antitoxin was not administered due to his rapid clinical improvement by the time C. diphtheriae was isolated. He was discharged from the Infectious Diseases Unit on 9 November 2019 with 500 mg erythromycin four times daily and 500 mg amoxicillin three times daily. A diphtheria toxoid vaccine booster was also given prior to discharge. Clearance swabs on 22 and 25 November 2019 were negative ().
Second case: The second case was a 45-year-old British female who travelled with the index case to Tunisia. She reported the onset of pharyngitis from 28 October 2019. She also had a full immunisation history, but with no additional boosters. Following confirmation of C. diphtheriae in the index case, nasopharyngeal and throat swabs were taken and she was commenced on prophylactic oral clarithromycin 500 mg twice daily from 3 November 2019.
On 6 November 2019, when C. diphtheriae was isolated, she was urgently assessed at the Infectious Diseases Unit and found to have only a mildly erythematous pharynx. Her CRP was 23 mg/l. She was discharged on the same day with advice to self-isolate and to complete 14 days of clarithromycin 500 mg twice daily. Diphtheria antitoxin (DAT) was not administered. Clearance swabs on 20 and 22 November 2019 were negative ().",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [48, 'years'], 'Temperature': [37.8, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True, 'Cough Absent': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 48 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 37.8 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at -1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at -1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score -1 + 1 = 0.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 0 + 1 = 1.
Hence, the Centor score for the patient is 1."
4455,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-7400,Extracted,"A 44-year-old man presents to a clinic for the evaluation of difficulty swallowing for the past few days. He says that he has noticed progressively worsening chest pain when he attempts to swallow solids or liquids. He works from a home office, has not had any recent sick contacts, and is currently not sexually active. His medical history includes AIDS. His current medications include emtricitabine, rilpivirine, and tenofovir. His temperature is 38.1°C (100.6°F),  pulse is 72/min, respirations are 18/min, and blood pressure is 136/84 mm Hg. A physical examination is notable for a dry mouth with red mucosa and no distinct plaques or patches, and a supple neck with no masses or cervical lymphadenopathy. An esophagogastroduodenoscopy shows small white patches within the esophageal lumen. A biopsy of one of the lesions is performed and the microscopic appearance of the finding is shown below.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [44, 'years'], 'Temperature': [38.1, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False, 'Cough Absent': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 44 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 38.1 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 1.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 1.
Hence, the Centor score for the patient is 1."
4456,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-2769310-1,Extracted,"A 25-year-old Caucasian male with a history of tobacco use, alcohol abuse, and gastroesophageal reflux disorder (GERD) was admitted to our hospital with a chief complaint of upper airway obstruction. He was initially seen one week prior to admission by his primary care physician for a complaint of back pain. At this visit, the patient reported recent contact with a co-worker who was recovering from mononucleosis and thus a blood smear was performed which revealed atypical lymphocytes. A subsequent Monospot test was positive for heterophile antibodies. Further blood tests for viral hepatitis were negative. He first began developing symptoms four days after diagnosis, which included fevers, nightsweats, diffuse body aches, and a sore throat. These continued to worsen in the following two days, so the patient sought attention at the urgent care clinic. Workup at this time for superimposed streptococcus infection was negative. The patient returned home without treatment. Symptoms worsened overnight including difficulty swallowing and handling oral secretions as well as fevers to 104°F. Two days later, the patient was short of breath with continued fevers, throat pain, and difficulty swallowing leading to one episode of blood-tinged emesis.
Medical history included GERD, anxiety, and moderate tobacco and alcohol use. He was on no medications. His family history was significant for epilepsy and hyperthyroidism. He was a student and worked as a manager of a restaurant. He drank five beers 3-4 times per week, smoked a ½ pack per day, and denied illicit drug use. The patient had no known drug allergies.
On physical exam, he was alert and awake with a flushed face and spoke with a hyponasal or raspy voice. This muffled vocal characterization is referred to as “hot potato voice” by some physicians []. He was in no apparent respiratory distress. Height was 72 inches and weight was 191 pounds. His vitals were T 99.3°F, P 106, R 24, BP 133/88, 96% on room air. Head and neck exam revealed tender cervical lymphadenopathy with erythematous, swollen tonsils that were in apposition with minimal white exudates. There was no evidence of inflammation in the internal auditory canal, sclera were non-injected, no stridor, no trismus, and the trachea was midline. Lung exam was clear to auscultation bilaterally. Heart sounds were regular without murmurs or clicks. The abdomen was soft, non-tender, and without hepatosplenomegaly. Extremities were without edema, clubbing, or cyanosis. Neurological exam revealed no focal deficits. Laboratory values were remarkable for a white blood cell count of 20 K/cmm with an absolute monocytosis of 2.97 K/cmm. Liver enzymes were elevated with an alkaline phosphatase of 270 U/L, AST 136 U/L, ALT 275 U/L.
In the emergency department, CT scan of the head and neck showed tonsillar swelling with lymphadenopathy ( & ). Laryngoscopy confirmed these findings and revealed no other causes of obstruction. He was treated with 10 mg intravenous dexamethasone and 3 g ampicillin/sulbactam with rapid improvement. The patient was then admitted to the medical service where steroid treatments were continued overnight and he was discharged the following day on no medications.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [25, 'years'], 'Temperature': [99.3, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True, 'Cough Absent': False}",2,2,2,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 25 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 99.3 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 67.3 = 37.38889 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 0.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 0.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 0 + 1 = 1.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 1 + 1 = 2.
Hence, the Centor score for the patient is 2."
4457,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-5965421-1,Extracted,"A 13-year-old African-American female presented to our pediatric emergency department (ED) with fever for eight days, as high as 103°F at home. Her fevers responded to antipyretics but would return without an identifiable pattern, often within a few hours, sometimes longer; but the fever would always return by the next day. She also complained of odynophagia, headache, fatigue, and dizziness. The patient had been seen in another ED two days prior for these symptoms. She had been diagnosed as having streptococcal pharyngitis because of a positive rapid test and was prescribed amoxicillin. She came into our ED because her symptoms had worsened despite compliance with her antibiotics. Specifically, the patient had developed gradually worsening joint pains in her ankles, knees and shoulders. Her mother noted the patient’s joints had become swollen that day and she had developed a facial rash. The patient denied any nausea, vomiting, diarrhea, abdominal pain, or respiratory symptoms such as coughing or wheezing.
Her past medical history included seizures of an unknown etiology occurring between birth and three years of age. She saw her pediatrician regularly. While she lacked a current influenza vaccination, all of her other immunizations were up to date. Her only medication was the amoxicillin she had been prescribed two days prior to presentation. She had no known drug allergies. Her family medical history was significant for a sibling with idiopathic pancreatitis and several family members with type 2 diabetes and hypertension. The patient had not travelled recently, she was post-menarchal, and was not sexually active. Her last menstrual period was two weeks prior to presentation. When questioned without family present, the patient denied any form of abuse.
At the time of her ED evaluation, the patient was afebrile (37.2°C) with a heart rate of 80 beats/minute, respiratory rate of 20 breaths/minute, blood pressure of 118/73 mmHg, and she had an oxygen saturation of 99% on room air. She was 5 feet 1 inch tall (1.35m) and weighed 90 pounds (41kg), giving her a body mass index of 17. This placed her at the 25th percentile for height and weight for her age.
Physical examination revealed a well-developed and nourished adolescent female in no acute distress who appeared fatigued. Her head was normocephalic and atraumatic with bilateral periorbital edema. Her conjunctiva and sclera were normal. Her mucous membranes were moist and she had no nasal discharge. The posterior oropharynx was erythematous without exudates. Her tongue was normal and no intra-oral lesions were seen. Her neck was supple with bilateral cervical lymphadenopathy, the largest node measuring 1.5cm in length. Her lungs were clear to auscultation bilaterally. Her heart was regular without murmurs, rubs or gallop. Her abdomen was soft and non-tender without organomegaly.
She had mild joint pain with passive movement of her extremities, but she had full range of motion except for pain-limited plantar and dorsiflexion of her ankles. There was bilateral pedal edema. Examination of her skin revealed an erythematous midface rash with nasolabial and perioral sparing. No rashes were present elsewhere. Her cranial nerves were intact. The patient had full motor strength throughout all of her extremities. Her coordination, balance, speech, and comprehension were all normal.
Her initial laboratory results are shown in and . Based on the suspicion of the clinician, an additional laboratory test was sent that confirmed the diagnosis.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [13, 'years'], 'Cough Absent': True, 'Temperature': [37.2, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 13 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 37.2 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 1.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 1 + 1 = 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 3.
Hence, the Centor score for the patient is 3."
4458,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-4776,Extracted,"A 5-year-old male is brought to the pediatrician with complaints of a painful mouth/gums, and vesicular lesions on the lips and buccal mucosa for the past 4 days. The patient has not been able to eat or drink due to the pain and has been irritable. The patient also reports muscle aches. His vital signs are as follows: T 39.1, HR 110, BP 90/62, RR 18, SpO2 99%. Physical examination is significant for vesicular lesions noted on the tongue, gingiva, and lips, with some vesicles having ruptured and ulcerated, as well as palpable cervical and submandibular lymphadenopathy.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [5, 'years'], 'Temperature': [39.1, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Cough Absent': False, 'Exudate or swelling on tonsils': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 5 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 39.1 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 1 + 1 = 2.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 3.
Hence, the Centor score for the patient is 3."
4459,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-6230353-1,Extracted,"A 58-year-old female smoker with a history of alcohol abuse presented to the ED at a community hospital with a chief complaint of shortness of breath, sore throat, and fever. She reported progressively worsening sore throat and odynophagia over the preceding two days as well as voice change and shortness of breath on the day of presentation to the ED. The patient admitted to fever, chills, diaphoresis, cough productive of phlegm, pain in the sides of her neck, and nausea. She denied sick contacts or recent travel.
On arrival to the ED, the patient’s vital signs were temperature 38.3° Celsius; pulse rate 130 beats per minute; blood pressure 118/72 millimeters of mercury; respiratory rate 20 breaths per minute; and pulse oximetry 99% on room air. The patient was acutely ill appearing with diaphoresis. She was able to phonate in complete sentences. She had full, active range of motion of her neck. On examination of the posterior oropharynx, there was no appreciable edema or peritonsillar abscess noted. She did have a small amount of frothy yellow phlegm in her posterior oropharynx and appeared unable to swallow these secretions. Auscultation of her lungs demonstrated diffuse rhonchi and slight expiratory wheeze.
Sepsis was suspected on arrival, and the ED sepsis protocol was initiated with a suspected source of community-acquired pneumonia. The sepsis protocol included administration of intravenous (IV) fluids at 30 milliliters (mL) per kilogram of body weight and broad-spectrum antibiotics. The patient was given two grams of IV ceftriaxone and 500 milligrams (mg) of IV azithromycin as well as 10 mg of IV dexamethasone. We ordered an albuterol and ipratropium nebulizer treatment as the patient was suspected to have undiagnosed, underlying chronic obstructive pulmonary disease given her smoking status and lung examination.
One hour after initial ED evaluation, the patient was receiving the nebulized breathing treatment when she was found to be sitting up on the side of her stretcher in acute respiratory distress with an oxygen saturation in the seventies. She was anxious appearing and unable to phonate. The patient was immediately transferred to a nearby resuscitation bay. She was placed on 15 L of oxygen by nasal cannula as well as on a non-rebreather mask. Materials for an emergent surgical airway were readied at bedside.
Staff included two nurses, a respiratory therapist, an emergency medicine (EM) attending physician, and two EM resident physicians. Rapid sequence intubation was initially attempted by the EM resident using video laryngoscopy. Upon visualization, we noted significant edema and purulence involving the epiglottis, arytenoids, and adjacent soft tissues causing severe deformity of normal anatomy, which obscured visualization of the glottis. There was pooling of secretions in the supraglottic region as well. The supraglottic tissues were bulbous and friable with diffuse exudates and active bleeding. While initial intubation attempts using the video laryngoscope and a bougie were unsuccessful, the attending physician was able to successfully secure the airway with an endotracheal tube placed with over-the-bougie technique. Fortunately, we were able to achieve adequate ventilation via bag-valve-mask between direct laryngoscopy attempts preventing need for a surgical airway.
Upon review of the laboratory results, the patient was noted to have a white blood cell count of 18,300 cells per microliter and an initial point of care lactic acid of 5.51 millimoles per liter (of note, value was obtained prior to treatment with albuterol). Group A streptococcal testing of the oropharynx was positive. Her troponin I level was elevated at 0.068 nanograms per mL and felt to be secondary to sepsis. Computed tomography (CT) of the chest with IV contrast demonstrated bilateral patchy consolidative changes in the lower lobes consistent with pneumonia, a thickened distal esophagus with retained fluid, multiple wedge-shaped hypodensities in the kidneys consistent with renal infarcts, and hepatic steatosis. A CT of the neck with IV contrast demonstrated enlargement of the tonsils with adjacent edema and narrowing of the airway without definite fluid collection. Following intubation the patient became hypotensive, necessitating placement of a central venous catheter and the use of norepinephrine for continued management of septic shock. The patient was admitted to the intensive care unit.
The patient was extubated the following day, and she was transferred to another facility two days following admission for otolaryngology evaluation. Upon arrival to the second hospital, the patient was evaluated by an otolaryngologist who performed flexible laryngoscopy, which demonstrated epiglottitis with a mottled epiglottis and fibrinous exudate that appeared to be consistent with early resolution of epiglottitis. The patient was continued on IV steroids as well as IV broad-spectrum antibiotics. She continued to require oxygen supplementation to maintain an oxygen saturation above 88%. Respiratory cultures and blood cultures were positive for Streptococcus pyogenes. The patient was discharged from the hospital 15 days following her initial presentation to the ED, the completion of the course of IV antibiotics and the resolution of hypoxia.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [58, 'years'], 'Cough Absent': False, 'Temperature': [38.3, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': True}",2,2,2,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 58 years old. Because the age is greater than 44 years, we decrease the score by one point, making the score 0 - 1 = -1.
The patient's temperature is 38.3 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score -1 + 1 = 0.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 0.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 0 + 1 = 1.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 1 + 1 = 2.
Hence, the Centor score for the patient is 2."
4460,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-6009,Extracted,"A 23-year-old man presents to student health for a cough. The patient states he has paroxysms of coughing followed by gasping for air. The patient is up to date on his vaccinations and is generally healthy. He states he has felt more stressed lately secondary to exams. His temperature is 101.0°F (38.3°C), blood pressure is 125/65 mmHg, pulse is 105/min, respirations are 14/min, and oxygen saturation is 98% on room air. Laboratory values are notable for the findings below.

Hemoglobin: 12 g/dL
Hematocrit: 36%
Leukocyte count: 13,500/mm^3 with a lymphocytosis
Platelet count: 197,000/mm^3

Physical exam is notable for clear breath sounds bilaterally.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [23, 'years'], 'Cough Absent': True, 'Temperature': [101.0, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",2,2,2,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 23 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 101.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 69.0 = 38.33333 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 1 + 1 = 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
Hence, the Centor score for the patient is 2."
4461,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-9267,Extracted,"A 19-year-old woman presents to the family medicine clinic for evaluation of a sore throat. The patient states that she does not have a runny nose, cough or itchy throat. The patient has no past medical history but she did have an appendectomy when she was 8 years old. She takes acetaminophen when she gets a headache and does not smoke cigarettes. Her vitals include: blood pressure 112/68 mm Hg, heart rate 72/min, respiratory rate 10/min and temperature 39.2°C (102.6°F). Physical examination reveals a patient who is uncomfortable but alert and oriented. Upon palpation, the physician notices swollen anterior cervical nodes. Inspection of the pharynx and tonsils does not reveal any erythema or exudate.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [19, 'years'], 'Cough Absent': True, 'Temperature': [39.2, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': True, 'Exudate or swelling on tonsils': False}",3,3,3,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 19 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 39.2 degrees celsius. The patient's temperature is greater than 38 degrees Celsius, and so we add one point to the score, making the current score 0 + 1 = 1.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 1 + 1 = 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as present for the patient. Hence, we increase the score by 1, making the current score 2 + 1 = 3.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 3.
Hence, the Centor score for the patient is 3."
4462,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,pmc-7700053-1,Extracted,"The patient was a 35-year-old Indian male with no significant medical history. He was born in Tamil Nadu, India, and emigrated to Singapore six years prior to presentation. He returns to India annually to visit friends and relatives, both in small towns and villages in rural areas with farms housing farm animals. He drank well water and ate local food during these trips back to India. He had no known personal or contact history of tuberculosis.
He presented to medical care after a first-onset seizure which was witnessed by his wife. The seizure was described as jerking movements of all four limbs, associated with uprolling of eyeballs, and a transient loss of consciousness lasting ten minutes. There were no preictal symptoms. Postictally, he was drowsy for another ten minutes and was unable to recall the events upon regaining consciousness. Prior to this seizure, he was generally well and did not report any constitutional symptoms such as fever, night sweats, weight loss, or anorexia.
On examination, he had a low-grade temperature of 37.8 degrees centigrade. Blood pressure, heart rate, and oxygen saturation were normal. Neurologic examination did not reveal any focal neurologic deficits, and there were no localising signs of infection. Laboratory investigations were significant for leukocytosis with a white blood cell count of 18.4 × 109/L. There was no peripheral eosinophilia. Renal and liver function tests were normal, as were routine biochemistry and serum electrolytes. Noncontrasted computed tomography scan of the brain revealed an ill-defined eight-millimetre hypodense lesion with a hyperdense rim in the left basal temporal region, with mild surrounding vasogenic edema. MRI of the brain further delineated this as a solitary ring-enhancing lesion measuring 1.2 by 1 centimetre (). Postcontrast images showed thick smooth peripheral enhancement, but no clearly-defined scolex or mural nodule consistent with a typical viable cyst of neurocysticercosis. Skull base artefacts limited assessment of the contents on diffusion-weighted images.
Human immunodeficiency virus serology was nonreactive. Two sets of blood cultures were negative, as was serum Cryptococcal antigen. Three sets of stool microscopy for ova, cyst, and parasites did not pick up any parasites. As there was no available serologic test for cysticercosis at our centre, a serum sample was sent to an overseas reference centre for serologic testing with an antibody-detecting ELISA-based assay.
After discussion with the managing neurosurgical team, the patient opted for brain biopsy for definitive diagnosis, in view of the broad range of differential diagnoses based on the neuroradiologic features. A left minicraniotomy was performed and identified a slightly hardened pale white to yellow lesion, with a milky white exudate upon breaching the lesion capsule. The entire cyst was excised and sent for histology and microbiologic evaluation.
Histology demonstrated granulomatous inflammation featuring aggregates of epithelioid histiocytes and multinucleated giant cells lining the fibrous cyst wall, accompanied by a mixed inflammatory infiltrate and necrosis. Features characteristic of a cysticercus were absent, and no viable larva was identified (). No fungi or acid-fast bacilli were found on Gomori methenamine silver (GMS) and Ziehl–Neelsen histochemical stains, respectively, and no Toxoplasma organisms were identified on immunohistochemical staining.
Microbiologic testing did not identify causative organisms on Gram stain, aerobic and anaerobic culture, fungal smear, acid-fast smear, and GeneXpert MTB/RIF assay (Cepheid Inc, Sunnyvale, CA, USA).
In view of nonspecific histologic and radiologic features, no definite diagnosis was made at this point. As histology showed granulomatous inflammation, and tuberculosis is endemic in the region, empiric combination ant-tuberculous therapy and a tapering corticosteroid regimen were initiated after discussion and shared decision-making between the patient and medical team while awaiting further diagnostic tests.
While awaiting ELISA serologic assay results, which later returned positive for cysticercosis, residual brain tissue was sent to the National Public Health Laboratory, a tertiary reference laboratory, for further molecular diagnostic testing. 25 milligrams of brain tissue was minced on dry-ice, lyzed in ATL buffer with proteinase K, and DNA was extracted using QIAmp® DNA Mini Kit (Qiagen, Hilden, Germany) according to the manufacturer's instructions. A Taenia solium-specific PCR targeting the pTsol9 repeat element based on a previous paper by Almeida and colleagues [] and a pan-Cestoda PCR targeting a fragment of the mitochondrial ribosomal RNA (16S rRNA – 12S rRNA) genes based on a paper by Le and colleagues [] were attempted. Capillary electrophoresis on QIAxcel® Advanced System (Qiagen, Hilden, Germany) equipped with DNA Fast Analysis Kit displayed multiple bands of expected sizes (120 bp, 280 bp, and 440 bp), corresponding to the amplification of 1, 2, and 3 repeat unit(s) of the pTsol9 element, respectively () and a single band of 810 bp for the 16S rRNA-12S rRNA genes. Purification, bidirectional Sanger sequencing, alignment, and cross-checking of the sequences were performed as previously described [] for the 16S rRNA-12S rRNA PCR products. A consensus fragment of the 16S rRNA-12S rRNA genes (808 bp) was obtained, compared by Basic Local Alignment Search Tool (BLAST) against GenBank (NCBI, Bethesda, MD, USA), showed 99.6% similarity (805/808) with sequence [AB086256], and thus ascertained that detected DNA was from T. solium. The sequence has been deposited in GenBank under the accession number (MT772182).
Upon molecular confirmation of neurocysticercosis, antituberculous therapy was stopped. The patient completed 14 days of oral albendazole together with a rapid taper of corticosteroids and has remained well since on subsequent follow-up.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [35, 'years'], 'Exudate or swelling on tonsils': True, 'Temperature': [37.8, 'degrees celsius'], 'Tender/swollen anterior cervical lymph nodes': False, 'Cough Absent': False}",1,1,1,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 35 years old. Because the age is in between 15 and 44 years, the score does not change, keeping the score at 0.
The patient's temperature is 37.8 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 0.
The patient note report reports that the patient is coughing and so we do not change the score, keeping the current score at 0.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 0.
The patient note reports 'exudate or swelling on tonsils' as present for the patient. Hence, we increase the score by 1, making the current score 0 + 1 = 1.
Hence, the Centor score for the patient is 1."
4463,20,Centor Score (Modified/McIsaac) for Strep Pharyngitis,severity,integer,usmle-6112,Extracted,"A 7-year-old boy is brought to his pediatrician's office by his mother with a new onset rash. His mother says that the rash appeared suddenly yesterday. He is otherwise well. His medical history is unremarkable except for a recent upper respiratory infection that resolved without intervention two weeks ago. His temperature is 98.2°F (36.8°C), blood pressure is 110/74 mmHg, pulse is 84/min, and respirations are 18/min. Physical exam shows a well appearing child with a diffuse petechial rash.",What is the patient's Centor Score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [7, 'years'], 'Cough Absent': True, 'Temperature': [98.2, 'degrees fahrenheit'], 'Tender/swollen anterior cervical lymph nodes': False, 'Exudate or swelling on tonsils': False}",2,2,2,"The criteria listed in the Centor Score formula are listed below:

1. Age: 3-14 years = +1 point, 15-44 years = 0 points, ≥45 years = -1 point
2. Exudate or swelling on tonsils: No = 0 points, Yes = +1 point
3. Tender/swollen anterior cervical lymph nodes: No = 0 points, Yes = +1 point
4. Temperature >38°C (100.4°F): No = 0 points, Yes = +1 point
5. Cough: Cough present = 0 points, Cough absent = +1 point

The Centor score is calculated by summing the points for each criterion.
    
The current Centor score is 0.
The patient is 7 years old. Because the age is between 3 and 14 years, we add one point to the score making current score 0 + 1 = 1.
The patient's temperature is 98.2 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 66.2 = 36.77778 degrees celsius. The patient's temperature is less than or equal to 38 degrees Celsius, and so we do not make any changes to the score, keeping the score at 1.
The patient note reports an absence of cough and so we add 1 point to the score, making the current score 1 + 1 = 2.
The patient note reports 'tender/swollen anterior cervical lymph nodes' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
The patient note reports 'exudate or swelling on tonsils' as absent for the patient. Hence, we do not change the score, keeping the current score at 2.
Hence, the Centor score for the patient is 2."
4464,22,Maintenance Fluids Calculations,physical,decimal,pmc-8443410-1,Extracted,"A 66-year-old man (body height, 168 cm; body weight, 88.5 kg) experienced dyspnea, a sensation of chest tightness, and back pain for a few days before he was brought to our hospital on an emergency basis. His symptoms became aggravated suddenly as he was about to get off a taxi on his way home from work. He presented with a history of close contact with a coworker with COVID-19 and was waiting for instructions from a public health center.
In the ambulance, the following conditions were documented: Glasgow Coma Scale score, E4V5M6; heart rate, 80/min and irregular; blood pressure, 100/60 mmHg; body temperature, 38.4ºC; oxygen saturation, 98% (O2 delivered with reservoir mask at a rate of 15 L/min). On admission, his white blood cell count was 22,300/µL; hemoglobin, 14.7 g/dL; platelet count, 35 × 104/µL; creatinine level, 2.23 mg/dL; creatine kinase level, 2582 IU/L; creatine kinase myocardial band level, 164 ng/mL; low-density lipoprotein cholesterol level, 97 mg/dL; high-density-lipoprotein cholesterol level, 19 mg/dL; triglyceride level, 173 mg/dL; hemoglobin A1c level, 7.9%; C-reactive protein level, 13.8 mg/dL; troponin T level, 9.640 ng/mL; N-terminal pro-brain natriuretic peptide level, 11753 pg/mL; procalcitonin level, 0.62 ng/mL; d-dimer level, 16.34 µg/mL; and soluble fibrin level, 113.1 µg/mL. An electrocardiogram showed atrial fibrillation; ST-elevation in II, III, aVF, and V2–V6 leads; and ST depression in aVR leads (Figure ). Echocardiography revealed severe hypokinesis extending from the anterior wall to the apex and the inferior wall in left ventricle, with an approximate ejection fraction of 20%. We diagnosed STEMI and decided to perform emergency coronary angiography (CAG). A chest radiograph showed infiltrative shadows in both lungs and tracheal intubation was performed in the emergency outpatient unit (Figure ). Continuous infusion of noradrenaline (0.1 μg/kg/min) was started because his systolic blood pressure dropped below 80 mmHg. After heparin (5,000 U) was administered intravenously, the patient was transferred to the cardiac catheterization room.
CAG was performed by cardiologists, emergency physicians, clinical engineers, nurses, and radiological technologists who donned appropriate personal protective equipment before entering the room. CAG revealed total occlusion of the middle of the right coronary artery (RCA) and left anterior descending artery (LAD; Figure ). After a loading dose of dual antiplatelet therapy (aspirin, 162 mg; clopidogrel, 300 mg), an intra-aortic balloon pump catheter was inserted, and a 7-Fr guiding catheter was inserted into the left coronary artery. We removed white material, which did not at a first glance appear to be a typical thrombus, with an aspiration catheter, but blood flow did not improve. The onset-to-device time and door-to-device time were 116 and 84 minutes, respectively. Subsequent intravascular ultrasonography (IVUS) revealed several structures, which were thought to be thrombi; therefore, we performed plain old balloon angioplasty (Figure ). After the balloon was expanded, blood flow improved slightly in the LAD but not distally. Next, we placed an everolimus-eluting stent (4.0 × 38 mm) in the middle of the LAD, but peripheral blood flow was still not observed. Repeated IVUS revealed severe stenosis caused by plaque with thrombi. An additional balloon was inflated at the distal site, and a cutting balloon was also used. Another everolimus-eluting stent (2.25 × 38 mm) was placed at the distal site, but no blood flow improvements were seen angiographically.
We moved a double-lumen catheter to the distal LAD and performed CAG from the distal LAD, which revealed retrograde blood flow up to the middle of the LAD and collateral circulation from the septal branch to the RCA. Repeated IVUS examination revealed thrombi and plaque at the distal end of the stent and no intrastent blood flow (Figure ). Then, we tried to perform PCI for the total occlusion of RCA, but it was unsuccessful. At this point, 7 hours passed since the patient entered the cardiac catheterization room, and so we finished the procedure. The levels of activated clotting time during PCI were maintained at 280–310 seconds. After PCI, pathological examination proved the aspirated white material was white thrombi. Chest computed tomography performed after PCI showed ground-glass opacities distributed unevenly in both the lungs, as well as left-sided pleural effusion (Figure ). After the patient was transferred to the intensive care unit, he showed pulseless electrical activity, and cardiopulmonary resuscitation (CPR) was initiated. Return of spontaneous circulation was achieved with 1 mg of epinephrine and one cycle of CPR. Veno-arterial extracorporeal membrane oxygenation was considered, but his family decided against it. The blood pressure was maintained through the continuous administration of noradrenaline, dobutamine, and adrenaline. His nasopharyngeal swab was tested with polymerase chain reaction for SARS-CoV-2, and COVID-19-related pneumonia was diagnosed. Remdesivir treatment was initiated at a dose of 200 mg/day on the 5th day of hospitalization and continued at 100 mg/day. Because of the possibility of concomitant bacterial pneumonia, ampicillin sodium/sulbactam sodium (9 g/day) was also administered. However, the patient's oxygenation level worsened, and he died on the 7th day. It was difficult to confirm a main cause of death because we were not permitted to dissect patients due to COVID-19. We assumed that he had died from both cardiogenic shock due to myocardial infarction and septic shock due to covid-19 infection.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [88.5, 'kg']}",128.5,122.075,134.925,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 88.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (88.5 kg - 20 kg) = 128.5 mL/hr.
Hence, the patient's fluid maintenance is 128.5 mL/hr."
4465,22,Maintenance Fluids Calculations,physical,decimal,pmc-1403776-1,Extracted,"A 20-years-old Caucasian male, presented to a district hospital with acute right lower quadrant pain from six hours before. Physical examination revealed abdominal pain, localized right lower quadrant abdominal tenderness, body temperature slightly elevated (37.7°C), blood pressure 120/90 mmHg and heart rate 110/min. Blood tests showed leukocyte count at 12600/μL, the differential white account showing 75% neutrophils and hematocrit 35.9%. Abdominal and chest radiographs were normal. The primary diagnosis was acute appendicitis and appendectomy was decided. Entering the peritoneal cavity from a McBurney incision, the surgeon found large amount of blood and the surgery was transformed to exploratory laparotomy through a midline incision. The findings were enormous hepatomegaly and bleeding due to spontaneous rupture of the IV lobe of the liver. Active bleeding was managed with direct suture of identifiable vessels and absorbable gauze mesh. Postoperative course was uneventful, except of a continuous elevated body temperature (up to 38.5°C). The patient, five days after surgery, was referred to us in order to undergo further examinations for the nature of the liver abnormality. His medical history was unremarkable. He was previously in good health. His family and past history were not contributory. The patient weighted 65 Kg with 1.75 m height. He was in his right senses and well nourished. Yellow skin, icteric sclera, spider naevi and palmar erythema were not founded. Cardiopulmonary examination was unremarkable. Chest radiograph revealed no pulmonary pathology. The abdomen was swollen with the liver palpable. Laboratory tests showed liver function tests normal (before the initial surgery however, after the surgery SGOT, SGPT, LDH were altered three times the normal range) hepatitis markers of HAV, HBV, HCV, and HIV were negative and alpha-fetoprotein (AFP) was 35 ng/ml. The patient underwent computed tomography (CT) of the abdomen that showed hepatomegaly and a large hypodense lesion of the liver with multicystic appearance with septations and solid portions (Figure ). Magnetic Resonance Imaging (MRI) in T2-weighted and Short Time Inversion Recovery (STIR) sequences revealing hyperdense areas with intermixed hypodense septa (Figure ), and a thrombus in the inferior vena cava (Figure ). The differential diagnosis by the CT and MRI findings was giant hemangioma or cystic malignant lesion. Due to the size of the lesion and the previous history of spontaneous bleeding, it was decided that the patient must undergo surgery. In order to prevent pulmonary embolism, an inferior vena cava filter was inserted and fixated just below the renal veins. Two days later the patient underwent surgery. Primarily, thrombectomy and reconstruction of the inferior vena cava with removal of the filter was performed, followed by hepatectomy of I–IV and VIII lobe of the liver. Intraoperative biopsy demonstrated malignancy or sarcoma of the liver. Frozen section on the remaining liver was performed and showed normal liver tissue. The patient after surgery presented with life threatening bleeding and protean coagulation abnormalities, symptoms of disseminated intravascular coagulation, due to massive blood transfusion. The patient died the second postoperative day due to uncontrolled bleeding caused of the developing of disseminated intravascular coagulation (DIC). Pathologic review of the specimen revealed a 1580 gm left and part of right hepatic lobe, with a 30 × 14 × 9 cm tumor mass and the histological examination showed malignant sarcomatous tissue with spares giant neoplastic cells (head arrow) and residual hepatocytes (arrow) suggestive of undifferentiated embryonal sarcoma (Figure ). Sarcomatous tissue with severe atypia of the neoplastic cells and focal presence of giant cells partially with myoblastic characteristics was also present (Figure ). Residual hepatocytes stained positive in immunohistochemical stain for cytoceratinin 8–18, and showed infiltration by the sarcomatous tissue (DAB technique).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [65.0, 'kg']}",105,99.75,110.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 65.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (65.0 kg - 20 kg) = 105.0 mL/hr.
Hence, the patient's fluid maintenance is 105.0 mL/hr."
4466,22,Maintenance Fluids Calculations,physical,decimal,pmc-2848065-1,Extracted,"A 42-year-old Caucasian Finnish woman was scheduled for laparoscopic cholecystectomy due to typical symptoms and radiological findings of gallstones. She was obese (89 kg, BMI = 33), even though she had managed to lose weight by 20 kg six months prior to presentation. She was using sibutramine and oral contraceptives as regular medication.
Surgery was uneventful, but on the second postoperative day, the general state of our patient started to deteriorate, resulting in anuria and difficulty of breathing, admission into the intensive care unit (ICU), endotracheal intubation, and mechanical ventilation. Endoscopic retrograde cholangiopancreatography (ERCP) was performed upon ICU admission because of suspected biliary tract leakage. However, no signs of leakage were observed. Computed tomography (CT) examination revealed fluid around her liver, while her pancreas could not be visualized. Her plasma amylase concentration was elevated, thus confirming the diagnosis of pancreatitis.
Due to decreased renal function, she was commenced on continuous hemodiafiltration therapy on the third day and continued until the 10th postoperative day. Propofol infusion for sedation, supplemented with intravenous oxycodone boluses, was started as part of our hospital's standard therapy in order to facilitate mechanical ventilation and other treatment procedures. Propofol sedation was continued until the 36th postoperative day. Upon the decision of weaning, her attending physician decided to add dexmedetomidine infusion into the sedation regimen 17 days after her surgery.
Weaning was not successful, and tracheostomy was performed on the 18th postoperative day. On the 19th postoperative day, esophagogastroduodenoscopy and explorative laparotomy were performed because the general condition of our patient again started to deteriorate. Hemorrhagic pancreatitis with severe inflammation of her abdominal cavity was discovered. This deterioration prevented further weaning. Our aim was to stop propofol infusion after starting her on dexmedetomidine, but in order to achieve the desired level of sedation (light to moderate, Sedation-Agitation Scale (SAS) levels 3 to 4 []), propofol infusion had to be continued despite the already high dose of dexmedetomidine she was receiving.
Our patient later required yet another laparotomy because of elevated abdominal pressure. This surgery did not reveal any additional findings, but this time her abdominal wall had to be left open, and sedation had to be continued. Vacuum-assisted closure therapy was established on the 22nd and continued until the 34th postoperative day. Weaning was started again on the 36th postoperative day. Clonidine infusion was started on the 40th postoperative day, while the dexmedetomidine infusion was discontinued on the following day, on the 24th day of its administration.
Our patient's abdominal wall was finally closed on the 47th day, and the clonidine infusion was stopped on the 51st postoperative day. The tracheostomy cannula was removed on the 54th day and she was admitted to a surgical ward on the 55th postoperative day for further recovery.
During dexmedetomidine sedation, her plasma albumin level was low (8.4 g/L to 11.6 g/L) and her creatinine level was slightly elevated (23 μmol/L to 126 μmol/L). Meanwhile, her bilirubin level and international normalized ratio (INR) were both normal at 5 μmol/L to 16 μmol/L and 1.1 to 1.4, respectively.
At 14 months later, her recovery is still incomplete. Already in the ICU she complained that her vision is impaired. According to the consulting ophthalmologist, this symptom is likely due to ischemic optic neuropathy. At present she can only see movement and light with her right eye. The vision of her left eye is also severely impaired, but she is able to read using special equipment for the visually impaired. Additionally, her everyday life is harmed by numbness and weakness of her extremities, which is caused by critical illness polyneuropathy. Despite these impairments, her aim is to return to work.
Samples for the measurement of dexmedetomidine concentrations in her plasma were drawn at 8-hour intervals as directed by the plan of the pharmacokinetic study she was recruited in. The concentrations were determined using reversed-phase high-performance liquid chromatography with tandem mass spectrometric detection (PE Sciex API4000 instrument; PE Sciex, Foster City, California, US) as described previously [].
The rates of the dexmedetomidine and propofol infusions, as well her plasma concentration results of dexmedetomidine, are presented in Figure . In calculating the dexmedetomidine dose, we used her preoperative weight of 89 kg.
Because the dose rate of dexmedetomidine remained constant for relatively long periods of time during three separate intervals, we calculated the plasma clearance of dexmedetomidine during these intervals by dividing the infusion rate by the plasma concentration. The calculated clearance was 55 L/h, 92 L/h and 87 L/h during the 2nd to 6th, 14th to 20th and 21st to 23rd day of the dexmedetomidine infusion, respectively. A list of drugs administered during her ICU stay is presented in Table .","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [89.0, 'kg']}",129,122.55,135.45,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 89.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (89.0 kg - 20 kg) = 129.0 mL/hr.
Hence, the patient's fluid maintenance is 129.0 mL/hr."
4467,22,Maintenance Fluids Calculations,physical,decimal,pmc-7785504-1,Extracted,"A 36-year-old Caucasian male, with a past medical history of bilateral lung transplant for cystic fibrosis in 2017 complicated by a rejection episode, cystic fibrosis-related diabetes, hypertension, pancreatic insufficiency, anxiety, gastroesophageal reflux disease, chronic rhinosinusitis, and peripheral neuropathy presented with an 18-month history of progressive muscle weakness. The patient had a double lung transplant three years prior to the start of the muscle weakness. He had excellent exercise performance from a few months post-transplant, riding a road bike regularly and even participating in the Transplant Olympics. He experienced an episode of rejection about three years and three months after his initial transplant and required treatment with anti-thymocyte globulin. Although lung function was reduced after his rejection episode, he was still biking regularly up to 15 miles at a time. A few months after this episode of rejection, he developed some peripheral neuropathy symptoms, and therapy with pregabalin at a dose of 100 mg twice daily was initiated. Weakness started within two months after pregabalin therapy was initiated and slowly progressed. He was no longer able to ride a bike and had difficulty rising from a squatted position, or standing up from a chair. He denied shortness of breath, chest pain, peripheral edema, orthopnea, or paroxysmal dyspnea. There were no symptoms of hypothyroidism and thyroid function was normal. His daily medications included mycophenolate, tacrolimus, prednisone, pregabalin azithromycin, pramipexole, ursodiol, trimethoprim-sulfamethoxazole, metoprolol, omeprazole, oxycodone, ativan, melatonin, simethicone, calcium, sertraline, Humalog insulin, pancrelipase, magnesium oxide, methylcobalamin, a multivitamin tablet, and tramadol on an as-needed basis.
Vital signs included a blood pressure of 120/82, a heart rate of 67, a respiratory rate of 18, and a temperature of 99 F. He weighed 76.6 kilograms with a BMI of 21.6, his oxygen saturation was 97% on room air. His general build and nourishment were normal, his fingernails showed mild clubbing. His neurological exam showed the presence of mild proximal muscle weakness; His heart had a regular rate and rhythm without murmurs. Peripheral pulses were normal. Lungs were clear to auscultation bilaterally. Laboratory testing revealed an elevated level of creatinine kinase and raised AST and ALT levels. The patient's pulmonary function tests showed a mild decrease in his FEV1 and FVC which subsequently improved while his muscle fatigue continued to worsen. A bronchoscopy performed to investigate his reduced exercise tolerance showed some purulent secretions and cultures grew methicillin-sensitive Staph aureus. Biopsy performed showed no evidence of rejection (ISHLT Grade A0, B0). Repeat labs drawn the next month showed a persistently elevated creatinine kinase level (Figure ).
A muscle biopsy was subsequently performed for further assessment. It showed scattered degenerating and necrotic muscle fibers with an associated macrophage infiltrate and phagocytic response. A prominent acute neutrophilic or chronic lymphocytic inflammatory reaction was not seen and centrally vacuolated myofibers were not identified. Taken together with the clinical history, these histologic findings were consistent with a drug-induced acute necrotizing myopathy (Figure ).
Upon reviewing the patient's medication for potential causes, mycophenolate and tacrolimus were viewed as the most likely causative agents, and the decision made to switch to cyclosporine and sirolimus. The patient did not report any improvement in his symptoms over a three-month time period. Creatinine kinase levels continued to rise despite the change in his medication regimen and the patient grew increasingly despondent. The decision was made to discontinue pregabalin. The patient noted a dramatic improvement in muscle weakness over the next few weeks and the creatinine kinase levels improved from 1023 U/L to 256 U/L (normal range: 49-320 U/L) within a month time period. Within 3 months, the patient was now able to walk on the treadmill for a half-hour and ride his bike again.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [76.6, 'kg']}",116.6,110.77,122.43,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 76.6 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (76.6 kg - 20 kg) = 116.6 mL/hr.
Hence, the patient's fluid maintenance is 116.6 mL/hr."
4468,22,Maintenance Fluids Calculations,physical,decimal,pmc-2965334-1,Extracted,"An 11-month old girl was admitted with severe kwashiorkor, acrodermatitis enteropathica, diarrhoea, and urinary tract infection. She had a three-week history of diarrhoea and four-day history of fever. She was born at term, following an uneventful pregnancy and delivery. She was almost exclusively breastfed during 11 months. Intake of solid foods was very poor. In the medical history, there was nothing eventful until three weeks before admission. Her parents were uneducated, appeared unaware of some basic elements of childcare, and their children did not receive regular medical care. They had not noticed when she began to show growth failure and insufficient weight gain. The parents were first cousins. They and their first child were healthy.
On examination, weight (6.470 kg), length (61 cm), and head circumference (42 cm) of the study girls were below the third centile for age. She had the typical features of kwashiorkor (generalized oedema, hypopigmented skin lesion on pretibial area, rotund sugar baby appearance, diaper dermatitis, abdominal distention, irritability, and thin, sparse hair) and rickets (obvious rachitic rosary, flaring of the wrists, craniotabes). Gross motor milestones were slightly retarded. There was no ataxia and nystagmus.
Laboratory evaluation was remarkable for a serum albumin of 2.6 g/dL, urea nitrogen of <6 mg/dL, and normocytic anaemia (7.5 g/dL). The serum alkaline phosphatase was markedly elevated, phosphorus was low, calcium was low normal, 25(OH)-vitamin D level was low, and the parathyroid hormone level was markedly elevated. Serum vitamin B12 and folate levels were normal. Evaluation for other causes of hypo-albuminaemia was negative.
Therapy for kwashiorkor was instituted, including gradual refeeding, initially via a nasogastric tube with a milk-based paediatric nutritional supplement. Supplements of vitamin D and calcium were provided. The oedema began to resolve after nutritional support. Serum zinc level was evaluated because an acrodermatitis enteropathica-like desquamative skin eruption persevered in the perineal areas (). Zinc level was in the normal range, and so, further investigation for a metabolic disorder was considered. After urine and blood samples were sent to the laboratory, our patient died on the seventh day of admission due to pneumonia. Chromatography of urinary amino acids revealed massive generalized neutral aminoaciduria and indicanuria. These amino acids were detected at low levels in the serum. Based on these findings, the diagnosis of Hartnup disease was made after her death.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.47, 'kg']}",25.88,24.586,27.174,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.47 kg. Hence, the patient's maintenance fluid is 6.47 kg * 4 mL/kg/hr = 25.88 mL/hr.
Hence, the patient's fluid maintenance is 25.88 mL/hr."
4469,22,Maintenance Fluids Calculations,physical,decimal,pmc-4421407-1,Extracted,"A male patient, born in 1990, first presented with a kidney stone when he was 10 years old, but the stone had passed spontaneously, and no further testing was done at that time. At the age of 20, he presented with a second episode of renal colic. Proteinuria and microscopic haematuria were also noticed, for which he was referred to a nephrologist.
On examination, he was a lean young man with normal height and stature. Height was 175 cm, and weight was 59 kg. Systemic examination was unremarkable. Blood pressure was 107/74 mmHg.
Laboratory examination showed an elevated serum creatinine of 130 μmol/L (1.44 mg/dL) (eGFR 62 mL/min/1.73 m2). Serum alkaline phosphatase level was 122 U/L with elevated bone fraction of alkaline phosphatase. Other blood tests were normal. Twenty-four-hour urine collection showed proteinuria of 2.981 g/day consisting mainly of low-molecular-weight proteins. Calciuria was 8.3 mmol/day (334 mg/day) or 5.7 mg/kg/day (normal < 4). Urine sediment analysis was normal ().
Ultrasonography, CT scan and MRI revealed normal kidney size and contour but bilateral multiple cysts. The cysts were mainly localized in the cortex, and they had a benign simple appearance. Furthermore, bilateral nephrolithiasis and intraparenchymal calcification consistent with nephrocalcinosis were seen ( and ).
Renal biopsy had been performed in another centre and had shown normal light microscopy, normal electron microscopy, and negative immunofluorescence.
After the acute renal colic, transurethral stone extraction was performed. Stone analysis showed a stone consisting of calcium phosphate and calcium oxalate.
Family history was negative for renal disease or renal colic. The patient had no siblings. The parents underwent a renal ultrasound examination: both had normal morphology of their kidneys without cysts, but one asymptomatic nephrolithiasis was found in the father.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [59.0, 'kg']}",99,94.05,103.95,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 59.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (59.0 kg - 20 kg) = 99.0 mL/hr.
Hence, the patient's fluid maintenance is 99.0 mL/hr."
4470,22,Maintenance Fluids Calculations,physical,decimal,pmc-8449714-1,Extracted,"This is a case of a 70-year-old Caucasian male with a medical history of hypertension and osteoarthritis who presented with a two-week history of dizziness. He also reported a few episodes of nonbloody, nonbilious emesis. Four days prior to presentation, he was unable to carry on with his daily activities due to generalized weakness which prompted him to seek medical attention. Upon further review of systems, he was admitted with night sweats, subjective fevers, and loss of appetite resulting in a 40-pound weight loss over the past few months.
On physical exam, the patient had skin and conjunctival pallor. Vitals revealed orthostatic hypotension. Laboratory investigations indicated significant microcytic anemia with a hemoglobin of 7.1 g/dL (14–18 g/dL), decreased from his baseline of 14.5 g/dL one year prior, and a MCV of 66 fL (79–93.9 fL). He had leukocytosis with a white blood cell count of 15.7 (4.5–11.0 K/UL) as well has thrombocytosis of 529 K/UL (130–400 K/UL). On chemistry, he was found to have acute kidney injury with a creatinine level of 1.42 mg/dL (0.7–1.3 mg/dL) and BUN of 34 mg/dL (9–23 mg/dL) from a baseline creatinine level of 0.9 mg/dL. He was also found to have hypokalemia with a potassium level of 3.2 mmol/L (3.5–5.1 mmol/L) and metabolic alkalosis with an elevated CO2 level of 34 mg/dL (9–23 mg/dL). Analysis of laboratory values (AKI, mildly elevated leukocytosis, metabolic alkalosis, and hypokalemia) hinted towards dehydration likely resulting volume depletion from vomiting. Laboratory values resolved with hydration. In addition, the patient had a positive stool guaiac suggestive of GI bleed. He was transfused with one unit of packed red blood cells. He denied recent history of hematemesis, melena, or hematochezia and had an unremarkable colonoscopy 5 years prior to presentation.
Due to symptomatic anemia, weight loss, and obstructive symptoms in the setting of a GI bleed, he underwent esophagogastroduodenoscopy (EGD) and colonoscopy. EGD revealed severe diffuse hemorrhagic gastritis () with biopsies consistent with chronic gastritis and no malignant features. Colonoscopy showed localized, severe colitis at the cecum that was erythematous, friable, and ulcerative (). There was also extraluminal compression of the cecum with protrusion of the ileocecal valve and luminal narrowing ().
Due to the extraluminal compression of the cecum, computed tomography (CT) of the abdomen and pelvis with intravenous and oral contrast was obtained. This ultimately revealed a cecal mass measuring 12 × 12 × 4.7 cm with the bulk of the mass protruding into the terminal ileum causing high-grade narrowing of the lumen (). Lymphadenopathy was localized to the right lower quadrant, and no distant lymphadenopathy was observed elsewhere (). CT of the chest (with and without IV contrast) that was also done did not show pulmonary nodules, pleural or pericardial effusions, or lymphadenopathy to suggest distant disease.
Subsequently, surgery was consulted, and due to his presentation with obstructive symptoms and symptomatic anemia secondary to the seen cecal mass, the patient underwent a right hemicolectomy. Pathology from both colonoscopy and right hemicolectomy showed MCL of cecum. The lymphoma cells expressed cyclin D, with characteristic cytogenetic abnormality of t (11; 14) (q13; q32). A high index of Ki-67 of 65% indicates adverse prognosis (Figures and ). MCL was also present in pericolonic lymph nodes.
Initially, the patient declined further workup and treatment including chemotherapy and bone marrow biopsy. Nonetheless, two months after discharge, he presented to the Oncology Clinic willing to undergo further evaluation and treatment. At this time, PET/CT scan revealed advanced disease with hypermetabolic lymph nodes within the mediastinum and retroperitoneum, as well as diffuse omental caking and bilateral malignant pleural effusions; no uptake on the bony structures was identified. The patient was now diagnosed with advanced disease and stage IV MCL, contrary to initial presentation where lymphadenopathy was limited to the right lower quadrant. The patient was started on chemotherapy consisting of rituximab and bendamustine of which he received 2 rounds before being lost to follow-up again.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [40.0, 'lbs']}",56.28736,53.47299,59.10173,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 40.0 lbs so this converts to 40.0 lbs * 0.453592 kg/lbs = 18.14368 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (18.14368 kg - 10 kg) = 56.28736 mL/hr.
Hence, the patient's fluid maintenance is 56.28736 mL/hr."
4471,22,Maintenance Fluids Calculations,physical,decimal,pmc-5496108-1,Extracted,"A 54-year-old man who recently immigrated from El-Salvador with a past medical history of Human Immunodeficiency Virus (HIV) presented with one-month progressive diarrhea, abdominal pain, subjective fevers, and 30-pound weight loss. There were no neurologic complaints. He was immunocompromised with an absolute CD4 count of 6 cells/μL after being off antiretroviral therapy for the past 10 years. He had been working full time as a car mechanic and reported having multiple indoor pet cats throughout his life. The patient was cachectic and frail appearing but with an otherwise unremarkable physical exam. Laboratory showed a HIV viral load of >130,000 copies/mL with Toxoplasma IgG > 700 IU/mL. Laboratory was unremarkable otherwise with Toxoplasma IgM < 3 AU/mL, no fecal ova or parasites observed, negative cryptococcal antigen, negative enteric cultures, and a nonreactive rapid plasma reagin. CT of the chest, abdomen, and pelvis demonstrated diffuse circumferential colonic wall thickening with prominent mesenteric lymph nodes (). Bidirectional endoscopy was performed with esophagogastroduodenoscopy showing large ulcerations in the gastric cardia and fundus. Severe inflammation and ulcerations in the right colon and cecum were noted on colonoscopy (). Biopsies were taken from both the gastric and colonic ulcerations. Histologic examination revealed markedly active gastritis and colitis with ulceration and ischemic changes (). Many free tachyzoites and encysted forms were identified in the lamina propria as well as the cytoplasm of epithelial, endothelial, and smooth muscle cells (Figures , , and ). Immunohistochemistry (polyclonal rabbit anti-Toxoplasma, 1 : 200; Dako Corporation, Carpinteria, Calif) confirmed the diagnosis of toxoplasmosis (). Follow-up CT head demonstrated a 1.6 cm peripherally enhancing lesion consistent with toxoplasmosis. There was subtle surrounding vasogenic edema without midline shift. The patient was diagnosed with disseminated toxoplasmosis and treatment was initiated with pyrimethamine, sulfadiazine, and leucovorin with subsequent resolution of his gastrointestinal and intracranial toxoplasmosis.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [30.0, 'lbs']}",47.21552,44.85474,49.5763,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 30.0 lbs so this converts to 30.0 lbs * 0.453592 kg/lbs = 13.60776 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.60776 kg - 10 kg) = 47.21552 mL/hr.
Hence, the patient's fluid maintenance is 47.21552 mL/hr."
4472,22,Maintenance Fluids Calculations,physical,decimal,pmc-5784682-2,Extracted,"The patient is a 13-years old female referred to our center for evaluation of dysmorphic features and congenital heart disease. She was born at term with uneventful prenatal and peripartum period. She was noticed after birth to have hypoplastic right thumb. Her parents, who are not related, have 4 other normal children. When she was initially evaluated in our center at the age of 6 and ½ years, her examination showed a head circumference of 45 cm (4.7 SD below the mean), a weight of 14.6 kg (4 SD below the mean) and a height of 100.5 cm (3 SD below the mean). She had upslanting palpebral fissures, bulbous nose, malformed right ear, retrognathia, low posterior hairline, webbed neck, and widely spaced nipples. The chest and abdominal examination was unremarkable. The cardiovascular examination revealed normal first heart sound, fixed split of second heart sound, and a systolic murmur grade 3/6 over the left upper sternal border. She had normal tone, power and deep tendon reflexes. The musculoskeletal examination revealed right thumb hypoplasia with absent thenar muscles, absent extensor pollicis longus, and thumb extensors. There was significant instability of the metacarpophalangeal joints of the right thumb. Skeletal survey revealed ankylosis between C3, C4 and C5 spine. The thoraacolumbar spine and the long tubular bones of both upper limbs were osteopenic. The right fifth metacarpal bone was short with hypoplasia of the first right metacarpal bone. The epiphysis of the first metacarpal bone was absent bilaterally. There was mild bilateral subluxation of the hip joints. The tibia and fibula were normal bilaterally. Hallux valgus at the interphalangeal joint was seen bilaterally. There was coning of the epiphysis of the second to fourth toes bilaterally. Echocardiogram revealed large secundum atrial septal defect measuring 12 mm with left to right shunt. Ultrasound of abdomen and pelvis indicated that the left kidney was rotated and ectopic lying down into the pelvis.
As part of routine diagnostic procedures a high-resolution GTW-banding study was carried on the patient’s sample. No gross abnormality was detected. Then, an aCGH experiment was performed as a further clinical screening and indicated an interstitial duplication pointed by 33 oligonucleotide probes on 5q35.2-q35.3. An interphase FISH using a probe (CTD-2301A4) within the duplicated interval re-confirmed the findings. To better characterize the duplication a high-resolution array (Cytogenetics Whole-Genome 2.7 M) from Affymetrix Inc. (Affymetrix Inc., San Paolo, CA, US) was utilized to further delineate the gain missed during the initial standard microscope based-karyotyping. This particular chip array utilizes 2.7 million markers including 400,000 SNP probes that provide whole-genome coverage with the one of the highest density coverage among the present platforms. Based on Affymetrix’s cytogenetic assay results, the duplication extends from 175,349,728 to 177,347,753 bp (hg19) and comprises 58 genes targeted by more than 600 SNP and copy number (CN) probes covering approximately 2.0 Mb (Fig. ). In comparison to the previously published duplications this duplication seems novel and does not share breakpoints with the compared cases.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [14.6, 'kg']}",49.2,46.74,51.66,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 14.6 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (14.6 kg - 10 kg) = 49.2 mL/hr.
Hence, the patient's fluid maintenance is 49.2 mL/hr."
4473,22,Maintenance Fluids Calculations,physical,decimal,pmc-8015191-1,Extracted,"A 5-month-old female presented with a 3-day history of coughing and recurrent vaginal discharge and poor weight over the last 3 months. The discharge was said to have been present since birth, on and off, and it had worsened in the 3 days prior to presentation. Of note was that the child had been treated for conjunctivitis when she was 4 days old and for an upper respiratory tract infection (URTI) at 10 weeks of age. She was exclusively breastfed and, despite adequate milk supply, was small for her age. The mother was HIV negative and had not been screened for syphilis during pregnancy. There is a history of maternal febrile illness during pregnancy that was nonspecific.
On examination, she was alert, pale, and small for her age (Wt 5.4 kg, length 64 cm, Z score: −3 SD to −2 SD). Vital signs were normal and, on respiratory examination, the child had bilateral crepitations. Abdominal and cardiovascular examinations were normal. Examination of the skin revealed generalized hyperpigmented spots (healing dermatitis). Genitourinary examination was also normal. RPR was reactive and with titers (1:4). FBC was done, and the patient was found to have microcytic hypochromic anemia (Hb 7.0 g/dL, MCV 59.7 fL, MCH 17.2 pg) and leukocytosis (WCC 15 × 103/uL). Differential count was normal.
She was admitted and given aqueous crystalline penicillin G (benzylpenicillin) 270,000 IU given IV four times daily for 10 days. On follow up, respiratory and genitourinary symptoms had resolved.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.4, 'kg']}",21.6,20.52,22.68,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.4 kg. Hence, the patient's maintenance fluid is 5.4 kg * 4 mL/kg/hr = 21.6 mL/hr.
Hence, the patient's fluid maintenance is 21.6 mL/hr."
4474,22,Maintenance Fluids Calculations,physical,decimal,pmc-8495192-1,Extracted,"A 7-day-old girl was admitted to our hospital with a fever and poor feeding. Her family history was unremarkable. Group B Streptococcus was not detected in the vaginal and stool culture of her mother before delivery. She denied any exposure to toxins, drugs, tobacco, or alcohol. The neonate was delivered by vacuum assisted vaginal delivery, at the gestational age of 40 weeks and 3 days. Her birth weight was 3,436 g and Apgar score was 2/9. Before her birth, her heart rate was low, and suction delivery was performed because of shoulder dystocia. To alleviate her respiratory distress, non-invasive positive pressure ventilation was performed, and her respiratory condition immediately improved. She did not receive any antibiotics or parenteral nutrition. Auditory brainstem response testing revealed no abnormal findings at 4 days of age. She was discharged without any complications from hospital. No other neonates presented P. aeruginosa infection in the hospital around the same time as this patient. She was fed expressed breast milk in a bottle. Cleaning of the milk bottle with an appropriate sanitizer such as a hypochlorite-based disinfectant, sufficient rinsing, and drying after each use were not being done at home. She developed fever and failure to thrive at 7 days of age and was admitted to our hospital. On examination, she was febrile with a temperature of 38.2°C, tachycardiac and tachypneic, lethargic, and showing a bulging fontanelle. Her umbilical cord had already fallen off and she had simple dimple. No external malformations could be observed. On admission, initial investigations revealed an elevated white blood cell (WBC) count of 29.1 × 109 cells/L (normal range 3.8–10.0 × 109 cells/L) and C-reactive protein at 23.8 mg/L (normal range <2.0 mg/L). The coagulation screen, liver function tests, and renal function tests were normal. The cerebrospinal fluid (CSF) showed a markedly increased WBC count (4.7 × 109 /L), elevated protein level (15.9 g/L), and low glucose (1.6 mmol/L) when compared with an elevated serum glucose level (4.3 mmol/L). A Gram stain of CSF showed no organism on admission. Transfontanellar ultrasound performed on the admission day revealed no abnormal findings. Empirical therapy for neonatal meningitis with intravenous ampicillin and cefotaxime combined with acyclovir was initiated. On the next day, a CSF culture was positive for P. aeruginosa, and no pathogens were isolated by blood culture and urine culture. We stopped the empiric therapy regimen and started meropenem monotherapy. Once antimicrobial susceptibility test () was confirmed, meropenem de-escalated to cefepime according to the Practical Guideline for Bacterial Meningitis 2014 in Japan. She developed agitation and myoclonus over the 3 days of cefepim treatment. We changed the antibiotic therapy to ceftazidime and continued for 3 weeks. We performed head MRI and whole body enhanced CT scans 12 days after admission. These images showed no findings of ventriculitis, hydrocephalus, brain abscess, or infarction. Structural defects of the cribriform plate, inner ear, or sinuses were also not detected. Her immunological status was assessed, and we found that the total absolute lymphocyte count, immunoglobulin levels, total complement measurement, lymphocyte analysis by flow cytometry, isohemagglutinins, response against lipopolysaccharide, and ability to produce reactive oxygen were all normal, except for slightly low immunoglobulin A level and natural killer cell count. Her clinical course was good, and she was discharged without any complications apart from a slight hearing disability for both ears detected on audiology testing. A brief summary has been shown in the timeline (shown in ). At the time of writing, 8 months after diagnosis, the patient is receiving outpatient follow-up without any problems. We investigated mother's breast skin, feeding bottle, breast pump milk collection kits, and related items as the source of infection. Pseudomonas aeruginosa was isolated from a cleaning sponge brush and had the same band pattern as the isolate obtained from CSF culture as shown by agarose gel electrophoresis patterns of the PCR-based open reading frame typing (POT) (shown in ).
The study protocol was approved by the Institutional Review Board of the Japanese Red Cross Wakayama Medical Center (no. 855).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3436.0, 'g']}",13.744,13.0568,14.4312,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3436.0 g so this converts to 3436.0 lbs * kg/1000 g = 3.436 kg. Hence, the patient's maintenance fluid is 3.436 kg * 4 mL/kg/hr = 13.744 mL/hr.
Hence, the patient's fluid maintenance is 13.744 mL/hr."
4475,22,Maintenance Fluids Calculations,physical,decimal,pmc-3819851-1,Extracted,"A 67-year-old woman, 55 kg was admitted to hospital with a 3-day history of abdominal pain, nausea and vomiting. She was diagnosed to have chronic obstructive pulmonary disease (COPD) 5 years ago and had four episodes of prior hospitalization secondary to acute exacerbation. She often required nebulisers and had an exercise tolerance of approximately 100 yards. In the week prior to admission she had received oral antibiotics and steroids for an infective exacerbation of COPD. On admission to the hospital she had signs of peritonitis and her abdomen was noted to be markedly distended. Ultrasonographic scan revealed a possible bowel (duodenal) perforation. She was tachypneic (RR 28/min) with evidence of accessory muscle use. Examination revealed reduced bi-basal air entry with crepitations all over the chest and chest X-ray showed consolidation of the right middle and lower lobe. Her arterial blood gas revealed type I respiratory failure (FiO2 0.60, pH 7.37, pO258 mmHg, pCO245 mmHg). Her heart rate was 112/min, and BP 90/60 mmHg. She was anemic with hemoglobin of 6 g%. S. urea - 102 and S. creatinine-2 g%. Intravenous acetaminophen was administered for pain relief, but despite this she could not cough or take deep inspiration due to ongoing pain. She was categorized as American society of anesthesiologists (ASA) physical status grade IV/E and was planned for emergency laparotomy. We planned to avoid general, epidural or spinal anesthesia, so we opted for TAP block under ultrasound guidance as a sole anesthetic technique. After proper explanation to the patient about the technique of TAP block, she was taken to operation theatre table and monitors attached. Pulse oximetry showed oxygen saturation of 88% on room air. Hence oxygen supplementation was carried out with venturi mask with oxygen flow at 6 L/min. Saturation improved to 92%. After securing an IV access with 18G (Gauge) needle on the right dorsum of the hand, she was sedated with intravenous dexmedetomidine infusion at 4 mcg/kg/min to make her comfortable, cooperative, and pain free for performing the block. Then she was laid supine with the anterolateral abdominal wall exposed bilaterally from the iliac crest to the sub-costal margins and scrubbed aseptically. The block was performed using an aseptic ultrasound guided in-plane technique (s-nerve sonosite, HFL38 (Company brand name of the 6.0 to 13.0 MHz linear probe) probe, 100 mm sonoplex needle). When the needle tip position is within the TAP neuro-fascial plane a mixture of 20 ml of 0.25% bupivacaine, 20 ml of 1% Lidocaine and 0.2 mg adrenaline was injected slowly through the needle. The same steps were repeated on the contra-lateral side. A remarkably good clinical effect was achieved within 30 min with almost complete resolution of pain. After 30 min, the abdominal incision was carried out without pain. All the vital signs remained normal intraoperatively. Effective coughing and deep breathing became possible and her tachypnea gradually resolved. Laparotomy revealed an ileal perforation, which was sealed with omentum. She made a slow post-operative recovery to be discharged from hospital 14 days after admission.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [55.0, 'kg']}",95,90.25,99.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 55.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (55.0 kg - 20 kg) = 95.0 mL/hr.
Hence, the patient's fluid maintenance is 95.0 mL/hr."
4476,22,Maintenance Fluids Calculations,physical,decimal,pmc-7422994-1,Extracted,"A 7-days-old female newborn was requested to visit our hospital due to an abnormal Pompe disease screening result []. She was born at full-term to a G1P1 mother with a birth bodyweight of 4380 gm. The parents denied poor feeding, poor activity, nor weak crying in this baby. NBS included Pompe disease, and other conditions were performed on her third day of life. On Day 4, our NBS laboratory received her sample. On Day 6, a high risk of Pompe disease was reported (GAA activity 0.18 uM/h (critical cutoff < 0.5); ratio 42.87 (critical cutoff acid β-glucosidase (ABG)/GAA ≥ 20) so an urgent visit to our hospital was arranged on Day 7. When we saw her, she had normal muscle power, normal reflex, no macroglossia, but her facial folds decrease slightly. Laboratory examination revealed an elevation of pro-BNP (8738 pg/mL), CK (722 U/L), and alanine aminotransferase (ALT) (112 U/L). A chest X-ray revealed mild cardiomegaly (). Echocardiography revealed moderate left ventricle (LV) and right ventricle (RV) hypertrophy, with a LV mass index (LVMI, measured by 2-D method) of 115.7 g/m2 (normal range < 65 g/m2). A whole blood sampling at Day 7 revealed deficient lymphocyte GAA activity (1.33 nmol/g pro/h, normal mean 66.7) and thus confirmed the diagnosis of IOPD. However, she did not have the common CRIM-positive Taiwan Pompe disease p.D645E variant, tested using DNA extracted from the first DBS. Although her CRIM status was unknown, her parents refused prophylactic immune modulation therapy. Western Blot analysis using the white blood cells as the material soon revealed the 110 kDa precursor GAA band (), suggesting a CRIM-positive status. She received her first dose of rhGAA (20 mg/kg) at the age of 8 days. Mutation analysis showed heterozygous c.2024_2026del (p.N675del) and c.2040+1G>T variants in trans, compatible with IOPD. There were no CRIM status predictions about these two variants [].
The study was approved by the ethical committee of National Taiwan University Hospital, Taipei, Taiwan (201906053RINB, 1st approved date 2019/08/05). The clinical information was gathered from the hospital medical records retrospectively, and no individual's consent was required.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4380.0, 'g']}",17.52,16.644,18.396,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4380.0 g so this converts to 4380.0 lbs * kg/1000 g = 4.38 kg. Hence, the patient's maintenance fluid is 4.38 kg * 4 mL/kg/hr = 17.52 mL/hr.
Hence, the patient's fluid maintenance is 17.52 mL/hr."
4477,22,Maintenance Fluids Calculations,physical,decimal,pmc-8552511-1,Extracted,"The patient is a six-year-old male, the third child in the family with a positive history of a first-degree consanguinity. The other two siblings are completely healthy and there is no family history of genetic disease. The mother is healthy and became pregnant at age 23. There were no complications during the pregnancy. She was positive for group B streptococcus and was adequately treated with antibiotics. The child is a product of full-term pregnancy, delivered through emergent cesarean section due to meconium-stained amniotic fluid and fetal distress. His Apgar score was nine at one minute and nine at five minutes. 3.1 kg (25th percentile), 49 cm (25th percentile), and 34 cm (25th percentile) are the weight, length, and head circumference measurements at birth, respectively. On initial examination, it showed dysmorphic features like deep-seated eyes, small palpebral fissure, low set of ears, high arched palate, short neck, and right-hand polydactyly. The patient was hypertonic on all four limbs. At 12 hours of life, precordial examination revealed a grade 2/6 systolic ejection murmur at the left lower sternal border. On pulmonary auscultation, he was ventilated on Assist-Control mode with equal bilateral air entry and no pathological sounds. Abdominal examination revealed umbilical hernia which resolved at seven months of age without any intervention, and normal male genitalia with both testicles present in the scrotum. Chromosomal analysis performed on a cultured peripheral blood sample revealed a mosaic result. Five cells showed an additional chromosome 13 (47, XY, +13). Another five cells showed numerical and structural normal male chromosomes (46, XY).
The patient stayed in the neonatal intensive care unit (NICU) for a month because of persistent hyperinsulinemic hypoglycemia, pericardial effusion, and respiratory distress. He was treated with polycose and diazoxide, and the goal was to maintain blood glucose level as 5-6 mmol/L. The pericardial effusion resolved on its own and did not need pericardiocentesis. Intubation was performed for respiratory distress because of worsening oxygen saturation. During his stay in the NICU, he was followed up by endocrinology and cardiology. Head and abdominal ultrasounds were normal and chest X-ray showed cardiomegaly. Echocardiogram showed patent foramen ovale and patent ductus arteriosus, both closed by themselves. Patent ductus arteriosus closed few days after birth and the patent foramen ovale closed at the age of nine months. MRI of the brain done on the 12th day of life showed no evidence of structural malformation and no masses or collections. At 15 months of age, he was referred to plastic surgery for removal of the postaxial polydactyly in the right hand.
The patient is currently being followed by a pediatrician for his asthma which is under control. At the age of 12 months, he presented to the emergency room (ER) for bronchopneumonia with hyperactive airway disease exacerbation. His hyperactive airway disease was controlled since. He is on salbutamol, taken as needed, and fluticasone 50 mcg twice daily with no day or night symptoms, no exercise-induced symptoms, and no ER visits. He used to follow with endocrinology for transient congenital hyperinsulinemia and he was on diazoxide. It resolved at the age of 18 months. Currently, he is being followed by otolaryngology because of snoring. Prescribed mometasone with the possibility of surgical removal of adenoid hypertrophy if not improved with medication.
At the age of two months, he was active, moving all four limbs, mildly holding his head. At age of seven months he was able to sit by himself. At 12 months he was able to cruise around furniture, holds a bottle, and say mama and dada. He was referred to physiotherapy because of balance issues when standing and walking, he showed poor knee control with partial flexion and bowing. According to the mother, his balance issues improved with physiotherapy sessions. At 15 months, he was able to get objects from the floor while standing without losing control and walk a long distance with no support. At 25 months, he was able to say multiple words but unable to form a sentence, he could run and climb up and down the stairs with on and off-balance issues. At four years and five months, he began care with developmental pediatric clinic. They have noticed that his motor activity improved with physical therapy, and he still used single words and no phrases, did not know body parts, was good with non-verbal expression, responds to name, and follows commands. He was noted to be a risk-taker with no sense of danger. The developmental pediatrician assessed his speech and motor skills to be at the level of a two-year-old child. At the age of six years, he continued to make slow progress and he gained new skills like using two to three words phrases and knows some colors and numbers. He is still not trained to use the toilet. The parents were advised to enrol their son in different special education centers to help with his developmental delay.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.1, 'kg']}",12.4,11.78,13.02,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.1 kg. Hence, the patient's maintenance fluid is 3.1 kg * 4 mL/kg/hr = 12.4 mL/hr.
Hence, the patient's fluid maintenance is 12.4 mL/hr."
4478,22,Maintenance Fluids Calculations,physical,decimal,pmc-7796768-2,Extracted,"A 48-year-old male patient (weight 84 kg, height 186 cm) was scheduled for an ileostomy reversal surgery. ESP block was performed from the left side at the Th8 level with 20 mL 0.25% bupivacaine. The total amount of given fentanyl was 400 μg. After the operation, the patient complained of having pain 5/10 and 1 g metamizole was given. 2 h after operation, the pain was 6 at rest and on coughing, thus, 1 g paracetamol was given. After 6 h, the pain was 3/10 at rest and on coughing, but after 12 h he received 100 mg tramadol (the pain was 6 at rest and 8 on coughing). After 24 h, the pain was 5/10 at rest and 6/10 on coughing, thus, 1 g paracetamol was given, and after 36 h, the pain was 2/10 at rest and on coughing. Pain scores 4/10 at rest and 5/10 on coughing were reported after 48 and 72 h, respectively and 1 g paracetamol was given.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [84.0, 'kg']}",124,117.8,130.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 84.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (84.0 kg - 20 kg) = 124.0 mL/hr.
Hence, the patient's fluid maintenance is 124.0 mL/hr."
4479,22,Maintenance Fluids Calculations,physical,decimal,pmc-8157604-3,Extracted,"A 34-year-old secundigravida, underwent fetal MRI at 30 weeks’ gestation confirming bilateral hydronephrosis, right dysplastic kidney, megacystis, and oligohydramnios. A male neonate, weighing 2.650 g, was delivered by elective C-section at 36 weeks’ gestation. Immediately after birth, he developed a mild pneumothorax with respiratory distress requiring nasal CPAP. Initial serum creatinine was 1.6 mg/dl. An initial attempt at transurethral catheterization using a 6 Fr Foley catheter was unsuccessful due to excessive resistance felt halfway through the urethra, and was followed by a self-limiting urethral bleeding. A 5 Fr umbilical catheter was therefore used to drain the bladder. Postnatal ultrasonography confirmed an enlarged and thick-walled bladder, associated with mild bilateral hydronephrosis, a dysplastic right kidney, and multiple small cysts with cortical subcapsular distribution in the contralateral left kidney. The umbilical catheter slipped out of the bladder after 72 h and was eventually replaced with a 6 Fr Foley catheter. On day-of-life 14, he was deemed fit enough to undergo VCUG. The test revealed a trabeculated bladder associated with a moderate posterior urethral dilatation and left-sided grade III vesicoureteral reflux. After catheter withdrawal, a good urinary stream and complete bladder emptying were documented during micturition (). The baby was ultimately discharge home on day-of-life 17, with a relatively stable renal function. Repeat VCUG at 9 months disclosed a less irregular bladder contour, gradual shrinking of the posterior urethral dilatation, and reflux disappearance. The bladder emptied rapidly, and postvoid residual urine volume was small. He is now 2 years old and, following a first episode of urinary tract infection, had undergone second look cystoscopy that ruled out obstructing residual valves. Follow-up ultrasonography showed progressive thinning of the bladder wall and minimal postvoid residual urine volume ().
Renal function remains stable with a serum creatinine of 0.53 mg/dl. However, eGFR (59 mL/min/1.73m2) falls within the range of stage 3 chronic kidney disease.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.65, 'kg']}",10.6,10.07,11.13,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.65 kg. Hence, the patient's maintenance fluid is 2.65 kg * 4 mL/kg/hr = 10.6 mL/hr.
Hence, the patient's fluid maintenance is 10.6 mL/hr."
4480,22,Maintenance Fluids Calculations,physical,decimal,pmc-3237160-1,Extracted,"A 6-month-old male infant, 3.5 kg in weight, presented with the history of refusal to feed, tender abdomen, swelling in the right groin and constipation since 3 days. Diagnosis of a right-sided obstructed, irreducible indirect inguinal hernia was made. The paediatric surgeons reduced the hernia and a semi-elective herniotomy was planned.
The child had a history of stridorous breathing since birth and was subsequently diagnosed as a case of congenital laryngomalacia. He was a full-term delivery by Caesarean section for meconium-stained liquor. The infant was kept in the intensive care unit (ICU) for 3 days post-delivery for breathing difficulties and neonatal jaundice. Anaesthesia pre-evaluation revealed microretrognathia []. The child underwent a High resolution computed tomography (HRCT) imaging of the chest along with virtual bronchoscopy to rule out any obstruction in the airway and there was a chance finding of three ununited rib fractures of the left side (4th, 5thand 6th) []. Subsequent paediatric, orthopaedic and ophthalmologic evaluations revealed blue sclera, spontaneous rib fractures, failure to thrive and multiple hernias (umbilical and right inguinal) because of the lax abdominal wall. Cardiac evaluation was unremarkable. A clinical diagnosis of congenital osteogenesis imperfecta type 1 was made by the paediatricians.
High-risk consent and consent for post-operative ventilation was obtained. The child was premedicated with inj. glycopyrolate 4 mcg/kg, inj. midazolam 0.03 mg/kg and inj. ketamine 0.5 mg/kg IV. Anaesthesia was induced with IV propofol 2 mg/kg. A paediatric fibreoptic bronchoscope was not available, so direct laryngoscopy was performed with a shoulder pad in place and intubation was achieved in the second attempt using size 1 Miller blade, and a 3.5-mm uncuffed enotracheal tube (ETT) was inserted. On direct laryngoscopy, the view was Cormack-Lehane Grade III. After confirmation of tube placement, inj. atracurium 0.5 mg/kg was administered and anaesthesia was maintained with oxygen, nitrous oxide, and sevoflurane. Monitoring devices included a pulse oximeter, cardioscope, non-invasive blood pressure monitor, temperature monitor and capnometer. Caudal block was administered with 2 cc of 0.25% bupivacaine. The patient was carefully repositioned supine and adequate padding was done. The surgery lasted 30 min and was uneventful. Post-surgery, neuromuscular blockade was reversed and the patient extubated. The patient was shifted to the ICU for observation. A quiet and pain-free post-operative period ensured that the patient did not have any breathing difficulties.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.5, 'kg']}",14,13.3,14.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.5 kg. Hence, the patient's maintenance fluid is 3.5 kg * 4 mL/kg/hr = 14.0 mL/hr.
Hence, the patient's fluid maintenance is 14.0 mL/hr."
4481,22,Maintenance Fluids Calculations,physical,decimal,pmc-4669602-1,Extracted,"A 30-year-old previously well Bangladeshi male was admitted to a local tertiary care hospital with a 20-day history of fever, chills, rigors, headache, myalgias, and anorexia. He had been suffering from nausea, vomiting, diarrhoea, jaundice with scleral icterus and dark urine for five days. One day prior to admission, he was diagnosed with malaria on thick smear at a private hospital, however parasite density result was unavailable. There he was treated with intravenous quinine (750 mg 8-hourly x five doses) and azithromycin, due to limited availability of first line therapy of artesunate, before being referred for further management.
Past medical history was significant for three prior malaria infections. His most recent episode of suspected vivax malaria was 30 days prior to admission, which was partially treated with an incomplete course of chloroquine. He had no history of jaundice, liver disease, transfusions, malignancy, or autoimmune disease. There was no family history of jaundice or iron treatments. He did not take any regular or traditional medicines. There was no history of betel nut consumption.
On admission, he had a temperature of 39.7 oC, Glasgow Coma Score (GCS) 15/15, blood pressure (BP) 127/60 mmHg, heart rate (HR) 127 beats per minute, a respiratory rate (RR) of 24 breaths per minute with oxygen saturation (SaO2) of 93 % on room air, and body weight of 65 kg. He appeared unwell with pronounced scleral icterus, black urine, hepatomegaly and splenomegaly (4 cm and 5 cm below the costal margin, respectively). There was no conjunctival suffusion or lymphadenopathy.
Admission peripheral blood smear confirmed a diagnosis of falciparum malaria (360 parasites/μl). Severity criteria included hyperlactataemia (lactate 6.8 mmol/L), hyperbilirubinaemia (total bilirubin 58 μmol/L), and 4+ haemoglobinuria (blackwater fever); hence the case was classified as severe malaria (Table ). He was promptly treated with intravenous artesunate 120 mg, 2.4 mg/kg body weight (Guilin Pharmaceuticals, China) at 0, 12, 24 and 48 h (four doses), in addition to empiric ceftriaxone 2,000 mg every 12 h, as per local hospital practice. After 30 h his peripheral parasites cleared with resolution of the fever and haemoglobinuria, and he was switched to oral artemether/lumefantrine (AL) combination 80/480 mg (Novartis, Switzerland).
On the third day of admission he developed fever, confusion, dyspnoea (RR 28, SaO2 90 %), tachycardia (HR 106), hypotension (BP 100/80 mmHg), recurrent 4+ haemoglobinuria with severe microcytic anaemia (haemoglobin of 32 g/L) accompanied by elevated lactate dehydrogenase and bilirubin, consistent with acute haemolytic anaemia (Table , Fig. ). Pre-transfusion peripheral blood smear showed no schistocytes and reticulocytes of 2 % (reticulocyte production index 0.15 (compared to RPI of 0.3 on day 3 in blackwater fever patients []). Direct antiglobulin test (DAT; anti-IgG and anti-C3d) was negative and indirect antiglobulin test (IAT) was positive. Glucose was normal. Blood and urine bacterial cultures were negative. Glucose-6-phosphate dehydrogenase testing and haemoglobin typing were not available. Human immunodeficiency virus, syphilis, hepatitis A, hepatitis B and hepatitis C serology were negative. Hepatitis B antigen was negative. He promptly received transfusion of three units matched whole blood. Intravenous artesunate was substituted for AL despite parasite clearance due to the notion that the recurrent fever must be due to malaria. In total, he received seven doses of artesunate (total dose of 840 mg) and three doses of AL (total dose of artemether 240 mg, and lumefantrine 1,440 mg). Empiric amikacin 500 mg, 7.5 mg/kg 8-hourly was added on day 6 to broaden antibacterial coverage for potential multi-drug resistant gram-negative bacteria given his ongoing fever despite negative blood and urine cultures. The haemolysis continued for nine days and he required a total of 10 transfusions (Fig. ).
On day 10, bone marrow biopsy revealed gross hypercellularity with erythroid hyperplasia and no evidence of lymphoma, leukaemia, or haemophagocytic syndrome. Meropenem (500 mg 8-hourly) was empirically substituted for amikacin and ceftriaxone given his renal dysfunction to cover potential extended-spectrum β-lactamase producers, and dexamethasone 5 mg 6-hourly was initiated for suspected autoimmune haemolytic anaemia. The haemoglobinuria resolved two days after steroid treatment and ceftriaxone discontinuation. His haemoglobin slowly recovered, reaching 76 g/L by day 20.
On day 16, he had ongoing fever with right-sided facial pain and swelling. A large, 3 × 2 cm ulcer on the right upper hard palate covered with yellow slough and an area of necrosis was observed (Fig. ). The right maxillary sinus was tender on palpation. He had pain with right eye extra-ocular movements but no ocular discharge, proptosis, pupil asymmetry, diplopia, or decreased visual acuity. There was no nasal or ear involvement. A swab of the hard palate ulceration revealed long, broad, aseptate hyphal elements displaying 90° branching consistent with Mucor, (Fig. ). Fungal cultures failed to grow. MRI showed extensive right-sided opacification and mucosal thickening of the maxillary and ethmoid sinuses with no radiographic evidence of orbital or cerebral extension (Fig. ). He underwent prompt surgical debridement of the oral ulcer and right maxillary sinus. His steroids were discontinued and he was started on oral itraconazole 100 mg 12-hourly until first line treatment with amphotericin B became available nine days later. Intravenous amphotericin B deoxycholate 50 mg daily, was continued for 14 days with improvement of his facial swelling and oral ulceration. The patient was pleased with his clinical improvement and hospital care, however due to a family emergency in his remote village he left hospital against medical advice and could not attend follow up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [65.0, 'kg']}",105,99.75,110.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 65.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (65.0 kg - 20 kg) = 105.0 mL/hr.
Hence, the patient's fluid maintenance is 105.0 mL/hr."
4482,22,Maintenance Fluids Calculations,physical,decimal,pmc-4528876-1,Extracted,"A 78-year-old man presented with 1-day history of nausea and vomiting. His symptoms started suddenly the night prior to presentation. The nausea was constant, to the point where he could no longer tolerate oral intake. Vomiting occurred 5 to 6 times throughout the evening, but there were no further episodes as of the morning of presentation. He endorsed very minimal epigastric burning, which he described as a “gas pain,” but he had no other abdominal symptoms. His bowel movements were normal. The patient was discharged from the hospital 10 days prior; during that hospitalization, he had symptomatic bradycardia felt to be secondary to his β-blocker. His dosage was reduced, his bradycardia improved, and he was discharged home. Since discharge, he noted persistent exertional dyspnea and bilateral lower extremity edema.
The past medical history was remarkable for type 2 diabetes mellitus, hyperlipidemia, paroxysmal atrial fibrillation, nonischemic cardiomyopathy (ejection fraction of approximately 40%) with stage III diastolic dysfunction, and chronic kidney disease (baseline creatinine 2.2). He smoked 4 cigarettes daily for 25 years, but not the last 20 years. His medications included aspirin, simvastatin, furosemide, metoprolol tartrate, and glipizide.
On examination, his blood pressure was 136/71 mmHg, heart rate 77 bpm, respiratory rate 16, temperature 36.1°C, oxygen saturation 100% (room air), weight 82 kg, and no orthostasis. In general, he was not in acute distress. There were no skin lesions. Mucous membranes were moist. Lung fields were clear to auscultation bilaterally. Heart was regular without murmurs, rubs, or gallops. He had jugular venous distention 4 cm above the sternal angle. His abdomen was benign. He had no tenderness over his liver and no hepatomegaly was present. He had minimal bilateral lower extremity edema.
The patient’s white blood cell count was 15 200/mm3. The hemoglobin was 13 g/dL, and the platelet count was 97 000/mm3. The total bilirubin was 3.3 mg/dL, direct bilirubin 1.3 µg/dL, aspartate aminotransferase (AST) 4725 IU/L (normal value = 12-38 IU/L), alanine aminotransferase (ALT) 3240 IU/L (normal value = 10-45 IU/L), alkaline phosphatase 110 IU/L (normal value = 25-100 IU/L), total protein 6.6 g/dL, and albumin 3.7 g/dL. The international normalized ratio (INR) was 2.6. His sodium was 134 mmol/L, potassium 5.6 mmol/L, bicarbonate 21 mmol/L, blood urea nitrogen 54 mg/dL, and creatinine 3.5 mg/dL. His brain-natriuretic peptide was 1040 pg/mL (normal = <100 pg/mL), and troponin was 0.50 ng/mL (normal = <0.09 mg/mL). His lipase was 49.0 IU/L (normal = 10-50 IU/L).
An abdominal ultrasound revealed increased echogenicity of the liver parenchyma, patent hepatic vasculature, and no dilated intrahepatic or extrahepatic ducts. The acetaminophen level was zero and the urine drug screen negative. Hepatitis A to C serologies were negative, and antinuclear antibody, antimitochondrial antibody, F-actin antibody, and liver-kidney microsome-1 antibody titers were all normal. Further review of his past records indicated that his liver tests were AST 47 IU/L and ALT 53 IU/L during his hospitalization 10 days ago.
The patient’s electrocardiogram (ECG; ) revealed multiple conduction defects including a right bundle branch block, left anterior fascicular block, and a first-degree atrioventricular block. He also had inferior Q waves and T wave inversions in leads I, aVL, and V3. These findings along with the conduction defects were all seen on previous ECGs. Review of prior records indicated that he had a left heart catheterization about 18 months prior to this admission. At that time was found to have nonobstructive coronary disease.
His most recent echocardiogram (), which was performed 2 weeks prior to this admission, showed a reduced ejection fraction (40%), biatrial enlargement (, RA and LA), and biventricular hypertrophy (, VS and PW; , arrows). There was also a granular or “speckled” appearance of the myocardium (, asterisk). The estimated peak right ventricular systolic pressure was 34 mm Hg based on an estimated right atrial pressure of 13 mm Hg, without primary valvular abnormalities. Mitral valve inflow Doppler and mitral annulus tissue Doppler () were consistent with severe left ventricular diastolic dysfunction. The E/e ratio was >15, consistent with an elevated left ventricular filling pressure. There was hypokinesis to akinesis of the inferior and septal walls.
The patient was monitored overnight and his symptoms resolved without intervention. His blood pressure remained within normal limits and he had normal urine output. The aminotransferases declined dramatically, to a level of 1070 IU/L within 48 hours. He was discharged home in baseline condition. One month later, he was seen in cardiology clinic during which time he had further evaluation with cardiac magnetic resonance imaging (MRI; ). This revealed diffuse myocardial thickening of both left and right ventricles with delayed hyperenhancement in a pattern consistent with amyloidosis ( and , asterisks). Both atria were dilated in size, with evidence of patchy subendocardial scar ( and , arrows). The patient declined endomyocardial biopsy and further invasive investigation or therapy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [82.0, 'kg']}",122,115.9,128.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 82.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (82.0 kg - 20 kg) = 122.0 mL/hr.
Hence, the patient's fluid maintenance is 122.0 mL/hr."
4483,22,Maintenance Fluids Calculations,physical,decimal,pmc-3350249-1,Extracted,"A 4.5-month-old female presented to hospital with a 2-day history of watery diarrhea and fever developed in the 12 hours before admission. The infant was reported to have had 10 watery stools over the previous 24 hours, during which she became quite unsettled, crying a lot, whilst drinking half her usual amount of liquids. There was no history of vomiting.
Her medical history revealed delivery at term via emergency cesarean section due to severe fetal distress, with a birth weight of 2910 g. Her Apgar score was 0-1 at one and five minutes, respectively, after delivery requiring tracheal intubation and transfer into neonatal intensive care unit. She was put into induced coma and active hypothermia for 72 hours. The infant was extubated on the fourth day of life, followed by reestablishment of enteral nutrition by day 5. She was fed exclusively on formula milk from birth. An MRI performed on day 5 showed signs of severe hypoxic-ischemic encephalopathy. Followup after discharge was very irregular and the infant did not receive any vaccines up until the current hospitalization episode. Her weight curve was a reason for concern; indeed, her weight two weeks before the current admission to hospital was 4390 g.
On the day of presentation, physical examination revealed an alert but irritable and ill-appearing infant with a temperature of 39.9°C, heart rate between 170 and 190 beats/min, respiratory rate between 40 and 80 breaths/min, blood pressure of 102/55 mmHg, and oxygen saturation by pulse oximetry of 100%. The child's weight at admission into hospital was 3990 g, meaning she lost 10% of the previous reported weight. The skin was pale grey, tenting skin turgor, dry lips and dry buccal mucosa, normal looking eyes but reduced tears, soft fontanele, and capillary refill time of 3 seconds. The urine output was also decreased. Heart and lung examination were normal except for tachycardia; the abdomen was swollen and slightly painful on palpation, no hepatosplenomegaly. Abdominal and thorax radiographs were normal. There were no signs of meningeal irritation. Laboratory tests showed hemoglobin 12.6 g/dL, white blood cells 11 970/mm3 (PMN = 7590), platelets 1 085 000/mm3, and C-reactive protein was less than 0.05 mg/dL (). Routine stool specimen tested positive for rotavirus antigen (Vikia Rota-Adeno, Biomerieux), whilst results for blood and urine culture were negative. Serum electrolytes were significant for a sodium concentration of 146 mEq/L and a bicarbonate level of 8 mEq/L. Blood urea nitrogen was 61 mg/dL.
The patient was admitted to the hospital and intravenous fluid therapy was promptly initiated to correct the infant's tachycardia, polypnea, and low blood pH, by attempting volume repletion with 2 subsequent doses of 0.9% sodium chloride at 20 mL/kg over 60 minutes. A solution containing dextrose 5% plus electrolytes was administered soon after the second dose of normal saline to attain the slow correction of hypernatremia. Diuresis was reestablished within four hours of rehydration therapy. Digestive losses of water and electrolytes were offset by oral rehydration solution (ORS), at an initial dose of 10 mL/kg and thereafter replaced volume per volume depending on the amount of stool losses. Enterol (yeast of Saccharomyces boulardii) was initiated as an adjuvant treatment to ORS. Metabolic acidosis was difficult to correct during the first 48 hours because of large liquid losses due to diarrhea. Despite the difficulties experienced to restore the electrolytic balance, the baby showed an outstanding digestive tolerance throughout the entire hospital stay, which allowed continuation of enteral nutrition with lactose-free formula milk (Novalac Diarinova).
At 24 hours after admission, hyperleukocytosis with neutrophilia and increased C-reactive protein in blood () prompted antibiotic treatment with ceftriaxone 100 mg/kg/day, which was suspended three days later due to negative bacterial culture results; stools were not tested for the presence of Clostridium difficile. Adjuvant treatment with gelatin tannate was initiated on the third day of hospitalization. Metabolic acidosis improved in the following 48 hours along with a substantial reduction in stool output. The baby was exclusively fed by oral route from the fifth day. The patient's history included also antiplatelet treatment (aspirin 5 mg/kg/day for one month) due to thrombocytosis.
Gelatin tannate was first administered in the afternoon of the third day of hospitalization, one sachet every 6 hours, five days after the start of diarrhea. The patient presented to hospital with a 2-day history of 10 watery stools a day, followed by a slight increase in the number of liquid stools during the first 4 days of hospitalization (). A considerable reduction of the total number of daily stools was registered in the first 24 hours after initiating antidiarrheal treatment with gelatin tannate, with four and three watery stools registered in the first 12 and 24 hours, respectively. The number and volume of stools continued to diminish substantially during the second day of treatment, with the diarrhea practically resolving by the third day of treatment with gelatin tannate (only three stools of almost normal consistency). Gelatin tannate was administered-dissolved in ORS, except for the first dose (dissolved in milk). The progress was favorable, however, the patient was discharged from hospital three days later in order to achieve optimum nutrition and to ensure vaccinations were up to date. Upon discharge from hospital the baby's weight was 4.640 kg.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.64, 'kg']}",18.56,17.632,19.488,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.64 kg. Hence, the patient's maintenance fluid is 4.64 kg * 4 mL/kg/hr = 18.56 mL/hr.
Hence, the patient's fluid maintenance is 18.56 mL/hr."
4484,22,Maintenance Fluids Calculations,physical,decimal,pmc-3263066-1,Extracted,"A 27-year-old man with end-stage kidney disease from chronic glomerulonephritis received a renal allograft from his mother in 2005 using prednisolone, cyclosporine and azathioprine, without induction therapy. During the immediate post transplant period, he received three intravenous pulses of methylprednisolone 1 g each daily for acute cellular rejection. He did not develop major infections till the current episode. His weight was 58 kg. He had stable graft function, with serum creatinine at 1.6 mg/dl and was on prednisolone 10 mg/d, azathioprine 100 mg/d and cyclosporine 175 mg/d, with the trough (C0) and 2-hour (C2) cyclosporine levels being 368 and 1280 ng/ml, respectively, at 6 months after transplantation.
Three years after transplantation, he presented to us with 4 months history of fever, weight loss of 16 kg in 4 months, episodic small volume diarrhea and diffuse abdominal pain with occasional hematochezia. He did not have pulmonary or other gastrointestinal symptoms. He discontinued cyclosporine 4 months prior to visiting our center. At presentation, he was on prednisolone (10 mg/d) and azathioprine (100 mg/d). On examination, his weight was 38 kg, and pulse rate, blood pressure, respiratory rate were normal. He was pale but did not have icterus or peripheral lymphadenopathy or allograft tenderness. He had a diffuse, ill-defined, firm, tender mass (9 × 7 cm) in the right hypochondrium. There was no hepatosplenomegaly or ascites.
Laboratory investigations revealed anemia (hemoglobin of 6.7 g/dl), a total leukocyte count of 4200/mm3, a normal platelet count and serum albumin of 2.2 g/dl. He had renal allograft dysfunction (serum creatinine of 3.1 mg/dl) with normal electrolyte profile and liver enzymes. His chest radiograph revealed an ill-defined minimal haziness in the right upper and midzones with minimal pleural effusion. Ultrasonogram of abdomen showed an intussusception mass measuring 7.1 × 5.0 × 10.1 cm in the right hypochondrium with a few enlarged mesenteric nodes and fat within and adjacent to it []. The renal allograft appeared normal. Computed tomogram (CT) scan of abdomen with rectal contrast revealed an ileocolic intussusception up to the hepatic flexure with multiple enlarged mesenteric nodes and mesenteric fat pulled into it []. The ascending colon was thick. The para-aortic, mesenteric and para-iliac nodes were enlarged and showed central necrosis.
The patient underwent an emergency exploratory laparotomy with resection of the ileocolic intussusception, the adjacent ascending colon and terminal ileum []. Histopathological examination of the ileocolic intussusception revealed fragments of a lymph node with extensive caseation necrosis and many acid-fast bacilli (AFB). The proximal polypoidal lesion of the intussusceptum and the mucosal ulcerations of the intussuscepient colonic segment revealed dense inflammatory infiltrates of lymphocytes and plasma cells, along with microabscesses in the submucosa and lamina propria, transmural granulomas with epitheloid histiocytes, lymphocytes; Langhans type multinucleated giant cells and central foci of caseation [Figure and ]. Long, curved and beaded AFB, morphologically typical of Mycobacterium tuberculosis (MTB), were detected in all the above-mentioned lesions [].
On the first postoperative day, the patient received hydrocortisone 100 mg thrice daily, but azathioprine was discontinued due to leukopenia (WBC count 1900/mm3). He received granulocyte colony stimulating factor for leukopenia. On the second postoperative day, he was weaned off mechanical ventilation. On the fourth postoperative day, he received ATT with isoniazid 300 mg/d, rifampicin 450 mg/d, pyrazinamide 750 mg/d and ethambutol 400 mg/d. On the fifth postoperative day, 36 hours after starting ATT, he developed tachycardia, tachypnea, hypotension, oliguria and worsening of pulmonary oxygenation [partial pressure to inspired fraction of oxygen ratio (P–F ratio)]. The chest radiograph revealed worsening of the preexisting haziness. However, there was no bacteremia or evidence of invasive fungal infection.The total leukocyte count had remained about 4500 cells/mm3 during this period. His condition subsequently worsened, and he received broad-spectrum antibiotics (piperacillin with tazobactam) while routine cultures remained sterile. A tracheal aspirate showed numerous AFB morphologically typical of MTB, though there was no growth in culture. In addition, tracheal aspirate grew mixture of non-fermenting gram negative bacilli and Candida glabrata, which were probably contaminants. He continued to develop worsening features of a systemic inflammatory response syndrome, lung infiltrates, and disseminated intravascular coagulation. Steroids were continued, antibiotics were changed empirically to meropenem with teicoplanin and liposomal amphotericin B. The patient died on the 11th postoperative day. The next of kin declined post-mortem examination.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [38.0, 'kg']}",78,74.1,81.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 38.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (38.0 kg - 20 kg) = 78.0 mL/hr.
Hence, the patient's fluid maintenance is 78.0 mL/hr."
4485,22,Maintenance Fluids Calculations,physical,decimal,pmc-6967328-1,Extracted,"A 68-year-old man (165 cm, 74 kg) was scheduled for transurethral resection of a bladder tumor using 5-ALA. He had been receiving amlodipine 5 mg and azilsartan 20 mg every morning orally for hypertension. His blood pressure was maintained around 130/70 mmHg. Since he had been diagnosed with pyogenic spondylodiscitis in the fourth/fifth lumber disk region in his forties, general anesthesia was preferred. During the pre-operative examination, chest X-ray, electrocardiogram, and laboratory test findings were normal.
The patient took only amlodipine besylate on the morning of the surgery. Three hours before anesthesia induction, 5-ALA 20 mg/kg (Alaglio, Chugai Pharmaceutical, Tokyo, Japan) was administrated orally. Just before anesthesia induction, the patient’s blood pressure was 98/61 mmHg and his heart rate 82 beats/min. Anesthesia was induced with propofol 100 mg, rocuronium 50 mg, fentanyl 100 μg, and remifentanil 0.4 μg/kg/min. After 5 min, just before tracheal intubation, his blood pressure decreased to 47/32 mmHg. There were no observed changes in his electrocardiogram, such as ST-T changes or arrhythmia. Although we used phenylephrine at a total dose of 0.2 mg and ephedrine at a total dose of 10 mg over 10 min, hypotension persisted at 50/33 mmHg. Wheezing and erythema were not observed. Administration of 100 mL hydroxyethyl starch bolus for a few minutes was unsuccessful in increasing blood pressure. Transthoracic cardiac ultrasonography revealed normal systolic function, no asynergy, and normal size of the inferior vena cava. Bolus administration of noradrenaline at a total dose of 30 μg over 6 min slightly increased blood pressure to 65/39 mmHg. Arterial blood gas analysis revealed the following: pH, 7.350; HCO3− concentration, 23.2 mmol/L; base excess, 2.3 mmol/L; and lactate concentration, 1.7 mmol/L. Following this, bolus administration of adrenaline at a total dose of 30 μg over 9 min elevated the blood pressure from 53/26 to 127/49 mmHg. We decided to perform surgery under continuous administration of adrenaline. Anesthesia was maintained with sevoflurane and remifentanil. The patient’s blood pressure and heart rate ranged from 72/31 to 94/40 mmHg and from 70 to 85 beats/min, respectively, under the administration of adrenaline at 0.01–0.07 μg/kg/min. On completion of the surgery, he was transferred to the intensive care unit under intubation. Twelve minutes after admission to the intensive care unit, he was extubated as his blood pressure had stabilized at 142/56 mmHg under the administration of adrenaline at 0.03 μg/kg/min. Ten minutes after extubation, adrenaline infusion was discontinued. Although his lactate concentration was 5.3 mmol/L at this time, it decreased to 2.7 mmol/L after 3 h. His blood pressure and heart rate were stable during his intensive care unit stay. The patient was then transferred to the general ward on day 1 postoperatively. He was discharged without any complications 6 days postoperatively. Three months later, dermatologists performed a skin-prick test on him for propofol, rocuronium, and 5-ALA, the results of which were negative. Five months later, he received TUR-Bt under general anesthesia without 5-ALA for recurrence of tumor. Although we used propofol and rocuronium, severe hypotension did not occur.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [74.0, 'kg']}",114,108.3,119.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 74.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (74.0 kg - 20 kg) = 114.0 mL/hr.
Hence, the patient's fluid maintenance is 114.0 mL/hr."
4486,22,Maintenance Fluids Calculations,physical,decimal,pmc-7233891-1,Extracted,"A 50-year-old male patient was admitted to our hospital with progressive dyspnea, cough, and cold sweats. He mentioned night sweating for a year and 15 kilograms weight loss. His medical history stated a human immunodeficiency virus (HIV) infection since 2003, with a double-sided pneumonia with Pneumocystis jirovecii (among other pathogens) at admittance, therefore diagnosed as acquired immunodeficiency syndrome (AIDS). Patient was treated with antiretroviral therapy with an undetectable viral load in 2012, but had stopped taking medication 1 year ago. He lived in a homeless shelter with his wife (who was also HIV positive); his children were accommodated elsewhere. There was no (intravenous) drug or alcohol use, and he had quit smoking 15 years ago. Physical examination on admission showed a non-acutely ill patient, tachypneic with an oxygen saturation of 88% on room air. His blood pressure was 130/80 mm Hg, heart rate 132 per minute, and temperature 38.2°C. Percussion of the lungs did not reveal any dullness, and at auscultation normal breath sounds were heard except for the left lower side. Other physical examination was unremarkable.
Relevant laboratory results on admission were hemoglobin 7.2 mmol/L, white blood cell count 6.6 × 109/L, platelets 214 × 109/L, and C-reactive protein (CRP) 64 mg/L. There was no renal or hepatic insufficiency. Immunology results were as follows: CD4: 0.039 × 109/L, CD8: 1.2 × 109/L, CD4/CD8 ratio: 0.033. A chest X-ray showed bilateral “cloudy” infiltrates.
The patient was treated according to the local sepsis protocol, with gentamicin 280 mg and amoxicillin/clavulanic acid 1200 mg intravenously in the emergency room. This was followed by cotrimoxazole (3 × 1920 mg) and prednisolone (2 × 40 mg) the next day for suspected PJP. Two days after admission, a bronchoscopy with bronchoalveolar lavage (BAL) was performed to confirm the diagnosis. Directly after this procedure, the patient became dyspneic, had low oxygen saturations (82%), and developed subcutaneous emphysema. Due to progressive respiratory insufficiency, endotracheal intubation and mechanical ventilation were necessary. Bronchoscopy-guided intubation was performed in the operating theater, which was uneventful. A computed tomography (CT) scan of the chest immediately after intubation showed subcutaneous and mediastinal emphysema without pneumothorax. Also, severe air bronchograms and bilateral infiltrations were seen. Patient was admitted to the intensive care unit (ICU) afterward.
During the (ventilatory) treatment on the ICU, the subcutaneous and mediastinal emphysema increased, resulting in swelling of the entire face, arms, and torso down to the scrotum (). Several bronchoscopies were performed to exclude tracheal injury that could have occurred during the BAL, but no injury was visualized. Despite efforts to treat patient with lung protective ventilation, using low tidal volumes and low airway pressures, the emphysema continued to increase. A new CT scan was performed 1 week after admission to the ICU, showing severe subcutaneous and mediastinal emphysema (). Treatment of the emphysema by skin incisions alone (“blow holes”) was considered but discarded due to the high HIV viral load (700,000 copies/mL) of the patient and the fear of viral spreading by blood spatters. Because of the severity and increase of the symptoms and no obvious tracheal injury (on subsequent bronchoscopies and CT scans), a search for other treatment options was performed. After elaborate consideration, it was decided to make two infraclavicular skin incisions and place VAC therapy on these incisions (ActiV.A.C., KCI Medical, –125 mm Hg; ). While the subcutaneous emphysema started to improve significantly, a gradual clinical improvement was seen in the first week. VAC therapy was ended 9 days after initiation. The subcutaneous emphysema continued to decrease after removal of the VAC therapy system.
During his stay on the ICU, inflammatory markers decreased together with the pulmonary infiltrations on the chest X-ray, implying adequate treatment of the PJP. Patient was extubated after 17 days of mechanical ventilation, with a significant ICU-acquired weakness. Furthermore, dysphonia was reported, possibly caused by emphysema of the larynx. The patient was discharged to the general ward 25 days after admission to the ICU. Antiretroviral medicine was restarted, and patient was finally discharged to a medical rehabilitation center for further recovery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15.0, 'kg']}",50,47.5,52.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.0 kg - 10 kg) = 50.0 mL/hr.
Hence, the patient's fluid maintenance is 50.0 mL/hr."
4487,22,Maintenance Fluids Calculations,physical,decimal,pmc-6191573-1,Extracted,"A 55-year-old man, with severe left main coronary artery disease (CAD), and with short stature (150 cm height) and 76 kg weight, was referred to our center for coronary artery bypass grafting (CABG). The patient scheduled for off-pump CABG (OPCAB).
Due to unstable hemodynamic condition, an IABP catheter (Datascope, procure, state, dual lumen, 9.5F, 34 ml, Datascope Inc., Montreal, NJ, United States) was inserted percutaneously through the right femoral artery, and was attached to the Datascope system via a console. Immediately after device insertion, with a counter pulsation and 100% augmentation, and a ratio of 1:1, the systolic blood pressure increased up to 90 mmHg, and urine output increased.
The patient underwent an OPCAB operation using conventional grafts such as the left internal thoracic artery and saphenous vein grafts. Following the extubation, urine output was decreased that managed by diuretic and fluid therapy. Although, laboratory examination showed abrupt increasing of the following test: blood urea nitrogen (BUN): 70 mg/dl, creatinine (CR): 1.6 mg/dl, aspartate transaminase (AST): 80 IU, alanine aminotransferase (ALT): 70 IU, and acetate dehydrogenase (LDH): 350 IU. AST, ALT, and LDH values elevated seriously to 1200, 3500, and 5500 IU, respectively. The BUN and creatinine also increased to 80 and 2.1 mg/dl, respectively. The mean elevation of total bilirubin was also noted (total bilirubin: 2.5 mg/dl).
The distension caused the failure of Doppler to reveal the condition of portal and liver venous and arterial flow blood flow, but showed the reduction of renal arterial blood flow. However, in a thoracic X-ray catheter’s tip was not detected, and an abdominal X-Ray showed that the balloon pump catheter’s tip was displaced distally; uncovering of catheter dressing in right thigh revealed loosing of fixation suture of catheter to the skin in its correct position ().
The improper mismatching of the IABP catheter size with the patient length may be another possible cause of the liver, renal, and mesenteric arterial malperfusion in this specific case. After IABP removal, the patient urine output was abruptly increased on the following hours. Then, the liver function tests, including ALT, AST, LDH, total bilirubin, and prothrombin time continued to reduce, and recovered drastically at the 10th day of catheter removal; liver function tests returned to normal value at time of hospital discharge, too.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [76.0, 'kg']}",116,110.2,121.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 76.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (76.0 kg - 20 kg) = 116.0 mL/hr.
Hence, the patient's fluid maintenance is 116.0 mL/hr."
4488,22,Maintenance Fluids Calculations,physical,decimal,pmc-8270611-1,Extracted,"An 8-month-old, 9-kg, and 70 cm-in-height male infant was diagnosed as congenital pulmonary airway malformation (CPAM) over left lower lobe and scheduled for lobectomy by Uniport VATS as the first case in this institution. After placement of regular monitors, anesthesia was inducted with thiamylal, fentanyl and atracurium, and the patient was then intubated with 5.0 mm uncuffed endotracheal tube. A 5 Fr Uniblocker tube (Fuji Systems Corporation, Tokyo, Japan) was inserted under the guide of a 2.0 mm-out diameter (OD) fiberoptic bronchoscope (Olympus America, Inc., Melville, NY) in the lumen of endotracheal tube. (Fig. ) The position of Uniblocker was checked by the bronchoscope to make sure the upper marker of the balloon was 1 to 2 mm just beneath the carina. (Fig. ) The balloon was gradually inflated with air until the breathing sound disappeared over left lung field. Two episodes of balloon dislodgement occurred before the surgical procedure per se, the first when changing position to the left decubitus position, and the second when inserting the surgical instrument into the port, presenting as oxygen desaturation and loss of corresponding lung collapse, respectively. In both episodes the position of Uniblocker was examined by bronchoscope and was adjusted inwards to the proper position. Then the surgical lung remained well collapsed all the time through resection of the left lower lobe, around 4 hours long. The ventilator was set at volume control mode with FiO2 100%, tidal volume 8 ml/kg, I.E. ratio 1:1.5, and respiratory rate 24 /min. End-Tidal CO2 was around 28 to 38 mmHg, and SpO2 was always above 97% during the rest course of one lung ventilation. At the timepoint when the surgeon stapled the bronchus, the bronchial balloon was deflated and the Uniblocker withdrawn into the tracheal tube to avoid incorporation with the surgical staple line.[ The whole surgical procedure was then finished smoothly, and two-lung ventilation was resumed, with a total one lung- ventilation period of 245 minutes and blood loss of 20 ml without blood transfusion. The Uniblocker tube was removed immediately after he was sent to the intensive care unit. The entotracheal tube was removed by the patient himself one day later, but was reinserted hours later for O2 desaturation. After 10 days of ICU care, the endotracheal tube was successfully weaned. Though subglottic tracheal stenosis occurred at 17 days, deemed to be due to tracheal re-intubation, this problem was solved by laser coagulation surgery, and he was discharged home on day 19 Table .","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [9.0, 'kg']}",36,34.2,37.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 9.0 kg. Hence, the patient's maintenance fluid is 9.0 kg * 4 mL/kg/hr = 36.0 mL/hr.
Hence, the patient's fluid maintenance is 36.0 mL/hr."
4489,22,Maintenance Fluids Calculations,physical,decimal,pmc-6202903-1,Extracted,"Male, 8-month-old patient, weighting 11 kg, living in the city of São Paulo (São
Paulo), was hospitalized in the pediatric emergency room presenting with laryngeal
inspiratory stridor associated with suprasternal notch and subdiaphragmatic
retraction, classified as severe (score 11) in the Westley’s scale (). He evolved to severe acute respiratory
failure, presenting respiratory frequency (RF) of 70 breaths per minute (bpm) and
heart rate (HR) higher than 200 beats per minute (bpm), requiring tracheal
intubation and being referred to the pediatric intensive care unit (ICU).
As personal history, the child was born in a C-section, at term, and was intubated
for 17 days in the pediatric ICU due to early respiratory distress. He presented
with tracheal extubation failure caused by high respiratory distress in that
hospitalization, evolving without intercurrences after that period.
In the pediatric ICU, dexamethasone (0.6 mg/kg/day) was introduced on the first day
of hospitalization, and the patient remained in mechanical ventilation, requiring
ventilator support: fraction of inspired oxygen (FiO2): 0.25; inspiratory
time: 0.79 seconds; RF: 30bpm; positive end expiratory pressure: 5 cmH2O;
pressure support: 14 cmH2O; pressure control: 16 cmH2O; and
current volume: 85 mL. He remained intubated, on midazolam (0.2 mg/kg/h) and
fentanyl (2 mcg/kg/h), without the need for vasoactive medication, remaining
clinically stable. Six days after hospitalization, flexible bronchoscopy was carried
out to assess the conditions of the mucosa before indicating extubation, since the
patient had been intubated for six days without signs of tracheal peri-cannula
ventilator escape. Bronchoscopy revealed “major mucosal edema, involving the
intratracheal cannula” (), so the
choice was to maintain the tracheal cannula, without progression of bronchoscopy
through the trachea. The infant was intubated, stable, on dexamethasone and
medication for sedation and analgesia. Seven days after bronchoscopy, he
demonstrated signs of escape through the tracheal cannula, shown by auscultation and
observed in the monitor of the ventilation equipment (Servo-i®, Maquet,
Rastatt, Germany). A new flexible bronchoscopy was carried out for the supervised
extubation. Bronchoscopy showed “larynx with discrete posterior wall edema, with
good mobilization of vocal folds and air escape between the tracheal cannula and the
larynx”.
For the programming of the tracheal extubation, a thoracic X-ray was performed and
did not show any abnormalities nor arterial blood gas (pH: 7.50; pO2: 120
mmHg; pCO2: 32 mmHg; sodium bicarbonate: 21 mEq/L; base excess: +1;
SatO2: 98%). Tracheal extubation was conducted and the use of nasal
oxygen catheter began, with 2 L/minute, presenting with mild laryngeal stridor, with
improvements after inhalation with one ampoule of budesonide (0.25 mg). Forty-eight
hours after the extubation, the patient evolved to severe acute respiratory failure,
with major laryngeal stridor, vacillation of the wings of the nose, and increased HR
until 167 bmp, and RF of 39 bpm, indicating a new tracheal intubation. The choice
was to start support with high-flow nasal cannula (Optiflow Junior®,
Fisher & Paykel, Auckland, New Zealand) at 15 L/minute, FiO2: 25%, with
significant improvement in the respiratory situation, as well as reduced HR and RF
(). The infant was comfortable in
the high-flow nasal cannula, preventing tracheal reintubation.
The patient remained with the high-flow nasal cannula for nine days, and showed
improvements in high respiratory discomfort. There was a transition from the
high-flow nasal cannula to nebulization with oxygen at 2 L/minute for one more day,
being discharged to pediatric nursery in good clinical conditions.
Before discharge, since the patient presented with persistent laryngeal stridor, and
because of the previous history of intubation for 17 days, and extubation failure in
the neonatal period, a new flexible bronchoscopy was performed to investigate the
after-effects in the airways, showing “hyperemia of the larynx and subglottic region
with edema and granular surface”.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [11.0, 'kg']}",42,39.9,44.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 11.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (11.0 kg - 10 kg) = 42.0 mL/hr.
Hence, the patient's fluid maintenance is 42.0 mL/hr."
4490,22,Maintenance Fluids Calculations,physical,decimal,pmc-6966759-1,Extracted,"A 48-year-old man (height 168 cm, weight 80 kg) with gastric cancer was scheduled for laparoscopic gastrectomy. He was on maintenance dialysis for chronic renal failure. His medical history included coronary artery bypass grafting for angina. Blood tests were done a day before surgery and prior to maintenance hemodialysis showed mild hyperkalemia (serum K+ 5.4 mEq/L). Serum K+ was not rechecked after hemodialysis.
In the operating room, after placing a thoracic epidural catheter, we induced general anesthesia by intravenous administration of propofol 60 mg, fentanyl 100 μg, and rocuronium 70 mg. A central venous catheter was placed via the internal jugular vein. Anesthesia was maintained with oxygen (40 to 50%), air and desflurane (4 to 5%); and a continuous infusion of remifentanil (0.1–0.2 μg/kg/min). Bolus 1.5% lidocaine epidural infusion and intravenous fentanyl infusion were added as needed. Circulation was supported by continuous nicorandil infusion and bolus phenylephrine. In addition to standard monitors, continuous arterial pressure was monitored via the radial artery.
Surgery was performed in the reverse Trendelenburg position. An hour into surgery, his arterial blood gas (ABG) analysis showed hyperkalemia serum K+ =6.3 mEq/L (Table ). The patient had received K+ free infusion since arriving in the operating room until then. The cause for hyperkalemia was unclear at that point in time. In the surgical field, the liver was enlarged and had been retracted for optimal exposure.
ABG analysis during the third hour of surgery showed a further increase in serum K+ to 7.0 mEq/L (Table ). Hence, we initiated an infusion of 50% glucose at 5 mL/h with insulin at 0.2 U/h. As serum K+ remained high, we increased the ratio and volume of the infusion gradually to 50% glucose at 20 mL/h with 2 U/h of insulin. When the K+ level exceeded 7 mEq/L during the fifth hour of surgery, sodium bicarbonate (120 mg) was administered. We reported the hyperkalemia to surgeons and discussed to arrange an emergency postoperative hemodialysis. They did not report any abnormal changes that could be the cause of the hyperkalemia in the surgical field, including color changes to the liver. The K+ level continued to remain high despite remedial measures. From the eighth hour onwards, the lactate level also increased (Table ). The total surgical duration was 601 min, and anesthesia time was 743 min.
The patient received a total of 900 mL of normal saline and 500 mL of 5% albumin during the procedure. His estimated blood loss was 350 mL. The patient was hemodynamically stable throughout the operation, with no abnormal findings on electrocardiogram (ECG). After the conclusion of the surgery, the patient was extubated in the operating room and transported to the intensive care unit.
Immediate postoperative blood analysis showed a significant rise in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) (Fig. ), suggestive of liver damage, most probably due to intraoperative liver retraction. We initiated glycyrrhizin infusion for suspected liver damage. Serum K+ decreased marginally to 6.7 mEq/L (Table ) because of continuous glucose-insulin infusion, and thus an emergency postoperative hemodialysis was avoided. However, we resumed hemodialysis on the first postoperative day (POD 1). Serum K+ was 7.0 mEq/L (Table ) despite hemodialysis and so he received continuous hemodiafiltration from POD 1 to POD 4. Serum K+, AST, and ALT peaked on POD 1 and then improved gradually with the above treatment measures (Fig. ). However, the patient developed a high-grade fever (39 °C) on POD 5. Emergent computed tomography (CT) showed a low-density area in the left lobe of the liver (Fig. ), suggestive of hepatic infarction. Treatment with antibiotic agent was initiated for presumed infection of the infarcted liver. The patient responded well to treatment. He was discharged 27 days after surgery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [80.0, 'kg']}",120,114,126,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 80.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (80.0 kg - 20 kg) = 120.0 mL/hr.
Hence, the patient's fluid maintenance is 120.0 mL/hr."
4491,22,Maintenance Fluids Calculations,physical,decimal,pmc-8175873-1,Extracted,"Written informed consent was obtained from the parent. The patient was a 6.5-year-old boy with PRS (height 110 cm, weight 15.46 kg) who was admitted due to persistent leakage at the closure site after percutaneous endoscopic gastrostomy removal. He had a history of failed intubation and emergent tracheostomy at birth due to severe micrognathia and glossoptosis. Granular tissue removal at the tracheostomy site was performed due to subglottic fibrosis four months after tracheostomy. Micrognathia and repaired cleft palate were identified by physical examination.
We decided to use 3D printed airway modeling, because there was a possibility of difficult intubation and it was difficult to predict the appropriate endotracheal tube size. The open-source program InVersalius (InVersalius 3.0, Renato Archer Information Technology Center, Brazil) was used for 3D printed airway modeling and for the generation of .stl files, and the 3D airway model was printed using CreatBot (CreatBot F430, Henan Suwei Electronic Technology Co., Ltd., China). The 3D printed airway model did not reveal airway narrowing (), and simulation of endotracheal intubation was successful with an internal diameter (ID) 5.5 sized cuffed endotracheal tube (Hi-contour oral cuffed tracheal tube, Covidien, USA) ().
The patient had a small chin and his range of movement from ear to orbit was estimated to be over 120 degrees (). General anesthesia induction and intubation were planned with reference to the difficult airway algorithm described in the 2013 American Society of Anesthesiologists guidelines []. Before the induction of anesthesia, ID 4.5, 5.0, 5.5, and 6.0 cuffed and uncuffed endotracheal tubes were secured, and pre-emptive preparations were made for laryngeal mask airway, video laryngoscope (KoMAC video laryngoscope, KoMAC Co., Ltd., Korea), stylet, nasopharyngeal airway, oropharyngeal airway, and fiberoptic bronchoscope. Mask ventilation was possible after the administration of intravenous thiopental 75 mg, followed by rocuronium 10 mg. Successful endotracheal intubation was performed via video laryngoscopy with a #2 blade, a stylet, and an ID 5.5 cuffed endotracheal tube. Ventilation was performed after confirming the suitability of the endotracheal tube using a leakage test. There were no subsequent complications, and he was discharged on postoperative day 6.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15.46, 'kg']}",50.92,48.374,53.466,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15.46 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.46 kg - 10 kg) = 50.92 mL/hr.
Hence, the patient's fluid maintenance is 50.92 mL/hr."
4492,22,Maintenance Fluids Calculations,physical,decimal,pmc-7419066-2,Extracted,"A 5-year old male entire Suri Alpaca (V. pacos) weighing 80 kg was referred to the Royal Veterinary College for a left hind lateral claw removal, following a previous diagnosis of squamous cell carcinoma of the claw.
Pre-anesthetic examination was considered unremarkable. The patient was starved, a jugular catheter placed and premedication performed as for case 1. The induction was performed 10 minutes later, with 3 mg/kg ketamine (Ketamidor® 100 mg/ml, Chanelle Pharma Group, Loughrea, Ireland) IV followed by intubation with a 12 mm ID cuffed endotracheal tube. The patient was connected to a circle rebreathing system and anesthesia was maintained with isoflurane in oxygen and air (0.8 and 0.2, respectively). Hartmann’s solution was infused at 2 ml/kg/hour. The animal was monitored as described in case 1 except for BP, which was measured invasively via a 20 g IV catheter placed in the right auricular artery. Mechanical ventilation was initiated immediately following the start of volatile anesthesia, with tidal volume and respiratory rate adjusted to maintain normocapnia.
The SN block was performed as described in case 1, using 0.1 ml/kg (0.75 mg/kg) of ropivacaine (Naropin® 0.75%, AstraZeneca, Cambridge, UK). The patient was transferred to the surgical theatre where claw amputation was performed. General anesthesia lasted 1 hour and 40 minutes. During this time, the patient experienced mild hypotension with a mean arterial pressure of 60 mmHg. An IV bolus of 0.1 mg/kg ephedrine (Ephedrine Hydrochloride, Martindale Pharmaceuticals, Buckinghamshire, UK) was given, increasing mean BP to ~95mmHg. Further vasopressor administration was not required. No changes in HR, BP, or RR (suggestive of either sympathetic stimulation or nociception) were observed. The ETiso concentration ranged from 0.87% to 1.3% throughout.
At the end of the procedure, the patient experienced an uneventful recovery. Post-operative analgesia was provided with 0.01 mg/kg buprenorphine (Buprecare® 0.3 mg/ml, Animalcare, York, UK) IV every 8 hours and 0.5 mg/kg meloxicam (Metacam® 20 mg/ml, Boehringer Ingelheim, Berkshire, UK) IV once daily. The patient was standing, passing feces, and showing an interest in food 90 minutes following the end of anesthesia. Based on physical and behavioral assessment from a specialist farm animal clinician, pain was deemed to be well controlled. Buprenorphine was discontinued 24 hours later, while meloxicam continued at the same dose. Due to reduced interest in food 72 hours post-operatively, a blood sample was taken that showed an elevation in potassium (5.9 mmol/l; reference range 2.5–5.2), aspartate aminotransferase (1,114 U/l; reference range 175–340), creatine kinase (4,271 U/l; reference range 120–470), urea (23.5 mmol/l; reference range 2.5–8.9), and creatinine (411 umol/l; reference range 53–194). At this stage, the patient was anuric and renal insufficiency was suspected; however, attempted medical treatment with IV isotonic fluid and IV furosemide administration was unsuccessful. Euthanasia was performed 6 days following surgery.
Post-mortem examination revealed reddened ileal and caecal mucosa, with fluid large intestinal contents. A moderate volume of serosanguineous peritoneal fluid was also present. On histopathology of the kidney, muscle, and liver, no signs of rhabdomyolysis were observed; however, changes were consistent with disseminated intravascular coagulation. This was likely secondary to bacterial toxins originating from the intestines. Renal insufficiency was most likely secondary to these findings.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [80.0, 'kg']}",120,114,126,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 80.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (80.0 kg - 20 kg) = 120.0 mL/hr.
Hence, the patient's fluid maintenance is 120.0 mL/hr."
4493,22,Maintenance Fluids Calculations,physical,decimal,usmle-3275,Extracted,"A previously healthy 14-year-old girl is brought to the emergency department by her mother because of abdominal pain, nausea, and vomiting for 6 hours. Over the past 6 weeks, she has also had increased frequency of urination, and she has been drinking more water than usual. She has lost 6 kg (13 lb) over the same time period despite having a good appetite. Her temperature is 37.1°C (98.8°F), pulse is 125/min, respirations are 32/min, and blood pressure is 94/58 mm Hg. She appears lethargic. Physical examination shows deep and labored breathing and dry mucous membranes. The abdomen is soft, and there is diffuse tenderness to palpation with no guarding or rebound. Urine dipstick is positive for ketones and glucose.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.0, 'kg']}",24,22.8,25.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.0 kg. Hence, the patient's maintenance fluid is 6.0 kg * 4 mL/kg/hr = 24.0 mL/hr.
Hence, the patient's fluid maintenance is 24.0 mL/hr."
4494,22,Maintenance Fluids Calculations,physical,decimal,pmc-5579860-1,Extracted,"A 6-month-old, 3 kg boy presented with resting tachypnoea and diaphoresis while feeding and failure to thrive. The heart rate (HR) was 160/min and blood pressure (BP) was 90/60 mmHg. No murmur was present. Electrocardiogram (ECG) showed T-wave inversion in lead II, III and AVF and chest radiograph showed significant cardiomegaly.
Transthoracic echocardiography revealed retrograde flow in LMCA draining into the PA. There was dilatation of left atrium and ventricle with Grade II mitral regurgitation (MR). There was severe left ventricular (LV) dysfunction with ejection fraction (EF) of 20%. Since the diagnosis was clear, cardiac catheterisation and angiography were not done. His medications included digoxin, spironolactone and ramipril.
The child was taken to operating room, where non -invasive monitors such as 5 lead ECG, Pulse oximetry and non-invasive BP (NIBP) were attached. BP was 90/50 mmHg, HR was 135/min and SpO2 was 100%. There was no evidence of ischaemia on ECG. General anaesthesia was induced with intravenous (iv) injection ketamine (2 mg/kg), followed by iv injection fentanyl (2 μg/kg) and iv injection atracurium (0.5 mg/kg) and the trachea was intubated with 4.0 mm cuffed endotracheal tube (CETT). The femoral artery was cannulated for invasive arterial BP monitoring, and the right internal jugular vein was cannulated for central venous pressure monitoring. Anaesthesia was maintained with isoflurane and intermittent fentanyl.
The ventilatory settings were aimed to prevent hypocarbia, hyperoxia and alkalosis. An FiO2 of 0.5 was targeted to maintain normoxia, with a PaO280-100mmHg which was used to maintain pulmonary vascular resistance (PVR). End-tidal carbon dioxide was maintained between 40 and 45 mmHg. Re-implantation of the LMCA was performed under cardiopulmonary bypass (CPB). During weaning from CPB, dopamine (5 μg/kg/min) and milrinone (0.33 μg/kg/min) were started. Patient remained haemodynamically stable throughout the perioperative period. The child was ventilated for 24 h and discharged to ward on 5th post-operative day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.0, 'kg']}",12,11.4,12.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.0 kg. Hence, the patient's maintenance fluid is 3.0 kg * 4 mL/kg/hr = 12.0 mL/hr.
Hence, the patient's fluid maintenance is 12.0 mL/hr."
4495,22,Maintenance Fluids Calculations,physical,decimal,pmc-6461826-1,Extracted,"A 68-year-old man with 21-year history of type 2 diabetes presented with an ulcer on the left heel. Height was 162 cm; body weight was 69 kg; body mass index was 26.3. The patient had been diagnosed with lower extremity atherosclerotic obliterans 7 years earlier. The left lower limb has been numb for 6 years, with intermittent claudication and rest pain for 1 year. The patient reported that his sleep was affected, but his degree of pain was decreased with the intermittent use of analgesic agents. For the left lower limb with claudication, walking distance was 90 m.
The patient was hospitalized on 10 July 2017. Twenty days before hospitalization, irritation and pain developed on the lateral skin of the toes of the left foot, with no obvious inducement. Purulent exudate was observed after skin ulceration, and the patient’s body temperature increased to 39.5 °C. During hospitalization, the five toes of the left foot were black, necrotic, and associated with aggravated rest pain. Although the dose of oral analgesics was increased, the patient’s pain was not relieved, and his sleep was severely affected.
The patient’s appearance on initial evaluation is shown in Fig. a and b. The five toes of the left foot were almost entirely black and necrotic. The skin extending from the bottom of the foot to the 5th metatarsophalangeal joint was red and swollen, with obvious tenderness; skin temperature was normal. The muscles of the left foot had clearly atrophied; the skin was thin, bright, and hypertonic. Incision and drainage (approx. 5.0-cm long) was immediately performed between the 4th and 5th toes. Necrotic tissue, minimal purulent exudation, and limited bleeding were observed.
The diagnostic results on obtained on July 13 are shown.Secretion cultures displayed Pseudomonas aeruginosa and Staphylococcus aureus. X-ray film showed in Fig. c and d revealed no obvious destruction in foot bone. The lower limb computed tomographic angiography (CTA) is shown in Fig. e.
The magnetic resonance imaging (MRI) of the foot obtained on July 14th is shown in Fig. f and g. Subcutaneous inflammatory tissue in the lateral 5th humerus bone was confirmed as an infectious submerged cavity (Fig. ). The first incision performed at the bedside resulted in limited purulent exudation, as well as decreased local tension and reduced foot swelling. However, progressive necrosis of the skin margin was noted (Fig. a and b).
On July 17, basal therapy consisted in controlling blood sugar with insulin (58 units/day). The initial antimicrobial application of ceftazidime infusion (2 g, twice daily) was replaced by the sensitive drug Sulperazon (Cefoperazone Sodium and Sulbactam Sodium for Injection, Pfizer), according to the bacterial culture result of the secretion, and the application of antibiotics was stopped after July 22. The patient showed improved circulation and blood pressure. Treatment was maintained with protein and iron supplements.
On July 18th, interventional therapy was performed on the lower limb. The balloon was expanded in the superficial femoral artery, anterior tibia artery, iliac artery, and tendon. A thrombus had formed in the lower segment of the superficial femoral artery. The catheter for thrombolysis was left in place until July 20 (Fig. c, d, e and f). Skin temperature in the left foot increased, and swelling extended to the center of the foot. The amount of purulent exudation increased, as did pain and body temperature. The foot was therefore incised and drained, once more. Multiple subcavities were found (Fig. ).
On July 21st, we performed patella truncation and debridement on toes 4 and 5. The procedure was performed in the operating room, with the patient under sciatic nerve block. Results are presented in Fig. . Submerged cavities were filled with povidone-iodine gauze. The amount of nonviable tissue in the submerged cavity gradually decreased. The submerged space became shallow, and the granulation filled. All subsequent treatments were performed in the outpatient department.
From July 25th to September 30th, the left foot plaster was fixed at a functional position and applied intermittently (Fig. a, b, c, d, e and f). After October 1st, the plaster was removed. The patient was given diabetic shoes, and walking was guided. The first signs of wound healing were observed on November 19 (Fig. g, h and i).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [69.0, 'kg']}",109,103.55,114.45,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 69.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (69.0 kg - 20 kg) = 109.0 mL/hr.
Hence, the patient's fluid maintenance is 109.0 mL/hr."
4496,22,Maintenance Fluids Calculations,physical,decimal,pmc-6577310-1,Extracted,"The patient is a 33-year-old, 182-pound (83 kg) Caucasian female (weight range 162–183 pounds; BMI 24.6–27.4 kg/m2) who presented to us in 2017 after presenting with partial complex seizures, posterior cyclitis, inflammatory polyarthritis, photosensitive rash, painful nasal and oral ulcers, malar rash, recurrent pleuritic chest pain, Raynaud’s phenomenon, 103°F (39°C) fever, severe fatigue, thrombocytopenia, lymphopenia, non-nephrotic range proteinuria and positive ANA 1:320 homogeneous pattern. Further rheumatological workup disclosed positive chromatin antibody; renal biopsy showed non-specific immunoglobulin M mesangial deposits, and a previous mesenteric lymph node biopsy was consistent with reactive adenitis. Dermatological evaluation agreed with a diagnosis of acute cutaneous lupus lesions by physical examination. Initial treatment consisted of HCQ (two 200 mg tablets taken once a day for a total of 4.8 mg/kg/day), mycophenolate mofetil and intermittent intramuscular corticosteroid injections; she was already on antiepileptic therapy by her neurologist and her 25-hydroxy (OH) vitamin D level was greater than 40 nmol/L while taking ergocalciferol 50 000 IU weekly. Her flares decreased in severity and frequency with this regimen but incompletely. Recurrent steroid-responsive severe headaches with her flares ended up requiring moderate doses of prednisone to provide relief. After several months, subcutaneous belimumab was added 200 mg a week. She continued to have flares with cutaneous, joint and constitutional symptoms. A blood HCQ level was obtained via liquid chromatography coupled with mass spectrometry (testing by Exagen Diagnostics) showing a subtherapeutic level of 593 ng/mL (a therapeutic level is considered ≥1000 ng/mL per Exagen). The patient verbally insisted on close to 100% adherence to taking her HCQ, and a verbal conversation between her rheumatologist and pharmacist disclosed regular on-time refills from her pharmacy suggesting excellent adherence. It was noted that she had previously had RYGB surgery in 2009 for the treatment of morbid obesity, so the possibility of malabsorption of HCQ was considered, and her dose was increased to 200 mg three times daily dosing (for a total of 7.4 mg/kg/day). A repeat level 3 months later showed a significantly improved level of 1684 ng/mL while taking 200 mg three times daily. However, she developed central nervous system (CNS) lupus complications at this visit requiring changing her immunosuppressant therapy. Due to having a high HCQ blood level on 200 mg three times daily, her dose was again adjusted to 200 mg twice daily. A repeat HCQ blood level 3 months later was again lower at 520 ng/mL after which we increased her HCQ dose to 500 mg daily (6.7 mg/kg/day) subsequently resulting in a blood level of 1032 ng/mL 3 months later. During all HCQ blood measurements, she had normal renal function with an estimated glomerular filtration rate (eGFR) range of 64–118 mL/min/1.73 m2 (normal is >59 mL/min118 mL/min/1.73 m2) and she did not have protein malnutrition from her RYGB (her serum albumin and protein levels were normal).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [83.0, 'kg']}",123,116.85,129.15,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 83.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (83.0 kg - 20 kg) = 123.0 mL/hr.
Hence, the patient's fluid maintenance is 123.0 mL/hr."
4497,22,Maintenance Fluids Calculations,physical,decimal,pmc-4714619-1,Extracted,"A neonate born at term to a 26-year-old primigravida by elective cesarean delivery was diagnosed with an intra-abdominal cystic mass at 35th week of pregnancy. A conservative management plan was undertaken with repeated ultrasonographic evaluations every two weeks. The pregnancy, medical history of the patient and birth were unremarkable. A female full-term infant of 39+5 week of gestation was delivered with a birth weight of 4160 gram. Physical examination was unremarkable. Post-delivery ultrasonography revealed an anechoic uncomplicated cystic mass measuring 5x3.5 cm located in the right pelvis and another semi-solid complicated cystic mass was located in the left pelvis with a measure of 5.4x3.8 cm, without any vascular signal. Both ovaries were not identified.
Laparoscopy revealed brown round smooth cystic mass with a tiny stalk nearly amputated from the left fallopian tube in the left pelvis. A loop of intestinal segment also twisted around this calcified tiny stalk of the mass (Fig. 1). Right ovary was also twisted with the cystic mass (Fig. 2). The right ovary was untwisted 2 times (360 degree) and left in the pelvis after cyst aspiration without excision and ovarian fixation. Then the left ovary examined and seemed to be nearly amputated from the adnexa. It was removed after cyst aspiration. The calcified stalk was separated from the bowel. The post-operative period was uneventful and the patient was discharged on the 2nd post-operative day. Follow-up at 1 month with ultrasonographic evaluations showed an18 mm right ovary and no cyst.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4160.0, 'g']}",16.64,15.808,17.472,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4160.0 g so this converts to 4160.0 lbs * kg/1000 g = 4.16 kg. Hence, the patient's maintenance fluid is 4.16 kg * 4 mL/kg/hr = 16.64 mL/hr.
Hence, the patient's fluid maintenance is 16.64 mL/hr."
4498,22,Maintenance Fluids Calculations,physical,decimal,pmc-6485526-1,Extracted,"A 49-year-old Hispanic female with no significant past medical history presented to the emergency department with progressive dysphagia to liquids and solids and 40-pound unintentional weight loss over the last eight months. She denied a history of alcohol abuse, herbals, supplements or environmental exposures. Upon presentation, blood pressure was 99/57 mmHg and the pulse rate was 122/minute. On examination, she was cachectic, had 4 to 4+ power in all extremities, bilateral wrist swelling, bi-basilar crackles, and bilateral pedal edema. Her body mass index (BMI) was 22; her BMI one year ago was 30. Liver enzymes, a year prior to the presentation, were normal.
Labs were significant for blood urea nitrogen 7 mg/dL, creatinine 0.3 mg/dL, albumin 1.6 g/dL, total bilirubin 1.2 mg/dL, direct bilirubin 0.9 mg/dL, alkaline phosphatase 722 units/L, gamma-glutamyl transferase 958 units/L, aspartate aminotransferase 325 units/L, alanine aminotransferase 82 units/L, hemoglobin 10.3 g/dL, ferritin 2468 ng/mL, transferrin saturation 85%. Her creatine kinase (CK) was 55 units/L (normal range 0-163), aldolase 10.4 units/L (normal range < 8.1) and C-reactive protein was 1.71 mg/dL (normal range < 0.6). Antinuclear antibody (ANA), anti-Jo-1, and anti-topoisomerase I antibody were negative. There were no documented liver function tests prior to presentation. Computed tomography (CT) of the chest, abdomen, and pelvis revealed ground glass opacities involving bilateral lung apices and dependent portions of the lower lobes, consistent with aspiration pneumonia, and hepatomegaly with hepatic steatosis (Figures -). Anti-mitochondrial antibody assay, HFE gene mutation analysis, ceruloplasmin, viral hepatitis panel, alpha-1 antitrypsin level and anti-smooth muscle antibody assay were sent to evaluate the elevated liver enzymes and were negative. Magnetic resonance cholangiopancreatography (MRCP) did not reveal any biliary pathology. A bedside swallow evaluation revealed oropharyngeal dysphagia and X-ray of the hands revealed juxta-articular osteopenia (Figure ).
An ultrasound-guided liver biopsy revealed severe diffuse macrovesicular hepatic steatohepatitis involving 80%-90% of the liver parenchyma, mild intracanalicular cholestasis, prominent Mallory-Denk bodies within ballooning hepatocytes and bridging fibrosis on trichrome stain (Figures -). Neurologic electrophysiology studies showed normal nerve conduction, fibrillation and positive waves in all muscles and low amplitude motor unit action potentials in the majority of the muscles studied, particularly in the proximal muscles. In summary, it showed electrophysiologic evidence of a diffuse myopathy with features of muscle membrane irritability. A subsequent muscle biopsy revealed atrophic fibers with a perimysial distribution (as seen in Figure ), increased immunohistochemistry (IHC) labeling for major histocompatibility complex (MHC) 1 (as seen in Figure ), and capillary complement staining (as seen in Figure ), suggesting an autoimmune myositis. There were no features to suggest autoimmune hepatitis. Near the end of her hospitalization, she developed confusion, progressive hypoxia, and succumbed to multi-organ dysfunction.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [40.0, 'lbs']}",56.28736,53.47299,59.10173,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 40.0 lbs so this converts to 40.0 lbs * 0.453592 kg/lbs = 18.14368 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (18.14368 kg - 10 kg) = 56.28736 mL/hr.
Hence, the patient's fluid maintenance is 56.28736 mL/hr."
4499,22,Maintenance Fluids Calculations,physical,decimal,pmc-4173623-1,Extracted,"A 3 year 2 months old male child, weighing 13 kg, presented to the emergency with history of sudden coughing and chocking while eating apple at home about 2 h back. As per his parents’ version, there was difficulty in breathing following cough and gradual bluish discoloration of lips and fingers. The child was rushed from the emergency department to the emergency operation theatre, monitors attached and resuscitated with 100% O2 through the mask with Jackson-Rees modification of Ayre's T-piece in semi-recumbent position to correct hypoxemia as much as possible. The child was comatosed, dehydrated, with gasping breath and central cyanosis. Pulse rate was 168/min, respiratory rate was 44/min with SpO2 of 44% and decreased respiratory movement of the right chest. On auscultation breath sound was decreased with wheeze and crepitations in the middle and lower part of the right chest. Owing to the rapidly declining physical condition of the child, no investigation was done and the diagnosis was made on the basis of history and clinical findings. Intravenous cannulation done with a 22G cannula and intravenous (IV) fluid started with Ringer lactate.
Injection glycopyrrolate 0.01 mg/kg and injection hydrocortisone 5 mg/kg were given IV We planned to maintain spontaneous ventilation throughout the operative procedure and not to increase the peak inspiratory pressure to avoid the dislodgement of the FB from its place. Anesthesia was commenced with sevoflurane 1 vol.% by mask when saturation improved to 90% and maintained with sevoflurane. Pediatric fiberoptic bronchoscope was not available in the department. Initial attempt was made by ear, nose, and throat surgeon with adult rigid bronchoscope with the idea to make a tight fit on the glottic opening maintaining anesthesia through the same and to assess the position of the FB in the respiratory tract. But there was difficulty found in fixing it tightly and negotiating the grasper. Patient was desaturating too. As the SpO2 was gradually declining, child was immediately intubated with a 4.5 mm cuffed endotracheal tube (ETT) and maintained on spontaneous ventilation with sevoflurane, O2, and N2O. He was maintaining SpO2 at around 94%. A tracheotome was made at the level of 3rd and 4th tracheal cartilage [] and an adult rigid nasal endoscope (4 mm, 70°) was introduced through the tracheotome by the side of the ETT [] with risk of airway being compromised as part of fresh gas flow was leaking and part of it going to the left lung. FB was found in the proximal part of right bronchus and removed with the help of a crocodile forceps. The FB was in the form of a piece of apple, with its skin, of size of about 2 cm × 1 cm []. Extubation was done with proper tracheobronchial suctioning at the end of the procedure and a metallic tracheostomy tube (26Fr) was placed in the tracheotome.
Postoperative period was uneventful and the child recovered gradually. Moist O2 inhalation at 2 l/min was given for that night. Antibiotic, nebulization with salbutamol thrice daily and hydrocortisone 5 mg/kg IV were continued for 2 days. Paracetamol suppository 15 mg/kg was prescribed for analgesia. Tracheostomy tube was removed after 2 days and skin was closed by primary closure. A chest X-ray done after 2 days was found normal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [13.0, 'kg']}",46,43.7,48.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 13.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.0 kg - 10 kg) = 46.0 mL/hr.
Hence, the patient's fluid maintenance is 46.0 mL/hr."
4500,22,Maintenance Fluids Calculations,physical,decimal,pmc-8610462-1,Extracted,"A 73-year-old female was brought by emergency medical services (EMS) to the emergency department (ED) after a motor vehicle collision (MVC). She was driving when her car crashed into a streetlamp at 40 miles per hour. The EMS team reported that the pole intruded into the passenger compartment and the patient required a prolonged extrication. She had a Glasgow Coma Scale score (GCS) of 11 when EMS arrived at the scene, which improved to a 15 after repeated evaluations. She was conscious, alert, and oriented at the scene and during transport.
The patient had difficulty recalling the events before the collision. She remembered feeling “like I was having a panic attack” just before the crash, and she did not recall the car impacting the streetlamp. In the ED, she complained of substernal chest pressure. The patient’s history was limited due to her continued difficulty recalling the events of the accident. The patient’s son was contacted and he stated that she lives alone and is active and independent. He stated that she had experienced syncopal episodes over the last several years, all associated with paroxysms of panic when driving, and she had undergone extensive workups without any clear etiology identified. She had magnetic resonance imaging (MRI) of her brain with and without contrast four years prior for stroke-like symptoms after a syncopal event. Per his report, no abnormalities were found.
The patient had a past medical history of anxiety, migraines, Hashimoto thyroiditis, and hyperlipidemia. She had been diagnosed with breast cancer in 2012, which was treated with a left mastectomy followed by five years of tamoxifen and letrozole treatment. She had a family history of dementia, diabetes, and heart disease. She denied using tobacco, alcohol, or illicit substances. She was prescribed, and was taking, the following medications: levothyroxine 25 micrograms daily; atorvastatin 20 milligrams (mg) nightly; rizatriptan 10 mg as needed for headaches; and multivitamins.
On physical exam, the patient’s temperature was 36.5° Celsius, her heart rate was 92 beats per minute, and her blood pressure was 142/72 millimeters of mercury. She was breathing at a rate of 21 breaths per minute with an oxygen saturation of 98% on room air. She weighed 125 pounds and was 5 feet, 3 inches tall, with a body mass index of 22.1 kilograms per meter squared. She did not appear to be in any acute distress, was healthy appearing, and was oriented to her name, date, and location. Her head was normocephalic and atraumatic; she had no Battle sign, raccoon eyes, or other signs of trauma. She had hearing aids in place bilaterally. She had normal extraocular movements with equal pupils that were reactive to light. She had a cervical collar in place. Later, when it was safe to remove her collar, her neck had a normal range of motion without rigidity or pain.
On auscultation, her heart had a regular S1 and S2 at a normal rate and was without murmurs. She had normal pulses bilaterally. Her lungs were clear without wheezing or rhonchi, and she was noted to have normal effort without respiratory distress. Her abdomen was soft and flat, without tenderness or guarding. Her musculoskeletal exam showed an overall normal range of motion without deformities. She had no step-offs of the spinous processes or tenderness along the midline spine. The remainder of her skeletal exam only revealed tenderness over the left wrist. She had a capillary refill of less than two seconds. On her skin exam, she had minor contusions to the left upper chest near the axilla with superficial abrasions along the left wrist. She was not diaphoretic. Neurologically she had no cranial nerve deficits, with no motor weakness or sensory deficits peripherally. She had a normal gait and normal coordination as well. She could not recall her birth date and had slow verbalization with some word-finding difficulty. Psychiatrically, she was normal in mood and behavior.
Point-of care-ultrasound did not find evidence of free fluid within the abdominal or thoracic cavities and was negative for a pericardial effusion. Point-of-care ultrasound examination of her chest revealed normal lung sliding bilaterally. Chest radiograph showed no acute abnormalities. A radiograph of her pelvis showed no fracture or malalignment of the bones. A computed tomography (CT) of her head and brain showed no intracranial injury. A CT of the cervical spine and chest with contrast in the arterial phase was performed, which showed normal vertebral body height and alignment without fracture. The CT did show some mild atherosclerosis of the carotid and vertebral arteries, but no vascular injury and no obvious narrowing. Her trachea and mainstem bronchi were patent, she had no mediastinal abnormalities, the thoracic aorta was normal in appearance, and she had no pericardial effusion or pneumothorax ().
A CT of her abdomen and pelvis with contrast in the venous phase was also performed, which showed patent vasculature including a normal caliber aorta and inferior vena cava, normal appearing spleen, pancreas, adrenal glands and kidneys/ureters, a small hiatal hernia but otherwise normal appearing bowel, and no ascites or pneumoperitoneum. The radiologist did not find any fractures on her imaging or any soft tissue injuries. Initial laboratory studies (), laboratory studies after administration of intravenous fluids (), and the patient’s electrocardiograms (ECG) () are shown. A test was then performed and a diagnosis was made.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [125.0, 'lbs']}",96.699,91.86405,101.53395,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 125.0 lbs so this converts to 125.0 lbs * 0.453592 kg/lbs = 56.699 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (56.699 kg - 20 kg) = 96.699 mL/hr.
Hence, the patient's fluid maintenance is 96.699 mL/hr."
4501,22,Maintenance Fluids Calculations,physical,decimal,pmc-6311974-1,Extracted,"A 38-year-old man presented to an emergency department with progressive weakness and decreased urine output after having vomited up to 20 times per day over a period of 7 days. The patient was referred to our intensive care unit. Before medical consultation, he was healthy, and no other symptoms were reported. Diarrhea, fever, chills, or abdominal pain was absent.
Clinical examination revealed a patient of normal weight (height: 180 cm, weight: 70 kg). Blood pressure and heart rate were elevated (150/80 mmHg, 105/min); the respiratory rate was normal (13/min), but oxygen saturation was low (89%). During blood pressure measurement, a positive Trousseau sign was noted. The mucous membranes were dry, and the physical examination was otherwise unremarkable.
Arterial blood gas analysis revealed a metabolic alkalosis with partial respiratory compensation (pH: 7.71 [7.35–7.45], base excess: 40.5 mmol/l [-2-3 mmol/l], pCO2: 56.1 mmHg [32–45 mmHg], pO2: 43.5 mmHg [83–108 mmHg], bicarbonate: 72.2 mmol/l [21–26 mmol/l], lactate: 2.8 mmol/l [0.5–1.6 mmol/l], chloride: 52 mmol/l [98–106 mmol/l], sodium: 130 mmol/l [136–146 mmol/l], potassium: 2.4 mmol/l [3.5–5.1 mmol/l], ionized calcium: 0.77 mmol/l [1.15–1.29 mmol/l] and glucose: 165 mg/dl [70–105 mg/dl]).
Ultrasound revealed a distended and full stomach; the inferior vena cava was collapsing on inspiration. Otherwise, the ultrasound was unremarkable. The electrocardiography [] showed a prolonged QT interval (QTc 547 ms).
Laboratory tests were consistent with acute kidney injury (creatinine: 5.2 mg/dl, urea: 176 mg/dl); liver function tests, coagulation tests, albumin, lipase, procalcitonin, total calcium, hemoglobin, and thyroid-stimulating hormone were normal. Leukocytes were minimally elevated (11500/μl).
We suspected a prerenal acute kidney injury and a hypochloremic metabolic alkalosis due to gastric losses of HCl and fluids. Initial management consisted of oxygen therapy to correct hypoxemia and intravenous fluid therapy with normal saline and potassium chloride. Initially, a balanced crystalloid solution was infused, and later normal saline with KCl (40 mmol/l) was used because of the higher chloride content. Metoclopramide was administered to promote gastric emptying. To prevent further gastric losses of HCl, a proton-pump inhibitor was given. The patient was put on nihil per os for 24 h.
After 24 h, a total of 4.5 l of crystalloid fluid was infused. There was no further vomiting. A repeated bedside ultrasound revealed an empty stomach. The pH was corrected to 7.49, bicarbonate was reduced to 48.6 mmol/l, base excess was 23.4, chloride was 69 mmol/l, and potassium was still low at 2.8 mmol/l. There was hypoventilation with a pCO2 of 68.4 mmHg. We noted onset of diuresis. After 72 h of fluid therapy, the acid-base and electrolyte status was normal. Creatinine had decreased to 3.5 mg/dl. Small meals were tolerated.
Since there was no evidence of an infectious etiology for the excessive vomiting and the ultrasound had shown a distended stomach, an upper gastrointestinal endoscopy was performed []. A significant stenosis of the duodenum was diagnosed. Although there was no ulcer visible, an occult ulcer was deemed to be possible. A portal hypertensive gastropathy was diagnosed while esophageal varices were absent. Helicobacter pylori testing was positive, so an eradication therapy was initiated. A repeated endoscopy confirmed the stenosis, but again, no ulcer was seen. Since a focused abdominal ultrasound did not reveal the reason for the stenosis, a magnetic resonance imaging scan was performed to rule out malignancy such as pancreatic or gallbladder cancer or a thrombosis of the mesenteric vein. There was no evidence of malignancy or cirrhosis. An endosonography was done without evidence of malignancy or mesenteric vein thrombosis. At that point, the stenosis had partly resolved, and endoscopic passage was possible. We concluded that the temporary duodenal stenosis was caused most likely by portal hypertension of unknown etiology, and our differential diagnosis included idiopathic noncirrhotic portal hypertension after exclusion of cirrhosis and portal vein obstruction.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [70.0, 'kg']}",110,104.5,115.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 70.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (70.0 kg - 20 kg) = 110.0 mL/hr.
Hence, the patient's fluid maintenance is 110.0 mL/hr."
4502,22,Maintenance Fluids Calculations,physical,decimal,pmc-6099373-2,Extracted,"The patient was a 9-year-old girl who was the elder sister of the patient in case one. At 2 years old, the patient suffered from cyanosis and dyspnea after physical activity. She had clubbed-finger. When the patient was 4 years old, herchest HRCT revealed crazy paving pattern (Fig. A). Using results of a lung biopsy, she was diagnosed with chronic interstitial pneumonia at a local hospital and was prescribed corticosteroid. At 8 years old, she stopped taking corticosteroid. Her physical activity is normal for her age group.
The patient's height was 142 cm, weight was 29 kg, BMI 14.4. Her height and weight were both below the 75th percentile within her age group. Her oxygen saturation was 98% without oxygen supplementation. Pulmonary auscultation revealed no abnormalities. Clubbed-finger was present but not as notably as in her younger sister.
We used lung tissue obtained from her previous biopsy to perform a PAS stain which had a positive result. Her chest HRCT showed patches and nodular opacities on the apicoposterior of the left lung lobe, multiple cystic lucency in subpleural of both upper lobes (Fig. B) . Like her sister, the patient had a mutation in the SLC7A7 gene including C.1387 del C and IVS4+1C>T. Her Lung function tests showed FVC at 69% of predicted, FEV1 at 73% of predicted, FEV1/FVC at 110%, DLCO at 56% of predicted. Abdominal ultrasonography revealed diffuse enlargement of the liver and spleen. Blood ammonia was 60 umol/L (11-40). Serum ferritin was 568.98 ng/mL (10-120). Metabolic disease screening by blood testing showed Citrulline was 33.25 umol/L (2.7-38), Arginine was 1.87 umol/L (0-50), Citrulline/Arginine was 17.71 (<7). Increased lysine was shown through urine tests. The patient was also diagnosed LPI with PAP. We recommended she restrict protein intake then supplement with vitamins and calcium. She chosen not to inhale rGM-CSF due to economic reasons. Eighteen months later, her lung function test result showed FVC at 68.2% of predicted, FEV1 at 74.9% of predicted, FEV1/FVC at 111.1%, DLCO at 64.5% of predicted. Her chest HRCT showed no improvement compared to her condition at admission (Fig. C). Blood ammonia was 40 umol/L (11-40).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [29.0, 'kg']}",69,65.55,72.45,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 29.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (29.0 kg - 20 kg) = 69.0 mL/hr.
Hence, the patient's fluid maintenance is 69.0 mL/hr."
4503,22,Maintenance Fluids Calculations,physical,decimal,pmc-4420373-1,Extracted,"A 4-day-old, 1.7kg weight male neonate, born at term to a primigravida mother by normal vaginal delivery conducted by an untrained birth attendant, was brought with complaints of abdominal distension from D2 of life. There was no antenatal checkup or tetanus immunization, although the pregnancy and delivery was reported as normal. Although he had passed meconium on D1 of life, he had not passed any meconium for the previous three days. On examination, he was sick looking and had tachycardia (PR=160/min.) and tachypneic (RR=60/min.). Abdomen was grossly distended and tense. Hematological and biochemical investigations were normal. Abdominal X-ray showed massive pneumoperitoneum (Fig. 1). A clinical diagnosis of necrotizing enterocolitis Bell’s stage III was made. Keeping in view of the respiratory distress resulting from massive pneumoperitoneum, bilateral peritoneal drains were immediately put to deflate the abdomen.
On exploration few hours later, there was gross contamination of peritoneal cavity with meconium. There was a rent in anterior wall of rectum reaching up to the peritoneal reflection; rest of the gut was normal. During surgery, a pack of cotton wool pack was found in the rectal lumen. Congenital rectal atresia was ruled out by passing a Hegar dilator from below. A proximal diverting colostomy at the level of sigmoid colon was done. Multiple sero-muscular colonic biopsies were taken just proximal and distal to this colostomy. No attempt was made to repair the rectal perforation.
The postoperative period was uneventful. The colonic biopsies ruled out Hirschsprung’s disease. The relatives denied any knowledge about how rectal perforation could have occurred or who left the cotton wool pack in the rectum.
The child was lost to follow up for a year. Per rectal examination revealed that rectum was totally obstructed about 4cm from anal verge. Distal cologram showed complete obstruction of rectum. The rectal obstruction was only few millimeters thick and simulated like congenital rectal atresia (Fig. 1).
Transanal, end-to-end, rectorectal anastomosis (TERA) was done for the membranous acquired rectal atresia. The passage created was dilated over next six weeks and this was followed by closure of colostomy. Both the surgeries went uneventfully and the child has been doing well on two year follow up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1.7, 'kg']}",6.8,6.46,7.14,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1.7 kg. Hence, the patient's maintenance fluid is 1.7 kg * 4 mL/kg/hr = 6.8 mL/hr.
Hence, the patient's fluid maintenance is 6.8 mL/hr."
4504,22,Maintenance Fluids Calculations,physical,decimal,pmc-4254080-2,Extracted,"A 26-year-old nulliparous Caucasian woman at 38 weeks of gestation came to the obstetric emergency room complaining of complete blindness and headache. She had gained 30 kilograms since the beginning of her pregnancy and weighted 120 kilograms (BMI = 44). Until then, her pregnancy had been free of complications. Her blood pressure was 205/105 mmHg and she had severe peripheral edema. Laboratory exams showed high LDH (271 mu/mL) without any other anomalies. Arterial hypertension was only partially controlled by oral nifedipine with intravenous infusion of labetalol and magnesium sulphate. Cesarean section was performed. Because of the predicted difficult management of airways (full stomach, obesity, and El Ganzouri score 6) and since she had a normal state of consciousness, single shot subarachnoid anesthesia was chosen (12 mg of hyperbaric 0,5% bupivacaine at L4-L5 level). The anesthetic sympathetic blockade, combined with the ongoing antihypertensive treatment, was associated with good control of blood pressure and no hypotension. No anesthetic or surgical complications occurred. The neonate weighed 3.8 kg and presented Apgar scores of 9 at 1 minute, and 10 at 5 minutes, with arterial pH 7.2 and base excess −6 millimoles/L. Brain CT showed hypodense occipital lesions (). The patient was transferred to the ICU, where intravenous nitroprusside was started because of recrudescence of hypertension. Four hours after the Cesarean section, the blindness had resolved, but right facial droop and mild paresis of the right leg were observed. Pheochromocytoma and kidney dysfunction were excluded by abdominal CT and hormonal assays. Three days later she was discharged from the ICU with normal blood pressure controlled by oral antihypertensive therapy and normal neurological findings. MRI including T2 FLAIR and DWI performed 7 days later was normal (). Diagnosis of PRES was made on the basis of the reversibility of symptoms and of the radiological lesions. On the sixteenth day she was discharged from the hospital in good health with antihypertensive therapy. Placental examination showed chronic hypoxia, intimal hyperplasia of stromal vessels, and intervillous thrombus.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [120.0, 'kg']}",160,152,168,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 120.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (120.0 kg - 20 kg) = 160.0 mL/hr.
Hence, the patient's fluid maintenance is 160.0 mL/hr."
4505,22,Maintenance Fluids Calculations,physical,decimal,pmc-6681613-1,Extracted,"A nine-year-old 7-kg (15.4-lb) spayed female mixed breed dog (dog one) was examined for a 4 day history of vomiting, lethargy, and anorexia. On initial physical examination, a grade III/VI systolic heart murmur was detected with maximum intensity over the mitral valve region. A complete blood count (CBC) revealed unremarkable findings. A serum biochemical analysis revealed a normal total bilirubin (0.5 mg/dL; reference range 0.1-0.6 mg/dL) and elevations in alkaline phosphate (ALP) (435 U/L; reference range 13-240 U/L), alanine transferase (ALT) (1259 U/L; reference range 18-100 U/L) and cholesterol (375 mg/dL; reference range 130-354 mg/dL).
The patient underwent standard three-view abdominal radiography, which revealed a 1.1 cm x 0.6 cm oval-shaped mineral opacity in the right cranial abdomen superimposed with the proximal descending duodenum (). Transabdominal ultrasonography was also performed, and findings included multiple hyperechoic structures with acoustic shadowing within the common bile duct (CBD) at the distal-most aspect adjacent to the major duodenal papilla with the largest one measuring approximately 1 cm in diameter. The CBD was found to be markedly distended along its entire length, measuring up to 8 mm in diameter. The average diameter of the normal canine CBD is 3 mm []. The gallbladder (GB) was markedly distended and the wall appeared thick and irregular. The canine GB wall typically measures 2-3 mm in thickness and wall thickening of the GB is diagnosed when the wall is thicker than 3-3.5 mm []. The GB lumen contained a large amount of variably echogenic debris. The majority of the debris was non-organized and collected in the dependent portion while some appeared adhered to the wall and was partially organized suggestive of early mucocele formation.
Based on clinical signs, clinicopathologic findings, and results of diagnostic imaging, the primary differential diagnosis was partial obstruction of the extrahepatic biliary tract due to choledocholithiasis [, ]. The dog's clinical signs improved with supportive care of intravenous fluid therapy, maropitant (1 mg/kg, IV, q 24 hr), and buprenorphine (0.02 mg/kg, IV, q 8 hr), and an abdominal ultrasound was performed the following day revealing the common bile duct to be slightly less distended measuring 4-5 mm in diameter with the previously described choledocholiths in a similar location. The dog was discharged with medical management including ursodeoxycholic acid (7.7 mg/kg, PO, q 12 hr), amoxicillin-clavulanic acid (16 mg/kg, PO, q 12 hr), tramadol (6.5 mg/kg, PO, q 8-12 hours) and s-adenosylmethionine and silybin (30 mg/kg, PO, q 24 hr).
The dog represented to the emergency service 3 days later for icterus, anorexia, and lethargy. On physical examination, the dog now exhibited generalized icterus and marked discomfort was elicited on deep palpation of the abdomen. A serum chemical analysis revealed elevations in ALP (903 U/L; reference range 13-240 U/L), ALT (1250 U/L; reference range 18-100 U/L), aspartate aminotransferase (AST) (80 U/L; reference range 9-63 U/L), cholesterol (557 mg/dL; reference range 130-354 mg/dL), and total bilirubin (7.6 mg/dL; reference range 0.1-0.6 mg/dL).
Transabdominal ultrasonography revealed the GB and CBD to be markedly distended with the CBD measuring up to 8 mm in diameter. Several choledocholiths were noted within the lumen of the cystic duct and CBD (). The wall of the distal CBD was markedly thickened and hyperechoic, measuring up to 3 mm in thickness. The wall of the canine CBD is often partially visualized with ultrasonography and should not exceed 1 mm in thickness []. In addition, mild dilation of several intrahepatic bile ducts with intraluminal choleliths was noted. The variably echogenic, partially organized, and adhered debris within the GB lumen was unchanged compared to the transabdominal ultrasound performed 3 days prior. The decision was made to perform an immediate exploratory laparotomy due to the suspicion of complete extrahepatic biliary tract obstruction from choledocholithiasis. Echocardiography demonstrated mild mitral and tricuspid regurgitation with normal chamber sizes and a normal left ventricular systolic function. A coagulation panel consisting of prothrombin time (PT) and partial prothrombin time (PTT) was done prior to surgery and both values were within normal reference ranges.
General anesthesia was induced with administration of fentanyl (5.0 mcg/kg, IV), ketamine (2 mg/kg, IV), and propofol (4 mg/kg, IV) to effect. An endotracheal tube was placed, and anesthesia was maintained with delivery of sevoflurane in oxygen, with a constant rate infusion (CRI) of fentanyl (3 to 5 mcg/kg/hr, IV) and lidocaine (25 to 50 mcg/kg/min, IV) for analgesia. After standard aseptic preparation for surgery, and with the patient positioned in dorsal recumbency, a ventral midline incision was made for exploratory celiotomy. An enlarged liver, a moderately distended GB, and markedly dilated CBD were noted during abdominal exploration.
Multiple stones were palpated within the lumen of the common bile duct. An antimesenteric duodenal incision measuring 2 cm in length was made with a #11 blade distal to the externally visible junction of the CBD and duodenum, and the major duodenal papilla was visualized. The largest choledocholith was isolated within the lumen of the common bile duct, and a #11 blade was used to make a 1 cm incision into the CBD over the choledocholith. The 1 cm in length choledocholith was removed and the CBD was gently compressed dislodging multiple stones for evacuation. A five French red rubber catheter (Covidien Dover Rob-Nel, Medtronic Covidien, Minneapolis, MN 55432) was placed through the major duodenal papilla, bypassing the choledochotomy, and the cystic and intrahepatic bile ducts were flushed copiously with sterile saline. This process was repeated multiple times alongside massaging the GB, cystic ducts, and intrahepatic bile ducts to dislodge and remove any remaining biliary sludge and stones. The CBD incision was closed with a single layer closure using monofilament absorbable suture (size 4-0 polydioxanone (PDS II, Ethicon, Johnson and Johnson, Somerville, NJ 08876)) in a simple continuous pattern. The red rubber catheter was then sutured to the lumen of the duodenum with a simple interrupted pattern of monofilament absorbable suture (size 3-0 polydioxanone (PDS II, Ethicon, Johnson and Johnson, Somerville, NJ 08876)) to act as a stent. The duodenal incision was closed with a modified Gambee pattern using monofilament absorbable suture (size 4-0 polydioxanone (PDS II, Ethicon, Johnson and Johnson, Somerville, NJ 08876)). A guillotine biopsy of the left medial liver lobe was collected and submitted for histopathologic examination. Choleliths and liver tissue were submitted for aerobic and anaerobic culture. Several of the choledocholiths were submitted for quantitative analysis. The abdomen was then copiously lavaged with sterile saline and then closed routinely. Postoperatively, the dog was treated with ampicillin (30 mg/kg, IV, q 8 hr) for 3 days for suspected cholecystitis. Pain was managed postoperatively with a fentanyl CRI (2-5 mcg/kg/hr, IV) that was tapered over 72 hours of hospitalization.
Histopathological examination of the liver revealed moderate multifocal hepatic glycogenosis with biliary hyperplasia. No organisms were detected with aerobic and anaerobic cultures of the liver and gallbladder. Composite analysis of the collected gallstones revealed the largest calculus to have a surface layer composed of 100% calcium carbonate with a homogeneous interior composed of 100% bilirubin.
Four days postoperative, a serum biochemical analysis revealed persistent but improved elevations in ALP (440 U/L; reference range 13-240 U/L) and ALT (330 U/L; reference range 18-100 U/L). The dog's hypercholesteremia, hyperbilirubinemia, and elevated AST had resolved, but the albumin had decreased (1.6 g/dL; reference range 3.2-4.3 g/dL). The dog was transitioned from intravenous to oral analgesics which included acetaminophen (10 mg/kg, PO, q 8 hr) and codeine (1.5 mg/kg, PO, q 8 hr). The clinical signs at presentation had resolved, the dog was eating and subsequently was discharged on day 4 postoperatively. Follow up information was obtained from a phone conversation with the dog's owners. The owners did not report any return of clinical signs related to biliary obstruction in the 16 months since surgery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.0, 'kg']}",28,26.6,29.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.0 kg. Hence, the patient's maintenance fluid is 7.0 kg * 4 mL/kg/hr = 28.0 mL/hr.
Hence, the patient's fluid maintenance is 28.0 mL/hr."
4506,22,Maintenance Fluids Calculations,physical,decimal,pmc-3580361-1,Extracted,"A 3-week-old boy weighing 2 kg, presented with inability to open mouth, difficulty in feeding, and failure to thrive. Antenatal and family history was normal. Contrast enhanced computerized tomography had revealed near complete fusion of jaws with normal palate []. Neonate was not fit for any anaesthesia. He was examined in operational theatre and was found to have complete fibrinous fusion of both jaws except 3 mm slit opening at canine region and obliteration of gingivobuccal sulcus posteriorly []. They were released with bipolar cautery after spraying the local anaesthesia. He also had right partial lateral ankyloblepharon and was released with blunt dissection []. Manual manipulation gradually increases inter- alveolar opening to 20 mm []. Genetic work up and ophthalmic examination were normal. Post-operatively, mother was able to feed the baby well [].","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.0, 'kg']}",8,7.6,8.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.0 kg. Hence, the patient's maintenance fluid is 2.0 kg * 4 mL/kg/hr = 8.0 mL/hr.
Hence, the patient's fluid maintenance is 8.0 mL/hr."
4507,22,Maintenance Fluids Calculations,physical,decimal,pmc-7793194-1,Extracted,"A 23-year-old previously healthy male was transferred to our hospital after the onset of diaphoresis, generalized weakness, and inability to rise from bed. He endorsed 35 kg of weight loss over the prior 3 months and having had a high-carbohydrate meal the evening prior to presentation. The patient was not on medications prior to presentation and denied palpitations, heat intolerance, tremor, dyspnoea, oedema, anxiety, vision change, and change in bowel habit prior to presentation.
On exam, he was in moderate distress with a heart rate of 152 b.p.m., blood pressure of 89/56 mmHg, respiratory rate of 28 breaths per minute, oxygen saturation of 98% on room air, and temperature of 37.8°C. The patient had an otherwise unremarkable cardiovascular examination, including the absence of abnormal heart sounds, jugular venous distention, and lower extremity oedema. His lungs were clear to auscultation. The patient had moist mucous membranes and an enlarged thyroid but no evidence of exophthalmos, tremor, or ophthalmoplegia. He was found to have generalized weakness, predominantly in the lower extremities. Laboratory studies were notable for a potassium of 1.9 mEq/L (normal 3.7–5.2 mEq/L), an undetectable thyroid-stimulating hormone, and free T4 of 3.2 ng/dL (normal 0.6–1.2 ng/dL). Initial ECG demonstrated sinus tachycardia with prolonged QT interval (QTc 652 ms) and minimal ST-elevations in V1–V3 (, top panel). He was admitted to the medical intensive care unit (ICU).
His weakness improved following potassium repletion and fluid resuscitation, but his tachycardia persisted. A second ECG was obtained and notable for anteroseptal (V1–V4) ST-elevations and resolution of QT prolongation (QTc 401 ms) (, bottom panel). He denied chest pain or pressure. Troponin-I was elevated to 7.97 ng/mL (normal <0.04 ng/mL), trending upwards to 18.98 ng/mL.
Treatment was initiated with aspirin, ticagrelor, and unfractionated heparin infusion. He was unable to acutely tolerate beta-blockade due to hypotension. Urgent echocardiogram () revealed a severely dilated left ventricle [left ventricular end-diastolic volume index (LVEDVi) 114 mL/m2] with severely reduced systolic function [ejection fraction (EF) 23%] and global hypokinesis. No focal wall-motion abnormalities were present.
Following initiation of propylthiouracil, potassium iodine solution, and stress-dosed steroids, his tachycardia and ST-elevations improved. Computed tomography (CT) coronary angiography () 2 days after presentation demonstrated no evidence of coronary artery atherosclerosis or stenosis. Additionally, cine cardiac CT images of the heart showed normal left ventricular systolic function (, Videos S). Aspirin, ticagrelor, and heparin were stopped at this time due to a low concern for type I MI. Thyrotropin receptor antibodies returned positive, consistent with Graves’ disease. Ultrasound of the thyroid gland showed thyromegaly (right lobe volume 32 cc, left lobe volume 26 cc) with heterogenous parenchyma and increased vascularity, also consistent with Graves’ disease. Prior to discharge, the patient endorsed improved but persistent fatigue and dyspnoea with exertion. He continued to be free of chest pain and remained normotensive throughout the remainder of his hospital stay. The patient was discharged on methimazole in addition to guideline-directed medical therapy for heart failure, including lisinopril 2.5 mg daily and metoprolol succinate 25 mg daily. Up-titration of his lisinopril and metoprolol dosages were limited by borderline-low blood pressures. He appeared euvolemic throughout the hospitalization, so diuretics were not initiated. Mineralocorticoid receptor antagonists were not prescribed upon discharge due to borderline hypotension, as well.
At 2-month follow-up, the patient’s left ventricle remained severely dilated (LVEDVi 126 mL/m2) but with recovered systolic function (EF 65%) (). He had returned to normal activities without functional limitations. He was initially continued on lisinopril and metoprolol, but both were eventually discontinued over the course of several months given the patient’s recovered left ventricular systolic function and successful treatment of his hyperthyroidism. He remained on methimazole and was clinically euthyroid on follow-up visits.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [35.0, 'kg']}",75,71.25,78.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 35.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (35.0 kg - 20 kg) = 75.0 mL/hr.
Hence, the patient's fluid maintenance is 75.0 mL/hr."
4508,22,Maintenance Fluids Calculations,physical,decimal,pmc-8692788-2,Extracted,"A 16-month-old neutered male rabbit weighting 1,380 g was presented to the clinic for a gradual decline in appetite and reduced faecal output over 3 days. It was fed on a commercial pelleted diet, vegetables, and hay ad libitum with no dietary changes. The rabbit had been examined 3 days previously by another practitioner because of mild apathy and reduced faecal output. At that time, blood sample results showed normal WBC, heteropenia, lymphocytosis, hyperglycaemia, and hyperproteinaemia (). The rabbit was treated with an oral analgesic drug meloxicam at 0.4 mg/kg q12h (Meloxoral 1.5 mg/ml, Le Vet B.V., Oudewater, Netherlands) and a prokinetic itopride at 10 mg/kg q12h (Itoprid, Pro Med, Hradec Kralove, Czech Republic). Syringe-feeding with a recovery diet for herbivores was advocated.
Three days later, the rabbit was referred to the authors' clinic, where clinical examination revealed active to hyperactive behaviour, normal body condition (BCS 2.5/5), tachycardia, tachypnoea, skin tenting (estimated dehydration 5%), severe discomfort on abdominal palpation, a full stomach with a small amount of gas, a palpable tubular abdominal structure in the mid-abdomen, and a rectal temperature of 39.6°C. Blood analyses showed leucocytosis, lymphocytosis, monocytosis, hyperglycaemia, and hyperglobulinaemia (). Urine analyses showed pH of 7 (). Radiography and abdominal ultrasound revealed a reduced amount of chymus in the stomach and intestines (). The tubular structure had a wall thickness of 4.2 mm with a rounded, closed end and a multilayered wall characteristic of the intestinal tract (). These findings were suggestive of appendicitis.
Supportive treatment was started immediately and consisted of intravenous fluid therapy at 15 ml/kg/h (Ringerfundin, B. Braun, Melsungen, Germany) and a 5-ml bolus of 5% glucose, analgesic drug buprenorphine at 0.03 mg/kg i.m. (Bupredine Multidose, Le Vet Beheer B.V., Netherlands), a prokinetic drug metoclopramide at 1 mg/kg i.m. (Degan, Eurovet Animal Health, Bladel, Netherlands), an appetite stimulant pro toto at 2 ml (Catosal 10%, Bayer, Leverkusen, Germany), an antiulcer drug famotidine at 1 mg/kg i.m. (Quamatel, Gedeon Richter, Budapest, Hungary), a hepatoprotective drug at 0.1 ml/kg/pro toto (acidum methylphenoxypropionicum, Hepagen, Biopharm, Ždár, Czech Republic), and vitamin C at 30 mg/kg s.c. (acidum ascorbicum Biotika, Biotika Bohemia, Prague, Czech Republic). Meloxicam at 0.8 mg/kg s.c. (Meloxidolor 5 mg/ml, Le Vet Beheer B.V., Netherlands) was administered 4 h after the patient admission to the clinic, when it was stabilised with intravenous fluid therapy.
Anaesthesia was induced with medetomidine at 0.02 mg/kg i.m. (Domitor, Pfizer, Berlin, Germany) and ketamine at 3 mg/kg i.m. (Narkamon, Bioveta, Ivanovice na Hané, Czech Republic) followed by propofol at 0.3 ml to effect (propofol 1% MCT/LCT Fresenius, Fresenius Pharma Austria GmbH, Vienna, Austria). The rabbit was intubated using over the endoscope technique, and anaesthesia was maintained with isoflurane at 1.5–3% (Isoflurane Rhodia, Torrex Pharma GmbH, Wien, Austria). Continual intravenous fluid therapy with Ringerfundin was administered throughout the surgical procedure at a rate of 10 ml/kg/h. Perioperative monitoring consisted of observing respiration by close inspection of the thoracic wall, lung and heart auscultation, ECG monitoring, and pO2 (mean value of 99%) measurement using a pulse oximeter (Eickemeyer LifeVet® monitor, Eickemeyer, Tuttlingen, Germany) attached to the hind-limb fingers.
A standard midline laparotomy confirmed a presence of small amount of free fluid in the abdomen (~10 ml) and a thickened sacculus rotundus and a thickened processus vermiformis caeci (appendix) with miliary yellowish lesions visible in the wall of these structures (). All the vessels in the cecocolic fold were ligated (PDS 5-0, Johnson & Johnson Ethicon, Cincinnati, OH, USA), and the caecal body was transfixed with a suture and then transected to free the vermiform process (appendix). The appendix was resected, and the distal opening of the caecum was closed in two layers by an inverted suture pattern using polydioxanone PDS 5-0, Ethicon. The patency of the caecum was confirmed by gentle palpation of the suture between the thumb and index finger. Other perioperative findings included yellow colour of the mesenteric fat and mild splenomegaly. No signs of enteritis or pancreatitis were seen. After copious abdominal lavage with sterile saline warmed to 39°C, the abdominal wall was closed routinely using polyglactin 910 (Vicryl 4-0, Ethicon). The skin was stitched with a modified intradermal suture using polymer of glycolic acid (PGA Resorba 5-0, Resorba Medical GmbH, Nuremberg, Germany). Atipamezole at 0.15 mg/kg i.m. (Antisedan, Pfizer, Germany) was administered after surgery.
In the 4 h following surgery, the rabbit started to recover and did not show extreme pain on gentle abdominal palpation. Intravenous fluid therapy was continued, and analgesics (buprenorphine at 0.03 mg/kg i.m. q6h, and meloxicam at 0.8 mg/kg s.c. q12h) were given. To support intestinal motility, apart from metoclopramide, oral itopride at 10 mg/kg q12h (Itoprid, Pro Med, Czech Republic) and intravenous lidocaine at 100 μg/ml/h (Lidocaine Egis, EGIS Pharmaceuticals, Hungary) were also administered. The preoperative supportive treatment was continued for 6 days with fluid therapy. As antibiotics, a combination of marbofloxacin at 10 mg/kg i.m. q24h (Quiflox inj., Krka, Novo Mesto, Slovenia) and metronidazole at 20 mg/kg i.v. q12h (Entizol, Krka, Slovenia) was used. The rabbit was syringe-fed with recovery diet (EmerAid IC Herbivore, EmerAid, Cornell, IL, USA) and Supreme Science Recovery Plus, Supreme Petfoods, Ipswich, UK). It started to eat on its own and produce faecal pellets 2 days after surgery.
After 6 days, the patient was sent to home care with oral itopride at 10 mg/kg q12h, oral meloxicam at 0.8 mg/kg q12h, and oral marbofloxacin at 10 mg/kg q24h, for the next 10 days. Follow-up examinations at 10 days, at 1 month, and at 11 months after the surgery did not show any abnormal clinical or laboratory findings.
Samples of the appendix wall and its necrotic contents were sent for histopathological and bacteriological testing. Histopathological examination of the appendix wall revealed the same findings as in the previous case (). Aerobic culture and biochemical identification (MALDI-TOF Mass Spectrometry) () of the bacterial pathogens performed at the human-accredited laboratory identified the presence of pure culture of Klebsiella variicola sensitive to enrofloxacin, marbofloxacin, tetracycline, cefuroxime, trimethoprim sulphonamide, neomycin, and gentamicin and resistance to penicillin G, amoxicillin clavulanate, and bacitracin. Bacteroides sp. was isolated in low amounts and was sensitive to enrofloxacin, marbofloxacin, clindamycin, and metronidazole and resistant to tetracycline, trimethoprim sulphonamide, and penicillin G.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1380.0, 'g']}",5.52,5.244,5.796,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1380.0 g so this converts to 1380.0 lbs * kg/1000 g = 1.38 kg. Hence, the patient's maintenance fluid is 1.38 kg * 4 mL/kg/hr = 5.52 mL/hr.
Hence, the patient's fluid maintenance is 5.52 mL/hr."
4509,22,Maintenance Fluids Calculations,physical,decimal,pmc-2722014-1,Extracted,"An 8-month-old boy () was admitted to our emergency room because of repeated seizures. A seizure had occurred a day prior to this presentation. It persisted for 30 min, and his parents observed upward eyeball fixation and tonicclonic movement of the extremities. However, treatment was not sought at the time. At his home on the day of this hospitalization, a seizure redeveloped, persisted for about an hour and then spontaneously stopped. Several hours later the third seizure occurred and did not stop. His parents then brought the patient to our emergency room where the seizure was observed by doctors. Pupils were fixed without deviation with nictitating of eyelids, lip smacking, and stiffness of the right extremities. The seizure stopped after a diazepam injection. Subsequently, seizures were controlled by valproic acid administration.
The patient had no relevant birth or family history. At the time of hospitalization, his body temperature was 36.6℃, pulse rate 128/min, and respiratory rate 28/min. In terms of body measurements, his body weight was 8.8 kg (20th percentile), height 75 cm (90th percentile), and head circumference 51 cm (more than the 97th percentile). Anterior fontanel was soft and flat, and he had macrocephaly and a projecting forehead, similar to that observed in hydrocephalus. Breathing sounds were clear and heart beat regular. Liver and spleen were not palpable and bowel sounds were normal. Light reflex was isocoric and prompt, and deep tendon reflexes were increased. Babinski sign was unremarkable and both ankles showed clonus. He was unable to control his head, and his language and social skills were at the 1-2 month post-natal level.
The complete blood count was within normal limits, and total protein/albumin was 6.2/4.3 g/dL, Na/K/Cl 138/4.9/104 mEq/L, blood sugar 100 mg/dL, BUN/Cr 11/0.4 mg/dL, and AST/ALT 26/22 IU/L, respectively. Normal finding was seen by 7.93 (4.9-20.5 mM/M creatinine) in N-acetylaspartic acid (NAA) of urine. Brain MRI showed an absence of myelination except in the frontal lobe and in a portion of the temporal lobe (). DNA analysis revealed that the 716th base sequence of the 4th exon of the GFAP gene showed thymine substituted for guanine (c.716G>T), which led to R239L missense mutation at the 239th amino acid involving the replace of arginine by leucine. Additionally, when we examined the DNA of his parents and older sister, it appeared that they had a normal base sequence (). Interictal waking electroencephalography (EEG) showed slow waves in the frontal lobe, but no epileptic discharge ().
Three months later, at the age of 11 months, infantile spasms of the flexor type developed accompanied with vocalization after waking up. Interictal sleep EEG showed hypsarrythmia (). The spasms came under control after starting vigabatrin (40 mg/kg/day) and after the third day of this medication, no more spasm was observed. A follow-up MRI at 24 months of age showed disease progression ().
Now, at age 30 months (), he is in good nutritional condition and has a relatively good cardiopulmonary function. However, he suffers from intermittent vomiting, dysphagia, irritability, easy startling, developmental retardation, slow progressive spasticity of the extremities, and seizures.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [8.8, 'kg']}",35.2,33.44,36.96,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 8.8 kg. Hence, the patient's maintenance fluid is 8.8 kg * 4 mL/kg/hr = 35.2 mL/hr.
Hence, the patient's fluid maintenance is 35.2 mL/hr."
4510,22,Maintenance Fluids Calculations,physical,decimal,pmc-5437990-1,Extracted,"A 2-year-old previously healthy male of Albanian decent presented to the emergency room with cough. He was diagnosed with a viral upper respiratory tract infection and discharged home. Two days later, he returned to the emergency room with a worsening cough, productive of white sputum, shortness of breath, and fever. On review of systems, he was also noted to have decreased oral intake and several episodes of emesis. There were no known sick contacts. On exam, he was febrile, tachycardic, and tachypneic. He was noted to be pale and mildly dehydrated. Decreased breath sounds were appreciated over the right lung field. Initial labs were as follows: hemoglobin of 8.7 g/dL, hematocrit 28.7%, platelet count 474,000 g/dL, sodium 134 meq/L, potassium 3.8 meq/L, chloride 98 meq/L, HCO3 15 meq/L, BUN 21 mg/dL, creatinine 0.5 mg/dL, glucose 67 mg/dL, calcium 9.3 mg/dL. His urinalysis showed specific gravity 1.016, trace ketones, 30 mg/dL protein, trace blood, and urine microscopy showed 4 WBCs and 2 RBCs. Initial chest X-ray showed a right sided middle and lower lobe pneumonia and a small right sided pleural effusion. In the emergency room, the patient was given a dose of ceftriaxone, started on oxygen for increased work of breathing, given an IV fluid bolus of normal saline and admitted to the general pediatric floor.
His past medical history was significant for iron deficiency anemia diagnosed at 11 months of age; he had a normal hemoglobin electrophoresis at that time. Family history and social history was non-contributory. The patient has no known drug allergies. He was noted to have normal growth and development.
On hospital day 3, the patient was noted to have increasing respiratory distress. Repeat chest X-ray and a chest sonogram showed a large right sided pleural effusion with multiple thick septations. He was treated with vancomycin and ceftriaxone for management of empyema. Concurrently, his BUN and creatinine increased to 67 mg/dL and 1.6 mg/dL, respectively, and his hemoglobin and platelet counts both decreased to 3.2 g/dL and 23 × 103/µL, respectively. Lactic dehydrogenase (LDH) was 5,850 U/L, total bilirubin 2.1 mg/dL and direct bilirubin 0.8 mg/dL. The partial thromboplastin time (PTT) was prolonged to 60.7 seconds. The patient was transferred to the PICU for further care.
Pediatric hematology, nephrology, and transfusion medicine were consulted. The peripheral smear was notable for toxic granulation in the neutrophils, large platelets, burr cells, target cells, microspherocytes, and schistocytes. Antibody screen was negative but the direct antiglobulin test was positive with both IgG and polyspecific antisera. Anti-I was identified at 4 °C. The patient’s RBCs mixed with 5 randomly selected, AB0-identical, antibody screen negative, normal adult serum samples showed strong agglutination (4+). This is consistent with T-antigen activation. Lectin agglutination was not done. Analysis for other etiologies of atypical HUS, including testing for Factor H and CH50, were not sent as these studies are not readily available at our institution. ADAMST13 testing was not performed as there was a low clinical suspicion for thrombotic thrombocytopenic purpura.
Due to urgent transfusion need, washed RBCs were not initially available and the patient was given a RBC transfusion with a resultant increase in the hemoglobin from 3.2 g/dL to 5.5 g/dL. Forced-air warming was initiated in an attempt to keep the patient warm.
On hospital day 4, he became oliguric. This coincided with a peak in his BUN and creatinine to 103 mg/dL and 2.8 mg/dL, respectively. A temporary hemodialysis catheter was placed and continuous veno venous hemodiafiltration (CVVHDF) was initiated. A right sided chest tube was placed. Blood cultures and pleural fluid cultures taken at two separate times during the hospitalization were negative, but the urine Streptococcus pneumoniae antigen was positive. His hemoglobin again dropped to 3.7 g/dL. At this time, he was transfused with washed RBCs. The hemoglobin was noted to increase to 8.4 g/dL and the platelet count to 22 × 103/µL. Despite this increase, the patient had persistent hemolysis, and the hemoglobin again decreased to a low of 5.6 g/dL by hospital day 5. He was given an additional washed RBC transfusion with an increase in hemoglobin to 10.1 g/dL and an increase in platelet count from 18 × 103/µL to 32 × 103/µL.
On hospital day 6, it was decided to initiate plasmapheresis secondary to pHUS disease progression. The patient weighed 14 kg and was 101 cm tall. The total blood volume was calculated as 1,442 mL. Because of the patient’s size, washed RBCs were used to prime the COBE® Spectra for the PE procedure. The apheresis machine was primed according to the manufacturer’s instructions with normal saline and anticoagulant citrate dextrose A (ACD-A) and subsequently primed a second time with 0.5 U of RBCs. 5% albumin (~ 1 L per procedure) was used as replacement fluid. The ACD-A to whole blood ratio was 1 : 15. The access was a right internal jugular Shiley catheter. After the first PE, the hemoglobin increased to a high of 12.1 g/dL and then gradually decreased to 7.6 g/dL by hospital day 9. The platelet count gradually increased from 32 × 103/µL immediately following PE, to 68 × 103/µL by hospital day 9. At this time, it was decided to perform a second PE using the same prime and replacement fluid. The following day, the hemoglobin rose to 9 g/dL, and by hospital day 11, the platelet count increased to 166 × 103/µL.
The hemoglobin gradually decreased following the second PE to 5 g/dL on hospital day 16. The patient was transfused with washed RBCs, after which the hemoglobin remained greater than 9 g/dL until discharge on hospital day 24. The platelet count remained stable from hospital day 11 until discharge. On the day of discharge, the hemoglobin and platelet count were 10 g/dL and 429 × 103/µL, respectively. The two values remained normal on follow-up ().
With respect to his renal course, the patient was transitioned to intermittent hemodialysis on hospital day 6. He received a total of five hemodialysis treatments, his last treatment on hospital day 12. His creatinine on hospital day 12 was 3.3 mg/dL and declined to 0.4 mg/dL on hospital day 24. He went home on amlodipine for hypertension.
The chest tube was removed on hospital day 11. On hospital day 15, the patient had significant desaturations with a new oxygen requirement. A chest CT revealed a large air cavity representing a pneumatocele of the right lung base. His antibiotic regimen was changed to zosyn and vancomycin. On hospital day 16 he had a right thoracotomy and decortication and placement of two chest tubes. Chest tubes were removed by hospital day 18. The patient was discharged from the hospital 5 days later on augmentin to complete a 3 week course.
Three months following initial diagnosis of pHUS, the patient developed cholelithiasis and chronic cholecystitis and underwent a laparoscopic cholecystectomy. He has, otherwise, had no complications during a 10 month follow-up period.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [14.0, 'kg']}",48,45.6,50.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 14.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (14.0 kg - 10 kg) = 48.0 mL/hr.
Hence, the patient's fluid maintenance is 48.0 mL/hr."
4511,22,Maintenance Fluids Calculations,physical,decimal,pmc-3485087-1,Extracted,"A hitherto healthy 23-year-old Caucasian male student reported a history of several intermittent episodes of absence for over a year. According to his family, such episodes recurred every 2 months. During the episodes, he was conscious, but felt sleepy, his vision was blurred and he was unable to talk. In addition, he suffered one episode of concomitant jaw paralysis. These episodes happened most frequently upon awakening, but sometimes also late in the afternoon. The family had noticed that his symptoms improved continuously within 30 minutes of having eaten honey, sugar or fruits. Every episode was usually followed by headaches. He also mentioned a weight gain of 6kg over the past year. His physical examination was normal and a magnetic resonance imaging (MRI) and electroencephalogram with sleep deprivation failed to demonstrate any abnormality. However, never was the patient evaluated while symptomatic. He was referred to our endocrinology out-patient clinic to exclude a metabolic disorder. He had no family history of any metabolic or endocrine disorders.
In the meantime, his general practitioner taught the patient to self-monitor his capillary blood glucose levels. While completely asymptomatic, his fasting glucose levels ranged between 2.3mmol/L and 3.0mmol/L. None of the blood glucose measures was done during an episode of absence.
Laboratory findings on two different occasions revealed low venous fasting plasma glucose concentrations (2.6mmol/L and 1.6mmol/L) with high insulin (15.5mU/L and 55.3mU/L) and C-peptide (0.762nmol/L and 0.53nmol/L) levels. A 72-hour fasting test had to be stopped after 18 hours because of a glucose level of 1.8mmol/L and a mini-mental state score (MMSE) of 24 out of 30. After an intravenous injection of 1mg of glucagon, the glucose level increased to 4.7mmol/L and the MMSE to 29 out of 30. A plasma sulfonylureas screen test at the beginning and at the end of the fasting study was negative. Anti-insulin antibodies were negative. Insulin and C-peptide levels increased during the fasting test. These results confirmed our clinical suspicion of an insulinoma.
An abdominal computed tomography (CT) and MRI did not reveal any lesions. A subsequent somatostatin receptor scintigraphy (SRS) performed 4 hours and 24 hours after injection of 190MBq 111In-pentetreotide (OctreoScan®) showed a faint but definite, albeit discrete, focal abnormality at the junction between the head and body of the pancreas, compatible with an insulinoma (Figure ). Nevertheless, endoscopic ultrasound of the pancreas failed to confirm this finding. We decided not to perform selective intra-arterial calcium stimulation with hepatic venous sampling at this stage because we relied on the results of the SRS. We initially planned to complete the investigations by performing a glucagon-like peptide-1 (GLP-1) receptor scintigraphy to confirm the lesion found only on SRS. The patient, nonetheless, refused this supplementary imaging procedure. After a multidisciplinary discussion, a 111In-pentetreotide radio-guided surgery was performed. The day before surgery, the patient received 200MBq of 111In-pentetreotide and single-photon emission computed tomography (SPECT) CT, which confirmed the focal uptake located between the head and the body of the pancreas described above. During surgery, the nuclear gamma probe detected the increased uptake that was suspected to be the lesion within the head and the body of the pancreas, but intraoperative ultrasound failed to detect any morphological abnormality. Biopsies were undertaken in the area of this maximal signal intensity detected by the gamma probe. However, the frozen sections were not conclusive for an insulinoma. Metallic clips were put around the biopsy site and the abdomen was closed. Another SRS was performed 2 weeks after this first intervention and confirmed that the uptake was located between the surgical clips, exactly at the same location as it had been seen on the first SPECTCT. As the tumor was located deeper in the head of the pancreas, a pylorus preserving duodenopancreatectomy was performed after having obtained the patient’s consent. Macroscopic examination of the resection specimen identified no tumor. Microscopically, the lobular architecture of the exocrine pancreas was preserved and no ductuloinsular complexes were observed in any specimens. Some of the islets were enlarged and varied in size; some measuring 0.2cm and randomly scattered throughout the pancreatic parenchyma. The outlines of the islets were more irregular than normal (Figure ). A consistent finding in all specimens was the presence of multiple enlarged islet cells showing increased nuclear size with prominent nucleoli and clear cytoplasm (Figure ). There was no mitotic activity. The enlarged and irregular islets were highlighted with immunohistochemical staining by using antibodies against chromogranin and synaptophysin (Figure ). Approximately half of all cells within the pancreatic islets were stained with insulin (Figure ). By contrast, glucagon and somatostatin cells did not have any cytologic abnormalities. Insulin-positive cells were also scattered throughout the parenchyma. These features, combined with the clinical and radiological findings, are consistent with diffuse nesidioblastosis.
Noting that multiple endocrine neoplasia mutations were described in conjunction with nesidioblastosis, a menin gene mutation with polymerase chain reaction enzymatic amplification was performed and was found to be negative. Calcium, prolactin and insulin-like growth factor 1 levels were within normal values.
Postoperative recovery was complicated by a wound infection. Following surgery, the hypoglycemic episodes continued and a diffuse nesidioblastosis of the pancreatic distal body and tail was suspected. The patient’s diet was adapted to provide regular intake of carbohydrates, especially early in the morning, but the patient’s symptoms persisted. To avoid further pancreatic resection in such a young patient, a verapamil treatment was initiated (40mg twice daily, increasing up to 80mg three times daily, over 1 week). The patient, however, experienced severe headaches and palpitation after 3 weeks and stopped the medication. Diazoxide was then introduced; initially 100mg twice daily, increasing to 100mg three times a day, which resulted in a normalization of his glucose level with peaks of up to 7.2mmol/L. A 72-hour subcutaneous glucose monitoring testing, undertaken through a glucosensor (CGMS Sensor®), revealed normal glycaemia levels.
Four months after surgery, the patient experienced abdominal pain, more frequent stools (three times a day) and weight loss (1kg/week). Stool examination showed high fat levels of 89g per 24 hours (normal value 5g to 7g per 24 hours). Therefore, an enzyme substitution was initiated and dietary advice provided in order to treat the postoperative malabsorption.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.0, 'kg']}",24,22.8,25.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.0 kg. Hence, the patient's maintenance fluid is 6.0 kg * 4 mL/kg/hr = 24.0 mL/hr.
Hence, the patient's fluid maintenance is 24.0 mL/hr."
4512,22,Maintenance Fluids Calculations,physical,decimal,pmc-4532870-1,Extracted,"In the summer of 2013, the pediatric intensive care unit (PICU) of a hospital in Hong Kong received an 8-year-old boy with central hypoventilation with respiratory infection and decompensation en route to Hong Kong on a make-a-wish campaign. He was diagnosed with central hypoventilation (medullary atrophy) or Ondine's curse and had been well managed in Toronto, Canada. He was ambulatory, only needed home ventilatory support at night via tracheostomy, and inhaled salbutamol puffs on a prn basis, and he was on PEG (percutaneous endoscopic gastrostomy) feeding with puree food. Advanced fitness for air-travel arrangement was well negotiated with the respective commercial airline. However, he developed symptoms of respiratory infections with intermittent fever (up to 39°C), cough, and sputum for 2 days prior to departure. The child was seen at the emergency department of a children's hospital in Toronto and was treated with an oral course of cefuroxime. During the long-haul flight, symptoms of respiratory infections persisted and desaturations (86%) developed. The patient had his own oxygen monitoring and air compressor on board which needed to be increased to 1 L/min. On arrival in Hong Kong, he was taken to the emergency department. His vital signs were as follows: tympanic temperature 38.6°C, heart rate 157/min, and SpO2 98% on own ventilator with flow 1 L/min. The home ventilator's electric plug was in Canadian style and did not fit the Hong Kong standard socket. Chest radiograph revealed mild right sided haziness. He was admitted to PICU for management. He weighed 23.2 kg and his vital signs were as follows: temperature 36.5°C, heart rate 121/min, respiratory rate 23/min, BP 97/57 mmHg, and SpO2 97% in room air on arrival at PICU. The child received physiotherapy and the tracheostomy was temporarily connected to the ICU ventilator on SIMV mode with pressure control (PC) and pressure support (PS). Settings were FiO2 0.25, inspiratory time (Ti) 0.9 seconds, intermittent mandatory ventilation (IMV) rate 20/min, positive end expiratory pressure (PEEP) 5 cm H2O, pressure control 15 cm H2O above PEEP, and PS 13 cm H2O above PEEP. There was no further desaturation, and the settings were gradually reduced to IMV 10/min and FiO2 of 0.21. The child gave a history of drug allergy to Ativan (lorazepam) and gluten sensitivity. Sedation was not needed. He received a course of intravenous amoxicillin/clavulanate (30 mg/kg/dose, 8 hourly). The patient remained playful, talkative, and not in distress. Laboratory data were normal complete blood count with white blood cell count of 16.1 × 109/L, neutrophil differential of 77%, and elevated C-reactive protein of 44.1 (normal < 9.9 mg/L). There was no bacterial or respiratory viral isolation in the tracheal aspirate. Blood culture was negative. The patient was discharged from the PICU 2 days later and went on with his make-a-wish journey to Disneyland in Hong Kong prior to returning home.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [23.2, 'kg']}",63.2,60.04,66.36,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 23.2 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (23.2 kg - 20 kg) = 63.2 mL/hr.
Hence, the patient's fluid maintenance is 63.2 mL/hr."
4513,22,Maintenance Fluids Calculations,physical,decimal,pmc-3822031-1,Extracted,"The patient was a 34-month-old girl with a height of 90 cm and weight of 12.5 kg who was diagnosed with Lennox-Gastaut syndrome who was scheduled for surgical treatment of a lower lid epiblepharon. She was born by normal spontaneous vaginal delivery with a weight 3.52 kg at 38 weeks 6 days and there were no specific abnormalities in the antenatal exam. At the age of 40 days, she began to show signs of generalized tonic-clonic seizures. At that time, there were no abnormalities in her EEG and magnetic resonance imaging (MRI), but video-electroencephalographic monitoring showed lateralized to midline central, regionalized to central. Repeated EEG and MRI were normal and an epilepsy monitoring unit showed hypermotor seizures in the left frontotemporal and central regions.
She displayed developmental delay when compared to toddlers in the same age group. Because of the ataxia and muscle atrophy, she had been bedridden. Although she took antiepileptic drugs (AEDs), the tonic seizures persisted. As an additional treatment, she had given a ketogenic diet for 2 months. However, it also had no effect and was stopped. The frequency of the seizure was about three to ten times per day. Her preoperative vital signs, chest X-ray and laboratory data were normal ().
The patient took phenobarbital (30 mg), vigabatrin (300 mg), carbamazepine (250-200-100 mg), levetiracetam (250 mg), leucovorin (5 mg), pyridoxine (12.5 mg), lamotrigine (chewable, 12.5 mg) until the morning of the day of operation. Midazolam (1.2 mg, 0.1 mg /kg) was administered intravenously for sedation upon entering the operating room. Before anesthesia, the blood pressure was 94/60 mmHg, heart rate was 89 beats/min and oxygen saturation was 100%. Anesthesia was induced with thiopental sodium (50 mg, 5 mg/kg) intravenously and mask ventilation was started with 5 vol% isoflurane and 100% oxygen. After checking that the mask ventilation was operating properly, rocuronium bromide (10 mg, 1 mg/kg) was administered. After a minute, proper muscle relaxation was verified and the glottis was exposed using a Machintosh laryngoscope number 2. The trachea was intubated with an endobronchial tube with a 4.5 mm envelope. Mechanical ventilation was started with pressurecontrolled ventilation at a pressure 14 cmH2O (a tidal volume 90-100 ml) and a respiratory rate of 18-20 beats/min. Anesthesia was maintained with isoflurane (1.0-1.2 vol %) in oxygen (40%). Monitors included electrocardiography, pulse oxymetry and capnography, and inspired and the end-tidal concentrations of isoflurane were measured. During the operation, the blood pressure was 85-100/40-50 mmHg, heart rate was 85-110 beats/min, oxygen saturation was 100% and body temperature was 36.1-36.7℃. The blood sugar level was 149 mg/dl during the middle of the operation. The operation lasted a total of about 2 hours and 150 ml Ringer's lactate solution was supplied. At the end of surgery, anesthetics were discontinued. She recovered spontaneous respiration and glycopyrrolate (0.1 mg, 0.01 mg/kg) and pyridostigmine (2.5 mg, 0.2 mg /kg) were intravenously injected. After extubation was performed, her respiratory and circulatory conditions were stable and she was transferred to the postanesthetic care unit (PACU). Forty minutes later, during her stay with her mother in the PACU, she had a tonic seizure attack with mild eyeball deviation. The duration of the seizure was thirty seconds and there was no saturation change during the convulsion. According to her mother, the seizure was similar to her usual symptoms. She was discharged from the hospital the following day without complications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.5, 'kg']}",45,42.75,47.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.5 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.5 kg - 10 kg) = 45.0 mL/hr.
Hence, the patient's fluid maintenance is 45.0 mL/hr."
4514,22,Maintenance Fluids Calculations,physical,decimal,pmc-4536722-1,Extracted,"A 26-year old primigravida woman was admitted to Severance Hospital for the evaluation of a secondary amenorrhea with galactorrhea. She had been well until 3 years earlier when amenorrhea first developed. Menarche was at the age of 15 with a regular interval of approximately 35–40 days between menstrual period, and a flow of 7 days duration, but menstruation stopped abruptly at the age of 23. Eight months before the amenorrhea was noticed, she had an artificial abortion of her first baby at 4 months IUP. For one year after the amenorrhea was first observed, she had taken shots of progesterone at local clinics and experienced withdrawal bleeding, without effecting a return of the normal menstrual cycle. In the meantime, she had suffered from intermittent headaches and galactorrhea for 3 years. Sudden impairment of visual acuity and diplopia developed 15 days before admission. One month prior to this admission, she had had an appendectomy. One week before this admission, she suddenly became lethargic. With a steroid treatment, she became alert.
Her temperature was 37.2 C; pulse, 76/min.; respiratory rate, 16/min.; and blood presssure 110/70 mmHg. She was 155cm tall and weighed 42 kg. On examination, the patient appeared to be pale, slender, and chronically ill. Her pubic hairs were scanty and axillary hairs were absent. Also, there was an impairment of upward gaze in the left eye.
The urine was normal. The hemoglobin was 10.5 g/dl; hematocrit, 32%; white cell count, 7500/mm3 with 82.4% neutrophils, 14% lymphocytes, and 3% monocytes; reticulocytes count, 0.6%. In the serum, the T3 level was 49.66 ng/dl (normal: 80–220 ng/dl); the T4 level, 2.2 ug/dl (normal: 5–13 ug/dl); free T4, 0.38 ng/dl (normal: 0.68–1.8 ng/dl); estradiol, less than 5 pg/dl (normal: 30–100 pg/dl); prolactin, 6.60 ng/ml (normal: 0–25 ng/ml); HCG, 10.06 mIU/ml (normal: less than 10 mIU/ml); and aFP, 1600 ng/ml. In the 24 hour urine collection, the 17-KS was 5.96 mg (normal: 4–10 mg/day) and the 17-OHCS was 1.86 mg (normal: 3–8 mg/day). Beta-endorphin was undetectable in the serum and in the CSF fluid. A combined pituitary function test was done (). Ventricular-evoked potential represented a bilateral optic nerve dysfunction.
Plain skull X-rays revealed a marked bony erosion of the dorsum of the sella. Cerebral arteriography showed a large pituitary tumor with some parasellar extension and a marked suprasellar extension. A C-T scan showed a pituitary tumor mass with a parasellar and a suprasellar extension, which was greater on the left side. Multiple low density areas were scattered in the tumor mass, representing probable tumor necrosis and hemorrhage ().
The pituitary fossa was explored through a trans-sphenoidal approaceh. A hard surfaced, encapsulated, somewhat whitish intrasellar mass was removed. Microscopic examination showed neuroectodermal tissue (80%), squamous epithelium, cartilage and skeletal muscle. The neuroectodermal tissue was composed of neuroepithelial elements and mature or anaplastic giant cells (). The post-operative course was complicated by transient diabetes insipidus, and regressive behavior. The follow-up ventricular-evoked potential which was done on the second post-operative day showed improved visual function.
On the 17th post-operative day, a course of chemotherapy was started with a PVB regimen under the direction of an oncologist (PVB : cisplatinum 120 mg for 1 days, VP-16 170 mg for 3 days, and bleomycin 30 mg for 1 days). After the chemotherapy, the patient was discharged.
Sixteen days after her first program of chemotherapy, she was readmitted for the second course of chemotherapy. Bilateral hemianopsia had disappeared with an improvement of visual acuity of 20/50 (O.U.). Galactorrhea disappeared, also, but the amenorrhea persisted. Alphafetoprotein became undetectable in the serum and CSF, and there was no elevation on HCG in either. On a follow-up C-T scan, the tumor mass was found to have shrunk ().
For 5 weeks, after two weeks of rest following the second course of chemotherapy, a course of radiotherapy, with 5,000 rads, was given.
Since the completion of the course of radiotherapy, she has been visiting the hospital periodically for hormone replacement therapy and maintenance chemotherapy with a PVB regimen.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [42.0, 'kg']}",82,77.9,86.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 42.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (42.0 kg - 20 kg) = 82.0 mL/hr.
Hence, the patient's fluid maintenance is 82.0 mL/hr."
4515,22,Maintenance Fluids Calculations,physical,decimal,pmc-6542123-1,Extracted,"A 6-month-old male neutered domestic shorthair cat weighing 2.5 kg was referred for imaging and evaluation owing to a 1 week history of abdominal distension and pain on abdominal palpation. Muscle atrophy at the hips was also noted. The cat presented from a rescue facility and patient history was limited; however, no known toxin exposure or trauma was noted in the month prior to presentation. Elevated blood urea nitrogen (BUN) and creatinine, hyperphosphatemia and monocytosis were noted by the referring veterinarian 4 days prior to presentation at our facility (see ).
On physical examination the kidneys were large and distorted, and the cat was moderately dehydrated. Hematology and biochemistry panels confirmed elevated BUN and creatinine, hyperphosphatemia and revealed a mild leukocytosis for the feline species (see ). The urine specific gravity was 1.018 with moderate protein and an inactive urine sediment; urine culture was negative for bacterial growth. A diagnosis of grade 3 non-oliguric acute kidney injury was made and the cat was started on intravenous fluids (lactated Ringer’s solution) at a rate of 4 ml/kg/h. A renal diet and/or a phosphate binding agent were not introduced at this time to avoid food aversion.
Abdominal radiographs followed by ultrasonography revealed large fluid-filled sacs surrounding both kidneys, consistent with bilateral PNPs. The cat was sedated with butorphanol 10 mg/ml 0.2 mg/kg intramuscularly (IM), ketamine 100 mg/ml 2 mg/kg IM and dexmedetomidine 0.5 mg/ml 0.1 mg/kg IM prior to each therapeutic aspiration and drainage of the PNPs. Both kidneys were hyperechoic with poor corticomedullary distinction and located within hypoechoic subcapsular fluid. Therapeutic ultrasound-guided aspiration of the PNPs was performed on presentation; 195 ml fluid was drained from the right cyst and 42 ml from the left.
The creatinine concentration of the fluid from the left and right pseudocysts was 11 mg/dl (838.75 µmol/l) and 8.6 mg/dl (655.75 µmol/l), respectively, vs 3.6 mg/dl (318.24 µmol/l) in the serum. The total protein content of the fluid collected was 0 g/dl (<2.5 g/dl), and the color was pale straw to light yellow. The fluid contained low cellularity, comprised predominantly of macrophages and neutrophils, with low numbers of small lymphocytes. Overall, the presence of a transudate was supported; however, the creatinine of the cystic fluid was more than twice the serum concentration, suggestive of a uriniferous fluid. No growth was detected on culture of the PNP fluid. Owing to the cat’s discomfort with increasing PNP distension/refilling, therapeutic PNP cystocentesis under IM sedation was necessary every 48 h prior to surgery (performed twice prior to the day of surgery). Sedation was not reversed to allow continued, lingering pain control between drainage (q48h) until surgical intervention could be performed. On the day of surgery, 50 ml of fluid was drained from each cyst immediately prior to surgery.
Laparoscopic fenestration of the PNPs was elected. The cat was premedicated with butorphanol 10 mg/ml 0.37 mg/kg IM, midazolam 5 mg/ml 0.19 mg/kg IM and oxymorphone 1 mg/ml 0.47 mg/kg IM 50 mins prior to induction. Butorphanol was used in an effort to prevent/antagonize the dysphoric, sedative and respiratory effects that some cats experience with full agonist while, in theory, sparing the analgesic effects. Oxymorphone was chosen for increased pain control. The cat was then induced with propofol 10 mg/ml 9.4 mg/kg intravenously. Postoperative pain control included placement of a fentanyl 12 µg patch at the inside of the left rear leg immediately following the procedure, and subcutaneous morphine 15 mg/ml 0.7 mg/kg 20 mins and 3 h postoperatively.
The cat was placed in dorsal recumbency and the surgical site was prepped. A ventral midline stab incision was made caudal to the umbilicus and a Veress needle was inserted. The abdomen was then insufflated with CO2 to a maximal pressure of 13 mmHg using a mechanical insufflator (Endoflator; Karl Storz Endoscopy). A trocar-cannula was placed using a 3.5 mm Karl Storz 30114GK Lightweight Trocar + Cannula W/Silicone Valve, and a 3 mm, 0°, 14 cm laparoscope (Hopkins; Karl Storz Endoscopy) was inserted at the location of the Veress needle. A second cannula was placed caudal to the umbilicus, and the palpation probe (Karl Storz 26167TS Palpation Probe With CM Markings 3 mm × 20 cm) was used to isolate the PNPs. A third cannula was placed through the left lateral body wall at the level of the left kidney. The left PNP was grasped and elevated with laparoscopic forceps (Karl Storz 30322 MDS Clickline Blakesley Dissecting and Biopsy Forceps). The PNP was then fenestrated and cauterized with laparoscopic scissors (Karl Storz 30321MWS Clickline Scissors). The right PNP was grasped, elevated and fenestrated in a similar manner. The dissected aspects of each capsule were placed lateral to the bladder and were retrieved prior to closure. The kidneys were not removed from their retroperitoneal attachments. As much of the ventral aspect of the pseudocyts as possible was resected bilaterally, creating a 3–4 cm fenestration at each site. The cannula sites were closed with two layers of cruciate sutures in the body wall and skin utilizing 4-0 polydioxanone suture (PDS II; Ethicon).
Histopathologic analysis of the capsular tissue was consistent with steatitis/fasciitis with mild granulomatous fibrosis also noted. Submitted tissue was negative for corona viral antigen utilizing immunohistochemistry, as feline infectious peritonitis may be associated with CKD and PNP development.
The cat was hospitalized 3 days postoperatively. Aluminum hydroxide powder was introduced (35 mg/kg with food q12h) as a phosphate binder once appetite returned postoperatively. A renal diet was deferred owing to the patient’s age and growth requirements. The cat was re-examined at 1 month, 6 months and 1 year postoperatively. BUN and phosphorus remained elevated on all occasions. Creatinine was elevated at 6 months and 1 year postoperatively. Creatinine was consistent with grade 3 acute kidney injury initially; 1 month postoperatively the patient was in stage 1 CKD. Biochemistry values were consistent with stage 2 CKD 6 months and 1 year postoperatively. Repeated abdominal ultrasound at subsequent visits revealed no evidence of cystic structures in the region of the kidneys, and no free fluid was noted in the abdomen.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.5, 'kg']}",10,9.5,10.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.5 kg. Hence, the patient's maintenance fluid is 2.5 kg * 4 mL/kg/hr = 10.0 mL/hr.
Hence, the patient's fluid maintenance is 10.0 mL/hr."
4516,22,Maintenance Fluids Calculations,physical,decimal,pmc-2663564-1,Extracted,"42 year old obese (BMI-38) caucasian male presented to his primary care provider with complaints of insidious onset of anorexia, nausea, jaundice, pale stools, dark urine and about 35 pound weight loss over the previous 3 weeks. Outpatient laboratory work up revealed normal complete blood counts and basic panel but deranged liver function tests suggestive of cholestatic jaundice. Patient was then referred to a regional medical center for imaging studies. Ultrasound of abdomen showed multiple hyperechoic and hypoechoic liver lesions all less than 1 cm in size. The CT scan of abdomen showed massive hepatomegaly with coarse echotexture with contracted gall bladder and normal sized common bile duct. A chest x-ray (Figure ) obtained at the same time revealed a huge mediastinal mass with evidence of mediastinal widening. CT scan of the chest (Figure ) showed 3 anterior mediastinal masses with the largest one being 16 cm × 10 cm. In view of these imaging studies, the patient was referred to a tertiary care center for further work up. Upon arrival, we found the patient to be significantly icteric with some abdominal distension. There was smooth, non-tender liver edge palpable 10 cm below the right costal margin. No peripheral lymphadenopathy was noticed. The laboratory work on admission showed normal CBC and basic panel but persistently deranged liver function tests (Table ).
Additional work up was ordered which showed ceruloplasmin 5 mg/dl, AFP <1.3 ng/dl and serum ferritin 4686 ng/ml. ANA, anti-smooth muscle antibodies, HIV, along with EBV and CMV antibodies were all negative. CT guided biopsy of the mediastinal mass (Figure ) showed features of malignant lymphoma characterized by a diffuse proliferation of medium sized lymphoid cells, which exhibited fine nuclear chromatin, inconspicuous nucleoli and scanty cytoplasm. Occasional mitosis with few scattered tangible body macrophages was noted. The neoplastic cells were positive for CD1a (Figure ), CD3 (Figure ), CD4, CD5, CD8 and CD43. The neoplastic T cells also expressed synaptophysin (Figure ). However, the tumor was negative for CD20, kappa and lambda light chain immunoglobulins, CD34, TDT, cytokeratin AE1/AE3, cytokeratin 5.2 and CD56. The proliferation fraction (Ki-67) was 100%. Next, a PET CT scan (Figure ) was ordered which again showed a very large anterior mediastinal mass extending across the mediastinum from left to right and superiorly into the supraclavicular area. Diffuse liver involvement and abnormal activity in axial bones were also noticed. CT guided liver biopsy (Figure ) and bone marrow biopsy (Figure ) revealed the same tumor cell morphology with identical immunohistochemistry. A 200-cell count with differential performed on bone marrow aspirate showed 85% lymphoblasts, 2% small mature lymphocytes, 6% segmented neutrophils, 2% intermediate granulocytic precursors and 5% erythroid precursors. Ultrasound of bilateral testes was negative. MRI brain showed no masses or infarcts. Lumbar puncture was normal with no lymphoblasts. Thus, the diagnosis of precursor T-ALL/T-LBL was made. Since this patient had more than 25 percent T lymphoblasts in his bone marrow aspirate, his disorder could be best described as precursor T-ALL. After having considered the highly deranged liver function tests, per the recommendations of the treating oncologist, the treatment was initiated with cisplatin and dexamethasone (CD) for a total of 3 cycles to be followed by 4 cycles of Hyper CVAD. Follow up on day 100 after the completion of 3 cycles of Hyper CVAD revealed a normal hepatic panel and normal LDH (Table ) with the patient scheduled for a fourth round of Hyper CVAD and a subsequent referral to a bone marrow transplant center.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [35.0, 'lbs']}",51.75144,49.16387,54.33901,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 35.0 lbs so this converts to 35.0 lbs * 0.453592 kg/lbs = 15.87572 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.87572 kg - 10 kg) = 51.75144 mL/hr.
Hence, the patient's fluid maintenance is 51.75144 mL/hr."
4517,22,Maintenance Fluids Calculations,physical,decimal,pmc-6687642-1,Extracted,"An 11-year-old boy was presented to our dermatology department for evaluation of diffuse follicular hyperkeratosis, alopecia, and photophobia. At the age of 3 months old, complete non-scarring alopecia including the lack of eyebrows and lashes was noted. Hyperpigmented scales with follicular hyperkeratosis appeared on his scalp, face and buttocks, which later progressed to the whole body. Hyperkeratotic plaques developed around the regions of his elbows, knees, and buttocks. There were prominent dystrophic and deformed nails. The patient was suggested to use moisturizers for his involved skin, but no improvement was reported. He had photophobia without structural abnormalities of the eyes at the age of 1 year. Between the age 1 to 7, he suffered from several epilepsy attacks and since then anticonvulsants were administered. During the last 4 years, he did not suffer from any seizures. He had mild mental retardation and did not cope well in school for his age. He had normal hearing, sweating secretion, and dentition development. He was the son of his nonconsanguineous parents born at term weighing 3.2 kg. The pregnancy history of his mother was unremarkable. His parents and two older sisters were healthy with none of the similar manifestations, whereas his grandmother had the history of dry skin and lamellar desquamation on the lower limbs since birth.
On admission, he was found to have short stature (132 cm) and low body weight (27 kg). Visual acuity was 0.25 in the left eye and 0.15 in the right eye. Ophthalmologic examination revealed conjunctival congestion and photophobia while cornea and ocular fundus were normal. He had slightly prominent ears. Dermatological examination revealed complete absence of hair, eyelashes, and eyebrows as well as chronic angular cheilitis around the mouth (Figure a). Generalized dry skin with widespread follicular papules involved his scalp, neck, trunk and extremities, giving a thorn-like sensation at palpation. Flaky scales developed on the extensor extremities (Figure b). There were hyperkeratotic psoriasis-like lesions on the elbows, knees, and buttocks and dark brown scales on the upper and lower limbs (Figure c). Histopathologic examination of a skin biopsy from the right limb showed hyperkeratosis, focal parakeratosis, and follicular plugging of the epidermis, absence of sebaceous glands and mild perivascular inflammatory infiltration in the dermis (Figure ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [27.0, 'kg']}",67,63.65,70.35,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 27.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (27.0 kg - 20 kg) = 67.0 mL/hr.
Hence, the patient's fluid maintenance is 67.0 mL/hr."
4518,22,Maintenance Fluids Calculations,physical,decimal,pmc-5059589-1,Extracted,"A 26-year-old woman, primigravida, with no significant past medical history was referred to our Prenatal Diagnosis Unit because in the 21-week ultrasound the sex was not clearly differentiated. Due to the ambiguity of the genitalia, a fetal karyotype in maternal blood was requested and it revealed a normal male karyotype (46XY). We performed a detailed fetal examination using ultrasound equipment Epiq 7 (Phillips Medical Systems, Bothell, WA, USA) with abdominal probes C5-1 and xMATRIX 6-1.
The fetal biometric measurements correlated with his estimated gestational age and showed no fetal anatomic abnormality except in the external genitalia.
In the external genitalia a shortened penis is observed with a ventral angulation between the two scrotal folds. The two testicles were properly descended into the scrotum (). 3D ultrasound was used to obtain a more precise diagnosis (). In the volumetric study and surface rendering mode we clearly visualized a shortened and curved but correctly formed penis, with a surplus foreskin at the tip forming the prepucial cap. We can guess the location of the urethral meatus, in the most anterior part of interscrotal fold. The diagnosis is supported by viewing the fetal micturition, showing a ventral jet from the shaft of the penis, near the base (). The exploration was compatible with a third-degree hypospadias.
The remaining ultrasounds performed during pregnancy showed no other relevant findings except for a fetal weight at the lower limit.
The patient was admitted at 37th week of gestation for a hypertension study. At 37 + 1 weeks a male of 2100 grams (percentile <3) was delivered by an induced vaginal delivery. The newborn was admitted to the Neonatal Unit because of low weight for gestational age. The exploration of the external genitalia confirmed the diagnosis of severe hypospadias with the urethral meatus at the base of the penis, almost interscrotal, a severe curvature, and a bifid scrotum with the testes in the bag, without other associated anomalies ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2100.0, 'g']}",8.4,7.98,8.82,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2100.0 g so this converts to 2100.0 lbs * kg/1000 g = 2.1 kg. Hence, the patient's maintenance fluid is 2.1 kg * 4 mL/kg/hr = 8.4 mL/hr.
Hence, the patient's fluid maintenance is 8.4 mL/hr."
4519,22,Maintenance Fluids Calculations,physical,decimal,pmc-3811799-1,Extracted,"A 29-year-old man presented at a emergency room in a stupor.
The patient had started psychiatric treatment after being diagnosed with personality disorder and hypochondriasis by the department of psychiatry in our hospital 4 years ago. After about 1 year of treatment, olanzapine was administered due to the patient's symptoms of social withdrawal and distrust of people. After the initiation of olanzapine, the patient's body weight increased by ≥30 kg, and hyperthermia occurred together with nausea and vomiting 1 week prior to the visit to our hospital. The patient received a prescription from a neighboring hospital and had taken antipyretics, but did not show any improvement. Then the patient showed mental deterioration and was admitted to our hospital via the emergency room.
Both parents were moderately built, and none of the family members, including siblings, had a metabolic disease such as diabetes.
The patient was on medication due to incidences of personality disorder, hypochondriasis, and psychotic tendency, taking olanzapine 10 mg, valproic acid 500 mg, clonazepam 0.5 mg, and lorazepam 1 mg on a daily basis. The aforementioned medication regimen was maintained for over 1 year without any dosage change, and the intake period of olanzapine was 32 months. There was no other underlying disease than the aforementioned, and there were no abnormal test results based on blood assay, including an assay for fasting plasma glucose, which was performed prior to administration of antipsychotics.
The patient had no history of smoking or alcohol drinking and was unemployed since completion of military service as social service personnel.
In physical examination, the patient showed acute signs of illness and was in a coma. His vital signs measured at the time of visit to our hospital were 110/70 mm Hg for blood pressure (BP), 120 beats per minute for pulse rate, 24 times per minute for respiratory rate, and 37.2℃ for body temperature. The patient's height was 181 cm, weight was 104 kg and body mass index (BMI) was 31.7 kg/m2. His consciousness state was stupor with normal light reflexes, and senses as well as spontaneous motions of extremities were maintained. Chest auscultation revealed that the heart rate was fast, but there was no murmur, and the patient had tachypnea, but had no crackles or wheezing sound auscultated. There was neither notable tenderness nor rebound tenderness from the abdomen. The patient's skin was dry overall.
Peripheral blood assay showed the following results: white blood cell 6,560/mm3 (neutrophil 72%), hemoglobin 20.2 g/dL, hematocrit 60.8%, and platelets 228,000/mm3. Taking the findings of physical examination into account, dehydration-induced hemoconcentration was suspected. The results of serum biochemical assay revealed that the plasma glucose level had increased to 1,216 mg/dL, the blood urea nitrogen level was 31 mg/dL, and creatinine level was 2.4 mg/dL. The result also showed the following: sodium, 149 mEq/L; potassium, 4.5 mEq/L; chloride, 96 mEq/L; total protein, 8.7 g/dL; albumin, 5.0 mg/dL; aspartate aminotransferase, 28 IU/L; alanine aminotransferase, 44 IU/L; total bilirubin, 0.6 mg/dL; calcium, 11.5 mg/dL; phosphate, 6.1 mg/dL; and creatine phosphokinase (CPK), 80 U/L (reference range, 30 to 170). Dipstick-utilized urine assay showed a positive reaction to ketone, and increases in amylase and lipase to 545 IU/L (reference range, 28 to 100) and 1,435 U/L (reference range, 13 to 60), respectively. Arterial blood gas analysis (ABGA) showed that the pH was 7.25, pCO2 was 18.9 mm Hg, pO2 was 86.1 mm Hg, HCO3- was 8.2 mEq/L, and oxygen saturation was 95.7%, presenting metabolic acidosis with 44.8 mEq/L of anion gap. The glycosylated hemoglobin level was 13.8%, while the serum C-peptide level tested during the administration of insulin were 0.38 ng/mL. So the patient was presumed to be in DKA and acute renal failure.
Electrocardiography findings showed sinus tachycardia with rate of 150 beats per minute.
There were no specific findings from the chest X-ray examination, and there was no evidence of ileus other than fecal impaction shown on abdominal X-ray examination. An abdominal computed tomography scan showed no findings of edema or necrosis or fluid retention in the pancreatic parenchyme and its periphery ().
Although there was no sign of BP reduction, the patient showed severe dehydration induced by extreme hyperglycemia and metabolic acidosis. We administered ≥4 L per day of fluid through intravenous infusion and immediately began insulin pump therapy. Within 24 hours of insulin therapy, the plasma glucose level was reduced to less than 300 mg/dL (), the anion gap level was reduced to normal range and ABGA showed that the patient was out of metabolic acidosis. But, in spite of fluid infusion of ≥2 L per day, hyperthermia occurred and the levels of CPK and creatinine began to increase rapidly to 16,161 U/L and 4.1 mg/dL, respectively, on the 3rd day of hospitalization. Also, the urinary myoglobin level was 1,879 ng/mL. In addition, the patient was in a confused mental state with severe muscle stiffness and rigidity, and increased uptake at upper and lower proximal limb was shown on bone scan (). Even with fluid treatment for acute renal failure, the level of creatinine continued to increase, so we started continuous renal replacement therapy (CRRT) on the 5th day of hospitalization (). After initiation of CRRT, the patient showed remarkable improvement in fever and consciousness, so we converted dialysis modality to intermittent hemodialysis 3 days later and maintained the treatment until the 12th day of hospitalization. The urine output was normalized and there was no additional elevation in creatinine and CPK concentrations, so we discontinued hemodialysis (). The patient presented consciousness deterioration, muscle stiffness, and high fever that did not respond to antipyretics and fluid infusion with history of taking antipsychotics, so we determined that the patient had NMS, and implemented supportive therapy including discontinuation of causative medication. We used the insulin pump for glycemic control in the early stage, and changed to multiple daily injections of insulin to manage the patient's condition. We could discontinue the administration of insulin on the 41st day after the first visit to our hospital as the insulin demand had gradually decreased. And we changed to metformin monotherapy. We stopped the administration of oral hypoglycemic agents on the 52nd day. On follow-up examination, we confirmed a notable reduction in glycosylated hemoglobin and a remarkable restoration of the serum C-peptide level (). Currently, the patient is maintaining very good glycemic control only by life style modification and is under prognostic observation as an outpatient.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [104.0, 'kg']}",144,136.8,151.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 104.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (104.0 kg - 20 kg) = 144.0 mL/hr.
Hence, the patient's fluid maintenance is 144.0 mL/hr."
4520,22,Maintenance Fluids Calculations,physical,decimal,pmc-7499275-1,Extracted,"A 5-month-old male was admitted with severe diarrhea and failure to thrive. The baby was born at term after an uneventful pregnancy and delivery with a birth weight of 2.97 kg. He was exclusively breast-fed. At 2-1/2 months of age, he developed frequent, large volume, watery stools with occasional blood streaks. There was no fever, emesis, or any infectious contacts. The family history was only significant for two paternal second-degree relatives with celiac disease and one-second degree relative with a thyroid disorder and type 1 diabetes mellitus.
On initial examination, the child appeared ill, pale, malnourished, and dehydrated. The weight was 5.19 kg (<3rd percentile), length was 59.7 cm (<3rd percentile), and head circumference was 40.5 cm (between 3rd and 10th percentile). Other than some diaper rashes, the physical examination was unremarkable with no atopic dermatitis or icthyosis.
The results of initial investigations are shown in . The absolute eosinophil count was only slightly elevated. Immunoglobulins including IgE were normal. The serum albumin was low, consistent with the protein losing enteropathy. Stool examination did not reveal any pathogens. Stool electrolytes showed secretory diarrhea. The antinuclear antibody and direct antiglobulin were negative.
Endoscopy and biopsies revealed acute and chronic inflammation, marked autoimmune enteropathy with total villous atrophy, and abundant CD3+ T- and CD20+ B-cell aggregates in the small intestine and colon.
Further immunological workup showed intact IL-10 receptor function since endotoxin-induced tumor necrosis factor (TNF) production in mononuclear cells was suppressed by IL-10. Initial T- and B-cell phenotype analysis was normal. The percentage of circulating Treg cells and FOXP3 protein expression in these cells measured by flow cytometry were also normal (Figures and ).
Analysis of all coding regions and exon/intron boundaries of the FOXP3 gene was carried out. This revealed a hemizygous missense mutation (c.1190G > A, p.Arg397Gln) which would result in a nonfunctional FOXP3 protein and Treg cells, similarly in the patient's mother, who is a healthy career. The anti-islet cell antibody was negative, insulin-like growth factor-1 level was normal, and the patient never developed type 1 diabetes mellitus. Thyroid function was also normal.
The patient required intensive resuscitation with intravenous fluids. He was then managed with parenteral nutrition and high-dose intravenous corticosteroids. He was maintained on oral prednisone and tacrolimus. The clinical condition gradually improved, and he was able to initiate oral intake with an elemental formula in a few weeks.
The patient had a matched unrelated hematopoietic stem cell transplant (HSCT) with reduced intensity conditioning including alemtuzumab, fludarabine, and melphalan at 8 months of age. Early transplant period was complicated with donor Epstein–Barr virus (EBV) reactivation treated with rituximab. He developed autoimmune hemolytic anemia. Initially, enteropathy significantly improved; however, colitis recurred 3 months after the transplant when, unfortunately, there was decreasing mixed chimerism and secondary bone marrow rejection. Donor lymphocyte infusions were unsuccessful, and the patient required a second transplant at 14 months of age from the same donor with busulfan, fludarabine, and alemtuzumab conditioning this time.
Two years after the second HSCT, the patient has mixed chimerism and 65% of donor haematopoiesis but 91% of donor Treg cells (). The gut function gradually recovered, and graft-versus-host disease was ruled out on repeated gut biopsies. Currently, he is doing well, except having eczema of typical distribution and morphology seen in toddlers and responding to high-potency topical corticosteroids. He is immunocompetent and has sustained protective antibody titres to several vaccine antigens.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.19, 'kg']}",20.76,19.722,21.798,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.19 kg. Hence, the patient's maintenance fluid is 5.19 kg * 4 mL/kg/hr = 20.76 mL/hr.
Hence, the patient's fluid maintenance is 20.76 mL/hr."
4521,22,Maintenance Fluids Calculations,physical,decimal,pmc-1523335-1,Extracted,"The patient is a 60-year old man who was diagnosed with type 2 diabetes in 1989 and had a family history of overweight and diabetes. Retinopathy was diagnosed in the mid-90s. The patient had been treated several times with focal laser photocoagulation. In 2003 he developed proliferative retinopathy and was treated with photocoagulation. In addition to glimepiride and the ACE-inhibitor quinapril, medication included metoprolol, furosemide, simvastatin and aspirin. In 1995–1997, his blood pressure (BP) was on average 125/90 mm Hg. Over the same period, the patient's bodyweight varied between 89 kg and 85 kg. Traditional dietary counselling for weight loss usually resulted in a short-term loss of a few kg, but the bodyweight soon increased again.
In July 1997 albuminuria was noted with a urine concentration of 116 mg/l. That year the patient's average body mass index (BMI) was 29.4 kg/m2 and the average bodyweight was 87.0 kg.
Insulin treatment was started four months later resulting in a temporary improvement of HbA1c but an increase in bodyweight. One year later, his BMI was 32.5 kg/m2 and his weight was 94 kg. The insulin dose was lowered in order to avoid further increase in bodyweight. In the years 1998–1999, following the weight increase and despite improved glycemic control, his BP increased to an average 145/90 mm Hg. Likewise, urine albumin increased as seen in the Figure. In 2000, despite a still reasonable glycemic control but following further weight increase, the albuminuria reached an average of more than 2000 mg/l and the BP was 160/90 mm Hg. Both were controlled by exchanging quinapril for the angiotensin II receptor antagonist candesartan, and by adding amlopidine. The BP has since been stable, averaging 130/76 (± 10/7) mm Hg, but the decline of renal function continued. The Figure shows the albuminuria record and the increase in HbA1c, serum creatinine and body weight with increasing insulin dosage.
In January 2004 his diet was changed radically by reducing dietary carbohydrates to 80–90 g per day, consisting only of vegetables and small amounts of hard bread (crisp bread). Potatoes, bread, pasta, rice and cereals were excluded, and the caloric requirements were covered by protein and fat. To ease the transition the patient was supplied with a number of meal recipes suggesting a caloric restriction to about 1800 calories per day. The per cent proportions of carbohydrates, fat and protein in the recipes were 20 : 50: 30.
Less than two weeks later the patient discontinued his insulin treatment and 6 months later his bodyweight had decreased by 19 kg. HbA1c had dropped to 6.5 % after 3 months, and the steady rise of his serum creatinine stopped. The creatinine has since – for two-and-a-half years – been stable as seen in the figure. When insulin was discontinued rosiglitazone was prescribed. In the Table measured parameters are shown before the dietary change, and now. As of late 2005 there was no sign of proliferative disease in the patient's retinopathy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [94.0, 'kg']}",134,127.3,140.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 94.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (94.0 kg - 20 kg) = 134.0 mL/hr.
Hence, the patient's fluid maintenance is 134.0 mL/hr."
4522,22,Maintenance Fluids Calculations,physical,decimal,pmc-6555724-1,Extracted,"The patient was a 45-year-old male who was admitted to our institution due to uremia. He had no diabetes and biliary tract disease history, and his BMI (body mass index) was 22.99 kg/m2 (183cm, 77 kg). He underwent kidney transplantation in our institution on 9th August, 2017. The donor was from donation after cardiac death (DCD). Before surgery, he received antilymphocyte therapy of basiliximab (20 mg i.v.). The surgery was successful and the initial immunosuppressive regimen consisted of tacrolimus (6 mg/day, 0.078 mg/kg/day), mycophenolate mofetil (1500 mg/day) and corticosteroids (initial dose 35 mg/day). The patient recovered well after surgery and was discharged on day 26+ with blood creatine level 156.6umol/L and trough concentration of tacrolimus 10.6 ng/ml then. After discharged, He reexamined in our institution once a week. From day 26+ to day 60+, the reexamine results showed his blood creatine level continued to decline to 101.7umol/L (day 60+), the dosage of corticosteroids was gradually tapered from 35 mg/day to 5 mg/day, and the dosage of tacrolimus was maintained at 6 mg/d with trough concentration ranged from 9.5–11.2 ng/ml. In addition, the recipient neither had a history of high fat diet nor presented hyperlipidemia from day 1+ to 67+ posttransplant, the laboratory analysis results showed the serum triglyceride (TG) level was in the range of 0.71–1.43 mmol/L while the cholesterol (CHOL) level was 3.3–4.5 mmol/L during the period.
On day 67+, he presented with acute abdominal pain in middle and left area of abdomen accompanied with nausea and vomiting. Physical examination showed diffuse abdominal tenderness with diminish bowel sound. Laboratory analysis showed WBC 9.16 × 109/L, neutrophils 7.98 × 109/L, hemoglobin 73 g/L, platelets 78 × 109/L, blood creatinine 147.4umol/L, blood urea nitrogen (BUN) 17.79 mmol/L, calcium 2.52 mmol/L, potassium 4.72 mmol/L, sodium 138 mmol/L, serum amylase 679.3 IU/L (normal 15–115), lipase 755 U/L (normal 6–51), trough concentration tacrolimus> 30 ng/ml (dosage was 6 mg/day) accompanied with elevated fasting blood glucose (29.49 mmol/L) and diabetic ketoacidosis (DKA) tendercy (blood ketone body test +). Abdominal computed tomography scan showed enlarged pancreatic head with peripancreatic inflammation and inflammatory exudate without dilatation of biliary tract (Fig. ). Pancreatitis diagnosis was made on the basis of the information all above.
Tacrolimus treatment was discontinued, somatostatin (3 mg, q12h, i.v.) was administrated to treat pancreatitis, other treatments included fluid replacement, insulin (i.v.) and imipenem (1 g, q12h, i.v.). Three days after somatostatin using (day 70+), patient’s condition improved significantly, abdomen symptoms relieved, blood amylase level were normalized (72 IU/L) and lipase level deceased to 69 U/L, blood glucose level maintained around 10–15 mmol/L. Cyclosporine (4 mg/kg/day) was administrated as an alternative for tacrolimus on day 75+, and the patient was discharged on day 80 + .
There was no recurrence of pancreatitis in 7 months follow up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [77.0, 'kg']}",117,111.15,122.85,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 77.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (77.0 kg - 20 kg) = 117.0 mL/hr.
Hence, the patient's fluid maintenance is 117.0 mL/hr."
4523,22,Maintenance Fluids Calculations,physical,decimal,pmc-4352369-1,Extracted,"A 77-year-old woman is brought by ambulance to the emergency room at 11 am for an edema of the tongue that started 2–3 h earlier. During the transfer in the ambulance, she was administered 125 mg of methylprednisolone and 0.5 mg of epinephrine subcutaneously. She said she never presented such symptoms. The apparition of the edema was brutal and it progressed rapidly. She had not eaten anything unusual. Her medical history revealed occasional and severe events of abdominal pain. She had recently been hospitalized to elucidate the origin of this pain but no etiology had been found. The woman had a morbid obesity (BMI = 38). Complete history included anxiety, depression, reflux esophagitis, ancient esophageal fungus, sigmoid diverticulosis, diabetes type 2, hypertension, hypercholesterolemia, left subacromial bursitis, and cholecystectomy (several years ago). Daily treatment of the patient was composed of gliclazide 60 mg, esomeprazole 20 mg, atenolol 100 mg, altizide 15 mg + spironolactone 25 mg, attapulgite 3 g, bromide otilonium 120 mg, acetylsalycilic acid 80 mg, rosuvastatin 20 mg, bromazepam 6 mg, and lisinopril 20 mg (she has been taking it since 2007). She had no known allergies. She did not smoke and she consumed liquor only on occasional circumstances. On the family level, we noted that her daughter suffered from a minor oropharyngeal edema which did not need medical treatment. Physical examination on admission revealed, in addition to edema, a blood pressure of 190/100 mmHg and a regular heart rate of 104 bpm. These parameters were related at least partly to the administration of epinephrine. She was afebrile and her saturation was 96%. She was polypneic (about 30 breaths per minute) and dysarthric. Her parameters were monitored regularly. The ear nose throat (ENT) specialist on duty was called because of the possibility of a difficult intubation or tracheotomy. Upon the ENT specialist's arrival, the patient had a lower blood pressure: 147/60 mmHg. The edema of the tongue was very important and slightly asymmetrical with a right predominance. The lips and mouth were also affected as well as the neck. The pharynx was not visible and palpation of the neck did not allow localizing the different osteochondral structures. The swelling was not itching and the symptoms were not relieved by the corticosteroids and adrenaline previously administered in the ambulance. Histamine-induced AE was then ruled out and a bradykinin-induced AE either drug induced or hereditary was diagnosed. A blood test containing chemistry, enzymology, glucose, hematology, coagulation, etc., was asked, with addition of the dosage of tryptase, complement, and C1 esterase inhibitor (quantity and activity). We did not perform flexible endoscopy for fear of increasing the swelling. Fresh frozen plasma was administered but there was no improvement after 4 h. Berinert® (manufactured by CSL Behring GmbH, King of Prussia, Pennsylvania, USA) was ordered at the pharmacy and subsequently administered after discussion with the family because of the uncertainty of reimbursement of the drug by medical insurance. According to the patient's weight (102 kg) four ampoules were injected (20 UI/Kg). In less than an hour, the swelling was absorbed and the patient remained in hospital for 48 h observation. The administration of corticosteroids resulted in hyperglycemia which justified the instauration of a temporary insulin regimen. ACEIs were prohibited (and even sartans because of the severity of the symptoms) and 40 mg omeprazole and tranexamic acid 1 g twice a day were added to the treatment. The patient was followed up in the outpatient department. We got the results of the blood tests a few days later. They were as follows: C3 complement was slightly increased (158 mg/dL), C4 complement was normal, and the antigen and the activity of C1 esterase inhibitor were normal (31 mg/dL and 130%). Allergy skin tests were negative and tranexamic acid was stopped since hereditary AE was excluded. A contact with the patient's former cardiologist revealed that the patient had experienced a chronic cough a few years before with another ACEI medicine (ramipril). The patient was lost to follow up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [102.0, 'kg']}",142,134.9,149.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 102.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (102.0 kg - 20 kg) = 142.0 mL/hr.
Hence, the patient's fluid maintenance is 142.0 mL/hr."
4524,22,Maintenance Fluids Calculations,physical,decimal,pmc-5349350-1,Extracted,"A 59 year old man who had undergone left total knee replacement in November 2008 in another institution presented with a 5 month history of left knee pain and persistent swelling. He complained of a restriction in the range of movement and morning stiffness. The pain was at the front of the knee and medially more than laterally. It was worse with stairs, getting up from a chair, kneeling, squatting, getting into and out of a car and exercising. Sitting, medication and icing made the pain better.
Clinical examination revealed that the patient was 71 inches tall and weighed 285 pounds. There was a marked effusion in the left knee. It was slightly warm but there was no redness. The knee had a 10 degree fixed flexion contracture and could bend to 100 degrees. There was no instability in the antero-posterior or medio-lateral directions. The neurological and vascular examinations in the extremity were normal.
Past medical history included a successful right total knee replacement in 2007, spinal surgery in 1989, adrenalectomy in 2011 and prostate surgery in 2010. He also had a history of hypertension, prior hepatitis and dyslipidemia
Radiographs showed an increase in patellofemoral joint space suggesting a marked effusion in the left knee and asymmetric medial joint space narrowing. There was the suggestion of internal rotation of the tibial component and periprosthetic lucency was noted in the posterior aspect of the medial and lateral tibial plateau, consistent with polyethylene wear and particle disease (). CT scan showed internal rotation of the tibial component and joint effusion. The patient had a posterior stabilized Triathlon TM knee (Stryker Corp, Kalamazoo, MI). Both femoral and tibial knee components were made of cobalt chrome alloy, with a polyethylene spacer.
Pre operative Complete Blood Count (CBC) was within normal limits. Erythrocyte Sedimentation Rate (ESR) was slightly raised at 28mm/hr and C reactive protein (CRP) was slightly elevated at 5.7 mg/L. Aspiration of the knee revealed cloudy fluid and gram stain, cell count with differential and cultures were negative for infection. Three phase bone scan showed increased uptake on the blood pool phase consistent with synovitis, and increased uptake in the left knee on the delayed images.
Therefore revision knee surgery was performed. There was a florid synovitis and the polyethylene component was fractured and worn posterolaterally. There was a 2 ⨯ 3 cm area of significant metallic wear on the postero-lateral aspect of the femoral component. The metallic tibial component was also worn posterolaterally and internally rotated. It appeared that metal-on-metal wear was occurring in this area. There was an adjacent soft tissue mass which resembled a pseudotumor. The femoral component was well fixed to the bone and well positioned. However significant wear and shape change of the lateral femoral component was noted and this mandated femoral component removal. Debridement and synovectomy was performed followed by revision of the femoral and tibial components and the polyethylene insert. The patellar prosthesis was well fixed and not damaged. Therefore the original patellar component was left in place. The patient had delayed wound healing, and small areas were left to granulate in successfully. The patient had a successful post operative recovery and was mobilizing well at the 6 month follow up. The range of movement of the knee was 0 – 110 degrees and the knee was stable.
Histology of the specimen revealed granulomatous inflammation, metallic and polyethylene wear debris, and areas of tissue necrosis and lymphocytic infiltration. () AFB and Gram staining were negative.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [285.0, 'lbs']}",169.27372,160.81003,177.73741,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 285.0 lbs so this converts to 285.0 lbs * 0.453592 kg/lbs = 129.27372 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (129.27372 kg - 20 kg) = 169.27372 mL/hr.
Hence, the patient's fluid maintenance is 169.27372 mL/hr."
4525,22,Maintenance Fluids Calculations,physical,decimal,pmc-8506145-1,Extracted,"A 24-year-old woman (gravida II, para 0) was referred at 21 weeks of gestation for genetic counseling including amniocentesis, as both unrelated parents suffered from heterozygous protein C deficiency. The woman had a history of thrombosis and lung embolism 4 years previously that had resulted in therapy with a vitamin K antagonist (phenprocoumon). During early pregnancy, the mother was treated with low-molecular weight heparin (5,000 IU dalteparin q24h). Genetic testing was initiated as part of the pregnancy counseling of the parents and revealed paternal heterozygous protein C mutation as well as a heterozygous factor V Leiden mutation despite no history of thrombosis up to this time (). Thrombosis or mutations in the PROC gene in other first-degree relatives of the parents were also not known. Amniocentesis was preceded by detailed counseling regarding the risks of pregnancy, the probability of disease, and the risk of mortality and morbidity of the child.
The results of the amniocentesis showed a heterozygous mutation in codon 325 (GTG□ATG) in exon 9 of the PROC gene with exchange of the amino acid valine against methionine (val325met-mutation) (maternal mutation) and heterozygous mutation in codon 343 (ATG□ATA) in exon 9 of the PROC gene with exchange of the amino acid methionine against isoleucine (met343ile-mutation) (paternal mutation). The fetus had inherited both mutations of his parents resulting in compound heterozygous protein C deficiency ().
The val325met-mutation has been described in patients with clinically apparent protein C deficiency (). In the absence of expression studies, there is only indirect evidence for a resulting protein C deficiency. The met343ile-mutation however is generally known to lead to protein C deficiency ().
After receiving the results of the amniocentesis, we performed weekly ultrasound examinations of the fetus as well as a fetal magnetic resonance imaging (MRI) at 28 weeks of gestation, which did not indicate any abnormalities.
As opposed to low-molecular weight heparin, which does not cross the placental barrier in significant amounts, treatment with vitamin K antagonists generates sufficient thrombosis prophylaxis for both mother and fetus (, ). After informed consent, we started oral anticoagulation with phenprocoumon the first days in overlap with heparin after 23+6 weeks of gestation to prevent intrauterine retinal detachment and fibrosis of the retinal membrane and cerebral thrombosis of the fetus. For the remaining pregnancy, the mother and the fetus were closely monitored as inpatients.
To achieve maximum safety for both mother and fetus, primary cesarean section was scheduled for 32 weeks of gestation but performed at 31+5 weeks of gestation due to premature rupture of membranes. The effects of phenprocoumon were antagonized several hours before surgery by substitution of 3,500 IU of PPSB (prothrombin complex, containing the factors II, VII, IX, and X) with 500 IU antithrombin and one platelet concentrate.
A male preterm infant was delivered (1,680 g, APGAR 7/7/8) and admitted to the neonatal intensive care unit (NICU) at Heidelberg University (level III perinatal center).
Postnatally, the infant displayed a normal ophthalmic examination, normal ultrasound of the brain, and no signs of purpura. The protein C activity was 0.9% (12–44%); D-dimers, 0.27 mg/L; elevated international normalized ratio (INR), 2.02; partial thromboplastin time, 55.7 s (27–75 s); antithrombin activity, 31% (14–62%); hemoglobin level, 14.6 g dl−1; white blood cell count, 5,900 μl−1; platelet count, 237,000 μl−1 ().
The newborn presented with respiratory distress syndrome. Initially, respiratory support by continuous positive airway pressure (CPAP) was delivered, at the age of 12 h, secondary intubation and surfactant application were performed. On the fifth day, the boy could be extubated successfully under caffeine therapy. He received the recommended neonatal vitamin K therapy right after birth as well as on days 5 and 28 of life.
Immediately after birth, 120 IU/kg protein C concentrate (Ceprotin®, Baxter Co., Germany) was infused over 10 min, via a peripheral venous line, followed by 60 IU/kg every 6 h, aiming at >30% physiological protein C activity (, , , , ) (). Sufficient activity levels were reached during the first day of life, and protein C concentrate was daily infused with increasing intervals from 6 over 8 to 12 h until the infant's weight was 3 kg. At 38 corrected weeks (days 50–51), subcutaneous infusion was started and overlapped with intravenous infusion for 2 days. Subcutaneous infusion (1 ml/h, i.e., 100 IU/ml) was carried out using an infusion set (DISETRONIC tender, Burgdorf, Switzerland) with a PEGA® plus box infusion pump (PEGASUS, Kiel, Germany). The subcutaneous needle (25G, initial 9 mm, later on 17 mm s.c. MediPro) was changed once or twice a week. The puncture site on the abdomen was rotated clockwise.
An attempt to prolong infusion intervals to every other day by increasing the amount of protein C concentrate from 154 to 300 IU/kg and the corresponding infusion time from 5 to 10 h (infusion rate of 1 ml/h) on the day of infusion (tested on days 58–59) did not result in sufficient basal protein C activity >30% after 42 h. Therefore, daily infusion was chosen for further treatment.
The infant was discharged on day 73 (corrected, 42 weeks; weight, 4.1 kg) with maintenance therapy of 1,000 IU/day protein C concentrate (243 IU/kg) administered by subcutaneous infusion pump for 10–12 h overnight (infusion rate 1 ml/h). Up to the date of discharge, the infant received a total of 34,560 IU of protein C.
At the age of 1 year, we stopped protein C substitution under prophylaxis of low-molecular weight heparin therapy (anti Xa activity 0.4–0.8) to test for baseline activity and half-life due to reports on maturation of protein C function over time (). After infusion of 1,000 IU protein C concentrate, protein C activity decreased from 75.4 to 38.7% after 16 h and to 24.8% after 38 h. After that, subcutaneous protein C substitution was reinitiated. The subcutaneous application half-life was 17 h on this day.
During the following years, no further baseline or half-life tests were performed. Treatment was monitored by regular measurements of protein C activity under substitution and the absence of thromboembolic events. D-dimers and fibrinogen, which are often used for monitoring, were measured regularly (). Except for occasional minor reddening of the skin at the injection site, which disappeared quickly after the needle was changed, there were no side effects associated with subcutaneous protein C substitution. Investigations to detect the occurrence of protein C inhibitory alloantibodies were performed at 1 year of age. After that, there was no need for regular testing. The protein C activities were always within the target range under constant dosage. The child received the first regular vaccination during the initial hospitalization and received all other vaccinations according to the recommendations of the Standing Committee on Vaccination (STIKO Germany). Because infections are known to be a trigger for thromboembolic events, protein C activity (trough and peak activity levels) were immediately monitored at the onset of fever or other signs of infection until recovery. A prophylactic increase of the daily protein C dose was not performed. In the context of a febrile obstructive bronchitis episode at the age of 10 months, the protein C activity measured at hospital admission was 38.4% (peak level), only slightly above the target range, so that the daily dose had to be increased from 100 to 150 IU/kg/day over 5 days. No bleeding or thrombotic events occurred during this episode; D-dimers, prothrombin, activated partial thromboplastin time (APTT), thrombin clotting time, and fibrinogen concentration were within physiological ranges at all times.
As of now, the child is 13 years old (weight, 59 kg) without any thrombotic events. Under subcutaneous substitution of 1,500 IU/day protein C (last 30 IE/kg) during a 10–12-h period overnight, baseline protein C activity of 25% could be reached. During the last months of subcutaneous therapy, pump alarms due to needle dislocation or technical problems increasingly disturbed the sleep of the young boy. The adolescent was increasingly dissatisfied with the current treatment regime, and compliance was likely to be compromised. The available treatment options, including continuation of the current therapy, the use of vitamin K antagonists, and the administration of direct oral anticoagulants (DOACs) as experimental individual therapy, were discussed with the parents and the adolescent, taking into account all risks, side effects, and benefits of the respective therapy. Together with the family, we reached informed consent to change therapy to DOAC (apixaban 3 × 5 mg/day). The switch in therapy was carried out under close monitoring (clinical and laboratory values) especially in trigger situations such as infections.
Up to the time of this report, ophthalmic examinations, 3D time-of-flight (TOF) MR angiography at 3.0 T of the circle of Willis, and MRIs of the brain were normal, and no episodes of purpura fulminans occurred. The boy has developed regularly and actively participates in sports.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [59.0, 'kg']}",99,94.05,103.95,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 59.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (59.0 kg - 20 kg) = 99.0 mL/hr.
Hence, the patient's fluid maintenance is 99.0 mL/hr."
4526,22,Maintenance Fluids Calculations,physical,decimal,pmc-5819630-1,Extracted,"Institutional Board Review is not required at Nationwide Children’s Hospital (Columbus, OH) for the presentation of a single case report.
The patient was a 25-year-old, 51.6 kg male, who was admitted for cardiothoracic surgery (Bentall procedure including composite graft replacement of the aortic valve, aortic root and ascending aorta, with re-implantation of the coronary arteries into the graft). He had a history of progressive aortic valve insufficiency due to bicuspid aortic valve and ascending aortic aneurysm. He was known to have DM type 1 (Steinert disease). Clinical examination revealed symmetrical facial weakness, ptosis with temporal balding and wasting. There was upper and lower limb muscle weakness. His family history was positive for other members with DM. Preoperative electrocardiogram (ECG) showed a sinus rhythm with a heart rate of 54 beats per minute (bpm), an intraventricular conduction delay, left ventricular hypertrophy, and early repolarization. Echocardiogram showed an abnormal bicuspid aortic valve, moderate aortic stenosis and regurgitation, severe aortic root and ascending aorta dilation, moderate-to-severe left ventricular enlargement, and qualitatively normal left ventricular systolic function. Laboratory evaluations, including complete blood count, electrolytes, renal function, and coagulation profile, were within normal limits. His current medications included cholecalciferol. The patient was held nil per os (NPO) for 6 h and transported to the operating room where American Society of Anesthesiologists’ (ASA) monitors were placed. A peripheral intravenous catheter was placed and a rapid sequence induction (RSI) with endotracheal intubation was carried out with the following medications: midazolam (2 mg), fentanyl (100 µg), etomidate (10 mg), propofol (30 mg), rocuronium (50 mg), and lidocaine (60 mg). Endotracheal intubation proceeded without difficulty. Maintenance anesthesia was provided with desflurane, dexmedetomidine (0.5 µg/kg/h), and intravenous fentanyl. Bilateral paravertebral blocks (total of 40 mL of 0.2% ropivacaine) were placed using ultrasound guidance for postoperative analgesia. A central venous catheter and a radial arterial line were placed. Cardiopulmonary bypass (CPB) time was 3 h 10 min with an aortic cross-clamp time of approximately 2 h. The patient weaned from CPB with epinephrine and milrinone infusions. The patient received a total of 110 mg of rocuronium during the surgery. After completion of the procedure, neuromuscular blockade was reversed with sugammadex (4 mg/kg). After return of appropriate strength and spontaneous ventilation, his trachea was extubated when he was awake in the operating room. He was transferred to the cardiothoracic intensive care unit in stable condition and his postoperative course was unremarkable.
Five weeks later, the patient returned for transesophageal echocardiography (TEE) and cardioversion due to atrial flutter with depressed myocardial function. His current medications included coumadin (2 mg PO every evening), enalapril 5 mg BID, and cholecalciferol. He was held NPO for 6 h and was transported to the cardiac procedure room where routine ASA monitors were placed. RSI with endotracheal intubation was performed with the following medications: etomidate (16 mg), fentanyl (25 µg), and rocuronium (50 mg). His trachea was intubated without difficulty and maintenance anesthesia provided with desflurane. TEE was performed, followed by electrical cardioversion, which resulted in a return to normal sinus rhythm. Forty-three minutes after the single dose of rocuronium, sugammadex (4 mg/kg) was administered. Within 10 min, he had return of baseline neuromuscular function and when awake, his trachea was extubated. His postoperative course was unremarkable.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [51.6, 'kg']}",91.6,87.02,96.18,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 51.6 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (51.6 kg - 20 kg) = 91.6 mL/hr.
Hence, the patient's fluid maintenance is 91.6 mL/hr."
4527,22,Maintenance Fluids Calculations,physical,decimal,pmc-3970085-1,Extracted,"A 41-year-old man with a weight of 70 kg and height of 163 cm underwent laparoscopic appendectomy for the diagnosis of acute appendicitis. He was generally healthy but had a history of asthma as a child. In the operating room, neuromuscular function was monitored using mechanomyography by train of four (TOF) built in the anesthesia monitor (S5 TM, GE Healthcare TM, Milwaukee, WI, USA). Calibration was performed at the right adductor pollicis. General anesthesia was induced by intravenous administration of propofol 120 mg and a bolus of remifentanil 0.05 mg followed by continuous infusion of remifentanil 0.2 μg/kg/min; rocuronium 60 mg facilitated tracheal intubation. Bilateral transversus abdominis plane (TAP) block using 0.375% ropivacaine (20 mL, each) was performed using the ultrasound technique. General anesthesia was maintained by sevoflurane 1–1.5% and continuous infusion of remifentanil 0.1-0.2 μg/kg/min, and an additional 10 mg bolus of rocuronium was given at the appearance of the second twitch of TOF. The duration of surgery was 51 minutes, and the surgery was finished uneventfully. At the time of skin closure, continuous administration of fentanyl 30 μg/hr was started for postoperative pain using a patient-controlled analgesia pump (Sylinjector PCA TM, Daiken TM, Tokyo, Japan). Forty-five minutes after the final administration of rocuronium, the fourth twitch of TOF was confirmed. Sugammadex, 140 mg (2 mg/kg), was given, and infusion of remifentanil as well as propofol was discontinued. The total dose of rocuronium administered during surgery was 70 mg. The patient began spontaneous ventilation, regained consciousness, and responded to commands. The value of the T4/T1 ratio in TOF was over 90%. Chest X-ray was obtained as a routine procedure in the hospital and showed no abnormal signs (). The tidal volume was over 400 mL and respiratory rate was over 15 breaths/min. After suctioning the sputum in the trachea and oropharynx, the trachea was extubated. Just after the extubation, the patient began to choke and developed marked respiratory depression. The airway was secured by jaw tilting, spontaneous respiration resumed with stridor, and the anesthesiologist began manual bag ventilation. Even though manual bag ventilation was possible, oxygen saturation remained at around 90%. Arterial blood gas analysis revealed marked hypercapnia and hypoxia (pH, 7.14; P
CO, 61.8 mmHg; P
O, 145.8 mmHg; Base Excess, −9.4, FiO2 = 1.0). Bilateral auscultation revealed abnormal breath sounds. During mask ventilation, frothy pink sputum was noted to be coming from the patient's mouth. A bolus of propofol 40 mg and the residual bolus of rocuronium 30 mg, which remained in the syringe, were given to reintubate.
The trachea was reintubated. High airway pressure was required to obtain adequate tidal volume. Chest X-ray obtained after reintubation revealed marked bilateral pulmonary edema (NPPE) (). Arterial blood gas analysis showed remarkable hypercapnia and hypoxia (pH, 7.18; P
CO, 60.0 mmHg; P
O, 240 mmHg; and Base Excess, −7.0, FiO2 = 1.0). The patient was admitted to the ICU and received continuous positive airway pressure ventilation and administration of furosemide for two days after the surgery. The trachea was extubated two days after surgery and no clinical problems remained.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [70.0, 'kg']}",110,104.5,115.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 70.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (70.0 kg - 20 kg) = 110.0 mL/hr.
Hence, the patient's fluid maintenance is 110.0 mL/hr."
4528,22,Maintenance Fluids Calculations,physical,decimal,pmc-8044679-1,Extracted,"A 39-year-old male was referred to our hospital's neurology department because of severe headache and numbness in the left side of his body with a partial seizure that lasts 1–2 min for 3–4 times a day. The complaint started two weeks before hospital admission and progressively worsened. He had been healthy until two months before. Recently, the patient presents complaining of several weeks of cough with generalized weakness and poor oral intake. He was a non-smoker and denied using illicit drugs or another relevant medical history. He had no family history of TB and denied contact with a person with a TB infection.
On admission, he appeared well: bodyweight, 52 kg; height, 162 cm; temperature, 36.5 °C; blood pressure, 120/80 mmHg; pulse, 72 beats/min; respirations rate, 24/min; oxygen saturation, 98% while breathing ambient air. The neurology examination showed a hemisensory syndrome and 4/5 as the muscle strength score on the upper and lower extremity, respectively, in the left side of the body. All of the cranial nerve examination results were normal.
A computed tomography (CT) scan of the head showed a hypodense lesion in the right parietal lobe. Chest radiograph showed uniform-sized small nodules randomly distributed diffusely throughout the lungs (). Laboratory results found HIV antibody test was positive using ELISA (enzyme-linked immunosorbent assay), and acid-fast bacilli from sputum produced positive results. His CD4 count was 84 cells/μL. We, therefore, diagnosed the patient with miliary TB.
The patient was treated daily with three tablets of a fixed-dose combination of antituberculous treatment consisted of isoniazid (225 mg), rifampicin (450 mg), ethambutol (825 mg), and pyrazinamide (1200 mg), and also streptomycin injection 15 mg/kg. He also received intravenous dexamethasone 0.4 mg/kg per day and mannitol and then tapered-off. Valproic acid was also given for his focal seizure. The symptoms began to improve within three days after he received the anti-TB agents, and he was discharged without any complications on day 10. We postponed the ARV (antiretroviral) therapy within two weeks after starting the Anti-TB medication.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [52.0, 'kg']}",92,87.4,96.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 52.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (52.0 kg - 20 kg) = 92.0 mL/hr.
Hence, the patient's fluid maintenance is 92.0 mL/hr."
4529,22,Maintenance Fluids Calculations,physical,decimal,pmc-8349667-1,Extracted,"The patient and her mother provided written informed consent to publish this report.
A 17-year-old girl (height, 170.8 cm; weight, 51.2 kg; body mass index, 17.55 kg/m2) was scheduled to undergo maxillary sinus floor elevation and tooth removal under general anesthesia. The patient was previously diagnosed with jaw deformity, excessive resorption of the maxillary alveolar ridge, and bilateral impacted mandibular wisdom teeth.
At the age of 15 years, the patient was diagnosed with hyperthyroidism which was being treated with 10 mg thiamazole orally. She had no reported drug or food allergies, but reported a history of administration of local anesthetic several times with no complications.
Initially, the surgery was postponed because of complications related to hyperthyroidism. During the preoperative examination, she was in a clinically euthyroid state. Laboratory tests showed a hemoglobin level of 10.2 g/dL (). No abnormalities were noted on other laboratory tests or chest radiographs. A 12-lead preoperative electrocardiogram showed normal sinus rhythm.
Given her hyperthyroidism, we planned to administer 3% prilocaine containing 0.03 IU/mL felypressin as a local anesthetic to avoid complications that may arise from adrenaline-containing drugs.
Her medications were continued orally until 14 h before surgery. Upon arrival in the operating room, her peripheral oxygen saturation (SpO2) on room air was 100%. General anesthesia was induced with 100 µg of fentanyl, target-controlled infusion of propofol with an initial target plasma concentration of 5.0 µg/mL, and 30 mg of rocuronium. The patient was intubated using a nasal endotracheal tube. Anesthesia was maintained using an intermittent bolus of fentanyl (total dose was 400 µg), propofol infusion (target plasma concentration of 2.8–3.2 µg/mL), and remifentanil (0.3–0.6 mg/h).
Approximately 61 min after inducing general anesthesia, the patient was administered 3.6 mL prilocaine with felypressin for infiltration anesthesia; the same dose was added 43 min later, which led to a gradual decrease in SpO2, even though the fraction of inspired oxygen was increased to 0.6 ().
Ninety-six minutes after the first administration of prilocaine, the SpO2 level decreased to 95%. Blood gas analysis showed that the MetHb value was 3.8% and fractional oxyhemoglobin was 93.9%, despite a partial pressure of oxygen of 327 mmHg (BGA#1 in ). Next, 50 mg of methylene blue was administered slowly, 127 min after the first administration of prilocaine. The SpO2 value improved gradually to 99%, and the MetHb value decreased to 1.2% (BGA#2 in ). SpO2remained above 99%, and the MetHb value 2.5 h after the administration of methylene blue was 1.6% (BGA#3 in ). No noteworthy adverse respiratory findings were observed during the perioperative period.
Upon returning to her room, the patient did not present with any symptoms of methemoglobinemia, and SpO2 remained above 99% for 2 h under oxygenation with a simple face mask at 3 L/min. After 2 h, she remained asymptomatic, and her SpO2 remained at 98% after the oxygen mask was removed. From that point until the next day, her SpO2 was measured intermittently and remained at 97%–98% on room air. The MetHb value 7 days after surgery was 1.2%, which is within normal limits, and congenital methemoglobinemia was ruled out.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [51.2, 'kg']}",91.2,86.64,95.76,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 51.2 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (51.2 kg - 20 kg) = 91.2 mL/hr.
Hence, the patient's fluid maintenance is 91.2 mL/hr."
4530,22,Maintenance Fluids Calculations,physical,decimal,pmc-4660716-1,Extracted,"3-year-old boy with 18 kg of weight, referred to our hospital 48 h after a circumcision. The boy had ongoing pain and examination revealed a significantly ischemic, poorly perfused, almost black, glans []. Surgical procedure had been classically performed without incidents. A dorsal penile nerve block was performed with local anesthesia to decrease postoperative discomfort. Described as 2 sub-pubic symmetrical 2 mL injections of 1% mepivacaine without adrenalin, 1 cm lateral to the midline and just below the lower border of the pubis symphysis.
Blood analysis showed important increase of white blood cells count > 25000/mm3.
In spite of a good micturition, a 8 Ch bladder Foley catheter was placed to prevent future urethral stenosis.
Under general anesthesia, surgical exploration and liberation of the suture was performed, with a posterior therapeutic caudal block using a 20G (0.9 mm × 50 mm) Tuohy-Weiss needle and 24G multiperforate catheter (Perifix ONE System, BRAUN©), with bupivacaine 0.25% 1 mL/kg in extreme sterility conditions, in order to reduce sympathetic tone and improve arterial supply, as well as venous drainage. After that, topic treatment with nitroglycerin and gentamicin and oral administration of pentoxifylline 60 mg/8 h and during were started and mantained hospital stay. Patient outcoming was very impressive with nearly total resolution of the black glans coloration and local pain []. The patient was discharged at 7 days without sequelae.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [18.0, 'kg']}",56,53.2,58.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 18.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (18.0 kg - 10 kg) = 56.0 mL/hr.
Hence, the patient's fluid maintenance is 56.0 mL/hr."
4531,22,Maintenance Fluids Calculations,physical,decimal,trec-ct-2021-73,Extracted,"The patient is a 3-day-old female infant with jaundice that started one day ago. She was born at 34w of gestation and kept in an incubator due to her gestational age. Vital signs were reported as: axillary temperature: 36.3°C, heart rate: 154 beats/min, respiratory rate: 37 breaths/min, and blood pressure: 65/33 mm Hg. Her weight is 2.1 kg, length is 45 cm, and head circumference 32 cm. She presents with yellow sclera and icteric body. Her liver and spleen are normal to palpation.
Laboratory results are as follows: 
Serum total bilirubin: 21.02 mg/dL
Direct bilirubin of 2.04 mg/dL
AST: 37 U/L
ALT: 20 U/L
GGT: 745 U/L
Alkaline phosphatase: 531 U/L
Creatinine: 0.3 mg/dL
Urea: 29 mg/dL
Na: 147 mEq/L
K: 4.5 mEq/L
CRP: 3 mg/L
Complete blood cell count within the normal range.
She is diagnosed with neonatal jaundice that may require phototherapy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.1, 'kg']}",8.4,7.98,8.82,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.1 kg. Hence, the patient's maintenance fluid is 2.1 kg * 4 mL/kg/hr = 8.4 mL/hr.
Hence, the patient's fluid maintenance is 8.4 mL/hr."
4532,22,Maintenance Fluids Calculations,physical,decimal,pmc-5609782-1,Extracted,"The patient was a 49-year-old Chinese female living in Shantou, China. Accompanied by her elder brother, she came (in March 2016) to the outpatient department of the Mental Health Center, Shantou University Medical College, for excessive talking, nosiness, rash spending, decreased need for sleep, and irritable mood that had persisted for 3 weeks.
The patient was 138 cm tall and had been diagnosed with TS, confirmed by the karyotype of 45, X/46, X, i(Xq). Physical findings included the following: short neck, multiple pigmented nevi over face, moderate hearing impairment in both ears, small breasts, flat nipples, and thin flat vulva, as well as sparse armpit and pubic hairs. The other systemic examinations were as follows: weight of 40 kg and blood pressure of 97/70 mmHg. Electrocardiogram showed inverted T waves in leads V3–V6, while electroencephalogram and magnetic resonance imaging of the brain seemed to be normal. Ultrasonography showed small ovaries and uterus, as well as smaller right kidney. Moreover, ultrasonography revealed diffuse hyperplasia in the thyroid glands although no abnormal blood flow signal was seen.
During the physical examination, the patient showed clear consciousness and good eye contact while talked about irrelevant issues, although she did demonstrate inattention by looking elsewhere during the interaction. The full-scale Wechsler IQ (Chinese version) score was 66, with performance IQ score of 73 and verbal IQ score of 75.
Laboratory findings included the following: decreased levels of estradiol (19 ng/L), progesterone (0.3 μg/L), and serum testosterone (0.07 μg/L) and normal levels of follicle-stimulating hormone (FSH; 69.8 IU/L), luteinizing hormone (LH; 14.1 IU/L), and cortisol (10.4 μg/dL). Her fasting blood sugar (8.5 mM/L) and glycosylated hemoglobin (7.5%) were higher although serum insulin (12.8 IU/mL) levels were within normal range. In addition, her total thyroxine (TT4; 66.6 μg/L) and total triiodothyronine (TT3; 0.9 ng/mL) were lower, while thyroid-stimulating hormone (TSH; 7.9 IU/mL) was higher along with high levels of autoantibody to thyroid peroxidase (TPO; 180 U/mL).
The patient had a full-term vaginal birth. Her mother took medicaments to attempt to abort the pregnancy. She was the youngest child of a lower class family with eight children. Of her seven siblings (four brothers and three sisters), two brothers had history of mood disorders, which had been successfully treated.
She developed slowly during childhood and was shorter compared to her peers of the same age. She had significant academic difficulties, did not finish primary education, and never had a job. She did not experience the onset of menstruation after puberty. She married when she was 32 years old, but never had children.
Because of amenorrhea and short stature, she gradually became depressed and self-blamed, had no self-confidence, and believed she was useless. She isolated herself at home and hesitated to meet others. She had poor appetite and sleep and tried to suicide. Because of these problems and symptoms, she was admitted to the mental health center in 1991. She was diagnosed with depression and secondary hypopituitarism and treated with doxepin, which did significantly improve her symptoms.
In November 1992, the patient was admitted to the center again for depressive mood and suspicion of others. She suspected that her home had been stolen by one of her sisters-in-law and showed lack of impulse control and loss of temper. She was diagnosed with depression and depression-induced psychotic disorder. After perphenazine (16 mg/day) and doxepin (100 mg/day) treatments, her symptoms improved, and she was discharged from the center. At home, she kept up with taking her medication.
In 1995, after the discontinuation of the medication, she was admitted to the center a third time for excessive talking, hyperactivity, buying things for others without reason, and excessive praying. At home, she had difficulty controlling herself and would have outbursts with shouting and crying and other disruptive behavior. She was diagnosed with affective disorder with manic episodes, pulmonary tuberculosis, which was shown in a chest X-ray, and hypopituitarism. Her symptoms improved after treatment with antituberculosis drugs and clozapine, after which, she was discharged from the center.
The patient was hospitalized in both 2001 and 2004, for the same manic episodes including excessive talking, hyperactivity, rash spending, and difficulty controlling herself.
In 2005, the patient became depressed and stupefied, slow in her movements, lazy, and maintained erratic hours. During hospitalization, a karyotypic analysis was performed and the karyotype of 45, X/46, X, i(Xq) was identified which led to the diagnosis of TS. An endocrinologist initiated estrogen and progestin replacement therapy, and sodium valproate (1.0 g/day) was also prescribed. The patient’s mood stabilized, and she was discharged from the center; however, she did not continue the estrogen and progestin replacement therapy. Menses was present during the second cycle of treatment.
In 2009, the patient was hospitalized again for a manic episode. During hospitalization, her fasting blood sugar was found to be high, leading to a diagnosis of diabetes mellitus for which metformin was prescribed, in addition to sodium valproate for the manic symptoms.
It was concluded that the previous diagnosis of hypopituitarism was incorrect as there was no laboratory evidence to support this diagnosis. Unfortunately, the misdiagnosis had not been corrected until 2005 when a karyotype of 45, X/46, X, i(Xq) was identified. It is likely that the psychiatric practitioner was not knowledgeable regarding TS and hypopituitarism.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [40.0, 'kg']}",80,76,84,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 40.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (40.0 kg - 20 kg) = 80.0 mL/hr.
Hence, the patient's fluid maintenance is 80.0 mL/hr."
4533,22,Maintenance Fluids Calculations,physical,decimal,pmc-4173468-1,Extracted,"Ten-year-old male child weighing 18 kg, recently diagnosed as Job's syndrome with severe mental retardation presented for recurrent abscess drainage. Physical examination revealed pallor++. Airway examination showed mouth opening of two finger breadths, high arched palate, crowding of teeth with presence of primary and secondary dentition, prognathism+. Head to toe examination revealed coarse facies, microcephaly, slanting and widely separated eyes, depressed nasal bridge, with multiple abscesses over chest, back, upper, and lower limbs, Scoliosis+. Respiratory and cardiovascular system were within normal limits. There was global developmental delay. Past history revealed multiple skin lesions since one year which were medically treated. Birth history and family history were uneventful. Investigations revealed microcytic hypochromic anemia (Hb 6 gm), leukocytosis. Chest x-ray and electrocardiogram, liver function test, renal function test were with in normal limits.
I/W consent of parents was obtained. Due to associated mental retardation child was sedated under vigilance with oral syrup midazolam 9 mg (oral dose is 0.5-0.75 mg/kg)[] and EMLA cream applied with occlusive dressing 30 min prior to shifting to OT. Upon arrival to the OT, pulse oximetry, noninvasive blood pressure, electrocardiogram, temperature probe, cardioscope were attached. Difficult airway cart was kept ready before induction in view of dental and oral manifestations. Inhalation induction done with sevoflurane and IV line secured with 22G cannula. Glycopyrolate 0.1 mg + fentanyl 30 mcg + propofol 30 mg given intravenously. General anesthesia was maintained with bag and mask ventilation with oxygen + nitrous oxide + sevoflurane with spontaneous ventilation. Ringer lactate weighing 230 mL was infused intraoperatively. Temperature was maintained with the help of warming blankets. Patient was shifted to PACU and monitored with ECG, NIBP, and Pulse oximetry. Intravenous fluids maintained at a rate of 56 mL/h. Paracetamol suppository 400 mg was used for postoperative analgesia. Postoperative period was uneventful.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [18.0, 'kg']}",56,53.2,58.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 18.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (18.0 kg - 10 kg) = 56.0 mL/hr.
Hence, the patient's fluid maintenance is 56.0 mL/hr."
4534,22,Maintenance Fluids Calculations,physical,decimal,pmc-6906581-1,Extracted,"A 41-year-old man presented with pain in the right lower posterior teeth, followed by swelling and pain in the oral and maxillofacial head and neck regions for 7 d, and difficulty in breathing and swallowing for 2 d.
One week before admission, due to pain in the right lower posterior teeth, the patient placed a cigarette butt dipped in the pesticide ""Miehailin"" into the ""dental cavity"" to relieve the pain. However, two days later, there was no significant improvement in dental pain and he visited a local community clinic where the doctors removed the cigarette butt and the patient received an infusion of anti-inflammatory drugs for 4 d. However, the odontogenic infections gradually became aggravated, and spread bilaterally to the floor of the mouth, submandibular space, neck, chest, waist, back, temporal and other areas. The patient also began to have difficulty in breathing, swallowing and eating. Due to these complications, the patient was transferred to our hospital for follow-up treatment as an emergency admission. Since the onset of illness, he had been mentally exhausted, with a poor diet, poor sleep, and weight loss of approximately 2.5 kg.
Healthy, with no specific diseases.
None.
Physical examination showed that the patient had an acutely painful face, extensive swelling and pneumatosis in the bilateral temporal, oral, maxillofacial, neck, chest, waist and back regions, combined with skin redness and high temperature. The submandibular space and neck regions pulsated when touched. Puncture revealed purulent fluid which was black, thin, with bubbles and had a foul odor. When the patient was admitted to hospital, mouth opening was less than 1 cm; therefore, the tooth lesion could not be examined properly.
Laboratory examination results on emergency admission were as follows: leukocyte count was 13.53 × 109/L, neutrophil ratio was 88.40%, hypersensitive C-reactive protein was > 180 mg/L, and procalcitonin was 9.8 ng/mL. Electrolyte results were: potassium was 5.65 mmol/L, sodium was 136.4 mmol/L, chlorine was 101.9 mmol/L, calcium was 1.91 mmol/L, and magnesium was 0.93 mmol/L. Liver and kidney function test results were as follows: alanine aminotransferase was 19 U/L, glutamic oxaloacetic aminotransferase was 23 U/L, creatinine was 94 µmol/L, and urea was 19.1 mmol/L. The platelet count was 41.0 × 109/L and the D-dimer level was 1184 ng/mL. The results of blood culture indicated infection with Streptococcus viridans. Drug sensitivity testing indicated that the organism was sensitive to penicillin antibiotics.
Computed tomography scans of the maxillofacial, neck and chest regions showed extensive swelling and pneumatosis in soft tissues bilaterally in the oral, maxillofacial, temporal, cervical, parapharyngeal space, chest, back, mediastinum and posterior abdominal wall regions (Figures and ). The upper respiratory tract was narrowed slightly and bilateral lung pneumothorax was observed. A small amount of effusion was seen bilaterally in the pleura and pericardium (Figure ). Lung pneumothorax was more serious on the left side and the compression ratio was approximately 20%-30% (Figure ). Pulmonary infection was seen in both lungs, particularly in the left lung.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.5, 'kg']}",10,9.5,10.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.5 kg. Hence, the patient's maintenance fluid is 2.5 kg * 4 mL/kg/hr = 10.0 mL/hr.
Hence, the patient's fluid maintenance is 10.0 mL/hr."
4535,22,Maintenance Fluids Calculations,physical,decimal,pmc-5803987-1,Extracted,"A 24-year-old G4P2 female presented for fetal arrhythmia at 33 weeks' gestation. Fetal ultrasound revealed enlarged heart with small periventricular effusion []. Detailed history revealed Group B Streptococcus (GBS) bacteriuria treated with a standard course of ampicillin between weeks 2 and 6 of gestation and upper respiratory infection at approximately 17–19 weeks gestation. The only other medication used was prenatal vitamins. Family history was negative for congenital heart disease or connective tissue disease. Pregnancy history was positive for a first trimester spontaneous abortion and two full-term vaginal deliveries, one of which was complicated by pregnancy-induced hypertension. A fetal echocardiogram revealed no arrhythmia with preserved ventricular function, and no LV aneurysm was appreciated at that time. She was followed with weekly nonstress tests, which remained normal. She did not have any further complications or exposures, and at 39 weeks' gestational age, she had an uncomplicated vaginal delivery of a 3.245 kg boy.
The infant continued to have irregular heart rate, and an electrocardiogram revealed frequent premature ventricular contractions but no runs of ventricular tachycardia. Vital signs were normal and physical examination noted a 2/6 systolic ejection murmur loudest at the left midsternal border with some radiation to the back. An echocardiogram revealed the presence of large LA appendage aneurysm and large LV free wall aneurysm with good biventricular function. He was started on Inderal and aspirin and was observed in the neonatal Intensive Care Unit with stable clinical course before repeat echocardiogram at 1 week of age showed the development of a large blood clot in the LA appendage. He was placed on enoxaparin sodium (Brand name - Lovenox, Manufacturer - Sanofi-aventis) and was transferred to a quaternary facility [].
Cardiac magnetic resonance imaging confirmed LA appendage aneurysm with blood clot and large left free wall LV aneurysm. Surgical LA aneurysm resection was performed, but the clot had already embolized to the left iliac bifurcation without evidence of limb ischemia [].
His initial postoperative course was uncomplicated, and he was discharged on Coumadin therapy. Postoperative echocardiogram revealed the development of a left ventricle apex pseudoaneurysm which required surgical plication [].
Coagulation workup was negative, and Coumadin was discontinued with continuation of aspirin therapy. Serial echocardiograms continue to show large aneurysm of the left ventricle free wall with good LV function []. The ventricular ectopy decreased, and beta-blockers were discontinued until the age of six when he developed dizziness and ventricular ectopy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.245, 'kg']}",12.98,12.331,13.629,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.245 kg. Hence, the patient's maintenance fluid is 3.245 kg * 4 mL/kg/hr = 12.98 mL/hr.
Hence, the patient's fluid maintenance is 12.98 mL/hr."
4536,22,Maintenance Fluids Calculations,physical,decimal,pmc-8664037-1,Extracted,"A 4-year 8-month-old girl born of third degree of consanguinity presented with cough and progressive breathlessness for 3 months. She was hypoxic for 2 weeks prior to presentation requiring oxygen support. She was admitted twice in the past 1 year for cough and breathlessness wherein a diagnosis of viral respiratory tract infection was made. Her birth, immunization, developmental, and family history were unremarkable. There was no significant family or personal history of asthma or allergy or any other respiratory illness.
Clinical examination on presentation to our hospital revealed the child with failure to thrive, with a weight of 12.1 kg (<first centile) and a height of 97 cm (<third centile). She was afebrile, had tachycardia (heart rate of 120/minute), and was tachypneic (respiratory rate of 46/minute). She had marked subcostal and intercostal retraction and a SpO2 of 93% on 10 L/minute of oxygen by a non-rebreathing mask. On systemic examination, the child had pectus excavatum with bilateral coarse crackles on auscultation, with the rest of the examination being normal.
Basic hematological workup done during her previous admission was normal. Arterial blood gas (ABG) on O2 of 10 L/minute showed PaO2—104 mm Hg, PaCO2—45.8 mm Hg, pH—7.31, and HCO3—22.4 mmol/L. Her thyroid function tests, electrocardiogram, and 2D echo were within normal limits. Human immunodeficiency virus was negative. Serum lactate dehydrogenase (LDH) was raised—694 U/L (140–280 U/L). X-ray of the chest showed bilateral reticular infiltrates, which showed a progressive worsening in serial X-rays () over the past 1 year, and computed tomography (CT) of the chest showed diffuse intralobular and interstitial thickening with ground-glass opacities (crazy-paving pattern) suggesting interstitial lung disease ( and ). Clinical and radiological features were suggestive of PAP, and further investigations were done to confirm the diagnosis.
The bronchoscopy and bronchoalveolar lavage done in her previous hospital admission were inconclusive. It was negative for acid-fast bacilli, Pneumocystis carinii, and aerobic cultures, and galactomannan test was also negative. An autoimmune etiology was ruled out as an antibody against granulocyte-macrophage colony-stimulating factor (GM-CSF) was negative, and serum GM-CSF concentration was raised. Next-generation sequencing showed contiguous homozygous deletion encompassing exonic regions 1 to 5 of CSF2RA gene, suggestive of pulmonary surfactant metabolism dysfunction 4, an X linked disorder confirming a diagnosis of PAP.
She was treated with steroids, antibiotics, and other supportive care. With a confirmed diagnosis of PAP due to CSF2RA gene mutation and the presence of severe respiratory insufficiency, a decision was made to perform a therapeutic WLL on ECMO.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.1, 'kg']}",44.2,41.99,46.41,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.1 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.1 kg - 10 kg) = 44.2 mL/hr.
Hence, the patient's fluid maintenance is 44.2 mL/hr."
4537,22,Maintenance Fluids Calculations,physical,decimal,pmc-4386196-1,Extracted,"A fifty two year old male was admitted via Emergency department with complaints of shortness of breath. Patient had history of intermittent episodes of shortness of breath for last two years with each episode being worsened from the previous one. The last episode started one month ago restricting his physical activity only to few steps; Shortness of breath is partially relieved by lying laterally. It was also associated with productive cough with white scanty, non-foul smelling sputum, occasionally mixed with blood. Patient also received ATT (anti tuberculosis therapy) for last fifteen days without any betterment in his status. He holds past two year record of admissions, where he was treated for pneumonia initially; later two admissions were done with extensive workup firstly in August 2012 and latter January 2013. Biopsies were done both the time and both confer the diagnosis of solitary fibrous tumor. Patient was advised for followup in both institutes, but never returned and finally landed in our institute in order to avoid a possible surgical resection.
Clinically patient was restless, tachycardic and tachypneic but maintained oxygen saturation on 3-4 liter of oxygen. His chest examination showed decrease right sided movements with dull percussion note, decrease breath sounds. Lab investigations further revealed anemia with Hemoglobin of 8.0 gm/dl, blood gases showed mild hypoxia with PO2 of 80mm Hg while rest of his metabolic panel & co-agulation profile were within normal limit.
Chest X-ray showed a large homogenous opacity on right side with mediastinal shift. CT Scan of chest confirmed the finding of a large heterogeneous mass with few sparks of calcification occupying almost whole of the right hemi thorax. Medially the mass was abutting and pushing superior vena cava, Aorta, right pulmonary artery and heart. Mass was also causing compression effects on the right hemi-diaphragm. It is displacing the mediastinal contents on to the left and caused compression collapse of right medial and lover lobe. Minimal pleural effusion with pleural thickening was also noted. ( and )
After thorough discussion and multiple settings; patient was counselled for surgical removal of the mass and its catastrophic outcome in case of further delay. Explorative thoracotomy was done and a huge extra pleural mass was removed. Right upper lobe of the lung was also adherent to the mass. Careful incision was performed to remove the mass preserving the surrounding vascular structures with minimal blood loss. The size of excised mass 24 x 20cm x 8cm and it was 3150gm in weight. (). The lower and middle lobe collapse was relieved partially and later fully. Two drains were placed and wound was approximated.
The pathological examination revealed a single multi nodular encpsulated pale white firm piece of tissue. On serial sectioning two collapsed cavities were also indentified with larger one measuring 5 x5 cm filled with yellow pleurant exudate. A flap of pleura id identified too measuring 12x6 cm.
Microscopic examination revealed demarcated lesion composed of spindloid cells. The nuclei are oval to elongated with evenly dispersed chromatin. Cytoplasm is abundant. Scattered mitotic figures are seen. Areas of hyalinization and fibrosis are noted. Conclude as neoplastic lesion; solitary fibrous tumor as possibility.
Patient was kept on mechanical ventilation, but, as per plan, the ICU team could not wean him off in next two days. Patient also developed fever spikes and later developed ventilator associated pneumonia. Tracheal cultures revealed acinetobacter. Intravenous anti-biotics were given as per sensitivity and after six days patient was finally extubated. Drains were removed on third day of surgery. Physical capacity continues to increase slowly and patient was able to walk short distances without any discomfort.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3150.0, 'g']}",12.6,11.97,13.23,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3150.0 g so this converts to 3150.0 lbs * kg/1000 g = 3.15 kg. Hence, the patient's maintenance fluid is 3.15 kg * 4 mL/kg/hr = 12.6 mL/hr.
Hence, the patient's fluid maintenance is 12.6 mL/hr."
4538,22,Maintenance Fluids Calculations,physical,decimal,pmc-3030069-1,Extracted,"A 178 cm, 64 kg and 67-year-old male patient, who suffered from continuous epigastric pain and nausea for about 1 month, was admitted. Stomach cancer was diagnosed from the endoscopic biopsy, so a total gastrectomy was decided. The patient had no past medical history other than an appendectomy.
To reduce the patient's anxiety, 2 mg of midazolam was administered intravenously. Once arriving at the operating room, standard monitoring of electrocardiogram, pulse oximetry, and noninvasive blood pressure were established before the induction of anesthesia. The initial vital signs were arterial pressure of 123/71 mmHg, pulse rate of 73 rate/min, and peripheral oxygen saturation (SpO2) of 100%. General anesthesia was induced with remifentanil and propofol at target effect-site concentrations of 3.0 ng/ml and 4.0 µg/ml, respectively, using target-controlled infusion device (Orchestra® infusion pump system, Fresenius vial, Brezins, France), and 40 mg of rocuronium was administered intravenously. After 2 min of manual ventilation, intubation was performed with a 7.5 mm diameter cuffed endotracheal tube. After tracheal intubation, mechanical ventilation was performed using oxygen and medical air (FiO2 = 0.5) to make an end-tidal carbon dioxide level between 30 and 35 mmHg. Anesthesia was maintained by propofol and remifentanil infusion. A 16 Fr Foley catheter was inserted and a nasopharyngeal thermometer was placed. Antibiotic drug, 1 g of cefazoline, was administered intravenously after the negative response was confirmed on an intradermal test.
Approximately 35 minutes after the induction of general anesthesia, the skin incision was started and 5 min later, the arterial pressure was suddenly dropped to 50/36 mmHg, SpO2 was reduced to 80%, and the pulse rate was elevated above 120 rates/min. The lungs were ventilated with oxygen (FiO2 = 1.0) and remifentanil infusion was stopped. Despite 10 mg ephedrine and 20 µg phenylephrine were administered intravenously to raise the arterial pressure, there were no changes in the arterial pressure or heart rate. Rale and wheezing in both lungs were heard upon auscultation of the chest, thus airway secretions were removed by tracheal suction and salbutamol sulfate (Ventolin™ inhaler, 100 µg/puff, GlaxoSmithKline, Madrid, Spain) was sprayed 2-3 times through the endotracheal tube. A 20 gauge catheter was placed on the right radial artery for continuous arterial pressure monitoring. An arterial blood gas analysis was performed, which showed pH 7.17, PaCO2 60.6 mmHg, PaO2 80.7 mmHg, HCO3 21.5 mmHg, SaO2 92.5%, Na+ 154.2 mmol/L, K+ 5.16 mmol/L, and Ca2+ 1.46 mmol/L. In addition, 20 µg phenylephrine was administered, and continuous infusion of 10 µg/kg/min dopamine and 0.02 µg/kg/min norepinephrine were started afterwards. Epinephrine (0.2 mg) was injected subcutaneously for bronchial dilation, and the broncho-tracheal suction and salbutamol sulfate treatment were performed repetitively. However the patient's hemodynamic vital signs did not improve, so a transesophageal echocardiogram was performed to evaluate cardiac function and to rule out thromoembolism. However, there were no structural or functional specific findings, and a simple chest X-ray also did not result in any specific abnormal findings.
An arterial blood gas analysis was performed again 50 min after the surgery, when the FiO2 was at 1.0, which showed pH 7.18, PaCO2 67.9 mmHg, and PaO2 141.7 mmHg. PaO2 had improved, but PaCO2 was still high. Large amount of secretion in the airway was revealed by bronchoscopy. The surgery was at dissection of omentum before starting the main procedure of a total gastrectomy. Despite the various managements, systolic arterial pressure remained below 80 mmHg, and pulse rate remained continuously above 125 rates/min. So judging that proceeding with the surgery would be risky for the patient, it was determined that the surgery was terminated and the patient should be transferred to the intensive care unit (ICU). Total anesthesia time was 95 min and total surgery time was 60 min with infused crystalloid solution, infused colloid solution, estimated blood loss, and urine volume of 1,000 ml, 500 ml, 100 ml and 400 ml, respectively. While the patient was being moved to the ICU, skin rash and urticaria were discovered on his chest and abdomen. So 4 mg of chlorpheniramine and 5 mg of dexamethasone were administered immediately. Upon arriving in the ICU, the patient's vital signs were as follows; arterial pressure of 117/67 mmHg, pulse rate 127 rates/min, and SpO2 of 95%. The patient's hemodynamic vital signs slowly stabilized and returned to the preoperative levels about 1 hr after. Skin rash and urticaria disappeared and the endotracheal tube was removed after the consciousness was recovered. The next day the patient was transferred to the ward.
The sudden occurrence of cardiovascular collapse and the outbreak of rash and urticaria led us to suspect anaphylaxis. A skin test was decided upon to identify the drugs that could have been the cause. After two weeks, a skin test had been performed, which showed only a strong positive response to latex. A weak positive response appeared just on the intradermal test when 10 mg/ml rocuronium was tested. Other than that, there were no specific responses to intraoperatively used anesthetic or antibiotic drug administered immediately before surgery. When rocuronium was administered, hemodynamic stability was maintained until before starting the surgery, however, several minutes into the surgery, the patient became hemodynamically unstable. That led us to strongly suspect that the anaphylaxis had been caused by latex rather than by rocuronium.
One week later, a total gastrectomy was performed again. Thirty mg of methylprednisolone was administered twice at 12 hr and 2 hr before surgery, and 4 mg of chlorpheniramine and 50 mg of ranitidine were administered 1 hr before surgery. To prevent exposure of the patient to latex during the whole time of anesthesia and surgery, the surgical gloves (Biogel® Skinsense, Mölnlycke Health Care, Norcross, GA, USA) and all other items were prepared with latex-free products. There was no latex-free Foley catheter, so it was not inserted. As rocuronium had shown a weak positive response on the intradermal test, atracurium was used instead, which showed a negative response. Propofol, remifentanil, and atracurium were used for general anesthesia, and the surgery proceeded uneventfully. The patient was discharged 7 days later in better condition.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [64.0, 'kg']}",104,98.8,109.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 64.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (64.0 kg - 20 kg) = 104.0 mL/hr.
Hence, the patient's fluid maintenance is 104.0 mL/hr."
4539,22,Maintenance Fluids Calculations,physical,decimal,pmc-5417264-3,Extracted,"The last patient was a 4-year-old female. Following an uncomplicated pregnancy with no ultrasound abnormalities or polyhydramnios, she was born to a G1P1 mother and nonconsanguineous parents. The patient’s mother had had a history of renal stones and recurrent urinary tract infections secondary to a vesicoureteral reflux. The maternal great uncle had received a renal transplant in his mid-40s, though the reason for the transplant was unknown. There was no other family history of renal disease or hearing loss. The child had a long-standing history of dysmorphic features and spastic dystonic diplegia. Her symptoms were consistent with those found on the Galloway-Mowat syndrome spectrum and included microcephaly, cerebellar atrophy, developmental delay and seizures, and proteinuria, with an absence of infantile nephrotic syndrome. Her dysmorphic features included prominent large ears, frontal bossing, a broad nasal bridge, a high arch palate, and scarce eyebrows. In the past, she had exhibited failure to thrive and developmental delay that had progressed since the age of 8 months. She was followed by the genetics clinic because of her developmental delay and her dysmorphic features, which could not be linked to a particular diagnosis or syndrome. She had no previous episodes of dehydration, polyuria, or polydipsia.
She initially presented with status epilepticus and hypomagnesemia at the age of 4. Her anthropomorphic parameters were within normal limits: weight (10.0 kg—below the 3rd percentile), height (94 cm—between the 3rd and 10th percentiles), and head circumference (44.5 cm—below the 3rd percentile). She was placed on valproic acid following her first seizure and experienced significant side effects including lethargy and severe drooling.
She had 2 subsequent hypomagnesemia-associated episodes of status epilepticus; her most recent episode had been complicated by an extended spectrum β-lactamase Escherichia coli urinary tract infection. Her lowest magnesium level was 0.31 mmol/L [reference interval 0.65-1.05] (0.75 mg/dL) and her calcium level was normal at 2.31 mmol/L [reference interval 2.15-2.55] (9.24 mg/dL). Her fractional excretion of magnesium was elevated at 26%. There was no evidence of hypercalciuria (calcium to creatinine ratio 0.35 [reference interval < 0.6] mmol/mmol). Aside from transiently low serum potassium, her serum bicarbonate level, urate level, and fractional potassium excretion were normal. Exome sequencing was performed to verify the CNNM2 mutation differential diagnosis, which is associated with hypomagnesemia and impaired brain development. This test was negative and there was no association with any other known magnesium-losing tubulopathies. No abnormalities were noted in the WDR73 gene, which is associated with Galloway-Mowat syndrome. A head MRI revealed diffuse cerebral white matter signal abnormalities evocative of demyelination along with progressive atrophy of the cerebellar hemispheres. The numerous EEGs that were performed while she took her maintenance antiepileptics showed that her epileptic activity ceased when her magnesium levels normalized. Her EEG had a background of δ grade II generalized activity, with suppression of grade I activity in the right hemisphere.
The patient’s seizures were difficult to control, requiring phenytoin (15 mg/kg loading dose) and intubation with a midazolam infusion during her episodes of status epilepticus. Her serum magnesium levels normalized after several days of magnesium sulfate infusions (14 mg/kg/h), after which she was switched to oral magnesium oxide (120 mg/kg/d). The addition of amiloride was necessary to maintain stable magnesium levels, and following another episode of status epilepticus, some of the magnesium oxide was replaced with magnesium bisglycinate to reduce diarrhea. If her magnesium levels fall below 0.65 mmol/L, she usually experiences seizures. She is also on enalapril to control her hypertension and proteinuria, which are commonly seen in Galloway-Mowat syndrome.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.0, 'kg']}",40,38,42,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.0 kg - 10 kg) = 40.0 mL/hr.
Hence, the patient's fluid maintenance is 40.0 mL/hr."
4540,22,Maintenance Fluids Calculations,physical,decimal,pmc-8571992-1,Extracted,"A 57-year-old woman presented to the emergency department (ED) – in December 2020 – with complaints of slurred speech, confusion, and left upper limb weakness. Her medical history included suffering from a persistent fever, severe headache, cough, fatigue, anosmia, dysgeusia, sore throat, vomiting, dizziness, fatigue, and bony pain, and the reverse transcription-polymerase chain reaction (RT-PCR) assay of nasopharyngeal swab sample was positive for SARS-CoV-2 from one week before presentation in ED. The patient also has diabetes mellites and hypertension in her medical history. All routine diagnostic tests were done, and the patient’s blood analysis showed an increase in red blood cells (RBCs), lymphocytes count, a marked increase in C-reactive protein (CRP), and D-dimer due to infection. She had a slightly decreasing mean corpuscular hemoglobin concentration and a marked increase in fasting blood glucose (FBS) as diabetes (). The patient weight was 70 kg; height: 150 cm; body mass index (BMI): 31 kg/m2; and the blood pressure: 140/100 mm Hg sitting. The pulse was 90/min, and oxygen saturation was 90%. Chest computed tomography (CT) and magnetic resonance imaging (MRI) on the brain were done for the patient. CT of the lung showed few right-side apical small ground-glass consolidation patches with bilateral mild subpleural lower lobar ground-glass haze more accentuated on the right side that scientifically reefed to right-side viral pneumonia because of COVID-19. Few scattered sub-centimetric emphysematous bullae were noted with fine scattered subpleural atelectatic bands. Mediastinal structures are normal with a patent tracheobronchial tree. There is no mediastinal, hilar adenopathy, or pleural effusion (). The scanned arterial tree, including the coronary vessels, involved advanced atherosclerotic changes and mild to moderate cardiac chamber enlargement. Visualized cuts of the upper abdomen revealed a well-defined right adrenal lesion with internal fat density measuring about 5.2 cm × 4 cm, primarily representing fat-rich adenoma with few bilateral simple cortical renal cysts ().
Brain MRI showed acute infarction of the right basal ganglia () and abnormal hyperintense signal along with the right caudate head and anterior limb of the internal capsule in (a) fluid-attenuated inversion recovery (FLAIR) sequence (arrow) associated with positive mass effect on the right lateral ventricle. The corresponding area of restricted diffusion was appreciated as a hyperintense signal in (b) diffusion-weighted imaging (DWI) and hypointense signal in (c) apparent diffusion coefficient (ADC) denoting restricted distribution in the DWI and ADC map, (d) perfusion-weighted imaging (PWI) showing corresponding markedly reduced perfusion in the affected area (circle) impressive of right caudate head/anterior limb of internal capsule acute infarction. The images were imported into the viewing software (OsiriX Lite®).
Intravenous recombinant tissue plasminogen activator (rt-PA) was given to patients within 3 hours after onset. In addition to starting the COVID-19 therapeutic course, the decision was taken to admit the patient to an intensive care unit (ICU) until stabilizing O2 saturation. We treated the patient with intravenous ceftriaxone (2 g/day for 14 days), methylprednisolone (60 mg daily over six months), and anticoagulation over three months. Symptoms resolved entirely within 72 h. The patient was discharged after two weeks of antibiotic therapy. During a follow-up period of two weeks, no new symptoms occurred, and the second nasopharyngeal swab by RT-PCR assay was negative for SARS-CoV-2.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [70.0, 'kg']}",110,104.5,115.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 70.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (70.0 kg - 20 kg) = 110.0 mL/hr.
Hence, the patient's fluid maintenance is 110.0 mL/hr."
4541,22,Maintenance Fluids Calculations,physical,decimal,pmc-7485990-2,Extracted,"Case 2 was a 10-year-old Japanese girl, with no significant past medical history. She was born at 39 weeks of gestational age, with a birth weight of 3202 g (+1.1 SD) and birth length of 49.5 cm (+0.4 SD). She had a height of 148.6 cm (+1.8 SD), body weight of 26.2 kg (-0.9 SD), and BMI of 11.9 kg/m2 (-3.6 SD). Her body weight was 31.1 kg one month prior to presentation There was no family history of DM. She was referred to our hospital after presenting with generalized fatigue, polydipsia, and polyuria. She was able to maintain conversation but was moderately restless in general. Her vital signs are shown in Table . A clinical examination revealed fruity breath odor, Kussmaul breathing, and lethargy. A diagnosis of DKA-HHS was made based on her laboratory findings (Table ).
We administered 0.58%-0.9% saline and insulin 0.05 U/kg/h via DIV. Finally, her sodium level returned to the normal range after 78 hours from admission (Figure ). She did not develop any neurological complications.
Six months postadmission, the patient is 146.4 cm (+1.2 SD) tall, with a body weight of 33.4 kg (-0.6 SD) and BMI of 13.6 kg/m2 (-2.1 SD). Her treatment consists of 10 units/day of insulin degludec and 19 units/day of insulin lispro (0.87 units/body weight/day). She was diagnosed with T1DM, complicated with DKA-HHS and severe hypernatremia.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [26.2, 'kg']}",66.2,62.89,69.51,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 26.2 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (26.2 kg - 20 kg) = 66.2 mL/hr.
Hence, the patient's fluid maintenance is 66.2 mL/hr."
4542,22,Maintenance Fluids Calculations,physical,decimal,usmle-1024,Extracted,"A 3100-g (6.9-lb) male newborn is brought to the emergency department by his mother because of fever and irritability. The newborn was delivered at home 15 hours ago. He was born at 39 weeks' gestation. The mother's last prenatal visit was at the beginning of the first trimester. She received all standard immunizations upon immigrating from Mexico two years ago. Seven weeks ago, she experienced an episode of painful, itching genital vesicles, which resolved spontaneously. Four hours before going into labor she noticed a gush of blood-tinged fluid from her vagina. The newborn is ill-appearing and lethargic. His temperature is 39.9°C (103.8°F), pulse is 170/min, respirations are 60/min, and blood pressure is 70/45 mm Hg. His skin is mildly icteric. Expiratory grunting is heard on auscultation. Skin turgor and muscle tone are decreased.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3100.0, 'g']}",12.4,11.78,13.02,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3100.0 g so this converts to 3100.0 lbs * kg/1000 g = 3.1 kg. Hence, the patient's maintenance fluid is 3.1 kg * 4 mL/kg/hr = 12.4 mL/hr.
Hence, the patient's fluid maintenance is 12.4 mL/hr."
4543,22,Maintenance Fluids Calculations,physical,decimal,pmc-4613638-1,Extracted,"We report a 28-year-old single man with bilateral breasts enlargement, which was noticed since the age of 15 years. At the onset, it was painful, but the pain disappeared with time. No history suggestive of headache, visual changes, testicular trauma, or systemic or sexually transmitted diseases. Family, surgical and drug histories were unrevealing. On examination, he was obese (weight 89.8 Kg, height 159 cm, body mass index 35.9) and has an arm span of 165 cm. Systemic examination was unremarkable apart from mild hepatomegaly. Local examination revealed bilateral soft breast enlargement 14×10×10 cm (), with non tender sub-areolar mass concentric, areola (3.5 x 3.5 cm), with regular borders, and free from underlying and overlying tissues. He has a little facial hair, scanty axillary and pubic hair, small and atrophic testes, and small non-buried penis. All routine biochemical reports were within normal limits. Hormonal assay revealed hypergonadotrophic hypogonadism on the basis of low serum total testosterone, high luteinizing hormone, and high follicle stimulating hormone with normal prolactin, estradiol, thyroid stimulating hormone, cortisol, beta human chorionic gonadotrophin, and alpha fetoprotein. Abdominal and pelvic CT was normal apart from fatty liver. Scrotal ultrasound showed significantly small testes, but with normal echotexture and shape. Bilateral ultrasound showed enlarged breasts, very small and difficulty visualized glandular tissue, normal nipples, areola, subcutaneous and fatty tissues, and axillary regions. Bilateral mammography showed predominantly fatty tissue and there were no masses, abnormal fibroglandular tissues, calcifications, or axillary lymph nodes. Semen analysis showed Azoospermia. Cytogenetic analysis, which showed 47 XXY karyotype diagnostic of Klinefelter’s syndrome (KS).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [89.8, 'kg']}",129.8,123.31,136.29,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 89.8 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (89.8 kg - 20 kg) = 129.8 mL/hr.
Hence, the patient's fluid maintenance is 129.8 mL/hr."
4544,22,Maintenance Fluids Calculations,physical,decimal,pmc-4747957-1,Extracted,"A 65-year-old woman suffered general fatigue, abdominal fullness, and dyspnea for a month and visited our hospital. The dyspnea had prevented her from sleeping for several days. She had hypertension and underwent laparoscopic cholecystectomy for cholecystitis 20 years earlier. She denied history of trauma. She was 146 cm tall and weighted 97 kg (body mass index, 45.5). Her blood pressure, pulse, and oxygen saturation were 96/59 mmHg, 85 beats/min, and 90 %, respectively. Her body temperature was 37.5 °C. Her abdomen was highly distended, and she could not lie supine because she felt harder to breathe. Abdominal tenderness, muscular defense, or Blumberg’s symptom were not observed. Laboratory examinations revealed general inflammation (leukocyte count, 15,700/μl; C-reactive protein level, 16.2 mg/dl), mild liver dysfunction (total bilirubin, 2.97 mg/dl; direct bilirubin, 0.81 mg/dl), and mild renal dysfunction (creatinine, 1.40 mg/dl). Anemia was not indicated (hemoglobin level, 13.3 g/dl). Computed tomography revealed giant polycystic liver which occupied the large part of the peritoneal cavity, much ascites in the lower abdomen, and highly elevated right diaphragm (Fig. a). Fractional liver parenchyma was detectable in the right lobe. Only two small cysts were observed in kidneys. Serological tests for Echinococcus antibody were negative. Abdominal paracentesis provided dark brown transparent ascites that showed no evidence of parasites or neoplasms. Any kinds of bacteria were not detected by culture of the ascites.
We diagnosed isolated polycystic liver disease (PCLD) and spontaneous rupture of the cysts. The cause of leukocytosis and high serum CRP values was not apparent, but we denied infectious peritonitis on the ground of physical findings and appearance of the ascites. We continuously drained the ascites whose volume was totally 16,000 ml in 25 days. Her dyspnea, general inflammation, and hepatorenal dysfunction were improved (oxygen saturation, 97 %; leukocyte count, 5920/μl; C-reactive protein level, 6.17 mg/dl; total bilirubin, 0.56 mg/dl; direct bilirubin, 0.17 mg/dl; creatinine, 0.56 mg/dl). Her weight and body mass index downed to 82 kg and 38.5, respectively. Despite those remarkable improvements, abdominal fullness remained after the drainage.
Twenty-five days after her visit to our hospital, resection of multiple liver cyst walls and left lateral segmentectomy were performed (Fig. ). We started the surgery by laparoscopic approach but switched to laparotomy to repair the left hepatic duct which was injured by the laparoscopic manipulation. Kinds of intracystic fluid varied between individual cysts; colorless transparent, dark-brownish transparent, bile-like transparent, or abscess-like muddy fluid were observed. Discharged fluid was totally 7500 ml. On gross examination, excised left lateral segment consisted almost entirely of cysts and resected all cyst walls were thickened without mural nodules (Fig. a). Histopathological examination of the specimens revealed simple columnar epithelia inside of cyst walls and fractional liver parenchyma between the cyst walls and showed no evidence of parasites or neoplasms (Fig. b). After the surgery, her abdominal fullness was greatly lessened and she has been asymptomatic for 10 months (Fig. b).
Simple liver cysts sometimes reach large sizes and cause pressure symptoms resulting from mass effect, vascular compression, and biliary obstruction []. In the present case, multiple and giant liver cysts occupied most of the abdomen. Initially, polycystic liver was considered to be associated with autosomal dominant polycystic kidney disease (ADPKD) []. In 2003, Tahvanainen et al. indicated that polycystic liver in some patients was genetically distinct from ADPKD; it is now known and described as PCLD []. PCLD has an autosomal dominant inheritance pattern as ADPKD does. Genetic mutation in PKD1 or PKD2 was observed in both PCLD and ADPKD, but genetic mutation in PRKCSH or SEC63 was specifically identified only in PCLD []. Although genetic examination was not performed, the present case was clinically diagnosed as PCLD according to the diagnostic algorithm devised by Lantinga et al. []. The present case provided unexplained inflammation which might reflect that some liver cysts were infectious because several cysts contained abscess-like fluid in the operation. PCLD is a rare condition and has prevalence of less than 0.01 % []. Similar to simple liver cysts, cysts in PCLD contain a clear, bile-like fluid, and pathologically consist of an inner lining of cholangiocytes []. PCLD can lead to massive hepatomegaly and cause pain or compression of the adjacent gastrointestinal organs, vasculature, and diaphragm []. Van Keimpema et al. examined clinical features of PCLD in their retrospective study (n = 137) []. In summary, they described that symptomatic PCLD patients were mainly females (86 %), most patients had more than 20 liver cysts (88 %), median diameter of the largest cyst was 9 cm, females and mutation carriers were younger at diagnosis and had more severe courses of disease, and PCLD-related mortality was 2 %. Hoevenaren et al. compared the clinical features of patients with PCLD (n = 19) with those of patients with ADPKD (n = 34) []. They concluded that the clinical course of PCLD was relatively benign compared with ADPKD, although PCLD was characterized by larger and greater number of liver cysts. While ADPKD is characterized by an increased risk of developing vascular manifestations such as hypertension, mitral valve prolapse, and intracranial aneurysms, several studies have shown that PCLD patients do not have the risk and targeted screening for those diseases is not advised for PCLD [, ]. For PCLD patients with pressure symptoms, surgical reduction of the volume of the liver cysts has been generally performed to diminish the mass effect [] and somatostatin analogues, lanreotide, and octreotide are expected to relieve the symptoms as optional therapies [].
Spontaneous rupture of simple liver cysts including polycystic liver is extremely rare, and only 14 cases have been reported including this case [–] (Table ). Median age of onset is 62.5. Male to female ratio of the patients is 5:9. Two patients had received maintenance hemodialysis for chronic renal failure due to ADPKD. Only our case was diagnosed as PCLD. Most of the patients complained of abdominal pain. Locations of ruptured cysts were the right lobe in six patients and the left lobe in eight patients. Median size of the ruptured cyst is 12.5 cm. In the present case, we could not identify a location of the ruptured cyst because our case had many cysts all over the liver and we did not perform an emergency surgery. Four of 14 cases (29 %) had hemorrhage with rupture. In most patients, the liver cyst ruptured into the peritoneal cavity while two cases ruptured into the common hepatic duct and the hepatic subcapsule [, ]. As treatments for the rupture of liver cysts, invasive procedures were mainly performed and they varied from percutaneous drainage to hepatectomy. Two of 14 cases (14 %) had recurrence of pressure symptom. In these two cases, marsupialization and percutaneous drainage were performed. In other eight cases, resection of cyst walls or hepatectomy was performed and no recurrence occurred. Basically, palliative reduction is thought to be appropriate for pressure symptoms of simple liver cysts [], but marsupialization or percutaneous drainage may be insufficient, and more invasive procedures such as cystic wall resection and hepatectomy may be recommended to prevent the recurrence of the symptoms. Only one case died of postoperative serious complications; the case had end-stage renal failure due to ADPKD and life-threatening hemorrhage from a ruptured liver cyst. Spontaneous rupture of simple liver cysts without hemorrhage may lead to favorable prognosis. In the present case, we temporarily carried out percutaneous drainage of the ascites to relieve dyspnea and performed surgical reduction of the liver cysts after general condition was improved and favorable outcome was obtained.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [97.0, 'kg']}",137,130.15,143.85,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 97.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (97.0 kg - 20 kg) = 137.0 mL/hr.
Hence, the patient's fluid maintenance is 137.0 mL/hr."
4545,22,Maintenance Fluids Calculations,physical,decimal,pmc-5374574-1,Extracted,"An 8-year-old Cameroonian boy with no significant past history was brought to our emergency service following a road traffic accident. On crossing a road, he was knocked down by an oncoming motorbike weighing approximately 125 kg, medium sized, and traveling at moderate speed. The motorbike fell on the boy with the handlebar catching him in the abdomen as its rider lost control. He sustained a lesion to the head with no initial loss of consciousness. On arrival, he complained of pain in his head and a swelling in the left upper quadrant of his abdomen.
On examination, he was conscious, with a Glasgow coma score of 15/15, blood pressure of 119/83 mmHg, pulse of 90 beats per minute, respiratory rate of 18 breaths per minute, temperature of 37.3 °C; he was 96 cm tall and weighed 26 kg. There was a 2 cm laceration in the occipital region of his head, and a swelling in his left lumbar region with mild bruising of the overlying skin (Fig. ). The swelling was reducible and disappeared in the supine position. There was no guarding and no rebound tenderness. He had normal bowel sounds on auscultation and the rest of the examination was unremarkable.
A diagnosis of mild head injury and a handlebar hernia was made. After resuscitation, his scalp laceration was closed with a one point suture and he was programmed for surgery for the handlebar hernia the next day. A surgical exploration of the area showed a 7 cm laceration of his lateral abdominal wall (Fig. ), running from the external oblique aponeurosis through all the muscle layers to his peritoneum with loops of small bowel present in the opening. There was no blood or feces in the area immediately surrounding the lesion. Exploration of the bowel loops closest to the opening did not reveal signs of intra-abdominal injury. The abdominal wall defect was repaired in layers. The abdominal incision was closed in a standard manner. His postoperative period was uneventful. He was discharged on postoperative day 9 and scheduled 2 weeks later for a follow-up visit, but unfortunately was lost to follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [26.0, 'kg']}",66,62.7,69.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 26.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (26.0 kg - 20 kg) = 66.0 mL/hr.
Hence, the patient's fluid maintenance is 66.0 mL/hr."
4546,22,Maintenance Fluids Calculations,physical,decimal,usmle-3483,Extracted,"Two days after undergoing abdominal surgery for lysis of adhesions, a 52-year-old man has nausea and one episode of bilious vomiting. The patient's nausea is somewhat alleviated in the prone position. The patient has had a 70-kg (154-lb) weight loss since undergoing bariatric surgery 1 year ago. Physical examination shows abdominal distention. Sudden movement of the patient elicits a sloshing sound on auscultation of the abdomen. An upper gastrointestinal series of the abdomen with oral contrast shows no passage of contrast past the third segment of the duodenum.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [70.0, 'kg']}",110,104.5,115.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 70.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (70.0 kg - 20 kg) = 110.0 mL/hr.
Hence, the patient's fluid maintenance is 110.0 mL/hr."
4547,22,Maintenance Fluids Calculations,physical,decimal,pmc-5650002-1,Extracted,"A 4-month-old male infant presented to the emergency department with a 3-day history of vomiting, diarrhea and difficulty breathing. Excessive and rapid weight gain was noted by the parents since the age of 2 months. The baby was previously healthy and born at term with a birth weight of 3.62 kg; the pregnancy and delivery were uncomplicated. There was no family history of consanguinity, malignancies, unexplained childhood deaths or stillbirth.
On a detailed physical exam, the baby was noted to have Cushingoid facies, poor muscle tone and excessive fat pad on the back and arms (). Notably, his length was 54 cm (below the 1st percentile) and the weight was disproportionately elevated at 6.7 kg (50th percentile). He was obese with weight for length ratio more than 99th percentile for the comparable age and sex. His blood pressure was elevated for age, ranging from 93 - 121 to 40 - 73 mm Hg. A large abdominal mass was palpable on the left lower quadrant and the borders were difficult to define. He had a prepubertal genital examination with no overt virilization; his phallus was typical in size but buried in the suprapubic fat pad. Neither acne, adult body odor, nor axillary hair was noted on examination.
In light of the respiratory distress, a chest radiograph was obtained and demonstrated bilateral upper lobe infiltrates, and henceforth he was admitted with a working diagnosis of pneumonia.
While being treated in the hospital for pneumonia, an evaluation was launched to delineate the etiology of the excessive weight gain, growth arrest, hypotonia and the abdominal mass. Laboratory evaluation revealed consistently elevated serum cortisol levels, irrespective of the time of the day with values of 73.0 μg/dL at 5:08 am and 68.6 μg/dL at 12:50 pm (normal range 4 - 22 μg/dL). Serum adrenocorticotropic hormone (ACTH) was suppressed at 7 pg/mL, at 5:16 am (normal range 0 - 60 pg/mL), suggestive of a primary adrenal cortisol hypersecretion. Dehydroepiandrosterone sulfate (DHEA-S) was mildly elevated at 115 μg/dL (normal range 16 - 96 μg/dL), but clinical features of hyperandrogenism were absent. The aldosterone level was normal at 23 ng/dL with a slightly elevated renin of 43.51 ng/mL/h. There was a slight increase in urine vanillylmandelic acid (VMA) and metanephrines, excluding a pheochromocytoma. An ultrasound demonstrated a 6.8 × 7.7 cm size solid mass at the upper pole of left kidney. A subsequent computerized tomography scan confirmed a large left-sided soft tissue mass with internal necrosis and a well-defined capsule abutting the left kidney with non-visualization of the left adrenal gland (). Henceforth, presumptive diagnosis of a functional cortisol producing adrenal tumor was made.
The baby underwent exploratory laparotomy and a left adrenalectomy was performed. Intraoperative findings revealed a 9.0 × 7.0 × 5.0 cm (315 cm3), well-encapsulated tumor weighing 180 g without breach of the capsule. The tumor was resected completely. There were no other signs of tumor spread including no liver metastasis or suspicious periaortic lymph nodes. Histological classification confirmed a high-grade adrenocortical carcinoma (24 mitotic figures/50 HPF) with a few pleomorphic nuclei (). The tumor was finally classified an adrenocortical carcinoma (ACC), stage 2 (based on combined American Joint Committee on Cancer (AJCC)/International Union Against Cancer (UICC) classification). During the perioperative period, the baby was treated with stress dosing of hydrocortisone and had an uneventful recovery. He continued to receive maintenance doses of hydrocortisone which were subsequently weaned. No adjuvant treatment with mitotane was done. During the recovery period, his linear growth velocity improved and his weight normalized (). Yearly follow-ups for the next 4 years and then most recently at 7 years and 10 months after treatment indicate continued health and successful recovery ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.7, 'kg']}",26.8,25.46,28.14,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.7 kg. Hence, the patient's maintenance fluid is 6.7 kg * 4 mL/kg/hr = 26.8 mL/hr.
Hence, the patient's fluid maintenance is 26.8 mL/hr."
4548,22,Maintenance Fluids Calculations,physical,decimal,pmc-7220329-1,Extracted,"A 71-year-old man, non-smoker (height: 155 cm; weight: 59 kg), was scheduled to receive video-assisted thoracoscopic extended thymectomy with the diagnosis of MG. Two months previously, he developed symptoms of right ptosis and progressive swallowing difficulty. Based on a positive response to edrophonium and increased titers of autoantibodies to acetylcholine receptor (19.3 nmol/L; normal < 0.2 nmol/L), he was diagnosed as having MG with severity belonging to Osserman's classification IIb (ie, generalized moderate weakness and/or bulbar dysfunction). Thoracic computed tomography demonstrated glandular hyperplasia of the thymus (Fig. A). The patient was started on prednisolone 20 mg daily and pyridostigmine 60 mg three times daily. His past history included hypertension without evidence of previous myasthenic crisis or thromboembolic events (eg, history of lower limb swelling). The results of electrocardiography, pulmonary function test [eg, vital capacity: 93%], echocardiography (eg, left ventricular ejection fraction: 85.1%), chest radiography (Fig. B), and laboratory studies (eg, coagulation test) were unremarkable. On the other hand, impaired renal function [i.e., serum creatinine: 1.42 mg/dL; eGFR: 49.1 mL/min/1.73 m2] was observed after admission.
Preoperative physical examination of the patient showed clear consciousness without respiratory distress. Vital signs included a blood pressure of 187/103 mm Hg, heart rate of 82 beats/min, and respiratory rate of 14 breaths/minute. Under real-time neuromuscular monitoring with a train-of-four (TOF) monitor (TOF-watch SX, N.V. Organon, Oss, Netherlands), anesthesia was induced with propofol (130 mg) and rocuronium (0.85 mg/kg). Following successful tracheal intubation with a double-lumen tracheal tube (Broncho-Cath; Mallinckrodt, Athlone, Ireland), general anesthesia was maintained with sevoflurane, rocuronium (total dosage: 40 mg), and a continuous infusion of remifentanil. An 18-gauge peripheral intravenous line and an arterial line were introduced. The surgical time was 4 hours 15 minutes with an estimated blood loss of 100 mL. Upon completion of surgery, sugammadex 4 mg/kg was administered to reverse neuromuscular blockade, with a maximum TOF ratio of 0.93 following reversal. Additionally, intravenous morphine 8 mg was given for postoperative analgesia. After successful extubation in the operating room and resumption of spontaneous breathing, he was transferred to the post-anesthesia care unit (PACU) for further care.
During the immediate postoperative period, the patient was hemodynamically stable without respiratory distress. Because of surgical pain with a numeric rating scale of 5 (scale of 0–10), intravenous morphine was titrated to a total dosage of 7 mg. Forty-five minutes later, respiratory distress with drowsiness was noted. Physical examination found pinpoint pupils with a TOF ratio of 0.9. Blood gas analysis demonstrated severe hypercapnia (arterial carbon dioxide pressure: 117.7 mm Hg) and acidosis (pH: 6.996, lactate levels: 3.3 mmol/L). On suspicion of morphine overdose, intravenous naloxone was administered twice (0.08 mg each time). After 20 minutes, the patient regained consciousness and normal respiratory pattern. Subsequent blood gas analysis demonstrated hyperlactatemia (lactate levels: 6.0 mmol/L) (Fig. ) despite improvement in arterial carbon dioxide pressure and arterial oxygen pressure after naloxone administration. Taking into account the overall clinical improvement, he was transferred to ward with spontaneous breathing and stable hemodynamics after observation for 100 minutes following initial reversal of opioid overdose.
However, one hour after being transferred to ward (ie, three hours after naloxone administration), he was found to exhibit consciousness loss, respiratory distress, and pinpoint pupils. Intravenous naloxone 0.4 mg was given, followed by endotracheal intubation and transfer to the intensive care unit for mechanical ventilatory support. Brain computed tomography showed no intracranial lesion. He regained consciousness two hours after naloxone administration in the intensive care unit without symptoms of opioid withdrawal (eg, pulmonary edema). As weaning from mechanical ventilation was difficult on POD 3, a diagnosis of POMC was made. Steroid therapy (prednisolone 40 mg twice daily) and pyridostigmine (60 mg 3 times a day) was initiated. The patient was extubated smoothly on POD 6 and was discharged from hospital on POD 12. The course of hyperlactatemia was shown in Figure . In addition, his eGFR increased from 49.1 mL/min/1.73 m2 at baseline to 88.9 ml/min/1.73m2 on POD 5. Pathological analysis of the specimen from thymectomy confirmed the diagnosis of type B2 thymoma according to the World Health Organization (WHO) classification.
The patient was readmitted on POD 24 because of left thigh swelling. Ultrasonographic examination showed evidence of DVT involving the left femoral and popliteal veins. Anticoagulant therapy with low-molecular-weight heparin (ie, subcutaneous Clexane 60 mg every 12 hours) was implemented immediately after hospitalization, and he was discharged without sequelae on POD 31. During hospitalization, his eGFR was 86.5 mL/min/1.73m2. There was no recurrence of myasthenic crisis or DVT up to 3 months of follow-ups.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [59.0, 'kg']}",99,94.05,103.95,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 59.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (59.0 kg - 20 kg) = 99.0 mL/hr.
Hence, the patient's fluid maintenance is 99.0 mL/hr."
4549,22,Maintenance Fluids Calculations,physical,decimal,pmc-6180689-1,Extracted,"A 72-year-old male patient weighing 65 kilograms with diagnosis of postlaminectomy kyphosis with compressive myelopathy was scheduled for C5–C6 corpectomy and instrumentation under general anesthesia. Past medical history revealed complete heart block, for which permanent pacemaker was implanted 8 months ago. Airway examination revealed modified Mallampati Class I with restricted neck movements indicating difficult airway. Hematological and biochemical investigation reports were within the normal limits. Two-dimensional echocardiography revealed concentric left ventricular hypertrophy with an ejection fraction of 60%. The pacemaker was identified to be VITATRON E50A1D (Medtronic Inc., USA) (MODE: DDDR), in proper working condition. It was reprogrammed to asynchronous DOOO mode on the day before surgery. Defibrillator and transcutaneous pacing equipment were checked and kept ready before induction of anesthesia. Difficult airway trolley and crash cart for resuscitation were arranged and checked for all its contents. Pads for transcutaneous pacing were appropriately placed for use in case of pacemaker failure. Grounding plate of unipolar cautery was placed on the thigh of the patient. After preoxygenation, general anesthesia was induced with fentanyl 150 mcg and thiopentone 250 mg. Rocuronium 50 mg IV was given to facilitate intubation. Intubation was done using video laryngoscopy with 8.0-sided cuffed endotracheal tube. Anesthesia was maintained with oxygen, nitrous oxide, sevoflurane, fentanyl, and rocuronium. Cannulation of the right radial artery was done after induction of anesthesia. Cardiac output monitoring was done using FloTrac (Edward Lifesciences, CA). Acid-base status and electrolytes remained within normal limits during the intraoperative period. Total duration of anesthesia was 4 h. A total of 2.5 liters of crystalloid and 500 ml of colloid (6% HES 130/0.4) were administered during the procedure. Blood loss was minimal, and there was no requirement for transfusion of blood products. Temperature monitoring was done and was maintained in normal range using forced air warmer. At the end of procedure, neuromuscular blockade was reversed with neostigmine and glycopyrrolate at the end of procedure. The patient was extubated when he was fully alert with adequate reversal of neuromuscular paralysis and shifted to postanesthesia recovery unit for further observation. The pacemaker was reprogrammed to DDDR mode the next day. Vigilant electrocardiogram (ECG) monitoring and availability of backup pacing equipment were ensured till reprogramming. Postoperative course remained uneventful, and the patient was discharged home on 8th postoperative day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [65.0, 'kg']}",105,99.75,110.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 65.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (65.0 kg - 20 kg) = 105.0 mL/hr.
Hence, the patient's fluid maintenance is 105.0 mL/hr."
4550,22,Maintenance Fluids Calculations,physical,decimal,pmc-5351162-1,Extracted,"A 24-year-old African woman, gravida 4 para 3, presented with a 2-week history of right upper quadrant pain and an 8 weeks and 5 days amenorrhea with spotting. She first consulted in a secondary health facility where her clinical evaluation revealed a hepatomegaly on abdominopelvic ultrasound and positive urinary pregnancy test without intrauterine or tubal gestational sac. These findings motivated the medical team to refer her to our tertiary center.
This was her first episode of such pain. She had no history of sexually transmitted diseases and no history of contraception. She had never had an operation. Her hepatitis B and C status were unknown. There was no dizziness, asthenia, or jaundice.
Her vital signs were stable: blood pressure of 120/60 mm Hg, pulse rate of 70 beats per minute, respiratory rate of 16 cycles per minute, and temperature at 36.5 °C. She weighed 59 kg. She was not pale. Her right upper quadrant was tender on deep palpation but not after deep breath. There was no guarding or rebound tenderness. Her uterus was of normal size and there were no adnexal masses noted. Her rectovaginal pouch was free and non-tender. We suspected acute cholecystitis or acute viral hepatitis in pregnancy.
On another abdominopelvic ultrasound, a heterogeneous poorly vascularized mass was visible under the right lobe of her liver, of size 42 × 38 mm. There was no hemoperitoneum and her uterus was empty without adnexal masses. On full blood count, there was mild microcytic and hypochromic anemia at 10.2 g per dL, with normal leukocyte and platelet counts. Her liver transaminases and renal function were normal. Her serum β-human chorionic gonadotropin (βhCG) titers rose from 200 mUI/mL to 3000 mUI/mL in 48 hours. No gestational sac was visible on concomitant pelvic ultrasound.
Our final diagnosis was hepatic pregnancy. We chose to administer 1 mg/kg of methotrexate intramuscularly since she was hemodynamically stable and the Fernandez score [] was in favor of medical treatment. Evolution was favorable and she was discharged at day 5. Two weeks later, her serum βhCG titer was 15 mUI/mL. She did not show up at 1-month appointment.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [59.0, 'kg']}",99,94.05,103.95,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 59.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (59.0 kg - 20 kg) = 99.0 mL/hr.
Hence, the patient's fluid maintenance is 99.0 mL/hr."
4551,22,Maintenance Fluids Calculations,physical,decimal,pmc-3591566-1,Extracted,"An 8-month-old infant, weighing 9 kg, a product of uneventful pregnancy and normal delivery presented with enlarging head and sunset appearance of the eyes. His development was within normal but has difficulty in turning due to heavy head. His head circumference was above the 97th percentile, and the anterior fontanele was wide, full and slightly tense. He had upward gaze palsy and the rest of neurological examination was otherwise normal. Radiological investigations showed obstructive hydrocephalus caused by a large posterior fossa arachnoid cyst, distorting and occluding the fourth ventricle outlet; and associated with downward herniation of the cerebellar tonsils through the foramen magnum [].
He underwent ETV through the right angle of the anterior fontanelle successfully. On an attempt to fenestrate the posterior fossa cyst through the lateral ventricle, he bled and the procedure had to be abandoned leaving an EVD in the lateral ventricle, which was kept opened at a level of 10-cm height from the patient's head. Anesthesia was induced with 7-8% sevoflurane in oxygen. Ventilation with face mask was found to be easy. Fentanyl 10 microgram (mcg) and Cisatracurium 1 mg were given intravenously (i.v.) to facilitate endotracheal (ET) intubation. First attempt was with 3.5-mm internal diameter noncuffed polyvenyl chloride (PVC) ET tube was not successful as the anesthetist found it to be grade 3 intubation (Cormack and Lehane Classification).[] The second anesthetist inserted the same ET tube after repositioning the shoulder roll resulting in improved glottic view. There was little leak of air around the ET tube on gentle intermittent positive pressure ventilation (IPPV). After intubation, 125 mg paracetamol suppository was inserted. Anesthesia was maintained with 2-3% sevoflurane in 50% oxygen air mixture and patient received an additional bolus of fentanyl in the dose of 5 mcg. Anesthesia course was uneventful except slight drop in body temperature to 34°C despite of the use of fluid and body warmers. After completion of the surgery, the patient was warmed to 36.5°C and inhalational anesthetic terminated. Residual neuromuscular block was reversed with mixture of neostigmine and atropine. Trachea of the patient was extubated when the patient was fully awake after attaining adequate respiration and shifted to postanesthesia care unit (PACU). During first hour of stay in PACU, the patient's vital were stable and no additional analgesic was needed. Before shifting the patient to ward, oxygen face mask was removed to assess breathing on room air, but oxygen saturation by pulse oximeter (SPO2) dropped to 90% and mild inspiratory stridor was noted. There were no signs of respiratory distress at that stage. The SPO2 improved to 98% when oxygen face mask with 5 liters/min flow was applied. The cause of inspiratory stridor was not obvious and intubation trauma secondary to two attempts at intubation was considered to be a possibility. There was no change in the vital signs or in the severity of stridor. It was decided to shift him to the pediatric intensive care unit (PICU) for observation and further management as it was not safe to send this patient to the ward. While waiting for PICU admission, the patient received 2.5 mg dexamethasone was given i.v. followed by 2.25% racemic epinephrine nebulization in the dose of 0.25 ml in 3-ml normal saline. It resulted in rise in heart rate from 125 to 150 beats/min; however, other vital signs were unchanged during this period. After 45 minutes of nebulization the patient rapidly developed difficulty in breathing and SPO2 dropped to 80%, which improved to 95% when IPPV and PEEP were applied through anesthesia face mask attached to Ayre's T-piece circuit connected with 100% oxygen with 8 liters/min flow. The trachea of the patient was reintubated with same size ET tube after administering 10 mcg fentanyl i.v. After ET intubation, the patient developed generalized tonic-clonic seizure, which was controlled with 0.5 mg Midazolam i.v. Another episode of seizure recurred after 10 minutes and controlled with an additional dose of 1 mg midazolam i.v. An emergency CT scan was done which showed marginally smaller lateral ventricles with extra-axial fluid collection, and crowded foramen magnum. There was some blood in the occipital horns and tip of the EVD was in the lateral ventricle []. The patient was then shifted to PICU and connected to mechanical ventilation.
He maintained his vital signs and was stable enough next morning to arrange an MRI scan, which revealed reduction in the size of the ventricles, wide supratentorial subdural space, along with marginal increase in the posterior fossa cyst and anterior displacement and compression of the brain stem against the clivus. The brain stem was kinked and compressed, and the foramen magnum was crowded by the cerebellar tonsils compromising the medulla [].
He was taken back to theater for craniocervical decompression; suboccipital craniectomy and removal of the posterior arch of Atlas, followed by durotomy and Gor-tex duroplasty, and insertion of cystoperitoneal shunt. Postoperatively, he recovered and his breathing improved dramatically that he could be weaned successfully off the ventilator and discharged of the hospital in a week's time.
He was seen in the outpatient clinic after 1 month, his parents reported improvement in his behavior and motor development, they also noticed slight reduction in the head size. A CT scan at that time showed stable ventricular size and subdural space, while posterior fossa cyst size was marginally smaller [].","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [9.0, 'kg']}",36,34.2,37.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 9.0 kg. Hence, the patient's maintenance fluid is 9.0 kg * 4 mL/kg/hr = 36.0 mL/hr.
Hence, the patient's fluid maintenance is 36.0 mL/hr."
4552,22,Maintenance Fluids Calculations,physical,decimal,pmc-6142625-1,Extracted,"Here we report a 36-year-old female nurse, working full-time 12-h night shifts in a busy intensive care service, with generalized (MGFA IIb) auto-immune MG, symptomatic and dependent on cholinesterase inhibitors. Past medical history includes eczema in her teens, she is a carrier for sickle disease (sickle cell trait (SCT)) and she carried two pregnancies to term. Red blood cells have slightly reduced mean corpuscular volume and mean corpuscular hemoglobin concentration, 75.5 fl and 25.7 pg, respectively. She has no clinical symptoms of anemia and no specific treatment or monitoring. Surgical history includes 1 cesarean (2004), linea alba repair (2011) and breast implant (2014). She is a nonsmoker and does not drink alcohol. She is right-handed. She has a normal body mass index, 20.3 kg/m2, weighing 52 kg for 1.60 m.
Despite already experiencing abnormal weakness, she began running a year before being diagnosed with MG. Prior to running, she played amateur level basketball however this became incompatible with working night-shifts. MG diagnosis was based on clinical signs (right hand weakness - difficulty brushing teeth and hair, carrying light loads, cutting meat, a heavy head, nasal voice, ptosis, diplopia, dysphagia and difficulty masticating and articulating), serum auto-antibodies against nicotinic acetylcholine receptors (AChR) (> 100 nmol/l) and significant decrement on repetitive nerve stimulation (3 Hz) EMG (50% right trapezius, 24% right anconeus, 15% left anconeus, 43% tongue/mouth (CN V/XII)). Myasthenic muscle score (MMS) was 65/100. Initial treatment consisted of intravenous immunoglobulins (2 g/kg over 3 days (100 g)) and 60 mg pyridostigmine (t.i.d). Thoracic CT scan did not show thymoma but was in favour of thymic hyperplasia. Thymectomy was not performed as per the patient’s request.
Despite the patient being informed at diagnosis that sport was contra-indicated, she kept running. Training consisted of 1–2 10 km weekly runs with the beginning being the most difficult. MG symptoms persisted including fatigue, dysphagia and episodes of diplopia at the end of pyridostigmine dose thus aziathoprine (100 mg) was introduced. She performed a half marathon 2 months later, followed by a full marathon and another half marathon. No major difficulty was experienced and performances significantly improved: 5h13mins (8.1 km/h) for a marathon pre-diagnosis to 4h51mins (8.7 km/h) post diagnosis (and treatment), Figs. & .
On clinical evaluation 1 year after MG diagnosis, she had above average respiratory strength (MIP and MEP 135% and 144% of theoretical) and normal respiratory function (FVC 95% of theoretical). On maximal voluntary testing, limb strength was normal (knee extensors and elbow flexors: 128% and 101% of theoretical, respectively and right handgrip strength: 88%). Walking endurance was also considered normal (92% of theoretical 6MWD). The MMS suffered from a ceiling effect with the patient achieving the maximal score of 100 and a score of 4 on the MG-ADL due to episodes of dysphagia, dyspnea with effort and UL fatigue with brushing her teeth and hair. She reported recurrent MG symptoms including loss of hand dexterity (difficulty manipulating medication at work), bulbar symptoms such as dysphagia on her own saliva, a nasal voice and ocular symptoms (ptosis and diplopia). MG-specific quality of life (MGQOL-15-F) was reduced (17/60) particularly with regards to professional and social aspects, reflected in the WHO-QOL Bref with the social relationship and physical health domains being reduced, 11/20 and 13/20 respectively [, ].
She continued regular running without any particular changes in her MG, recurrent right hand weakness persisted and she experienced occasional ocular and bulbar symptoms primarily at the end of pyrodistigmine dose. Quality of life improved significantly over time (Fig. ) and strength remained stable (knee extensors and elbow flexors: 128% and 100% of theoretical, respectively, right handgrip strength: 93%). She discontinued aziathoprine (treatment duration 14 months) and remained exclusively treated with cholinesterase inhibitors (60 mg, b.i.d).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [52.0, 'kg']}",92,87.4,96.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 52.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (52.0 kg - 20 kg) = 92.0 mL/hr.
Hence, the patient's fluid maintenance is 92.0 mL/hr."
4553,22,Maintenance Fluids Calculations,physical,decimal,pmc-4937533-1,Extracted,"A seven-year-old, intact male, mixed breed dog weighing 8.1 kg was presented to the Emergency Service of the Department of Clinical Science of Companion Animals of the Faculty of Veterinary Medicine, Utrecht University with a 2 weeks history of lethargy, progressive dyspnea and coughing. The dog previously lived in the Cape Verdean islands for approximately 3 years and returned to the Netherlands 10 months before presentation. In the past 2 years, the dog had showed chronic mild exercise intolerance and had a few episodes of diarrhea that resolved with symptomatic therapy. The dog was up-to date with his vaccinations and anthelminthic treatments.
Physical examination showed generalized weakness and decrease mental state. Cardiovascular examination revealed tachycardia, weak peripheral pulses, pale mucous membranes, prolonged capillary refill time, jugular distensions and venous pulses, and a grade three out of six systolic murmur with the point of maximal intensity over the right cardiac apex. The dog was also severely dyspneic and demonstrated harsh lung sounds on auscultation. The abdomen was distended and positive undulation was detected. These findings were consistent with pulmonary disease, right-sided heart failure and poor peripheral perfusion.
Complete blood count (CBC) showed a moderate microcytic, hypochromic anemia, moderate leukocytosis with a marked left shift and a severe thrombocytopenia. Biochemistry showed severe hyperproteinemia, hyperglobulinemia and a mild hypoalbuminemia. Serum protein electrophoresis showed a polyclonal peak in the gamma globulin region. Arterial blood gas analysis showed a severe hypoxemia with hypocapnia. Urinalysis showed mild hemoglobinuria, glucosuria and proteinuria. Blood samples were submitted for serological and molecular biological testing. Immunofluorescence antibody test (IFAT) for E. canis (MegaFLUO Ehrlichia canis®, Mega Cor Diagnostik GmbH, Hörbranz, Austria) was positive (IgG titer >2560), but polymerase chain reaction (PCR) amplification for Ehrlichia genus (real-time PCR, Light Cycler® 2.0, Roche Diagnostics GmBH, Mannheim, Germany, primers used as described previously []) was negative. Serology for Leishmania sp. (Dog-DAT®, Leishmania specific antibody detection kit, Koninklijk Instituut voor de Tropen, Amsterdam, the Netherlands) and B.
canis. (MegaFLUO Babesis canis®, Mega Cor Diagnostik GmbH, Hörbranz, Austria) and antigen snap tests for A. vasorum (Angio Detect™ Test, IDEXX Laboratories) and Dirofilaria immitis (SNAP® Heartworm RT Test, IDEXX Laboratories) were also negative. Laboratory results are summarized in Table .
On thoracic radiographs, a mild diffuse increase in pulmonary opacity with an interstitial lung pattern and mild peribronchial cuffing was seen, which was most accentuated in the caudodorsal lung lobes. Thin pleural fissure lines were noted between all lung lobes. The cardiac silhouette showed signs of right-sided cardiomegaly (vertebral heart score (VHS): 11.0, reference interval <9.7 ± 0.5) and a main pulmonary artery knuckle was present on the dorsoventral view (Fig. ).
Echocardiography showed dilation of the right ventricle and the pulmonary artery, septal flattening and a severe tricuspid regurgitation. The left ventricle was severely under filled (Fig. ). Congenital defects and left heart disease were excluded. The maximal tricuspid systolic velocity was 5.83 m/s, indicating a peak tricuspid gradient of approximately 136 mm Hg which is graded as severe PH (reference <40 mm Hg, severe >75 mm Hg) [], (Fig. ).
To address the severe hypoxemia and PH the dog was placed in an oxygen cage with an inspired concentration of oxygen between 40 and 50 %. The clinical signs of the dog did not improve markedly with the extra oxygen supplementation. Because anemia could have contributed to the cardiovascular signs and the poor tissue oxygenation, a typed packed red blood cell transfusion was administered. Based on the travel history, the abnormalities within the CBC and biochemical analysis and the positive serology for E. canis, an infection with CME was suspected. Treatment with doxycycline (5 mg/kg, orally twice daily) (Doxoral®, AST Farma, Oudewater, the Netherlands), pimobendan (0.3 mg/kg, orally twice daily) (Cardisure® Flavour, Eurovet Animal Health BV, Bladel, the Netherlands) and sildenafil (1.5 mg/kg, orally twice daily) (Viagra®, Pfizer, New York, USA) was initiated.
The hematocrit increased from 20 to 36 % after the blood transfusion and the dog’s clinical condition improved remarkably. However, the dog remained moderately dyspneic and severely hypoxic (PaO2: 46.5 mm Hg, reference interval: 85.0–103.3 mm Hg). The dyspnea gradually improved and the dog seemed comfortable outside the oxygen cage after 6 days of treatment, although the improvement of the hypoxemia was only minimal (PaO2: 55 mm Hg, reference interval: 85–103.3 mm Hg, Table ). Because of financial limitations of the owner, the dog was discharged with the above-mentioned therapies at that time.
Seventeen days after initiation of treatment, the dog was admitted via the cardiology polyclinics of the same university and re-examined. At that time, there was complete resolution of all clinical signs and physical examination was completely unremarkable. CBC showed normal platelet counts and leukogram, with only a very mild microcytic hypochromic anemia. Biochemical analysis again showed severe hyperproteinemia and hyperglobulinemia. The albumin concentration normalized. The IgG titer for E. canis (IFAT) was again very high (IgG titer 2560) (Table ). Thoracic radiography showed marked improvement with resolution of cardiomegaly (VHS: 10.2, reference interval 9.7 ± 0.5) and only a very mild interstitial pattern of the caudodorsal lung lobes and a very mild dilation of the pulmonary artery (Fig. ) as remaining abnormalities. Echocardiography also showed a remarkable improvement. Tricuspid regurgitation was no longer present and only a very mild uniform dilation of the pulmonary artery was still present (Fig. ). Therapy with pimobendan and sildenafil were discontinued and the treatment with doxycycline was continued for another 5 weeks.
The dog was reevaluated 4 weeks later and was clinically doing very well. Nevertheless, the dog again developed mild anemia and the hyperproteinemia persisted. Proteinuria had resolved at that time (Table ). Doxycycline therapy was continued for another 4 weeks and another re-examination was advised. Unfortunately, the dog was lost to follow–up at that time.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [8.1, 'kg']}",32.4,30.78,34.02,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 8.1 kg. Hence, the patient's maintenance fluid is 8.1 kg * 4 mL/kg/hr = 32.4 mL/hr.
Hence, the patient's fluid maintenance is 32.4 mL/hr."
4554,22,Maintenance Fluids Calculations,physical,decimal,pmc-5412554-1,Extracted,"A 67-year-old woman (56 kg with a body mass index of 21.1 kg/m2) presented with 1-day history of abdominal pain, vomit and constipation in the local clinic. CT of the abdomen showed features of upper gastrointestinal obstruction with a suspicion of intussusception of a duodenum segment. The patient was transferred to our hospital for further treatment on October 16, 2016. She had a 5-year history of epigastric fullness and intermittent upper abdominal pain. She denied the history of hematemesis, melena, change in bowel habit or significant recent weight change. She did not have surgical history in the past. She denied family history of neoplasia. She was a non-smoker and non-alcoholic drinker. On admission, she showed improvement in her symptoms and there were no significant findings except epigastric tenderness on physical examination. Hematological and biochemical parameters were normal except for Hb: 95 g/L (normal range: 110 - 150 g/L), neutrophil ratios: 90.4% (normal range: 50-70%), and C-reactive protein: 7.89 mg/L (normal range: < 5 mg/L). Plain radiography of the abdomen showed bowel dilatation with air-fluid levels. CT of the abdomen revealed hypodense lesions with CT value of -64 Housefield Units (HU) to -138 HU located from the descending part of the duodenum to the proximal jejunum, which was suggestive of lipomas (). She was initially managed with fluid replacement and nasogastric aspiration and subsequently underwent MRI of the abdomen, which showed fat-containing mass lesions from the descending part of the duodenum to the proximal jejunum. The lesions were high-intensity on T1-weighted () and intermediately intense on T2-weighted images, with a drop in signal on T1 and T2-weighted fat-suppressed images (), consistent with a diagnosis of duodenal lipomas. As the obstruction did not fully resolve, we carried out an exploratory laparotomy under general anesthesia. On entering the peritoneal cavity, there was no obvious intussusception of the duodenum. Intraoperatively, multiple, giant lipomas could be palpated in second, third and fourth part of duodenum and proximal jejunum and the rest of the bowel appeared normal. Duodenum 4 cm distal to ampulla was excised along with 14 cm of proximal jejunum (). Intestinal continuity was maintained by end-to-end duodenojejunal hand-sewn anastomosis. Gastrostomy, jejunostomy and T tube in the common duct were performed in the meanwhile to prevent the anastomotic leakage. The patient was discharged from the hospital with successful recovery. The macroscopic appearance of the lesion is shown in . Final histopathological analysis confirmed the diagnosis of multiple, submucosal lipomas with sizes varying from 1.3 to 11.0 cm in maximal dimensions.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [56.0, 'kg']}",96,91.2,100.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 56.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (56.0 kg - 20 kg) = 96.0 mL/hr.
Hence, the patient's fluid maintenance is 96.0 mL/hr."
4555,22,Maintenance Fluids Calculations,physical,decimal,pmc-2771803-1,Extracted,"A 59-year-old woman was admitted to the hospital because of progressive dyspnea, peripheral edema, and general weakness. She had a six-year history of end-stage renal disease and peritoneal dialysis. She also had a history of diabetes mellitus, hypertension, and parathyroidectomy due to parathyroid adenoma. She denied alcohol use and corticosteroid use and had no history of tuberculous infection or tuberous sclerosis.
She was 156 cm tall and weighed 72 kg, with a body mass index of 29.6 kg/m2. Her blood pressure was 90/60 mmHg, and her pulse rate was 95 beats/min. Facial edema and neck vein distension were noted on physical examination. No palpable masses were found in the neck, trunk, or axillae. Respiratory examination revealed clear breathing sound bilaterally, with no crackles or wheezes. Heart sounds were decreased, but no murmur or pericardial rub was heard. Pitting edema was noted in both legs. The electrocardiogram was within normal limits. Laboratory examination showed evidence of end-stage renal disease, including blood urea nitrogen of 50.8 mg/dL and creatinine of 9.13 mg/dL. The other laboratory parameters, including autoantibodies, were unremarkable.
Chest radiography revealed cardiomegaly and bilateral obliteration of the costophrenic angles, indicating the presence of a pleural effusion (). TTE showed a small pericardial effusion and a diffuse, circumferential echogenic mass in the epicardium, suggesting massive fat infiltration. There were no significant abnormalities in systolic or diastolic function. The left ventricular (LV) ejection fraction was estimated to be 68% (). There was no evidence of right ventricular (RV) dysfunction, based on fractional area change.
The patient underwent high concentrative peritoneal dialysis and additional hemodialysis to control uremia and hypervolemia. Despite management over a two-week period, her symptoms and signs of hemodynamic instability failed to improve. Follow-up TTE revealed no residual pericardial effusion, but continued to show diffuse, massive fat infiltration. Moreover, the patient had pericardial thickening and adhesions, interventricular septum bouncing, inferior vena cava plethora, diastolic reversal of hepatic venous flow, and respiratory variations on transmitral inflow (), suggesting the presence of constrictive pericarditis. On tissue Doppler imaging, the average of the pulsed Doppler-derived E' velocity at the septal corner was 5 m/s (). Multislice CT of the heart confirmed thickened pericardium (7-11 mm) and diffuse, extensive fat infiltration of the whole pericardium, with a density similar to that of fat (). We measured the volume of the epicardial adipose tissue using 3-mm thick axial slices. We manually traced the epicardial fat in every slice, working from the aortic root to the apex. The number of manually traced slices was 37. The measured volume of epicardial fat in this patient was 487 mL.
Coronary angiography and left ventriculogram showed minimal intracoronary stenosis and normal systolic function, but also showed decreased normal inward systolic motion of the coronary arteries, caused by interference from massive surrounding fat tissues. Cardiac catheterization showed diastolic pressure equalization, ""dip and plateau"" feature on simultaneous right ventricular and left ventricular pressure tracings (), equalization of right atrium and left ventricular pressures on simultaneous right atrial and left ventricular pressure tracings, and marked x & y descent on right atrial pressure tracings (). These findings were compatible with constrictive pericarditis.
We therefore diagnosed this patient with constrictive pericarditis that may have been promoted by massive epicardial fat. We prepared the patient for pericardiectomy to improve hemodynamics, after consultation with the department of cardiac surgery. The patient developed sudden exacerbation of hemodynamic instability during preparation. Pericardiectomy could not be performed, and the patient expired.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [72.0, 'kg']}",112,106.4,117.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 72.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (72.0 kg - 20 kg) = 112.0 mL/hr.
Hence, the patient's fluid maintenance is 112.0 mL/hr."
4556,22,Maintenance Fluids Calculations,physical,decimal,pmc-5690740-1,Extracted,"A boy was delivered at 38 weeks of gestation to a 25-year-old gravida1 paral1 by emergency cesarean section soon after the coagulation function of his mother had become normal. His mother had bled from oral mucosa for 3 days because of an unknown reason. Blood tests showed a prolonged prothrombin time (PT) exceeding 70 s (normal: 10.4–12.6 s) and activated partial thromboplastin time (aPTT) of 110.5 s (normal: 74.0–110.0 s). The addition of normal plasma in a 1:1 ratio resulted in complete correction of the coagulation abnormalities, and a coagulation factor deficiency was suspected. The results of factor assay were associated with vitamin K deficiency: the levels of factor II, factor VII, factor IV, and factor X were sharply low, but factor V and factor VIII were within normal ranges. The mother was given vitamin K intravenously, and the oral bleeding stopped after 8 hours. Serum screening for toxicant by using gas chromatography/mass spectrometry (GC/MS) was taken 6 hours after admission and the result showed a bromadiolone level of 126 ng/mL.[ She denied intentional ingestion of any kind of rodenticides. The most likely route of exposure might be ingestion of the food contaminated by bromadiolone.
The boy's APGAR scores[ were 2 (Pulse: 2), 5 (Activity: 1;Pulse: 2;Grimace: 1;and Respiratory effort: 1), and 5 (Activity: 1;Pulse: 2;Grimace: 1;Respiratory effort: 1) at 1, 5, and 10 minutes respectively. Blood gas analysis showed pH of 7.249, PCO2of 55.9mmHg, PO2of 32mmHg, and BE of −4.2mmol/L. Immediate intubation and resuscitation was necessary. The boy showed poor respiratory effort, decreased muscle tone, and pallor. He was transferred to the neonatal intensive care unit for further treatment. The patient presented no history of trauma and bleeding diathesis.
Upon admission, the boy's measurements were as follows: weight 3120 g; length 48 cm; and fronto-occipital head circumference 37 cm. All of these measurements were appropriate for the boy's gestational age. The boy presented with bulging anterior fontanelle, a heart rate of 169 bpm, and blood pressure of 68/40 mmHg. No external signs of spontaneous hemorrhage were noted. The pupils were dilated and fixed to light. Corneal, Moro, and rooting reflexes were absent. Hepatomegaly and splenomegaly were not found.
Laboratory tests revealed hemoglobin level of 74 g/L, white blood cell count of 17.57 × 109/L, and platelet count of 264 × 109/L. PT exceeded 70 s (upper limit of reference), and aPTT was greater than 150 s (upper limit of reference). Fibrinogen (3.02 g/L) and thrombin time (16.4 s) were normal. Serology assay showed the following values: ALT: 5U/L; Alb: 28 g/L; TBil: 27.4 μmol/L; Cr: 57 μmol/L; CK: 353U/L; and CKMB: 6.3 μg/L.
The neonate was treated with vitamin K, fresh-frozen plasma, and red blood cells. His oral mucosa started to bleed at 2 hours after birth. Muscle tone increased at 4 hours after birth. Generalized seizures started on day 1 of life. A head computed tomography showed a severe subdural hematoma causing midline shift, bilateral intraventricular hemorrhage, and subarachnoid hemorrhage (Fig. ). Serum from cord blood was screened for toxicants. The result showed bromadiolone level of 94 ng/mL. His parents requested to stop all treatment, and the neonate died shortly after. Autopsy was not obtained from the parents.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3120.0, 'g']}",12.48,11.856,13.104,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3120.0 g so this converts to 3120.0 lbs * kg/1000 g = 3.12 kg. Hence, the patient's maintenance fluid is 3.12 kg * 4 mL/kg/hr = 12.48 mL/hr.
Hence, the patient's fluid maintenance is 12.48 mL/hr."
4557,22,Maintenance Fluids Calculations,physical,decimal,pmc-4670978-1,Extracted,"This report is on a 10 months old male infant who was born through normal vaginal delivery with birth weight of 2900 grams (gm), head circumference of 33 centimeters (cm) and height of 49.5 cm. He was the first child of consanguineous parents (first cousin) and his mother had no previous history of abortion or dead fetus. The child was nearly normal until the age of 3 months when he gradually developed lethargy, poor feeding, and inability to hold his neck with progressive increase in his head circumference. On physical exam at the age of 10 months, the child had poor weight gain (weight: 6.6 kg), large (48 cm) head circumference (above 95% percentile), visual problem (poor eye contact and impaired fixing and following), and a sluggish response to sound along with poor feeding. Based on his mother’s statements the child had been floppy at the onset of the disease, but at the age of 10 months, he became spastic with bilateral extensor plantar response and inability to sit. The patient was investigated for possible neurodegenerative disease and metabolic work-ups such as serum ammonia, lactate, pyruvate, blood gas, tandem mass metabolic screening (MS/MS), urine organic acid profile and plasma amino acids profile through HPLC method were requested. All the findings were normal except for an increased N-Acetyl-L-Aspartic Acid in urine. However, an audio metric brainstem response (ABR) and visual evoked potential (VEP) tests have shown abnormal findings. Magnetic resonance imaging (MRI) of the brain revealed diffuse symmetrical white matter of centrum semiovale and involvement of subcortical U fibers, along with some degree of hyper intensity in the thalamus, basal ganglia, periventricular white matter, brainstem and cerebellum. Because of the suspicion of Canavan disease on physical examination, further laboratory investigation, brain imaging and the Aspartoacylase enzyme activity test on the skin culture fibroblast were found in favor of the Canavan disease. ASPA-specific genomic DNA fragments were amplified by PCR method using specific sets of primers (). DNA sample from the patient was investigated by sequencing method. A homozygous missense mutation as C.202G>A in exon 1 was found (). This finding has not been reported in literatures. The parent’s DNA investigation was not done due to refusal of the parents.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.6, 'kg']}",26.4,25.08,27.72,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.6 kg. Hence, the patient's maintenance fluid is 6.6 kg * 4 mL/kg/hr = 26.4 mL/hr.
Hence, the patient's fluid maintenance is 26.4 mL/hr."
4558,22,Maintenance Fluids Calculations,physical,decimal,pmc-5297160-1,Extracted,"A 61-year-old woman was admitted because of sudden onset of confusion and slurred speech. In preparation for an elective outpatient colonoscopy she had commenced bowel preparation four hours earlier with sodium picosulfate/magnesium citrate (PICOLAX ®). As instructed, she had ingested two liters of water and two liters of tea, albeit within two hours. Shortly thereafter, she felt nauseous, dizzy and vomited repeatedly. Her husband found her confused with unintelligible speech and unsteady gait and called the ambulance.
On physical examination, the patient appeared agitated and her speech was incomprehensible. She weighed 56 kg and her height was 168 cm (BMI 19.9 kg/m2). Vital signs were as follows: Afebrile, blood pressure 132/66 mmHg, pulse 82 beats/min. The patient was clinically euvolemic and could follow verbal commands. No lateralizing signs were found on neurological examination but generalized tremor was present. Acute CT scanning of the brain did not reveal any abnormalities.
Her medical records showed a history of hypothyroidism for which she took levothyroxine. She was a non-smoker and did not drink alcohol. Family history was unremarkable and there was no history of diuretic use or anorexia, as corroborated by her husband.
In the emergency department, biochemistry results were as follows: Serum sodium 122 mmol/l, potassium 3.1 mmol/l, chloride 87 mmol/l, BUN 14.8 mg/dl, creatinine 1.1 mg/dl, uric acid 4.1 mg/dl, glucose 108 mg/dl. Serum osmolality was 251 mOsm/kg. In view of the patient’s symptoms and the clear time of onset, acute hyponatremia was deemed likely and treatment with hypertonic saline (3%) at a rate of 50 ml/h was commenced. Urine osmolality was not done on admission but was 232 mOsm/kg with a urinary sodium of 39 mmol/l when tested two hours later. Thyroid-stimulating hormone was suppressed under replacement therapy. The sodium level increased to 128 mmol/l within the ensuing four hours. In parallel, the patient’s symptoms abated. Twelve hours after admission, she had voided 2600 ml of urine and her mentation and electrolytes had normalized.
On further questioning, it transpired that the patient had had very limited food intake prior to the scheduled procedure. On the day before admission (two days before the endoscopy appointment), her diet consisted of carrot-ginger soup with white bread for lunch and rusk with tea for dinner. The next day, a breakfast consisting of two slices of plain toast and a cup of coffee, followed by a broth at lunchtime, was all she had to eat. No additional salt had been added to her meals. Furthermore, the patient had been taking a nonsteroidal anti-inflammatory drug (NSAID) for the last five days because of shoulder pain (Diclofenac 50 mg bid). A diagnosis of hyponatremic encephalopathy due to acute water intoxication facilitated by poor dietary solute intake was made. On follow-up appointment 1 week later, the patient was well and electrolytes were normal. Adrenal function was tested and found to be intact.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [56.0, 'kg']}",96,91.2,100.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 56.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (56.0 kg - 20 kg) = 96.0 mL/hr.
Hence, the patient's fluid maintenance is 96.0 mL/hr."
4559,22,Maintenance Fluids Calculations,physical,decimal,pmc-6919956-1,Extracted,"An eight-year-old boy was brought to the casualty department attached to the Prathima Institute of Medical Sciences with the chief complaints of fever, malaise, vomiting, and difficulty in swallowing. The boy was admitted to the pediatric intensive care unit (PICU) for further evaluation. The boy’s parents complained of acute onset of low-grade fever three days back. The boy was previously normal and was going to school regularly. The fever episodes were not associated with any type of skin rash. Three to four episodes of vomiting per day were noted along with the fever. The vomiting was non-projectile, non-bilious, blood-tinged, and was stimulated by both solid and liquid food intake. The boy also complained of pain in the throat and had difficulty swallowing. The patient had a loss of appetite, gave a history of high-colored urine, and had generalized weakness.
No previous history of similar complaints in the patient, as well as his two other siblings, was reported. There was no documented evidence/medical record that the patient was immunized with DPT although the parents claimed that the patient was immunized according to the national immunization schedule.
On clinical examination, the patient’s vitals were all good. A noisy breath, probably due to the infection in the throat, was noted, without any dyspnoea. Clinical examination of the pharynx showed grade IV tonsillitis with a grayish-white membranous patch covering the tonsil, which was extending towards the soft palate. The posterior pharyngeal wall revealed congestion, with both sides of the tonsil showing enlargement. The uvula was central, oedematous, showed congestion, and was bleeding on touch.
General physical examination of the patient revealed sunken eyes, loss of the buccal pad of fat, a prominent maxilla, and a scaphoid abdomen. The patient was noted to be underweight (20 kg) as against the recommended weight at the same age (32 kg) and was 133 cm tall as against the recommended height (140 cm) at a corresponding age.
The patient’s parents reported a low-calorie intake of 1200 KCal/day as against the recommended 1920 KCal/day. Also, the patient was only taking 24 g of protein against the daily recommended intake of 38.4 g/day. Considering this, the patient was diagnosed/categorized as suffering from protein-energy malnutrition.
The complete blood picture showed neutrophilic leucocytosis, and borderline platelet counts (1.5 lakh cells/mm3). The patient had raised C-reactive protein (CRP) (2.4 mg/dL) and erythrocyte sedimentation rate (ESR) (40 mm).
A preliminary diagnosis of grade IV tonsillitis was made, and a throat swab was sent to the clinical microbiology laboratory for a direct Gram's stain, culture, and sensitivity. On direct Gram’s stain of the throat swab, plenty of Gram-positive bacilli were observed, with occasional Gram-positive cocci, as shown in Figure .
Culture on blood agar showed 2-3 millimeter, small, round, white-cream-colored non-hemolytic colonies along with 1-2-millimeter, pinpoint, translucent beta-hemolytic colonies, as shown in Figure .
Gram’s stain of the small and the pinpoint colonies revealed gram-positive bacilli and gram-positive cocci in pairs respectively as shown in Figure .
The colonies on blood agar were non-hemolytic (C. diphtheriae forms hemolytic colonies), glossy (gravis type is matt-like) in appearance, raised (intermedius are flat), and were glistening and butyrous (butter-like) in texture, as shown in Figure .
They were catalase-positive, non-motile, and non-fermenters on triple sugar iron agar (TSI). The Gram-positive bacilli were identified as morphologically and biochemically resembling C. diphtheriae. The gram-positive cocci were catalase-negative and were identified as Streptococcus species (Streptococcus Spp).
Both the gram-positive cocci and the bacilli showed varied sensitivity patterns using the Kirby-Bauer disk diffusion method. The antimicrobial susceptibility pattern of gram-positive bacilli showed sensitivity to vancomycin, linezolid, tetracycline, and ofloxacin. Resistance was observed against penicillin, oxacillin, clindamycin, ciprofloxacin, cefotaxime, cefepime, cefoperazone, ceftriaxone, ceftazidime, amikacin, gentamicin, and piperacillin-tazobactam, as shown in Figure .
The Streptococcus spp. isolated was sensitive to amikacin, gentamicin, ciprofloxacin, ofloxacin, trimethoprim-sulfamethoxazole, vancomycin, linezolid, tetracycline, and piperacillin-tazobactam. Resistance was noted against penicillin, erythromycin, clindamycin, oxacillin, cefotaxime, cefepime, cefoperazone, ceftriaxone, and ceftazidime, as shown in Figure .
Considering the transmissibility of the infection, the patient was put under isolation. Treatment was initiated with 80,000 units of diphtheria antitoxin through the intravenous route. Since the isolated organisms were resistant both to penicillin and erythromycin, the drugs of choice in the case of suspected diphtheria, and because the patient also had beta-hemolytic Streptococci, the patient was started on a course of piperacillin-tazobactam and amikacin. The patient had a gradual and uneventful recovery.
The bacterium morphologically resembling C. diphtheriae was not confirmed using the standard anti-toxin by the Elek’s gel precipitation test due to the unavailability of a suitable identification system. Also, the close household contacts were neither screened nor administered prophylactic antibiotics as suggested/recommended by the World Health Organization (WHO) because of the non-cooperation of the patient's parents.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [20.0, 'kg']}",60,57,63,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 20.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (20.0 kg - 10 kg) = 60.0 mL/hr.
Hence, the patient's fluid maintenance is 60.0 mL/hr."
4560,22,Maintenance Fluids Calculations,physical,decimal,pmc-7549992-1,Extracted,"A 60-year-old Caucasian gentleman with a past medical history significant for hypertension and diabetes presented to his primary care physician with abdominal pain for one month. The pain was insidious in onset and associated with poor oral intake, nausea, and vomiting. His diet had been restricted to clear liquids due to unremitting nausea and vomiting, resulting in 32 pounds of weight loss. He denied recent sick contacts, diarrhea, fever, chills, dysuria, or hematuria. Family and social history were insignificant. Examination revealed a blood pressure of 177/94 mmHg, a pulse rate of 87 beats per minute, afebrile, and epigastric tenderness with no other focal systemic findings.
Initial laboratory workup revealed hemoglobin of 10 mg/dL, platelet count of 250,000 cell/µL, creatinine of 3.32 mg/dL (baseline creatinine 1.13 mg/dL), calcium of 13.8 mg/dL, and phosphorous of 2.5 mg/dL. Initial evaluation for hypercalcemia revealed low parathyroid hormone (PTH) level of 11.3 pg/mL, parathyroid hormone-related peptide (PTHrP) of 1 pmol/L, 25-hydroxyvitamin D level of 17 ng/mL, and a 1,25-dihydroxyvitamin D level elevated to 68 pg/mL. The constellation of abdominal pain, anemia, acute kidney injury, and hypercalcemia guided further evaluation for multiple myeloma. Serum protein electrophoresis and urine protein electrophoresis revealed no monoclonality. Serum immunofixation revealed imperceptible free lambda light chains and elevation in both kappa and lambda free light chains with a ratio of 1.73. A bone marrow biopsy revealed normal cellularity, no significant increase in plasma cells, and no plasma monoclonality. He was started on intravenous fluids, pamidronate, and calcitonin for hypercalcemia. Due to worsening renal function, a renal biopsy was obtained which revealed acute tubular injury with chronic and subacute thrombotic microangiopathy, but no evidence of multiple myeloma or sarcoidosis. He was briefly started on steroids for possible sarcoidosis with improvement in serum calcium; however, a normal serum angiotensin-converting enzyme (ACE) level and lack of granulomas on biopsy arrested concerns for sarcoidosis. Due to microangiopathy on renal biopsy, workup including autoimmune antibody, rheumatoid factor, anti-double-stranded DNA antibody, anti-Sjogren's syndrome A (anti-SSA) antibody, anti-Sjogren's syndrome B (anti-SSB) antibody, and lactate dehydrogenase were all negative. CT of his chest revealed small bilateral pleural effusions and pulmonary edema (Figure ). CT abdomen revealed enlarged inguinal lymph nodes that were thought to be reactive.
His calcium and creatinine improved with a dose of denosumab, and he was discharged home with outpatient follow-up. However, due to rising outpatient calcium levels a positron emission tomography (PET) scan was obtained, which revealed multiple tiny fluorodeoxyglucose (FDG)-avid lymph nodes in the chest, abdomen, and pelvis, as well as abnormal FDG labeling in the liver and spleen. Due to concerns for lymphoma, he underwent biopsy of an inguinal lymph node which revealed noncaseating granulomas with giant cells (Figure ). He was diagnosed with extrapulmonary sarcoidosis, and was subsequently started on steroids with improvement in his hypercalcemia.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [32.0, 'lbs']}",49.02988,46.57839,51.48137,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 32.0 lbs so this converts to 32.0 lbs * 0.453592 kg/lbs = 14.51494 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (14.51494 kg - 10 kg) = 49.02988 mL/hr.
Hence, the patient's fluid maintenance is 49.02988 mL/hr."
4561,22,Maintenance Fluids Calculations,physical,decimal,pmc-7034198-1,Extracted,"A 29-year-old male patient weighing 57 kg who was diagnosed to have hemophilia type A since 13 years of age and was on intermittent blood and factor VIII (FVIII) transfusions presented with complaints of chest pain, breathlessness, and palpitations since 4 months which suddenly increased to Grade IV dyspnea since 15 days before admission.
On examination, he had elevated jugular venous distension, wide pulse pressure, epigastric pulsations, and a continuous murmur best heard over left sternal border. His electrocardiography (ECG) showed left ventricular hypertrophy with tall P-wave in lead II and a bifid P wave in lead V. Cardiac computed tomography angiography was performed wherein the aortic annulus was 25 mm, sinus - 37 mm, ascending aorta - 24 mm, and the noncoronary sinus showed a focal dilation (15 mm × 12 mm) protruding into the right atrium suggestive of RSOV of noncoronary sinus.
Laboratory investigations revealed hemoglobin of 14 g/dl and platelet count 2 lakhs/cumm. His coagulation profile including prothrombin time and activated partial thromboplastin time was within normal limits except for FVIII level, for which FVIII assay was done, which was 1% of normal. His disseminated intravascular coagulation profile (platelet counts, fibrin degradation products, etc.) was repeated after injecting 3000 units of FVIII and his FVIII level increased to 100% of normal.
A hematology consultation was sought, and the patient was planned for device closure of the RSOV under general anesthesia in catheterization laboratory by cardiologist, especially in view of Hemophilia type A to avoid risks associated with surgical repair of the RSOV. On of the cardiac surgery operation theater was kept on standby until the completion of the interventional procedure.
Preoperative anesthetic evaluation was done. Oral premedication in the form of tablet diazepam 5 mg HS and tablet alprazolam 0.5 mg an hour before the procedure were given. Premedication in the form of intramuscular injections were avoided for fear of an intra-muscular hematoma. Three thousand units of FVIII (Eloctate®, antihemophilic factor, Fc Fusion protein, Biogen, USA) were given intravenous (IV) 1 day before the procedure and another 3000 units were given 30 min before the procedure on the day of intervention as advised by the hematologist.
Four units of packed red blood cell, 4 units of platelet concentrate and 4 units of cryoprecipitate were arranged. Three vials of 3000 unit each were also arranged and the plan was to repeat 3000 units in the evening in case surgery was needed.
The patient was taken up for the procedure early morning as the first case. Monitoring included pulse oximetry, ECG, and noninvasive blood pressure. Intravenous cannulation was performed using 16 G cannula after local infiltration with insulin syringe. Injection midazolam 1 mg and injection fentanyl 100 μg were given intravenously. Anesthesia was induced with injection etomidate 20 mg and atracurium 40 mg IV was used as muscle relaxant. Trachea was intubated with 8.0 mm ID cuffed endotracheal tube and fixed at 22 cm. Anesthesia was maintained with oxygen, air, and isoflurane. End-tidal CO2 monitoring was attached. Transesophageal echocardiography (TEE) probe was inserted gently avoiding any trauma []. Injection paracetamol 1 g IV was administered 30 min before the completion of procedure for adequate analgesia.
Catheters for loading the device were inserted through the femoral artery and the device was successfully deployed under fluoroscopic guidance []. The procedure lasted for about 2 h and was uneventful. An occluder device (Amplatzer, 2.5 mm) was successfully placed to occlude the ruptured aneurysm [ and ]. The patient was extubated in the cath lab table and was shifted to the ward in a stable condition. No intraprocedure blood or blood product transfusions were required. Postprocedure FVIII levels were maintained for at least 7 days.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [57.0, 'kg']}",97,92.15,101.85,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 57.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (57.0 kg - 20 kg) = 97.0 mL/hr.
Hence, the patient's fluid maintenance is 97.0 mL/hr."
4562,22,Maintenance Fluids Calculations,physical,decimal,pmc-8134852-1,Extracted,"A 30-year-old woman presented to our hospital complaining of swallowing difficulty.
A patient had a violation of physical development and constipation from an early age. At the age of 7 years, she was diagnosed with partial bilateral symmetric ptosis. At the age of 8 years, she was referred to the hospital with diagnoses of generalized viral infection of unspecified etiology, postinfectious encephalopathy, cerebro-asthenic syndrome, neurosis, urinary bladder and gut atony, chronic pyelonephritis, mydriasis, semiptosis, and dystrophy. At the age of 9 years, she had suspected high intestinal obstruction which was followed by surgery. The obstruction was not revealed during the surgery. In the postoperative period, signs of intestinal obstruction persisted, and they were managed conservatively. After the surgery, she developed meningeal signs, gaze paresis, double vision, and reduced vision. Electrocardiogram showed an incomplete type of blockade of the right branch of the bundle of His. Esophagogastroduodenoscopy (EGD) showed gastric hypotony. Computed tomography scans of the head revealed moderate diffuse cortex atrophy. Cerebrospinal fluid was clear with 0.066. The patient was seen by a neurologist, ophthalmologist, infectious diseases specialist, and neurosurgeon. However, the diagnosis remained unclear. The following pathologies were excluded: neuro infections, intestinal infections, oncohematology, and endocrine pathologies. Further generalized pathology persisted. At the age of 10 years, a second laparotomy was performed followed by a temporary ileostomy because of signs of acute intestinal obstruction. From the ages of 11 years to 14 years, the patient was annually referred to the surgery department with signs of acute intestinal obstruction, which were managed conservatively. At the age of 11 years, she was diagnosed with intestinal pseudo-obstruction. From the age of 11 years, paradontosis began. From the age of 14 years, the patient had daily dysphagia while eating solid and liquid food. She lost 5 kg and began feeling weak and fatigued. At the age of 15 years, resection of the jejunum was performed two times with an overall resection length of 90 cm because of acute intestinal obstruction which was not managed conservatively. The patient was dystrophic, which was thought to be because of malabsorption as a consequence of the resection of the jejunum. At the age of 25 years, the patient lost all her teeth because of progressive paradontosis. From the age of 26 years, she developed amenorrhea. At the age of 29 years, esophagography showed signs of achalasia, gastroptosis, and delayed gastric and duodenum emptying time. At the age of 30 years, the patient was referred to the endoscopy department of Pavlov Medical University for achalasia treatment.
History of present illness includes the patient’s entire life. That is why we suppose that this part is irrelevant in this case.
The mother, father, and sister are healthy. There was no family history of GI or autoimmune pathologies or allergic disorders. The niece (4 years of age) had sensorineural hearing loss.
Eckardt score was 4. Her weight was 38 kg. Her body mass index was 16.9, and she had protein energy malnutrition. During preoperative preparation, the patient was revealed to be 16 wk pregnant. She was not aware of the pregnancy. In addition, intraventricular blockage was diagnosed. High-resolution esophageal manometry showed achalasia type I (Figure ). Hemoglobin and total blood protein levels were 106 g/L and 64 g/L, respectively. Creatine phosphokinase and lactate levels were normal. Neurologic and ophthalmologic disorders were not observed. Considering all data, we suspected mitochondrial disease: incomplete Kearns-Sayre syndrome (KSS) or mitochondrial neurogastrointestinal encephalopathy (MNGIE) disease.
Histology of the esophageal muscular layer specimens: There were myocytes of different thicknesses with sites of wave-like deformation and dystrophic changes. There were also single myocytes with necrobiotic changes and small vessels with “edge standing” leukocytes (Figure and ).
Genetic testing of mitochondrial DNA (lymphocytic): It showed segment deletion in mitochondrial DNA (mDNA) which affected the genes RNR1 (MTRNR1) and RNR2 (MTRNR2). This aberration is considered to be pathogenic and most frequently observed in patients with KSS[]. Unfortunately, after discharge, the patient refused further genetic testing.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [38.0, 'kg']}",78,74.1,81.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 38.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (38.0 kg - 20 kg) = 78.0 mL/hr.
Hence, the patient's fluid maintenance is 78.0 mL/hr."
4563,22,Maintenance Fluids Calculations,physical,decimal,usmle-8188,Extracted,"A 55-year-old female comes to see her doctor for a rapidly enlarging abdomen and swelling of both legs. She was hospitalized 2 weeks ago for an upper gastrointestinal bleeding episode. On that occasion, her esophagogastroduodenoscopy showed grade 1 esophageal varices and a 1 cm clean-based antral ulcer. The patient was discharged on omeprazole. Review of symptoms shows that the patient is forgetful, does not sleep well, and is drowsy and fatigued during the day which prevents her from working full-time. She denies abdominal pain. The patient has a 10-year history of type 2 diabetes mellitus, hypertension, and hypercholesterolemia but no history of angina or coronary heart disease. She drank alcohol moderately heavy in her twenties and currently drinks less than 3 drinks per week and does not smoke. Her family history is unremarkable. On physical examination, her blood pressure is 132/82 mm Hg, pulse is 88/min, and her temperature is 37.0°C (98.6°F). She weighs 106.6 kg (235 lb) and her BMI is 33. She is alert, oriented to person, place, year, and month but not to the day. Her sclerae are nonicteric. Her pulmonary and cardiovascular exam are normal but her abdomen is distended with a fluid wave and mild tenderness to palpation. There is no hepatosplenomegaly. There is a 2+ edema to mid-calf and pedal pulses are barely palpable. Her neurological exam is without motor or sensory deficits but she demonstrates flapping tremor of her hands while asked to hold them in front of her for a few seconds and her skin exam shows a few spider telangiectasias on her face and upper chest. After an initial evaluation, lab tests were obtained:
Serum sodium 133 mEq/L
Serum potassium 3.8 mEq/L
BUN 8 mg/dL
Serum creatinine 1.0 mg/dL
Serum albumin 2.5 mg/dL
Aspartate aminotransferase 68 IU/ml
Alanine aminotransferase  46 IU/ml
Alkaline phosphatase  130 IU/ml
Total bilirubin  1.8 mg/dL
 WBC count 4,200/mm3
Platelets 94,000/mm3
Hematocrit 35.5%
Prothrombin time (INR) 1.5
A liver biopsy is performed and the results are pending.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [106.6, 'kg']}",146.6,139.27,153.93,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 106.6 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (106.6 kg - 20 kg) = 146.6 mL/hr.
Hence, the patient's fluid maintenance is 146.6 mL/hr."
4564,22,Maintenance Fluids Calculations,physical,decimal,pmc-2824987-1,Extracted,"A 12-year-old female patient weighing 35kg was admitted to hospital with complaints of behavioral disturbances since last six weeks. Her past medical history revealed that 14 weeks ago she was hospitalized following three episodes of seizures in a day with up rolling of eyeballs, confusion and limbs stiffness. A diagnosis of complex partial seizure with secondary generalized seizure disorder was made. She was treated with tablet valproic acid 200 mg twice daily and tablet clobazam 5mg at night during her hospital stay. After 5 days of treatment she was discharged with refilled prescription of valproic acid and clobazam and advised for monthly visits. Patient was otherwise normal and had no known psychiatric history or previous episodes of abnormal behavior.
After 13 weeks of treatment with valproic acid and clobazam, she was hospitalized with complaints of irrelevant talk, talking to self, wandering and singing devotional songs, decreased food intake and insomnia since about five weeks i.e. about eight weeks after initiation of valproic acid therapy. Upon hospitalization, tablet chlorpromazine 100mg once daily, tablet olanzapine 5mg thrice daily, tablet risperidone 3mg twice daily were started while she continued to receive valproic acid and clobazam at the same dose. She was discharged on day three of hospitalization with an advice to continue all medications prescribed during the hospital stay at same doses for 15 days. However, her complaints of wandering, insomnia and decreased food intake continued to persist and she was readmitted to the hospital after a week.
During the present hospital admission patient was under observation and continued to receive valproic acid and clobazam. The antipsychotics were discontinued. As there was no improvement in behavior, valproic acid was suspected as a causative agent for abnormal behavior and was replaced with tablet carbamazepine 200 mg twice daily on day six of her hospital stay. Three days after the withdrawal of valproic acid her sleep pattern, food intake and speech improved significantly. A week later she was discharged with carbamazepine and clobazam with an advice for the review after two weeks. She recovered completely after 12 weeks. Later she continued to receive only carbamazepine for her seizure disorder.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [35.0, 'kg']}",75,71.25,78.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 35.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (35.0 kg - 20 kg) = 75.0 mL/hr.
Hence, the patient's fluid maintenance is 75.0 mL/hr."
4565,22,Maintenance Fluids Calculations,physical,decimal,pmc-6078740-1,Extracted,"A 66-year-old man was hospitalized in April 2017 for a weight loss of 7 kg and a nocturnal low-grade fever evolving since January 2017. The patient reported clinical tuberculosis in childhood. His medical history included arterial hypertension, dyslipidemia, coronary artery disease, and tobacco smoking. A bladder cancer diagnosed in 2015 had been treated with local resection and weekly intravesical instillation of BCG (BCG-MEDAC, strain RIVM 1173-P2, MEDAC, Lyon, France) for 6 weeks. In April 2017, a thoraco-abdomino-pelvic computerized tomography scan diagnosed pulmonary embolism, a sub-renal septic aneurysm and a collection in the right psoas muscle (Fig. A). A 2-deoxy-2-[fluorine-18]fluoro-D-glucose positron emission tomography combined with computed tomography (18FDG PET/CT) was subsequently performed and showed an intense hypermetabolism of the aortic aneurysm, with no other embolic foci (Fig. B). Physical examination found dyspnea and diffuse abdominal pain. Remarkable biological parameters included hemoglobin concentration of 10.8 g/dL (normal value, 13–16 g/dL), 0.7 G/L lymphocytes (normal value, 1–4 G/L), and a C-reactive protein of 60 mg/L (normal value, 0–5 mg/L). Surgical flattening of the aneurysm was immediately performed which showed rupture on the right flank of the aorta, explaining the psoas hematoma. Postoperative probabilistic therapy included 4 g tazocillin 3 times a day and 1 bolus of 320 mg gentamicin. Routine bacteriological investigations of an aneurysm specimen collected during surgery remained negative. Pathological examination yielded chronic granulomatous inflammation of the vascular wall leading to a differential diagnosis of BCG aneurysm. While routine microscopic examination after Ziehl-Neelsen staining (Kit Quick-TB, RAL DIAGNOSTICS, Martillac, France) remained inconclusive, the surgical specimen was examined by using fluorescence in situ hybridization specifically targeting the M tuberculosis complex rpoB gene. Briefly, the fresh specimen was cut and an imprint slide was prepared by dabbing the cut surface of the biopsy against a clean glass slide after 3 washes with Dulbecco's phosphate-buffered saline (DPBS) (Thermo Fisher Scientific, Illkirch, France), then heat-fixed at 90 °C for 5 minutes and flooded with 70% ethanol for 10 minutes. The slide was covered with 10 mg/mL lysozyme (37 °C for 30 minutes), then with 5 μg/mL proteinase K (37 °C for 5 minutes) and finally with 10 μL of solution containing the rpoBMTC probe. After hybridization and appropriate washings, the slide was stained with Ziehl-Neelsen staining in a dark room and observed under 100 times magnification using a red filter and a fluorescent microscope. The overall procedure took 20 hours. Combining rpoBMTC-FISH and Ziehl-Neelsen-staining yielded specific detection of tuberculous mycobacteria as red fluorescent Ziehl-Neelsen-positive bacteria (Fig. ). Identification at the species level was confirmed by multiplex polymerase chain reaction (PCR) amplification of regions of differences (RD) RD1, RD4, RD9, and RD12 as previously described[; and by PCR-sequencing of the rpoB gene which detected M bovis BCG with 99% sequence similarity with the reference species (GenBank AM408590.1).[ Culture for mycobacteria remained sterile. Tazocillin was discontinued and an anti-tuberculous treatment including ethambutol 500 mg 3 times a day plus an oral combination of isoniazid and rifampicin was continued for 2 months then relayed by an oral combination of rifampicin and isoniazid for 8 months. A CT scan performed at 6-month follow-up showed the absence of relapse of the aortic collection while the 18FDG PET/CT showed a reduction of the size and of the metabolism of the aortic aneurysm (Fig. C). A 9-month clinical follow-up indicated a favorable clinical and biological evolution.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.0, 'kg']}",28,26.6,29.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.0 kg. Hence, the patient's maintenance fluid is 7.0 kg * 4 mL/kg/hr = 28.0 mL/hr.
Hence, the patient's fluid maintenance is 28.0 mL/hr."
4566,22,Maintenance Fluids Calculations,physical,decimal,pmc-4198860-1,Extracted,"A 12-year-old female with tuberous sclerosis and associated psychiatric symptoms was admitted on February 6th, 2011 to the Kangning Psychiatric Hospital. The history of the development of her condition was as follows.
Born by normal delivery at full-term, her early childhood development was unremarkable. Facial erythema appeared when she was 3 years of age and subsequently expanded to cover the skin on her head and neck in elevated stripes; but it had never been painful so it was not treated. At the age of six she starting having frequent 30 to 60-second episodes (usually more than 12 times a day) during which her hands twitched, her head and neck were askew, she was non-responsive and she foamed at the mouth. After detailed assessments at several hospitals, a diagnosis of tuberous sclerosis was made. She was treated with 100 mg/d topiramate and 0.5g/d clonazepam for her seizures; these medications decreased the frequency of the seizures but did not eliminate them completely. She continued to have very brief seizures twice daily during which her eyes looked to one side and her hands twitched.
She completed the first two years of elementary school without trouble, but in the third year her scores in math and Chinese dropped significantly and she was no longer able to complete math problems that she had been able to complete in grades 1 and 2. At the same time she became introverted. Two years prior to the current admission (when she was 10 years old) her behavior changed; she became temperamental, attacked others with little provocation, and cried out repeatedly.
Three months prior to the current admission, she started treatment with 500 mg/d vigabatrin. This treatment gradually reduced her twitching and seizures (she had had none in the 6 weeks prior to admission), but in the month before admission she became increasingly moody, angry, impulsive and aggressive; this included biting her hands and scratching family members. Unable to manage this behavior, the family decided to admit her to a psychiatric hospital.
The patient's mother had condyloma acuminatum during pregnancy, but there was no family history of mental disorders.
At the time of admission her height and weight were 159 cm and 70 kg. She had normal vital signs and normal consciousness. Covering the head and neck she had elevated red erythema which did not fade when pressed. There were also more than a dozen lipoadenomas which were soft in texture and did not produce pain on palpation. She had depigmented spots of 0.5cm × 0.5cm scattered on the skin of her torso. On her abdomen and thighs there were streak-shaped pigmentations similar to striae gravidarum. On the second joint of her ring finger of the right hand there was a 0.5cm × 0.5cm painless nodule which was hard in texture, had clear border lines, and could not be moved. She had a supple neck and did not have abnormalities in her lungs or heart. Her abdomen was extended resembling pregnancy; she was not cooperative with the examination of her liver and spleen but no abnormalities were detected.
Her consciousness was clear but she was uncooperative, crying and shouting during the examination. Her speech and mannerisms were age inappropriate, similar to those of a much younger child. There were no evident hallucinations or delusions. She had poor attention. Her memory, ability to do simple calculations, comprehension, judgment and overall intelligence were all impaired. She had immobile facial features and labile emotions. She was self-centered and stubborn. She was capable of basic self-care but was impulsive, destructive and aggressive. She had no insight into her condition and had only passively accepted the need for psychiatric help.
Electrolytes and liver and renal function tests were normal. Serum calcium level was 2.68mmol/L. She had a normal electroencephalography and a normal echocardiography, but the computerized tomography of her head showed several nodular calcifications of different sizes bilaterally distributed under the ependymal or the lateral ventricle. An abdominal ultrasound revealed a fatty liver and hamartomas in both kidneys. On the Wechsler Intelligence Scale for Adults her scores were 49 for verbal intelligence and 62 for performance intelligence.
She was diagnosed as having a mental disorder due to a medical condition (tuberous sclerosis). Taking into consideration the patient's young age, obesity, and the intracerebral nodules, we decided to provide symptomatic treatment with quetiapine, an antipsychotic that has relatively little effect on prolactin, body weight and the extrapyramidal system. The low starting dose of 25mg/d was gradually increased to 200mg/d and she was maintained on her antiepileptic medication (vigabatrin). This regimen lead to improvement in her disruptive and argumentative behavior so she was discharged two weeks after admission. She continued this dosage and was seen as an outpatient each month. At the time of the last follow-up in the end of October 2011 her condition had stabilized and she was able to undertake simple self-care at home.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [70.0, 'kg']}",110,104.5,115.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 70.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (70.0 kg - 20 kg) = 110.0 mL/hr.
Hence, the patient's fluid maintenance is 110.0 mL/hr."
4567,22,Maintenance Fluids Calculations,physical,decimal,pmc-8708697-1,Extracted,"A five-month-old, female, domestic shorthaired cat, weighing 1.65 kg, was referred to the Veterinary Teaching Hospital of the University of Padua with a two-month history of recurrent episodes of respiratory distress. The cat had been treated in the previous 10 days with doxycycline 10 mg/kg PO q24 h and inhaled beclomethasone with only partial relief of the respiratory signs.
On physical examination, the cat was alert but panting with open mouth breathing. The mucous membranes were pink-pale and the respiratory rate was 80 breaths/min with a restrictive respiratory pattern. Thoracic auscultation revealed respiratory crackles on both side of the thorax without appreciable cardiac murmur. The heart rate was 190 bpm. The laboratory work-up included serology for feline leukemia virus antigen and feline immunodeficiency virus (FIV) antibodies and both tests were negative, results of complete blood count were unremarkable. To minimize the respiratory distress, successive diagnostic procedures were performed with the cat under sedation with butorphanol (0.2 mg/kg IV), dexmedetomidine (5 μg/kg IV), propofol IV to effect, and oxygen delivery.
Thoracic radiography showed subjective generalized cardiomegaly with prominent right-sided cardiac chambers and a vertebral heart score of 10.0 (A,B). The right cranial and caudal pulmonary artery were prominent while the left pulmonary arteries were barely appreciable suggesting left lung hypoerfusion. In the lungs, an interstitial pulmonary pattern was found in the right caudal lung lobe. A gas filled stomach was an additional radiographic finding, likely due to aerophagia associated with respiratory distress.
Trans-thoracic echocardiography revealed severe right atrial and ventricular dilatation and reduced left ventricular cavity (right atrial diameter = 1.5 cm; right ventricular diastolic diameter = 1.13 cm, left ventricular diastolic diameter = 0.56 cm) (A,B). The right ventricular free wall was hypertrophic (diastolic thickness = 0.49 cm) and interventricular septal flattening was evident (diastolic interventricular septum thickness = 0.45 cm). The cardiac septa were intact, and the left atrium (LA) was not enlarged (LA to aortic root ratio = 1.36, normal value < 1.6). No obstruction of the right ventricular outflow tract was found. The pulmonic valve was normal, and the pulmonary blood flow was laminar with a sharp peak (type II pulmonary blood flow) on pulsed-wave Doppler interrogation, suggesting increased pulmonary artery pressure (C). The pulmonary acceleration time (AT) and ejection time (ET) were 45 ms and 153 ms, respectively with an AT to ET ratio (AT/ET) of 0.29. Moderate-severe tricuspid regurgitation (TR) was found on color flow Doppler (D) with a peak systolic velocity of 5.57 m/s corresponding to an estimated pressure gradient of 133 mmHg using a modified Bernoulli equation. The pulmonary trunk appeared dilated, but evaluation of the main PAs was not feasible. A bubble test was performed using 2 mL of saline solution with 0.5 mL of air agitated forcefully between two syringes connected with a three-way stopcock and rapidly injected in the left cephalic vein trough a 22G catheter. As no echo contrast was detected in the left heart and in the abdominal aorta, intracardiac or vascular extra cardiac right-to-left shunts were excluded.
A presumptive diagnosis of severe right sided cardiac remodeling due to precapillary PH, left lung hypoperfusion, and pneumonia was made. In addition to pneumonia, other differential diagnoses for precapillary PH included distal PA stenosis, pulmonary parasitic disease, and pulmonary capillary hemangiomatosis. Selective angiogram and computed tomography scan were proposed to refine the diagnosis but were denied by the owner. The cat was discharged on doxycycline 10 mg/kg PO q24 h and sildenafil 0.5 mg/kg PO q12 h. Two days after our visit the cat was presented to the Emergency Service because of worsening of respiratory signs that prompted sudden death because of cardiorespiratory arrest.
On gross pathology, multifocal, compact, and brownish-yellow pulmonary areas associated with severe reactive enlargement of the tracheobronchial lymph nodes were found. The heart demonstrated severely increased right ventricular volume and severe dilatation of the right atrium and auricle. The PA was markedly dilated at the level of the main trunk and right branch, with severe and diffuse hypoplasia of the left branch (A). The examination of the PA cavity showed an atresia of the origin of its left branch (B). The right ventricular outflow tract and tricuspid valve had no lesion. The cross section of the ventricles showed severe concentric right ventricular hypertrophy with a thickness of the free wall and interventricular septum of about 0.6–0.7 cm and 0.5–0.6 cm, respectively.
Multiple samples of lung, tracheobronchial lymph nodes, right ventricle, and left PA branch were examined histologically according to routine techniques. In the right lung, severe macrophagic pneumonia, characterized by alveolar infiltration of activated macrophages with wide and granular cytoplasm often containing optically empty vacuoles, and eosinophilic granular material was found. In the left lung, multifocal and severe lymphocytic interstitial infiltrates and a mild mid-intimal hypertrophy of medium-caliber arteries were present. Severe reactive hyperplasia of the tracheobronchial lymph nodes was an additional finding. The right ventricle showed severe hypertrophy of myocardiocytes with multifocal and minimal interstitial fibrosis. The longitudinal section of the PA showed complete atresia and occlusion of the origin of the left branch by fibromyxoid tissue along the endothelial layer. The left branch of the PA had a voluminous thrombus in the residual cavity of its first portion ().
The final diagnosis was left PA coarctation associated with pneumonia, pre-capillary PH, and severe right-sided cardiac remodeling.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1.65, 'kg']}",6.6,6.27,6.93,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1.65 kg. Hence, the patient's maintenance fluid is 1.65 kg * 4 mL/kg/hr = 6.6 mL/hr.
Hence, the patient's fluid maintenance is 6.6 mL/hr."
4568,22,Maintenance Fluids Calculations,physical,decimal,pmc-5885127-5,Extracted,"A 13-year-old girl weighing 18 kg presented with lumbosacral meningomyelocele. She had no sensory deficit over the anterior abdominal wall. Her medical history included scoliosis, hydrocephalus, and spina bifida. She was scheduled for laparoscopic insertion of a peritoneal dialysis catheter. Her physical examination did not reveal any significant findings. Hemoglobin, hematocrit, platelet count, coagulation profile, liver enzymes, bilirubin levels, blood glucose level, serum sodium and potassium levels were within normal limits in preoperative investigations. Blood urea level was 74 mg/dl and serum creatinine level was 2.1 mg/dl. Her preoperative chest x-ray revealed scoliosis. Pulmonary function tests were within normal limits (). Preoperative investigations revealed elevated urea and creatinine levels.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [18.0, 'kg']}",56,53.2,58.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 18.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (18.0 kg - 10 kg) = 56.0 mL/hr.
Hence, the patient's fluid maintenance is 56.0 mL/hr."
4569,22,Maintenance Fluids Calculations,physical,decimal,pmc-7204778-1,Extracted,"A 55-year-old man with a previous surgical history of distal gastrectomy with antecolic Roux-en Y reconstruction performed 3 years previously for gastric cancer (tub2, T1, N0, M0, pStage IA) presented with a rapidly growing intraabdominal mass that had developed during the postoperative course. The patient had not undergone adjuvant chemotherapy and had no medical or surgical history other than that of gastric cancer.
On admission, his height was 167 cm, weight was 49 kg, blood pressure was 118/73 mm Hg, heart rate was 67 beats/min, and body temperature was 36.6°C. The abdomen was soft and flat with a midline incision scar. A mobile, elastic, hard mass was palpable on the left side of the abdomen. His complete blood count and serum chemistry results were normal, and all of the examined tumor markers (carbohydrate antigen 19-9, carcinoembryonic antigen, α-fetoprotein, neuron-specific enolase, cytokeratin 19 fragment, and soluble interleukin-2 receptor) were within their normal limits.
Abdominal contrast-enhanced computed tomography (CT) initially detected a newly appearing small mass measuring 14 mm, neighboring the Roux-en-Y limb anastomosis without invasion into the small bowel 22 months previously (although this was confirmed only via retrospective observation). The mass had increased in size from 33 mm (6 months before) to 82 mm at the time of the operation (Fig. ). On the preoperative CT, the tumor was 82 × 75 mm in size, and it appeared to originate from the mesentery of the small intestine. We determined the most likely differential diagnosis of gastrointestinal stromal tumor and lymph node recurrence of the gastric cancer, and DF was not included in the list. 18F-2-fluoro-2-deoxyglucose positron emission tomography (PET) revealed a heterogeneously enhanced uptake on the lesion (SUVmax = 4.40) in the lower abdomen. The mobility of the tumor from the previous CTs also supported the origin of the mesentery. Apart from this, there were no significant findings that indicated metastasis or any other lesions (Fig. ). Biopsy was considered because chemotherapy, not surgery, may be needed in case of recurrence of the gastric cancer. However, this strategy was abandoned owing to the lack of a suitable route for a percutaneous or endoscopy-assisted approach.
Overall, we suspected that a malignant lesion was located in the mesentery near the Roux-en-Y limb that was responsible for its rapid growth. There was no other lesion elsewhere; therefore, we decided to perform resection for both diagnosis and treatment.
Laparotomy showed that the tumor was located in the mesentery of the small intestine near the Roux-en-Y limb. The feeding vessels for the Roux-en-Y limb anastomotic site were partly involved by the tumor; therefore, the anastomotic site was resected en bloc with the tumor, and the whole Roux-en-Y limb was reconstructed with functional end-to-end anastomosis using a linear stapler. No intraperitoneal dissemination or distant metastasis was observed during the surgery.
Macroscopically, the resected specimen was a 10 × 9 × 8 cm-sized solid lesion with no necrosis or bleeding (Fig. ). No exposure to the mucosa of the adjacent small intestine was observed, indicating its origin in the mesentery. Histopathological findings revealed that the tumor was located in the mesentery of the small intestine, and spindle-shaped cells resembling fibroblasts or myofibroblasts proliferated sparsely with intervening collagen fibers. Invasive proliferation into the surrounding fat tissue was observed in the marginal area of the tumor (Fig. ). The immunohistochemistry results were negative for desmin, α-smooth muscle actin, CD34, and c-kit. Moreover, positivity for the nuclear accumulation of β-catenin was observed (Fig. ). In accordance with our findings, DF of the mesentery was diagnosed.
The postoperative course was uneventful, and the patient was discharged on postoperative day 13. At the time of writing of this report, the patient was free from recurrence with no adjuvant treatment and was being carefully followed up with CT.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [49.0, 'kg']}",89,84.55,93.45,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 49.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (49.0 kg - 20 kg) = 89.0 mL/hr.
Hence, the patient's fluid maintenance is 89.0 mL/hr."
4570,22,Maintenance Fluids Calculations,physical,decimal,pmc-7213769-1,Extracted,"A 71-year-old male patient presented in July 2019 with abdominal pain of unknown duration, 107-pound weight loss over one year, and recent history of altered bowel habits. The abdominal pain was generalized, non-radiating, and not associated with alleviating or aggravating factors. The patient denied any nausea, vomiting, fevers, bone pain, or night sweats. The patient was also experiencing constipation with stools that were small and black. His past medical history is significant for KS, congenital unilateral cryptorchidism (right), a left atrophic testicle, cerebrovascular accident (CVA) in 2015, hypertension (HTN), chronic obstructive pulmonary disease (COPD), and benign prostatic hyperplasia (BPH). On physical examination, the patient was thin, appeared older than his age, and had mild abdominal distention, bilateral inguinal lymphadenopathy, and gynecomastia.
This constellation of symptoms necessitated an extensive workup. CT scan of the chest (Figure ) revealed a posterior mediastinal mass and mediastinal lymphadenopathy (LAD). CT scan of the abdomen and pelvis (Figure ) revealed large retroperitoneal masses measuring up to 11.9 cm with significant LAD, central hypo-density (necrosis) in bilateral iliac chains, and involvement of the perivertebral space. Multiple large inguinal lymph nodes with central necrosis were also seen. The above features with the history of KS and unilateral cryptorchidism were highly suggestive of germ cell tumors. Imaging showed no evidence of any anterior mediastinal masses, pulmonary metastasis, or liver metastasis, and a CT scan of the brain did not reveal any leptomeningeal metastasis.
Serum lab profile [including complete blood count (CBC), comprehensive metabolic panel (CMP), coagulation studies], fecal occult blood test (FOBT), and serum tumor markers [including alpha-fetoprotein (AFP), beta human chorionic gonadotropin (β-HCG), lactate dehydrogenase (LDH), and placental alkaline phosphatase (PLAP)] were positive only for mild anemia (Hct 34.1 & Hb 10.8) as well as elevated LDH level of 714. The remainder were negative or normal.
Colonoscopy with biopsy was performed, which did not reveal any malignant transformation or colorectal cancer.
The surgical team was consulted to perform an excisional biopsy of the inguinal lymph nodes. The resultant tissue samples revealed a poorly differentiated embryonal cell carcinoma. Morphologic review of the slides demonstrates high-grade/poorly differentiated malignant neoplasm with necrosis replacing most portions of the lymph node. Immunohistochemistry (IHC) studies revealed strong expression of tumor cells for keratin OSCAR, SALL4, and focal expression for keratin-7, along with a rare expression for OCT3/4. Tumor cells showed a lack of expression for CD30, PLAP, TTF1, CDX2, GATA-3, Calretinin, HCG, Inhibin, and SATB2 (Table and Figure ).
Positron emission tomography-computed tomography (PET-CT) was subsequently obtained which revealed extensive FDG-avid LAD seen throughout the body (axillary, mediastinal, paraesophageal, retrocrural, mesenteric, inguinal) with the exception of the neck (Figure ). There was extensive FDG-avid retroperitoneal LAD encasing the aorta and likely displacing the inferior vena cava (IVC). LAD was also noted to extend into the bilateral common and external iliac chains as well as to the right inguinal region.
Staging (2017 AJCC TNM Classification System for Testicular Cancer; Table ):
pTx: primary tumor cannot be assessed
pN3: metastasis with a lymph node mass >5 cm in the greatest dimension
M1b: distant metastases other than non-regional nodal or lung
S2: LDH 1.5-10.0 × ULN or HCG 5,000-50,000 mIU/ml or AFP 1,000-10,000 ng/ml
Given the above parameters, an initial diagnosis of advanced stage IIIC testicular embryonal germ cell tumor was made (Table ).
In light of advanced metastatic disease, chemotherapy was planned. A regimen of bleomycin, etoposide and platinum (BEP regimen) × 4 cycles of 21 days was ordered (Bleomycin 30U IV Weekly on days 1, 8 and 15; etoposide 100 mg/m² on day #1-5 day and cisplatin 20 mg/m² on day #1-5).
During cycle 1, day 15, the patient's treatment course was complicated by chemotherapy-induced severe neutropenia, with weakness, fatigue, diarrhea, and decreased breath sounds. As such, his day 15 dose was delayed and he was transferred to the ER and admitted. A complete infectious workup was initiated and he was started on empiric antibiotics as well as Neupogen 300 mcg SQ daily for five days. He reported significant improvement in symptoms and remained afebrile with improvement in his neutropenia throughout the remainder of his treatment course. Bleomycin was discontinued in the fourth cycle due to concerns regarding developing interstitial lung disease.
After completing four cycles of chemotherapy, a repeat CT abdomen and pelvis was obtained (Figures , ) in October 2019 to evaluate his response to treatment. It yielded redemonstration of multiple large retroperitoneal masses including a heterogeneous mass adjacent to the aorta to the right of midline at the level of the kidneys again measuring up to 11.9 cm. Additionally, it showed a 5.1 × 4.1 cm heterogenous mass just lateral to the right iliac artery abutting the right iliopsoas muscle. New findings included multiple mildly enlarged mesenteric lymph nodes measuring up to 1.3 cm. When compared to prior imaging, there was no significant decrease in the size of the masses or lymph nodes on follow-up imaging. Follow-up CT chest also revealed new bilateral diffuse ground-glass opacifications which were attributed to bleomycin toxicity.
The patient was readmitted in December 2019 for bilious vomiting and right leg pain. He was found to have a right superficial and common femoral vein deep vein thrombosis (DVT) attributed to compression from the right iliac tumor. Additionally a workup for small bowel obstruction necessitated surgical exploration. He was optimized and the surgical team planned to perform a diagnostic laparoscopy for the obstruction. Furthermore, a multi-disciplinary decision was made that the patient would benefit from tumor debulking if possible, considering he was non-responsive to chemotherapy.
On laparoscopic exploration there were no findings that could explain a small bowel obstruction. A retroperitoneal dissection was begun for tumor debulking, and was eventually converted to an open right retroperitoneal dissection (Figure ). Although the tumor was noted to be encasing the right iliac vessels, we were successfully able to debulk this portion of tumor (Figure ). Additional tumor was encountered along the proximal right iliac vein and encasing the IVC, which was ultimately deemed unresectable. The repeat staining and immunohistochemistry of the right iliac tumor was entirely unchanged from the initial tumor biopsy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [107.0, 'lbs']}",88.53434,84.10762,92.96106,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 107.0 lbs so this converts to 107.0 lbs * 0.453592 kg/lbs = 48.53434 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (48.53434 kg - 20 kg) = 88.53434 mL/hr.
Hence, the patient's fluid maintenance is 88.53434 mL/hr."
4571,22,Maintenance Fluids Calculations,physical,decimal,pmc-5483845-2,Extracted,"Case 2: A 61 years old male (weight 75 kg, ASA status III) suffered from AS for 20 years, and was scheduled for left total hip arthroplasty (THA). He had a history of coronary heart disease and received coronary stent implantation 7 years ago. A physical examination revealed rigidity of cervical and lumbar spine, severe press pain and immobilization of left hip joints. An X-ray of the neck, chest and lower back revealed bamboo-like changes of the spine. CT of the hip joints reported necrosis of the left femoral head, and ankylosis of left hip joint. He had taken aspirin for anticoagulation therapy for a long term, and was replaced by low molecular weight heparin.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [75.0, 'kg']}",115,109.25,120.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 75.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (75.0 kg - 20 kg) = 115.0 mL/hr.
Hence, the patient's fluid maintenance is 115.0 mL/hr."
4572,22,Maintenance Fluids Calculations,physical,decimal,pmc-2815825-1,Extracted,"A 35-year-old man presented with a 1-month history of dizziness, palpitation and indigestion. He had a feeling of fullness in his epigastrium and he had esperienced a weight loss (5 Kg/month). On physical examination, the patient was pale with a blood pressure of 130/70 mmHg. The admission laboratory tests revealed a Hb of 9.1 g/dL, a Hct of 30%, normal platelets and normal coagulation parameters. The stool was positive for blood, but there is no bleeding focus in esophagogastroduodenoscopy, and colonoscopy. A CT scan was performed for further evaluation, and it showed a mass in the lumen of the jejunum with subtle contrast enhancement. Minimal bowel dilation was also seen proximal to the jejunal mass (). Enteroclysis revealed a short segment of jejunal stricture with central ulceration (). The angiogram did not show any extravasation or staining. Segmental resection of the jejunum was then done. There was a jejunal mass with stricture and adhesion, and the surgical pathology revealed a large caliber persistent submucosal artery protruding through a mucosal defect ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.0, 'kg']}",20,19,21,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.0 kg. Hence, the patient's maintenance fluid is 5.0 kg * 4 mL/kg/hr = 20.0 mL/hr.
Hence, the patient's fluid maintenance is 20.0 mL/hr."
4573,22,Maintenance Fluids Calculations,physical,decimal,pmc-2876934-2,Extracted,"The second patient was an 83-year-old, 76 kg man with a past medical history of hypertension treated with lisinopril and hydrochlorothiazide and a distant history of tobacco use. During an evaluation for headaches, an MRI revealed an aneurysm of the left internal carotid artery (LICA) in the supraclinoid territory. There was no history of previous CVA or SAH. The morning of surgery, the patient's BP was 134/51 mmHg and the HR was 71 beats/minute. The patient had not taken his routine antihypertensive medications the morning of surgery. The treatment plan was for coiling of LICA aneurysm in the interventional radiology suite under general anesthesia. Preoperatively, an 18 gauge IV cannula and premedication provided by intravenous midazolam (2 mg). An arterial cannula was placed in the right radial arterial. The patient was transported to the interventional radiology suite and positioned to comfort. Standard ASA monitors were applied and the patient was pre-oxygenated with 100% oxygen. Anesthesia was induced with lidocaine (100 mg), fentanyl (100 μg), and propofol (total dose of 80 mg). Neuromuscular blockade was provided by vecuronium (10 mg). Immediately after endotracheal intubation, the BP was 105/70 mmHg with a HR of 60 beats/minute. Anesthesia was maintained with desflurane (expired concentration 4-6%) and 100 mg of fentanyl. The procedure lasted approximately one hour and twenty minutes. The vital signs remained within 20% of baseline throughout the procedure. Secondary to the anatomy of the aneurysm, coiling could not be accomplished. The patient's trachea was extubated during spontaneous ventilation with an expired concentration of 1 MAC of desflurane. Following tracheal extubation, the desflurane was discontinued. The SBP increased to 150-170 mmHg with a heart rate of 80-90 beats/minute. A clevidipine infusion was started at 2 mg/hour. Within 5-7 minutes, the sBP decreased to the 110-120 mmHg with an increase in the HR to 90-94 beats/minute. The patient was transferred to PACU with the clevidipine infusion at 2 mg/hr. The infusion was weaned over the next 30 minutes in 1 mg/hr increments in the PACU. He remained stable with the sBP ranging from 110-120 mmHg. The patient was discharged home the next day without complications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [76.0, 'kg']}",116,110.2,121.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 76.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (76.0 kg - 20 kg) = 116.0 mL/hr.
Hence, the patient's fluid maintenance is 116.0 mL/hr."
4574,22,Maintenance Fluids Calculations,physical,decimal,pmc-4531775-1,Extracted,"A 56-year-old woman was referred to our hospital with complaints of chronic diarrhea, weight loss, indigestion and abdominal pain lasting for 11 months. Before admission, the patient visited a private clinic and underwent gastroscopic and colonoscopic examinations. Gastroscopic examination showed small gastric ulcerations on the antrum and colonoscopic examination showed multiple punched-out ulcerations and erosions on the entire colon, including the sigmoid colon to the terminal ileum. Biopsy results were not diagnostic at that time. Under the clinical impression of intestinal tuberculosis, she received 2 months of antituberculosis medication without improvement of symptoms. The follow-up biopsy result of colonoscopic examination showed intestinal lymphoma of T-cell type. The patient was then referred for further evaluation. On admission, the patient looked pale, emaciated and dehydrated. An eleven kg weight loss was noted during the last 6 months (47kg--> 36kg). She denied fever or night sweating except complained of profuse watery diarrhea (5–6/day) and indigestion. She denied aggravation of diarrhea symptoms after wheat ingestion. No improvement of diarrhea was found by withdrawal of wheat intake. There was no palpable lymphadenopathy or hepatosplenomegaly. Diffuse abdominal tenderness on the whole abdomen was noted on abdominal physical examination. Initial laboratory findings were as follows: WBC 8,300/mm3, Hb 10.7 g/dL, Hct 32.6%, platelet 409,000/mm3, urine analysis was normal, stool occult blood was negative, serum total protein 5.2 mg/dL, albumin 2.3 mg/dL, serum LDH 128 IU, calcium 7.9 mg/dL, phosphorous 4.4 mg/dL, ALT/AST 12/13 U, cholesterol 101 mg/dL, BUN 13 mg/dL and creatinine 1.0 mg/dL. Chest X-ray was normal. Gastroscopic examination showed diffuse irregular nodular and depressed lesions on the angle and the lower body and multiple red spots on the antrum, suggesting erosive gastritis. But esophagus and stomach biopsies showed diffuse infiltration of lymphoma cells with epitheliotropic features (, ). Duodenal biopsy also revealed lymphoma cell infiltration, and villous atrophy and blunting were found. Colonoscopic findings were the same as noted previously () and the biopsy showed diffuse infiltration of small to medium-sized lymphoma cells (). The infiltrated lymphoma cells were immunostained for UCHL-1 (+), CD 3 (+), MT-1 (+), L-26 (−) and MB-2 (−) (Figure 1.2.4). Small bowel series also showed chronic granulomatous lesions on the cecum and the distal ileum. Abdominal CT scan revealed diffuse wall thickening of the bowels, including the esophagus, the stomach and parts of the small bowel and colonic loop. There was no evidence of involvement of lymphoma on bilateral bone marrow biopsies. Finally, the patient was diagnosed as primary intestinal T-cell lymphoma involving the entire gastrointestinal tract (Ann Arbor Stage IVB) with malabsorption. She was treated with combination chemotherapy including cyclophosphamide, adriamycin, vincristine and prednisone (CHOP). Although after two cycles of chemotherapy the initially observed bowel wall thickening disappeared on follow-up abdominal CT scan and no definitive nodular or ulcerative lesions were noted, on follow-up gastro-and colonoscopic examinations lymphoma cells remained on the biopsy. Despite further treatment with 4 cycles of systemic chemotherapy, only a partial response was achieved.
The patient was readmitted to our hospital with complaints of hematochezia. Colonoscopic examination showed internal hemorrhoid and diffuse hyperemic mucosa and multiple ulcerations were noted throughout the rectum to cecal area, suggesting relapse of lymphoma. After two cycles of salvage chemotherapy with etoposide, dexamethasone, adriamycin and cisplatin (EDAP), the bowel lesions were slightly improved but lymphoma cells were still found, indicating refractory to chemotherapeutic agents, agten then, the patient was treated without a specific treatment except supportive care. Eventually, the patient died of spontaneous bowel perforation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [36.0, 'kg']}",76,72.2,79.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 36.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (36.0 kg - 20 kg) = 76.0 mL/hr.
Hence, the patient's fluid maintenance is 76.0 mL/hr."
4575,22,Maintenance Fluids Calculations,physical,decimal,pmc-8049380-1,Extracted,"An 81-year-old female weighing 67kg with a past medical history of hypertension, hyperlipidemia, hypothyroidism, COPD and 40 pack-years of smoking, presented to the emergency room with shortness of breath. She was found to have Covid-19 pneumonia and admitted for management of hypoxic respiratory failure. Biomarkers upon admission included a ferritin of 1,462 ng/mL (reference range 12-150), creatine kinase of 114 U/L (reference range 30-135), procalcitonin of 0.56 ug/L (reference range <0.5), D-dimer of 21 mcg/mL (reference range <0.4), and C-reactive protein of 63 mg/L (reference range 0.3-10). Her platelet count (reference range 150-400 × 10(3)/mcL) and hemoglobin (Hgb) (reference range 11.5-17.3 g/dL) were within normal limits and her creatinine clearance was 29 mL/min (reference range >60). As per hospital Covid-19 protocol, she was started on an elevated prophylactic dose of 40mg of Lovenox twice daily (BID). She took Aspirin 81 mg daily at home and was started on Aspirin 325 mg in the hospital. Her respiratory status was initially stable on nasal cannula oxygen.
On hospital day 5 she experienced hypoxia which resulted in her transfer to the medical intensive care unit. The patient's Lovenox dose was empirically increased to 60 mg BID out of concern for pulmonary embolism (PE). Subsequent CT angiography (CTA) of the chest was negative for PE, with incidental findings of a small amount of fluid in the LUQ of unclear etiology (seen only on the very last slice of the CTA). Later that day, the patient became obtunded, pale, and hypotensive. She was intubated for airway protection, and developed shock requiring vasopressors. Arterial blood gas demonstrated profound acidosis and Hgb of 3.7 g/dL. This was a large drop from Hgb of 11.5 g/dL just 20 hours prior. Her lactic acid was 19.0 mmol/L (reference range 0.4-2.0). Physical exam, including nasogastric lavage, showed no obvious source of bleeding. Her abdomen was soft, nontender, nondistended. After transfusion of 2 units of packed red blood cells (pRBCs), her Hgb improved to 8.5 g/dL. However, the patient continued to require pressor support and transfusion of additional blood products. All anticoagulants and antiplatelet agents were stopped.
On day 6 she further destabilized and required greater volume of blood products. The patient developed multi-organ failure secondary to profound hypoperfusion evidenced by derangements on complete metabolic panel and worsening coagulopathy. Non-contrast CT performed late that night demonstrated a large left retroperitoneal hematoma measuring up to 25cm in greatest diameter. CTA performed in the early morning hours of hospital day 7 demonstrated active extravasation of contrast into the expanding left retroperitoneal hematoma, now measuring up to 31cm (). That morning she was then taken to interventional radiology and had technically successful embolization of multiple bleeding lumbar arteries ( and ). She was briefly stabilized during the day, but that night experienced another large drop in Hgb from 11.5 g/dL to 5.0 g/dL and died in the early hours of hospital day 8.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [67.0, 'kg']}",107,101.65,112.35,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 67.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (67.0 kg - 20 kg) = 107.0 mL/hr.
Hence, the patient's fluid maintenance is 107.0 mL/hr."
4576,22,Maintenance Fluids Calculations,physical,decimal,pmc-4982779-1,Extracted,"A 75-year-old man sought the medical facility complaining of diffuse abdominal pain, abdominal distension, postprandial fullness, hypersalivation, nausea, and frequent vomiting over the last 6 months. He referred some relief of symptoms with the use of a proton pump inhibitor and lost 10 kg of weight during this period. He was diagnosed with hemorrhoids 2 months ago and has been presenting episodes of hematochezia since then. He denied hematemesis and dysphagia. His relatives referred an altered sleep–wake cycle and periods of fluctuating levels of consciousness over the past few days. His medical history included dyslipidemia, and a recent diagnosis of chronic liver disease of undetermined etiology. He was taking furosemide, cholestyramine, chlortalidone, and pantoprazole. He was a smoker (60 packs/year) and a social drinker. He came from an endemic region of schistosomiasis and his wife recently had been diagnosed with the intestinal form of this disease.
The physical examination revealed an ill-looking patient, icteric, and dehydrated. He was afebrile, his blood pressure was 80/60 mmHg, his pulse was a regular 72 beats per minute, and his room air oximetry was 97%. He was lucid and oriented in time and space, and the Glasgow Coma Scale was 15. The neurologic examination was normal. He had a jugular venous distension at 45 degrees, and lower limbs edema was present. The pulmonary examination disclosed bilateral diffuse crackles and hypophonesis of the heart sounds. The abdomen was distended; the liver was palpable until 7 cm below the xiphoid appendix (left liver lobe enlargement); and large ascites was present. The laboratory work-up is shown in .
Other examinations included: ANA – HEp-2 = 1/320, nucleolar pattern, normal determination of complement fractions C3 and C4. Urinalysis showed proteinuria, 37,000 erythrocytes/ mm3, hyaline, and granular casts, and 24-hour urine protein was 7 g. Hepatitis B and C, and HIV serologies were negative. The anti-mitochondria antibody was negative, and ceruloplasmin and copper determinations were within the normal range. The rectum biopsy was negative for Schistosoma sp eggs. The monoclonal component was identified in the serum protein electrophoresis as a lambda chain by immunofixation.
The abdominal ultrasound (US) showed an enlarged liver with a globular shape, and nonspecific heterogeneous echotexture of the parenchyma. The biliary system, pancreas, and kidneys were normal. A huge amount of free ascitic fluid and bilateral pleural effusion were present. The hepatic Doppler US showed a normal gauge of the hepatic veins with multiphasic hepatofugal blood flow. The portal and superior mesenteric veins were enlarged with reduced velocity hepatopetal blood flow. The upper digestive endoscopy disclosed small and medium caliber esophageal varices, hypertensive gastritis, and a healing duodenal ulcer. The abdominal computed tomography showed an enlarged liver at the expense of the left and caudate lobes, plus splenomegaly, and ascites. Doppler echocardiography showed a mild double aortic lesion (mean systolic left ventricular/aortic gradient of 9 mmHg), mild diastolic left ventricular dysfunction, and preserved systolic function. Renal biopsy was not performed due to the patient's critical clinical status. A diagnostic paracentesis was undertaken and the results were consistent with portal hypertension (serum-ascites albumin gradient = 2.37 g/dL) and a high number of neutrophils consistent with the diagnosis of spontaneous bacterial peritonitis, which was treated with the administration of albumin and ceftriaxone. The patient's condition evolved with persistent altered mental status, and after 2 weeks of hospitalization he suddenly presented thoracic pain with no ischemic electrocardiogram changes nor elevation in myocardial necrosis markers. Two days after this complaint he presented cardiac arrest and died. An autopsy was performed.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [65.0, 'kg']}",105,99.75,110.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 65.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (65.0 kg - 20 kg) = 105.0 mL/hr.
Hence, the patient's fluid maintenance is 105.0 mL/hr."
4577,22,Maintenance Fluids Calculations,physical,decimal,pmc-7370336-1,Extracted,"A 48-year-old woman, Jehovah’s Witness, presents to the outpatient of pulmonology service, with 8-year history of chronic cough and dyspnea, along with a progressive deterioration of her functional class (NYHA IV), along with permanent requirement of oxygen therapy and decline in the quality of life. Computed tomography scan of the chest revealed interstitial lung disease (see and ). Rheumatoid factor was positive and anticardiolipin antibodies were in indeterminate range; rest of autoimmune profile was negative. The patient did not present with clinical features of autoimmune disease. A diagnosis of autoimmune featured interstitial lung disease was made; cyclophosphamide cycle was administered without improvement of symptoms. Lung biopsy was taken via video-assisted pulmonary wedge resection, under general anesthesia. Pathology showed a histologic pattern consistent with usual interstitial pneumonia. Due to failure of medical therapy, the patient was accepted as a transplant candidate. However, due to religious beliefs, the patient stated that she does not accept blood products. Pulmonary function tests revealed a forced vital capacity (FCV) of 1.33 (44%), a forced expiratory volume in one second (FEV1) of 1.10 (44%), FEV1/FVC ratio of 83%, partial pressure of oxygen (PO2) of 91.3 mmHg and partial pressure of carbon dioxide (PCO2) of 55.1 mmHg, diffusing capacity for carbon monoxide (DLCO) 8.1 mL/mmHg/min (31%), 6-minute walk distance of 422 meters (73%), and a minimal oxygen saturation of 76 % without oxygen therapy.
Several months later, and after meticulous case review held by the lung transplant board (anesthesia, thoracic surgery, pulmonology), abdominal organ transplant board, and ethics committee, the patient was admitted for single-lung transplantation. She signed an informed consent declining transfusion of blood components, however agreeing to continuous cell-saver use. In the case of major perioperative bleeding, the patient also accepted the use of a prothrombin complex concentrate (which has advantages over fresh frozen plasma as it allows rapid correction of coagulation factor deficits with less volume infusion) and desmopressin. Blood loss during surgery was planned to be restored with 5% lactalbumin, in order to reduce the use of crystalloids in the event of significant bleeding.
The patient’s anthropometrics were 71 kg weight and 160 cm height. Regarding general procedure information, length of the procedure was 135 minutes. Cold Ischemia time was 230 minutes; there was no need for ECMO support. Bleeding during the procedure was estimated at 300 mL. Pulmonary artery pressure (PAP) was continuously measured, achieving a mean PAP of 18 mmHg in average during surgery.
Regarding hemostatic perioperative management for this patient, recommendations established in the current literature within the “Patient Blood Management” at the time were taken into account. Since preoperative hemoglobin was within normal values (14.6 g/dL), no additional measures were taken to optimize erythropoiesis. To minimize bleeding in the intraoperative setting, blood preservation methods were used: prophylactic use of antifibrinolytics was planned preoperatively, using an initial bolus of tranexamic acid 1 g, followed by continuous infusion during surgery. Fluids were adjusted at 2 to 4 cc/kg/h and readjusted according to intraoperative hemodynamic and metabolic variables. Insensible fluid loss was restored infusing a total of 870 cc of Ringer’s lactate. Normothermia was maintained with the use of Blanketrol heating system, and electrocautery scalpels were used to obtain a thorough surgical hemostasis with the help of topical hemostatic agents (tissue sealant/Surgicel). The patient agreed to intraoperative closed-system cell salvage, as it did not represent a conflict with her religious beliefs. Bleeding during surgery was calculated as of 300 cc, from which 120 cc were reinfused postoperatively. Finally, during the postoperative period, a drainage thoracostomy was positioned for a better quantification of postoperative bleeding and adequate blood evacuation from the lung. Erythropoietin was initiated during hospitalization.
After surgery, the patient was admitted to the intensive care unit, early extubation was successfully achieved, and there was no need of vasopressors or inotropes. PaO2/FiO2 ratio of 480 mmHg. Chest radiography revealed right perihilar infiltrates. The previous findings suggested a primary graft dysfunction grade 1 (see and ). Intensive care unit length of stay was 4 days, and total hospitalization length of stay was 13 days. Hemoglobin levels decreased at the end of hospitalization (see ). The patient was discharged without further complications with hemoglobin levels of 10.6 g/dL, which was treated in the outpatient setting with subcutaneous erythropoietin 2000 IU 3 times per week as ordered by internal medicine and pulmonology physicians. Hemoglobin levels increased to 11.4 g/dL at 1-week follow-up.
Pulmonary function tests after LT revealed FVC of 1.88 (53%), FEV1 of 1.73 (59%), FEV1/FVC of 92%, 6-minute walk distance of 353 meters (67%), and a minimal oxygen saturation of 94% without oxygen therapy. The patient final hemoglobin level was 11.4 g/dL.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [71.0, 'kg']}",111,105.45,116.55,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 71.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (71.0 kg - 20 kg) = 111.0 mL/hr.
Hence, the patient's fluid maintenance is 111.0 mL/hr."
4578,22,Maintenance Fluids Calculations,physical,decimal,pmc-7001364-1,Extracted,"A set of female twin neonates was seen at the clinic as 19-day-old term babies delivered in primary health center. They had bilateral ear piercing without adherence to asepsis on the 9th day of life. No extreme pressure was applied to the ear during or after the procedure. The procedure was uneventful until 4 days after the procedure when the lobules were noticed to have swollen and darkened. There was no discharge from the wound, fever or refusal of feeds. There was no known history of atopy in the older siblings.
The mother removed the earrings on the fourth day after the ear piercing and noticed rims of demarcated dark tissues. Subsequently, the ears of the first twin developed abnormally large buttonholes instead of the earring pinhole. The second twin had some degree of distortion which necessitated presentation to a tertiary hospital.
Babies were delivered at 38 weeks of gestation without any preceding history of premature rupture of membrane or vaginal discharge in the mother. Babies were on exclusive breastfeeding. Examination revealed a 2.7 kg first twin (T1) with a temperature of 37.5 °C, pulse rate of 118 pm and respiratory rate of 56 cpm. The right ear showed a buttonhole ulcer about 0.5 cm in the widest dimension with inflamed surrounding skin. The left ear showed a smaller buttonhole ulcer measuring 0.4 cm in the widest dimension (Fig. ).
The second twin (T2) weighed 3.7 kg with a temperature of 37.5 °C, pulse rate of 120 pulsations per minute and respiratory rate of 60 cpm. The right ear showed a 2cmx0.2 cm ulcer along the rim of the lobule with a necrotic bed and inflamed surrounding skin. The left ear had an ulcer measuring about 3cmx2cmx1cm affecting whole thickness of the lobule. The edge was undermined and the surrounding skin inflamed (Fig. ).
A diagnosis of necrotizing soft tissue infection of both ears was made for each twin. They were admitted, wound swab and tissue specimen were sent for microscopy, culture and sensitivity (MCS) and histology respectively for the both twin. Erythromycin and metronidazole syrups were commenced empirically while awaiting sensitivity results. Wound care was provided by dressing wound with 5% povidone-iodine ointment.
T1 wound swab MCS showed growth of Staphylococcus aureus sensitive to erythromycin and ceftazidime but resistant to vancomycin and ampicillin, amoxicillin, and augmentin. T2 wound swab MCS yielded Saureus and Pseudomonas aeruginosa which were sensitive to ceftazidime, levofloxacin, augmentin but resistant to erythromycin.
After 2 days on admission, the parents declined further inpatient treatment on financial grounds and returned home on oral drugs. However, on telephone follow-up, the wounds were noted to have healed well and the twins remained healthy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.7, 'kg']}",10.8,10.26,11.34,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.7 kg. Hence, the patient's maintenance fluid is 2.7 kg * 4 mL/kg/hr = 10.8 mL/hr.
Hence, the patient's fluid maintenance is 10.8 mL/hr."
4579,22,Maintenance Fluids Calculations,physical,decimal,pmc-5698679-1,Extracted,"A 22-month-old girl diagnosed with Sandhoff disease was referred to our hospital with chief complaints of spasticity and swallowing difficulty as well as difficulty with head control. She was born at full term through normal vaginal delivery. She was able to stand while holding on to something at 8 months of age, which suggested normal development. However, developmental arrest occurred at 13 months of age. Spasticity and genu recurvatum were observed while standing and holding on to something. The patient showed a progressive motor regression pattern, and at 18 months of age, she could barely maintain a propped sitting position. At 20 months of age, she showed symptoms of aspiration while swallowing and prolonged feeding time.
Brain magnetic resonance imaging scans obtained at 15 months of age did not show delayed myelination or abnormal enhancement (). Developmental regression was similar to that in GM2 gangliosidosis, such as Tay-Sachs disease and Sandhoff disease. The patient underwent hexosaminidase assay in white blood cells, which showed increased hexosaminidase A (%) and decreased total hexosaminidase. The total hexosaminidase A & B and hexosaminidase A levels were 321.2 nmol/hr/mg (reference range, 620–1,000 nmol/hr/mg) and 74.3% (reference range, 55%–72%), respectively. Based on these findings, the patient was diagnosed with Sandhoff disease. However, the patient did not show cherry red spot on fundoscopy.
At the time of admission, physical examination revealed grade 3 and 2 muscle strength in the upper and lower extremities, respectively. Neurological examination showed sustained ankle clonus and increased deep tendon reflexes in all extremities as well as hypertonicity and decerebrate posture manifested by an exaggerated extensor posture of all extremities, while crying and/or when she was irritable (). In terms of spasticity, her four extremities scored grade 2 based on the modified Ashworth scale (MAS).
Overall, the patient had developmental regression. Especially, she showed a delay in development by 1 month in gross-motor domain, by 3 months in language and fine motor domain, and by 2 months in personal-social interaction domain in the Denver Developmental Screening Test II.
Dietary assessment revealed that the patient irregularly ingested a soft and blended diet of 70–130 kcal, five times a day, and the mean eating duration was approximately 1 hour. She had difficulty in eating and she showed signs of aspiration (e.g., coughing, gagging). Moreover, she had a poor feeding posture with inadequate trunk and head support.
Oral motor function assessment showed that the patient had increased tone and decreased movement of the tongue and hypersensitivity in the oral and perioral areas. The patient underwent videofluoroscopic swallowing study (VFSS), and was given barium-containing free water, yogurt (thick liquid), and rice porridge (soft). In the oral phase, motor control, including lip sealing, tongue control, and mastication, was inadequate with delayed oral transit time (1.3 seconds) and premature bolus loss []. In the pharyngeal phase, a delayed swallow reflex was observed without aspiration or penetration during or after swallowing ().
The patient's height and body weight were 85.0 cm and 11.6 kg, respectively. Her weight-for-height Z-score (−0.3) was in the 15th–50th percentile of the World Health Organization (WHO) growth standards []. Nutritional evaluation showed that the patient needed a regular daily intake of 989 kcal. However, she could only consume 700 kcal/day, which was less than the required caloric intake. The patient was given supplementary balanced nutrition twice a day.
The patient received an intensive dysphagia rehabilitation program for 30 minutes a day, five times a week, for 6 weeks, and it comprised both direct and indirect interventions, such as oromotor facilitation, thermo-tactile stimulation, and lip strengthening, and compensatory techniques, such as postural modification and alteration of the feeding utensil to facilitate swallowing []. She was given anti-spasticity drugs for managing spasticity and achieving a stable posture during feeding. After the treatment, she was fed in a semi-reclined position, which reduced the signs of aspiration and the amount of food or liquid leakage from the mouth.
However, her nutritional status showed no improvement, with her daily calorie intake decreasing to 600 kcal/day after 4 weeks of admission. At 6 weeks postadmission, her total intake further decreased to 392 kcal/day. Her body weight continuously declined from 11.6 kg to 10.5 kg, and her weight-for-height Z-score (−1.6) decreased to the 3rd–15th percentile of the WHO growth standards, which was a sharp decrease of one major percentile line in a short period [].
Gastrostomy was therefore recommended, but her parents refused the procedure. She was then referred to another hospital for treatment of deconditioning due to dehydration, and she received gastrostomy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [11.6, 'kg']}",43.2,41.04,45.36,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 11.6 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (11.6 kg - 10 kg) = 43.2 mL/hr.
Hence, the patient's fluid maintenance is 43.2 mL/hr."
4580,22,Maintenance Fluids Calculations,physical,decimal,pmc-6215987-1,Extracted,"A 32-year-old homosexual man, infected with human immunodeficiency virus (HIV) in 2005, was admitted in May 2015 for suspected acute prosthetic left knee infection. He had a history of left femoral osteosarcoma in 1996, treated with chemotherapy and resection surgery. Moderate chronic renal insufficiency developed after chemotherapy (creatinine clearance 60 ml/min). A knee megaprosthesis, implanted in 1997, was exchanged in 2006 because of loosening.
In May 2015, he developed acute left knee inflammatory pain, swelling, functional impairment and high fever (40°C), and was hospitalized. No source of infection was found on clinical examination. Blood tests revealed no hyperleukocytosis but elevated C-reactive protein (CRP; 169 mg/liter). Knee aspiration revealed a turbid joint fluid containing 5500 leukocytes/mm3, with a differential of 75% neutrophils. Joint fluid and blood cultures remained sterile. X-ray of the knee showed no signs of osteitis but radiolucency under the internal tibial plateau was seen. CD4-lymphocyte count was 370/mm3 and HIV load was 4.4 log10/ml. Empirical intravenous (IV) vancomycin, ceftriaxone and rifampicin were prescribed. Surgery with debridement and implant retention (DAIR) without exchange of mobile parts was performed 2 days after admission. A broad-range polymerase chain reaction (16S rRNA) on joint fluid was performed with the universal primers E8F (5-AGAGTTTGATCMTGGCTAG-3) and 357R (5-TGCTGCCTCCCGTAGGAGT-3) using a sample-specific multiplex identifier for pyrosequencing that confirmed infection with Helicobacter cinaedi
. After one week of IV therapy (vancomycin, ceftriaxone, rifampin), treatment was switched for oral doxycycline and clindamycin for 3 months with a favorable outcome. Antiretroviral therapy with abacavir, lamivudine, dolutegravir was begun in May 2015. In April 2017, his CD4 count was 1200/mm3 and HIV load undetectable. The patient remained asymptomatic for 2 years, CRP was normal.
Two years later, on 1st of May 2017, he again suddenly developed similar symptoms (pain, swelling, functional impairment, high fever) in his left knee. CRP was 200 mg/liter. He was admitted in our unit where knee aspiration showed 13,500 leukocytes/mm3, with a differential of 93% neutrophils. Prolonged culture in enriched medium remained sterile, as did blood cultures. X-rays of the left lower limb showed evident osteolysis under the internal and external tibial plateau but no sign of chronic osteitis (no periosteal bone construction or endosteal osteolysis). The patient underwent a second DAIR without exchange of mobile parts, because of the acute onset, sterile joint-fluid cultures and the difficult-to-change arthroplasty. He received continuous intravenous meropenem (6 g/24 hours for a 55-kg patient) for 2 weeks, followed by an oral regimen with minocycline (300 mg/day) for 10 more weeks. Finally, PCR on joint fluid was positive for Helicobacter DNA and sequencing of the gyrA gene (F2-QRDR-Hspe TGGGTGATGTRATYGGTAAAT R1-QRDR-Hspe TGATTAAGCCCTCYAARATATG 939 bp) confirmed the presence of H. cinaedi. The patient had owned a cat for many years. Cultures of the patient's and the cat's feces, did not grow H. cinaedi. In July 2018, more than one year after the second episode, the patient is doing well, he walks more than one kilometer without a stick.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [55.0, 'kg']}",95,90.25,99.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 55.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (55.0 kg - 20 kg) = 95.0 mL/hr.
Hence, the patient's fluid maintenance is 95.0 mL/hr."
4581,22,Maintenance Fluids Calculations,physical,decimal,pmc-6579323-1,Extracted,"A three-year-old male child was admitted to the pediatric ward of Dr. Ruth KM Pfau, Civil Hospital Karachi (CHK) with a one-year history of generalized weakness, loose motions, decreased appetite and intermittent fever not associated with rigors, chills or night sweats, an eight-month history of inability to walk and sit, polydipsia, polyurea, abdominal distention and loss of neck holding for 14 days. He had a previous history of hospitalization six months ago due to the same complaints. The patient was accompanied by his mother. He weighed 6 kg, is the 7th born child to his parents and was delivered at term to a 37-year-old G7P7 mother via normal vaginal delivery. The mother did not report any complications or illnesses during pregnancy. He cried immediately after birth, and there were no complications during or after birth. There is no consanguinity between mother and father. The child was vaccinated but was malnourished, with an unremarkable family history.
The patient also developed diarrhea which was bulky in consistency, green in color with seven episodes per day after every meal intake. Diarrhea was associated with abdominal distention and vomiting. The mother then started giving him a combination of trimethoprim-sulfamethoxazole, after which diarrhea subsided. The child developed neck holding at four years of age, he started sitting at eight months and started walking with support at 12 months of age. The child was first breastfed within three hours of delivery and was exclusively breastfed up to six months. Complimentary feeding was started after six months with pulses, mashed potatoes, porridge and chicken. Breastfeeding was continued up to two years. Currently, the child takes 1-2 feeds per day. The personal history revealed that the patient was sleeping normally, but the appetite was decreased. The mother also noticed a weight loss, altered bowel habits, and micturition was normal.
On examination (O/E), the patient was lying on the bed irritated, severely wasted and emaciated with visible bony deformities. Initial vitals included blood pressure (BP) 110/70 mmHg, a regular pulse of 90 beats/min, a respiratory rate of 20 breaths/min, and a low-grade fever of 100° F. The patient was anemic and dehydrated, while, there was no presence of edema, clubbing, cyanosis, and lymphadenopathy. On further examination, parietal and frontal bossing, rachitic rosary (Figure ), widening of wrists and knock knees (it's a valgus deformity in which legs curve inwards so that the feet are apart when the knees are touching) were found as well. On abdominal examination, it was soft, non-tender, distended with mild tenderness on both flank regions, with a centrally placed umbilicus. The liver was palpable three fingers below the right costal margin. Gut sounds were audible 3-4 sounds/min. All other systems were unremarkable.
The anthropometric measures of the child are as follows: weight = 6.5 kg, occipitofrontal circumference = 49.5 cm, height = 72.5 cm, mid-upper arm circumference = 8 cm, upper segment = 45 cm, lower segment = 27.5 cm, weight for height = 6.5/9 *100 = 72.2 (moderately low) and height for age = 72.5/94.6*100 = 76.6 (severely low).
On investigations performed, complete blood count (CBC) showed a hemoglobin (Hb) of 5.4 gm/dl, mean corpuscular volume (MCV) of 82 fl and a platelet count of 187,000/mL. The total leukocyte count (TLC) was 10.6 x 109/L, including 39% neutrophils and 48% lymphocytes. His inflammatory markers were raised with a C-reactive protein (CRP) of 23 mg/L [Normal (N) = 3] and an elevated erythrocyte sedimentation rate (ESR) of 115 mm/hr (N = 0-22) for men and (N = 0-29) for women. The clotting profile showed an international normalized ratio (INR) of 1.01, while prothrombin time (PT) was 10.6 seconds.
The urea creatinine electrolytes (UCE) were within normal range except decreased potassium levels of 2.8 mEq/L. The levels of calcium, magnesium and phosphate in blood were 15.1, 1.9 and 4 mg/dL, respectively. The blood culture showed a growth of Burkholderia species. The urinalysis showed a pH of 5.0, specific gravity of 1.025, with the presence of protein and blood. Additionally, numerous red cells were seen along with yeast and 4-6 pus cells per high power field (HPF). The urine culture showed growth of Candida species. The stool analysis showed that the stool was hard, acidic, brown in color with 1-2 pus cells per HPF. His vitamin D levels came out to be 54.29 ng/mL, and parathyroid levels were 8.36 pg/ml. Liver function tests showed a total bilirubin of 0.28 mg/dL, direct bilirubin of 0.21 mg/dL and levels of alkaline phosphate alanine aminotransferase were 368 and 3 units per liter, respectively.
The X-rays of the chest (Figure ), skull (Figure ) and femur (Figure ) are attached below. Additionally, ultrasound of kidney ureters and bladder (KUB) showed an incidental finding of bilateral renal calculi (right kidney at lower pole measuring 0.7 cm, in the left kidney at mid pole measuring 0.7 cm), along with bilateral grade 2 renal parenchymal changes. The urinary bladder was normal in thickness with no presence of focal mass, calculus or diverticulum.
Considering the diagnosis of OI, an ophthalmology review was done to look for lens dislocation and blue sclera, but neither was present in both eyes. However, the left eye showed a corneal thinning nasally, temporally and inferiorly.
During the hospital stay, the patient was intravenously given cefotaxime 220 mg, piperacillin-tazobactam 700 mg, and meropenem three times a day. Additionally, linezolid 70 mg was injected every eight hours, along with injections of bisphosphonate 7 mg for three days, amikacin 55 mg twice a day for 14 days and fluconazole 85 mg loading dose, 45 mg once a day for 10 days. The patient was also given a teaspoon of the combination (artemether and lumefantrine) once a day. Three pints of red blood cells were transfused as well, after which his Hb became 10.6 mg/dL. During the stay, the child had a prolonged course of fever with pancytopenia, which improved on injections of meropenem, amikacin, and fluconazole.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.0, 'kg']}",24,22.8,25.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.0 kg. Hence, the patient's maintenance fluid is 6.0 kg * 4 mL/kg/hr = 24.0 mL/hr.
Hence, the patient's fluid maintenance is 24.0 mL/hr."
4582,22,Maintenance Fluids Calculations,physical,decimal,pmc-8238612-1,Extracted,"We discuss the case of a 44.5 kg, 8-year-old female with no significant past medical history who presented with abdominal pain and distension accompanied by nausea and vomiting. An ultrasound revealed a mixed solid and cystic 17 × 9 cm mass in the right liver lobe with compression of the IVC (see ). In light of worsening abdominal distention with concern for abdominal compartment syndrome, biopsy and drain placement of the mass was performed on hospital day 7. Over the next several days, persistent sanguineous drain output and resultant anemia were concerning for hemorrhage. CT revealed an infrarenal IVC thrombus (see ) and near-occlusive embolus distal to the left pulmonary artery. TTE was obtained revealing compression of the distal IVC at the right atrial junction with normal biventricular function and no evidence of elevated right heart pressures. Although heparin was initiated, there was significant difficulty in maintaining therapeutic anticoagulation in light of the underlying hemorrhagic liver mass as well as coagulopathy in the setting of synthetic liver dysfunction.
On hospital day 15, the patient underwent right hepatectomy with caudate lobe resection. In light of the patient's coagulopathy, IVC thrombus, pulmonary embolus (PE), and the anticipated use of intraoperative TEE, a pediatric cardiac anesthesiologist was requested. In addition, extracorporeal membrane oxygenation, a perfusionist, and the cardiac surgical team were also on standby. Blood products were placed on hold, and a rapid transfusion device was readied in the OR. The patient arrived to the OR with a double lumen PICC and two 20-gauge PIVs in situ. After preoxygenation, rapid sequence induction of anesthesia was performed with propofol 100 mg, ketamine 20 mg, fentanyl 100mcg, and rocuronium 60 mg. She was intubated without difficulty using a Mac 2 laryngoscope and 5.5 endotracheal tube. Anesthesia was maintained with sevoflurane at 1.4–1.8% with intermittent opioid boluses.
Subsequently, further invasive access was achieved with 6 F left internal jugular vein central line, 2.5 F left radial arterial line, and 16-gauge peripheral IV. In addition to standard ASA monitors, invasive arterial blood pressure and central venous pressure were monitored throughout the case. A TEE probe was utilized to assess the patient's cardiac function intermittently. These invasive monitoring modalities were chosen in light of the risk for significant rapid blood loss as well as potential embolization of the IVC thrombus and propagation of her existing PE.
Surgical preparation was performed in a manner leaving her neck, chest, abdomen, and pelvis exposed for emergent intervention if necessary. Of note, her initial CVP was elevated to 17-18 mmHg but improved significantly to 1–3 mmHg after abdominal incision was made, likely due to the large size of the abdominal tumor and relief of pressure from abdominal ascites. In order to maintain oxygenation in light of the patient's PE, she was maintained on FiO2 of 1.0 throughout the case. Intraoperative TEE was utilized to monitor for right ventricle (RV) dysfunction and propagation or dislodgement of the IVC thrombus. In addition, the RV pressure gradient (PG) across the tricuspid valve was monitored to evaluate potential RV strain from a subsequent PE. At the initial exam, no thrombus was visualized in the RA and IVC on midesophageal (ME) bicaval view (see ).
Her intraoperative course was uncomplicated, and the patient remained hemodynamically stable throughout. Rotational thromboelastometry was sent off intraoperatively, and the patient was transfused 2 units of red blood cells and 1 unit of fresh frozen plasma. She also received 250 mL 5% albumin due to large volume ascites that was evacuated upon entrance into the abdomen. As the incision was being closed, a dexmedetomidine infusion was initiated at 1 mcg/kg/min. The patient was brought to the intensive care unit intubated and sedated on dexmedetomidine at 0.5 mcg/kg/min. She was extubated later that evening without complication. The patient was discharged on hospital day 28, with plans for initiation of a chemotherapeutic regimen.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [44.5, 'kg']}",84.5,80.275,88.725,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 44.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (44.5 kg - 20 kg) = 84.5 mL/hr.
Hence, the patient's fluid maintenance is 84.5 mL/hr."
4583,22,Maintenance Fluids Calculations,physical,decimal,pmc-4972726-1,Extracted,"A male patient aged 58 years visited our hospital because of right hip joint pain. In the past, he underwent bipolar hemiarthroplasty on the right hip due to osteonecrosis of femoral head 11 years ago and total hip arthroplasty on left hip due to same disease 3 years ago. The patient weighted 52 kg and had BMI of 19.6 kg/m2. On plain film, there was stem loosening at right bipolar hemiarthroplasty. So, we decided to revise the right hip. In 2005, we revised with 54-mm acetabular cup (Trilogy; Zimmer, Warsaw, IN, USA) and 36-mm metal head mated against HXLPE (Longevity; Zimmer) as bearing surface. As to a femoral stem, we revised with 11 mm beaded full coating, non-cemented revision femoral stem (Versys; Zimmer). Post-operative radiograph showed a cup abduction angle of 50° and 23.4° anteversion respectively (). After 10 days since index operation, patient took a weight-bearing within the limits of tolerance, and discharged without any event. After 6 years since 1st revision, the patient visited our center complaining an abrupt right hip pain developed without recent trauma history. Radiographs demonstrated eccentric femoral head position within acetabular cup and radiopacity suggesting tines of the locking mechanism on the infero-medial side of right hip joint (). On the basis of this finding, we suspected a liner breakage. In the 2nd revision, we identified metallosis (). Also, we found a fragmentation of the Longevity liner at the superior quadrant (), severe scratch damages in just below the neck portion of femoral stem and superior quadrant area of liner. After checking stable fixation status of femoral stem, and no damages in Morse taper of femoral stem, we conducted 2nd revision with 56-mm acetabular cup (Trilogy) and 36-mm metal head mated with HXLPE (Longevity) as bearing surface remaining femoral stem. Since leaving the hospital, there have not been special events.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [52.0, 'kg']}",92,87.4,96.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 52.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (52.0 kg - 20 kg) = 92.0 mL/hr.
Hence, the patient's fluid maintenance is 92.0 mL/hr."
4584,22,Maintenance Fluids Calculations,physical,decimal,pmc-3611080-1,Extracted,"A 32-year-old, 162 cm, 68 kg, gravida 1, para 1, pregnant woman received cesarean delivery due to failure of labor progression at 33 weeks and 6 days of pregnancy. The patient was diagnosed with gestational diabetes mellitus at 27 weeks of pregnancy with insulin therapy. She had a history of gastroenteritis at 17 weeks from gestation. Dysarthria and diplopia occurred after recovery from the gastroenteritis (18 weeks from gestation) and she was admitted to the emergency room (ER) and was diagnosed with Guillain-Barré syndrome. In the ER, the patient suffered from ongoing respiratory insufficiency (decreased oxygen saturation and CO2 retention) along with mental decline. She was intubated shortly after admission, transferred to the intensive care unit (ICU) and received mechanical ventilator care (Pressure controlled ventilation with synchronized intermittent mandatory ventilation mode, pressure support 8 cmH2O, tidal volume 600 ml, frequency 12 per minute, FiO2 0.4). TPN started at 19 weeks from gestation for expecting prolonged fasting period. At 20 weeks from gestation, she eventually received tracheostomy (T-cannula I.D. 7.0) for prolonged ventilator care due to progressive respiratory muscle weakness. At 27 weeks from gestation, mechanical ventilaton was converted to home ventilation Bi-level positive airway pressure (BPAP, BiPAP®). The setting was inspiratory positive air way pressure (IPAP) 8 cmH2O, expiratory positive airway pressure (EPAP) 4 cmH2O . And gradually started intermittent BPAP during night (29 weeks from gestation). At 33 weeks from gestation patient presented dyspnea and desaturation then continous BPAP ventilation was applied again until delivery.
She underwent intravenous immunoglobulin (IVIG) therapy twice to prevent disease progression and enoxaparin therapy for the prevention of thrombosis. However, enoxaparin therapy was stopped due to the elevation of liver enzymes at 28 weeks from gestation. The patient suffered from various neurologic symptoms including binocular diplopia, dysarthria, facial diplegia and muscle weakness in upper and lower extremities (both upper and lower extremities: 3 to 4 of 5, Medical research council scale for muscle strength). The nerve conduction study showed electrophysiologic abnormalities suggesting motor-dominant polyneuropathy in bilateral upper and lower extremities. In the cerebrospinal fluid study, albumin level was 13.1 (10-30) mg/dl, and IgG 2.17 (0-8) mg/dl. Magnesium infusion started at 34 weeks from gestation for prevention of eclamptic seizure.
At 34 weeks from gestation the attending obstetrician judged that it was no longer possible to maintain the pregnancy due to further mental decline, elevation of liver enzymes, and respiratory difficulty. At first, induction of delivery was tried, but emergency cesarean section was decided to be performed with retardation of fetal heart rate. Preoperative evaluation was within normal limits, except elevation of liver enzymes (AST/ALT 372/458) and sinus tachycardia (120 beats per minute) on electrocardiogram.
Without premedication the patient was transferred from ICU to the operating room with manual ventilation via tracheostomy. Standard monitoring including electrocardiogram, pulse oxymeter and noninvasive blood pressure measurement was started. Upon arrival at the operating room, the blood pressure was 124/90 mmHg, heart rate was 118 beat per minute with pulse oxygen 98%. A bispectral index (BIS) was placed on the patient's forehead to monitor depth of anesthesia and the leads for the nerve stimulator were placed at the ulnar side of the patient's left forearm to monitor muscle relaxation. Under gentle manual assisted ventilation with 100% oxygen, approximately 500 ml of gastric juice was aspirated from the nasogastric tube. After the sterile surgical drape was confirmed, 250 mg of thiopental was injected via the intravenous line and ventilated manually with sevoflurane 1.5 vol% and oxygen. Muscle relaxation was checked with a nerve stimulator on 40mV stimulus. When the train of four (TOF) count of 4/4 was confirmed, 10 mg of rocuronium was administered and mechanical ventilation via tracheostomy was started, after the TOF count was 0/4 and BIS score was 55. Arterial catheter was placed at the patient's right radial artery with a 20 Gage angiocatheter to monitor arterial blood pressure. Anesthesia was maintained with oxygen, medical air and sevoflurane 1.5 vol% on mechanical ventilation (tidal volume: 500 ml, frequency: 12/min, FiO2: 0.5). The BIS score and TOF count were serially monitored ().
The baby (3,390 g, Apgar score; 5-7) was delivered at 8 minutes from the start of the surgery, and the placenta was extracted 2 minutes later. Oxytocin 30 IU (mixed with normal saline 100 ml) was administered intravenously slowly. Arterial blood gas analysis and blood sugar test (glucose 137 mg/dl) were performed 20 minutes after the induction of anesthesia. Arterial blood gas analysis data and other electrolyte levels were in the normal range (pO2 146.3 mmHg, pCO2 40.7 mmHg, pH 7.425 at FiO2 0.5, EtCO2 35 mmHg). Intraoperative hemodynamic changes are shown in . No additional muscle relaxant was administered during surgery. Post-surgery TOF count was 4/4 and atropine 1 mg, and neostigmine 1.5 mg was administered to reverse the muscle relaxation. Fifteen minute after administration of reverse agents, patient's spontaneous ventilation was recovered and she was sent to the ICU with assisted manual ventilation. The motor score evaluated upon ICU arrival was 3 to 4 in all extremity, similar to that of preoperative values. Total operation time was 55 minutes and anesthesia time was 75 minutes. Total infused crystalloid, colloid, estimated blood loss, and urine output were 200 ml, 500 ml, 500 ml and 100 ml, respectively.
Weaning of mechanical ventilation was tried on postoperative day (POD) 7 and successfully done on POD 25. Abrupt chest pain and respiratory difficulty with desaturation occurred on POD 32. CT angiography showed severe pulmonary thrombosis in both pulmonary arteries and deep vein thrombosis in the left lower extremity. She was diagnosed with pulmonary thromboembolism and treated with warfarin targeted at INR 2-2.5. Two months later, she was discharged and has been on outpatient department follow-up to the department of internal medicine, neurology, and rehabilitation medicine.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [68.0, 'kg']}",108,102.6,113.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 68.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (68.0 kg - 20 kg) = 108.0 mL/hr.
Hence, the patient's fluid maintenance is 108.0 mL/hr."
4585,22,Maintenance Fluids Calculations,physical,decimal,usmle-2795,Extracted,"A 15-year-old girl is brought to the physician for her annual physical examination. Breast and pubic hair development began at the age of 12 years, but menses have not yet occurred. She is 160 cm (5 ft 3 in) tall and weighs 54 kg (120 lb); BMI is 21 kg/m2. Physical examination shows normal external genitalia. Breast and pubic hair development are Tanner stage 5. A pelvic ultrasound shows normal ovaries but an absent uterus.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [54.0, 'kg']}",94,89.3,98.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 54.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (54.0 kg - 20 kg) = 94.0 mL/hr.
Hence, the patient's fluid maintenance is 94.0 mL/hr."
4586,22,Maintenance Fluids Calculations,physical,decimal,pmc-3269350-1,Extracted,"A 10-year-old Egyptian boy was referred to our institution for an evaluation of recurrent attacks of muscle cramps, paresthesia of the fingertips and perioral numbness of two months duration. Apart from drug treatment for hypercholesterolemia, he was not receiving any other medication. He was the second-born male child to consanguineous Egyptian parents, with the other sibling being normal. His prenatal history was uneventful. He was delivered at term by Caesarean delivery and cried immediately after birth. He was apparently normal until two years of age. His mental development was normal. No other family members were affected with similar complaints. His mother noticed that he was not gaining weight and had decreased scalp hair growth. On examination, his weight was 11.5 kg (below the third centile), his height was 102 cm (below the third centile) and his head circumference was 52 cm. He had prominent dilated veins present over his scalp with alopecia and frontal bossing, a beaked nose, thin lips, protruding ears, a high pitched voice, sparse hair over the eyebrows and eyelashes, micrognathia but normal dentition and his eyes appeared prominent. There were multiple patches of coarse and thickened skin, especially over the dorsum of his hands and shoulders. He appeared to have poor sexual development. The terminal ends of his fingers appeared broad and stubby and his nails were dystrophic. His limbs were thin with bilateral contracture of both knee joints. Based on his history and the clinical findings, a provisional diagnosis of progeria was made. The diagnosis was confirmed genetically by detection of mutations (G608G) in the laminin A gene (Lmna). He had no signs of rickets. His blood pressure was normal. Chvostek's and Trousseau's sign were positive. He had no hypopigmentation of his skin or oral thrush. Investigations revealed that a hemogram, liver function tests, renal function tests, his lipid profile, fasting blood sugar, sodium, potassium and magnesium levels, blood gases, a urinary aminoacidogram, thyroid function tests, an electrocardiogram, an echocardiogram, an abdominal ultrasound, an electroencephalogram and a computerized tomography scan of his brain were all normal. He had low total calcium 5.4 mg/dL (normal range, 8.5 mg/dL to 10.5 mg/dL), low ionized calcium 2.3 mg/dL (normal range, 4.5 mg/dL to 5.6 mg/dL), raised serum phosphate 7.2 mg/dL (normal range, 2.4 mgdL to 4.1 mg/dL), raised alkaline phosphatase 118 U/L (normal range, 30 U/L to 95 U/L) and low intact PTH 1.2 pg/mL (normal range, 12 pg/mL to 72 pg/mL). A radiograph of his hands and feet revealed resorption of the terminal phalanges with osteoporosis. He was started on oral calcium salt and vitamin D; his symptoms improved with the treatment and his serum calcium, urinary calcium and alkaline phosphates levels were monitored every three months to ensure adequacy of therapy and to avoid hypercalcemia.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [11.5, 'kg']}",43,40.85,45.15,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 11.5 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (11.5 kg - 10 kg) = 43.0 mL/hr.
Hence, the patient's fluid maintenance is 43.0 mL/hr."
4587,22,Maintenance Fluids Calculations,physical,decimal,pmc-3790037-1,Extracted,"A 32-year-old man (height 168 cm, weight 66 kg) was presented for a hand-assisted laparoscopic left nephrectomy for renal cell carcinoma. He has suffered from ulcerative colitis for 2 years and taken oral mesalazine daily. He was also diagnosed with diabetes mellitus 6 months ago, and his blood sugar levels have been well controlled by metformin. There was no history of allergies to food or drugs. He fasted for more than 8 hours before surgery and was given no sedative or opioid premedication.
When arriving at an operating room, the patient was monitored with an electrocardiogram, a non-invasive arterial blood pressure monitor and a pulse oximeter. Anesthesia was induced intravenously with thiopental sodium 350 mg, following preoxygenation with 100% oxygen. After confirming the loss of consciousness and self respiration, we mask-ventilate the patient with oxygen. Mask ventilation was performed without difficulty, and he did not show any signs of airway irritation including cough. Vecuronium 10 mg was given for neuromuscular block, and then fentanyl 100 µg was administered. After a few seconds after the injection of fentanyl, the patient began to cough suddenly and vigorously. Coughing has persisted for about 30 seconds until he vomited a large volume of greenish fluid around the face mask. His head was immediately turned to the left and head down tilt of the table was applied. When vomiting ceased, after suctioning of the oral cavity and oropharynx, endotracheal intubation was achieved. During this episode, the arterial oxygen saturation transiently decreased to 93%, but soon recovered to 98%. Anesthesia was maintained with sevoflurane and 50% oxygen in air. A nasogastric tube was placed, and nearly 100 ml of bile-stained gastric fluid was drained. A small amount of greenish fluid was aspirated out of the endotracheal tube. Then, the surgery started with the patient in the right lateral decubitus position. After peritoneal insufflation with carbon dioxide (CO2), the peak inspiratory pressure increased from 21 to 26 mmHg. His arterial oxygen saturation has gradually fallen from 98 to 92% since the introduction of CO2. Although no more gastric fluids or secretions were suctioned through the endotracheal tube, a coarse crackle was heard throughout the right lung field on auscultation. The patient was placed on 100% oxygen and positive end-expiratory pressure of 5 mmHg was applied. The arterial oxygen saturation rose to 95%. An arterial blood gas analysis, checked at this time on a FiO2 of 1.0 and an ETCO2 of 37, was as follows: pH 7.334, PaO2 82.2 mmHg, PaCO2 44.2 mmHg, bicarbonate 24.9 mEq/L and SaO2 95.4%. Surgery proceeded uneventfully and vital signs were stable during the operation. The total anesthetic time was 255 minutes and blood loss was estimated at 300 ml. The patient was transferred to the intensive care unit and his arterial oxygen saturation which ranged between 93 and 95% with mechanical ventilation with a FiO2 of 1.0. Chest radiography taken postoperatively has shown patchy consolidation at the right lower lung field and decreased volume of the right lung, suggestive of pulmonary aspiration and atelectasis (). Fiberoptic bronchoscopic examination revealed a large amount of bile-stained fluid and some undigested food particles around the trachea, right main bronchus and lower lobar bronchi, which was aspirated and removed. The arterial oxygen saturation increased to 99-100% thereafter. His body temperature rose to 38.6℃ and antimicrobial therapy was initiated. Suction through the endotracheal tube and chest percussions were also frequently applied. On the next day, his temperature dropped to 36.5℃ and a radiologic improvement on the chest X-ray was observed. The patient was extubated and transferred to a general ward. Supplemental oxygen was delivered via the nasal prong at a rate of 3 L/min. He did not complain of dyspnea, productive cough or purulent sputum any more. Over the ensuing five days, mild cough and sputum left over were relieved, the arterial hypoxemia resolved and pulmonary infiltration was much improved (). The patient was discharged home seven days after surgery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [66.0, 'kg']}",106,100.7,111.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 66.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (66.0 kg - 20 kg) = 106.0 mL/hr.
Hence, the patient's fluid maintenance is 106.0 mL/hr."
4588,22,Maintenance Fluids Calculations,physical,decimal,pmc-5791498-1,Extracted,"A 7-year-old girl, weighing 16 kg, with the diagnosis of TOF, and a history of right-sided modified Blalock-Taussig (BT) shunt 4 years back, was scheduled for corrective surgery. On examination, she had pulse rate of 80 beats/min, sinus rhythm, arterial blood pressure 90/60 mm of Hg, and a Grade II ejection systolic murmur heard in the second left intercostal space. The peripheral oxygen saturation was 88% on room air. She was on Tablet propranolol 10 mg every 12 h. Preoperative hemoglobin was 18.2 g/dL with a platelet count of 269,000/μL. Chest X-ray postero-anterior view showed a boot-shaped heart with normal transverse diameter and clear lung fields. Electrocardiography showed sinus rhythm with right ventricular hypertrophy.
Preoperative echocardiography showed situs solitus, atrioventricular and ventriculoarterial concordance, large, nonrestrictive malaligned ventricular septal defect (VSD) of 20 mm size, with the right to left shunt and 50% aortic over-ride. There was severe infundibular and valvular pulmonary stenosis. The peak gradient across the right ventricular outflow tract was 90 mm of Hg. Pulmonary arteries were small and confluent with Mc Goon ratio of 0.7. The right ventricle was moderately hypertrophied. Ventricular function was good with an ejection fraction of 61%. The great vessels were normally related with a left aortic arch.
Cardiac catheterization confirmed the diagnosis. The coronaries were normal. Descending aortogram did not reveal any significant aortopulmonary collaterals []. However, injection into the right subclavian artery showed multiple small collaterals feeding the right upper lobe. Reformation of only a distal right upper lobe branch of PA was seen []. Injection into right modified BT shunt showed filling of confluent pulmonary arteries. Mild narrowing of right pulmonary artery (RPA) at right modified BT shunt anastomosis site was appreciated and the upper lobe branch of RPA was cutoff [].
In the operating room, induction of anesthesia was done with sevoflurane in 100% oxygen followed by administration of injection ketamine 2 mg/kg, fentanyl 3 μg/kg, and rocuronium bromide 1 mg/kg. A smooth direct laryngoscopy was performed and the trachea intubated with a 5.5 cuffed endotracheal tube (ETT). A pediatric transesophageal echocardiography (TEE) probe and temperature probe were gently placed followed by the acquisition of left radial artery and right internal jugular central venous access. Median sternotomy was done, and right modified BT shunt takedown was performed, followed by systemic heparinization. CPB was initiated after aortic and bicaval cannulation and an adequate activated coagulation time (ACT). The CPB lasted for 124 min with aortic cross-clamp duration of 66 min. The surgical field did repeatedly flood with blood during the CPB, which was managed with frequent venting.
After satisfactory correction, on resuming gentle ventilation, the aortic cross-clamp was released. Thereafter, lungs became progressively heavy, and ventilation was barely possible even at high airway pressures in spite of a patent ETT and circuit. The patient was nebulized with short acting β agonists. Injection deriphyllin, methylprednisolone, and hydrocortisone were added to the CPB reservoir. The difficulty in ventilation persisted. Soon, endotracheal bleed became apparent. The oral cavity was free from any bleeding. Gentle ETT suctioning was mandatory to allow any ventilation signifying a substantial bleed. About 100–150 ml of blood was suctioned from the ETT, and ventilation was then possible.
Once we were able to ventilate with an acceptable tidal volume, we came off CPB. On TEE, an adequate surgical repair was confirmed, demonstrating a good contractility with no right ventricular outflow tract obstruction or residual VSD. We could maintain hemodynamics on inotropic support of dopamine 5 μg/kg/min, dobutamine 5 μg/kg/min, and noradrenaline 0.1 μg/kg/min and peripheral oxygen saturation between 90% and 97% on 100% oxygen. Even, after adequate reversal of heparin with protamine, the ETT bleed continued. Adrenaline-saline (1:200,000) irrigation, gentle ETT suction of blood and intermittent ventilation was alternated. A post-CPB bolus dose of epsilon aminocaproic acid (EACA) 100 mg/kg was followed by an infusion of EACA. 20 ml/kg fresh frozen plasma, 0.1 U/kg platelet concentrates and packed red blood cell corpuscles were transfused to maintain a minimum hematocrit of 36%, in view of ongoing lung bleed. The sonoclot signature and the ACT were normal ruling out a medical cause of bleed. The above-mentioned measures were continued for an hour to achieve hemostasis. The amount of bleed had decreased sizeably but did not subside completely.
The immediate postoperative chest X-Ray demonstrated haziness in right upper and middle zone of the lung []. In the intensive care unit, we followed a comprehensive three-pronged management approach that constituted (i) lung protective ventilatory strategy with a low tidal volume, high frequency, minimizing the airway pressures, addition of positive end-expiratory pressure, recruitment manoeuvres with minimal and gentle suctioning, (ii) delayed sternal closure, and (iii) pharmacological control of bleeding and airway hyperreactivity with antifibrinolytics, nebulization, and steroids, respectively. The blood and blood products were transfused to maintain a minimum hematocrit of 36% and coagulation parameters within normal range. The patient was successfully weaned off and extubated on the third postoperative day and discharged on the tenth postoperative day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [16.0, 'kg']}",52,49.4,54.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 16.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (16.0 kg - 10 kg) = 52.0 mL/hr.
Hence, the patient's fluid maintenance is 52.0 mL/hr."
4589,22,Maintenance Fluids Calculations,physical,decimal,pmc-3101731-1,Extracted,"A 5-day-old male neonate presented with generalized jaundice. He had been born by vaginal delivery at term with a birth weight about 2100 g. The mother (gravida: 6, para: 6, living: 6) was healthy with no significant past medical history other than mild photosensitivity. The baby had no history of passing clay-colored stools or of fever and had not been given any drugs.
On admission, physical examination revealed pale conjunctiva, icteric sclera, generalized jaundice, a few erythematous lesions in the periorbital areas, and mild splenomegaly. He had an irregular pulse, with a heart rate of about 75 beats per minute. The electrocardiogram showed third-degree atrioventricular block; echocardiography showed a patent foramen ovale but no other abnormality. Hematological investigation revealed anemia (hemoglobin 9 g/dL) and thrombocytopenia (platelets 80 000/mm3). A blood smear showed erythrocyte hypochromia, anisocytosis, and poikilocytosis. The reticulocyte index, C-reactive protein, and erythrocyte sedimentation rate were normal. Liver function tests showed increased values, as follows: aspartate aminotransferase (AST), 760 U/L (normal:1-46 U/L); alanine aminotransferse (ALT), 187 U/L (normal: 1-49 U/L); alkaline phosphate, 2045 U/L (normal: 64-306 U/L); total bilirubin, 12.4 mg/dL (normal: 0.1-1.3 mg/dL); and direct bilirubin, 6.2 mg/dL (normal: 0.1-1.3 mg/dL). Prothrombin time and partial thromboplastin time were not prolonged. TORCH titers, viral hepatitis markers, and thyroid function tests were normal. For both mother and neonate, blood and urine cultures were negative. Tests for metabolic diseases, including galactosemia, tyrosinemia, and phenylketonuria, were negative.
Abdominal ultrasound revealed a normal-sized liver and gall bladder, no bile duct dilation, and no sludge in the biliary tree. The spleen was mildly enlarged but showed a normal echo pattern. Hepatobiliary scintigraphy showed decreased hepatic uptake, with no passage through the intrahepatic bile ducts.
At first, the cutaneous lesions consisted of a few nonscarring erythematous annular plaques in the periorbital areas. Over the next few days, they spread to the nasal bridge and the upper parts of the cheeks and had sharp and slightly hyperkeratotic borders.
Serologic studies of the infant and mother were positive for antinuclear antibodies (ANA; 1: 640), anti-Ro/SSA: >4 index (normal: <1 index) and anti-La/SSB antibodies: >4 index (normal: <1 index). Anti-ds DNA antibodies, anti-SM antibodies, anti-U RNP antibodies were not detected. More detailed studies in the mother revealed a low C3 level of 0.71 g/dL (normal: 0.9-1.87 g/dL), leukopenia (WBC: 2900 mm3), and anemia (hemoglobin: 10.6 mg/dL).
We diagnosed NLE. Earlier studies have reported beneficial effects of glucocorticoids on different manifestations of NLE such as thrombocytopenia and cholestasis, and we therefore prescribed prednisolone (2 mg/kg/day) for 2 weeks along with ursodeoxycholic acid. The parents were advised to avoid exposing the neonate to the sun and to use sunscreen agents and topical hydrocortisone creams. After the platelet count had returned to normal the patient was discharged and was then followed up in the outpatient clinic. Within 2 months both the jaundice and the skin rashes had resolved. At 6 months of age, liver function tests were normal. During the follow-up period, the patient had a normal heart rate and there was no evidence of heart failure.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2100.0, 'g']}",8.4,7.98,8.82,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2100.0 g so this converts to 2100.0 lbs * kg/1000 g = 2.1 kg. Hence, the patient's maintenance fluid is 2.1 kg * 4 mL/kg/hr = 8.4 mL/hr.
Hence, the patient's fluid maintenance is 8.4 mL/hr."
4590,22,Maintenance Fluids Calculations,physical,decimal,usmle-3776,Extracted,"A 2850-g (6-lb 5-oz) newborn is delivered at term to a 19-year-old primigravid woman via normal spontaneous vaginal delivery. The mother has had no prenatal care. Examination of the newborn in the delivery room shows a small, retracted jaw and hypoplasia of the zygomatic arch.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2850.0, 'g']}",11.4,10.83,11.97,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2850.0 g so this converts to 2850.0 lbs * kg/1000 g = 2.85 kg. Hence, the patient's maintenance fluid is 2.85 kg * 4 mL/kg/hr = 11.4 mL/hr.
Hence, the patient's fluid maintenance is 11.4 mL/hr."
4591,22,Maintenance Fluids Calculations,physical,decimal,pmc-7526953-1,Extracted,"An 80-year-old male with a past medical history of Crohn's disease presented to the emergency department with complaints of nausea and multiple episodes of coffee-ground emesis for one day and was initially diagnosed with upper gastrointestinal bleed. His prior medical conditions included longstanding Crohn's disease, hypertension, diabetes, and coronary artery disease. He had undergone previous abdominal surgery for the complication of small intestinal obstruction due to Crohn's disease in 2017. On initial evaluation, he had a blood pressure of 159/74 mmHg, pulse of 84 per minute, respiratory rate of 18 per minute, oxygen saturation levels (SpO2) of 98% on room air, and body weight 125 pounds. On physical examination, the patient was noted to have a mildly tense and tender abdomen with hyperactive bowel sound. The fluid thrill and shifting dullness were negative.
His blood work revealed creatinine of 1.27 mg/dL, blood urea nitrogen of 27 mg/dL, sodium of 147 mmol/L, potassium of 3.6 mmol/L, chloride of 103 mmol/L, bicarbonate of 27 mmol/L, bilirubin of 2.3 mg/dL, lactate of 1.3 mg/dL, cardiac troponins of <0.10 (normal), WBC of 22,000 cells/mm3, and hemoglobin of 14.2 mg/dL. Imaging studies included CT abdomen and pelvis, which showed a markedly distended stomach filled with the enteric contrast, rotated in mesenteroaxial (MA) rotation, and localized fluid in the left upper quadrant with the caudal displacement of the spleen due to left upward stomach (Figures , ). The gastric outflow tract was pinched to the left of the midline superior to the esophagogastric junction related to the gastric volvulus, with a small amount of contrast material passing into the small intestine, suggesting a short segment of focal narrowing at the level of antrum or proximal duodenum (Figures , ). This was consistent with the diagnosis of gastric volvulus. After the initial resuscitation, the gastroenterologist decided to perform endoscopic detorsion, which was unsuccessful due to the twisting of the distal stomach in the antrum and stricture at the level of the antrum. The area was traversed multiple times without achieving clear untwisting due to adhesions.
The patient was taken to the operating room and laparoscopy was performed to find a redundant stomach without adhesions or masses. The stomach was detorsed. The gastroenterologist was consulted in the operating room and endoscopy was performed. The narrowing at the junction of the antrum and proximal duodenum was identified. Gastric and duodenal mucosa were healthy, without lesions or masses, and gastropexy was performed. Postoperatively, the patient was kept under observation for one week and was discharged home with outpatient follow-up. At his biweekly follow up, the patient was found to be doing well.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [125.0, 'lbs']}",96.699,91.86405,101.53395,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 125.0 lbs so this converts to 125.0 lbs * 0.453592 kg/lbs = 56.699 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (56.699 kg - 20 kg) = 96.699 mL/hr.
Hence, the patient's fluid maintenance is 96.699 mL/hr."
4592,22,Maintenance Fluids Calculations,physical,decimal,pmc-7705384-1,Extracted,"A 5-month-old girl presented with a 3-month history of growth retardation and slightly low muscle tension in the lower limbs. Her mother had a history of hydramnios in the third trimester of pregnancy. The girl’s body weight at birth was 3.2 kg, and her development score as a newborn was normal. Physical examination showed that her motor evaluation was equivalent to that of 2- to 3-month-old children, and fine motor and motor growth retardation were observed. Electromyography of the lower limbs showed no abnormalities. Magnetic resonance imaging of the skull showed widening of the left anterior temporal subarachnoid space and bilateral lateral fissure cisterns. She was diagnosed with cerebral palsy. Nutritional nerve therapy and hyperbaric oxygen therapy were given.
The child was readmitted at 10 months of age because of aggravated nausea and vomiting accompanied by malnutrition and mild to moderate dehydration during the rehabilitation training and treatment. Electrolyte measurement revealed a potassium level of 1.24 mmol/L, sodium level of 110.3 mmol/L, chloride level of 60.5 mmol/L, magnesium level of 0.72 mmol/L, and calcium level of 1.17 mmol/L. Blood gas analysis showed a blood pH of 7.602, oxygen partial pressure of 76.3 mmHg, carbon dioxide partial pressure of 37.4 mmHg, bicarbonate of 36.1 mmol/L, and base excess of 13.6. Her serum creatinine level and estimated glomerular filtration rate were normal. The hypokalemia could not be corrected even with venous potassium supplementation at high concentrations. Urine electrolyte measurement showed a urinary potassium level of > 20 mmol/L and high urinary calcium level. Her parathyroid hormone level and blood pressure were normal. Abdominal ultrasound, computed tomography, and renal artery angiography showed no abnormalities. Her renin, angiotensin II, and aldosterone levels were significantly higher than normal (). The possibility of BS was considered at this point, and the initial diagnosis of cerebral palsy was suspected to be incorrect.
Next-generation sequencing of the proband (355 genes) showed that the patient carried two known heterozygous pathogenic mutations: c.88C > T (p.Arg30*) and c.1313G > A (p.Arg438His). Thus, she was diagnosed with typical BS (type III), namely that with the CLCNKB mutant genotype. Sanger sequencing of the patient’s family further showed that the mother carried CLCNKB c.1313G > A (p.Arg438His), which was a missense mutation. The patient’s father carried CLCNKB c.88c > T (p.Arg30*), a nonsense mutation that has been previously reported. The Sanger sequencing diagram is shown in , and the family tree is shown in .
The patient was given oral potassium chloride (4–6 mmol/kg per day), indomethacin enteric-coated tablets (1–2 mg/kg per day), and antiseton (1–3 mg/kg per day) to reduce potassium loss. The electrolyte disturbance was corrected, and the serum potassium concentration was maintained at a slightly lower level than normal accompanied by correction of alkalosis (). The patient maintained normal growth and development after treatment ().
Indomethacin was selected for this patient’s treatment because it is small enough to be crushed and dissolved in milk for infants to drink. After 10 years of long-term treatment with indomethacin, the child began to show adverse effects including upper abdominal pain with acid regurgitation, nausea, and vomiting. Considering the gastrointestinal adverse effects of indomethacin, we changed the patient’s treatment to ibuprofen sustained-release tablets (6–30 mg/kg per day) at 0.3 g twice per day, continuation of potassium chloride sustained-release tablets (5–10 mmol/kg per day) at 3.5 g twice per day, spironolactone (1–3 mg/kg per day) at 60 mg per day, and discontinuation of captopril tablets. We monitored her fasting electrolyte levels, which were maintained at a slightly lower level than normal. At the time of this writing, 4 years had passed since the change in the combined drug treatments, and no obvious gastrointestinal adverse effects had occurred.
The patient’s electrolyte disturbances were basically corrected with potassium supplementation combined with a cyclooxygenase inhibitor. Her overall growth and development were maintained within the normal range. At the time of this writing, she was 14 years old, was 155 cm tall, and weighed 48 kg. Treatment of type III BS with indomethacin in this patient increased her body weight to the level of normal development (). Consent for publication of this paper was provided by the patient’s mother.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [48.0, 'kg']}",88,83.6,92.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 48.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (48.0 kg - 20 kg) = 88.0 mL/hr.
Hence, the patient's fluid maintenance is 88.0 mL/hr."
4593,22,Maintenance Fluids Calculations,physical,decimal,pmc-7882788-1,Extracted,"A 31-year-old Gravida III and Para II mother came to the outpatient clinic of the University of Gondar specialized hospital, North West Ethiopia, in January 2019 complaining of pruritus (mainly under the breasts, on the neck, palms of the hands and soles of the feet) along with jaundice at 24 weeks gestational age (GA). She had a history of antenatal care follow up at a nearby health center. She presented to us with singleton and intrauterine pregnancy.
On arrival, she was screened for both subjective and objective data for her current and past obstetric, medical, surgical, gynecological, social, personal and family history. She had a history of early neonatal loss and one living child, her bilirubin value was elevated, she suffered pruritus and hepatomegaly in her previous pregnancies. She had a personal and family history of pruritus during pregnancy. From her previous personal history, she reported a history of similar features that resembled her current clinical presentation. The rest of her laboratory investigations and physical examination results, including vital signs (blood pressure 100/70 mmHg), were in their normal range and she arranged for her next follow up after being provided with an antihistamine drug and offered counseling and health education to ensure the best outcome for her pregnancy. At 30 weeks GA, she was assessed for any complaints, including the worsening of pruritus and underwent liver biochemistry tests. Based on this, her bilirubin total and bilirubin direct tests were 4.52 mg/dl and 3.45 mg/dl respectively. Other complete blood count tests and urinalysis were within the normal range. The progress of the pregnancy was also assessed using ultrasound and showed no any abnormality. At 34 weeks GA her bilirubin values became elevated, whereas her liver function test on both alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were 83U/L and 75 U/L, respectively. The value of prothrombin time (PT) and partial thromboplastin time (PTT) were 12.2 and 34.6 seconds, respectively. Urine bilirubin, urobilinogen, urine nitrite, and Hepatitis B surface antigen (HBS-antigen) tests were negative. But there was no opportunity for a TBA laboratory test.
As a result of having some abnormally elevated liver biochemistry tests, and the clinical features of the patient's current and past obstetric history, a decision was made to admitthe patient to the obstetric ward after a diagnosis of ICP was made. After admission various checks were carried out, including: weekly fetal surveillance with ultrasound and using a kick chart; administration of four doses of dexamethasone 12 hours apart to accelerate fetal lung maturation at 33 weeks GA; administration of antihistamine drugs to alleviate the suffering from pruritus; and psychological reassurance of the patient. The patient's clinical symptoms were not improved after administering antihistamine drugs and she suffered from severe pruritus following the administration of dexamethasone. At 37 weeks GA, the obstetrician and midwives had a detailed discussion and decided to deliver the baby. Initially the cervix was ripened with a Foley catheter so as to have an acceptable BISHOP score and then induction of labor with oxytocin was carried out. During this time a non-reassuring fetal heart rate pattern was detected with a cardiotocograph (CTG) and was confirmed with ultrasound. Finally, a successful caesarean section was done performed to deliver a 2.8 kg live female baby with an APGAR score of 8 and 9 in the 1st and 5th minutes, respectively. Following delivery, the patient remained inhospital for a week and was discharged to home with both mother and baby in stable conditions. The evaluation of the patient during the puerperium two weeks after giving birth was good, with the normalization of the liver biochemistry tests and the disappearance of the pruritus. The bilirubin total, ALT and AST decreased to 1.1 mg/dl, 32 U/L, and 31 U/L respectively. The evaluation of the baby was also good, with normal physical development.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.8, 'kg']}",11.2,10.64,11.76,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.8 kg. Hence, the patient's maintenance fluid is 2.8 kg * 4 mL/kg/hr = 11.2 mL/hr.
Hence, the patient's fluid maintenance is 11.2 mL/hr."
4594,22,Maintenance Fluids Calculations,physical,decimal,pmc-5362012-1,Extracted,"A 10-month-old female spayed domestic shorthair cat was referred for urinary incontinence of 3 months’ duration. The cat was dribbling urine, and damp bedding was noticed following sleep. The cat had been spayed 122 days prior with no complications reported. Sixty-four days after ovariohysterectomy (OHE), pollakiuria with stranguria and haematuria was observed over a 2 day period. Treatment was provided with oral amoxicillin–clavulanic acid (Clavulox; Pfizer) 12.5 mg/kg PO q12h for 1 week. Haematuria had resolved at a recheck 3 weeks later but pollakiuria remained. At 1 week prior to referral serum biochemical analysis revealed azotaemia (), urine specific gravity was 1.028 and urine dipstick findings included 2+ red blood cells and a pH of 6.5. No crystals were identified on microscopy and culture was not performed. Oral marbofloxacin (Zeniquin; Pfizer) 3.3 mg/kg q24h was prescribed for 14 days and proprietary renal diet initiated (k/d, Hill’s Pet Nutrition).
At presentation the cat had lost 0.66 kg, down from 3.94 kg 2 months earlier. No abnormalities were identified on physical examination. Abnormal laboratory findings included a packed cell volume of 28% (reference interval [RI] 30–45%) and azotaemia (). Abdominal ultrasound showed bilateral hydronephrosis and hydroureter (). The urinary bladder appeared normal. The urethral lumen was variably distended measuring between 4.5 mm and 6.0 mm along its length. Computer tomographic (CT) contrast pyelography was recommended to investigate the cause of urinary tract distension, with ureteral ectopia the primary differential; however, this was declined by the owner. Urine culture was not performed owing to antibiotic use. The cat was discharged with advice to continue antibiotic therapy for possible associated pyelonephritis.
At 245 days post-spay the cat represented to the original referring practice with pollakiuria and stranguria. A large bladder was palpated. Clinical signs resolved after 2 days on oral diazepam (Valium; Roche) 0.25 mg/kg q12h and prazosin (Minipress; Pfizer) 0.125 mg/kg q12h.
The cat was presented for further investigation at 18 months of age, 298 days post-spay. Voluntary urination appeared normal; however, there were episodes of apparent incontinence immediately after urinating and occasional stranguria. Diazepam and prazosin were ongoing. Blood testing was performed ().
A CT study was performed to evaluate the urinary tract. The cat was imaged in sternal recumbency and a survey scan in a soft tissue algorithm (WL 30 and WW 350) with 2.00 mm slice thickness was performed. Iodinated contrast agent (Omnipaque 240 mg/ml; GE Healthcare Australia Pty) was administered intravenously at a reduced dose of 240 mg/kg. A second scan was obtained after a delay of 3 mins with a soft tissue algorithm (WL 30 and WW 350) and a slice thickness of 1.50 mm.
This examination identified moderate bilateral hydronephrosis and diffuse mild-to-moderate hydroureter (; ,). On the postcontrast images there was a normal parenchymal phase; however, the excretory phase was delayed.
The apex of the urinary bladder had a moderately distended lumen apically; however, it tapered sharply just prior to the trigone region and was clearly torsed at this level (). In the region of the trigone the lumen became distended again before tapering towards the urethral sphincter at the level of the pelvic brim (). The distal ureters could be observed extending to the level of the trigone but their terminations could not be determined.
Aerobic urine culture was performed with no bacteria isolated after 48 h. The reversibility of renal compromise was unknown; however, surgery was advised to document and correct the suspect bladder torsion.
At 315 days postspay midline laparotomy was performed and marked adhesions of the greater omentum to the bladder apex were identified (). Dissection allowed identification of torsion of the bladder neck of approximately 150º such that the left ureter passed over the dorsal surface of the bladder neck to insert on the right side, and the right ureter inserted on the ventral bladder neck (). The bladder was de-rotated; however, the omental adhesions caused the bladder to return to a torsed state so the adhesions were broken down. A right paramedian incisional cystopexy was performed with 4-0 glyconate (Monosyn; B Braun). The abdomen was closed routinely.
Postoperative analgesia was provided with 0.02 mg/kg buprenorphine q8h (Temgesic; Reckitt Benckiser) sublingually. The cat was maintained on intravenous compound sodium lactate solution (Hartman’s solution; Baxter) at 2.5 ml/kg/h. In hospital, urination was regularly observed in the litter tray but not on bedding. Azotaemia improved through the period of hospitalisation ().
Ten days postoperatively all clinical signs were reported to have resolved. Ten weeks postoperatively (449 days after spay) the cat was reported to be active and eating well, although still polydipsic. Laboratory findings were recorded (). Urine dipstick was negative for proteinuria and testing of systolic blood pressure revealed normotension on repeated assessments. During ultrasound examination both kidneys exhibited much reduced pylectasia and the ureters could not be identified (). The urinary bladder appeared within normal limits.
At this visit a recheck CT examination was performed in sternal recumbency with a plain survey study followed by sequential postcontrast studies acquired 3, 5 and 11 mins postadministration of iodinated contrast agent (240 mg/kg). There was evidence of reduced hydronephrosis and the kidneys had reduced in size (). The cortical margins were undulating, giving the kidneys a slightly lobulated structure. In the postcontrast series there was a homogeneous parenchymal phase and normal progression to the excretory phase. The ureters had a reduction in diameter and demonstrated evidence of peristalsis (). There was normal ureteral insertion into the trigone. There was some residual narrowing of the trigonal lumen at the site of the previous torsion. The cat was assessed as having near complete resolution of structural urinary tract changes as a result of surgery so no subsequent deterioration in renal function due to obstruction was anticipated. The cat was deemed to have stage 2 chronic kidney disease according to the IRIS guidelines, and was discharged with advice to feed a proprietary renal diet and seek repeat assessment of renal parameters every 3 months.
At day 469 after OHE serum creatinine was within the RI and urine specific gravity was measured at 1.034 ().
At day 603 after OHE (8 months postcorrective surgery) all serum biochemical parameters were within the RI (). The cat was receiving a renal diet and no clinical concerns were noted.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.28, 'kg']}",13.12,12.464,13.776,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.28 kg. Hence, the patient's maintenance fluid is 3.28 kg * 4 mL/kg/hr = 13.12 mL/hr.
Hence, the patient's fluid maintenance is 13.12 mL/hr."
4595,22,Maintenance Fluids Calculations,physical,decimal,pmc-6693048-1,Extracted,"An 83-year-old female patient presented to our clinic with abdominal pain, lack of appetite, nausea, weight loss, and fatigue. The patient had lost nearly 12 kilograms in the past 6 months. Abdominal pain was localized in the right upper quadrant. She had obtuse pain that had no relation to food. It was found that the patient had osteoporosis in her history but did not receive any treatment. In the physical examination of the patient, who did not present any characteristics in her family history, the liver extended to 2 cm below the costal margin. She did not have ascites or splenomegaly. Heart and lung examinations were normal. Laboratory tests presented a normal hemogram. Biochemical tests revealed an aspartate aminotransferase (AST) level of 50 U/L, alanine aminotransferase (ALT) level of 20 U/L, total bilirubin level of 1.3 mg/dL, alkaline phosphatase (ALP) level of 101 U/L, gamma-glutamyltransferase level of 227 U/L, albumin level of 2.6 g/dL, total protein level of 4.9 g/dL, calcium level of 12,35 mg/dL, and a phosphate level of 2.6 mg/dL. The patient was hospitalized in order to investigate the etiology of hypercalcemia. The patient had a parathormone level of 9.5 pg/mL. These results excluded a diagnosis of primary hyperparathyroidism. The patient who was thought to have malignant hypercalcemia was started on intravenous fluid replacement and furosemide treatment. The patient who manifested a creatinine clearance of 55.5 mL/min/1.73 m2 was started on 2 mg zoledronic acid treatment. Tomography scans demonstrated no osteolytic bone lesions. During follow-up, the patient's calcium levels regressed to 9.7 mg/dL with the specified treatment. Abdominal ultrasonography performed due to right upper quadrant pain and hepatomegaly revealed multiple hypoechoic images in the liver, of which the largest was 1.5 cm in size, and a coarsely granular parenchyma. The dynamic CT of the patient demonstrated hypodense lesions with multiple areas of peripheral contrast enhancement that were particularly congregated in the right lobe, the largest of which had a size of 47 × 32 mm, and this was interpreted as metastasis (Figure ).
Levels of alpha-fetoprotein were determined as 91 ng/mL, cancer antigen (CA-125) as 258.6 U/mL, carcinoembryonic antigen (CEA) as 0.82 ng/mL, and cancer antigen 19-9 (CA19-9) as 2.1 U/mL. A biopsy was performed on the mass in the liver for diagnosis. Pathology result indicated cholangiocellular cancer (Figure ). The patient did not consent to surgical resection; therefore, a monthly zoledronic acid treatment was planned for pain palpation and hypercalcemia.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.0, 'kg']}",44,41.8,46.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.0 kg - 10 kg) = 44.0 mL/hr.
Hence, the patient's fluid maintenance is 44.0 mL/hr."
4596,22,Maintenance Fluids Calculations,physical,decimal,pmc-7396112-1,Extracted,"The patient was a healthy 46-year-old female with no significant medical history (patient weight: 90.1 kg and height: 67 inches) who presented with a lateral malleolus fracture after a fall. She underwent an ORIF ankle, and surgery lasted about an hour and half. Her baseline preoperative pain score was 0, and she had no sensory or motor deficits. Preoperative nerve block placement was uneventful, and the patient received 20 mL of EXPAREL® 1.3% 20 ml (266 mg). On arrival to the PACU, she reported no cold sensation in the targeted dermatome areas; however, she reported 10/10 pain on VAS. In addition, the patient complained of pruritis, and she received 0.5 mg hydromorphone IV and diphenhydramine 50 mg IV. Her followed-up pain scores were 3/10 and 0/10 at 60 minutes and 120 minutes, respectively. On POD #1, the patient recorded a highest pain score of 8/10 and required 2 doses of Percocet 5/325 total for the day. On POD #2, the patient recorded a highest pain score of 10/10, so she took Advil for breakthrough pain as she reported pruritus after taking Percocet. On POD #3, her highest pain score was 4/10, and she continued to take Advil for breakthrough with two doses total for the day. The patient reported a 4/5 overall satisfaction score.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [90.1, 'kg']}",130.1,123.595,136.605,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 90.1 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (90.1 kg - 20 kg) = 130.1 mL/hr.
Hence, the patient's fluid maintenance is 130.1 mL/hr."
4597,22,Maintenance Fluids Calculations,physical,decimal,pmc-7092595-1,Extracted,"A 15-year-old patient with a female phenotype (Fig. ) presented at our hospital with a chief complaint of short stature for 9 years. She was the first full-term child born to her parents; the mother was healthy during pregnancy and had no history of illness or medication. Her father was 167 cm in height; he began to develop at the age of 14 and had his first spermatorrhea at 18 years. Her mother was 157 cm in height, and her menarche began at the age of 12 years. Both parents stated no history of other hereditary and infectious diseases.
The patient was delivered via cesarean section, no postpartum asphyxia or hypoxia and no abnormal Apgar score. Her birth weight and length were 3.3 kg and 48 cm, respectively. She had normal teething, and mental and physical development before the age of 6 in line with her healthy peers. At the age of 6 years, she showed a slow growth rate, growing approximately 1–2 cm every year, with a gradual decline in intelligence, understanding, and learning ability. Five years ago, at the age of 10, her bone age was determined to be 8 years. The patient was then diagnosed with “dwarf syndrome” and treated with growth hormone. However, no height growth was obvious, and thus the treatment was terminated after 1–2 months.
Upon physical examination, the patient’s height was 136 cm and the weight was 29 kg, which are both below the third percentile of children of the same age and gender. The patient was lean, with a short neck, many moles, an epicanthic fold, tall palatine arches, a shield-like chest, wide breast distance, evident breath sounds in lungs, and no dry and wet rales. The heart rate was 86 beats per minute, with a regular rhythm. No murmur was heard in each valve auscultation area. The abdomen was soft, with no tenderness, rebound tenderness, and muscle tension, and there was no palpable swelling in the liver or spleen. Cubitus valgus was present. The 4th and 5th metacarpals were short, and no edema was detected in either of the lower limbs. In terms of sex development, she doesn’t have normal breast development. If the Tanner stage is adopted, the patient’s breast is stage I, which does not match the age. The patient had a young vulva and a small clitoris. There was no mass in the inguinal and labia majora area, and no pubic hair or armpit hair.
Blood, urine, and stool analyses were unremarkable. Liver function, renal function, blood lipids, electrolytes, blood sugar, and thyroid function were all normal. Hepatitis tests revealed hepatitis A virus IgM antibody (−), hepatitis B surface antigen (−), hepatitis C virus antibody (−), and hepatitis E virus IgM antibody (−). Thyroid function and antibody were normal. Six sex hormones were analyzed: luteinizing hormone (LH), 17.5(0.1–11.9) mIU/ml; follicle-stimulating hormone (FSH), 103.50(2.1–11.1)mIU/ml; testosterone 0.09(0.00–2.39) nmol/l; progesterone, 1.50 (0.98–4.83)nmol/l; prolactin, 292.50 (6.68–53.44)μIU/ml, and estradiol < 18.35 (48.00–521.00)pmol/l, prolactin levels increased, but other biochemical and imaging tests were normal, which may be related to the patient’s nervousness, the above results suggest that the patient has hypergonadotrophic hypogonadism (gonadal failure/lack of functioning). Insulin-like growth factor-1 was 172.00 ng/ml. The 24-h urine free cortisol was normal. Karyotype analysis (400 belt, G belt) showed 47,XYY (Fig. ). Further chromosomal microarray examination showed a chimera of the karyotype 46,XY/47,XYY. The ratio was approximately 2:1, and the Y chromosome contained the SRY gene.
Pituitary magnetic resonance imaging and chest X-rays showed no abnormalities. The bone age was approximately 13 years of age (Fig. ). Ultrasound examination of the uterus and double attachment revealed an approximately 1.1 × 0.9 × 0.6-cm hypoecho, similar to a uterine echo. There was no endometrial echo and both ovaries were unclear. Cardiac ultrasonography showed no abnormalities in the intracardiac structure nor aortic stenosis. Abdominal color Doppler showed no abnormalities in the structures of the liver, gallbladder, pancreas, spleen, and kidneys.
Next-generation sequencing showed no mutations in the 65 genes associated with disorders of sex development, and no large missing or repeated segments of sex-reversal-related genes (NROB1, WNT4, NR5A1, SOX9, AMH, SF1, FGF9, FOXL2) were detected by multiplex ligation-dependent probe amplification.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [29.0, 'kg']}",69,65.55,72.45,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 29.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (29.0 kg - 20 kg) = 69.0 mL/hr.
Hence, the patient's fluid maintenance is 69.0 mL/hr."
4598,22,Maintenance Fluids Calculations,physical,decimal,pmc-5175312-1,Extracted,"A 12-month-old baby boy of African descent presented to us with a history of global developmental delay, erratic sleep patterns, and poor weight gain. He was the first born to a 28-year-old woman with type 1 diabetes mellitus diagnosed at the age of 9. The mother attended antenatal clinic from the 16th week of gestation and received all routine antenatal care as per the Tanzanian protocol (antihelminthics, antimalarial medications, hematinics, and tetanus toxoid). She tested negative for human immunodeficiency virus (HIV), hepatitis B and C, and syphilis. The mother denied history of toxoplasmosis, other (syphilis, varicella-zoster, parvovirus B19), rubella, cytomegalovirus, and herpes (TORCH) infections, trauma, or chronic drug use; however, she had a urinary tract infection during her first trimester which was successfully treated with oral cephalexin 500 mg four times a day for 5 days. Apart from the insulin-dependent diabetes mellitus, no other history of familial genetic disorders was elicited. Sonographic evaluation at 16th and 36th week of gestation revealed a normal singleton pregnancy. Despite a fairly good sugar control before pregnancy, the mother had poor glycemic control during pregnancy and her glycated hemoglobin (HbA1C) taken at 7 and 29 weeks of gestation was 8.3% and 7.9% respectively. She gave birth at 39+ weeks by emergency cesarean section due to fetal distress and breech presentation. The baby weighed 2315 g and had Apgar scores of 6/10 and 8/10 at 1 and 5 minutes respectively. His head circumference at birth was 38.9 cm (97th percentile). Chromosome analysis (karyotyping) is not a routine practice in Tanzania and it was not performed.
The boy weighed 8.5 kg at 6 months, which was the exact same weight measured during his visit to our institution at 12 months of age. His head circumference at 1 year was 49.1 cm (99th percentile). He had stable vital signs but a physical examination revealed a small-for-age child with conjunctival and palmar pallor. All his growth parameters were below the 5th percentile and he had a developmental age of 2 months. He scored 4 on neurocognitive assessment using the Carter Neurocognitive Assessment Severity Scale. He had normal facies but a neurological examination revealed hypotonia in all four limbs. Other systemic examinations were unremarkable. He underwent a series of blood work-up, cardiac echocardiography (ECHO), and renal ultrasound all of which revealed normal findings except for iron deficiency anemia: hemoglobin (Hb) 8.7 g/dL, mean corpuscular hemoglobin (MCH) 21 pg/cell, mean corpuscular volume (MCV) 69 fL, and red cell distribution width (RDW) 15.1%. The child also underwent MRI of his brain which revealed an incompletely formed interhemispheric fissure, a monoventricle with partially developed temporal and occipital horns, partial fusion of his frontal lobe, hypoplastic corpus callosum, and volume loss bilaterally at temporal lobes (Figs. , , and ). His cerebellum and brain stem appeared normal. Based on the clinical presentation and MRI findings the diagnosis of semilobar HPE was entertained. The child was treated for iron deficiency anemia with Hemovit syrup (ferric ammonium citrate, folic acid, pyridoxine hydrochloride, cyanocobalamin, and zinc sulfate) 10 ml thrice daily, ferrous sulfate 10 mg once daily, folic acid 1 mg once daily, and multivitamin syrup 5 ml once daily. Furthermore, nutritional and genetic counseling was offered to his parents.
The child continued to be attended by a developmental pediatrician and pediatric dietician on a regular basis at our institution. An assessment conducted at 12 months post-initial visit showed improvement in his neurocognitive status (Carter Neurocognitive Assessment Severity Scale score = 2). Furthermore, he had attained an acceptable weight for his age (12.6 kg) and his sleeping pattern was stable. In the long run, he is scheduled for both physical and occupational therapy aiming to enhance his motor skills and maximize functional independence.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.6, 'kg']}",45.2,42.94,47.46,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.6 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.6 kg - 10 kg) = 45.2 mL/hr.
Hence, the patient's fluid maintenance is 45.2 mL/hr."
4599,22,Maintenance Fluids Calculations,physical,decimal,pmc-7576439-2,Extracted,"A 34 years old Nepalese man with no previous illnesses, presented to the emergency department with a 5 days history of fever, productive cough, shortness of breath, diarrhoea, generalized fatigue and myalgia. On admission he was febrile at 39.3 °C with a respiratory rate of 35 breaths/min. He required 10 L of oxygen to maintain saturations of 94%. He was a never smoker and his chest examination revealed bilateral crepitations. His height was 175cm with a weight of 92kg (BMI 30). Blood workup showed a CRP of 44 mg/L, D dimer 0.67mg/L (peak 1.41 mg/L), WBC 7.1 × 103/μL, lymphocyte count of 1 × 103/μL. He tested positive for Covid-19 by rRT-PCR with a cyclic threshold of 25.7. His CXR revealed bilateral lower zone non-homogenous infiltrates (). He was commenced on treatment in accordance with the local hospital guidelines. He improved gradually and was weaned off oxygen over the next few days, however, on Day 7 he developed a right sided pleuritic pain and worsening shortness of breath with stable vital signs and oxygen saturations. A CT chest was requested which revealed a large right sided pneumothorax, consolidation of the right basal segments, and multifocal bilateral ground glass opacities in both lungs. (B). Subsequently a chest drain on the right side was inserted, resulting in full resolution of the pneumothorax in 6 days when the drain was removed and the patient was discharged home with a follow up. Of note was the fact that the patient gave a history of similar symptoms with ‘air in his chest’ ipsilaterally 3 years ago, managed with simple aspiration in his home country.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [92.0, 'kg']}",132,125.4,138.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 92.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (92.0 kg - 20 kg) = 132.0 mL/hr.
Hence, the patient's fluid maintenance is 132.0 mL/hr."
4600,22,Maintenance Fluids Calculations,physical,decimal,pmc-3785335-1,Extracted,"A four-year-old girl was admitted because of fever and vomiting. Her family and past histories were unremarkable except for bronchial asthma of her father. She had frequent and periodic fever since she was two years old. She had been admitted five times because of prolonged fever, and diagnosed as pneumonia, tonsillitis, acute otitis media and sinusitis. She had febrile periods (38 °–40 °C) lasting 4 to 7 days every 4 to 8 weeks. She often complained of mild arthralgia in knee joints and had diarrhea frequently. She often showed cervical lymphoadenopathy, tonsillitis and hepatomegaly without stomatitis. She was admitted at this time because of fever which continued for 5 days, vomiting and increased acute inflammatory laboratory data (white blood cell 11.000/μl, CRP 8.9 mg/dl). She also complained of sore throat and diarrhea.
Her height was 104 cm (+0.93SD), and weight was 14 kg (−0.66SD). Her blood pressure was 114/72 mmHg, and heart rate was 128 per minutes, respiratory rate was 26 per minutes. Her tonsil was reddish and enlarged. Cervical lymphoadnopahty was accompanied without hepatosplenomegaly. Her laboratory findings were not remarkable except for increased acute inflammatory responses. All bacterial cultures were negative. Her urinalysis was normal. Chest and sinusoidal X-ray, abdomen and heart echogram were all normal. Without antibiotics her fever decreased naturally after 8 days, and her CRP and count of White blood cells normalized. Her IgD was extremely high as 25.69 mg/dl (181.9 IU/ml). Other laboratory findings were as follows: white blood cells 11.000/μl (neutrophiles 78.9%, eosininophile 0.0%, basophile 0.3%, lymphocytes 13.9%, monocytes 6.9%), red blood cells 4.15 × 106/μl, Hemoglobin 11.0 g/dl, hematocrit 33.8%, platelets 196 × 103/μl, total protein 7.3 g/dl, albumin 4.1 g/dl, aspartate transaminase (AST) 28 U/L, alanine aminotransferase (ALT) 3 U/L, Lactate Dehydrogenase (LDH) 521 U/L, alkaline phosphatase 278 U/L, γ-glutamyltranspeptidase (GTP) 10 U/L, Total birilubin 0.51 mg/dl, BUN 8.7 mg/dl, Creatinin 0.22 mg/dl, beta-2 microglobulin 1.14 mg/l, ferritin 126.1 ng/dl, CRP 8.9 mg/dl, Erythrocyte Sedimentation Rate 91 mm/hour, 2–5 oligoadenylate synthetase 180 pmol/dl, IL-6 15 pg/ml, Serum Amyloid A (SAA) 1100 μg/l (<8 μg/l), IgG 1488.0 mg/dl, IgA 127.0 mg/dl, IgM 180.0 mg/dl, IgE 848.1 IU/ml. IgG subclass were within normal range. RAST was positive for egg white. C3, C4 and CH50 were 167 mg/dl, 44 mg/dl, 52.3 U/ml, respectively. Anti-nuclear antibody, anti-DNA antibody and LE factor were negative. ASLO was below 60 IU/ml. The titer for adenovirus (CF) was below ×4. EBV-VCA IgM and EBV-EBNA were below ×10. EB virus DNA was below 2.0 × 10/106cells. Mevalonic acid showed 10 ng/ml in serum, and 115 ng/ml in urine, respectively. Both levels were higher than those of healthy controls. Restriction Fragment Length Polymorphism (RFLP) and direct sequencing for V377I and I268T were negative []. From the data of high IgD and her clinical symptoms she was diagnosed as non-classic HIDS. Without tonsillectomy ibuprofen (20 mg/kg) was effective to shorten the duration of febrile episodes (from 7 to 2–3 days) for 3 years. However, the levels of IgD were constantly high without any other symptoms. The levels of IgD were normal before 4 years earlier, which are shown in .","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [14.0, 'kg']}",48,45.6,50.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 14.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (14.0 kg - 10 kg) = 48.0 mL/hr.
Hence, the patient's fluid maintenance is 48.0 mL/hr."
4601,22,Maintenance Fluids Calculations,physical,decimal,pmc-4496068-1,Extracted,"A 2-year 1-month-old girl presented to hospital with fever, at which point she was noted to have short stature, alopecia (), and gait instability. Her parents were non-consanguineous and approximately 30 years old when she was born. She had no family history of rickets or unresolved pain. Her mother got a natural conception, and the pregnancy and delivery was uneventful. Her birth weight was 2,868 g (-0.8 standard deviations [SD]), birth length 51 cm (+0.6 SD), gestational age 41 weeks. She had no episode of convulsion and her psychomotor development was normal until she started walking alone at 1 year 3 months of age, but she could not run by age 2. Her body height at presentation was 74.8 cm (−3.5 SD), and her body weight, 9.7 kg (−1.2 SD). She had symptoms of rickets such as bow-legs and enlargement of the limb joints, but had no other external malformation, dysmorphic features, or ataxia. Her verbal developmental quotient (DQ) was 81 and cognitive DQ 94.
Laboratory data revealed hypocalcemia (7.7; reference: 8.5–10.5 mg/dL), hypophosphatemia (3.0; reference: 4.5–6.5 mg/dL), markedly elevated levels of serum alkaline phosphatase (8,891; reference: 300–1,239 IU/L), and intact parathyroid hormone (PTH) levels (576; reference: 10−65 pg/mL). Her serum 1,25(OH)2D level was high (137; reference: 20–70 pg/mL) with a normal 25(OH)D level (20.1 ng/mL). Serum levels of fibroblast growth factor 23 (FGF23) were low (<10 pg/mL), and a bone roentgenogram showed characteristic findings of rickets (). From these findings, she was clinically diagnosed as having HVDRR.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [9.7, 'kg']}",38.8,36.86,40.74,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 9.7 kg. Hence, the patient's maintenance fluid is 9.7 kg * 4 mL/kg/hr = 38.8 mL/hr.
Hence, the patient's fluid maintenance is 38.8 mL/hr."
4602,22,Maintenance Fluids Calculations,physical,decimal,pmc-8024095-1,Extracted,"A 5-year-old intact male mixed breed dog (body weight = 28.0 kg) was presented with two wide dorsal ulcers: the dimension of the thoracolumbar lesion was 10.0 cm × 9.0 cm and the circular lumbosacral lesion a diameter of 15.8 cm (). Overlying skin of the affected areas sloughed off, according to history, exposing a crust-coated reddened subcutaneous and deep fascia tissue (). History also indicated no antimicrobial or prolonged immunosuppressive drug therapy. Affected areas were highly sensitive to touch, inciting intense painful reactions from the patient. The patient was depressed, lethargic, hyperpneic, and feverish (40.2°C). After clinical examination and shaving of the dorsal thorax, this area showed crepitating cyanotic patches of necrotizing skin ().
Using 13 × 150 mm sterile swab sticks (Hangzhou Co. Ltd., China), deep wound swabs were obtained for bacterial culture and sensitivity testing; afterwards, skin biopsy was taken for histopathology. Complete blood count depicted leukocytosis characterized by (i) marked monocytosis, indicating tissue necrosis; (ii) intense neutrophilia, indicative of stress or infection; and (iii) mild basophilia (). The overall leukocyte pattern suggested an acute inflammatory response with tissue necrosis. Serum biochemistry analysis was unremarkable, except for hyperbilirubinemia, mild hyponatremia, mild hypochloremia, and increased ALP and AST levels ().
WBC: white blood cell; PLT: platelet; RBC: red blood cell; HGB: hemoglobin; HCT: hematocrit; MCV: mean corpuscular volume; MCH: mean corpuscular hemoglobin; MCHC: mean corpuscular hemoglobin concentration; RDW: red cell distribution width.
AST: aspartate aminotransaminase; ALT: alanine aminotransaminase; ALP: alkaline phosphatase; GGT: gamma glutamyl transferase.
With bacterial culture and histopathology results pending, treatment of the patient commenced. Wounds were debrided and clean-disinfected under general anesthesia (xylazine, 2.2 mg/kg; plus ketamine 3 mg/kg; Sigma-Aldrich, India); and during the procedure, the patient received a polyionic isotonic fluid (Ringer's lactate IV; Nirlife-Aculife, Sachana, India) at a rate of 1.8 mL/kg/h IV. Amoxicillin, (20 mg/kg) (Interchemie, Venray, Holland) and enrofloxacin (5 mg/kg) (Tradeon Band, Dombivli, India) were administered, all IM, and metamizole 30 mg/kg IV (Sigma-Aldrich, India) for analgesia, postdebridement. Unceremoniously, the dog was euthanized the following day at the request of the owner.
Nonetheless, using the Bruker MALDI Biotyper, Macrococcus caseolyticus (score value: 1.84), Proteus mirabilis (score value: 2.14), and Escherichia coli (score value: 2.22) were later identified ().
Tet: tetracycline; Cot: cotrimoxazole; Crx: cefuroxime; Gen: gentamycin; Ery: erythromycin; Flx: flucloxacillin; Pen: penicillin; Amp: ampicillin; R: resistant; +: intermediate susceptibility, results are equivocal; ++: moderately susceptible, may be inhibited provided a higher dosage is used; +++: susceptible, infection may respond to treatment at normal dosage.
Histopathology demonstrated superficial fascia necrosis, mild dermal fibrosis, orthokeratotic and parakeratotic hyperkeratosis, moderate histiocytic and polymorphonuclear cell infiltration of the dermis and fascia, and presence of bacteria within the damaged fascia and dermis (Figures and ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [28.0, 'kg']}",68,64.6,71.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 28.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (28.0 kg - 20 kg) = 68.0 mL/hr.
Hence, the patient's fluid maintenance is 68.0 mL/hr."
4603,22,Maintenance Fluids Calculations,physical,decimal,pmc-5490109-1,Extracted,"A 65-year-old, 50 kg, female presented with the complaints of progressive pain and swelling over the right lower limb for the past one week following a thorn prick. This was associated with a history of high-grade fever, chills, rigor, productive cough, and mild dyspnea. She was a known case of type 2 diabetes mellitus, for which she was taking oral hypoglycemic drugs. Laboratory workup showed that the wound was infected with methicillin-resistant Staphylococcus aureus and hence, intravenous linezolid was started. Further, the wound infection was spreading upward until the knee joint hence decided for above knee amputation. On examination, the patient was conscious, drowsy, responding to commands. She was pale, febrile with temperature of 101 F, pulse rate 113/min, blood pressure 130/80 mmHg, with a mild tachypnea. Her central nervous system and cardiovascular examination were normal. Her investigations showed that she was anemic with Hb 7.8, total count was 32,500, and her platelet count was 63,000. Her renal parameters were mildly elevated with a prothrombin time (international normalized ratio) of 1.4. Her glycemic control was poor capillary blood glucose trending >250 mg/dL. On considering ongoing sepsis in the presence of active infectious focus, it was considered to do above knee amputation for infection control and as a lifesaving procedure. Central neuraxial anesthesia was deferred because of low platelet count and lack of time of correction with platelet infusions. However, in view of difficult airway with active respiratory tract infection and severe wheeze, general anesthesia was considered relatively unsafe. We administered nebulized salmeterol with budesonide to optimize the respiratory system. We planned to take up this case under peripheral nerve block alone. Hence, we did femoral nerve and lateral femoral cutaneous nerve (LFCN) blocks in supine position and sciatic nerve block in prone position with a mixture of local anesthetics. Fifteen milliliters of 0.5% bupivacaine with 15 ml 2% lignocaine 1:200,000 adrenaline and 10 ml of normal saline was prepared. We used 15 ml (femoral), 15 ml (sciatic), and 3 ml (LFCN) of the mixture, respectively, under ultrasound guidance. Regarding femoral nerve, the ultrasound probe was placed just above inguinal ligament and the nerve was blocked 2 cm above the inguinal ligament. LFCN was blocked according to classically described technique. Switching the patient to prone position, the sciatic nerve was visualized at the subgluteal region between the ischial tuberosity and greater trochanter of the femur. On checking the sensory and motor components of two major nerves were blocked satisfactorily. On specific checking for obturator nerve, there was a loss of sensation on the medial side of the knee with decreased power of adductors. Surgery was uneventful with a minimal discomfort during maneuvering of the lateral thigh which settled with 40 mg of intravenous pethidine. Intraoperative one unit packed cell, with two units each of fresh frozen plasma and platelets, was transfused. Glycemic control was achieved with intravenous short-acting insulin, and further, it was maintained with sliding scale of short-acting insulin to keep random blood glucose at 150 mg%. Nebulized drugs were continued. Platelet count improved to 100,000 the next day. Her postoperative period was uneventful.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [50.0, 'kg']}",90,85.5,94.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 50.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (50.0 kg - 20 kg) = 90.0 mL/hr.
Hence, the patient's fluid maintenance is 90.0 mL/hr."
4604,22,Maintenance Fluids Calculations,physical,decimal,pmc-6425306-1,Extracted,"A 22-year-old female was referred to our endocrine clinic with 2-year history of gradually progressive proximal muscle pain and weakness involving both upper and lower extremities. Her pediatrician had treated her with prednisone for a period of two months without any improvement. MRI of pelvis and thighs completed before her referral had shown linear hypointense foci in both proximal medial femoral necks and the right ischium consistent with insufficiency fractures. She had a normal childhood development and pubertal growth and at presentation had a height of 154cm and a body weight of 57.1kg. There was no reported family history of rickets, osteomalacia, or any other metabolic bone disease. Her menstrual history was unremarkable.
Past medical history was significant for a diagnosis of carnitine palmitoyl transferase 2 (CPT2) deficiency at the age of 14 which was diagnosed in the context of a work-up for diffuse muscle pain and weakness. At that time, she was evaluated in the Neurology clinic and was found to have low serum carnitine levels, elevated serum alanine, normal lactate, and low pyruvate levels. C16, C18:2, C18:1, and C18 levels were elevated suggesting carnitine palmitoyltransferase II deficiency. However, genetic testing was negative for the S113L variant. Results of other biochemical testing at that time were not available in her medical records. Her symptoms had reportedly completely resolved a few months after she was started on oral carnitine replacement therapy.
Physical exam did not show any apparent kyphosis or scoliosis of spine, vertebral tenderness, or hyperextensibility of joints. There were no lower extremity deformities. She had proximal muscle weakness with 4/5 strength in upper and 3/5 in the lower extremities. There was tenderness in the thighs. Her neurological exam was otherwise normal. She had a waddling gait.
Laboratory work-up revealed the following results: calcium, 9.1 (ref: 8.6-10.2 mg/dl); phosphate level, 2.0 (ref: 2.5-4.5 mg/dl); alkaline phosphatase, 243 (ref: 39-136 Units/L); bone specific alkaline phosphatase, 119.6 (ref: 0-21.3 mg/dl); 25-hydroxy vitamin D, 8.2 (ref: 30-100 ng/ml); and PTH, 145 (ref: 22-84 pg/ml). A bone density scan showed an abnormally low bone density matched for age, gender, and ethnicity with the lowest Z score of -3.3 at the left femoral neck. Vertebral fracture assessment score was within normal limits.
A 24-hour urine collection revealed low calcium of 27.6 (ref: 100-300.0 mg/24 hr) and inappropriately normal urine phosphate excretion of 445 mg/dL (ref: 400.0-1300.0 mg/24 hr). Fractional excretion of phosphate was inappropriately normal at 19% (ref: 15–20%). Renal tubular reabsorption of phosphate (TmP/GFR) was low at 0.50 (ref: 3.18-6.41 for 16- to 25-year-old females). These results suggested renal phosphate wasting as a potential etiology for osteomalacia and we considered Tumor-Induced Osteomalacia (TIO) and Hereditary Hypophosphatemic Rickets (HRR) as diagnostic possibilities. However, in the absence of any family history of rickets and her normal childhood growth and stature, rickets appeared to be less likely and subsequent work-up was directed at ruling out TIO. An Octreotide scan with SPECT imaging came back negative and was followed by F-18 FDG PET/CT scan, which too failed to reveal any tumor. However, an FGF-23 level was found to be elevated at 580 (ref: 44-215 RU/mL). The assay used is a second-generation C-terminal assay that measures both the intact FGF-23 and its C-terminal fragments. At this stage, following the negative localization studies for TIO, the patient was counseled on genetic testing to look for the possibility of hereditary hypophosphatemic rickets. She consented for the genetic testing which revealed a heterozygous known pathogenic missense variant in FGF23: c.527 G>A p. Arg176Gln (R176Q) consistent with a diagnosis of “Autosomal Dominant Hypophosphatemic Rickets”.
Genetic screens for variants in PHEX (X-linked Hypophosphatemic Rickets) and DMP-1 (Autosomal Recessive Hypophosphatemic Rickets 1) were negative. These results were therefore consistent with a diagnosis of Autosomal Dominant Hypophosphatemic Rickets (ADHR) caused by a mutant FGF23. When we informed the patient about the genetic diagnosis, she did some further research regarding her family history and found out that her father's maternal aunt and grandfather had ‘bone disorder' and were wheelchair-bound in early adulthood but her mother remained in good health and had no symptoms
She was started on Ergocalciferol 50,000 IU weekly and was encouraged to increase her dietary calcium to 1000 mg daily. She was also prescribed Potassium-Sodium-Phosphate 250 mg (8 mmol) 4 times a day. She continued to have pain and discomfort in her inner thighs. She was prescribed Diclofenac and Flexeril for pain. MRI of the pelvis was repeated to follow up on the insufficiency fractures and showed persistent bilateral femoral stress insufficiency fractures (). She was referred to orthopedic surgery and underwent pinning of bilateral femoral necks. She had significant improvement in pain and discomfort in the right thigh and groin region but still had some discomfort in the left upper thigh.
Her 25(OH)D levels normalized to 46.2 ng/ml as did her serum phosphate level (2.7 mg/dL) with oral replacement therapy.
Due to persistent pain in her left groin, she was prescribed narcotic analgesics and underwent a steroid injection of the psoas muscle by orthopedics with no relief. A repeat X-ray of pelvis showed new insufficiency fractures of the left superior and inferior rami ().
The patient had difficulty adhering to the regimen of potassium-sodium-phosphate 250 mg (8 mmol) four times daily. Therefore, she was started on calcitriol 0.25 mcg once a day. The dose of calcitriol was gradually increased up to 2 mcg per day. The patient reported significant improvement in her pain after the introduction of calcitriol to her regimen.
Although she missed a few follow-up appointments in the endocrine clinic, she was eventually seen a year later and reported feeling significantly better on the same treatment regimen of calcitriol 2 mcg daily, potassium-sodium-phosphate 250 mg (8 mmol) twice daily, vitamin D3 2000 units daily, and 600 mg of calcium supplement daily. She had complete resolution of her pain and was not on any pain medications. Her physical exam showed normal strength in the upper and lower extremities and no tenderness. Laboratory work-up at that time showed complete resolution of the previous abnormalities: serum phosphate level was 3.3 (ref: 2.5- 4.5 mg/dl); calcium, 9.4 (ref: 8.6-10.2 mg/dl); alkaline phosphatase, 88 (ref: 39-136 units/l); and 25(OH)D, 44.6 (ref: 30-100 ng/ml). A repeat X-ray of pelvis showed resolution of the previous left superior and inferior pubic rami fractures.
The patient subsequently enrolled in a clinical trial of iron supplementation for patients with ADHR at another institution. Correspondence received from that institution showed a hemoglobin 10.1 (ref: 12-15.5 g/dl), hematocrit 31 (ref: 39.4-44.5%), MCV 78 (80-96 fL), platelets 313, 000 (ref: 150,000-400,000/ml), WBC 8.400 (ref: 4,000-11,000 ml), Total Iron Binding Capacity (TIBC) 378 (ref: 240-450 mcg/dl), ferritin 6.4 (ref: 12-300 ng/ml), and percent iron saturation 3% (ref: 25-35%). These results are consistent with iron deficiency anemia. The patient has not followed up with our endocrine clinic since then and we have not been able to reach her despite multiple attempts to obtain any update on her condition following iron supplementation trial.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [57.1, 'kg']}",97.1,92.245,101.955,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 57.1 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (57.1 kg - 20 kg) = 97.1 mL/hr.
Hence, the patient's fluid maintenance is 97.1 mL/hr."
4605,22,Maintenance Fluids Calculations,physical,decimal,pmc-6414298-1,Extracted,"A 67-year-old, 115.3 kg, 157-cm female patient with papillary serous adenocarcinoma of the uterine adnexa and uterine masses was brought to the operating room for an exam under anesthesia, exploratory laparotomy, total abdominal hysterectomy, bilateral salpingo-oophorectomy, omentectomy, debulking, and lymph node dissection. Her medical history included hypertension, hemorrhoids, morbid obesity (body mass index (BMI) 46.8), and a pulmonary embolism three months prior to surgery. Enoxaparin sodium was stopped two days prior to surgery. The patient’s functional capacity was moderate to excellent at greater than or equal to four metabolic equivalents (METS). She reported completion of all household chores, cycled three to five miles daily and was capable of climbing two flights of stairs. She reported no history of anesthetic complications and no family history of anesthetic complications. Her surgical history included one previous colonoscopy, for which she received deep sedation.
The patient's home medications included prochlorperazine 10 mg as needed after chemotherapy, dexamethasone 4 mg for three days only after chemotherapy, rivaroxaban 20 mg daily, and enoxaparin 120 mg/0.8 mL solution subcutaneous (held two days prior to surgery). In addition, hydrochlorothiazide-valsartan 12.5-320 mg was taken by the patient daily for control of essential hypertension. A non-smoker, the patient reported one alcoholic beverage an average of four times per month. Her medication allergies consisted of benazepril (tachycardia), ezetimibe (myalgias), simvastatin (myalgias), and triamterene (myalgias).
Premedication for anxiolysis was accomplished with 2 mg midazolam. In the operating room, standard anesthesia monitors were applied, including non-invasive blood pressure measurement, electrocardiogram, peripheral oxygen saturation, and a temperature-sensing Foley catheter. Her baseline vital signs were a temperature of 36.94 degrees Celsius, blood pressure 138/80 mm Hg, heart rate 81 beats/min, and oxygen saturation (SaO2) 99%. Induction of general anesthesia proceeded with the administration of 180 mg of 1% propofol, 70 mg lidocaine, and 50 mcg fentanyl after preoxygenation with 100% oxygen. Tracheal intubation was facilitated with the administration of 40 mg rocuronium. A 7.0 mm cuffed oral endotracheal tube was placed with one attempt and then secured at 22 cm. The maintenance of anesthesia with sevoflurane was initiated and the patient received 10 mg of intravenous (IV) dexamethasone after the start of surgery. Mechanical ventilation with volume control was selected with 6 mL/kg and a fraction of inspired oxygen (FiO2) of 0.5. A second 18 g IV was started in the left hand and an arterial line was placed in the right radial artery with one attempt.
At the conclusion of the surgery, 400 mg IV sugammadex (3.74 mg/kg) was given as reversal for the neuromuscular blockade (the train-of-four was 0/4). Within 60 seconds, her blood pressure dropped to 58/39 mm Hg, heart rate remained stable at 80, and SpO2 dropped to 94%. Phenylephrine was titrated in 0.2 mg doses for a total of 1 mg. Intravenous fluids were administered liberally and the surgical team notified of intractable hypotension. Ischemic changes were observed in electrocardiogram (ECG) leads II and V at the same time that the heart rate began to increase. Given the presentation of symptoms in close proximity to the administration of sugammadex, the possibility of anaphylaxis was considered. At this time, 150 mcg IV epinephrine was given followed an additional dose of 100 mcg. Vasopressin two units IV was then administered to restore the blood pressure to baseline in the setting of epinephrine-induced tachycardia. Auscultation revealed clear breath sounds and there was no increase in airway pressures noted. However, a maculopapular rash was noted over the upper thorax. Greater attention was given to the possibility of anaphylaxis at this point and diphenhydramine 50 mg and famotidine 20 mg were administered. A serum tryptase level was sent to the laboratory to assist with determining the cause of the patient's symptoms. After her condition was stabilized, the patient was successfully extubated and transferred to the recovery room. A 12-lead electrocardiogram showed sinus tachycardia and a prolongation of the corrected QT (QTc) interval (Figure ).
Cardiology was consulted and the patient was observed in the intensive care unit overnight as a precaution. Dermatological manifestations resolved within a few hours. Serum tryptase from the time of the episode returned at 62 ng/mL (normal < 11.4 ng/mL), which effectively confirms that the cause of this patient's symptoms was consistent with an anaphylactic reaction. She was discharged home on postoperative Day 4 with a recommendation for follow-up with her primary care physician.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [115.3, 'kg']}",155.3,147.535,163.065,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 115.3 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (115.3 kg - 20 kg) = 155.3 mL/hr.
Hence, the patient's fluid maintenance is 155.3 mL/hr."
4606,22,Maintenance Fluids Calculations,physical,decimal,pmc-6112933-1,Extracted,"A 5-month-old girl was referred to our department for treatment of chylous ascites. She was born at full-term through vaginal delivery and bottle-fed. Her non-consanguineous parents complained that her abdomen had been presenting with gradual distension since the age of 2 months. She had received intermittent treatment at a local hospital, by receiving TPN and drainage of ascitic fluid, but was not effective. Her body weight was 5.0 kg compared to the birth weight of 3.0 kg. On examination, she presented with intensive ascites that progressed to severe respiratory distress without obvious edema (Fig. ). Erythema spots (nevus flammeus) were noticed on the chest, upper limbs, hypogastrium, and a large area of the dorsum after birth. Besides these, demarcated grayish-blue hyperpigmentations with clear-cut edges (Mongolian spots) on the back region of the shoulder, dorsum, buttocks, and lower limbs were also noticed (Fig. ). These lesions were unchanged and asymptomatic since the time of presentation. An ophthalmic examination showed bilateral blue spots on the sclera and conjunctiva (Fig. ). The extremities were symmetrical, and no hypertrophy and atrophy signs were noticed on soft tissues. Abdominal ultrasonography depicted normal findings other than the presence of massive ascites. To rule out tethered cord, we also performed spinal ultrasonography, which showed that no abnormalities were observed in the spine. A biochemical examination revealed the following: total protein, 47.5 g/L; albumin, 30 g/L; and white cell count, 4.5 × 109 cells/L with 12.2% lymphocytes. Abdominal paracentesis was performed immediately when the infant was admitted to hospital and 300 mL of straw-colored fluid was slowly aspirated (Fig. ). Routine analysis of the peritoneal fluid showed: Rivalta test (±); white blood cell count, 2683 × 106 cells/L; mononuclear leucocyte proportion, 90%; multinuclear cell proportion, 10%; and peritoneal fluid culture negative.
After the diagnosis of CCA was made, bottle feeding was stopped. At the beginning of treatment, the patient's nutrition was maintained with oral MCT-based diet. This feeding regimen can fulfill the amount of required calorie intake based on the current body weight. However, it failed to improve the condition and the patient needed repeated paracentesis every 3 to 5 days and about 300 to 500 mL straw-colored fluid was aspirated out every time. The patient was then initiated on somatostatin by continuous intravenous infusion at a rate of 4 μg/kg/h, with a subsequent plan for TPN, if the ascites did not decrease. A peripheral intravenous central catheter was inserted and TPN was started. The weight and the abdominal girth were measured every day. The abdominal girth reduced markedly from 48 cm to 40 cm during 20 days. Then we attempted to return to oral intake; however, ascites rapidly increased again and we performed repeat paracentesis. Furthermore, we completed 99mTc-human serum albumin (HAS) intestinal protein losing detection which indicated that there were no obvious signs of intestinal protein losing. Therefore, we highly suspected that the patient had a lymphatic deformity. The patient was referred to the lymphatic specialist for further investigation and treatment. Direct lymphangiography showed that the trunk of the thoracic duct was obviously dilated, and the terminal structure of the thoracic duct was chaotic. As no contrast agent was found in the blood, thoracic duct exploratory operation was conducted. Dense fibrous adhesions between the ampullary region and Pirogoff angle were found during the procedure and it was believed to result in obstruction of the thoracic duct. After removing the cellulose belt, the chylous fluid flowed from the thoracic duct into the Pirogoff angle. However, abdominal distention, caused by chylous ascites, still remained after surgery. Other unknown abnormalities of the lymphatic system were considered. However, reoperation at this tender age would have presented great risks for our patient. The child was advised to be discharged from the hospital 9 days after surgery and to continue conservative treatment. She was continually treated by abdominal cavity aspiration, and low-fat diet feeding, and the infection was controlled at the local hospital. However, she eventually died of severe peritoneal cavity infection, electrolyte imbalance, and severe malnutrition three months after being discharged from the hospital.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.0, 'kg']}",20,19,21,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.0 kg. Hence, the patient's maintenance fluid is 5.0 kg * 4 mL/kg/hr = 20.0 mL/hr.
Hence, the patient's fluid maintenance is 20.0 mL/hr."
4607,22,Maintenance Fluids Calculations,physical,decimal,pmc-3696269-1,Extracted,"A 10-year-old female patient weighing 25 kg presented with the complaints of painful swelling over lateral aspect of right chest wall and high-grade fever for past 4 days. She had tachycardia (PR 128/min) with normal blood pressure (114/71 mmHg). Her airway assessment revealed Mallampati class II, adequate mouth opening and short neck with limited head and neck movement. Local examination revealed a tense and tender swelling present over lateral aspect of right chest wall. On systemic examination, no abnormality was detected. Her investigations revealed anaemia (haemoglobin: 8.6 gm%) and leucocytosis (total leucocyte count: 19,500/mm3). A clinical diagnosis of an abscess (?pyogenic) over right chest wall was made and patient was scheduled for incision and drainage under general anaesthesia.
In the operating room, monitoring for electrocardiography, pulse oximetry and noninvasive blood pressure (by oscillometry method) was commenced by using COLIN-306 monitor. Anaesthesia was induced with fentanyl 2 μg/kg and propofol 2.5 mg/kg, and maintained with sevoflurane 1-2% in oxygen and nitrous oxide (1:1) with spontaneous ventilation on face mask through Magill's circuit. PLMA size 2.5 was inserted without muscle relaxant and cuff was inflated with 14 ml air. The bite block was kept between the incisors. Following insertion of PLMA, difficulty in spontaneous ventilation was observed with chest retraction due to airway obstruction. Her head was almost in neutral position as sniffing position was not possible due to restricted movement of head and neck. Three attempts were made to correct the position of PLMA with restricted movement of head and neck to get an unobstructed clear airway, but no success was achieved. Resistance was felt in the bag when assisted ventilation was tried following each attempt. The value of partial pressure of end-tidal carbon dioxide (PEtCO2) was zero and tracing line was touching to the base of the capnograph. The whole event of correction of position and observation of respiration took about 2 min. Meanwhile, SpO2 started dropping to a minimum of 92% on inspired fraction of oxygen (FiO2) 0.5. PLMA was removed and no difficulty on mask ventilation was observed. Her trachea was then intubated with 5.5-mm-ID cuffed endotracheal tube under the effect of atracurium (0.5 mg/kg) and intermittent positive pressure ventilation (IPPV) was started. Following intubation, anaesthesia was maintained with oxygen and nitrous oxide (1:1) with halothane (0.5-1%) through Bain's circuit. After tracheal intubation, PEtCO2 initially observed was 47 mmHg, which later on came down to 42 mmHg with normal waveform of capnograph. However, there was no improvement in SpO2 even on IPPV with FiO2 0.5. Surgery was continued. On auscultation of chest, extensive coarse crepts were observed bilaterally. After few minutes, pink frothy secretions appeared in the endotracheal tube and breathing circuit with further fall in SpO2 to a minimum value of 86% on FiO2 1. Clinical diagnosis of pulmonary oedema was made and managed with diuretic, narcotic and IPPV under atracurium.
After surgery, she was put on ventilator for IPPV with positive end expiratory pressure (PEEP) in ICU. She responded well to the therapy. She was weaned off from ventilator and her trachea was extubated after 11 h of mechanical ventilation. Her 12-lead electrocardiogram, arterial blood gas analysis (PaO2 111 mmHg, PaCO2 31 mmHg, pH 7.37) and X-ray chest were within normal limits. She was discharged from ICU after 24 h in a satisfactory condition.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [25.0, 'kg']}",65,61.75,68.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 25.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (25.0 kg - 20 kg) = 65.0 mL/hr.
Hence, the patient's fluid maintenance is 65.0 mL/hr."
4608,22,Maintenance Fluids Calculations,physical,decimal,pmc-4975905-2,Extracted,"The younger sister of the proband is a 20-month-old girl who was born after uneventful pregnancy and delivery. She presented with abnormal movement at the age of 7 weeks, in the form of focal tonic contraction on the right side with deviation of the mouth lasting from few seconds to 10 min associated with lip smacking and drooling. Antiepileptic medications including phenobarbitone, clobazam and topiramate showed partial response. The seizure attacks progressed for which she needed repeated hospital admissions. Developmentally, she could not roll, weak grasp for object and poor eye contact. Examination at 6 months of age, weight was 5.95 (−2.2 SD) length was 63.5 cm (−0.99 SD) and head circumference was 42 cm (0.16 SD). She had no dysmorphic features, no facial asymmetry. There was poor head control with increased tone and brisk reflexes in all limbs. At 8 months, she was admitted with acute bronchiolitis needing PICU admission for non-invasive ventilation; she had swallowing assessment for which she was started on nasogastric tube feeding. Currently, she is having severe psychomotor retardation and epileptic encephalopathy. Brain MRI showed progressive demyelination and atrophy of both frontal and temporal areas. (Fig. , ).
At 16-month of age, she was admitted to PICU due to fever, acute respiratory failure and intractable Epilepsy. During this admission, she was seen by Gastroenterology team due to history of choking, gagging and aspiration. She had a G-tube and is currently entirely fed through a G-tube and nothing by mouth. In addition, she also seen by Orthopedics due to her healing right proximal humerus fracture and was noted to have mild neurogenic scoliosis. On exam, length was 85.1 cm, weight was 15.2 kg and head circumference was 48.5 cm. She had contractures of all 4 limbs. She was alert, but not interactive, sitting in a wheelchair. Strength was 2 in all extremities with normal muscle bulk and tone. Deep tendon reflexes were 2+ in the upper and lower extremities, and 3+ reflexes in the ankles with sustained clonus at the left and right. She had positive Babinski bilaterally.
She had plasma lactate, T4, TSH, AST, ALT, vitamin D, urine for organic acids, plasma and urine amino acids, CGH array, all were normal. EEG showed electro-clinical generalized tonic seizure, multiple myoclonic generalized seizures, multifocal spikes, generalized fast spikes, continuous generalized slowing, lack of normal sleep elements, and diffuse encephalopathy. A 24-h EEG showed 8 generalized spasms or tonic seizures per hour with multi-focal spikes while awake, and discontinuity of the background during sleep.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15.2, 'kg']}",50.4,47.88,52.92,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15.2 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.2 kg - 10 kg) = 50.4 mL/hr.
Hence, the patient's fluid maintenance is 50.4 mL/hr."
4609,22,Maintenance Fluids Calculations,physical,decimal,usmle-1385,Extracted,"A 34-year-old woman with HIV comes to the emergency department because of a 2-week history of diarrhea and abdominal cramping. She has had up to 10 watery stools per day. She also has anorexia and nausea. She returned from a trip to Mexico 4 weeks ago where she went on two hiking trips and often drank from spring water. She was diagnosed with HIV 12 years ago. She says that she has been noncompliant with her therapy. Her last CD4+ T-lymphocyte count was 85/mm3. She appears thin. She is 175 cm (5 ft 9 in) tall and weighs 50 kg (110 lb); BMI is 16.3 kg/m2. Her temperature is 38.3°C (100.9°F), pulse is 115/min, and blood pressure is 85/65 mm Hg. Examination shows dry mucous membranes. The abdomen is soft, and there is diffuse tenderness to palpation with no guarding or rebound. Bowel sounds are hyperactive. Microscopy of a modified acid-fast stain on a stool sample reveals oocysts.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [50.0, 'kg']}",90,85.5,94.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 50.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (50.0 kg - 20 kg) = 90.0 mL/hr.
Hence, the patient's fluid maintenance is 90.0 mL/hr."
4610,22,Maintenance Fluids Calculations,physical,decimal,pmc-7728615-1,Extracted,"A 10-week-old female African leopard, weighing 3.2 kg, was referred for a 40-day history of lameness in the right pelvic limb, with no description of trauma. Clinical examination under mild sedation of intramuscular combination of dexmedetomidine 5 μg/kg and ketamine 1 mg/kg revealed swelling at the cranio-medial aspect of the right tibial. Medio-lateral and caudo-cranial radiography views of the right pelvic limb confirmed a malunion of tibial and fibular diaphyseal fractures resulting in a tibial varus/procurvatum deformity, probably due to nutritional secondary hyperparathyroidism. On the basis of physical examination, hematology and biochemistry, and echocardiography, the leopard was deemed healthy (American Society of Anesthesiologists status II). Closing wedge osteotomy and internal fixation with a 2.7 locking plate system (Synthes, Ltd.) were scheduled 10 days after admission. Meanwhile, confinement in a small and controlled area, oral gabapentin (10 mg/kg twice daily) for analgesia, and administration of specific diet to correct nutritional hyperparathyroidism were instituted.
On the day of surgery, food was withheld for 4 h and water was not restricted prior to general anesthesia. The leopard (weighing 3.8 kg) received an intramuscular combination of 5 μg/kg dexmedetomidine, 2 mg/kg of ketamine, and 0.2 mg/kg of methadone, using a squeeze cage for feral cats, to achieve sufficient sedation to allow intravenous (IV) cephalic catheter (20 G) placement.
General anesthesia was induced with IV propofol 1% (1.8 mg/kg) to enable tracheal intubation with a 5-mm cuffed endotracheal tube (ETT). The ETT was connected, via a heat and moisture exchanger/filter (HME), to a rebreathing circuit and mechanical ventilation was provided with a small animal ventilator (Merlin Small Animal Ventilator) using a volume-cycled mode with f r set to maintain PECO2 between 35 and 42 mmHg with a tidal volume (VT) of 35 ml. Peak inspiratory pressure (PIP) was maintained below 10 cmH2O and isoflurane in 60% oxygen was administered to maintain anesthesia, guided by a neuronal function monitor (SEDLine™, Masimo, Irvine, CA), throughout surgery.
A multiparameter monitor (S5 Compact Anesthesia Monitor; Datex-Ohmeda, Florida, USA) was used throughout the anesthetic period to monitor lead II electrocardiogram, capnography, end-tidal isoflurane, pulse-oximetry, esophageal temperature, and non-invasive arterial blood pressure until cannulation of the left dorsal pedal artery with a 22-gauge catheter permitted invasive arterial blood pressure measurement. A Masimo Radical 7 monitor was used to measure perfusion index (Pi) and Patient State index (PSi). Body temperature was maintained between 36 and 37.5°C using a warm air blanket (Bair Hugger 505 Warming Unit, 3M, Germany). Physiological parameters recorded during general anesthesia are summarized in . Ringer lactate solution was administered IV at 3 ml/kg/h. Intraoperative rescue analgesia was planned as bolus administration of fentanyl (3 μg/kg IV) in response to an increase of HR or mean invasive blood pressure (mIBP) >20%.
Anesthetic depth was monitored using PSi (SEDLine™, Masimo monitor) and by evaluating clinical signs such as palpebral reflex, eye position, and ear twitch reflex. After aseptic preparation of the lateral and medial thigh area, sciatic, and saphenous nerve blocks were performed.
To provide perioperative analgesia, US-guided sciatic and saphenous nerve blocks were attempted as previously described (). An US machine (Sonosite® M-Turbo, Fujifilm, Netherlands) equipped with a 25 mm linear-array transducer (10–6 MHz) was used.
The sciatic nerve block was performed with the leopard positioned in left lateral recumbency. The probe (10 MHz) was positioned distal to the femoral greater trochanter, with a transverse orientation to the long axis of the limb. The sciatic nerve showed two components, the tibial and common peroneal nerves, that appeared as round to oval, hypoechoic structures surrounded by hyperechoic connective tissue positioned cranially to greater trochanter. The needle (Bbrown® 0.7 ×50 mm, 21-gauge ×30°), connected to a peripheral nerve stimulator (Plexygon Nerve Stimulator, Vygon®, France), was introduced in-plane and advanced in a cranial direction through the semitendinosus muscle, until its tip was positioned close to the sciatic perineural tissues and the threshold current for stimulation was >0.3 and <0.5 mA (). Ropivacaine 0.5% (0.15 mg/kg) was administered after a negative aspiration test and in the absence of resistance to injection ().
The saphenous nerve block was performed with the leopard in the same position, with the right pelvic limb abducted 90° and extended caudally. The probe (10 MHz) was placed perpendicular to the long axis of the limb, at the medial part of the limb at the level of the middle third of the femur. The femoral artery and vein were localized, and the saphenous nerve cranial to them. The needle (Bbrown® 0.7 ×50 mm, 21-gauge ×30°) was introduced in an in-plane approach and advanced in a craniocaudal direction (). Ropivacaine 0.5% (0.15 ml/kg) was administered after a negative aspiration test and in the absence of resistance to injection ().
Physiological parameters remained stable intra-operatively (), and end-tidal isoflurane concentration ranged between 0.6 and 0.9%. The anesthetic plane was considered light during the surgical procedure, with persistent slight palpebral reflex, ventral rotation of the eye, and absence of swallowing reflex, muscle movement, lacrimation, and ear twitch reflex. However, rescue analgesic administration of fentanyl was not required. Total duration of anesthesia was 150 min, and surgery lasted 100 min. The ETT was removed 12 min after discontinuing isoflurane, when swallowing reflex appeared, and then the leopard was transferred to a dedicated cage to fully recover from anesthesia. Recovery was uneventful and no clear signs of discomfort or licking of the right pelvic limb were observed. Motor function of the quadriceps muscle appeared not to be affected, while paralysis and proprioception deficit distal to the stifle suggested motor and sensory blockade lasting for 6 h postoperatively. Postsurgical analgesia was achieved through a single injection of IM buprenorphine (15 μg/kg) and subcutaneous meloxicam (0.1 mg/kg), administered immediately after extubation. Gabapentin (10 mg/kg orally twice daily) was administered for 10 days, starting the day after surgery. Amoxicillin and clavulanic acid (20 mg/kg) were administered IV after placing the intravenous catheter and administered orally twice for 5 days after surgery. The postoperative physical and radiographic check at 6 weeks after surgery demonstrated correct position of the implant and bone healing, and the animal was no longer lame.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.8, 'kg']}",15.2,14.44,15.96,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.8 kg. Hence, the patient's maintenance fluid is 3.8 kg * 4 mL/kg/hr = 15.2 mL/hr.
Hence, the patient's fluid maintenance is 15.2 mL/hr."
4611,22,Maintenance Fluids Calculations,physical,decimal,pmc-3284047-1,Extracted,"A 5-month-old male patient weighing 6.78 kg was admitted with a complaint of generalized tonic–clonic seizure for 4–5 times per day for 5 days in pediatric ward of Sir Takhtsinhji General Hospital, Bhavnagar, Gujarat. The patient had an altered sensorium with normal pulse and respiratory rate. Pupil was constricted and poorly reacting to light. Parents revealed the history. The child was vaccinated for the first dose of DPT before 16 days. After 3 days of vaccination, the child developed seizures and admitted to the nearby community health center (CHC) for 9 days. The patient was discharged after the control of seizures and was at home for 3 days without any treatment. Treatment detail is not available on admission at CHC. Reappearance of seizures occurred at home. After that the patient was admitted and treated with phenytoin, methyl prednisolone, and levetiracetam in private hospital at Bhavnagar. Afterward the patient was transferred to our center for further management. There was no history of head injury, trauma, tuberculosis, febrile convulsion, and ear discharge. There was no previous history of seizure before DPT vaccination. Provisional diagnosis as postvaccination encephalopathy was made. Investigations, such as total leukocyte count, differential leukocyte count, red blood cell (RBC) count, packed cell volume, RBC indices, platelet count, erythrocyte sedimentation rate, peripheral smear examination, random blood sugar, liver function tests, renal function tests, and cerebrospinal fluid examination were normal except hemoglobin (10.5 g/dL; reference value: 12.0–18.0 g/dL), LDH (439 IU/L; reference value: 180–360 IU/L), CK-MB (95 IU/L; reference value 18–51 IU/L), and ionized calcium (1.06 mmol/L; reference value: 1.16–1.32 mmol/L). Postreaction CT-scan of brain, MRI of brain and electroencephalogram were normal. The patient was treated with midazolam, phenytoin, levetiracetam, phenobarbitone, and clobazam. After omitting clobazam, clonazepam was added to control seizures at day 5. Acyclovir and methyl prednisolone were started as empirical therapy on the 2nd day of admission. From 7th day onward prednisolone was started. Seizure frequency reduced from 2nd day and last episode occurred on the 13th day. The patient became fully conscious on 8th day. The patient was discharged on 15th day. The patient was followed at 3 months and found without any neurological sequel.
Naranjo's scale showed that the relationship between DPT and acute encephalopathy was probable.[] According to Brighton criteria for vaccine-induced encephalopathy, the present adverse event was of level 3.[] According to Modified Schumock and Thornton's criteria, this reaction was definitely preventable and Modified Hartwig and Siegel's scale showed that the reaction was moderately severe.[]","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.78, 'kg']}",27.12,25.764,28.476,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.78 kg. Hence, the patient's maintenance fluid is 6.78 kg * 4 mL/kg/hr = 27.12 mL/hr.
Hence, the patient's fluid maintenance is 27.12 mL/hr."
4612,22,Maintenance Fluids Calculations,physical,decimal,pmc-8588840-1,Extracted,"A 14 week-old, 10.8 kg male intact American Pit Bull Terrier was evaluated for suspect pit viper envenomation. The puppy was unsupervised outside for 2 h and found limping on his left hindlimb with two bleeding punctures over his fourth digit. Physical examination revealed left pelvic limb weight-bearing lameness with hemorrhagic lymphedema around two punctures on the left hind paw. The mentation and vitals were normal. A pain score (Colorado State University Acute Pain Scale) of 1/4 was assigned. Clinicopathologic abnormalities included: mild hyponatremia (140 mmol/L, reference range 146–151 mmol/L), mild hypochloremia (105 mmol/L, reference range 108.5–116 mmol/L), mild anemia [packed cell volume (PCV) 32%, reference range 33–55%] without hemolysis, and moderate hypoproteinemia [total solids (TS): 48 g/L (reference range 65–80 g/L); 4.8 g/dL (reference 6.5–8 g/dL)]. The activated clotting time (ACT) was normal (96 s (s); reference range 80–120 s). A snakebite severity score (SSS) was 1/20. One vial of F(ab)2 antivenom (VenomVet®, MT Venom, LLC) was diluted in 60 mL 0.9% saline (0.9% sodium chloride, Abbott Laboratories) and administered intravenously (IV) over an hour as the potential envenomation occurred within 30 min to 2 h prior to presentation and there was concern for progression in the subacute setting. Six hours later, the SSS was 2/20. The puppy was maintained on IV lactated Ringer's solution (LRS) (Lactated Ringer's Solution, Baxter Laboratories) at 4 mL/kg/h and methadone (Methadone hydrochloride, Mallinckrodt Inc) (0.25 mg/kg IV) when pain scores exceeded 1.5/4. No progression of envenomation or adverse reactions to antivenom occurred and the puppy was discharged 20 h later.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.8, 'kg']}",41.6,39.52,43.68,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.8 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.8 kg - 10 kg) = 41.6 mL/hr.
Hence, the patient's fluid maintenance is 41.6 mL/hr."
4613,22,Maintenance Fluids Calculations,physical,decimal,pmc-4152690-2,Extracted,"The second case is a 66-year-old, 115 kg man, BMI 30, was transferred, from an outside hospital, on vasopressors for hypotension during a flare of ulcerative colitis. His comorbidities included multi-vessel coronary artery disease status post-myocardial infarction with left anterior descending stent 14 years prior. He also had chronic systolic heart failure with an ejection fraction of 30%, an automatic implantable cardioverter defibrillator for ventricular tachycardia, obstructive sleep apnea, ulcerative colitis, hyperlipidemia, gastro-esophageal reflux disease (GERD), chronic anemia, osteoarthritis and an abdominal aortic aneurysm. Medications included chronic steroids, a beta blocker, aspirin, a statin, amiodarone, an immunomodulator and nitrates. His hospital course included a hospital acquired pneumonia requiring 3 days on a ventilator and diuresis for volume overload. He also developed bilateral pulmonary emboli, a gastrointestinal (GI) bleed after heparinization and underwent inferior vena cava filter placement. After he was stabilized, extubated and weaned from pressors, he underwent a loop ileostomy under TAP block.
His TAP block was performed, using a 20 gauge, 8 cm Stimuplex needle, with one attempt. A total of 60 mL of local anesthetic was injected in divided doses. This included a 30 mL mixture of 0.25% ropivicaine and 1% lidocaine in a 50/50 mix on each side. The block was successfully performed by a 1st year anesthesia resident without any complications. Total procedure time from preparation for the block to completion of the block was 10 min. During the block itself, the patient received intravenous sedation, including 2 mg midazolam and 75 mcg fentanyl. He received no further sedation during the 1.5 h surgery. The patient remained hemodynamically stable throughout the procedure. His diet was advanced on the first post-operative day and he was discharged home on the post-operative day 7.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [115.0, 'kg']}",155,147.25,162.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 115.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (115.0 kg - 20 kg) = 155.0 mL/hr.
Hence, the patient's fluid maintenance is 155.0 mL/hr."
4614,22,Maintenance Fluids Calculations,physical,decimal,pmc-4154290-1,Extracted,"An eighteen year old boy, born out of non-consangious marriage, first in birth order, born at term by vaginal delivery with normal perinatal history and normal motor and mental mile stones, was admitted in accident and emergency department with history of progressively worsening crampy leg pain from one month, increased frequency of micturation and increased thirst for last three weeks. There was history of inability to move his limbs from last 3 days. There was no history of rash, headache, fever, vomiting, diarrhea, and weight loss and bladder or bowel incontinence. There was no history of any drug or herbal medicine intake. On examination, patient was conscious, cooperative and well oriented in time, place and person. General physical examination revealed pulse 92 per minute, blood pressure 110/70mmHg and respiratory rate of 16 per minute. There were bony deformities in the form of widening of bilateral wrists and bilateral knock-knees. Chest, cardiovascular and abdominal examinations were unremarkable. Nervous system examination revealed normal higher mental functions and no cranial nerve deficit. Motor examination revealed hypotonia and a power grade of 3/5 in both arms and 2/5 in both lower limbs. Deep tendon reflexes were depressed all over and bilateral planter response was flexor. Differential diagnosis in our patient included hypokalemic periodic paralysis, myositis and renal tubular acidosis. Laboratory investigation revealed random blood glucose of 112 mg/dl, serum sodium 144 mmol/liter, serum potassium 1.3 mmol/liter, pH 7.30, serum bicarbonate 20.3 mmol/liter, serum chloride 112 mmol/liter, partial pressure oxygen 83 mmHg, oxygen saturation of 93% and partial pressure carbon dioxide 34 mmHg. Haemogram, kidney function and liver function tests at presentation are depicted in (). Muscle enzymes in the form of Creatine phosphokinase (CPK) were 1823 U/liter (0-195) and Lactate dehydrogenase (LDH) 886 U/liter (100-235). In view of severe hpokalemia, patient was immediately started on intravenous potassium chloride infusion at a rate of 30 meq/hour and oral potassium was started simultaneously in a dose of 20 meq 6 hourly. There was a predictable improvement in muscle weakness after initiation of potassium therapy and patient became ambulatory after 24 hours of treatment. In view of severe hypokalemia, systemic acidosis and skeletal deformities, a strong possibility of renal tubular acidosis was made. Subsequently, patient was subjected to anthropometric examination which revealed severe disproportionate short stature () with height of 144 cm (<3rd centile, standard deviation score (SDS)=-4.30), upper segment (74 cm), lower segment (70 cm), upper segment to lower segment ratio (1.05), arm span (142 cm), head circumference (52 cm) and mid parental height of 162 cm. Patient´s weight was 33 kg with a body mass index (BMI) of 15.9 kg/m² (<3rd centile, SDS=-2.85). Patient had well developed secondary sexual characters in the form of pubic hair stage 5, stretched penile length (SPL 10 cm), bilateral testicular volume >15ml. Hearing tests in the form of Rinne and Weber and ophthalmic tests including Schirmer’s test were unrevealing. 24 hour urinary calcium was 472 mg per day, urinary creatinine 702 mg per day, urinary phosphorus 824 mg per day and urinary protein of <50mg per day and no glycosuria. After correcting hypokalemia, there was further fall in serum pH to 7.27 with serum bicarbonate of 16.5 mmol/litre. Urinary pH at this time was 7.0.Abdominal ultrasonography (USG) revealed bilateral medullary nephrocalcinosis. Digital abdominal X- ray revealed fine calcified foci in bilateral renal area (). Skeletal survey revealed widening of both wrists and bilateral knock knees (). In view of severe hypokalemia and normal anion gap (12 mmol/litre) hyperchloremic metabolic acidosis and inability to acidify urine with associated hypercalciurea and no apparent secondary cause, a diagnosis of primary distal renal tubular acidosis was made. However exact etiological diagnosis could not be established because of unavailibity of genetic testing in our Centre.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [33.0, 'kg']}",73,69.35,76.65,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 33.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (33.0 kg - 20 kg) = 73.0 mL/hr.
Hence, the patient's fluid maintenance is 73.0 mL/hr."
4615,22,Maintenance Fluids Calculations,physical,decimal,pmc-5859759-1,Extracted,"A 57-year-old gravida 6, para 3, Asian Taiwanese woman presented to our hospital for scheduled surgery due to endometrial cancer. At admission, her body temperature was 36.8 °C, pulse rate 78 beats/minute, respiratory rate 20/minute, and blood pressure 136/98 mmHg. Her family and environmental history were unremarkable. She did not receive surgery before nor take any medication for systemic disease, such as diabetes mellitus or hypertension. She was a housekeeper. She did not smoke tobacco or consume alcohol. On physical examination, she had normal breathing sound, without wheezing or crackle, and a regular heartbeat without murmur. Her abdomen was soft with normoactive bowel sound on auscultation. Her extremities were freely moveable without edema. She exhibited severe morbid obesity (body weight, 128.4 kg; height, 155.7 cm; BMI, 52.9 kg/m2). Her daily activities were independent most of the time, except for some episodes of exertional dyspnea. Computed tomography (CT) revealed a ventral hernia with a large fascial defect (Fig. ). There were no clinical symptoms, such as abdominal pain or tenderness. She underwent total abdominal hysterectomy, bilateral salpingo-oophorectomy, and ventral herniorrhaphy with Goretex mesh (GORE DUALMESH®).
Her early postoperative course was smooth. She consumed water on postoperative day (POD) 3, a clear-liquid diet on POD5, and a semi-liquid diet on POD7. She began bedside ambulation, and half of her stitches were removed on POD10. However, progressive dyspnea was noted after bedside ambulation. Intra-abdominal free air with elevation of right-side hemidiaphragm was noted by chest X-ray (Fig. ) on POD14. There was no abdominal tenderness or rebounding pain, but there was moderate abdominal distension. She was kept under close observation and began nil by mouth (NPO) for possible visceral perforation.
Two days later (POD16), severe dyspnea and extensive abdominal distention were noted. Her respiratory rate was elevated to 26/minute with accessory muscle use. Arterial blood gas analysis (under simple O2 mask, 10 L/minute) showed: pH, 7.42; partial pressure of carbon dioxide in arterial blood (PaCO2), 44.8 (mmHg); partial pressure of oxygen in arterial blood (PaO2), 86.2 (mmHg); bicarbonate (HCO3-), 28.5 (mmol/L); blood oxygen saturation (SpO2), 96.7%; and blood pressure, 102/75 mmHg. Laboratory tests revealed leukocytosis with a white blood cell (WBC) count of 12,900/uL, hemoglobin (Hb) 12.6 g/dL, and platelet count 310,000/uL. Her C-reactive protein (CRP) was elevated at 165.7 mg/dL. Serum creatinine was 0.99 mg/dL, while serum sodium was 131 mmol/L, and potassium was 3.9 mmol/l. A physical examination showed severe abdominal distension without rebound pain. A pelvic examination demonstrated good healing of the vaginal cuff without leakage. CT showed a large amount of intra-peritoneal free air with little ascites (Fig. ). Because clinical visceral perforation was less likely, under the impression of pneumoperitoneum, in this emergent situation, an 8-Fr. pigtail catheter was inserted under CT guidance for decompression. A massive amount of gas was drained. Subsequently, her dyspnea and abdominal distention dramatically subsided. She re-started oral intake on POD20, and the abdominal pigtail catheter was removed on POD24 after no more free air was revealed by chest X-ray. No further abdominal distention was noted, and she was discharged on POD28. The clinical course of the endometrial cancer and repaired hernia were well at the 1-year follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [128.4, 'kg']}",168.4,159.98,176.82,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 128.4 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (128.4 kg - 20 kg) = 168.4 mL/hr.
Hence, the patient's fluid maintenance is 168.4 mL/hr."
4616,22,Maintenance Fluids Calculations,physical,decimal,pmc-7737305-1,Extracted,"A 37-year-old man who was 172 cm tall and weighed 62 kg, BMI 21.5 kg/m2 underwent video-assisted thoracoscopic right upper posterior segmentectomy with systematic mediastinal lymphadenectomy. His had no history or ongoing (chronic) health problems like hypertension, diabetes mellitus, cerebrovascular disease and atrial fibrillation (AF). He had a smoking history of 15 pack-years. A an 8-mm ground-glass opacity (GGO) lesion had been identifed at the posterior segment (S2) of the right upper lobe during incidental computed tomography (CT) screening 6 months prior to his presentation to us. The ground-glass nodules grew slightly during the follow-up period (Fig. a). Results of all preoperative laboratory tests including electrocardiogram, blood examination and urine examination were within normal limits. Platelet function tests were not performed.
During the surgery, the patient was placed in the left lateral decubitus position with the arms extended to 90°. General anesthesia was induced, and intubation was achieved via a double-lumen endobronchial tube. The first stage of this operation was opening the oblique fissure. Incomplete oblique fissure was divided via endoscopic stapler (Ethicon ECHELON FLEX™ ENDOPATH EC60A stapler, blue staples). We exposed the central vein, V2a and V2b but not found and isolated the draining veins of posterior segment (S2) specifically (Fig. b). Next the pulmonary artery was dissected distal to expose the posterior segmental artery(A []). The A2 was then dissected, and ligated by hemolok. Then the posterior segmental bronchus was dissected from right superior lobar bronchus. Before closing the bronchus with the stapler, we ventilated the right lung to confirm the target bronchus. The B2 was then transected by stapler (Ethicon ECHELON FLEX™ ENDOPATH EC60A stapler, green staples). Then, the S2 parenchyma was divided followed the inflation-deflation method by stapler (Ethicon ECHELON FLEX™ ENDOPATH EC60A stapler, blue staples) []. The specimen was retrieved in a self-made bag using a surgical glove. Examination of a frozen section confirmed lung adenocarcinoma; Systematic mediastinal lymphadenectomy was then performed. The total operation time was 1 h, 15 min. The postoperation pathological diagnosis of the tumor was adenocarcinoma (pT1aN0M0-stage IA1 as defined by the 8th Edition of TNM classification (TNM8) of lung cancer) [].
After surgery the patient returned to the intensive care unit. 20 h later, Mild consciousness disturbance [Glasgow Coma Scale, 11 points (E3V2M6)], conjugate deviation of the eyes to the left, right hemiplegia (Manual Muscle Testing upper limbs score of 1 of 5 and lower limbs score of 0 of 5), mixed aphasia were observed, with National Institutes of Health Stroke Scale score of 23. His vital signs were a blood pressure of 118/67 mmHg, a heart rate of 107 /min, a respiration rate of 17 /min and SpO2 of 100% with nasal catheter oxygen at 4 L/min. Emergent head enhanced CT showed left middle cerebral artery M1 occlusion (Fig. a). The left middle cerebral artery were not visualized in intracranial vascular computed tomography angiography (CTA). Considered the risk of hemorrhage in the postoperative period, we decided to perform IAMT. Trombus at the M1 branch of the middle cerebral artery were removed successfully, and successful recanalization was achieved (Fig. b, c). A pathological examination after the operation showed the thrombus were mainly composed of laminar fibrin, abundant neutrophils, and erythrocytes (Fig. ).
The patient was observed in the intensive care unit for 3 days. The patient’s Mental status and motor function gradually improved. During this time, We performed some physiological examinations including Holter electrocardiography, transthoracic echocardiography, venous ultrasonography, carotid artery ultrasonography, and also checked blood tests such as coagulation function, and autoantibodies of collagen diseases. However, no anatomic abnormality or thrombophilia factors were observed. Three days after thrombus removal, his NIHSS score was 0. Follow up brain CT were done, and there was no significant findings. The patient was discharged without major complications after rehabilitation training for 7 days.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [62.0, 'kg']}",102,96.9,107.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 62.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (62.0 kg - 20 kg) = 102.0 mL/hr.
Hence, the patient's fluid maintenance is 102.0 mL/hr."
4617,22,Maintenance Fluids Calculations,physical,decimal,pmc-7213938-2,Extracted,"GBSA, a female of 61 years old with ESRD due to hypertensive nephrosclerosis, underwent deceased donor KTx in December 2015. She received antithymocyte globulin induction immunosuppression at a total dose of 6 mg/kg body weight, 3 plasmapheresis sessions, and IVIG at total dose of 2 g/kg, as well as maintenance therapy with tacrolimus, everolimus, and prednisone, progressing without complications until hospital discharge.
About one year after KTx, she was admitted to the hospital with dry cough, low fever, hyporexia, asthenia, and polyarthralgia for 1 month; she had lost approximately 6 kilos in this period. Previous examinations revealed anemia and thrombocytopenia (). She was then hospitalized for evaluation, diagnosis, and clinical support.
At admission, the patient was feverish, tachypneic, tachycardic, and pale. She had lung auscultation crackles in the lower right third and abdomen dullness to percussion over Traube’s space. Antibiotic therapy was started with levofloxacin after evaluation and suspected diagnosis of community-acquired pneumonia. Admission examinations revealed persistence of bicytopenia, in addition to hyperferritinemia and hypertriglyceridemia. Renal function was preserved. Total abdominal ultrasonography confirmed the presence of homogeneous splenomegaly. The patient followed with progressive clinical worsening (persistence of fever, tachycardia, and hypotension). Antibiotic therapy with piperacillin-tazobactam and later with meropenem was scaled-up due to unsatisfactory clinical response. Given the cytopenia, a myelogram was performed two weeks after admission, which revealed hypercellularity and hematopoiesis, increased macrophage activity, and bone marrow with reactive characteristics (). HLH secondary to an unknown infectious process was diagnosed. Mycoculture was negative. Concomitantly, increasing levels of galactomannan in blood led to the initiation of antifungal therapy with voriconazole for aspergillosis. Therefore, IVIG at 2 g/kg body weight, divided into 3 doses, was initiated combined with the specific therapy, and immunosuppression was reduced (suspension of everolimus and maintenance of tacrolimus and prednisone).
After these measures, the patient clinical status improved significantly, with reduction of inflammatory markers and gradual improvement of hematological dysfunction ().
However, after 40 days of hospitalization, the patient had a massive pulmonary aspiration, clinical worsening, and death one week after the event.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.0, 'kg']}",24,22.8,25.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.0 kg. Hence, the patient's maintenance fluid is 6.0 kg * 4 mL/kg/hr = 24.0 mL/hr.
Hence, the patient's fluid maintenance is 24.0 mL/hr."
4618,22,Maintenance Fluids Calculations,physical,decimal,pmc-6319055-1,Extracted,"A 52-year-old menopausal female weighing 50 kg (body mass index [BMI] = 21.5 kg/m2) posted for tonsillectomy and adenoid resection was referred by the ear, nose, and throat surgery department to the anesthesia preoperative clinic for evaluation. The patient presented with chief complaints of snoring, difficulty in breathing during sleeping, and irritation of the throat for 5 months. In addition, she also complained of dyspnea on exertion with mild-to-moderate activity. The patient was a tobacco chewer for 40 years and had undergone tubal ligation in the past which was uneventful.
Airway examination revealed a mouth opening of three fingers, a Mallampati grade of 3 with bilateral tonsillar enlargement, and a normal thyromental distance. There was no restriction in movement at the joints in the neck/spine. The cervical spine X-ray in the lateral view revealed enlarged adenoids.
Inside the operation theater after attaching the monitors for plethysmograph, capnograph, electrocardiogram, and noninvasive blood pressure, the patient was preoxygenated. The patient was then premedicated with injections glycopyrrolate (0.2 mg), midazolam (1 mg), and fentanyl (2 μg/kg) intravenously, followed by induction with propofol (2 mg/kg) intravenously. After checking for adequate ventilation, the patient was given muscle relaxant intravenous succinylcholine (100 mg). A direct laryngoscopy was performed with Macintosh blade size 4, but the vocal cords were not visualized. The patient was mask ventilated, followed by a direct laryngoscopy with McCoy blade size 4, and tracheal intubation was attempted with the help of a gum-elastic bougie that failed. The patient was mask ventilated again, and AmbuR aView™(Ambu A/S, Baltorpbakken) was used through the nasal approach that failed to be negotiated. The patient was mask ventilated again followed by negotiation of AmbuR aView™(Ambu A/S, Baltorpbakken) through the mouth where the epiglottis was seen, but the vocal cords were not clearly visualized as a result of the surrounding edema. A cuffed endotracheal tube of size 7.5 mm was threaded over the AmbuR aView™(Ambu A/S, Baltorpbakken) and was successfully placed. During the surgery, adenoid resection was performed with tonsillectomy. At 6 weeks' follow-up, the patient reported moderate improvement in the symptoms of snoring and difficulty in breathing during sleeping.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [50.0, 'kg']}",90,85.5,94.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 50.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (50.0 kg - 20 kg) = 90.0 mL/hr.
Hence, the patient's fluid maintenance is 90.0 mL/hr."
4619,22,Maintenance Fluids Calculations,physical,decimal,pmc-2769482-1,Extracted,"A 73-year-old Caucasian male presented to the Emergency Department (ED) in June 2008 with a history of collapse without loss of consciousness while mobilizing to the toilet in the early hours of the morning. This occurred on the background of a 6 day history of general unwellness. He was conscious and orientated on arrival but was slightly drowsy. Other than clinical features of dehydration and mild central abdominal adiposity with a waist: hip ratio of 1.04, there were no other significant clinical signs. His random plasma glucose (RPG) on arrival was 59.1 mmol/L. His height was 1.76 meters (m) and weight was 90 kilograms (kg) making the body mass index (BMI) 29.0 kg/m2. The patient was previously fit and well without any known co-morbidities. He was on no regular medication. There was no family history of diabetes or other significant conditions. He was a non-smoker and consumed no alcohol. He works as a farm equipment evaluator. There was no history of specific weight loss over the preceding months. His general practitioner (GP) had performed a fasting plasma glucose test on him in February 2008 which showed a value of 6.4 mmol/L. This was repeated within 2 weeks and the repeated value was 6.1 mmol/L. Glycosylated haemoglobin (HbA1c) was also done and was 6.3%. Subsequent 75 gram (g) oral glucose tolerance test (OGTT) produced a value of 15.3 mmol/L, 14.1 mmol/L and 7.6 mmol/L 30 minutes, 1-hour and 2-hours post glucose load respectively. He was managed with dietary modification and exercise.
His sodium (Na) was 150 mmol/L, potassium (K) 4.6 mmol/L, urea 26.1 mmol/L and creatinine (Cr) 237 micromol/L. Calculated osmolality was 394.4 mOsm/kg. Arterial blood gas sampling (ABG) showed a pH of 7.36, pCO2 4.9 kPa, pO2 11.0 kPa, bicarbonate 20 mmol/L and BE -1 mmol/L. Lactate was mildly elevated at 1.4 mmol/L. β-hydroxybutyrate (β-OHB) was slightly elevated at 3.67 mmol/L. Repeat HBA1c was 8.1%. Besides a small amount of ketones and glycosuria, urine testing revealed nil else of concern. Full septic screen was done; white cell count (WCC) and differential showed mildly raised WCC at 12.5 × 109 and neutrophils at 10.9 × 109 with the rest of differential count being normal, CRP was 4, urine microscopy, culture and sensitivity was normal and chest radiograph was normal. Thyroid function was normal. Lipid profile was also normal.
The patient was diagnosed with T2DM based on his presentation, age and absence of anti-Glutamic Acid Decarboxylase 65 (Anti-GAD 65), Insulinoma Antigen-2 (IA-2) and Islet Cell (ICA) antibodies. His acute presentation was consistent with hyperglycaemic hyperosmolar state (HHS) and acute renal failure secondary to dehydration. He was treated with intravenous insulin and intensively rehydrated with close attention to electrolyte balance. He improved considerably and renal function normalized. He was started on Metformin 500 mg twice daily (BID) increasing to 1 g BD and Penmix 30 subcutaneous insulin at a dose of 12 units BD increasing to 30 units BD. 5 days after the acute event, a 1 mg intravenous (IV) glucagon stimulation test was done at 9.00 am with blood samples for glucose and C-peptide taken at baseline, 5, 10 and 15 minutes.
Patient had been fasted for 15 hours overnight and medications were withheld until after the test. The glucose values were 6.3 mmol/L, 15.1 mmol/L, 16.3 mmol/L and 16.6 mmol/L at baseline, 5, 10 and 15 minutes respectively. Corresponding C-peptide values were 0.21 nmol/L, 0.42 nmol/L, 0.47 nmol/L and 0.51 nmol/L respectively. He was finally discharged after 7 days of hospital care with clinic follow up in 2 months. His average capillary blood glucose (CBG) was 6.7 mmol/L and range 6.5-7.7 mmol/L on discharge.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [90.0, 'kg']}",130,123.5,136.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 90.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (90.0 kg - 20 kg) = 130.0 mL/hr.
Hence, the patient's fluid maintenance is 130.0 mL/hr."
4620,22,Maintenance Fluids Calculations,physical,decimal,pmc-5412738-1,Extracted,"A 67-year-old male patient (height 165 cm; body weight 88 kg), without previous cardiological history, was admitted to our emergency room for paroxysmal nocturnal dyspnea. The patient had reduction of functional capability and dyspnea (New York Heart Association functional class III) in the preceding months. He was on chronic therapy with enalapril for systemic hypertension. Electrocardiogram on admission showed atrial fibrillation with ventricular rate response of 100 beats/min, right bundle branch block and diffuse repolarization abnormalities. Physical examination revealed a 2/6 L holosystolic murmur over the aortic area, a fixed split of the second heartbeat and mild signs of pulmonary congestion. Transthoracic echocardiography showed normal size of the left ventricle, which was hypertrophic and with normal ejection fraction. Color-Doppler evaluation revealed left to right shunt in the basal portion of the interatrial septum without the involvement of the interventricular septum [] and moderate mitral valve regurgitation. Right atrium was dilated, right ventricle was hypertrophic and mildly dilated (telediastolic diameter 49 mm) with moderate to severe tricuspid regurgitation. Systolic pulmonary artery pressure was 40 mmHg. Chest X-ray showed posterior bilateral pleural effusion, diffuse thickening of the interstitial peribronchial vascular tissue and enlargement of the cardiac shadow. For further evaluation, a transesophageal echocardiography was performed, confirming an atrial septal defect, ostium primum type, with left-to-right shunt []. Mitral valve appeared dysmorphic, fibrocalcific (compatible with a cleft of mitral valve's anterior leaflet) with moderate regurgitation. Subsequently, coronary angiography revealed no coronary artery disease. The patient underwent surgical closure with autologous pericardium patch (intraoperative measurement of the defect was 1,9 × 3 cm, localized in the caudal portion of the septum). During surgery, the patient developed complete atrioventricular block requiring permanent epicardial pacemaker implantation. Postoperative transthoracic echocardiography showed no residual atrial communication, with a slight reduction of the right sections dimensions and mild mitral regurgitation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [88.0, 'kg']}",128,121.6,134.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 88.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (88.0 kg - 20 kg) = 128.0 mL/hr.
Hence, the patient's fluid maintenance is 128.0 mL/hr."
4621,22,Maintenance Fluids Calculations,physical,decimal,pmc-6120405-1,Extracted,"In February 2018, a 60-year-old woman with fistulizing CD for about 40 years came to our attention because of the appearance of worsening asthenia and abdominal pain. Her past medical history was positive for left colon resection with colostomy packaged about 20 years before, for ileocecectomy carried out in 2005 due to adhesion syndrome, and for fistulotomy in 2015 because of multiple rectovaginal and rectocutaneous fistula. The patient was considerably underweight (45 kg). Objective examination of heart, chest, and hypochondriac organs was negative. The abdomen was flat and manageable, painless with torpid peristalsis. The ostomy appeared retracted and stenotic into the left site were not evaluable. At the perianal level, it was possible to appreciate multiple fistulous ostia with presence of minimal granulation tissue and abundant mucous-purulent secretions that also involved the labia majora. The perineum appeared completely destructured. The patient regularly took prednisone (5 mg), lansoprazole (30 mg), and ciprofloxacin (500 mg). She had suspended mesalazine (800 mg) because of the appearance of a probably drug-related skin rash. Abdominal CT, carried out in order to restage the disease and evaluate perianal involvement, showed, on the lateral and posterolateral right side of the anal canal, a 21 × 21 mm hyperdense thickening also extending to the levator ani muscle of the omolateral side, probably representing an abscess. In addition, at the anal level there was a fluid and gaseous collection of 27 × 81 mm, extending also to the vagina and major labia. MRI of the lower abdomen showed two subtle striae hyperintense on T2-weighted sequences fat-sat, localized posteriorly and in the left subsphincter region; these findings were evaluated as fistulas. After evaluating the objective exam as well as hematochemical and instrumental examinations, we proposed to the patient, in agreement with our gastroenterologists, a multidisciplinary therapeutic program that included initial surgical drainage of the perianal fistulas with the Miles technique and repackaging of the retracted ostomy, followed by medical therapy. The surgery involved two stages, one abdominal and the other perineal. The surgeon accessed the abdominal cavity through a xipho-pubic incision. After viscerolysis the sigmoid ostomy was isolated and dissected. We identified the rectosigmoid stump that was isolated up to the rectum wings. A left ovarosalpingectomy was necessary due to adherences which evolved in an abscess probably coming from the rectal stump. Then 10 cm of sigma were resected after mobilization of the splenic flexure which involved a necessary splenectomy. The remaining colon was mobilized up to half of the transverse colon. The ostomy was packaged on the distal transverse side at the level of the right iliac fossa because of the presence of multiple abscesses and cutaneous ulcers at the site of the previous ostomy. The reconstruction of the pelvic floor and the excision of the preexisting ostomy were carried out with biopsy of the peristomal cutaneous lesion. Two drainages were applied: an upper one in the splenic loggia and a lower one in the neo-Douglas. After repeated washings and hemostasis control, the surgical breaches were synthesized and the ostomy was opened. Later we performed an excision of the anorectal canal as the perineum was deconstructed. We proceeded to the partial closure of the ischiorectal excavation with placement of a perineal drainage. The removed material was sent to the anatomopathologists (Fig. ). The postoperative course was regular. The final histological examination showed normal findings as concerned the ovary, the spleen, the ostomy, the colon, and the parastomal skin, while it showed adenocarcinoma of the large intestine as regards the sigmarectoanal canal specimen. This was an adenocarcinoma arising from flat low-grade and high-grade dysplasia, infiltrating the wall up to the subserous adipose tissue (pT3) with a maximum extension of 3 mm from the outer limit of the muscle membrane in the perivisceral adipose tissue. The neoplasia showed infiltrative growth with abundant single cells and poor peri- and intratumoral lymphocytic infiltration. In the wall and in the adipose tissue underlying the neoplasia, numerous lymphoid aggregates and gigantocellular granulomas (compatible with CD) were observed. On the serosa, bleeding as well as granulocytic and histiocytic inflammatory infiltrates could be observed to configure a picture of localized peritonitis. Neoplastic invasion of the sphincter muscle was not observed. As regards grading, the neoplasia was classified as G3 and according to Dukes' classification as B2. High-grade tumor budding was present and was evaluated with anticytokine antibodies AE1 and AE3. Vascular invasion was not documented while perineural invasion was present and widespread. The expression of the protein product encoded by DNA repair genes was also evaluated: MSH-6 and PMS-2 were conserved, while CDX-2 had a partial loss of nuclear positivity (Fig. ). The eight isolated pericolic lymph nodes were disease-free. The proximal margin and the distal margin sampled on the operating piece were disease-free. The radial margin showed a distance of 1 mm from the neoplasm. After evaluating the new clinical situation, we contacted our oncologist for postoperative staging of the neoplasm and evaluation of a possible antitumor therapy. In consideration of stage II of the disease, the most appropriate therapy involved postoperative radiotherapy (45 Gy) associated with capecitabine chemotherapy 1,650 mg/m2/day within 2.5 months after surgery. The patient refused any kind of treatment and only accepted perineum dressings.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [45.0, 'kg']}",85,80.75,89.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 45.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (45.0 kg - 20 kg) = 85.0 mL/hr.
Hence, the patient's fluid maintenance is 85.0 mL/hr."
4622,22,Maintenance Fluids Calculations,physical,decimal,pmc-4255135-1,Extracted,"A 25-year-old male was referred to our surgical department for investigation of 3 months of progressive gastric outlet obstruction. At presentation, the patient was unable to tolerate oral intake other than minimal amounts of water. There was a 13-kg weight loss over this 3-month period (weight 79 kg at presentation).
Gastroenterology work up was undertaken shortly after the onset of symptoms. Endoscopy at that time showed non-specific duodenitis, with biopsies taken from the gastric antrum and body as well as the duodenum. Gastric mucosa showed a mild-to-moderate increase in chronic inflammatory cells in the lamina propria with few focal polymorphs. Helicobacter pylori were present. No epithelial dysplasia or malignancy was reported. Duodenal biopsy showed no evidence of increased lymphocytes, parasites, dysplasia or malignancy. Triple therapy was initiated to eradicate H. pylori. CT did not reveal any abnormality of the gastrointestinal tract. Symptoms improved with eradication therapy. While subsequently on holiday in Taiwan the symptoms returned, prompting further investigation. Endoscopy identified a possible submucosal lesion in the duodenum. Endoscopic ultrasound suggested a duodenal lesion (suboptimal study). Inflammatory markers were raised at this point. As the patient remained unwell, he returned to New Zealand for further evaluation in our centre.
The patient was a previously well non-smoker, with no significant medical or surgical history, taking only omeprazole (prescribed during the prior work up). There was a family history of Crohn's disease in a maternal aunt.
On admission, the patient was haemodynamically normal, oliguric and afebrile with mild peripheral oedema. Abdominal examination revealed a soft, non-tender abdomen with no masses.
On admission C-reactive protein was 19, with a normal white cell count (8.56 × 109/l). The patient was noted to be hypokalaemic. IV fluids were given initially, and on Day 3 of admission, a nasojejunal tube was placed endoscopically for enteric feeding. Endoscopy revealed a clear fluid in the gastric body, with acquired stenosis noted in the duodenal bulb, which was biopsied. Endoscopic images are shown in Fig. .
Biopsy revealed non-specific inflammation, with Brunner gland hyperplasia and foveolar metaplasia, reported as non-specific peptic duodenitis with no malignancy identified. Repeat endoscopy 3 days later reported malignant looking severe stenosis of the prepyloric region. Endoscopic images are shown in Fig. . No biopsy was taken at this time.
Endoscopic ultrasound was undertaken on Day 8 of admission, which showed generalized thickening of the prepyloric deep mucosa with no discreet mass. Biopsy again showed non-specific inflammation without evidence of granuloma or malignancy. After discussion with a multidisciplinary team and subsequently with the patient and family, a decision was made for distal gastrectomy. On Day 16 of admission, the patient underwent a Billroth II distal gastrectomy with retrocolic gastrojejunostomy. During the operation, a nodular lesion was noted in the pylorus which did not appear to involve the duodenum. Several small lymph nodes were identified. No other abdominal abnormalities were observed. On Day 7 post-operatively, a histological diagnosis was made of Crohn's disease of the stomach, involving the duodenum. Histopathological images are shown in Fig. .
The patient was discharged 14 days after the operation when he was able to tolerate adequate oral intake for nutritional need. Subsequent anti-saccharomyces cerevisiae antibodies testing was positive for both IgG (66 units/ml) and IgA (171 units/ml). The patient was subsequently started on azathioprine. Colonoscopy and gastroduodenoscopy with multiple biopsies have failed to show any evidence of further disease.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [79.0, 'kg']}",119,113.05,124.95,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 79.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (79.0 kg - 20 kg) = 119.0 mL/hr.
Hence, the patient's fluid maintenance is 119.0 mL/hr."
4623,22,Maintenance Fluids Calculations,physical,decimal,pmc-5597920-1,Extracted,"A 37-year-old woman suffering from morbid obesity without comorbidities underwent LSG and lost 57 lbs (25.8 kg) over a 2-month period (her body mass index was reduced from 43 to 35). At 3 weeks postoperatively, she presented to the emergency room with epigastric abdominal pain, dysphagia, and elevated serum levels of amylase and lipase that were attributed to a small pseudocyst demonstrated by an abdominal computed tomography scan. Under conservative treatment her symptoms gradually subsided, and she was discharged in a satisfactory condition. However, the patient did not maintain a balanced nutrition and was not compliant with the vitamin supplementation that was recommended after surgery. She then returned at 10 weeks postoperatively with poor oral intake, confusion, postural imbalance (requiring a wheelchair for ambulation), and visual impairment.
There was no history of any systemic disorders, including hypertension and diabetes, as well as any ophthalmic disorders. She denied fever, headaches, abdominal pain, nausea, vomiting, or heartburn. Alcohol use was ruled out. On ophthalmologic examination, extraocular movements were not limited, but a bilateral horizontal nystagmus was present. Visual acuity was 20/20 in both eyes, and anterior segments were normal. Pupil function tests were normal, and no relative afferent pupillary defect was present. Dilated exam showed bilateral optic disc swelling with an adjacent preretinal hemorrhage in the left eye (Fig. ). Workup included normal laboratory tests except for low thiamine levels (13.9 ng/mL, normal range 32–95 ng/mL). These findings supported the diagnosis of WE, and she began intravenous thiamine replacement therapy. The nystagmus had regressed a few days after the initiation of thiamine supplementation, and the fundus findings had resolved completely by 3 months.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [25.8, 'kg']}",65.8,62.51,69.09,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 25.8 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (25.8 kg - 20 kg) = 65.8 mL/hr.
Hence, the patient's fluid maintenance is 65.8 mL/hr."
4624,22,Maintenance Fluids Calculations,physical,decimal,pmc-6453847-1,Extracted,"A 61-year-old male smoker and alcoholic was referred to our center for diagnosis and treatment of a pancreatic mass. He had consulted at his local hospital for a 30-pound weight loss and epigastric pain radiating to the back for 3 months. Laboratory tests and tumor markers were within normal limits. Magnetic resonance cholangiopancreatography showed a poorly defined mass of 25×21×41 mm compromising the pancreatic head and pancreatoduodenal groove, with cystic areas and thickening of the first and second duodenal portions. A normal pancreatic body and tail were observed, with a non-dilated pancreatic duct and no compression of the bile duct, which was slightly deformed (-). EUS showed diffuse chronic pancreatitis with focal hypoechogenicity and nodularity in the head, but without compromise of the intrapancreatic bile duct or pancreatic duct. The duodenal wall was thickened by a hypoechoic formation compromising the pancreatic parenchyma, and an anechoic lesion of 15 mm was compatible with an intraparietal duodenal cyst. FNA was performed on the focal area for histopathological examination, and the cyst for physical-chemical and cytological analysis. Endoscopically, edematous mucosa with a polypoid appearance and narrowing of the second part of the duodenum was observed, and biopsies were performed (-). Histopathological examination of the focal mass revealed acini in the context of an acute inflammatory infiltrate, and accumulation of fusiform cells without atypical epithelial cells. Vimentin and synaptophysin were expressed but pan-cytokeratin AE1-AE3 was not detected in spindle cells. The duodenum showed chronic bulboduodenitis and foveolar metaplasia without dysplasia; cyst analysis revealed a CEA of <0.5 ng/mL and negative cytology. With the diagnosis of chronic pancreatitis and acute compromise of the gastroduodenal groove, pancreatic enzymes and elimination of risk factors were indicated with good clinical response, weight gain, and normalization of imaging findings 6 months later.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [30.0, 'lbs']}",47.21552,44.85474,49.5763,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 30.0 lbs so this converts to 30.0 lbs * 0.453592 kg/lbs = 13.60776 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.60776 kg - 10 kg) = 47.21552 mL/hr.
Hence, the patient's fluid maintenance is 47.21552 mL/hr."
4625,22,Maintenance Fluids Calculations,physical,decimal,pmc-6300820-1,Extracted,"We report a case of an 81-year-old woman with valvular heart disease (previous mitral valve replacement) that presented with increased dyspnoea, abdominal discomfort, and 1.5 kg weight gain. Ambulatory daily heart failure treatment was bisoprolol 1.25 mg, furosemide 160 mg, chlorthalidone 25 mg, acetazolamide 125 mg, and spironolactone 12.5 mg. No evident cause for clinical decompensation was noted. Vital signs at presentation were as follows: heart rate 69 bpm, arterial blood pressure 90/56 mmHg (usual values and no signs of hypoperfusion), respiration rate 19 per minute, and capillary Sa02 96%. The physical examination revealed abdominal and jugular venous distension, positive hepatojugular reflux, but no peripheral oedema nor rales. Echocardiography showed a normally functioning prosthetic mechanical mitral valve, preserved left ventricular ejection fraction, dilated right ventricle with preserved systolic function (tricuspid annulus plane systolic excursion of 20 mm), a moderate tricuspid regurgitation with an estimated pulmonary artery systolic pressure of 65 mmHg, and a severely dilated inferior vena cava (Figure
A). Given that the patient had a mechanical mitral valve, echocardiographic assessment of left ventricular end diastolic pressures was not possible. The laboratory analysis showed an N-terminal prohormone of brain natriuretic peptide of 3205 pg/mL and WRF, with an increase in serum creatinine from 1.23 to 1.81 mg/dL (a decline in estimated glomerular filtration rate from 45 to 27 mL/min/1.73 m2). A Doppler ultrasonography evaluating renal interlobar venous flow showed a monophasic pattern (Figure
B), suggesting a severe elevation in intrarenal venous pressures.
In this case, according to physical and Doppler findings, renal venous congestion appeared to be casually linked to the occurrence of WRF. Accordingly, we started an aggressive intravenous diuretic treatment during the first 48 h (cumulative furosemide dose of 500 mg). At this time, we reassessed the echo-Doppler, registering a reduction of the diameter of inferior vena cava (Figure
C) and a change from monophasic to biphasic venous flow pattern in the intrarenal ultrasonography (Figure
D), indicating an improvement in venous flow and, therefore, a reduction of venous pressures. Importantly, this change occurred in parallel with clinical improvement (resolution of abdominal discomfort, 2 kg weight loss) and an improvement in renal function (serum creatinine and estimated glomerular filtration rate changed from 1.81 to 1.44 mg/dL and from 27 to 38 mL/min/1.73 m2, respectively). Changes in laboratory parameters after diuretic treatment are shown in Figure .","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1.5, 'kg']}",6,5.7,6.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1.5 kg. Hence, the patient's maintenance fluid is 1.5 kg * 4 mL/kg/hr = 6.0 mL/hr.
Hence, the patient's fluid maintenance is 6.0 mL/hr."
4626,22,Maintenance Fluids Calculations,physical,decimal,pmc-7506226-1,Extracted,"A 67-year-old male was referred from a local medical center and admitted to our hospital for body weight loss of approximately 10 kg over 2 months (from 81 to 71 kg). He denied fever or chills and had no abdominal pain. Abdominal computed tomography (CT) performed at a local medical center showed a 53 × 39 mm, exophytic low-density mass in the uncinate process of the pancreas (Fig. ) and a 19 × 14 mm, low-density mass in the body of the pancreas (Fig. ). The patient was taking medication for hypertension and type 2 diabetes mellitus. He reported consuming one bottle of an alcoholic beverage per day and had never smoked. Vital signs were as follows: blood pressure 110/65 mm Hg, pulse rate 77/min, respiratory rate 18/min, and body temperature 36.4°C. On physical examination, the patient appeared to have anicteric sclera, and his abdomen was soft and flat without tenderness. The laboratory findings were as follows: white blood cell count 7,060/µL (neutrophil 69.3%), hemoglobin 12.3 g/dL, platelet count 300,000/µL, aspartic acid aminotransferase 14 IU/L, alanine aminotransferase 17 IU/L, blood urea nitrogen 12.4 mg/dL, creatinine 0.79 mg/dL, C-reactive protein 2.62 mg/dL, carcinoembryonic antigen 5.9 ng/mL, carbohydrate antigen 19-9 48.35 U/mL, fasting serum glucose 367 mg/dL, and hemoglobin A1c 11.6%.
Since pancreatic cancer was suspected, the patient was evaluated for surgical treatment based on the CT findings. The mass in the pancreatic body seemed to abut the superior mesenteric artery. On the day after admission, magnetic resonance imaging (MRI) was performed to further characterize the pancreatic lesion. The interval between the MRI and the previous CT was 21 days. On MRI, the mass in the uncinate process decreased from 53 to 35 mm, while the mass in the body increased from 19 mm to 40 mm (Fig. ). Based on the MRI findings, we predicted that the pancreatic lesions are atypical inflammations, such as tuberculosis.
Endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) was planned to differentiate this atypical inflammatory lesion. On the 6th day of hospitalization, one day prior to EUS-FNA, the patient developed a fever of 37.9°C and was treated with intravenous third-generation cephalosporin. The next day, EUS-FNA (GF-UCT 260; Olympus Co., Tokyo, Japan, and 22-gauge needle, Mediglobe; Mediglobe Co., Achenmuehle, Germany) was performed according to our previous plan. The mass of the body of the pancreas was irregular in shape, and the margin was unclear; moreover, a low echoic lesion was identified in the center. Pus-like fluid was aspirated from the tissue by EUS-FNA. However, the abscess of the pancreatic body lesion was ruptured to the peripancreatic area just after EUS-FNA. The EUS-FNA procedure was aborted, and the patient was closely monitored in the ward. The aspirated fluid was not sent for culture sensitivity. Later, a cytological examination only revealed the presence of inflammatory cells within the pancreas parenchyma (Fig. ). Fever had subsided after 4 days of intravenous antibiotic treatment. After treatment with intravenous antibiotics for 11 days, the patient was discharged with per-oral antibiotics for 7 days. After 1 month, the follow-up abdominal CT demonstrated that the mass in the uncinate process decreased to 8 mm, and the mass in the body was no longer present. The patient has been compliant and has continued with follow-up as of now.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [71.0, 'kg']}",111,105.45,116.55,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 71.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (71.0 kg - 20 kg) = 111.0 mL/hr.
Hence, the patient's fluid maintenance is 111.0 mL/hr."
4627,22,Maintenance Fluids Calculations,physical,decimal,pmc-6727096-1,Extracted,"A 2.5-year-old (3.5 kg) female intact Bengal queen was referred for a possible uterine prolapse during parturition, which had started approximately 12 h before presentation. The owner found the cat after it had delivered three healthy kittens, hiding and showing aggressive behavior. Upon examination, they noticed a mass protruding from the vulva that was thought to be another kitten. The owner manipulated the protruding mass as if it was an obstructed kitten, but this provoked profuse bleeding, which prompted the owner to seek emergency veterinary consultation.
On presentation, physical examination revealed mild tachypnea (48 respirations/min), mild tachycardia (200 beats/min) and mild dehydration (estimated 5%), the mucous membranes were pale and lacked observable capillary refill, and pulses were weak. The abdomen was distended, and signs of pain were elicited on palpation. Indirect blood pressure measured using Doppler ultrasonography was mildly decreased (systolic blood pressure 80–90 mmHg; reference interval [RI] 110.0–180.0 mmHg). What was thought to be a uterine prolapse was an evisceration of most of the uterus through the vulva. The distal region of the uterine body was torn 360º, and the edge was everted showing the uterine mucosa, which had signs of necrosis. Both uterine horns were eviscerated, almost entirely, through the vulva ().
A serum biochemical analysis was performed and showed: low packed cell volume (22%; RI 25–45%) and normal proteinemia (6 g/dl; RI 6.0–7.9 g/dl) attributed to subacute bleeding; mildly increased glucose concentration (14.3 mmol/l; RI 3.3–6.7 mmol/l) attributed to stress; normal creatinine (102 µmol/l; RI 80–194 µmol/l); and mildly increased blood urea nitrogen (30–40 mg/dl; RI 14–36 mg/dl) attributed to mild dehydration. A metabolic acidosis (pH 7.1; RI pH 7.27–7.40) with hyperlactatemia (6.2 mmol/l; RI 0.37–2.81 mmol/l) was present. An abdominal ultrasound limited to the reproductive system was able to identify only a uterine horn containing a dead fetus, and a small amount of free abdominal fluid.
For stabilization and in preparation for an emergency surgical procedure, ampicillin 22 mg/kg (Ampicillin Sodium; Novopharm) and two boluses of lactated Ringer’s solution, 10 ml/kg in 15 mins and 5 ml/kg in 10 mins (Plasma-Lyte A; Baxter), were administered intravenously (IV). The patient’s systolic blood pressure increased to 110 mmHg. Analgesia was administered (hydromorphone 0.05 mg/kg IM [HYDROmorphone; Sandoz]; remifentanil 5 µg/kg/h continuous rate infusion IV [Remifentanil Hydrochloride; SteriMax]) and pre-oxygenation was performed via a facemask.
Anesthesia was induced with midazolam 0.2 mg/kg IV (Midazolam Injection; Sandoz) and propofol 1 mg/kg IV (PropoFlo; Zoetis), and the queen was intubated with a cuffed endotracheal tube that had an inner diameter of 4.5 mm. Anesthesia was maintained with isofluorane (Isoflurane; Fresenius Kabi), and intraoperative monitoring included capnography, electrocardiogram and pulse oximetry performed with a multiparameter patient monitor (Life Window; DigiCare Animal Health). Intraoperative analgesia was provided with epidural locoregional analgesia (bupivacaine 0.5 mg/kg epidural [Bupivacaine Injection; SteriMax]) and an infusion of remifentanil 5–7 µg/kg/h IV. Because of the preoperative anemia and hypotension during anesthesia (systolic blood pressure 50 mmHg), dopamine 5–7 µg/kg/min (Dopamine; Baxter) and norepinephrine 0.1 µg/kg/min (Norepinephrine; Sandoz) IV infusions were initiated at the time of induction, a blood transfusion was given (11 ml/kg of whole blood, type A, IV transfusion over 4 h) and fluid therapy intraoperatively consisted of crystalloids 6 ml/kg/h IV (Plasma-Lyte A; Baxter), and a bolus of colloids 10 ml/kg IV over 10 mins (Voluven; Fresenius Kabi Canada).
A midline laparotomy was performed. There was a moderate amount of blood in the abdomen, with some blood clots located in the caudal abdomen dorsal to the urinary bladder. The right uterine horn was identified with a dead fetus inside (). The left uterine horn and left ovary were absent, and the ovarian pedicle was not ruptured, but the left suspensory ligament with its ovarian artery and vein were severely elongated (). The right and left ovarian pedicles were ligated and transected. The right uterine horn was double ligated and transected distal to the location of the fetus to separate the intra-abdominal and eviscerated parts and remove the uterus. Once the left ovarian pedicle and the right uterine horn were ligated and transected, gentle retraction allowed exteriorization of the rest of the uterus and the left ovary from the vulva. Upon manipulation of the uterine stump dorsal to the bladder, urine extravasation was noted. A small cystotomy was performed to introduce a 5 F urinary catheter (Covidien) in a normograde manner to help to identify the urethra during correction of the vaginal tear. The remnant of the vaginal vault was severely damaged making it difficult to identify its margins (). Careful closure of the vaginal tear was performed with absorbable sutures (polydioxanone 3-0) making sure not to compromise the urethra. The abdomen was lavaged with warm saline and abdominal wall closure was routine.
The queen recovered well from anesthesia and was hospitalized for a total of 5 days. Postoperative care included fluid therapy with crystalloids 2 ml/kg/h IV, remifentanil 5–7 µg/kg/h IV, enrofloxacin 5 ml/kg slow IV q24h (Baytril; Bayer), ampicillin 22 mg/kg IV q8h and maropitant 1 mg/kg IV once (Cerenia; Zoetis). A 5 F urinary catheter was left in place for the first 3 days, and the cat was able to urinate voluntarily thereafter without difficulty. The intravenous analgesia was progressively transitioned to sublingual buprenorphine 0.02 mg/kg q8–12h (Vetergesic Multidose; Champion Alstoe Animal Health). Intravenous antibiotics were discontinued and the queen was prescribed amoxicillin–clavulanic acid 62.5 mg PO q12h (Clavaseptin; Vetoquinol) to complete a total of 10 days of antibiotherapy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.5, 'kg']}",14,13.3,14.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.5 kg. Hence, the patient's maintenance fluid is 3.5 kg * 4 mL/kg/hr = 14.0 mL/hr.
Hence, the patient's fluid maintenance is 14.0 mL/hr."
4628,22,Maintenance Fluids Calculations,physical,decimal,usmle-3296,Extracted,"A previously healthy 13-year-old girl is brought to the physician for evaluation of a 2-month history of fatigue. She reports recurrent episodes of pain in her right wrist and left knee. During this period, she has had a 4-kg (8.8-lb) weight loss. Her mother has rheumatoid arthritis. Her temperature is 38°C (100.4°F). Examination shows diffuse lymphadenopathy. Oral examination shows several painless oral ulcers. The right wrist and the left knee are swollen and tender. Laboratory studies show a hemoglobin concentration of 9.8 g/dL, a leukocyte count of 2,000/mm3, and a platelet count of 75,000/mm3. Urinalysis shows excessive protein.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.0, 'kg']}",16,15.2,16.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.0 kg. Hence, the patient's maintenance fluid is 4.0 kg * 4 mL/kg/hr = 16.0 mL/hr.
Hence, the patient's fluid maintenance is 16.0 mL/hr."
4629,22,Maintenance Fluids Calculations,physical,decimal,pmc-6230409-1,Extracted,"A 46-year-old female presented with complaints of fever, breathlessness on minimal exertion, vomiting, abdominal pain, and reduced appetite since 10 days. She also complained of weight loss of 10 kilograms in the last 6 months. She was diagnosed with HIV-1 infection, 1 month prior, and was prescribed tenofovir, lamivudine, and efavirenz fixed-dose combination single-pill regimen. Her baseline CD4 count was 68 cells/mm3, and plasma HIV-1 viral load was 867,000 copies/ml. She had no comorbidities or prior significant medical history. On examination, she was febrile (temperature: 100 degrees Fahrenheit) with pulse (100/min), blood pressure (110/60 mm Hg), and respiratory rate (24/min). Respiratory examination revealed crepitations in bilateral inframammary, infraaxillary, and infrascapular areas. There was diffuse abdominal tenderness but no organomegaly. Rest of the examination including fundoscopy was unremarkable. Hemoglobin was 8.3 g/dl while rest of the biochemical investigations was normal. CD4 count and plasma HIV-1 viral load after 1 month of ART was 190 cells/mm3 and 9,500 copies/ml, respectively, suggesting satisfactory immune reconstitution. The arterial blood gas (ABG) was suggestive of hypoxia (pO2-63 mm Hg) on room air. Chest X-ray was suggestive of bilateral, extensive, and patchy consolidation suggestive of infective etiology (). Sonography of abdomen showed multiple mesenteric nodes with the largest size of 21 mm by 17 mm, grade 2 fatty liver, and dilated portal vein. The CT scan of chest revealed bilateral ground glass haziness suggestive of pneumocystis carinii pneumonia (PCP). CT abdomen showed biliary dilatation due to distal CBD stricture, mesenteric lymphadenopathy and mild diffuse thickening of the caecum, and ascending and transverse colon. 2D echocardiography of the heart was normal. Blood culture was sterile, and serum procalcitonin was normal. Keeping a provisional diagnosis of IRIS to Pneumocystis jirovecii or Mycobacterium tuberculosis in mind, she was started on high-dose trimethoprim-sulphamethoxazole (TMP-SMX), oral steroids, and empirical antitubercular therapy (ATT) in addition to ART. She had diarrhea on admission, which subsided in 2 days after taking loperamide. Stool routine and modified Ziehl–Neelsen (ZN) examination was unremarkable. Due to a suspicion of CMV enterocolitis, she was also started on empirical oral valgancyclovir. Bronchoscopy with BAL was attempted but had to be aborted in view of worsening hypoxia during procedure. For establishing diagnosis, upper GI endoscopy and colonoscopy were attempted. Upper GI endoscopy revealed diffuse gastroduodenitis. Colonoscopy showed patchy colitis. Duodenal biopsy revealed focal blunting, ulceration, and neutrophilic exudates (). The surface epithelium showed several eggs, larvae, and adult forms of S. stercoralis (). Lamina propria showed moderate mononuclear inflammatory infiltrate with lymphoid follicle formation and many admixed eosinophils (Figures and ). There was no evidence of tuberculosis or malignancy. Induced sputum also demonstrated larvae of S. stercoralis. As a result, diagnosis of SHS as a manifestation of IRIS was made, and she was started on an oral combination of albendazole (400 mg twice a day) and ivermectin (200 µg/kg). Inspite of antihelminthic treatment, her dyspnea worsened. Her repeat ABG showed hypoxia (PO2 –47 mm Hg, Spo2 89%) and respiratory alkalosis. She developed hypotension (blood pressure 80/60 mm Hg) and altered sensorium in the form of increasing drowsiness (Glasgow Coma Scale 12/15). She was shifted to the Intensive Care Unit (ICU) for the same. MRI brain and CSF examination were normal while serum sodium level had dropped to 125 mEq/L. Noradrenaline infusion and noninvasive BIPAP ventilation were started. She was initiated on intravenous (i.v.) meropenem, i.v. teicoplanin, and i.v. fluconazole in addition to antihelminthic agents, steroids (in tapering doses), and ART. ATT and valganciclovir were withdrawn while TMP-SMX was reduced to prophylactic dose. She gradually started improving over the next 7 days with improvement in sensorium and reduction in breathlessness. She was shifted out of the ICU by day 21 of admission. Her CXR showed complete resolution of pneumonic consolidation. She was discharged on oral antihelminthic treatment which she continued for another 8 weeks. Follow-up endoscopy studies showed complete clearance of S. stercoralis.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.0, 'kg']}",40,38,42,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.0 kg - 10 kg) = 40.0 mL/hr.
Hence, the patient's fluid maintenance is 40.0 mL/hr."
4630,22,Maintenance Fluids Calculations,physical,decimal,pmc-6057286-1,Extracted,"A 3-month-old Japanese boy was admitted because of poor body weight gain, vomiting, and fever that had persisted for one week. He was born as a full-term infant with no complications during pregnancy.
At the time of admission, he had polyuria with a urine volume of 700–800 mL/d. Results of laboratory examinations are shown in . Findings of brain magnetic resonance imaging (MRI) were normal. Based on the polyuria and the high serum ADH level, the infant was diagnosed as having NDI, and hydrochlorothiazide was initiated. Spironolactone and potassium supplementation was added when he was 2 years old and 4 years old, respectively, and indomethacin and a protein-restricted diet were initiated when he was 6 years old. He is currently 13 years old. His height is 150 cm (−0.8 SD), and his weight is 37 kg (−0.6 SD). His urine volume is approximately 7 L/day. He has mild hydronephrosis in the right kidney. His mother is asymptomatic. The family tree of Case 1 is shown in .","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [37.0, 'kg']}",77,73.15,80.85,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 37.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (37.0 kg - 20 kg) = 77.0 mL/hr.
Hence, the patient's fluid maintenance is 77.0 mL/hr."
4631,22,Maintenance Fluids Calculations,physical,decimal,pmc-7413470-1,Extracted,"A 2-month-old male infant was hospitalized with progressive, multiple erythematous, crusted, and glazed dermatitic lesions predominantly involving buttocks, perianal area, scrotum and prepuce [], cheeks, chin, pinnae, neck fold, and nostrils [] symmetrically for 15 days suggestive of acrodermatitis enteropathica. Few similar lesions were also distributed widely over trunk and extremities, fingers [], ankles, and popliteal fossae. Historically, initial lesions had developed over perianal skin and involved other sites within a week. He had poor sleep, 4-5 loose stools per day, and aversion for feeds for past 1 week. He was first child born normally to otherwise healthy non-consanguineous parents after an uneventful gestation and full-term pregnancy. No similar problem was reported in any other family offsprings. He was exclusively breastfed, weighed 4.5 kg, immunized for his age, and had normal mental and developmental milestones. He was afebrile, irritable, had minimal pallor, oral thrush, photophobia, and paronychia. He had no lymphadenopathy, hair or nail abnormality. Systemic examination and baseline laboratory investigations showed no significant abnormality []. KOH mount and aerobic culture from skin lesions showed no fungus or bacterial growth. His serum zinc levels were 0.8μg/dl (normal 70–115 μg/dl) estimated colorimetrically (ERBACHEM-7 Spectrophotometer) by nitro-PAPS (2-(5-nitro-2-pyridylazo)-5-(N-propyl-N-sulfopropylamino) phenol) method usingin vitro kits from AGAPPE Diagnostics Ltd., India. The zinc levels in mother's serum were 12 μg/dl (normal 70–115 μg/dl) and 14 μg/dl in the breast milk (normal 16.0–536.0 μg/dl, median 166.0 μg/dl at two months of postpartum).[] Her complete blood counts and serum biochemistry including serum calcium (9.2 mg/dl), magnesium (2.1 mg/dl), albumin (3.9 gdl), and alkaline phosphatase (88 U//l) levels were within the reference range.
Treatment with oral zinc 1 mg/kg/day of elemental zinc (zinc gluconate oral solution containing elemental zinc ≡ 4 mg/ml) in two divided doses was initiated overnight along with bland emollients topically. Mother was also given elemental zinc (1 mg/kg/day) orally as zinc sulfate 220 mg ≡ 50 mg elemental zinc, and advised to continue breastfeeding. Clinical symptoms of irritability, photophobia, diarrhea, sleep, and acceptance for feed improved rapidly by next morning after first dose itself. The serum zinc levels improved to 8.2 μg/dl after 2 doses of oral zinc. His skin lesions resolved completely [Figure -] and serum zinc levels were 110 μg/dl after 1 week at discharge from hospital. The serum and milk zinc levels in mother also improved to 166 μg/dl and 160 μg/dl, respectively, after 1 week of zinc supplementation. The baby was completely normal on follow-up visit after 2 months. Both had discontinued zinc supplementation a month after leaving the hospital. However, zinc levels in serum or breast milk could not be re-estimated. The mother was advised to wean the baby at 6 month onwards. They did not follow-up further.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.5, 'kg']}",18,17.1,18.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.5 kg. Hence, the patient's maintenance fluid is 4.5 kg * 4 mL/kg/hr = 18.0 mL/hr.
Hence, the patient's fluid maintenance is 18.0 mL/hr."
4632,22,Maintenance Fluids Calculations,physical,decimal,pmc-4408828-1,Extracted,"A 16 months old female patient was admitted to our clinic with diagnosis of aortic
coarctation and descending aortic aneurysm. She presented with poor feeding and failure
to thrive (body weight: 8 kg). The prenatal and postnatal history was unremarkable; any
umbilical vascular catheterization was not performed. Physical examination revealed 80
mmHg systolic pressure difference between upper and lower extremities. Femoral pulses
were weak but palpable. There was a systolic murmur (3/6) at the left sternal border
which was also heard at the interscapular area. The leukocyte count, C-reactive protein
level and erythrocyte sedimentation rate were all within normal limits. The patient had
been admitted to another clinic a few months ago and transthoracic echocardiography had
demonstrated aortic coarctation with 60mmHg peak systolic gradient. Any intracardiac
pathology had not been encountered. Cardiac catheterization had been performed in order
to confirm the diagnosis and perform a balloon angioplasty if possible; however the
catheterization had revealed a segment of coarctation and saccular aneurysm in the
descending aorta (). Therefore, the
patient was referred to our clinic for surgical repair.
The patient was operated under general anesthesia and a left posterolateral thoracotomy
was performed at the 4th intercostal space. A 3x2 cm aneurysm which embraces
the coarcted segment in descending aorta was encountered (). Descending aorta was mobilized, resection and end-to-end
anastomosis was performed with 6/0 polyprolene suture. The sutures were continuous at
the posterior wall, whereas they were interrupted at the anterior wall of the
anastomosis, in order to provide potential for growth. Residual gradient was less than 5
mmHg. The resected specimen was examined by the pathology department. Gross and
microscopic cross sectional examination of the coarctation area revealed the segments of
both coarctation and aneurysm formation. Basophilic degeneration and vacuole formation
were remarkable (). The postoperative
period was uneventful and the patient was discharged at the sixth postoperative day
without any complication. At the sixth postoperative month, a second intervention was
performed because of recoarctation. The MR angiography revealed a recoarctation at the
descending aorta, in which balloon dilatation was performed with a residual gradient of
25 mmHg (). The patient is followed up by
echocardiographic evaluations with regular intervals.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [8.0, 'kg']}",32,30.4,33.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 8.0 kg. Hence, the patient's maintenance fluid is 8.0 kg * 4 mL/kg/hr = 32.0 mL/hr.
Hence, the patient's fluid maintenance is 32.0 mL/hr."
4633,22,Maintenance Fluids Calculations,physical,decimal,pmc-3772920-1,Extracted,"Nineteen year-old-man, known case of Type 2 Diabetes mellitus for 4 y on 1 g metformin twice daily since diagnosis of his diabetes. He was in his usual state of health till he presented to the emergency department reporting nausea, vomiting and epigastric pain for 3 d.
On physical examination, his height was 170 cm and body weight 99 kg; body mass index (BMI) 34.3 kg/m2, looked mildly dehydrated. Vitals signs were stable. Systemic examination was unremarkable, apart from mild epigastric tenderness.
Laboratory investigations showed HbA1c 7.7%, Creatinine 58 µmol/L, Amylase 462 units/l (normal range < 100), Lipase 1378 units/l (0–60), white blood cells 16.8/mm3 (4–11) 80% of which was neutrophils, CRP 258 mg/l (0–5), Mg 0.76 mmol/l (0.7–1.05), Ca 2.17 mmol/l (2.2–2.6), AST 18 units/l (< 39), ALT 34 units/l (< 41), TG 0.95 mmol/l (< 2.3), Lactate 1.4 mmol/l (0.5–1.6). Abdominal Ultrasound and ERCP were done for the patient, results showed no gallstones and clear biliary tract, respectively. CT confirmed the diagnosis of acute pancreatitis, with no identifiable cause.
The patient was admitted to ICU for close monitoring and further investigation. Normalization of Amylase and Lipase was reached after Metformin cessation, and Supportive treatment in the form of IV insulin and IV fluids. Other potential causes of pancreatitis were excluded. Patient was discharged home in stable condition after 2 weeks.
Few days later, after re-exposure to Metformin, he presented with recurrence of his previous symptoms, and elevation of Amylase and Lipase was documented.
As a result, Metformin was suspended with improvement of his symptoms and biochemical profile.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [99.0, 'kg']}",139,132.05,145.95,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 99.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (99.0 kg - 20 kg) = 139.0 mL/hr.
Hence, the patient's fluid maintenance is 139.0 mL/hr."
4634,22,Maintenance Fluids Calculations,physical,decimal,pmc-8180584-1,Extracted,"A 64-year-old male presented to the emergency department with a 6-month history of gradual onset of joint pain, swelling, and morning stiffness involving the wrists, metacarpophalangeal (MCP) joints, proximal interphalangeal (PIP) joints, and ankles. In addition, he complained of occasional vomiting, anorexia, progressive fatigue, and unintentional 12 kg of weight loss. His arthralgia was progressive and debilitating, and had a poor response to non-steroidal anti-inflammatory drugs (NSAIDs), acetaminophen, and opioid analgesics (tramadol 200 mg daily).
His past medical history and medication were irrelevant besides being an ex-smoker (10 pack-years, stopped 10 years ago). He had a family history of gastrointestinal and pulmonary malignancies. He denied any oral ulcers, dry eyes, rash, fever, night sweats, gastrointestinal bleeding, or other complaints. On physical examination, arthritis of the wrists, MCP joints, PIP joints, and ankles, and a positive metatarsal squeeze test were noted. The rest of the examination was unremarkable.
The initial laboratory investigations uncovered a microcytic and hypochromic anemia (hemoglobin 7.9 g/dl), leukocytosis (12.7 × 109/L), thrombocytosis (904 × 109/L), and elevation of C-reactive protein (CRP; 17.3 mg/dl) and erythrocyte sedimentation rate (ESR; 94 mm/h). Renal and liver profiles were normal, and an infection screen was negative. An anemia investigation showed low serum iron (9.6 μg/dl) and transferrin saturation (4%), and normal ferritin (74.1 ng/dl), cyanocobalamin (465 pg/ml), and folate (5 ng/ml) levels. Radiographic evaluation of the affected joints and chest was unremarkable. The RF and ACPA were significantly elevated at 215 IU/ml (0–14 IU/ml) and 156.9 IU/ml (<20 IU/ml), respectively.
Upper gastrointestinal endoscopy exhibited on the lesser curvature and antrum of the stomach a hard and friable mass with areas of necrosis that conditioned luminal stenosis (). Endoscopy ultrasound of the upper gastrointestinal tract revealed a mass extending 17 mm to the serosa layer with regional involvement of four lymph nodes. Endoscopy biopsy specimens showed a gastric adenocarcinoma with poor differentiation. Contrast-enhanced chest–abdomen–pelvis computed tomography confirmed the gastric mass with no evidence of other adenopathy or distant metastasis (), and the tumor was rated T3N2M0, G3. Chest evaluation showed slight changes compatible with emphysema.
During the hospitalization, while the malignancy workout was ongoing, polyarthritis was treated with a short course of corticosteroids (dexamethasone 5 mg daily) with good clinical response, and the dose was quickly tapered. However, a few weeks later, his symptoms recurred, and he was readmitted due to severe polyarthritis with disabling gait. Corticosteroid therapy was reintroduced (prednisolone 20 mg daily), and hydroxychloroquine (200 mg daily) was also added. However, full adherence to the therapeutic regimen was only possible after a few months and only then was a complete resolution of polyarthritis achieved ().
He was referred to oncology and proposed for gastrectomy. During the laparotomy procedure, extensive peritoneal carcinomatosis was detected, whereby he underwent gastrojejunostomy. The patient started palliative chemotherapy with cisplatin and fluorouracil, and after HER2 overexpression was documented, trastuzumab was added. Cisplatin and fluorouracil were stopped after 8 months, but cancer progression was documented and were reintroduced later on, with little effect on arthritis control. After 18 months of follow-up, he remained alive, with sustained arthritis remission for over 9 months (documented clinically and using ultrasound) and without radiological detectable erosions, under treatment with low-dose prednisolone (<7.5 mg daily) and hydroxychloroquine (300 mg daily), despite the absence of a curative cancer treatment.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.0, 'kg']}",44,41.8,46.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.0 kg - 10 kg) = 44.0 mL/hr.
Hence, the patient's fluid maintenance is 44.0 mL/hr."
4635,22,Maintenance Fluids Calculations,physical,decimal,pmc-4050942-1,Extracted,"A 55-year-old man weighing 50 kg and 160 cm tall, non-smoker, presented with cough with expectoration and shortness of breath on exertion since 3 years. He also gave a history of intermittent diarrhoea and flushing of the face and upper body since 3 months, precipitated by alcohol intake. He was a known hypertensive on tablet amlodipine 10 mg OD since 10 years.
Clinical examination revealed decreased air entry over left upper lung zone. Chest radiograph showed a mass in left suprahilar region. Computerised tomographic scan (CT scan) of the chest revealed a large, lobulated, heterogeneous enhancing mass lesion measuring 8.6 cm × 5.5 cm in left suprahilar region extending to left upper lobe bronchus [].
CT guided biopsy on histopathology showed a typical lung carcinoid. Blood chemistry, electrocardiogram (ECG) and echocardiogram were normal. His pulmonary function testing, arterial blood gas (ABG) analysis and breath holding time showed a predicted post-operative forced expiratory volume in 1 s of 54%, PaO2 of 93 mmHg, PaCO2 of 40 mmHg and breath holding time of 24 s. Urinary 5-hydroxy-3-indole acetic acid was 50 mg/day (n ≤ 10 mg/day). A diagnosis of left upper lobe bronchial carcinoid with carcinoid syndrome was made. Pre-operative preparation with subcutaneous (SC) octreotide 100 μg TDS relieved symptoms of flushing and diarrhoea. After 10 days, patient was scheduled for left upper lobectomy.
Premedication included tablet midazolam 7.5 mg and tablet ranitidine 150 mg at night and 1 h before surgery. On the morning of surgery, inj.octreotide 250 μg was given as an intravenous (IV) bolus followed by continuous infusion of 100 μg/h. An epidural catheter was sited at T7-T8 interspace and after test dose of 3 ml 2% lignocaine, 50 μg fentanyl in 6 ml saline was administered. Under local anaesthesia a radial artery catheter and right internal jugular line was inserted. Drugs for emergency use, octreotide, phenylephrine, glyceryl trinitrate, esmolol, corticosteroids and antihistaminics were kept handy. Anaesthesia was induced with fentanyl 100 μg, propofol 75 mg with preadministration of Inj. lignocaine 60 mg. Using vecuronium, Portex® right sided double lumen tube (DLT) 37 FG was inserted and position was confirmed by fibreoptic bronchoscope. Oxygen saturation (SpO2), end tidal CO2 (EtCO2), invasive blood pressure, ECG, central venous pressure, temperature and airway pressures were monitored throughout the procedure.
Anaesthesia was maintained with vecuronium and sevoflurane 1-1.2% in O2/N2O mixture. During surgical manipulation of tumour, there was sudden rise in peak airway pressure (P peak) from 20 to 35 cm H2O then to 42 cm of H2O and EtCO2, from 36 to 47 mmHg, then to 50 mmHg, accompanied by fall in SpO2 from 97% to 80%. On auscultation, there was marked reduction in breath sounds, with rhonchi. Flushing was observed all over the chest and face. Acute carcinoid induced bronchospasm was suspected. Surgical manipulation was stopped and N2O was discontinued. Octreotide 250 μg IV bolus was given and infusion rate was increased to 200 μg/h and inj. hydrocortisone 200 mg and chlorpheniramine 25 mg were administered IV.
Position of DLT was rechecked and ABG sample was taken. Clinical improvement was seen within 60 s of octreotide bolus and within 5 min respiratory parameters were normal. During this episode patient remained haemodynamically stable and decision was made to proceed with surgery.
Extubation was uneventful and post-operative analgesia was provided with bupivacaine and fentanyl. In the recovery room patient's SpO2 remained 97% on room air with no evidence of wheezing. Inj. octreotide infusion was tapered off over next 24 h. Histological examination of resected specimen confirmed diagnosis of carcinoid tumour.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [50.0, 'kg']}",90,85.5,94.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 50.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (50.0 kg - 20 kg) = 90.0 mL/hr.
Hence, the patient's fluid maintenance is 90.0 mL/hr."
4636,22,Maintenance Fluids Calculations,physical,decimal,pmc-2778135-1,Extracted,"A previously healthy 9-year-old boy (whose mother was recently found to be HIV-positive) presented to the hospital with 1 week of right-sided hemiplegia and right-sided facial palsy. Past medical history included psoriasis, diagnosed 4 years prior. His only HIV exposure was perinatal. On exam the patient weighed 22 kilograms, and vitals signs were within normal limits. He was alert and oriented with a normal level of consciousness and responded appropriately to questions. His speech was slowed and slurred, but this was his baseline according to his mother. He had right-sided facial palsy and right-sided tongue deviation; otherwise cranial nerves were intact. The boy had 3/5 strength in the right upper extremity and 4/5 strength in the right lower extremity. Left-sided strength was 5/5. The patient was able to walk with limited difficulty. Deep tendon reflexes were 2+ and 3+ throughout. Babinski's sign showed dorsiflexion of the right 1st toe. Sensation was intact throughout. The patient also had clusters of 1-2 mm skin colored papules on his forehead and left cheek in addition to diffuse mild psoriatic scaling. Immunizations were up to date. The patient was admitted for a workup of these symptoms.
Laboratory studies showed complete blood count: hematocrit 31.6%, hemoglobin 10.5 g/dL, white blood cell count 5000 cells/μL (N 41%, L 35%, E 12%, M 6%, B 1%, atypical L 1%), and 157 000 platelets/μL. HIV-antibody test was positive with a CD4 T-cell 0.21% (4 cells/μL) and plasma HIV RNA virus of 185 976 copies/mL (log 5.27). Tests for Cryptococcus antigen, Toxoplasmosis antigen, Ebstein Barr virus IgG and IgM, Cytomegalovirus IgG and IgM, Hepes Simplex virus polymerase chain reaction (PCR), Japanese encephalitis as well as cultures for tuberculosis and fungi (plasma and cerebrospinal fluid, CSF) were all negative. Plasma and CSF samples were positive for JCV by real time PCR with a plasma RNA level of 226 copies/mL.
Three days after admission a brain computerized tomography (CT) scan was performed and showed frond-like hypodense lesion at the left frontal lobe with mild effacement of the left frontal horn of the lateral ventricle. Highly active antiretroviral therapy (HAART) regimen was subsequently started 10 days after admission, consisting of GPOvir-Z (coformulated zidovudine 250 mg, lamivudine 150 mg, and nevirapine 200 mg) []. Clinically, the patient deteriorated during the 1st and 2nd weeks of HAART with fever and increased right leg weakness, but immunologic and virologic improvement was seen (CD4 T-cell count 0.8%, 10 cells/μL, and a plasma HIV RNA viral level of 26 532 copies/mL, log 4.42). CT () and brain magnetic resonance imaging (MRI; ) scans were subsequently performed. The scans showed progressive of white matter lesions with asymmetrical deep and subcortical white matter lesions over the left frontotemporoparietal region and the right frontal lobe. The lesion on the left hemisphere involved internal capsule, lentiform nucleus, thalamus, and genu of corpus callosum and anterior cerebellar hemisphere. There were no enhanced areas after the contrast study.
The patient was discharged 7 weeks after the first admission. Upon discharge he was able to walk with assistance, but was unable to speak.
The patient was readmitted one day after discharge due to autonomic nervous system dysfunction (nausea, vomiting, and loss of bowel and bladder tone). Deep tendon reflexes were 4+ throughout, and Babinski was positive bilaterally. Continued improvement of immunologic (CD4 T-cell count 2.0%, 30 cells/μL) and virologic (HIV RNA level 3220 copies/mL, log 3.51) measures were seen. Due to progressive neurologic symptoms HAART was ceased. The second MRI () scan was performed and showed a progressive lesion in the same regions as described in the previous MRI, but also found new lesions over the midbrain, pons, and medulla predominantly on the left. The patient was discharged approximately 3 weeks after admission.
The patient was readmitted 1 month later (100 days after onset of symptoms). Immune Reconstitution Inflammatory Syndrome (IRIS) was suspected, and the boy was treated with methylprednisolone (2 mg/kg/day) for 5 days. Despite HAART suspension and administration of steroids, his clinical symptoms worsened. The third MRI () scan showed new lesions in the regions of the right brainstem and right hemisphere with gyral enhancement. The patient's mother refused further treatment, he was discharged home, and he subsequently died 1 year later.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [22.0, 'kg']}",62,58.9,65.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 22.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (22.0 kg - 20 kg) = 62.0 mL/hr.
Hence, the patient's fluid maintenance is 62.0 mL/hr."
4637,22,Maintenance Fluids Calculations,physical,decimal,pmc-3384799-1,Extracted,"A 29-year-old woman (height, 164 cm; weight, 85 kg; gravid 2; parity 0) underwent cesarean delivery at 23 weeks' gestation. She had a history of antiphospholipid syndrome diagnosed by her rheumatologist 11 years ago. She experienced deep vein thrombosis with antiphospholipid antibodies and was lupus anticoagulant positive in that time. She was taking Astrix (100 mg/day). Six days before operation, she was admitted due to persistant epigastric pain. Blood pressure was 120/80 mm Hg, heart rate was 72 beats/min and body temperature was 36.8℃. Blood laboratory data were as follows: serum aspartate aminotransaminase (AST) 549 IU/L, serum alanine aminotransaminase (ALT) 489 IU/L, serum lactate dehydrogenase (LDH) 790 IU/L, blood urea nitrogen (BUN) 17.5 mg/dl, creatinine 0.5 mg/dl, hematocrit 29.7%, platelet count 54 × 103/ml, prothrombin time (PT) 12 sec and activated partial thromboplastin time (aPTT) 82.4 sec. A urine specimen demonstrated proteinuria (1+). Transabdominal ultrasound showed weak portal vein flow (main, 18.4 cm/sec; right, 30 cm/sec; left, 29 cm/sec) with a small amount of ascites. The obstetrician suggested autoimmune hepatitis or portal vein thrombosis was complicating antiphospholipid syndrome rather than HELLP syndrome because of the early gestational period and normal blood pressure. Repeated daily blood chemistries revealed an aPTT of 41-60 sec and therefore 1,000 unit/hour of heparin was initiated to reach the target aPTT of 80-100 seconds and 40 mg of prednisolone was added as treatment. For evaluating autoimmune hepatitis, auto-antibodies were checked. Anti-cardiolipin antibodies were examined by enzyme linked immunosorbent assay (ELISA). The IgG (51.8 GPL units/ml) was positive and IgM (2.76 MPL units/ml) was negative. A lupus anticoagulant test was also positive (control ratio of 2.67). Other laboratory investigations were unremarkable. On the morning of the operation, she had abrupt vomiting with generalized tonic-clonic seizures with eyeball deviations of 30-40 sec; she recovered spontaneously. One hour after the 1st seizure attack, she had another seizure attack with high blood pressure (200/100 mmHg); hydralazine and diazepam was given. The laboratory findings revealed AST/ALT 1,459/1,108 IU/L, LDH 1,424 IU/L, hematocrit 30%, platelet count 43 × 103/ml, aPTT 87.6 sec and urine protein (4+).
An emergency cesarean delivery was scheduled, she was not premedicated and upon arrival to the operating room, standard monitoring devices were applied. Vital signs were blood pressure 190/120 mmHg, heart rate 110 beats/min and pulse oxymetry revealed 99% oxygen saturation before anesthetic induction. The patient already received heparin and therefore, the patient did not wear a compression stocking as this could increase arterial blood pressure with increased venous return. Anesthesia was induced with 300 mg of pentothal sodium and 50 mg of rocuronium. Tracheal intubation was performed using a single lumen internal diameter (ID) 6.5 mm tube in one attempt without difficulty. Anesthesia was maintained with sevoflurane (1-2%) within BIS between 30-60. Systolic blood pressure was maintained about 140-160 mmHg using intravenous nicardipine (100-300 ug bolus) and body temperature was maintained about 36.8-37.3℃. A cesarean delivery was performed by a Pfannenstiel incision and a 470 gram live-born male infant was delivered (APGAR score; at 1 min, 3 and at 5 min, 7). Intravenous magnesium sulfate (170 mg/hour) and alfentanyl (1,000 ug) were given to the patient. The cesarean delivery proceeded without an event. The patient received fentanyl (1,000 ug) in 100 ml of normal saline for 48 h using patient controlled intravenous analgesia. At the end of surgery, all anesthetic agents were discontinued and the residual neuromuscular blockade was reversed with pyridostigmine and glycopyrrolate. Estimated blood loss was 500 ml and she was not transfused with blood components. The tracheal tube was removed when the patient responded to verbal commands and showed sufficient spontaneous respiration and neuromuscular function. There were no signs of uterine atony or bleeding. Pathologic observation of the placenta revealed mulifocal infarction involving up to 40% of the placenta. The patient remained in the post-anesthetic care unit for 1 hour event free and was then transferred to the intensive care unit. Intravenous magnesium sulfate used for 24 hours and she was transferred to the general ward at postoperative day 1. She had an uneventful recovery with improved liver function and platelet counts () and was discharged on postoperative day 8.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [85.0, 'kg']}",125,118.75,131.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 85.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (85.0 kg - 20 kg) = 125.0 mL/hr.
Hence, the patient's fluid maintenance is 125.0 mL/hr."
4638,22,Maintenance Fluids Calculations,physical,decimal,pmc-8429817-1,Extracted,"An 11-year-old Chinese girl was admitted to our hospital who presented with nephrotic syndrome. She weighed 49 kg and her blood pressure was 120/80 mmHg. Physical examination at admission revealed mild edema of the lower limbs with no associated corneal arcus or xanthoma. Laboratory investigations showed anemia (98 g/L), elevated serum urea (6.7 mmol/L) and creatinine (58 μmol/L), and decreased albumin (21 g/L). Urinalysis revealed proteinuria (4+) and microscopic hematuria (3+). Urinary protein was 2.06 g/24 h. Lipid profile showed elevated total cholesterol (5.04 mmol/L), elevated triglyceride (2.18 mmol/L), and normal LDL-cholesterol (2.24 mmol/L).
Based on laboratory findings, secondary causes of NS were excluded. Anti-nuclear, anti-cardiolipin, anti-neutrophil cytoplasmic, and anti-glomerular basement membrane antibodies were negative. Rheumatoid factor was also negative. Hepatitis B and C serology were negative. In addition, complement C3 and C4 levels were normal. Renal ultrasonography revealed normal-sized kidneys. These findings were consistent with the diagnosis of primary NS.
Despite treatment with prednisone (60 mg/day) and captopril (60 mg/day) for 2 months, her massive proteinuria and microscopic hematuria persisted, thereby prompting further evaluation via percutaneous renal biopsy. Light microscopy showed segmental glomerulosclerosis in three out of nine samples and mild-to-moderate proliferation of the mesangial cells and matrix (). The capillary lumina were dilated due to the presence of lipoprotein thrombi with pale staining on periodic acid-methenamine silver (). Oil red O staining confirmed the presence of intraluminal lipid droplets (). Immunofluorescence microscopy revealed that immunoglobulins (i.e., IgG, IgA, and IgM) and complement factor 1q (C1q) were negative. These findings were highly suggestive of LPG.
Genetic testing confirmed the presence of the c.127C>T (p.R43C) or Kyoto mutation of the APOE gene (). Her parents refused to undergo genetic screening. Therefore, her grandparents were investigated and underwent genetic screening. Her grandfather was asymptomatic and her grandmother was otherwise healthy. The APOE mutation in the patient and her grandfather were heterozygous (). In addition, the patient did not have any siblings.
All of these findings were consistent with the diagnosis of LPG. Prednisone was gradually tapered. Ideally, the patient should have been given captopril and a lipid-lowering agent. However, her grandfather refused the latter.
A 2-year follow-up revealed that her serum creatinine (102 μmol/L) and urine protein levels (3.2 g/24 h) were elevated. Moreover, her lipid profile showed elevated total cholesterol 6.56 mmol/L, triglyceride (2.82 mmol/L), and LDL-cholesterol (3.87 mmol/L).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [49.0, 'kg']}",89,84.55,93.45,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 49.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (49.0 kg - 20 kg) = 89.0 mL/hr.
Hence, the patient's fluid maintenance is 89.0 mL/hr."
4639,22,Maintenance Fluids Calculations,physical,decimal,pmc-5337310-1,Extracted,"A 42-year-old Caucasian female, gravida 3 para 1 (1 spontaneous vaginal delivery and 2 elective abortions), was admitted with a 2-month history of diffuse abdominal pain, decreased appetite, nausea, vomiting, abdominal distention, weakness, and a twenty-pound unintentional weight loss. Her history was significant for a twenty-eight-pack-year tobacco use and a copper IUD placed approximately fifteen years earlier.
On admission, the patient was found to be cachectic, tachycardic, and tachypneic but afebrile. Her abdomen was moderately distended, tender to palpation throughout but without acute peritoneal signs. It was diffusely tympanic but dull over bilateral lower quadrants, with hypoactive bowel sounds. External genitalia and vagina were normal. Cervix was parous in appearance with two strings visualized from the cervical os; IUD was removed and sent for microbiologic studies. Uterus was difficult to palpate secondary to pain and adnexal tenderness. Adnexa were diffusely tender with bilateral fullness. Rectal exam showed normal tone and normal rectovaginal septum with fullness palpated anteriorly.
The patient's initial laboratory evaluation showed marked leukocytosis (WBC: 29,000), anemia (Hgb: 10.9), hypoalbuminemia (albumin: 2.2), and mildly elevated CA 125 (54). AST/ALT, CEA, and CA 19-9 were normal. No infectious disease was found per evaluation via urine and blood cultures, gonorrhea, chlamydia, vaginitis panel (testing for trichomoniasis, candida, and bacterial vaginosis), tuberculin test, HIV, or hepatitis B and hepatitis C.
CT of the abdomen demonstrated marked bowel distention and a complex cystic mass within the left pelvis with enhancing septations measuring 8.2 × 6.7 × 9.8 cm, retroperitoneal lymphadenopathy, and small ascites with peritoneal enhancement. Large distended bowel loops surrounded the heterogeneous lesion peripherally ().
Parenteral antibiotics (Meropenem and Vancomycin) were started for coverage of pelvic abscess of unknown etiology with noted improvement in leukocytosis after 72 hours. Nasogastric tube was placed for upper GI decompression and control of emesis for suspected partial small bowel obstruction. Total parenteral nutrition was also started to improve her malnourished state. Gynecologic oncology was consulted and concluded that the likelihood of carcinomatosis was very low based on the patient's age, absence of omental caking or peritoneal implants on CT, and only mildly elevated CA-125. In the presence of a neglected IUD for 15 years with low suspicion for malignancy, actinomycosis was a likely diagnosis. CT-guided diagnostic paracentesis was performed after bowel decompression was achieved with NG tube. Purulent peritoneal fluid was obtained which was negative for malignancy, yet positive for Actinomyces (). Copper IUD was removed and culture grew Micromonas micros and Actinomyces ().
One week after initiation of antibiotic therapy, repeat CT of abdomen and pelvis showed stable to slightly improved fluid collections compared to prior exams. As final laboratory diagnosis was achieved, Vancomycin and Meropenem were discontinued after 8 and 11 days of treatment, respectively.
The patient was started on Ampicillin-Sulbactam 3 g IV every 6 hours, which helped control her leukocytosis. On day five of the Ampicillin-Sulbactam, AST and ALT values were 209 and 148, respectively, and patient was diagnosed with transaminitis secondary to the Ampicillin-Sulbactam. The Ampicillin-Sulbactam was discontinued, which improved the transaminitis, and the patient was started on Penicillin 3 million units IV every 4 hours, which was continued for a total of 4 weeks.
After 3 weeks of in-hospital management, patient was tolerating regular diet with regular bowel movements and improved pain control. Patient was discharged home with close outpatient follow-up arranged. At her outpatient follow-up four weeks later, she was transitioned to Penicillin 500 mg PO four times daily. Patient continued Penicillin orally for 1 year, during which she was gaining the strength and weight back with assistance of nutrition and occupational therapy professionals.
Repeat CT of abdomen and pelvis 1 year after initiation of treatment demonstrated complete resolution of bowel distention, ascites, and adenopathy; the left adnexal mass had more than 50% size reduction, measuring 3.9 × 3.2 cm (). The patient was found to have complete resolution of pain and abdominal distention, as well as 21 lbs weight gain since treatment was initiated.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [21.0, 'lbs']}",38.10172,36.19663,40.00681,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 21.0 lbs so this converts to 21.0 lbs * 0.453592 kg/lbs = 9.52543 kg. Hence, the patient's maintenance fluid is 9.52543 kg * 4 mL/kg/hr = 38.10172 mL/hr.
Hence, the patient's fluid maintenance is 38.10172 mL/hr."
4640,22,Maintenance Fluids Calculations,physical,decimal,pmc-6675956-1,Extracted,"A 42-year-old male whose Crohn's disease had been controlled with medications for more than 19 years visited the emergency room (ER) with small bowel dilation and mechanical ileus in October 2018. Emergency surgery was performed because the ileus became exacerbated and small intestinal perforation was suspected. A severe adhesion and a fistula were found at the 200 cm point (in the Treitz ligament) and another severe adhesion was evident in the distal ileum. Bowel segments about 80 cm in length both proximal and distal to the lesion were resected and then loop ileostomy was formed. The remaining small bowel was 160 cm in length.
At the time of ER admission, an initial nutritional assessment was conducted. He was moderately malnourished based on the American Society for Parenteral and Enteral Nutrition (ASPEN)/Academy of Nutrition and Dietetics (AND) malnutrition criteria []. His estimated nutritional need was 25–30 kcal/kg usual body weight (UBW)/day with 1.2–2.0 g protein/kg UBW/day based on guidelines for the adult critically ill patient []. Because of the mechanical ileus, total PN was initiated with a target of 25 kcal/kg UBW/day and 1.4 g protein/kg UBW/day. PN was customized to prevent the development of electrolyte imbalances.
After extensive small bowel resection, the estimated energy requirement was 1,500 kcal/day (derived using the Penn State equation). In order to decrease stomal output and allow persistent luminal stimulation, continuous tube feeding with a low-residual formula (500 kcal) was initiated at 20 mL/hr over 24 hours. When he could tolerate 1,200 kcal/day at 50 mL/hr over 24 hours, he was weaned off PN (1,058 kcal/day, protein 58 g/day). According to evaluations about 1 month after surgery (postoperative day [POD] #30), he had continued to lose weight; he weighed 41.1 kg (body mass index [BMI] 13.9 kg/m2) which meant he had lost 21.6% of his body weight at admission. HOS (about 3,000 ml/day) and elevated blood urea nitrogen (24.0 mg/dL) and creatinine (1.6 mg/dL) were observed, so the risk of dehydration was high. Although on POD #30 magnesium concentration was not measured, it was 1.5 mEq/dL on POD #14, and since it was the marginal level and PN was suspended, deficiency of micronutrient was also expected. Intake via tube feeding was 1,400 kcal/day (34 kcal/kg current body weight [CBW]) and protein 56 g/day (1.35 g/kg CBW). Our NST decided to increase the enteral nutrition (EN) supply to the target calorie level and to provide supplemental PN (commercial 3-in-1 PN with multivitamins and trace elements, 345 kcal/day, protein 16 g/day) to replenish nutrients lost. Total amount supplied, including EN and PN, was 1845 kcal/day (45 kcal/kg CBW) and protein 75.8 g/day (1.85 g/kg CBW).
He commenced an oral diet 6 weeks after operation (POD #43) and was again weaned from PN. A dietitian evaluated dietary intake, and assessed stomal output volume and consistency. The estimated dietary intake was 1400 kcal/day with protein 80 g/day. The stomal output was approximately 3,000 mL/day (the bag was emptied 10 times/day) of watery diarrhea. The dietitian educated the patient on the need for frequent small meals, the sipping of fluid between meals (thus not with meals) to ensure hydration, and the avoidance of foods containing high levels of fiber and sugary beverages, which might exacerbate stomal output. Multivitamins and multiminerals were recommended. As a typical Korean meal includes a bowl of vegetable soup and several vegetable side dishes, the need to strictly avoid soup and vegetables was emphasized. The guidelines recommend commencing vegetables 6–8 weeks after operation. However, given his HOS status, a vegetable-free diet was maintained until the stomal output fell to below 2,000 mL/day, even 8 weeks after the operation. To enhance compliance and to help him understand the principles of food selection, the dietitian visited him 4 times.
As discharge approached, the dietitian conducted a nutritional re-assessment. The patient exhibited severe malnutrition based on the ASPEN/AND criteria []. He had lost 25.4% of his body weight and exhibited moderate loss of muscle mass and body fat. His estimated nutritional requirements were 35–45 kcal/kg UBW/day and 1.5–2.0 g protein/kg UBW/day. He was taking 1,800 kcal and 90 g protein/day but still losing weight. To increase his weight and improve his nutritional status, home PN support was recommended. The NST planned home PN three times/week (commercial 3-in-1 PN with multivitamins and trace elements, 578 kcal, protein 26 g).
When he was re-admitted 1 month after discharge (POD #106), nutritional re-assessment was performed. His percent of ideal body weight value was 71.6%, his BMI was 15.8 kg/m2, and the nutritional intake met his requirements; his nutritional status had improved compared to that 1 month earlier. His progress is summarized in .
The energy intakes from both EN and PN after loop ileostomy are shown in . Two months after operation (POD #60), his body weight was 40.3 kg at discharge. He maintained the oral intake that he had established in the hospital, and received home PN, for 2 months after discharge. About 18 weeks after the operation (POD #106), he was re-admitted to manage necrosis of both feet and hands associated with use of an inotropic agent in the intensive care unit. His body weight was 46.6 kg (BMI 15.8 kg/m2), and had thus increased by 15.6% since discharge.
After ileostomy, intravenous PN and/or fluids were administered for about 18 weeks. lists the laboratory data, stomal output volumes, and the PN infusion details. Although a large stomal output (about 3,000 mL/day) of watery diarrhea was observed in the early postoperative period, the electrolyte balance was optimized via infusion therapy. When he was re-admitted (POD #106), his stomal output was slightly reduced but the consistency had thickened significantly.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [46.6, 'kg']}",86.6,82.27,90.93,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 46.6 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (46.6 kg - 20 kg) = 86.6 mL/hr.
Hence, the patient's fluid maintenance is 86.6 mL/hr."
4641,22,Maintenance Fluids Calculations,physical,decimal,pmc-3031022-1,Extracted,"This 41-week-gestation male was born to a 30-yr-old mother with good health by normal spontaneous vaginal delivery in November 2009. His birth weight was 3,140 gm. There was no maternal complication during pregnancy. There was neither family history of congenital anomalies nor maternal exposure to drugs during pregnancy. The baby had APGAR scores of 7 and 5 at 1 and 5 min, respectively. He needed positive pressure ventilation with intubation because of progressive respiratory difficulties and hypoxia. The baby was immediately transferred to our hospital for further evaluation and management after stabilization.
The physical examination and laboratory findings for the baby were unremarkable on admission. He had the surfactant replacement therapy for acute respiratory failure. For the next few days, we tried extubation several times, but failed to succeed because the baby suffered from recurrent apnea and hypercarbia leading to the clinical suspicious of CCHS. On day 8 of life, a cranial ultrasound study was performed and it did not show evidence of hemorrhage or mass lesions.
During the second day of life, it was noted that the patient had distended abdomen and was unable to pass meconium without rectal stimulation. A gastrografin contrast enema study showed multiple meconium plugs in the colon suggesting meconium plug syndrome (). Meconium was passed and abdominal distension was relieved after contrast study. On day 6 of life, he showed sustained abdominal distension with poor bowel movement. A barium contrast enema study was needed to rule out other causes of lower gastrointestinal obstruction. It showed a transition zone in rectosigmoid colon suggesting HD. The diagnosis was confirmed by rectal suction biopsy with acetylcholinesterase immunohistochemistry (). The infant underwent an open laparotomy on day 12. He was noted to have long segment HD with a transition zone at mid descending colon. Seromuscular biopsies of the bowel taken 3cm proximal and distal to the transition zone revealed the presence of ganglion cells in the proximal biopsy specimen only. A descending loop colostomy was done at the 2 cm from proximal biopsy site. After the diagnosis, the patient was transferred to another hospital for the treatment. The patient had a tracheostomy to provide the necessary assisted ventilation. Laparoscopic Pull through Procedure was carried out for the treatment of HD. After the discharge, he has been followed up until now.
The cytogenetic study was performed clinically in the infant and his parents and their karyotypes were normal. Genomic DNA of the patient and his parents was isolated from peripheral blood using the Wizard Genomic DNA Purification Kit according to the manufacturer's instructions (Promega, Madison, WI, USA). Amplification of the coding sequence of the PHOX2B gene by polymerase chain reaction (PCR) was carried out as previously described with minor modifications (). Polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP) was performed as previously described (). PCR products in the patient, his parents, and normal controls were electrophoresed through 8 and 10% polyacryamide gels (). In patient, a mutant band was found, however, his parents had no mutant band. To determine the sequences of the DNA sample showing the mutant band, direct sequencing was performed by Macrogen Inc, in Korea. However, the quality of the result was not clear. To get apparent result of sequencing, PCR products were cloned by TOPO TA cloning (Invitrogen Ltd., Paisley, United Kingdom) and 10 single colonies were collected for extracting plasmid DNA. Direct sequencing revealed expanded alleles containing polyalanine 26 repeats in exon 3 of the PHOX2B gene, further supporting the diagnosis CCHS ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.14, 'kg']}",12.56,11.932,13.188,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.14 kg. Hence, the patient's maintenance fluid is 3.14 kg * 4 mL/kg/hr = 12.56 mL/hr.
Hence, the patient's fluid maintenance is 12.56 mL/hr."
4642,22,Maintenance Fluids Calculations,physical,decimal,pmc-8185152-1,Extracted,"A 7-month-old girl presented to the Department of Gastroenterology because of recurrent episodes of fever, abdominal pain, diarrhea, and failure to thrive for 4 months. The girl was born at 40 weeks with a birth weight of 3,000 g. The family history was unremarkable. At the age of 3 months, she was admitted to the pediatric intensive care unit (PICU) due to 8 days of unexplained fever, vomiting, severe diarrhea, spasmodic cough, and aggravated shortness of breath for half a day. The patient was given intravenous administration of broad-spectrum antibiotics for clinical sepsis and supportive treatment for other symptoms in the PICU. After discharge from the PICU, the patient still suffered from multiple episodes of fever, diarrhea, and failure to gain weight. On admission, she had a weight of 4.3 kg (<1st percentile, Z score, −5.10) and a height of 56 cm (<1st percentile, Z score, −5.20). Diffuse small miliary red papules around the skin of the mouth and a white ulcer (3*2 mm) on the right-side buccal mucosa of the mouth were observed. Furthermore, she suffered from perianal ulcers and vulvar abscesses. Laboratory tests showed low levels of total protein (44.89 g/L, reference range: 60–80 g/L) and albumin (25.13 g/L, reference range: 38–54 g/L), elevated white blood cells (WBCs, 17.89*10∧9/L, reference range: 8–12*10∧9/L), an elevated erythrocyte sedimentation rate (ESR, 120 mm/h, reference range: 0–20 mm/h), and elevated procalcitonin (PCT, 8.98 ng/ml, reference range: <0.1 ng/ml), and C-reactive protein (CRP, 89 mg/L, reference range: <5 mg/L) levels. The liver biochemical profile was normal. Lymphocyte subset analysis was normal. Slightly elevated levels of immunoglobulin G (IgG), IgA, IgM, and IgE were detected. Endoscopy and colonoscopy were abandoned due to the low weight of the patient. An abdominal computed tomography (CT) scan revealed bowel wall thickening and pneumatosis. The patient was treated with montmorillonite powder, total parental nutrition (TPN), methylprednisolone, thalidomide, and intravenous administration of broad-spectrum antibiotics. She was discharged with some symptomatic improvement. However, the patient still suffered from recurrent episodes of fever, abdominal pain, and diarrhea. Therefore, she was suspected to have a primary immunodeficiency disease and was recommended for genetic testing.
To identify the genetic cause of the suspected primary immunodeficiency disease, whole-exome sequencing (WES) was performed using genomic DNA extracted from peripheral blood of the patient and her parents. A novel compound heterozygous mutation c.395T>G (p.Leu132Arg)/ex.1del (p.?) in the IL-10RA gene of the patient was identified, which was inherited from her mother and father. The p.Leu132Arg mutation is located on the “C” beta-strand within the D2 region of the extracellular domain of IL-10RA (). In silico prediction tools predicted that the c.395T>G (p.Leu132Arg) missense variant was deleterious (SIFT score, −4.712; PolyPhen-2 score, 1.000), and it was defined as a likely pathogenic variant according to American College of Medical Genetics and Genomics (ACMG) guidelines (). The ex.1del variant leads to a deletion of exon 1 of IL-10RA and is predicted to cause a loss of function of IL-10RA (SIFT score, −22.749). The ex.1del mutation was classified as a damaging variant according to ACMG guidelines. Furthermore, two IL-10RA variants were confirmed by Sanger sequencing () or quantitative PCR (). Neither variant has been reported previously.
To demonstrate a functional defect in the IL-10 signaling pathway caused by the identified novel IL-10RA mutation in the patient, PBMCs were isolated via Ficoll-Paque centrifugation and stimulated with recombinant human IL-6 (100 ng/ml) or IL-10 (100 ng/ml) for 30 min. Cell lysates were collected for immunoblotting to detect STAT3 phosphorylation. As shown in , IL-10 treatment failed to activate STAT3 phosphorylation, whereas IL-6 induced the phosphorylation of STAT3 in PBMCs from the patient. Both IL-10 and IL-6 were able to induce the phosphorylation of STAT3 in PBMCs from healthy control and the patient's father and mother (). Taken together, the patient was diagnosed with VEO-IBD caused by a novel compound heterozygous IL-10RA mutation.
After a diagnosis of VEO-IBD caused by IL-10RA deficiency, the patient was recommended for HSCT. During a long period of 10 months of management before HSCT, the patient presented with persistent symptoms of fever, abdominal pain, diarrhea, skin rashes, vulvar abscesses, and oral and perianal ulcers. The patient was admitted to our department repeatedly and was managed with symptomatic treatments, including broad-spectrum antibiotics for bacterial infection, acyclovir for viral infection, methylprednisolone for intestinal inflammation, thalidomide for immunosuppression, montmorillonite powder for diarrhea and nutritional support with TPN. At the age of 19 months, the patient underwent matched unrelated peripheral blood HSCT using reduced-intensity conditioning with busulfan, fludarabine, cyclophosphamide, and antithymocyte globulin. The CD34 cell dose was 7.5 × 106 cells/kg, the number of mononuclear cells was 15.39 × 108 cells/kg, and the platelet count was 202 × 109/L. The patient was given methotrexate (3.5 mg/day) and cyclosporine A (40 mg/day) for 4 days to prevent graft-vs.-host disease. On day +14 post-HSCT, the short tandem repeat test of the blood showed that she engrafted with 94.6% of the donor cells. Currently, the patient's clinical manifestations are dramatically improved, including relieved abdominal pain and diarrhea (<4 times per day) and full recovery of skin papules, vulvar abscesses and perianal ulcers after 1 month of HSCT.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.3, 'kg']}",17.2,16.34,18.06,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.3 kg. Hence, the patient's maintenance fluid is 4.3 kg * 4 mL/kg/hr = 17.2 mL/hr.
Hence, the patient's fluid maintenance is 17.2 mL/hr."
4643,22,Maintenance Fluids Calculations,physical,decimal,pmc-4173390-1,Extracted,"A 12-year-old boy presented to the oral and maxillofacial surgery department of our institution with swelling in lower jaw since 6 months, which progressively increased in size and was painful. It was diagnosed to be dentigerous cyst that required excision due to its painful symptomatology. He was an established case of Duchenne muscular dystrophy since childhood and was confined to wheel chair since then. The child had no history of recent upper respiratory tract infection or previous anesthetic exposures. On physical examination, the weight of the child was measured to be 48 kg and he had wasting of muscles in both the lower limbs with motor power of grade II. Airway examination revealed mouth opening of >3 cm with modified Mallampati grade of II, normal thyromental and mento-hyoid distance and normal range of neck movements []. Examination of the back revealed a mild scoliosis involving the thoraco-lumbar region with convexity toward the right side. Cardiovascular and respiratory system examination was unremarkable. The laboratory investigations were all within normal limits except for raised creatine kinase levels of 1823 IU/L (normal 75–230). The electrocardiography showed sinus tachycardia and biventricular hypertrophy and findings of echocardiography revealed an ejection fraction of 32% with moderate depression of the left ventricular systolic function. The child was planned for excision of dentigerous cyst. During the preoperative visit, the child and the parents were highly anxious about the procedure but after careful counseling and discussion of various implications and the risks associated with general anesthesia, the parents and the child agreed to undergo the procedure under procedural sedation. The child was given nil per oral instructions according to the standard protocol and was advised tab. ranitidine 150 mg PO and tab. metoclopramide 10 mg PO in the night and in the morning 2 h before the planned procedure. On the day of procedure, the anesthesia machine was properly checked and flushed to remove any traces of inhalational agents and all vaporizers were removed. The child was shifted to the operating room and an intravenous line was secured and preloading done with 400 mL of the normal saline solution. The monitoring included five lead electrocardiography, noninvasive blood pressure (NIBP) and pulse oximetry. The child was then premedicated with glycopyrrolate 0.2 mg intravenously (IV) and fentanyl 1 μg/kg was given IV to achieve analgesia. Dexmedetomidine was administered slowly with a loading dose of 1 μg/kg over 15 min followed by a continuous infusion at 0.5 μg/kg/h throughout the surgical procedure. Lignocaine with 1 in 2 lakh adrenaline was used for local infiltration and the child was given supplemental oxygen through nasal prongs at 3 L/min. The child remained calm and comfortable throughout the procedure which lasted for 40 min and did not complain of any pain. At the end of procedure, the dexmedetomidine infusion was discontinued and the child remained sedated but arousable to verbal commands. Postoperatively, the child was observed in a high dependency unit for 2 h. The recovery period was uneventful and the child was discharged after 6 h when fully awake and responding.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [48.0, 'kg']}",88,83.6,92.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 48.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (48.0 kg - 20 kg) = 88.0 mL/hr.
Hence, the patient's fluid maintenance is 88.0 mL/hr."
4644,22,Maintenance Fluids Calculations,physical,decimal,pmc-2778868-1,Extracted,"A 40-week, 2884 g, female infant was delivered via
cesarean section to a 41-year-old primigravida after arrest of descent and
failed vacuum extraction. Complications of the pregnancy included a history of
infertility, gestational diabetes (glyburide controlled), prolonged rupture of
membranes, and chorioamnionitis. Apgar scores were 1, 7, and 8. Umbilical
artery and venous pH were 6.94 and 7.06, respectively. Initial blood testing
was nonspecific. Physical examination was significant for a large left caput
succedaneum with a soft and flat anterior fontanel. Neurological examination
demonstrated mild hypotonia. At approximately 36 hours of age, the patient had
seizure activity consisting of eye fluttering, bilateral clonic movements of
the upper extremities, and tongue thrusting. Two separate events occurred, each
lasting less than three minutes.
Repeat blood testing revealed a normal
glucose level, no significant electrolyte abnormalities, a white blood count of 9.8 × 103/mm3, and hematocrit of 46.8%. The platelet count had
decreased from 155 (initial) to 119 × 103/mm3 with subsequent drop to 109 × 103/mm3 twenty four hours later. Cerebrospinal fluid evaluation revealed
(traumatic lumbar puncture) 115 000/mm3 red blood cells, 50/mm3 white blood cells with 87% polys and 12% lymphs. 
The patient was given a loading dose of phenobarbital, and ampicillin and gentamicin
had been started shortly after birth.
Magnetic resonance imaging (MRI) of the
brain () demonstrated bilateral multifocal regions of increased signal
on diffusion-weighted imaging in the left pons, left occipital lobe, left
thalamus, left and right frontal lobes, and left and right frontoparietal
regions. No evidence indicated hemorrhage, and all of the lesions were dark on apparent
diffusion coefficient of water (ADC) mapping indicating that they were acute in
nature (within 1 week). A transthoracic echocardiogram demonstrated normal
cardiac anatomy with no intracardiac thrombus or vegetation. Magnetic resonance
angiography (MRA) of the head and neck without contrast () demonstrated
occlusion of the right internal carotid artery (ICA) at its origin without distal
reconstitution. Collateral flow directed blood through the anterior
communicating artery to the right anterior cerebral artery (ACA) and right
middle cerebral artery (MCA). The vertebral arteries were diminutive and the
basilar artery was occluded. The posterior communicating arteries and PCAs were
not visualized. With this extent of vessel occlusion, even more widespread
brain infarction might be expected. However, the complex distribution of the
infarcts demonstrated on diffusion-weighted images can be explained by the
relative robustness of the patient's leptomeningeal collateral vessels. EEG
evaluation demonstrated left parieto-occipital spike wave discharges with
associated slowing, excessive subtransients for age, and mild slowing and
suppression of background activity.
Bacterial
and viral studies were negative. Placental pathology demonstrated a third
trimester placenta with acute necrotizing chorioamnionitis and a three-vessel
cord with acute funisitis (inflammation of the umbilical cord). Extensive thrombophilia
evaluation performed on day of life four () failed to identify any
inherited or acquired prothrombotic risk factors. However, other than negative
DNA mutation analysis, definitive protein abnormalities could not be ruled out
until repeat evaluation performed at 3–6 month of life []. State metabolic screening through the State of
Florida was negative.
Prior 
to the results of the thrombophilia evaluation, we decided to anticoagulate the
patient with LMWH. We based this decision on the occlusion of multiple large
blood vessels with evidence of multifocal cerebral infarctions, a pattern
indicative of an embolic process. Our rationale for choosing LMWH was to
decrease the risk of clot extension, which was suggested by the progressive
thrombocytopenia. LMWH was initiated, using a therapeutic antifactor Xa level
of 0.5–1.0 IU/mL.
The patient had no further seizure
activity, and gradually improved during her admission. The platelet count
increased after starting therapy to 156 × 103/mm3 and then 253 × 103/mm3, at 48 hours
and 96 hours, respectively. She was discharged home on day of life 13 from the
neonatal intensive care unit taking full oral feedings, and her family was
instructed to continue phenobarbital and LMWH with scheduled follow-up.
MRI evaluation at four months of age
demonstrated bilateral encephalomalacia in areas of prior infarction with no
evidence of current or prior hemorrhage. Mild encephalomalacia was also seen in
the right PCA territory, which was not ischemic on the initial MRI. This likely
reflected an additional infarct which most likely occurred during or soon after
the initial scan, possibly before the initiation of LMWH. MRA evaluation
() revealed resolution of the right ICA thrombus with overall decreased
caliber of the vessel compared to the left, and residual irregularity and
narrowing at the superior cervical segment. The intracranial vessels were all
patent, although the right PCA was diminutive. Repeat thrombophilia assessment at four months of life was negative ().
We
discontinued LMWH treatment after obtaining the results of the repeat MRI, MRA,
and thrombophilia evaluations. Neurological evaluation at 4.5 months of age
demonstrated asymmetric tracking and blinking to confrontation which was worse
on the left, mildly increased flexor tone of the left upper extremity, normal
lower extremity tone and reflexes bilaterally, and age appropriate milestones
for gross motor, fine motor, and social interaction. No seizure activity has
been observed or suggested on EEG evaluation, and phenobarbital has been
weaned. Neuro-ophthalmological examination at 6 months of age demonstrated
normal visual acuity for age and normal blinking to confrontation. The patient continues to thrive and develop
at home.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2884.0, 'g']}",11.536,10.9592,12.1128,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2884.0 g so this converts to 2884.0 lbs * kg/1000 g = 2.884 kg. Hence, the patient's maintenance fluid is 2.884 kg * 4 mL/kg/hr = 11.536 mL/hr.
Hence, the patient's fluid maintenance is 11.536 mL/hr."
4645,22,Maintenance Fluids Calculations,physical,decimal,pmc-3915732-2,Extracted,"A 5-year-old girl was hospitalized because of abdominal distention and severe bilious vomiting. Her defecation was not changed but was loose. She had history of anorexia, poor weight gain and abdominal distention since infancy but had not have visited previously. She was toxic, febrile and cachectic with weight of 12 kg (<3% weight percentile for age for girls) and height of 96 cm (<5% height percentile for age for girls). Her lung was normal but heart was tachycardic. Abdomen was distended with hyperactive bowel sound, and diffuse tenderness was noted on palpation. Her abdominal X-ray revealed air-fluid levels, indicative of bowel obstruction. Abdominal ultrasonography revealed gas distention of bowel loops and reductable transient intussusceptions with donuts appearance on the right side of the abdomen (). Nasogastric tube was inserted. After three days of serum therapy and administration of antibiotics, vomiting had stopped and abdominal distention decreased gradually. Laboratory tests revealed leukocytosis (18,400/mm3) with polyneucleosis (11,800/mm3), anemia (hemoglobin, 8.4 g/dL), normal serum electrolytes, tTG IgA >800 U/mL, and tTG IgG >200 U/mL. Diagnosis of celiac disease was confirmed with endoscopic duodenal biopsies, showing histopathology of marsh III (). After six months GFD, she had got good appetite and gained 6 kg of weight and her distention was resolved near completely.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.0, 'kg']}",44,41.8,46.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.0 kg - 10 kg) = 44.0 mL/hr.
Hence, the patient's fluid maintenance is 44.0 mL/hr."
4646,22,Maintenance Fluids Calculations,physical,decimal,pmc-6206789-1,Extracted,"A 70-year-old male, weighing 62 kg, with no comorbid illness, presented to us with complaints of chest pain and breathlessness following road traffic accidents (RTAs). Chest X-ray showed mediastinal widening []. The CECT chest showed dissection of DTA just distal to the left subclavian artery, extending over a length of 4 cm with a para-aortic hematoma []. He was planned for surgical resection of dissection and end-to-end anastomosis of DTA through left posterolateral thoracotomy using left heart bypass. In the operation theater, general anesthesia was induced with balanced anesthesia technique. A 37 F left-sided double-lumen tube was inserted for the isolation of the left lung. TEE examination confirmed the dissection in DTA. Midesophageal descending thoracic aorta long axis view showed a large lacerated flap in the DTA opening into a large (4 cm × 5 cm) pseudoaneurysm cavity. Color flow Doppler showed free flow of blood from the lumen of DTA to the aneurysm. Careful look demonstrated another tear in the wall of DTA few centimeters below the large dissection flap []. Color flow Doppler showed turbulent jet originating from DTA lumen and entering into the same aneurysm cavity. The finding was discussed with the surgeon, and the surgical approach for left heart bypass was modified. Left heart bypass was instituted with cannulation of the left atrium and femoral artery instead of direct cannulation of DTA. A cross-clamp on DTA was applied such that it remains well below the lower margin of the 2nd intimal tear and enough margin of healthy DTA remains available for the anastomosis. Diseased part of DTA was resected, and a Dacron graft was used as a conduit for the anastomosis between proximal and distal end of DTA. After surgery, the patient was shifted to the Intensive Care Unit and extubated after 2 h. The patient had uneventful postoperative course and was discharged from the hospital after 3 days.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [62.0, 'kg']}",102,96.9,107.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 62.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (62.0 kg - 20 kg) = 102.0 mL/hr.
Hence, the patient's fluid maintenance is 102.0 mL/hr."
4647,22,Maintenance Fluids Calculations,physical,decimal,pmc-6567292-1,Extracted,"A 39-year-old man was referred to our clinic due to infertility. His height and weight were 175 cm and 82 kg, respectively. The patient left school when he was in the third grade of primary school because of learning issues. He was unable to read and write properly, and had deficits in intellectual ability like reasoning or problem solving. Currently, the patient was working as a cleaner in a factory. He was noted to have mild ID.
On physical examination, the patient had no dysmorphic features. He was married for 8 years; he and his wife were not consanguineous. His parents had two children and the family history of the patient was remarkable for a deceased brother at the age of 15 years, who had also ID (
). Since there was no history of spontaneous pregnancy during his marriage, the patient was considered to represent a case of primary infertility who had also mild ID. Sperm analysis showed complete azoospermia.
In vitro fertilization was performed four times by testicular sperm extraction without success. Luteinizing hormone, follicular stimulating hormone and testosterone levels were compatible with hypergonadotropic hypogonadism (
). Y micro-deletion analysis demonstrated that AZFa, AZFb and AZFc regions on the Y chromosome were intact. After conventional cytogenetic analysis, we performed array conventional cytogenetic technique (aCGH). Karyotype analysis could not be performed for the parents or the patient’s brother, since they were not alive.
Conventional cytogenetic technique: Peripheral blood lymphocytes were used for a 72-hour culture. Chromosome analysis was performed on phyto-haemagglutinin-induced peripheral blood lymphocytes. Metaphase plaques were analyzed using the GTG banding method at almost 500–550 band resolution.
aCGH: An Agilent SurePrint G3 CGH+SNP Microarray Kit (4x180K) was used for genetic analysis of the patient. Microarray data were analyzed using Feature Extraction and Agilent Cytogenomics v4.0.3.12 software. Log ratios between -0.5 – 0.5 and variations with less than 5 consecutive probes were excluded. Genomic positions were based on GRCh37/hg19
Homo sapiens assembly.
Conventional cytogenetic analysis revealed that the patient had an insertional translocation: 46, XY, inv ins(18;2)(q11.2;q13q22) (
). Array CGH did not show any deletion or duplication (
).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [82.0, 'kg']}",122,115.9,128.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 82.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (82.0 kg - 20 kg) = 122.0 mL/hr.
Hence, the patient's fluid maintenance is 122.0 mL/hr."
4648,22,Maintenance Fluids Calculations,physical,decimal,pmc-3814067-1,Extracted,"An obese, 16-year-old, Caucasian female with a 4-year history of T2DM presented to our endocrinology practice for a follow-up visit on October 26th, 2012. She was diagnosed with diabetes at the age of 12 and has a significant family history for Type 2 diabetes and obesity. Her medical history is significant for T2DM complicated by microalbuminuria, depression, and type IV hyperlipidemia. She was referred to the practice for management of T2DM at the age of 14 with a hemoglobin A1c (HbA1c) of 11.47. Her HbA1c has not been below 11% in the past 2 years, including an A1C of 13.4% in July 2012.
In September 2012, the patient presented with her mother for a follow-up visit. The patient stated she tries to control her blood sugar and weight but gets frustrated and reverts to poor habits. Her parents are not helpful in assisting her in managing her medical problems or establishing healthy eating habits. Her weight at this visit was 244 lbs. With a height of 66 inches; her BMI was 39.4 kg/m2. Prior to this visit, she managed her diabetes with insulin glargine 75 units subcutaneously in the morning and 25 units at night, metformin ER 2000 mg once daily, and insulin aspart at mealtime using a coverage scale, as the patient and parents were reluctant to use scheduled mealtime insulin doses. Her HbA1c was 11.19% at this visit. After careful consideration and dutiful explanation to the patient and her mother (including the fact that no other medication is currently approved for use in pediatric patients), consent was given, and liraglutide 0.6 mg subcutaneously daily was added to the patient's diabetes regimen. The patient was instructed to titrate the dose of liraglutide up to 1.8 mg daily over a three-week period.
On October 26th, 2012, the patient returned to the office for a 1-month follow-up visit since the initiation of liraglutide; she was currently using 1.8 mg subcutaneously daily. She reported no adverse effects from the medication and no symptoms of hyperglycemia or hypoglycemia. During this time her HbA1c decreased by 1.53% to 9.66%. In addition, her total daily basal insulin requirement decreased 20% from baseline and she rarely needed insulin aspart for mealtime coverage of glucose excursions. Weight was 11 pounds higher than at her previous visit. Nutritional counseling was again addressed. On November 27th, 2012, the patient returned to the office for a follow-up visit two months after initiation of liraglutide. The patient stated that she has not experienced any symptoms of hypoglycemia or hyperglycemia. Her HbA1c decreased an additional 0.82% to 8.84%, representing a total A1C reduction of 2.35%. The patient's diabetes regimen included liraglutide 1.8 mg subcutaneously prior to dinner, insulin glargine 60 units subcutaneously at bedtime, and metformin ER 2000 mg with the evening meal. Since the initiation of liraglutide the patient's basal insulin requirement has decreased by 40%, and she no longer requires the use of mealtime insulin. Weight at this visit was increased, however, by 1.8 pounds (up to 256.8 pounds and a BMI of 41.4 kg/m2).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [256.8, 'lbs']}",156.48243,148.65831,164.30655,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 256.8 lbs so this converts to 256.8 lbs * 0.453592 kg/lbs = 116.48243 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (116.48243 kg - 20 kg) = 156.48243 mL/hr.
Hence, the patient's fluid maintenance is 156.48243 mL/hr."
4649,22,Maintenance Fluids Calculations,physical,decimal,pmc-4667149-2,Extracted,"A 1-month-old boy weighing 1700 g underwent ophthalmological screen for ROP. He was born at 25 weeks gestation and weighed 1000 g. His Apgar scores were 8 at 1 min and 9 at 5 min. His neonatal problems included PDA, which required pharmacological management. He required 3 weeks of nasal CPAP therapy for respiratory distress syndrome and was ultimately diagnosed with moderate grade BPD, which required supplemental oxygen. The nasal CPAP was discontinued 1 week before the examination. The chest radiograph demonstrated diffuse haziness in both the lungs. For mydriasis, one drop of 1% tropicamide followed 30 s later by one drop of 2.5% phenylephrine was instilled in each eye. At that time he was receiving O2 (1 L/min via nasal cannula). Five minutes later, a second drop of both tropicamide and phynylephrine were instilled in each eye. About 10 min later, his saturation on pulse oximetry was slowly decreased from 94 to 88%, and mild wheezing was detected on both lung fields. Blood pressure was 75/40 mmHg and heart rate was 135 beats/min. During preparation of the nebulizer, he received O2 at a rate of 8 L/min through a face mask, followed by inhaled salbutamol while positioned slightly head-up position with O2 supplied continuously through the nasal cannula. The saturation was restored to 93-94% and the wheezing was resolved after 20 min. Follow-up chest radiograph revealed no interval changes. At the next eye review, only 1% tropicamide was used for mydriasis and there was no adverse event.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1700.0, 'g']}",6.8,6.46,7.14,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1700.0 g so this converts to 1700.0 lbs * kg/1000 g = 1.7 kg. Hence, the patient's maintenance fluid is 1.7 kg * 4 mL/kg/hr = 6.8 mL/hr.
Hence, the patient's fluid maintenance is 6.8 mL/hr."
4650,22,Maintenance Fluids Calculations,physical,decimal,pmc-4574787-1,Extracted,"Baby D, was a female baby, born at 36 4/7 weeks of gestation, with a birth weight of 3350 g, by spontaneous vaginal delivery to a 30-year-old, gravida 2, healthy mother. Apgar scores at 1 and 5 min were 9 and 10 and physical examination was normal. The blood group of the mother was ORh (+). The blood group of the baby was B Rh(+), with a hemoglobin level of 17.4 g/dL, hematocrit 52%, direct Coombs test (+++), reticulocyte count 6.2%. At the 6th postnatal hour the bilirubin level was 2.8 mg/dL, which corresponded to a pathologic rate of increase (0.46 mg/dL/h). These findings were in accordance with an immune hemolysis due to ABO incompatibility and IVIG infusion was started to be given over 4 h. The patient was monitored during the infusion and 75 min after the start of the treatment, the heart rate suddenly increased to 260 beats/min. The electrocardiography showed narrow QRS supraventricular tachycardia (SVT). After the administration of adenosine 0.1 mg/kg, her heart rate returned to normal (144/min) (Fig.). An echocardiography was performed which showed patent foramen ovale and small patent ductus arteriosus. The patient was monitored for 2 days in the NICU and SVT episodes did not recur either during the hospitalization or the outpatient follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3350.0, 'g']}",13.4,12.73,14.07,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3350.0 g so this converts to 3350.0 lbs * kg/1000 g = 3.35 kg. Hence, the patient's maintenance fluid is 3.35 kg * 4 mL/kg/hr = 13.4 mL/hr.
Hence, the patient's fluid maintenance is 13.4 mL/hr."
4651,22,Maintenance Fluids Calculations,physical,decimal,pmc-5814473-1,Extracted,"A 58-year-old man (height, 160 cm; weight, 64 kg) presented with exertional dyspnea 6 months ago. Cardiac catheterization showed a 90% stenosis at each branch of left and right coronary arteries. The patient responded to medical therapy; thus, elective on-pump coronary artery bypass grafting (CABG) was scheduled.
He had a history of deep vein thrombosis and multiple cerebral infarctions at 46 years of age. Screening for a thrombophilic diathesis was performed at that time and showed a reduced PS activity level of 33.7% (reference range, 70–160%), while the PC activity level was normal at 123% (reference range, 70–130%). The significant difference between the PS and PC activity levels strongly suggested PS deficiency. He had no comorbidities to which acquired PS deficiency could be attributed; therefore, the hereditary form was suspected.
After admission, an echocardiogram showed an ejection fraction of 50% and abnormal wall motion with mild aortic and mitral valve regurgitation. His hemoglobin concentration was 11.3 g/dL, platelet count was 170,000/mm3, prothrombin time-international normalized ratio (PT-INR) was 2.54, and activated partial thromboplastin time (aPTT) was 43.6 s (control, 30 s). Warfarin was stopped 7 days before surgery, and the patient was started on intravenous unfractionated heparin to maintain an aPTT of 45 to 75 s (1.5–2.5 times control). Heparin was stopped 5 h before surgery. After anesthetic induction, the activated clotting time (ACT) was 142 s.
The patient received 720 mL of FFP prior to heparinization. Its volume was determined by taking the patient’s urine output into consideration to avoid heart congestion. Before the initiation of CPB, 300 units/kg of heparin was administered and the ACT was 536 s. The left and right internal thoracic arteries were grafted to the left posterolateral branch and the left anterior descending artery, respectively. The total CPB time was 138 min with an aortic cross-clamp time of 102 min, and the patient was weaned from bypass without complications. After a protamine dose of 3 mg/kg, the ACT was 126 s, while the bilateral internal thoracic artery graft flow was maintained at > 50 mL/min. An additional 1200 mL of FFP was transfused after protamine administration until the end of surgery. Its volume was decided, considering the CPB ultrafiltration volume. The amount of bleeding was 1200 mL and total intraoperative transfusion comprised 2240 mL of packed red blood cells, 1920 mL of FFP, and 200 mL of packed platelets.
In the intensive care unit, an additional 360 mL of FFP was administered. Nineteen hours postoperatively, the patient had no bleeding, and the heparin infusion was resumed with a dose adjustment to achieve an aPTT of 45 to 75 s. Warfarin was restarted 3 days after the surgery and adjusted to maintain a PT-INR of 1.5 to 2.5. The heparin infusion was discontinued after the PT-INR became stable. The postoperative period was uneventful, and the patient was discharged without any complications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [64.0, 'kg']}",104,98.8,109.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 64.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (64.0 kg - 20 kg) = 104.0 mL/hr.
Hence, the patient's fluid maintenance is 104.0 mL/hr."
4652,22,Maintenance Fluids Calculations,physical,decimal,pmc-6425374-1,Extracted,"A 74-year-old woman with a history of SLE on hydroxychloroquine without known renal involvement, chronic kidney disease stage (CKD) IIIa, heart failure with reduced ejection fraction, hypertension, and type 2 diabetes mellitus (T2DM) presented to the emergency department with progressive chest “heaviness” which had started several days prior to admission. In addition, she complained of swelling in both feet and at least three-pound weight gain.
Upon admission she was afebrile, blood pressure ranged 150-180/70-80 mm Hg, heart rate was about 50 bpm, and oxygen saturation was above 95% on room air. She was a well-developed, nonobese woman in no significant distress and nontachypneic. Pertinent physical exam findings included no jugular venous distention, no crackles audible at base of lungs, heart with regular rate and rhythm with no extra sounds or murmurs, nondistended abdomen, trace peripheral leg edema, and no visible rashes. Laboratory tests were significant for sodium 129 mEq/L, potassium 4.2 mEq/L, chloride 98 mEq/L, CO2 20 mEq/L, BUN 46 mg/dL, and creatinine 3.4 mg/dL. Her baseline creatinine based on the most recent reading one month prior to admission was 1.1 mg/dL. Urinalysis was significant for a specific gravity of 1.006, RBC 142, and WBC 8 per HPF. No casts of dysmorphic cells were seen. Proteinuria was 2+, and a random urine protein-to-creatinine ratio was 1.48.
Her creatinine continued to rise rapidly, and by day 6 of hospitalization it was 6.4 mg/dL. Due to these findings, a renal biopsy was performed. Up to 21 glomeruli were present per tissue section, and two of them showed global sclerosis. Two other glomeruli showed segmental sclerosis and the remaining glomeruli were open. There was global diffuse marked mesangial sclerosis and hypercellularity, and there was no obvious endocapillary cell proliferation or inflammatory cell infiltrate. Three of the open glomeruli also displayed segmental or circumferential predominantly cellular crescent. There was multifocal chronic tubulointerstitial injury characterized by atrophic tubules, interstitial fibrosis, and mild mononuclear inflammatory cell infiltrate, all which accounted for about 20-40% of the cortical tissue area. Figures and are biopsies seen in light microscopy with the former showing mesangial proliferation and the latter demonstrating a crescent on silver stain. Immunofluorescent staining showed marked IgA and C3 mesangial deposition, weak linear IgG staining of the glomerular basement membrane, and absence of C4 and C1q which was consistent with IgA nephropathy. There are also changes suggestive of diabetic nephropathy, in keeping with the clinical history of diabetes. These changes include thickened lamina densa and linear IgG of the glomerular basement membrane and mesangial sclerosis. Immunofluorescent staining positive for IgA and C3 is seen in Figures and , respectively. Staining for C4 and C1q was both negative with the latter seen on . In addition, electron microscopy showed uniform thickening of lamina densa of glomerular basement membrane, marked mesangial sclerosis, and hypercellularity, and some electron dense deposits were identified in the mesangial areas and subepithelial location which can be seen in Figures and . Ultimately, given the histological findings, the biopsy was diagnosed as mesangial proliferative glomerulonephritis with crescent formation. Findings were not comparable with lupus nephritis, especially the immunofluorescent findings. The significant mesangial IgA staining raised the likelihood of IgA nephropathy.
Her serologic work-up included anti-dsDNA antibody (1:80), ANA (1:320), and normal serum complement levels. With these biopsy results in the setting of worsening kidney function, she was diagnosed with immune complex RPGN secondary to IgAN.
She subsequently received intravenous methylprednisolone 500 mg daily for three days and five rounds of plasmapheresis. Unfortunately, her renal function continued to deteriorate, and she was started on hemodialysis. She was discharged with instructions to take prednisone 60 mg daily for one month with a taper. Her clinical symptoms showed mild improvement, however, there was no significant recovery in kidney function, and she was declared to have end-stage renal disease (ESRD).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.0, 'lbs']}",5.44312,5.17096,5.71528,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.0 lbs so this converts to 3.0 lbs * 0.453592 kg/lbs = 1.36078 kg. Hence, the patient's maintenance fluid is 1.36078 kg * 4 mL/kg/hr = 5.44312 mL/hr.
Hence, the patient's fluid maintenance is 5.44312 mL/hr."
4653,22,Maintenance Fluids Calculations,physical,decimal,pmc-3935113-1,Extracted,"A 21 day-old girl was transferred to Samsung Medical Center due to extubation failure. The baby was born at the 35+1 weeks of gestation by emergency cesarean section due to spontaneous rupture of the membranes and premature labor. Apgar scores were 2 at 1 minute and 8 at 5 minutes. When the baby was born, she did not cry and became cyanotic and lethargic. Positive pressure ventilation was not effective, so endotracheal intubation was performed in the delivery room. At birth, weight, length, and head circumference were 2,030 g (25th percentile), 49 cm (75th-90th percentile), and 35 cm (>90th percentile), and she had low set ears. A large patent ductus arteriosus (PDA) was found and ligated 12 days after birth.
We conducted osteomeatal unit computed tomography (CT) to find the cause of extubation failure. CT scan showed bilateral choanal atresia, atresia of the left external auditory canal, and stenosis of the right auditory canal (). Thirty-five days after birth, she underwent a repair operation of the choanae, and we tried to extubate again. However, she was reintubated with an endotracheal tube because of sustained desaturation and tachypnea. We considered that the cause of extubation failure was an upper airway problem. She was identified to have postglottic stenosis through laryngomicrosurgery (). Forty-two days after birth, a tracheostomy was performed, and respiration stabilized without respiratory support.
The patient had a left aortic arch with aberrant origin of the right subclavian artery on chest CT and minimal left pulmonary artery hypoplasia without focal stenosis on echocardiography. Based on these results, we conducted the ophthalmic examination to identify other features of CHARGE syndrome, and found coloboma in her both eyes. Because she met two out of the three major criteria and two of the five minor diagnostic criteria, we concluded that she had typical CHARGE syndrome.
Written informed consent was obtained for a molecular genetic analysis of the CHD7 gene mutation from the parents. Direct sequencing analysis of the CHD7 gene was performed with genomic DNA isolated from peripheral blood leukocytes. As a result, a c.3896T>C (p. leu1299Pro) missense mutation in exon 16 of the CHD7 gene was detected, which has not been reported previously (). A familial study revealed that neither of the parents had the mutation. The polymorphism phenotyping program and the sorting intolerant from tolerant program predicted ""possibly damaging"" and ""not tolerated."" The amino acid residue L1299 is highly conserved across different species, and the L1299P variation does not occur in 200 control chromosomes from 100 healthy individuals.
After discharge at 2 months of age, she has been followed up at the outpatient clinic regularly. At present, she is 11 months old and is using a hearing aid because of sensorineural hearing loss. Since she has had recurrent aspiration; thus G-tube feeding is required. Her height was 10th-25th percentile, body weight was 5th-10th percentile, and head circumference was 10th-25th percentile. The patient can sit alone but cannot stand with support. Hypoplasia of both kidneys was identified by abdominal ultrasonography, which was performed at 5 months of age. She has met two of the three major criteria and four of the five minor diagnostic criteria for CHARGE syndrome.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2030.0, 'g']}",8.12,7.714,8.526,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2030.0 g so this converts to 2030.0 lbs * kg/1000 g = 2.03 kg. Hence, the patient's maintenance fluid is 2.03 kg * 4 mL/kg/hr = 8.12 mL/hr.
Hence, the patient's fluid maintenance is 8.12 mL/hr."
4654,22,Maintenance Fluids Calculations,physical,decimal,pmc-8325382-1,Extracted,"A 39-year-old Asian female presented to our hospital with nausea, vomiting, sweating, dyspnea, and generalized weakness. She had been diagnosed with type 2 DM six days prior by her primary care physician (PCP), with elevated HbA1c (13.0%) and hyperglycemia (300 mg/dl). She had been advised to start a low carbohydrate diet and daily exercise and had been started on dapagliflozin (5 mg). However, this had resulted in strict avoidance of carbohydrates on her part. Two days after the initiation of dapagliflozin, she had developed nausea, vomiting, and loss of appetite. Due to severe fatigue, she had been evaluated both in the local ER and by her PCP who had assured her that her blood glucose level was unremarkable, and her symptoms might be due to hyperventilation and dehydration. However, her symptoms had continued to worsen, and she came to our ER the following day.
The patient had no fever, chills, abdominal pain, alcohol intake history, nor any history of recent surgery. On physical examination, the patient was drowsy, but alert and oriented to time, place, and person. Her vital signs were as follows: blood pressure of 108/83 mmHg, heart rate of 114 beats/minute, respiratory rate of 20 breaths/minute, and temperature within normal limits. Oxygen saturation was 98% on room air. Her height was 155 cm, and her weight was 63 kg (body mass index of 26.2 kg/m2). Oral mucosa was dry but otherwise unremarkable. Initial laboratory data showed significant metabolic acidosis with a blood pH of 7.19, bicarbonate level of 10.4 mmol/L, and anion gap of 25.0 mmol/L without an elevation in lactate. Her blood glucose was 181 mg/dl and her HbA1c was 12.6%. Urinalysis showed 4+ ketones and glucose >1000 mg/dl. The anti-insulin antibody was negative. Other laboratory data on admission are shown in Table . She was admitted to the ICU with a diagnosis of euDKA related to SGLT2 inhibitor use. Her glucose levels were monitored on an hourly basis, and her basic metabolic panel and venous blood gas were monitored until the gap was closed. Seven hours after admission, the anion gap was closed. On day two of admission, she was able to start having meals and her laboratory abnormalities were found rectified. We provided diabetic education including home blood sugar monitoring and discharged the patient with insulin glargine 10 units every evening and glucose tablets in case of hypoglycemia. The patient was followed up by a local diabetologist. Insulin was discontinued with the initiation of metformin a week after the discharge. Anti-glutamic acid decarboxylase (GAD) antibody was investigated by the specialist and was found negative. Her DM has been well controlled since her discharge without any recurrent episodes of ketoacidosis.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [63.0, 'kg']}",103,97.85,108.15,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 63.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (63.0 kg - 20 kg) = 103.0 mL/hr.
Hence, the patient's fluid maintenance is 103.0 mL/hr."
4655,22,Maintenance Fluids Calculations,physical,decimal,pmc-3466864-1,Extracted,"We present a 23-month-old girl admitted for the evaluation of a cardiac murmur with a history of one episode of syncope two months before admission. She had no positive history for syncope and no positive family history for congenital heart diseases or any kind of cardiac tumors.
On physical examination, her growth and development were within normal limits (height = 85 cm, weight = 11 kg). The central and peripheral pulses were normal and no cyanosis was detected. Her blood pressure was 90/60 mmHg. On heart auscultation, there was a grade 3/6 systolic ejection murmur at the second right inter-costal space with radiation to the neck. Electrocardiography revealed normal sinus rhythm with left ventricular hypertrophy. Her heart rate was 110 beats per minute. The chest X-ray showed mild cardiomegaly with normal vascular markings.
Transthoracic echocardiography demonstrated mild left ventricular hypertrophy and a large intraluminal mass in the ascending aorta, but its borders were not obvious. Doppler interrogation of the ascending aorta showed a turbulent, high-velocity ante grade flow with a 66 mmHg peak pressure gradient and a 46 mmHg mean pressure gradient. By color mapping, turbulency began at the level of the aortic valve.
In order to confirm the transthoracic echocardiography findings, transesophageal echocardiography was performed, which confirmed the presence of a large intraluminal mass in the ascending aorta. The mass was elongated and occupied about 60% of the ascending aorta’s area (3 cm × 1 cm × 1 cm). It was heterogeneous, lobulated, and immobile. The mass had attachments to the anterior cusp of the bicuspid aortic valve. The turbulent antegrade flow around the margins of the mass was obvious and there was no more adherence. The distal end of the mass juxtaposed the initiation of the transverse aorta ().
The high likelihood of the mass being tumoral and its hazardous location precluded catheterization, and the child underwent surgery for mass resection. Given the position of the mass, cannulation via the femoral artery, inferior vena cava, and superior vena cava was done. With cerebral protection during cardiopulmonary bypass, the arteriotomy of the ascending aorta was preformed. The mass was found to be entirely within the ascending aorta with firm adherence to the anterior leaflet of the bicuspid aortic valve ().
The tumor was excised subtotaly because it could not be detached from the aortic valve leaflet. The arteriotomy was closed, and the child was weaned from the cardiopulmonary bypass machine without any difficulty.
Repeat transthoracic echocardiograms following the operation did not reveal any evidence of residual supravalvular aortic stenosis and there was no aortic insufficiency.
In gross pathology description, the mass was solid, firm, and creamy with a nodular appearance (3 × 1 × 1 cm). Microscopic sections showed a benign neoplasm composed of fascicles of fibroblasts with variable amounts of collagen and a scanty number of lymphocytes arranged in a focally myxomatous stroma without any evidence of malignancy such as increased mitotic figures or areas of necrosis ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [11.0, 'kg']}",42,39.9,44.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 11.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (11.0 kg - 10 kg) = 42.0 mL/hr.
Hence, the patient's fluid maintenance is 42.0 mL/hr."
4656,22,Maintenance Fluids Calculations,physical,decimal,pmc-5828046-1,Extracted,"A 96-year-old woman was prescribed garenoxacin for 8 days after complaining of a bad cough, dyspnea, and anorexia at a nearby clinic. This was despite a simple laboratory blood test revealing a white blood cell (WBC) count of 7920/μL (55% neutrophils) and a C-reactive protein (CRP) level of 0.33 mg/dL, findings that were unremarkable. However, she developed high-grade fever on the following day, and intravenous ceftriaxone (1 g daily for 6 days) was added to her treatment regime two days after prescribing garenoxacin. After 5 days of therapy with ceftriaxone, a follow-up laboratory blood test performed showed a WBC count of 1050/μL (0% neutrophils) and a CRP level of 6.67 mg/dL. Severe leucopenia was suspected, and she was referred to our hospital for evaluation.
During presentation, her blood pressure was 136/99 mmHg, her pulse rate was 87 beats per minute, and her body temperature was 37.4°C. Her respiratory rate was 20 breaths per minute and peripheral oxygen saturation 97%. Chest sounds were normal, and other findings of physical examination were unremarkable. She was 150 cm in height with mild kyphosis and weighed 40 kg. She had a medical history of atrial fibrillation, stroke, hypertension, hypotonic urinary bladder, lower back pain, and gastritis. Her daily medications included candesartan, lansoprazole, amlodipine, carbocysteine, zaltoprofen, tranexamic acid, rivaroxaban, bisoprolol, brotizolam, and celecoxib.
Full blood count performed at our hospital revealed severe leucopenia with a WBC count of 830/µL (neutrophils 7/µL, eosinophils 8/μL, basophils 18/μL, monocytes 378/μL, and lymphocytes 415/μL). Other laboratory data are shown in . A chest radiograph and computed tomography showed mild infiltrative shadow on her left lung. However, both blood and sputum culture results were negative.
She was diagnosed with drug-induced agranulocytosis (presumably from antibiotics used) with mild pneumonia and admitted to an isolated room. Candesartan, lansoprazole, amlodipine, and celecoxib were discontinued because they are also known to cause agranulocytosis. She was given meropenem hydrate intravenously (2 g/day) and levofloxacin hydrate orally (500 mg/day) for 10 days, after which a short course of sulfamethoxazole/trimethoprim (4 g/day) was administered. Subcutaneous injection of filgrastim (recombinant human G-CSF, 75 µg/day) was also given to treat her neutropenia.
Filgrastim was administered for 6 days before the neutrophil count normalized to 2539/µL on day 6. Although her neutrophil count increased to 12,940/µL on day 9, it eventually stabilized around 3000 to 4000/µL after day 13. summarizes the changes in WBC count, neutrophil count, and CRP levels during her hospitalization. Her fever receded after day 10, and she was discharged on day 18 without further complications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [40.0, 'kg']}",80,76,84,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 40.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (40.0 kg - 20 kg) = 80.0 mL/hr.
Hence, the patient's fluid maintenance is 80.0 mL/hr."
4657,22,Maintenance Fluids Calculations,physical,decimal,pmc-4532033-1,Extracted,"A 44-year-old woman was admitted to our hospital for the evaluation of Cushing’s syndrome. She was diagnosed as hypertension at a local clinic in 1986 but recieved no antihypertensive medication. She developed headache, nausea and vomiting in Feb, 1990 and was admitted to the department of neurosurgery with diagnosis of Rt. cerebellar hemorrhage. After discharge, she has been followed for treatment of hypertension. During the follow-up period, she was found to have the Cushingoid features and transferred to the Department of Internal Medicine for the evaluation of Cushing’s syndrome.
The family and other past medical history were not contributory.
On admission, blood pressure was 150/110 mmHg, pulse rate 78/min, body temperature 36.5°C, respiration rate 18/min and height was 164cm and body weight was 77kg.
On physical examination, she was shown to have central obesity. Her face was round and plethoric. She had pink conjunctivae and white sclerae.
On auscultation of the chest, breathing sounds were normal and the heart sound was regular without murmur. On examination of the abdomen, she was found to have striae. Further examination revealed no abnormal finding.
Laboratory studies included hemoglobin 12.7g/dl, WBC 6700/mm3 with 75% neutrophils and 23% lymphocytes, platelet 261,000/mm3, total protein 7.2g/dl, albumin 4.2g/dl, total bilirubin 0.7mg/dl, direct bilirubin 0.3mg/dl, ALT 17unit, AST 19 unit, alkaline phosphatase 65U/L, BUN 20mg/dl and creatinine 1.1mg/dl. The concentrations of Na, K, CI and Ca were normal. FBS was 116mg/dl and HbA1c was 3.1%. Urinalysis was normal.
The results of low and high dose dexamethasone suppression test were shown in .
Chest PA and skull series revealed no abnormal findings.
By her history and physical examination, we suspect she had Cushing’s syndrome and then measured 24hr urine free cortisol and performed low dose dexamethasone suppression test. After this study, high dose dexamethasone suppression test was done to differentiate the etiology of Cushing’s syndrome. The levels of plasma cortisol were not suppressed and plasma ACTH level was very low. Abdominal CT scanning was done under the impression of adrenocortical tumor but revealed no abnormal mass in the adreanal gland first. Therefore we performed pituitary fossa MRI to rule out Cushing’s disease associated with micronodular adrenal hyperplasia. MRI reveals atrophic pituitary gland with empty sella. At that time, we didn’t decide the treatment modality for this patient because of poor general condition.
Instead, follow-up study was recommended. Follow-up abdominal CT scan, 3 years after the first study, revealed 2cm-sized hypodense mass in the upper pole of lt, adrenal gland (). So, explorative laparotomy was done under the impression of lt, adrenal adenoma. At operation field, no abnormal adrenal mass was found but the surgeon performed lt, adrenalectomy. The cut surface of surgical specimen showed multiple black pigmented nodules with pale atrophic cortex ().
On the microscopic finding, pigmented micronodular dysplasia with cortical atrophy was found (, ).
After operation, her blood pressure was normalized, and follow-up hormonal levels were also improved.
We concluded that her Cushing’s syndrome resulted from primary pigmented nodular adrenocortical disease and we plan the contralateral adrenalectomy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [77.0, 'kg']}",117,111.15,122.85,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 77.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (77.0 kg - 20 kg) = 117.0 mL/hr.
Hence, the patient's fluid maintenance is 117.0 mL/hr."
4658,22,Maintenance Fluids Calculations,physical,decimal,pmc-4737662-1,Extracted,"A 24-year-old Korean male visited the emergency room (ER) of our hospital on April 1, 2015 with pain in both flanks. The initial impression was ureter stone due to his symptom; thus, a computerized tomography (CT) of his abdomen was performed. Abdomen CT showed a decreased enhancement of both kidneys but no evidence of urolithiasis. After ruling out urolithiasis, the patient was admitted for diagnostic evaluation. Upon history taking, he stated that he had suffered from urolithiasis 4 years prior, and had passed the stone spontaneously. He also stated that his mother had a history of AKI, and both his aunt and uncle, had a history of urolithiasis. Despite the patient's mother's AKI history, no other specific medical history was noted with familial history taking (). His blood pressure was 130/70mmHg, and his weight and height were 78 kg and 170 cm, respectively. The patient showed pain in both flanks. Laboratory tests on admission revealed the following results: Cr, 1.6mg/dL; blood urea nitrogen (BUN), 17mg/dL; C-reactive protein, 1.40 mg/dL; white blood cell count, 11,380/µL; potassium, 4.0 mmol/L; lactate dehydrogenase, 494 U/L (normal range: 263-450 U/L), creatine kinase, 86 U/L (normal range; 60- 220 U/L); total CO2, 24.8mmol/L; and a low uric acid level of 0.5mg/dL. The urinalysis revealed a specific gravity of 1.012, a pH of 5.0, and 0-1 red blood cells/µL. No glycosuria, aminoaciduria was found. The 24-hour urinary protein was 17mg. The following parameters were within normal limits or negative: serum immunoglobulin; serum complement; antinuclear antibody; perinuclear/ cytosolic-antineutrophil cytoplasmic antibody; and HIV, HBsAg, and hepatitis C antibodies. Fractional excretion of uric acid (FeUA) was 23.95%. Abdominal ultrasonography was unremarkable. After conventional causes of Cr elevation were ruled out, the patient's history was taken again, during which he stated that he had been swimming prior to the flank pain event. The patient was suspected to have familial renal hypouricemia based on, the exclusion of other causes of hypouricemia, familial histories of AKI and urolithiasis, and decreased renal enhancement on abdominal CT (). Thus, the patient was also suspected to be in an EIAKI state. Therefore, genetic analysis for SLC22A12 mutations was conducted. The patient was discharged 6 days after admission. During the outpatient follow up, the patient was stable and the Cr level was maintained at <1.0mg/dL.
AKI recurred 10 weeks after the first episode. On June 17, 2015, the patient was admitted to our hospital via the ER due to pain in both flanks that occurred following swimming. The physical examination did not reveal abnormalities. The patient's blood pressure was 120/80 mmHg, his 24-hour urine protein excretion was 718mg. In addition, serum Cr was 2.2mg/dL, BUN was 21mg/dL, and uric acid was 2.4mg/dL. The renal ultrasound showed increased echogenicity of both kidneys, but structural abnormalities were not observed. We again performed a FeUA and the result was 14.61%. The history of flank pain after swimming may indicate recurrent EIAKI. Hydration and symptomatic treatment were performed during the admission. The symptoms of the patient resolved upon treatment and the serum Cr level decreased gradually. The patient was discharged on day 9 of hospitalization. Anaerobic exertion was prohibited including swimming. At the time of the 1-month follow up, the patient had a normal serum Cr level of 1.0mg/dL, but his hypouricemia (uric acid, 0.7mg/dL) remained. No further episode of EIAKI was noted.
Sequence analysis of the SLC22A12 gene was performed on the patient and his mother due to the suspicion of EIAKI associated with familial renal hypouricemia. T he sequence analysis of SLC22A12 revealed a mutation of c.774 G>A (p.[Trp258Ter]:[Trp258Ter]), or homozygous W258X, which causes renal hypouricemia. The patient's mother exhibited a heterozygous mutation of W258X, making her a carrier of renal hypouricemia; her results were consistent with autosomal recessive inheritance of the disease (). We also proposed another molecular biologic analysis to the patient's father, but the father refused further genotyping since he had normal uric acid level and the cost.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [78.0, 'kg']}",118,112.1,123.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 78.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (78.0 kg - 20 kg) = 118.0 mL/hr.
Hence, the patient's fluid maintenance is 118.0 mL/hr."
4659,22,Maintenance Fluids Calculations,physical,decimal,pmc-6300189-1,Extracted,"This is a case of a 59-year-old morbidly obese female with situs inversus totalis who presented for a laparoscopic sleeve gastrectomy. Her BMI was 38 (height 4 ft 11.5 inches, weight 188.2 pounds), and she had a lifelong history of morbid obesity and obesity-related comorbidities, including obstructive sleep apnea requiring a continuous positive airway pressure machine, an elevated hemoglobin A1c (5.8) and a fasting blood glucose increasing her risk of developing diabetes mellitus, and degenerative joint disease which significantly impacted her ability to exercise. The main challenges she identified in losing weight involved eating carbohydrate rich foods, overeating during meals and limited activity due to musculoskeletal pain. The patient had made multiple attempts to lose weight through commercial dieting programs but had been unsuccessful. The patient also completed a six-month medically supervised diet through her primary care provider, which also included working closely with a bariatric registered dietician, following a strict diet of about 1800 calories/day and performing modified exercise, about 120 minutes/week. Despite these intense medical weight loss efforts, she was unable to maintain a healthy weight. The patient was motivated to try bariatric surgery after she witnessed the significant weight loss success her daughters had from this intervention. Her greatest hope from the bariatric surgery was to be healthier and to alleviate her obesity-related comorbidities.
The patient’s surgical history included cesarean section and evacuation of an ectopic pregnancy. She was a former smoker, quitting over 25 years ago, and has no other history of substance or alcohol use. Family history is positive for obesity, diabetes, hypertension, coronary artery disease and hypercholesterolemia. She did not take any medications, including supplements, except for Ibuprofen 800 mg 1–3/daily for musculoskeletal pain.
The patient underwent a comprehensive evaluation and treatment plan prior to the surgery including: psychiatric evaluation and clearance, nutritional consultation with a registered dietician, education about bariatric surgery and pre/post op expectations, routine preoperative labs, UGI, esophagogastroduodenoscopy (EGD), pulmonary function analysis, and a cardiovascular exam. Situs inversus totalis was confirmed with abdominal X-ray and CT, and echocardiogram. Pre-procedural evaluation with UGI revealed mild gastroesophageal reflux observed to the level of the distal one-third esophagus and small sliding-type hiatal hernia. EGD revealed normal esophagus and duodenum. Stomach biopsy was obtained for antral gastritis, and no helicobacter organism was identified. Abdominal ultrasound confirmed fatty liver disease. Pulmonary function analysis including spirometry, lung volumes and diffusion was normal. A pre-procedural cardiovascular exam was performed due to dextrocardia to exclude other structural cardiac abnormalities. 2-D echocardiography with M-mode demonstrated a left ventricular ejection fraction of 60%, no structural abnormalities in the aortic, pulmonic, tricuspid and mitral valve, or right and left atrium and ventricles. Color Doppler and continuous and pulse wave Doppler demonstrated mild pulmonic regurgitation and mild tricuspid regurgitation.
The patient discontinued the Ibuprofen more than one month before her surgery and began a low-calorie liquid diet two weeks prior to surgery. On the day of surgery, preoperative antibiotics, Cefazolin, were given within 60 minutes before the first incision. Prior to induction, the patient received 5000 units of heparin subcutaneously and sequential compression device (SCD) boots were placed for deep vein thrombosis (DVT) prophylaxis. No beta-blockers were administered. The patient was placed in the supine position and general anesthesia was induced. A Foley catheter was placed and the patient was supported with positioning devices including: arms on padded arm boards, gel pad under left axilla, footboard with gel pads, hover mat and a bariatric safety belt over patient’s thighs. The abdomen was then prepped and draped in the standard surgical fashion.
A Veress needle was used in the right upper quadrant to access the abdomen and insufflation was created to 15 mmHg. Veress was removed and replaced with a 5 mm trocar and the scope was placed. Additional trocars were placed in the following position: right and left 5 mm lateral trocars, right and left 12 and 15 mm supra-umbilical trocars. The placement of all retractors and graspers was adjusted accordingly to the mirror image anatomy of the intraabdominal organs. The primary surgeon was positioned on the left side of the patient and the assisting surgeon on right side of the patient. Situs inversus totalis was confirmed with the majority of the liver oriented to the patient’s right, spleen on the right, greater curvature of the stomach on the right and gallbladder on the left.
The operating table was placed in the reverse Trendelenburg position. The patient’s right-sided half of the liver was retracted cephalically using a Nathanson retractor to expose the vicinity of the esophageal hiatus. The peritoneum over the cardia was incised using the Ethicon Harmonic scalpel, and the plane between the cardia and the left crus of the diaphragm was opened to expose the right diaphragmatic crus. No hiatal hernia was present. A point 5 cm proximal to the pylorus along the greater curvature of the stomach was marked corresponding to the incisura angularis just proximal to the crow’s foot of Latarjet’s nerve. The vessels along the greater curvature and all the short gastric vessels were sealed and divided using the Ethicon Harmonic scalpel, freeing the greater curvature and the fundus of the stomach. A 42-French bougie was placed and oriented towards the antrum along the lesser curvature (Figure ). The stomach was stapled and divided alongside the tube in a vertical fashion towards the angle of His (Figures -).
An Ethicon Echelon Flex triple staple line power stapler with a total of one black, three green, and one gold staple loads was used. All staple loads were 60 millimeters in length with staple line bio-absorbable reinforcement. Hemostasis at the external staple line was achieved (Figure ). The stomach was removed from the abdomen via the left-sided 15 mm trocar (Figures , ). Intraoperative endoscopy was performed using a 5 mm Olympus Ultrathin gastroscope revealing no areas of stenosis, internal staple line bleeding, nor staple malformation or leak seen. Total operation time was 108 minutes. There were no post-operative complications.
Post-operative care included pain management and DVT prophylaxis with SCD, heparin and early ambulation four hours post-surgery. A UGI was performed on post-op day 2 with normal findings for a post-bariatric surgery evaluation and clear fluids were started. The patient was discharged on post-op day 3 without any complications. Upon discharge, the patient had a treatment plan that was previously discussed that included instructions for diet and medications, including vitamin supplementation and antacids. At her three-month follow-up, the patient was still without complications and very pleased with her weight loss of 46.2 lbs, weighing 142 lbs (BMI 29).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [188.2, 'lbs']}",125.36601,119.09771,131.63431,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 188.2 lbs so this converts to 188.2 lbs * 0.453592 kg/lbs = 85.36601 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (85.36601 kg - 20 kg) = 125.36601 mL/hr.
Hence, the patient's fluid maintenance is 125.36601 mL/hr."
4660,22,Maintenance Fluids Calculations,physical,decimal,pmc-2740044-1,Extracted,"A 37-year-old Caucasian Brazilian male patient was admitted to the hospital with a 4-month history of cough with purulent sputum, hemoptysis, fever, and weight loss of 5 kg. He was diagnosed with AIDS 2 years earlier, and was taking his antiretroviral medications irregularly. On examination he appeared pale and emaciate, but not cyanotic. His vital signs included a blood pressure of 120/80mmHg, a heart rate of 98 bpm and a respiratory rate of 26 breaths/min. Chest auscultation revealed a condensation syndrome in the upper third of the right hemithorax; cardiac auscultation showed no abnormalities, and the remainder of the physical examination was normal. Laboratory evaluation revealed a red blood cell (RBC) count of 3.46 × 106/mm3, hemoglobin level of 10 g/dL, hematocrit of 27%. His WBC count was 11 × 103/mm3 (band 4%, mon 64%, eos 1%, lymph 10%). The CD4 + T-cell count was of 228 cell/mL and the plasma viral load was of 12,000 copies/mL.
Chest radiograph demonstrated consolidation in the upper lobe of right lung, and computed tomography (CT) revealed the presence of areas of consolidation with air bronchograms and airspace nodules (). Several sputum samples were collected and tested for the presence of acid-fast bacilli, but all smears were negative. The patient then underwent bronchoscopy with bronchoalveolar lavage (BAL), and aspirated material was negative for tuberculosis, fungi (including Pneumocystis jirovecii), and malignancy. Because of progressive worsening of clinical status, a new bronchoscopy with bronchoalveolar lavage was performed, and this new BAL fluid revealed the presence of filamentous Gram-positive structures compatible with Nocardia species.
The patient was started on trimethoprim-sulfamethoxazole, and his antiretroviral therapy was changed to stavudine, lamivudine and nelfinavir. After four weeks of treatment the patient showed a complete regression of symptoms and radiological findings. Six months later the patient was again admitted to the hospital for other complications related to AIDS, and rapidly progressed to death. No autopsy was performed.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.0, 'kg']}",20,19,21,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.0 kg. Hence, the patient's maintenance fluid is 5.0 kg * 4 mL/kg/hr = 20.0 mL/hr.
Hence, the patient's fluid maintenance is 20.0 mL/hr."
4661,22,Maintenance Fluids Calculations,physical,decimal,pmc-4075270-1,Extracted,"A 67-year-old woman was diagnosed oseteoporosis and treated with oral Risedronate (150 mg/month for 2 years), Ibandronate (150 mg/month for 2 years) and Alendronate (70 mg/week for 3 years) for 7 years. She presented with sudden developed right hip pain despite no evidence of definite trauma. On the radiograph, transverse, noncomminuted subtrochanteric fracture with medical beak was noted. She was treated with closed reduction using long proximal femoral nail (Long Gamma-3 nail, Stryker) in the regional hospital (). Osteoporosis treatment has been discontinued. But from 6 months after the surgery she discontinued the schedule of our out-patient department. After three years of operation, she showed up at our out-patient department with pain in the right hip joint while walking despite no evidence of trauma. On the radiograph, nonunion of subtrochanteric fracture and breakage of long Gamma-3 nail was noticed (). Her height was 145 cm, body weight 55 kg, and body mass index (BMI) 26.1 kg/m2. The bone mineral density (BMD) of lumbar spine measured by dual energy X-ray absorptiometry (Discovery™, Hologic, Bedford, MA, USA) was 0.490 g/cm2, of which the T score was -3.6 and the Z score -1.2. The levels of serum calcium and phosphorus were 9.1 mg/dL (normal 8.6-10.0 mg/dL) and 4.5 mg/dL (normal 2.8-4.5 mg/dL), respectively. The serum C-terminal telopeptides of type I collagen (CTx) and urinary N-terminal telopeptides of type I collagen (NTx) levels measured by enzyme-linked immunosorbent assay (ELISA) were 55.7 nmoL bone collagen equivalents (BCE)/mmoL Cr (normal 6.0-125.7 nmoL BCE/mmoL Cr) and 0.26 ng/mL (normal 0.11-1.00 ng/mL). We removed the broken nail and exchanged to cephalomedullary nailing and autogenous iliac bone graft was done (Zimmer Natural Nail Cephalomedullary nail, Zimmer). We performed osteotomy at lateral cortex below the lag screw to making a notch for sliding (). After the revision operation, she was treated with daily subcutaneous injection of teriparatide (recombinant human parathyroid hormone 1-34) at a dose of 20 µg per day and her symptom resolved gradually for 6 months. She underwent outpatient follow up of dental clinic due to extraction of the mandibular right lateral incisor, right central incisor, left central incisor 1 year before visit to our outpatients department (OPD) clinic, following which the extraction socket never healed and pain and pus discharge for 2 months (). Oral antibiotics treatment and local debridement were ineffective. Sequestrectomy of mandible and incision and drainage of submental abscess was done. Intravenous antibiotics for 2 weeks and oral antibiotics for 10 weeks were administrated postoperatively. No more abscess drainage oral cavity and no more pain was complaint. BRONJ was diagnosed at 9 years after the osteoporosis treatment.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [55.0, 'kg']}",95,90.25,99.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 55.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (55.0 kg - 20 kg) = 95.0 mL/hr.
Hence, the patient's fluid maintenance is 95.0 mL/hr."
4662,22,Maintenance Fluids Calculations,physical,decimal,pmc-6354114-1,Extracted,"A 60-yr-old African American female with a remote medical history of breast cancer, status post double mastectomy, presented with 1 wk of bilateral lower abdominal pain that was associated with diarrhea, early satiety, and a 30 lb. weight loss (over 3 mo).
A computed tomography (CT) scan revealed a large circumferential mass involving the transverse colon which extended approximately 14 cm in length (Figure A, B, and C). On physical exam, her vitals were stable. Her abdominal exam was soft and non-distended, with mild pain to palpation to her lower abdomen. Her laboratory work-up was notable for a mild leukocytosis (white blood count 13.4 bil/L, hemoglobin 15.7 g/dL, platelets 404 bil/L), hyponatremia and acute kidney injury ( sodium 123 mmol/L and creatinine 2.52 mg/dL (baseline creatinine was normal)). Her liver function tests (including albumin and protein level), lactic acid, lipase, infectious stool studies (i.e., Clostridium difficile infection, ova and parasites, Shiga toxin producing Escherichia coli, Salmonella, Shigella, Campylobacter, or Escherichia coli O157) were all normal.
She underwent an esophagogastroduodenoscopy (EGD) and colonoscopy. EGD was notable for non-erosive gastropathy and normal appearing duodenum for which biopsies were obtained. Colonoscopy was notable for nodular ileal and colonic mucosa with multiple colonic polyps (Figure ). In addition, she had a 15 cm malignant appearing stricture in the transverse colon (Figure ). The largest colonic polyp was approximately 2.5 cm in her rectum (Figure ). Pathology results of her stomach, duodenum, terminal ileum, colon, transverse stricture and all of her colonic polyps were notable for MEITL (Figure ). There was no evidence of celiac disease on duodenal biopsy. There was no evidence of adenocarcinoma throughout her colon.
For the patient’s newly diagnosed high grade EATL, she underwent staging bone marrow biopsy and positron emission tomography (PET)/CT scan. Bone marrow biopsy was without overt morphologic or flow cytometry evidence of T-cell lymphoma or metastatic malignancy. PET/CT scan with abnormal F-18 fluorodeoxyglucose (FDG) activity associated with the transverse colonic mass, mesenteric lymphadenopathy, focal uptake within the rectum, intense uptake throughout the bone marrow, and portions of the spleen.
The patient was started on chemotherapy with EOCH (Etoposide, Oncovin, Cyclophosphamide, and Hydroxydaunorubicin). She was not a candidate for HCT given her functional status. Unfortunately, despite her aggressive chemotherapy regimen, her disease persisted. At her 6-month follow-up, her repeat PET/CT scan with abnormal FDG activity associated with the transverse colon and rectum. Repeat colonoscopy noted a large lymphoma polyploidy lesion.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [30.0, 'lbs']}",47.21552,44.85474,49.5763,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 30.0 lbs so this converts to 30.0 lbs * 0.453592 kg/lbs = 13.60776 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.60776 kg - 10 kg) = 47.21552 mL/hr.
Hence, the patient's fluid maintenance is 47.21552 mL/hr."
4663,22,Maintenance Fluids Calculations,physical,decimal,pmc-6158940-1,Extracted,"A 24-year-old male with a past medical history of HIV not on antiretroviral treatment presented to the emergency department of a large community hospital with complaints of bilateral lower extremity swelling of two weeks duration and worsening abdominal discomfort. He reported a 6-month history of mild to moderate constant abdominal pain, dull in nature, associated with distention and early satiety. He denied pain in the lower extremities. A review of systems was positive for night sweats, intermittent dry cough, shortness of breath on exertion, fatigue, poor appetite, and a 30-pound weight loss. The patient admitted to drinking alcoholic beverages on social occasions but denied tobacco or illicit drug use. He had previously been diagnosed with HIV at another hospital three years prior, but he had not been taking the antiretroviral treatment (ART) for two years.
In the emergency department, the patient's vital signs were normal and there were no signs of hypotension, sepsis, or hypoxia. On physical examination he appeared cachectic and had oral candidiasis and a large protuberant abdomen. On abdominal examination there was a large, firm, nontender mass palpated extending from the epigastrium to the periumbilical region, as well as hepatomegaly and right upper quadrant tenderness. Marked bilateral lower extremity edema up to the knee level was also noted.
Initial laboratory tests demonstrated an anion gap metabolic acidosis (anion gap 17 and HCO3 23 meq/L). Venous lactate and lactate dehydrogenase levels were both markedly elevated at 9.4 mmol /L (normal range = 0.5-1.0 mmol/L) and 2445 U/L, respectively. Aspartate aminotransferase (AST) was elevated at 63 U/L, but alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were within normal limits. Uric acid was measured as 9.6 mg/dL. The remainder of the metabolic panel, including creatinine and glomerular filtration rate (GFR), was normal. The patient's renal function remained stable throughout the course of his hospital admission. Complete blood count demonstrated a normocytic anemia (white blood cells 4.2 cells/μL, hemoglobin 8.1 g/dL, platelet count 176 platelets/μL, and mean corpuscular volume 85 fL), likely due to chronic disease. Lab results also showed a CD4 count of 38 cells/μL (3.0%), a CD8 count of 1023 cells/μL (84.0%), and an HIV viral load of 354,120 copies/mL, consistent with acquired immunodeficiency syndrome (AIDS). Infectious disease was consulted for recommendations, and the patient was started on ART (dolutegravir, tenofovir, and emtricitabine) on hospital day 3.
Computed tomography (CT) with contrast of the abdomen revealed a large soft-tissue mass (16.3 cm × 14.1 cm × 20 cm) with internal vascularity that appeared to arise from the left hepatic lobe (). Additional findings included innumerable small hypodense lesions throughout the liver parenchyma and mass effect on the inferior vena cava (IVC) by a 3.6 cm × 2.9 cm aortocaval lymph node. Additionally, there appeared to be bilateral suprarenal soft-tissue masses and sclerotic lesions within the pelvis and lower thoracic spine, suggestive of metastatic disease with bone involvement. A chest radiograph demonstrated left hilar adenopathy, a small left pleural effusion, and a left lower lobe nodular opacity. Ultrasound-guided core biopsy of the hepatic mass was performed and revealed a high-grade diffuse large B-cell lymphoma (DLBCL) (CD19+/CD20+/ CD34-/KAPPA+) with germinal center formation (FIGURE). Immunohistochemistry was positive for C-MYC, and ki-67 reactivity was greater than 90%. A bone marrow biopsy demonstrated severe hypocellularity (<5% cellularity) with atypical lymphoid infiltrate.
On hospital day 5, the patient was started on his first cycle of chemotherapy consisting of etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, and a double dose of rituximab (EPOCH-RR). Given that bone marrow involvement was present, he also received intrathecal methotrexate. By hospital day #8 the lactic acidosis resolved and was measured as 1.0 mmol/L (normal value = 0.5-1.0 mmol/L). He subsequently developed neutropenia and neuropathic pain of the hands and feet within several days of initiating chemotherapy and was treated with G-CSF until the neutropenia resolved. The patient was discharged on hospital day #26 but was readmitted the following day after an echocardiogram showed a left ventricular ejection fraction (LVEF) of 20% (normal range = 55-70%) which had decreased from 49% obtained 3 weeks earlier. He was started on Carvedilol and Lisinopril for Doxorubicin induced cardiomyopathy.
The patient completed cycles 2 and 3 of EPOC-RR without doxorubicin (due to induced cardiomyopathy) and doses of cyclophosphamide and etoposide were increased by 20% with no complications. Repeat echocardiogram also showed improvement in LVEF to 45-49% and he was discharged in stable condition. Outpatient PET-CT after the third cycle of chemotherapy showed a complete radiologic response with no remaining FDG-avid lesions. Given the complete radiologic response, the patient completed one additional cycle of EPOC-RR (fourth cycle) and was advised to follow-up with medical oncology in 3 months.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [30.0, 'lbs']}",47.21552,44.85474,49.5763,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 30.0 lbs so this converts to 30.0 lbs * 0.453592 kg/lbs = 13.60776 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.60776 kg - 10 kg) = 47.21552 mL/hr.
Hence, the patient's fluid maintenance is 47.21552 mL/hr."
4664,22,Maintenance Fluids Calculations,physical,decimal,pmc-7580351-1,Extracted,"A five and half year-old girl, from Cozy corner, L Maavah, Maldives presented to Emergency unit. She presented with cough, Dyspnea, Irritability, and fatigue. She had no fever. She was diagnosed case of Beta Thalassemia. She was diagnosed at the age of 2 years. She was diagnosed and lost to follow up. Her family history was not significant for any blood related disorder or any genetic disease.
On physical examination patient was ill looking. Her vitals were stable. She was clinically anemic with brittle hair and nail. Patient’s finger nails and skin extremities exhibited whitish tinge and sclera showed pallor. Her skin was ashen grey in color. She appeared dehydrated and had a body weight of 13.11 kg. She was underbuilt, under-nourished with a short stature, with evident icterus, and yellow tinged fingernails. Decayed upper tooth, not associated with pain or swelling. Head and Neck examination showed maxillary expansion, retracted upper lip and saddle nose; all together depicting the classical “Chipmunk facies”. Also noted yellowish tinge at the junction of hard and soft palate. Intraoral examination, localized periodontitis and broken teeth in lower anterior aspect as shown (). Her abdominal examination didn’t show and sign of enlargement of spleen. Her ophthalmologic and audiologic examination were done and were within normal limits.
Haematological examination was performed. Her haemoglobin was 4.5 gm/dl. Hematologic investigation revealed microcytic hypochromic anaemia with anisocy-tosis, poikilocytosis, nucleated Red Blood Cells (RBC). The impression drawn from the peripheral smear study was that of haemolytic anaemia favouring Thalassemia going for haemolytic crisis. Later Haemoglobin (Hb) electrophoresis was done which too was in favor of Beta Thalassemia major. Her Human immunodeficiency Virus (HIV), Hepatitis B, and Hepatitis C was negative. Liver function test and Renal function test were within normal limit.
She was planned for blood transfusion. She was given 3 pints of packed cell. She was given each packed cell at the rate of 220 ml in every 4 hours. Her vitals were monitored regularly during the transfusion to see any transfusion related complications. No complication ware obtained during transfusion. Then she was investigated for Haemoglobin (Hb) and found out to be 9.5 gm/dl. She was then discharged and advised to follow up in 15 days. In follow up visit her ferritin was investigated and was found to be 3562.69 ng/ml. Then she was started on iron chelating agent. She was kept on Deferoxamine B(DFO) 2 gm per dose at the rate of 4 times in a week and oral Deferasirox 400 mg once in a day dose. Her Hb was 7.5 mg/dl, she was transfused with a pint of packed cell and discharged hose with a follow up in 20 days for transfusion. She is hospitalized every 20 days for transfusion of packed RBC. She is investigated for Liver function test and thyroid function testis every 20 days. Her growth and development is assessed in every OPD visit for follow up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [13.11, 'kg']}",46.22,43.909,48.531,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 13.11 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.11 kg - 10 kg) = 46.22 mL/hr.
Hence, the patient's fluid maintenance is 46.22 mL/hr."
4665,22,Maintenance Fluids Calculations,physical,decimal,pmc-8296537-1,Extracted,"A 3-year-old 55-kg neutered male Tibetan Mastiff was evaluated because of a 1-month history of progressive signs including ataxia, lethargy and behaviour changes. At 6-months-old, the dog manifested clusters of generalized seizures. A diagnosis of IE was suspected because of normal blood analyses, unremarkable brain computed tomography (CT) scan and cerebrospinal fluid (CSF) analysis. At first, PB was prescribed as monotherapy (5 mg/kg, PO, q 12 h). Because of the appearance of adverse effects early after treatment initiation, the pet-owners arbitrarily decided to lower the PB dose (2.3 mg/kg/ PO, q 12 h). Four months later, because of cluster seizures still occurring every 7 to 20 days, KBr was introduced as additional antiepileptic drug (40 mg/kg, PO, q 24 h). After seven months of combined therapy, seizure clusters resolved with a single episode of seizure reported. Despite the improvement of seizure control, the dog presented mild hyporexia and marked 4-limbs ataxia as a consequence of the combined anticonvulsant therapy. Because the drugs’ secondary effects were deemed unacceptable by the pet-owners, KBr dosage was decreased by 17 % (33 mg/kg, PO, q 24 h). Four months later (eight months before presentation), a seizure-free status was achieved, paralleled by a reduction of the aforementioned adverse effects. Ataxia was still present, therefore KBr treatment was again lowered by 15 % (28 mg/kg, PO, q 24 h). Complete resolution of neurological signs was progressively achieved within a month. Six months prior to presentation, according to the owners’ perception, the dog’s gait, behaviour and appetite were considered completely normal. A 6-kg weight gain was reported.
Because of a history of chronic diarrhoea, at the time of the first reduction of KBr, the dog was transitioned to a dry hydrolysed diet (Pet Food A). Gastrointestinal signs were positively affected by the highly digestible kibbles. Prompted by almost one year with no diarrhoea, two months before presentation, the owners decided to switch the dog’s back to an over-the-counter adult dry diet (Pet food B).
Antiepileptic treatment, clinical signs, seizure frequency, and diet prior to presentation, are summarized in Fig. .
Physical examination at presentation was unremarkable. Over an 8-month period, a total 12-kg weight gain was registered. Body condition was scored 6 on the 9-point scale []. Neurological examination revealed an abnormal gait, with severe symmetric 4-limbs ataxia and frequent falls. The dog showed behavioural changes during consultation, such as aggression (e.g. attempt to bite when handled) and disorientation. Furthermore, outbursts of hyperactivity were displayed through attempts to jump and climb on doors and windows.
Postural reactions were abnormal on all four limbs, with pelvic limbs more affected (in particular hopping reactions). Spinal reflexes were normal. Cranial nerves examination did not reveal any significant abnormality. Neurological examination was consistent with upper motor neuron (UMN) tetraparesis.
The pet-owners did not consent to a brain magnetic resonance imaging (MRI), which was proposed in completion to the diagnostic work-up that previously brought to the presumptive diagnosis of IE.
Present antiepileptic treatment consisted in the combination of PB (2.3 mg/kg, PO, q 12 h) and KBr (28 mg/kg, PO, q 24 h).
Results of complete blood count and serum biochemical analysis were within reference ranges, except for a high serum alkaline phosphatase activity (1450 U/L; reference range, 20 to 155 U/L), which is a common finding with long-term administration of PB. Markers of renal function were normal and similar to previous measurements (Creatinine, 65.9 [59.2–71.7] µmol/L; reference range, 44 to 133 µmol/L). Serum chloride concentration was markedly high (> 128 mmol/L; reference range, 115 to 128 mmol/L) paralleled by a normal serum sodium level (143 mmol/L; reference range, 138 to 148 mmol/L). Pseudohyperchloremia was suspected secondary to KBr treatment.
Serum PB concentration was 20 µg/mL (therapeutic range, 15 to 35 µg/mL) [, ], while serum bromide was 2800 mg/L. The latter showed a 103 % increase since last follow-up 8 months ago (1380 mg/L). Analyses of serum PB and bromide were always processed at the same laboratory.
Analysis of chloride content in both Pet Food A and B was obtained via potentiometric titration at an external certified private laboratory. Results showed 1.91 and 1.01 g/1000 kcal ME (0.46 and 0.24 g/MJ ME) of chloride in Pet Food A and B, respectively (Table ). Considering that daily energy intake did not significantly differ from before and after dietary transition, a 53 % decrease of dietary chloride was found between the two dry diets.
Bromide toxicosis (bromism) was suspected, due to bromide reduced clearance secondary to the decreased dietary chloride content.
Hospitalization and parenteral infusion with saline solution were proposed as first line treatment to increase bromide renal clearance. The owners refused the approach, knowing that the dog will have suffered being alone in the stressful environment of the hospital.
To address the clinical manifestations, it was decided to lower by a 15 % KBr (24 mg/kg, PO, q 24 h) treatment while leaving unchanged PB. The 1-year period without seizure was considered enough to justify the avoidance of a novel antiepileptic drug. Pet-owners were advised to strictly avoid any further dietary change.
Ataxia and behaviour changes progressively improved without seizure recurrence. After two months, mild symmetric ataxia was still observed, but otherwise neurological examination was unremarkable. Serum bromide concentration lowered (1500 mg/L) to the same level measured before dietary modification, while serum PB kept stable (17 µg/ml) (Fig. ).
Despite lowered since first evaluation, serum alkaline phosphatase remained moderately high (650 U/L; reference range, 20 to 155 U/L).
According to the pet-owners, four months after reduction of the KBr treatment, the dog’s gait and behaviour were completely normal and no seizure was recorded.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [55.0, 'kg']}",95,90.25,99.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 55.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (55.0 kg - 20 kg) = 95.0 mL/hr.
Hence, the patient's fluid maintenance is 95.0 mL/hr."
4666,22,Maintenance Fluids Calculations,physical,decimal,pmc-3221158-3,Extracted,"This was a 3-month-old girl whose parents refused surgery for left diaphragmatic hernia at an earlier age, and who was subsequently brought for sudden-onset abdominal distension and vomiting []. At laparotomy, mesenterico axial type of gastric volvulus was corrected and Bochdalek's hernia was repaired. The stomach initially appeared dusky, but regained color and was hence repositioned and the child was discharged on oral feeds. The child developed progressive dysphagia and intolerance of oral feeds. Barium contrast study revealed distended lower esophagus with stricture and no contrast entering the stomach []. An endoscopy performed did not allow even a guide wire. Laparotomy revealed dense adhesions and small receptacle of stomach, opening into the duodenum, and feeding gastrostomy was carried out. Definitive repair was done after 8 months (weight – 7 kg), and it revealed a blind-ending esophagus and a distal remnant of stomach, with no communication between them. A Hunt Lawrence jejunal pouch was created and anastomosed to the lower esophagus. Contrast study revealed good flow of contrast into the jejunal pouch with no leak or reflux. The child was discharged on oral feeds and had a weight gain of 600 g in 2 months. The child is tolerating the oral diet and does not have any dysphagia or reflux.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.0, 'kg']}",28,26.6,29.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.0 kg. Hence, the patient's maintenance fluid is 7.0 kg * 4 mL/kg/hr = 28.0 mL/hr.
Hence, the patient's fluid maintenance is 28.0 mL/hr."
4667,22,Maintenance Fluids Calculations,physical,decimal,pmc-5908590-1,Extracted,"A 5-month-old female infant with a history of overeating, hirsutism, and excessive weight gain over the previous 2 months was referred to our hospital. The infant was born to Bangladeshi parents at 37 + 2 weeks with a birth weight of 3100 g via Cesarean section at a local hospital. A maternal history of polycystic ovary syndrome and oligohydramnios was reported. The infant was healthy with no unusual medical history, and her development was normal. There was no medical history of disorders such as metabolic or endocrine diseases, cancer, and genetic diseases. Written informed consent was obtained from the patient's parents. Institutional ethics review board approval is not required for observational case reports that do not alter patient management.
Physical examination revealed a overweight baby with a moon face, buffalo hump, and protruding abdomen (Fig. ). Increased body hair was also noted. The patient's body length was 61.0 cm (5–10th percentile) and her weight was 10.4 kg (>97th percentile). Her blood pressure was within the normal range (100/60 mm Hg).
Complete blood cell counts showed leukocytosis (white blood cell count of 29,220 cells/μL, 44% lymphocytes), but the other cell counts were all normal. The results of the blood chemistry analysis, including serum glucose levels and liver and kidney function tests, were normal. After a low-dose (1 mg) dexamethasone suppression test, a morning serum cortisol level of 49.7 μg/dL was obtained, which showed no suppression (cut-off point, <1.8 μg/dL). An elevated 24-hour urinary free cortisol level was noted (872.4 μg/d), and the concomitant plasma adrenocorticotropic hormone (ACTH) level was within the lower limits of the normal range (12.1 pg/mL). These results were compatible with a diagnosis of ACTH-independent CS.
Regarding the results of the imaging studies, a chest x-ray showed nonspecific findings with normal thymic and cardiac shadows. However, abdominal magnetic resonance imaging (MRI) revealed a 3.8 × 2.8 cm right adrenal mass with homogenous enhancement and diffusion restriction. The margin was smooth with distinct borders, showing no invasion to adjacent organs, which was suggestive of adrenocortical adenoma; however, adrenocortical carcinoma could not be fully excluded due to restrictions in diffusion (Fig. ). The patient also underwent MRI to exclude sellar lesions. However, results showed a normal pituitary gland.
The right adrenalectomy revealed a soft, movable suprarenal mass that measured 4.2 × 3.9 × 2.4 cm with a dystrophic calcification of the capsule (Fig. ). No lymphadenopathy or adhesions to the adjacent organs were observed. Histopathology revealed findings suggestive of adrenal adenoma, including adrenal cells with uniform round nuclei and increased nucleocytoplasmic ratio separated by fibrous septae. No evidence of necrosis or infiltration was found (Fig. ).[
Postoperatively, the patient was administered hydrocortisone via intravenous infusion for 2 days; the treatment was then changed to an oral physiologic replacement dose (10 mg/m2/d) with sequential tapering and was discontinued after 6 months. The patient was regularly followed up at our oncology department and showed clinical improvement with weight normalization and resolution of her Cushingoid appearance over the next 4 months. The elevated cortisol level had also returned to normal at 18.2 μg/dL at the 4-month follow-up.
Six months after adrenalectomy, a mediastinal mass, which was previously nonexistent, was detected on a routine chest x-ray (Fig. ). For further evaluation, chest CT was performed and an enlargement of the left thymic lobe (45.51 × 72.97 × 51.76 mm) with homogenous attenuation was confirmed. To exclude the possibility of a residual adrenal lesion or misdiagnosis, an abdomen CT scan was performed and showed no abnormal findings. To further investigate the mass, a fine needle aspiration (FNA) biopsy was performed. Histopathology revealed benign thymic tissue without evidence of malignancy. Thymic architecture consisting of corticomedullary differentiation with presence of Hassall corpuscles in the medulla was conserved, thus confirming that the thymic tissue was benign, which is characteristic of RTH (Fig. ). Thereafter, she did not undergo surgical exploration and only basic assessments were performed during regular follow-up check-ups.
The 6-month follow-up chest x-ray after the diagnosis of RTH still showed mediastinal widening. However, at the 1-year follow-up, the chest x-ray showed resolution of the RTH (Fig. ). In addition, the size of the thymus on the follow-up CT findings has gradually decreased since the diagnosis. After 1 year, the size of the thymus had decreased from 45.51 × 72.97 × 51.76 mm to 37.01 × 61.99 × 41.24 mm (Fig. ). The length and width were measured perpendicularly as the maximum diameter, and the height was measured from the sternoclavicular junction level based on the proximal clavicular end.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.4, 'kg']}",40.8,38.76,42.84,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.4 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.4 kg - 10 kg) = 40.8 mL/hr.
Hence, the patient's fluid maintenance is 40.8 mL/hr."
4668,22,Maintenance Fluids Calculations,physical,decimal,pmc-3542923-1,Extracted,"We report the case of an athletic 49-year-old female with no medical records who has run the 2011 Marathon of Paris (42.195 Km). In view of the marathon, the patient started to train a few months ahead as per two to three runs weekly. She completed the marathon within 5 h 30, with an average speed of 7.5 Km/h, on a warm day (27 degrees celsius). Along the run, she drunk 4 L of mineral water (5 mg/L NaCl), and had some energy bars at the various feeding stations. Four hours after completion of the marathon, the patient felt dizzy and nauseous, with a strong asthenia and encompassed three vomiting periods associated with disorientation and confusion. She was then admitted to the emergency room 7 hours after the afore-mentioned symptoms occurred.
Upon admission, the patient was conscious but disoriented, clouded, with a Glasgow coma score of 13. She was apyretic and presented no circulatory failure. The neurological examination revealed acute spreadover of osteotendinous reflexes the four limbs, no systematic deficiencies and cutaneous plantar reflexes in flexion, isochoric and reactive pupils. Her body weight was 53.4 Kg (normal average body weight of 50 Kg).
The patient was then transferred to the intensive care unit (ICU) for diagnosis and treatment. Four hours later, the patient had a generalized tonic-clonic seizure that resolved following 1 mg clonazepam IV injection. The cerebral CT-scan showed a diffused supratentorial cerebral oedema (). The initial biological parameters were natremia 121 mmol/L, chloremia 88 mmol/L, protidemia 70 g/L, glycemia 8.5 mmol/L, kalemia 3.3 mmol/L, bicarbonates 18 mmol/L, blood urea nitrogen 3.7 mmol/L, creatinemia 68 μmol/L, blood urea nitrogen 2.9 mmol/L, uric acid 214 mmol/L, Glycemia 6.6 mmol/L, calcemia 1.8 mmol/L, phosphorus 0.87 mmol/L, magnesemia 1.04 mmol/L, CPK 14486 UI/L, Hb 10.1 g/dL, platelet count 172 G/L, and leukocytes 11.06 G/L. The calculated osmolality was 260 mosm/kg and the measured osmolality was 246 mosm/kg. Arterial blood gases showed a respiratory alkalosis to compensate an increased plasmatic anion gap metabolic acidosis, with initial blood lactate 10.5 mmol/L. The initial collection of a urine sample showed an urinary osmolality of 489 mosm/L. We report a natriuresis and kaliuresis of 86 and 75 mmol/L, respectively. The measure of the free cortisol was 1250 nmol/L at 8 am, and 1350 nmol/L following the ACTH test, by which therefore eliminate an adrenal origin of hyponatremia.
The patient was given a calculated bolus of isotonic saline as per the Adrogue formula. As no further clinical improvements followed, with a persistent hyponatremiaof 121 mmol/L, the patient was given a treatment based on 3% hypertonic saline solution. Natremia was recorded and indicated 128 mmol/L and 136 mmol/L at 4 hours and 7 hours after beginning of the treatment, respectively. Despite a rapid correction of natremia abnormalities, biological improvement was associated with the resolution of the neurological perturbations without apparition of new neurological symptoms.
The patient was discharged after 7 days following complete resolution of clinical and biological disorders.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [53.4, 'kg']}",93.4,88.73,98.07,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 53.4 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (53.4 kg - 20 kg) = 93.4 mL/hr.
Hence, the patient's fluid maintenance is 93.4 mL/hr."
4669,22,Maintenance Fluids Calculations,physical,decimal,pmc-3167144-1,Extracted,"A 20-month-old boy, weighing 12.5 kg, was admitted to the hospital due to cyanosis and a persistent cough following ingestion of a peanut. Upon arrival at the hospital, his arterial blood gas analysis (ABGA) revealed the following results: pH 7.24, PCO2 58 mmHg, PO2 50 mmHg, oxygen saturation 77%, and his chest X-ray showed air trapping in the left lung, suggesting a check-valve obstruction. His past history and lab test results were unremarkable.
Emergency rigid bronchoscopy was performed under general anesthesia. Anesthesia was induced with thiopental (50 mg) and rocuronium (7 mg); it was maintained with 50% oxygen, 50% nitrous oxide, and sevoflurane. The patient's initial oxygen saturation was 80%, but after intubation and 100% oxygen administration, the saturation level increased to 100%. Even when 50% oxygen was applied, the saturation was 100%. The oncall otolaryngologist identified peanut pieces at the carina and at the right main bronchus by rigid bronchoscopy (Doesel-Huzly bronchoscope, size 3 and 3.5, Karl Storz GmbH & Co. KG, Tuttlingen, Germany), and the pieces were removed using forceps. The ventilation port was opened to introduce the forceps, and during the apnea period, which lasted for 10-15 s, the oxygen saturation dropped to 80%. A rigid bronchoscopic examination performed after foreign body removal revealed no residual peanut pieces, and the patient was intubated with an endotracheal tube (ID 4.0 Sheridan® uncuffed™, Teleflex Medical, Durham, USA). Oxygen saturation remained at 99% during the remainder of the procedure.
However, 2 days later, the patient was still coughing and developed a mild fever. Follow-up chest radiographs showed unresolved air trapping and pneumonia in the left lung. A computed tomography (CT) scan revealed a low-density lesion in the left main bronchus. The patient was referred to our department, and an airway exploration with flexible bronchoscopy (size 1.8 mm LF-P, intubation fiberscope, Olympus, Shinjuku-ku, Tokyo, Japan) under general anesthesia was planned. After preoxygenation with 100% oxygen, general anesthesia was induced with thiopental (50 mg) and rocuronium (7 mg). A slightly large ETT (ID 5.0 Sheridan Sheridan® uncuffed™, Teleflex Medical, Durham, USA) was chosen for the procedure. A modified connector with two ports was attached to the ETT which allowed the passage of instruments with no interruption in ventilation (). Flexible bronchoscopic exam by anesthesiologists revealed a remnant foreign body at the distal end of the left main bronchus. A Fogarty balloon catheter (3-Fr arterial embolectomy catheter, Edwards Lifesciences Corporation of Puerto Rico, Irvine, CA, USA) was then tied to the flexible bronchoscope and passed through a slit between the foreign body and the bronchial wall. The Fogarty catheter balloon was dilated with 0.6 ml of saline and used to gently pull the foreign body toward the carina. The foreign body was removed with grasping forceps (5-Fr Richard Wolf Medical instruments Co., Vernon Hills, IL, USA). There was no interruption in ventilation during the procedure. The patient's oxygen saturation was maintained at 99%, and the end tidal carbon dioxide was maintained at about 35 mmHg. The initial airway pressure was 12 mmHg, and increased to 18 mmHg when instruments were introduced into the ETT. The diameter of the ETT, flexible bronchoscope, Fogarty catheter and grasping forceps were 5 mm, 1.8 mm, 1 mm, and 1.67 mm, respectively. The patient was treated with antibiotics and discharged 13 days later with no complications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.5, 'kg']}",45,42.75,47.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.5 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.5 kg - 10 kg) = 45.0 mL/hr.
Hence, the patient's fluid maintenance is 45.0 mL/hr."
4670,22,Maintenance Fluids Calculations,physical,decimal,pmc-8080733-1,Extracted,"A 22-year-old female Caucasian patient was diagnosed with UC 3 mo ago, complaining of bloody diarrhea, abdominal pain and weight loss, and discontinued mesalamine due to the gastric intolerance. The patient underwent a colonoscopy 2 wk before the admission to the hospital, which revealed lesions consistent with UC of moderate endoscopic activity (Mayo endoscopic score 2).
She was admitted to the emergency department in due to frequent liquid and bloody stool and intense abdominal pain for 2 mo, with worsening of the symptoms during the last week, in poor condition with nausea, vomiting, and weight loss (10 kg) and without the improvement from the previous use of antibiotics.
At hospital admission (day 1 of hospital admission), the patient presented in poor condition, dehydrated, tachycardic (110 beat/min), blood pressure 100/60 mmHg, temperature > 37.8 °C, with distended and diffusely painful abdomen, and rebound tenderness.
Laboratory tests showed inflammatory process (C-reactive protein 20.3 mg/dL) and anemia (hematocrit 25.8%, hemoglobin 8.1 g/dL) at admission (Table ).
Abdominal X-ray revealed colonic dilation of 7 cm, consistent with megacolon (Figure ).
Clostridium difficile (C. difficile) A and B toxin was positive, and the treatment with oral vancomycin 250 mg qid was initiated. However, the patient presented with worsening of diarrhea and rectal bleeding (> 10 episodes/d), increased abdominal distension, and fever. A flexible sigmoidoscopy was performed (day 4 of hospital admission) and inserted up to 25 cm with no insufflation, showing ulcers covered by fibrin, mucosal friability, edema, and intense enanthem with spontaneous bleeding in sigmoid and rectum, consistent with UC of severe activity (Mayo endoscopic score 3) (Figure ). Histopathological evaluation showed chronic colitis in intense activity with structural abnormalities of the mucosa, presence of crypt micro-abscesses and plasmacytosis, consistent with severe inflammatory activity without the evidence of C. difficile or cytomegalovirus infection.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.0, 'kg']}",40,38,42,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.0 kg - 10 kg) = 40.0 mL/hr.
Hence, the patient's fluid maintenance is 40.0 mL/hr."
4671,22,Maintenance Fluids Calculations,physical,decimal,pmc-6411594-1,Extracted,"A 5-day-old girl was referred to us with bilious vomiting and abdominal distention since birth. The baby was born at term by caesarean section to a 30 year old primigravida mother. The baby weighed 2.79 kg at birth. Antenatal ultrasonography at 32 weeks gestation had revealed multiple, dilated, fluid filled bowel loops. At admission, the baby was dehydrated with a distended abdomen. Rest of the systemic examination was unremarkable. Blood investigations were within normal range. X-ray abdomen revealed few dilated bowel loops, paucity of distal gas shadows and nasogastric tube in the right upper quadrant of abdomen (). Ultrasound abdomen revealed liver predominantly on the left side of abdomen, multiple spleen like structures on the right side with distended bowel loops. Echocardiography revealed ostium secundum atrial septal defect of 5 mm with levocardia.
Since pre-operative diagnosis of abdominal situs inversus was known, a left upper quadrant transverse incision was given in contrast to the classical right upper quadrant transverse incision. Laparotomy confirmed situs inversus abdominis with the liver and duodenal C loop on the left side (a). The baby had three spleens on the right side (b). The proximal jejunum was massively dilated and there were multiple jejunal atresias (5 in number) starting from about 45 cm from the duodenojejunal flexure (a). The entire distal small bowel was supplied by a single branch of the ileo-colic artery and had apple peel appearance. There were several Ladd’s bands crossing the second part of duodenum with narrow base mesentery. The segment of jejunum containing the atretic segments was excised and cut back of the bulbous proximal jejunal end was done. End to side jejuno-ileal anastomosis was done (b), Ladd’s procedure done and a trans-gastric trans-anastomotic feeding jejunostomy done. The residual small bowel length was about 145 cm.
Post-operatively the child was shifted to newborn ICU. Immediate post-op period was uneventful. The baby was started on tube feeds by post-op day (POD) 3, however oral feeds were not tolerated till POD 14. This may be due to hypo-peristalsis in the dilated proximal jejunum. Full oral feeds were reached by POD 28 and the baby was discharged. At 18 months follow up, the baby is thriving well and is asymptomatic.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.79, 'kg']}",11.16,10.602,11.718,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.79 kg. Hence, the patient's maintenance fluid is 2.79 kg * 4 mL/kg/hr = 11.16 mL/hr.
Hence, the patient's fluid maintenance is 11.16 mL/hr."
4672,22,Maintenance Fluids Calculations,physical,decimal,pmc-3030059-1,Extracted,"A 35-year-old, 157 cm, 52 kg, woman was hospitalized for surgical treatment of peroneal tendonitis in her right foot. She had no significant medical history, allergy, or previous neurological disease. She underwent surgery for the same condition 1 year earlier at another hospital. Spinal anesthesia was performed and the operation was uneventful. After transferring to the general ward, the patient's right leg began moving involuntarily. The movement was rhythmic and was limited to the right leg. The transient movement disappeared completely after 30 min, and no complication resulted. A specific diagnosis for the movement was not determined. The patient experienced no further problem.
On a preoperative visit to our hospital, she expressed no fear regarding spinal anesthesia and agreed to undergo spinal anesthesia again.
Premedication consisted of 2.5 mg of midazolam, administered intramuscularly 30 min before surgery. In the operating room, standard monitoring (non-invasive blood pressure, peripheral oxygen saturation, and electrocardiogram) was used. The patient was placed in the right lateral decubitus position, and lumbar puncture was performed without difficulty at L3-4. After free-flowing cerebrospinal fluid was obtained, 9 mg of heavy bupivacaine 0.5% (Marcaine Spinal 0.5% Heavy®, AstraZeneca, Sweden) and 0.2 mg of epinephrine were administered via a 25 G spinal needle. The procedure was performed without complication. Sensory input to T10 was blocked, and the surgery was completed uneventfully in approximately 50 min.
After surgery, the patient was transferred to a recovery room. Approximately 100 min after administration of anesthesia, she began to experience bilateral, involuntary myoclonic movement of both legs and arms. Sensory function in her arms was intact, and the rhythm of the movement varied widely in rate. She was conscious, oriented, and calm. At that point, 2 mg of midazolam was administered intravenously. Approximately 10 min later, she was treated with 0.5 mg of oral clonazepam and 2 mg of IV midazolam. The myoclonic movement diminished slightly, but persisted. A neurology consult was obtained. There was no evidence of weakness or impairment of cerebellar or cranial nerve dysfunction. Thus, these movements were clinically defined as spinal myoclonus. After approximately 1 h, 0.5 mg of clonazepam was administered again. The myoclonic movement disappeared completely at 4 h after its onset. Postoperative laboratory findings, including serum electrolytes and glucose, were within normal limits. When she was examined again the following day, no abnormal neurologic finding was evident. One month later, she visited the hospital again; no recurrence of spinal myoclonus had occurred.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [52.0, 'kg']}",92,87.4,96.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 52.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (52.0 kg - 20 kg) = 92.0 mL/hr.
Hence, the patient's fluid maintenance is 92.0 mL/hr."
4673,22,Maintenance Fluids Calculations,physical,decimal,pmc-4400503-1,Extracted,"A 21-year-old African American male presented to our hospital in November 2010 with a 1-week history of hematuria, bilateral pedal edema, flank pain and vomiting. He also noted a weight gain of 9 kg over the past 5 months. About 2 months prior to admission, the patient had stopped his highly active antiretroviral therapy (HAART) and lisinopril citing insurance reasons.
Past medical history was significant for vertically transmitted HIV infection and hypertension. In 2006, he was found to have an elevated creatinine of 132.6 μmol/L and underwent a renal biopsy, which was consistent with lupus-like glomerulonephritis. At that time, he was on HAART and his CD4 count was 494 cells/μL with HIV viral load of 107 copies/mL.
Physical examination was significant for periorbital edema, 2+ pitting peripheral edema, bilateral costovertebral angle tenderness and palpable lymphadenopathy. Initial laboratory workup revealed a serum creatinine of 875.16 μmol/L (baseline creatinine was 132.6 μmol/L); estimated glomerular filtration rate (eGFR) 6.7 mL/min/1.73m2 (0.11 mL/s/1.73m2) calculated using the four-variable Modification of Diet in Renal Disease Study equation. Urine analysis showed 3+ protein, 2+ blood, 6–10 red blood cell and was negative for esterase and nitrite. Serum albumin was 2.1 g/dL, low-density lipoprotein was 176 mg/dL and 24-h urinary protein was 22 g. Complement levels were within normal limits. Serological workup for anti-streptolysin O antibody, anti-DNase B, double-stranded DNA and anti-nuclear antibodies (ANA) was negative. CD4 count was 420 cells/μL and HIV viral load was 79 998 copies/mL. Renal ultrasonography showed normal sized kidneys with no mass or obstruction.
The following differential diagnoses were considered: (i) HIV nephropathy, (ii) rapidly progressive glomerulonephritis, (iii) acute tubular injury due to nephrotoxic HIV medications or volume depletion and (iv) lupus-like glomerulonephritis. The patient underwent percutaneous kidney biopsy, which was diagnostic of lupus-like proliferative glomerulonephritis ().
HAART was restarted and he was given Lasix and intravenous Solumedrol. The edema became refractory to diuretics and serum creatinine trended to 1095.16 μmol/L eGFR 5.2 mL/min/1.73m2 (0.086 mL/s/1.73m2)] at which time hemodialysis was initiated.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [9.0, 'kg']}",36,34.2,37.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 9.0 kg. Hence, the patient's maintenance fluid is 9.0 kg * 4 mL/kg/hr = 36.0 mL/hr.
Hence, the patient's fluid maintenance is 36.0 mL/hr."
4674,22,Maintenance Fluids Calculations,physical,decimal,pmc-8681225-1,Extracted,"A 48-year-old man with a past medical history of hypertension, alcohol dependence, macrocytic anemia (secondary to a well-established clinical entity of monoclonal gammopathy associated with B-cell lymphoma, with an elevated IgG kappa level of 1380 mg/dL on immunoelectrophoresis), and a smoking history presents to the emergency department with multiple complaints including severe weight loss, poor appetite, fatigue, and nonproductive cough with sinus drainage for the past month. According to the patient, he has lost around 50 pounds in the span of four to five months and has been complaining of early satiety for the past two months. The patient denied any abdominal pain, dysphagia, or odynophagia and denies any history of esophagogastroduodenoscopy (EGD) or colonoscopy in the past. The patient admits to drinking more than one pint of hard liquor a day for the past four years and has been smoking half a pack a day for the past 30+ years. The patient had no family history of cancer. The patient is a homosexual and has multiple sexual partners and does not use protection. During his visit to the emergency department, the patient had two episodes of vomitus with large bright red blood; the patient denies any history of varices or variceal bleeding.
Initially, the patient had a WBC count of 10.37 k/mcl (Normal: 4-11) with a hemoglobin of 4.8 g/dL (Normal: 13.5-17.5) and MCV of 117.5 fl (Normal: 80-100) with a platelet count of 72 k/mcl (Normal: 150-450). The patient's creatinine was 2.64 mg/dl (Normal: 0.70-1.5) with an unknown baseline with a sodium of 124 mmol/L (Normal: 135-145), potassium 3.1 mmol/L (Normal: 3.5-5.4), and alkaline phosphatase of 226 IU/L (Normal: 20-130) with AST of 94 IU/L (Normal: 0-45), and a total protein of 9.8 g/dL (Normal: 6.2-8.1). The patient's urine drug analysis was negative and tested negative for coronavirus/SARS-CoV-2 (COVID-19). Vital signs show a heart rate of 120 beats/minute and were afebrile, and the rest of the vital signs were within normal limits. Physical exam showed that the patient was cachectic but not in acute distress. No enlarged lymph nodes were appreciated. Cardiovascular examination showed S1 plus S2 with no audible murmurs, and lungs were clear to auscultation bilaterally. Gastrointestinal examination showed a soft, non-tender abdomen with positive bowel sounds. The patient had 5/5 strength in the upper and lower extremities. Rectal examination showed multiple genital warts, which were coliform in nature, and the guaiac test was negative for any bleeding. Initially, the chest x-ray showed no acute disease; however, an abdominal ultrasound showed fatty changes in the liver but was negative for any gallbladder pathology. Computed tomography (CT) scan of the abdomen/pelvis without contrast was initially done and was negative for any acute pathology. The patient was resuscitated with intravenous (IV) fluids and two units of packed red blood cells and was started on octreotide drip for possible variceal bleed. The patient subsequently underwent EGD for his hematemesis, and a friable, ulcerated circumferential mass lesion was seen in the distal esophagus extending from 28 to 40 cm from the incisors with active oozing that was seen from the mass (Figure , Panels A and B).
Multiple biopsies were obtained and sent to pathology. Oncology was subsequently consulted. Moreover, the patient’s syphilis screen was nonreactive, he had a normal thyroid-stimulating hormone (TSH) level, hepatitis panel was negative, and tested negative for cytomegalovirus (CMV). Furthermore, the patient was tested for HIV which was positive with a viral load of 219,000 cpy/mL, with appropriate HIV 1 genotyping. The absolute lymphocyte number was 0.93 k/mcl with an absolute CD4 T-helper count of 24 /mm3. The patient subsequently underwent CT of the chest abdomen pelvis with IV contrast, which demonstrated a distended esophagus to about 2.5-3 cm with an air-fluid level (Figure ) and a subcarinal mass-like encirclement of the esophagus with splaying of the carina and mass-effect along the left atrium and inferior pulmonary veins, measuring 7.36 x 5.38 cm in the greatest transverse and anterior/posterior dimensions (Figure ). Pathologic analysis of esophageal biopsy showed a diffuse perforation of the large, atypical cells associated with brisk mitotic activity consistent with plasmablastic lymphoma (Figure ). Immunohistochemical (IHC) stains were positive for CD79a, CD138, MUM-1, and CD10 (Figures -, respectively) and were negative for CD20, PAX-5, CD3, CD5, BCL6, BCL2, cyclin D1, CD30, anaplastic lymphoma kinase (ALK), and epithelial membrane antigen (EMA). C-MYC by immunohistochemistry was positive and in-situ hybridization for Epstein-Barr virus (EBV) was positive (Figure ). The patient also underwent a bone marrow biopsy, which showed hypercellular marrow with 90% cellularity and decreased trilineage hematopoiesis, plasma cells, histiocytes, and lymphocytes. Immunohistochemistry showed the CD-79a highlights with scattered B cells and numerous plasma cells, which were also highlighted by CD-138. Flow cytometry showed CD45-positive lymphocytes and was negative for CD20, CD10, CD 200, CD5, and lambda light chain. The patient was started on chemotherapy with dose-adjusted etoposide, prednisolone, vincristine, cyclophosphamide, doxorubicin (V-EPOCH) and highly active antiretroviral therapy (HAART) with Truvada and Dolutegravir. The patient underwent a total of six cycles of V-EPOCH with dose-adjusted cyclophosphamide due to elevated bilirubin and low CD4 counts. Therapy was complicated by multiple episodes of febrile neutropenia requiring hospitalization and severe peripheral neuropathy requiring multiple dose adjustments; however, the patient tolerated therapy generally well and is now discussing the option of allogeneic bone marrow transplantation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [50.0, 'lbs']}",62.6796,59.54562,65.81358,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 50.0 lbs so this converts to 50.0 lbs * 0.453592 kg/lbs = 22.6796 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (22.6796 kg - 20 kg) = 62.6796 mL/hr.
Hence, the patient's fluid maintenance is 62.6796 mL/hr."
4675,22,Maintenance Fluids Calculations,physical,decimal,pmc-4005616-1,Extracted,"A five year old male neutered cairn terrier was presented to the primary veterinarian for an acute onset of lethargy, vomiting, and inappetence. The dog had no travel history outside of Pennsylvania and was vaccinated as per American Animal Hospital Association recommendations, not including vaccination for leptospirosis []. A complete blood count (CBC) and serum biochemistry panel were performed with the significant abnormality being mild thrombocytopenia (Table ). The dog was treated supportively with 20 ml/kg lactated Ringer’s solutiona subcutaneously. The dog’s clinical signs continued and it was presented to Veterinary Specialty and Emergency Center (VSEC) on day four. A physical examination revealed mild dehydration estimated at 5% without other abnormalities. An electrolyte panel was performed, revealing mild hypokalemia (Table ). An abdominal ultrasound showed mild thickening of the gastric body and diffuse hyperechoic mucosal speckling of the small intestines. The patient was given supportive care for non-specific gastroenteritis with dolasetronb (0.5 mg/kg intravenously [IV] q 24 h), famotidinec (0.5 mg/kg IV q 24 h), metronidazoled (10 mg/kg IV q 12 h), mirtazapinee (7.5 mg per os [PO] q 24 h), and IV lactated Ringer’s solution at a rate of 4 ml/kg. The dog was discharged to the owner on day five with no further vomiting and an improved appetite. Treatment was continued at home with maropitant citratef (2.4 mg/kg PO q 24 h × 4 days), metronidazoleg (12.5 mg/kg PO q 12 h × 14 days), famotidineh (0.5 mg/kg PO q 24 h × 7 days), mirtazapine (0.75 mg/kg PO q 24 h as needed for inappetance), and the patient was placed on a hydrolyzed dieti.
On day 24, the dog was presented to VSEC for re-evaluation after the owner noted an increased thirst and inappropriate urination in the house since day 18, without hematuria, stranguria, or pollakiuria. There was no recurrence of the gastrointestinal signs and the dog’s appetite remained good. Physical examination was unremarkable. A CBC showed persistent mild thrombocytopenia. A serum biochemistry panel showed mild increases in alkaline phosphatase, cholesterol and globulins, mild hypokalemia, and other non-specific abnormalities as shown in Table . Urine was hyposthenuric (urine specific gravity [USG] 1.002) with trace protein on urine dipstick (Table ) and an unremarkable urine sediment. A urine culture was submitted to rule out an occult urinary tract infection.
Given the history, marked hyposthenuria, and absence of azotemia and hyperglycemia, psychogenic (primary) polydipsia, polydipsia secondary to gastrointestinal disease, and diabetes insipidus were amongst the primary differentials []. Polydipsia secondary to gastrointestinal disease was considered unlikely given the lack of resolution with treatment of the gastrointestinal signs []. Renal insufficiency was excluded at that time based on the presence of hyposthenuria, suggesting active dilution of the urine []. The owner was asked to collect a series of at-home urine samples from the dog over the following week to evaluate for evidence of any spontaneous concentrating ability that would support a diagnosis of psychogenic polydipsia.
The dog was re-evaluated on day 29. The polyuria had persisted but the dog was now lethargic, inappetent, was intermittently vomiting, and had had a significantly reduced thirst over the past 5 days. On physical examination, tacky mucous membranes and decreased skin turgor were noted; based on these findings and a decrease in weight from 9.5 kg to 8.6 kg, the dog was estimated to be 10% dehydrated. No other new physical examination findings were noted. A serum biochemistry panel revealed moderate azotemia (Table ). Urine specific gravity was 1.006 on a urinalysis with 2+ protein and 3+ blood (Table ). Abdominal ultrasound revealed mild to moderate bilateral renomegaly (left kidney measured 5.8 cm in craniocaudal dimension versus 5.3 cm on day 4; right - 6.1 cm versus 4.8 cm). The kidneys had a rounded, swollen appearance with increased echogenicity of the medullae. The liver was also mildly enlarged and diffusely hypoechoic. The ultrasonographic changes to the gastrointestinal tract persisted, but were improved compared to day 4. Resting cortisol was 6.1 μg/dL, excluding a diagnosis of hypoadrenocorticism []. The urine protein: creatinine ratio was 4.5. The urine culture from day 24 showed no bacterial growth. Serum was submitted for microscopic agglutination test (MAT) against a panel of seven leptospiral serogroups.
The patient was admitted to the hospital, and treatment with IV lactated Ringer’s solution, ampicillinj (20 mg/kg IV q 8 hr), doxycyclinek (10 mg/kg IV q 24 hr), dolasetron (0.5 mg/kg IV q 24 hr), and famotidine (0.5 mg/kg IV q 24 hr) was initiated. An indwelling urinary catheter was placed to measure urine output and to protect hospital staff and clients against exposure to potentially infectious leptospires in the urine. On day 31, the dog had a decline in urine output (from 3.1 ml/kg/hr on day 30 to 1.8 mls/kg/hr on day 31) and developed hypertension (200 mmHg systolic measured by noninvasive doppler). The azotemia had significantly worsened (Table ). The urine output did not increase after boluses of furosemidel (1 mg/kg IV) and mannitolm (0.5 g/kg IV twice) and the owners elected to have the dog euthanized. The MAT results were received after the dog was euthanized and showed high titres against multiple serovars (Table ). Given the clinical signs and absence of vaccination against leptospirosis, the markedly elevated MAT in this case was considered to confirm a diagnosis of leptospirosis [,]. Since multiple serovars had a titre >1:3200, the causative serovar could not be determined.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [8.6, 'kg']}",34.4,32.68,36.12,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 8.6 kg. Hence, the patient's maintenance fluid is 8.6 kg * 4 mL/kg/hr = 34.4 mL/hr.
Hence, the patient's fluid maintenance is 34.4 mL/hr."
4676,22,Maintenance Fluids Calculations,physical,decimal,pmc-2872854-1,Extracted,"A 81-year-old woman (height: 150 cm, body weight: 49 kg) was admitted to an intensive care unit because of respiratory failure and generalized edema. She was followed up in our hospital because of hypertension, congestive heart failure, asthma and a destroyed lung due to having pulmonary tuberculosis for 9 years. She was admitted in an intensive care unit and she received controlled mechanical ventilation because of the aggressive generalized edema and respiratory failure caused by the corpulmonale and congestive heart failure. The controlled ventilation was maintained with a tidal volume of 380-440 ml, a respiratory rate (RR) of 16-24 bpm and an FiO2 of 35% and a positive end expiratory pressure (PEEP) of 5 cmH2O. She developed tracheomegaly during the 53 days of mechanical ventilation. She was impossible to wean off the mechanical ventilator, so she was planned to undergo tracheostomy. On the chest radiography, the maximum transverse diameter of the trachea was measured to be 50.3 mm (); on the thoracic CT, the maximum diameter of the trachea was measured to be 51.3 mm and 48.8 mm, respectively, in the sagittal and transverse directions ().
The patient was premedicated with 0.2 mg of glycopyrrolate IM at 30 minutes pre-op. She was transported in the operating room and her trachea was intubated with a 6.5 mm internal diameter endotracheal tube. We connected the breathing circuits and the endotracheal tube, we monitored the electrocardiography and performed noninvasive blood pressure monitoring, pulse oximetry and capnography. At arrival in the operation room, the patients was drowsy and her vital signs were blood pressure: 130/80 mmHg, heart rate: 130 rate/min, O2 saturation: 72% and end-tidal carbon dioxide (ETCO2): 56 mmHg. After hyperventilation by using ambu-bagging with 100% O2 6 L/min, the O2 saturation and ETCO2 reached 95-96% and 43-46 mmHg respectively.
Anesthesia was induced with 5 mg of midazolam IV and 15 mg of rocuronium bromide IV after loss of conscienceness and the 0.05-0.1 µg/kg/min of remifentanil was continuously infused. Anesthesia was maintained with sevoflurane 1-1.5 Vol%, The FiO2 was 60%, and fresh oxygen was given at 4 L/min. Pressure controlled ventilation via a ventilator (Cato® edition, Dräger Medical AG, Germany) was provided with a peak airway pressure of 25 mmHg, The RR was 15-20 bpm and the PEEP was 5 cmH2O. After tracheostomy, we extubated the endotracheal tube and then a 7 mm cuffed tracheostomy tube was inserted. We inflated the cuff with 10 ml air via a pilot balloon of the tracheostomytube, but tidal volume was very small because of the significant peritubal leakage during the ambu-bagging. Despite of inflating the cuff with 15 ml air via a pilot balloon, after the 8 mm tracheostomy tube re-intubated, we couldn't control the ventilation because of peritubal air leakage. The ETCO2 continued to increase to 55-60 mmHg.
The arterial blood gas showed severe hypercapnia: pH 7.09, PaCO2 97.2 mmHg, PaO2 78 mmHg and HCO3- 29.7 mEq/L. We observed the nasal and oropharyngeal air leakage, so we compressed the above site of the thyroid cartilage and we then confirmed the reduced air leakage. We packed the larynx with wet gauze using an intubating blade and forceps to prevent gas leakage. But the tidal volume was 100-150 ml and air leakage was still present. To preventing laryngeal air leakage, we intubated with a 4 sized Proseal® laryngeal mask airway after sealing the connector with tape. We could control the ventilation as the the air leakage was reduced and tidal volume was more than 200 ml, so we brought the patient back to consciousness with 100% oxygen. At this point, the patient's vital signs were: blood pressure: 100/70 mmHg, heart rate: 100-110 rate/min, O2 saturation: 95-96%, ETCO2: 43 mmHg. But as the patient awoke and she recovered her laryngeal reflex, the laryngeal mask airway was displaced, so we couldn't controlled the ventilation. Once more the ETCO2 increased to 55-60 mmHg, and we planned endotracheal reintubation. After IV midazolam 3 mg and remifentanil 60 µg, the tracheostomy tube was extubated. We intubated her with a 6.5 mm endotracheal tube and inflated the cuff to 25 cmH2O with a cuff pressure manometer (VBM Medizintechnik GmbH, Germany). The endotracheal tube depth was 23 cm at the patient's upper lip. Chest auscultation revealed symmetrical and little air leakage was present. But the tidal volume measured over 300 ml for ambu-bagging. The incision site of the tracheostomy was sutured. After hyperventilation with ambu-bagging, the ETCO2 measured 38-42 mmHg. The arterial blood gases were a pH of 7.29, a PaCO2 of 46.2 mmHg, a PaO2 of 78 mmHg and a HCO3- of 29.7 mEq/L. The patient's vital signs were a blood pressure of 105/40 mmHg, a heart rate of 105 beats/min and an O2 saturation of 97%. The patient was moved ICU with ambu-bagging while she was unconscience.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [49.0, 'kg']}",89,84.55,93.45,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 49.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (49.0 kg - 20 kg) = 89.0 mL/hr.
Hence, the patient's fluid maintenance is 89.0 mL/hr."
4677,22,Maintenance Fluids Calculations,physical,decimal,pmc-4209027-3,Extracted,"A 34-year old, 62 kg, 159 cm man underwent left pansinectomy for sinobronchitis. Anesthesia was induced with 100 mg propofol, 0.25 μg/kg/min remifentanil, and 40 mg rocuronium. Following tracheal intubation, anesthesia was maintained with sevoflurane and remifentanil. During induction and maintenance of anesthesia, BP, oxygen saturation, and ETCO2 were within normal ranges. The total operation time was 59 minutes. At the end of surgery, 50 mg flurbiprofen axetil, 15 mg pentazocine, and sugammadex 3.2 mg/kg were injected. One minute after the injection but before extubation, the patient developed intense erythema all over the body, especially on the face and chest. Simultaneously, BP decreased from 100/60 to 70/40 mmHg, with no respiratory symptoms. BP recovered to 100/60 mmHg after 4 mg ephedrine hydrochloride injection, and the patient was transferred to the recovery unit. Erythema disappeared after treatment with 5 mg chlorpheniramine maleate and 50 mg ranitidine hydrochloride administered intravenously. The patient was transferred out of the recovery room 1 hour after the event and discharged home 6 days later. An intradermal test for flurbiprofen axetil, pentazocine, and sugammadex allergy was performed about 7 weeks after the operation. As shown in Table , a 1:1000 dilution of sugammadex induced flare, while a 1:100 dilution of sugammadex induced both flare and wheal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [62.0, 'kg']}",102,96.9,107.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 62.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (62.0 kg - 20 kg) = 102.0 mL/hr.
Hence, the patient's fluid maintenance is 102.0 mL/hr."
4678,22,Maintenance Fluids Calculations,physical,decimal,usmle-1140,Extracted,"A 2800-g (6-lb 3-oz), 3-day-old newborn is in the intensive care unit for fever, vomiting, tremors, cyanotic episodes, and seizures. She was born at 36 weeks to a 25-year-old primigravid woman. Spontaneous vaginal delivery was complicated by maternal fever and chorioamnionitis. Apgar scores were 6 at 1 minute and 7 at 5 minutes, respectively. Shortly after delivery, the child had seizures and high-grade fever with poor feeding and hypotonia. She was intubated for respiratory distress. Her temperature is 39°C (102.3°F), pulse is 180/min, and respirations are 60/min. Physical exam shows grunting breath sounds, an enlarged liver palpable 3 cm below the right costal margin, and lethargy. A CT scan of the chest, abdomen, and pelvis shows multiple pulmonary and hepatic granulomas.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2800.0, 'g']}",11.2,10.64,11.76,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2800.0 g so this converts to 2800.0 lbs * kg/1000 g = 2.8 kg. Hence, the patient's maintenance fluid is 2.8 kg * 4 mL/kg/hr = 11.2 mL/hr.
Hence, the patient's fluid maintenance is 11.2 mL/hr."
4679,22,Maintenance Fluids Calculations,physical,decimal,pmc-4121498-1,Extracted,"A 73-year-old female patient was diagnosed with spinal stenosis on L1-L5, and it was decided to perform posterior lumbar spinal fusion. The patient had height of 154 cm and weight of 72 kg. Except for hypertension, no other specific medical history was known. Prior to surgery, there were no abnormal findings in the complete blood count, and electrolyte and blood coagulation tests.
Before anesthetic induction, the patient's blood pressure was 150/70 mmHg, heart rate was 82 beats/min, and oxygen saturation was 98%. Anesthetic induction was conducted with injection of propofol 120 mg and rocuronium 50 mg, followed by endotracheal intubation. General anesthesia was maintained through sevoflurane (1-1.5 %)-O2(2 L/min)-N2O (2 L/min). For direct measurement of the arterial pressure, right radial artery cannulation was performed. It was planned that the patient would be managed in the intensive care unit for a few days after the surgery, and at the request of the orthopedic surgeon, a subclavian venous catheter, which is comparatively convenient for long term maintenance, was to be inserted. Due to a skin lesion in the right subclavian area, central venous catheter insertion was conducted in the left subclavian vein with a two-lumen CVC set (Arrow International, Inc., Reading, PA, USA). The catheter was fixed at a depth of 15 cm while the intravenous supply after blood regurgitation was confirmed. Afterwards, the patient was turned into the prone position on the Wilson frame (OSI, Union City, CA, USA) for the surgery (). After changing the position, the upper chest area from above the nipples and including the subclavian area showed overall compression. In order to prevent pressure by compression, a surgical cotton pad was applied to the applicable area, and free flow of fluid through the CVC was checked before commencing the operation. During the whole operating time of 4 hours and 45 minutes, the mean arterial blood pressure and the heart rate were maintained at 65-75 mmHg and 60-75 beats/min, respectively, showing stable vital signs. Total fluid input during the surgery amounted to 1,200 ml of normal saline, 500 ml of colloid, 5 units of packed red blood cell and 3 units of fresh frozen plasma, and the actual blood loss amounted to 1,500 ml and the urine output was 850 ml. After the operation, the patient was transferred to the intensive care unit. The patient was mentally alert, with a blood pressure of 130/80 mmHg and heart rate of 61 beats/min. In the blood coagulation test carried out immediately after the operation, the prothrombin time (INR) was measured at 1.13 and activated partial thromboplastin time was 42.3 seconds.
On the next day, there was a sudden occurrence of severe edema in the patient's left arm, and the fingertips of her left hand felt cold. The CVC was removed from the patient immediately. A blood test conducted on the day of the symptom showed that D-dimer had increased above 20 g/ml, which led to the suspicion of deep vein thrombosis. To suppress the swelling, the patient's left arm was wrapped with a pressure bandage, and ultrasonography and computed tomography scan were performed on the patient. On ultrasonography, extensive deep vein thrombosis was observed in the left subclavian vein and caudal branch () while on computed tomography, thrombosis was found in the left brachiocephalic vein and subclavian vein (). Immediately, thrombolysis was conducted in the upper left arm through a venogram (). Over the next 3 days after the thrombolysis, anticoagulation therapy was carried out by concurrently administering heparin 500 IU/h and urokinase 100,000 IU/h, and over the next 6 days, urokinase was stopped and only heparin was administered. The patient showed no more particular complications, and was discharged from the hospital 2 weeks after the treatment.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [72.0, 'kg']}",112,106.4,117.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 72.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (72.0 kg - 20 kg) = 112.0 mL/hr.
Hence, the patient's fluid maintenance is 112.0 mL/hr."
4680,22,Maintenance Fluids Calculations,physical,decimal,pmc-8039748-1,Extracted,"A 4-year-old girl visited our hospital because of colicky abdominal pain. The patient complained of abdominal pain 1 day ago. The pain was throbbing and localized in the periumbilical area. She refused to eat her meal due to aggravation of the abdominal pain and was seldom able to move. Fever, vomiting, or diarrhea was absent. Furthermore, no history of previous medical problem, surgery, or abdominal trauma was present. The mother had several silent stones in the gallbladder (GB), which were detected during routine health checkup.
The patient’s weight and height were 18 kg (50–75th percentile) and 103.1 cm (50–75th percentile), respectively. Vital signs were relatively stable, with a blood pressure of 100/70 mm Hg, heart rate of 104 beats/min, respiratory rate of 28 breaths/min, and body temperature of 36.5°C. Physical examination revealed decreased bowel sound and abdominal tenderness on the periumbilical area.
The hemoglobin, white blood cell, and platelet counts were 13.1 g/dL, 8,210/mm3, and 310×106/mm3, respectively. Hemolysis was not noted. Blood chemistries were as follows: cholesterol 157 mg/dL (reference range, 120–200 mg/dL), total protein 7.9 mg/dL (6.1–7.9 mg/dL), albumin 4.9 mg/dL (3.5–5.6 mg/dL), alkaline phosphatase 294 U/L (134–386 U/L), aspartate aminotransferase (AST) 271 U/L (15–40 U/L), alanine aminotransferase level (ALT) 115 U/L (5–45 U/L), gamma glutamyl transpeptidase (GGT) 202 U/L (5–32 U/L), total bilirubin 0.63 mg/dL (<2.0 mg/dL), amylase 320 U/L (16–91 U/L), and lipase of 567 mg/dL (4–29 mg/dL).
Abdominal X-ray showed focal ileus in the central part of the abdomen. Abdominal ultrasonography (USG) revealed a swollen pancreas, dilated intrahepatic bile duct, and a CBD 0.94 cm in diameter and a 4.7-mm-sized echogenic focus in the distal CBD (, ). The echogenic focus was suggested to be a CBD stone without posterior shadow. A septum in the CBD was noted on the coronal view of pancreaticobiliary computed tomography (CT; ). Acute pancreatitis, with biliary obstruction due to the stone and web-like structure in the CBD, was diagnosed. Non per oral diet, intravenous hydration, pain killers, and antibiotics (cefotaxime and metronidazole) were started. We decided to perform ERCP to evaluate and manage the stones and septum in the CBD. Endoscopic procedure was performed on the 6th day of admission under general anesthesia when the serum amylase and lipase levels decreased to 75 U/L and 32 mg/dL, respectively. A squashed muddy stone was extracted from the CBD (). A thin narrowing and a shelf-like linear contrast shadow in the distal CBD as well as proximal bile duct dilatation were observed on ERCP (). The CBD patency was re-established by balloon dilation (), and an abnormal pancreaticobiliary junction of the common channel was suspected (). Post-ERCP pancreatitis occurred, and the serum amylase and lipase levels increased to 1,749 U/L and >700 mg/dL, respectively. Conservative treatment was started again. After regression of the post-ERCP pancreatitis, the patient was discharged in good general condition on the 15th day of hospitalization. After 11 months, the patient visited our hospital again due to pancreatitis and biliary tract dilation caused by distal CBD stricture, probably due to previously incomplete recanalization (, ). ERCP with balloon dilation was performed, and the child was discharged on the 5th day of re-hospitalization with improvement of pancreatitis and distal CBD stricture (). She has been doing well for 4 years since then.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [18.0, 'kg']}",56,53.2,58.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 18.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (18.0 kg - 10 kg) = 56.0 mL/hr.
Hence, the patient's fluid maintenance is 56.0 mL/hr."
4681,22,Maintenance Fluids Calculations,physical,decimal,pmc-7403119-1,Extracted,"This study was approved by St.Mary's Hospital, The Catholic University of Korea (SC19ZESE0137).
A 60-year-old male (weight: 64 kg, height: 159 cm) was scheduled for emergency incision, drainage, and flap coverage on soft tissue infection of the right hand. He had amputation of the right index finger at another hospital 26 years ago, and had middle finger amputation and flap coverage in our orthopedic department seven years ago. Both surgeries were performed under general anesthesia without exposure to sugammadex. He had hypertension that was not treated. He did not have allergy history.
After he entered the operating room with anxiety, blood pressure (BP) 220/118 mmHg, heart rate 55 beats per minute (bpm), and O2 saturation by pulse oximetry 97% at room air were measured. Because a long time operation was scheduled and the patient refused regional anesthesia, we decided to perform general anesthesia. Within 5 min after we injected midazolam 3 mg and nicardipine 0.5 mg, he became comfortable and his BP decreased to 155/99 mmHg. After preoxygenation, general anesthesia was induced with propofol 120 mg and succinylcholine 70 mg using rapid sequence technique with supplemental remifentanil infusion. Following endotracheal intubation, we maintained anesthesia with inhalational gas mixture of oxygen (FiO2 0.4)-air-desflurane (6 vol%), supplementary remifentanil infusion at a rate of 0.03–0.07 μg/kg/min, and neuromuscular blocking agent rocuronium (EsmeronⓇ, MSD, the Netherlands) 40 mg. At 30 min after the operation, only a biopsy was performed and the operation was terminated because the malignancy was strongly suspected. Total anesthetic duration was 40 min. We discontinued the administration of all anesthetics. Sugammadex (Bridion®, MSD, the Netherlands) 200 mg was used to antagonize neuromuscular blockade at a train of four count of two monitored with a peripheral nerve stimulator (TOF watch®, Organon, Ireland). The patient started to breathe spontaneously while BP increased up to 207/119 mmHg concurrently that was treated with nicardipine 0.5 mg again. About 3 min after extubation while we prepared to transport the patient, his BP decreased suddenly to 78/38 mmHg. After 10 mg of ephedrine and 100 μg of phenylephrine injection to compensate suspicious nicardipine overdose, BP rose to 93/48 mmHg. He was transferred to the post anesthetic care unit (PACU).
During transport, he complained of itching sense at the buttock area. Just after arrival at the PACU, we found urticarial rashes on the neck, chest, and buttock. Soon, he became rapidly hypotensive (66/41 mmHg) and tachycardic (104–105 bpm). In turn, he developed generalized urticaria over the whole body. An anaphylactic shock was strongly suspected on the basis of hemodynamic data and skin manifestation. We rapidly elevated his both legs, increased fluid infusion rate, and started infusion of epinephrine. We added norepinephrine to increase BP effectively. Also, methylprednisolone 125 mg, hydrocortisone 100 mg, and pheniramine 4 mg were given intravenously. Portable echocardiography showed no abnormal wall motion except dehydration. Arterial blood gas analysis was normal. After 30 min, his condition improved with a stable vital sign. After we explained anaphylaxis to the patient, he was transported to the intensive care unit for overnight observation. His serum mast cell tryptase level was 2.4 μg/L at 12 h and 5.8 μg/L at 36 h post-event (reference value: < 11.0 μg/L). His levels of immunoglobulins E, G, A, and M were normal.
After one month from anaphylaxis, he was scheduled for an elective operation on the right first and third metacarpal bone resection. His hypertension was treated with atenolol. The plan of regional anesthesia was denied by the patient. After informed consent, an intradermal skin test was performed under general anesthesia. We anesthetized the patient in the same manner as prior anesthesia, but we used vecuronium (instead of rocuronium) and anticholinesterase (neostigmine 1.5 mg) with anticholinergics (glycopyrrolate 0.4 mg).
For the intradermal test, we prepared dilutions of test drugs: nicardipine 1 mg/ml (diluted 1 : 100), rocuronium 10 mg/ml (diluted 1 : 100), and sugammadex 100 mg/ml (diluted 1 : 100, 1 : 1000). We also prepared a mixture of rocuronium and sugammadex to test the sugammadex-rocuronium complex. Sugammadex (1 : 500 dilution) was mixed with the same volume of rocuronium (1 : 50 dilution). Thus, the final dilutions of the two drugs were 1 : 1000 and 1 : 100, respectively. This complex is known to have very few free sugammadex molecules. We used histamine (0.01%) as positive control and normal saline as negative control. Intradermal testing was conducted according to standard protocol on the patient’s volar forearm with a 25 G needle, resulting in a 5 mm wheal, 30 mm apart from each other. After 20 min, we evaluated the intradermal skin test results.
The skin tests were positive to 1 : 100 (20 × 10 mm wheal, 44 × 38 mm flare) and 1 : 1000 (14 × 9 mm wheal, 43 × 47 mm flare) dilutions of sugammadex. Sugammadex-rocuronium complex site also showed a positive reaction (24 × 10 mm wheal, 50 × 35 mm flare) (). Reactions to normal saline, nicardipine, and rocuronium were negative. There was no systemic allergic reaction during the test.
He received one more general anesthesia for vitrectomy due to retinal detachment. We avoided the use of sugammadex again. Currently he is on treatment of primary cancer of skin appendage, lung cancer, and bone metastasis.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [64.0, 'kg']}",104,98.8,109.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 64.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (64.0 kg - 20 kg) = 104.0 mL/hr.
Hence, the patient's fluid maintenance is 104.0 mL/hr."
4682,22,Maintenance Fluids Calculations,physical,decimal,pmc-3535728-1,Extracted,"A 4-week-old male infant was brought to the emergency room for a 3-day history of non bilious, non bloody emesis with feeds as well as fussiness and tachypnea. The frequency of emesis had increased to after almost every feeding, and he had decreased urine output. He otherwise had no fever, upper respiratory tract symptoms, diarrhea, or sick contacts. He was born at term via uncomplicated vaginal delivery and had previously been well.
On initial physical examination, his weight was 3.9 kg, temperature was 36.5°C, heart rate was 147 bpm, blood pressure was 78/44 mmHg, respiratory rate was 70 breaths/min, and oxygen saturation was 100% on room air. He had mild tachypnea and mild abdominal distention with the liver edge palpated below the costal margin. The remainder of the exam including heart and lungs was within normal limits.
An abdominal ultrasound showed no evidence of pyloric stenosis. Therefore, an oral feeding trial was attempted. Upon reassessment, however, the infant was found to be in moderate respiratory distress. He was placed on oxygen, and a chest X-ray revealed mild cardiomegaly and mild pulmonary edema. A capillary blood gas revealed a pH 6.84, PCO2 64 mmHg, HCO3 11 mEq/L, and base deficit of 24. The infant was intubated, and two normal saline fluid boluses of 20 mL/kg were given.
An echocardiogram showed a structurally normal heart but with severely decreased right and left ventricular systolic function and a left ventricular shortening fraction of 13% (normal range: 28–44%). The cardiac size was normal with a left ventricular end-diastolic diameter of 2 cm (Z score −0.6). Because of the finding of severe ventricular dysfunction, the patient was transferred to the neonatal intensive care unit and started on inotropic support with dopamine and milrinone infusions.
Upon admission, a 12-lead electrocardiogram (ECG) was obtained and showed sinus rhythm with a rate of 150 bpm. A short PR interval of 50 ms was seen as well as a delta wave resulting in a prolonged QRS duration of 110 ms (). These findings were consistent with ventricular preexcitation, and a diagnosis of Wolff-Parkinson-White (WPW) syndrome was made. Due to the lack of tachycardia observed at initial presentation, however, a diagnosis of tachycardia-induced cardiomyopathy was suspected but could not be confirmed. Laboratory testing to evaluate inborn errors of metabolism and specific viral serology, and PCR was therefore ordered to possibly delineate an additional underlying diagnosis.
A follow-up echocardiogram was done on hospital day (HD) 2 that showed complete normalization of ventricular function with an LV shortening fraction of 44%. The patient was therefore weaned off inotropic support and successfully extubated the next day. Later on HD 3, however, the patient had multiple episodes of supraventricular tachycardia (SVT) to rates of 260 bpm (). Vagal maneuvers (application of ice to the face) did not affect the rhythm, and IV adenosine was needed to terminate the SVT. Thereafter, multiple recurrences of sustained SVT occurred over the next 24 hours requiring intervention with ice and/or adenosine.
Oral propranolol was initially started, but, due to persistent episodes of SVT, oral flecainide was initiated on HD 6 (~100 mg/m2/day). Except for one very brief self-limited episode of SVT, there were no further sustained tachycardia episodes observed after starting flecainide, and the patient was discharged home on HD 10. He has not had any recurrences on flecainide therapy and has been feeding well without respiratory symptoms. Follow-up echocardiograms have continued to show normal biventricular function. This course confirmed the diagnosis of tachycardia-induced cardiomyopathy due to supraventricular tachycardia in a patient with underlying Wolff-Parkinson-White syndrome.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.9, 'kg']}",15.6,14.82,16.38,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.9 kg. Hence, the patient's maintenance fluid is 3.9 kg * 4 mL/kg/hr = 15.6 mL/hr.
Hence, the patient's fluid maintenance is 15.6 mL/hr."
4683,22,Maintenance Fluids Calculations,physical,decimal,pmc-5558357-1,Extracted,"A nulliparous woman aged 30 years was referred to our perinatology unit for evaluation because of oligohydramnios at 12 weeks of gestation. An antenatal ultrasonographic scan revealed a single live fetus with oligohydramnios. The upper half of the fetus appeared normal with both upper extremities seen separately and moving normally. However, the lower extremities appeared to be fused together in fixed extension and mobility at the hip and knee joints was restricted (). A single umbilical artery was demonstrated using color Doppler (). Thus, the diagnosis of sirenomelia was made prenatally. Medical termination of pregnancy was performed with the informed decision of the parents. On postnatal examination, the fetus weighed 150 grams. External examination revealed fusion of both lower extremities (). Based on the external examination, sirenomelia was diagnosed.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [150.0, 'g']}",0.6,0.57,0.63,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 150.0 g so this converts to 150.0 lbs * kg/1000 g = 0.15 kg. Hence, the patient's maintenance fluid is 0.15 kg * 4 mL/kg/hr = 0.6 mL/hr.
Hence, the patient's fluid maintenance is 0.6 mL/hr."
4684,22,Maintenance Fluids Calculations,physical,decimal,pmc-8605914-1,Extracted,"This is a case of a 95-year-old female, 140 cm tall, weighing 42 kg. She underwent artificial head replacement for a fracture of the right femoral neck when she was 92 years old. Other pertinent history included traumatic subdural hemorrhage and hypertension. Her current medical history included asymptomatic gross hematuria, and transurethral resection of bladder tumor (TUR-BT) was scheduled to closely examine a papillary bladder tumor. Preoperative examination showed anemia with a hemoglobin of 8.2; hence, 2 units of red blood cells were transfused. Coagulation function was normal, but the D-dimer level was elevated at 2.29. Ultrasound of the lower leg was performed, and DVT was noted in the lateral branch of the left soleus vein. No anticoagulant therapy was administered due to the anemia as a sequela of the bladder tumor.
Spinal anesthesia and right obturator nerve block were planned to resect the tumor close to the right ureteral ostium. Spinal anesthesia was performed using a 25-gauge Quinke needle from L3/4, and 2.4 mL of 0.5% high specific gravity bupivacaine was injected. Right obturator nerve block was performed using a Sonokolect Needle™ (manufactured by Hakko Co., Ltd., Medical Device Division) using a nerve stimulator. Puncture was performed 2 cm to the right and 2 cm caudal to the pubic symphysis, and twitch of adductor muscles at 0.5 mA was observed at the 3rd attempt. 20 mL of 1.5% mepivacaine was injected after negative aspiration. Surgery time was 50 minutes, and the anesthesia time was 81 minutes.
On postoperative day (POD) 1, subcutaneous hemorrhage was observed on the inner aspect of the lower right thigh. Hemoglobin decreased from 8.2 to 6.7; therefore, 2 units of RBC were transfused. Postoperative urine color was pale yellow, and no bladder bleeding was demonstrated. On POD 2, swelling was observed from the anterior aspect of the right inguinal region to the inner aspect of the thigh and the popliteal fossa. Contrast-enhanced CT performed on POD 4 revealed a hematoma spreading anteriorly from the right pubis to the inner aspect of the thigh (). Hemoglobin was still low, and another RBC unit was transfused. Thereafter, the hematoma and subcutaneous hemorrhage advanced to the medial thigh to the popliteal fossa extending to the back of the lower leg, and hematoma did not expand on POD 9 (). To reassess the hematoma, a follow-up blood test and CT were conducted, and there was no exacerbation. She was discharged on POD 17. The hematoma and subcutaneous bleeding disappeared on POD 53 ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [42.0, 'kg']}",82,77.9,86.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 42.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (42.0 kg - 20 kg) = 82.0 mL/hr.
Hence, the patient's fluid maintenance is 82.0 mL/hr."
4685,22,Maintenance Fluids Calculations,physical,decimal,pmc-3835393-1,Extracted,"An 84-year-old female was admitted to our institution with a complaint of nausea and vomiting. Her medical history included cataract surgery, hypertension, and multiple lacunar infarctions. The patient had no history of smoking or alcohol intake. On admission, her blood pressure was 150/74 mmHg, heart rate was 86 beats/min, body temperature was 36.5°C, and oxygen saturation level was 98% in room air. On initial clinical examination, her weight was 44.5 kg, height was 142 cm and body mass index (BMI) was 22.1 kg/m2. Inspection of her palpebral conjunctiva revealed no evidence of anemia. Chest auscultation revealed no evidence of abnormal heart murmurs and no rales or other abnormal respiratory sounds. The abdomen was slightly distended, but normal peristalsis was evident. Mild tenderness was detected in her upper abdomen. No masses were palpable, and no signs of peritoneal irritation were detected. A physical examination revealed no edema or cyanosis. Although the chest radiography revealed a normal cardiothoracic ratio of 59.5%, the abdomen was markedly dilated and bloated, which was subsequently identified to be caused by the gastric antrum and duodenum incarcerated behind the heart. Abdominal computed tomography revealed an esophageal hiatal hernia with incarceration of the gastric antrum and duodenal bulb (Figure a and b). Blood chemistry analysis revealed an elevated white blood cell count (12,000/μL), normal C-reactive protein levels (0.1 mg/dL), an elevated glucose level (206 mg/dL), mild hypoproteinemia (6.5 g/dl), mild hypoalbuminemia (3.6 g/dl), and evidence of coagulation dysfunction (prothrombin time, 75%; international normalized ratio, 1.19). Upper gastroendoscopy revealed severe deformation of the stomach and the presence of massive contents within. Stenosis was evident in the region prior to the descending portion of the duodenum. Therefore, gastrofluorography under gastroendoscopic guidance was performed. Gastrofluorography confirmed the prolapse of the antrum and duodenal bulb into the esophageal hernial sac (Figure a and b). Although repositioning of the prolapse was successfully performed under gastroendoscopic guidance, reprolapse occurred immediately. Therefore, the following surgical treatment was performed on Day 11 of hospitalization.
The upper median laparotomic approach was used to expose the peritoneal cavity. The triangular ligament of the liver was incised to facilitate mobilization and rightward displacement of the left lobe of the liver. The gastric antrum and duodenal bulb involved in the paraesophageal hernia were noted on the right side of the esophagus (Figure ). First, the gastric antrum was relocated to its normal position. Then the median arcuate ligament was exposed anterior to the right and left crura of the diaphragm and above the celiac artery. After exfoliating the tissue around the esophagus, the position of vagus nerve was confirmed. The median arcuate ligament was fixed to the anterior and posterior walls of the lesser curvature of the upper body of the stomach without damage to the vagus nerve. Finally, the right and left crura of the diaphragm were sutured using absorbable sutures, and the hiatal hernia was successfully corrected. The patient’s postoperative course was uneventful. On postoperative Day 7, plain abdominal computed tomography and gastrofluorography revealed a normal stomach, which was not dilated. The patient was ambulatory at discharge.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [44.5, 'kg']}",84.5,80.275,88.725,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 44.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (44.5 kg - 20 kg) = 84.5 mL/hr.
Hence, the patient's fluid maintenance is 84.5 mL/hr."
4686,22,Maintenance Fluids Calculations,physical,decimal,pmc-8663912-1,Extracted,"A 2-month-old, 3.9-kg male infant was scheduled to undergo surgery for inguinal hernia and undescended testis with general anesthesia. The baby was delivered 38 + 6 weeks of gestation and a weight of 2440 g via cesarean section. During his hospital stay, the patient had subcostal retraction while breathing and frequent oxygen desaturation events. An otolaryngologist diagnosed laryngomalacia by evaluating the larynx with fiberscopy and finding an omega-shaped epiglottis (Fig. A and B). Even after 2 months of observation, the patient displayed laryngomalacia, showing supraglottic edema. However, because the respiratory pattern and the laryngeal edema were improved, an otolaryngologist agreed to pursue surgery with general anesthesia.
Upon arrival to the operating room, the patient was arranged to receive oxygen supply with HFNC (Optiflow System; Fisher and Paekel, Auckland, New Zealand). After vital signs in the normal ranges were confirmed and initial oxygen saturation (SpO2) was confirmed at 99%, preoxygenation with 100% oxygen was delivered using a face mask at a rate of 6 L/min for 3 minutes. The patient was then anesthetized with 0.05 mg/kg of midazolam and 0.5 mcg/kg of fentanyl intravenously and, after sedation, 2 L/kg/min of oxygen was delivered via HFNC. The initial 2 attempts of endotracheal intubation with a rigid laryngoscope without a neuromuscular blocking agent (NMBA) were unsuccessful because the vocal cords were obscured by the epiglottis. After deeper sedation was performed with 0.05 mg/kg of midazolam, another intubation attempt was successfully made with a 3.0-sized, uncuffed endotracheal tube within 20 minutes after the initial attempt (Fig. C). During intubation, the oxygen saturation was maintained at greater than 98%. NMBA was achieved with 0.6 mg/kg of rocuronium and anesthesia was maintained with sevoflurane in 50% O2-air. At the end of the surgery, 0.1 mg/kg of pyridostigmine, and 0.008 mg/kg of glycopyrrolate were administered intravenously to antagonize the residual neuromuscular blockade. After spontaneous breathing had returned, the patient was transferred to the ICU with the endotracheal tube maintained. Dexamethasone (0.2 mg/kg) was injected to prevent airway edema. The next day, the patient showed no desaturation after extubation, although he had chest retraction. The patient was discharged 5 days after surgery without any adverse side effects.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.9, 'kg']}",15.6,14.82,16.38,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.9 kg. Hence, the patient's maintenance fluid is 3.9 kg * 4 mL/kg/hr = 15.6 mL/hr.
Hence, the patient's fluid maintenance is 15.6 mL/hr."
4687,22,Maintenance Fluids Calculations,physical,decimal,pmc-3420620-1,Extracted,"A 53-year-old postmenopausal woman, with a history of hypertension and fibromyalgia, presented with 1 month of intermittent chest pain, mild nonproductive cough, dyspnea on exertion, and a 22 lb weight loss over 4 months. Complete blood count revealed a macrocytic anemia with a mean corpuscular volume (MCV) as high as 108, with normal cobalamin and red blood cell folate. Coombs testing was negative, and her levels of lactate dehydrogenase (LDH), haptoglobin, and unconjugated bilirubin were normal. The peripheral blood smear showed dysplastic changes in all hematopoietic lineages including hypogranulation and hypersegmentation of the neutrophils and rare teardrop-shaped red cells, prompting a bone marrow evaluation. Bone marrow aspirate yielded a diagnosis of MDS, refractory anemia with excess blasts (RAEB-1; 8% blasts) with karyotype 46,XX,+1,der(1;7)(q10;p10)[20], resulting in the loss of 7q in 20/20 cells on examination of 20 metaphases. She required transfusion support for symptomatic anemia and became red blood cell transfusion dependent over the next several months.
As she presented with shortness of breath and pleuritic chest pain, a computed tomography (CT) scan of the chest was performed at initial presentation which revealed multiple, calcified, slightly enlarged mediastinal, and hilar lymph nodes as well as scattered ground-glass linear and nodular opacities. Bronchoalveolar lavage was suggestive, but not diagnostic, of alveolar proteinosis. Transbronchial biopsy and wedge resection by video-assisted thoracic surgery (VATS) procedure were also nondiagnostic.
Two months later the patient presented with severe bilateral eye pain, marked eyelid swelling, high fever, and a blanching rash on the upper and lower extremities. Lacrimal gland biopsy showed prominent acute and chronic inflammatory infiltration with focal abscess formation, few macrophages, and perivascular inflammatory cuffing, diagnostic of lacrimal gland pseudotumor. Gram stain, acid-fast bacilli (AFB) stain, and fungal stains were negative. Skin biopsy revealed panicular hemorrhage without signs of panniculitis or vasculitis. Repeat chest CT showed increase in size and number of pulmonary nodules. Repeat VATS procedure with wedge resection of the lung now revealed a diagnosis of acute fibrinous and organizing pneumonia (AFOP) which is a rare form of acute lung injury distinct from both diffuse alveolar damage (DAD) and organizing pneumonia.
Initiation of intravenous Solumedrol 100 mg daily led to improved orbital and respiratory symptoms within 6 weeks. A repeat chest CT scan showed almost complete resolution of pulmonary nodules. Her transfusion requirements also declined while on high dose steroids. She was eventually placed on Prednisone 80 mg daily, which was decreased by 10 mg per week to a maintenance dose of 20 mg. Subsequently, treatment with Decitabine 20 mg/m2 (a hypomethylating agent) was initiated for her MDS. Four months later, while on Prednisone 20 mg daily and after completing her third cycle of Decitabine 20 mg/m2, she presented with high fevers, severe bitemporal headaches, and exertional dyspnea. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were elevated to 140 mm/hr and 54.83 mg/L, respectively. A left temporal artery biopsy performed to assess for giant cell arteritis (GCA) was nondiagnostic. However, magnetic resonance imaging (MRI) of the head showed thickening of the temporal arteries. Blood and urine cultures were sterile. Antinuclear antibody (ANA), cytoplasmic antineutrophil cytoplasmic antibody (c-ANCA), and perinuclear cytoplasmic antibodies (p-ANCA) tests were negative. Chest CT scan performed due to increasing dyspnea showed recurrent pulmonary nodules. Intravenous Solumedrol 100 mg was resumed as there remained clinical concern for GCA. She experienced a brisk improvement in her symptoms, and her ESR decreased. She was discharged on Prednisone 100 mg with plan to taper the dose by 10 mg every 2 weeks.
Over the next few months, and as Prednisone was decreased to 40 mg daily, the patient presented with recurrent high fevers, flares of bilateral temporal headaches, and exquisite tenderness over the temporal regions. She also complained of blurred vision and jaw claudication during her second admission. Right temporal artery biopsy was again nondiagnostic for vasculitis. Extensive workup for infection, including CT scans, transesophageal echocardiogram, and tagged white blood cell scan were unrevealing. Repeat bone marrow aspirate and biopsy showed persistent MDS with the emergence of a new clone that expressed the trisomy 8 marker. Fluorescent in situ hybridization (FISH) detected nuc ish(D7S486x1)[151/200]/(D8Z2x3)[131/200]. There was doubling of the original abnormal clone in approximately 94 chromosomes. Aneuploidy of chromosomes 7q, 8, and 20q but not 5q was identified. Her symptoms again improved on high dose steroids. The patient was therefore started on oral methotrexate (MTx) 15 mg weekly, as she continued to manifest a dominant autoimmune phenotype. She defervesced after two doses, but MTx was promptly discontinued due to myelosuppression.
In the next few months, she was repeatedly admitted to the hospital with fevers, pancytopenia, fatigue, severe myalgias, and arthralgias. A repeat bone marrow biopsy during her final hospitalization revealed markedly hypocellular bone marrow (<5%) without increase in white cell blasts. There was overall clinical deterioration due to bone marrow failure, progressive dyspnea and hypoxemia with progressive lung infiltrates, and intractable, generalized bone pain. The decision was made to institute comfort care measures, and the patient succumbed to her illness several days later. Postmortem exam was not allowed by the family.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [22.0, 'lbs']}",39.91608,37.92028,41.91188,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 22.0 lbs so this converts to 22.0 lbs * 0.453592 kg/lbs = 9.97902 kg. Hence, the patient's maintenance fluid is 9.97902 kg * 4 mL/kg/hr = 39.91608 mL/hr.
Hence, the patient's fluid maintenance is 39.91608 mL/hr."
4688,22,Maintenance Fluids Calculations,physical,decimal,pmc-2946039-1,Extracted,"A 62-year-old, weight 50 kg, height 158 cm woman was scheduled for microdisckectomy for herniated nucleus pulposus at L5S1. She had a 5-year and 3-year history of type 2 diabetes mellitus (DM) and hypertension respectively. Her past surgical history was left total knee replacement due to osteoarthritis two years ago. Her laboratory examination showed normal fasting serum glucose at 109 mg/dl, platelet 234 × 109/L, prothrombin time 9.8 sec, activated partial prothrombin time 20.0 sec except rheumatoid factor positive and protein 6.1 g/dl. Preoperatively, she took an antihypertensive drug in the morning of the operation day.
The patient was taken to a standard American Standards Association monitor upon arrival in the operating room. An appropriately sized BP cuff was placed on her left arm above the elbow. Her BP was monitored at 5-minute intervals. Her pre-induction BP was 150/95 mmHg. Anesthetic induction was performed using fentanyl 50 µg, lidocaine 40 mg, propofol 100 mg, rocuronium 30 mg and anesthesia was maintained by 2 vol% sevoflurane-O2 2 L/min-N2O 2 L/min.
Post-induction, a rash was noted on her left arm during inflation of BP cuff, which diminished immediately. The cause of the rash was an initially thought to be due to increased venous pressure, and a transient phenomenon without serious consequences. The patient's BP stabilized in the prone position, and her arm was covered by a sterilized sheet to prevent a fall in body temperature. During the operation, the patient showed severe BP fluctuations, ranging from 80-140/55-85 mmHg. For the purpose of maintaining a stable BP and postoperative pain control, we set up patient-controlled analgesia using fentanyl 1,000 µg, ketorolac 120 mg and ondansetron 8 mg 20 min before the end of the operation. Operation time was 60 minute, the anesthetics took 90 min. When the sterilized sheet was removed from the patient at the end of the operation, a severe rash with petechiae on the left arm was noted associated with facial flushing in the supine position ().
The patient's facial flushing diminished in the recovery room. Once recovered from anesthesia, the patient did not complain about pain in the affected extremity. All motor and sensory function appeared intact. The petechiae and rash of the forearm resolved spontaneously within ten days.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [50.0, 'kg']}",90,85.5,94.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 50.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (50.0 kg - 20 kg) = 90.0 mL/hr.
Hence, the patient's fluid maintenance is 90.0 mL/hr."
4689,22,Maintenance Fluids Calculations,physical,decimal,pmc-8654073-1,Extracted,"An 11-year-old boy was diagnosed with Crohn’s disease at the age of nine years. Since then, he was on a regular infliximab transfusion regimen at monthly intervals at a dose of 5 mg/kg for maintenance of remission of disease as symptoms relapse by the end of each month. He presented to the Maternity and Children Hospital in Al-Ahsa, Eastern Province in Saudi Arabia, complaining of palpitation for one year. The palpitations were intermittent at the beginning of the year but then worsen progressively over the last month. They were associated with easy fatigability and chest discomfort, with no history of cyanosis or chest pain. There was no history of a similar condition or history of cardiac disease or sudden death in the family. In addition, these symptoms occur with the manifestation of tachycardia during infliximab transfusion with no respiratory or mucocutaneous involvement or other signs of anaphylaxis. This transfusion reaction is managed by slowing the transfusion rate and premedication with steroids and antihistamines.
Upon examination of the child, he appeared pale, underweight (with weight of 18 kg below the third centile) but not distressed. He had sinus tachycardia (150-160 beats/min) with maintained blood pressure (98/59 mmHg). chest examination revealed hyperdynamic precordium with pan-systolic murmur grade III out of VI at the apex with radiation to left mid-axillary line with no thrill. Rest of the examinations were unremarkable. Laboratory investigations showed microcytic hypochromic anemia related to the drop of iron profile and thrombocytosis, with positive anti-Saccharomyces cerevisiae antibodies for Crohn’s disease and negative antibodies for infliximab (Table ). ECG and Holter 24 hours monitor were done and showed intermittent sinus tachycardia with no dysrhythmias (Figure ). Echocardiography showed dilated left ventricle with ejection fraction of 21% and fraction of shorting of 10% associated with severe mitral regurgitation (Figure and Video ). The patient was diagnosed with acute heart failure secondary to dilated cardiomyopathy. He started on anti-failure medications controlling three parameters pre-load, after-load, and enhancing myocardial contractility by diuretics furosemide (1 mg/kg/dose twice a day initially), spironolactone (1 mg/kg/dose twice a day), enalapril (0.35 mg/kg/day divided three times a day) and digitoxin (2.5 mcg/kg/day once daily), respectively. Aspirin was added as an anticoagulant. In addition, the patient started on intravenous iron to improve anemia which was not responding to oral iron supplementations or dietary management. The patient was discharged home with the previous plan and kept on regular follow-up with pediatric cardiology with no need for cardiac surgery at the present time. In addition, he kept on regular follow up with pediatric hematology to assess the improvement in hemoglobin and response parental iron. Finally, the patient referred to a tertiary hospital for further follow-up with pediatric gastroenterology and the possibility of starting a different anti-tumor necrosis factor agent ustekinumab.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [18.0, 'kg']}",56,53.2,58.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 18.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (18.0 kg - 10 kg) = 56.0 mL/hr.
Hence, the patient's fluid maintenance is 56.0 mL/hr."
4690,22,Maintenance Fluids Calculations,physical,decimal,pmc-6463096-1,Extracted,"A 59-year-old Brazilian man presented cachexia and disseminated and ulcerated skin lesions with one-year evolution (A). Before his illness, he worked as an agriculturist, truck driver and a sewerage system cleaner in his town. During his last professional activity, he was continuously exposed to polluted water. Eight months earlier, the diagnosis of leprosy was made without any microbiological evidence and he was unsuccessfully treated with rifampin, dapsone and clofazimine. Six months ago, HIV infection was detected and lamivudine, tenofovir and efavirenz were added. At admission, he was depressed, febrile and complaining of pain. His body weight was 40 kg, and, besides the cutaneous clinical manifestations, there were no signs of internal organ involvement. The main laboratory findings included anemia with hemoglobin of 9.1 g/dL, leukocytosis (12,100 cell/μL) and protein chain reaction (PCR) of 11mg/L. HIV test was positive with CD4 cell count of 584 cells/mm3and viral load of 1558 copies/mL (log 3.1). A skin biopsy depicted a mixed exudative and granulomatous cellular infiltrate with a few round to elongated yeast cells (B). The cultures of biopsy fragments yielded a dimorphic fungus phenotypically identified as Sporothrix sp., later identified by DNA sequence as S. schenckii. The anti-lepromatous therapy was stopped and the patient was treated with itraconazole, 400 mg per day, and cotrimoxazole 360mg/800mg per day for secondary bacterial infection. Because IRIS was suspected, prednisone at the daily dose of 20 mg per day was added and ART was changed to atazanavir/ritonavir due to probable drug-to-drug interactions between itraconazole and the previous antiretrovirals. He improved gradually and corticosteroid and cotrimoxazole were discontinued. After three months of therapy, itraconazole was reduced to 200 mg per day and discontinued after six months. The patient presented complete clinical and mycological responses. (C).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [40.0, 'kg']}",80,76,84,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 40.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (40.0 kg - 20 kg) = 80.0 mL/hr.
Hence, the patient's fluid maintenance is 80.0 mL/hr."
4691,22,Maintenance Fluids Calculations,physical,decimal,pmc-8152383-3,Extracted,"A 39-year-old female was diagnosed with PNH in 2013 (aged 32 years), manifesting with fatigability, skin thrombophlebitis and PNH on WBC clone size was 80.6%. The patient refused treatment with eculizumab at that time. However, she had a history of severe aplastic anemia for couple of years controlled on cyclosporine and aspirin (81 mg) because of worsening of her cytopenia. She had a history of four abortions, three intrauterine fetal deaths (IUFD) and one stillbirth due to brain atrophy.
In 2017, the patient became pregnant, and enoxaparin 40 mg and folic acid supplement were added to aspirin; however, cyclosporine was discontinued to avoid its teratogenicity. The antepartum period was complicated with bone marrow suppression, mild vaginal bleeding, frequent hemolysis and dropping of platelets level, and thus she required frequent RBC and platelet transfusion, glucocorticoid and intravenous immunoglobulin therapy. At 31-week of gestation, 600 mg eculizumab was started as she presented with low platelets and low hemoglobin. Enoxaparin was switched to prophylactic fondaparinux (2.5 mg) because the patient developed heparin-induced thrombocytopenia (HIT). However, fetal US showed normal interval growth and normal blood flow.
Preterm rupture of membranes occurred at 36 weeks of gestation, then induction of labor started and eventually progressed with spontaneous vaginal delivery. The infant was full term and stable, weighted 2320 grams, the Apgar score was 9, and had no complications that required NICU admissions. Postpartum period was completed with no complications and she was continued on eculizumab and fondaparinux for 6 weeks.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2320.0, 'g']}",9.28,8.816,9.744,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2320.0 g so this converts to 2320.0 lbs * kg/1000 g = 2.32 kg. Hence, the patient's maintenance fluid is 2.32 kg * 4 mL/kg/hr = 9.28 mL/hr.
Hence, the patient's fluid maintenance is 9.28 mL/hr."
4692,22,Maintenance Fluids Calculations,physical,decimal,pmc-4472390-1,Extracted,"A fit and healthy 12-year-old white boy (height 150cm, weight 40kg) underwent elective removal of a 2×2cm benign skin lesion from his anterior abdominal wall. He had no past medical history and was not on any medications. His physical examination preoperatively was normal. Surgery was scheduled for the late afternoon. He was fasted for 6h for solids and 2h for clear fluids. The World Health Organization surgical checklist for safety in the operating room [] was complied with intraoperatively, which included the prohibition of jewellery and other constrictive clothing items worn during surgery. After establishing intravenous access with a 22-guage cannula in a vein in the cubital fossa of his left arm, anaesthesia was induced with propofol (140mg) and fentanyl (50ug). A size 3 classic laryngeal mask was inserted for airway management, and spontaneous ventilation was maintained with 1 minimum alveolar concentration sevoflurane in a 50% oxygen to air mixture. Five millilitres of a local anaesthesia solution (lignocaine 2% with 1:200,000 adrenalin) was injected into the surgical area for local anaesthesia and postoperative analgesia. During surgery both of his arms were positioned by his side in a neutral position, supported by foam padding on the operating table to minimise pressure. The abdominal lesion was removed uneventfully and the procedure took 22min. Continuous electrocardiography, pulse saturation monitoring, and intermittent blood pressure measurements every 3min were normal. After uneventful emergence from anaesthesia, the laryngeal mask was removed, and he was transferred to the postoperative recovery unit for a 30-min observation period. He was haemodynamically stable, with normal arousal to voice and command. He required no further analgesia and was transferred to the ward at 1830 hours. On the ward his observations remained stable. After a light meal and when completely conversant and cooperative, he was discharged home under parental supervision.
He presented with his parents to the emergency department the following morning complaining of severe pain, paraesthesia and weakness of the right hand. A clinical examination revealed a circumferential wristwatch pressure imprint over his anterior and posterior distal right forearm (Figs. and ), as a result of sleeping with his wristwatch on. His hand was erythematous, swollen and painful to touch. There were complete sensory and motor deficits involving his right hand in a glove and stocking distribution from the wristwatch pressure imprint distally, including involvement of all five digits. A neurological examination showed inability to differentiate cooling and heat, sharp and dull, and there was a deficit in 2-point discrimination in the radial, median and ulnar nerve root distributions, most severe in the territory of the superficial cutaneous branch of the radial nerve. In addition there was complete motor deficit in the median, radial and ulnar nerve distributions.
He was admitted to the overnight short stay unit where his hand was elevated. A non-steroidal anti-inflammatory analgesic (ibuprofen 400mg) was prescribed 8 hourly for analgesia. Movement of his left hand was encouraged, and over the following 12h the oedema and erythema resolved completely, with complete return of motor function. After 18h, the sensory deficit had also completely recovered. In view of the rapid neurological recovery, quantitative nerve function assessments, for example nerve conduction studies, were not performed. He was discharged home and reviewed 24h later at the surgical out-patients clinic where his hand function examination remained normal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [40.0, 'kg']}",80,76,84,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 40.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (40.0 kg - 20 kg) = 80.0 mL/hr.
Hence, the patient's fluid maintenance is 80.0 mL/hr."
4693,22,Maintenance Fluids Calculations,physical,decimal,pmc-4325654-1,Extracted,"A 49-year-old female patient came to the outpatient clinic with complaint of general weakness, mild discomfort and heat sensation in the abdomen. Diagnosed with PNET with multiple liver metastases at another hospital, she was transferred to our clinic for bloodless surgery owing to the patient's religious faith. The patient's height was 152 cm and weight was 53.6 kg. She didn't have any other underlying medical diseases such as hypertension, diabetes, hepatitis, tuberculosis and so on. Physical exams revealed mildly distended abdomen and a non-tender palpable intraabdominal mass. The serum tumor markers including CEA, CA 19-9, and α-FP were within normal limits, whereas liver function test levels including total bilirubin (1.3 mg/dL), aspartate transaminase (58 U/L), and alanine transaminase (49 U/L) were slightly elevated. Radiological tools including abdominal-pelvic CT scan, biliary and pancreas dynamic MRI with contrast, PET/CT scan, and bone scan contributed to diagnosis and therapeutic plan. According to the results of radiological imaging studies, a huge well capsulated tumor (about 8-cm diameter on the longest distance) was located in the pancreatic body and tail, which was highly enhanced by the contrast material. Multiple hepatic metastases were found in both lobes ().
Sono-guided biopsies on liver and pancreas showed proliferation of uniform round cells in ribbon, consistent with metastatic well-differentiated PNET from the pancreas. Results revealed positive staining of chromogranin A and cytokeratin (CK). Ki67 labeling index was about 4%-5% that corresponded to grade 2. For treatment of PNET with multiple liver metastases, serial therapies were scheduled. First of all, transarterial chemoembolization (TACE) was performed prior to surgery. The interventional radiologist performed TACE with mitomycin and lipiolol, which were injected to the patient's metastatic hepatic tumors. After a total of 3 sessions of successful TACE for multiple liver metastases over 4 months (), the size of multiple liver metastases decreased dramatically in the following abdomen CT (). Meanwhile, the patient suffered from liver failure with total bilirubin increased up to 23 mg/dL. Careful conservative management without transfusion was carried out for treatment of liver impairment. For the systemic treatment, octreotide acetate injection was given before surgery. Initial dose was 0.1 mg via subcutaneous injection every 8 hours over 3 days for response test, and then 4 injections at 20 mg were given daily via intramuscular route per 28 days.
The attending surgeon and anesthesiologist discussed the risks of bloodless major operations. The patient signed a consent form for the operation without the use of blood products. She allowed albumin and acute normovolemic hemodilution (ANH). Considering that it was a cancer surgery, Cell Saver was not allowed due to risk of shed cancer cells. The preoperative albumin level was 3.7 g/dL, hemoglobin was 12.6 mg/dL, and hematocrit was 36.8%. The dissection of RAMPS procedure started from the left side, which is the neck of the pancreas, to the right side with splenic vessels and celiac node dissection. Afterwards, the plane of dissection proceeded posteriorly in a sagittal plane along the celiac artery and the superior mesenteric artery down to the level of the aorta, in sequence, going on laterally to the left adrenal gland (). There was severe adhesion of omentum to the hepatic tumors and pancreatic tumor, however, the celiac trunk and the superior mesenteric artery were relatively well isolated from the tumor. The pancreatic tumor was well vascularized, capsulated, and abutted to the renal arteries and veins, but not invading (). Histological diagnosis was consistent with well-differentiated pancreatic neuroendocrine carcinoma with negative resection margin but extending to the peripancreatic soft tissue and splenic venous wall. It showed angioinvasion and neural invasion containing ischemic necrosis. Immunohistochemical examination revealed that chromogranin A, CD56, CD10, and CK were positive (). Pathologic staging was T3N0M1 stage IV according to American Joint Committee on Cancer/Union for International Cancer Control TNM staging for pancreatic tumors.
Total operative time was 4 hours 30 minutes. Estimated blood loss was 800 mL and while the patient received 3 pints of ANH and intravenous dextran during the operation. The postoperative albumin was 2.8 g/dL, hemoglobin 11.5 mg/dL, hematocrit 33.8%, and fibrinogen 248 mg/dL. As an assistant therapy for a transfusion free patient, recombinant human erythropoietin 4,000 IU and 1 ample of iron hydroxide sucrose complex were given daily for five days after surgery. Postoperative abdominal CT scan didn't show any evidence of pancreatic fistula or fluid collections around the pancreatic resection margin.
The patient took a sip of water on day 2 and began a soft diet on day 4, postoperatively. She was discharged 12 days after the operation. We had future plans to give octreotide acetate injection for the systemic treatment and additional TACE for liver metastasis","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [53.6, 'kg']}",93.6,88.92,98.28,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 53.6 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (53.6 kg - 20 kg) = 93.6 mL/hr.
Hence, the patient's fluid maintenance is 93.6 mL/hr."
4694,22,Maintenance Fluids Calculations,physical,decimal,pmc-5138453-1,Extracted,"A fourteen-year-old boy from South America was transferred to the burn unit at our institution for severe malnutrition. The patient had sustained second-degree burns (>25% BSA) two years prior to admission. He did not receive adequate nutrition and medical care because of poverty and limited resources in his home country. He was noted to be severely cachectic and malnourished at a local hospital and was transferred to the United States by a charity organization for higher level of care.
Initial assessment was significant for a weight of 19 kg (<3rd percentile on WHO growth chart), height of 141 cm (BMI 9.6 kg/m2, z score −12.42), blood pressure of 92/63 mmHg, and a heart rate of 140 bpm. He experienced shortness of breath with minimal physical activity. Physical examination revealed severe cachexia with atrophy of all muscles without peripheral edema. He was also noted to be moderately dehydrated. Initial investigations were significant for mild hyponatremia [133 mmol/L (NL 135–145 mmol/L)], severe hypoalbuminemia [0.2 g/dL (NL 3.5–5.0 g/dL)], hypocalcemia [ionized calcium 3.2 mg/dL (NL 4.5–5.3 mg/dL)], severe iron deficiency anemia [hemoglobin/hematocrit 6.7 gm/dL/24.8%, MCV 69.3 FL], and selenium deficiency [32 ug/L]. The reported normal serum selenium levels in the United States ranges from 50 to 150 ug/L [] while the normal serum levels of selenium in his country of origin is reported to be 80.6–199 ug/L []. The carnitine level was normal.
Immediate intravenous fluid resuscitation was initiated. Since he was severely malnourished and had limited ability for oral intake, high calorie enteral nutrition was administered via a nasogastric tube. An initial echocardiogram (echo) showed a globular dilated left ventricle with a severely depressed systolic function [ejection fraction (EF) < 25%] consistent with dilated cardiomyopathy. He was initially treated with furosemide and enalapril, and carvedilol was added a week later since there was minimal improvement in cardiac function in addition to selenium replacement [200 mcg (2.5 umol) twice daily intravenously]. He received two blood transfusions and repeated albumin infusions within the first five days. One week later, his cardiac function dramatically improved [EF 46%]. His selenium level, as well as other labs, normalized within two weeks. The cardiac function normalized within four weeks. His weight continued to increase and reached 30 kg [BMI 15.1 kg/m2, z score −2.40] within four months (). All cardiac medications were then discontinued. The patient's stamina continues to improve, and he is able to tolerate full oral intake.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [19.0, 'kg']}",58,55.1,60.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 19.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (19.0 kg - 10 kg) = 58.0 mL/hr.
Hence, the patient's fluid maintenance is 58.0 mL/hr."
4695,22,Maintenance Fluids Calculations,physical,decimal,pmc-6332958-1,Extracted,"A 16-year-old Samoan male with a history of RHD, diagnosed in 2013, subsequently developed SLE in 2018. His initial presentation of RHD included mild aortic insufficiency, arthritis to his fifth metatarsal, positive streptozyme test, anti-DNase B 789 U/ml (normal < 170), ANA < 40, negative rheumatoid factor, and sedimentation rate up to 93 mm/hr. Two days after admission, he had a C-reactive protein 75.9 mg/L (normal < 1). Once his rheumatic fever resolved, he was placed on monthly parenteral benzathine penicillin G prophylaxis (BPG) for which he had incomplete compliance. He remained asymptomatic until he developed SLE five years later.
In January 2018, he developed fever, oral ulcers, pancreatitis, elevated ANA titers, elevated anti-Sm, elevated dsDNA, pancytopenia, and proteinuria. He initially presented after having a fever, coryza, and cough with a sore and hoarse throat. He then developed cold sores on his lips and roof of his mouth. After several days, the cough, runny nose, and fever resolved, but his sore throat persisted with subsequent lip swelling and redness accompanied with painful ulcers on lips and palate. Throughout this period, his solid food intake decreased and he reported a 30-pound weight loss.
He was evaluated in the outpatient setting after developing diffuse abdominal pain without fever, nausea, vomiting, or jaundice. The pain gradually became more constant and localized to the midepigastric and right upper quadrant of his abdomen with a noted blood pressure (BP) of 60/40, but no interventions were reported by his mother. He returned and saw his primary care physician who noted a BP of 84/52. Thus, he was transported to the hospital by ambulance, given a fluid bolus, and admitted for hypotension for potential sepsis and further workup.
His only previous significant medical history, aside from RHD, was stage 1 hypertension resolved at his last cardiology follow-up. Reviewing his outpatient records revealed sporadic BPG administration.
A general physical exam was significant for a fever of 38.3°C, ulcers with erythema on the hard palate, left lower, and upper lip, and oropharynx with petechial spots. Additionally, there was a blanching scaly rash noted to his helices and postauricular areas of ears with extension to the adjacent scalp on the left side. Although his overall abdomen was soft without organomegaly, he possessed tenderness to palpation of his upper quadrants. The lymphadenopathy of his superior left posterior cervical chain was unusual with a small 1-2 centimeter lymph node tender to palpation as well as a small, mobile, nontender lymph node of his left axilla. Further physical exam was otherwise normal.
Initial laboratory findings upon admission were significant for pancreatitis with a lipase of 3,140 U/L (normal < 58), transaminitis (AST 367 U/L and ALT 166 U/L) with elevated PTT, and pancytopenia with mild normocytic anemia, leukopenia, and thrombocytopenia. Bone marrow biopsy was normal after an elevated ferritin level of 2,159 mg/ml (reference range 36–311 ng/mL) was found. Multiple triglyceride and fibrinogen levels were found to be within the normal range which made hemophagocytosis less likely. Urinalysis results revealed proteinuria and trace leukocyte esterase. Initial infectious workup was unremarkable with negative antibodies toward viruses known to cause hepatitis. However, initial imaging on the ultrasound showed mild bilateral kidney enlargement but was otherwise unremarkable.
He was started on piperacillin-tazobactam for a four-day course due to progressive pancytopenia. His serum returned positive for salmonella, typhi, and paratyphi antibodies, so he was started on daily ceftriaxone until gastrointestinal PCR returned negative for salmonella. Rheumatologic workup was as follows: ANA of 1,280, anti-dsDNA of 20,480 (normal < 10), and anti-Sm antibodies elevated at >8. He completed four days of pulse steroids before initiation of steroid taper regimen. Nephrology followed him for lupus nephritis with proteinuria and an initial random protein-creatinine ratio at 610. Despite initiation of steroids, proteinuria persisted. For his pancreatitis, he was first placed on a clear diet, which he did not tolerate, and the diet was changed to nothing by mouth. He was started on partial parenteral nutrition and eventually total parenteral nutrition until he could tolerate diet. Finally, he received his monthly BPG prior to discharge.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [30.0, 'lbs']}",47.21552,44.85474,49.5763,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 30.0 lbs so this converts to 30.0 lbs * 0.453592 kg/lbs = 13.60776 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.60776 kg - 10 kg) = 47.21552 mL/hr.
Hence, the patient's fluid maintenance is 47.21552 mL/hr."
4696,22,Maintenance Fluids Calculations,physical,decimal,pmc-5117279-2,Extracted,"A 2-day-old, preterm female neonate, weighing 1.9 kg, 1st in birth order was born by vaginal delivery. He presented to our institute with bilious vomiting; there was no delayed passage of meconium. On examination, child was hemodynamically stable, anicteric, mildly dehydrated. Abdominal signs included mild epigastric distension, soft on palpation and absent bowel sounds; nasogastric aspirate was bilious. Laboratory tests were normal. Abdominal ultrasonography (USG) was not conclusive. Upper gastro-intestinal contrast study was performed which suggested duodenal obstruction (Fig.1B). Laparotomy revealed dilated stomach and duodenum till third part, with a change in the caliber beyond it (Fig.3). C-loop of the duodenum was exposed. Palpation of palpable fibrotic ring extra-luminally at third part of duodenum was done. Enterotomy and circumferential excision of web (membrane) at the third part of duodenum was carried out (Fig.3). The postoperative course was uneventful and the child is doing well at follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1.9, 'kg']}",7.6,7.22,7.98,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1.9 kg. Hence, the patient's maintenance fluid is 1.9 kg * 4 mL/kg/hr = 7.6 mL/hr.
Hence, the patient's fluid maintenance is 7.6 mL/hr."
4697,22,Maintenance Fluids Calculations,physical,decimal,pmc-6028443-1,Extracted,"Our case was a 28-year-old male heavy smoker with morbid obesity (initial weight = 150 kg, height = 180 cm BMI = 46 kg/m2) that was operated with a LSG at another institution with a stable postoperative course. He reported chronic dysphagia and vomiting despite normal postop imaging (upper GI series and CT scan). Patient has lost the foreseen weight at 6 months (50 kg, BMI = 30.86 kg/m2, %EWL = 72.5%), but he presented to our institution 8 months later with a left pleuritic chest pain, nonradiating in nature associated with left shoulder pain, dyspnea, fever, chills, and decrease food intake (he stopped eating well 2 weeks prior to presentation because of described odynophagia and took multiple doses of IV NSAIDS). Upon admission, patient was hypotensive with a deteriorating general status (anxious, nadir GCS was 11, hypotensive, tachycardic) and a bad respiratory status (dyspnea, tachypnea, crackles on physical exam specially in the left side, with decrease left sided air entry). A chest x-ray showed a left massive pleural effusion with left lower lobe consolidation (effusion + pneumonia) (Fig. ). In an effort to explain the cause of the effusion, a CT scan chest, abdomen and pelvis with IV and oral contrast, showed a proximal stomach (gastro-esophageal junction) staple line fistula that was draining to what was first described as a left upper quadrant abscess later found to be a GC fistula causing a left pleural effusion (reactional effusion) (Figs. and ). He had a chest tube placed immediately that drained nonpurulent sero-sanguinous liquid of which one set of culture was taken. He was then started on empiric antibiotics, ceftriaxone, and levofloxacin, after cultures were taken and the patient was kept NPO. Four days later, chest tube was removed, and conservative management was continued. Total parenteral nutrition was started because the patient was malnourished, with low serum albumin, low iron, and evident muscular wasting (although he maintained a BMI of 26). Results of new cultures were out and showed no growth. Patient's antibiotics were switched to piperacillin/tazobactam and fluconazole. He was scheduled for a salvage surgery with a laparoscopic esophagogastrectomy with a Roux-en-Y esophagojejunal reconstruction when his nutritional status was adequate enough for the procedure, and after resolution of his infection. Ten days after, a repeat CT scan was done that showed a smaller residual left pleural effusion plus enhancement of the visceral and peritoneal pleura, and persistence of the gastro-colic fistula (Fig. ). GP fistula was excluded and GC fistula was confirmed. Patient was discharged home with a naso-jejunal tube (placed 1 day before discharge) for enteral feeding with high protein shakes (1500 mL Fresubin HP and 10 scoops of Protiphar/day to compensate for his daily caloric needs of 2400 kcal per day) and was kept on PO antibiotics (co-amoxiclav). A total of 14 days of IV antibiotics and another 2 weeks of PO antibiotics were taken. Upon many outpatients’ consultations, the patient family was concerned with the possible risks and benefits of the reoperation that was thoroughly explained to them and to the patient with multiple counseling sessions. They opted to continue conservative treatment (antibiotics + naso-jejunal enteral nutrition) in an attempt for the fistula to resolve without surgery because they feared the possible outcomes. The patient was carefully monitored over the course of 8 weeks with serial CT scans and outpatient visits, and finally on the last CT scan, the GC fistula had completely resolved (Fig. ), with no evidence of pleural effusion and the patient was started on a progressive oral diet after removal of the Naso-Jejunal tube. On future follow-ups, the patient seemed to do well, with adequate nutrition and good quality of life.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [150.0, 'kg']}",190,180.5,199.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 150.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (150.0 kg - 20 kg) = 190.0 mL/hr.
Hence, the patient's fluid maintenance is 190.0 mL/hr."
4698,22,Maintenance Fluids Calculations,physical,decimal,pmc-6441210-1,Extracted,"A boy aged 2 years and 8 months with a history of episodic fatigue and weakness was admitted for the evaluation of symptomatic hypoglycemic episodes. The patient was the first child of unrelated Chinese parents. The boy was born by a full-term normal vaginal delivery after 40 weeks of gestation, with a birth weight of 3.3 kg and a birth length of 49 cm. His pre- and postnatal periods and developmental milestones were normal, and his parents and younger sister were healthy. The symptomatic hypoglycemic episodes were first noted when he was 2 years old. Physical examination showed a non-dysmorphic boy with a height of 97 cm (0SD~ + 1SD), a weight of 15.5 kg (0SD~ + 1SD), and no palpable liver enlargement. He displayed normal muscle strength according to the MRC scale.
The patient’s biochemical characteristics are listed in Table . Urine ketone bodies were positive. His liver size was normal on ultrasonography with no liver hyperechogenicity or hypoechogenicity. His electroencephalography, social life ability and intelligence development were normal. His Peabody developmental motor scale presented a motor delay [Gross Motor Quotient (78); Fine Motor Quotient (87); Total Motor Quotient (83)] [].
Consent and Ethics:
Written informed consent was provided by the parents. This study was approved by the ethics committee of Peking Union Medical College Hospital, China.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15.5, 'kg']}",51,48.45,53.55,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15.5 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.5 kg - 10 kg) = 51.0 mL/hr.
Hence, the patient's fluid maintenance is 51.0 mL/hr."
4699,22,Maintenance Fluids Calculations,physical,decimal,pmc-5813771-1,Extracted,"The patient was a 68-year-old man of 166 cm height and 60 kg weight who was diagnosed with an esophageal carcinoma (T3N1M0, stage III). We performed video-assisted thoracoscopic esophagectomy followed by posterior mediastinal gastric tube reconstruction. There was no indication of coagulopathy prior to surgery. The activated partial thromboplastin time (APTT) was 27.2 s (reference range 23–35 s), prothrombin time (PT) was 108.0% (reference range 75–130%), and platelet count was 24.4 × 104/μL (reference range 14–34 × 104/μL).
Anesthesia was provided using a combination of general and epidural anesthesia. For the latter, the epidural catheter was inserted at the Th6–7 level and advanced approximately 5 cm into the epidural space. We did not observe any neurological symptoms, hemorrhage, or dural puncture during catheter implantation. Propofol and fentanyl were administered intravenously to induce anesthesia, and endotracheal intubation was carried out after rocuronium administration. Anesthesia was maintained using oxygen/air/desflurane with additional rocuronium as needed. For intraoperative analgesia, a total of 20 mL of 1.5% lidocaine was administered via the epidural catheter. Following video-assisted thoracoscopic resection of the esophagus, we reconstructed the gastric tube through laparotomy and performed cervical esophageal anastomosis using the posterior mediastinal route. In addition, we also performed regional lymphadenectomy (in three nodal regions) and enterostomy. The operation time and anesthesia time were 405 and 536 min, respectively. Blood loss during surgery was 221 mL.
After surgery, the patient was moved to the general intensive care unit and was extubated the following day; no neurological deficits were observed at this point. Two days after surgery, APTT, PT, and platelet count were within normal limits. However, high levels of d-dimer (36.9 μg/mL; reference range 0–0.9 μg/mL) indicated a need to prevent thrombosis, and we decided to administer enoxaparin sodium (Clexane™, SANOFI, Tokyo, Japan), a low-molecular-weight heparin, as an anticoagulant. At that time, fibrinogen level was 419 mg/dL (reference range 150–350 mg/dL), APTT was 29.1 s, PT was 81.4%, and platelet count was 5.4 × 104/μL. The epidural catheter was removed 2 h before the scheduled administration of enoxaparin sodium. The patient was placed in the decubitus position for catheter removal, and the catheter was removed smoothly without resistance.
Fifteen minutes after catheter removal, the patient complained of a complete lack of strength in both of his lower extremities. The patient had a manual muscle testing score of 1 (out of a possible 5), and he reported a lack of touch sensation and cold sensation below Th4. Due to this unexpected development, an emergency magnetic resonance imaging (MRI) scan was performed 2 h after catheter removal, which indicated a possible spinal epidural hematoma spreading from Th3 to Th6 (Fig. ). As shown in Fig. , the hematoma was pressing the spinal cord toward the ventral side. The patient experienced involuntary movements in his lower extremities during MRI scanning. Three hours after catheter removal, we began emergency surgery to remove the hematoma. Within an hour, we had confirmed and removed a hematoma that spanned from Th3 to Th7; the hematoma had spread to another spinal segment since the MRI scan had been performed. After surgery, the patient demonstrated gradual improvements in touch sensation, cold sensation, and motor function. The patient was able to walk 2 days after hematoma removal, and involuntary movements ceased after 7 days.
Catheter-associated spinal epidural hematomas can occur during catheter placement or removal, and incidence has been reported to range from 2 to 20 cases per 100,000 epidural procedures [, , ]. Despite their relatively low incidence, these hematomas are widely recognized by anesthesiologists as a possible deleterious complication of epidural anesthesia. Furthermore, the development and progression of hematomas associated with epidural anesthesia is relatively slow and is generally characterized by symptoms such as dorsalgia, impaired motor function (paraplegia), and sensory abnormalities; intense pain also occurs in many cases []. In the present case, the patient rapidly developed paraplegia and sensory abnormalities without any intense back pain. Rapid diagnosis was facilitated through the use of T2-weighted MRI, which produced clear visualization of the hematoma. Previous investigations of the time course of spinal epidural hematoma development reported that paraplegia can occur as early as 1 h after catheter removal, with some cases developing symptoms after more than 24 h [, ]. In contrast, the case described here is unusual in the rapid manifestation of neurological symptoms after catheter removal.
The epidural cavity, which lies between the lamina externa and lamina interna, contains loose connective tissue, adipose tissue, and venous plexuses. Therefore, the veins in the epidural cavity constitute the primary source of epidural hematomas. In the report by Gulur et al., epidural hematomas occurred in patients with abnormal coagulation parameters after the epidural catheter had been removed [], indicating the importance of conducting follow-up examinations. Although our case patient did not develop paraplegia or sensory abnormalities during the 2 days when the epidural catheter was implanted, these symptoms rapidly developed after catheter removal, suggesting that a venous plexus was damaged during the removal process. This supposition was supported by the absence of arterial hemorrhage or arteriovenous malformation during surgery. However, it is interesting that the degree of hemorrhage from a vein could result in such rapid onset of neurological symptoms.
The following abnormal coagulation parameters during the perioperative period have been identified as risk factors for epidural hematoma occurrence: APTT >35 s, international normalized ratio of PT >1.5, and platelet count <10 × 104/μL []. However, our case patient fulfilled none of these criteria for abnormal parameters. The levels of d-dimers, a fibrin degradation product, generally increase in patients with thrombotic disease or after undergoing surgery []. Despite the usefulness of d-dimer levels in the exclusion of deep-vein thrombosis [], there is also a need to perform ultrasonography of the veins in the lower extremities for accurate diagnoses. Although our case patient underwent ultrasound scanning, the field of view did not indicate any sign of thrombosis.
Studies have shown that patients with epidural hematomas should undergo surgical intervention within 8 h from the onset of symptoms to allow for neurological recovery []. In our case patient, we had detected and surgically evacuated the hematoma within 4 h after catheter removal. It is likely that the rapid response and surgical intervention were crucial in facilitating neurological recovery.
It should be noted that the increasingly prevalent use of postoperative anticoagulation therapy in recent years has provided the option of utilizing nerve blocks in place of epidural anesthesia. Peng and Wang reported that the use of a thoracic paravertebral intercostal nerve block was able to achieve satisfactory postoperative analgesia in esophageal cancer patients []. In our institution, however, analgesia control for thoracoabdominal surgery is generally performed using epidural anesthesia. The guidelines of the American Society of Regional Anesthesia and Pain Medicine for anticoagulant therapy recommend the use of a low-molecular-weight heparin (such as enoxaparin sodium) at least 4 h after epidural catheter removal []. In accordance with this practice, we had planned to remove the epidural catheter before administering the anticoagulant.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.0, 'kg']}",100,95,105,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.0 kg - 20 kg) = 100.0 mL/hr.
Hence, the patient's fluid maintenance is 100.0 mL/hr."
4700,22,Maintenance Fluids Calculations,physical,decimal,pmc-6610259-1,Extracted,"A 32-year-old woman was referred to our hospital with severe psychosis. Three months previously, her family recognized emotional changes in the patient, such as euphoria and/or depression. She progressed to cognitive decline, insomnia, and whole-body edema developed one week before visiting another hospital. On admission to the other hospital, initial endocrine investigations revealed high ACTH (545 pg/mL) and cortisol (136 μg/dL) levels. Computed tomography (CT) showed an anterior mediastinal mass and multiple pulmonary nodules (Fig a,b). As ectopic ACTH-producing mediastinal tumor with pulmonary metastasis was suspected, metyrapone was administered at an initial dose at 250 mg/day, which was gradually increased to 750 mg/day. However, she lost the ability to communicate due to consciousness disturbance within one week of hospitalization. Therefore, she was transferred to the emergency unit of our hospital. Physical examination on admission revealed moon face and proximal muscle weakness. Body height and weight were 164 cm and 55 kg, respectively and her bodyweight had not altered during the previous few months. Blood pressure was 116/61 mmHg. She had emotional lability and impaired memory. Laboratory findings at our hospital demonstrated severe hypokalemia and metabolic alkalosis, in addition to the increase in serum ACTH and cortisol levels (Table ). She showed self-injurious behavior, and attempted to bite her tongue. Due to her severe psychosis and consciousness disturbance, intubation was required and she was sedated in the intensive care unit. Metyrapone was increased to the maximal dose of 4000 mg/day via nasogastric tube. In addition, potassium supplementation was performed at 200 mEq/day and spironolactone was used to control low potassium levels. On day 8, we added perospirone hydrochloride hydrate to propofol sedation to suppress restlessness (Fig ). Thoracic surgery was performed for the lung nodule. Hematoxylin and eosin staining of the resected specimen indicated irregularly-shaped sheets and nests of tumor cells, and a diagnosis of NET was made (Fig ). Immunohistochemical staining revealed tumor cells positive for ACTH, chromogranin A, and synaptophysin. The Ki-67 labeling index was <1%., indicating that cancer staging by the WHO classification was neuroendocrine tumor G1. The time course of changes in serum cortisol levels is shown in Figure . As cortisol levels decreased after initiation of metyrapone, her conscious disturbance improved. She became able to communicate and was extubated on day 14 of hospitalization. Somatostatin receptor scintigraphy was performed and showed abnormal accumulation in the anterior mediastinal mass (Fig a) but not in the pulmonary nodules (Fig b). There were no other metastatic organs, including the brain. Resection of the anterior mediastinal tumor and the largest metastatic lesion of the right lung were subsequently performed through a median sternotomy to decrease serum ACTH level as much as possible. The pathological findings, including immunological staining, in the mediastinal tumor were similar to the initially resected left lung tumor and confirmed that the tumor was thymic in origin. Thus, according to the WHO classification in 2018, a diagnosis of NET of the thymus (typical carcinoid) with multiple pulmonary metastases was made. Postoperatively, a combination of octreotide long-acting repeatable (LAR; 30 mg) every four weeks and everolimus (10 mg/day) therapy has been continued, and ACTH and cortisol levels have remained stable. There was no personal or family history of multiple endocrine neoplasia type I in the present case.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [55.0, 'kg']}",95,90.25,99.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 55.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (55.0 kg - 20 kg) = 95.0 mL/hr.
Hence, the patient's fluid maintenance is 95.0 mL/hr."
4701,22,Maintenance Fluids Calculations,physical,decimal,usmle-3821,Extracted,"A 19-year-old woman comes to the physician because of a 1-year history of severe abdominal pain, bloating, and episodic diarrhea. She has also has a 10-kg (22-lb) weight loss over the past 10 months. Physical examination shows a mildly distended abdomen, diffuse abdominal tenderness, and multiple erythematous, tender nodules on the anterior aspect of both legs. There is a small draining lesion in the perianal region.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.0, 'kg']}",40,38,42,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.0 kg - 10 kg) = 40.0 mL/hr.
Hence, the patient's fluid maintenance is 40.0 mL/hr."
4702,22,Maintenance Fluids Calculations,physical,decimal,pmc-5596813-2,Extracted,"This 5-year-old boy developed chronic euvolemic hyponatremia due to SIADH after neurosurgical partial removal of a hypothalamic-chiasmatic astrocytoma. Post-surgical chemotherapy regimen treatment was started and an endocrinological follow-up was established to evaluate hypothalamic-pituitary axis functionality. At this time, he had asymptomatic hyponatremia with serum sodium levels ranging from 123 mmol/L to 130 mmol/L. As he developed central hypothyroidism and secondary adrenal insufficiency, a substitutive treatment for these conditions was started. He also developed central precocious puberty for which a LHRH-analogue treatment was started. At age 8 years, after the beginning of a second chemotherapy regimen treatment due to tumour size increase, hyponatremia became symptomatic with headache, nausea, asthenia, and seizures which persisted after chemotherapy withdrawal. Corticosteroid dosage increase (oral cortone acetate 40-50 mg/m2/day), mineralocorticoid treatment (oral fludrocortisone, 0.1 mg/day), and salt supplement (oral NaCl 3 g/day) were not sufficient to maintain serum sodium at acceptable levels, thus we started low-dose tolvaptan treatment (3.75 mg/day, 0.05 mg/kg/day, weight 83 kg) with prompt normalization of serum sodium (136-141 mmol/L) as shown in .
After 3 months, the tolvaptan dosage has been increased to 7.5 mg (0.09 mg/kg/day), the corticosteroid dosage was reduced to a substitutive range (10-15 mg/m2/day), the mineralocorticoid treatment and the supplemented salt were discontinued, with serum sodium levels remaining stable at 135-144 mmol/L.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [83.0, 'kg']}",123,116.85,129.15,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 83.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (83.0 kg - 20 kg) = 123.0 mL/hr.
Hence, the patient's fluid maintenance is 123.0 mL/hr."
4703,22,Maintenance Fluids Calculations,physical,decimal,pmc-5937564-1,Extracted,"An 11-year-old Thai boy presented with progressive abdominal distension for one month prior to admission. He had a significant weight loss up to 8 kg within one month, but had no fever or jaundice. There is a history of eating habits: eating uncooked fish, meat, and beef. He also had polyuria upon admission. On physical examination, it was found that he was cachexic. His weight was in the 3rd percentile. Generalized lymphadenopathy and marked hepatosplenomegaly were detected. Neurological examination was within the normal limit.
His laboratory data revealed that the hemoglobin level was 13.3 g/dl, the hematocrit value was 41.5 volume %, the WBC count was 15,100 cells/mm3 (neutrophil 60%, lymphocyte 30%, monocyte 9%, and basophil 1%), and the platelets count was 304,000 cells/mm3. Peripheral blood smears were normochromic and normocytic red blood cells, without blasts cells. Bone marrow examination and biopsy were normal. The chromosome study reviewed 46 XY, normal male karyotype. The liver function test revealed that the level of albumin was 4.9 g/dl, total bilirubin 0.3 mg/dl, direct bilirubin 0.2 mg/dl, SGOT 73 U/L, SGPT 46 U/L, and alkaline phosphatase 339 U/L. Uric acid level was 6.1 mg/dl. The amount of lactate dehydrogenase (LDH) was 149 U/L. Serum electrolytes showed that the level of sodium was 134 mmol/l, potassium 3.82 mmol/l, chloride 98.5 mmol/l, and bicarbonate 26.3 mmol/l. Hypercalcemia and hypophosphatemia were detected; the serum calcium level had increased to 13.6 mg/dl and the phosphate level to 2.3 mg/dl. The blood urea nitrogen level was 11.7 mg/dl and creatinine 0.5 mg/dl. Serum amylase was 37 U/L, and serum lipase was higher than normal of 96 U/L. The amount of gamma-glutamyl transpeptidase (GGT) was 630 (normal range 15–85) U/L. Stool examination revealed blastocystis hominis. Chest X-ray showed generalized osteopenia (). The bone scan showed no evidence of active bone lesion.
CT chest and whole abdomen (Figures and ) revealed hepatomegaly and numerous heterogeneous low-attenuation centers varying in size, with peripheral rim-enhancing masses scattered in both hepatic lobes, and the largest one was 8 × 7.5 × 11.6 cm in size. No dilatation of intrahepatic duct and CBD was seen. The spleen was enlarged, and the hypodensity mass size was 1.4 × 1.9 cm. The pancreas was enlarged with an ill-defined irregular hypodensity mass at the pancreatic body, and the tail size was 2.2 × 4.7 × 2.8 cm. Enlarged portal and para-aortic nodes were observed.
Investigations for hypercalcemia were performed. The intact parathyroid hormone (iPTH) level was very low 6.33 (normal range 15–65) pg/ml, while the 25-OH vitamin D level was 27 (normal range 30–100) ng/ml. It was shown that secondary hypercalcemia developed due to malignancy that is most likely from the parathyroid hormone- (PTH-) related protein (PTHrP) producing tumor.
The level of serum tumor markers such as alpha fetoprotein was 78.52 ng/ml, CA 19-9 was 360.8 U/ml, and CA 125 was 267.10 U/ml while the CEA and β-hCG were normal.
Liver biopsy was performed for diagnosis. Histological examinations of fine-needle biopsy showed poorly differentiated tubular adenocarcinoma ().
In regard to immunohistochemistry, the tumor cells diffuse positive for cytokeratin 7 and 19 (), negative for cytokeratin 20 and synaptophysin, and lacked mCEA and pCEA ().
The patient was treated with vigorous hydration and diuretic; 20 mg of furosemide was given intravenously every 8 hours until the serum calcium level became lower than 12 mg/dl. He was placed on systemic chemotherapy; cisplatin (25 mg/m2) and gemcitabine (1,000 mg/m2) were administered intravenously on days 1 and 8 every 3 weeks for 8 cycles (24 weeks).
The patient was followed up with pediatric hemato-oncologists regularly. Physical examination and laboratory evaluation after the completion of the first cycle of chemotherapy revealed liver span, and the spleen decreased in size from 20 cm to 8 cm and 4 cm below left costal margin to just palpable. , respectively Also, the serum calcium level had decreased to 12.1 mg/dl, the phosphate level increased to 3.4 mg/dl, and the intact parathyroid hormone (iPTH) level had increased to 7.75 (normal range 15–65) pg/ml. However, he discontinued hydration therapy and diuretics.
Repeated CT chest and whole abdomen after the completion of the fourth cycle of chemotherapy for 12th and 24th weeks showed a decrease in size of the infiltrative mass in both hepatic lobes, the spleen, the pancreas, and intra-abdominal lymph nodes.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [8.0, 'kg']}",32,30.4,33.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 8.0 kg. Hence, the patient's maintenance fluid is 8.0 kg * 4 mL/kg/hr = 32.0 mL/hr.
Hence, the patient's fluid maintenance is 32.0 mL/hr."
4704,22,Maintenance Fluids Calculations,physical,decimal,pmc-7542866-1,Extracted,"A 78-year-old man presented at the emergency department with increasingly disabling lower back pain. His past medical history revealed transurethral resection of the prostate and lumbar spinal stenosis. In addition, he was recently diagnosed with acute myeloid leukemia for which he received induction chemotherapy 1 month earlier. During this course, he developed a perforated diverticulitis for which he underwent resection of the sigmoid. Subsequently, he developed a candidemia with C. krusei and micafungin treatment was started. Since ophthalmoscopy, echocardiography and ultrasound of the liver did not reveal any signs of septic foci, micafungin was continued until 14 days after the last positive blood culture. After the first cycle of chemotherapy a complete remission was achieved.
His current complaints started 3 weeks before presentation. He noticed progressive lower back pain radiating to the buttocks and hips hampering his walking. He did not experience loss of motor or sensory function. On presentation, the patient was hemodynamically stable without fever. Neurological and physical examination were normal except for a rigid gait. The patient weight was 77 kg. Blood chemistry showed a slightly elevated CRP of 38 mg/L (normal range < 8 mg/L) and a mild leukocytosis of 12.9 × 109/L (normal range 4–10 × 109/L). An MRI of the lower lumbar spine showed a spondylitis of the L4 and L5 vertebral bodies with remarkable sparing of the intervertebral disc (Fig. a). Furthermore, intraspinal epidural expansion of inflammation with an abscess in the posterior epidural space was revealed with notable involvement of the posterior elements (Fig. b). A small second abscess in the right erector spinae muscle was punctured and aspirated for culture (Fig. c). After puncture, empirical treatment with flucloxacillin (6000 mg/24 h IV) was started. In addition, with his recent candidemia in mind and MRI findings suggesting an atypical pathogen, anidulafungin (loading dose of 200 mg IV, followed by 100 mg/day IV) was added to the treatment. After 6 days culture of the abscess showed C. krusei. Susceptibility testing showed the following minimal inhibitory concentrations (MIC): for amphotericin B MIC 0.5 mg/ml, anidulafungin 0.023 mg/L and voriconazole 0.5 mg/mL. Antimicrobial therapy was narrowed to anidulafungin. Because of the low bone penetration of anidulafungin, oral voriconazole (200 mg/twice daily) was added. Considering the infection and risk of derailment upon chemotherapy induced neutropenia, further treatment for acute myeloid leukemia was halted.
Three months after starting the anidulafungin plus voriconazole regimen with adequately controlled serum levels, a gradual increase in backpain and expansion of inflammation on MR-imaging warranted posterior decompression and stabilization from the L2 vertebra to the pelvis. Voriconazole was switched to liposomal amphotericin B (3 mg/kg). Culture of a peroperative bone biopsy (level L4–5) showed persistent infection with C. krusei, sensitive to anidulafungin (MIC 0.016 mg/L) and with a low MIC for voriconazol (MIC ≤0.12 mg/L, no clinical breakpoint for C. krusei). In this material, no anidulafungin could be detected by high-performance liquid chromatography, suggesting insufficient penetration in bone. Concentrations of voriconazol were not measured due to limited available biopsy material. Determing levels of liposomal amphoterocin B seemed redundant, as this had not been started at the time of biopsy. Nevertheless, due to severe muscle cramps, amphotericin B therapy was switched back to voriconazole, with a trough concentration of 3 mg/l, and the daily dose of anidulafungin was increased to 300 mg. As serum concentration of anidulafungin did not correlate to bone concentration there was no target concentration. Serum levels were monitored through concentrations. At a anidulafungin dose of 300 mg/day the trough concentrations were between 9.9 and 18.7 mg/L. This in contrast to through concentrations of 2.8 to 3.5 mg/L when anidulafungin was dosed 100 mg/day. This treatment will be continued until 6 months after surgery. Complete relieve of symptoms was noted after surgery and the patient experiences no side effects of the current treatment. Unfortunately, 7 months after initial chemotherapeutic treatment his acute myeloid leukemia relapsed. He currently undergoes treatment with azacitidine.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [77.0, 'kg']}",117,111.15,122.85,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 77.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (77.0 kg - 20 kg) = 117.0 mL/hr.
Hence, the patient's fluid maintenance is 117.0 mL/hr."
4705,22,Maintenance Fluids Calculations,physical,decimal,pmc-6937415-1,Extracted,"We report a 15-year-old girl who presented with recurrent headaches, arterial hypertension, and a systolic murmur.
Echocardiographic examination in a medical practice had revealed a potential coarctation of the aorta.
The patient had no history of serious illness.
There were no medically relevant aspects from the patient’s personal history. Other than arterial hypertension and coronary artery disease in the patient’s grandfather, there was no known cardiac disease within the family.
The patient presented in good general condition. Body weight was 61 kg and height were 172 cm. Her blood pressure in the right arm with 144/86 [MAP (mean arterial pressure) 110 mmHg] was significantly higher than that in the left arm [118/82 (MAP 96) mmHg] and of the right leg [118/72 (MAP 91) mmHg]. We consistently felt an unequal pulse between the right and left radial arteries (right stronger than left). A 2/6 systolic murmur was identified ventrally in the second and third left intercostal space, and, less prominently, dorsally between the shoulder blades. All other aspects of the physical examination were normal.
No laboratory examinations were done in the diagnostic work-up.
Echocardiography and cardiac MRI revealed a hypoplastic native aortic arch with a bi-carotid trunk and a segment just proximal of the left subclavian artery which was stenosed by 75% ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [61.0, 'kg']}",101,95.95,106.05,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 61.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (61.0 kg - 20 kg) = 101.0 mL/hr.
Hence, the patient's fluid maintenance is 101.0 mL/hr."
4706,22,Maintenance Fluids Calculations,physical,decimal,pmc-7745487-1,Extracted,"A 16-year-old male soccer player on an amateur team who was a resident of a rural community with limited access to medical services presented to the trauma emergency room with a 6 d history of evolution, pain, swelling in the left knee and the inability to bear weight.
The patient’s injury occurred while he was playing soccer; his right leg was fixed in extension when he kicked a ball with his left foot. Subsequently, the patient experienced severe pain in the left knee, fell directly onto the ground from a standing position, and could not bear weight on the foot. He was immobilized and treated with non-steroidal anti-inflammatory drugs (NSAIDs), rested and physical measures; however, when the symptoms persisted, the patient was transferred to our trauma center. He was initially assessed in our center 6 d after the incident.
The patient had no significant previous illnesses.
The patient exhibited grade 2 obesity (weight: 102 kg, height: 1.65 cm, body mass index: 37.50 kg/m2), and there were no relevant items in the medical history.
In the examination, the skin on the left knee was intact, without abrasions or wounds, and the patient showed a diffuse increase in soft tissue around the left knee, moderate joint effusion (grade 3), and a knee attitude in flexion. He was also unable to actively perform knee extension. The patient experienced severe pain during palpation of the TT (8/10 in the visual analogue scale). The injured patella was also asymmetrically elevated compared to the contralateral patella (Figure ). The Lachman test result was negative, and no knee instability was confirmed on the physical exam. Distally, he demonstrated to the ability to completely plantarflex and dorsiflex the ankle and flex and extend the fingers.
This patient had routine blood tests including complete blood count, blood clotting, blood group, basic metabolic panel, C-reactive protein and erythrocyte sedimentation rate tests. These results did not reveal any abnormalities.
The radiographs revealed a displaced avulsion fracture of the TT extending to the level of the proximal tibial physis (Ogden type 2B) with 180º of rotation in the fragment and a concomitant high-riding patella (Caton-Desahmps index: 1.47) (Figure and ). Given the latter finding, concern was raised for PT injury; a magnetic resonance imaging (MRI) scan was performed, and the results demonstrated a complete distal rupture of the PT (which was retracted in the lower pole of the patella) (Figures and ), reclassifying the lesion as an Ogden 2C type lesion. A computed tomography (CT) scan of the knee was performed, which revealed a large anterior fragment displaced by 13.14 mm (Figures and ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [102.0, 'kg']}",142,134.9,149.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 102.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (102.0 kg - 20 kg) = 142.0 mL/hr.
Hence, the patient's fluid maintenance is 142.0 mL/hr."
4707,22,Maintenance Fluids Calculations,physical,decimal,pmc-7683876-1,Extracted,"We present a case of a two-month-old girl born at 33 weeks gestation by cesarean section due to severe maternal pre-eclampsia with a weight of 1.98 kg. She was admitted to the neonatal intensive care unit for three weeks and discharge, she remained healthy on breastfeeding. She was brought by her mother to the accident and emergency department with a one-month history of skin lesions that involved the perioral region, hands, and skin folds including napkin area. This was associated with cracked lips, hair loss, and diarrhea more than seven times per day. The mother noticed that her daughter was excessively crying, lethargic, and febrile. The patient was admitted previously to another hospital with superinfected skin lesions, which was treated with intravenous antibiotics for four days. At the initial assessment of the patient, she looked lethargic and dehydrated. Skin examination revealed erythematous scaly patches on the neck and nappy area as well as vesiculopustular lesions predominantly on the perioral region []. Alopecia was noticed as well. We considered the diagnosis of AE, and the patient was hospitalized. Laboratory tests were sent, which showed normal inflammatory markers, anti-tissue trans glutamine for celiac disease, β-lactoglobulin for cow’s milk protein intolerance, and immunoglobulins but low alkaline phosphatase (ALP) (45 IU/L). Zinc level was sent to a laboratory in France. While waiting for blood culture, urine cultures, and swabs from the lesions, the patient was started on intravenous cloxacillin, cefotaxime, and zinc therapy. Zinc therapy was started at a dose of 3 mg/kg daily of elemental zinc. During admission, the patient’s diarrhea stopped, and her skin lesions started to become paler and smaller after three to four days. All cultures and swabs did not reveal any growth. She completed 14 days of intravenous antibiotics and was discharged home to continue daily zinc therapy with a follow-up appointment at the pediatric dermatology clinic. The patient did not undergo genetic testing because of logistical reasons as it is only available in a single health care institution across the country.
At the follow-up appointment, we reported her zinc level as < 1.9 µmol/L. The patient improved, and complete remission of skin lesions and alopecia were noticed []. Her dose was adjusted to 0.5 mg/kg/day according to her weight. She was advised to continue with her zinc therapy and to continue regular follow-up visits with the pediatric gastroenterology and dermatology clinic at the regional hospital.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1.98, 'kg']}",7.92,7.524,8.316,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1.98 kg. Hence, the patient's maintenance fluid is 1.98 kg * 4 mL/kg/hr = 7.92 mL/hr.
Hence, the patient's fluid maintenance is 7.92 mL/hr."
4708,22,Maintenance Fluids Calculations,physical,decimal,pmc-5369859-1,Extracted,"An 80-year-old Japanese woman presented to the Dermatology Department of the Showa General Hospital on day 0 with a 1-month history of spreading ulcers due to pyoderma gangrenosum. Her past medical history included pyoderma gangrenosum, diabetes mellitus, and rheumatoid arthritis. Her daily medications included alfacalcidol, salazosulfapyridine, polaprezinc, methotrexate, lansoprazole, folic acid, diclofenac, and felbinac.
On initial physical examination, she had a temperature of 37.0 °C (98.6 °F) and a blood pressure of 111/45 mmHg, with a heart rate of 51 beats per minute. Her height was 145.5 cm, and her body weight was 45.5 kg. The patient presented with several ulcers on all her extremities but had otherwise unremarkable findings. The initial laboratory workup (day 0) showed hyperglycemia of 237 mg/dL, leukocytosis (white blood cell count [WBC], 16,040/µL), and abnormal renal function (blood urea nitrogen [BUN], 39.6 mg/dL; creatinine 1.64 mg/dL). An echocardiogram showed a heart rate of 38 beats per minute and a complete atrioventricular block.
The clinical course is shown in . The patient was treated with prednisolone 40 mg/day for pyoderma gangrenosum; moreover, tazobactam/piperacillin was administered since an infection of the ulcers was suspected. On day +19, a pacemaker was implanted to treat the complete atrioventricular block. On day +23, Gram staining of the blood culture showed numerous yeast cells that were identified as C. glabrata (), on API® ID32C (API-bioMérieux France). Micafungin 250 mg/day was administered (starting on day +23) followed by 150 mg/day (starting on day +29) after exclusion of fungal endophthalmitis. The pacemaker was removed to remove a possible source of infection on day +23. On day +30, a central venous (CV) catheter was inserted; it was subsequently removed and reinserted on day +38. On days +40 and +54, skin grafting was performed for the ulcers. As guidelines state that antifungal treatment should be completed >2 weeks after a negative blood culture (on day +31), micafungin therapy was discontinued on day +77 after a total of 54 days of treatment. On day +88, the CV catheter was removed and then reinserted. On day +105, Gram staining of the blood culture showed the recurrence of numerous yeast cells that were again identified as C. glabrata (). As this was a recurrence of the C. glabrata BSI, we re-administered micafungin 150 mg/day and removed and reinserted the CV catheter. On day+109, another skin grafting procedure was performed. On day +120, Gram staining of the blood culture showed numerous yeast cells yet again; consequently, the micafungin dose was increased to 250 mg/day and the CV catheter was removed and then reinserted. On day +127, the blood culture and the CV catheter culture tested positive for C. parapsilosis (), identified by API® ID32C (API-bioMérieux France).
Micafungin was switched to liposomal amphotericin B (3 mg/kg/day), as this medication is effective for both C. glabrata and C. parapsilosis. On day+155, liposomal amphotericin B therapy was discontinued after a total treatment duration of 28 days, as the treatment had been provided >2 weeks after the negative blood culture result (day+134). On day+156, the CV catheter was removed and the patient was discharged from the hospital after successful treatment.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [45.5, 'kg']}",85.5,81.225,89.775,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 45.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (45.5 kg - 20 kg) = 85.5 mL/hr.
Hence, the patient's fluid maintenance is 85.5 mL/hr."
4709,22,Maintenance Fluids Calculations,physical,decimal,pmc-5936485-1,Extracted,"A 20-day-old male neonate was referred from a private hospital with a case of hypoplastic aortic arch syndrome. He was born full term via normal vaginal delivery to a primiparous mother with a birth weight of 3.4 kg and a normal Apgar score. Antenatal examinations including an abdominal ultrasound were completely unremarkable. He had no neonatal intensive care admissions, and on routine clinical examination, a cardiac murmur was detected. A cardiac echocardiogram confirmed the diagnosis of the hypoplastic aortic arch syndrome. He was started on prostaglandin E1 infusion and referred to King Abdulaziz Medical City Hospital at 15 days of age for further management. On physical examination, the patient had mild central cyanosis, soft, systolic ejection murmur at the left sternal border and high-pitched systolic murmur at the lower left sternal border. His vital signs were completely normal. Initial laboratory tests revealed that blood urea nitrogen (BUN) was 7.84 mg/dL (normal range: 7–20 mg/dL) and serum creatinine was 0.452 mg/dL (0.2–0.7 mg/dL). Electrolytes and blood gas analyses were within normal limits. A complete blood count showed a hemoglobin level of 14.1 g/dL (normal range: 10–12 g/dL), normal leukocytes count, and a platelet count of 742 × 109/L (normal range: 150–400 × 109/L). There was no serological evidence of hepatitis B and C or viral infections. Blood and urine cultures were negative. Abdominal ultrasound and the chromosomal analysis including fluorescence in situ hybridization were normal. An electrocardiogram revealed the absence of Q waves in the inferior and lateral leads. An initial chest X-ray revealed mild cardiomegaly with the prominent bilateral pulmonary vasculature. Repeated cardiac echocardiogram showed a hypoplastic aortic arch, a small left ventricular outflow tract, an aortic annulus, large muscular ventricular septal defects with inlet extension, a restrictive patent foramen ovale, and a large patent ductus arteriosus.
The patient underwent surgical correction on day 20 of his life. Intraoperatively, a median sternotomy with aortic and bicaval cannulation was performed using 14 and 10 French catheters, respectively. A cardiopulmonary bypass with systemic cooling was instituted. The patent ductus arteriosus was divided, the ventricular septal defect was closed using a Gore-Tex patch, and an aortic arch reconstruction was performed using a pulmonary homograft patch. An atrial septectomy and a tricuspid valve commissuroplasty were performed. The Damus–Kaye–Stansel procedure was constructed in a side-to-side fashion and connected to the reconstructed aorta under circulatory arrest with antegrade cerebral perfusion. A 4 mm size Blalock–Thomas–Taussig shunt was constructed between the base of the innominate artery and the central pulmonary artery. A transesophageal echocardiogram was performed, which did not show any significant residual lesions. However, oxygen saturation declined, and the patient was placed on venoarterial ECMO (Quadrox-i pediatric; Maquet Getinge Group, Rastatt, Germany) to control the hemodynamics, allow the heart to rest, and the pulmonary vascular resistance to drop. The patient was transferred to the pediatric cardiac intensive care unit with an ECMO and ventilator support. The targeted ECMO blood flow was 70–100 mL/kg/minute with the initial flow started at ∼0.5 L/minute. The heparin dose was adjusted to maintain an activated clotting time between 180 and 220 seconds. Details of the ECMO and ventilation parameters during the hospital stay are illustrated in . In addition, the patient had severe hypotension and bleeding necessitating multiple courses of fresh frozen plasma, platelets, blood transfusions, and inotropes. Postoperatively, he was noted to be anuric and clinically had significant fluid overload and poor diffusive clearance. His chest X-ray showed significant fluid overload (). Renal replacement therapy was initiated using an inline hemofilter (Maquet hemofilter) directly into the ECMO circuit (). The priming volume of the hemofilter is 18 mL with a surface area of 0.25 m2 and designed using polypropylene fiber material. The hemofilter is incorporated after the pump and before the membrane oxygenator. After delivery through the hemofilter, the blood returned to the pre-pump limb of the circuit. Efficient ultrafiltration was balanced using a standard intravenous infusion pump connected to the effluent port of the hemofilter. The ultrafiltration was equal to the rate programmed into the infusion device. On follow-up, the patient had stable electrolyte parameters, balanced fluid removal, and efficient diffusive clearance (). He was decannulated from ECMO therapy after 9 days without any complications related to the IHS. Repeated chest X-rays showed significant improvement in relation to fluid overload ().
Written informed consent for the publication of this case report and any accompanying images has been obtained from the patient’s father.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.4, 'kg']}",13.6,12.92,14.28,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.4 kg. Hence, the patient's maintenance fluid is 3.4 kg * 4 mL/kg/hr = 13.6 mL/hr.
Hence, the patient's fluid maintenance is 13.6 mL/hr."
4710,22,Maintenance Fluids Calculations,physical,decimal,pmc-7669430-1,Extracted,"A 25-year-old African American male with no known past medical history presented with a 1-week history of intermittent headaches, constant diplopia, and dysconjugate gaze. No prior history of these symptoms was reported. The patient did not regularly see a physician. Upon admission, the vitals were BP −196/108 mm Hg, HR −89/min, RR −20/min, SpO2 −98% on room air, and a weight of 351 lbs (BMI 64 kg/m2). On fundoscopic examination, he had papilledema, but his vision was grossly normal. Cardiovascular examination revealed no murmurs and 1-2+ edema in lower extremities. His central nervous system examination revealed a 6th nerve palsy on the left, dysconjugate gaze, facial symmetry, and midline tongue. The remainder of the examination was unremarkable. There was no personal or family history of sickle cell anemia.
Laboratory data are shown in Table . Urinalysis was suggestive of protein >300 without any evidence of infection or blood. CT scan of the head was suggestive of partially empty sella turcica and no evidence of acute intracranial process. The patient's blood pressure improved shortly after admission. He underwent lumbar puncture (LP) which was suggestive of pseudotumor cerebri, and treatment with acetazolamide was initiated. Nephrology was consulted for an incidental finding of acute kidney injury (AKI) and proteinuria. The patient's kidney function was within normal limits based on the laboratories obtained from outside hospital during an ER visit 1 week prior to the current admission. He was diagnosed with urinary tract infection (UTI) and was prescribed Bactrim (trimethoprim and sulfamethoxazole)-DS (double strength), one tablet twice a day for a week. Unfortunately, we were unable to obtain the results of urinalysis or any other clinical details of his ER visit, and there were no prior laboratories on our system to assess for baseline urine proteinuria. The only information we had was, he was prescribed antibiotics for UTI and the kidney functions were essentially in the normal range. The patient's history was negative for any risk factors for AKI or chronic kidney disease (CKD). Peripheral smear did not reveal any schistocytes. The spot urine protein: 369, urine creatinine: 93 (protein/creatinine ratio = 4 gm/gm). Urine microscopy did not reveal red blood cell (RBC) casts or dysmorphic RBCs. HIV antigen/antibody was negative, and the viral load was <40. Antinuclear antibody (ANA) was 1:40 speckled. Anti-Ro, anti-La, anti-Smith, and anti-dsDNA were negative. The complements C3 was within normal limits and C4 was elevated. Evaluation for infectious causes including Cytomegalovirus (CMV), Epstein Barr Virus (EBV), Parvovirus, and Hepatitis virus was all negative. C reactive protein (CRP) and erythrocyte sedimentation rate (ESR) levels were elevated at 3.243 mg/dL and 120 mm/hr respectively. Renal ultrasound revealed a 15.4 cm right kidney and 15.2 cm left kidney with increased echogenicity bilaterally without any evidence of cortical thinning or suspicious cysts, masses, or hydronephrosis. Except for the recent exposure to Bactrim, the patient was not on any other medication that could explain the cause of his AKI. Given the presentation of AKI, nephrotic range proteinuria, and negative serologic workup, a renal biopsy was obtained as shown in the image. (Figure ). Light microscopy showed up to four glomeruli with no globally sclerotic glomeruli were identified per level. Three of the glomeruli show capillary tuft collapse with podocyte hypertrophy and numerous protein reabsorption droplets. No necrosis or crescent formation was identified. There was mild interstitial fibrosis. Many of the tubules showed dilatation with proteinaceous casts. There is a patchy, lymphoplasmacytic interstitial infiltrate. The vasculature is unremarkable. Immunofluorescence showed limited deposition of C3 within the glomeruli. Podocyte protein reabsorption droplets were seen, and ultrastructural evaluation revealed extensive podocyte foot process effacement. Electron microscopy showed hypertrophic podocytes with extensive podocyte foot process effacement without any definitive immune complex dense deposits. The glomerular basement membranes are irregularly thickened with an expansion of the lamina densa which is of unclear significance. There was no evidence of acute tubular necrosis (ATN) on the biopsy.
Treatment involved administration of 120 mg of oral Prednisone every other day, and the patient was discharged without any evidence suggesting the need to initiate dialysis as he remained nonoliguric during the entire hospital stay. Hyponatremia was corrected at an appropriate rate. Subsequent nephrology clinic visits revealed improving renal indices. One week after the discharge, patient's laboratories revealed BUN of 55 mg/dL with a Cr of 4.52 mg/dL. Three months after discharge, his BUN was 17 mg/dL with a creatinine of 1.67 mg/dL at which point steroid taper was initiated. The spot urine protein: 769 and spot urine creatinine: 321.5 (protein/creatinine ratio = 2.39 gm/gm). 24-hour urine collection was not performed.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [351.0, 'lbs']}",199.21079,189.25025,209.17133,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 351.0 lbs so this converts to 351.0 lbs * 0.453592 kg/lbs = 159.21079 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (159.21079 kg - 20 kg) = 199.21079 mL/hr.
Hence, the patient's fluid maintenance is 199.21079 mL/hr."
4711,22,Maintenance Fluids Calculations,physical,decimal,pmc-2740157-1,Extracted,"A 6-year-old male child born of a non-consanguineous marriage from a middle class family of a rural area of Burdwan admitted in the emergency pediatrics ward with the history of convulsion associated with frequent vomiting. According to the mother the problem had started since 4th month of age which was initially more on the right side gradually progressing to affect whole of the body. The vomiting occurred frequently with or without convulsion.
The child was developmentally lacking behind other children of the same age and sex of the community. He was not able to speak and communicate till now, very much sleepy and did abnormal behavior frequently.
Mother noticed changes in the skin since 4th year of age, there were multiple tiny pink nodules on the nose and malar prominences which later coalesced to form fleshy appearances. There are hyperpigmented patches on left forehead and right malar regions. Patchy hypopigmented areas were present on both front and back of the trunk.
There was no other member of the family suffering from the disease.
On examination, the child was found dull, indifferent and expressionless with an average built having weight 20 kg, height 122 cm, head circumference 52 cm and chest circumference 61 cm. There were extensive facial angiofibromatosis with butterfly distribution covering nose and spreading to cheeks (), two prominent hyperpigmented plaques were seen, one on left forehead covering a wide area () and one on right cheek. There were hypopigmented patches abundant on both sides of the trunk.
The child had disturbances of higher function like orientation in time and place, speech and language as well as intelligence. His cranial nerves and motor functions were normal. Other neurological and systemic examinations appeared to be normal.
Psychiatric assessment with the help of Vineland Social Maturity Scale and Conner’s Autism Rating Scale revealed the child was suffering from autism along with severe mental retardation with intelligent score was about 25 to 30.
C T scan of the brain showed multiple foci of Subependymal calcification looked like candle-dripping appearances; they were also present in both basal ganglia, both temporal and left parietal regions ().
Ultrasonography of kidneys and liver showed no abnormality, Echocardiography of heart revealed no rhabdomyoma of cardiac muscle. Opthalmolscopic examination was also normal.
The child was treated with higher doses of sodium valproate and the convulsion was controlled. He was referred to the Psychiatric department for necessary measures.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [20.0, 'kg']}",60,57,63,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 20.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (20.0 kg - 10 kg) = 60.0 mL/hr.
Hence, the patient's fluid maintenance is 60.0 mL/hr."
4712,22,Maintenance Fluids Calculations,physical,decimal,pmc-5564197-1,Extracted,"A 20-year-old man (height, 177 cm; weight, 60 kg) was hospitalized for an orthognathic surgery. He was diagnosed with bilateral CLP and mandibular prognathism associated with midface deficiency, and was scheduled to undergo LeFort I osteotomy, right iliac block bone graft procedure, and bilateral sagittal split osteotomy. He had previously undergone cheiloplasty, palatoplasty, cleft maxillary repair, and pharyngoplasty to correct the CLP. Preoperative laboratory findings, chest X-ray image, and electrocardiogram were normal. He had no other diseases, including upper airway obstruction or obstructive sleep apnea symptoms.
He had maxillary deficiency with malocclusion, mandibular prognathism, a scar due to a pharyngeal flap, and cheiloplasty. As a premedication, glycopyrolate (0.2 mg) was injected intramuscularly. Standard monitoring was performed in the operating room. After preoxygenation with 100% oxygen, general anesthesia was induced with remifentanil (1 µg/kg), propofol (120 mg), and rocuronium (50 mg). After providing adequate muscle relaxation, flexible fiberoptic bronchoscope (FFB)-guided NTI was attempted using a nasotracheal tube (NTT) of 6.5 mm internal diameter; this procedure was performed instead of a direct rigid laryngoscope because FFB technique and smaller sized NTT are more suitable for adults who have intact pharyngeal flaps. The FFB was inserted into the both nostrils for examination and passed through the posterior pharynx; we observed that the velopharyngeal port (between the nasopharynx and oropharynx) was divided into two small-sized pharyngeal ports by the pharyngeal flap (). Because right side of pharyngeal port was a little wider, a scope was passed carefully through the right side pharyngeal port and vocal cords to the carina; NTT was passed over the FFB smoothly. There was no specific resistance during NTT insertion, but minor bleeding appeared on the nasopharynx. After the intubation, the patient was mechanically ventilated to administer desflurane (6 vol%), with a fresh gas flow rate of 3 L/min and 50% oxygen in air. After the induction of anesthesia, active bleeding was observed in the mouth immediately. To assess the bleeding focus, we examined the oral cavity with a dental mirror, and bleeding was seen at the pharyngeal flap. The flap was probably torn at the time of the NTI. Subsequently, hemostasis was achieved using a 4 × 4 gauze moistened with 1:1000 epinephrine solution. After the bleeding was controlled, cotton swabs soaked in 2% lidocaine and 1:1000 epinephrine were inserted into the torn flap and nostril. Subsequently, the pharyngeal bleeding stopped, and the surgery was completed without further complications. After the surgery, the patient recovered without any problems. A follow-up examination using a nasendoscopic view that was performed two years later showed that the pharyngeal flap remained intact after the recovery (). For this case presentation, we received consent from the patient.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.0, 'kg']}",100,95,105,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.0 kg - 20 kg) = 100.0 mL/hr.
Hence, the patient's fluid maintenance is 100.0 mL/hr."
4713,22,Maintenance Fluids Calculations,physical,decimal,pmc-2933487-1,Extracted,"A one-and-half-year-old girl weighing 7.5 kg was admitted with a history of fever and cough since 15 days, neck swelling and difficulty in swallowing and mouth opening since 1 week. Diagnosis of retropharyngeal abscess was made using neck X-ray and computed tomography (CT) scan.
The X-ray showed widened prevertebral soft tissue shadow []. CT scan showed fairly large collection with enhancing thin walls in the prevertebral region, extending from base of skull to carina measuring 44 × 20 × 105 mm, suggestive of an abscess []. Laryngeal airways were clear. Laryngeal cartilage and hyoid bone were intact. Carotid arteries and jugular veins were found to be normal. Trachea and main bronchi were clear. No hilar or mediastinal lymphadenopathy was present. Cardia, pericardium and great vessels were normal. Lung fields were clear, and there was no pleural effusion.
Investigations were within normal limits except for raised erythrocyte sedimentation rate (ESR) and leucocytosis. The patient was put on IV cefotaxime 250mg twice daily (BD) and diclofenac suppository. The patient was taken up for intraoral drainage on emergency basis.
Preanaesthetic evaluation was done on the patient She was febrile. There was a neck swelling on the left side. Her pulse was 140 beats/minute, and the SPO2 was 98% with room air. Her mouth opening was restricted to one finger. She had difficulty in closing her mouth as well. Mallampati score could not be assessed. Only the upper and lower central incisors were present. Cervical spine was normal.
The respiratory system had the following features. Trachea was central. Air entry was equal, bilateral crepitations and occasional ronchi were present. Rest of the examination was unremarkable.
In view of the anticipated difficult mask ventilation and intubation, all equipments for difficult airway management were kept ready, including that for emergency tracheostomy.
In the operation theatre, IV line was secured with 22-Gauge cannula connected to isolyte P solution. Heart rate, oxygen saturation, respiratory rate and electrocardiogram (ECG) were monitored. Head low position was given to prevent aspiration of abscess contents. The patient was premedicated with inj. midazolam 0.5 mg, inj. pentazocin 4 mg and inj. hydrocortisone 50 mg. In view of the anticipated difficult mask ventilation and intubation, an inhalational induction was planned. Preoxygenation was done for 3 minutes, and anaesthesia was induced with incremental doses of halothane in a mixture of 50% oxygen and 50% nitrous oxide. Under deep inhalational anaesthesia, direct laryngoscopy was done with external laryngeal manipulation to visualise the vocal cords. As Cormach-Lehane grade was 3, i.e. only tip of the epiglottis was visualised, 3.5 mm portex uncuffed endotracheal tube was intubated in the second attempt. The tube was fixed after confirming bilateral air entry. There was pus leak due to trauma during larygoscopy and intubation. After thorough suctioning, throat pack was done to prevent aspiration of blood, pus and secretions. Anaesthesia was maintained with halothane in oxygen and nitrous oxide.
Inj. atracurium 0.5 mg/kg was given. The patient was ventilated manually throughout the procedure. Intraoral drainage of the abscess was done and 10F size Foleys catheter was placed in the abscess cavity and the bulb inflated with 3ml distilled water [Figures and ]. Nasogastric tube was inserted. After the patient’s adequate breathing efforts were confirmed, she was reversed using 0.05 mg/kg neostigmine, 0.02 mg/kg atropine, and extubated. Postoperatively, the patient was conscious, alert, breathing adequately, maintaining saturation in room air and haemodynamically stable. The patient was shifted to postoperative ward.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.5, 'kg']}",30,28.5,31.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.5 kg. Hence, the patient's maintenance fluid is 7.5 kg * 4 mL/kg/hr = 30.0 mL/hr.
Hence, the patient's fluid maintenance is 30.0 mL/hr."
4714,22,Maintenance Fluids Calculations,physical,decimal,pmc-7718048-1,Extracted,"We describe a case of a 21-year-old obese Chinese man with underlying nephrotic syndrome (NS) secondary to renal biopsy-proven minimal change disease who suffered from a right middle cerebral artery territory infarct.
He was initially admitted to our hospital six months prior to stroke, with a complaint of generalized body swelling and shortness of breath for one month. Twenty months prior to the weakness of limbs, he received treatment in a private clinic, but subsequently defaulted. Clinical examination revealed anasarca.
His initial workup for NS revealed that his urea was 10.7 mmol/L, serum creatinine was 134 μmol/L, and serum albumin was 7 g/L. His urinalysis results showed protein 4+ and blood 2+. His 24-hour urine protein was 32.3 g/24 hours. Both kidneys were normal in size and echogenic, with preserved cortical thickness on ultrasound. The bipolar length of the right kidney was 10.3 cm and that of the left kidney was 10.4 cm. Ultrasound Doppler of bilateral kidneys showed no evidence of renal vein thrombosis. Autoimmune workup including ANA, Jo-1, La, Ro, U1RNP, Scl, and SM was negative. He had no history of illicit drug abuse or smoking. His hepatitis B, hepatitis C, and HIV serology were negative. Renal biopsy was planned upon improving his edematous state.
He required temporary haemodialysis alternate with ultrafiltration for 6-week duration due to fluid overload and worsening of kidney function (creatinine up to 282 μmol/L and urea of 17.3 mmol/L). He was started on prednisolone 80 mg per day, furosemide 80 mg three times per day, and cyclosporine 25 mg twice per day.
At the second month of treatment, his kidney function improved with the creatinine level of 97 μmol/L and urea of 9.9 mmol/L. He had weight reduction from 120 kg (BMI: 41.5 kg/m2) to 100 kg (BMI: 34.6 kg/m2). His haemodialysis was withheld. Renal biopsy was performed and was highly suggestive of minimal change disease. His medications were changed to furosemide 40 mg once per day, prednisolone tapering dose to 20 mg once per day, and cyclosporine 50 mg twice per day.
At the fourth month of treatment, his kidney function further deteriorated with the serum creatinine level of 264 μmol/L and urea of 9.0 mmol/L. His albumin was 12 g/L, and 24-hour urine protein was 19.8 g/24 hours. His weight increased to 115 kg (BMI: 39.8 kg/m2). The patient was admitted and reassessed. He was not responding to intravenous steroids and diuretics. His immunosuppressive medication was switched from cyclosporin to mycophenolate mofetil (MMF) 500 mg twice per day due to deterioration of renal function.
He visited us in the clinic at the fifth month of treatment, and he was unable to tolerate MMF due to nausea. He was started on tacrolimus 1 g twice per day. His albumin was 10 g/L, serum creatinine was 278 μmol/L, and 24-hour urine protein was 26.4 g/24 hours. Weight remained the same.
At the sixth month of treatment, he presented to the hospital with left hemiparesis. He was afebrile, vital signs were stable, Glasgow Coma Scale of 15/15, blood glucose was 6.0 mmol/L, and NIHSS score of 12 (left facial palsy: 2 marks, left upper limb: 4 marks, left lower limb: 3 marks, left side sensory: 1 mark, dysarthria: 1 mark, and inattention: 1 mark). Muscle power of the left upper limb was graded 0/5 and that of the left lower limb was 2/5, with reduced sensation over the left upper and lower limbs.
Blood investigation revealed: hemoglobin, 8.8 g/dL (normochromic and normocytic); platelet, 580 × 103/μL; WBC, 13.9 × 103/μL; urea, 6.0 mmol/L; creatinine, 316 μmol/L; INR, 1.2; PT, 15.8 sec; and aPTT, 15.8 sec. Venous blood gas revealed metabolic acidosis, with a pH of 7.25 and HCO3 of 13.7 mmol/L. Toxicology screening was not done.
Plain CT brain at 210 minutes poststroke onset showed a normal CT brain (), and he was given intravenous thrombolysis with alteplase of a dose of 0.9 mg/kg.
MRI and MRA brain scan at 375 minutes poststroke onset and 135 minutes post-rTPA thrombolysis revealed that he had a right middle cerebral artery territory infarct and stenosis at distal M1 segment of the right middle cerebral artery (Figures –). Mechanical thrombectomy was carried out with partial recanalization of M2 segment of the right middle cerebral artery.
His kidney function deteriorated further postcontrast when serum creatinine peaked at 528 μmol/L. He was intubated for respiratory distress as he developed fluid overload. After intubation, he was nursed in intensive care unit and required haemodialysis via a temporary femoral catheter. He also required a tracheostomy to sustain his airway.
He was further evaluated. He had normal C3 and C4 levels, and cANCA and pANCA were negative. Echocardiogram, electrocardiogram, and Doppler ultrasound of carotid arteries were normal. However, his repeated lupus anticoagulant (LA) titre was detected. Hence, the diagnosis of concomitant APS with NS was made. He was subsequently started on vitamin K antagonist (VKA) anticoagulant.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [115.0, 'kg']}",155,147.25,162.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 115.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (115.0 kg - 20 kg) = 155.0 mL/hr.
Hence, the patient's fluid maintenance is 155.0 mL/hr."
4715,22,Maintenance Fluids Calculations,physical,decimal,pmc-3030066-1,Extracted,"A 67-year-old man, 164.5 cm in height and 64.7 kg in weight, was admitted to the hospital for investigation of abnormal shadows on chest X-ray in both lungs. Approximately 3 months before admission, he was diagnosed with pancreatic ductal adenocarcinoma and underwent surgery, which consisted of a distal pancreatectomy, splenectomy, and left adrenalectomy. The patient did not have hypertension, diabetes mellitus, cardiovascular disease or other associated disorder. No abnormal findings were detected in the preoperative physical examination, electrocardiography, pulmonary function test or echocardiography. On admission, he had no symptoms related to respiration or speech. His chest X-ray and computed tomography scan revealed multiple pulmonary small nodules in both lungs. Hematogenous pulmonary metastasis of pancreatic ductal carcinoma was highly suspected, and pulmonary wedge resection of the left upper lobe by VATS was scheduled for tissue confirmation.
Surgery was performed under general anesthesia using a DLT (Bronchocath left 37F; Mallinckrodt Medical, Athlone, Ireland). We confirmed indirectly that the endotracheal and endobronchial cuffs were not overinflated by palpation of the pilot balloon. The correct placement of the tube was confirmed by fiberoptic bronchoscopy (FOB). After the patient's position was changed to right lateral decubitus, the inflation of the endotracheal and endobronchial cuffs were reconfirmed as above, and the placement of the tube was again confirmed by FOB. We also confirmed that the cuffs were not overinflated before and after one-lung ventilation. Anesthesia was maintained with 2-3% isoflurane with O2 and air, 1 L/min each during two-lung ventilation. One-lung ventilation was provided in volume control mode with 400 ml tidal volume. The FiO2 was 1.0, respiratory rate was 12 breaths/min and peak airway pressure was maintained at less than 18 cmH2O. The left upper lobe wedge resection was performed without complications. During the operation, the surgeon confirmed that the left recurrent laryngeal nerve was left untouched and remained preserved. The operation time was approximately 1 hour.
At the end of the surgery, glycopyrrolate 0.4 mg and pyridostigmine 15 mg were given after confirming 4 twitches in train-of-four (TOF) stimulation of the ulnar nerve. The tidal volume was 150-250 ml, and the patient was able to open his eyes following a verbal order, so extubation was performed. Severe stridor was immediately heard and the patient became irritable. The TOF ratio was greater than 0.9 at that time. Thinking this was due to upper airway spasm following the stress of extubation or vocal cord edema, we applied a jaw thrust maneuver with 10 L/min of oxygen via facial mask. The tidal volume was checked and was half of the pre-extubation level. Both lung sounds were decreased, but the peripheral arterial oxygen saturation by pulse oximetry (SpO2) was 100%. A salbutamol sulfate puff was applied twice. In addition, solumedrol 125 mg and dexamethasone 10 mg were intravenously injected. Five minutes later, the stridor had not abated, but the patient seemed to breathe well without the jaw thrust maneuver, so he was transferred to the postanesthesia care unit (PACU) without reintubation.
In the PACU, an electrocardiogram, non-invasive blood pressure, and SpO2 were monitored, and 10 L/min O2 was applied to the patient via facial mask. Severe stridor developed, however, although the SpO2 remained at 100%. We began to suspect that the patient might have other reasons besides laryngeal spasm or vocal cord edema for his stridor. An otolaryngologist examined the patient with a fiberoptic nasopharyngolaryngoscopy and diagnosed him with bilateral vocal cord paralysis of median type with a 1 mm gap. The otolaryngologist also observed that the vocal cords were not edematous. We planned a tracheostomy, but an arterial blood gas analysis showed mild hypercapnia and normal arterial oxygen pressure (PaCO2 54 mmHg, PaO2 223 mmHg), and the surgeon persistently opposed any invasive procedure. We decided to monitor him in the intensive care unit (ICU), keeping in mind the possibility of an emergency tracheostomy.
In the ICU, 1 mg of midazolam was given intravenously by a pulmonologist, based on his experience with previous patients. After the midazolam injection, the patient became sedated and the stridor diminished. Two hours later, the patient became fully awake and was able to say ""Ah"". The stridor had completely vanished three and a half hours after extubation. The otolaryngologist's laryngoscope examination was again performed. Bilateral vocal cord paralysis was present, however, and identical to the patient's last examination. The next day, inspection of the vocal cords was again performed and revealed fully recovered vocal cord movement. Thereafter, the patient was transferred to the general ward and discharged six days after surgery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [64.7, 'kg']}",104.7,99.465,109.935,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 64.7 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (64.7 kg - 20 kg) = 104.7 mL/hr.
Hence, the patient's fluid maintenance is 104.7 mL/hr."
4716,22,Maintenance Fluids Calculations,physical,decimal,pmc-5624261-1,Extracted,"A 66-year-old male patient with a history of CD presented to our clinic with chronic abdominal pain and diarrhea. He had been experiencing intermittent crampy, diffuse abdominal pain associated with 3–4 daily episodes of loose bowel movements for the previous 3 months. Since the diagnosis of CD 5 years earlier, he had intermittently been adherent to a GFD. On questioning, he stated that he had been completely nonadherent to GFD for the previous 5 months. His weight had decreased from 175 to 165 lb (5.7% loss) over the previous 3 months.
A physical examination showed normal results except for mild diffuse abdominal tenderness. A laboratory workup revealed a white blood cell count of 7,900/µL and a hemoglobin level of 13.2 g/dL, with the remainder of the parameters within normal limits. Stool Clostridium difficile PCR and ova, parasites, and cultures were all negative. Celiac serology was found to be positive for IgA antiendomysial antibodies (titer 1:160) and IgA tissue transglutaminase (87 positive >8), reflecting his dietary noncompliance.
A CT scan of the abdomen showed a 5 × 4 cm mass which seemed to be arising from the second part of the duodenum (Fig. ). It was unclear if it was arising from the duodenum or was a mesenteric node close to the wall. Given this uncertainty, an esophagogastroduodenoscopy was performed, which revealed duodenal mucosal atrophy; however, no mass was seen invading the lumen. Endoscopic ultrasound revealed a hypoechoic, poorly demarcated, heterogeneous 53 × 42 mm mass which was thought to be arising from the duodenal wall at the junction of the second and third part. Fine needle aspiration was performed, and histology revealed clusters of epithelioid histiocytes with nucleomegaly, nuclear pleomorphism in a background of macrophages, and multinucleate giant cells (Fig. , Fig. ). This finding was consistent with a reactive inflammatory mass comprising BSCs. There was no evidence of systemic granulomatous diseases such as sarcoidosis, tuberculosis, or fungal infection in this patient.
It was concluded that an inflammatory reaction because of uncontrolled CD resulted in the formation of this walled-off inflammatory mass. It was decided to monitor this mass with periodic CT scans, and the patient was advised to strictly adhere to a GFD. Follow-up CT scans of the abdomen at 9 and 16 months revealed that the mass had shrunken to 3 × 3 cm and 1 × 1 cm (Fig. ), respectively. The patient reported strict adherence to the GFD during this period and reported no recurrence of symptoms of the disease.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [165.0, 'lbs']}",114.84268,109.10055,120.58481,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 165.0 lbs so this converts to 165.0 lbs * 0.453592 kg/lbs = 74.84268 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (74.84268 kg - 20 kg) = 114.84268 mL/hr.
Hence, the patient's fluid maintenance is 114.84268 mL/hr."
4717,22,Maintenance Fluids Calculations,physical,decimal,pmc-5278591-1,Extracted,"A 23-year-old male was brought to the General Hospital at Mahad, with complaints of difficulty in speaking, inability to swallow saliva, and continuous spitting. He strongly rejected taking sips of water and was afraid of water like a hydrophobic patient. He gave no history of snake bite or ptosis. The posterior pharynx could not be visualized, even after repeated attempts with depression of the tongue with a spatula. The uvula and surrounding structures, including the soft palate, were edematous. The uvula was touching the base of the tongue [].
He was weighing 80 kg, conscious cooperative and well oriented. His blood pressure was 120/80 mmHg; pulse was 88 beats/min and regular. His extremities were warm, the electrocardiograph was within normal limits, and SpO2 was 98% on ambient air. The patient said that he ate only Chinese triple fried rice for dinner the previous night 10 hours earlier. Within an hour of eating, he had giddiness, sweating, and itching all over the body which subsided without any medication. Two hours earlier he had woken up due to difficulty in swallowing and speaking out a few words. He communicated with his family with hand gestures regarding his inability to speak and swallow. There was no history of allergy or bronchial asthma.
The hemoglobin was 14 mg/dl, white cell count 13,000 per cu mm (normal 5000–10,000), eosinophils 1% (normal 1–9), neutrophils 90.9%, random blood sugar 135 mg/dl (normal 70–140), and serum IgE 917.021 IU/ml (normal 3–188).
The patient was admitted and given intravenous crystalline solution of 40mg methyl prednisolone and was monitored continuously for oxygen saturation.
There was no improvement over half an hour, so 0.30 mg of adrenaline was administered as a deep intramuscular injection over the lateral side of the thigh. The swelling of the uvula and surroundings gradually regressed. The patient no longer had drooling of saliva and was able to speak a few words. His throat looked angry around the uvula and surrounding.
On account of raised leukocyte count with neutrophilia, the patient was treated with oral Amoxycillin with clavulinate. At 16 h after the initiation of treatment, he started normal oral communication and was able to swallow liquid.
On the following day, there was a gradual reduction in the size of the uvula and surrounding inflammation. 2 days from admission, the uvula and surrounding structures including the palate returned to normal and he could swallow solids [].","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [80.0, 'kg']}",120,114,126,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 80.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (80.0 kg - 20 kg) = 120.0 mL/hr.
Hence, the patient's fluid maintenance is 120.0 mL/hr."
4718,22,Maintenance Fluids Calculations,physical,decimal,usmle-625,Extracted,"A 7-year-old boy is brought to the physician by his parents because of a 4.5-kg (10-lb) weight loss during the last 3 months. During this period, he has complained of abdominal pain and fullness, and his parents feel that he has been eating less. His parents also report that his urine has appeared pink for several weeks. He has been performing poorly in school lately, with reports from teachers that he has not been paying attention in class and has been distracting to other students. He was born at term and has been healthy except for a history of several infantile seizures. His vital signs are within normal limits. He is at the 60th percentile for height and 20th percentile for weight. Physical examination shows a palpable abdominal mass, abdominal tenderness in the left upper quadrant, and left costovertebral angle tenderness. There are several ellipsoid, hypopigmented macules on the back and legs and a 4-cm raised plaque of rough, dimpled skin on the right lower back that is the same color as the surrounding skin.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.5, 'kg']}",18,17.1,18.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.5 kg. Hence, the patient's maintenance fluid is 4.5 kg * 4 mL/kg/hr = 18.0 mL/hr.
Hence, the patient's fluid maintenance is 18.0 mL/hr."
4719,22,Maintenance Fluids Calculations,physical,decimal,usmle-8558,Extracted,"A 57-year-old man presents to his physician with dyspnea on exertion and rapid heartbeat. He denies any pain during these episodes. He works as a machine operator at a solar panels manufacturer. He has a 21-pack-year history of smoking. The medical history is significant for a perforated ulcer, in which he had to undergo gastric resection and bypass. He also has a history of depression, and he is currently taking escitalopram. The family history is unremarkable. The patient weighs 69 kg (152 lb). His height is 169 cm (5 ft 7 in). The vital signs include: blood pressure 140/90 mm Hg, heart rate 95/min, respiratory rate 12/min, and temperature 36.6℃ (97.9℉). Lung auscultation reveals widespread wheezes. Cardiac auscultation shows decreased S1 and grade 1/6 midsystolic murmur best heard at the apex. Abdominal and neurological examinations show no abnormalities. A subsequent echocardiogram shows increased left ventricular mass and an ejection fraction of 50%.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [69.0, 'kg']}",109,103.55,114.45,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 69.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (69.0 kg - 20 kg) = 109.0 mL/hr.
Hence, the patient's fluid maintenance is 109.0 mL/hr."
4720,22,Maintenance Fluids Calculations,physical,decimal,pmc-8107897-1,Extracted,"A 47-year-old Chinese man presented to the hospital with frequent watery diarrhoea.
The patient had no history of prior illness and no family history of any similar disease.
The patient’s symptoms had started 3 mo prior with frequent watery diarrhoea (4-5 times/d). For nearly a month, there was apparent blood in the diarrhoea and positive faecal occult blood with acid regurgitation, eructation, occasional nausea, and a weight loss of 10 kg within 2 mo. The patient was treated with symptomatic therapies, such as spasmolytics and antibiotics, which were ineffective in alleviating his symptoms.
The patient had no history of prior illness and no family history of any similar disease.
A physical examination revealed marked alopecia; brownish macular pigmentation of the facial region, palms and soles; and onychodystrophy of the fingernails and toenails (Figure ).
The laboratory findings included a positive faecal occult blood showing 0-2 red blood cells/haptoglobin, an albumin concentration of 32.7 g/L (normal range 40-55 g/L), and cytoplasmic antinuclear antibody positivity with a titre of 1:320.
Gastroscopy revealed multiple polyps in the stomach and duodenum (Figure ). Endoscopic ultrasonography revealed diffuse thickening of the gastric mucosa to 8.5 mm (i.e. massive enlargement of the mucosa and submucosa), and the polyps originated from the mucosa, which was internally hyperechoic and inhomogeneous (Figure ). Colonoscopy revealed numerous polyps occupying the colonic and rectal mucosa (Figure ).
Histological examination of biopsy specimens obtained from the colon and the stomach was consistent with hyperplastic polyps, and immunoglobulin G 4 staining was negative.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.0, 'kg']}",40,38,42,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.0 kg - 10 kg) = 40.0 mL/hr.
Hence, the patient's fluid maintenance is 40.0 mL/hr."
4721,22,Maintenance Fluids Calculations,physical,decimal,pmc-8081011-1,Extracted,"A 13-year-old Syrian male presented to the pediatric gastroenterology clinic with a history of recurrent episodes of epigastric and peri-umbilical abdominal pain for 3 years, which were exacerbated by food and partly controlled with analgesics. The episodes were associated with anorexia and pallor. There was no significant past medical or family history. During that period, the child was diagnosed with iron deficiency anemia [hemoglobin (Hb) 8.9 g/dl, Mean corpuscular volume (MCV) 69 fl] with no response to iron supplemental therapy. Anti-gliadin antibodies IgA, IgG (AGA IgA, IgG), Anti-tissue transglutaminase Antibodies IgA (anti-TTG IgA) were markedly elevated (more than 100 U/mL). An Esophagogastroduodenoscopy (EGD) had been performed a year pirior to admission, with normal findings, and the duodenal biopsies had shown CeD type 3a according to the Marsh classification (partially atrophic villi with lymphocytic exocytosis at 56 lymphocytes/100 enterocytes in the lamina properia) (). The patient was treated with a gluten-free diet without improvement in abdominal pain.
On physical examination, his body weight was 23 kg (SD –4) and his height was 137 cm (SD –2). He was pale, but his observations were stable and he appeared generally well. The patient underwent multiple investigations that showed hypochromic microcytic anemia [Hb 8.6 g/dl, MCV 68 fl] associated with an inflammatory respond [C- reactive protein (CRP) 81 mg/l, erythrocyte sedimentation rate (ESR) 40 mm at the end of 1st hour] and hypoalbuminemia (Alb 3,2 g/dl). AGA (IgA, IgG) and anti-TTG IgA were within the normal range on this admission. Investigations including hepatic and renal function, blood glucose, urinary investigations and an abdominal ultrasound were all normal. Therefore, an EGD was repeated showing diffuse scattered nonbleeding ulcers, covered with fibrinous membranes in the esophagus, antrum, and duodenum. Histological examination of stomach biopsies showed chronic active ulcerated gastritis with diffuse lymphocytic infiltration in the lamina properia and stomach abscesses (). Duodenal biopsies showed uncertain chronic duodenal mucosa inflammation. The ileocolonoscopy showed regions of congestive mucosa in the rectum, colon, caecum, and ileum with longitudinal ulcers alternating with healthy mucosa (). Histological study of colonic and ileal biopsies showed focal erosions, crypitis, crypt abscesses with fissures, and non-caseating granulomas which correlates with active Crohn’s disease ().
The patient was treated with a gluten-free, low fiber, high caloric diet, and a course of oral corticosteroid (Prednisolone 2 mg/kg/day) with progressive tapering after 3 weeks.
After about one month of initiation treatment, the patient had significant clinical improvement. His symptoms improved markedly, and he gained 3 kg in weight. We then added 5-aminosalicylic acid (Mesalamine) 25 mg/kg/day, vitamins, and iron supplements.
We followed the patient for 3 years after initial treatment. During these years, the steroid was gradually reduced until it was discontinued after 6 months of treatment at full dose. Currently, the patient is treated with a gluten-free, low fiber, high caloric diet, mesalamine 25 mg/kg/day and vitamins. His CD remains in remission and he now has a normal growth rate with normal pubertal development.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [23.0, 'kg']}",63,59.85,66.15,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 23.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (23.0 kg - 20 kg) = 63.0 mL/hr.
Hence, the patient's fluid maintenance is 63.0 mL/hr."
4722,22,Maintenance Fluids Calculations,physical,decimal,pmc-6362890-1,Extracted,"A 70-year-old man underwent a colonoscopy after having episodes of bright red stool per rectum and diarrhea. A lower rectal cancer was diagnosed based on a histology obtained through a biopsy of the rectal lesions (Rb, T2N0M0 cStageI (UICC Classification, 7th ed)). The past medical history was notable for hypertension untreated and smoking 50 pack year. His height was 173 cm, and weight was 73 kg with body mass index of 24.4. The creatinine clearance was 87 ml/min. Although the preoperative history talking failed to recognize the symptoms of intermittent claudication and sensory impairment of his lower extremities, a preoperative contrast enhanced computed tomography (CT) scan demonstrated a significant stenosis in bilateral external iliac artery due to arteriosclerosis obliterans (ASO) (Fig. ) and occlusions of bilateral internal iliac artery. There was no coagulation abnormality in his blood test or atrial fibrillation on an electrocardiogram.
He underwent an elective laparoscopic abdominoperineal resection with a lithotomy position. There was no vascular injury or compression with laparoscopic forceps as far as we were able to recognize retrospectively based on the laparoscopic video and the memory. The duration of surgery was 4 hours and 48 minutes. Blood loss was estimated 100 ml, the urine volume was only 50 ml during the operation. In-out balance during operation divided body weight and time of operation was 6.38 ml/kg/h. The patient reported a severe pain in the left leg, when he woke up post-operatively. The left leg was pale and cold, associating sensory abnormality and motor dysfunction; left pedal and popliteal pulses were absent. A CT scan revealed the contrast interruption of left common iliac artery (CIA) over 11.5 cm and suspected to be due to an arterial thrombosis (Fig. ). Under the local anesthetic technique, the left femoral artery was exposed and performed thrombectomy with a 5Fr Fogarty catheter. After a new clot was removed, aortography revealed persistent stenosis in left iliac artery. Consequently, a Percutaneous transluminal angioplasty (PTA) with stent (Express LD 8 × 37 mm) was added (Fig. ) via left femoral artery. Blood perfusion in his left leg improved markedly immediately post PTA. The patient was transferred to the intensive care unit for two days due to the complications with a rhabdomyolysis (creatinine phosphokinase up to 23 598 IU/l). The patient started walking 5 days post-surgery, however, the patient was left with the numbness in his left lower leg. A heparinization had been commenced on the postoperative day 1, then this was switched to the cilostazol prior to the discharge for home. We note that the patient continued reporting the left lower leg numbness even one year past the surgery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [73.0, 'kg']}",113,107.35,118.65,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 73.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (73.0 kg - 20 kg) = 113.0 mL/hr.
Hence, the patient's fluid maintenance is 113.0 mL/hr."
4723,22,Maintenance Fluids Calculations,physical,decimal,pmc-7448144-1,Extracted,"A 57-year-old man presented with a 3-week history of yellow sclera and dark urine. He had undergone a 5 kg weight loss over the past three months. Ultrasound examination performed at a local hospital showed enlargement of the intra and extrahepatic bile duct. Contrast-enhanced computed tomography (CT) showed a lesion in the duodenal ampullary region. The patient was referred to our hospital for further treatment.
The patient had no family history of cancer but he had been a smoker and drinker for more than 50 years. Physical examination showed mild yellow sclera and upper abdominal tenderness. Laboratory test findings were as follows: total bilirubin, 90.8 µmol/l (normal range 0–21.0 µmol/l); conjugated bilirubin 81.3 µmol/l (normal range : 0–6.8 µmol/l); unconjugated bilirubin 9.5 µmol/l (normal range : 5.1–21.4 µmol/l); aspartate aminotransferase, 111 U/l; (normal range: 13.0–35.0 U/l); alanine aminotransferase, 136 U/l; (normal range: 7.0–40.0 U/l); alkaline phosphatase, 882 U/l (normal range: 50.0–135.0 U/l). The serum levels of several common tumour markers were within normal ranges. Abdominal triple-phase contrast CT showed enlargement of the intra and extrahepatic bile ducts and the presence of a local nodule at the end of the common bile duct which was indistinguishable from the adjacent head of the pancreas and duodenum. There was a strong possibility that the lesion was ampullary carcinoma ().
A pancreaticoduodenectomy was performed and a cauliflower-like mass (4 × 5 cm) invading the ampulla of Vater was discovered (). An enlarged lymph node, approximately 2 × 2 cm was found beside the left renal artery. Pathology of the resected specimen showed that the tumour had two elements: Small cell neuroendocrine carcinoma (NEC) was the main component (approximately 70%) and the remainder was a moderately differentiated adenocarcinoma. (). The mitotic rate of the small cell NEC component was 20 cells per 10 high power fields (). The tumour had infiltrated the duodenum and the pancreatic parenchyma. Lymphatic and venous but no apparent perineural infiltration was seen. The local mucosal epithelium at the margins of the pancreas and the common hepatic duct showed mild to moderate dysplasia.
Surgical resection margins were free of neoplastic lesion. The small cell NEC components were recognized on standard histology and confirmed with immunohistochemistry by detection of specific endocrine markers (i.e., synaptophysin and CD56) (). There was a negative reaction to Chromogranin A (CgA). The Ki-67 labelling index was 40% indicating strong proliferative activity (). The adenocarcinoma neoplastic cells showed positive expression of pan-cytokeratin (CK-pan), but were negative for other neuroendocrine markers such as CD56, CgA and synaptophysin. The tumour was classified as a grade G3 NEC because its mitotic and Ki-67 labelling indices were high and the patient was classified as having a T3N1M0 (Stage IIIB) cancer.
According to the histological findings, the diagnosis of MANEC in the ampulla of Vater was confirmed. The patient refused chemotherapy and died from metastatic disease 14 months after the initial surgery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.0, 'kg']}",20,19,21,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.0 kg. Hence, the patient's maintenance fluid is 5.0 kg * 4 mL/kg/hr = 20.0 mL/hr.
Hence, the patient's fluid maintenance is 20.0 mL/hr."
4724,22,Maintenance Fluids Calculations,physical,decimal,pmc-6894892-1,Extracted,"A 69-year-old female, with height 5’6” and weight 56.7 kg, without significant past medical history, originally presented for bilateral skin-sparing mastectomies/right-sided axillary lymph node dissection/expander placement due to right-sided breast lobular carcinoma.
Bilateral T4 single-injection paravertebral blocks were performed preoperatively using 3.5 cm 22G TuohyTM needles under standard landmark technique with 20 ml 0.2% ropivacaine and 20 mg methylprednisolone acetate on each side. General anesthesia with an endotracheal tube was induced. During this 7.5-hour-surgery, the patient received 300 mcg fentanyl, 1.4 mg hydromorphone, 50 mg ketamine, and 165 mcg dexmedetomidine. Upon emergence, the patient reported no pain. She continued to have no pain until postoperative day (POD) 2 on discharge. She was discharged home with a 10-day course of pregabalin 100 mg twice daily, diazepam 5 mg every eight hours as needed, and oxycodone 5 mg (total 30) every four hours as needed. Telephone correspondence with the patient revealed that she continued to have no need for oxycodone at home until POD 7 when diffuse pain slowly came back. She experienced such a high level of satisfaction with the paravertebral block that before her subsequent bilateral implant exchange (four months after the original surgery), she called the anesthesia department to ensure she would receive the same block.
For the second surgery, she indeed received bilateral T4 paravertebral blocks under the same technique except with 20cc 0.25% bupivacaine and 4 mg dexamethasone sodium phosphate on each side. General anesthesia with endotracheal tube was again induced and the patient received 150 mcg fentanyl and 0.4 mg hydromorphone intraoperatively for the 1.5-hour surgery. She was discharged home on the day of surgery with tramadol 50 mg (total 30) every six hours as needed. On telephone follow-up, the patient stated that she needed to take opioids much earlier, on POD 1 following the secondary surgery instead of POD 7 in the original surgery, to be precise. She had no residual sensory or motor deficits after block wore off for each surgery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [56.7, 'kg']}",96.7,91.865,101.535,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 56.7 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (56.7 kg - 20 kg) = 96.7 mL/hr.
Hence, the patient's fluid maintenance is 96.7 mL/hr."
4725,22,Maintenance Fluids Calculations,physical,decimal,pmc-3237174-1,Extracted,"Miss AB, a 20-year-old female, attended our outpatients’ department (OPD) on 16 August 2007 with complaints of lump lower abdomen for last two months []. She also complained of nausea and vomiting for the last few days. She had history of primary amenorrhea and poorly developed secondary sexual characteristics. There was no history of cyclic abdominal pain, hormonal intake, radiation exposure or any chemotherapy. There was no history of significant trauma and medical or surgical illness. There was no history of any major disease in the family. She is the second child of her mother being delivered vaginally at the age of 29 years. The mother reported that the pediatrician after examining the baby told the parents that the external genitalia of the baby were inadequately developed and advised the mother to return after one year if there was no adequate development. Over time they did not turn up and she started growing up as a female although with very poor development of her secondary sex characters. She has one brother and one sister. All of them attained puberty normally and are enjoying good health.
On general examination her condition was fair, height 146 cm and weight 42 kg. She had mild pallor. There was no cyanosis, clubbing, edema, obesity, acne, hirsutism, thyroid swelling or cushingoid features; her breast was small, underdeveloped with hypopigmented areola (Tanner Stage II). There was no axillary or pubic hair. Her systemic examination including chest and Cardiovascular system were within normal limits. Per abdomen examination revealed lump in lower abdomen, there was no visible swelling in the inguinal region. Her external genitalia were infantile. There were hypertrophied clitoris resembling like a micropenis. She had inadequately developed vulva with small vaginal pit [].
Her blood group was A +ve, H aemoglobin percentage 7.5 g% and all other routine blood tests were within normal limits. Her S. AFP was 48815.2 IU/ml (normal range <7.22 IU/ml), serum beta hCG=1.24 mIU/ml (normal range <6.15 mIU/ml), serum prolactin and thyroid profile were within normal limits, serum testosterone level 924 ng/dl (normal range 300-1000 ng/dl), serum estradiol 31.18 pg/ml, serum calcium 7.6 mg% and Parathyroid hormone level 9.69 pg/ml. Karyotyping showed 46 xy pattern. A whole abdomen ultrasonography (USG) showed no uterus and ovaries. There was a lower abdominal mass approx 15 cm × 15 cm × 10 cm, probably neoplastic changes in an intra-abdominal testis, with mild ascites.
A USG-guided fine needle aspiration cytology (FNAC) from the tumor mass reported the possibility of non-seminomatous germ cell tumor, possibly embryonal carcinoma. Smear from ascitic fluid was suggestive of metastatic adenocarcinoma. Computed tomography (CT) scan of brain revealed normal findings. PA view chest X-ray was normal.
A diagnosis of Stage IIIC malignant germ cell tumor (embryonal carcinoma) of undescended (intra-abdominal) gonad was made. The tumor board of our Institute decided to go in for laparotomy following a few courses of neoadjuvant chemotherapy.
She received three cycles of neoadjuvant chemotherapy (Regime Bleomycin, Etoposide and Cisplatin). Post chemotherapy an assessment of the disease status was done by a CT scan whole abdomen, which revealed an oval-shaped residual solid mass arising from the left side of the pelvis and externally to the lower abdominal cavity; the size of the mass was 12 × 7.2 cm × 9.5 cm. No adjacent organ infiltration was noted. No ascitis, vascular or ureteric encasement was seen. No hepatic secondary or significant lymphadenopathy was noted. Serum AFP came down to 3.4 IU/ml and S. B. hCG: 3.24 mIU/ml. After proper counseling and written and informed consent, laparotomy was done on 10 December 2007 under general anesthesia. The findings were: left testis was enlarged, 15×10 cm, right testis was of normal size, no uterus/ovaries detected.
At laparotomy (L) orchidectomy with removal of tumor, (R) orchidectomy, omentectomy and appendisectomy was performed [Figures –]. Histopathological examination of the excised specimens: Left testis: embryonal cell carcinoma, Right testis– normal, omentum – metastatic deposit, appendix- chronic appendicitis. Her postoperative recovery was uneventful. She was discharged on 18– December 2007 and advised to attend the Gynecology OPD after three weeks at which her S AFP level was 2.3 IU/ml.
Postoperatively she received two more cycles of adjuvant chemotherapy of the same regime.
On 25 February 2008 repeat total S. testosterone was 120 ng/dl and free testosterone 940 ng/dl.
Over four months after operation she was doing well and her secondary sexual characters were developing (breast development Tanner Stage III) after taking hormonal supplementation advised by the endocrinologist. She is on regular follow-up, she attended our OPD for checkup on 20 October 2009 with no evidence of disease clinically, USG was within normal limits and normal S. AFP.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [42.0, 'kg']}",82,77.9,86.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 42.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (42.0 kg - 20 kg) = 82.0 mL/hr.
Hence, the patient's fluid maintenance is 82.0 mL/hr."
4726,22,Maintenance Fluids Calculations,physical,decimal,pmc-5073164-2,Extracted,"A 17-year-old female patient was admitted due to cough, chest pain, dyspnea, and swelling in the abdomen. On physical examination, height was 140 cm (–3.5 SD), and weight was 43 kg (–2 SD). She had severe short stature and 2 years retarded bone age. She was pale and somnolent. Her score on the Glasgow Coma Scale was 11 points. She was dyspneic and cyanotic. Oxygen saturation was 65%, respiratory rate was 24/min, and pulse rate was 120/min. She had hypotension (80/60 mmHg) and subfebrile fever (37.4℃). Her mucous membranes were dry. She had dry skin, sparse hair, and goiter. Cardiovascular examination revealed deep heart sounds. A chest X-ray showed a ""tents heart"" (). On echocardiography, a massive PE was found. She was taken to undergo urgent pericardiocentesis, removing 1,000 mL of fluid. Blood investigations, including complete blood count, erythrocyte sedimentation rate, and serologic markers of viral pathogens and autoimmune diseases, were within normal limits. All work up of the fluid for the etiology of the PE was normal. Although pericardiocentesis was performed, hypotension did not recover. Thyroid function analysis showed raised TSH (>100 µU/mL; normal range, 0.35–5 µU/mL), decreased fT3 (0.9 pg/mL; normal range 2.3–5 pg/mL), and decreased fT4 (<0.25 ng/dL; normal range, 0.8–2 ng/dL) (). Antithyroglobulin antibody (87 IU/mL) and anti-TPO (860 IU/mL) were positive. Thyroid USG showed thyroiditis. After thyroid replacement therapy was started with an oral formulation, because intravenous thyroxine was unavailable in our country, hypotension and other complaints were resolved. We were unable to follow up her, because she did not apply to our outpatient clinic.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [43.0, 'kg']}",83,78.85,87.15,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 43.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (43.0 kg - 20 kg) = 83.0 mL/hr.
Hence, the patient's fluid maintenance is 83.0 mL/hr."
4727,22,Maintenance Fluids Calculations,physical,decimal,pmc-6200485-1,Extracted,"A 69-year-old female patient (148 cm; 45 kg; American Society of Anesthesiologists physical status III) was scheduled to undergo bipolar hip arthroplasty for a fracture of the neck of femur on the left side. She had undergone a left partial mastectomy at the age of 67 and was diagnosed to have metastatic disease of the lumbar spine owing to breast cancer at the age of 68. She was hypertensive and had severe heart failure with an ejection fraction of 33%.
We were reluctant to administer spinal anesthesia because of lumbar spine metastasis. Besides, optimal pain management was required in the perioperative period because of severe heart failure. Therefore, we decided to administer a peripheral nerve block combined with sedation. The extent of analgesia required for the surgery involved block of the femoral and the LFN s. Therefore, we performed a fascia iliaca block. In contrast to the conventional approach (inguinal or infra-inguinal), we used the new supra-inguinal approach.
The patient had a baseline blood pressure of 130/64 mmHg, heart rate of 66 beats/min, and oxygen saturation of 97% upon arrival in the operating room. She was positioned supine, followed by standard monitoring with electrocardiography, pulse oximetry, and noninvasive blood pressure. Supplemental oxygen was administered by face mask at 3l/min. A high-frequency linear array transducer was placed horizontally at the left inguinal region and moved cranially by a few centimeters (Fig. ). A 20-gauge, 8-cm nerve block needle was advanced superficial to the iliac muscle by ultrasound guidance (Fig. ). A local anesthetic solution of 20 mL of 0.5% levobupivacaine was administered superficial to the iliac muscle after infiltration anesthesia (Fig. ). After 20 minutes, analgesia was confirmed along the distribution of the femoral and the LFN s. We used an infusion of dexmedetomidine (0.2–0.7 μg/kg/h) for sedation during the procedure. No additional analgesia was used in the intraoperative period.
No additional analgesia was required in the postoperative period. Rehabilitation was commenced from the day after surgery. The patient was discharged after 2 weeks.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [45.0, 'kg']}",85,80.75,89.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 45.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (45.0 kg - 20 kg) = 85.0 mL/hr.
Hence, the patient's fluid maintenance is 85.0 mL/hr."
4728,22,Maintenance Fluids Calculations,physical,decimal,pmc-7718669-1,Extracted,"A 14-year-old previously healthy male was admitted with a 3-week history of daily emesis, constipation, and lethargy. He had a decreased appetite and 3 kg weight loss in the preceding weeks. He described vague periumbilical pain and his family noticed a recent depressive change in his mood, including a fatigued appearance, low mood, and withdrawn behaviour. He had no joint or bone pain and denied fever or night sweats. Past medical history was unremarkable. He was on no medications. The family had recently immigrated from the Philippines one-week prior to the onset of symptoms. On exam, he appeared unwell and cachectic with a weight of 37 kg (-2.1 standard deviation (S.D.)) and a body mass index (BMI) of 14.1 kg/m² (<-3 S.D.). He was alert, oriented and cooperative. Neurological exam was unremarkable with normal deep tendon reflexes, bilateral flexor plantar reflexes, a normal gait and normal strength. A large, irregular, tender, mobile abdominal mass of 10 × 5 cm was palpable in the left lower quadrant.
Initial laboratory testing demonstrated severe hypercalcemia and hypophosphatemia, with a corrected total serum calcium of 4.30 mmol/L (N: 2.14–2.65 mmol/L) and a phosphate of 0.58 mmol/L (N: 0.74–1.52 mmol/L). Initial serum intact parathyroid hormone (PTH) was elevated at 51.70 pmol/L (N: 1.30–6.80 pmol/L), later peaking at 70.2 pmol/L. Additional biochemical evaluation on presentation is provided in Table .
Given the palpable mass and reported symptoms of emesis and constipation, a plain film abdominal radiograph was performed on admission to evaluate the abdominal mass and assess for possible obstruction. This identified large fecal loading of the colon and a lytic lesion within the left iliac wing (Fig. ). Subsequent computed tomography (CT) and magnetic resonance imaging (MRI) imaging showed the lesion arising within the bone, measuring 13 × 5.1 × 5.8 cm and a scalloped appearance with a T2 intense soft tissue component slightly projecting beyond the anterior table of the iliac bone (Fig. ). Thyroid ultrasound and Nuclear Medicine technetium 99 m Sestamibi scan were consistent with the identification of a solitary left superior parathyroid adenoma (Fig. ).
No further bony lesions were identified with full body skeletal survey radiographs and scintigraphy. Renal ultrasound was unremarkable with no nephrocalcinosis nor nephrolithiasis. Bone mineral densitometry (BMD) demonstrated lumbar spine, whole body and left distal forearm Z-scores of -0.2, -1.1, and − 1.7, respectively.
CT guided core needle biopsy of the iliac bone lesion was performed and underwent histological assessment demonstrating viable bone surrounded by moderately cellular spindle cells with hemosiderin, hemorrhage, and rare osteoclast-like giant cells, consistent with osteitis fibrosa cystica (Fig. ).
Prior to surgical treatment, hypercalcemia was treated with intravenous (IV) normal saline, multiple doses of subcutaneous (SC) calcitonin and a single dose of IV Zoledronic acid (0.025 mg/kg). The patient underwent surgical excision of a left superior parathyroid gland (2.0 × 1.6 × 0.4 cm; 0.9 g) with histology consistent with a parathyroid adenoma (Fig. ). The postoperative course was complicated by prolonged, recurrent hypocalcaemia with a total serum calcium nadir of 1.98 mmol/L, consistent with “hungry bone syndrome”. He required IV and oral replacement of calcium for 6 days. He was later discharged to home with oral supplementation of calcium carbonate and cholecalciferol.
In the subsequent 8 months post-parathyroidectomy, his weight increased 17 kg to 54 kg (-0.4 S.D.) and BMI to 19.8 kg/m² (0.0 S.D.). Serum biochemistry was maintained with gradual weaning and discontinuation of supplementation of calcium and vitamin D; serum total calcium 2.43 mmol/L, phosphate 1.66 mmol/L, and PTH 6.2 pmol/L. Repeat pelvic MRI within 12-months post-parathyroidectomy demonstrated complete resolution of pelvic lesion.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [37.0, 'kg']}",77,73.15,80.85,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 37.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (37.0 kg - 20 kg) = 77.0 mL/hr.
Hence, the patient's fluid maintenance is 77.0 mL/hr."
4729,22,Maintenance Fluids Calculations,physical,decimal,pmc-2438313-1,Extracted,"A 45-year-old male patient experienced an epigastric ache and distended stomach for 7 years. During abdominal ultrasonography (USG), a tumor was diagnosed in the right suprarenal fossa. He did not use any drugs and there was no characteristic of past medical and family illness history. He was 1.74 cm and weighted 81 kg, with a body mass index (BMI) of 26.5 kg/m2. His right hand tension arteriel was 110/70 mmHg and his left hand tension arterial was 115/70 mmHg; when standing, these values were 110/70 and 110/70 mmHg, respectively. Heart rate was 80 beats/minute, and no pathologic data was found in the system examination. The laboratory data showed that hemogram and urine findings were normal. His lipid profile was normal. Other findings were as in Table .
Plasma cortisol was under 1.00 μg/dL after low dose (1 mg) overnight dexamethasone suppression test. 24 hours urinary catecholamines level were vanil mandilic acid (VMA) 8.90 mg/day (normal range, 3 to 90 mg/day), metanefrin 330 μg/day (normal range, 52 to 341 μg/day), epinefrin 13 μg/day (normal range, 2 to 24 μg/day), norepinefrin 41 μg/day (normal range; 15 to 100 μg/day). Hormonal levels were as in Table .
There was a 34 × 26 mm solid lesion in the right perirenal space.
Liver parenchyma was homogeneous. In the right lobe of the liver, there was a two millimeter subcapsular calcification. A regular-shaped mass (dimension 36 × 35 × 35 mm) with a homogeneous and solid structure was diagnosed at the right suprarenal fossa. The density of the mass was 80 Hounsfield units (HU) in postcontrast CT and 40 HU without contrast CT [Fig. ].
After all these examinations, the patient was given a diagnosis of a non-functional adrenal incidental lesion. Because it was 80 HU in contrast CT, 40 HU without contrast CT, and 36 × 35 × 35 mm, the patient underwent a right adrenalectomy [Fig. ]. There were no clinical problems during, before, or after the surgery. The pathology examination confirmed the mass as being pheochromocytoma [Fig ]. The patient was discharged after 5 days.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [81.0, 'kg']}",121,114.95,127.05,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 81.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (81.0 kg - 20 kg) = 121.0 mL/hr.
Hence, the patient's fluid maintenance is 121.0 mL/hr."
4730,22,Maintenance Fluids Calculations,physical,decimal,usmle-5867,Extracted,"A 1-hour-old newborn male is evaluated in the delivery room. The infant was born at 37 weeks gestation to a 39-year-old G3. The mother initially labored at home with a midwife but was transferred to the hospital for failure to progress. The infant was eventually delivered via Caesarean section. The mother declined all prenatal screening during this pregnancy. Upon delivery, the infant is found to have a 3 cm full-thickness defect in the abdominal wall to the right of the umbilicus with evisceration of a loop of bowel. His Apgar scores were 7 and 8 at 1 and 5 minutes, respectively. His weight is 3.0 kg (6.6 lb), and his height and head circumference are in the 30th and 40th percentiles, respectively.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.0, 'kg']}",12,11.4,12.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.0 kg. Hence, the patient's maintenance fluid is 3.0 kg * 4 mL/kg/hr = 12.0 mL/hr.
Hence, the patient's fluid maintenance is 12.0 mL/hr."
4731,22,Maintenance Fluids Calculations,physical,decimal,pmc-8557646-1,Extracted,"A 1-year-old-male baby was presented to the hospital with a history of an abdominal mass. A local pediatrician in the outpatient clinic incidentally discovered it when he was examining the child for a complaint of distention and chronic diarrhea.
The child was referred to the hospital and was admitted to the Pediatric Surgery Department. Physical examination indicated the mass was painless and mobile. The palpable mass was nontender and extended from the upper left quadrant to the umbilicus. Vital signs were normal, and the child was asymptomatic with a good appetite. He did not complain of vomiting, constipation or abdominal pain. His weight at admission was 9 kg. Laboratory tests were normal. Abdominal ultrasound showed a hyperechoic soft tissue lesion with a maximum diameter of ~10 cm, pushing the intestine to the right without obstruction of the intestinal lumen.
Computed tomography (CT) of the abdomen revealed a homogeneous, well vascularized mass measuring 9.4 × 10.6 cm and encapsulated with thin septation in its medial part. The mass was located in the upper left quadrant and extended to the pelvis with an oval appearance (). Other abdominal findings were normal. Under general anesthesia, an incision was made in the midline above the umbilical region. The findings were a soft, yellow mass with defined margins, originating from the small intestine’s mesentery, 30 cm from Treitz ligament ( and ). Complete excision of the mass was performed without intestinal resection ( and ). Histopathology showed a normal adipose tissue composed of mature adipocytes with no evidence of mitosis or nuclear atypia, which confirmed the presence of the mesenteric lipoma (). Oral feeding was started 2 days after the operation, and the patient stayed in hospital for 5 days. He was discharged in a good condition with normal bowel movement. The child was evaluated 4 months after the procedure. He had no complains, and abdominal ultrasound revealed normal findings.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [9.0, 'kg']}",36,34.2,37.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 9.0 kg. Hence, the patient's maintenance fluid is 9.0 kg * 4 mL/kg/hr = 36.0 mL/hr.
Hence, the patient's fluid maintenance is 36.0 mL/hr."
4732,22,Maintenance Fluids Calculations,physical,decimal,pmc-2698207-1,Extracted,"A healthy 51-yr-old, 60 kg woman with an endometrial mass was scheduled for a hysteroscopic endometrial biopsy and resection under general anesthesia. Apart from a history of exploratory laparotomy that was performed 35 yr ago, her medical history was unremarkable. The preoperative laboratory tests were normal; the patient was premedicated with midazolam and atropine. Anesthesia was induced with thiopental, midazolam and fentanyl. The tracheal intubation was facilitated with rocuronium. The anesthesia was maintained with 50% N2O in oxygen, fentanyl, enflurane and rocuronium. The patient was placed in the lithotomy position with a slight Trendelenberg tilting. During hysteroscopy, the uterus was distended with Urosol® (a mixture of 2.7% sorbitol and 0.54% mannitol, CJ Pharma, Seoul, Korea) at a height of 135 cm above the operating table. Forty minutes after the initiation of hysteroscopy, the amount of the absorbed Urosol® was estimated to be approximately 7 L, based on the uterine inflow and outflow. Radial atery cannulation was performed for continuous monitoring of blood pressure, and for serial blood gas analysis (). The serum sodium level was <100 mEq/L when measured using a blood gas/electrolyte analyzer in the operating room (GEM Premier 3000, Instrumentation Laboratory, Lexington, MA, U.S.A.), but it was 89 mEq/L when measured again at the central laboratory. The ionized calcium level was 0.53 mM/L. A diagnosis of TURP syndrome was made on the basis of severe hyponatremia. The patient received a total of 100 mg of furosemide in divided doses. One hour after the start of surgery, arterial blood gas analysis showed a severe acidosis (pH 7.19; pCO2, 39 mmHg; HCO3-, 17 mM/L; and base excess, -12.6 mM/L). Although 80 mL of 8.4% sodium bicarbonate was administered over 90 min, the pH value persisted at a value of ≤7.35. Since the blood pressure also decreased to 62/40 mmHg at 105 min after the start of surgery, 10 mg of ephedrine was intravenously administered and dopamine was infused at a rate of 10 µg/kg/min, but the blood pressure did not rise. However, after administration of 40 mL of 3% calcium chloride, the blood pressure increased to preoperative value. The ionized calcium level increased to 0.83 mM/L but a prolonged QT interval on ECG was noted. Two hours after the start of surgery, the PaO2 level gradually decreased to 87 mmHg when FiO2 was at 0.75, and the SaO2 level decreased to 95%. Adhesiolysis of intrauterine synechia was failed due to bleeding from the opened vessel. Two hours and 30 min after the start of surgery, the hysteroscopic procedure was stopped and transabdominal hysterectomy was performed instead. Because the repeated measurements of serum sodium persisted at the level of <100 mEq/L, 2% saline was infused at a rate of 2 mL/kg/hr and thereafter normal saline was infused after the serum sodium level became 103 mEq/L. During surgery, 1,500 mL of normal saline, 160 mL of packed red blood cells and 150 mL of hetastarch were infused. Additionally, since the blood glucose gradually increased to ≥300 mg% (), 5 units of regular insulin were intravenously administered. The lactate level increased to 7.1 mM/L when surgery was completed.
At the completion of surgery, the patient regained full consciousness. Postoperatively, chest radiography and arterial blood gas analysis did not exhibit findings of pulmonary edema. The patient was admitted to intensive care unit for close observation. Normal saline was infused with the maintenance of a central venous pressure at 4 to 6 mmHg in intensive care unit. The ionized calcium returned to normal 6 hr later and serum sodium level returned to normal 24 hr later. The patient recovered uneventfully and was discharged from the hospital.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.0, 'kg']}",100,95,105,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.0 kg - 20 kg) = 100.0 mL/hr.
Hence, the patient's fluid maintenance is 100.0 mL/hr."
4733,22,Maintenance Fluids Calculations,physical,decimal,pmc-4612481-1,Extracted,"Forty-five-year-old male shelter resident, chronic alcoholic, chronic smoker, and marijuana abuser presented to emergency department (ED) with complaints of intermittent fever with night sweats and productive-cough for 10 days with yellowish sputum associated with pleuritic chest pain. Patient reported a single episode of minimal amount of hemoptysis. He complained of generalized weakness and decreased appetite and claimed to have lost approximately 10 pounds in 2 weeks.
Physical examination including respiratory system was unremarkable. Patient had high grade fever of 102°F and tachycardia of 110–122/min on admission.
Laboratory results showed leukocytosis of 17,000/mm3 with neutrophil differential of 11,200/mm3 (65%) with band neutrophils of 10%. Comprehensive metabolic panel was normal. Urine toxicology panel was positive for cannabinoids. Chest radiograph was reported as right middle lobe consolidation but careful observation revealed a foreign body (FB), likely a tooth in the right bronchus intermedius (). CT scan of chest showed a well calcified FB likely a tooth at the level of carina obstructing right intermedius bronchus and consolidation in right lower lobe indicating post-obstructive pneumonia (). Patient was admitted and prescribed intravenous antibiotics targeting Gram-negative organisms and anaerobes. His fever subsided within 48 h of starting antibiotics.
Bronchoscopy was planned for the removal of FB from the right intermedius bronchus.
Deep conscious sedation was achieved by propofol infusion in the presence of an anesthesiologist and cardiothoracic surgery backup. Bronchoscopy showed tooth in right intermediate bronchus with ~75% occlusion, and purulent secretions from the right main stem (Figs. –). The FB was removed successfully with rat tooth forceps ( and ). No significant bleeding was noted at the site of removal. Post bronchoscopy inspection showed right main stem, bronchus intermedius, and right middle and lower lobe bronchi to be well patent. Granulation tissue was noted around previous embedded FB site. Broncho-alveolar lavage was performed, the results of which were negative.
Upon further questioning, the patient said that he did not remember having aspirated the tooth and hence the duration of aspiration could not be known. He was discharged home on oral antibiotics a couple of days after the bronchoscopy and counseled to quit alcohol and drugs.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.0, 'lbs']}",18.14368,17.2365,19.05086,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.0 lbs so this converts to 10.0 lbs * 0.453592 kg/lbs = 4.53592 kg. Hence, the patient's maintenance fluid is 4.53592 kg * 4 mL/kg/hr = 18.14368 mL/hr.
Hence, the patient's fluid maintenance is 18.14368 mL/hr."
4734,22,Maintenance Fluids Calculations,physical,decimal,pmc-7536457-2,Extracted,"Case 2 – Three years after the presentation of the first patient, an elder sibling, a 15-year-old adolescent girl presented with vertigo, nausea, and plethora. The physical examination was normal except plethora. Vital functions were normal and peripheral capillary oxygen saturation was 95%. Her height was 161 cm, and body weight 53.5 kg. Blood counts were Hb 19.4 g/dL, Hct 64.6%, MCV 87fL, leucocyte 6.500/mcL, absolute neutrophyl count 4010/mcL, thrombocyte 168 000/mcL. The serum EPO level was 6.44 mU/mL, serum ferritin level was 4.1 mU/mL, and Hb electrophoresis using HPLC showed no abnormality (HbA 83%, HbA2 2.3%, HbF 0). Analysis of JAK2 and BCR/ABL revealed no mutation. Phlebotomy (450 mL) was performed, acetylsalicylic acid 100 mg/day and oral ferro-sulfate was started. In the following year, she presented with similar symptoms twice and two more phlebotomies were performed. Her Hb was between 20.4–18.4 g/dL when she had some symptoms. She is aged 23 years now and says that her plethora increases after a bath but she is well and she refused phlebotomy in recent years.
The patients reported that their father was aged 45 years and had tinnitus and erythrocytosis. The grandmother died of stroke at the age of 52 years. The paternal aunt also died at the age of 52 years. It is not clear whether the grandmother and aunt also had erythrocytosis.
Written consents of the patients were obtained for the genetic study, which revealed that the siblings were both heterozygous for the EPOR nonsense mutation c.1316G>A (p.Trp439Term).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [53.5, 'kg']}",93.5,88.825,98.175,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 53.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (53.5 kg - 20 kg) = 93.5 mL/hr.
Hence, the patient's fluid maintenance is 93.5 mL/hr."
4735,22,Maintenance Fluids Calculations,physical,decimal,pmc-4989072-1,Extracted,"A 46-year-old male presented with progressive, mostly postprandial abdominal pain, and significant weight loss of almost 44 lb. in a six-month period.
His medical history was notable for heavy smoking for the past 30 years and cholelithiasis. His medications included 40 mg esomeprazole once a day.
Four months prior to presentation, he underwent an esophagogastroduodenoscopy (EGD) to evaluate similar complaints and was diagnosed with peptic ulcer disease (PUD) with positive HP. No improvement followed a course of a high dosage of esomeprazole and Helicobacter eradication therapy.
On admission the patient was stable, with a heart rate of 65 beats/min., blood pressure of 110/60 mmHg, and oxygen saturation of 98%. His physical examination was unremarkable except for epigastric tenderness and bilateral temporal and extremities wasting. Laboratory tests revealed normal CBC, kidney, and liver function. His C-reactive protein and erythrocyte sedimentation rate were also unremarkable.
Upon admission, a review of a computed tomography (CT) scan was done in an outpatient setting and revealed fatty liver, thickened gastric wall (), and a hypodense area in the stomach; however no revision of the gastrointestinal arterial vasculature was done at that time. The patient underwent second EGD that revealed mildly erythematous antral mucosa. An immunohistochemical stain for HP was negative. Random gastric biopsies showed mild chronic active gastritis. The patient was discharged with the impression that he is suffering from active nonspecific gastritis. The dosage of esomeprazole was escalated to 40 mg twice a day. Due to the continuity of his symptoms, a third EGD was performed that showed hyperemic erythematous gastric mucosa with few longitudinal ulcerations that were located on the greater curvature on a preantral location. The pathology examination from gastric biopsies revealed a single focus of markedly atypical glands with necrotic material in the lumen, suspicious of a malignancy. A week later, a fourth EGD showed large ulcerations on the preantral greater and lesser curvatures () with hyperemic intervening mucosa. A pathological examination showed acute gastritis and duodenitis, reactive atypia, negative stain for HP, and no signs of intestinal metaplasia or malignancy.
Six weeks later, he was admitted again due to worsening of epigastric pain and further weight loss, overall losing 66 lbs. over 9 months. During the third hospitalization, a diagnosis of ischemia was considered. A CT angiogram showed significant gastric pyloric wall thickening and surrounding small lymphadenopathy, several new splenic infarcts, and significant narrowing and obstruction in the origin of the superior mesenteric artery (SMA) and the origin of the celiac trunk with mild stenosis of the inferior mesenteric artery (IMA) origin (). A vascular surgery consult was obtained and open surgical revascularization was recommended given our patient's young age and lack of comorbidities. The patient underwent a surgical bypass with expanded polytetrafluoroethylene (ePTFE) graft between the right common iliac artery and the SMA with extension graft to the hepatic artery that resulted in significant clinical improvement and weight gain. Repeat EGD following the surgical bypass revealed mild gastritis and duodenitis with resolution of the gastric ulcers.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [66.0, 'lbs']}",69.93707,66.44022,73.43392,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 66.0 lbs so this converts to 66.0 lbs * 0.453592 kg/lbs = 29.93707 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (29.93707 kg - 20 kg) = 69.93707 mL/hr.
Hence, the patient's fluid maintenance is 69.93707 mL/hr."
4736,22,Maintenance Fluids Calculations,physical,decimal,pmc-5063890-1,Extracted,"A 27-year-old female presented to the Gout Clinic of Peking Union Medical College Hospital with recurrent arthritis and infertility. Fourteen years before presentation, she noticed protrusion of her right ankle but did not undergo evaluation at a hospital. Eight years before presentation, at age 19, she experienced acute pain and swelling of her right ankle. The pain resolved spontaneously but recurred 6 to 7 times/year, involving the bilateral metatarsophalangeal (MTP) joints, bilateral ankles, and right knee. Her serum urate level (SUA) was elevated to 789 μmol/L. A diagnosis of gout was made, and she was prescribed NSAIDs for pain relief and allopurinol and benzbromarone to lower her urate level. However, she discontinued allopurinol and benzbromarone on her own as these medications triggered acute flares. Five years before presentation, she noticed multiple nodules in her MTP joints, ankles, and fingers. The nodules on her feet interfered with normal walking. She also complained of the inability to conceive after 3 years of attempts. Her age at menarche was 14 years, and her cycles were irregular. She was reported to prefer snacks and fatty food during her childhood. Her father had hypertension. Her grandfather had an SUA level greater than 400 μmol/L but without gout. On physical examination, the patient was generally healthy, with a height of 168 cm and a weight of 55 kg. Her blood pressure was 120/80 mmHg. Cardiac and pulmonary examinations were normal. On abdominal palpation, the liver was enlarged with a normal soft texture. A joint examination revealed multiple nodules on the bilateral MTP1 joints, ankles, and fingers.
A serological examination after overnight fasting revealed a SUA level of 548 μmol/L, serum creatinine (Cr) level of 49 μmol/L, fasting glucose level of 3.6 mmol/L, total triglyceride level of 6.22 mmol/L, and total cholesterol level of 6.60 mmol/L. Her resting lactate level was 7.4 mmol/L. Her 24-h urine urate level was 2.262 mmol/24 h, and her fractional excretion of uric acid (FE-UA) was 2.48 %. Her liver enzymes were normal. The estrogen level and basal body temperature curve were normal for her age and menstrual status. Renal ultrasonography revealed normal kidney size with possible calcium deposits in the bilateral renal medulla. Computed tomography (CT) imaging of her abdomen showed hepatomegaly without nodules. The pelvic ultrasonography and salpingography findings were normal. Serum examinations of her parents and her husband were normal.
Whole blood DNA was extracted from all four family members (the patient, both parents, and her husband) after signing an informed consent form. A genetic study was first conducted with a target gene sequencing approach. A search of the OMIM, NIH, and PubMed databases using the key words “FEMALE,” “GOUT,” and “HYPERLACTACIDEMIA” indicated familial juvenile hyperuricaemic nephropathy, glycogen storage disease type I, and glycogen storage disease type II. Next-generation sequencing was used to sequence each of the exons of the UMOD, RENIN, G6PC, SLC37A4, and GAA genes, as well as two SNP loci (rs2231142 and rs72552713) of ABCG2 found in our previous report of a family including a female with gout.
The genetic sequencing results showed that UMOD, RENIN, SLC37A4, GAA and rs72552713 of ABCG2 were all normal in the patient and her family. Sequencing of the G6PC gene revealed composite heterozygous c.190G>T/c.508C>T mutations in the patient, a heterozygous c.190G>T mutation in her father, and a heterozygous c.508C>T mutation in her mother. The genetic analysis of her husband was normal. The c.190G>T mutation was located on exon 1 and encoded a missense mutation of p.V64L, whereas the c.508C>T mutation was located on exon 4 and encoded a nonsense mutation of p.R170X (Fig. ). Sequencing of 50 healthy females and 100 healthy males at the two loci produced normal results. To our knowledge, the c.190G>T mutation has not been reported in previous literature.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [55.0, 'kg']}",95,90.25,99.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 55.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (55.0 kg - 20 kg) = 95.0 mL/hr.
Hence, the patient's fluid maintenance is 95.0 mL/hr."
4737,22,Maintenance Fluids Calculations,physical,decimal,pmc-3603068-1,Extracted,"A 60-year-old lady, presented with tremulousness of hands for 1 month and palpitation with excessive sweating for 3 months. She had a history of weight loss for 6 months, and gradually enlarging neck swelling for 3 years. She was nervous, irritable, and emotionally labile. Her weight was 46 kg, BMI 17, afebrile, pulse rate: 110/min/regular, blood pressure: 140/56 mm of Hg. Her thyroid gland was symmetrically enlarged, firm in consistency, nodular/lobular surface and mildly tender without any bruit. Palms were warm and sweaty with fine tremor in hands. All reflexes were exaggerated. There were no occular manifestations.
Initial thyroid function tests (TFT) revealed high T3: 3.80 ng/ml (0.80-2.10), T4: 12.40 ug/dl (5.10-12) with a low TSH: 0.20 mU/L (0.70-5). Her TSH receptor antibody (TSAb): 25 U/L (Normal [nl.] <1), anti TPO antibody: 374 IU/ml (nl. <35) and thyroglobulin antibody: 268 IU/ml (nl. <65) were all strongly positive. Complete hemogram and ESR-18 mm/h (nl.-1-25) were normal. Ultrasonogram of thyroid revealed an enlarged gland with hypoechoic parenchyma with fibrous septa.99mTc pertechnetate scan (Tc99m scan) revealed enlarged thyroid gland with diffusely increased uptake of radiocontrast: 17% (nl. 0.4-4%) with some patchy defects in both lower poles. Thyroid FNAC showed sheets of Hurthle cells with abdunce of lymphocytes and sheets of regular follicular cells, indicating HT. She was observed on beta blockers. Repeat TFT, 3 months later showed: T3: 4.20 ng/ml, T4: 14.40 ug/dl, TSH: 0.001 μU. Repeat 99mTc pertechnetate scan was done, which again revealed enlarged thyroid gland with diffusely increased uptake of radiocontrast: 21% (nl. 0.4-4%) with same patchy defects in both lower poles. Antithyroid medication carbimazole was started.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [46.0, 'kg']}",86,81.7,90.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 46.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (46.0 kg - 20 kg) = 86.0 mL/hr.
Hence, the patient's fluid maintenance is 86.0 mL/hr."
4738,22,Maintenance Fluids Calculations,physical,decimal,pmc-3418045-1,Extracted,"A 4-month-old male baby presented to our hospital with the complaint of palpable mass in the right hemi-abdomen noted by the parents one day back. The patient was born at full term with uneventful birth history. The baby achieved milestones normally. Abdominal examination revealed a non-tender mass with vague margins in the right hemi-abdomen. Laboratory investigations including alpha-fetoprotein were within normal limits. X-ray abdomen showed mass impression pushing the gut shadows to one side. Bones and calcifications were also evident in the right hemi-abdomen. Ultrasound of the abdomen revealed a heterogeneous mass with calcifications suggestive of teratoma. Abdominal CT scan showed a 9.2cm × 10.0cm heterogeneous mass containing fat, bones and soft tissues. The various bones were vertebrae, long bones like femur, tibia and fibula, and bones of hand/feet (Fig.1). Provisional diagnosis of FIF was made.
At operation, a mass covered in whitish-gray membrane, pushing the gut loops to the opposite side in the upper retroperitoneum, was found (Fig.2). The membrane was incised to find a fetiform mass floating in clear fluid having a few well differentiated and other rudimentary organs. The fetiform mass was suspended in the amnion like cavity with an umbilical cord like stalk (Fig.3). The mass with sac was mobilized and excised completely.
Post operative recovery was uneventful. Patient was allowed orally on 3rd and discharged on 7th post operative day. The patient is currently being followed with alpha-fetoprotein and ultrasound abdomen. At six months follow up patient is doing well.
The FIF was of 13.75cm×12.5cm×6.25cm size with a weight of 500 grams. It was anencephalic having otic and nasal placodes and optic vesicles. The left upper limb was meromelic; lower limbs were sirenomelic. The umbilical cord had two vessels in it. The FIF had a scrotum like skin at the site of genitalia that lacked gonad in it. The FIF also lacked anus and genitalia (Fig.4). Plain radiography of the specimen revealed axial skeleton in the form of vertebrae, along with ribs, long bones of upper and lower limbs, and facial bones (Fig.5).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [500.0, 'g']}",2,1.9,2.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 500.0 g so this converts to 500.0 lbs * kg/1000 g = 0.5 kg. Hence, the patient's maintenance fluid is 0.5 kg * 4 mL/kg/hr = 2.0 mL/hr.
Hence, the patient's fluid maintenance is 2.0 mL/hr."
4739,22,Maintenance Fluids Calculations,physical,decimal,pmc-5362000-1,Extracted,"A 14-year-old, 4.02 kg, spayed female domestic shorthair cat was referred to the Oncology Service at the University of Florida Small Animal Hospital with an 8 month history of increased vocalization, urination, food and water intake, and two episodes of hematuria. The referring veterinarian identified a right adrenal mass (3.57 cm × 2.71 cm) on ultrasound (), and cytology of the mass was consistent with adrenocortical tumor. At the time of presentation, the cat was being medicated with amlodipine (1.5 mg PO q24h) for hypertension and with a potassium supplement (Tumil-K Powder 4 mEq PO q24h) for hypokalemia.
At presentation the cat was alert and responsive. Physical examination revealed tachycardia (220 beats/min) with a gallop rhythm and synchronous femoral pulse. The cat had a cardiovascular consult, which revealed no abnormalities (including hypertrophy). Capillary refill time was < 2 s and the respiratory rate was 35 breaths/min. A pendulous abdomen, prominent dermal blood vessels and muscle atrophy along the epaxial muscles were observed. A complete blood count showed mild neutrophilia (13 × 103/µl; reference interval [RI] 2.3–9.8 × 103/µl) and lymphopenia (0.43 × 103/µl; RI 0.9–5.5 × 103/µl). Serum biochemical abnormalities included hyperglycemia (171 mg/dl; RI 70–140 mg/dl), mild decrease in alanine aminotransferase activity (27 U/l; RI 32–83 U/l), and normal potassium (3.9 mEq/l; RI 3.5–5.0 mEq/l). Urine specific gravity was 1.019 and urinalysis was otherwise unremarkable. Venous blood gas analysis was consistent with a metabolic alkalosis (pH 7.341, HCO3 29.2 mmol/l) with respiratory compensation (partial pressure of carbon dioxide 53.4 mmHg). Subsequent venous blood gas analyses were in the normal range for cats. Computed tomography of the abdomen and thorax identified the left adrenal gland < 5 mm and the right adrenal gland as a 3.8 × 3.2 × 2.8 cm mass, which caused ventromedial deviation of the vena cava, as well as caudal displacement of the right renal artery and vein (). There was no evidence of local vascular invasion or pulmonary metastasis.
An adrenocorticotropin hormone stimulation test (ACTH-ST) was performed. The baseline cortisol concentration was 6.59 µg/dl (RI 0.8–5.0 µg/dl) and 1 h postcortisol concentration was 20.0 µg/dl (RI 3.6–10.0 µg/dl). A blood sample was submitted to the University of Tennessee for measurement of adrenal sex hormone concentration. The endocrinology panel showed an increased concentration of aldosterone (> 1376 ng/ml; RI 11.3–294.3 ng/ml) and progesterone (2.59 ng/ml; RI 0.03–0.40 ng/ml). Normal levels of 17 OH progesterone (0.12 ng/ml; RI 0.08–0.20 ng/ml), androstenedione (0.20 ng/ml; RI 0.1–0.3 ng/ml) and testosterone (0.02 ng/ml; RI 0.02–0.30 ng/ml) were observed; estradiol concentration was 27.3 pg/ml (RI 50.3–84.0 pg/ml) and cortisol was 2.1 ng/ml (reference range 5.2–54.4 ng/ml).
A presumptive diagnosis of a cortisol, aldosterone and progesterone co-secreting tumor of the right adrenal gland was made. With no signs of macroscopic metastasis or vena cava invasion, adrenalectomy was considered the treatment of choice. The calcium channel blocker (amlodipine) and the potassium supplement were discontinued immediately prior to surgery. General anesthesia was induced with propofol (6 mg/kg IV) and was maintained with isoflurane and fentanyl in 100% oxygen. Postoperative analgesia was maintained with methadone (0.3mg/kg IV q4h) and buprenorphine (0.1 mg/kg IV q6h). A dose of dexamethasone (1 mg/kg IV) was slowly administered during surgery. A right adrenalectomy was performed without complications; the adrenal mass seemed encapsulated and it was closely associated with the vena cava. The phrenicoabdominal vein was doubly clipped and transected; the tumor was excised with a combination of blunt dissection and electrocautery. No gross metastasis was observed to other abdominal organs and the left adrenal gland was considered grossly atrophied. Histopathology of the right adrenal gland was consistent with an adrenocortical tumor. Anisocytosis and anisokaryosis are mild to moderate, and one mitotic figure was observed in ten 400× fields. Postoperative therapy consisted of intravenous (IV) fluid therapy (lactated Ringer’s solution at 10 ml/h), methadone (0.3 mg/kg IV q3–6h), amoxicillin and clavulanic acid (15 mg/kg IV or PO q12h) and one dose of desoxycorticosterone pivalate (DOCP; 2 mg/kg SC).
Twenty-four hours after surgery, venous blood gas analysis (pH 7.411) and blood pressure (90 mmHg) were in the normal range. Serum biochemical was unremarkable (blood glucose 134 mg/dl [RI 70–140 mg/dl]; potassium 3.54 mEq/l [RI 3.5–5.0 mEq/l]; sodium 154.9 mEq/l [RI 148–156 mEq/l]; creatinine 1.6 mg/dl [RI 1.0–2.1 mg/dl]; blood urea nitrogen 37 mg/dl [RI 17–40 mg/dl]). An ACTH-ST was performed, which showed a baseline cortisol concentration of <0.1 µg/dl (RI 0.8–5.0 µg/dl), and 1 hour postcortisol concentration was 0.146 µg/dl (RI 3.6–10.0 µg/dl), indicating a need for corticosteroid supplementation. The cat received one dose of DOCP (2.2 mg/kg SC) and oral administration of prednisolone solution (0.2 mg/kg q12h) was started as the cat was eating and drinking. The cat was discharged 4 days after surgery, with an improved attitude and appetite. On the day of discharge serum biochemical analysis showed hypokalemia (2.8 mEq/l; RI 3.5–5.0 mEq/l), normal systolic blood pressure (115 mmHg) and normal venous blood gas analysis (pH 7.406). The owner was instructed to start oral potassium supplementation and to maintain oral prednisolone.
Over the following 2 weeks, the cat showed progressive clinical improvement with normal food intake and a good activity level at home. Three weeks after surgery, potassium supplementation was discontinued as serum potassium concentration was consistently within the RI (between 4.1 and 4.5 mmol/l; RI 3.5–5.8 nmol/l) and aldosterone concentration was less than the RI (112 pmol/l; RI 194–338 pmol/l), and prednisolone were gradually tapered down and it was discontinued. Eighteen months after surgical removal of a hormone-secreting adrenal cortical tumor the cat is doing well. All laboratory values in both US and International System of Units are shown in .","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.02, 'kg']}",16.08,15.276,16.884,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.02 kg. Hence, the patient's maintenance fluid is 4.02 kg * 4 mL/kg/hr = 16.08 mL/hr.
Hence, the patient's fluid maintenance is 16.08 mL/hr."
4740,22,Maintenance Fluids Calculations,physical,decimal,usmle-9832,Extracted,"A 70-year-old man presents to the physician with a 1-month history of severe fatigue. During this time, he has unintentionally lost 2 kg (4.4 lb). Currently, he takes no medications other than aspirin for occasional knee pain. He does not smoke or drink alcohol. His vital signs are within the normal range. On physical examination, the conjunctivae are pale. Petechiae are present on the distal lower extremities and on the soft and hard palates. Palpation reveals bilateral painless cervical lymphadenopathy. Examination of the lungs, heart, and abdomen shows no abnormalities.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [70.0, 'kg']}",110,104.5,115.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 70.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (70.0 kg - 20 kg) = 110.0 mL/hr.
Hence, the patient's fluid maintenance is 110.0 mL/hr."
4741,22,Maintenance Fluids Calculations,physical,decimal,pmc-3170808-1,Extracted,"A 49-year-old male patient presented to our hospital because of abdominal pain, nausea-vomiting, lack of appetite, and weight loss (4 kg in the past month). He had been suffering abdominal pain in the past 3 weeks, which was localized in the right-lower quadrant, and it was relievable by defecation. During the past month, he had started to suffer diarrhea with no mucus and occasional appearance of fresh blood in the stool 2-3 times a day along with vomiting 1-2 times a day. His history revealed no remarkable event other than a hydatid cyst and simultaneous cholecystectomy operation 12 years previously. He had no history of immunosuppressive treatment. Physical examination revealed an incisional scar of 20 cm in length starting from the xiphoid process and extending parallel to the costal arch and towards the right axillary line, along with a mass lesion of 22 × 14 cm in size with an upper border 3 cm above the umbilicus and a lower border extending to the suprapubic region which was solid, deep, and painful upon palpation.
CBC results were as follows: WBC: 8400/μL; lymphocyte count: 1800/μL; Hb: 10.20 g/dL; MCV: 84.1 fL; platelet: 527000/mm3. Biochemical profile was normal. Sedimentation rate was 60 mm/h, and CRP was 50 mg/L. There was no occult blood or parasite in the stool. Fecal culture showed no pathogenic bacterial growth. CEA, CA19-9, and CA 72-4 values were normal. The patient was seronegative for anti-HIV antibody and anti-EBV IgM and IgG. The patient was admitted to our hospital based on the presumptive diagnosis of Crohn's disease, lymphoma, colon cancer, or abscess.
Abdominal ultrasonography displayed calcifications located in the segment VI of the liver (postoperative changes?) and a 12 cm long intestinal segment of 5 cm total diameter and 1.6 cm thickness which was located superior to the bladder over the midline and left aspect of the midline ().
Abdominal tomography demonstrated coarse calcifications associated with the previous operation in the posterior aspect of the left liver lobe along with a heterogenous and solid area of 11 × 6 cm in size showing mild enhancement after intravenous contrast administration around which the adjacent adipose tissue had a streaky appearance (). The center of the above-described lesion exhibited luminal enhancement in the intestines. Since the lumen of the small bowel was symmetrical, inflammation of the terminal ileum and its complications were considered first. Adenocarcinoma was ruled out based on the absence of luminal stenosis and lack of marked contrast enhancement.
The patient was subjected to total colonoscopy. Ileocecal valve was observed to be patent, and mucosa was found to be edematous and mildly irregular. Terminal ileal mucosa was severely edematous and granular. Due to the severe edema in the terminal ileum, the colonoscope could not be advanced further than 5 cm. There was no ulcer in the terminal ileum or ileocecal valve. Many biopsy samples were acquired from the ileocecal valve and terminal ileum. The lumen and mucosa of cecum, ascending colon, transverse colon, descending colon, sigmoid colon, and rectum were normal. Anal canal displayed internal hemorrhoids.
Biopsies derived from ileum and ileocecal valve revealed chronic active nonspecific changes in two biopsy fragments and ulceration on the surface. Other fragments demonstrated edema and nonspecific inflammatory alterations. Although there was no granuloma, focal active inflammation was thought to be consistent with the Crohn's disease.
Examination of the small bowel by barium contrast revealed an approximately 4 cm long segment that was extending proximally from cecum within the terminal ileum over which adjacent intestinal segments were pushed away, valvulae conniventes were indistinct, and small bowel mucosa had a patchy irregular appearance. Radiographic findings were thought to be consistent with Crohn's disease as well ().
Mesalazine therapy was started at a dose of 4 g/day. During the treatment of the patient, abdominal pain and diarrhea showed a regression; however, they recurred after 2-3 days of improvement. Inspections carried out on a daily basis revealed a remarkable and progressive increase in the size of the palpable mass over the right-lower quadrant. Lower extremity Doppler USG was performed due to diameter difference in favour of the right leg. Doppler USG depicted thrombosis in the right main femoral vein, deep femoral vein, proximal aspect of the superficial femoral vein, and proximal aspect of the great saphenous vein. A filter was placed into the vena cava inferior and low-molecular-weight heparin therapy was started. Because overall health status of the patient began to deteriorate progressively, he was transferred to surgery department for laparotomy. During the laparotomy, a tumoral lesion of approximately 20 cm in size was encountered in the ileum and resected (). Histopathologic analysis of the resected material showed a malignant lymphoma consistent with CD20-positive atypical Burkitt's lymphoma.The patient died on the third postoperative day due to acute myocardial infarction and cardiac arrest which did not respond to cardiopulmonary resuscitation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.0, 'kg']}",16,15.2,16.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.0 kg. Hence, the patient's maintenance fluid is 4.0 kg * 4 mL/kg/hr = 16.0 mL/hr.
Hence, the patient's fluid maintenance is 16.0 mL/hr."
4742,22,Maintenance Fluids Calculations,physical,decimal,pmc-5538601-1,Extracted,"A full term 2-day-old female neonate with birth weight 2 kg, born by normal vaginal delivery was referred with history of abdominal distension and recurrent bilious vomiting. The child had not passed meconium and had continuous bilious nasogastric aspirates. Examination revealed gross abdominal distension while on infantogram dextrocardia along with gas under both diaphragms was seen. On exploration, a pin point gastric perforation at fundus near lesser curvature was noted along with situs inversus. The stomach and spleen were found on right side while liver on left side of abdomen. There was incomplete gut rotation along with shortened mesentery. The stomach was normal sized and distal bowel was unused and small in calibre. The cecum and appendix were located in left lumbar region. Primary two layered closure of gastric perforation was done along with straightening of duodenum and widening of mesentery. In postoperative period, child passed stools and discharged on full breast feeds. But after two weeks, child was readmitted with intolerance to feeds and recurrent bilious vomiting. Initially managed with total parenteral nutrition and trial of feeds was subsequently started. The child was accepting feeds infrequently. Hence an upper GI contrast study was done which revealed partial duodenal obstruction (Fig.. Re-exploration confirmed duodenal web with central aperture between 2nd and 3rd part of duodenum (Fig.. A diamond shaped duodeno-duodenostomy was done. The child was kept on total parenteral nutrition and intravenous antibiotics. Postoperative period was uneventful and baby was discharged on full feeds on 7th postoperative day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.0, 'kg']}",8,7.6,8.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.0 kg. Hence, the patient's maintenance fluid is 2.0 kg * 4 mL/kg/hr = 8.0 mL/hr.
Hence, the patient's fluid maintenance is 8.0 mL/hr."
4743,22,Maintenance Fluids Calculations,physical,decimal,pmc-8362796-1,Extracted,"A 52-year-old man with a history of hypertension, hyperlipidemia, obesity, gastroesophageal reflux disease (GERD), and non-insulin-dependent diabetes mellitus (NIDDM) presented to the ICU with a 10-day onset of dyspnea and a dry cough. He was a former cigarette smoker with a 10-year history of 15 packs per day but had stopped for the past two years. He stood 180.3 cm tall and weighed 151.5 kg for a body mass index (BMI) of 46.6. EMS reported the patient’s O2 saturation at 57% room air and immediately placed him on BiPap for supplemental oxygen therapy upon arrival. The patient reported his shortness of breath had worsened in the last 24 hours. Aggravating factors included exertion and an attempt to speak. A positive PCR test confirmed the patient’s diagnosis for COVID-19 on April 10, 2021, approximately eight days after he was exposed by a co-worker on April 2, 2021 (Table ). These sequences of events occurred following his administration of the J&J vaccine on March 31, 2021 (Table ). His review of systems was remarkable for exacerbating chest pain and a dry cough with a worsened shortness of breath. He had a family history significant for hypertension. He denies any tobacco, alcohol, or drug abuse. He had no known drug allergies (NKDA). His regularly prescribed medications included Atorvastatin, Metoprolol, and Pantoprazole.
An electrocardiogram (ECG) obtained en route reported regular rhythm with sinus tachycardia with no signs of ectopy. The PR, QRS, and T-waves were normal with no changes to his ST-wave. On arrival, he displayed severe respiratory deterioration with dyspnea and hyperventilation with measured pulse oximetry of room air at 67%. Cardiac defibrillation was successfully performed by endotracheal tube (ET) intubation; 40 mg of propofol, 4 mg versed, and 50 mg of rocuronium were administered to sedate the patient.
Physical examination was notable for a heart rate of 136 beats per minute, a respiration rate of 40 breaths per minute, and hypertension (174 mmHg/104 mmHg). The cardiovascular examination was significant for rhythm sinus tachycardia with S1 and S2 heart tones present. For his pulmonary examination, he required mechanical ventilation at a rate of 15 liters per minute, 100% BiPap, and 5 cmH2O for positive end-expiratory pressure (PEEP). Bilateral crackle sounds were heard, along with an observed asymmetrical chest mount and intercostal retractions. The use of his accessory muscles was noted.
Given the report of a positive COVID-19 diagnosis with severe dyspnea and hyperventilation, there was high suspicion for SARS-associated pneumonia as the cause for his ARDS. He received an RNA nose swab and was started on a combination of Remdesivir, Rocephin, Zithromax, and Decadron (6 mg IV q 12 hours). Vaportherm was provided for additional oxygenation along with normal saline 150 cc/hour for sepsis. He was emergently taken to radiology for suspected pulmonary masses. Chest X-rays revealed bilateral airspace consolidations with no acute osseous abnormalities to confirm lateral airspace disease (Figure ). These consolidations would likely be a result of an infection/inflammation due to sepsis or viral pneumonia. The catheterization lab revealed an elevated filling pressure on the right side of his heart with a right atrial pressure of 21 mmHg and a pulmonary capillary wedge pressure of 14 mmHg. A computed tomography (CT) angiogram revealed a thrombus crossing the bifurcation that extended into the right upper, middle, and lower lobe segmental branches with a greater thrombus burden on the left pulmonary arteries and the right ventricle (Figure ). Minimal atheromatous plaques were found with no dissection or thoracic aortic aneurysm. Bilateral ground-glass consolidations with interstitial thickening were discovered in the lungs with an increased right to left heart ratio suggesting an underlying right heart strain to a certain degree. Upper and lower extremity Doppler ultrasounds showed occlusive and non-occlusive thrombus bilaterally on the patient’s lower extremity veins (Figure ).
Laboratory analysis displayed in Table was conducted upon the patient’s arrival. It showed increased concentrations of glucose (164 mg/dL), alanine (82 U/liter), and aspartate aminotransferase (43 U/liter) with a low platelet count of 100,000 μL. Low levels of fibrinogen at 132 mg/dl were measured. Elevated prothrombin time (PT) and partial-thromboplastin (PTT) were measured at 16.4 and 37 seconds, respectively. Elevated acidity levels were observed for the patient with increased lactic acid levels from 9.0 mmol/L to 10.3 mmol/L (Table ) and a decreased pH from 7.455 to 7.255 (Table ). The patient’s arterial blood gas values in Table revealed a low partial pressure of oxygen (pO2) of 58.3 mmHg and increased partial pressure of carbon dioxide (pCO2) of 40.2 mmHg. These blood gas values put the patient at a higher risk for respiratory failure with a decreased PaO2/FiO2 ratio of 58.3 mmHg/100%. This ratio meets the threshold feature for increased severity of ARDS []. Severe hypoxia with a PaO2/FiO2 ratio less than 250 is associated with community-acquired pneumonia (CAP) []. He had an abnormally elevated D-dimer level at 3.6 μg/mL (Table ).
The patient continued hyperventilating with a decline in oxygen saturation from 90% to 76.1% (Table ). He was deemed critical but in stable condition within the capability of the ICU. The attending physician explained to the patient and his family the status of his continued respiratory failure by the findings of the DVT and PE. The patient was transferred upon recommendations made by his attending physician and the intensivist to a nearby healthcare facility for higher-level (tertiary) care for further management. He underwent radiological intervention two days later to remove the clots from his lungs. The patient, unfortunately, continued to experience worsened dyspnea with no significant improvement, which resulted in his expiration approximately one month following his initial admission.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [151.5, 'kg']}",191.5,181.925,201.075,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 151.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (151.5 kg - 20 kg) = 191.5 mL/hr.
Hence, the patient's fluid maintenance is 191.5 mL/hr."
4744,22,Maintenance Fluids Calculations,physical,decimal,pmc-6580501-1,Extracted,"Our patient’s mother, 22-year-old previously healthy multigravida woman (Para 4, Gravida 6, Abortion 1, Live children 4) was admitted to the Beni General Hospital Ebola Treatment Center 2 days after onset of symptoms (fever, vomiting and malaise) and was confirmed positive for EBOV by polymerase chain reaction (PCR). She reported a 34 week pregnancy and confirmed that the previous pregnancy follow up was uneventful. She was discharged after 1 week of management made of rehydration, Cefixime, Paracétamol and other supportive measures.
At the gestational age of 38 weeks, vaginal delivery occurred after a 10 h labor, the foetus was in breech presentation with meconial amniotic fluid and a normal placenta. The female newborn baby did well initially with an Apgar score of 8/9/10. General and neurologic examination did not reveal any pathology. The vital signs and anthropometric parameters at birth were as follows: temperature 36.5 °C, regular breathing at 52 cycles per minute and heart rate 146 beats per minute; weight of 3500 g, head circumference of 36 cm and height of 53 cm. The haemoglobin level was 16 g / dl; the umbilical cord blood PCR, the blood and salivary swabs were negative for the Ebola virus disease. She was subjected to an antibiotic therapy made of cefotaxime (3x200mg/day) and was discharged after 5 days.
At 1 month and 6 days of age, the baby was growing normally, she weighed 4100 g (versus 4400 g ideally), she was being breastfed and her mother reported no illness in the past days of her life.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4100.0, 'g']}",16.4,15.58,17.22,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4100.0 g so this converts to 4100.0 lbs * kg/1000 g = 4.1 kg. Hence, the patient's maintenance fluid is 4.1 kg * 4 mL/kg/hr = 16.4 mL/hr.
Hence, the patient's fluid maintenance is 16.4 mL/hr."
4745,22,Maintenance Fluids Calculations,physical,decimal,pmc-7234858-1,Extracted,"On April 6, 2018, a 49-year-old Korean man with end stage renal disease (ESRD) was transferred to our hospital for kidney transplantation. He visited emergency room at local hospital due to nausea and vomiting one month ago. Laboratory findings revealed renal failure (blood urea nitrogen 137 mg/dL, serum creatinine 20.5 mg/dL) and anemia (hemoglobin 9.1 g/dL) and metabolic acidosis on arterial blood gas analysis (pH 7.3, bicarbonate 16.4 mEq/L). Routine urinalysis revealed no proteinuria or hematuria. Complement levels were normal range and autoantibodies (Antinuclear antibody and antineutrophil cytoplasmic antibody) were negative. Chest PA showed no cardiomegaly or pulmonary edema, and Kidney-Ureter-Bladder radiography (KUB) was non-specific. Kidney ultrasonography revealed diffusely increased echogenicity and kidney size was smaller than normal (8.2 × 5.0 cm). The abdominal computed tomography showed no evidence of stone in both kidneys ().
Due to uremic symptoms, emergency hemodialysis was started and the kidney biopsy was performed to identify the cause of ESRD. The kidney biopsy showed foci of tubular damage with deposition of translucent crystals of different shapes which are predominantly intraluminal, and confirmed these crystals as calcium oxalate crystals using polarized light (). Final report of pathology was chronic tubulointerstitial nephritis with oxalate crystal deposits and a change of ESRD.
He was an office worker. He received regular national health examination including renal function and urinalysis, and both results were normal until two years before admission. His height and body weight were 167 cm and 70 kg. Body mass index was 25 kg/m2. Review of medical history revealed no history of kidney stone, diabetes, hypertension and operation. He had no medical family history. From the drug history, he had taken Chaga mushroom powder for 5 years due to atopic dermatitis. Initially, he had taken 3 g daily for 4 years following company's recommendation and 9 g of powder for another year because his symptom did not improve.
Based on pathologic finding (oxalate nephropathy) and drug history (long-term exposure to Chaga mushroom), we suspected the association between Chaga mushroom and oxalate nephropathy in our case. Thus, we requested oxalate content of remained Chaga mushroom to researcher/clinical pharmacology division of Catholic Medical center clinical research coordinating center of Korea. Measurement of oxalate was performed by high performance liquid chromatography (HPLC), and analysis revealed extremely high content of oxalate in Chaga mushroom powder (0.14 g of oxalate per 1 g of Chaga mushroom powder).
We finally diagnosed this case as Chaga mushroom-induced oxalate nephropathy with kidney biopsy findings, drug history and high content of oxalate. Clinical course of our case was unfavorable. Renal function has not recovered and he is on maintenance hemodialysis for 18 months.
This study was approved by the Institutional Review Board (IRB) of the Catholic University of Korea (IRB No. 2019-3713-0001) and an informed consent was received from the patient and a caregiver. The images are published under agreement of the patient.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [70.0, 'kg']}",110,104.5,115.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 70.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (70.0 kg - 20 kg) = 110.0 mL/hr.
Hence, the patient's fluid maintenance is 110.0 mL/hr."
4746,22,Maintenance Fluids Calculations,physical,decimal,pmc-3438423-1,Extracted,"A 30-month-old female was brought to the emergency department after a brief (<5 minutes) generalized convulsive seizure. The patient had displayed a fever for the 3 days before admission, had vomited approximately 15 times, and had experienced 2 or 3 episodes of watery diarrhea on the day of admission. Before arrival at the emergency department, the patient experienced an episode of shaking of the arms and legs, with the eyes rolling upward. The witnesses' descriptions were consistent with a generalized tonic-clonic seizure. The patient's past medical history, family history, growth history, and developmental history were otherwise unremarkable. The patient's temperature was 37.5℃, heart rate 110, respiratory rate 28, weight 13.1 kg (50-75th percentile) and length 96.7 cm (95-97th percentile). The patient exhibited a drowsy mental status, but other neurological examinations did not reveal other defined abnormal findings. The patient underwent extensive diagnostic evaluations. The results of lab tests performed on admission were positive for rotavirus antigen in stool. Laboratory findings included a WBC count of 12,600/µl and platelet count of 905,000/µl; both were mildly elevated from normal. There were non-specific findings on all other laboratory tests, including a comprehensive metabolic panel, spinal fluid, blood culture, and urine culture. The patient was diagnosed with RE by a pediatric neurologist. The patient received effective replacement of fluids and electrolytes. Anticonvulsant medication was not taken without recurrent seizures. After one week, the patient displayed a much improved condition and was discharged 2 weeks after onset. Brain MRI, including DTI, was performed at onset and one week after onset. Lesions were well defined and ovoid in the SCC. The SCC lesion was homogeneously hyperintense on T2-weighted images and isointense or slightly hypointense on T1-weighted images; the lesion was not detected in MRI conducted one week later (). DTI data were acquired twice simultaneously with a conventional MRI (onset and one week after onset) using a 1.5-T Philips Gyroscan Intera system equipped with a multi-channel head coil with a single-shot spin echo-planar imaging sequence. For each of the 32 non-collinear and non-coplanar diffusion-sensitizing gradients, 60 contiguous slices were acquired parallel to the anterior commissure-posterior commissure line. Imaging parameters were as follows: matrix=128×128 matrix; field of view=221×221 mm2; TE=76 ms; TR=10,726 ms; SENSE factor=2; EPI factor=49; b=1,000 mm2 s-1; NEX=1; and a slice thickness of 2.3 mm. Eddy current image distortions and motion artifacts were removed using affine multiscale 2-dimensional registration, which was performed using the Oxford Centre for Functional Magnetic Resonance Imaging of Brain (FMRIB) Software Library (FSL, ). The analysis for callosal projections was conducted using a single region of interest (ROI) approach using DTI-studio software CMRM (Johns Hopkins Medical Institute, Baltimore, USA). A callosal ROI was defined manually at the red portion of the midsagittal plane on the color map. Additional fiber tracking for the fornix and the cingulum were identified using fibers passing through two ROIs on the color map. The seed ROI of the fornix was placed on the junction between the column and body, and the target ROI was the junction between the body and crus. For the cingulum, the seed ROI was located in the green portion of the anterior cingulum areas and the target ROI was in the green portion of the posterior cingulum areas on the coronal slice. Fiber tracking was initiated at the center of a seed voxel with a fractional anisotropy (FA) >0.2 and ended at a voxel with a fiber assignment of FA <0.2 and a tract turning-angle of <60 degrees. Also, the FA values of cingulum, corpus callosum and fornix were measured. The whole corpus callosum was divided into 5 regions (genu, rostral body, body, isthmus and splenium) according to a well-established protocol, with 7 subdivisions of the corpus callosum, and FA and apparent diffusion coefficient (ADC) values of each of the 5 regions of the corpus callosum were measured. We evaluated the FA and ADC values of 3 divided regions of the fornix (column, body and crus) ().
The initial FA value of SCC at onset (0.66) was noticeably lower than that of follow-up FA value at one week after onset (0.77). However, the other regions of the corpus callosum showed no definite differences in FA values between the initial and follow-up data. For the fornix, only the region of the right crus had prominent interval changes between initial (0.33) and follow-up value (0.40). The cingulum showed no definite differences between initial and follow-up data. The initial ADC value was decreased and the follow-up value was increased, in the SCC and right fornical crus regions. For the other regions, there were no definite differences between initial and follow-up ADC values. The results of initial DTT demonstrated spared integrity of the corpus callosum, although a splenial lesion was apparent on conventional MRI. However, fornix revealed discontinuity of the right fornical crus. On the follow-up DTT at one week after onset, the interrupted right fonical crus was restored. In the cingulum, there were no definite abnormal findings at onset or at follow-up DTT (, ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [13.1, 'kg']}",46.2,43.89,48.51,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 13.1 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.1 kg - 10 kg) = 46.2 mL/hr.
Hence, the patient's fluid maintenance is 46.2 mL/hr."
4747,22,Maintenance Fluids Calculations,physical,decimal,pmc-5828416-1,Extracted,"A seventeen-year-old African-American female with mood disorder, infrequent migraine without aura, GERD, and ulcerative colitis presented to the emergency department with four weeks of abdominal pain, hematochezia, and an unintentional 28-pound weight loss over those four weeks. She had been poorly compliant with her medications and follow-up. MRI of the abdomen was notable for diffuse mucosal enhancement of the colon, which contained numerous air fluid levels, consistent with ulcerative colitis exacerbation. Colonoscopy showed multiple ulcerations of the transverse and distal colon. She was hospitalized for three weeks and failed medical management with two rounds of infliximab. Additionally, she required blood transfusions due to intractable bloody diarrhea. Ultimately, the decision was made to proceed with total colectomy and ileostomy, which she tolerated without incident.
Notably, on her fourth day of hospitalization, she was found down in her bathroom. She was disoriented and complained of a headache. Initial head CT without contrast noted a small subdural hematoma overlying the high bilateral frontal lobes and along the falx. She was transferred to the pediatric ICU, where she subsequently suffered three witnessed tonic-clonic seizures over a twenty-four-hour period. She was treated acutely with lorazepam and loaded on both Keppra and fosphenytoin, and her seizures stopped. The following morning, her repeat CT of the head noted hyperdensity of the superior sagittal, right transverse, and right sigmoid sinuses, raising the suspicion of a venous sinus thrombosis. MRI, MRA, and MRV were therefore obtained. MRA was unremarkable. Her MRI and MRV are shown below in Figures and , respectively.
She was started on therapeutic Lovenox with goal Factor Xa level 0.6 since she was anemic from the ulcerative colitis flare. A hypercoagulable panel was negative for protein C deficiency, protein S deficiency, Factor V Leiden, antithrombin deficiency, factor II mutation, and antiphospholipid antibody panel. She was not taking medications prior to hospitalization. She denied a smoking history. Her only known risk factor was ulcerative colitis.
The patient was seen by pediatric neurology while being in the PICU, and her EEG was notable for bifrontal sharps with occasional right temporal sharp complexes. Since her seizures stopped within twenty-four hours, fosphenytoin was discontinued after its load. She was continued on Keppra. Repeat imaging one week later showed significantly improved flow in all three involved sinuses and resolution of the right frontal intraparenchymal and bifrontal subdural hemorrhages.
She was hospitalized for nearly one month for management of the ulcerative colitis flare, which ultimately required total colectomy and ileostomy. At follow-up, she was doing well. She was continued on Keppra and Lovenox. At that time repeat MRV was notable only for a small residual thrombus in the superior sagittal sinus, as seen in .","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [28.0, 'lbs']}",45.40116,43.1311,47.67122,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 28.0 lbs so this converts to 28.0 lbs * 0.453592 kg/lbs = 12.70058 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.70058 kg - 10 kg) = 45.40116 mL/hr.
Hence, the patient's fluid maintenance is 45.40116 mL/hr."
4748,22,Maintenance Fluids Calculations,physical,decimal,pmc-2847967-1,Extracted,"A 53-year-old Caucasian male with a history of heavy nonsteroidal anti-inflammatory drug (NSAID) usage and chronic alcohol abuse presented to the emergency room with a four-month history of dysphagia, 45-pound weight loss, coffee-ground vomitus and upper abdominal pain. Physical examination was normal, except for nonspecific epigastric tenderness, as were routine laboratory studies including CBC, chemistries and liver function studies. Although chest X-rays showed only mild perihilar consolidation, esophagogastroduodenoscopy (EGD) confirmed the presence of a large, intrathoracic, cystic structure, partially filled with necrotic debris, arising from a large entry orifice just above the gastroesophegal junction. Computed tomography (CT) of the chest demonstrated bilateral pleural effusions, pneumomediastinum, and a 6.7 cm diameter, fluid-filled diverticulum extending from the esophagus into the posteromedial left hemithorax, Fluoroscopy, performed during injection of barium through a nasogastric tube positioned in the distal esophagus, showed contrast extravasation from the distal esophagus into this cavity in the left chest.
The patient was treated with targeted drainage, intravenous antibiotics, nasogastric decompression, and enteral nutrition. However, he became septic two days after the EGD, and required emergency thoracotomy with distal esophagectomy following several days later. After ashort term of ventilator support and parenteral nutrition, he was weaned off of fboth, and was discharged with a PEG tube for enteral feedings, and is currently being evaluated for esophagostomy reversal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [45.0, 'lbs']}",60.41164,57.39106,63.43222,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 45.0 lbs so this converts to 45.0 lbs * 0.453592 kg/lbs = 20.41164 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (20.41164 kg - 20 kg) = 60.41164 mL/hr.
Hence, the patient's fluid maintenance is 60.41164 mL/hr."
4749,22,Maintenance Fluids Calculations,physical,decimal,pmc-2943703-1,Extracted,"An 8-year-old, 17-kg girl child suffering from Bartter’s syndrome (BS) with a history of gall stones was posted for laparoscopic cholecystectomy. She had been diagnosed with BS 1.5 months before and was on oral potassium chloride. A history of maternal polyhydramnios and premature birth was present. No haemolytic and metabolic disorders that could contribute to gall stone formation were found. History of excessive fatigue during physical stress, poor growth and increased thirst was present. Serum potassium during the first evaluation was 2.9 mmol/l with increased 24-h urinary potassium and chlorides []. Electrocardiogram and renal and liver functions were within normal limits. The younger sibling of the patient was also suffering from BS.
Pre-operatively, serum potassium was 3.5 mmol/l but urinary potassium and chloride remained high []. The patient was premedicated with oral trichlofos and ondansetron. Her arterial pressure (BP) was 108/60 mmHg and pulse 88/min. We started two intravenous infusions: one of 10 mmol of potassium chloride in 250 ml of Ringer lactate, at 40 ml/h, and second of normal saline, for maintaining hourly volume requirement. Preoxygenation was followed by induction with inj. propofol 40 mg with 1% lignocaine; endotracheal intubation was performed after administering succinyl choline 30 mg; anaesthesia was maintained with oxygen-nitrous oxide (33%:66%), vecuronium, sevoflurane 0.5-1 % and IPPV to maintain end-tidal CO2 (EtCO2) of not less than 5.3 kPa. Entry points of laparoscopic cannulae were infiltrated with 0.25% bupivacaine. The patient was positioned for cholecystectomy (anti-Trendelenberg of 20° and left tilt of 15°). Monitoring consisted of pulse oximetry, non-invasive blood pressure, ECG, temperature, capnography, urine output, blood gas analysis and electrolytes. Nasogastric tube, Foley’s catheter and radial arterial line were inserted after induction.
Haemodynamics were stable intra-operatively but for increased heart rate and BP during the establishment of pneumoperitoneum which needed increased sevoflurane concentration and temporary hyperventilation. The ABG sample showed slight alkalosis and the rate of ventilation was adjusted to maintain EtCO2 of 5.3 kPa. Intra-abdominal pressure was limited to 1.87 kPa (14 mmHg). Neuromuscular blockade reversal and extubation were uneventful. Rectal diclofenac (25 mg) was inserted for post-operative analgesia. The procedure was completed in exactly 55 min and the patient was repositioned flat on the operating table. BP and heart rate were normal and the respiratory rate was 16 per min. Ten minutes after extubation, serum potassium was 2.3 mmol/l with mixed metabolic and respiratory alkalosis [Table and ]. The rate of infusion of the Ringer lactate and potassium chloride solution was increased (60ml/h, so as to provide 2.4 mmol/h of potassium). Haemodynamic parameters remained normal subsequently and the respiratory rate stabilized at 14 per minute. ABG after 3 and 6 h showed persistent metabolic alkalosis, with normal potassium levels (3.6 mmol/l and 3.4 mmol/l). The urine output was adequate throughout; the patient was allowed liquids orally after 6 h. Oral potassium chloride was resumed. The patient was discharged on the second day, without complications. Gall stone analysis showed the presence of organic matter, calcium, bile pigment, traces of carbonate and cholesterol. At 3-week follow-up, serum potassium was 1.8 mmol/l with no symptoms; oral potassium chloride was increased as per paediatrician’s advice.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [17.0, 'kg']}",54,51.3,56.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 17.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (17.0 kg - 10 kg) = 54.0 mL/hr.
Hence, the patient's fluid maintenance is 54.0 mL/hr."
4750,22,Maintenance Fluids Calculations,physical,decimal,pmc-4297396-1,Extracted,"A 2.5-year-old caucasian boy presented to the Pediatric Emergency Department with a one-day history of lethargy and two episodes of bilious vomiting during the past three hours, without any fever. The symptoms appeared two days after he had returned from a 10-day holiday in Crete (Greece), where he ate seafood and fish every day. A cefpodoxime treatment had been introduced 9 days before the admission for an upper respiratory tract infection.
His past medical history revealed mild developmental delay and poorly controlled focal epilepsy, despite valproic acid and clobazam treatment, secondary to an ischemic episode in the neonatal period. No fever or modification of the seizure pattern had been noted by the parents.
Clinical examination revealed a 15.3 kg body weight conscious but lethargic child lying still in a fetal position. Temperature was 37°C, heart rate 105/min, and blood pressure 135/88 mmHg. Palpation of the abdomen was tender and bowel sounds were absent. However, no guarding or rebound tenderness was observed. Laboratory work-up showed the following results: white blood cell count 24.8 G/L with immature neutrophils 6.2 G/L, normal CRP, procalcitonin, AST, ALT and electrolytes. Intravenous lactates were 2.3 mmol/L, and amylase and lipase were elevated (561 U/L and 1074 U/L respectively).
Abdominal ultrasound showed severe thickening of the intestinal walls in the right lower quadrant, with a large amount of multiloculated peritoneal fluid and hyperechogenic mesenteric fat. The ileocecal valve was hypervascularized. The visualized proximal part of the appendix showed no abnormality and the pancreas also had a normal aspect.
Laparoscopy did not reveal any intra-abdominal abnormality, especially no intestinal wall perforation, but the presence of abundant purulent abdominal fluid and fibrinous membranes in the lower abdomen, thus confirming the diagnosis of primary peritonitis. The appendix was removed. Histology showed no sign of acute appendicitis (Figure ). The peritoneal fluid grew for a gram-positive, coccoid, aerobic, coagulase-negative, non-encapsulated germ, identified as a Kocuria marina. The organism was grown on BHI (brain heart infusion), a highly nutritious growth medium for fastidious and non-fastidious microorganisms. Blood culture was negative. Unfortunately, peritoneal fluid could not be sent for PCR. Blood PCR was negative for K. marina.
The patient was post-operatively admitted to the intensive care unit and treated with intravenous broad spectrum antibiotics (piperacillin and tazobactam) during 7 days. He gradually improved and was discharged on day 7, with a supplemental 7-day course of oral ciprofloxacin.
SBP is a rare presentation of peritonitis in childhood. Most cases are due to Streptococcus pneumoniae, Escherichia coli or staphylococcal strains []. However, in few cases no pathogen can be identified []. To our knowledge, this is both the first description of SBP caused by Kocuria marina in a child, and the first description of a K. marina SBP in a patient with no underlying risk factor.
Kocuria spp are members of the Micrococcaceae family. They are gram-positive, usually aerobic, coccoid, non-encapsulated bacteria. Seventeen species have been recognized so far []. They are environmental bacteria that can be encountered in mammals including humans’ skin and in the commensal flora of the oropharynx. Certain species (but not K. marina) have been isolated from traditional Korean fermented seafood []. Kocuria-related infections are rare. Bacteremia, peritonitis, brain abscess, endocarditis, cholecystitis and UTI have been described with K. rosea, K. kristinae, K. varians, and K. rhizophila (Table ).
Kocuria marina has been isolated from marine sediments and first identified in 2004 []. In 2009, Lee et al. described two cases of primary peritonitis caused by K. marina in adult patients undergoing peritoneal dialysis []. A small case series reported a positive K. marina blood culture in a 57 year-old oncologic patient with a central venous catheter []. However, it was considered a contaminant by the authors. We did not find any other report of K. marina infection.
In our patient, the organism was identified on peritoneal fluid samples, obtained at the time of surgery. Contamination of the fluid from the skin or from the intestinal content seems very unlikely because of the sterile skin condition at the time of surgery and the absence of visible intestinal perforation. The sample was seeded on the surface of a 5% sheep blood agar and incubated at 35°C in 5% CO2. After 48 h of incubation, the isolate was identified as Kocuria marina by MALDI-TOF mass spectrometry (score value = 2.014). MALDI target plates were inoculated by picking a freshly grown overnight colony with the tip of a sterile toothpick and smearing the specimen directly onto a ground steel MALDI target plate in a thin film. The microbial film was then overlaid with 1.5 μl of a MALDI matrix (a saturated solution of α-cyano-4-hydroxy-cinnamic acid in 50% acetonitrile–2.5% trifluoroacetic acid) and allowed to dry at room temperature. Mass spectra were acquired using the MALDI-TOF spectrometer in a linear positive mode (Microflex; Bruker Daltonics). Measured mass spectra ranged from 2,000 to 20,000 Da. Extraction of the peaks from the generated mass spectra and their matching against the reference spectra of the integrated database provided by the manufacturer was performed with MALDI Biotyper software (Bruker Daltonics). Unfortunately, the peritoneal fluid could not be sent for PCR-based confirmation of the species and antibiotic susceptibilities were not performed.
According to a 2010 review [] which focuses on antibiotic susceptibilities for Kocuria species, K. marina should respond to ampicillin and other betalactam-based antibiotics while showing a relative resistance to penicillin []. At the time of presentation our patient had been treated with oral cephalosporin for 9 days, which might have covered early symptoms and might explain the acute severe clinical presentation.
Another interesting finding is the description of the presence of K. marina in seafood and marine sediments. We can assume a potential relationship between the daily fish and seafood consumption over the 10-day period preceding the symptoms in our patient and the peritoneal infection due to this bacterium. Indeed, haematogenous dissemination is frequently described with Kocuria species. In our patient, the pathogen might have been ingested with sea-food, then translocated to mesenteric lymph nodes and to the peritoneal cavity. However, other pathophysiologic mechanisms are possible. Indeed, transient bacteremia following upper respiratory tract colonisation in the context of the upper respiratory tract infection preceding the peritonitis may also be encountered, even if less probable and not documented in this case.
Direct infection through cutaneous breaches associated with sea-bathing seems unlikely in our patient [].","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15.3, 'kg']}",50.6,48.07,53.13,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15.3 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.3 kg - 10 kg) = 50.6 mL/hr.
Hence, the patient's fluid maintenance is 50.6 mL/hr."
4751,22,Maintenance Fluids Calculations,physical,decimal,pmc-7397898-1,Extracted,"A 2-year-old, 4.4 kg, intact female Persian cat was presented at the Small Animal Teaching Hospital, Faculty of Veterinary Science, Chulalongkorn University as the normal volunteer for another research. All processes of the study were conducted under the approval by The Institution Animal Care and Use Committee of Faculty of Veterinary Science, Chulalongkorn University (CU-IACUC), approval number: 1631073. After history taking, physical examination, routine laboratory tests and the test for feline leukaemia virus (FeLV) and feline immunodeficiency virus (FIV) (Witness® Zoetis) were done and normal ranges of former tests were achieved, the cat was subjected to perform abdominal radiography, ultrasonography and computed tomography (CT), using the previous study protocol (Darawiroj & Choisunirachon, ).
The abdominal radiograph includes lateral and ventrodorsal projections was performed using the digital radiograph (Brivo DR-F, GE, USA; 65 kVp and 10 mAs) without sedation or anaesthesia. In brief, the cat was pre-medicated with acepromazine maleate (0.03 mg/kg, Combistress® Belgium) and tramadol hydrochloride (2 mg/kg, Tramache®). Subsequently, the anaesthetic induction was performed using propofol (2–4 mg/kg, Lipuro®) prior endotracheal tabulation. The anaesthesia was maintained by isoflurane (2%–5%, AERRANE®). CT was conducted using a 64-slice, CT scanner (Optima CT660) in prone position with the head point into the gantry and the field of view was set to be covered the whole abdomen. After the pre-contrast CT (pcCT) images of abdomen were obtained, iohexol contrast medium (600 mgI/kg, Omnipaque 300®) was intravenously administrated. Contrast-enhanced CT images (cCT) were then performed using a low-pass filter, 1.25-mm slice thickness, collimator pitch at 0.531, matrix of 512 × 512, peak kilovoltage of 120 kVp and automated amperage.
All imaging data were collected as the Digital and Communication in Medicine (DICOM) files and reanalysed by DICOM viewer software (OsiriX®). The cCT was displayed using a soft tissue window at 350 Hounsfield Unit (HU) of window width (WW) and 40 HU of window level (WL). After the abnormality of ureter was detected, maximum intensity projection (MIP) was applied to clearly unveil morphology and location of ureter.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.4, 'kg']}",17.6,16.72,18.48,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.4 kg. Hence, the patient's maintenance fluid is 4.4 kg * 4 mL/kg/hr = 17.6 mL/hr.
Hence, the patient's fluid maintenance is 17.6 mL/hr."
4752,22,Maintenance Fluids Calculations,physical,decimal,pmc-5458028-1,Extracted,"A 58-year-old male with dyslipidemia, an eight-year history of T2DM, a family history, his mother, of T2DM, with no known micro- or macrovascular complications, was admitted to the emergency department for malaise, epigastric pain, polyuria, and progressive dyspnea which had begun 10 h ago. He had experienced a 2-kg weight loss over the last few days. His usual medications included aspirin 100 mg q24 h, atorvastatin 40 mg q24 h, and metformin 850 mg q8 h, which had been switched to dapagliflozin 20 days before, due to poor glycemic control, with HbA1c 12% (108 mmol/mol). His vital signs included a heart rate of 122 bpm, respiratory rate 33 rpm, blood pressure 142/70 mmHg, temperature 36.1°C, and body mass index 22.5 kg/m2. On physical examination, somnolence, dry skin and mucous membranes, a Kussmaul breathing pattern, and a capillary refill of 3 sec were observed. Blood tests revealed hemoglobin 17.1 g/dL (13.5–18), leukocytes 19.5 × 103 (4–10 × 103), platelets 296 × 103 (150–450 × 103), glucose 248 mg/dL (60–100), creatinine 0.97 mg/dL (0.67–1.17), sodium 136 mmol/L (135–145), potassium 4.7 mmol/L (3.5–5.5), chloride 101 mmol/L (95–112), phosphate 4.9 mg/dL (2.5–4.5), amylase 70 U/L (10–115), lipase 28 U/L (1–67), pH 6.95 (7.35–7.45), pCO2 23 mmHg (35–45), HCO3 5 mmol/L (22–26), lactate 1.8 mmol/L (0–1.5), urine ketone bodies >150 mg/dL (0–0), CK 112 U/L (1–190), CK-MB 7.3 ng/mL (0.1–5), and troponin I 0.07 ng/mL (0.001–0.05). The electrocardiogram (EKG) showed sinus rhythm with right bundle branch block, and nonspecific repolarization abnormalities. Because of the right bundle branch block was not previously known, a new troponin test was performed six hours later with a peak value of 4.28 ng/mL. Treatment with crystalloids, continuous infusion of intravenous insulin, and administration of potassium and sodium bicarbonate were begun in the emergency room (ER). Due to a poor response over the first two hours, with the persistence of lactic acidosis, the patient was transferred to the intensive care unit (ICU), where more aggressive rehydration with crystalloids was started, without further modifications of the original therapeutic plan.
Two days later, the patient was discharged from the ICU to the endocrinology ward. Because of his coronary risk factors and the elevated troponin on admission, a coronary angiography was performed, showing triple-vessel disease. Successful bypass surgery without extracorporeal circulation was performed a few days later, with internal mammary artery grafts to the anterior descendent and marginal obtuse arteries and a saphenous vein graft to the right coronary artery. He was discharged 3 days later on Lantus™ Sanofi-aventis S.p.a Valcanello,03012 Anagni (FR), Italia (insulin glargine) 20 IU and Insulina Novorapid™: Novo Nordisk A/S. Hallas Allé, DK-4400. Kalundborg, Dinamarca (insulin aspart) 6-4-4-0 IU subcutaneous insulin, aspirin, clopidogrel, enalapril, bisoprolol, atorvastatin, and furosemide. The oral antidiabetic treatment with dapagliflozin was not restarted. During follow-up by endocrinology, C-peptide, anti-GAD, and IA-2 antibodies were required due to normal BMI and lack of family history suggested T1DM or a latent autoimmune diabetes of adults (LADA) rather than T2DM as etiology of his diabetes. C-peptide was 1 mg/dL (0.9–7.1) with glycemia 214 mg/dL (60–100), anti-GAD <5 U/mL (0–12.5), and anti-IA-2 <7.5 U/mL (0–7.5).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.0, 'kg']}",8,7.6,8.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.0 kg. Hence, the patient's maintenance fluid is 2.0 kg * 4 mL/kg/hr = 8.0 mL/hr.
Hence, the patient's fluid maintenance is 8.0 mL/hr."
4753,22,Maintenance Fluids Calculations,physical,decimal,pmc-3375196-1,Extracted,"A 33-year-old man was admitted to our hospital because of generalized weakness, emaciation and anorexia 12 years after massive small bowel resection. Our patient underwent massive small bowel and ileocecal resection because of small bowel volvulus 12 years ago. An end-to-side anastomosis was performed between his proximal jejunum and his ascending colon, with only 40 cm of his small bowel remaining. Subsequent bowel rehabilitation therapy, which included enteral nutrition with dietary fiber, recombinant human growth hormone and glutamine, was instituted for four weeks []. Our patient was weaned from total parenteral nutrition (TPN) and had a normal diet up to the present.
One month ago, our patient developed diarrhea and weight loss of 7 kg with no obvious predisposing cause; he felt weak, anorexic and dizzy, and became progressively cachexic. Urinary volume was reduced, while stool volume was increased. On admission, our patient's body weight was 36 kg, body mass index (BMI) 12.2 kg/m2, heart rate 80 beats per minute (bpm), blood pressure 70/50 mmHg, and respiratory rate 18 bpm. He was oriented and cognitively intact. Pitting edema appeared in his lower extremities. An abdominal examination revealed previous surgery scarring, thin skin, a scaphoid abdomen, and negative shifting dullness. A chest X-ray showed a high density shadow of a nodule outside his right upper lung, considered to be rib calcification. A lower limb X-ray and ultrasound of both kidneys and ureters were normal. An ultrasound of his gallbladder showed gallbladder atrophy. An electrocardiogram showed normal sinus rhythm with T wave changes (II/III/avF/v4-6 flat, inversion), with incomplete right bundle branch block. All laboratory values are presented in Table .
Our patient was diagnosed with severe malnutrition and was supported by blood transfusion, parenteral nutrition (500 kcal/day), fluid, electrolyte, trace element and multi-vitamin supplementation (one ampoule each of Soluvit® and Addamel® daily), along with thiamine 100 mg intravenously prophylactically. Our patient's physical strength improved after these treatments, and pitting edema of the lower extremities decreased. Within 24 hours, our patient presented with profound fatigue and flaccid weakness of all four limbs. His heart rate was 98 bpm, respiration was normal, but biochemical investigation showed severe hypophosphatemia 0.05 mmol/L (Table ), hence a clinical diagnosis of RFS was made, and immediately the patient was transferred to the intensive care unit (ICU) for closer monitoring. Parenteral and enteral nutrition were interrupted and intravenous supplementation with phosphate polyfusor (120 mmol on the first day, then 60 mmol per day intravenously or enterally for five days) was initiated, along with enteral and parenteral multi-vitamins and trace elements (two ampoules each of Soluvit®, Vitalipid® and Addamel® daily for two days, thereafter one ampoule of each daily). He also received a once daily intramuscular dose of Vitamin B12 0.1 mg and thiamine 100 mg. In addition, a hydrocortisone injection 100 mg was given to prevent adrenal insufficiency on the fifth day. A plasma transfusion was given to expand blood volume because blood pressure fell to 97/60 mmHg temporarily.
On the seventh day, our patient had numbness of his limbs, diarrhea and dyspnea. At the same time, a chest X-ray indicated right middle lobe pneumonia. Respiratory muscle weakness was considered to be the reason, and an emergency tracheotomy with mechanical ventilation was done, and sputum aspiration was regularly performed. Anti-diarrhea (diphenoxylate 1 pill three times a day by mouth), anti-infection (moxifloxacin 0.4 g/day intravenously), and antacid (omeprazole 40 mg intravenously twice daily) therapy were given immediately.
On the ninth day, when his blood chemistry became normal, enteral nutrition was resumed at 500 kcal/day and increased gradually. On the twelfth day, total enteral nutrition was well tolerated with improved pulmonary symptoms, and our patient was successfully weaned from mechanical ventilator support. Subsequently, he received recombinant human growth hormone therapy (10 u/d) and total enteral nutritional support for one month and recovered uneventfully with a weight of 45 kg (gain of 9 kg) and a BMI of 15.2 kg/m2.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [45.0, 'kg']}",85,80.75,89.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 45.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (45.0 kg - 20 kg) = 85.0 mL/hr.
Hence, the patient's fluid maintenance is 85.0 mL/hr."
4754,22,Maintenance Fluids Calculations,physical,decimal,pmc-5008484-1,Extracted,"A 43-year-old, 101 kg, body mass index (BMI) 31.2, Caucasian male was scheduled for an elective right frontal craniotomy for a meningioma excision. The patient presented with right-sided headache (no signs of raised intracranial pressure), hypothyroidism, and mild obstructive sleep apnea (OSA). All laboratory investigations were unremarkable. Patient's pre-op vitals were HR 60 beats/min, BP 112/73, and 98% oxygen saturation on room air. Electrocardiogram (ECG) showed a normal sinus rhythm with a baseline heart rate of 50 beats per minute. All the standard monitors were attached and the preinduction invasive arterial line was also inserted. The patient was induced with remifentanil 1 mcg/kg bolus, propofol 200 mg, and rocuronium 60 mg intravenously, and tracheal was intubated with 8 mm cuffed endotracheal tube. Anesthesia was maintained on propofol infusion at 100 to 150 mcg/kg/min. This was supplemented with remifentanil 0.05 to 0.15 mcg/kg/min and desflurane at 3% end tidal concentration in oxygen and air (1:1). During the time of dural separation from tumor, the patient developed 2 episodes of severe bradycardia. Each time the heart rate went down to 35 to 37 beats/min lasting around 36 s; however, the blood pressure was maintained at the baseline. Surgeon was notified; however, there was no other option left except to continue separating dura from the tumor. We therefore decided to increase the depth of anesthesia. Each episode of bradycardia was terminated with a bolus of 50 mg of propofol intravenously. At the end of the procedure the muscle relaxant was reversed with neostigmine 2.5 mg and 0.4 mg glycopyrrolate. The patient was successfully extubated and transferred to postanesthesia care unit for further observation. The further clinical follow-up was uneventful.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [101.0, 'kg']}",141,133.95,148.05,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 101.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (101.0 kg - 20 kg) = 141.0 mL/hr.
Hence, the patient's fluid maintenance is 141.0 mL/hr."
4755,22,Maintenance Fluids Calculations,physical,decimal,pmc-7843668-1,Extracted,"A 55-year-old, 168-cm, 88.3-kg male with a body mass index (BMI) of 31.3 kg/m2 was scheduled to undergo RARC for bladder cancer. He had diabetes mellitus and a history of smoking.
After placement of a lower thoracic epidural catheter, general anesthesia was induced. Anesthesia was maintained with combined general and epidural anesthesia. The FloTracTM system (Edwards Lifesciences, Irvine, CA, USA) was used to achieve adequate fluid management. The patient was placed in the lithotomy position with stirrups (Levitator®, Mizuho Medical, Tokyo, Japan), after elastic stockings (ES; Comprinet Pro® Size 3, Terumo, Tokyo, Japan) and intermittent pneumatic compression (IPC) devices (Flowtron Excel®, Muranaka, Osaka, Japan) were applied to prevent deep vein thrombosis (DVT). Intraoperatively, phenylephrine was infused at 0.5–1 mg/h to maintain mean blood pressure (BP) above 60 mmHg. Heart rate was kept stable between 50 and 90 beats/min and SpO2 was maintained at 98% or more.
RARC was performed using the da Vinci Xi surgical system® (Intuitive Surgical Inc., Sunnyvale, CA, USA). Total cystectomy, extended pelvic lymph node dissection, and intracorporeal urinary diversion with an ileal conduit were performed uneventfully. However, the surgical duration was prolonged as long as 481 min due to expansion of lymph node dissection. Total blood loss, including urine volume, and total infusion volume were 300 ml and 5560 ml, respectively. The patient remained in the lithotomy position for 515 min, during which he remained in an extreme 25-degree Trendelenburg position for 201 min. He was extubated immediately after the surgery and was transferred to the intensive care unit.
At 3 h postoperatively, he complained of paresthesia and pain over the right calf. The epidural infusion was discontinued because the paresthesia might result from the effect of epidural analgesia. However, the paresthesia and pain were exacerbated 1 h after suspension of the epidural infusion. Urgent blood examinations revealed an elevated level of creatine kinase (CK) (15,800 U/l). Computed tomography (CT) revealed swelling of the right calf (Fig. a). He was diagnosed with WLCS and transferred back to the operating theater for urgent fasciotomy at 7 h postoperatively.
Compartment pressures of the right calf measured under general anesthesia with a needle manometer (TraWave®, Edwards Lifesciences, Irvine, CA, USA) were high at 38, 19, and 14 mmHg in the anterior, lateral, and posterior compartments, respectively. Fasciotomies performed on both sides of the calf reduced compartment pressures to 18, 14, and 12 mmHg, respectively (Fig. b). Subsequent hematological examinations indicated a return of CK to a normal level (218 U/l) by postoperative day 15.
After the fasciotomy, he required debridement procedures twice due to local infection, followed by a skin graft to compensate for the skin defect 43 days after RARC. He was finally discharged from hospital 78 days after RARC without any neuromuscular disorders and in an ambulatory condition.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [88.3, 'kg']}",128.3,121.885,134.715,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 88.3 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (88.3 kg - 20 kg) = 128.3 mL/hr.
Hence, the patient's fluid maintenance is 128.3 mL/hr."
4756,22,Maintenance Fluids Calculations,physical,decimal,pmc-6392699-1,Extracted,"A 37-year-old man presented to our hospital with abdominal pain for 2 weeks. The pain was periumbilical, nonradiating, 4/10 in intensity, intermittent with no aggravating or relieving factors. The abdominal pain was associated with nausea, vomiting, loss of appetite, and chronic diarrhea. He did not notice blood or mucous in his stool. The diarrhea was associated with a 50-pound weight loss over the past 6 months. Review of system was significant for persistent frontal headaches with on and off dizziness over the last few weeks. He did not have fever, neck stiffness, blurry vision, rash, trauma, or any other sick contacts.
Patient was recently admitted to another hospital with similar symptoms, and as per the records received, was treated for hypo-osmolar hyponatremia and discharged after the symptoms had improved. His past medical history was significant for hypertension. He had no previous surgical history. Family history was significant for hypertension in both parents. He drank 3 to 4 beers every weekend. He was born and raised in Honduras, came to the United States in 2004, and had recently moved from Connecticut to New York about 7 months ago. He had not traveled outside United States since he came to the United States and was living with his 2 sisters; none of whom had any similar symptoms.
On presentation the patient was afebrile, with heart rate of 89 beats/min, with blood pressure of 120/62 mm Hg, and an oxygen saturation of 98% on ambient air. On examination, he was cachectic, alert, and oriented, and had dry oral mucosa, sunken eyes, and appeared dehydrated. His cardiorespiratory examination was unremarkable. His abdomen was soft, mildly tender in the periumbilical area with hypoactive bowel sounds. Neurological examination was unremarkable. The initial labs on presentation are tabulated in Table .
He was started initially on hypertonic saline for hyponateremia and possible neurological manifestations secondary to hypovolemic hyponateremia secondary to gastrointestinal losses and later switched to 0.9% normal saline once the serum sodium had improved with resolution of headache and dizziness. The patient was started on antiemetics for vomiting and antibiotics (metronidazole and ciprofloxacin) for diarrhea. Stool studies could not be collected due to patients’ noncooperation and later the diarrhea resolved after 2 days of hospitalization. He also had improvement in his vomiting.
His serum sodium levels did not improve to normal values despite medical therapy (Fig. ). To evaluate the cause of his persistent hyponatremia, further work up was done that revealed a serum osmolarity of 246 mOsm/kg (275–295 mOsm/kg), urine osmolality 177 mOsm/kg water (300–900 mOsm/kg water), urine sodium <20 meq/L (40–220 meq/L). He had subclinical hyperthyroidism (low TSH, normal T3, and free thyroxine levels). A cortisol stimulation test was done to rule out any adrenal insufficiency as a cause of hyponatremia, which showed appropriate response. The serum sodium levels during the hospitalization are shown in Figure .
The results were consistent with the presence of syndrome of inappropriate antidiuretic hormone secretion (SIADH) as the etiology of this patient's hyponateremia, in addition to the gastrointestinal losses; 0.9% normal saline was discontinued, and he was started on free water restriction. To evaluate the cause of SIADH, further work up including CT scan of head and chest to rule out potential causes of SIADH was performed which were unremarkable. The human immunodeficiency virus (HIV) and rapid plasma reagin (RPR) testing were also negative. His hospital course was complicated with sudden worsening of vomiting and diffuse abdominal pain. A CT scan of abdomen was done for further evaluation, which showed partial small bowel obstruction without any mass. A nasogastric tube was placed, and he was managed conservatively with resolution of the obstruction, but he persistently had intractable vomiting. Considering the history of chronic diarrhea, weight loss, intractable vomiting, he underwent an esophagogastroduodenoscopy (EGD) to evaluate for a possible small bowel pathology. Interestingly, we found edema and widespread whitish spots consistent with intestinal lymphangiectasia in the duodenum (Fig. ). Biopsies were taken from the stomach and small bowel. He was started on restrictive medium chain triglyceride (MCT) diet (low fat, high protein diet). The pathology report from the GI biopsies was reported as presence of extensive strongyloidosis infection with lymphocytic and focal eosinophilic infiltrate (Figs. and ). He was started on ivermectin. It was recognized that he had systemic strongyloidosis with extensive gastrointestinal involvement as well as being the cause of his SIADH. We wanted to further evaluate the reason of systemic strongyloidosis as it is usually associated with immunosuppression. A human T-cell lymphotropic virus (HTLV) 1 and 2 serology was sent that was reported as positive. After starting treatment with ivermectin patient's symptoms improved with increase in serum sodium and patient was able to tolerate regular oral diet.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [50.0, 'lbs']}",62.6796,59.54562,65.81358,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 50.0 lbs so this converts to 50.0 lbs * 0.453592 kg/lbs = 22.6796 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (22.6796 kg - 20 kg) = 62.6796 mL/hr.
Hence, the patient's fluid maintenance is 62.6796 mL/hr."
4757,22,Maintenance Fluids Calculations,physical,decimal,pmc-6905252-1,Extracted,"A 30-year-old pregnant woman, P1 (previous cesarean delivery), referred to Ain Shams University Fetal Care Unit as pregnant female 34 weeks + 2 days’ gestation with fetal umbilical cord mass for further evaluation. Further evaluation showed that she is pregnant 35 weeks’ gestation ± 1 week with estimated fetal weight of 2.639 kg, good amniotic fluid volume, normal umbilical cord, and a well-defined mass measuring 6.47 cm × 5.7 cm arising from the fetal oral cavity [].
The color flow mapping showed that the mass was well vascularized, especially in its center [Figures and ], and its blood supply was originated from the fetal oral cavity [].
The studied case managed by multidisciplinary team consists of senior obstetrician, neonatologist, anesthetist, and pediatric surgeon.
Fetal MRI was done before delivery to study the relation of the mass to the fetal airways and to exclude intracranial extension of the mass.[] T2-weighted MRI showed a hyperintense mass with a stalk projecting from the palate and upper lip, measuring 6.7 cm × 5.7 cm in size with no evidence of fetal airway obstruction and/or intracranial extension or central nervous system-related anomalies.
She delivered by elective cesarean section a baby boy – 3.550 kg and Apgar score 7, 8, and 9 at 1, 5, and 10 min, respectively, at 39 weeks’ gestation[] according to the hospital protocol with the prescribed oral mass by ultrasound protruding from the newborn oral cavity [Figures and ].
Immediately after delivery and neonatal resuscitation, the mass was surgically excised 6–8 h after delivery [].
The histopathological microscopic examination of the excised mass showed the presence of hair follicles with mature adipocytes and keratinized squamous epithelium consistent with mature fetal enigmatic teratoma or epignathus.
The newborn admitted to the neonatal subcare unit for 2 postoperative days and discharged from the neonatal subcare unit in good general condition without any postoperative complications after chromosomal studies which showed (46, XY) normal karyotype.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.55, 'kg']}",14.2,13.49,14.91,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.55 kg. Hence, the patient's maintenance fluid is 3.55 kg * 4 mL/kg/hr = 14.2 mL/hr.
Hence, the patient's fluid maintenance is 14.2 mL/hr."
4758,22,Maintenance Fluids Calculations,physical,decimal,pmc-8345747-1,Extracted,"A 9-year-old, previously healthy Caucasian girl was referred to the Department of Pediatric and Oncological Surgery, Urology and Hand Surgery of the Pomeranian Medical University in Szczecin from a district hospital. The patient’s body weight was 41 kg, her height 140 cm and BMI (body mass index) 20.92 kg/m2, which indicated that she was overweight.
On admission, the patient presented with severe epigastric pain lasting for 3 days. In addition, the parents reported one episode of vomiting and stool retention lasting 2 days. The girl had no fever. On physical examination, the abdomen was distended. On palpation, significant pain, with increased tension of abdominal integuments in the right and central epigastrium, was observed. The lower quadrants of the abdomen were soft with mild tenderness, with palpable stool masses in the lower left iliac fossa. The percussion examination was impaired by the excess amount of subcutaneous tissue with tympanitic sounds in the epigastrium and slightly dull sounds over the left iliac region. Peristalsis was heard in the umbilical region. The pain intensified with changes in position. Diagnostics for acute abdominal diseases were implemented. The differential diagnosis included acute pancreatitis, gastrointestinal obstruction, gastrointestinal perforation (including duodenal perforation) and acute appendicitis. Laboratory tests showed elevated inflammatory parameters: CRP (C-reactive protein) at 69.42 mg/L, insignificant leukocytosis with a WBC (white blood cell count) of 10.65 thousand/μL, with a neutrophil predominance of 71%, and fibrinogen at 524.7 mg/dL; the serum amylase and lipase levels were within normal limits. As for imaging examinations, a plain abdominal X-ray was initially performed, which showed no signs of obstruction or perforation of the gastrointestinal tract but did show fecal masses in the ascending colon and rectum ().
An abdominal ultrasound was then performed () and showed mesenteric adipose tissue along the right flank, with increased echogenicity. There was fluid in the pouch of Douglas, with a layer thickness of up to 25 mm, along with a trace of free fluid, both interloop and perihepatic. The appendix was not visualized, which prompted a further diagnostic work-up.
As the ultrasound examination was inconclusive, a team of doctors consisting of a pediatric surgeon, a pediatric gastrologist and a radiologist decided to expand the diagnostics with a non-contrast CT of the abdomen and pelvis. The examination showed a focal area of fat stranding, measuring 58 × 20 mm (transverse dimension), in the right epigastrium, anterior to the site of the gastric connection to the duodenum, along with small-banded thickenings along both flanks and in the lower abdomen. In addition, there was no free gas in the abdominal or pelvic cavities and the appendix presented with no signs of inflammation ().
The clinical picture, along with laboratory and imaging investigations, led to the diagnosis of omental infarction. Conservative treatment was introduced. Enema was performed with a good effect. Antibiotic therapy (cefuroxime), analgesic treatment and fluid therapy were implemented. During hospitalization, the subsidence of clinical symptoms and a decline of the inflammatory parameters were observed. In the control abdominal ultrasound, performed on the seventh day of hospitalization, a partial regression of lesions was noted ().
The patient was discharged after 7 days of hospitalization. Oral antibiotic therapy was continued for the next 5 days. Two weeks after the hospitalization, a follow-up visit to the pediatric surgery outpatient clinic took place. The patient did not report any complaints. A follow-up ultrasound examination two weeks after hospitalization showed regression of the abdominal lesions—adipose tissue in the middle-right epigastrium had still partially increased echogenicity, but with neither increased vascularity on Doppler nor fluid collections ().
The long-term follow-up of the patient showed no complications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [41.0, 'kg']}",81,76.95,85.05,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 41.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (41.0 kg - 20 kg) = 81.0 mL/hr.
Hence, the patient's fluid maintenance is 81.0 mL/hr."
4759,22,Maintenance Fluids Calculations,physical,decimal,pmc-6297984-1,Extracted,"The proband was a 2-year and six-month-old female patient from healthy unrelated parents at full-term normal delivery and with a birth of weight of 3.2 kg. Her perinatal period was unremarkable. At around 4 months of age, she was admitted to the local hospital due to vomiting. At that time, the laboratory finding showed that she suffered from metabolic acidosis and hypokalemia (Table ). She accepted the supplementary treatment of potassium chloride and sodium bicarbonate for a short time and then therapy was discontinued. At about 2.5 years old, she was hospitalized in our renal unit because of recurrent hypokalemia, hyperchloremic metabolic acidosis and growth retardation. Physical examinations on admission showed height (84.0 cm, <3rd percentile) and weight (10.1 kg, <3rd percentile) were lower than normal. Clinical features and biochemical data revealed that the patient presented hypokalemia (2.7 mmol/l, normal 3.5–5.5 mmol/l),hyperchloremic (115 mmol/l, normal 99-110 mmol/l), metabolic acidosis (pH 7.28, normal7.35–7.45) and paradoxical alkali urine (Urinary pH > 6.0 while CO2CP < 18 mmol/l) (Table ). Thus, the clinical and biochemical features of this patient suggested a diagnosis of dRTA.
To make a definite diagnosis, renal ultrasound and audiological assessment were performed. Renal ultrasound indicated bilateral nephrocalcinosis. Automated auditory brainstem response (AABR) test revealed that bilateral sensorineural hearing loss, with moderately severe (45 dB) on the left ear and severe (80 dB) on the right ear, which was accompanied with EVA on both sides determined by high-resolution computed tomography (HR-CT) (Fig. ).
To identify the pathogenic gene mutation, Genomic DNA was extracted from the peripheral blood of the patient and her parents using Blood genome DNA Extraction kit (TaKaRa, Japan). Both ATP6V1B1 and ATP6V0A4 genes were preferentially screened in this study. If inconclusive (no mutation or only one was identified in either gene) then SLC4A1 gene should be analyzed for further verification. Direct sequencing analysis was employed to screen both of ATP6V1B1 and ATP6V0A4 genes, and two novel mutations were identified in ATP6V1B1. One mutation was a successive 2-nucleotide deletion in exon 2(c.133-134delTG)(Fig. ), which resulted in a frame shift mutation (p.Cys45Glnfs*37) and was expected to produce a truncated protein. The other mutation was a guanine to adenine substitution of the first nucleotide within the intron 8(c.785 + 1 G > A)(Fig. ). No mutation was found in ATP6V0A4 and we did not perform the SLC4A1 gene analysis since the causal mutations have been found.
For the mutation in the first nucleotide of intron 8(c.785 + 1 G > A), which just located in the 5′-splice donor site, splicing prediction programs presumed this mutation cause the disability of donor site and skipping exon 8with the on-line software BDGP (Score decreases from 0.92 to 0), NetGene2 (Confidence decreases from 0.88 to 0) and Spliceview (Score decreases from 85.6 to 0), respectively.
To verify this mutation really led to exon 8 skipping in vivo, the cDNA from the peripheral blood of the patient was amplified by nested PCR with primers spanning exon 7 to exon 9 (Table ). By direct PCR products sequencing, the exon 8-excluded transcript was visualized, while the normal was not (Fig. ). Of note, the absence of RT-PCR product corresponding to the allele harboring c.133-134delTG from this patient might suggest a marked nonsense mediated mRNA decay (NMD). The parents of this patient gave their informed consent. The study protocol was approved by the Ethics Committee of the affiliated hospital of Qingdao University.
A systematic treatment was performed by administration of sodium citrate (0.7 mmol/kg/day), potassium citrate (0.65 mmol/kg/day), and citric acid (0.62 mmol/kg/day) to correct metabolic acidosis and hypokalemia in this patient, and her normal growth was also restored in about 2 years (Fig. ). However, during the follow-up period, from the age of 2.5 to the age of 4.5 years, her hearing decreased gradually with fluctuating exacerbation which was associated with common cold infections. Finally, she had to accept the use of bilateral hearing aids.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.1, 'kg']}",40.2,38.19,42.21,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.1 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.1 kg - 10 kg) = 40.2 mL/hr.
Hence, the patient's fluid maintenance is 40.2 mL/hr."
4760,22,Maintenance Fluids Calculations,physical,decimal,pmc-7706278-1,Extracted,"A 45-year-old man with a history of hypertension, dyslipidemia, and habitual drinking visited our hospital with complaints of severe chest pain, back pain, bilateral shoulder pain, and vomiting. He fell ill after heavily consuming alcohol for a day. Three and a half hours prior to his arrival, he experienced discomfort in his chest followed by vomiting. Two hours and 20 min prior to his arrival, he felt nauseated, describing a feeling of sudden stiffness throughout his entire upper body. On arrival, he was alert, his blood pressure was 139/98 mmHg, pulse rate was 64/min and regular, body temperature was 36.5 °C, respiratory rate was 20/min, and oxygen saturation was 95%. He was 173 cm tall and weighed 73.1 kg. No abnormalities other than cold sweat and epigastric tenderness were noted on physical examination. Chest radiography of the lateral view (seated position) showed several areas of free-air just below the diaphragm (Fig. ). Contrast-enhanced computed tomography (CT) showed free-air, bilateral pleural effusion, and a dilated esophagus and stomach (Fig. ). Based on these findings, an esophageal rupture with mediastinitis was the definitive conclusion and he was thus diagnosed with Boerhaave syndrome. A subsequent esophagogram further confirmed the diagnosis. Nine hours after the onset of the rupture, an emergency operation was performed as follows. Through a left thoracoabdominal incision, closure of the perforation and drainage of both the mediastinum and thoracic/abdominal cavities were performed in succession. The penetrating laceration was approximately 3 cm in length vertically on the left posterior wall of the distal esophagus and was patched with the patient’s omentum. Although the patient had a complication of anastomotic insufficiency on the 16th day, it was ultimately resolved. The patient was then administered a liquid diet on the 35th day, and he was discharged on the 41st day. Upper gastrointestinal endoscopy was performed on the 98th day, and a scar due to the suture was observed in the same location as the previous perforation (Fig. ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [73.1, 'kg']}",113.1,107.445,118.755,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 73.1 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (73.1 kg - 20 kg) = 113.1 mL/hr.
Hence, the patient's fluid maintenance is 113.1 mL/hr."
4761,22,Maintenance Fluids Calculations,physical,decimal,pmc-1950509-2,Extracted,"A 72-year old male patient with phthisical right eye had phacoemulsification and IOL implantation for senile cataract of the left eye. The patient, weighing only 36 kg, was cachectic secondary to eating problems (nausea and vomiting) due to gastrectomy operation. He underwent this operation five years ago. He had received oral supplementation (with high protein content) before the cataract surgery. Fundus examination showed ""dry type"" age related macular degeneration. Preoperative visual acuity was 0.1 (based on Snellen chart) and achieved 0.5 (based on Snellen chart) after an uneventful phacoemulsification surgery. Topical steroid and ciprofloxacin treatment was started postoperatively. These medications were gradually reduced over a period of one month and stopped. The patient was referred to us for uveitis at postoperative third month. He was suffered from decreased vision and pain. Topical steroid drops had been prescribed. Visual acuity limited to hand motion and biomicroscopic examination showed inflammatory reaction in the anterior chamber. There was a little improvement of the symptoms with steroid treatment. However, complaints were eventually intensified. Fibrinoid inflammatory reaction and membrane formation were noted around the pupil and the anterior chamber. Considering endophthalmitis, anterior chamber lavage was performed. Necrosis of and defect in iris were observed beneath the membrane. Samples of anterior chamber fluid were cultured. Vitreous was clean. Vancomycin (1 mg/0.1 cc) and amphotericin-B (5 μg/0.1 cc) were administered into the anterior chamber. The patient was treated empirically with topical fortified gentamicin and vancomycin ophthalmic solutions, oral ciprofloxacin (750 mg, b.i.d), intravenous (IV) vancomycin (500 mg, q.i.d) and meropenem (1 g, t.i.d). Due to suspicious fungal growth in culture, IV liposomal amphotericin-B (3 mg/kg/day) was started. Secondary to recurrence of dense fibrinoid inflammatory reaction, IOL extraction, vitrectomy and silicon oil injection were performed. Cornea was also edematous. Voriconazole (2.5 μg/0.1 cc) was given into the silicon-filled vitreous space and amphotericin-B (5 μg/0.1 cc) into the anterior chamber. Culture results yielded Scopulariopsis spp. In vitro susceptibility with E test revealed that the infecting organism had a MIC of >32 μg/ml for amphotericin-B. MIC for voriconazole (VFEND®-Pfizer) was found 8 μg/ml with susceptibility test using dilution method and MIC for caspofungin (Cancidas®-MERCK SHARP & DOHME) was 4 μg/ml. Henceforth, IV amphotericin-B was stopped and IV voriconazole (4 mg/kg, b.i.d) and caspofungin (50 mg/day) were started. Voriconazole (2.5 μg/0.1 cc) was injected into the silicon-filled vitreous space. Topical voriconazole (0.01 mg/cc) ophthalmic solution was started. As the hepatic enzymes elevated on the tenth day of the treatment, IV voriconazole was stopped and topical voriconazole and IV caspofungin were administered for a course of 8-weeks. Visual acuity improved to counting finger from 3 meters at the postoperative 2nd month. Fungal endophthalmitis did not recur during the 4 months follow-up period. Corneal edema was still present and visual acuity remained unchanged.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [36.0, 'kg']}",76,72.2,79.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 36.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (36.0 kg - 20 kg) = 76.0 mL/hr.
Hence, the patient's fluid maintenance is 76.0 mL/hr."
4762,22,Maintenance Fluids Calculations,physical,decimal,pmc-3781627-1,Extracted,"A 3-d-old full-term girl born to consanguineous (firstdegree cousins) parents was admitted to our neonatal intensive care unit with jaundice and fever (37.6 °C). Her birth weight was normal (3300 g) and had jaundice and poor feeding 1 day prior to admission. She was the offspring of the mother’s second gravida. The first gravida was terminated via abortion. Prenatal history, mother’s laboratory findings, and family history were unremarkable. The patient was delivered via Caesarian section and had normal APGAR scores.
On physical examination she weighed 3000 g and her vital signs were stable. She had icterus, lethargy, and weak sucking. The remainder of the physical examination was unremarkable. Initial laboratory findings were as follows: white blood cell (WBC) count: 10.3 x 109/L; hemoglobin (Hb): 15.7 g/dL; red blood cell (RBC) count: 4.68 x 1012/L; platelet (Plt) count: 233x109/L; C-reactive protein (CRP): 3.34 mg/dL; total bilirubin: 15.6 mg/dL: direct bilirubin: 1 mg/dL; aspartate aminotransferase (AST): 1367 U/L; alanine aminotransferase (ALT): 504 U/L; prothrombin time (PT): >60 s; international normalized ratio (INR): >6; activated partial thromboplastin time (aPTT): 88 s. The blood of the patient and her mother was O Rh +; Coombs test was negative. Serum sodium, potassium, and creatinine were 147 mEq/L, 4.5 mEq/L, and 0.46 mg/dL, respectively. Microbiological work-up, including blood culture, was performed and ampicillin-gentamicin was empirically started.
The patient received supportive treatment with vitamin K and fresh frozen plasma due to acute liver failure (ALF). The patient’s clinical condition deteriorated on d 2 of hospitalization and her body temperature increased to 39 °C. Due to upper gastrointestinal bleeding oral feeding was stopped. The following screening tests performed due to elevated liver enzymes and coagulopathy were negative: Epstein-Barr virus, toxoplasma, rubella, cytomegalovirus, herpes simplex virus, human immunodeficiency virus, human parvovirus B19, treponema pallidum, and hepatitis A, B, and C. The patient’s ferritin level was 5644 ng/ mL, and her fibrinogen level was 147 mg/dL, despite fresh frozen plasma treatment. During this period the patient was given an anti-oxidant cocktail that included selenium, n- acetylcysteine, vitamin E, and desferrioxamine due to the possibility of hemochromatosis, but there was no improvement in clinical or laboratory parameters. For the differential diagnosis of neonatal hemochromatosis buccal biopsy was performed, but no evidence of hemochromatosis was observed.
On d 12 of hospitalization hepatosplenomegaly was noted on physical examination and the patient’s WBC count, Hb, and Plt count decreased to 3.8 x 109/L, 6.5 g/ dL, and 48 x 109/L, respectively. Hemophagocytosis was observed in her bone marrow aspirate () and CRP increased to 19 mg/dL. The patient was diagnosed as HLH based on fulfillment of 6 diagnostic criteria (fever, hemophagocytosis, hypofibrinogenemia, pancytopenia, splenomegaly, and hyperferritinemia). Antibiotic treatment was changed to imipenem due to suspected sepsis, and then vancomycin was added. Blood cultures were negative and the patient was given high-dose (1 mg/kg) intravenous immunoglobulin (IVIG) to stop the inflammatory cascade, because diverse bacterial infections were suspected to have caused HLH. Her work-up for inborn errors of metabolism showed non-specific changes, except for urine, which was positive for reducing substance; however, thin layer sugar chromatography was negative on 3 separate occasions. Liver histology showed focal hepatic necrosis, macrovesicular steatosis, vacuolar degeneration, and canalicular cholestasis.
Due to the possibility of galactosemia, lactose-free formula was commenced together with the second dose of IVIG, after which time the patient’s clinical and laboratory findings improved. As galactose-1-phosphate uridyl transferase (GALT) enzyme analysis would have been noninformative due to previous erythrocyte transfusion during hospitalization, her GALT enzyme level was evaluated at age 3 months (72 U/L [n > 262]) and the diagnosis of galactosemia was confirmed. At age 5 months the patient’s physical examination and laboratory findings were normal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3000.0, 'g']}",12,11.4,12.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3000.0 g so this converts to 3000.0 lbs * kg/1000 g = 3.0 kg. Hence, the patient's maintenance fluid is 3.0 kg * 4 mL/kg/hr = 12.0 mL/hr.
Hence, the patient's fluid maintenance is 12.0 mL/hr."
4763,22,Maintenance Fluids Calculations,physical,decimal,usmle-264,Extracted,"A 5-year-old African-American boy is brought to the physician because of fatigue and night sweats for the past month. During this time, he has also lost 3 kg (6.6 lbs). Before the onset of symptoms, he had been healthy except for a febrile seizure as an infant. His brother had chickenpox 2 months ago. He is at the 75th percentile for height and 50th percentile for weight. He appears markedly fatigued. His temperature is 38°C (100.4°F), pulse is 95/min, respirations are 19/min, and blood pressure is 100/60 mm Hg. Lung and cardiac examination is normal. There are enlarged, nontender lymph nodes bilaterally in the neck. The abdomen is soft and nontender. A complete blood count shows:
Leukocyte count 8,000/mm3
Hemoglobin 9.1 g/dL
Hematocrit 26.9%
Platelet count 34,000/mm3
Serum
Na+ 135 mEq/L
K+ 4.5 mEq/L
Cl- 101 mEq/L
HCO3- 27 mEq/L
Urea nitrogen 9 g/dL
Creatinine 0.7 g/dL
Ca2+ 8.8 mg/dL
PCR testing demonstrates a 9:22 chromosomal translocation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.0, 'kg']}",12,11.4,12.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.0 kg. Hence, the patient's maintenance fluid is 3.0 kg * 4 mL/kg/hr = 12.0 mL/hr.
Hence, the patient's fluid maintenance is 12.0 mL/hr."
4764,22,Maintenance Fluids Calculations,physical,decimal,pmc-2726488-1,Extracted,"A 50-day-old Egyptian Caucasian girl was referred to our department for persistent vomiting, dehydration and disturbed conscious level. The patient was born full term, 3500 kg (+1 SD) by normal vaginal delivery, with a cephalic presentation. Her mother is 26 years old, G3P3 with no family history of renal diseases and her husband is a first cousin. The mother reported the death of her second offspring, a girl, at the age of 3 months due to fever, vomiting and diarrhea. The condition appeared to be gastroenteritis but no medical or laboratory records are available. The first offspring of the parents is a 4-year-old healthy living girl.
Our patient's complaint started with persistent vomiting and dehydration when she was 15 days old. She was admitted to the neonatal intensive care unit (NICU) for 4 days with no significant improvement. Soon after discharge, her mother noticed an increase in her child's rate of breathing and presented to the medical facility again. Only serum ammonia was available during this period: 109 μmol/L (N: < 81 μmol/L).
At the age of 45 days, the patient's conscious level deteriorated, suckling decreased and she was admitted to the pediatric intensive care unit (PICU). On admission, her modified Glasgow Coma Scale (GCS) was 12, she had severe dehydration with dry mucous membranes, poor perfusion (capillary refill: 5 s), a temperature of 38.2°;C, weight 3300 kg (-2.8 SD) and bilateral diffuse sonorous rhonchi over her chest. Her complete blood count showed mild absolute neutrophilia with neutrophils (NE) 63%, C-reactive protein (CRP) 24 mg/dL (N < 6), chest anteroposterior (AP)/lateral X-ray images were free from pneumonic patches, serum creatinine 1.1 mg/dL (N: 0.3 to 1.0), and blood urea nitrogen (BUN) 31 mg/dL (N: 7 to 22). Her chest infection and dehydration were successfully treated with third generation cephalosporins and intravenous fluids.
Our patient was then strongly considered to have distal renal tubular acidosis (dRTA) based on the presence of the following: failure to thrive, growth retardation, hyperchloremic metabolic acidosis with respiratory alkalosis and persistent alkaline urine (pH > 7). Urine and blood tests were performed to confirm the diagnosis and distinguish between proximal and distal renal tubular acidosis (Table ).
She started to receive intravenous bicarbonate infusion and potassium supplementation with partial response. Pelvi-abdominal ultrasound (U/S) revealed bilateral nephrocalcinosis and left renal increased medullary echogenicity with a picture suggestive of medullary sponge kidney (Figures and ). She had no abnormality in auditory brainstem response and in a skeletal survey. After 1 month of treatment with oral bicarbonate 3 meq/kg/day, KCl 2 meq/kg/day, patient vomiting and weight improved. The last laboratory tests were as follows: pH 7.435 (N: 7.35 to 7.45), HCO3- 20.9 mmol/L (N: 21 to 28), PvCO2 29.6 mmHg (N: 37 to 47), Cl- 110 meq/L (N: 96 to 106), Na+ 134 meq/L (N: 138 to 145), K+ 3.9 meq/L (N: 3.5 to 5.0), serum creatinine 0.3 mg/dL (N: 0.3 to 1.0). Her growth over 6 months of follow-up after treatment showed a marked improvement (Figure ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3300.0, 'kg']}",3340,3173,3507,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3300.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (3300.0 kg - 20 kg) = 3340.0 mL/hr.
Hence, the patient's fluid maintenance is 3340.0 mL/hr."
4765,22,Maintenance Fluids Calculations,physical,decimal,pmc-4234798-1,Extracted,"This was a case of a 22-year-old male patient, weighing 18 kg, diagnosed with FOP, presenting with severe pneumonia progressing to respiratory failure. His clinical features included severe kyphoscoliosis with restrictive lung disease, necessitating non-invasive bi-level positive airway pressure (BIPAP) therapy (settings of 5/4 cm H2O), critical temporomandibular joint (TMJ) ossification causing restricted mouth opening (<1 cm) and consequent severe malnutrition from poor feeding, chronic gastro esophageal reflux, multiple musculoskeletal deformities, including multiple contractures of arms and legs and chronic pain syndrome. His medications included baclofen, fentanyl patch, oxycodone, omeprazole, metoclopramide and albuterol and fluticasone/salmeterol inhalers.
Physical examination revealed an emaciated patient weighing 18 kg non responsive to verbal commands with a Glasgow coma scale of 11. His neck was fixed in moderate flexion. O2 saturation ranged between 88% and 96% despite oxygen administration (FiO2 100%) with BIPAP support of 18/5 mm Hg. Arterial blood gas showed severe respiratory acidosis, with pH of 6.98, PaCO2 136 mm Hg and PaO2 99 mmHg. The chest X-ray was difficult to interpret due to extensive kyphoscoliosis, but did reveal right sided tracheal deviation []. Patient was kept nil per os and maintained on intravenous fluids. An anesthesia consultation was initiated to evaluate the patient for tracheal intubation and positive pressure ventilation.
In the operating room, with an ENT team available to perform an emergent tracheostomy should that be absolutely necessary, an airway endoscopy mask (VBM mask; # 3, child; hole 3 mm; ref: 30-40-333) [] was used to intubate the trachea with a fiber-optic intubation videoscope (Olympus LF-V) while maintaining him on pressure support of 18 mm Hg and positive end-expiratory pressure of 5 mm Hg with 100% oxygen through the anesthesia machine.
The patient was positioned with pillows and blankets under the right thorax and head to get optimal access to the airway and prevent any ossification from pressure injuries. Electrocardiogram (ECG), pulse oximetry and non-invasive blood pressure monitoring were instituted. An intravenous bolus of 10 mcg dexmedetomidine was infused over 5 min and 10 mg ketamine was administered intravenously. Nostrils were prepared with xylometazoline drops and dilated with a 20 mm nasopharyngeal airway. Fiber-optic bronchoscopy was performed through the airway endoscopy mask to determine the degree of visualization of the glottic aperture. The vocal cords were visualized with some difficulty. There appeared to be some subglottic stenosis. A further bolus of 10 mg of ketamine was administered intravenously. The bronchoscope was removed and reintroduced with a 5.0 mm cuffed microlaryngeal tube threaded over it. The endotracheal tube was carefully guided through the vocal cords. Rocuronium 20 mg was administered intravenously after intubation. Brownish secretions, which could have been due to aspiration, were noted in the tube. The patient remained hemodynamically stable and oxygen saturations were maintained between 82% and 96% during the procedure. The endotracheal tube appeared to be endobronchial but could not be withdrawn, probably due to airway edema. Dexamethasone (8 mg) was administered and the tube was pulled back into the trachea a few hours later in the intensive care unit.
The patient was discharged with the endotracheal tube and home ventilation 36 days after intubation. Tracheostomy was not performed.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [18.0, 'kg']}",56,53.2,58.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 18.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (18.0 kg - 10 kg) = 56.0 mL/hr.
Hence, the patient's fluid maintenance is 56.0 mL/hr."
4766,22,Maintenance Fluids Calculations,physical,decimal,pmc-5437522-1,Extracted,"The patient is a 57-year-old Caucasian male (May 2015) with a height of 180 cm and a weight of 82 kg, in whom eosinophilia was first detected in August 2003 and has remained almost constantly present until today (Fig. ). Eosinophilia from chronic infection, worms, fungi, drugs, toxins, or allergy was excluded. His individual history was positive for several items. In 1990, he had to undergo surgery for spontaneous left-sided Achilles tendon rupture. Since at least October 1999, hyperlipidemia has been noteworthy (Fig. ), which was treated successively with fluvastatin, bezafibrate, atorvastatin, and since March 2015 with ezetimibe (10 mg/day). At the same time (October 1999), hyperuricemia was noted. In July 2001, mild renal insufficiency became apparent which has persisted until today. In June 2007, L-thyroxine was prescribed to prevent the growth of diffuse and nodular goiter but was discontinued by the patient. Later, he developed autoimmune hypothyroidism requiring L-thyroxine since March 2013. Since March 2006, elevation of the γ-glutamyl-transpeptidase has been noted. Since 2009, he has suffered from recurrent exanthema of the buttocks. In June 2013, he experienced pneumonia.
Neurologic symptoms were noticed in 2002 when he recognized double vision for 3–4 min upon strenuous fixation of objects, an abnormality that has been inducible until today. In July 2005, he experienced a left-sided transient peripheral facial palsy. Since then, he has complained about mild memory impairment. At that time, also hyper-CK-emia was first recognized and has remained present until today with a tendency to increase. The maximal value was 2,088 U/l (Fig. ). In November 2005, his wife noted a seizure-like event with a vacant stare lasting for a few seconds. In January 2006, he experienced a first tonic-clonic seizure, and carbamazepine was given. Because carbamazepine caused generalized fatigue, it was replaced by lamotrigine in April 2006. Despite changing the antiepileptic regimen, he experienced a second tonic-clonic seizure in September 2006, and lamotrigine was increased. Since then, he has only experienced recurrent focal seizures, manifesting as ascending sensory disturbance, deja vus, or smacking, with a frequency of 6 per year, and a third tonic-clonic seizure in July 2009. Since April 2006, he has recognized muscle aching after mild exercise. Neurologic exam at that time only revealed sore neck muscles and mild postural tremor. Neurologic exam in March 2009 additionally revealed reduced Achilles tendon reflexes. Electroencephalography in December 2010 was normal. In September 2013, after cardiac surgery, he experienced transient weakness for right foot extension and transient numbness of the left digit 5. Neurologic exam in November 2013 revealed mild hypoacusis, bilateral ptosis, lid edema, mild weakness for right foot extension, reduced Achilles tendon reflexes bilaterally, an exaggerated left patella tendon reflex, and postural tremor. Neurologic exam in March 2015 revealed mild hypoacusis, exaggerated tendon reflexes on the right arm, bradydiadochokinesis bilaterally with right-sided predominance, wasting of the thighs, and reduced Achilles tendon reflexes bilaterally.
Cardiologically, he has required treatment for arterial hypertension since April 2006. Echocardiography in October 2007 revealed mitral insufficiency grade 3. Since May 2013, he has developed resting and exertional dyspnea. Echocardiography in May 2013 revealed mitral insufficiency grade 4 and mitral stenosis. Heart failure and atrial fibrillation were diagnosed, and heart failure therapy and phenprocoumon were initiated. Echocardiography revealed pulmonary hypertension (60 mm Hg) and combined mitral valve stenosis and mitral valve insufficiency grade 4; therefore, he underwent mitral valve replacement therapy (St. Jude Medical 29-mm mechanical valves) in September 2013. Coronary angiography and carotid ultrasound before surgery showed only minimal atherosclerotic alterations. Four months after cardiac surgery, he required implantation of a pacemaker because of atrioventricular block III (January 2010). Stress testing during rehabilitation after cardiac surgery had to be interrupted 2 times because of early muscle fatigue.
He had a 40-pack-year history of smoking cigarettes. The family history was positive for pulmonary embolism (father), hyperlipidemia (mother, sister), hyperuricemia (mother, sister), hypothyroidism (mother, sister, sister of mother), cataract (sister), stroke (mother), thyroid cancer (mother), osteoporosis (mother), arthrosis (mother, sister), liver cirrhosis (sister of mother), colon cancer (grandmother from the mother's side), ovarian cancer (grandmother from the mother's side), and breast cancer (grandmother from the mother's side, mother, sister of mother). His medication in April 2015 included phenprocoumon, L-thyroxine (87.5 μg/day), nebivolol (10 mg/day), lamotrigine (700 mg/day), and ezetimibe (10 mg/day). The patient did not consent with genetic diagnostics for suspected MID.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [82.0, 'kg']}",122,115.9,128.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 82.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (82.0 kg - 20 kg) = 122.0 mL/hr.
Hence, the patient's fluid maintenance is 122.0 mL/hr."
4767,22,Maintenance Fluids Calculations,physical,decimal,pmc-2633086-1,Extracted,"A 26-year old woman was admitted to our hospital for further evaluation of a perirenal mass. Five days earlier, she had visited an outside emergency department with complaints of a high fever and left flank pain, which radiated to the iliac fossa and posterior back. An abdominal ultrasound (US) revealed a left perinephric mass (). The abdominal computed tomography (CT) scan revealed a perirenal hematoma confined to the left kidney. However, other perinephric structures, including the pancreas, adrenal grand, and additional vasculature, remained unaffected ().
The patient had a long history of insulin dependent diabetes mellitus (IDDM), and had been treated with insulin since the age of 16. She had no other medical illness (i.e. vasculitis, immunodeficiency, hypertension, or tuberculosis) and had no relevant medication history (i.e. aspirin or non-steroid anti-inflammatory drugs (NSAIDs)). However, in an attempt to lose weight, the patient had been exercising 30 minutes daily for about six months, using a hula-hoop. She recalled experiencing intermittent left flank pain whilst exercising with the hula-hoop.
A physical examination revealed an ill-appearing woman with a body temperature of 38℃, blood pressure of 130/80mmHg, and a heart rate of 98 beats/min. Her body weight was 54kg, and her height was 162cm (BMI, 20.1kg/m2). Her abdomen was soft, not distended, and remarkable for left costovertebral angle tenderness.
Laboratory examination revealed a WBC of 11,700/mm2 (64.5% segmental neutrophils and 10.9% lymphocytes), hemoglobin of 11.1g/dL, hematocrit of 34.8%, platelet 340 × 103, fasting blood glucose of 99mg/dL, postprandial glucose of 207mg/dL, hemoglobin A1C of 16.2%, serum sodium of 143mmol/L, potassium of 4.6mmol/L, blood urea nitrogen of 19mg/dL, creatinine 0.9 of mg/dL, lipase 78 of IU/L and a lactate dehydrogenase of (LDH) 396IU/L. Urine analysis was negative for blood and protein, and showed 0-1 WBC and 0-1 RBC. The 24-hour total protein was 473mg/day, and creatinine clearance was 77 mL/min/1.73m2. Coagulation parameters and the liver functions were normal.
An abdominal US was rechecked at our hospital. The US showed a 1.2cm diameter mass encircling the left kidney (). The size of the left perirenal hematoma was smaller than the previous image, which was conducted at a previous hospital about five days prior. Signs of persistent bleeding were absent, and the left kidney was well preserved and encapsulated. No vascular malformation was identified. She was treated with hydration and intravenous antibiotics (cephazedone, 2g/day), and her blood glucose level was well-controlled with insulin. Four days later, her fever subsided and her general condition improved. She was discharged, and a third abdominal US was repeated 20 days later in an outpatient setting. The US revealed an overall reduction in the size of the perirenal hematoma ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [54.0, 'kg']}",94,89.3,98.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 54.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (54.0 kg - 20 kg) = 94.0 mL/hr.
Hence, the patient's fluid maintenance is 94.0 mL/hr."
4768,22,Maintenance Fluids Calculations,physical,decimal,pmc-8490116-1,Extracted,"A 67-year-old male patient was admitted to the department of pulmonology with symptoms of dyspnea, fever, and cough with massive sputum. The patient had a history of non-small cell lung cancer (clinical stage IIIA, T2N2M0) and underwent right upper lobe lobectomy 6 years ago. The patient then received adjuvant chemo-radiotherapy. He had type 2 diabetes mellitus, with a hemoglobin A1c level of 8.8%, seemed undernourished (168 cm in height, 54 kg in weight, and a serum albumin level of 2.4 g/dL) and he had smoked for 40 years. After cancer treatment, the patient was repeatedly hospitalized and discharged due to recurrent pneumonia and empyema. Broad-spectrum systemic antibiotic therapy was started from the day of admission. After identification of Mycobacterium abscessus from the sputum, a triple antibiotic regimen (clarithromycin, imipenem/cilastatin, and amikacin) was started. Under fiberoptic bronchoscopy examination, the patient was found to have a BPF (1.2 cm in diameter) at the right superior lobar bronchial stump. On computed tomography (CT) imaging, a huge dead space (8.8 × 7.4 × 9.1 cm3) was observed in the right upper pleural cavity (). He was then referred to the department of plastic and reconstructive surgery and the department of thoracic surgery for surgical intervention.
Under general anesthesia, intubated with a double-lumen endotracheal tube, the patient was laid in the left decubitus position. In a collaborative procedure with the thoracic surgery team, thoracostomy was performed through previous thoracostomy scar. Using video-assisted thoracoscopy, the thoracic surgeons identified the BPF site and closed it primarily, followed by decortication of the pleura and debridement of the infected tissues. Next, the plastic surgeons harvested a pedicled LDMC flap with an 8 × 25 cm skin paddle. De-epithelization of the skin flap was performed due to its deciduousness. The LDMC flap was transposed into the pleural cavity to obliterate the dead space. Due to the limited view of the pleural space, the fixation of the LDMC flap to the pleural space and BPF stump was performed under a video-assisted thoracoscopic view. Air leakage was excluded by the Valsalva test. The thoracostomy and donor site wounds were closed after inserting 28-Fr chest tubes (). The patient was extubated immediately after the operation. On postoperative chest CT, the pleural cavity was completely obliterated (). Postoperative bronchoscopy confirmed a water-tight seal of the fistula. At a 1-month postoperative followup, the patient was in good condition without donor site complications or recurrence of the fistula.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [54.0, 'kg']}",94,89.3,98.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 54.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (54.0 kg - 20 kg) = 94.0 mL/hr.
Hence, the patient's fluid maintenance is 94.0 mL/hr."
4769,22,Maintenance Fluids Calculations,physical,decimal,pmc-8168026-1,Extracted,"A 7-month-old intact female Maine Coon was referred for further evaluation of a 2-month history of severe regurgitations, involving both kibble and water, occurring seconds to minutes after food intake (about twice a week to twice a day). Weight loss was reported over the previous 2 months. No improvement was noted after symptomatic treatment, including maropitant, cimetidine and amoxicillin/clavulanic acid, or with gastrointestinal diet trials. The cat showed a normal appetite and water consumption, as well as a normal level of activity. Review of the patient’s medical history revealed chronic vomiting of undigested food and bile from the age of 3–5 months, and an episode of self-resolving acute vomiting (about three times a day, for 10 days), when it was 5 months old. No episode of regurgitation or vomiting was reported before the age of 3 months. The referring veterinarian had performed thoracic radiographs, taken before and after oral administration of contrast medium mixed with canned food, which demonstrated a generalised oesophageal distension. As a significant amount of residual ingesta was observed in the oesophageal lumen several minutes after swallowing, oesophageal motility was subjectively considered reduced (). No evidence of aspiration pneumonia was noted.
At the time of presentation, the cat was bright, alert and responsive, with a body weight of 2.5 kg and a body condition score of 2/9. Stunted growth was noted. The remainder of the physical examination was unremarkable.
Because of the previously mentioned loss of continuity between the distal oesophagus and the stomach on contrast lateral thoracic radiographs, endoscopy was performed to evaluate the oesophagogastric mucosa and to investigate a potential distal oesophageal obstruction (eg, stricture or foreign body). After premedication with methadone (0.2 mg/kg [Comfortan; Dechra]) and dexmedetomidine (5 µg/kg [Sedadex; Dechra]), general anaesthesia was induced by an intravenous injection of propofol and ketamine (1 mg/kg each [Propovet; Abbott] [Imalgene; Merial]), followed by endotracheal intubation for anaesthetic maintenance by isoflurane. The oesophagoscopy was performed using an 8.8 mm external diameter videogastroscope: a diffusely dilated oesophagus was noted, with oral to an annular luminal narrowing adjacent to the cardia. Only a 2.8 mm biopsy forceps could be passed through the stricture. A small distal oesophageal diverticulum was noted laterally to the narrowing, probably resulting from the food accumulation in the distal oesophagus. In this context, endoscopic examination of the stomach was not possible. Taken together, these findings were consistent with a severe lower oesophageal stricture.
Attempts to pass an endoscopy-guided balloon dilator entirely throughout the stricture were unsuccessful. Balloons were partially inserted into the stenotic canal and filled up to reach their maximum burst pressure, which was held for 120 s, and no significant improvement of the stricture was noted (). Therefore, the procedure was discontinued and another approach was decided.
The cat underwent coeliotomy for a transgastric retrograde approach of the gastroesophageal junction a few days after the endoscopic examination. After cranioventral body gastrotomy, the stricture was visualised intraluminally throughout the cardia. Four radial full-thickness mucosal incisions were performed using an #11 scalpel blade; each incision was performed so as to reach only the submucosa, taking care not to breach the oesophageal wall. Incisions were approximately 1 cm in length. These allowed an initial progressive dilation, and further dilation was obtained first with gentle finger manipulation (bougienage), and then using balloon dilators of increasing sizes. The stricture diameter reached 20 mm after the last dilation. To reduce the risk of recurrence, four injections of triamcinolone acetonide (0.25 mg each [Kenacort; Bristol-Myers Squibb]) were performed during surgery in the submucosa within the site of the stricture. Two incisional biopsies of the gastric fundus were performed at the time of gastrotomy to query underlying gastric disease, and histological analysis revealed no significant abnormality. After gastric closure, a left gastropexy was performed to exert traction on the distal oesophagus, with the aim of reducing the oesophageal diverticulum. An 18 Fr latex oesophagostomy feeding tube was placed to extend across the gastroesophageal junction and approximately 10 cm into the lumen of the stomach, to feed the patient while protecting oesophageal wounds, and keeping the stricture open and dilated. Overall anaesthesia and procedure durations were 140 and 80 mins, respectively.
Postoperative analgesia (buprenorphine 20 µg/kg IV q8h [Bupaq; Virbac]) was administered for 3 days. Treatment including maropitant (1 mg/kg IV q24h [Cerenia; Zoétis]), pantoprazole (1 mg/kg IV q12h [Inipomp, Takeda]) and sucralfate (0.5 g PO q8h [Ulcar; Sanofi]) was started immediately after surgery. A nutritional plan was prescribed, divided into four feedings a day of Recovery Liquid (Royal Canin) as a total of 150 ml a day through the oesophagostomy tube for 15 days. Recovery from surgery was otherwise uneventful. Follow-up endoscopy at 6 days postoperatively revealed no procedural complication (eg, mural necrosis and leakage) (). The endoscope was passed easily through the cardia. Mucosal healing was judged to be satisfactory and the cat was discharged from hospital.
The patient was reported to be stable at home. The oesophagostomy feeding tube was removed after a period of 15 days, following which the cat appeared to be comfortable. The cat was able to eat wet and dry food without regurgitating, and is still doing so at the time of writing this report (12-month follow-up). As food-responsive gastropathy was suspected, a dietary change for a hydrolysed source of protein (Specific FDD HY; Dechra) was implemented. Marked weight gain (2 kg) was reported. Follow-up endoscopic examinations were performed both 1 and 3 months after surgery. No stricture was noted, and the oesophageal diverticulum was no longer noticeable. The endoscope was passed easily through the cardia at both time points (). Moreover, at the 1-month follow-up, serial contrasted thoracic radiographs taken by the referring veterinarian showed reduction of the oesophageal distension (). Antacid treatment was discontinued 6 weeks postoperatively.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.5, 'kg']}",10,9.5,10.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.5 kg. Hence, the patient's maintenance fluid is 2.5 kg * 4 mL/kg/hr = 10.0 mL/hr.
Hence, the patient's fluid maintenance is 10.0 mL/hr."
4770,22,Maintenance Fluids Calculations,physical,decimal,usmle-5862,Extracted,"A 52-year-old woman with hypertension presents to your clinic complaining of swelling in the front of her neck that has been increasing in size for the last six months. She also endorses a recent decrease in weight of 10 lbs in the last month, which she attributes to her new diet, as well as hot flashes that have been interfering with her sleep. She says that she sometimes feels anxious about losing her new job, but denies headaches, palpitations, tremors, or abdominal symptoms. Her temperature is 98°F (36.7°C), pulse is 88/min, blood pressure is 142/82 mmHg, respirations are 12/min, and oxygen saturation is 100% on room air. On physical exam, there is a palpable, non-tender nodule at the anterior aspect of her neck, which moves upon swallowing. No cervical adenopathy is appreciated.

Routine labs and thyroid function tests were performed with the following findings:

Serum:
Na+: 142 mEq/L
K+: 4.1 mEq/L
Cl-: 88 mEq/L
HCO3-: 24 mEq/L
Blood urea nitrogen: 11 mg/dL
Creatinine: 1.2 mg/dL
Thyroid stimulating hormone: 3.0 mIU/L
Free T4: 1.0 ng/dL

Hemoglobin: 13.5 g/dL
Leukocyte count: 6,000/mm^3
Platelet count: 250,000/mm^3

A fine-needle aspiration (FNA) of the mass is shown in Figure A.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.0, 'lbs']}",18.14368,17.2365,19.05086,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.0 lbs so this converts to 10.0 lbs * 0.453592 kg/lbs = 4.53592 kg. Hence, the patient's maintenance fluid is 4.53592 kg * 4 mL/kg/hr = 18.14368 mL/hr.
Hence, the patient's fluid maintenance is 18.14368 mL/hr."
4771,22,Maintenance Fluids Calculations,physical,decimal,pmc-6966733-1,Extracted,"The patient was a 6-year-old boy of height 107.7 cm and weight 17.7 kg. He was born by scheduled Cesarean delivery after gestation of 38 weeks and 2 days, with weight 3026 g and height 45.5 cm, because his mother was after hysteromyctomy. At 1 day old, he was diagnosed with tetralogy of Fallot (TOF), and he received palliative surgery at another hospital at 6 weeks. At 1 year, more than 50% thrombocytopenia and upper extremity movement disorder appeared after catheterization, and he was diagnosed with HIT II because his functional assay was positive for HIT antibodies. Therefore, radical intracardiac repair with administration of argatroban was performed at the hospital. After this surgery, aortic regurgitation and residual defect of the ventricular septum were confirmed. Follow-up observation was performed for these symptoms, in addition to pulmonary stenosis and regurgitation, which were associated with TOF.
Based on a desire for treatment at our hospital, the patient underwent a cardiac catheter test, which showed progression of pulmonary valve insufficiency. Thus, reoperation was scheduled for aortic valvuloplasty, pulmonary valve replacement, and repair of ventricular septal defect. Anesthesia was performed with slow induction of sevoflurane and maintained with fentanyl and sevoflurane/midazolam. No abnormalities were found on the coagulation test and HIT antibody had become negative, but argatroban and nafamostat mesilate were used as anticoagulants because some reports suggest that HIT II can redevelop due to heparin re-administration []. During surgery, we measured Celite ACT and kaolin ACT, which do and do not reflect the effect of nafamostat mesilate, respectively (Fig. ). Physiological saline was used for the blood pressure line. The blood samples were collected from the arterial pressure line placed in the radial artery, but from the blood supply circuit only during cardiopulmonary bypass, because blood in the blood supply circuit most reflects the activation of the coagulation system by the cardiopulmonary bypass circuit. Therefore, there may be slight differences in ACT measurement values depending on the sampling line.
After thoracotomy, a 5-mg argatroban bolus was administered and continuous argatroban was started at 12 mg/h, which was then decreased to 3 mg/h because the activated partial thromboplastin time (APTT) was 136.6 s. However, since kaolin ACT decreased from 352 to 217 s, the dose was increased again to 12 mg/h and bolus administration of 2.5 mg was added. After kaolin ACT reached 501 s and the patient was placed on cardiopulmonary bypass, continuous administration of nafamostat mesilate was started at 50 mg/h, concomitantly with argatroban. ACT was continuously prolonged, and Celite ACT and kaolin ACT were 1500 and 600 s, respectively, at 3.5 h before weaning from cardiopulmonary bypass. Therefore, administration of argatroban was discontinued after the dose was decreased by half. ACT continued to be prolonged, although with some shortening, and thus the dose of nafamostat mesilate was decreased to 30 mg/h until weaning from cardiopulmonary bypass. Upon weaning, Celite ACT and kaolin ACT were 533 and 399 s, respectively.
ACT decreased to ≤ 200 s (177 s) for the first time at 5 h and 1.5 h after discontinuation of argatroban and nafamostat mesilate, respectively. Operation and anesthesia times were 10 h 9 min and 11 h 36 min, respectively. Intraoperative hemorrhage was about 1000 ml, and 560 ml of red blood cells (RBCs), 520 ml of fresh frozen plasma (FFP), and 250 ml of platelet concentrate (PC) were transfused. There was no significant postoperative bleeding. Extubation was performed on the day after surgery and the patient was discharged on postoperative day 11.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [17.7, 'kg']}",55.4,52.63,58.17,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 17.7 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (17.7 kg - 10 kg) = 55.4 mL/hr.
Hence, the patient's fluid maintenance is 55.4 mL/hr."
4772,22,Maintenance Fluids Calculations,physical,decimal,pmc-5073164-1,Extracted,"A 10-years-old girl presented with complaints of muscle pain, malaise, coldness in the hands and feet, color changes in her finger in response to cold, and bruising after blanching. Previous medical history revealed no trauma, vigorous exercise, infection, or any medication usage. On physical examination, her height was 124 cm (–2.7 standard deviation [SD]), and her weight was 27 kg (–1.2 SD). She had severe short stature. Her bone age was 8 years. She had normal heart rate (84/min), respiratory rate (30/min), and, blood pressure (95/50 mmHg). Her skin showed diffuse dryness. Coldness in the hands and feet, nonpitting leg edema, and periorbital edema were present. Neurological examination showed weakness of proximal muscles of both upper and lower extremities. She had no sign of joint swelling or arthritis and had normal range of motion of all joints.
A pediatric rheumatologist had performed initial laboratory evaluations and found elevated levels of creatine kinase (CK) (2,039 U/L). A normal electromyogram had been obtained. It had been thought to be systemic sclerosis (SS) among connective tissue disease (CTD). Prolonged gastric emptying time supported this diagnosis. Although, rheumatologic markers, including antinuclear antibody, anti–double-stranded DNA, antineutrophilic cytoplasmic antibody, cytoplasmic, and antiextractable nuclear antigen (anti-Ro, anti-La, anti-Sm, anti-RNP, anti-Scl-70, anti-Jo-1), were all negative, a pediatric rheumatologist started the patient on naproxen and a calcium channel blocker. The patient had no improvement. When it was realized that she had goiter, the patient was sent to a pediatric endocrinologist.
In the thyroid function test, thyroid stimulating hormone (TSH) was elevated (>100 µIU/mL; normal range, 0.35–5 µU/mL), and fT4 was decreased (<0.25 ng/dL; normal range, 0.8–2 ng/dL). Thyroid-peroxidase antibodies (anti-TPO) were present in high titers (201 IU/mL). Thyroid ultrasonography (USG) was consistent with thyroiditis. These findings were also consistent with the diagnosis of autoimmune thyroiditis or HT with associated hypothyroidism. After treatment with L-thyroxine, her muscle strength gradually improved, other clinical symptoms regressed, thyroid function tests, CK levels returned to normal within a few weeks. Thyroid function test were presented in . Her height progressively increased, after 3 years of L-thyroxine treatment she gained 2.9 SD of height and she attained midparental height percentile (). Bone age was appropriate with chronological age.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [27.0, 'kg']}",67,63.65,70.35,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 27.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (27.0 kg - 20 kg) = 67.0 mL/hr.
Hence, the patient's fluid maintenance is 67.0 mL/hr."
4773,22,Maintenance Fluids Calculations,physical,decimal,pmc-3917483-1,Extracted,"An eight-year-old boy was visited in endocrinology clinic of the Kashan University of Medical Sciences. He was 15.5 kg in weight (3.5 standard deviation below mean) and his height was 92 cm (7 standard deviation below mean). Based on the available documents, he weighed 3.65 kg (50th centile) at birth, with a crown to heel length of 47 cm (10th centile). He had shown abdominal distention and vomiting in his neonatal period and eventually diagnosed asHirschsprung disease that was confirmed using biopsy.
In physical examination he had severe short stature, disproportionate short-limbed dwarfism, short and puffy hands, and genu varum deformity. The sternum was abnormally prominent. Hyperextensibility of the joints was not detected.
His scalp hairs, eyebrows, and eyelashes were fair, very fine and sparse (). While no nail dysplasia or dental abnormality was found, intellectual development was normal for his age and no clinical evidence of immunodeficiency was observed. However he developed hypothyroidism in the age of 6 years. A 3-mm kidney stone was detected when he was 3 years old that enlarged to 8mm in size at the age of 8 and treated by lithotripsy.
Skeletal X-rays revealed typical metaphyseal dysostosis, including widening, cupping, and defective mineralization in the metaphysis of the tubular bones (). Vesicouretral reflux was detected in his voiding vesicocyctogram. Complete blood count, electrolytes, and renal function tests were normal. Sterile pyuria was found in several samples of urinalysis that may be as a result of the vesicouretral reflux or renal stone. Microscopic stool examination detected no fat globules. The patient had been assessed for celiac disease and cystic fibrosis during his infancy that was negative.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15.5, 'kg']}",51,48.45,53.55,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15.5 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.5 kg - 10 kg) = 51.0 mL/hr.
Hence, the patient's fluid maintenance is 51.0 mL/hr."
4774,22,Maintenance Fluids Calculations,physical,decimal,pmc-3250004-1,Extracted,"A 3-year-old male child was referred to casualty department with a thread protruding from mouth. On examination, he was 14 kg in weight and 88 cm in height. No sign of malnutrition was apparent and there was no alopecia. Abdominal examination revealed a non-tender smooth abdominal mass in the left upper quadrant emerging from beneath the left costal margin and extending over the midline. Rigid esophagoscopy was done and a bunch of hair about 50 g was found in esophagus which was extended into stomach. Laparotomy was planned and was carried out through an upper midline incision. A large 10×4 cm J-shaped foul-smelling black bunch of hairs, about 200 g, was retrieved through a longitudinal anterior gastrotomy [Figures and ]. There was also a daughter bezoar of 6×4 cm in size and about 100 g in jejunum about 30 cm away from duodenojejunal junction which was retrieved through enterotomy. Tail of the daughter bezoar was seen to have gone through the duodenum to jejunum. Abdomen was closed and patient was shifted to post-anesthesia care unit and then to surgical ward. His postoperative recovery was good and uneventful. He was discharged on 10th postoperative day. Psychiatric consultation was advised and child was followed up for a period of 1 year. No recurrence occurred.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [14.0, 'kg']}",48,45.6,50.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 14.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (14.0 kg - 10 kg) = 48.0 mL/hr.
Hence, the patient's fluid maintenance is 48.0 mL/hr."
4775,22,Maintenance Fluids Calculations,physical,decimal,pmc-7547417-1,Extracted,"We present a case of a 6.8-kg, 5-month-old Hispanic girl who was brought to the emergency room for 1 day of fever, vomiting, seizures, and leftward gaze deviation. Initial computed tomography revealed a large hemorrhagic intracranial mass in the suprasellar and third ventricular region causing obstructive hydrocephalus. An emergent extraventricular drain was placed, a magnetic resonance imaging study was obtained, and the girl was admitted to the pediatric intensive care unit (PICU). Other than left gaze preference and clonus, the result of her examination was unremarkable, with normal capillary refill and no sunken fontanels, though a full examination was limited by sedation and her hydrocephalus. On hospital day 3, the mass was surgically resected, and its pathology was consistent with stage IV glioblastoma.
Prior to resection, she developed CDI, and a vasopressin infusion was initiated. Vasopressin was titrated to maintain urine output between 2 and 4 ml/kg/hour and was discontinued on postoperative day (POD) 1. On POD 3, she became hyponatremic with low to normal urine output, thought to be SIADH. On POD 7, she again became polyuric, but with continued hyponatremia and elevated urine sodium. She was started on sodium and fluid supplementation in the form of 0.9% NaCl, 3% NaCl, and enteral NaCl tablets to treat CSW. On POD 8, she developed brisk and dilute urine output, with serum hypernatremia, requiring reinitiation of a vasopressin infusion and temporary cessation of sodium supplementation for CDI (Fig. ). By the next day, she became hyponatremic with continued polyuria, suggestive of concurrent ongoing CSW, and sodium supplementation was resumed.
She fluctuated between hypo-osmolar and hyperosmolar polyuria. Trials of discontinuing vasopressin only resulted in worsened polyuria, so she remained on a vasopressin infusion. To promote renal sodium retention, fludrocortisone was started at 0.025 mg twice daily on POD 11 and increased to three times daily on POD 17 [, ]. Sodium supplementation was adjusted to maintain normonatremia. Urine output in excess of 4 ml/kg/hour was replaced with lactated Ringer solution, 0.45% NaCl, and 0.9% NaCl respective of her urine sodium content. A timeline of various fluid and sodium treatments and examples of laboratory findings that guided treatment are described in Fig. . It was presumed that the component CSW would resolve over time. Her serum sodium concentration remained generally stable, with urine output ranging from 2 to 8 ml/kg/hour. Her fluid balance was nearly even, although maintaining this balance required aggressive and frequent fluid replacement.
On POD 20, her urine output began increasing precipitously, reaching over 40 ml/kg/hour in the following days. Her vasopressin infusion was increased accordingly, with no effect in slowing her output (Fig. ). By this time, her acute neurosurgical issues had otherwise resolved, but she remained in the PICU for fluid management and vasopressin. Her fluid volume status was again maintained, with moist mucous membranes and flat fontanels observed on examination, though she required progressively larger fluid replacement to match her rising urine output. This pronounced polyuria, and apparent inefficacy of increased vasopressin prompted consultation with pediatric nephrology on POD 27.
She had previously responded well to vasopressin; she was given no known medications associated with NDI; her electrolytes other than sodium and chloride were within normal limits; and her creatinine was appropriate for her age, ranging from 0.06 to 0.12 mg/dl, ruling out most acute and congenital causes of NDI. Other causes of urinary concentration defects were therefore considered. Her total protein upon admission was normal, but her serum albumin had decreased from 3.7 mg/dl upon admission to 2.9 mg/dl. In the days prior to consultation, her hemoglobin decreased from 11.5 to 8.5 g/dl. Her blood urea nitrogen (BUN) became undetectable, which was thought to reflect a protein deficiency and depleted renal urea gradient (Fig. ). Prolonged increased fluid and solute intake with hypertension and daily sodium intake of 20 mEq/kg/day were also thought to exacerbate her polyuria, further depleting her osmotic gradient. As such, her fluid replacement was incrementally decreased by 2 ml/kg/hour each day, and she was started on enteral protein supplementation to restore her osmotic gradient. Within 4 days of treatment, her BUN increased, and her urine output, vasopressin needs, and fluid replacement dramatically decreased (Fig. ). Fludrocortisone was discontinued; protein supplementation was stopped by POD 31. She then exhibited a singular CDI physiology and remained only on vasopressin without need for frequent fluid replacements. She was transitioned to subcutaneous desmopressin on POD 33 and transferred to the general ward on POD 39. After hospital discharge, she remained on desmopressin long term.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.8, 'kg']}",27.2,25.84,28.56,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.8 kg. Hence, the patient's maintenance fluid is 6.8 kg * 4 mL/kg/hr = 27.2 mL/hr.
Hence, the patient's fluid maintenance is 27.2 mL/hr."
4776,22,Maintenance Fluids Calculations,physical,decimal,pmc-4797444-1,Extracted,"The 5-month-old previously normal, well-growing [weight = 5.3 kg, length = 60 cm, weight/height = -1 SD to -2 SD as per the World Health Organization (WHO) growth chart, head circumference = 40.5 cm] immunized female child presented with fever since 6 days followed by fast breathing for 2 days. Roentgenogram of the patient's chest [] showed left-sided large pneumothorax with shift of the mediastinum on the right and was referred to our center for further management.
On admission, she was euthermic, irritable [heart rate = 168/min, respiratory rate = 68 bpm, blood pressure = 98/60 mmHg, peripheral capillary oxygen saturation (SpO2)=88% on room air] with reduced chest expansion on the left side. Her breath sounds were decreased on the left side with a hyperresonant note. She was started on high-flow oxygen and was shifted to the pediatric intensive care unit (PICU). On admission to PICU, the left-sided intercostal drainage tube was placed [], which drained gush of air followed by thick, white-colored pleural fluid that was exudative. The complete blood picture of the patient showed hemoglobin level = 10 gm%, total leukocyte count (TLC) =37,400/mm3 (P 80% and L 15%), and C-reactive protein (CRP) level was positive (18.3 mg/dL), human immunodeficiency virus enzyme-linked immunosorbent assay (HIV ELISA) was negative. Ceftriaxone injection, Ampiclox, and Clindamycin were started, along with other supportive measures.
Gradually, her respiratory distress was alleviated over a period of next 24 h but roentgenogram [] of the chest showed incomplete expansion of the left side with multiple cavitations even after 5 days, hence computed tomography (CT) scan of the chest [] was done that showed collapse consolidation of the left lung with multiple cavitations and some cavity in the lower lobe communicating with pleural cavity and suspected to be CCAM. Left thoracotomy with decortication with lower lobe lobectomy was done in view of suspected CCAM. Gross surgical sample [] revealed a wedge of lung measuring 10 cm × 8 cm × 5 cm. Pleural surface was congested and cut surface was firm with no or little normal looking lung parenchyma. Microscopic examination [] of the patient showed signs of pleuritis with underlying suppurative inflammation of the lung indicative of abscess. Adjacent lung tissue showed vague lobulated architecture with interlobular fibrosis, definite increase in the number of bronchiolar structures, and small alveolar spaces lined by plump cuboidal epithelium. Overall symptoms in correlation with clinical and radiological findings were consistent with type III CCAM.
Later, she became hemodynamically stable with improved air entry to the left side of the chest. Roentgenogram of the chest [] showed resolution of the pneumothorax following which the implantable cardioverter defibrillator (ICD) tube was removed. Later blood and pleural fluid cultures were sterile; hence, the patient was started on oral antibiotics and was discharged after pneumococcal and flu vaccination. On follow-up after 4 weeks, her growth and respiratory functions were found to be normal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.3, 'kg']}",21.2,20.14,22.26,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.3 kg. Hence, the patient's maintenance fluid is 5.3 kg * 4 mL/kg/hr = 21.2 mL/hr.
Hence, the patient's fluid maintenance is 21.2 mL/hr."
4777,22,Maintenance Fluids Calculations,physical,decimal,pmc-8064790-1,Extracted,"Our patient was a 61-year-old Hispanic man who had not seen a health care provider in many years and presented with one month history of vague abdominal pain, 20 pound weight loss in 1 month, and generalized weakness with malaise as well as occasional cough that worsened and became productive of clear sputum over the last week before presentation. He also reported occasional episodes of nausea and nonbloody diarrhea. He denied any fevers, chills, or rash but reported some arthralgias. The patient was born in Chihuahua, Mexico, but had lived in Texas, USA, since age seven. He was divorced, estranged from his children, and lived alone. There was no significant tobacco or alcohol use but he confirmed exposure to high intensity dust when he used to work in a ceramic and tile factory without wearing a mask for the last five years.
He was evaluated by a private community physician a few days before presentation to our hospital who prescribed for him a combination of oral ciprofloxacin and metronidazole without specific diagnostic testing. The patient did not have any improvement so he presented to the emergency room.
In the emergency department, his temperature was 98.3 F, blood pressure 84/61 mmHg, pulse rate 128/minute, and respiratory rate 27/minute with pulse oximetry 92% on ambient air. He was acutely ill-looking but alert. While lung examination was limited on admission due to COVID-19 restrictions and the use of disposable stethoscopes, there were decreased air sounds but no rales. His abdominal examination was benign but positive findings were significant for large lymph nodes in the cervical, supraclavicular, inguinal, and axillary areas, some measuring more than 3 cm in diameter. Laboratory findings on admission showed white blood cell count was 8,900/mm3 with 80% neutrophils, 0.5% band forms, and 11% eosinophils, hemoglobin was 8.9 gm/dL, hematocrit was 27.6%, and platelet count was 447,000/mm3. Electrolytes showed bicarbonate of 17, blood urea 54, creatinine 1.5, albumin 2.2, lipase 14, lactic acid 2.5, ALT 57, and AST 139. Procalcitonin was 6.1.
His chest film on admission showed a diffuse micronodular pattern which triggered testing for COVID-19 which turned out to be negative. CT scan of the chest without contrast revealed extensive diffuse bilateral micronodules in a miliary pattern, mediastinal and axillary lymphadenopathy with pericardial thickening, while the CT scan of abdomen and pelvis revealed enlarged lymph nodes in the para-aortic, gastrohepatic, inguinal, external, and internal iliac chains (Figures and ). While the patient was seen by many physicians to rule out lymphoma and tuberculosis, as well as to manage his respiratory failure, acute renal failure, and septic shock, the infectious disease physician suspected coccidioidomycosis and began a work up for the patient with serologic testing.
Since he was in shock, blood and urine cultures were sent and he was treated with IV isotonic fluid resuscitation with empiric intravenous vancomycin and cefepime along with intravenous methylprednisolone 60 mg every 8 hours and admitted to the intensive unit. Further testing showed that he was positive for HIV-1 with viral load 309,000 and CD4 count 38. We did not begin antifungal medications at the outset because we did not have a diagnosis of HIV at the time. Upon a diagnosis of HIV in the hospital, we expanded our differentials to miliary tuberculosis, histoplasmosis, and coccidioidomycosis. Histoplasmosis antigen, acid fast bacilli (AFB), and Cryptococcus antibody tests did not yield a positive result; however, sputum culture was positive for Candida albicans. Despite aggressive treatment with vasopressors, mechanical ventilation, and continuous renal replacement therapy, the patient died on hospital day 3. The family agreed to an autopsy which showed diffuse coccidioidomycosis with negative AFB stain and no evidence of malignancy. The cause of death was acute respiratory distress syndrome (ARDS) secondary to disseminated coccidioidomycosis secondary to HIV/AIDS infection.
At autopsy, there were bilateral pleural lung effusions (left: 300ml, right: 400ml), congestion of the lungs with areas of consolidation, and extensive intra-alveolar edema. There were innumerable diffuse tan nodules showing miliary spread in the upper and lower lung lobes with predominance in the upper lobes in the lungs bilaterally (see Figures and . These nodules microscopically consisted of granulomatous inflammation. The lung alveolar spaces were filled with proteinaceous material and Coccidioides fungal microorganisms. Coccidioides fungal microorganisms have spherules that may be empty or filled with endospores. Coccidioides fungal microorganisms are accentuated with Grocott-Gomori's methenamine silver stain (GMS) (see Figures and ).The decedent grossly had extensive cervical, supraclavicular, inguinal, and axillary lymphadenopathy. The lymph nodes grossly showed a cut tan surface (see ). Microscopically, normal lymph node architecture was replaced with caseating granulomas with Coccidioides fungal microorganisms that are accentuated with Grocott-Gomori's methenamine silver stain (GMS) (See Figures and ). It should be noted that acid fast bacilli (AFB) stain was performed and was negative for acid fast microorganisms on both lung and lymph node sections.
Autopsy Findings and Figures are presented in .","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [20.0, 'lbs']}",36.28736,34.47299,38.10173,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 20.0 lbs so this converts to 20.0 lbs * 0.453592 kg/lbs = 9.07184 kg. Hence, the patient's maintenance fluid is 9.07184 kg * 4 mL/kg/hr = 36.28736 mL/hr.
Hence, the patient's fluid maintenance is 36.28736 mL/hr."
4778,22,Maintenance Fluids Calculations,physical,decimal,pmc-6754913-1,Extracted,"A previously healthy 5-year-old girl of African origin presented to the Emergency Department (ED) with macroscopic hematuria appeared 24 hours before presentation and isolated abdominal pain for one month previously. There was no history of fever, vomiting, urinary or systemic symptoms, weight loss, or abdominal trauma.
The patient had no significant medical history, in particular, head injuries such as trauma, hemorrhage, or infection, and did not take any medications. Family history was unremarkable, with no antecedents of neoplasm or precocious puberty. Her mother was not taking any contraceptive hormonal medications, and there was no history of any other source of exposure to hormonal drugs.
On physical examination, the child appeared well. Her anthropometric parameters were as follows: weight 21 kg (50th percentile); height 117 cm (50–75th percentile). Her vital signs were normal, except for blood pressure at 130/90 mm Hg (>99th percentile for sex and height). She had neither dysmorphic features nor skin lesions (café-au-lait spots, facial acne). On abdominal examination, we palpated a mass, measuring 6 cm with regularly margins in the right upper quadrant. There was no central nervous system dysfunction (headache, vomiting or visual abnormalities). She had bilateral, symmetrical nontender enlargement of breast buds corresponding to stage 2 of the Tanner classification. There was no pubic or axillary hair, and her thyroid was normal on clinical inspection.
Laboratory work-up in the ED included a complete blood count, metabolic panel, and urinalysis. Her hematologic and basic metabolic panel, serum electrolytes, and liver and renal function tests were normal. Urinalysis confirmed hematuria. The child underwent an ultrasonography, which revealed a well-circumscribed heterogeneous echogenic mass, measuring 9.2 × 9.5 cm, in the right renal fossa. With suspicion of Wilms tumor, the child was admitted into the Oncology Department. On abdominal and pulmonary computerized tomography (CT), a high suspicion of nephroblastoma was made. Histological examination confirmed the diagnosis of intermediary-risk nephroblastoma stage I.
The first endocrine work-up revealed a normal thyroid function and prepubertal gonadotropin levels (see ). Ultrasonography excluded ovarian and adrenal masses and showed infantile ovaries and uterus. Bone age was not performed. The endocrine diagnosis was bilateral PT.
The International Society of Pediatric Oncology (SIOP) 2001 chemotherapy protocol (dactinomycin/vincristine) was commenced, with complete excision of the tumor performed 4 weeks later. Additional chemotherapy cycles were provided after surgery, for a total duration of 3 months. The clinical tolerance and response were excellent, without any side effects or signs of residual tumor.
A second endocrine assessment was performed at the end of chemotherapy. Surprisingly, we identified an accelerated linear growth (a gain of 3 cm in 4 months) in the context of rapid breast development (passage from stage 2 to stage 3 over 4 months) with no axillary or pubic hair. The second hormonal work-up found an activated pituitary-gonadal axis () along with advanced skeletal maturation and ultrasound signs of uterine hormonal impregnation. A gonadotropin-releasing hormone analog (GnRHa) stimulation test was carried out and showed a pubertal response, confirming gonadotropin-dependent puberty ().
Magnetic resonance imaging (MRI) of the brain showed a morphologically normal pituitary, but of pubertal size (pituitary height of 6 mm and marked convexity of the upper surface) and no congenital or acquired lesions in the pineal or hypothalamic-optic region (). Human chorionic gonadotropin (hCG) levels (repeated twice at different time points) were normal. hCG-secreting tumor was considered as potential etiology of PP, but this diagnosis was excluded on both biological (high LH and FSH levels, normal hCG) and radiological arguments (no tumor in liver, mediastinum, ovaries, or CNS).
The definitive diagnosis of idiopathic CPP was made, and we began treatment with GnRHa (11.25 mg every 3 months, intramuscularly). Six months later, we noted a reassuring clinical evolution, with partial regression of breast development, reduction in growth velocity (2 cm/6 months), and increasingly random LH level at 3.4 IU/L. Recently, a prospective study [] showed that this biological evolution, with incomplete suppression of LH levels, is common in children with CPP under treatment. In a patient with a favorable clinical response (neither clinical pubertal progression, nor an advancement of bone age), this biological evolution should not be interpreted as indicative of treatment failure.
The global evolution of our patient, from oncological diagnosis up to 6 months after the beginning of CPP treatment, is depicted in .","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [21.0, 'kg']}",61,57.95,64.05,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 21.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (21.0 kg - 20 kg) = 61.0 mL/hr.
Hence, the patient's fluid maintenance is 61.0 mL/hr."
4779,22,Maintenance Fluids Calculations,physical,decimal,pmc-4697249-1,Extracted,"A 21-year-old male patient, suffering from TS, weighing 58 kg presented with complaints of abdominal pain for the past 3 years. He had seizures in childhood and the last episode was at the age of seven after which he was not on any medication. There was no history of hypertension, haematuria, mental retardation or developmental delay. Family history was unremarkable.
Physical examination revealed adenoma sebaceum in the face [], ash leaf spots in the back and hyper-pigmentation of gums. Laboratory investigations revealed haemoglobin of 9.0 g% and all other parameters including renal function tests were within normal limits. Fundus examination revealed left eye astrocytoma. Echocardiography showed normal left ventricular function. Contrast-enhanced computed tomography (CECT) abdomen showed multiple angiomyolipomas with the largest measuring 8 cm involving the right kidney []. CECT thorax showed multiple small, well-defined nodules in bilateral lung fields and sclerotic lytic lesions involving vertebrae. CECT brain revealed multiple subependymal calcifications along with a cystic lesion in the posterior fossa. He was followed up with serial ultrasounds to assess the size of the tumour and right partial nephrectomy was planned as the right kidney increased in size significantly.
He was pre-medicated with tablet diazepam 10 mg and tablet famotidine 20 mg in the night and the morning before surgery. On arrival at the operation theatre, after attaching monitors, anaesthesia was induced with injection fentanyl 100 μg and injection propofol 100 mg intravenously (IV). Injection atracurium 25 mg. IV facilitated tracheal Intubation and was followed by maintenance with air and oxygen with 1.5% isoflurane and injection morphine 6 mg IV was used for intraoperative analgesia.
Throughout the intraoperative period, haemodynamics remained stable and peak inspiratory pressure was maintained at 15 cm H2 O by using pressure-controlled ventilation mode on Datex-Aestiva/5® (Datex-Ohmeda Ltd, Hatfield, UK) anaesthesia machine. Partial nephrectomy of the right kidney with excision of the angiomyolipoma was done. Intraoperative blood loss of 800 ml was managed with transfusion of two units of packed cells, and adequate urine output was maintained. He was extubated at the end of the surgery and shifted to post-anaesthesia care unit for monitoring. IV morphine through patient-controlled analgesia pump was administered for post-operative analgesia. His entire post-operative period remained uneventful and he was discharged on 7th post-operative day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [58.0, 'kg']}",98,93.1,102.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 58.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (58.0 kg - 20 kg) = 98.0 mL/hr.
Hence, the patient's fluid maintenance is 98.0 mL/hr."
4780,22,Maintenance Fluids Calculations,physical,decimal,pmc-6168055-1,Extracted,"A 78-year-old African-American man weighing 53 kilograms with a past medical history significant for chronic lymphocytic leukemia (CLL), hyperuricemia with chronic gouty arthropathy, chronic kidney disease (CKD) stage 3 presented to the Emergency Department (ED) with the chief complaint of shortness of breath and fatigue for one day. His outpatient medication included ibrutinib 420 milligrams (mg) and allopurinol 300 mg daily. He was diagnosed with CLL two years prior to presentation. Initially, he was started on bendamustine with an appropriate response. However, an escalation in his lymphocyte count was appreciated one month prior to presentation and ibrutinib was initiated for CLL progression. One day prior to admission to the hospital, the patient was evaluated by his primary oncologist at an outpatient visit. He was febrile with a temperature of 101.6 degrees fahrenheit (°F) but otherwise asymptomatic. Blood and urine cultures were obtained and was started on oral levofloxacin empirically. His labs were significant for worsening hyperuricemia with a uric acid level of 13.0 milligram per deciliter (mg/dl). A single dose of intravenous rasburicase 3 mg was then administered.The following day, he presented to the ED complaining of significant fatigue associated with dry nonproductive cough of one day duration. Examination was remarkable for a fever of 102.8°F, an oxygen saturation (SPO2) of 85% on room air, conjunctival pallor and scleral icterus. A left lower lobe infiltrate was observed on his computed tomography (CT) angiogram of the chest (Figure ). Laboratory results were noteworthy for a drop-in hemoglobin (4.9 mg/dL), indirect hyperbilirubinemia (7.2 mg/dL), low haptoglobin (<10 mg/dL) and elevated lactate dehydrogenase of 1611 International Units per liter (IU/L) compared to (756 IU/L) the day before; depicting acute hemolytic anemia. SPO2 persisted at 85% despite the use of nasal cannula, nonrebreather and non-invasive positive pressure ventilation. The patient was admitted to the intensive care unit (ICU). Arterial blood gas on 50% fraction of inspired oxygen (FiO2) was significant for an arterial oxygen level (PO2) of 222 millimeters mercury (mm Hg) and an oxyhemoglobin of 85.9%. Co-oximetry was then obtained and methemoglobin level was 13.4%. The patient was started on vancomycin and cefepime and transfused with three units of packed red blood cells. Methylene blue was not administered as the patient was assumed to have G6PD deficiency given his race and this episode of hemolysis.
After an ICU stay of two days, the patient clinically improved, SpO2 normalized, his hemoglobin levels improved, methemoglobin levels trended down and was transferred back to the floor (Table ). A G6PD level sent during the acute attack yielded a result within the normal range. In addition, mycoplasma serum antibodies were negative. Despite broad spectrum antibiotic coverage, the patient continued to spike fevers as high as 102.7°F from day one to day four. He subsequently started complaining of right knee pain associated with right knee swelling and tenderness on examination. Arthrocentesis revealed monosodium urate crystals and was started on colchicine and prednisone. Fever, knee pain, swelling and tenderness resolved. The patient was discharged to a skilled nursing facility on prednisone taper, allopurinol and colchicine. He was continued on ibrutinib to date (five months later) and his white blood cell count is currently within normal limits. A repeat CT chest performed three monthts later documented resolution of the previously seen left lower lobe pulmonary inifiltrate.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [53.0, 'kg']}",93,88.35,97.65,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 53.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (53.0 kg - 20 kg) = 93.0 mL/hr.
Hence, the patient's fluid maintenance is 93.0 mL/hr."
4781,22,Maintenance Fluids Calculations,physical,decimal,pmc-3474965-1,Extracted,"A 38-year-old unbooked gravida 3 Para 2+0 two alive woman with no formal education was booked at the antenatal clinic for elective caesarean section at 32 weeks for severe pre-eclampsia. Blood pressure at booking was 220/160 mmhg. Patient later went into spontaneous labour on the same day and developed cord prolapse for which she was booked for emergency caesarean section. On examination, she was in painful distress, anasarca, sacral oedema, bilateral pitting pedal oedema up to the knee joint, and periorbital oedema. Weight was 195 kg, height 1.7 m, pulse rate 100 beats per minute, and blood pressure 210/160 mmhg after receiving three doses of 5 mg diazepam, 10 mg hydralazine, and 25 mg magnesium sulphate. Auscultation of the chest was vesicular breath sounds. She was pale, anicteric, and febrile to touch. Urinalysis showed protein ++ and glucose +. Radom blood sugar was 6 mmol/dL. The temporomandibular joint was mobile with mallampati IV. Packed cell volume was 34%. An assessment of ASA IIIE with severe preeclampsia and prematurity in morbidly obese obstetric patient was made. The patient was counselled for surgery and informed consent obtained. Spinal anaesthesia was administered after several attempts with 2 mLs of hypobaric bupivacaine and L4, L5 interspace. The height of block was T4. She was given oxygen by facemask. During surgery, a male baby was extracted birth weight 2.1 kg, Apgar score [, ]. Blood pressure at the end of surgery was 200/160 mmhg. She spent several days in hospital because of poor wound healing and the blood pressure was persistently high despite administration of antihypertensive. She was discharged home 18 days postoperative due to industrial action by the hospital medical staff.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [195.0, 'kg']}",235,223.25,246.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 195.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (195.0 kg - 20 kg) = 235.0 mL/hr.
Hence, the patient's fluid maintenance is 235.0 mL/hr."
4782,22,Maintenance Fluids Calculations,physical,decimal,pmc-6798273-1,Extracted,"A 5-year-old boy presented with fever for 12 days, progressive motor weakness in lower limbs for 9 days, and retention of urine and constipation for 6 days. The patient was treated elsewhere for fever for three days. However, on the fourth day of the illness, the child developed progressive symmetrical lower limb weakness causing difficulty in standing, sitting, and turning from side to side. Over the next three days, he developed retention of urine and constipation, hence was referred to our hospital for further management.
There was no history of headache, vomiting, altered sensorium, cranial nerve or sensory deficit, recent immunization, and head or spine trauma. The patient had no tuberculosis (TB) in the past nor TB contact.
At admission, his pulse rate was 88/min, respiratory rate was 32/min, and blood pressure was 90/60 mm of Hg. Bacillus Calmette Guerine vaccine scar was seen. Spine palpation revealed no tenderness or deformity. His weight (16kg) and height (106cm) both were between the 10th and 25th centiles for his age and sex. His higher mental functions, cranial nerves, and sensory examination were normal, and papilledema was absent. Tone, power, and reflexes of both upper limbs were normal. Both lower limbs had hypotonia, power grade 2/5, and exaggerated (3+) deep tendon reflexes. Abdominal and cremasteric reflexes were absent and plantar reflexes were extensor bilaterally. Meningeal signs were absent. The patient had mild firm hepatomegaly (2cm) and a palpable distended urinary bladder. Respiratory and cardiovascular system examination was normal.
His initial investigations showed iron deficiency anemia and elevated Erythrocyte sedimentation rate (25 mm at 1h), a negative Mantoux test, normal chest radiograph, and gastric aspirate negative for acid-fast bacilli. Enzyme-linked immunosorbent assay was negative for human immunodeficiency virus infection. MRI of dorsal spine (P + C) showed a well-defined oval T2 hypointense ring-enhancing lesion (4.5 × 2.5 mm) in the thoracic cord at D4-D5 level, with mild perilesional edema from D3 to D5 level suggestive of IMT []. MRI of brain revealed few tiny T2/fluid attenuation inversion recovery (FLAIR) hyperintense enhancing foci in left frontal white matter and subependymal region of the left ventricle. Minimal focal subcortical white matter edema was observed in right frontal lobe suggestive of tuberculoma [].
The patient was started on ATT regime containing two months of Isoniazid (H), Rifampicin (R), pyrazinamide (Z) and Ethambutol (E) followed by 7 months of Isoniazid (H), Rifampicin (R) and Ethambutol (E) therapy (2HRZE +7HRE) with steroids for four weeks. Parenteral dexamethasone was given for two days followed by oral prednisolone for a total of four weeks. He showed clinical improvement in three days and had complete clinical recovery by nine days. Meanwhile, family screening for TB detected sputum positive for pulmonary TB in father. His father was enrolled and started on standard ATT, the younger sibling was started on isoniazid prophylaxis as per Revised National Tuberculosis Control Program guidelines. On follow-up, the patient was found to be compliant with ATT and clinically well without adverse effects.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [16.0, 'kg']}",52,49.4,54.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 16.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (16.0 kg - 10 kg) = 52.0 mL/hr.
Hence, the patient's fluid maintenance is 52.0 mL/hr."
4783,22,Maintenance Fluids Calculations,physical,decimal,pmc-5073778-1,Extracted,"A 50-year-old man presented to the emergency department with stridor of 1-week duration. He also complained of progressive cough and breathlessness for 2 months. There was a significant reduction in appetite and he had lost 5 kg of his body weight. On admission to our facility, the patient was drowsy. Physical examination revealed an afebrile patient with a heart rate of 120 beats/min, respiratory rate of 38 breaths/min, and blood pressure of 80/50 mmHg. His oxygen saturation was 91% while breathing 40% oxygen. Contrast-enhanced computed tomography (CT) of his chest revealed the presence of a mass in the subcarinal region encasing the lower trachea and main bronchi and consolidation in the right upper lobe [].
The patient was intubated with an endotracheal tube (7.0 mm internal diameter) and mechanically ventilated. Resuscitation with fluids and vasopressors was performed. He was initiated on intravenous co-amoxiclav (1.2 g thrice a day). Shock recovered after 48 h and tachycardia resolved. However, the patient could not be weaned off the ventilator over the next 5 days. On the 6th day, EUS-B-FNA of the subcarinal mass was performed. Cytological examination showed loosely cohesive clusters and dispersed population of small-sized tumor cells with hyperchromatic nuclei showing focal nuclear molding suggestive of small cell carcinoma of the lung [].
The final clinicoradiological stage was IIIb (T4 N3 M0), but the patient had a poor performance status (Eastern cooperative oncology group score of 4). Placement of a metallic tracheobronchial Y-stent was considered but was not performed as the patient's legal representative refused consent. Chemotherapy with cisplatin 100 mg (85% of 60 mg/m2 of body surface area [BSA]) and irinotecan 160 mg (90% of 100 mg/m2 of BSA) were administered. After a week, the patient was successfully weaned off the ventilator and was discharged to home care. The patient received three more cycles of chemotherapy. However, the disease progressed and the patient succumbed to his illness 3 months after the diagnosis.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.0, 'kg']}",20,19,21,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.0 kg. Hence, the patient's maintenance fluid is 5.0 kg * 4 mL/kg/hr = 20.0 mL/hr.
Hence, the patient's fluid maintenance is 20.0 mL/hr."
4784,22,Maintenance Fluids Calculations,physical,decimal,pmc-4947274-1,Extracted,"The proband (Fig. , V: 2) is 1-month-old Saudi boy born normally at term to first 24-year- old parents. Four maternal aunts (Fig. , IV: 1, 4, 7, 8.) had died at the age of four, five, three and six weeks respectively, in a remote medical facility with no available records. However, all are said to have presented with microcephaly and abnormal movements similar to the index (see below). The mother was G2P1 (IUFD at 28 weeks gestation) +0. No history of exposures. Antenatal ultrasound (US) scan showed microcephaly. Apgar score was 9 and 10 at one and five minutes, respectively. Birth weight 2675gm (10th percentile), head circumference 29 cm (−3SD). Examination showed microcephaly, sloping forehead, short neck, and micrognathia (Fig. ). Shortly after birth, he developed abnormal movements in the form of bursts of tonic/clonic movements provoked by non-habituating glabellar and root of the nose tapping, sound and light (see Additional files , and ). There was hyperreflexia, hypertonia and arthrogryposis of the lower limbs. He developed frequent apneas necessitating mechanical ventilation. Treatment with clonazepam was initiated and later phenobarbitone was added to control the abnormal movements. Laboratory investigations (Table ) showed normal metabolic screen including plasma and CSF asparagine, glutamine, aspartate and glutamate.CSF neurotransmitters, 5HIAA, 3-OMD, and HVA were normal. Brain MRI (Fig. ) revealed cerebral atrophy, simplified gyral pattern and hypoplastic cerebellum and pons. EEG showed multifocal discharges, fast spiking in the left hemisphere favoring cortical dysplasia, and frontal spikes. The findings favor epileptic encephalopathy in a transitional phase with predominant seizure burdens. Whole exome sequence (WES) revealed nonsense mutation in the ASNS gene, (NM_001178076.1: c.970C > T p. (Arg324*). He died at the age of six weeks in status epilepticus.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2675.0, 'g']}",10.7,10.165,11.235,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2675.0 g so this converts to 2675.0 lbs * kg/1000 g = 2.675 kg. Hence, the patient's maintenance fluid is 2.675 kg * 4 mL/kg/hr = 10.7 mL/hr.
Hence, the patient's fluid maintenance is 10.7 mL/hr."
4785,22,Maintenance Fluids Calculations,physical,decimal,trec-ct-2022-48,Extracted,A 20-year-old man comes to the emergency due to bleeding after a tooth extraction.  The bleeding has persisted for approximately 30 minutes despite constant direct pressure.  He is a known case of Hemophilia type A treated with FVIII. Blood pressure is 95/60 mm Hg and pulse is 105/min. His weight is 70 Kg. Family history is positive for Hemophilia type A in his maternal uncle. He also has a lipoma on his left arm which he plans to remove surgically. His FVIII activity is 40%.,"Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [70.0, 'kg']}",110,104.5,115.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 70.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (70.0 kg - 20 kg) = 110.0 mL/hr.
Hence, the patient's fluid maintenance is 110.0 mL/hr."
4786,22,Maintenance Fluids Calculations,physical,decimal,pmc-4320515-1,Extracted,"A one-month-old Moroccan baby boy was referred to our institute for a medical genetic consultation with a chief complaint of malformations diagnosed as popliteal pterygium syndrome. He was the fourth liveborn child of a healthy nonconsanguineous couple, aged 35 for the mother and 49 for the father, with no particular familial history. On clinical examination, both the parents and other siblings were normal. During pregnancy, the mother had no history of drug ingestion, abdominal trauma, or radiographic examination. The pregnancy was not medically followed, but it was reported without complications. The baby was born at term by vaginal delivery. His Apgar score was good. At birth, he weighed 3,500g; his length was 52cm; his head circumference was 36cm. On general physical examination, our patient had a bilateral cleft lip and palate with two large pits on the lower lip and oral synechias that did not restrict feeding (Figure ). He presented several achromic spots of different shapes and sizes on his face. They were irregular but with a well-defined border. On Wood lamp examination, they appeared off-white. There was an asymmetrical large-size pigmented nevus on the sole of his right foot, without relevant nails anomalies (Figures and ). He also had right popliteal pterygium and bilateral syndactyly of four to five toes (Figure ). The urogenital examination showed a phimosis. X-rays of the skull, transfontanellar, abdomino-genitourinary and cardiac ultrasonography were normal. The results of all laboratory examinations were within normal limits. Informed consent was obtained from the proband’s parents prior to molecular analysis. Peripheral blood was collected from the affected child and his parents. Molecular genetic testing for suspected PPS was performed by Sanger sequencing of the entire coding region and flanking introns of the IRF6 gene (NM_006147.3). This led to the identification of the heterozygous c.250C>T; p.Arg84Cys mutation in exon 4 (Figure ). This mutation occurred de novo, as it was not revealed in the hematologic cells of the parents.
Our patient was scheduled for reconstructive surgery of his cleft lip and palate, oral synechiae and popliteal pterygium.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.5, 'kg']}",14,13.3,14.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.5 kg. Hence, the patient's maintenance fluid is 3.5 kg * 4 mL/kg/hr = 14.0 mL/hr.
Hence, the patient's fluid maintenance is 14.0 mL/hr."
4787,22,Maintenance Fluids Calculations,physical,decimal,pmc-2804722-1,Extracted,"A 38 year-old caucasian male, heavy smoker (40 pack/year), was presented to the emergency department (ED) with a painful swelling of the left lower limb of 15 days duration. He also complained of productive cough, anorexia and weight loss within the past 6 months. He was not on any medications and had no allergies. At that moment, he was an unemployed construction worker and a moderate alcohol consumer. General physical examination revealed a poorly built, malnourished man weighing 47 Kg. He was febrile (axilar temperature 38.3°C), taquicardic (pulse 102 bpm) and normotensive. Pulse oximetry (FiO2 21%) was 96% and chest auscultation revealed bilateral rhonchi. Cardiovascular and abdominal examination was normal. His left leg was swollen and tender to touch.
Arterial blood gas analysis (FiO2 = 21%) showed hypoxemia (pO2 = 89 mmHg). Laboratory findings on admission revealed a normal WBC count (7.9 G/mm3), a low hemoglobin level (11.3 g/dL), macrocytosis (MGV 106.2 fL), normal platelet count (397.000/mm3), hiponatremia (131 mEq/L) and elevated CRP (5.20 mg/dl) and d-dimer levels (5.51 ug/ml - normal < 0.5). Plasma fibrinogen level was also high (455 mg/dl - normal range 200-400).
Chest X-ray demonstrated bilateral infiltrations and multiple cavitary lesions in both lungs (Figure ). Deep venous thrombosis was confirmed by leg ultrasound.
Chest CT angiography performed showed occlusion of distal segment of left pulmonary artery and right basal segmental branches, compatible with bilateral pulmonary embolism. There were also findings consistent with severe pulmonary tuberculosis (Figure ).
Mycobacterium tuberculosis (MT) infection was confirmed by culture on Lowenstein-Jensen agar and MT organisms were found to be sensitive to all first-line anti-tuberculosis drugs. Serologic testing for HIV, HBV and HCV were negative.
Standard ATT was initiated adjusted to weight: isoniazid (200 mg/day), rifampin (480 mg/day), pyrazinamid (1200 mg/day) and ethambutol (800 mg/day). The patient was treated with low-molecular-weight heparin (60 mg twice daily) and 3 days later, warfarin (5 mg/day) was started with a target International Normalized Ratio (INR) of 2.0-3.0.
On ATT his general state improved and he responded well to anticoagulation therapy. No adverse effects were seen. He was discharged 14 days after admission to continue follow-up at the Pneumology Diagnostic Centre. The patient has now finished two months on ATT regimen with isoniazid (200 mg/day) and rifampin (480 mg/day) with a good clinical response.
A 51 year-old male, ex-smoker, presented to the ED with a 3-week history of anorexia, productive cough with yellow sputum and weight loss. He also complained of night sweats and vomiting in the last 3 days. There was no prior history of other diseases but he had contacted in the last few months with a patient with TB. There was no history of alcohol abuse or sexual risk behaviors.
Clinical examination, revealed a thin, ill-appearing-man, weighing 40 kg. He was febrile (axilar temperature 38.4°C), hypotensive (BP 90/53 mmHg) and tachycardic (pulse 118 bpm). His respiratory rate was normal with an oxygen saturation of 98% (FiO2 = 21%). Examination of chest and abdomen was unremarkable. No peripheral edema was found.
Routine investigations revealed anemia (Hb 10.5 g/dl), leucocytosis (WBC 13.8 G/L) and a high platelet count (635.000/mm3). Other abnormal results included hiponatremia (129 mEq/L), high CRP (18.09 mg/dL) and fibrinogen levels (668 mg/dl). Arterial blood gas analysis (FiO2 21%) showed: pH 7.47; pO2 92 mmHg; pCO2 33.8 mmHg; HCO3 24.3 mmol/L; oxygen saturation 98.5%.
Chest X-ray demonstrated a heterogeneous consolidation of both lung fields, mainly in the upper 2/3, consistent with tuberculosis (Figure ).
Sputum was found to contain acid-fast bacilli (> 36 bacilli/field) and MT subsequently cultured and found to be susceptible to all first line drugs. Serologic tests for HIV, HBV e HCV were negative.
ATT including isoniazid (250 mg/day), rifampicin (600 mg/day), pyrazinamid (1500 mg/day), ethambutol (1200 mg/day) and piridoxin (40 mg/day) was started. After two weeks in hospital, patient presented favorable response with improvement in constitutional symptoms and was discharged to continue ATT at the Diagnostic Pneumology Centre. He returned to the ED complaining of pain and swelling in his left limb 13 days later. Ultrasound revealed a femoropopliteal thrombosis. He was put on low-molecular-weight heparin (60 mg twice daily) and warfarin (5 mg/day) on the same day. Since therapeutic INR level was difficult to maintain with high doses (15 mg) of warfarin, acenocumarol was initiated.
Chest CT showed multiple confluent cavitary lesions mainly in the upper lobes, consolidation and micronodules, consistent with extensive pulmonary tuberculosis. A right hilar adenopathy (17 mm) and mediastinal adenopathies (some larger than 10 mm) were also observed. Abdominal and pelvic CT was performed and revealed homogeneous hepatomegaly and no focal parenchymal lesions. Tumor makers were negative. Since his bacteriological and radiological response (Figure ) to ATT was slow, he had to complete an 18-month therapy regimen.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [47.0, 'kg']}",87,82.65,91.35,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 47.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (47.0 kg - 20 kg) = 87.0 mL/hr.
Hence, the patient's fluid maintenance is 87.0 mL/hr."
4788,22,Maintenance Fluids Calculations,physical,decimal,pmc-2633182-1,Extracted,"A 2 months old male infant was admitted to a local hospital due to generalized edema. On prenatal examination, high α-fetoprotein (AFP) level (20.85 MoM) in the maternal serum was detected at the 18th gestational week. The baby was born at 36 weeks of gestational age with a birth weight of 2.57 kg. The weight of placenta was reported to be normal. Apgar scores at 1 and 5 min were 9 and 10 points, respectively. However, he showed shortness of breath and abdominal distension soon after the birth. He has normal male external genitalia. Laboratory tests revealed markedly hypoalbuminemia (serum albumin 1.2 g/dL), massive proteinuria (urinary protein excretion 7,959 mg/m2/day), and hypothyroidism. There was no evidence of congenital infection. The parents and his older brother are all healthy except that his mother is a hepatitis B virus antigen carrier. Captopril (0.1 mg/kg/day) and synthyroid (2.7 µg/kg/day) were started as well as intermittent albumin infusions. However, generalized edema was aggravated with frequent need of albumin infusion. At 2 months of age, he was transferred to Seoul National University Children's Hospital because of intractable generalized edema and respiratory difficulty. On admission, his body weight was 4.49 kg (3-10 percentile), and height was 52 cm (<3 percentile). He showed mild chest retraction, and breathing sound was coarse with crackles on both lung fields. The serum albumin was 1.6 g/dL, serum creatinine was 0.3 mg/dL, random urine protein/creatinine ratio was 110 mg/mg, platelet count was 888×103/µL, and serum immunoglobulin G level was 64 mg/dL (normal range, 176-201 mg/dL). The nasopharyngeal aspirate was positive for human respiratory syncytial virus A. Thus, in addition to supportive lung care, intravenous immune globulin (0.5 g/kg) was given. He was medicated with indomethacin (4 mg/kg/day), captopril (4.7 mg/kg/day), dipyridamole (3 mg/kg/day), warfarin, and synthyroid as well as high protein (up to 4 mg/kg/day) and high calorie diet (120 Cal/kg/day). However, frequent albumin infusion (2 g/kg/day) had to be continued to control respiratory problem and generalized edema, and a Chemoport® was implanted into right atrium via right external jugular vein to secure a central venous line. An open renal biopsy was performed at 4 months of age, which showed diffuse mesangial proliferation (, ). Genetic analysis of the NPHS1 gene revealed compound heterozygous frame-shifting mutations, 8-bp deletion in exon 16 (c.2156_2163 delTGCACTGC causing p.L719DfsX4), and 1-bp insertion in exon 24 (c.3250_3251insG causing p.V1084-GfsX12) (). The former mutation was inherited from mother, and the latter from father. During follow-up, he was admitted 2 more times due to central line infections. Thus, at 8 months of age, Chemoport® removal and unilateral nephrectomy were done to control the recurrent infections and to reduce the degree of proteinuria and the need of albumin infusions, respectively.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.49, 'kg']}",17.96,17.062,18.858,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.49 kg. Hence, the patient's maintenance fluid is 4.49 kg * 4 mL/kg/hr = 17.96 mL/hr.
Hence, the patient's fluid maintenance is 17.96 mL/hr."
4789,22,Maintenance Fluids Calculations,physical,decimal,pmc-3008953-1,Extracted,"A 23-year-old female was referred from the Urology clinic as a case of solitary pelvic kidney and azotemia. She had history of primary amenorrhea, recurrent urinary tract infections and recent onset hypertension. Examination revealed her to be of average built (body weight of 62 kg and height of 168cms), euvolemic, with no pallor, BP- 110/70 mm of Hg (on medication), and no gross skeletal abnormality or hearing defects. Her cardiovascular, abdominal and respiratory examination was normal. She had feminine body features. Her gynecological examination showed a small vaginal pouch of about 2.5 cm ending blindly. There was no family history of any gynecological or renal abnormalities.
Investigations showed hemoglobin 117g/dL, WBC count- 7.5×103/dmm3, platelets - 3.55×109/mm3, urea-4.3 mmol/L, Creatinine 2mg/dl, albumin - 3.5g/dL, Calcium 9mg/dl, phosphorus- 6.5 mg/dL, sodium - 140 mmol/L, potassium- 4.8 mmol/L, PTH- 29 pmol/L. Urine examination showed 2+ proteins, leucocytes 4-6/HPF, no RBCs, 24-hour urinary protein of 1.2 gram and a creatinine clearance of 38ml/min (24-hour urinary creatinine estimation). Her hormonal profile was within normal limits. Detailed ultrasound revealed left kidney not localized, a 9.5 cm right pelvic kidney, with increased echotexture, loss of cortico-medullary differentiation, few cortical cysts and mild hydronephrosis Uterus was not seen but both ovaries were present []. A Magnetic Resonance Imaging (MRI) scan revealed solitary pelvic kidney in relation to right internal iliac vessels and gynecological abnormalities were confirmed [Figures –]. Tc 99 DMSA scan showed a poorly outlined right pelvic kidney showing nonhomogenous tracer uptake by functional parenchymal tissue. Left kidney was not visualized. A cystoscopy done by urologists prior to her referral had shown only right ureteric orifice and absent left ureteric orifice. Genetic study revealed 46 XX karyotype.
The features are consistent with type 2 MRKH syndrome with chronic kidney disease (CKD)-stage 3. Her CKD is likely because of chronic pyelonephritis secondary to anomalies of her urinary tract. She was counseled and is on regular follow-up in renal and gynecological clinics. Because of the social stigma she refused to be assessed by a plastic surgeon as was advised by her gynecologist. She is on conservative measures for her CKD but her follow-up in renal clinic is erratic.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [62.0, 'kg']}",102,96.9,107.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 62.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (62.0 kg - 20 kg) = 102.0 mL/hr.
Hence, the patient's fluid maintenance is 102.0 mL/hr."
4790,22,Maintenance Fluids Calculations,physical,decimal,pmc-6312918-1,Extracted,"A 1-month-old girl was referred to the genetics clinic of our hospital for evaluation of testicle-like masses observed during herniorrhaphy. Bilateral inguinal hernias were noted just after birth and laparoscopic herniorrhaphy was performed at a local clinic when the patient was 1 month old. Laparoscopy showed that there was no uterus, and testicle-like masses were found around the openings of bilateral inguinal canals. This child was born at a gestational age of 38 weeks with a birth weight of 3.8 kg (90th–97th percentile) and had no specific prenatal or perinatal history. She was the second child of healthy nonconsanguineous parents, and her 4-year-old sister was also healthy. There were no abnormal results from the newborn screening for inherited metabolic disorders.
A physical examination performed at her first visit showed that her height and body weight were 58.3 cm (50th–75th percentile) and 5.7 kg (50th–75th percentile), respectively. She showed good activity and did not have either hyperpigmentation or hypertension. A testicle-like mass was palpable in the left but not the right inguinal area. Her external genitalia showed a complete female phenotype and there was only one external opening.
The results of hormonal studies are shown in . Baseline serum concentrations of adrenocorticotropic hormone (ACTH) and luteinizing hormone (LH), follicle stimulating hormone (FSH), estradiol, and testosterone were no higher than those of normal male infants. Anti-Müllerian hormone (AMH) was also within the normal range for male infants.
No fistula was detected when contrast medium was injected into the common urethra and a blind short vaginal pouch (3.8 cm in length) was found on genitography (). Pelvis sonography revealed that the right testis (0.87 cm×0.15 cm×0.76 cm) was located in the right lower quadrant of the abdomen and the left testis (1.07 cm×0.45 cm×0.64 cm) was located in the proximal inguinal canal. No uterus, ovaries, or other internal female genital organs were identified ().
The patient’s karyotype was that of a normal male, i.e., 46,XY. Genetic analysis of AR and SRD5A2 was performed, and a hemizygous mutation (c.2324G>A, p.Arg775His) was identified in AR. No mutation was found in SRD5A2. Family screening for genetic counseling was performed, and the same AR mutation was also found in the child’s mother, who was a heterozygous female carrier. The child’s elder sister had a normal female karyotype of 46,XX and did not have the AR mutation ().
The patient was referred to the pediatric urology clinic for surgical treatment. Laparoscopic bilateral gonadectomy was performed when the child was 8 months old, to avoid the risk of malignancy in the undescended testicles. Both testes were dissected and removed (). No spermatic fascia was observed in the gross examination of the specimen, although testes and epididymides were present. Histopathological findings revealed an immature testis and epididymis with indistinct lumina and maturation arrest of germ cells ().
The patient was confirmed to have CAIS caused by an AR mutation and is being raised as a girl. She is now 31 months old and shows typical developmental milestones.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.7, 'kg']}",22.8,21.66,23.94,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.7 kg. Hence, the patient's maintenance fluid is 5.7 kg * 4 mL/kg/hr = 22.8 mL/hr.
Hence, the patient's fluid maintenance is 22.8 mL/hr."
4791,22,Maintenance Fluids Calculations,physical,decimal,pmc-2516517-1,Extracted,"The above patient is a 2-year-old boy with a peculiar facies and psychomotor retardation, especially gross motor retardation and speech delay. His weight is 11.700 gr (25th centile), the height 86 cm (50th centile), and the head circumference 49 cm (75th centile). He was born by a caesarean section at 35 weeks' gestation with a small weight for gestational age (1.880 gr, <3rd centile). As an infant the patient presented hypotonia in association with severe recurrent episodes of apnea, bradycardia and cyanosis, almost on a daily base. Patient's dysmorphic features include frontal bossing with narrow biparietal diameter, prominent eyes with blue sclerae, broad nasal bridge, low set ears, high narrow palate, retrognathia, upsweep of frontal scalp hair, abnormal palmar creases, bilateral overlapping toes, and omphalocele. In addition, the patient has gastro-esophageal reflux, a small atrial septal defect, and a right renal rotation around its elongated axis.
Chromosomal and FISH [subtelomeric and whole chromosome paint (wcp)] analyses of this patient showed an apparently balanced de novo translocation between chromosomes 9 and 15. The initial karyotype was designated as 46,XY,t(9;15)(q31;q26.1)dn. Array-CGH though revealed an ~6.1 Mb duplication on chromosome 9 at 9q34.2-q34.3 and deletions on three regions of chromosome 15 adding to ~10 Mb (Figure ). A fourth region also appeared deleted on chromosome 15 but FISH analysis using the corresponding BAC clone showed normal signals. The imbalances detected by array-CGH were on the same chromosomes involved in the translocation but not directly associated with them. The array-CGH findings were confirmed using FISH with 14 region-specific BAC clones. During confirmation of the array findings, the rearrangement was found to be even more complex with additional breakpoints (at least 5 breakpoints) and an inversion was unexpectedly identified involving chromosome 15 with breakpoints at q21.1 and q21.2. FISH using the same BAC clones was also performed for the parents of the patients and normal results were obtained.
Revised karyotype after FISH confirmation of the array results:
46,XY,t(9;15)(q31;q26.1).ish dup(9)(q34.1q34.3)(RP11-295G24++, RP11-417A4++),del(15)(q21.2q21.3)(RP11-32N2-),del(15)(q22.31q23)(RP11-321F6-, RP11-540N15-, RP11-375D9-),del(15)(q25.1q25.2)(RP11-2E17-), inv(15)(q21.1q21.2)(RP11-90J19st,RP11-353B9mv,RP11-105D1mv, RP11-313P18mv)dn.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [11.7, 'kg']}",43.4,41.23,45.57,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 11.7 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (11.7 kg - 10 kg) = 43.4 mL/hr.
Hence, the patient's fluid maintenance is 43.4 mL/hr."
4792,22,Maintenance Fluids Calculations,physical,decimal,pmc-8523337-1,Extracted,"A 16-year-old male presented to the sleep lab for routine nocturnal polysomnography (PSG) ordered by the pediatrician followed by the sleep specialist consultation with a working diagnosis of frequent night terrors that were provided from another sleep center. These episodes began two years ago and were initially occurring once or twice weekly but were getting more frequently now occurring few times every night. The child would wake up screaming and shaking for few minutes before going back to sleep, with no recollection of these events. Epworth Sleepiness Scale (ESS) assessment was 8/24. He did snore with occasional reported respiratory pauses, raising concerns for underlying obstructive sleep apnea, for which the pediatrician, primarily, ordered the PSG. At bedtime (10 pm), he would fall asleep within 15 minutes; in the morning, he would wake up at 7:30- 8:00 am, with no daily naps. There was no other significant medical history and no family history of parasomnias or seizures.
Examination revealed patient weight at 73.3 kg; height, 165.5 cm. Z-scores of 0.79 (79%) and -1.25 (10%) were based on CDC 2-20 years weight-for-age, and stature-for-age data, respectively. Body mass index was 26.76 kg/ (m2) (Z score: 1.44, 93rd percentile). He had a Mallampati score of 1; tonsil size of 1+. The remainder of the physical examination was normal.
The PSG revealed total sleep time as 322.7 minutes; lights-off time, 10:15 pm; lights-on time, 6:12 am. The obstructive apnea-hypopnea index was 0.4 events/h, the lowest oxygen saturation was 94%, and the mean end-tidal carbon dioxide (EtCO2) was 40.4 mmHg. Periodic limb movement index was 1.0 events/h. However, during the PSG, the patient had three typical events at 3:05 am, 4:44 am and 6:01 am. During these events, the patient would wake up confused with the extension of his left arm, head rotation to the left, flexion of the right arm, and abduction of the right shoulder. Each episode lasts for 10-15 seconds, followed by falling back to sleep. The following changes were seen on the EEG in a 30 seconds window on the sleep study (Figure ).
The diagnosis is SHE seizures, also known as nocturnal frontal lobe epilepsy (NFLE). Figure above demonstrates a 30 seconds window of the EEG portion on the sleep study with (1a) onset of event from N3; (1b) continuation and (1c) end of the event. Asterisks in Figure (1b/1c) refer to the individual epileptiform discharges. The semiology with the “fencing posture” described above is a classic manifestation of seizures arising from the supplementary sensorimotor area of the frontal lobe and in the context of the EEG findings exhibited above will support the diagnosis. The most appropriate next step is to rule out any structural cerebral abnormalities that might cause the SHE, a form of focal epilepsy, and to start an antiepileptic medication (carbamazepine).
Follow up
The patient was admitted to the hospital for further evaluation, where his brain MRI was found normal. He also had additional inpatient standard video EEG monitoring during which his seizures were demonstrated again (Figure ). His seizures were heralded by fast beta activity at the right frontal region (FP2-F4 electrodes) that then evolved to the left frontal region (FP1-F3 electrodes/FP1-F7 electrodes) with rhythmic delta and theta activity. This subsequently evolved over the next 5-10 seconds to rapid rhythmic generalized epileptiform discharges (highlighted with asterisks). The patient was started on carbamazepine. The patient tolerated his medication well and reported no side effects on the three-month follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [73.3, 'kg']}",113.3,107.635,118.965,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 73.3 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (73.3 kg - 20 kg) = 113.3 mL/hr.
Hence, the patient's fluid maintenance is 113.3 mL/hr."
4793,22,Maintenance Fluids Calculations,physical,decimal,pmc-3683218-1,Extracted,"A 61-year-old, married lady, was referred to our Endocrine Clinic by a general practitioner, with a background of hypertension (untreated, since four years) and right hemi-thyroidectomy (performed 15 years ago for multinodular goiter), with complaints of persistent lower backache (non-radicular) and generalized severe body ache that had worsened after she was put on teriparatide (since four months). The teriparatide was started by the primary care physician for severe osteoporosis that was thought to be due to premature menopause (achieved at the age of 35 years). She was a vegetarian, non-smoker, non-ethanolic without any significant family history or drug history.
Examination revealed a lady withdrawn in pain, weighing 61 kg, with a body mass index of 27.5 kg/m2. The blood pressure was 160/92 mm of Hg supine and 170/106 mm of Hg when sitting, without any postural fall. The proximal muscle weakness was 4/5 in all four limbs. General and systemic examination was otherwise normal.
Biochemistry was unremarkable, except for mild hyponatremia (sodium 130 mmol/L) and elevated alkaline phosphatase 140 IU/L (50-136), which was associated with a corrected calcium of 9.7 mg/dl (calcium 10.1 mg/dL, albumin 4.5 gm %) and normal liver function. Although teriparatide therapy could possibly have accounted for these changes, we chose to look at her previous results, with a suspicion of a possible secondary cause for the elevated high alkaline phosphatase on the background of worsening symptoms.
It was noted that she had corrected calcium as high as 10.3 mg% on review of her previous results, which we thought was significantly elevated, especially as her diet was poor in calcium. Further enquiry suggested large volumes of fluid intake (free water) approximately 4-5 liters/day, which the patient put down to persistent thirst, which we considered to be secondary to polydipsia. The adrenal and thyroid screen (TSH: 1.14 mIU/ml) screen was normal
Subsequent specialized testing revealed an elevated parathormone 166 pg/mL (11-54), insufficient vitamin D3 27 ng/L (11-42), and hypercalciurea (24-hour urine calcium 624 mg % (50-300 mg%)), and thus a PTH-dependant etiology for hypercalcemia was considered.
Plain x-ray of the chest was normal. A s keletal survey revealed spondylolisthesis of L4 over L5, without any obvious fractures. Dual Energy X-Ray Absorptiometry (DEXA) densitometry showed a worsening T-score at the spine (T-scores, hip — 2.3, spine — 3.9, forearm — 4.5), compared to the previous results. The echocardiogram was consistent with evidence of systemic hypertension showing diastolic dysfunction with mild concentric left ventricular hypertrophy. A fundoscopy revealed evidence of early hypertensive changes.
Specialized imaging in the form of Doppler ultrasound of the neck suggested a mass at the inferior pole of the right lobe of the thyroid gland (most likely a parathyroid adenoma). The SESTAMIBI scan confirmed the presence of a right inferior parathyroid adenoma as localized by ultrasonography.
A minimal invasive parathyroidectomy was undertaken. A mass 1.5 × 1.0 cm was removed that was consistent with parathyroid adenoma. Microscopy showed an encapsulated lesion composed of a diffuse proliferation of chief cells with surrounding delicate capillary network []. The patient continued to remain well with corrected calcium of 9.3 mg%, with a plan of yearly zolendronic acid infusions for a total of five infusions","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [61.0, 'kg']}",101,95.95,106.05,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 61.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (61.0 kg - 20 kg) = 101.0 mL/hr.
Hence, the patient's fluid maintenance is 101.0 mL/hr."
4794,22,Maintenance Fluids Calculations,physical,decimal,pmc-3030010-1,Extracted,"A 39-year-old man (weight 65 kg; height 168 cm) was scheduled to undergo endoscopic pansinus surgery for the treatment of chronic sinusitis. With the exception of well-controlled hypertension, he was in good health, and the routine preoperative laboratory tests, chest radiography and electrocardiography were normal.
In the preanesthetic room, after confirming negativity by the skin testing, ceftizoxime 1 g was injected intravenously. Intravenous midazolam 2 mg was then injected as a premedication, and he was transferred to the operating room. However, while being moved to an operating bed, he complained of dyspnea. Without delay, oxygen was supplied via a facial mask at 5 L/min. Arterial pulse oxygen saturation, electrocardiography and noninvasive blood pressure were monitored. Blood pressure was 203/105 mmHg and heart rate was 110 beats/min, but despite this oxygen supply, his oxygen saturation decreased gradually to 90%. To secure an airway without resorting to muscle relaxant, propofol 60 mg was administered, and manual ventilation with oxygen initiated. After confirming loss of consciousness, a laryngeal mask airway was inserted. One hour later, the patient recovered and was fully awake. The laryngeal mask airway was then removed and he was transported from the operating room to a postanesthetic room for further care. IgE immunoassays for penicilloyl G and penicilloyl V returned normal results. Total IgE was slightly elevated at 102 IU/ml (normal range: 0-100 IU/ml). The operation was postponed, and he was discharged two days later without any sequelae.
Skin prick and intradermal tests for midazolam and ceftizoxime were conducted three months after the event. The intradermal test revealed a positive reaction to midazolam. The patient was diagnosed as having midazolam hypersensitivity. Four months later, the operation was performed uneventfully without the use of midazolam.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [65.0, 'kg']}",105,99.75,110.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 65.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (65.0 kg - 20 kg) = 105.0 mL/hr.
Hence, the patient's fluid maintenance is 105.0 mL/hr."
4795,22,Maintenance Fluids Calculations,physical,decimal,pmc-8241635-1,Extracted,"We present a 41-year-old man with a past medical history of chronic New York Heart Association (NYHA) Class II-III heart failure with reduced ejection fraction (HFrEF), non-ischemic cardiomyopathy, obstructive sleep apnea, chronic kidney disease and gastroesophageal reflux disease. His home medications were Entresto 24/26mg orally twice daily, carvedilol 3.125mg orally twice daily, pantoprazole 40mg orally twice daily and Maalox 30cc orally every six hours as needed for indigestion. There was no known family history of heart disease, sudden or premature death. He is a former smoker and does use alcohol or illicit drugs, and had serum ethanol less than 10 and urine drug screen negative. He was initially diagnosed with cardiomyopathy of uncertain etiology, HFrEF and he was told that his ejection fraction (EF) was 20%-25% (no records available), two years prior at another facility. There was no ischemic workup at that time and he was discharged on carvedilol, furosemide, lisinopril and metoprolol tartrate (unknown dosages of medications). Subsequently, he had his first presentation to our institution with exertional dyspnea in the context of decompensated HFrEF. At that time, he underwent cardiac catheterization which revealed no significant coronary artery disease (Figures -). Thereafter, he was discharged on low-dose carvedilol, as needed torsemide and Entresto. Aldactone was withheld due to hypotensive episodes. He was advised to have a repeat transthoracic echocardiogram in three months to assess left ventricular systolic function on optimized medical therapy but this was not done. Additionally, he was recommended for outpatient cardiac magnetic resonance imaging to delineate a possible etiology for his nonischemic cardiomyopathy. Seven months later, he underwent cardiac magnetic resonance imaging, which showed a non-compacted (NC) to compacted myocardium ratio of greater than 2.3 (Figure ).
Thereafter, he re-presented with two weeks of worsening dyspnea on exertion, bilateral lower extremity swelling and significant weight gain. On presentation, vital signs were as follows, blood pressure 125/80mmHg (mean arterial pressure of 88mmHg), regular heart rate of 76 beats per minute with increased pulse volume, respiratory rate 24 breaths per minute, temperature 98.2F and SpO2 99% on ambient air. His normal dry weight was approximately 330lbs (149.7kg) and his weight at the time of presentation was 350lbs (158.8kg). Physical examination revealed reduced breath sounds bilaterally with significant rales, along with bilateral lower extremity pitting edema. The remainder of his systems examination was within normal limits. EKG demonstrated normal sinus rhythm at 73 beats per minute, ventricular trigeminy, no pathologic Q-waves, left axis deviation, possible left atrial enlargement, poor precordial R-wave progression and nonspecific T-wave abnormality (Figure ). Subsequent transthoracic echocardiogram with definity echo contrast revealed severe LV systolic dysfunction, EF 25%-30% (Video ).
The patient presented with clinical features consistent with decompensated heart failure. As such, he was diuresed successfully to euvolemia with intravenous furosemide. He experienced persistent sinus bradycardia with a nadir of 40 beats per minute likely of multifactorial origin - deoxygenation from congestive heart failure [], superimposed on obesity hypoventilation and inadequately treated obstructive sleep apnea. Even after aggressive diuresis and improved oxygenation with the utilization of continuous positive airway pressure therapy his bradycardia persisted. Our thought process was that the patient would not be able to tolerate maintenance beta-blockade (necessary guideline-directed medical therapy [GDMT] for his heart failure) given his persistent nocturnal sinus bradycardia into the 40s. Concurrently he had symptomatic salvos of nonsustained ventricular tachycardia. In this setting and combined with the fact that he had been on GDMT, he received a dual-chamber cardiac defibrillator system (ICD). Ultimately, we opted for implantation of a dual-chamber cardiac defibrillator system in the setting of sinus node dysfunction, as he benefited from atrial pacing capability to allow better titration of his carvedilol. Repeat EKG post ICD implantation revealed an atrial-paced rhythm (Figure ). Given his diagnosis of non-compaction and deep trabeculations he was continued on therapeutic anticoagulation. However, there was mild hypotension limiting the intensification of GDMT. He was discharged on torsemide, carvedilol, apixaban, low-dose Entresto and spironolactone in a stable condition.
At two months post dual-chamber cardiac defibrillator system placement and GDMT, the patient was asymptomatic and euvolemic with adequate perfusion. However, there was persistent hypotension limiting the use of afterload reducing agents and this will be followed closely in the outpatient setting. On discharge, we recommended that his first-degree relatives, his children, be screened. Additionally, his outpatient cardiologist will arrange for potential genetic testing of the patient.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [158.8, 'kg']}",198.8,188.86,208.74,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 158.8 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (158.8 kg - 20 kg) = 198.8 mL/hr.
Hence, the patient's fluid maintenance is 198.8 mL/hr."
4796,22,Maintenance Fluids Calculations,physical,decimal,pmc-3253671-1,Extracted,20 year old female (upon admission). Diagnosed of Graves' disease the previous year but presented allergic urticaria to both propylthiouracil and methimazole. Thyroid function was controlled with potassium iodide until surgery. She had a history of anorexia bulimia and was hospitalized for cognitive behavioral therapy at age 18. Her eating behavior was stable as well as her thyroid function at the time of surgery at age 20. There is no record of the use of SSRIs in the treatment of anorexia nervosa. Her height was 154.2 cm and body weight was 53 kg (BMI 22.3) at the time of surgery. Post operatively she was placed on 50 mcg of levothyroxine daily which maintained her thyroid function within normal levels. There was no relapse of her anorexia bulimia and her body weight was maintained over the next five years.,"Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [53.0, 'kg']}",93,88.35,97.65,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 53.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (53.0 kg - 20 kg) = 93.0 mL/hr.
Hence, the patient's fluid maintenance is 93.0 mL/hr."
4797,22,Maintenance Fluids Calculations,physical,decimal,pmc-8251549-1,Extracted,"Patient 1 was a 6-year-old female who was the first child of healthy and nonconsanguineous Japanese parents. She was born after an uncomplicated pregnancy at 35 weeks and 4 days of gestation. Her weight at birth was 2142 g (−0.5 SD), length was 43 cm (−1.2 SD), and head circumstance was 33 cm (+0.8 SD). After birth, she showed tachycardia. Head ultrasound showed ventricular enlargement and intraventricular hemorrhage. She had been in neonatal intensive care unit since 34-day-old. After discharge, she attended her hospital regularly due to cerebral palsy and global developmental delay. At 2 years of age, she underwent an operation for exotropia. She had congenital hearing loss and wore hearing aids at 5 years of age. Head magnetic resonance imaging (MRI) at 5 years of age showed thin corpus callosum, cyst of septi pellucidi, ventricular wall irregularity, and periventricular leukomalacia (Figure ). She showed distinctive dysmorphic features with high hairline, small eyes, anteverted nares, a depressed nasal bridge, a broad columella, a thin upper-lip, and high-arched palate (Figure ). Her developmental milestones were delayed. She started to walk at the age of 3 years. She also stated to speak her words at the age of 3 years and spoke only few words at the age of 6 years. Her developmental quotient as assessed using the WISC-IV test was 23. Her physical growth was also delayed. At 6 years of age, her weight was 15.9 kg (−1.3 SD), height was 102.4 cm (−2.4 SD), and head circumference was 54.5 cm (+2.4 SD). She had no urogenital anomalies.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15.9, 'kg']}",51.8,49.21,54.39,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15.9 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.9 kg - 10 kg) = 51.8 mL/hr.
Hence, the patient's fluid maintenance is 51.8 mL/hr."
4798,22,Maintenance Fluids Calculations,physical,decimal,pmc-3932357-1,Extracted,"A 64-year-old man presented with a four-year history of globus sensation. He was referred for intractable symptoms despite having taken reflux medication for two months. Despite continued medication, his symptoms developed to dysphagia, even when swallowing liquid. He denied hoarseness or dyspnea. His medical history included a transurethral resection for bladder cancer 3 years previously. He had experienced weight loss of 3 kg over the previous 2 months. On his first presentation, flexible fiberoptic laryngoscopy showed pooling saliva, but no mass-like lesion in the hypopharynx. Vocal fold mobility was intact. The patient underwent a double-contrast pharyngoesophagogram due to persistent symptoms. An ovoid submucosal mass with a smooth contour in the left pyriform sinus was revealed (). Subsequently, computed tomography (CT) scans showed a 3×4 cm mass with central low attenuation in the left hypopharynx (). With the patient under general anesthesia, the lesion was removed via direct laryngoscopy using a microdissection electrode for endoscopic electrosurgery. The mass originated from the lateral wall of the pyriform sinus. It appeared as a pedunculated mass with a smooth, well-encapsulated surface. It was removed by means of submucosal dissection with the microelectrode. The resected specimen consisted of a 2×3×4 cm cystic mass with proteinaceous fluid (). Histologic examination showed a true epithelial-lined cyst consisting of cuboidal epithelium (). The final diagnosis, made by a pathologist, was a ductal cyst of the hypopharynx. Postoperative recovery of the patient was uneventful. The patient was free of symptoms after one month. Five years of follow-up showed no tumor recurrence and normal swallowing.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.0, 'kg']}",12,11.4,12.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.0 kg. Hence, the patient's maintenance fluid is 3.0 kg * 4 mL/kg/hr = 12.0 mL/hr.
Hence, the patient's fluid maintenance is 12.0 mL/hr."
4799,22,Maintenance Fluids Calculations,physical,decimal,pmc-6506424-1,Extracted,"The first patient was a 16-year-old female (height: 1.58 m, weight: 41.7 kg) with a recent diagnosis of CD, who two days prior had received her first infusion of infliximab. She was admitted to the gastroenterology service for severe abdominal pain which began that morning. The patient was unable to tolerate anything by mouth due to severe nausea. At that time, the grayscale US demonstrated a narrowing of the terminal ileum, with a thickened submucosal layer and decreased peristalsis. Contrast US showed avid contrast enhancement of the narrowed terminal ileum. Quantitative evaluation of the terminal ileum, compared to the jejunum as an internal control, demonstrated more prompt wash-in, higher peak intensity, and higher area under the curve. The kinetic perfusion parameters are reported in . Average elastography value of the terminal ileum was 0.64 m/s. MRE demonstrated wall thickening and inflammation in the terminal ileum, resulting in narrowing and proximal dilation in the distal ileal segments. Adjacent to the terminal ileum, there was mesenteric inflammation as evidenced by contrast enhancement (). Given the patient's MRE findings and her clinical improvement with a second infusion of infliximab, her flair was determined to be acute inflammation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [41.7, 'kg']}",81.7,77.615,85.785,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 41.7 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (41.7 kg - 20 kg) = 81.7 mL/hr.
Hence, the patient's fluid maintenance is 81.7 mL/hr."
4800,22,Maintenance Fluids Calculations,physical,decimal,pmc-6043999-1,Extracted,"A 12-year-old boy (height: 51 in.; weight; 44 lbs. 1.5 oz. [20.0 kg]; BMI: 11.93 kg/m2) with a history of Lesch-Nyhan syndrome presented to our office with a 1 ½ month history of dysuria, hematuria, and pain secondary to nephrolithiasis. He suffered from a non-verbal learning disorder associated with a developmental delay, was wheelchair-dependent, and had undergone extraction of 10 teeth due to biting and grinding his teeth. Due to his self-mutilating behavior, he wore braces on his arms and had surgery of his left thumb as a result of biting himself. Two years prior to presentation, the patient underwent a cystoscopy with bilateral ureteroscopy due to xanthine stones. He was stone free following the procedure. The patient’s mother denied a family history of kidney stones, thromboembolism and gout. At the age of 18 months, the boy underwent a test for organic acids in his urine which revealed highly elevated hypoxanthine without an elevation of xanthine and with a slight elevation of uracil. He was diagnosed clinically with Lesch-Nyhan syndrome at that time based on a triad of uric acid overproduction, neurologic dysfunction, and cognitive and behavioral disturbances.
Uric acid crystals were noted intermittently in the patient’s diaper which had increased significantly in the preceding days. He had been treated with the medication allopurinol since he was 2 years old. At the time of presentation, the dose of allopurinol was 200 mg administered once per day. He had never experienced gout. The patient was prescribed potassium citrate.
A renal ultrasound demonstrated multiple calculi in both kidneys with the largest measuring 1.8 cm in the right kidney as well as echogenic material in the medullary pyramids bilaterally suggesting nephrocalcinosis (Fig. ). There were no masses, hydronephrosis, or hydroureter. A urinalysis revealed the following: specific gravity = 1.010; pH = 7.0; leukocyte esterase = 500; trace microscopic hematuria; and negative nitrite. The urine culture was negative. The uric acid level in blood was 2.9 mg/dL (Normal range: 2.5–8.5 mg/dL). Uric acid levels in blood collected in the previous 2 years were all in the normal range, specifically, 5.0 mg/dL, 2.6 mg/dL, and 3.2 mg/dL. There was no evidence of renal failure. The patient underwent six separate urinalyses between the ages of 9 and 12, all of which demonstrated a pH of either 6 or 7.
A CT scan of the abdomen and pelvis demonstrated staghorn calculi in both kidneys, involving all calyces.
The patient underwent a right percutaneous nephrolithotomy (PCNL) 2 months after presentation. During the hospital stay, the patient was noted to be anemic and received 5 days of epogen and iron supplementation. He developed a thrombus in the right cephalic vein and was diagnosed with heterozygous Factor V Leiden with elevated homocysteine (16.2 umol/L [Normal range: 6.6–14.8 umol/L]). The methylene tetrahydrofolate reductase (MTHFR) and prothrombin genes were negative. Folic acid was initiated. The Factor V Leiden mutation was detected through a polymerase chain reaction (PCR) test that utilized microarray-based oligonucleotide hybridization and signal amplification to detect the Factor V Leiden mutation.
Seven weeks later, the patient began experiencing aspiration of liquids, gastroesophageal reflux, and markedly delayed gastric emptying, necessitating a laparoscopic Nissen fundoplication with gastrostomy tube and open pyloroplasty. The patient continued to suffer from nephrolithiasis, with visualization of a left renal calculus greater than 2 cm. A CT scan demonstrated staghorn calculi in the left kidney (Fig. ). He underwent a left PCNL and left nephrostomy tube exchange 6 months after the right-sided procedure. A nephrogram revealed evidence of a filling defect in the lower pole calyx which may represent organizing blood clot or residual stone. Renal ultrasounds performed 6 and 9 months later demonstrated extensive bilateral nephrocalcinosis without hydronephrosis or hydroureter. There was no evidence of calculi in the collecting systems.
The calculi that were removed during the ureteroscopies, the ones that the patient had passed while seen as an outpatient, and those that were sent for analysis following the PCNL were all consistent with xanthine calculi.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [20.0, 'kg']}",60,57,63,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 20.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (20.0 kg - 10 kg) = 60.0 mL/hr.
Hence, the patient's fluid maintenance is 60.0 mL/hr."
4801,22,Maintenance Fluids Calculations,physical,decimal,pmc-8637043-2,Extracted,"A 48-years-old, 140 kg, 164 cm, BMI 52.1 kg/m2, ASA III female. She was hospitalized for symptomatic angina. Owing to a gigantic appetite mainly on rice and pasta, her weight gradually increased in the past 20 years. Both her parents and sibling 3 were over obese. She had a history of hypertension (Bisoprolol 5 mg, Amlodipine 10 mg, and Olmesartan 40 mg), OSA, Diabetes, fatty liver and umbilical hernia, aortic stenosis and hypercholesterolemia. Preoperative airway assessment included a Mallampati class III, a 7.0 cm thyromental distance, a 5 cm interincisor distance and a 41 cm neck circumference. Physical examination showed nutritional obesity and mild cyanosis of the lips. Hematologic tests shows: WBC 10.93 × 109 /L, NEU% 0.798, CRP 11.7 mg/mL. CT showed fatty liver, umbilical hernia and dilatation of surrounding intestine. Admission diagnosis: Morbid obesity, Umbilical hernia, Hypertension, Fatty liver.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [140.0, 'kg']}",180,171,189,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 140.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (140.0 kg - 20 kg) = 180.0 mL/hr.
Hence, the patient's fluid maintenance is 180.0 mL/hr."
4802,22,Maintenance Fluids Calculations,physical,decimal,pmc-7576439-1,Extracted,"A 49 years old gentleman confirmed to have Covid-19 by RT-PCR five days ago, was brought in via ambulance to the emergency department from quarantine with worsening cough, shortness of breath and a high-grade fever. He was a never smoker and a driver by profession. His past medical history was unremarkable. On examination, he was tachypnoeic with a respiratory rate of 22 breaths/min, febrile at 39.1 °C, normotensive at 115/65 mmHg and hypoxic with oxygen saturations of 85% on room air. General physical examination was unremarkable, his height was 161 cm with a weight of 66 kg and body mass index (BMI) of 25.5. Chest examination revealed bilateral basal crepitations with the chest radiograph showing bilateral lower zone infiltrates consistent with a diagnosis of Covid-19 pneumonia. Notable lab investigations included a white blood cell count (WBC) of 10.2 × 103/μL with a lymphocyte count of 0.8 × 103/μL, D-dimer of 1.47 mg/L (peak 2.96), CRP of 133 mg/L, peak Lactate Dehydrogenase (LDH) of 436 U/L and a ferritin of 8352 mcg/L. He required 10 L of oxygen to maintain oxygen saturation of 95% and was treated initially as per the local guidelines for Covid-19 and later received IV tocilizumab, convalescent plasma and IV methylprednisolone in view of risk of rapid deterioration. He gradually improved and was weaned off of oxygen over a period of 12 days without needing mechanical ventilation. A day later he complained of right sided chest pain and increasing shortness of breath requiring 5 L of oxygen to maintain saturations of 95%. Chest x-ray identified a large right sided pneumothorax with mediastinal shift towards the left. () A right sided intercoastal chest drain was inserted. After another 5 days he complained of left sided chest pain and a chest radiograph this time confirmed a large left sided pneumothorax (). Subsequently a left sided intercostal chest tube was inserted. A CT chest was performed which showed bilateral pneumatoceles/bullous disease with a pneumatocele/bullae in right and left lower lobes respectively (). Further investigation revealed a normal serum Alpha −1 antitrypsin level. The right lung gradually expanded and the drain was removed after a period of two weeks while the left sided chest tube remained in situ for 16 days due to a persistent air leak until lung expansion whilst awaiting surgical intervention.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [66.0, 'kg']}",106,100.7,111.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 66.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (66.0 kg - 20 kg) = 106.0 mL/hr.
Hence, the patient's fluid maintenance is 106.0 mL/hr."
4803,22,Maintenance Fluids Calculations,physical,decimal,pmc-3101761-1,Extracted,"An 11-month-old male child was brought to the plastic surgery OPD of our institute by his parents with the chief complaints of increase in size of a swelling over upper lip with difficulty in oral intake for the last 1 week. On eliciting the history, it was revealed that the lesion was present since birth and had been gradually enlarging. The size of the lesion was measured to be 5.5×3.5×1.5 cm and was diagnosed as a case of hemangioma upper lip [Figures and ]. Previously, the patient did not have much difficulty in feeding but the difficulty rose since 1 week as the lesion had suddenly enlarged. He was being fed by the spoon from the angle of the mouth. Considering the age of the child, size of the lesion and most importantly the site of the hemangioma, it was planned to ablate and strangulate the vessels during the first stage so as to decrease the size of lesion before proceeding for surgical excision. Preanesthetic assessment revealed a very narrow mouth opening with difficulty in assessing the mallampatti grading [Figures and ]. All the investigations were within normal limits including the coagulogarm and weight of the child was found to be 8 kg.
General anesthesia was planned for the child with main stress upon airway management. The child was kept in a fasting state for 6 hours and was administered 2 mg of syrup midazolam 30 minutes before the surgical procedure. Airway trolley was made ready with all the pediatric airway equipment including the fibreoptic bronchoscope of 2.4 mm diameter. The child was taken to the operation theatre by one female staff who had been with him for the last half-an-hour and had developed a good rapport with the child. Pulse oximetry probe was attached to the great toe of right foot and a pediatric stethoscope was fixed on the precordium. Induction of anesthesia was achieved with sevoflurane in 6 L of oxygen administered through number 3 face mask attached to Jackson Rees circuit while covering the eyes with soft cotton pad to prevent injury to the eyes. A good intravenous access was secured with 22 G venflow and after establishing a good breathing pattern evident from the bag movements we administered 15 mg of ketamine. When we were sure that we can easily ventilate the patient, we administered 20 mg of succinylcholine while sevoflurane was kept at 2.5% during this stage. Gentle positive pressure ventilation was carried out for 1 minute. Laryngoscopy was done with miller blade size 2 from the left corner of the mouth and tongue was lifted in a diagonal manner and we were able to see the full view of glottis. During the whole exercise of laryngoscopy the fulcrum on the upper teeth was never made rather a forward and upward pressure was maintained without even touching the mass. An oral RAE endotracheal tube number 4.5 mm (internal diameter) was inserted from the right corner of the mouths while an assistant helped continuously in raising the mass with a soft cotton pad with gentle force so as to enable laryngoscopy and a good intraoral view. After checking the equal air entry bilaterally, we packed the oral cavity with a roll gauge to prevent any aspiration of secretions or possibly blood as the tube was without a protective cuff. The child was then paralyzed with 3 mg of injection atracurium and positive pressure ventilation was carried out throughout the procedure with Jackson Rees circuit with nitrous oxide and oxygen in the ratio of 60:40. Right from the beginning a team of plastic surgeon, a general surgeon and an otorhinolaryngeologist were scrubbed and ready with their equipment. Surgical procedure was initiated and peripheral surgical ablation of the feeding vessels was done with electric cauterization. Thereafter the intralesional injection of steroid was administered. The surgical procedure lasted for 15 minutes and at the end of surgery the child was reversed with 0.5 mg of injection neostigmine and 0.1 mg of glycopyrrolate. The dry intraoral roll gauge pack was removed and the child was extubated in a fully awake state after establishment of adequate and rhythmic respiratory efforts with good tidal volume and flexion of legs at the hip joint. He was given rectal suppository of 150 mg paracetamol for postoperative pain relief after induction of anesthesia. The child was kept in the recovery ward for 2 hours and later on shifted to the pediatric wing of the plastic surgery ward where he was kept for another 1 day and was discharged after an uneventful recovery period during the hospital stay. The parents were instructed for follow-up of the child after 15 days.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [8.0, 'kg']}",32,30.4,33.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 8.0 kg. Hence, the patient's maintenance fluid is 8.0 kg * 4 mL/kg/hr = 32.0 mL/hr.
Hence, the patient's fluid maintenance is 32.0 mL/hr."
4804,22,Maintenance Fluids Calculations,physical,decimal,pmc-4172948-1,Extracted,"The patient, a 26-year-old woman with a diagnosis of hypopituitarism, hypothyroidism and binocular blindness in the course of septo-ocular dysplasia was admitted to the Clinic of Urology because of a large tumor of the left kidney. The patient was 139 cm tall, weighed 52 kg and her BMI amounted to 27 kg/m2. Her blood pressure was 120/70 mmHg, heart rate 70/minute, creatinine levels 66 μmol/l, and her electrolytes, blood count and urinalysis were normal. The lesion had been diagnosed incidentally in another medical centre during investigation of persistent stomach ache with a suspicion of pyelonephritis. During case examination a perceptible mobile pathological resistance was reported on the left side of the stomach from the costal arch up to the iliac fossa. On abdominal ultrasonography (USG) examination, a large, intra-abdominal and left flank heterogeneous tumor with dimensions 170 × 78 mm, mostly hyperechogenic (consisting probably of adipose tissue with little vascularization observed in Doppler color) and probably coming out of the left kidney, was reported. The right kidney was 108 mm long, with no urinary retention and no deposits. The diagnostics were extended by computer tomography (CT) angiography of the abdomen with contrast, in which the following was stated: numerous AMLs in the left kidney, the biggest coming out from its lower part and affecting the whole paranephric space and going down to the level of iliac fossa with dimensions of about 226 × 95 × 104 mm. Except for this the other intra-abdominal organs revealed no abnormalities (Figures , ). The patient qualified for surgical treatment. The whole kidney with the entire tumor was removed (Figure and Figure ) by performing a median transperitoneal incision. Due to the risk of serious bleeding, the priority was to reach the renal vessels. The procedure was performed without any complications with the loss of 100 ml of blood. Further recovery proceeded without any complications. Histopathological examination confirmed the diagnosis of AML.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [52.0, 'kg']}",92,87.4,96.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 52.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (52.0 kg - 20 kg) = 92.0 mL/hr.
Hence, the patient's fluid maintenance is 92.0 mL/hr."
4805,22,Maintenance Fluids Calculations,physical,decimal,pmc-6078880-1,Extracted,"A 65-year-old male patient (height: 165.2 cm; body weight: 55 kg) visited the general surgery outpatient clinic for presumptive cholangiocarcinoma. He was previously healthy with an unremarkable medical history. The patient underwent a series of preoperative evaluations. Laboratory values including complete blood cell counts (CBCs) and chemistry were within normal limits except C-reactive protein (CRP), which was elevated at 2.19 mg/dl (normal range: 0–0.3 mg/dl). Total bilirubin was 0.6 mg/dl (normal range: 0.2–1.5 mg/dl), direct bilirubin 0.3 mg/dl (normal range: 0–0.5 mg/dl), and the patient’s Model for End-Stage Liver Disease (MELD) score was 6 []. Vital signs were within normal limits including axillary body temperature (36.7°C). Preoperative chest radiography and transthoracic echocardiography showed no abnormal findings. The imaging studies indicated a 5.1-cm-sized tumor involving both the right and left intrahepatic bile duct and common bile duct and a 2.6-cm-sized enlarged lymph node around the common hepatic artery, suggesting probable metastasis (). Owing to bilateral invasion of the bile duct, the tumor was unresectable. Therefore, the general surgery team planned to perform LDLT unless the patient had lymphovascular metastasis. The surgical plan was to begin the donor hepatectomy after confirming no metastasis via intraoperative frozen biopsy.
To the recipient, anesthesia was induced with intravenous thiopental sodium 350 mg, atracurium 30 mg, and sevoflurane. After endotracheal intubation, sevoflurane was used for anesthetic maintenance. Bispectral index (BISⓇ, Medtronic, USA) was monitored, with a target intraoperative maintenance value of 40–60. The right radial artery, right femoral artery, and right femoral vein were cannulated. To prevent intraoperative hypothermia, a warming blanket (Blanketrol IIⓇ, CSZ medical, USA) was applied. The ambient and warming blanket temperatures were set at 25 and 40°C, respectively, and a fluid warming system (Level 1Ⓡ H-1200 Fast Flow Fluid Warmer, Smiths Medical, USA) was also prepared. The patient’s body temperature was monitored on his forehead with an infrared thermometer (FS-100Ⓡ, HuBDIC, Korea) at 10-min intervals. The body temperature was initially 36.7°C and showed little variation until the operation began. After the surgeon placed the retractor, the inhalant anesthetic was changed from sevoflurane to isoflurane and anesthesia was maintained with continuous infusion of remifentanil (0.03–0.1 μg/kg/min) and atracurium (7 μg/kg/min) [4–6]. Concentrations of the inhalant anesthetics were changed depending on the patient’s hemodynamics and BIS. The sevoflurane gas was completely eliminated before reperfusion; thus, the graft was not affected. A lymph node adjacent to the common hepatic artery and a segment of the common bile duct were excised for frozen biopsy, and at this time, the surgeon clamped the common bile duct as a portion of it was resected (, 09:20 am). Fortunately, both specimens were negative for cancer cells, and the LDLT was continued.
After induction of the donor, a nasogastric tube was placed and a 9 Fr AVA (Advanced Venous AccessⓇ, Edward Lifesciences, USA) catheter was inserted into the right internal jugular vein of the recipient. A pulmonary artery catheter (Swan-Ganz CCOmbo VⓇ, Edward Lifesciences, USA) was inserted to monitor pulmonary artery pressure, continuous cardiac output, and mixed venous oxygen saturation. During insertion of the AVA and pulmonary artery catheter, because of the aseptic procedure, the recipient’s body temperature was not measured on the forehead for half an hour, and the last recorded skin temperature was 36.9°C (, 10:30 am). Subsequently, measurement of CBT with the pulmonary artery catheter was begun, and the initial CBT was 37.6°C (, 11:00 am). The fluid warming system was turned off immediately, and the warming blanket was set to cooling mode (25°C) while the room temperature was adjusted to the lowest possible setting (22°C).
Donor hepatectomy was initially scheduled with a laparoscopic approach. However, mobilization of the liver was difficult, and massive bleeding occurred from the inferior vena cava. Therefore, the laparoscopic surgery was converted to open hepatectomy. As a result, more time than usual was required to harvest the graft. During donor hepatectomy, the recipient’s CBT continuously rose to 39.5°C despite our efforts. Vital signs and monitoring parameters including end-tidal carbon dioxide (ETCO2) were within normal range with the exception of mild reactive tachycardia (100–110 beats/min). No blood products or medicine except anesthetics were administered. We considered the possibility of malignant hyperthermia, but there were no signs of this condition other than hyperthermia and tachycardia. ETCO2 was within the normal range (35–38 mmHg), and arterial blood gas analysis showed no acidosis, hypoxemia, or hyperkalemia. Allergic reactions could be ruled out owing to the absence of skin rash. We considered device error, but the patient’s skin was actually hot to the touch. In addition, his preoperative CBCs, vital signs, and chest radiographs did not show any evidence of infection, and thyroid function tests were also normal. Adequate depth of anesthesia appeared to be achieved, as BIS was monitored. We discussed the hyperthermia with the operating surgeon, and he suggested that clamping of the common bile duct could be the reason for this unexplained hyperthermia. The surgeon drained the congested bile and CBT rapidly declined (, 14:30 pm). Total duration of the clamping of the bile duct was about 5 h (09:20 am–14:30 pm). Intraoperative bile duct clamping during an unexpectedly prolonged donor hepatectomy resulted in biliary congestion.
The anhepatic phase began 2.5 h after declamping of the common bile duct, at which time the recipient’s CBT was 37.5°C (, 17:00 pm). CBT decreased further to 36.9°C within the first hour of the anhepatic phase. We turned on the warming blanket (40°C) and fluid warming system and set the room temperature at 25°C again. CBT was maintained at 36.7–37.3°C during the remainder of LDLT. The anesthesia time was 14 h, and the patient received about 8,300 ml of crystalloid, 500 ml of colloid solution, 1,450 ml of 5% albumin, and 248 ml of cell saver blood, and urine output was 2,165 ml. No other blood products were transfused during the operation.
The patient was transferred to the intensive care unit, at which time body temperature at the tympanic membrane was 37.6°C. Laboratory exams performed immediately revealed that WBC count was slightly increased compared to preoperative results (9.34 × 103/μl → 11.59 × 103/μl), in contrast to CRP (2.19 mg/dl → 2.12 mg/dl). Total and direct bilirubin were also slightly increased though they were still within the normal range (0.6 mg/dl → 1.3 mg/dl, 0.3 mg/dl → 0.9 mg/dl, respectively). Postoperative chest radiographs did not show remarkable interval change since the preoperative studies. All cultures, including blood, fluid from Jackson-Pratt drains, urine, stool, throat swab, and catheter tips, showed no growth of bacteria or fungus. The patient was transferred to the general ward on the fifth postoperative day with no complications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [55.0, 'kg']}",95,90.25,99.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 55.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (55.0 kg - 20 kg) = 95.0 mL/hr.
Hence, the patient's fluid maintenance is 95.0 mL/hr."
4806,22,Maintenance Fluids Calculations,physical,decimal,pmc-7233890-1,Extracted,"A 7-year-old boy of Han ethnicity, weighing 23.5 kg, was admitted to hospital with recurrent episodes of joint swelling and severe pain for 1 year. He had two surgeries in the prior year for suppurative knee arthritis. There was no obvious trauma before the onset of each episode, and no pyoderma, acne, suppurative hidradenitis, systemic infection, or fever during the course of the disease. Physical examination showed that the right knee joint of the child was more swollen than the left, with higher skin temperature and tenderness, but no obvious sense of fluctuation upon palpation. His right knee movement was restricted with flexion less than 40° and stretching up to 0°. Internal and external rotation of the right knee joint was also slightly limited and the floating patella test was negative. No abnormalities were found in the other limb joints.
At the time of admission, the total number of white blood cells (11.08 × 109/L) in the peripheral blood was high, mainly comprising neutrophils (7.89 × 109/L, 71.2%). The erythrocyte sedimentation rate (ESR) was elevated (73 mm/h). Liver and kidney function showed no obvious abnormality. C-reactive protein (CRP, 123 mg/L), procalcitonin (PCT, 0.10 ng/mL), and interleukin-6 (IL-6, 73.25 pg/mL) were all increased. The levels of interleukin-1β (IL-1β, <5.0 pg/mL), interleukin-8 (IL-8, 15.6 pg/mL), and interleukin-10 (IL-10, <5.0 pg/mL) were normal. Rheumatoid factor (RF) antibody levels (IgG 26.08 AU/mL, IgA 4.12 AU/mL, and IgM 2.41 IU/mL) were within the normal range, too. Autoimmune antibodies such as anti-keratin antibodies (AKA), antinuclear antibodies (ANA), anti-double-stranded DNA (anti-dsDNA) antibodies, anti-Smith antibodies, and anti-neutrophil cytoplasmic antibodies (ANCA, including p-ANCA, c-ANCA, myeloperoxidase, and proteinase-3) were all negative, as was human leucocyte antigen (HLA-B27). Articular cavity effusion was thick and turbid with a high number of nucleated cells (3+/HPF) and pus cells (1+/HPF), 98% of which were multi-nucleated cells. No bacterial growth was observed in either culture of articular cavity effusion (microbiology cultures were saved for 28 days). The patient’s blood coagulation function and viral screening (human immunodeficiency virus (HIV), syphilis, and hepatitis) were normal.
The boy underwent arthroscopic knee debridement and peri-knee abscess resection. He was treated with vancomycin and rifampicin after each operation, but his arthritis continued to intermittently attack. Upon further inquiry, we found that the patient’s 5-year-old brother had the same history of arthritis in his right elbow and left ankle. The boy’s grandfather also had a history of recurrent pyoderma. We recommended that the whole family undergo genetic testing, which revealed that the patient, his brother, and his father were all heterozygous for the PSTPIP1 gene mutation, which was found in the exon region (c.36+68 G>A, c.137+47 G>C, and c.562+114C>G het). These three mutated sites have not been reported in the previous literature, among which the first and second mutated sites were highly expressed in the sequencing of 1000 normal subjects, while the third mutated site was not reported in the normal genome database, so it may be a possible deleterious mutated site. Although the father was a carrier, he never showed signs of the syndrome. The grandfather declined genetic testing. After the diagnosis of PAPA was made, the boy was treated with naproxen (0.2 g per time, four times a day), high-dose prednisone (1–2 mg/kg/day), and methotrexate (10 mg/m2/week). However, due to poor efficacy of the medication combination and elevation of IL-6, we switched to intravenous infusion of tocilizumab once every 4 weeks at a dose of 8 mg/kg. The boy had received four treatments with tocilizumab and did not develop suppurative arthritis for the duration of treatment. The CRP (27.40 mg/L), PCT (0.04 ng/mL), and IL-6 (23.88 pg/mL) levels were restored or nearly normal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [23.5, 'kg']}",63.5,60.325,66.675,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 23.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (23.5 kg - 20 kg) = 63.5 mL/hr.
Hence, the patient's fluid maintenance is 63.5 mL/hr."
4807,22,Maintenance Fluids Calculations,physical,decimal,pmc-6946536-1,Extracted,"A 36-year-old pregnant woman with a history of paranoid schizophrenia for more than 10 years and syphilis for 2 years presented at 38+ weeks gestational age having drank 1 mouthful (about 20 ml) of paraquat solution 10 hours earlier in an apparent suicide attempt. Before admission to our hospital, the patient was taken to the local hospital for gastric lavage. On admission, the patient had a burning sensation in the throat accompanied by nausea and vomiting with blood but had no chest distress, dyspnea or palpitations, abdominal pain, or vaginal bleeding. However, 4 hours after admission, chest tightness, shortness of breath, and dyspnea were observed.
On initial evaluation, her body weight was 55 kg and vital signs were as follows: temperature 37.1°C, heart rate (HR) 115 beats/minute, respiration (RR) 25 per minute, blood pressure 132/70 mm Hg, and oxygen saturation 98% on room air. Physical examination showed that she was clear minded but had several visible ulcers on the tongue and oral mucosa. Moreover, her heart and lungs were normal and there was no jaundice of the skin or sclera. An abdominal examination showed absence of tenderness and a third trimester pregnancy, with the uterine height being consistent with the estimated gestational age. Babinski sign showed negative results.
Paraquat level in blood determined by high performance liquid chromatography (HPLC) at the 10th hour of poisoning was 0.547 μg/ml and the urine dithionate test showed light blue color (Fig. ). Initial laboratory tests revealed the following: white blood count 19,290 cells/μl (84% neutrophils), hemoglobin 9.3 g/dl, and platelets 231,000/ml. Serum chemistry showed high creatinine 138 μmol/L (normal: 46–106 μmmol/L), uric acid (UA) 456 μmmol/L (normal: 149–446 μmmol/L), aspartate transaminase (AST) 46 μ/L (normal 14–36 u/L), creatine kinase (CK) 399 μ/L (normal: 30–135 μ/L), creatinine kinase MB isoenzyme (CK-MB) 14.5 ng/ml (normal: 0.3–4 ng/ml), lactate dehydrogenase (LDH) 634 u/L (normal: 313–618 μ/L), amylase 221 mmol/L (normal: 30–110 mmol/L). However, total bilirubin (TBIL) level was within the normal range. Arterial blood gas analysis on room air revealed the following: partial pressure of oxygen (PO2) 125 mm Hg, partial pressure of carbon dioxide (PCO2) 20 mm Hg, Lactic acid 1.6 mmol/L, buffer excess (BE) −11.2 mmol/L, bicarbonate (HCO3−) 12.1 mmol/L. However, after 6 hours, creatinine, AST, and TBIL had risen to 192 μmmol/L, 68 μ/L, and 36 μmol/L, respectively, which suggested a deterioration in liver and kidney function.
Without prior antenatal examination, the patient received a prenatal ultrasound which showed an intrauterine singleton pregnancy in breech presentation with a bi-parietal diameter (BPD) of 91 mm and femur length (FL) of 61 mm. Worse still, the placenta was located in the front wall of the uterus with its lower margin covering the cervix, grade I+ (Fig. ). In addition, low echoes in the parenchyma of placenta had also been explored. The fetal heart sounds were audible with a rate of approximately 142 beats/minute and the amniotic fluid was 6.4 cm but had poor internal sound.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [55.0, 'kg']}",95,90.25,99.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 55.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (55.0 kg - 20 kg) = 95.0 mL/hr.
Hence, the patient's fluid maintenance is 95.0 mL/hr."
4808,22,Maintenance Fluids Calculations,physical,decimal,pmc-6908478-1,Extracted,"We report an 11-year-old male patient who was hospitalized on January 23rd, 2019 and found to have elevated serum calcium for 4 months. Two years ago (December 2016), due to proteinuria, hypocomplementemia, anti-nuclear antibody, and positive anti-dsDNA, he was diagnosed as SLE and LN. The treatment of high dose methylprednisolone plus high dose cyclophosphamide and plasma exchange did not improve his condition. Urinary protein continued to be 4+~5+. Then mycophenolate mofetil (MMF) plus tacrolimus (FK 506) were used to treat. Glucocorticoid was gradually decreased during this period. MMF (0.375 g q12h, concentration of MMF is 53.741 ug/ml), FK 506 (1.5 mg qm and 1.0 mg qn, concentration of FK506 is 4.8 ug/L), and prednisone (10 mg qd) were being taken to treat LN. He had no history of taking excessive calcium and vitamin D preparations. There was no clinical manifestation of hypercalcemia at admission. At admission, SLE was in remission, urinary protein was negative, and SLEDAI score was 2 points (positive for anti-dsDNA). Physical examination: height 144 cm, weight 47.5 kg, body surface area 1.33 m2, no edema, superficial lymph node swelling, cardiopulmonary abdominal examination no abnormalities.
Laboratory examination at admission: hypercalcemia (2.88–3.09 mmol/L, normal range 2.1–2.6), low blood phosphorus (1.16 mmol/L, normal range 1.29–1.94), high iPTH (110.4 pg/mL, normal range 12–88), 25-hydroxyvitamin D deficiency (11 ng/mL, normal range > 25), normal alkaline phosphatase (224 U/L, normal range 0–110), magnesium (0.64 mmol/L, normal range 0.7–1.0), Leukocyte count was 11.54 × 109/L (normal range 4.0-10.0), hemoglobin was 14.6 g/dL (normal range 12.0–15.0), and platelet count was 444 × 109/L (normal range 100–300); blood Urea Nitrogen (BUN) was 6.1 mmol/L (normal, 2.9–8.6), creatinine (CR) was 80 umol/L (normal, 53–115), creatinine clearance rate (CCR) 129.04 ml/min.1.73 m2. Thyroid function is normal. The level of anti-dsDNA was 14.01 IU/mL (normal range 0–12), and the anti-nuclear antibody was normal. Blood complement C3 and C4 were normal. Renal biopsy: immunocomplex nephritis, lupus nephritis, segmental mesangial proliferation, mild activity, LN III(A/C).
Erythrocyte sedimentation rate was normal. Urinary protein was negative. Twenty four hours urinary calcium was 4.07 mmol (normal range 2.5–7.5). His electrocardiogram was normal. Chest X-ray showed no abnormality in cardiopulmonary septum. CT scan of parathyroid imaging showed that SPECT/CT imaging was performed 15 and 120 min after intravenous injection of 99mTc-MIBI; 15 min showed that the left lobe of thyroid was irregular in shape; Radioactive aggregation could be seen at the lower pole of left lobe, and the right lobe of thyroid was normal; 120 min showed that the bilateral thyroid became pale obviously, and radioactivity could still be seen at the lower pole of the original left lobe. CT tomography and fusion images showed uniform low-density abnormal shadow of about 8 mm *7 mm in size below the left thyroid lobe, about the level of the first thoracic vertebra, with relatively uniform internal density, no obvious calcification, CT value of about 34 HU, slight abnormal 99mTc-MIBI concentration in the corresponding part of the fusion image; parathyroid imaging (posterior lower left lobe) Yang Sex. SPECT/CT indicated hyperplasia of the parathyroid gland. Ultrasound showed hyperplasia of the parathyroid gland. Hypercalcemia caused by malignant tumors has been excluded during hospitalization.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [47.5, 'kg']}",87.5,83.125,91.875,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 47.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (47.5 kg - 20 kg) = 87.5 mL/hr.
Hence, the patient's fluid maintenance is 87.5 mL/hr."
4809,22,Maintenance Fluids Calculations,physical,decimal,pmc-4660009-1,Extracted,"An 18-year-old previously healthy woman presented at our institution after a four-year history of hyporexia, polydipsia, weight loss, growth retardation, and poor academic performance. One month prior to presentation, outpatient laboratory analysis revealed increased serum calcium and parathyroid hormone (PTH). She did not have any other significant personal or family history.
She was admitted to our hospital in February 2010. On physical examination her height was 1.40 m and weight was 30 kg. Her vital signs were within normal limits. She presented with a marked cervical kyphosis.
Relevant laboratory results showed hypercalcemia (13.36 mg/dL, normal 8.6–9.9 mg/dL), elevated PTH (2551 pg/mL, normal 12–88 pg/mL), elevated alkaline phosphatase level (4410 IU/L, normal 34–104 IU/L), hypercalciuria (urinary calcium of 213 mg/24 H, normal 100–250 mg/24 H), low creatinine clearance (25.84 mL/min/1.73 m2, normal ≥90 mL/min/1.73 m2), and low 25[OH]D3 circulating level (13 ng/mL, normal 30–100 ng/mL). The laboratory findings at hospital admission and last follow-up visit are summarized in . Biochemical approach was further completed with prolactin 12.6 ng/mL, FSH 4.4 mIU/mL, LH 17 mIU/mL, estradiol 36.13 pg/mL, T3 1.78 nmol/L, T4 69.33 nmol/L, TSH 1.85 μUI/mL, thyroglobulin 5.7 ng/mL, ACTH 19 pg/mL, and morning cortisol 15.76 μg/dL, all within normal limits.
Skeletal X-rays showed skull with “salt and pepper” lesions, vertebral compression fractures, brown tumors within the left humerus, and profuse calcifications within the pancreas and kidneys (). The patient did not refer to abdominal pain, nor any symptomatology related to endocrine and exocrine pancreatic insufficiency. The electrocardiogram was unremarkable. Abdominal ultrasound revealed kidney stones causing bilateral dilation of the renal pelvis. Neck ultrasonography showed microcalcifications within a large echogenic mass, posterior to the right lobe of the thyroid gland of 33 × 14 × 14 mm, . A 25 mCi 99Tc-sestamibi scintigraphy reported persistence of the radionuclide material at 120 minutes in the right inferior parathyroid gland at the same location of the mass shown in the US, . Bone densitometry showed decreased Z-Score values (total lumbar Z-Score of −4.2), . Primary hyperparathyroidism secondary to a large parathyroid tumor was diagnosed.
For HBS prophylaxis, before surgery, she received a 400,000 IU of vitamin D2 (Drisdol) (ergocalciferol) and 1 mg of calcitriol. Right hemithyroidectomy with right lower parathyroidectomy was performed. A tumor of 2.8 cm with 3.8 g of weight was resected. Pathological revision reported a focal lesion containing parathyroid tissue; it infiltrated the nodule capsule, without trespassing it, and the diagnosis was consistent with an atypical parathyroid adenoma. Two lymph nodes demonstrated follicular hyperplasia. Despite the administration of vitamin D (50,000 per week) and calcitriol 0.75 mg per day after surgery, the 25-hydroxyvitamin D levels never reached a value above 30. 1,25-dihydroxy vitamin D was not measured.
Postsurgical laboratory analysis showed PTH values of 31.3 pg/mL, serum calcium of 8.5 mg/dL, phosphate of 1.9 mg/dL, and magnesium of 1.8 mg/dL; on physical examination she presented upper extremity distal contractures, oromandibular dystonia, Chvostek and Trousseau signs, and QTc interval prolongation. PTH levels reached up to 48.6 pg/mL after 1 month, coexisting with hypophosphatemia of 2.7 mg/dL. At last follow-up, PTH serum levels were between 80 and 90 pg/mL, . She developed a prolonged and severe HBS that required 3 months with oral and intravenous calcium supplementation. The calcium IV infusion was stopped three months later. High PTH levels with hypocalcemia but also hypophosphatemia ruled out hypoparathyroidism. “Protracted” HBS was therefore diagnosed. During her hospitalization she underwent two episodes of lithotripsy as treatment for the kidney stones. Serum calcium, phosphate, and magnesium levels during hospitalization and follow-up are shown in .
After 42 months of treatment, bone densitometry scores improved within normal limits, . As an outpatient since 2010 she has been receiving an average of 1197 mg of oral elemental calcium, 1600 units of vitamin D, and 3 grams of magnesium sulfate per day. She was kept under close medical evaluation as an outpatient. Unfortunately in November 2013 the patient stopped coming to our institution with no clear reason, .","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [30.0, 'kg']}",70,66.5,73.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 30.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (30.0 kg - 20 kg) = 70.0 mL/hr.
Hence, the patient's fluid maintenance is 70.0 mL/hr."
4810,22,Maintenance Fluids Calculations,physical,decimal,pmc-3364630-2,Extracted,"A 23-year-old Japanese female (gravida 1, parity 0) complained of excessive salivation (approximately 1-1.5 L/day) accompanied by severe nausea and vomiting during the first trimester of pregnancy. Her medical and genetic histories were unremarkable. Her appetite returned at 10-12 weeks’ gestation; however, ptyalism persisted. Although she was treated with phenobarbital, piperidolate HCL and alpinia oxyphylla, salivation continued until delivery. Her total weight gain during pregnancy was 6.3 kg. At 39 weeks’ gestation, she gave birth normally to a male infant with a birth weight of 2895 g (appropriate for gestational age). Ptyalism recovered spontaneously after delivery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.3, 'kg']}",25.2,23.94,26.46,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.3 kg. Hence, the patient's maintenance fluid is 6.3 kg * 4 mL/kg/hr = 25.2 mL/hr.
Hence, the patient's fluid maintenance is 25.2 mL/hr."
4811,22,Maintenance Fluids Calculations,physical,decimal,pmc-5341637-1,Extracted,"A 48-year-old male weighing 60 kg presented to surgery outdoor with chief complaint of progressive swelling in the right side of the neck since last 3 months following trauma. The swelling was initially of small size which gradually progressed to the current size. On the basis of clinical finding and radiological report, it was diagnosed as subclavian artery aneurysm and surgical intervention was advised. The patient also had a history of angina 4 months back for which he was hospitalized and treated. He was advised tablet aspirin 75 mg and tablet clopidogrel 75 mg once daily on a regular basis. On local examination, the mass was around 3 cm × 3 cm × 4 cm, diffuse, pulsatile, soft in consistency, and mobile []. Magnetic resonance imaging angiography of the neck showed the aneurysm of subclavian artery, 1 cm lateral to the origin of internal carotid artery []. On two-dimensional echocardiography an ejection fraction of around 30% with mild left ventricular hypokinesia and grade 2 diastolic dysfunction was found. In view of poor cardiac functional status of the patient, RA with CEA was planned as the anesthetic technique. The patient was advised to stop tablet clopidogrel 7 days before the day of surgery. Coagulation profile was done, and it was found to be within the normal limit. Informed and written consent were obtained and the patient was explained about nil per oral. Tablet alprazolam 0.5 mg and tablet ranitidine 150 mg were advised to be taken on the night before and morning on the day of surgery. After taking the patient to the operation theater, all standard ASA monitors were attached and vitals were continuously recorded. Heart Rate was 100/min and electrocardiogram showed sinus rhythm, blood pressure was 140/80 mmHg, and SpO2 of 99% on room air. An 18-gauge intravenous cannula was inserted and ringer lactate drip was started. The patient was placed in the sitting position with the head flexed and resting on the thorax, to open the lowest cervical interspaces. After achieving cutaneous local anesthesia by injecting 3 ml of 2% lignocaine with adrenaline (1:200,000), an 18-gauge Tuohy needle was inserted through the midline approach into the C7-T1 interspace. The needle was advanced slowly, and epidural space was identified by the loss of resistance technique with a glass syringe []. Careful aspiration ensured that the needle had neither entered the subarachnoid space nor penetrated any epidural vein. Then, 8 ml of injection ropivacaine 0.5% with injection fentanyl 50 µg/kg was given in graded doses over 10 min and was left for 15 min after which the effect was checked. The upper limit and lower limit of the block were achieved from C3 to T4, respectively. The surgery was proceeded during which vitals remained stable throughout and the patient was comfortable.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.0, 'kg']}",100,95,105,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.0 kg - 20 kg) = 100.0 mL/hr.
Hence, the patient's fluid maintenance is 100.0 mL/hr."
4812,22,Maintenance Fluids Calculations,physical,decimal,pmc-7402778-1,Extracted,"A 35-year-old woman (height 1.682 m, body weight 173.4 kg, BMI 61.3 kg/m2) visited our hospital for selective cesarean section at a gestational age of 37 weeks. Three years previously, the patient was diagnosed with diabetes, which was controlled with insulin. Preoperative obstetric ultrasonography confirmed normal amniotic fluid amounts and transverse presentation of the fetus. Vital signs at the time of admission were as follows: blood pressure 145/90 mm Hg, heart rate 92 beats/min, respiratory rate 20 breaths/min, and body temperature 36.8°C. The chest radiograph showed no active lesion in the lung, and electrocardiography showed a normal sinus rhythm. The results of arterial blood gas analysis, complete blood count, coagulation test, urine test, and liver function test were in the normal range. In preoperative anesthetic evaluation, spinal anesthesia was selected because of the high possibility of endotracheal intubation failure due to super morbid obesity.
The patient entered the operating room after an intramuscular injection of 0.2 mg of glycopyrrolate after 8 hours of fasting. The vital signs measured before induction of anesthesia were as follows: blood pressure 155/78 mm Hg, heart rate 84 beats/min, body temperature 37.0°C, respiratory rate 18 breaths/min, and pulse oxygen saturation level 97%. Considering the possibility of hypotension, an arterial cannula was placed in the right radial artery for invasive arterial pressure monitoring during spinal anesthesia. The patient was placed in a sitting position for easy confirmation of landmarks, and the anesthesiologist explored the surface anatomy. The L3–4 and L4–5 interspinous spaces were palpable. After sterile preparation, the skin was locally anesthetized with 20 mg of 2% liodcaine, and spinal anesthesia was performed through the L3–4 interspinous space using a 89 mm 24-gauge spinal needle. After dura puncture, cerebrospinal fluid was confirmed, and 9 mg of 0.5% hyperbaric bupivacaine and 20 μg of fentanyl were injected into the subarachnoid space. The patient was then placed in a supine position, and the block level of spinal anesthesia was checked. A sensory block test to cold alcohol pads confirmed nerve block to the T8 dermatome level. Immediately after spinal anesthesia, invasive arterial blood pressure was measured as 156/85 mm Hg and heart rate as 99 beats/min. Seven minutes after the operation began, a boy weighing 4.170 kg was delivered; the baby had Apgar scores of 7 and 9 at 1 and 5 minutes, respectively. Invasive arterial blood pressure was maintained between 165/85 and 94/38 mm Hg and heart rate was maintained between 69 and 105 beats/min. The surgery was completed uneventfully with an estimated blood loss of 600 mL. The intravenous fluids injected intravenously during surgery were 500 mL of colloid and 150 mL of crystalloid. The total operation time was 68 minutes. The block level of spinal anesthesia was maintained at the T8 dermatome level during the operation and was also confirmed at the end of operation. The patient did not experience intraoperative pain. At the end of surgery, the blood glucose level was 95 mg/dL. After confirming normal vital signs, the mother was transferred to the recovery room, and vital signs in the recovery room were normal. The patient was discharged on postoperative day 5.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [173.4, 'kg']}",213.4,202.73,224.07,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 173.4 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (173.4 kg - 20 kg) = 213.4 mL/hr.
Hence, the patient's fluid maintenance is 213.4 mL/hr."
4813,22,Maintenance Fluids Calculations,physical,decimal,pmc-4166385-1,Extracted,"A 77-year-old woman (height, 155 cm; weight, 50 kg) with severe back pain and radiating pain in both legs was scheduled for lumbar discectomy under the diagnosis of L4-5 spinal stenosis. She had been able to perform basic activities of daily living despite a functional capacity of less than 4 metabolic equivalents and she had had no cardiac symptoms other than shortness of breath on exertion before the neurologic symptoms occurred. Upon preoperative evaluation, a 2-dimensional (2-D) echocardiography showed severe AS (aortic valve area = 0.79 cm2, pressure gradient = 88/53 mmHg) and concentric LV hypertrophy. However, no LV outlet obstruction and LV dilatation was observed and the LV contractility, stroke volume, and ejection fraction were normal. The necessity of cardiac surgery before lumber discectomy and the possibility that the lumbar surgery could be delayed were discussed with neurosurgeons and cardiologists taking into consideration the anesthetic and surgical risks. Considering the condition of her AS, the cardiac surgery should have been performed first. However, the patient refused the cardiac surgery for financial reasons and because of her fears relating to cardiac surgery. The lumbar surgery was required to prevent aggravation of her neurologic symptoms/deficits. Therefore, we decided that CSEA was the safest anesthetic method to use after considering the potential risks of GA that can occur in AS patients with diminished cardiac reserve (mentioned above), the patient's cardiac condition and functional capacity, and the characteristics of the operation.
On the day of surgery, the patient was very nervous despite being premedicated with intramuscular midazolam 2 mg; her blood pressure (BP) and heart rate (HR) were 160/70 mmHg and 95 bpm, respectively. Before performing anesthesia, the patient was sufficiently hydrated and elastic stockings were applied to both legs to minimize blood pooling. Electrocardiography, pulse oximetry, and continuous invasive arterial and central venous pressures were monitored. The CO was not monitored because noninvasive CO monitoring was not available in this regional anesthesia case and the Swan-Ganz catheter was considered too invasive for this case. Cardiac drugs including phenylephrine and epinephrine were kept ready. The patient received a rapid infusion of 500 ml lactated Ringer's solution. Thereafter, her urinary bladder was catheterized and 2 L/min of oxygen was administered via a nasal cannula. The patient was placed in the left lateral decubitus position, and after sterilization and numbing of the skin with local anesthesia, a 17-gauge Tuohy needle was placed at the L1-2 intervertebral space. After the epidural space was identified using the loss-of-resistance technique, a catheter was inserted 3 cm in the cephalad direction and a test dose of 2% lidocaine 3 ml was injected via the catheter since neither blood nor cerebrospinal fluid was obtained on aspiration. Subsequently, a 25-gauge spinal needle was inserted at the L4-5 intervertebral space and 0.5% hyperbaric bupivacaine 8 mg was injected into the subarachnoid space. The patient was then immediately turned to a supine, reverse Trendelenburg position. Ten minutes later, the sensory block had reached the T11 dermatome, and her BP and HR were 145/70 mmHg and 90 bpm, respectively. Thereafter, 0.19% ropivacaine 8 ml plus dexmedetomidine 50 µg was divided in half and administered in separate doses through the epidural catheter with a 10-min interval between doses. Twenty minutes later, the sensory block had reached the T9 dermatome, and her HR had decreased to 70 bpm, but her BP was maintained at 130-140/65-70 mmHg. After she was turned to the prone position, the patient's BP and HR remained unchanged and surgery was initiated. The skin incision site was over the T10-11 dermatomes.
Throughout the surgery, the patient did not complain of pain and her vital signs were stable. The duration of the operation was 90 min. Blood loss was minimal, and her urine output was about 350 ml; 850 ml of crystalloid solution was administered. The central venous pressure was little changed during the perioperative period, and her cardiac enzymes levels were normal on postoperative day 1. The patient was discharged without any hemodynamic instability or cardiovascular/neurologic complications on postoperative day 10.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [50.0, 'kg']}",90,85.5,94.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 50.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (50.0 kg - 20 kg) = 90.0 mL/hr.
Hence, the patient's fluid maintenance is 90.0 mL/hr."
4814,22,Maintenance Fluids Calculations,physical,decimal,pmc-4857576-1,Extracted,"An 18-year-old female student, a never smoker, HIV-negative, was referred to our Institute for evaluation of exertional breathlessness, cough with minimal mucoid sputum and fever of 1.5 years duration. She had lost 15 kg weight over the past 6 months. Prior to the presentation, based on her clinical and radiological profile, she had received antituberculous therapy for 4 months with no relief.
On examination, she was tachypnoeic and dyspnoeic but afebrile. Digital clubbing was observed. Vesicular breath sounds with fine inspiratory crackles were audible in all areas of the chest wall. Oxygen saturation on room air was 54%. Arterial blood gas analysis on oxygen (4 lt/min) showed pH 7.40, PCO238.7 mmHg, PO257.6 mmHg, and SaO2 of 90%. The total leucocyte count was 5.43 × 103 cells/μL with a normal differential count.
Chest radiograph is shown in and high resolution computed tomography (HRCT) of the thorax is shown in . Sputum stains and cultures for Mycobacterium tuberculosis, fungi and other aerobic organisms were negative. Fiber-optic bronchoscopy did not visualize any gross abnormality. Bronchoalveolar lavage (BAL) was milky in appearance but stains and cultures were negative for aerobic organisms including M. tuberculosis and pathogenic fungi. The BAL fluid was sent for a special investigation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15.0, 'kg']}",50,47.5,52.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.0 kg - 10 kg) = 50.0 mL/hr.
Hence, the patient's fluid maintenance is 50.0 mL/hr."
4815,22,Maintenance Fluids Calculations,physical,decimal,pmc-6775407-1,Extracted,"A 19-month-old male child was brought to our pediatric hematology-oncology outpatient clinic for the management of recurrent anemia of unknown cause. There was a history of hydrops fetalis being detected on the patient's fetal ultrasound examination. The patient weight 2.29 kg at birth and had been delivered at 39 + 4 weeks’ gestational age via a vaginal delivery. As a newborn delivery, the patient had cried weakly and had a pale appearance and was consequently diagnosed with respiratory distress syndrome and anemia. He was treated with a surfactant and underwent 6 packed red blood cell (PRBC) transfusions in the neonatal intensive care unit within the first month of his birth. Subsequently, he continued to receive a PRBC transfusion every 3 to 4 weeks for persistent anemia, until he reached 3 months of age. Fortunately, his hemoglobin levels were sustained >9.0 g/dL from the age of 4 months. However, the patient continued to experience wheezing along with repeated episodes of upper respiratory tract infections. At the age of 19 months, there was a recurrence of anemia and he was transferred to the hematology-oncology outpatient clinic. The father informed us regarding the patient's course of admission in a neonatal intensive care unit for the first few months of his life for the management of persistent anemia of an undetermined cause. Other medical history included 2 operations, one each for inguinal hernia and congenital cataract at the ages of 3 and 7 months, respectively. On eliciting the family history, he also disclosed that an older male sibling to the patient had died of apnea at the age of 5 months.
On examination, the patient was severely anemic but anicteric. The patient weighted 7.2 kg, had a 75 cm, and his head circumference was 43.5 cm (all parameters <3rd centile for age). His right eye showed strabismus. The systemic examination revealed no abnormalities including hepatosplenomegaly. The developmental milestones for motor skills and language were found to be delayed for age. The patient's hemoglobin (5.4 g/dL; normal range [NR]: 10.5–14.0 g/dL), hematocrit (18.5%; NR: 32–42%), and the reticulocyte count (0.9%; NR: 0.5–1.5%) levels were severely decreased, whereas the mean corpuscular volume was elevated (105.9 fL; NR: 70–90 fL). The total white blood cell and platelet count were normal. On hemoglobin electrophoresis, hemoglobin F level was found to be elevated (12.1%; NR: <1%), along with an increase in the erythrocyte adenosine deaminase level (60.2 IU/L; NR: 8–19 IU/L). The patient's parvovirus B19 serological test (IgM and IgG) results were negative. A computed tomography (CT) scan of the abdomen was performed to rule out other causes of anemia. CT revealed a herniation of stomach and spleen into the thoracic cavity the posteromedial aspect of left hemidiaphragm, and the patient was therefore diagnosed with Bochdalek hernia (Fig. ). No foci of bleeding and other abnormalities were detected in the CT scan. The bone marrow study revealed a normocellular structure with a very high myeloid-to-erythroid ratio of 18:1 (NR: 1.2:1 to 5:1). The erythropoietic cells were observed to be markedly decreased in number, whereas other cell lines were unaffected. The patient's karyotype was 46XY. An echocardiogram showed an atrial septal defect of 5.58 × 3.77 mm in size. The patient's genetic analysis revealed a heterozygous RPS19 gene mutation, designated as c.380G>A (p.Gly127Glu), leading to a diagnosis of DBA. The parents refused genetic testing of the other family members. A PRBC transfusion was administered as the initial treatment, following which oral prednisone was administered at a dose of 2 mg/kg/day for 4 weeks and then tapered slowly. The patient was continued on maintenance oral prednisone at a dose of 0.3 mg/kg on alternate days and has since been observed to sustain a hemoglobin level of >9.0 g/dL without receiving further transfusions. As an operative repair of the CDH was not performed at the time, a follow-up of the condition was planned on outpatient basis.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.2, 'kg']}",28.8,27.36,30.24,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.2 kg. Hence, the patient's maintenance fluid is 7.2 kg * 4 mL/kg/hr = 28.8 mL/hr.
Hence, the patient's fluid maintenance is 28.8 mL/hr."
4816,22,Maintenance Fluids Calculations,physical,decimal,pmc-5626156-1,Extracted,"The patient of the present case was a 70-year-old man (height: 170 cm; weight: 66 kg) with a history of chronic obstructive pulmonary disease (COPD), intermediate emphysema, chronic bronchitis, hypertension, type 2 diabetes mellitus, and L3-L4 lumbar intervertebral disc herniation. Chest x-ray during routine physical examination revealed a solitary pulmonary nodule in the left lower lobe. Computed tomography (CT) confirmed a 1.5 × 1.2 × 2.4 cm solid nodule in the left lower lobe, which became larger after 3 months.
His medications included tiotropium and salbutamol nebulization for COPD, amlodipine besylate and losartan for hypertension, and acarbose and repaglinide tablets for diabetes mellitus. Preoperative pulmonary function tests revealed a forced expiratory volume in 1 second of 1.25 L, whereas the ratio of forced expiratory volume in 1 second to forced vital capacity was 55%. The diffuse capacity of the lung for carbon monoxide was 12.3 mL/min/mm Hg (72% of predicted value). His preoperative vital signs were as follows: blood pressure, 135/80 mm Hg; heart rate, 62 beats/minute; temperature, 36.5°C; and respiratory rate, 18–20 beat/min. Modified Mallampati airway classification was grade II. The patient exhibited a moderate barrel chest and diminished breath sounds, although no cardiac murmurs were observed.
Electrocardiography, pulse oximetry, blood pressure measurements, and end-tidal carbon dioxide waveforms were evaluated prior to surgery. A cannula was inserted into the right radial artery. Preoxygenation (6 L/min) was performed via a disposable face mask. General anesthesia was induced via an intravenous injection of midazolam, lidocaine, propofol, sufentanil, and rocuronium. The patient was intubated with a left-sided 37-French, Robershaw double-lumen tube using a stylet. The stylet was removed immediately after the tip of the tube had passed beyond the vocal cords. The tube was advanced by rotating counterclockwise at 90 degrees. The tube was inserted smoothly, and no resistance was encountered at any time during placement. Proper bronchial tube position was confirmed through a fiberoptic bronchoscope (FOB). Satisfactory positioning was attained with the proximal edge of the bronchial cuff at least 0.5 cm below the carina in the left bronchus. The left bronchial cuff was inflated with 2 mL of air, whereas the tracheal cuff was inflated with 6 mL of air. Cuff pressure was not measured during the procedure. The patient was then transferred to the right lateral decubitus position. During this change in position, the bronchial cuff was completely deflated, whereas the tracheal cuff was inflated. The FOB was used to reconfirm bronchial tube position following the change in posture. No bleeding or secretions were observed, and satisfactory positioning was confirmed. Anesthesia was maintained using propofol (effect site concentration: 2.5 to 4.0 μg/mL) and remifentanil (effect site concentration: 4.5 to 6.0 ng/mL) under target-controlled infusion. A bispectral index monitoring system (Aspect Medical System, MA) was utilized to maintain an anesthesia depth between 50 and 60.
Left lower lobectomy was performed via video-assisted thoracoscopy (VATS). When the thoracoscope entered the thoracic cavity, the surgeon observed that the left lung was not fully collapsed due to concurrent COPD-decreased lung recoil and emphysema, whereas the right lung was normally ventilated. The nondependent lung was suctioned. Observation through the inserted FOB revealed that the bronchial tube was in the appropriate place. Following consultation with experts in thoracic surgery, carbon dioxide was insufflated into the left cavity via the thoracoscope to compress the left lung and improve surgical access, whereas the left bronchus was simultaneously suctioned using a suction catheter. However, this intervention only partially collapsed the aerated left alveolar tissue. To further improve surgical access, forceps were used to oppress and torque the left lung. After several attempts, a relatively satisfactory condition was achieved, and the left lower lobe was successfully excised under VATS, following which the bronchial stump was clamped using 2 titanium clips. Peak airway pressure was maintained at 30 cm H2O under manual ventilation in order to verify the safety and integrity of the bronchial stump. An obvious air leakage and continuous air bubbling were observed in the left cavity under manual ventilation. Unfortunately, we were unable to mechanically ventilate the lung due to the extent of air leakage. Manual ventilation was then performed for the right lung. As no air leakage was observed, these findings confirmed left lung leakage. To identify the site of leakage, the surgeon further mobilized the tracheobronchial tree. An irregular, circular, horizontal, and full-thickness left main bronchus rupture (1.2 cm) was observed at the tip of the bronchial tube, although the bronchial balloon remained intact.
The rupture was repaired via primary suturing with 4–0 prolene thread and secondary reinforcement with a pericardial flap through a left thoracotomy. The integrity of the repair was evaluated on the table. Following surgery, the double-lumen tube was removed, and the patient was re-intubated with a single-lumen tube (7.5 mm). The patient was transferred to the ICU for mechanical ventilation. Twenty-four hours postoperatively, his vital signs were stable. ICU physicians removed the tube after the patient had recovered the ability for spontaneous respiration. Repeated bronchoscopy revealed tight sutures and mild bronchial contraction 3 and 10 days following surgery, respectively. The patient was discharged 15 days after surgery and remained in good condition at the 2-month follow-up.
The patient provided informed consent for the publication of his clinical data. Medical Ethical Committee approval of the report was waived by Shaoxing People's Hospital (Shaoxing Hospital of Zhejiang University).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [66.0, 'kg']}",106,100.7,111.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 66.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (66.0 kg - 20 kg) = 106.0 mL/hr.
Hence, the patient's fluid maintenance is 106.0 mL/hr."
4817,22,Maintenance Fluids Calculations,physical,decimal,pmc-7724123-1,Extracted,"The patient was a 37-year-old man (148 kg, 183 cm, body mass index [BMI] 44.2 kg/m2) with a history of tracheostomy due to hypertensive intracranial hemorrhage that occurred 4 years ago. He was diagnosed with grade I tracheal stenosis above the tracheostomy site 2 years ago. Despite conservative treatment, dyspnea developed and the patient underwent endoscopic tracheal dilatation under general anesthesia. Baseline peripheral capillary O2 saturation (SpO2) was 94% and Cormack-Lehane grade was 3 at the time of intubation. Surgery was performed using the intermittent apnea technique with extubation, and a total of six apnea events occurred, with a mean duration of apnea was 147 s. The lowest SpO2 was 64%, and SpO2 recovered to 96–98% after manual ventilation via endotracheal tube. The patient had been treated conservatively after balloon dilatation with portable O2 at home. Dyspnea worsened again 1 year ago, despite O2 therapy, and serial fiberoptic steroid injections to the subglottic stenosis site were planned. In our hospital, fiberoptic steroid injections are usually performed according to the following steps. Topical anesthesia at nostrils is followed by sedation, applied by surgeon. The fiberscope is inserted through the nostril, and the glottis and lesion are sprayed with additional local anesthetics. Then, the lesion is injected with steroid. The otolaryngologist consulted us for safe sedation and monitoring due to the possibility of emergency caused by airway edema or airway obstruction. Considering the patient’s general condition, symptoms, and experience of previous surgery, we decided to perform the operation under general anesthesia with spontaneous breathing in preparation for airway manipulation, because general anesthesia using the intermittent apnea technique could limit the view of surgical field and damage the larynx and subglottic lesions.
On entering the operating room, the patient was placed in a 30° sitting position for the first steroid injection. Standard American Society of Anesthesiologists monitoring (non-invasive blood pressure [NIBP], electrocardiogram, and SpO2) and bispectral index (BIS) monitoring were applied. The baseline vital signs were as follows: BP, 105/52 mmHg; heart rate (HR), 66 beats per minute (beats/min); SpO2, 95%. Oxygenation was applied at 6 L/min O2 through a standard facial mask. End-tidal CO2 (EtCO2) was monitored continuously by capnography to confirm self-respiration. Dexmedetomidine was used for sedation. After delivering a loading dose of 1 μg/kg over 10 min, continuous infusion of 0.6 μg/kg/h was maintained. During infusion of the loading dose, the EtCO2 level decreased gradually until apnea was induced. An oral airway was inserted and the jaw-thrust maneuver was applied to maintain airway patency and support self-respiration. After confirming that the patient was unresponsive to verbal commands and tactile stimulus, the surgery was started while self-respiration was maintained. The surgeon requested lowering of the facial mask so that it would not interfere with the procedure and applied topical anesthesia by packing gauze soaked with Bosmin® (0.1% epinephrine) and Beracaine® (10% lidocaine) into both nostrils. The fiberscope was passed through the nostril to access the glottic and subglottic lesions, and additional 2% lidocaine was sprayed around glottis and lesions, and 3 ml of tamcetone® (Triamcinolone 40 mg/ml) was then injected. The procedure was interrupted by bag-valve-mask ventilation because SpO2 fell to 86%. After ventilator assistance for 117 s, SpO2 recovered to 96%. During surgery, HR remained within 20% of the baseline, but BP increased by more than 20% of the baseline. However, systolic BP remained below 160 mmHg, so no additional drug administration was necessary. The value of BIS was maintained between 55 and 80. The total surgery time was 20 min and the total anesthesia time was 40 min. The patient was discharged after 1 day of monitoring in the Intensive Care Unit (ICU), without dyspnea or complications.
Dyspnea improved noticeably, but on physical examination, grade II subglottic stenosis and stridor remained, thus necessitating a second steroid injection 1 month later. Based on our previous experience, we considered that there was a need to improve oxygenation during the procedure, so we decided to apply Optiflow®. In the same manner as in the first operation, the patient was placed in the 30° sitting position, and standard American Society of Anesthesiologists and BIS monitoring were applied. Baseline vital signs were as follows: BP, 102/58 mmHg; HR, 70 beats/min; and SpO2, 94%. O2 (100% warmed, humidified) was supplied through a nasal cannula at a rate of 30 L/min for preoxygenation. The patient tolerated this well, without any complaints. Dexmedetomidine was used for sedation at the same dose as before. Once the patient was unconscious, the O2 flow rate was raised to 70 L/min. EtCO2 was monitored by placing the EtCO2 sampling line at the nostril next to the Optiflow® nasal cannula; however, a low value was obtained, so we could only confirm self-respiration by monitoring the shape of the waveform (). Topical anesthesia was applied by packing gauze into both nostrils. This disturbed the O2 supply through the Optiflow® nasal cannula; therefore, we inserted an oral airway to maintain airway patency, and the Optiflow® nasal cannula was transferred to the opening of the oral airway. The EtCO2 line was also transferred to the opening of the oral airway, but it still showed a low value; thus, only the shape of waveform was monitored (). SpO2 was maintained at 98–100%, and no intervention, such as mask ventilation or jet ventilation, was required during surgery. Despite self-respiration, there was a drop in SpO2 to 86% () due to O2 leakage; the Optiflow® nasal cannula dislocated from the airway opening. After fixing the nasal cannula to the airway with plaster (), SpO2 immediately recovered to 99% and no additional desaturation events occurred. The vital signs were stable within 20% of baseline. Additional bolus of midazolam was injected to prevent the event of awareness because the value of BIS was maintained between 70 and 79 when the procedure was performed; 1mg for oral airway insertion, 2 mg for gauze packing into both nostrils. During the operation, the value of BIS was well maintained between 35 and 50, and spontaneous breathing was generally maintained well. The patient endured the surgical stimuli without coughing and movement throughout entire operation. The total operation time was 15 min and total anesthesia time was 40 min. The surgeon had prepared jet ventilation because of the experience during the previous surgery, but ultimately did not use it; thus, the surgeon was highly satisfied with THRIVE. After the surgery, the patient was transferred to the ICU. Arterial Blood Gas Analysis (aBGA) was performed after arrival in the ICU; partial pressure of O2, 94 mmHg; partial pressure of CO2 (PaCO2), 49 mmHg; pH, 7.30; bicarbonate, 21.3 mEq/L. The patient was discharged after 1 day of monitoring without complications.
This study was approved by the Institutional Review Board of Soonchunhyang University Bucheon Hospital (IRB No. 2020-02-026-001). And written informed consent, included the consent to publish images, was obtained from the patient in this study.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [148.0, 'kg']}",188,178.6,197.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 148.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (148.0 kg - 20 kg) = 188.0 mL/hr.
Hence, the patient's fluid maintenance is 188.0 mL/hr."
4818,22,Maintenance Fluids Calculations,physical,decimal,pmc-3932572-1,Extracted,"A 16-month-old girl child from North east district of India presented to the emergency department with multiple erythematous nodules and ulcers in the skin [Figure and ], difficulty in breathing, and fever since 5 days. The parents gave history of near drowning in drain water 7 days prior to the onset of illness. The birth history was unremarkable.
On general physical examination, the child was conscious, irritable, febrile with toxic look, had tachypnea and tachycardia, and weighed 8 kg (Grade I malnutrition for age). Multiple erythematous nodules and ulcers (ecthyma gangrenosum) were noted in the skin, with few eschars [Figure and ]. Her pulse was 100/min and BP 90/56 mm Hg. Routine blood examinations revealed raised leukocyte count (14,500/mm3), neutrophilia (89%), elevated C-reactive protein (CRP; 68 mg/l) and procalcitonin (2.56 ng/dl) levels. The liver enzymes were mildly elevated [aspartate transaminase (AST) 138 IU/l; alanine transaminase (ALT) 99 IU/l; alkaline phosphatase (ALP) 363 IU/l] and renal function tests were unremarkable. The blood sugar level was within normal limits. ELISA test for the qualitative determination of antibodies to human immunodeficiency virus (HIV) type 1 and 2 viruses was non reactive. On examining the respiratory system, coarse crepitations and rhonchi were noted bilaterally.
Initial empirical antibiotic therapy was initiated with intravenous (IV) injections of Piperacillin + Tazobactum and Netilmicin. However, there was progressive deterioration of the patient's general condition with appearance of new skin lesions during the course of treatment.
An anterior–posterior (AP) view of chest radiograph [] revealed multiple patchy consolidations with air bronchogram in the left upper-mid zone and right mid and lower zones, with cavitations in few of them.
High-resolution computed tomography (HRCT) and contrast-enhanced computed tomography (CECT) of the thorax was done on 64 slice MDCT scanner, (Aquilion 64, Toshiba Medical Systems Corporation, Japan) [Figures –] which revealed multiple variable-sized segmental and subsegmental air-space consolidations scattered in bilateral lung parenchyma, more on the right side where few of them showed areas of eccentrically located breakdown and cavitations. Multiple relatively larger nodular lesions were also noted in parenchyma of both the lungs. Most of the cavitary lesions showed dependant intracavitary low-density collections. No mediastinal lymphadenopathy was noted. Based on the imaging findings, an initial diagnosis of septic pyogenic pneumonic abscesses with differential diagnosis of pulmonary tuberculosis was given.
However, a diagnosis of tuberculosis did not correlate well with the atypical skin lesions, the acute presentation, and the rapidly progressing clinical deterioration of the child. A fine-needle aspiration cytology (FNAC) from a nodule in the left forearm revealed frank pus [Figures and ]. A blood culture was done which showed growth of colonies of B. pseudomallei within 3 days, which established the diagnosis of melioidosis.
Based on the culture and sensitivity reports, specific antibiotic therapy was started with IV Meropenam, along with nebulization. However, despite intensive care and antibiotic therapy unfortunately, the child died 2 days later due to septicemic pneumonia (1 week since admission).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [8.0, 'kg']}",32,30.4,33.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 8.0 kg. Hence, the patient's maintenance fluid is 8.0 kg * 4 mL/kg/hr = 32.0 mL/hr.
Hence, the patient's fluid maintenance is 32.0 mL/hr."
4819,22,Maintenance Fluids Calculations,physical,decimal,pmc-2687548-2,Extracted,"A 16 month-old girl was evaluated for DD and seizures. She was born at 37 weeks of gestation by spontaneous delivery after an uneventful pregnancy. Neonatal weight was 2.49 kg (25th percentile), length 47.8 cm (25th percentile), head circumference 32.2 cm (3rd percentile). APGAR scores were 9 at the first and fifth minute. At birth, a ventricular septal defect (VSD) and a bicuspid aortic valve were detected by ecochardiogram. She was able to sit alone at 7 months, but indipendent walking was still not achieved at 16 months. At 10 months she presented generalized seizures characterized by gaze, circumoral cyanosis, masticatory movements. Right temporal spike and wave activity, associated with irritative multifocal anomalies were recorded on EEG; even if valproic acid therapy was subsequently undertaken, EEG anomalies persisted for 1 year and the children experienced febrile seizures during the second year of life. Moreover, external hydrocephalus was detected by MRI. On physical examination at 16 months, weight was 10.3 kg (10th–25th percentile), head circumference 47 cm (50th percentile), length 80 cm (50th percentile); straight eyebrows, deep set eyes and divergent strabismus were noted. Ophtalmological examination revealed bilateral nystagmus and hypermetropic astigmatism. Subtelomeric FISH analysis revealed a de novo terminal deletion of chromosome 1p (46, XX, ish.del (1p)(pVYS218C-)).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.3, 'kg']}",40.6,38.57,42.63,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.3 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.3 kg - 10 kg) = 40.6 mL/hr.
Hence, the patient's fluid maintenance is 40.6 mL/hr."
4820,22,Maintenance Fluids Calculations,physical,decimal,pmc-5894924-1,Extracted,"A previously healthy 7-month-old intact male domestic shorthair cat was evaluated 4 h after being hit by a car. It weighed 3.64 kg, presented laterally recumbent with pale mucous membranes, was hypothermic (35.0°C [95.0°F]) and mildly bradycardic (150 beats per min). Respiratory rate and effort were within normal limits. Several loops of bowel were palpated along the proximal medial aspect of the left pelvic limb. The skin was intact, but mild bruising was evident on the caudal abdomen. Several superficial abrasions were noted along the distal pelvic limbs.
The cat received a 13.7 ml/kg crystalloid fluid bolus (Lactated Ringer’s Solution [LRS]; Abbott Laboratories) over 30 mins, buprenorphine (0.24 mg/kg SC [Simbadol; Zoetis]), and thermal support was provided via forced air warmer (Bair Hugger; 3M). Its temperature rose to 36.9°C (98.4°F) over the next 3 h and it became more responsive. Femoral pulses were moderate in quality and mucous membrane color was pale pink. A blood pressure was not obtained.
Following initial stabilization, a complete blood count (CBC), biochemical profile and chest and abdominal radiographs were performed. Abdominal radiographs showed appropriate serosal detail with several gas-filled loops of bowel outside the abdominal cavity and tracking along the left medial thigh (,). The stomach was dilated with gas and contained a small amount of mineral opaque material. The thoracic cavity was unremarkable. No evidence of appendicular or axial fractures was detected. The radiographs were supportive of a diagnosis of inguinal herniation.
Following resuscitation, the hematocrit was 36.5% (reference interval [RI] 30.3–52.3%). Abnormalities included a mild neutrophilic leukocytosis with a left shift (white blood cell count 26.39 × 109/l [26,390/μl]; RI 2.87–17.02 × 109/l [2870–17,020/μl]), neutrophilia (14.41 × 109/l [14,410/μl]; RI 1.48–10.29 × 109/l [1480–10,290/μl]) and lymphocytosis (11.3 × 109/l [11,300/μl]; RI 0.92–6.88 × 109/l [920–6880/μl]). Clinically relevant findings on serum biochemistry included an increased blood urea nitrogen (19.99 mmol/l [56 mg/dl]); RI 3.57–10.71 mmol/l [10–30 mg/dl]), a normal creatinine (106.08 mmol/l [1.2 mg/dl]); RI 26.52–185.64 mmol/l [0.3–2.1 mg/dl]), an increased alanine aminotransferase (ALT; 1440 U/l [24.05 μkat/l]); RI 20–100 U/l [0.33–1.67 μkat/l]) and a normal blood glucose (109 mg/dl [6.05 mmol/l]); RI 70–150 mg/dl [3.9–8.32 mmol/l]).
The cat received LRS 3 ml/kg/h and ampicillin-sulbactam (30 mg/kg IV q8h [Unasyn; Pfizer]). The cat was able to maintain a sternal body position and was mentally appropriate. Its pulse quality and mucous membrane color remained moderate and pale pink. An abdominal exploratory celiotomy was performed the following morning.
The cat was induced with propofol (7 mg/kg IV [Propoflo; Abbott Laboratories]) and anesthesia was maintained with sevoflurane in oxygen (SevoFlo; Abbott Laboratories). The abdomen was aseptically prepared, and a 12 cm ventral midline incision was made extending from 2 cm cranial to the umbilicus caudally to the pubis. A full abdominal exploratory was performed. The urinary bladder was intact but deviated caudally and was entrapped in a left inguinal hernia. The left inguinal hernia measured approximately 3 cm and also contained approximately one- third of the mid-jejunum and a small portion of the colon. The bowel was examined closely, and no evidence of perforation or ischemic injury was evident at time of surgery. The intestines were normal in color, had strong mesenteric pulses and exhibited normal peristalsis. A mesenteric hematoma was evident adjacent to a 4 cm rent in the mesentery, and the crura of the superficial inguinal ring and aponeurosis of the external abdominal oblique muscle were entirely avulsed from the pubis. Hemorrhage was evident along the left retroperitoneal space. Otherwise, the abdominal contents were within normal limits.
The mesenteric rent and medial crus of the left inguinal hernia were closed in simple continuous pattern with 3-0 polydioxanone suture (PDS; Ethicon). The right inguinal musculature had entirely avulsed from its bony insertion, so the detached rectus abdominus muscle was sutured to fragments of remaining pubic periosteum using 3-0 PDS in a simple continuous pattern. The intestines were lavaged with sterile saline (0.9% NaCl Solution; Abbott Laboratories) and the abdominal cavity was dried using laparotomy sponges before routine closure using 3-0 polydioxanone suture in a simple continuous pattern to close the linea and 3-0 poliglecaprone suture in a buried intradermal pattern to close the skin (Monocryl; Ethicon).
Blood pressure trends were obtained with an oscillometric measurement device (SurgiVet; Smiths Medical) with an intraoperative reported mean arterial pressure range of 35–55 mmHg. Intraoperative intravenous fluid support included an initial LRS rate of 8.5 ml/kg/h with subsequent hydroxyethyl starch boluses totaling 5 ml/kg (Hetastarch 6% in 0.9% NaCl; Hospira) provided in response to decreasing blood pressure trends. Heart rate ranged from 125 - 150 beats per min (bpm), but temperature fell from 39.1°C (102.4°F) preoperatively to 34.1°C (93.4°F) immediately postoperatively, even though thermal support via a forced air warmer had been provided throughout. Recovery from anesthesia was uneventful and normothermia was achieved with additional external thermal support. The cat had a body temperature of 39.5°C (103.2°F), heart rate of 160 bpm and a respiratory rate of 24 breaths per min 8 h after surgery.
Postoperatively, the cat received LRS at 3 ml/kg/h, buprenorphine (0.24 mg/kg SC q12h) and ampicillin-sulbactam (30mg/kg IV q8h), and continued to recover well. Intravenous fluids were continued until the cat began eating and drinking approximately 8 h postoperatively. It began self-grooming 12 h after surgery. The following morning, it was ambulatory in the cage and was bright and alert, purring and interacting comfortably when held and manipulated. Its mucous membranes were pink and its femoral pulses were strong and synchronous. Body temperature was 39.3°C (102.7°F), the abdominal incision was clean and dry and abdominal palpation was non-painful.
Approximately 48 h postoperatively (72 h after initial injury), the cat’s respiratory rate and effort increased suddenly. It became less responsive to normal stimuli and showed pain on abdominal palpation. A CBC and biochemical profile were unremarkable aside from an elevation in ALT (252 U/l; RI 20–100 U/l), though this had decreased significantly from presentation. A lateral abdominal radiograph showed loss of abdominal detail and evidence of free gas (). Abdominal ultrasound showed a moderate amount of fluid in the abdomen. Blind abdominocentesis yielded a yellow–green-colored turbid fluid that contained grossly visible debris. Fluid cytology was supportive of acute bowel perforation with myriad polymorphic bacteria admixed with plant fragments and amorphous basophilic granular material.
Owing to the cat’s rapid clinical deterioration, the decision was made to euthanize. Immediately following euthanasia with 3 ml euthanasia solution (Euthanasia Solution; VetOne) intravenously, an abdominally focused post-mortem examination was performed and revealed two 1 cm perforations in the anti-mesenteric wall of the mid-jejunum (,). The intestine, approximately 3 cm oral and aboral of both perforations, was deep purple in color, but the rest of the bowel was pink with the serosa being slightly hyperemic and fibrin coated in response to peritonitis. There was no obvious evidence of mesenteric thrombosis, and the mesenteric tissue was pink in color. The hernia repair sites were still intact. Full necropsy and histopathology were not performed.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.64, 'kg']}",14.56,13.832,15.288,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.64 kg. Hence, the patient's maintenance fluid is 3.64 kg * 4 mL/kg/hr = 14.56 mL/hr.
Hence, the patient's fluid maintenance is 14.56 mL/hr."
4821,22,Maintenance Fluids Calculations,physical,decimal,pmc-7268772-1,Extracted,"A 31-year-old woman (G1, P0) had been diagnosed with Graves’ disease at 16 years of age. She discontinued treatment at her own discretion but was advised to resume treatment when she expressed her desire to become pregnant. At the time treatment had resumed, her TRAb (second generation) level was 211 IU/L (normal range: < 1.75 IU/L). Her family history was negative.
The patient became pregnant naturally, at a time when her thyroid function was not satisfactorily controlled by a high dose of propylthiouracil (PTU). An alternative treatment (isotope therapy or surgery) was being considered. Because of hyperemesis gravidarum, oral medications were no longer an option, resulting in her thyroid function deteriorating during week 13 of her pregnancy. Her TRAb level was 43.6 IU/L at that time, and a daily dose of 50 mg potassium iodide (KI) was administered. As a result, her thyroid function was under control, and KI administration was discontinued at week 17. The patient’s FT3 level fluctuated between normal and elevated, whereas her FT4 and TSH levels were low. Her TRAb level gradually declined but was still high at week 33 (18.4 IU/L).
At 33 weeks and 5 days of gestation, the amniotic pocket and the cervical lengths were 8.1 and 2.6 cm, respectively, indicating worsening hydramnios and threatened premature labor. A blood test showed that the patient’s TSH level had increased to within the normal range. Because pre-pregnancy reduction in her antithyroid medication caused sudden worsening of her thyroid function, she was prescribed a daily supplementary course of 25 μg levothyroxine. At 34 weeks of gestation, she was admitted for hydramnios management and prevention of threatened premature labor.
On admission, blood sampling showed an increased TSH level; thus, her thyroid function had improved. Because she was experiencing frequent uterine contractions, we consulted the Department of Diabetes and Endocrinology at our hospital and initiated a continuous drip of ritodrine hydrochloride under careful monitoring for aggravation of hyperthyroidism. At 34 weeks and 4 days of gestation, a transabdominal ultrasound indicated enlargement of the fetal thyroid. It showed a transverse diameter and circumference of 58.4 and 178 mm, respectively (mean values at the 35th week of pregnancy: 18.9 mm and 51.1 mm respectively []) (Fig. a). The blood flow was diffusely increased (Fig. b), and hydramnios was observed. In addition, the epiphyseal nucleus of the distal femur could not be confirmed. The fetus was in face presentation (Fig. a). We assumed that the cause of the hydramnios was the inability to swallow the amniotic fluid due to the size of the thyroid. We suspected that the PTU had crossed the placenta and migrated to the fetus, causing fetal goiter; therefore, we initiated a reduced dose of antithyroid medication for the mother at 34 weeks and 5 days of gestation. After reducing the PTU dose from 200 to 100 mg/day, neither the mother nor the fetus showed signs of hyperthyroidism. The dose of PTU was gradually reduced to 50 mg/day, while the levothyroxine dose was increased to 100 μg/day. The fetal thyroid showed a shrinking tendency, as magnetic resonance imaging (MRI) performed at 36 weeks and 3 days of gestation showed a 3-cm fetal thyroid transverse diameter (transverse section; Fig. b). The next day, an ultrasound indicated that the AFI had decreased from 24 to 15 cm, and that the fetus’ thyroid blood flow had returned to normal (restricted to the thyroid margins). The fetus had moved into a normal flexion position.
Because of the goiter, we were unable to confirm that there would be a patent airway after delivery. Therefore, we speculated that a tracheotomy would be necessary. After consultation with both the Department of Neonatal Medicine and the Department of Pediatric Surgery, an elective cesarean delivery was performed at 36 weeks and 5 days of gestation. On day 7 after delivery, the mother showed signs of hyperthyroidism, which necessitated an increase in her PTU dose.
A diagram describing the therapeutic course from pre-pregnancy to postpartum is shown in Fig. .
The infant was a male, weighing 2817 g, with Apgar scores of 8 and 9 at 1 and 5 min, respectively. His umbilical aortic blood pH was 7.26. The anterior cervical region had a transverse diameter of 40 mm, indicating an enlarged thyroid gland (Fig. ). Crying was normal, and no resuscitation was necessary. The infant was admitted to the neonatal intensive care unit (NICU) immediately after birth because of premature delivery and goiter. No bradycardia was observed, and other than the goiter, no external deformities that would suggest congenital hypothyroidism, such as megaloglossia or umbilical hernia, were observed.
A sonography indicated that the thyroid gland had a left-to-right transverse diameter of 41.4 mm (normal range [mean ± 2SD]: 13.9 ± 4.0 mm []) and an isthmus of 5.2 mm, indicating enlargement. An ultrasound showed no increased blood flow. Radiographs indicated no epiphyseal nucleus of the distal femur, which showed that fetal bone maturation was delayed because of the fetal hypothyroidism.
Thyroid function tests were conducted using the umbilical blood at delivery, and the results were as follows: FT3, 1.7 pg/mL (normal range [mean ± SD]: 1.70 ± 0.034 pg/ml); FT4, 1.6 ng/dL (normal: 1.17 ± 0.14 ng/dl); and TSH, 25.18 μIU/mL (normal: 10.27 ± 6.31 μIU/mL) []. The TRAb level was 17.4 IU/L. No treatment was given until 5 days of age, when thyroid function tests indicated a tendency toward hyperthyroidism, (FT3 = 3.5 pg/mL, FT4 = 2.7 ng/dL, and TSH = 2.56 μIU/mL). The infant was administered a course of thiamazole (MMI) (0.5 mg/kg/day). No major changes in the size of the infant’s thyroid gland were observed during the hospital stay. Because of neonatal jaundice, the infant was treated with 24-h phototherapy starting at 4 days of age. His progress was stable, and he was discharged at 18 days of age, weighing 3.1 kg. Following discharge, the MMI dose was gradually decreased as TRAb levels dropped, and it was discontinued at 51 days of age. At 10 months of age, the infant’s thyroid function was normal, despite persistent goiter. There was no evidence of any developmental delays. Currently, the infant is under the continuous care of the Department of Pediatrics.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2817.0, 'g']}",11.268,10.7046,11.8314,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2817.0 g so this converts to 2817.0 lbs * kg/1000 g = 2.817 kg. Hence, the patient's maintenance fluid is 2.817 kg * 4 mL/kg/hr = 11.268 mL/hr.
Hence, the patient's fluid maintenance is 11.268 mL/hr."
4822,22,Maintenance Fluids Calculations,physical,decimal,pmc-5027064-1,Extracted,"An 8-year-old boy presented with on and off abdominal pain for four months which increased in frequency and intensity 24 hours before presentation. Pain used to worsen on oral intake and was occasionally associated with non-bilious vomiting. There were no other significant symptoms. He had been evaluated elsewhere with a normally reported contrast follow-through study done three months earlier.
On examination patient weighed 20 kg and was dehydrated. There was no pallor and the patient was afebrile. Abdomen was soft, non-distended and non-tender without any palpable mass. Bowel sounds were increased. Per rectal examination was normal. After admission, he had episodes of agonizing abdominal pain. Nasogastric tube revealed non bilious aspirate. Routine blood investigations were within normal limits with baseline hemoglobin of 10.4 g/dl. Abdominal x-ray did not reveal any pathology. Abdominal ultrasound (USG) showed positive whirlpool sign. CT scan of the abdomen confirmed the USG findings and showed the abnormal relationship of superior mesenteric vein and artery (Fig.1). Considering the acute symptoms and the radiological findings, patient was taken up for emergency surgery. At laparotomy, midgut volvulus with malrotation was found. Derotation of the twisted small bowel loops was done. Bowel loops were healthy and viable. Thick Ladd’s bands with narrow small bowel mesentery were present. Ladd’s bands were divided and mesentery widened. Approximately 40 cm distal to the duodeno-jejunal flexure, a 10cm x 5cm tubular jejunal duplication on the mesenteric side was found (Fig. 2). It communicated with the normal jejunum through a narrow opening. Resection of the involved segment with end to end jejuno-jejunal anastomosis was performed. Resected specimen was sent for histopathological examination. Postoperative period was uneventful. Patient has been asymptomatic in the follow up period. Histopathological examination showed normal small intestinal features with ectopic gastric mucosa.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [20.0, 'kg']}",60,57,63,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 20.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (20.0 kg - 10 kg) = 60.0 mL/hr.
Hence, the patient's fluid maintenance is 60.0 mL/hr."
4823,22,Maintenance Fluids Calculations,physical,decimal,pmc-7783360-2,Extracted,"A 64-year-old female presented in July 2018 with progressive abdominal pain, nausea, 40-pound weight loss, and new cough. She was found to have a palpable right upper quadrant mass with CT scan revealing an 11 x 9.3 cm heterogeneously enhancing mass replacing the majority of the right kidney (). CT scan also showed associated inferior vena cava tumor thrombus, a T10 lytic lesion, and innumerable pulmonary nodules in the bilateral lung bases concerning for metastatic disease (). Pathology from a CT-guided pulmonary biopsy confirmed clear-cell RCC. Baseline labs showed WBC 11.5 K/ul, ANC 9.30 (H) K/ul, hemoglobin 8.0 g/dL, platelets 520 K/ul, Ca 12.0 mg/dL, and creatinine of 1.47 mg/dL. Her IMDC category criteria was poor-risk. She was initially started on cabozantinib 60 mg daily and denosumab at an outside hospital. Unfortunately, repeat imaging eight weeks later showed similar appearing pulmonary nodules and renal mass along with enlarging T10 vertebrae metastasis and new hepatic lesions consistent with additional metastases. She subsequently relocated to Tennessee and sought oncology consultation at the Vanderbilt-Ingram Cancer Center. At her initial consultation, she was wheelchair-dependent with a KPS of 40%. Cabozantinib was discontinued, and she was subsequently started on nivolumab 240 mg every two-weeks. At her first follow up appointment she reported cessation of her nausea along with significant improvement in her abdominal pain and appetite. Her performance status continued to improve and her first repeat imaging scan at eight weeks showed significant improvement in her bilateral pulmonary nodules, sclerosis of the T10 vertebral lesion, resolution of previously seen hepatic metastases, and reduction in the size of the right renal mass to 8.1 x 4.2 cm. During her course of treatment, two doses of nivolumab were held secondary to Common Terminology Criteria for Adverse Events (CTCAE) grade-1 hepatitis, and she required initiation of levothyroxine for CTCAE grade-2 hypothyroidism. She experienced no additional immune related adverse events while on treatment. Her CT scans continued to show further improvement and her KPS returned to 100%, allowing her to return to work. After 13 total doses of nivolumab, her renal mass measured 3.9 x 3.2 cm (65% decreased from baseline, ), and she underwent right radical nephrectomy two weeks later in September of 2019. The nephrectomy specimen was independently reviewed by two board-certified pathologists with expertise in genitourinary malignancies. Sections showed no residual tumor, indicating a complete pathologic response to therapy (). The previous tumor bed was replaced by an acellular dense hyalinized tissue with sparse lymphocytic infiltrate extending into the perinephric fat. In areas, the fibrous tissue was loose and edematous with rare hemosiderin-laden macrophages. The adjacent renal parenchyma showed chronic interstitial nephritis with extensive interstitial fibrosis, tubular atrophy and glomerulosclerosis. The interstitial infiltrate was predominantly lymphocytic with rare plasma cells. She elected to continue nivolumab monotherapy with her most recent CT scan, over one year post-nephrectomy, showing stable pulmonary nodules (largest 7 mm) and no other evidence of disease.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [40.0, 'lbs']}",56.28736,53.47299,59.10173,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 40.0 lbs so this converts to 40.0 lbs * 0.453592 kg/lbs = 18.14368 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (18.14368 kg - 10 kg) = 56.28736 mL/hr.
Hence, the patient's fluid maintenance is 56.28736 mL/hr."
4824,22,Maintenance Fluids Calculations,physical,decimal,pmc-7896659-1,Extracted,"A 50-year-old female who had a history of positive hepatitis B surface antigen for more than 10 years presented to The Infectious Department of our hospital complaining of aggravating anorexia and fatigue. During her presentation in The Infectious Department, she had nausea and vomit symptoms.
The patient’s symptoms started a week ago with gradually increasing gastrointestinal symptoms including anorexia and nausea. Her liver function tests showed elevated transaminases.
She had a past medical history of being a carrier of HBV for more than 10 years without antiviral treatment. She had no cardiac function abnormalities, arterial hypertension or diabetes mellitus. She had no negative drug history, and no alcohol intake.
The patient reported that her four siblings were infected with HBV, her mother died from hepatocellular carcinoma, and her father was in good physical condition.
After admission, the patient’s temperature was 36.6 °C, heart rate was 91 bpm, respiratory rate was 20 breaths per minute, blood pressure was 145/104 mmHg and oxygen saturation in room air was 99%. The patient was 160 cm tall and weighed 53 kg. The clinical examination revealed light scleral icterus without any other pathological signs.
Laboratory values on admission and during hospitalization are shown in Table . A series of tests were performed after admission to The Infectious Disease Department. Blood analysis revealed the following: Alanine aminotransferase, 575 U/L; Aspartate aminotransferase, 593 U/L; Total bilirubin, 108.3 μmol/L; Alkaline phosphatase 116 IU/L; Positive hepatitis B surface antigen, anti-LKM-1 > 1:80; Positive anti-soluble liver antigen/liver-pancreas; Positive anti-mitochondrial antibody; and Positive anti-SSA antibody and anti-SSB antibody.
The hematoxylin and eosin staining of liver tissue: The structure of hepatic lobules is unclear. The hematoxylin and eosin staining showed varying degrees of hepatocyte edema with moderate to severe piecemeal necrosis and scattered eosinophilic bodies (Figure , arrows). Small bile duct in the portal area was accompanied by lymphocyte-predominant inflammation with a small amount of eosinophil infiltration (Figure , filled triangles).
Immunohistochemistry analysis of liver tissue: The proliferation of small bile ducts in the portal area were obvious (Figure , arrows), with more infiltration of lymphocytes and plasma cells and positive marker detection including hepatitis B surface antigen (+), HBcAg (+-), bile duct epithelium (CK19+), IgG (+), and IgG4 (-) combined hepatocellular and cholangiocarcinoma. Findings were consistent with mild chronic hepatitis compatible with HBV infection, without histological stigmata of autoimmunity (Figure ).
Mesh fiber staining of liver tissue: The reticular fiber staining showed that the hepatic lobular stent was significantly damaged (Figure , arrows). The characteristic floral ring structure of AIH was not seen (Figure ).
Masson staining of liver tissue: The portal area was enlarged with fibrosis, the formation of bridging fiber band was visible in the focal area, and collagen fiber proliferated in the portal area by Masson staining (Figure , arrows).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [53.0, 'kg']}",93,88.35,97.65,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 53.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (53.0 kg - 20 kg) = 93.0 mL/hr.
Hence, the patient's fluid maintenance is 93.0 mL/hr."
4825,22,Maintenance Fluids Calculations,physical,decimal,pmc-6240425-2,Extracted,"Patient 2(III:15) was a 10 years old male, wheelchair bound, measuring 18 kg in weight, 107 cm in height and 51 cm in head circumference. Pregnancy and delivery were uneventful. Parents were also distant cousins (IBD proportion ~ 6%).His health remained poor since birth. He was able to walk but never became able to run. At the age of 8 years he sustained fractures of right humerus and right tibia and femur after trivial traumas (Fig. ). Clinical examination showed triangular face, normal teeth, right eye squint, normal sclerae, and wide protruding chest with increased antero-posterior diameter. Extremities were thin and showed bilateral mild angulation of proximal humeri and marked bowing of right femur. His feet were flat. Radiological examination showed generalized osteopenia, platyspondyli in all vertebrae, narrowing of inter-costal spaces, globular pelvis, bowing of distal parts of right tibia and fibula, and mild bowing of right radius and ulna (Fig. and ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [18.0, 'kg']}",56,53.2,58.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 18.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (18.0 kg - 10 kg) = 56.0 mL/hr.
Hence, the patient's fluid maintenance is 56.0 mL/hr."
4826,22,Maintenance Fluids Calculations,physical,decimal,pmc-3324737-1,Extracted,"A 69 year old male patient, with height at 172 cm and weight at 70 kg, visited the hospital with gait abnormality in his right leg and pain in the pelvic joint area, which had continuously continued since its occurrence two years ago. The patient had a history of undergoing low anterior resection, radiation treatment, and chemotherapy four years prior for rectal cancer, and was taking insulin and oral hypoglycemics for diabetes. Since two years ago, the patient's leg could not be straightened properly when walking and pain in the pelvic area occurred when there was sudden movement. He had visited pain clinics, rehabilitation clinics, neurology, and orthopedics, but did not receive any specific diagnosis and had endured with the aid of physical and drug treatments. The degree of pain was 4-5/10 in the visual analog scale (VAS), and the symptoms were pain in the right pelvic joint when walking, and when lying down, the pubic area felt tight and painful when the leg was completely straightened, with pain subsiding when the leg was bent.
During the physical examination, the straight leg raising test was 90/90, but there was pain in both thighs, and the Patrick test indicated that both sides were positive. The Ganslene test was also positive in both sides, but the pain was worse in the right. There was tenderness in the spinous process of L3, and there were no tender points in the facet joints. The patient also complained of tenderness in sacroiliac joints, gluteus medius, and piriformis. In the magnetic resonance image (MRI), there were no metastasis or recurrence observed, but the disc between L2 and 3 had been herniated to the right and was pressing the right psoas ().
Hence, the gait abnormality and pain was considered to be caused by the laterally herniated intervertebral disc that compressed the right psoas muscle, and so a right psoas compartment blockade was performed. First, the patient was laid prone and the skin was sterilized. Under C-arm guidance, the transverse processes of the L3 were confirmed and an approach was made with a 22-G Tuohy needle (ARROW®, Arrow International Inc., USA). At the position where resistance ceased, was the location after the psoas muscle was observed with the contrast medium, which was shown when 0.25% levobupivacaine (Chirocaine®, Abbott, Elverum, Norway) 10 ml and triamcinolone diacetonide 5 mg were injected (). The patient stated that there were no effects from the drug therapy received at another hospital, so in order to discern the effects of the blockade no other particular oral medication was prescribed. When the patient visited the outpatient clinic one week after the procedure, periods without pain had continued for two to three days and gait abnormality had also disappeared during this period, but at the time of visit, a pain of VAS 5/10 was experienced by the patient. Hence, it was decided that the psoas compartment blockade was effective, so it was performed three times in two week intervals. As a result, the patient has shown improvements in pain of about VAS 3/10, so we are still monitoring his progress.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [70.0, 'kg']}",110,104.5,115.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 70.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (70.0 kg - 20 kg) = 110.0 mL/hr.
Hence, the patient's fluid maintenance is 110.0 mL/hr."
4827,22,Maintenance Fluids Calculations,physical,decimal,pmc-2687570-1,Extracted,"A two month old boy was admitted to our institution with symptoms of a fever, poor oral intake, lethargy, and hazy urine. Initial urinalysis performed in the out-patient department showed many white blood cells in the urine, making the diagnosis of a urinary tract infection a highly likely cause of the boy's ailments. Among blood relatives, there was no known history of genetic, hepatic, or renal diseases. His past medical records were unremarkable. Upon physical examination, the patient was acutely ill-looking and slightly lethargic, but otherwise appeared normal. He suffered from a high fever that exceeded 38℃ and had no detectable hepatosplenomegaly or costovertebral angle tenderness. No icterus was present and his abdomen was unremarkable, without signs of portal hypertensions, such as ascites or distension of abdominal veins. Edema and oliguria were both absent. His weight was 6.3 kg, which was more than the 95 percentile for his age.
Laboratory studies revealed a hemoglobin level of 9.2 g/dL, leukocyte count of 4420/µL, platelet count of 388,000/µL, total serum bilirubin of 0.4 mg/dL, and direct bilirubin level of 0.2 mg/dL. Serum alanine aminotransferase level was 26 IU/L, aspartate aminotransferase level was 10 IU/L, alkaline phosphatase was 274 U/L, total protein was 4.5 g/dL, and albumin was 3.2 g/dL. Blood urea nitrogen level was 10.9 mg/dL and creatinine level was 0.4 mg/dL. Abdominal ultrasonography (US) was performed for renal evaluation, which revealed a large kidney (Length; Rt - 8.63 cm, Lt - 8.31 cm) with increased cortical echoes and multiple small cysts in the medulla and cortex of both kidneys (). Dilatation of intrahepatic and common bile ducts were noted coincidentally and ARPKD, with Caroli's disease fell under suspicion.
The patient's older brother and both parents were examined ultrasonographically for the presence of renal anomalies, which turned out to be negative. The patient underwent a DMSA scan and a MAG3 diuretic renogram for the functional evaluation of the dysplastic kidneys. The DMSA scan revealed a split renal function of 51.8% on the right and 48.2% on the left kidney. The MAG3 diuretics renogram showed a decrease in both the flow and function of both kidneys. Abdominal MRI showed large, multicystic dysplastic kidneys, fusiform dilatation of the common bile duct, and small, round, and tubular dilatation of the intrahepatic bile ducts (). Needle biopsy of the liver revealed fibrotic changes, a finding that suggested congenital hepatic fibrosis (). Based on these findings, the diagnosis of Caroli's syndrome with ARPKD was made. The patient was put on broad-spectrum antibiotic therapy consisting of ampicillin-sulbactam and cefotaxime. His pyuria persisted, but all his culture studies - including three consecutive urine cultures - proved negative. His fever subsided two days after the initiation of antibiotic therapy and the patient required red blood cell transfusion after the hepatic needle biopsy, but his stay in the hospital was otherwise uneventful. As no overt symptoms remained, the patient was discharged after the fever and other initial symptoms had subsided and is currently being followed up through the out-patient department.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.3, 'kg']}",25.2,23.94,26.46,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.3 kg. Hence, the patient's maintenance fluid is 6.3 kg * 4 mL/kg/hr = 25.2 mL/hr.
Hence, the patient's fluid maintenance is 25.2 mL/hr."
4828,22,Maintenance Fluids Calculations,physical,decimal,pmc-8530501-1,Extracted,"A 26-year-old man who was 50 kg in weight and 140 cm in height was scheduled for debridement of cellulitis, extending proximally from the sole of his right foot up to the middle third of his calf in the surgical unit. He developed sepsis and was consequently being treated with broad-spectrum antibiotics, which later changed to culture-sensitive antibiotics. The patient’s condition progressively deteriorated. Subsequently, on the 13th day of stay in the surgical unit, his vitals became unstable and his GCS score dropped. The department of anesthesia was called for the critical care and airway management of the patient.
Upon assessment, the patient had a GCS score of 6/15 (E2V1M3), blood pressure of 80/40 mmHg, heart rate of 148 bpm, respiratory rate of 40 breaths/min, and oxygen saturation of 80% while on 15 liters of supplemental oxygen using a non-rebreather mask. On examination, his spine had curvature disorder with mild cervical kyphosis, severe thoracic kyphoscoliosis, and moderate lumbar lordosis resulting in the upper body contorting towards the left side and severe restriction of neck movements (Figures , ). On auscultation, his cardiovascular examination was unremarkable. The chest examination revealed bilateral basal coarse crackles. The hematological and biochemical parameters were significant for leukocytosis, severe metabolic acidosis with a lactate of 5.8 mmol/L, and hypoxemia with a partial pressure of oxygen of 46 mmHg. Chest X-ray showed tracheal deviation toward the left side of the chest and a Cobb angle of 55° (Figure ). The electrocardiogram (ECG) revealed a right axis deviation with T-wave inversion.
Emergency intubation was planned, along with resuscitation. The airway examination revealed a Mallampati classification of II and a restricted range of neck movement, especially during flexion. A team of anesthetists and assistants prepared the patient, attached the monitors, and checked the equipment for difficult intubation. Besides, the otorhinolaryngology (ENT) department was briefed about the case. Their team prepared for the ""can't intubate can't ventilate"" scenario and were in the standby position. The patient was propped with cushions below his left shoulder and the left lumbar region to optimize his position. He was given bag-mask ventilation initially but it was not effective as he started to desaturate. One of the anesthetists administered 2 mg of midazolam and 100 mg of suxamethonium before intubation. Subsequently, the senior anesthetist performed direct laryngoscopy using a size four blade and noted a Cormack-Lehane grade III view. A video laryngoscope was not employed due to a lack of availability. The tip of the epiglottis was marginally visualized and a gum elastic bougie (50 mm x 200 mm) was passed. Then an endotracheal tube of size 7.0 mm was railroad over the bougie. The chest was examined for the bilateral rise and auscultated for equal air entry in both lung fields. Due to unavailability, the capnometer was not utilized. Next, the endotracheal tube was fixed at 20 cm near the right oral commissure by an assistant. For management with ventilatory and vasopressor support, the patient was shifted to the intensive care unit.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [50.0, 'kg']}",90,85.5,94.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 50.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (50.0 kg - 20 kg) = 90.0 mL/hr.
Hence, the patient's fluid maintenance is 90.0 mL/hr."
4829,22,Maintenance Fluids Calculations,physical,decimal,pmc-4837260-1,Extracted,"A male infant was vaginally delivered to a 24-year-old G2P2 mother at 30 weeks of gestation. Apgar scores were 6 and 8 at 1 and 5 minutes, respectively. The infant required respiratory support and was transferred to the neonatal intensive care unit where he was intubated and ventilated. A chest radiograph displayed respiratory distress syndrome and surfactant replacement therapy was given. In accordance with our units' policy, the infant's skin and blood cultures were taken immediately after delivery and the baby was given amoxicillin and gentamicin. At birth, his birth weight was 1450 g (10–25 percentiles), height was 40.5 cm (25–50 percentiles), and his head circumference was 28 cm (25–50 percentiles). On third day of life, these antibiotics were discontinued when the cultures were found to be negative. On 5th day of life, he was seen to clinically deteriorate. Because there was the suspicion of sepsis, he was given vancomycin, amikacin, and topical gentamicin and cultures for blood, urine, and skin lesions were taken and biochemical tests were performed. Biochemical laboratory examinations revealed C-reactive protein (CRP) to be 100 mg/dL (normal range: 0–5 mg/dL), the platelet count was 14 × 103/mm3, and the white blood cell count was 9.2 × 102/mm3; all other parameters were normal. The next day, rapidly progressive edematous, erythematous, and necrotic plaques with bullae were observed to form on his lips, soft palate, and tongue (). Simultaneously, similar lesions developed on his back, gluteal region, and both lower extremities. Three days later, the blood and skin lesion cultures were found to be positive for PA, but the urine culture was negative. According to the results of the culture antibiogram, vancomycin was stopped and ceftazidime was added to the treatment regimen because Gram-negative bacteria are sensitive to ceftazidime, and then the patient started to recover. Five days after the treatment initiation the skin lesions started to improve and on the 10th day of treatment these lesions disappeared; however, due to the loss of tissue in the lips, soft palate, and tongue, the patient developed difficulty in the functions of sucking and swallowing (). Because of this dysfunction, the patient was fed with an orogastric tube. He was discharged in good general condition 63 days after birth.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1450.0, 'g']}",5.8,5.51,6.09,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1450.0 g so this converts to 1450.0 lbs * kg/1000 g = 1.45 kg. Hence, the patient's maintenance fluid is 1.45 kg * 4 mL/kg/hr = 5.8 mL/hr.
Hence, the patient's fluid maintenance is 5.8 mL/hr."
4830,22,Maintenance Fluids Calculations,physical,decimal,pmc-3603067-1,Extracted,"A 22-year-old male was brought to our Endocrine clinic by his brother due to his “not growing up.” The patient was 83 cm in height (SDS – 16.98) and weighed 13.9 kg (<3rd percentile). He had dull look, puffy face with thick lips, macroglosia, and umbilical hernia. There was sexual infancy with prepubertal testes (<3 ml). He could sit without support, but could not stand or walk without support, and could only talk in monosyllables. He was born full term by normal vaginal delivery, and cried immediately after birth. The developmental milestones were delayed and not achieved till the date. He is the eldest of seven siblings, rest six of whom have no complaints. An X-ray of hand was done showing bone age of less than 1 year. A thyroid profile showed thyroid stimulating hormone (TSH) >150 IU/ml, free T4 and T3 were below the assay range. Ultrasound of neck showed absent thyroid tissue in neck. Iodine-131 uptake scan was consistent with thyroid aplasia. Diagnosis was myxematous cretinism due to thyroid aplasia was made, and patient was started on thyroxine supplementation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [13.9, 'kg']}",47.8,45.41,50.19,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 13.9 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.9 kg - 10 kg) = 47.8 mL/hr.
Hence, the patient's fluid maintenance is 47.8 mL/hr."
4831,22,Maintenance Fluids Calculations,physical,decimal,pmc-7416821-1,Extracted,"A 31-year old 4-month postpartum female, weighing 75 kg, presented to the emergency department with a history of drowsiness, fatigue, shortness of breath, vomiting and progressive confusion for two consecutive days prior to admission. She had initiated the LCHF diet about 2 weeks prior to admission while breastfeeding, in order to lose weight accumulated during pregnancy. She successfully lost 5 kg in 2 weeks following severe restriction of dietary carbohydrates. She denied any alcohol or drug use. She reported no known allergies or chronic conditions (including diabetes) except for mild asthma.
Her initial examination in the emergency department revealed a blood pressure of 133/89 mmHg, a heart rate of 126 beats/min, a respiratory rate of 30 breaths/min, oxygen saturation of 100% on room air, a temperature of 36.2°C and a haemoglucotest of 6.7 mmol/L. The pH on the arterial blood gases was 7.128; the pCO2 was 6.7 mmHg and the pO2 was 119 mmHg. Her lactate was 2.4 mmol/L (reference range 0.5–1.2 mmol/L) and glucose 9.1 mmol/L. Her urine dipstick chemistry revealed a pH of 5.5, ketones 4+ positive, blood 3+ positive and protein 1+ positive. Physical examination of her abdomen and chest were normal. Apart from her confusion, her central nervous system examination was normal with no localizing signs. Her blood results are explained in Table .
These results confirmed a non-diabetic ketoacidosis with acute kidney injury. Serum toxicology (benzodiazepines, barbiturates, paracetamol, salicylate, tricyclic antidepressants) results were negative.
She was admitted to the adult intensive care unit and received haemodialysis at the speed of QB 200 ml/min and QD 500 ml/min for 4 h. A high potassium bath was added as the serum potassium was found to be low [2.5 mmol/L (reference range 3.5–5.1 mmol/L)]. An insulin infusion was started at 5 units/h with a total of 45 units administered intravenously. This was followed by 6 units of insulin subcutaneously. Simultaneously, 5% dextrose water with 40 mmol potassium chloride was administered at 160 ml/h for 9 h, reduced to 100 ml/h for 5 h and then further reduced to 80 ml/h. Her acidosis was reversed after 24 h.
Empiric antibiotic therapy was administered to cover the possibility of sepsis although the CRP was only marginally elevated [22 mg/l (reference range >5 mg/l)], with a white blood cell count of 26.92 10^9/l (reference range 3.92–9.88 10^9/l), with neutrophils comprising 23.85 10^9/l (reference range 2.00–7.50 10^9/l) and monocytes 1.72 10^9/l (reference range 0.18–1.00 10^9/l) of the total cells.
Thyroid ultrasound showed increased vascularity of the thyroid gland. Levothyroxine 100 mcg twice daily was administered orally while she was admitted. Her thyroid hormone levels are depicted in Table .
The amylase and lipase 48 h after admission were elevated at 98 U/L (reference range <100 U/L) and 299 U/L (reference range 13–60 U/L), respectively. These decreased during her admission. A sonar exam of the abdomen and pelvis showed no abnormalities. A chest X-ray and brain CT scan revealed no abnormalities as did the cardiac echo.
The lipogram profile (as shown in Table ) was measured 2 days after admission and showed an elevated LDL cholesterol and non-HDL cholesterol both of which normalized 48 h after admission without pharmacological treatment. The triglyceride levels were also slightly elevated (still within the normal range) and decreased to 1.0 mmol/L on discharge.
The patient recovered fully and was discharged after 4 days. She received a prescription for levothyroxine 100 mcg once daily orally but without insulin or oral hypoglycemics. Four follow-up visits post discharge showed normalization of amylase and lipase levels and thyroid and kidney function.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [75.0, 'kg']}",115,109.25,120.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 75.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (75.0 kg - 20 kg) = 115.0 mL/hr.
Hence, the patient's fluid maintenance is 115.0 mL/hr."
4832,22,Maintenance Fluids Calculations,physical,decimal,pmc-4173354-1,Extracted,"A morbidly obese 80-year-old female [weight 102.1 kg, height 157.5 cm, body mass index (BMI) of 41] presented with mouth pain, and multiple carious teeth were scheduled for teeth extraction with an alveoplasty. She had a past medical history of Cerebrovascular accident (CVA), transient ischemic attack (TIA), congestive heart failure (CHF), hypertension, and myocardial infarction (MI). Electrocardiogram (ECG) showed first-degree heart block, prolonged QT interval with anterolateral infarct. Echocardiograph (ECHO) showed an ejection fraction of 45–50%, left atrial enlargement, mild pulmonary hypertension, and trace mitral regurgitation.
Preoperative airway assessment revealed a Mallampati score of IV, three finger breadth mouth opening, slight limitation of neck movement, and loose carious teeth. With this assessment, the patient was predicted to be difficult to intubate. The anesthetic plan included management of the predicted difficult intubation with the GlideScope® with other usual backup planes for difficult intubation.
Anesthesia was induced with fentanyl 150 µg, lidocaine 100 mg, propofol 150 mg and succinylcholine 100 mg.
The GlideScope® blade tip was placed in the vallecula and the vocal cords and epiglottis were seen. A size 7 endotracheal tube (ETT) was mounted in the GlideRite® rigid stylet and then passed into the oral cavity for intubation. The endotracheal tube (ETT appeared to slide into the oropharynx with relative ease and the endotracheal tube was placed into the trachea. The stylet was removed, and positive EtCO2 and equal bilateral breath sounds was confirmed. A successful GlideScope® intubation was assumed.
As the surgeon began the procedure, he noticed that ETT had pierced and entered the tissue of the retromolar trigonum (the same space which holds the lingual nerve), and then proceeded to pass through the oropharyngeal space and re-enter the vocal cords [Figure and ].
We decided to remove ETT rather than cutting the tissues to free it, to avoid trauma to lingual nerve. We re-inserted another size 7 ETT with the aid of the GlideScope® camera. Positive EtCO2 and equal bilateral breath sounds was confirmed. Surgery was completed uneventfully; however, the surgeon stated multiple times that the patient's oral mucosa was very fragile and easily torn. The patient was easily extubated and transported to post anesthesia care unit (PACU). Both intubations were performed by the student registered nurse anesthetist (SRNA).
PACU staff was instructed to look for signs of lingual nerve injury (numbness in the tongue, loss of ability to taste, tingling sensation in the tongue, pain, burning, or electric shock sensations in the tongue, speech impairment and drooling).
The PACU stay was uneventful, the patient denied any of the above mentioned symptoms, and was discharged.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [102.1, 'kg']}",142.1,134.995,149.205,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 102.1 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (102.1 kg - 20 kg) = 142.1 mL/hr.
Hence, the patient's fluid maintenance is 142.1 mL/hr."
4833,22,Maintenance Fluids Calculations,physical,decimal,usmle-9222,Extracted,"A 65-year-old man presents to his primary care provider with excessive fatigue, weight loss, and multiple small bruises on his arms and abdomen. These symptoms started several months ago. He reports worsening fatigue and a 20-pound (9 kg) weight loss in the past month. Past medical history is significant for an asymptomatic lymphocytosis noted 6 months ago on a yearly physical. On review of systems, he denies chest pain, difficulty breathing, swelling in the extremities, or change in bowel habits. Vitals include: temperature 37.0°C (98.6°F), blood pressure 110/75 mm Hg, pulse 99/min, respirations 20/min, and oxygen saturation 91% on room air. On physical exam, the patient is listless. The cardiac exam is normal. Lungs are clear to auscultation. The abdominal exam is significant for mild splenomegaly. Scleral icterus is present and there is prominent generalized non-tender lymphadenopathy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [9.0, 'kg']}",36,34.2,37.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 9.0 kg. Hence, the patient's maintenance fluid is 9.0 kg * 4 mL/kg/hr = 36.0 mL/hr.
Hence, the patient's fluid maintenance is 36.0 mL/hr."
4834,22,Maintenance Fluids Calculations,physical,decimal,pmc-5418708-1,Extracted,"We describe the case of a premature Bahraini girl born at 29 weeks of gestation by spontaneous vaginal delivery, to a 39-year-old gravida 6 para 5 mother. She was born “flat” with an APGAR score of 4 and 9 at 1 and 5 minutes respectively and a birth weight of 910 g. Ventilatory support was required during her first 6 days of life, with a dose of surfactant. She had an uneventful Neonatal Intensive care stay, tolerating breast milk and was gaining weight at a steady pace. On her 47th day of life she developed sepsis and required repeated ventilator support for 3 days. At day 51 she weighed 1400 g, but developed abdominal distension and feed intolerance. She was referred to the pediatric surgeon on day 54 when pneumoperitoneum was detected by a shoot-through lateral plain abdominal film (Fig. ). Our examination showed her abdomen to be distended but soft with mild diffuse tenderness and no signs of peritonitis. There was no abdominal wall erythema or visible bowel loops. We did not find any hernias or abdominal masses. Her C-reactive protein (CRP) was 37 mg/L which is 12 times higher than the normal range. In view of pneumoperitoneum, she was taken for exploratory laparotomy. A classic right transverse upper abdominal incision was used to open her abdomen as the diagnosis was NEC. Her entire small and large bowel was healthy and normal in appearance (Fig. ). Her appendix measured approximately 2 cm in length and was acutely inflamed with a perforation at the tip. Except for the site of perforation, there was no other evidence of gangrene (Fig. ). The findings were consistent with a perforated appendix with no evidence of peritonitis or NEC. An appendectomy was performed. She had a smooth postoperative recovery where she was started on breast milk on the second postoperative day and her CRP was normal on the eighth postoperative day. Histology demonstrated mucosal ulceration of her appendiceal wall, marked acute transmural inflammation, and necrotic wall at the perforated end (Fig. ) but the rest had intact mucosal lining (Fig. ). A neuron-specific enolase (NSE) immunohistochemical stain showed positive staining for nerve fibers (Fig. ) which excluded Hirschsprung’s disease. She was discharged home at day 120 of life and was thriving at 2-year follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1400.0, 'g']}",5.6,5.32,5.88,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1400.0 g so this converts to 1400.0 lbs * kg/1000 g = 1.4 kg. Hence, the patient's maintenance fluid is 1.4 kg * 4 mL/kg/hr = 5.6 mL/hr.
Hence, the patient's fluid maintenance is 5.6 mL/hr."
4835,22,Maintenance Fluids Calculations,physical,decimal,pmc-8718300-1,Extracted,"A 49-year-old Caucasian male with a history of tobacco and alcohol abuse presented with worsening headaches, unintentional weight loss, and left-hand weakness. He reported a one-month history of worsening and persistent headaches as well as 30 lbs. of unintentional weight loss. He then developed left hand weakness approximately 2 weeks prior to presentation; he also reported increased left hand dyscoordination, which led him to dropping things often. He was taken to the emergency room by a coworker when he became unresponsive. His neurological exam on presentation was significant for 4/5 strength as well as a subtle drift in his left upper extremity. The rest of his physical exam was unremarkable. MRI brain showed a 4.4 x 4.0 x 3.7 cm right frontal mass with associated 1.3 cm right to left midline shift (Figure ); the patient did not undergo positron emission tomography (PET) scan.
The patient was admitted to the neurosurgery service and underwent a right craniotomy due to initial suspicion of a high-grade glioma. However, pathology of the resected mass showed adenocarcinoma with an immunohistochemical profile most consistent with colorectal primary malignancy. Further review of systems revealed eight months of non-bloody diarrhea associated with fecal urgency. He did not have a family history of colorectal cancer in any first-degree relative. Carcinoembryonic antigen was elevated at 4.6 ng/mL. CT imaging of the chest, abdomen and pelvis showed ill-defined, nodular wall thickening of the rectum and sigmoid colon, sub-centimeter presacral and lower para-aortic lymph nodes and no other distant metastatic lesions. Flexible sigmoidoscopy demonstrated a partially obstructing rectal mass (Figure ) with biopsies consistent with rectal adenocarcinoma. Immunohistochemistry showed microsatellite stability and molecular studies for KRAS, NRAS, and BRAF mutations were negative. He was referred to oncology and a repeat MRI brain did not show any evidence of any new intracranial metastases. The patient is awaiting systemic palliative chemotherapy with FOLFOX and bevacizumab.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [30.0, 'lbs']}",47.21552,44.85474,49.5763,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 30.0 lbs so this converts to 30.0 lbs * 0.453592 kg/lbs = 13.60776 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.60776 kg - 10 kg) = 47.21552 mL/hr.
Hence, the patient's fluid maintenance is 47.21552 mL/hr."
4836,22,Maintenance Fluids Calculations,physical,decimal,pmc-5413680-1,Extracted,"A 38-year-old Japanese female smoker with a previous history of OC use visited the emergency department with a chief complaint of a sudden onset of severe left flank pain. Her present history started with exacerbation of dysmenorrhea, which induced her to take loxoprofen sodium 60 mg tid for the previous 10 days. Five days prior to admission, she also restarted taking an OC, drospirenone/ethinyl estradiol (YAZ), for dysmenorrhea due to adenomyosis uteri. On the morning of admission, she was awoken by severe left flank pain, a continuous aching pain, roughly 6/10 on the conventional pain scale. She also had nausea that started immediately after the onset of the chief compliant. She had noticed dyspnea on effort during the previous 3 months but denied other symptoms such as chest pain, back pain, constipation, diarrhea, tarry stools, or hematochezia. A review of her symptoms revealed anorexia accompanied by a 5-kg loss of body weight over the previous 3 months.
Two years prior to her emergency department visit, the patient was diagnosed with adenomyosis uteri, myoma uteri, and iron deficiency anemia due to hypermenorrhea at that time. One year prior, she was prescribed YAZ, a low-dose OC, for dysmenorrhea and hypermenorrhea due to adenomyosis, but discontinued this medication 4 months before admission due to diminished symptoms, until 5 days prior to her hospital visit. She had tried to take iron tablets 2 years prior, but failed due to nausea. She had one induced abortion at the age of 18. Her recent menstruations were regular, the last starting 2 weeks prior and finishing 1 week prior to admission, 2 days before she started taking OC again. She was currently a smoker, and had smoked ten cigarettes per day for 10 years. She denied smoking more than 15 cigarettes per day. She had divorced several years prior and currently lived with her parents. She managed a bar and consumed a large amount of alcohol every night at the bar. She had no family history of thromboembolic disorders or malignancies.
The patient’s height was 160 cm, body weight 47.4 kg, and body mass index 18.5 kg/m2. She was alert and cooperative but annoyed by her pain and appeared ill. Her blood pressure was 126/70 mmHg, pulse regular at 86 beats per min, respiration 24 breaths per min, body temperature 37.2 °C, and blood oxygen saturation level on room air was 100 %. Her face and conjunctivae appeared pale, but not icteric, and her oral cavity showed no aphthae or petechiae. There was no lymphadenopathy, bruits, or venous hum, her heart sounds were regular, without murmur or gallops, and lung sounds indicated a bilaterally clear condition. Abdominal findings showed tenderness at the left flank area with obvious rebound and muscular guarding. Light percussion at the left costovertebral angle provoked knocking pain. No edema, petechiae, or peripheral signs were observed.
Laboratory data (Table ) was remarkable for severe anemia. Other routine data, including renal function, liver function, and electrolytes, were normal. Urinalysis revealed proteinuria (1.4 g/gCr) and microhematuria. Urine sediment showed 1–4 neutrophils, 10–19 red cells, and 1–4 squamous epitheliums per high-powered field (HPF), without bacteria or casts. Left renal vein thrombosis was seen on computed tomographic (CT) scan with contrast material and echogram of the abdomen (Fig. a, b). No other thrombi, masses, or apparent compression of the renal vein suggesting nutcracker syndrome were seen.
Drospirenone/ethinyl estradiol was discontinued immediately and acetaminophen was administered instead of loxoprofen sodium. Anticoagulation therapy with continuous intravenous heparin and subsequent oral warfarin was initiated immediately after laboratory specimens were submitted to evaluate underlying thrombophilic predispositions. Concentrated red cells were transfused for symptomatic anemia and a tolerable dosage of iron tablets was started.
Due to the patient’s anorexia and body weight loss, we performed upper and lower gastrointestinal endoscopy, but there were no findings suggesting ulcers, inflammation, active bleeding, or malignancies. Gynecological examination and transvaginal echogram found no malignancies. Blood examinations submitted before these procedures revealed no underlying thrombophilia such as connective tissue diseases, vasculitis syndromes, anti-phospholipid syndrome, factor V Leiden deficiency, anti-thrombin deficiency, protein S deficiency, protein C deficiency, or disseminated intravascular coagulation (Table ). Repeated urinalysis and normal serum albumin excluded nephrotic syndrome. Abdominal ultrasound, performed after admission, confirmed the thrombus at the left renal vein and excluded other thromboembolism or findings of nutcracker syndrome.
The patient’s flank pain and anorexia improved soon after treatment was begun. A CT scan performed 2 weeks after admission showed remarkable volume reduction of the thrombus and the patient was discharged, with instructions to continue warfarin and iron supplement administration. Although transient breakthrough bleeding and macrohematuria continued for a few days after admission, no complications such as pulmonary embolism or persistent bleeding occurred during treatment. The patient’s urine findings were normalized, with hemoglobin at 12.5 g/dL and PT-INR extended to 3.0 at the time of discharge, 18 days after admission (Table ). Elevated transaminases at the day of discharge were spontaneously normalized at the outpatient clinic without any intervention. The patient stopped smoking, took no OC after admission, and was in good condition during our continuous observation at the outpatient clinic.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [47.4, 'kg']}",87.4,83.03,91.77,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 47.4 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (47.4 kg - 20 kg) = 87.4 mL/hr.
Hence, the patient's fluid maintenance is 87.4 mL/hr."
4837,22,Maintenance Fluids Calculations,physical,decimal,usmle-1049,Extracted,"A 36-year-old man is brought to the emergency department because of multiple episodes of nonbilious emesis for 3 days. The vomitus consists of undigested food and he has also had dark brown emesis twice today. He has been having early satiety during this period. He has had progressive severe episodic epigastric pain and dyspepsia for the past week. The pain is partially relieved with food or over-the-counter antacids, but worsens at night and several hours after eating. He has also had a weight gain of 2 kg (4.4 lbs) during this period. His father underwent surgery for colon cancer 3 years ago. He has smoked one pack of cigarettes daily for the last 15 years. He drinks two to three beers daily. His temperature is 37.1°C (98.8°F), pulse is 106/min and blood pressure is 108/68 mm Hg. Examination shows dry mucous membranes. The abdomen is mildly tender to palpation in the left upper quadrant; there is a tympanitic mass in the epigastrium. A succussion splash is heard with a stethoscope when the patient is rocked back and forth at the hips. Bowel sounds are reduced. Rectal examination is unremarkable. Test of the stool for occult blood is positive. The remainder of the examination shows no abnormalities.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.0, 'kg']}",8,7.6,8.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.0 kg. Hence, the patient's maintenance fluid is 2.0 kg * 4 mL/kg/hr = 8.0 mL/hr.
Hence, the patient's fluid maintenance is 8.0 mL/hr."
4838,22,Maintenance Fluids Calculations,physical,decimal,pmc-7322092-1,Extracted,"A 40-year-old woman (height:5′0″ and weight: 125lbs) was brought to our Level II trauma center following a motor vehicle collision in mid-May of 2018. She was a restrained driver in the crash and denied losing consciousness. Her Glasgow coma scale (GCS) was 15. She reported abdominal pain and had abrasions over her left clavicle and lower abdomen in a seatbelt sign pattern, contusions over her right thigh and left hip and a laceration over her right knee revealing the joint. CT scan of the head, chest, abdomen, and pelvis was performed, and small foci of air was seen under the diaphragm which was indicative for small bowel perforation. A CT Scan of the head without IV contrast revealed no acute processes, including intracranial hemorrhage or cerebral contusions. The patient was emergently taken to the operating room for an exploratory laparotomy and irrigation and debridement of the right lower extremity.
The patient’s prior past medical history was significant for hypothyroidism and medications prescribed were Synthroid 88 mg once daily. The patient reported that she was compliant with her medication. She denied any hypertension, cardiac, pulmonary, renal, neurological or substance use history. The patient had a normal sinus rhythm and a normal ECG with all intervals within normal limits.
On anesthesia pre-operative exam, the patient’s vital signs were within normal limits. The patient underwent an exploratory laparotomy for a perforation in the jejunum and a tear in the mesentery followed by an irrigation and debridement for the open laceration in the right knee. Intraoperatively, the patient’s vitals fluctuated. The patient’s blood pressure ranged from 80 to 140/ 38 to 69 mmHg. The heart rate ranged from 79 to 125 beats per minute (bpm). The patient received 160mcg of phenylephrine at induction,and received 10 mg of ephedrine and 240mcg of phenylephrine when her blood pressure dropped to 90/39 mmHg.
In recovery, the patient’s vital signs were as follows: blood pressure of 93/71 mmHg, heart rate of 104 beats per minute, respiratory rate of 19 breaths per minute, and an O2 saturation of 96% on room air. The patient’s vital signs were monitored continuously in the post anesthesia care unit. On discharge from the recovery room, her vitals were as follows: blood pressure of 136/69 mmHg, 98 bpm, 18 breaths per minute with a 96% O2 saturation on room air.
The patient’s hospital course was prolonged due to a tarsometatarsal fracture which required an open reduction internal fixation. Preoperatively, the patient’s vitals were as follows: blood pressure of 116/58 mmHg, heart rate of 101 bpm, 16 breaths per minute and saturating 94% on room air. Intraoperatively, the patient’s vital signs fluctuated, with her blood pressure ranging from 85 to 150/41 to 78 mmHg. Her heart rate ranged from 60 to 130 bpm. The patient received 80mcg of phenylephrine when her blood pressure dropped to 85/42 mmHg.
In recovery, the patient’s vital signs were as follows: blood pressure of 135/77 mmHg, heart rate of 95 beats per minute, respiratory rate of 24 breaths per minute, and an O2 saturation of 96% on room air. The patient’s vital signs were monitored continuously in the post anesthesia care unit. Her vitals were blood pressure of 123/74 mmHg, 89 beats per minute, 17 breaths per minute with a 96% O2 saturation on room air prior to discharge from the recovery room.
During her stay, her vital signs were within normal limits with the exception of episodes of sinus tachycardia as high as 119. The patient’s blood pressure was well controlled, and her systolic pressure never was higher than 140.
On post exploratory laparotomy day 3, the patient developed a headache and visual changes manifesting as central blurriness. Ophthalmology was consulted and attributed the cause of visual changes to macular edema. No intervention was recommended due to their belief that it would resolve on its own. The headache and visual disturbances persisted through day 7 and now progressed to right sided hemianopsia. An MRI of the brain, MRA of the head without contrast and MRA of the neck with contrast were ordered to rule out stroke and intracranial hemorrhage. The MRA of the head and neck showed no findings, however the MRI brain showed some patchy T2 areas and diffusion hyperintensity in the periphery of both occipital lobes and adjacent cerebellar hemispheres. These hyperintensities extended superiorly on the right side into the parieto-occipital junction while the left hyperintensity appeared to spread more inferiorly and laterally (See
). These findings were consistent with posterior reversible encephalopathy syndrome.
Over the next 3 days, the patient received an open reduction internal fixation for the tarsometatarsal fracture and was discharged to rehabilitation. The patient reports that her hemianopsia resolved in mid-July of 2018.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [125.0, 'lbs']}",96.699,91.86405,101.53395,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 125.0 lbs so this converts to 125.0 lbs * 0.453592 kg/lbs = 56.699 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (56.699 kg - 20 kg) = 96.699 mL/hr.
Hence, the patient's fluid maintenance is 96.699 mL/hr."
4839,22,Maintenance Fluids Calculations,physical,decimal,pmc-6935665-1,Extracted,"A 71-year-old man with a 50-year history of tobacco and alcohol abuse presented to the emergency department with a focal to bilateral tonic-clonic seizure, lasting 2-3 minutes, followed by drowsiness and confusion. He had a 6-month history of dysphagia, dyspnea, and 22-kg weight loss, along with hoarseness since last month. His past medical history was otherwise normal.
On examination, he was cachectic and had an evident inspiratory stridor and a painless forehead lump. Apart from that, chest X-ray and laboratory results were normal, except for an elevation of creatine kinase (553 IU/L) and white blood cell count (11.5 × 103/µL), probably due to the seizure.
Given a patient presenting with a first-ever seizure, and considering the possible existence of an underlying brain neoplasm due to smoking, drinking, and weight-loss patient's history, a brain computed tomography (CT) scan was obtained, showing a frontal osteolytic mass (Figure A) and ring-enhancing lesions in the left frontoparietal region (Figure B).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [22.0, 'kg']}",62,58.9,65.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 22.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (22.0 kg - 20 kg) = 62.0 mL/hr.
Hence, the patient's fluid maintenance is 62.0 mL/hr."
4840,22,Maintenance Fluids Calculations,physical,decimal,pmc-5540456-1,Extracted,"A 41-year-old woman (G3P2L2Ab1) was referred to gynecology clinic with chief complaints of abdominal distension and localized abdominal pruritus for three months. To rule out gastrointestinal disorders, she had visited a general physician given her symptoms. But she found no response to the drugs in spite of a long-term usage and was referred to our clinic after taking ultrasonography. Her past history showed menorrhagia but not menstrual irregularity and dysmenorrhea for several months. Laboratory tests including hemoglobin at 8 g/dl, hematocrit at 28,7%, ferritin at 6 ng/ml, and iron at 29 mcg/dl approved this claim but the patient had not expressed it initially as a complaint. Vital signs were in normal limits. In general appearance, the patient was not cachectic with full activity without vertigo, impairing appetite, constipation, nausea, vomiting, and urinary symptoms, but a distended abdomen that lacks rebound and tenderness. The origin of the mass was not detectable by vaginal examination. Ultrasonography had revealed a huge multicystic septated mass, 40 cm in diameter in abdominal cavity, probably a serous cystadenoma originating from ovary that was extended to epigastric area. Uterine and bladder were reported normal; however, these were impressed by extrinsic pressure of the mass. Uterine observation was not possible with vaginal sonography due to huge ovarian tumor. Tumor markers including cancer antigen-125, carcinoembryonic antigen, αFP, and CA19-9 were all within normal limits. Further assessment by computed tomography (CT) scan was done to show the nature of tumor which approved the diagnosis of ovarian serous cyst adenoma (); other viscera like kidneys, spleen, and liver were all in normal status; no free fluid and no lymphadenopathy were observed in abdominal cavity. Chest X-ray also did not show any lesion. The patient was hospitalized and advised with operation. The surgery was performed under general anesthesia through a vertical incision. Laparotomy revealed a huge multilocular mass with firm consistency, originating from pelvic with extension to adjacent tissues like ureter and upward to diaphragm with adhesion to ovaries and uterine. Obviously, gentle adhesiolysis to avoid damage to ureter and intestine took a long time. The whole solid-multicystic tumor measuring 40 cm and weighing 10 kg and with attached uterine and ovaries was removed (). Lymph nodes and other visceral organs were normal. Regarding previous chronic anemia of the patient, transfusion of two-packed cell-blood was done. Patient's weight was 82 kg before operation and 69 kg subsequently. Three days later, the patient was discharged in a good health status. Pathology report showed uterine leiomyosarcoma (). The CT scan for patient's follow-up presents no metastatic mass and lymph node involvement. The patient is under observation and has no problem in one year.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [82.0, 'kg']}",122,115.9,128.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 82.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (82.0 kg - 20 kg) = 122.0 mL/hr.
Hence, the patient's fluid maintenance is 122.0 mL/hr."
4841,22,Maintenance Fluids Calculations,physical,decimal,usmle-9594,Extracted,"A 13-year-old girl is referred to an oral surgeon after complaining of tooth pain, especially in the upper jaw. A review of her medical history reveals status post-surgical repair of a patent ductus arteriosus when she was 6 years old. At the clinic, her temperature is 37.0ºC (98.6°F), pulse is 90/min, respirations are 18/min, and blood pressure is 110/78 mm Hg. On physical examination, her height is 157.5 cm (5 ft 2 in), her weight is 50 kg (110 lb) and her arms seem disproportionately long for her trunk. She also has arachnodactyly and moderate joint laxity. Intraoral examination reveals crowded teeth and a high arched palate.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [50.0, 'kg']}",90,85.5,94.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 50.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (50.0 kg - 20 kg) = 90.0 mL/hr.
Hence, the patient's fluid maintenance is 90.0 mL/hr."
4842,22,Maintenance Fluids Calculations,physical,decimal,pmc-6694688-1,Extracted,"A 15-year-old girl was posted for cortical mastoidectomy with tympanoplasty for chronic suppurative otitis media under general anesthesia. She was thin built with body weight of 40 kg and body mass index 18 kg/m2, American Society of Anesthesiologists Physical Status (ASA-PS) I, with no significant family or personal medical history. Preoperative investigations were unremarkable. She was anxious about the surgery, for which she was counselled and advised oral diazepam 5 mg on the night before and 2 h prior to surgery.
The patient was still anxious when she arrived in the operation theatre, so she was again counselled and reassured. Anesthesia was induced with intravenous (IV) fentanyl 80 μg, propofol 80 mg and vecuronium 4 mg. After tracheal intubation, anesthesia was maintained with isoflurane in 50% oxygen in air, with supplemental doses of vecuronium to maintain muscle relaxation. Paracetamol 750 mg IV infusion and IV dexamethasone 4 mg was given after induction of anesthesia. During the 2 h of surgical period her vital signs were stable. Ventilation was adjusted to keep end tidal CO2 (ETCO2) between 35 and 40 mmHg. She received 600 ml of Ringers lactate intraoperatively, and the blood loss was insignificant. IV ondansetron 4 mg was given at the end of the surgery. After the completion of surgery, residual neuromuscular blockade was reversed with IV neostigmine 2 mg and glycopyrrolate 0.4 mg. Once she regained consciousness, obeyed commands, and had regular spontaneous respiration with adequate tidal volume, her trachea was extubated and she was shifted to the PACU. Supplemental oxygen at 5 L/min was provided via facemask.
After 15 min in the PACU, the patient complained of difficulty in breathing and became agitated. She started hyperventilating with deep breaths at the respiratory rate (RR) of 60–70 breaths/min. Her heart rate (HR) and blood pressure (BP) started to increase and reached a maximum of 180 beats/min and 180/70 mmHg respectively. Initially, we suspected it to be agitation due to pain and gave her fentanyl 20 μg IV bolus, but there was no improvement. We tried to support the ventilation using Bain’s circuit and anatomical face mask with oxygen flow at 10 L/min. Suspecting recurarization, 0.5 mg neostigmine and 0.1 mg glycopyrrolate IV was given. But her respiratory rate did not settle. So, we planned to sedate her with IV propofol 20 mg. She became calm with normal breathing pattern and her HR settled to 100–110 beats/min. But once the patient was awake from the effect of propofol, the symptoms reoccurred. Suspecting full bladder, bladder catheterization was done and urine was drained. As the symptom did not improve, IV propofol 20 mg was repeated. Although the symptom was relieved for a few minutes, she started to hyperventilate again after the effect of propofol wore off. This time, after an episode of hyperventilation, she developed apnea. She was unresponsive to verbal and painful stimuli. Oxygen saturation started to fall and reached up to 80%. Oxygenation and ventilation was quickly supported with bag and mask ventilation, limiting the RR to 10 breaths/min. After about 10 manual breaths, she resumed spontaneous respiration but soon started to hyperventilate. The series of hyperventilation, breath holding, desaturation, bag and mask ventilation and resumption of spontaneous respiration occurred for 3 cycles. Meanwhile, blood sample was sent for arterial blood gas (ABG) analysis. IV haloperidol 2.5 mg was given and repeated after 5 min. Finally, the patient became sedated and calm. HR settled to 90 beats/min and respiratory pattern normalized with RR of 14–16 breaths/min. Thirty minutes later, she regained consciousness. This time her respiratory pattern and vital signs continued to remain normal.
The ABG analysis revealed severe respiratory alkalosis with pH 7.672, pCO2 13.6 mmHg, pO2 129 mmHg, HCO3− 18.9 mEq/L, base excess − 1.7 mmol/L and lactate 3.1 mmol/L. Electrolytes and blood glucose were within normal range. She was shifted to ICU for monitoring and further management. Haloperidol 2.5 mg IV was advised as needed for recurrence of symptom. During her stay in ICU, she remained conscious, cooperative, and had stable vital signs. Deranged ABG returned to normal. When enquired later about her experience of the event, she remembered that she felt difficulty in breathing. Apart from that she did not have any intraoperative recall or any memory of events in the PACU.
Psychiatric consultation suggested a diagnosis of acute stress reaction. No significant personal or family history of conversion disorder, panic attack, schizophrenia, depression or mania was found. She was advised oral lorazepam at bedtime. The next day she was shifted to inpatient unit and discharged from the hospital on the third postoperative day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [40.0, 'kg']}",80,76,84,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 40.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (40.0 kg - 20 kg) = 80.0 mL/hr.
Hence, the patient's fluid maintenance is 80.0 mL/hr."
4843,22,Maintenance Fluids Calculations,physical,decimal,pmc-7323263-1,Extracted,"A 45-year-old man presented with polydipsia, polyuria, and weight loss for 6 months. Headache, dizziness, nausea, vomiting, blurred vision, and visual field defect were denied. His body mass index (BMI) was 28.7 kg/m2 with height of 170 cm and weight of 83 kg. No enlarged lymph nodes or swelling of salivary glands were noted. His past medical history included chronic obstructive pulmonary disease, obsolete tuberculosis, and thymic cyst surgery. He denied any history of autoimmune disease.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [83.0, 'kg']}",123,116.85,129.15,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 83.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (83.0 kg - 20 kg) = 123.0 mL/hr.
Hence, the patient's fluid maintenance is 123.0 mL/hr."
4844,22,Maintenance Fluids Calculations,physical,decimal,pmc-3899554-1,Extracted,"A 62-year-old non-diabetic, non-alcoholic male patient attended to our out-patient department with the complaint of dull aching pain in the right upper part of the abdomen. He was suffering from such pain since last 1 month. Pain responded to analgesic. He lost around 3 kg weight in last 1 month. He lost appetite also.
Abdominal ultrasonography was performed, which suggested HCC with ascites. Triple phase contrast enhanced computer tomography (CECT scan) revealed HCC of 12 cm × 15 cm size in segments 6 and 7 of liver []. Computer tomography also showed typical radiological characteristics of HCC (arterial enhancement of liver mass and wash out on delayed phase, arterioportal shunt [Figures –], portal vein thrombosis). There was gross ascites. No extravasation of dye seen. Ruptured tumor through liver capsule [] was seen with necrosis and hemorrhage in the center of the tumor.
Patient was admitted for evaluation. His blood pressure and heart rate was normal. Peritoneal tapping was performed for ascetic fluid analysis. Ascetic fluid was clear, exudative in nature with serum to ascetic fluid albumin gradient less than 1.1. Cytological examination ascetic fluid revealed no tumor cell.
On evaluation for chronic liver disease, all viral markers were negative. Upper gastrointestinal endoscopy showed non-bleeding grade II esophageal varices. On biochemical analysis of blood total and direct bilirubins were 1.98 and 0.48 respectively. Liver enzymes were raised (Aspartate transaminase-51 IU/ml and alanine amino transferase -55 IU/ml) with normal total protein and albumin. His hemoglobin was 12.4 g% and cell counts were normal. Alpha fetoprotein was high (424 ng/ml; normal range 0-8.5) and carcinoembryonic antigen was normal.
The disease was in advanced staged to be cured by surgery and portal vein thrombosis excluded TACE from treatment options; therefore, transarterial radioembolization was offered, but patient refused it.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.0, 'kg']}",12,11.4,12.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.0 kg. Hence, the patient's maintenance fluid is 3.0 kg * 4 mL/kg/hr = 12.0 mL/hr.
Hence, the patient's fluid maintenance is 12.0 mL/hr."
4845,22,Maintenance Fluids Calculations,physical,decimal,pmc-7369305-1,Extracted,"A 75-year-old male (American Society of Anesthesiologists physical status, class III; height, 176 cm; weight, 94 kg; body mass index, 30) presented for right total hip arthroplasty revision due to severe pain. His medical history was significant for diabetes mellitus type II (on insulin and metformin), hyperlipidemia, obstructive sleep apnea (non-compliant with CPAP therapy), and slowly progressive dementia (managed with donepezil; his caretaker is his wife). With respect to his dementia, the patient was diagnosed with mild cognitive impairment 6 years before surgery after taking the Montreal Cognitive Assessment test; however, his symptoms had gradually progressed to a moderate cognitive decline prior to surgery.
The following details the sequence of events: 1 year prior to surgery, his wife first noticed a change in the patient’s gait described as shuffling steps. Subsequently, 5 months prior to surgery, the patient started complaining of pain in his thighs and difficulty standing up from a seated position, and 2 months prior to surgery, the patient experienced several falls attributed to frequent tripping. A neurologist was consulted a few days prior to surgery for further evaluation. Physical exam revealed diffusely brisk deep tendon reflexes in upper and lower extremities (Mayo Clinic scale for tendon reflex assessment −4 to +4; + 1 (brisk) for biceps, brachioradialis, triceps, quadriceps with crossed adductor response, and Achilles reflexes) with negative Hoffman sign, Babinski sign absent on right and equivocal on left, and visible fasciculations of right external rotators, right deltoid, bilateral gastrocnemius and quadriceps muscles. Motor testing demonstrated mild motor weakness of upper (Medical Research Council scale for muscle power 0 to 5, Right Side/Left Side: external rotators 4/4, deltoid 4/5, biceps 4/5, triceps 4/5, wrist extension 4/5, wrist flexion 5/5, finger extension 4/4, interossei 4/4, abductor pollicis brevis 4/5) and lower extremities (Medical Research Council scale for muscle power 0 to 5, Right Side/Left Side: Iliopsoas 4/4, thigh adductor 5/5, thigh abductors 5/5, quadriceps 5/4, hamstrings 5/5, tibialis anterior 5/5, gastrocsoleus 5/5, foot inversion 5/5, foot eversion 4/4, toe extension 4/4, toe flexion 4/4). Sensory testing was notable for mildly decreased vibration and pinprick sensation in great toes. During gait testing, the patient was slow to stand up, unable to stand on his heels, and was walking with a slight wide-based stance with steppage on the left leg. The patient denied any problems with breathing, chewing, or swallowing. His speech and language were normal, palate elevation was symmetric, and there were no tongue fasciculation. Serology demonstrated an elevated creatine kinase levels up to 1825 U/L (reference level 39–308 U/L). Electromyography study showed neurogenic changes with active denervation in the cervical, thoracic, and lumbosacral segments. Magnetic resonance imaging revealed normal morphology of the spinal cord, conus medullaris, and cauda equina with mild to moderate cervical spondylosis and foraminal stenosis. Head computed tomography taken during evaluation for a recent fall showed mild brain parenchymal volume loss. Electrocardiogram demonstrated sinus bradycardia which was unchanged from a previous electrocardiogram 13 years prior. Given these findings, the patient’s clinical and pathological features were highly suspicious for ALS. Of note, he had a hip replacement 10 years ago at an outside hospital with no reported complications; however, the patient was unable to recall the type of anesthetic he received.
On the day of surgery, the patient appropriately fasted for at least 8 hours, and his vital signs were heart rate 97, blood pressure 152/93, oxygen saturation 96%, and respiratory rate 20. After a multidisciplinary team discussion involving the surgical and anesthesia team, the patient elected to have spinal anesthesia due to potential concerns of postoperative respiratory failure associated with ALS. In the operating room, an 18-gauge IV was established, and standard anesthetic monitoring was applied (5-lead electrocardiogram, blood pressure, pulse-oximeter, temperature, and capnography), and intravenous midazolam (2 mg) and fentanyl (50 mcg) were administered for sedation during the spinal procedure. A 1-liter fluid bolus of lactated ringers was administered during the regional anesthesia procedure. The patient was positioned in the lateral decubitus position, and an intrathecal injection of 1.8 mL of 0.75% isobaric bupivacaine was administered using a 22-gauge, 3.5-inch Whitacre needle at L3-L4 via midline approach under sterile conditions. During the surgical procedure the patient received mild sedation with a propofol infusion (10 to 30 mcg/kg/min) titrated to a Richmond Agitation-Sedation Scale of −1, and the patient was spontaneously breathing with a nasal cannula for oxygen support. Intravenous dexamethasone (4 mg), cefazolin (2 g), tranexamic acid (2 g), and ephedrine (25 mg in divided doses) were also administered intraoperatively. The surgeon performed a peri-articular block using a ropivacaine solution for postoperative analgesia., Surgery was uneventful with a total procedure time of approximately 2 hours. The patient remained hemodynamically stable (heart rate 60 to 70, respiratory rate 14 to 16, oxygen saturation 100%, non-invasive blood pressure mean 65 to 80, skin temperature 36°C) during the intraoperative period with minimal fluctuation in vitals for the exception of periodic low blood pressure readings which was responsive to small doses of ephedrine. In the recovery unit, the patient had minimal pain and he did not experience nausea. He was discharged from the recovery unit within 1 hour of arrival, and his vital signs prior to discharge was heart rate 78, blood pressure 158/86, respiratory rate 14, oxygen saturation 98% on room air, temperature 36.4 °C. Postoperatively, the patient was able to slowly ambulate and participate in physical therapy (Activity Measure for Post-Acute Care Inpatient Short Form during hospitalization: Basic Mobility Raw Score increased from 14 to 18, and Daily Activities Raw Score increased from 16 to 17). He was discharged from the hospital on postoperative day 7 to a skilled nurse facility for ongoing rehabilitation. No neurological complications were noted during his hospitalization and at a 6-month follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [94.0, 'kg']}",134,127.3,140.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 94.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (94.0 kg - 20 kg) = 134.0 mL/hr.
Hence, the patient's fluid maintenance is 134.0 mL/hr."
4846,22,Maintenance Fluids Calculations,physical,decimal,pmc-7544284-1,Extracted,"A 66-year-old female patient had no obvious cause of abdominal distension that started more than 3 years ago, and she experienced an increase in abdominal circumference (not controlled by diet); however, the patient was not admitted to the hospital for examination and treatment.
Recently, the patient felt that the bloating was aggravated, she could not be in a supine position, and she had difficulty breathing after physical activity. The patient chose to be admitted to the hospital.
The patient was usually healthy and had no other diseases. She was 161 cm tall, weighed 68 kg, and had an abdominal girth of 110 cm. She was G3P1A2. The admission test showed a cancer antigen (CA)125 level of 75.13 U/mL. Her hematological investigations were within normal limits, albumin 30 g/L and hemoglobin 109 g/L in the blood. Her liver, renal functions were also in normal values
The patient's urinary system ultrasound showed right hydronephrosis and right ureteral dilatation. A chest computerized tomography (CT) scan showed coronary calcification and left pleural effusion. The abdominal enhanced CT showed a bulky cystic mass that arose from the left ovary and occupied the whole abdominal and pelvic cavity (Fig. ). Her electrocardiogram showed sinus tachycardia. An examination of her cardiovascular system showed no abnormalities. Physical examination revealed mild edema of the lower extremity, and the patient reported that the urine volume decreased.
To prevent potential complications during the perioperative period, the gynecology team organized preoperative multidisciplinary teamwork (MDT) based on the patient's condition. The preoperative MDT included members of the gynecology, oncology, medical imaging, anesthesiology, urology, pathology, intensive care, and gastrointestinal surgery departments and operating room care units who convened before surgery to discuss the tumor pathology type, surgical technique, anesthesia protocol, physiologic considerations, assessment of other organ functions, postoperative recovery, and logistical support issues.
Considering the specific physical condition of the patient, we performed a full preoperative evaluation. Preoperative pulmonary function tests indicated restrictive impairment. On the basis of the assessment of the patient's condition and physical condition, we determined that the patient's was American Society of Anaesthesiologists (ASA) grade III.
Before surgery, 6 units of blood were ordered, and the availability of fresh frozen plasma and platelets was confirmed. The patient fasted from the day before surgery. Preoperative intramuscular injection of midazolam was treated as premedication in order to relieve the patient's anxiety. From admission to removing giant tumor, the patient received treatment in the mild left lateral position to avoid inferior vena cava compression (10∼20°). As prophylaxis against thromboembolism, the patient wore elastic support stockings before surgery.
Standard monitors were applied in the operating room. Noninvasive blood pressure (NIBP), bispectral index (BIS), and temperature monitors were connected. The baseline vital signs showed the following: BP: 128/88 mm Hg, heart rate (HR): 114 beats/min, breathing rate: 26 times/min, and body temperature: 36.3°C. A catheter was placed in the left radial artery and the right internal jugular vein under ultrasound guidance to monitor arterial blood pressure (ABP) and central venous pressure (CVP). We successfully performed epidural catheterization in the L1-2 segment of the lumbar spine for postoperative epidural analgesia.
Because heat loss was anticipated from the large surface area of the operation site, we used a heater to keep the patient warm. All intravenous fluids were warmed before administration. The operating theater temperature was maintained at 24°C, and the operating room doors were kept closed. The oropharyngeal temperature was measured continuously.
The patient with a large abdominal tumor could be treated as a full stomach. First, a dexmedetomidine infusion was administered for sedation at 1 μg/kg for 10 minutes along with 3 L/min O2 via a face mask, which was then followed by a rapid induction through a vein: etomidate: 20 mg, sufentanil: 15 μg, and rocuronium 42 mg with cricoid pressure. A tracheal tube with an internal diameter (ID) of 7.0 mm was successfully inserted under the guidance of a video laryngoscope. Intraoperative anesthesia was maintained by a continuous infusion of propofol according to the BIS target; sufentanil was added intermittently as needed to obtain a clinically adequate depth of anesthesia, and cisatracurium was continuously administered at 0.08 mg/kg/h. These drugs were chosen for their minimal and predictable effects on cardiovascular stability and their suitability for use during postoperative ventilation. We injected the patient with 50 mg flurbiprofen and 40 mg antiemetic ondansetron before the surgery was over.
After inducing anesthesia, the inspired oxygen fraction (FIO2) was 0.5. The tidal volume (TV) was set at 7 mL/kg predicted body weight with an initial respiratory frequency of 12 breaths/min and positive end-expiratory pressure (PEEP) of 5 cmH2O. The respiratory rate was adjusted to maintain an end-tidal carbon dioxide (PETCO2) of 35 to 45 mm Hg. The inspiratory/expiratory ratio was 1:2, and the patient's airway pressure was 23 cmH2O. Once an abdominal midline incision was made by the surgeon, the TV was reduced gradually by anesthesiologist to preventing pulmonary edema. During the operation, the patient's airway pressure further decreased and stabilized as the tumor fluid was expelled.
The patient's pulse and BP remained stable until the peritoneal cavity was opened and the was cyst punctured. After anesthesia was induced, a catheter was inserted into the tumor from the lower abdomen to discharge the ovarian contents, and the suction speed was set to 1 L/min. In total, 23 L liquid was extracted over 30 minutes. During fluid extraction, the patient's ABP gradually decreased.
To maintain a stable patent's cardiac output and stroke volume, dopamine was started at 15 μg/kg/min and was then tapered to 5 μg/kg/min after the BP had stabilized. During this period, ephedrine and norepinephrine was administered as appropriate.
During aspiration, although the patient's BP fluctuated greatly, the CVP changed insignificantly from 6 to 8 cmH2O. In addition, to prevent postoperative atelectasis, the PEEP was 5 cmH2O. The ventilator mode was set to pressure-controlled ventilation, and the same TV was maintained with a lower inspiratory pressure and PEEP to prevent re-expansion pulmonary edema (RPE). During the aspiration process, SpO2 was maintained at approximately 100%; draining the tumor fluid improved respiratory compliance, and the patient slowly lifted her head. In the process of removing the ovarian tumor, broad adhesiolysis between the tumor wall and abdominal wall required a long period time and resulted in excessive blood loss. After the tumor was removed, persistent bleeding and low ABP and CVP were observed. After a period of fluid resuscitation and the use of vasoactive drugs, the blood volume was gradually restored, and the HR, arterial pressure and CVP began to return to normal values. To prevent critical intestinal distension and facilitate breathing, an abdominal binder was applied postoperatively, and the patient returned to the intensive care unit (ICU) with an endotracheal tube (Fig. ). During the operation, the patient's oropharyngeal temperature was in the normal range, and the acid-base balance and electrolyte of the blood gas analysis were normal after transferred to the ICU. Pathologically, the tumor was a mucinous cystadenoma of the left ovary. Intraoperative blood loss was estimated at 1000 mL, 3U RBC, 500 mL fresh frozen plasma, 2000 mL crystal solution, and 500 mL colloidal solution were injected. The duration of surgery was 300 minutes.
Postoperatively, the patient was transferred to the ICU for further monitoring. We used multimodal analgesia after surgery: epidural analgesia assisted nonsteroidal anti-inflammatory analgesics. To avoid RPE, ventilation was provided with an inspiratory pressure of 18 cmH2O and PEEP of 8 cmH2O, which resulted in a TV of 400 mL. After the patient recovered to spontaneous respiration, she was ventilated with pressure support and PEEP to maintain a TV of 350 to 400 mL. Her respiratory status was good thereafter. The patient was able to generate TVs of 500 mL. The arterial oxygen tension (PaO2) was 12 kPa with an inspired oxygen concentration of 30%. The tracheal catheter was removed on postoperative day 2. The postoperative chest X-ray showed no evidence of lung oedema.
After the drainage of large ovarian cysts during surgery, patients are prone to developing RPE postoperative. Therefore, the CVP, arterial pressure, and pulse rate were monitored continuously. Daily estimations of hemoglobin, urea, electrolytes, and serum albumin were made. The patient's basic vital signs remained stable after surgery. In the ICU, we monitored the patient's body temperature, and her armpit temperature was 37.5°C. The arterial blood gas analysis demonstrated normal acid-base balance.
The patient returned to the general ward on postoperative day 3. The epidural catheter was removed before the patient returned to the ward. As patients are at high risk for perioperative thrombosis, low-molecular-weight heparin was administered by subcutaneous injection for symptomatic treatment starting on the third postoperative day.
In addition to low-grade fevers caused by atelectasis, the patient felt considerable abdominal distention on postoperative day 7 and underwent abdominal enhanced CT, which showed a large amount of gas in the abdominal cavity (Fig. ). As we believed that the patient may have intestinal distension, even though the patient was on a liquid diet, the patient was given a diet restriction. Abdominal distension and abdominal pain were improved by fasting, inserting a nasogastric tube, injecting omeprazole and somatostatin. On postoperative day 10, the patient's abdominal distension significantly improved compared with her previous condition. After a period of observation, the patient was in stable condition, and was discharged 22 days after surgery and was followed up regularly.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [68.0, 'kg']}",108,102.6,113.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 68.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (68.0 kg - 20 kg) = 108.0 mL/hr.
Hence, the patient's fluid maintenance is 108.0 mL/hr."
4847,22,Maintenance Fluids Calculations,physical,decimal,pmc-5497433-2,Extracted,"On December 14, 2015, a 34-year-old man was transferred to our department due to the sudden onset of upper abdominal pain for one day. He had a history of hepatitis B virus infection. He denied any history of alcohol or drug abuse. At his local hospital, laboratory tests were performed on December 13, 2015, demonstrating that the white blood cell count was 10.3 × 109/l, neutrophil percentage was 81.3%, serum amylase was 67 U/l (reference range at his local hospital: 40-129 U/l), and serum lipase was 167.2 U/l (reference range at his local hospital: 0-60 U/l). Additionally, based on the findings of CT scans, acute pancreatitis was also suspected. Nasogastric tube insertion, antibiotics, protease inhibitors, and fluid therapy were given.
On admission, physical examinations demonstrated that his weight was 79 kg, height was 175 cm, heart rate was 76 times/min, temperature was 36.5°C, blood pressure was 143/97 mmHg, respiratory rate was 17 times/min, and upper abdominal tenderness was positive without any rebound or tension. On December 14, 2015, blood tests were performed. White blood cell count was 7.6 × 109/l, neutrophil percentage was 61.0%, platelet count was 139 × 109/l, serum amylase was 38.6 U/l (reference range: 22-80 U/l), serum lipase was 235 U/l (reference range: 23-300 U/l), C-reactive protein was 73.6 mg/l (reference range: 0-8 mg/l), fasting glucose was 14.25 mmol/l (reference range: 3.9-6.1 mmol/l), triglyceride was 15.03 mmol/l (reference range: 0.45-1.7 mmol/l), cholesterol was 7.71 mmol/l (reference range: 2.85-5.7 mmol/l), procalcitonin was 0.091 ng/ml (reference range: 0-0.05 ng/ml), total bilirubin was 14.9 μmol/l (reference range: 5.1-22.2 μmol/l), alanine aminotransferase was 14.9 μmol/l (reference range: 5.1-22.2 μmol/l), alkaline phosphatase was 73.00 U/l (reference range: 45-125 U/l), albumin was 43.7 g/l (reference range: 40-55 g/l), creatinine was 73.39 μmol/l (reference range: 44-133 μmol/l), and prothrombin time was 12.2 s (reference range: 11.5-14.5 s). HBsAg, HBeAb, and HbcAb-IgG were positive, and HBV DNA was 3.2 × 103 copies/ml (reference range: < 1.0 × 103 copies/ml). Non-enhanced CT scans demonstrated that the pancreatic edge was coarse and peripancreatic fat was vague, suggesting mild acute pancreatitis related to hypertriglyceridemia. Additionally, the ratio of liver to spleen density in CT scans was less than 0.5, suggesting the presence of severe fatty liver disease (). Lipid- and glucose-lowing treatment was also added.
On December 16, 2015, abdominal pain was rapidly alleviated. Blood tests were performed again. White blood cell count was 7.0 × 109/l, neutrophil percentage was 66.7%, serum amylase was 42.6 U/l (reference range: 22-80 U/l), serum lipase was 78 U/l (reference range: 23-300 U/l), fasting glucose was 8.21 mmol/l (reference range: 3.9-6.1 mmol/l), triglyceride was 5.48 mmol/l (reference range: 0.45-1.7 mmol/l), and cholesterol was 7.13 mmol/l (reference range: 2.85-5.7 mmol/l). Liver and renal function remained within the normal range.
On December 21, 2015, abdominal discomfort completely disappeared. Serum amylase was 49.5 U/l (reference range: 22-80 U/l), serum lipase was 171.0 U/l (reference range: 23-300 U/l), fasting glucose was 7.70 mmol/l (reference range: 3.9-6.1 mmol/l), triglyceride was 3.19 mmol/l (reference range: 0.45-1.7 mmol/l), and cholesterol was 6.43 mmol/l (reference range: 2.85-5.7 mmol/l). Thus, he was discharged without any complaints.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [79.0, 'kg']}",119,113.05,124.95,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 79.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (79.0 kg - 20 kg) = 119.0 mL/hr.
Hence, the patient's fluid maintenance is 119.0 mL/hr."
4848,22,Maintenance Fluids Calculations,physical,decimal,pmc-7322153-1,Extracted,"A 10-year-old boy with a background of double inlet left ventricle, pulmonary atresia, atrial septal defect, and a right aortic arch originally presented to cardiology at 8 months of life due to chronic respiratory issues and cyanosis. He proceeded to have a bidirectional Glenn procedure and completed a total cavopulmonary connection via an extracardiac fenestrated Fontan surgery at 3 years and 10 months.
His last outpatient visit was 1 month prior to developing COVID-19, at which point, his oxygen saturations were 98%, heart rate 83 bpm, and blood pressure (BP) 124/60. His weight was 78.23 kg, height was 150.2 cm2, and BMI 34.7 kg/m2 (>99.6th centile).
He was initially presented to his local hospital with symptoms of fever, red eyes, lethargy, and mild cough. His initial presentation was prompted as his parents were positive for SARS-COV-2 and his contact tracing swab was positive. He was well with normal saturations and was discharged home. He re-presented 4 days later with increased work of breathing, worsening cough, and persistent fever. He had an oxygen requirement (0·5 L/min) at this stage to maintain oxygen saturations >90%.
On day 7 of his illness, he deteriorated requiring an increase in his oxygen requirement to 1 L/min, and his chest x-ray showed significant left mid and lower zone consolidation (Fig ). He was commenced on intravenous cephalosporin and oral macrolide antibiotics. There had been ongoing liaison since his initial presentation with paediatric cardiology and respiratory specialists, and it was decided with the deterioration to transfer to a tertiary paediatric hospital.
His oxygen requirement increased to a peak of 3 L/min from day 8 to 10 of illness. His chest x-ray, however, on day 9 was unchanged (Fig ). His full blood count showed haemoglobin 125 g/L, platelets 144 × 109/L, and total white cell count 2.4 × 109/L with neutrophils 1.67 × 109/L and lymphocytes 0.56 × 109/L. His C-reactive protein was 13. He had a normal renal profile and normal liver profile. Further escalation of ventilatory support was not required, and he remained at ward level care for the duration of his admission. Intravenous antibiotics were stopped after 7 days, and no further medicines were prescribed. He was transferred back to his local hospital on day 14 of his illness self-ventilating in room air prior to his discharge home.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [78.23, 'kg']}",118.23,112.3185,124.1415,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 78.23 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (78.23 kg - 20 kg) = 118.23 mL/hr.
Hence, the patient's fluid maintenance is 118.23 mL/hr."
4849,22,Maintenance Fluids Calculations,physical,decimal,pmc-2769385-1,Extracted,"A previously fit and healthy 34-year-old middle eastern Kuwaiti female presented with right lower quadrant pain of four days duration radiating to the back. It was associated with nausea and vomiting. She was a house wife and married with four healthy children. She had a recent urinary tract infection treated with antibiotics. She had an intrauterine contraceptive device (IUCD) and gave a history of brownish vaginal discharge. There was no family history of relevance. On examination she was febrile (38 degrees Celsius). Her weight was 90 kilograms and her height was 160 cm. Abdominal examination revealed tenderness and guarding in right iliac fossa (RIF) and right lumber region. Her laboratory investigation showed a leucocytosis with normal urine routine microscopy. Her liver function test and C-reactive protein was normal.
Abdominal ultrasound showed a thin rim of free intra-abdominal fluid in RIF with no masses or localized collection. A trans-vaginal ultrasound showed normal ovaries with an IUCD in situ. We proceeded with diagnostic laparoscopy which revealed serous collection in the right side of the abdomen with a normal-looking appendix. Her caecum was noted to be inflamed. The procedure was then converted to laparotomy through a lower mid-line incision which revealed an inflamed caecal wall with localized perforation. There were no masses palpable in the lumen. We performed an ileocaecal resection with side to side anastomosis.
Postoperative recovery was smooth with no complications and the patient was discharged home on 6th postoperative day. She remained well three months later. Histologically, there was a marked acute inflammatory exudate around the caecum forming an inflammatory mass (). A residual diverticulum was seen within the inflammatory mass with pieces of colon contents and fecal material seen within pericolic fat indicating site of perforation (). The colon, terminal ileum and appendix were unremarkable.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [90.0, 'kg']}",130,123.5,136.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 90.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (90.0 kg - 20 kg) = 130.0 mL/hr.
Hence, the patient's fluid maintenance is 130.0 mL/hr."
4850,22,Maintenance Fluids Calculations,physical,decimal,pmc-8399293-1,Extracted,"This 27-year-old Saudi male was not known to have any medical illness; he presented to the emergency department with a history of epigastric pain that started two days before admission. The pain was continuous, started suddenly with severity of 10/10 according to the patient with no diurnal variation or radiation. Moreover, it was sharp in nature, aggravated by movement and relieved by rest. The pain was associated with nausea and vomiting (gastric content). There was no history of change in bowel habits, urine, nor cardiopulmonary symptoms. The patient consumes alcohol on rare occasions, approximately one to two cups per month, and is known to be a smoker. The patient denied any history of abdominal trauma, scorpion bites, current medication use, or previous similar complaint. Family history was insignificant of autoimmune disease, inherited diseases, or similar complaints. The patient's surgical history was unremarkable. The patient was known to have morbid obesity, for which he underwent a minimally invasive procedure; an IGB was inserted seven months ago. As a result, he lost 17 kg, from 98 kg to 81 kg.
On examination, the patient was hemodynamically and vitally stable. The abdominal examination revealed severe epigastric tenderness, with typical bowel sounds and soft lax consistency in other regions. Systemic examination was unremarkable.
On investigations, laboratory, complete blood count, renal and liver function tests were within normal limits. Amylase and lipase were above the average level with the values of 327 and 2,000, respectively (Table ). Imaging showed ultrasound was nil for gallbladder stones and common bile duct dilatation. CT scan of the abdomen showed necrotizing pancreatitis with compression of the pancreas by IGB (Figure ).
The patient was treated conservatively under nothing per oral, intravenous fluids, antiemetics, and analgesia. The patient improved clinically and was discharged after three days of hospitalization without the removal of IGB.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [81.0, 'kg']}",121,114.95,127.05,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 81.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (81.0 kg - 20 kg) = 121.0 mL/hr.
Hence, the patient's fluid maintenance is 121.0 mL/hr."
4851,22,Maintenance Fluids Calculations,physical,decimal,pmc-6671882-1,Extracted,"A 36-week-gestation male neonate weighing 2230 g was born to a 29-year-old female patient, primipara, by vaginal labor induced with oxytocin. The mother’s medical history was unremarkable, except for two episodes of urinary tract infection and a morphologic ultrasound examination at 19 weeks’ gestation showing exencephaly, medial labial cleft, and edema. After a breech delivery with a laceration of the umbilical cord during birth, a neonate with multiple malformations was born, with an Apgar score of 8/9/9. The neonate was referred to the neonatal ICU for palliative care. The parents were aware of the prognosis, with the malformations being incompatible with life. The karyotype analysis was normal, 46 XY (20 cells analyzed). During the ICU stay, the neonate was placed in a heated crib, prescribed serum, analgesic, fentanyl, and midazolam. The physical examination presented heart rate of 180 beats per minute and room air oximetry of 100%. The newborn evolved with grunting and died with 29 hours. An autopsy was performed.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2230.0, 'g']}",8.92,8.474,9.366,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2230.0 g so this converts to 2230.0 lbs * kg/1000 g = 2.23 kg. Hence, the patient's maintenance fluid is 2.23 kg * 4 mL/kg/hr = 8.92 mL/hr.
Hence, the patient's fluid maintenance is 8.92 mL/hr."
4852,22,Maintenance Fluids Calculations,physical,decimal,pmc-3223352-1,Extracted,"A previously healthy 5-month-old female infant was brought to the emergency department for progressive proptosis. Her parents denied any history of trauma or fever episode in the previous 1 month, and there was no regular medication being taken. She was a full-term infant without any birth defects, and vaccinations were received regularly. Physical examination revealed a well-developed infant with a weight of 3,200 g, a pulse of 100 beats per minute, a respiratory rate of 24 per minute, and a temperature of 36°C. Her left periorbital region showed swelling, redness, and tenderness to palpation. In addition, the conjunctiva of the left eye was swollen, and increased tears were observed (Fig. ). Laboratory investigations revealed a white blood cell count of 36,100/μL and a C-reactive protein of 42.5 mg/dL. Soft tissue infection of the left periorbital region was suspected, and therefore, the patient underwent an orbital computed tomography (CT) scan. CT images demonstrated a heterogenous lesion in the left orbit with adjacent soft tissue swelling (Fig. ) and opacified left ethmoid and maxillary sinuses, which was diagnosed as an orbital abscess and sinusitis of the ethmoid and maxillary sinuses.
The patient underwent decompression surgery of the left orbit using an external approach, and 10 ml of pus was drained out. Bacteriological culture of the pus revealed MRSA, and the results from blood culture were negative. After a 10-day course of intravenous vancomycin treatment, the patient was discharged home without permanent visual damage upon follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3200.0, 'g']}",12.8,12.16,13.44,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3200.0 g so this converts to 3200.0 lbs * kg/1000 g = 3.2 kg. Hence, the patient's maintenance fluid is 3.2 kg * 4 mL/kg/hr = 12.8 mL/hr.
Hence, the patient's fluid maintenance is 12.8 mL/hr."
4853,22,Maintenance Fluids Calculations,physical,decimal,pmc-5586030-1,Extracted,"A 2280-g Hispanic preterm female was born at 32 weeks of gestation to a 29-year-old gravida (G) 2 para (P) 1 woman by spontaneous vaginal delivery. At delivery, the AF was noted to be “meconium stained.” A total of 35 mL of greenish AF was aspirated from the baby’s stomach (Fig. ). She had Apgar scores of 9 and 9 at 1 and 5 minutes respectively. The pregnancy was significant for prenatal diagnosis of small bowel obstruction at 31 weeks of gestation. A physical examination revealed a weight of 2280 g (85th centile), length of 48 cm (95th centile), and head circumference of 29 cm (40th centile). She did not have any respiratory distress and there was no abdominal distension. An additional 35 mL of greenish fluid was aspirated from her stomach in the neonatal intensive care unit (NICU). She had her first bowel movement at 48 hours of age; the stool appeared sticky and white (Fig. ). An upper gastrointestinal (UGI) series and a Gastrografin (sodium diatrizoate and meglumine diatrizoate) enema showed jejunal atresia and microcolon. She underwent exploratory laparotomy on the 3rd day of life. An intervening segment was noted between the two proximal jejunal atresias measuring approximately 10 cm. The jejunal atretic segment was resected and a tapering enteroplasty of that jejunal segment was performed. Her postoperative course was uneventful; she was discharged home at 31 days of age.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2280.0, 'g']}",9.12,8.664,9.576,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2280.0 g so this converts to 2280.0 lbs * kg/1000 g = 2.28 kg. Hence, the patient's maintenance fluid is 2.28 kg * 4 mL/kg/hr = 9.12 mL/hr.
Hence, the patient's fluid maintenance is 9.12 mL/hr."
4854,22,Maintenance Fluids Calculations,physical,decimal,pmc-8171158-1,Extracted,"An 83-year-old female underwent perspective endoscopic nephroureterectomy; lymphadenectomy at the hilum of the kidney; and partial bladder resection for right advanced renal pelvis, ureteral cancer, and bladder cancer 10 months ago. The pathology report showed that the right renal pelvis and ureteral were invasive urothelial carcinoma and noninvasive high-grade papillary urothelial carcinoma, respectively. She had relapsing urothelial carcinoma in the urinary bladder 6 months prior. She underwent posterior spinal fusion and received radiation therapy for spine metastasis 4 months ago.
Liver metastasis was observed 3 months ago. She initiated chemotherapy with the one-cool combination of gemcitabine and carboplatin 2 months ago, and stopped this combination therapy due to the elevation of biliary enzyme and the judgment of progressive disease (PD) using Response Evaluation Criteria in Solid Tumors (RECIST) criteria. She received 200 mg pembrolizumab therapy 1 month ago. Due to liver failure with severe transaminase elevation and coagulopathy, she was admitted to our hospital. To our surprise, she was asymptomatic without complaint and was fully conscious and alert. Her body length, body weight, and body mass index were 1.48 m, 66.9 kg, and 30.7 kg/m2, respectively. Her body temperature, blood pressure, pulse rate, and blood oxygen saturation (at room air) were 36.4°C, 127/60 mmHg, 73 beat per minute, and 96%, respectively. She had no anemia, jaundice, or abnormal findings on chest or abdomen. She had slight edema and a scar from the operation on both legs and her back, respectively. Her performance status was Grade 2, according to the Eastern Cooperative Oncology Group (ECOG) performance status classification.
She had a history of cataract, hypertension, ovarian cyst, and boundary intelligence. She was not a drinker of alcohol or a smoker. Her family history was as follows: her father, cerebral infarction; her brother, gastric cancer; and her sister, uterine cancer. She had taken several drugs: amlodipine besilate (5 mg daily), lafutidine (20 mg daily), tramadol hydrochloride (37.5 mg/tablet) acetaminophen (325 mg/tablet) (four tablets daily), mirogabalin besilate (20 mg daily), celecoxib (200 mg daily), precipitated calcium carbonate, cholecalciferol, magnesium carbonate (two tablets daily), and furosemide (20 mg daily). She had also taken ursodeoxycholic acid (UDCA) 300 mg daily and glutathione 150 mg daily for biliary enzyme elevation due to the combination treatment of gemcitabine and carboplatin. She had no history of drug allergy.
Her laboratory data on admission to our department are shown in Table , Figure A, B. Marked elevation of serum transaminase and coagulopathy were noted. The chest X-ray showed no lung metastasis. The electrocardiogram and echocardiogram showed no sign of heart diseases. Findings of computed tomography (CT) and abdominal ultrasound showed multiple liver metastases with mild ascites (Fig. C). Magnetic resonance cholangiopancreatography (MRCP) did not show dilatation of the bile duct (Fig. D). Therefore, the diagnosis was liver failure with liver metastasis and ICI-induced hepatitis associated with the use of pembrolizumab as an acute insult.
As hepatic toxicity was Grade 3, according to the Common Terminology Criteria for Adverse Events (CTCAE) v5.0 classification, we stopped using pembrolizumab and administered 40 mg daily prednisolone. On day 22, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were improved. However, on day 37, she died due to primary disease.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [66.9, 'kg']}",106.9,101.555,112.245,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 66.9 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (66.9 kg - 20 kg) = 106.9 mL/hr.
Hence, the patient's fluid maintenance is 106.9 mL/hr."
4855,22,Maintenance Fluids Calculations,physical,decimal,pmc-6967019-1,Extracted,"A 75-year-old man (height 165 cm, weight 63 kg) was scheduled to undergo his third TURBT. For prostatic hyperplasia, he was prescribed 5α-reductase inhibitor. Preoperative examinations were within the normal ranges. Systolic blood pressure (S-BP) was about 140 mmHg at home. On the patient’s request, general anesthesia was planned. On the day of the operation, the BP was 139/82 mmHg. A nitroglycerin transdermal patch (nitroglycerin 25 mg) was used at the start of preoperative crystalloid infusion (100 mL/hr) as a routine medication against perioperative myocardial ischemia. For the first time in his life, the patient took a 5-ALA (1.5 g) solution 3 h before TURBT but felt sick afterwards. About 2 h later, the patient walked to the lavatory, but upon returning, he could not sit by himself and had a severe staggered feeling and nausea. Although his S-BP was 42 mmHg, he was fully conscious. The patient had cold sweats and a pulse rate (PR) of 70–80 bpm, but other skin symptoms were absent. The blood glucose level was 146 mg/dL. Placing the patient in the Trendelenburg position with fluid resuscitation brought recovery from the shock. Before entering the operating room, the BP and PR were 96/55 mmHg and 67 bpm, respectively. General anesthesia was induced with atropine (0.5 mg), propofol (80 mg), and rocuronium (30 mg). Anesthesia was maintained with sevoflurane (1.0–1.5%) and remifentanil (100–300 μg/h). Although ephedrine (total dose 15 mg) and phenylephrine (total dose 0.2 mg) were necessary to maintain S-BP above 80 mmHg, abnormal hypotension did not develop during the PDD surgery. The operation was completed without any incident, and the postoperative course was uneventful. However, the pathology report suggested the need for a future PDD surgery. With the nitroglycerin patch attached, the hypotension seemed non-ischemic. Although the nitroglycerin patch could have affected the preoperative BP, it was difficult to conclude that the patch caused the severe hypotension.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [63.0, 'kg']}",103,97.85,108.15,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 63.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (63.0 kg - 20 kg) = 103.0 mL/hr.
Hence, the patient's fluid maintenance is 103.0 mL/hr."
4856,22,Maintenance Fluids Calculations,physical,decimal,pmc-5457868-1,Extracted,"The patient was a 5-year-old Chinese woman. She presented to the emergency department with complaints of cough for 2 weeks and fever for 5 days. She also had headache, vomiting, and altered interactions with her parents for 1 day. She was admitted to the pediatric intensive care unit. She hailed from a large island in East China Sea (6-hours drive to the mainland city center). She had an uncomplicated birth and roughly normal growth during the first 3 years of life but retarded height growth and decreased activity in the recent 2 years (as reported by her parents) without further medical assessment. The patient had no history of medication. On physical examination, the patient's height and weight were 109 cm and 22 kg (z = 0.5 and −1, respectively). Her vital signs included temperature of 38.7 °C, heart rate of 105 beats per minute, respiratory rate of 35 breaths per minute, and blood pressure of 90/55 mmHg. Her oxyhemoglobin saturation was 90% in room air. She showed generalized puffiness and non-pitting edema of the face and extremities capillary refilled time was >3 seconds (Fig. ). Rales were found on the auscultation of both lungs. The cardiac auscultation was normal. Her abdomen was soft, mildly distended with normal bowel sounds. Neurological examination revealed that the patient was slightly confused and could not properly respond to commands.
Additional laboratory examinations were conducted immediately after admission. A complete blood count showed hemoglobin level of 97 g/L, white blood cell count of 2.5 × 109/L, with 70% neutrophils and blood platelet was 75 × 109/L. The levels of electrolytes, glucose, albumin, and creatine kinase were normal. The blood gas was also normal at admission. Chest computed tomographic (CT) scan confirmed left lobe pneumonia and mild pleural effusion (Fig. ). The echocardiogram showed mild pericardial effusion with normal cardiac ejection fraction. The magnetic resonance imaging (MRI) scan of the brain and cerebrospinal fluid exam was normal. The patient was initially diagnosed as pneumonia and sepsis. Empiric antibiotic therapy, immunoglobulin supply (IVIG 2 g/kg) as immune supportive therapy, and restricted fluid administration were given immediately after admission.
Her mental status subsequently deteriorated. She became comatose on the second day after the admission, her temperature dropped to 35 °C. She also developed hypotension, arrhythmia, and hypoxia with SaO2 decreased to 75% (Fig. ). Electrocardiogram confirmed prolonged Q–T interval (Fig. ). Thyroid studies were ordered at admission due to the retarded growth. The thyroid test results were received on the next day while the patient developed coma. Thyroxin (T4) was undetectable in the plasma (reference range, 58.1–140.6 nmol/L, Table ). The thyroid stimulating hormone (TSH) level was extremely high (>150 uIU/mL; reference range, 0.55–4.78 uIU/mL). Laboratory results revealed extremely elevated anti-thyroid peroxidase (TPO-Ab) and anti-thyroglobulin (TgAb) levels in plasma (Table ) after 2 days. Ultrasound of the thyroid revealed mild bilateral enlargement with small tubercles in the left side.
The patient was diagnosed with MC complicated with untreated hypothyroidism on the second day after her admission. The thyroid test indicated that the hypothyroidism was secondary to autoimmune thyroiditis (Hashimoto's thyroiditis). Hormone replacement was immediately started. Intravenous dexamethasone at a dosage of 0.3 mg/kg/d divided every 12 hours was administered for the stressed state early morning on the second day of admission. Later that day, once the thyroid test results were obtained, oral levothyroxine was administered at a dose of 100 μg/m2/d (4 μg/kg/d) once daily by nasogastric tube. The patient also received vasopressor, mechanical ventilation, and continuous renal replacement treatment for hypotension, hypoxemia, and anuria, respectively. Two days after starting levothyroxine, her consciousness was restored and temperature returned to normal. She was extubated on the fifth day after the initial hormone administration (Fig. ).
The dosage of oral levothyroxine was reduced to 3 μg/kg/d once daily 2 weeks after initial administration (Fig. ). She was discharged on this regimen and continues to do well (Fig. ).
Eight months after discharge, her height reached 118 cm, and had increased 9 cm since the initial hormone therapy. She was also reported to be more active than before. Her family was recommended to undergo thyroid tests. Her father and grandmother were confirmed with Hashimoto's thyroiditis as well.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [22.0, 'kg']}",62,58.9,65.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 22.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (22.0 kg - 20 kg) = 62.0 mL/hr.
Hence, the patient's fluid maintenance is 62.0 mL/hr."
4857,22,Maintenance Fluids Calculations,physical,decimal,pmc-5104873-2,Extracted,"A 25-year-old, 60-kg male patient was scheduled to undergo high Le Fort I osteotomy, BSSO, genioplasty, and malar augmentation for a mandibular prognathism with midface deficiency. His medical history was unremarkable except for a history of pneumonia two years previous. The patient was taking no medications and reported no allergies. The preanesthetic evaluation findings were all normal.
He was not premedicated, and his preanesthetic vital signs were BP of 128/70 mmHg, HR of 98 bpm, and SpO2 of 99%. General anesthesia was induced with intravenous thiopental sodium (300 mg), 2% lidocaine (60 mg), rocuronium (50 mg), and remifentanil (0.15 µg/kg/min), and nasotracheal intubation was performed. General anesthesia was maintained with sevoflurane (1.5-2.5 vol%), O2 (1.5 L/min), N2O (1.5 L/min), and remifentanil (0.05-0.13 µg/kg/min). After radial artery catheterization, the patient's first ABGA results were pH 7.44, PaO2 350 mmHg, PaCO2 37 mmHg, HCO3– 25.1 mEq/L, BE 0.9 mEq/L, glucose 95 mg/dL, lactate 1.6 mmol/L, and normal electrolytes.
Submucosal infiltration of 2% lidocaine with 1:100,000 epinephrine was performed in the upper vestibular area before the first surgical incision. During the operation, an additional injection was administered in the lower vestibule before each surgical incision. In all, 18 mL of 2% lidocaine along with 1:100,000 epinephrine (180 µg epinephrine) were injected submucosally. In addition, gauze soaked with 25 mL of 0.01% epinephrine was used for dense packing at the bleeding site in the operative field until the bleeding stopped. Intraoperatively, the patient's vital signs were BP of 105-140 mmHg/50-70 mmHg and HR of 95-110 bpm. However, the patient's BP and HR increased to 160-170 mmHg/65-100 mmHg and 105-128 bpm, respectively, after intermittent injections of lidocaine containing 1:100,000 epinephrine. To maintain stable vital signs, a calcium channel blocker and dose increases of remifentanil were applied.
One hour after the first incision, the ABGA was pH 7.3, PaCO2 43 mmHg, PaO2 296 mmHg, HCO3– 21.2 mEq/L, BE –5.2 mEq/L, glucose 277 mg/dL, and lactate 5.3 mmol/L. These findings implied the presence of lactic acidosis and hyperglycemia. After the first hour, ABGA measurements were repeated at one-hour intervals during the procedure. The ABGA results worsened over time, showing maximum change three hours after the surgery began. The pH, HCO3–, and BE decreased to pH 7.29, 18.3 mEq/L, and –8.3 mEq/L, respectively, while the glucose and lactate increased to 331 mg/dL and 9.9 mmol/L. The surgery was successful, and the patient was transferred to the ICU in a sedated and intubated state. Serial ABGA findings subsequently improved dramatically and returned to normal two hours after the end of the surgery with fluid resuscitation.() He was extubated 19 hours after surgery end and discharged from the hospital with no complications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.0, 'kg']}",100,95,105,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.0 kg - 20 kg) = 100.0 mL/hr.
Hence, the patient's fluid maintenance is 100.0 mL/hr."
4858,22,Maintenance Fluids Calculations,physical,decimal,pmc-8716636-1,Extracted,"A 60-year-old Black male with a past medical history of HIV infection with a CD4 T cell count of 351 cells/mm3 on HAART, HIV encephalopathy, hyperthyroidism, BMI 18.2 kg/m2 (height 1.7 cm and weight 52 Kg) with no previous history of lung disease such as chronic obstructive pulmonary disease (COPD) or opportunistic disease documented and no active smoking or respiratory disease presented to the hospital due to worsening confusion, cough, and generalized weakness. Initial vital signs included temperature of 36.9°C, blood pressure (BP) 95/77 mmHg, heart rate (HR) 110 beats/min, respiratory rate (RR) 18 breaths/min, and oxygen saturation of 97% on room air.
On physical exam, the patient was noted to be frail, tachycardic, and demonstrated appreciable scattered rhonchi on auscultation. Laboratory testing was remarkable for leukocytosis 11.6 K/μL (normal 4.8–10.8 K/μL), D-Dimer 4 μg/ml (normal <0.4 μg/ml), fibrinogen 980 mg/dL (normal 196–493 mg/dL), erythrocyte sedimentation rate (ESR) 76 mm/h (normal 0–20 mm/h), C-reactive protein (CRP) 26 mg/L (normal 0–0.6 mg/L), lactate dehydrogenase (LDH) 322 u/L (normal 140–280 u/L), CD4 T cell count 351 cells/mm3 (normal 500–1,500 cells/mm3), CD4% of 23%, CD8 T cell count 258 cells/mm3 (150–1,000 cells/mm3), undetectable HIV viral load, procalcitonin 0.88 ng/ml (normal <0.1 ng/ml), and serum (1,3)—Beta-D-glucan <31 pg/mL (negative) on early admission. HAART treatment with dolutegravir, emtricitabine, and tenofovir alafenamide was continued throughout the admission without interruptions. The chest x-ray showed diffuse parenchymal infiltrates bilaterally with some sparing of the right upper lobe. SARS-CoV-2 PCR test resulted positive, and he was started on hydroxychloroquine therapy, which was the standard of care at that time.
During the hospital course, febrile episodes, typical of SARS-CoV-2 infection, over 38.4°C were noted. On the fourth day of admission, the patient had worsening dyspnea prompting repeat chest x-ray, which revealed bilateral 20% apical pneumothoraces without tension (). His respiratory status continued to decline with worsening tachypnea and he was transferred to the intensive care unit with oxygen therapy via non-rebreather mask at a flow rate of 12 L/min (). After ICU transfer, the patient's oxygen saturation dropped to 85%, with BP of 107/77 mmHg, RR range of 31–37 breaths/min, HR of 115 beats/min, and was found to have a left-sided tension pneumothorax. Subsequently, a 20 French (FR) of chest tube was placed on fourth mid-axillary line and connected securely with tape to a chest drainage system after verified by chest x-ray; however the patient's oxygen requirements continued to increase. Arterial blood gas (ABG) showed a pH 7.49, partial pressure of carbon dioxide (PaCO2) 36.8 mmHg, partial pressure of oxygen (PaO2) 64 mmHg. Patient was intubated and mechanical ventilator started on volume control/assisted control (VC/AC), RR 12, tidal volume (TV) 262 ml (6 ml/kg), peak-end-expiratory pressure (PEEP) 8 cmH2o, and fractioned of inspired oxygen (FiO2) 100%. On the ninth day of admission, the patient's oxygen saturation declined again and pulmonary CT and CTA was performed to rule out another etiology, such as a pulmonary embolism (PE). CT confirmed the presence of a left pneumothorax with 10% of hemithorax volume in size mostly in the inferior costophrenic sulcus and PE was ruled out (). On hospital day 18, after remaining hemodynamically stable, pneumothorax was reabsorbed and the patient was extubated and transferred to the inpatient medical floor, and 11 days later was discharged in stable condition breathing on room air.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [52.0, 'kg']}",92,87.4,96.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 52.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (52.0 kg - 20 kg) = 92.0 mL/hr.
Hence, the patient's fluid maintenance is 92.0 mL/hr."
4859,22,Maintenance Fluids Calculations,physical,decimal,pmc-6650173-1,Extracted,"A 62-year-old female presented with a three-month history of bilateral flank pain associated with unintentional weight loss of 25 pounds. Physical examination revealed flank tenderness bilaterally without guarding or rigidity and temporal muscle wasting. Computed tomography (CT) scan of the abdomen showed a 3-centimeter (cm) mass in the pancreatic tail suspicious for malignancy associated with retroperitoneal and bilateral inguinal adenopathy without ascites (Figure ). CT scan of the chest done did not show any metastases. Endoscopic ultrasound (EUS) revealed a 3-cm pancreatic tail mass invading the splenic artery at the superior pole of the left kidney. EUS-guided fine needle aspiration (FNA) demonstrated malignant tumor with prominent multinucleate-cell component and readily identifiable mitotic activity. Positron emission tomography (PET) scan did not show a fluorodeoxyglucose (FDG) avid lesion. The patient underwent distal pancreatectomy, splenectomy, and left partial adrenalectomy. Histopathological examination revealed UC-OGC (Figure ). The carcinoma was associated with bone formation and extended into peri-pancreatic soft tissue. The tumor showed fibrosis and old hemorrhage, lymphovascular invasion, and had negative resection margins and no nodal metastases. The patient was started on adjuvant chemotherapy with gemcitabine and capecitabine but she did not tolerate the first cycle. She developed significant colitis. Given her significant colitis, we discontinued capecitabine and she is currently receiving gemcitabine as an adjuvant chemotherapy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [25.0, 'lbs']}",42.6796,40.54562,44.81358,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 25.0 lbs so this converts to 25.0 lbs * 0.453592 kg/lbs = 11.3398 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (11.3398 kg - 10 kg) = 42.6796 mL/hr.
Hence, the patient's fluid maintenance is 42.6796 mL/hr."
4860,22,Maintenance Fluids Calculations,physical,decimal,pmc-4767072-1,Extracted,"A term 2-day-old female child weighing 3 kg presented to the emergency ward with complaints of respiratory distress. There was no significant antenatal history. Apgar score at birth was 6/10. On examination, the child had rapid breathing with peripheral cyanosis. On auscultation, there was diminished bilateral air entry in lower lung zones. Heart rate was 160/min and respiratory rate was more than 60/min. Oxygen saturation (SpO2) on room air was 92% but improved to 100% with 4 L of oxygen. Blood gas analysis on room air showed pH 7.46, PO2 74 mm Hg and PCO2 40 mm Hg. Chest X-ray revealed bilateral eventration of the diaphragm []. Computed tomography (CT) of the chest showed bilateral eventration of the diaphragm with high placed subdiaphragmatic liver and a gastric lumen in lower thoracic cavity []. There were no congenital heart defects or significant pulmonary hypertension on echocardiography.
It was decided to do a staged repair of bilateral eventration of the diaphragm. Thoracoscopic repair of left diaphragmatic eventration was planned on the 2nd day of life. The child was preoxygenated for 3 min with 100% oxygen. Standard American Society of Anaesthesiologists monitoring with an electrocardiogram, noninvasive blood pressure, SPO2, temperature, end-tidal carbon dioxide (EtCO2), and precordial stethoscope over dependent lung was employed. The child was premedicated with intravenous glycopyrrolate 0.05 mg and fentanyl 6 mcg. The child was induced with increasing concentration of sevoflurane from 2% to 4%. Intubation was facilitated by intravenous atracurium 1.5 mg. The child was intubated with 4 mm cuffed endotracheal tube taking care to confirm bilateral equal air entry. Anesthesia was maintained with manual ventilation on air, oxygen and sevoflurane 2–3%. Ventilation with 100% oxygen was attempted whenever SPO2 dropped below 90%.
The child was placed in right lateral decubitus position taking care to protect the pressure areas and confirming bilateral equal air entry. A 5 mm port with 30° telescope was inserted in the midaxillary line at the 4th intercostal space and two 5 mm ports were inserted in anterior and posterior axillary line at the 5th intercostal space. CO2 was insufflated into the left chest at a pressure of 5 mm Hg and flow of 0.5–1 L/min. There was herniation of stomach, left lobe of liver and spleen into the left thoracic cavity which were reduced. The left hemidiaphragm was thin and paper like which was plicated with 2-0 polypropylene interrupted sutures tied extracorporeally and pushed down with knot pusher. No clamp or retractor was used, and the intercostal drain was introduced. The port and drain site was infiltrated with 0.125% bupivacaine. The duration of the surgical procedure was 2 h.
After the reversal, the child was conscious having good respiratory effort. We decided to go for extubation with all precautions. The child tolerated extubation well and had an uneventful immediate postoperative course managing well on oxygen support. The child was started on nasogastric feeds on the 2nd postoperative day (POD), which was well tolerated.
In view of uneventful postoperative course, it was decided to go for thoracoscopic repair of eventration of the right diaphragm 5 days later. A part of the liver was inside the right thoracic cavity which was pushed, and diaphragmatic plication was done. The child had an uneventful postoperative course []. The child was started on nasogastric feeds on 2nd POD, and intercostal drains were removed on 4th POD. The child was discharged on 10th POD and is on regular follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.0, 'kg']}",12,11.4,12.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.0 kg. Hence, the patient's maintenance fluid is 3.0 kg * 4 mL/kg/hr = 12.0 mL/hr.
Hence, the patient's fluid maintenance is 12.0 mL/hr."
4861,22,Maintenance Fluids Calculations,physical,decimal,pmc-7599373-1,Extracted,"A 72-year-old Caucasian man was referred for evaluation of jaundice. He had been experiencing postural abdominal pain for more than 1 year. In the past month, the pain was getting worse and he experienced heartburn. He noticed loss of appetite in the past 2 months and lost 8 pounds of bodyweight. During the last weeks, jaundice developed, his urine became dark, and he began having gray-colored stool in the absence of fever, chills, or vomiting. There was no history of hepatitis, nor recent travel outside of the Netherlands. Previous medical history included a transient ischemic attack in 2010. He stopped smoking 15 years ago. Up to 2 months ago he drank 3 glasses of wine a day. Medication included a statin and dual antiplatelet therapy, none of which is known to cause jaundice as a possible side effect.
An outpatient ultrasound examination showed a large aneurysm of 10 cm central in the liver hilum; there were no gallstones. On admission, his vital signs were normal. Physical examination revealed an abdominal mass with an audible murmur in the epigastric region. There were no signs of hepatomegaly. Laboratory findings showed elevated levels of total bilirubin (114 μmol/L), aspartate aminotransferase (AST; 198 U/L), alanine aminotransferase (ALT; 472 U/L), AF (1508 U/L), gamma-glutamyl transferase (1742 U/L), C-reactive protein (33.9 mg/L), and normal white blood count (8.5 109/L).
A triple-phased contrast-enhanced computed tomography (CTa) scan revealed a true aneurysm starting in the distal common hepatic artery, reaching up to the bifurcation of the proper hepatic artery of almost 13 cm, causing compression of the common bile duct with intrahepatic bile duct dilatation (, A and B). Also, a small subthreshold infrarenal aortic aneurysm of 5.1 cm was seen. No other intra-abdominal abnormalities were found. Semiacute reconstruction of the hepatic artery was performed. A bypass was created from the common hepatic artery to the bifurcation of the proper hepatic artery, using a reversed autologous saphenous vein graft. Clamping time to the liver was approximately 45 minutes. Arterial flow in the right and left hepatic arteries was preserved, but the gastroduodenal artery had to be sacrificed owing to dissection and subsequent thrombosis.
The total blood loss was 1.5 L; there were no perioperative complications. One day after surgery the total bilirubin level decreased to 50 U/L and the jaundice resolved. AST and ALT levels improved direct after the surgery (AST 109 U/L; ALT 266 U/L), suggesting no significant ischemia of the liver had occurred. He was discharged on postoperative day 5 and further recovery was uneventful. Duplex ultrasound examination 1 week after discharge and a CTa scan 4 weeks after discharge showed a patent reconstruction without complications (, C).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [8.0, 'lbs']}",14.51496,13.78921,15.24071,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 8.0 lbs so this converts to 8.0 lbs * 0.453592 kg/lbs = 3.62874 kg. Hence, the patient's maintenance fluid is 3.62874 kg * 4 mL/kg/hr = 14.51496 mL/hr.
Hence, the patient's fluid maintenance is 14.51496 mL/hr."
4862,22,Maintenance Fluids Calculations,physical,decimal,usmle-1818,Extracted,"A 61-year-old man comes to the physician because of progressively worsening swelling of his ankles. He says he has felt exhausted lately. Over the past 3 months, he has gained 5 kg. He has smoked one pack of cigarettes daily for 30 years. His pulse is 75/min and his blood pressure is 140/90 mmHg. Examination shows 2+ pitting edema in the lower extremities. Neurologic exam shows diminished two-point discrimination in the fingers and toes. A urine sample is noted to be foamy. Laboratory studies show a hemoglobin A1c of 7.9% and creatinine of 1.9 mg/dL.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.0, 'kg']}",20,19,21,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.0 kg. Hence, the patient's maintenance fluid is 5.0 kg * 4 mL/kg/hr = 20.0 mL/hr.
Hence, the patient's fluid maintenance is 20.0 mL/hr."
4863,22,Maintenance Fluids Calculations,physical,decimal,pmc-5547087-2,Extracted,"A 23-year-old woman underwent evaluation for primary amenorrhea. She had a surgical history of inguinal hernia at the age of 8 years. Her weight was 62 kg, height was 160 cm, and body mass index was 24.2 kg/m2. The patient had no axillary hair, Tanner stage 3 breast development, and Tanner stage 1 pubic hair growth. Inspection of her external genitalia showed normal appearing labia majora and minora. However, a short, blind vaginal pouch was detected with a depth of 4 cm. Inguinal masses were palpable on both sides and identified in MRI as testis-like gonads located at the inguinal canal. Transvaginal ultrasonography and MRI showed the absence of a uterus, fallopian tubes, and ovaries. Laboratory evaluation revealed follicle-stimulating hormone, luteinizing hormone and estradiol serum levels of 21.2 mIL/mL, 22.6 mIL/mL, and 46.5 pg/mL, respectively. Serum testosterone was elevated at 1,032 ng/dL, and chromosomal analysis confirmed a normal male 46, XY karyotype. The patient was diagnosed with CAIS. Gonadectomy was recommended because of the malignant transformation potential of occult testicular elements. We performed bilateral gonadectomy through the inguinal approach, which allowed easy access to the testes in both inguinal canals. The surgery was uncomplicated, and pathological examination of the gonads showed Leydig cell hyperplasia and only Sertoli cells in the seminiferous tubules at both sides (). The patient was started on estrogen therapy for breast development and bone health.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [62.0, 'kg']}",102,96.9,107.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 62.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (62.0 kg - 20 kg) = 102.0 mL/hr.
Hence, the patient's fluid maintenance is 102.0 mL/hr."
4864,22,Maintenance Fluids Calculations,physical,decimal,pmc-4455014-1,Extracted,"Mrs. A. A, a 40-year-old Para 2-+-0 with no living child, (last child birth was 3 years and last menstrual period was 2 weeks prior to presentation) was seen at gynecological clinic with a history of abdominal distension of 3 years duration. The distension started gradually in the suprapubic region: - it later progressed to involve the entire abdomen. There was no change in the menstrual period and cycle. There was no change in urinary or bowel habit. There was no vomiting, cough, jaundice or abnormal vaginal bleeding. There was associated with mild abdominal discomfort and weight loss. She had been taking herbal medications since the onset of the above problem. When the mass became very large, it prevented the patient from carrying out her normal activities. The patient sought medical care at Awka General Hospital where a diagnosis of ovarian tumor was made. She was subsequently referred to Nnamdi Azikiwe University Teaching Hospital, Nnewi for expert management. She attained the age of menarche at 14 years. She was neither aware of Pap smear nor contraceptives. The past medical history was not contributory. There was no family history of such ailment. She was the third wife of her husband who was a farmer. She did not take alcohol or tobacco in any form.
On examination, she was chronically ill looking and pale. She was neither jaundice nor febrile. The pulse rate, blood pressure, and temperature were normal. Her body weight and height were 63 kg, and 160 cm, respectively. The cardiovascular and respiratory systems were normal. Abdominal examination revealed grossly distended abdomen, which was tense and visible veins [Figures and ]. The abdominal circumference was 126 cm measured at the level of the umbilicus. The liver, spleen and kidneys were difficult to assess due to the tensed abdomen. On vaginal examination, the vulva, vaginal and cervix appeared normal. The uterine size and adnexae were also difficult to assess because of the tensed abdomen. Abdomino-pelvic ultrasound revealed huge well circumscribed cystic mass with internal echoes arising from the pelvis. There were echogenic crystal-like solid components. The mass extended from the pelvis to the epigastrium and bowel loops were displaced posteriorly. There was no ascites. The liver, spleen and kidneys were normal from ultrasonography. Huge ovarian mass was a provisional diagnosis. The uterus was obscured by the cyst and could not be visualized; however, it appeared normal on transvaginal ultrasound. The urinalysis, completed blood count, liver function test, blood urea nitrogen, electrolyte and creatinine were normal. Her blood group was B Rhesus D- negative. She was admitted and worked up for laparotomy.
She underwent exploratory laparotomy on May 28, 2011 via low midline incision with upward extension up to about 6 cm below the xiphisternum. After laparotomy, a large tense smooth surfaced cystic mass that obliterated the peritoneal cavity was seen. There were no ascites. The intracystic fluid was drained through a small hole made on the mass. Approximate 20 L of straw colored thick fluid with debris was drained. Attempt to remove the mass with an intact capsule failed because it was adherent to the anterior abdominal wall and to loops of bowel posteriorly []. The cyst wall was eventually separated from the anterior abdominal wall by blunt dissection. The mass originated from the right ovary. It contained some debris. The left tube and ovary were normal. Ovarian cyst was removed by ipsilateral salpingo-oophorectomy. Estimated blood loss was 700 ml; two units of blood were transfused intraoperatively. The pathologists confirmed Mucinous cystadenoma of the right ovary was later confirmed from histopathology The post- operative period was uneventful and she was discharged on the 9th post-operative day.
She was followed up for 1 year and did not develop any symptom suggestive of pseudomyxoma peritonei. She was later lost to follow up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [63.0, 'kg']}",103,97.85,108.15,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 63.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (63.0 kg - 20 kg) = 103.0 mL/hr.
Hence, the patient's fluid maintenance is 103.0 mL/hr."
4865,22,Maintenance Fluids Calculations,physical,decimal,pmc-4420434-1,Extracted,"A 1350-g male child of 32 weeks gestation age was born to a 25-year-old mother by spontaneously vaginal delivery. Apgar scores were 6 and 9 at 1 and 5 min, respectively. He did not require artificial ventilation support. The post-natal period was uneventful till day 8, and enteral feeding had been started successfully. On the 8th day of life, he presented with a distended abdomen but soft and lax, without any redness of abdominal wall. Although he had bowel sounds in this process, but stool was not passed. Abdominal X-rays showed distended intestinal loops and a marked pneumoperitoneum bilaterally. Clinical diagnosis of perforation peritonitis was done at this instance and his enteral feeding was stopped along with insertion of NG tube. Biochemical examinations were normal. Total parenteral nutrition and antibiotics were started. Exploratory laparotomy revealed meconium peritonitis and a focal perforation on the 1/3 distal part of sigmoid colon (0.5x0.5 cm, the size of perforation range) (Fig. 1). Full-thickness rectal biopsy on frozen section examination was reported to have normal ganglion cells. The colon size was normal. Margins of the perforation were freshed and closed primarily. Histopathological examination of the margins of perforation was normal. The patient recovered promptly. He is doing fine on follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1350.0, 'g']}",5.4,5.13,5.67,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1350.0 g so this converts to 1350.0 lbs * kg/1000 g = 1.35 kg. Hence, the patient's maintenance fluid is 1.35 kg * 4 mL/kg/hr = 5.4 mL/hr.
Hence, the patient's fluid maintenance is 5.4 mL/hr."
4866,22,Maintenance Fluids Calculations,physical,decimal,pmc-5644516-1,Extracted,"An eight-year-old girl presented with a two-week history of fever, abdominal pain, passage of watery stool and recurrent vomiting. There was also a history of frequent micturition with occasional dysuria but neither haematuria nor passage of dark-coloured urine. Prior to presentation in the teaching hospital, she had been admitted to a distant private hospital for five days, where she was treated with amoxicillin, ciprofloxacin and artesunate (doses and duration of treatment are unknown). She was discharged from that hospital because her state of health was not improving significantly and also because of the need for better family support. There was no other history of hospital admission or blood transfusion and no history suggestive of haemoglobinopathy. Immunisation and nutritional history were essentially normal.
General physical examination revealed a conscious but ill-looking, somewhat pale, febrile (temperature 38.5 °C) girl. She was moderately dehydrated and jaundiced. Her weight was 22 kg (86% of expected weight for age). There was no facial or pedal oedema. The respiratory rate was 32 cycles per min and breathing was regular; pulse regular at 120 beats per min and with good volume. Her blood pressure was 90/50 mmHg. The significant systemic findings on examination at admission were severe suprapubic tenderness, moderate hepatosplenomegaly (firm, not tender) and negative renal angle tenderness. All other systems were normal.
Conventional blood cultures were done at five different times after admission. There was a growth of Klebsiella sp. on three occassions. Once, the isolate was sensitive to gentamicin and ceftriaxone but resistant to all available antibiotics tested on the other two occasions. Urine and stool cultures did not yield growth of any pathogens. Screening for human immunodeficiency virus (HIV), hepatitis C virus (HCV) and hepatitis B surface antigen (HBsAg) was negative.
Full blood counts showed a haematocrit ranged between 14% and 30%, white cell counts of 8 x 10/L – 9.2 x 10/L and an essentially normal platelet count (260 x 10/L). The erythrocyte sedimentation rate was 80 mm/hr (Westergreen method) and the haemoglobin phenotype (by electrophoresis) was AS. Serum biochemistry parameters were all normal except for conjugated hyperbilirubinaemia. Repeated abdominal ultrasonography showed findings that are consistent with hepatosplenomegaly in a septicaemic patient.
Whilst in hospital and when fever was uncontrolled and persistent, the patient was given fresh whole blood transfusions thrice and exchange blood transfusions twice, amongst other forms of treatment.
Fever remained persistent for five weeks following admission, despite different courses of antibiotics involving ciprofloxacin, gentamicin, ceftazidime, ceftriaxone and amoxicillin-clavulanic acid (). It was only at this point that the possibility of infection with an ESBL-producing organism was considered. ESBL-producers are not routinely sought in the diagnostic laboratory. During the sixth week, the Klebsiella sp. isolate from the patient was tested and confirmed to be producing an ESBL. Immediately following this test result, treatment was commenced with imipenem (not routinely available in the hospital) and there was dramatic resolution of fever. The patient remained free of fever for one week after receiving imipenem and was subsequently discharged. Two weeks later, when she reported for follow-up, she was still fever-free and healthy.
The Klebsiella sp. isolate was identified as Klebsiella pneumoniae subspecies pneumoniae using the API 20E identification strips for Enterobacteriaceae (bioMérieux, Marcy-l’Étoile, France). Presumptive ESBL phenotypic testing and confirmation in the organism was performed by disc diffusion tests on Mueller Hinton agar by employing ceftazidime (30 µg) and cefpodoxime (10 µg) alone and in combination with clavulanic acid as ceftazidime-clavulanic acid (30/10 µg) and cefpodoxime-clavulanic acid (10/1 µg) respectively. Results were interpreted using the Clinical and Laboratory Standards Institute (CLSI) criteria for disc diffusion. Antimicrobial susceptibility testing for the organism was carried out by the disc diffusion technique according to the guidelines and recommendations of CLSI. The isolate was resistant to streptomycin, gentamicin, chloramphenicol, tetracycline, nalidixic acid, ciprofloxacin, ampicillin, trimethoprim, sulphamethoxazole, ceftriaxone, cefepime and amoxicillin-clavulanic acid, but susceptible to imipenem.
Genomic DNA was extracted from the isolate using the Wizard genomic extraction kit (Promega) according to the manufacturer’s directions and used as template for PCR reactions targeting resistance elements and genes. Platinum PCR Supermix (Invitrogen) was used for all reactions, and PCR cycle conditions were as recorded in the original articles describing the primers (). We employed oligonucleotides that prime the conserved ends of the cassette regions of class 1 and 2 integrons respectively to screen for these elements (). As shown in , we were able to determine that the strain harboured a class 1, but not a class 2 integron. Sequencing of the 1.6 kb amplified class 1 cassette region revealed that it was identical to the cassette region of plasmid pIP1206 (Genbank Accession number NC_010558), containing two integrated cassettes: a dfrA17 cassette encoding resistance to trimethoprim, and an aadA4 aminoglycoside resistance cassette. Since the integron did not contain an ESBL cassette, we screened the isolate for blaCTX-M type genes, employing primers that amplify an internal fragment from multiple blaCTX-M alleles (). The resulting 550 bp product shown in was sequenced and found to be identical to the corresponding region of blaCTX-M-15.
The cost of repeated investigations () was N14 000.00 ($90.92), which is more than a tenfold increase on projected diagnostic expenses, had a diagnosis estimate been made immediately on admission. Antibiotics and fresh whole blood transfusions (thrice) as well as exchange blood transfusions (twice) cost N89 900.00 ($583.77). These and other treatment interventions effectively doubled the cost of treatment as compared to that for what would normally have been appropriate therapy after admission. Finally, prolonged hospital accommodation, feeding and nursing care over 48 days amounted to N20 400.00 ($132.46) in contrast to N2975.00 ($19.32) for admission for one week, an almost tenfold increase.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [22.0, 'kg']}",62,58.9,65.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 22.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (22.0 kg - 20 kg) = 62.0 mL/hr.
Hence, the patient's fluid maintenance is 62.0 mL/hr."
4867,22,Maintenance Fluids Calculations,physical,decimal,pmc-3724097-1,Extracted,"A 2.5-month-old girl was admitted to our hospital for evaluation of abnormal respiratory pattern (episodic tachypnea and/or apnea) and hypotonia. She was the first child of healthy consanguineous parents. The baby was born at term by vaginal delivery after an uneventful pregnancy and did not cry immediately after birth. On admission to the hospital, the baby was found to have episodes of breathlessness, with a respiratory rate of up to 100 breaths/min, alternating with apnea lasting for 15-20 s with cyanosis. On physical examination, her weight was 2500 g (<3rd percentile), her length was 47 cm (<3rd percentile) and her head circumference was 36.5 cm (3rd percentile). Facial features include broad forehead, arched eyebrows, left-sided squint, epicanthic folds and widely spaced eyes (hypertelorism). Examination of the oral cavity revealed midline upper lip cleft and bilateral fleshy nodules on the under surface of the tongue, bumps of the lower alveolar ridge and high-arched palate []. Skeletal examination revealed post-axial as well as mesaxial (an extra digit between the middle digits) polydactyly of both hands and pre-axial polydactyly of both feet []. Other physical examination, findings were normal. Laboratory investigations including complete blood count (CBC), hepatic enzymes, blood urea nitrogen, creatinine, electrolytes, blood sugar and urine analysis were normal. Echocardiography, abdominal ultrasonography, especially of the kidney, ureter and bladder (KUB) region, and ophthalmological examination were found to be normal, except squint on the left side. X-ray of both hands documented mesaxial polydactyly as evident with Y-shaped metacarpal []. Magnetic resonance imaging showed hypoplasia of the cerebellar hemispheres and vermis and a narrowed isthmus of the mid brain with a characteristic “molar tooth appearance” []. The infant was discharged home and advised to attend the follow-up clinic.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2500.0, 'g']}",10,9.5,10.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2500.0 g so this converts to 2500.0 lbs * kg/1000 g = 2.5 kg. Hence, the patient's maintenance fluid is 2.5 kg * 4 mL/kg/hr = 10.0 mL/hr.
Hence, the patient's fluid maintenance is 10.0 mL/hr."
4868,22,Maintenance Fluids Calculations,physical,decimal,pmc-2481241-1,Extracted,"A 52-year-old white male with O2-dependent COPD, hypertension, GERD, idiopathic gastroparesis, and chronic low back pain was noted to have persistent hypokalemia in the 2.7–3.3 meq/L range over more than 2 years. He complained also of chronic generalized weakness and fatigue. He denied nausea or vomiting, but did have occasional loose stools. The hypokalemia persisted despite discontinuation of diuretic treatment for hypertension and fludrocortisone that had been prescribed briefly for orthostatic hypotension. There was no improvement with aggressive oral potassium supplementation in amounts up to 120 meq per day. The patient's serum potassium level normalized on three occasions when he was hospitalized and given supplemental potassium (COPD exacerbations in 7/06 and 1/07, pseudoseizures in 7/07), but the hypokalemia promptly recurred after discharge from the hospital (Figure ). His medications were paroxetine, trazodone, pregabalin, sustained-release morphine, loratadine, isosorbide mononitrate, lisinopril, metoprolol, simvastatin, omeprazole, metoclopramide, potassium chloride, calcium/vitamin D tablets, alendronate, and mometasone, tiotropium, and albuterol inhalers. He smoked one-half pack of cigarettes per day and did not drink alcohol.
On physical examination, he was a chronically ill-appearing man wearing a nasal cannula. Height was 69 inches, weight 205 pounds. There were no cushingoid facies, buffalo hump, or abdominal striae. Vital signs were temperature 98.6 degrees, pulse 95, respiratory rate 14, blood pressure 128/73. There was no thyromegaly or lymphadenopathy. Lungs showed decreased breath sounds and mild expiratory wheezes bilaterally. Heart sounds were regular with no murmurs, rubs, or gallops. The abdomen was soft and non-tender, with no masses or organomegaly. Extremities showed no edema, clubbing or cyanosis. The neurologic examination revealed mild generalized muscular weakness (4+/5) and normal deep tendon reflexes.
Laboratory results include serum sodium 137 mg/dL, potassium 3.0 mg/dL, chloride 95 mmol/L, CO2 30.0 mmol/L, blood urea nitrogen 5 mg/dL, creatinine 0.8 mg/dL, calcium 9.3 mg/dL, phosphorus 4.1 mg/dL, albumin 3.6 g/dL, ferritin 126 ng/mL, hemoglobin 12.7 g/dL, white blood cell count 10.6 K/cmm, and platelet count 160 K/cmm. Serum aldosterone was 4.8 ng/dL (normal 4–31 ng/dL) and the plasma renin activity was 0.33 ng/mL/hr (normal 1.31–3.96 ng/mL/hr upright, 0.15–2.33 ng/mL/hr supine). Spot urine potassium was 8.6 mEq/L, urine sodium was < 10 mEq/L, and urine chloride was 16 mmol/L.
In the absence of a clear explanation for this patient's chronic hypokalemia, he was asked to give the details of his diet. He admitted to drinking 4 liters of Pepsi-Cola per day for the past several years. It was his habit to sip cola slowly but almost continuously, throughout the day. When hospitalized, he had stopped drinking cola and his potassium levels had temporarily normalized. In early May 2008, he decreased his cola intake to 2 liters per day, with a resultant increase in the serum potassium from 3.0 to 3.5 mg/dL (Figure ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [205.0, 'lbs']}",132.98636,126.33704,139.63568,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 205.0 lbs so this converts to 205.0 lbs * 0.453592 kg/lbs = 92.98636 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (92.98636 kg - 20 kg) = 132.98636 mL/hr.
Hence, the patient's fluid maintenance is 132.98636 mL/hr."
4869,22,Maintenance Fluids Calculations,physical,decimal,pmc-4188769-1,Extracted,"A 57-year-old male, 75 kg in weight and 167 cm in height, diagnosed with an unruptured aneurysm of the right anterior communicating artery measuring 5.3 × 3.8 mm underwent surgical clipping of the aneurysm. He had no previous medical history of hypertension, coagulopathy, or any hematologic abnormality. Anesthesia was induced with thiopental and maintained under endotracheal intubation with 0.6-1.0 MAC of desflurane in air and 0.05-0.15 µg/kg/min of remifentanil infusion.
A left pterional craniotomy (slight rotation and accentuated extension of the head) was performed with intraoperative monitoring of the somatosensory evoked potential. During the operation, 2,500 ml of crystalloid fluid was given, and 930 ml of urine output was measured. Five hundred milliliters of blood loss was measured. At the end of the surgical procedure, ketorolac 60 mg and ondansetron 4 mg were given intravenously. The surgical and anesthetic durations were 280 and 470 minutes, respectively. The patient was hemodynamically very stable during the whole anesthetic procedure. The patient regained consciousness without any neurologic deterioration after completion of the surgery and was transferred to the postanesthetic care unit (PACU). The course of anesthetic recovery was even, except that the patient complained of a strange feeling in his right eye when he blinked at about 2 hours after operation. A postoperative brain CT scan was then taken, and it revealed a small amount of parenchymal intracranial hemorrhage (ICH) with swelling in the right frontal lobe and left cerebellar hemisphere (). On postoperative day 1, the patient became slightly lethargic and complained of dizziness, nausea, vomiting, and headache. He was treated conservatively. A brain CT scan taken on postoperative day 4 revealed an increased amount of acute ICH in the left cerebellar hemisphere (), but he was still alert without any focal neurologic deficit. On postoperative day 7, the hematoma on the left cerebellum and right frontal lobe resolved partially. On postoperative day 14, ICH on both sides resolved further (), and the patient was discharged without any neurologic deficits.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [75.0, 'kg']}",115,109.25,120.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 75.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (75.0 kg - 20 kg) = 115.0 mL/hr.
Hence, the patient's fluid maintenance is 115.0 mL/hr."
4870,22,Maintenance Fluids Calculations,physical,decimal,pmc-3465941-1,Extracted,"The patient was a 75-year-old female with an 8-month history of worsening dysphagia, to both solids and liquids and epigastric pain, burning in nature, radiating to the chest, costal margin, and back. Just before presentation, she experienced nausea and frequent (10–30 minutes) episodes of projectile vomiting, not related to oral intake. The patient had suffered from diarrhoea for a week prior to presentation, with no reports of blood or mucous in her stool. Generalised weakness, lethargy, reduced appetite, and a weight loss of 16 Kgs in 6 months were also reported. Past medical history was significant for hypertension and chronic obstructive pulmonary disease (COPD) under medical control.
During the clinical examination, the patient was found to have a distended, but soft abdomen. Generalised tenderness, mainly to the right side and particularly during deep palpation, was noted. No organomegaly or masses were detected. Bowel sounds were present and active. Rectal examination was unremarkable. The rest of the clinical examination only revealed bilateral pitting oedema of the ankles and swollen hands with “sausage-like” digits.
The patient was initially investigated with an oesophagogastroduodenoscopy (OGD), which diagnosed Candida oesophagitis (possibly due to the inhaled steroids for the COPD) and mild chronic non-active inflammation of the gastric mucosa on biopsy. However, it also identified an extrinsic compression of the gastric antrum and therefore a computer tomography (CT) of the abdomen and pelvis was performed. The CT showed moderately dilated small bowel loops with gas within the intestinal wall (). Since the patient's clinical condition was stable and did not demonstrate signs of peritonism, a decision for conservative management was made. After excluding life-threatening and acute causes of PI, such as infection or ischemia, further investigations were performed guided towards the more uncommon pathologies. A screen for autoimmune diseases showed positive results for the anticentromeric and antinuclear antibodies and the diagnosis of systemic sclerosis was made. With the diagnosis confirmed, a more detailed medical history was obtained, specifically guided to reveal any symptoms of systemic sclerosis, with no success. Similarly, no signs related to the disease, such as skin thickening, calcinosis, or telangiectasia, were identified. The patient improved on methotrexate and was discharged after a total of 4 weeks hospital stay with appropriate outpatient follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [16.0, 'kg']}",52,49.4,54.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 16.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (16.0 kg - 10 kg) = 52.0 mL/hr.
Hence, the patient's fluid maintenance is 52.0 mL/hr."
4871,22,Maintenance Fluids Calculations,physical,decimal,pmc-5815706-1,Extracted,"A 69-year-old patient (G6 P6) (height, 155 cm; weight, 66 kg) reported vaginal prolapse for several years and incontinence, abdominal pain and hematuria. Comorbidities: type 2 diabetes for 20 years, circulatory failure, paroxysmal atrial fibrillation, anaemia, urinary tract infection, hypertension, chronic biliary gastritis, cervical osteoarthritis.
Physical examination on admission revealed anterior vaginal and uterine walls prolapse, with 8 cm in diameter large ulcerated lesion (Fig. ) located on the anterior vaginal wall. Diagnostic biopsy of the lesion revealed squamous cell carcinoma (Fig. ).
Additional tests: hemoglobin 11.0 g/dL (12.0–16.0); hematocrit 33.9% (37.0–47.0); erythrocytes 4.34 × 106/uL (4.00–5.00); MCV 78.1 fL (80–94); MCH 25.3 pg (27.0–31.0); MCHC 32.4 g/dL 931.0–37.0); RDW-SD 48.3 fL (36.4–46.3); RDW-CV 17.7% (11.7–14.4); Blood Plate 296 × 103/Ul (140–400); plate distribution width (PDW) 11.6 fL (9.80–16.20); MPV 9.8 fL (9.40–12.50); platelet large cell ratio (P-LCR) 24.1% (19.10–46.60); WBC 8.12 × 103/ul (4.0–10.0); Macro R 6.7%; Micro R 7.9%; total protein 7.1 g/dL (range 6.3–8.2); chlorides 112.0 mmol/L (98.0–107.0); activated partial thromboplastin time (APTT) 29.0 s (25.9–36.6); prothrombin time 9.2 s (7.6–11.4); Prothrombin index 103.7% (80.0–120.0); INR 1.0 (0.9–1.3); D-dimer 2 208.8 ng/mL (<500.0); fibrinogen 503.9 mg/dL (180.0–400.0); glomerular filtration rate (GFR) 27 mL/min/1.73 m2 (>60.0); glucose 115 mg/dL (70–99); creatinine 1.85 mg/dL (0.52–1.04); urea 66 mg/dL (15–43); potassium 4.9 mmol/L (3.5–5.1); sodium 144.0 mmol/L (137.0–145.0); TSH 0.50 uIU/mL (0.27–4.20).
Sagittal pelvic CT showed protruded vagina, infiltrated bladder wall, uterus, and rectum. In frontal CT scan of abdomen, enlarged pelvic iliac nodes, hydronephrosis of the left kidney with left hydroureter, in the right kidney nephrostomic catheter were observed (Fig. ).
Cystoscopy-mucosal lesions were found in the bladder (Fig. ). The diagnostic biopsies were collected from the urethra and the bladder (Fig. ).
Symptomatic treatment included: InsulinueGensulin R t.i.d. (2–6 units)sc, Amlodypinum 2 × 10 mg, 0.9%NaCl 2 × 500 ml iv., Clexan (Enoxaparinumnatricum) 2 × 0.6 sc, Ramiprilum 5 mg 1 × 1, Captoprilum 25 mg 1 × 1.
The patient was disqualified from surgery due to the severity of the disease, lymph node metastases, and coexisting comorbidities. Only palliative nephrostomy was performed.
The patient signed informed consents. In our case the patient accepted regular and proved diagnosis and therapy in Clinical Department of Urology, so the ethical approval was not necessary.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [66.0, 'kg']}",106,100.7,111.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 66.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (66.0 kg - 20 kg) = 106.0 mL/hr.
Hence, the patient's fluid maintenance is 106.0 mL/hr."
4872,22,Maintenance Fluids Calculations,physical,decimal,pmc-4070198-2,Extracted,"A 3-year-old boy weighing 12 kg was diagnosed as congenital complete heart block (CHB) with a moderate PDA. The clinical evaluation showed heart rate of 70 bpm and continuous murmur on auscultation. The electrocardiogram (ECG) showed narrow QRS CHB. The TTE showed a 3 mm PDA with continuous left to right shunt. The aortogram in lateral view showed a 2.8 mm type ‘A’ PDA with good ampulla. The PA pressures were normal. A 6F delivery sheath was placed in the descending aorta and a 6/4 Amplatzer duct occluder (ADO) was used for the closure. The device was positioned in the ampulla and planned to release in right anterior oblique view []. The ADO was embolized into descending aorta instantaneously. Careful subsequent evaluation revealed improperly positioned device as there was gap between the aortic retention disc and ampulla.
The device retention screw in the descending aorta was facing cranially and felt unfavorable for the retrieval. And hence, a pigtail catheter was used from the pulmonary artery through PDA into descending aorta to manipulate the device keeping an 8 mm inflated Tyshak balloon (NuMED Canada Inc. Cornwall, ON, Canada) below the device to avoid further dislodgment. The device was manipulated to direct the retention screw to face caudally. A 7F long primary sheath was exchanged in the femoral artery and gradually advanced close to the retention screw using anteroposterior and lateral fluoroscopy views. Now a 6F secondary sheath was taken into the previously placed sheath and advanced gradually into the retention screw. A 3F delivery cable was advanced in the sheath and re-screwed the device gradually by clock-wise rotation like in the case 1. Now the same retrieved device was taken and repositioned properly with a constant pull into the PA. The angiogram in lateral view showed well-positioned device []. The follow-up assessment showed no residual shunt or malposition of the device.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.0, 'kg']}",44,41.8,46.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.0 kg - 10 kg) = 44.0 mL/hr.
Hence, the patient's fluid maintenance is 44.0 mL/hr."
4873,22,Maintenance Fluids Calculations,physical,decimal,pmc-3943037-1,Extracted,"A previously healthy, 12-kg, 22-month-old female toddler was referred to us with high fever, non-bloody and non-xanthic jumpy vomiting, and non-bloody watery diarrhea following a trip. Her height was 80 cm (below the percentile 25%) and head circumference was 47 cm (percentile 50%). Several hours later, her level of consciousness decreased (Glasgow coma scale=7), she developed generalized tonic-clonic seizures, and was transferred to PICU. Quadripelagic spasms with greater intensity in the right upper and lower limbs as well as spasity and severe dystonia were then noted. In the course of the disease, she was transferred to Amirkola Children Hospital in Babol. On the first examination after admission to this center, her complete blood count, PT, PTT, and urine analysis were normal. C reactive protein, erythrocyte sedimentation rate, blood sugar, blood urea nitrogen, creatinine, calcium, sodium, potassium, aspartate transaminase, alanine transaminase, alkaline phosphatase, total bilirubin, and direct bilirubin were reported to be 2 mg/dL, 7 mm/hr, 94 mg/dL, 9.2 mg/dL, 0.6 mg/dL, 9.4 mg/dL, 140 mEq/L, 5.2 mEq/L, 100 U/L, 119 U/L, 247U/L, 1.1 mg/dL, and 0.5 mg/dL, respectively. Evaluation of the cerebrospinal fluid (CSF), blood ammonia, lactate, and pyruvate were also normal. Urine reducing substances, amino acids chromatography and blood gas were normal. Anticonvulsant therapy with phenytoin, Phenobarbital, and midazolam drip was begun. Respiratory support by mechanical ventilation was also initiated. Acyclovir (Zovirax), dexamethasone, intravenous immunoglobulin (IVIG), amikacin (for UTI), and imipenem were prescribed.
Diazepam (0.2 mgr /kgr q6h), levodopa(10mgr/day), and trihexifenidilo(2mgr/6h) were used to treat dystonia. Although dystonia and spasity gradually declined, mental and physical sequelae developed. She therefore became a candidate for percutaneous endoscopic gastrostomy (PEG). MRI revealed increased T2 signal intensity in the thalami, basal ganglia (putamen and globus pallidus), and periventricular white matter presenting hemorrhage accompanied with necrosis in those regions ().
The patient underwent supportive care including physiotherapy, speech therapy, and outpatient supports.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.0, 'kg']}",44,41.8,46.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.0 kg - 10 kg) = 44.0 mL/hr.
Hence, the patient's fluid maintenance is 44.0 mL/hr."
4874,22,Maintenance Fluids Calculations,physical,decimal,pmc-4320605-1,Extracted,"The patient was a 61-year-old male of Japanese ethnicity. He was 167cm tall, weighed 42kg, and had a body mass index (BMI) of 15kg/m2. He was admitted to our hospital to undergo surgery for multiple colorectal tumors. Colonoscopy revealed sigmoid colon cancer, an early cancer in the transverse colon, and several adenomas across the length of the entire colon (Figure ). Laparoscopic subtotal colectomy was performed under general and epidural anesthesia, after informed consent was obtained from the patient. The inferior mesenteric artery and vein were resected distal the left colic artery branch. The right and left side of the colon and each mesentery and the hepatic and splenic flexure were mobilized after the area between the transverse colon and the greater omentum was resected. During detachment of the splenic flexure, all layers of the transverse colon were damaged and the intestinal contents flowed out. The ileocolic artery and vein, and the right colic and middle colic vessels were resected at each trunk. The rectum was detached up to the peritoneal reflection. Ten centimeters of the colon to the anal side of the sigmoid colon cancer was transected using a linear stapler (Echelon Flex™ Powered Endopath® Stapler 60; Ethicon, USA). After the colon was pulled out from the umbilical region and the ileum end was transected, the colon was excised. Side-to-end ileorectal anastomosis was performed using a circular stapler (Proximate* ILS CDH 29; Ethicon, USA) (Figure ). Penrose drains were inserted below the left crus of the diaphragm and at the posterior surface of the anastomosis after the peritoneal cavity was washed with 3,000 cc of warm physiological saline. The small bowel was returned to its original position, antiadhesive material was placed inside the cavity, and the abdomen was closed. The duration of surgery was 8 h and 22 min, with 200 cc of blood loss.
The final diagnosis was T2N0M0 stage I moderately differentiated adenocarcinoma for the sigmoid colon cancer, stage 0 (TisN0M0) well differentiated adenocarcinoma for the transverse colon cancer, and tubular adenomas (10 low grade adenomas, 3 high grade adenomas) for other polyps. Bowel obstruction developed on the sixth day after surgery (Figure ) and did not improve, even after an ileus tube was inserted and conservative treatment was performed. He had fever and abdominal distension. Blood tests (Table ) revealed an elevated inflammatory response, hypoalbuminemia, impaired liver function, and coagulation system abnormalities.
Emergency surgery was performed because bowel obstruction caused by internal hernia was suspected based on abdominal computed tomography (CT) findings (Figure ). The upper part of the small bowel was dilated because the ileum had protruded into the mesenteric defect, leading to an internal hernia. The tip of the ileus tube had stopped at the oral side of the incarcerated herniated intestine (Figures and ). The area around the anastomosis had hardened and was determined to be an anastomotic stricture. The incarcerated herniated bowel was 30cm long, whereas the ileum to the oral side of the ileorectal anastomosis to the anal side was 40cm long. Re-anastomosis was performed after hernia repair because the situation was treated as a stenosis, even though circulation to the bowel of the ileorectal anastomosis was not interrupted. The mesenteric defect was closed using 3–0 Vicryl, and a Penrose drain was inserted into the posterior of the anastomosis. A loop ileostomy was them constructed. The patient began eating on the third day after emergency surgery and recovered with no major problems. He was discharged 28 days after surgery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [42.0, 'kg']}",82,77.9,86.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 42.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (42.0 kg - 20 kg) = 82.0 mL/hr.
Hence, the patient's fluid maintenance is 82.0 mL/hr."
4875,22,Maintenance Fluids Calculations,physical,decimal,pmc-7076047-1,Extracted,"A 13-month-old, male, Sphynx cat weighing 3.0 kg was referred to the Small Animal Clinic of the Faculty of Veterinary Medicine of the University of Liege for investigation of heart murmur, cough, dyspnea and weakness. Cardiac ultrasonography, performed by a board-certified cardiologist, revealed a left-to-right PDA associated with an enlargement of the left atrium (left atrium to aorta ratio of 2.3), the left ventricle and the pulmonary trunk. Moreover, turbulent blood flow at the aortic valve, increased peak systolic velocity of forward blood flow across the aortic valve (2.7 m/s) and smoke-like echo in the left atrium were observed. Thoracic radiographs confirmed the severe cardiomegaly (vertebral heart size of 11.4) and the dilation of the pulmonary trunk. Furthermore, radiographs demonstrated a dilation of the aortic arch, an increased pulmonary vascularity and were suggestive of a pulmonary edema. Thoracic computed tomography angiography showed a short and large PDA and supported the severe cardiomegaly, the dilation of the pulmonary trunk as well as the increased pulmonary vascularity. All these findings were compatible with a left-to-right PDA associated with a severe cardiomegaly and a left-sided congestive heart failure. The cat was discharged immediately after examination and prescribed furosemide (Furosoral; Dechra) 5 mg PO q12h, clopidogrel (Plavix; Sanofi) 19 mg PO q24h and pimobendan (Vetmedin; Boehringer Ingelhein) 0.9 mg PO q12h; and the surgery was scheduled for 10 days later. In the meantime, dyspnea and weakness improved but coughing frequency increased.
Food and water were withheld for 12 h prior to surgery. A 20 G intravenous catheter was placed in the left cephalic vein and lactated Ringer's solution (Vetivex; Dechra) was infused at a rate of 2 ml/kg/h to replace oral fluid intake. Furosemide, clopidogrel, and pimobendan were administered the evening before surgery. Although the combination of IV fluid therapy and furosemide might seem counterintuitive, it aimed at maintaining normal hydration status without running the risk of worsening congestive heart failure. Preanesthetic physical examination revealed tachycardia [196 beats per minute (bpm)], tachypnea [48 respirations per minute (rpm)], a grade 5/6 heart murmur, a bounding pulse, a strongly positive laryngeal reflex and a body condition score of 4/9; the rest of the examination was unremarkable and the patient was assigned a grade IV according to the ASA health status classification system. Increasing coughing frequency, strongly positive laryngeal reflex and tachypnea were highly suggestive of cardiomegaly and left-sided congestive heart failure. Laboratory analyses were not performed prior to anesthesia.
Methadone (Comfortan; Dechra) (0.2 mg/kg IV) was administered as preanesthetic medication. Anesthesia was induced with midazolam (Midazolam; Mylan) (0.2 mg/kg IV) and alfaxalone (Alfaxan; Dechra) (2 mg/kg IV) and the trachea was intubated with a 3 mm cuffed endotracheal tube. The cat was positioned in right lateral recumbency and connected to a rebreathing circuit. Isoflurane (IsoFlo Vet; Abbott) was delivered in 100% oxygen and pressure-controlled ventilation (Neptune; Medec) was used during the whole procedure to maintain end-tidal carbon dioxide partial pressure below 60 mmHg (respiratory rate: 20–30 rpm, peak inspiratory pressure: 7–12 mmHg, end-expiratory pressure: 0–2 mmHg, tidal volume: 25–40 ml). Mild hypercapnia was tolerated to meet surgical needs. Indeed, increasing minute ventilation, by increasing either respiratory rate or tidal volume, would have prevented surgical access to the PDA. Non-invasive arterial blood pressure was monitored every 5 min using Doppler ultrasonic method (811-B Ultrasonic Doppler Flow Detector; Parks Medical Electronics). Pulse oximetry, electrocardiogram, tidal volume, inspired and expired percentages of oxygen and isoflurane, inspired and expired carbon dioxide partial pressures and esophageal temperature were continuously recorded using a multiparameter monitor (Compact 5S; Datex-Ohmeda).
The cat received alfaxalone (1 mg/kg) to increase the anesthetic depth before the surgery started. Fentanyl (Fentanyl-Janssen; Janssen-Cilag) (3 μg/kg IV) was administered prior to skin incision and infused thereafter throughout the whole procedure (5 μg/kg/h). End-tidal percentage of isoflurane was maintained between 0.7 and 1.4%. A left thoracotomy via the fourth intercostal space was performed and the PDA was ligated within 120 min after induction. Cefazoline (Cefazoline; Sandoz) (20 mg/kg IV) was administered every 90 min until the procedure was completed. Heart rate oscillated between 140 and 180 bpm, systolic arterial blood pressure ranged between 75 and 90 mmHg, peripheral oxygen saturation varied between 99 and 100% and lactated Ringer's solution was infused at a rate of 5 ml/kg/h until the PDA was ligated.
A 14 G guidewire chest tube (guidewire inserted chest tube; Mila) was then inserted using the Seldinger technique. The tube was introduced through a skin incision in the 10th intercostal space and advanced subcutaneously until it reached the 7th intercostal space where it entered the thorax. Immediately after placement of the tube, severe intrathoracic bleeding was observed and the tube was removed. Because surgeons were unable to identify the origin of the hemorrhage, a second thoracotomy was performed via the 7th intercostal space. It allowed identifying the caudal intercostal artery as responsible site for the bleeding. This vessel was thermo-cauterized, which efficiently terminated the hemorrhage. Meanwhile, systolic arterial blood pressure dropped to 40 mmHg, heart rate increased up to 230 bpm and pulse oximeter stopped giving a signal of peripheral oxygen saturation. Two boluses of tetrastarch colloid (Voluven 6%; Fresenius Kabi) (2 ml/kg) and one bolus of lactated Ringer's solution (10 ml/kg) were administered while patient's blood was typed (QuickVet/RapidVet Feline Blood Typing; Zoetis). Systolic arterial blood pressure reached 100 mmHg but the improvement lasted for only 10 min. Blood type was A but there was no feline blood available and it was decided to give untyped canine fresh whole blood that was purposely collected, and given immediately after collection, without performing neither minor nor major cross-match tests. Lactated Ringer's solution infusion was discontinued and transfusion rate started at 5 ml/kg/h and was doubled after 20 min. During transfusion, body temperature, mucous membrane color, capillary refill time, peripheral oxygen saturation, pulse quality, heart rate, heart rhythm, further decrease in arterial blood pressure and possible vomiting, diarrhea, hives, erythema, facial swelling and muscle tremors were closely monitored. At the end of surgery, vacuum was restored in the chest with a 3.5 Fr small animal urinary catheter (Tomcat; Mila) and levobupivacaine (Chirocaine; Abbvie) (1 mg/kg) was instilled through this catheter, which was removed immediately thereafter. Methadone (0.2 mg/kg IV) was administered and the cat recovered in the intensive care unit. The esophageal temperature was 37.5°C after the total anesthesia time of 270 min. The cat became cyanotic after the trachea was extubated, which was efficiently resolved with flow-by oxygen administration. The total amount of blood loss was estimated at 131 ml by weighing soaked compresses and estimating aspirated blood. The cat received 24 ml of blood during surgery and the transfusion was maintained postoperatively until he received the 131 ml in order to match the estimated amount of blood loss. Although the cat remained hemodynamically unstable while receiving blood under general anesthesia (systolic arterial blood pressure as low as 40 mmHg, heart rate of up to 230 bpm and loss of peripheral oxygen saturation signal), it gradually improved and normalized its parameters after transfusion of the whole blood volume. Furthermore, it never showed any sign of fluid overload. Methadone (0.2 mg/kg IV q4 h) was first administered but the analgesic plan was modified and an infusion of fentanyl (2 μg/kg/h) was started 12 h after surgery. Fentanyl infusion was maintained until the third day after surgery where the analgesic protocol was continued with buprenorphine (Vetergesic; Ecuphar) (0.02 mg/kg IV q8h). Furosemide (5 mg PO q12h), clopidogrel (19 mg PO q24h) and pimobendan (0.9 mg PO q12h) were maintained after surgery.
The cat was discharged 3 days after surgery at the owner's request. At that time, it did not show any abnormal clinical sign nor any sign of hemolysis. Hematology revealed a packed cell volume (PCV) of 36% and an absolute reticulocyte count of 142, 000/μL.
The cat was presented for an echocardiographic follow-up at 1 and 2 months after surgery. Although it had developed a hypertrophic cardiomyopathy at that time, it has improved clinically and never showed signs of hemolysis or anemia.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.0, 'kg']}",12,11.4,12.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.0 kg. Hence, the patient's maintenance fluid is 3.0 kg * 4 mL/kg/hr = 12.0 mL/hr.
Hence, the patient's fluid maintenance is 12.0 mL/hr."
4876,22,Maintenance Fluids Calculations,physical,decimal,pmc-5301991-1,Extracted,"A 34-year-old female (162 cm, 42 kg) underwent kidney transplantation due to end-stage renal disease at the Gachon university Gil medical center (1600-bed tertiary referral hospital), Incheon, South Korea during year 2015. She had a history of long-term laxative ingestion due to chronic constipation. Eight months pre-transplantation, she was diagnosed with renal insufficiency with hypokalemia, but did not experience any subjective symptom. Profound hypochloremic metabolic alkalosis persisted, as determined by monthly laboratory follow-up visits, despite regular oral potassium supplementation (). Peritoneal dialysis was started six months before transplantation. The patient was determined to undergo kidney transplantation from her sister and started plasma exchange/plasma pheresis using 12 units of AB+ fresh frozen plasma due to ABO incompatibility (Donor, AB+; Recipient O+). Anti-A and -B were reduced from 1:16 and 1:4 to 1:1 and 1: 1, respectively, after four plasma exchanges. She was taking mycophenolate sodium, tacrolimus, intravenous immunoglobulin and corticosteroid after applying rituximab. Prior to transplantation, her mental status was alert. Preoperative electrocardiography and chest x-ray were normal, and blood pressure, heart rate, and body temperature were 105/65 mmHg, 84 beats/minute, and 36.4oC, respectively. Preoperative laboratory data were as follows: hematocrit 26.6%, platelet count 267 × 103/mL, Blood Urea Nitrogen (BUN) 46.2 mg/dL, Creatinine (Cr) 6.1 mg/dL, tCO2 53.8 mEq/L, potassium (K+) 3.8 mEq/L, chloride (Cl-) 74 mEq/L, Prothrombin Time (PT) 9.2 seconds and activated Partial Thromboplastin Time (aPTT) 27.8 seconds. Parathyroid hormone was 298.6 pg/mL (normal range 10 - 65 pg/mL). Arterial blood gas analysis in the preanesthetic room revealed pH 7.56, PaO2 88 mmHg, PaCO2 71 mmHg, bicarbonate (HCO3-) 60 mEq/L, and base excess 30 mEq/L. All analyzers for serum variables (TBA-200FR NEO, Toshiba, Tokyo, Japan) and arterial blood gas analysis (GEM Premier 3000, Instrumentation Laboratory, MA, USA) were calibrated periodically and the measuring variables were selected as preoperative evaluation protocol of our institute. The samples were analyzed for pH, PaCO2 (standard electrodes), and the base excess and HCO3- were taken from the arterial blood gas analyzer, which uses the Henderson–Hasselbalch equation and the van Slyke equation. Additionally, the concentrations of serum values, including K+, Cl- (ion-selective electrode) and tCO2, were measured using the same blood samples. Remifentanil 40 μg, lidocaine 40 mg, propofol 80 mg, and cis-atracurium 5 mg were administered for anesthetic induction. To maintain a Bispectral Index (BIS) score between 40 and 60, anesthesia was maintained with desflurane at 4 - 7 vol% and remifentanil at 0.05 - 0.1 µg/kg/minute. A 20-G right radial arterial catheter and a 16-Fr right internal jugular venous catheter were inserted. During transplantation, vital signs were maintained at blood pressure 97/55 - 130/78 mmHg, heart rate 72 - 91 beats/minute, and central venous pressure 2 - 9 mmHg without transfusion of blood components. The total amount of infused fluid was 3800 mL, estimated blood loss was 350 mL and urine output was 1110 mL, during the six-hour operation. The ABGA values during the operation are provided in . During the 70-minute post-anesthetic care unit stay, urine output was 850 mL, and vital signs were stable with alert mentality despite a PaCO2 value of 64 mmHg ().
The patient was discharged on postoperative day 15 without complication and remained asymptomatic at her 12-month follow-up without an electrolyte abnormality or sign of rejection.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [42.0, 'kg']}",82,77.9,86.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 42.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (42.0 kg - 20 kg) = 82.0 mL/hr.
Hence, the patient's fluid maintenance is 82.0 mL/hr."
4877,22,Maintenance Fluids Calculations,physical,decimal,pmc-3492090-1,Extracted,"A 1-day-old, 420g, Japanese boy was born through Cesarean section after a 25-week gestation to a 34-year-old, gravida 2, para 1 mother with pregnancy-induced hypertension. The Apgar scores of the baby were 4 and 8 at 1 and 5 minutes, respectively. He was placed on mechanical ventilation, and surfactant replacement therapy was administered for RDS. However, he developed pulmonary hemorrhage, and a chest X-ray revealed the deterioration of lung aeration. Surfactant replacement therapy was administered again, resulting in an improvement in oxygenation.
A chest X-ray obtained on postnatal day 2 revealed PIE in the right lung. High-frequency oscillatory (HFO) ventilation was initiated to prevent the progression of PIE. However, his condition gradually progressed over his entire right lung field (Figure ). He was treated with right lateral decubitus positioning from day 8 and steroid therapy (hydrocortisone, 2mg/kg per day for 3 days) from day 10. However, the PIE worsened progressively and growing diffuse pseudocystic changes occured (Figure ). Additional nitric oxide inhalation therapy was administered from day 13. Unfortunately, a sudden deterioration occurred at postnatal day 16. His systemic blood pressure (measured in millimeters of mercury) decreased from the 60s to the 40s, and his blood oxygen saturation at 100% fractional inspired oxygen concentration fell to 80%. A chest X-ray revealed progressively expanding PIE on the right side and a marked shift of the mediastinum to the left (Figure ).
His clinical condition rapidly deteriorated to the same pathophysiological condition as that of tension pneumothorax. Therefore, we chose to evacuate the PIE by percutaneous lung puncture. A peripheral intravenous catheter (24 gauge; Terumo, Tokyo, Japan) was inserted into his right lower lung. However, evacuation with this catheter was insufficient, and an Argyle™ trocar catheter (10 French; Nippon Sherwood Medical Industries Ltd, Tokyo, Japan) was inserted into the same location. A total of 24cm of water was suctioned with the trocar catheter, resulting in adequate evacuation of the PIE, resolution of the mediastinal shift, and dramatic improvement in clinical condition (Figure ). We used thoracic transillumination to monitor both the effectiveness of evacuation and the development of accidental pneumothorax. The drainage was discontinued 5 days after the lung puncture, and there was no PIE recurrence (Figure ). After complete resolution of PIE, bilateral bubbling shadows gradually appeared on chest X-rays. Chronic lung disease was diagnosed, and systemic and inhaled steroids were administered. He was weaned from HFO ventilation on day 34 and from ventilatory support on day 68.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [420.0, 'g']}",1.68,1.596,1.764,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 420.0 g so this converts to 420.0 lbs * kg/1000 g = 0.42 kg. Hence, the patient's maintenance fluid is 0.42 kg * 4 mL/kg/hr = 1.68 mL/hr.
Hence, the patient's fluid maintenance is 1.68 mL/hr."
4878,22,Maintenance Fluids Calculations,physical,decimal,pmc-3198695-1,Extracted,"A 34-year-old man with no history of systemic disease presented with fever; he had lost 8 kg during the week before presentation. Physical examination revealed no significant findings. Laboratory investigation showed several abnormal findings, including leukocytosis (14500 cells/μL; reference range [RR], 4500-11000 cells/μL) and elevated aspartate aminotransferase (61 U/L; RR, 10-42 U/L) and alanine aminotransferase (75 U/L; RR, 10-40 U/L) levels. Ultrasonography of the abdomen revealed marked thickening of the gallbladder wall. However, serum bilirubin (0.4 mg/dL; RR, < 1.5 mg/dL), alkaline phosphatase (140 U/L; RR, 40-140 U/L), and gamma-glutamyl transpeptidase (59 U/L; RR, 8-61 U/L) levels were normal. Initially, acute atypical cholecystitis with fever as the only symptom was diagnosed, and empirical antibiotic therapy was indicated (intravenous infusion of ceftazidime [2000 mg] 3 times per day). The fever persisted even after 1 week of antibiotic therapy, and blood culture was negative. A subsequent gallium-67 scan revealed a rim-like, gallium-avid lesion in the upper right quadrant of the abdomen (Figure ). Magnetic resonance imaging (MRI) was performed to clarify the nature of the gallbladder lesion and showed evident thickening of the epithelial and muscular elements and multiple intramural cysts of various sizes in the gallbladder wall (Figure ). GAM with intramural Rokitansky-Aschoff sinuses was suspected; however, the possibility of a malignant gallbladder tumor could not be ruled out entirely.
Exploratory laparotomy with cholecystectomy revealed an enlarged gallbladder (approximately 11 cm in diameter) with abscess formation in the gallbladder wall (Figure ). Pathological tests revealed extensive inflammatory cell infiltration and caseous-like necrosis consisting of chronic granulomatous inflammation with acute necrotizing inflammation. Mycobacterium tuberculosis culture of the specimen revealed negative results. The fever subsided after the cholecystectomy, and the patient was discharged uneventfully 10 days after the operation. He was followed up at our outpatient department more than 3 years later; he was well and did not have a fever.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [8.0, 'kg']}",32,30.4,33.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 8.0 kg. Hence, the patient's maintenance fluid is 8.0 kg * 4 mL/kg/hr = 32.0 mL/hr.
Hence, the patient's fluid maintenance is 32.0 mL/hr."
4879,22,Maintenance Fluids Calculations,physical,decimal,pmc-3146124-1,Extracted,"A 20 days old, full term, male baby weighing 3 kg delivered vaginally at a peripheral maternity hospital to a primigravida mother, presented to our hospital with respiratory distress since birth. The baby had cried immediately after birth, color was pink and peripheries were warm. The heart rate was 140/min and respiratory rate was 40/min. However, soon after birth were he started developing respiratory distress with suprasternal and intercostal recession. On auscultation, air entry on left side of the chest was decreased, heart sounds better heard on the right side. Pulse oximeter showed a saturation of 85% while using an oxygen hood.
A chest x ray () reported left pneumothorax with consolidation on the right side. Consequently, a chest tube was put in the left 4th intercostal space. However, the distress remained and the intercostal tube column was not moving. Repositioning it did not improve the status. Since respiratory distress persisted with antibiotics and other standard care the child was referred to our hospital. A CT scan () was performed which revealed gross mediastinal shift to the right side. The heart and other mediastinal contents appeared to be normal. There was evidence of collapse consolidation in right upper and left lower lung lobes with emphysema in left upper lobe and no pneumothorax. The chest tube was reported to be lying in emphysematous LUL. A diagnosis of congenital lobar emphysema was made and surgery was planned. The preoperative blood investigations revealed Hb of 11.9 g%, normal leukocyte, platelet counts and normal biochemistry. ABG analysis revealed a pH of 7.48, pO2 of 55 mmHg and pCO2 of 26 mmHg on FiO2 of 0.4. Echocardiography was normal. In the pre anesthesia check up, the baby had respiratory distress with RR of 56/min with suprasternal and intercostal recession. The saturation with an oxyhood was 85% and on room air was 75%. The air entry was decreased on left side and intercostal tube was in situ. The child was scheduled for left lobectomy on the next day, blood was ordered and no sedative premedication was prescribed.
In the OT, ECG, saturation and temperature monitoring was started and a peripheral line secured. Standard precautions to avoid hypothermia were taken and premedication with iv atropine 0.03mg and fentanyl 0.006 mg was given. A surgeon was washed up and ready to perform an emergency thoracotomy if the need arose. Induction was done by a mask with 100% O2 and sevoflurane 2-4%. After achieving an adequate depth of anaesthesia, trachea was intubated with size 3.0mm ETT fixed at 9 cm. Gentle assisted ventilation was done with hand using a Jackson Rees circuit, neonate placed in the right lateral position and anaesthesia maintained with sevoflurane 2-3% in 100% O2. Local anaesthetic 0.25% (2 ml) bupivacaine was infiltrated in the line of incision before starting surgery. Intraoperative analgesia was provided with intravenous ketamine given to a total of 10 mg in divided doses. A left upper lobectomy was performed through the 4th intercostal space with stable hemodynamics throughout the two hour surgical procedure. After lobectomy, the left lower lobe was expanded using gentle manual recruitment maneuver. Blood and fluid loss monitored and replaced with 120 ml of warmed Ringer's Lactate and 20 ml of fresh whole blood. At the end of the surgery, an intercostal block was given by the surgeon under direct vision using 2 ml of 0.25% bupivacaine. The saturation rose up to 100% after the lobectomy and the trachea was extubated after discontinuation of sevoflurane when full airway reflexes had returned. The baby was shifted to the post anesthesia care unit with no evidence of respiratory distress. Post operative analgesia was provided by rectal paracetamol. The patient made a rapid uneventful recovery and was discharged on 7th post operative day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.0, 'kg']}",12,11.4,12.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.0 kg. Hence, the patient's maintenance fluid is 3.0 kg * 4 mL/kg/hr = 12.0 mL/hr.
Hence, the patient's fluid maintenance is 12.0 mL/hr."
4880,22,Maintenance Fluids Calculations,physical,decimal,pmc-3475018-1,Extracted,"A 16 years old boy came to our attention because of polyuria (about eight liters of urine) and polydipsia associated with asthenia. There was family history of diabetes mellitus for the father and allergy to inhalants from the mother. He was second-born by normal delivery of consanguineous parents (first degree cousins); weight at birth was 3015 gr. From the age of five, the symptoms of polydipsia and polyuria have increased. At 10 years old, he suffered from a fracture of his left foot after a trauma of mild intensity. A physical examination revealed evidence of growth cessation. The patient’s weight and height were below the third percentile of growth (35, 4 Kg; 143 cm) and delayed puberty was diagnosed (absent pubarche, testicular volume 6-8 cc, penis stage was the third). At the time of admission, the patient’s clinical condition was poor, skin turgor was reduced, muscles appeared norm tonic but slightly hypertrophic. Thoracic, cardiac and abdominal examinations were normal. There was no clinical sign of neurologic diseases. Speech ability and school performance were good. Laboratory findings at admission were normal; the only abnormal values were hypophosphatemia, hypokalemia and hyper transaminasemia: (Aspartate Aminotransferase (AST) 47 U/L and Alanine Aminotransferase (ALT) 81 U/L while the normal ranges are 5-42). The diagnostic work-up for growth cessation and delayed puberty were initiated, but all of the findings were normal: thyroid hormones, gonadotropins, and IGF-1 and anti-transglutaminase antibodies. Hand and wrist x-rays confirmed the development of ossification centers in relation to chronological age (the corresponding skeletal age was 13 years old). Because of the presence of polyuria, urine specimens were examined for spot and a 24-hour sample confirmed intense polyuria (6000 ml), high urinary calcium level (670 mg; v.n. 100-300) , with normal excretion of other electrolytes, and low urinary creatinine (660 mg/24 h; v.n. 800-2000). Creatinine clearance was reduced: 70 ml/min (v.n. >100 ml/min). We tested the plasma and urinary osmolarity which were normal; the ultrasonography of abdomen showed hyper echogenic liver and pyramidal calcification of kidneys with enhanced corticomidollary differentiation features suggestive of medullary nephrocalcinosis (), and gallbladder lithiasis. Brain and pituitary gland magnetic resonance imaging did not reveal abnormality, neither in brain parenchyma nor Sella and parasellar regions. We checked calcitonin, parathyroid hormone, renin angiotensin aldosterone system and all results were found normal. Plasmatic, urinary amino acid levels and urinary acid organics did not reveal an abnormal pattern. In order to assess a possible cause for hyper transaminasemia lipid subset, alpha 1 antitrypsin, and liver kidney microsome tests were done. The complete infectivological panel did not reveal any abnormalities. The blood gas analysis showed a normal pH and bicarbonate level. The characteristics were compatible with an incomplete distal renal tubular acidosis that is the sign of WD. Finally the levels of serum concentration of copper and ceruloplasmin were 21 mcg/dl, v.n. 70-140 and 4 mg/dl v.n. 22-58 respectively which is another possible suggestion of WD. This suspicion was confirmed by elevated copper urinary excretion (111.30 mcg/24 hours’ urine; v.n. 0-50). Liver biopsy showed typical signs of WD when viewed on an electron microscope: mild lymphocytic infiltrate and eosinophilia granulocyte, no piecemeal necrosis, fatty liver degeneration (steatosis) to medium and small lipid droplets with moderate diffuse nuclear glycogenation, numerous Mallory bodies and lobular activity. Copper’s content was 270 μg/g dry weight of liver. Slit-lamp eye examination did not reveal the presence of typical Kayser-Fleischer ring, while a bone density scan revealed significant bone demineralization (). Molecular tests confirmed, through direct DNA sequencing, the presence of a mutation in homozygosis N1270S (belong to exon 18). We started therapy with D-Penicillamine (20 mg/Kg/day) given in three doses, one hour prior meals, B-vitamin complex and a low copper diet. Moreover, we initiated therapy for osteoporosis with Alendronate (70 mg/weekly) and calcium and D vitamin complex. After two months a decrease in urinary copper and calcium excretion were revealed. The ultrasonography features of mild hepatitis responded to treatment and hypercalciuria was slightly decreased while nephrocalcinosis was unchanged.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [35.4, 'kg']}",75.4,71.63,79.17,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 35.4 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (35.4 kg - 20 kg) = 75.4 mL/hr.
Hence, the patient's fluid maintenance is 75.4 mL/hr."
4881,22,Maintenance Fluids Calculations,physical,decimal,pmc-3127313-1,Extracted,"A 2-month-old 4.3 kg male child was diagnosed as extrahepatic biliary atresia and was scheduled for laparotomy. The child was brought to the pediatrics clinics 2 weeks earlier with complaints of rapid breathing since 12 days, vomiting (non bilious) since 8 days, and decreased oral intake since 1 day. The child was passing clay colored stools and dark colored urine. There was yellow discoloration of skin since 2 weeks, which was progressively increasing. The mother revealed the presence of recurrent rhinorrhoea from the first day of life.
Examination revealed icterus. Abdomen examination showed hepatospenomegaly (liver on left side and spleen on right side) and umbilical hernia. Electrocardiogram (ECG) displayed inverted P waves in I, aVL and aVR, which were suggestive of situs inversus. Chest X-ray revealed evidence of bronchopneumonia and the cardiac shadow was on the right side. Ultrasonography abdomen also indicated situs inversus. Echocardiography was suggestive of situs inversus with dextrocardia with normal cardiac anatomy. Hepatobiliary iminodiacetic acid (HIDA) scan was indicative of extra hepatic biliary atresia (EHBA) with the liver in left upper abdomen. Child was diagnosed as situs inversus with dextrocardia, bronchopneumonia, and extrahepatic biliary atresia.
Bronchopneumonia was managed with intravenous antibiotics, paracetamol, and steam inhalation. The child was placed on therapy with oral phenoparbitone 10 mg twice a day and intravenous Vitamin K 5 mg once a day for 10 days. Investigations revealed hemoglobin 9.5 g/dL, total leucocyte count (TLC) 17400/mm3, platelet count 4.5 lac/mm3, serum sodium 131 meq/L, serum potassium 4.4 meq/L, random blood sugar 70 mg/dL, serum bilirubin 19.2 mg/dL (normal 0.2-1.2) (direct-12, indirect 7.2), SGOT 148IU/L (normal 15-50) , SGPT 93 IU/L (normal 15-50), alkaline phosphatase 1232 IU/L (normal 50-300), blood urea 18 mg/dL (15-45), serum creatinine 0.6 mg/dL (0.6-1.2), prothrombin time (PT) 11.3 sec (test), 12 sec (control), and aPTT test 38.7 sec Control 29 sec (normal 20-40 sec). The child was listed for corrective biliary surgery.
The operating room was kept warm prior to shifting of the child. In the operating room, routine monitors (electrocardiogram, pulse oximeter, non invasive blood pressure) were attached. Left-sided ECG leads were attached on the right side and vice versa. Anesthesia was induced with intravenous fentanyl (9 μg) and thiopentone (25 mg), and lungs were ventilated with isoflurane in oxygen and nitrous oxide (50:50) (MAC 1.2) using Jackson Rees modification of Ayre's T piece. After achieving neuromuscular blockade with atracurium (2.5 mg), trachea was intubated with endotracheal tube size 3.5 mm ID. Capnography and temperature monitoring was also initiated. Urethra was catheterized and urinary output was monitored. Anesthesia was maintained with desflurane in oxygen and nitrous oxide (50:50) (MAC 1) using paediatric close circuit along with boluses of atracurium (0.5 mg) and fentanyl (1 μg) as required. The child was kept warm using warm fluids, warming mattress and by adequately covering the child with cotton.
The surgeon found the liver on left side with right lobe on the left side, malrotated gut (caecum, appendix on the left side), two atretic gall bladders, annular pancreas with preduodenal portal vein, cirrhotic enlarged liver, and a multi-lobulated spleen. Hepatic roux-en-y portoenterostomy with Ladd's procedure was done. The surgical incision site was infiltrated with 6 mL of 0.125% bupivacaine. The hydration was maintained using normal saline. The surgery lasted 5 hours, and blood loss of 100 mL was replaced with packed red blood cells.
At the end of surgery, the airway resistance increased. The airway pressures increased from 18 cm H2O to 28 cm H2O. Endotracheal tube suctioning was done. On auscultation, breath sound was reduced on the right lung fields. Repeat suction was done. We suspected a mucus plug to be obstructing the endotracheal tube and changed the tube after repeat laryngoscopy. A mucus plug was seen at the tip of the tube. The ventilation became better. Residual neuromuscular blockade was reversed and trachea was extubated. The child had good respiratory efforts with bilateral equal air entry. The child was shifted to the pediatric intensive care unit for further management. The child was nursed in the incubator and ECG and pulse oximeter monitoring were continued. The vitals and urinary output were within normal limits. The humidified oxygen was supplemented using an oxygen hood. The postoperative hemoglobin was 9.9 g/dL. The serum electrolytes were normal. The analgesia was provided with rectal paracetamol suppository. The child had an uneventful recovery and was discharged on the 18th postoperative day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.3, 'kg']}",17.2,16.34,18.06,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.3 kg. Hence, the patient's maintenance fluid is 4.3 kg * 4 mL/kg/hr = 17.2 mL/hr.
Hence, the patient's fluid maintenance is 17.2 mL/hr."
4882,22,Maintenance Fluids Calculations,physical,decimal,pmc-8215124-2,Extracted,"A 14.5-year-old, 87.5-kg female with 1p36 deletion syndrome and associated developmental delays presented in cardiorespiratory failure. Upon admission to our institution, she was diagnosed with LVNC cardiomyopathy with severely depressed left ventricle function. She had a history of low muscle tone and some congenital hypotonia, feeding difficulties, mild facial dysmorphism, underlying gross and global developmental delay, and partial hearing loss. There was no known 1p36 deletion family history.
She had been in her usual state of health without cardiac issues until 1 week prior to presentation when she developed persistent abdominal pain, worsening appetite, and orthopnea. She presented to local emergency department, and given sepsis concern, she was transferred to an acute hospital where she was intubated and started on dopamine and milrinone due to EF of 23%. She was then transferred to our institution for further stabilization of her heart failure as well as evaluation for cardiac transplantation or LVAD.
The echocardiogram at admission showed LVNC cardiomyopathy with decreased left-ventricular systolic function with EF of 34%. The patient was found to be in ventricular tachycardia with hemodynamic compromise, likely secondary to heart failure and volume overload. The arrhythmia was resolved with pleural effusion drainage and weaning of inotropic support, and it did not recur prior to transplantation. Computed tomography angiography (CTA) showed increased trabeculations in the left ventricle, particularly in the midsections and apex with a non-compacted to compacted ratio of 2.5 (). Extubation was attempted, but ultimately, she failed due to poor cardiac function. Right heart catheterization revealed favorable Pulmonary vascular resistance (PVR), while on inotropic drips. The patient was listed for cardiac transplantation, and 2 days later, a suitable organ donor became available, and the patient was successfully transplanted.
As of this writing, the patient is now 1 year 8 months after cardiac transplantation and has done well from a cardiac perspective with normal function and no history of rejection ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [87.5, 'kg']}",127.5,121.125,133.875,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 87.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (87.5 kg - 20 kg) = 127.5 mL/hr.
Hence, the patient's fluid maintenance is 127.5 mL/hr."
4883,22,Maintenance Fluids Calculations,physical,decimal,pmc-8436272-1,Extracted,"The first patient, an 8.5-year-old female, was referred to the endocrinology clinic to be evaluated for short stature. She was born at term from healthy consanguineous parents (first cousin).
On examination, her height was 97 cm (−6.4SD), weight 17.2 kg (−3.4SD) and Tanner stage 1. Her blood pressure was 110/70 mmHg with a heart rate of 85 bpm. She had a prominent forehead, flattened nasal bridge, hypertelorism and short limbs concerning trunk length (). There were no goiter, hepatosplenomegaly or skin manifestations. Her biochemical workup tests () showed normal levels of thyroid-stimulating hormone (TSH) and cortisol, a low level of insulin-like growth factor (IGF1) and a high level of fasting growth hormone (GH). GH stimulating test with insulin (0.1 U/Kg/IV) showed high levels of GH post-stimulation. Her bone age was 5 years, the combination of typical features, low level of IGF1 and elevated levels of fasting and post-stimulating GH to lead to the diagnosis of LS (index case). At the age of 9.5 years, she developed subclinical hypothyroidism (TSH: 8 UL/mL with normal free thyroxine FT4: 8.4 μg/dL and thyroid peroxidase antibodies (TPOAb): 21 IU/mL), treated with levothyroxine (3 mcg/kg/day).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [17.2, 'kg']}",54.4,51.68,57.12,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 17.2 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (17.2 kg - 10 kg) = 54.4 mL/hr.
Hence, the patient's fluid maintenance is 54.4 mL/hr."
4884,22,Maintenance Fluids Calculations,physical,decimal,pmc-6900420-1,Extracted,"A 70-year-old man (weight 70 kg, body mass index 25.7 kg/m2) with underlying hypertension and dyslipidemia underwent an elective open hernioplasty for right inguinal hernia under ambulatory surgery. He had normal airway features: good mouth opening, Mallampati score of 1, thyromental distance > 6 cm and normal tongue protrusion. General anesthesia was induced with intravenous propofol 200 mg plus fentanyl 100 μg and a size 4 LMA ProtectorTM Airway was placed smoothly in a single attempt by a senior resident. The cuff was inflated with 25 ml of air and the black line indicator on the cuff pilot valve remained within the green zone throughout the surgery. However, we did not check the intra-cuff pressure using manometry. The oropharyngeal leak pressure was 25 cmH2O. The sternal notch test and bubble test were performed after insertion to confirm the placement of the LMA protector []. Anesthesia was maintained with a mixture of sevoflurane and oxygen/air. The patient’s breathing was supported with a pressure support of 8 cmH2O, which generated a tidal volume of 400–450 ml and the maximum minute ventilation attained was 12 L/min with peak pressures of 8–10 cmH2O. He was placed in a supine position with standard American Society of Anesthesiologists monitoring for the surgery which lasted for 180 minutes. The surgery was uneventful, and the patient’s vital signs were stable throughout. Postoperatively, the LMA was removed smoothly when he was awake. Moreover, blood stains or minimal secretions were not observed on the device.
At the post anesthesia care unit, the patient complained of difficulty in chewing food and a weird tongue movement. He had no voice changes or altered taste sensation. On examination, the patient’s tongue was seen to be deviated to the left during active protrusion (). All sensations of the tongue were intact and there were no tongue fasciculations or wasting. The neurological examination revealed no lateralizing signs or limb weakness. The gag and cough reflexes as well as other cranial nerves were normal. The patient was referred to the ENT surgeon the same day. The nasoendoscopy examination was unremarkable. The working diagnosis was that of an isolated left hypoglossal nerve palsy or neuropraxia. He was allowed to go home the same day with reassurance, oral prednisolone for one week, and instructed for follow up at the ENT outpatient clinic. Neuroimaging was not required. He achieved complete recovery 3 months after the injury (, ) and was subsequently discharged from the follow-up clinic.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [70.0, 'kg']}",110,104.5,115.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 70.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (70.0 kg - 20 kg) = 110.0 mL/hr.
Hence, the patient's fluid maintenance is 110.0 mL/hr."
4885,22,Maintenance Fluids Calculations,physical,decimal,pmc-7831216-1,Extracted,"A 43-year-old man with a 20-year history of bipolar disorder attempted suicide by ingesting pills containing 20 g caffeine. He arrived at our hospital 100 min after ingestion. Vital signs included: respiratory rate, 30 breaths/min; SpO2, 97% (ambient air); heart rate, 130 b.p.m.; blood pressure, 126/69 mmHg; and Glasgow Coma Scale score, E4V5M6. The patient had 10 bouts of watery vomit. He was 176 cm tall and weighed 60 kg.
Premature ventricular contractions were observed on electrocardiography (Fig. ). Blood examination revealed: white blood cell count, 7500/μL; creatine phosphokinase, 66 IU/I; and potassium, 2.6 mEq/L. Arterial blood gas analysis revealed respiratory alkalosis and metabolic acidosis: pH 7.43; PCO2, 27.3 mmHg; PO2, 124 mmHg; HCO3, 17.7 nEq/L; and lactate, 6.5 mmol/L. He had ingested 333 mg/kg of caffeine, with blood levels showing 42 μg/mL (poisoning range ≥25 μg/mL) 2 h after ingestion. Blood theophylline levels, a metabolite of caffeine, were at or below measurement sensitivity (poisoning range ≥20 μg/mL). Although a normal blood pressure at arrival was maintained, a wide QRS complex and a pulse rate of 130 b.p.m. were observed.
At 50 min after arrival, a flexible double-lumen catheter was placed in the right internal jugular for emergency hemodialysis. Sixty minutes after arrival, when the arrhythmia occurred, a catheter sheath was placed in the right femoral vein and left femoral artery to enable rapid introduction of extracorporeal membrane oxygenation (ECMO). Sixty-five minutes after arrival, midazolam (10 mg), fentanyl (0.1 mg), and rocuronium (50 mg) were used to initiate tracheal intubation and artificial respiratory management. Eighty minutes after arrival, when he was placed in the left lateral decubitus position during endoscopy, he developed pulseless ventricular tachycardia. Eighty-two minutes after arrival, chest compressions and defibrillation yielded successful return of spontaneous circulation; however, he developed ventricular fibrillation. Eighty-five minutes after arrival, VA-ECMO was introduced from the sheath catheter site, ensuring a blood supply of 3.5 L/min at 2000 rpm. Because potassium levels were low, they were replenished, which eliminated premature ventricular contractions. One hundred minutes after arrival, hemodialysis was introduced at a flow rate of 100 mL/min from the flexible double-lumen catheter and a dialysate flow rate of 4000 mL/h. After hemodialysis, the patient’s tachycardia began to improve. Sixteen hours after arrival, the premature ventricular contractions decreased and hemodialysis was terminated. The premature ventricular contractions did not reappear after termination of dialysis, and his heart rate maintained a sinus rhythm at 90 b.p.m. Dialysis was terminated when the PaO2/FiO2 ratio was at 450 mmHg, and the patient was weaned off ECMO. On hospital day 2, ECMO was terminated when the patient had a heart rate of 70 b.p.m., blood pressure of 130/80 mmHg, respiration rate of 16 breaths/min, and electrocardiographic waveform with sinus rhythm, suggesting he had escaped the acute poisoning state (Fig. ). He also returned to a lucid state of consciousness. Extubation was carried out on hospital day 4, and the serum caffeine level was 5.5 μg/mL, with a serum theophylline level of 3.7 μg/mL (Fig. ). Rehabilitation was started on the day of extubation, and he was transferred to a psychiatric hospital on day 21.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.0, 'kg']}",100,95,105,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.0 kg - 20 kg) = 100.0 mL/hr.
Hence, the patient's fluid maintenance is 100.0 mL/hr."
4886,22,Maintenance Fluids Calculations,physical,decimal,pmc-4183039-1,Extracted,"Black female patient, aged 4 years and 6 months, hospitalized for surgical correction
of a heart defect. She was the only daughter of a non-consanguineous couple, aged 27
(mother) and 23 (father). The mother had three other healthy children from two
previous marriages. There was no history of congenital heart disease in the family.
The mother reported occasional alcohol intake during pregnancy. Syphilis was
diagnosed in the 4th month of gestation and treated with Penicillin. The patient also
had loss of amniotic fluid during pregnancy. The child was born by caesarean section,
cephalic presentation, 30 weeks preterm, weighing 2,075g, measuring 42,5 cm, head
circumference of 31cm, and had Apgar scores at 1 and 5 minutes, of 8 and 9
respectively. The child cried immediately after birth and was not cyanotic. The
screening test was normal. Congenital heart disease was discovered at 4 months of
life. The neuropsychomotor development was normal and there were no behavior
problems.
On physical examination, at 4 years and 6 months old, the patient presented weight of
17,500g (50-75th percentile), height of 105cm (50-75th percentile), and head
circumference of 48.5cm (2-50th percentile) (anthropometric measures evaluated
according the CDC Growth Charts -
http://www.cdc.gov/nchs/data/series/sr_11/sr11_246.pdf). The patient was not
syndromic but had dysmorphic features that included bilateral epicanthal folds, broad
nasal root with bulbous nose, high arcade palate, large mouth with thick lips,
pectus carinatum, cubitus valgus, and clinodactyly of fifth
fingers. On the skin, there were many (more than six) café-au-lait spots measuring
about 2-3cm in the trunk and limbs and freckles in the axillary and inguinal regions
(). Family history revealed that the
father had similar skin findings (multiple café-au-lait spots and freckles in the
axillary/inguinal regions). This enabled the diagnosis of NF1, which was also
confirmed by dermatological evaluation. Ophthalmologic examination was normal.
Cardiac evaluation of the child by echocardiography revealed unroofed coronary sinus
atrial septal defect. There was no persistence of left superior vena cava. These
cardiac findings were confirmed at surgery. The procedure consisted of repair of
atrial septal defect with autologous pericardium. Abdominal ultrasonography and spine
radiography were normal. The high-resolution karyotype by GTG banding and
fluorescence in situ hybridization for 22q11 microdeletion (using the probe TelVysion
TM TUPLE 1, Abbott Molecular Inc.) were also normal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [17500.0, 'g']}",55,52.25,57.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 17500.0 g so this converts to 17500.0 lbs * kg/1000 g = 17.5 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (17.5 kg - 10 kg) = 55.0 mL/hr.
Hence, the patient's fluid maintenance is 55.0 mL/hr."
4887,22,Maintenance Fluids Calculations,physical,decimal,pmc-7888275-1,Extracted,"A male infant was born to a 30-years-old mother with no significant medical history (gravida 0, para 0, abortus 0) who became pregnant via natural insemination. At 23 weeks of gestation, the mother was referred to our hospital because of severe fetal growth restriction caused by utero-placental insufficiency and was treated with antenatal steroids. Fetal maturity was ascertained by calculating from the mother's last menstrual period and was confirmed by prenatal ultrasound. Prenatal counseling was conducted for the parents, and they requested to give birth by cesarean section. At 24 weeks and 0 days of gestation, the infant was delivered by emergency cesarean section because of interrupted blood flow in the umbilical cord; there was no umbilical cord coiling or amniotic fluid staining. The weight of the placenta was 60 g. Placental pathology revealed infarction. No findings of chorioamnionitis were observed. Immediately after birth, he was wrapped using a plastic bag on a prewarmed radiant warmer. The ambient temperature of the operating room was set to 27°C (). He was intubated in the operation room with a 2-mm endotracheal tube and transferred to the NICU in an incubator. The admission temperature at the axilla was 35.8°C. The humidity in the incubator was set at 90% on day 0 in order to reduce insensible water loss, and it was lowered by 5% daily to 60% (). His Apgar score was 2 at 1 min after birth, 6 at 5 min, and 6 at 10 min. Apart from his size, his physical examination and laboratory test results were unremarkable. Postnatal maturation assessment was adequate for a preterm infant born at 24 weeks of gestation. Genetic disorders were ruled out as a cause of intrauterine growth restriction based on the findings of physical examination and ultrasonography and the results of blood examination including blood gas, complete blood count, and biochemistry. Hence, genetic testing was not performed. His birth weight was 268 g (−3.92 SD). In order to prioritize stabilization, his head circumference and length were not measured at birth; when they were measured for the first time on postnatal day 16 (postmenstrual age 26 weeks, 2 days), his head circumference was 18.5 cm (−3.03 SD) and his length was 24.0 cm (−3.7 SD). On arrival to the NICU, he was placed on high-frequency oscillatory ventilation because of low pulmonary compliance, and a surfactant was administered on days 0 and 2. Sedation was not performed. Anhydrous caffeine was started from day 0. Prophylactic antibiotics (ampicillin, gentamicin, and fosfluconazole) were administered after birth and continued until day 6. Because the umbilical artery was narrow, an umbilical artery catheter could not be inserted. The infant's blood pressure was measured after birth via a 24G peripheral arterial catheter to avoid the risk of damage that a cuff would pose to his immature skin and was the approximate value expected for his gestational age; thus, no inotropes were administered. After the catheter occluded on day 8, we assessed his blood pressure mainly by physical examination. The target ranges of osmotic agents were set with reference to previous studies, and his albumin level was kept above 2.5 g/dL to maintain osmotic pressure (–). Echocardiography was performed to diagnose patent ductus arteriosus (PDA) on day 1. We administered 0.1 mg/kg per dose of indomethacin, because echocardiography represented an increased shunt volume of PDA (, ). PDA closed after indomethacin administration on day 1. He required 45 days of mechanical ventilation, including 40 days of high-frequency oscillation (). He was extubated on day 45 (30 weeks and 3 days of postmenstrual day) when we confirmed that the prongs of our continuous positive airway pressure machine fit his nose. His body weight when measured after extubation was 518 g on day 51 (31 weeks and 2 days of postmenstrual day). From day 42, he received a systemic steroid (dexamethasone) for 10 days, as advised by Doyle et al. (). After successful extubation, he required nasal continuous positive airway pressure for 7 days and a high-flow nasal cannula for 116 days. Target SpO2 was set at 85–95% before 34 weeks of postmenstrual age and above 95% afterward.
Parenteral nutrition was started on day 0 via an 18G umbilical venous catheter. After this catheter became occluded on day 12, a 27G peripherally inserted central venous catheter was used, but it also became occluded on day 19. From then on, parenteral nutrition was continued via a peripheral venous catheter. On day 1, oral administration of the mother's breast milk using a cotton swab was performed by the parents, and trophic feeding via nasogastric tube was started. A maximum of 3 mL/kg of 5-fold-diluted amidotrizoic acid was rectally administered for 1 week starting on day 1, resulting in successful defecation. After 3 days of trophic feeds, enteral feeding was stopped because the infant's abdomen was gradually becoming distended. His daily abdominal X-ray indicated significantly expanding intestinal gas, and we diagnosed him with meconium-related ileus. Intragastric administration of 3 mL/kg 5-fold-diluted amidotrizoic acid succeeded in triggering mass excretion of feces, as described in previous studies (–). Subsequently, abdominal distention improved, and enteral feeding was resumed. Fortified breast milk was used from day 20 when the infant's breast milk consumption reached 100 mL/kg per day. We maintained him on a breast milk diet for most of his hospital stay, adding medium-chain triglyceride oil from day 94 to 133 for calorie enrichment. The calorie goal was set at 120–140 kcal/kg/day. Oral feeding was initiated on day 98, and the gastric tube was removed on day 137. During the treatment, blood glucose was managed within the reference range with glucose administration and enteral feeding only, except for insulin administration at day 1 and from day 5 to 6. Fluid intake was determined from vital signs and physical findings, fluid balance, and blood test results. Fluid intake was relatively restricted in expectation of reducing risk of morbidities and complications (). Transepidermal water loss was estimated based on the sodium levels, fluid intake, urine output, and previous reports (). Total fluid volume administered on day 0 was 65 mL/kg; for most of the period after the patient stabilized, it was maintained between 130 and 160 mL/kg per day. Minimal handling was conducted in all aspects of the patient's management. As described above, anthropometric measurements were kept to a minimum, and our patient's weight was estimated from fluids and nutritional balance and was adjusted on the day it was measured. After his first weighing on day 0, he was not weighed again until day 30 to confirm the anticipated growth. His body weight, length, and head circumference were measured every 2 weeks after that. Until day 42, we kept him in a prone position without postural change, aiming to prevent both gastroesophageal reflux and unplanned extubation. During that period, we undertook careful skin management, making sure to give him proper support to prevent bedsores. Although minimizing postural change may increase the risk of skin and pulmonary infection, there were only two events after the day of birth when we had to administer antibiotics: from day 38 to 45 for suspected aspiration pneumonia and from day 66 to 76 for cellulitis due to methicillin-sensitive Staphylococcus aureus at the site of the removed peripheral catheter. Blood sampling was also minimized to reduce the frequency of painful procedures and the risk of iatrogenic anemia. For a month after birth, heel sticks were performed as little as once per day to analyze blood gas, electrolytes, metabolic factors (glucose, lactate), and biochemical factors (albumin, phosphate, C-reactive protein). We performed a comprehensive blood examination (complete blood count and biochemical tests) only once every week or two ().
In addition to minimal handling, we encouraged parental involvement from the day of birth. Shortly after the infant was born, the family began to talk to him and hold him. The parents frequently visited our NICU to engage in physical contact with him, including breastfeeding, which was performed from day 1 ().
Magnetic resonance imaging of the head at 45 weeks of postmenstrual age revealed no detectable abnormalities. An automated auditory brainstem response test was bilaterally passed. However, the infant developed bilateral retinopathy of prematurity (stages 2–3), requiring laser treatment. He was discharged from the hospital on day 176 (postmenstrual age, 49 weeks and 1 day) without any requirement for home oxygen therapy or tube feeding. His body weight at discharge was 3,238 g (−3.41 SD), his head circumference was 35.5 cm (−1.31 SD), and his length was 46.8 cm (−4.55 SD) () (). The patient's mother said that she could only say how happy she was that he had grown so much.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [268.0, 'g']}",1.072,1.0184,1.1256,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 268.0 g so this converts to 268.0 lbs * kg/1000 g = 0.268 kg. Hence, the patient's maintenance fluid is 0.268 kg * 4 mL/kg/hr = 1.072 mL/hr.
Hence, the patient's fluid maintenance is 1.072 mL/hr."
4888,22,Maintenance Fluids Calculations,physical,decimal,pmc-4127409-1,Extracted,"A 54-year-old Korean man presented with a month-long history of cough and yellowish sputum, an 8-kg weight loss over the course of three months and Modified Medical Research Council Dyspnea Scale grade 1 dyspnea. He had no history of surgery or other medical illness and he was a current smoker (30 pack-years). On examination, his blood pressure was 100/80 mm Hg, pulse rate was 76 beats/min, respiratory rate was 24 breaths/min, and body temperature was 36.5℃. On chest auscultation, breathing sounds were abnormal with coarse rales in both upper lung fields. Initial arterial blood gas results were pH 7.428, pCO2 32.8 mm Hg, pO2 85.1 mm Hg, HCO3- 21.2 mmol/L, and SaO2, 97.8% in ambient air. Blood tests showed a white blood cell count of 6,700/mm3 (normal, 4000-10000/mm3), hemoglobin of 12.8 g/dL (normal, 12.5-15 g/dL), and a platelet count of 178/mm3 (normal, 150-450/mm3). The C-reactive protein level was found to be 5.23 mg/L (normal, 0-0.75 mg/L). A blood chemistry panel revealed a blood urea nitrogen level of 45.3 mg/dL (normal, 7-20 mg/dL), creatinine of 1.0 mg/dL (normal, 0.5-1.5 mg/dL), total protein of 8.3 g/dL (normal, 6.0-8.3 g/dL), albumin of 3.2 g/dL (normal, 3.5-4.5 mg/dL), and aspartate aminotransferase/alanine aminotransferase of 78/54 IU/L (normal, 8-40/5-35, respectively). Cardiac enzyme labs were found to be elevated: CK-MB, 33.21 ng/mL (normal, 0-5 ng/mL); troponin-I, 0.904 ng/mL (normal, 0.0-0.2 ng/mL); and brain natriuretic peptide, 183.20 pg/mL (normal, 0-99 pg/mL). Electrocardiography (ECG) revealed nonspecific ST- or T-wave abnormalities. Initial chest radiographs showed numerous nodules in both apices suggestive of active pulmonary tuberculosis (). Chest computed tomography (CT) showed two large cavities in the right upper lobe and small nodules in both lungs (). There were no abnormal lesions present in either adrenal gland. There was a 1.9-cm ovoid filling defect in the apex of the left ventricle (LV) suggestive of a thrombus (). Echocardiography showed a balloon-like akinesia of the apex wall (), a 1.65×1.21-cm apical thrombus (), and the left ventricular ejection fraction was 56.7%.
We started anticoagulation with low molecular weight heparin for the LV thrombus. Coronary CT angiography showed normal epicardial coronary arteries. The next day, CK-MB and troponin I levels normalized to 1.09 ng/mL and 0.267 ng/mL, respectively. Follow-up ECG showed T-wave inversion at the V3-V6 leads in contrast to the normal initial ECG. Sputum studies showed positive results for acid fast stain and polymerase chain reaction for mycobacterium tuberculosis. We started first-line anti-tuberculosis medication (rifampin, isoniazid, ethambutol, and pyrazinamide) immediately. Ten days later, follow-up echocardiography showed normalized LV apical wall motion and no evidence of akinesia of the apex wall (). The left ventricular ejection fraction was 58%. The LV thrombus was still noted on imaging, but decreased in size (). Seventeen days later, we confirmed a diagnosis of pulmonary tuberculosis through positive tuberculosis culture. Drug susceptibility test revealed all sensitive results. He completed a six months of treatment with rifampin, isoniazid, ethambutol and pyrazinamide for two months, followed by rifampin and isoniazid for four months. During the follow-up period, there was no physical evidence of recurrence in TTC.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [8.0, 'kg']}",32,30.4,33.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 8.0 kg. Hence, the patient's maintenance fluid is 8.0 kg * 4 mL/kg/hr = 32.0 mL/hr.
Hence, the patient's fluid maintenance is 32.0 mL/hr."
4889,22,Maintenance Fluids Calculations,physical,decimal,pmc-6381853-1,Extracted,"A 42-year-old Saudi male from Jizan, with a comorbidity of hypertension and type 2 diabetes mellitus diagnosed 6 years prior (well controlled by oral antidiabetic agents: metformin 1000 mg twice daily and gliclazide 30 mg once daily), presented with impaired renal function and hematuria. After basic laboratory investigations, kidney biopsy was performed. Histological examination with light microscope revealed a global sclerosed glomeruli, minimal interstitial fibrosis and tubular atrophy []. A diagnosis of glomerulonephritis of unknown etiology was made and treatment with mycophenolate (1 g PO twice daily) and prednisone (20 mg PO once daily) was initiated.
After 3 months, the patient presented with a 3-week history of fever, abdominal pain and fatigue. The fever was subjective, intermittent, associated with chills and rigors, especially at night, and not relieved by paracetamol. The abdominal pain was intermittent, diffuse and colicky in nature and was associated with nausea and vomiting without blood (2–3 times/day). During these 3 weeks, the patient's appetite decreased, owing to which he lost 7 kg in weight. In addition, the patient reported a history of animal contact (goat and sheep), ingestion of raw goat milk and swimming in the valley water. There was no history of rash, cough, hemoptysis, jaundice, diarrhea, constipation, dysuria, change in urine color, arthralgia, visual disturbances, oral ulcers, genital rash, discharge or contact with tuberculosis patients.
On physical examination, the patient was found to be obese, sweating, not jaundiced or cyanosed. He was conscious, alert and oriented to time, place and person. His vital signs were as follows: body temperature, 38.6°C; pulse rate, 98 beats/min; respiratory rate, 24 breaths/min; blood pressure, 125/85 mmHg; and oxygen saturation, 100% on room air. He was pale, with normal jugular venous pressure and no oral ulcers or thrush. Abdominal examination revealed mild epigastric tenderness and a palpable liver 4 cm below the costal margin with a 15-cm liver span. The rest of the examinations were within normal limits.
Laboratory investigations on admission revealed a white blood cell (WBC) count of 2.65/mcL (neutrophils, 72.1%; lymphocytes, 23.2%; monocytes, 4%; and eosinophils, 0.7%). Results of other hematological examinations were as follows: hemoglobin level, 8.8 g/L; erythrocyte sedimentation rate, 88 mm/h; platelet count, 87,000/mcL; and reticulocyte count, 1.28%. Level of ferritin was 1000 ng/mL, with a transferrin saturation of 11.22 mg/dL. Estimation of electrolytes showed sodium 138 mEq/L, potassium 3.2 mEq/L and bicarbonate 25 mmol/L. Liver function tests showed that total protein was 6.1 g/dL, albumin 3.2 g/dL, total bilirubin 1.2 mg/dL, alanine transaminase 71 IU/L, aspartate transaminase 42 IU/L, alkaline phosphatase 179 IU/L and gamma-glutamyl transferase 447 IU/L. International normalized ratio was 0.8. Renal function tests showed that blood urea nitrogen was 12 mg/dL and creatinine 2.15 mg/dL. Level of lactate dehydrogenase was 732 U/L and C-reactive protein 53 mg/L. Urine analysis showed 2–5 WBCs/high-power field and 10–25 red blood cells/high-power field with no nitrites. Sickling test and direct/indirect Coombs test were negative, and the stool test result was normal.
Chest X-ray and electrocardiogram were normal. Abdominal ultrasound showed an enlarged liver (16.2-cm liver span) and a mildly enlarged spleen (14 cm in length). Kidneys were normal in size, with a mild increase in the echogenicity of renal parenchyma, but no hydronephrosis or ascites.
The serological tests for viral hepatitis, human immunodeficiency virus, Epstein–Barr virus, cytomegalovirus, Toxoplasma and Brucella were negative. Rheumatoid factor, antinuclear antibody, antineutrophil cytoplasmic antibody, antiglomerular basement membrane antibody, anti-Sjögren's syndrome A and B antibodies and cryoglobulin were negative. Malaria smear and blood cultures were also negative.
The patient's condition continued to deteriorate and he developed continuous fever of up to 40.5°C. Repeated tests after 5 days revealed the following: WBC, 1.4/mcL; hemoglobin, 6.7 g/dL; platelet, 55,000/mcL; creatinine, 3.3 mg/dL; C-reactive protein, 151 mg/L; total bilirubin, 2.9 mg/dL; alkaline phosphatase, 460 IU/L; alanine aminotransferase, 80 IU/L; aspartate aminotransferase, 138 IU/L; gamma-glutamyl transferase, 651 IU/L; albumin, 2.5 g/dL; and lactate dehydrogenase, 1400 U/L.
Bone marrow aspirate showed mild hypocellular marrow with no evidence of dysplasia or malignancy. Bone marrow culture for Brucella was negative. Further, Leishman-Donovan bodies were not detected by light microscope. Polymerase-chain reaction test for the diagnosis of tuberculosis, serological tests for dengue fever and Q fever as well as β-D-Glucan and galactomannan antigen tests were all negative. Liver biopsy showed granulomatous hepatitis with extramedullary hematopoiesis. After 1 week of admission, the patient was treated empirically with broad-spectrum antibiotic (meropenem intravenously, 1 g every 8 h for 6 days); however, there was no improvement.
Additional serological testing using enzyme-linked immunosorbent assay (ELISA) releveled the presence of anti-Leishmania antibodies. Based on this, the patient was started on liposomal amphotericin B course as a treatment for VL (4 mg/kg intravenous on Days 1–5, 10, 17, 24, 31 and 38), despite the lack of a definitive diagnosis. After 1 week, the patient improved clinically, the fever subsided, the laboratory parameters began to improve and at the end of liposomal amphotericin B course, all tests returned to normal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.0, 'kg']}",28,26.6,29.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.0 kg. Hence, the patient's maintenance fluid is 7.0 kg * 4 mL/kg/hr = 28.0 mL/hr.
Hence, the patient's fluid maintenance is 28.0 mL/hr."
4890,22,Maintenance Fluids Calculations,physical,decimal,usmle-3901,Extracted,A 65-year-old African-American man comes to the physician for a follow-up examination after presenting with elevated blood pressure readings during his last visit. He has no history of major medical illness and takes no medications. He is 180 cm (5 ft 9 in) tall and weighs 68 kg (150 lb); BMI is 22 kg/m2. His pulse is 80/min and blood pressure is 155/90 mm Hg. Laboratory studies show no abnormalities.,"Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [68.0, 'kg']}",108,102.6,113.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 68.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (68.0 kg - 20 kg) = 108.0 mL/hr.
Hence, the patient's fluid maintenance is 108.0 mL/hr."
4891,22,Maintenance Fluids Calculations,physical,decimal,pmc-6042642-1,Extracted,"A 7-month-old male, intact, 18 kg (39.6 lb) Labrador mix presented for acute vomiting, rigidity, and dull mentation. The owners had not been home for 14 h prior. When they returned, they found the dog laterally recumbent, rigid, but conscious, with vomit, and a chewed lamotrigine (GlaxoSmithKline plc, Lamotrigine [Lamictal XR Extended Release], Brentford, London, UK) bottle nearby. The dog ingested approximately fifty 100 mg tablets. The estimated oral dose ingested was 278 mg/kg (611.6 mg/lb). There were no other animals in the household. The dog had been healthy with no previous illnesses.
On presentation, the dog had a rectal temperature of 39.4°C (103.0°F). On physical examination, the dog had good body condition. He was tachypneic at 60 breaths per minute with clear lung fields. The mouth was rigidly closed. Abdominal palpation was soft with no intra-abdominal masses. Rectal examination revealed normal, brown stool. Neurological examination revealed a dull mentation, vertical nystagmus, severe alligator rolling with extensor rigidity in all four limbs. Cardiac examination revealed a heart rate of 160 beats per minute, and he had pale pink mucous membranes with a capillary refill time of 2 s. An intermittently irregular heart rhythm was noted.
Diagnostic testing upon presentation included an electrocardiogram and blood pressure measurement. This identified the arrhythmia as multifocal ventricular tachycardia (). The blood pressure was found to be 104 mmHg. An intravenous (IV) catheter was placed, and a balanced electrolyte solution (Plasmalyte A; Baxter International Inc, Deerfield, IL, USA) was started at three times maintenance (180 mL/kg/day). Because of the patient’s abnormal mentation and neurologic status on presentation, oral medication could not be administered and also an IV catheter could not be placed safely initially. Methocarbamol (Auxilium Pharmaceuticals, Inc, Chesterbrook, PA, USA) was administered (100 mg/kg [220 mg/lb], rectally) mixed with 3 mL of saline. A lidocaine (Lidocaine hydrochloride; Amphastar Pharmaceuticals, Inc, Rancho Cucamonga, CA, USA; 2 mg/kg [4.4 mg/lb], IV) bolus was administered IV soon thereafter converting electrocardiogram to a normal sinus rhythm.
The dog was hospitalized for supportive care and monitoring. After the single methocarbamol and lidocaine doses, three times maintenance IV fluid therapy was continued; however, no further methocarbamol doses or lidocaine boluses were administered. Two hours after presentation, the patient was able to stand and ambulate with mild ataxia. A mild head tremor lastinĝ45 s was recorded at that time, which resolved on its own. Three hours after presentation, another electrocardiogram was taken, which revealed a normal heart rate, 136 beats per minute, with occasional ventricular premature complexes. Blood gas was evaluated to be normal (). Low–normal potassium was noted at 3.7 meq/L (reference range 3.6–4.9 meq/L). The dog began to eat within the first 4 h of presentation and had no further vomiting.
Three times maintenance IV fluids were administered until that evening when they were decreased to two times maintenance (120 mL/kg/day). The following day, another blood gas was taken, which revealed that all values remained within the normal limits (). An electrocardiogram was also repeated and found to have normal rate and rhythm (). By 48 h after presentation, fluids were decreased to 60 mL/kg/day, and the patient was discharged soon thereafter.
The dog was presented for recheck 72 h after original presentation. He was presented with a rectal temperature of 39.6°C (103.2°F). On physical examination, the dog was found to be in good body condition. He was panting at 60 breaths per minute. His heart rate was 125 beats per minute, and he had pink mucous membranes with a capillary refill time of 2 s. Neurological examination revealed normal mentation, normal spinal reflexes, and placing reflexes. Cardiac examination revealed normal sinus rhythm. No further arrhythmias were noted on electrocardiogram.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [18.0, 'kg']}",56,53.2,58.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 18.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (18.0 kg - 10 kg) = 56.0 mL/hr.
Hence, the patient's fluid maintenance is 56.0 mL/hr."
4892,22,Maintenance Fluids Calculations,physical,decimal,pmc-6153526-1,Extracted,"The patient was 4 years old girl, born at 37 weeks gestation age through cesarean section
and weighed 2850 kilograms. She was born in a nonconsanguineous family with nonremarkable
family history. She developed severe global developmental delay from the age of 3 months
which was accompanied by recurrent respiratory tract infections, abnormal behavior, and
stereotypic movement, that is, shaking and clapping hands. On examination, she had
microcephaly (-3SD), normal length, round face, short nose with broad nasal tip, ears with
thin helices, hypertelorism, long and smooth philtrum, wide spaced teeth, thin vermilion
borders, micrognathia, strawberry naevus in the trunk, bilateral clinodactyly, and small
puffy feet with metatarsus varus (). Ophthalmologic and audiologic examination revealed no abnormalities. She
developed focal epilepsy, which was fever related from the age of 10 months and it was not
controlled by valporic acid, topiramate, and levetiracetam. She was also noticed to have
speech delay, and dysmorphic features became more prominent as she was growing up.
Examination of the heart and kidney revealed no abnormalities, however, brain magnetic
resonance imaging revealed mild brain atrophy. Electroencephalography revealed multifocal
discharge arising from both hemisphere characterized by spike-wave complex. Metabolic tests
were negative. Low-depth whole-genome sequencing was performed whereby she was found to have
4 de novo copy number variations: 1q44q44 deletion (4.6 Mb) spanning HNRNPU,
HNRNPU-AS1, COX20, and NLRP3 genes, 3q29-q29 duplication (880
Kb) spanning CEP19, PCYT1A, RNF168, TCTEX1D2, and TFRC
genes, 8p11.21-p11.1 duplication (100 Kb) spanning part of HGSNAT gene, and
11p15.4-p15.4 duplication (190 Kb) spanning PGAP2 and
STIM1 genes. Low-depth whole-genome sequencing was also performed for
both parents in order to identify whether they are de novo or inherited. The 4 copy number
variations were not found in either of the parent, hence they were considered as de novo.
The classification of the identified copy number variations was done according to the
American College of Medical Genetics (ACMG) guideline for interpretation of postnatal copy
number variations. Two de novo copy number variations which represent 2 separate syndromes, that is,
1q43q44 microdeletion and 3q29 microduplication syndromes, were classified as pathogenic,
while the other 2 de novo duplications were classified as variant of unknown significance
().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2850.0, 'kg']}",2890,2745.5,3034.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2850.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (2850.0 kg - 20 kg) = 2890.0 mL/hr.
Hence, the patient's fluid maintenance is 2890.0 mL/hr."
4893,22,Maintenance Fluids Calculations,physical,decimal,pmc-7204776-1,Extracted,"A 75-year-old woman was admitted to our hospital with a 1-week history of appetite loss, diarrhea, dyspnea, and oliguria. She had a medical history of hypertension and bronchial asthma for 9 years. Both were well controlled with antihypertensive agents (irbesartan and amlodipine combination) and an anti-asthmatic drug (inhalation of a combination drug containing vilanterol trifenatate and fluticasone furoate), respectively. Her renal function was previously unremarkable. Upon admission, her blood pressure was 137/63 mm Hg, her pulse rate was 81 beats/min, and her temperature was 35.8°C. She was 131.3 cm tall and weighed 58.9 kg. She was neither pale nor icteric. A physical examination of the chest and abdomen revealed unremarkable findings, and no lymphadenopathy or skin lesions were observed. She had generalized edema.
Laboratory data upon admission are shown in Table . Proteinuria (9.38 g/gCr), hypoalbuminemia (serum albumin, 2.4 g/dL), and renal dysfunction (blood urea nitrogen, 182.0 mg/dL; creatinine [Cr], 7.70 mg/dL) were noted, while anti-neutrophil cytoplasmic antibodies were negative. The serum brain natriuretic peptide (BNP) level was 88.5 pg/mL. Chest radiography revealed slight right pleural effusion, and electrocardiography revealed an incomplete right bundle branch block. Abdominal computed tomography showed slight enlargement of both kidneys. These findings led to the diagnosis of AKI and NS.
Despite infusion of a hypotonic electrolyte solution and discontinuation of the antihypertensive medication (which contained irbesartan, an angiotensin II receptor blocker), diuresis was not accomplished, and her serum Cr level rose to 8.25 mg/dL. On admission day 2, urinary protein excretion was 3–20 g/gCr, which was within the nephrotic range, and hemodialysis was initiated.
On admission day 10, a kidney biopsy was performed to investigate the etiology of AKI and NS. Her serum Cr level was 4.38 mg/dL at that time. Light microscopy of the biopsied sample showed 18 glomeruli, of which 2 were obsolescent. The glomeruli showed minor abnormalities, including very mild segmental mesangial expansion (Fig. ). Interstitial edema and tubular necrosis were not observed. Moderate arterial hyalinosis was observed. Immunofluorescence analysis revealed faint and segmental mesangial deposits of IgA, IgG, and C3 (Fig. ). Electron microscopy revealed diffuse effacement of podocyte foot processes, with microvillus transformation. Electron-dense deposits were seen in the paramesangial areas, and they were less frequent and of lower density than those observed in typical IgA nephropathy (Fig. ). On the basis of these pathological findings, a diagnosis of MCNS associated with faint mesangial IgA deposits was made.
Oliguria continued for approximately 2 weeks, and cardiomegaly and anasarca deteriorated. Her BNP level increased to 325.8 pg/mL. Therefore, we attempted aggressive fluid removal by hemodialysis for approximately 20 days. This reduced her weight by 10 kg, and her urine output gradually increased to 700–1,000 mL/day. Her serum Cr level improved to 1.9 mg/dL, and hemodialysis was discontinued on admission day 23. As diuresis was achieved, she had severe proteinuria, with massive protein secretion of 6–8 g/day. Her kidney biopsy revealed slight mesangial proliferation and absence of severe histological changes, such as adhesion or crescentic lesions, which are observed in progressive IgA nephropathy with severe proteinuria or AKI. She had very mild microscopic hematuria and mesangial deposits of IgA, which are occasionally observed in patients with minimal change disease (MCD). She had no history of macroscopic hematuria, which is often associated with reversible AKI in patients with IgA nephropathy. Clinical and pathological findings led to a diagnosis of AKI from MCD with mesangial IgA deposition. On admission day 25, intravenous methylprednisolone pulses (500 mg) were started, followed by 30 mg of oral prednisolone. At the beginning of steroid administration, her serum Cr and urine protein levels were 1.54 mg/dL and 6.4 g/day, respectively. One week thereafter, her urinary protein had decreased to <0.1 g/day, and the generalized edema had completely resolved. Her prednisolone dosage was tapered gradually over several months, and she has remained in complete remission without relapse (Fig. ). Her serum Cr level improved to 0.9 mg/dL without a re-exacerbation of AKI.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [58.9, 'kg']}",98.9,93.955,103.845,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 58.9 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (58.9 kg - 20 kg) = 98.9 mL/hr.
Hence, the patient's fluid maintenance is 98.9 mL/hr."
4894,22,Maintenance Fluids Calculations,physical,decimal,usmle-1564,Extracted,"A 76-year-old woman is brought to the physician by her daughter for evaluation of progressive cognitive decline and a 1-year history of incontinence. She was diagnosed with dementia, Alzheimer type, 5 years ago. The daughter has noticed that in the past 2 years, her mother has had increasing word-finding difficulties and forgetfulness. She was previously independent but now lives with her daughter and requires assistance with all activities of daily living. Over the past year, she has had decreased appetite, poor oral intake, and sometimes regurgitates her food. During this time, she has had a 12-kg (26-lb) weight loss. She was treated twice for aspiration pneumonia and now her diet mainly consists of pureed food. She has no advance directives and her daughter says that when her mother was independent the patient mentioned that she would not want any resuscitation or life-sustaining measures if the need arose. The daughter wants to continue taking care of her mother but is concerned about her ability to do so. The patient has hypertension and hyperlipidemia. Current medications include amlodipine and atorvastatin. Vital signs are within normal limits. She appears malnourished but is well-groomed. The patient is oriented to self and recognizes her daughter by name, but she is unaware of the place or year. Mini-Mental State Examination score is 17/30. Physical and neurologic examinations show no other abnormalities. A complete blood count and serum concentrations of creatinine, urea nitrogen, TSH, and vitamin B12 levels are within the reference range. Her serum albumin is 3 g/dL. Urinalysis shows no abnormalities.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.0, 'kg']}",44,41.8,46.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.0 kg - 10 kg) = 44.0 mL/hr.
Hence, the patient's fluid maintenance is 44.0 mL/hr."
4895,22,Maintenance Fluids Calculations,physical,decimal,pmc-7813047-1,Extracted,"We present a case of a 3.5-year-old girl who complained of central cyanosis since birth. Her mother reported exertional fatigue and recurrent respiratory infections. Based on her central cyanosis since birth, the differential diagnosis in this girl includes the following: congenital cyanotic heart diseases as DTGA (D-transposition of great arteries), TOF (tetralogy of fallot), pulmonary atresia, single ventricle, and truncus arteriosus. Also, chest diseases including pulmonary arteriovenous fistulas and hemoglobin disorders like methemoglobinemia should be considered.
On clinical examination, she had severe cyanosis with grade Ⅲ clubbing in both fingers and toes, and resting oxygen saturation was 74% in room air. Her weight was 13 Kg, and her height was 89 cm. On cardiovascular examination, we found normal heart sounds with a mild systolic heart murmur on the left sternal border. Heart rate was 110 beats/minute. Pulse was palpable and symmetrical in the four limbs.
Pectus excavatum was appreciated on chest examination. The examination of the nervous system was normal.
The mental growth development was appropriate for the child's age. We mention some developmental milestones observed in this child: Language Milestones (Can say her name and age and Speak in sentences of 5-6 words), Cognitive Milestones (Can correctly name familiar colors and count), Movement Milestones (Can walk up and down stairs, walk forward and backward easily, help put on, and remove clothing), and emotional and social Milestones (Can imitate parents and friends, Understands the idea of ""mine"" and ""his/hers"").
The child had frequent respiratory infections and a hospital admission for pneumonia 1 year ago. Her complete blood count (CBC) showed erythrocytosis with hemoglobin concentration of 18 g/dL. ECG (electrocardiography) showed normal sinus rhythm with no abnormalities. CXR (chest X-ray) showed increased vascularity with an abnormal paracardiac shadow in the right lung.
We found a secondary ASD 6.5 mm in diameter with a left to right shunt and enlargement of the main pulmonary trunk and the right pulmonary artery. The rest of the echo was normal.
Contrast echo confirmed the abnormal connection between the pulmonary arteries and the left atrium through the visualization of bubbles in the left atrium.
Cardiac catheterization was performed, where the presence of the fistula was confirmed between the right pulmonary artery and the left atrium (Figure ).
Multislice CT shows that the pulmonary artery branch supplying the middle right lobe drains directly into the left atrium through a large fistula taking the form of a large aneurysm accompanied by an absence of the upper right pulmonary vein (Figure ).
The surgery was performed under general anesthesia through a median sternotomy. Cardiopulmonary bypass was established, and following cardioplegic arrest, 32˚C blood-body temperature was provided. Following right atriotomy, the atrial septal defect was found measuring 7 mm, and it was expanded and its edges hung. Through the ASD, the fistula's orifice was seen to measure 20-25 mm connecting the right pulmonary artery and the left atrium at the point where the right upper pulmonary vein usually opens into the atrium, and the right upper pulmonary vein was absent; then, the fistula's ostium was closed by means of a biological patch using a continuous suture technique with 5/0 prolene. Afterward, the ASD was closed by a biological patch using a continuous suture technique with 5/0 prolene. Other than the ASD, no other shunts or malformations were found during the surgery. (Figure ).
Oxygen saturation improved to 95% immediately after surgery. On follow-up after 6 months, the patient was asymptomatic and the clinical examination was normal. (Figure ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [13.0, 'kg']}",46,43.7,48.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 13.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.0 kg - 10 kg) = 46.0 mL/hr.
Hence, the patient's fluid maintenance is 46.0 mL/hr."
4896,22,Maintenance Fluids Calculations,physical,decimal,pmc-3784102-2,Extracted,"A 32-year-old woman, gravida 2, para 0, was admitted to Seoul National University Bundang Hospital at 35 weeks and 5 days gestational age with symptoms of vaginal bleeding in October 2011. Trans-vaginal ultrasonography revealed that the placenta completely covered the internal os. Approximately two thirds of the placenta was located in the posterior wall of the uterus and the remaining portion was located in the anterior lower segment of uterus. When the patient and her husband were counseled about the risk of hysterectomy, they strongly requested preservation of the uterus for future fertility. Therefore, a Cesarean section with prophylactic intraoperative UAE was planned. Under spinal anesthesia, a uterine incision was made transversely at the lower uterine segment. The surgeon could not avoid tearing the placenta before the female newborn weighing 2,465 g was delivered. The torn placental margins and the cut edges of the uterus were clamped by Allis forceps. During the interventional radiologist tried to insert an angiographic catheter into the right femoral artery for four minutes, the surgeon found a diffuse hemorrhage from the torn placental margin and cut edges of the uterus. At this point, the surgeon abandoned the plan of a prophylactic UAE. The surgeon removed the placenta manually and profuse hemorrhage from the placental bed sites developed. Although the implantation site was repeatedly over-sewn with 0-monofilament absorbable suture, bleeding was quite severe, thus a Cesarean hysterectomy was indicated. However, it was decided that intraoperative UAE would be attempted once more before the Cesarean hysterectomy since massive transfusion was successful. The interventional radiologist inserted an angiographic catheter into the right femoral artery and approached both uterine arteries. Embolization with gelfoam was performed under fluoroscopic guidance for bilateral enlarged tortuous uterine arteries (). Fortunately, blood flow decreased on angiography and bleeding through the vagina decreased. At this point it seemed possible to avoid a hysterectomy. The uterine wall was repaired after an additional intraoperative UAE. Estimated blood loss was 5,000 mL and massive transfusion (9 packs of RBC and 3 packs of FFP) was performed during the operation. Although bleeding decreased markedly after two attempts of intraoperative UAE, the patient was transferred to the angiography room for another attempt at UAE. Embolization of the uterine artery was performed with a coil in the angiography room () and then the patient was transferred to the intensive care unit (ICU) for close observation. While in the ICU, the patient received three more packs of RBC and six more packs of FFP as well as cryoprecipitate and platelet. The next day, her hemoglobin level was 10.2 g/dL and vital signs were stable. She was transferred to the general ward for further postoperative care. On the second day after surgery, the patient presented with a fever of 39.1℃ and after a full fever study, her antibiotic regimen was changed. The fever resolved on the fourth day and the patient was discharged from the hospital 10 days after surgery with no other complications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2465.0, 'g']}",9.86,9.367,10.353,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2465.0 g so this converts to 2465.0 lbs * kg/1000 g = 2.465 kg. Hence, the patient's maintenance fluid is 2.465 kg * 4 mL/kg/hr = 9.86 mL/hr.
Hence, the patient's fluid maintenance is 9.86 mL/hr."
4897,22,Maintenance Fluids Calculations,physical,decimal,pmc-4895744-1,Extracted,"A 7-year-old boy from overseas was referred to us with corrosive stricture esophagus. The child had ingested corrosive 2 years back. This was followed by more than twenty attempts at esophageal dilatation in Pakistan and India at several centers. After each session of dilatation, he was able to take liquids for 4-6 weeks. In the last attempt at dilatation, he had developed a diverticulum with failure of even a guidewire to go through the stricture. Unfortunately, throughout these 2 years of endoscopic attempts, he had no significant nutritional support and was weighing (7 years, 14 kg) less than the third centile for his age.
The child was evaluated with a contrast swallow and esophagoscopy. The stricture was long with multiple pseudodiverticula. The thinnest guidewire (0.18 mm, Terumo) was not negotiable across the stricture. Since he had arrived in dehydrated emaciated state, he was kept on intravenous fluids for a week. This was followed by laparoscopic feeding gastrostomy, and he was nutritionally built up for the procedure for 1 week.
A week later, he was taken up for laparoscopic transhiatal esophagectomy and esophageal substitution with stomach. After endotracheal intubation and general anesthesia, the child was placed at the foot end of the table in low lithotomy position. The camera port was placed at the umbilicus and pneumoperitoneum created at a pressure of 10 mmHg. Two working ports were placed on the right and the left iliac fossa in the midclavicular line at the level of the umbilicus. The procedure was started with mobilization of the gastrostomy and closure of the gastrostomy site by intracorporeal suturing. The gastrostomy site at the left hypochondrium was used for retraction of the liver to aid in transhiatal dissection. There were dense adhesions around the esophageal hiatus of the diaphragm. The diaphragmatic crura were divided and scarred, and fibrosed esophagus was dissected from mediastinal adhesions.
The retromediastinal dissection was challenging due to dense postcorrosive ingestion adhesions and loss of tissue planes. During the difficult dissection at the lower end of the esophagus, a small tear was inadvertently created in the left hemidiaphragm. The small rent in the diaphragm was closed with interrupted sutures. The lower two-third of the esophagus was mobilized by the transhiatal route. The cervical esophagus was exposed through the neck incision and the upper esophagus mobilized, and entire esophagus was delivered through the neck wound.
The stomach and duodenum were mobilized by the division of short gastric vessels with kocherization and ligation of the left gastric artery. The posterior mediastinal gastric transposition was completed with the esophagogastric anastomosis in the neck.
The child was ventilated for 48 h and contrast swallow was done on the 7th day which showed wide patent neck anastomosis, no leak, and prompt gastric emptying []. He was started on semisolid diet, which he began to tolerate without any symptom. Later in the evening, he started developing progressive respiratory distress. The child was placed on oxygen by mask and close monitoring. A chest X-ray on the same evening revealed a diaphragmatic hernia with hugely dilated colon [].
In view of the high risk of strangulation and gangrene of the herniated loop of large bowel, he was taken up for surgery immediately. Laparoscopy was done through the same port sites used for transhiatal esophagectomy and esophageal substitution. The hiatal access was difficult with omentum, small bowel and large bowel adhesions blocking the approach to the hiatal area. Gentle traction and separation of adhesion led to definition of the hiatus, demonstrating snugly fitting lower end of the stomach. In the parahiatal region, the central tendon had a small rent where the repair of the iatrogenic injury had given way allowing colon to migrate up. The hugely dilated and obstructed, congested transverse colon was reduced back into the abdomen. The diaphragmatic defect was repaired by intracorporeal interrupted mattress suturing. Postoperative period was unremarkable with quick recovery and he was discharged 2 days later. He remains well on follow-up 1-year after surgery having gained significant weight.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [14.0, 'kg']}",48,45.6,50.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 14.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (14.0 kg - 10 kg) = 48.0 mL/hr.
Hence, the patient's fluid maintenance is 48.0 mL/hr."
4898,22,Maintenance Fluids Calculations,physical,decimal,pmc-8683236-1,Extracted,"A 35-year-old female presented to the Emergency Department (ED) for evaluation of 3 months of worsening exertional dyspnea and bilateral lower extremity edema. The patient initially noted mild dyspnea on exertion, which gradually progressed to the point of being unable to climb a single flight of stairs without stopping to rest. The patient endorsed a nonproductive cough, pleuritic chest pain, occasional orthopnea, and an unintentional 20-pound (9.1 kg) weight loss over a one-month period. She denied any associated fevers, chills, or night sweats; had no nausea or vomiting; and had no easy bruising or bleeding. The patient denied any other recent illness and also denied any significant exposures or risk factors for tuberculosis. She had no significant past medical history including any previous cardiac pathology, thromboembolic disease, structural heart disease, indwelling catheters, or asthma. She denied any current or prior intravenous drug use (IVDU). Family and surgical history was also noncontributory.
Physical exam demonstrated a nontoxic appearing patient sitting comfortably in bed. Vital signs included a temperature of 98.1°F (36.7°C) with mild tachycardia at 109 beats per minute, blood pressure of 107/64 mmHg, and respiratory rate of 20 breaths per minute. Pulmonary examination revealed lungs clear to auscultation bilaterally without adventitious sounds or retractions; however, the patient was only able to speak in 4–5-word sentences with effortless tachypnea and no accessory muscle use. Cardiac examination demonstrated mild tachycardia without murmurs, rubs, or gallops; no jugular venous distention; and no carotid bruits. Extremity examination was notable for symmetric 2+ pitting edema to the midshin of both lower extremities. Skin exam revealed no purpura, Osler nodes, Janeway lesions, splinter hemorrhages, or track marks. Abdominal exam was nontender, and neurological examination was nonfocal.
Multiple laboratory studies including 2 sets of blood cultures were obtained () and remarkable only for mild hyponatremia with a sodium of 127 mEq/L, a chloride of 90 mEq/L, and mild anemia with a hemoglobin of 8.5 g/dL. There was no leukocytosis, troponin was undetectable, and brain-natriuretic peptide was within the normal range. These laboratory findings were not suggestive of any particular pathological processes. The finding of anemia was noted, but the lack of any corresponding elevation in bilirubin made acute hemolysis less likely. The hyponatremia was felt to be consistent with the patient's hypervolemic clinical picture. The lack of leukocytosis was noted, though limited inferences can be made from this value in isolation. Overall, the laboratory results made acute decompensated congestive heart failure and bacterial pneumonia lower on the differential.
A 12-lead electrocardiogram revealed sinus tachycardia with normal axis and intervals, with no acute injury pattern and no evidence of right-heart strain. A chest radiograph was obtained () and was interpreted by the radiologist as demonstrating “bilateral patchy atelectasis”—however, the emergency physicians felt it demonstrated a pleural-based wedge-like consolidation in the right inferior lobe consistent with Hampton's Hump. The initial differential considered by the providers included pulmonary embolus, pneumonia, congestive heart failure, pulmonary hypertension, cardiomyopathy, and infectious endocarditis. At this time, a third set of blood cultures were added to the patient's workup.
A limited bedside transthoracic echocardiogram (Figures and ) in the ED revealed findings concerning for tricuspid valve vegetations as well as a slightly enlarged right ventricle without any D-sign (i.e., a D-shaped left ventricle on parasternal short-axis view, consistent with right ventricular strain causing shift of the ventricular septum). Cardiology was consulted for concern for potential IE. A CT-angiogram (CTA) of the chest was ordered to assess for pulmonary embolism and further characterize the pulmonary lesions seen on radiography, and the patient received intravenous (IV) ceftriaxone and azithromycin to cover possible community-acquired pneumonia while the CTA was pending. The CTA revealed findings consistent with multiple septic emboli and mycotic aneurysms (Figures and ), as well as multiple segmental pulmonary arterial occlusions with associated infarcts or hemorrhage. A stat formal echocardiogram was obtained and interpreted at bedside by the cardiology fellow, confirming the presence of tricuspid vegetations as well as moderate tricuspid regurgitation, with no evidence of right ventricular strain.
The patient was treated with IV vancomycin, gentamycin, and ciprofloxacin to provide coverage for possible MRSA endocarditis, due to the concern for possible undisclosed IVDU, and was admitted with consultation of Cardiothoracic Surgery and Infectious Disease (ID).
The patient was maintained on IV gentamycin and vancomycin and underwent a transesophageal echocardiogram (TEE) on hospital day 2 which revealed a large 2.0 × 2.1 cm posterior leaflet tricuspid valve vegetation with severe tricuspid regurgitation. On hospital day 5, the patient admitted to a history of heroin IVDU but was not forthcoming about the date of her most recent use, and a urine toxicologic screen was negative. The patient underwent a tricuspid valve annuloplasty and reconstruction using autologous pericardial tissue by Cardiothoracic Surgery on hospital day 8. The patient's blood cultures remained negative on hospital day 9, at which time ID recommended the patient receive ceftriaxone 2 g IV daily for 6 weeks. Pathology of the valve leaflets resulted on hospital day 10 and indicated granulation tissue with focal areas of bacterial colonization without bacterial identification. The remainder of the patient's postoperative course was uncomplicated, and on hospital day 15, she was transferred in good condition to a skilled nursing facility to complete her 6-week course of IV ceftriaxone. The blood cultures remained negative, and the causative pathogen was not identified.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [9.1, 'kg']}",36.4,34.58,38.22,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 9.1 kg. Hence, the patient's maintenance fluid is 9.1 kg * 4 mL/kg/hr = 36.4 mL/hr.
Hence, the patient's fluid maintenance is 36.4 mL/hr."
4899,22,Maintenance Fluids Calculations,physical,decimal,pmc-8330006-1,Extracted,"A 1-day-old female African newborn weighing 3500 g was referred for management of a large oral mass that protruded from the mouth and caused maxillary protrusion and flattening of the nose. The patient was having difficulty breathing (Fig. ).
She was born by spontaneous vaginal delivery to a mother who was unaware of the date of her last menstrual period. She had no prenatal medical care, so there was no opportunity for prenatal diagnosis.
Initial examination revealed a mass that occupied the majority of the oral cavity and protruded from the mouth. On palpation, the mass appeared to arise from one side of the palate, and there was an adjacent palpable cleft. No other congenital anomalies were evident on physical examination.
The patient had some breathing difficulty, but the airway was patent. She was administered oxygen and intravenous fluids, and a nasogastric feeding tube was successfully placed. Feeding was commenced at 35 ml, eight times per day, and she stabilized.
On day 5, she was taken to surgery. Laryngoscopy was performed using a standard Macintosh blade size 1, and an easy intubation with a 2.5 endotracheal tube. The mass was excised under general anesthesia, Good hemostasis was achieved, and complete resection of the tumor was accomplished. There were no immediate postoperative complications.
Gross examination revealed a large fibrocystic tumor involving the oral and nasal cavities with its base originating from the hard palate. It measured 6 × 5 × 4.5 cm and was well circumscribed (Fig. ).
Histopathologic examination revealed a congenital primarily epidermal teratoma.
She had an uneventful postoperative course, although a palatal defect remained (Fig. ). She had no difficulty opening or closing her mouth. Bottle feeding with expressed breast milk was initiated shortly after surgery and was well tolerated. She was able to breastfeed by postoperative day 5.
On postoperative day 30, the patient was taken back to surgery, where she underwent successful palatoplasty (Fig. ). She was discharged home with her mother on postoperative day 9 after palatoplasty (Fig. ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3500.0, 'g']}",14,13.3,14.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3500.0 g so this converts to 3500.0 lbs * kg/1000 g = 3.5 kg. Hence, the patient's maintenance fluid is 3.5 kg * 4 mL/kg/hr = 14.0 mL/hr.
Hence, the patient's fluid maintenance is 14.0 mL/hr."
4900,22,Maintenance Fluids Calculations,physical,decimal,pmc-3039606-1,Extracted,"A 24-year-old Caucasian man, a full-time student, 1.8 m tall, 77 kg in weight, with no significant medical history, a non-smoker, taking no medications and with no substance misuse, was riding a motorcycle while wearing a helmet; he collided with a moving automobile and was ejected over 30 m into the air. He sustained multiple injuries including a large chest wall avulsion and a severe partial amputation of the left arm. The limb was not salvageable, requiring amputation, with a small residual fragment of the left scapula remaining (Figure ). Left scapulothoracic dislocation and severed left brachial plexus were also found intra-operatively. His head, right arm and lower extremities were grossly intact.
He received 10 weeks of acute care in our surgical medical unit, where surgical intervention included repair of the chest wall and internal organs, after which he was transferred to the acute rehabilitation unit where, almost immediately, phantom limb pain became his major issue.
He reported his pain episodes as variable in number, ranging from three to six per day. Described as searing, aching or cramping as if his missing hand was clenched in a fist formation, the pain episodes often occurred at random intervals during the day, ranging from 15 minutes to up to an hour and a half. On average, he rated the pain at between 8 to 10 out of 10 on a visual analog scale (VAS).
As his entire left upper limb was missing, including the shoulder and parts of the clavicle and scapula, 'stump' pain did not actually apply to his description. Instead, he consistently experienced the feeling that his left fist was severely clenched and he could not release it from the cramping that became a burning, searing pain.
This persisted despite a series of aggressive pain management methods through the administration of naproxen 250 mg three times a day, tramadol 50 mg four times a day, extended release morphine 150 mg twice a day, hydrocodone/acetaminophen 5/500 mg every four hours as needed, lidocaine patches (two patches every 24 hours), gabapentin 400 mg four times a day and the use of a transcutaneous electrical nerve stimulation (TENS) unit. At this point our pain clinic was consulted for possible nerve block, which was deemed not appropriate. The pain was so severe that it affected patient's blood pressure as well. He required treatment with clonidine 0.4 mg twice daily, metoprolol 125 mg twice daily, and lisinopril 20 mg once daily. Over the course of two weeks, it was suggested that the employment of mirror therapy might provide some measure of relief. A vertically supported mirror in a frame was fashioned for easy positioning against his midline chest with him seated in a chair. In leaning slightly forward, he was able to watch the reflection of his right arm during motions as if doing biceps curls, opening and closing the fist, pronating and supinating the outstretched 'arms', while attempting to concentrate on doing these movements as if bilaterally. He performed these maneuvers for 15 minutes at a time at least twice daily. Although not significant in the first week to week and a half, he began to report some decrease in the intensity of the left upper extremity phantom limb pain by the end of the second week of the mirror therapy. He rated his maximal pain as 6 out of 10 on the VAS. All pain medications except gabapentin were gradually discontinued over two weeks of mirror therapy. Gabapentin was decreased to 400 mg three times a day.
His blood pressure also decreased after two days of mirror therapy. At the end of the third week he was only on lisinopril 20 mg daily.
During the mirror therapy course his mother participated by clapping her hands in synchrony with his movement of his hand towards the mirror, giving the illusion of not only seeing but also hearing hand clapping. We encouraged this form of auditory feedback and it was continued throughout his acute rehabilitation stay. Although MVF was started initially for the treatment of this patient's PLP, auditory feedback, at first performed unintentionally by his mother, was thereafter simultaneously performed along with the mirror therapy.
His other rehabilitation goals were met sooner than initially projected, and he was determined to be appropriate for discharge home with continuation of out-patient mirror and auditory feedback therapy, as well as further out-patient therapy care.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [77.0, 'kg']}",117,111.15,122.85,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 77.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (77.0 kg - 20 kg) = 117.0 mL/hr.
Hence, the patient's fluid maintenance is 117.0 mL/hr."
4901,22,Maintenance Fluids Calculations,physical,decimal,pmc-8558014-1,Extracted,"A 79-year-old woman (height: 158 cm and weight: 65 kg) visited the emergency room with bilateral leg motor weakness (grade 4/4) and back pain. All her vital signs were stable; however, she had mild fever (37.9°C). She had a medical history rheumatoid arthritis and type 2 diabetes mellitus.
She had previously undergone acupuncture or epidural blocks in the lumbar region occasionally at a local pain clinic. Blood test results showed a markedly elevated white cell count of 14,360 cells/mm3, a C-reactive protein level of 7.57 mg/dL, and an erythrocyte sedimentation rat of 83 mm/h. Magnetic resonance imaging (MRI) of the entire spine revealed dorsal compression of the spinal cord and cauda equina by an epidural abscess extending from the apex of T3 to L5 ().
Two separate midline incisions were made over the T8-T9 and T12-L1 areas. We performed bilateral laminotomy at T8 and T12. On the laminotomy at each level, yellowish pus was gushed out (), and swabs were sent for culture. A 5-Fr pediatric feeding tube () was advanced from the laminotomy level superiorly and then inferiorly into the dorsal epidural space, and vancomycin mixed with saline was irrigated through the pediatric feeding tube, resulting in further irrigation of portions of the epidural abscess not exposed via laminotomy. Two inflow irrigation tips (Hemovac pp 400 mL, 1.6 mm) were inserted into the epidural space, and 2 outflow tips (Hemovac ps 400 L, 2.8 mm) were inserted in each epidural space (). The irrigation system was maintained for 48 h, and when the color of the outflow was clear, it removed to prevent secondary infection. The pus culture revealed methicillin-resistant Staphylococcus aureus (MRSA) as the causative agent. The patient was initiated on intravenous vancomycin. Blood cultures also showed MRSA positivity; therefore, she was transferred to infection internal medicine department for further antibiotic treatment. Follow-up MRI performed 21 days after surgery showed that the abscess in the thoracic spine was completely removed, with a small residual abscess in the lumbar spine (). After 3 months of follow-up, the motor strength of both lower extremities improved (G5/G5), and she could walk without any assistance.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [65.0, 'kg']}",105,99.75,110.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 65.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (65.0 kg - 20 kg) = 105.0 mL/hr.
Hence, the patient's fluid maintenance is 105.0 mL/hr."
4902,22,Maintenance Fluids Calculations,physical,decimal,pmc-3928270-1,Extracted,"A 10-year-old boy (height, 120 cm; weight, 20 kg) presented with an 8-year history of arteriovenous malformation (AVM) involving the right lower limb. He had been started on sclerotherapy 4 years earlier because of leg length discrepancy causing gait disturbance. However, this treatment was stopped because there was no remarkable improvement. A year before presentation, the AVM had undergone rapid expansion causing significant pain and high-output cardiac failure. Therefore, an amputation of the affected lower limb was recommended at the other hospital.
On admission to Kyungpook National University Hospital, an examination revealed that AVM with soft tissue hypertrophy had spread all over the right leg (). A chest X-ray showed marked cardiomegaly with increased pulmonary vascularities (). Electrocardiography showed normal sinus rhythm with right ventricular hypertrophy. Two-dimensional echocardiography showed an enlarged right atrium, right ventricle, and left ventricle, but relatively good left ventricular contractility. The pulmonary artery was also enlarged, but there was no pulmonary edema. Computed tomographic (CT) angiography of the right lower extremity revealed extensive AVM with feeding arteries from the branches of the right profunda femoris and superficial femoral arteries. The venous drainage was through the superficial femoral and deep femoral veins, and there was a marked dilatation of the pelvic vein and inferior vena cava (). The blood investigations were found to be normal.
One week before surgery, the patient was scheduled to receive preoperative selective embolization to reduce the size of the AVM and minimize the risk of uncontrolled intraoperative bleeding. For embolization, the radiologist performed catheterization through the left common femoral artery and installed a tourniquet over the right proximal thigh. Soon after, remarkable bradycardia developed due to a baroreceptor reflex-induced abrupt increase in the systemic vascular resistance (SVR), and this procedure was cancelled. After a thorough discussion with the plastic surgeons, orthopedic surgeons, and vascular surgeons, right hip disarticulation was considered to be the best option for improving the patient's quality of life. It was anticipated that the large feeding vessel branches of the right profunda femoris artery, superficial femoral artery, and the large veins draining the limb would be difficult to control during a hip disarticulation. To minimize the chances of torrential hemorrhage, a disarticulation was planned under cardiopulmonary bypass.
After anesthetic induction, an intra-arterial catheter 22G was inserted into the left radial artery to check the invasive arterial pressure and cardiac output by using an arterial pressure waveform-derived cardiac index sensor (FloTrac; Edward Lifesciences LLC, Irvine, CA, USA) and monitor (Vigileo, Edward Lifesciences LLC). Further, a central venous catheter was positioned into the left subclavian vein.
After induction, the mean arterial pressure was maintained between 60 and 80 mmHg. The cardiac index (CI) and the central venous pressure (CVP) were recorded at 10 and 18, respectively, which were considered to be high.
After heparinization, the right iliac artery was cannulated using an 18 French (Fr) cannula, and a 24 Fr venous cannula was placed through the right iliac vein. Partial cardiopulmonary bypass (CPB) was commenced at a flow rate of 1,200 mL/m2/min. The patient's body was maintained at a normal temperature, and the activated clotting time was greater than 400 seconds throughout the CPB. During a partial CPB, a continuous intravenous infusion of milrinone 0.5 µg/kg/min was used to improve the right ventricle function by decreasing the pulmonary vascular resistance. After the initiation of CPB, the CI and CVP were lowered to 2.5 and 3, respectively. The amputation was performed at the level of the proximal one-third of the right femur. The CPB time was 180 minutes. After heparin neutralization using protamine, the patient was weaned off of the bypass with 0.1 µg/kg/min of norepinephrine and 0.5 µg/kg/min of milrinone. Despite the use of CPB, the blood loss was extensive, and a transfusion of 8 units of packed red cells, 6 units of fresh frozen plasma, and 5 units of cryoprecipitate was required.
He was extubated on the following day. The postoperative period was uneventful, and he recovered fully with no neurologic deficit. A two-dimensional echocardiography, which was performed a week after surgery, showed a significantly smaller cardiac chamber. Two months after surgery, no residual lesion was observed in a CT angiography (), and a chest X-ray was unremarkable without cardiomegaly ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [20.0, 'kg']}",60,57,63,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 20.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (20.0 kg - 10 kg) = 60.0 mL/hr.
Hence, the patient's fluid maintenance is 60.0 mL/hr."
4903,22,Maintenance Fluids Calculations,physical,decimal,pmc-7727885-1,Extracted,"A 34 year old male presented to the emergency department with a history of hemoptysis since 5 days. He had a history of loss of weight and appetite. He had no history of tuberculosis (TB) or TB contact, smoking, fever, or drugs. He also had a history of the inability to father a child and have never sought medical treatment for the same. There was no history of loss of libido, hypothyroidism, radiation to head or neck, surgery to head or abdomen, or symptoms of raised intracranial tension. On examination, his height was 156 cm and weight was 45 kg. His vitals were stable. He had pallor and digital clubbing. External genital examination showed genital ambiguity in the form of bifid scrotum, which was rugose and pigmented with a phallus of length 9 cm with well-formed glands []. The right gonads were not palpable in labioscrotal fold or elsewhere and the left gonads were palpable in the left inguinal region. There was no vaginal opening. Sexual maturity rate (SMR) P2 B1 with no axillary hair. He had poor facial and body hair. A natal history was later reviewed with him and there was no history of salt-wasting crisis, maternal virilization, or history of sex reversal. We considered the possibility of 46XY disorder of sex development (DSD), MGD, or ovotesticular DSD.
Laboratory investigations included hemoglobin of 8 g/dl, total leukocyte count of 8000/mm3, platelet count of 4.5 lakhs, and erythrocyte sedimentation rate of 60. Liver function test (LFT), renal function test (RFT), blood glucose, serum electrolytes, cortisol (8 am cortisol 16.08 mcg/dl), and 17-OH-progesterone were normal (1.1 ng/ml). Pooled follicle-stimulating hormone and luteinizing hormone levels were 14 mIU/mL and 9 mIU/mL, respectively; thyroid-stimulating hormone: 3.8 mIU/L, T4: 130 nmol/L (60–140), basal total testosterone: 240 ng/dL, estradiol 20 pg/ml (normal male: 10–50 pg/ml), prolactin 12 ng/ml (5–20 ng/ml), and inhibin B 156 ng/ml (80–300 ng/ml). Work up for tuberculosis (TB) which includes sputum acid fast bacilli and TB polymerase chain reaction study with sputum and blood specimens were negative. Chest-X ray was normal.
High-resolution computed tomography chest showed irregular solid lesions in the right upper lobe suggestive of a lung metastasis. Search for primary malignancy was done and investigations included upper endoscopy, colonoscopy, USG abdomen and pelvis, and tumor markers study (alpha fetoprotein, lactate dehydrogenase, carcinoembryonic antigen, and prostate-specific antigen levels). Ultrasound of the pelvis showed hypoplastic uterus with no gonads visualized. Tumor markers and gastrointestinal study were normal. Karyotyping (30 cells and 100 cells) revealed 45, X genotype. In view of the possibility of malignancy arising from a dysgenetic gonad and the inability to localize primary malignancy from the initial evaluation, we proceeded with a laparoscopy. Laparoscopic examination was done and visualized the right gonads and ducts. Laparoscopy showed enlarged right gonads in the ovarian fossa with bilateral fallopian tubes and hypoplastic uterus []. The right gonad was adhering to the adjacent peritoneum. The left gonad was visualized in the left inguinal region and biopsy was taken to confirm the type of gonad. The right gonad with fallopian tubes and rudimentary uterus was removed. A thorough histopathological examination of the right gonad showed dysgerminoma, and the left gonad showed testicular tissue (seminiferous tubules and Leydig cells). Dysgerminoma arising from the right gonad showed sheets or nests of large, uniform polygonal cells with clear or eosinophilic cytoplasm with distinct squared off cell membranes and with loose stroma []. No ovarian tissue was noted in these sections. Fluorescence in situ hybridization (FISH) for the identification of Y chromosome was done in gonadal tissue. FISH showed mosaic pattern with 90% cells of 45, X and 10% showing X and Y chromosomes 45, X/46, XY.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [45.0, 'kg']}",85,80.75,89.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 45.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (45.0 kg - 20 kg) = 85.0 mL/hr.
Hence, the patient's fluid maintenance is 85.0 mL/hr."
4904,22,Maintenance Fluids Calculations,physical,decimal,pmc-5681726-1,Extracted,"An 11-year-old, 6 Kg, neutered male domestic shorthair cat was referred for lethargy, weight loss, occasional vomiting and polyuria/polydipsia lasting for three weeks. The cat had no history of previous medical problems. Upon physical examination, a body condition score of 7/9, depressed mental status and bright pink mucous membranes were noticed. No signs of clinically detactable dehydration were present. An irregular mass was palpated in the cranial right side of the abdomen. Non-invasive blood pressure (BP) measurement using a veterinary oscillometric device (petMAP™ graphic, Ramsey Medical, Inc., Tampa, F, USA) revealed high-risk hypertension (210/110 mmHg). Complete blood count (CBC) (ADVIA 2120, Siemens Healthcare Diagnostics, Tarrytown NY, USA) revealed marked erythrocytosis with increased RBC (16.2x106/μL, RI 5.0-10.0x106/μL), hematocrit (HCT) (64.8%, RI 24-45%) and hemoglobin concentration (20.6 g/dL, RI 8.0-15.0 g/dL) above the RI. Complete hematologic profile is reported in .
The evaluation of the blood film revealed mild anisocytosis and minimal polychromasia, numerous platelet clumps and large platelets. Chemistry profile (OLYMPUS AU 400, Beckman Coulter/OLYMPUS, Munich, Germany) showed azotemia (creatinine 2.5 mg/dL, RI 0.8-1.8; urea 104 mg/dL, RI 15-60) and mild hyperproteinemia (total protein 8.35 g/dL, RI 6-8; albumin 3.85 g/dL, RI 2.90-3.60). Ionized calcium results and coagulation profile were within the RI.
A free-catch midstream urine specimen was submitted to urinalysis, which revealed a urinary specific gravity (USG) of 1024, pH of 5.5 and unremarkable sediment. The urinary protein to creatinine ratio was normal (0.1; RI 0-0.4). Thoracic radiographs were unremarkable. Abdominal ultrasound showed a 4.6 x 2.3 cm, round and patchy mass in the cranial pole of the right kidney. An ultrasound-guided fine-needle aspiration (BD Spinal needle 25 GA 3.00 IN 0.50 x 75 mm, Becton Dickinson SA, S. Augustin del Guadalix Madrid, Spain) of the mass was performed, and smears were stained with May Grunwald-Giemsa (Merck KGaA, 64271 Darmstadt, Germany). Cytologic samples were markedly hemodiluted, and displayed three-dimensional clusters of moderately pleomorphic epithelial cells with variable nucleus/cytoplasmic ratio, round to oval central nuclei with lacy reticular chromatin and prominent nucleoli (). Although anisocytosis and anisokaryosis were mild, cytology was considered consistent with carcinoma, and presumptive diagnosis was renal cell carcinoma. Differential diagnoses included transitional cell carcinoma of the renal pelvis and metastatic carcinoma.
A high performance liquid chromatography method (High performance liquid chromatography, Water Corp HPLC system, Waters PDA Detector [Water Corp., Milford, MA, USA], Acquity UPLC System [Waters Corporation, Manchester England]) for erythropoietin (EPO) measurement in serum sample was used for the case reported.
The sample was analyzed in liquid chromatography coupled UV detection. EPO measured upon admission in our case was above the RI (0.54 mUI/mL, RI 0.39-0.51). These findings supported the diagnosis of SIE associated with renal neoplasia, in response to abnormal production of EPO or EPO-like substances.
The cat was hospitalized and stabilized with intravenous fluids and supportive care. Since the lack of clinically evident dehydration and the presence of high-risk systemic hypertension, a conservative fluid therapy regimen (Lactate Ringer’s solution, 2 mL/kg/h) was elected. A re-evaluation of the packed cell volume (PCV) after 10 hours of fluid therapy administration showed no significant change (63%). Due to the persistence of marked erythrocytosis and the lack of clinical improvement, manual erythrocytapheresis was performed: 15 mL/kg of whole blood were drawn from the jugular vein, similarly to previously reported (Lucas et al., 2004). Collected blood (Terumo CPDA-1 Double Blood Bag, Terumo Europe N.V., Interleuvenlaan 40, 3001 Leuven, Belgium) was processed using a refrigerated centrifuge (CRIOFUGE 6000i, Heraeus, Kendro Laboratory Products GmbH, Langenselbold, Germany) (3500g for 10 minutes including acceleration time, temperature: +4-6°C). After separation (Separation Stand, Terumo Corporation, Hatagaya, Shibuya-ku, Tokyo, Japan), 30 mL of fresh plasma were returned to the patient.
A marked improvement in the general condition of the cat was noticed, and BP reduced to 160/90 mmHg. After this procedure, the PCV was significantly reduced (53%; RI 24-45%). The patient was discharged, and re-hospitalized in view of surgery two weeks later. Blood exams at that time revealed a HCT of 56.7%, and a significant reduction in serum creatinine concentration compared to the previous baseline (1.98 mg/dL, RI 0.8-1.8). Due to the type of lesion, a nephrectomy of the right kidney was performed. Grossly, the resected kidney revealed a 4 x 2.5 x 3 cm reddish mass at the cranial pole, non-capsulated, irregularly lobulated, invading both the cortex and the medulla ().
The histologic examination of hematoxylin and eosin stained sections from selected portions of the tumor mass demonstrated tubular and papillary formations of neoplastic epithelial cells, with cuboidal to columnar shape, eosinophilic cytoplasm, vesicular nuclei and prominent nucleoli. The diagnosis was well differentiated tubulo-papillary renal cell carcinoma.
Replicate sections were then immunostained with an anti-EPO antibody (Rabbit IgG polyclonal anti-EPO antibody, clone H-162, Santa Cruz Biotechnology, Inc.) using the labeled avidin-biotin (LAB). In detail, slides were steamed in 0.01 moL/L sodium citrate buffer, pH 6, in a microwave oven. Endogenous peroxidase activity was quenched by 0.3% hydrogen peroxide in methanol while non-specific binding of immunoglobulins and tissue proteins were blocked by incubation with either 5% non-fat dry milk or 2.5% goat normal serum. Slides were then incubated overnight at 4°C with an anti-EPO antibody at a final concentration of 1:200, followed by incubation at room temperature with a goat anti-rabbit biotinylated IgG (Goat anti-rabbit biotinylated IgG, Biospa, Milan, Italy) and with an avidin peroxidase complex (Avidin peroxidase complex, Biospa, Milan, Italy). The reaction was developed with the DAB Peroxidase (HRP) Substrate Kit, 3.3’-diaminobenzidine (DAB Peroxidase HRP Substrate Kit, 3.3’-diaminobenzidine, Vector Laboratories Inc. Burlingame, CA, USA) and counterstained with hematoxylin. Negative controls were also performed by omission of primary antibodies, substitution of primary antibodies with normal serum, substitution of primary antibodies with non-reactive antibodies of the same species and immunoglobulin class. Replicates were also developed using a horseradish peroxidase (HRP) secondary antibody to confirm results and exclude nonspecific biotin bound. The immunohistochemical stain was interpreted by assessing the intensity of labeling. Cytoplasmic and/or membrane immunoreactivity was considered positive. In the case here reported, an intense and diffuse cytoplasmic positivity of tumor cells was demonstrated ().
The cat remained hospitalized in order to receive supportive therapy and clinical and clinicopathological monitoring.
Over the postoperative period (day 2), a gradual decline in PCV and serum creatinine concentration was observed (38%, RI 24-45%; 1.92 mgdL, RI 0.8-1-8 mg/dL, respectively). CBC was within the RI (RBC 9.3x106/μL, RI 5.0-10.0x 106/μL; HCT 35.4%, RI 24-45%; hemoglobin concentration 11.5 g/dL, RI 8.0-15.0), and serum creatinine and EPO concentrations decreased until normalization (1.76 mg/dL, RI 0.8-1.8 and 0.28 mUI/mL RI 0.39-0.51; respectively) in the next two weeks. The cat remained clinically stable for eight months postoperatively; additional re-checks showed the resolution of the polyuria/polydipsia (USG of 1080), and CBC and chemistry profile results were within RI.
At nine months postoperatively, the cat was evaluated for anorexia and mental disorientation. Physical examination revealed anisocoria and multiple cranial nerve defects. BP was 190/100 mmHg, while the fundus examination showed no abnormalities. Thoracic radiographs, abdominal ultrasound, CBC and chemistry were unremarkable.
Metastatic intracranial disease was suspected but the owner declined further imaging studies. The patient’s conditions progressively worsened until euthanasia was elected. Due to the owner’s objection, necropsy was not performed.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.0, 'kg']}",24,22.8,25.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.0 kg. Hence, the patient's maintenance fluid is 6.0 kg * 4 mL/kg/hr = 24.0 mL/hr.
Hence, the patient's fluid maintenance is 24.0 mL/hr."
4905,22,Maintenance Fluids Calculations,physical,decimal,pmc-4093547-1,Extracted,"We present a case of a 12 year old male who presented with
swelling and a non-healing sinus in the dorsum of the left
wrist joint of 5 months’ duration. The patient gave
a history of intermittent low grade fever associated with
significant weight loss (5kg) over the last 5 months. There
was a history of purulent discharge from the sinus. Patient
was on broad spectrum antibiotics at presentation.
Examination revealed the wrist mildly swollen and tender
but not warm. A single sinus was present in the dorsum of the
wrist. Systemic examination including the respiratory
system was essentially normal.
The blood invesigations revealed anemia (haemoglobin-9.2
mg/dl), elevated E.S.R of 52 mm/hr and a Mantoux test of
22mm by 22mm. C- reactive protein was positive (17 mg/l).
Radiograph of the wrist at presentation suggested osteopenia
of carpal bones with a lytic lesion of the capitate . Other
carpal boness were relatively spared. and MRI
showed increased signal intensity in the capitate with
surrounding soft tissue edema in T2 weighted images. suggesting an infective etiology
Histopathology of intra-osseous tissue removed at biopsy
confirmed the diagnosis of bone tuberculosis, with typical
caseous necrosis surrounded by epithelioid and giant-cell
follicles. Synovial biopsy revealed non-specific chronic
synovitis. No organisms were cultured in the purulent
material.
The patient was started on multidrug chemotherapy isoniazid
5mg/kg, rifampicin 10mg/kg, pyrazinamide 25mg/kg and
ethambutol 15mg/kg. The antitubercular drug was continued
for one year. Pyrazinamide was stopped after 3 months and
ethambutol at 6 months. The sinus healed in 10 weeks. The
wrist became non tender and regained excellent range of
motion. Subsequent radiographs showed remineralisation of
bone with increasing sclerosis. At 18 months follow up there
was no sign of reactivation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.0, 'kg']}",20,19,21,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.0 kg. Hence, the patient's maintenance fluid is 5.0 kg * 4 mL/kg/hr = 20.0 mL/hr.
Hence, the patient's fluid maintenance is 20.0 mL/hr."
4906,22,Maintenance Fluids Calculations,physical,decimal,pmc-6552343-1,Extracted,"A 32-year-old male with BS and a past medical history significant for well-differentiated pancreatic adenocarcinoma, diabetes mellitus type II, and restrictive lung disease presented for a consultation and annual checkup at the Integrated Cancer Prevention Center (ICPC) at Tel Aviv Medical Center.
At presentation, he was 147 cm and 33.4 kg (body mass index (BMI) 15.5). He was presented with no complaints and his physical examination was unremarkable, except for severe cachexia. He was examined, as all patients are at the ICPC, by specialists in internal medicine, surgery, plastic surgery, urology, oral surgery, and gastroenterology. He also underwent routine imaging (US abdomen) and blood tests.
A well-differentiated pancreatic adenocarcinoma (T2N0M0) was diagnosed on March 2018 by abdominal computed tomography (CT) and increased blood levels of carcinoembryonic antigen (CEA) and CA19-9. He underwent near total pancreatectomy. Histology was positive for CA19-9 and CEA, and negative for P53 and SMAD4. No tumor-based genetic testing was done.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [33.4, 'kg']}",73.4,69.73,77.07,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 33.4 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (33.4 kg - 20 kg) = 73.4 mL/hr.
Hence, the patient's fluid maintenance is 73.4 mL/hr."
4907,22,Maintenance Fluids Calculations,physical,decimal,pmc-8716121-1,Extracted,"An eight-year-old, well-thriving female from Dhaka, weighing 34 kg, was admitted to the pediatric intensive care unit (PICU) with a four-day high-grade, continued fever and abdominal pain, diarrhea, and non-bilious vomiting, as well as a headache for the past three days. She has a history of contact with a family member with COVID-19 infection within a month of presenting illness. She had no previous history of dengue fever. On the second day of fever, nonstructural protein 1 antigen (NS1 Ag) for dengue was positive.
On examination, the patient was febrile, with a temperature of 102°F, and tachypnea (42/minute) and tachycardia (160/minute) were present, with low volume pulse and narrow pulse pressure of 60/45 mm Hg. Auscultation of lungs revealed coarse crepitations in both lungs with poor air entry, especially on the right middle and lower lung fields. The abdomen was distended with mild tenderness on the whole abdomen. Flanks were full, with no organomegaly. She had mucosal bleeding, petechial rashes on extremities, and generalized edema, with no lymphadenopathy. Oxygen saturation (SpO2) was 90% in room air and 96% with a face mask (5 L/minute oxygen). Initial investigations showed markedly reduced platelet counts and raised inflammatory markers. Serum calcium and albumin levels were low. Liver functions were altered with alteration of coagulation profiles (Table ). Serum electrolytes and renal functions were within the normal range. The chest X-ray (CXR) revealed pulmonary infiltrations with pleural effusion (Figure ).
Blood, urine, stool, and throat swab culture were sent and came back with negative results. Nasopharyngeal swab for reverse transcription-polymerase chain reaction (RT-PCR) for SARS-CoV-2 was positive with a cycle threshold (CT) value of 32.9. The patient was isolated and treated for expanded dengue syndrome with plasma leakage with SARS-CoV-2 infection accordingly, with intravenous (IV) broad-spectrum antibiotics, inotropes, crystalloids, and colloids. Echocardiography on admission was normal with good biventricular systolic functions (ejection fraction (EF): 70%).
Pleural effusion was resolving, but on the seventh day of fever, the patient developed a cough and increasing respiratory distress, with pulmonary hemorrhage. She was still febrile and hemodynamically unstable. Immediately, the patient was intubated and kept on a mechanical ventilator. Chest radiograph at that time revealed alveolar opacities and patchy infiltrations on both lungs (Figure ).
ECG was done and was still within normal limits. Dengue IgM was positive after seven days of fever. However, echocardiography on the seventh day revealed dilated coronary arteries (left main coronary artery (LMCA): 5 mm (+3 standard deviations (SD)); left coronary artery (LCA): 4.8 mm (+2.5 SD)), with the loss of distal tapering and perivascular brightness (Figure ) and fair biventricular systolic functions (EF: 66%) (Figure ).
Serum D-dimer and ferritin levels were noticeably increased with markedly raised cardiac enzymes (Table ). Consultations were obtained from pediatric cardiologists, and we administered one dose of intravenous immunoglobulin (IVIG) 2 g/kg over 24 hours. Thereafter, methylprednisolone was added.
Meanwhile, the patient became afebrile and was hemodynamically stable with cessation of pulmonary hemorrhage. Chest radiographs showed improvements. Three days after ventilatory support, the patient was gradually extubated. General conditions were improving with normal vitals without inotropes, and SpO2 was 98% in room air with a gradual return of appetite. Inflammatory markers and cardiac enzymes were reduced. Hematocrit came to baseline with gradually corrected thrombocytopenia (Table ) and coagulopathy. Aspirin was added subsequently.
At this point, the patient was transferred to the ward and thereafter discharged with the required and necessary advice and scheduled follow-ups.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [34.0, 'kg']}",74,70.3,77.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 34.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (34.0 kg - 20 kg) = 74.0 mL/hr.
Hence, the patient's fluid maintenance is 74.0 mL/hr."
4908,22,Maintenance Fluids Calculations,physical,decimal,pmc-5047988-1,Extracted,"A 59-year-old male, height 170 cm and weight 68 kg, was admitted for open reduction and internal fixation of ankle fracture. The patient underwent an open reduction and internal fixation of ankle fracture under spinal anesthesia with bupivacaine 2 years ago. During the surgery, he was sedated by intravenously administered midazolam without premedication and the anesthesia- or surgery-related complications were not reported. He has not experienced sedation management with the exception of the surgery. There was no known history of atopy, asthma, or allergies. Preoperative evaluations such as laboratory tests, electrocardiography, and chest radiography were normal.
For the preoperative treatment, atropine 0.5 mg and midazolam 3.0 mg were intramuscularly administered 30 minutes before the operation. His blood pressure was 122/75 mmHg with a heart rate of 85 beats/min, and a respiratory rate of 16 breaths/min before he transferred to the operation room. After his arrival in the operating room, the patient's vital signs were monitored by noninvasive blood pressure measurement, electrocardiography, and pulse oxymetry. Before induction of general anesthesia, he complained generalized pruritus. Urticarial skin rashes of upper and lower extremity and an angioedema of face and tongue were observed.
Because an anaphylactic reaction was suspected judging from these generalized skin symptoms, the operation was delayed and he was moved to the recovery room. Although 250 mg of methylprednisolone and 40 mg peniramin were injected intravenously to treat the anaphylactic reaction, his blood pressure decreased to 70/40 mmHg with heart rate of 98 beats/min and pulse oxygen saturation on pulse oximetry (SpO2) of 90% 25 minutes after skin symptoms (). Although he began to experience mild dyspnea, the sound of wheezing was not auscultated. The patient was given 100% oxygen via face mask. Simultaneously, epinephrine 50 µg and hydrocortisone 100 mg were injected intravenously with plasmalyte solution (Plasma Solution-A, CJ Pharma, Seoul, Korea) hydration. And then, the serum tryptase level and the total serum immunoglobulin E (IgE) level were measured for confirming anaphylaxis. After transient tachycardia of heart rate of 130 beats/min, heart rate decreased to 100 beats/min within 10 minutes and the blood pressure increased to 90/60 mmHg, SpO2 to 95%. Except the tachycardia, other specific changes of electrocardiography were not observed. During the rest of the period, vital status was stably maintained without medication other than intramuscular epinephrine 0.3 mg. The elevated tryptase level to 29.9 µg/L (normal range: 0–11 µg/L) was detected from laboratory test. Except that systemic erythematous rash and swelling of the skin around the eyes could still be seen, there were no other abnormal findings. The skin symptoms resolved after 2 hours in the recovery room. Arterial blood gas analysis (ABGA) gave pH 7.32, pCO2 44 mmHg, pO2 155 mmHg, and BE 0.5 mM at fraction of inspired oxygen 0.3. Since the results of ABGA and chest radiography were normal and there were no further specific clinical presentations, the patient was transferred to a general ward.
After 2 months, skin prick and intradermal tests were performed to establish the allergen. As a result, midazolam was identified as a cause of anaphylactic shock () and the patient was informed to avoid this agent. The patient underwent an open reduction and internal fixation of ankle fracture under spinal anesthesia without sedation. After one week following surgery, the patient was discharged without any other problems.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [68.0, 'kg']}",108,102.6,113.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 68.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (68.0 kg - 20 kg) = 108.0 mL/hr.
Hence, the patient's fluid maintenance is 108.0 mL/hr."
4909,22,Maintenance Fluids Calculations,physical,decimal,pmc-5484263-1,Extracted,"A 7-year-old girl visited the emergency department with severe polyuria. She had a 3-day history of frequent urination (3–4 times every hour), polydipsia, and lethargy. Although she drank more beverage than usual, she felt excessive thirst and lost weight from 22 to 19.6 kg in 7 days. She had recently moved to a new house and was having a hard time fitting in at the new school. She was previously healthy with no past admissions or serious illness. She had no change of eating habits and lifestyle recently. No history or family history of endocrine disease including diabetes mellitus was reported. At admission, her height was 127.4 cm (50th–75th percentile), weight was 19.6 kg (5th–10th percentile), and body mass index (BMI) was 12.08 kg/m2 (<first percentile). Her temperature was 37.2°C, heart rate was 88 beats/min, respiratory rate was 18 beats/min, blood pressure was 100/60 mm Hg, and pulse oximetry was 100% on room air. Her mental status was alert, sensation was intact, and motor strength was quite good considering her condition. However, she looked cachectic and lethargic. Her glucose level was too high to check with a capillary blood glucose meter, so a blood test was performed and rehydration therapy with intravenous fluid (isotonic saline 10 mL/kg loading dose for 1 hour) was started immediately (Table ). Initial biochemistry results demonstrated severe hyperglycemia (1167 mg/dL), hyperosmolality of 350 mOsm/kg (effective osmolality 311 mOsm/kg), mild acidosis (venous pH 7.34), hyponatremia (sodium 123 mmol/L; corrected for blood glucose: 140 mmol/L), severe glycosuria, and mild ketonuria.
On the basis of the laboratory results, intensive intravenous fluid and regular insulin were administered and laboratory examinations were performed every 2 hours to check and modulate electrolyte changes. Serum glucose level decreased approximately 60 mg/dL/h and normalized to 115 mg/dL 17 hours after treatment started, which led a gradual decrease in serum osmolality (Fig. ). No evidence of acidosis or severe ketosis confirmed the diagnosis of HHS. A neurological examination and brain computed tomography scan were performed to check for complications of HHS, but no cerebral edema was found.
The laboratory results that confirmed the diagnosis of T1DM were as follows: glycated hemoglobin (HbA1c), 15.6% (reference, <5.6%); C-peptide, 0.12 ng/mL (reference, 1.10–4.40 ng/ml); anti-GAD antibody, 2.4 U/mL (reference, ≤9.0 U/mL); anti-insulin antibody, 4.9% (reference, ≤7.0%); anti-islet cell antibody, negative; and 24-hour urine c-peptide, 4.5 μg/day (reference, 17.2–181.0 μg/day). All parameters of other hormone group were within normal range; triiodothyronine, 86.23 ng/dL (reference, 80.00–200.00 ng/dL); free thyroxine, 1.40 ng/dL (reference, 0.70–2.00 ng/dL); thyroid-stimulating hormone (TSH), 2.78 μIU/mL (reference, 0.5–4.5 μIU/mL); anti-thyroglobulin, 25.30 IU/mL (reference, ≤115.00 IU/mL); anti-microsome, 5.19 IU/mL (reference, ≤34.0 IU/mL); anti-TSH receptor 0.40 IU/L (reference, ≤1.75 IU/L).
After a 13-day hospital stay that included blood glucose control and T1DM education, she was discharged without any symptoms. Anthropometric measurements at discharge were height, 127.0 cm (50th–75th percentile); weight, 24.0 kg (25th–50th percentile); and BMI, 14.88 (29th percentile). She is being followed-up in the outpatient clinic regularly with split insulin therapy (Neutral protamine Hagedorn and regular insulins) and self-glucose monitoring. At recent visits (4 months after discharge), her HbA1c level was 7.1%, and she was maintaining blood glucose within the target range.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [19.6, 'kg']}",59.2,56.24,62.16,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 19.6 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (19.6 kg - 10 kg) = 59.2 mL/hr.
Hence, the patient's fluid maintenance is 59.2 mL/hr."
4910,22,Maintenance Fluids Calculations,physical,decimal,pmc-6702657-2,Extracted,"The second case was a 64-year-old woman diagnosed with PBC in June 2010, when she started UDCA 750 mg/d. Some months later, she was started on endoscopic sclerotherapy and injection of cyanoacrylate glue for gastric fundal varices. In December 2017, gastroesophageal varicose vein ligation and stripping were demonstrated for uncontrolled gastric bleeding. She had a 3-year history of type 2 diabetes mellitus, treated by keeping an appropriate diet for blood sugar. She developed dysphonia and weakness of the hands 3 months before admission. The symptoms gradually progressed. Two months later, she presented weakness in her lower limbs, therefore, she was admitted to our hospital in May 2018. She had lost 10 kg of weight over 3 months. She had no family history of neurodegenerative diseases.
Upon physical examination, muscle atrophy was observed bilaterally in the first dorsal interosseous muscles and the thenar, hypothenar muscles. Fasciculations and atrophy were evident in the tongue. Power was MRC grade 3/5 in the upper limbs and 4/5 in the lower limbs bilaterally. Deep tendon reflexes were brisk in all extremities. Positive bilateral Hoffman signs and hyperreflexia in the pharyngeal muscles were observed. No abnormality was observed in sensations and cerebellar function. AMA (>1:40) and ANA (1:320) were both positive. Hepatitis markers were negative, so were tumor markers. The levels of white blood cell count (1.80*109/L), red blood cell count (3.11*1012/L), hemoglobin (105 g/L), and platelet (30*109/L) all decreased. The biochemical results showed aspartate aminotransferase (AST) 41.3U/L and total bilirubin (TBIL) 26.0 umol/L. Baseline data of the patient was as follows (). There were some lacunar infarctions in bilateral frontal, temporal lobes, and left basilar ganglia on brain MRI. A thyroid ultrasound scan showed small nodules on the left and right lobes (). Clear lungs were observed on her chest CT. Abdominal ultrasound visualized out of proportion hepatic lobes, mild heterogeneous decrease in echogenicity of the portal vein consistent with mural thrombus, splenomegaly () and dilated splenic vein, neither biliary obstruction nor space-occupied lesions. The CMAP amplitudes of right median and ulnar nerve decreased on NCS. EMG revealed florid active denervation changes in bulbar muscles and all limbs. Lumbar puncture was not executed because of her low platelet count. She was given UDCA, riluzole, and edaravone (Radicava), a new medication for ALS in 2017 approved by Food and Drug Administration (FDA) (). At the follow-up, she had indwelled gastric tube and difficulty in ambulation in 8 months.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.0, 'kg']}",40,38,42,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.0 kg - 10 kg) = 40.0 mL/hr.
Hence, the patient's fluid maintenance is 40.0 mL/hr."
4911,22,Maintenance Fluids Calculations,physical,decimal,usmle-5732,Extracted,"A 55-year-old man presents to his primary care physician for fatigue. He states he has not felt like himself recently and had to take a few days off of work secondary to fatigue. He has lost 10 pounds over the past month. He drinks 4 drinks per day and smokes 1 pack of cigarettes per day, which he has done for the past 20 years. His temperature is 99.0°F (37.2°C), blood pressure is 128/65 mmHg, pulse is 100/min, respirations are 11/min, and oxygen saturation is 98% on room air. Laboratory values are ordered as seen below.

Hemoglobin: 9 g/dL
Hematocrit: 27%
Leukocyte count: 2,500/mm^3 with normal differential
Platelet count: 293,000/mm^3

A biopsy of the bone marrow is performed which demonstrates hypocellular and fibrotic bone marrow and a peripheral smear is performed as seen in Figure A.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.0, 'lbs']}",18.14368,17.2365,19.05086,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.0 lbs so this converts to 10.0 lbs * 0.453592 kg/lbs = 4.53592 kg. Hence, the patient's maintenance fluid is 4.53592 kg * 4 mL/kg/hr = 18.14368 mL/hr.
Hence, the patient's fluid maintenance is 18.14368 mL/hr."
4912,22,Maintenance Fluids Calculations,physical,decimal,pmc-7642508-1,Extracted,"A previously healthy, 17-year-old 86.3 kg male presented due to refractory hypotension requiring vasopressor support. Initially, the patient reported loss of smell and taste about 4 weeks prior to presentation. Two weeks prior to admission, the patient was noted to be COVID-19 positive, with intermittent fevers, progressively worsening cough, and shortness of breath, as well as an evanescent rash. Following a two-week quarantine, symptoms resolved until presentation, when the patient developed neck tenderness, vomiting, diarrhoea, and syncope. The patient was seen at an emergency department on multiple occasions for symptoms and discharged home with the diagnosis of COVID-19 and given Azithromycin for an unclear diagnosis, without resolution of symptoms. During the 24 hours prior to admission, the patient endorsed blurry vision, eye redness, chest pain, nausea, and vomiting. En route to the hospital, the patient complained of dizziness and reported syncope. On arrival, the patient was hypotensive to the 80s/40s. On initial physical exam, the patient was ill-appearing, with no significant respiratory impairment, pale and diaphoretic, tachycardic to 120s with sinus rhythm, and had a hyper-dynamic precordium. Mild hepatomegaly was noted. The conjunctiva was injected and tongue erythematous, and a blanching rash was noted on palms and wrists. Criteria were met for severe multi-system inflammatory syndrome in children given the cardiovascular, renal, gastrointestinal, mucocutaneous, and pulmonary involvement with history of COVID-19 infection.
He received a 3 L normal saline bolus, but continued to be hypotensive despite norepinephrine, before quickly changed to epinephrine for concerns of cardiogenic shock. Electrocardiogram at presentation showed sinus tachycardia. A blood gas was notable for respiratory acidosis with mild metabolic compensation and lactic acidosis, troponin and brain natriuretic peptide were elevated; he had evidence of acute kidney injury, and inflammatory markers were elevated (Table ). Cardiology, Infectious Disease, and Rheumatology were consulted. Given the severity of symptoms and refractory shock, the patient was admitted to the paediatric ICU.
He was started on pulse solumedrol 30 mg/kg/day for 3 days per rheumatology recommendations, followed by tapered doses. The patient received recommended intravenous immunoglobulin treatment for multi-system inflammatory syndrome in children (100 g, weight-based maximum). Milrinone 0.5 mcg/kg/min and Aspirin 81 mg were started. Serial troponin continued to be elevated, however, down trending throughout admission. Multiple echocardiograms were obtained and significant for small pericardial effusion, but normal cardiac function, ejection fraction, and no sign of pulmonary hypertension. No coronary abnormalities were noted. On hospital day 1, the patient complained of acute chest pain without hypoxia that improved with morphine. CT chest was done and did not show evidence of pulmonary embolus. No evidence of strain on telemetry. He remained persistently hypotensive. On day 2, the patient was started on a 5-day course of biologic therapy with recombinant IL-1 antagonist Anakinra, 100 mg twice per day given the severity of presentation with elevated inflammatory markers suggesting cytokine storm. On day 3, premature atrial contractions were noted on telemetry with subsequent atrial fibrillation requiring cardioversion with 100 J and 150 J (Fig a). He remained stable until day 4 with new episode of atrial fibrillation requiring cardioversion with 150 J (Fig b) and a bolus dose of amiodarone. Low-dose epinephrine 0.02–0.05 was necessary even with sinus rhythm for refractory hypotension with orthostatic hypotension out of proportion to his clinical picture. The patient remained on sinus rhythm, but noted to have a 5 beat run of wide complex tachycardia on day 11.
Repeat labs showed improvement, with down trending inflammatory markers, troponin, and brain natriuretic peptide. The patient was transitioned to acute care floor on day 14 with the resolution of cardiac arrhythmias. He continued to have dysautonomia with orthostatic hypotension, and fludrocortisone and midodrine were started with improvement in blood pressure. Rehabilitation medicine was consulted for therapy given severe de-conditioning. He was discharged on day 16 with follow-up in Cardiology, Rheumatology and Physical/Occupational Therapy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [86.3, 'kg']}",126.3,119.985,132.615,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 86.3 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (86.3 kg - 20 kg) = 126.3 mL/hr.
Hence, the patient's fluid maintenance is 126.3 mL/hr."
4913,22,Maintenance Fluids Calculations,physical,decimal,pmc-2800015-1,Extracted,"A 9-month-old female infant was admitted to our hospital because of greasy stools and failure to thrive. She had been well until two months of age, when a productive cough and fever developed. She was hospitalized twice with recurrent pneumonia, which was treated with antibiotics. At three months of age, failure to thrive was noted and methicillin-resistant Staphylococcus aureus (MRSA) was isolated from sputum cultures obtained by ventilating bronchoscopy. At seven months of age, her parents were aware of her greasy and foul-smelling loose stools that were often pale; the infant also showed poor appetite. The patient had been born to a nonconsanguineous healthy couple by normal spontaneous vaginal delivery at 40 weeks of gestation. The patient's birth weight was 2.60 kg and there was no history of delayed passage of meconium. She had a 6-yr-old brother and the family history was unremarkable.
On admission, the infant appeared to be malnourished but was not in acute distress. The body weight was 4.5 kg (<3rd percentile for age), height 54.7 cm (<3rd percentile), and head circumference 33 cm (<3 percentile). The patient's vital signs included a temperature of 36.9℃, heart rate of 130 beats per minute and respiratory rate of 40 per minute. Her chest was not retracted and her breathing sounds were clear. The abdomen was not distended and the bowel sounds were normal. There was no organomegaly. No digital clubbing was found and a neurologic examination was negative.
A complete blood count and serum electrolytes were all within the normal limits. The serum albumin level was 2.6 g/dL and cholesterol was 100 mg/dL. AST and ALT levels were 36 U/L and 14 U/L, respectively. Plasma carotene level was 22.5 µg/dL (reference range 50-250 µg/dL). Immunologic studies of the patient were unremarkable, including normal proportions of polymorphonuclear cells, B cells, CD4 and CD8 T cells, and normal immunoglobulin levels. Stool fat was demonstrated microscopically. To confirm the presence of steatorrhea and estimate the quantity of stool fat, an acidified steatocrit test was performed: this gave a value of 33.3% (reference range; 0-6.5%). Stool alpha-1 antitrypsin clearance was 0.49 mL over 24 hr, which was within the normal limits. Chest radiographs and computed tomography (CT) scans revealed segmental atelectasis and patchy infiltration. An abdomen CT scan showed normal pancreas and hepatobiliary systems.
CF was suspected on the basis of isolation of MRSA in the respiratory tract, recurrent respiratory infection, and fat malabsorption. A quantitative pilocarpine iontophoresis sweat test was performed, showing the average sweat chloride concentration on both thighs to be 102.0 mM/L (reference limit <40 mM/L). After obtaining informed consent from the parents, genomic DNA was extracted from peripheral blood leukocytes. Direct sequence analysis of the CF transmembrane conductance regulator (CFTR) gene was performed as described (). This identified compound heterozygous mutations composed of a novel splicing mutation in intron 12 (c.1766+2T>C) and a 1-bp duplication in exon 21 resulting in a frameshift mutation (c.3908dupA; Asn1303LysfsX6) (). The parents declined further genetic analysis and sweat testing of the family.
Pancreatic enzymes (lipase 25,000 IU), fat-soluble vitamins, and long-chain polyunsaturated fatty acids were given to treat the infant's pancreatic insufficiency. She was fed with breast milk and standard infant formula. With pancreatic enzyme replacement, the steatorrhea improved and the infant gained weight slowly. She was thriving and passing formed stools by one year after hospital discharge. Her weight was at the 3rd percentile for age and her height was at the 10th percentile.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.5, 'kg']}",18,17.1,18.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.5 kg. Hence, the patient's maintenance fluid is 4.5 kg * 4 mL/kg/hr = 18.0 mL/hr.
Hence, the patient's fluid maintenance is 18.0 mL/hr."
4914,22,Maintenance Fluids Calculations,physical,decimal,pmc-6458504-1,Extracted,"A 13-year-old boy (height: 163 kg; weight: 54 kg) was admitted because of fractures of the left femur and ulna and the nasal bone as well as a blowout fracture after a car accident; he also had contusions to the chest wall, heart, and liver. According to his medical history, he had been diagnosed with DMD when he was three years old and had taken steroids. He had mild weakness in his lower limbs, but he could walk normally, and he did not complain of any respiratory distress. We referred the patient to the pediatric department for a preoperative evaluation, and he had no cardiac complications; his electrocardiogram (ECG) also showed normal sinus rhythm with right ventricular hypertrophy. Most of the laboratory findings were normal, but his abnormal findings were as follows: aspartate transaminase, 156.0 U/L; alanine transaminase, 215.7 U/L; creatine kinase (CK), 11196 U/L; CK-MB, 132.6 ng/ml. Mild rhabdomyolysis due to trauma was suspected, and the patient received hydration therapy. His K+ level was 4.00 mEq/L, and his urine output was more than 800 ml/day before surgery. The orthopedic surgeon planned to delay the operation until the swelling subsided and laboratory findings improved; however, he decided to conduct emergency surgery only for the femur fracture because of the risk of nonunion.
Three days after the accident, the patient was transferred to the operating room (OR) for the emergent surgery; baseline measurements were oxygen saturation (SpO2) 100%, noninvasive blood pressure 120/80 mmHg, heart rate (HR) 120 beats/min, end-tidal CO2 (ETCO2) 39 mmHg, and esophageal temperature 37.4oC. Anesthesia was induced using 250 mg of thiopental sodium and 35 mg of rocuronium and was maintained using 1% vol of sevoflurane with a fresh gas flow of 3 L/min of N2O/oxygen mixture. At the end of surgery, he recovered adequate respiration (train-of-four > 99%) with 10 mg of pyridostigmine and 0.4 mg of glycopyrrolate. The surgery time was 2 hours, and the administered fluid and estimated blood loss were 600 ml and 20 ml, respectively. All of his vital signs were maintained within 20% of the baseline, and there were no changes on the ECG or specific complications during the surgery. The patient’s mental state was clear, and he was transferred to the recovery room.
On arrival in the recovery room, the patient could answer questions, and he complained of pain in his leg. His vital signs were noninvasive blood pressure 119/70 mmHg, HR 90 beats/min, SpO2 98%, and ear temperature 36.3oC (). Approximately 2 minutes later, he became cyanotic and apneic, and his HR on the ECG showed 7 beats/min; the ECG showed an irregular ventricular wide-complex sine wave without a p wave. CPR was started, and 1 mg of epinephrine was administered. During the CPR, the patient underwent endotracheal intubation and arterial blood gas analysis (ABGA), and the ABGA was repeated approximately every 15 minutes after the CPR. An arterial blood gas test revealed pH 6.530, PaO2 38.9 mmHg, PaCO2 97.8 mmHg, base excess (BE) −32.4 mEq/L, Na+ 132.8 mEq/L, K+ 9.60 mEq/L, and hematocrit 38% (). Cardiac arrest due to hyperkalemia was suspected, and 20 ml of 3% calcium chloride, 10 unit of regular insulin, and 80 mEq of sodium bicarbonate were administered (); the patient achieved return of spontaneous circulation, and his blood pressure and heart rate became 80/35 mmHg and 40 beats/min, respectively. He was moved back to the OR for further monitoring and management and for effective CPR. External pacing was attempted, but there was no response. Continuous infusions of dobutamine, norepinephrine, and vasopressin were started, and mechanical ventilation (MV) was maintained with 5 L/min of 100% O2. However, cardiovascular collapse developed again about 5 minutes later and CPR was applied. Despite treatment with multiple doses of insulin, calcium chloride, and sodium bicarbonate, the patient’s K+ concentration did not reduce below 8.06 mmol/Eq, and the cardiovascular collapse repeated itself. Moreover, pulmonary edema developed, and peak inspiratory pressure increased more than 40 mmHg. The ABGA showed sustained acidosis (pH < 7.0), hypercarbia (PaCO2 > 90 mmHg), hypoxia (PaO2 < 50 mmHg), and hyperkalemia (K+ > 8.06 mEq/L).
After the fourth cardiovascular collapse, we decided to apply ECMO. We consulted with the cardiothoracic surgeon about using ECMO not only for cardiac and respiratory support but also to eliminate excess K+ using hemofiltration. The cardiothoracic surgeon suggested the use of in-line hemofiltration with ECMO and prepared for surgery; arterial and venous cannulas (Biomedicus®, Medtronic, USA) were inserted into the patient’s right femoral artery and vein. The hemofilter (Hemofiltration kit, Dideco, Italy) was connected between the pump and the arterial line of the ECMO circuit to remove excess K+ and water. ECMO was started 90 minutes after the first cardiac arrest, and blood flow was maintained about 3.0 L/min.
About 30 minutes after starting ECMO, laboratory results showed significant improvement and there was no further cardiac arrest ( and ). About 1 hour after the ECMO, ABGA showed almost normal pH (7.289), PaCO2 (38.9 mmHg), and PaO2 (200.8 mmHg), and lower serum K+ concentration (5.97 mEq/L). During the CPR and surgery for ECMO, 3,000 ml of fluids were administered, urine output was 300 ml, and estimated volume of bleeding was 200 ml. Then, the patient was transferred to the intensive care unit (ICU) and sedated using dexmedetomidine and remifentanil. Under suspicion of severe rhabdomyolysis, the patient’s serum CK, myoglobin, and urine myoglobin were measured. CK had increased to 242,340 U/L after cardiac arrest and decreased to 539 U/L after 26 days of treatment (), and serum and urine myoglobin had increased by more than 3,000 and 20,000 ng/ml, respectively, both of which exceeded the measurable value, and decreased to 2,359 and 1,438 ng/ml after 20 days, also respectively ().
In the ICU, the patient remained on ECMO support for 3 days. Although he had suffered from pneumonia, his vital signs were improving, but AKI secondary to myoglobinemia developed. At first, the patient maintained urine output more than 500 ml/h, but urine output decreased to less than 80 ml/h on the 3rd day after the ECMO. Moreover, intra-arterial thrombosis of the right femoral artery developed. Thus, we weaned the patient from the ECMO and MV, performed angioplasty of the femoral artery, and applied continuous renal replacement therapy (CRRT) simultaneously because his vital signs stabilized. The patient was successfully weaned from ECMO and MV, and CRRT was started with a newly inserted central venous catheter in the left internal jugular vein. His condition improved daily, and all inotropics and vasopressors were stopped on the 5th day. After 10 days from the start of CRRT, the patient’s renal functions had recovered, and he was successfully weaned from CRRT.
The patient was discharged from the ICU after 21 days of treatment and moved to the ward. Unfortunately, he required surgical disarticulation of his right leg because of angiopathy following the ECMO and the long rehabilitation treatment. However, he successfully recovered from the cardiac arrest by hyperkalemia due to massive rhabdomyolysis with the combination of ECMO and in-line hemofiltration.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [54.0, 'kg']}",94,89.3,98.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 54.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (54.0 kg - 20 kg) = 94.0 mL/hr.
Hence, the patient's fluid maintenance is 94.0 mL/hr."
4915,22,Maintenance Fluids Calculations,physical,decimal,pmc-3872382-3,Extracted,"The 3rd Case. A 57-year-old female patient arrived at the service referring abdominal pain and jaundice three months before and a gradual weight loss starting 6 months ago (total of 12 kg). The patient also referred asthenia, tiredness, and night fever, making it hard for her to perform daily chores 3 months before the admission.
At physical examination the patient was pale (2+/4+) and showed no signs of jaundice. Abdominal ultrasound showed a heterogeneous mass of 6.4 cm × 5.8 cm, close to the head of the pancreas; as well as thickening of the intra and extra-hepatic biliary tract, consistent with inflammation. A CT with intravenous contrast was performed, showing enlargement of periaortic lymph nodes near the hepatic hilum, with some as large as 2 cm. An abdominal MRI showed enlarged lymph nodes at the hepatic hilum, the hepatic gastric ligament, portocaval space, peripancreatic and interaortocaval regions, measuring up to 2.8 cm, leading to a main hypothesis of lymphoproliferative disease.
At EUS, the same enlarged lymph nodes were shown and EUS-guided fine needle aspiration (EUS-FNA biopsy) of the hepatic hilum was chosen for sampling with a 22-gauge needle. Histological analysis of the obtained samples showed necrotic tissue accompanied by round blast-like structures of multiple sizes and favoring fungal infection. Grocott stain confirmed the presence of fungi with morphological features consistent with Paracoccidioides brasiliensis (Figures and ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.0, 'kg']}",44,41.8,46.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.0 kg - 10 kg) = 44.0 mL/hr.
Hence, the patient's fluid maintenance is 44.0 mL/hr."
4916,22,Maintenance Fluids Calculations,physical,decimal,pmc-3192208-1,Extracted,"A 46-year-old man presented with a 3-month history of dyspepsia and a 7-kg weight loss. He had no history of any disease. He did not smoke and drank alcoholic beverages in moderation. On admission, the patient's vital signs were stable. His family history was negative for malignancy. Direct tenderness was noted over the right upper quadrant area of the abdomen, but rebound tenderness and Murphy's sign were absent. The remainder of the examination was unremarkable. The complete blood count showed a white cell count of 7,800/mm3 (70.9% neutrophils), hemoglobin 10.3 g/dL, hematocrit 29.2%, and platelet count of 283,000/mm3. The blood chemistry showed a fasting glucose level of 107 mg/dL, urea nitrogen 19 mg/dL, creatinine 0.8 mg/dL, total protein 6.1 g/dL, albumin 4.0 g/dL, aspartate transaminase 13 IU/L, alanine aminotransferase 12 IU/L, alkaline phosphatase 238 IU/L, total bilirubin 0.6 mg/dL, total cholesterol 170 mg/dL, and triglyceride 64 mg/dL. The serum amylase was elevated slightly to 170 U/L, and the serum lipase to 338 U/L. The carcinoembryonic antigen (CEA) was 3.3 ng/mL, α-fetoprotein was 1.5 ng/mL, and the CA 19-9 was elevated to 566.7 ng/mL. Gastroduodenoscopy showed a hard ulceroinfiltrative mass with a yellowish exudate that bled readily on touch at the second portion of the duodenum (). Initially, we thought that he had duodenal cancer. However, a biopsy of the duodenum showed adenosquamous cell carcinoma (). Abdominal computed tomography showed a 7.1 × 6.3-cm heterogeneously enhancing mass in the pancreatic head. The main pancreatic duct was dilated due to compression by the mass. The tumor mass invaded the duodenum, gastric antrum, and gastroduodenal artery sheath. Multiple enlarged lymph nodes were seen around the left gastric vessel, greater omentum, and small bowel mesentery (). Fine-needle aspiration biopsy of the pancreatic mass revealed adenosquamous cell carcinoma, anaplastic type (). We diagnosed primary adenosquamous cell carcinoma of the pancreas that had invaded the duodenum, resulting in an ulceroinfiltrative lesion. The patient refused palliative management and was discharged.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.0, 'kg']}",28,26.6,29.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.0 kg. Hence, the patient's maintenance fluid is 7.0 kg * 4 mL/kg/hr = 28.0 mL/hr.
Hence, the patient's fluid maintenance is 28.0 mL/hr."
4917,22,Maintenance Fluids Calculations,physical,decimal,pmc-6007484-1,Extracted,"A 14-year-old African–American female presented as a referral for evaluation of short stature. She has a history of basal meningoencephalocele [repaired during infancy], left-eye blindness due to morning glory disc anomaly, and cleft lip and palate [repaired during infancy]. Growth curves showed all of her growth parameters below −5 SD. Her estimated growth velocity was ~1 cm per year, annualized over 6 months. The mother reported normal growth during early infancy that slowed as she neared the age of 1 year. She was referred to another endocrinology group for growth failure at the age of 2 years.
On physical exam she was noted to have Tanner stage 1 breast development with lipomastia. No pubic hair or body odour was noted. She reported being premenarchal. She appeared small for age but exhibited a proportional habitus. Height 118.9 cm [−6.5 SD], weight 27.0 kg [−5 SD], BMI 19.1 kg/m2 [−0.2 SD], arm span 118.2 cm, upper segment 61 cm. Healed facial burns were noted from a scald injury during early childhood. Cardiac, respiratory, abdominal and genitourinary exam were unremarkable.
She denied symptoms and did not exhibit any manifestations of hypothyroidism except for dry skin. She also denied symptoms of adrenal insufficiency including hypoglycemic, hypotension and syncopal events. Mother noted that the patient had hypoglycemic during early childhood but this is now resolved. She denied any symptoms of diabetes insipidus including polyuria and polydipsia.
The patient was previously evaluated by endocrinology at 2 years of age but had been lost to follow-up at around the age of 3 years. During this time, she was diagnosed with growth hormone deficiency and hypothyroidism. Treatments were stopped as she was lost to follow-up. She had a non-contrast MRI of the brain at the age of 4 years, performed at our institution, that showed ‘broad depression of the sphenoid planum with meningoencephalocele’. The pituitary could not be visualized in full.
She has a history of left-eye blindness diagnosed at the age of 2 years. The mother stated that this was diagnosed by an optometrist. Records from her primary care provider confirm that she has a morning glory disc anomaly of the left eye.
She was the product of a full-term birth, with an uncomplicated pregnancy with good prenatal care. Antenatal course was complicated by cleft lip and cleft palate. Birth weight was 6 pounds and 14 ounces. Mother did not recall her birth length. The patient was in the NICU for feeding issues surrounding cleft lip and cleft palate. She also underwent cleft lip and cleft palate repair with simultaneous repair of her basal meningoencephalocele.
Family history includes a reported maternal height of 5 feet and 6 inches and reported paternal height 6 feet and 2 inches. Maternal onset of menarche was at 15 years old. Timing for paternal onset of puberty is unknown. Mother denied issues with infertility or consanguinity. No previous family history of genetic syndromes, short stature, endocrine disorders or autoimmune conditions.
The patient had multiple risk factors for having hypopituitarism that prompted endocrine testing, this included documented growth failure, previous diagnosis of growth hormone deficiency, previous diagnosis of hypothyroidism, coarse facial features, mid-line defects [cleft-lip and cleft palate] and pubertal delay.
Endocrine testing was obtained to screen for secondary/tertiary endocrinopathies. Cortisol level [8am]: 3.31 µg/dL [<10], 250 µg cosyntropin stimulation test peak cortisol level: 19.50 µg/dL [>18], ACTH level: 39 pg/mL [6–48], TSH: 2.110 mcIU/mL [0.5–4.5], free T4: 0.48 ng/dL [0.8–2.0], LH: 0.091 mIU/mL [0.4–11.7], FSH: 0.609 mIU/mL [1.0–9.2], insulin-like growth factor I [IGF-I]: 24 ng/mL [211–547], IGF binding protein 3 [IGFBP-3]: 0.7 mg/L [2.2–5.9]. Microarray showed normal female genotype, 46XX. Bone age according to standards of Greulich and Pyle is 8 years 10 months and 10 years for a chronologic age of 14 years 3 months [−5 SD].
As the patient was found to have hypopituitarism, contrast and non-contrast MRI of the brain and pituitary were obtained that revealed a craniopharyngeal canal (Fig. ). Extension of CSF, meninges and the sellar contents into the craniopharyngeal canal was visualized although no intrasellar adenohypophyseal or neurohypophyseal tissue was identified. The transverse dimension of the defect was 6 mm and the oblique craniocaudal dimension was 7 mm. Her previously diagnosed morning glory disc anomaly was also seen. She was also noted to have a smaller than expected caliber of the orbital segment of the left optic nerve. Irregular appearance and caudal position of the cribriform plate, as well as the right fovea ethmoidalis, was also noted. Caudal protrusion of the right gyrus rectus and medial orbital gyrus was noted. The olfactory bulb could not be visualized. The patient has an intact sense of smell.
An MR angiogram was also obtained to help exclude Moyamoya disease, which has been associated with morning glory disc anomaly. Her MR angiogram was normal.
Unfortunately, the patient has been lost to follow-up despite multiple attempts to reach the family after her diagnosis. Therefore, we were unable to initiate therapy for any of her endocrinopthies.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [27.0, 'kg']}",67,63.65,70.35,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 27.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (27.0 kg - 20 kg) = 67.0 mL/hr.
Hence, the patient's fluid maintenance is 67.0 mL/hr."
4918,22,Maintenance Fluids Calculations,physical,decimal,pmc-5635439-1,Extracted,"Here we report a case of a seven-month-old boy, born out of a third degree consanguineous marriage, with a history of recurrent episodes of pneumonia, acute otitis media, diarrhea and oral thrush since two months of age. The child was pale, emaciated, febrile, and had respiratory distress with lower chest retractions. He was in compensated shock. There was no clubbing, cyanosis or lymphadenopathy. There was no facial dysmorphism, and skin and hair were normal. He weighed 5.4 kg; measured 64 cm in length and head circumference was 39.5 cm; all below the 3rd centile as per WHO Child Growth Standards. Examination of the chest showed evidence of bronchopneumonia while there was no evidence of congenital heart disease or neurological deficits. There was mild hepatomegaly with a liver span of 6.5 cm.
The baby was normal in the perinatal and postnatal period. His birth weight was normal (3.04 kg) and was asymptomatic until 2 months of age. There was a history of admission to pediatric intensive care unit (PICU) and artificial ventilation for severe pneumonia at the age of 2 months. He was admitted for 22 days during that episode. The child had gross motor developmental delay and no adverse events following immunization. He had a male sibling who expired at seven months of age due to persistent pneumonia and two unaffected female siblings, apart from a half-brother and half-sister both of whom were asymptomatic (
).
On investigation, the child was found to have hypochromic microcytic anemia, lymphocytopenia, and a normal eosinophil count and platelet count. Liver and renal function tests were normal. The ionized calcium was 0.28mmol/L. Blood culture was positive for Enterobacter species. The child’s mother was HIV ELISA negative and the child had a negative Mantoux test and negative gastric acid AFB stain. His chest X-Ray’s lateral view showed absence of the thymus shadow apart from evidence of bronchopneumonia.
A close workup of the immunoglobulin profile revealed hypogammaglobulinemia-IgA 23 mg%, IgG 44 mg% and IgM 26 mg%. IgE was 1 IU/L. The absolute CD3 count was 464 cells/ul (normal range 1,460–5,440 cells/ul), absolute CD19 lymphocyte count was 12 cells/ul (normal 430–3,300 cells/ul) and absolute NK cell count was 1,328 cells/ul (normal 80–340 cells/ul). Flow cytometry suggested absent B and markedly reduced T cell populations suggestive of B- T- NK+ SCID.
The child was treated with piperacillin (80mg/kg/dose Q8H), vancomycin (15 mg/kg/dose Q6H), dopamine (10 mic/kg/min), intravenous immunoglobulin (IVIG) and other supportive measures and was put on cotrimoxazole (6 mg/kg/day OD) prophylaxis. He was treated with ganciclovir for CMV infection and for staphylococcal pneumonia.
The child was referred for a bone marrow transplant, since SCID is not compatible with life beyond infancy. The patient underwent a matched sibling donor bone marrow transplant at the age of 1 year and 3 months. The conditioning regimen used was Fludarbine 40mg/M2 for 4 days, and Treosulphan 12 gm/M2 for 3 days. GVHD prophylaxis was provided with Methotrexate 10 mg/M2 on days 1, 3 and 6 following transplant, along with Tacrolimus on day 0. Leuconostoc sepsis was treated with intravenous Amoxicillin and Clavulanic acid. Chimerism was assessed using whole blood by fluorescence
in situ hybridization (FISH) as the transplant was sex mismatched. At 6 months post- transplant, chimerism was down to 28%, and hence 2 donor lymphocyte infusions were given. The last assessment was done at 1 year by T and B cell markers and serum immunoglobulins, and these were found to be within the normal range. The chilld is now one year three months post-transplant and off all medications including immunosuppressive therapy.
The clinical diagnosis of SCID and family history of sibling death prompted us to investigate the molecular genetic correlates of the disease. Since over 13 genes are implicated in SCID and regular molecular testing was not readily available for the genes, we resorted to whole exome sequencing.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.4, 'kg']}",21.6,20.52,22.68,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.4 kg. Hence, the patient's maintenance fluid is 5.4 kg * 4 mL/kg/hr = 21.6 mL/hr.
Hence, the patient's fluid maintenance is 21.6 mL/hr."
4919,22,Maintenance Fluids Calculations,physical,decimal,pmc-7937578-1,Extracted,"The patient was a 71-year-old woman (body weight, 49 kg; height, 148 cm) with a history of hypertension. THA was performed due to osteoarthritis of the hip using a posterolateral approach. General anesthesia was maintained by propofol (TCI, 2.3–3.3 μg/mL) and remifentanil (0.15 μg/kg/h) with stable hemodynamics. A total of 200 μg of fentanyl was used during surgery. Postoperatively, the patient developed mild pain upon movement in the outer side of the thighs but did not require additional pain management. The patient was able to start using a walker and increase loading on the affected side from POD1, with a Bromage score of 0 (Table ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [49.0, 'kg']}",89,84.55,93.45,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 49.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (49.0 kg - 20 kg) = 89.0 mL/hr.
Hence, the patient's fluid maintenance is 89.0 mL/hr."
4920,22,Maintenance Fluids Calculations,physical,decimal,pmc-4560322-1,Extracted,"A 52-year-old Caucasian woman was admitted to our hospital from the nursing home due to refusal of percutaneous endoscopic gastrostomy tube feeding and altered mental status, which was attributed to hypoglycemia and urinary tract infection. Her medical history was significant for long-standing severe anorexia nervosa, depression and recent percutaneous endoscopic gastrostomy tube placement for nutritional support at another hospital. She was allergic to ciprofloxacin and penicillin and her nursing home medications included multivitamin, megestrol, ferrous sulfate, calcium carbonate, ranitidine, thiamine, folic acid, and olanzapine.
Upon admission, her weight was 21 kg and her BMI was 7.9, which amounted to approximately 40%percnt; of her ideal body weight. The vital signs were normal. The patient was bed bound, alert and well oriented. The physical exam revealed dry skin, excoriations all over the body, brittle nails, pallor and profound emaciation with bitemporal wasting. Her abdomen was scaphoid without organomegaly, and she had a percutaneous endoscopic gastrostomy tube with granulation tissue surrounding the stoma. There were no stigmata of chronic liver disease. The remainder of her physical examination was unremarkable.
Laboratory investigations revealed hemoglobin of 8.4 g/dl, white cell count of 3.5 k/μl, platelet count of 230 k/μl, prothrombin time of 12 s and activated partial thromboplastin time of 29 s, normal serum electrolytes except for a blood sugar level of 56. Her liver function tests showed serum alanine aminotransferase of 32 units/l, serum aspartate aminotransferase of 32 units/l and serum total bilirubin of 0.6 mg/dl.
She continued to refuse oral and tube feeding and she had intermittent episodes of hypoglycemia. She was evaluated by psychiatrists and was deemed to lack decisional capacity. It was recommended that percutaneous endoscopic gastrostomy tube feeding be imposed for nutritional support. After consultation with the nutritional team, tube feeding was begun at 400 kcal/day and advanced gradually over the next 5 days to 900 kcal/day.
Five days after the initiation of feeding, she developed tachycardia and lab work revealed electrolyte abnormalities such as hypophosphatemia (phosphorus 0.8 mg/dl) and hypokalemia (potassium 2.9 mEq/l) (fig. ). An electrocardiogram was done, which showed sinus tachycardia with some premature ventricular complexes and prolonged QT interval (QTc 472). She was then evaluated by cardiologists and nutritional teams. A diagnosis of refeeding syndrome was made, and the patient was transferred to the telemetry unit for further management. Further laboratory tests revealed elevated transaminases (alanine aminotransferase 193 units/l, aspartate aminotransferase 173 units/l), alkaline phosphatase (392 IU/l) and bilirubin (1.4 mg/dl), which were normal upon admission (fig. ). A consultation with a gastroenterologist was called. Viral hepatitis was excluded by serological tests and autoimmune workup, including anti-smooth muscle antibody, anti-liver/kidney microsomal antibody, antinuclear antibody and antimitochondrial antibody, was negative. Serum ceruloplasmin level was normal. Other causes of hepatitis such as hepatotoxic drugs were excluded. The liver and pancreas appeared normal on a computed tomogram. An abdominal ultrasound revealed normal echotexture of the liver without intra- or extrahepatic biliary dilatation and normal Doppler evaluation of the hepatic and portal vein blood flow.
Infusions of potassium phosphate and magnesium sulfate were administered in addition to oral potassium phosphate supplements. Intravenous thiamine was given. Her enteral intake was reduced and daily electrolyte levels were obtained along with regular monitoring of the liver function tests. The liver enzymes started improving after reduction of the tube feeding rate. Electrolytes also normalized over the next few days and the patient was eventually discharged.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [21.0, 'kg']}",61,57.95,64.05,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 21.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (21.0 kg - 20 kg) = 61.0 mL/hr.
Hence, the patient's fluid maintenance is 61.0 mL/hr."
4921,22,Maintenance Fluids Calculations,physical,decimal,pmc-4610393-1,Extracted,"A 43-year-old homeless African-American man presented to the intensive care unit with severe jaundice and altered mental status. The patient had an unintentional 100 lb. weight loss over the previous 6 months, along with rapid heart rate, extreme fatigue, and frequent diarrhea. Two weeks prior to admission, the patient was evaluated for nausea, vomiting, jaundice, and dehydration and was discharged home to arrange outpatient follow-up of an unspecified hepatic and thyroid defect. He had no previous history of liver disease, exposure to jaundiced people or hepatitis, exposure to hepatotoxins (such as acetaminophen), alcohol ingestion, or drug abuse and was not taking any medications. Physical examination revealed an ill-appearing, cachectic man with temporal wasting who was unresponsive to external stimuli. His pulse was 150 beats/min and irregular; blood pressure 140/70 mmHg, temperature 36.7 °C, and weight 146 lb. Sclerae were icteric, but without proptosis or exophthalmos. His thyroid gland was diffusely enlarged (40 g by palpation) with a palpable thyroid thrill and audible thyroid bruit. There were no palpable thyroid nodules. Cardiovascular examination revealed an irregular rate and rhythm, no jugular venous distension, and no murmurs. The patient had a tender right upper quadrant on palpation of his abdomen, with hepatomegaly palpable 4–5 cm below the costal margin and no ascites. Neurologic examination revealed a resting tremor with hyperreflexia.
Laboratory data was remarkable for an elevated total bilirubin of 47.4 mg/dL (normal range: 0.2–1.2 with direct bilirubin of 44.6 mg/dL, delta bilirubin of 18.5 mg/dL, conjugated bilirubin of 26.1 mg/dL, unconjugated bilirubin of 2.8 mg/dL); aspartate aminotransferase of 259 U/L (AST; normal range: 8–60); alanine aminotransferase 142 U/L (ALT: normal range 14–78), alkaline phosphatase 307 U/L (normal range: 38–126 U/L); albumin 3.3 mg/dL (normal range 3.5–5.0); and prothrombin time (PT) >90 s. Complete blood count, platelets, and reticulocyte count were within reference ranges. Blood and urine toxicology (including alcohol), hepatitis A/B/C serologies, antinuclear antibodies, anti-mitochondrial antibodies, anti-gliadin antibodies, and HIV serology results were negative. Serum haptoglobin, ceruloplasmin, CEA, CA 19–9, AFP measurements were within normal limits. Electrocardiogram revealed atrial fibrillation and echocardiogram demonstrated tachycardia, preserved cardiac function with an ejection fraction of 70 %, and no evidence of congestive heart failure. Abdominal CT imaging revealed hepatomegaly without evidence of focal hepatic mass, inflammation, or vascular obstruction. The lack of a specific diagnostic cause for fulminant liver failure led to planning for hepatic biopsy to determine a potential pathologic liver defect.
Thyroid function studies revealed a thyroid-stimulating hormone of 0.20 μU/mL (TSH; normal range: 0.4–4.0); total thyroxine 15.2 μg/dL (total T4; normal range 4.5–12.5); free thyroxine 9.0 ng/dL (free T4; normal range 0.89–1.80); T3 uptake 1.98 (normal range 0.9–1.3 TBI); and total triiodothyronine 3.2 ng/mL (total T3; normal range 0.6–1.71). The patient’s history of homelessness as well as reported contact with rodents (and thus rodent antigens) raised the suspicion that measured TSH values were falsely elevated due to heterophile antibody interference with the TSH assay. Heterophile antibodies consist of natural antibodies that are weak and polyspecific antibodies capable of interference with immunoassays, such as TSH []. Following removal of human anti-mouse antibodies (HAMA) by precipitation, subsequent measurement of TSH concentration was <0.01 mU/L. Furthermore, a screen for HAMA was positive.
Based on previously published diagnostic guidelines [], a clinical and laboratory diagnosis of thyroid storm due to Graves’ disease was made and treatment with propylthiouracil (PTU; 400 mg every 6 h), potassium iodide, corticosteroids, and beta blockers was initiated by the end of the second day of hospitalization. After 24 h of treatment, free T4 and total T3 levels began to decline, while total T4 levels rose, potentially related to the acute inhibitory activity of PTU on type 1 deiodinase [, ]. Within 2–3 days of therapy, liver function studies began to improve, along with improvement of T4 levels. By day 5 of therapy, mental status and functioning improved. Corticosteroids were discontinued within 10 days of treatment. Scleral icterus and jaundice resolved by day 15 of treatment. From days 10–25, thyroxine levels dropped below normal control concentrations, and thionamides and iodide were briefly discontinued. Of note, thionamide therapy with PTU was initiated at the outset of treatment, but briefly substituted with methimazole due to concern over hepatic toxicity. These concerns were ultimately unfounded, as a lower dosage of PTU (200 mg every 8 h) was reintroduced by one month after treatment initiation and was maintained with dramatic improvement of total bilirubin, AST, and ALT levels (detailed in Fig. ). Hepatic synthetic activity also dramatically improved as prothrombin time and albumin concentrations returned to reference ranges within 2–3 weeks. Alkaline phosphatase concentrations improved by one month of treatment, but not completely to normal ranges, prompting an evaluation of bone and liver isoenzymes, which were both elevated; bone-specific alkaline phosphatase of 88 IU/L (normal range: 0–55) and liver-specific alkaline phosphatase of 278 IU/L (normal range: 16–70) by 2 weeks of therapy. By 4 weeks after treatment, the patient was moved to an inpatient rehabilitation facility, where he subsequently gained weight and improved his functional conditioning while continuing PTU therapy. Prior to discharge from the hospital, an I-123 uptake and nuclear scan was performed revealing diffuse 74 % uptake at 2 h and 43 % uptake at 24 h. He was subsequently treated with 18.7 mCi of I-131 for ablative therapy.
Given his severe liver failure during thyrotoxicosis, previous studies have suggested that an underlying defect in bilirubin metabolism could be aggravated by thyrotoxicosis [, ]. In order to test for the presence of genetic mutations affecting bilirubin metabolism, genomic DNA was extracted from peripheral blood using a commercially available kit (Genetra systems, Inc.) and followed by automated DNA sequencing [] at a reference laboratory at the Children’s Hospital of Philadelphia. The patient was found to be heterozygous for Gilbert’s syndrome, an autosomal recessive disorder, which is characterized by mild, unconjugated hyperbilirubinemia in the absence of liver disease or hemolysis. Gilbert’s syndrome is due to the presence of genetic defects in the promoter region of the UGT1A1 gene, which encodes the UDP-glucuronosyltransferase enzyme and is a key component for efficient biliary excretion of bilirubin []. Patients with Gilbert’s syndrome possess an additional TA repeat in the TATAA element of the 5′ promoter of the gene ((TA)7TAA rather than the normal (TA)6TAA), but patients with heterozygous mutations for Gilbert’s syndrome are often asymptomatic and do not exhibit hyperbilirubinemia. Furthermore, the patient did not have suppression or absence of albumin-bound delta bilirubin, a phenomenon reported during hyperbilirubinemia secondary to hemolysis or Gilbert’s syndrome [].","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [146.0, 'lbs']}",106.22443,100.91321,111.53565,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 146.0 lbs so this converts to 146.0 lbs * 0.453592 kg/lbs = 66.22443 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (66.22443 kg - 20 kg) = 106.22443 mL/hr.
Hence, the patient's fluid maintenance is 106.22443 mL/hr."
4922,22,Maintenance Fluids Calculations,physical,decimal,pmc-8040449-1,Extracted,"The patient is a 3-year-old boy diagnosed with congenital PA, complicated by metabolic strokes with neurologic sequelae (seizures, developmental delay, non-verbal communication, non-ambulatory). He received tube feedings through a G-tube five times a day. He also had a left subclavian vein subcutaneous port that was placed 2 years ago. He presented to the emergency department with acute encephalopathy after experiencing cough, congestion and non-bloody, non-bilious post-tussive emesis in the previous 24 h. He was reported to be in his usual state of health prior to these symptoms. On examination, he was found to be markedly lethargic, hypotonic, normotensive, with a low-grade fever (38 °C), tachycardic (128 bpm) and tachypneic (34 breaths/min). Review of medical history and previous records revealed the patient had a recent hospital admission 3 months prior for status epilepticus, for which he was tracheally intubated for several days and discharged home with anti-seizure medications. Interview of his parents also revealed that both his mother and father, as well as his aunt, were diagnosed with SARS-CoV-2 infection 3 weeks prior. All of them completed self-quarantine and had since recovered.
Laboratory workup in the emergency department showed results consistent with an episode of hyperammonemic metabolic acidotic crisis, including a pH of 6.95, bicarbonate level of 5 (hospital normal range: 18 - 27 mmol/L), glucose of 47 (range: 70 - 105 mg/mL), ammonia of 190 (range: 18 - 72 µmol/L) and white blood cell count of 16.7 (range: 4.5 - 14 × 109/L). Chest radiograph appeared normal. Blood cultures from his central port as well as from new venous sites were obtained, all of which grew gram-positive cocci that speciated into S. epidermidis. SARS-CoV-2 PCR assay was positive, while the remainder of his viral and bacterial respiratory panels were negative. A transthoracic echocardiogram was obtained revealing normal biventricular systolic function and no pathologic valve stenosis or regurgitation was seen.
The patient was admitted to the pediatric intensive care unit (PICU) and was treated with ammonia-scavenging drugs (a combination of sodium benzoate and sodium phenylacetate), carglumic acid, levocarnitine, biotin, serum acid buffering with sodium bicarbonate, glucose delivery and aggressive fluid hydration. Enteral feeding with low-protein formula was initiated through his G-tube. His anti-seizure medications (clonazepam and lamotrigine) were also continued. IVIG for SARS-CoV-2 infection and broad-spectrum intravenous antibiotics (vancomycin, clindamycin and piperacillin-tazobactam) were initiated per the infectious disease team recommendations.
The patient’s metabolic crisis was attributed to a possible central venous port infection and co-infection with SARS-CoV-2. He was slated for the OR 2 days after his initial presentation and was scheduled for removal of his central port, as well as placement of a peripherally placed central catheter (PICC). A preoperative anesthetic evaluation revealed a 13.9-kg male with a blood pressure of 98/78 mm Hg, a heart rate of 120 bpm and respiratory rate of 35 breaths/min. Auscultation of the heart and lungs revealed no abnormalities. Laboratory values at this time were normalized from his treatments and were as follows: pH of 7.47, bicarbonate of 25 mmol/L, glucose of 75 mg/mL, ammonia of 55 µmol/L, white blood cell count of 11 × 109/L, in addition to normal serum creatinine, blood urea nitrogen (BUN), aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), hemoglobin and platelet levels.
He was nil per os (NPO) for 6 h for enteral feedings. At least one functioning intravenous cannula was verified. To avoid worsening of his metabolic crisis due to catabolic processes, maintenance with intravenous fluid consisting of D5 ½ NS with 20 mEq KCl/L and 27 mEq NaHCO3/L was initiated immediately after the discontinuation of enteral feeds. Because of the patient’s positive SARS-CoV-2 status, he was taken to a negative-pressure OR for his procedure. Routine monitors were used, including pulse-oximetry, electrocardiography, non-invasive blood pressure, end-tidal CO2 and skin temperature. An attending anesthesiologist and a resident anesthesiologist both donned controlled air-purifying respirators (CAPRs) while the rest of the OR personnel wore N95 masks. Rapid sequence induction and intubation were performed without difficulty using indirect visualization with a video-laryngoscope. To limit the exposure of OR personnel to respiratory droplets and aerosols that may carry SARS-CoV-2, non-anesthesiology staff were asked to leave for the induction and intubation period. The patient was given 2 mg of intravenous midazolam. A bolus dose of propofol (1.5 mg/kg), fentanyl (1 µg/kg) and rocuronium (1.2 mg/kg) were given on induction, and anesthesia was maintained with 1.8-2.2% sevoflurane in 50% oxygen. Before the start of the procedure, another intravenous line was placed, as well as an arterial line for continuous blood pressure monitoring.
Upon removal of the port, significant bleeding occurred where the previous catheter entered the venous system, at the junction of the subclavian and internal jugular veins. About 350 mL of blood was lost before hemostasis of the venotomy was achieved. The patient was rapidly transfused 120 mL of packed red blood cells (PRBCs). Vital signs remained normal throughout the procedure, however. Upon the completion of the procedure, he was transported back to the PICU and was extubated there without issues. The patient remained hemodynamically stable throughout the remainder of his stay in the PICU, and was discharged home 3 days after his procedure with instructions to continue intravenous vancomycin (following S. epidermidis susceptibility results) for 6 weeks. Another SARS-Co-V-2 PCR test was obtained 2 weeks after he was discharged, which resulted negative.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [13.9, 'kg']}",47.8,45.41,50.19,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 13.9 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.9 kg - 10 kg) = 47.8 mL/hr.
Hence, the patient's fluid maintenance is 47.8 mL/hr."
4923,22,Maintenance Fluids Calculations,physical,decimal,pmc-5235654-1,Extracted,"A 15-year-old adolescent male from Punjab, Pakistan presented to the gastroenterology clinic with nausea, vomiting, and diarrhea for a week. He vomited two to three times per day, often after a meal. The vomits were not bloody or bilious and contained only food particles. The diarrhea was semi-solid to watery without any mucus or blood. He had these episodes three to four times a day. There was no fever or any abdominal pain. On general physical examination, he had a swollen face, puffy eyes, and peripheral edema. There was pallor. His pulse was 80/minute, blood pressure 120/70 mm hg, respiratory rate 16/minute, he was afebrile and weighed 65 kg. An abdominal examination revealed distention and shifting dullness. There was no visceromegaly. The examinations of the respiratory, cardiovascular, and neurological systems were unremarkable.
His initial laboratory parameters are tabulated in Table .
An ultrasound scan of the abdomen revealed a coarse heterogeneous outline of the liver and moderate ascites. A urine examination revealed three plus proteinuria. He was referred to the nephrology clinic. A urine protein creatinine ratio (PCR) was performed, which estimated about 17 grams of proteinuria per 24 hours. The results are tabulated at various stages of patient treatment. The serum complement levels were within normal range.
Meanwhile, a workup for the chronic liver disease was sent. His markers for viral hepatitis was negative. The workup for autoimmune hepatitis was negative. Anti-nuclear antibody was also negative. The serum ceruloplasmin levels were 9 mg/dL (20-60 mg/dL). The 24-hour urine copper excretion revealed 272 micrograms of copper excreted per day (normally less than 60 micrograms/day). His ophthalmological examination was normal. On the basis of all these parameters, he was diagnosed as a case of Wilson’s disease by the consultant gastroenterologist. There was no history of this disease or related manifestations in the family.
He was started on tablet penicillamine 250 mg twice daily along with pyridoxine. Meanwhile, he was given a trial of oral prednisolone at 20 mg twice daily for a month and started on spironolactone at 50 mg/day, which was later increased to 100 mg/day. He was initiated on a salt restricted diet and started on atorvastatin 5 mg once daily. On the follow-up visit, he was found to have persistent proteinuria as tabulated. A renal biopsy was performed after informed consent was obtained. Light microscopy (LM) revealed focally increased mesangium and cellularity in the glomeruli (Figure ). Immunofluorescence (IF) showed 3+ fine granular deposits of IgM in the mesangium (Figure ).
The patient was then subjected to three doses of intravenous cyclophosphamide separated one month apart. The doses were 300 mg for the first and 400 mg each for the second and third cycle, respectively. Corticosteroids were continued at the same dosage along with atorvastatin at 5 mg daily.
The patient had regular follow-up visits in gastroenterology and nephrology clinics and he showed significant improvement after the third dose of intravenous (IV) cyclophosphamide. The urine PCR declined to 0.5 and the serum albumin rose to 3.8 g/dL. His edema resolved completely and he came off diuretic treatment. A year after these events he developed a relapse of the disease, which was treated successfully with corticosteroids and mycophenolate mofetil. Currently, he is on disease remission with no proteinuria or edema and enjoying good health.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [65.0, 'kg']}",105,99.75,110.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 65.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (65.0 kg - 20 kg) = 105.0 mL/hr.
Hence, the patient's fluid maintenance is 105.0 mL/hr."
4924,22,Maintenance Fluids Calculations,physical,decimal,pmc-6036857-1,Extracted,"A 47-year-old patient with an enormous uterine leiomyoma reaching beyond the navel and up to the costal arch was admitted. During the 14 years since its detection, because of the patient's extreme fear of an abdominal incision, the myoma was merely monitored and all suggested laparotomies thus far had been refused. At the moment of admission, the patient only agreed to a minimally invasive surgery. She was informed in detail about all risks, side effects, and alternatives as well as the potential risk for an emergency open abdominal surgery. Before surgery, we performed imaging diagnostics by means of computed tomography (CT) of the abdomen ().
When performing a hysterectomy of a very large uterus (>2500 g), the anatomical changes in the abdomen caused by the size of the uterus need to be taken into account. The large uterus divides the abdominal area, and only 3 narrow spaces are left to manipulate surgical instruments: between the left uterine wall and left abdominal wall, between the right uterine wall and right abdominal wall, and between the fundus uteri and liver and diaphragm. Successful surgery is only feasible when both instruments (forceps and coagulator or scissors) are in the same space simultaneously. Hence, we performed LASH with the “changeover technique” as described previously []. As such, we inserted 6 trocars including 3 on the left: one trocar in the lower, one in the middle, and one in the upper abdomen, allowing access to the left narrow space ().
The 3 trocars on the right side were placed in a mirror-like fashion. Surgery was initiated at the patient's left side, using the upper left trocar to introduce the camera () and the other two left-located trocars to introduce forceps and coagulator or scissors.
The patient was slightly tilted to the opposite side to facilitate visualization and preparation of structures. For uterus manipulation and movement, we used blunt forceps and palpation probes. After parameterization and resection of the uterine adnexa on the patient's left side, the plica vesicouterina was exposed and the bladder was pushed caudally.
Next, the surgeon and his team switched sides positioning to the right side of the patient, thus accessing the narrow space on the right side in between the right uterine wall and right abdominal wall (). Again, the patient was slightly tilted to the opposite side, enabling better exposure and preparation of organ structures.
The procedure continued analogically as on the left side. As was seen on the CT scan, multinodal, intraligamentary, and parametric myomas were found on the right side. Consequently, further exposure and protection of the ureter was done by visualizing followed by preparing or abscising the right adnexa, parametria, and blood vessels ().
The corpus uteri were removed from the abdominal cavity by power morcellation. The entire procedure lasted 4 hours and 53 minutes, of which surgery on the uterus took 2 hours and morcellation 2 hours and 53 minutes. No postoperative complications occurred, and the patient was taken to outpatient care 2 days after surgery. Before discharge, a vaginal and renal ultrasound did not reveal any conspicuous intra-abdominal findings. Because of the young age of our patient, a very slow growth of the leiomyoma (over 14 years), and negative Doppler test results before surgery, we assumed no presence of malignancy. Histological analysis of the removed specimen confirmed this assumption. Furthermore, to prevent morcellation-induced spreading of occult malignancy, the patient was alternately tilted from a head-down to head-up position, after which we extensively rinsed the abdominal cavity with Ringer's lactate solution, a routine postsurgical measure at our facility. The total weight of the uterus was 4065 g (Institute for Pathology PPO Berlin; Mona Tawfik, M.D.; 06.05.2014).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4065.0, 'g']}",16.26,15.447,17.073,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4065.0 g so this converts to 4065.0 lbs * kg/1000 g = 4.065 kg. Hence, the patient's maintenance fluid is 4.065 kg * 4 mL/kg/hr = 16.26 mL/hr.
Hence, the patient's fluid maintenance is 16.26 mL/hr."
4925,22,Maintenance Fluids Calculations,physical,decimal,pmc-5343247-1,Extracted,"A 27-year-old African American male with a history of morbid obesity status post-Roux-en-Y gastric bypass 9 years prior presented with painful nonbloody mucoid diarrhea, icterus, and dark urine of four-day duration. He described recent travel with family to a beach resort in the United States during which he noted that two family members had developed a self-limited diarrheal illness. Three days after exposure, he noted abdominal cramps followed by hourly watery yellow stools without blood. He also had intermittent nausea and an episode of bilious vomiting and reports not eating since onset of diarrheal illness. He noticed a 17-pound weight loss over 1 week. He had no fevers, chills, or rash. There was no preceding history of eating uncooked fish or meats and he had no tick exposure. Medication history included Lisinopril and Amlodipine, and he denied any new medications or alcohol use. He admitted to homosexual intercourse.
He was acutely ill-looking with icteric sclera and dry mucus membranes. Vitals signs showed low-grade fever of 100.2°F and pulse rate of 126 beats per minute. Cardiac, lung, and skin examinations were unremarkable. Abdomen was diffusely tender with hyperactive bowel sounds without peritoneal signs.
Laboratory data was remarkable for leukopenia of 2200/μL, hemoglobin of 12.7 g/dL, normal platelet of 158,000/μL, sodium of 128 meq/L and potassium of 3.2 meq/L, acute kidney injury with creatinine of 1.59 mg/dL (baseline of 0.63 mg/dL), BUN of 41 mg/dL, and anion gap of 19. After intravenous hydration, hemoglobin dropped to 10.1 g/dL and platelet to 96,000/μL. Sodium, BUN, and creatinine also improved with rehydration. He was also noted to have elevated transaminases AST 201 IU/L and ALT 73 IU/L, elevated total bilirubin of 8.2 mg/dL, direct bilirubin of 4.4 mg/dL, normal alkaline phosphatase of 66 IU/L, albumin of 3.2 g/dL, normal lipase of 40 U/L, and elevated lactate of 3.5 meq/L. INR was elevated to 1.8; however, he had normal haptoglobin 236 mg/dL (36–195 mg/dL) and LDH 177 IU/L (normal: 94–202 IU/L). Hepatitis panel was negative. Patient also tested negative for HIV, CMV, EBV, and Parvovirus B19 infection. Tylenol level was normal. Urinalysis showed moderate bilirubinuria. Stool study was positive for Shigella sonnei but was otherwise negative for bacteria, ova, or parasites. Rickettsia rickettsii IgM was positive and he was treated with Doxycycline. Other workup for tick-borne infection including Lyme, Babesia, Ehrlichia, and Anaplasma was negative. Autoimmune workups including ANA, antismooth muscle, liver/kidney microsome, and mitochondrial antibodies were negative. Alpha-1 antitrypsin and ceruloplasmin were also normal.
Abdominal ultrasound showed a diffusely increased heterogeneous liver echogenicity with underlying hepatomegaly consistent with hepatic steatosis. Hepatoportal duplex showed patent portal vein and hepatic artery. Computed tomography of the abdomen and pelvis was significant for hepatic steatosis, hepatomegaly, mild right colitis, and absence of gallstones. Magnetic resonance cholangiopancreatography (MRCP) was unremarkable with normal intra- and extrahepatic biliary tree.
During his hospital course, bilirubin trended up to 9 mg/dL and INR peaked at 2.9. Patient was not encephalopathic. Given impending hepatic failure, recommendation was made to transfer the patient to a transplant center but he declined. He was treated with N-acetylcysteine. Blood culture initially reported as Gram-negative rods presumptively Escherichia coli (E. coli) was later confirmed to be Shigella sonnei. Urine culture remained negative. He was treated with ciprofloxacin based on sensitivity results with an improvement in diarrhea frequency and downward trend in transaminases. He remained stable and was discharged home on Day 8. He was doing well 4 months later with normal cell counts, normal liver, and kidney function.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [17.0, 'lbs']}",30.84424,29.30203,32.38645,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 17.0 lbs so this converts to 17.0 lbs * 0.453592 kg/lbs = 7.71106 kg. Hence, the patient's maintenance fluid is 7.71106 kg * 4 mL/kg/hr = 30.84424 mL/hr.
Hence, the patient's fluid maintenance is 30.84424 mL/hr."
4926,22,Maintenance Fluids Calculations,physical,decimal,pmc-8417986-1,Extracted,"A 14-year-old white girl with unilateral anterior uveitis and abnormal urinalysis was referred from the ophthalmological care to our nephrology unit in November 2018. She had been seen at our out-patient clinic at the age of 12 years in 2016. Her family history was positive for elevated blood pressure. She was the first child of an uneventful pregnancy, born at 40 weeks gestation with a birth weight of 3990 g and birth length of 53 cm.
Upon visit, she was seen due to elevated blood pressure with occasional tension-type headaches, obesity, impaired glucose tolerance, and hyperlipidemia, which were a result of a sedentary lifestyle and unhealthy eating habits. She reported no first-degree family members with metabolic syndrome or its complications. Ambulatory blood pressure monitor values were within reference ranges (average 24-hour systolic and diastolic blood pressure 117 and 66 mmHg, respectively), so we implemented nonpharmacological lifestyle approaches. During follow-up, she received extensive evaluation, including endocrinological and dietary assessment, and was continued to be seen by our pediatric nephrologist twice per year.
In October 2018, aged 14 years, she presented to the Department of Ophthalmology with 1 week of redness, pain, epiphora, and loss of visual acuity of the right eye. She denied any recent drug exposure, allergy, infection, or symptoms of systemic illness. A diagnosis of acute anterior uveitis was made, followed by topical corticosteroid and cycloplegic treatment, which led to symptom alleviation.
A broad diagnostic work-up was performed. Renal ultrasound was normal. Also, chest radiography was also normal (Fig. ), which in conjunction with a normal serum angiotensin-converting enzyme level and absence of cough excluded sarcoidosis, a known oculorenal offender. However, upon laboratory evaluation, marked elevation in erythrocyte sedimentation rate (ESR, 98 mm/hour), mild elevation of serum C-reactive protein (CRP, 13 mg/L), mild normocytic anemia (Hb, 113 g/L), elevated serum creatinine (80 µmol/L), mild proteinuria (0.38 g/day), microalbuminuria (urine albumin-to-creatinine ratio, 58 mg/g), elevated values of alpha-1 microglobulin (urine alpha-1-microglobulin-to-creatinine ratio, 3.24 mg/g), and normoglycemic glycosuria (1+) were observed. Immunological screening revealed elevated C3 complement fraction (C3, 2.01 g/L), with negative antinuclear antibodies (ANA), anti-extractable nuclear antigen antibodies (ENA), anti-deoxyribonucleic acid antibodies (anti-DNA) and antineutrophil cytoplasmic antibodies (ANCA) antibodies. These values indicated mild renal involvement and prompted a referral to our nephrology unit.
Upon admission, she had no history of unexplained fevers, weight-loss, or other systemic symptoms. She had a pulse of 100 beats/minute, blood pressure of 126/81 mmHg, and body temperature of 36.5 °C. Her review of systems was negative, with a gradual improvement of symptoms and vision of the right eye. She continued both-sided topical cycloplegic and topical corticosteroid therapy. Borderline blood pressure values with repeated and persistent abnormal values of ESR, serum urea and creatinine, proteinuria, and glucosuria, indicating kidney injury, prompted a kidney biopsy.
Histopathology revealed focal tubulointerstitial nephritis. Interstitial inflammatory cell infiltrate was composed of lymphocytes, macrophages, fewer neutrophils, eosinophils, and plasma cells and rare noncaseating granulomata, with foci of invasion of lymphocytes into the tubules (tubulitis). Tubules in the affected areas showed signs of acute tubular injury—flattened, irregular, and vacuolated tubular epithelium. Glomeruli and vessels were unremarkable (Figs. , ). Immunofluorescence was negative. Electron microscopy showed no specific pathological findings. On the day of renal biopsy, 1 month after first symptom presentation, she also developed contralateral, left-sided anterior uveitis. A diagnosis of TINU syndrome was confirmed, based upon histopathological findings.
DNA typing of HLA loci showed the subtype HLA-B *07, *51; DRB1 *11, *13; DQA1 *05:05/05:09; DQB1 *03:01, negative for uveitis-related HLA-B27 genotype. Next-generation sequencing did not demonstrate any disease-related variants.
The patient was started on methylprednisolone 60 mg daily, which improved the laboratory markers of kidney injury and allowed us to continue an alternate-day corticosteroid therapy regimen. She also received pantoprazole 40 mg daily, trimetoprim–sulfametoxazole 480 mg twice daily every other day for Pneumocystis carinii pneumonia prevention, and vitamin D supplementation 2000 units daily, together with topical ocular therapy (scopolamine, nepafenac, dexamethasone). Because of elevated blood-pressure readings, she began therapy with ramipril 2.5 mg and later 5 mg daily and received regular follow-up.
After 3 months, upon evaluation at our out-patient clinic, her ocular symptoms improved, although she started having pain in her lumbar spine. Clinical examination showed a Cushingoid appearance with a 4 kg increase in body weight since discharge. Blood pressure values with antihypertensive therapy were normal. Lumbosacral spine X-ray imaging was normal, without signs of osteopenia (Fig. ). This allowed a slow reduction in corticosteroid therapy upon following weeks and motivated her for implementation of healthy lifestyle measures.
At the most recent ambulatory office visit, two and a half years after onset of TINU, the patient denied any further ocular exacerbations, but she gained weight and had a body mass index of almost 35 kg/m2. Her 24-hour ambulatory blood pressure values were normal, as well as renal ultrasound examination, without presence of renal scarring. She was receiving ramipril 2.5 mg and metformin 500 mg twice daily each, together with education on necessary lifestyle changes.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [35.0, 'kg']}",75,71.25,78.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 35.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (35.0 kg - 20 kg) = 75.0 mL/hr.
Hence, the patient's fluid maintenance is 75.0 mL/hr."
4927,22,Maintenance Fluids Calculations,physical,decimal,pmc-5410879-1,Extracted,"In June 2014, a 50-year-old man was brought to the emergency room with pain abdomen, high-grade fever with chills, generalized malaise, night sweats and significant weight loss (>10 kg in 45 days). The patient is a milk vendor by occupation in rural Bangalore and routinely consumes unpasteurized or raw milk due to a belief that raw milk is healthier. The patient is an ex-smoker and alcoholic with consuming about 20 g (whiskey) per day from 10 years. Patient's medical records and history from relatives revealed fever with night sweats and pain abdomen from 2 months for which he was evaluated as fever of unknown origin. The patient denied any recent travel or contact with persons having a similar illness.
His physical examination during admission was remarkable for fever (40°C), hypotension (BP: 86/60 mmHg), and increased respiratory (30 min–1) and heart (120 min–1) rates. He was severely dehydrated and pale, but no scleral icterus, clubbing, cyanosis, edema or lymphadenopathy was noted. Systemic examination of the abdomen showed tenderness in the left hypochondriac region. The liver was nontender with normal span. The spleen was not palpable but castell's sign was elicited (dullness noted in lower eighth intercostal space on inspiration). Cardiovascular and respiratory system examination was normal. Nervous system examination was normal.
Investigations revealed total white blood cell count of 32 100 mm–3 (neutrophils 64%, lymphocytes 30%, eosinophils 3% and monocytes 3%), ESR of 100 mm/h, C-reactive protein of 92 mg/l, hemoglobin of 10 mg/dl and platelet count was 199 000 μm–1. The arterial blood gasses had pH of 7.36, a PO2 of 68 mmHg, PCO2 of 35.5 mmHg and 17.9 mmol/l of bicarbonate. Renal function test was abnormal with creatinine of 2.0 mg/dl and blood urea of 70 mg/dl. Liver function test was normal. Electrocardiogram showed tachycardia and nonspecific ST–T changes in leads 2 and aVF. Echocardiography was normal with the ejection fraction of 60% and no features of endocarditis were found.
Brucella slide and tube agglutination tests (Wright, at 1/640) were positive. Ultrasound abdomen and computerized tomography of the abdomen showed splenomegaly and well-demarcated hypodense lesion, which is nonenhancing and measuring 3.2 × 2.8 × 2.8 cm in the upper pole of spleen with perisplenic fat stranding. Blood cultures confirmed infection by Brucella melitensis on Day 1 and Day 3. Chest radiograph showed bilateral pleural effusion with basal atelectasis. Upper gastrointestinal (GI) endoscopy was normal. The patient was treated with percutaneous drainage along with oral doxycycline (200 mg/day) and rifampin (600 mg/day) for 6 weeks.
The patient improved symptomatically over a period of 10 days with the absence of fever and reduction of pain abdomen. The patient was discharged on Day 10 with advice for review ultrasound abdomen examinations. The patient remained asymptomatic without recurrence at 6 months after completion of treatment. Repeat ultrasound abdomen showed mild splenomegaly without any other abnormalities.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.0, 'kg']}",40,38,42,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.0 kg - 10 kg) = 40.0 mL/hr.
Hence, the patient's fluid maintenance is 40.0 mL/hr."
4928,22,Maintenance Fluids Calculations,physical,decimal,pmc-4337035-1,Extracted,"A 13-year-old girl with no past medical history, complained for 2 years of chronic diarrhea with no other clinical signs, and this has necessitated several visits to pediatricians without improvement under symptomatic treatment. Due to the persistence of diarrhea associated with growth retardation (weight and height were at minus 2 standard deviations (SD)) with a bone age corresponding to 10 years; celiac disease was suspected; antitransglutaminase and antiendomysium antibodies were negative; jejunal biopsy with histological study was read as villous atrophy II. The patient was put on gluten-free diet for 6 months without improvement. The evolution was marked by the persistence of diarrhea and the appearance of an intermittent fever, ranging between 37.8 and 38.5°C, asthenia, anorexia, weight loss, night sweats, and a deterioration of the general state. Second gastric and duodenal biopsies with histological study were read to show a nonspecific chronic interstitial duodenitis. The search of Koch's bacillus in sputum and tuberculin skin test was negative. Six months later, the patient developed insidiously growing abdominal mass; lymphoma was suspected, so she was transferred to our department for evaluation.
Clinical examination at admission revealed a febrile patient at 38.5°C, in poor physical condition, pale, and with a growth retardation; her body weight was 24 Kg (minus 3 SD); and the body height was 138 cm (minus 3 SD). Abdominal palpation revealed a hepatomegaly (4 cm below the costal margin), a splenomegaly (2 fingerbreadth from the flange left costal), and a painless paraumbilical mass which was slightly mobile, measuring about 6 cm of diameter. The rest of the physical examination demonstrated lenticular inguinal and cervical lymph nodes. Abdominal ultrasound followed by thoracoabdominal-pelvic computed tomography revealed a hepatosplenomegaly, a multiple mesenteric lymph nodes (the largest measures 19 mm in diameter), and a soft tissue mass roughly rounded shape, well limited, enhanced moderately and homogeneously by the product of contrast and measuring 40 × 65 × 56 mm in diameter. This mass has an intimate contact with the gallbladder without signs of invasion, and a contact with the antropyloric region of the stomach, with a significant infiltration of the surrounding fat (). The chest X-ray was normal. The biological investigations revealed microcytic hypochromic anemia (hemoglobin = 7 g/dL) (normal range 10.5–13.5 g/dL), thrombocytosis (platelet count = 489,000/mm3) (normal range 150000–450000/mm3), and elevated inflammatory markers: erythrocytes sedimentation rate (ESR) = 145 mm in the first hour (normal range < 16 mm), c-reactive protein = 252 mg/L (normal range 0–6 mg/L), fibrinogen = 7.1 g/L (normal range 2–4 g/L), ferritin = 527.9 µg/L (normal range 20–250 µg/L), serum iron = 0.10 mg/L (normal range 0.6–1.9 mg/L), hypoalbuminemia (22 g/L) (normal range 33–50 g/L), an increase of alpha 1 globulin (5.6 g/L) (normal range 1.2–4 g/L), alpha 2 globulin (14.4 g/L) (normal range 4–8 g/L), beta 2 globulin (6.7 g/L) (normal range 1–4 g/L), and hypergammaglobulinemia (37.5 g/L) (normal range 6–12 g/L). The insulin-like growth factor (IGF1) was low (26.5 ng/mL) (normal range 220–972 ng/mL) without abnormal secretion of growth hormone in the insulin stimulation test. The hepatic transaminases and lactate dehydrogenase were normal. The bacteriological, viral (Epstein Barr virus, cytomegalovirus, human immunodeficiency virus, hepatitis B and hepatitis C, and human herpes virus 8 (HHV8)), and parasite evaluation were negative. Immune and thyroid function tests were normal.
A scan-guided biopsy of the abdominal mass was performed. Microscopic examination revealed normal lymph node tissue architecture, with hyperplastic lymphoid follicles made of elements of variable size; in some areas they look like an onion bulb. In the interfollicular areas, a marked proliferation of plasma cells was identified. An immune-staining by the anti-CD20 and anti-CD3 shows a normal distribution of the lymphoid population. The anti-CD138 antibody shows a wealth of interfollicular tissue into mature plasma cells. These findings were compatible with the plasma cell form of CD. Because of the rarity of this disease, a study of the biopsy by another pathologist confirmed this result. The myelogram performed during general anesthesia was normal.
The patient received oral corticosteroid (prednisone) for a one month with a minimal response (20% the reduction of the size of the mass); thus she received chemotherapy based on 2 courses of VAMP (vinblastine, doxorubicin, methotrexate, and prednisone) that allowed a 62% reduction in the size of the mass, permitted to perform a total tumorectomy. The outcome was favorable with the disappearance of fever, night sweats, diarrhea, hepatosplenomegaly, and normalization of inflammatory markers. Currently we are at 26-month follow-up; the child is asymptomatic, starting to catch up the height and weight growth (minus 1.5 SD).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [24.0, 'kg']}",64,60.8,67.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 24.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (24.0 kg - 20 kg) = 64.0 mL/hr.
Hence, the patient's fluid maintenance is 64.0 mL/hr."
4929,22,Maintenance Fluids Calculations,physical,decimal,pmc-6682344-1,Extracted,"A 50-year-old female presented to our hospital with generalized abdominal pain. The pain had been intermittent and was occurring spontaneously, every two to three weeks, for the last year. Her current episode spanned over 15 days and had gradually been increasing in intensity. The pain radiated to the back and was associated with three episodes of non-projectile, non-bilious vomiting. The pain had no association with meals. The review of systems revealed undocumented weight loss and reduced appetite. She had a history of Grade 3 ductal carcinoma of the left breast, treated with mastectomy and chemoradiotherapy 10 years previously. She had also undergone a laparoscopic cholecystectomy 15 years ago. Family history was not significant for any illness. At the time of presentation, she was being treated for Helicobacter pylori gastritis with triple therapy. There was no history of smoking, drug, or alcohol use.
At the time of presentation to the emergency room (ER), the patient was in severe pain. The patient was of short stature and lean, and was visibly distressed. At the time of presentation to the ER, she was hypotensive with a systolic blood pressure (SBP) ranging from 64 to 81 mm Hg and a diastolic blood pressure (DBP) of 30-40 mm Hg and tachycardic (Pulse = 131-150 bpm). She was afebrile. General physical examination revealed pallor and dehydration of conjunctival and oral mucosae. On abdominal examination, there was generalized tenderness but no guarding. Gut sounds were audible. The remaining physical examination was unremarkable. Resuscitation with intravenous fluids was initiated. A central venous catheter was placed to monitor fluid status and for the administration of norepinephrine. Tramadol was given to manage the pain and heparin sodium subcutaneously for deep venous thrombosis (DVT) prophylaxis.
Laboratory investigations revealed anemia (hemoglobin 8.9 gm/dl) and renal dysfunction (creatinine 2.2 mg/dl). Arterial blood gas suggested metabolic acidosis with respiratory compensation. The calculated serum osmolarity was 288 mOsm/kg and anion gap (corrected for albumin) was 26 (Table ).
Following volume resuscitation, she underwent a contrast-enhanced CT scan that showed significantly distorted bowel anatomy with abnormally dilated enhancing proximal and mid-jejunal loops. The presence of a midgut volvulus, affirmed by the presence of the whirlpool sign was noted (Figure ). No congenital malrotation could be identified. The superior mesenteric artery was significantly attenuated representing occlusion, and there was non-enhancement of distal jejunal and ileal loops. These findings suggested mesenteric ischemia. There was no evidence of pneumatosis intestinalis or pneumoperitoneum. The liver was unremarkable.
Following successful resuscitation, an emergency laparotomy was performed. No underlying anatomic abnormality that could direct us towards the cause of the volvulus could be identified. Therefore, a presumptive diagnosis of primary midgut volvulus was made. Approximately 250 cm of gangrenous distal jejunum, ileum and cecum were resected (Figure ). Seventy-five centimeters of duodenojejunum remained but had questionable viability in some areas. The abdomen was irrigated with three liters of fluid. The two stapled ends were left in place without an anastomosis. The fascia was not closed and the skin was approximated using towel clips.
The patient was shifted to the intensive care unit (ICU) and extubated. During the next 48 hours, she remained hemodynamically stable off vasopressors. She was afebrile, required minimal supplemental oxygen, and produced adequate urine. Anticoagulation was maintained via heparin sodium infusion.
She underwent a re-look laparotomy 48 hours later. Approximately 100 cc of thin murky fluid was found in the peritoneal cavity. The residual small bowel was viable with pulsatile mesenteric vessels throughout the remaining mesentery. There were no areas of necrosis identified. A side to side functional end to end stapled anastomosis was created between the mid jejunum and ascending colon. The fascia was closed and the skin left open.
She was again shifted to the ICU, and extubated a day later. Total parenteral nutrition (TPN) was initiated. The surgical wound was open and daily dressings were done. She was transferred to a special care unit (SCU) on day 5 of admission where she remained for a day before being shifted to the ward (day 6). She maintained adequate urine output and had multiple bowel movements every day from the sixth day of admission.
A complete nutritional assessment for this patient was done. She weighed 40 kg with a height of 155 cm, BMI of 18 kg/m2, and an ideal body weight of 48 kg. To meet her nutritional requirements, it was determined that she needed 1400-1800 kcal/day (35-45 kcal/kg/day). This was further split into 80 gm of protein, 175 gm of carbohydrates and 42 gm of fat. She was kept nil per oral (NPO) till the 2nd post-operative day, following the re-look procedure. During this time, she was kept on a TPN formula consisting of 10 gm of nitrogen, 200 gm of dextrose and 20 gm of fat, with a caloric value of 1130 kcal. Her TPN formula was subsequently adjusted to include 12 gm of nitrogen, 20 gm of fat, 260 gm of dextrose, 10 ml of multivitamin and 5 ml zinc sulfate, amounting to 1384 kcal. She was started on a soft diet on the 3rd post-operative day along with the new TPN formula. She was then progressed to a regular diet along with TPN. On the 6th post-operative day, TPN was discontinued and oral intake was supplemented with full-strength Ensure, at 200 ml twice a day. She was discharged on the 9th post-operative day on a regular diet, along with Ensure.
On her first visit to the outpatient clinic four days post-discharge, her weight was 35 kg and she was documented to have had multiple bowel movements (an average of four per day) at home. On subsequent monthly visits that continued for the next eight months, her weight remained fairly stable, going up to 36 kg; and she was found to be tolerating her diet well. She had no active complaints during these visits and her physical examination revealed adequate granulation tissue developing at the wound site.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [35.0, 'kg']}",75,71.25,78.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 35.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (35.0 kg - 20 kg) = 75.0 mL/hr.
Hence, the patient's fluid maintenance is 75.0 mL/hr."
4930,22,Maintenance Fluids Calculations,physical,decimal,pmc-7869126-1,Extracted,"A 1-year-old male child presented to the outpatient department with complaints of bluish discoloration of the body and fast breathing for last 1 month. Bluish discoloration was sudden in onset involving nail beds and lips. It was associated with fast breathing which was sudden in onset, progressive and increased during evening. On examination, he presented severe dyspnea with nasal flaring, subcostal and intercostal indrawing and retraction of sternal notch. He was cyanosed and afebrile. His heart rate was 110 bpm and respiratory rate 45 bpm. Blood pressure was recorded at 85/35 mm Hg and oxygen saturation 70% in room air. All peripheral pulses were palpable. Cardiac examination revealed normal first and second heart sounds and a systolic murmur at the left upper parasternal area. The child was managed with prostaglandin infusion which mildly improved his condition. The child had normal term vaginal delivery with birth weight of 2.6 kgs. He cried immediately after birth. The pregnancy was uneventful. No family history of congenital heart disease was present.
The initial transthoracic echocardiographic assessment revealed: criss-cross heart with discordant atrioventricular connections, double outlet right ventricle, large ventricular septal defect, and subvalvular pulmonary stenosis.
CT was done on 128 slice Dual Energy CT scanner (SOMATOM Definition Flash; Siemens, Erlangen, Germany). CT data were obtained with the following parameters: 3 mm slice thickness, 3 mm increment, 0.28 s rotation time, 0.38 pitch and reconstructed images of 0.6 mm slice thickness and 0.6 mm increment. A low effective radiation dose of 0.2 milli Sieverts was given to the patient. A volume of 2 ml kg−1 bodyweight of non-ionic iodinated contrast agent was administered through IV cannula at a rate of 2 ml s−1 via a power injector. Care bolus tracking technique was employed with the region of interest placed within the descending thoracic aorta, at the level of the carina and scan threshold set at 100 Hounsefield units (HU). Contrast saline solution of 50% dilution was utilized in bolus chasing technique to improve contrast within the cardiac chambers. ECG synchronized retrospective gating technique was employed for cardiovascular evaluation.
Cardiac CT revealed atria in solitus position with morphological right atrium on right side and morphologic left atrium on left side (). Dextro-loop topology was noted with morphological right ventricle to the right of morphological left ventricle (). Left atrium and right atrium were noted in supero-inferior relationship, respectively (). Crossing axes of atrioventricular connections and atrioventricular discordance showing the right atrium draining into morphological left ventricle and left atrium draining into morphological right ventricle were seen (). Both aorta and main pulmonary artery were noted arising from right ventricle s/o double outlet right ventricle (). Aortic was located anterior and slightly to the right of main pulmonary artery s/o dextro-malposed great arteries (). Significant subvalvular pulmonary stenosis was noted. Aortopulmonary collaterals were noted (). These were seen arising from right subclavian artery and descending thoracic aorta. Large inlet ventricular septal defect with extension into outlet beneath pulmonary valve was noted. Double superior vena cava was present. Left superior vena cava drained into right atrium through coronary sinus. The above described case represented atrial situs solitus, criss-cross-atrioventricular connections with atrioventricular discordance, double outlet right ventricle, dextro-malposed great arteries, ventricular septal defect and subvalvular pulmonary stenosis. Fontan procedure was performed. The definitive repair included closure of ventricular septal defect, ligation of the proximal pulmonary trunk and a conduit was placed between the left ventricle and the distal pulmonary trunk. Post-operative period was uneventful. The patient’s condition was satisfactory at discharge.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.6, 'kg']}",10.4,9.88,10.92,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.6 kg. Hence, the patient's maintenance fluid is 2.6 kg * 4 mL/kg/hr = 10.4 mL/hr.
Hence, the patient's fluid maintenance is 10.4 mL/hr."
4931,22,Maintenance Fluids Calculations,physical,decimal,pmc-4822278-6,Extracted,"Patient 6 is a 39-year-old woman, born to non-consanguineous parents. Normal vaginal delivery took place at full term. Birth measurements were in the normal range. Her parents, sister and brother were unaffected, similar to her first son. Her second son was affected (see patient 7). Congenital club feet were treated with tenotomy of Achilles tendon. Bilateral hip dislocation was treated with several orthopedic surgeries. In early childhood, she could walk with braces. She still had club feet deformity. At the age of 29, she became wheelchair-dependent due to hip dislocation and club feet.
At the age of 39 years, physical examination revealed height of 145 cm (−3.5 SD), OFC of 57 cm (−1.8 SD), and weight of 85 kg (+1.8 SD). She had prominent forehead, depressed nasal bridge, long philtrum, and telecanthus (Fig. ). She had bilateral dislocated elbows (Fig. ) and cylindrical fingers with short and broad fingertips and spatulate thumbs (Fig. ). She had bilateral fixed clubfeet deformities with partial syndactyly of toes 2/3 on the right (Fig. ). Wrist joints were normal and there was no pectus deformity. Teeth and nails were normal. Hearing was normal. Numbness of the upper extremities was suggestive of compressive myelopathy. Radiographs confirmed bilateral dislocated elbows (Fig. ), hip dislocation with ossified right hip joint (Fig. ), and deformities of cervical vertebral bodies (Fig. ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [85.0, 'kg']}",125,118.75,131.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 85.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (85.0 kg - 20 kg) = 125.0 mL/hr.
Hence, the patient's fluid maintenance is 125.0 mL/hr."
4932,22,Maintenance Fluids Calculations,physical,decimal,pmc-4607000-1,Extracted,"A 14-year-old girl was consulted for psychiatric assessment at the department of paediatric ward of JUTH. She was assessed for a cluster of symptoms including intractable vomiting, inability to eat and walk, and significant loss of weight with emaciation.
Greatly concerned, her father had taken her to the nearby hospital, a health care facility three hundred kilometres from Jimma town. From there, she was referred to Addis Ababa, which is approximately 650 kilometres from her home. She was then taken to various prestigious public and private health care institutions, where she was examined for a number of possible medical complaints by methods including CT scans and MRI examination of the spinal cord. All results were normal. The family incurred huge expenses from these tests, and yet her condition remained unexplained, and she did not receive the necessary help. In desperation, and losing hope, her father took her back to the first hospital, and from there, she was referred to JUTH. At JUTH, she was first contacted and admitted to the paediatric ward, from which she was finally transferred to the psychiatry clinic through a consultation process.
The examining clinician noted sunken eyeballs, generalised body weakness, and significantly decreased overall muscular mass. Slight abdominal tenderness was detected during physical examination and vital signs were within normal range. With support, she was able to sit and stand upright, but was not able to take a single step, or stand for long. At admission, her weight was 22 kg, her height 132 cm, and body mass index 12.6, which was below the 3rd percentile []. Consequently, a nasogastric tube was inserted for feeding and treatment for suspected Peptic Ulcer Disease commenced. It was observed that she was able to move her legs to some degree whenever she was distracted. After 2 weeks of thorough investigation, including neurological examination, there were no findings suggestive of any medically explained illnesses, and as she appeared severely mentally disturbed, she was transferred to the psychiatric ward. The referral diagnosis was suspected as early onset schizophrenia, and the differential diagnosis was conversion disorder.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [22.0, 'kg']}",62,58.9,65.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 22.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (22.0 kg - 20 kg) = 62.0 mL/hr.
Hence, the patient's fluid maintenance is 62.0 mL/hr."
4933,22,Maintenance Fluids Calculations,physical,decimal,pmc-3412705-1,Extracted,"A 61-year-old male presented with chronic cough and breathlessness. Chest CT revealed a well enhanced giant mass, approximately 18 cm in diameter in the right thoracic cavity (Figure ). FDG-PET showed that the SUVmax of the tumor was 5.0 in the center and almost 2.5 in the surrounding areas (Figure ). A trans-bronchial biopsy was performed and atypical cells were detected from the giant tumor. An intrathoracic malignant tumor was suspected, therefore surgical resection was performed. The CT findings suggested that the mass had not invaded surrounding organs, but had some adhesion to the right lung and superior vena cava. Surgical access to the mass was accomplished through a median sternotomy with a 4th intercostal thoracotomy of the right chest wall. A well-defined giant mass measuring 18 × 14.5 × 11 cm was found in the right thoracic cavity. The feeding vessels of the tumor were branching from internal thoracic vessels and collateral blood vessels were extensive surrounding the giant tumor. The tumor was completely resected without combined resection of the other organs. The weight of the tumor was 1350 g. The cut surface of tumor revealed a light brown color, an internal lobulated structure with a portion of capsulation invasion (Figure ). A microscopic examination showed the tumor to contain spindle shaped cells with a lymphocyte rich component (Figure ). Immunohistochemistry showed predominantly lymphocytes expressing CD1a, TdT and CD5. The spindle cells of the tumor were all negative for EMA, cytokeratin, CAM5.2,αSMA, S100, CD5, TTF-1 and CD34. These histopathological findings indicated that the tumor was a type AB thymoma according to the World Health Organization classification and Masaoka stage IIB. The postoperative course was uneventful, and there has been no evidence of recurrence 6 months after the surgery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1350.0, 'g']}",5.4,5.13,5.67,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1350.0 g so this converts to 1350.0 lbs * kg/1000 g = 1.35 kg. Hence, the patient's maintenance fluid is 1.35 kg * 4 mL/kg/hr = 5.4 mL/hr.
Hence, the patient's fluid maintenance is 5.4 mL/hr."
4934,22,Maintenance Fluids Calculations,physical,decimal,pmc-8077912-1,Extracted,"A 53-year-old man with normal height (175 cm) and overweight (102 kg, body mass index = 33.3 kg/cm2) initially presented with low back pain and bilateral legs pain for 4 years and bilateral lower limps numbness for 2 years.
Four years ago, this patient gradually developed low back pain, radiating to hip and lateral side of both legs. The pain worsened after long time standing, walking and working and relieved when bending and crouching. Numerical rating scale (NRS, an 11-point scale where 0 = no pain and 10 = the worst pain) scored 4. The patient tried some unknown painkillers but they did not work. The intermittent pain lasted for years until 2 years ago when he started to have numbness of both lower limps, ranging from both sides of calfs to the dorsum of feet. Intermittent claudication occurs within 500 m’ walking. No cauda equina syndrome (CES) appeared. It should be noticed that this man gained 55 kg in weight during the past 20 years. Relevant history included hypertension for 10 years, smoking for 30 years and drinking for 30 years. In recent two weeks there was a fluctuation of blood sugar but no formal monitoring record was available. This patient had never received steroids medications.
A full endocrinologic workup was conducted in patient to rule out underlying endocrine abnormalities and type 2 diabetes mellitus was diagnosed. On physical exam, the patient showed 5/5 strength, normal muscle tone and intact superficial sensation in the upper and lower extremities bilaterally. Tendon reflexes of the right knee was absent and several myelopathic signs were recorded as follows: Chaddock sign ( +) on the left, Oppenheim sign ( +) on the left and Babinski sign suspected ( +) on both sides. CT scan indicated typical signs of LSS: intervertebral foraminal stenosis, ligamentum flavum hypertrophy, disc paracentral herniation and spinal stenosis from L2 to L5 (Fig. ), and MRI showed epidural abnormal fat deposition in the spinal canal from L2–L5 (Fig. ). According to a previous study of Borre et al., SEL could be graded on basis of the degree of epidural adipose tissue occupying the spinal canal (extradural fat [EF]-to spinal canal [SC] ratio); grade I, 41–50% of the canal; grade II, 51–74% of the canal; and grade III, > 75% of the canal []. This patient’s imaging revealed grade II (60% EF/SC ratio) lumbar epidural lipomatosis (Fig. d).
Based on the patient’s symptoms, history, physical examination and radiological imaging, a primary diagnosis of LSS and obesity-induced idiopathic SEL from L2–L5 was proposed. The compression of the cauda equina came from anterior protruding lumbar disc and posterior adipose tissue and ligamentum flavum, and pressure on nerve root is caused by intervertebral foraminal bony stenosis. Since refractory radiculopathic symptoms had appeared, indication of surgery was clear. Mimimally invasive surgery like endoscopic technique was insufficient to relieve bony stenosis, so extensive decompression was necessary. Internal fixation and bone graft fusion were adopted to maintain the stability of responsible vertebrae. Although the modified articular fusion had never been reported in such a rare disease, it was performed successfully in a large amount of obese patients with lumbar degenerative disease only. This was our first application of this modified surgical style on obesity SEL.
After a preoperative use of prophylactic antibiotics (cefuroxime 1.5 g, intravenous), the operation was performed under general anesthesia and in a prone position. Following careful stripping of the paraspinal muscles, spinous process, bilateral articular processes and roots of transverse processes were exposed. Afterwards, titanium polyaxial pedicle screws (6.5 mm in diameter, 50 mm long, Legacy, Medtronic, USA) were inserted bipedicularly from the L2 to L5 vertebrae. We chose used F4 reverse thread screws providing a tightening power in horizontal direction and minimizes the possibility of pulling out. This is quite important for such a patient with hight body weight. Then, pre-bended titanium rods were implanted and intraoperative fluoroscopy confirmed satisfactory position and length of screws. The resection range included spinous processes (L3, L4 and small portion of L2 and L5), 2/3 of the inferior L2 lamina, L3 and L4 lamina and 1/5 of upper L5 lamina, as well as the corresponding supraspinous ligament, interspinous ligament, ligamentum flavum and joint capsule. Then hyperplastic medial portion of facet joints, atrophic ligamentum flavum, stenosis of lumbar lateral recess and accumulation of epidural adipose tissue contributing to dural sac compression was visible (Fig. a). Decompression range of L2–L3 included medial 2/3 of the L2 bilateral inferior articular process, 1/3 of the medial side of bilateral superior articular processes of L5 and hyperplastic medial portion of L3 superior articular processes. Medial 2/3 of the bilateral L2 inferior articular process and 1/3 of the medial side of bilateral superior articular processes of L3 was carried out with a chisel and the lateral 2/3 portion was preserved for bone grafting. Management of L3–L4 and L4–L5 was the same as the above description. Following the decompression was resection of epidural adipose tissue with bipolar cautery (Fig. b).
Subsequently, inspection verified an adequate relaxation of nerve root and full decompression of dural sac. Removed tissue (Fig. c) had the appearance of normal adipose tissue. A round head grinding drill was then used to prepare the inter-articular space as grafting bed for autograft and allograft cancellous bone. After that, the surgery field was rinsed with saline before bone graft was pressed into the inter-articular space. Finally, a drainage tube was put in place and the wound was closed up. Intraoperative hemorrhage was 586 mL.
The patient showed full muscle strength and sensation once regained consciousness. Preoperative symptoms relieved obviously during the following days, and NRS scored 1. We removed the drainage tube and encouraged the patient to stand and walk on the third day after operation. Radiographs of lumbar spine were taken to verify the good location of screws and rods (Fig. ), and MRI confirmed complete decompression and elimination of excessive fat tissue (Fig. ). The patient was permitted to discharge with referral for outpatient rehabilitation. We also mobilized this patient to lose weight.
By now the man has come back for follow-up regularly and his low back and radiating leg pain has completely resolved, and NRS scored 0. X-Ray, CT and MRI at different follow-up time points showed persistent stability and graft and satisfactory fusion rate, and no evidence of reoccurred SEL was detected (Figs. and ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [102.0, 'kg']}",142,134.9,149.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 102.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (102.0 kg - 20 kg) = 142.0 mL/hr.
Hence, the patient's fluid maintenance is 142.0 mL/hr."
4935,22,Maintenance Fluids Calculations,physical,decimal,pmc-2992660-1,Extracted,"A 3-day-old female child, (full-term, normal delivery) weighing 2.75 kg at birth with stable vitals, moderate abdominal distension and history of not being able to pass meconium was referred to us. Examination showed normal anal opening but red rubber catheter could not be passed beyond 3 cm of anal verge. Spine and external genitalia were normal. X-ray (invertogram with red rubber catheter passed through anal opening) showed catheter abutting the air column in the bowel) [].
With anal retractors anal canal was opened but upper-end of membrane could not be seen.
An endoscopy was done with a 7.5F cystoscope. About 3 cm from the anal verge, the anal canal ended blindly and a membrane was visualized at the blind end. We incised the outer mucosal membrane, i.e. of the distal pouch with a bugbee, but the vision was lost due to technical reasons. Then anal retractors were used, and after the incision on the mucosa of the distal pouch, the inner mucosal membrane was seen bulging significantly due to meconium within it [].
Transanal membranotomy was done. Postoperatively, on day one, dye study was done and feeds were started. Patient was discharged on day 4.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.75, 'kg']}",11,10.45,11.55,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.75 kg. Hence, the patient's maintenance fluid is 2.75 kg * 4 mL/kg/hr = 11.0 mL/hr.
Hence, the patient's fluid maintenance is 11.0 mL/hr."
4936,22,Maintenance Fluids Calculations,physical,decimal,pmc-3236149-1,Extracted,"A 23-year-old previously healthy Caucasian woman, G2P0A1, presented at 36 weeks gestation to the emergency department (ED) after sudden onset of dyspnea, nausea, and vomiting for 5 minutes, then collapse and unresponsiveness. Her pregnancy had been complicated by pregnancy-induced hypertension treated with labetalol 400 mg 3 times daily. She had no other medical, surgical, or drug-use history. On arrival, she was agitated, altered, uncooperative, and moving all extremities. Her heart rate was 151 beats per minute, blood pressure 118/78 mmHg, respiratory rate 32 breaths per minute, with SpO2 86% on a nonrebreather mask. The patient did not appear Marfanoid or dysmorphic, with a height of 5′7″ and weight 147 lbs. On physical exam, the patient had perioral cyanosis, tachycardia with distant heart sounds, no edema, and gravid abdomen.
The patient immediately underwent rapid sequence orotracheal intubation and was mechanically ventilated. Her initial hemoglobin (HemoCue) was 12.5 g/dL. The patient quickly became pulseless with pulseless electrical activity (PEA). Chest compressions were initiated. A bedside ultrasound examination showed a large clot inside the pericardium, pericardial fluid, and empty, poorly contracting ventricles. A pericardiocentesis was performed with 5 mL of blood aspirated. A thoracotomy was immediately performed by the ED physicians. The obstetrical team concurrently performed an emergent perimortem cesarean delivery. A baby boy was delivered, intubated, and transferred to the Neonatal Intensive Care Unit.
The thoracotomy had findings of blood in the pericardial sac and a boggy, fibrillating heart with no evidence of active bleeding or cardiac injury. Cardiac massage was initiated resulting in palpable carotid pulses. This was followed by intracardiac epinephrine injection, internal defibrillation, and intravenous bicarbonate infusion.
At this time, the cardiothoracic surgical team arrived. On further exploration of the chest cavity, the source of bleeding could not be isolated. The cardiothoracic surgeons then inserted a thoracostomy tube into the right chest, which drained 100 mL of serous fluid. The patient continued to decompensate and was pronounced dead 1 hour after her initial presentation to the ED.
On autopsy, the patient was found to have a 0.5-cm tear in the aortic adventitial tissue and a 3-cm ragged tear in the posterolateral aorta superior to the aortic valve and extending 3 cm vertically. The tear was not consistent with chest compressions performed during cardiopulmonary resuscitation. The heart had severe left ventricle hypertrophy and weighed 450 gm, which was much larger than the expected 250 gm.
The baby boy was discharged a month later to the care of his father.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [147.0, 'lbs']}",106.67802,101.34412,112.01192,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 147.0 lbs so this converts to 147.0 lbs * 0.453592 kg/lbs = 66.67802 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (66.67802 kg - 20 kg) = 106.67802 mL/hr.
Hence, the patient's fluid maintenance is 106.67802 mL/hr."
4937,22,Maintenance Fluids Calculations,physical,decimal,pmc-7927550-2,Extracted,"A 10 years old girl presented in the emergency department with a history respiratory distress since the last few days and polyuria, polydipsia and nocturia for 2 weeks. Recent medical history revealed fatigue with onset since at least one month, and a weight loss of 4 kg in the last 2 months. Moreover, the child was treated with topic antimycotic agent for genital candidiasis with poor response one month before the admission.
On examination, she presented with polypnea and dyspnea due to Kussmaul’s breathing and severe dehydration (skin pallor, sunken eyes, dry mucous membrane, cold extremities, capillary refill time about 3 seconds). Her heart rate was 111 ppm, her blood pressure 123/79 mmHg.
Laboratory findings on admission are summarized in consistent with a diagnosis of moderate diabetic ketoacidosis (DKA).
Intravenous fluids, insulin and potassium replacement were started according to the local protocol for the management of DKA ().
DKA correction was achieved within 12 hours after treatment was commenced and she was the started on insulin subcutaneous treatment with a basal-bolus regimen.
Patient and caregiver had nasopharyngeal and oropharyngeal swab sampling, testing SARS-CoV-2 nucleic acid using reverse-transcriptase quantitative PCR assay, and resulted negative. Positive anti-GAD65 and anti-IA2 antibodies confirmed the diagnosis of type 1 diabetes.
Parents admitted that the danger and fear of contracting SARS-CoV-2 pandemic outbreak was responsible for the delay in the access to medical services.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.0, 'kg']}",16,15.2,16.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.0 kg. Hence, the patient's maintenance fluid is 4.0 kg * 4 mL/kg/hr = 16.0 mL/hr.
Hence, the patient's fluid maintenance is 16.0 mL/hr."
4938,22,Maintenance Fluids Calculations,physical,decimal,pmc-7291651-1,Extracted,"A 1-month old male infant weighing 3.6 kg was referred to our institution with symptoms of tachypnea and cyanosis. The patient’s mother refused to do the prenatal examination causing a delayed diagnosis. Echocardiography and computed tomography angiography (CTA) which are routinly peformed in our center for complex anatomical patterns before the operation revealed TGA with anterior-posterior-oriented great arteries, wide patent ductus arteriosus (PDA), type B IAA, ventricular septal defect (VSD) and pulmonary arterial hypertension (PHT), Fig. .
In October 2019, the patient underwent a single-stage primary surgical repair. The proximal descending aorta was separated from the distal aortic arch by approximately 2.6 cm. The left subclavian artery originated from the descending aorta which was perfused by a patent ductus arteriosus of 3.9 mm. Marked vessel discrepancy between the hypoplastic ascending aorta and the dilated main pulmonary artery (PA) due to the double size of PA than the ascending aorta was observed. No hypoplasia was noted in the right ventricle (RV) and the normal coronary pattern was observed.
A single-stage primary repair was performed through the midline sternotomy. Cardiopulmonary bypass (CPB) was introduced as both the ascending aorta and the PA which perfused the descending aorta through the wide patent ductus arteriosus were cannulated using a Y-shaped aortic inflow line. Cannulations of caval veins were then peformed with a right angle cannulation for the superior vena cava and a straight cannulation for the inferior vena cava. The aorta was cross-clamped at 30.2 °C core temperature during the systemic cooling and the myocardial protection was performed through infusions of the histidine-tryptophan-ketoglutarate (HTK) cardioplegic solution into the aortic root. The left heart venting was started by making a small incision on the atrial septum as there was no patent foramen ovale. As the RV was well developed, transpulmonary VSD closure was performed with a bovine pericardial patch after transecting the pulmonary trunk 5 mm above the annulus during the cooling process. At 20.5 °C the extracorporeal perfusion was stopped, and the arterial cannula was withdrawn from the pulmonary trunk. The aortic arch was then reconstructed under hypothermic circulatory arrest (HCA). The left subclavian artery was doubly ligated and transected during the reconstruction with the aim to relieve the tension of anastomosis. After complete excision of the ductal tissue, a longitudinal aortotomy was performed on the inner curvature of the ascending aorta. The end of the descending aorta was then directly anastomosed with the ascending aorta. After the completion of the aortic arch reconstruction systemic arterial perfusion was resumed.
The ascending aorta was then transected 5 mm above the coronary artery (CA) to perform an arterial switch operation of the transposed great arteries. As there were no variable coronary patterns both CA were excised with buttons of the aortic wall and implanted again to the proximal neoaorta. The miss-match between the two ends of neoaorta was then corrected during the anastomosis of neoaorta with an elliptical patch of bovine pericardium used for enlargement of the distal part of the ascending aorta. For next step, the incision of atrial septum was totally closed. Anastomosis of the neo-pulmonary trunk was at last accomplished using a glutaraldehyde-treated autologous pericardium leaving the neoaorta behind the pulmonary bifurcation, which adopted the Lecompte Manouvre. The patient was transferred to the intensive care unit with an open sternum and a peritoneal dialysis catheter placed in the abdominal cavity. The by-pass, cross-clamping and circulatory arrest times were 265, 184, and 33 min, respectively.
The vasoactive-inotropic score (VIS), a predictor of morbidity and mortality in infants after cardiopulmonary bypass [] was 17.5 (adrenaline 0.10μg/kg.min, noradrenaline 0.05μg/kg.min, isoprenaline 0.025μg/kg.min) at the first hour after the operation and 16 (adrenaline 0.10μg/kg.min, noradrenaline 0.03μg/kg.min, milrinone 0.3μg/kg.min) after 24 h. Nitroprusside was used to reduce afterload. N-terminal pro-brain natriuretic peptide (NT-proBNP) was 22,914.00 pg/ml the first day after the operation and decreased to 7101.00 pg/ml after 2 days. The ventilation time was 91 h and the patient stayed in the ICU for 12 days. Postoperative echocardiography and CTA showed excellent results as the systolic function of both ventricles was normal and there were no aortic or pulmonary regurgitations, Fig. . A maximum velocity of 1.7 m/s and 2.4 m/s was recorded at the neoaorta and neopulmonary anastomosis, respectively. The patient remained asymptomatic at 3 months after surgery confirmed with echocardiography demonstrating the normal systolic function of ventricles and trivial regurgitation for both aortic and pulmonary valves. The maximum velocity at the neoaorta and neopulmonary anastomosis was 1.8 m/s and 2.4 m/s, respectively.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.6, 'kg']}",14.4,13.68,15.12,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.6 kg. Hence, the patient's maintenance fluid is 3.6 kg * 4 mL/kg/hr = 14.4 mL/hr.
Hence, the patient's fluid maintenance is 14.4 mL/hr."
4939,22,Maintenance Fluids Calculations,physical,decimal,pmc-5564119-1,Extracted,"The patient was a 50-year-old man (height 159 cm, weight 69 kg) scheduled for extraction of impacted wisdom teeth (#18, 28, 38, and 48) and saucerization owing to chronic osteomyelitis in the right mandibular molar area. The patient had a history of heavy snoring, but was otherwise in good health. However, he had an extreme phobia of tooth extraction. The oral surgeon also determined that the procedure would be highly invasive; as a result, intravenous sedation was requested from the department of dental anesthesiology. We planned conscious sedation using dexmedetomidine to help secure the patient's airway during the extraction procedure. The authors also planned PCS for adequate titration of sedation levels. The patient received an explanation about the dental procedure under sedation, after which he provided written consents for the procedure and the case report.
The results of the pre-anesthesia examination performed the day before the surgery after the patient was admitted showed no specific findings, except eosinophil levels elevated to 13% in the blood test. He was given instruction for NPO for eight hours before the procedure and was sent to the operating room after securing an 18-gauge intravenous line in his left arm.
The PCS pump used was a Perfusor® Space PCA Infusion Pump System (B. Braun Medical Inc., Germany). Dexmedetomidine (Precedex 200 µg/2 ml) was diluted in normal saline to prepare a 50 ml solution at 4 µg/ml. Without setting a basal infusion dose in the PCS pump, the bolus dose, lock-out time, and injection speed were set to 0.1 µg/kg, 1 min, and 1,500 ml/h, respectively.
Electrocardiogram, noninvasive blood pressure, oxygen saturation, and bispectral index (BIS) monitors were attached to the patient. The patient held the PCS demand button in one hand and the patient was instructed to push the button if he felt any anxiety or pain. Oxygen was supplied through a nasal canula, while capnography measurements were obtained simultaneously ().
The sedation procedure took a total of 100 min, and the procedure included saucerization of the region around #37 and extraction of impacted wisdom teeth (#18, 28, 38, and 48). The single dose administered when the patient pushed the button was 1.73 ml, equivalent to 6.93 µg. The patient pushed the button a total of 13 times, but was pushed four times within the lock-out time; therefore, the drug was actually administered nine times, totaling 15.6 ml (62.4 µg).
The patient maintained his state of consciousness and was able to respond to commands. His respiratory rate and vital signs also remained within a normal range (). During the operation, the button was pushed several times during painful procedures. Afterwards, the BIS value dropped to around 60 once, but was maintained around 90 throughout. The serum dexmedetomidine concentrations calculated from the patient and the number of times the button was pushed are shown in . The patient was discharged the next day without any complications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [69.0, 'kg']}",109,103.55,114.45,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 69.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (69.0 kg - 20 kg) = 109.0 mL/hr.
Hence, the patient's fluid maintenance is 109.0 mL/hr."
4940,22,Maintenance Fluids Calculations,physical,decimal,pmc-7085946-1,Extracted,"A 48-year-old female with obesity and with various comorbidities.
A 48-year-old female with obesity was referred for consideration of ESG. She had a medical history significant for hypertension that was controlled with oral agents. She had no prior history of bariatric surgery. At initial presentation, her weight was 93 kg, with a body mass index of 31.4 kg/m2, despite lifestyle changes and prior placement of a gastric balloon.
The patient gave written informed consent, after which she underwent ESG at a private hospital (Hospital Meridional, Cariacica, ES, Brazil). This was the first ESG performed at this center. There were no immediate procedural related complications. The procedure was performed under general anesthesia, with an endoscopic suturing system (OverStitch endosuturing device; Apollo Endosurgery, Austin, TX, United States) coupled to a dual-channel endoscope (GIF-2T160; Olympus America, Center Valley, PA, United States). Carbon dioxide insufflation was used. A full thickness U-shaped suture pattern was used by the physician to perform ESG, as previously described[] (Figure ). A total of five sutures were used.
In the immediate postoperative period, the patient was treated daily with antiemetics (ondansetron, dimenhydrinate, dexamethasone, and scopolamine), as well as dipyrone and omeprazole. The patient was discharged on post-operative day 1, in good condition and without any complaints, with prescriptions for omeprazole, ondansetron, dipyrone, scopolamine, and codeine phosphate combined with acetaminophen if necessary.
On postoperative day 3, the patient developed abdominal pain which continued to worsen over the next 24 h; thus, she was referred to the emergency department for further evaluation.
Obesity and hypertension.
Physical examination was normal preoperatively. On the fourth postoperative day, the patient had a rigid abdomen with signs of peritoneal irritation.
On the fourth postoperative day and admission to the emergency department, the patient had significant leukocytosis (19800 × 103 leukocytes/µL) and an increased C-reactive protein level (147 mg/L).
At the emergency entrance, computed tomography imaging revealed free fluid in the peritoneal cavity (Figure ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [93.0, 'kg']}",133,126.35,139.65,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 93.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (93.0 kg - 20 kg) = 133.0 mL/hr.
Hence, the patient's fluid maintenance is 133.0 mL/hr."
4941,22,Maintenance Fluids Calculations,physical,decimal,pmc-5177704-1,Extracted,"An 11-year-old boy was referred to the pediatric neurology clinic in Konyang University Hospital for evaluation of severe mental retardation, developmental delay, and seizures.
At the time of referral, although his movements were not impaired, he showed overactivity and attention-deficit nature. On physical examination, his weight was 23 kg (less than 3th percentile), height was 120.4 cm (less than 3th percentile), and occipitofrontal circumference (OFC) was 48.5 cm (90th to 95th percentile). He had small deep-set eyes with an apparent hypertelorism, a thin upper lip, a thick and everted lower lip, maxillary micrognathia, and short neck (). He was able to express himself using less than 2 words in incomplete sentences, each made of a word, or repetitive monosyllables. He could not understand demands and these speech-language functions were consistent with the age of 13 months. His cognitive development was uneven, as evidenced by his scores on the Korean Wechsler Intelligence Scale for Children III, which was performed at the age of 10. The verbal intelligence quotient (IQ) scores ranged from 36 on arithmetic to 42 on comprehension, and the performance IQ scores ranged from 43 on block design to 47 on coding, with a full-scale IQ of 31. Ultrasonography of the abdomen was normal and the electrocardiogram revealed an intermittently incomplete atrial-ventricular block. The electroencephalogram showed frequent left central and temporal slow waves (). There were dental anomalies with hypodontia, including all second permanent molars and left mandibular second permanent premolar, and agenesis of all wisdom teeth in a panoramic radiograph (). In addition, delayed eruption of maxillary first permanent molars and poor development of maxillary bones were noticed. His bone age was consistent with his chronological age. Chromosomal microarray (CMA) analysis was performed because of facial dysmorphisms, severe mental retardation, developmental delay, and seizure occurrence.
His medical histories are as follows. He was the third child of healthy, nonconsanguineous parents, a 34-year-old father and a 31-year-old mother at the time of his birth. His mother did not take any medications during the pregnancy and no prenatal growth retardation was observed. There was no known inherited disorder in the family. He was born at a gestational age of 42+0 weeks by vaginal delivery, with a birth weight of 2.9 kg (10th to 25th percentile) and had no perinatal problems. His length was 48 cm (10th to 25th percentile) and his OFC was 32 cm (10th to 25th percentile). His Apgar score was 7 at 1 minute and 8 at 5 minutes. After birth, he was hospitalized because of poor oral intake and fever. He showed subsequent improvement and was discharged without any problems within the next few days. At the time, the hospital records described that he showed facial dysmorphisms such as small eyes with hypertelorism, open mouth, and pectus excavatum. However, he had no symptoms of muscular hypotonia. Excluding chromosomal analysis, no other abnormalities were identified from the laboratory findings. We reviewed his standard chromosomal analysis of peripheral blood lymphocytes, G-banded karyotyping, based on the medical records from the neonatal period. Our analysis revealed that an add(5) was present in all analyzed cells, specifically the 46,XY,add(5)(q31) variant (). However, although a deletion of chromosome 5 at 5q33.3q.35.1 was suspected, unfortunately, it could not be confirmed at that time because of relatively low resolution of G-banded karyotyping. Ultrasonography of the brain revealed the presence of small bilateral cysts in the choroid plexus. A small-sized patent ductus arteriosus was detected in the echocardiogram; however, it was found to have closed spontaneously during follow-up visits. Nuss operation for pectus excavatum was performed at 4 years of age because he intermittently suffered from respiratory discomfort. He also had a follow-up visit for subclinical hypothyroidism.
At 6 months of age, a gradual delay in global development was noticed. For example, he could sit up by the age of 10 months and walk at 3 years. Until 1 year of age, he showed no response in brain stem audiometry. Speech development was also delayed; he started uttering single words only when he turned 4 years old. His first epileptic seizure occurred with fever when he was 3 years old and was first erroneously interpreted as febrile convulsion. Later, the recurrent nature of these seizures became apparent until the age of 8. After treatment with antiepileptic medications, the patient reached a seizure-free state. Magnetic resonance imaging at 8 years of age showed unremarkable findings.
The parents provided a formal informed consent that permitted the use of peripheral blood sampling and genetic testing. We performed high-resolution CMA analysis to specify the breakpoint. The genomic DNA was analyzed using a Cytoscan 750K array and the chromosome analysis suite software package (Affymetrix, Santa Clara, CA, US) using genome build Hg19. The results showed a 16-Mb deletion of 5q33.3q35.11 and an array aberration with 5q33.3q35.1(156,409,412-172,584,708)x1 (). His parents had apparently normal chromosomes. Consequently, the patient was diagnosed as having a de novo deletion in the 5q33.3q35.1 chromosome.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [23.0, 'kg']}",63,59.85,66.15,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 23.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (23.0 kg - 20 kg) = 63.0 mL/hr.
Hence, the patient's fluid maintenance is 63.0 mL/hr."
4942,22,Maintenance Fluids Calculations,physical,decimal,pmc-2239218-1,Extracted,"A 57-year-old woman (180 cm, 60 kg) was presented to the emergency department with upper abdominal pain and left-sided chest discomfort for a couple of days. In addition, she reported of nausea. Upon physical examination, percussion sounds over the left lower thorax were a bit dull and cervical lymph nodes were palpable with a size of up to 1 cm. The abdomen was generally tender without signs of peritonitis; bowel sounds were normal. The ECG showed no abnormalities. Routine laboratory tests revealed mild leucocytosis and a slightly elevated C-reactive protein level. Troponin, myoglobine, and creatine kinase levels were within normal limits. An upper gastrointestinal endoscopy was performed. Whereas the oesophagus, the lower stomach, and the duodenum were
without abnormalities, a small hole in the fundus was visible after inversion of the scope ().
The “hole in the stomach” was intubated with a catheter and contrast dye was administered. Fluoroscopy revealed a diaphragmatic hernia with a large herniation of the gastric fundus (). Immediate laparotomy showed a 3 cm orifice of the
diaphragm (). The orifice was widened and a partial necrosis of the incarcerated fundus was resected (). The diaphragmatic orifice was covered with polydioxanone. The patient recovered fully and 
was discharged 12 days after laparotomy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.0, 'kg']}",100,95,105,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.0 kg - 20 kg) = 100.0 mL/hr.
Hence, the patient's fluid maintenance is 100.0 mL/hr."
4943,22,Maintenance Fluids Calculations,physical,decimal,pmc-6787412-1,Extracted,"A 75-year-old man was admitted to our hospital for further evaluation of subacute renal failure. He had no past history associated with bronchial asthma or drug administration and no other medical problems, history of smoking, habitual drinking, or family history of renal disease. Upon admission, his body weight was 51.0 kg, height was 171.0 cm (body mass index 17.4), temperature was 36.8°C, and blood pressure was 125/74 mm Hg. The lymph nodes were not palpable, and there were no signs of leg edema. The peripheral white blood cell count was 4,600/mm3, with 3,450 neutrophils/mm3 and 92 eosinophils/mm3; the hematocrit was 27.1′; the red blood cell count was 2,710,000/mm3, hemoglobin was 8.9 g/dL, and the platelet count was 156,000/mm3. Laboratory serological findings were as follows: total protein 7.5 g/dL, albumin 4.4 g/dL, creatinine 3.3 mg/dL, urea nitrogen 46.9 mg/dL, and C-reactive protein 0.6 mg/dL. The serum IgG and IgG4 levels were 1,614.0 and 235.0 mg/dL, respectively. Serum protein electrophoresis showed no signs of gammopathy. Slight hypocomplementemia in C4 (C3 83 mg/dL, C4 21.7 mg/dL, CH50 49 U/mL) was also observed. Antinuclear and antineutrophil cytoplasmic antibodies, antiglomerular basement membrane antibody, SS-A and SS-B antibodies, as well as cryoglobulin were all negative. Serum angiotensin-converting enzyme, soluble interleukin-2 receptor, and tumor marker levels were within normal limits. Urinalysis showed proteinuria of 0.9 g/day without hematuria and increasing levels of NAG (22.8 IU/L) and α1-MG (85 mg/L). Whole-body CT and magnetic resonance imaging showed no pleural effusion, ascites, lymph node swelling, or enlargement of organs, except for diffuse enlargement of the kidneys (Fig. ). The longest diameter of the kidneys was > 12 cm. A whole-body gallium scan showed no abnormal accumulation.
Percutaneous renal needle biopsy showed diffuse infiltration of abundant lymphocytes and IgG4-positive plasma cells and storiform fibrosis, which is specific to IgG4-RKD, in the interstitium on light microscopy. There were no signs of injury of the glomeruli or basement membrane. No crescent forms were observed in glomeruli. Slight linear deposition of C3 was observed in the tubules on immunofluorescence microscopy, and no electron-dense deposits were observed (Fig. ). Immunohistochemically, IgG4-positive plasma cells were markedly observed in the interstitium (> 10 IgG4-positive plasma cells/high-power field), and the ratio of IgG4-positive plasma cells to IgG-positive plasma cells was > 90′ (Fig. ).
The diagnosis of IgG4-RKD was reached based upon the above-described findings, and the patient was started on prednisolone at a dose of 0.6 mg/kg/day (30 mg/day). Serum IgG4 and creatinine levels and urinary α1-MG level improved temporarily; however, renal insufficiency continued to advance as the prednisolone was tapered. It became necessary to decrease the dose of the steroid after the onset of severe steroid psychosis. He lost his appetite and became malnourished, and we abandoned the additional therapy because of the risk of infection. The renal function did not improve and maintenance dialysis was initiated. Serum creatinine as well as urinary NAG and α1-MG levels became exacerbated as the prednisolone was tapered. However, the serum IgG4 level continued to decline. Moreover, the diffuse enlargement of kidneys, which was detected by CT, did not improve from the initiation of steroid therapy to the initiation of hemodialysis.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [51.0, 'kg']}",91,86.45,95.55,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 51.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (51.0 kg - 20 kg) = 91.0 mL/hr.
Hence, the patient's fluid maintenance is 91.0 mL/hr."
4944,22,Maintenance Fluids Calculations,physical,decimal,usmle-300,Extracted,"A 29-year-old, gravida 1 para 0, at 10 weeks' gestation comes to the physician for progressively worsening emesis, nausea, and a 2-kg (4.7-lb) weight loss over the past 2 weeks. The most recent bouts of vomiting occur around 3–4 times a day, and she is stressed that she had to take a sick leave from work the last 2 days. She is currently taking ginger and vitamin B6 with limited relief. Her pulse is 80/min, blood pressure is 100/60 mmHg, and respiratory rate is 13/min. Orthostatic vital signs are within normal limits. The patient is alert and oriented. Her abdomen is soft and nontender. Urinalysis shows no abnormalities. Her hematocrit is 40%.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.0, 'kg']}",8,7.6,8.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.0 kg. Hence, the patient's maintenance fluid is 2.0 kg * 4 mL/kg/hr = 8.0 mL/hr.
Hence, the patient's fluid maintenance is 8.0 mL/hr."
4945,22,Maintenance Fluids Calculations,physical,decimal,pmc-5971357-1,Extracted,"A 50-year-old, 50-kg, 152-cm man with aortic and mitral valvular disease was scheduled for a double valve replacement. He had been diagnosed with Hunter syndrome at the age of 40 years and had received enzyme replacement therapy with idursulfase infusion. He had undergone general anesthesia 3 months previously for cervical laminoplasty at another hospital, and his airway had been managed uneventfully at that time with a reinforced tracheal tube of 7-mm inner diameter (ID). He showed the distinctive features of a short neck, jaw deformation, and macroglossia, and he had slight cervical motor restriction and a Mallampati classification of Ш. Preoperative flexible fiberoptic laryngoscopy 2 week previously showed that the patency of the upper respiratory tract was kept though oropharyngeal soft tissue thickening was recognized. However, chest computed tomography (CT) 1.5 months previously showed tracheal stenosis that had flattened the lumen (). The narrowest part above the tracheal bifurcation was 2 cm long and the anteroposterior diameter was ≤6 mm, but the patency of the upper part of the trachea was adequate for insertion of a tracheal tube of 7-mm ID. Cardiac ultrasound demonstrated severe aortic valve stenosis, moderate aortic valve regurgitation, and mild mitral valve regurgitation. The aortic valve area was 0.53 cm2. The maximum and mean aortic valve pressure gradients were 106 and 67 mmHg, respectively. The left ventricle was generally enlarged and the ejection fraction was 71% (Simpson's method). Abdominal CT showed hepatosplenomegaly. All blood parameters were within the normal ranges. During a preoperative conference, we assessed that his airway could be managed in the same way as during the previous anesthetic procedure because the patient had not felt difficulty in breathing.
At the time of admission, his blood pressure was 139/47 mmHg, heart rate was 65 beats/min, and peripheral oxygen saturation was 97%. After cannulation to the left radial artery for continuous monitoring of arterial blood pressure, 3 mg of midazolam and 200 μg of fentanyl were administered for induction of anesthesia. After confirming mask ventilation, 60 mg of rocuronium bromide was provided for neuromuscular blockade. The glottis was easily confirmed using the Airway Scope (Pentax-AWS®; Hoya, Tokyo, Japan), and a tracheal tube of 7-mm ID was inserted into the trachea. However, the tube could not be advanced more than 3 cm from the glottis. The tube was removed. The upper airway was then secured using an i-gel #4 (Nihon Kohden, Tokyo, Japan), and bronchoscopic examination was performed through the breathing channel of the i-gel. Tracheal stenosis that gradually became more severe from under the glottis was revealed (). Therefore, a tracheal tube of 6-mm ID was inserted using the Airway Scope. We felt slight resistance during insertion of the tube, but an audible leak around the tube with an inspiratory pressure of 20 cmH2O was heard when the cuff was deflated. The tube was secured at the 22-cm mark at the alveolar ridge. Pressure-controlled ventilation was started with a peak inspiratory pressure of 20 cmH2O and a respiratory rate of 12 breaths/min, and a tidal volume of about 450 ml was obtained. Although a transesophageal echocardiography (TEE) probe was inserted, the tidal volume did not change.
The aortic and mitral valve replacement was uneventfully performed under cardiopulmonary bypass. After aortic declamping, the patient was easily weaned from cardiopulmonary bypass with a 5-μg/kg/min dopamine infusion. Cardiac function after weaning was good. However, the tidal volume suddenly decreased from 450 to 120 ml at sternal closure, and the end-expiratory carbon dioxide pressure increased from 39 to 71 mmHg. Bronchoscopic examination showed that the stenosis became more severe than that after induction of anesthesia, and the part of the tracheal bifurcation was almost occluded. The tidal volume was hardly obtained in spite of a peak inspiratory pressure of >30 cmH2O. Therefore, we tried to remove the TEE probe because it might have been exacerbating the tracheal stenosis by pushing the trachea adjacent to the esophagus. As a result, a tidal volume of 400 ml was obtained with a peak inspiratory pressure of 25 cmH2O by improving the severe stenosis of the tracheal bifurcation, and the end-expiratory carbon dioxide pressure decreased to 43 mmHg. In addition, 125 mg of methylprednisolone was administered intravenously to reduce edema in the lower respiratory tract. Extubation was performed on the second postoperative day. After extubation, the patient's oxygenation was good but wheezing and dyspnea were noted. Procaterol inhalation and noninvasive positive-pressure ventilation were administered for 3 days. After his breathing had become stable, the patient was discharged from the hospital on the 25th postoperative day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [50.0, 'kg']}",90,85.5,94.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 50.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (50.0 kg - 20 kg) = 90.0 mL/hr.
Hence, the patient's fluid maintenance is 90.0 mL/hr."
4946,22,Maintenance Fluids Calculations,physical,decimal,pmc-6220405-1,Extracted,"A 17-year-old nonobese Caucasian female who had a history of a medulloblastoma diagnosed at 7 years of age was treated with radiation therapy. She subsequently developed TSH and GnRH deficiencies. Though GHD was suspected based on height (z-score of – 3.1; see ), treatment had not been initiated based on the initial management focus being to treat her medulloblastoma. At 15 years of age when her bone age showed full skeletal maturity, her parents were informed that GH therapy could not be pursued because her linear growth was complete.
On presentation, the patient's height was 141.3 cm (z= -3.1) and weight was 53 kgs (36th percentile for age). Body mass index was 25.8 kg/m−2 (86th percentile for age). Surveillance labs done at the oncology clinic showed glucosuria. Further testing showed HbA1c of 9.6% and on another day her fasting glucose was 277 mg/dL. Based on these results, diabetes mellitus was diagnosed.
When glutamic acid decarboxylase (GAD-65; Esoterix), islet-cell (Esoterix), insulin (Esoterix), and zinc transporter 8 (ARUP Laboratories) antibodies as well as DNA panel for maturity onset diabetes of youth (MODY) genes (HNF4α, GCK, IPF1, HNF1α, and HNF1β, [Athena Diagnostics]) returned all negative along with an elevated fasting C-peptide level of 3 ng/mL (normal: 0.4 - 2.1), T2DM was diagnosed. With the initiation of traditional basal/bolus insulin therapy using conventional dosing, a rapid escalation to peak total daily insulin dose of 2.9 units/kg/day (~ 155 units/day) was required to treat her refractory hyperglycemia. Treatment nonadherence was thought to be the unlikely cause of her increased insulin requirements based on the agreement between her insulin dosing and prescription refill data.
A comprehensive evaluation for conditions associated with IR was negative. However, based on Arginine/Clonidine stimulation testing showing peak GH level of 0.8 (normal: ≥ 10 ng/mL), a diagnosis of GHD was made. GH supplementation was initiated at 0.3 mgs daily and titrated based on IGF-1 levels.
After GH was started, her systolic and diastolic blood pressures (BP) which were mildly elevated between 124-136 and 77-89, respectively, became more normal. Despite this, lisinopril 5 mgs once daily was added for microalbuminuria.
With the diagnosis of T2DM and our patient having a significant family history of adverse cardiovascular risk factors, she was started on atorvastatin 10 mgs once daily. Within 2 months of therapy, her LDL cholesterol (LDL-C) decreased to 74 mg/dL. shows serial lipid profiles.
Though her diabetes was not fully reversed with GH, her HbA1c decreased to 5.9% and 5.8% at 6 and 19 months, respectively. Her insulin therapy requirement decreased to 1.9 units/kg/day (~ 100 units) at 12 months after the start of GH.
Magnetic Resonance Imaging (MRI) of the brain and abdomen indicated a small anterior pituitary gland and liver masses, respectively. Liver biopsy showed steatohepatitis with bridging fibrosis (). With GH therapy, her liver transaminases trended to normalcy (). Repeat MRI abdomen at 20 months after the start of GH showed stability of the liver lesions when compared to that done at 14 months. These hyperintense lesions like the initial ones were located in the liver's parenchyma and the appearance of the liver was otherwise normal.
With GH therapy, the patient's stamina improved. She was now able to work for 20 hours weekly without becoming fully exhausted and her Quality of Life-Assessment of Growth Hormone Deficiency in Adults (QoL-AGHDA) and Quality of Life Satisfaction (QLS) scores, both questionnaire-based, improved ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [53.0, 'kg']}",93,88.35,97.65,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 53.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (53.0 kg - 20 kg) = 93.0 mL/hr.
Hence, the patient's fluid maintenance is 93.0 mL/hr."
4947,22,Maintenance Fluids Calculations,physical,decimal,pmc-7383637-1,Extracted,"A 71-year-old right-handed man [height: 185 cm; body weight: 87 kg; body mass index (BMI) 25.4 kg/m2] presented at the emergency department following involuntary movement of the left arm for 1 week. He had no history of diabetes but experienced polydipsia, polyuria, and a weight loss of about 10 kg in the previous month. He also reported a 24-year history of well-controlled hypertension and a 4-year history of percutaneous coronary intervention. He was on regular medication for the above two diseases. He had been diagnosed with lung adenocarcinoma 4 years before presentation and had been receiving icotinib (125 mg tid) since then. On neurological examination, muscle tone and strength of extremities were generally normal. No cranial nerve impairment or sensory disturbance was identified. Routine laboratory evaluation revealed random serum glucose up to 42.05 mmol/l with normal serum osmolarity (304.5 mmol/l). The artery gas analysis was normal. His urine glucose was positive (+++) and ketone was negative. His A1C (HbA1c) was 14% (130 mmol/mol). Cerebral CT was arranged instead of MRI because of the metal coronary stent and revealed a hyperdense lesion in the right basal ganglia (). After neurology and endocrinology consultation, other etiologies for HH including cerebrovascular condition, infection, and neurodegenerative disorders were excluded. The patient was diagnosed with diabetic HH and referred to the endocrinology department for further therapy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [87.0, 'kg']}",127,120.65,133.35,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 87.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (87.0 kg - 20 kg) = 127.0 mL/hr.
Hence, the patient's fluid maintenance is 127.0 mL/hr."
4948,22,Maintenance Fluids Calculations,physical,decimal,pmc-8361718-3,Extracted,"Patient 3 was the product of a naturally-conceived pregnancy to a then 21-year-old G2P0➔1 mother. Both parents were from the Dominican Republic. Family history was notable for consanguinity with the mother's maternal grandfather and the father's paternal grandmother being siblings (second-cousin union) and for a prior pregnancy terminated for multiple congenital anomalies, including lemon-shaped head with frontal bossing, posterior fossa cyst, encephalocele, and arthrogryposis with bilateral talipes equinovarus. Microarray and exome sequencing were nondiagnostic.
Pregnancy was complicated by prenatal ultrasound concerning for multiple congenital anomalies, prompting fetal MRI, which demonstrated bilateral ventriculomegaly, dandy-walker malformation, occipital meningocele, ambiguous genitalia, bilateral talipes equinovarus, and shortened long bones. Patient was born at 36 weeks gestational age via caesarian section for fetal macrocephaly. APGARs were 2 and 8 and 1 and 5-min of life, respectively. Birth weight was 3.17 kg (75%), birth length was 45 cm (20%), and head circumference was 42 cm (>97%). He was diagnosed postnatally with cleft palate and four-extremity polydactyly. He developed respiratory distress in the delivery room requiring positive pressure ventilation, and was intubated shortly thereafter for persistent apneas and desaturations.
He was evaluated by Genetics on day of life 3. Physical examination was notable for macrocephaly with prominent forehead and occiput, down-slanting palpebral fissures, hypertelorism, nasal milia, bifid tongue, lingual hamartomas, micrognathia, four-extremity postaxial polydactyly, micropenis and hypotonia. Due to concern for OFDS, an abdominal ultrasound, echocardiogram, brain MRI and ophthalmology examination were requested. Abdominal ultrasound showed structurally normal liver and kidneys, echocardiogram showed a structurally normal heart, ophthalmology examination showed bilateral optic nerve colobomas, and brain MRI showed dandy-walker malformation, left parasagittal occipital encephalocele, possible ectopic posterior pituitary gland, possible left frontal lobe cleft, and small optic nerves.
Patient is currently 8-months of age. Growth parameters are notable for a weight of 10.5 kg (95%), a height of 61 cm (<3%; 50% for 2.5 months of age), and a head circumference of 46 cm (>97%). Physical examination is largely unchanged. Patient's clinical course has been complicated by hydrocephalus status post shunt placement complicated by multiple shunt infections, respiratory failure status post tracheostomy placement, G-tube dependence, cortical visual impairment, neuro-irritability, spasticity, central adrenal insufficiency, and profound developmental delay.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.5, 'kg']}",41,38.95,43.05,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.5 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.5 kg - 10 kg) = 41.0 mL/hr.
Hence, the patient's fluid maintenance is 41.0 mL/hr."
4949,22,Maintenance Fluids Calculations,physical,decimal,pmc-3139320-1,Extracted,"A 38-year-old woman (weighing 62 kg), with abnormal bleeding, was scheduled for an abdominal hysterectomy. Clinical history, physical examination, and biochemical tests showed normal values. We planned to use spinal anesthesia for her operation. After transferring her to the Operation Room, the intravenous (IV) line was accessed, with an 18 G angiocath, and 1.5 mg midazolam was injected intravenous and 500 ml of crystalloid fluid was administered. The electrocardiogram (ECG), noninvasive blood pressure (NIBP), heart rate (HR), and peripheral oxygen saturation (SpO2) were measured with Saadat monitoring (Poyandegan). The Mean Arterial Pressure (MAP) and HR were 85 mmHg and 64 beat per minute, respectively. After explaining the procedure, the patient was laid down in the left lateral position. After aseptic preparation, local anesthesia was administered using 2 cc lidocaine 1%, and then a 25-gauge spinal needle was administrated in the subarachnoid space at the L3–L4 interspace, using a median approach. Appearance of CSF through the needle was confirmed by the subarachnoid position.
The drug ampoule, mistakenly containing 25 mg of tracurium (rather than a hyperbaric 0.5% bupivacaine solution, Marcaine-Spinal 0.5%; Astrazeneca AB. Sodertalje. Sweden) was drawn into the syringe and injected into the spinal space. This mistake was committed due to the similarity between the tracurium 25 mg ampoule (Glaxo Wellcome Company) and the bupivacaine solution. The active substance of the tracurium ampoule is atracurium besilate. The other ingredients are benzene sulfonic acid and water.
The patient was turned to the supine position, without a pillow under her head, and was observed for development of sensory and motor block. An assessment of the level of analgesia, through a pinprick test, was made five minutes later; at this time it was apparent there was no analgesia. After ten minutes, no sensory or motor block was yet seen, and at this point, we realized that the wrong ampoule had been injected, as the empty ampoule of tracurium (Glaxo Wellcome Company) was discovered.
At this stage, the patient was comfortable and without hemodynamic instability. MAP and HR were 80 mmHg and 78 beats per minute, respectively, and the patient was warmed with a blanket. Force, tonicity of peripheral extremity muscles, and reflex were evaluated, as well as upper and lower senses (with pinpricking and temperature tests); her spontaneous movements were normal, and the train of four (TOF) ratio was 60%. The patient's ability to breathe, to open her eyes, to protrude her tongue, and to swallow saliva was not affected. Intravenous crystalloid was infused as soon as possible. Monitoring was continued and the patient was observed for untoward signs and symptoms for 40 minutes and at that time the TOF ratio was at 75% and all clinical signs were normal. MAP and HR were normal, and the patient was comfortable. As the bleeding was modest, we decided to induce general anesthesia and operate on her once the TOF ratio reached more than 90% (at almost 50 minutes). Pre-induction MAP and HR were 75 mmHg and 74 beats per minute. Induction of anesthesia was done with thiopental Na 300 mg, fentanyl 150 μg, and tracurium 30 mg, and titrated with TOF monitoring, and when a TOF response was not seen, the patient was intubated. Anesthesia was maintained with propofol 100 μg/kg/minute, N2O, and O2 50%. Fentanyl 50 μg was administered every 25 – 30 minutes. The patient's muscular relaxation was monitored with a TOF with the Stimuplex HNS 11 nerve stimulator; a B-Braun Company device, every five minutes. During the operation, when the fourth TOF stimulus response appeared, we injected tracurium 10 mg. The intraoperative course was uneventful and the vital signs remained stable.
At the end of the surgery, at the appearance of the fourth response, the reverse of neuromuscular blockade (neostigmine 2.5 mg and atropine 1 mg) was administered. When an 80% TOF ratio was reached, the patient's trachea was extubated. In the recovery room the patient's ability to breathe, lift her head, and bend her knees was evaluated, and a tongue-depressor test was administered. When the TOF response was restored to >90%, the patient was transferred to the surgical ward and examined at one, two, twenty-four, and forty-eight hours, with all examinations reporting normal results. Sensory (pinpricking and temperature test), motor (spontaneous movement), and reflex maneuvers (upper and lower limbs) were evaluated at one week, two weeks, and one month.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [62.0, 'kg']}",102,96.9,107.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 62.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (62.0 kg - 20 kg) = 102.0 mL/hr.
Hence, the patient's fluid maintenance is 102.0 mL/hr."
4950,22,Maintenance Fluids Calculations,physical,decimal,pmc-4860440-1,Extracted,"The patient, a 44-year-old non-smoking woman with obesity (weight: 115 kg, BMI: 45.5) was admitted to the hospital due to numerous round shadows in both lungs, revealed incidentally during a control radiological examination. The patient did not report any ailments.
Her medical history included gynecological surgery to remove uterine myomas 13 years earlier. At that time, her gynecologist recommended to her the contraceptive Cilest (0.25 mg norgestimate and 0.035 mg ethinylestradiol), which she continued to take without interruption. Her medical history also featured an appendectomy, a bilateral procedure for carpal tunnel syndrome, and arterial hypertension treated with Ramipril (1 x 5 mg) and Metoprolol (1 x 50 mg).
The patient was the mother of 3 healthy children. Her first period occurred at the age of 11. The periods were regular: every 28 days for 4 days. Before the uterine myoma surgery, the periods had been very profuse.
Physical examination revealed bradycardia (approx. 52 bpm), arterial pressure: 140/90, onychomycosis affecting the toenails (during topical treatment), and postoperative scars on the hypogastrium.
Laboratory tests demonstrated that the level of alanine aminotransferase (ALAT) was increased to 89.5 IU/l.
Chest X-ray and computed tomography (CT) visualized numerous (several dozen) well-defined round shadows of varying diameter (2-32 mm) in both lung fields, enhanced after the addition of contrast (). No comparisons could be made with previous X-ray photographs, as the patient had not been examined radiologically for the previous 26 years.
The results of respiratory function tests (arterial blood gas, spirometry) were normal. The patient did not consent to bronchofiberoscopy.
She was qualified for right-sided videothoracoscopy; during the procedure, a marginal resection of a fragment of the right lung's lower lobe with a grey-white nodule (7 mm in diameter) was performed.
The ensuing pathomorphological investigation identified the tumor as an adenomyoma, which was confirmed by immunohistochemical tests. Proliferation index Ki-67 was positive in approx. 1% of cells. Actin (+), desmin (+), S-100 (–), and TTF-1 (+) were also labelled. Furthermore, positive expression of estrogen and progesterone receptors was detected: ER (+), PR (+).
The patient did not report for a control examination scheduled at the Thoracic Surgery Clinic; after 2 years, she was referred to the hospital by a pulmonologist in order to undergo invasive diagnostics and possibly treatment of suspected metastatic lesions in the lungs.
Right-sided thoracotomy was performed, and several solid nodules (8-25 mm in diameter) were enucleated from each lobe of the right lung. The postoperative course was uneventful. The result of pathomorphological investigation, benign metastasizing leiomyoma, was supplemented with a repeated analysis of samples from the uterine myomas removed 15 years earlier. The control pathomorphological analysis confirmed the previous diagnosis: leiomyoma cellulare, mitotic index: MI 3/10 HPF, positive Ki-67 proliferation index in approx. 1% of cells, presence of estrogen receptors (+) and progesterone receptors (+ + +).
After a gynecological consultation, the contraceptive Cilest, which the patient had been taking for the past 15 years, was discontinued; the patient had her last period during the next month.
She was qualified by an oncologist for treatment with a gonadotropin-releasing hormone (GnRH) analog – Diphereline (Triptorelin). Chest CT images obtained after 3 and 6 months showed that the nodular lesions remained stable. The patient was offered hysterectomy and adnexectomy, but she is yet to make a final decision.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [115.0, 'kg']}",155,147.25,162.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 115.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (115.0 kg - 20 kg) = 155.0 mL/hr.
Hence, the patient's fluid maintenance is 155.0 mL/hr."
4951,22,Maintenance Fluids Calculations,physical,decimal,pmc-5820982-3,Extracted,"A six-month-old girl was born after the first full-term pregnancy via spontaneous vaginal delivery, weighting 2840 g. The pregnancy was complicated by exacerbation of herpes infection in the second month of the pregnancy. Congenital heart defect (tetralogy of Fallot [TF]) was diagnosed antenatally. Second-level examinations, such as amniocentesis and genetic analysis, were not offered to the parents during the pregnancy. Apgar scores were 7 per 1 minute and 7 per 5 minutes. The general condition of the patient after the birth was grave due to respiratory and cardiovascular disorders. Family history is not clear, but there were some neonatal period deaths and incidences of heart disease in close relatives.
Congenital heart defect – TF was confirmed in the first day of life. Nasal regurgitation was observed in the first months. There was physical development retardation. At the age of 11 months her weight was 6150 g. There was a mild motor delay. Dysmorphic findings were mild.
Laboratory findings showed normal serum ionised calcium level. The thymus was not visualised by computed tomography scanning. Immunological studies revealed low levels of CD3+ (by percentage) and CD4+ (by percentage and absolute numbers) T lymphocytes. Other subtypes of T lymphocytes (by percentage and absolute numbers) and immunoglobulins were normal (). Recurrent infections were not observed ().
At the age of three weeks FISH analysis revealed chromosome micro-deletions in 22 q11.2 locus, female karyotype: 46,XX.ish del(22)(q11.2)(HIRA-).
Vaccinations of hepatitis B and pneumococcal infections were carried out.
At the age of five months radical correction of the heart defect was performed.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6150.0, 'g']}",24.6,23.37,25.83,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6150.0 g so this converts to 6150.0 lbs * kg/1000 g = 6.15 kg. Hence, the patient's maintenance fluid is 6.15 kg * 4 mL/kg/hr = 24.6 mL/hr.
Hence, the patient's fluid maintenance is 24.6 mL/hr."
4952,22,Maintenance Fluids Calculations,physical,decimal,pmc-7034498-1,Extracted,"Patient 1 (T3188) is a 23-year-old man with lifelong weakness of distal limbs, abnormal gait, and congenital foot malformation. He was born of full-term spontaneous vaginal delivery with normal birth weight (3.1 kg). Bilateral clubfoot was observed at birth. He achieved sitting and standing at 10 months and 2 years old, respectively. At the age of three years, he learned to walk alone but was unstable, with falling every 5–6 steps. Orthotics surgeries were performed on feet twice at the age of 1 and 6 years, respectively. Hands are clumsy since childhood, especially for delicate manipulating. At the age of 16 years, the muscle twitching on both thighs appeared. Wearing the orthopedic shoes, he may walk slowly and vacillatingly. However, distal dominant limb weakness and muscle atrophy slowly progressed without any sensory disturbances. At the age of 23 years, he was 180 cm in height with body weight 52 kg, clear in speech and alert in recognition. Upon evaluation, tongue fasciculations was continuous when stuck out. He had normal strength in neck flexion and proximal limbs (5/5 rated on a scale of 0/5–5/5), but reduced strength of grip (4/5). Muscle tone in four limbs was normal. Fingers could not be straightened with limited interphalangeal joint extension, obvious interosseous, and thenar muscle atrophy (Fig. A and B) as well as postural tremor. Muscle atrophy below knee was eye-catching. Foot deformity was composed of Achilles tendon contracture as well as toe varus (Fig. C and D). Tendon reflexes were brisk in four limbs. Patellar clonus was positive on the right side. The pathological plantar reflex examination was not completed due to unsatisfactory cooperation. Ptosis, nystagmus, dysarthria, dysphagia, ataxia, muscle pain, and dyspnea were not noticed. Mental psychological and cognitive tests were normal. He has been training in backstroke team for six years mainly depending on arm strength. The electrophysiologic showed nerve conduction velocity was normal. Compound muscle action potential (CMAP) was decreased in nervus peroneus communis (0.96 mV), median nerve (1.27 mV), and ulnar nerve (4.4 mV). The duration and amplitude of motor unit potential (MUP) and multiphase potentials were increased, without spontaneous activity, indicating extensive chronic neurogenic lesions. Figure E showed the X-ray photography of distal extremities at the age of 23 years.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [52.0, 'kg']}",92,87.4,96.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 52.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (52.0 kg - 20 kg) = 92.0 mL/hr.
Hence, the patient's fluid maintenance is 92.0 mL/hr."
4953,22,Maintenance Fluids Calculations,physical,decimal,pmc-5963038-1,Extracted,"A 52-year-old black man with no relevant past medical history was referred to our centre for the management of cellulitis. He presented with a swollen erythematous and painful right leg that progressed to formation of blebs, suppurating ulcers and a wet gangrene. This started at knee joint 8 days prior to presentation and was initially managed with over-the-counter amoxicillin and diclofenac. The swelling later progressed to involve the right leg with development of blister-like lesions 4 days following the onset of symptoms. The patient also developed generalised pruritic rash prompting consultation at the regional hospital and there, a diagnosis of a sepsis secondary to a cellulitis was made. Initial work-up at the regional hospital comprised of a complete blood count which revealed leucocytosis (white cell count of 53.9 × 109/l) with neutrophil predominance, normocytic normochromic anaemia (haemoglobin of 3.9 g/dl) and thrombocytosis (platelet count of 880 × 109/l). The blood urea nitrogen was 114 mg/dl and serum creatinine was 2.1 mg/dl (l84.8 µmol/l). The patient was initially managed with intravenous ceftriaxone 1 g 12 hourly, intravenous metronidazole 500 mg 8 hourly and subcutaneous enoxaparin 4000 IU 24 hourly and was also transfused two units of compatible whole blood. The patients’ stay at the regional hospital was marked by persistence of fever, progressive ulceration of the leg, bullae formation and the onset of gangrene prompting referral to Saint Elizabeth Catholic General Hospital Shisong following 4 days of hospitalisation.
Physical examination upon arrival at our centre revealed a temperature of 38.9 °c, respiratory rate of 23 breaths/min, blood pressure of 99/70 mmHg and a pulse rate of 114 beats/min. The patient was alert with pale conjunctivae and anicteric sclerae and his weight was 66 kg. His left leg was swollen, warm, fluctuant with ulcerated skin and necrosis to the level of the knee joint (Fig. ). All digits of the right foot were pale and cold with absent posterior tibial pulse. The following investigations were conducted: a random blood glucose was 150 mg/dl (8.3 mmol/l) and a fasting blood glucose done 16 h later was 117 mg/dl (6.5 mmol/l). A complete blood count revealed a white cell count of 16.4 × 109/l with neutrophil predominance, a microcytic hypochromic anaemia with haemoglobin level of 7.2 g/dl and platelet count of 569 × 109/l. A diagnosis of fulminant necrotizing fasciitis was made.
The following parenteral antibiotics were given upon admission: ampicillin 1 g 6 hourly, gentamycin 80 mg 12 hourly and metronidazole 500 mg 8 hourly; analgesia included intravenous paracetamol 1 g 6 hourly and fluids. After counselling and consent, surgical debridement was done under general anesthesia 12 h following hospitalization. Visualization during surgical exploration confirmed the diagnosis of NF (Figs. and ). Debridement was repeated on day 3 and day 7 of hospitalization. After debridement, the wound was washed and dressed 12 hourly with Dakin’s solution and normal saline. A wound swab was sent for culture and sensitivity and Proteus mirabilis and E. coli were isolated. Necrosis progressed despite multiple and aggressive surgical debridement resulting to an above-knee amputation. Two units of compatible whole blood were transfused during surgery. The patient continued having swinging pyrexia (Fig. ) and on post-operative day 6, the stump started producing purulent discharges (Fig. ). The second wound swab was collected and sent for culture and sensitivity and it still revealed P. mirabilis and E. coli were isolated. Proteus mirabilis was sensitive only to the carbapenems (imipenem and meropenem) while E. coli was additionally sensitive to ofloxacin and ornidazole (Table ).
Further management involved removal of sutures, debridement of necrosed tissue and initiation of parenteral meropenem 1 g given 8 hourly. Clinical progress was marked by formation of granulation tissue. The wound was closed up 6 days later and the patient was eventually discharged after 7 weeks of hospitalization.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [66.0, 'kg']}",106,100.7,111.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 66.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (66.0 kg - 20 kg) = 106.0 mL/hr.
Hence, the patient's fluid maintenance is 106.0 mL/hr."
4954,22,Maintenance Fluids Calculations,physical,decimal,pmc-4881626-5,Extracted,"A 2.9-year-old female child weighing 12.5 kg with a diagnosis of TOF was scheduled for total correction. Clinical reason for the operation was increase in frequency of cyanotic spells. Room air saturations were 72% and Hb of 17.2 g/dl. The patient was operated with the standard anesthetic technique. Pump time and CXT time was 125 and 73 min, respectively. At the end of the procedure, the patient was extubated on the table after fulfillment of the standard extubation criteria. Postoperative events included increased drain output at 3–4 mL/kg/h for few hours. She was transfused with PRBCs (15 mL/kg), FFP (15 mL/kg) and transamine. She was shifted on 3rd postoperative day after chest drain removal to step down.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.5, 'kg']}",45,42.75,47.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.5 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.5 kg - 10 kg) = 45.0 mL/hr.
Hence, the patient's fluid maintenance is 45.0 mL/hr."
4955,22,Maintenance Fluids Calculations,physical,decimal,pmc-8021304-1,Extracted,"A 16-month-old boy was transferred from an outside hospital because of a high fever and skin rash. He was born via normal vaginal delivery at 40 weeks of gestation, with a birth weight of 3670 g. He was previously healthy except for atopic dermatitis and a history of suspected viral meningitis at the age of 100 days, which was resolved without complication. Age-appropriate vaccination was done without specific adverse events following the administration of the vaccines, which included the Bacillus Calmette–Guérin (BCG), measles/mumps/rubella, and varicella vaccines. His language and motor development were within the normal ranges. On the day of admission, he had a weight of 11.5 kg (50th–75th percentile) and a height of 81.9 cm (50th–75th percentile).
He was admitted to the outside hospital because of a high fever of up to 40°C for 3 days. On physical examination, abnormal findings were not shown other than hand and foot swelling. The initial complete blood count (CBC), blood urea nitrogen (BUN), creatinine (Cr), and serum albumin levels were normal. However, his C-reactive protein (CRP) level was high, at 10.37 mg/dL (the normal level is < 0.5 mg/dL). He was treated with an initial empiric antibiotic of intravenous cefotaxime. On his third day of hospitalization, perioral ecchymosis and mild coagulopathy developed, with a prothrombin time (PT) international normalized ratio (INR) of 1.30, activated partial thromboplastin time (aPTT) of 67.0 seconds, and D-dimer of > 1000 ng/mL. No bacterial or viral pathogens were identified in the initial blood culture and respiratory viral polymerase chain reaction (PCR), respectively. Besides, oliguria (urination of 0.5 cc/kg/h) developed, along with persistent high fever and swollen extremities. He was transferred to our hospital on the sixth day of fever.
On the first day at our hospital, his vital signs were as follows: a blood pressure of 149/91 mm Hg (reference: 86–103/40–55); a pulse of 189 bpm (reference: 70–160); and a body temperature of 38.2°C. He appeared acutely ill. Generalized edema, oral ulcers, and multiple purpura, including perioral ecchymosis, were observed on physical examination (Fig. ). His blood count showed bicytopenia with hemoglobin of 9.5 g/dL, platelet count of 120,000/μL, and white blood cell (WBC) count of 7200/μL, of which 70.7% were neutrophils, 15.8% were lymphocytes, and 4.8% were eosinophils. Other blood laboratory findings were as follows: CRP of 11.14 mg/dL, BUN/Cr of 3 mg/dL / 0.17 mg/dL, albumin of 2.3 mg/dL, PT INR of 1.22, aPTT of 47.8 seconds, fibrinogen of 372 mg/dL, D-dimer of 5.82 μg/mL, and fibrin degradation product of 33 μg/mL. The cerebrospinal fluid profile and urinalysis were unremarkable. Under the impression of serious bacterial infection, he was given vancomycin (60 mg/kg/day, intravenous) and meropenem (60 mg/kg/day, intravenous) as empiric antibiotics. However, repeated culture studies showed no definite pathogens. On the third day, new ecchymosis around his right ear and forehead developed, and a high spiking fever persisted.
To exclude other etiology of fever of an unknown origin, a peripheral blood smear, bone marrow examination, and bone scan were done, which showed no specific abnormalities suggesting malignancies. The immunoglobulin (Ig) G, M, and A levels were normal [at 969 mg/dL (normal: 345–1236), 242 mg/dL (normal: 43–207), and 74.3 mg/dL (normal: 14–159), respectively]. However, the immunoglobulin E (IgE) level was high, at 1679 kU/L (normal: 0–230), and the complement fractions C3, C4, and CH50 were low, at 80.0 mg/dL (normal: 77–195), 6.7 mg/dL (normal: 7–40), and 13.3 U/mL, respectively. The antinuclear antibody (ANA) was positive, at 1:320 with homogenous fluorescence, and the anti-double stranded (anti-ds) DNA antibody was also positive, at 10.8 IU/mL. The tests for anti-SSA, anti-SSB, anti-ribonucleoprotein, anti-scleroderma 70, and anti Jo1 antibodies were all negative.
Two weeks after he was hospitalized, leukopenia developed, and thrombocytopenia became worse, along with the persistent fever. The complement fractions were decreased to 37.9 mg/dL of C3, < 1.5 mg/dL of C4, and under 10.0 U/mL of CH50, respectively. The ANA titer increased to 1:1280 with homogenous fluorescence, and the anti-ds DNA antibody level increased to 84.4 IU/mL. The lupus anticoagulant and anticardiolipin antibody were all positive, while other autoantibodies were all negative. To control the fever, he was started on naproxen on the 30th day of fever, and his fever subsided from 32nd day of fever. He definitively satisfied the 2015 American College of Rheumatology (ACR)/Systemic Lupus Erythematosus International Collaborating Clinics (SLICC) revised criteria for the diagnosis of SLE (7 points out of 16); therefore, he was treated with a steroid (methylprednisolone, 2 mg/kg/day, intravenous). The anti-ds DNA antibody level and complement fractions were improved after steroid therapy, and his fever did not recur.
Approximately 1 week after starting steroid treatment, his steroid dose was reduced to 1.0 mg/kg/day, orally. Two weeks after the first dose reduction, his steroid dose was again reduced to 0.5 mg/kg/day. However, at this point, his fever returned, and his anti-ds DNA antibody titer increased. Accordingly, his steroid dose was increased to 1.0 mg/kg/day, and his fever disappeared. One week later, fever, the swelling of the hand and foot, and proteinuria (Urine Protein/Creatinine ratio of 0.484 mg/mg) appeared again. A renal biopsy confirmed the diagnosis of lupus nephritis (focal lupus nephritis, class III). Transthoracic echocardiography showed vegetation in the tricuspid valve, which was thought to be indicative of Libman-Sacks endocarditis. He was treated with intravenous methylprednisolone (1.0 g/m2) for 3 days, followed by cyclophosphamide (500 mg/m2). Then, steroid (deflazacort), mycophenolate mofetil, and cyclosporin were used for his SLE, and the disease was well controlled.
Considering the early-onset SLE, partial exome sequencing for 4813 OMIM genes was performed in his peripheral leukocytes. Exomes were captured using the TruSight One Panel (Illumina Inc.), which enriches a 12 Mb region spanning 4813 genes. Sequencing was performed using the NextSeq platform (Illumina Inc.). Sequence reads were aligned to the reference genome, hg19, using a Burrows–Wheeler aligner (BWA) (v0.7.12, MEM algorithm). The mean depth of coverage was 90× (> 10× = 98%). One heterozygous missense variant, c.5536A>G (p.Lys1846Glu), was found, which was inherited from his father. This variant was not reported previously. The mutation was confirmed using in silico prediction tools, such as PolyPhen-2 (, score 1.00) and SIFT (, score 0.00). This variant has been classified as likely to be pathogenic, according to the American College of Medical Genetics and Genomics (ACMG).[ To rule out the possibility of a large exonic deletion of DOCK8, multiple ligation-dependent probe amplification (MLPA) analysis (P385-A2, MRC Holland, Amsterdam, the Netherlands) was done in the peripheral leukocytes of both the patient and his parents, which revealed a heterozygous deletion of exon 1 to 8 in the patient and his mother. Through the results of the genetic testing, he was confirmed to have DOCK8 deficiency.
At the age of 22 months, when the patient's anti-ds DNA antibody titer and complement levels were normal as a result of the use of immunosuppressants, he newly experienced skin and soft tissue infections and bacteremia caused by Pseudomonas aeruginosa and received cefepime (60 mg/kg/day, intravenous). From that point, he experienced skin and soft tissue infections several times, which is compatible with ecthyma gangrenosum.
At the age of 28 months, he received haploidentical hematopoietic stem cell transplantation (HSCT) from his mother as a donor, with a non-myeloablative conditioning regimen that included antithymocyte globulin, thiosulfan, and fludarabine. WBCs were grafted on the 10th day following HSCT, and no significant HSCT-related morbidity, including graft versus host disease (GvHD), occurred during a follow-up period of 1-year post-HSCT. At 1 month post-HSCT, the complement fractions C3, C4, and CH50 were normal, at 113.0 mg/dL, 22.7 mg/dL, and 51.2 U/mL, respectively. The ANA was positive at 1:160, with homogenous fluorescence, and the anti-ds DNA antibody level had decreased to 13.0. The IgE level was high, at 526 kU/L. However, the anti-ds DNA antibody normalized at 3 months post-HSCT, and the ANA and IgE became normal at 6 months post-HSCT. He had 20% and 33% donor T-cell chimerism at 3 months and 6 months post-HSCT, respectively. Currently, at 12 months post-HSCT, he is doing well, without any autoimmune features or recurrent infections (Fig. ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [11.5, 'kg']}",43,40.85,45.15,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 11.5 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (11.5 kg - 10 kg) = 43.0 mL/hr.
Hence, the patient's fluid maintenance is 43.0 mL/hr."
4956,22,Maintenance Fluids Calculations,physical,decimal,pmc-6639066-1,Extracted,"A 59-year-old male presented with a history of untreated Hepatitis C and 50 pack-year smoking. He presented to the emergency department with black tarry loose bowel movements that started five days before the presentation. The melena was associated with cramping generalized abdominal pain and diarrhea. On review of systems, he complained of palpitation but denied any chest pain, shortness of breath, or lower limb swelling. He also mentioned that he noticed more than 20 pounds of weight loss in the last three months. Physical examination was remarkable for tachycardia with a regular rhythm, normal heart sounds, and no murmurs. On abdominal examination, he had epigastric tenderness on palpation, and he had non-tender hepatomegaly. Signs of liver cirrhosis were found on examination, such as spider angioma, gynecomastia, and mild palmar erythema.
Due to concerns of variceal bleeding, two large-bore intravenous catheters were inserted, a cross-match was done, and two units of packed red blood cell units were prepared. The patient was immediately started on octreotide and pantoprazole infusions with prophylactic ceftriaxone, and he was admitted directly to the intensive care unit. Gastroenterology team was consulted, and they performed an urgent esophagogastroduodenoscopy (EGD) that showed grade 3 esophageal varices with findings suggestive of recent bleeding associated with a large amount of blood in the gastric body that required banding (Figures -).
Upon further evaluation, the patient had a computed tomography (CT) of the abdomen and pelvis, which revealed multiple liver masses with an intraluminal IVC mass extending from the hepatic vein into the right atrium. This mass was thought to be a tumor thrombus that is extending up to the right atrium. Subsequently, a CT scan of the chest was done, and it confirmed the presence of a tumor thrombus in the IVC extending to the right atrium (Figures -).
On further workup, his alpha-fetoprotein level was 53,320 ng/ml. Magnetic resonance imaging (MRI) of the abdomen confirmed the diagnosis of HCC. Oncology team evaluated the patient, and they determined that the patient was not a candidate for surgical or ablative therapies. The patient’s wishes were to avoid any invasive intervention for his thrombus and cancer. Therefore, he was discharged with a plan to receive palliative treatment with sorafenib as an outpatient. After two months of palliative treatment, the patient condition deteriorated, and he decided to switch to hospice, and he passed shortly after that.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [20.0, 'lbs']}",36.28736,34.47299,38.10173,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 20.0 lbs so this converts to 20.0 lbs * 0.453592 kg/lbs = 9.07184 kg. Hence, the patient's maintenance fluid is 9.07184 kg * 4 mL/kg/hr = 36.28736 mL/hr.
Hence, the patient's fluid maintenance is 36.28736 mL/hr."
4957,22,Maintenance Fluids Calculations,physical,decimal,pmc-6753395-1,Extracted,"Chief complaint: A 67-year-old female presented to the emergency department with progressively worsening shortness of breath and fever.
History of present illness: The patient complained of twenty pounds’ weight loss over three months. She had shortness of breath, fever and productive cough for a duration of four weeks.
History of past illness: She had medical conditions of hypertension, chronic obstructive pulmonary disease, gastroesophageal reflux disease, gout and a 40-pack year history of smoking. She lived at home and had a history of exposure to TB when she was 9 years old as well as a known positive tuberculin skin test. She had never traveled outside the country.
Physical examination: Her vital signs were significant for low-grade fever of 37.9 °C, heart rate of 110 beats per minute, blood pressure of 165/100 mm of Hg and oxygen saturation of 96% on room air. She had bilateral rales on lung auscultation and rest of the physical exam was unremarkable
Laboratory examinations: Blood analysis was significant for hyponatremia (sodium 118 mEq/L) and anemia (Hemoglobin 7.3g/dL).
Imaging examinations: Chest X-ray and computed tomography (CT) scan on admission showed bilateral patchy infiltrates predominantly in the upper lobes (Figure ).
Treatment: Ceftriaxone and azithromycin were initiated for community-acquired pneumonia (CAP), and she was admitted to intensive care unit (ICU) for sepsis and hyponatremia. She was also placed in respiratory isolation due to high suspicion for TB. On day 2 of admission, sputum acid fast bacilli (AFB) stain was reported positive, and the patient was started on isoniazid, rifampin, ethambutol, and pyrazinamide (RIPE) for Mycobacterium tuberculosis. Human immunodeficiency virus (HIV) test was negative. Mycobacterium tuberculosis was confirmed by polymerase chain reaction (PCR) before the final culture report. Subsequently, she became progressively more hypoxic and hypotensive requiring mechanical ventilation and vasopressor support. Chest X-ray after intubation showed worsening of bilateral lung infiltrates (Figure ). She developed multi-organ failure secondary to shock including hepatic and renal dysfunction requiring hemodialysis. Patient was also initiated on high dose steroids, and antibiotic coverage was broadened with no significant improvement in hemodynamic status.
Final diagnosis: Septic shock due to Mycobacterium tuberculosis.
Outcome and follow up: Due to poor prognosis and no improvement in the patient’s condition, the family wished for transfer to hospice care and patient died on day 22 of hospitalization. Final culture and susceptibility reports confirmed sensitivity to RIPE.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [20.0, 'lbs']}",36.28736,34.47299,38.10173,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 20.0 lbs so this converts to 20.0 lbs * 0.453592 kg/lbs = 9.07184 kg. Hence, the patient's maintenance fluid is 9.07184 kg * 4 mL/kg/hr = 36.28736 mL/hr.
Hence, the patient's fluid maintenance is 36.28736 mL/hr."
4958,22,Maintenance Fluids Calculations,physical,decimal,pmc-3349517-1,Extracted,"A 22-year-old girl, born from unrelated healthy parents of Tunisian origin, during the neonatal period had received BCG immunization without any local or systemic responses. From 6 months of age she had recurrent episodes of bronchopulmonary and gastrointestinal infections. At 10 years, she was referred to our hospital for the first time. On physical examination, she was growth retarded with a weight of 20 kg (-2.2SD) and height of 121 cm (-2SD). Tuberculin skin test was negative. Immunologic examination revealed decreased serum IgG levels: 5 g/l (5.6-16.1), low serum IgA: 0.4 g/l (0.5-2.5), and serum IgM levels within the normal range of age: 0.8 g/l (0.5-1.8). Lymphocyte subsets produced the following: CD3 = 2 × 109cells/L (1.2-2.6), CD4 = 1 × 109cells/L (0.65-1.5), CD8 = 1 × 109cells/L (0.37-1.1), CD19 = 0.374 × 109cells/L (0.27-0.86). The diagnosis of MHC class II deficiency was established on the basis of the loss of MHC II expression on peripheral blood lymphocytes and PHA activated T cells related to homozygous 752delG25 mutation in the RFXANK gene (Figure ). She was started on intravenous immunoglobulin (0.4 g/kg by 3 weeks) and cotrimoxazole sulfamethoxazole prophylaxis (25 mg/kg, 3 times a week). Bone marrow transplantation could not be performed because no compatible donor was identified. At the age of 12, she had multiple, pale, painless, lesions on her buccal mucosa (Figure ). The lesions were firm on palpation, covered by healthy, normal appearing mucosa, neither ulcerated nor inflamed, but her dental hygiene was poor. Sexual abuse was denied by the patient. A biopsy of the oral lesions with histological examination was performed; HPV infection was diagnosed. HPV typing performed on the tissue obtained at biopsy showed HPV type 6. HLA typing revealed an HLA DQB1*0301phenotype. The patient was treated by laser with partial response. She has a Karnofsky Performance Scale Index score of 50%.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [20.0, 'kg']}",60,57,63,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 20.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (20.0 kg - 10 kg) = 60.0 mL/hr.
Hence, the patient's fluid maintenance is 60.0 mL/hr."
4959,22,Maintenance Fluids Calculations,physical,decimal,pmc-7919995-1,Extracted,"An 87-year-old man (weight 80.9 kg, height 1.79 m and BMI 25.3 kg/m2) presented with a syncope and fall at the emergency department. Upon arrival (at 4 p.m.) he was well oriented; BP (seated) was 168/59 mmHg with a regular pulse at 65/min (auscultatory). He had dyspnea (respiratory rate 15/min) with an arterial O2 saturation of 89 % (98 % after oxygen administration). His mouth mucosa was dry and he had bilateral pulmonary stasis, but no jugular tumescence. There was a slight degree of peripheral pitting edema and he had a urethral catheter. The neurologic examination was repeatedly normal; his MMSE score was 25/30. His basic ADL (Katz-scale) was 8/24; the instrumental ADL score (Lawton) was 15/27. He was mobile with a four-wheel walker under supervision from his wife. He was a previous smoker and admitted drinking three alcohol consumptions per day on average. His non-fasting glycemia was 107 mg/dL (fasting reference values 70–100 mg/dL) and follow-up revealed neither hyper- nor hypoglycemia; his hemoglobinemia was 12.6 g/dL (reference values: 13.0- 16.5 g/dL).
OH had been documented since approximately three years, with a systolic BP varying between 73 and 93 mmHg. An orthostatic test, two years before the present admission, had shown a BP of 184/111 mmHg and a heart rate (HR) of 73/min. in supine position. After standing one minute, BP was 98/70 mmHg and pulse rate 85/min; after three minutes 99/71 mmHg and 82/min.; after five minutes 98/63 mmHg and 78/min. He presented almost weekly syncopes and falls, mainly occurring after meals or physical effort. Convulsions, lasting ± 30 seconds, had been observed once. His medical history mentioned atrial fibrillation (with periods of slow ventricular response), bronchiectasis, colon diverticulosis, urge incontinence and urine retention, treated by trans-urethral catheter, and bilateral hip prosthesis for osteoporotic fractures after falls. Three months earlier, during a hospitalization for OH (86/53 mmHg), a discrete rigidity of the right arm and a slight bilateral tremor of the hands had been noted, suggesting an essential tremor or a beginning PD. It had been concluded that he suffered from severe OH, mainly due to sodium and fluid deficit, resulting in cerebral hypoperfusion. Several investigations had already been completed recently. A transthoracic cardiac ultrasound examination had shown no signs of cardiac amyloidosis, and a primary adrenal cortical failure was excluded.
His medication upon arrival consisted of rivaroxaban 15 mg q.d., amiodarone 200 mg q.d., bumetanide 1 mg q.d., spironolactone 25 mg q.d., fludrocortisone 0.1 mg b.i.d., finasteride 5 mg q.d., folic acid 4 mg q.d., calcium carbonate 1000 mg q.d., cholecalciferol 800 IE q.d., zolendronate 5 mg i.v. once a year, and paracetamol 1 g if necessary. He had been advised to wear elastic stockings, rise slowly, apply a mild anti-Trendelenburg position during the night, avoid large meals, and drink sufficiently.
Upon admission to the geriatric ward amiodarone and finasteride were stopped. He developed a pneumonia, empirically treated with piperacilline and tazobactam. This treatment was successful, but he developed heart failure, necessitating fludrocortisone to be stopped.
A CT scan of the brain showed slight cortico-subcortical and cerebellar atrophy, and some small lacunar infarctions in the basal ganglia. An EEG was normal. Given the history of syncopes, hypotension, and bradycardia, the cardiologist advised a coronaroangiography that showed only a moderate stenosis at two sites. An ultrasound examination of the neck showed no arterial stenosis, but revealed a multinodular thyroid goiter (thyroid hormone levels were found to be normal). An electromyography showed signs of length-dependent chronic axonal sensory-motoric polyneuropathy.
He had a calculated MDRD of 40ml/min, with normal renal ultrasound examination and no signs of renal artery stenosis. Continuous ECG registration confirmed a regular sinus rhythm with an average frequency of 52/min, (33–61/min) and a second degree A-V block Mobitz type II. Placing of a pacemaker normalized the heart rhythm, but syncopes and daytime OH persisted.
24-hours BP registration revealed a reversal of the day-night rhythm with hypotension during the day and hypertension during the night (see Fig. ). The daytime average systolic, diastolic, and mean arterial pressures (StDev) were respectively 98 (33.7), 59 (19.2), and 72 (24.0) mm Hg; during the night these values were respectively 147 (17.0), 85 (8.8), and 106 (11.4) mm Hg. Trying to control the BP, bumetanide and spironolactone were stopped, and fludrocortisone (0.5 mg) was given in the morning and captopril (12.5 mg) in the evening. With this treatment, BP values varied between 80 and 180 mmHg with a tendency for improvement towards the end of his hospitalization that continued afterwards.
A PET brain scan showed no arguments for Lewy body disease. An 18 FDG PET CT brain scan demonstrated cerebellar hypometabolism, arguing in favour of MSA.
Due to the 2020 Covid 19 pandemic, we could not realize a follow-up 24 h BP registration. However, the patient reported a clear improvement with a significant reduction of symptomatic events.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [80.9, 'kg']}",120.9,114.855,126.945,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 80.9 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (80.9 kg - 20 kg) = 120.9 mL/hr.
Hence, the patient's fluid maintenance is 120.9 mL/hr."
4960,22,Maintenance Fluids Calculations,physical,decimal,pmc-5013576-1,Extracted,"A previously healthy 36 year-old Caribbean woman, G4P2012, presented at 8 weeks gestation, with a 1-week history of worsening swelling in her hands and feet. Her prior pregnancies were without complication, and she took no medications other than prenatal vitamins. She had no personal or family history of kidney disease or immunodeficiency. Her prenatal workup was unremarkable and HIV test negative. Her physical exam on presentation was significant for a blood pressure of 146/95 mmHg, and 3+ pitting edema up to her knees. Approximately 1 month prior to presentation, her 4-year-old daughter had experienced a classic presentation of “Fifth disease” from parvovirus B19. On admission, an obstetrical ultrasound revealed fetal demise and she underwent a dilation and curettage procedure. Products of conception were not sent for parvovirus staining as the obstetrical team felt her presentation was entirely consistent with acute parvovirus infection.
Notable laboratory and imaging results included serum creatinine concentration (SCr) of 557 umol/L (6.3 mg/dL), blood urea nitrogen of 15.3 mmol/l (43 mg/dL), serum albumin 15 g/L (1.5 g/dL), total cholesterol 10.55 mmol/L (408 mg/dL), triglycerides 7.01 mmol/L (621 mg/dL), LDL 7.86 mmol/L (304 mg/dL), INR 0.96, PTT 33 s, and PT 10.7 s. A spot urine protein:creatinine ratio was 20.8 g/g. Urine microscopy revealed 2–5 white blood cells per high power field and maltese crosses were diffusely present upon polarization. Further serologic workup was negative, including ANA, anti-dsDNA, repeat HIV test, and for hepatitis B and C. Serum parvovirus B19 qPCR detected the parvoviral genome with a modest viral load of approximately 2000 copies, and parvovirus serologies both IgM and IgG were elevated demonstrating acute infection. While, “undetected” would be the reported result for unexposed individuals, the clinical virology lab reports that their sensitive qPCR assay allows for viral load quantification from approximately 200 copies to over 1X1010 (with the higher values only seen in immunocompromised and sickle cell patients who present early and without adequate immune response). Renal ultrasound revealed normal sized kidneys bilaterally and slight increase in echogenicity, but without hydronephrosis, cysts, or calcifications.
The patient underwent renal biopsy (Fig. ) on day 3 of presentation, with a limited biopsy sample revealing 10 mostly unremarkable glomeruli aside from few swollen and vacuolated podocytes found focally and segmentally. There was acute tubular injury with simplification of tubular epithelium, loss of brush border staining, and dilated tubular lumina, as well as a moderate interstitial inflammatory infiltrate without significant tubulointerstitial scarring. Immunofluorescence was not done due to sample inadequacy. Electron microscopy demonstrated patent capillary loops with minor basement membrane irregularity, but no immune complex deposits or tubuloreticular inclusions. There was global podocyte foot process effacement. Immunohistochemistry for parvoviral proteins (Cell Marque R29F6 mouse monoclonal antibody [, ], 1:100 dilution, with appropriate negative controls) was performed after the time of clinical care, and demonstrated positivity in hypertrophic podocytes, parietal epithelial cells, and tubular cells (Fig. ). Given her clinical diagnosis of acute parvovirus infection, and the glomerular changes along with the microcystically dilated tubules, the biopsy was interpreted as showing changes suggestive of Collapsing Glomerulopathy with acute tubular injury and mild active interstitial nephritis. The hope was that, if attributable to parvovirus, this injury would improve with self-limited resolution of viral infection over time. She was treated with oral prednisone (60 mg daily) for the interstitial nephritis. Her SCr did not improve, and peripheral edema worsened despite diuretics. Two weeks later, she was re-biopsied to determine a more definitive diagnosis. A total of nine glomeruli were present, two segmentally sclerotic with more pronounced podocyte hypertrophy and hyperplasia, and prominent microcystically dilated tubules. Immunofluorescence microscopy was performed and was negative for immune reactants. A diagnosis of CG, likely virally-mediated, was made.
She was discharged home after 3 weeks of hospitalization, with tapering prednisone and an aggressive diuretic regimen. She returned 6 days later with orthostatic hypotension despite persistent anasarca (80+ pounds above her baseline). Her serum albumin was 10 g/L (1.0 g/dL). Water immersion therapy with diuresis was attempted in an effort to alleviate the patient’s edema, but had little effect.
Her SCr had improved to 309 umol/L (3.5 mg/dl) by 5 weeks after presentation, but she then developed pancytopenia. Serum hemoglobin fell to 50 g/L (5 g/dL), platelet count to 15,000/uL, and ANC as low as 1700/uL with an inadequate rise in reticulocyte count. Serum lactate dehydrogenase and haptoglobin remained normal. Bone marrow biopsy showed a markedly hypocellular marrow with mild dyserythropoesis. While no viral inclusions or hemophagocystosis were found, her serum ferritin rose to 2260 ug/L. This was proposed to be from parvovirus-related inflammation, which has been reported previously []. Repeat parvoviral testing showed persistently detectable low levels of virus in the 200–1000 copy range. Intravenous immunoglobulin (IVIG) was started for multi-organ complications of parvovirus, despite low copy numbers. Preparations of IVIG contain parvovirus specific antibodies at concentrations capable of neutralizing parvoviral antigens [, ] and have been shown to be helpful in eradicating parvovirus B19-associated anemia [, ]. IVIG dosing was empiric, and notably, most of the infusion was lost in the urine (proteinuria up to 60 g/day following infusion). Dosing was continued at 1 g/kg every other day, and eventually quantitative PCR showed estimated viral copy number less than 200 copies, although persistently detected. Because she had no initial response to the IVIG and her pancytopenia was severe, she also received intravenous solumedrol (60 mg daily for 2 weeks, then tapering). After a total of 1 month of hematologic issues, cell counts returned to normal. Initially after beginning IVIG treatment, the SCr reached a nadir of 256 umol/L (2.9 mg/dl), but with her worsening pancytopenia, kidney function worsened, and SCr rose to over 530 umol/L (6 mg/dl).
A third renal biopsy was undertaken 10.5 weeks after initial presentation to help decide whether to consider cytotoxic therapy for FSGS in a now fairly debilitated young woman. Due to the extent of disease progression on this biopsy, the decision was made to forego any cytotoxic therapy and to initiate dialysis for uremia and volume management.
Given the uncommon severity of this case and the possibility of African ancestry given her Caribbean origin [], the possibility of a genetic susceptibility to podocyte injury was considered. To investigate this, venous blood was collected in the setting of an IRB-approved research protocol and genomic DNA was extracted and sent for whole exome sequencing by Illumina HiSeq 2000 technology. The authors used well validated scripts made available by the Yale Genetics/Yale Center for Genomic Analysis [] to curate, align, and annotate the sequencing data. Mean coverage was 57.4 reads, and there was 92.4 % 10x coverage. As hypothesized may be the case, our patient carries two APOL1 risk alleles (homozygous missense variants p.S342G and p.I384M which together comprise the G1 risk allele). For completeness, the following 50 additional genes with published association with glomerular diseases were also assessed: ACTN4, ADCK4, ALG1, ALMS1, ANLN, APOA1, APOL1, ARHGAP24, ARHGDIA, ATGB4, B2M, CD151, CD2AP, CFH, COL4A3, COL4A4, COQ2, COQ6, CRB2, CUBN, DGKE1, EMP2, FGA, FN1, GLA, INF2, ITGA3, ITGB4, LAMB2, LMX1B, LYZ, MEFV, MYH9, MYO1E, NEIL1, NLRP3, NPHS1, NPHS2, PAX2, PDSS2, PLCE1, PLCG2, PMM2, PTPRO, SCARB2, SMARCAL1, TRPC6, WDR73, WT1, ZMPSTE24. There were no loss of function (nonsense, frameshift, splice site) variants, nor were there any rare non-synonomous variants with predicted deleterious consequence in these genes.
Over the subsequent 2 months on hemodialysis, the patient became anuric. Her serum albumin climbed to 3.0 g/L (by 5 months after her initial presentation). She was evaluated for transplantation, and successfully received a living donor kidney transplant from her sister 8.5 months after initial presentation and 6 months after starting hemodialysis. Our findings of the patient’s APOL1 genotype were made available to transplant physicians during transplant evaluation and clinical genetic testing was suggested to the patient’s donor (sister) but she declined. As there are no established guidelines in place for APOL1 testing of donor organs, the donation was accepted. With over 6 months of follow-up, her renal function fortunately remains excellent, with <500 mg proteinuria, and no anemia.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [80.0, 'lbs']}",76.28736,72.47299,80.10173,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 80.0 lbs so this converts to 80.0 lbs * 0.453592 kg/lbs = 36.28736 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (36.28736 kg - 20 kg) = 76.28736 mL/hr.
Hence, the patient's fluid maintenance is 76.28736 mL/hr."
4961,22,Maintenance Fluids Calculations,physical,decimal,pmc-5362839-1,Extracted,"A 5-month-old female intact feral kitten presented to the local animal shelter unable to ambulate after being trapped underneath a garage door. A board-certified neurologist (KMV) localized the lesion to the C5 to brainstem region. Cervical and thoracic radiographs showed no evidence of cervical fracture, but a mild bronchointerstitial pulmonary pattern was noted. As per routine protocol of the shelter, imidacloprid/moxidectin (Advantage Multi for Cats; Bayer) was applied to the kitten and a 5 day course of fenbendazole was initiated at 50 mg/kg PO q24h.
The kitten was placed in foster care once able to ambulate 5 days later, and although it continued to improve neurologically, respiratory signs of tachypnea, cough and wheezing suddenly worsened in frequency and severity 9 days later. On day 10, the cat presented to the University of California, Davis, William R Pritchard Veterinary Medicine Teaching Hospital for a further diagnostic work-up. On physical examination the kitten weighed 1.7 kg, heart rate was 180 beats per minute, respiratory rate was 70 breaths per minute with wheezing and rectal temperature was 103.0ºF. Complete blood count results included a mild normocytic normochromic non-regenerative anaemia, likely age related (haematocrit 27%; reference interval [RI] 30–50%), and a white blood cell count of 6098/μl with neutrophils (4025/μl; RI 2000–9000/μl), lymphocytes (1342/μl; RI 1000–7000/μl) and eosinophils (305/μl; RI 150–1100/μl) within RIs, and a slight left shift (band neutrophils 183/μl; RI 0/μl). Serum biochemistry results included hyperkalemia (5.3 mmol/l; RI 3.6–4.9 mmol/l), hypochloremia (115 mmol/l; RI 117–126 mmol/l), hyperphosphatemia (9.0 mg/dl; RI 3.2–6.3 mg/dl) and increased alanine aminotransferase (103 IU/l; RI 27–101 IU/l) and creatine kinase (722 IU/l; RI 73–260 IU/l).
Thoracic radiographs revealed a severe diffuse bronchointerstitial pulmonary pattern with peribronchial cuffing and ill-defined pulmonary nodules. Soft-tissue opacities dorsal to the carina and the second and third sternebrae were interpreted as lymphadenomegaly (). Differentials included infectious etiologies such as toxoplasmosis, feline infectious peritonitis and cryptococcosis. Serology was considered but was thought less likely to be helpful in the diagnosis. Parasitic pulmonary disease was considered less likely due to previous treatment with fenbendazole and neoplasia (lymphoma) was also lower on the differential list.
Given the severity of thoracic radiographic findings, the kitten was prepped for anesthesia to undergo a laryngoscopy/bronchoscopy and bronchoalveolar lavage (BAL). Premedication was provided with butorphanol 0.6 mg/kg (1.03 mg) subcutaneously, flow-by 100% oxygen was provided and induction was performed with alfaxalone 1.0 mg/kg (1.7 mg) and midazolam 0.3 mg/kg (0.5 mg) intravenously. A jet ventilator was used to provide oxygenation at 180 pulses per minute, and anaesthesia maintained with an alfaxalone constant rate infusion to effect (4.12 mg/kg infused). A 2.8mm outer diameter video-endoscope (Flex XC; Karl Storz Veterinary Endoscopy) was utilized for bronchoscopy. Moderate laryngeal, tracheal and bronchial hyperemia was noted along with excessive mucus accumulation (). BAL was performed in the left and right caudal lung lobes and was submitted for cytologic evaluation. Copious amounts of tracheal mucus were expectorated and a swab collected from the oropharynx was also submitted for cytologic evaluation.
BAL fluid was hypercellular (1010 and 1100 cells/µl, right and left, respectively; RI 300–400/μl) with 62% and 50% neutrophils (normal 5–8%) and 22% and 25% eosinophils (normal <20%) (). Increased numbers of multinucleate giant cells, goblet cells and mast cells were also present, along with epithelial hyperplasia. Swabs of oropharyngeal mucus revealed a dense background of mucus with neutrophilic and eosinophilic inflammation, numerous free mucus granules and evidence of mineralization. Five large parasitic (helminth) larvae were observed on one slide (), including one that appeared to have a dorsal spine on the tail. The oropharyngeal sample was submitted to the University of Teramo for molecular identification of larvae. DNA was extracted using a commercially available kit (QIAgen Mini Kit; Qiagen), and nested PCR was performed targeting the ITS2 region of Aelurostrongylus abstrusus and Troglostrongylus brevior, as previously described. PCR was positive for A abstrusus at the 233 base-pair region and negative for T brevior at the 356 base-pair region ().
The kitten was discharged with application of a second dose of imidiclopid/moxidectin, and fenbendazole was prescribed at 50 mg/kg PO q24h for 10 days. Three weeks later, the kitten was doing clinically well at home but still coughing intermittently. Radiographs revealed marked resolution in the bronchial pattern with partial resolution of peribronchial cuffing and ill-defined nodules (). Fenbendazole was prescribed for an additional 5 days at 50 mg/kg/day. All respiratory signs had resolved at the time of ovariohysterectomy 3 weeks later, and radiographs 2 months after the final treatment were normal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1.7, 'kg']}",6.8,6.46,7.14,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1.7 kg. Hence, the patient's maintenance fluid is 1.7 kg * 4 mL/kg/hr = 6.8 mL/hr.
Hence, the patient's fluid maintenance is 6.8 mL/hr."
4962,22,Maintenance Fluids Calculations,physical,decimal,usmle-1786,Extracted,"A 72-year-old man comes to the emergency department for progressively worsening abdominal pain. The pain began 2 weeks ago and is localized to the right upper quadrant. He feels sick and fatigued. He also reports breathlessness when climbing the stairs to his first-floor apartment. He is a retired painter. He has hypertension and type 2 diabetes mellitus. He is sexually active with one female partner and does not use condoms consistently. He began having sexual relations with his most recent partner 2 months ago. He smoked 1 pack of cigarettes daily for 40 years but quit 10 years ago. He does not drink alcohol. Current medications include insulin and enalapril. He is 181 cm (5 ft 11 in) tall and weighs 110 kg (264 lb); BMI is 33.5 kg/m2. His vital signs are within normal limits. Physical examination shows jaundice, a distended abdomen, and tender hepatomegaly. There is no jugular venous distention. A grade 2/6 systolic ejection murmur is heard along the right upper sternal border.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [110.0, 'kg']}",150,142.5,157.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 110.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (110.0 kg - 20 kg) = 150.0 mL/hr.
Hence, the patient's fluid maintenance is 150.0 mL/hr."
4963,22,Maintenance Fluids Calculations,physical,decimal,pmc-5070337-1,Extracted,"A 22-year-old, 48-kg female patient with a 6-month history of temporomandibular joint pain was scheduled for bilateral temporomandibular meniscopexy. The patient underwent an uneventful general anesthesia for an appendectomy at age 10.
The patient was admitted to surgery with a heart rate of 92 bpm, respiratory rate of 16 breaths per minute, blood pressure of 128/78 mmHg, and oxygen saturation on room air at 91%. Preoxygenation was performed, and induction was begun with midazolam 2 mg, intravenous (IV), remifentanil 0.14 µg/kg/min IV, propofol 140 mg IV, and rocuronium 35 mg IV. Following intranasal application of oxymetazoline HCl 0.025%, five drops, and topical lidocaine gel, the nasotracheal tube was inserted, with confirmation of proper placement through symmetrical auscultation and capnography. As the nasotracheal tube was being fixed, the patient presented sinus bradycardia associated with ST changes, which rapidly progressed to supraventricular tachycardia with a heart rate of 168 bpm, hypotension, desaturation, and piloerection with persistence of ST changes. Increased airway pressure associated with rhonchi was noted, and therefore, bronchospasm was considered to be a possible etiology. After four puffs of salbutamol and 100 mg hydrocortisone IV, bloody material was seen coming from the nasotracheal tube, compatible with pulmonary edema. A chest X-ray was ordered, which showed severe bilateral pulmonary edema []. In the light of these findings, an emergency TEE was performed.
The TEE showed severe left ventricular dysfunction with akinesia of the apical and mid segments of the anterolateral and septal walls, hypokinesia of the anterior and anteroseptal walls, with spared of the basal segments of the septal and inferior septal and inferior walls. The right ventricle was moderate dilated with a mild dysfunction and moderate tricuspid regurgitation. The cardiac output was calculated at 1.8 l/min with Left ventricular outflow tract velocity time integral method [ and ]. Vasopressor support was begun with noradrenaline at 0.1 µg/kg/min IV, with which the patient improved slowly, reaching a heart rate of 103 bpm, blood pressure of 94/66 mmHg, and oxygen saturation at 92 at 100% FiO2%. Vasopressor support was continued, surgery was canceled, and the patient was transferred to the Intensive Care Unit (ICU) for stabilization.
In the ICU, a pulmonary artery catheter was placed, showing a cardiac index of 1.63 l/min/m2, and a wedge pressure of 20 mmHg, with normal systemic and pulmonary resistance. A transthoracic echocardiogram reported severe biventricular dysfunction with hypokinesia of the distal third of the anterior and inferior septum, and therefore, treatment was started with milrinone at 0.5 µg/kg/min IV []. troponin I on the day one was 3.7 ng/mL, and the troponin on the second day was 0.7 ng/mL (normal value <0.1 ng/mL). The patient continued a gradually favorable course with a progressive increase in the cardiac index to 3.1 l/min/m2, and an ejection fraction up to 60% [ and ]. She was weaned from mechanical ventilation on the second day and discharged from the ICU on the 6th day postoperative. The following day, cardiac catheterization was performed, in which no coronary disease was found [].","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [48.0, 'kg']}",88,83.6,92.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 48.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (48.0 kg - 20 kg) = 88.0 mL/hr.
Hence, the patient's fluid maintenance is 88.0 mL/hr."
4964,22,Maintenance Fluids Calculations,physical,decimal,pmc-3498671-1,Extracted,"A 4-year-old, male patient, 18.4 kg in weight, physical status I according to the classification system of the American Society of Anesthesiologists (ASA) was admitted to our institution for right retinal detachment surgery. On admission, there was no significant past or family history of medical diseases and no evidence of pulmonary or cardiac disease on physical examination. Preoperative vital signs were as such blood pressure of 100/65 mmHg, heart rate 92 and O2 saturation (SpO2) 100% on room air. The patient was premedicated with oral midazolam 0.5 mg/kg. In the operating room, standard intraoperative monitoring three-lead electrocardiogram (ECG), noninvasive blood pressure, end-tidal carbon dioxide (EtCO2), peripheral nerve stimulator, temperature probe and pulse oximetry were applied. Anesthesia was induced with sevoflurane in oxygen. Following insertion of a 22-gauge cannula, he received glycopyrrolate (5.0 μg/kg), propofol 25 mg, fentanyl 50 mg and cis-atracurium 0.15 mg/kg intravenously. After induction of anesthesia, paracetamol suppositories 500 mg were given. Anesthesia was maintained with sevoflurane 2-2.5% in a mixture of nitrous oxide and oxygen (60%:40%). Intermittent doses of cis-atracurium (0.03 mg/kg) every 20-40 min were injected as needed to keep muscle relaxation based on neuromuscular stimulation. The patient was mechanically ventilated, and it was adjusted to provide an end tidal CO2 concentration of 30–35 mmHg, maintain peak airway pressure below 15 cm H2O and an oxygen saturation of ≥98% with 40% oxygen. Ringer's lactate solution was administered according to the standard fluid administration guidelines during anesthesia. Normothermia was maintained during the whole procedure by the use of a forced air warming device. Few minutes later, after start of surgery, the noninvasive blood pressure, which was around 90/55 mmHg, suddenly rose to 220/120 mmHg and the heart rate, previously around 75 beats/min, increased to 140 beats/min (sinus rhythm). Initially, the inspired sevoflurane concentration was increased to increase the depth of anesthesia. On questioning the surgeon, the earlier administration of two drops of 10% ocular phenylephrine to the right eye was confirmed for further dilation of inadequate dilated pupil. A diagnosis of severe hypertension secondary to systemic absorption of ocular phenylephrine was suspected. Subsequently, while preparing the antihypertensive medication, the monitors displayed increased airway pressure and oxygen saturation drop from 99% (with an inspired oxygen concentration (FiO2) of 0.4) to 82%. Auscultation revealed crepitations throughout the chest and a blood-stained frothy fluid was aspirated from the trachea. There was neither clinical evidence of airway obstruction nor aspiration on examination and a diagnosis of pulmonary edema was justified at that time. Therefore, fluid administration was stopped, hydralazine (5 mg) and furosemide (10 mg) were administered intravenously, manual ventilation with 100% oxygen was commenced and suctioning via the tracheal tube was performed several times. Seven minutes later, the blood pressure returned to normal and SpO2 increased to 92%, with decreased intratracheal secretions. After approximately 20 min, the SpO2 had improved to 99% (with a FiO2 of 1.0), the blood pressure was 109/63 mmHg and the heart rate was 121 beats/min. A Foley catheter was inserted and the urine output was 280 mL. Surgery was completed, mechanical ventilation was regained with a positive end expiratory pressure (PEEP) of 5 cm H2O and FiO2 gradually reduced back to 0.4 over 30 min with no further desaturation. After surgical closure, auscultation of the chest revealed no crepitations. Then, inhalational anesthetic was discontinued, the fresh gas rate was changed to 6 L/min of oxygen and neuromuscular block was reversed with neostigmine (0.04 mg/kg) and atropine (0.02 mg/kg). Tracheal extubation was done when the train-of-four response was 90% and the patient demonstrated facial grimace and spontaneous opening of his eyes with adequate tidal volume and respiratory rate. The patient was transferred to the post anesthesia care unit (PACU) with oxygen via a face mask. A postoperative 12-lead ECG showed sinus rhythm and chest radiography revealed no evidence of pulmonary edema. Oxygen 3 L/min was administered through a face mask for 5 h postoperatively and then the patient was discharged from the PACU to the ward conscious and oriented, with a blood pressure of approximately 100/55 mmHg and O2 saturation of 98% on room air and normal chest auscultation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [18.4, 'kg']}",56.8,53.96,59.64,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 18.4 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (18.4 kg - 10 kg) = 56.8 mL/hr.
Hence, the patient's fluid maintenance is 56.8 mL/hr."
4965,22,Maintenance Fluids Calculations,physical,decimal,pmc-1488855-1,Extracted,"A 51-year-old HIV-positive homosexual man, who has been followed at our hospital since 1992 for HIV, was admitted in June 2004 for persistent low-grade fever, night sweats and a 12 kilogram weight loss over one year. He was treated with antiretroviral therapy since 1995 and HAART since 1997. Unfortunately, the emergence of HIV variants with multiple resistance gene mutations resulted in a high HIV load and low CD4+ T cell count. At the time of admission, the patient's CD4+ T cell count was 8 cells/μl, and his HIV RNA level was 792,000 copies/ml. The body temperature ranged from 37°C to 38°5C. Physical examination revealed an enlarged liver and an extensive well-demarcated, violaceous plaque on the left ankle with 5 additional small violaceous nodules disseminated on the head, trunk and left leg, suggesting a diagnosis of bacillary angiomatosis (BA). A chest CT scan revealed a left lower-lobe density and sputum smears were positive for acid-fast bacilli (AFB). Pelvic CT scan revealed an inflammatory swelling within the right gluteus muscle that was biopsied as were the cutaneous lesion of the left ankle and the bone marrow.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.0, 'kg']}",44,41.8,46.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.0 kg - 10 kg) = 44.0 mL/hr.
Hence, the patient's fluid maintenance is 44.0 mL/hr."
4966,22,Maintenance Fluids Calculations,physical,decimal,pmc-8210642-1,Extracted,"A 58-year-old male patient presented with symmetrical edema of the upper limbs (), lower limbs (), and scrotum, in conjunction with chronic diarrhea. He weighed 48 kg, with a height of 1.58 m, giving a body mass index (BMI) of 19.2 kg/m2, and his primary complaints were paroxysmal nocturnal dyspnea when in decubitus and impaired quality of life because of dyspnea and food intolerance.
The patient had a prior history of congenital edema of the lower limbs and refractory ascites in childhood, associated with diarrhea with food intolerance to any type of diet with lipid components, which still remains. He also had a history of peritoneal tuberculosis that had been treated 30 years previously and an enlarged prostate.
Laboratory tests conducted in June 2019 revealed below normal serum levels of the following elements: zinc, ionic calcium, and magnesium. The patient brought abdominal tomography showing thin and wrinkled jejunal mucosa and prominent Kerckring folds in the ileum, with an appearance suggestive of jejunization of the ileum, bilateral pleural thickening, with costophrenic angle blunting, free liquid in the abdominal cavity, and multiple calcifications distributed throughout the peritoneal cavity, with appearance compatible with remnants of the prior tuberculosis.
Computed tomography with contrast () showed evidence of edema of small intestine loops. Colonoscopy () was able to identify lymphatic congestion in the ascending colon and lymphatic hyperplasia in the ileum.
Lymphoscintigraphy () showed non-obstructive dysfunction of lymphatic drainage of the lower limbs, lateral dermal backflow and rapid ascent of lymph through the lower limbs, but did not identify lymph vessels. Serum tests conducted in August 2019 showed complement, globulins, serology, triglycerides, total and partial cholesterol, and fecal fat tests.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [48.0, 'kg']}",88,83.6,92.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 48.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (48.0 kg - 20 kg) = 88.0 mL/hr.
Hence, the patient's fluid maintenance is 88.0 mL/hr."
4967,22,Maintenance Fluids Calculations,physical,decimal,pmc-5662356-1,Extracted,"A 12-year-old boy presented with recurrent fever for more than 2 years and was referred to Peking Union Medical College Hospital in 2014. The recurrent fever began without obvious predisposition and lasted 4 to 14 days per attack. The intervals between episodes range from 4 to 20 days. Temperature peak was up to 40°C. No cough, expectoration, rash, joint pain, or other discomfort appeared. He was referred to local clinics and had been diagnosed with Epstein–Barr virus (EBV) infection many times with positive EBV antibodies (EBV-Ab) and elevated plasma virus copies. Details of his physical examination, laboratory results, and therapies were unavailable.
He visited a hospital in Beijing owing to another fever in February 2014. Enlargement of lymph nodes and hepatosplenomegaly were discovered in physical examination. Assay of EBV-Ab and virus copies were performed, which indicated that IgA/early antigen (EA), IgA/viral capsid antigen (VCA), IgG/VCA, NA-IgG were positive and the virus copies were elevated to 3.45 × 10^5/mL. Diagnosis of EBV infection was made and then ganciclovir was employed, which ameliorated his symptoms and reduced the virus copies.
In May 2014, his fever relapsed and then he was referred to Peking Union Medical College Hospital for further treatment. Reviewing the history of the patient before the onset of recurrent fever, we found that he had frequent respiratory infections with twice a month. Physical examination indicated that his growth and development were within normal limits, weighing 38.5 kg and 146 cm in height (both in the range of the tenth percentile to the twenty-fifth percentile). Ichthyosis rash could be seen on his lower limbs. Several enlarged lymph nodes were palpable in the anterior region of the neck. No erythema or exudate of the throat or enlargement of tonsils was observed. There were no obvious abnormalities with cardiopulmonary examination. On the abdominal physical examination, hepatomegaly was found with 2 cm below the ribs, medial hardness, and a clear margin. Spleen could not be palpated. No deformity of joints was found as well.
On laboratory examination, peripheral blood count showed a decreased number of neutrophils and proportions of lymphocytes and neutrophils were inverse (63.2% and 25.9%, respectively). Acute phase reactants increased (erythrocyte sedimentation rate was 34 mm/h and C reactive protein was 15 mg/L). Liver function tests revealed slightly elevated glutamic oxaloacetic transaminase (AST) and normal alanine aminotransferase (ALT) (see Fig. ). Serum immunoglobulin was normal (IgG, 16.44 g/L; IgA, 5.24 g/L; IgM, 0.75 g/L) with decreased T cells in the peripheral blood (see Table ). Table summarizes the values of lymphocyte subsets changing with time and therapy. The numbers of CD3+ T cell especially the CD4+ T cell markedly decreased, while NK cell significantly increased. These abnormal results persisted despite treatment with cyclosporine A for 4 months from July 2015 to November 2015. Recombinant human interferon α-2a began to be used in November 2015 with a dose of 1 MU, 3 times a week. Four months later in February 2016, the above abnormality still existed despite the remission of his symptoms and improvement of other laboratory examinations. Dosage of recombinant human interferon α-2a was then added to 2 MU, 3 times a week. Henceforward, the values of lymphocyte subsets gradually returned to normal level. Positivity of EBV-Ab (see Table ) and elevated virus copies (1.5 × 10^6 copies/mL, see Fig. ) were observed. As we can see in Table , IgA/EA, IgA/VCA, IgG/VCA, NA-IgG were persistently positive no matter what treatment was used. Abdominal ultrasonography indicated hepatosplenomegaly (oblique diameter of right lobe of liver was 13.0 cm and spleen diameter was 14.3 cm). Cardiac ultrasound showed that he had patent ductus arteriosus.
His symptoms, abnormal signs, and laboratory indexes repeatedly occurred during the follow-up, which were improved with repeated treatment of ganciclovir. The diagnosis of CAEBV was established on the basis of diagnostics guideline proposed by Okano et al.[ The following aspects of our patient fulfilled the Okano guideline: recurrent infectious mononucleosis-like symptom include fever, swelling of lymph nodes, and hepatosplenomegaly; unusual pattern of anti-EBV antibodies with raised anti-VCA and anti-EA, and detection of increased EBV genomes in the peripheral blood; and exclusion of other chronic illness such as other infections, autoimmune diseases, and neoplastic diseases upon completion of related examinations.
The repeated use of ganciclovir could not prevent the frequent relapses of EBV infection for our patient. The combination of cyclosporine A for 4 months could not reduce the virus copies to normal level as well. With the possibility of immunodeficiency disease, next-generation sequencing (NGS) was performed to analyze all known PID genes followed by Sanger sequencing to verify results. The patient possessed 2 novel compound heterozygous mutations of JAK3 (see Fig. ). The p.H27Q mutation came from his father, while p. R222H from his mother. Thus, his diagnosis was corrected for JAK3-deficiency PID and CAEBV. Antiviral therapy was replaced with subcutaneous injection of recombinant human interferon α-2a with 1 to 2 MU, 3 times a week since November 2015. The virus copies gradually decreased to the normal level and his symptoms ameliorated significantly. Moreover, ALT decreased to normal level after 3 months. His latest follow-up was in February 2017. He has hardly had a fever for nearly 1 year and the virus copies and ALT were normal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [38.5, 'kg']}",78.5,74.575,82.425,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 38.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (38.5 kg - 20 kg) = 78.5 mL/hr.
Hence, the patient's fluid maintenance is 78.5 mL/hr."
4968,22,Maintenance Fluids Calculations,physical,decimal,pmc-7748566-1,Extracted,"A three-day-old male neonate presented to the pediatric ER with a one-day history of lethargy, reluctance to feed, and respiratory distress. He was born of a consanguineous marriage at 39 weeks’ gestation via a normal spontaneous vaginal delivery at home. According to the maternal report, she had no antenatal visits and delivery was uneventful. On further inquiry, it was found that the patient had three male siblings who expired in the early neonatal period, succumbing to similar complaints as that of the patient. The cause of their death was, however, unidentified.
On arrival in the ER, the child was noted to be a plethoric, macrosomic baby with no dysmorphism weighing 4 kilograms (90th percentile) with length and head circumference within the normal limits. On physical examination, the patient looked sick, jaundiced, and drowsy, with the following vital signs: temperature 37°C, respiratory rate 62 breaths per minute, pulse 140 beats per minute, oxygen saturation of 94%, and capillary blood sugar of 22 mg/dL. Palpation of the abdomen revealed a firm, non-tender, enlarged liver, 5 cm below the costal margin. No other viscera were palpable. Neurological examination showed poor neonatal reflexes. Respiratory examination revealed tachypnea, subcostal recessions, and bilateral equal entry of air. The remainder of the physical examination was normal.
The patient was admitted to the neonatal intensive care unit (NICU) and baseline investigations were run. Complete blood counts and renal function tests returned within the normal ranges. Liver function tests revealed conjugated hyperbilirubinemia (direct bilirubin = 61.5 μmol/L), mildly elevated liver enzymes (alanine aminotransferase (ALT) = 106 U/L), and deranged coagulation profile (international normalised ratio (INR) = 1.8). For detailed results at admission, see Table . Results of the laboratory evaluation were notable for hypoglycemia (blood sugar level = 18 mg/dL; 0.999 mmol/L) and a high anion gap metabolic acidosis (anion gap = 24). Blood was drawn during the period of hypoglycemia and sent for insulin levels and serum ketones. First voided urine during the hypoglycemic episode, requesting glucose, ketones, and reducing substances was also sent.
An intravenous bolus of 10% dextrose at the rate of 2 mL/kg was given to correct the hypoglycemia. Vitamin K was administered to treat the raised INR. Intravenous antibiotics were empirically started to cover for presumed sepsis. Despite the above measures, his hypoglycemic state persisted along with a reluctance to feed, therefore, 10% dextrose at the rate of 60 mL/kg/day was intravenously started. The glucose infusion rate was eventually raised to 17 mg/kg/min to maintain his blood sugar levels. Critical samples sent during the hypoglycemic episode yielded negative serum ketones and a serum insulin level of 5 μU/mL (34.7 pmol/L). Urine samples returned negative for ketones and reducing sugar as well. Results of critical samples are mentioned below in Table . Oral diazoxide was started at a dosage of 5 mg/kg/day to treat the hyperinsulinemia. The dosage was later increased to 15 mg/kg/day to meet the patients’ requirements.
Suspicion was high for a metabolic disorder therefore further investigations were run. Urine samples for organic acid chromatography yielded two peaks of succinyl acetoacetate, confirming the diagnosis of hereditary tyrosinemia. Plasma tyrosine and methionine levels were 400 μmol/L and 437 μmol/L, respectively. Serum alpha-fetoprotein (AFP) levels were also raised (AFP = 450 ng/mL). Parents were counseled about the treatment options including dietary management with tyrosine- and phenylalanine-restricted formula and medical management with nitisinone, which is an effective treatment if started early in life. Late complications and the grave consequences, if left untreated, resulting in liver failure and the need for liver transplant in the future were also discussed. At the time of writing the report, the patient was transferred to a tertiary care hospital and was being managed with oral diazoxide at a dosage of 15 mg/kg/day along with a tyrosine- and phenylalanine-restricted formula. The patients' family, however, refused treatment with nitisinone due to the high cost. Genetic counseling was done regarding the risk of disease in future pregnancies and the role of DNA mutation analysis along with measuring succinyl acetoacetate in amniotic fluid during the antenatal period for prenatal diagnosis was highlighted to the family.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.0, 'kg']}",16,15.2,16.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.0 kg. Hence, the patient's maintenance fluid is 4.0 kg * 4 mL/kg/hr = 16.0 mL/hr.
Hence, the patient's fluid maintenance is 16.0 mL/hr."
4969,22,Maintenance Fluids Calculations,physical,decimal,pmc-4753200-1,Extracted,"A 14-year-old girl was admitted to the hospital with fever, chills, malaise, fatigue, and a dull pain in the right subcostal area. She had lost 5 kg in bodyweight in the preceding 3 months. Ten days prior to presentation, she had complained of a remittent fever, with temperatures of up to 39.5℃. Two days prior to presentation, a dry cough and epistaxis had developed. There was no known history of contact with tuberculosis patients. Physical examination revealed a temperature of 38.8℃, cutaneous pallor, and mild tenderness on the right upper quadrant of the abdomen. Lymphadenopathy was detected on the both sides of the neck (a single matted lymph nodes in both side, more than 20 mm ×10 mm in the size that were firm with mild tenderness but not erytherma). There was no splenomegaly or hepatomegaly. Examination of the other systems revealed no abnormalities.
Laboratory investigations undertaken at the initial assessment revealed microcytic hypochromic anemia (hemoglobin, 10.2 g/dL), leukocytopenia (2,020 cells/µL), thrombocytopenia (52,000 cells/µL) with poikilocytosis and atypical lymphocytosis identified in the peripheral smears. The erythrocyte sedimentation rate was increased to 26 mm/hr and the C-reactive protein level was slightly increased to 0.86 mg/L (normal range, <0.5 mg/L). Liver function tests revealed mild abnormalities (alanine transaminase, 54 U/L; aspartate aminotransferase, 153 U/L). We also observed mild hypocalcemia (8.0 mg/dL) with normal phosphorous (2.9 mg/dL) and alkaline phosphatase levels (61.0 U/L). Serum lactate dehydrogenase was 1535 U/L (reference range, 240–480 U/L). The chest radiograph did not reveal any suspicious abnormalities usually associated with pulmonary tuberculosis or pneumonia.
During observation, the fever persisted with a remittent pattern. Pancytopenia was aggravated, and neutropenia was particularly aggravated (neutrophil count, 520 cells/µL). We evaluated the potential causes of the fever of unknown origin (FUO). We started treatment with cefepime for neutropenic fever on the second day. Further laboratory tests revealed elevated levels of lactate dehydrogenase (1,690 IU/L), hypertriglyceridemia (229 mg/dL), and hyperferritinemia (1,420 ng/mL). Multiple lymph node enlargements were detected on abdominal computed tomography (CT). We noted a hypocellular bone marrow with high numbers of histiocytes and marked hemophagocytosis on the bone marrow biopsy performed on day 7 after hospitalization (). The ratio of CD3CD4/CD3CD8 was reduced to 0.53 (normal range, 0.9–3.6) while CD16+CD56+ (natural killer cell activity) was within the normal range. However, caseous granuloma was not noted in the bone marrow specimen. The Mantoux test, acid-fast bacterium stain and culture of sputum revealed negative at that time. Results of several virus tests, including hepatitis A virus (negative for IgM and IgG), cytomegalovirus (negative for IgM, positive for IgG), EBV (negative for viral capsid antigen [VCA] IgM, early antigen R&D IgM and IgG, positive for VCA IgG and Epstein-Barr nuclear antigen IgG), and human immunodeficiency virus tests (negative for antihuman immunodeficiency virus), did not suggest acute infection. Only the venereal disease research laboratory test result was positive. However, the Treponema pallidum hemagglutination assay and fluorescent treponemal antibody-absorption test results were both negative. Results of fluorescent antinuclear antibody test was positive (1:1,280) but those of the rheumatoid arthritis factor test and anti-Smith antibody assay were both negative.
On the basis of these findings, a diagnosis of HLH was made and treatment with high-dose dexamethasone (0.3 mg/kg/day for 7 days and tapering thereafter) and intravenous immunoglobulin (0.5 g/kg/day for 2 days) began on day 8 after hospitalization. At that time, the patient's activated partial thromboplastin time began to prolong to 44.3 seconds (normal range, 29.0–42.0 seconds) and fibrin degradation product was positive. After immune modulation, the fever subsided on day 9 after hospitalization, pancytopenia improved and ferritin level decreased to within the normal range. The PCR tests (AdvanSure TB/NTM real-time PCR using M. tuberculosis complex specific IS6110 and ITS specific primer) with both the bone marrow aspiration and sputum samples were reported to be positive for tuberculosis on day 10 after hospitalization. An antitubercular therapy regimen including 4 drugs—isoniazid 300 mg/day, rifampicin 450 mg/day, ethambutol 500 mg/day, and pyrazinamide 100 mg/day—was immediately started.
On day 17 after hospitalization, the results of all laboratory tests were normalized. After 3 weeks of follow-up, cellularity was restored to normal level and no hemophagocytosis was observed at bone marrow biopsy (). Results of PCR with both the bone marrow aspiration and sputum samples were also negative for tuberculosis. The previously detected multiple lymph node enlargements were decreased in size on the follow-up abdominal CT. After 6 months of antitubercular therapy, the patient was healthy with no signs of disease.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.0, 'kg']}",20,19,21,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.0 kg. Hence, the patient's maintenance fluid is 5.0 kg * 4 mL/kg/hr = 20.0 mL/hr.
Hence, the patient's fluid maintenance is 20.0 mL/hr."
4970,22,Maintenance Fluids Calculations,physical,decimal,pmc-7591194-1,Extracted,"We present a case of a 25-year-old male patient, shepherd by occupation, native of Balaghat, Madhya Pradesh. He presented to our clinic with complaints of difficulty in walking and convulsions for the past 20 years. For all these years, he was being treated by a local physician and was misdiagnosed as a case of poliomyelitis. Neurological examination had revealed muscle wasting and contracture of both limbs on the right side. Power was grade four. Speech and vision were normal. No other deficit was found. A noncontrast computed tomography (CT) of the brain revealed a well-defined spherical nonenhancing, hypodense, well-circumscribed, peripherally calcified 7 cm × 8 cm size space occupying lesion in the left frontoparietal region []. A contrast-enhanced magnetic resonance imaging (MRI) of the brain revealed nonenhancing intra-axial focal lesion with calcified walls [Figure and ]. No restriction on diffusion was observed. Cyst wall appeared hypo-intense in all sequences with blooming area, suggestive of calcification. No perilesional edema was seen. Complete work-up of the patient was done but there was no presence of primary disease in other organs. The patient was operated with frontoparieto-temporal craniotomy. The mass was totally calcified and loosely adherent to dura matter. Through simple dissection, mass was excised in one piece without rupture and spillage. The weight of the cyst was around 300 g []. The longest and shortest diameter of the cyst were 25.4 cm and 23.9 cm, respectively [Figure and ]. The cavity was then irrigated with hypertonic saline jet. Ventricle was incidentally punctured leading to spilling of cerebrospinal fluid. Dura was closed primarily. There was no postoperative new neurological deficit. Histopathological examination revealed calcified hydatid cyst. The patient was discharged on 10th postoperative day after removal of the sutures and was prescribed tablet albendazole 400 mg BD for a month and advised regular follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [300.0, 'g']}",1.2,1.14,1.26,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 300.0 g so this converts to 300.0 lbs * kg/1000 g = 0.3 kg. Hence, the patient's maintenance fluid is 0.3 kg * 4 mL/kg/hr = 1.2 mL/hr.
Hence, the patient's fluid maintenance is 1.2 mL/hr."
4971,22,Maintenance Fluids Calculations,physical,decimal,pmc-7427458-1,Extracted,"A 79-year-old male with a past medical history of CMML diagnosed 4 years prior, anemia related to CMML and CKD receiving erythropoiesis-stimulating agent, hypertension, and chronic kidney disease stage 3 (baseline creatinine 1.8 mg/dL) presented with one day of decreased urination and an unintentional 20 pound weight loss and fatigue over the preceding three months.
The patient’s blood pressure was 141/84 mmHg, pulse 104 beats per minute, respiratory rate 16 respirations per minute, SpO2 96%, and temperature of 36.6°C. The physical exam did not reveal any abdominal tenderness to palpation but did reveal splenomegaly. There was no palpable cervical, supraclavicular, axillary, or inguinal lymphadenopathy.
Laboratory evaluation was significant for profound leukocytosis, 88.5 × 103 cells per mm3, with 24.0% monocytes compared to his baseline WBC 4.5–7 × 103 cells per mm3 over the preceding 4 years. Additional laboratory abnormalities were significant for uric acid 19.8 mg/dL and creatinine 2.94 mg/dL as well as potassium 4 mmol/L, phosphorus 4 mg/dL, calcium 9.2 mg/dL, and albumin 3.2 g/dL. Urinalysis was significant for protein 200 mg/dL, 20/LPF granular casts, and 7/LPF hyaline casts. A renal ultrasound measured the left kidney as 10.2 cm long, with at least two cysts the largest at 3.5 cm, and without hydronephrosis. The right kidney measured as 10.5 cm long, with one cyst at 2 cm, and also without hydronephrosis. The CT of the chest, abdomen, and pelvis identified splenomegaly with a splenic diameter of 14.6 cm. No renal calculi were appreciated. Also visualized were several borderline subcentimeter retroperitoneal and pelvic lymph nodes.
Peripheral blood smear was performed and revealed a myeloid predominance with left shift and a small blast population (0.6%) as well as monocytic phenotypic aberrance (see ). Subsequently, a bone marrow biopsy was performed which identified 20–25% of CD 34+ blasts and morphologic features consistent with AML with monocytic differentiation (see and ). Flow cytometry showed prominent monocytes which demonstrated loss of expression of HLA-DR and CD14 as well as coexpression of CD56. Next generation sequencing (NGS) revealed a pathogenic mutation in the NPM1 gene.
With presenting hyperuricemia and acute on chronic kidney injury, he received one dose of rasburicase 3 mg IV given concern for early TLS with concomitant initiation of daily allopurinol. He commenced cytoreduction with hydroxyurea 1000 mg twice daily and after 48 hours, his white blood cell count and uric acid down-trended to 48.5 × 103 cells per mm3 and 5.5 mg/dL respectively. Creatinine also trended down to 1.98 mg/dL.
Due to the patient’s performance status and age, hematology offered reduced-intensity therapy consisting of azacitidine with or without venetoclax or best supportive care rather than intensive induction chemotherapy. Ultimately, the patient elected for home hospice services and passed away 10 days later.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [20.0, 'lbs']}",36.28736,34.47299,38.10173,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 20.0 lbs so this converts to 20.0 lbs * 0.453592 kg/lbs = 9.07184 kg. Hence, the patient's maintenance fluid is 9.07184 kg * 4 mL/kg/hr = 36.28736 mL/hr.
Hence, the patient's fluid maintenance is 36.28736 mL/hr."
4972,22,Maintenance Fluids Calculations,physical,decimal,pmc-8367440-1,Extracted,"A 79-year-old female patient, referred to the outpatient surgical department, presenting with acute onset of dyspnea during minor exercise, fatigue, angina and diffuse intermittent abdominal pain. She mentioned loss of appetite and more than 15-kg weight loss during a 3-month span. Her past medical history was unremarkable. She claimed no systematic use of medication. Her vital signs and electrocardiogram (ECG) had no pathological findings. Clinical examination revealed diffuse abdominal pain during deep palpation, reduced lung sounds and presence of bowel sounds in the left hemithorax and tympanic sound during percussion ipsilaterally. Blood sampling for a full blood count and biochemistry was performed. Results appeared to be within normal range, except from a slight platelet count (PLT) elevation (583 K/μl). Chest X-ray revealed the presence of large intestine and gastric bubble within the left hemithorax. Full cardiologic workup was conducted, with no pathological findings. A contrast-enhanced computed tomography (CT) of the chest and abdomen was performed. A left hemidiaphragm elevation was revealed, with part of the stomach, transverse and left colon and spleen herniating in the left chest trough a left posterior diaphragmatic defect. All signs were compatible with a Bochdalek hernia ().
Patient was subjected to a robotic-assisted mesh surgical repair. Four-trocar setup was used: one 8-mm trocar was placed above the umbilicus (optic camera), two 8-mm working ports were placed in the right- and left-midclavicular lines above the umbilicus, respectively, and one 5-mm port was placed at the left axillary line at the level of the umbilicus for the first assistant. The patient was placed in a steep reverse Trendelenberg position (35°).
During the first assessment of the abdominal cavity utilizing the optic camera, two remarkable findings were revealed. The heart and pericardium shifted to the contralateral side of the thorax due to compression from the hernial sac. This was depicted clearly via the pulsating heart over the right diaphragm. Additionally, an anatomical variation was encountered at the diaphragmatic border of the liver, where a steep ridge was formed at the area where the heart was beating and was chronically compressing the liver parenchyma, forming a pocket in the hepatic tissue.
After mobilization of the left liver lobe, visualization of the hiatus was achieved. A two silk suture was placed through the avascular hepatogastric ligament and outside the patient’s anterior abdomen with an extracorporeal knot in order to assure atraumatic elevation-retraction of the liver. Space was created in the surgical field due to the absence of a retracting surgical instrument within the abdominal cavity. The hernia’s sac was then dissected with use of energy device and bipolar cautery with minimal traumatic tissue handling; the herniated stomach, transverse and left colon, omentum and finally spleen were dissected free (). Due to the atypical clinical symptomatology as well as increased PLT, the suspicion of chronic ischemia of the herniated organs was raised. ICG was administered to assess the patency of blood supply in the herniated organs and specially to the spleen; blood supply was excellent and as a result, no further resections were needed (). An 8- × 4-cm posterolateral diaphragmatic defect was revealed; the defect was repaired with the use of ProGrip mesh and was supported by a continuous V-loc suture for fixation. The patient resuscitated from anesthesia in great condition and returned to the ward, with an uneventful course. A post-operative upper GI fluoroscopy was conducted at the second post-operative day (POD), and oral diet was commenced ().
An episode of paroxysmal supraventricular tachycardia appeared during the third POD. The arrhythmia was controlled spontaneously. The patient was discharged from the hospital during the fifth POD. Patient is followed-up for 1 year with no signs of recurrence.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15.0, 'kg']}",50,47.5,52.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.0 kg - 10 kg) = 50.0 mL/hr.
Hence, the patient's fluid maintenance is 50.0 mL/hr."
4973,22,Maintenance Fluids Calculations,physical,decimal,pmc-8310603-1,Extracted,"A Caucasian 59-year-old man with a history of hypothyroidy and fatty liver was diagnosed in 2018 with a myelodysplastic syndrome with multilineage dysplasia (MDS-MLD) [] and a very low risk by the R-IPSS at our facility. There was no family medical history. The patient was married, had two children, and worked as a social worker. He did not consume alcohol nor tobacco. The only treatment was l-thyroxine 50 µg/day.
Laboratory tests showed a leukocyte count of 3.9 × 109L, with neutrophils at 1.5 × 109/L and monocytes at 1.49 × 109/L, a platelet count of 113 × 109/L, and hemoglobin at 115 g/L. The bone-marrow blast count was 1.4%, and cytogenetics were normal, with no Philadelphia chromosome. Next-generation sequencing (NGS) detected a SETBP1 mutation, with a variant allelic fraction (VAF) of 0.21%. Biological and clinical monitoring was decided.
In December 2019, a brutal deterioration of the general state, with a loss of 13 kg, night sweats, major fatigue, and loss of appetite, raised doubts about the diagnosis. The patient’s body temperature was 36.7 °C, heart rate 95 beats per minute, blood pressure 103/64 mmHg, and oxygen saturation at 100% on ambient air. Cardiopulmonary auscultation was normal. He was conscious, oriented, and had a Glasgow score of 15, without detectable abnormalities on neurological clinical examination. His weight was 60.5 kg. Laboratory tests showed a leukocyte count of 29.7 × 109/L, with neutrophils at 23.46 × 109/L and monocytes at 1.78 × 109/L, a platelet count of 83 × 109/L, and hemoglobin at 78 g/L. Another medullary aspiration was performed and showed major dysplasia without excess blasts and a cytological aspect of CMML-0. Immunophenotyping showed a near-absence of type MO3 monocytes, consistent with a diagnosis of CMML. A PET scan was performed and detected several deep lymphadenopathies with moderate hypermetabolism [maximum standardized uptake value (SUV) 3.6]. They had a maximum size of 12 mm and were not puncturable. There was no evidence of another cancer. Treatment with hydroxyurea (three tablets per day) was introduced for the hyperleukocytosis and was administered over 3 weeks.
In January 2020, the appearance of psychomotor slowdown led to admission to the hematology department of Tours Hospital. Subsequently, the patient’s condition quickly worsened with the occurrence of severe problems of alertness and aphasia. At this time, clinical examination showed a Glasgow score of 11 (M6V2E3), with bilateral nonreactive myosis and right central facial paralysis. There was no motor or sensory deficit of the limbs within the limits of clinical examination in such a state of consciousness.
Laboratory tests showed a hemoglobin level of 77 g/L, a platelet count of 36 × 109/L, and a leukocyte count of 37 × 109/L, with neutrophils at 31 × 109/L and monocytes at 3 × 109/L (Table ). Infectious assessment was negative, with sterile hemocultures in bacteriology and mycology and negative serologies for Cryptococcus, Toxoplasma, HIV, HBV, HBC, CMV, EBV, and syphilis. Beta-d-glucan assessment was negative. Autoimmune assessment, including for ANA, was also negative. Cerebral CT showed multiple hemorrhagic nodular lesions (Fig. A). On MRI (Fig. B–C) these CNS lesions were heterogeneous, without enhancement after gadolinium administration. The MRI also showed multiple supra- and infratentorial hemorrhagic lesions of varying age, in favor of leukemic infiltration as well as the beginning of left temporal engagement (Fig. B–D). We could not perform a lumbar puncture because of the risk of engagement. Treatment with high-dose corticosteroids, consisting of 100 mg intravenous methylprednisolone per day, was introduced, and the patient was transferred to intensive care because of his worsening state of consciousness. A neurosurgical diagnosis could not be performed owing to the nontissular hemorrhagic description of the lesions by imaging. The patient died on 15 January 2020.
An autopsy was performed. Macroscopic sections of the brain showed multiple hemorrhagic lesions (Fig. A). Microscopic analyses showed infiltration by relatively immature myeloid elements and hemorrhagic phenomena (Fig. B). Immunohistochemistry analyses of the brain tissue showed positivity of the lesion for antibodies against CD15 (Fig. C) and MPO (Fig. D). No megakaryocytic or erythrocytic precursors were found in the brain (not shown). However, adenopathy (Fig. E) exhibited a predominance of myeloid polymorphic localization and mature elements with megakaryocytes (Fig. F–G), and elements of erythrocytic lineage (not shown) were also found. No blastic elements were found in the node (Fig. H) or other localizations (not shown). The bone marrow (Fig. I–J) exhibited a predominance of a myelomonocytic line, but no immature cells. The spleen, lungs, and liver contained mostly myeloid and monocytic elements, without megakaryocytes (not shown). These various elements suggest brain, splenic, liver, lung, and lymph node localization of myelomonocytic leukemia, without any evidence for evolution of the CMML to acute leukemia.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.5, 'kg']}",100.5,95.475,105.525,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.5 kg - 20 kg) = 100.5 mL/hr.
Hence, the patient's fluid maintenance is 100.5 mL/hr."
4974,22,Maintenance Fluids Calculations,physical,decimal,pmc-7087373-1,Extracted,"A male infant presented with vomiting, abdominal distension and watery diarrhea at the age of 2 weeks old. His vomiting was aggravated when he was 1 month old, and the episodes of vomiting were often occurred after feeding. At 2 months of age, he was admitted to our department. He was the first child of his mother, and he was born at term with a birth weight of 2.95 kg after an uneventful pregnancy. The parents were nonconsanguineous and healthy. There were no similar diseases occurred in his family history. When he was admitted, he had severe malnutrition, while his vital signs were stable. His weight was 3.42 kg, and the Z score of the weight for age (ZWFA) was below -3SD; his length was 55.5 cm, and the Z score of the height for age (ZHFA) was below -2SD. He had stable breathing, and lungs auscultation was normal, the rhythm and strength of the heart beat were normal. Neither abdominal tenderness nor hepatosplenomegaly was observed. No edema was observed. The complete blood count showed the following: a white blood cell count of 10.58 × 109/L (65.7% lymphocytes), a hemoglobin level of 105 g/L, a platelet count of 628 × 109 /L, a hypersensitive C-reactive protein level of 3 mg/L. The immunoglobulin (Ig) levels were within the normal range: Ig G 6 g/L, Ig A 0.36 g/L, Ig M 0.3 g/L, and Ig E < 17.9 IU/mL, and the serum albumin level and liver function were normal. The stool etiology examinations were all negative. Blood Analysis of blood tandem mass spectrometry did not indicate any metabolic disease. Gastrointestinal contrast revealed a horizontal transverse stomach and the ileum was segmental slightly extended. The patient was diagnosed with intestinal malabsorptive syndrome, severe malnutrition and growth failure according to the clinical and laboratory findings.
The patient was given partial parenteral nutrition and enteral nutrition with deep-hydrolysis formula during hospitalization. The daily amount of the stool was between 30 g per kilogram to 40 g per kilogram, and the largest amount of stool was 80 g per kilogram every day. The amount of stool decreased after hospitalization for 13 months, however there was only a minimal gain of weight from 3.42 kg to 4.88 kg, and the body height increased from 55.5 cm to 64.3 cm. The child was advised to perform an endoscopy procedure and genetic tests for suspecting congenital diarrhea and enteropathy. However, his parents refused to perform these examinations strongly. When he was discharged at 1-year-3-month old, the amount of formula he can take was about 700 ml per day. He was advised to continue parenteral nutrition treatment intermittently, but his parents did not take the doctor’s advice.
When the patient was 1 year and 6 months old, his diarrhea increased again. The episodes of stool were about five to six times a day. His mother added rice paste in his diet when he was 1 year and 8 months old. Half a month later, an edema was observed in the lower limbs and he had coughing as well. He was taken to the emergency room and the blood testing found hypoglycemia with blood glucose level of 1.2 mmol/L. Laboratory examinations showed the following: slightly decreased potassium ion level of 3.4 mmol/L, normal sodium ion level was normal, decreased calcium ion level of 0.56 mmol/L; a white blood cells count was 9.01 × 109 /L (49.4% lymphocytes), a hemoglobin level was 122 g/L, platelets count was 202 × 109 /L, normal hypersensitive C-reactive protein of 3 mg/L, normal serum albumin level of 34.4 g/L, slightly increased total bilirubin level of 31.0 μmol/L, increased alanine aminotransferase level of 119 U/L, an increased hypersensitive troponin T level of 0.165 ng/mL, an increased N-terminal B-type natriuretic peptide level more than 35,000 pg/mL. Chest X-ray showed pneumonia, multiple fractures of the ribs, narrowing of vertebral bodies and osteoporosis of various bones. An Echo ultrasound revealed decreased systolic function of left ventricular with EF level of 0.39. After admission, his general condition deteriorated quickly, and he developed sepsis and multiple organ failure. Finally, he had cardiac arrest and he needed repeated cardiopulmonary resuscitation. His parents gave up further treatment at last.
Due to intractable diarrhea, growth failure and intestinal absorptive dysfunction, he was strongly suspected to have congenital diarrhea and entropy. He was advised to perform the genetic test again. Therefore, peripheral heparin anticoagulation blood was taken from him and his parents, and exon detection V2 which included over 4400 genes was performed at Beijing Mackinaw Medical Laboratory. The candidate genes of primary immunodeficiency diseases prone to refractory diarrhea including IL-2 receptor common gamma chain, ZAP70, ORAI-1 and ITK, and those also associated with congenital diarrheas and enteropathies such as DGAT1, SKIV2L, TTC7A, MYO5B, FOXP3, STAT3, IL10, IL10RA, IL10RB, NEMO, and STAT1 et al. were all analyzed. Genetic analysis revealed: two disease-related gene mutations in this patient, one homozygous mutation of EpCAM gene and the nucleotide number 491 + 1 in the coding region was changed from guanine to adenine, resulting in amino acid changes. One splicing mutation was derived from his mother, and his father was suspected to have a heterozygous deletion mutation of the gene. This homozygous gene mutation was associated with CTE and was functionally verified to be a causative gene []. The second mutation was a TTC7A gene complex heterozygous mutation, c.291_292insTACG, which was derived from his mother. He also had a mutation of c.335G > A, which was derived from his father. The compound heterozygous mutation was a suspected pathogenic mutation associated with multiple intestinal atresia (MIA) and chronic diarrhea. The patient was diagnosed with CTE (MIM 613217) in combination of clinical manifestations and genetic testing results.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.42, 'kg']}",13.68,12.996,14.364,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.42 kg. Hence, the patient's maintenance fluid is 3.42 kg * 4 mL/kg/hr = 13.68 mL/hr.
Hence, the patient's fluid maintenance is 13.68 mL/hr."
4975,22,Maintenance Fluids Calculations,physical,decimal,pmc-6029183-1,Extracted,"The male neonate was born at 40 + 1 weeks'gestational age to a 30-year-old mother, gravida 1, para 0 with a birth weight of 3030 g through cesarean section. The pregnancy had been complicated by maternal right Bell's palsy during gestation 30–35 weeks, and the delivery course was prolonged for 24 h, yet the Apgar scores were 9 at 1 min and 10 at 5 min, respectively. The neonate received prophylactic intramuscular Vitamin K after birth. The patient was well-being initially, but on the 5th postpartal day, he was noted to have fever and convulsion with limbs extension, accompanied with desaturation, and decreased activity. Neonatal seizure was suspected, and after loading dose of luminal at the local clinic, he was transferred to our hospital.
His maternal uncle had a history of unknown congenital disease with mental retardation; otherwise, the family history was unremarkable.
On physical examination, he had body temperature 38.5°C, pulse 173 beats/min, respiratory rate 50 breaths/min, blood pressure 96/66 mmHg, oxygen saturation 98%–99% on room air, and his body weight 2800 g. The anterior fontanelle was flat, and his activity decreased with hypotonia. There was polydactyly of the right hand. The remainder of the physical examination was unremarkable.
The initial laboratory tests showed hemoglobin 12.5 g/dL and platelet count 322 K/uL. The spinal tapping for ruled out central nerve infection showed bloody cerebral spinal fluid. The cranial USG was arranged on admission day 1 after the cerebrospinal fluid (CSF) study. The coronal view along the plane of the choroid plexus and the midline sagittal view through the anterior fontanel [] revealed obstructive hydrocephalus with enlarged bilateral lateral and 3rd ventricles and ill-defined hyperechoic density over the cerebellum with upward compression of the 3rd ventricle and the 4th ventricle hardly to identified. The resistive index (RI) was 0.63 (normal range: 0.6–0.9), which is through the midline sagittal view and spectral waveforms of the anterior cerebral artery. Magnetic resonance imaging (MRI) of the head [Figures and ] was soon arranged and revealed a subdural hematoma in the region of the left cerebellar hemisphere causing compression and displacement of the 4th ventricle and resulted in obstructive hydrocephalus with dilatation of the lateral and 3rd ventricles.
The patient was intubated with ventilator support due to frequent apnea and cyanosis. Bleeding diathesis evaluation showed his prothrombin time was 10.9 s (reference range: 8.0–12 s), and an activated partial thromboplastin time was >120 s (reference range: 23.9–35.5 s). Factor VIII (FVIII) activity was <6.6% (reference range: 60%–150%). Hemophilia A was diagnosed.
Owing to personal reasons and the economic conditions of family, the parents refused surgical treatment and recombinant FVIII concentrate therapy. The patient was expired at 15-day-old unfortunately.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2800.0, 'g']}",11.2,10.64,11.76,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2800.0 g so this converts to 2800.0 lbs * kg/1000 g = 2.8 kg. Hence, the patient's maintenance fluid is 2.8 kg * 4 mL/kg/hr = 11.2 mL/hr.
Hence, the patient's fluid maintenance is 11.2 mL/hr."
4976,22,Maintenance Fluids Calculations,physical,decimal,pmc-8270611-2,Extracted,"A 9-month-old, 8-kg and 72 cm-in-height male infant was diagnosed as CPAM over right lower lobe. He was also scheduled for lobectomy under Uniport VATS. Anesthesia was inducted with thiamylal, fentanyl and cisatracurium, and the patient was intubated with a 5.0 mm uncuffed endotracheal tube. Sevoflurane was used to maintain anesthesia. Then, a 5 Fr Uniblocker tube was inserted through the endotracheal tube into the right main bronchus with the guidance of a fiberoptic bronchoscope, and the balloon of the Uniblocker tube just lay beneath the carina (Fig. -B). The balloon volume was titrated gradually until the breathing sound over the right lung field vanished. The three lobes of the right lung collapsed quite well during surgery.
One episode of Uniblocker balloon dislodgement occurred in the beginning of lung manipulation, presenting as inability to ventilate. After confirmed by fiberoptic bronchoscopy, the problem was solved by repositioning of the balloon under fiberoptic bronchoscope guidance, with well lung collapse regained throughout the 4-hr surgical time. The ventilator was set at volume control mode with FiO2 100%, tidal volume 6 ml/kg, I.E. ratio 1:1.5, and respiratory rate 28 /min. End-Tidal CO2 was around 33 to 39 mmHg. SpO2 was above 95% during the whole 270-minute course of one-lung ventilation. Overall blood loss was 80 ml, and 80 ml of packed red blood cell was transfused. The postoperative course was acceptable. Endotracheal tube was removed on day 3, and he was discharged at 8 days uneventfully.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [8.0, 'kg']}",32,30.4,33.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 8.0 kg. Hence, the patient's maintenance fluid is 8.0 kg * 4 mL/kg/hr = 32.0 mL/hr.
Hence, the patient's fluid maintenance is 32.0 mL/hr."
4977,22,Maintenance Fluids Calculations,physical,decimal,pmc-5470561-2,Extracted,"A 20-year-old male patient sought the emergency unit complaining of high-grade fever and chills accompanied by malaise, headache, and weakness during the last 10 days. He referred loss of appetite and consequently 3 kg of weight loss (5% of total body weight). His physical examination was normal, as well as the ophthalmoscopy. Laboratory workup showed normal renal function, glucose determination, electrolytes, hepatic enzymes, liver function tests, protein electrophoresis, and urinalysis. Serology for HIV, hepatitis B and C, toxoplasmosis, EBV, syphilis, leptospirosis, and dengue fever were negative. Rubella and cytomegalovirus serologies showed IgG positive but IgM negative. Tests for antinuclear antibody, anti-neutrophil cytoplasmic antibody, and rheumatoid factor were also negative. The tuberculin skin test was negative as well as the acid-fast bacilli research in the sputum. The thoracic CT was normal and echodoppler of the lower limbs ruled out the diagnosis of deep venous thrombosis. The cerebrospinal fluid (CSF) examination was normal. Four sets of blood samples, urine, and CSF cultures were negative for bacteria, fungus, and acid-fast bacilli. The patient remained hospitalized presenting a daily temperature of 38.5 °C and 39 °C and was recorded as a fever of unknown origin (FUO). In this setting, he underwent a transesophageal echodopplercardiogram, which was normal. The determination of a high titer of ferritin was odd, which was interpreted as an inflammatory marker or even the possibility of Still’s disease, without other diagnostic criteria. The abdominal ultrasound and CT were normal despite the progressive raising determination of liver enzymes (AST, ALT, APh and γGT) and LDHi. Nevertheless he was submitted to a wedge liver biopsy through laparoscopy, which did not detect any abnormality in the abdominal cavity. The histological examination of the liver specimen showed non-specific findings: preserved lobular architecture, with moderate neutrophilic infiltration of portal tract with histiocytes, mild biliary ductal proliferation. The hepatocytes, Kupfer cells, as well as the central veins were also preserved. Bone marrow aspiration resulted in dry tap, which was followed by a bone marrow biopsy, which showed hypoplasia of the all hematopoietic series and focal infiltration by large lymphoid cells, with nuclear pleomorphism, atypia and evident nucleoli.
The patient evolved with lower limb cellulitis and septic shock, and died before the complete diagnostic work up has been completed. Unfortunately the bone marrow biopsy was not prioritized over the other examinations, being undertaken lately in the course of the disease. The diagnosis was confirmed by the immunohistochemical report, which showed a profile consistent with ALK+ ALCL: (positive for CD30, ALK, and EMA, and negative for CD20, CD3, CD15, CD43, CD34, CD31, and myeloperoxidase) ().
The autopsy revealed generalized lymphadenopathy (lymph nodes measuring up to 2 cm) involving the axillary, mediastinal, abdominal, and lower limb chains, which showed sinusoidal infiltration by large, atypical multinucleated cells ().
The lungs, liver, and spleen also showed lymphomatous infiltration (). The final diagnosis was ALK+ ALCL and the immediate cause of death was septic shock with massive bilateral pulmonary hemorrhage.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.0, 'kg']}",12,11.4,12.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.0 kg. Hence, the patient's maintenance fluid is 3.0 kg * 4 mL/kg/hr = 12.0 mL/hr.
Hence, the patient's fluid maintenance is 12.0 mL/hr."
4978,22,Maintenance Fluids Calculations,physical,decimal,pmc-4904662-1,Extracted,"A 47-year-old man presented with a three-month history of anorexia, nausea, vomiting, diarrhea, and weight loss of 30 kg. His bowel movements occurred 12–15 times daily, with abdominal cramps but no gastrointestinal bleeding. No infectious, extraintestinal, or other constitutional symptoms were present. His past medical history included remote peptic ulcer disease (PUD) diagnosed 15 years earlier, for which he was on no current medical therapy, untreated hepatitis C, and intravenous drug use. His sole medication was methadone. The patient's in-hospital course was complicated by pneumonia and sepsis requiring intubation, from which he eventually recovered. Upon recovery from his critical illness, his gastrointestinal symptoms and failure to thrive persisted despite high-calorie enteral feeds via nasogastric tube. The gastroenterology team was involved at this point. Vital signs were stable; physical examination revealed cachexia, minimal shoulder and thigh muscle bulk, thinning hair, fissured nails, and bilateral pitting peripheral edema. Abdominal exam revealed a sunken abdomen and visible ribs, with bulging flanks and a positive fluid level.
Laboratory investigations revealed serum potassium of 1.9 mmol/L (normal 3.5–5.0 mmol/L), bicarbonate of 41 mmol/L (normal 22–29 mmol/L), albumin of 9 g/L (normal 35–50 g/L), and creatinine of 35 μmol/L (normal 64–111 μmol/L), along with other markers of malnutrition and hypovitaminosis. Serum and stool workups for infectious causes of diarrhea and celiac disease were negative. The patient underwent gastroscopy and colonoscopy. On gastroscopy, a superfluous lumen was identified proximal to the pylorus (), which could not be probed. No surrounding erythema or ulceration was noted (). On colonoscopy, a structure with a luminal appearance was identified proximal to the splenic flexure (). Upon advancing the colonoscope through this structure inadvertently (), gastric rugae were ultimately identified, which suggested the presence of a gastrocolic fistula (GCF). No features suggestive of inflammatory bowel disease (IBD) were identified on endoscopy.
A barium study revealed immediate filling of the fistula tract from the stomach into the transverse colon (). Computed tomography confirmed the results. The patient subsequently received parenteral nutrition and underwent distal gastrectomy and resection of the transverse colon with primary anastomosis. His postoperative course was complicated by bleeding from the colonic anastomosis. He underwent repeat laparotomy; hemostasis was secured and an end colostomy was performed. The patient recovered fully. Final pathology revealed acute and chronic inflammation with ulceration, without features of malignancy or IBD. Repeat endoscopic evaluation 6 months after surgery revealed healthy anastomoses. Successful closure of his colostomy was subsequently performed.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [30.0, 'kg']}",70,66.5,73.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 30.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (30.0 kg - 20 kg) = 70.0 mL/hr.
Hence, the patient's fluid maintenance is 70.0 mL/hr."
4979,22,Maintenance Fluids Calculations,physical,decimal,pmc-7511065-1,Extracted,"A 25-year-old non-smoking male with a history of chest wall myoepithelial carcinoma status post excision, chemotherapy, and radiation therapy with relapse in and progression of disease on pembrolizumab presents to the emergency department (ED) with 10 days of progressive dyspnea on exertion, palpitations, and 45-pound weight loss over the past three months.
Initial evaluation consisted of a chest x-ray and CT of the chest with contrast, which revealed metastatic spread to the patient’s lungs including spread to the epicardium, and a new pericardial effusion (Figures , ).
Diagnostic transthoracic echocardiogram was then performed, which showed a very large circumferential pericardial effusion, measuring up to 4 cm along the right ventricular free wall, with associated findings concerning for tamponade physiology (Figure ).
Urgent fluoroscopic-guided pericardiocentesis was then performed, removing 590 mL of serosanguinous fluid. A pigtail catheter drain was left in place for residual effusion, and subsequent serial echocardiography was performed, revealing a persistent small-to-moderate sized pericardial effusion with continued respirophasic septal shifting, and annulus reversus on tissue Doppler imaging suggestive for ECP as the underlying cause for this clinical presentation (Figures -).
Following the discovery of his ECP and the terminal nature of his malignancy, the patient wished to defer further procedures and definitive management for the ECP and was discharged to home hospice.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [45.0, 'lbs']}",60.41164,57.39106,63.43222,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 45.0 lbs so this converts to 45.0 lbs * 0.453592 kg/lbs = 20.41164 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (20.41164 kg - 20 kg) = 60.41164 mL/hr.
Hence, the patient's fluid maintenance is 60.41164 mL/hr."
4980,22,Maintenance Fluids Calculations,physical,decimal,pmc-7279891-1,Extracted,"A 2 year-old boy presented to pediatric neurology investigation due to global developmental delay associated with multiple congenital anomalies.
The patient was born from the first pregnancy of healthy, consanguineous (parents are first-degree cousins). At the time of pregnancy, the mother was 24-year-old and the father, 36 years old. No history of previous miscarriages, no report of use of prescribed or over-the-counter medicines, and no history of exposure to possible teratogenic products during pregnancy.
The pregnancy was complicated by ventricle enlargement detect by ultrasound at 5 months of gestation. The patient was born preterm, gestational age of 7 months, cesarean delivery. Birth weight was 1,720g (<3th centile), length was 39cm (<3th centile) and occipitofrontal circumference (OFC) was 31cm (<3th centile).
The patient was hospitalized four times at early infancy, twice due to pulmonary infection, once at 6 months of age for surgical removement of an extra toe on his left foot and for undescended testicles, and a last time, at 8 months, for a ventriculoperitoneal shunt surgery because of hydrocephalus.
Early global delay of developmental milestones was present. He kept the head up at the age of 12 months, sat at 16 months.
Currently, at 24 months, the patient presents failure to thrive, weight 10.6kg (5th percentile); length 78cm (<5th percentile) and OFC 48cm (50th percentile). Physical features were significant for large anterior fontanelle and slight coarsening of facial appearance. He had a short nose with anteverted nares and smooth philtrum (). The ears were normally set and normal in size and configuration. Palate was narrow with thick gums. The patient also presented fifth-finger clinodactyly and polydactyly on the left foot ().
The neurological evaluation was noteworthy for severe agitation associated with a self-aggressive behavior characterized by head banging leading to severe self-inflicted injuries. The patient presented spastic hypertonus and brisk tendon reflexes, being unable to walk independently or speak.
Cranial magnetic resonance imaging revealed supratentorial hydrocephalus, ballooning of the chiasmatic recess, corpus callosum thin, dilatation of the lateral ventricles and of the third ventricle, absence of septum pellucidum, and cerebral hypomyelination ().
The Human Genome CGH Microarray 60K (Agilent Technologies™) revealed an terminal deletion, starting from the middle of 12q24.31, between the genomic positions (123.309.075bp) to the near end of the q arm (132.283.607bp), arr[NCBI36/Hg18] 12q24.31-q24.33(123.309.075-132.283.607)X1, confirming the diagnosis of 12q deletion syndrome. The exam was performed in 2011 by the Human Genome Studies Center (Institute of Biosciences – Universidade de São Paulo).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.6, 'kg']}",41.2,39.14,43.26,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.6 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.6 kg - 10 kg) = 41.2 mL/hr.
Hence, the patient's fluid maintenance is 41.2 mL/hr."
4981,22,Maintenance Fluids Calculations,physical,decimal,pmc-4173396-1,Extracted,"We discuss a case of 65-year-old, ASA II, 63-kg male posted for left-sided laparoscopic radical nephrectomy due to renal cell carcinoma. Patient was a known case of lepromatous leprosy and was on medications rifampicin, dapsone and clofazimine since 7 months. At first preanesthetic check-up (PAC) visit he was found to be a known case of chronic obstructive pulmonary disease on derriphyline and inhalers of budesonide and ipatropium bromide. Patient was also chronic smoker since 20 years. He was having bilateral basal coarse crepitations for which advised incentive spirometry, steam inhalation and prescribed antibiotics and nebulization with bronchodilator. He was examined to rule out cardiac dysautonomia (by normal 2D-Echo, Valsalva response, ECG changes to respiration and blood pressure changes related to posture and hyperventilation, all were within normal limits) and respiratory dysautonomia [by breath holding time 30 sec, pulmonary function test (PFT); values was showing obstructive pattern and sleep study were acceptable as per age]. Rest of his general examination and biochemical (liver and kidney functions test) investigations were within normal limits. On PAC review patient clinically improved and chest X-ray and PFT were acceptable. On night before surgery patient was given tablet rantidine 150 mg and lorazepam 1 mg perorally and advised to continue with respiratory medications.
In operation theatre monitoring was applied and large bore IV line was secured after local anesthetic application. Anesthesia was induced with propofol 150 mg after midazolam 2 mg and fentanyl 120 mcg and was intubated with size 8.5 cuffed endotracheal tube after administration of muscle relaxant; atracurium 50 mg. Anesthesia was maintained with oxygen, air (50:50) with sevoflurane, fentanyl, atracurium and propofol infusion. Central venous catheter was placed in right IJV for CVP monitoring and fluid management. Radial artery was cannulised to know beat to beat variability, invasive blood pressure monitoring and serial ABG analysis. Standard monitoring like ECG, SPO2, ETCO2, temperature, urine output were done. While making left sided kidney positioning nerve and joints injury protection by adequate padding were done. All the universsal principals of anesthesia for laparoscopic surgery were followed. Patient remained hemodynamically stable intraoperatively. At the end of surgery anesthesia was reversed with neostigmine 2.5 mg and glycopyrrolate 0.4 mg. Extubation was smooth done after giving xylocard 60 mg. Post operative analgesia was maintained with IV paracetamol 1 gm\6 hrly and vitals monitored in postoperative care unit.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [63.0, 'kg']}",103,97.85,108.15,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 63.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (63.0 kg - 20 kg) = 103.0 mL/hr.
Hence, the patient's fluid maintenance is 103.0 mL/hr."
4982,22,Maintenance Fluids Calculations,physical,decimal,pmc-5796925-1,Extracted,"The first subject was a 53-year-old Korean woman who had not been diagnosed with diabetes. The subject visited the medical center at December 2016. Then subject was 163.7 cm in height and 63.5 kg in weight (BMI, 23.7 kg/m2; overweight by Asian standards). Her glycated hemoglobin (HbA1c) level was 6.1% and her fasting glucose sugar level was 104 mg/dL ().
Three months before the visit to the medical center, the weight of the subject had increased to 68 kg because of increased intake of snacks, including late-night snacks. After that, the subject had adjusted the diet and reduced the weight by 3 kg. The subejct preferred to eat dairy products (e.g., whole milk and cream cheese), bread (e.g., red bean bread and cream bread), and snacks. At first visit, the subject was sufficiently motivated for weight management and was aware of the necessity of weight loss. Two months ago, the subject had tried to refrain from snacking and regularly ate three meals a day. The subject usually ate meals with side dishes of vegetables and fish of equal size at home. The subject's breakfast comprised cereal, fruits, tofu, and vegetables. Usual energy intake was approximately 1,400–1,500 kcal/day (). The subject engaged in a low level of physical activity, but had recently started walking. We provided information on appropriate calorie intake and identified a target weight to be achieved by the next visit. We also provided calorie information in foods the subject regularly consumed as snacks and how to choose appropriate snacks, including how to read the Nutrition Facts label when buying processed foods. We also explained the benefits of regular exercise and encouraged the subject to engage in it.
In January 2017, four weeks after the first visit, the body weight of the subject was 59.5 kg. This was approximately 4 kg less than the weight at the time of the first visit (). The subject had regularly consumed three meals a day over the past 4 weeks. In addition, the subject had consumed 100–150 g of vegetables and 50 g of fish and meat for every meal. The subject had not eaten any snacks or sweet bread, and the subject drank a cup of black coffee or low-fat latte a day. The subject walked for exercise about 1 hour a day for more than 4 days a week. The subject was proud of the weight loss that she had achieved over the 4 weeks with a steady diet and exercise and demonstrated a commitment to maintaining improved eating habits in the future. We affirmed the weight loss success and explained that it was very important to ensure that the weight did not increase again. We also encouraged the subject to maintain her improved eating and exercise habits.
In March 2017, the subject made third time visit to our medical center. The weight was 57.7 kg, which was 5.8 kg less than the weight at the time of the first visit (). The subject had tried to maintain a balanced diet in every meal and to maintain the weight loss. However, since February, the subject had had frequent meetings and her consumption of high-calorie and high-fat foods (e.g., pork belly, gimbap, and tteok-bokki) had become more frequent. The subject had been eating snacks such as bread, corn, chocolate, and jelly more frequently than at the time of the last visit. However, on the days that the subject ate out or engaged in overeating, the subject walked from 20,000 to 30,000 steps more than 4 times a week. We provided an information on the challenge of calorie consumption and strategies on appropriate eating when eating out.
In June 2017, the subject's weight was 57 kg, which was 6.5 kg less than the weight at the time of the first visit (). Over the past 6 months, the subject had managed to lose approximately 10% of the initial weight. However, the subject had not been able to consistently manage the diet over the past 3 months. Dietary diary analysis showed that the average calorie intake was approximately 1,700 kcal (). In particular, over the past 3 months the subject had often eaten out. When eating out, the subject often ate high-calorie foods such as pasta, pizza, and hamburgers. Despite of increasing calorie intake, the subject had been frequently exercising, such as walking and cycling. We encouraged the success in achieving a weight loss of 10% over 6 months and commended the subject to maintain the healthy eating and regular exercise.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [57.0, 'kg']}",97,92.15,101.85,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 57.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (57.0 kg - 20 kg) = 97.0 mL/hr.
Hence, the patient's fluid maintenance is 97.0 mL/hr."
4983,22,Maintenance Fluids Calculations,physical,decimal,pmc-6083477-1,Extracted,"We present a 9-year-old girl with newly diagnosed DM1, DKA, brain edema, multifocal vasogenic brain lesions and lower limb paresis.
The patient was reported to have polyuria and polydipsia over the past week and a weight loss of 3 kg over the previous month. The patient was admitted to the district hospital in a serious clinical condition with severe dehydration. Initial intravenous fluid therapy included infusion of 15 mL/kg of 0.9% sodium chloride during the first 90 minutes. The total volume of fluids administered during the first 12 hours and consisting of 1250 mL 0.9% sodium chloride (NaCI) and 1000 mL of 5% dextrose with 0.9% NaCI (2:1 proportion, sodium concentration-51.34 mEq/L) was 65 mL/kg (patient’s weight-34.6 kg). Intravenous insulin therapy was introduced in an initial dose of 0.05 units/kg/hour in order to prevent a rapid decrease of glycaemia. After three hours, the patient’s medical state and neurological condition was reported to deteriorate. She experienced motor restlessness and agitation followed by upper limb spasms. At the end of the first day of treatment the patient was transferred to the Intensive Care Unit (ICU) of the Children’s Memorial Health Institute in Warsaw with a Glasgow Coma Scale (GCS) score of 13 points. Results of laboratory tests are shown in .
Six hours after admission to the ICU, her clinical state was deteriorating rapidly and the GCS score had decreased to 7 points. Computed tomography scan revealed brain edema and a 13-mm hypodense lesion in the left temporal region ().
The patient was sedated and intubated. Insulin infusion was continued and intravenous fluid administration was diminished. Anti-edematous treatment was introduced (Mannitol 0.3 g/kg/dose, three times per day). The patient’s state showed a gradual improvement. After four days, she was extubated. Subsequently the patient was transferred to the Department of Endocrinology and Diabetology. Despite improvement in her clinical condition, the patient was found to have developed symmetric lower limbs paresis. Brain magnetic resonance imaging (MRI) revealed numerous, diffuse lesions (, ). Presence of infection and neoplasm of CNS were ruled out.
Lower limb nerve conduction studies (NCS) revealed damage to the motor neuron in both lower extremities with dysfunction in both peroneal nerves and in the right tibial nerve. Neurological opinion was that the etiology of the multifocal brain lesions was vasogenic. However, the cause of neuropathy was not fully clear. Presence of DKA and peripheral ischemia were given as the probable factors leading to development of the neuropathy.
Alpha lipoic acid and vitamins B1, B6 and B12 were introduced to the therapeutic regimen and the patient underwent intensive physiotherapy, which led to improvement of left lower limb motor function.
Brain MRI was performed three months later in which no progression in size and number of the brain lesions was observed. NCS revealed normalization of the left peroneal nerve parameters. However, findings indicative of deep motor neuropathy of the right lower limb was found to persist. An informed consent form for publication was given by the parents.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [34.6, 'kg']}",74.6,70.87,78.33,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 34.6 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (34.6 kg - 20 kg) = 74.6 mL/hr.
Hence, the patient's fluid maintenance is 74.6 mL/hr."
4984,22,Maintenance Fluids Calculations,physical,decimal,pmc-3915077-1,Extracted,"A 30-year-old female with acute hepatitis was referred to our hospital in 1995. She had been asymptomatic until the disease onset. She had no history of significant medical condition, blood transfusion, or daily intake of medicine and did not consume alcohol. Her serum alanine aminotransferase (ALT) level had fluctuated from 300 to 1116 IU/L for 3 months before admission. On admission, laboratory examinations revealed total bilirubin 2.5 mg/dL, aspartate transaminase (AST) 842 IU/L, ALT 956 IU/L, alkaline phosphatase 153 IU/L, γ-glutamyl transpeptidase 68 IU/L, γ-globulin 2.3 g/dL, and immunoglobulin G 2,710 mg/dL. Hepatitis B virus surface antigen and hepatitis C virus antibody were negative, antinuclear antibody was weakly positive (1:40, homogeneous), anti-smooth muscle antibody was positive (1:320), and anti-mitochondrial antibody was negative. Human leukocyte antigen was positive for DR-4. Histological analysis of the liver revealed marked interface hepatitis with rosette formation in the parenchyma. On the basis of these findings, she was diagnosed with autoimmune hepatitis and started on prednisolone (30 mg/day). Her serum ALT level gradually declined. Her prednisolone dose was tapered to 10–15 mg/day, which was administered with ursodeoxycholic acid (UDCA; 600 mg/day) to maintain her ALT level <40 IU/L. Since 2002, she had been treated by a doctor at home, and the aforementioned regimen was continued. In 2008, she developed steroid-induced cataract and was referred to our hospital to consult about treatment options for autoimmune hepatitis. At the time of referral, she was 150 cm in height and weighed 43.5 kg (body mass index 19.3 kg/m2), and she was being administered 12.5 mg/day of prednisolone and 600 mg/day of UDCA, and her serum AST and ALT levels were 23 and 34 IU/L, respectively. We added azathioprine (100 mg/day) to this regimen and gradually tapered the prednisolone dose to 10 mg/day; her ALT level was maintained between 22 and 40 IU/L with occasional mild flare-ups. In May 2012, she complained shortness of breath and easy fatigability and significant pallor was noted on physical examination. A hemogram revealed hemoglobin 6.4 g/dL, mean red cell volume 117.3 fL, reticulocyte count 0.6 %, white blood cell count 2,600 cells/μL, and platelet count 207,000 cells/μL. Laboratory serum analyses revealed total protein 6.0 g/dL, albumin 3.7 g/dL, AST 32 IU/L, ALT 42 IU/L, lactic acid dehydrogenase 221 IU/L, and normal bilirubin and alkaline phosphatase levels. Her serum iron level was 214 μg/dL, erythropoietin level was 3,750 mIU (normal 9.1–32.8 mIU), and vitamin B12 and folic acid levels were 307 pg/mL (normal 233–914 pg/mL) and 3.3 ng/mL (normal 3.6–12.9 ng/mL), respectively. She showed no symptoms of recent infection, such as fever or myalgia, and gastrointestinal endoscopy showed no evidence of hemorrhagic lesions. She was initially suspected of having azathioprine-induced anemia; therefore, azathioprine was discontinued. A red cell transfusion was performed, which increased her hemoglobin level to 8.3 g/dL; however, after 4 weeks, her hemoglobin levels decreased to 6.1 g/dL (Fig. ). Another transfusion was performed; however, severe anemia kept recurring and repeat transfusions were required. Her reticulocyte count was consistently low (0.2–0.6 %) except just after transfusion. In July 2012, bone marrow aspiration was performed, which revealed hypocellular bone marrow with an absence of erythroblasts. Giant proerythroblast was not observed and her serum was negative for immunoglobulin (Ig)M antibody to parvovirus B19, although viral DNA was not examined. Therefore, she was diagnosed with acquired PRCA on the basis of these findings, and CsA was administered on September 2012 at an initial dose of 6 mg/kg/day (250 mg/day). After 7 weeks, her hemoglobin level and reticulocyte count both showed considerable improvement (12.4 g/dL and 2.4 %, respectively). The CsA dose was gradually reduced and maintained at 1.6 mg/kg/day (70 mg/day) since April 2013, without relapse of anemia. Her cyclosporine trough blood level has ranged from 69 to 88 ng/mL. In October 2012, UDCA was discontinued and the prednisolone dose was tapered to 9 mg/day; prednisolone has been maintained at 8 mg/day since January 2013. The mild fluctuations in serum AST and ALT levels noted after azathioprine discontinuation ceased after initiating CsA therapy. Her AST and ALT levels have remained <20 IU/L for 8 months since the initiation of therapy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [43.5, 'kg']}",83.5,79.325,87.675,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 43.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (43.5 kg - 20 kg) = 83.5 mL/hr.
Hence, the patient's fluid maintenance is 83.5 mL/hr."
4985,22,Maintenance Fluids Calculations,physical,decimal,pmc-7089734-1,Extracted,"A 30-month-old male with a body weight of 12 kg was admitted to our clinic. There was no other pathology in his physical examination except central cyanosis (72% with pulse oximetry). Normal sinus rhythm with a right axis and right ventricular (RV) dominance were present in the electrocardiographic evaluation. Transthoracic echocardiography demonstrated TGA and an atrial septal defect of 10 mm in diameter with color Doppler ultrasonography. There was no left ventricular (LV) systolic dysfunction or outflow obstruction (). There was a banana-shaped LV involution. The LV end-diastolic posterior wall thickness was 3 mm (z score: -1.59), end-diastolic interventricular septum thickness was 6 mm (z score: 0.6), end-diastolic LV diameter was 20 mm (z score: -4), and LV mass index (LVMI) was 24.7 gram/m2 (z score: -2.7). The measured LV/RV pressure ratio was 0.5 at the angiography. It was decided to proceed with an arterial switch procedure.
The operation was conducted with cardiopulmonary bypass (CPB) through aortic and bicaval cannulation. Mild hypothermia and del Nido cardioplegia were utilized. Following the preparation of coronaries as small buttons, the LeCompte maneuver was done and ascending aorta was reconstructed via an end-to-end anastomosis. Then, the aortic cross-clamp was released, allowing the neo-aortic root to distend. The ideal locations for the coronary arteries on the neo-aorta were marked with a sterile pen. Stab wounds were made at these marks, taking care not to injure the previously marked anterior neo-aortic commissure, which was marked with a Prolene® suture. Following this, the aortic cross-clamp was reapplied. The location of the anterior neo-aortic commissure was confirmed through the holes, and the openings were enlarged to accommodate the coronary buttons. Pulmonary artery reconstruction was performed after the removal of the cross-clamp with a single autologous pericardial patch that had been treated with glutaraldehyde for three minutes. Ultrafiltration during bypass and modified ultrafiltration after bypass were used. A left atrial pressure monitoring line was inserted through the right superior pulmonary vein before weaning from CPB support.
The perioperative scores of the patient were 4, 12, and Class II (adequate minor residua) in the Risk Adjustment in Congenital Heart Surgery (RACHS-1) score, the Aristotle Comprehensive Complexity (ACC) score, and the Technical Performance Score (TPS), respectively.
Due to insufficient LV contractions and hypotensive progress following weaning from CPB, the patient was switched to ECMO support at the postoperative 2nd hour in the intensive care unit. Neck cannulation was performed. He was cannulated from the right carotid artery, for the arterial flow, and from the right atrium, for the venous flow. An additional 50 to 100 IU/kg of heparin was introduced according to the initial activated clotting time (ACT). Continued heparin infusion was initiated at a dosage to maintain the ACT at 180 to 200 seconds, and the dosage was titrated. The ECMO pump flow was initiated at 100 ml/kg/min. The pump flow was rearranged after the maintenance of end organ perfusion was ensured, along with the increase in systemic venous oxygen saturation (SO2) and decrease in lactic acidosis.
Inotropic support was administered as milrinone (0.5 µg/kg/min) and a low dose of epinephrine (0.05 µg/kg/min) for the first few postoperative hours. Noradrenaline treatment was added if the coronary perfusion pressure was less than 20 mmHg. Fentanyl and dexmedetomidine were used for sedation and analgesia.
Cardiac functions were evaluated daily by echocardiography. Mechanical ventilation was initiated for oxygenation and to prevent atelectasis. Generally, the frequency was set at 10 to 12 breaths/min, fraction inspired oxygen (FiO2) at 0.35 to 0.45, and positive end-expiratory pressure (PEEP) at 5 to 10 cmH2O to provide a peak inspiratory pressure (PIP) <20 cmH2O.
The patient was monitored with daily echocardiographic examinations, electrocardiography (ECG), and hemodynamic findings. The ECMO support was reduced gradually, and the patient was disconnected from it at the end of one week. On the 10th day postoperatively, the general condition of the patient was good, and the LV had returned to the normal shape from the original banana shape (). There was no systolic dysfunction, as confirmed by ECG. The pro B-type natriuretic peptide (BNP) level decreased from > 35,000 pg/L to 2,100 pg/L.
As the patient’s hemodynamic variables progressed to normal values, medical inotropic support was gradually reduced and discontinued completely. Echocardiographic examinations on the 16th day postoperatively demonstrated normal systolic functions with mild insufficiency of the neo-aortic valve and a small left-to-right shunting through the opening left on the atrial septum. The patient was discharged without any neurological sequelae on the 20th day postoperatively ().
In the follow-up conducted one month after discharge, the patient was hospitalized again with a diagnosis of pneumonia. Echocardiography revealed moderate mitral and aortic regurgitation with a reduced contraction fraction (20%). The mean pulmonary artery pressure measured by pulmonary regurgitation was 50 mmHg. The patient was treated with antibiotics for three weeks. After treatment, sildenafil, enalapril, and furosemide were initiated due to ongoing pulmonary hypertension and heart failure findings. At the seven-month follow-up, it was observed that regurgitations were reduced, pulmonary artery pressure decreased, and cardiac function normalized (contraction fraction: 30 to 35%, ejection fraction: 60%). One year after the operation, the patient had no issues.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.0, 'kg']}",44,41.8,46.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.0 kg - 10 kg) = 44.0 mL/hr.
Hence, the patient's fluid maintenance is 44.0 mL/hr."
4986,22,Maintenance Fluids Calculations,physical,decimal,pmc-2786190-1,Extracted,"An 8-month-old male infant came to our observation for multiple food intolerance and failure to thrive.
He had been exclusively breast fed until the age of 4 months, when a partially hydrolyzed cow based whey formula (Humana HA, Humana, Italy) was introduced by the pediatrician due to the mother's agalactia and family history of atopy. The child started to present vomiting and diarrhea after each feeding and a progressive failure to thrive. Blood, feces, and urine exams did not show any sign of infection, blood loss, or anaemia. Suspecting a milk intolerance, an extensively hydrolyzed whey formula (Nutrilon peptiplus, Nutricia, Italy) was introduced with resolution of the symptoms. Between age of 5 to 7 months, wheat baby cereals and various fruits were introduced without reaction. At the age of 7 months, 50 g of boiled rice was given for the first time. After 4 hours the child had severe vomiting, diarrhea, apnea, and lethargy. The parents took the child to the Emergency Room of a local hospital, where a new feed with 10 g of boiled rice caused the previously described symptoms. The child received intravenous fluid resuscitation and was then transferred to our hospital, Meyer Children's Hospital, University of Florence, Italy, for further evaluation.
At admission he was in good general condition, afebrile. His weight was 6920 g (3 percentile) and his height was 71 cm (50 percentile).
The physical and neurological exams were irrelevant. Routine blood exams were unremarkable, in particular total IgE level (1 IU/mL), antibodies against endomisius, IgA anti-alpha gliadine and IgG anti-alpha gliadine, ammonium, lactic acid, sweat test, and hemogas analysis were normal. Skin prick test (Lofarma, Milan, Italy) and RAST (Unicap System, Pharmacia) for major foods (milk, soy, egg white, cod fish, wheat, rice, peanut, tomato, rabbit meat, chicken meat), thorax X-Ray, and abdomen sonogram were negative. An endoscopy with duodenal biopsy showed aspecific signs of inflammation.
During the hospitalization, open challenges [] with rice and rabbit meat resulted in vomiting and diarrhea within 4 hours, while lamb and pork meat, apple, and corn were tolerated. This study was approved by the Ethics Committee of Meyer Children Hospital, and informed consent was obtained from the child's parents.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6920.0, 'g']}",27.68,26.296,29.064,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6920.0 g so this converts to 6920.0 lbs * kg/1000 g = 6.92 kg. Hence, the patient's maintenance fluid is 6.92 kg * 4 mL/kg/hr = 27.68 mL/hr.
Hence, the patient's fluid maintenance is 27.68 mL/hr."
4987,22,Maintenance Fluids Calculations,physical,decimal,pmc-5359794-1,Extracted,"A 12 year-old, male neutered, domestic shorthair cat was referred to the Valentine Charlton Cat Centre for investigation of persistent hypokalaemia (2.5–3.3 mmol/l; reference interval [RI] 3.5–5.8 mmol/l), hypertension, hindlimb ataxia and weakness of approximately 1 month’s duration. A palpable, left-sided, cranial abdominal mass localised to the left adrenal gland was identified on abdominal ultrasound.
On presentation at referral, the cat was agitated, vocalising and pacing compulsively in wide circles to the left. The cat weighed 6.45 kg (body condition score [BCS] 3/5) and had lost 500 g in body weight over the previous 2 months. On physical examination vital parameters were normal. A grade III/VI left parasternal systolic heart murmur was auscultated and systolic arterial blood pressure was 220 mmHg (Doppler method). A neurological examination revealed an absent right menace response and a proprioceptive deficit on the right forelimb. Cranial nerves and spinal reflexes were assessed to be normal. On fundoscopy, there was evidence of hypertensive chorioretinopathy, including a focal, hyper-reflective bullous lesion in the left tapetal fundus and tortuous retinal vessels.
An aldosterone-secreting adrenal neoplasm was suspected, based on clinical history, hypokalaemia, systemic hypertension with evidence of end-organ damage and sonographic findings. Abnormalities on repeat haematology and serum biochemistry were confined to hypokalaemia (2.5 mmol/l; RI 3.5–5.8 mmol/l), metabolic alkalosis (bicarbonate 25 mmol/l; RI 17–21 mmol/l) and mildly elevated creatinine kinase (460 U/l; RI 64–400 U/l). Serum total thyroxine was within normal limits (37 nmol/l; RI 10-60 nmol/l). Plasma aldosterone concentration was markedly elevated (>3465 pmol/l; RI 110–540 pmol/l), while plasma renin activity was low (<40 fmol/l/s; RI 60–630 fmol/l/s). An adrenocorticotropic hormone (ACTH) stimulation test was performed using 125 µg cosyntropin (Synacthen; Novartis) administered intravenously. Progesterone was increased at time zero (16.1 nmol/l; RI 0.19–2.22 nmol/l) and 1 h post-ACTH administration (23.2 nmol/l; RI 2.86–14.62 nmol/l). Based on these results, an aldosterone and progesterone-secreting adrenal neoplasm was diagnosed.
A repeat abdominal ultrasound confirmed the presence of a 3.1 cm diameter, circumscribed, hypoechoic mass involving the left adrenal gland, with no evidence of metastases or vascular or renal parenchymal invasion. The right adrenal gland was of normal dimensions and appearance (3.9 mm diameter).
The neurological abnormalities were suggestive of a concurrent left forebrain lesion. It was difficult to determine the clinical course of the neurological signs because profound weakness from hypokalaemia was also present. However, major differential diagnoses included metastasis from an adrenal carcinoma, a primary meningioma or a vascular accident secondary to hypertension.
The cat underwent computed tomography (CT) of the abdomen, thorax and skull under general anaesthesia (). There was no evidence of vascular invasion of adjacent blood vessels by the adrenal mass. There was no evidence of metastatic disease within the thorax. On CT of the skull, an extra-axial, rim-enhancing, left forebrain lesion was evident after the administration of iohexol (2 ml/kg, Omnipaque 350; GE Healthcare). Meningioma was suspected and magnetic resonance imaging (MRI) was performed to further characterise the lesion and to confirm that the tumour was solitary, prior to surgical excision ().
On MRI the forebrain mass (2 cm × 1.5 cm) was well demarcated and had a broad base towards the periphery associated with the left parietal lobe causing a midline shift and impingement of the left lateral ventricle. The mass was isointense to grey matter in the T1-weighted sequence and hyperintense in T2-weighted and FLAIR sequences. There was transtentorial herniation of part of the mesencephalon into the caudal fossa and obliteration of the subarachnoid space between the cerebellum and medulla. There was evidence of mild peritumoural oedema. These findings were consistent with a single meningioma.
Anaesthetic recovery was unremarkable and the cat was discharged on amlodipine besylate (1.25 mg q24h PO, Norvasc; Pfizer), spironolactone (6.25 mg q24h PO, Aldactone; Pfizer) and potassium gluconate (156 mg q12h PO, Hypokal; Mavlab). Prednisolone (7.5 mg q12h PO, Pred-X 5; Apex Laboratories) was given to treat suspected cerebral oedema.
Twenty-four hours after discharge the cat re-presented with recurrent vocalisation, a left body turn, stilted hindlimb gait and hindlimb weakness. Serum acid–base and electrolytes showed persistent hypokalaemia (2.9 mmol/l) and metabolic alkalosis (pH 7.482 [RI: 7.31–7.46]; bicarbonate 31.3 mmol/l [RI 17–21 mmol/l]). A potassium chloride infusion (0.5 mmol/kg/h IV) was given, as well as mannitol (0.25 g/kg IV over 1 h) for suspected increased intracranial pressure. Phenobarbitone (15 mg q12h PO, Phenomav; Mavlab) was also commenced. After stabilisation, the intracranial mass was removed 3 days later via a rostrotentorial craniotomy with no complications (). On histopathology the mass was composed of spindle cells with ovoid plump nuclei, vesiculate chromatin and small multiple nucleoli. There were distinct cell boundaries with moderate eosinophilic cytoplasm. Psammoma bodies were evident between cell aggregates. A diagnosis of psammomatous meningioma was made. Immuno-histochemical staining of the meningioma using a mouse monoclonal antibody to human PR previously validated for use in the cat (Bio-Genex InSite PR antibody [Clone PR88]; Bio-Genex) was performed. There was strong positive labelling of PRs in the meningioma tissue (). Mammary adenocarcinoma tissue was utilised as a positive tissue control, and an affinity-purified normal mouse IgG reagent control (preimmune serum) supplied by the manufacturer was used as the negative control.
Postoperative recovery from the craniotomy was uneventful and neurological status markedly improved over the next 2 weeks, except for persistent weakness. Hypokalaemia (2.3–2.9 mmol/l), and metabolic alkalosis (bicarbonate 29.0 mmol/l) and hypertension persisted, while hypertension was controlled (systolic blood pressure 150 mmHg). Left adrenalectomy was performed 2 weeks after the craniotomy. A typed blood transfusion was required postoperatively to treat intra-abdominal haemorrhage. Hypokalaemia and hypertension resolved and oral potassium, spironolactone and amlodipine were weaned. The patient was discharged from hospital 5 days after surgery. Histopathology of the adrenal tumour was consistent with a low-grade, encapsulated, adrenocortical carcinoma.
At a recheck, 2 weeks after adrenalectomy, serum biochemistry was suggestive of mineralocorticoid deficiency (mild hyperkalaemia [5.9 mmol/l; RI 3.7–5.4 mmol/l], normal sodium [146 mmol/l; RI 144–158 mmol/l] and low Na:K [24.7; RI >29.0]). Fludrocortisone (0.15 mg daily divided dosage PO, Florinef; Aspen Pharma) was administered. This medication was tapered and then ceased over a 3 week period. A week after stopping the fludrocortisone, serum potassium was normal and the cat continued to gain weight. All neurological deficits had resolved.
Two years post-initial presentation the cat was clinically normal, normotensive and 1 kg heavier (7.5 kg, BCS 4/5). Electrolytes, urea and creatinine were within RIs. No neurological deficits were detected on examination.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.45, 'kg']}",25.8,24.51,27.09,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.45 kg. Hence, the patient's maintenance fluid is 6.45 kg * 4 mL/kg/hr = 25.8 mL/hr.
Hence, the patient's fluid maintenance is 25.8 mL/hr."
4988,22,Maintenance Fluids Calculations,physical,decimal,pmc-4870951-1,Extracted,"An 86-year-old female weighing 58 kg, with controlled hypertension underwent elective choledochoduodenostomy under general anaesthesia with endotracheal intubation. Before induction of general anaesthesia, an epidural catheter was inserted uneventfully at T7-8 intervertebral level using 18 gauge Tuohy needle with 20 Gauge catheter; epidural space was identified using loss of resistance to air in the first attempt, with no blood seen through epidural needle and catheter. A test dose of 3 ml 2% lignocaine with adrenaline 1:200,000 was used to test to exclude intravascular and intrathecal placement of epidural catheter. Pre-operative investigations were within normal limits including creatinine (0.97 mg/dl), prothrombin time, activated partial thromboplastin time and platelet count.
Post-operative analgesia was provided with continuous epidural infusion of bupivacaine 0.125% along with fentanyl 2 μg/ml at the rate of 4-8 ml/h. Mechanical thromboprophylaxis (pneumatic pump) was started pre-operatively with addition of a single daily dose of fractionated heparin (dalteparin sodium 2500 U) subcutaneously after 12 h post-operatively. Post-operative course was uneventful. On the 4th post-operative day, 12 h after the last dose of fractionated heparin, the epidural catheter was removed. Four hours after removal of the epidural catheter, the patient complained of severe backache with radiating pain and weakness in the lower limbs. Clinical examination revealed hypoesthesia and muscle power of grade 3/5 in the left lower limb and 4/5 in the right lower limb. With a high index of suspicion for SEH causing spinal cord compression, the patient was started on intravenous (IV) methylprednisolone, and further dosage of heparin was withheld. A magnetic resonant imaging (MRI) scan was deferred after discussion with radiologist and surgeon as the patient had staples at skin incision site. Computed tomography thorax was done which revealed partial collapse of L1-3 vertebrae, and vague intraspinal soft tissue lesion in L1 extending to T11-L2 level. On the 6th post-operative day (48 h after symptoms were noted) after removing the skin staples, an MRI scan was done. MRI revealed epidural haematoma at T11-L1 level with cord compression with no significant cord lesion [Figures and ].
The patient was taken up for emergency laminectomy and decompression under general anaesthesia. The haematoma was meticulously evacuated, and no active bleeding vessel could be identified.
Her neurological status remained unchanged for first 2 days; however, the radiating pain had disappeared. On the 3rd post-operative day, improvement in muscle power was seen. On the 5th post-operative day, the patient regained normal muscle power of both lower limbs. She was discharged home on the 6th post-operative day; subsequent follow-up on weekly basis did not reveal any sensory-motor abnormality.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [58.0, 'kg']}",98,93.1,102.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 58.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (58.0 kg - 20 kg) = 98.0 mL/hr.
Hence, the patient's fluid maintenance is 98.0 mL/hr."
4989,22,Maintenance Fluids Calculations,physical,decimal,pmc-8026832-1,Extracted,"A 37-year-old woman was admitted to our hospital on September 15, 2020 due to recurrent cough for more than 10 mo.
The patient developed a paroxysmal cough accompanied by a small amount of white sputum 10 mo ago. She had no chills, fever, chest pain, hemoptysis, or shortness of breath. She received symptomatic treatment such as anti-infection at a local hospital but her symptoms persisted during this period. The above symptoms recurred 1 mo ago with a little yellow sputum. Fever and hemoptysis were absent. The patient was admitted to our hospital for further treatment.
The patient was thin and weighed only 40 kg (Body mass index: 15.6). Her temperature was 37.4 °C, pulse rate was 99 bpm, respiratory rate was 19 breaths/min, and blood pressure was 100/63 mmHg. No clubbing of fingers, icterus, or generalized lymphadenopathy were observed. Clinical examinations of the cardiovascular, gastrointestinal, and nervous systems were normal, but crackles were found in the lower lobe of the left lung during lung auscultation.
Laboratory studies showed normal white blood cells (8.6 × 109/L), and the neutrophil ratio was 83.0%. Erythrocyte sedimentation rate was 26 mm/h (normal value < 15 mm/h), and high-sensitivity C-reactive protein was 8.2 mg/L (normal value < 8.0 mg/L). Arterial partial pressure of oxygen was 91 mmHg (partial pressure of oxygen/fraction of inspiration O2 433.3 mmHg), and arterial partial pressure of carbon dioxide was 41 mmHg. The 1,3-β-D-glucan test and galactomannan test were both negative.
Enhanced computed tomography images revealed a honeycomb lesion in the lower lobe of the left lung, and an enhanced vascular shadow was seen in the descending aorta, which was consistent with pulmonary sequestration (Figure ).
We also performed bronchoscopic alveolar lavage in the posterior basal segment of the left lower lobe. Gram-positive bacilli were detected in the bronchoalveolar lavage fluid (BALF) (Figure ). The modified acid-fast staining of BALF was weakly positive, and the possible presence of Nocardia species was considered. Following culture of BALF, N. cyriacigeorgica was identified (Figure ), which was confirmed by matrix-assisted laser desorption ionization-time of flight mass spectrometry (matrix-assisted laser desorption/ ionization-time of flight; VITEK MS, bioMérieux, Craponne, France) ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [40.0, 'kg']}",80,76,84,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 40.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (40.0 kg - 20 kg) = 80.0 mL/hr.
Hence, the patient's fluid maintenance is 80.0 mL/hr."
4990,22,Maintenance Fluids Calculations,physical,decimal,pmc-6943102-1,Extracted,"A one year and eleven months old boy weighing 7.2 kilograms (kgs) was referred to Emergency with complaints of vomiting after corrosive ingestion one month previously. The child drunk from a soda bottle in which toilet cleaner had been stored. He was initially taken to a local hospital in his native town from where he was discharged after 24 hours of observation and good oral intake. He started vomiting 10 days after ingestion. His upper GI contrast study showed near total obstruction for which surgery was advised and the child was referred to TIH. Here we performed fiberoptic endoscopy after initial assessment and workup. The esophagus and stomach appeared normal, but the pylorus was scarred and completely obliterated such that even a guidewire could not be passed. Subsequently, the family was counseled and surgery planned. Intraoperatively, an isolated pyloric stricture was identified whilst the duodenum and antrum were normal. Heineke-Mikulicz pyloroplasty was performed, leaving a trans-anastomotic jejunal tube through which feeding was started 24 hours later. The child was discharged three days later when he tolerated full feed. He was followed up and nine months post-surgery, he was tolerating oral diet well and gaining weight.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.2, 'kg']}",28.8,27.36,30.24,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.2 kg. Hence, the patient's maintenance fluid is 7.2 kg * 4 mL/kg/hr = 28.8 mL/hr.
Hence, the patient's fluid maintenance is 28.8 mL/hr."
4991,22,Maintenance Fluids Calculations,physical,decimal,pmc-4683492-1,Extracted,"An 8-year-old (21 kg) boy presented to us with the deterioration of consciousness, seizures, and vomiting for 8 days. On clinical examination, the child was drowsy with Glassgow Coma Score of 12, had central cyanosis, grade II clubbing, fever, and bradycardia. Cardiovascular system examination revealed single loud second heart sound. Child's history was remarkable for diagnosis of cyanotic CHD at birth and episodes of cyanotic spells on crying and exercise. His hemoglobin was 146 g/L, hematocrit 56%, and total leukocyte count 16.0 × 109/L. Other hematological and biochemical investigations including platelet count and coagulation profile were within normal limits. Chest radiograph showed ""egg-shaped"" cardiac shadow and increased pulmonary vascular markings []. Right axis deviation and right ventricular hypertrophy were seen in electrocardiography. His computerized tomography scan showed brain abscess (44 mm × 32 mm) in right thalamic-ganglion region with 6.6 mm midline shift. Due to worsening of symptoms 3 months back cardiology consultation was done and his echocardiography revealed D-TGA with discordant ventricular – great artery relation, fossa ovalis ASD with bidirectional shunt, inlet VSD with bidirectional shunting, and infundibular pulmonary stenosis (PS) with gradient of 64 mmHg. No surgical correction was done, and the patient was not taking any medications at the time of presentation.
Emergency craniotomy and drainage of brain abscess were planned under general anesthesia. The preoperative temperature was 37.8°C, heart rate 55/min, blood pressure 96/70 mmHg, and oxygen saturation (SpO2) 82% on room air. Intramuscular paracetamol 15 mg/kg (2 ml) was given preoperatively as the patient had a fever. After preoxygenation SpO2 increased to 93%. Injection normal saline was started through 21 gauge intravenous (i.v.) cannula after meticulously flushing to remove any air bubbles. Ceftriaxone 50 mg/kg i.v. was given 30 min before skin incision. Patient was premedicated with i.v. glycopyrrolate 0.2 mg, midazolam 1 mg, and fentanyl 2 µg/kg. Induction and intubation were done using thiopentone sodium titrated to effect and rocuronium 0.9 mg/kg, respectively. Patient was intubated with cuffed endotracheal tube size 6.0 mm without much hemodynamic variation or hypoxia. Anesthesia was maintained using sevoflurane in 100% oxygen to maintain a minimum alveolar concentration (MAC) of 1.2. Volume control ventilation without positive end-expiratory pressure (PEEP) was used and end-tidal carbondioxide was maintained between 30 and 35 mmHg. Injection mannitol 0.5 gm/kg i.v. was given after adequate hydration. Hemodynamic parameters and SpO2 remained stable during the entire course of surgery, which lasted for 40 min. All anesthetic agents were stopped; neuromuscular blockade was reversed using neostigmine, and glycopyrrolate and the child was extubated after the return of adequate muscle power. After ensuring the patient was hemodynamically stable and maintaining SpO2 above 90% with oxygen by venturi mask he was transferred to the intensive care unit. The postoperative course was uneventful, and the child was discharged on the seventh postoperative day with advice to consult a pediatric cardiologist.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [21.0, 'kg']}",61,57.95,64.05,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 21.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (21.0 kg - 20 kg) = 61.0 mL/hr.
Hence, the patient's fluid maintenance is 61.0 mL/hr."
4992,22,Maintenance Fluids Calculations,physical,decimal,pmc-6143370-1,Extracted,"A 32-year-old woman (59 kg, 1.68 m) with a five-year history of generalized tonic-clonic seizures presented to Inova Loudoun Hospital's emergency room on June 6, 2016. Upon presentation, the patient suffered a generalized tonic-clonic seizure that lasted for more than one minute. She recently immigrated from Honduras, had no US medical insurance, and reported a history of nonadherence to her antiepilepsy medications. Currently, the patients were not on any routine home medications as an outpatient and denied any known treatment for NCC. The patient admitted that she had a seizure episode in Honduras three years ago, which was treated with intravenous (IV) fosphenytoin at the time. She had been seizure-free since.
In the emergency department, a computed tomography (CT) scan of the brain was performed without remarkable findings. The patient was loaded with a single dose of IV levetiracetam 1000 mg and then started on oral levetiracetam 500 mg twice a day after admission to the hospital. Given her prior seizure history, a magnetic resonance imaging (MRI) scan of the brain was requested to rule out any space-occupying vascular or ischemic insult. An electroencephalogram (EEG) was also requested. The patient was afebrile with mild leucocytosis (WBC 11.02) and elevated creatinine kinase (CK) of 1.6. The liver panel was normal. The physical exam and review of systems were noncontributory.
On hospital day 2, the MRI scan of the brain revealed a 5 mm ring-enhancing lesion in the posterior right frontal lobe of the cerebral cortex, with surrounding vasogenic edema, suggestive of an infective neurocysticercosis lesion. CT scan and EEG were normal. A positive serological antibody test utilizing a western blot assay for cysticercosis immunoglobulin G (IgG) antibody established the diagnosis of parenchymal neurocysticercosis. The patient was commenced on oral ABZ 400 mg twice daily plus oral PZQ 1,200 mg three times daily, dexamethasone 6 mg IV daily, and oral levetiracetam 500 mg twice daily.
On hospital day 3, no recurrent seizure episodes were observed. Leucocytosis and elevated CK resolved. On hospital day 4, the patient was discharged and given further instructions to continue taking oral ABZ 400 mg twice daily in combination with oral PZQ 1,200 mg three times daily for a total of 14 days, oral dexamethasone 6 mg daily for a total of 14 days, and oral levetiracetam 500 mg twice daily for one year. Follow-up appointments at the neurology clinic were scheduled on a monthly basis to evaluate the resolution of neurocysticercosis cysts, the presence of any seizure episodes, and other associated symptoms. The first follow-up visit in three weeks revealed no recurrent seizure episodes. The patient had finished and tolerated well the 14-day course of combination ABZ plus PZQ. Physical exam and labs were normal. A repeat MRI scan of the brain confirmed the complete resolution of cysticerci. The patient continues to be seizure free and is being monitored for one year.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [59.0, 'kg']}",99,94.05,103.95,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 59.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (59.0 kg - 20 kg) = 99.0 mL/hr.
Hence, the patient's fluid maintenance is 99.0 mL/hr."
4993,22,Maintenance Fluids Calculations,physical,decimal,pmc-4420291-1,Extracted,"A 3-day-old male neonate, delivered at term by vaginal delivery, weighing 2.75kg, as referred to our institute with antenatal diagnosis of duodenal atresia. Mother was a non-diabetic and had polyhydramnios. Antenatal scan in the second trimester had shown the presence of duodenal atresia; the gall bladder was reported normal. On examination, child was hemodynamically stable with mild icterus. Nasogastric aspirate was dark bilious. X-ray of the abdomen showed classic double bubble sign. After initial resuscitation, the child was taken up for laparotomy. Classic type 3 duodenal atresia was noted. This was associated with a duplicated Boyden type D gall bladder (Fig. 1). No other anomalies were detected. Kimura’s diamond shaped duodeno-duodenostomy was carried out. Since the child was small and there was no problem in biliary drainage, cholecystectomy was not done. The post operative course was uneventful. Child was started oral feeds on post operative day 6 and discharged on post operative day 8. Retrospectively, after reviewing the literature on gall bladder duplications, we felt cholecystectomy should have been done to prevent future complications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.75, 'kg']}",11,10.45,11.55,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.75 kg. Hence, the patient's maintenance fluid is 2.75 kg * 4 mL/kg/hr = 11.0 mL/hr.
Hence, the patient's fluid maintenance is 11.0 mL/hr."
4994,22,Maintenance Fluids Calculations,physical,decimal,pmc-2499992-1,Extracted,"A 12 hour old male neonate presented to the department with complaint of two episodes of bilious vomiting in last two hours. The patient was a full term normal vaginal delivery, delivered in the hospital. The family history was non contributing.
On examination, the general condition of the patient was good. His weight was 2.75 kg. There was no obvious congenital anomaly. On examination of the abdomen a cystic structure was felt in the right lumbar segment. X-Ray of the abdomen revealed three gas shadows in the left hypochondrium with no other gas shadow. A diagnosis of proximal small bowel atresia was made. No other investigation was done.
The patient was managed by nil by mouth and nasogastric tube placement. He was given intravenous (IV) fluid. The antibiotics given were ceftriaxone (75 mg/kg IV 12 hourly), amikacin(7 mg/kg IV 12 hourly) and metronidazole (7.5 mg/kg IV 12 hourly).
The patient was operated after about 24 hours of presentation. Under general anesthesia, the right transverse supraumbilical incision was made. On exploration of the peritoneal cavity there was presence of a mesenteric cyst in the jejunal mesentery that was felt as the cystic structure on abdominal examination (figure ). The jejunum associated with the mesenteric cyst was having a single type I atresia. The presence of atresia was 15 cm from the dudenojejunal flexure. The proximal bowel was dilated. The treatment included resection of the cyst along with the atretic bowel and proximal 7.5 cm of the dilated bowel and end to end single layer anastomosis by vicryl 5-0.
The post operative period was uneventful. The patient was allowed orally on 11th post operative day. IV antibiotics were continued for 11 days followed by oral cefixime (4 mg/kg BD) for seven days. He was discharged on 14th post operative day in satisfactory condition. The follow up of the patient is also satisfactory.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.75, 'kg']}",11,10.45,11.55,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.75 kg. Hence, the patient's maintenance fluid is 2.75 kg * 4 mL/kg/hr = 11.0 mL/hr.
Hence, the patient's fluid maintenance is 11.0 mL/hr."
4995,22,Maintenance Fluids Calculations,physical,decimal,pmc-8547604-1,Extracted,"In February, 2018, a 58-year-old Japanese male was diagnosed with malignant melanoma (pT4b, N3, M0, stage IIIC) in the right toe in our dermatology. Tumor resection was performed. He did not have any medical history relevant to this disease and adverse effects. However, since multiple lung and liver metastases were found during the Feron maintenance therapy after the operation, this subject was treated with nivolumab in July 2018 (week 0) (). The PD-L1 level at the time of treatment was less than 1%, and BRAF was negative in this case. About 4 weeks later, thyrotoxicosis was induced [free T4 (FT4) = 3.67 ng/dl, thyroid-stimulating hormone (TSH) < 0.01 μU/ml], and about 10 weeks later, hypothyroidism was observed (FT4 = 0.55 ng/dl, TSH = 22.10 μU/ml) (). Therefore, we diagnosed him with nivolumab-induced destructive thyroiditis and started replacement therapy with 50 μg/day of levothyroxine, increasing up to 100 μg/day ().
In November 2018, nivolumab monotherapy was changed to a combination therapy of nivolumab and ipilimumab in order to enhance the antitumor effect of such medication (). About 4 weeks later, he had fever and a headache. In the cerebrospinal fluid test, a mononucleosis-dominated cell number increase was observed. Thereby, he was diagnosed with aseptic meningitis induced by the combination therapy of nivolumab and ipilimumab (). We stopped both drugs and started steroid therapy with 30 mg of prednisolone. We gradually decreased the dose of prednisolone and stopped it in April 2019. Thereafter, we started nivolumab once more because the metastatic tumors were not altered. At that time, we started nivolumab together with prednisolone, just in case, in order to reduce the possibility of recurrence of the adverse effects triggered by nivolumab (). After stopping prednisolone, however, he felt general fatigue, appetite loss, and nausea, and he had fluid replacement therapy in an outpatient department. Also, the percentage of eosinophils gradually increased up to 10.5% ().
About 9 months after starting nivolumab, he was hospitalized due to pneumonia. After admission, adrenal insufficiency and hypoglycemia were observed [adrenocorticotropic hormone (ACTH) < 1.5 pg/ml, cortisol = 3.3 μg/dl, postprandial plasma glucose = 64 mg/dl]. Eosinophil was increased to 9.3% [white blood cell (WBC) = 5,390/μl]. In addition, in the rapid ACTH load test, there was no cortisol response. After the diagnosis of adrenal insufficiency, we started replacement therapy with 15 mg of hydrocortisone. After recovery from pneumonia, he was discharged. Since the metastatic tumors in this subject were substantially reduced by the above-mentioned immune checkpoint inhibitors, it seemed that the pathological course of malignant melanoma was relatively favorable, except for the appearance of several adverse effects with the use of such inhibitors.
Thereafter, he was hospitalized again for further examination of adrenal deficiency. On admission, he continued to take 15 mg (10 mg in the morning and 5 mg in the evening) of hydrocortisone and 100 μg of levothyroxine. His height, body weight, and BMI were 168.3 cm, 86.8 kg, and 30.6 kg/m2, respectively. The blood pressure, heart rate, and body temperature were 166/99 mmHg, 88bpm, and 36.9°C, respectively. The clinical parameters on admission under replacement therapy with hydrocortisone were as follows: eosinophil, 4.5% (WBC = 7,930/ml); plasma glucose, 95 mg/dl; and HbA1c, 5.5%. Slight hypokalemia was observed (3.3 mmol/L), but renal and liver functions were normal and the lipid parameters were within the normal range. Endocrine system tests at rest revealed low levels of ACTH (<1.5 pg/ml), cortisol (0.3 μg/dl), and dehydroepiandrosterone sulfate (DHEA-S; 6 μg/dl); high levels of luteinizing hormone (LH; 9.77 mIU/ml) and follicle-stimulating hormone (FSH; 26.8 mIU/ml); and normal levels of TSH (4.54 μIU/ml), growth hormone (GH; 0.04 ng/ml), and prolactin (12.1 ng/ml). There was no abnormality in the chest X-ray and electrocardiogram. In sonography, the thyroid size was at the lower limit of normal, and the echo levels were low. In brain computer tomography at the onset of aseptic meningitis, there were no intracranial hemorrhage, space-occupying lesions, or other abnormalities. In contrast-enhanced magnetic resonance imaging (MRI), there were no signs of pituitary swelling, stalk thickness, or space-occupying lesions.
All load tests were performed in the morning in a fasting state. As shown in , in the corticotropin-releasing hormone (CRH) stimulation test, there was no reaction in both the ACTH and cortisol levels, which was compatible with ACTH deficiency. In the GH-releasing peptide 2 (GHRP2) load test, GH showed a normal response, but ACTH did not respond at all, which was also compatible with ACTH deficiency. In addition, as shown in , in the thyrotropin-releasing hormone (TRH) load test, excess reaction of TSH and normal reaction of prolactin were observed. No increase in FT3 secretion was observed in response to TRH. In the gonadotropin-releasing hormone (GnRH) load test, the levels of LH and FSH were normally increased. Based on these findings, we diagnosed this subject with isolated ACTH deficiency and destructive thyroiditis induced by immune checkpoint inhibitors taken for malignant melanoma.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [86.8, 'kg']}",126.8,120.46,133.14,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 86.8 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (86.8 kg - 20 kg) = 126.8 mL/hr.
Hence, the patient's fluid maintenance is 126.8 mL/hr."
4996,22,Maintenance Fluids Calculations,physical,decimal,pmc-6414314-1,Extracted,"A 22-year-old male patient visited the renal department of Chonnam National University Hospital for evaluation of an abnormal computed tomography (CT) finding. His height was 179 cm, body weight was 58 kg, and body mass index was 18 kg/m2. There was no history of any underlying disease and, at the time, he was not taking any medication. His family history was non-specific. Initial laboratory findings were all within normal range. Laboratory investigations showed leukocyte count, 9,500 cells/mL; hemoglobin, 13.0 g/dL; platelet count, 340,000 cells/mL; blood urea nitrogen level, 16.1 mg/dL; creatinine, 0.75 mg/dL; estimated glomerular filtration rate, 130.2 mL/min/1.73 m2 (which was calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula: mL/min/1.73 m2=141 × minimum(creatinine/k, 1)α × maximum (creatinine/k, 1)−1.209 × 0.993age × 1.018 (if female) × 1.159 (if black), where κ is 0.7 for women and 0.9 for men, and α is −0.329 for women and −0.411 for men; sodium level, 138 mEq/L; potassium level, 4.0 mEq/L; chloride level, 114 mEq/L; magnesium level, 2.0 mg/dL; total calcium level, 8.4 mg/dL; and serum osmolality, 290 mOsmol/kg. Urine analysis showed the following values: urine osmolality, 312 mOsmol/kg; random urine sodium, 120 mEq/L; random urine potassium, 30.4 mEq/L; random urine chloride, 61 mEq/L; and urinary pH, 7.0. Urine analysis did not show any proteinuria, hematuria, or glucosuria. Contrast-enhanced CT of the abdomen () was performed. Over 20 cysts were detected in both kidneys and in the liver. The right kidney size was 171.30mm (length) × 120.29 mm(width) × 65.80 mm(depth), and the left kidney size was 163.42 mm(length) × 101.88 mm(width) × 79.86mm(depth).
Genetic analysis was performed using Sanger's method. Direct sequencing revealed that the 22nd intron had translocated from G to A, which was previously reported as a pathogenic variant, but the change in amino acid was unknown ().
An angiotensin-converting enzyme inhibitor treatment was started and a follow-up CT was performed after 2 years (). The volume of each kidney was as follows: right kidney volume, 828 mL; left kidney volume, 791 mL; total kidney volume (TKV), 1,620 mL; and height-adjusted total kidney volume (HtTKV), 905 mL/m. The CT showed that the growth rate of the HtTKV was 7.33% per year.
From May 2017, tolvaptan therapy was initiated at a dose of 60 mg per day, with morning and afternoon doses at 45 mg and 15mg, respectively. Monthly checks of the body weight, blood pressure, and laboratory tests including complete blood count, renal function test, electrolyte text, liver function test, random urine electrolytes, and osmolality were performed. Further clinical course was uneventful and the electrolyte levels remained unremarkable. The patient did not report any specific side effects of the tolvaptan therapy, except polyuria and polydipsia. The liver enzyme profile and serum sodium level and osmolality remained within normal range. The serum creatinine was 0.97 mg/dL after 1 year of the tolvaptan therapy (). The urine osmolality decreased to less than 300 mOsmol/kg and urine sodium was less than 100 mOsmol/kg.
Another follow-up abdominal CT was performed 11 months after commencement of tolvaptan therapy (). The size of each kidney was as follows: right kidney volume, 837 mL; left kidney volume, 792 mL; TKV, 1,629 mL; and HtTKV, 910 mL/m. The growth rate of HtTKV decreased from 7.33% to 0.66%(). Till the foreseeable future, the plan is to maintain the current tolvaptan therapy with its same dosage, unless a specific problem occurs.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [58.0, 'kg']}",98,93.1,102.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 58.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (58.0 kg - 20 kg) = 98.0 mL/hr.
Hence, the patient's fluid maintenance is 98.0 mL/hr."
4997,22,Maintenance Fluids Calculations,physical,decimal,pmc-6444971-1,Extracted,"A 64-year-old male who complained of headache for 1 day underwent an emergency intracranial aneurysm clipping after subarachnoid hemorrhage from rupture of posterior communicating artery aneurysm. His body weight was 60 kg and height was 169 cm. He was previously healthy, but a smoker (10 cigarettes a day for 40 years) without drug abuse and remarkable family history. Physical examination revealed axillary temperature of 37°C, blood pressure 140/90 mmHg, heart rate 106 bpm, respiratory rate 20 bpm, and oxygen saturation 95% on room air. He was drowsy without nausea or vomiting. Glasgow coma scale score was 15. Blood routine showed that white blood cell count was 15.63 × 109/L. Thoracic computerized tomography which was taken a day before the surgery revealed bullae and low attenuation area in bilateral lower lobes []. Written consent of publishing of this paper was obtained from the patient when he was discharged.
The patient was positioned supine in the operating room. Anesthesia was managed with etomidate, fentanyl, propofol, remifentanil, and cisatracurium. After successful intubation on one attempt, chest auscultation revealed bilateral equal breath sounds without rales or wheezing. Vital volume was set at 450 mL and respiratory rate 12 bpm without positive end-expiratory pressure. The central vein was not punctured or catheterized. During surgery, the artery aneurysm was clipped with Sugita Titanium Aneurysm Clip (17-001-86, MIZUHO Corporation, Tokyo, Japan). The surgery lasted for 3 h and finished uneventfully without awakening the patient during the surgery. There was no blood transfusion. A total of 1000 mL lactated Ringer's solution was given. Urine output was 300 mL.
The spontaneous breath was back 10 min after the surgery, so mechanical ventilation was stopped. Twenty min later, the patient developed a sudden dry cough without consciousness or extubation. Soon after the cough, oxygen saturation began to decline, so assisted ventilation was intermittently used to keep oxygen saturation more than 90%. In the meantime, subcutaneous emphysema was noted over his neck and chest. His blood pressure was 150/90 mmHg and heart rate was 70 bpm. A bolus of 50 mg propofol was given intravenously. Diminished breath sounds were detected in the left lung on auscultation. The patient's blood pressure and heart rate began to decrease. A thoracic surgeon was invited for consultation immediately and arrived 10 min later. After physical examination, needle aspiration was performed under local anesthesia in the left midaxillary line and in the fifth intercostal space, and then a large of tensioned air was immediately released, so tube thoracostomy was undergone at the same site. The procedures were followed by immediate improvement in oxygen saturation. During the whole period, heart rate was once decreased to 40 bpm, so a total of 1 mg atropine was administered intravenously and blood pressure was reduced to 70/40 mmHg, so 10 mg dopamine was given. No tear of the trachea or endotracheal tube obstruction was found under fiberoptic bronchoscopy. When his status was stable, the patient was taken to take cerebral and thoracic computerized tomography scan with oxygen supplementation. The thoracic computerized tomography demonstrated bilateral pneumothorax, pneumomediastinum, and subcutaneous emphysema in the neck and chest []. The patient was transferred to the intensive care unit.
Two days later, the patient was sober and extubated. His oxygen saturation was around 95% with oxygen administration by a venturi mask. Oxygen saturation could be kept above 95% on room air on the next day. The intercostal tube was removed on postoperative day 12. Follow-up chest radiograph on postoperative day 13 showed resolved pneumothorax and pneumomediastinum with residual subcutaneous emphysema in the neck and left chest wall []. The postoperative course was uneventful, and the patient was discharged with a little subcutaneous emphysema on postoperative day 17.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.0, 'kg']}",100,95,105,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.0 kg - 20 kg) = 100.0 mL/hr.
Hence, the patient's fluid maintenance is 100.0 mL/hr."
4998,22,Maintenance Fluids Calculations,physical,decimal,pmc-3404937-1,Extracted,"The patient is a 63-year-old Caucasian man. He is 1.61 meters tall and weighs 66 kilograms. After working as a car mechanic for 36 years, he had been receiving disability benefits for 11 years. He was working part-time as a caretaker averaging 10 hours per week until two and a half years ago. At the age of 35, the patient began having bouts of severe back pain approximately twice a year. When these episodes occurred, he took non-steroidal anti-inflammatory drugs for three to four weeks for pain relief. At the age of 40, lumbar spondylolisthesis was diagnosed by radiography. At the age of 50, he suddenly developed severe right hip pain. He suffered from substantial arthrosis on the right side, which was treated with a total hip replacement one year later.
Three years ago, he began to develop neurological symptoms in both hands. Pain and loss of function of his fingers prevented him from working as a caretaker. The pain radiated from his neck bilaterally down to his fingers and was described as parasthesia-like in nature. He also complained of weakness in his hands. Left hand digit flexion was classified as J1 and right hand as J4. Digit extension was classified as J4 on the left and J2 on the right and abduction on the left was classified as J0 and on the right as J1. The patient also had difficulty walking (Nurick 4, EMS 10/18) as he had to support himself using his surroundings in order to stand upright and was unable to walk unassisted. He was referred to a neurologist by his general practitioner who in turn referred him to a neurosurgeon. Radiographs (Figure ) magnetic resonance imaging (Figure ) and computed tomography (CT) revealed a spondylolisthesis between C7 and T1. Using the Meyerding classification [], which was initially developed for grading the degree of lumbar spondylolisthesis, the patient would have been diagnosed with a cervico-thoracic spondylolisthesis of the second or third degree. The spondylolisthesis, measured using the method developed by Kawasaki et al. [], was 13 mm. In view of the special nature of the case, a collaborative treatment between neurosurgeons and orthopedic surgeons was favored and subsequently implemented.
The surgical management was performed as follows:
The patient was placed in the supine position. The intervertebral disk at C7-T1 was exposed using blunt dissection. The disk was then removed to the point of the ligamentum flavum. A subsequent resection of the lateral parts of the intervertebral discs significantly mobilized the spondylolisthesis.
The wound was closed and the patient was rotated to the prone position. First, the dislocation between vertebras C7 and T1 was reduced while positioning the head.
Subsequently, the lateral masses were prepared from a dorsal approach between C5 and T3. Then, lateral mass-screws were inserted into C5 and C6. We had noticed considerable laxity between C6 and C7. In addition, C5 and C6 were naturally fused and we decided to include them in the instrumentation. There was also a rigid displacement between C7 and T1.
Bicortical screws were then inserted into the transverse processes of T2 and T3. These were inserted into at least two segments from both sides in divergent directions. The length of these screws was 10 to 12 mm, with a diameter of 3.2 mm.
This was followed by a laminectomy. Since the roots of C7 and C8 were exposed, the lateral masses of C7 and C8 had to be resected. Longitudinal rods were placed. Proper reduction in lordosis and the preservation of a 5 mm intervertebral space between C7 and T1 were confirmed by radiograph. Set screws were used to fix the instrumentation in the desired position. Chips of cortical and cancellous bone were placed lateral to the longitudinal rods.
The dorsal wound was then closed. The patient was again rotated to the supine position to reopen the ventral wound. Now, instead of the previously seen displacement, a large gap was visible between C7 and T1. The endplates between C7 and T1 were milled and the ligamentum flavum was resected using punches. Then, the spinal canal was exposed completely, using a Caspar opener.
Subsequently, a Harms basket, filled with autograft bone chips, was inserted into the intervertebral space. Three drains were placed and the wound was closed. For prophylactic infection control, the patient was perioperatively given intravenous 1.5 g cefuroxime twice a day for the next four days. Intraoperative and postoperative radiographs (Figure and ) were taken to confirm correct placement of the instrumentation.
Following the operation, the patient was transferred to the intensive care unit. His vital signs were stable enough for him to be transferred to the general postoperative recovery ward on the fourth postoperative day. Eleven days after surgery, the patient left the hospital and entered an orthopedic and neurologic rehabilitation program.
The pain and parasthesias in his fingers resolved after the operation. Two months postoperatively, his ability to walk had noticeably improved after completing his rehabilitation program (Nurick 3).
Today, two years postoperatively, the patient is able to walk without assistance (Nurick 2). Flexion of the fingers on his left hand was graded as J3 and as J5 on the right hand. Extension of the fingers on his left hand was graded as J4 and as J2 on the right. Abduction was graded as J4 for his left hand and as J2 for his right hand (EMS 14/18).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [66.0, 'kg']}",106,100.7,111.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 66.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (66.0 kg - 20 kg) = 106.0 mL/hr.
Hence, the patient's fluid maintenance is 106.0 mL/hr."
4999,22,Maintenance Fluids Calculations,physical,decimal,pmc-5796503-1,Extracted,"A 25-year-old man was referred to vascular medicine clinic because of pain in the left calf while running, which had been occurring for the past 4 years.
This patient practiced almost daily physical activity that involved both combative and running (over 8 h per week), and he competed at a regional level (with a personal best of running of 36min12s/10000 m). In 2012, the patient had reported left calf pain when running, forcing him to stop. He described a calf swelling sensation that gradually increased with the intensity of running. While in the past he could easily run 15–20 km, the patient reported at that date that he could not run more than 2 km before having to stop. After stopping, the pain was deep and persisted for several minutes; it was also associated with swelling of the calf. This pain had led him to change his occupation to a less physically demanding job (military officer in the past, and now security officer). The consequences were a weight gain of 8 kg, and a cessation of all physical activity (running, fight sports). The patient also reported a loss of self-esteem.
Over a period of 4 years, the patient was seen by two general physicians, a rheumatologist, a neurologist, a sports physician and a vascular physician. Many explorations were carried out (spinal and pelvic x-ray, pelvic and lumbar spine scan, venous duplex scan, arterial duplex scan, and electromyography), all of which revealed no sign of dysfunction. The sports physician raised the possibility of diagnosis of a compartment syndrome, but the patient refused to submit to investigation of intramuscular pressure taken at rest and in immediately post exercise. Different therapies were proposed, including anti-inflammatory drugs, paracetamol and compression stockings (Class 2).
The patient interview revealed that a proximal deep vein thrombosis DVT (thrombosis in the iliac, femoral and popliteal veins) of the left lower limb had been diagnosed in 2012 and treated for 6 months by direct oral anticoagulant therapy (Rivaroxaban, Xarelto 20 mg per day) combined with compression stockings french class 3 worn (20–36 mmHg) for 6 months and then class 2 compression socks (15–20 mmHg) thereafter. This episode of DVT occurred spontaneously without major or minor contributing factors. There was no family history of venous thromboembolism disease. Clinical and laboratory tests had found no neoplasia. The biological thrombophilia test at distance of anticoagulation was negative.
The patient was 1.78 m and 79 kg (body mass index = 24.9 kg/m2). He was afebrile, and his brachial blood pressure was 120/70 mmHg. Upon examination the legs were hot and there was no trophic disorder. There was a difference in the circumference of the calves (left calf 2 cm > right calf). There were no visible or palpable varicose veins. Peripheral pulses were present and there was no sign of Lassegue. Palpation of the major lower limb joints (ankles, knees, hips) was not painful. Calves were flexible, painless, with good trophicity. No lymphadenopathy was found and no local inflammatory signs. When examined by auscultation, there were no vascular sounds along the vascular axes.
All Doppler ultrasound measurements were performed with a high-resolution ultrasound machine (Affiniti 70, Philips, Amsterdam, The Netherlands). The deep venous system was free and compressible when compressed by the ultrasound probe at calf level (posterior tibial veins, peroneal, gastrocnemius and soleus), at femoral popliteal level (popliteal veins, femoral and common femoral) and at ilio-cava level with no sign of recent deep vein thrombosis. There was wall thickening at the left common femoral vein CFV (anterior posterior diameter APD under compression = 3.9 mm) and at the left external iliac vein (APD under compression = 3.6 mm); this finding had already been highlighted when vascular physician examined the patient in 2013.
The Doppler examination showed a clear asymmetry of the respiratory modulations of blood velocity between right and left CFV. In the left CVT, respiratory modulations were almost absent and blood volume flow was not as high as on the right side. We found a reflux into the left internal iliac vein and dilation of the left gonadal vein. While standing, there was no significant deep venous reflux (> 1 s) at the popliteal vein (functional venous valves). The superficial venous system (great and small saphenous veins) was compressible and continent.
The diagnostic hypothesis of MTS was issued at the end of this first consultation, taking into account the following clinical and hemodynamic arguments:▪ History of the left proximal DVT without predisposing factor. ▪ Symptoms of left calf venous claudication due to effort (+/− associated with unilateral edema reported by the patient). ▪ Asymmetry respiratory modulation and venous blood volume flow at the left proximal deep vein (as a result of a downstream obstacle).
Additional morphological exploration was requested computed tomography angiography (CTA) and a surgical opinion was recommended and requested.
The CTA revealed compression of the left common iliac vein (CIV) between the right common iliac artery (CIA) and lumbar spine (Fig. ) and intraluminal spurs. There was also dissimilar venous systems collatorally with that was more highly developed on the left iliac axis relative to the right iliac axis, reflecting the need to create a system of substitution.
In this context of symptomatic MTS with compatible imaging, venography was performed in order to confirm the diagnosis and to treat the MTS at the same time. Venography showed patency of the left venous axis iliac featuring endoluminal spurs and a footprint at the terminal portion of the iliac vein (Fig. ).
Endovascular support was carried out with introduction of two Wallstent endo prostheses (Boston Scientific) into the common iliac and external iliac veins, associated with angioplasty intra stent to modulate the different areas of overlap, the diameters and lengths to achieve a harmonious assembly. The phlebographic control carried out at the end of the procedure was satisfactory.
At 3 and 6 months, the patient reported an improvement in symptoms. The patient restarted running, and initially venous claudication was not felt and the patient was once more able to run more than 10 km. He currently wears a compression class III especially during physical activity, as advised.
Angiographic assessment found normal stent patency at the iliac vein, with symmetrical respiratory modulations. It was also decided to carry out a duplex ultrasound scan at 3 months. At this scanning session the stents were in place and permeable. Pharmacological treatment in the form of an anti platelet (Clopidogrel 75 mg) was prescribed.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [79.0, 'kg']}",119,113.05,124.95,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 79.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (79.0 kg - 20 kg) = 119.0 mL/hr.
Hence, the patient's fluid maintenance is 119.0 mL/hr."
5000,22,Maintenance Fluids Calculations,physical,decimal,pmc-8213290-1,Extracted,"The patient, a teenage male, 16 years old, mainly having a short penis for (16 years), was suffering from progressive weight gain (for 9 years), unstable walking (for more than 1 month). The mother did not take drugs during her pregnancy, and there was no history of exposure to any poisonous and radioactive substances. He is an off-spring of non-consanguineous parents, born full-term normal delivery, with cephalic presentation, no history of hypoxia, birth weight 3.3 kg, no complications such as obvious hypotonia and feeding difficulties after birth (The birth length is not known). The child was breastfed till he turned 2 years old, and while he started walking at 2 years old, he commenced talking later than his peers. The child also showed slow reaction since childhood, poor academic performance, mild intellectual disability and social fear. Movement disorder was noted in July 2020, needing a visual reference when he walks, otherwise he walked unsteadily. The patient was 155 cm tall and weighed 105 kg, and his BMI was, therefore, 43.70 kg/m2. According to the percentile curve of height and weight of boys aged 2 to 18 years old obtained from the physical development survey of 9 provinces and cities in China in 2005, the patient's height is less than 3% of the same age and sex in the same region, and his weight is more than 97%. Further, he had thick and black hair with a thick posterior hairline to the neck, thick eyebrows, wide eye-distance, collapsed nose, some beard scattered around the mouth, no Adam's apple, changed voice, armpit hair, and smaller hands and feet when compared to his peers. There was no breast development on either side. He had a thick vulva and pubic hair and pigmentation in the penis and scrotum, but there had been no obvious enlargement of his penis since he turned 9 years old, no morning erection and no spermatorrhea. The penis was found to be about 4 cm long in the non-erected state, and the left testicle's volume was found to be about 1 mL. The right testis was not palpable.
Based on the patient's medical history, imaging examination and molecular genetic testing results, the diagnosis was SYS. Patient was advised to reduce weight, control blood lipids, blood glucose through appropriate strengthening of exercise and diet control in the future. At the same time, the family members were advised to provide mental training to the patients to strengthen their contact and communication with the outside world and improve the autistic symptoms of the patient. Because of the patient's bilateral cryptorchidism, it is recommended that the patient should be treated with bilateral cryptorchidism reduction fixation in the department of urology. After a follow-up of the patient for 2 months, the patient is still walking unsteadily and requires an auxiliary reference material to walk normally. There is no significant change in height compared to before, and the weight has dropped by about 2 kg in the past 2 months. The rest of the physical examination did not show significant changes. The symptoms of autism have improved slightly. The patient is willing to communicate with outsiders, his intelligence has not improved significantly, and his academic performance in school is still at the middle and lower levels.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [105.0, 'kg']}",145,137.75,152.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 105.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (105.0 kg - 20 kg) = 145.0 mL/hr.
Hence, the patient's fluid maintenance is 145.0 mL/hr."
5001,22,Maintenance Fluids Calculations,physical,decimal,pmc-8187023-1,Extracted,"A 25-year-old male with American Society of Anesthesiologists class III physical status and body mass index (height 167 cm, weight 65 kg) 23.3, was admitted for surgery for squamous cell carcinoma (SCC) of tongue.
The patient had been diagnosed with hemophilia 15 y ago. The previous medical history had no other abnormalities. Three months before being admitted, the patient had visited another hospital with complaints of intense pain on right tongue lesion. The patient had severe hemophilia A and required red blood cell transfusion because of bleeding after a swap test and incisional biopsy. The bleeding stopped within 30 min following an injection of factor VIII concentrate. Histological examination of the swab specimen revealed an atypical squamous cell carcinoma. The patient was then transferred to the Oral and Maxillofacial Surgery Department, Seoul National University Dental Hospital for surgery.
On examination using CT and MRI, an ulcerative lesion of 2.9 × 1.5 cm sized was seen on the right mid posterolateral border of tongue (). On clinical examination, the tumor showed endophytic growth, and the depth of the ulcer was >10 mm. Enhanced computational tomography (CT) image () revealed the depth of invasion to be 19 mm, and a suspicious metastatic lymph node was observed on the right level IIa. Due to swab test, there was prolonged bleeding and oozing on the swab site. The Human papillomavirus (HPV) infection status was tested using intraoral mucosal swab and the result showed HPV16 (−), HPV 18 (−), other high risk (−). After the swab test at the outpatient department, as hemostasis was not achieved the patient was moved to the day-surgery unit. Hemostasis was then achieved by application of bipolar electrocauterization, Surgicel® (Ethicon SARL, Puits-Godet 20, Swizerland) (oxidized regenerated cellulose); gauze biting was also performed. After discharge, factor VIII concentrate injection was needed again due to the swab site bleeding. The patient was scheduled to undergo partial glossectomy, selective neck dissection, and reconstruction with a lateral arm free flap.
A preoperative electrocardiogram (ECG) showed normal sinus rhythm and the chest radiography was unremarkable. Preoperative hemoglobin (Hb), hematocrit (Hct), and platelet count was 10.5 g/dl, 32.1, and 401 × 103/µl respectively. The coagulation profile showed that the prothrombin time (PT) international normalized ratio (INR) was 0.95, which was within the normal range of 0.8 to 1.2, and the activated partial thromboplastin time (aPTT) was 48.3 s, which was longer than the normal range of 26.7 to 36.6 s. The activity of coagulation factor VIII was reduced by 11%.
According to the answers of the consultation with the Hematology Department at Seoul National University Hospital, the patient was preoperatively injected with monoclonal antibody-purified factor VIII concentrate (GreenMono®, GC Pharma, Yongin, Republic of Korea, 2892 International Unit [IVS]) 1 h before the surgery. Twelve hours after the initial injection, another injection of the same amount of GreenMono® was administered. Thereafter, the injection was administered at every 12 h interval. Considering the extent of reconstructive surgery, the administration was recommended for 7 to 14 d so as to achieve sufficient hemostasis. In case of insufficient hemostasis after the injection of GreenMono®, 500 mg of tranexamic acid was recommended every 8 h.
General anesthesia was induced after routine monitoring (pulse oximetry, end-tidal CO2, ECG lead II with continuous ST-segment analysis, and noninvasive blood pressure monitoring) in the patient. His preoperative blood pressure (BP) was 121/65 mmHg, heart rate (HR) was 102 beats/min, body temperature was 36.1℃, and oxygen saturation (SpO2) was 100%. After sufficient preoxygenation, anesthesia was induced with lidocaine (30 mg), propofol (120 mg), and cisatracurium (16 mg). Nasotracheal intubation with an endotracheal tube (right angle endotracheal tubes, cuffed, 7.0 mm) was performed using fiberoptic bronchoscopy. Anesthesia was maintained with an O2/air mixture (fraction of inspired oxygen 50%) and adjusted for desflurane (4.5–8% vol). The patient was maintained on volume-controlled mechanical ventilation with a mean arterial pressure of 60–80 mmHg for a normal and regular heart rate. An additional neuromuscular blocker was administered, as needed. The tidal volume was 6–8 ml/kg, and positive end-expiratory pressure (5 cmH2O) was utilized. The respiratory rate was adjusted to maintain the partial pressure of end-tidal CO2 at 30–35 mmHg. Invasive BP monitoring and arterial blood gas analysis (ABGA) were performed with the catheter in the left dorsalis pedis artery. ABGA was performed every two hours after the surgery began ().
Non-invasive continuous monitoring of total hemoglobin (SpHb; Masimo, Irvine, CA, USA) was also performed. Though this is not as accurate as the laboratory hemoglobin, it is used to identify relative numerical changes due to the serial measurements obtained. The initial value was 11.1, and 10.1 was the lowest value measured.
Central catheterization of the right femoral vein was performed to gain venous access because of the known bleeding tendency. During the reconstruction procedure, when the systolic blood pressure dropped to less than 120 mmHg, ephedrine 5–10 mg was injected twice, followed by dopamine, which was continuously injected for 275 min at a rate of 3.2–10 mcg/kg/min. This permitted maintaining the systolic blood pressure of 130–150 mmHg.
The routine surgical field was draped with povidoneiodine in the orofacial and neck areas. The tongue lesion was grossly marked with a surgical marking pen. Partial glossectomy was performed for a 1 cm safety margin (). Muscular bleeding during partial glossectomy was controlled using bipolar electrocautery. Frozen biopsies were performed around the marked margin. While waiting for the biopsy result, selective neck dissection was initiated. The internal jugular vein, carotid artery, vagus nerve, and spinal accessory nerves were isolated and preserved. Right levels I, II, III, and IV lymphatic chains were resected (). Meticulous bleeding control was performed using electrocautery, vascular tying, and collagen sponge. The right side of the retromandibular vein branch and facial artery were isolated for vessel anastomosis. After confirmation of negative frozen biopsy results, lateral arm fasciocutaneous free flap harvesting was initiated. Skin incision and subcutaneous dissection were performed up to the junction of the radial collateral arteries. The branch and veins of the distal part of the posterior radial collateral artery were clamped and cut. The lateral arm fasciocutaneous free flap was transferred to the tongue to fit the defective region. The flap inset was closed with 4-0 Dafilon. Vessel anastomosis was performed using a microscope. The anastomosis of the posterior radial collateral artery with the facial artery and that of vena comitans with the retromandibular vein branch was performed via the end-to-end mode (). All surgical sites were closed layer by layer, and the surgery was completed by suction drain and pressure dressing.
The surgery was uneventful. At the end of the surgery, 125 mg of methylprednisolone mixed with 50 ml of normal saline was injected. The total anesthesia time was 535 min, and the total surgery lasted for 500 min. During the operation, 5500 ml of crystalloid was administered and the total urine output was 2350 mL. The estimated blood loss was 400 ml. Following recovery at recover room for 40 minutes in the intubated state, the patient was transferred to the intensive care unit (ICU) and after 11 h, was transferred to the recovery room for extubation. The oxygen was supplied as 5 L/min through the T-piece. Oral and endotracheal tube suction was performed with routine monitoring. During the leakage test, the oxygen saturation was maintained at 99%. After extubation, the patient was monitored, and oxygen support by a reservoir bag mask was provided.
Monoclonal-antibody-purified Factor VIII Concentrate (GreenMono®) 6000IU (3000IU Bis in die, bid) was used on the day of surgery. From the first postoperative day (POD) and up to the next 15 days, 3000 U (1500 U bid, 8:30am, 8:30pm) were administered daily and then discontinued. On POD 18, a total of 1500 IU of GreenMono® was used before and after dental scaling, #26 distal caries resin restoration, #28, and #38 surgical extraction. No additional hemostatic agents, such as tranexamic acid, were used. Following administration of GreenMono® after the surgery (), the aPTT level was rarely out of the normal range, and there were no bleeding-related symptoms or complications. The patient was discharged without any postoperative complications on POD 25.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [65.0, 'kg']}",105,99.75,110.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 65.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (65.0 kg - 20 kg) = 105.0 mL/hr.
Hence, the patient's fluid maintenance is 105.0 mL/hr."
5002,22,Maintenance Fluids Calculations,physical,decimal,pmc-4877834-1,Extracted,"A 4 year old male child was scheduled for a repeat single-staged bladder exstrophy repair. Patient had a previous 1st stage surgery at 3rd week of life under general endotracheal anaesthesia. There were no documented anaesthetic complications; however, postoperatively the patient developed leakage of urine at the bladder neck and separation of the pubic bones necessitating a repeat surgery.
The preoperative review revealed no other problems except a lower abdominal scar with suprapubic defect draining urine, pubic diasthesis approximately 5 cm and an epispadias. He weighed 12 Kg and his packed cell volume was 38%, other investigations including intravenous urogram, serum electrolyte, urea and creatinine and renal scan were normal.
Anaesthesia plan consisted of general endotracheal anaesthesia and caudal epidural anaesthesia/analgesia. A multiparameter monitor comprising non-invasive blood pressure (NIBP) and pulse oximeter were attached to the patient and baseline vital signs recorded as follows: pulse rate- 96/m, BP-112/62 mmHg and SP02 -100% on air.
The patient was preoxygenated for 5minutes and premedicated with 0.24 mg of atropine. Anaesthesia was induced with 50 mg of sodium thiopentone, halothane at 1-2%, and 18 mg of Suxamethonium was given to facilitate endotracheal intubation with size 5mm cuffed endotracheal tube. Caudal epidural anaesthesia was performed using a size 16G tuohy epidural needle. Approximately 4 cm of the catheter was left in the epidural space and loading dose of 8 mls of 1% lidocaine with adrenaline was injected. Halothane was reduced to 0.5%, 6 mg of pentazocine and 0.6 mg of pancuronium were given and surgery was commenced.
Intraoperatively, several procedures were performed by a team of orthopaedic, urologic and paediatric surgeons, these included bilateral anterior innominate bone osteotomy, followed by dissection and delineation of the bladder, insertion of ureteric stents and bladder catheters, repair of the bladder, approximation of pubic bones and epispadias repair.
Surgery lasted for 10 hrs, the estimated blood loss from gauze count and suction bottle was 250 ml, a total of 250 ml of blood was transfused in 20-40 ml aliquots, approximately 1500 ml of Ringers lactate was used and 1 mg/kg of furosemide was given. At the end of surgery, muscle paralysis was reversed with neostigmine/atropine combination and 150 mg of intravenous paracetamol was given. Patient was extubated in the theatre fully awake and was transferred to the recovery room.
Postoperatively, the patient was managed in the paediatric surgical ward; skin traction was applied to both legs and tied to the foot of the bed. Intravenous fluid and antibiotics were continued, analgesia was maintained with epidural top-up injections using 6ml of 0.125% bupivacaine plus fentanyl 1 µg/ml 6 hrly for 48 hr, rectal diclofenac and intravenous paracetamol. The epidural catheter was removed on the 3rd postoperative day; further analgesia was maintained with oral paracetamol, rectal dicIofenac and intravenous pentazocine as per the surgeon’s order. On the 9th postoperative day, patient developed abdominal wound dehiscence and vesicocutaneous fistula and were managed conservatively to complete healing","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.0, 'kg']}",44,41.8,46.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.0 kg - 10 kg) = 44.0 mL/hr.
Hence, the patient's fluid maintenance is 44.0 mL/hr."
5003,22,Maintenance Fluids Calculations,physical,decimal,pmc-4667049-1,Extracted,"C. K., a 53-year-old Caucasian female, was referred by her primary care physician for abnormal liver function tests. She was first diagnosed with HCV exposure in 2005 with genotype 3a and had undergone pegylated interferon monotherapy weekly for six months. She achieved end of treatment response. Subsequently, she continued to use intravenous drugs. On presentation to our clinic on 05/04/2011, patient was found to have reinfection with genotype 1a with an HCV viral load of 29,000 IU/mL. She had no nausea, vomiting, heartburn, abdominal pain, or dysphagia. She had lost some weight but she was dieting. She denied any intravenous drug and alcohol use in last 3 years.
Her past medical history was notable for methicillin resistant staphylococcus aureus (MRSA) endocarditis, vertebral osteomyelitis, hyperlipidemia, diverticulosis, and Helicobacter pylori gastritis. There was no family history of celiac disease, type 1 diabetes or any other autoimmune diseases. She is a former smoker. Her medications included butalbital/acetaminophen/caffeine, simvastatin, and esomeprazole.
Initial physical examination showed temperature of 98.2°F, pulse of 72 beats/minute, BP of 116/70 mm/Hg, and weight of 146 pounds. Physical examination was normal “without stigmata of liver disease or malnutrition and so forth.”
Laboratory data on initial visit showed normal complete blood count (CBC), complete metabolic profile (CMP), and iron studies. Pt was found to have HCV viral load of 4,515,392 IU/ml and genotype 1a. Other causes of liver disease including hepatitis B, autoimmune hepatitis, Wilson disease, and HIV were ruled out. The patient underwent a liver biopsy which showed Metavir grade 2 inflammatory activity and stage 1 fibrosis ().
Colonoscopy was also done on 6/25/2008 at different facility, which did not show any polyps but showed diverticular disease of descending colon and sigmoid colon. The patient underwent upper gastrointestinal endoscopy (EGD) done on 10/7/2009 which was unremarkable.
Treatment was initiated on dual therapy with pegylated interferon alfa-2a at 180 μg subcutaneous weekly plus ribavirin 600 mg orally twice per day for a 4-week lead-in phase, followed by triple therapy using boceprevir (BOC) 800 mg orally three times per day for total of 28 weeks. HCV viral loads which were collected at weeks 4, 8, 12, 21, and 24 were undetectable by polymerase chain reaction. During treatment, the patient developed neutropenia and anemia, which were treated with pegfilgrastim and darbepoetin alfa.
Approximately 4 weeks after initiation of triple therapy the patient developed loose nonbloody bowel movements, which was not reported at the time. She experienced nausea and decreased appetite but no vomiting or abdominal pain. Occasionally she felt bloated. There was no fever, chills, or skin rash.
Three months following cessation of treatment the patient complained of ongoing weakness and dyspnea on exertion which had begun after the initiation of therapy but which had not resolved completely. She had ten-pound weight loss during treatment which persisted, but she also now admitted to having 5-6 watery loose bowel movements for the preceding five months. Repeat CBC showed low hemoglobin of 10.7 g/dL (baseline 14 g/dL). The patient failed to give stool samples for analysis. She underwent an EGD and colonoscopy. During EGD, mucosa in the stomach and second and third part of duodenum appeared normal but biopsies from second portion of the duodenum revealed mild villous blunting, mild crypt hyperplasia, and minimal intraepithelial lymphocytes consistent with CD (). The tissue transglutaminase IgA was 85 U/mL. The patient was started on gluten-free diet. Her intestinal symptoms improved and the hemoglobin returned to normal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [146.0, 'lbs']}",106.22443,100.91321,111.53565,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 146.0 lbs so this converts to 146.0 lbs * 0.453592 kg/lbs = 66.22443 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (66.22443 kg - 20 kg) = 106.22443 mL/hr.
Hence, the patient's fluid maintenance is 106.22443 mL/hr."
5004,22,Maintenance Fluids Calculations,physical,decimal,pmc-5564854-1,Extracted,"A 34-year-old African woman was diagnosed with HIV infection when she attended for sexually transmitted infection screen in 2006. She was commenced on abacavir, lamivudine, and nevirapine, as her nadir CD4 count was 90 cells/mm3. Her last HIV RNA level was <70 IU/mL, and CD4 counts were persistently over 600 cells/mm3. She had a history of recurrent painful vulval ulcers. Her last documented clinical episode of genital herpes was in 2014. However, the vulval swab for the polymerase chain reaction (PCR) of herpes simplex virus (HSV) DNA 1 and 2 were negative.
In May 2016, she was admitted to a medical admission unit with a 4-day history of fever, headache with neck pain, and intolerance to light. She did not give any history of recent clinical features of mucocutaneous herpes infection. She did not have any previous history of viral meningitis. She was born in Kenya and living in the United Kingdom for 26 years. She had been to Kenya 3 years prior to her hospital admission on holiday. Examination revealed marked neck stiffness, with positive Kernig’s sign. Her temperature was 38.7°C. She was alert with a Glasgow Coma Scale (GCS) of 15/15. There were no focal neurological signs.
Investigations showed that her total white blood cells were 5.7 × 109/L, with neutrophils of 3.0 × 109/L. C-reactive protein (CRP) was <5 mg/L. Blood cultures were sterile. Chest radiograph and computed tomography (CT) of the head were reported as normal. Cerebrospinal fluid (CSF) analysis showed total white blood cells of 396 × 106/L, with 100% of lymphocytes and raised CSF protein of 0.88 g/L. The Gram stain did not show any organisms. Serum glucose was 5.1 mmol/L with CSF glucose of 2.9 mmol/L. She was treated with intravenous aciclovir, 800 mg three times a day, and cefotaxime 2 g stat. Her weight was 82.3 kg. Subsequent CSF PCR for herpes simplex type 2 DNA was positive. Herpes simplex type 1 DNA, meningococcal DNA, pneumococcal DNA, and enterovirus DNA were all negative. Cefotaxime was stopped. She was discharged home 3 days after intravenous aciclovir. She was given a 2-week course of oral valaciclovir, 1 g three times a day.
She was reviewed at an outpatient clinic a week later. She remained asymptomatic. She had been advised about the possibility of similar illnesses recurring and reminded to seek medical advice promptly.
She was readmitted with a similar illness 5 months after her last admission. She was alert with GCS of 15/15. She had neck stiffness. Her CD4 counts were 612 cells/mm3. Her repeat CSF showed white blood cell counts of 151/106/L with 90% lymphocyte count and raised protein of 0.66 g/L. Herpes simplex type 2 DNA was detected; by contrast, Herpes simplex type 1 DNA, meningococcal DNA, pneumococcal DNA, and enterovirus DNA were all negative. CSF HIV RNA level was not done.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [82.3, 'kg']}",122.3,116.185,128.415,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 82.3 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (82.3 kg - 20 kg) = 122.3 mL/hr.
Hence, the patient's fluid maintenance is 122.3 mL/hr."
5005,22,Maintenance Fluids Calculations,physical,decimal,pmc-3905649-1,Extracted,"A one month and twenty-five days old baby girl from a low-income family, with monthly family income of TK 5,000, living in a slum area of Dhaka city was brought to Dhaka Hospital of icddr,b on 6 September 2011. She was the 4th issue of her non-consanguineous parents. Her mother was a 35 years old healthy woman, and her antenatal period was uneventful. The baby was delivered at home at full term but her birthweight and height were not recorded. She was fed diluted formula milk, along with breastmilk since birth. The girl was not vaccinated against any infectious diseases. She did not have a history of contact with any person known or suspected to have tuberculosis, and her family members were healthy. The parents were non-literate, the father was a watchman, and the mother was a housewife. The baby girl was admitted with a history of watery diarrhoea and occasional vomiting for 7 days, low-grade fever and breathing difficulty for 3 days, and reluctance to eat for 2 days. Her stool frequency was 5-6 times per day, copious in amount but there was no visible blood or mucous. There was no convulsion or rash. She received properly-prepared oral rehydration salts (ORS) solution at home.
One month ago, she had been admitted into the same hospital with similar complaints. At that time, she was diagnosed as a case of neonatal sepsis complicated by septic shock and sclerema. Her blood culture grew coagulase-negative Staphylococcus (CNS), and urine culture revealed Escherichia coli (colony count >105). She received two boluses of intravenous fluid resuscitation (20 mL/kg/bolus), intravenous antibiotics (ampicillin 200 mg/kg/day and gentamicin 5 mg/kg/day), inotropic support, and two units of blood. Fourteen days later, she had fully recovered and was discharged with a follow-up plan.
On second admission, the girl was lethargic and mildly pale, and her rectal temperature was 37.8 ˚C. Her radial pulse was feeble, and blood pressure was unrecordable, capillary refilling time was 5 seconds, and extremities were cold. She had severe dehydration assessed according to the Dhaka Method (). The infant weighed 1.8 kg, with a length of 45 cm, and her anthropometric measurements showed a z-score of <-3 for all three indices—weight-for-age, weight-for-length, and length-for-age of the WHO median. She did not have cyanosis, jaundice, oedema, or clubbing. The girl was tachypneic, with a respiratory rate of 60 per minute. She had lower chest wall in-drawing but no nasal flaring, head nodding, stridor, wheezing, or grunting respiration. Her breathing sounds were vesicular with no added sounds (rales, ronchi, or pleural rub). She had oral thrush with angular stomatitis, the abdomen was mildly distended with active bowel sound, and there was no organomegaly. Other systemic examination of the infant was unremarkable.
Her blood glucose, measured at the bedside, was 3.8 mmol/L, and her arterial oxygen saturation (SPO2) was 97% in room air (WHO defines SPO2 of <90% at sea-level as hypoxaemia).
The initial problems were: (a) acute watery diarrhoea with severe dehydration; (b) severe malnutrition; (c) reduced activity (the differentials included dehydration, dyselectrolytaemia, severe pneumonia, and severe sepsis).
The laboratory workup included: complete blood count, blood culture and sensitivity, serum electrolytes, creatinine, rectal swab culture for isolation and identification of enteric pathogens, urine culture and sensitivity, and a chest x-ray to confirm pneumonia. Initially, intravenous rehydration therapy was started for correction of severe dehydration by using half-strength acetate with 5% dextrose with 13 mmol/L of potassium chloride. Subsequently, she was managed as a case of severe sepsis; a fluid bolus was given (@ 20 mL/kg) following the standard sepsis guideline of the hospital; wide antimicrobial coverage was initiated using parenteral ampicillin and gentamicin. The infant was also provided with micronutrients, vitamins and minerals, and feeds according to the hospital's standard protocolized management of severe malnutrition and diarrhoea.
Her total WBC was 20,000/mm3, with 50% neutrophils, no bands, and 48% lymphocytes. Serum creatinine was 118.3 umol/L, TCO2 was 6.9 mmol/L, serum sodium was 143 mmol/L, and serum potassium level was 4.74 mmol/L, and total calcium was 1.8 mmol/L. The chest x-ray revealed patchy opacities in the right perihilar and pericardiac areas.
Twelve hours after admission, she was still lethargic, with little voluntary movement. There was a hardening of the skin and subcutaneous tissues of her both buttocks and thighs. She voided urine 8 hours after admission. Twenty-four hours later, the baby became extremely listless and hypotensive (BP 60/30 mmHg, respiration rate 60/min, pulse rate 150/min, low volume, capillary refilling time 4 sec, with cold extremities, SPO2 88% in room air). She was transferred to the Intensive Care Unit of the hospital. She looked pale, puffy, and oedematous, even though pitting oedema was absent. Her hands and feet looked waxy white, and the limbs were tallow-hard. The sclerema became more extensive involving both buttocks and extremities, and, to a lesser extent, abdomen, chest, and face (ascending type). It did not involve the palms, soles or genitalia. Her reflexes were depressed, the abdomen became distended and tense, and she was not tolerating oral feeds. At that time, the problem list was revised to severe sepsis, very severe pneumonia, ileus, and sclerema. In the Intensive Care Unit, ampicillin and gentamicin were substituted for ceftazidime and amikacin as the patient's condition had deteriorated; another fluid bolus (20 mL/kg) was given, after which her blood pressure recovered, and she was given nothing orally.
In spite of adequate antimicrobials and supportive therapies, the baby's condition progressively deteriorated. At this point, forty-eight hours after admission, it was decided that she might benefit from blood transfusion. So, a fresh blood transfusion was arranged (10 mL/kg), and she received a transfusion daily in the next five days. On the fourth day of hospital stay after her second transfusion, her general condition started to improve; she became alert but the sclerema persisted. Feeding through nasogastric tube was started and well-tolerated. A marked improvement was noticed at the end of the fifth transfusion; the sclerema had softened, and the skin looked pink. The baby became more active and subsequently breastfeeding was re-established. All cultures (blood, urine, and stool) were negative. Parenteral antimicrobials were continued for 10 days. The child was discharged after full resolution of the sclerema two weeks after admission, and her parents were counselled on breastfeeding, immunization, and subsequent follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1.8, 'kg']}",7.2,6.84,7.56,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1.8 kg. Hence, the patient's maintenance fluid is 1.8 kg * 4 mL/kg/hr = 7.2 mL/hr.
Hence, the patient's fluid maintenance is 7.2 mL/hr."
5006,22,Maintenance Fluids Calculations,physical,decimal,pmc-7690928-1,Extracted,"A 2-month-old female infant previously healthy, presented to the pediatric emergency department. The infant's mother reported weight loss, colic, crying for feeding alternating with lethargy, mild diarrhea and worsening of vomiting beginning 5 days before ( ). Previously, she reported nasal congestion, sporadic cough, conjunctivitis, small skin vesicles on the chest and no fever. The real time reverse transcription-polymerase chain reaction (RT-PCR) SARS-CoV-2 nasopharyngeal test result was positive ( ). The mother had been infected with SARS-CoV-2 10 days before the child. On physical examination, the infant was markedly irritable alternating with lethargy, with painful facies suggestive of abdominal colic associated to interruption of feeding several times, moderate dehydration, and hypothermia (<36°C). Her weight was 4.8kg, she had a mottled skin, prolonged capillary refill and a decreased urine output. Pulse rate was 125 beats/minute, respiratory rate was 54 breaths/minute, and oxygen saturation by pulse oximetry of 97% in room air. She was transferred to the pediatric intensive care unit (PICU) after fluid resuscitation.
The patient was born at term, had no pre-existing medical conditions or use of antibiotics, and had been breastfed and complemented with infant formula since the second week of life.
summarizes data on blood biochemistry, urine, stool analysis, coagulation tests and infection biomarker tests performed after confirming SARS-CoV-2 infection by RT-PCR upon admission, and in follow-up. Serology for SARS-CoV-2 was IgM positive (2.11AU/mL, with normal range <0.90) and IgG was negative. The SARS-CoV-2 PCR persisted positive in fecal samples for more than 27 days, although the respiratory tract test was negative. Additional viral panel testing, urine and fecal culture were negative, and only the nucleic acid amplification test (NAAT or PCR) was positive for C. difficile .
The helical multislice chest computed tomography (CT) scan, Doppler echocardiography and abdominal ultrasonography were normal.
During 4 days of hospitalization in the PICU, the patient persisted with abdominal colic, and required additional intravenous fluids due poor acceptance of breast milk or infant formula. The proton pump inhibitor initially prescribed was withdrawn. The patient was not prescribed antivirals, glycocorticoids or antimicrobials.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.8, 'kg']}",19.2,18.24,20.16,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.8 kg. Hence, the patient's maintenance fluid is 4.8 kg * 4 mL/kg/hr = 19.2 mL/hr.
Hence, the patient's fluid maintenance is 19.2 mL/hr."
5007,22,Maintenance Fluids Calculations,physical,decimal,pmc-6260546-1,Extracted,"A 34-year-old primipara with pycnodysostosis was scheduled for an elective caesarean delivery in week 37 + 4 of pregnancy. The patient was 140 cm in height and weighted 60kg. She had no known allergies apart from nonsteroidal anti-inflammatory drugs and was not taking any prescribed medication. She had a history of multiple fractures, including 8 vertebral compression fractures in the thoracic and lumbar spine, but was otherwise healthy. Prior general anesthetics involving intubations had been without complications.
Prior to the caesarean delivery the patient was evaluated in a preoperative assessment by an experienced anesthesiologist.
The airway was assessed using the Simplified Airway Risk Assessment (SARI), which consist of 7 parameters: mouth opening, thyromental distance, Mallampati score, movement of the neck, ability to protrude the jaw, body weight, and a history of previous difficult intubation. A summed SARI score >3 indicates possible difficult intubation []. The patient had a SARI score of 3, due to inability to protrude her jaw (1 point) and a thyromental distance less than 6 cm (2 points). She had a modified Mallampati score of II. The overall dental status was good and she had no prior dental work done.
Physical examination of the spine revealed a slightly accentuated lumbar lordosis, which reduced with flexion. No scoliosis was detected.
Given her medical history, current pregnancy, and physical examination the initial plan was spinal anesthesia. Patient was also consented for general anesthesia. On the day of surgery the anesthesiologist responsible for the operation chose neuraxial anesthesia with an epidural approach. The patient was monitored with 3-lead electrocardiography, pulse oximetry and noninvasive blood pressure. The vital signs were all within normal ranges. Intravenous access was secured with an 18-gauge (G) cannula. Cefuroxime 1.5g and 1000 mL of Ringers-Acetate were administered. The epidural catheter was placed preoperative by an experienced anesthesiologist. Under strict aseptic conditions the epidural catheter was inserted at the L2-L3 level with an 18G Tuohy needle with the patient in the sitting position. The catheter was inserted via midline approach using the loss of resistance to saline technique. Loss of resistance was obtained at 5.5 cm, and the catheter was placed 3.5 cm into the epidural space. The procedure was uncomplicated. During the procedure the patient experienced a short period of paraesthesia in the left leg, which quickly resolved. There was negative aspiration for blood and cerebrospinal fluid. The catheter was tested with 2 mL of 2% lidocaine without onset of spinal anesthesia.
Epidural anesthesia was preformed with incremental doses of a solution consisting of 2% lidocaine with epinephrine 5μg/mL, sodium bicarbonate 8.4mg/mL, and fentanyl 3.75μg/mL. The epidural was dosed in aliquots with intermittent aspiration; a total of 6 mL was administered. The patient achieved satisfying level of analgesia above the Th4 level and the caesarean delivery was performed. It took 4 minutes from the beginning of the procedure to the delivery of a healthy boy. 10 international units of syntocinon were administered. Perioperative bleeding was estimated at 300 mL. The entire procedure took 26 minutes. The postoperative period was without complications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.0, 'kg']}",100,95,105,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.0 kg - 20 kg) = 100.0 mL/hr.
Hence, the patient's fluid maintenance is 100.0 mL/hr."
5008,22,Maintenance Fluids Calculations,physical,decimal,pmc-3725030-1,Extracted,"An 18-year-old female presented with a painful swelling in the left upper quadrant of her abdomen. She became aware of this problem 4 days before presentation. There was no history of previous illness, nor did she take any medication. Physical examination revealed a tender, painful spot and palpable mass in the left upper quadrant of the abdomen.
Biochemistry indicated an elevated C-reactive protein value (14 mg/dl, normal <1). Tumor marker carbohydrate antigen (CA) 125 was within normal range and the lactate dehydrogenase value was not elevated.
Ultrasonographic evaluation revealed a structure in the left upper quadrant, inferior to the left kidney measuring 7 × 9.5 cm. There were calcifications visible and the study in Doppler mode revealed no apparent blood flow.
Subsequent abdominal computed tomography (CT; fig. , fig. ) confirmed a nodular mass in the left upper quadrant measuring 6.5 × 7.5 × 10 cm. The mass was partially solid, partially cystic and had some calcifications. This mass was situated inferior to the left kidney. The spleen and pancreas were situated superior to this structure, the descending colon was posterior to this lesion and was closely related to it. The medial border of this mass was in close contact with the distal part of the transverse colon and the stomach. There was also contact with the jejunal part of the small intestine and a diffuse infiltration of the surrounding fatty tissue. There was no obvious lymphadenopathy and there were no intra-abdominal metastases.
A CT scan of the thorax did not detect thoracic metastases. Colonoscopy was normal except for a small nodule at the cecum, which anatomopathological investigations confirmed to be a submucosal lymphoid nodule.
Excisional surgery was planned and median laparotomy was performed. Exploration revealed that the tumor was located partially in the omentum majus and partially fixed in the retroperitoneum inferior to the spleen. There was no evidence of peritoneal or hepatic metastases during surgery, nor a connection with the small or large intestine. A wide excision of the lesion with a surrounding envelope of fatty tissue was performed. Perioperative frozen section after resection suggested the presence of a mesenchymal tumor.
The specimen weighted 260 g. It consisted of omental fat and peritoneum with a well-defined, encapsulated multinodular mass of 9 × 5.5 × 5.5 cm. Cross-section revealed a solid washed-out lesion with inlying yellow zones and a macroscopic aspect of necrosis.
The tumor was well defined with large inlying islands of necrosis. The tumor cells were monotonous and were closely packed together. The nuclei were of oval shape, irregular and had a notch. There was a moderate mitotic activity. The cytoplasm was vacuolated or lucid. Some cells were separated by connective tissue. Some tumor cells contained periodic acid-Schiff (PAS)-positive granules in the cytoplasm (fig. ).
The tumor that was resected during the laparotomy was positive for vimentin (fig. ) and CD99 (fig. ) (membranous) and negative for keratin, S-100, WT1, neuroendocrine marker (synaptophysin), inhibin, CD45, calretinin, CD117, CD34 and muscle markers (smooth cell actin and desmin). The morphologic and immunophenotype was consistent with ES. Molecular analysis by fluorescent in situ hybridization (FISH) confirmed an ES gene (EWS) rearrangement.
There were no postoperative complications. The patient was discharged from the hospital in good health on the 4th postoperative day. A whole-body positron emission tomography (PET)/CT scan was performed 4 weeks after surgery, which revealed no evidence for hypermetabolic activity.
Two months after treatment, the patient underwent laparoscopic resection of the left adnexa for cryopreservation. During this laparoscopy, 2 lesions of endometriosis were discovered and excised. The adjuvant chemotherapy regimen consisted of a 3-drug regimen including vincristine, ifosfamide and doxorubicin. There were 8 cycles planned every 3 weeks. After the first cycle, the patient had neutropenic fever which necessitated intravenous antibiotics. The subsequent second cycle was given in combination with neurokinine-1 receptor antagonist and granulocyte colony-stimulating factor (pegfilgrastim).
A CT scan of the thorax and abdomen 3 months after surgery revealed no recurrence.
After the third cycle, the patient had neutropenic fever and severe thrombopenia. The patient received intravenous antibiotics and a pool of thrombocytes. There were no other problems reported during the last 5 cycles of chemotherapy. The 6th cycle was one with a dose reduction of doxorubicin and ifosfamide (80%). During this regimen, she received intramuscular injections of luteinizing hormone releasing hormone to protect the right ovary.
The PET/CT scan performed 6 months after chemotherapy revealed no evidence for local, lymphatic or hematogenic recurrence. Ultrasound evaluation of the abdomen and X-ray of the chest revealed no recurrence 14 months after surgery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [260.0, 'g']}",1.04,0.988,1.092,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 260.0 g so this converts to 260.0 lbs * kg/1000 g = 0.26 kg. Hence, the patient's maintenance fluid is 0.26 kg * 4 mL/kg/hr = 1.04 mL/hr.
Hence, the patient's fluid maintenance is 1.04 mL/hr."
5009,22,Maintenance Fluids Calculations,physical,decimal,pmc-6448431-1,Extracted,"A 56-year-old female weighing 45 kg, diagnosed case of carcinoma ovary with pleural metastases and malignant right pleural effusion, was posted for CRS with HIPEC together with thoracotomy and HITHOC. She had received three cycles of paclitaxel and carboplatin-based chemotherapy 6 months back. Patient had no other medical comorbidities. Airway and systemic examination were normal except for reduced air entry in the right infra-axillary and infra-scapular areas. Investigations including hemogram, coagulation tests, liver function test, renal function test, and electrocardiogram (ECG) were normal. Chest X-ray was suggestive of right-sided pleural effusion with collapsed right lung []. Contrast enhanced computed tomography chest revealed moderate-to-gross loculated right pleural effusion with pleural thickening and nodularity suggestive of pleural metastases. Omental metastases, minimal pelvic-free fluid, and bulky ovaries were also present. Pulmonary function test revealed restrictive pattern with FEV1 55.21%, FVC 60.76%, and FEV1/FVC 95.77%. Cardiopulmonary exercise testing showed VO2 (rest 247 ml/min, warm-up 357 ml/min, anerobic threshold 483), VO2/kg (rest 5 ml/kg/min, warm-up 7.4 ml/kg/min, anerobic threshold 10.1), metabolic equivalent (rest 1.4, warm-up 2.1), and heart rate (rest 111, warm-up 116). Her room air oxygen saturation was 94%. Preoperatively, deep breathing exercise, incentive spirometry, and steam inhalation were started. She was kept nil orally for 8 h and was advised oral ranitidine 150 mg in night and morning of surgery with sip of water.
In the operating room, monitoring included five lead ECGs, noninvasive blood pressure, pulse oximetry, capnography, nasopharyngeal temperature, invasive arterial blood pressure, and central venous pressure. Intravenous access was secured with a 16-G cannulae. After epidural puncture at L3–L4 level, 300 μg morphine with 5 mg of 0.5% bupivacaine heavy given intrathecally followed by epidural catheter placement. After preoxygenation, anesthesia was induced with intravenous morphine 6 mg, propofol 100 mg, and atracurium 30 mg. A 35-Fr left double lumen tube was placed and position confirmed by fiberoptic bronchoscopy. Deep venous thrombosis (DVT) pump was placed. Anesthesia was maintained using oxygen, air, and desflurane (end-tidal concentration of 0.8%). Intravenous morphine and atracurium were administered as and when required.
During CRS, blood loss was approximately 2 l replaced with 2 units of packed red blood cells (PRBC) and ringer lactate. Temperature was around 35°C using forced air warmer and fluid warmer. The cytoreductive phase which lasted for 5 h consisted of total abdominal hysterectomy with bilateral salpingo-oophorectomy, lymph node dissection, and total omentectomy. The diaphragm was opened via abdominal approach to excise pleural-based nodule and hemorrhagic pleural fluid drained. As the patient developed hypotension (BP 80/60 mmHg) intra-operatively, bolus of ringer lactate was administered, and subsequently, noradrenaline infusion with a dose ranging from 0.04 to 0.2 mcg/kg/min was administered to maintain a mean arterial pressure >65 mmHg. As the pleural-based nodule could be excised via abdominal approach, thoracotomy was not required. Fluid management was guided by urine output, pulse pressure variation, and arterial blood gas analysis (ABG) []. Urine output was maintained at 0.5–1 ml/kg/h during CRS phase and 2–3 ml/kg/h during HIPEC phase. Before the start of HIPEC and HITHOC phase, forced air warmer was kept on ambient mode and fluid warmer switched off. Cold intravenous fluids were administered. Semi-Open technique (Coliseum) using cisplatin 100 mg in 2.5 l dialysate at 41°C was circulated for 60 min in the peritoneal cavity and right hemithorax through the diaphragmatic defect at a rate of 1.5 l/min using Sunchip roller pump. Temperature, urine output, hemodynamics, and ABG were monitored. The temperature increased from 35.2°C in the beginning of HIPEC to 38.3°C by the end of the procedure. The ventilatory parameters were adjusted to achieve end-tidal concentration of carbon dioxide between 35 and 40 mmHg. Lung protective ventilation strategies in the form of low tidal volume, recruitment maneuvers were used. Positive end expiratory pressure (PEEP) of 5 cmH2O was provided to prevent atelectasis and also to increase the surface area of contact between circulating dialysate containing cisplatin and the diseased pleura. Intravenous furosemide and cold ringer lactate were administered to maintain urine output of 2 ml/kg/h. Following the procedure, the diaphragmatic defect was closed, chest and abdominal drains were inserted, and abdomen was closed. The total duration of procedure was 8 h. The total fluids administered were 5000 ml of balanced salt solution along with 2 units of PRBC.
Postoperatively, patient was shifted to intensive care unit in view of hemodynamic and metabolic derangements. Vasopressor support was gradually tapered and stopped. Patient developed mild renal dysfunction from second postoperative day (POD) which was normalized by fourth to fifth POD []. Coagulation parameters were also deranged coagulation and fresh frozen plasma was transfused for the same. She was extubated on second POD. Chest physiotherapy and incentive spirometry were started post-extubation []. Analgesia was achieved with epidural morphine and intravenous acetaminophen. She was shifted back to ward on POD 4 and discharged from the hospital on POD 9.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [45.0, 'kg']}",85,80.75,89.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 45.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (45.0 kg - 20 kg) = 85.0 mL/hr.
Hence, the patient's fluid maintenance is 85.0 mL/hr."
5010,22,Maintenance Fluids Calculations,physical,decimal,pmc-5495012-1,Extracted,"A 41-year-old male originally from West Africa with a questionable history of ventriculoseptal defect (VSD), presented with worsening exertional dyspnea and palpitations, loss of appetite, lower extremity edema and a 30 pounds weight loss over 6 weeks. On admission, his temperature was 98.8°F (37.1°C), blood pressure of 104/50 mm Hg, heart rate of 120/min, respiratory rate of 18/min and an oxygen saturation of 98% on room air. His physical examination was significant for chronically ill cachexic male with a BMI of 21 kg/m2, jugular venous distension, bilateral rales, tachycardia, RV heave and 4/6 pan-systolic murmur with a palpable thrill throughout the precordium. Blood cultures were obtained for suspected endocarditis and empiric intravenous antibiotics were started. An initial transthoracic echocardiogram and subsequent transesophageal echocardiogram demonstrated a large mass attached to the aortic valve leaflet measuring 3.2 × 0.6 cm (Supplementary Videos 1–2), severe aortic regurgitation with holodiastolic flow reversal in the aorta (Fig. ), mass attached to the flail anterior mitral valve leaflet resulting in severe mitral regurgitation (Figs –, –, Supplementary Videos 4–7), mass attached to pulmonic valve, significant pulmonic regurgitation (Figs , , ) and severe pulmonary hypertension with Pulmonary Artery Systolic Pressure of 65 mm Hg. Additionally, dilatation of the aortic root along with fistula between the aortic sinus and the RV outflow tract was seen (Figs , , , , ). Within 24 h, blood culture revealed gram-positive cocci in two out of two bottles, subsequently identified as Abiotrophia species. Patient was transferred to a tertiary care center for further management. He underwent right heart catheterization demonstrating elevated filling pressures, low cardiac index and shunt fraction of 2.1. Emergent surgery revealed an aortic root abscess. He underwent prophylactic grafting of the left anterior descending coronary artery and obtuse marginal artery as the left main coronary Os was close to the aortic annulus. Patient also underwent bio-prosthetic pulmonary and mitral valve replacement, closure of the congenital VSD and closure of aorto-RV fistula using bovine pericardial patches in addition to an aortic root replacement with porcine root prosthesis. Post-operatively, patient developed atrial fibrillation and was subsequently started on amiodarone therapy. He was on intravenous penicillin and gentamycin during his hospitalization. Transesophageal echocardiogram, post intervention, revealed mild left ventricular dysfunction with an ejection fraction of 45% and competent bio-prosthetic valves. Repeat blood cultures remained negative and patient was discharged on intravenous vancomycin via peripherally inserted central catheter.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [30.0, 'lbs']}",47.21552,44.85474,49.5763,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 30.0 lbs so this converts to 30.0 lbs * 0.453592 kg/lbs = 13.60776 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.60776 kg - 10 kg) = 47.21552 mL/hr.
Hence, the patient's fluid maintenance is 47.21552 mL/hr."
5011,22,Maintenance Fluids Calculations,physical,decimal,pmc-7441615-1,Extracted,"A 79-year-old woman (height, 140.1 cm; body weight, 38.5 kg; body surface area, 1.22 m2; EuroSCORE II, 2.93%) with aortic valve stenosis, hypertension, and paroxysmal atrial fibrillation was referred to our hospital. Chest X-ray revealed concentric cardiomegaly. Electrocardiogram demonstrated regular sinus rhythm with 53 beats per min, and complete right bundle branch blockage. Transthoracic echocardiography showed an ejection fraction of 69%, thickening and normal motion of the left ventricular wall, severe aortic valve stenosis, and severe tricuspid valve regurgitation. The aortic valve area, as calculated using the continuity equation, was 0.54 cm2, while the peak aortic velocity, and mean pressure gradient were 4.4 m/s and 37 mmHg, respectively. Coronary angiography did not demonstrate any significant stenotic lesions. Medications included amlodipine besylate (2.5 mg), azosemide (30 mg), carvedilol (2.5 mg), and apixaban (5 mg). She was scheduled to undergo surgical aortic valve replacement (AVR) and tricuspid valve annuloplasty (TAP) with MAZE procedure under CPB six weeks later. Her blood type was A RhD(+); however, antibody screening was positive, and the subsequent direct antiglobulin test was negative, indicating the presence of isolated antibodies in the plasma. Consequently, her Ok blood phenotype was revealed to be Ok(a−) and the antibody was anti-Oka.
The preoperative hemoglobin (Hb) levels fluctuated between 10 and 11 g/dL. Furthermore, since Ok(a−) is an extremely rare phenotype, obtaining sufficient amounts of Ok(a−) red blood cell products for the surgery, was a significant concern. From a regional blood center, eight units of frozen thawed red cells (FTRCs) and six units of red blood cells (RBCs) were collected on the day of surgery. The RBCs were donated by three discrete Ok(a−) individuals a few days prior to surgery. Apixaban was stopped two days before surgery. The results of blood tests performed one day before surgery, were not remarkable except for the Hb level being 10.7 g/dL, hematocrit (Hct) 34.4% (Table ), and N-terminal pro-brain-type natriuretic peptide (NT-pro BNP) 3848 pg/mL (normal, < 55 pg/mL).
In addition to standard monitoring, regional cerebral oxygen saturation levels (INVOS™ 5100C, Edwards Lifesciences, Irvine, CA, US) were monitored. An arterial catheter was inserted in the radial artery, and remifentanil was infused at 0.4 μg/kg/min, followed by administration of 500 μg fentanyl. General anesthesia was induced with 7 mg midazolam and 40 mg rocuronium. After tracheal intubation, transesophageal echocardiography was performed. A central venous catheter and a pulmonary artery catheter were inserted, and mixed venous oxygen saturation and cardiac output were monitored thereafter (VigilanceII™, Edwards Lifesciences, Irvine, CA, US). Acute normovolemic hemodilution (ANH) was conducted; 400 mL of autologous whole blood was collected via arterial pressure catheter, and 300 mL of crystalloid was rapidly infused. The Hb and Hct levels after ANH were 10.3 g/dL and 31.9%, respectively (Table ). Anesthesia was maintained with sevoflurane and continuous infusion of remifentanil. Blood pressure and systemic vascular resistance were maintained by norepinephrine (0.02 μg/kg/min) and dopamine (1–3 μg/kg/min) infusion with several boluses of ephedrine (4 mg) and phenylephrine (0.05 mg), until the initiation of CPB. The Hb and Hct levels, immediately after initiating surgery, were 9.7 g/dL and 30.1%, respectively (Table ), and pre-bypass fluid administration was restricted to 400 mL of crystalloid, including 300 mL for ANH. Tranexamic acid (2000 mg) was administered to suppress hyperfibrinolysis.
The baseline activated coagulation time (ACT) was 158 s. After administration of 12,000 units of heparin, an arterial cannula was inserted into the ascending aorta, followed by cannulation of both the superior and inferior vena cava. CPB, under mild hypothermia, was initiated with spontaneous beating retained. Thereafter, general anesthesia was maintained with a target-controlled-infusion of propofol and an effect-site concentration set at 1.3 μg/mL, along with remifentanil infusion, to maintain the bispectral index (BIS™, Medtronic, Minneapolis, MN, US) between 40 and 60. In advance, four units of FTRCs were loaded in the CPB priming solution (Table ) to avoid excessive hemodilution, and the Hb and Hct levels immediately after CPB initiation were 8.0 g/dL and 25.0%, respectively (Table ). ACT was 1000 s, and no additional heparin administration was required during CPB (the shortest value of ACT was 401). After approximately 30 min, body temperature in both bladder and esophagus was stabilized at 30.0 °C. After 1 h from CPB initiation, the Hb and Hct levels decreased to 7.3 g/dL and 22.9%, respectively, and two units of FTRCs were transfused from the CPB circuit, which raised both to 9.0 g/dL and 27.8%, respectively (Table ). Pulmonary vein isolation and left atrial appendage closure were completed and the ascending aorta was cross-clamped, followed by cardiac arrest that was introduced via antegrade infusion of cardioplegia. After AVR with a biological valve was completed, re-warming was initiated, and TAP was conducted uneventfully. During the valve replacement, cardiac arrest was maintained with intermittent selective and retrograde infusion of cardioplegia. Spontaneous circulation was promptly restored after aortic de-clamping, and CPB was terminated with a dopamine infusion of 5 μg/kg/min. The aortic cross-clamp time was 111 min, and total CPB time was 170 min. Blood tests performed after aortic de-clamping gave the following results: Hb, 8.6 g/dL; Hct, 27.4% (Table ); platelet count, 12.8 × 104/μL; international normalized ratio of prothrombin time (PT-INR), 1.81; and fibrinogen, 491 mg/dL.
After confirming that ACT had returned to 143 s by 120 mg protamine, two units of FTRCs were transfused. In addition, four units of FFP and ten units of PC, as planned prior to surgery, were intensively transfused, facilitating both prompt surgical hemostasis and stable hemodynamics. Oxidized regenerated cellulose (SURGICEL® FIBRILLAR™, Johnson & Johnson, New Brunswick, NJ, US) and human fibrinogen (Beriplast® P Combi-Set Tissue adhesion, CLS Behring, King of Prussia, PA, US) were applied to minimize suture-line oozing of the aorta and right atrium. Minimal bleeding was observed in the surgical field, and 316 mL of salvaged blood, primarily collected from the residual blood in the CPB circuit, was subsequently transfused. Thus, the Hb and Hct levels were maintained above 8.0 g/dL and 27%, respectively, after CPB termination (Table ). Dopamine infusion was slowly tapered to 1 μg/kg/min, until the end of surgery. The operation duration was 319 min, and total time of anesthesia was 402 min with a total fluid balance of + 546 mL. After the surgery, the patient was transferred to the intensive care unit under intubation, wherein both carbazochrome sodium sulfonate hydrate (25 mg) and tranexamic acid (1000 mg) were administered. Approximately 400 mL of the autologous whole blood was returned to the patient, which raised the Hb and Hct levels to 11.0 g/dL and 32.6%, respectively (Table ). Patient was extubated at postoperative hour 6, with no neurological deficits. Until postoperative day (POD) 1, blood drainage from pericardium and anterior mediastinum were 80 mL and 50 mL, respectively. The Hct level was consistently maintained above 25%, and thereafter, no additional blood transfusion was conducted throughout the hospital stay. The patient had a good postoperative course, and was discharged on POD 17. We ensured that the six unused units of Ok(a−) RBCs were transfused to other hospitalized Ok(a+) patients within the expiration date.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [38.5, 'kg']}",78.5,74.575,82.425,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 38.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (38.5 kg - 20 kg) = 78.5 mL/hr.
Hence, the patient's fluid maintenance is 78.5 mL/hr."
5012,22,Maintenance Fluids Calculations,physical,decimal,pmc-5784969-1,Extracted,"A 24-year-old male was admitted to Peking Union Medical College Hospital, Beijing, China, on 13 May 2015 because he had been experiencing intermittent fever with chills and fatigue for six months. Antibiotic therapy (lack of detailed information) prescribed by the community hospital was completed before he came to our hospital, but the symptoms persisted. On physical examinations, the patient was revealed to be healthy except for an unstable temperature with intermittent fever, hypotension [103/38 mmHg] and weight loss of 15 kg during the course of illness. Laboratory tests revealed that the patient had an increased erythrocyte sedimentation rate (ESR) of >140 mm/h and suspected anemia with Hb of 57 g/L. His symptoms were slightly alleviated after a blood transfusion with 2 units of condensed erythrocytes. Cardiac auscultation revealed consecutive murmurs in the second aortic valve area. Echocardiography was prescribed to determine the cause of the murmurs. Congenital heart disease (CHD) of patent ductus arteriosus (PDA) and IE were diagnosed with evidence of aortic regurgitation and multiple vegetations on the pulmonary valve and pulmonary artery wall. Based on the above evidence and the current physical condition, the patient was hospitalized in the cardiac surgery department on 26 May, and a cardiac surgical operation was performed to rectify the CHD and IE condition on 1 June 2015. A peripheral blood sample was sent to microbiology laboratory for blood culture testing on 26 May and was positive; the pathogen from the blood culture was revealed to be a novel species of the family Flavobacteriaceae on 6 June. Empirical treatment with ceftriaxone (IV, 2 g, qd) for 2 weeks during his hospitalization was prescribed. The patient recovered well after the operation and was discharged on 10 June 2015 with prolonged antibiotic treatment with ceftriaxone for 5 weeks. Since he was discharged, no significant clinical events have occurred during follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15.0, 'kg']}",50,47.5,52.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.0 kg - 10 kg) = 50.0 mL/hr.
Hence, the patient's fluid maintenance is 50.0 mL/hr."
5013,22,Maintenance Fluids Calculations,physical,decimal,pmc-8502456-1,Extracted,"A 48-year-old South African woman presented with a left neck mass for 1 year with cosmetic concerns and no compressive symptoms. She reported no significant history of cardiovascular disease, and no history of food or drug allergies. No family history of any thyroid diseases and any allergies was reported. She was admitted to the hospital for a tentative thyroid radiofrequency ablation.
Her body mass index was 24.5 kg/m2 (weight 66.7 kg; height 165 cm), and her blood pressure, heartbeat, SpO2, and body temperature were normal (113/71 mmHg, 70 beats/min, 96%, and 37.2°C, respectively). On physical examination, there was a soft mass in the left thyroid lobe, which was moving on swallowing (Figure ). Her report was no compressive symptoms, with a symptom score of 5/10 on a visual analog scale and a cosmetic score of ¾. The physical examination of heart, lung, abdomen, and CNS was normal.
Before the procedure, thyroid function tests (FT4, thyrotropin) and other tests (CBC, liver, and renal function tests, prothrombin time) were normal with serum FT4 1.16 ng/dl (normal range [NR] 0.93–2.22); thyrotropin 4.17 microUI/ml (NR 0.27–4.2); prothrombin time 111%, and INR 1.0. Her chest X-ray showed no abnormal findings. ECG showed normal sinus rhythm at a rate of 73 bpm. The thyroid ultrasonography showed a single, mixed echogenicity mass (cystic part of 50%) on the left thyroid lobe, with no calcification, no vascularity, and no lymph node involvement (Figure ). Nodule volume was 6.2 ml (W × H × D: 22.8 × 20.1 × 25.7 mm). 2 separate FNAs of the thyroid nodule revealed a colloid nodular hyperplasia with hyperplastic thyrocytes and fluid colloid (Bethesda II) affirmed the diagnosis of the large benign thyroid nodule. Because of her fear of surgery complications, we proposed RFA of the nodule.
In a preliminary assessment, a procedure safety checklist (medical conditions, drugs using, allergies) and written informed consent for the procedure (efficacy, possible complications) were obtained. The emergency drug box (including methylprednisolone, epinephrine, diphenhydramine, and lipofundin 20% (lipid emulsion)) and the vital signs monitor machine were routinely prepared. The patient underwent an intravenous infusion in 500 ml of 0.9% saline during and after thyroid RFA. In the RFA procedure, after finishing skin sterilization and careful local anesthesia with 10 ml of 2% lidocaine at the needle-puncture site and peri-thyroidal area under ultrasound guidance (Figure ), complete fluid aspiration was performed before ablating the nodule and its vascularity via the trans-isthmic approach and the moving-shot technique.
After 15 min of ablation, the patient started feeling circumoral numbness, dizziness, nausea, and blurred vision. Her skin became cold, and no rash appeared. Shortly, she was hypotensive, bradycardia, and hypoxia with a blood pressure of 80/60 mmHg, a heartbeat of 34 bpm, and SpO2 of 74%. The ablation procedure was aborted immediately. Emergency management was rapidly started including “call help” with red code, nasal cannula oxygen therapy to maintain SpO2 of 100%, monitor the cardiovascular system, and support the patient with keeping rapid intravenous fluids flow (0.9% saline). At the same time, we administrated of lipid emulsion therapy (lipofundin 20%) in different intravenous way: first, intravenous bolus 1.5 ml/kg over 1–2 min (100 ml) and then intravenous infusion 0.25 ml/kg/min (~17 ml/min). The normal sinus rhythm and blood pressure were restored within 5 min of intravenous lipid injection with 60 bpm and 110/80 mmHg. Her mental status became stable. The total used volume of lipofundin 20% was 500 ml. The patient was subsequently transferred to our intensive care unit for follow-up and supportive treatment. She was discharged 12 h later.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [66.7, 'kg']}",106.7,101.365,112.035,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 66.7 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (66.7 kg - 20 kg) = 106.7 mL/hr.
Hence, the patient's fluid maintenance is 106.7 mL/hr."
5014,22,Maintenance Fluids Calculations,physical,decimal,pmc-2672220-1,Extracted,"A 28-year-old female physician presented to the ED with nausea and vomiting for three days with epigastric pain and decreased urination. The vomiting was non-bloody and non-bilious, occurred four times per day, and the patient was unable to tolerate liquids. The epigastric pain was mild, constant, and sharp. The patient felt a rapid pulse. She denied fever, chills, diarrhea, melena, or prior similar episodes. The past medical history was unremarkable with no prior surgeries, medical problems, or medications. The family history was documented as noncontributory and the patient denied pregnancy and alcohol, tobacco or drug use.
The physical exam revealed an oral temperature of 36.7° C, heart rate at 131 beats/min, respirations at 18 breaths/min, blood pressure at 128/75 mm Hg, and room air oxygen saturation (O2 sat) at 100%. The patient weighed 52.3 kg with a height of 157.5cm. She was alert and oriented, nontoxic and in no distress. The eye exam was normal without exophthalmos. There was no lymphadenopathy, no goiter was noted, and a thyroid exam was not documented. The lungs were clear and the cardiac exam was normal other than tachycardia. The abdomen was soft with normal bowel sounds, with mild tenderness in the epigastrium but no rebound or guarding. The neurological exam revealed normal cranial nerve function, full strength and sensation, and a normal gait. Deep tendon reflexes were not documented.
A metabolic panel including electrolytes, glucose, BUN and creatinine were normal. Liver function tests showed albumin at 3.6 g/dL(normal 3.2–5.5), AST at 118 IU/L(normal 8–40), ALT at 197 IU/L(normal 0–60), alkaline phosphatase at 51 IU/L(normal 26–110), and total bilirubin at 1.5 mg/dL(normal 0–1.4). The lipase level and complete blood count with differential were normal. A voided urinalysis showed specific gravity of 1.024, pH at 7.30, ketones at 150 mg/dL, small bilirubin, urobilinogen at 8 mg/dL, 2 red blood cells/high power field (hpf), 3 white blood cells/hpf, 6 epithelial cells/hpf, moderate bacteria, and no hemoglobin, leukocyte esterase, nitrite, protein, glucose, or crystals. A urine pregnancy test was negative. Bedside ED ultrasound by the EP showed no evidence of cholecystitis.
The patient received two liters IV normal saline and two doses of antiemetics. She then tolerated an oral liquid challenge, felt better and requested to be sent home. The discharge diagnosis was possible gastritis versus viral hepatitis. Lansoprazole 15 mg once daily was prescribed, with primary care physician (PCP) follow up in 1–2 days. A repeat set of vital signs was not documented.
Seven days later, the patient returned. She had seen her PCP who referred her for an esophagogastroduodenoscopy (EGD). She had not eaten or drunk for 20 hours prior to the procedure. The EGD, done with fentanyl and midazolam sedation, found a small hiatal hernia with no other abnormalities. Because of persistent tachycardia in the 140s/minute with intractable vomiting, the patient was sent directly to the ED. The patient stated the vomiting had resolved since the last ED visit and only started again after the EGD. The epigastric pain persisted without change and the only additional complaint was tremulousness. She continued to deny fever, chills, diarrhea, and melena.
The physical exam showed an oral temperature of 36.3° C, heart rate at 143 beats/min, respirations at 20 breaths/min, blood pressure at 125/61 mm Hg and O2 sat at 100% on 2L/min oxygen per nasal cannula. The patient weighed 50 kg (a 2.3 kg weight loss in one week). The patient was alert, tremulous and appeared fatigued. The remainder of the exam was unchanged. She received supplemental oxygen, three liters IV normal saline, and cardiac monitoring.
A repeat complete metabolic panel showed normal glucose and electrolytes except for bicarbonate at 19 mEq/L(normal 25–34), magnesium at 1.8 mg/dL(normal 1.8 – 2.5), albumin at 3.2 g/dL, AST at 83 IU/L, ALT at 87 IU/L, alkaline phosphatase at 48 IU/L, and total bilirubin at 0.8 mg/dL. A serum lipase level and complete blood count with differential were within normal limits. The erythrocyte sedimentation rate and C-reactive protein were normal. A urinalysis was not repeated. An EKG showed a narrow-complex sinus tachycardia at a rate of 152 beats/min with no ischemic ST or T wave changes. In addition, she had thyroid function tests sent, which are performed once daily by our institution’s laboratory. The patient tolerated oral liquids after antiemetics. Despite hydration, the patient’s tachycardia persisted at 130 beats/min. She appeared fatigued but had resolution of all other presenting symptoms. The patient was admitted to the internal medicine service on a telemetry floor.
Overnight she received two more liters IV normal saline, followed by maintenance rate. A right upper quadrant ultrasound showed a markedly thickened gallbladder wall without gallstones, a small amount of pericholecystic fluid, and a normal common bile duct. Radiology recommended a CT scan of the abdomen and pelvis, which showed small bilateral pleural effusions, periportal edema, upper abdominal ascites, marked gallbladder wall thickening, and moderate amount of free fluid in pelvis.
The next day general surgery recommended an exploratory laparoscopy. This procedure was delayed because the patient ate breakfast. The first two thyroid function panels sent from the ED and on hospital day two were invalid due to hemolysis, but a third set showed a free thyroxine (T4) level greater than 6 ng/dL(normal 0.8–1.9) and an undetectable thyroid-stimulating hormone (normal 0.5–5 mIU/L). After atenolol and methimazole, the patient improved and was discharged on the third hospital day with diagnoses of new onset thyrotoxicosis, dehydration, liver hemangioma, and small hiatal hernia.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [50.0, 'kg']}",90,85.5,94.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 50.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (50.0 kg - 20 kg) = 90.0 mL/hr.
Hence, the patient's fluid maintenance is 90.0 mL/hr."
5015,22,Maintenance Fluids Calculations,physical,decimal,pmc-8709556-3,Extracted,"Male, 44 years old, referred to our division from another island with a huge mass on his penis and scrotum. He was injected with olive oil several times a couple of years ago. Due to the paraffinoma mass reported a heavy feeling in his scrotal and penile areas (). He also had repeated blisters at the bilateral inguinal that caused him pain and made walking difficult. He complained of pain upon erection, and the swollen mass rendered him unable to achieve satisfactory sexual intercourse. He could still urinate but had a trapped feeling about the paraffinoma mass around the penoscrotal area. The mass excision was performed by our colleagues from the Urology Division to the penis and scrotal area. The excised paraffinoma mass was firm, yellow in color, and almost 1 kilogram in weight (). The scrotal area was reconstructed with the healthy surrounding tissue and left to vacuum drain for 3 days. The penis was resurfaced with a one-sheet spiraling FTSG from the right inguinal (). The surgical technique was the same as cases no. 1 and 2. The patient also received other drugs such as antibiotics, analgesics, albumin, and vitamins. One week after the surgery, the patient had five HBOT sessions with 2.0 ATA (). The patient was discharged from the hospital on the 14th postoperative day with outpatient follow-up twice per week. After 1 year, the patient had no complaints and was satisfied with the surgical results.
Soft tissue filler is a critical component of aesthetic dermatologic surgery. In soft tissue augmentation, a variety of temporary and permanent filler compounds have been used. Paraffin, Vaseline, and liquid injectable silicone are the most commonly used. Extruded polytetrafluoroethylene and Silastic (strong silicone) implants are the simplest permanent filler fabrics approved for use in the US In the past, liquid silicone was utilized for permanent soft tissue augmentation, but the FDA has not approved the forms of liquid silicone available for medical usage in the US. Liquid silicone is injected intradermally and subcutaneously in animals and people since it is predictable, self-restricted, nonirritating, and nearly noninflammatory. It can be visualized under the microscope as dispersed vacuolization or encapsulated by collagen deposition and fibrosis. Around the silicone droplets, phagocytes and other large cell responses are occasionally detected. The tissue enlargement when silicone is injected is caused by collagen deposition and fibrosis. In these paraffinoma patients, fibrotic tissue almost surrounded the penile area, and removing the fibrous tissue without damaging the surrounding tissue was challenging. Despite its reputation as a chemically inert material, liquid silicone has been associated with severe inflammatory reactions, including tissue damage. When substances are injected into the penis for augmentation, granulomatous and fibrotic reactions occur in the subcutaneous fat region, resulting in the formation of a lipogranuloma, which appears as a firm disfiguring subcutaneous mass with surrounding skin fibrosis and thickening, giving the impression of a larger penis. Pain, erythema, foreign object reaction, ecchymosis, cellulitis, tissue damage, scarring, ulceration, and even discomfort for their sexual partner are some of the local complications. We can use several methods to treat paraffinoma, including a one-sheet full-thickness skin graft. This technique has some advantages, namely, starting from a not extensive scar, a lower secondary contraction rate than a split-thickness skin graft, and a reduced occurrence of hypertrophy and keloids.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1.0, 'kg']}",4,3.8,4.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1.0 kg. Hence, the patient's maintenance fluid is 1.0 kg * 4 mL/kg/hr = 4.0 mL/hr.
Hence, the patient's fluid maintenance is 4.0 mL/hr."
5016,22,Maintenance Fluids Calculations,physical,decimal,pmc-4891544-1,Extracted,"A 39-year-old woman (gravida 2 para 1) had reversetranscription polymerase chain reaction (RT-PCR)-confirmed MERS-CoV at 35 + 4 weeks of gestation. This patient had gestational-related diabetes, but it was well-controlled by diet without medication. She was admitted to obstetrics ward of our institution on April 19 due to premature labor. During the 6-week admission period, she visited her mother who was hospitalized in the emergency department of the same institution on May 27 and 28, which was the same time that a known MERS-CoV super-spreader patient was treated there. Her mother developed illness with fever on day 7 after contacting the super-spreader and was confirmed positive by MERS-CoV RT-PCR.
Our case complained of severe myalgia without fever on June 8 and was admitted to the isolation ward 5 days after discharge. Her sputum sample was positive for MERS-CoV by RT-PCR. Creactive protein (CRP) was elevated to 1.95 mg/dl and a chest X-ray revealed patchy opacity in both lower lobes, suggesting bronchopneumonia (). A chest X-ray taken 4 days later was improved and CRP had decreased to a value within the normal range (0.15 mg/dl). However, she complained persistently of episodes of dyspnea, sputum, and myalgia without fever. She was provided supportive treatment, but no antiviral agent or steroid because the disease was not progressing. Fetal growth was within normal gestational limits, and she recovered gradually from the myalgia and other symptoms. The results of RT-PCR follow-up tests performed on June 19 and 21 were all negative in sputum samples. The Division of Infectious Diseases confirmed a full recovery, and she moved to the obstetrics ward on June 22 where she was expected to have a normal delivery. However, she began sudden bleeding with abdominal pain on the day after recovery was declared. A pelvic examination with a speculum confirmed the vaginal bleeding. However, the transabdominal ultrasonography did not detect any placental problems or hidden hemorrhaging. Baseline fetal heart rate (FHR) was 120–130 bpm with moderate variability. An obstetrician diagnosed placental abruption based on the symptoms and physical examinations. We considered spread of MERS-CoV because her symptom onset was very recent, and delivery would involve a large volume of contagious body fluids. An emergency C-sec under combined spinal-epidural anesthesia (CSE) was scheduled with precautions. The surgery was performed in a designated negative pressure-ventilated isolation operating room. All designated specialized infection control personnel prepared for the surgery and wore enhanced personal protective equipment (PPE) ().
A medical worker with PPE transferred the patient on an exclusive elevator. She was very anxious in the operating room, so we provided emotional support but no premedication. She was 167 cm tall and weighed 79 kg (body mass index, 28.33 kg/m2). Her baseline blood pressure and heart rate were 120/50 mmHg and 82 beats/min, respectively. SpO2 was 100% on room air and electrocardiograph results showed normal sinus rhythm. The patient was placed in the right lateral decubitus position, and epidural anesthesia was attempted with a 17-gauge Tuohy needle via the median approach at L3–4. The epidural space was detected using the loss-of-resistance technique, and a 22-gauge epidural catheter was inserted (). A lumbar puncture was performed with a 25-gauge Whitacre spinal needle at the L4–5 interspace, and 6 mg of 0.2% ropivacaine and 20 µg fentanyl were injected intrathecally. Levobupivacaine (0.25%, 10 ml) was administered through the epidural catheter. The patient was placed in the supine position with a left lateral tilt to avoid aortocaval compression. Anesthesia was assessed bilaterally using cold and light touch, and the spinal injection produced a T4 block after 10 min. The C-sec was performed uneventfully without pain or discomfort. The baby was 3.14 kg, with Apgar scores at 1 and 5 min of 9 and 10. Umbilical vein pH was 7.363. A 10 × 10 cm blood clot was extracted and approximately 20% of the placenta appeared to be abrupted.
Total operation time was 150 min, with an estimated blood loss of 700 ml. A total of 2700 ml of crystalloid solution and 1000 ml of colloid were administered during the surgery. An infusion of oxytocin (10 units/1000 ml Ringer's lactate solution) and carbetocin (1000 µg/10 ml normal saline) was administered to produce uterine contractions and minimize blood loss, respectively.
She was administered in the operating room until a recovery block to T8, then the patient was transferred directly to a single room on the obstetrics ward. The baby was isolated in the intensive care unit, and a MERS-CoV test was negative. Maternal serum and the placenta were MERS-CoV negative. Breastfeeding was allowed by pumping instead of sucking. She was discharged on postoperative day 7. The mother and baby are doing well.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [79.0, 'kg']}",119,113.05,124.95,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 79.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (79.0 kg - 20 kg) = 119.0 mL/hr.
Hence, the patient's fluid maintenance is 119.0 mL/hr."
5017,22,Maintenance Fluids Calculations,physical,decimal,pmc-3966100-1,Extracted,"The present case is about a 11-year-old Saudi boy who was referred to our service for bilateral adrenalectomy. The patient had been diagnosed by the pediatric endocrinologist with cycling Cushing disease. He presented with a history of rapid weight gain, decreased school performance and emotional disturbances in the previous 18 months. These complaints came in cycles, each lasting 2-4 months before the patient returned to normal. Adrenal ultrasound and computed tomography scan showed normal adrenal glands, magnetic resonance imaging of the brain also showed normal pituitary and hypothalamic area. During one of these cycles, his weight increased by 4 kg, blood pressure was 140/100 and he exhibited the typical signs of Cushing's disease. Blood work confirmed Cushing's disease. His serum cortisol at 1 PM was elevated at 16.6 mcg/dL. Electrolytes showed sodium 143 mEq/L, potassium 4 mEq/L, chloride 103 mEq/L, total CO2 27, blood urea nitrogen 9 mg/dL and creatinine 0.3 mg/dL. 24 h urine for free cortisol was high at 542 mcg/24 h (normal 5-55 mcg/24 h). At 2 months later, the patient presented with a third episode and was admitted for a full work-up. Urine free cortisol was elevated at 350 mcg/24 h, at midnight serum cortisol was 19.9 mcg/dL and serum adrenocorticotropic hormone (ACTH) was <4 pg/ml. Am cortisol was 15.7 mcg/dL and ACTH was 5.4 pg/ml. The patient was subjected to small and high doses of dexamethasone suppression tests (1 mg and 5 mg respectively) but there was no change in cortisol or ACTH serum levels. These findings confirmed a diagnosis of Cushing's disease of adrenal origin and its cyclic nature presented Carney's complex syndrome as a possibility. Further investigations to exclude Endocrine and cardiac tumors as part of Carney's complex included ultrasound of the thyroid and echocardiography which were normal. Ultrasound of the testes showed bilateral diffuse macro-calcification as well as 0.8 × 0.8 cm hypo-echoic mass within the left testicle, which strengthened the diagnosis of Carney's complex. The patient had no abnormal skin rash and the family history was negative for any endocrine problems. Deoxyribonucleic acid analysis on our patient did not show the known mutation in Carney's complex (PRKAR1A) which is found in only 50% of those patients.
Bilateral adrenalectomy was the treatment of choice in this patient. The plan was to start with right laparoscopic adrenalectomy and proceed to left adrenalectomy with the possibility of converting to open. The patient underwent a successful simultaneous bilateral adrenalectomy; the operative time was 3 h and 30 min. The estimated blood loss was 50 ml. The patient resumed his diet and ambulated on the 1st post-operative day and was discharged from hospital on the 2nd post-operative day. The post-operative course was smooth and uneventful and he was started on replacement therapy post-operatively. At 3 months later, he was doing well with a remarkable improvement in his behavior and school performance. Histopathology report of his adrenal gland was consistent with micronodular adrenocortical hyperplasia.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.0, 'kg']}",16,15.2,16.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.0 kg. Hence, the patient's maintenance fluid is 4.0 kg * 4 mL/kg/hr = 16.0 mL/hr.
Hence, the patient's fluid maintenance is 16.0 mL/hr."
5018,22,Maintenance Fluids Calculations,physical,decimal,pmc-5028855-1,Extracted,"A 5-month-old girl was referred for recurrent infections of respiratory and genitourinary tract, chronic diarrhea, and hyperemic skin lesions. She was born at term with 3650 gr of birthweight, to second-degree consanguineous healthy parents. Her elder siblings were lost at 4 months of age due to sepsis and 1 year of age due to inflammatory bowel disease, respectively. She had two cousins dead at early infancy with unknown reasons. Pedigree is shown in .
Her past medical history was loaded with frequent and severe infections. She was hospitalized at 10th day of life for sepsis, diarrhea (7-8 times a day), extensive skin rash on face and scalp, respiratory distress, fever, and urinary tract infection with Klebsiella pneumoniae. At 4 months of age, she had a gluteal abscess; Klebsiella pneumoniae was isolated from draining material. She was hospitalized at a public hospital for pneumonia and gastroenteritis at 5 months of age.
Her weight was 6.5 kg (10 percentile), height was 63 cm (3–10 percentile), and vital signs were normal at admission to our department at the age of 5 months. She had extensive erythematous skin lesions, coarse crackles on both chest areas, and anal fissure. Complete blood count was as follows: white blood cell (WBC) 20700/mm3 (normal WBC count for age: 6000–14000/mm3) (polymorphonuclear leukocytes 35.6%, lymphocytes 54.9%, monocytes 4.7%, and eosinophils 3.5%), hemoglobin 9.3 g/dL (normal: 10.5–14 g/dL), hematocrit 28.3% (normal: 32–42%), mean corpuscular volume 60.9 fL (normal: 72–88 fL), and platelet 577000/mm3 (normal: 150000–450000/mm3). Biochemical parameters were within normal ranges. C-reactive protein was 2.3 mg/dL (normal: <0.3 mg/dL), and erythrocyte sedimentation rate was 22 mm/hour (normal: <20 mm/hour). Urine analysis showed plenty of bacteria. Extended spectrum beta lactamase positive E. coli grew in the urine culture. High resolution computerized tomography revealed subsegmental atelectasis in right upper lobe apical and posterior segments. Abdominal ultrasonography was normal.
Primary immune deficiencies were first to be suspected in differential diagnosis because of her past clinical and familial medical history. Immunglobulins (IgG: 537 mg/dL, IgM: 52.6 mg/dL, IgA: 25.6 mg/dL, and IgE: 26.2 IU/mL) (age-related reference values; IgG 619 ± 208 mg/dL, IgM 78 ± 39 mg/dL, IgA 34 ± 25 mg/dL, and IgE <100 IU/mL) and complement levels (C3: 130 mg/dL, C4: 25 mg/dL) were normal for age. Percentages of lymphocyte subgroups were normal (CD3: 65.1% (normal: 51–79%), CD19: 18.6% (normal: 14–44%), CD3+CD4+: 47.7% (normal: 31–54%), CD3+CD8+: 13.9% (normal: 10–31%), and CD3-CD16+56+: 12.5% (normal: 5–23%)). Naive and memory T helper cell levels were normal for age. She did not have any elevation in TCR-gamma delta T cells. Transplacental maternal T cell engraftment was excluded by genetic analysis (PCR). In vitro T cell proliferation response to mitogens (PHA) was low. The quantitative determination of oxidative burst was normal, excluding chronic granulomatous disease. Foxp3 expression on CD4+CD25+ cells was normal. EBV and CMV-DNA were negative. Autoantibodies (anti-nuclear antibody, direct coombs test) were negative. Her immunoglobulin levels, although mostly normal initially, showed a fluctuating pattern with some lower values requiring intravenous immunoglobulin (IVIG) replacement regularly.
She had ongoing diarrhea during follow-up. Stool investigations for bacteria, virus (rotavirus, adenovirus, and enterovirus), fungi, and parasites yielded negative results. Refractory diarrhea caused dehydration leading to central venous catheter replacement many times and several line infections with gram negative rods and Candida species, which prolonged hospitalization. The family noticed stool discharge through the vagina. Fistulography showed a rectovaginal fistula, which was treated by fistulectomy and anoplasty. Healing with scarred tissue led to colostomy decision. Although there was no blood in her stool, early-onset inflammatory bowel disease was considered because of refractory diarrhea, perianal disease, and positive family history. Colonoscopy revealed granularity of the right colon, exudative mucosal ulceration, pseudopolyps, laceration, and loss of haustration of the left colon, which was compatible with colitis (). Histopathologic examination showed irregular architectural changes on the right colon and plasma cells in the lamina propria of the left colon. Macroscopic examination of the upper gastrointestinal tract by endoscopy was normal, while histopathology showed esophagitis, chronic active gastritis, and erosive bulbitis.
Recurrent infections, intermittent folliculitis, early onset colitis, and perianal disease leading to fistula formation and colostomy requirement together with positive family history in this patient suggested probable IL-10/IL-10R defects. A mutation at position c.G477A in exon of the IL10RB gene results in a stop codon at position p.W159X. This mutation has previously been published by Glocker et al. and STAT3 phosphorylation by IL-10 was shown to be abrogated [].
She underwent hematopoietic stem cell transplantation with 10/10 HLA (high resolution) matched related father at 11 months of age. She received myeloablative conditioning with the use of busulfan 4 mg/kg/day on days −5 to −2 and fludarabine 40 mg/m2/day on days −5 to −2, with rabbit ATG (Fresenius) 10 mg/kg/day on days −3 to −1. Gut decolonization was performed with the use of oral ciprofloxacin. Infection prophylaxis was intensified with acyclovir and amphotericin B (3 mg/kg/day). Enteral nutrition was given during the peritransplantation period. Cyclosporin A and short term methotrexate were used for graft versus host disease prophylaxis. Stem cell source was bone marrow. Counts of total nucleated and CD34+ cells were 4 × 108/kg and 14 × 106/kg, respectively. Neutrophil engraftment occurred at day +16. She was discharged at day +28. No severe complications were noted and perianal lesions, chronic diarrhea, and recurrent infections resolved (). Tapering of cyclosporine was started at day +100 by 10% every week. Hematopoietic chimerism was determined using restriction fragment length polymorphism. She has full donor chimerism and is in excellent health condition after one year of HSCT.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.5, 'kg']}",26,24.7,27.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.5 kg. Hence, the patient's maintenance fluid is 6.5 kg * 4 mL/kg/hr = 26.0 mL/hr.
Hence, the patient's fluid maintenance is 26.0 mL/hr."
5019,22,Maintenance Fluids Calculations,physical,decimal,pmc-5564138-1,Extracted,"A 7-year-old boy, 107 cm in height and 17 kg in weight, had been previously presented with fever and convulsion and was diagnosed with acute encephalopathy at the age of 3 years. Dental treatment at our hospital was scheduled under general anesthesia due to his multiple caries and uncooperative behavior.
At 1 month after his initial diagnosis, the patient had received a tracheotomy for chronic respiratory failure, and at 5 years of age, he received trachea closure surgery because his respiratory condition stabilized. After computed tomography (CT) confirmation of tracheal granulation tissue under the vocal cords at 7 years of age, the patient regularly received follow-up observations (). The neurological status of the patient was poor with severe mental retardation and cerebral paralysis. He could not speak or walk without support and we could not communicate with him. The patient had been taking antiepileptic drugs daily and was without seizure activity for more than two years. However, due to tracheal granulation, the patient had a few episodes of wheezing and stridor. On admission, clinical assessment of his airway was difficult, but his respiratory condition was stable and his oxygen saturation (SpO2) was 98% in room air. No abnormal findings were observed on a chest X-ray, in laboratory data, or in cardiac function.
On the day of dental treatment, no premedication was administered, and the patient was transferred to the operating room. Anesthesia was induced with inhalation of sevoflurane at 1–8% in oxygen after the initiation of noninvasive monitoring for SpO2 (100%). After the loss of consciousness, mask ventilation with an oral airway was uncomplicated, and we began electrocardiogram (ECG; sinus rhythm), blood pressure (BP; 90/58 mmHg), and heart rate (HR; 105 bpm) monitoring. Atropine at 100 mcg and rocuronium at 6 mg were administered after peripheral intravenous access was obtained. Insertion was carried out without difficulty with a size 2 FLMA (). Anesthesia was maintained with sevoflurane at 1–3% in air and oxygen. Blood pressure was maintained at 85–110/38–68 mmHg and HR was 80–100 bpm with acetaminophen. In the surgical field, a rubber dam isolation technique was used to prevent contamination due to saliva or hemorrhage. The conservative treatment and tooth extraction were completed in 135 min without any surgical or anesthetic problems. Blood loss was minimal during the operation and the patient received a total of 436 mL of lactated Ringer's solution with 1% glucose. Urine volume was 60 mL. The respiratory condition was stable after removing the FLMA. The patient left the hospital one day after the dental surgery, and no remarkable changes or complications have occurred thereafter.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [17.0, 'kg']}",54,51.3,56.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 17.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (17.0 kg - 10 kg) = 54.0 mL/hr.
Hence, the patient's fluid maintenance is 54.0 mL/hr."
5020,22,Maintenance Fluids Calculations,physical,decimal,usmle-4111,Extracted,"A 2710-g (6-lb) male newborn is delivered at 38 weeks of gestation to a 26-year-old woman, gravida 2, para 2. The pregnancy, labor, and delivery were uncomplicated. Breastfeeding is initiated.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2710.0, 'g']}",10.84,10.298,11.382,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2710.0 g so this converts to 2710.0 lbs * kg/1000 g = 2.71 kg. Hence, the patient's maintenance fluid is 2.71 kg * 4 mL/kg/hr = 10.84 mL/hr.
Hence, the patient's fluid maintenance is 10.84 mL/hr."
5021,22,Maintenance Fluids Calculations,physical,decimal,pmc-8713580-1,Extracted,"A 17-year-old female presented to us with anasarca developed over the past 2 months, which started with bipedal edema gradually developing into anasarca for the last 15 days associated with intermittent fever for the same. Tracing backward this patient had a history of progressive exertional breathlessness for the past 5 years and had a history of weakness of the right side of the body and facial deviation of angle of mouth to the left, which recovered spontaneously within 24 h, suggestive of transient ischemic attack (TIA), 1 month back. She also had developed jaundice throughout the last 2 weeks and orthopnea in the last 1 week.
Fever was associated with productive cough and expectoration. There was no history of rash, diarrhea, vomiting, joint pain, dysuria, hematemesis, melena, altered sensorium, renal failure or proteinuria. Her birth history was uneventful, developmental milestones were delayed along with poor scholastic performance and she didn’t achieve her menarche yet.
On examination, she had sinus tachycardia, pallor, fever with 100.8°F, anasarca, suffering from cardiogenic shock with a blood pressure of 70/40 mm of Hg, raised Jugular Venous Pressure (JVP) and poor capillary filling. Cardiological auscultation revealed a systolic murmur of grade III over the left parasternal area with loud P2; chest auscultation revealed basal crepitations. She was malnourished with stunted growth. There was no organomegaly or clubbing or any abnormal fundoscopic picture. The patient was resuscitated, vasopressors added, blood cultures sent, empirical intravenous antibiotics started and urgent echocardiography planned in accordance with the infective endocarditis protocol. Electrocardiogram showed sinus tachycardia with features of biatrial enlargement. Echocardiogram revealed levocardia with situs solitus; a 1.8 cm × 1.8-cm sized mass suggestive of thrombus within the left ventricular (LV) cavity near apex was found with dilated all four cardiac chambers with no evidence of vegetation. Global hypokinesia of LV, right ventricular free wall with left ventricular ejection fraction of 21% associated with severe tricuspid regurgitation and severe pulmonary arterial hypertension were found. No abnormalities were found in the aortic valve cusp or aortic root. ().
Given the working diagnosis of heart failure due to DCM with intracardiac thrombus, we started the patient on anticoagulation with low molecular weight heparin 20 unit subcutaneously twice daily. After initial stabilization, we searched for the underlying etiology behind this early DCM and intracardiac thrombus. Anti-Nuclear Antibody (ANA)-Hep2 and anticardiolipin, antibeta-2glycoprotein antibody was negative along with normal protein C, S values, which ruled out some common causes of the thrombotic phenomenon.
On detailed anthropometric analysis, she had short stature (height 125 cm), underweight (17.5 kg), upper segment:lower segment of 0.87 and arm span being 110 cm. Other notable findings were short fourth toe in the bilateral lower limb and low intelligence [Intelligence Quotient (IQ) 72 (borderline) as per Wechsler Adult Intelligence Scale (WAIS-IV) classification] []. There was a history of amenorrhea, associated with scanty axillary and pubic hairs and breast development showed tanner stage 1 with widely spaced nipples. She had a low posterior hairline with micrognathia, a webbed neck and cubitus valgus (). Hormonal assay revealed normal levels of estradiol (129 pg/ml), follicle-stimulating hormone (6.21 mIU/ml), luteinizing hormone (0.56 mIU/ml) and low insulin-like growth factor-1 level (102 pg/ml).
The skeletal survey revealed short fourth metacarpal and metatarsal in all four limbs. We had ruled out pseudohypoparathyroidism with normal serum calcium, phosphate and iPTH values along with the absence of other classical Albright’s hereditary osteodystrophy phenotype morphology (early obesity, round face, heterotopic calcification) and sent sample for karyotyping from the blood that showed a mosaic pattern, with 45, X/46, X,r(X)(p22.3q28); i.e. Turner syndrome karyotype with a very rare variety that is ring chromosome [] ().
She was treated for heart failure with reduced ejection fraction as per standard protocol conservatively, with subsequent anticoagulation. The patient was cured of intracardiac thrombi and congestive cardiac failure and finally was discharged with oral contraceptive pills for secondary sexual character development, iron-folic acid supplementation therapy for iron deficiency anemia, was put on dabigatran for 3 months and regular follow-up is being done periodically.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [17.5, 'kg']}",55,52.25,57.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 17.5 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (17.5 kg - 10 kg) = 55.0 mL/hr.
Hence, the patient's fluid maintenance is 55.0 mL/hr."
5022,22,Maintenance Fluids Calculations,physical,decimal,pmc-7132803-1,Extracted,"A 62-year-old Chinese man was scheduled for combined dissection of the tongue, mandible, and neck, right forearm free flap transplantation, mandibular titanium plate implantation, and tracheotomy. He was a smoker, 170 cm in height, and 51 kg in weight. Except for hypertension, which was treated with losartan potassium, the patient had no other medical history and denied any allergies. Two sessions of chemotherapy (docetaxel injection 120 mg, nedaplatin injection 120 mg) were completed before admission. The patient provided consent for publication of this case report, and the Institutional Review Board of the University of the Chinese Academy Of Sciences (Ningbo No. 2 Hospital) granted approval for the study protocol (YJ-KYSB-NBEY-2019-120-01).
On the day of surgery, the patient received 2 mg of intravenous midazolam as preoperative medication. Standard American Society of Anesthesiologists monitors were applied and a loading dose of dexmedetomidine was intravenously infused at 0.6 µg/kg over 10 minutes before induction. Induction was performed by propofol (80 mg), sufentanil (20 µg), and rocuronium (50 mg) followed by tracheal intubation. An invasive arterial catheter and an internal jugular vein catheter were placed. Anesthesia was maintained with sevoflurane (1% to 2%), propofol (150–200 mg/hour), and intermittent sufentanil 10 µg and rocuronium 10 mg, which were titrated to hemodynamic status and surgical requirements.
Urine output increased 30 minutes after the dexmedetomidine infusion was completed, reaching approximately 1900 mL within 2 hours. Pituitrin 2 U/hour was infused intravenously and changed to 3 U/hour 30 minutes later until the operation was over. Urine output showed a downward trend since the pituitrin treatment, and decreased to 500 ml/hour 2 hours later. Serial urine output is shown in .
The surgery lasted for 14 hours, during which time the patient received 5500 mL of lactated Ringer’s solution, 2000 mL of hydroxyethyl starch (130/0.4), and 375 mL of packed red blood cells. The estimated blood loss was 600 mL and the total urine output was 7150 mL.
The patient’s serum sodium level was 135 mmol/L 5 days before surgery and rose to 143 mmol/L intraoperatively. The patient’s serum osmolality was within normal limits at 2 hours after surgery (). The patient was hemodynamically stable throughout the procedure without major episodes of hypotension or tachycardia.
The patient was transferred to the intensive care unit after the operation with no diuresis or abnormal electrolyte and plasma osmotic pressure. He was discharged on postoperative day 18 without further related complications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [51.0, 'kg']}",91,86.45,95.55,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 51.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (51.0 kg - 20 kg) = 91.0 mL/hr.
Hence, the patient's fluid maintenance is 91.0 mL/hr."
5023,22,Maintenance Fluids Calculations,physical,decimal,pmc-4147201-1,Extracted,"A 65-year-old African-American man with a history of hypertension, reflux disease, allergic rhinitis, and peptic ulcer disease presented to the emergency department with dull, nonradiating, right-sided abdominal pain, watery diarrhea, nausea, and poor appetite for seven days. He also complained of a thirteen-pound weight loss over the eleven months prior to admission. He denied chest pain, shortness of breath, rashes, dysuria, melena, hematochezia, arthralgias, or myalgias. The patient denied tobacco, alcohol, or illicit drug use, and he had no recent domestic or exotic travel. He admitted to having a blood transfusion in 1975. He was also evaluated by an oral surgeon and had a tooth extraction approximately eleven months prior to hospitalization, in addition to a dental cleaning 1.5 months ago. No prophylactic antibiotics were given prior to these procedures.
Family history was significant for a mother with coronary disease and a sister with diabetes. He reported having four healthy children, living alone, and working from home. Medications included fluticasone nasal spray daily, losartan 100 mg daily, ranitidine 150 mg twice daily, and pantoprazole 40 mg twice daily. He develops a diffuse rash with penicillin use.
Of note, he was treated for cholecystitis and choledocholithiasis after presenting with obstructive jaundice, transaminitis, and abdominal pain over 1.5 years earlier. MRCP showed multiple stones within the extrahepatic biliary ductal system consistent with choledocholithiasis and mild dilation of both the intra- and extrahepatic bile ducts suggestive of biliary obstruction. He was afebrile and there was no evidence of acute cholecystitis on imaging, but he was treated prophylactically with ciprofloxacin and metronidazole due to positive Murphy's sign and transaminitis (AST 260 IU/L, ALT 396 IU/L, total bilirubin 7.0 mg/dL). Gastroenterology performed two successive ERCPs due to difficulty with cannulation related to obstructive stones. The first entailed partial sphincterotomy and prophylactic 5Fr 3 cm pancreatic duct (PD) stent placement. The following day, the PD stent was removed, the common bile duct (CBD) was dilated to 12 mm, and the sphincterotomy was extended to allow the extraction of four stones. Occlusion cholangiogram revealed one retained stone in the cystic duct, and a 10F 5 cm stent was placed in the CBD to ensure proper drainage. A trickle of blood was observed at the upper margin of the sphincterotomy but abated with the spraying of epinephrine. Laparoscopic cholecystectomy was performed two days later, and he was discharged home on postoperative day number one. H. pylori stool antigen was also found to be positive, so he was discharged to complete a two-week course of triple antibiotic therapy (clarithromycin 500 mg po twice daily, omeprazole 20 mg po twice daily, and metronidazole 500 mg po twice daily). Repeat ERCP was performed approximately a month later with the removal of the single residual stone and extraction of the CBD stent without complication.
On his presentation to our team, temperature was 102.8 F, pulse 85, respirations 16, and blood pressure 116/66 mmHg. Physical exam revealed a well-nourished man in no acute distress that appeared in his stated age. Eyes were anicteric. There were multiple silver and gold tooth fillings but no evidence of dental caries, periodontitis, or oral abscess was found. Cardiovascular exam was negative for murmurs, and there was no lower extremity edema. Lungs were clear to auscultation bilaterally. Abdomen was obese without fluid wave. There was moderate tenderness to palpation at the right upper quadrant with negative Murphy's sign. There was also no rebound, guarding, hepatosplenomegaly, rash, or jaundice.
Laboratory data showed WBC 23.2 k/μL, hemoglobin 12.2 gm/dL, platelets 442 k/μL, creatinine 1.6 mg/dL, AST 138 IU/L, ALT 136 IU/L, alkaline phosphatase 176 μ/L, total bilirubin 2.4 mg/dL, albumin 2.5 gm/dL, lipase 90 μ/L, amylase 58 μ/L, and negative urinalysis, and coagulation studies were within normal limits. Acute hepatitis panel was negative, and urine drug screen was negative other than for opiates which he received in the emergency department. Right upper quadrant ultrasound () showed a homogenous liver and a complex, predominant cystic lesion measuring 10.2 × 7.4 × 9.4 cm within the right hepatic lobe demonstrating multiple internal thickened septations with color Doppler flow as well as debris. The common bile duct was within normal limits, and the gallbladder was surgically absent. Blood cultures were drawn, and he was empirically placed on ciprofloxacin 400 mg intravenous (IV) every 12 hours and metronidazole 500 mg IV every 8 hours due to history of penicillin allergy without anaphylaxis.
Contrasted CT imaging was initially deferred so that intravenous fluids could be given to improve the patient's creatinine. After the creatinine normalized, three-phase CT of the abdomen with delayed imaging () was obtained demonstrating a 13.0 × 10.2 × 7.8 cm cystic, heterogeneously arterially enhancing lesion involving segments VI and VII of the liver with multiple enhancing septations with peripheral enhancement on the arterial phase and partial venous and delayed phase washout. There was also a focus of gas within the porta hepatis. Findings were thought to be most consistent with hepatic abscess; however, necrotic neoplasm could not be excluded.
A CT-guided drain was placed with the expression of blood-tinged, purulent fluid which was sent for multiple studies. In the meantime, blood cultures which were obtained on admission resulted positive with gram positive cocci in pairs and chains, so antibiotics were switched to ceftriaxone 2 gm IV daily with metronidazole 500 mg IV every 8 hours. In addition, AFP < 2.0 ng/mL and Entamoeba histolytica IgG was negative. Both blood and fluid cultures eventually grew Streptococcus intermedius. This was isolated using blood and chocolate agar medium and a VITEK 2 gram positive card. Fungal culture was negative. Susceptibility studies revealed sensitivities and MIC values as follows: cefotaxime 0.019, ceftriaxone 0.125, penicillin 0.064, and vancomycin 1.0. Transthoracic echocardiogram was later performed showing ejection fraction 60–65% and no discrete valvular lesions. He refused to submit to HIV testing.
The patient's clinical status improved, and repeat blood cultures were negative. He was discharged with the hepatic drain in place with plans for removal in outpatient clinic in one week's time. A PICC line was inserted, and he was placed on ceftriaxone 2 gm IV daily to complete a four-week course of intravenous therapy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [13.0, 'lbs']}",23.5868,22.40746,24.76614,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 13.0 lbs so this converts to 13.0 lbs * 0.453592 kg/lbs = 5.8967 kg. Hence, the patient's maintenance fluid is 5.8967 kg * 4 mL/kg/hr = 23.5868 mL/hr.
Hence, the patient's fluid maintenance is 23.5868 mL/hr."
5024,22,Maintenance Fluids Calculations,physical,decimal,pmc-6967330-1,Extracted,"A 169-cm, 65-kg, 51-year-old, right-handed man with right-side hemiparesis and dysarthria underwent screening magnetic resonance imaging (MRI) 2 years before craniotomy: a diffuse parietal tumor was misdiagnosed as cerebral infarction. Anticonvulsant polytherapy (carbamazepine, 200 mg daily; levetiracetam, 1000 mg daily) was started for symptomatic epilepsy. Right-hand and oro-facial motor paresis worsened beginning 4 months before surgery, and he was diagnosed with malignant glioma. He was referred to our institution 2 months before surgery. MRI demonstrated a T1 hypointense, T2/fluid-attenuated inversion recovery hyperintense area in the left lower parietal lobe with a gadolinium-positive mass in the postcentral gyrus. 11C-methionine positron emission tomography showed a high accumulation of methionine mainly in the postcentral gyrus. The results of a manual muscle test (MMT) showed reduced function (3/5) in his right-upper extremity.
The patient’s hypertension was well-controlled with telmisartan (40 mg, daily) and hydrochlorothiazide (12.5 mg, daily). Diabetes was treated with glimepiride (1 mg, daily) and anagliptin (400 mg, daily). Obstructive sleep apnea syndrome (OSAS) was suspected due to a history of snoring. Electrolyte imbalance was not observed. Although carbamazepine was increased to 400 mg daily beginning 17 days before surgery, epileptic seizure in his right-upper limb occurred every 2–3 days. Levetiracetam was increased to 2000 mg daily upon admission 4 days before surgery.
The lesion, suspected grade III glioma according to the World Health Organization (WHO) guidelines [], was distributed throughout the primary motor and sensory areas of his dominant hemisphere. We chose awake craniotomy using the “Asleep-Awake-Asleep” technique combined with intraoperative MRI for removal of his glioma. Uncontrollable seizure suggested rapid growth of the tumor. The patient was evaluated as American Society of Anesthesiologists (ASA) Physical Status Class 2. While the preoperative blood examination at admission indicated that his plasma sodium level (reference 136–145 mEq/L) had decreased from 140 to 130 mEq/L, he was asymptomatic. Preoperative correction of hyponatremia was ruled out to avoid neurological deterioration due to further growth of the glioma. Additional blood or urine examinations were not performed.
No premedication was given. Besides standard ASA monitoring, invasive arterial pressure and processed electroencephalogram monitoring were adopted. Following the intravenous administration of 100 μg fentanyl, general anesthesia was commenced and maintained with the target-controlled infusion of propofol (4.0 μg/mL) and the continuous infusion of remifentanil (0.5 μg/kg/min). After several attempts, a supraglottic airway (SGA) was inserted without muscle relaxant. Ventilation was adjusted to maintain an EtCO2 level around 35 mmHg. Normal saline and bicarbonate Ringer’s solution were given. Scalp blocks and infiltration analgesia were provided with 60 mL of 0.3% ropivacaine and 20 mL of 1% lidocaine with 0.01% epinephrine, respectively. Arterial blood gas (ABG) analysis (STAT PROFILE® Critical Care Express; Nova Biomedical, Waltham, MA) after induction showed mild hyponatremia (Table , T1).
Hypotension followed by induction was stabilized by three boluses each of ephedrine 4 mg and phenylephrine 0.1 mg until the beginning of surgery. Before dural incision, 200 mL of 20% mannitol was administered over 10 min. ABG analysis 117 min after induction, 25 min into mannitol infusion, revealed hyponatremia with hyperkalemia (Table , T2). Neither pathological electrocardiogram changes nor arrhythmia was observed. Sodium bicarbonate 2.8 g was given. Glucose-insulin (40 mL of 50% glucose containing 8 units of insulin) was infused simultaneously with another ABG analysis, which was performed to exclude mechanical failure (Table , T3). Hyponatremia was not treated promptly because of the risk of central pontine myelinolysis. ABG analysis 191 min from induction indicated persistent hyponatremia without hyperkalemia (Table , T4). In the planned transition to the awake phase, we anticipated insufficient wakefulness, intractable seizure, and deterioration of upper airway patency. Thus, the entire procedure was performed under general anesthesia. The remaining operation was uneventful, although the plasma sodium level remained less than 125 mEq/L (Table , T5–7). Anesthetics were discontinued, and SGA was removed 415 min after induction. The patient’s cardiorespiratory status was stable, but the patient could not follow orders. An intravenous transfusion of 1500 mL bicarbonate Ringer’s solution, 300 mL 1% glucose-containing acetated Ringer’s solution, 650 mL normal saline, and 200 mL mannitol was given. Total urine output was 1300 mL, and estimated blood loss was 36 mL. Surgery and anesthesia lasted 433 and 354 min, respectively.
The patient regained consciousness 1 h after the operation. MMTs of his right upper and lower extremities showed 1/5 and 3/5, respectively. Motor aphasia persisted until eight postoperative days (POD), and he walked unaided on POD 24. His plasma sodium concentration normalized by POD 35, before discharge on POD 39. MMTs at discharge were 2/5 and 4/5, respectively. Since the pathological examination revealed an oligoastrocytoma (WHO grade II), he received adjuvant chemotherapy. Prophylactic anticonvulsant polytherapy was continued, and there was no evidence of tumor recurrence at 36 months follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [65.0, 'kg']}",105,99.75,110.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 65.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (65.0 kg - 20 kg) = 105.0 mL/hr.
Hence, the patient's fluid maintenance is 105.0 mL/hr."
5025,22,Maintenance Fluids Calculations,physical,decimal,pmc-7713837-1,Extracted,"A 75-year-old male (body weight 71.6 kg, height 159.3 cm, body mass index [BMI] 28.22 kg/m2) came to emergency room with right lower quadrant pain that had started 2 days previously. We diagnosed him with acute appendicitis and decided to do a laparoscopic appendectomy. He had undergone a radical prostatectomy five years previously for prostate cancer. The patient took oral medications for hypertension and Parkinson’s disease. His neck was a little bit rigid. The thyromental distance was 7 cm. His mouth opening was 2.5 fingerbreadths. The Mallampati score was a class III. There were no loose, chipped, or damaged teeth. Although there was a concern about airway difficulties on physical examination, we decided to proceed with general anesthesia because there had been no airway issues in previous surgeries.
After giving consent for general anesthesia, the patient entered the operating room. The patient’s vital signs were stable prior to general anesthesia. We applied standard monitoring, including electrocardiogram, pulse oximetry, and noninvasive blood measurement. The patient was preoxygenated with 4 L/min oxygen via facial mask. General anesthesia was induced with propofol 120 mg and rocuronium 50 mg. We inserted the oral airway into the oral cavity. There was no difficulty in mask ventilation. We attempted direct laryngoscopy to visualize the patient’s larynx. But after several attempts, it turned out that it was impossible to insert the direct laryngoscope deep enough for vocal cord visualization without damaging his teeth because of a limited mouth opening.
We decided to do a fiberoptic intubation. We expected the laryngeal view on fiberoptic intubation to be bad because the patient had a high BMI (28.22 kg/m2) and was fully relaxed. We decided to use the modified Guedel airway that we had made earlier for difficult fiberoptic intubations.
We modified the regular Guedel airway by making a longitudinal channel at the convex side to facilitate airway removal after intubation and opened the distal lingual end for a better laryngeal view ().
We inserted the sterilized modified Guedel airway into the mouth. We inserted a fiberoptic bronchoscope (5.2 mm diameter, Olympus LF-TP, Japan) into the lubricated 7.5-mm endotracheal tube. An assistant lifted the jaw for a better laryngeal view. We advanced the fiberoptic cable through the modified Guedel airway until the glottis was visualized. The fiberoptic cable advanced through the vocal cord until the carina was seen (). The airway was removed gently from the oral cavity. The endotracheal tube was inserted into the trachea along the fiberoptic cable.
We completed the laparoscopic appendectomy under general anesthesia without any problems. Following surgery, we infused 200 mg of sugammadex via the intravenous route after we had confirmed four twitches in a train-of-four stimulation. We performed extubation when the patient was fully awake. No specific event was reported after extubation.
After the operation, the patient provided written informed consent to have his case details and the accompanying images published.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [71.6, 'kg']}",111.6,106.02,117.18,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 71.6 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (71.6 kg - 20 kg) = 111.6 mL/hr.
Hence, the patient's fluid maintenance is 111.6 mL/hr."
5026,22,Maintenance Fluids Calculations,physical,decimal,pmc-4162970-1,Extracted,"A 66-year-old man (height 172 cm, weight 92 kg) presented with diabetic nephropathy for planned living donor kidney transplantation. He suffered from CAD, hypertension, hypercholesterolemia, insulin dependent diabetes mellitus II and a chronic obstructive pulmonary disease. He had undergone coronary artery bypass surgery in a different hospital 7 months before (left internal mammary artery (LIMA) to left anterior descending (LAD) and saphenous vein graft to the ramus diagonalis). The ramus circumflexus (RCX) was not accessible to revascularization during bypass operation according to the documents of the different hospital. The LAD was supplied with a drug-eluting stent three years before. The RCX was supplied with a bare-metal stent one year before and, because of an in-stent restenosis, 5 month before with a Genous stent in a different hospital. Additionally another Genous stent was placed distally to the previous stent area.
The patients’ wife was intended to serve as the organ donor. She had a history of severe chronic obstructive pulmonary disease with intercurrent infectious exacerbation, why the transplantation had been called off twice, yet. Prior to the planned date of transplantation she was in good condition.On account of the medical history of the recipient and according to the pre-transplantation guidelines of our institution with regard to high-risk patients a cardiac catheterization was carried out 5 days before transplantation. Here an in-stent restenosis of the proximal ramus circumflexus, which had already been supplied with drug-eluting and bare metal stents two times before, was observed (see Figure ). After intensive discussion between the cardiologist, the surgeon and the anaesthesiologist the following therapeutic plan was made: the stenosis was dilated with a 3.0/15 mm drug-eluting balloon (Inc. Braun, Germany) followed by anticoagulation with tirofiban and aspirin until surgery. The post-interventional angiography showed a very good result after PTCA (see Figure ). Definitive stenting was planned after full recovery from the kidney transplantation.
Five days later the planned kidney transplantation was carried out. Medication including aspirin and tirofiban was continued up to the day of operation. In the operating room (OR) induction with sufentanil 0.33 μg kg-1, propofol 1.6 mg kg-1 and rocuronium 0.33 mg kg-1 was performed. Anaesthesia was maintained with sevofluoran 1.6 Vol%. During whole operation mean arterial pressure was above 70 mmHg with a heart rate between 50 and 60 bpm. The patient received norepinephrine with a maximum dose of 0.11 μg kg-1 min. Intraoperative blood loss was 800 ml, and the lowest level of haemoglobin was 12.2 g/l. The patient received 2500 ml of crystalloid solution. After successful kidney transplantation he was extubated in the OR and transferred to the intensive care unit (ICU).One hour after admission to the intensive care unit (ICU) the patient developed pectanginous symptoms. The ECG at 10 minutes after clinical presentation of angina revealed no significant abnormalities. The cardiac troponin I was initial negative and 13.9 pg/ml after 4 hours with a peak level of >50.0 pg/ml 7 hours after admission. Cardiac catheterization, carried out 20 minutes after the first complaint of angina by the patient presented a sub-acute in-stent thrombosis of the RCX stent which had been dilated preoperatively with a drug-eluting balloon (see Figure ). After PTCA with a 2.0 mm balloon the implantation of a 3.0/24 mm drug-eluting stent (Medtronic Endeavor Resolute, Medtronic, Germany) followed. The angiography again showed a good result (see Figure ). Postinterventionally, after consultation of the surgeons, anticoagulation with tirofiban over 3 days was started followed by prasugrel for 12 months and aspirin. During anticoagulation only minor skin bleeding appeared. 12 days after kidney transplantation the patient could be dismissed home in a good state and is still well after three years.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [92.0, 'kg']}",132,125.4,138.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 92.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (92.0 kg - 20 kg) = 132.0 mL/hr.
Hence, the patient's fluid maintenance is 132.0 mL/hr."
5027,22,Maintenance Fluids Calculations,physical,decimal,pmc-8716839-1,Extracted,"A 56-year-old Caucasian nulliparous female presented to our outpatient clinic with left lower quadrant abdominal discomfort. The discomfort was described as a fluid wave that radiates from the left lower quadrant to the umbilicus, which was worse after eating. For the past 6 years, she had suffered from a 4/10 chronic flank pain. She has a history of ADPKD, multiple liver cysts along with other complications of ADPKD including stage 3 CKD, nephrolithiasis, constipation, mitral valve prolapse, pelvic organ prolapse. Ten years ago she had a total hysterectomy with bilateral salpingo-oophorectomy. Six months ago, she underwent robotic-assisted laparoscopic sacral colpopexy, paravaginal defect repair with cystocele repair, rectocele repair with perineorrhaphy using mesh. She has no children. Family history is significant with a father with polycystic kidney disease, hypertension, aneurysm, and heart disease, a mother with ovarian cancer. Her vital signs were unremarkable with weight 116 lb (52.6 kg), pulse 68 BPM, temperature 98.8℉ (37.1 ℃), blood pressure 108/62 mmHG, BMI of 20.34 (18.5-24.9) and hyposthenia body habitus. On the physical exam, she had a +3 systolic murmur with a mid-systolic click at the apex; the abdomen was diffusely distended with two-third of the abdomen filled with palpable masses from the liver and kidney cysts and tenderness to palpation.
Labs showed elevated blood urea nitrogen (BUN) of 51 mg/dl (7-18 mg/dL), creatinine of 2.14 mg/dL (0.6-1.2 mg/dL), decreased eGFR of 24ml/min (120−130 mL/min), and low sodium of 133 mEq/L (136-146 mEq/L). Complete blood count shows low RBCs of 3.94*10^6/µL (4.10-5.10*10^6/µL), and hemoglobin of 11.9 g/dL (12-16 g/dL). Renal ultrasound showed enumerable simple and complex cysts in bilateral kidneys, with kidneys measuring 13.7 x 7.6 x 7.2 cm on the left and 12.2 x 6.1 x 6.3 on the right. Abdominal ultrasound shows liver size measuring 20.4 in the cranial-caudal direction, with innumerable simple cysts seen throughout the liver. An echocardiogram showed mildly dilated left atrium with impaired diastolic dysfunction. Moderate to severe mitral valve prolapse and mitral regurgitation is also appreciated. Non-contrast Computed tomography (CT) scan of the abdomen and pelvis showed extensive cysts with coarse calcifications in bilateral kidneys (Figures , ) and numerous simple cysts throughout the liver parenchyma (Figures , ). Her blood pressure is medically controlled with 160 mg of amlodipine-valsartan and 2.5 mg of Nebivolol. She was also in 50 mg of tramadol as needed for pain for the past one year.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [52.6, 'kg']}",92.6,87.97,97.23,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 52.6 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (52.6 kg - 20 kg) = 92.6 mL/hr.
Hence, the patient's fluid maintenance is 92.6 mL/hr."
5028,22,Maintenance Fluids Calculations,physical,decimal,pmc-3474230-1,Extracted,"A 6 days old full-term, female infant presented with complaints of restricted movements of upper extremities. The infant was born at home through vaginal route and was third in birth order. The infant cried at birth and was exclusively breastfed. On the third day of life, the mother noticed swelling of both the elbow joints. There was no history of trauma, bleeding from any site, bruising, fever, seizures, or altered sensorium.
On examination the infant weighed 2.4 kg and was moderately active but irritable. There was mild icterus with no pallor, lymphadenopathy, or rash. Both the upper limbs were in adduction with flexion at elbow joints. There was swelling of both elbow joints () and the right knee joint () along with painful limitation of movements. There was no local rise of temperature or erythema. Marked paucity of spontaneous movements of both upper limbs was observed, and the infant cried on passive movement of the joints (Parrot's pseudoparalysis). The neonate did not have any snuffles or feeding difficulty. Anterior fontanel was flat, and there was no asymmetry of movements or cranial nerve palsy. A differential diagnosis of septic arthritis and traumatic arthritis (Battered Baby Syndrome) was considered. As there was no organomegaly or rash, congenital TORCH infections were not entertained.
History revealed an uncomplicated antenatal period. The mother was VDRL and HIV negative when screened for in the first trimester. Mother's examination during first visit was noncontributory. The previous two siblings are healthy.
Investigations revealed normal blood picture and C-reactive protein (CRP). Blood culture was sterile. Neurosonogram and Ultrasound scan of the abdomen were also normal. An Infantogram revealed osteolytic erosions with indistinct cortical outlines of the ulnar ends of both the humerus. Stippling and erosions of the humeral end of left ulna were also visible (). The upper metaphyseal ends of both tibias revealed a typical moth eaten appearance along the medial sides (Wimberger's sign). These changes are classical of congenital syphilis (Figures and ).
Further, VDRL (Venereal Disease Research Laboratory) test was positive in the baby and the mother with titers being 1 : 2048 and 1 : 128, respectively. Father's VDRL test was negative. CSF VDRL test was positive. Cerebrospinal fluid analysis showed normal sugar and proteins with lymphocytosis. The Treponema pallidum haemagglutination (TPHA) test was positive in the baby, mother, and father. As the father tested negative for the VDRL test but positive for the TPHA test, on further probing it was revealed that the father had undergone treatment for genital ulcers during the first trimester of his wife's most recent pregnancy. Based on the clinical manifestations along with pseudoparalysis, typical radiological findings of osteochondritis, positive VDRL and TPHA tests, a diagnosis of congenital syphilis was made. The infant was managed with crystalline penicillin 50,000 units/kg/dose three times a day for a total of 10 days. The baby became asymptomatic and repeat, VDRL titers were conducted after three months, which were found to be negative. Posttreatment of the radiograph of the long bones showed sclerotic metaphysis with clear bony margins suggestive of resolving metaphysitis. The infant weighed 3.5 kg at followup (). Mother was treated by the STD department of the institute as per the protocol.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.4, 'kg']}",9.6,9.12,10.08,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.4 kg. Hence, the patient's maintenance fluid is 2.4 kg * 4 mL/kg/hr = 9.6 mL/hr.
Hence, the patient's fluid maintenance is 9.6 mL/hr."
5029,22,Maintenance Fluids Calculations,physical,decimal,pmc-2693556-1,Extracted,"A 23-yr-old woman to be in gravida 3, para 1 was referred to the Chosun University Hospital due to a cyst in the abdomen of fetus on routine US from private clinic. We performed ultrasound which showed a 56×47 mm cyst suspected to be a mesenteric cyst or ovarian cyst (). The size of the cyst did not change during follow up US and the fetus showed a normal development. Spontaneous labor was at 38 weeks' gestation. The healthy female neonate weighing 3.6 kg with 49 cm height was born via spontaneous vaginal delivery. The newborn was admitted to nursery after birth to examine the cyst observed through prenatal US and underwent routine biochemical, hematologic tests, chromosome study and MRI. The biochemical, hematologic and chromosome studies were normal. MRI revealed a 56×47 mm homogenous cyst in the right posterior retroperitoneal space. This cyst showed low signal density on T1 weighed images and high signal intensity on T2 weighted images (). No enhancement was seen after the use of intravenous contrast enhancer. This cyst was pressing against the tail of pancreas and inferior vena cava. The neonate underwent surgery to remove the cyst. The excision of the cystic mass originating from the pancreatic tail was performed with distal pancreatectomy (). The cyst contained amylase (30 U/L). Gross examination of the cyst showed a 8×8 cm fresh cyst containing clear fluid inside. In immunohistochemical stains, calretinin and CD 34 were negative and cytokeratin was positive (). The histopathologic diagnosis was pancreatic cyst. The baby recovered well after operation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.6, 'kg']}",14.4,13.68,15.12,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.6 kg. Hence, the patient's maintenance fluid is 3.6 kg * 4 mL/kg/hr = 14.4 mL/hr.
Hence, the patient's fluid maintenance is 14.4 mL/hr."
5030,22,Maintenance Fluids Calculations,physical,decimal,pmc-6188736-1,Extracted,"The patient was a 60-year-old man who was diagnosed with alcoholic liver cirrhosis and type 2 diabetes when he was 50 years old. His drinking history was 540–720 mL Japanese sake per day for 35 years, and his smoking history was 30 cigarettes per day for 30 years. His ascites increased in 2008 when he was 57 years old, and he repeatedly exhibited symptoms of hepatic encephalopathy. Due to the liver cirrhosis symptoms, the patient was treated with several medications including furosemide, spironolactone, lactulose, and total amino acid preparation. To prevent the complications of liver cirrhosis, coil embolization to a portal venous shunt was performed twice. The patient was admitted to our hospital in June 2012 because of slowly progressive renal impairment and nephrotic syndrome.
Upon admission, the patient's height and weight were 166 cm and 64 kg, respectively. His body temperature was 36.7°C and his blood pressure was 150/60 mmHg. His consciousness was clear. His abdomen was slightly expanded but exhibited no tenderness. The liver and spleen were not palpable. No rash or purpura was noted on the skin. Diabetic and/or hypertensive changes were not observed in the ocular fundus.
The laboratory findings on admission were hemoglobin level of 9.4 g/dL (normal range 13.5–17.6 g/dL), platelet count of 11x104/μL (normal range, 13.1–36.2x104/μL), prothrombin time measurement of 68% (normal range, 70–130%), total bilirubin level of 0.9 mg/dL (normal range, 0.3–1.2 mg/dL), NH3 level of 85 mg/dL (normal range, 30–80 mg/dL), blood urea nitrogen level of 41 mg/dL (normal range, 8–20 mg/dL), serum creatinine concentration of 1.77 mg/dL (normal range, 0.5–1.1 mg/dL), serum total protein level of 5.7 g/dL (normal range, 6.7–8.3 g/dL), serum albumin level of 2.1 g/dL (normal range, 3.5–5.2 g/dL), total cholesterol of 188 mg/dL (normal range, 120–219 mg/dL), and HbA1c of 5.8% (normal range, 4.3–5.8%). The serum levels of IgG were 1558 mg/dL (normal range, 870–1700 mg/dL), of IgA were 481 mg/dL (normal range, 110–410 mg/dL), of IgA1 were 398 mg/dL (normal range, 50–314 mg/dL), of IgA2 were 83 mg/dL (normal range, 10–156 mg/dL), and of IgM were 219 mg/dL (normal range, 35–220 mg/dL). The serum levels of free κ and λ light chains were 149.0 mg/L (normal range, 3.3–19.4 mg/L) and 106.0 mg/L (normal range, 5.7–26.3 mg/L). The serum free light chain ratio was within normal range. The serum level of complement factor C3 was 79 mg/dL (normal range, 65–135 mg/dL), of C4 was 17 mg/dL (normal range, 13–35 mg/dL), and of CH50 was 41.1 U/mL (normal range, 30–50 U/mL). All of the other serology findings including anti-nuclear antibody, hepatitis B virus surface antigen, hepatitis C virus antibody, anti-neutrophil cytoplasmic antibody, and anti-glomerular basement membrane antibody were negative. There was no M-spike on serum and urine protein electrophoresis. A serum test for a cryoglobulin precipitation was negative.
The urinary sediments showed many red blood cells in high power fields together with granular casts and dysmorphic red blood cells. The urinary protein excretion was 4.7 g/day. The 24-hour creatinine clearance was 45 mL/min. Computed tomography revealed liver deformity with moderate accumulation of ascites. The kidneys were normal in size and there were no signs of urinary tract obstruction.
The renal biopsy specimens contained a total 28 glomeruli, 12 of which were globally sclerotic. The degree of interstitial fibrosis/tubular atrophy was 50–60% of the total biopsy specimen identified. Moderate fibrous intimal hyperplasia was observed in the arcuate artery. Diffuse segmental double-contours of the glomerular basement membrane and mesangial cell hypercellularity were identified in nonsclerotic glomeruli, exhibiting a membranoproliferative glomerulonephritis-like pattern (). Some glomeruli showed moderate-to-severe endocapillary hypercellularity, accompanied by fibrocellular crescents (). Fluorescent immunostaining showed granular staining of IgA and C3, but not of IgG, IgM, or C1q, on glomerular capillaries and some mesangial areas (Figures –). Among the IgA subtypes, staining of IgA1 (GenWay Biotech, San Diego, CA, USA) was observed, but staining of IgA2 (GenWay Biotech) was not identified (Figures and ). With light chain immunostaining, only κ (SouthernBiotech, Birmingham, AL, USA) was identified and no λ staining (SouthernBiotech) was seen (Figures and ). On electron microscopy, the glomerular capillary walls showed double contours. Electron-dense deposits were found in the paramesangium and around the subendothelial space of the glomeruli (). No organized structure deposits were identified (). Based on these findings, this case was histologically diagnosed as diffuse membranoproliferative glomerulonephritis with monoclonal IgA1-κ deposits.
Because this case was accompanied by moderately advanced decompensated liver cirrhosis, there was a concern that the patient may have serious side effects due to aggressive treatment such as the administration of corticosteroids. Thus, supportive treatment based on medications such as RAS inhibitors/diuretics, in addition to dietary therapy including salt restriction/branched-chain amino acid administration, was selected. Although these treatments led to a modest decrease in the urinary protein excretion, the patient's renal dysfunction slowly progressed and finally resulted in end-stage renal failure and initiation of dialysis therapy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [64.0, 'kg']}",104,98.8,109.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 64.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (64.0 kg - 20 kg) = 104.0 mL/hr.
Hence, the patient's fluid maintenance is 104.0 mL/hr."
5031,22,Maintenance Fluids Calculations,physical,decimal,pmc-4049498-1,Extracted,"Patient: Male, 57 years old.
Hospital “A”
Chief complaint: Continuous cough for 1 month
History of the present illness: Pneumonitis (for which differential diagnosis of pulmonary tuberculosis was needed) was diagnosed by plain chest radiography carried out in a nearby hospital due to continuous cough for 1 month. The patient visited the Division of Pulmonology at the “A” University Hospital on the same day and was hospitalized.
Past medical history: No special findings.
Personal history and family disease: The patient had been smoking a pack of cigarettes daily for 40 years, and did not drink alcohol. There was no notable family disease.
Physical examination: Enlarged cervical lymph nodes were found bilaterally.
Blood test: Hemoglobin (Hb) was measured to be 12.6 g/dl in the complete blood cell count (CBC), which was a slightly decreased concentration, while the total proteins and albumin were in the normal range. The erythrocyte sedimentation rate (ESR) increased to 73 mm/h.
Tumor marker: Carcinoembryonic antigen (CEA) was 0.66 ng/ml, which was at the normal level, while neuron-specific enolase (NSE) increased to 19.31 ng/ml.
Chest images: In the plain chest x-ray, potential pneumonitis or pulmonary tuberculosis was found bilaterally in the upper lobes of the lungs (discernment of a lung tumor on the right upper lobe was required) (Figure -A). Pneumonitis was most suspicious bilaterally on the upper part of the lungs from the chest computed tomography (CT). Based on the imaging study, we concluded that complicated silicosis was accompanied by pneumonitis. Sarcoidosis or pulmonary tuberculosis had to be considered if this pneumonitis was to be classified as a tumor.
Findings from thyroid and cervical ultrasound: There were no abnormal findings in the thyroid. The cervical level IV and VI lymph nodes and supraclavicular lymph nodes on both sides were enlarged, which raised a suspicion of cancer metastasis (Figure ).
Findings in excision biopsy of cervical lymph nodes: Excision biopsy of the enlarged lymph nodes showed reactive hyperplasia and anthracosis.
Bronchoscopic findings: No endobronchial lesions were observed. The bronchial washing test gave negative results for acid-fast bacillus (AFB), AFB polymerase chain reaction (PCR), AFB culture test, and microscopic cytology. In the endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA), atypical cells were observed on the right bronchial tubes. Immunohistochemistry (IHC) on the reactive lymphoid tissue of 2 lymph nodes produced negative results for CD 56, chromogranin A, and synaptophysin.
CT-guided percutaneous needle biopsy (PCNB): In a biopsy of the lungs, malignant neoplasm was not found while fibrosis and anthracosilicosis were observed.
Pulmonary function test: The forced vital capacity (FVC) was 67%, and forced expiratory volume in one second (FEV1) 59%, and FEV1/FVC (%) 64%, indicating a mixed ventilatory defect.
Diagnosis and progress: Lung cancer was suspected, accompanied by pneumonitis. As the dyspnea symptoms had improved somewhat, the patient was discharged and positron emission tomography - computed tomography (PET-CT) was planned as an outpatient follow-up examination. However, the patient has not returned to Hospital “A” since then.
Hospital “B” (7 months later)
Chief complaints: cough, dyspnea (repeated worsening and improving for 7 months)
History of the present illness: The patient had been discharged from Hospital “A” voluntarily without a definitive diagnosis during the medical evaluation he was undergoing due to continuing symptoms of dyspnea, cough, and fatigue during exercise that had started 7–8 months before. Then he visited the Department of Pulmonology of Hospital “B” in August 2012 with repeated worsening of symptoms.
Physical examination: At the time of admission, his body temperature was 36.5°C, pulse 98 beats/min, blood pressure 105/60 mmHg, respiration rate 20 breaths/min, and with decreased bilateral respiratory sounds in the lungs. While his nutritional status was good and mental status was normal, he looked chronically ill and his whole body was weak. He had difficulty in breathing even when sitting still, and the symptoms worsened when he lay on the left side. He had lost 5 kg—from 55 kg to 50 kg—since January 2012.
Chest images: Small opacities were observed throughout the whole lung in plain chest radiographic images, and a large opacity was observed in the right upper lung, interpreted to be pneumoconiosis (ILO classification u/u, 2/3, A) (Figure -B). Pneumonic infiltration was observed around the large opacity. Pneumoconiosis (silicosis pattern) accompanied by progressive massive fibrosis, along with reactive lymph nodes, were found in the chest CT, which, in addition, required the discernment of lung cancer. Nodules characteristic of silicosis were observed in the centrilobular and subpleural parts of the lung in the chest high resolution CT (HRCT) (Figure -D).
Pulmonary function test: The forced vital capacity (FVC) was 57%, and forced expiratory volume in one second (FEV1) 47%, and FEV1/FVC (%) 66%, indicating a mixed ventilatory defect. The carbon monoxide diffusing capacity (DL,CO) was decreased to 61%.
Findings from electrocardiogram and echocardiography: The ejection fraction (EF) was normal at 60-64%, and there were no specific findings regarding cardiomobility.
Blood test: HB was slightly below normal at 11.9 g/dl, and the erythrocyte sedimentation rate (ESR) was 120 mm/h and c-reactive protein (CRP) 4.31 mg/dL.
Bronchoscopic findings: The segmental bronchi within the right middle, right upper, and left upper lobes had become narrower (Figure ), and a malignant cell test, AFB smear and culture tests, and AFB PCR test in broncho-alveolar lavage fluid were performed, all of which were negative.
Job history and work environment (based on personal statement): The patient was referred to the Division of Occupational and Environmental Medicine and applied for occupational accident coverage since silicosis was suspected after excluding lung cancer. The patient's job history showed that he had been working in rice farming and greenhouse strawberry farming until 1992, and at the time, there had been no facilities that could expose him to dust, such as a cement factory or mine near the residence or farmland. For approximately 20 years since then, he had been engaged in the task of blending raw materials for manufacturing glass containers, and he stopped working in glass manufacturing after being admitted to Hospital “A”.
His main task was to put silicon dioxide, the major material comprising glass containers, along with additives including soda and calcium carbonate, into an automatic mixer, and to operate the machine 1–2 times a day for about 10 minutes. He was also engaged in other tasks such as product packaging and transport in addition to blending work, while neither grinding nor cutting glass was included in the manufacturing process.
The blender was placed indoors and the ceiling of the workshop was partially open. The workers used a dust mask onto which a handkerchief was attached during work.
Diagnosis and progress: The patient had been diagnosed with silicosis, and was discharged since the dyspnea symptoms had improved. He received outpatient treatment at the Division of Pulmonology and underwent a consultation on the occupational accident in the Department of Occupational and Environmental Medicine.
Hospital “B” (12 months later)
Chief Complaint: Acute dyspnea had occurred a week earlier.
History of the present illness: The patient presented to the emergency room because acute dyspnea had occurred while having suffered a severe cough due to a cold for 4—5 days.
Past medical history: The patient had been undergoing regular examinations due to pneumoconiosis (silicosis) accompanied by progressive massive fibrosis.
Physical examinations: When the patient came to the emergency room, he was clearly conscious with the temperature of 36.2°C, a pulse rate of 102 beats/min, blood pressure of 110/70 mmHg, a respiration rate of 20 breathes/min, 97% oxygen saturation of arterial blood. The height was 164 cm and the weight 48 kg, which had been reduced by 2 kg since August 2012.
Arterial blood gas analysis (emergency room): The analysis showed that the pH was 7.419, pO2 69.8 mmHg, pCO2 32.7 mmHg, bicarbonate 20.7 mEq/L, O2 saturation 93.3%, and base excess −3.0 mEq/L.
Chest Images: In the chest X-ray images, pneumothorax on the right side and pneumoconiosis were observed (Figure -C). In the chest CT, pneumothorax on the right side, localized pulmonary edema in various sites, complicated pneumoconiosis accompanied by progressive massive fibrosis, and mediastinal reactive lymph nodes were observed.
Examination findings: An AFB smear examination of sputum, AFB culture test, and sputum culture test all gave negative results.
Pulmonary function test (after treating pneumothorax): The FEV1/FVC (%) was 63.8%, FVC 75.0%, and FEV1 59.1%, indicating mixed ventilatory defects
Clinical progress: Pneumothorax and other symptoms have been improved by the oxygen therapy, and thus the patient was discharged after the 7 days of hospitalization. Follow-up examinations ensued, and the patient applied for occupational accident rehabilitation coverage.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [48.0, 'kg']}",88,83.6,92.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 48.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (48.0 kg - 20 kg) = 88.0 mL/hr.
Hence, the patient's fluid maintenance is 88.0 mL/hr."
5032,22,Maintenance Fluids Calculations,physical,decimal,pmc-5463292-1,Extracted,"The proband was a 2.5-year-old female child who was admitted to our hospital for evaluation of her seizures, deformities of lower extremities, failure to thrive, and alopecia. She was born to consanguineous parents as a full-term infant by normal spontaneous vaginal delivery, with a birth weight of 3250 g and a birth length of 50 cm. Her mother had received prenatal care and had taken vitamins regularly. The patient had been almost exclusively breastfed since birth up to 15 months. In addition, she had received 25-hydroxyvitamin D3 [25(OH)D3] 400 IU per day for one year. At presentation, her height was 83 cm (3-10% p), her weight was 10.7 kg (weight for height: 25% p), and head circumstance was 47 cm (3-97% p). She had rachitic rosary over the chest wall, widening of wrists and ankles, and “X” deformity of lower extremities. Her head appeared disproportionately large, but head circumference was within the normal range with an open anterior fontanel and frontal bossing. She was able to sit without support, but her ability to stand and walk were restricted due to the “X” deformity of the legs. She had frontal bossing, near total alopecia, and sparse eyebrows and eyelashes (). Laboratory results revealed normal levels for serum electrolytes, serum albumin, blood urea nitrogen (BUN), and creatinine. Other laboratory results were as follows: serum calcium (Ca): 7.5 mg/dL (8.8-10.8), serum phosphorus (P): 2.3 mg/dL (4.5-5.5), ALP: 2278 U/L (80-220), intact PTH: 1194 pg/mL (10-71 pg/mL), 25(OH)D3: 25.2 ng/mL (10-44 ng/mL), 1,25(OH)2D3: 59 pg/mL (16-65 pg/mL). Serum Ca, P, and ALP were determined by spectrophotometric method (Abbott, Architect C 16.000, IL, USA), intact PTH by chemiluminescent method (Beckman Caulter DxI800), and 25(OH)D3 by electro chemiluminescent method (Roche, Cobas e-411). Serum electrolytes, albumin, BUN, and creatinine levels were within normal ranges. Serum 1,25(OH)2D3 level was in the upper limit of the normal range. The skeletal survey showed generalized osteopenia with advanced features of rickets manifested by cupping and fraying at the metaphyseal ends of long bones of upper and lower extremities (). VDR gene sequence analysis was performed by using MiSeq next-generation sequencing (NGS) platform, a Food and Drug Administration-approved diagnostic system (IIIumina, San Diego, CA, USA), and it was shown as a homozygote stop-codon mutation (c.148C>T) with mutation number: NM-001017535 (). This mutation was described previously (). Parents were heterozygous for the same mutation.
As shown in , the patient was initially treated with high doses of oral calcium (elemental Ca: 2 g/day), phosphate (1 g/day), and calcitriol [1α-25(OH)D3] (2 µg/day). Elemental calcium and calcitriol were subsequently increased to 4 g/day and 6 µg/day, respectively. After 8 weeks of this protocol, serum Ca concentration became close to normal levels, but PTH was not suppressed and ALP was still high, and no radiological improvement was observed. Treatment was continued with high-dose oral calcium and calcitriol. After 6 weeks, the patient was admitted to hospital again with hypocalcemic seizures. During this period, HVDRR was confirmed by VDR gene mutation and intravenous calcium infusion was initiated. Elemental calcium was administrated at 150 mg/kg/day, infused via central line over a period of 10 hours for five days in a month. She has been on this treatment for 4 months. We observed a decrease in PTH and ALP levels and normalization of serum P levels only during the periods of intravenous calcium infusion administration. After 4 steps of i.v. calcium infusion, partial healing in skeletal bone rickets findings were observed (); however, when the calcium infusion was stopped, secondary hPTH, increased ALP levels, and hypophosphatemia developed again and rachitic bone features became more apparent in the radiograms. After 4 months of intermittent calcium infusion, serum PTH and ALP levels decreased to near normal levels and radiological improvements were detected, secondary hPTH was normalized temporarily but not improved completely. After these improvements, intravenous calcium treatment was stopped and oral calcium and calcitriol treatment in high doses was administered again. However, after a while, serum PTH and ALP levels started rising again, serum Ca and P levels tended to decrease. We started cinacalcet (0.25 mg/kg) once a day along with high doses of oral calcium (4 g/day) and calcitriol (6 µg/day) and the cinacalcet dose was incrementally increased based on serum calcium and PTH levels, reaching 0.4 mg/kg/day over the next 2 weeks. We observed a temporary hypocalcemia during cinacalcet therapy. After 4 months of cinacalcet, serum Ca and P levels were within normal limits and we also observed sustained control of serum PTH and ALP levels and healing of the radiological rickets findings (). Treatment has been continued with a decreased dose of calcitriol (2 µg/day) and oral Ca (2 g/day) along with low-dose cinacalcet.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.7, 'kg']}",41.4,39.33,43.47,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.7 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.7 kg - 10 kg) = 41.4 mL/hr.
Hence, the patient's fluid maintenance is 41.4 mL/hr."
5033,22,Maintenance Fluids Calculations,physical,decimal,pmc-4541194-1,Extracted,"A female patient aged 18 years weighing 35 kg was admitted to the Intensive Care Unit (ICU) in our hospital with complains of diffused dull aching abdominal pain, not related to food habit with occasional nausea and vomiting from 2 months. She was treated with proton pump inhibitors (tablet pentoprazole 40 mg twice daily) and antispasmodic medication (dicyclomin). Gradually she also developed diarrhea, vomiting and progressive weakness of her lower limbs and finally flaccid quadriparesis. At the time of presentation to ICU, she was conscious, oriented, Glasgow coma score (GCS) 15/15, pulse rate 100/min, blood pressure (BP)-130/80 mmHg, normal respiratory and cardiovascular system and flaccid quadriplegia. There was also a history of two episodes of seizure last night. She gave no history of accidental or intentional ingestion of any poisonous substances. Her family history was unremarkable. Initial laboratory investigations showed total leucocyte count 12.0 × 109/L with neutrophil 80%, sodium 128 meq/L, chloride 96 meq/L and normal magnetic resonance imaging cervical spine and cerebrospinal fluid analysis. Treatment was started with anticonvulsants (injection phenytoin 100 mg 3 times a day), antibiotics (injection ceftriaxone 1 g twice daily) and correction of the electrolyte imbalance. Over the next 15 days, she developed respiratory muscle paralysis, was intubated and put on mechanical ventilation. Despite all measures she continued to have seizures and labile BP. Gradually she also became delirious with deterioration of GCS to 10. No improvement was observed in her laboratory parameters also. Finally urine PBG was done which was found positive. Electromyography results also demonstrated the presence of severe sensory motor axonal polyneuropathy. Immediately, all porphyrogenic drugs were stopped, phenytoin was replaced by gabapentin and a high-carbohydrate diet (400 to 450 g/day) was started. Treatment with hematin could not be started, due to the difficulty in obtaining the drug. Even after 1-week of therapy there was no improvement in her clinical condition and a decision was made to try hemodialysis. However, eventually she developed sepsis requiring high-ionotropic support which precluded further leading to her demise.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [35.0, 'kg']}",75,71.25,78.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 35.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (35.0 kg - 20 kg) = 75.0 mL/hr.
Hence, the patient's fluid maintenance is 75.0 mL/hr."
5034,22,Maintenance Fluids Calculations,physical,decimal,pmc-8239477-1,Extracted,"The patient was a girl child aged two years and nine months, who presented with persistent left otorrhea for one month. The otorrhea was foul-smelling and copious in nature, which was preceded by bouts of rhinorrhea, without fever or symptoms to suggest intracranial complications. There were no symptoms to suggest upper respiratory obstruction. She was diagnosed with acute otitis media with mastoiditis, with suspicion of congenital cholesteatoma. The child had been born full-term with a good birth weight of 3.5 kg. Both her antenatal and postnatal histories were unremarkable.
On examination, the child was found to be active with no facial asymmetry. The external ear and neck examinations were unremarkable. On otoscopy, there was foul-smelling mucopus in the left external auditory canal (EAC) with a dull, bulging TM and a pinhole perforation seen at the posteroinferior quadrant of the TM. Neither posterior wall-sagging nor keratin debris was observed.
Nasoendoscopy was not performed at the time of the initial examination. Play audiometry revealed left mild to moderate conductive hearing loss (CHL) with an average air-bone gap of 36 dB (Figure ).
The high-resolution CT (HRCT) temporal bone (Figures , ) showed soft tissue occupying the bony part of left EAC, middle ear, and mastoid air cells with extension into parapharyngeal space. The floor of the left middle ear was eroded.
MRI of the neck showed a well-encapsulated lesion within the left parapharyngeal space with heterogenous hyperintensities on T1WI (Figure ) and T2WI (Figure ), which was suppressed on fat saturation sequences with similar signal intensities in keeping with the fat content. The lesion measured 1.8 x 3.0 x 2.8 cm, laterally abutting the deep lobe of the left parotid gland with its epicenter located at the ET, extending superiorly and widening the floor of the hypotympanum, suggestive of DC of ET.
The patient underwent left canal wall up mastoid exploration and myringotomy and grommet insertion. Intraoperatively, the left mastoid was found sclerotic, with granulation tissues and pus in the mastoid cavity and middle ear. The dome of the lateral semicircular canal (SCC) was flattened. The DC was neither seen at the nasopharynx nor the middle ear. A final diagnosis of left COM with mastoid abscess secondary to DC of ET was made following pre and intraoperative evaluations.
Histopathological examination of the mastoid and middle ear lesion showed features of an acute on chronic inflammatory process. Pus culture grown did not show any bacterial growth, and tissue specimens were negative for Mycobacterium tuberculosis infection. At the two-week follow-up after the operation, the patient was found to be doing well with no complications. Subsequently, she was lost to follow-up due to the coronavirus disease 2019 (COVID-19) pandemic. However, upon communication with her mother via phone, the child reportedly went on to develop recurrent left otorrhea three months after the operation. Her speech is normal with no obvious reduced hearing noted by the family. She is scheduled for a repeat MRI and hearing assessment at her next follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.5, 'kg']}",14,13.3,14.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.5 kg. Hence, the patient's maintenance fluid is 3.5 kg * 4 mL/kg/hr = 14.0 mL/hr.
Hence, the patient's fluid maintenance is 14.0 mL/hr."
5035,22,Maintenance Fluids Calculations,physical,decimal,pmc-5198007-2,Extracted,"A male infant delivered at term at another facility to a 33-year-old primigravida was brought to medical attention on the 18th postnatal day for reduced breastfeeding, vomiting, and weight loss. There was no history of parental consanguinity. There were no similar cases in the pedigree. His birth weight was 3100 g, but at presentation, his weight was 2400 g (<3rd percentile). His length was 52 cm (25th-50th percentile) and head circumference 37 cm (50th percentile). The infant had dysmorphic facial features and was dehydrated (). Laboratory values included serum glucose: 52 mg/dL, sodium: 124 mmol/L, potassium: 7.4 mmol/L, ACTH: 628 pg/mL, cortisol: 20.6 µg/dL, 17-OHP: 6.04 ng/mL. The adrenal glands could not be visualized by ultrasonography. Fluid and electrolyte therapy along with hydrocortisone and fludrocortisone replacement were initiated. Serum triglyceride level was 761 mg/dL, CPK was 28.134 U/L, and CK-MB was 592 U/L (normal range: 0-25). Routine karyotype was consistent with normal 46,XY constitution; however, CGH showed a 3.88 Mb deletion encompassing part of the DMD gene (exon 45 extending through 3’ end) and three additional disease-associated genes (NR0B1, GK, and IL1RAPL1) ().
The patient was discharged with oral hydrocortisone, fludrocortisone, and salt supplementation when 42 days old.
Informed consent was obtained from the parents of the two children studied for further investigation. DNA was extracted by standard methodology and CGH.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2400.0, 'g']}",9.6,9.12,10.08,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2400.0 g so this converts to 2400.0 lbs * kg/1000 g = 2.4 kg. Hence, the patient's maintenance fluid is 2.4 kg * 4 mL/kg/hr = 9.6 mL/hr.
Hence, the patient's fluid maintenance is 9.6 mL/hr."
5036,22,Maintenance Fluids Calculations,physical,decimal,pmc-7102488-1,Extracted,"An 11-week-old female ex-premature infant (corrected gestational age 6 weeks) presented to a peripheral hospital with respiratory distress and a three-day history of cyanotic episodes, following three weeks of upper respiratory tract infection symptoms. The infant was born at 35 weeks' gestation, weighing 2489 g, and did not require resuscitation or respiratory support at birth. The newborn had a 5-day admission to the special care unit for feeding establishment and observation prior to being discharged home well on day 7 of life. The child's mother had received six cycles of R-CHOP for NHL between 17 and 33 weeks of gestation.
The infant was tachypneic and hypoxic, was commenced on high flow nasal cannula support, intravenous (IV) ampicillin and gentamicin, and managed at the peripheral hospital's critical care unit. Over the next two days, respiratory support was escalated to noninvasive ventilation, and antibiotics were changed to IV cefotaxime (D1–D8) and IV azithromycin (D3–D5).
Nasopharyngeal aspirate (NPA) was negative for eight respiratory viruses. Respiratory virus detection for influenza A, influenza B, parainfluenza 1, 2, and 3, respiratory syncytial virus (RSV), and adenovirus was performed using an in-house respiratory virus multiplex real-time RT-PCR assay [], while human metapneumovirus (HMPV) was tested with the in-house real-time RT-PCR assay utilising oligonucleotides []. Testing for Pneumocystis jirovecii was also requested on the NPA specimen and performed using an in-house real-time RT-PCR assay []. A synthetic reference standard was also utilised to enable quantification. Human immunodeficiency virus (HIV) serology was negative. A chest X-ray revealed diffuse bilateral ground glass changes ().
As the hypoxic respiratory failure worsened, atypical infections and possible childhood interstitial lung disease (ChILD) were considered and pulse IV methylprednisolone was commenced. The NPA was subsequently positive for Pneumocystis jirovecii DNA at 2.0 × 106 copies/mL. Oral co-trimoxazole 20 mg/kg/day (D4) was commenced and transitioned to IV co-trimoxazole (D8) due to clinical deterioration.
On day 9, the infant developed a left pneumothorax and pneumomediastinum, requiring intercostal drainage. The child was intubated, ventilated, and retrieved to our Pediatric Intensive Care Unit (PICU) due to worsening respiratory failure. In addition to IV co-trimoxazole, IV lincomycin and primaquine were commenced as second-line PCP therapy due to the clinical deterioration [], and antimicrobial cover was broadened to IV piperacillin-tazobactam.
Steroids were weaned over the next 10 days (D4–D14). All other microbiological and virological testing were negative. The immune screen revealed mild pan lymphocytopenia, severe hypogammaglobulinemia, and neutropenia, suggestive of a combined immunodeficiency (). The infant was commenced on fungal (fluconazole) and viral (valaciclovir) prophylaxis as well as immunoglobulin replacement therapy (IRT) and intravenous immunoglobulin (IVIg) at 0.4 g/kg. Granulocyte-colony stimulating factor (G-CSF) was also administered.
The patient's respiratory failure continued to worsen, and the infant subsequently developed acute respiratory distress syndrome (ARDS). An attempt at high-frequency oscillatory ventilation was ineffective. The infant was then placed on VV-ECMO on day 15 of the presentation. Bronchoscopy performed on day 16 was still positive for Pneumocystis jirovecii DNA at 1.6 × 105 copies/mL.
From day 40 (24 days after commencement of VV-ECMO) until day 42, the infant received three doses of poractant alfa (Curosurf) via the endotracheal tube. The patient was also commenced on IV hydrocortisone (1 mg/kg 6 hourly) on day 41, which was slowly weaned off over a two-week period. The child was successfully decannulated to conventional ventilation (D46) and extubated on day 53. Subsequent immunological assessment revealed adequate lymphoproliferation responses to phytohemagglutinin (PHA) and adequate levels of recent thymic emigrants. The lymphocyte counts slowly normalised, confirming a secondary combined immune deficiency.
The infant improved clinically, was stepped down to oral antimicrobials, and was discharged home on day 103 with supplemental oxygen. The patient remained on supplementary oxygen at home, IRT, and antimicrobial prophylaxis including oral valaciclovir, fluconazole, and co-trimoxazole until the age of 6 months. The timeline of events is summarised in . The infant's mother remained well throughout and did not have any investigations for Pneumocystis jirovecii. Informed consent was obtained from the infant's parent for this case report.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2489.0, 'g']}",9.956,9.4582,10.4538,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2489.0 g so this converts to 2489.0 lbs * kg/1000 g = 2.489 kg. Hence, the patient's maintenance fluid is 2.489 kg * 4 mL/kg/hr = 9.956 mL/hr.
Hence, the patient's fluid maintenance is 9.956 mL/hr."
5037,22,Maintenance Fluids Calculations,physical,decimal,pmc-4420314-1,Extracted,"A 1-day-old (weight 2.5kg) male neonate, born out of non consanguineous marriage by full term vaginal delivery was referred to us with distension of abdomen and failure to pass meconium since birth. No antenatal details were available. On examination neonate was hemodynamically stable. Abdomen was grossly distended with stretched shiny skin. Erythema was present in the periumbilical region indicating underlying peritonitis.
Both the scrotal sacs were filled with fluid. Routine hematology investigations were within normal limits. Erect X-ray abdomen revealed single air fluid level in the Lt. Upper quadrant with rest of abdomen having ground glass appearance with specks of calcification seen in left flank area (Fig. 1).
Baby was resuscitated with nasogastric tube drainage, IV fluids and antibiotics. Provisional diagnosis of upper gastro-intestinal obstruction with associated peritonitis was made. At operation the peritoneal cavity was filled with meconium stained fluid. Small bowel, caecum and part of ascending colon were dilated. A large perforation was noticed on the anti-mesenteric border of the ascending colon. Multiple colonic atresias were present distal to the perforation site, near the hepatic flexure and in transverse colon (intra luminal webs Type I) (Fig. 2).
Two more Type II atresias were noticed near the recto sigmoid junction. Resection of atretic segments with end to back anastomosis at three sites and removal of intra luminal web were done along with covering ileostomy.
Gastrotomy done proximal to the pylorus revealed type I A pyloric atresia (complete Web). There was no discon­tinuity at pylorus. Resection of pyloric web with pyloroplasty (Heineke-Mikulicz) was done. Gastrostomy was done by putting 8-Fr Malecot’s catheter. Bilateral flank drains were inserted.
Post operatively baby required ventilator support and frequent assessment for fluid and electrolyte levels. Feeds were started through gastrostomy tube on 10th post operative and drain removed on 10th postoperative day. The patient is doing well and on follow up for ileostomy reversal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.5, 'kg']}",10,9.5,10.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.5 kg. Hence, the patient's maintenance fluid is 2.5 kg * 4 mL/kg/hr = 10.0 mL/hr.
Hence, the patient's fluid maintenance is 10.0 mL/hr."
5038,22,Maintenance Fluids Calculations,physical,decimal,pmc-6710092-1,Extracted,"A 9-year-old girl (height = 120 cm, weight = 16 kg) with Down's syndrome was referred to our institution with a butterfly-shaped congenital sternal cleft. The patient had been operated for a congenital heart defect (cor triatriatum) in the 1st week of life which left this unhealed congenital sternal cleft. As often in neonatal cardiac surgery, chest closure was delayed a few days and then, sternal rims were just sealed and the cleft was left open because of the cardiac surgery.
Cardiac echocardiogram was normal at readmission. A midline defect with visible chest pulsations caused serious esthetical concerns and hard school integration (
). Because of intellectual impairment related to Down's syndrome, respiratory function testing was not available.
As shown in
, the previous cardiac surgery scar went on a skin raphe, as sometimes described in this rare congenital defect (failure of midline development). Clinical findings were confirmed by chest tomodensitometry (
). To preserve chest wall stability, optimize growth evolution, and avoid some pitfall of other techniques, we choose a ceramic prosthesis (Sternum Ceramil, I.Ceram, Limoges, France) for surgical repair. As at this time, the European Certification was not yet obtained, the surgery was performed thanks to a waiver from the French Agency for Health Security (ANSM) and the patient's parents who gave their consent for this surgery. Since this surgery this device has been CE marked.
At surgery, prior cutaneous scar was excised as much as possible. Pectoralis major muscle was elevated on either side from their sternal origin.
Costal cartilages were gently and softly excavated to leave space for prosthetic sternum implantation. This stage was simplified using the trial implant which allowed removing only the necessary amount of cartilages. The trial implant has the same shape and size as the ceramic but is in stainless steel. It is used to choose the size and to prepare the area of implantation. The preperforated prosthetic ceramic sternum (size 1) was anchored to cartilages with eight nonabsorbable 3/0 polyester sutures (
). Closed suction drains were placed above and below the sternum. The pectoralis major muscles were approximated medially and the skin was closed with subcutaneous and cutaneous continuous sutures.
Chest drains were removed on day 3 and the patient was discharged on day 7. Early and long-term postoperative pain was limited. At the last follow-up visit (month 12), the patient was doing well and the scar was totally healed, clean, and dry (
,
), as it was since the first outpatient visit at day 10.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [16.0, 'kg']}",52,49.4,54.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 16.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (16.0 kg - 10 kg) = 52.0 mL/hr.
Hence, the patient's fluid maintenance is 52.0 mL/hr."
5039,22,Maintenance Fluids Calculations,physical,decimal,pmc-3161441-1,Extracted,"A 10-year-old boy had been admitted at a nephrology clinic for generalized edema, hypertension, and fatigue that appeared 3 weeks before. His medical past was unremarkable and immunization status was complete. His mother reported baths in stagnant water 5 years ago in their village. But, there was neither personal nor familial history of hematuria or edema. Physical examination showed height 130 cm, weight 30 kg, temperature 37°C, high blood pressure (150/90 mmHg), tachycardia (100 beats/min), and edema over face, back, limbs, and mild ascites. Cardiac and pulmonary auscultation was normal and there was neither arthritis, nor skin abnormality.
Laboratory findings are represented in . Serologies for hepatitis B, C, and HIV were negative and serum complement (CH50) was slightly low. Cryoglobulins, and anti-DNA and anti-streptococcal antibodies were not found. Ultrasound examination of kidneys and the lower urinary tract was strictly normal.
Diagnosis of nephrotic syndrome was made and the patient was treated with oral prednisolone (2 mg/kg/day) combined with captopril (50 mg/day), salt-free diet, furosemide (60 mg/day), and oral supplementation with potassium, calcium, and vitamin D3. Four weeks later, edema decreased slightly and urine albumin excretion slowed down at 187 mg/kg/day. Urine sediment was still unremarkable. A second 4-week period of oral prednisolone was started after three daily IV pulses of methylprednisolone (10 mg/kg/day). However, clinical and biological findings did not improve at the end of this cure. Then, renal biopsy was performed and showed type 1 membranoproliferative glomerulonephritis (MPGN) [] with mild tubulointerstitial fibrosis and a granuloma made of histiocytes and giant cells surrounding an egg of S. hematobium []. Congo red staining was negative and immunofluorescence did not find any deposition. Circulating IgG antibodies against schistosomal antigens were high (1/250). A final diagnosis of type 1 MPGN secondary to S. hematobium was made. The histological findings corresponded to class III–IV of the African Association of Nephrology (AFRAN) classification.[] Despite the absence of adult worms in urine and renal parenchyma, treatment with praziquantel was given (single 40 mg/kg dose per os) to ensure complete cure. After 1 month, there was no improvement in renal function. Then, oral cyclophosphamide (2 mg/kg/day) was added to corticosteroids with supportive therapy (salt-free diet, captopril, furosemide, calcium, and vitamin D3) for 6 months. Nevertheless, the patient reached end-stage renal disease (ESRD) 1 year later and had to start hemodialysis.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [30.0, 'kg']}",70,66.5,73.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 30.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (30.0 kg - 20 kg) = 70.0 mL/hr.
Hence, the patient's fluid maintenance is 70.0 mL/hr."
5040,22,Maintenance Fluids Calculations,physical,decimal,pmc-7369677-1,Extracted,"A 35-year-old 105.5 kg male with a previous history of ALS for 7 years, history of respiratory insufficiency with a tracheostomy, and PEG for over two years, was admitted from a nursing home after a cardiac arrest. The return of spontaneous circulation (ROSC) was 12 minutes, and the patient was treated for aspiration pneumonia and urinary tract infection. In the past, he has had three previous cardiac arrests associated with respiratory insufficiency. Cardiac echocardiogram revealed a normal left and right ventricular function. Serum albumin was 3.1 g/dl. The patient has had quadriplegia felt secondary to his ALS and multiple cardiac arrests and has always stabilized and been treated for various infections. Neurologically, the patient still had a pupillary reflex on the left with spontaneous eye movement and he had partial mouth opening and closing. The patient does not visibly respond to pain. No gag or corneal reflexes were noted by the ICU team or neurology.
Over the last several years, the family was approached by the health care team on multiple occasions regarding consideration of Do Not Resuscitate (DNR). The family was told that the overall situation was hopeless due to his underlying primary disease. Despite this, the family always had hope that an ALS cure would be found and always wanted everything done.
Initially, a 24 hr urine creatinine was collected (patient with indwelling foley catheter) and was 172 mg. This was repeated since the value was very low but still came back 199 mg of urinary creatinine in 24 hr. The coefficient of variation was 10%, and the average was 186 mg of urinary creatinine excreted in 24 hr (see for data summary). In addition, the patient's height was 185 cm.
The patient was treated successfully over several weeks in the ICU and was eventually transferred back to his nursing facility. Within one month after discharge, the patient died at another facility.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [105.5, 'kg']}",145.5,138.225,152.775,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 105.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (105.5 kg - 20 kg) = 145.5 mL/hr.
Hence, the patient's fluid maintenance is 145.5 mL/hr."
5041,22,Maintenance Fluids Calculations,physical,decimal,pmc-8436629-1,Extracted,"A 36-year-old woman was referred to our hospital for treatment of decompensated cirrhosis C. She had been diagnosed with intractable epilepsy and cerebral palsy at birth. At age 1 year, she was found to have a varicella zoster virus infection followed by thrombotic thrombocytopenic purpura and was treated with red blood cell transfusion, which probably resulted in HCV infection at that time. She had been fed by central venous nutrition and nasal enteral feeding for decades. She had no history of alcohol drinking, and her family had no history of liver diseases. She had a persistent HCV infection, with HCV-RNA viral loads of 4.7 logIU/mL at age 32 years and 4.5 logIU/mL at age 33 years. Treatment for HCV infection was therefore considered at age 34 years, at which time she was being treated with clobazam, zonisamide, and carbamazepine (CBZ) for her intractable epilepsy. Because of harmful drug interactions between CBZ and some DAAs for HCV, her antiepileptic regimen was changed to levetiracetam (LEV). Although LEV was found to control her epilepsy, she developed thrombocytopenia (platelet count: 4–6 × 104/µl, Fig. ). LEV was therefore discontinued, and she was started on valproic acid (VPA).
Her thrombocytopenia was not accompanied by coagulation abnormalities. The activity of a disintegrin and metalloproteinase with thrombospondin type 1 motifs 13 was not decreased, being ≥101% (normal range ≥10%). The concentration of platelet-associated IgG (PA-IgG) was 606.1 ng/107 cells, markedly higher than normal (≤30.2 ng/107 cells). Moreover, examination of a bone marrow aspirate showed reactive small megakaryocytes without abnormal cells or blast cells, suggesting that thrombocytopenia in this patient was due to reactive secondary immune thrombocytopenia (ITP). Although her platelet count was as low as 2 × 104/µl, it generally fluctuated from 4 to 6 × 104/µL (Fig. ).
The patient subsequently developed pneumonia and showed decreased activity. Her VPA dose was reduced, and she was started on clarithromycin, which improved her systemic condition. However, her serum albumin concentration remained below 3.0 g/dL, and she developed leg edema and ascites, which did not improve. Despite her nutrition intake by central venous feeding and a nasal gastric tube being stable and maintained as usual, her pancytopenia, leg edema, and ascites did not improve. Ascites was also not improved by administration of diuretics through a nasal gastric tube, albumin infusion, venous administration of diuretics, or administration of tolvaptan through a nasal gastric tube (Fig. ). Examination of ascites fluid showed transudation but no evidence of infection. The increase in liver fibrosis markers indicated that the refractory ascites in this patient was due to decompensated cirrhosis C.
This patient was transferred to our department for treatment of HCV infection. Physical examination showed that her body weight was 54 kg (47 kg 1 year earlier), and her body temperature was normal. She showed massive ascites and leg edema. Laboratory data examination showed a marked reduction in serum albumin concentration and increase in fibrosis markers (Table ). CT showed liver deformity, mild splenomegaly, and massive ascites (Fig. ). Although her viral load was not very high, she was found to have sustained infection with HCV serotype 2 (Table ).
The indication for HCV eradication was carefully considered. Although she had been bedridden, this patient showed sustained HCV infection, and her ascites, which was caused by HCV-derived cirrhosis, was refractory to conservative treatment including albumin infusion. Her epilepsy was well controlled at that time, and her intake of nutrition via central venous nutrition and nasal gastric tube feeding was stable. After obtaining repeated informed consent from her mother, the patient was started on SOF/VEL for 12 weeks. Because she could not swallow tablets due to dysphagia, she was administered crushed SOF/VEL through the nasal gastric tube. Despite co-administration of antiepilepsy drugs, this patient did not experience any adverse effects of crushed SOF/VEL. HCV-RNA disappeared after 2 weeks of SOF/VEL administration. She completed 12 weeks of SOF/VEL treatment without any adverse events, and her ascites and edema were improved (Fig. ). At the end of treatment, her liver function and thrombocytopenia were improved, and CT showed no evidence of ascites (Fig. ). She was confirmed as having achieved SVR at both 12 and 24 weeks after treatment. Twelve weeks after treatment, her platelet count was 13.8 × 104/µL, her serum albumin concentration was 3.4 g/dL, her Mac2 binding protein glycan isomer (M2BPGi) concentration was 1.98 cutoff index (COI), and her type IV collagen concentration was 179 ng/mL. At 24 weeks after the end of treatment, her platelet count was 16.6 × 104/µL, her serum albumin concentration was 4.0 g/dL, her M2BPGi concentration was 1.84 COI, her type IV collagen concentration was 159 ng/mL, and her PA-IgG concentration was 86.6 ng/107 cells, and she was in good condition.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [54.0, 'kg']}",94,89.3,98.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 54.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (54.0 kg - 20 kg) = 94.0 mL/hr.
Hence, the patient's fluid maintenance is 94.0 mL/hr."
5042,22,Maintenance Fluids Calculations,physical,decimal,pmc-6806403-1,Extracted,"A 54-year-old Chinese gentleman presented to the hospital for palpitations and exertional dyspnoea over 3 months. He was initially reviewed by a cardiologist and a transthoracic echocardiography performed showed a 3.9 cm × 4.2 cm mass posterior to the left atrium. He was also found to be anaemic with a haemoglobin of 5.9 g/dL. Upon further questioning, he denied any symptoms of dysphagia, abdominal or chest discomfort, reflux/regurgitation and respiratory symptoms. He did however note a loss of weight of 5 kg over the same duration with no loss of appetite.
A CT scan of the thorax, abdomen and pelvis was performed which showed a markedly dilated oesophagus with large intraluminal masses extending from proximal thoracic oesophagus to cardioesophageal junction (CEJ). There appeared to be 2 masses in close proximity measuring 4.5 cm × 7.2 cm and 5.8 cm × 14.4 cm, with a stalk arising from the cervical oesophagus. The proximal mass was noted to be predominantly fat whilst the distal mass was of a mixed fat and soft tissue attenuation. There was no invasion of adjacent structures and no enlarged lymph nodes or distant metastases. Oesophagogastroduodenoscopy (OGD) performed showed one giant, pedunculated polyp distending the oesophageal diameter and extending from the cervical oesophagus to CEJ. The polyp also appeared to be bilobed with mucosal ulceration at its distal aspect (, , , ).
An endoscopic ultrasound (EUS) was also performed, which showed a large submucosal pedunculated multilobed mass with some lobular lipomatous regions (hyperechoic). A vascular stalk was seen at the proximal oesophagus. Core biopsy of the mass however only revealed rare groups of spindle cells with no malignant cells seen.
In view of occult bleeding (and resultant anaemia) from ulceration on the distal polyp, resection was advised. Endoscopic resection was deemed not suitable in view of a highly vascular 1 cm stalk and large size of polyp. He subsequently underwent surgical resection and intraoperative findings were that of a large multiloculated heterogenous oesophageal polyp (arising from a 1 cm-wide stalk in cervical oesophagus) spanning up to the CEJ. Total polyp length was 24 by 6 cm with the cut end of stalk to base of polyp being 3.5 cm.
The cervical oesophagus was mobilised via a left neck skin crease incision. Longitudinal cervical oesophagostomy was performed on the left side and the polyp stalk on the opposite wall was ligated and oversewn with PDS 3/0 for haemostasis. The polyp diameter was deemed too large for transoral retrieval. A 5 cm left upper quadrant abdominal incision was made and a gastrostomy was performed near the greater curve of the stomach. An Applied medical GelPOINT® port was inserted into the stomach to enable trans-gastric retrieval of the giant oesophageal polyp. Both the cervical oesophagostomy and gastrostomy were closed with PDS 3/0 (, , , , ).
The patient’s post-operative recovery was uneventful and he was progressed to diet on POD 3 and discharged well on POD 4. He was well on follow up post-operatively with no evidence of recurrence.
Final histology of the oesophageal polyp showed a dedifferentiated liposarcoma arising within a giant fibrovascular polyp, FNCLCC grade 2, measuring 17.5 cm in size. Stalk margin was clear of tumour. FISH (Fluoresence in situ hybridisation) was positive for MDM2. Immunohistochemistry was positive for CD34, SMA and desmin, but negative for STAT 6, ALK-1, S100, AE1/3 and MNF116 (, ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.0, 'kg']}",20,19,21,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.0 kg. Hence, the patient's maintenance fluid is 5.0 kg * 4 mL/kg/hr = 20.0 mL/hr.
Hence, the patient's fluid maintenance is 20.0 mL/hr."
5043,22,Maintenance Fluids Calculations,physical,decimal,pmc-3704905-1,Extracted,"A 13 year-old boy was admitted for Addison’s disease, dysphagia, muscle weakness, excessive fatigue and recent onset gait ataxia. He was born by natural delivery, after an uneventful 40 week gestation. Birth weight was 3.3 kg, birth length 50 cm, Apgar score was 9/9. Parents were apparently healthy Caucasians of Italian ancestry, coming from the same small village of Puglia region - southern Italy. Parental consanguinity was not recognized. The younger brother of the proband was apparently healthy. As shown in Figure , the first son of the maternal uncle of the proband was affected by X-linked adrenoleukodystrophy (ALD). One sister of the paternal grandmother was affected by progressive spastic paresis due to a thoracic syringomyelia diagnosed at the age of 60 years.
Bilateral cryptorchidism and inguinal hernia associated with hypospadia were noted at birth, surgically repaired at the age of 6 years. At the age of 2 years, recurrent vomiting, failure to thrive and progressive skin pigmentation became evident. Gastro-esophageal reflux was diagnosed and treatment with ranitidine and domperidone was started. At the age of 4 years, he presented recurrent episodes of hypotonia, hypoglycemia and hypothermia. Addison’s disease was diagnosed and the patient was started on hydrocortisone replacement therapy.
Early developmental milestones appeared normal, with autonomous sitting at 7 months, initial speech at 12 months, walking at 14 months. A global developmental delay became evident afterwards. Psycho-educational assessment, performed when he was 9 year-old, indicated mild mental retardation.
He had a history of deficiency in tear production, dating back to early infancy, his mother described that he had always “cried without tears”.
At the age of 13 years (our first observation), height was 160 cm (0.42 SDS), weight was 71 kg (3.55 SDS), BMI: 27.73 (2.04 SDS), pubertal stage II according to Tanner, with testicular volume 6 ml bilaterally. Severe hyper-pigmentation and hyper-keratosis of elbows and knuckles were evident. Facial appearance was characterized by malar hypoplasia and prognathism, with dysartria and nasal speech. Permanent teeth were normal. Eye movements were saccadic with horizontal gaze nystagmus. Pupils were bilaterally dilated, with poor response to direct light and accommodation. Fundoscopy revealed mild bilateral optic atrophy. Distal muscle weakness and wasting were evident in the arms, more marked distally (hypothenar prominence wasting). A milder pyramidal weakness, without relevant muscle wasting was evident in the legs. He showed unsteady walking on his toes. He was unable to tandem walk and stand on either foot for more than 2 to 3 seconds. Cerebellar examination was otherwise normal. Deep tendon reflexes were hyperactive and extensor planter response was present bilaterally. Light touch, pain and temperature sensation was apparently intact.
At admission in our hospital, plasma ACTH levels were markedly elevated (1494 pg/ml – normal range: 5–46 pg/ml). Serum electrolyte levels were normal, as were serum aldosterone levels (184 pg/ml – normal values: 75–455 pg/ml) and plasma renin levels (16 pg/ml – normal values: 5–90 pg/ml). Isolated glucocorticoid deficiency, with normal mineralcorticoid balance, was confirmed and hydrocortisone therapy continued. Although X-linked ALD could be reasonably excluded from the observation of the family pedigree (Figure ), plasma levels of very long chain fatty acids (VLCFA) were analyzed and were found normal (C26:0: 0.9 micromol/l – C26:0/C22:0: 0.008 – C24:0/C22:0: 0,77). Bone mineral density, analyzed by Dual Energy X-ray Absorptiometry (DEXA) of the lumbar spine was found normal (Z score: -0.6). Body composition analysis by DEXA showed an apparently normal proportion of lean (muscle) mass of the limbs, with increased central and peripheral fat mass.
Nerve conduction studies showed reduced sensory and motor conduction velocities in the upper and lower extremities, reduced motor responses and chronic denervation changes, consistently with a widespread peripheral sensory-motor neuropathy.
Visual evoked potentials showed marked bilateral delay and reduced amplitude. Brain stem auditory evoked potentials were normal. Somatosensory evoked potentials from the lower limbs showed mild bilateral delay and reduced amplitude.
Brain magnetic resonance imaging (MRI) was found normal. Functional spectroscopy study showed normal levels of the main metabolites. Spine MRI (Figures A and B) showed a cystic cavity within the spinal cord (syringomyelia), localized between the sixth cervical vertebra (C6) and the first thoracic vertebra (T1). Maximal diameters of the cavity were mm 30 longitudinally, mm 5 front-back, mm 6 laterally. In addition, cerebellar tonsils descended 7 mm caudal to foramen magnum, consistently with a mild type 1 Chiari malformation. Mild posterior inter-vertebral disk protrusions were evident between T9 and T10 and between L4 and L5.
Our patient had manifested severe and progressive dysphagia, starting from the age of 11 years. At admission in our Hospital (aged 13) he could not swallow food without drinking. Barium swallow showed dilated esophagus and absent peristalsis. Esophageal manometry showed elevated lower esophageal sphincter (LES) pressure (54 mmHg), poor relaxation to swallow and absent body peristalsis, consistent with achalasia. He underwent Heller’s myotomy of the cardias, with good clinical results.
The genomic DNA was isolated from whole blood by proteinase K digestion and phenol/chloroform extraction. The methods of DNA amplification and sequence analysis of the AAAS gene have been previously reported in detail []. The analysis of the AAAS gene revealed a homozygous missense mutation in exon 12. It is a T > G transversion at nucleotide position 1224 resulting in a change of leucine at amino acid position 381 into arginine (Leu381Arg or L381R). Both parents were found heterozygous for the same mutation. No further mutations were found in the different exons or flanking intronic regions.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [71.0, 'kg']}",111,105.45,116.55,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 71.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (71.0 kg - 20 kg) = 111.0 mL/hr.
Hence, the patient's fluid maintenance is 111.0 mL/hr."
5044,22,Maintenance Fluids Calculations,physical,decimal,pmc-6900415-1,Extracted,"Our first case has been previously described []. He was a 42-year-old man, weighing 160 kg, BMI 54 kg/m2, scheduled for total thyroidectomy and bilateral neck dissection for metastatic papillary thyroid cancer with paratracheal lymph node and left recurrent laryngeal nerve involvement. His co-morbidities included asthma and hypertension. He had a Mallampati score of 3, large thick neck, and severe obstructive sleep apnea (OSA). Flexible nasendoscopy showed a narrow velopharynx and left vocal cord palsy. Due to his morbid obesity, predictors of difficult intubation, and difficult front-of-neck access, we secured his airway using awake SAGFBI.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [160.0, 'kg']}",200,190,210,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 160.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (160.0 kg - 20 kg) = 200.0 mL/hr.
Hence, the patient's fluid maintenance is 200.0 mL/hr."
5045,22,Maintenance Fluids Calculations,physical,decimal,pmc-4316414-1,Extracted,"A 17-year-old girl visited the hospital with the chief compliant of goiter with acute onset. She was born via spontaneous vaginal delivery at 37-week gestation, weighing 2.6 kg. She was the second child of unrelated healthy parents. Her father was 171 cm tall and her mother was 158 cm tall. Midparental height was 158 cm.
She had visited our clinic for growth evaluation at 11 years 10 months of age, when her height was 141.2 cm (10th-25th percentile) and her weight was 39.7 kg (50th percentile). Tanner stage was breast 4 and pubic hair 4. Her bone age was approximately 13 years and her height for bone age was <3rd percentile. Menstruation had been started at 10 years 9 months of age. According to her school record, she was short before pubertal onset, but her height and weight were relatively normal during puberty (). So, idiopathic short stature and early normal puberty were diagnosed at 11 years 10 months of age.
At the age of 17 years, goiter developed abruptly, and the patient visited the hospital again. She was short in stature and of normal weight, measuring 144.7 cm (<3rd percentile) and weighing 44 kg (3rd-5th percentile). She showed no signs of TS, such as webbed neck, short neck, cubitus valgus, high arched palate, and shield chest deformity, except for short stature. Her menstrual cycle was regular. Tanner stage was breast 5 and pubic hair 5. She had normal intelligence and high grades in school.
The laboratory profiles demonstrated normal complete blood count, chemistry panel, and electrolytes. The thyroid function test showed: thyroid stimulating hormone (TSH), 0.01 mIU/L (reference, 0.25-4.0 mIU/L); free thyroxine, 7.3 ng/dL (reference, 0.7-2.0 ng/dL); triiodothyronine, 680 ng/dL (reference, 60-190 ng/dL), thyroglobuin antibody, 7.06 U/mL (reference, 0-0.3 U/mL); thyroid stimulating immunoglobulin, 22.7% (reference, 0%-15%); microsomal antibody, 1.45 U/mL (reference, 0-0.3 U/mL), suggesting Graves disease. On thyroid ultrasonography, enlargement of both thyroid glands with increased vascularity was observed. A Technetium-99m thyroid scan showed diffuse, enlarged thyroid glands with markedly increased uptake. Other results were as follows: luteinizing hormone (LH), 14.65 mIU/mL (reference: follicular phase, 0.6-6.2 mIU/mL; luteal phase, 0-6.0 mIU/mL); follicle stimulating hormone (FSH), 7.78 mIU/mL (reference: follicular phase, 3.3-8.8 mIU/mL; luteal phase, 1.6-8.7 mIU/mL); and estradiol, 156.99 pg/mL (reference: follicular phase, 60-200 pg/mL; luteal phase, 60-260 pg/mL), without evidence of ovarian failure. Because the final height was below the 3rd percentile with coexisting thyroid dysfunction and autoimmunity, chromosome analysis was performed. The karyotype was 46,X,del(X)(p22.1), one of the form of TS (). Methimazole was prescribed for the patient and a regular thyroid function test was performed.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [44.0, 'kg']}",84,79.8,88.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 44.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (44.0 kg - 20 kg) = 84.0 mL/hr.
Hence, the patient's fluid maintenance is 84.0 mL/hr."
5046,22,Maintenance Fluids Calculations,physical,decimal,pmc-4501070-1,Extracted,"The proposita is a 10.5 year-old girl, second born of non-consanguineous healthy parents. Her elder brother is referred to be healthy and his stature is 150 cm at 14 years (5th centile for age) (National Center for Health Statistics in collaboration with the National Center for Chronic Disease Prevention and Health Promotion (2000) []), with pubertal development of PH3 G3 following Tanner stage. A third pregnancy hesitated in a spontaneous abortion. Her father is 169 cm whereas her mother is 150 cm high.
She was born at 39 gestational weeks, after normal pregnancy, by Caesarian section. Intrauterine growth retardation was detected during last weeks of gestation and her neonatal weight was 2.400 Kg, with a stature of 48 cm and an occipito-frontal circumference of 33 cm. In neonatal period, because of heart murmur, she underwent echocardiographic evaluation that evidenced an ostium secundum interatrial defect, spontaneously closed at 2 years. At 7 years slight hairs covered her back and arms, and overweigh was noted. Her parents reported slowdown in growth curve in the last 6 months despite a rapid increase in body weight.
Anthropometric values and clinical findings at 7 years were: stature 114.6 cm (3-10th centile), weight 25 kg (75th centile), BMI 19 (90-95th centile). Pubertal development was PH1 B1 following Tanner stage; genetic target was cm 153.5 + 6. At a further observation at 8 years, she presented with healthy condition, short stature (height cm 116 – below 3rd centile), overweight (weight kg 29 – 75th centile, BMI 21.55 – above 95th centile), hypertrichosis with slightly hairy legs and back, mild short neck, very mild valgus elbow, and small joint hyperlaxity, shortening of the fifth metacarpal with syndactyly of 2th and 3th of the toes.
At a first examination, laboratory tests evidenced: FSH: 12.3 mIU/ml; LH: 0.8 mIU/ml; Estradiol 10.2 pg/ml. Adrenal and thyroid profiles were within the normal range for age. Abdominal ultrasound revealed normal kidney, and pelvic echography showed reduced ovarian size range for age (right ovary 15 mm × 8 mm × 12 mm; left 13 mm × 7.4 mm × 10 mm). Because of hairiness increase, a new serum hormonal evaluation was performed at 7.5 years: laboratory tests showed elevated FSH values (31.3 mUI/ml) with normal prepuberal values of LH (0,7 mUI/ml) and Estradiol (13.2 pg/ml); a further pelvic ultrasound revealed infantile uterus and confirmed size reduced ovaries.
Analysis of FMR1 triplet repeat sizes in the proband by repeat primed PCR [] revealed sizes in the normal range (20 to 33 CGG repeats) (data not shown).
During 1-year follow-up period, a POI was suspected according to high FSH and LH levels and low Estradiol, inhibin B and AMH levels. Serum FSH and LH values increased to 179.90 mlU/ml and 40.30 mlU/ml respectively, while Estradiol decreased to 10 pg/ml. Inhibin B showed a level <20 pg/ml and AMH serum levels were 0.4 ng/ml, well below the normal range.
Bone age of 6 years was assessed by radiological examination of the left-hand wrist (Tanner e Whitehouse (TW2) method), despite a chronological age of 8 years. Stimulation tests for growth hormone (GH) reserve were performed because of deceleration of growth curve, increased gap from the stature target, and retardation of bone age. Testing for GH revealed a 1.4 ng/ml peak after arginine injection (0.5 g Arginina/kg in vein infusion in 30 minutes) and a 4.5 ng/ml peak after clonidine administration (100 mcg/m2 per os). Replacement therapy with rh-GH at standard dose for GHD patient was started (0.23 mg/kg/week). During GH-replacement therapy follow-up a gain of growth rate (25-50th centile) with achievement of target height in the first 6 months of therapy was observed. Any side effect was reported.
Pubertal induction with estroprogestin hormones was considered in long-term follow-up to prevent the ovarian failure that often occurs in majority cases before puberty and leads to infertility.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [25.0, 'kg']}",65,61.75,68.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 25.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (25.0 kg - 20 kg) = 65.0 mL/hr.
Hence, the patient's fluid maintenance is 65.0 mL/hr."
5047,22,Maintenance Fluids Calculations,physical,decimal,pmc-7562874-1,Extracted,"A 26-year-old woman with a normal medical history presented with a complaint of watery stools.
She was a nonsmoker and an occasional drinker. The patient had consumed raw spring rolls at a restaurant 2 days prior. The patient developed a fever 2 days after the meal (Day 1 of onset of illness), excreted approximately 10 watery stools, and experienced lower abdominal pain starting on the next day. On Day 3 of the onset of illness, bloody stools and vomiting were observed; on Day 4, the patient underwent a check-up at Hospital A. The patient was diagnosed with infectious gastroenteritis and was prescribed 500 mg/d of levofloxacin for 3 days. Although her bloody stools and vomiting improved, the patient could not eat and was still having a few watery stools per day. The patient was referred to our department on Day 7 of the onset of illness because EHEC O157 (positive for verotoxins type 1 and 2) was detected in the stool culture at Hospital A. The physical findings were as follows: height, 160 cm, and weight, 49 kg (no weight loss observed). Her vital signs were as follows: body temperature, 36.7°C; blood pressure, 114/74 mm Hg; pulse, 112 beats/min; respiratory rate, 16 breaths/min; and consciousness, clear. Dry mouth was not observed. The abdomen was flat and soft, with mild epigastric tenderness but no rebound tenderness. Intestinal peristalsis was reduced, and the capillary refill time was <2 seconds.
Her hematology and chemistry test findings are shown in Table . In the urinalysis, the specific gravity was 1.013, protein was 3+, occult blood was ±, ketone bodies were +, and erythrocytes in sediment were 30-49/high power field.
The patient's diarrhea had almost completely resolved at the time of admission; however, her food intake remained poor, and based on her positive urine ketones, we concluded that she was dehydrated. Thus, fluid therapy was administered during hospitalization as a symptomatic treatment. At the time of admission, measures to prevent contact infection (based on the hospital manual) were taken by the infection control team of the hospital. Initially, the dehydration was considered to be due to the protein 3+ and occult blood ± findings. The patient's diarrhea had completely resolved by Day 8 of the onset of illness. After admission, the patient had no subjective symptoms, appeared well, and was not critical. However, blood tests revealed thrombocytopenia, advanced anemia, an increase in lactate dehydrogenase (LDH) level, and a predominant increase in indirect bilirubin level over time. On Day 11 of the onset of illness, fragmented RBCs were observed, the LDH was 862 mg/dL, the total bilirubin level had increased to 3.9 mg/dL (direct bilirubin was 0.9 mg/dL), and the platelet count was the lowest at 22 000/μL. In addition, the direct Coombs test was negative, haptoglobin level was <10 mg/dL (n: 19-170), and a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13) activity was 41% (normal range: >10). On the same day (Day 9), the urinary protein was 3+, the urinary occult blood worsened to 3+, and the serum creatinine (Cr) was 1.03 mg/dL, all of which indicated renal dysfunction. The three criteria for HUS, ie, hemolytic anemia, thrombocytopenia, and acute renal injury (which increased from 0.68 mg/dL to 1.03 mg/dL, 1.5-fold from baseline) were met, and delayed onset HUS was diagnosed on Day 11. The platelet count was lowest on Day 11 and the Hb levels dropped to 7.0 g/dL on Day 15 as a result of the hemolytic anemia (Figure ). An infusion of 2000-3000 mL/d of extracellular fluid was started on Day 11, and the laboratory findings gradually improved (Figure ). Although slight headache and nausea were observed for approximately 4 days beginning on Day 12, the patient's general condition was good and she was discharged on Day 17. Figure shows the changes in platelet counts, Hb, LDH, Cr, and qualitative urinalysis findings.
On Day 26, during an outpatient consultation, it was confirmed that the patient was cured based on the improvement of her symptoms and positive laboratory test results, including hematology, chemistry, and urinalysis. The Cr value was 0.68 mg/dL. At a later date, the health center reported that two other people had been infected with O157 after eating at the same restaurant 2 days prior to the onset of the current patient's symptoms.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [49.0, 'kg']}",89,84.55,93.45,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 49.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (49.0 kg - 20 kg) = 89.0 mL/hr.
Hence, the patient's fluid maintenance is 89.0 mL/hr."
5048,22,Maintenance Fluids Calculations,physical,decimal,pmc-7359153-3,Extracted,"Severe vasogenic hypertension with severely impaired cardiac function.
A 33-year-old obese mother (162 cm, 95.5 kg, BSA 2.14 m2) with 3 prior pregnancy’s complicated by moderate hypertension, presented at 32 weeks gestational age with severe hypertension, BP 165/95 (MAP = 118) and increasing oedema and leg pitting. The patient was scheduled for a therapeutic induction at 32 weeks gestational age.
Caesarean section delivered small for dates baby, 1550 g at 32 weeks gestational age with an Apgar score at 1 min of 9, at 5 min 7, and at 10 min 9, followed by a 3-day ICU stay.
Summary—Severe vasogenic hypertension, with a severely elevated SVR (2332 v normal 1100 dyne s cm−5). Additionally, there was severe impairment of the SV (46 v normal 79 ml), CO (4 v 6.9 L/min), SMII (1.1 v 2.0 W/m2) and, importantly, DO2 was approximately 60% of normal (594 v 900 ml/m2) (Fig. ).
Physiologically guided therapy would have targeted reducing the SVR with a vasodilator, and an inotrope to stimulate the LV function.
Outcome—The baby, after Caesarean birth, had a depressed 5 point APGAR score, which recovered over the first hour, while the mother required 3 days of ICU care. It is probable that this significant haemodynamic dysfunction would have been expressed in the first trimester and would have been detected by haemodynamic monitoring. This may have led to improved physiologically targeted management and a more stable haemodynamic course through pregnancy and improved outcome.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [95.5, 'kg']}",135.5,128.725,142.275,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 95.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (95.5 kg - 20 kg) = 135.5 mL/hr.
Hence, the patient's fluid maintenance is 135.5 mL/hr."
5049,22,Maintenance Fluids Calculations,physical,decimal,pmc-6507145-1,Extracted,"A 6-year old domestic huacaya alpaca non-pregnant mare with a body mass of 53 kg, was referred to the Clinic for Ruminants, Vetsuisse-Faculty, University of Bern, Switzerland for further diagnostic investigation. For 6 weeks, the mare had shown respiratory symptoms such as forced breathing but with no fever. Although the mare always had a good appetite, significant weight loss occurred during this time. A treatment by the referring veterinarian did not improve the symptoms.
At clinical examination, the alpaca was alert, nervous and in poor general condition. Body condition was moderate (bodyweight 53 kg: reference range55-90 kg) with a body condition score of 1 out of 5 (body condition score of the Australian Alpaca Association []). Its rectal temperature was 38.3 °C (reference range: 37.5–38.9 °C), heart rate 72 beats per minute (reference range: 60-80beats per minute) and respiratory rate 60 breaths per minute (reference range: 10–30 breaths per minute). The mare showed dyspnea with an abdominally reinforced breathing and bilateral dilated nostrils. There was no spontaneous nor provoked cough or evidence of nasal discharge. Auscultation of its lungs revealed bilateral ventrally scratching and crackling sounds, on the left dorsal aspect respiration sounds were focally absent. Further clinical examination showed no abnormalities, the alpaca had a good appetite once back in the stable, although dyspnea was still present.
Clinicopathological tests included a complete blood cell count and a blood chemistry panel. A neutrophilia (9.37 × 109/l, reference interval: 3.4–9.1 × 109/l) with left shift was present. Blood chemistry showed low potassium (3.64 mmol/l, reference interval: 4–5.2 mmol/l) and magnesium (0.71 mmol/l, reference interval: 0.8–1.1 mmol/l) values. Parasitological examination of a fecal sample revealed no endoparasite eggs or lungworm larvae.
Ultrasonographic examination (Esaote piemedical®, 10mHz linear probe) of the lungs revealed on the day of admission several comet-tail-artefacts over the whole lung field. The left dorsal lung surface was focally retracted and a moderate amount of gas was visualized in the pleural space. An area of increased density of the lung parenchyma was visible. There was no evidence of pleural effusion.
Laterolateral radiographs of the lungs were taken on the day of admission (Fig. ) and four days after admission (Fig. ). On both occasions, a bilateral pneumothorax with retracted lung lobes, mild on one and moderate on the other side, was diagnosed. Due to a mild retraction of lung lobes in the cardiophrenic angle in combination with focal effacement of the contours of the diaphragm and the cardiac silhouette, a very mild amount of pleural effusion was suspected. A focal lesion (17x22mm) located dorsally in the less retracted caudal lung lobe was observed with ill-defined borders, associated with a focal indentation of the lung surface. In the dorsal part of the lung field, several small gas lucent (6-15 mm diameter) lesions without a wall were suspected. In the central parts of the lung field, the opacity was diffusely increased with an ill-defined mixed reticular and bronchial pattern. However, it remained unclear, if this represented a pathology or was a consequence of partially collapsed lungs due to the pneumothorax. In the follow-up radiographs four days after admission, stripy increased opacities were observed in the cardiophrenic angle (Fig. ).
Differential diagnosis included neoplasia, fungal granulomas or tuberculosis. To obtain a better characterization of the lung pathology, a computed tomography scan(CT-scan) of the lungs in general anesthesia was performed.
The CT-scan revealed multiple focal bronchocentric part-solid spiculate nodules with internal air bronchograms in all lung lobes. The pneumothorax was confirmed. [Figures. and ].
Based on history, physical examination, available laboratory results and diagnostic imaging the main differential diagnosis was a pulmonary neoplasia. To distinguish between neoplasia and the other differentials as fungal granulomas or infectious agents (i.e. tuberculosis), the option of performing a fine needle aspiration or a biopsy was discussed.
Over 4 days of hospitalization, the general state and respiratory distress of the animal worsened progressively. Therapeutic options like undertaking pleural drainage to restore the pneumothorax were also discussed, but due to the poor prognosis, the owners elected for euthanasia of the alpaca. The animal was euthanized with an intravenous injection of pentobarbital (Esconarkon ad us.vet., Streuli Pharma AG, Uznach, Switzerland) in a dosage of 150 mg/kg bodyweight.
The postmortem examination, revealed the following findings: Affecting the cranial and caudal lung lobes there were multiple, approximately 1 cm × 0.5 cm × 0.5 cm, nodular, poorly demarcated, non-encapsulated, whitish to yellowish masses. No extra-pulmonary involvement was observed. There were multifocal areas of bullous emphysema within dorsally parts of the right and left cranial lobes. Other remarkable gross findings were multifocal, 1 cm in diameter nodular, centrally mineralized parenchymal masses in the liver and multifocal mucosal ulceration within compartment 3 of the forestomaches. The other examined organs were macroscopically unremarkable and no pathological alteration could be detected.
Samples of the lung and liver were fixed in 10% neutral buffered formalin for histological examination. The samples were routinely processed; paraffin wax embedded, stained with hematoxylin and eosin (HE), sections of 3 μm were cut and observed by standard light microscopy for histological examination.
Microscopically, the pulmonary nodules consisted of unencapsulated, poorly demarcated and infiltrative growing neoplastic masses. The epithelial neoplastic masses showed lepidic growth along pre-existing alveolar walls, which was cuboidal to low columnar with mostly distinguished cell borders, scant to moderate amounts of eosinophilic cytoplasm, mostly basally placed, round nuclei with coarse-stippled chromatin pattern and up to 1 nucleoli. The stroma separating the neoplastic acinar structures was abundant and poorly cellular consisting of plump spindle cells and extracellular deposition of collagen. Occasionally, there were areas of squamous epithelial cells differentiation with central keratin pearls and no apparent acinar formation [Fig. ]. Mitoses were very rare. Multifocal small areas of necrosis were present.The adjacent lung parenchyma showed a diffuse thickening of the alveolar septum characterized by infiltration with small numbers of lymphocytes, plasma cells and scattered macrophages. Alveolar spaces were emphysematous or multifocal filled with small numbers of foamy macrophages and few neutrophils.
The liver lesions were histologically compatible with a chronic, granulomatous and eosinophilic cholangiohepatitis. No trematodes could be observed within the examined sections and Ziehl-Neelsen-stain was negative. There was no evidence of fungal organism in the histopathological examination of liver and lung samples.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [53.0, 'kg']}",93,88.35,97.65,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 53.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (53.0 kg - 20 kg) = 93.0 mL/hr.
Hence, the patient's fluid maintenance is 93.0 mL/hr."
5050,22,Maintenance Fluids Calculations,physical,decimal,pmc-7872487-1,Extracted,"A 57-year-old African American female with a history of GERD and stroke was referred for two months of dysphagia to solids, unintentional weight loss of 30 lbs, and an abnormal barium swallow. The patient denied alcohol use and smoking. Barium swallow from the referring facility showed segmental narrowing and a long irregular distal esophageal stricture. Upper endoscopy revealed a circumferential ulcerated mass extending from 25 cm to 32 cm from the incisors, precluding passage of an adult gastroscope. The exchange for a pediatric gastroscope allowed for further evaluation and revealed a patch of nodular mucosa with ulceration at 23 cm from the incisors (Figure ). In addition, a deep invasive, large bulky ulcerated fungating mass was seen (Figure ). Pathology showed moderately to poorly differentiated basaloid SCC (Figure ). The patient was referred to oncology and CT imaging was ordered for staging. Unfortunately, the patient also developed septic shock from which she eventually suffered a cardiac arrest, and thus CT imaging for staging was unable to be completed.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [30.0, 'lbs']}",47.21552,44.85474,49.5763,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 30.0 lbs so this converts to 30.0 lbs * 0.453592 kg/lbs = 13.60776 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.60776 kg - 10 kg) = 47.21552 mL/hr.
Hence, the patient's fluid maintenance is 47.21552 mL/hr."
5051,22,Maintenance Fluids Calculations,physical,decimal,pmc-8628241-1,Extracted,"We report the case of a 9-year-old boy weighing 35 kg, with blood group AB RhD positive diagnosed to have acute lymphoblastic leukemia (B-ALL) with extramedullary relapse and was receiving BFM ALL-REZ protocol at our institute. He was admitted for fever and was evaluated for the focus of infection. The treating physician ordered three units of PC on day 4 of admission for platelet count of 10 × 103/μl []. During transfusion of three units of PC among which one was group O Rh positive and other two were B Rh positive, the patient developed rash over the face and scalp, generalized itching, chills, and fever. The patient was managed conservatively with injection chlorpheniramine and paracetamol infusion. Few hours after transfusion, the patient passed bright red urine suggestive of hemoglobinuria with complaints of pain in the chest and back.
ABO and RhD testing of the patient's posttransfusion sample were consistent with the pretransfusion sample. Pre- and posttransfusion sample was negative for DAT by polyspecific IgG and C3d gel card and was negative for antibody screening (ScreenLyse, Diagast). Patients posttransfusion Hb dropped to 5.6 g/dL from 6.8 g/dL with the presence of jaundice, fluid retention, elevated lactate dehydrogenase levels 340 U/L (normal 120–240U/L), and borderline RFT. There was no visible hemolysis in the supernatant of posttransfusion sample. The patient was managed symptomatically and discharged on day 6 of admission.
The donors of three PC units were called back and tested for high titer ABO antibodies. The donor sample from O PC revealed an antibody titer of 1:128 at room temperature for both anti-A and anti-B. The hemolysin test was positive for both A and B cells in the O group donor. The second donor (B positive) had anti-A titer of 1:32 and the third donor (B positive) did not turn up for testing. These findings along with the clinical symptoms and signs of acute hemolysis following transfusion can be presumably caused because of high antibody titer of anti-A and anti-B from group O PC.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [35.0, 'kg']}",75,71.25,78.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 35.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (35.0 kg - 20 kg) = 75.0 mL/hr.
Hence, the patient's fluid maintenance is 75.0 mL/hr."
5052,22,Maintenance Fluids Calculations,physical,decimal,pmc-4438664-1,Extracted,"An 11 months 22 days old partially-breastfed female baby was admitted with the complaints of the passage of loose stool since birth, occasional vomiting, and failure to thrive. The stool was watery in nature; frequency was 8-10 times per day, and was not associated with blood or mucous. The parents were healthy but their marriage was consanguineous. Antenatal and birth history included polyhydramniosis and premature delivery at 35 weeks of gestation. The baby's birthweight was 2.1 kg. During her neonatal period, she was admitted to another hospital due to sepsis and hyperbillirubinaemia. Moreover, she had several episodes of hospitalization for the management of persistent diarrhoea before coming to our hospital. There was no history of cyanosis or congenital heart disease. On admission, the patient appeared toxic, had reduced activity, and signs of some dehydration [assessed by Dhaka Method () recommended by WHO]. Her weight on admission was 3.8 kg, and length was 61 cm. Pulse rate was 118/minute with BP 90/50 mm of Hg, temperature 36.8 oC, respiration rate 48/minute, oxygen saturation (SpO2) 99% without applied oxygen on admission. On examination, no chest indrawing was observed, lungs were clear on auscultation, abdomen was soft, mildly distended but bowel sounds were present. She also showed signs of motor delay (neck control was not yet established).
Initially, the patient was managed as a case of chronic diarrhoea with some dehydration and severe acute malnutrition. We also suspected that her reduced activity might be due to electrolyte imbalance or sepsis. Hence, the following investigations were done: complete blood count (CBC), serum electrolyte and creatinine, blood and stool for culture and sensitivity (C/S), routine microscopic examination (RME) of stool and urine, and chest x-ray. The test report for electrolytes showed hypochloraemic hypokalaemia with alkalosis ( and ) which, thereafter, became persistent. Based on these findings, our differential diagnosis now included gastric outlet obstruction, cystic fibrosis, Bartter Syndrome, and congenital chloride diarrhoea (CCD). Subsequent investigations showed normal chloride level in sweat, normal routine microscopy of stool, urinary Na+ was 16 mmol/L (reference value 54-150), K+ 24.52 mmol/L (reference value 20-80), and Cl- 12 mmol/L (reference value 110-250). Tissue transglutaminase immunoglobulin (TtG-IgA) and IgG antibodies were negative, with plasma total protein 86.47 g/L (reference value 64.0-82.0), albumin 48.97 g/L (reference value 34.0-50.0), globulin 37.5 g/L (reference value 23.0-35.0), albumin and globulin ratio 1.31 (reference value 1.10-1.80). Chloride level in stool was 126.6 mmol/L (normal range 6-17 mmol/L), potassium 30.9 mmol/L, and sodium 82.9 mmol/L (normal range 50-60 mmol/L). The diagnosis of CCD was made on the basis of the results of faecal chloride content of >90 mmol/L and faecal chloride more than the sum of faecal Na and K contents and exclusion of other suspected diseases. Genetic testing could not be done due to its unavailability in Bangladesh. Urine and stool culture showed no growth of pathogens. We started oral NaCl and KCl supplementation and commercially-available oral formulation of Omeprazole. Other recommended treatment (with oral butyrate) was not applied as it was not available in Bangladesh. After 15 days of hospitalization, the patient developed fever and respiratory distress. The respiration rate was 64/minute, she was tachycardic (175 beats per minute), and the chest x-ray was suggestive of pulmonary infiltrates. So, we suspected that this was most likely due to a hospital-acquired infection and, initially, the patient was treated with injection Ceftazidime and injection Amikacin. However, no improvement was seen even after 5 days of treatment and, subsequently, the antibiotic was changed to injection Imipenem instead of ongoing medication. In the meantime, the blood C/S report was available, and it showed Acinetobacter species sensitive to Polymyxin B. Therefore, we started injection Polymyxin B. At that time, the patient also developed a changing murmur in addition to fever and anaemia, which raised the possibility of infective endocarditis. We, therefore, arranged an echocardiogram that showed mild coarctation of aorta, mild mitral regurgitation Grade 1, and mild pulmonary hypertension with normal ejection fraction (EF) of 70%. We added Captopril to protect heart failure. After adding Captopril, we found, to our surprise, that the stool output significantly reduced, and serum potassium increased. In response to this observation, we reduced the dose of supplemental KCL and NaCL and continued the treatment with Captopril. This decision was expedited by the fact that the overall condition of the patient was improving. The stool output and consistency was also improving. The patient attended regular follow-up with us, and the electrolyte profile had been normal in the next 6 months. In the first and second follow-up visit, we used Captopril with KCl (), and it showed that the diarrhoea was resolved and serum chloride and total carbon dioxide were also normal. The mother of the patient did not provide Captopril in the preceding one week prior to the third visit according to the advice of the local cardiologist, and the patient again developed alkalosis and hypokalaemia (). The most recent echocardiogram showed trivial MR, good biventricular function: left ventricular ejection fraction (LVEF) 69%, FS 34% left ventricular internal dimension in systole (LVIDs) 15 mm, left ventricular internal dimension in diastole (LVIDd) 24 mm trivial TR were noticed, along with peak pressure gradient (PPG) 10 mmHg, intact interatrial septum (IAS), and interventricular septum (IVS). No PDA or coarctation was seen. No intra-cardiac mass or vegetation was seen. Chamber dimensions and wall motion were normal. All valves were normal. No pericardial effusion was seen; biventricular function was good and, finally, the cardiac anatomy showed normal findings. The patient was gradually gaining weight from 3.8 kg to 7.1 kg in 7 months, and control over her neck was then completely normal. Her blood pressure was normal throughout the follow-up period.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.1, 'kg']}",28.4,26.98,29.82,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.1 kg. Hence, the patient's maintenance fluid is 7.1 kg * 4 mL/kg/hr = 28.4 mL/hr.
Hence, the patient's fluid maintenance is 28.4 mL/hr."
5053,22,Maintenance Fluids Calculations,physical,decimal,pmc-7953405-1,Extracted,"A 58-year-old male was referred to the department of rehabilitation medicine for an electromyography (EMG) study for symptoms of bilateral foot drop that appeared 25 d after the first biliary surgery.
The patient was diagnosed with acute cholecystitis and then underwent a laparoscopic cholecystectomy. Nine days after the first operation, the patient developed complications and underwent second common bile duct resection with Roux-en-Y hepaticojejunostomy. During the hospitalization for the two surgeries, the patient had no unconscious time other than surgery. After the two operations, however, he rarely ate oral meals for approximately 10 d because of nausea, vomiting, and anorexia; instead, he received conservative treatment only with Hartman solution or dextrose fluid, and thus lost weight rapidly. Before the surgery, the patient was 168 cm tall and weighed 68 kg [body mass index (BMI), 24.1 kg/m2], but after the two surgeries, his body weight was reduced to 58 kg for 24 d (0.42 kg/day; BMI, 20.5 kg/m2).
After the second operation, early ambulation was recommended, but during the first postoperative week, he was unable to walk properly because of the pain of operation site and discomfort caused by the tube inserted in his body. When he tried walking in the ward 2 wk after the operation, but he noticed that both ankles, especially the left ankle, were dragged, accompanied by numbness in both feet.
There was no illness in previous medical history.
No abnormalities.
In a physical examination before the EMG study on the 105th day after the first operation, the patient showed the obvious bilateral weakness of ankle dorsiflexor (right: 2/5 and left: 0/5), big toe extensor (right: 1/5 and left: 0/5), and foot everter (right: 2/5 and left: 0/5). In addition, the sensation was decreased in the anterolateral aspect of the calf, the dorsal surface of the foot, and the first web space of foot. Tinel’s sign was positive in the area around both fibular heads.
In the motor nerve conduction study, the amplitude of the deep peroneal nerve recorded in the extensor digitorum brevis was reduced on both sides as compared with the normal lower limits, and conduction block on the area around both fibular heads was found using the “inching” technique. The amplitude of the compound motor action potential (CMAP) measured in the tibialis anterior was also significantly reduced on the left side. In the sensory nerve conduction study, no action potential was induced in the left superficial peroneal nerve (Table ). On the needle EMG, abnormal spontaneous activity was observed in both tibialis anterior, peroneus longus, and extensor digitorum brevis. In particular, no motor unit action potential was observed in the left tibialis anterior during contraction. All the other nerve conduction studies (median, ulnar, tibial, and sural nerves) showed normal findings. The EMG study was consistent with bilateral common peroneal neuropathy around the fibular heads. In addition, blood tests were conducted to detect DM, thyroid dysfunction, vitamin (B1, B6, and B12) deficiency, or folate deficiency, which may cause non-compressive peroneal neuropathy; however, all test results were normal.
There were no abnormal findings on magnetic resonance image (MRI) study of the lumbar spine that was performed to rule out the possibility of paralysis of both lower extremities due to lumbosacral lesions. Ultrasonography revealed no tumors or cysts along the course of the sciatic nerve and peroneal nerve from the hip to the lower leg.
On left knee MRI, no structure was found around the fibular head that could cause entrapment of the peroneal nerve, and volume loss and edema were observed with the signal change by the nerve denervation in the anterior and lateral muscular compartments of the left lower leg (Figure ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [58.0, 'kg']}",98,93.1,102.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 58.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (58.0 kg - 20 kg) = 98.0 mL/hr.
Hence, the patient's fluid maintenance is 98.0 mL/hr."
5054,22,Maintenance Fluids Calculations,physical,decimal,pmc-5324033-1,Extracted,"A 67-year-old Caucasian male presented to the emergency department at a local hospital for left lower abdominal tenderness. The patient had undergone a living unrelated kidney transplant into his left iliac fossa 12 years prior due to chronic glomerulonephritis. His stable immunosuppression regimen included tacrolimus (1 mg every 12 h), mycophenolate mofetil (500 mg every 12 h), and prednisone (5 mg daily). Except for one episode of acute cellar rejection a month after kidney transplantation, he had been doing well with a baseline serum creatinine level of 2.0 mg/dL. On arrival, his body temperature was 36.6 °C, blood pressure was 163/54 mmHg, and pulse was 61 beats/min. He reported that he had been active until the day before without noticing any injuries, but he recalled his cat, weighing 15 lbs, jumped on his abdomen seven days prior. On physical examination, his abdomen was soft and flat without rebound or guarding, except for a small tender mass noticed at the incisional site of the kidney transplant. His hemoglobin was 7.1 g/dL. His serum creatinine level was elevated from his baseline to 2.5 mg/dL. He was producing a normal amount of urine without hematuria. Computed tomography (CT) without intravenous contrast revealed a 12 cm × 2.5 cm subcapsular hematoma around the transplanted kidney (Figure ). Urology was consulted, and the decision was made to conservatively observe the patient, as he met criteria of a renal trauma grade II according to the renal trauma grading system by the American Association for the Surgery of Trauma.
On admission, the patient received a red blood cell transfusion and was started on labetalol for hypertension. His systolic blood pressure was controlled within a range of 110-140. Within three days, his serum creatinine level increased to 5.4 mg/dL and his urine output decreased. His blood pressure was elevated up to 156/80 mmHg. The patient was transferred to a transplant center for further treatment.
At the transplant center, Doppler ultrasound (US) demonstrated an extensive peri-allograft hypoechoic area, abnormal arterial waveforms with absent diastolic flow in the arcuate arteries and a patent renal vein (Figure ). He underwent emergent laparotomy for hematoma decompression. A substantial portion of the hematoma was evacuated by capsulotomy. Concurrent kidney biopsy showed no evidence of rejection. His postoperative course was uncomplicated and uneventful. The patient resumed tacrolimus, mycophenolate mofetil, and prednisone. However, his kidney function continued to deteriorate and he became dependent on hemodialysis. He is currently maintained with mycophenolate mofetil monotherapy and is awaiting a second kidney transplant.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15.0, 'lbs']}",27.21552,25.85474,28.5763,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15.0 lbs so this converts to 15.0 lbs * 0.453592 kg/lbs = 6.80388 kg. Hence, the patient's maintenance fluid is 6.80388 kg * 4 mL/kg/hr = 27.21552 mL/hr.
Hence, the patient's fluid maintenance is 27.21552 mL/hr."
5055,22,Maintenance Fluids Calculations,physical,decimal,pmc-3195142-1,Extracted,"A 3-day-old male neonate was presented with complaints of poor feeding and respiratory distress in the form of fast breathing and retractions for 2 days duration.
The baby was born at term, to a primi-gravida mother by spontaneous vaginal delivery following an uneventful antenatal period with birth weight 2.7 kg. The mother was booked and immunized with two doses of tetanus toxoid during pregnancy. The baby cried immediately after birth and colostrum was given. Baby was apparently normal for 24 hours following which the symptoms started. There was no history of seizures, jaundice, or poor sensorium. There was no history of allergy in the mother or family. On examination, baby had tachypnea with mild grunting, scattered crepitations, and conducted sounds on respiratory examination. Other systems were within normal limits. Initial septic screen was negative. Chest X-ray showed bilateral para-cardiac infiltrates. A diagnosis of early-onset sepsis with pneumonia was made. The child was supplemented with oxygen and was put on intravenous cefotaxime and gentamicin. Cefotaxime was given at a dose of 100 mg/kg/day in two divided doses and gentamicin at a single morning dose of 4 mg/kg. Symptoms improved within 3 days of antibiotic therapy and feeds were started. Blood culture was sterile. The child was shifted to general ward from neonatal intensive care unit (NICU) for completion of antibiotic course. On day 6 of antibiotic therapy, child developed sudden poor sensorium, flaccidity, apnea, and cyanosis within seconds following administration of a night dose of cefotaxime. There was no evidence of extravasation of the drug. On examination, child had feeble respiratory attempts and bradycardia. Baby was given 100 mg of intramuscular adrenaline and cardiopulmonary resuscitation was done. Child was intubated and artificial ventilation was given for 10 minutes. Heart rate picked up as spontaneous respirations appeared regularly. Child was extubated immediately and readmitted in NICU and was monitored for the next 48 hours. Subsequent doses of cefotaxime were withheld and steroids were added. Child improved well and was shifted to the general ward after 2 days and discharged.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.7, 'kg']}",10.8,10.26,11.34,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.7 kg. Hence, the patient's maintenance fluid is 2.7 kg * 4 mL/kg/hr = 10.8 mL/hr.
Hence, the patient's fluid maintenance is 10.8 mL/hr."
5056,22,Maintenance Fluids Calculations,physical,decimal,pmc-4663799-1,Extracted,"A 5-year-old, 2.5 Kg, spayed female, domestic European short hair cat, was presented for twitching and muscle tremors after the owner applied a topical permethrin flea product containing 1 gr/Lt imidacloprid and 500 g/Lt of permethrin in a 1 ml pipette (Advantix spot-on for 4-10 kg dogs. Bayer AG, Leverkusen, Germany) 2 hours prior to presentation, for a total toxic dose of permethrin of 200 mg/kg. At presentation the cat was tachypnoic (respiratory rate of 52 breaths per minute), heart rhythm was 128 beats per minute, oral membranes were pink and rectal temperature was 38.5°C (). The cat was depressed and indifferent and had convulsions after few minutes (). Cat was washed with a mild detergent and two endovenous catheters were placed at both cephalic veins. Micro-Hct and total protein were evaluated (). Ringer lactate solution infusion was started at 3 times the maintenance dose (6 ml/kg/h) for maintaining hydration and promote diuresis. Due to the severity of tremors, a single IV bolus of propofol (Proposure 10 mg/ml solution, Merial Italia, Milano- Italy) was given at 1 mg/kg. Then DXMDT (Dexdomitor 0.5 mg/ml solution for dogs and cats. Orion Corporation, Espoo, Finland) was administered IV at 1 µg/kg. After administration cat was quieter and tremors were reduced. Oxygen was given via face mask and it was well tolerated. ILE (Intralipid 20% IV Fat Emulsion, Fresenius Kabi, Canada) bolus was administered using the second venous access at 2 ml/kg in 3 minutes, followed by a constant rate infusion at 4 ml/kg/h for one hour. After the first hour the cat was reassessed and, because of persisting twitching, ILE infusion continued again for 2 hours. Two hours later facial twitching reduced, respiratory rhythm slowed to 40 bpm and rectal temperature reduced to 37.9 °C. As the cat was not able to stand up, still unresponsive to surrounding stimulus, with mild tremors, ILE infusion was still continued for another 2 hours at 2 ml/kg/h, for a total time of 5 hours (). After this time neurological symptoms improved and temperature, heart rate, mucous membranes were within normal limit. Little facial twitching was still present and the animal was ataxic. On day 2 the cat still presented facial twitching, presented mild ataxia no tremors were observed and the animal was alert and eating without any problems. In the afternoon of the same day the cat was discharged after 26 hours after presentation. During hospitalization the cat also received: amoxicilline and clavulanic acid (Synulox injectable suspension, 140 mg/ml amoxicilline+ 35 mg/ml clavulanic acid, Pfizer Italia Srl, Rome-Italy) at 12.5 mg/kg and ranitidine (Ranitidine 50 mg/5ml injectable solution, HEXAL S.p.a, Agrate Brianza (MB), Italy) at 2 mg/kg. Cat was discharged with antibiotic therapy (amoxicilline and clavulanic 12.5 mg/kg for a week). On follow-up for 10 months later, the owner had not noticed any abnormalities and the cat was well.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.5, 'kg']}",10,9.5,10.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.5 kg. Hence, the patient's maintenance fluid is 2.5 kg * 4 mL/kg/hr = 10.0 mL/hr.
Hence, the patient's fluid maintenance is 10.0 mL/hr."
5057,22,Maintenance Fluids Calculations,physical,decimal,pmc-3546245-1,Extracted,"A 17-year-old girl with severe kyphoscoliosis presented with breathlessness and productive cough of one week duration. She was referred to our institute as a case of non-resolving left pneumothorax. Significant history included open heart surgery for ventricular septal defect closure at 4 years of age and spinal instrumentation for correction of kyphoscoliosis at the age of 15 years. On examination, she was emaciated, weighing 35 kg, and had severe thoracic kyphoscoliosis and generalized muscle wasting. Airway evaluation revealed limited mouth opening with inter-incisor distance of 1 cm, Mallampati Score was IV, and Atlanto-occipital joint extension was grade IV (<12). Respiratory system examination revealed a decreased air entry on the left chest. Chest radiography and computed tomography displayed a large pneumothorax with complete atelectasis of the left lung and airway distortion with deviated trachea and bilaterally narrowed bronchi []. Transthoracic echocardiography showed good biventricular function with no evidence of pulmonary hypertension.
Despite conservative management for two weeks, which involved insertion of intercostal drains, there was no improvement in the left lung status. The possible aetiology for the non-resolving left pneumothorax was multiple bullae in a hypoplastic lung. The hypoplasia of the left lung was probably due to the spinal deformity that the patient had. Due to the non-resolving nature of the left pneumothorax, an informed consent was obtained and the patient was taken up for a pleurectomy.
In view of anticipated difficult airway access, an awake fiberoptic tracheal intubation was planned. After premedication with oral midazolam, under standard American Society of Anaesthesia (ASA) monitoring guidelines, the right radial artery was cannulated under topical anesthesia for invasive arterial pressure monitoring. Despite topicalization of the upper airways with local anesthetic, the patient remained uncooperative for any kind of airway instrumentation. After further sedation with intravenous fentanyl (50 μg) and midazolam (1 mg), general anesthesia was induced with titrated concentrations of sevoflurane taking care to maintain spontaneous breathing. A lubricated nasopharyngeal airway was inserted in the left nostril to administer oxygen and sevoflurane. A 7.0-size cuffed endotracheal tube was successfully introduced into the patient's trachea through the right nostril under the guidance of a 4.0-mm diameter fiberoptic scope (LF-1 Olympus).
Once airway control was achieved, a muscle relaxant (cis-atracurium) was administered. In view of distorted trachea & bronchi it was decided to use an endobronchial blocker for achieving OLV as was the request from the surgical side. Using the special multiport adaptor provided, a five-size Arndt wire-guided endobronchial blocker (Cook, Inc., Bloomington, IN) was introduced coaxially through the nasotracheal tube. Under fiberoptic guidance, the blocker was placed in the left main bronchus. A left thoracotomy was performed. Standard lung-deflation technique was used and OLV was instituted. The surgical procedure proceeded uneventfully with good visualization of the operative field. Pressure control ventilation with positive end expiratory pressure (4 cm H2O) and peak airway pressures up to 24 cm H2O were used throughout the surgery. Inspired oxygen concentration (FiO2) and the respiratory rate were adjusted based on serial arterial blood gas analysis, pulse oximetry (SpO2) and end tidal carbon dioxide concentration (EtCO2) values during both lung ventilation and OLV. The patient remained haemodynamically stable with adequate oxygenation and ventilation. After completion of surgery, the blocker balloon was deflated and the left lung was expanded. The blocker was then removed with the nasotracheal tube left in situ.
In view of the chest deformities and difficulties with airway access, the patient was gradually weaned off artificial ventilation after four hours of elective mechanical ventilation in the post-cardiothoracic surgery intensive care unit. Postoperative analgesia was provided with fentanyl infusion and the patient's trachea was extubated successfully with satisfactory arterial blood gases. Serial chest radiographs showed good left lung expansion and, after an uneventful postoperative course, the patient was discharged home on seventh postoperative day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [35.0, 'kg']}",75,71.25,78.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 35.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (35.0 kg - 20 kg) = 75.0 mL/hr.
Hence, the patient's fluid maintenance is 75.0 mL/hr."
5058,22,Maintenance Fluids Calculations,physical,decimal,pmc-8411534-1,Extracted,"The proband, a 1-year-9-months old female, was admitted to the hospital in March 2019 for “growth retardation of more than one year”. She was born at term gestation to a G1P1(G is gravida, meaning the number of pregnancies; P is pregnancy, indicating the number of births) mother via cesarean section delivery. Her birth weight was 3.05 kg (25th–50th centile), and her birth height was 49.0 cm (25th–50th centile). She was breastfed to the age of one year, then fed with a combination of breastfeeding and formula. The child’s appetite was normal. However, she experienced postnatal jaundice when consuming breast milk that lasted for approximately two months. The child’s comprehension and memory were normal.
The child’s parents were from two unrelated families, and there was no family history of inherited or metabolic diseases. The heights of her father and mother were 171.0 cm and 167.0 cm, respectively. The body length of the child was monitored by her parents for the first nine months after birth, as seen in Table .
The child’s height at the time of admission was 61.0 cm (− 7.24 SD), and her weight was 6.4 kg (− 1.50 SD). Specific physical characteristics included yellowish hair, large and unclosed anterior fontanelles, a raised forehead, a low and flat nose, and 12 erupted baby teeth. No apparent abnormalities were observed during cardiopulmonary auscultation. Her abdomen was soft, and her liver and spleen were palpable and exhibited normal size, smoothness, and firmness.
No discernible abnormalities were found in the blood gas analysis, liver and kidney function assays, and serum electrolytes. The thyroid function indicators, including total triiodothyronine (TT3) (2.06 nmol/l), total thyroxine (TT4) (107.00 nmol/l), and free thyroxine (FT4) (1.15 ng/dl), were in the normal range. However, the TSH (6.97 mIU/l) level was elevated. The serum ACTH (29.80 pg/ml) and cortisol (414.16 nmol/l) levels were normal, but the IGF-1 (16.99 ng/ml) level was low, and the level of growth hormone was exceedingly low (< 0.05 μg/l). Fasting blood glucose (3.44 mmol/l) and insulin (0.16 mIU/l) levels also were low. The child's karyotype was determined to be 46, XX.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.4, 'kg']}",25.6,24.32,26.88,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.4 kg. Hence, the patient's maintenance fluid is 6.4 kg * 4 mL/kg/hr = 25.6 mL/hr.
Hence, the patient's fluid maintenance is 25.6 mL/hr."
5059,22,Maintenance Fluids Calculations,physical,decimal,pmc-6473657-1,Extracted,"A 22-year-old African-American man presented to the Emergency Department complaining of bright red blood per rectum, diffuse abdominal pain, dark-colored urine, malaise, and 30-pound weight loss in the last month. Bowel habits were unchanged. There was no hematemesis or dysphagia. He also reported vomiting and subjective fevers, but denied dyspnea, cough, night sweats, arthralgia, dysuria, or prior bleeding events. There were no episodes of recurrent infections. His past medical history was unremarkable and he denied taking any medications. He did not report any substance abuse. His sexual history was significant for unprotected same-sex intercourse, with the last encounter two weeks prior to presentation. He reported no recent travels or sick contacts. On physical exam, the patient appeared emaciated and lethargic. There was no pallor, icterus, adenopathy, or rash. Oral examination revealed gingivitis but no thrush or sores. Abdomen was soft and diffusely tender with no distension or guarding. A large, posterior anal fissure was noted on rectal exam with minimal amount of blood. The remainder of examination was unremarkable. No genital ulcers or urethral discharge was noted.
Laboratory studies revealed normal hemoglobin at presentation, but during the course of his hospital stay, he had a significant drop from 14.7 g/dL to 10.3 g/dL over the course of two days (NR 12.9–16.8 g/dL) despite no further bleeding, reaching as low as 8.4 g/dL after the first week. The elevated lactate dehydrogenase of 2100 u/L (NR 85–210 U/L) and slightly increased bilirubin (1.3 mg/dL, NR 0.2–1.2 mg/dL) was suggestive of hemolysis (performed on Beckman Coulter AU 5800). Haptoglobin was found to be low (<6 mg/dL), with a negative direct Coombs test and no schistocytes on the peripheral blood smear. Glucose-6-phosphate dehydrogenase (G6PD) was significantly decreased at 0.4 units/g Hgb (reference range: 4.6 to 13.5 units/gram of hemoglobin). Reticulocyte production index was inappropriately low at 0.48. Vitamin B12 and folate levels were normal, but ferritin was greater than 7500 ng/mL (performed on Beckman Coulter AU 640, NV 23.90–336.20 ng/mL). Platelets were mildly decreased (114 × 103/μL) and white count was within normal limits. He also developed acute kidney injury with creatinine of 1.9 mg/dL upon admission, which resolved two days after fluid resuscitation. Urinalysis revealed a large amount of blood but just one red blood cell per high power field. Urobilinogen was positive and there was also proteinuria 30 mg/dL. Meanwhile he was also worked-up for his abdominal pain with computed tomography (CT) scan, magnetic resonance imaging (MRI), endoscopy, and colonoscopy, all of which were unrevealing.
The patient consented to testing for human immunodeficiency virus (HIV) testing, which revealed positive fourth-generation screening but negative confirmatory results by the western blot technique. Viral load was above the detection limit of two million copies/mL. CD4 lymphocyte count was 456 cells/μL. He was screened for other sexually-transmitted infections with negative hepatitis panel but positive urethral swab for Chlamydia trachomatis and Neisseria gonorrhoeae, for which he received a single dose of ceftriaxone 250 mg and azithromycin 1g. Further infectious work-up that included quantiferon-TB gold, toxoplasmosis serology, and Histoplasma urine antigen were all negative. Epstein–Barr serum DNA and Cytomegalovirus IgM were both negative. The patient received supportive and symptomatic treatment with no blood transfusions. He was started on antiretroviral therapy with dolutegravir, tenofovir alafenamide, and emtricitabine prior to discharge. His hemoglobin remained stable at 7.7 g/dL and his LDH and indirect bilirubin were down-trending after treatment.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [30.0, 'lbs']}",47.21552,44.85474,49.5763,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 30.0 lbs so this converts to 30.0 lbs * 0.453592 kg/lbs = 13.60776 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.60776 kg - 10 kg) = 47.21552 mL/hr.
Hence, the patient's fluid maintenance is 47.21552 mL/hr."
5060,22,Maintenance Fluids Calculations,physical,decimal,pmc-8581785-1,Extracted,"A 14-year-old male castrated Cornish Rex cat weighing 6.9 kg (15.2 lb) presented to a private referral and emergency clinic in a state of hypotensive and anaemic shock. The cat had presented to its primary veterinarian the prior afternoon for the second injection of pentosan polysulfate (Synovan; Ceva) of a four-weekly course, and was not on any other medications. The cat was previously clinically healthy apart from chronic mobility issues; haematology and biochemistry panels from 10 months prior were normal.
The injection was reportedly given at 3 mg/kg SC over the cervical region and the cat displayed a severe adverse and apparently painful reaction to this injection, which had not occurred at any previous injection (the cat had previously completed 4-week courses of pentosan polysulfate both 18 months and 10 months prior, which were temporarily effective for chronic elbow and stifle arthritis). Immediately after returning home the cat was noticed to be very restless, weak in the hindlimbs and a painful swelling was noted over the neck at the injection site. Over the next 5 h this progressed to lethargy, tachypnoea, vocalisation and eventually collapse with altered mentation.
The cat initially presented to a different after-hours veterinary clinic the day of the injection.
Reported physical examination findings included hyperaesthesia, particularly over the neck and hindlimbs, pale mucous membranes, hypotension (Doppler blood pressure 74 mmHg) and hypothermia of 35.1ºC (95.2ºF). The cat was treated supportively overnight with intravenous fluid therapy, buprenorphine, dexamethasone and active warming. Haematology and serum biochemistry performed in house the following morning showed a severe non- or pre-regenerative anaemia with a haematocrit of 11.4% and absolute reticulocyte count of 26.2 K/µl (reference interval [RI] 3.0–50.0), a mature neutrophilia of 18.8 × 109/l (RI 2.50–12.50), normal platelet count of 183 K/µl (RI 175–600), hyperglycaemia of 10.52 mmol/l (RI 3.95–8.84), mild panhypoproteinaemia of 47 g/l (RI 57–89) and mild hypophosphataemia of 0.89 mmol/l (RI 1.00–2.42). At this point, approximately 24 h post-injection, the cat was transferred to the tertiary referral clinic for further evaluation and care.
On arrival, the cat was dull but hyper-responsive to stimuli, and was painful around the injection site. Mucous membranes were pale and pulses were weak. A gallop sound was heard on cardiac auscultation. Packed cell volume (PCV) was 5% on presentation and adequate blood to perform clotting times was not obtainable. Non-pitting interstitial oedema was noted on the shoulders, ventral thorax, neck and chin. A blood transfusion (50 ml whole blood over 4 h) was performed following blood typing (type A); however, a cross-match was not performed owing to the severity of the cat’s clinical signs and lack of prior transfusion history. The cat’s vital signs remained stable and 100% oxygenation measured via pulse oximetry was maintained throughout the transfusion. A post-transfusion PCV of 15% was achieved. Mentation initially improved following transfusion but subsequently deteriorated again. The cat was stabilised in an oxygen tent with intravenous fluid therapy, maropitant (1 mg/kg IV), dexamethasone (0.23 mg/kg IV) and subcutaneous vitamin B12 injection (0.25 mg/cat) overnight, prior to further diagnostics.
An echocardiogram was performed by a board-certified cardiologist around 12 h after presentation, which documented severe left atrial enlargement, moderate right atrial enlargement and discrete upper septal thickening (DUST). There was small-volume pericardial and pleural effusion, which together with the cardiac changes was consistent with heart failure, a finding that complicated but did not explain the severe anaemia.
Abdominal ultrasound identified a mild peritoneal effusion, as well as mildly increased intestinal thickness and mildly altered layering. Thoracic radiographs interpreted by a board-certified radiologist reported a normal heart size with dilation of the pulmonary arteries and veins. A bronchointerstitial, but no alveolar, lung pattern was identified. Owing to the cat’s normal respiratory rate and character at the time of these diagnostic tests and no evidence of pulmonary oedema on radiographs, the anaemia and subsequent blood transfusion and fluid therapy were considered as a possible cause of acute exacerbation of heart disease, so the initial recommendation was to discontinue fluid therapy before initiating diuretics or any cardiac medications. The cat was maintained in an oxygen tent.
The cat’s condition deteriorated rapidly later that evening, despite oxygen therapy, becoming increasingly dyspnoeic. Venous blood gas analysis showed a severe respiratory acidosis (pH 7.074) and hypercapnia (PvCO2 73.3 mmHg). The owners were considering humane euthanasia, owing to a perceived poor prognosis, and elected for this at this time as a result of the cat’s unstable condition, rather than attempting further therapeutics such as thoracocentesis.
The presence of widespread non-pitting interstitial oedema and anaemia prompted a suspicion for internal haemorrhage, and the body was sent to an external laboratory for post-mortem examination. The examination was performed by a board-certified anatomical pathologist, and significant post-mortem findings were as follows. (1) Large amounts of subcutaneous and intermuscular haemorrhage circumferentially around the neck (particularly ventrally), caudal head and mandibular skin and over the dorsal thorax. The haemorrhage extended between dorsal and left lateral thoracic muscle layers, and between the left scapula and the body wall, as well as over both proximal forelimbs (). (2) Retropharyngeal haemorrhage with extension between hypaxial muscles and the oesophagus into the mediastinum and pericardium (). (3) Retropharyngeal haemorrhage with extension between hypaxial muscles and the oesophagus into the mediastinum and pericardium (). (4) Subcutaneous oedema without haemorrhage in the distal left forelimb. (5) Red serous fluid (100–200 ml) within the pleural cavity, and 1–2 ml of red serous fluid within the pericardial cavity (). (6) The lung parenchyma ranged from light to dark red and oedematous (). (7) Two small liver nodules (5 mm and 10 mm, respectively). No other gross abnormalities were identified, including no cutaneous petechiae or ecchymoses, and no evidence of haemorrhage from recent blood sampling and catheter sites.
Gross diagnoses were: (1) severe cervical and thoracic subcutaneous, intermuscular, mediastinal and pericardial haemorrhage, and forelimb oedema; (2) pleural and pericardial effusion; (3) pulmonary oedema, congestion and possible haemorrhage; and (4) hepatic nodular hyperplasia or neoplasia.
Testing was also carried out on a post-mortem liver sample for coumarin anticoagulants using the liquid chromatography–mass spectrometry method to rule out rat bait poisoning as a cause of the haemorrhage. There were no levels of brodifacoum, bromadiolone, coumatetralyl or flocoumafen detected, with a limit of detection of 0.005 µg/g using this method.
Histopathology was performed on tissue samples taken as part of the necropsy. This confirmed the presence of interstitial haemorrhage between muscle fibres and adipose tissue with a mild mixed inflammatory infiltrate, and evidence of myofibre regeneration in a sample from the typical site for an injection. This was presumed to be related to the first injection of pentosan polysulfate administered 1 week prior. Sections of the heart, particularly in the basal interventricular septum and left ventricular free wall, were characterised by large areas of interstitial fibrosis and small areas of neutrophilic and lymphocytic subendocardial and interstitial inflammation, which was considered to be consistent with the DUST finding on echocardiography and confirmed a pre-existing cardiomyopathy and endomyocarditis. The liver also had small-to-large areas of centrilobular hepatocellular necrosis and vacuolation; one large area of necrosis was related to a liver nodule, but an underlying neoplastic cause of nodule formation was not obvious. The necrosis and vacuolation were felt by the histopathologist to be most likely attributable to tissue hypoxia related to the hypotension and anaemia. The lungs were congested, and contained interstitial oedema, with no evidence of microthrombi. There were no other significant microscopic findings.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.9, 'kg']}",27.6,26.22,28.98,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.9 kg. Hence, the patient's maintenance fluid is 6.9 kg * 4 mL/kg/hr = 27.6 mL/hr.
Hence, the patient's fluid maintenance is 27.6 mL/hr."
5061,22,Maintenance Fluids Calculations,physical,decimal,pmc-6723212-1,Extracted,"A 67-year-old woman with a 5-year history of T2D presented to the emergency department (ED) of a public hospital because of abdominal pain and impaired conscious level (Glasgow Coma Scale: 12), occurring after one week of fever, malaise, and dyspnea. Family reported that the patient was not a smoker nor was used to drink alcohol and had normal blood pressure. Clinical charts showed that she was free of cardiovascular disease and had albuminuria (800–1100 mg/g creatinine) with estimated glomerular filtration rate (eGFR) 75–85 mL/min/1.73 m2. In the last month, due to worsening glycemic control, the diabetologist prescribed a lower intake of calories and added empagliflozin 25 mg/day on top of usual treatment (metformin 1700 mg/day). The new therapy led to 14-kg body weight loss (from 67 to 53 kg). Family also mentioned bis-in-die therapy with nonsteroid anti-inflammatory agents (NSAID) for a joint pain throughout the two weeks before hospitalization. At presentation, BMI was 21.5 kg/m2. Vital signs were temperature 37.2 °C, pulse rate 110 beats/min, blood pressure (BP) 90/60 mmHg, respiratory rate 40 breaths/min, and urinary output 100 mL/h. Physical examination showed dehydration and no relevant findings at objective examination of lungs and abdomen. reports main lab data during hospitalization.
In ED, diagnosis was “metabolic acidosis and hyperkalemia in diabetic patient with acute kidney injury (AKI) likely related to NSAIDs”, and treatment was intravenous (iv) bolus (140 mmol) of sodium bicarbonate 1.4% followed by continuous iv infusion of normal saline 0.9% and sodium bicarbonate 1.4% at the rate for either solution of 125 mL/h. In the subsequent 6 h, acidosis status slightly improved, thus leading to reduction of bicarbonate rate to 20 mL/h.
After 12 h of infusion, a renal consultant was called because of hypernatremia onset and persistent acidosis. Nephrologist asked for urinalysis, not included in the initial screening, that disclosed very high glucose and ketones levels. The consultant diagnosis was “AKI and DKA related to SGLT2-I”. Therefore, SGLT2-I therapy and bicarbonate infusion were discontinued, iv infusion of Lispro, a rapid-acting insulin analog (0.1 UI/kg/h) was started, and KCl 20 mmol/h was added to the normal saline infusion. In the same day, due to severity of acidosis and hypernatremia onset coupled with worsening of hemodynamics (BP 80/60 mmHg) and mental status, the patient was transferred to the nephrology department. She underwent 4-h treatment with bicarbonate hemodialysis for two consecutive days with ultrafiltration rate adjusted to allow volume expansion of 2.0 L/session. After the first session, urinary output increased up to about 500 mL/h due to repletion of extracellular volume, concomitant increase of BP (130/60 mmHg), and persistent glycosuria. Within few days, a significant improvement was observed in mental status, systemic hemodynamics, renal function, and hydroelectrolyte homeostasis. Insulin infusion continued for one week. Additional lab exams obtained in the nephrology ward demonstrated mycotic and bacterial infection of urinary tract associated with high procalcitonin (up to 7.7 ng/mL-normal <0.05 ng/mL) that was efficaciously treated by culture-guided therapy. Lab tests also showed high glycated hemoglobin (HbA1c 12%), very low fasting C-peptide (0.43 ng/mL), and absence of autoantibodies against insulinoma-associated protein 2 (IA-2 6.3 U/mL) and glutamic acid decarboxylase (GAD 4 U/mL) suggestive for latent autoimmune diabetes in adults (LADA). Following the complete resolution of the clinical picture, a kidney biopsy was performed at day 15 because of high albuminuria (942 mg/g) not readily attributable to diabetic nephropathy according to the relatively short duration of T2D and the absence of diabetic retinopathy. Histopathology, however, revealed overt diabetic nephropathy ().
The patient was discharged after recovery of renal function, volemia, and metabolic control. Diagnosis was “euDKA related to SGLT2-I associated with AKI due to osmotic diuresis-induced volume depletion in patient with type 2 diabetic nephropathy”. The patient was switched on chronic insulin therapy and regular nephrology follow-up was indicated.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [53.0, 'kg']}",93,88.35,97.65,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 53.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (53.0 kg - 20 kg) = 93.0 mL/hr.
Hence, the patient's fluid maintenance is 93.0 mL/hr."
5062,22,Maintenance Fluids Calculations,physical,decimal,pmc-8440148-1,Extracted,"A 14-year-old boy was admitted for bilateral scrotal masses for 11 years in our outpatient department. According to the previous documents provided by his family, his parents were normal but his elder brother showed same scrotal masses.When they were 3 years old,the elder brother,who is 10 years older than the younger, accepted serious hypospadias repair surgery in 1999 while the younger in 2009 at Wuhan Children’s Hosptial. In the short postoperative period, this younger child’s skin color became tanned and the color deepen. Although parents noticed that his testicles were slightly larger than peers in progressive pigmented stage, occasionally even with orchialgia, same to childhood of his elder brother, they still ignore it and did not take him to medical treatment until oversize bilateral lumps 5 years later. Thus his parents sent them to Tongji Hosiptal affiliated to Middle China University in Wuhan, and both were diagnosed as TARTs with 3β-2HSD by routine hormone examination(see in Fig. ) and recommended gene analysis(see in Supplementary Fig. 1).In addition, tumor tissue biopsy approved by custodians also supported TARTs diagnosis. The markedly elevated androgen, ACTH and 17-OHP levels and actual bone age(15-year-old) indicated only hydrocortisone(HC) supplementary therapy feasible when they refused surgerical excision. In long-term follow-up, HC dosage(15 mg/m2·d) was gradually adjusted to 23 mg/m2·d, which was proven effective by diminshed tumor size. While two siblings often forgot to take medicine on time for one year and did not seek for regular examination due to COVID-19 epidemic in Wuhan. The bilateral TARTs size became slightly larger than pre-treatment and seemed insensitive to HC.
In the second admission to Shenzhen Children’s Hospital, we conducted sonography and computed tomography(CT)(show in Fig. ).The Physical examinations details included:Height_145.4 cm(-3.4 SD), Sitting Height_84.6 cm, Weight_55.7 kg, Pigmented Skin(see Supplementary Fig. 2). Tanner staging: breast B1, armpit hair A2,pubis PH5,penis 6 cm*2.7 cm.
With slowly increased height about 1.2 cm since first admission 5 years ago, we replaced HC with dexamethasone(DXMS) to control the disease. The CT image suggested that testis tumor nearly replaced normal testicles tissue and hyperplasia in bilateral adrenal cortex. After Multi-disciplinary discussion, the tumor was proposed to excise to avoid growing up and his parents accepted our advice.
After the incision into tunica vaginalis in each side, there is an obvious characteristic that cavity of tunica vaginalis disappeared, we can noticed two hard giant tumors(see Fig. ) with several sporadic bean-like tubercles and cannot clearly distinguished structure of epididymis and testis. Finally,we stripped the tumor and suture incision by rolling residual testicular tissue and tunicae vaginalis.The tumors were demonstrated TARTs by pathology results (see in Supplementary Fig. 3 and Table 1 ) with no existence of Reinke crystals.
In the postoperative week,bilateral scrotum skin folds gradually resumed with subsidence of scrotum swelling and bilateral size obviously decreased comparing with primary manifestation.
During the third admission to Shenzhen Children’s Hospital in 2021 July, physical examinations included:Height_146.2 cm(-3 SD), Sitting Height_85.3 cm, Weight_64.5 kg, Pigmented Skin color improved. Tanner staging: breast B1,armpit hair A2,pubis hair PH5,penis 1 cm*3.5 cm.The surgery incision recovered well and bilateral testis unltrasound show Left volume was 11.59ml and Right was 10.79ml. Adrenal hormone profile shows ACTH 4.090pg/ml, testosterone 7.54nmol/L,17-OHP 0.47nmol/L, serum cortisol is 0.000ug/dl and follow-up is necessary for long-term prognosis.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [64.5, 'kg']}",104.5,99.275,109.725,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 64.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (64.5 kg - 20 kg) = 104.5 mL/hr.
Hence, the patient's fluid maintenance is 104.5 mL/hr."
5063,22,Maintenance Fluids Calculations,physical,decimal,pmc-7717086-1,Extracted,"A 47-year-old male, otherwise healthy, was diagnosed with a localized 9.8 cm high-grade malignant peripheral nerve sheath tumor (MPNST) in his right axilla involving his brachial plexus and subclavian artery (Figure ). He was 5’10” and weighed 68 kg. He received neoadjuvant radiation and concomitant chemotherapy. His preoperative Hemoglobin (Hgb) was 13.1 g/dL (ref: 12.6 - 17.4 g/dL). A central line and peripheral IVs were established and 600 ml of autologous blood was drawn, lowering his Hgb to 12.0 g/dL. With hemodilution and an estimated blood loss of 450 ml, his Hgb fell to 9.5 g/dL at mid-surgery and 8.9 g/dL at the conclusion of surgery. He received a total of 4.5L of crystalloid and the 600 ml of autologous blood was reinfused during wound closure. The duration of surgery was approximately six hours and included dissection of the tumor en-bloc away from numerous major nerves and an end-to-end vascular graft anastomosis for the axillary artery. The final margins were R0. The Hgb on postoperative day (POD) one was 10.5 g/dL and he was discharged on POD two with a Hgb of 11.0 g/dL. The patient consented to the publication of the details of his case.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [68.0, 'kg']}",108,102.6,113.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 68.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (68.0 kg - 20 kg) = 108.0 mL/hr.
Hence, the patient's fluid maintenance is 108.0 mL/hr."
5064,22,Maintenance Fluids Calculations,physical,decimal,pmc-7838352-1,Extracted,"A 2-year-old, 22.6 kg castrated male Vietnamese Potbellied pig presented to the Food Animal and Camelid Hospital at Iowa State University's College of Veterinary Medicine for a 2 week history of “toe-touching” lameness. Two weeks prior, the pig was noted to have fallen while running across a wood floor and was immediately lame afterward. Other than recent lameness, the pig had an episode of suspected erythema multiformae that resolved without treatment 1 year prior.
Examination was within normal limits with exception of lameness. On presentation, the right pelvic limb was noted as Grade 4/5 lame with occasional toe-touching, but no absolute weight-bearing observed. On palpation, the patella was permanently luxated and could be manipulated in a medial fashion back into the groove (Grade 3/4) (). The pig was bright, alert and responsive, and had an appropriate body condition score (2/5). Radiographs taken by the referring veterinarian displayed no evidence of fracture.
Based on the confirmation of the patellar luxation and overall health of the patient, a surgical correction was planned for the next day. A single radiograph taken by the referring veterinarian showed no evidence of fracture or other orthopedic disease (). The patient was withheld from food and water starting at midnight prior to the surgery.
The patient was classified as ASA 2 according to the American Society of Anesthesiologists. Food was withheld for 18 h and water for 10 h, respectively, prior to anesthesia. Premedication included morphine at 0.4 mg/kg, dexmedetomidine at 0.005 mg/kg and midazolam at 0.5 mg/kg administered intramuscularly (IM). An intravenous catheter was placed in the right auricular vein and the patient was induced with propofol and ketamine, each at 1.1 mg/kg intravenously. The larynx was sprayed with 2% lidocaine prior to intubation with an 8 mm internal diameter cuffed endotracheal tube. Cardiovascular and respiratory monitoring was performed with a multiparametric monitor. Oxygen saturation using pulse oximetry, continuous electrocardiography, body temperature, oscillometric blood pressure, end-tidal carbon dioxide (EtCO2) using side-stream capnography, and gas analysis were measured; cardiovascular and respiratory parameters were recorded every 5 min. Anesthesia was maintained with isoflurane in oxygen delivered via a circle system. Mechanical intermittent positive pressure ventilation was instituted soon after intubation to maintain normocapnia (EtCO2 35–45 mmHg) with a tidal volume of ~8 mL/kg and a peak inspiratory pressure of 16 cm H2O. A lumbosacral spinal epidural was performed using 0.15 mg/kg preservative free morphine and 2 mg/kg lidocaine for additional analgesia. The patient was placed in dorsal recumbency for the surgical procedure. Lactated Ringers Solution was administered at ~5 mL/kg/hr intraoperatively. Warming therapy included a forced-air warming blanket (Bair HuggerTM, 3M, Maplewood, MN, US) and warming blanket (HotDog®, Augustine Surgical Inc, Eden Prairie, MN, US) to minimize intraoperative hypothermia. Tulathromycin (Draxxin, Zoetis, Parsippany, NJ, US) at 2.5 mg/kg was administered IM shortly after induction for antimicrobial prophylaxis. Intraoperative complications included hypotension which was managed with fluid boluses, an anticholinergic, and a dopamine and dobutamine constant rate infusion at 10 mcg/kg/min. Total anesthetic time was 2 h and 15 min with surgical time being 63 min. The patient recovered unremarkably.
The patient was placed in dorsal recumbency. The right pelvic limb was clipped and aseptically prepared using the hanging leg technique. A #10 scalpel blade was used to make a 20 cm craniolateral skin incision on the stifle. The incision extended from proximal to the patella to the level of the proximal third of the tibia. Metzenbaum scissors were used to incise the subcutaneous tissue. A #15 blade was used to incise the retinacular fascia on the lateral aspect of the joint and a #15 blade was used to make a stab incision into the joint capsule. Curved Mayo scissors were used to extend the arthrotomy and the patella was luxated medially (). Hemorrhage was controlled using radiopaque gauze sponges and electrocautery throughout the procedure. The joint was inspected. Cruciate ligaments were intact and meniscal cartilages were normal. The trochlear groove was extremely shallow. The articular cartilage appeared mildly hyperemic with several streaks of reddened foci apparent.
A #15 blade was used to score the trochlear ridges of the femur for planned wedge recession. A reciprocating saw (Micro 100, Hall Surgical, Largo, Florida, US) was used to perform a wedge recession. Sufficient depth of the groove was confirmed by replacing the patella into the groove and afterwards ensuring a sufficient portion of the wedge was seated within the groove (). The cranial tibial muscle was elevated from the lateral aspect of the tibial tuberosity and the fascia from the medial aspect of the proximal tibial was sharply reflected for planned tibial tuberosity transposition. The osteotomy was performed with the reciprocating saw. The tibial tuberosity was transposed ~0.75 cm laterally, a small K wire was placed. Two 0.0625 inch K wires were placed in the proximal tibia, and an 18 gauge tension band placed routinely (). The stifle was reassessed for patellar luxation and no luxation in flexion or extension was noted. The joint capsule was closed with 0 polydioxanone (PDS, Ethicon inc, Somerville, NJ, US) using a horizontal mattress pattern. The lateral fascia was closed and imbricated with #0 polydioxanone in a mayo mattress pattern. The subcutaneous layer was closed with #2-0 poliglecaprone 25 suture (Monocryl, Ethicon inc) in a simple continuous pattern. The skin was closed with surgical staples. The incision was then covered with an aluminum aerosol bandage afterwards. Post-operative radiographs of the image were obtained ().
Post-operative analgesia was administered by placing a fentanyl transdermal patch (50 mcg/kg/h) 7 h after the pre-anesthetic medications were administered. The next morning the patch was displaced by the patient. Repeated attempts to replace the patch were met with the patient removing the patches. Based on patient demeanor and attitude the patch was discontinued. Inflammation was managed postoperatively with meloxicam (0.5 mg/kg orally every 24 h).
During the first 24 h postoperative, the pig was confined to a 3 × 2 m stall divided in two, the one side bedded with hay. The other side was used to allow for the pig to defecate and urinate, as the patient was a house-trained companion animal. During recovery at the hospital the pig did not bear weight on his right pelvic limb, but was able to ambulate. The pig appeared to be otherwise doing well, not showing any obvious signs of pain or discomfort. Cryo-therapy (towel-wrapped ice pack applied for 15–20 min) was held against the incision every 6 h post-operatively. The pig was discharged 5 days post-operatively. Seven days post-operatively a second dose of tulathromycin (2.5 mg/kg, IM) was administered by the referring veterinarian. Meloxicam (generic, 0.5 mg/kg orally, q 24–48 h) was administered as needed, with the clients reporting no doses given after 3 weeks post-repair.
Initial physical restrictions involved putting the patient in a small room or crate when not being monitored as well as placing sections of carpet on the wood floor to minimize the risk of further slipping. The pig was also separated from other companion animals during this time. Physical rehabilitation therapy was performed during the first month postoperatively by focusing on massage of the limb (15 min intervals), immediately followed by 15 min of range of motion stretches. During stretching, care was taken to extend and flex the limb over a 15 s time period. The massage/stretching sessions were done three times daily for the first 4 weeks postoperatively. During this time, attempts were made to periodically and gently push the pig from the opposite rear limb in order to encourage bearing weight on the right pelvic limb. After 4 weeks the pig was reluctant to allow physical therapy for the full length of time previously described, and was also noted to be bearing more weight when walking. Approximately 5 weeks postoperatively, the pig was noted to spontaneously run around the house as he would before the incident.
At recheck examination ~7 weeks post-surgery, the pig's vital parameters were within normal limits on physical examination. Occasionally, the pig would guard the right pelvic limb while standing, however no abnormal gait or posture was noted on ambulation. The clients reported at this time that the pig had resumed normal levels of activity compared to before the injury. Post-operative radiographs were obtained and considered normal ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [22.6, 'kg']}",62.6,59.47,65.73,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 22.6 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (22.6 kg - 20 kg) = 62.6 mL/hr.
Hence, the patient's fluid maintenance is 62.6 mL/hr."
5065,22,Maintenance Fluids Calculations,physical,decimal,pmc-5586869-1,Extracted,"A 110-kg 28-year-old male was admitted to the Emergency Department for subtrochanteric fracture of the right thigh following a road traffic accident. Besides the injured thigh, there was no complaint of pain at any other site. There was no associated injury and any other comorbid conditions. The patient was obese with a body mass index of 37 and no other comorbidities. He had no history of veno-occlusive disease, and all the preoperative laboratory evaluations were normal. Antegrade interlocking nailing was planned as a treatment strategy. He was taken into the operating theatre within 48 h of the trauma after adequate resuscitation. The surgery was carried out under general anaesthesia, with epidural analgesia. The patient was positioned on a fracture table. The well leg was placed in hemilithotomy position in 70° flexion and 40° abduction, and it was placed on a leg holder. The patient was maintained in this position throughout the procedure. Following closed reduction of the fracture, nailing was attempted. But the failure to obtain acceptable reduction initially increased the surgical time; the intraoperative plan was changed and fixation with a dynamic condylar screw (DCS) was performed (fig. ). The total surgical time was 2 h and 30 min. There was 650 ml of blood loss and 1 unit of whole blood was transfused intraoperatively. The patient's arterial blood pressure was maintained by the anaesthetists at 94/60 mm Hg or above throughout the procedure as a preventive measure to reduce bleeding at the operative site. The intraoperative traction was released after 2 h for 5 min. When the procedure was nearing completion, a dose of epidural analgesia was given to relieve the patient of any possible postoperative pain. The patient was shifted to the ward after the completion of surgery.
In the postoperative rounds, the distal pulses of the operated extremity were palpable and any neural deficit could not be assessed as the patient was under the effect of epidural analgesia. The well leg was not examined by the surgeon and the nurse. Four hours after the end of surgery, the patient complained of severe pain in the well leg. A tense and firm swelling was found and stretch pain was present (fig. ). On physical examination, there was paraesthesia on the lateral aspect of the foot. A diagnosis of well-leg compartment syndrome was made. An urgent radiograph of the well leg was taken to exclude any bone injury which might have been missed. The radiographs revealed no bone injury, and the patient was treated with an immediate fasciotomy. A double-incision fasciotomy was performed. Vacuum-assisted closure suction was applied over the fasciotomy wound (fig. ). His wounds healed without difficulty and he regained normal strength and sensation in the lower extremity. The patient was discharged on the 20th postoperative day. The fracture united both clinically and radiologically at the 12th week. At the last follow-up at the end of 1 year, the patient had resumed his occupation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [110.0, 'kg']}",150,142.5,157.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 110.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (110.0 kg - 20 kg) = 150.0 mL/hr.
Hence, the patient's fluid maintenance is 150.0 mL/hr."
5066,22,Maintenance Fluids Calculations,physical,decimal,usmle-1957,Extracted,"Two hours after undergoing laparoscopic roux-en-Y gastric bypass surgery, a 44-year-old man complains of pain in the site of surgery and nausea. He has vomited twice in the past hour. He has hypertension, type 2 diabetes mellitus, and hypercholesterolemia. Current medications include insulin, atorvastatin, hydrochlorothiazide, acetaminophen, and prophylactic subcutaneous heparin. He drinks two to three beers daily and occasionally more on weekends. He is 177 cm (5 ft 10 in) tall and weighs 130 kg (286 lb); BMI is 41.5 kg/m2. His temperature is 37.3°C (99.1°F), pulse is 103/min, and blood pressure is 122/82 mm Hg. Examination shows five laparoscopic incisions with no erythema or discharge. The abdomen is soft and non-distended. There is slight diffuse tenderness to palpation. Bowel sounds are reduced.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [130.0, 'kg']}",170,161.5,178.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 130.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (130.0 kg - 20 kg) = 170.0 mL/hr.
Hence, the patient's fluid maintenance is 170.0 mL/hr."
5067,22,Maintenance Fluids Calculations,physical,decimal,pmc-4870949-1,Extracted,"A 13-year-old Asian girl weighing 24 kg was admitted with progressive thoracolumbar kyphoscoliosis deformity since 2 years. She underwent tracheostomy 6 years before, related to severe bronchopneumonia management. Since then, she continued to require ventilatory support at night. Genetic study confirmed PD and she was started on ERT. Her motor milestones were delayed with progressive deterioration. At admission, she was on tracheostomy and required ventilatory support during sleep with BIPAP mode. She was not able to stand and walk.
She was conscious, oriented with normal higher mental functions. She had thoracolumbar kyphoscoliosis extending from D1 to L4 level. She had wasting of the lower limb and paraspinal muscles with 3/5 motor power. She had varus deformity of the left foot, bilateral fixed flexor deformity of lower limbs. Upper limb showed normal muscle power with no wasting. On auscultation, chest was clear with no added sounds. Oxygen saturation was 95% on room air. Blood gases were within normal limits. Chest X-ray showed normal lung fields. Her cardiovascular system and electrocardiogram (ECG) were normal. Echocardiography showed normal ventricles with ejection fraction of 54% with no evidence of hypertrophy or obstructive cardiomyopathy. Serum creatinine kinase was raised. She was prepared with chest physiotherapy and salbutamol nebulisation.
General anaesthesia was planned. No pre-medication was given. Monitoring included ECG, non-invasive blood pressure, pulse oximetry (SpO2), end-tidal CO2, central venous pressure, depth of anaesthesia monitoring (Entropy͹), temperature and urine output. After adequate pre-oxygenation, anaesthesia was induced with dexmedetomidine infusion 1 μg/kg over 10 min, ketamine 50 mg and morphine 2 mg. Anaesthesia was maintained with dexmedetomidine infusion at 0.5 μg/kg/h, oxygen in air (50:50%) and sevoflurane 1-2% as required. The child remained haemodynamically stable. Body temperature was maintained around 36°C by active forced hot air blankets. Motor evoked potential (MEP) monitoring was used during correction of kyphoscoliosis. The total blood loss was about 1.1 L. Under central venous pressure monitoring, 450 ml of blood along with 2.3 L of Ringers lactate were infused. At the end of the surgery, child was conscious; breathing appeared shallow and hence was shifted to paediatric intensive care unit for elective post-operative ventilation. Post-operative pain was treated with fentanyl infusion.
On the 2nd post-operative day, she developed bilateral mild pleural effusion which was treated with diuretics and antibiotics. On the 5th post-operative day, patient was weaned off from ventilator. However, she continued to require nocturnal ventilatory support. Rest of the hospital stay was uneventful and she was discharged on the 10th day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [24.0, 'kg']}",64,60.8,67.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 24.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (24.0 kg - 20 kg) = 64.0 mL/hr.
Hence, the patient's fluid maintenance is 64.0 mL/hr."
5068,22,Maintenance Fluids Calculations,physical,decimal,pmc-5857148-5,Extracted,"This case is especially interesting. This is because a 63-year-old obese male (1.78 m, 119 kg) who was admitted to the hospital with hoarseness was examined by an ENT surgeon (indirect laryngoscopy). He was not sure whether the patient had a polyp or a tumor of the entry to larynx. Laryngoscopy was performed with the C-MAC videolaryngoscope using a standard size three blade after premedication and a topical anesthetic of the upper airway. Laryngoscopy confirmed the tumor of the vocal cords.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [119.0, 'kg']}",159,151.05,166.95,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 119.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (119.0 kg - 20 kg) = 159.0 mL/hr.
Hence, the patient's fluid maintenance is 159.0 mL/hr."
5069,22,Maintenance Fluids Calculations,physical,decimal,pmc-4967636-1,Extracted,"A 13-day-old, 3.4 kg male infant with Pierre Robin Sequence born at 39 weeks by Cesarean-section was scheduled for mandibular distractor placement due to ongoing respiratory distress with intermittent airway obstruction. The infant had to be maintained in the prone position with nasal cannula oxygen to avoid respiratory decompensation. The patient was transported to the operating room (OR) in the prone position with supplemental oxygen and a 24 G IV in place. In the OR prior to induction the infant was premedicated with 80 µg of atropine IV. The patient was placed in the lateral position and an LMA Classic™ #1 was easily inserted into the patient awake. This was well tolerated by the infant. The LMA Classic™ was then connected via a standard pediatric circle system to the anesthesia machine. The patient continued to ventilate spontaneously with an appropriate end tidal carbon dioxide (ETCO2) tracing and no physical signs of upper airway obstruction. The patient was then moved to the supine position. The fresh gas flow was set at 6 L/min of oxygen. After 1 minute of preoxygenation via the LMA Classic™, the sevoflurane vaporizer was turned to 8%. The infant continued to breathe spontaneously and after approximately 1 minute his heart rate began to decrease and spontaneous movements of his extremities ceased. At this point the patient's ventilation was assisted. Once the ability to ventilate via the LMA Classic™ was assured, rocuronium 3 mg IV was administered to facilitate placement of the Air-Q® and intubation. The sevoflurane concentration was reduced to 1.2%. The LMA Classic™ was removed and was immediately replaced with an Air-Q® 1.0. No attempt was made to mask ventilate the patient. The patient was ventilated via the Air-Q®, and adequate chest excursion and good ETCO2 were noted. A 2.8-mm inner diameter Karl-Storz FFB was loaded with a 3.5 uncuffed endotracheal tube (ETT) []. The ETT was easily placed in the trachea via the Air-Q®. The FFB was removed and the ETT adapter was replaced to confirm endotracheal placement of the ETT. Good chest excursion and ETCO2 were observed. The Air-Q® ""Pusher"" was used to hold the ETT in place as the Air-Q® was removed. The adapter was replaced and ETT was secured at 10.5 cm at the alveolar ridge. Once secured, the surgery proceeded as planned. At no time during induction or intubation was the patient difficult to ventilate, and the patient remained well saturated throughout.
The patient remained intubated following the procedure and was extubated without event 6 days later.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.4, 'kg']}",13.6,12.92,14.28,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.4 kg. Hence, the patient's maintenance fluid is 3.4 kg * 4 mL/kg/hr = 13.6 mL/hr.
Hence, the patient's fluid maintenance is 13.6 mL/hr."
5070,22,Maintenance Fluids Calculations,physical,decimal,pmc-3669543-1,Extracted,"A 2 month old female infant, weighing 3.7kg presented with history of breathlessness, feeding difficulty and cyanosis. She was a second product of non-consanguineous marriage and born by normal vaginal delivery. There was no family history of congenital heart disease. Physical examination was remarkable with evidence of pallor, cyanosis and dysmorphic facies. Her heart rate and respiratory rates were 154/min. & 60/min. respectively. Blood pressure was recorded at 75/35 mmHg and oxygen saturation 85% in room air. There was evidence of respiratory distress. All the peripheral pulses were well felt. Cardiac auscultation revealed normal first and second heart sound along with a grade 3/6 ejection systolic murmur audible best at the left upper parasternal area. The third heart sound was audible.
Chest roentgenogram revealed an enlarged heart (cardiothoracic ratio 0.6) with pulmonary plethora. The two-dimensional echocardiography, subcostal coronal views demonstrated the connection of the left-sided left atrium and the right-sided left ventricle through the mitral valve and the right-sided right atrium to be connected to the left-sided right ventricle through the tricuspid valve by anterior angulation of the transducer. It also shows the two great arteries arising from the right ventricle ().
2-D and color Doppler imaging revealed the crossing of the atrioventricular connections. Short-axis views shows the right ventricle was superior and left ventricle was inferior with horizontal position of the ventricular septum ().
The standard 4-chamber view was not showing simultaneously all four chambers and both atrioventricular valves ().
Parasternal short axis view shows malposed great arteries ().
A large size inlet type of ventricular septal defect (bidirectional shunt) and a moderate size ostium secundum atrial septal defect (bidirectional shunt) were present. Biventricular function was normal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.7, 'kg']}",14.8,14.06,15.54,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.7 kg. Hence, the patient's maintenance fluid is 3.7 kg * 4 mL/kg/hr = 14.8 mL/hr.
Hence, the patient's fluid maintenance is 14.8 mL/hr."
5071,22,Maintenance Fluids Calculations,physical,decimal,pmc-7727036-1,Extracted,"The patient was a 26-year-old Caucasian man of 74 kg with a past medical history of epilepsy with low convulsive threshold since the age of 19 and viral meningitis in childhood. His medications included levetiracetam, lamotrigine, and lacosamide. Two years earlier, an AKI episode following a GTCS was treated in another hospital. At that time, SCr reached 252 μmol/L without significant CK elevation. The uric acid level was not measured, and the SCr returned to baseline within 3 days with no clear etiology. At that time, SCr after discharge was 94 µmol/L (eGFR 97 mL/min/1.73 m2) with normal urine dipstick.
More recently, the patient was transported to the ER following a 2-minute witnessed GTCS. In the ER, second and third GTCS episodes of respectively 2- and 1-minute duration occurred, with incomplete return to baseline neurological state between episodes. His blood pressure was 123/68 mmHg and his oral temperature was 35°C. On physical examination, the patient had no sign of meningism or trauma. The cerebral scan was within normal limits. The initial laboratory workup revealed the following: severe lactate acidosis at 22.8 mmol/L (reference range: <2.4 mmol/L) with serum bicarbonate at 5.1 mmol/L (reference range: 21.0-28.0 mmol/L), elevated SCr at 134 µmol/L, serum electrolytes within normal limits and leukocytosis at 33 × 109/L (reference range: 4.0-11 × 109/L). The patient’s hemodynamic and vital parameters remained stable throughout the hospitalization. A lumbar puncture demonstrated the absence of white blood cells in the cerebrospinal fluid and bacterial culture and polymerase chain reaction (PCR) for all common viral infection of the central nervous system were negative. He was admitted to the neurology unit following a 24-hour surveillance at the ER, with a diagnosis of a resolved status epilepticus secondary to limited drug compliance and acute lack of sleep.
The SCr reached 213 µmol/L the following day and a nephrology consultation was requested for nonoliguric AKI. Common etiologies were eliminated following an adequate clinical evaluation, and renal ultrasound showing no abnormality. The fractional excretion of sodium (FENa) was 2.64% without urine dipstick anomalies. Based on these findings, no urine microscopy was performed at that time. The patient had no exposure to non-steroidal anti-inflammatory drug (NSAID) or intravenous contrast. Relevant laboratory measurements during the first 5 days of hospitalization are shown in . The first result of serum uric acid, taken 36-hour after the convulsive episode, demonstrated hyperuricemia at 782 µmol/L (reference range: 206-441 µmol/L) and a slight CK elevation, with no acidosis on blood gas at that time. The uric acid to creatinine ratio on urine was 0.57 (reference range for urate nephropathy: ≥1.0 mg/mg (13)), but was collected only at day 3 while the patient was already receiving intravenous hydration. Since the severe hyperuricemia could not be explained by a prerenal disease with increased tubular reabsorption and no other AKI etiology seemed compatible, a presumptive diagnosis of uric acid nephropathy was made.
Urine alkalinization treatment based on intravenous bicarbonate (150 mmol/L) was quickly initiated until the value of uric acid fell in the reference range. Target urinary pH was maintained ≥7.0 during treatment with urine output of 5 to 6 L/day during the first 3 days. Allopurinol was initiated at the same time. Uric acid level and kidney function rapidly improved. Noteworthily, a delayed increase in CK levels occurred 2 days after as showed in , while creatinine was already going down. Intravenous hydration was changed to 0.9% NaCl, and the flow was adjusted to obtain a urine output of ~4 L/day to prevent additional CK-induced tubulotoxicity. Due to the rapid improvement of AKI once the treatment introduced, no renal biopsy was performed to confirm the suspected etiology. The patient was discharged at day-6 with a follow up at the outpatient nephrology clinic 3 months later where the SCr was 87 µmol/L.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [74.0, 'kg']}",114,108.3,119.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 74.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (74.0 kg - 20 kg) = 114.0 mL/hr.
Hence, the patient's fluid maintenance is 114.0 mL/hr."
5072,22,Maintenance Fluids Calculations,physical,decimal,pmc-5890561-1,Extracted,"A 33-week gestation preterm male delivered through precipitous vaginal delivery in the emergency department to a 21-year-old G2P1 female presenting with acute onset of labor with rupture of membranes at home. Birth weight was 1870 g and Apgar scores were 7 at 1 min and 8 at 5 min. Due to immediate respiratory distress, the infant was intubated and mechanically ventilated. One dose of surfactant was given and he was transferred to the neonatal intensive care unit. Caffeine was administered for apnea of prematurity, and ampicillin and amikacin were initiated for concern of neonatal sepsis due to preterm labor and delivery. Within hours, the infant became hypotensive requiring normal saline boluses and a dobutamine drip, prompting an increased concern for sepsis and the addition of cefepime. However, after 3 days, blood cultures were negative, and the clinical condition had improved. Therefore, the antibiotics were discontinued.
On the day of life three, a routine cranial ultrasound was found to be normal. Echocardiogram was also normal with no structural abnormalities. The initial cranial circumference was 31 cm, and the neurological examination after resolution of hypotension was normal with no focal findings. On the day of life six, significant abdominal distention occurred with pain elicited on examination. Necrotizing enterocolitis was suspected, so empiric intravenous vancomycin and meropenem were initiated. However, pneumatosis intestinalis and portal venous gas were not observed on serial abdominal X-rays, and blood cultures never isolated a pathogen. Due to clinical severity, 2 weeks of antimicrobial treatment was given with clinical improvement and enteral feedings by nasogastric tube were started.
On the 18th day of life, the cranial circumference suddenly increased 34 cm. On examination, the anterior fontanelle was bulging, despite the child being alert and active with a normal neurological examination. Cefipime was initiated out of concern of neonatal sepsis and meningitis. Laboratory evaluation for possible sepsis found hypernatremia that was treated with an enteral sterile water drip. The ventricular puncture was performed and cerebrospinal fluid (CSF) collected. No leukocytes were seen in the CSF sample, but glucose was decreased at 20 mg/dl and protein elevated at 128 mg/dl. Cranial ultrasound revealed significant hydrocephalus with no intraventricular hemorrhage or mass seen. Magnetic resonance imaging (MRI) was performed revealing hydrocephalus [] and an apparent right frontoparietal cerebral arteriovenous malformation. MR angiography was performed and confirmed a large saccular aneurysm of the right middle cerebral artery []. Three days after collection of the CSF, Candida lusitaniae was isolated, and the blood culture identified methicillin-resistant Staphylococcus epidermidis. Antimicrobial coverage was changed from cefepime to vancomycin and amphotericin B. For a suspected large mycotic aneurysm of the right middle cerebral artery, neurosurgery was consulted. During the period of surgical consideration, the infant abruptly experienced severe apnea, hypotonia, and lethargy with aggressive attempts at resuscitation failing. Rupture of an aneurysm was the suspected cause of death due to the rapid onset of cardiovascular and neurological demise, but an autopsy was refused by the infant’s mother.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1870.0, 'g']}",7.48,7.106,7.854,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1870.0 g so this converts to 1870.0 lbs * kg/1000 g = 1.87 kg. Hence, the patient's maintenance fluid is 1.87 kg * 4 mL/kg/hr = 7.48 mL/hr.
Hence, the patient's fluid maintenance is 7.48 mL/hr."
5073,22,Maintenance Fluids Calculations,physical,decimal,pmc-3970335-1,Extracted,"A 16-year-old girl was admitted to the surgical ward for evaluation of recurrent vomiting of 3-week duration. Past medical history was noted for congenital multiple intestinal atresia and bilateral clubfeet. She had a prolonged hospitalization for multiple intestinal resections and she was on total parenteral nutrition for few months. She was followed by the pediatric gastrointestinal service and she was noticed to have failure to thrive. Her weight and height were below 3rd percentile throughout her childhood. She was on normal diet and was not compliant to her dietary supplements to increase her weight. She had normal cognitive function and attended ordinary schools. She had menarche in time. Her clubfeet, which was secondary to hereditary in nature according to the pediatrician's notes, did not interfere with her daily activities. According to the pediatrics' notes, her yearly follow-up revealed borderline iron deficiency anemia and low vitamin D levels. Her previous investigations revealed partial intestinal obstruction secondary to adhesions related to her previous intestinal surgeries.
Upon admission, she was kept nil by mouth and she was given intravenous fluids only. There was no history of confabulation or fluctuation in the level of consciousness. One week later, she developed acute diplopia, vertigo, and ataxia. Her general examination was unremarkable except for poor growth (height: 143 cm, weight: 34 kg; both were below the 5th percentile). On neurological examination, she was fully conscious oriented with normal speech and language. Cranial nerve examination revealed symmetric pupillary reaction to light and accommodation with normal fundoscopy. She had impaired bilateral horizontal gaze secondary to bilateral CN VI paresis. The rest of cranial nerve examination was unremarkable. Motor exam revealed normal tone and power but her deep tendon reflexes were diminished and planters were down-going. Sensory exam was unremarkable. Bilateral upper limb dysmetria was noted with normal gait.
Considering her prior history of poor nutrition and acute neurological presentation following recurrent vomiting, the possibility of vitamin deficiency was considered. She was given IV thiamine 200 mg once daily for a week along with injectable Vitamin B12 1000 ugm and oral folic acid 5 mg once daily. Laboratory investigations revealed Hb = 11.0/l, RBC = 3.66 × 1012/L (3.8–4.8), MCV = 90 (83–101), MCH = 30 pg (27–32), MCHC = 335 (315–345), and WBC = 8.4. Several vitamin levels were subsequently measured revealing the following results: B1 = 125 ng/mL (20–100), B2 = 231 ng/mL (75–300), B6 = 15.4 ng/mL (7–30), Vitamin C < 5.7 umol/L (> 11.4) and Vitamin D = 22 (30–75) which was measured 3 months prior to her admission. MRI brain was unremarkable. She started to improve in 48 hours. Diplopia completely resolved along with her eye movements within a week except for bilateral gaze-evoked-horizontal nystagmus. She was discharged without any neurological symptoms on oral thiamine 50 mg once a day.
Four months later, she presented to the emergency department with 2-week history of severe headache, tinnitus, bilateral hearing impairment and diplopia, which were preceded by recurrent vomiting for 10 days. There was no history of confabulation or any change in the level of consciousness. She was mildly dehydrated, afebrile and had normal ear, nose and throat examinations. There were no meningeal irritations. On neurological examination, she was fully conscious, alert and oriented to time and place. Cranial nerve examination was noted for bilateral lateral rectus paresis (secondary to bilateral CN VI palsies) and bilateral severe sensorineural deafness. Her blood parameters revealed the following: hemoglobin 14.0, RBC 4.61, MCV 88, MCH 30, MCHC 347, WBC 8.2. Serum electrolytes and renal and liver function tests were within normal limits. Urgent noncontrast CT brain showed symmetrical bilateral caudate nucleus hypodensities (). Due to her headache and bilateral subcortical lesions, the possibility of cortical venous thrombosis was considered and CT venography was ordered and it was negative. She was given IV thiamine 100 mg once daily for five days along with intensive hydration. Her headache disappeared by the next day and the tinnitus and diplopia improved within two days while deafness persisted. MRI brain revealed T2/FLAIR hyperintense signals of bilateral caudate nucleus, mamillary body, periaqueductal region and vermis (). In addition, hyperintensity of caudate nuclei in Diffusion Weighted Images (DWI) and gadolinium enhancement of vermis and maxillary bodies were noted (). Deafness persisted till her 4-month follow-up. Audiometry indicated severe bilateral hearing impairment (). A follow-up MRI 4 months later, revealed partial resolution of vermian lesion, with atrophy of mamillary body ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [34.0, 'kg']}",74,70.3,77.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 34.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (34.0 kg - 20 kg) = 74.0 mL/hr.
Hence, the patient's fluid maintenance is 74.0 mL/hr."
5074,22,Maintenance Fluids Calculations,physical,decimal,pmc-4085269-1,Extracted,"A 6-year-old girl 102 cm tall and weighing 17 kg, with chronic intestinal pseudo-obstruction was scheduled for multivisceral organ transplantation. Four-years earlier, she visited a hospital for abdominal distention and was diagnosed with gastric volvulus and congenital megacolon, for which she underwent gastropexy and segmental resection of the transverse colon. Since her symptoms did not improve over the next year, she was referred to our center and underwent a transverse colostomy. After that, she was repeatedly hospitalized and maintained on total parenteral nutrition due to continuously recurring mechanical ileus, malnutrition, and electrolyte imbalance. Two months before surgery, she was admitted due to abdominal distension and a malfunctioning colostomy. The colostomy function was normalized 2 days later, and she received conservative medical care, including total parenteral nutrition.
The patient was scheduled for multivisceral organ transplantation, including seven abdominal organs, the liver, spleen, stomach, duodenum, small bowel, colon and pancreas. Cadaveric donor was 5-year-old female 110 cm tall and weighed 21 kg, who had brain death due to increased intracranial pressure caused by medulloblastoma. Histidine-tryptophan-ketoglutarate solution was used as preservation solution and ischemic time was 170 min. Intraoperative gross finding of the grafts showed no significant abnormality. The recipient was not premedicated and arrived at the operating room with her father. Her blood pressure was 120/64 mmHg, her heart rate was 120 beats/min, and her oxygen saturation on pulse oxymetry was 100% before induction of anesthesia. Pre-operative blood laboratory data were within normal ranges, including hemoglobin (9.4 g/dl), Na+ (142 mmol/L), K+ (3.7 mmol/L), creatinine (0.34 mg/dl), aspartate transaminase (AST; 43 IU/L), alanine transaminase (ALT; 35 IU/L), total bilirubin (0.5 mg/dl), albumin (4.4 g/dl), and prothrombin time (1.00 INR). Anesthesia was induced with 75 mg of pentothal sodium, 15 mg of rocuronium, and 50 µg of fentanyl. After tracheal intubation, anesthesia was maintained with 1% sevoflurane in 50% oxygen in air and continuous infusion of fentanyl (100 µg/h) and vecuronium (2 mg/h). Her brachial artery was cannulated for continuous arterial blood pressure monitoring. A central venous catheter was inserted into her right internal jugular vein and a second into her subclavian vein to monitor central venous pressure and venous oxygen saturation. Femoral venous pressure was also monitored. Ten minutes before graft reperfusion, her vital signs and arterial gas analysis were as follows; mean arterial blood pressure (MAP) was 86 mmHg, heart rate was 90 bpm, central venous pressure was 4 mmHg, femoral venous pressure was 16 mmHg, and body temperature was 36.7℃, pH was 7.32 with a base excess of -9.5 mEq/L, arterial lactate concentration was 5.6 mmol/L, Na+ was 142 mmol/L, K+ was 2.5 mmol/L, Ca2+ was 0.83 mmol/L, hemoglobin was 10.8 g/dl, and blood glucose was 98 mg/dl.
After injection of 20 mEq of NaHCO3, graft reperfusion was performed. Just after reperfusion, MAP rapidly decreased to 39 mmHg. Femoral venous pressure decreased after IVC unclamping from 16 mmHg to 4 mmHg and central venous pressure was maintained around 4 mmHg. Because the decrease of arterial pressure was too severe to expect spontaneous recovery and met the definition of PRS (≥ 30% decrease in MAP occurring within 5 minutes after reperfusion and lasting for at least 1 minute). She was immediately administered 5 µg of epinephrine, resulting in an MAP of 44 mmHg. However, repeated injections of 10 µg epinephrine and volume replacement were required to increase her MAP due to prolonged hypotension. Hypotension was sustained over 10 minutes, during which her averaged arterial pressure was 38 mmHg despite intermittent surge of MAP > 60 mmHg (). Arterial blood gas analysis 5 minutes after reperfusion showed severe metabolic acidosis, with a arterial blood pH of 7.09 with a base excess of -17.9 mEq/L, and the arterial lactate concentration was 8.5 mmol/L, K+ was 4.8 mmol/L, Ca2+ was 0.84 mmol/L, glucose was 114 mg/dl, and hemoglobin was 8.5 g/dl. To correct metabolic acidosis and hypotension, she was immediately and repeatedly injected with 30 mEq of NaHCO3 and 10 µg of epinephrine. Her body temperature had decreased to 33.4℃ just after reperfusion, with hypothermia sustained for 30 min (nadir body temperature: 33.0℃) despite active warming with an air warmer. Subsequently, continuous infusion of norepinephrine (0.1 µg/kg/min) until the end of the operation was required to maintain her MAP within an acceptable range. At the end of surgery, her body temperature increased to 35.7℃, but metabolic acidosis was sustained despite frequent administration of NaHCO3 (arterial pH: 7.23; base excess: -10.0 mEq/L). During the surgery, the patient was infused with a total of 2,900 ml of fluid, including 1,500 ml of balanced crystalloid solution, 100 ml of half-normal saline, 300 ml of 5% dextrose water, and 1,000 ml of 5% albumin, as well as 2 units of packed red blood cells. After 9 hours of surgery, the patient was transferred to intensive care unit. Hemodynamic and laboratory changes during the operation are shown in .
After surgery, the AST and ALT concentrations of the patient increased rapidly (immediate postoperative AST 2,108 IU/L and ALT 2,351 IU/L), reaching 7,300 IU/L and 6,400 IU/L, respectively, on the second day after the operation. She required continuous infusion of fresh frozen plasma due to prolongation of prothrombin time (3.07-5.69 INR). Her total bilirubin concentration, which was 0.5 mg/dl preoperatively, increased to 3.4 mg/dl postoperatively. The patient was diagnosed with primary hepatic graft failure and scheduled for re-transplantation of the liver. An adult to child living donor liver transplantation was performed on the third day after multivisceral transplantation. During this operation, the patient's vital signs remained stable until reperfusion, including a MAP of 70-80 mmHg. Ten minutes before reperfusion, her arterial blood pH was 7.49 with a base excess of -0.1 mEq/L, arterial lactate concentration was 3.8 mmol/L, Na+ was 137 mmol/L, K+ was 3.3 mmol/L, Ca2+ was 0.97 mmol/L, hemoglobin was 8.2 g/dl, and blood glucose was 170 mg/dl. After reperfusion, PRS developed again and lasted over 1 min. She received three injections each of 4 µg epinephrine and 20 µg of phenylephrine to maintain MAP within an acceptable level. Her arterial lactate concentration was 3.1 mmol/L at pH 7.44 with a base excess of -2.2 mEq/L, Na+ concentration was 138 mmol/L, K+ was 2.9 mmol/L, Ca2+ was 1.00 mmol/L, and hemoglobin was 6.8 g/dl. After transfusion of one unit of packed red blood cells, her vital signs remained stable (MAP: 70-76 mmHg) until the end of the operation. At that time, plasma hemoglobin concentration was 11.9 g/dl, AST was 453 IU/L, ALT was 695 IU/L, total bilirubin was 3.6 mg/dl, creatinine was 0.6 mg/dl, albumin was 2.9 g/dl, and prothrombin time was 1.74 INR. Her serum AST and ALT concentrations decreased gradually. On the seventh day after liver transplantation, AST and ALT concentrations had declined to 69 IU/L and 150 IU/L, respectively, her total bilirubin was 1.4 mg/dl, prothrombin time was 1.07 INR, and feeding through gastrostomy tube was started. The patient was managed conservatively for 3 months including 50 day stay in the Intensive Care Unit and discharged in an improved condition 139 days after multivisceral transplantation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [17.0, 'kg']}",54,51.3,56.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 17.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (17.0 kg - 10 kg) = 54.0 mL/hr.
Hence, the patient's fluid maintenance is 54.0 mL/hr."
5075,22,Maintenance Fluids Calculations,physical,decimal,pmc-8662753-1,Extracted,"A 17-year-old male with UC was referred to Kyungpook National University Children's Hospital due to acute pancreatitis. He had been diagnosed with UC a year prior to admission and remission had been induced and maintained by medications including prednisolone, mesalazine, and azathioprine. All drugs were sequentially stopped in consideration of drug-induced pancreatitis; however, pancreatitis recurred with development of symptoms of mild abdominal pain and intermittent hematochezia. Family and past medical histories were unremarkable.
On admission, his vital signs were stable and within normal limits. Physical examination revealed rapid weight loss of 23 kg over 1 year. Initial laboratory tests demonstrated the following: white blood cell count 5,170/μL; hemoglobin level, 14.7 g/dL; platelet count, 251,000/μL; erythrocyte sedimentation rate (ESR), 58 mm/h; C-reactive protein (CRP) level, 0.35 mg/dL; amylase, 1,319 U/L; and lipase, 809 U/L. Fecal immunochemical testing (FIT) was positive. The fecal calprotectin (FC) level was 814 mg/kg. Other laboratory findings, including IgG, antinuclear antibody, anti-smooth muscle antibody, and anti-mitochondrial antibody, were all within the normal range. Sigmoidoscopy showed superficial ulcers and erosions confined to the rectum (). These findings were improved when compared to his initial colonoscopy at time of diagnosis which had revealed pancolitis. Abdominal computed tomography (CT) demonstrated peripancreatic fat stranding and a perisplenic pseudocyst (). Diagnostic exome sequencing of genetic mutations of CFTR, SPINK1, and PRSS1, revealed no pathological variants. No congenital abnormalities were seen on magnetic resonance cholangiopantcreatography. Methylprednisolone was started at a dose of 30 mg/day. Despite corticosteroid treatment, pancreatitis persisted and hematochezia worsened. Corticosteroids were stopped and treatment with infliximab (IFX) was started.
After the second dose of IFX infusion, mild decreases in amylase and lipase levels were seen. However, at the visit for his third IFX infusion, laboratory tests were as follows: ESR, 59 mm/h; CRP level, 0.05 mg/dL; amylase, 1,083 U/L; and lipase, 2,040 U/L. FIT was negative. The FC level was 63 mg/kg. Magnetic resonance imaging showed a focal mass-forming inflammatory lesion in the pancreatic tail (). Endoscopic ultrasound (EUS)-guided fine needle aspiration (FNA) was used to sample the pancreatic mass (). Histology revealed atypical cells. In addition, serum carbohydrate antigen (CA) 19-9 was elevated at 415.94 U/mL. Considering the possibility of pancreatic cancer, surgery was scheduled. Preoperative positron emission tomography-CT showed no abnormal uptake other than by the inflammatory pancreatic lesions. Chest CT was normal. Laparoscopic distal pancreatosplenectomy was conducted (). Histological analysis of the surgical specimen revealed chronic pancreatitis with storiform fibrosis and infiltration of IgG4-positive cells ().
After surgery, amylase and lipase levels decreased to 55 U/L and 45 U/L, respectively. Serum CA 19-9 normalized to 29.64 U/mL. The patient is currently 18 years old and is in clinical and biochemical remission on IFX at a dose of 5 mg/g at 8-week intervals for maintenance treatment of UC. No recurrence of pancreatitis has occurred at 9 months postoperatively.
This case report was approved by the Institutional Review Board of Kyungpook National University Chilgok Hospital (No. 2021-07-012). All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and national research committees and with the Helsinki Declaration (as revised in 2013). Written informed consent was obtained from the patient.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [23.0, 'kg']}",63,59.85,66.15,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 23.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (23.0 kg - 20 kg) = 63.0 mL/hr.
Hence, the patient's fluid maintenance is 63.0 mL/hr."
5076,22,Maintenance Fluids Calculations,physical,decimal,pmc-3189476-1,Extracted,"A 62-year-old male, who had been subjected to a left nephrectomy due to a traffic accident at the age of 24, was admitted for treatment of a right renal cell carcinoma, which measured 11 cm in diameter. Partial nephrectomy was performed that included 25 minutes of warm ischemic time. Histologically, the tumor was a clear cell RCC without perinephric fat or microvascular invasions.
Two years after the surgery, abdominal CT revealed para-aortic lymph node metastasis, 2.5 cm in diameter, which was confirmed histologically by CT-guided biopsy. During the two years after the partial nephrectomy, serum creatinine had increased gradually from 2.0 mg/dL to 2.9 mg/dL together with the appearance of proteinuria.
Sorafenib, 400 mg/day, was started but after only a week of administration a fever developed and sorafenib was stopped. Although he was normotensive after the cessation of sorafenib, serum creatinine increased to 3.83 mg/dL and serum albumin decreased from 1.8 g/L to 1.0 g/L. Proteinuria also worsened; the amount of urinary protein was 27.5 g/day. He became edematous and his body weight increased from 53.5 kg to 57.6 kg. Ascites and cardiac effusions also appeared.
He was diagnosed with nephrotic syndrome. With sodium restriction, supplementation of albumin, and administration of diuretics, his edema, ascites, and cardiac effusions were improved. The amount of urinary protein was also reduced to 9.4 g/day.
Renal biopsy was not performed because of the possible complications that could progress to deterioration of renal function. A retrospective review of the histology of the partial nephrectomy revealed no change in the glomeruli ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [57.6, 'kg']}",97.6,92.72,102.48,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 57.6 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (57.6 kg - 20 kg) = 97.6 mL/hr.
Hence, the patient's fluid maintenance is 97.6 mL/hr."
5077,22,Maintenance Fluids Calculations,physical,decimal,usmle-3517,Extracted,"A 58-year-old man is brought to the emergency department after a witnessed tonic-clonic seizure. His wife says he has had a persistent dry cough for 6 months. During this time period, he has also had fatigue and a 4.5-kg (10-lb) weight loss. The patient has no history of serious illness and does not take any medications. He has smoked 1 pack of cigarettes daily for 35 years. He is confused and oriented only to person. Laboratory studies show a serum sodium concentration of 119 mEq/L and glucose concentration of 102 mg/dL. An x-ray of the chest shows an irregular, poorly demarcated density at the right hilum.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.5, 'kg']}",18,17.1,18.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.5 kg. Hence, the patient's maintenance fluid is 4.5 kg * 4 mL/kg/hr = 18.0 mL/hr.
Hence, the patient's fluid maintenance is 18.0 mL/hr."
5078,22,Maintenance Fluids Calculations,physical,decimal,pmc-2876702-1,Extracted,"A 14-year-old boy was referred with history of dry cough, dyspnea, and fever of three months' duration, with seizure disorder since the age of two years. He also had delayed developmental milestones and poor scholastic performance. Physical examination revealed height and weight of 147 cm and 47 kg, respectively, which were below 5 percentile for his age. There was presence of gynacomastia. Vital parameters were within normal limits. Respiratory examination showed bulging of the chest wall with decreased breath sounds all over the right hemithorax. On further examination, a testicular swelling was noted.
Investigations showed hemoglobin - 10.6 g/dL, white blood count - 12600/μL, blood urea nitrogen- 10 mg%, Lactate dehydrogenase (LDH) – 827IU/L; human immunodeficiency virus (HIV) was nonreactive. Chest X-ray showed anterosuperior mediastinal mass []. Ultrasonography (USG) showed large hypo-echoic mass with anechoic areas within it. On computed tomography (CT) of thorax, there was inhomogeneously enhancing mass lesion 31-36 HU and 95 HU on contrast study [], almost involving the entire right lung, with relative sparing of the apex, extending into the prevascular space and partially compressing the right main bronchus. Ultrasonography of scrotum showed left testis measuring 2.5 × 1.7 × 0.7 cm with 6 × 6 mm well-defined hypo-echoic lesion with specks of calcification in the wall. Right testis measured 2.2 × 1.6 × 0.9 cm with few specks of calcification. Fine-needle aspiration biopsy of the mediastinal mass showed malignant cells with large nuclei and high nucleo-cytoplasmic ratio and hyperchromatic nuclei, suggestive of nonseminomatous germ cell tumor [Figures and ]. Human chorionic gonadotropin (HCG) hormone and alfa fetoproteins (AFPs) were 1.65 mIU/ mL and 6553.94 ng/mL, respectively. Intelligence quotient analysis score was 70, suggestive of mild mental retardation. He was subsequently investigated for history of seizure disorder, delayed developmental milestones, poor scholastic performance, mental retardation, and gynacomastia. Electroencephalogram showed normal wave pattern. Chromosomal analysis done using GTG-banding technique using Giemsa showed cytogenic profile of 3 sex chromosomes and 44 autosomes, with karyotype 47 XXY in all metaphases studied, suggestive of Klinefelter syndrome. The patient expired after five cycles of chemotherapy with bleomycin, cisplatin, etoposide.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [47.0, 'kg']}",87,82.65,91.35,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 47.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (47.0 kg - 20 kg) = 87.0 mL/hr.
Hence, the patient's fluid maintenance is 87.0 mL/hr."
5079,22,Maintenance Fluids Calculations,physical,decimal,pmc-4976162-1,Extracted,"Patient's written consent was obtained and any information, including illustrations, was anonymized as far as possible.
A 32-year-old male patient having 180 cm height and 75 kg weight (BMI 23.1) presented to the Emergency Department (ED) of General Hospital of Filiates complaining from a gunshot penetrating injury at left lower anterior abdominal wall.
The patients vital signs were BP 120/80 mm, Hg HR 80/min, and Glasgow Coma Scale (GCS) 15/15. On clinical examination 1 cm diameter entry wound was revealed at the left lower abdominal wall. There was no exit wound. On palpation the abdomen was soft with mild tenderness. The Complete Blood Count (CBC) and urinalysis were normal. Abdominal X-rays showed the bullet in the pelvic cavity (Figures and ). Chest X-ray did not show free air under the diaphragm. After these examinations, abdominal CT scan was scheduled to identify any serious damage. The CT scan identified the bullet lying in the peritoneal-pelvic cavity and intraperitoneal and retroperitoneal visceral structures were identified to be normal with no injury ().
After conservative treatment and vital signs follow-up for the first 24 hours and series of clinical examinations, an EL was scheduled. EL identified the bullet in the peritoneal cavity, with no other damages. Finally, the bullet was removed laparoscopically (). The patient remained for 24 hours in the surgical department and was discharged from hospital in good conditions.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [75.0, 'kg']}",115,109.25,120.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 75.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (75.0 kg - 20 kg) = 115.0 mL/hr.
Hence, the patient's fluid maintenance is 115.0 mL/hr."
5080,22,Maintenance Fluids Calculations,physical,decimal,pmc-7329962-2,Extracted,"Case 2: a 65-year-old female (153 cm, 39 kg) was diagnosed with recurrence of esophageal cancer and metastasis of lung and bone. She was receiving intravenous oxycodone which was gradually increased for 18 days to 4.5 mg/h for her pain due to metastasis of her right sacral bone. Femoral trochanteric fracture was diagnosed after tumbling on the floor and she was planned for intramedullary nailing. As her preoperative chest x-ray revealed narrowing of the trachea due to lung metastasis (Fig. a), regional anesthesia with spinal anesthesia was selected. Isobaric 0.5% bupivacaine 2 ml completely treated her pain due to both fracture and bone metastasis (no record of anesthesia level). Oxycodone was continued during the surgery (surgery time, 1 h 48 min) and continuous RR and end-tidal CO2 monitoring was applied in accordance with the standard monitoring of ECG, SpO2, and BP. No respiratory event was recorded throughout the surgery (Fig. b) with average RR of 18 ± 6/min.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [39.0, 'kg']}",79,75.05,82.95,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 39.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (39.0 kg - 20 kg) = 79.0 mL/hr.
Hence, the patient's fluid maintenance is 79.0 mL/hr."
5081,22,Maintenance Fluids Calculations,physical,decimal,pmc-8527088-1,Extracted,"A 1.5-month-old girl was admitted to our hospital due to persistent diarrhea and failure to thrive. She was the only child of her non-consanguineous parents without any familial history of diarrhea. She had experienced no recurrent infections before. She was born at 39 gestational weeks. Her birth height was 48 cm (10th percentile), and her birth weight was 2.5 kg (below the 3rd percentile) (intrauterine growth retardation). She received mixed feeding (regular formula and breast milk) at birth but was stunted at 1.5 months of age (height, 50 cm, below the 3rd percentile; weight, 3.16 kg, below the 3rd percentile) (). She had non-bloody watery stools seven to eight times a day and poor weight gain since birth. Deep hydrolysis formula and amino-acid formula were administered after diagnosis of allergy to cow-milk protein. However, her condition did not improve.
Physical examination showed that the infant was weak and displayed a severe loss of subcutaneous fat. Her hair was short and sparse (woolly and brittle) (). No abnormalities were observed on the skin. Normal results were shown in all laboratory and imagological examinations.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.16, 'kg']}",12.64,12.008,13.272,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.16 kg. Hence, the patient's maintenance fluid is 3.16 kg * 4 mL/kg/hr = 12.64 mL/hr.
Hence, the patient's fluid maintenance is 12.64 mL/hr."
5082,22,Maintenance Fluids Calculations,physical,decimal,pmc-5605339-1,Extracted,"A 54-year-old female presented to the emergency department with intermittent dysphagia and a 60-pound weight loss within a 3-mo period. The patient denied any complaints of nausea or vomiting. Computerized tomography (CT) (Figure ) of the abdomen revealed a mass in the head of the pancreas, a dilated common bile duct, and a dilated pancreatic duct. Her past surgical history included a total hysterectomy and bilateral tubal ligation. There was no family history to suggest a genetic hereditary disease. Laboratory tests showed mild elevation of transaminases, significant elevation of alkaline phosphatase and direct hyperbilirubinemia, indicating obstructive jaundice. Carbohydrate antigen 19-9 was elevated (380 IU/mL) and carcinoembryonic antigen was unremarkable. Endoscopic retrograde cholangiopancreatography (ERCP) showed a large 2.5 cm irregular, ill-defined mass at the head of the pancreas causing complete bile and pancreatic duct obstruction. Endoscopic ultrasound (EUS) (Figure ) showed a 2.5 cm × 2.2 cm hypoechoic mass in the head of the pancreas causing extrahepatic biliary obstruction and pancreatic ductal dilation. Marked edematous and inflammatory changes were noted around this area. A fine needle aspiration of the pancreatic mass showed predominantly fibrotic, bland spindle cells with scattered normal skeletal muscle components. Immunohistochemical stains for CD117, CD34, and Pancytokeratin were negative. No pancreatic epithelial elements or significant inflammatory infiltrates were noted. Surgery was recommended on the suspicion of a reactive fibroinflammatory pseudotumor. However, surgery was deferred due to underlying pancreatitis.
Two months after the emergency department admission, she underwent a new abdominal CT scan, which showed an enlarging of 5.2 cm × 4.2 cm in the pancreatic head. This had not changed significantly on a repeat CT scan after seven weeks. A repeat EUS guided fine needle aspiration was performed due to high suspicion of malignancy. Cytological examination was again negative for epithelial malignancy. Four months after initial presentation, the patient underwent a Whipple procedure with end-to-end pancreaticojejunostomy, cholecystectomy, an end-to-side choledochojejunostomy, a wedge liver biopsy of segment 3, a biopsy of the superior pancreatic lymph node, and a retrocolic end-to-end gastrojejunostomy. The procedure was successful, and a feeding jejunal tube was placed. On pathologic microscopic examination, the surgical margins of the liver and lymph node biopsies were negative for a tumor. The pancreatic head lesion showed typical features of DTF. A poorly circumscribed uniform fascicular spindle cell proliferation infiltrates the pancreatic parenchyma among remnants of normal pancreatic epithelial structures (Figure ). The spindled myofibroblasts exhibit low cellularity and bland cytology (no atypia, no mitosis) with scattered keloid-like collagen and minimal inflammation within a collagenous stroma (Figure ). Immunohistochemistry demonstrated positive Vimentin (mesenchymal marker) and Actin (focal, patchy, myofibroblast marker). Markers for myogenic cells (Desmin), stromal cells (CD117, CD34), neural cells (S-100) and epithelial cells (Pancytokeratin) were all negative. An initial pathologic impression of inflammatory myofibroblastic tumor was made after an additional immunohistochemical stain for ALK-1 was interpreted as showing “staining of spindle cells within the lesion”. However, further consultative review (Gerardo G Vergara) disclosed histologic features more consistent with DTF and the ALK-1 immunostain (faint, patchy staining of spindle cells) was essentially negative. An additional immunostain for Beta-catenin was diffusely nuclear positive (Figure ), supportive and diagnostic of DTF.
Inflammatory Myofibroblastic Tumor exhibits more cellularity, cellular atypia, more inflammation, and ALK-1 positivity. In reactive fibroblastic/myofibroblastic proliferative lesion, cells are cytologically indistinguishable but architecturally different from fibromatosis and are B-catenin negative. The final diagnosis was therefore changed to DTF.
Recognizing and distinguishing between these lesions are clinically important due to different prognostic and treatment implications, which is key in our case. The patient received no additional therapy after surgery. The patient’s liver function tests normalized within nine days after surgery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.0, 'lbs']}",67.21552,63.85474,70.5763,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.0 lbs so this converts to 60.0 lbs * 0.453592 kg/lbs = 27.21552 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (27.21552 kg - 20 kg) = 67.21552 mL/hr.
Hence, the patient's fluid maintenance is 67.21552 mL/hr."
5083,22,Maintenance Fluids Calculations,physical,decimal,pmc-7064856-1,Extracted,"The patient is a 49-year-old male, with height 161 cm, weight 85 kg, and a history of preterm birth at gestational week 34 from nonconsanguineous parents, congenital anisocoria, developmental delay, hypoacusis, and tetra-ataxia (). During childhood general downslowing, chronic fatigue, and sicca syndrome of the eyes occurred. He repeatedly experienced respiratory infections and oral herpetic infections and once painless desquamation of the hands and foot soles (). He was successfully trained and worked as a hairdresser until the age of 38 years in his parent's hair saloon and retired at the age of 40 years.
At age of 30 years, left anterior hemiblock and right bundle-branch-block were recorded. Since age 35, recurrent mild elevation of creatine-kinase (CK) was noted. Aldolase and myoglobin were also elevated. Since age 35, recurrent electrolyte disturbances (hypokalemia and hyponatremia) and hyperuricemia developed. At age 36, he experienced a first episode of disorientation, impaired cognition, bradyphrenia, and secessus urinae. Clinical exam revealed bilateral ophthalmoparesis and dysarthria. Magnetic resonance imaging (MRI) showed subcortical hyperintensities in a nonvascular distribution, which were hyperintens on diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) (). Neuropsychological testing revealed attention deficits, disability of encoding visual contents, adjustment disorder, and depression. The patient was diagnosed with suspected Bickerstaff encephalitis and questionable seizures. Following these episodes, his gait became disturbed with occasional falls due to increased ataxia. At age 37, he experienced an untriggered rhabdomyolysis. Muscle biopsy from the deltoid muscle suggested muscular dystrophy as only fat but no muscle tissue was detected (). At age 38, he underwent a second muscle biopsy from the left lateral vastus muscle which showed cytochrome-C-oxidase (COX)-negative fibers (), glycogen depositions (), fiber splitting, and ragged-red fibers (). Electron microscopy showed abnormally shaped and structured mitochondria, megaconia, abnormal glycogen and lipid depositions, and dark bodies (Figures and ). At age 44, migraine developed. At age 47, he underwent cataract surgery bilaterally (). At age 49, diabetes was diagnosed. Transthoracic echocardiography was normal except for mild enlargement of the ascending aorta ().
The family history was positive for hypotonia (mother), diabetes (father, brother of father, grandmother from the father's side, grand-grandfather from the father's side), carcinoma (father), and stroke (father). Neurological exam at age 49, revealed short stature, microcephaly, facial dysmorphism, myopathic face, ophthalmoparesis, pupils nonreactive to light, anisocoria (left: 5 mm, right: 3 mm, unrounded), divergence of bulbs, ophthalmoparesis (abduction right bulb 60° abduction left bulb: 15° vertical movements impossible), bilateral ptosis (right > left), reduced corneal reflexes, hypoacusis requiring bilateral hearing devices, dysarthria, dropped head, weakness for right elbow extension and flexion, reduced tendon reflexes on the upper limbs, ataxia and brady-dysdiadochokinesia on the upper limbs, marked wasting of the thighs, ataxia on the lower limbs, truncal ataxia, and ataxic stance, and gait. Gnome calves bilaterally, which were described at age 38 were no longer present. The last medication included indapamide, furosemide/spironolactone, simvastatin, NaCl, KCl, coenzyme-Q (60 mg/d), and vitamin-D.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [85.0, 'kg']}",125,118.75,131.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 85.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (85.0 kg - 20 kg) = 125.0 mL/hr.
Hence, the patient's fluid maintenance is 125.0 mL/hr."
5084,22,Maintenance Fluids Calculations,physical,decimal,pmc-8048214-1,Extracted,"A 28 months-old boy presented to our emergency department for evaluation of recurrent upper airway infections in the six weeks prior to admission, non-icteric pruritus, and progressive tiredness. He refused to walk although he was described to have been an active child before. He had lost more than 10% of his body weight within 2.5 months. Body weight at presentation was 10.3 kg (5th percentile). Previous history included a heminephrectomy at age 5 months due to a double kidney. The surgery had to be postponed due to a pathologic prothrombin time. As this responded well to a single dose of vitamin K no further evaluation was initiated. Family history was unremarkable.
On clinical examination, hepatomegaly without splenomegaly was noted. The skin was pale; he showed no signs of dehydration and no signs of pathologic coagulation. Clinical examination was normal otherwise. Laboratory parameters at presentation are shown in Table . The patient was admitted for further diagnostics and therapy. Infectious causes including CMV, EBV, HSV, hepatitis A-C, and HIV were excluded serologically. Acute phase proteins were normal. No evidence for alpha 1-antitrypsin deficiency, autoimmune hepatitis, or Wilson’s disease was found. Celiac disease was excluded by serological testing. A sweat test yielded no result as the child did not sweat. Vitamin K concentration in serum was again decreased (Table ), as were other fat-soluble vitamins. Supplementation of vitamin K and other fat-soluble vitamins was started.
After admission, severe hypoglycemia (minimum 1.4 mmol/L) was noted. Due to the combination of hepatomegaly, dystrophy and fasting hypoglycemia with only mildly elevated lactate and no cardiac or muscular involvement, a glycogen storage disorder was suspected. A broad metabolic work-up was initiated: Glycogen storage disorders III and IX were excluded. Acid lysosomal lipase activity, a marker for Wolman disease, was within normal ranges. Tyrosinemia type 1 was excluded. Total cholesterol was reduced (Table ) but a defect of the cholesterol biosynthesis (Smith-Lemli-Opitz syndrome) could be excluded. We performed an isotransferrin electrophoresis to check for congenital disorders of glycosylation. The result was inconclusive, further investigations were initiated and finally, a congenital disorder of glycosylation was ruled out. Hypoglycemia recurred and a diet with frequent carbohydrate-rich meals during the day was initiated. To prevent fasting hypoglycemia, the child was given several doses of uncooked corn starch during the day and at night via nasogastric tube. Hypoglycemia could be controlled and the patient was discharged.
Four weeks later, the patient was admitted with bacterial pneumonia. The parents reported recurrent soft and fatty stools. Elastase was tested in three separate stool samples and was markedly reduced to less than 15 U/L. Sweat test was repeated and showed a markedly increased sweat chloride concentration of 87 mmol/L, which was confirmed by a second sweat test (Cl− 94 mmol/L). Genetic analysis revealed Phe508del (c.1521_1523delCTT) and Arg1066Cys (c.3196C > T) mutations in the CFTR gene, confirming the diagnosis of cystic fibrosis.
Appropriate therapy with supplementation of pancreas enzymes, inhalation therapy, and physiotherapy was initiated, and vitamin supplementation was continued. Under this regimen appropriate weight gain could be recorded (see Fig. ). Morning fasting blood glucose normalized and nocturnal corn starch supplementation could be stopped after four months of therapy. Since then, the patient had one pneumonia, treated with oral antibiotics, but otherwise an unremarkable course. Lung function at age 6 years was normal with a Forced Expiratory Volume in 1 s (FEV-1) of 104.4 predicted. Transaminases have been in the normal range for almost five years and hepatomegaly resolved slowly over 9 months.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.3, 'kg']}",40.6,38.57,42.63,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.3 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.3 kg - 10 kg) = 40.6 mL/hr.
Hence, the patient's fluid maintenance is 40.6 mL/hr."
5085,22,Maintenance Fluids Calculations,physical,decimal,pmc-6903892-1,Extracted,"A 19-year-old female was in her usual state of health until she developed sudden-onset nausea, vomiting, and abdominal pain. She had been unable to tolerate any oral intake without emesis. She subsequently sought treatment at an outside facility emergency department. Her history was notable for bipolar disorder and a 61 lb (27.7 kg) weight loss in the past year with about 30 lb (13.6 kg) lost in the prior month. Physical examination was notable for tachycardia at 105 beats per minute, a body mass index (BMI) of 19.05 kg/m2, and generalized abdominal tenderness. Initial laboratory evaluation revealed an elevated white blood cell count (WBC) at 18,600 per µL (normal limit: 4,000-11,000 per µL) with 16,400 per µL neutrophils (normal limit: 1,800-8,000 per µL) and a urine drug screen positive for methamphetamines, marijuana, and MDMA. A urinalysis was negative for nitrites or leukocyte esterase. Despite meeting systemic inflammatory response syndrome/sepsis criteria at this time, she did not receive further work-up or antibiotic treatment. She was given intravenous (IV) fluids and ondansetron with alleviation of her symptoms and tolerance of oral intake. She was subsequently discharged home.
She returned to the emergency department the following day with a recurrence of postprandial nausea, vomiting, and severe abdominal pain. She was again unable to tolerate any oral intake without emesis. Physical examination demonstrated a BMI of 18.03 kg/m2, decreased bowel sounds, and diffuse abdominal tenderness. She was given IV fluids and ondansetron with fentanyl for pain control. Repeat laboratory work was significant for an elevated WBC of 26,500 per µL. A lactic acid was normal at 1.0 mmol/L (normal limit: 0.4-2.0 mmol/L). Blood cultures were obtained, and a one-time dose of ceftriaxone was subsequently administered. A computed tomography (CT) scan of the abdomen and pelvis with intravenous contrast was obtained to assess possible intussusception as she was unable to tolerate any oral contrast.
CT revealed a severely distended stomach and proximal duodenum with air-fluid levels and a transition point from dilated to decompressed duodenum at the midline as the third portion of the duodenum passed inferior to the SMA (Figures , ). The aortomesenteric angle measured 8 degrees (normal limit: 38-65 degrees) with an aortomesenteric distance of 6.0 mm (normal limit: 10-28 mm) which was consistent with SMA syndrome (Figure ).
She was transferred and admitted to the hospital for nasogastric decompression, fluid, and electrolyte support. The patient admitted to restrictive eating behavior in the months prior in addition to methamphetamine use for weight loss that psychiatry felt was consistent with anorexia nervosa. Gastroenterology performed an esophagogastroduodenoscopy, which revealed a dilated deformity of the first, second, and third portions of the duodenum. The fourth portion of the duodenum required abdominal pressure to advance the scope but was otherwise normal. Her symptoms began to improve throughout her hospital stay. On day 4 of her hospitalization, the nasogastric tube was discontinued, and her diet advanced as tolerated without return of her symptoms. She was discharged with close primary care and psychiatric follow-up. She returned to clinic one week after discharge and had already gained 5 lb (2.3 kg).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.3, 'kg']}",9.2,8.74,9.66,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.3 kg. Hence, the patient's maintenance fluid is 2.3 kg * 4 mL/kg/hr = 9.2 mL/hr.
Hence, the patient's fluid maintenance is 9.2 mL/hr."
5086,22,Maintenance Fluids Calculations,physical,decimal,pmc-6411848-1,Extracted,"The 3rd patient of the family (IV:4) is a 10 years old boy who has had similar clinical course and manifestations as his two older cousins. Presently, his height is 111 cm (Z-score -3.7) and weight 33 kg (Z-score -0.4). Delayed milestones and multiple compression fractures were apparent at the age of 9 months. His first femoral fracture occurred at the age of 18 months and generalized osteopenia was observed; multiple other fractures have occurred thereafter. Physical evaluation revealed a low posterior hairline, short and webbed neck, low set ears, shield chest, long fingers and toes. Sclerae and teeth were normal. Radiographs revealed moderate thoracic kyphosis and platyspondyly. He started intravenous pamidronate treatment at the age of 3 years which improved the compression fractures but did not completely prevent new fractures. Along with skeletal problems he was also diagnosed with hearing loss and visual impairment at the age of 5 years. He was operated on for bilateral cataract. Learning difficulties were observed since early childhood. Blood biochemistry for calcium, alkaline phosphatase, creatinine and 25-OH-vitamin D was normal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [33.0, 'kg']}",73,69.35,76.65,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 33.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (33.0 kg - 20 kg) = 73.0 mL/hr.
Hence, the patient's fluid maintenance is 73.0 mL/hr."
5087,22,Maintenance Fluids Calculations,physical,decimal,pmc-4027082-1,Extracted,"A 13-year-old boy presented with sudden palsy of the left side of the face. Prednisolone (60 mg/day) and acyclovir (800 mg/day) were prescribed, however, the patient's facial palsy did not improve completely as we expected it was Bell palsy. He appeared lethargic and pale, and his parents suspected he had gained weight over the past two years. They also suspected his chronic fatigue was due to the weight gain.
The patient had no history of a viral infection, exposure to high levels of iodide or any medication. He was born at term weighing 3,500 g by spontaneous vaginal delivery without complication, and is the first child of unrelated parents. He also had no family history of any autoimmune or thyroid disease. His father's height was 176 cm. Mother's height was 155 cm, The mid parental height was 172 cm. His blood pressure was 100/60 mmHg, and ha had pulse rate of 70 beats/min.
Upon physical examination, he was found to be myxedematous with coarse facial features including dry and thickened skin. However, no goiter was found. His weight, height, and body mass index (BMI) were 68.5 kg (90-95 percentile), 155 cm (50th percentile), and 28.5 kg/m2 (>97th percentile), respectively. Pubertal development was also noted (penis, Tanner stage 2-3; pubic hair, Tanner stage 1; testis, 6-8 mL). Ophthalmological examinations, including a visual field test, revealed no abnormal findings.
Laboratory data revealed normocytic normochromic anemia (hemoglobin, 10.3 g/dL), and increased aspartate transaminase (68 IU/L), and alanine transaminase (139 IU/L), hypercholesteremia (total cholesterol, 378 mg/dL), hypertriglycemia (409 mg/dL), and increased creatine kinase (912.2 IU/L) levels (). Endocrinological testing showed severe primary hypothyroidism, elevated thyroid stimulating hormone level (TSH>100 µIU/mL) (normal range, 0.5 to 4.8 µIU/mL), decreased total thyroxine level (1.04 µg/dL) (4.5 to 12.0 µg/dL), decreased total triiodothyronine level (0.31 ng/mL) (1.19 to 2.18 ng/mL) and decreased free thyroxine level (0.07 ng/dL) (0.8 to 2.3 ng/dL), In addition, elevated levels of serum antithyroid peroxidase antibodies (1,933.39 IU/mL) (<10 IU/mL), antithyroglobulin antibodes (848.16 IU/mL) (<100 IU/mL), and TSH receptor antibodies (immunoassay>40 IU/L) (0.3 to 1.22 IU/L) were found. The results of the bioassay were negative for TSH receptor stimulating antibodies ().
Additional results of the laboratory analysis are as follows: prolactin, 29.04 ng/mL (3 to 18 ng/mL); morning serum cortisol, 6.69 µg/dL (3 to 21 µg/dL); adrenocorticotropic hormone, 20.31 pg/mL (10 to 60 pg/mL); growth hormone, 0.08 ng/mL (0.07 to 5.68 ng/mL); insulin like growth factor-I (IGF-I), 105.0 ng/mL (145.2 to 647.8 ng/mL); IGF binding protein-3 (IGFBP-3), 3,270 ng/mL (2,200 to 4,490 ng/mL); luteinizing hormone, 1.32 mIU/mL (0.2 to 4.9 mIU/mL); follicle stimulating hormone, 4.29 mIU/mL (1.8 to 3.2 mIU/mL); and testosterone, 0.2 ng/mL (0.18 to 1.5 ng/mL) (). According to the Greulich-Pyle method, bone age was 12.5 years (chronological age, 13 years). Thyroid sonography revealed a heterogenous internal structure; neither the size nor the vascularity of the bilateral gland was increased (). Thyroid scintigraphy with 99mTc revealed a substantially decreased uptake in both lobes (). Magnetic resonance images displayed an enlarged pituitary gland, with upward convexity, measuring 13.0 mm in height and a transverse diameter of 8 mm ().
After L-thyroxin treatment was initiated, the symptoms of facial palsy and the patient's clinical condition improved (, ). After 3 months, the second magnetic resonance images revealed a regression of the pituitary hyperplasia and a smaller pituitary gland than that from the first round of images. This condition was described as reactive hyperplasia caused by primary hypothyroidism. After 8 months, follow-up thyroid sonography revealed that the parenchymal echogenicity was coarse, and had decreased in size. However, changes to the size or echogenicity of the thyroid gland were not significant.
After 1 year, the patient's height was 166.2 cm (50-75th percentile), which is an 11 cm gain in height and his weight was 66 kg (75-90th percentile). His BMI also improved to 23.9 kg/m2 (75-85th percentile). Bone age was 14.5 years with the chronological age of 14 years. He was performing well academically.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [68.5, 'kg']}",108.5,103.075,113.925,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 68.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (68.5 kg - 20 kg) = 108.5 mL/hr.
Hence, the patient's fluid maintenance is 108.5 mL/hr."
5088,22,Maintenance Fluids Calculations,physical,decimal,pmc-5337861-1,Extracted,"Our patient is a 58-year-old Caucasian man weighing 92.9 kg, 175 cm tall, with a history of type 1 DM who presented for repair of a hip labral tear. His past medical history was significant for obstructive sleep apnea (OSA), gastroesophageal reflux disease, bicuspid aortic valve, bipolar disorder, obsessive-compulsive disorder, and cataracts. His only prior anesthetic exposure was for cataract surgery and he had no complications. However, the patient's daughter, who also had DM, experienced severe respiratory depression following general anesthesia, requiring intensive care unit (ICU) admission postoperatively. Primary considerations in relation to anesthesia include the disease's association with cardiomyopathy and cardiac conduction abnormalities, sensitivity to respiratory depression and ventilatory weakness, prolonged gastric emptying, and myoclonus triggered by stimuli such as hypothermia and specific medications.
Following the application of standard ASA monitors, a combined spinal and epidural anesthetic technique was performed successfully. Fifteen mg of isobaric bupivacaine was injected into the subarachnoid space at the L4-L5 interspace and an epidural catheter was inserted immediately. The spinal level was tested and found to be at a T10 dermatomal level. External pacer/defibrillator pads were applied and an arterial line was used for continuous blood pressure monitoring and to facilitate arterial blood gas measurements in the event of pulmonary compromise. A thermometer was placed in the patient's axilla for continuous monitoring. The operating room's ambient temperature was increased, a forced-air warming blanket was applied to the patient, and a fluid warmer was connected to his intravenous line. Intraoperatively, the patient received small (0.5 to 1 mg) boluses of midazolam titrated for a Richmond Agitation-Sedation Scale (RASS) of −3. For the 3 hour and 43 minute procedure, the patient received a total of 10 mg of midazolam and 50 mcg of fentanyl. Forty-five minutes into the surgical procedure the surgeon requested further relaxation of the patient's hip muscles and the epidural catheter was subsequently bolused with 5 mL of 2% lidocaine. Two hours into the procedure, another 5 mL of 2% lidocaine was bolused into the epidural. No complications were noted in the intraoperative period. The patient was transported to the postanesthesia care unit (PACU) with continuous SpO2, ECG, and blood pressure monitoring. A written consent was obtained from the patient for this case report.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [92.9, 'kg']}",132.9,126.255,139.545,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 92.9 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (92.9 kg - 20 kg) = 132.9 mL/hr.
Hence, the patient's fluid maintenance is 132.9 mL/hr."
5089,22,Maintenance Fluids Calculations,physical,decimal,pmc-4623346-1,Extracted,"A 10-year-and-4-month-old boy (height 150 cm, 75-95 percentile, weight 67 kg, >97 percentile) was admitted to the intensive care unit via the emergency center with a chief complaint of mental change after one episode of generalized tonic-clonic seizure.
Prior medical history revealed that the patient had had one suspicious episode of seizure 6 years before, and had received an evaluation including blood tests, brain computed tomography (CT) scanning and electroencephalogram (EEG). All of the results were normal except for a subtle abnormality in the EEG, which was considered clinically insignificant. He had shown no more suspicious seizure events since that time without medication. He has been diagnosed with intellectual disability (intelligence quotient score of 44) and attention deficit hyperactivity disorder (ADHD) in a local psychiatric clinic. Medications included methylphenidate, atomoxetine, aripiprazole, fluvoxamine, benztropine, and topiramate on a daily basis. There was not any notable family history.
The physical examination revealed that the patient was in a comatose state, not responding to any noxious stimuli. Pupils were fixed and equal with a diameter of 5 mm each. Lung sounds were decreased on auscultation and the heart examination was normal. The abdomen was soft and not distended, and hypoactive bowel sounds were present. Rectal examination revealed hypotonic sphincter tone. Admission vital signs were as follows: pulse of 75 beats per minute, abnormally high blood pressure of 167/118 mmHg, respirations of 22 per minute, and temperature of 36.2℃.
Initial chest x-ray and chest CT scan showed findings compatible with pulmonary edema, and brain CT scan revealed severe brain swelling. Brain magnetic resonance imaging (MRI) showed severe brain swelling with tonsillar and uncal herniation ().
Although the laboratory findings 3 months prior to admission, performed when he visited our emergency center due to cervical lymphadenopathy, showed no abnormal findings, on the admission day, severe hypo-osmolar hyponatremia (serum Na, 101 mmol/L [basal reference values {BRV}, 135-145 mmol/L]; serum osmolality, 215 mOsm/kg [BRV, 289-308 mOsm/kg]) was found on the initial laboratory examination, along with low urine osmolality and low spot urinary sodium concentration (urine osmolality, 108 mOsm/kg [BRV, 50-1,200 mOsm/kg]; urine Na, 19 mmol/L). Serum glucose, total protein, albumin, blood urea nitrogen, and creatinine levels were all within normal range. The plasma adrenocorticotropin level was slightly low (5.54 pg/mL [BRV, 7.2-63.3 pg/mL]), while the serum cortisol level was in the normal range (12.5 µg/dL [BRV, 6.7-22.6 µg/dL]). Thyroid hormones were in the normal range (T3, 0.67 ng/mL [BRV, 0.58-1.59 ng/mL]; free T4, 0.97 ng/dL [BRV, 0.7-1.48 ng/dL]; thyroid-stimulating hormone, 2.97 µIU/mL [BRV, 0.35-4.94 µIU/mL]). The antidiuretic hormone (ADH) level was mildly elevated (13.34 pg/mL [BRV, 0-6.7 pg/mL]).
Shortly after admission, the patient experienced respiratory arrest. Endotracheal intubation was immediately done, and the patient was put on mechanical ventilation. After intubation, his blood pressure fell to 64/39 mmHg, and intravenous inotropics were administered. During the first 3 hours after admission, the patient showed polyuria with urination of 700 mL in 3 hours. After 3 hours, however, oliguria developed with sudden decrease in urination to 30 mL/hr even though diuretics were administered. The patient was put on continuous renal replacement therapy (CRRT) using continuous veno-venous hemodialysis.
After acute management, further past history was taken from the patient's mother, and it was revealed that for several months prior to admission, he had suffered from worsening of inattention, impulsivity, and hyperactivity, which led to him dropping out of school in the prior month. He also had difficulty controlling impulsive eating, and ate one type of food in excessive amounts for a period time. For example, he ate a lot of toothpaste for a while, and there was also a period of time when he ate a lot of soap. Since around 2 to 3 months prior to the event, his mother noticed that the patient drank excessive amounts of water, even drinking water directly from the shower tap, but she had not yet reported this change to the psychiatrist. The polydipsia had become worse in the previous few days, resulting in water regurgitation from his stomach when he lay down, as well as frequent bed-wetting.
Together with the patient's history and laboratory results, we concluded that the patient was in hypotonic hyponatremia due to psychogenic polydipsia.
For the treatment of brain edema, intravenous mannitol was administered. For hyponatremia, increment of serum sodium concentration was done by administration of hypertonic saline solution and intravenous furosemide, and fluid restriction. Using 3% sodium chloride fluid and normal saline solution together, 5.5 mEq/kg of sodium was first administered, and the sodium concentration of the fluid and fluid balance target were continuously adjusted according to the patient's serum electrolytes that were measured every 2 to 4 hours. The patient's serum sodium level had increased from 101 to 108 mmol/L by 8 hours after admission, and the subsequent serum sodium concentration were 110 mmol/L at 24 hours after admission, 117 mmol/L at 48 hours after admission, 127 mmol/L at 72 hours after admission, and reached the normal range at 96 hours after admission at 139 mmol/L ().
On the third day of his admission, a sudden increase in urine output (>350 mL/hr) occurred, with an increase in serum osmolality (291 mOsm/kg) and a decrease in urine osmolality (67 mOsm/kg). With the impression of central diabetes insipidus (DI), desmopressin acetate (Minirin, Ferring pharmaceuticals, Saint-Prex, Switzerland) was subsequently started, and CRRT was discontinued. The patient remained on desmopressin acetate after that, and his electrolytes were kept stable.
An EEG was performed on the fourth day of admission, and showed extremely low voltage and featureless background rhythms. The patient did not show self-respiration during an apnea test. On the 20th day of admission, after thorough neurological examinations together with the results of the EEG and brain MRI, the patient was declared to be in a state of brain death by a panel of neurologists.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [67.0, 'kg']}",107,101.65,112.35,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 67.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (67.0 kg - 20 kg) = 107.0 mL/hr.
Hence, the patient's fluid maintenance is 107.0 mL/hr."
5090,22,Maintenance Fluids Calculations,physical,decimal,usmle-118,Extracted,"A 43-year-old woman comes to the physician because of a 2-month history of chest pain. She describes the pain as intermittent and burning-like. She states that she has tried using proton pump inhibitors but has had no relief of her symptoms. She has had a 5-kg (11-lb) weight loss over the past 2 months. Her temperature is 36.7°C (98.1°F), pulse is 75/min, and blood pressure is 150/80 mm Hg. Examination shows tightness of the skin of the fingers; there are small nonhealing, nonpurulent ulcers over thickened skin on the fingertips. Fine inspiratory crackles are heard at both lung bases. There is mild tenderness to palpation of the epigastrium.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.0, 'kg']}",20,19,21,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.0 kg. Hence, the patient's maintenance fluid is 5.0 kg * 4 mL/kg/hr = 20.0 mL/hr.
Hence, the patient's fluid maintenance is 20.0 mL/hr."
5091,22,Maintenance Fluids Calculations,physical,decimal,pmc-2876914-1,Extracted,"A 56-year-old male weighing 60 kg was scheduled for live related allograft kidney transplantation. He was diagnosed to have end-stage renal disease and was on regular bi-weekly maintenance haemodialysis. The patient was on regular medications like antihypertensive drugs, calcium and phosphorous supplements. He had an adequate cardio-respiratory reserve with a normal chest X-ray, ECG and resting 2-D echocardiogram. All investigations, except an Hb level of 8.5 gm% and serum creatinine of 5.8 mg/dl, were within normal limits.
The patient was haemodialysed the previous day and premedicated with tablet alprazolam 0.25 mg orally the night before the operation and on the morning of surgery. The morning doses of antihypertensive drugs were also given with a few sips of water. His preoperative pulse rate, BP, RR, SpO2 were 80/min, 140/80 mm of Hg, 14/min and 98% respectively.
General anaesthesia was induced with fentanyl 100 μg, midazolam 1 mg, thiopentone 250 mg and atracurium 30 mg IV. Trachea was intubated with cuffed ETT of 8.5 mm ID and anaesthesia was maintained with O2: air (40:60), isoflurane 0.6-1% and atracurium infusion @ 0.5 mg/kg/hr. For invasive monitoring triple lumen CVP catheter was placed via the right internal jugular vein approach and right radial artery was cannulated. The surgery was proceeding uneventfully with continuous monitoring of pulse, SpO2 EtCO2, ECG, ST analysis, temperature, IBP, CVP and intermittent ABG analysis (which were all within normal limits). Vascular anastomoses were being done after clamping the external iliac artery and vein. The base line CVP of 8 mm Hg was raised up to 20 mm Hg by rapid infusion of normal saline (collapsible IV bags) with the help of pressure infuser bags and simultaneous 20% albumin infusion. This was done to achieve supranormal intravascular volume to ensure adequate perfusion to the new renal graft. Just after unclamping of the vascular clamps there was a sudden decrease in EtCO2 from 32mm Hg to 15mm Hg followed by decrease in the SpO2 from 98 to 66% with significant bradycardia (HR <45/min) and hypotension. Since there was a clinical suspicion of sudden air embolism (most probably due to entrainment of air in the IVC), immediate resuscitative measures including flooding of operative site with saline, head down with left lateral tilt (Durrant's position), IV atropine 0.6 mg, ventilation with 100% O2 and aspiration of air through distal lumen of CVP line were tried. No obvious air was seen on aspiration and SpO2 returned to 100% with normal EtCO2 tracing within a minute.
The surgery proceeded uneventfully with an adequate urine output. The trachea was extubated on the operating table and the patient was shifted to kidney transplant ICU for observation and further management. However, the surgeon was doubtful about entrainment of air into IVC as there was no leak around the anastomotic site. Subsequently we observed that one of the IV sets connected to the proximal lumen of CVP line had air in it and the IV fluid bag inside the pressure infuser bag was empty.
On retrospective analysis, it was realized that the self collapsible one litre NS bag was disconnected during the infusion and IV mannitol was connected in that line. Later, after the mannitol infusion, the same NS bag was reconnected and the pressure infuser bag was applied to it for the rapid infusion which resulted in air embolism as the saline infusion had finished unnoticed and the pressurized air entered through the central venous catheter leading to sudden fall in EtCO2, HR, BP and SpO2.
As this life threatening situation was immediately recognized due to standard monitoring protocols, the resuscitation measures were started. Left lateral tilt might have allowed the air bubble obstructing the RV outflow tract to be shifted to the superiorly placed right atrium, thereby, allowing the oxygenation and circulation to be restored. The drop in saturation level could have been attributed to overloading with IV fluids, but it would not have been as sudden as in our case. Moreover, the SpO2 in Durrant's position would have worsened in case of fluid overload. Hence fluid overload was unlikely in our case. We established this as the possible cause by simulating the same scenario in vitro.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.0, 'kg']}",100,95,105,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.0 kg - 20 kg) = 100.0 mL/hr.
Hence, the patient's fluid maintenance is 100.0 mL/hr."
5092,22,Maintenance Fluids Calculations,physical,decimal,pmc-4208431-1,Extracted,"A 24-year-old woman was admitted for severe malnutrition and dehydration in the context of anorexia nervosa that was diagnosed one year ago. During this time, she had been hospitalized during 4 months with a transitory gain of six kilograms. She was treated with serotonin reuptake inhibitor and denied taking illicit drug or potentially harmful products. On admission, she presented hypotension (90/50 mmHg), sinus bradycardia (40 bpm), slight hypoglycemia (3.9 mmol/L), and hypothermia (35.7°C). She measured 160 cm and her body weight was 36 kg, corresponding to a body mass index (BMI) of 14 kg/m2. At physical examination she was oriented but lethargic and slightly jaundiced. The abdomen was slightly tender without ascites. The liver was not enlarged.
Laboratory data at admission demonstrated the following: glycemia (3.5 mmol/L), Na+ 137 mmol/L (N: 136–144), K+ 3.7 mmol/L (3.6–4.6), total Ca2+ 2.34 mmol/L (N: 2.2–2.52), Mg2+ 1.10 mmol/L (N: 0.65–1.05), P2− 1.22 (N: 0.8–1.5), and osmolality 289 mOsm/kg. Platelets were at 144 G/L (N: 150–350), hemoglobin was at 133 g/L (N: 120–160), and leucocytes were at 6.6 G/L (N: 4–11). The liver function tests was abnormal with a factor V at 33% (N: >70%). Serum aminotransferase levels were increased as follow: AST 208 U/L (N: 11–42), ALT 341 (N: 9–42), and total bilirubin 65 μmol/L (N: 7–25). The vitamin C was normal at 78 umol/L (N: 17–85) as was the thiamine at 208 umol/L (N: 65–200).
She was treated with serotonin reuptake inhibitor and denied taking illicit drug or potentially harmful products. Her treatment was stopped, but laboratory tests continued to deteriorate.
After one week, the laboratory routine tests revealed abnormal hematological tests with hemoglobin at 114 g/L, leucopenia at 2.5 G/L, and thrombocytopenia at 52 G/L. Additional investigations included prealbumin: 121 mg/L (N: 223–380) and albumin: 36 g/L (N: 35–48). Electrolytes remained normal. Renal and thyroid functions were unremarkable. Liver tests were as follows: AST 1088 U/L, ALT 1868 U/L, GGT 138 U/L, PA 102 U/L, and total bilirubin 66 μmol/L. INR was at 1.02 and factor V at 85%. Additional laboratory tests were performed to exclude all possible causes of liver injury. Hepatitis A, B, C, and E, CMV, and HIV tests were negative. Autoantibodies were absent; iron studies and ceruloplasmin were normal. At abdominal ultrasound the liver appeared normal with no ascites. Portal and hepatic veins were unremarkable. Thus, a diagnosis of acute liver injury associated with anorexia nervosa was considered the most plausible diagnosis.
A careful and progressive refeeding was performed, but liver transaminases remained abnormal. Thus, 10 days after hospital admission, a liver biopsy was performed by the transjugular route.
At histology, architecture of the liver was normal without fibrosis. Portal tracts and biliary and vascular structures were normal. Cytoplasm of hepatocytes was clarified and some acidophil bodies were found predominant in the centrilobular region. In addition, ceroid pigments at the apical pole of the hepatocytes were observed ().
An electron microscopy study was also performed in a fragment of liver biopsy, which showed features that strongly suggested a phenomenon of autophagocytosis: the density of glycogen particles in the hepatocytes was very low, consistent with cytoplasm clarification on PAS staining at the optical microscopy. In addition, the number of both mitochondria and rough endoplasmic reticulum appeared to be reduced. This observation contrasts with an increased number of Golgi bodies and smooth endoplasmic reticulum as well as primary and secondary lysosomes containing digested material (). Eight weeks after admission, with progressive refeeding the test returned back to normal ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [36.0, 'kg']}",76,72.2,79.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 36.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (36.0 kg - 20 kg) = 76.0 mL/hr.
Hence, the patient's fluid maintenance is 76.0 mL/hr."
5093,22,Maintenance Fluids Calculations,physical,decimal,pmc-5538095-2,Extracted,"A 10-year-old boy with no previous comorbidities, presented with high-grade fever and chills for 15 days, pain abdomen for 10 days; more on the left side and radiating to the back. A week later, he developed oliguria followed by anuria. There was no history of gross hematuria, altered sensorium, or seizures. He was treated at another hospital with peritoneal dialysis 3 days before referral to our center.
At admission, the child was pale, restless, and febrile with respiratory distress (weight: 30 kg). He had abdominal distention and tenderness, more prominent in the left flank region, with free fluid. No organomegaly was noted. Investigations revealed anemia, neutrophilic leukocytosis, thrombocytopenia, and elevated procalcitonin. Blood biochemistry revealed raised urea nitrogen and creatinine, mild transaminitis, and deranged coagulation profile. Chest radiograph revealed bilateral pleural effusions and increased perihilar opacities suggestive of pulmonary edema. Abdominal ultrasound showed bilateral bulky kidneys with mild hydronephrosis and ascites. Workup for tropical diseases and immunological conditions was negative. Serology for HIV, HBsAg, and HCV was negative. The child was started on hemodialysis, empiric broad-spectrum antibiotics, and antifungal fluconazole along with supportive treatment. His clinical condition deteriorated with seizure and respiratory failure requiring invasive mechanical ventilation, and he was shifted to ICU. His subsequent course was complicated by septic shock requiring vasopressors and inotropes, severe metabolic acidosis with electrolyte disturbances requiring renal replacement therapy, and disseminated intravascular coagulation requiring transfusions of multiple blood products. Echocardiography revealed global hypokinesia with left ventricle ejection fraction of 20%. The child succumbed to his illness on day 4 of admission. Blood cultures were sterile for bacteria and fungus. Postmortem kidney biopsy revealed acute necrosis of renal parenchyma with ghost cell outlines of glomeruli and tubules and fragments of aseptate fungal hyphae in the lumen of blood vessels and glomeruli suggestive of zygomycosis with infarct.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [30.0, 'kg']}",70,66.5,73.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 30.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (30.0 kg - 20 kg) = 70.0 mL/hr.
Hence, the patient's fluid maintenance is 70.0 mL/hr."
5094,22,Maintenance Fluids Calculations,physical,decimal,pmc-5396431-1,Extracted,"A 56-year-old female with a history of pulmonary embolism, myotonic dystrophy, and complete heart block on pacemaker presented to the emergency department (ED) with sudden onset shortness of breath and substernal chest pain radiating to the back. There was no history of fever, chills, cough, sore throat, or chest trauma. Her history was negative for any gastrointestinal, musculoskeletal, or neurological symptoms. She was taking rivaroxaban 20 mg once daily for deep vein thrombosis of the left axillary vein diagnosed 7 weeks ago. There was no prior history of tuberculosis, chest irradiation, or chemotherapy. She had a history of pulmonary embolism in 2007 for which she was on coumadin for a year. She had a biventricular pacemaker placed in 2008 for complete heart block induced nonischemic cardiomyopathy. Complete heart block was diagnosed at the same time and was believed to be secondary to myotonic dystrophy. The pacemaker device reached elective replacement indicator and was replaced with a Medtronic Protecta D314TRG device in 3/2012. She was on Tylenol 500 mg as needed for back pain, levocetirizine 5 mg twice daily for seasonal allergies, and rivaroxaban and zolpidem 5 mg nightly as needed. The above-listed medications do not have p-glycoprotein altering activity or CYP3A4/5 or CYP2J2 inhibiting activity [, ]. The past surgical history and family history were unremarkable.
In the ED, her blood pressure was 78/48 mm Hg, pulse 106/minute, temperature 36.5°F, and respiratory rate 18/min with saturation of 87%. Her height and weight were 1.7 m and 180 lbs, respectively. Cardiac examination was normal. Chest examination was significant for bibasilar rales. Electrocardiogram revealed ventricular paced rhythm. There was no associated electrical alternans. Lab tests revealed negative troponin, INR of 1.3, and PTT of 28 s. Complete blood count and basic metabolic profile were unremarkable. Computed tomography (CT) on chest showed no pulmonary embolism but revealed a large hyperdense pericardial effusion (). Echocardiogram showed moderate-sized circumferential effusion with a swinging heart consistent with pericardial effusion (prior echo 4 years ago showed no pericardial effusion) (). Inferior vena cava was dilated with no respiratory collapse and right ventricle outflow tract collapsed in diastole. With the diagnosis of cardiac tamponade, emergency subxiphoid pericardial window was performed and a total of 300 mL of bloody pericardial fluid was drained. Hemostasis was achieved and was satisfactory. Transesophageal echocardiogram confirmed emptying of the collection as well as improved cardiac function. There was immediate improvement in her hemodynamic status. Postprocedure images showed complete resolution of the effusion. Further etiologic workup was unrevealing. Pericardial fluid culture was negative with normal cytology. Pericardial tissue biopsy was negative for malignancy. Thyroid and liver function tests were normal. ANA, rheumatoid factor, anti-saccharomyces cerevisae antibody, anti-mitochondrial antibody, C3, C4, and anti-liver-kidney-muscle antibody were negative making the autoimmune cause unlikely. Myotonic dystrophy was considered to be an unlikely cause of her hemopericardium as pericardial involvement has not been reported with it []. In addition, her previous echo was negative for pericardial effusion. There was no temporal relation to the axillary vein DVT and the pacemaker lead implantation as CT scan done in 2013 and echocardiogram done in 2015 mentioned a normal pericardium with appropriately implanted leads. Intraoperatively, there was no mention of pacemaker lead induced pericardial perforation. Further hospital course, unfortunately, was complicated by healthcare associated pneumonia with septic shock and multiorgan failure. The autopsy was not done.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [180.0, 'lbs']}",121.64656,115.56423,127.72889,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 180.0 lbs so this converts to 180.0 lbs * 0.453592 kg/lbs = 81.64656 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (81.64656 kg - 20 kg) = 121.64656 mL/hr.
Hence, the patient's fluid maintenance is 121.64656 mL/hr."
5095,22,Maintenance Fluids Calculations,physical,decimal,pmc-3277472-1,Extracted,"MR was a 14-year-old Muslim Kurdish student living in Sulimania, northeast of Iraq. His parents were of an educated middle class family who enjoyed good health and stable relationships. He was brought by his mother to the hospital on 18th July 2010 for refusing to eat, which had led to severe weight loss and generalized weakness. His condition began seven months prior when his friends teased him about his plumpness and greedy appetite. Consequently, he started restricting his food intake, avoiding high-calorie foods and indulging routinely in extensive exercise. His parents tried to convince him to eat regular meals, but he refused. He was obsessed about his body shape and measured his waist and thigh circumferences regularly. His food intake decreased rapidly until his daily meal became no more than a cup of yogurt and pieces of cucumber. A few weeks before his visit to the hospital, he experienced severe fatigue, headaches, joints aches and attacks of epigastric pain followed by vomiting. He was treated by the local doctor with multivitamins, anti-emetics and anti-spasmodics, but without improvement.
The patient seemed to be overprotected by his mother. He was the youngest of seven siblings and a clever boy. She described him as being a graceful and obedient child, but somewhat of a perfectionist. There was neither a history of physical or mental illness nor sexual abuse during childhood.
On admission to the hospital, he appeared to be severely ill. He was pale, emaciated and dehydrated. He had lost about 20 kg during the past four months, according to his mother, who reported episodes of irritability and depressed mood with the decrease in weight. His body weight was 28 kg and height 147 cm, which is below the 2nd percentile for his age according to the growth chart. His BMI was 13.0, reflecting a 37% deficit in weight for his height [].
Upon examination, he showed generalized muscle wasting, and his skin was dry and covered by lanugo hair. His chest was clear, and he had a scaphoid soft abdomen. His blood pressure was 90/60 mmHg, heart rate 55 bpm and body temperature 37.8°C. Laboratory tests were as follows: blood glucose: 60 mg/dl, blood urea: 18 mg/d, serum sodium: 136 mg/dl, serum creatinine: 0.6 mg/dl, serum cholesterol: 147 mg/dl, WBC: 2200, platelet count: 150000, ESR: 1, and HB: 12 mg/dl. Blood proteins were low with slightly elevated liver enzymes. The blood culture was negative. Thyroid functions tests and steroid hormones were normal. General urine examination and culture revealed an acute bacterial infection, which accounted for his fever. Skull, spine and chest x-ray, brain scan and abdominal ultrasound were all normal. A previous gastroscopy at another hospital showed mild mucosal atrophy. An ECG revealed sinus bradycardia. The patient was smaller and shorter than his matching peers. He looked attentive but indifferent to his serious condition. His speech was rational and did not reveal delusions or hallucinations. However, he expressed strong denial of his body appearance and insisted he had a normal body shape. His mood was depressed, but he denied suicidal ideation.
The patient was admitted on 18th July 2010 to Sulimania General Hospital and was referred later for psychiatric consultation. A liaison treatment plan was designed by the attending physician, psychiatrist and dietitian focusing on scheduled feeding under the dietitian's advice, which was to be achieved through a nasogastric tube. Caloric intake was measured to reach 2000 calories per day, and he was instructed to rest in bed under a nurse's supervision. This ameliorated his previous hypoglycemic attacks. He was prescribed oral cephalosporin 250 mg qds to treat his urinary infection. On the second day of his admission, the psychiatrist prescribed a 20 mg daily dose of fluoxetine to treat his depressed mood and food-related obsessions. A 5 mg nightly dose of olanzapine was prescribed to resolve the distorted thoughts about his body image and promote sedation. Nasogastric refeeding was continued for the first week in the hospital until oral feeding was established. The tube was removed on the 6th day. In addition, a few sessions of cognitive psychotherapy were conducted with the patient.
At the end of the third week, he became more realistic and rational about his body weight and was more compliant with eating normal meals. His mood and irritability improved. He was discharged after 24 days in the hospital, advised to abide by the regulations of the dietitian and continue his medication for three months. He was to report to the psychiatry clinic on alternate weeks. His body weight had increased to 30 kg.
He did not keep his appointments and appeared six months later at the clinic weighing 38 kg. He was enjoying better health, although he was still having eating peculiarities. He had maintained his daily exercise but was reluctant to gain more weight. After consultation, he was advised to continue on fluoxetine for another three months. The family was advised to escort him regularly for psychotherapy sessions and watch his dietary intake.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [38.0, 'kg']}",78,74.1,81.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 38.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (38.0 kg - 20 kg) = 78.0 mL/hr.
Hence, the patient's fluid maintenance is 78.0 mL/hr."
5096,22,Maintenance Fluids Calculations,physical,decimal,pmc-8672657-1,Extracted,"A 44-year-old female with a past medical history of hyperlipidaemia and Laing distal myopathy diagnosed at age 32, began experiencing intermittent episodes of pre-syncope and palpitations which occurred intermittently after swallowing, predominantly during deglutition with food. Episodes of palpitations and pre-syncope post-deglutition occurred mostly with warm liquids or food intake and less frequently with cold liquids. There was no accompanying chest pain, shortness of breath, or odynophagia. She did not consume alcohol, caffeine and was a non-smoker. An ambulatory 30-day patient triggered event monitor recorded episodes of atrial fibrillation with rapid ventricular response () and wide-complex tachycardia with heart rates up to 242 b.p.m. (). Each patient triggered event occurred after eating, associated with lightheadedness and/or palpitations. Family history was significant for Laing distal myopathy in her father who is still alive at 72 years old and atrial fibrillation in her mother.
Given the findings on ambulatory event monitoring, she was admitted to our hospital for further evaluation. Patient blood pressure on presentation was 123/64 mmHg, pulse 76 b.p.m. and regular, respiration rate 18 breaths/minute, weight 109 pounds, and body mass index of 22.07 kg/m2. Oxygen saturation was 100% on ambient air. Remainder of the physical exam including respiratory exam was unremarkable. Laboratory data including a complete metabolic panel, troponin I, N-terminal prohormone of brain natriuretic peptide, and thyroid function tests were within normal limits.
Resting baseline electrocardiogram demonstrated sinus rhythm, right axis deviation. Transthoracic echocardiogram and cardiac magnetic resonance imaging were normal. An exercise treadmill SPECT Imaging stress test revealed normal left ventricular systolic function and no evidence of ischaemia or infarction. A fluoroscopic oesophagram revealed a mild oesophageal dysmotility.
During hospitalization, she had several episodes of atrial fibrillation with rapid ventricular response which coincided with deglutination. She was initially placed on metoprolol tartrate 12.5 mg twice daily with mild improvement of palpitations; however, she was still experiencing episodes of atrial fibrillation with rapid ventricular response after deglutination. Metoprolol tartrate was subsequently discontinued, and she was started on flecainide 50 mg p.o. every 8 h and verapamil 40 mg p.o. every 8 h. During her hospitalization, there were no recorded episodes of ventricular tachycardia. After initiation of flecainide and verapamil, there has been no documented recurrence of atrial fibrillation and her symptoms of palpitations have resolved.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [109.0, 'lbs']}",89.44153,84.96945,93.91361,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 109.0 lbs so this converts to 109.0 lbs * 0.453592 kg/lbs = 49.44153 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (49.44153 kg - 20 kg) = 89.44153 mL/hr.
Hence, the patient's fluid maintenance is 89.44153 mL/hr."
5097,22,Maintenance Fluids Calculations,physical,decimal,usmle-3266,Extracted,"A 48-year old man comes to the physician for the evaluation of an 8-month history of fatigue and profuse, watery, odorless diarrhea. He reports that he has had a 10.5-kg (23-lb) weight loss during this time. Physical examination shows conjunctival pallor and poor skin turgor. Laboratory studies show:
Hemoglobin 9.8 g/dl
Serum
Glucose (fasting) 130 mg/dl
K+ 2.5 mEq/L
Ca2+ 12 mg/dl
A CT scan of the abdomen with contrast shows a 3.0 × 3.2 × 4.4 cm, well-defined, enhancing lesion in the pancreatic tail.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.5, 'kg']}",41,38.95,43.05,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.5 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.5 kg - 10 kg) = 41.0 mL/hr.
Hence, the patient's fluid maintenance is 41.0 mL/hr."
5098,22,Maintenance Fluids Calculations,physical,decimal,pmc-5652124-1,Extracted,"A 68-year-old male was seen in the Emergency Department for evaluation of altered mental status and personality changes. His initial work up included a computerized tomography (CT) scan of his head, which was concerning for an intracranial aneurysm. There was no evidence of subarachnoid hemorrhage. A diagnostic angiogram revealed an anterior communicating artery aneurysm directed anteriorly, superiorly, and medially and measuring 17.3 mm × 15.4 mm × 15.0 mm with a 3.5 mm neck [].
Past medical history included well-controlled hypertension, bipolar disorder and relapsing alcohol abuse. Physical examination revealed a well-appearing man in no distress. He was 178 cm and 100 kg. His blood pressure was 110/65 mmHg, heart rate 111 beats/min and regular, and his oxygen saturation was 98% on room air. He was alert and oriented to person, place, date, and situation. He had no neurological deficits.
The patient was brought to the operating room for elective clip ligation of the aneurysm. Anesthesia was induced with lidocaine, fentanyl, propofol, and succinylcholine and maintained with propofol/remifentanil infusion following endotracheal intubation. A left radial arterial catheter and a left subclavian central venous catheter were placed. Defibrillating/pacing pads were placed as a routine in our institution when intraoperative adenosine administration is anticipated. A standard right fronto-temporal craniotomy was performed to approach the aneurysm. Burst-suppression was induced with a propofol bolus of 150 mg and an increase in its infusion to 250 mcg/kg/min 5 min before the anticipated temporary clipping of the aneurysm feeding branches []. The decision to use adenosine was made due to the challenging size and location of the aneurysm that would allow for a transient circulatory arrest, which would aid in the dissection and treatment of the aneurysm.[] The dose of adenosine was quickly escalated from 6 to 18, 30, and 60 mg due to inadequate response (our institutional goal is 30 s of cardiac asystole/severe hypotension). With the adenosine dose of 60 mg, the asystole only lasted for 2–3 s or appeared as a few skipped beats, and the systolic blood pressure decreased to about 60 mmHg and lasted for about 20 s before a quick and complete recovery. The decision to administer 90 mg of adenosine was then made. This resulted in a 5 s asystolic period and a decrease in systolic blood pressure to about 45 mmHg for approximately 30 s. No further escalation in adenosine dose was attempted even though this response was not considered optimal. After the first 90 mg of adenosine, the surgeon discovered that there was significant calcification at the aneurysm neck, and the transition zone between the calcified wall and normal endothelial surface was friable. The aneurysm ruptured during the course of clip reconstruction of the flow. During the ensuing course, 6 additional doses of 90 mg adenosine were administered. The intervals between the adjacent doses were 17, 12, 4, 7, 5, and 14 min (6 intervals for 7 doses). The responses to each succeeding adenosine (90 mg) were similar to the first dose. A full hemodynamic recovery (of the hypotension) was achieved before each re-dosing. Phenylephrine infusion continued, and intermittent boluses were given for blood pressure support. Burst-suppression based on bispectral electroencephalogram monitoring was maintained throughout []. Shortly following the last dose of adenosine, the surgeon was able to finish the microsurgical clip to a satisfactory result. A total of 744 mg of adenosine was administered. The patient was kept intubated overnight and extubated the next day. The patient did not have focal neurological deficits and was transferred out of intensive care unit on postoperative day 3 and discharged home 5 days later.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [100.0, 'kg']}",140,133,147,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 100.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (100.0 kg - 20 kg) = 140.0 mL/hr.
Hence, the patient's fluid maintenance is 140.0 mL/hr."
5099,22,Maintenance Fluids Calculations,physical,decimal,pmc-6721907-1,Extracted,"A 19-year-old female, a diagnosed case of atypical bilateral trigeminal neuralgia, primary Raynaud's phenomenon, and endometriosis presented to our tertiary care setup after being referred for intractable nausea and vomiting with excruciating abdominal pain. Initially, these symptoms seem to have started when she had episodes of trigeminal neuralgia, which started three years back, however, all of her symptoms have progressed and occurred out of the window of neuralgia. Vomiting, in particular, worsened after microvascular decompression surgery for atypical trigeminal neuralgia, two years before presentation to our hospital. She had 25 episodes of forceful, projectile, watery, nonmucoid, and bilious vomiting with associated nausea and shortness of breath. She also had some blood streaks in her vomitus on hospital admission. It peculiarly aggravated on eating and relieved to a slighter extent on fasting. Her normal baseline for vomiting was six episodes per day. During such episodes, she felt as if she was going to die. She did not feel nauseous in between the episodes. Her abdominal pain was constant and mainly located in the epigastrium and left upper quadrant. It was a sharp, non-radiating, and lancinating pain with a severity of nine on the standard numeric pain scale. It got worse on eating food and even by drinking water. The pain was not relieved on lying prone, in the left lateral decubitus, or in the knee-chest position. She also felt bloated all the time but had no change in bowel habits. The abdominal pain and vomiting were trialed with amitriptyline, metoclopramide, pregabalin, ketorolac, sucralfate, ranitidine, omeprazole, and antacids, but none were successful. Her weight dropped from 154 pounds to 110 pounds within six months before presentation. There was no associated fever, vertigo, nystagmus, night sweats, dysphagia, melena, or feculent material in the vomitus.
On admission, she looked frail, wasted, and in significant discomfort but was alert and fully oriented with no mood alterations. The patient was afebrile, with a pulse of 102 beats per minute (bpm), blood pressure of 103/62 mmHg, and respiratory rate of 20 per min. Her abdomen was scaphoid, tender to light and deep palpation over the epigastrium and left upper quadrant. Bowel sounds were normoactive in all four quadrants with no signs of hepatosplenomegaly. The patient has no lymphadenopathy, edema, cyanosis, clubbing, oral rashes, or thrush. There were, however, severe conjunctival pallor and delayed capillary refill. The cardiovascular system was significant for early systolic murmur in the pulmonic area, signifying an innocent murmur secondary to anemia. The respiratory and nervous system were normal on physical examination.
The complete blood count (CBC) showed a total leukocyte count (TLC) of 2.6 x 109/L, with neutrophils being 40.2% and lymphocytes being 50.3%. Platelets were 183 x 109/L. Red blood cell (RBC) count was 3.07 x 106/ mL (normal: 4.0-5.0 x 106/ mL) with low hemoglobin and hematocrit of 7.1 g/dl and 23%, respectively. The erythrocyte sedimentation rate and C reactive protein levels were within normal limits. The coagulation profile was normal as well. The electrolyte panel indicated a sodium level of 137 mEq/L (normal: 136-146 mEq/L), chloride of 106 mEq/L (normal: 94-107 mEq/L), and potassium of 3.1 mEq/L (normal: 3.5-5.0 mEq/L). The glycosylated hemoglobin (HbA1c) level was 4.2%, with a random blood sugar level of 97 mg/dl (normal: 79-160 mg/dl). Total serum protein was 5.2 g/dl (normal: 6-8.3 g/dl). The blood urea nitrogen and creatinine ratio was marginally elevated.
Non-invasive imaging was done, which included abdominal ultrasound and plain supine abdominal radiograph (AXR). The ultrasound was insignificant while AXR showed gastric distension. Gastric emptying studies with barium swallow were initially not conducted, as the patient was not able to co-operate because of an aversion to liquids. Esophagogastroduodenoscopy (EGD) was performed, which showed mild erythema consistent with reflux and retained gastric content in the stomach, findings suggestive of gastroparesis. Computed tomography (CT) with oral contrast and intravenous (IV) contrast was performed. Axial and sagittal sections were obtained, which showed gastric distension with extrinsic compression of the third part of the duodenum by the SMA, with retained fluid, consistent with findings of SMA syndrome (Figures -).
CT sagittal view showed reduced aortomesenteric distance and angle of about 3.4 mm (normal: 10-28 mm) and 12 degrees (normal: 38-65 degrees) respectively (Figure ).
Imaging was obtained with the help of the granisetron patch to keep the patient from any emetic episode while imaging.
Supportive and medical treatment was initiated with close liaison between gastroenterologists and nutritionists. To counter the drastic weight loss, the patient was started on total parenteral nutrition (TPN) via a peripherally inserted central catheter (PICC), with dextrose 8%, amino acids 4.3%, sodium acetate 110 mEq at 84 ml/hr and fat emulsion 20% at 6 ml/hr for 24 hours. This diverted the nutritional flow from the gut and helped in pain relief. Nasogastric decompression could not be performed, as it would have aggravated trigeminal neuralgia. Electrolytes were corrected and a jejunostomy feeding tube was used as a possible intervention to improve the metabolism of the patient. She was then followed up for nine months and showed massive improvement in her weight and symptoms.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [110.0, 'lbs']}",89.89512,85.40036,94.38988,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 110.0 lbs so this converts to 110.0 lbs * 0.453592 kg/lbs = 49.89512 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (49.89512 kg - 20 kg) = 89.89512 mL/hr.
Hence, the patient's fluid maintenance is 89.89512 mL/hr."
5100,22,Maintenance Fluids Calculations,physical,decimal,pmc-6967102-1,Extracted,"A 62-year-old woman (height 163 cm, weight 59 kg, BMI 22 kg/m2) with no previous medical history or history of medications was scheduled to undergo hysterectomy, total cystectomy, and ileal conduit surgery for bladder cancer. The patient was managed by epidural anesthesia (Th12/L1) and general anesthesia. Just after massive intraoperative bleeding, 1500 mL of colloid fluid, 8 units of red blood cells (RBCs) and 6 units of fresh frozen plasma (FFP) were administered. The total amount of bleeding was 3640 mL. After the surgery, she woke up smoothly, and extubation was performed in the operating room. She was then admitted to the intensive care unit (ICU). During her stay in the ICU, 2 more units of RBCs were provided. ICU staff noted that pain control by epidural anesthesia was sufficient, but she complained of nausea once. She was discharged from the ICU on postoperative day 1 (POD 1), and urologists started to manage her on their own ward (Table ). She did not receive antithrombotic therapy for prevention of venous thrombosis postoperatively.
On POD 4, she complained of severe abdominal pain (numerical rating scale (NRS) score: 10/10) 40 min after removal of the epidural catheter. She was unable to walk or eat despite pain relief provided by intravenous infusion of acetaminophen and NSAIDs. On POD 12, computed tomography (CT) showed a hematoma extending from inside the rectus muscle to subcutaneous tissue, and the surgeon started to administer tramadol (50 mg/day). On POD 16, CT showed that the size of the RSH was unchanged (Fig. ), and the NRS score was high (resting: 2/10, moving: 10/10). The anesthesiologists were consulted regarding pain management. On POD 17, a rectus sheath catheter was placed under ultrasound guidance. A high-frequency linear probe was placed transversely with the rectus muscle immediately lateral to the umbilicus. An 18-G Tuohy needle was inserted in-plane to the US transducer and advanced until the tip had reached the posterior rectus sheath. Then, 20 mL of 0.375% ropivacaine were injected, and the catheter was passed through the needle to 5 cm within the rectus sheath. A total of 150 mL of analgesics (146 mL of 0.2% ropivacaine and 4 mL of fentanyl at 200 μg) were continuously administered at a rate of 4 mL/h. The NRS score decreased immediately just after ropivacaine injection (resting 0/10, moving 2 or 3/10), and she was able to walk and eat. She had no further need for oral or intravenous analgesics after the block procedure. After removing the catheter on POD 28, she had no complaints of abdominal pain and was discharged from the hospital without catheter site infection.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [59.0, 'kg']}",99,94.05,103.95,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 59.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (59.0 kg - 20 kg) = 99.0 mL/hr.
Hence, the patient's fluid maintenance is 99.0 mL/hr."
5101,22,Maintenance Fluids Calculations,physical,decimal,pmc-4337264-1,Extracted,"A 52-year-old male presented to the hospital with 2 months of fevers of up to 40 degrees Celsius, weakness, and a 15 kg weight loss over 6 months. His past medical history was notable for a cadaveric renal transplant of over 20 years for which he had been on immunosuppressant therapy, mycophenolate, sirolimus, and prednisone. On admission, he was found to have profound anemia with hemoglobin of 4.9 g/dL, a platelet count of 50,000/uL, and ferritin above 22470 mmol/L. He also had elevated liver transaminases fluctuating between 100 and 200 mmol/L. A bone marrow biopsy was performed to look for other causes of his cytopenias such as infectious infiltration; he was found to have hemophagocytosis involving 50% of the histiocytes (). Further workup revealed a triglyceride level of 9.04 mmol/L, LDH of 2000 mmol/L, and a soluble IL-2 level of 23,690 pg/mL. Given his history of being on immunosuppressants, an infectious workup for opportunistic infections was investigated upon admission to the hospital. All microbiological cultures were negative. However, he was later found to have profound Epstein-Barr virus infection with 9,380,000 copies/mL in his peripheral blood, as well as EBV positivity in his cerebrospinal fluid. CT of chest, abdomen, and pelvis did not show masses or lymphadenopathy, so we ruled out posttransplant lymphoproliferative disorder. The diagnosis of HLH was made as he met the diagnostic criteria: fever, hemophagocytosis on bone marrow biopsy, elevated ferritin, cytopenias, hypertriglyceridemia, and high soluble IL-2 level.
The patient's outpatient immunosuppressants were held. He was begun on dexamethasone 10 mg/m2/day according to the HLH-94 protocol []. After being on therapy for 3 days, his fevers and cytopenias did not improve. Due to his abnormal kidney and liver function, we did not start conventional chemotherapy (etoposide) [] and gave him instead rituximab weekly for the EBV infection (375 mg/m2 intravenously). This was based on the knowledge regarding the relationship between EBV infections and HLH [].
Within one week following the first dose, his fevers, cytopenias, liver function tests, and inflammatory markers improved significantly. He was given his second dose of rituximab in the hospital setting and discharged safely to continue his third and fourth doses of rituximab in the outpatient setting. During 3-month follow-up period, the patient remained in complete remission. His counts normalized with the exception of his hemoglobin, as he remained mildly anemic due to his transplanted kidney failure and the initiation of dialysis. EBV viral load was checked 7 weeks after finishing treatment, and it was undetectable ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15.0, 'kg']}",50,47.5,52.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.0 kg - 10 kg) = 50.0 mL/hr.
Hence, the patient's fluid maintenance is 50.0 mL/hr."
5102,22,Maintenance Fluids Calculations,physical,decimal,pmc-6967366-1,Extracted,"A 46-year-old female weighing 60 kg, a diagnosed case of Gilbert syndrome was posted for MVR. Her liver function profile [] revealed total bilirubin of 20.6 mg/dl with unconjugated bilirubin of 19.8 mg/dl. Preoperative echocardiography showed severe mitral stenosis, moderate tricuspid regurgitation (TR), moderate pulmonary hypertension with mild right ventricular (RV) dysfunction, and a left ventricular ejection fraction of 65%.
She was premedicated with oral. alprazolam 0.25 mg and fasted for 8 h but allowed clear water up to 2 hours before surgery. 5% dextrose infusion was started in the morning. Standard monitors including 5 lead electrocardiogram, invasive arterial blood pressure, and pulse oximetry were attached to the patient before general anaesthesia (GA) induction. With patient in left lateral decubitus position under aseptic precautions, 10cc of normal saline containing 250 μg morphine and 25μg fentanyl was injected into the intrathecal space with a 26 G Quincke spinal needle in the L3-L4 intervertebral space. GA was induced with titrated doses of fentanyl and propofol intravenously (IV). Transoesophageal echocardiography (TOE) revealed a clot in left atrial appendage and dilated inferior vena. The average hepatic blood flow was estimated to be 192 ml/min before CPB.
After systemic heparinisation with 4 mg/kg of injection heparin, cannulation was performed. Proper position of IVC cannula was confirmed by TOE. Normothermic (35°C–36°C) CPB was maintained with flow of 2.2-2.5 L/min/m2, and a mean arterial pressure of 70-80 mmHg. The mitral valve was replaced with 29 mm St. Jude's mechanical valve. Total ischaemia time and CPB time were 78 and 98 min, respectively. The patient was weaned from CPB with inotropic support of inj. milrinone 0.3 μg/kg/min and noradrenaline 0.05 μg/kg/min. Post CPB TOE showed mild right ventricular dysfunction and moderate tricuspid regurgitation, normal mitral prosthetic valve function, and hepatic blood flow was 175 ml/min. The patient was extubated after 4 h of ventilation and allowed orally 2 h after extubation. Postoperative pain was managed with inj. diclofenac 50 mg twice daily (IV) and intermitted boluses of inj. fentanyl with total opioid of 130 μg over next 48 h. Patient was discharged from intensive care unit after 5 days and hospital after 8 days.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.0, 'kg']}",100,95,105,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.0 kg - 20 kg) = 100.0 mL/hr.
Hence, the patient's fluid maintenance is 100.0 mL/hr."
5103,22,Maintenance Fluids Calculations,physical,decimal,pmc-4823413-1,Extracted,"A 69-year-old female patient (59.3 kg, 154.6 cm, body mass index 24.8) was scheduled for total knee replacement (TKR). Past medical history revealed that the patient underwent general anesthesia for prior TKR of the other knee three years at another hospital, and the patient failed to recall any specific events associated with anesthesia other than a sore throat, which is fairly common after intubation. The patient complained of occasional mild dyspnea during exercise, but chest radiographic readings by radiology were non-specific and we pursued further testing. Spirometry (FEV 2.27 liters (L), FEV1 1.84 L, FVC/FEV1 81%) and arterial blood gas analysis showed normal results. Both lung sounds were clear and no chest abnormalities were observed.
Upon entering the operating room, the patient was monitored with electrocardiograph electrodes, pulse oximeter, bispectral monitoring, and noninvasive blood pressure. After 3 minutes of pre-oxygenation with 100% oxygen, she was anesthetically induced with propofol (60 mg) and rocuronium (30 mg). After ventilating the lungs with a facial mask for two minutes without any difficulties, initial intubation was attempted with a conventional laryngoscope with the aim of inserting a 7.0 mm internal diameter endotracheal tube (ETT), which failed to pass the larynx. After a second attempt failed with a 6.5 mm internal diameter ETT due to continuous resistance when passing the vocal cords, we used a GlideScope® (Verathon Inc., Burnaby, Canada) to visualize and identify the source of the resistance. The GlideScope® view indicated that the subglottic area was divided into two sections with a septum (). A laryngeal mask airway (LMA, i-gel®, 4.0, Intersurgical Ltd., Wokingham, UK) was inserted for temporary ventilation with a tidal volume of 7 ml/kg and 12 breaths/min, but peak airway pressures of 30 mmHg did not improve even after injection of additional neuromuscular blockade. Predicting inadequate ventilation over several hours of anesthesia with i-gel® inevitably resulted in the attending anesthesiologist awakening the patient and postponing surgery until further evaluation. After reversing the neuromuscular blockade with sugammadex (Bridion®, MSD, Kenilworth, NJ, USA) 200 mg, the patient regained consciousness without any respiratory symptoms and the i-gel® was removed.
Neck computed tomography () and fiberoptic endoscopy () performed consecutively after surgery revealed fibrous tissue at the glottic level dividing the anterior and posterior portion into 5.8 mm and 1.7 mm lengths, respectively. An initial chest radiograph revealed evident narrowing at the level of the glottis (), with a post-anesthesia chest radiograph confirming the initial findings. Re-questioning the patient regarding any discomfort or complications from the previous surgery revealed that the patient suffered from severe dyspnea and dysphagia after surgery 3 years ago, which lasted several weeks. Afterwards, she complained of continuous mild dyspnea on exertion, but did not consider these symptoms to be anesthetic sequelae. An otorhinolaryngologist consulted for treatment diagnosed post-intubation tracheal stenosis, but did not recommend aggressive or invasive treatment. After constructing a plan including the use of a supraglottic airway (SGA) or smaller diameter ETT in case of failed regional anesthesia, the patient underwent successful surgery with continuous epidural block.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [59.3, 'kg']}",99.3,94.335,104.265,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 59.3 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (59.3 kg - 20 kg) = 99.3 mL/hr.
Hence, the patient's fluid maintenance is 99.3 mL/hr."
5104,22,Maintenance Fluids Calculations,physical,decimal,pmc-5738592-2,Extracted,"A 12-year-old female wire hair fox terrier (9.5 kg) presented to its local (UK-based) veterinary surgery on September 21, 2016 suffering from conjunctivitis of the left eye. The dog had been seen 20 days previously for this complaint by a veterinarian in Italy when a topical course of chloromycetin (unspecified) had been prescribed. On clinical examination worms were detected on the conjunctiva of the affected eye and the animal was admitted for further examination. Following sedation with medetomidine and butorphanol (0.24 mg, Domitor 1 mg/ml solution for injection, Vetoquinol UK; and 0.95 mg, Torbugesic 10 mg/ml solution for injection, Zoetis UK, respectively), approximately 10 nematodes were manually recovered from beneath the nictitating membrane and conjunctival sac, following which the sedation was reversed with atipamezole (125 µg/kg, Antisedan 5 mg/ml solution for injection; Zoetis UK). Based on the suspicion of ocular thelaziosis, an oral dose of milbemycin and praziquantel (5 and 50 mg, respectively, Milbemax tablets for small dogs and puppies; Novartis Animal Health UK) was administered, and topical fusidic acid (one drop twice daily, Isathal 10 mg/g eye drops; Dechra Veterinary Products) was prescribed with a seven-day course for the affected left eye. Two nematodes were placed in physiological saline and submitted to LVPD via Axiom Laboratories (Newton Abbot, Devon, UK) for identification (see below). No further worms were detected at a seven-day follow-up appointment. At this time the topical course of fusidic acid course was extended for a further seven days, and an additional treatment with imidacloprid and moxidectin (100 and 25 mg, respectively, Advocate Spot-On Solution for Medium Dogs; Bayer) was also administered. No further problems have been reported since.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [9.5, 'kg']}",38,36.1,39.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 9.5 kg. Hence, the patient's maintenance fluid is 9.5 kg * 4 mL/kg/hr = 38.0 mL/hr.
Hence, the patient's fluid maintenance is 38.0 mL/hr."
5105,22,Maintenance Fluids Calculations,physical,decimal,pmc-3160386-1,Extracted,"A 54-year-old Caucasian man with a history of ischemic stroke and ischemic cardiomyopathy presented to our emergency department with constant left-sided lower abdominal pain and decrease in urination of one week's duration. Four months prior to presentation, he had noticed pain and swelling in his left groin. Because of his concerns of a hernia, he sought clinical evaluation. His family physician sent him for an ultrasound of the scrotum, which revealed a left-sided varicocele. He was then referred to a urologist. For one week, he developed continuous, unrelenting left-sided abdominal pain localized primarily in the left lower quadrant. He had diminished appetite and noted a 12-pound weight loss during the prior one month. Because of decreased urinary frequency, he came to our emergency department for evaluation. His family history was negative for malignancy. His physical examination revealed a hard mass occupying the entire left abdomen, crossing the midline, and extending to the pelvic brim, as well as the presence of a left-sided varicocele. He had no lymphadenopathy or hepatomegaly and no clinical signs of hormone access of 1.7 from a baseline of 1.0, hyponatremia (serum sodium 130 mmol/L), and normocytic anemia (hemoglobin 10.9 g/dL, hematocrit 34.5%, mean corpuscular volume 82.5 fL, and mean corpuscular hemoglobin 26.1 pg.) His hormonal evaluations, including fasting blood glucose, serum potassium, adrenocorticotropic hormone (ACTH), morning serum cortisol, and androgen levels, were normal. Renal ultrasound showed that the left kidney was inferiorly displaced by what was thought to be an enlarged spleen. His home medication of lisinopril was discontinued. Intravenous fluid was started. Contrast-enhanced computed tomography (CT) of the abdomen and pelvis performed after the patient's renal function improved showed a large retroperitoneal mass on the left side displacing the left kidney inferiorly and the spleen superiorly with T5 epidural compression (Figures and Figure ). Thrombus was also identified in the left renal vein extending into the inferior vena cava. A CT chest scan showed bilateral pulmonary nodules compatible with metastasis. Anti-coagulation therapy, a 5 mg/day dose of warfarin adjusted according to International Normalized Ratio levels and five days of 1 mg/kg enoxaparin administered subcutaneously every 12 hours for bridging therapy were initiated because of thrombosis of the blood vessels. The patient's acute kidney injury improved after intravenous fluid and anti-coagulation treatment. During the course of his hospitalization, he was seen by our medical oncologist, who managed his anti-coagulation therapy and arranged for the biopsy. A CT-guided biopsy of the abdominal mass was performed. Immunohistochemistry showed malignant cells with abundant amounts of eosinophilic cytoplasm and a rosette pattern of the cells around his blood vessels. Occasional, very enlarged, bizarre nuclei were observed. Mitoses were rare but could be identified (Figures and ). Immunohistochemistry performed to detect primary adrenal origin was positive for calretinin, melan-A, vimentin, and synaptophysin. His Ki-67 proliferation index was 12%. This presentation was consistent with primary ACC. The diagnosis of ACC stage IV was made. Laboratory tests performed for hormornal evaluation, including fasting blood glucose, serum potassium, cortisol, and urinary metanephrine levels, were normal. A nuclear cardiac stress test was performed, which showed borderline anterior ischemia and mild to moderate systolic dysfunction with a left ventricular ejection fraction of 38%. Unfortunately, the adrenal mass was determined to be unresectable because of local unresectability and metastatic disease.
Mitotane, an adrenocorticolytic drug, was started at an initial dose of 1 g/day and the dose was later increased to maintain plasma levels between 14 μg/mL and 20 μg/mL, which was well tolerated. Irradiation of the lesion at T5 that was causing the epidural compression was followed by combination chemotherapy consisting of etoposide, doxorubicin, and cisplatin. The patient understood that the goal of therapy was to control his symptoms and hopefully to achieve better quality of life and prolonged survival.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.0, 'lbs']}",21.7724,20.68378,22.86102,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.0 lbs so this converts to 12.0 lbs * 0.453592 kg/lbs = 5.4431 kg. Hence, the patient's maintenance fluid is 5.4431 kg * 4 mL/kg/hr = 21.7724 mL/hr.
Hence, the patient's fluid maintenance is 21.7724 mL/hr."
5106,22,Maintenance Fluids Calculations,physical,decimal,usmle-7581,Extracted,"A 61-year-old man presents to the clinic with complaints of excessive thirst, frequent urination, and partial visual loss in both eyes for 1 day. His family history is significant for type 2 diabetes mellitus in his mother and cousin. His weight is 112 kg ( 246.9 lb), height 187 cm (6 ft 1 in), blood pressure: 150/90 mm Hg, heart rate: 89/min, respiratory rate: 14/min, and temperature: 36.7℃ (98.4℉). The physical examination is significant for dry skin, a pustular rash over the patient’s shoulders and back, an accentuated second heart sound (S2) best heard in the second intercostal space at the right sternal border, and distal loss of vibration sensitivity in both feet. A fundoscopic examination shows small red dots in the superficial retinal layers suggestive of microaneurysms.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [112.0, 'kg']}",152,144.4,159.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 112.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (112.0 kg - 20 kg) = 152.0 mL/hr.
Hence, the patient's fluid maintenance is 152.0 mL/hr."
5107,22,Maintenance Fluids Calculations,physical,decimal,pmc-3737702-1,Extracted,"A 24-year-old male with fracture upper third shaft of left humerus was posted for open reduction and internal fixation. Patient had an insignificant post-anesthetic exposure for left inguinohernioplasty under spinal anesthesia. Patient was explained about the option of regional anesthesia for the above surgery and also about the possible complications. He agreed for the brachial plexus block. Patient was 152 cm tall, weighed 70 kg with no coexisting disease, and had normal physical examination and routine investigation.
A left brachial plexus block was performed under aseptic precautions by interscalene approach using a 22-guage, 2-inch insulated needle with extension tube assembly (Stimuplex®, B Braun, Melsungen AG, 34209, Melsungen, Germany) after localizing the plexus with the help of the nerve stimulator by eliciting motor response at shoulder and upper arm at 0.5 mA. With all standard monitors, 40 ml of local anesthetic solution containing 200 mg of lignocaine with 50 μg adrenaline and 50 mg of bupivacaine was injected slowly over 5 min. Adequate sensory and motor block was achieved. But within 10 min after injection of local anesthetic solution, patient complained of increased sweating in the face and diminished vision in the left eye. On examination, sweating was confined to the left half of the face with widened palpebral fissure of the left eye and the left pupil was dilated in comparison to the right pupil (4 mm/2 mm). Patient was reassured and the surgery was completed successfully. These symptoms resolved when the plexus functions returned to normal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [70.0, 'kg']}",110,104.5,115.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 70.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (70.0 kg - 20 kg) = 110.0 mL/hr.
Hence, the patient's fluid maintenance is 110.0 mL/hr."
5108,22,Maintenance Fluids Calculations,physical,decimal,pmc-8329389-1,Extracted,"A 51-year-old healthy Korean man without comorbid diseases was admitted to our hospital with complaints of generalized edema on May 12, 2021. On April 13, 2021, he received Ad26.COV.2. The next day after vaccination, he had fatigue and mild myalgia, then he did not feel any discomfort and did not take analgesics or herbal medication. After seven days of vaccination, he recognized peripheral edema on both lower extremities and edema had been aggravated. As edema developed, the total daily amount of urine decreased by a quarter of the usual amount. On May 3, 2021 (20 days after vaccination), his body weight increased from 77 kg to 91 kg. He visited the local nephrology clinic, and urinalysis revealed protein 4+ and urinary sediment revealed 3−5 red blood cells per high power field. Serum albumin level was 1.6 g/dL and creatinine level was 1.13 mg/dL. The nephrologist suspected nephrotic syndrome and transferred him to the tertiary referral hospital.
He was admitted 28 days after vaccination and the clinical course is shown in . His body weight increased to 98 kg with generalized edema, including lower and upper extremities, trunk, and face in a physical examination. Initial blood pressure was 146/98 mmHg; pulse rate, 60 beats/min; and axillary temperature, 36.5ºC. Abdominal computed tomography revealed a normal size and shape of both kidneys. In the laboratory findings to identify glomerulonephritis, anti-nuclear antibody, anti-neutrophil cytoplasmic antibody, anti-glomerular basement membrane (GBM) antibody, and anti-phospholipase A2 receptor antibody were all negative. Both complement C3 and C4 levels were within the normal range. Hepatitis B surface antigen, hepatitis C antibody, and human immunodeficiency virus antigen/antibody tests were negative. Serum immunoglobulin (Ig) G level decreased to 578.0 mg/dL (reference: 700−1,600 mg/dL). Real-time reverse transcriptase-polymerase chain reaction assay for SARS-CoV-2 (Seegen, Seoul, Korea) was negative. Total amount of collected 24-h urinary protein was 8,600.0 mg/day. Serum total cholesterol level was 416.0 mg/dL, albumin level was 1.6 g/dL, and creatinine level was 1.54 mg/dL.
To control edema, intravenous furosemide was applied, then daily urine volume increased to over 2,000.0 mL/day, and edema gradually improved. However, his creatinine level increased to 1.96 mg/dL for seven days, and a kidney biopsy was performed 33 days after vaccination (). In the periodic acid-Schiff stain, there were 28 glomeruli having a normal appearance. In the interstitium, there was no inflammation or injury; and no chronic changes, such as tubular atrophy and interstitial fibrosis in the cortex and medulla were observed. Some proximal tubules contained protein droplets. Immunofluorescence revealed that IgG, IgA, IgM, C3, and fibrinogen were all negative. Electron microscopy revealed that GBM thickness was normal (average 375.2 nm) with diffuse effacement of the podocyte foot processes. There was no electron-dense deposit. According to the histopathological findings, he was diagnosed with MCD.
High-dose steroid therapy was initiated immediately after checking the histopathology result by light microscopy. Considering the body weight, 64 mg parenteral methylprednisolone (the equivalence of 1 mg/kg prednisone) was administered. At three days after steroid use, his serum creatinine level started to improve. He was discharged at nine days after kidney biopsy (42 days after vaccination) with oral steroids. Two week after discharge, the follow-up examination showed decreased serum creatinine level to 0.95 mg/dL, increased serum albumin to 2.7 g/dL, and decreased spot urine protein-to-creatinine ratio to 0.2 g/g.
Informed consent for data collection and publication of the study was obtained from the patient.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [98.0, 'kg']}",138,131.1,144.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 98.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (98.0 kg - 20 kg) = 138.0 mL/hr.
Hence, the patient's fluid maintenance is 138.0 mL/hr."
5109,22,Maintenance Fluids Calculations,physical,decimal,pmc-8236333-1,Extracted,"A 7-year-old Asian female presented to our outpatient clinic with intermittent fevers and left-sided neck swelling. She had low-grade fevers (100.40 F-1020F) recurring periodically over the last four months, accompanied by night sweats, fatigue, and weight loss. She had stopped attending school due to her illness. The painless swelling in her neck persisted for three months. However, few weeks prior to the presentation, there had been a gradual and progressive increase in its size. Her past medical history was significant for steroid-sensitive nephrotic syndrome diagnosed about two years ago, and since then, she has had frequent relapses of the disease. At the time of presentation, she was in remission for nephrotic syndrome and was not taking any medications. She also complained of abdominal pain, loss of appetite, dry cough, headache, and unintentional 3 kg weight loss in the past four months. She denied any history of chest pain, palpitations, dyspnea, visual changes, rashes, hematuria, urinary frequency, joint pain, and body aches.
Physical examination was significant for a 5 cm swelling in her left neck and palpable left-sided non-tender, matted, and rubbery supraclavicular lymphadenopathy with freely mobile and smooth overlying skin. There was reduced air entry on the left side with no wheezing or added sounds on chest examination. The rest of the physical examination was unremarkable. The baseline complete blood count test showed mild neutrophilia and thrombocytosis as the only abnormalities. Her chest x-ray revealed a large mediastinal mass (Figure ). Other baseline investigations, including urea, creatinine, urine analysis, and hepatic function panel, were within normal limits. The patient was hospitalized for an excisional biopsy of the left supraclavicular lymph node, and the histopathology report confirmed a classical Hodgkin lymphoma of mixed cellularity type.
To further investigate for spread and appropriate staging, she was scheduled for a bone marrow biopsy, CT, and positron emission tomography (PET) scan. The biopsy report did not reveal any evidence of bone marrow involvement. However, staging CT and PET scan reports concluded a bulky mediastinal nodal disease which caused left lung upper lobe collapse and minor left-sided pleural effusion, along with the involvement of spleen and splenic hilar nodes (Figure ). Although imaging did not clearly exhibit hypodense renal lesions, both kidneys were also suspected to be involved in the disease. Based on these results, a diagnosis of stage 4 Hodgkin's lymphoma was made.
The patient was admitted to the hospital for the treatment of malignant lymphoma. On the second day of hospitalization, before initiation of chemotherapy, she was vitally and clinically stable with the exception of mild dehydration (dry oral mucous membranes with the capillary refill of 2-3 seconds, and normal urinary output). Her laboratory findings were consistent with metabolic acidosis (HCO3 16mEq/L, Normal Range 22-28 mEq/L), elevated LDH (496U/L, Normal range 120-200), hyperuricemia (10 mg/dl, Normal range 2-6mg/dl), hyperkalemia (5.74 mmol/L, Normal range 3.3-5.1), hypocalcemia (8.73 mg/dl, Normal range 8.8-10.8), and hyperphosphatemia (7 mg/dl, Normal range 2.5-6.0). The diagnosis of spontaneous tumor lysis syndrome was suspected (extremely rare in patients with Hodgkin's lymphoma), and she immediately received intravenous fluids, allopurinol, urine alkalization, and forced diuresis therapy. The patient responded well to the treatment and recovered without developing further complications. Finally, under oncology care, the patient received multiple cycles of chemotherapy (ABVE-PC Regimen) followed by radiation therapy. The mediastinal mass showed a significant reduction in size after receiving chemotherapy (Figure ). The blood counts returned to normal levels within three months.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.0, 'kg']}",12,11.4,12.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.0 kg. Hence, the patient's maintenance fluid is 3.0 kg * 4 mL/kg/hr = 12.0 mL/hr.
Hence, the patient's fluid maintenance is 12.0 mL/hr."
5110,22,Maintenance Fluids Calculations,physical,decimal,pmc-7667200-1,Extracted,"A 12-year-old girl with KOS (weight 30 kg, height 140 cm) was scheduled for a pectus excavatum repair for cosmetic reasons. She has a family history of KOS. She was born at 30 weeks gestation with a birth weight of 1546 g, and had been kept in a neonatal intensive care unit (NICU) for 4 months. During her NICU stay, she presented with respiratory failure from her thoracic configuration and required mechanical ventilation. She underwent a tracheostomy at 3 months and a gastrostomy for feeding at 3 years. At 6 years of age, the tracheostomy was closed and the gastrostomy tube was removed. These procedures were all uneventful.
She had no physical symptoms and complications associated with the prior tracheostomy. Several craniofaciocervical features were noted such as frontal bossing, depressed nasal bridge, full cheeks, anteverted nares, protruding philtrum, micrognathia. and short webbed neck. Although she had mental retardation, she was able to follow simple instructions given by us and make simple conversation. She did not have symptoms such as dyspnea, fatigue, or precordial pain after exercise despite remarkable chest wall asymmetry (Fig. ). Sternocostal elevation was scheduled for pectus excavatum.
Anesthesia was planned as a combination of general and epidural anesthesia. With no premedication, general anesthesia was induced with 8 % sevoflurane with 6 L/min O2 via a facemask. Snoring occurred during a slow inhalation induction. The endotracheal tube (φ5.5 cm) was easily inserted. Under general anesthesia, an epidural catheter was inserted via the T7–T8 intervertebral space without any difficulty. General anesthesia was maintained with 2% sevoflurane, remifentanil, and rocuronium. Local anesthetics (0.25% levobupivacaine and 0.2% ropivacaine) were administered from the epidural catheter, a total of 29 ml of levobupivacaine was administered intermittently during operation. Epidural patient-controlled analgesia was initiated with 5 ml/h of 0.2% ropivacaine, with a 3 ml bolus dose and 30-min lockout time. The volume of 0.2% ropivacaine injected during operation was 18 ml.
Her sternocostal elevation was initiated with a median vertical incision. Pediatric surgeons resected parts of her costal cartilages (3rd to 8th on the right; 2nd to 8th on the left), adjusted them to appropriate lengths, and reattached them to the sternum. Then, the lower part of the sternum was resected. The surgery was uneventful and lasted 4 h 40 min. Blood loss was 202 ml.
We measured her spontaneous breathing pattern, while keeping a sufficient depth of anesthesia (2% sevoflurane and 0.7 μg/kg/h dexmedetomidine). At the end of surgery, we used 60 mg sugammadex to reverse the neuromuscular block. She presented with respiratory rate of 20 breaths/min, tidal volume of 200 ml, and end tidal CO2 of 43 mmHg. Her respiratory status was stable. Before extubation, we performed a bronchoscope to confirm edema and/or stenosis in the pharyngolaryngeal region. Bronchoscopic examination did not show pharyngolaryngeal edema and stenosis.
Tracheal extubation was performed 30 min after administering 0.7 μg/kg/h dexmedetomidine. Bronchoscopy was performed soon after extubation to evaluate vocal cords and detect laryngomalacia. Dexmedetomidine was continued for sedation and analgesia during bronchoscopic examination. The movement of the vocal cords and larynx was normal; a floppy epiglottis was not observed. She was then transferred to the ward. The anesthesia time was 6 h 25 min. Her post-operative recovery was uneventful. She was discharged on the 9th day after her surgery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [30.0, 'kg']}",70,66.5,73.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 30.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (30.0 kg - 20 kg) = 70.0 mL/hr.
Hence, the patient's fluid maintenance is 70.0 mL/hr."
5111,22,Maintenance Fluids Calculations,physical,decimal,pmc-7759049-1,Extracted,"On April 6th, 2020, a 64-year-old man (weight 78 kg; height 170 cm, and body surface area 1.89 m2) presented to the outpatient clinic with the symptoms of COVID-19 infection complaining of intermittent fever (maximal temperature: 38.2°C), postnasal discharge, and myalgias. He denied cough, sore throat, shortness of breath, gastrointestinal symptoms, or anosmia. He had a history of orthotopic heart transplantation bridged from veno-arterial extracorporeal membrane oxygenation (VA-ECMO) for post-infarction refractory cardiogenic shock in December 2013. The marginal donor was a 58-year-old male with a history of hypertension and left ventricular hypertrophy. His post-transplant course was unremarkable except for hypertension, with no episodes of rejection. On further discussion with the patient, he stated that his wife was a pharmacist and COVID-19-positive for two days. Nasopharyngeal and oropharyngeal swabs tested negative for severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) by real-time reverse-transcriptase-polymerase-chainreaction (RT-PCR) assay. No compliant finding with COVID-19 was detected on chest radiograph or computed tomography (CT) (Figure ). Electrocardiography showed sinus rhythm, 76 bpm with the previously confirmed right bundle branch block. The complete blood count analysis revealed mild leukopenia and lymphopenia. C-reactive protein (CRP) was mildly elevated to 6.1 mg/L (normal range: 0 to 5 mg/L) (Table ). Considering the history of his close contact, we commenced on hydroxychloroquine 200 mg q12h, selfisolated in a separate home from his wife - the treatment targeted for symptomatic relief at this stage under close follow-up with self-measured pulse oximeter.
The repeated RT-PCR assay of a nasopharyngeal swab on April 7th, 2020 tested positive for SARS-CoV-2 and the patient was hospitalized and isolated. On arrival, the body temperature was 36.8°C with a pulse rate of 82 bpm, a blood pressure of 130/80 mmHg, a respiratory rate of 20 breaths/min, and an oxygen saturation of 97% on room air. Auscultation of the chest revealed natural breathing sounds. He did not require oxygen supplementation. According to the blood chemistry tests, mild leukopenia and lymphopenia persisted. Laboratory results showed normal renal and hepatic function. His immunosuppressive regimen consisted of cyclosporine A 100 mg q12h and mycophenolic acid 360 mg q12h. The dose of cyclosporine was adjusted as 75 mg q12h to achieve a cyclosporine level between 400 and 600 ng/mL at 2h. Other medications were pantoprazole 40 mg per day, acetylsalicylic acid 100 mg per day, candesartan 8 mg per day, and pravastatin sodium 20 mg per day.
Following hospitalization, hydroxychloroquine therapy was discontinued. After a loading dose of favipiravir 1,600 mg b.i.d., 600 mg q12h maintenance dose was initiated under the recommendations of the Coronavirus Scientific Advisory Board of the Tr MoH. Prophylactically, subcutaneous enoxaparin sodium 0.4 mL was commenced q12. Daily electrocardiogram monitoring was performed with particular attention to QT prolongation, and no additional findings were detected. Handheld portable echocardiography revealed a mildly dilated left atrium, hypertrophic myocardium, and abnormal interventricular septal movement with normal left ventricular function. The need for oxygen did not arise. Favipiravir treatment was completed in five days and discontinued thereafter. On Day 23 of the disease, two PCR tests-24-h apart-were negative for COVID-19. The patient was discharged on mycophenolate sodium 360 mg b.i.d. and cyclosporine 100 mg b.i.d.
A written informed consent was obtained from the patient.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [78.0, 'kg']}",118,112.1,123.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 78.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (78.0 kg - 20 kg) = 118.0 mL/hr.
Hence, the patient's fluid maintenance is 118.0 mL/hr."
5112,22,Maintenance Fluids Calculations,physical,decimal,pmc-3809310-1,Extracted,"A one-day old, full term male, weighing 2.6 kg, was referred with a swelling at umbilical region. Baby was delivered at a local hospital through spontaneous vaginal delivery. On arrival, he had normal morphological features. There was a large omphalocele about 10 x 12 cm, covered with a thin, intact, semi-transparent membrane with a narrow pedicle of around 3 cm diameter (
). Umbilical clamp was well away from the omphalocele. The small bowel loops and a thick sac like structure were visible through the thin membrane. Rest of the neonatal examination was unremarkable.
Echocardiography showed a large ventricular septal defect with overriding of aorta, hypertrophied right ventricle, infundibular pulmonary stenosis and bunching of atrial septum – correlated with Tetralogy of Fallot. After optimization of the general condition surgery was done. At surgery, a 10 x 12 cm meconium filled cyst located at the distal ileum was found as the major content of the sac, along with small intestinal loops. The proximal and distal ileal loops were communicating with the cyst. (
 and 
) Rest of the bowel had no gross anomaly. Excision of cyst with primary end-to-end ileo-ileal anastomosis was performed.
Post operative course was stormy. During his stay at PICU the baby developed uncontrolled septicaemia and died in spite of best of efforts. Histopathology of the excised specimen revealed wall of small intestine with thin walled blood vessels surrounded by fibromyxomatous tissue. Ectopic mucosa was not identified.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.6, 'kg']}",10.4,9.88,10.92,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.6 kg. Hence, the patient's maintenance fluid is 2.6 kg * 4 mL/kg/hr = 10.4 mL/hr.
Hence, the patient's fluid maintenance is 10.4 mL/hr."
5113,22,Maintenance Fluids Calculations,physical,decimal,usmle-2148,Extracted,"A 3200-g (7.1-lb) female newborn is delivered at 38 weeks' gestation to a 24-year-old woman. The mother had regular prenatal visits throughout the pregnancy. The newborn's blood pressure is 53/35 mm Hg. Examination in the delivery room shows clitoromegaly and posterior labial fusion. One day later, serum studies show:
Na+ 131 mEq/L
K+ 5.4 mEq/L
Cl− 102 mEq/L
Urea nitrogen 15 mg/dL
Creatinine 0.8 mg/dL
Ultrasound of the abdomen and pelvis shows a normal uterus and ovaries.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.2, 'kg']}",12.8,12.16,13.44,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.2 kg. Hence, the patient's maintenance fluid is 3.2 kg * 4 mL/kg/hr = 12.8 mL/hr.
Hence, the patient's fluid maintenance is 12.8 mL/hr."
5114,22,Maintenance Fluids Calculations,physical,decimal,pmc-5789473-1,Extracted,"A 14-year-old male, American Society of Anesthesiologists (ASA) status III, with SJS and epilepsy, was scheduled for multiple dental extractions and alveoloplasty under general anesthesia.
He had no history of previous anesthesias or known allergies.
His usual medication was carbamazepine 200 mg BID for his epilepsy, which was under control. Family history revealed that his mother and brother were diagnosed with the same condition.
Physical examination showed a patient with a weight of 35 kg, a height of 130 cm, and a short stature compared with other children with the same age. He had an unusual facies, muscle stiffness, and rigidity. Vital signs and remaining physical examination were normal.
The patient was scheduled as the first one of the day. Before his arrival to the operating theater, the circuit of the anesthetic workstation was flushed and we guaranteed that dantrolene and cooling devices were available. Difficult airway devices were readily accessible should any problem with the endotracheal intubation arise.
Before induction, a peripheral venous catheter was placed. No premedication was administered. He was monitored under the ASA standards plus core temperature measurement and bispectral index monitoring (BIS). After 3 min of preoxygenation with oxygen (O2) at 100%, induction of anesthesia was accomplished with a propofol bolus at a 2 mg/kg dosage. We had no difficulties with mask ventilation. Direct laryngoscopy was attempted. His Cormack–Lehane grade was III, and we performed two attempts of tracheal intubation with a Macintosh Blade No. 3 with no success. We decided to interrupt laryngoscopy and ventilate the child with the facial mask. Afterward, a new attempt with a C-MAC® videolaryngoscope was performed. We visualized 60% of the glottis, but inserting the endotracheal tube was impossible. We decided to introduce a wireframe laryngeal mask (LM) that allowed an adequate ventilation. After discussing the case with the surgical team, we carried out the procedure using the frame LM for airway (LMA) management with pressure-controlled ventilation targeted to 4–6 mL/kg and a respiratory frequency adjusted to achieve an end-tidal CO2 (EtCO2) of 35–40 mmHg. Maintenance of anesthesia was accomplished with a propofol infusion at 5 mg/kg/h and local anesthetic infiltration. Fifteen minutes before the end, paracetamol 425 mg intravenously was administered to provide postoperative analgesia. The procedure lasted 2 h and underwent without any clinical events. The patient remained hemodynamically stable, with no significant fluctuations in blood pressure, pulse, or peripheral O2 saturation. His core temperature remained within the normal range. Blood loss was minimal. When the surgery ended, we stopped the propofol infusion. As soon as he regained consciousness, airway reflexes, and spontaneous breathing, with adequate lung volumes per minute, the LMA was removed. The patient was transferred to the postanesthetic care unit, with normal vital signs and painless, where he remained for 24 h under observation. In the next day, he was discharged home without any anesthetic or surgical complications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [35.0, 'kg']}",75,71.25,78.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 35.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (35.0 kg - 20 kg) = 75.0 mL/hr.
Hence, the patient's fluid maintenance is 75.0 mL/hr."
5115,22,Maintenance Fluids Calculations,physical,decimal,pmc-5633263-1,Extracted,"A 46-year-old female with an eight-year history of hypertension was referred to our surgical outpatient clinic upon detection of a large abdominal mass noted on a computed tomography (CT) scan of her abdomen and pelvis done during workup for nausea and vomiting. Her symproms also included 35 lb weight loss, palpitations, chest heaviness, sweating, facial flushing, flushing of skin, fatigue with slight exertion, and intermittent headaches over a period of three months. She is a current smoker. Physical examination revealed hypertension and sinus tachycardia, but no facial flushing. There was a flushed look to the forearms, hands, and pretibial lower extremities from the distal third of the lower extremities bilaterally. The abdomen was soft and nontender without masses; the rest of the exam was unremarkable.
The CT scan revealed a large right adrenal mass measuring 11.5 x 6 x 9 cm with compression of the vena cava and displacement of the right kidney (Figure ).
A positive emission tomography scan combined with CT (PET/CT) in March 2016 revealed heterogenous moderate fluorodeoxyglucose (FDG) uptake in the large right adrenal lesion. There was intense FDG uptake localizing to the unusual and abnormal nodularity and low soft tissue densities surrounding both kidneys, with a standardized uptake value (SUV) of 10.2 (Figure ).
Biochemical investigations revealed an elevation in serum total metanephrine greater than 13,000 pg/mL, normetanephrine greater than 13,000 pg/mL, plasma renin 175 ng/dL/h, and cortisol of 2.7 ug/dL (ref range 4.5-22.7 ug/dL) after dexamethasone suppression (Table ).
The patient was presented at our multidisciplinary tumor board. Upon further review of the imaging studies, the finding on the PET scan suggested the possibility of diffuse brown fat development and evidence of hypermetabolism, symmetric in the neck, retroperitoneum, and inguinal regions. Overall, this appearance was consistent with pheochromocytoma with brown fat stimulation and less likely suggestive of metastatic pheochromocytoma. Preoperatively, adequate catecholamine blockade was achieved using alpha adrenergic blocker and beta blockage. Her symptoms improved.
A repeat PET/CT in April 2016 after adequate alpha and beta blockade revealed the stable size of the large heterogeneous right adrenal mass with moderate FDG uptake with areas of central photopenia, which likely correspond to central necrosis. No significant retroperitoneal or intra-abdominal lymphadenopathy was noted (Figure ).
The patient was taken to the operating room in May 2016. An open right adrenalectomy was performed through right subcostal incision with extension up the midline to the xiphoid. A large adrenal mass was noted with significant periadrenal gland fibrosis. The mass was resected en bloc with a portion of the right hemidiaphragm. Intraoperatively, there were significant fluctuations in the patient’s blood pressure, which was appropriately managed by the anesthesia team. There were no other significant surgical complications, and the patient made an uneventful recovery. She was discharged on postoperative day 10. Five months later, the patient remained stable and had no symptom to suggest recurrence. A PET/CT scan in October 2016 revealed no focal abnormality in the resection bed, no gross evidence of metastatic disease, no significant retroperitoneal or intra-abdominal lymphadenopathy (Figure ). Given the risk of recurrence, long-term follow-up with CT scan of the chest, abdomen, and pelvis, and serum metanephrine studies is recommended.
Pathological examination of the surgical specimen revealed an ovoid soft tissue mass measuring 12 x 9.3 x 5 cm and weighed 270 g. The capsule appeared intact. Sectioning revealed a red-brown-yellow, soft and lobulated cut surface with fibrous septae and focal areas of hemorrhagic degeneration. Immunohistochemistry revealed tumor cells positive for chromogranin and synaptophysin. The final pathologic diagnosis was pheo of the right adrenal gland with lymphovascular invasion and no perineural invasion; inked margin was uninvolved.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [270.0, 'g']}",1.08,1.026,1.134,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 270.0 g so this converts to 270.0 lbs * kg/1000 g = 0.27 kg. Hence, the patient's maintenance fluid is 0.27 kg * 4 mL/kg/hr = 1.08 mL/hr.
Hence, the patient's fluid maintenance is 1.08 mL/hr."
5116,22,Maintenance Fluids Calculations,physical,decimal,pmc-6872624-1,Extracted,"An 8-year-old 24.6 kg male mixed breed dog presented for bronchoscopy for evaluation of a chronic gradually progressive cough. The dog had been treated for heartworm disease 7 years earlier before adoption. Annual heartworm antigen testing thereafter remained negative. Two years before presentation, the dog developed a nonproductive cough, occurring once a month. Laboratory testing, including heartworm testing, was normal. Thoracic radiographs and echocardiography were performed and documented changes resulting from previous heartworm disease, including mild right heart enlargement, and mild pulmonary artery enlargement with an estimated pulmonary artery pressure based upon calculation of the tricuspid regurgitant velocity via Doppler echocardiography of 47 mm Hg (reference range < 30 mm Hg). The dog was administered fenbendazole (50 mg/kg PO q24h × 14 days), doxycycline (5 mg/kg PO q12 × 21 days) and clopidogrel (1.7 mg/kg PO q24 indefinitely).
A month before presentation, the cough had progressed from once monthly to 2–3 times per month. This change had gradually occurred over approximately 2–3 months' time. Abnormalities were not detected on physical examination. Because of the subtle worsening of his respiratory signs, a bronchoscopy and an airway wash were planned in attempt to better define an etiology. Repeat thoracic radiographs documented a diffuse and patchy bronchointerstitial pattern with mild right-sided cardiomegaly. The pulmonary arteries were assessed as slightly enlarged and tortuous. The baseline PCV/TS was 44% and 6.7 g/dL. The last dose of clopidogrel was administered 24 hours before the procedure. The dog was premedicated with acepromazine (0.02 mg/kg) and butorphanol (0.15 mg/kg) IM, and propofol was administered to effect to allow for tracheal intubation. Bronchoscopy, using a 5.2 mm flexible bronchoscope (Karl Storz Endoscopy-America, Inc, El Segundo, California) was performed through the endotracheal tube while using an bronchoscopic adaptor. Bronchoscopy documented a cobblestone and irregular appearance to the mucosal region in the intra-thoracic trachea and mainstem bronchi (Figure ). A bronchoalveolar lavage was performed, subsequently documenting limited cellularity, with only ciliated columnar epithelial cells, and a rare neutrophil observed. A biopsy, using 2 mm clamshell biopsy device, was obtained from an area of mucosal irregularity, near the junction of the left and right mainstem bronchi. Immediately after biopsy, a large volume of hemorrhage appeared, first visualized at the biopsy site, and subsequently grossly within the endotracheal tube.
Dilute (1:10) phenylephrine was applied to the region, and the endotracheal tube was replaced with a longer tube that would reach the level of the carina. The cuff was inflated in an attempt to provide direct pressure to the biopsy site. As the biopsy was in the middle of the carina, the tube was advanced as far as possible with the intent of being able to apply pressure. However, blood continued to pour from the endotracheal tube. A recheck PCV/TS 10 minutes after hemorrhage began showed a decrease to 35% and 5.2 g/dL, with a lactate of 2.0 mmol/L. A fluid bolus (25 mL/kg lactated ringers solution) was provided, and a type-specific transfusion (15 mL/kg) of packed red blood cells and 10 mL/kg of fresh frozen plasma was started. The dog continued to hemorrhage, and despite rapid transfusion, the PCV/TS fell to 32%/4.8 g/dL over the next 60 minutes.
Without recovering the dog from anesthesia, a multiphase thoracic CT angiogram (Toshiba Aquilon 16 CT; Canon Medical Systems, Glen Mills, Pennsylvania) was performed to attempt to clarify any specific abnormalities. The angiogram was performed using a power injector, using 2.2 mL/kg of contrast (Iohexol 300, GE Healthcare, Marlborough, Massachusetts) diluted to 96 mL, at a rate of 3 mL/s. The region of interest was the main pulmonary artery, and the threshold HU was 150. Slices were 3 mm. Apnea was induced with hyperventilation; 5 cmH2O positive end expiratory pressure was applied. The CT scan did not identify a clear source of hemorrhage, but did identify enlarged and tortuous arteries, suspected to be the bronchial and possibly pulmonary arteries; intraluminal noncontrast enhancing amorphous material (30-35HU) within bronchi, consistent with clot; and evidence of prior heartworm infection, including main pulmonary artery enlargement, enlarged, tortuous and blunted pulmonary arteries, and mineral foci within vessels (Figure ). Kaolin-activated thromboelastography to evaluate global coagulation status was unremarkable, and TEG platelet mapping was not performed.
Over the next hour, the dog continued to hemorrhage. The volume of hemorrhage was not able to be precisely quantified, but filled several anesthesia circuits, was well as about 500 mL into a suction canister, and about a 3 m radius of the floor. Surgical exploration was elected, and the dog was placed in dorsal recumbency to prepare for a median sternotomy. At this point, the hemorrhage suddenly ceased, and surgical exploration was canceled. The dog was placed in the intensive care unit, with the goal of keeping the dog sedated and intubated so clot formation could mature. Overnight, the dog was hemodynamically stable. No additional hemorrhage was evident either grossly and serial laboratory evaluations supported that that PCV/TS/lactate were stable. Sedation was maintained with fentanyl and midazolam. Supplemental humidified oxygen was provided. After 19 hours of intubation, sedation was slowly weaned and the dog was extubated and placed into a run.
Approximately 20 minutes after extubation, the dog coughed twice, and a large volume of hemorrhage was noted from the mouth. The dog was promptly induced and re-intubated; however, the hemorrhage continued at a high rate. The dog was positioned in dorsal recumbency. Crystalloid treatment (30 mL/kg IV) was administered, as was 3 whole units of pBRCs, 1 unit of fresh whole blood, and 2 units of fresh frozen plasma, for a total volume of 1650 mL (67 mL/kg) within 2 hours, and 95 mL/kg over 12 hours. One unit of commercially available cryoprecipitate (Cryoprecipitate, Hemopet, Garden Grove, California) reconstituted with 60 mL 0.9% NaCl was administered via the endotracheal tube with an attempt to provide topical clotting factors. Emergent surgical intervention was again planned, but the dog died before completing presurgical preparation.
A necropsy was performed. Cause of death was confirmed to be exsanguination (Figures and ). Extensively throughout the trachea and bronchi were mucosal ulcerations along with prominent submucosal vessels. The biopsy site was identified histopathologically and was consistent with mechanical removal of tissue over a submucosal vessel, suspected to be a branch of a bronchial artery. The adjacent tracheal mucosa had multifocal regions of tracheal necrosis and ulceration with submucosal edema and infiltration of neutrophils. Histopathology of the main pulmonary artery showed a long-standing proliferative arteritis from previous heartworm infection and enlargement of the pulmonary arteries (Figure ). Bacterial and mycoplasma cultures were negative.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [24.6, 'kg']}",64.6,61.37,67.83,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 24.6 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (24.6 kg - 20 kg) = 64.6 mL/hr.
Hence, the patient's fluid maintenance is 64.6 mL/hr."
5117,22,Maintenance Fluids Calculations,physical,decimal,pmc-5818772-1,Extracted,"The Institutional Review Board of Fukuoka Dental College approved this study.
The patient was a 14-year-old boy (height = 150 cm, weight = 54 kg) with Down syndrome, atrial septal defect (ASD), ventricular septal defect (VSD), and patent ductus arteriosus (PDA). His congenital heart defects were surgically repaired at 5 months of age. Thereafter, he was followed up once a month with echocardiography. No structural or mechanical problems and dysfunction were noted in his cardiovascular system, such as a left-right shunt. The most recent findings of his echocardiogram were as follows: all chambers were balanced; good wall motion; no asynergy; normal interventricular septum; left ventricular ejection fraction, 85 %; left ventricular end-diastolic dimension, 42 mm; no valve regurgitations; and no abnormal flow resulting from the ASD, VSD, and PDA. The attending physician of the pediatric cardiology section categorized the patient’s condition as grade 1 heart failure according to the New York Heart Association functional classification system. Therefore, we assessed the patient in accordance with the diagnosis of the attending physician. The patient’s intelligence quotient was 35, and his intellectual level was that of a 1.5-year-old child.
The patient had many dental caries, as observed during examination at the Fukuoka Dental College Hospital. However, because he was uncooperative owing to his condition and our attempts at physical restraint had failed (he violently refused our intervention), he was scheduled for dental treatment under general anesthesia. At our hospital, we recommend that all patients undergo routine checkup, including blood tests, elective cardiograms, chest radiography, and urine tests. However, because of the patient’s violent behavior, we were unable to perform any of the aforementioned tests. Therefore, we referred to the data obtained by the attending physician during the routine checkup of his cardiac condition. According to the preanesthetic examination that was performed at the other institution, the patient had no abnormalities in his blood or urine. A complete right bundle branch block (RBBB) was the only abnormality observed on the electrocardiogram (ECG) (Fig. ). The patient was not regularly taking prescription medication for his congenital heart disease. His blood pressure (BP), heart rate (HR), peripheral oxygen saturation (SpO2), and body temperature could not be measured because of his violent behavior.
The patient’s parents were informed about the risks of general anesthesia before they provided consent. We determined that the perioperative risk in this patient was similar to that in other patients who had undergone corrective surgery for ASD, VSD, and PDA because there were no structural or mechanical problems with his cardiovascular system. He did not present with any risk factors for complications resulting from intubation, such as macroglossia, micronesia, and brevicollis. Although we did not check for dislocation of the first cervical vertebra, it did not seem necessary to restrain his head for airway management. He consumed no food for 6 h and no liquid for 2 h before the operation. We decided to intramuscularly inject midazolam before surgery and to gradually and incrementally induce anesthesia by means of inhalation of sevoflurane with oxygen and nitrous oxide through a face mask, after which an intravenous catheter and arterial line were inserted. To prevent infective endocarditis, we also planned to administer intravenous antibiotics during the operation.
At 9:30 a.m. on the day of the operation, the patient was administered 10 mg midazolam intramuscularly as a sedative. At 10:00 a.m., he was brought to the operating room on a gurney. However, he was not sedated because the midazolam had not taken effect. Moreover, because of his inability to emotionally cope with the environmental change, he acted violently against physical restraint and was in danger of falling from the operating table; therefore, it became necessary to perform anesthesia induction immediately. We therefore administered sevoflurane (5 %) to induce general anesthesia as rapidly as possible. We intended to decrease the concentration of sevoflurane as soon as the patient’s movements were controlled. Because of the patient’s violent behavior, we could not measure his BP, HR, SpO2, and body temperature and could not perform the cardiac evaluation with insertion of an intravenous catheter and arterial line before the induction. The anesthetist who performed the anesthesia induction had 15 years of experience at the time. Three anesthetists, who are all co-authors of this paper, performed the anesthesia induction.
Approximately 1 min after the induction, the patient’s consciousness and combative behavior gradually decreased. His respiration ratio did not change, and his tidal volume progressively subsided. We then began performing assisted ventilation, which was achieved by using a face mask (Fig. ). The initial vital signs were as follows: BP = 90/42 mm Hg, HR = 75 beats per minute (bpm), and SpO2 = 100 %. The ECG initially showed a normal sinus rhythm (Fig. ). However, a few seconds later, his ECG indicated severe bradycardia (HR of <30 bpm) and gradually showed prolonged R-R intervals, immediately followed by asystole (Fig. ). Although we could manage his airway and ventilation, we did not detect a pulse in the carotid artery. We immediately ceased the administration of sevoflurane and nitrous oxide and began cardiopulmonary resuscitation (CPR) with a combination of 15 chest compressions and two ventilations (Fig. ). We thought that it was unnecessary to perform tracheal intubation during the initial ventilation because controlled ventilation was achievable through a face mask during CPR. Therefore, we performed tracheal intubation during the switch between rescuers in order to minimize interruptions in the chest compressions. A few minutes after CPR, the previous chest compression waveform on the ECG changed, as the patient’s heartbeat and breathing returned (Fig. ). We therefore stopped CPR, inserted an intravenous catheter in the antecubital vein, and continued ventilation and monitoring until the patient regained consciousness. Throughout this incident, his SpO2 did not decrease (Fig. ). After conferring with the operating dentist, we decided to stop the operation under general anesthesia. After the return of his spontaneous circulation, we decided to perform tracheal intubation while the patient was still unconscious and not spontaneously breathing. The patient regained consciousness relatively early because he only inhaled sevoflurane for a short period. Thereafter, he was transported to the recovery room of the ward (Fig. ). He was monitored for 1 day at our hospital and was then discharged the next morning without any sequelae. Even after consulting with pediatricians and cardiologists at our hospital, the cause of his cardiac arrest remains unclear.
After this incident, the operating dentist scheduled his dental treatment under sedation using midazolam and physical restraint.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [54.0, 'kg']}",94,89.3,98.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 54.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (54.0 kg - 20 kg) = 94.0 mL/hr.
Hence, the patient's fluid maintenance is 94.0 mL/hr."
5118,22,Maintenance Fluids Calculations,physical,decimal,pmc-4988024-2,Extracted,"A 24-year-old female Chinese patient presented with repeated episodes of swelling and pain of her chin for 2 years. The patient had a history of premature loss of some deciduous teeth before 6-year-old and accidental leg fracture at 10-year-old. Family history revealed that her mother lost several teeth at 40-year-old. The patient was 160 cm height and 39 kg weight, with a BMI of 15.23. Intraoral examination (Fig. ) and CBCT showed enamel hypoplasia in most of her residual teeth. Teeth #14 and # 31 were missing. No fistula or pus was noted.
The panoramic film (Fig. ) revealed that all the roots were short, and multiple well defined radiolucencies were shown at the apices of teeth #25, #26, #32–35, and #41–46. Furthermore, alveolar bone height reduction was observed as well. CBCT proved that most of the root lengths were shorter than normal (Table ). Skeletal radiography didn’t show any obvious changes. The laboratory examination results were unremarkable except that the serum ALP level was 35.0 U/L (normal range 45.0–125.0 U/L).
The patient was diagnosed as HPP (odontohypophosphatasia form) and multiple radicular cysts []. Root canal therapy of teeth #25, #26, #33–35, and #41–44 was performed before enucleation of the radicular cysts. In addition, teeth #32, #45, and #46 were extracted. Pathological report confirmed the diagnosis of radicular cysts (Fig. ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [39.0, 'kg']}",79,75.05,82.95,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 39.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (39.0 kg - 20 kg) = 79.0 mL/hr.
Hence, the patient's fluid maintenance is 79.0 mL/hr."
5119,22,Maintenance Fluids Calculations,physical,decimal,pmc-8223890-1,Extracted,"A 56-year-old man weighing 102 kg and 188 cm tall (Figure ) was referred to our hospital because of an evident thickening around the neck. He had had the enlargement for the last 10 years and lately, the condition worsened. He was also a heavy alcohol drinker for the last 30 years and had 50 pack-years of smoking upon presentation. He was employed as a farmer and construction worker and had never demanded health care for his condition in the past.
More specifically, during the last 3 years, the enlargement became a collar-like mass around the neck and dyspnea crises with cough and upper airway excretions appeared, especially when bending the neck. He was relieved after some minutes of neck extension. The patient reported progressive difficulty sleeping due to extensive bulk of the mass, while he never had a problem of snoring, sleep deprivation, or other sleep apnea-associated symptoms. Additionally, he complained of weakness and chronic fatigue during these last years. The mass presented with cervical pain upon weight lifting, while he did not have any signs of neuropathy.
He referred a known history of hypertension with frequent hypertensive crises with systolic blood pressures of 220-230 mm Hg after heavy drinking, for which he used an angiotensin II receptor blocker (ARB) and hydrochlorothiazide and was usually referred to the local hospital. The cardiac assessment was normal. He had suffered from hypothyroidism for the last 15 years.
Upon examination, he had a circular mass of the neck, semi-hard on the anterior and hard on the posterior in a double oval-shaped configuration. The mass was not fixed to the overlying skin. His articulation was disturbed, and he had stridor while bending the head. Interestingly enough, we noticed that his legs and arms had lipohypertrophic along with lipoatrophic areas and that his supraclavicular regions were hypertrophic. The identification of the “pseudoathletic” type of Madelung's disease (type I), and hence, the diagnosis was delayed because the patient's physique was attributed to his occupation as a construction worker. Neurological examination was normal.
High values of uric acid, cholesterol, triglycerides, CPK, and LDH were reported. A slight elevation of SGOT along with a double γ-GT price was compatible with alcohol abuse.
A facial, cervical, and thoracic computed tomography (CT) showed a bilateral and symmetrical fat mass of the posterior and anterior region of the neck and of the upper trunk, without displacement or infiltration of the trachea (Figure ). Based on these findings, the diagnosis of Madelung's disease was made and we decided to treat the patient surgically.
Two different operations took place. In the first one, orotracheal intubation was impossible, so nasotracheal intubation was performed. A Gluck-Sorenson incision was performed, and fat tissue was excised in a similar fashion as in bilateral functional lymph node neck dissection with preservation of the accessory and marginal and cervical branches of the facial nerves. More specifically, we dissected levels I-V on the right side and levels I-VI on the left side. The dissection of the tissue in the carotid triangles was laborious (the fat tissue had septa that extended between the structures). The excised specimen's size was 27 × 12 × 18 cm, and its weight was 627 g (Figure ). A tracheostomy was performed before completion.
In the second operation, which took place 3 weeks later, the patient was placed in a prone position. The fat masses of the cervical, occipital, suboccipital, retro-auricular, and upper dorsal regions were removed surgically and with liposuction. The weight of the fat tissue was 114gram. We continued with removing the fat mass from the upper anterior cervical region. Part of the skin was removed because of its excess. The tracheostomy from the first operation remained and was finally removed 6 days after the second operation.
Histological examination after both the operations confirmed the initial diagnosis.
During the next 6 months, we suggested the use of a soft collar because we desired extra tension of the musculocutaneous tissue over the neck triangles for better healing. The patient did not follow our orders for alcohol abstinence.
In Figure , we can see the final result three months later.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [102.0, 'kg']}",142,134.9,149.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 102.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (102.0 kg - 20 kg) = 142.0 mL/hr.
Hence, the patient's fluid maintenance is 142.0 mL/hr."
5120,22,Maintenance Fluids Calculations,physical,decimal,usmle-1951,Extracted,"A 53-year-old man comes to the physician for recurring fever and night sweats for the past 6 months. The fevers persist for 7 to 10 days and then subside completely for about a week before returning again. During this period, he has also noticed two painless lumps on his neck that have gradually increased in size. Over the past year, he has had an 8.2-kg (18.1 lbs) weight loss. Two years ago, he had a severe sore throat and fever, which was diagnosed as infectious mononucleosis. He has smoked a pack of cigarettes daily for the past 10 years. He does not drink alcohol. His job involves monthly international travel to Asia and Africa. He takes no medications. His temperature is 39°C (102.2°F), pulse is 90/min, respirations are 22/min, and blood pressure is 105/60 mm Hg. Physical examination shows 2 enlarged, nontender, fixed cervical lymph nodes on each side of the neck. Microscopic examination of a specimen obtained on biopsy of a cervical lymph node is shown.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [8.2, 'kg']}",32.8,31.16,34.44,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 8.2 kg. Hence, the patient's maintenance fluid is 8.2 kg * 4 mL/kg/hr = 32.8 mL/hr.
Hence, the patient's fluid maintenance is 32.8 mL/hr."
5121,22,Maintenance Fluids Calculations,physical,decimal,pmc-7458169-1,Extracted,"A 17-year-old woman with a 3-month history of thirst, polydipsia, and polyuria underwent urine glucose screening at school where glucosuria was detected for the first time. The patient underwent surgery at birth to correct congenital ileal atresia, but had no history of hearing loss. She underwent examination at a clinic where her fasting plasma glucose (FPG) level and glycated hemoglobin (HbA1c) value were found to be 276 mg/dL and 9.7%, respectively. Based on her young age and absence of obesity, the patient was diagnosed with type 1 diabetes and insulin glargine 300 U/mL (Gla-U300) was started at 14 units/d. The treatment failed to sufficiently control the blood glucose level and the patient was admitted to our hospital for diabetes treatment as well as for education. Her family history is shown in Figure . Her mother and maternal grandmother developed diabetes at the age of 32 and 50, respectively, and were treated with oral medication. Her mother and maternal aunt had bicornuate uterus, and the latter also had unilateral aplasia of the kidneys. There was no family history of hearing loss. The patient's height was 154 cm and her weight was 41.4 kg (body mass index of 17.3 kg/m2). Physical examination revealed no abnormalities. Laboratory investigations revealed an FPG level of 80 mg/dL and HbA1c value of 9.5% (Table ). Glucagon stimulation test under a stable blood glucose level revealed that serum C-peptide immunoreactivity (CPR) was 1.01 ng/mL (PG 92 mg/dL) and 2.53 ng/mL (PG 117 mg/dL), before and 6 minutes after glucagon stimulation, respectively (ΔCPR of 1.52 ng/mL). According to these data, her endogenous insulin secretion remained in addition, she displayed low levels of serum potassium (3.0 mEq/L) and serum magnesium (1.0 mg/dL). No islet-related autoantibodies, including insulin autoantibodies, anti-glutamic acid decarboxylase antibodies, anti-insulinoma-associated protein-2 antibodies, or anti-zinc transporter-8 antibodies, were detected in her blood, suggesting the absence of autoimmune diabetes. As serum lactate and pyruvate were within normal limits, and mitochondrial DNA point mutations, including A3242G, were not detected in genetic screening tests targeting 10 point mutations, mitochondrial diabetes was excluded.
Contrast-enhanced computed tomography was performed to assess the morphology of the pancreas. The images showed defects in the pancreatic body and tail, as well as the presence of multiple renal cysts (Fig. ). Contrast-enhanced magnetic resonance imaging revealed that the partial pancreatic defects were due to agenesis of the dorsal pancreas, rather than fat displacement. The p-aminobenzoic acid excretion index was 35.4%, indicating insufficiency of exocrine pancreatic function. Based on these findings, and the patient's hypopotassemia, hypomagnesaemia, agenesis of dorsal pancreas, multiple renal cysts, and family history of diabetes, and renal and urogenital abnormalities, MODY 5 was suspected. Screening of MODY-related genes using multiple ligation-dependent probe amplification detected a heterozygous deletion of HNF1B (Fig. ), leading to a definitive diagnosis of MODY 5.
Immediately following admission to our hospital, multiple-dose injection therapy with insulin lispro (maximum requirement was 9 units/d) and Gla-U300 (maximum requirement was 13 units/d) was commenced. After 9 days of insulin therapy, the patient was started on liraglutide to prevent dysfunction of the remaining pancreatic beta cells. According to flash glucose monitoring (FreeStyle Libre, Abott Japan, Japan) data, before liraglutide was administered, the patient's blood glucose was within the target range (80–140 mg/dL) 39% of the time under the treatment with 9 units/d of insulin lispro and 13 units of Gla-U300 (Fig. A). After 6 days of liraglutide treatment, this value improved to 65% (Fig. B), under the treatment with just 7 units/d of Gla-U300, indicating a reduction of 15 units in the total daily insulin dosage, and 0.9 mg/d of liraglutide. Notably, HbA1c was maintained below 7% for at least for 12 months after the patient was discharged with 0.6 mg of liraglutide a day (a higher dose was not tolerated by the patient due to nausea), without any insulin injections. Serum CPR level was 1.15 ng/mL (FPG 135 mg/dL) and 1.91 ng/mL (FPG 115 mg/dL) after 6 and 12 months of liraglutide therapy, respectively, indicating that endogenous insulin secretion was maintained during the treatment period.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [41.4, 'kg']}",81.4,77.33,85.47,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 41.4 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (41.4 kg - 20 kg) = 81.4 mL/hr.
Hence, the patient's fluid maintenance is 81.4 mL/hr."
5122,22,Maintenance Fluids Calculations,physical,decimal,pmc-4070326-1,Extracted,"Thirty-eight-year-old woman with 162 cm height and 76 kg weight was admitted to our outpatient clinic with the complaint of renal colic. She had a history of renal stone diseases for 6 times in the last 6 months with 20–40 days of intermittences. Her stones were white in color and they were easily dispersible with a diameter of 3–5 mm approximately (). She had collected her stones and Fourier transform infrared spectroscopy (FTIR) was performed to the stones for the analysis (). The results of the analysis revealed that 45.1% of the stones were aluminum hydroxide and 44.9% were carbonate apatite and protein. Metabolic investigations were made both in serum and 24-hour urine in order to determine the etiology of stone (). Serum aluminum was determined as 32 μg/L (1–14) and calcium was 9.87 mg/dL (8.8–10.2), while urinary calcium excretion was 0.38 g/day (0.1–0.3). In her history it was determined that she was using a roll-on deodorant that was containing aluminum. After 2-month period of dismissing this deodorant, her serum aluminum level was 12 μg/L (1–14) and her urinary aluminum excretion was in normal limits (3.67 μg/day, reference range: <50).
She was evaluated with urinary ultrasound and tomography for the presence of stone disease and they were all normal. In approximately 5 months of follow-up, she did not have any renal colic attacks.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [76.0, 'kg']}",116,110.2,121.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 76.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (76.0 kg - 20 kg) = 116.0 mL/hr.
Hence, the patient's fluid maintenance is 116.0 mL/hr."
5123,22,Maintenance Fluids Calculations,physical,decimal,pmc-3356519-1,Extracted,"A 4-year-old girl with chronic renal failure due to vesicoureteral reflux was admitted our hospital with fever, cough, fatigue, and unconsciousness complaints. Her symptoms had started 3 days ago. Two family members also had the same symptoms. Salicylates and salicylate-containing products had not been administered for the last days.
On physical examination, her body weight was 11 kg (<3%), body temperature was 39.5°C, blood pressure was 100/60 mmHg. Her pharynx was hyperemic. Respiratory and cardiovascular systems were normal. She was unconscious. She had mild increased deep tendon reflex and extensor plantar responses. No focal neurological signs were noted.
At the second day of admission, she had generalized tonic–clonic seizures for three times which was controlled by IV phenytoin.
Laboratory studies showed white blood cells of 6,000 × 103 per liter, platelet count of 117,000 × 103 per liter, and hemoglobin level of 8.0 g/dl. Serum electrolytes, bilirubin, metabolic screening of urine and blood were normal. Serum BUN 88 mg/dl, creatinine 1.7 mg/dl, AST/ALT 273/219 U/l, ammonia 177 μmol/l, glucose 23 mg/dl, and prothrombin time 35/1.66 were noted. Moreover, serological studies for Epstein–Barr virus, cytomegalovirus, herpes simplex virus, rubella virus, hepatitis A–C virus, and toxoplasma gondii were negative. Toxicologic studies were also negative. Magnetic resonance imaging (MRI) of the brain on the second day showed hyperintense changes in the thalami bilaterally, brain stem, cerebellum, and subcortical cortex (Fig. ). However, we could not perform lumbar function and electroencephalography because of her poor clinical conduction.
Under the impression of Reye or Reye-like syndrome, she was given intravenous glucose infusion and hypertonic saline treatment. Broad spectrum IV antibiotic (ceftriaxone) and acyclovir treatment were initiated. On the third day, her conduction was deteriorated and intubated patient was mechanically ventilated by conventional mechanical ventilation. Novel influenza A (H1N1) virus was positive on her nasal and throat swabs and started oseltamivir. But she died on the same day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [11.0, 'kg']}",42,39.9,44.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 11.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (11.0 kg - 10 kg) = 42.0 mL/hr.
Hence, the patient's fluid maintenance is 42.0 mL/hr."
5124,22,Maintenance Fluids Calculations,physical,decimal,pmc-3459717-1,Extracted,"A 29-year-old, Nigerian Igbo woman who had not pre-registered at a hospital and who was in her fourth pregnancy presented at the labor ward at a gestational age of 31 weeks with a two-hour history of spontaneous drainage of liquor and subsequent vaginal bleeding. She has had three consecutive deliveries of dead achondroplastic babies and had no living child. The vaginal bleeding was moderate, and there was no dizziness or fainting spells. There was no history of bleeding from other sites, abdominal pain, trauma, fever, dysuria, vaginal discharge, or chronic cough. She was not known to be hypertensive or diabetic. She had no history of surgery or radiation exposure. There was no family history of achondroplasia.
The index pregnancy was spontaneously conceived and was supported by her husband, who was a 34-year-old trader. She booked at a gestational age of 13 weeks in a private hospital and her booking parameters were said to be normal. There was no previous ultrasound examination, and the pregnancy had been uneventful until presentation. She was referred to the teaching hospital because of the spontaneous rupture of membranes (SROM) and vaginal bleeding.
Her first confinement was in 2005. She had SROM at a gestational age of 30 weeks and delivered a live achondroplastic female baby in a private hospital. However, the baby died a few minutes after delivery.
Her second confinement was in January 2008. She had ultrasound diagnoses of gross fetal abnormality and achondroplasia in a private hospital. The pregnancy was consequently terminated by using intra-vaginal misoprostol at a gestational age of 25 weeks.
The third confinement was in January 2009. She booked at the teaching hospital at a gestational age of 28 weeks. Her hemoglobin genotype is AA and her blood group is O Rhesus D-positive. The result of a veneral disease research laboratory test was non-reactive. The results of a test for human immunodeficiency virus I and II were negative. The results of fasting blood sugar and two-hour postprandial tests were normal. She received one course each of intermittent preventive therapy for malaria and tetanus toxoid at 28 weeks of gestation. An abdominal ultrasonography scan at 30 weeks revealed features of fetal achondroplasia and polyhydramnios. She had a premature rupture of membranes at 31 weeks of gestation. She had an intra-uterine fetal death while on conservative management and subsequently a spontaneous vertex delivery of a fresh stillborn boy that weighed 1.2kg. The following features were noted: short upper and lower limbs, a relatively large head circumference, a conjoined and patent anterior fontanelle, and a gangrenous intestine. An anatomical diagnosis of achondroplasia was made at autopsy.
A clinical examination revealed a woman who was in painful distress, afebrile, and anicteric but pale. There was no pedal edema. Her height was 1.68m and her body weight was 60kg. The height of her husband was 1.70m. Neither had any features of achondroplasia. Her abdomen was enlarged and moved with respiration. There was generalized tenderness in her abdomen. The symphysiofundal height was 28cm. The abdomen was hard, and the fetal parts were not easily discernible. The fetal heart rate was 160 beats per minute.
The urgent packed cell volume was 30%, and the results of urine analysis and clotting time were normal. The transabdominal ultrasound examination at the labor ward revealed oligohydramnios and a viable fetus with achondroplasia. The placenta was fundal with small retroplacental blood collection. A diagnosis of abruptio placentae grade 1 was made. Our patient and her husband were counseled on the diagnosis and options of delivery. They consented to delivery via Cesarean section.
The intra-operative findings included an achondroplastic live male baby who had Apgar scores of 4 at one minute and 5 at 10 minutes and who weighed 1.1kg. The baby had a relatively large head circumference, normal length of trunk, short limbs, and broad hands and feet (rhizomelic) as well as a protruding tongue, a large defect joining anterior and posterior fontanelles, hepatosplenomegaly, and low-set ears. However, the baby died 30 minutes after birth. The estimated blood loss was 400mL, excluding a retroplacental clot of about 100mL. Her post-operative recovery was satisfactory. A diagnosis of recurrent achondroplasia was made.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.0, 'kg']}",100,95,105,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.0 kg - 20 kg) = 100.0 mL/hr.
Hence, the patient's fluid maintenance is 100.0 mL/hr."
5125,22,Maintenance Fluids Calculations,physical,decimal,pmc-3030067-1,Extracted,"A 3-year-old boy, weighing 18 kg, ASA physical status I, required surgery for a fracture of the lower third of the left humerus. After a thorough discussion of the risks and benefits with his parents, who then provided written informed consent, a USG supraclavicular brachial plexus block was undertaken. After inducing general anesthesia with 1 mg/kg of ketamine, a laryngeal mask airway (LMA) was inserted and ventilation was spontaneous.
A portable system with a linear array 5-10 MHz transducer (SonoSite® 180plus, Bothell, USA) was used for the USG supraclavicular brachial plexus block. The probe was placed in the coronal-oblique plane in the supraclavicular fossa and the puncture was in-plane (IP) from the lateral to medial (). The brachial plexus was identified as hypoechoic nodules surrounded by a hyperreflective fascial sheath, superior and lateral to the subclavian artery (). After infiltrating the adjacent skin and subcutaneous tissue, a 25-gauge 50-mm insulated block needle (UniPlex NanoLine, Pajunk®, Germany) was advanced along the long axis of the probe in plane with US beam guidance. When the brachial plexus bundle () was reached, the nerve stimulator (Stimuplex® HNS 12, B/Braun, Germany) was turned on, starting from 1.0 mA and decreasing by 0.5 mA to elicit a muscle twitch. After injecting 1ml of 0.5% ropivacaine, the muscle twitch disappeared and local anesthetic spread at the time of injection was observed in real time. Nine ml of 0.5% ropivacaine was injected after a negative aspiration test.
The patient underwent a closed reduction and percutaneous pinning of the distal humerus. Maintenance of anesthesia was carried out with sevoflurane 1.5 vol% in 50% oxygen/air until the end of the surgery. His vital signs did not change and no opioid supplementation was administered during surgery. The child did not require rescue analgesia in the postoperative period and no adverse effects were noted.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [18.0, 'kg']}",56,53.2,58.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 18.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (18.0 kg - 10 kg) = 56.0 mL/hr.
Hence, the patient's fluid maintenance is 56.0 mL/hr."
5126,22,Maintenance Fluids Calculations,physical,decimal,pmc-3888708-1,Extracted,"With approval of the local ethics committee (application number: 263/11, ethics committee of the University of Wuerzburg), we report the case of a 21-year-old male patient weighting 100 kg, who was scheduled for elective shoulder arthroscopy. Neither the patient nor his family had any history of neuromuscular disease or MH. According to the medical records, the patient underwent two uneventful anesthesias using halothane combined with oxygen (O2) and nitrous oxide (N2O) for cleft lip revision at the age of 5 months and at the age of 4 years, respectively. The preoperative laboratory examinations were within normal values. Initial heart rate (95 bpm), blood pressure (145/80 mmHg), and peripheral oxygen saturation (96%) were unremarkable. Anesthesia was induced by intravenous application of 0.1 mg/kg piritramid, an initial bolus of 2.5 mg/kg propofol followed by an additional application of 1.5 mg/kg propofol, and 1.5 mg/kg succinylcholine. To secure patient's airways, a size 8,0 mm cuffed endotracheal tube was inserted after direct laryngoscopy. Afterwards, anesthesia was maintained by sevoflurane 1.5 vol% supplemented by O2/N2O and application of 0.05 mg/kg piritramid if needed. During the initial period of surgery, hemodynamic and metabolic parameters were within normal limits with end-tidal carbon dioxide values between 38 and 39 mmHg. Suddenly, after 290 min a slightly increase of heart rate from 60 bpm to 80 bpm and a rise in systolic blood pressure from 120 mmHg to 135 mmHg were noticed. Furthermore, end-tidal carbon dioxide concentration rapidly increased from 39 mmHg to 85 mmHg within 5 min after the onset of sinus tachycardia. Simultaneously, oxygen saturation decreased from 98% to 93%. Unfortunately, there was no monitoring of body temperature, but the attending anesthesiologist observed and documented warming of head and chest during this episode. After MH was suspected, the anesthesiologist immediately stopped sevoflurane and hyperventilated the patient with 100% oxygen (25 L/min). In addition, 240 mg dantrolene was applied twice and anesthesia was continued intravenously by infusion of 5 mg/kg/h propofol and repeated fentanyl applications. After these interventions, hemodynamic and metabolic parameters were stabilized within 10 min. The surgical procedure was stopped, and the patient was transferred to the intensive care unit (ICU) in stable conditions.
Laboratory analyses performed after admission to the ICU detected a significant rhabdomyolysis with creatine kinase levels about 20.000 U/L and a hyperkalemia (6.4 mmol/L). Further laboratory data were unremarkable. Interestingly, blood gas analysis drawn one hour after the MH suspected event did not show signs of metabolic or respiratory acidosis. Four hours after the admission, the patient was extubated without neurological deficits.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [100.0, 'kg']}",140,133,147,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 100.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (100.0 kg - 20 kg) = 140.0 mL/hr.
Hence, the patient's fluid maintenance is 140.0 mL/hr."
5127,22,Maintenance Fluids Calculations,physical,decimal,pmc-4377388-1,Extracted,"A 30-year-old multiparous woman was admitted at the 41 weeks of her pregnancy for the purpose of labor induction. It had been pointed out that she had a uterine myoma with a diameter of 7 cm and her placenta was low-lying since 22 weeks of gestation. But the myoma did not obstruct the birth canal, and the placenta was located at least 2 cm apart from the internal uterine os just prior to delivery. With labor induction by oxytocin infusion, she delivered normally a healthy female infant weighing 4,056 g with Apgar scores of 8 and 9 after 1 and 5 minutes.
After delivery of the placenta, excessive hemorrhage occurred and could not be controlled by total 40 units of oxytocin infusion with intravenous fluids, vigorous uterine massage, and bimanual uterine compression. We diagnosed uterine atony after excluding placental retention, cervical or vaginal laceration, and uterine rupture by inspection, palpation, and ultrasound.
The total blood loss was estimated at 2,800 mL or more. Although her consciousness was still clear, her systolic blood pressure temporarily dropped to 80 mmHg and tachycardia (136 bpm) was also observed. The hemoglobin level decreased from 11.0 g/dL before labor to 6.5 g/dL at 2 hours after delivery on laboratory examination. The data on coagulating system including plasma fibrinogen levels (210 mg/dL) were almost normal.
Then, we tried a modified method of UBT after verbal informed consent of the patient. We used an intrauterine balloon catheter called “Cervical Balloon” (Utsunomiya Seisaku Co., Ltd.), which was produced for the purpose of cervical dilation prior to labor induction. Its balloon part was wrapped in gauze impregnated with 20 mL of 5% tranexamic acid solution (=1 gram of TXA), inserted through the cervix into the uterus and inflated with sterile water (210 mL) until the lowest part of the balloon was fitted just to internal uterine os (Figures –). In addition, a one-meter long normal gauze was packed in the vagina to prevent the balloon from slipping out. A blood transfusion with 6 units each of packed red cells and fresh frozen plasma was performed in parallel. Oxytocin and crystalloid fluid were infused continuously and intravenous antibiotics were given to prevent infection.
Afterwards, the bleeding abated immediately and stopped completely by the next day, when the balloon and gauze were removed after 20 hours of indwelling. She was discharged with her newborn in good condition on the fifth postpartum day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4056.0, 'g']}",16.224,15.4128,17.0352,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4056.0 g so this converts to 4056.0 lbs * kg/1000 g = 4.056 kg. Hence, the patient's maintenance fluid is 4.056 kg * 4 mL/kg/hr = 16.224 mL/hr.
Hence, the patient's fluid maintenance is 16.224 mL/hr."
5128,22,Maintenance Fluids Calculations,physical,decimal,pmc-4439900-1,Extracted,"A 24-day-old male infant was referred to our endocrine and metabolic center because of conjugated bilirubinemia, elevated liver enzymes and hepatomegaly. The patient had been admitted to another hospital on the 7th day of life with complaints of poor feeding and jaundice.
The infant was born by spontaneous vaginal delivery at 40 weeks following an uneventful gestation. His birth weight was 3280 g. Parents were second cousins. The family history revealed a sibling who had the same clinical features and died on the 10th day of life from a condition of unknown etiology.
On physical examination at presentation, weight was 3660 g (10th-25th p), length was 54 cm (25th-50th p) and head circumference was 36 cm (5th-10th p). The sclera and skin were icteric. Lenticular opacity (cataract) and hepatomegaly were noted. Other system examinations were normal. Laboratory investigations performed at admission revealed elevated liver enzymes [alanine aminotransferase: 194 IU/L (N: 0-41); aspartate aminotransferase: 224 IU/L (N: 0-41)] and a high level of conjugated bilirubin (2.8 mg/dL). During follow-up, the bedside capillary blood glucose level was measured as 369 mg/dL, 367 mg/dL and 342 mg/dL on three occasions. Despite high capillary blood glucose, urinalysis showed no glucosuria. Biochemical glucose measurement was also normal (71 mg/dL). Test results for urinary reducing agents was (+++) and urinary sugar chromatography showed (++) galactosuria. Galactose level was 514.2 mg/dL (N<10.00) with an inappropriately low galactose-1-phosphate uridyl transferase level [0.86 U/g Hb (N>5.00)], as shown in .
Based on presence of conjugated hyperbilirubinemia, hepatomegaly, cataract, reducing agents in the urine, galactose on sugar chromatography and a low blood galactose-1-phosphate uridyl transferase activity, a diagnosis of classical galactosemia was considered. The infant was weaned from breastfeeding and started on a lactose-free formula. Following this change in diet, the bedside capillary blood glucose measurements decreased to the normal range and were even in the low normal range ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3660.0, 'g']}",14.64,13.908,15.372,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3660.0 g so this converts to 3660.0 lbs * kg/1000 g = 3.66 kg. Hence, the patient's maintenance fluid is 3.66 kg * 4 mL/kg/hr = 14.64 mL/hr.
Hence, the patient's fluid maintenance is 14.64 mL/hr."
5129,22,Maintenance Fluids Calculations,physical,decimal,pmc-2810825-1,Extracted,"A 10-day-old male neonate weighing around 3 kg presented with minimal respiratory distress with persistent non-bilious vomiting since birth. On examination, there was tachypnea and tachycardia with dehydration and mild fullness in the epigastric region.
Plain X-ray of the chest showed the presence of an abnormal gas shadow in the right paravertebral region in the lower chest []. Ryle's tube was passed and it drained non-bilious aspirate. Barium contrast study revealed the dilatation of the esophagus with stomach in the right side of thorax in a state of volvulus with some contrast passing distally [].
After the correction of dehydration, the patient was taken for an emergency surgery. On exploration, the stomach was not found in the abdominal cavity and the gastroesophageal junction was at its normal site (). Further exploration confirmed the presence of the entire stomach within the chest cavity. Herniation of the stomach had occurred in the midline through an enlarged esophageal hiatus with the stomach in a state of mesenterioaxial volvulus. The gastric volvulus was reduced followed by the repair of the hiatal defect with gastropexy. The infant recovered well.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.0, 'kg']}",12,11.4,12.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.0 kg. Hence, the patient's maintenance fluid is 3.0 kg * 4 mL/kg/hr = 12.0 mL/hr.
Hence, the patient's fluid maintenance is 12.0 mL/hr."
5130,22,Maintenance Fluids Calculations,physical,decimal,pmc-6823080-1,Extracted,"A one-year-old female infant presented to the pediatric out patient clinic of Dr. Ruth KM Pfau, Civil Hospital Karachi (CHK) with a past four-day history of difficulty in breathing, which worsened over time, and high-grade continuous fever without rigors or chills. The fever was not associated with any diarrhea, vomiting, fits or jaundice.The child was accompanied by her mother. As stated by the mother, her child had been gaining excessive weight from the age of four months while maintaining normal appetite and diet. She was exclusively breast-fed for the first four months, her mother started introducing fruit, vegetables and meat into her diet from the age of five months. A significant weight gain was observed during her first year of life, at four months she weighed 6400 g, at 11 months she weighed 14500 g (>95th percentile). The mother did not report any complications or illnesses during pregnancy. Her baby cried immediately after birth, and there were no complications during or after delivery. There is no consanguinity between mother and father. Immunization status was up to date. There was no significant family history except for her elder sibling who was obese, polydactyly of the right hand and a vision problem.
On examination, the patient was lying on a bed depicting several abnormalities, including obesity with a weight of 15000 g (>95th percentile) (Figure ), high weight for height (>98th percentile), a body mass index (BMI) was 18 (85th percentile), and also polydactyly of the left foot (Figure ).
Her length and head circumferences were 83 cm and 46 cm respectively. She showed obvious signs of respiratory distress with a respiratory rate of 55 breaths/min and a heart rate of 112 beats/min. Her blood pressure was 127/77 mmHg. Chest examination revealed bilateral coarse crepitation with prominent subcostal and intercostal recessions. Central nervous system (CNS) examination was unremarkable with no spasticity or paraparesis. Her pupils were equally reactive to light however they were not following it. The ability of a child to follow a target with her eyes was impaired suggestive of reduced visual acuity. Rest of the systemic examination was unremarkable.
BBS, LMS and Cohen’s syndrome were among the differential diagnoses until further investigations were carried out. Laboratory investigation showed an elevated creatinine of 1.3 mg/dL [Normal (N) = 0.3 to 0.7], blood urea nitrogen (BUN) of 38 mg/dL (N = 4-15) and a creatinine clearance of 25.5 ml/min suggesting renal pathology. The total leukocyte count (TLC) was 14.0 x 109/L, with 40% neutrophils and 48% lymphocytes. Her inflammatory marker was also raised with a C-reactive protein (CRP) of 8.3 mg/L (N = 3) suggestive of infection. Bilateral sensory-neural hearing loss was confirmed by Brainstem Evoked Response Audiometry (BERA). The ultrasound of kidneys, ureters and bladder (KUB) showed left dysplastic kidney (Figure ).
Fundoscopy showed retinal pigmentary changes showing dark intraretinal pigments indicative of early stages of retinitis pigmentosa. The X-ray of the chest (Figure ) confirmed the presence of bronchopneumonia. The above findings were most likely indicative of BBS in our patient.
The patient was initially treated with oxygen via continuous positive airway pressure along with intravenous (IV) amoxicillin/clavulanic acid and acetaminophen. She was nebulized with ipratropium bromide and albuterol. Her hypertension was managed by enalapril and amlodipine. She improved over a period of three days and is under regular follow up with no recurrence of respiratory complications. Interactive and play therapy was encouraged since the child was mentally challenged. She was referred to the nephrology department for the consideration of dialysis and is being evaluated by specialists to provide visual aids, hearing aids (for bilateral sensorineural hearing loss), mobility training and speech therapy. Furthermore, early intervention for the management of obesity was accomplished through proper diet and by maintaining normal appetite. The mother of a child was thoroughly counseled about these interventions.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15000.0, 'g']}",50,47.5,52.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15000.0 g so this converts to 15000.0 lbs * kg/1000 g = 15.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.0 kg - 10 kg) = 50.0 mL/hr.
Hence, the patient's fluid maintenance is 50.0 mL/hr."
5131,22,Maintenance Fluids Calculations,physical,decimal,pmc-7752288-1,Extracted,"In November 2012, a 45-year-old Caucasian woman presented to her primary care physician with lower abdominal pain. At the time of presentation, her medical history was notable for obesity (weight = 183.2 kg and body mass index (BMI) 61.6 mg/m2), type 2 diabetes mellitus (hemoglobin A1C (HbA1C) = 7.5%), hypertension, and recurrent episodes of cellulitis. A contrast-enhanced CT scan of the abdomen and pelvis in the portal venous phase was obtained that showed no source for her abdominal pain but did note an incidental 5.5 × 4.0 cm left adrenal tumor containing macroscopic fat and reported as a myelolipoma (). This tumor had grown from a CT scan in April 2007, where it measured 4.4 × 3.3 cm (). The right adrenal appeared normal on both scans.
In September 2014, the patient was referred to an endocrinologist for worsening diabetes mellitus. At this visit, her weight was 184.7 kg with a BMI of 61.9 mg/m2 and HbA1C of 9.2%. Because of clinical concern for hypercortisolism, a functional workup was initiated. A 1 mg dexamethasone suppression test revealed a postsuppression cortisol of 9.3 µg/d (reference range <1.8 µg/dL). Serum aldosterone was 4.7 ng/dL with a renin activity of 0.3 ng/ml/hr. Plasma free metanephrines were less than the upper limit of normal, and a morning adrenocorticotropic hormone (ACTH) was 16 ng/L (reference range 6–50 ng/L). The patient was lost to follow-up before completing further testing.
In June 2015, she reestablished care with her endocrinologist. Physical exam was notable for obesity, but without other clinical signs of Cushing's syndrome, including moon facies, buffalo hump, or striae. A dual-energy X-ray absorptiometry (DEXA) scan showed normal bone health. The 24-hour urine cortisol level was 54.1 µg/day (reference range <45 µg/day). Repeat 24-hour urine cortisol was again elevated at 47.5 µg/day. ACTH was 8 ng/L (reference range 6–50 ng/L) and dehydroepiandrosterone sulfate (DHEAS) was suppressed at <15 µg/dL (reference range 32–240 µg/dL). Repeat 1-mg dexamethasone suppression test was elevated at 13.5 µg/dL (reference range <1.8 µg/dL). BMI was 62.4 kg/m2 (weight 186.1 kg), and HgA1C was 9.0%. Given continued symptomatology and positive lab values, the patient was then referred to endocrine surgery with suspicion for Cushing's syndrome from her left adrenal myelolipoma but failed to make her appointments.
In March 2016, the patient was seen by endocrine surgery for consideration of a laparoscopic left adrenalectomy for Cushing's syndrome. A repeat CT showed the tumor had increased in size to 5.8 cm and was still partially composed of macroscopic fat and consistent with a myelolipoma (). BMI was 65.1 kg/m2 (weight = 188.7 kg) and HbA1C was 10.0%. She underwent an uncomplicated laparoscopic adrenalectomy in October 2017. The case was performed via a standard transabdominal approach. The patient had a generous amount of intraabdominal fat which was mobilized with the colon and spleen from the left adrenal gland. She required an increased pneumoperitoneum pressure to facilitate exposure (17 cm of water). The remainder of her case and postoperative course were unremarkable. On surgical pathology, she was noted to have a 6.7 cm adrenal collision tumor comprised of a 4 cm adrenocortical adenoma and a 2.7 cm myelolipoma (). Postoperatively, the patient was placed on corticosteroid replacement, which was tapered over the course of a year and a half without significant symptoms of adrenal insufficiency. 24 hour urine cortisol following discontinuation of steroids normalized to 7.6 µg/24 hours. Her weight decreased to 149.4 kg with a BMI of 51.6 and HbA1c of 7.3% ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [188.7, 'kg']}",228.7,217.265,240.135,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 188.7 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (188.7 kg - 20 kg) = 228.7 mL/hr.
Hence, the patient's fluid maintenance is 228.7 mL/hr."
5132,22,Maintenance Fluids Calculations,physical,decimal,usmle-596,Extracted,"A 62-year-old man comes to the physician for a follow-up examination after having been diagnosed with stage II adenocarcinoma of the left lower lung lobe without evidence of distant metastases 1 week ago following an evaluation for a chronic cough. He has hypertension and type 2 diabetes mellitus. He has smoked one pack of cigarettes daily for the past 40 years. His current medications include metformin, sitagliptin, and enalapril. He is 177 cm (5 ft 10 in) tall and weighs 65 kg (143 lb); BMI is 20.7 kg/m2. He appears lethargic. Vital signs are within normal limits. Pulse oximetry shows an oxygen saturation of 98%. Examination shows inspiratory wheezing at the left lung base. The remainder of the examination shows no abnormalities. A complete blood count and serum concentrations of electrolytes, creatinine, glucose, and liver enzymes are within the reference range. Spirometry shows an FEV1 of 1.6 L. The diffusing lung capacity for carbon monoxide (DLCO) is 66% of predicted.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [65.0, 'kg']}",105,99.75,110.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 65.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (65.0 kg - 20 kg) = 105.0 mL/hr.
Hence, the patient's fluid maintenance is 105.0 mL/hr."
5133,22,Maintenance Fluids Calculations,physical,decimal,pmc-3799273-1,Extracted,"A 24-year-old woman who lived in Saitama, Japan had three pregnancies, two childbirths, body mass index (BMI) of 22.3, and unremarkable past medical and family histories. Furthermore, her pre pregnancy weight was 55 kg and her height 163 cm.
She also had an uneventful first trimester, but developed a fever of >39°C at 22nd week, 1st day of pregnancy. Because of prolonged headache and nausea, she was referred to our hospital in Saitama for complete physical examination on October 2008. On admission, she had blood pressure of 103/51 mmHg, heart rate of 100 beats per min (bpm), body temperature of 39.0°C, mild stiffness in the neck, and cold extremities. No neurological abnormalities, such as consciousness disturbance or paralysis, were observed. However, brain computed tomography (CT) for the prolonged headache revealed a 1.5 cm mass in the right frontal lobe, while hematological analysis showed an elevated white blood cell count of 12,400 cells/µl (neutrophils, 87.7%). Cerebrospinal fluid findings were positive for gram-positive bacteria, an increased cell count (especially for neutrophils) of 2,332 cells/µl, and a low glucose concentration of 30 mg/dl. Brain MRI revealed a 1.5 cm mass with a high intensity signal inside and a low intensity T2 signal on the margin in the deep white matter of the right frontal lobe. Based on the above findings and a high intensity zone surrounding the mass on diffusion-weighted images, she was immediately placed on intensive therapy with concurrent administration of antibiotics cefotaxime (2 g/day) and meropenem (3 g/day), as well as glycerin 20 g/day to reduce intracranial pressure. shows a list of examinations performed in search of causal factors, while the results show the isolation of methicillin-sensitive Staphylococcus aureus (MSSA) from the throat. On the other hand, she had no dental problems. Because of unremarkable upper gastrointestinal endoscopy findings and a negative fecal occult blood test result, the possibility of brain metastasis of a malignant tumor was ruled out. After six weeks of intensive therapy with concurrent administration of two antibiotics and glycerin, the headache and nausea disappeared along with a reduction in the number of white blood cells. Subsequent brain MRI at 28th week, 4th day of pregnancy showed no enlargement of the abscess and disappearance of the surrounding edema, with no indication of puncture drainage. At this point, she was switched to oral administration of amoxicillin 750 mg/day for four weeks and was discharged at 29th week, 3rd day of pregnancy. shows the post admission course.
She vaginally delivered a 2,890 g girl baby at 38th week, 5th day of pregnancy, with no abnormalities. No neurological abnormalities were evident during a five-year follow-up observation conducted over the phone.
MRI findings at the 22nd and 28th week of pregnancy are shown in .","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [55.0, 'kg']}",95,90.25,99.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 55.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (55.0 kg - 20 kg) = 95.0 mL/hr.
Hence, the patient's fluid maintenance is 95.0 mL/hr."
5134,22,Maintenance Fluids Calculations,physical,decimal,usmle-907,Extracted,"A 33-year-old woman comes to the emergency department because of severe right flank pain for 2 hours. The pain is colicky in nature and she describes it as 9 out of 10 in intensity. She has had 2 episodes of vomiting. She has no history of similar episodes in the past. She is 160 cm (5 ft 3 in) tall and weighs 104 kg (229 lb); BMI is 41 kg/m2. Her temperature is 37.3°C (99.1°F), pulse is 96/min, respirations are 16/min and blood pressure is 116/76 mm Hg. The abdomen is soft and there is mild tenderness to palpation in the right lower quadrant. Bowel sounds are reduced. The remainder of the examination shows no abnormalities. Her leukocyte count is 7,400/mm3. A low-dose CT scan of the abdomen and pelvis shows a round 12-mm stone in the distal right ureter. Urine dipstick is mildly positive for blood. Microscopic examination of the urine shows RBCs and no WBCs. 0.9% saline infusion is begun and intravenous ketorolac is administered.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [104.0, 'kg']}",144,136.8,151.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 104.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (104.0 kg - 20 kg) = 144.0 mL/hr.
Hence, the patient's fluid maintenance is 144.0 mL/hr."
5135,22,Maintenance Fluids Calculations,physical,decimal,pmc-7947137-1,Extracted,"A 61-year-old woman was admitted to our hospital for treatment of gastric cancer. Preoperative examination showed that the tumor was located in the middle part of the stomach and had invaded the muscularis propria (MP) but without lymph node metastasis. She underwent LADG with extragastric lymph node dissection (D2) [] using laparoscopic ultrasonic shears (Harmonic Scalpel; Ethicon Endo-Surgery, Cincinnati, OH, USA). Billroth I gastroduodenostomy was performed, and a drain was placed under the left lobe of the liver from the right upper abdomen. On postoperative day 2, the patient was allowed oral intake of food. The drain was removed at postoperative day 3. The postoperative course was uneventful and she was discharged at postoperative day 14. Histological tumor findings were M, Less, Type 2, 50 × 20 mm, por > sig, pT1b (SM2), pN1 (2/47), pStage IB [].
Two months after LADG, she was readmitted to hospital because of abdominal distension. Her weight was 55.0 kg, a gain of 0.8 kg since discharge. Physical examination revealed increasing abdominal girth and bilateral leg edema. The serum albumin concentration was 3.0 g/dL, showing hypoalbuminemia. Ultrasound examination confirmed diffuse ascites. A percutaneous peritoneal drainage catheter was placed in the peritoneal cavity under ultrasonographic imaging, and 7100 mL of white-milky fluid was drained which had a high triglyceride level of 1320 mg/dL. Cytological examination of the ascites showed it to be class IIb. Bacterial culture was negative. We therefore made a diagnosis of chylous ascites.
Although a fat-restricted diet was initiated, abdominal girth gradually increased. Oral intake was discontinued and total parenteral nutrition started on the 5th day, but increasing body weight and decreasing serum albumin concentration was not controlled. Because no improvement was observed, PTTDE was performed on the 8th day.
Ultrasound-guided access to the left inguinal lymph nodes was achieved with a 26G needle. Lipiodol was slowly administered to the lymph nodes. Fluoroscopic imaging showed an accumulation of Lipiodol in the left lumbar lymphatic channels (Fig. ) and the thoracic duct. Fluoroscopic imaging indicated the leakage site to be in the upper abdominal thoracic duct (Fig. ).
Percutaneous transabdominal thoracic duct cannulation was performed using a 21G Chiba needle at the level of the navel under fluoroscopic guidance, and a V-18 peripheral guidewire was used to probe for the duct. Once the thoracic duct had been accessed, a microcatheter (Prominent Raptor) was passed over the guide wire into the upper thoracic duct. Thoracic duct embolization was then performed. First, microcoils (AZUR CX 6 mm–20 cm and 5 mm–15 cm) were positioned to provide a matrix for glue polymerization on the thoracic part of the thoracic duct, after which 20% n-butyl cyanoacrylate (NBCA) diluted with Lipiodol was used for embolization (Fig. ). Abdominal CT scan obtained immediately after lymphangiography and PTTDE showed contrast pooling between the abdominal aorta and the pancreas head and contrast extravasations accumulating at Morrison’s pouch (Fig. ).
Two days after thoracic duct embolization, her body weight showed a progressive decrease and inversely, her serum albumin concentration increased. Five days after thoracic duct embolization, oral intake was resumed and on the 24th day (17 days after thoracic duct embolization), she was discharged without recurrence of ascites (Fig. ). She has remained asymptomatic.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [55.0, 'kg']}",95,90.25,99.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 55.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (55.0 kg - 20 kg) = 95.0 mL/hr.
Hence, the patient's fluid maintenance is 95.0 mL/hr."
5136,22,Maintenance Fluids Calculations,physical,decimal,pmc-6615582-1,Extracted,"A 40-year-old Hispanic woman was admitted to University Medical Center New Orleans, Louisiana in August 2017 for evaluation of progressively worsening abdominal pain of eight months duration with associated intermittent nausea and vomiting. The patient also reported losing approximately 30 kilograms in weight. She denied any associated fever, night sweats, change in bowel habits, rash, enlarged lumps or palpable masses. She was previously healthy and denied any personal or family history of malignancy. She never smoked and used alcohol sparingly. She had no known allergies.
On physical exam, the patient’s body temperature was 98.6°F, blood pressure was 100/60 mmHg, and heart rate was 120/min. Cardiovascular and pulmonary exams were unremarkable. The abdomen was soft and mildly tender. A palpable mass was appreciated in the right periumbilical region. No cervical, axillary or inguinal lymphadenopathy was appreciated. Laboratory analysis showed severe metabolic derangements as follows: sodium of 121 mEq/L (reference range, 135-145 mEq/L), potassium of 2.2 mEq/L (reference range, 3.5-5.5 mEq/L), blood urea nitrogen of 61 mg/dL (reference range, 7-20 mg/dL), and serum creatinine of 3.03 mg/dL (reference range, 0.6-1.2 mg/dL). Liver and pancreatic enzymes were in the normal limits. The hematologic panel was consistent with mild normocytic anemia with a hemoglobin of 11.2 g/dL along with leukocytosis with a white blood cell count of 16.6 × 109/L. Platelet count was normal at 299 × 109/L. A peripheral blood smear was within normal limits. A chest radiograph was unremarkable. A non-contrast computed tomography (CT) scan of the abdomen revealed fluid-filled distention of the stomach and proximal duodenum with concern for proximal small bowel obstruction.
The patient was admitted to the intensive care unit given her various metabolic disturbances and was treated conservatively for partial small bowel obstruction. After optimization of her kidney function, a repeat scan of the abdomen with contrast was performed. An irregular mass-like thickening at the level of the second/third portion of the duodenum was identified resulting in severe luminal narrowing. Also, peritoneal ""carcinomatosis"" with multiple target lesions was noted (Figure ). The overall picture was concerning for metastatic carcinoma. Later, serum carcinoembryonic antigen (CEA) and Ca 19-9 levels were checked and were within normal limits.
An upper endoscopy was performed the following day revealing a frond-like friable obstructing mass in the second portion of the duodenum of which biopsies were taken (Figure ). Large-sized lymphocytes were seen (Figure ).
Immunohistochemical stains demonstrated that these cells were strongly and diffusely positive for cluster of differentiation (CD)20 and CD79a, and negative for CD3, CD5, CD10, CD30, B-cell lymphoma 2 (Bcl-2) and pan-cytokeratin. Additionally, nuclear staining in about 40% of the neoplastic cells was present for c-Myc and in more than 30% of cells for Bcl-6. A diagnosis of DLBCL with germinal center immunophenotype was made (CD10 negative, Bcl-6 positive, MUM-1 negative). The Ki-67 index was elevated within the B cell population at 60%-70%. No assay specific abnormalities were detected by Bcl-2, Bcl-6, and c-Myc fluorescence in situ hybridization (FISH) probes. Completion staging with neck, chest, and pelvic CT scans failed to demonstrate any additional evidence of disease. A bone marrow examination showed no involvement by lymphoma. Human immunodeficiency virus (HIV) and hepatitis serologies were negative. Serum lactate dehydrogenase was mildly elevated at 318 U/L. Given the patient’s peritoneal lymphomatosis and weight loss, she was diagnosed with stage IV B lymphoma by Ann Arbor staging.
Given the aggressive presentation with evidence of bowel obstruction and peritoneal involvement (along with markedly elevated Ki-67), the decision was made to start treatment as an inpatient. Therefore, cycle 1 of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) was administered, and the patient tolerated the treatment well. Central nervous system (CNS) analysis and chemoprophylaxis were not performed as she was considered intermediate-risk for CNS involvement. A few days after the completion of cycle 1, she was able to tolerate oral feeding and she was discharged home. She received the remainder of her treatment as an outpatient and completed a total of six cycles of systemic chemotherapy. She exhibited significant clinical and radiographic improvement throughout her treatment. In fact, a repeat scan after six cycles showed improved luminal duodenal narrowing with resolution of the peritoneal deposits (Figure ). A push enteroscopy was also performed to assess for local response and demonstrated no evidence of disease. She remains now disease-free 15 months after her diagnosis and 10 months after completion of her treatment.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [30.0, 'kg']}",70,66.5,73.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 30.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (30.0 kg - 20 kg) = 70.0 mL/hr.
Hence, the patient's fluid maintenance is 70.0 mL/hr."
5137,22,Maintenance Fluids Calculations,physical,decimal,pmc-4989811-1,Extracted,"A 54-year-old woman (height, 169 cm and weight, 74 kg) underwent elective surgery for a left posterior parietal meningioma. Her medical history consisted of arterial hypertension well controlled by nebivolol therapy (10 mg/day) that was not interrupted before surgery. The patient was free of visual complaints before surgery. The pre-operative anaesthesia evaluation found her to be in excellent condition. The patient was accepted in the American Society of Anesthesiologists’ physical status 1 with a Lee's cardiac risk index of 1. Pre-operative laboratory investigations were within normal limits. Pre-operative arterial blood pressure was 160/80 mm Hg. Haemoglobin concentration at the beginning of surgery, however, was 11.2 g/dL and haematocrit 35%. She was induced with controlled administration of propofol and sevoflurane. Cisatracurium was used to achieve orotracheal intubation with the help of a No. 8 endotracheal tube. Anaesthesia was maintained with propofol target-controlled infusion (target: 4-6 μg/ml) and continuous infusion of remifentanil (0.5-1 μg/kg/min). Central venous pressure (CVP) and arterial pressure were monitored after cannulation. She was then positioned for surgery in the prone position, with a mild inclination of the table towards a reverse Trendelenburg position. Her head was maintained in a Mayfield frame, with a mild flexion. There was no external compression of the ocular globes. During anaesthesia, end tidal CO2 was continuously kept in the range of 30 mm Hg and oxygen saturation always above 95%. The patient received 200 ml mannitol 15% for brain relaxation 1 h after the beginning of surgery. Her systolic and mean blood pressure was maintained in the range of 80-100 mm Hg and around 60 mm Hg, respectively, throughout the surgery []. Total duration of anaesthesia was 7 h and the patient remained in prone position for 6 h. Total blood loss was around 50 ml. Total fluid infused was 2000 ml crystalloids and intraoperative urine output was 700 ml. There was no use of vasopressors at any point. Extubation was performed 49 min after the surgery. The patient did not receive neuromuscular reversal agents. At the end of surgery, the haemoglobin concentration was 11.7 g/dL and the haematocrit was 36%. The patient was then transferred to Intensive Care Unit (ICU) for further management. On admission, her CVP was 8 mm Hg, systolic arterial pressure 135 mm Hg and mean pressure 85 mm Hg, and these values were maintained during the whole ICU stay. Fluid balance over the first 24 h was slightly negative (−300 mL). After recovery from anaesthesia in ICU, the patient began complaining of a significant decrease in visual acuity without any ocular pain. She was unable to count fingers at a distance of 2 m. The ophthalmological examination was otherwise unremarkable, except for a sluggish pupillary light reflex. There was no evidence of papilloedema on fundoscopy. Intraocular pressure was within normal range. The post-operative brain computed tomography ruled out ischaemic or haemorrhagic complications. The patient was assessed with VEPs on the 1st post-operative day. The examination consisted of flash VEPs (fVEPs) (day 1) and monocular pattern reversal VEPs (pVEPs) (day 1 and 5). The fVEPs were elicited by light-emitting diode goggles (monocular stimulation; red light; flash duration: 1000 μsec; rate: 1.7 Hz; analysis time 500 ms) and recorded at left and right occipital location (O1 and O2). The pVEPS were obtained on day 1 and day 5 by reversal of a black-and-white checkerboard (monocular stimulation, using 3 check sizes, respectively, of 1΀, 30’ and 15’ of arc, at a rate of 1.7 Hz). The pVEPs were recorded at the medial occipital location (Oz) referred to the central medial location (Cz). The fVEPs remained normal at day 1 and were not retested (data not shown). In contrast, the latency of the pVEPs showed significant slowing in both eyes, irrespective of the check size, with a typical paramacular profile (positivity-negativity-positivity) [ above panel]. This alteration in the structure of the VEPs suggested that all nervous fibres in the optic nerve were not affected to the same extent. The latency and structure of pVEPs were normalised by day 5 [, lower panel].
Starting from post-operative day 2, the patient made a complete recovery of visual acuity. This was confirmed by ophthalmological examination at discharge.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [74.0, 'kg']}",114,108.3,119.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 74.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (74.0 kg - 20 kg) = 114.0 mL/hr.
Hence, the patient's fluid maintenance is 114.0 mL/hr."
5138,22,Maintenance Fluids Calculations,physical,decimal,pmc-6075625-1,Extracted,"A 21-year-old female presented to the Case Western Reserve University School of Dental Medicine Clinic in Cleveland, Ohio. Her chief complaint was a slowly growing painless swelling involving the right side of the mandible that had started one year previously. Her past medical history revealed no previous surgeries or diseases. Her vital signs were recorded as 120/80 mmHg blood pressure, a pulse of 103 beats per minute (bpm), 15 respirations per minute, height - 5.1 ft, weight - 165 lb, and a calculated body mass index (BMI) of 23.71. No other medical conditions were identified, and the patient did not report taking any medications. Clinical examination revealed an intraoral swelling involving the posterior part of the body of the mandible and extending to the ramus on the right side. On palpation, the lesion was hard in consistency, except for select areas which exhibited a softer texture.
The patient was referred to a private dental imaging center for a CBCT scan to evaluate the extent of the lesion. A board-certified oral and maxillofacial radiologist performed the radiographic interpretation of the CBCT scan. The scan revealed a well-defined radiolucent lesion ranging from the interdental bone in between the second and third right molars and extending to the ramus of the mandible posteriorly in the anteroposterior direction. The lesion extended from the alveolar crest to the inferior border of the mandible in the superior-inferior direction (Figure ).
Osteolytic changes of the alveolar crest margin distal to the third molar were noted and displaced the roots of the third molar more distally. The sagittal cut showed that the lesion had a multilocular appearance with an incomplete internal septal structure, demonstrating wispy-like septations. The inferior border of the mandible showed some resorption with undulating borders (Figure ). The lesion showed expansion of the alveolar crest. In axial cuts, the lesion involved the ramus of the mandible, and expansion and thinning of the inner cortical plate were noted.
Extending more medially, the borders of the lesion showed fine wispy-like septations with undulating borders (Figure ). Coronal slices demonstrated the resorption of the outer cortical boundary, a multilocular appearance, an expansible nature, and thinning and resorption of the inner cortical boundary. The presence of an intact (albeit thinning) border, wispy septations, and expansion led to a provisional diagnosis of an aggressive benign tumor. Central giant cell granuloma, ameloblastoma, and keratocystic odontogenic tumor (KOT) were considered in the differential. However, the presence of fine, wispy septations and undulating borders favored a CGCG diagnosis.
An incisional biopsy was performed, and the histopathological report for the lesion revealed a giant cell reparative granuloma formed of proliferating spindle cells, multinucleated giant cells, extravasated red blood cells (RBCs), and mononuclear cells. No specific inflammatory granuloma or significant nuclear anaplasia and mitosis or other evidence of malignancy were noticed. This information, along with clinical and radiological features, was suggestive for CGCG and hyperparathyroidism (because of similar histopathological features). Laboratory investigations showed that the parathyroid hormone, alkaline phosphates, and calcium levels were all within normal limits. This excluded hyperparathyroidism as a possible diagnosis. The patient underwent surgical resection of the lesion. The surgery and recovery were uneventful.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [165.0, 'lbs']}",114.84268,109.10055,120.58481,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 165.0 lbs so this converts to 165.0 lbs * 0.453592 kg/lbs = 74.84268 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (74.84268 kg - 20 kg) = 114.84268 mL/hr.
Hence, the patient's fluid maintenance is 114.84268 mL/hr."
5139,22,Maintenance Fluids Calculations,physical,decimal,pmc-7396326-1,Extracted,"The patient was a 0-day-old male neonate with left isolated CDH. The diagnosis of CDH was made prenatally, and 46, XY, der(21)t(1;21)(q42.3;q22.2) was diagnosed via examination using the amniotic fluid. Fetal ultrasonic testing showed a lung thorax transverse area (LT) ratio of 0.10. He was born at full term, 38 weeks and 2 days, through vaginal delivery in the delivery room. The birth weight was 2105 g. After birth, intubation (uncuffed endotracheal tube, 3.5 mm, Smiths Medical, USA) was performed immediately. After admission to the neonatal intensive care unit (NICU), the piston HFOV (calliope-alpha, Metran, Japan) was started as the initial ventilation. At the initial settings, the MAP was 14 cmH2O, the stroke volume (SV) 20 ml, and the frequency 12 Hz. Inhaled nitric monoxide (iNO) was used at 20 ppm because of the persistent pulmonary hypertension of the newborn (PPHN) (Fig. ). Fourteen hours after birth, PPHN increased and Lipo-prostaglandin E1 (Lipo-PGE1) was administered to keep the arterial duct open and maintain blood flow to the pulmonary artery. After administration of Lipo-PGE1, the level of saturation was increased both pre-ductally and post-ductally, and the saturation was kept around 95% for the next 30 h. The level of saturation decreased, and the dissociation of pre-ductal and post-ductal saturation re-occurred 44 h after birth. Increasing the iNO concentration and MAP was ineffective. Blood gas analysis revealed an alveolar-arterial oxygen difference (AaDO2) of 500 Torr, and oxygenation index (OI) of 20. The PaO2/FiO2 (P/F) ratio was 58.8 (Fig. a–c), which required considering the introduction of extra-corporeal membrane oxygenation (ECMO) to save the patient’s life. Before introducing the ECMO, we inspected the pulmonary function tests results. The static pulmonary function was measured by occlusion method using ARFEL III (Aivision, Japan), which adapted a Fleischer type of pneumotachograph. Because under HFOV, pulmonary function tests cannot be performed accurately, we changed ventilator mode from HFOV to CMV, and used muscle relaxant to rule out the effects of spontaneous breathing just before running the test. The occlusion valve operation was measured with 4–5 breaths to confirm reproducibility. The respiratory-system compliance (Crs) level was 0.29 ml/cmH2O/kg and the respiratory-system resistance (Rrs) level was 515 cmH2O·kg/L/s. Because the Rrs level was elevated, we made the decision to shift the ventilator mode from HFOV to CMV at the ventilator settings of PIP 20 cmH2O, PEEP 5 cmH2O, and ventilator rate of 40/min. After switching to CMV, the patient’s heart rate rose from 159 bpm to 169 bpm, and saturation rose from 89 to 96% immediately. Thirty minutes after switching to CMV, blood gas tests revealed that the AaDO2 dropped to 275 and the OI to 7.3, while the P/F ratio increased (Fig. a–c). At 55 h after birth, the operation for repairing the diaphragm was performed. The patient was then discharged from our hospital at 1 month of age with an uneventful course of treatment.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2105.0, 'g']}",8.42,7.999,8.841,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2105.0 g so this converts to 2105.0 lbs * kg/1000 g = 2.105 kg. Hence, the patient's maintenance fluid is 2.105 kg * 4 mL/kg/hr = 8.42 mL/hr.
Hence, the patient's fluid maintenance is 8.42 mL/hr."
5140,22,Maintenance Fluids Calculations,physical,decimal,pmc-5649119-1,Extracted,"A female child of Chinese descent was conceived by a 37 year old G
1P
1→2 woman by
in-vitro fertilization and born at 33
+1 weeks’ gestational age with a birth weight of 1315g (2
nd percentile, UK-WHO growth charts
). At three weeks of age, acholic stools were noted and she was found to have cholestatic jaundice (total bilirubin 6.9 mg/dL, reference range [RR] <1 mg/dL; direct bilirubin 4.4 mg/dL, RR <0.4 mg/dL), elevated transaminases (AST 159 U/L, RR <63 U/L; ALT 54 U/L, RR <32 U/L) and alkaline phosphatase (422 U/L, RR <321 U/L) with normal γ-glutamyl transpeptidase (33 IU/L, RR <50 IU/L). Coagulation times and blood counts were normal: prothrombin time international ratio was 1.0 (RR <1.2), partial thromboplastin time 37.4 s (RR <40), and platelet count 216 k/µL (RR 150 – 200 k/µL).
Imaging studies included an abdominal ultrasound that demonstrated hepatosplenomegaly and normal hepatobiliary anatomy, as well as a cholescintigraphy scan that failed to identify tracer excretion into the gallbladder. She subsequently underwent an intraoperative cholangiogram that was normal; liver biopsy was also obtained showing severe intercanalicular cholestasis, hepatocyte ballooning with giant cell formation, portal inflammation, and extramedullary hematopoiesis. UDCA 30 mg/kg/day was started for treatment of cholestatic jaundice at age four weeks.
Biochemical investigations ruled out galactosemia, hepatorenal tyrosinemia, fatty acid oxidation disorders, organic acidemias, amino acidopathies, congenital disorders of glycosylation, peroxisomal disorders, disorders of polyol metabolism, mucopolysaccharidosis type VII, oligosaccharidoses, Farber disease, and lysosomal acid lipase deficiency. Of note, her acid lipase activity was above normal range, at 681 nM/punch*hr (RR 79.9 – 378.6 nM/punch*hr). Post-biopsy, she could not tolerate attempts at extubation, and a tracheostomy was placed at five weeks of life. Mechanical ventilation was difficult, initially requiring high positive end-expiratory pressures (PEEP) of +7 cm H
2O due to atelectasis from hepatosplenomegaly and abdominal distension, and often exacerbated by recurrent bacterial tracheitis. Her direct bilirubin ranged between 4 – 7 mg/dL and total bilirubin between 7 – 10 mg/dL, peaking during episodes of tracheitis. Advancement of enteral feedings was frequently interrupted by abdominal distension and emesis. Ventilation and feeding intolerance gradually improved, so that by 3 months she was at normal PEEP of +5 cm H
2O, and tolerating 100 mL/kg/day of 0.73 kcal/mL elemental formula.
A urine bile acid profile obtained at age 2 months while on UDCA was consistent with mild-to-moderate cholestasis, but because of potential masking of a bile acid synthetic defect by UDCA, the bile acid profile was repeated at 3 months of age, off UDCA therapy for 5 days. This profile indicated a potential bile acid synthesis defect in 3β-hydroxy-Δ(5)-C(27)-steroid oxidoreductase encoded by the
HSD3B7 gene, and treatment with cholic acid (CA) was suggested at age 4 months to suppress endogenous bile acid synthesis. Pending
HSD3B7 molecular sequencing, the patient was consented under Cincinnati Children’s Hospital Study #2011-2448 to participate in an emergency compassionate use, open-label study of enteral CA (Asklepion Pharmaceuticals, Baltimore, MD, USA) under protocol #CAC-002-01. The CHOC Children’s Institutional Review Board was consulted due to her severely ill condition, and allowed emergency access for the patient to be CA contingent upon parental consent to the Cincinnati Children’s Study.
At 4.5 months of age, the patient began CA, 15 mg/kg/day. Her stable pre-CA elevation in transaminase and bilirubin levels began to increase 7 days after initiation of CA, and continued to increase (See
 and
). She also developed worsening hepatosplenomegaly, vomiting, and increase in abdominal girth from 39 cm pre-CA to 46 cm. Twenty-five days after CA initation, she began to have bradycardic / desaturation events without signs of infection. The levels of PEEP required to prevent bronchospasm increased from +5 to +10, and eventually +15 cm H
2O. She remained on CA therapy for a total of 37 days; due to worsening of clinical and laboratory parameters and no mutations identified in
HSD3B7, CA was discontinued and UDCA restarted at 30 mg/kg/day (
 and
). She was transferred to another centre for consideration of orthotopic liver transplantation, where UDCA and high ventilator support was continued. Her PEEP was slowly titrated downwards, eventually reaching +6 cm H
2O at age 8 months. At age 12 months, whole exome sequencing identified compound heterozygous pathogenic
NPC1 mutations (c.2213C>A / c.3234_3237dupATTT) and the decision was made not to proceed with liver transplantation due to the NPC1 diagnosis.
Subsequently, she was enrolled in an emergency compassionate use, single-patient Investigational New Drug study (CHOC Children’s study #140223) of open-label intravenous and intrathecal 2-hydroxypropyl-β-cyclodextrin (HPβCD; Janssen Research & Development). To date, she has safely received 148 intravenous treatments that started at 500 mg/kg/week and escalated to her current 2000 mg/kg/week dose by 14 weeks of treatment. Her initial intrathecal dose was 175 mg monthly, delivered via lumbar puncture, and gradually escalated to her current dose of 300 mg every other week. She has received 57 intrathecal treatments to date. Plasma cholestane-3β,5α,6β-triol dropped from 0.34 nmol/mL (pre-treatment) to 0.04 nmol/mL; RR <0.02 nmol/mL. Her latest total bilirubin was 0.6 mg/dL, AST 51 U/L, ALT 28 U/L, alkaline phosphatase 149 U/L, prothrombin time international ratio of 1.10, and fibrinogen of 251 mg/dL (all normal). Her γ-glutamyl transpeptidase is now elevated at 120 IU/L and partial thromboplastin time prolonged at 44.1 s. Her NPC Severity Score, which assesses a broad range of symptoms and level of neurologic function and increases with worsening disease
, was 30 prior to initiation of HPβCD, 24 in Year 1, and 26 by Year 2. Developmentally, she is delayed, but currently sitting up without support, speaking several words, waving hello and goodbye, flipping book pages, and taking steps with assistive device support.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1315.0, 'g']}",5.26,4.997,5.523,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1315.0 g so this converts to 1315.0 lbs * kg/1000 g = 1.315 kg. Hence, the patient's maintenance fluid is 1.315 kg * 4 mL/kg/hr = 5.26 mL/hr.
Hence, the patient's fluid maintenance is 5.26 mL/hr."
5141,22,Maintenance Fluids Calculations,physical,decimal,pmc-6157329-1,Extracted,"A 54-years old male, weighing 66 kg, with tobacco use for 30 years, had undergone the primary partial laryngectomy 13 months before. He was scheduled for total laryngectomy and neck dissection. No abnormality was detected with preoperative physical examination and CT scan showed increased lung markings without metastasis. It also demonstrated moderate general condition with 3 cm of mouth opening, ECG with right bundle block, Malampatti grade II, without complaint of apnea or major depression signs. There was an 8 cm healed scar of a previous surgical incision along the cervical midline but with normal neck extension. Routine non-invasive blood pressure, ECG, and SPO2 were monitored. General anesthesia was induced with midazolam (1 mg), sufentanil (20μg), vecuronium (8 mg) and propofol (120 mg) followed by an attempted tracheal intubation using Macintosh laryngoscopy after preoxygenation. Nonetheless, the epiglottis and glottis were not viewed under Macintosh laryngoscopy, and then SPO2 dropped to 85% from 98%. Meanwhile, no effective ventilation was obtained by mask ventilation. The subsequent placement of neither an oropharyngeal airway nor a laryngeal mask airway (LMA) could resolve the difficult ventilation, which was accompanied by a quick drop of SPO2 to 25%, and an increased heart rate to 150 beats per minutes. In a short time, urgent tracheostomy was performed by a standby otolaryngologist, and then SPO2 and heart rate recovered after oxygen delivery through the placement of a coiled tracheal tube of 7.0 mm diameter. Anesthesia was maintained with continuous infusion of propofol, remifentanil, and inhalational sevoflurane. The patient emerged without sequelae from the short episode of hypoxia after the surgery was over.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [66.0, 'kg']}",106,100.7,111.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 66.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (66.0 kg - 20 kg) = 106.0 mL/hr.
Hence, the patient's fluid maintenance is 106.0 mL/hr."
5142,22,Maintenance Fluids Calculations,physical,decimal,pmc-7054071-1,Extracted,"The patient was a 24-year-old woman, who was diagnosed with CdCS in infancy. She had grade 1 intellectual disability and abnormal gait due to neuromotor malfunction. General anesthesia was advised, because oral examination was not possible owing to the intellectual disability.
The caregiver stated that internal organ malformations were absent. She was 150 cm tall and weighed 42 kg. Only partial airway evaluation and parental interviews were performed, since preoperative examinations including blood tests were not possible because of poor coordination. Although the American Society of Anesthesiologists (ASA) physical status classification could not be made accurately, it was estimated to be ASA 2, because the patient appeared physically was healthy and had no other medical condition disease. No abnormalities were noted in with the aperture and cervical spine; However, she had a difficult airway, which was caused by class 2 malocclusion and micrognathia, with a broad nasal bridge and epicanthal folds, which are characteristic of CdCS.
Dental examinations and treatments were planned under outpatient general anesthesia, and the following procedure was used for inducing general anesthesia.
The patient refused to sit on the dental chair, but her parents managed to soothe her and mask induction was started with inhalation of 50% nitrous oxide and oxygen and sevoflurane (4 vol%), followed by sedation. Airway obstruction occurred as the patient calmed down. Thus, positive pressure ventilation was performed using the oropharyngeal airway. Patient monitors for evaluating blood pressure in a noninvasive manner, temperature, pulse oximetry, and electrocardiography were attached simultaneously. An intravenous line was obtained and rocuronium 20 mg was injected. A cotton swab soaked with epinephrine (Bosmin®R) (1 mg/1 cc) was applied to both nasal cavities to facilitate smooth nasotracheal intubation.
Nasotracheal intubation was performed after sufficient neuromuscular blockade. First, the endotracheal tube (ETT) was passed through the left nostril, using a laryngoscope with a size 3 Macintosh curved blade. However, intubation was impossible due to a Cormack-Lehane grade of 4, i.e., the vocal cord was not exposed (). After immediate removal of the instrument, oxygen supply and anesthesia depth were maintained using 100% oxygen and 4 vol% of sevoflurane. Subsequently, video laryngoscopes (AceScope, Acemedical Co., Korea) were prepared, and the vocal cord was easily exposed using the same laryngoscope blade ().
The ETT was too thick to pass through the vocal cord but could pass through the nostrils, even though an ETT with an inner diameter (ID) of 6.0 mm and outer diameter (OD) of 8.6 mm was selected after considering patient's age, sex, and height. Intubation was possible with an ETT with an ID of 5.5 mm, although it was difficult due to the wider OD of the anterior part of the balloon (). An inflation pressure of 30 cmH2O was applied without inflating the balloon after intubation. Thus, we decided to replace the ETT with one with a smaller OD because absolutely no air leaked was observed. Nonetheless, we proceeded with the intubated tube, since the expected treatment time was short and repeated intubation attempts were considered to be detrimental to the patient. Dexamethasone 10 mg was administered to prevent post-intubation stridor. Desaturation or bleeding were not observed during the induction process.
The ETT was placed at a depth of 23 cm from thenares. Anesthesia was maintained with 50% nitrous oxide, oxygen, and 2 vol% of sevoflurane. The peak airway pressure was between 15 and 17 cmH2O when the partial pressure of end tidal carbon dioxide was maintained at approximately 30 mmHg using the volume control mode. A dentist from the department of preventive dentistry performed the oral examination. The patient's oral hygiene was very poor: extensive calculus deposition was observed. Oral prophylaxis was performed with an ultrasonic scaler. The follow-up visit was planned after 18 months.
A neuromuscular-blocking reversal agent was administered after the procedure. Extubation was performed with a positive pressure of 30 cmH2O, following recovery from anesthesia and confirmation of spontaneous breathing and eye opening. Vital signs were observed within approximately 3 min while providing 100% oxygen, and the patient was shifted to the recovery room. For the dental treatment procedure required 95 min and 130 min for anesthesia. No complications were observed during recovery and the patient was discharged.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [42.0, 'kg']}",82,77.9,86.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 42.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (42.0 kg - 20 kg) = 82.0 mL/hr.
Hence, the patient's fluid maintenance is 82.0 mL/hr."
5143,22,Maintenance Fluids Calculations,physical,decimal,pmc-6827696-1,Extracted,"A 25-year-old woman with GPA, chronic ear and sinus infection, and a known sellar mass presented to the emergency department with recurrent headache and vomiting (Poster: Sachin Gadani, Fahid Alghanim, Annika Windon, Lisa Rooper, Rohini Nadgir, and Karan Desai. Granulomatosis with polyangiitis manifesting as a symptomatic sellar mass in a young woman. Society of General Internal Medicine; 5/2019). GPA had been diagnosed one year prior through sinus biopsy, and she has been maintained on prednisone and methotrexate. At the time, she was known to have upper respiratory tract involvement mainly within her sinuses and ears. The day prior to admission, she developed a left-sided headache and subjective fever followed by nausea and profuse vomiting. She stated that these symptoms, with the exception of fever, were consistent with her typical GPA flares, which she had been experiencing weekly for the past several months. Rarely the symptoms did not resolve and she would present to the emergency department, with her last presentation assumed to be a GPA flare and managed successfully with diphenhydramine and methylprednisolone.
During examination, the patient also revealed eight months of amenorrhea, fatigue, cold intolerance, 20 lb of weight gain, and constipation. She was febrile to 38.3°C with otherwise normal vital signs. Physical examination showed no meningismus, papilledema, or visual field deficit. She refused lumbar puncture because the symptoms were similar to those of her regular GPA flares. Blood cultures were negative. Thyroid function studies showed a TSH level of 0.06 uIU/mL (0.4-4.0), free T4 level of 0.4 ng/dL (0.9-2.4), and total T3 level of 0.49 ng/mL (2.3-6.2), indicating central hypothyroidism. Further testing showed a low prolactin level of 0.1 ng/mL (2-29), luteinizing hormone level of 0.4 mIU/mL (0.5-76.3), and follicle-stimulating hormone (FSH) level of 2.5 mIU/mL (15-20), consistent with central hypogonadism. Insulin-like growth factor-1 (IGF-1) was within normal range at 108 ng/mL (63-373). Morning cortisol was measured as 0.7 ng/dL (10-20) but confounded by chronic prednisone use. There was no clinical evidence of anti-diuretic hormone (ADH) deficiency.
Her presentation of recurrent headache, nausea/vomiting, and hypopituitarism led to a further investigation of her known sellar mass. Ten months prior to admission, a cystic, non-enhancing sellar lesion with suprasellar extension was seen incidentally on an MRI performed to investigate mastoiditis (Figure ). At that time, it measured 1.2 x 1.6 x 1.5 cm (AP x TR x CC [anteroposterior x transverse x craniocaudal]), did not cause mass effect, and was thought to likely represent Rathke’s cleft cyst. A repeat MRI scan showed an interval enlargement of the lesion, now 1.5 x 1.6 x 2.4 cm and extending posteriorly into the clivus and superiorly into the hypothalamus (Figure ). The lesion showed T1 hypointensity, T2 heterogeneity, and mild diffusion restriction, and was notably enhancing internally post-contrast (Figures , ). These interval changes were not consistent with Rathke’s cleft cyst, and, instead, possible etiologies considered were insidious infection, pituitary macroadenoma, and GPA-related inflammation.
To define the underlying pathology, a transsphenoidal biopsy of the sellar mass and the adjacent bone was performed. Histopathology of the mass demonstrated acute and chronic inflammation. There were prominent reactive macrophages and few PMNs (polymorphonuclear leukocytes) with large areas of fibrosis and necrosis (Figure ). Gram, PAS, and Giemsa stains were negative for bacterial or fungal organisms, AFB (acid-fast-bacillus) was negative for mycobacteria, and Whipple stain was negative. There was no evidence of vasculitis. Bone histopathology showed evidence of chronic inflammation. Given the prominently activated immune cells without evidence of infection, the most likely diagnosis was autoimmune inflammation related to GPA.
In the immediate postoperative period, she developed central diabetes insipidus, with increased urinary frequency, urgency, and thirst, which did not resolve in the months following surgery. Pituitary hormone deficiency was treated with prednisone, levothyroxine, vasopressin, and a combined oral contraceptive pill. Her presenting symptoms of headache, nausea, and vomiting had significantly improved. She was aggressively immunosuppressed with prednisone 60 mg daily and cyclophosphamide 1 mg/kg (75 mg) daily, with a plan to increase the dose to 2 mg/kg (150 mg). At a dose of 2 mg/kg of cyclophosphamide, she developed mild transaminitis (AST [aspartate transaminase] and ALT [alanine transaminase] elevation), and thus the dose was decreased to 1.25 mg/kg daily. Two months later, the patient requested to be transitioned from cyclophosphamide to rituximab due to concerns regarding fertility. She was weaned from cyclophosphamide and has been on a slow steroid taper and rituximab. At her last clinic visit, she was without any significant GPA flare or progression of pituitary involvement for nine months after initiating rituximab. She continued to have occasional headaches, sinus pressure, and fatigue.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [20.0, 'lbs']}",36.28736,34.47299,38.10173,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 20.0 lbs so this converts to 20.0 lbs * 0.453592 kg/lbs = 9.07184 kg. Hence, the patient's maintenance fluid is 9.07184 kg * 4 mL/kg/hr = 36.28736 mL/hr.
Hence, the patient's fluid maintenance is 36.28736 mL/hr."
5144,22,Maintenance Fluids Calculations,physical,decimal,pmc-8080741-1,Extracted,"The patient was a 43-year-old woman that consulted the Mie University Hospital because of fatigue and vomiting.
The patient first consulted a medical practitioner because of sudden malaise, thirst, and vomiting in April 2019. A laboratory analysis disclosed increased blood glucose levels (428 mg/dL), a mild increase of hemoglobin A1c (6.6%), and increased ketone bodies in urine. She received insulin therapy for four days. Because the serum anti-glutamic acid decarboxylase antibody was negative, she was diagnosed with type 2 diabetes mellitus. The treatment was then switched from insulin therapy to oral medication with metformin 500 mg/d, empagliflozin 10 mg/d, and vildagliptin 100 mg/d. The patient's general condition improved, and she was discharged two days after switching to oral treatment when her one-point blood glucose level decreased to 203 mg/dL.
Two days after discharge from the medical practitioner's clinic, she consulted Mie University Hospital's outpatient department complaining of fatigue and vomiting. The clinical findings on examination were as follows: Height 159.3 cm; body weight 58.6 kg, body mass index 23.0 kg/m2, blood pressure 128/83 mmHg, heart rate 107 beats/min, body temperature 37.4 ˚C, and peripheral oxygen saturation (SpO2; normal level > 95%) at room air 98 %.
She had no medical history of any disease.
The patient's physical examination showed notable dryness of the oral cavity.
Table showed the results of the laboratory analysis performed at Mie University Hospital. Arterial blood gases demonstrated metabolic acidosis (pH, 7.18; pCO2, 18 mmHg; HCO3, 6.6 mEq/L; base excess, -19.3 mmol/L; A-gap, 27.6 mmol/L), with normal level of lactic acid (1.0 mmol/L). Fasting blood glucose (184 mg/dL) was mildly elevated with increased glycated hemoglobin/hemoglobin A1c (HbA1c) (7.3%). Urinalysis showed high levels of glucose (2000 mg/dL) and ketone bodies (3+). The plasma levels of 3-hydroxybutyric acid (6585 μmol/L) were markedly high. The renal function markers (blood urea nitrogen 9.1 mg/dL; serum creatinine 0.40 mg/dL) were within the normal range. These findings were compatible with the diagnosis of diabetic ketoacidosis with mild hyperglycemia.
Additional laboratory analysis showed reduced urinary C-peptide level (8.6 μg/d) and decreased fasting serum C-peptide level (0.3 ng/mL). However, islet-related autoantibodies, including anti-glutamic acid decarboxylase antibody, insulin autoantibody, islet cell antibody, insulinoma-associated protein-2 antibody, and zinc transporter-8 autoantibody, were undetectable. An abdominal computed tomography showed a normal pancreas, and the blood level of pancreas exocrine enzymes, including amylase and lipase, were within the normal range.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [58.6, 'kg']}",98.6,93.67,103.53,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 58.6 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (58.6 kg - 20 kg) = 98.6 mL/hr.
Hence, the patient's fluid maintenance is 98.6 mL/hr."
5145,22,Maintenance Fluids Calculations,physical,decimal,pmc-8489187-1,Extracted,"A previously healthy 67-year-old Caucasian male was admitted to the outpatient service of Neurology Division in April 2015, complaining of numbness of hands and feet, and inability to walk that had started two years before with progressive worsening, associated with weight loss of 14kg. He denied dry mouth and eyes or sweating, gastrointestinal or sexual dysfunction, previous diseases, and any relevant familial medical history. No abnormalities were found on general clinical examination, but skinny complexion. At neurological assessment, Medical Research Council scale (MRC) was grade 5 in all muscles, except grade 1 for flexion and extension of the feet; slight atrophy was found in feet intrinsic muscle added to global areflexia, positive Romberg sign, superficial hypoesthesia at toes, severe loss of vibratory sensation up to elbows and knees. Blood pressure and heart rate were 130x82 mmHg and 83 bpm, respectively, on supine position, and 125x80 mmHg and 92 bpm, respectively, after 3 minutes on standing position; cranial nerves were preserved; 51 points on Neuropathy Impairment Score (NIS); score 2 for upper (U) and 2 for lower (L) limbs (L) on Overall Neurological Limitation Scale (ONLS). Except for IgA lambda-MG in serum immunofixation, a slightly elevated serum beta-2 microglobulin of 2.0 mg/mL (RR = 1.0-1.7 mg/mL) and mild anemia (hemoglobin of 11,5 g/dL, RR = 13-18 g/dL), other laboratory tests were normal, including complete blood count, vitamin B12 and folic acid serum levels, serum kappa and lambda free light-chains ratio, liver, renal and thyroid functions, blood glucose, lactic dehydrogenase, calcium, serology for infectious diseases (HIV, B, and C hepatitis, VDRL), antinuclear and rheumatoid factors, antineutrophil cytoplasmic antibodies, anti-SSA/SSB, total complement and fractions, anti-cardiolipin, prostatic specific antigen, carcinoembryonic antigen, alpha fetus protein, and urinalysis with protein electrophoresis and immunofixation. Computed tomography (CT) of chest, abdomen, and pelvis were normal, and 99mTc-MDP scintigraphy (SC) did not show abnormal uptake in bones. Bone marrow aspirate was normal. The CSF showed 1 cell/mm3 and 88 mg/dL (RR < 45mg/dL) of protein with 16% gamma (RR < 14%). Anti-nerve antibodies detection was not available. An external ENMG showed longer motor distal and F wave latencies, moderately reduced motor nerve conduction velocity, no conduction block or abnormal temporal dispersion, slightly reduced motor amplitude data, and was interpreted as a primarily demyelinating process with slight secondary axonal degeneration fulfilling demyelination criteria of EFNS/PNS.
DADS with IgA lambda-MGUS was diagnosed, and the patient started on monthly pulse therapy with intravenous (iv) methylprednisolone (MP, 1000 mg/day/3days) from May to October 2015. No clinical-laboratory evidence of any systemic disease arose, NIS remained unchanged, but worsening in ONLS (2 UL and 3 LL) lead to the addition of monthly cyclophosphamide (1g/iv/month) to MP from December 2015 to May 2016, and then changed to oral methotrexate (15 mg/week) for 7 months.
In March 2016, under immunosuppressive therapy, the patient started with sexual distress complaints. Except for the IgA lambda-MG, extensive serum reinvestigation and thoracic and abdominal CT remained normal. The ENMG () was remade and showed unexpected and marked axonal impairment.
Autonomic evaluation disclosed the absence of cutaneous sympathetic reflex in all limbs and reduced cardiac variability at rest and with a deep breath and Valsalva maneuver (RR interval = 901.2 ± 4.6 ms). The uptake in fifth and seventh ribs observed in 99mTC-MDP SC () was not confirmed in 99mTC-MIBI SC (). No plasmacytosis or other alterations were seen in bone marrow aspirate, and a subcutaneous (SC) tissue biopsy resulted negative for amyloid deposition under Congo red staining.
Despite the negative SC biopsy result, AL was still suspected associated with the IgA lambda component. Due to the marked motor worsening (NIS 88.5, ONLS 3 UL and 5 LL) and the onset of pain and other autonomic complaints (orthostatic intolerance and voiding dysfunction), Fludarabine (100 mg/iv/monthly) was prescribed from December 2016 to April 2017, resulting in slight improvement (NIS 83.5, ONLS 3 UL and 4 LL) and disappearance of bone uptake in coastal arches but showing distension of urinary tract ().
A sural nerve biopsy (February 2018) revealed amyloid deposition () with IgA positivity and non-specific lambda light-chain staining by immunohistochemistry (IHC) (-). Kidney dysfunction started in 2018 with a protein/creatinine ratio of 1,59 (RR = 0.06 – 0.35). Imaging studies showed renal parenchyma with normal thickness and echotexture associated with dilatation of urinary tract and thickened and trabeculated bladder walls (data not shown).
Still denying any suspected familial history, the patient brought us in October 2018 a photograph of his mother at the age of 60 years old showing a very lean lady with atrophic hands, who was bedridden for several years and died at 82 years old due to a non-confirmed bone malignancy. This information led us to search for a mutation in the TTR gene to find a heterozygous Val30Met mutation. At the age of 69 years, a liver transplant was not indicated due to the risk associated with age, low body mass index, and renal dysfunction. Tafamidis was also not indicated due to familial amyloidosis staging system score of II (ambulatory but require assistance) and IIIb at polyneuropathy disability score (walking with the help of two sticks). Only in 2019 was it possible to carry out an IHC staining for TTR in the stored nerve tissue biopsy, which showed positive staining at the same sites of previous IgA deposition ().
Tc99m-pyrophosphate SC showed strong diffuse uptake in ventricular walls in February 2019 (), with heart/contralateral area ratio of 1.9 and 1.7 after 1 and 3 hours, respectively, highly suggestive of ATTR. At the last follow-up in April 2019, the patient reported a stable neurological condition, sporadic pain in lower limbs, and denied any autonomic symptoms; NIS and ONLS had not changed since 2017. The patient deceased in July 2019 of undetermined cause in another medical service where the autopsy was not performed.
Being performed in January 2021, under research settings, laser microdissection and mass spectrometry analysis (LC/MS) showed only TTR in amyloid on nerve biopsy ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [14.0, 'kg']}",48,45.6,50.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 14.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (14.0 kg - 10 kg) = 48.0 mL/hr.
Hence, the patient's fluid maintenance is 48.0 mL/hr."
5146,22,Maintenance Fluids Calculations,physical,decimal,pmc-6969991-2,Extracted,"An 82-year-old man with a history of cerebral infarction sequelae and dementia of the Alzheimer's type was treated for 2 weeks with antibiotics after a diagnosis of mesenteric panniculitis. One month after discharge from the hospital, the patient gained weight and experienced fatigue, upon which he visited the hospital. He was diagnosed with ascites, pleural effusion, and pericardial effusion, and he was then readmitted to the hospital.
The patient's height was 163 cm and his weight was 59.5 kg. There was no noise in the heart sound. Abdominal distension and lower leg edema were observed. Blood test findings were somewhat low ().
An abdominal CT image showed a large amount of ascites (), and a test puncture revealed its milky appearance. A bacterial culture of the ascites was negative, and cytology showed it to be Class I of the Papanicolaou classification.
Initially, we placed the patient on a fat-restricted diet (1400 kcal and lipid 40 g per day), furosemide 10 mg/day, and a single dose of elemental diet, Elental, but improvements in weight and waist circumference were poor. Oral administration of Elental did not cause any side effects.
After that, we stopped the fat-restricted diet and increased the amount of Elental to 3 times a day. In addition, peripheral parenteral nutrition was administered by infusion. The patient's body weight then decreased from 62 to 53 kg in 25 days, and his abdominal girth improved from 90 to 70 cm ().
After that, we restarted the patient on a fat-restricted diet at 900 kcal divided into morning and evening, and lipid at 20 g/day, and the patient also consumed 2 bottles of Elental daily at noon.
Ultimately, oral nutrition and a small amount of diuretic administered orally resulted in better control of weight and abdominal girth. Abdominal CT also showed a marked improvement in ascites (). He was discharged from the hospital and continued treatment on an outpatient basis.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [59.5, 'kg']}",99.5,94.525,104.475,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 59.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (59.5 kg - 20 kg) = 99.5 mL/hr.
Hence, the patient's fluid maintenance is 99.5 mL/hr."
5147,22,Maintenance Fluids Calculations,physical,decimal,pmc-6867740-1,Extracted,"A 11-year-old boy was referred to our hospital for liver enlargement with significantly elevated transaminase levels.
The patient went to a local hospital after experiencing nausea for no obvious cause for a period of 6 months. Examinations revealed liver enlargement and elevated transaminase levels. The patient subsequently took Chinese medicinal herbs (uncertain dose and composition) for 2 months, and his symptoms improved. A follow-up examination showed that the liver was still enlarged. The patient's chief complaint at that time was slight upper abdominal discomfort on the right side. The patient was then received by our hospital for further diagnosis and treatment. The patient was healthy before experiencing his current symptoms, and factors that might cause liver injury, including infection, autoimmune disease, alcohol consumption, or ingestion of other chemical drugs and poisons, were excluded.
The patient was 130 cm tall, weighed 31 kg, and displayed dysplasia of the teeth and abnormal relaxation of the ligament of the metacarpophalangeal joint. The superficial abdominal veins could be exposed by palpitation, and the liver edge could be felt 8 cm below the costal margin and 7 cm below the xiphoid (Fig. ).
Blood tests confirmed that the patient had elevated aminotransferase levels (aspartate aminotransferase 77 U/L, alanine aminotransferase 102.7 U/L). An abdominal noncontrast computed tomography (CT) scan was performed, which showed only a marked enlargement of the liver (Figs. and ). We tested for infectious factors that might cause liver injury, including hepatitis virus, Epstein-Barr virus, cytomegalovirus, and parasites, and found no signs of infection. Tests for autoimmune disease-related antibodies conducted at follow-up examinations were negative. On the basis of the patient's age, history, symptoms, and test results, we suspected a genetic or metabolic disease. We screened for abnormal copper and iron metabolism, but the related biomarkers were all normal. During the patient's stay in our hospital, we noted a slightly low fasting blood glucose level, which was still within the normal range (3.69 mmol/L), and a high blood triglyceride level (2.17 mmol/L). Repeated tests produced the same results of high triglyceride level and slightly low glucose level, which suggested abnormal glucose metabolism and the possibility that the patient had GSD. After obtaining permission from the patient's parents, we performed an ultrasound-guided liver biopsy. Histopathological examination of the biopsy sample with periodic acid-Schiff staining showed massive accumulation of glycogen in the hepatic tissue (Figs. –), leading to a final diagnosis of GSD. With further consent from the patient and the patient's mother, we performed whole-genome sequencing on the patient and the patent's mother to get the exact genotype underlying the GSD. Analysis of the patient's genetic sequences revealed a mutation known to cause GSD; the cytosine at nucleotide position 133 in the PHKA2 gene on the X-chromosome was replaced by thymidine (c.133C>T), resulting in a change from arginine (Arg) to tryptophan (Trp) at amino acid position 45 in the PhK protein. The patient's mother was also found to carry the c.133C>T mutation in PHKA2, indicating that the patient inherited the mutation from his mother (Fig. ).
We placed the patient on a high-protein, high-starch diet and provided hepatoprotective and supportive therapy. The patient attended regular follow-up visits with careful re-examinations from June 2018 until March 2019.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [31.0, 'kg']}",71,67.45,74.55,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 31.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (31.0 kg - 20 kg) = 71.0 mL/hr.
Hence, the patient's fluid maintenance is 71.0 mL/hr."
5148,22,Maintenance Fluids Calculations,physical,decimal,pmc-4745298-1,Extracted,"This report concerns a ten-year-old Mauritanian female child, who was referred by orthopedics service for assessment of fragility fractures. She was born to consanguineous parents. Congenital blindness was diagnosed at birth. She then presented with five broken limbs (humerus, wrist, ankle, and femur) after a fall from standing height, which premiered at the age of 5 years. Since femur fracture, she did not walk again. On clinical examination, we observed microphthalmia, corneal opacity (), dorsal kyphosis, and incurvation of tibias and lower limb length inequality (Summarized ). Her weight was 15 kg and size was 117 cm, both far below the second percentile for her age. Neurological examination was normal. Serum calcium, phosphate, alkaline phosphatase, creatinine, and 25 OH vitamin D3 were all normal. Radiographs showed diffuse bone demineralization, multiple vertebral fractures, and platyspondyly (). Bone mineral density (BMD) revealed a Z score of −5.5 at the spine.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15.0, 'kg']}",50,47.5,52.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.0 kg - 10 kg) = 50.0 mL/hr.
Hence, the patient's fluid maintenance is 50.0 mL/hr."
5149,22,Maintenance Fluids Calculations,physical,decimal,usmle-3672,Extracted,"A 45-year-old man comes to the emergency department because of a 1-day history of black, tarry stools. He has also had upper abdominal pain that occurs immediately after eating and a 4.4-kg (9.7-lb) weight loss in the past 6 months. He has no history of major medical illness but drinks 3 beers daily. His only medication is acetaminophen. He is a financial consultant and travels often for work. Physical examination shows pallor and mild epigastric pain. Esophagogastroduodenoscopy shows a bleeding 15-mm ulcer in the antrum of the stomach.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.4, 'kg']}",17.6,16.72,18.48,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.4 kg. Hence, the patient's maintenance fluid is 4.4 kg * 4 mL/kg/hr = 17.6 mL/hr.
Hence, the patient's fluid maintenance is 17.6 mL/hr."
5150,22,Maintenance Fluids Calculations,physical,decimal,pmc-4232227-1,Extracted,"A 38-year-old Caucasian woman was diagnosed with a left-sided neck nodule six months after undergoing RYGB to treat obesity. She recalled palpating a vague mass on the cervical site before her RYGB, but this mass became more pronounced only after she lost 33kg. (Her body mass index (BMI) had changed from 43.5kg/m2 to 30.5kg/m2). She reported a past history (prior to her RYGB) of a right lobectomy of the thyroid to treat a benign nodule, as well as hypertension and obstructive sleep apnea. Before undergoing the second thyroid surgery and during her first visit at our clinic, she brought laboratory results showing normal levels of calcium, phosphorus, 25-hydroxyvitamin D (25(OH)D), PTH and thyroid-stimulating hormone (TSH).
To investigate the cervical mass, a thyroid ultrasound was performed. The scan showed a 3.1×2.2×2.0cm hypoechoic nodule on the left lobe. Subsequently an aspirative biopsy was obtained. Cytopathology suggested a Hurthle cell lesion. Total thyroidectomy was indicated and hence carried out, and the diagnosis of Hurthle cell adenoma was confirmed. Immediately after surgery, the patient had hypocalcemia and required an intravenous calcium gluconate infusion to stabilize her calcemia. All of the laboratory data obtained during clinical management are provided in Table .
Two months after her total thyroidectomy, she was referred to our unit’s care center by the surgeons because of difficulties in the clinical management of hypoparathyroidism. Meanwhile, she was admitted several times to an emergency room to reverse hypocalcemia with intravenous calcium infusions. During her visit at our unit, she reported paresthesias, muscle cramps and tingling in the mouth. A physical examination revealed that she had positive Chvostek’s and Trousseau’s signs. Her serum calcium and phosphorus levels were 5.9mg/dl and 7.1mg/dl, respectively. Her TSH level was 16.6μUI/ml. She was being treated with levothyroxine 100μg/day, calcium carbonate 7.5g/day, oral calcitriol 2.0μg twice daily and a multivitamin tablet. Doses of levothyroxine and calcium carbonate were increased to 150μg/day and 12g/day, respectively, and magnesium oxide 400mg tablet three times per day was added. Strict instructions about sunlight exposure (20min/day) and diet were given. All these measures improved her calcium homeostasis and avoided any further hospitalization. At her three-month follow-up examination, it was discovered that her calcium level had increased and her phosphorus level had decreased (see Table ). She had a low PTH level and a normal TSH level. Her magnesium and albumin levels and renal and hepatic function were within normal ranges (NRs). We decided to change calcium carbonate to citrate (12g/day) and to add cholecalciferol (12,000IU/day).
One month later, her symptoms were partially improved, and she reported that our advice about sunlight exposure was not being completely followed. Minimal changes in laboratory data were noticed, and her urinary calcium/creatinine ratio was 0.09 (NR<0.20). Because of the large amount of tablets/pills needed for daily intake at that time, we speculated that she could be a candidate for surgical reversal of the bariatric procedure; however, she definitively rejected it, fearing weight regain. Facing this challenge, and without financial resources to cope with synthetic PTH hormone treatment, we hypothesized that the use of pancrelipase could improve fat absorption at the alimentary tract with possible positive effects on vitamin D absorption and subsequently on calcium homeostasis. To test our hypothesis, pancrelipase was added at mealtime (three times per day) (compound capsule containing 10,000 USP units of lipase, 37,500 USP units of protease and 33,200 USP units of amylase). After continuous use of pancrelipase without side effects, her symptoms gradually improved until she became totally asymptomatic. Two months later, she had serum calcium and phosphorus levels of 7.2mg/dl and 5.0mg/dl, respectively. We increased her calcium citrate dosage to 14g/day. After two months, her levels of calcium, phosphorus and 25(OH)D were 7.8mg/dl, 5.2mg/dl and 67.9μg/L, respectively. At that time, her calciuria was 62.6mg/24h (NR, 50mg/24h to 250mg/24h), and her phosphaturia was 405mg/24h (NR, 340mg/24h to 1300mg/24h). Calcitriol was subsequently reduced to 1.5μg three times daily.
Her symptoms had completely remitted at 10 months after thyroidectomy. Her levels of calcium were within, and eventually slightly below, the NR. She became pregnant, and, during the second trimester, although asymptomatic, she had hypocalcemia with normal levels of phosphorus and 25(OH)D (Table , 14 months). Calcium citrate was increased to 18g/day, which stabilized calcium homeostasis from the sixth month of pregnancy until delivery. She gave birth to a healthy newborn at term and breastfed her baby during the first six months. At present, her symptoms have remitted and her calcium, phosphorus and 25(OH)D levels are within NR. However, she still ingests an excessive daily number of tablets and/or pills (a total of 45/day). She has not regained weight (65kg; BMI, 25.7kg/m2).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [65.0, 'kg']}",105,99.75,110.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 65.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (65.0 kg - 20 kg) = 105.0 mL/hr.
Hence, the patient's fluid maintenance is 105.0 mL/hr."
5151,22,Maintenance Fluids Calculations,physical,decimal,pmc-7836275-1,Extracted,"In 2018, a 46-year-old male was admitted to the Department of Internal Medicine with a one-month history of progressing dyspnoea at rest. The patient reported cough with mucus and severe exercise intolerance. In the last year he had weight loss of 15 kilograms. The patient had no past history of either pulmonary or heart problems. He was a heavy smoker for 17 years and a stonemason by profession. Because of an occupational hazard, pneumoconiosis was initially suspected.
On examination the patient was tachycardiac with normal blood pressure (120/78 mm Hg), tachypnoeic and hypoxic (SpO2 93.7% in room air). Mild exercise induced oxygen desaturation. Laboratory tests indicated acute inflammation. Spirometry demonstrated mild lung restriction. Bronchoscopy did not reveal any relevant anomalies. Microbiological analysis of the aspirate provided negative results. No significant abnormalities were detected by abdominal ultrasound, electrocardiography or echocardiography. Pulmonary angiography disclosed no evidence of emboli. X-ray imaging showed several pathologic features such as fluid in pleural space, loss of pulmonary lobes volume and reticular opacification (). High-resolution computed tomography (HRCT) () displayed left lung base atelectasis, interlobular septal thickening and pleural effusion (left space – 65 ml, right space – 20 ml). The HRCT also detected an elevation of the left hemidiaphragm and mediastinal nodes enlargement. Subsequently, thoracentesis was performed to aspirate exudative fluid from the pleural cavity (2650 ml). The patient received antibiotics and oxygen therapy, but no improvement was observed. Based on the clinical presentation as well as on the CT scan, the differential diagnosis included sarcoidosis, silicosis and lymphangitic carcinomatosis. In search for a specific causal factor the patient was further subjected to video-assisted thoracoscopic surgery (VATS), during which pleurodesis was performed and biopsies of both parietal pleura and lung parenchyma were taken.
Results of histopathological examination excluded all initially suggested underlying conditions. On high magnification, multiple emboli of atypical epithelial cells were found in pulmonary blood vessels (). The cells had a characteristic signet – ring shape with a central, optically clear droplet of cytoplasmic mucin and eccentrically displaced nucleus (). Immunohistochemistry (IHC) revealed i) positivity for cytokeratin 7, cytokeratin 20, cytokeratin 19, Ki67, high molecular weight cytokeratin and cytokeratin AE1/AE3 () and ii) negativity for CD68, thyroid transcription factor 1 (TTF1), cytokeratin 5/6, p63, synaptophysin, CD10, napsin A, PAX-8, prostate specific membrane antigen (PSMA), adult renal cell carcinoma (RCC), CD56 and chromogranin A. Results for CDX2 were heterogenous (). In addition, the biopsy was found positive for mucin.
Since the IHC data strongly suggested the gastrointestinal (GI) tract as the origin of cells, GI endoscopy was conducted. Inflammatory changes within the gastric mucosa were observed. Two ulcers covered with fibrin measuring approximately 6 mm and 10 mm in diameter were detected in the stomach. Biopsy was taken and histopathology confirmed the diagnosis of signet ring cell gastric adenocarcinoma () with haematogenous dissemination involving pulmonary vessels. The patient was referred for palliative EOX (epirubicin, oxaliplatin, capecitabine) chemotherapy. After completing two treatment cycles he reached partial remission and stabilisation of the disease. One month later his condition deteriorated and because of exacerbation of dyspnoea, he required an oxygen concentrator. He received four cycles of docetaxel, but pleural effusion was constantly increasing. The patient underwent several thoracenteses. There was no improvement and he died within two months from the first chemotherapy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15.0, 'kg']}",50,47.5,52.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.0 kg - 10 kg) = 50.0 mL/hr.
Hence, the patient's fluid maintenance is 50.0 mL/hr."
5152,22,Maintenance Fluids Calculations,physical,decimal,pmc-4966356-2,Extracted,"A 60-year-old female patient weighing 55 kg presented with huge colloid goitre with stridor in the emergency department. She had no other symptoms and was clinically and biochemically euthyroid. The swelling was 12 cm × 10 cm × 12 cm in size extending from the angle of the mandible on the right side to the anterior border of the left sternocleidomastoid transversely and from the lower end of the jaw to the suprasternal notch vertically. The patient was extremely uncooperative. Airway examination revealed adequate mouth opening, prominent incisors, modified Mallampati grading III, restricted neck flexion and tracheal deviation to left. Radiological examination of the swelling showed lateral displacement of the trachea on antero-posterior view [] and no tracheal compression on lateral view. Telelaryngoscopic examination revealed the larynx being pushed towards the left lateral pharyngeal wall with a bulge in the posterior pharyngeal wall. Right aryepiglottic fold was seen prolapsing into the glottic inlet with inspiration. The vocal cords on both sides were hidden by the aryepiglottic folds and appeared mobile with normal and symmetrical mucosal wave pattern [].
Awake nasotracheal fibreoptic intubation was planned and the procedure was explained to the patient. Difficult airway cart including a rigid bronchoscope was kept ready in the operating room. After attaching monitors, oropharynx was sprayed with 10% lignocaine. The patient was positioned in a partial reclining position, and 7.0 mm polyvinyl chloride reinforced tube was mounted on the flexible fibrescope. Several attempts to negotiate the flexible tip across the glottis were unsuccessful. Visibility of vocal cords was hampered due to poor patient co-operation and continuous movement of the aryepiglottic folds which prevented the passage of flexible tip. An attempt was made to induce anaesthesia with sevoflurane, but the patient developed airway obstruction and there was difficulty in mask ventilation also. Inhalational agent was discontinued and the patient was awakened on 100% oxygen. 70° nasendoscope with Frova was considered as plan B intubation option. Image of the glottis was similar to that obtained with flexible fibrescope, but Frova intubating introducer could be guided across the glottis under direct vision as the view did not disappear even when the vocal folds were collapsing together. After confirming the correct placement of Frova with capnograph, lignocaine 2% was sprayed through the Frova, and 7.0 mm reinforced tracheal tube was railroaded over the Frova into the trachea. Surgery lasted for three hours and was uneventful. At the end of the surgery, when the patient was fully awake, trachea was extubated with the use of an airway exchange catheter.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [55.0, 'kg']}",95,90.25,99.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 55.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (55.0 kg - 20 kg) = 95.0 mL/hr.
Hence, the patient's fluid maintenance is 95.0 mL/hr."
5153,22,Maintenance Fluids Calculations,physical,decimal,pmc-4722418-1,Extracted,"A 31-year-old woman was diagnosed with hypertension by a private clinic in August 2013, based upon a systolic blood pressure of 160 mm Hg and she was prescribed antihypertensive drugs to treat the condition. Initial therapy consisted of hydrochlorothiazide 12.5 mg and losartan 50 mg daily. After 1 week, her blood pressure was still high, so the doctor changed her medication to amlodipine 5 mg, losartan 100 mg, and indapamide 2.5 mg per day. Five days after initiating this second regimen of drugs, she developed pretibial pitting edema, and thorough workup was done for the symptom. There were bilateral adrenal masses on abdominal-pelvic computed tomography (CT). Routine blood tests revealed the following: potassium 2.2 mmol/L, plasma renin activity (PRA) 0.12 ng/mL/hr, plasma aldosterone concentration (PAC) 16.76 ng/dL, and an aldosterone/renin ratio (PAC/PRA) >30, indicative of primary hyperaldosteronism.
Following her possible diagnosis of primary hyperaldosteronism, the patient was referred to our hospital for additional testing. At the time of admission, her blood pressure was 155/111 mm Hg, height was 164.5 cm, and weight was 63.5 kg (body mass index, 23.47 kg/m2). Pretibial pitting edemas were detected, but no physical signs of Cushing syndrome were observed.
A routine blood test at the time of admission showed the following: white blood cell 6,900/µL, hemoglobin 13.5 g/dL, platelet 351,000/µL, total protein 6.9 g/dL, albumin 4.1 g/dL, aspartate aminotransferase 76 U/L, alanine aminotransferase 126 U/L, blood urea nitrogen 7.3 mg/dL, creatinine 0.71 mg/dL, sodium 141 mmol/L, potassium 2.9 mmol/L, chloride 101 mmol/L, total cholesterol 210 mg/dL, triglyceride 104 mg/dL, high density lipoprotein 50 mg/dL, low density lipoprotein 141 mg/dL, and hemoglobin A1c 5.9%. Biochemical evaluation of pheochromocytoma showed no excessive catecholamine production. The transtubular potassium concentration gradient was 12.64%, suggesting the possibility of hyperaldosteronism or hypercortisolism. PAC and PRA were 24.4 ng/dL and 0.76 ng/mL/hr, respectively, and the PAC/PRA ratio was 32.11 (). After correcting for hypokalemia, a saline loading test was performed, which revealed no suppression of the aldosterone level after saline administration, consistent with a diagnosis of hyperaldosteronism (the basal PAC 24.4 ng/dL increased to 27.3 ng/dL after a 2 L saline infusion). Dexamethasone suppression tests (DSTs) resulted in no suppression of cortisol levels (). Adrenal CT demonstrated two bilateral adrenal masses in each of the adrenal glands, including a 1.6-cm mass on the right and a 2-cm mass on the left adrenal gland (). An adrenal cortical scan using iodine-131-6β-iodomethyl-19-norcholesterol (NP-59) showed focally increased radioactive uptakes in the bilateral adrenal gland areas, with a substantially higher uptake on the left side ().
Bilateral adrenal venous sampling (AVS) with adrenocorticotropic hormone (ACTH) stimulation () revealed inadequate right adrenal venous blood sampling (right adrenal vein cortisol level/peripheral blood cortisol level [CRt/CP] <10), whereas the cortisol concentration in the left adrenal venous blood showed successful sampling on the left side. One explanation for this difference may be that the low level of CRt was the result of suppressed cortisol secretion due to excessive cortisol secretion from the left adrenal mass. The left adrenal vein aldosterone/cortisol (ALt/CLt) ratio was lower than that of peripheral blood, implying the possibility of suppressed aldosterone secretion from this side caused by a contralateral adrenal mass which might secrete excessive aldosterone []. Four days after the first AVS, a second AVS was performed using low-dose DST but without ACTH infusion (). This time, we also measured the epinephrine levels in the both adrenal veins and peripheral blood; a large peripheral-to-adrenal gradient of epinephrine assured successful catheterization on both sides []. CLt/CP testing confirmed that the left adrenal mass was a cortisol-secreting adenoma [].
Even though those two AVS results appeared to provide clear evidence of the lateralization of functioning adrenal masses, such an independent functioning of bilateral masses was highly suspicious. We therefore concluded that sequential adrenalectomies, rather than concurrent operations, would be beneficial for making a definitive diagnosis. Moreover, the patient agreed to do sequential operations. The first procedure was a laparoscopic partial adrenalectomy of the right adrenal gland to remove the putative aldosterone-producing mass, with the goal of controlling hypertension and hypokalemia. A firm, 1.5-cm ovoid, well-circumscribed, bright yellow tumor mass lacking necrosis or hemorrhage was arising from the cortex of the adrenal gland in the pathologic specimen. Within 24 hours after surgery, the patient's blood pressure had fallen to 110/80 mm Hg without antihypertensive medication, serum potassium normalized at 4.5 mmol/L, and PAC decreased to 3 ng/dL. These large postoperative changes strongly suggested that the right adrenal adenoma was producing excessive aldosterone. By day 3, an overnight DST continued to show no cortisol suppression, indicating persistent secretion of corticosteroid from the left adrenal mass. To limit the likelihood of subclinical Cushing syndrome progressing to overt Cushing syndrome, we opted to completely remove the left adrenal gland as a means of controlling hypercortisolism. The excised portion of the adrenal mass contained an encapsulated brown solid mass.
The patient began taking prednisolone 10 mg once a day for steroid replacement 1 day after the second surgery. By 2 months she had lost 5 kg of body weight. At that time, a rapid ACTH test revealed adrenal insufficiency (). At 16 months after surgery, the patient has gradually reduced her prednisolone intake to 5 mg every other day. Her blood pressure and serum potassium levels have remained within normal ranges, without the need for additional antihypertensive medications or potassium supplements.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [63.5, 'kg']}",103.5,98.325,108.675,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 63.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (63.5 kg - 20 kg) = 103.5 mL/hr.
Hence, the patient's fluid maintenance is 103.5 mL/hr."
5154,22,Maintenance Fluids Calculations,physical,decimal,pmc-5735466-1,Extracted,"A 26-year-old female patient weighing 35 kg, presented with strangulated umbilical hernia. Her previous medical records revealed she was a known case of DCMP and chronic kidney disease since 2 years. She was presently on treatment with tablet digoxin 0.25 mg, tablet furosemide 40 mg, and tablet carvedilol 12.5 mg once a day. She gave a history of repeated hospital admissions in the past 2 years with features suggestive of congestive heart failure (CHF) and was on regular twice weekly maintenance hemodialysis, last being 2 days before the surgery.
On preanesthetic evaluation, her heart rate was 96 beats/min, regular; blood pressure was 106/72 mmHg; respiratory rate was 16 breaths/min. On auscultation grade, three ejection systolic murmurs were audible. There were no rhonchi or crepitations. Air entry was equal bilaterally. There was no hepatomegaly, ascitis, or pedal edema. The skin overlying the hernia appeared necrosed.
The preoperative 12 lead electrocardiogram (ECG) revealed normal sinus rhythm. Echocardiography demonstrated global hypokinesia, poor systolic function with LVEF of 28%, all 4 chambers dilated, severe mitral regurgitation, tricuspid regurgitation, pulmonary regurgitation, and moderate pulmonary artery hypertension. Chest radiograph revealed cardiomegaly with normal lung fields. Her investigations showed Hb 7.9 g/dl, total leukocyte count TLC 12.9 × 1000/μl, platelet count 219 × 1000/mm3, urea 28.9 mg/dl, creatinine 3.6 mg/dl, sodium 138 mEq/L, potassium 4.5 mEq/L, international normalized ratio of 1.05.
A high-risk written and informed consent was obtained in view of cardiac and renal disease. After shifting to the operating room, an 18-gauge intravenous (IV) cannula was secured. Under strict aseptic precautions, an 18-gauge epidural catheter was inserted into the epidural space at T10-11 interspace using loss of resistance to air technique. A 22-gauge right radial arterial cannula was secured since the left hand had an arteriovenous fistula. Under local anesthesia, a 7 Fr, 15 cm triple lumen central venous catheter was inserted into a right internal jugular vein under ultrasound guidance for intensive hemodynamic monitoring.
The following parameters were monitored: Two lead ECG (II and V5), invasive blood pressure, central venous pressure (CVP), oxygen saturation by pulse oximetry, end-tidal carbon dioxide, body temperature, and urine output. FloTrac® continuous cardiac monitoring was done to monitor cardiac output, cardiac index and stroke volume variability (SVV).
Anesthesia was induced with injection etomidate 0.2 mg/kg, injection fentany l 3 μg/kg. Injection cisatracurium 0.15 mg/kg IV was given to facilitate intubation with size 7.0 mm endotracheal tube. Anesthesia was maintained with 50% air in oxygen, desflurane 4%–6%, and intermittent boluses of 1 mg cisatracurium. An epidural infusion of 0.05% ropivacaine with 2 μg/ml fentanyl was started at 5 ml/h. The CVP was maintained between 8 and 10 cmH2O, cardiac output of 6.8 L/min, cardiac index of 5.5 L/min/m2, and systemic vascular resistance (SVR) of 835 dyne/s/cm5. Arterial blood gas revealed a pH of 7.381, pO2193 mmHg, pCO232.1 mmHg, base excess - 5.8 mmol/L, HCO3− 18.6 mmol/L.
We started injection noradrenaline infusion at 0.08 μg/kg/min and injection dobutamine infusion at 5 μg/kg/min which were tapered slowly towards the end of surgery. Surgeons found only ascitic fluid as the sac contents which was then aspirated. There was no bowel or omentum. The neck of the hernia was found to be very narrow, and defect was closed without a mesh. The procedure lasted for 90 min. Blood loss was about 100 ml. Intraoperatively, a total of 400 ml of normal saline was given. Paracetamol 500 mg IV was given as a means to achieve multimodal analgesia. At the end of surgery, after the return of respiratory efforts, the residual neuromuscular blockade was reversed with injection glycopyrrolate 0.01 mg/kg and injection neostigmine 0.05 mg/kg and extubated. The patient had stable hemodynamics throughout the procedure []. The patient was shifted to surgical recovery room, and all the intraoperative monitoring was continued postoperatively. A continuous epidural infusion of 0.05% ropivacaine with 1 μg/ml fentanyl was continued postoperatively.
All her preoperative medications were continued as per the recommended scheduled dosing and timing. The patient was shifted from the recovery room after 4 h. She underwent dialysis on the postoperative day 1 and was then discharged on postoperative day 4.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [35.0, 'kg']}",75,71.25,78.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 35.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (35.0 kg - 20 kg) = 75.0 mL/hr.
Hence, the patient's fluid maintenance is 75.0 mL/hr."
5155,22,Maintenance Fluids Calculations,physical,decimal,pmc-2994119-1,Extracted,"An 18-year-old male patient was admitted to our institution with principal complaints of short stature, prepubertal sexual maturation, and exertional dyspnea, for 1 year. He was severely anemic, with a hemoglobin level of 3.3 g/dL. He had a history of small bowel resection from 50 cm below the Treitz ligament to 5 cm above the ileocecal valve, necessitated by midgut volvulus in the neonatal period. No other abnormal congenital or genetic condition was detected. After surgery he experienced short bowel syndrome (SBS) as a sequela, and total parenteral nutrition had been supplied, which was gradually replaced by enteral feeding. Chronic abdominal pain, intermittent diarrhea, and vomiting had persisted for several years but eventually improved. At 4 years of age, his feeding mode was entirely enteral, and he was lost to follow-up until his recent visit. His family history was unremarkable. He denied use of any abusive substance and was not sexually active.
Review of system on admission revealed long-lasting dizziness and dyspnea on exertion, and these symptoms had become aggravated in the past year. He also complained of early satiety during meals, but denied gastrointestinal symptoms such as abdominal pain, constipation, or diarrhea.
On physical examination, he was alert, but chronically ill-looking and very pale. His blood pressure was 113/77 mmHg, his pulse rate 95/min, his respiratory rate 20/min, and his body temperature 36.1℃. His height was 137.7 cm (below the 3rd percentile for his age) and his weight 28.9 kg (also below the 3rd percentile for his age). His pubic hair was of Tanner stage I, as was his genital development (testis volume <4 mL). Other physical and neurologic examination findings were unremarkable.
The results of initial laboratory studies are listed in . The complete blood count showed hemoglobin of 3.3 g/dL, hematocrit of 12.5%, mean corpuscular volume (MCV) of 86.2 fl, mean corpuscular hemoglobin (MCH) of 22.8 pg, red cell distribution width (RDW) of 22.2%, and reticulocyte count of 0.59% (reticulocyte production index 0.16). The white blood cell count was 4,900/mm3 with a differential count of 45% neutrophils, 47% lymphocytes, 7% monocytes, and 1% eosinophils. The platelet count was 182,000/mm3. Serum iron was 23 µg/dL (normal 50-170 µg/dL), TIBC was 534 µg/dL (normal 280-400 µg/dL), and serum ferritin was 2.5 ng/mL (normal 20-320 ng/mL). Serum vitamin B12 was 60 pg/mL (normal 211-911 pg/mL) and serum folic acid was 11.3 ng/mL (normal >5.4 ng/mL). Peripheral blood cell morphology () showed normocytic hypochromic anemia, marked anisocytosis, mild poikilocytosis, hypersegmented neutrophils, and mild thrombocytopenia. Bone marrow aspiration and biopsy revealed normal cellularity (90%) with an myeloid : erythroid (M : E) ratio of 2:1. Dyserythropoiesis, including changes in megaloblastoid levels, decreased amounts of hemosiderin particles, and sideroblasts, were also found. The cytogenetic study revealed a normal 46,XY karyotype. Because our patient was of short stature and was sexually underdeveloped, we performed a hormonal evaluation. Luteinizing hormone (LH) and follicular stimulating hormone (FSH) levels were 3.1 mIU/mL (normal 1.5-9.0 mIU/mL) and 2.0 mIU/mL (normal 2.0-9.2 mIU/mL) respectively, both of which were at prepubertal levels. Testosterone was 0.34 ng/mL (normal 3.5-9.7 ng/mL), insulin-like growth factor-1 (IGF-1) 83.6 ng/mL (normal 239-630 ng/mL), and insulin-like growth factor binding protein (IGFBP-1) 3,565 ng/mL (normal 1,820-6,990 ng/mL). On simple chest radiography, the heart size was normal. Bone age was about 12 years by wrist x-ray (). Bone mineral density (BMD) measured by dual energy x-ray absorptiometry was very low, and the Z score (with respect to bone age) of the BMD of the lumbar spine was -3.9.
Based on these findings, the patient was diagnosed with anemia caused by a combined vitamin B12 and iron deficiency attributable to impaired absorption caused by SBS. Parenteral vitamin B12 and iron treatment was initiated. Vitamin B12, as cobalamin, was administrated via intramuscular injection of 100 µg daily for 14 days, followed by 50 µg every other week. Our patient was also given 3 mg/kg elemental iron (ferric form) intravenously every other day for 14 days, followed by the same dose weekly. He was initially placed on a high potassium diet to avoid the transient hypokalemia that could result from rapid erythropoiesis.
The hematologic indices responded immediately to therapy (). The reticulocyte count peaked at 14.9% on the 6th day of parenteral vitamin B12 and iron therapy. Ten days after treatment began, the hemoglobin concentration had increased to 7.7 g/dL, the hematocrit to 29.2%, vitamin B12 to 1,389 pg/mL, and serum iron to 47 µg/dL. He was discharged on the 10th day after admission with improvement in his dizziness and exertional dyspnea. After discharge, he was maintained on parenteral vitamin B12 and iron supplementation in the outpatient clinic. At 3 months after discharge, his hemoglobin level and hematocrit were 12.3 g/dL and 39%, respectively. Treatment was maintained for 17 months and the level of hemoglobin stabilized at around 12 g/dL. Two years after treatment began, the patient's weight and height had increased to 42.3 kg and 154.2 cm (below the 3rd percentile for his age). He has also attained puberty, with Tanner stage 4 pubic hair and a testicular volume of more than 10 mL.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [28.9, 'kg']}",68.9,65.455,72.345,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 28.9 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (28.9 kg - 20 kg) = 68.9 mL/hr.
Hence, the patient's fluid maintenance is 68.9 mL/hr."
5156,22,Maintenance Fluids Calculations,physical,decimal,pmc-6259516-1,Extracted,"An 11-month-old female baby had presented with weakness involving both lower limbs and left upper limb. There was a small cutaneous mole at the back of the child just above the buttock, which was present since birth. The parents had noticed that around the age of 7 months she could not sit without support and could barely move the lower limbs. Subsequently, the weakness progressed, gradually involving the left hand. The baby was born by normal vaginal delivery at term weighing 2.7 kg. There was no other birth history available except that the baby had cried immediately following birth. The baby had three attacks of documented urinary tract infection in the previous 4 months and was treated with oral antibiotics as per urine culture sensitivity.
On examination the baby was irritable. Her weight was 7.1 kg and occipitofrontal circumference was 41 cm. There was marked spastic paraparesis of both lower limbs with exaggerated deep tendon reflexes. There was weakness of the left upper limb and some bite marks (self-inflicted as reported by the parents) in both hands.
Investigations revealed a significant (colony count >100,000) pure growth of multiresistant E. coli in her urine. This was treated with broad spectrum intravenous antibiotics. MRI of spine revealed extensive hyperintense signals involving the entire spinal cord with inhomogeneous enhancement and diffuse altered signals in lumbar thecal sac []. The cauda equina roots could not be identified and a loculated cystic lesion at the level of L5-S1 was identified []. There was significant intramedullary extension of a dermal sinus tract in the sagittal view [Figures and ].
In view of the MRI findings and the presenting clinical signs, neurosurgical opinion was sought. The entire dermal sinus was removed. The histopathological examination of the cystic lesion confirmed the diagnosis of epidermoid cyst, which was infected resulting in an abscess formation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.1, 'kg']}",28.4,26.98,29.82,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.1 kg. Hence, the patient's maintenance fluid is 7.1 kg * 4 mL/kg/hr = 28.4 mL/hr.
Hence, the patient's fluid maintenance is 28.4 mL/hr."
5157,22,Maintenance Fluids Calculations,physical,decimal,usmle-549,Extracted,"A 40-year-old man with AIDS comes to the physician because of a 3-week history of intermittent fever, abdominal pain, and diarrhea. He has also had a nonproductive cough and a 3.6-kg (8-lb) weight loss in this period. He was treated for pneumocystis pneumonia 2 years ago. He has had skin lesions on his chest for 6 months. Five weeks ago, he went on a week-long hiking trip in Oregon. Current medications include efavirenz, tenofovir, and emtricitabine. He says he has had trouble adhering to his medication. His temperature is 38.3°C (100.9°F), pulse is 96/min, and blood pressure is 110/70 mm Hg. Examination shows oral thrush on his palate and a white, non-scrapable plaque on the left side of the tongue. There is axillary and inguinal lymphadenopathy. There are multiple violaceous plaques on the chest. Crackles are heard on auscultation of the chest. Abdominal examination shows mild, diffuse tenderness throughout the lower quadrants. The liver is palpated 2 to 3 cm below the right costal margin, and the spleen is palpated 1 to 2 cm below the left costal margin. Laboratory studies show:
Hemoglobin 12.2 g/dL
Leukocyte count 4,800/mm3
CD4+ T-lymphocytes 44/mm3 (Normal ≥ 500 mm3)
Platelet count 258,000/mm3
Serum
Na+ 137 mEq/L
Cl- 102 mEq/L
K+ 4.9 mEq/L
Alkaline phosphatase 202 U/L
One set of blood culture grows acid-fast organisms. A PPD skin test shows 4 mm of induration.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.6, 'kg']}",14.4,13.68,15.12,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.6 kg. Hence, the patient's maintenance fluid is 3.6 kg * 4 mL/kg/hr = 14.4 mL/hr.
Hence, the patient's fluid maintenance is 14.4 mL/hr."
5158,22,Maintenance Fluids Calculations,physical,decimal,pmc-3540378-1,Extracted,"A 68-year-old female patient presented with abdominal distension of one month duration and slurred speech for one day. She had been diagnosed with pancreatic cancer 5 months previously, and had subsequently undergone pancreaticoduodenectomy. In the operation field, the pancreatic consistency was intermediate and pancreatic resection line was conducted on, but not including, the portal vein. During operation, no hypotension or massive bleeding was encountered. The surgical pathologic finding was ductal adenocarcinoma and complete tumor resection (safety margins of 2 and 3 cm from the duodenum and common bile duct, respectively). However, since pancreaticoduodenectomy, she suffered a loss of appetite and consequently her body weight reduced from 51 kg to 44 kg over 3 months (body mass index from 22.1 to 19.0 kg/m2), even though she had experienced no postoperative diarrhea or obstructive gastrointestinal symptoms. A routine check of pancreas by dynamic CT at three months after surgery revealed severe fatty liver but no tumor recurrence (). At that time, the CT value of liver parenchyma had decreased from 50 Hounsfield units (HU) by preoperative CT to -30 HU.
The patient began to develop abdominal distension one month before presentation, and as a result, her body weight increased from 44 to 55 kg at presentation. At admission, vital signs were as follows; blood pressure 110/60 mmHg, heart rate 90/min, and body temperature 36.0℃. In addition, she complained of cold sensation. Pertinent physical findings included shifting dullness with abdominal distension, anemic conjunctivae, pretibial pitting edema, and flapping tremor with slurred speech. summarizes laboratory findings, which showed anemia with a chronic illness pattern, prolonged prothrombin time, hypoalbuminemia, markedly depressed lipid profiles, and slight decreases in level of calcium and phosphorus. To evaluate the presence of steatorrhea, a stool study was performed, and did not show stool fat. Hemoglobin A1c was 6.0% without anti-diabetics, although she had been diagnosed with diabetes two years prior to the pancreaticoduodenectomy. Viral markers for hepatitis B and C were negative. Carbohydrate antigen (CA) 19-9 had been maintained within the normal range post-pancreaticoduodenectomy. Infectious and autoimmune causes of liver disease and functional abnormalities of the thyroid and adrenal glands were excluded by laboratory testing. She denied alcohol intake and taking any other medicine, including herbal medicine, except supportive pancreatic enzyme. Follow-up liver dynamic CT at this presentation also revealed marked fatty liver and newly developed moderate amounts of ascites (). There was no evidence of local tumor recurrence or lymph node enlargement. The ascites was tapped and proved to be transudate (serum-ascites albumin gradient 1.5) free of malignant cells. It was then controlled with diuretic agents. Her slurred speech, disorientation, and flapping tremor improved within 1-2 days of frequent laxative administration (lactulose). Although her laboratory findings showed mild metabolic alkalosis (pH 7.52, PCO2 33 mmHg, PO2 66 mmHg, HCO3 26.9 mmol/L, O2 saturation 95.0%) in blood gas analysis, mild electrolyte imbalances and no electroencephalographic study was performed, the neurologist checked our patient and there was no organic problem explaining her mental state except hepatic encephalopathy. A liver biopsy was performed to exclude other causes of liver parenchymal disease, and its findings were consistent with severe steatohepatitis which of NAFLD activity score 7 (NAS; macrovesicular steatosis (3), lobular inflammation (2) and hepatocellular ballooning (2)) and a fibrosis score of 1 (). In addition, a Mallory's body was observed in the high power field ().
The patient was hydrated with saline at 20-30 mL/kg/day and then parenteral and enteral feeding was started at 10 kcal/kg/day for 3 days and then increased to 20-25 kcal/kg/day, in view of the risk of refeeding syndrome. In addition, she was administered multi-vitamins including folic acid, thiamine, and zinc and selenium. Her electrolyte levels, body weight, and urine output were checked daily. After 3 months of nutritional support, follow-up CT showed some regression of fatty liver (CT value 10 HU) and near complete regression of the ascites (no diuretic was administered; ). After 7 months of controlled oral nutritional intake, she was free of symptoms of ascites and encephalopathy and her liver function tests and lipid profiles were improved without evidence of tumor recurrence ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [55.0, 'kg']}",95,90.25,99.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 55.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (55.0 kg - 20 kg) = 95.0 mL/hr.
Hence, the patient's fluid maintenance is 95.0 mL/hr."
5159,22,Maintenance Fluids Calculations,physical,decimal,pmc-8631462-1,Extracted,"This is a case of a 40-year-old female known HIV/AIDS patient who has been on ART for the last 14 years with good adherence and regular follow-up, and who is now on 3rd line ART medication with TLD+DRR/r (on her 11th month) after being diagnosed with second-line treatment failure.
After 6 months and 1 week of therapy, the viral load (VL) was sent, and the result was undetectable. The CD4 cell count is currently 950 cells/mm3. The patient’s clinical conditions had greatly improved. She was on second line ART with TDF/3TC/LPV/r since 21/8/2019 with good adherence and follow up for one year prior to the current regimen.
She was on AZT/3TC/NVP at the start of ART (since 18/7/2006), with good adherence and regular follow-up. The CD4 and VL baseline levels were 52 cells/mm3 and 129,988 copies/mL, respectively. When she was switched to the second line, her CD4 and VL levels were 15 cells/mm3 and 98,136 copies/mL, respectively. Prior to one year before treatment failure, both were non-revealing, with the lowest CD of 570 cells/mm3 and the highest VL of 270 copies/mL. To put it another way, there have been no problems with treatment failure in the last 12 years, with all virologic and immunologic results falling within acceptable ranges.
She was acute on chronic sick looking when she arrived, and all of her vital signs were within normal ranges. Her height was 160 cm, her weight was 38, and her BMI was 14.8 kg/m2.
The pertinent findings were as follows: CBC=WBC=2.2103 with Neutrophil of 87.1, and Lymphocytes of 3.4, Eosinophil of 0.3 and Basophil of 0.3%, Haemoglobin=7 mg/dl, and Haematocrit=22%, and the Platelet count was 66, 000, and the conclusion is Pancytopenia, and the Stool Examination re Modified Acid Fast Bacilli was also performed, and an oocyte of C. parvum was noticed (treated).
With this, she was managed for medical complications and was linked to an ART clinic, where her regimen was changed to TLD+ DRV/r with the diagnosis of second-line treatment failure and she was seen after two weeks, and she was fine, and she was seen again after a month with strict adherence. She took her medication monthly for the first month, then every three months after that.
Currently on third-line ART with TLD plus ritonavir-boosted darunavir, the VL is undetectable, and the CD4 count is 950 cells/mm3.The complete blood count (CBC) parameters were also checked, and they were all within acceptable bounds.
Clinically, she is doing a lot better than she was before, and she is now a determined and upbeat client who has an appointment at our hospital every three months.
She is the mother of three children, the oldest of whom is 21 years old and the youngest of whom is 8 years old, and all of her children have negative RVI (Retroviral Infection) serostatus. Her husband is also an RVI patient who takes his medication on a regular basis and has a viral load that is undetectable. They work as elementary school teachers and claim that their monthly salary is sufficient to support their family.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [38.0, 'kg']}",78,74.1,81.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 38.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (38.0 kg - 20 kg) = 78.0 mL/hr.
Hence, the patient's fluid maintenance is 78.0 mL/hr."
5160,22,Maintenance Fluids Calculations,physical,decimal,pmc-8613585-1,Extracted,"A 47-year-old male presented to a UK teaching hospital with a 1-week history of melaena, passing 2 dark, tarry stools per day. He had also experienced 7 months of proximal muscle weakness associated with 12 kg of weight loss, equating to approximately 13% loss of his total baseline weight. On presentation, he was using a walking stick to compensate for ongoing right hip pain following a low energy fall from a bicycle 6 weeks beforehand. Pre-morbidly, he had never had any issues with mobility and had been a keen cyclist and runner.
He had a medical history of a grade 1 pancreatic head neuroendocrine tumour, staged at T3N1M0 with a Ki-67 index of <2% on biopsy. The tumour was non-functional with measured serum chromogranin A (CgA), chromogranin B (CgB), and gut hormone levels all within the normal range (CgA 1.8 nmol/L [<6 nmol/L], CgB 1.5 nmol/L [<3 nmol/L], VIP 5 pmol/L [<30 pmol/L], somatostatin 52 pmol/L [<150 pmol/L], pancreatic polypeptide 28 pmol/L [<300 pmol/L], glucagon 21 pmol/L [<50 pmol/L], and gastrin 9 pmol/L [<40 pmol/L]). This was diagnosed and surgically managed 6 years prior with a curative pylorus-preserving pancreaticoduodenectomy. His medication history therefore included pancreatin and a basal-bolus insulin regime of insulin glargine at night and insulin aspart with meals. He did not take any anticoagulant, antiplatelet, or non-steroidal anti-inflammatory medications. He was a non-smoker and consumed minimal alcohol, revealing no obvious precipitant for UGI bleeding.
On admission, the patient had a sinus tachycardia of 115 beats per minute with a blood pressure of 128/63 mm Hg. Physical examination revealed no peripheral stigmata of chronic liver disease; however, there was new bilateral pitting oedema to the mid-thigh. His abdomen was soft and non-tender to palpation with no appreciable hepatosplenomegaly. Digital rectal examination confirmed the presence of melaena.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.0, 'kg']}",44,41.8,46.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.0 kg - 10 kg) = 44.0 mL/hr.
Hence, the patient's fluid maintenance is 44.0 mL/hr."
5161,22,Maintenance Fluids Calculations,physical,decimal,pmc-8173422-1,Extracted,"A 40-year-old woman at 26-wk gestation was admitted to the hospital for hematemesis, hematochezia, and abdominal pain for 10 h.
Abdominal color Doppler ultrasonography showed portal vein thrombosis, splenomegaly, intrauterine pregnancy, and intrauterine fetal death
The patient had no significant past medical history.
The patient had no history of smoking or alcohol consumption. She had no relevant family history.
The physical examination revealed that the patient had normal vital signs, a body weight of 56 kg, a height of 1.58 m, a body mass index of 22.4 kg/m2, an anemic appearance, and lower abdominal distension, and had no abdominal shiftiness sound.
The laboratory examination was otherwise unremarkable. The laboratory assessment included an initial blood test of the complete blood count (hemoglobin level, 76 g/L), liver test (albumin level, 29.9 g/L), and tumor markers (alpha-fetoprotein level, 179.60 ng/mL; cancer antigen 125 level, 209.40 U/mL; and cancer antigen 199 level, 168.20 U/mL). Viral hepatitis markers were negative. Glucose and serum insulin levels were normal.
Esophagogastroduodenoscopy revealed esophageal and gastric varicose veins and portal hypertensive gastropathy (Figure ). Contrast-enhanced computed tomography (CT) demonstrated multiple emboli formation in the portal vein and splenic vein, multiple round shadows in the liver with a slightly lower density (metastatic tumors were mostly considered), portal vein broadening, varicose veins in the lower esophagus and gastric fundus, splenomegaly, bilateral pleural effusion, ascites and pelvic effusion, broadening of the common bile duct, and increased uterine volume. Ultrasound-guided fine-needle aspiration biopsy of the liver tumor was performed. Histologically, the tumor consisted of heterogeneous cells arranged in nests, with a small cell extraction volume, short spindle or polygonal, unclear cell boundary, eosinophilic cytoplasm, increased nucleoplasmic ratio, and varying degrees of nuclear atypia. Immunohistochemical staining revealed that the tumor cells were positive for CKp, synaptophysin (Syn), chromogranin A (CgA), CD10, CD56, CDX-2, CEA, and Ki67 (40%+) (Figure ). To identify the primary lesion, 18F-fluorodeoxyglucose Positron emission tomography/computed tomography (18F-FDG-PET-CT) was performed and showed multiple metabolic elevations in the pancreatic tail area, intrahepatic portal vein, and adjacent mesenteric and splenic veins. Considering the pathological tendency, it was considered that there was a high possibility of primary lesions of pNEC, secondary intrahepatic metastasis, venous cancer thrombogenesis, and corresponding varicose veins. No other metastatic lesions were found (Figure ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [56.0, 'kg']}",96,91.2,100.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 56.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (56.0 kg - 20 kg) = 96.0 mL/hr.
Hence, the patient's fluid maintenance is 96.0 mL/hr."
5162,22,Maintenance Fluids Calculations,physical,decimal,pmc-5749102-2,Extracted,"A 3-year 4-month-old male child presented with left-sided hemiparesis and right-sided facial weakness for 15 days. He had recurrent bilateral otorrhea for 5 months. There was no fever, altered sensorium or other illnesses in the past. He was a full term normal delivery with birth weight of 1.75 kg and required Neonatal Intensive Care Unit stay for 25 days for neonatal hyperbilirubinemia. His milestones and immunization were appropriate for age. On examination, weight was 10 kg and height was 81 cm. He had large hepatomegaly and mild splenomegaly. On CNS examination, he had left-sided hemiparesis with hypertonia and brisk deep tendon reflexes on the left side. There were no meningeal signs. MRI brain showed right basal ganglia, internal capsule, corona radiata, perisylvian fronto-temporoparietal cortical, and subcortical acute and subacute infarcts. CSF was normal. His antiphospholipid antibody IgM and IgG were positive (17.4 and 19.2 mg/dl, respectively). USG Abdomen showed hepatosplenomegaly. Parents subsequently gave a history of both being HIV infected. The child was also tested for HIV and was found to be HIV infected. His CD4 count was 1645 (28%) cells/cumm. He was started on ART consisting of stavudine (d4T), lamivudine (3TC), and nevirapine, following which he had complete recovery of his hemiparesis. He is currently 5 years old, weights 14 kg and is on regular follow-up and CD4 is 2335 (58.86%) cells/cumm with CD4: CD8 = 1.44.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [14.0, 'kg']}",48,45.6,50.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 14.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (14.0 kg - 10 kg) = 48.0 mL/hr.
Hence, the patient's fluid maintenance is 48.0 mL/hr."
5163,22,Maintenance Fluids Calculations,physical,decimal,pmc-4543188-1,Extracted,"A male patient aged four years and 10 months was brought in with a complaint of short stature. It was indicated that although his development was normal until 12 months of age, it halted afterwards. It was found out that the patient was born at term in breech position through cesarean section with a normal Apgar score and birth weight of 3,750 g, hospitalized postnatally for five days due to birth in breech position and was not noted to be hypothermic and hypoglycemic, was diagnosed with LCP at four years of age following detailed examination due to complaints of pain in the hips, and consequently underwent surgery (). Family history indicated that the patient's parents were related to each other within the second degree of consanguinity. His first sibling was being followed up for Tangier disease, and his second sibling was being followed up for hyperlipidemia by the Department of Pediatric Metabolism. Physical examination findings showed that the patient was prepubertal, and that he had a height of 96 cm (standard deviation score [SDS], -3.2), body weight of 14.6 kg (SDS, -1.9), 2 cm shorter left leg compared to right leg, a surgical scar in the left inguinal region, and stretched penile length of 4.5 cm. Other systemic examination findings were normal. While the patient's chronological age was four years and 10 months, his bone age was consistent with a 2-year-old's (according to Greulich and Pyle).
Laboratory tests yielded the following results: white blood cell count, 11,300/mm3; hemoglobin, 12.1 g/dL; thrombocyte, 320,000/mm3; urea, 7 mg/dL; creatinine, 0.9 ml/dL; serum sodium, 148 mmol/L; potassium, 4.3 mmol/L; chloride, 102 mmol/L; calcium, 9.7 mg/dL; phosphorus, 4.4 mg/dL; normal liver function; fasting blood glucose, 92 mg/dL; total cholesterol, 130 mg/dL; high-density lipoprotein, 41 mg/dL; low density lipoprotein cholesterol, 69 mg/dL; triglyceride, 50 mg/dL; and urine density, 1,022 g/cm3.
Detailed laboratory analyses showed thyroid function consistent with central hypothyroidism (sT4, 0.49 ng/dL [0.8-1.9 ng/dL]; thyroid-stimulating hormone, 2.57 mU/L [0.5-5 mU/L]). The patient was also determined to have hypocortisolemia (basal serum cortisol level of 2.75 g/dL, stimulated serum cortisol level of 5.71 g/dL [with low-dose adrenocorticotropic hormone]) and GHD (peak GH values in glucagon and levodopa tests while the patient was euthyroid were 0.257 and 0.46 ng/mL, respectively). Serum IGF-1 level was 15 ng/mL (SDS, -3) and Insulin-like growth factor binding protein-3 (IGFBP3) level was 900 ng/mL (SDS, -2.6). An etiology-oriented hypophyseal magnetic resonance imaging was performed due to high prolactin levels (37.4 ng/mL [normal range, 0-25 ng/mL]), which revealed in the sellar cavity center that the adenohypophyseal gland height was 3 mm, neurohypophyseal localization was abnormal, and that there was no signal intensity. In addition, T1A hyperintense nodular appearance with dimensions of 3 mm×2.5 mm showing diffused homogeneous contrast retention following injection of contrast agent was observed at the median eminence level (ectopic neurohypophysis). The pituitary stalk was not identified as a separate structure (). Considering the patient's medical history, it was deduced and evaluated as a pituitary stalk interruption syndrome due to difficult birth. The patient was sequentially started on hydrocortisone, L-thyroxin, and GH therapy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [14.6, 'kg']}",49.2,46.74,51.66,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 14.6 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (14.6 kg - 10 kg) = 49.2 mL/hr.
Hence, the patient's fluid maintenance is 49.2 mL/hr."
5164,22,Maintenance Fluids Calculations,physical,decimal,pmc-7271108-1,Extracted,"A 10-year old boy transferred to Vinmec Hospital (Hanoi, Vietnam) due to a huge mass on the right liver. His height of 137 cm, weight 24.6 kg, BMI 13.11 kg/m2. Medical history of congenital cardiac anomaly, diagnosed at 20 days after birth (atrial and ventricular septal defects; pulmonary hypertension up to 50 mmHg). During childhood he had to admit to hospital frequently (5-6 episodes per year) due to severe pneumonia. Under medical treatment and follow-up, all cardiac septal defects recovered spontaneously and pulmonary hypertension resolved. Since 4 years old, severe pneumonia became less frequent with 1-2 episodes per year. Skeletal anomaly particular noted with agenesis bilateral 5th toes.
On referral, his serum biochemical panel from previous hospital show intermittent disorders of liver function as in .
On admission at our hospital, he presented growth retardation and mild mental impairement, transient postprandial drowsiness, and loss of concentration. His height was in standard range, but his weight was 6.1 kg less than standard reference (comparable with 8 year-old boy) and was evaluated as Tanner stage 1. For mental problem, he had trouble to cope with his friends and stayed at class level 1 elementary school while his friends went to the 4th class. He can still remember simple things like parents name, his home address and so on; but got a long and hard for simple summation (within 10), can only spell but didn’t read well. On psychology examination, he was evaluated with Raven Colour Test: IQ 80 (ICD-10-CM: F70 - Mild intellectual disabilities) and Vineland Test 90 points.
Clinically, there were abdomen discomfort due to mild hepato-splenomegaly.
His total and direct bilirubin was 49.8 and 24.8 µmol/L (our hospital normal range was <21 and 5.1, respectively). AST 133.5 U/L and ALT 135.5 U/L (<35 and 35). GGT: 526 U/L (<55); ALP 676 U/L (30-120). NH3 90.6 µg/dl (18.7-86.9). AFP 2.29 (<9 ng/ml); PIVKA II 81.8 (0-40 mAU/ml). Liver virus panel and HIV negative. Platelet 326 G/L. INR (International normalized ratio) 1.04. PELD score: 2.8; Child Pugh Score 7 (Grade B). Cardiosonography found no more congenital defects, with EF 68%, without pulmonary hypertension.
Living donor liver transplantation underwent using right lobe from his mother on 22 August 2018. Operation time was 430 minutes, anhepatic phase: 73 minutes. Warm ischemic time (graft out from cold preserve solution for RHV and portal vein reconstruction): 28 minutes; Cold ischemic time: 82 minutes. Portal vein clamping time: 16 minutes. Blood loss 550 ml; Red blood cell transfused: 350 ml. Graft weight: 549 gr; GRWR (Graft to Recipient Weight Ratio): 2,2%; G/SLV (Graft/Standard Liver Volume): 80%.
Intraoperative we found the native liver was almost dominated by a huge mass (mainly in the right liver). Mobilizing the whole liver from its ligaments, we confirmed that the patient had no right hepatic vein, the middle and left hepatic vein joined into a common trunk, draining into the IVC. The superior mesenteric vein confluenced with splenic vein before draining directly into the inferior vena cava (Abernethy anomaly type 1b), just 3 cm below and to the left of the draining site of hepatic vein complex into the IVC. The so-called portal vein measured of 10mm diameter and ran a 3 cm distance to the IVC (-). Anatomopathology findings of the native liver showed chronic hepatitis with cirrhosis 4/6 Knodel-Ishak ().
The immunosuppressive inducted by basiliximab, then maintained with tacrolimus and mycophenolate.
The post operative course was uneventful; the allograft function’s well with normalization of total bilirubin within 3 days, and AST/ALT down under 2N (upper normal value) within 9 days. CT Scan control 3 weeks postopratively showed all hepatic vessels patent with good flow (). Patient was discharged 28 days postoperatively. He was doing well at the follow-up 12 months later. His mentality was much improved according to his parents.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [24.6, 'kg']}",64.6,61.37,67.83,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 24.6 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (24.6 kg - 20 kg) = 64.6 mL/hr.
Hence, the patient's fluid maintenance is 64.6 mL/hr."
5165,22,Maintenance Fluids Calculations,physical,decimal,trec-ct-2021-39,Extracted,"A 3-day-old Asian female infant presents with jaundice that started a day ago. She was born at 38w3d of gestation, after an uncomplicated pregnancy. The family history is unremarkable. The baby is breastfed.
Vital signs are reported as: axillary temperature: 36.3°C, heart rate: 154 beats/min, respiratory rate: 37 breaths/min, and blood pressure: 65/33 mm Hg. Her weight is 3.2 kg, length is 53 cm, and head circumference 36 cm. Her sclera are yellow and her body is icteric. No murmurs or any other abnormalities are  detected in the heart and lung auscultation. Her liver and spleen are normal on palpation.
Laboratory results are as follows: 
Serum total bilirubin: 21.02 mg/dL
Direct bilirubin of 2.04 mg/dL
AST: 37 U/L
ALT: 20 U/L
GGT: 745 U/L
Alkaline phosphatase: 531 U/L
Creatinine: 0.3 mg/dL
Urea: 29 mg/dL
Na: 147 mEq/L
K: 4.5 mEq/L
CRP: 3 mg/L
Complete blood cell count within the normal range.
She is diagnosed with uncomplicated neonatal jaundice that may require phototherapy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.2, 'kg']}",12.8,12.16,13.44,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.2 kg. Hence, the patient's maintenance fluid is 3.2 kg * 4 mL/kg/hr = 12.8 mL/hr.
Hence, the patient's fluid maintenance is 12.8 mL/hr."
5166,22,Maintenance Fluids Calculations,physical,decimal,pmc-3701922-3,Extracted,"A one-year-old boy was admitted with complaints of irritation, constipation, loss of appetite, and vomiting for 20 days. Patient history revealed regular consumption of a multivitamin preparation, 5 mL per day known to contain 200 IU vitamin D, in the past ten days, prescribed as a dietary supplement. Body weight was 10 kg (-0.14 SDS), and height was 80 cm (+1.65 SDS). Systemic signs were normal. Laboratory parameters were Ca: 13.7 mg/dL, P: 4.1 mg/dL, creatinine: 0.46 mg/dL, PTH <3 pg/mL, 25(OH) vitamin D >160 ng/mL, and urinary Ca/creatinine ratio: 1.2 mg/mg. The patient received therapy with 3000 mL/m2/day IV hydration and 1 mg/kg/day furosemide with dietary restrictions for two days. Renal ultrasonography showed an image consistent with bilateral nephrocalcinosis. Serum Ca level was 14.1 mg/dL at 24 hours. Prednisolone 1 mg/kg/day was also added. Patient was discharged on day 3 with a serum Ca level of 11 mg/dL. Serum Ca and vitamin levels were within the normal range at the follow-up visit.The biochemical findings in the 3 patients are given in .","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.0, 'kg']}",40,38,42,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.0 kg - 10 kg) = 40.0 mL/hr.
Hence, the patient's fluid maintenance is 40.0 mL/hr."
5167,22,Maintenance Fluids Calculations,physical,decimal,pmc-4942313-1,Extracted,"A 13-year-old boy was admitted because of right upper abdominal pain accompanied by vomiting and diarrhea that developed 3 days before admission. No history of a specific disease, abdominal trauma, or surgery was revealed. Family history was unremarkable. His height was 156.5 cm (50-75 p), weight was 60.3 kg (90-97 p), and BMI was 24.8 kg/m2. Vital signs were normal except for low-grade fever (37.6℃), and tenderness over the right upper abdomen was noted without a palpable mass on a physical examination.
A blood test revealed the following: white blood cells (WBCs), 15,100/µL (neutrophils, 72.9%; lymphocytes, 18.2%); platelets, 454,000/µL; erythrocyte sedimentation rate, 29 mm/h; and C-reactive protein (CRP), 5.45 mg/dL. Liver function tests, amylase, lipase, ammonia, prothrombin time, partial thromboplastin time, antinuclear antibody, and antineutrophil cytoplasmic antibody were all negative. A chest radiograph showed no abnormalities. An abdominal computed tomography (CT) scan revealed increased attenuation and enhancement of the omental fat between the gall bladder and epigastric midline, as well as anterior peritoneal wall thickening and enhancement, suggesting omental fat inflammation or infarction (). Laparoscopic biopsy was performed on hospital day (HD) 5, and the pathology showed mesenteric panniculitis with chronic inflammation, adiponecrosis, and moderate septal fibrosis (). Nested polymerase chain reaction for Mycobacterium tuberculosis and special immunohistochemical staining for β-catenin, calretinin, Ki-67, and P53 for malignancy were all negative.
Prednisolone was started (30 mg/d) on HD 6, and the abdominal pain subsided within 4 days. The blood tests showed improvement: WBCs, 7,320/µL (neutrophils, 55.6%; lymphocytes, 31.7%) and CRP, 1.65 mg/dL. He was discharged on prednisolone (30 mg/d) on HD 12, and the prednisolone was tapered to 10 mg/d over 1 month and continued at that dose for 7 months. An abdominal CT scan performed 8 months after discharge showed improvement from the previous abnormal findings without any significant sequelae (). Follow-up blood testing was normal. The patient remained in good health after the 2 year clinical follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.3, 'kg']}",100.3,95.285,105.315,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.3 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.3 kg - 20 kg) = 100.3 mL/hr.
Hence, the patient's fluid maintenance is 100.3 mL/hr."
5168,22,Maintenance Fluids Calculations,physical,decimal,usmle-5664,Extracted,"A 4-day-old male presents to the pediatrician with his mother for his first well visit. The patient was born at 36 weeks gestation to a 26-year-old primigravid via cesarean section for cervical incompetence. The patient required no resuscitation at birth, and both mother and child were discharged from the hospital at two days of life. The patient has been exclusively breastfed since birth, and his mother reports that he feeds for 20-30 minutes every two hours. The patient urinates 3-4 times per day and has begun passing 2-3 stools per day that his mother describes as “grainy” and the color of “mustard.” His birth weight was 3670 g (8 lb 1 oz), and his current weight is 3487 (7 lb 11 oz). His temperature is 97.1°F (36.2°C), blood pressure is 57/42 mmHg, pulse is 140/min, and respirations are 38/min. On physical exam, the patient’s anterior fontanelle is soft and flat, and his eyes are moderately icteric. His abdomen is soft and non-distended. The patient has the physical exam finding seen in Figure A. His diaper can be seen in Figure B.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3487.0, 'g']}",13.948,13.2506,14.6454,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3487.0 g so this converts to 3487.0 lbs * kg/1000 g = 3.487 kg. Hence, the patient's maintenance fluid is 3.487 kg * 4 mL/kg/hr = 13.948 mL/hr.
Hence, the patient's fluid maintenance is 13.948 mL/hr."
5169,22,Maintenance Fluids Calculations,physical,decimal,pmc-3354781-1,Extracted,"A twenty-day-old boy who was second child of healthy unrelated parents was brought to our department. Child was born after 38 weeks of gestation and weighing 2 kg at the time of birth, without any complications during pregnancy and delivery and no anomaly was detected during routine prenatal examinations. The chief complaint was nasal regurgitation of milk in supine position. On oral examination, child was seen to have a complete cleft lip and palate on right side and cleft of hard and soft palate on left side without involvement of alveolus [Figures and ]. On extraoral examination, ectrodactyly of both hands [] and feet [] was seen. Both hands showed claw shaped deformity with only two non-fused fingers present. Radiograph showed only two phalanges in each finger with normal development of other bones in hand []. Feet had three toes with absence of 2nd and 3rd toe. There was syndactyly between 4th and 5th toe. Radiograph showed presence of phalanges of all toes, except 2nd toe which was incompletely formed []. Abnormal continuous discharge from eyes of infant was noted which may be due to nasolacrimal duct anomaly. But, no other anomaly indicating ectodermal dysplasia was seen in hairs or nails. Complete medical investigations were done which revealed no genitourinary or other systemic abnormality. To treat his chief complaint, an impression of the palatal defect was made using elastomeric impression material and an obturator was constructed using cold cure acrylic material which was later relined using soft tissue liner []. Patient is scheduled for primary cheilioplasty around 4 months and surgical repair of palate around 18 months of age.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.0, 'kg']}",8,7.6,8.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.0 kg. Hence, the patient's maintenance fluid is 2.0 kg * 4 mL/kg/hr = 8.0 mL/hr.
Hence, the patient's fluid maintenance is 8.0 mL/hr."
5170,22,Maintenance Fluids Calculations,physical,decimal,pmc-5796925-2,Extracted,"The second subject was a 46-year-old Korean man who had not been diagnosed with diabetes. The subject visited our medical center in January 2017. The subject was 181.7 cm in height and 87.1 kg in weight (BMI, 26.4 kg/m2). The HbA1c level was 5.7% and the fasting glucose sugar level was 107 mg/dL ().
The subject had a high standard of education and was interested in weight loss, and as such, the subject had tried various diets in the past, but had never been successful in losing weight. At the time of first visit, the subject recognized the necessity of weight control, but did not translatethe recognition into obvious action. The subject usually had frequent company meetings, and often ate meat or raw fish when eating out. The subject drank alcohol more than 4 times a week and drank a variety of drinks, including soju, whiskey, liquor, and beer. The subject drank more than 4 cups of alcohol each time. Over the past 3 days, the subject had consumed only yogurt and vegetable juice for weight control. The subject engaged in a low level of physical activity, but had recently started doing core exercises for 30 minutes a day at home. We provided information on appropriate calorie intake and identified a target weight to be achieved by the next visit. We also provided calorie information of alcoholic drinks and foods often consumed and explained how to make appropriate menu choices when eating out. In addition, we explained the benefits of limiting alcohol intake and encouraged the subject to stop drinking.
In February 2017, 4 weeks after the first visit, the weight of the subject was 85.0 kg, which was approximately 2 kg less than the weight at the time of the first visit (). The subject ate lunch and dinner outside, usually eating a lunch box or a one-dish meal at a cafeteria. The subject had tried to reduce the amount of rice he consumed. The subject still had many dinner engagements for work, but the frequency of the alcohol consumption had decreased to once a week. However, the amount of alcohol consumed each time had increased from four glasses of soju and beer to eight glasses when the subject had a meat as a main dish. For snacks, the subject had been having a latte and a small amount of nuts. The physical activity had increased; the subject walked a lot on days that he overate and had maintained thecore exercises at home. Still the subject had ate out many times since last visit to the center, and the subject was stressed whenever he ate out. The subject still had a lot of interest in weight loss, but the actual willingness to act seemed to be weaker. The subject also showed a lot of interest in nutritional counseling. We again gave him a calorie information of the foods often consumed when eating out, how to make appropriate menu choices, and how to reduce calorie intake upon eating out. We reiterated the appropriate amount of drinking and encouraged the subject to stop drinking. In addition, we encouraged the subject to continue walking and the core exercises.
In March 2017, the subject's weight was 82.9 kg, which was 4.2 kg less than the weight at the time of the first visit (). The subject had tried to eat regularly, and the subject's calorie intake was lower than that of the second visit. When the subject was too busy to eat breakfast, the subject consumed a bread with coffee. The amount and frequency of snacking had greatly reduced. However, as the subject's work became busy, the subject was not able to exercise as much as he had before. We affirmed the weight loss of the subject and encouraged the subject to ensure that the weight had not increased again.
The subject visited our medical center for the fourth time in July 2017. The weight was 84.9 kg, which was 2.2 kg less than the weight at the time of the first visit (). The subject had finally managed to lose 2.5% of thr weight at the time of the first visit over the course of 6 months. Since the last month before this visit, the subject had had many dinner engagements with friends and colleagues and had eaten more high-calorie foods such as high-fat meats and stews. In addition, the frequency and amount of the alcohol consumption had significantly increased since the time of the last visit. Dietary diary analysis showed that the subject's average calorie intake was approximately 2,100 kcal, and the proportion of fat was 43%. Both the calorie and fat intake rates were higher than those at the time of the last visit (). Also, it is important to note was that the subject's calorie intake did not reflect the alcohol intake. In an interview, we estimated the calorie intake from each time the subject consumed alcohol to be approximately 1,100 kcal. The intake of high-fat foods and overconsumption of alcohol were due to the subject's frequent dinner appointments, which had been a problem since the time of the subject's first visit. This had not been improved significantly. Moreover, the subject had ceased exercising. We analyzed obstacles to address these problems and set goals that could be implemented to overcome these obstacles. In addition, we provided the subject an information on ingestion tips to maintain progress of these goals.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [87.1, 'kg']}",127.1,120.745,133.455,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 87.1 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (87.1 kg - 20 kg) = 127.1 mL/hr.
Hence, the patient's fluid maintenance is 127.1 mL/hr."
5171,22,Maintenance Fluids Calculations,physical,decimal,pmc-2808565-1,Extracted,"A 9 yr-old girl was admitted to Samsung Medical Center due to chronic productive cough and shortness of breath. During the infancy she developed cough and sputum, which was associated with frequent respiratory tract infection. Diarrhea persisted from 1 month of age regardless of the dietary formula and is unresponsive to antibiotics. Diarrhea led to poor weight gain and generalized edema, which necessitates hospitalization twice. Mantoux test performed at 10 months of her age because of chronic cough was positive (15×15 mm). Hence she was treated with anti-tuberculosis regimen for 9 months, but her symptoms did not improve. When she was 2 yr old, clubbing fingers were noticed, and at 5 yr of age, she received ventilator care due to severe respiratory distress. At that time, Pseudomonas aeruginosa was isolated from her sputum. Since then, her respiratory symptoms were waxed and waned, and she had been hospitalized several times.
She was born by vaginal delivery without any perinatal problems. Her birth weight was 2.4 kg, which was small for her gestational age (37 weeks). Vaccination was done as scheduled. She had a 7-yr old younger brother, and family history was unremarkable. Besides chronic productive cough and respiratory difficulty, she complained of the intermittent abdominal pain or chest discomfort. She also presented diarrhea after fat-rich meal. Other symptoms were denied.
On admission, her blood pressure was 104/49 mmHg, heart rate 90 beats/min, respiratory rate 26/min and the body temperature 37℃. Her body weight was 19.1 kg (<3 percentile) and her height was 118 cm (<3 percentile). She had chronic ill-looking appearance and her mentality was alert. Both chest walls expanded symmetrically with mild intercostal retraction. Coarse breathing sound and crackles were heard on both lung fields. The heart beats were regular and murmur was not heard. There was hepatomegaly but the spleen was not palpable. Clubbing fingers were noted with cyanosis. There was no specific finding on neurologic examination.
The diseases such as immunodeficiency, allergic disease, congenital heart disease and ciliary dyskinesia were ruled out by her normal complete blood cell count (CBC), serum immunoglobulin levels, specific IgE levels, echocardiogram and bronchial mucosal biopsy. Stool examination showed 30 neutral fat droplets and 60 fatty acid droplets per high power field. Chest and abdomen computed tomography (CT) scan demonstrated the bronchiectasis in both lung fields () and fatty replacement of pancreas with severe atrophy (). Inflammatory change in maxillary, frontal, ethmoid sinuses and polyposis in the right maxillary sinus were found in CT scan of paranasal sinuses. P. aeruginosa was cultured from her sputum.
The sweat chloride concentration was measured by a quantitative pilocarpine iontophoresis sweat test recommended by National Committee for Clinical Laboratory Standards (National Committee for Clinical Laboratory Standards. Sweat Testing: Sample Collection and Quantitative Analysis: Approved Guideline. Villnova, Pa: National Committee for Clinical Laboratory Standards; 1997 NCCLS document C34-A.). The test was performed repeatedly on separate days to confirm the diagnosis. The skin of her both forearms was stimulated with pilocarpine and an electrical current of 4 mA for 5 min. The sweat specimens were collected on a gauze pad for 30 min preventing evaporation. The weight of the samples and the chloride concentration was measured according to the mercuriometric titration method (). The average weights of the sweat samples from both forearms were 131.5 mg in the first test and 134.5 mg in the second test. The average sweat chloride concentrations on both forearms were 108.1 mM/L and 96.7 mM/L in separate occasions performed 2 weeks interval. Intrassay coefficients of variation ranged from 2.8-18.4% for both forearms. Patient's brother showed negative sweat test (25.3 mM/L), while sweat chloride concentration of her mother was 42.6 mM/L. Patient's father did not perform sweat test.
Eleven mutation/polymorphism loci of CFTR gene previously found in a Korean population and ten most common disease-associated loci in Caucasians were screened using SNaP-Shot method as previously detailed (). In addition, denaturing gradient gel electrophoresis (DGGE) and subsequent nucleotide sequencings were performed to find unknown CFTR mutations. Two disease-related mutations were identified in this patient: Q1291X and IVS8 T5-M470V. Haplotyping using the method described by Lee et al. () revealed that the two mutations were located in different alleles. Finally, it was identified that Q1291X was from her father and IVS8 T5-M470V was from her mother in the genetic analyses of family members ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [19.1, 'kg']}",58.2,55.29,61.11,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 19.1 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (19.1 kg - 10 kg) = 58.2 mL/hr.
Hence, the patient's fluid maintenance is 58.2 mL/hr."
5172,22,Maintenance Fluids Calculations,physical,decimal,pmc-4330610-1,Extracted,"A 4-year-old boy with 25 kg weight presented to the Emergency Department of Imam Hospital of Sari in December 2013 due to tonic-clonic generalized seizures approximately 30 min ago. 3 h before seizure, his mother mistakenly gave him 2 spoons (amount 20–25 cc) lidocaine hydrochloride 2% solution instead of pediatric gripe. Seizure with generalized tonic-clonic occurred 3 times in home. On arrival at our Emergency Department, she was agitated and had confused speech with Glasgow coma scale score of 14/15. His initial blood pressure was 90/55 mmHg with a pulse rate of 130 beats/min.
His temperature was 36.9°C axial. Respiratory rate was 20 per min with a SpO2 of 96% on 2 L of nasal oxygen. Twitching movement with muscle spasm was noticed in the limbs. The pupils were 4 mm in diameter, equal and reactive, and no focal neurological deficit was found. His skin was normal. Bowel sound was normal, and the bladder was not palpable. An electrocardiogram (ECG) showed sinus tachycardia with a heart rate of 139 beats/min, and QT interval was 0.89 s. Neurologic examination was essentially unremarkable except for the depressed level of consciousness. The personal and medical history was unremarkable; including the absence of birthing trauma or febrile seizures. He had no history of use of other drugs.
Laboratory studies while the patient received supplemental oxygen included an arterial blood gas with pH 7.30; pO2104 mm Hg; pCO239 mmHg; and HCO321. A complete blood count revealed white blood cells 10,400/mm3(31% polymorphonuclear leukocytes, 64% lymphocytes, 5% monocytes); hemoglobin 12 g; and hematocrit 35%. Blood chemistry studies were unremarkable except for an elevated glucose (219 mg %) obtained while the patient was receiving an IV line with 5% glucose. One day after admission; a repeat glucose level was 89 mg%.
Shortly after arrival at the Emergency Department, he developed one episode of brief generalized convulsion with upward gaze and episode lasting for around 30 s, 5 mg of IV diazepam was administered and a contrast-enhanced computed tomography (CT) scan of the brain was promptly performed. The latter showed no evidence of intracranial ischemic or hemorrhagic lesions. Serum lidocaine concentration 30 min after the onset of seizures was 5.1 μg/ml. There were no further seizures; the patient remained stable and was discharged 2 days after admission.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [25.0, 'kg']}",65,61.75,68.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 25.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (25.0 kg - 20 kg) = 65.0 mL/hr.
Hence, the patient's fluid maintenance is 65.0 mL/hr."
5173,22,Maintenance Fluids Calculations,physical,decimal,pmc-5063483-1,Extracted,"A 56-year-old female patient, who weighed 66 kg, was 158 cm tall and had American Society of Anesthesiologists’ physical status I, was diagnosed with advanced right breast carcinoma. She presented 4 months prior to the surgery with a history of right breast lump; incisional biopsy revealed invasive ductal carcinoma. She was then commenced on neoadjuvant chemotherapy. Two years prior to this, she had total thyroidectomy under GA for simple multinodular goiter complicated with stridor, hypoxia, and hoarseness of voice, secondary to vocal cord palsy, which was managed with tracheostomy. The tracheostomy tube was removed 8 months later, leaving the patient with a persistent hoarseness of voice and defective left vocal cord. She was worked up for surgery after completion of neoadjuvant chemotherapy. Her serum biochemistry, hematology, electrocardiogram (ECG), and chest X-ray results were normal. She was instructed on the visual analog scale for pain intensity, where 0 meant no pain and 10 meant the worst pain imaginable. The anesthetic plan was explained to and discussed with the patient.
In the theater, intravenous (IV) access was established with 18 G cannula on the left hand, and 500 mL normal saline solution was set up. Using the Classic-120 Multiparameter® monitor (Health-Care Equipment and Supplies Co. Ltd, Surrey, UK), noninvasive blood pressure (BP), pulse oximetry, and continuous ECG were monitored. Her baseline pulse rate was 83 beats/min (bpm), BP was 146/86 mmHg, and arterial oxygen saturation (SaO2) was 98%, breathing room air. Verbal contact was maintained throughout the block placement and surgery. With the patient sitting up on the operating table, a right-sided TPVB using Jüttner et al’s modification of Pfeiffer et al’s lamina technique was performed. The C7–T6 vertebral spinous processes were palpated and marked. Her T3 spinous process was identified using the scapular spine as a landmark, and 1.5 cm from the midline on the right side was marked as the needle entry point (). Povidone iodine (10%) solution was used for skin preparation, followed by infiltration of the injection site using 2 mL 1% lidocaine with 1:200,000 epinephrine. An 18 G Tuohy needle (Portex; Smiths Medical, Ashford, UK) was inserted and advanced in a paramedian sagittal plane at 45° to the skin in the cranial direction until contact was made with the vertebral lamina at a depth of 4 cm. With a negative test aspiration of air, blood, and cerebrospinal fluid, 6 mL 1% lidocaine with 1:200,000 epinephrine was injected to facilitate insertion of the 20 G epidural catheter (Portex) 3.0 cm beyond the needle tip into the paravertebral space. The catheter was secured, and the patient was placed supine on the operating table. Test dose comprising 5 mL 1% lidocaine with 1:200,000 epinephrine was administered via the catheter while monitoring the patient’s pulse rate, BP, respiration, and consciousness to exclude pneumothorax, epidural, or subarachnoid injection. Thereafter, 7 mL 1% lidocaine with 1:200,000 epinephrine and 20 mL 0.5% bupivacaine with 1:200,000 epinephrine were injected over 10 minutes. The block was completed within 28 minutes (catheter was removed after the local anesthetic [LA] injection) and was deemed adequate in 16 minutes by loss-of-cold and pinprick sensation (by the surgeon) over the operative area. The patient was observed to be shivering, but she was reassured and received IV fentanyl 50 μg and midazolam 2 mg. Then a mixture of propofol 150 mg and ketamine 100 mg (ketofol) in 500 mL normal saline solution was infused at 2–4 mL/min to achieve a Ramsey sedation score of 3–4. Supplemental oxygen at 4 L/min via nasal prongs was commenced. The surgical incision was elliptical, which included the nipple–areolar complex and the underlying 14 cm ×16 cm breast mass. The incision at the sternal border elicited pain, for which 10 mL 0.5% lidocaine with 1:200,000 epinephrine was infiltrated by the surgeon. Superior and inferior skin flaps were raised to the level of the clavicle and the lower coastal margins, respectively. The breast tissue was dissected off and the axilla was accessed through the same incision. The skin was closed over a drain. The duration of surgery was 95 minutes. A total of 245 mL ketofol was employed for conscious sedation. The blood loss was 150 mL; intraoperative fluid administered was 500 mL normal saline and 500 mL Gelofusine. The patient’s vital signs throughout surgery were as follows: pulse rate 60–82 bpm, BP 90/50–130/80 mmHg, and SaO2 100% at 4 L/min oxygen via nasal prongs.
At the end of surgery, the patient was transferred awake to the recovery room, and IV paracetamol 600 mg was administered. She was commenced on oral feeding 8 hours after surgery with good effect. On the ward in the first 24 hours, she had IV paracetamol 1 g, IV pentazocine 30 mg, and oral Celebrex 200 mg; her pain score was 2–3. In the next 24 hours, the pain score remained low; analgesics via oral route comprised Celebrex 400 mg and paracetamol 3 g in divided doses. She was discharged home on the sixth day. Both the surgeon and patient described the anesthesia and pain control as satisfactory.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [66.0, 'kg']}",106,100.7,111.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 66.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (66.0 kg - 20 kg) = 106.0 mL/hr.
Hence, the patient's fluid maintenance is 106.0 mL/hr."
5174,22,Maintenance Fluids Calculations,physical,decimal,pmc-3611078-1,Extracted,"A 51-year-old male, 50 kg in weight who had been diagnosed with Huntington's chorea at the 41 years-of-age was admitted for an emergency laparoscopic hernia repair. On physical examination, the patient displayed choreic movements in all limbs, swallowing dysfunction and excessive oral secretions. Laboratory values were all within normal limits, except for leukocytosis. A chest radiograph did not show any abnormal finding and the electrocardiogram (ECG) revealed left ventricular hypertrophy. The patient was transferred to the operating room without being pre-medicated. Routine monitoring included pulse oximetry, ECG, noninvasive blood pressure and end-tidal carbon dioxide and gas monitoring. To check the depth of anesthesia during the operation, A BIS sensor (BISquatro™, Aspect® Medical Systems, Inc., USA) was attached and measurements were taken when the signal quality index (SQI) was above 95. Muscle relaxation was monitored using an electrical stimulator (Relaxograph®, Datex Relaxograph, Finland) by applying the train of four (TOF) on the wrist's ulnar nerve and measuring the contraction of the adductor pollicis muscle. To avoid possible pulmonary aspiration, awake fiberoptic intubation was planned by an expert. The procedure and need to be intubated while awake was explained to the patient. The base of the tongue and pharyngeal walls were anesthetized with 10% xylocaine spray and 4% lidocaine was injected trans-tracheally to anesthetise the trachea. The fiberoptic bronchoscope (LF-TP, Olympus, Japan) was checked and loaded with a cuffed endotracheal tube with an inner diameter (ID) of 7.5 mm. The vocal cords were visualized and the tube was passed over the fiberscope into the trachea without difficulty. After confirmation of tracheal intubation by viewing the tube tip inside the trachea using fiberoptics, tube fogging, the inability of the patient to vocalize and end-tidal carbon dioxide, anesthesia was induced with an intravenous computer-controlled infusion pump (Orchestra® Base Primea, Fresenius Vial, France) of 2% propofol with a target of 4 µg/ml and remifentanil with a target of 4 ng/ml, and an intravenous bolus of 0.5 mg/kg rocuronium. The radial artery cannula was inserted for invasive blood pressure monitoring. The TOF ratio was zero after induction.
During the surgery, the concentrations of propofol and remifentanil were regulated according to the BIS and mean arterial pressure. Anesthesia was maintained with a TCI of propofol and adequate concentrations to maintain the BIS between 40 and 60. The mean arterial pressure and heart rate remained within normal limits during the procedure. Four twitches were detected on TOF at 60 and 90 minutes after induction and rocuronium 5 mg was administered each time. The surgery lasted 105 minutes. Ondansetron 4 mg was administered to reduce postoperative nausea and vomiting.
The infusions of remifentanil and propofol were discontinued at the end of the procedure and a neuromuscular blockade was reversed with pyridostigmine 15 mg and glycopyrrolate 0.4 mg. Spontaneous respiration and consciousness returned after 9 minutes, at which time the endotracheal tube was removed. The postoperative course was uneventful and there were no complications such as nausea, vomiting or shivering. The patient was transferred to a general ward and discharged from the hospital after 3 uneventful days.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [50.0, 'kg']}",90,85.5,94.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 50.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (50.0 kg - 20 kg) = 90.0 mL/hr.
Hence, the patient's fluid maintenance is 90.0 mL/hr."
5175,22,Maintenance Fluids Calculations,physical,decimal,pmc-5266800-1,Extracted,"This 11-month-old girl is the first child of healthy nonconsanguineous parents, neither having a Marfan diagnosis (although not formally tested). There is no other family history of Marfan disease, aortic disease, or sudden death.
The pregnancy was planned. Anomaly scans at 33 weeks showed increased leg length, and repeat scans at 37 weeks demonstrated oligohydramnios. This resulted in steroid induction at 37 + 2 weeks. After birth, she did not require any resuscitation or special care but was found to have positional talipes. At birth, her length was 49.6 cm (>75th centile) and head circumference 33 cm (50th centile). Her birth weight was 2.335 kg (9th centile).
She was referred to a genetics clinic at 6 weeks due to concern over her physical features. On examination, her head circumference was 39 cm (99.6th centile) and length was 55 cm (75th–91st centile). Her head was plagiocephalic with prominent coronal sutures and a posteriorly positioned anterior fontanelle, and her posterior skull was turricephalic with a cone shape (see ). Her zygomatic arches were prominent.
Her fingers and toes appeared elongated (arachnodactyly), although lengths were not objectively measured, and her thumb held abducted (see ). She had clicky joints in her legs and was unable to fully extend her knees. Her feet bent up so that the top of her foot touched her shin. She had kyphoscoliosis.
There was presence of a divergent squint, although eye exam was otherwise unremarkable, with no lenticular dislocation nor iridodonesis noted. Her palate was normal. Her right nipple was positioned more laterally compared to the left and her ribs were more prominent on the right. The remainder of the clinical examination was unremarkable.
In light of the dysmorphic features identified, genetic investigations were carried out on suspicion of nMFS. There was confirmation of an FBN1 gene mutation (exon 26, c.3143T>C). Echocardiography was performed which showed aortic root dilatation at 5 months of age, with a maximum diameter of 18 mm (Z + 4.3). In addition, echocardiography demonstrated atrioventricular valve prolapse, tricuspid regurgitation, a dysplastic mitral valve with mitral regurgitation, an increase in right ventricular pressure, and pulmonary hypertension (see ).
At 5 months of age, she was admitted due to signs of heart failure and respiratory distress, with a click and pansystolic murmur of mitral regurgitation on cardiac auscultation. She was started on medical heart failure therapy (captopril, spironolactone, and furosemide) and was discharged home following improvement. The child was started on captopril (an ACE inhibitor) instead of an alternative angiotensin receptor blocker, as this was consistent with local trust guidelines.
Worsening respiratory function at 7 months required further admission to rule out bronchiolitis and pneumonia, although no formal lung function tests were carried out. Our patient was commenced on sildenafil in light of the clinical picture and previous echocardiographic demonstration of pulmonary hypertension.
Echocardiogram revealed worsening regurgitation, dilated pulmonary arteries, and pulmonary hypertension and a CT scan additionally demonstrated right sided cardiac enlargement, an atrial septal defect, and a patent ductus arteriosus (see ). At 8 months of age she required intubation and mechanical ventilation for further deteriorations. Our patient was started on the phosphodiesterase-3 inhibitor milrinone, and captopril was converted to irbesartan on the advice of the intensive care unit. Since then, she remained on mechanical ventilation due to a combination of cardiac failure and a restrictive lung physiology related to scoliosis and severe hypotonia. Digoxin was started one month later due to persistent cardiac failure.
A multidisciplinary team (MDT) meeting discussed the feasibility of cardiac surgery given the severity of congestive cardiac failure, and it was concluded that surgery would not be in the patient's best interests. The nMFS presentation, severe hypotonia, and its impact on early and late postoperative morbidity were the main concern, with the comorbidities preventing a good long-term outcome.
A second opinion concerning cardiac surgery was requested by the parents. A clinical geneticist's view was sought and they emphasised that the main prognosis for this child was dependent upon her life limiting cardiovascular status and that disease related complications would be manageable after surgery and compatible with a good quality of life. Consequently, it was decided that cardiac surgery would be in the patient's best interests. It is important to note that this view was subjective but discussed and agreed on by an MDT including cardiologists and cardiovascular surgeons. In preparation for surgery, and in light of worsening cardiovascular and respiratory function, the patient was given a tracheostomy to facilitate long-term ventilation.
The patient underwent tricuspid valve repair (leaflet repair and partial annuloplasty), mitral valve repair (leaflet chordae shortening and partial annuloplasty), and ASD closure at 11 months of age. Direct inspection of her lungs showed very significant pulmonary emphysema. The surgery was uneventful with no bleeding and no rhythm issues apart from slow sinus rhythm. She was admitted to PICU in a stable condition. Nasogastric feeding was resumed 2 days after surgery.
From a cardiovascular point of view, the patient remained stable following the surgery. She required inotropic support with adrenaline for 2 hours and required pacing via epicardial pacemaker for 24 hours due to slow sinus rhythm. A postoperative transthoracic echo in PICU confirmed good surgical results with good biventricular function, mild mitral regurgitation, and mild-moderate tricuspid regurgitation (see ).
Following surgery, the patient remains ventilated through a tracheostomy but has had gradually increasing periods off ventilator (30 minutes–1 hour every 2-3 hours). She developed frequent daily vomiting due to gastrooesophageal reflux disease, which was treated with omeprazole. Due to feeding difficulties, a PEG was inserted. Since then she has been progressing well and is gaining weight. Immediately before operation, at 11 months of age, the patient weighed 5.80 kg (<0.4th centile). At 14 months of age she weighed 8 kg (2nd–9th centile).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [8.0, 'kg']}",32,30.4,33.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 8.0 kg. Hence, the patient's maintenance fluid is 8.0 kg * 4 mL/kg/hr = 32.0 mL/hr.
Hence, the patient's fluid maintenance is 32.0 mL/hr."
5176,22,Maintenance Fluids Calculations,physical,decimal,pmc-4916277-1,Extracted,"A 33-year-old gentleman was referred from adult psychiatrist to genetic clinic for assessment of his intellectual disability. He was the first child of a nonconsanguineous Chinese couple, born at full term with birth weight of 3 kg (10–25th percentile) through normal vaginal delivery in rural hospital of China. His neonatal course was complicated with poor feeding and bilateral undescended testis. His failure to thrive and hypotonia were gradually improved during early infancy. The growth parameters and appetite were increased significantly in early childhood that he became obese afterwards. He had developmental delay and studied in special school till the age of 12. He came to Hong Kong at the age of 20 and developed type 2 diabetes mellitus since he was 22 years old. He was regularly followed up in endocrine clinic for his diabetes and obesity. Endocrine investigation showed borderline low testosterone level of 200 ng/dL (normal 240–950 ng/dL) with HbA1c of 9.4% (normal < 6%). His intellectual function assessed by Wechsler Adult Intelligence Scale-Fourth Edition (Hong Kong) showed he had severe grade mental retardation. He also had obsessive compulsive behavior that required psychotherapy.
Clinical assessment in genetic clinic showed he was obese with body weight of 76.8 kg (90–97th percentile), body height of 152 cm (6 cm < 3th percentile), and the BMI of 33.2 Kg/m2. There were no facial dysmorphic features except that he had fair complexion. He had bilateral gynecomastia. Both hands and feet were relative small (). There was only scanty axillary and pubic hair. Stretched penile length was 4 cm and two 5 mL testes were palpable. There were no acanthosis nigricans or other evidence of insulin resistance. The rest of the physical examination was essentially normal. Based on the medical history and physical findings, Prader-Willi syndrome (PWS) was suspected. Methylation study using SALSA MLPA ME028 Prader-Willi/Angelman probemix kit from MRC-Holland (Amsterdam, Netherlands) was performed. It showed heterozygous deletion and hypermethylation of SNRPN locus. The 15q11–13 deletion was confirmed by FISH study; thus the diagnosis of Prader-Willi syndrome due to paternal deletion of SNRPN locus was substantiated. He was then referred to endocrine clinic for assessment of growth hormone usage and testosterone replacement.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [76.8, 'kg']}",116.8,110.96,122.64,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 76.8 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (76.8 kg - 20 kg) = 116.8 mL/hr.
Hence, the patient's fluid maintenance is 116.8 mL/hr."
5177,22,Maintenance Fluids Calculations,physical,decimal,pmc-8191279-1,Extracted,"A 52-year-old male obese patient (weight 115 kg, height 181 cm), with history of hypertension, analgesics abuse due to chronic back pain, came to Emergency Department for repeated massive hematemesis episodes. Upon arrival, the patient was conscious, with slightly reduced response to painful stimulation and regularly reflexive pupils; vital signs were recorded: heart rate was 145 bpm, non-invasive blood pressure 80/45 mmHg, SpO2 86% in room air. Blood tests were performed, urinary catheter and indwelling arterial line for blood pressure monitoring and serial blood gas measurements were placed. After anamnesis excluded presence of active liver disease and esophageal varices, the patients signed the informed consent so that a gastric tube was gently positioned to drain blood from stomach, and immediately after a Sengstaken Blackmore tube to in an attempt to stop bleeding.
Emergency endoscopy was arranged and performed with locally sprayed 10% lidocaine and minimal sedation with midazolam 1 mg, resulting in failure to identify and control active source of bleeding with endoscopic treatment. Following the worsening of hemodynamic conditions and impossibility to stop bleeding, immediate surgical access was scheduled. Patient was moved to operatory room and, under vital parameters monitoring and 3 minutes preoxygenation in 100% oxygen, a rapid sequence induction was performed with etomidate 0.2 mg*kg-1, suxamethonium 1 mg*kg-1, and fentanil 100 mcg. Cricoid pressure (CP) was applied in order to decrease the risk of regurgitation. Before the procedure, patient was not carefully studied for airway management, due to urgent setting, but a Mallampati 3 score and slightly reduced neck movement were recorded. At a first direct laryngoscopy, no glottic structures were visible; a second attempt, after aspiration of blood and releasing of CP, showed a Cormack-Lehane 3 grade with partial view of lingual border of epiglottis.
Intubation was attempted blindly twice with styletted tube, unsuccessfully, whereas ventilation by face-mask was getting quickly worse. As the oxygen saturation was descending rapidly (spO2 60%), a number 4 classic LMA was placed after repeated mouth aspiration. Mask was inflated accordingly to manufacturers' instruction (25 ml of air) and manual ventilation was obtained via gentle but frequent insufflation with 100% Oxygen. Once saturation was fully recovered, considering emergency surgery and aspiration risk, the decision to intubate through LMA was taken.
Optical instruments (video/fiberoptical) were not available. We then inserted a 16 Fr standard nasogastric tube (NGT) blindly through LMA, finding indirect sign of passage in trachea in easy advancement without resistance and repeated free air aspiration. Then, we cut proximal tip of NGT and kept granting ventilation passing proximal end of NGT via holed catheter mount. Next, proximal part of LMA with glued connector was cut and removed to allow passage of a 7,5 mm endotracheal tube (ET) through LMA by railroading on NGT [].
Before removing the LMA, the ET cuff was inflated and position confirmed by capnography.
After successful intubation, surgery started and patient was successfully treated for duodenal ulcer. Vital parameters were stable throughout the operation, but blood and plasma transfusion were necessary according to blood test results. At the end of the surgery, the patient was moved to intensive care unit for postoperative monitoring and uneventfully extubated the day after using a safe extubation technique.[]","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [115.0, 'kg']}",155,147.25,162.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 115.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (115.0 kg - 20 kg) = 155.0 mL/hr.
Hence, the patient's fluid maintenance is 155.0 mL/hr."
5178,22,Maintenance Fluids Calculations,physical,decimal,pmc-4823429-2,Extracted,"A 54-year-old 175 cm tall man weighing 84 kg underwent right craniotomy for clipping of an unruptured middle cerebral artery aneurysm. A Spetzler catheter inserted at L4-5 interspace drained 100 mL of CSF, and was removed post-craniotomy. The patient did well initially, however, on POD 3, he developed a partial right third nerve palsy and lethargy. A Head CT revealed midline shift with an epidural air collection (). Re-exploration was performed to address the mass effect attributed to the epidural collection. At craniotomy, however, the dura and brain were depressed and not under pressure. Postoperatively, upright intracranial pressure (ICP) was -14 mmHg, and increased to 0 with supine positioning. Arteriography demonstrated no vasospasm; although the basilar artery was kinked (). A head CT revealed an oval shape midbrain (), consistent with brain sag. Two days after re-exploration, he was awake but confused, oriented to self, following only simple commands. His right pupil was dilated and nonreactive to light. He remained too lethargic to complain of positional headache but became more alert while supine.
Brain sag was confirmed by the constellation of persistent lethargy, third nerve palsy, radiographic findings and low ICP (0-3 mmHg). Seven days after aneurysm clipping, a L4-5 EBP was performed with 25 mL of blood. Within the hour, he became more awake and appropriate. Within four hours, he engaged in a telephone conversation and fully recovered to baseline neurological state. One day after EBP, he was ready for transfer to rehabilitation medicine and remained neurologically intact thereafter.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [84.0, 'kg']}",124,117.8,130.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 84.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (84.0 kg - 20 kg) = 124.0 mL/hr.
Hence, the patient's fluid maintenance is 124.0 mL/hr."
5179,22,Maintenance Fluids Calculations,physical,decimal,pmc-3663318-1,Extracted,"A 4-year-old 19-kg male child suffered from sudden onset of abdominal pain and fever for about 5 days. Parents reported no significant past medical or surgical history. On arrival at our hospital, the patient had stable hemodynamics with a body temperature of 37.4 °C, a pulse rate of 94 beats per minute, a blood pressure of 124/79mm Hg, and a decreased urine output. On physical examination, the abdomen was distended mildly, and bowel sound was absent. Abdominal tenderness to deep palpation in the right upper quadrant without rebounding pain was found. Rectal examination showed yellowish stool that was Hemoccult-negative. Laboratory data were as follows: total white blood cell count, 17.2×109/L with a significant left shift; hematocrit, 34.9%; serum amylase, 61U/L; serum lipase, 19U/L and serum C-reactive protein, 78.21 mg/mL. The abdominal radiograph showed normal bowel gas pattern and no abnormal free air was identified. Abdominal sonography showed a hypoechoic mass with debris. A computed tomographic scan of the abdomen with intravenous contrast showed an abscess measuring 22×25×24 mm in the small bowel mesentery (). The appendix was not swelling.
In light of the abnormal image findings, it was decided that a surgical intervention should be performed; and a laparoscopic approach was elected. Laparoscopy was performed in supine position with a 5-mm Hasson port at the umbilicus and two 5-mm ports at the right upper and left lower quadrants. Video laparoscopy was performed with a 5-mm 30° laparoscope (Karl Storz GmbH, Tuttlingen, Germany). The cecum was initially identified and the entire small bowel was examined. Some serous fluid was observed in the peritoneal cavity. There was an abscess located in the small bowel mesentery right side of the abdomen. Then, the cavity of the abscess was opened attentively and the content was sucked out completely. A piece of peanut was found lying free in the cavity of the abscess (), and the ileal loop and omentum had walled off an inflamed and perforated Meckel's diverticulum (). Diverticulectomy and wedge resection of the ileum were performed. The anastomosis of the ileum was performed intracorporeally.
Histology confirmed the diagnosis of a perforated Meckel's diverticulitis with abscess formation. Macroscopically, the specimen consisted of one enteric segment measuring 50 mm in length and maximal 20 mm in diameter (). A perforation was found at the tip. On microscopic examination, it showed ulcerative intestinal mucosa with diffusely necrotizing inflammation, with acute and chronic inflammatory cells infiltrating transmurally and fibrinoid substance coating on the serosa. No recognizable ectopic mucosa was identified. The patient was discharged 4 days after operation and remains healthy without any sequelae on one-year follow-up at our outpatient clinic.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [19.0, 'kg']}",58,55.1,60.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 19.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (19.0 kg - 10 kg) = 58.0 mL/hr.
Hence, the patient's fluid maintenance is 58.0 mL/hr."
5180,22,Maintenance Fluids Calculations,physical,decimal,pmc-3475915-1,Extracted,"A 32-month-old Egyptian girl was referred to our pediatric endocrinology unit for evaluation of poor growth. She was the second-born female child to consanguineous Egyptian parents with the other sibling being normal. She was borne at term by normal vaginal delivery in a private hospital and cried immediately at birth. Her birth weight was 1.5 kg and length was 35 cm.At the age of 12 days, she developed multifocal seizures and hypocalcemia was detected at that time. Serum parathormone (PTH) level was not checked due to lack of facilities.The seizures were controlled with intravenous calcium infusions. Later, she required calcium and alfacalcidol to maintain her calcium levels. She has been on calcium and vitamin D supplements since then. At the age of one year her weight was 4.800 kg and height was 48 cm. She was thriving poorly in spite of her good appetite.. There was no history of recurrent infection or previous hospital admission. On examination, she was found to be severely growth retarded with normal mentality, her weight was 7 kg, height 60 cm, and head circumference 38 cm (all far bellow third percentile) [], the upper segment to lower ratio was normal, dysmorphic facies: (microcephaly, deep-set eyes, peaked nose, thin lips, micrognathia, low set ears, depressed nasal bridge) []. Systemic examination including the cardiovascular system was within normal limits. Ophthalmic examination did not reveal any abnormality. Investigations revealed that hemogram, liver, renal function, and urine analysis were normal. She had low total calcium 7.4 mg/dL (normal range, 8.5 mg/dL to 10.5 mg/dL), low ionized calcium 3.3 mg/dL (normal range, 4.5 mg/dL to 5.6 mg/ dL), raised serum phosphate 8.2 mg/dL (normal range, 2.4 mg/dL to 4.1 mg / dL), raised alkaline phosphatase 344 U/L (normal range, 30 U/L to 95 U/L) and low intact PTH 6.2 pg/ mL (normal range, 12 pg/mL to 72 pg/mL). Abdominal ultrasound was normal. Radiograph of long bones showed cortical thickening with medullary stenosis, and skull X-ray revealed absent diploic space in the skull bones [Figures and ], Computed tomographic scan of brain was normal. Cytogenetic and fluorescent in situ hybridization studies were normal. The diagnosis was confirmed genetically by detection of homozygous deletion of 12 bp (155-166 del) in exon 3 of the tubulin specific chaperone E gene (TBCE gene). The parents were heterozygous carriers of this mutation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.0, 'kg']}",28,26.6,29.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.0 kg. Hence, the patient's maintenance fluid is 7.0 kg * 4 mL/kg/hr = 28.0 mL/hr.
Hence, the patient's fluid maintenance is 28.0 mL/hr."
5181,22,Maintenance Fluids Calculations,physical,decimal,pmc-3094288-1,Extracted,"A 17-year-old Caucasian female presented to local hospital with a history of acute alcohol intoxication and ingestion of large quantities of acetaminophen. The patient complained of nausea for 2 days and subjective increase in thirst and urine output for a day. She did not notice any dysuria, abdominal pain or change in the colour of her urine. She did however report a remarkable increase in lower back pain that she had attributed to strenuous exercise.
Two days prior to her presentation to the emergency department, the young lady had attended a party where she consumed over 300 mL of vodka and ingested twenty 500 mg tablets of acetaminophen later that night.
Past medical history revealed that she had experienced an episode of rash after having taken liquid acetaminophen as a child. She had not taken acetaminophen since infancy and also denied regular use of any other analgesic. Family history was non-contributory for relevant physiological and psychological illness. The patient reported feeling stressed due to a recent slip in school grades, however denied any suicidal ideation.
Physical examination in the emergency department revealed blood pressure of 140/92 mmHg, pulse 80 bpm, temperature 36.9°C, respiratory rate of 16 breaths per minute and oxygen saturation of 100% at room air. Height and weight were recorded at 170 cm and 63 kg. Physical examination was otherwise unremarkable. No rash, joint swelling or sign of dehydration was detected.
Initial renal function tests at the local hospital revealed serum creatinine and BUN levels of 1.6 mg/dL and 19.3 mg/dL, respectively. Other laboratory results included: glucose 112 mg/dL, sodium 141 mEq/L, potassium 4.3 mEq/L, chloride 104 mEq/L, bicarbonate 29 mEq/L, albumin 43 g/L, aspartate transaminase 20 IU/L, alkaline phosphate 66 IU/L and total bilirubin 1.11 mg/dL. Her INR was reported to be normal at 0.9. Toxicity screens on admission showed acetaminophen level at 9.06 μg/mL. Urine dipstick showed trace amount of blood and 2 plus protein. Microscopy revealed 25 red blood cells per high power field and was otherwise non-contributory. Abdominal ultrasound revealed increased hepatic echogenicity and the kidneys were normal in appearance.
At the outside hospital, she was given morphine, ondansetron and lansoprazole for her back pain and gastrointestinal symptoms. Acetylcysteine was not administered as the patient presented more than 24 hours after the ingestion of acetaminophen.
Renal function tests were repeated later that evening and monitored frequently thereafter. Over the course of 36 hours, the patient's serum creatinine and BUN levels elevated from 1.6 mg/dL and 19.3 mg/dL to 5.7 mg/dL and 49.6 mg/dL, respectively. Urine output was reported to be 2.7 mL/kg/hour. At this time, the patient was transferred to our Children's Hospital for rapidly progressive renal insufficiency.
Physical examination upon admission showed normal vital signs: blood pressure 115/74 mmHg, pulse 60 bpm, temperature 36.6°C, respiratory rate 16 breaths per minute and 100% oxygen saturation at room air. Serum creatinine and BUN levels were measured at 6.3 mg/dL and 52.4 mg/dL, respectively. Furthermore, her electrolytes were recorded as follows: random glucose 86 mg/dL, sodium 134 mEq/L, potassium 5.7 mEq/L, chloride 104 mEq/L and bicarbonate 22 mEq/L. Coagulation study revealed an INR of 1.0 and an APTT of 28 seconds. Other investigations including blood counts and liver functions tests were within normal range. The patient's daily urine output was 3.3 mL/kg/hour at this time. Urinalysis revealed small amounts of protein and blood in her urine. Staining for eosinophils on the random urine sample was positive.
Renal biopsy was performed to further delineate the underlying cause of rapidly progressive renal insufficiency. Figure depicts the histological findings. The biopsy showed no evidence of glomerulonephritis. The interstitium was mildly edematous with small aggregates of inflammatory cells, mainly lymphocytes and eosinophils. Immunofluorescence and electron microscopy were both negative for immune deposits. The histological findings were compatible with acute interstitial nephritis.
The patient was managed supportively by careful monitoring of fluid intake and output. Corticosteroids therapy was considered if no improvement of her renal function was observed. However, her serum creatinine and BUN levels peaked at 7.0 mg/dL and 60 mg/dL two days after admission then began to improve without further medical intervention. Her serum creatinine and BUN levels upon discharge were 4.7 mg/dL and 48 mg/dL respectively. Outpatient follow-up at two weeks after discharge showed that she had completely recovered; her creatinine was 1 mg/dL and BUN was 18 mg/dL.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [63.0, 'kg']}",103,97.85,108.15,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 63.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (63.0 kg - 20 kg) = 103.0 mL/hr.
Hence, the patient's fluid maintenance is 103.0 mL/hr."
5182,22,Maintenance Fluids Calculations,physical,decimal,pmc-6114031-1,Extracted,"A 19-year-old male presented to the emergency department at 10:42 a.m.,42 min after the sudden onset of slurred speech with weakness of his right upper and lower extremities. He reported no headache, dizziness, nausea, vomiting, fever, or convulsions. He denied any significant medical history, drug abuse, or high-risk sexual behaviors. He had no history of migraines, trauma, insect bites, exposure to chemicals, or use of medications. Apart from cigarette smoking for 1 year, he denied other risk factors for stroke. There was no history of early cardiovascular disease in the family.
On physical examination, the patient’s vital signs were normal. His weight was 65 kg (69 kg, 3 weeks ago), body mass index (BMI) 21.47 kg/m2. His chest examination was clear, and no additional murmurs were detected upon cardiac examinations. The liver, spleen and cervical lymph nodes were not enlarged; no skin or mucosal lesions were seen.He was alert and oriented to person, place, and time. The pupils were equal and reactive to light and accommodation. He had mild right hemiplegia with strength of 4:5 in the right upper and lower extremities; slight dysarthria and right lower facial paresis were also noted. The neurologic examination was otherwise unremarkable. The National Institutes of Health Stroke Scale (NIHSS) score was 3.
Rapid blood glucose was in the normal range (6.3 mmol/L). Complete blood count results showed white blood cell (WBC) count 3.0 × 109/L, hemoglobin 11.9 g/dL, and platelets 273 × 1012/L. Stroke was first considered. As he was then in the 4.5-h time window for IV-rtPA, an urgent brain CT with computed tomography angiography (CTA) of intra–extracranial vessels and whole-brain computed tomography perfusion (CTP) imaging were performed in the emergency department. The nonenhanced CT (NECT) scan (Fig. ) and CTA (Fig. ) were normal. CTP showed hypoperfusion in the left hemisphere with prolonged mean transit time (MTT) and time-to-peak (TTP), slightly increased cerebral blood volume (CBV), and relatively preserved cerebral blood flow (CBF) (Fig. -). A diagnosis of acute ischemic stroke was made. After excluding absolute contraindications for intravenous thrombolysis, 58.5 mg (0.9 mg/kg) rtPA was given at 12:30 a.m., immediately after the patient signed the informed consent. After 1 h of rtPA, his symptoms were alleviated, and the NIHSS score was decreased to 1, with slight asymmetry of the nasolabial sulcus. The patient was then admitted to the department of neurology for further investigations and treatment. Within 60 min after admission, the clinical neurological examination had completely normalized.
On the next day, the patient had no complaints of discomfort. The NIHSS score was 0. Cerebral magnetic resonance imaging (MRI) was performed, and no acute lesion was seen in the diffusion-weighted image (DWI) sequences (Fig. ). Doppler ultrasonography of carotidal and intracranial arteries showed no abnormality. Electrocardiogram, electroencephalogram (EEG) and chest CT scan were all normal. Echocardiography showed that the left and right heart chambers were within normal size and function(left ventricle ejection fraction 70%). His laboratory tests showed WBC count 2.2 × 109/L, hemoglobin 10.4 g/dL, platelets 210 × 1012/L, ESR 18 mm/h (normal 0–15.0), CRP 0.66 mg/L (normal 0–8.0), homocystein 10.4 umol/L (normal < 15.0), and mild impairment of liver function (ALT 132 U/L (normal 5–40), AST 106 U/L (normal 8–40), GGT 257 U/L (normal 11–50), ALP 127 U/L (normal 40–150)). Serologies showed the following: rapid plasma reagin, negative; antinuclear antibody and antineutrophil cytoplasmic antibody, negative; complement level including C3, C4 levels, normal; anticardiolipin immunoglobulin G(ACL-IgG), ACL-IgM, and ACL-IgA antibody levels, normal; β2 glycoprotein I immunoglobulin G (β2-GP1- IgG) and β2-GP1- IgM antibody levels, normal; high β2-GP I-IgA antibody level, 67.16 units/mL (normal 0–18). HIV enzyme-linked immunosorbent assay and Western blot confirmed HIV infection with CD4 cell count of 7 cells/uL; the CD4:CD8 T cell ratio was 0.04 (7/173). Hepatitis B virus surface antigen and hepatitis C antibody were unremarkable.
On the third day of admission, the patient received a lumbar puncture with pressure of 140 mmH2O. Cerebrospinal fluid (CSF) studies showed normal-range white cell and red cell counts but a high protein level at 1185 mg/L. The CSF glucose and chloride were in the normal range. CSF viral PCRs (including herpes simplex virus, varicella zoster, Epstein Barr, cytomegalovirus and JC virus), cryptococcal antigen, and bacterial and fungal cultures were all negative. CSF syphilis TRUST and TPPA tests were also negative. There was no meninges or brain parenchymal enhancement on his brain contrast-enhanced MRI (Fig. ).
The patient was diagnosed with aborted stroke and HIV infection. Oral aspirin 100 mg and atorvastatin calcium 20 mg daily were given. For further treatment, the patient was transferred to the HIV/AIDS ward on the fourth day of admission. On follow up 2 months later, he reported no similar symptoms.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [65.0, 'kg']}",105,99.75,110.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 65.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (65.0 kg - 20 kg) = 105.0 mL/hr.
Hence, the patient's fluid maintenance is 105.0 mL/hr."
5183,22,Maintenance Fluids Calculations,physical,decimal,pmc-7331840-1,Extracted,"An 8-month-old male infant weighing 7.7 kg was referred with the diagnosis of VT and LV dysfunction. The infant presented with a history of poor oral intake and breathing difficulty of 1-week duration. There was no history of fever and no clinical or laboratory evidence of systemic infection. He was treated initially with tablet diltiazem (1 mg/kg/dose eight hourly) and subsequently with amiodarone infusion (up to 15 mcg/kg/min) with no response. At the time of admission to our unit, the heart rate was 200/min, with low-volume pulses and mean blood pressure of 40 mmHg. There were palpable congestive hepatomegaly and LV S3 with a gallop. Chest X-ray showed a Cardio-Thoracic ratio of 0.65 and pulmonary venous congestion. Echocardiography revealed a severe LV systolic dysfunction (LV ejection fraction [EF]: 30%). Electrocardiography showed a ventricular rate of 200/min, relatively narrow QRS complexes with right bundle branch block (RBBB) morphology, right axis deviation, and Ventriculo-Atrial (V-A) Dissociation suggestive of fascicular VT []. A diagnosis of tachycardiomyopathy due to incessant fascicular VT was made. He was started on inotropic support and diuretics. Electrical cardioversion was tried multiple times with a dose of 2 J/kg without any success. Intravenous verapamil with a dose of 0.1–0.2 mg/kg followed by 5 mcg/kg/min and xylocard were tried without any response. In view of incessant VT unresponsive to drugs and cardioversion, radiofrequency ablation was planned. After taking informed consent from the parents, ablation was successfully performed with no further recurrence of VT. Infant improved symptomatically, and EF normalized after ablation and discharged in a stable condition. The child has not had a recurrence at 2 years of follow-up and is off medications.
The child was brought into the electrophysiology laboratory in incessant VT, with RBBB morphology, left superior, and relatively narrow QRS with VA dissociation []. The procedure was done under controlled general anesthesia. Vascular access was obtained through the right femoral vein and artery and the right internal jugular vein. Catheters were placed in the coronary sinus, His bundle region and single catheter in right ventricle (RV) & Right atrium (not shown in figure). Heparin bolus of 100u/kg was administered, and activated clotting time (ACT) was maintained consistently over 300 s with repetitive heparin boluses. By retrograde approach, a 5Fr mapping catheter (nonirrigated Biosense Webster) was introduced into the left ventricle []. Careful mapping of the posterior LV septum was done to identify the earliest Purkinje potential (PP). Earliest PP preceded QRS by 40 ms. This area was carefully mapped to identify pre-PP or diastolic potentials []. Concealed entrainment with a postpacing interval-tachycardia cycle length of <10 ms was demonstrated. The delivery of radiofrequency lesion of 55 watts at 55°C, almost immediately terminated tachycardia []. Lesions linearly were delivered both apically and basally. Postablation sinus rhythm was restored. Programmed electrical stimulation with single and double extrastimuli from RV and LV, and burst pacing from RV and LV did not induce tachycardia. The protocol was repeated with isoprenaline infusion without inducing VT. No further recurrence of VT occurred.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.7, 'kg']}",30.8,29.26,32.34,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.7 kg. Hence, the patient's maintenance fluid is 7.7 kg * 4 mL/kg/hr = 30.8 mL/hr.
Hence, the patient's fluid maintenance is 30.8 mL/hr."
5184,22,Maintenance Fluids Calculations,physical,decimal,pmc-8287740-1,Extracted,"A 23-year-old Asian female presented to rheumatology in February 2020 following GP referral with history of worsening pain and paraesthesia of the right upper limb since 2018. She was managing with simple analgesics and physiotherapy under care of musculoskeletal and neurology team. Her symptoms were initially intermittent but became persistent from August 2019 and had progressed to involve the neck, upper-back and left arm. The severity of pain was disrupting her daily activities and sleep.
She was a non-smoker and non-drinker. There was no significant past medical history, except migraine.
She had a family history of Type 2 diabetes mellitus, hypertension and cancer, including thyroid and prostate cancer.
She was born in the UK to parents of Indian origin and had received the Bacillus Calmette-Guérin (BCG) vaccine at birth. She travelled to India every other year to visit relatives. She had no known contacts of TB.
Her weight was 54 kg, and body mass index (BMI) was 21. On examination, there was slightly reduced power noted in the right upper limb and myofascial tenderness over the cervical and thoracic spine, but range of motion and reflexes remained fully intact.
Initial blood tests demonstrated elevated white cell count (WCC) of 14.8 × 109/L (normal range (NR) 4–11 × 109/L) with neutrophilia (12.0 × 109/L; NR 2–7.5 × 109/L), elevated C-reactive protein(CRP) (31.4 mg/L; NR < 5 mg/L), elevated total protein (89 g/L; NR 60–83 g/L) with hypergammaglobulinaemia (49 g/L; NR 7–16 g/L), alongside low vitamin D (63.4 nmol/L; NR > 70nmol/L). Auto-antibody screen including anti-nuclear antibody, rheumatoid factor and anti-citrullinated protein antibodies were negative.
Previous electromyography and nerve conduction studies in February 2019 reported no evidence of nerve lesions and no myopathic features at the time. In December 2019, neurologist arranged magnetic resonance imaging (MRI) of cervical spine, thoracic spine and brachial plexus which was initially reported as normal with respect to the spine and brachial plexus (Fig. ). However, on further review of MRI at rheumatology multi-disciplinary team (MDT) meeting, an anterior mediastinal mass and lung shadowing was noted. Subsequent contrast-enhanced computed tomography (CT) of neck, thorax, abdomen and pelvis (Fig. ) demonstrated a cystic anterior mediastinal mass measuring 3.3 × 3.8 cm thought to be a necrotic node which is typical of TB. There was evidence of consolidation in the right upper lobe with ‘tree-in-bud’ appearance. ‘Tree-in-bud’ refers to involvement of the smaller airways—a finding commonly seen in TB. The case was referred to chest MDT and was diagnosed as likely pulmonary TB. However, in view of the clinical-radiological correlation, she did not have symptoms of cough, fever or chest pain at this time.
Although blood tests for enzyme-linked immune absorbent spot assay (ELISpot®) were negative for TB and bronchoalveolar lavage (BAL) smear was negative for acid fast bacilli (AFB), she was treated empirically with the quadruple-antitubercular treatment Voractive® (combined tablet of rifampicin, isoniazid, pyrazinamide and ethambutol) with 10 mg pyridoxine. The plan was to continue treatment and follow-up with repeat imaging in 2 months.
Within 2 weeks of commencing treatment, the woman developed continuous cough unable to sleep lying flat. She was advised to take simple cough linctus and continue with the treatment. However, her cough worsened, with progressive retrosternal discomfort.
Her care was transferred to a hospital closer to her home. The four-drug regimen was continued for 2 months followed by 1 month of Rifinah® (rifampicin and isoniazid) with pyridoxine 10 mg. Her cough and chest discomfort did not improve. Repeat blood tests performed in April and May 2020 showed haemoglobin fell from 117 g/L to 101 g/L, WCC was persistently elevated at 25.1 × 109/L and 20.2 × 109/L with raised neutrophils of 22.49 × 109/L and 19.62 × 109/L respectively. Follow-up chest X-rays (CXR) and repeat CT scan demonstrated new cavitating lesions in the right lung with further enlargement of the mediastinal mass (Fig. ). Sputum samples and repeat BAL sent for microscopy, culture and sensitivities (MC&S) and polymerase chain reaction (PCR) with GeneXpert® testing again yielded negative results for TB. A CT-guided needle biopsy of the lung and fluid aspiration of the mediastinal mass was performed. This yielded necrotic tissue on histology with negative AFB smear, negative GeneXpert® and microbiology. Following this, a whole-body fluorodeoxyglucose—positron emission tomography (FDG-PET)-CT scan was performed demonstrating metabolically active necrotic lesions in the mediastinum and lung parenchyma (Fig. A and B).
Histological analysis of mediastinotomy-derived lung biopsies demonstrated samples contained a nodular infiltrate of lymphoid cells admixed with bands of sclerotic tissue. The lymphoid tissue was polymorphous composed of small mature lymphoid cells admixed with histiocytes, eosinophils, neutrophils and some larger cells showing prominent nucleoli, binucleate forms and smudge cells. On immunohistochemistry, the large atypical cells were positive for CD30, CD15, MUM1, PAX5 and p53. They were negative for CD45, CD20, CD79a and CD3. The imaging and histological findings confirmed a diagnosis of Stage IVA classical Hodgkin’s lymphoma (nodular sclerosing subtype) in June 2020.
TB treatment was discontinued and the patient was urgently referred to the haemato-oncology team and commenced on the escalated BEACOP-DAC regimen (bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, prednisolone and dacarbazine, with granulocyte colony stimulating factor). As time was of the essence, the option of cryopreservation of ova prior commencing chemotherapy was not possible. However, gonadotrophin releasing hormone (GnRH) analogue was offered. The FDG-PET-CT scan following the first two cycles demonstrated good response to chemotherapy (Deauville Score 3). Therefore, only two more cycles of escalated BEACOP-DAC were given. The post-chemotherapy FDG-PET-CT scan (Fig. C and D) showed resolution of disease, so no further treatment was indicated. At the time of writing, the patient was well and plan was to follow-up in haemato-oncology clinic.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [54.0, 'kg']}",94,89.3,98.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 54.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (54.0 kg - 20 kg) = 94.0 mL/hr.
Hence, the patient's fluid maintenance is 94.0 mL/hr."
5185,22,Maintenance Fluids Calculations,physical,decimal,pmc-7825155-1,Extracted,"A Korean male infant with a weight of 2980 g (91st percentile) was born to a 37-year-old woman (gravida 2 and para 2) at 34+ 5 weeks’ gestation via normal spontaneous vaginal delivery. Apgar scores were 8 and 9 at 1 and 5 min after birth, respectively. The mother and other family members had no known allergies and no other particular medical history including the maternal history of diabetes, hypertension, dyslipidemia, and neurologic disease, with the mother’s consumption of a small amount of cow’s milk only as food additives during pregnancy. The pregnancy was not complicated by any abnormalities encompassing maternal fever, gestational diabetes, preeclampsia, premature or prolonged rupture of membranes, and placental abruption. The placental examination was unremarkable. The infant’s general condition was good and oral intake commenced with a total of 60 ml of preterm formula milk. Four hours after initial feeding, three episodes of non-projectile, non-bilious emesis developed with approximately 5 ml milky vomitus on each occasion, followed by hematochezia 5 h later. Table shows the flow of the infant’s laboratory and clinical data. Initial laboratory evaluation demonstrated a mild leukocytosis (white blood cells 11,400/μL) and eosinophilia (eosinophil fraction 14% and eosinophils 1530/μL), raised D-dimer 1718.3 vs. control < 500 ng/mL DDU, and mild conjugated hyperbilirubinemia (total bilirubin 1.5 mg/dL with the direct fraction 40%), with the other following data (hemoglobin 13.0 g/dL, hematocrit 37.7%, platelets 274,000/μL, C-reactive protein 0.04 mg/dL, prothrombin time 13.4 vs. 10.1–12.6 s with the international normalized ratio 1.19 vs. 0.93–1.13, partial thromboplastin time 42.8 vs. 23.6–31.1 s, antithrombin III 43%, and fibrinogen 256 vs. 180–350 mg/dL). Serum total immunoglobulin E (IgE) was 0.1 IU/ml (normal values < 5.0) and specific IgEs to cow’s milk proteins (CMPs) were negative. The Apt test for fresh blood in the stools did not change color and fecal occult blood was positive. A chest-abdomen plain radiograph showed a normal bowel gas pattern without other abnormalities. Oral feeds were discontinued from postnatal day 1. Total parenteral nutrition was instituted on day 2 and maintained until day 9. The stools mixed with macroscopic bleeding more than in the form of spots persisted during the first 3 days of life. From day 5, oral feedings were reintroduced with breast milk without maternal diet modification and/or casein hydrolyzed milk, which were tolerable without reactions including gastrointestinal symptoms and metabolic acidosis. On day 6, abdominal ultrasonography revealed a non-obstructive thrombus within the umbilico-portal confluence of the left portal vein as a hypoechoic tubular structure (Fig. a and b). On day 19, the peak eosinophil count of 3790/μL was observed with a low serum 25-hydroxyvitamin D 16.1 ng/mL (insufficiency < 30 and deficiency < 10). On day 75, the eosinophil count decreased to 590/μL and a supervised oral challenge to cow’s milk was performed. Feeding intolerance with vomiting and blood-tinged stools was noted and the feeding was changed back to the casein-hydrolyzed formula. At 6 months of age, oral re-challenge to regular cow’s milk feeding was attempted and no reaction was observed. The sonographic signal of the intraluminal thrombus gradually decreased in size and became heterogeneously hyperechoic over time (Fig. ). At 1 year of age of the last follow-up ultrasonography, the thrombus completely resolved. The infant showed good weight gain with well-tolerated formula feeds.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2980.0, 'g']}",11.92,11.324,12.516,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2980.0 g so this converts to 2980.0 lbs * kg/1000 g = 2.98 kg. Hence, the patient's maintenance fluid is 2.98 kg * 4 mL/kg/hr = 11.92 mL/hr.
Hence, the patient's fluid maintenance is 11.92 mL/hr."
5186,22,Maintenance Fluids Calculations,physical,decimal,usmle-7084,Extracted,"A 47-year-old woman with a history of recent gastric bypass surgery presents for a follow-up visit. 8 months ago, she underwent gastric bypass surgery because she was struggling with maintaining her BMI below 42 kg/m². She previously weighed 120 kg (265 lb), and now she weighs 74.8 kg (165 lb). She says that she has low energy and is easily fatigued. These symptoms have become progressively worse over the past month. She is struggling to get through the day and sometimes has to nap before she can continue with her work. She has also recently noticed that she gets cramps in her legs, especially after a long day. The patient is afebrile and vital signs are within normal limits. Physical examination is unremarkable. Her hemoglobin is 9.5 mg/dL with an MCV of 75 fl. Her peripheral smear is shown in the exhibit.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [74.8, 'kg']}",114.8,109.06,120.54,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 74.8 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (74.8 kg - 20 kg) = 114.8 mL/hr.
Hence, the patient's fluid maintenance is 114.8 mL/hr."
5187,22,Maintenance Fluids Calculations,physical,decimal,pmc-6449622-1,Extracted,"A 13-year-old male patient presented with complaints of new-onset polydipsia, excessive urination, and weight loss. The patient stated he had lost 7 kg over a period of 2 months. His past medical history included neurosensory hearing loss from birth and patent ductus arteriosus that was discovered at three months of age in the Pediatric Cardiology Department. He had no response to voice warnings at 3 months of age, and his neurosensory hearing loss was diagnosed with an auditory brainstem evoked responses test. In addition, the patient was followed by the Child and Adolescent Psychiatry Department due to behavioral problems and learning disabilities; he had been diagnosed with autistic spectrum disorder. There was no kinship between his parents. The patient's mother had a fever and a red rash on her face during the second trimester of pregnancy, although she was not diagnosed with rubella infection at that time.
On physical examination, the patient's weight was 42.7 kg (25th–50th percentile), height was 153.2 cm (25th–50th percentile), and his head circumference was 46 cm (<3rd percentile). A 2/6 cardiac murmur and hearing aid were noted. Laboratory examinations revealed blood glucose was 619 mg/dL, urine ketone was +3, blood gas showed metabolic acidosis (pH, 6.92; HCO3, 4 mEq/L; PaCO2, 24 mmHg), insulin was 4.1 IU/mL (range, 2–18 IU/mL), and serum C-peptide level was 1.23 ng/mL (range, 1.1–4.4 ng/mL). The patient's glycosylated hemoglobin value was 15.9%, anti-insulin antibody was 0.78 U/mL (range, 0–0.5U), anti-GAD was 22.8 U/mL (<1U/mL), and the islet cell antibody was positive. Orbital magnetic resonance imaging demonstrated no optic atrophy and normal optic nerve thickness, so Wolfram syndrome was excluded. In addition, genetic analysis for Wolfram's syndrome was normal.
The patient was diagnosed with immune-mediated type I DM, and intravenous fluid and insulin therapy were started according to the degree of dehydration. After the patient's metabolic acidity was corrected and blood glucose regulation was achieved, his medication was switched to subcutaneous insulin therapy 1.2 units/kg/day. Considering the patient’s patent ductus arteriosus, microcephaly, and neurosensory hearing loss, his immune-mediated type 1 diabetes was thought to be associated with a congenital rubella infection following his mother’s febrile rash illness during pregnancy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [42.7, 'kg']}",82.7,78.565,86.835,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 42.7 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (42.7 kg - 20 kg) = 82.7 mL/hr.
Hence, the patient's fluid maintenance is 82.7 mL/hr."
5188,22,Maintenance Fluids Calculations,physical,decimal,pmc-5412170-1,Extracted,"A 6-day-old girl presented with vomiting, lethargy, and severe dehydration. Physical examination showed an ill appearing infant with pale skin, poor perfusion, and sunken eyes. She was born full-term with birth weight 3.0 kg to consanguineous parents of Pakistani origin, with pregnancy complicated only by gestational diabetes requiring insulin. She had normal genitalia without clitoromegaly, labial fusion, or hyperpigmentation and no palpable abdominal mass. Laboratory evaluation showed hyponatremia Na+ 124 mEq/L, hyperkalemia K+ 10 mEq/L, metabolic acidosis HCO3− 10 mEq/L, urine Na+ 150 mEq/L, elevated serum aldosterone 8.97 nmol/L (normal range 0–6 nmol/L for term infants), plasma renin activity 13.39 ng/mL/hr (normal range 2–35 ng/mL/hr for infants 1–7 days, though some labs use reference range 1.4–7.8 ng/mL/hr for this age), normal serum cortisol 634.8 nmol/L (normal >500 nmol/L during acute stress), and normal 17-hydroxyprogesterone 0.7 nmol/L (normal range 0.2–2.3 nmol/L for term infants). A sweat test showed elevated sweat Cl− 34 mEq/L (normal range 0–29 mEq/L for infants 0–4 months). She had a normal renal ultrasound.
She required two normal saline boluses, oxygen, and several doses of Kayexalate and NaHCO3 as well as an insulin drip and glucose to correct electrolyte abnormalities. Sodium and potassium normalized within 2 days. She subsequently developed right lower lobe pneumonia requiring antibiotics and intubation, as well as Klebsiella and Enterococcus sepsis from her femoral line. She was discharged from the hospital after 4 weeks but then developed ventricular tachycardia requiring cardioversion due to hyperkalemia with K+ >9 mEq/L. Potassium levels normalized after increasing Kayexalate. She was then maintained on sodium supplementation of 49 mEq/kg/day as well as Kayexalate 3 grams every 8 hours.
Full sequencing of the SCNN1A gene that encodes the alpha subunit of ENaC was performed at Johns Hopkins University. Reported test methods were DNA extraction from whole blood, amplification of the coding sequence of SCNN1G by polymerase chain reaction in 14 segments, cycle sequencing of each segment in the forward and reverse directions, and analysis of each sequence by capillary electrophoresis. This showed a known mutation Nt1685C->T causing replacement of leucine for serine at position 562 in exon 13, which forms the 2nd transmembrane subunit of the alpha chain of ENaC. This mutation was previously reported in a patient with systemic PHA type I [] and confirmed the diagnosis in our patient. The testing was unable to determine if the mutation was present in two copies (homozygous) or one copy with a deletion of the 2nd allele (hemizygous). Sequencing of parental genes was not done.
The patient began developing the characteristic pulmonary symptoms at age of 2 years with recurrent pneumonia related to chronic bronchorrhea requiring intermittent treatment with Atrovent (Ipratropium). She had 7 episodes of pneumonia between ages of 2 and 3 years. These symptoms improved with age and frequency of infections decreased. Repeat sweat test at age of 3 years showed elevated sweat Cl− 133 mEq/L (normal range 0–39 mEq/L for patients >4 months). At her last follow-up at 5 and 5/12 years of age, she was receiving Kayexalate, NaCl, and NaHCO3 for a total dose of 23 mEq/kg/day of sodium. She has not had any recurrent salt wasting crises. Her height was 103.8 cm (−1.5 SDS), weight 13.4 kg (−3.1 SDS), and BMI 12.4 kg/m2 (−3.2 SDS). Labs at that time showed normal electrolytes with Na+ 135 mEq/L and K+ 4.4 mEq/L.
The patient had 2 younger siblings born to the same mother and father. The first sibling was clinically unaffected, and genetic testing showed that he was a carrier of the mutation in the SCNN1A gene. The second sibling developed salt wasting with Na+ 131 mEq/L, K+ 7.1 mEq/L, and HCO3− 13 mEq/L at 4 days of life. Physical exam showed a dusky appearing newborn with poor tone. She was started on Kayexalate (3 grams every 8 hours) in addition to NaCl and NaHCO3 supplements at a total dose of 60 mEq/kg/day of sodium. Genetic testing revealed the same SCNN1A mutation as her sister described above, confirming the diagnosis of systemic PHA type I. Her course was uncomplicated and she was discharged from the NICU at 10 days of life. Sodium doses were titrated based on serum levels with eventual decrease to 26 mEq/kg/day of sodium by 21 days of life.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [13.4, 'kg']}",46.8,44.46,49.14,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 13.4 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.4 kg - 10 kg) = 46.8 mL/hr.
Hence, the patient's fluid maintenance is 46.8 mL/hr."
5189,22,Maintenance Fluids Calculations,physical,decimal,pmc-5075604-1,Extracted,"After HIV infection was diagnosed, an 8-month-old boy with worsening pneumonia and respiratory distress was transferred to the University Hospital for Infectious Diseases, Zagreb, Croatia (UHID), on November 4, 2011. The child had previously been hospitalized two times in his local hospital for diarrhoea and pneumonia. His mother had not been tested for HIV while pregnant. There was no family history of tuberculosis (TB), but immunization with Statens Serum Institut (Danish strain) BCG vaccine at birth had left a nonhealing ulcer on the deltoid region of the left arm.
On presentation, the infant was receiving mechanical ventilation and was overall in poor condition. He weighed 7.4 kg and was 42.5 cm long. On physical examination he had tachycardia, hepatosplenomegaly, and oedema of the lower extremities. There was also an ulcer at the site of BCG immunization with a palpable ipsilateral 1 cm axillary lymph node. His chest X-ray showed diffuse bilateral interstitial infiltrates with a slightly enlarged cardiac silhouette.
Results of laboratory studies on admission showed an erythrocyte sedimentation rate of 5 mm per first hour, serum procalcitonin level of 0.844 µg/L, hemoglobin concentration of 130 g/L, leukocyte count of 10.4 × 109/L, and platelet count of 51 × 109/L. His CD4 cell count was 5.9% (24 cells per µL) and his plasma HIV-1 RNA was 4.96 million copies/mL. An overview of the major clinical and laboratory findings is presented on .
He was immediately given high-dose co-trimoxazole and steroids for presumed Pneumocystis jirovecii pneumonia as well as piperacillin-tazobactam for probable hospital acquired infection. Anti-TB therapy consisting of isoniazid, ethambutol, and rifampicin, which had been started the day before transfer to our hospital, was continued. On the third hospital day at UHID he developed signs of hepatitis; his serum bilirubin climbed to 116.5 µmol/L (conjugated bilirubin 66.9 µmol/L), his aspartate aminotransferase (AST) was 1952 IU/L, his alanine aminotransferase (ALT) was 365 IU/L, and his lactate dehydrogenase level was 2948 IU/L. His prothrombin time was prolonged (international normalized ratio value 2.7). All TB medications were stopped and liver function tests gradually returned to normal over the next three weeks.
Tracheal aspirate taken on the day of admission was positive for Pneumocystis jirovecii DNA on polymerase chain reaction and also grew Pseudomonas aeruginosa on culture. Antiretroviral therapy (ART) was started two weeks after admission to UHID with a combination of zidovudine, lamivudine, and lopinavir/ritonavir. There was no HIV drug resistance found in the blood sample obtained prior to initiation of ART. Steroids were stopped after 21 days of therapy and at that point co-trimoxazole was switched to a prophylactic oral dose. The breathing had significantly improved so he was weaned from mechanical ventilation 4 weeks after admission to our hospital. We performed an interferon-gamma release assay (QuantiFERON®); the result was negative. In light of the clinical improvement and prior signs of severe, presumably toxic hepatitis, the decision was made not to give TB treatment.
Two months after admission an abdominal ultrasound revealed multiple small (up to 8 mm) hypoechogenic splenic lesions. Two weeks later signs of BCG infection were again present with prominent ipsilateral axillary lymph node enlargement. An attempt was made to restart anti-TB medications. However, an urticarial rash developed after isoniazid was started, so the drug was discontinued; the patient was treated with amikacin for one week and clarithromycin, ciprofloxacin, and prednisolone for 4 weeks. This treatment regimen led to regression in lymph node size. At this time, zidovudine was replaced by abacavir due to anaemia ().
In the fourth month of care, the child developed multiple skin lesions on his head and limbs that started as erythematous papules and turned into subcutaneous abscesses. A repeated QuantiFERON test was now positive. Mycobacterial cultures from the disseminated skin lesions were taken and subsequently grew M. bovis. At this point we learned that mycobacterial cultures from the site of BCG application (left deltoid muscle) and tracheal aspirate were taken at the local hospital about one week prior to transfer to our hospital. These cultures also grew M. bovis, but the staff at UHID was not aware of the positive results. Initially the samples were cultured on solid (Loewenstein and Stonebrink) and liquid MGIT (Mycobacteria Growth Indicator Tube, the BD BACTEC™ MGIT™ 960 System) media. The identification of the cultured M. bovis BCG strain was done using the commercially available line probe assay, GenoType MTBC Kit (Hain Lifescience, Nehren, Germany).
Drugs with antimycobacterial activity (amikacin, ciprofloxacin, and azithromycin) were reintroduced (). Multiple cystic bone lesions were noted in the skull and in the bones of both arms, both hands, and both legs (). As fever and skin lesions persisted, ethambutol, linezolid (10–12 mg/kg orally three times per day), and isoniazid were sequentially added to his anti-TB regimen (). This time neither rash nor toxic hepatitis developed. Because we wanted to give rifampicin again and rifabutin was not available at that time, we replaced lopinavir/ritonavir with nevirapine. However, two weeks later there was an increase in serum liver enzymes (AST 113 IU/L and ALT 122 IU/L), so nevirapine was stopped and standard dose lopinavir/ritonavir was reintroduced. Amikacin, azithromycin, ciprofloxacin, and ethambutol were discontinued as shown in . After a 10-month hospital stay the patient was discharged on linezolid, isoniazid, abacavir, lamivudine, and lopinavir/ritonavir.
However, fever reappeared, new skin lesions were still developing, and bone lesions were growing. A bone biopsy of the right tibia was done on 12th month of care at UHID (). Histopathological findings revealed inflammatory tissue with microscopic characteristics of granulomata and foci of necrosis, which grew acid-fast bacilli identified as M. bovis. At this point ethambutol and rifabutin (dosed at 5 mg/kg three times per week) were added to the TB regimen, and after six weeks the frequency of rifabutin dosing was increased to daily administration (once daily 7 days per week) (). After rifabutin was given dosed at 5 mg/kg/day every day the patient remained without fever. The child's complete blood count was monitored; after rifabutin was given 3 times weekly his lowest observed leukocyte count was 4.1 × 109/L with an absolute neutrophil count (ANC) of 1.3 × 109/L (1300 per µL) on the 18th day of administration. After rifabutin was given daily, the lowest leukocyte count was observed after one month of therapy (1.9 × 109/L with an ANC of 0.7 × 109/L (700 per µL)). However, this neutropenia was transient; after six days the ANC was 3300 per µL without any intervention. Since the response to ART was not optimal (), a resistance test was done which showed reverse transcriptase mutations associated with nevirapine (Y181C) and lamivudine (M184V) resistance (16th month of care). To optimize the virological response to ART, abacavir was replaced by zidovudine and raltegravir granules were added to the antiretroviral regimen. After 16 months in care a skin lesion and a lymph node aspirate failed to grow mycobacteria for the first time, and one month later the child became consistently afebrile. At this point ethambutol treatment had reached 6 months, and it was discontinued. Two months later linezolid was stopped after a total of 13 months of therapy. At follow-up 12 months from the first negative skin lesion culture the child was clinically stable and radiographs of the lower limb showed signs of bone healing. Anti-TB therapy was stopped at this time (). The child reached an undetectable HIV-1 RNA viral load measured by the Abbott assay (detection limit 40 copies/mL) only after 36 months of ART on a regimen of tenofovir, lamivudine, lopinavir/ritonavir, and raltegravir.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.4, 'kg']}",29.6,28.12,31.08,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.4 kg. Hence, the patient's maintenance fluid is 7.4 kg * 4 mL/kg/hr = 29.6 mL/hr.
Hence, the patient's fluid maintenance is 29.6 mL/hr."
5190,22,Maintenance Fluids Calculations,physical,decimal,pmc-8531789-1,Extracted,"We report a 23-year-old African American male with a medical history of pediatric DDRT secondary to left-sided dysplastic kidney and right-sided obstructive uropathy. He presented to the emergency department with a one-week history of decreasing urine output, increased shortness of breath, generalized weakness, and nausea. He initially received his DDKT in 2010, which has been complicated by multiple episodes of both acute T cell-mediated and acute antibody-mediated rejection. The patient admitted to a two-month history of immunosuppressive medication nonadherence with tacrolimus, mycophenolate, and prednisone.
Physical examination revealed a young male, in no distress, weighing 142 pounds. He had a blood pressure of 153/102 mmHg and a heart rate of 77 beats/min. Exam findings are as follows: pale conjunctiva, lungs clear to auscultation, regular heart rate and rhythm, active bowel sounds, no abdominal tenderness, and no focal neurological deficit. Admission labs included a serum creatinine of 64.6 mg/dL (0.67–1.17 mg/dL) with a blood urea nitrogen (BUN) of 212 mg/dL (6–20 mg/dL), which increased to a serum creatinine of 73.8 mg/dL and BUN of 244 mg/dL prior to initiation of emergent dialysis. Serum chemistry included sodium 137 mmol/L (136–145 mmol/L), potassium 6.0 mmol/L (3.5–5.1 mmol/L), chloride 98 mmol/L (98–107 mmol/L), total carbon dioxide 7 mmol/L (22–29 mmol/L), glucose 68 mg/dL (74–106 mg/dL), and phosphorus 14.7 mg/dL (2.7–4.5 mg/dL).
The patient was initiated on emergent dialysis via a temporary dialysis catheter. Dialysis was complicated by new onset of seizures, initially thought to be secondary to dialysis disequilibrium syndrome. An electroencephalogram (EEG) was performed showing right temporal spikes epileptiform discharges with intermittent slow waves lateralized to the right hemisphere. Patient was thought to have epilepsy with initial seizure exacerbation secondary to severe metabolic derangements in setting of acute renal failure and severe azotemia. He was initiated on daily levetiracetam with resolution of seizures.
Patient received continuous renal replacement therapy (CRRT) while in the intensive care unit. After stabilization of his acute medical issues, a tunneled dialysis catheter was placed in his right internal jugular vein prior to discharge. Ultimately, the patient was diagnosed with renal allograft failure secondary to medication nonadherence and was discharged home on intermittent hemodialysis with improvement in serum creatinine to 23.8 mg/dL and BUN of 76 mg/dL at time of discharge, after completion of four hemodialysis sessions.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [142.0, 'lbs']}",104.41006,99.18956,109.63056,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 142.0 lbs so this converts to 142.0 lbs * 0.453592 kg/lbs = 64.41006 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (64.41006 kg - 20 kg) = 104.41006 mL/hr.
Hence, the patient's fluid maintenance is 104.41006 mL/hr."
5191,22,Maintenance Fluids Calculations,physical,decimal,pmc-4209027-2,Extracted,"A 75-year-old, 71 kg, 152 cm woman underwent left knee arthroplasty. General anesthesia was induced with 130 mg propofol, 0.2 μg/kg/min remifentanil, and 40 mg rocuronium. Following tracheal intubation, anesthesia was maintained with sevoflurane and remifentanil. Ten minutes after induction of general anesthesia, her BP and HR decreased to 70/50 mmHg and 50 bpm, respectively. Incremental doses of ephedrine (8 mg × 2), 0.2 mg phenylephrine and 0.5 mg atropine were administered intravenously. Both BP and HR responded well to these treatments and increased to 150/70 mm Hg and 75 bpm, respectively. Twenty minutes before the end of surgery, 50 mg flurbiprofen axetil was administered. The total operation time was 99 minutes. Before extubation, sugammadex 2.8 mg/kg was administered. Three minutes after the injection of sugammadex, her systolic BP fell to 40/undetectable mm Hg, together with thoracic erythema, with no response to 0.2 mg phenylephrine injection. No respiratory symptoms, such as wheezing and high airway resistance, were observed. Suspecting a possible allergic reaction to sugammadex, we intravenously administered 0.5 mg adrenaline, 5 mg chlorpheniramine maleate, 50 mg ranitidine hydrochloride, and 300 mg hydrocortisone. Her BP gradually increased to 160/80 mmHg after these treatments. The patient was transferred to the intensive care unit (ICU) without extubation. Her trachea was extubated 15 hours later in the ICU when she was fully awake and hemodynamically stable. She was transferred out of the ICU the following morning. Four weeks after the operation, an intradermal allergy test with dilutions of propofol, rocuronium, flurbiprofen axetil, and sugammadex was performed. A 1:1000 dilution of all the drugs showed a negative reaction. However, a 1:100 dilution of sugammadex resulted in a positive reaction (Table ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [71.0, 'kg']}",111,105.45,116.55,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 71.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (71.0 kg - 20 kg) = 111.0 mL/hr.
Hence, the patient's fluid maintenance is 111.0 mL/hr."
5192,22,Maintenance Fluids Calculations,physical,decimal,pmc-7769771-1,Extracted,"A 30-month-old 6.4 kg 71 cm boy with autosomal recessive polycystic kidney disease was maintained on dialysis since the second month of his life. Significant developmental deterioration was observed during the previous 12 months of his life. The patient lost his walking ability, needed intermittent mechanical ventilation that led to a tracheostomy 6 months prior to transplantation. One week prior to transplantation anti-A isoagglutinin titer was 1:16, anti-B isoagglutinin titer was 1:2. Extracorporeal isoagglutinin removal was not performed. Immunosuppression induction was alemtuzumab and eculizumab; maintenance immunosuppression was tacrolimus and mycophenolate mofetil (MMF) in regimens previously described in publications (, ). We performed a bilateral nephrectomy and a right kidney transplant from his ABOi 63-year-old grandmother, AB to O.
Patient suffered a cardiac arrest due to hyperkalemia (12.9 mmol/l) during the advanced stage of surgery prior to graft reperfusion. As the standard CPR was ineffective, the child was started on ECMO with the right common carotid artery and jugular vein cannulation. Centrifugal pump (Deltastream DP3, oxygenator Hilite 2400 LT, Medos Medizintechnik, Germany), rotation of 4,500–6,000/min allowed blood flow of 1.5–2.5 l/min/m2. After 27 min of ECMO sinus rhythm recovered. Vascular anastomoses were completed, and graft reperfusion started while on ECMO. The abdomen was left open to reduce abdominal pressure and restore venous return. Upon ICU admission the ECMO flow was suboptimal (1.4 L/min/m2), inotrope support included high doses of dopamine (15 mcg/kg/min) and epinephrine (0.6 mcg/kg/min). The blood pressure was 95/78 with a mean arterial pressure of 83 mmHg, heart rate was 135/min. The child had a low cardiac index (1.35–1.5 L/min/m2) and severe coagulopathy (INR 2.52, aPTT 104.7 s, fibrinogen 0.6 g/L); there was bleeding from the cannulas exit sites and the surgical wound.
Despite severe IRI, we maintained adequate brain and kidney graft perfusion (assessed by near infrared spectroscopy, ). Severe IRI resulted in elevated ALT, AST, LDH, and CK levels, blood counts revealed thrombocytopenia 29 × 109/L and low hemoglobin 76 g/L. Defibrillation was required twice during the first 24 h post-op for ventricular tachycardia. It took us 15 h to achieve adequate ECMO flow and stable hemodynamics with fluid loading, vasopressor infusions, blood components transfusion, and other such methods.
Plasma exchange (PE) was started as soon as hemodynamics were stabilized. The purpose was to prevent thrombocytopenia—associated multiorgan failure (TAMOF) and to decrease ALT, AST, LDH, and CK levels. PE was performed according to the institutional protocol: two volumes 16 h after the ECMO start, and one volume 40 h since the ECMO initiation. To keep up the immunosuppression we infused additional 300 mg of eculizumab after each PE session. CRRT in CVVHD mode (Fresenius Medical Care, hemofilter Ultraflux AVpaed) was started 18 h after the ECMO initiation. The CRRT circuit was pre-filled with erythrocytes and crystalloids—this helped to reduce additional eculizumab dosages as plasma transfusions were not needed between extracorporeal detoxication sessions. We used a restrictive transfusion strategy in this clinical case with goal Hb level 70–90 g/L and used transfusion for extracorporeal circuit and the detoxication devices volume compensation only.
The therapeutic effect of PE was insufficient (a slight decrease in ALT, LDH, rise of AST, CK, CRP, PCT, and vasopressor requirement) and blood purification with CytoSorb (Cytosorbents, USA) was initiated on POD 2. The goal was to stabilize hemodynamics, reduce vasopressor requirement and eliminate high concentrations of inflammatory mediators and ECMO-induced free hemoglobin. CytoSorb was installed into the CRRT circuit before the hemofilter. The CRRT access line was connected to the ECMO venous line and the return flow was through the CRRT venous line to the oxygenator bubble trap. The blood flow rate for CytoSorb was 80 ml/min; the procedure duration was 21 h (): for 12 h on POD2 and 9 h on POD3.
While the CytoSorb therapy successfully suppressed inflammation (measured by CRP and PCT decrease), but the increased inotropic requirements suggested uncontrolled infection (later identified as abdominal translocation of polyresistant Klebsiella Pneumoniae, discovered in feces). The suspected infection was treated with antibiotic regimen escalation, Colistin was added to Tienam/Linezolid and three sessions of lipopolysaccharides adsorption with the PMX-20R column (Toray, Japan) to avoid lipopolisaccharides endotoxic action () on POD 3, POD 4 and POD 10 (as PCT level rose again 3 days after the abdomen closure) (). The PMX-20R column was installed into the circuit pre-hemofilter in the same way as described above. The blood flow rate was 100 ml/min. The procedure duration was 8 h.
The use of these extracorporeal therapies and appropriate antibiotic regime controlled the infection. The hemodynamics stabilized quickly and inotrope index decreased from 165 to 10 within 2 days, ECMO could be discontinued on POD 6, decannulation was uncomplicated. We closed the abdomen on POD 7, diuresis restored on POD 8. CRRT could be discontinued on POD 15, ventilation could be ceased on POD 60.
The total ICU stay was 92 days, the patient was discharged from hospital on POD 116 with a moderate neurological deficit and a stable graft function (creatinine 51 mcmol/l, proteinuria 9 mg/l). In follow-up observation (1 year after surgery) the kidney graft function remained stable all this time: creatinine level 54 mcmol/l, proteinuria 8 mg/days. Despite much secondary damage to the kidney graft it functioned well on standard immunosuppression: tacrolimus 0.5 mg × 3 times/day to reach blood concentrations of 3–4 ng/ml, MMF 125 mg × 2 times daily.
Twelve months after surgery the neurological improvement was evident, though pre-transplant co-morbidities hindered the recovery (osteoporosis prevented walking, tracheostomy complicated speech). The patient could sit, monitor the surroundings, actively used a spoon, entertained toys and examined pictures in children books. He maturely showed emotions, recognized and differentiated his father and mother and related negatively to staff.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.4, 'kg']}",25.6,24.32,26.88,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.4 kg. Hence, the patient's maintenance fluid is 6.4 kg * 4 mL/kg/hr = 25.6 mL/hr.
Hence, the patient's fluid maintenance is 25.6 mL/hr."
5193,22,Maintenance Fluids Calculations,physical,decimal,pmc-4091002-1,Extracted,"A 32-year-old male patient, weighing 86 kg (body mass index 30 kg/m2) diagnosed as a case of bipolar disorder 5 months ago was started on lithium 400 mg daily initially. Even with an incremental dose of lithium over 2 months, he had not improved. Therefore, olanzapine (Oleanz®, SUN Pharmaceutical Industries Ltd., Mumbai, India) 5 mg twice daily was added to his regimen. He had no other co-morbidities and no previous medication history. He was non-alcoholic and non-smoker. He was also complaining of weight gain. After 2 months of starting olanzapine, he developed nausea, vomiting, and severe epigastric pain without any history of haematemesis, melaena and jaundice. There was no previous history of pancreatitis and gall stone disease. Family history for diabetes was negative. On examination, he had a heart rate of 105-115/min with blood pressure 110/56 mm Hg and respiratory rate of 24-28/min and was febrile. Abdominal examination demonstrated epigastric tenderness with guarding including normal liver dullness on percussion and absent bowel sound. Ultrasonography (USG) showed bulky pancreas with pancreatic oedema with no peripancreatic collection. Upper gastrointestinal (GI) endoscopy showed no abnormality. His pain was increasing in intensity and referred to back. On the 10th day of pain abdomen, he developed breathlessness and admitted to intensive care unit in view of low arterial O2 saturation and dyspnoea. All drugs he was on were stopped. Blood investigation showed serum lipase 900 U/L (normal level 10-140 U/L), serum triglyceride 560 mg/dL (normal level <150 mg/dL) and blood sugar (fasting and postprandial) were 230 and 478 mg/dL, respectively with normal serum calcium level. Mild derangement in liver function tests was noticed. His HIV serology status was nonreactive. The patient was put on mask oxygen, later on intubated as arterial blood gas was unfavourable and kept on mechanical ventilation with lung protective strategy. Chest X-ray showed left sided pleural effusion []. Contrast enhanced computed tomography scan abdomen (CECT) on 13th day showed pancreatic necrosis (15%) with oedema and peripancreatic collection, no cholelithiasis or choledocholithiasis with a large pelvic fluid collection[]. Pleural effusion was managed with left sided percutaneous drain and pelvic collection with USG guided percutaneous drainage. Inotropic and vasopressor support were continued for 7 days. Repeat CECT on 21th day showed pancreatic necrosis (40-50%) with gas formation in pancreas and peripancreatic areas, suggesting CT severity index 6-7/10 []. The diagnosis of EP was made. Sepsis was managed with appropriate antibiotics. Peripancreatic drain was inserted and culture report from drained fluid showed anaerobic enteric organisms. Intravenous imipenem and clindamycin were administered initially. Later on peripancreatic region was irrigated with metronidazole through percutaneous drain for few days. The patient required sustained low efficiency dialysis on alternate days for acute kidney injury. Hyperglycaemia was controlled with regular insulin infusion. He was extubated after 13 days of mechanical ventilation. Enteral feeding (nasojejunal) was started gradually. On stabilisation, the patient was discharged from the hospital on the 48th day with drug and life style advice for correcting dysglycaemia, dyslipidaemia and increased body weight. Olanzapine was replaced by other drugs. Subsequently, the patient lost about 15 kg body weight and did not develop symptoms/signs of pancreatitis.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [86.0, 'kg']}",126,119.7,132.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 86.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (86.0 kg - 20 kg) = 126.0 mL/hr.
Hence, the patient's fluid maintenance is 126.0 mL/hr."
5194,22,Maintenance Fluids Calculations,physical,decimal,pmc-4241730-1,Extracted,"A 33-year-old primigravida woman in her third trimester of pregnancy presented to the obstetrics department with severe itching. Examination of the patient confirmed a single, live intrauterine pregnancy of 33 gestational weeks. A widespread erythematous rash was also evident, with tense fluid-filled blisters accompanied by severe itching. The patient indicated these symptoms had begun two weeks previously. The patient was referred to the dermatology polyclinic, where examination showed erythematous maculae scattered over the arms, legs, trunk, and neck (Figures , , , , and ), some with burst and crusted tense blisters on them. The patient's personal history was unremarkable. Routine hemogram and biochemical tests produced normal results, and vitamin B12, folic acid, thyroid hormones, and antibody levels were all within normal ranges. Anti-BP 180-NC16 could not be obtained because this test could not be carried out in the biochemical laboratory of our hospital. Subepidermal disintegration was detected by means of punch biopsy (). Direct immunofluorescence showed linear C3 deposition () and weak IgG deposition () at the basement-membrane zone. A diagnosis of PG was made from these findings. Systemic corticosteroid treatment was initiated at a dose of 40 mg/day prednisolone. Since a regression was observed in the lesions of the patient after two weeks, the prednisolone dose was reduced gradually. No new blister formation was observed during hospitalization. Prednisolone treatment was started at a dose of 10 mg/day on the 15th day of hospitalization and the patient was then discharged. The patient had a mild relapse after 10 days, prednisolone dose was increased to 20 mg/day, and an improvement was observed. The dose was reduced after one week and maintained at 10 mg/day. The remaining follow-up period of the pregnancy was uneventful and the patient gave birth to a live baby measuring 3600 g in weight and 50 cm in length through vaginal delivery in the 39th gestational week. No abnormality was detected at the newborn examination. Treatment was maintained until 6 weeks after delivery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3600.0, 'g']}",14.4,13.68,15.12,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3600.0 g so this converts to 3600.0 lbs * kg/1000 g = 3.6 kg. Hence, the patient's maintenance fluid is 3.6 kg * 4 mL/kg/hr = 14.4 mL/hr.
Hence, the patient's fluid maintenance is 14.4 mL/hr."
5195,22,Maintenance Fluids Calculations,physical,decimal,usmle-8942,Extracted,"A 69-year-old woman presents to her physician’s office with cough, increasing fatigue, and reports an alarming loss of 15 kg (33 lb) weight over the last 4 months. She says that she has observed this fatigue and cough to be present over the past year, but pushed it aside citing her age as a reason. The cough has been progressing and the weight loss is really worrying her. She also observed blood-tinged sputum twice over the last week. Past medical history is noncontributory. She does not smoke and does not use recreational drugs. She is relatively active and follows a healthy diet. Today, her vitals are normal. On examination, she appears frail and pale. At auscultation, her lung has a slight expiratory wheeze. A chest X-ray shows a coin-shaped lesion in the periphery of the middle lobe of the right lung. The nodule is biopsied by interventional radiology (see image).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15.0, 'kg']}",50,47.5,52.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.0 kg - 10 kg) = 50.0 mL/hr.
Hence, the patient's fluid maintenance is 50.0 mL/hr."
5196,22,Maintenance Fluids Calculations,physical,decimal,pmc-6213993-1,Extracted,"Our patient was a 4-year-old Italian boy who visited our pediatric hospital for incidental head trauma with a linear fracture of the right parietal bone and a small hematoma. He presented with a Glasgow Coma Scale of 15/15 and normal neurological testing. His weight was 21 kg (>97th percentile), height was 113 cm (>97th percentile), and head circumference was 54.5 cm (>97th percentile). The patient exhibited dysmorphic facial appearance with trigonocephaly, frontal bossing, large ears, prominent chin, and high palate with dental malposition. Physical examination of the skin found one “café-au-lait” spot on the right hemithorax (2 cm × 0.5 cm) and an irregular skin lesion with a rubbery consistency and fibrosis (3 cm × 4 cm) on the right femoral side. He also exhibited syndactyly of the second and third right toes and learning difficulties. He was born at full-term via caesarean section because of macrosomia. His birth weight was 4.050 g (>97th percentile). His parents were healthy and unrelated. His older brother was also healthy and had normal development. His grandfather died at the age of sixty to chronic lung disease ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [21.0, 'kg']}",61,57.95,64.05,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 21.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (21.0 kg - 20 kg) = 61.0 mL/hr.
Hence, the patient's fluid maintenance is 61.0 mL/hr."
5197,22,Maintenance Fluids Calculations,physical,decimal,pmc-8594314-1,Extracted,"A 35-year-old Caucasian male weighing 124 kg (body mass index: 34 kg/m2) with a history of epilepsy was admitted to the ICU with generalized seizures. On arrival, the patient was unresponsive, and his body temperature was 35.9 °C. His blood pressure was 194/119 mmHg, pulse rate was 100/minute, and respiratory rate was 18/minute. The clinical assessment of disease severity according to the APACHE IV score was 92. Renal and liver tests were normal. Endotracheal intubation was performed. Lacosamide and levetiracetam were administered intravenously twice daily (50 mg and 1,500 mg, respectively). On day 4, due to increased antiepileptic activity, 250 mg topiramate twice daily was prescribed.
Due to miscommunication, a dose of 2,500 mg topiramate was administered by a nasogastric tube. The next day, the prescription error was discovered but a toxicity syndrome was already suspected. Prompt gastrointestinal decontamination, including active charcoal, was initiated within 12 hours from administration. A laxative (sodium thiosulphate) was administered every 4 hours to prevent drug absorption. No seizures were recorded on the EEG. The patient recovered fully and was discharged on day 6.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [124.0, 'kg']}",164,155.8,172.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 124.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (124.0 kg - 20 kg) = 164.0 mL/hr.
Hence, the patient's fluid maintenance is 164.0 mL/hr."
5198,22,Maintenance Fluids Calculations,physical,decimal,pmc-4770651-1,Extracted,"A 6-month-old, 5 kg, male patient presented with a history of swelling in dorsolumbar region (7 cm × 9 cm) since birth and progressive weakness of bilateral lower limbs. He was diagnosed to have of MMC with ACM for which ventriculoperitoneal shunting was done at postnatal age of 20 days. On examination, the infant was playful with a head circumference of 39 cm, and no movement in bilateral lower limbs. The child also had dorsal kyphoscoliosis. Laboratory investigations including hematology and biochemical parameters were within normal limits. Electrocardiogram and chest X-ray were unremarkable. Magnetic resonance imaging confirmed dorsolumbar spinal dysraphism, MMC, ACM (type II), and a ventriculoperitoneal shunt in situ [].
The infant was posted for excision and repair of dorsolumbar MMC under general anesthesia. Monitoring included 5 lead electrocardiography, noninvasive blood pressure, and pulse oximetry. Induction of anesthesia was achieved using increasing concentration of sevoflurane in oxygen with patient in supine position and the swelling placed in a donut. After securing an intravenous access fentanyl (2 mcg/kg) and rocuronium (1 mg/kg) were administered intravenously, and trachea was intubated with a 3.5 mm (internal diameter) microcuff endotracheal tube and bilaterally equal air entry were confirmed. Anesthesia was maintained with sevoflurane in O2:N2O (50:50) and intermittent boluses of rocuronium and fentanyl. Volume controlled mode (tidal volume – 40 ml and respiratory rate 22/min) was used. After induction invasive blood pressure, esophageal temperature and urinary output recording were also started. Thereafter, the child was placed in prone position. The incision of around 10 cm was made, and surgical repair included excision of the sac and dural repair. Postexcision, as the defect was large - a bilateral latissimus dorsi flap was used to achieve closure. During application of wound dressing, peak airway pressures increased up to 25 mm of Hg (from 12 to 13) associated with progressive bradycardia up to 65/min from 110/min, arterial hypotension 50/34 mmHg (from 74/38 mmHg), and desaturation up to 89% (from 99% to 100% on FiO2 0.5). There was no mechanical obstruction in breathing circuit or endotracheal tube. Chest auscultation revealed bilaterally equal but reduced air entry. The surgeon was immediately informed, and 100% oxygen was started. Intravenous atropine 0.2 mg and mephentermine 1.0 mg was administered, which temporary improved the hemodynamic status (BP 82/46 mmHg). The patient was turned supine and re-evaluated. Tracheal suction was done. Oxygen saturation came up to 93–94% (on FiO2 1.0) but peak airway pressures were still on the higher side (20–22 cm H2O). The total duration of surgery was 5 h, estimated blood loss 200 ml, total fluid intake was 400 ml, blood transfusion 170 ml, and urine output 20 ml. Neuromuscular blockade was not reversed, and he was shifted to neurosurgical Intensive Care Unit for further evaluation and management.
The child was nursed in lateral position and pressure control mode (inspiratory pressure of 18 cm H2O and respiratory rate of 26 breaths/min) was used for ventilation. The patient had poor lung compliance and soon there was fall in tidal volume delivered to patient and O2 saturation. The abdomen was tense so a nasogastric tube was placed, and 10 ml gastric contents were aspirated. It relieved the abdominal distension and slightly improved the respiratory compliance. Digital evacuation of impacted stools gave symptomatic benefit for another few hours. However, this was followed by bradycardia (57 bpm) along with fall in oxygen saturation to 80%. There was also associated drop in urine output. Tracheal tube was changed to rule out blockade along with necessary resuscitative measures for bradycardia and hypoxia were taken. Now, the flap was considered as prime culprit for decreased intra-abdominal volume, and the consequences. The lateral sutures of flap were removed which relieved abdominal distension and gradually patient's hemodynamic parameters and pulmonary compliance improved. The child was eventually extubated on the 2nd postoperative day and was fully intact neurologically. In following days, the defect was covered by skin graft and infant was discharged from the hospital on the 10th postoperative day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.0, 'kg']}",20,19,21,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.0 kg. Hence, the patient's maintenance fluid is 5.0 kg * 4 mL/kg/hr = 20.0 mL/hr.
Hence, the patient's fluid maintenance is 20.0 mL/hr."
5199,22,Maintenance Fluids Calculations,physical,decimal,pmc-3656535-1,Extracted,"A 17-day-old girl was admitted with chief complaint of episodic respiratory distress noted since the second day of her life. The baby was born out of nonconsanguinous marriage, by normal delivery at term, to a primigravida mother with an uneventful pregnancy, and cried immediately after birth. There was no maternal history of teratogenic drug or radiation exposure. No antenatal ultrasonography was done. After her birth (weight 2000 g) in a rural hospital, congenital malformations were first noted. The family history was negative for congenital anomaly and mental retardation. On admission her weight was 1750 g (SGA), length 42 cm (<5th centile), OFC 32 cm (<5th centile), and respiratory rate was 42/min with episodic panting type of respiration, with rate up to 100/min lasting for 1-3 minutes, followed by apnea for 12-15 s without bradycardia or cyanosis. In addition, physical examinations revealed posteriorly rotated low set ears, prominent upper forehead, sublingual nodules, bimanual heptadactyly, bilateral hallucal polysyndactyly, and an accessory right postaxial toe, coarse crepitations on the right chest, and generalized hypotonia with diminished deep tendon jerks. Neonatal reflexes were depressed. The other findings were unremarkable and fundoscopic examination was normal. The following investigations were done and found to be normal-routine blood and urine, serum CRP, blood sugar, blood urea, SGPT, serum calcium, X-rays of pelvis and skull, abdominal ultrasonography, and echocardiography [Figures and ]. Radiography of chest revealed pneumonitic changes in the right mid- and upper zones. X-ray of the hands showed y-shaped right third, left fourth and left fifth metacarpals with bimanual central polydactyly, a right postminimus, and a left postaxial extra digit. In addition, X-ray revealed short middle phalanx of all fingers. X-rays of the feet showed duplication of the first metatarsal and hallucal phalanges, an extra epiphysis in the soft-tissue hallux between normal and accessory bony hallux and syndactyly of first three toes, bilaterally. MRI of brain demonstrated a hypoplastic cerebellar vermis with a molar tooth sign (which consists of deepened interpeduncular fossa, thickened superior cerebellar peduncles and hypoplasia of cerebellar vermis) on axial image at the level of the isthmus. The diagnosis was reached based on clinicoradiological findings. She was treated conservatively and episodic tachypnea-apnea gradually decreased at 1 month of age. The child was then discharged and advised to seek regular follow-up for further evaluation and possible supportive interventions. Although advised, VEP and BAER test were not carried out. A chromosomal study (conventional G-banding) showed a normal karyotype (46, XX). At 2½ months of age, examination revealed growth failure (weight 2500 g), feeding difficulty, hypotonia, absent social smile, poor visual fixation and occasional episodic tachypnea.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2500.0, 'g']}",10,9.5,10.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2500.0 g so this converts to 2500.0 lbs * kg/1000 g = 2.5 kg. Hence, the patient's maintenance fluid is 2.5 kg * 4 mL/kg/hr = 10.0 mL/hr.
Hence, the patient's fluid maintenance is 10.0 mL/hr."
5200,22,Maintenance Fluids Calculations,physical,decimal,pmc-6685243-1,Extracted,"Our patient was a 27-year-old Javanese man with borderline intellectual functioning and striking dysmorphisms. Both his parents were Javanese, normal, non-consanguineous, and in their sixth decade of life. He was the third child born after a normal third pregnancy and he had two sisters who were normal. His mother had a cesarean delivery with no history of trauma, infection, or drug use during the term. No family history of similar complaints or any other congenital abnormality was reported. Our patient was born at term after an uneventful pregnancy.
He is a slow learner and attends a school for children with special needs in Cirebon, West Java, Indonesia. There he began to socialize, play with other classmates, and he likes to draw and enjoys music. The dysmorphisms found are very characteristic. On physical examination, his weight was 36 kg, height 158 cm, and occipital frontal circumference 54 cm. It was observed that he displayed hypertelorism, down-slanting palpebral fissure, strabismus, ocular proptosis, depressed nasal bridge, short philtrum, and low-set ears. In addition, acrocephaly, asymmetrical flat facies, nasal deformity, and prominent jaw were present (Fig. ). His oral deformities showed maxilla hypoplasia with high arch palate. His V-shaped maxillary arch was filled with double rows of teeth. In addition, there was a dental fusion between maxillary premolar and first molar. Panoramic radiographs were performed for confirmation (Fig. ). Other abnormalities found were mild scoliosis and mild pectus excavatum. Symmetrical cutaneous bilateral syndactyly involving his four fingers, his palms were spoon-shaped with an inwardly placed thumb, was present (type 2). Both feet showed type 2 symmetrical cutaneous syndactyly of the first to fifth toes. Radiographs of both hands and feet confirmed soft tissue syndactyly (Fig. ). He had corrective surgery twice on both hands to correct for joint contractures. There was no postoperative complication. Six months after the second surgery, he could start using his fingers. A clinical diagnosis of AS was previously made based on these clinical features, as earlier mentioned in our study describing clinical manifestations of this patient []. Furthermore, Pictures of Standard Syndromes and Undiagnosed Malformations (POSSUM) software () was used before molecular analysis and the result showed suspected AS with a cut-off point of 14. Ethical clearance for genetic testing was obtained according to the research ethic committee of Faculty of Medicine, Swadaya Gunung Jati University, Indonesia.
Mutation analysis was conducted for our patient. DNA was isolated from peripheral blood using the salt saturation method, as previously described by Miller et al. []. Molecular genetics analysis of FGFR2, targeting exon 7, was performed by direct sequencing at the Laboratory of Neurovascular Unit and Cognitive Impairments, University of Poitiers, France. The reference genomic DNA sequence used was NM_000141.4. Polymerase chain reaction (PCR) amplification of exon 7 from the FGFR2 gene was performed using the primers FGFR2-F 5-CCGGCAGTCTCCTTTGAAGT-3′ and FGFR2-R 5′-GATCTGTTAATTCCTTAGAACACTCTCT-3′, resulting in a 525 bp fragment. Approximately 50 ng of DNA solution (2.5 μl) was added to 22.5 μl of PCR mixture. This PCR mixture contained 0.25 μl of 25 mM deoxyribonucleotide triphosphates (dNTPs), 3 μl of 25 mM MgCl2, 0.25 μl of each 20 μM primer, 2.5 μl of 10× PCR buffer, 0.125 μl of 5 U/μl Diamond® high fidelity Taq DNA polymerase (Eurogentec), and 16.13 μl of H2O. PCR was initiated with denaturation at 95 °C for 3 minutes, followed by 35 PCR cycles (at 95 °C for 30 seconds, 60 °C for 30 seconds, and 72 °C for 30 seconds) and 7 minutes final elongation at 72 °C. The amplified products were detected by electrophoresis on a 1.5% agarose gel with 0.5 mg/ml ethidium bromide and visualized under ultraviolet (UV) light. Furthermore, 5 μl of the PCR product was cleaned up with 2 μl ExoSAP reagent (ThermoFisher) according to the manufacturer’s instructions, to remove excess primers and unincorporated nucleotides enzymatically. Finally, 2 μl of the PCR product was used for the sequence reaction (BigDye Terminator Cycle Sequencing Kit Version 3.3; Applied Biosystems), which was run on an ABI PRISM® 310 Genetic Analyzer (Applied Biosystems), following the manufacturer’s directions. Sequencing was performed bidirectionally using the forward and reverse PCR primers. The sequence result was compared with the published reference sequence using Chromas software version 2.6.4. In this patient, we detected a missense mutation, changing a TCG codon (coding for a serine) into a TGG (coding for a tryptophan): p.Ser252Trp (c.755C>G) (Fig. ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [36.0, 'kg']}",76,72.2,79.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 36.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (36.0 kg - 20 kg) = 76.0 mL/hr.
Hence, the patient's fluid maintenance is 76.0 mL/hr."
5201,22,Maintenance Fluids Calculations,physical,decimal,pmc-4868013-1,Extracted,"Our patient, a 2-year-old girl, was the third child of healthy nonconsanguineous parents of Moroccan origin, born at term after an uneventful 39-week gestation and normal delivery; she was admitted for genetic evaluation because of psychomotor delay and failure to thrive. Her birth weight was 2500 g (3rd centile), length was 46 cm (3rd centile), and head circumference was 32 cm (3rd centile). Her family history was unremarkable for developmental delay or recurrent miscarriages. The proposita sat at 18 months, but her walking and language acquisition were delayed. On clinical examination, her length, weight, and head circumference at 2 years old were as follows: 68 cm (<3rd centile), 8 kg (<3rd centile) and 44 cm (<3rd centile). She had mild dysmorphic features similar to that of the 9p duplication syndrome. She had hypertelorism, deep-set eyes, broad nasal bridge and bulbous nasal tip, short philtrum, downturned mouth, retrognathia, and short neck. Additional findings included large anterior fontanelle, fifth finger clinodactyly, left equinus foot, and umbilical hernia. Further evaluation revealed growth hormone deficiency with decreased serum level of IGF-1, estimated at 47 ng/mL; whereas normal values are between 51 and 327 ng/mL. Magnetic resonance imaging (MRI) scan of pituitary gland was normal.
Chromosomal analysis was performed on cultured peripheral lymphocytes of our patient and her parents according to standard methods. R banding at the resolution level of 400 bands was performed, as well as C banding after barium hydroxide treatment. RHG analysis (R-banding of human chromosomes by heat denaturation and Giemsa staining) showed a derivative of chromosome 9 with a 9p arm notably expanded. The extra band was C banding negative, thus excluding pericentric inversion of the 9qh region. This was interpreted as representing either a 9p duplication or some other rearrangement. Since parental karyotypes were both normal, our patient’s karyotype was designated as 46,XX,der(9)?dn (Fig. ).
Thereafter, fluorescence in situ hybridization (FISH) test was done, applying multicolor banding probe set for chromosome 9 []. Probe labeling, hybridization post washing, signal detection, and image acquisition were performed as previously reported [, ]. For characterization of the heteromorphic patterns of chromosome 9, further probe set was applied [, ].
FISH experiments identified the extra segment as a duplication of 9p24 to 9p12. The karyotype could be characterized after the application of the probes mentioned above. There was a partial trisomy 9p24 to 9p12. The region 9p24 to 9p12 was duplicated and inserted inverted in 9p12~13 (Fig. ). The final karyotype was designated as follows: 46,XX,der(9)(pter->p12~13::p12->p24::p12~13->qter)dn.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [8.0, 'kg']}",32,30.4,33.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 8.0 kg. Hence, the patient's maintenance fluid is 8.0 kg * 4 mL/kg/hr = 32.0 mL/hr.
Hence, the patient's fluid maintenance is 32.0 mL/hr."
5202,22,Maintenance Fluids Calculations,physical,decimal,pmc-4897161-1,Extracted,"A 33-month-old girl presented with edema and proteinuria. Following clinical diagnosis of NS, she was treated with prednisolone (60 mg/m2/day) for 4 weeks, but NS has been persistent. When the patient was transferred to our hospital, physical examination revealed generalized edema, but no evidence of thromboembolism. Her vital signs were stable, with a blood pressure of 103/66 mmHg. Her weight was 12 kg (25th–50th percentile) and her height was 91 cm (25th–50th percentile). Laboratory studies revealed a white blood cell count of 8.38×109/L, hemoglobin level of 15.9 g/dL, hematocrit level of 46.1%, and platelet count of 284×109/L. Biochemistry showed the following: total protein, 5 g/dL; albumin 2.5 g/dL; total cholesterol, 235 g/dL; blood urea nitrogen, 11 mg/dL; creatinine, 0.3 mg/dL; calcium, 8.7 mg/dL; phosphorus, 5.7 mg/dL, and normal electrolyte level. Prothrombin time and activated partial thromboplastin time were both within normal range. Urinalysis revealed proteinuria of 4+ and the spot urine protein-to-creatinine ratio was 31.23 g/g Cr. Test results for antinuclear antibody and antineutrophil cytoplasmic antibody were negative, and the IgG, IgA, and IgM levels were 391.0 mg/dL, 82.0 mg/dL, and 142.0 mg/dL, respectively. Ultrasonography revealed normal-sized kidneys with diffuse increased renal parenchymal echogenicity. Renal biopsy revealed a collapsing variant of focal segmental glomerulosclerosis (FSGS) ().
To manage the patient's steroid-resistant NS, high-dose intravenous methylprednisolone (MP) pulse therapy at a dose of 30 mg/kg was administered every 2 days. Angiotensin-converting enzyme inhibitor and intermittent albumin replacement followed by diuretics were also prescribed. After the first dose of MP, she complained of intermittent left lower leg pain, which was assumed to be a side effect of MP. After the third round of MP, her lower leg pain became continuous, progressed to both legs, and caused her to stop walking. The skin on the dorsum of her feet was pale and cold and capillary refill was slow. The dorsalis pedis pulse, posterior tibialis pulse, and popliteal pulse were palpable but not strong. Emergency Doppler ultrasonography of her lower extremities revealed turbulent flow in both her femoral and popliteal arteries. Magnetic resonance angiography showed multifocal segmental luminal occlusion of the common iliac arteries, external iliac arteries, and popliteal arteries (). The lumen of the common femoral arteries and superficial femoral arteries were relatively patent with distal flow reconstitution. The hemostasis study was as follows: thrombin time, 19.9 seconds (control, 17.0 seconds); fibrinogen, 362 mg/dL (reference, 180–380 mg/dL); D-dimer, 0.48 µg/mL (reference, 0–0.4 µg/mL); plasminogen activator, 86% (reference, 70%–140%); factor VIII, 214% (reference, 52%–190%); antithrombin (AT)-III activity, 91% (reference, 80%–120%); protein C, 243% (reference, 70%–140%); and protein S, 97% (reference, 65%–116%). Test results for anticardiolipin and anti-β2-glycoprotein-I antibodies were all negative. The factor V Leiden (1691G>A) mutation was absent.
TEC was suspected, and MP pulse therapy was discontinued and heparinization started, followed by mechanical thrombectomy of both iliac arteries and popliteal arteries using Forgarty balloon catheters. Thrombus cultures were obtained during mechanical thrombectomy despite the absence of clinical infection. Staphylococcus hominis subspecies hominis (S. hominis subsp. hominis) was isolated, which was found to be ampicillin-resistant and vancomycin-susceptible. Since peripheral blood culture results were negative, systemic antibiotics were not administered. Anticoagulant treatment was continued for 8 months with warfarin. Two months later, a follow-up Doppler ultrasonography of her lower extremities showed patent lumen and intact flow patterns in the common femoral arteries, superficial femoral arteries, and popliteal arteries. The severity of proteinuria, which was consistent with NS, persisted despite various combinations of oral steroids, cyclosporine A, tacrolimus, and rituximab. The patient's renal function deteriorated and progressed to end-stage renal failure, and renal replacement therapy of peritoneal dialysis was started 22 months after TEC onset.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [12.0, 'kg']}",44,41.8,46.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 12.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (12.0 kg - 10 kg) = 44.0 mL/hr.
Hence, the patient's fluid maintenance is 44.0 mL/hr."
5203,22,Maintenance Fluids Calculations,physical,decimal,pmc-5891917-1,Extracted,"A 47-year-old Japanese woman with aphasia and gait difficulty was admitted for the evaluation of a brain magnetic resonance imaging (MRI) abnormality. She had gradually developed aphasia and gait difficulty 2 months before admission. Her medical history included an invasive thymoma diagnosed at 24 years old, MG (Myasthenia Gravis Foundation of America clinical classification IIa) at 35 years old, cryptococcal meningoencephalitis at 36 years old, and erythrodermic psoriasis at 46 years old. The time course of her medical history and treatments are shown in Fig. . Ptosis and limb weakness, as MG symptoms, had completely recovered. She demonstrated chemotherapy-induced immunosuppression, and the invasive thymoma (Masaoka stage IVB) was refractory to shrinkage by multiple chemotherapies. The invasive thymoma had also seeded intraperitoneally. She had received her last chemotherapy (cyclophosphamide, 500 mg; doxorubicin, 50 mg; cisplatin, 50 mg) 16 months before admission, and had been taking prednisolone (12.5 mg/day) from 44 years of age. Her family history was unremarkable.
On admission, her body weight was 39.5 kg and she was 151.7 cm tall (body mass index of 17.2 kg/m2). Her vital signs were normal and her Glasgow coma scale score was 12 (E4V2M6). Physical examination revealed widespread erythema with scaling and exfoliation of the skin due to erythrodermic psoriasis, and an invasive thymoma in the left lower chest wall. She had a central venous port for chemotherapy in her left upper chest wall. Neurological examination revealed motor aphasia and central facial weakness on the right side. Barré’s sign for the upper extremities and Mingazzini’s sign for the lower extremities were negative. Finger-to-nose and heel-to-knee tests demonstrated no abnormalities. Bilateral deep tendon reflexes were normal, but bilateral plantar responses were extensor.
Laboratory studies showed the following results: hematocrit, 32.6%; hemoglobin, 10.7 g/dL; red blood cell count, 3.74 × 106/μL; mean corpuscular volume, 87.1 fL; platelet count, 22.7 × 104/μL; and white blood cell count, 8.2 × 103/μL, with 0.9% lymphocytes (74 cells/μL). Lymphocyte subgroups were as follows: CD4, 14.9% (normal range 25.0%–54.0%); CD8, 25.0% (normal range 2.0%–56.0%); CD4/CD8 ratio, 0.6; CD19, 0.4% (normal range 5.0%–24.0%); and CD20, 1.1% (normal range 3.0%–20.0%). Her total IgG level was 282 mg/dL (normal range 870–1700 mg/dL), IgA level was 58 mg/dL (normal range 110–410 mg/dL), and IgM level was 15 mg/dL (normal range 35–220 mg/dL). Serology for HIV type 1/2, human T-lymphotropic virus type 1, Candida, Aspergillus, Toxoplasma, and Mycobacterium tuberculosis were all negative. Anti-acetylcholine receptor (AchR) antibodies were positive (0.4 nmol/L: normal range < 0.3 nmol/L). Cerebrospinal fluid (CSF) analysis revealed a normal cell count, protein, and glucose, but an elevated IgG index (1.1) and elevated myelin basic protein levels (238 pg/mL). Oligoclonal bands and CSF cytology were negative. CSF cultures for bacteria, fungi, and M. tuberculosis were negative. CSF polymerase chain reaction (PCR) tests for M. tuberculosis, herpes simplex virus, varicella-zoster virus, Epstein-Barr virus, and cytomegalovirus were all negative, but CSF real-time PCR for JCV was positive, showing 6,283,000 copies/mL. Brain MRI showed hyperintense lesions in the left frontal white matter on T2-weighted images and fluid-attenuated inversion recovery images (Fig. ). These lesions were hypointense without contrast enhancement on T1-weighted images (Fig. ). Diffusion-weighted images (DWI) demonstrated a hyperintense lesion in the margin of left frontal white matter (Fig. ). Arterial spin labeling revealed hyperperfusion in the DWI hyperintense lesion (Fig. ). Magnetic resonance spectroscopy showed a decrease in N-acetylaspartate and increased lactate in the lesions (Fig. ). Thallium-201 single photon emission computed tomography revealed no uptake in the lesions (Fig. ). Based on the results of clinical features, imaging findings, and CSF PCR for JCV, the patient was finally diagnosed with non-HIV-related PML due to chemotherapy-induced immunodeficiency and GS [, ].
Monthly intravenous immunoglobulin (IVIg) therapy for hypogammaglobulinemia was started 10 days after admission. After the diagnosis of non-HIV-related PML, mirtazapine 15 mg/day was started 24 days after admission, and oral mefloquine 275 mg/day was also started for 3 days on day 25, followed by 275 mg once weekly. We also tapered her prednisolone to 10 mg/day on day 44. She had no deterioration of neurological symptoms indicating immune reconstitution inflammatory syndrome. However, she developed central venous port-related infections with no improvement of neurological symptoms, and received antibiotic and antifungal treatments on day 39. Although we tried to remove the central venous port, it could not be withdrawn without a risk of vascular injury. The above treatments were continued, but the patient unfortunately died of sepsis due to Candida albicans and Staphylococcus epidermis, as determined by blood culture on day 46.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [39.5, 'kg']}",79.5,75.525,83.475,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 39.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (39.5 kg - 20 kg) = 79.5 mL/hr.
Hence, the patient's fluid maintenance is 79.5 mL/hr."
5204,22,Maintenance Fluids Calculations,physical,decimal,pmc-3754395-1,Extracted,"A 4050-gram male newborn was delivered vaginally to a 20-year-old mother at 413/7 gestational weeks with no dysmorphic features and discharged on the postnatal day two. On the postnatal day six, a distended abdomen was noticed and baby was admitted to another hospital for investigations. On abdominal examination firm mass was palpable. The liver was occupying the entire abdomen. The patient also had edema of the lower extremities and mild respiratory distress.
Initial laboratory findings including complete blood count (hemoglobin: 14.6 g/dl, white blood count: 22,800 /l, platelet count: 330,000/l), electrolytes and renal function tests were within normal range. Alanine aminotransferase level (19 U/l, N: <45 U/l) was normal. However aspartate aminotransferase (85 U/l, N: <41 U/l), gamma glutamyl transferase (238 U/l, N: 8-61 U/l) and total/direct bilirubin levels (3/1.6 mg/dl, N: <1.1/<0.3 mg/dl) were high. Serological evaluation for toxoplasma gondii, rubella, cytomegalovirus, herpes simplex, Epstein–Barr virus and parvovirus were all negative. Abdominal ultrasonography (USG) revealed hepatomegaly with a heterogeneous liver parenchyma and a 39x31 mm hypo-echoic solitary non-calcified mass in the right adrenal region. A computed tomography scan revealed a right adrenal soft tissue mass (4.8x3.6 cm) with no calcification and contrast uptake, and significant hepatomegaly. The spleen appeared to be in normal size but was replaced inferiorly because of the massive hepatomegaly. Serum neuron-specific enolase level was higher, 60 ng/mL (normal range: <10 ng/mL), and alpha feto protein level (22754 ng/mL, N: >45000 ng/mL at birth) was normal. Urine vanillylmandelic acid and serum ferritin levels were 5718 mg/day (N: 0.5-2 mg/day) and 531 ng/mL (N: 24-336 ng/mL) retrospectively. Bone marrow aspiration revealed no malignant infiltration, no rosette forming and no storage cells. On the postnatal day eighteen, doppler USG showed decreased flow in the IVC, secondary to compression. Based on clinical presentation and imaging modalities, the presumptive diagnosis of NBL was made and the case was referred to our neonatal intensive care unit (NICU) on the postnatal day twenty.
On admission to our NICU, he had respiratory distress with 40% O2 requirement and significant abdominal distension with visible thin venous vessels through his abdominal skin (Fig. 1a). He had tachypnea besides edema of lower extremities, scrotum and penile area. Complete blood count revealed anemia (hemoglobin: 9.5 g/dl), leukocytosis (33.300 /l) and mild thrombocytosis (536.000/l). Serum sodium (128 mEq/l), chloride (94 mEq/l), calcium (7 mg/dl) and phosphorus (0.7 mg/dl) concentrations were low. Serum uric acid and renal function tests revealed normal results (uric acid: 5.8 mg/dl, blood urea nitrogen: 9 mg/dl, creatinine: 0.43 mg/dl). Liver function tests revealed cholestasis (alanine aminotransferase: 40 U/l, aspartate aminotransferase: 101 U/l, γ-glutamyltransferase: 463 U/l, total/direct bilirubin: 3.05/2.02 mg/dl) and hypoproteinemia (total protein: 3.4 g/dl and albumin: 1.8 g/dl). Clotting studies demonstrated prolonged prothrombin time (PT) as 16 seconds (N: 9.4 to 12.5 seconds) and low fibrinogen level (0.89 g/dl, N: 2.38–4.98).
Second abdominal USG evaluation showed right suprarenal mass which was about 5 cm in diameter, severely diffuse hepatomegaly and ascites. After pediatric oncology consultation, the patient underwent hydration, chemotherapy and allopurinol treatments between the postnatal days 20–23. The patient received modified VEC (vincristine, etoposide, carboplatin) protocol due to poor clinical condition. In spite of the received chemotherapy, his clinical condition worsened progressively. The abdominal distention was so increased that he required high frequency oscillatory ventilation support. However, he did not develop signs of tumor lysis syndrome. The patient was accepted as chemotherapy-resistant NBL due to clinical deterioration with massive liver involvement on the 3rd day of treatment and surgical excision was performed (Fig. 1b, 1c). Pathology revealed intra-adrenal tumor with wide-spread expression of bcl 2 in addition to distant metastases in the liver and minimal lymphocytic infiltration. MYC-N amplification obtained from adrenal specimen revealed <3 copies. IVC compression directly observed during the surgery resulted in severe circulation collapse and the patient died due to hypotensive shock and disseminated intravascular coagulation just two hours after the operation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4050.0, 'g']}",16.2,15.39,17.01,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4050.0 g so this converts to 4050.0 lbs * kg/1000 g = 4.05 kg. Hence, the patient's maintenance fluid is 4.05 kg * 4 mL/kg/hr = 16.2 mL/hr.
Hence, the patient's fluid maintenance is 16.2 mL/hr."
5205,22,Maintenance Fluids Calculations,physical,decimal,pmc-7752325-2,Extracted,"A 47-year-old woman with a body weight of 98.5 kg (BMI: 39 kg/m2) and body fat 48.5% and, no liver or renal function complications (AST and creatinine values of 30 IU/mL and 0.75 mg/dL, respectively), was first admitted in our institution in April 2017. Her glucose and insulin blood basal levels were 240 mg/dL and 5.0 µIU/mL, respectively. The temporal glucose and insulin values after an oral challenge with 75 g of glucose are showed in Figure A-B (triangles) and the HbA1c value was 7.4% (Table , Case 2). These results confirmed the type 2 diabetes state with hyperglycemia (Figure , triangles), and hypoinsulinemia (reduced insulin response during oral glucose-tolerance test, Figure , triangles). The patient was medicated with 1 g/day of metformin and a low-fat/low-caloric diet based on proteins and carbohydrates of low glycemic index. The treatment was followed during 1 (one) year with by-monthly controls. After the year, the patient increased her body weight and body fat (99.1 kg and 50.5%, respectively). Importantly, the diabetic state of the patient did not improve (Figure A-B, circles) and glucose and insulin levels remained pathologic (220 mg/dL and 4.9 µIU/mL, respectively). In agreement with these results, the levels of HbA1c after the 1 year treatment remained abnormally high (Table , Case 2). Therefore, we prescribed a daily dose of 2 mL (approximately 40 drops) of B subtilis natto DG101 at a concentration of 1 × 108 CFU (Colony Forming Units) per mL, 1 g/day of metformin and the same type of low-fat/low-caloric diet based on proteins and carbohydrates of low glycemic index, plus bimonthly controls. Interestingly, after 4 months of treatment with the probiotic supplement (plus metformin and the modified diet), the blood levels of glucose decreased to normal values, 95 mg/dL without an increase in insulin production, (Figure , squares), and the HbA1c level decreased to a normal value (Table , Case 2). The body weight and body fat of the patient at the end of treatment were 98.0 kg and 47.2%, respectively. During the period of treatment, the patient had normal liver and renal functions, and no adverse events were observed.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [98.5, 'kg']}",138.5,131.575,145.425,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 98.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (98.5 kg - 20 kg) = 138.5 mL/hr.
Hence, the patient's fluid maintenance is 138.5 mL/hr."
5206,22,Maintenance Fluids Calculations,physical,decimal,usmle-8500,Extracted,"A 25-year-old G1P0 woman at 22 weeks’ gestation presents to the emergency department with persistent vomiting over the past 8 weeks which has resulted in 5.5 kg (12.1 lb) of unintentional weight loss. She has not received any routine prenatal care to this point. She reports having tried diet modification and over-the-counter remedies with no improvement. The patient's blood pressure is 103/75 mm Hg, pulse is 93/min, respiratory rate is 15/min, and temperature is 36.7°C (98.1°F). Physical examination reveals an anxious and fatigued-appearing young woman, but whose findings are otherwise within normal limits.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.5, 'kg']}",22,20.9,23.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.5 kg. Hence, the patient's maintenance fluid is 5.5 kg * 4 mL/kg/hr = 22.0 mL/hr.
Hence, the patient's fluid maintenance is 22.0 mL/hr."
5207,22,Maintenance Fluids Calculations,physical,decimal,pmc-6617628-1,Extracted,"A 30-year old woman was admitted to our hospital to undergo renal biopsy. According to her medical records, microscopic hematuria was detected on every urine analysis since her birth. At 16-years-old, the potential causes were closely examined. However, no diagnosis was made. Renal biopsy was not performed at that time because the patient’s manifestation was only microscopic hematuria without increased urinary protein or other signs of renal dysfunction. A few years later, she chose to stop her regular visits to the doctor. When she was 27-years old, she became pregnant. Upon her initial visit at the department of obstetrics and gynecology, she tested positive for hematuria. In the 30th week of pregnancy, her urine tested positive for the presence of protein but the results returned to normal after puerperium. Further, the patient experienced hypertension soon after delivery, but her blood pressure was normotensive during all other periods. Through entire pregnancy and post-partum, evidence of hematuria remained upon testing her urine samples.
The patient did not experience any subjective or objective symptoms associated with kidney disorders such as, fever, deafness, hemoptysis, or rash. In addition, she was not taking any medication. Her urinary findings did not change over 2-years. The urinary protein level was 60 and 40 mg/day in 2016 and 2018, respectively. Hematuria was assessed using a urinary occult blood test resulting in 3+ and 2+ in 2016 and 2018, respectively. In addition, the urinary dysmorphic red blood cell (RBC) sediment was 50–99/high power field (HPF) and 30–49/HPF in 2016 and 2018, respectively. In contrast, serum creatinine levels increased from 0.57 mg/dl to 0.86 mg/dl during the same 2-years, without special events.
The patient had a history of far-sightedness, astigmatism, and strabismus from birth as well as polycystic ovarian syndrome diagnosed at the age of 27-years. Her family history included a paternal grandmother with a subarachnoid hemorrhage and a father with hypertension. There was no family history of renal dysfunction or urinary abnormalities.
Physical examination results on admission were as follows: height 152 cm, weight 42.0 kg, body mass index (BMI) 18.2 kg/m2, body temperature 36.8 °C, blood pressure 99/76 mmHg, and pulse of 73 beats/min. Hearing loss, skin manifestations, and joint symptoms were not detected. In addition, the patient’s respiratory sounds were normal and abdominal tenderness was not detected. Laboratory data showed renal insufficiency [serum creatinine, 0.86 mg/dl; estimated glomerular filtration rate (eGFR), 64 ml/min/1.73 m2] and hematuria (urinary occult blood, 3+; urinary dysmorphic RBC sediment, 11.3/HPF) (Table ). eGFR was calculated by serum creatinine concentrations using the Japanese eGFR equation []. The patient’s urinary protein level was 60 mg/day, which is classified as normal to mildly increased proteinuria according to the Kidney Disease: Improving Global Outcomes 2012 Clinical Practice Guidelines []. Immunological testing showed no abnormal findings (Table ).
The kidney size was within normal limits (right: 109 × 58 mm; left, 108 × 62 mm) and compression of the left renal vein between the aorta and proximal superior mesenteric artery, which would suggest Nutcracker syndrome, was not detected on abdominal computed tomography (CT). However, the density of the renal cortex was remarkably low (Fig. a). In addition, numerous small high-intensity spots were distributed within the subcapsular cortex on magnetic resonance imaging T2-weighted image (Fig. b).
The differential diagnosis of hematuria from early childhood include IgA nephropathy, Alport syndrome, and TBMN. Therefore, we performed renal biopsy the day after admission. Renal histological examination revealed global sclerosis in 5 of 22 glomeruli, cystic dilatation of the Bowman’s capsule in 3 of 22 glomeruli (14.1%), and atrophy of the glomerular tufts (Fig. a and b). Immunofluorescence studies indicated no deposition of immunoglobulins or complement proteins. Type IV collagen staining showed normal expression levels of the α5 chain in the GBM and Bowman’s capsule (Fig. c to e). The renal biopsy samples obtained for electron microscopy examination did not contain cystic glomeruli and therefore, the detailed appearance of cystic glomeruli could not be evaluated. Electron microscopy revealed thinning of the GBM. The width of the GBM was measured at 30 random points to calculate the average value. The average thickness of the GBM was 191 nm, which exceeded criteria set forth by Haas et al. for the lower limit of normal thickness (215 nm for females) [] (Fig. f and g). Other morphological abnormalities, including electron-dense deposits and foot process effacement, were not identified on electron microscopy. Based on the above findings, the patient was diagnosed with TBMN accompanied by GCKD.
Although this patient had no recorded family history of GCKD, we examined whether there were any associations with known genetic mutations using next-generation sequencing. There were no pathogenic mutations of UMOD, MUC1, or SEC61A1, encoding uromodulin, mucin1, or Sec61 translocon alpha 1 subunit, which are causative proteins of autosomal dominant tubulointerstitial kidney disease, including GCKD. No pathogenic mutations of COL4A3 and COL4A4, encoding type IV collagen α3 and α4 of the GBM, were detected. Based on these results, we diagnosed the patient with TBMN coexistent with sporadic GCKD. The patient was discharged and followed closely without intervention.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [42.0, 'kg']}",82,77.9,86.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 42.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (42.0 kg - 20 kg) = 82.0 mL/hr.
Hence, the patient's fluid maintenance is 82.0 mL/hr."
5208,22,Maintenance Fluids Calculations,physical,decimal,usmle-7586,Extracted,"A 17-year-old girl presents with significant weight loss over the last few months. There is a positive family history of Hodgkin lymphoma and hyperthyroidism. Her blood pressure is 100/65 mm Hg, pulse rate is 60/min, and respiratory rate is 17/min. Her weight is 41 kg and height is 165 cm. On physical examination, the patient is ill-appearing. Her skin is dry, and there are several patches of thin hair on her arm. No parotid gland enlargement is noted and her knuckles show no signs of trauma.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [41.0, 'kg']}",81,76.95,85.05,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 41.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (41.0 kg - 20 kg) = 81.0 mL/hr.
Hence, the patient's fluid maintenance is 81.0 mL/hr."
5209,22,Maintenance Fluids Calculations,physical,decimal,pmc-7388081-1,Extracted,"A 55-year-old male was admitted to the Department of Hematology of The First
Affiliated Hospital of Guangzhou University of Chinese Medicine because of atony
of both lower extremities and malaise for more than 6 months. The patient
reported increased fatigue and thirst during the last 2 months and described
perspiring during sleep. He also had an associated weight loss of 5 kg during 6
months, and fever. Physical examination revealed splenomegaly.
Laboratory examination of peripheral blood showed hyperleukocytosis with white
blood cell (WBC) counts of 38.22 × 109/l and a platelet (PLT) counts
of 390 × 109/l, and serum biochemical analysis showed lactate
dehydrogenase (LDH) levels of 1122 U/l. Morphological examination of bone marrow
(BM) aspirate showed a thrombocytosis and hypercellular marrow with high degree
of dysgranulopoiesis, including 0.5% myeloblasts, 3.5% promyelocytes, 9%
myelocytes, 3% metamyelocytes, 10% eosinophils, 4.5% lymphocyte, 2% nucleated
red blood cells, and 9.5% monocytes (). Manual differential count of
peripheral blood also revealed a granulocytosis (). BM biopsy analysis revealed
hypercellular marrow, including neutrophilic leukocytosis to 84% with left shift
and immature granulocytes, mean counts of 6–8 megakaryocytes/high power field
combined with cell enlargement, and a lack of karyolobism. Immunohistochemical
analysis identified myeloperoxidase (MPO)+, CD71+,
CD61+, CD117−, and CD34+/− cells.
Meshinprotein staining was consistent with grade 1 BM fibrosis (). Molecular
analyses of BCR/ABL fusion gene was negative
and positive for JAK2 V617F. Cytogenetic analysis revealed a
normal karyotype (46, XY). A preliminary diagnosis of prefibrotic primary
myelofibrosis (pre-PMF) was considered with other myeloid neoplasms needing to
be excluded. Next-generation sequencing was performed, and the results
identified the JAK2 V617F variant (51% mutations load) along with three
additional gene variants, additional sex combs like 1 (ASXL1) G645fs (36.09%),
SETBP1 D868N (46.00%), and splicing factor, arginine/serine-rich 2 (SRSF2)
P95_R102del (33.56%). Considering the SETBP1 expression, we retested peripheral
blood cell morphology and performed a manual differential count that revealed
65% neutrophils, 10% metamyelocyte, 10% myelocytes, 2% promyelocytes, 8%
monocytes, 2% basophilic granulocytes, 6% eosinophilic granulocytes, and 3%
lymphocytes. Dysgranulopoiesis demonstrated abnormal nuclear segmentation, with
31% neutrophilic granulocyte band forms and 31% nuclear hyper-segmentation.
Based on patient medical history, peripheral blood cell morphology, BM
pathology, and genetic testing, the most appropriate diagnosis was atypical
chronic myeloid leukemia with the coexistence of JAK2, SETBP1,
ASXL1, and SRSF2 variants.
Considering the fact that allogeneic HSCT is the only potentially curative
treatment for aCML, we recommended HSCT to the patient. However, taking into
account the risks and costs of transplantation, the patient refused allogeneic
HSCT and opted for treatment with lower risk and minimal pain. According to
presence of the JAK2 mutation, a targeted therapy of
ruxolitinib combined with symptomatic treatment was recommended since June 2019.
For the first 5 months, the therapy consisted of ruxolitinib (40 mg/day).
However, there was an aggravation of leukocytosis (from 38.22 g/l to 47.82 g/l),
which, combined with the JAK2 mutation, motivated a change in
treatment. Since 8 November 2019, Azacytidine (100 mg/day) was added to the
treatment protocol daily for 7 days followed by 1× every 30 days. After four
courses of therapy, the patient demonstrated a positive response, with effective
symptomatic control and small improvement of thrombocythemia (from
368 × 109/l to 208 × 109/l). The most significant
evolution was marked reduction in spleen size (thickness from 68 mm to 51 mm;
length diameter from 173 mm to 145 mm) and decreased WBC counts from
38.22 × 109/l to 10.79 × 109/l. The JAK2 V617F
mutations load dropped from 51% to 44.4%. However, the WBC counts rose again
after the fourth course of azacytidine in March this year. A comprehensive
follow-up examination on 18 March suggested that white blood cells are
15.54 × 109/l, hemoglobin is 139g/l, and PLT count is 248×
109/l. The results of BM and peripheral blood smears indicate
that the granulocyte system is actively proliferating, accounting for 59.5% of
nuclear cells. Peripheral blood neutrophil revealed a nucleus left shift,
including 7% myelocyte, 6% metagranulocyte, 12% segmented neutrocyte, and 24%
band form neutrophilic granulocyte. Eosinophils and basophils are easy to see.
BM pathology results revealed that BM fibrosis has progressed to grade 3. Two
additional gene mutations of NRAS and KRAS were found through another
second-generation sequencing. And the JAK2 V617F mutations load raised to 46.2%.
The spleen was more swollen than before, the long diameter increased to 168mm,
and the thickness increased to 65mm. The above examination results indicate that
the disease has progressed.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.0, 'kg']}",20,19,21,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.0 kg. Hence, the patient's maintenance fluid is 5.0 kg * 4 mL/kg/hr = 20.0 mL/hr.
Hence, the patient's fluid maintenance is 20.0 mL/hr."
5210,22,Maintenance Fluids Calculations,physical,decimal,pmc-4069804-1,Extracted,"A 62-year-old female patient was referred to the digestive system department of our hospital because of progressive abdominal distension for 1.5 years and edema of bilateral lower limbs for one month. The patient presented with the following symptoms upon admission: malaise, weight loss (10 kg), intermittent upper abdominal pain, watery diarrhea (three to four times daily), oliguria (500 mL/day), and transient skin flushes. The patient’s blood pressure declined from 120/90 mmHg to 100/70 mmHg. She did not receive any therapy before admission. Her medical history revealed that she had tuberculosis for 40 years and other unremarkable symptoms.
After physical examination, abdominal ultrasonography, and computed tomography (CT) scan, the following symptoms were detected: liver palm (palmar erythema), pot belly, bilateral lower limb edema, hepatomegaly (4 cm below the costal margin), mild splenomegaly, ascites, and nodular infiltration of the liver. Skin lesions, rashes, and superficial lymphadenopathy were absent.
Results of the laboratory examination performed at admission revealed a white blood cell count of 5.4×109/L with a normal differential count, hemoglobin level of 107 g/L, and platelet count of 249×109/L. The patient had a serum sodium level of 126 mmol/L (normal: 137-150 mmol/L), albumin level of 31.6 g/L (normal: 37-53 g/L), aspartate aminotransferase level of 12.9 U/L (normal: 0-40 U/L), alanine aminotransferase level of 13.2 U/L (normal: 0-40 U/L), gamma-glutamyltransferase level of 93 U/L (normal: 0-50 U/L), alkaline phosphatase level of 148 U/L (normal: 42-128 U/L), total bilirubin level of 6.5 µmol/L (normal: 0-20 µmol/L), direct bilirubin level of 1.4 µmol/L (normal: 1.7-6.8 µmol/L), and prothrombin time of 24.3 s (normal: 12-16 s). The tumor marker CA125 was present at a level of 207.6 U/mL (normal: <35 U/mL). Serological testing for hepatitis A, B, and C and HIV showed negative results. Autoimmune markers, other tumor markers, and blood and fecal cultures were negative.
A preliminary diagnosis based on clinical symptoms and laboratory examination results of the patient was made by the physician as follows: “hepatic cirrhosis, decompensated phase, however, etiology was not clear. In addition, given the tumor marker CA125 was in high level, exclude other abdominal or gynecological tumor was necessary.”
The patient underwent upper and lower gastrointestinal endoscopy three times during hospitalization because of persistent and intermittent diarrhea. She also underwent a liver biopsy. Subsequently, the patient developed anemia (hemoglobin level of 98 g/L). Bone marrow aspiration was performed, and results show an abundance of atypical hypogranulated round or spindle-shaped cells. The abundance of such cells conﬁrmed the presence of mast cell differentiation. Further immunohistochemical staining was performed on cells. Diffuse CD25 and CD117 in tryptase-positive mast cells infiltrated the gastric and colonic mucosa. Sheets of mast cells were present in the portal tract of the liver.
The liver biopsy highlighted an area of extinction comprising a large amount of spindled mast cells, fibrous tissue, entrapped hepatocytes, ductular reactions, and a portal spanning the width of the needle’s core (). Mast cells were positive for CD117 () and CD25, but negative for CD30. The mast cells were loosely scattered in the hepatic sinusoids within the hepatic parenchyma.
A diffuse hyperemia with superficial erosions was present. The mucosa showed a slightly raised appearance, which mimics the proliferative polyp found by upper and lower gastrointestinal endoscopy (). The results of histological analysis were as follows. Mucosal erosion and gland expansion and distortion were observed. Diffuse spindled mast cell infiltration in the gastric and colonic lamina propria was characterized by cells with small, elongated, and baculiform nuclei, inconspicuous nucleoli, and pale cytoplasm (). These cells were admixed with some lymphocytes and plasma cells. The tumor cells were positive for CD117 (), and showed abnormal surface molecular expression of CD25. However, tumor cells were negative for CD30.
These ﬁndings were fully consistent with ASM according to the WHO criteria, and a diagnosis of ASM with extensive involvement of the liver and gastrointestinal tract was made. The patient received H1 and H2 histamine antagonists with improvement in diarrhea. The patient was discharged upon the demand of her family and the patient herself. The patient died after one month.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.0, 'kg']}",40,38,42,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.0 kg - 10 kg) = 40.0 mL/hr.
Hence, the patient's fluid maintenance is 40.0 mL/hr."
5211,22,Maintenance Fluids Calculations,physical,decimal,pmc-2881526-1,Extracted,"A 67-year-old man weighing 80 kg had no other notable findings than a history of diabetes mellitus, and the patient visited the emergency care center with a chief complaint of hemoperitonium occurring after a fall injury from a 3 m height. At the time of admission, the patient had a clear mentality and spontaneous respirations. Due to persistent intra-abdominal bleeding, the patient had the following findings: blood pressure (BP), 85/50 mmHg; and heart rate (HR), 110 beats/min. During treatment at the emergency care center, the patient aspirated gastric contents, which led to tracheal intubation. Despite the infusion of dopamine (20 µg/kg/min), the patient remained hypotensive. To stop the abdominal bleeding, emergency surgery was performed. Sedation was continued post-operatively, and the patient was transferred to the ICU intubated. On postoperative day 1, during treatment with sedation and ventilator care in the ICU, hemodialysis was performed due to the occurrence of sepsis and acute renal failure (ARF). This was followed by the occurrence of ARDS due to pulmonary aspiration (). Controlled mechanical ventilation (CMV) was initiated with the following settings: tidal volume (TV), 480 ml; respiratory rate (RR), 20 breaths/min; FiO2, 1.0; and positive end expiratory pressure (PEEP), 15 mmHg. An arterial blood gas analysis (ABGA) was performed which showed the following: pH, 7.01; PaCO2, 60 mmHg; PaO2, 47 mmHg; HCO3-, 15.1 mmol/L; and SaO2, 58%. To improve oxygenation, NO was administered at a dose of NO from 3:00 pm on post-operative day 1 ().
Until post-operative day 2 following the use of NO, an ABGA was performed under the following CMV settings: TV, 450 ml; RR, 22 breaths/min; FiO2, 1.0; and PEEP, 20 mmHg. The ABGA showed as the following: pH, 7.27; PaCO2, 46.1 mmHg; PaO2, 126.7 mmHg; HCO3-, 20.7 mmol/L; and SaO2, 98.4%. Thus, oxygenation was gradually improving (). Due to the persistent presence of abdominal bleeding, an emergency repeat surgery was performed. While maintaining NO inhalation, the patient was transferred to the operating room ().
Upon arrival in the operating room, the patient had the following implants: a catheter in the right subclavian vein for central venous pressure (CVP) monitoring, a catheter in the right femoral vein for fluid supply, a catheter in the right radial artery for a continuous arterial blood pressure monitoring, and a colostomy. To maintain vital signs, the patient received an infusion of vasopressin (1 unit/hr), dopamine (15 µg/kg/min), norepinephrine (0.8 µg/kg/min), and bicarbonate (20 mEq/hr). The patient also had a BP of 103/55 mmHg, a HR of 110 beats/min, and a CVP of 21 mmHg. Mechanical ventilation was performed using a ventilator (Savina, Drager, Germany) which was used in the ICU. With continued CMV (TV, 400 ml; RR, 22 breaths/min; FiO2, 1.0; and PEEP, 18 mmHg), the measurements were as follows SaO2, 85-90%; and a peak inspiratory pressure (PIP), 34 mmHg. NO was infused to the area which was 30 cm remote from the Y-piece of the inspiratory limb of the ventilator using a NO delivery system (HY-1002; Metran Co., Germany). In the connecting part between the Y-piece and inspiratory limb, using an expiratory gas analyzer (PrinterNOx; Micro Medical Ltd., England), the concentrations of NO and NO2 were measured ( and ).
The patient's mental status was sedated with midazolam, which was used in the ICU (the bispectral index [BIS] was 8). Because the ventilator which was used in the ICU was also used in the operating room, due to a lack of availability of a vaporizer, the induction and maintenance of anesthesia were performed using total intravenous anesthesia. With reference to BIS measurements, a small dose of propofol (2.0 µg/ml) and remifentanil (2.0 ng/ml) were administered using a target-controlled infusion (Orchestra™; Fresenius Vial, France). A muscle relaxant, atracurium, was intravenously adminsitered at a dose of 20 mg/hr. Intra-operatively, BIS was abruptly increased from approximately 10 to 35. Because the BP was not sufficiently higher for the enhancement of the propofol infusion, to maintain the depth of anesthesia, midazolam was intravenously injected twice at a dose of 1 mg. Intra-operatively, the concentration of NO was maintained at 5.0-9.5 ppm, and NO2 was 0-0.8 ppm. With aggravation of the patient's vital signs, a Swan-Ganz catheter for pulmonary artery pressure (PAP) monitoring was not placed. Following the initiation of surgery, abdominal decompression was performed. Meanwhile, the BP decreased from 120/50 mmHg to 95/40 mmHg. The CVP decreased from 21 mmHg to 15 mmHg. The SaO2 increased from 90% to 100%. The PIP decreased from 34 mmHg to 24 mmHg. Blood was used as fluid therapy and an intravenous infusion of phenylephrine resulted in an elevation of BP to approximately 110/50 mmHg. Thereafter, during the surgery, there were no notable changes in the patient's status. At the time the surgical procedure was completed, with a continuous infusion of vasopressin (1 unit/hr), dopamine (15 µg/kg/min), norepinephrine (0.8 µg/kg/min) and bicarbonate (20 mEq/hr), the BP was 123/56 mmHg, the HR was 78 beats/min, and the CVP was 13 mmHg. Mechanical ventilation was finally set at a TV of 500 ml, a RR of 16 breaths/min, a FiO2 of 0.8 (O2, 3.2 L/min; and N2O, 0.8 L/min), and a PEEP of 10 mmHg in an effort to not further increase the PIP, TV, and minute volume. With the maintenance of the concentration of NO at 5.0-10 ppm, an ABGA was performed, and showed the following: pH, 7.18; PaCO2, 45 mmHg; PaO2, 430 mmHg; HCO3-, 16.8 mmol/L; SaO2, 100%; and PIP, 25 mmHg (). At this time, the BIS was 13-20. The intra-operative blood loss was 1,000 ml. With the transfusion of PRC (4 units), FFP (6 units), and PC (10 units), the Hb was maintained at 9.2 mg/dl. The anesthetic and surgical time was 2 hours and 50 minutes and 2 hours and 20 minutes, respectively.
Following surgery, the patient was transferred to the ICU. The CMV settings were as follows: TV, 550 ml; RR, 16 breaths/min; FiO2, 0.8; and PEEP, 10 mmHg. An ABGA analysis showed as the following: pH, 7.20; PaCO2, 39 mmHg; PaO2, 305 mmHg; HCO3-, 15.2 mmol/L; and SaO2, 100% (). The patient's status was considered to be improved. The use of NO was therefore discontinued (). Following the repeat surgery, however, the abdominal bleeding persisted. There were no further improvements in ARDS. On post-operative day 1, at approximately 5:00 pm, with the following CMV settings: TV, 500 ml; RR, 20 breaths/min; FiO2, 1.0; and PEEP, 20 mmHg, an ABGA was obtained (pH, 7.29; PaCO2, 42 mmHg; PaO2, 71 mmHg; HCO3-, 20.2 mmol/L; and SaO2, 92%; ). Due to a lack of response to an increased dose of epinephrine and norepinephrine, systolic blood pressure was not maintained at >80 mmHg. At dawn on post-operative day 2, due to multiple organ failure, including ARF, sepsis, aspiration pneumonia, and respiratory failure, the patient expired.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [80.0, 'kg']}",120,114,126,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 80.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (80.0 kg - 20 kg) = 120.0 mL/hr.
Hence, the patient's fluid maintenance is 120.0 mL/hr."
5212,22,Maintenance Fluids Calculations,physical,decimal,pmc-4082921-1,Extracted,"53-year-old man was admitted to our clinic at February 2012 with symptoms of general fatigue, anorexia, weight loss, nausea, and vomiting. His past history was unremarkable and he only complained of 20 kilos' weight loss extending over 4 months. Physical examination was unremarkable other than an enlarged liver extending to 5 cm below the right costal margin. Laboratory tests showed WBC of 9430 K/μL, hbg of 12.4 g/dL, hct of 36.2%, plt of 2000 K/μL, calcium of 14.9 mg/dL (8.6–10.2), phosphate of 1.8 mg/dL (2.6–4.5), albumin of 3.4 g/dL, alkaline phosphatase (ALP) of 295 (40–130), and gamma-glutamyl transferase (GGT) of 363 U/L (0–60). PTH was suppressed to 5 pg/dL (15–65), and CA 19-9 was as high as 2384 U/mL (<27). Patient consulted endocrinology and hematology departments and medical treatment was applied. Peripheral blood smear staining showed thrombocytopenia. Thorax and abdominal CT, abdominal MRI, and FDG-PET studies were performed. Abdominal USG showed a large tumor with hypoechogen pattern in right lobe of the liver. CT revealed 20 × 14 cm size hypoattenuating multinodular tumor mainly filling the right lobe of the liver with irregular boundaries (). Thorax and brain CT were normal. T1-weighted MR images showed the tumor as a hypointense area and T2-weighted images showed it as a slightly hyperintense area with contrast enhancement of peripheral zone being liable to confluent multiple lesions in right lobe of liver with retrocaval and aortocaval multiple metastatic lymphadenopathy and metastatic lesions on right iliac and right femoral bones (). Fluorodeoxyglucose-positron emission tomography (FDG-PET) showed pathological signal intensity of 10.7 of a standardized uptake value in CC of liver, in renal hilum, in bilateral aortocaval lymph nodes, and in six places of bones as C-5, T-11, and S-1 vertebral corpus, right iliac bone, and left and right ischium ().
The patient was treated with IV saline, furosemide, and calcitonin. After the 8th day of treatment, calcium level, thrombocytopenia, and other clinical symptoms were normalized (). After the patient stability and normal platelet count were obtained, we performed USG guided trucut liver biopsy. USG guided trucut liver biopsy confirmed the diagnosis of CC. Neoplastic cells stained positively by cytokeratins 7 and 19. Patient was evaluated surgically as inoperable with evidence of radiological and pathological findings and was directed to medical oncology department for purpose of palliative chemotherapy with intended radiotherapy for bone metastasis (Figures , , and ).
At the end of first month of the oncologic treatment, patient was readmitted to hospital with worsening of consciousness state and relapsed hypercalcemia (11.5 mg/dL), while thrombocyte count was normal. Calcium level was higher than normal levels but not as high as first admittance to lead to thrombocytopenia again. Medical treatment of hypercalcemia rapidly stabilized the patient consciousness state. In spite of the chemoradiation treatment, disseminated metastasis developed and patient died in the 5th month of diagnosis.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [20.0, 'kg']}",60,57,63,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 20.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (20.0 kg - 10 kg) = 60.0 mL/hr.
Hence, the patient's fluid maintenance is 60.0 mL/hr."
5213,22,Maintenance Fluids Calculations,physical,decimal,pmc-8488087-1,Extracted,"A 15-year-old female was referred to the cardiology clinic with tachycardia, murmur and known hyperthyroidism. She had been suffering from fatigue, heat intolerance and nonspecific myalgias for six months, and subsequently developed shortness of breath on exertion. Her past medical history was unremarkable and there was no known family history of AF.
On initial visit, her weight was 53.9 kg (57.6th percentile, +0.19 SDs) and height was 158.8 cm (31.9th percentile, -0.47 SDs). Heart rate was 148 beats per minute and irregular, with a blood pressure of 138/72 mmHg. The precordium was hyperdynamic with normal first and second heart sounds, and a gallop rhythm. There was a grade II/VI systolic regurgitant murmur audible at the left lower sternal border and over the apex. Her thyroid was moderately enlarged with no palpable nodules. There was no peripheral edema or hepatosplenomegaly.
An electrocardiogram (ECG) showed AF with an average ventricular rate of 141 beats per minute, with irregular conduction and left ventricular hypertrophy (). Laboratory studies revealed a TSH of 0.01mU/L, free T4 of 75.4 pmol/L, free T3 of >30.8 pmol/L, thyroperoxidase antibodies of 114 IU/mL, and TSH receptor antibody of 25 U/L. She had a normal complete blood count, electrolytes and renal function (). An echocardiogram revealed an enlarged left atrium, left ventricle (>6cm), moderate mitral regurgitation and mild mitral valve prolapse with low normal cardiac function ().
The patient had a transesophageal echocardiogram that demonstrated no thrombus in the left atrium. She underwent synchronized cardioversion as daycare procedure, and successfully reverted to normal sinus rhythm at a rate of 90 beats per minute (). Warfarin was started post cardioversion and anticoagulation was discontinued after evidence of persistent sinus rhythm. Low dose aspirin was added as part of our institutional practice to use aspirin for patients with AF at low risk of an embolic event. Her medical management included methimazole at a dose of 0.5 mg/kg/day and bisoprolol 2.5mg once daily. A euthyroid state was achieved, and AF did not recur. She was seen in follow-up clinic in a week, a month, 6 months and 1 year period. She continued to be in sinus rhythm. Bisoprolol was discontinued 4 months after her initial presentation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [53.9, 'kg']}",93.9,89.205,98.595,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 53.9 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (53.9 kg - 20 kg) = 93.9 mL/hr.
Hence, the patient's fluid maintenance is 93.9 mL/hr."
5214,22,Maintenance Fluids Calculations,physical,decimal,pmc-8009447-1,Extracted,"We report a case of a healthy 64-year-old female who originally presented to an outside emergency department with low-grade fever and a two-week history of worsening lower abdominal pain. She denied any nausea, vomiting, loss of appetite, diarrhea, constipation, melena, hematochezia, urinary dysuria, frequency, vaginal bleeding, or discharge. She denied any family history of colon cancer or inflammatory bowel disease. Past surgical history includes tubal ligation, and past medical history includes hypercholesterolemia, hypothyroidism, and lung adenocarcinoma years ago that resulted in a left lobectomy. She reported having a previous colonoscopy many years ago without any signs of polyps or masses.
Vitals included height 1.676 m (5' 6""), weight 57 kg (126 lbs.), and BMI 20 kg/m². Physical exam was benign except for the following findings: fever of 38.0°C, moderate-to-severe tenderness with rebound and guarding in the lower abdomen and suprapubic region (right greater than left), and positive McBurney's point. As seen in Figure , the CT scan obtained in the emergency department showed findings concerning perforated appendicitis with subsequent abscess formation in the right lower quadrant.
Once the diagnosis was confirmed clinically and via radiographic imaging, she was transferred for definitive surgical and medical management. On hospital day 1, a percutaneous drain was placed with radiographic assistance with the return of purulent and serosanguineous fluid. Over the following days, her diet was slowly advanced and a repeat CT scan was obtained a few days after the original, as seen in Figure , which showed resolution of the right lower quadrant abscess collection. The drain was removed at that time, and the patient was discharged home with a course of oral antibiotics and plans for colonoscopy evaluation and ultimately an interval appendectomy.
The patient was seen three weeks post inpatient hospitalization to discuss the possible surgical intervention. At that time, the patient was feeling much better and tolerating a normal diet. She had appropriate bowel and bladder function and denied any pain, redness, fever, chills, or gastrointestinal symptoms. On physical exam, the abdomen was soft and supple without any tenderness, distention, or masses present. The patient agreed on obtaining a colonoscopy in four weeks, which aligned with the standard of care of obtaining one 6-8 weeks after an acute perforation of the appendix.
Figures , demonstrate the colonoscopy findings that showed a tumor at the appendiceal orifice with pathology consistent with that of a tubulovillous adenoma. The patient met the surgeon the following week to discuss the findings and agreed on a right laparoscopic hemicolectomy in four weeks for a cancerous peri-appendiceal mass. Figure illustrates a staging CT scan that was obtained prior to the operation.
Laparoscopic exploration of the abdominal cavity revealed evidence of a grossly inflamed appendix with the adhesion of the appendiceal tip to the anterior abdominal wall, bladder dome, and right ureter. The surgeon performed a partial appendectomy with associated right hemicolectomy for oncological purposes with clip placement at the anterior abdominal wall for future identification of appendicular tip should cancer or positive margins be encountered. A functional anastomosis between the distal ileum and transverse colon was successfully completed. Visualization of the peritoneal cavity during the procedure showed no evidence of carcinomatosis, obvious metastatic disease, or malignant ascites.
The patient returned to the office two weeks after the surgery. Pathology from the procedure showed moderately differentiated adenocarcinoma involving the appendix with invasion through the muscularis propria into at least the peri-appendiceal adipose tissue. Carcinoma was present at the mesenteric margin as a solitary tumor deposit, which was felt to be the transected appendiceal tip margin. Perineural and lymphovascular invasion was present. Fifteen lymph nodes were found to be negative for metastatic carcinoma (0/15). Tumor was staged at least a T3 given uncertain involvement of the appendiceal tip and bladder wall. On physical examination, the abdomen was soft, non-tender, non-distended, and had no signs of masses or hernias. The surgical incisions were all clean, dry, and intact without any signs of infection or erythema.
The patient's care was then transferred to an outside hospital for evaluation by Surgical Oncology and discussion of further treatment options. A discussion was held to obtain repeat PET/CT imaging in three months to further evaluate the tumor for possible future en bloc resection with or without hyperthermic intraperitoneal chemotherapy (HIPEC).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [57.0, 'kg']}",97,92.15,101.85,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 57.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (57.0 kg - 20 kg) = 97.0 mL/hr.
Hence, the patient's fluid maintenance is 97.0 mL/hr."
5215,22,Maintenance Fluids Calculations,physical,decimal,pmc-8426069-1,Extracted,"An 83-year-old female presented to the operating room to undergo an elective suprapubic catheter placement for chronic urinary retention secondary to a hypotonic bladder. Past medical history included hypertension, aortic stenosis, atrial fibrillation, transient ischemic attack, peripheral vascular disease, five vaginal deliveries, and longstanding pelvic floor dysfunction. The patient weighed 53 kilograms. Preoperative cystoscopy revealed a grossly trabeculated bladder consistent with long-standing urinary retention. A trial of clean intermittent catheterization was found undesirable by the patient, and a urethral catheter was placed. After discussion regarding long-term options, the patient decided to proceed with SPC.
In the operating room, cefazolin 1 g was administered intravenously on induction of procedural sedation. The bladder was distended with approximately 500 mL of normal saline instilled through a urethral catheter and adequately palpated. A spinal needle was used to infiltrate the tract with 0.5% Marcaine without epinephrine. The spinal needle was then advanced into the bladder, and urine was aspirated. A trocar was passed, and an 18 French Foley catheter was advanced into the bladder. Hematuria was noted, and continuous bladder irrigation (CBI) was started through the urethral catheter. The patient was transferred to the post anesthesia care unit (PACU) in stable condition. Within one hour of surgery, nausea, vomiting, rigors, pyrexia (temperature 39°C), and significant hypertension (229/165 mmHg) became apparent. On examination, the patient was alert and the abdomen was moderately distended and firm. Intravenous labetalol was administered, and a stat computed-tomography (CT) scan of the abdomen and pelvis was ordered to rule out bowel injury. Marked hypotension (82/50 mmHg) was then noted, and blood cultures as well as intravenous crystalloid resuscitation were ordered. The CT scan showed no evidence of bowel puncture and confirmed appropriate placement of the suprapubic catheter tip within the bladder.
The patient was then transferred to the intensive care unit (ICU) for management of postoperative septicemia. Fluid resuscitation and empirical antibiotics were administered until blood cultures and sensitivities were available. Vasopressors were required overnight and discontinued on postoperative day one, as was the CBI and the urethral catheter. The suprapubic catheter was well positioned and draining clear, yellow urine. White blood cell counts peaked at 30.6 × 109/L. Blood cultures were positive for Enterococcus faecalis and Proteus mirabilis, for which the patient completed a seven-day course of piperacillin-tazobactam. P. mirabilis was sensitive to ampicillin, cefazolin, ciprofloxacin, gentamicin, and trimethoprim/sulfa, while E. faecalis showed sensitivity to ampicillin, gentamicin synergy, streptomycin synergy, and vancomycin.
The admission was further complicated by increased left ventricular afterload in the context of aortic stenosis, leading to poor coronary perfusion (postoperative troponin I peaking at 1917 ng/L) during the hypertensive episode in PACU. Coronary angiography was performed, and severe disease in the first obtuse marginal artery was treated with a drug-eluting stent. The patient was discharged in stable condition on postoperative day ten.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [53.0, 'kg']}",93,88.35,97.65,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 53.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (53.0 kg - 20 kg) = 93.0 mL/hr.
Hence, the patient's fluid maintenance is 93.0 mL/hr."
5216,22,Maintenance Fluids Calculations,physical,decimal,pmc-3141155-1,Extracted,"A 6-week-old male term infant, weighing 3.7 kg, presented to the accident and emergency ward with a history of fever, difficulty in feeding and rapid breathing rate for last 7 days. He was delivered by forceps at 39 weeks, was breastfed and suffered no medical problems until the presenting episode. He was treated in a peripheral hospital initially for pneumonia. However, there was no improvement even after medical therapy. He was then referred to the present hospital.
On examination, the baby was pale with poor capillary return and oxygen saturation of 80% on air and was in respiratory distress with intercostal retraction and tachypnoea of 60–64 per minute. On auscultation, air entry was decreased in the left lung and bronchial breathing over right haemithorax. Blood pressure was 90/50 mm Hg and heart rate was 180 beats per minute. Capillary blood gas analysis demonstrated respiratory acidosis with pH 7.2, pCO2 60 mm Hg, pO2 101 mm Hg and base excess of –1.3. Chest radiography [] demonstrated partial collapse of right lung with hyperinflation of left upper lobe and marked mediastinal shift across to the right. A clinical diagnosis of CLE was made and treatment started in the neonatal intensive care unit (NICU) with IV antibiotics, bronchodilators, and nebulisation and chest physiotherapy. Fluid resuscitation was commenced with 20 ml/kg N/5 dextrose solution that restored capillary return to normal, although tachypnoea remained. The baby was nursed on his left side overnight with supplemental oxygen delivered to a head box.
Computed tomography (CT) scan [] done on the next day confirmed the diagnosis of CLE of left upper lobe with gross mediastinal shift. Left upper lobectomy was planned under general anaesthesia the following day.
In the operation theatre, monitoring was established with pulse oxymetry (SPO2), electrocardiogram (ECG) and noninvasive blood pressure (NIBP) monitoring. Intravenous access was checked. Patient was induced with Sevoflurane 8% in oxygen, and tracheal intubation was secured after spraying the vocal cord with 10% Lidocaine spray with a 2.5-mm portex nasal tube. The tube was passed through the vocal cord down into the right main bronchus and fixed at 12 cm at nose. Right-sided endobronchial tube position was confirmed by auscultation.
For analgesia, a mixture of 5 ml 0.25% Bupivacaine and 0.2 mg Morphine was given via caudal epidural route. Rectal Paracetamol suppositories 125 mg were also inserted. SpO2, ECG, NIBP, capnography and temperature were monitored. Once oxygen saturation and heart rate settled during intermittent positive pressure ventilation IPPV, Atracurium 3 mg and Fentantyl 3 μg were given. Anaesthesia was maintained with oxygen, air and Isoflurane (0.7–1.5%) via Drager Fabius Medical Systems ventilator, and a peak inspiratory pressure of 20 cm was maintained. During the initial period of left thoracotomy position, an oxygen concentration of 100% was required to maintain an oxygen saturation of 99%. As soon as the left upper lobe was isolated and clamped and branch pulmonary artery and vein were ligated and divided, oxygen saturation stabilised at 97% on 40%. Oxygen and N2O were then started. During the surgical procedure, tracheal suctioning was required repeatedly.
After the removal of the emphysematous left upper lobe, the tracheal tube was withdrawn up to the carina and ventilation of both the lungs was started. IV fluid was maintained with N/5 dextrose solutions 16 ml/hour. Blood loss was insignificant. A left chest drain was left in situ. The baby was electively ventilated in the NICU for 12 hours and weaned off successfully. Postoperatively, the chest radiograph [] was repeated in the evening and revealed complete correction of the mediastinal shift and marked expansion of the right lung. Oral intake was started on the 3rd day and the baby was discharged uneventfully on the 7th postoperative day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.7, 'kg']}",14.8,14.06,15.54,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.7 kg. Hence, the patient's maintenance fluid is 3.7 kg * 4 mL/kg/hr = 14.8 mL/hr.
Hence, the patient's fluid maintenance is 14.8 mL/hr."
5217,22,Maintenance Fluids Calculations,physical,decimal,pmc-8290566-1,Extracted,"A 44-year-old Moroccan Jew woman (gravida 4, para 4) was admitted to an internal medicine ward for general weakness and drowsiness, which began 2 days before admission. Her past medical history included morbid obesity and related complications of type 2 diabetes, which were controlled by metformin treatment; dyslipidemia, which was treated with atorvastatin; gastroesophageal reflux disease, which was not being managed with regular treatment; and fatty liver disease with no other known comorbidities. Her family history included untimely deaths of two of her four children, whose symptoms were similar to those in Leigh’s disease; her other two children are alive and healthy. Aiming to lose weight and control additional comorbidities, she underwent gastric band surgery at the age of 30 years. At the age of 38 years, owing to insufficient weight loss, she underwent gastric sleeve bariatric surgery, which resulted in a weight loss of 30 kg; however, she rapidly regained the lost weight. She subsequently remained morbidly obese, with a body mass index of 48.4. She was approved for a third bariatric surgery involving gastric bypass, and was admitted at the age of 44 years, weighing 126 kg. The surgery began with a laparoscopic approach, but, because of bleeding and gastrointestinal leakage, the procedure was converted to an open laparotomy. The procedure included an omega loop gastric bypass and an elective gallbladder resection, but was complicated by heavy postoperative bleeding. During the next several months, she underwent prolonged hospitalization with continuous mechanical ventilation, which required insertion of a tracheostomy tube, several recurring surgeries for peritoneal lavage, and repeated abscess drainage from the internal abdomen and abdominal wall. During this period, the patient also experienced recurrent episodes of sepsis, which required treatment with multiple courses of broad-spectrum antibiotics. Eventually, after 8 months of postoperative hospitalization, she recovered and was transferred to the rehabilitation department.
After 44 days in the rehabilitation department, she gradually developed new symptoms including slow psychomotor response, weakness, worsening peripheral edema, and drowsiness. Her vital signs on admission to the internal medicine department were unremarkable: temperature 36.4 °C, blood pressure 110/72 mmHg, pulse rate 84 beats per minute, respiratory rate 22 breaths per minute, and oxygen saturation on room air 97%. Her weight was 95 kg. Physical examination revealed grade 3 encephalopathy with asterixis, and neurological evaluation revealed hyporeflexia with symmetric weakness and decreased muscle tone. Other findings included peripheral edema grade 3. The surgical wounds in the abdominal wall had closed, and no signs of infection were seen. No tenderness was observed during abdominal palpation. Laboratory blood examinations showed an elevated international normalized ratio (1.6; normal range: below 1.1), severe hypoalbuminemia (1.5 g/dL; normal range: 3.4–5.4 g/dL), and highly elevated blood ammonia (285 µg/dL; normal range: 15–45 µg/dL). Other results included hemoglobin 9.2 g/L, white blood cell count 7200/µL, platelets 234,000/µL, glucose 91 mg/dL, urea 33 mg/dL, creatinine 0.7 mg/dL, sodium 137 mmol/L, potassium 4.3 mmol/L, magnesium 2.4 mmol/L, calcium 7.2 mmol/L, phosphorus 3.4 mmol/L, aspartate aminotransferase (AST) 28 IU/L, alanine aminotransferase (ALT) 31 IU/L, alkaline phosphatase 131 IU/L, gamma glutamyl transpeptidase 34 IU/L, lactate dehydrogenase 413 IU/L, total bilirubin 0.9 mg/dL, creatine phosphokinase 89 IU/L, pH 7.34, bicarbonate 23 mg/dL and PCO2 39.6 mmHg. Her C-reactive protein level was 1.2 mg/L (normal: 0–0.5 mg/L), and her blood ketones were negative. Further laboratory tests revealed normal levels of factor 5 and normal lactate levels (0.6 mg/dL). Imaging studies, including abdominal ultrasound and computerized tomography (CT), did not reveal any signs of cirrhosis; apart from previously known postsurgical changes, only diffuse fatty infiltrates of the liver were found (Fig. ). Brain CT, including venography and angiography, showed no signs of intracranial pathology, ischemia, or early or late enhancement. Her electroencephalographic findings supported the diagnosis of encephalopathy.
The most likely diagnosis was urea cycle disorder (UCD), as supported by the high ammonia levels, low blood protein levels, and advanced encephalopathy. Imaging studies showed no signs of cirrhosis, and laboratory investigations excluded hepatocellular injury. Hepatic cellular function was preserved, as reflected by standard factor 5 levels. Plasma amino acid analysis revealed a decrease in levels of several amino acid: taurine 17 µM, aspartate 13 µM, citrulline 4 µM, valine 105 µM, leucine 14 µM, tyrosine 25 µM, and histidine 58 µM. Other amino acids were in normal ranges. An acylcarnitine profile showed elevated carnitine with no further abnormalities. The urine organic acid profile revealed markedly elevated 4-hydroxyphenyllactate, but this test was inconclusive because the high levels of antibiotics in the blood might have influenced the results. Karyotyping revealed no irregularities.
Empirical treatments with the ammonia scavenger sodium benzoate, N-carbamylglutamate, l-arginine, carnitine, and low-protein total parenteral nutrition were administered in addition to nutritional supplements, which included thiamine, zinc, and vitamins C, B, and E. The patient’s encephalopathy condition continued to deteriorate, with new-onset fever and hemodynamic instability combined with respiratory failure. She was placed on mechanical ventilation, supported by vasopressors, started on a course of broad-spectrum antibiotics, and transferred to the internal intensive care unit, where a second ammonia level test was conducted and indicated a marked increase to 455 µg/dL. Her high ammonia levels were controlled by hemofiltration, in addition to the above treatment, and by administration of supplemental intravenous amino acids. Hemofiltration helped control her ammonia levels, which gradually decreased to baseline levels within 5 days.
A sepsis investigation began after fever and hemodynamic instability further complicated her condition, but no infectious source was found, and all cultures were negative. Total body CT and cardiac echocardiography were performed and yielded normal results.
With the resolution of systemic inflammatory response syndrome (SIRS), our patient was gradually weaned from mechanical ventilation and vasopressors, and her nutrition was steadily shifted from parenteral nutrition to enteral nutrition, and later to oral nutrition. The patient recovered neurologically and regained normal cognitive function. She subsequently developed critical care polyneuropathy, owing to the use of muscle relaxants, and was discharged to undergo rehabilitation in a designated hospital without a further need for nutritional supplements.
After 2 months in the rehabilitation department, she was discharged home. At a 2-year follow up after the hospitalization described above, her hyperammonemia had not recurred, and she had recovered from critical care polyneuropathy. During the follow-up period, no liver disease was found, and her ammonia levels remained stable and in the normal range, as did all other examined blood measurements.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [95.0, 'kg']}",135,128.25,141.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 95.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (95.0 kg - 20 kg) = 135.0 mL/hr.
Hence, the patient's fluid maintenance is 135.0 mL/hr."
5218,22,Maintenance Fluids Calculations,physical,decimal,pmc-4811070-1,Extracted,"In January 2014, a 23-year-old unmarried woman consulted gynecology department of the “Sylvanus Olympio Teaching Hospital in Lomé” for a painful swelling of the major labia of the vulva. She had her first menstruations at 16 years of age and her first sexual intercourse at 20 years of age. She did not report any history of sexually transmitted infections. She did not smoke, nor take alcohol, nor take contraceptive pill.
Clinical examination revealed axillary temperature of 37°C, body weight of 75 Kg, and height of 1.65 m. Gynecological examination noted, at the major labia of the vulva, a firm swelling of about 2 cm, with regular contours. The major labium of the vulva was painful at contact. There were no satellite adenopathies.
Clinicians established an initial diagnosis of inflammation of Bartholin gland. A tumorectomy was done in February 2014 and the removed piece was sent for histological analysis. Conventional histological analysis of a biopsy performed in February 2014 concluded to a botryoid sarcoma of the vulva. Also, paraffin blocks were sent to France for specific examinations.
Immunohistochemistry investigations showed positivity of anti-epithelial membrane antigen (EMA) markers and anti-pancytokeratin 1 markers of tumor cells, but they were negative for anti-smooth muscle actin and desmin protein S100 ones (Figures , , and ).
In situ hybridization revealed the HPV 16/18 and 6/11 genotypes. The diagnosis of squamous cell carcinoma with poorly differentiated sequences of HPV was established. Chemotherapy was instituted.
One year after the beginning of chemotherapy, the patient complained of abdominal and bone pain. Thoracolumbar spine scan showed a metastatic osteolysis of vertebral spondyle and spinous process of the twelfth thoracic vertebra (). Abdominal ultrasound had shown no abnormalities. After multidisciplinary discussions, radiotherapy was decided in addition to the chemotherapy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [75.0, 'kg']}",115,109.25,120.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 75.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (75.0 kg - 20 kg) = 115.0 mL/hr.
Hence, the patient's fluid maintenance is 115.0 mL/hr."
5219,22,Maintenance Fluids Calculations,physical,decimal,pmc-5490844-4,Extracted,"An 11-year-old male castrated, indoor-only DSH cat was presented for evaluation of 1 week of lethargy with previous chronic history of vomiting, weight loss despite normal appetite and intermittent diarrhea. The owner also reported intermittent sneezing and increased upper respiratory noise. Abnormalities on physical examination included poor body condition (BCS 1/9, body weight 2.5 kg), unkempt haircoat, pale, tacky mucus membranes, cranial organomegaly, suspected pain on abdominal palpation, moderate serous nasal discharge and referred upper airway sounds on thoracic auscultation.
Blood work revealed a mild anemia (HCT 28%; RI 30–50%), elevated liver enzyme activities (ALT [195 U/l; RI 25–145 U/l], AST [106 U/l; RI 5–42 U/l], ALP [91 U/l; RI 10–79 U/l] and GGT [23 U/l; RI 0-5 U/l]) and low creatinine (0.4 mg/dl; RI 0.9–2.1 mg/dl). Total bilirubin was within normal limits. A complete blood count showed leukocytosis (white blood cells 19.7 K/μl; RI 4.5–15.7 K/μl) with a mature neutrophilia (segmented cells 17.8 K/μl; RI 2.1–10.0 K/μl).
On abdominal ultrasound the liver was enlarged and hyperechoic. The GB was not reliably identified. There was a large (approximately 3.2 cm diameter × 5.0 cm length), fusiform, focal dilatation of the proximal aspect of the CBD (,). The most distal 2–3 cm of the CBD was tubular in shape and mildly dilated (5.7 mm diameter). The DP was within normal limits. There was concurrent diffuse, marked, tubular-to-saccular dilatation of intrahepatic bile ducts (up to 8 mm diameter). Extrahepatic bile ducts were diffusely, markedly dilated and saccular in appearance (up to 1 cm diameter). Diffusely throughout the biliary tree there was a small amount of echogenic sediment. A small volume of anechoic peritoneal effusion was noted.
An EHBDO was ruled out owing to normal total bilirubin. Cholecystocentesis and bile culture were recommended but declined. Given the concurrent diffuse, saccular intrahepatic dilatation, and the absence of EHBDO, medical management was favored. The cat was medically managed for presumptive cholangitis/cholangiohepatitis; it was treated with antibiotics (amoxicillin–trihydrate/clavulanate potassium, 15 mg/kg PO q12h; metronidazole 10 mg/kg PO q12), liver protectants (s-adenosylmethionine, 35 mg/kg PO q24h), antacids (omeprazole, 2 mg/kg PO q24h) and antiemetics (maropitant citrate, 1 mg/kg PO q12h). The owner reported improved appetite but persistent diarrhea 1 week following initial examination. Additional follow-up information was not available for this cat; however, the referring veterinarian records indicated that the cat was euthanized within 1 month.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.5, 'kg']}",10,9.5,10.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.5 kg. Hence, the patient's maintenance fluid is 2.5 kg * 4 mL/kg/hr = 10.0 mL/hr.
Hence, the patient's fluid maintenance is 10.0 mL/hr."
5220,22,Maintenance Fluids Calculations,physical,decimal,usmle-1230,Extracted,"A 30-year-old woman comes to the physician because of severe headaches and lightheadedness for 2 months. She has also been hearing a 'swoosh' sound in her left ear for the past month. She has allergic rhinitis and acne. Her sister is being treated for thyroid cancer. Current medications include levocetirizine, topical clindamycin, and azelastine-fluticasone nasal spray. She appears anxious. She is 155 cm (5 ft 1 in) tall and weighs 77 kg (170 lb); BMI is 32 kg/m2. Her temperature is 37°C (98.6°F), pulse is 96/min, respirations are 14/min, and blood pressure is 168/96 mm Hg. Examination shows cystic acne over the face and back. The pupils are equal and reactive. There is a bruit on the left side of the neck. The lungs are clear to auscultation. Cardiac examination shows no murmurs, rubs, or gallops. The abdomen is soft and nontender. There is an abdominal bruit on the left side. Neurologic examination shows no focal findings.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [77.0, 'kg']}",117,111.15,122.85,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 77.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (77.0 kg - 20 kg) = 117.0 mL/hr.
Hence, the patient's fluid maintenance is 117.0 mL/hr."
5221,22,Maintenance Fluids Calculations,physical,decimal,pmc-4555212-1,Extracted,"A 65-year-old Japanese woman was admitted to our hospital for the evaluation of rapidly progressive renal dysfunction. At the age of 60 years (April 2000), hypertension was detected, and treatment with amlodipine was started. Subsequently, proteinuria (41 mg/dl) was noted, and serum creatinine (Cre) was 0.94 mg/dl. On September 3, 2005, edema of the bilateral lower extremities was noted with exacerbation of hypertension (200/110 mm Hg). She was admitted to hospital 2 days later on September 5.
On admission, her height was 154 cm, her weight was 48.2 kg, her blood pressure was 152/92 mm Hg, and her temperature was 35.9°C. No enlarged lymph nodes were palpable. Inspiratory and expiratory sounds were normal on auscultation. Both neurological examination and cutaneous examination revealed no abnormalities. There was pitting edema of the bilateral lower extremities. Laboratory findings are shown in table . Urea nitrogen was 41 mg/dl, and Cre was 2.7 mg/dl. CRP was 0.1 mg/dl, and the erythrocyte sedimentation rate was 53 mm/h. Soluble interleukin-2 receptor was elevated to 1,680 U/ml (normal range: 250–590). Urine sediment contained 6–10 erythrocytes per high-power field. Examination of a 24-hour urine specimen revealed excretion of 1.51 g of protein.
Computed tomography showed a normal liver and spleen with no lymphadenopathy. Both kidneys were small with a long axis of 9 cm bilaterally (fig. ). Echogenicity of the renal cortex was increased on ultrasonography (fig. ). Scintigraphy with 67Ga-citrate only showed positive uptake by the kidneys.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [48.2, 'kg']}",88.2,83.79,92.61,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 48.2 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (48.2 kg - 20 kg) = 88.2 mL/hr.
Hence, the patient's fluid maintenance is 88.2 mL/hr."
5222,22,Maintenance Fluids Calculations,physical,decimal,pmc-5473308-1,Extracted,"A 1-year-old male child of 7 kg weight reported with a history of abdominal distension since day one of life. The child was full term and had passed meconium on day 1 of life. The abdominal distension and gradually and progressively increased in size to its present status. The child was evaluated with ultrasound abdomen and contrast-enhanced computerized tomography scan of the abdomen which showed a 10 cm × 7.8 cm × 9 cm hypodense lesion in retroperitoneum in the infrarenal location. The mass was seen extending from L1 to L5 vertebrae, abutting abdominal wall anteriorly, and vertebral column posteriorly []. On Doppler evaluation, the mass had some color flow suggestive of pseudoaneurysm, but both common iliac and external iliac were patent with normal flow pattern.
Abdominal exploration through a midline laparotomy incision revealed a large abdominal aortic aneurysm extending from the infrarenal up to the bifurcation of aorta []. The left kidney was compressed with the aneurysm and left renal artery and vein were stretched out. Suprarenal aorta was of normal caliber, but part of the abdominal aorta at proximal junction of the aneurysm was of pinhole caliber suggestive of inflow agenesis. Celiac artery, superior mesenteric artery, and bilateral common iliac arteries were looped, and aneurysm wall was opened. The wall of the aneurysm was densely calcified with extensive intramural thrombus. Partial excision of the wall was done [], and the infrarenal aorta was replaced with 10 mm Dacron graft []. Postoperatively, the child had an uneventful recovery and a computed tomography (CT) angio performed in the follow-up showed that the graft was patent with good distal run off [].","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.0, 'kg']}",28,26.6,29.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.0 kg. Hence, the patient's maintenance fluid is 7.0 kg * 4 mL/kg/hr = 28.0 mL/hr.
Hence, the patient's fluid maintenance is 28.0 mL/hr."
5223,22,Maintenance Fluids Calculations,physical,decimal,pmc-8260192-1,Extracted,"A 44-year-old male with past history of mutism was brought in by his family for significant weight loss with associated intermittent abdominal pain, weakness and lethargy over a period of years. Per the family, he used to be overweight four years ago. The patient has been living in Haiti his entire life and recently migrated to the United States one month ago. Per the patient’s family, he has had chronic abdominal pain for five years associated with weight loss of nearly 100 lbs. His family also reported that he had poor nutritional intake; he could only eat a small amount before he seemed to be in pain, and eventually refused to eat. He also exhibited constipation, passing small hard stools once every few days. He had no other prior medical history, no family history of malignancy, no history of trauma or surgeries, no history of smoking or substance use, and did not take any medications. The gastroenterology team was consulted to investigate the etiology of abdominal pain and chronic weight loss.
 
The patient was non-verbal but did follow some commands. When asked to point to the area of pain, he pointed to his epigastrium. He was unable to assist much further in answering questions.
His vital signs were normal. His height was 5’ 8”, weight was 90 lbs, and body mass index (BMI) was 13.7 kg/m2. Physical exam revealed a thin cachectic male with a scaphoid abdomen and mild tenderness in the epigastrium. His abdomen was otherwise soft and non-distended with normal bowel sounds, no guarding or rebound tenderness, and Murphy’s sign could not be elicited. No abdominal bruit could be heard on auscultation. His skin was dry with tenting and his mucous membranes were dry. There was no scleral icterus. Cardiopulmonary exam was normal. He was nonverbal, but cooperative and calm, with spontaneous movement observed in all extremities without evidence of focal weakness. There were no signs of skin rash or bruising.
Labs were significant for mild normocytic anemia with hemoglobin 13.1 g/dL. Chemistry panel was normal. Hepatic function panel showed a mildly elevated aspartate aminotransferase and alanine aminotransferase at 60 U/L and 74 U/L, respectively, mildly reduced albumin at 3.4 g/dL and elevated alkaline phosphatase at 199 U/L. Lactic acid, amylase, lipase, erythrocyte sedimentation rate and c-reactive protein were normal. Stool samples were negative for bacteria, viruses, ova and parasites. Abdominal X-ray revealed a normal bowel gas pattern without signs of obstruction.
Abdominal duplex and computed tomography abdominal angiography were performed (Figures -).
The mesenteric vascular duplex revealed patency of the abdominal aorta with a peak velocity of 152 cm/second (Figure ), whereas examination of the celiac trunk demonstrated severe grade stenosis with a pre-stenotic velocity of 152 cm/second and a remarkably high post-stenotic velocity of 520 cm/second (Figure ). The pre-stenosis velocity to post-stenosis velocity ratio was greater than 3:1. Interestingly, the peak velocity did not vary significantly with respiration, which may have indicated chronic fibrotic changes in the wall of the celiac artery secondary to compression over time. Subsequently, contrast-enhanced computed tomography angiography of the abdomen revealed acute angle J-configuration of the takeoff of the celiac axis, with stenosis (red arrow) at its origin and focal post-stenotic dilatation (Figure ). Thus, the diagnosis of celiac artery compression syndrome was made. The patient is currently pending evaluation for surgical division of the median arcuate ligament in order to decompress the stenosis at the origin of the celiac artery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [90.0, 'lbs']}",80.82328,76.78212,84.86444,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 90.0 lbs so this converts to 90.0 lbs * 0.453592 kg/lbs = 40.82328 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (40.82328 kg - 20 kg) = 80.82328 mL/hr.
Hence, the patient's fluid maintenance is 80.82328 mL/hr."
5224,22,Maintenance Fluids Calculations,physical,decimal,pmc-7250996-1,Extracted,"A 2670-gram male boy was a product of consanguineous marriage born to a 25-year-old gravida 4, para 3 mother at 40 weeks of gestation by cesarean section due to decreased fetal movement and late deceleration CTG findings.
There was no history of chronic illness or drug intake and no radiation exposure.
Baby delivered with Apgar scores 5; 7 and 7 on 1; 5 and 10 minutes, respectively.
Positive pressure ventilation was initiated due to mild respiratory distress. Venous cord gases were within the normal range. The baby shifted to the neonatal intensive care unit where was intubated due to worsening respiratory distress and started on conventional ventilation.
On examination, there were no apparent dysmorphic features.
To achieve oxygen saturation, 95% baby was needed FIO2 40%. There was mild intercostal retraction and tachypnea with respiratory rate range around 70 breath per min.
The abdomen was significantly distended with bluish discoloration and tense.
Chest radiography showed bilateral hazy lung appearance.
The abdominal radiography revealed a central gastric bubble with the displacement of the orogastric tube to the right side with no visible bowel pattern (Figure ).
Ultrasound abdomen showed a huge distended stomach with the displaced liver. Spleen could not be visualized (Figure ).
Upper gastrointestinal contrast study findings revealed incomplete gastric volvulus and malrotation of C-loop of the duodenum but no obstruction (Figure ).
Echocardiography showed hypoplastic left heart syndrome, mitral atresia, large ventricular septal defect (VSD), and interrupted aortic arch. Prostaglandin E1 continuous infusion was started.
After summarizing all available data, we considered that most probably the patient has heterotaxy right isomerism (asplenia), complex congenital heart disease, and malrotation.
Laparotomy performed on the 1st day of life showed malrotation with multiple jejunal atresia (sausage bowel), nonretracting dusky bowel with short mesentery, abnormal central position of the liver, and no spleen could be detected during the surgical procedure. The jejune-jejunal anastomosis was performed after resection of dead bowel with preserved 35 cm of bowel remaining from the duodenojejunal junction and 35 cm from the distal part.
A peripheral blood smear was undertaken to check for the presence of Howell-Jolly bodies to ascertain that there is no splenic function but the result did not demonstrate Howell-Jolly bodies.
For confirmation of the diagnosis of asplenia, a computed tomography abdomen was requested that reported the presence of the spleen in form of five well-defined small cysts like appearance located in the right upper quadrant lateral to the right suprarenal gland, below and medial to the right hepatic lobe suggestive of polysplenia syndrome. Hepatic parenchyma was homogeneously enhanced and the liver enlarged, measuring 9.4 cm in length. The kidneys and pancreas were normal. Bilateral slightly prominent adrenal glands with no focal lesion were reported. The intrahepatic portion of inferior vena cava was visualized and normal. The visualized lung bases and bony skeleton are grossly unremarkable (Figure ).
Standard spleen scan using 99mTc-Sulfur-colloid showed evidence of focal area of intense activity in the right upper quadrant of the abdomen, highly suggestive of polysplenia with adequate functional status (Figure ).
The baby was gradually weaned from ventilatory support and extubated day 7 of life to nasal cannulae and then to room air.
Feeding was started that gradually increased until he received full maintenance feeds.
The case was referred to the higher cardiac center for cardiac defect repair but rejected due to poor outcome of repair hypoplastic left heart syndrome and palliative care was applied.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2670.0, 'g']}",10.68,10.146,11.214,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2670.0 g so this converts to 2670.0 lbs * kg/1000 g = 2.67 kg. Hence, the patient's maintenance fluid is 2.67 kg * 4 mL/kg/hr = 10.68 mL/hr.
Hence, the patient's fluid maintenance is 10.68 mL/hr."
5225,22,Maintenance Fluids Calculations,physical,decimal,pmc-7713836-1,Extracted,"Written informed consent was obtained from the patient for the presentation and publication of this case report.
A 40-year-old, 56-kg Korean woman (gravida 4, para 2) was scheduled for an emergency cesarean section at 35 weeks and 3 days of gestation for preterm labor. Her medical history included one abortion and two prior cesarean sections for placenta previa.
In the preoperative laboratory tests, her hemoglobin (Hb) was 11.4 g/dl and platelet count was 247,000/μl. Other laboratory findings, including coagulation tests, were within the normal range. On her ultrasound examination, the placenta was suggestive of placenta previa totalis, with possible placenta accreta ().
In the operating room, spinal anesthesia was performed at the L3–4 intervertebral space of the patient. After confirming the spontaneous flow of cerebrospinal fluid, 10 mg of 0.5% heavy bupivacaine and 10 μg of fentanyl were intrathecally injected using a 27-gauge (G) needle. The maximum sensory blockade level of anesthesia was T4. To prepare for arterial blood pressure monitoring, a 22 G angiocatheter was inserted into the right radial artery. Two 18 G intravenous lines were secured in both arms.
Three minutes after starting the operation, a female baby (2,590 g) was delivered with Apgar scores of 7 and 8 at 1 and 5 min, respectively. After the baby was delivered, the patient’s blood pressure suddenly decreased to about 60/40 mmHg and her heart rate was 70 beats/min. Massive bleeding was found in the surgical field. Her Hb level was 6.8 mg/dl at that time. The surgeon diagnosed the degree of placental adhesion as percreta, which had invaded the bladder and surrounding tissues. The bleeding was so extensive that the surgeon decided to perform a hysterectomy. Because of profound hypotension with a reduction in consciousness, the anesthetic method was changed to general anesthesia. Tracheal intubation was performed to secure the airway with rapid sequence intubation. An additional intravenous line was secured at the right external jugular vein, and rapid volume infusions and transfusions were performed using a rapid blood infuser (FMS 2000® fluid management system, Belmont Instrument Corp., USA). Despite attempts to ligate the uterine arteries, bleeding obscured the surgical field and resulted in further hemodynamic instability. The surgeon wished to perform a uterine artery embolization for bleeding control but it was difficult to maintain stability of the vital signs while transferring the patient to the intervention room. We, therefore, decided to implement a REBOA in the operation room to prevent hypovolemic shock. The acute care surgeon accessed the left femoral artery for the REBOA using a 7-French sheath (standard kit, Terumo, Vietnam) and inserted a balloon catheter (occlusion balloon catheter, Tokai Medical Products, Inc., Japan). After measuring the distance to the navel, 25 cm in this patient, they slid the balloon tip up to 25 cm from the punctured site and placed the balloon approximately between the infrarenal aorta and the bifurcation of the aorta. It was difficult to obtain radiologic confirmation of the balloon position because of the patient’s unstable vital signs. After balloon occlusion was accomplished, the systolic blood pressure immediately improved from 65 mmHg to 100 mmHg and the surgical field also improved (). REBOA was intermittently performed during the surgery and the balloon was sometimes partially deflated to identify the focus of the bleeding. During complete and partial inflation, ligation of both the uterine artery and internal iliac artery were performed. And the bleeding control was in progress by removing surrounding tissues where the placenta was invaded. The total duration of the occlusion was 75 min (divided over several occlusion times). The total operative time was 263 min and the total anesthesia time was 290 min. The estimated amount of blood volume lost was over 20,000 ml. Massive transfusions, including 36 units of packed red blood cells, 26 units of fresh-frozen plasma, and 10 units of platelets were administered.
Upon admission to the intensive care unit after embolization of the branch of the internal iliac artery, the patient was hemodynamically stable without any inotropes or vasopressors. No further transfusions were performed after surgery. The patient’s Hb was 12.2 g/dl, platelets were 89,000/μl, and prothrombin time (PT, international normalized ratio) and activated partial thromboplastin time (aPTT) were 13.9 s (1.23) and 39.1 s, respectively. The patient was extubated the same day and the femoral artery sheath was removed the next day. At postoperative day two, she was transferred to the ward and subsequently discharged on day 15 without complications. Neither the mother nor the baby experienced any complications after discharge.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [56.0, 'kg']}",96,91.2,100.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 56.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (56.0 kg - 20 kg) = 96.0 mL/hr.
Hence, the patient's fluid maintenance is 96.0 mL/hr."
5226,22,Maintenance Fluids Calculations,physical,decimal,pmc-5890554-1,Extracted,"A 9-month-old female infant was initially admitted to our hospital due to acute bronchiolitis. In her history, she was born with a sacral myelomeningocele and had undergone surgery for this condition at the age of 1 week, but a ventriculoperitoneal shunt was not required. The patient was the first child of unrelated Turkish parents. She was born at term after an uneventful gestational delivery. She also had no history of repeated infections, cardiac anomalies, or seizures. A physical examination demonstrated a weight and head circumference of 6 kg (3rd percentile) and 40 cm (3rd percentile), respectively, and her height was 68 cm (50th percentile). She showed atypical facial features, hypertelorism, short philtrum, micrognathia, low set ears, fish-like mouth, and a wide nasal bridge. A neurological examination revealed hypotonia, with no movement in the bilateral lower limbs, and a surgical scar was found surrounding the region of the repaired myelomeningocele. Her cardiac examination was normal. Laboratory investigations including a thyroid function test, parathyroid hormone levels, and other routine hematology and biochemical parameters were within normal limits. In the chest X-ray, the thymus could not be identified. The echocardiogram was unremarkable. There were no renal anomalies on clinical or ultrasound examinations. Peripheral lymphocyte subsets revealed a mild T-cell deficiency with CD3 (28%), CD4 (21.5%), CD8 (10.5%), CD 19 (38%), and normal levels of immunoglobulins. Her mother’s facial features appeared mildly dysmorphic. She had mild mental retardation with learning disabilities, a nasal voice, and hypothyroidism. She had no history of seizures or repeated infections. Her serum calcium, parathyroid hormone levels and echocardiography were normal. In view of the facial dysmorphism in both the patient and her mother and the presence of a T-cell deficiency, we suspected DGS. Both the patient’s and mother’s chromosomal examinations with fluorescence in situ hybridization analysis showed a chromosome 22q11.2 deletion. On the basis of these results, we accepted the diagnosis of DGS. At the age of 1 year, the patient experienced a clonic seizure while calcium concentration was normal. An electroencephalogram and brain magnetic resonance imaging were within normal limits. The seizure repeated a second time after 1 month while serum calcium concentrations were normal limits. Antiepileptic medications controlled the seizure.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.0, 'kg']}",24,22.8,25.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.0 kg. Hence, the patient's maintenance fluid is 6.0 kg * 4 mL/kg/hr = 24.0 mL/hr.
Hence, the patient's fluid maintenance is 24.0 mL/hr."
5227,22,Maintenance Fluids Calculations,physical,decimal,pmc-6230595-1,Extracted,"A 45-year-old male with no past medical history was transferred to our tertiary care facility after presenting to a community hospital with a one-week history of generalized abdominal pain, jaundice, dark urine, and lower extremity edema. His initial evaluation revealed severe hyperbilirubinemia and elevated transaminases, prompting his transfer. He denied any alcohol consumption for the previous twenty years or intravenous drug use. He had no medical history, was taking no medications prior to presentation, except a multivitamin. He denied taking any herbal supplements and his family history was unremarkable. He was married and employed as an auto mechanic.
On examination, he was notably jaundiced and cachectic in appearance with a height of 1.7 m, weight of 82.5 kg, and body mass index (BMI) of 28.3 kg/m2. He was afebrile with a pulse of 95 beats per minute, respiratory rate of 16 breaths per minute, and pulse oxygen saturation of 95% while on room air. He had marked scleral icterus; proptosis was noted. On thyroid examination, he had a large symmetrical, non-tender goiter with audible bruit. Heartbeat was irregularly irregular. His abdomen was mildly tender diffusely without ascites or organomegaly. Mild bilateral lower extremity edema was present. Skin was warm to the touch. A fine tremor was noted; asterixis of hands was intermittently present.
Initial laboratory evaluation revealed a hemoglobin of 12.1 g/dL (13.5-16.5), platelet count of 115 k/µL (150-400), and white blood cell count of 11.8 k/µL (4.5-11). His international normalized ratio (INR) was 2.4. His serum sodium was 128 mmol/L (137-147), potassium of 4.3 mmol/L (3.5-5.1) with creatinine of 1.77 mg/dL (0.4-1.24), blood urea nitrogen (BUN) of 57 mg/dL (7-25) and serum glucose 159 mg/dL (70-100). Notably, his total bilirubin was 19.8 mg/dL (0.3-1.2), direct bilirubin 13.8 mg/dL (<0.4), alkaline phosphatase 332 U/L (25-110), aspartate aminotransferase (AST) 86 U/L (7-40), and alanine aminotransferase (ALT) 50 U/L (7-56). His gamma-glutamyltransferase was 20 U/L (9-64). Total iron was 32 mcg/dL (50-185), percent iron saturation 11% (28%-42%), total iron binding capacity (TIBC) was 283 mcg/dL (270-380), and ferritin 121 ng/mL (30-300). The patient also had negative serology for hepatitis A, B, and C.
A workup for thyroid dysfunction demonstrated a thyroid-stimulating hormone (TSH) of 0.026 mcg/mL (0.35-5.00) with a free T4 of 4.3 ng/dL (0.6-1.6), free T3 4.6 pg/mL (2.1-3.9), and total T3 125 ng/dL (87-180). TSH receptor antibody was>40 IU/L (0.00 −1.75) and thyroid peroxidase (TPO) antibody was >1000 IU/mL (<5.61). An ultrasound of the patient's thyroid was notable for a mildly enlarged heterogeneous and hypervascular thyroid without nodularity. Based on these findings along with his presenting symptoms and signs, the patient was diagnosed with Graves’ disease.
In light of worsening cholestatic jaundice (Figure ), a thorough hepatology evaluation was undertaken for potential autoimmune, infectious, and primary hepatobiliary causes of cholestasis. The laboratory testing were all negative. Cardiac evaluation was notable for an ejection fraction of 55%-60% with right ventricular dilation and moderate mitral regurgitation. Moderate left atrial and severe right atrial enlargement was found with elevated central venous pressure as well as pulmonary artery pressure. Abdominal ultrasound demonstrated increase echogenicity of the liver and revealed trace abdominal and pelvic ascites. Further workup for cholestatic jaundice included a computed tomography scan of the abdomen and pelvis, which was notable for fatty liver, cardiomegaly, and diffuse irregular appearance of bones with prominent trabecula. Endoscopic retrograde cholangiopancreatography (ERCP) showed normal caliber common bile duct and common hepatic duct with normal intrahepatic ducts, without filling defects, strictures, or stenosis. Endoscopic ultrasound (EUS) was notable for normal pancreatic parenchyma as well as normal pancreatic and common bile ducts. The patient subsequently underwent transjugular liver biopsy with unremarkable hepatic vein pressures and a corrected sinusoidal pressure gradient of 5-6 mm Hg (normal). Pathology showed cholestasis and mild ductal proliferation with focal pericholangitis but no hepatic steatosis, fibrosis, hepatocellular injury, or necrosis. Periodic acid-Schiff (PAS) diastase digestion showed normal glycogen content without unusual intrahepatic inclusions; hepatic iron stores were normal.
Prior to transfer to our facility, he was initially stabilized with intravenous diltiazem drip 5 mg per hour titrated for rate control of his atrial fibrillation with rapid ventricular response, in combination with hydrocortisone 50 mg every eight hours and propylthiouracil (PTU) 150 mg every six hours for management of thyrotoxicosis. Due to concern for fulminant liver failure, urgent transfer was pursued to our facility. Upon arrival, the patient's thyrotoxicosis and resultant atrial fibrillation and diastolic heart failure were managed aggressively given his calculated Burch-Wartofsky score of 45. PTU was stopped in light of FDA black box warning, and methimazole was initiated at a dose of 20 mg every 8 hours; corticosteroids were continued for management of thyroid storm until normalization of total T3. The patient experienced gradual improvement in his free T4 (Figure ). His atrial fibrillation was managed with oral digoxin 125 µg after digitalizing doses and metoprolol 100 mg oral twice daily.
While the index of concern for acute liver failure prompted a swift and extensive investigation, it was entirely negative for primary hepatobiliary causes of his cholestasis including ERCP, EUS, and transjugular liver biopsy. Based on negative rheumatologic, autoimmune, and infectious causes workup, it was concluded that his cholestatic jaundice was related to Graves’ disease related thyrotoxicosis. This clinical hunch was further solidified with his clinical and metabolic improvement (Table ). Total bilirubin was 13.9 mg/dL on admission to the outside facility, peaking 17 days later at 39.1 mg/dL and improving to 14.0 mg/dL two weeks following discharge. An important point that needs to be made was his high bone-specific alkaline phosphatase, which was markedly elevated at 103 mcg/L (0-20), demonstrating a high bone turnover state related to his hyperthyroidism. The patient was discharged two weeks after his hospitalization with plans for definitive outpatient management of Graves’ disease.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [82.5, 'kg']}",122.5,116.375,128.625,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 82.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (82.5 kg - 20 kg) = 122.5 mL/hr.
Hence, the patient's fluid maintenance is 122.5 mL/hr."
5228,22,Maintenance Fluids Calculations,physical,decimal,usmle-259,Extracted,"A 38-year-old woman, gravida 4, para 3, at 20 weeks' gestation comes to the physician for a prenatal care visit. She used fertility enhancing treatment for her current pregnancy. Her other children were born before 37 weeks' gestation. She is 170 cm (5 ft 7 in) tall and weighs 82 kg (180 lb); BMI is 28.4 kg/m2. Her vital signs are within normal limits. The abdomen is nontender, and no contractions are felt. Ultrasonography shows a cervical length of 22 mm and a fetal heart rate of 140/min.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [82.0, 'kg']}",122,115.9,128.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 82.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (82.0 kg - 20 kg) = 122.0 mL/hr.
Hence, the patient's fluid maintenance is 122.0 mL/hr."
5229,22,Maintenance Fluids Calculations,physical,decimal,pmc-2740003-1,Extracted,"A 23-year-old gravida 0, para 0, Caucasian female graduate student weighing 55 kg and 160 cm in height presented to her primary care physician with discolored digits (1 through 3) on both of her feet. She also complained that her toes were painful, blistered, and intermittently pruritic. She stated her symptoms had begun the day after receiving a pedicure before going out to a university event that same evening. The patient's vital signs were blood pressure 120/62 mm Hg, heart rate of 70 beats per minute, and respirations 14 per minute. Physical examination of her heart and lungs was unremarkable. Her medical and surgical histories were negative. She was a non-smoker and consumed less than 6 ounces of alcohol per week. She had no allergies. The primary care physician prescribed cephalexin 500 mg by mouth daily for 10 days for a presumed bacterial infection.
Ten days later she still complained of discoloration, blisters and pain, and decided to visit an Emergency Department (ED) for a second opinion. The ED physician diagnosed CA-MRSA based on the physical presentations of the lesions and the increased incidence of MRSA in the community. Trimethoprim-sulfamethoxazole double strength (160 mg/800 mg) orally every 12 hours for 10 days was prescribed. The symptoms and signs persisted and the patient arranged to see a dermatologist, who performed a biopsy of the third digit (left foot). The dermatologist declined to prescribe further treatment until the biopsy returned. The biopsy revealed a histological diagnosis of perniosis (see ,). On further inquiry by the dermatologist, the patient stated that the evening after her pedicure she had spent several hours walking outdoors before the aforementioned university event. She had worn open-toed shoes and the wind chill factor that evening had gone as low as 0° F.
The patient was counseled to keep her feet warm and avoid damp conditions. No other medications were administered and the symptoms resolved three weeks later (mid-April) with conservative care and the return of warmer ambient temperatures.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [55.0, 'kg']}",95,90.25,99.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 55.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (55.0 kg - 20 kg) = 95.0 mL/hr.
Hence, the patient's fluid maintenance is 95.0 mL/hr."
5230,22,Maintenance Fluids Calculations,physical,decimal,pmc-5353830-1,Extracted,"A 7-month-old male child presented with jaundice along with high-colored urine and clay-colored stools since birth. There were no antenatal problems and birth was uneventful with birth weight of 3 kg. He was on exclusive breast feeds. At 5 months of age, he had been hospitalized and a liver biopsy had been done that showed cholestasis with vacuolated appearance of hepatocytes and mild bile duct proliferation with cholangioles, showing bile and thrombi suggestive of primary sclerosing cholangitis. His serial liver function tests are depicted in . On examination, weight was 5.9 kg and height was 67 cm. He was deeply jaundiced and had hepatosplenomegaly and ascites with palmar erythema. Other systems were normal. Ultrasound of the abdomen showed coarse echotexture of the liver, with normal gallbladder and common bile duct. He was started on Vitamins A, D, E, and K along with spironolactone and ursodeoxycholic acid and advised regarding liver transplant.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.9, 'kg']}",23.6,22.42,24.78,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.9 kg. Hence, the patient's maintenance fluid is 5.9 kg * 4 mL/kg/hr = 23.6 mL/hr.
Hence, the patient's fluid maintenance is 23.6 mL/hr."
5231,22,Maintenance Fluids Calculations,physical,decimal,pmc-5995021-1,Extracted,"A 47-year-old female patient with a nine-month history of growing thyroid goiter causing dyspnea was evaluated for total thyroidectomy. Laboratory examination, chest X-ray, and electrocardiography revealed no abnormality. The patient had hypertension, hypothyroidism, and severe obesity (body mass index 39.8 kg/m2, height 152 cm, weight 92 kg). She was suffering from severe obstructive sleep apnea that was intolerable in supine position.
Pre-operative airway assessment revealed several challenging aspects that strongly suggested difficult airway management. Her neck circumference was 51 cm with a huge thyroid goiter covering the entire anterior portion of the neck. Thickness of soft tissue measured from neck computer tomography (CT) was 49 mm that made palpation of the thyroid cartilage from the skin impossible. On neck CT, trachea was compressed bilaterally and posteriorly with slight deviation to the right side by the huge thyroid mass (). Her mouth opening was 3 cm, and thyromental distance could not be measured. Range of motion of the neck was 70 degrees from full flexion to full extension. Patient’s Mallampati class was IV. All options to secure the airway, from cricothyrotomy to laryngeal mask airway, were considered. However, due to location and size of the goiter and instability of the airway considering surgery, direct orotracheal intubation was inevitable.
On the day of surgery, we prepared the McGrath® MAC video laryngoscope (Aircraft Medical, UK), a fiberoptic bronchoscope (Olympus Optical, Japan), a laryngeal mask airway (LMA), and a cricothyrotomy set (Cook® Medical, USA) in case of intubation failure. On arrival in the operating room (OR), non-invasive blood pressure monitoring, electrocardiogram, and pulse oximetry were established. The monitoring revealed initial blood pressure of 159/89 mmHg, heart rate of 83 beats/min, and peripheral arterial oxygen saturation (SpO2) of 93% while breathing room air. In head up position (30 degrees), pre-oxygenation with 100% oxygen was conducted for three minutes, achieving saturation of 99%. Induction was conducted with intravenous injection of propofol 200 mg and succinylcholine 100 mg. Initial attempt with direct laryngoscopy failed due to grade IV difficulty. Following attempt with the McGrath® MAC video laryngoscope (blade size 3) with application of cricoid pressure also failed due to small oral cavity, visual field being limited to posterior part of arytenoid, and arytenoid cartilage edema () that made access to vocal cords more difficult. As our third choice, we planned awake intubation with fiberoptic bronchoscope. Hydrocortisone 100 mg was injected to prevent further airway edema and 4% lidocaine was sprayed to anesthetize the airway. During the procedure, we had to apply mask ventilation periodically because the patient presented hypoxia. Due to unpredictable airway movement caused by spontaneous breathing, low patient compliance, and small oral cavity along with progression of airway edema including epiglottis, our attempt at intubation failed again. We had to abort the procedure as patient revealed signs of respiratory failure including hypoxia (SpO2 88%) and hypercapnia (end tidal CO2 62 mmHg). After injecting second dose of hydrocortisone 100 mg, we secured the airway with air-Q® intubating LMA (Cookgas®LLC, USA). Intubation of endotracheal tube (ETT) was attempted through LMA, but the tube could not be advanced due to edema of glottal area caused by multiple intubation trials. After confirming adequate ventilation with capnography, we transferred patient to surgical intensive care unit (SICU) under assisted ventilation with ambu bag and conducted respiratory care with a mechanical ventilator. Arterial blood gas analysis was pH 7.21, PaCO2 52 mmHg, PaO2 93 mmHg, base excess −7.7, and SaO2 95%. As patient’s condition improved on monitoring and arterial blood gas analysis, LMA was removed. After two days, patient was sent to a general ward.
After nine days, patient returned to the OR. Routine monitoring was established along with left radial artery cannulation under local anesthetic. After preparation of the airway with solucotef nebulizer, two trials of awake intubation with fiberoptic bronchoscope and video laryngoscope were attempted but failed again. We applied a fiberoptic bronchoscope (external diameter 5.9 mm; Olympus Optical, Japan) and the McGrath® MAC video laryngoscope (blade size 3) simultaneously (). Due to increasing discomfort and incompliance of the patient, intravenous injection of propofol 150 mg and succinylcholine 90 mg was administered. Intubation was conducted by two anesthesiologists. We secured oral cavity space with a video laryngoscope, thus improving visual field of the airway and simultaneously and manipulated fiberoptic bronchoscopy into the vocal cord. Visual confirmation of intra-tracheal placement of the fiberoptic scope was made on both sides, and ETT was pushed in along the fiberoptic bronchoscope. After confirming adequate ventilation with capnography and pulse oximetry, patient underwent total thyroidectomy as planned. After removing 220 g and 250 g of goiters from right and left side the patient was sent to SICU with spontaneous ventilation through ETT. Extubation was conducted after a day, and the patient was discharged after 10 days without complications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [92.0, 'kg']}",132,125.4,138.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 92.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (92.0 kg - 20 kg) = 132.0 mL/hr.
Hence, the patient's fluid maintenance is 132.0 mL/hr."
5232,22,Maintenance Fluids Calculations,physical,decimal,pmc-3024961-1,Extracted,"A 43-year old Caucasian male with no remarkable medical history, was referred to our clinic with intermittent jaundice and a 1-month history of nausea, vomiting, pruritus, dark urine, clay-colored stools and weight loss of 5 kg. The patient did not report abdominal pain or decreased appetite.
On admission, the patient's liver function tests (LFTs) were abnormal; aspartate aminotransferase (AST) 78 IU/L (normal, < 45 IU/L), alanine aminotransferase (ALT) 109 IU/L (normal, < 45 IU/L), alkaline phosphatase (ALP) 226 IU/L (normal, 40-150 IU/L), γ-glutamyl transpeptidase (γGT) 932 IU/L (normal, 10-55 IU/L), total bilirubin 1.3 mg/dl (normal, 0.21-1.2 mg/dl) and direct bilirubin 0.9 mg/dl (normal, < 0.5 mg/dl), while the tumour markers CEA, CA 19-9 and AFP were within normal range.
Contrast enhanced computed tomography (CT) of the abdomen revealed dilatation of the biliary tree, with the hepatic duct measuring a diameter of 1.8 cm. Neither lymph node enlargement nor splenomegaly was demonstrated. Magnetic resonance cholangiopancreatography (MRCP) showed dilated intrahepatic and extrahepatic bile ducts including the cystic duct and the gallbladder. The common bile duct (CBD) measured 1.4 cm in diameter with an abrupt concentric stenosis in its lower third and a cut-off point located 1 cm distally to the duodenal ampulla. The pancreatic duct was depicted as normal (Figure ).
Endoscopic ultrasonography (EUS) demonstrated the duodenal ampulla of Vater thickened and the CBD dilated with the presence of thick content.
The patient underwent an endoscopic retrograde cholangiopancreatography (ERCP). The ampulla of Vater was depicted as being infiltrated by the neoplasm. An endoscopic sphincterotomy was carried out, thus letting us better view and sample the region, and the biopsies taken revealed the presence of an undifferentiated neoplasm, but no definitive diagnosis was made.
Taking into consideration the aforementioned findings, our decision was to operate on the patient, and we performed a pylorus-preserving pancreaticoduodenectomy with the en bloc resection of the area in question and surrounding structures, including the regional lymph nodes.
Histopathological and immunohistochemical study of the surgical specimen revealed infiltration of the duodenum by a non-Hodgkin B cell lymphoma, predominantly of nodular type, with characteristics of grade I follicular lymphoma [World Health Organization (WHO) classification] with G(λ)+ clonicity and indicative immunohistochemical examination (CD 10+, bcl-2-) (Figure ). In addition, an intramucosal carcinoid of the CBD, measuring a diameter of 0.3 cm, was identified. All eight excised lymph nodes were normal (Figure ).
Postoperatively, the patient was further staged. Regarding the lymphoma, we conducted a CT scan of the neck and chest as well as a bone marrow biopsy to exclude extra-enteric lesions, and we proceeded with a video capsule endoscopy in order to exclude multifocal involvement of the small intestine []. All these additional exams yielded no findings. As far as the carcinoid was concerned, the levels of the neuroendocrine markers 5-HIAA (5-hydroxyindoleacetic acid), CgA (chromogranin A) and NSE (neuron-specific enolase) were found within normal range. Because of the small size and histology of the carcinoid, no other imaging modalities such as Octreoscan or MIBG (meta-iodobenzylguanidine) scintigraphy were used [].
The follow-up of the patient includes a complete blood count, routine biochemical exams and an abdominal CT scan every six months after surgery, supported with an annual evaluation of CgA levels [,]. Eighteen months after the resection, neither the lab tests nor the imaging techniques have revealed any recurrence of the disease nor has the patient referred any symptoms.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.0, 'kg']}",20,19,21,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.0 kg. Hence, the patient's maintenance fluid is 5.0 kg * 4 mL/kg/hr = 20.0 mL/hr.
Hence, the patient's fluid maintenance is 20.0 mL/hr."
5233,22,Maintenance Fluids Calculations,physical,decimal,pmc-6016000-1,Extracted,"A nine-year-old girl presented to the emergency department with abdominal pain and distention for the past one week, with sudden increase in intensity of pain for the last four hours. The patient had not yet reached the age of menarche. There was no associated nausea or vomiting and her bowel habits were not affected. Past medical, surgical, and family history was also insignificant. An abdominal examination revealed tenderness in the lower abdomen with a firm palpable mass occupying the right side of the abdomen. Her blood counts showed an elevated total leukocyte count of 13,000 cells/dL with neutrophilic predominance. Initial clinical assessment raised the possibility of an appendicular mass.
The patient therefore immediately underwent a contrast-enhanced computed tomography (CT) scan of the abdomen and pelvis, which revealed a large soft tissue mass measuring approximately 80 x 150 x 170 mm in anteroposterior, transverse, and craniocaudal dimensions, respectively, and was predominantly occupying the right mid and lower quadrant. The mass showed some areas of low attenuation, suggestive of necrosis/intratumoral edema (Figure ). There was free fluid noted adjacent to the lesion and in the pelvis (Figure ). The right ovary was separately identified and appeared normal (Figure ).
Anteromedially, the mass had a tortuous, twisted vascular pedicle that was likely originating from the left adnexa (Figure ).
Additionally, few speckled calcifications were noted in the mass (Figure ). No enhancing fibrovascular septa were noted in the lesion.
No evidence of regional lymphadenopathy or distant metastases was found on the CT examination. On the basis of the radiological picture, an impression of left ovarian tumor with torsion was suggested.
The patient then underwent an exploratory laparotomy and left salpingo-oophorectomy along with partial omentectomy. Intraoperative findings included a large bilobed edematous mass weighing approximately 1.5 kg with a twisted, thickened vascular pedicle and varicosed vessels. The left fallopian tube was slightly thickened as well. No lymphadenopathy or invasion into the surrounding structures was seen.
The surgically resected specimen was then sent for histopathological analysis, which revealed a neoplastic lesion in the left ovary arranged in nests and trabeculae separated by fibrous septa. The cells were polygonal with moderate amount of clear to eosinophilic cytoplasm. The nuclei were round to oval, showed moderate plemorphism with prominent eosinophilic nucleoli and frequently visible mitotic activity. Scattered plasma cells and lymphocytes were present within the fibrous septa. In areas, tumor cells were seen scattered against edematous stroma. Thin-walled dilated and congested blood vessels were seen, suggestive of vascular compromise secondary to torsion. The neoplastic cells showed diffuse nuclear positive expression for octamer-binding transcription (OCT) 3/4 immunohistochemical stain. Intracytoplasmic glycogen was highlighted on Periodic acid-Schiff special stain (Figure ).
The overall findings confirmed mature ovarian dysgerminoma that was limited to the left ovary without capsular invasion (TNM stage: T1A, N0, M0 according to FIGO staging). The excised left fallopian tube, omentum, and peritoneal washout were all negative for malignancy.
Postoperatively, the patient showed satisfactory progress and was therefore discharged in a stable condition. She is planned for on oncology follow-up visit as an outpatient.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1.5, 'kg']}",6,5.7,6.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1.5 kg. Hence, the patient's maintenance fluid is 1.5 kg * 4 mL/kg/hr = 6.0 mL/hr.
Hence, the patient's fluid maintenance is 6.0 mL/hr."
5234,22,Maintenance Fluids Calculations,physical,decimal,pmc-7303259-3,Extracted,"A 3 year-old female intact Australian Shepherd (19 kg) was presented for investigation of a 1-month history of a progressive left head tilt in spite of treatment for possible inner ear disease (antibiotics, steroids, and myringotomy). Physical examination was unremarkable. Abnormal findings on the neurological examination included vestibular ataxia, left sided circling, marked left head tilt, and rotary nystagmus (fast phase left). Postural reactions were delayed in all limbs, but worse on the left side. A neuroanatomical localization was assigned to the brainstem and cerebellum (central vestibular dysfunction). Differential diagnoses were the same as for case 1 and 2.
A complete blood count and serum biochemistry had been performed by the referring veterinarian, was reportedly normal but was unavailable for review at the time of writing of this manuscript.
Magnetic resonance imaging of the brain and cranial cervical spine was performed using a 1.5T system (Siemens Espree; Siemens Medical Solutions, Malvern, PA, USA). Sequences included sagittal T2W, transverse T2W, T1W, T2W-FLAIR, and T2*-weighted gradient recalled echo (GRE), diffusion weighted imaging, post contrast transverse T1-weighted thin section GRE images with fat suppression (“volume interpolated breathhold examination”; “VIBE”), and post contrast T1W spin echo sequences in three planes.
On pre-contrast images there were heterogeneous T2W hyperintensities in the cranial aspect of the pons and along the lateral portion of the brainstem, more extensive on the left, and subtle optic nerve enlargement bilaterally. A small intraparenchymal area of heterogeneous T2 hyperintensity and mild syringomyelia were seen in the cranial cervical spine. Following contrast medium administration there was variable degree contrast enhancement of the orbital fissure (oculomotor, trochlear, and abducens nerves) and the optic, oculomotor, trigeminal, facial, and vestibulocochlearnerves (, Case 3). There was mild multifocal meningeal contrast enhancement as well as multifocal intramedullary and meningeal enhancement associated with the cranial cervical spine (). Cisternal CSF analysis revealed a marked mixed cell pleocytosis, which was predominantly lymphocytic (nucleated cell count of 304 cell/mm3, red blood cell count of 1 cell/mm3, and total protein of 202.7 mg/dL).
The patient was discharged with doxycycline (4 mg/kg PO q12h), clindamycin (12 mg/kg PO q12h), and prednisone (0.8 mg/kg PO q24h). She showed moderate improvement with decreased circling and an improved head tilt. Negative infectious tests were obtained 14 days later (Tick panel PCR, serology for Neospora antibodies, and Cryptococcus antigen latex). Testing for CDV was not submitted due to the same rationale provided in case 1 and 2. In turn, doxycycline and clindamycin were discontinued, and her prednisone dose was increased (to 1.6 mg/kg PO q24h).
At the time of her next recheck examination 2.5 months later, her neurological examination was unremarkable apart from a persistent mild left head tilt, and occasional circling to the left. Additional immunosuppressive medications were discussed, but declined at the time due to financial constraints. Additional recheck examinations have not been performed and the patient was lost to follow up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [19.0, 'kg']}",58,55.1,60.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 19.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (19.0 kg - 10 kg) = 58.0 mL/hr.
Hence, the patient's fluid maintenance is 58.0 mL/hr."
5235,22,Maintenance Fluids Calculations,physical,decimal,pmc-5411391-1,Extracted,"A 74-year-old female who had undergone RYGB in 1975, with lung cancer in remission and vaginal cancer complicated by rectovaginal fistula requiring colostomy diversion, presented with one month of early satiety, 40-pound weight loss, and left upper quadrant abdominal pain. Her physical exam was notable for fullness and tenderness to palpation of the abdominal left upper quadrant. Laboratory testing was notable for a normocytic anemia with hemoglobin of 8.4 g/dL and normal iron studies. Her white blood cell count, liver function tests, and lipase were within normal limits. Abdominal computed tomography (CT) revealed severe dilation of the stomach, with thickening of the pylorus and duodenal bulb consistent with gastric outlet obstruction of the excluded stomach (). Per-oral single-balloon enteroscopy was performed and revealed a normal gastric pouch and gastrojejunal anastomosis, but was unable to reach the excluded stomach because of sharp angulations of the small bowel, probably due to abdominal adhesions.
The patient was evaluated by the surgical service, who deemed her a poor surgical candidate for laparoscopic exploration. An ultrasound-guided 12-French (Fr) gastrostomy tube was placed percutaneously by interventional radiology into the excluded stomach for decompression of the gastric outlet obstruction of the excluded stomach. In subsequent months, upsizing of the gastrostomy tube tract was performed until a 24-Fr tube was in place. She then underwent endoscopic evaluation under moderate sedation using a pediatric gastroscope (EVIS EXERA III GIF-XP190N gastroscope) with an outer diameter of 5.4 mm. For this procedure, carbon dioxide was used for insufflation but no trocar was used. The patient’s existing 24-Fr gastrostomy tube was deflated and easily removed through the tract. A guidewire was coiled into the excluded stomach under endoscopic guidance. The pediatric gastroscope was advanced alongside the guidewire into the excluded stomach. A large, friable, ulcerated mass () was identified and multiple biopsies were taken, later identified as poorly differentiated adenocarcinoma with signet ring and mucinous features consistent with primary gastrointestinal malignancy. After removal of the gastroscope, a new 24-Fr gastrostomy tube was advanced without difficulty into the excluded tract and its position was confirmed via injection of contrast through the tube. She was deemed a poor surgical and chemotherapy candidate, eventually passing away in a hospice.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [40.0, 'lbs']}",56.28736,53.47299,59.10173,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 40.0 lbs so this converts to 40.0 lbs * 0.453592 kg/lbs = 18.14368 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (18.14368 kg - 10 kg) = 56.28736 mL/hr.
Hence, the patient's fluid maintenance is 56.28736 mL/hr."
5236,22,Maintenance Fluids Calculations,physical,decimal,pmc-8339415-1,Extracted,"A 67-year-old female patient presented with increasing pain in the right groin and severe weakness in the ipsilateral lower extremity, rendering her unable to bear weight or walk for 4 days. She underwent coronary angiography via a right groin puncture 4 days prior to admission in another hospital. She had a history of hypertension, coronary artery disease, and a body mass index of 32 (weight, 74 kg; height, 152 cm). She was not on anticoagulants. The medical records confirmed that femoral artery access was difficult and that it was performed without ultrasound guidance and required multiple puncture attempts. No closure device was used. However, it was noted that she was asymptomatic at the time of discharge.
Physical examination revealed tender induration and bruising in the right groin with no unusual pulsations or bruits. The patient was unable to extend her knee straight () and demonstrated significant weakness of the quadriceps femoris muscles with only grade 1/5 power according to the Medical Research Council scale of muscle strength. Numbness and tingling were also noted on the anteromedial aspect of the thigh and upper leg, suggesting severe femoral nerve dysfunction. The adductor and extensor compartments of the thigh did not exhibit any dysfunction. The increasing severity of local pain despite four analgesics and the onset of paralysis at 4 days post-puncture were suggestive of an expanding pseudoaneurysm stretching the adjacent femoral nerve rather than an intraprocedural direct nerve injury. Computed tomography angiography confirmed a DFA pseudoaneurysm measuring 4 cm×5.5 cm deep to the proximal part of the DFA ().
Based on the perceived need to evacuate the hematoma and release compression on the nerve, we proceeded with urgent open surgery rather than an endovascular treatment. Surgical exploration confirmed that the underlying pseudoaneurysm had overstretched the entire femoral neurovascular bundle. The common femoral artery (CFA) and superficial femoral artery (SFA) were dissected off the floor of the femoral triangle and controlled with clamps. A direct incision was used to evacuate the bulging hematoma, and the bleeding DFA branch was sutured and ligated (). The surgical site healed without any complications. Following intensive rehabilitation with electrical stimulation and quadriceps strengthening exercises, complete muscle recovery was achieved in 12 weeks ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [74.0, 'kg']}",114,108.3,119.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 74.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (74.0 kg - 20 kg) = 114.0 mL/hr.
Hence, the patient's fluid maintenance is 114.0 mL/hr."
5237,22,Maintenance Fluids Calculations,physical,decimal,pmc-6856499-1,Extracted,"A 32-year-old multigravida woman, married nonconsanguineously, came to us for counselling at 31 weeks of gestation. Antenatal scan at 25 weeks was suggestive of isolated ascites with an abdominal circumference >95th percentile. The mother was Rh positive and the Doppler middle cerebral artery peak systolic velocity was normal, ruling out the possibility of incompatibility or anemia. Amniocentesis was performed. The sample was sent for karyotyping and Toxoplasmosis, Others (Syphilis, Varicella-zoster, parvovirus B19), Rubella, Cytomegalovirus and Herpes infection workup. However, the reports came back normal. Similarly, the fetal echo was normal with no other structural abnormalities. Subsequent scan at 31 weeks of gestation showed features of hydrops fetalis like polyhydramnios, pleural effusion, gross ascites, and skin and scalp edema. Bilateral lungs were hypoplastic, secondary to an elevated diaphragm. The small bowel was echogenic and matted. Internal echoes were present in the ascites. There was a history of perinatal asphyxia and developmental delay in the previous baby. Therefore, metabolic causes for hydrops fetalis were also a possibility.
A 2,300 g hydropic female baby was delivered by caesarean section at 32 weeks of gestation suspecting preterm premature rupture of membranes. The baby did not cry at birth and required resuscitation in the form of positive pressure ventilation and intubation. The baby had scalp edema, generalized skin edema, ascites, and vulvar edema (). Her birth weight and head circumference were >90th percentile, and length was between the 10th–50th percentile according to the Fenton's growth chart.
Abdominal radiograph revealed intra-abdominal calcification scattered over the bilateral hypochondrium and flanks (). Abdomen ultrasound revealed massive ascites with internal echoes suggestive of calcification and inferior vena cava compression. Based on these findings, meconium peritonitis was maintained as a working diagnosis. Emergency laparotomy and exploration were performed on the first day of life. Intra-operatively, there was a 10-cm perforation proximal to the ileocecal valve with matted bowel forming an abdominal cocoon with interloop adhesions. Meconium pellets were seen in the proximal ileum with calcifications over the liver, spleen, and bowel (). Ileal resection was performed with a double-barrel ileostomy. Histopathology of the resected bowel revealed the healed perforation with granulation tissue. Immunoreactive trypsinogen level was normal.
There is a very low incidence of cystic fibrosis in our local population and the parents in this case did not consent to further cystic fibrosis genetic workup.
Ileostomy started functioning. Feeds were initiated and gradually increased to full feeds by 7 days of life. The baby also had inguinal hernia and was subsequently operated on. She started gaining weight steadily and was discharged home. Ileostomy closure was performed at the 5-month follow-up. Her condition is good and at 8 months, she is developmentally appropriate based on the Developmental assessment scales for Indian infants [].","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2300.0, 'g']}",9.2,8.74,9.66,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2300.0 g so this converts to 2300.0 lbs * kg/1000 g = 2.3 kg. Hence, the patient's maintenance fluid is 2.3 kg * 4 mL/kg/hr = 9.2 mL/hr.
Hence, the patient's fluid maintenance is 9.2 mL/hr."
5238,22,Maintenance Fluids Calculations,physical,decimal,pmc-8015191-2,Extracted,"A male infant, 2 months old, presented with a history of breathing difficulty, coryza, and cough for 1 week, with symptoms becoming progressively worse in the last 2 days
On examination, the child appeared ill and tachypneic, and was neither pale nor jaundiced. The child also had oral candidiasis and inguinal lymphadenopathy. His weight and length were 3.8 kg and 53 cm, respectively, with an axillary temperature of 36.6 ℃. Examination of the respiratory system revealed flaring of nostrils, as well as subcostal and intercostal recessions with bilateral crepitations. Other systems were normal.
The child was diagnosed with pneumonia with RVD exposure, and he was admitted for further management including administration of intravenous benzylpenicillin 6 hourly, oxygen by nasal prongs, and suctioning of oral and nasal secretions. RPR test was done on both the mother and infant and was found to be positive. The child was admitted to the Children’s Hospital at the UTH for 10 days, and on follow-up visits the child was well and symptoms had resolved.
Among the seven confirmed cases of congenital syphilis, coryzal symptoms were the most common and were observed in 6/7 cases. Skin lesions and anemia were present in 4/7 cases while conjunctivitis occurred in 3/7 (Table ).
Clinical characteristics of the case studies are described in Table . Symptoms involving the upper respiratory tract were the most common presenting symptom, and the age at diagnosis ranged from 30–180 days (median = 42 days, interquartile range (IQR) 5–105 days).
Three of the infants were HIV exposed, and there was only one case in which the mother had been screened for syphilis during antenatal care with the self-reported result being negative.
Regarding the nutritional status of the cases, three of the children were wasted (≤ 2 SD WHZ) and underweight (≤ 2 SD WAZ) at the time of diagnosis, and in all the five cases where full blood count was done the children were found to be anemic (microcytic hypochromic anemia) with a raised total white cell count. Of the two cases where TPHA titers were measured, only one had titers above 1:8, which is the point at which it is a true reactive test.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.8, 'kg']}",15.2,14.44,15.96,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.8 kg. Hence, the patient's maintenance fluid is 3.8 kg * 4 mL/kg/hr = 15.2 mL/hr.
Hence, the patient's fluid maintenance is 15.2 mL/hr."
5239,22,Maintenance Fluids Calculations,physical,decimal,pmc-3970461-1,Extracted,"A 67-year-old male presented with fatigue, anemia, and weight loss of 30 pounds in the last 3 months. He denied history of alcohol consumption and endorsed history of travel to Philippines. On physical examination he had pale conjunctiva bilaterally and shifting dullness on abdomen and rest of his physical examination was normal. Initial laboratory studies revealed Hb of 6.1 gm/dL, MCV 58 FL, creatinine 1.50 mg/dL, albumin 3.3 gm/dL, INR 0.77, normal ALT/AST/ALP, and total bilirubin. CXR did not reveal any infiltrates (). CT abdomen showed moderate amount of ascites with diffuse thickening of peritoneal surfaces suggestive of peritoneal carcinomatosis (). Due to these CT abdomen findings and history of recent weight loss, he underwent a work-up for malignancy with a possible gastrointestinal origin in mind. He underwent diagnostic paracentesis, which revealed WBC of 2,500, with 98% lymphocytes. Cytology was negative for malignancy. No acid-fast bacilli were seen by microscopic exam and culture was negative. PPD was negative. Carcinoembriogenic antigen (CEA) and alpha fetoprotein (AFP) were normal, 1.1 ng/mL and 2.4 IU/mL, respectively. Hepatitis B virus and hepatitis C virus antibodies were negative. EGD revealed duodenal bulbar ulceration, which was ablated, and biopsies were negative for malignancy. Colonoscopy was incomplete due to fixation of the sigmoid colon. Double contrast barium enema was normal. The patient underwent exploratory laparotomy with round ligament and peritoneal biopsies, which revealed numerous necrotizing granulomas. (). AFB stain of round ligament revealed single acid-fast bacilli consistent with mycobacterium (). PCR analysis was performed and found to be positive for M. tuberculosis complex DNA. Final culture results revealed that mycobacterium tuberculosis was sensitive to Rifampin, Isoniazid, Ethambutol, and Pyrazinamide. He was started on treatment for M. tuberculosis and completed the course. His repeat ultrasound of the abdomen after 6 months showed resolution of ascites and peritoneal carcinomatosis. Currently he is asymptomatic and hemoglobin level has normalized.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [30.0, 'lbs']}",47.21552,44.85474,49.5763,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 30.0 lbs so this converts to 30.0 lbs * 0.453592 kg/lbs = 13.60776 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (13.60776 kg - 10 kg) = 47.21552 mL/hr.
Hence, the patient's fluid maintenance is 47.21552 mL/hr."
5240,22,Maintenance Fluids Calculations,physical,decimal,pmc-6018093-1,Extracted,"A 10 year old male was referred to endocrinology clinic for evaluation of obesity, rapid weight gain, and growth deceleration. His mother noted he was previously one of the tallest children in his class, but now was one of the shortest. Review of previous growth charts revealed growth at the 90th percentile for height at 8 years of age with decrease to the 75th percentile at 9 years, and the 50th percentile by 10 years. His weight was consistently at the 95th percentile, but he had gained 5.5 kg (12 lbs) in the past year with weight now at the 97th percentile and body mass index (BMI) 27.5 kg/m2 at the 99th percentile, meeting criteria for extreme obesity.
His mother noted he had been markedly hyperactive as a child and that this behavior had decreased over the past 1–2 years with great improvement in his grades over the past year. His medical history was unremarkable and he did not take medication. Review of systems was unremarkable and he denied fatigue, muscle weakness, constipation, or cold intolerance. He had a good energy level and there were no recent changes in appetite or concentration. He had occasional dry skin. Family history was remarkable for maternal grandmother and mother with hypothyroidism. His midparental target height was 176.5 cm (69.5 inches) at the 50th percentile for height.
On physical examination, the patient measured 134.9 cm (26th percentile) and weighed 50.2 kg (97th percentile) with BMI 27.5 kg/m2 (99th percentile). He had a normal blood pressure 104/55 mm Hg and heart rate of 84 bpm. The patient was well appearing without dysmorphic features and had a normal affect. He had cherubic facies and fundi appeared normal. His thyroid was palpable and smooth with right and left lobe each measuring 4 cm with no lymphadenopathy. His chest, heart, and abdomen were normal. He had Tanner stage 1 genital development with 3 cc testes and no pubic hair. Skin examination was negative for rash, acanthosis, or striae.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [50.2, 'kg']}",90.2,85.69,94.71,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 50.2 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (50.2 kg - 20 kg) = 90.2 mL/hr.
Hence, the patient's fluid maintenance is 90.2 mL/hr."
5241,22,Maintenance Fluids Calculations,physical,decimal,pmc-6944968-1,Extracted,"A 24-year-old G4 P3 Caucasian female with a history of hypertension and type II diabetes mellitus presented to the emergency room with vaginal bleeding at 13 weeks of gestation. On presentation, she reported dizziness, diaphoresis, tremors, anxiety, palpitations, nausea, and leg swelling. Review of system was negative for headache or scotomas. Her vital signs showed blood pressure 141/80 mmHg, heart rate 97 beats per minute, respiratory rate 20 per minute, and temperature 98.4°F. Physical examination was significant for gravid uterus and bilateral lower extremity edema and had fine tremors of both hands. Thyroid gland was normal in size without any nodules. Laboratory studies (Tables and ) revealed suppressed TSH, elevated free T4, and absence of thyroid antibodies including thyrotropin-receptor antibodies (TRAb), thyroperoxidase antibodies (TPOAb), and thyroglobulin antibodies (TgAb). 24 hour urine protein was 200 mg/day and urine protein/creatinine ratio 0.2 in a random urine specimen. Pelvic ultrasound showed twin gestation with one complete HM and one coexisting normal fetus (Figures –). Based on clinical and biochemical evidence of hyperthyroidism with elevated human chorionic gonadotrophin (hCG) levels in the absence of autoantibodies, a diagnosis of GTH was made.
After extensive discussion regarding risk of developing complications associated with molar pregnancy [], she preferred to proceed with her current pregnancy until viability of fetus. As she was into her 2nd trimester of pregnancy, she was started on methimazole and the dose was titrated to achieve a goal free T4 in the upper range of normal (normal range = 0.8–1.7 ng/dL) to prevent fetal hypothyroidism. She was also on metoprolol 25 mg daily for chronic hypertension which was continued throughout the pregnancy. She also developed preeclampsia at 16 weeks of pregnancy with 24 hr urine protein of 3729 mg/day. She was again recommended termination of pregnancy, but she preferred to proceed with her pregnancy. At 24th weeks of gestation, pregnancy was complicated by worsening preeclampsia and she eventually underwent a lower segment cesarean section with delivery of a viable fetus and evacuation of molar pregnancy. The weight of the baby was 645 gram, and APGAR score was 1 at 1 minute, 2 at 5 minutes, and 3 at 10 minutes. Postoperatively, gross examination of the tissue revealed fragments of pink-red spongy soft tissue without any fetal parts or abnormal Z line, while microscopic examination revealed hydropic villi and trophoblastic proliferation confirming the diagnosis of a complete mole (Figures –). Histopathology of placenta revealed a singleton placenta weighing 156 grams and measuring 13.8 × 11.3 × 2.6 cm. At the time of delivery, she was on very low dose of methimazole, and therefore, it was discontinued. She remained clinically and biochemically euthyroid in the postpartum period. Her hCG gradually trended to a normal range of 17 weeks after delivery, and she had spontaneous remission of molar pregnancy as supported by low hCG levels at 1-year follow-up (). The preterm infant did not have any gross abnormalities, and screening for congenital hypothyroidism was negative both at birth with TSH < 2.91 μU/mL (normal range < 20 μU/mL) and free T4 8.2 μg/dL (normal range ≥ 5 μg/dL) and at two months postdelivery with TSH < 2.91 μU/mL (normal range < 20 μU/mL) and free T4 6.7 μg/dL (normal range ≥ 5°μg/dL). Unfortunately, the baby needed mechanical ventilation for respiratory distress syndrome and gradually developed bronchopulmonary dysplasia requiring need for prolonged mechanical ventilation and underwent tracheostomy. He was transferred to a long-term care facility.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [645.0, 'g']}",2.58,2.451,2.709,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 645.0 g so this converts to 645.0 lbs * kg/1000 g = 0.645 kg. Hence, the patient's maintenance fluid is 0.645 kg * 4 mL/kg/hr = 2.58 mL/hr.
Hence, the patient's fluid maintenance is 2.58 mL/hr."
5242,22,Maintenance Fluids Calculations,physical,decimal,usmle-7286,Extracted,"A 40-year-old man visits the office with complaints of fever and abdominal pain for the past 6 days. He is also concerned about his weight loss as he weighs 3.6 kg (8 lb) less, today, than he did 2 months ago. He has a previous history of being admitted to the hospital for recurrent cholangitis. The vital signs include: heart rate 97/min, respiratory rate 17/min, temperature 39.0°C (102.2°F), and blood pressure 114/70 mm Hg. On physical examination, there is tenderness on palpation of the right upper quadrant. The laboratory results are as follows:
Hemoglobin 16 g/dL
Hematocrit 44%
Leukocyte count 18,000/mm3
Neutrophils  60%
Bands 4%
Eosinophils 2%
Basophils 1%
Lymphocytes  27%
Monocytes 6%
Platelet count 345,000/mm3
Aspartate aminotransferase (AST)  57 IU/L
Alanine aminotransferase (ALT) 70 IU/L
Alkaline phosphatase 140 U/L
Total bilirubin 8 mg/dL
Direct bilirubin 5 mg/dL
An ultrasound is also done to the patient which is shown in the picture.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.6, 'kg']}",14.4,13.68,15.12,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.6 kg. Hence, the patient's maintenance fluid is 3.6 kg * 4 mL/kg/hr = 14.4 mL/hr.
Hence, the patient's fluid maintenance is 14.4 mL/hr."
5243,22,Maintenance Fluids Calculations,physical,decimal,pmc-6996534-1,Extracted,"A 14-day-old male newborn, weighing 3 kg, born of a nonconsanguineous marriage to a 25-year-old mother (gravida four, para three) by normal vaginal delivery, presented with severe anemia. There were no significant events during the antenatal period. The child was born in good condition, and there were no signs of jaundice, cyanosis, respiratory distress, haematoma, or fits during the immediate postnatal period. On examination, the child had severe anemia, tachypnea, tachycardia, and hepatosplenomegaly. On admission, his hemoglobin was 5.8 g/dL (reference range, 14-24 g/dL); his reticulocyte count (corrected) was 12% (reference range, 1%-2%), and his mean corpuscular volume was 105.3 fL (reference range, 96-108 fL). A peripheral smear showed polychromasia, dimorphic red blood cells (RBCs), target cells, acanthocytes, and spherocytes. His total serum bilirubin concentration was 0.89 mg/dL (reference range, 0.3-1.0 mg/dL), and his direct bilirubin concentration was 0.15 mg/dL (reference range, 0.1-0.3 mg/dL). A full septic work-up was negative for an underlying infectious pathology. The child was strongly positive on a direct Coombs test. Blood typing showed the baby was O-positive, the mother was O-negative, and the father was O-positive. The mother was positive on an indirect Coombs test. The anti-D antibody titers of the mother were also positive, which resulted in a diagnosis of HDN secondary to Rh isoimmunization with anti-D antibodies.
The mother had conceived three times before this pregnancy; all were uneventful normal vaginal deliveries. She had declined anti-D prophylaxis during all her previous pregnancies. All her previous children were born healthy with blood group O-positive and no postnatal complications. The infant diagnosed with HDN was transfused with packed RBCs, but his post-transfusion hemoglobin concentration dropped again to 5.5 g/dL. On day 17, packed RBCs were again transfused, after which his hemoglobin increased slightly to 6.3 g/dL. Two more units of packed RBCs were transfused on days 19 and 22, resulting in a dramatic increase in hemoglobin levels. The infant was finally discharged on day 24 with hemoglobin of 13.6 g/dL and a negative result on a direct Coombs test. The parents were counseled on the nature of their child’s illness, the implications of refusing anti-D prophylaxis, and a high risk of complications during subsequent pregnancies. Contraception was advised. Follow-up visits after one week and monthly for two months showed that the child was thriving well and his hemoglobin concentrations were within the reference range.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.0, 'kg']}",12,11.4,12.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.0 kg. Hence, the patient's maintenance fluid is 3.0 kg * 4 mL/kg/hr = 12.0 mL/hr.
Hence, the patient's fluid maintenance is 12.0 mL/hr."
5244,22,Maintenance Fluids Calculations,physical,decimal,pmc-5984920-1,Extracted,"A 45-year-old Caucasian woman presented with abdominal pain, nausea, and vomiting for 17 h. At 22 h prior to admission, she went out to dinner and drank one glass of wine. A few hours after the meal, she developed epigastric and left upper quadrant abdominal pain that was moderate, persistent, cramping, and aching; the pain radiated to her left middle back and arm without exacerbating or alleviating factors. The pain was associated with nausea, vomiting, and she could not tolerate any oral intake. She felt thirsty and had polyuria and positional lightheadedness. She reported no fever, chills, chest pain, cough, sputum production, dysuria, hematuria, diarrhea, hematochezia, and melena.
On further questioning, the patient shared that she had a history of gestational glucose intolerance 6 years ago, and has had occasional impaired fasting glucose of 81–107 mg/dL for the past 6 years. She began following an American Diabetes Association (ADA) diet 2 years ago and lost 25 lb. Additionally, she had a past medical history of supraventricular tachycardia, irritable bowel syndrome, social alcohol use, cholecystectomy, and thyroid papillary adenocarcinoma status post partial thyroidectomy complicated by postsurgical hypothyroidism. Home medications included metoprolol tartrate, levothyroxine, and meloxicam. The patient reported no family history of diabetes.
Temperature 97.7 °F, pulse 130 bpm, respiratory rate 28 bpm, BP 134/71 mmHg, weight 87 kg, height 1.68 m, BMI 31 kg/m2, SpO2 99% on room air.
The patient was in moderate distress. There was no acanthosis nigricans. Cardiovascular system revealed tachycardia. A pulmonary exam revealed tachypnea, accessory muscle usage with moderate respiratory distress. Abdominal exam revealed central obesity, normoactive bowel sounds, left upper quadrant and epigastric tenderness to palpation, no rigidity or guarding. No costovertebral angle tenderness.
CBC: WBC 25.9 × 109/L, hemoglobin 14.7 g/dL, hematocrit 45.8%, platelet 386 × 109/L, MCV 100.2 µm3. BMP: sodium 135 mmol/L, potassium 7.4 mmol/L, chloride 89 mmol/L, bicarbonate 5 mmol/L, BUN 37 mg/dL, creatinine 1.27 mg/dL, glucose 931 mg/dL, eGFR 46 mL/min.
Liver chemistry: Total bilirubin 0.2 mg/dL, AST 23 U/L, ALT 54 U/L, ALP 138 U/L, total protein 7.5 g/dL, albumin 4.5 g/dL. Calcium 8.7 mg/dL, phosphate 1.4 mg/dL, magnesium 2.1 mg/dL. VBG: pH 6.92. Repeated ABG 2 h later: pH 7.21, pCO2 16 mmHg, pO2 129 mmHg, HCO3− 6.4 mmol/L, SaO2 98% on 2 L/min oxygen by nasal cannula. Beta-hydroxybutyrate 28 mmol/L, lactic acid 4.0 mmol/L. Urinalysis showed urine ketones 80 mg/dL, leukocyte esterase negative, urine culture no growth. HbA1c 6.4%. Lipid profile: triglycerides 89 mg/dL, total cholesterol 144 mg/dL, LDL 91 mg/dL, HDL 35 mg/dL. TSH 3.12 mIU/mL, free T4 1.26 ng/dL. Troponin I < 0.01 ng/mL.
Ultrasonography of the abdomen revealed mild hepatic steatosis, incidental mild to moderate right-sided hydronephrosis, status post cholecystectomy. ECG on admission: sinus rhythm, HR 126 bpm, peaked T waves at lead V2–V6 consistent with hyperkalemia, no ischemic changes.
All procedures performed in this study were in compliance with the ethical standards of the institutional and/or national research committee and with the 1964 Declaration of Helsinki and its later amendments or comparable ethical standards. Informed consent was obtained from the individual participant for being included in the study.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [87.0, 'kg']}",127,120.65,133.35,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 87.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (87.0 kg - 20 kg) = 127.0 mL/hr.
Hence, the patient's fluid maintenance is 127.0 mL/hr."
5245,22,Maintenance Fluids Calculations,physical,decimal,pmc-7733524-1,Extracted,"A 22 kg 6-year-old, American Society of Anesthesiologists (ASA) 2 girl with suspicion of Down syndrome was operated for strabismus under general anesthesia (GA). She was hospitalized thrice for both acute otitis media and pneumonia since birth. Her past surgical, social and family history was uneventful. GA was induced with fentanyl 44 μg, propofol 66 mg and suxamethonium 22 mg followed by orotracheal intubation. GA was maintained using halothane at 1–2%. About 90 min postoperatively, her pulse and temperature suddenly rose from 126 to 166 beats per minute and 37 to 42°C associated with generalized muscular rigidity, and consecutively an episode of generalized tonic convulsions, bradycardia then cardiac arrest. Management involved cardiopulmonary resuscitation and cooling. Dantrolene was not available in the hospital. The patient had a fatal outcome within 30 min of cardiac arrest.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [22.0, 'kg']}",62,58.9,65.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 22.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (22.0 kg - 20 kg) = 62.0 mL/hr.
Hence, the patient's fluid maintenance is 62.0 mL/hr."
5246,22,Maintenance Fluids Calculations,physical,decimal,pmc-8463003-2,Extracted,"Patient 2 was a 43-year-old, 111.7 kg, white female with a BMI of 40.67 kg/m2 with a past medical history of asthma, bipolar disorder, hidradenitis suppurativa, insomnia, onychomycosis, panic disorder, paresthesia, PTSD, and type 2 diabetes mellitus. The patient presented to our facility with worsening depression, anxiety, irritability, and difficulty sleeping. The patient's symptoms during decompensation included recurrence of previous self-harm and escalation of suicidal ideation; with stressors being chronic, a TEAE was suspected. Laboratories relevant to this patient include serum creatinine 0.76 mg/dL, albumin 3.3 g/dL, ALT 16 U/L, and AST 12 U/L. Medications on admission were adalimumab 40 mg every week, aripiprazole 15 mg daily, clonazepam 2 mg twice daily as needed for anxiety or panic, diclofenac 75 mg twice daily, doxepin 6 mg nightly, dulaglutide 0.75 mg every week, ergocalciferol 50 000 units twice a week, escitalopram 20 mg daily, fexofenadine 60 mg twice daily, fluticasone propionate/salmeterol inhaler (250-50 mcg/dose) twice daily, glipizide 10 mg daily, lisinopril 10 mg daily, omeprazole 20 mg daily, pramipexole 0.125 mg nightly, and terbinafine 250 mg daily. Available evidence indicated the patient was medication adherent, and a possible DDI was suspected between aripiprazole and terbinafine.
Based on EPCD and chart review, this patient was taking aripiprazole for several months, and terbinafine was started approximately 2 weeks prior to admission. A serum trough aripiprazole concentration was ordered and obtained the second day of hospitalization. The aripiprazole serum trough at Css was 278.9 ng/mL. Serum concentrations were quantified using liquid chromatography-tandem mass spectrometry at LabCorp Laboratories. The patient discontinued terbinafine during hospitalization and continued aripiprazole. No long-term outcomes of these changes are known due to the patient receiving care outside our health system.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [111.7, 'kg']}",151.7,144.115,159.285,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 111.7 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (111.7 kg - 20 kg) = 151.7 mL/hr.
Hence, the patient's fluid maintenance is 151.7 mL/hr."
5247,22,Maintenance Fluids Calculations,physical,decimal,pmc-6251820-1,Extracted,"A 25-day-old female baby, born to a non-consanguineous couple of low socioeconomic status, was antenatally detected to have tumour in the mediastinum and referred to our hospital for further work-up. The baby was delivered by normal spontaneous vaginal delivery with a birth weight of 2.8 kg. She was asymptomatic after birth until now. On examination, oxygen saturation was 98% in room air. Cardiovascular system examination was unremarkable. Chest X-ray showed cardiomegaly suggestive of pericardial effusion. Neonatal echocardiography (Fig. ) and computed tomography (Fig. ) of the chest identified a large intra-pericardial tumour (5 × 6 cm), possibly teratoma, seen beside the right atrium and superior vena cava compressing the the right atrium and adherent to the ascending aorta with moderate pericardial effusion. After a multidisciplinary team meeting, the child was taken up for surgery.
Median sternotomy was done. Moderate pericardial effusion was drained. There was a large intrapericardial tumour attached to the ascending aorta (Fig. a). The tumour was seen to be arising from the tunica media of the ascending aorta to which it was densely adherent. It was, therefore, decided to electively perform cardiopulmonary bypass. Cardiopulmonary bypass was established with aortic and right atrium cannulation. The tumour was completely dissected from the aorta and was removed (Fig. b). There were tears at the site where the tumour was attached to the aorta. Those areas in the ascending aorta were repaired with 6-0 polypropelene sutures, thereby securing haemostasis. Histopathology examination of the mass confirmed the diagnosis of intrapericardial teratoma.
Post procedure, the patient's condition improved, and she was extubated on the 1st post-operative day and discharged on the 5th postoperative day. The child was asymptomatic with normal echocardiogram at 1-month follow-up.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.8, 'kg']}",11.2,10.64,11.76,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.8 kg. Hence, the patient's maintenance fluid is 2.8 kg * 4 mL/kg/hr = 11.2 mL/hr.
Hence, the patient's fluid maintenance is 11.2 mL/hr."
5248,22,Maintenance Fluids Calculations,physical,decimal,pmc-6743036-1,Extracted,"A 3-year-old male Australian Shepherd (weight: 17 kg) was presented at the Veterinary Clinic Norderstedt with generalized tremor, agitation, and panting, which occurred after oral treatment with two Profender® tablets for medium dogs (10 mg EMO plus 50 mg PZQ). The owner had received the product from a veterinarian without any further instructions on fasting, so the dog received a handful (30 g) of dry dog food (Bosch Active) about half an hour before the Profender® administration. Two and a half hours after drug application, the dog showed progressive tremor and severe panting. Furthermore, he developed excessive drooling and salivation and became ataxic.
Therefore, the dog was presented at a veterinary clinic immediately. Initial physical examination revealed a rectal temperature of 40.2°C (104.4°F), heart rate of 136/min, red mucous membranes and a normal capillary refill time of 1 s. The dog showed agitated general condition, panting, and generalized tremor, but was able to stand and walk on his own. Results of further neurological examination were unremarkable. As the patient's condition was stable, the treating veterinarian decided to perform no further clinical examinations (e.g., blood or urine analysis) and symptomatic treatment was initiated.
The dog was admitted to the intensive care unit and possible seizure activity, body temperature, and intravenous fluid therapy were monitored closely. An IV catheter (Vasofix® Braunüle®, Braun Melsungen) was placed in the right cephalic vein. The patient obtained an intravenous lipid emulsion (Lipofundin® MCT/LCT 20%, Braun Melsungen) as an IV bolus of 2.0 mL/kg followed by an infusion of 210 mL for the next hour. IV fluid therapy (Sterofundin® Iso, Braun Melsungen) was also administered at a maintenance rate of 10.0 mL/kg for 3 h, followed by 2.0 mL/kg/h until the next day. Additionally, 1.0 mg/kg diazepam (Ziapam®, 5 mg/ml, Ecuphar) was administered IV to treat the generalized tremor. Since no clinical improvements were noted, 0.2 mL acepromazine (Vetranquil® 1%, Ceva) were administered IM. Subsequently, the patient's condition improved and the generalized tremor changed to a slight trembling within an hour. Body temperature normalized after 4 h to 38.1°C (100.6°F).
One day following admission, no abnormalities were detected at the physical examination. The dog was alert, mucous membranes were pink and moist, heart rate was 84/min, the respiratory rate was 24/min, the rectal temperature was 38.6°C (101.5°F), the abdomen was slightly tensed and rectal examination was unremarkable. No defecation was observed during the hospitalization, but appetite and urination were normal. Neurological examination was also unremarkable and the dog was discharged to his owner without further medication. The owner reported that the dog vomited multiple times the week after discharge. Apart from that, the dog's behavior had recovered completely.
Since Australian Shepherds are predisposed to carry the nt230(del4) MDR1 mutation, which is associated with increased susceptibility against several MDR1 reactive drugs, including EMO, MDR1-genotyping was performed (TransMIT GmbH, Giessen, Germany). The dog showed the homozygous mutant MDR1−/− genotype, resulting in a complete loss of MDR1-mediated drug efflux at the blood-brain barrier.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [17.0, 'kg']}",54,51.3,56.7,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 17.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (17.0 kg - 10 kg) = 54.0 mL/hr.
Hence, the patient's fluid maintenance is 54.0 mL/hr."
5249,22,Maintenance Fluids Calculations,physical,decimal,usmle-7134,Extracted,"A 3-year-old boy presents with episodic diarrhea with malodorous stools, stunted growth, occasional abdominal cramps, and an itchy rash. His mother says that these symptoms developed approximately 2 years ago. The patient was exclusively breastfed up to the age of 7 months. Supplementary feeding was started with non-starchy vegetable followed by starchy vegetables, meat, fish, eggs, and bread. Bread and cookies were the last product to be introduced at the age of 12 months. The patient’s mother tried to withdraw dairy products from the patient’s diet because she heard that lactose can cause such symptoms, but it did not help. The patient’s vital signs include: blood pressure 90/55 mm Hg, heart rate 101/min, respiratory rate 19/min, and temperature 36.3℃ (97.3℉). His weight is 11 kg (24.2 lb, -2 SD) and height is 90 cm (2 ft 11 in, -1 SD). On physical examination, the patient’s skin is pale with a papulovesicular rash on his abdomen and back. There are a few aphthous ulcers in the oral cavity. The abdomen is distended but no tenderness to palpation. No hepatosplenomegaly. An immunological assay is performed and shows positive anti-transglutaminase and anti-endomysial antibodies.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [11.0, 'kg']}",42,39.9,44.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 11.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (11.0 kg - 10 kg) = 42.0 mL/hr.
Hence, the patient's fluid maintenance is 42.0 mL/hr."
5250,22,Maintenance Fluids Calculations,physical,decimal,pmc-8032910-1,Extracted,"A two-day old female preterm neonate with gestational age of 34 weeks birth weighting 2,450 grams was admitted in the neonatal intensive care unit (NICU) of Ali Asghar Children's Hospital with omphalocele. Her mother was premature rupture of membrane (PROM) for more than 24 hours before caesarian section. She was evaluated in order to find the associated anomalies and had ventricular septal defect (VSD), patent ductus arteriosus (PDA) which was closed spontaneously and mild enlargement of the left atrium but normal ejection fraction on the echocardiography. Ultrasonography of the urinary tract revealed malrotation of kidneys and the right pelvis diameter of 7 mm. Her omphalocele was repaired with the primary closure and she was intubated and mechanically ventilated for four days and needed supplemental oxygen therapy for two other days before clinical deterioration. She had a peripherally inserted central catheter (PICC) from the first day of admission. On the seventh day of the post-operation, she unexpectedly became mottled, febrile and cyanotic. She had poor feeding and vomiting. Her blood pressure was in the normal range but she had tachycardia. Except in the decreased neonatal reflexes, there was no other neurological sign. Moreover; she had one episode of apnea that responded to skin stimulation. The full sepsis work up was conducted and her laboratory data was as follows: white blood cell (WBC) 15,700/mm3 (neutrophil 80%, Band 3%, lymphocyte 16%), hemoglobin (Hb) 8.6 g/dl, platelet 386,000/mm3, and C-reactive protein (CRP) 119 mg/L. CSF analysis showed WBC 7,200/mm3 (neutrophil 41%, lymphocyte 59%), glucose 15 mg/dl and protein 157 mg/dl. Blood and wound culture were negative but throat and CSF culture were positive for A. baumannii and the antibiotic susceptibility test by the disk diffusion method showed resistance to cefuroxime, ceftazidime, ceftriaxone, cefepime, imipenem, ciprofloxacin, cotrimoxazole, piperacillin/tazobactam, amikacin and sensitivity only to colistin. OXA _ Gyr _VER- AMP- KPC -VIMNDM- IMP resistance genes were detected by a multiplex PCR method.
The brain ultrasonography was normal but the brain CT scan without contrast revealed a diffuse cerebral white matter hypodensity in favor of edema. The ventricles and subarachnoid spaces were normal in the appearance and there was no midline shift.
Regarding first diagnosis of nosocomial septicemia, she was treated empirically using vancomycin and meropenem and then switched to IV colistin, meropenem and rifampin, when the result of antibiotic sensitivity test showed a pan- resistant strain only susceptible to colistin.
The dosage of colistin and meropenem administered was 20,000 unit/kg every 8 hours and 40 mg/kg every 12 hours parenterally infused in one hour respectively. Rifampin was infused at a dosage of 10 mg/kg every 12 hours for 30 minutes and CRP reached <1 mg/L within 7 days. The patient was treated for 21 days and CSF analysis at termination of treatment revealed WBC 0/mm3, glucose 21 mg/dl and protein 107 mg/dl. The results of CSF analysis of the serial lumbar punctures are shown in the . Six months of follow up showed the normal auditory brain stem response and normal neurodevelopment.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2450.0, 'g']}",9.8,9.31,10.29,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2450.0 g so this converts to 2450.0 lbs * kg/1000 g = 2.45 kg. Hence, the patient's maintenance fluid is 2.45 kg * 4 mL/kg/hr = 9.8 mL/hr.
Hence, the patient's fluid maintenance is 9.8 mL/hr."
5251,22,Maintenance Fluids Calculations,physical,decimal,pmc-6020266-3,Extracted,"Patient 3 was a 4-year old boy, the third child of healthy, non-consanguineous parents. There was no family history of bone fragility or autism. Bowing of the lower limbs observed on the anomaly scan raised antenatal suspicion of a campomelic dysplasia. The patient was born by normal vaginal delivery at term. He weighed 3.74 kg (50th centile) with a head circumference of 34 cm (25th centile). He suffered mild respiratory distress at birth but did not require ventilatory support.
A skeletal survey performed after birth demonstrated a normal thoracic cage volume, bowing of the long bones with abnormal metaphyses and a fractured ulna. The patient suffered fractures to his left humerus and right forearm. He was subsequently diagnosed with severe osteogenesis imperfecta.
By 4-years of age, he had suffered multiple fractures of his ulnas and humeri, a femoral fracture and multiple vertebral wedge fractures. He has undergone bilateral osteotomies and rodding of his femurs and tibias at 2 and 3 years of age, respectively. He received 3-monthly pamidronate infusions.
This patient was developmentally delayed, sat independently from 2 years and walked with aids from 2.5 years of age. He had delayed speech and required intervention from speech and language therapists at age 21 months. He has demonstrated “rocking” behaviour from 2.5 years of age but did not have a clinical diagnosis of ASD before recruitment to the study.
On genetic assessment, he was noted to have a ‘triangular’ face, blue sclerae, high-pitched voice in keeping with a diagnosis of ‘Classical OI’. He went on to have testing for COL1A1/A2 and was found to have a pathogenic c.902G>A variant in COL1A2. This pathogenic mutation is predicted to replace glycine at position 301 with a glutamic acid. Glycine substitutions are well-recognised as a cause of OI. This confirmed his clinical diagnosis of OI.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.74, 'kg']}",14.96,14.212,15.708,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.74 kg. Hence, the patient's maintenance fluid is 3.74 kg * 4 mL/kg/hr = 14.96 mL/hr.
Hence, the patient's fluid maintenance is 14.96 mL/hr."
5252,22,Maintenance Fluids Calculations,physical,decimal,pmc-3853599-1,Extracted,"A 26-year-old male presented with a primary complaint of swelling and discharge in the upper part of sternum since last 6 months []. There was history of development of discharging sinus and fistula following pus aspiration from swelling. He also complained of intermittent fever, anorexia and weight loss of nearly 7 kg during last 6 months. There was no past history of Koch's. On examination, there was a discharging sinus in upper part of the sternum. Rest general physical and systemic examination was within normal limits. Routine blood investigations-complete blood count, kidney function test, liver function test, random blood sugar and serum electrolytes were within normal limits; hemoglobin was 11 g/dl; erythrocyte sedimentation rate-64 mm/h; Mantoux-15 mm × 15 mm; chest radiograph was normal; patient was non-reactive to HIV test; ultrasound chest revealed two hypoechoic linear tracts communicating with skin; pus aspirate was positive for acid fast bacilli on Ziehl-Neelsen staining; Contrast enhanced computed tomography (CECT) of the thorax [Figures and ] showed peripherally enhancing hypodense collection seen in the subcutaneous plane with underlying irregularity of body of sternum-caries of sternum with few calcified lymph node noticed in paratracheal region; underlying lung parenchyma appeared normal. Patient was counseled and started on anti-tubercular therapy under directly observed therapy short course (DOTS) of alternate day regime prescribed under Revised National Tuberculosis Control Program, i.e., isoniazid (600 mg), rifampicin (450 mg), pyrazinamide (1500 mg) and ethambutol (1200 mg). The patient is under follow up and has improved clinically with afibrile status, weight gain, resolution of pus and healing of sinuses. It is planned to administer intermittent therapy under DOTS for 9 months.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.0, 'kg']}",28,26.6,29.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.0 kg. Hence, the patient's maintenance fluid is 7.0 kg * 4 mL/kg/hr = 28.0 mL/hr.
Hence, the patient's fluid maintenance is 28.0 mL/hr."
5253,22,Maintenance Fluids Calculations,physical,decimal,pmc-4173411-1,Extracted,"A 70-year-old woman presented with cellulitis of the left upper limb. There was no other relevant medical or surgical history. The patient denied a previous history of bronchial asthma. On examination, she was febrile, her weight was 45 kg, heart rate was 110/ min and blood pressure in the right upper limb in supine position was 168/96 mmHg. Respiratory and cardiovascular systems were unremarkable. Laboratory investigations showed leucocytosis with neutrophilia and other parameters were within normal limits. ECG showed sinus tachycardia. Oxyhaemoglobin saturation (SpO2) on room air was 96%. She was scheduled to undergo an emergency debridement of the left upper limb.
Regional anaesthesia was planned and left brachial plexus block was performed uneventfully via the supraclavicular approach. Lignocaine (2%) with adrenaline (5 μg/ml) 10 ml and bupivacaine (0.5%) 10 ml was injected after eliciting paresthesia and careful aspiration. The patient developed adequate anaesthesia of the left upper limb within 10 minutes and the heart rate decreased to 80/min. The surgery lasted for 20 minutes and the further intra-operative period was uneventful.
In the post-operative care unit, 30 minutes later, the patient complained of difficulty in breathing and the SpO2 decreased to 88% with O2 4 L/min by face mask. She was using accessory muscles of respiration. The heart rate increased to 120/min. On auscultation, there was reduced air entry bilaterally and rhonchi were heard all over the chest. She was treated with propped-up position, supplemental oxygen, salbutamol nebulization and intravenous hydrocortisone 100 mg. A chest screening done subsequently with a C-arm was normal. ECG showed no fresh changes. At this time, the right upper limb was also examined for any sensory/motor deficit which the patient could not differentiate due to the respiratory distress. A repeat examination of the right upper limb 1 hour later did not reveal any sensory/motor deficit while the left still had adequate anaesthesia. The patient improved with the above treatment and rest of her hospital stay was uneventful.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [45.0, 'kg']}",85,80.75,89.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 45.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (45.0 kg - 20 kg) = 85.0 mL/hr.
Hence, the patient's fluid maintenance is 85.0 mL/hr."
5254,22,Maintenance Fluids Calculations,physical,decimal,pmc-8319662-1,Extracted,"A 66-year-old woman presented to the emergency department with complaints of shortness of breath and chest pain for the preceding 2 days.
She had a history of rheumatoid arthritis (RA) and systemic lupus erythematous (SLE), taking oral prednisolone (6 mg/day) and hydroxychloroquine (200 mg/day). She was a housewife and frequently worked with potting soils in her garden. She also had orange-coloured sputum (Figure ). Her vital signs upon admission were as follows: temperature, 36.1°C; blood pressure, 109/69 mmHg; pulse rate, 111 beats/min; respiratory rate, 30/min; and oxygen saturation, 96% on 9 L/min of oxygen mask with reservoir bags. She had clear consciousness. She had coarse crackles bilaterally.
Laboratory findings were as follows: white blood cell count 30,510/μl (neutrophils 99.5%), haemoglobin 10.1 g/dl, platelet count 5.0 × 104/μl, lactate dehydrogenase 341 U/L, urea nitrogen 30 mg/dl, creatinine 1.21 mg/dl and C-reactive protein 41.06 mg/dl. Blood gas analysis showed the following: pH 7.397, pCO2 34.4 torr, pO2 46.5 torr and HCO3
− 21.8 mEq/L (with room air).
Her chest x-ray showed consolidation in the upper and middle lung fields bilaterally (Figure ). Computed tomography (CT) of the chest showed consolidation of the right upper, middle and lower lobes and the left upper, and atelectasis of the left lower lobe (Figure ). Sputum Gram stain showed very few epithelial cells and some neutrophils, but not satisfactory to estimate causative bacteria. Both the BinaxNOW™ pneumococcal and Legionella urinary antigen test (Abott) were negative.
We suspected severe pneumonia and started with intravenous levofloxacin (500 mg q24h) and meropenem (500 mg q6h) empirically. Given her history of RA and SLE, and immunosuppressive state, we thought that viral/fungal infections, alveolar haemorrhage and interstitial pneumonia were important differential diagnoses. Thus, she underwent BAL by bronchoscopy under intubation. The colour of BALF was also orange (Figure ) and the cellular pattern was neutrophil predominant (90.0%) suggestive of bacterial infection. But, Gram stain of the BALF results was negative. Cytology of BALF revealed numerous neutrophils and a few macrophages which were not hemosiderin-laden. Because it has been clinically suggested that the colour of sputum obtained from patients with pneumonia caused by L. pneumophila is orange, we suspected non-pneumophila Legionella species pneumonia. We switched meropenem to azithromycin (500 mg q24h) and increased levofloxacin to maximum dose (750 mg q24h) targeting Legionella species pneumonia. Acid-fast bacillus cultures of sputum resulted negative. Two sets of blood cultures were negative. Polymerase chain reactions (PCR) for Pneumocystis, cytomegalovirus and SARS-CoV-2 were all negative. On the fifth day, mass spectrometry analysis of colonies obtained by culturing in BCYEα medium from BALF identified the presence of Legionella longbeachae.
On the sixth day, her respiratory condition deteriorated and contrast-enhanced CT showed exacerbation of ground-glass opacity (GGO) without pulmonary thromboembolism. We suspected organizing pneumonia secondary to L. longbeachae and started high-dose pulse intravenous steroid treatment with 1 g methylprednisolone for 3 days followed by prednisolone 1 mg/kg (60 mg/day) alongside levofloxacin that was administered 21 days in total. The following days she recovered gradually and she was extubated on Day 12. Eventually, consolidation and GGO improved on her chest CT of Day 23 and she was discharged home without oxygen on Day 34.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.0, 'kg']}",100,95,105,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.0 kg - 20 kg) = 100.0 mL/hr.
Hence, the patient's fluid maintenance is 100.0 mL/hr."
5255,22,Maintenance Fluids Calculations,physical,decimal,pmc-4078017-1,Extracted,"A 3-year-old, 3.7 kg intact female Miniature Poodle was taken to the Ai’ xin Small Animal Hospital (Cixi, Zhejiang, China), with a heart rate of 138, respiratory rate of 62, rectal temperature of 42°C, and intermittent seizures. The owners initially presented a conflicting and unclear history. The dog received external cooling without any other examination or treatment after admission. After continued conversation with the owners it became clear that the dog may have been intentionally fed an unknown amount of a crystalline-like substance by their friends in a nightclub approximately 1 hour before presentation. They suggested that ‘ice’, the street name of methamphetamine, may have been present in the nightclub. The dog had no medical records in the hospital, but, according to the owner’s description, had no other remarkable past history. After revealing a possible methamphetamine ingestion history the owners disappeared, leaving the dog at the hospital.
The dog was taken to the Veterinary Teaching Hospital of Zhejiang University by a referral veterinarian, and was provided with continuing external cooling (ice packs). By this time it was about 2.5 hours beyond ingestion when the dog was finally presented at the emergency room. The referral veterinarian reported that the dog was progressively displaying flushed skin and extensive petechiae in abdominal region (Figure 
). It also had started to develop watery bloody diarrhea, and had had 3 short seizures (about 50 seconds for each time seizure) on the way to the hospital. Physical examination revealed a rectal temperature of 41.5°C, heart rate of 186 beats per minute with no premature ventricular contractions or other arrhythmias, panting respiration, systolic blood pressure of 166 mmHg, diastolic blood pressure of 117 mmHg, and mean arterial pressure of 137 mmHg. The dog was alert, responsive and extremely agitated. It had bilaterally dilated pupils and displayed rotational locomoter activity (repeatedly circling in an anticlockwise direction) (Additional file
: Movie 1).
Blood samples were collected by cephalic venipuncture and placed in different sets of tubes, with or without anticoagulant, for a complete blood count (CBC), a biochemical profile panel and coagulation tests. All these tests were performed by IDEXX In-house Diagnostics Station (IDEXX Laboratories, Sacramento, CA). Hematological findings included white blood cell count 21,000/μL (reference range 5,050-16,760/μL), red blood cell count 5.1 M/μL (reference range 5.65-8.87 M/μL), red blood cell specific volume 31.2% (reference range 37.3%-61.7%), platelets 55,000/μL (reference range 148,000-484,000/μL), lymphocytes 5,300/μL (reference range 1,050-5,100/μL), and neutrophils 15,000 (reference range 2,950-11,640/μL) with normal segmented neutrophils. The results of the biochemical panel revealed mildly elevated alanine aminotranferease (ALT; 112 U/L, reference range is 10-100 U/L) and mildly elevated alkaline phosphatase (ALKP; 238 U/L, reference range is 23-212U/L) concentrations, with mildly decreased glucose (70 mg/dL, reference range 74-143 mg/dL). The prothrombin time (PT) was 16.8 seconds (reference range 11.0-14.0 seconds) and the activated partial thromboplastin time (aPTT) was 125.0 seconds (reference range 60.0-93.0).
Blood gas was also evaluated by electrolyte analysis and a blood gas analyzer (IDEXX Laboratories, Sacramento, CA) and the results revealed a pH of 7.20 (reference range 7.31-7.42) and a base deficit of 17.8 mmol/L (HCO3-, reference range 20.0-29.0 mmol/L), with unremarkable potassium, chloride and sodium concentrations. An x-ray of the chest and abdomen appeared normal with exception of severe distension of the stomach and small intestinal tract with air. Portions of the colon were also air filled. Presumptive diagnosis was functional or paralytic ileus (Figure 
). The urine test was unremarkable without any pathologic casts.At the time of presentation at the emergency unit, a preliminary drug screen on urine was performed using rapid competitive immunochromatographic screening tests (ABON Biopharm, Zhejiang, China) for the detection of ketamine, methamphetamine, methadone, or morphine. The screening tests showed positive results only for methamphetamine (Figure 
A). At the same time, the blood and urine samples were collected and submitted to Zhejiang Forensic Medical Examination Center (Hangzhou, Zhejiang, China) for the confirmation and quantification of the methamphetamine present in blood using gas chromatography mass spectrometry (GC-MS). The GC-MS results were provided by the police reports. Quantitative test revealed that the methamphetamine concentrations in serum and urine were 0.32 μg/mL and 2.35 μg/mL, respectively.
After the blood samples were taken, the dog was placed in a quiet room with minimum external stimulation. In order to treat the hyperthermia and maintain an adequate urine output, a venous catheter (Introcan; B. Braun Trading Corp, Shanghai, China) was placed in one cephalic vein for fluid administration, using 0.9% Sodium Chloride Solution. External cooling was continued using ice packs, and the rectal temperature was continually monitored to prevent possible hypothermia. The dog was given 3.6 mEq of intravenous sodium bicarbonate to correct the base deficit over the first 12 hours. The dosage then was adjusted according to the subsequent blood gas analysis. An intermittent intravenous injection of 50% Glucose Solution was given as appropriate based on continuous monitoring of serum glucose for the regulation of mild hypoglycemia. Subcutaneous amoxicillin and clavulanate potassium (7 mg/kg amoxicillin and 1.75 mg/kg clavulanate potassium as effective; Synulox Injection, Pfizer, New York) was begun on admission, and withdrawn within 4 days after the white blood cell count returned to normal and after confirming that urine cultures proved no growth of bacteria. Intravenous phenobarbital (4 mg/kg; Sodium Phenobarbital Injection, Tianjin Pharma., Tianjin, China) and acepromazine (0.05 mg/kg; Acepromazine injection, Mavlab Pty Ltd, Queensland, Australia) were given to control seizures and agitation. The dog was started on low-molecular-weight heparin to control coagulation abnormalities, supported with intravenous fluids for maintaining sufficient microvascular perfusion.
Over the initial 24 hours of hospitalization, the dog demonstrated progressive improvement, with the high fever resolved (between 36.5 and 37.6°C), normal serum glucose concentration, and sufficient urine output. After administration of phenobarbital and acepromazine the dog was lay down in the cage and ceased its repetitive circling. Nevertheless, it still had several short seizures and displayed occasional muscle twitching. Following the repetitive administration of phenobarbital and acepromazine no more seizures, muscle twitching, or repetitive circling behaviors were observed (beyond 48 hours after hospitalization). Urine was screened again on day 3 using the same rapid assay and at that time failed to reveal the presence of methamphetamine. By the sixth day of hospitalization the dog was clinically well (no diarrhea, no petechiae, no pupillary dilation, and eating and drinking well) and all laboratory data had returned to normal with the exception of a mildly elevated ALKP (220 U/L, reference range 23-212 U/L). The dog was sent to local veterinary hospital with no further medications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.7, 'kg']}",14.8,14.06,15.54,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.7 kg. Hence, the patient's maintenance fluid is 3.7 kg * 4 mL/kg/hr = 14.8 mL/hr.
Hence, the patient's fluid maintenance is 14.8 mL/hr."
5256,22,Maintenance Fluids Calculations,physical,decimal,pmc-6849168-1,Extracted,"In August 2018, a 58-year-old man [height: 169 cm, body weight: 56 kg, and body mass index (BMI): 19.6 kg/m2] was admitted to our emergency department with upper abdominal pain, hyperglycaemia and metabolic acidosis. He had lived with type 2 diabetes for 16 years and had no history of any allergy, hypertension, hyperlipidaemia or renal diseases. Five months prior to admission, he initiated subcutaneous insulin administration (SIA) with the biphasic insulin analogue aspart after failure of sitagliptin and metformin therapies (HbA1c: 8.07% [65 mmol/mol]). Glycaemic control did not improve (HbA1c: 10.2% [88 mmol/mol]; total daily insulin dose was 20 UI), and aspart administration caused mild allergic symptoms. Aspart was then substituted by biphasic human insulin in which the total daily insulin dose increased up to 37 units. However, 5 months after the initiation of these regimens, he developed a pruritic wheal, especially distinct at the injection site (Fig. a). Pruritic wheals appeared within 10 min of injection and lasted over 24 h. The levels of fasting blood glucose and HbA1c deteriorated to 8.6 mmol/litre and 11.2% (99 mmol/mol), respectively. An allergy to insulin was then suspected. A skin prick test was carried out with different types of insulin [insulin aspart (NovoRapid®), recombinant human insulin (Actrapid® and Insulatard®), insulin glargine (Lantus Solostar®), and insulin lispro (Humalog®, Humalog mix®)] in which the test was positive for all of these types. Two days before admission, he stopped SIA because of an allergic reaction and was treated with anti-allergic drugs.
One day later, he experienced weakness and upper abdominal pain. On admission, clinical examination revealed a dehydrated patient with a heart rate (HR) of 130 beats/minute, a temperature of 37 °C and a systolic/diastolic blood pressure (BP) of 150/90 mmHg. He was tachypnoeic and dyspnoeic with a respiratory rate (RR) of 28 breaths/minute. He had hot and dry skin without pruritic wheals, isochoric pupils, and had no focal neurological deficit. He had normal breath sounds and a soft and non-tender abdomen. Electrocardiogram showed sinus tachycardia at a rate of 130 beats/minute. Echocardiography revealed normal chamber size and systolic function, without valvular lesions. Laboratory tests revealed high anion gap metabolic acidosis with an arterial blood pH of 6.984, bicarbonate of 2.5 mmol/litre and a serum anion gap (AG) of 26.4 mmol/litre. The arterial PO2 and PCO2 levels were 164.3 mmHg and 10.5 mmHg, respectively. Serum glucose was 20.79 mmol/litre, serum lactate was 1.5 mmol/litre, and urinary ketone was 11.44 mmol/litre. Serum potassium, sodium and chloride levels were 5.7 mmol/litre, 137.4 mmol/litre and 114.2 mmol/litre, respectively. Liver and renal function tests were normal, and there was a slightly elevated white blood cell count of 14.1 × 109/l. He was admitted to our emergency ICU with a diagnosis of severe DKA in a patient with type 2 diabetes with an insulin allergy. Intravenous (IV) fluids, bicarbonate and potassium replacement and intermittent haemodialysis (IHD) were initiated. During the first 12 h, he received an initial 1 litre IV bolus of normal saline (0.9% NaCl) in the first hour, followed by a rate of 250 mL/hour, with 26 mmol of potassium chloride added per litre of normal saline. He also received 500 mL of sodium bicarbonate 1.4% solution over 2 h and then repeated as needed. However, his tachypnoea (35 breaths/minute) and metabolic acidosis persisted (arterial blood pH of 7.192, bicarbonate of 4.0 mmol/litre, PO2 of 156.1 mmHg, PCO2 of 10.3 mmHg, AG of 24.69 mmol/litre), prompting the initiation of CVVHDF using the Prismaflex® system (Gambro Lundia AB, Sweden) at the following settings: blood flow, 160 mL/minute; replacement volume, 1200 mL/hour; and dialysate, 1200 mL/hour. After 24 h of fluid resuscitation (6500 mL), he was haemodynamically stable and had 3500 mL of urinary output. However, he developed a decreased level of consciousness, agitation, and fatigue of his respiratory muscles. He was intubated for airway protection and was mechanically ventilated for respiratory support. Furthermore, hypotension (HR and BP were 120 beats/minute and 80/40 mmHg, respectively) occurred after intubation. A bolus of normal saline (1000 mL) was provided, and norepinephrine was administered at a rate of 0.3 μg/kg/minute. Haemodynamic stability was recovered after 1 h, with a HR of 110 beats/minute, BP of 120/60 mmHg, and measured CVP value of 8 cmH2O. Arterial blood gases revealed a worsening metabolic acidosis with an arterial blood pH of 7.022, bicarbonate of 2.5 mmol/litre and a serum AG of 25.75 mmol/litre. Renal function declined with a serum creatinine level of 198 μmol/litre. Serum glucose, potassium, sodium and chloride levels were 23.32 mmol/litre, 4.35 mmol/litre, 140.5 mmol/litre and 116.6 mmol/litre, respectively. CVVHDF and IV fluids and potassium replacement were continued. Although haemodynamic and respiratory stabilities were maintained, metabolic acidosis persisted. Further skin prick testing with different types of insulin [insulin aspart (NovoRapid®), recombinant human insulin (Actrapid®, Insulatard®, Mixtard®, Humulin R®, and Humulin N®), and insulin glargine (Lantus®)] only showed positivity to two (aspart, human) of these types. However, the intradermal test with these types was positive (the time of testing as shown in Additional file ). A 40 mg dose of methylprednisolone sodium succinate and 10 mg of diphenhydramine were given in the event of the possible occurrence of a severe allergic reaction, and continuous IV infusion of recombinant human insulin was initiated at a rate of 0.1 units/kg/hour. Approximately 60 min after continuous IV infusion of insulin, he developed hypotension without any signs or symptoms of allergic reactions of the skin and mucosa, and the HR was 115 beats/minute and BP was 80/40 mmHg. Infusion of insulin was temporarily stopped followed by intravenous epinephrine administration at a starting rate of 0.15 μg/kg/minute in addition to an IV bolus of 1000 mL of normal saline. He regained haemodynamic stability after 30 min, including a HR of 110 beats/minute and a BP of 120/70 mmHg, and did not require any additional administration of epinephrine after 5 h. Continuous IV infusion of recombinant human insulin at a rate of 0.1 units/kg/hour continued without any events such as signs or symptoms of allergic reactions and hypotension.
On day 5 of follow-up, ketonaemia, metabolic acidosis (arterial blood pH of 7.465, bicarbonate of 18.4 mmol/litre and AG of 12.73 mmol/litre), and renal dysfunction (serum creatinine of 108 μmol/litre) had almost resolved, and CVVHDF was withdrawn. He did not require vasoconstrictors. Continuous IV infusion of recombinant human insulin continued and was adjusted according to blood glucose levels measured with a portable blood glucose meter. He was extubated on day 7 and transitioned from continuous IV insulin infusion to subcutaneous insulin (combined regular human insulin with insulin glargine) administration on day 14. He was discharged on day 21 with SIA (combined regular human insulin with insulin glargine) in combination with an oral antidiabetic drug (sitagliptin and metformin). Three months later, glycaemic control was gradually restored (HbA1c: 8.3% [67 mmol/mol]; total daily insulin dose was up to 44 UI); he still appeared to have mild allergic symptoms, such as local erythaema and swelling, especially distinct at the injection site of insulin glargine (Fig. b).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [56.0, 'kg']}",96,91.2,100.8,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 56.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (56.0 kg - 20 kg) = 96.0 mL/hr.
Hence, the patient's fluid maintenance is 96.0 mL/hr."
5257,22,Maintenance Fluids Calculations,physical,decimal,pmc-4859119-1,Extracted,"On October 11, 2011, a 23-year-old G3P2 (both alive) woman was referred to our department on a suspicion of a malignant ovarian disease. She had presented at the referring clinic 2 weeks earlier with abdominal distension, pain, dyspnea, nausea, and vomiting. She was 10 weeks pregnant; her last menstrual period was on August 1, 2011. The abdominal pain had increased 2 days prior to referral despite taking analgesics (paracetamol). She did not have any previous medical or surgical disease, and her gynecological history was unremarkable. Menarche was at the age of 12, and menstrual cycles were regular. She had two normal vaginal deliveries at term, in 2008 and 2010.
She was well-nourished and weighed 58 kg, in acute distress and mild dyspnea. Temperature, pulse rate, and blood pressure were within normal limits. Her physical examination revealed a moderately distended, tender, and tense abdomen with positive shifting dullness on percussion. The bowel sounds were normal. On pelvic examination, the uterine size and ovaries could not be made out because of the distention and tenderness, but bilateral irregular and mobile adnexal masses could be palpated with difficulty. Pelvic ultrasound revealed a single viable fetus at 11 weeks (crown-rump length 38 mm), with bilateral multilocular cystic ovarian masses, measuring 18.7 cm × 13.1 cm on the right and 14.6 cm × 12.6 cm on the left, associated with the moderate generalized peritoneal free fluid collection. The liver, gall bladder, spleen, and both kidneys were normal [].
Laboratory studies revealed: Hemoglobin; 12.1 g/dl, hematocrit (Hct); 35.5%, white blood cell; 8700, platelet; 406,000, Na; 133 mEq/L, K; 4.5 mEq/L, blood urea nitrogen; 23 mg/dl, creatinine; 0.5 mg/dl, fasting blood sugar; 90 mg/dl, aspartate aminotransferase; 44 U/l, alanine aminotransferase; 23 U/l, alkaline phosphatase; 105 U/l. Total protein; 5.6 g/dl, albumin 3.2 g/dl, liver function tests, prothrombin time, partial thromboplastin time, tests were also normal. Blood group was B rhesus positive and genotype AA.
A diagnosis of severe OHSS, with viable intrauterine pregnancy, was made. She was admitted for monitoring and supportive therapy. She had intravenous fluid (normal saline) at least 2000 ml per day, and liberal oral fluid intake encouraged. Medications included oral bromocriptine 2.5 mg daily for 5 days in addition to oral tramadol, piriton, metoclopramide, vasoprin, and ranitidine. During hospitalization, daily weighing, and abdominal girth measurements showed an increase from 58–63 kg to 89–92 cm, respectively, but there were no respiratory difficulties and her vital signs remained stable, the daily urine out-put was satisfactory. She responded well to treatment and at discharge, after 7 days; a full blood count, electrolytes, liver function, and coagulation profile gave results within normal limits. Hct was 34%; she weighed 63 kg, and abdominal girth was 88 cm.
She was seen weekly at the clinic. Resolution of the ascites and decrease in follicular size occurred gradually, demonstrated by clinical and ultrasonographic studies. On November 01, 2011; she had no complaints, she weighed 60 kg, abdominal girth was 84 cm and Hct; 32%, ultrasonography revealed a single active fetus of 13 weeks gestation, with regressed adnexal masses with no ascites []. She remained stable, and at 26 weeks gestation ultrasound showed normal sized ovaries and there was no free fluid in the abdomen and pelvis. The fetus was compatible with 27 weeks of gestation, and no gross anomaly noted, the placenta was posteriorly located. Amniotic fluid was also within normal limits [].
The pregnancy proceeded normally and at 39 weeks of gestation, the patient had spontaneous onset labor and underwent an uncomplicated vaginal delivery of male new born weighing 3.4 kg.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [58.0, 'kg']}",98,93.1,102.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 58.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (58.0 kg - 20 kg) = 98.0 mL/hr.
Hence, the patient's fluid maintenance is 98.0 mL/hr."
5258,22,Maintenance Fluids Calculations,physical,decimal,pmc-7449603-1,Extracted,"A 3-day-old female baby was admitted to our center due to a 2-day history of postprandial vomiting of the ingested breast milk, which was of non-projectile. It was also associated with passage of black stools that were ‘sticky’ in nature as reported by the mother, low-grade fever which responded to paracetamol suspension and gradual abdominal distension. The baby was born normally via spontaneous vaginal delivery at term with a birth weight of 2.5 kg. The mother reported normal pregnancy.
Upon examination, an active baby with hemodynamic stable vitals. The abdomen was symmetrically distended with visible superficial blood veins, tender to palpate all over and reduced bowel sounds on auscultation. The respiratory, cardiovascular, genitourinary and nervous systems examination was essentially normal.
Provisional diagnosis of intestinal obstruction due to necrotizing enterocolitis with early neonatal sepsis was made. Initial blood investigations showed hemoglobin of 15.4 g/dl, BUN of 1.72 mmol/l and a serum creatinine of 72 μmol/l. Abdominal-pelvic ultrasound w revealed focal dilated bowel loops with poor peristalsis, free intraabdominal fluid. The liver, spleen and kidneys had normal echo-texture and impression of pneumoperitoneum was made. Plain abdominal X-ray showed features of pneumoperitoneum ().
The baby was prepared and taken for an emergency laparotomy whereby intraoperatively, a gastric perforation was found measuring 0.5 by 0.5 cm, circumferential and located on the anterior aspect of the stomach body near the pylorus (). There was also about 50 ml of amber-colored ascites. The perforation was repaired and Grahm’s patch was put, thorough abdominal lavage and the abdomen was closed in layers. Biopsy from the perforation site revealed non-necrotizing mild chronic gastritis, not otherwise specified with ulcerations ( and ).
Postoperatively the baby faired well, started oral feeds on day-2 and tolerated. The baby developed mild surgical site infection on day 6 that was treated with daily dressing and systemic antibiotics and discharged on day 28.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.5, 'kg']}",10,9.5,10.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.5 kg. Hence, the patient's maintenance fluid is 2.5 kg * 4 mL/kg/hr = 10.0 mL/hr.
Hence, the patient's fluid maintenance is 10.0 mL/hr."
5259,22,Maintenance Fluids Calculations,physical,decimal,pmc-4152687-2,Extracted,"A 65-year-old female weighing 50 kg, presented to the emergency department with acute hydrocephalus secondary to subarachnoid hemorrhage (World federation of Neurologic Surgeon Grade 5, Fischer Grade 4). Her admission GCS was 5/15. Her past medical history included hypertension on oral anti-hypertensive medications. She was intubated and arterial line was started and shifted to the operating room for insertion of an external ventricular drain (EVD).
Upon arrival to the operating room, her initial blood pressure was 190/85 with heart rate of 90 beats/min. Initial entropy readings (RE/SE) were 56/50. Patient was connected to the ventilator and hyperventilated to achieve an EtCO2 level of 30 mmHg. Patient received 25 mcg of fentanyl, 30 mg of rocuronium and a propofol infusion was started at 20-30 mcg/kg/min was started. Scalp infiltration was done with 2% xylocaine with adrenaline. Anesthesia was titrated to keep the entropy of 40-60. Blood pressure remained elevated and entropy readings were consistent during initial stages of surgical exposure.
Immediately following the insertion of the EVD, both RE and SE values increased by 20 points (58-80 for RE and 51-72 for SE) and there was a mild reduction in blood pressure (205/99-176/80) []. Propofol infusion rate was increased to 50 mcg/kg/min and this subsequently decreased the entropy values to 40-60. Post-operatively patient was transferred to NICU and then discharged to a rehabilitation center in her local town.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [50.0, 'kg']}",90,85.5,94.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 50.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (50.0 kg - 20 kg) = 90.0 mL/hr.
Hence, the patient's fluid maintenance is 90.0 mL/hr."
5260,22,Maintenance Fluids Calculations,physical,decimal,pmc-4339194-2,Extracted,"The second case (GS0155) is a 27-year-old female. She had had some episodes of right hemiparesis and a bowel volvulus in pediatric age. She was studied in the Neurology Unit after an episode of right hemiparesis, paresthesia and a visual field deficit. Imaging studies did not show any significant alteration. Biochemical analysis showed calcium values in the lower limit of normality (8.5–9.3mg/dl) and elevated PTH (200–300pg/ml), so she was diagnosed of pseudohypoparathyroidism. She did not present any symptom of Albright’s hereditary osteodystrophy (height 1.65m; weight 68.5kg; BMI: 25.1). No other hormone deficit was detected (TSH, 3μU/ml). She referred regular periods. Calcium and vitamin D supplements (both cholecalciferol and calcifediol) were prescribed, although she is not properly following the treatment.
In the last visit, she referred paresthesia in upper extremities with no calcium supplementation for a month. She brought a report with analytical levels: Ca, 8.7mg/dl; P, 3.9mg/dl; Mg, 2.4mg/dl, TSH, 4.15μU/ml; PTH, 349pg/dl; 25(OH)D, 37.2 ng/ml; urine Ca, 76mg/day; CLcr, 177ml/min; Dual-energy X-ray absorptiometry (DXA) with a lumbar T score of -0.7 SD and a femoral T score of -0.3 SD. She is clinically stable, with no symptoms of latent tetany. Biochemical analysis were performed: Ca, 8.9mg/dl; P, 3.7mg/dl; HbA1c 5.4%, PTH, 417pg/dl; 25(OH)D, 44 ng/ml.
Her mother was diagnosed at age 48 years with a multinodular toxic goitre. She was treated with I131 that caused iatrogenic hypothyroidism, so she was prescribed levothyroxine 125μg/day. Her past clinical history showed symptoms of generalized anxiety, being followed in the Mental Health Unit. She does not present any characteristic phenotype, with a normal physic exploration (height 1.64m; weight 70kg; BMI: 26).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [68.5, 'kg']}",108.5,103.075,113.925,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 68.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (68.5 kg - 20 kg) = 108.5 mL/hr.
Hence, the patient's fluid maintenance is 108.5 mL/hr."
5261,22,Maintenance Fluids Calculations,physical,decimal,pmc-6736139-2,Extracted,"A 29-year-old woman presented to our hospital on February 12, 2013 at a gestational age of 40+2 weeks, combined with less amniotic fluid for 1 day. Two years ago, left ovarian cyst about 5.0 cm in size was found and no treatment was given. Membrane ruptured naturally at 19:45 on February 12, 2013. Oxytocin intravenous drip was given to strengthen uterine contractions at 8:45 on February 13. Fetal heart monitoring showed that the fetal heart decelerated with a ratio of 69 to 88 bpm. Oxytocin intravenous drip was terminated immediately. Persistent oxygen inhalation of oxygen was performed accordingly. The fetal heart continued to slow down, and fetal distress was considered. Cesarean section was performed in the transverse incision of lower segment of uterus under local anesthesia. About 1500 ml intraoperative hemoperitoneum was found in the operation. A full-term male infant was delivered. Left appendage and the left posterior wall of the uterus were adhered to the posterior wall of the pelvic and abdominal cavity. Meanwhile, multiple blood clot and active bleeding were seen. Combined with the medical history, intraperitoneal hemorrhage was suspected. The causes were unknown. Then the patient was transferred to abdominopelvic cavity exploration. Diffuse adhesion zone and blood clot were found in the posterior wall of uterus during the operation. The left ovary was adhered to the left posterior wall of the uterus and the posterior lobe of the broad ligament. The diameter of endometriosis cyst in left ovary was about 3 × 4 × 5 cm, and the rupture showed a length of 2 cm. There was no active bleeding. No chocolate like liquid was seen around the left ovary. Chocolate-like liquid was seen in the content of the capsule. Multiple inflammatory adhesions were found in the left posterior wall of the uterus, the blood vessel on the surface was opened. Multiple active bleeding was seen, and a local hematoma of 4 × 4 × 11 cm was formed on the serosal surface of the uterus. Then the left ovarian cyst was removed. The volume of hemorrhage and blood transfusion were about 2000 ml and 800 ml, respectively. The weight of the newborn was 3390 g, the 1-minute Apgar score was 6 (muscle tension- 2, breath-1, heart rate-1), the 5-minute and 10-minute Apgar score were 9 (muscle tension-1). The mother and child were recovered and discharged.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3390.0, 'g']}",13.56,12.882,14.238,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3390.0 g so this converts to 3390.0 lbs * kg/1000 g = 3.39 kg. Hence, the patient's maintenance fluid is 3.39 kg * 4 mL/kg/hr = 13.56 mL/hr.
Hence, the patient's fluid maintenance is 13.56 mL/hr."
5262,22,Maintenance Fluids Calculations,physical,decimal,pmc-3173914-1,Extracted,"A 19-month-old female child presented to the hospital with complaints of constipation since 6 months of age and difficulty in passing urine for last 6 months. Parents had noticed lower abdominal fullness for last 1 year. The child was born out of non-consanguineous marriage between young parents at full term by an uncomplicated vaginal delivery. Antenatal ultrasound screening had not been performed. There was no history suggestive of birth asphyxia or trauma. The parents gave history of increasing constipation for which laxatives and enemas had been advised but did not provide relief. The child passed small amounts of urine at short intervals.
The child weighed 7.2 kg and other anthropometric parameters including head circumference were appropriate for age. Chest examination revealed multiple rib defects on both sides but air entry was normal without any added sounds. Abdominal examination revealed a cystic mass in the suprapubic region arising out of pelvis and reaching up to umbilicus. Digital rectal examination showed normal tone of the normally placed anus but a large cystic mass was felt posteriorly which precluded higher examination. Examination of the spine at the back did not show any bony defects. There was no neurological deficit.
Hematological investigations showed hemoglobin of 11.2 g/dL, TLC of 12,000 per cc and platelets of 117×103 per mm3. Kidney function tests were normal.
X-ray chest [] showed multiple segmentation anomalies of cervicodorsal vertebrae along with fusion anomalies of ribs on both sides. Echocardiogram did not show any associated cardiac anomaly. Ultrasound of abdomen demonstrated a cystic lesion posterior to urinary bladder measuring 9×4 cm with well-defined dome shaped upper margin and tapering inferiorly. No internal echoes were seen within the lesion. Urinary bladder was pushed anteriorly. There was no evidence of hydroureteronephrosis. Barium enema demonstrated Scimitar sign along with increased presacral space, displacement of the rectum anteriorly and sigmoid colon to the right [Figure and ]. Computed tomography [Figure and ] showed an anterior sacral dysraphic defect with large cystic mass in presacral region displacing the urinary bladder anteriorly and to the right side. Posteriorly, mass was seen entering the spinal canal through large sacral bone defect. There was no hydrocephalus. Both the kidneys were displaced and rotated through their axis but there was no evidence of hydronephrosis.
An exploratory laparotomy was performed by a suprapubic transverse incision with intent to excise the meningocele from anterior route. A cystic lesion measuring about 8×4 was seen emerging within the leaves of sigmoid mesocolon from the anterior part of sacrum in the pelvis. The sigmoid colon was pushed to the right while urinary bladder was pushed to the left side []. The sac was dissected till the base. The sac was opened at the apex, clear cerebrospinal fluid (CSF) was aspirated and the sac was excised with watertight closure of the tapering base saving the nerve roots and controlling epidural veins. Closed dural defect was checked for leakage of CSF and hemostasis and then covered with local tissue. CSF was sent for culture and sac was sent for histopathological examination (HPE). The CSF culture was reported as sterile while HPE report showed fibrocollagenous and fibrofatty tissue with few entrapped blood vessels and occasional nerve fibers.
There was no neurological deficit in the immediate postoperative period. There was no evidence of constipation, urinary complaints or hydrocephalus at 6 months of follow-up. Although the rib defects have not caused any clinical problem till now, the child remains in follow-up to manage if need arises.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.2, 'kg']}",28.8,27.36,30.24,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.2 kg. Hence, the patient's maintenance fluid is 7.2 kg * 4 mL/kg/hr = 28.8 mL/hr.
Hence, the patient's fluid maintenance is 28.8 mL/hr."
5263,22,Maintenance Fluids Calculations,physical,decimal,usmle-528,Extracted,"A 40-year-old woman comes to the physician because of a 2 week history of anorexia and a feeling of dryness in the mouth; she has had a 5.8-kg (12.8-lb) weight loss during this period. She also complains of fatigue and inability to carry out daily chores. One year ago, she was diagnosed with advanced cervical carcinoma, metastatic to the pancreas, and is being treated with combination chemotherapy. She is 157 cm (5 ft 2 in) tall and weighs 47 kg (103.6 lb); BMI is 19.1 kg/m2. She appears thin and pale. Her temperature is 37.7°C (99.8°F), blood pressure is 110/68 mm Hg, pulse is 105/min, and respirations are 28/min. There is generalized weakness and atrophy of the skeletal muscles.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [47.0, 'kg']}",87,82.65,91.35,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 47.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (47.0 kg - 20 kg) = 87.0 mL/hr.
Hence, the patient's fluid maintenance is 87.0 mL/hr."
5264,22,Maintenance Fluids Calculations,physical,decimal,pmc-3503352-1,Extracted,"An 8-month-old boy, 6 kg, was referred to our hospital with a history of recurrent upper and lower respiratory infections, progressive tachypnea, and obvious chest retraction at rest and heart murmurs. In last examination his specialist hearing a suspicious moderate continious murmur and refer him to us. Cardiomegaly and pulmonary congestion were seen in chest X-ray. His cardiothoracic ratio was near 65% in chest X-ray. Transtorasic echocardiography showed moderate degree of mitral regurgitation (MR), dilated left atrium and left ventricle, severe turbulence flow in pulmonary artery and large APW (7-8 mm) and “T” artifact at the edge of the defect that distinguishes it from normal dropout [].
At cardiac catheterization we found a large APW with pulmonary to aortic flow ratio above 3 and elevated pulmonary pressure (70% of systemic arterial pressure) [].
The patient was operated after diagnosis by transaortic approach using a median sternotomy and cardiopulmonary bypass. The patient had good recovery from operation. His respiratory symptoms decreased after surgery. Echocardiography was performed and showed normal left ventricular function, and no residual aortopulmonary defect. No evidence of narrowing or stenosis of aorta and pulmonary arteries and no distortion of semilunar valve were found by echocardiographic study. Our patient had trivial to mild MR after operation. He is active and asymptomatic at follow-up period (one year). His mild mitral regurgitation is decreased to trivial regurgitation and cardiac function is normal.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6.0, 'kg']}",24,22.8,25.2,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6.0 kg. Hence, the patient's maintenance fluid is 6.0 kg * 4 mL/kg/hr = 24.0 mL/hr.
Hence, the patient's fluid maintenance is 24.0 mL/hr."
5265,22,Maintenance Fluids Calculations,physical,decimal,pmc-4934552-1,Extracted,"The patient was a 47 year-old female who was 5 ft. tall and 175 lbs. with a body mass index of 34. She had a five-plus year history of a full-thickness DFU on the left plantar mid-foot. Her DFU had been managed by her podiatrist throughout its course and the patient reported that the wound had been open continuously during this time. Previous interventions included reconstructive surgery for Charcot foot deformity of the left foot six years previously, regular sharp debridement, use of a platelet-derived growth factor (Becaplermin Gel, 0.01%) topically, offloading via total contact casting initially and the use of an offloading walker boot and wheelchair more recently. Reportedly, TCC was discontinued because the patient felt unsteady and declined further use. Other past medical history was significant for Type 1 diabetes mellitus (DM) for 41 years, left eye blindness due to diabetic retinopathy, hypothyroidism and hypertension (HTN). She had a history of cataract surgery on her right eye two years previously. Medications included Synthroid for hypothyroidism, Lisinopril for HTN, and Humulin-N and insulin for DM. The patient was a home-maker and resided with her husband and their three children in a one-level home. She denied use of tobacco or alcohol. She was frustrated by her lack of progress toward wound healing and self-referred to the outpatient wound clinic in order to obtain a second opinion.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [175.0, 'lbs']}",119.3786,113.40967,125.34753,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 175.0 lbs so this converts to 175.0 lbs * 0.453592 kg/lbs = 79.3786 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (79.3786 kg - 20 kg) = 119.3786 mL/hr.
Hence, the patient's fluid maintenance is 119.3786 mL/hr."
5266,22,Maintenance Fluids Calculations,physical,decimal,pmc-7160728-1,Extracted,"A 50-year-old woman was admitted to our outpatient clinic for medical workup of a severe form of postprandial hypoglycaemia. Seven years earlier, a Roux-Y gastric bypass was performed due to morbid obesity (preoperative BMI 44.7 kg/m2and weight 129 kg). Within two years, the patient lost 57 kg (BMI 25.5 kg/m2). A year later, the patient noticed, for the first time, hypoglycaemic episodes 1-2 hours after meal intake, which were mainly characterized by loss of concentration, severe fatigue, and auditory and visual impairment that quickly resolved after intake of carbohydrates. An oral glucose tolerance test, at that time, confirmed the presence of symptomatic postprandial hypoglycaemia (2.9 mmol/l). Symptoms persisted despite dietary modifications of up to twelve small meals, each containing a maximum of 20 g of carbohydrates. Off-label treatment with acarbose, saxagliptin, and metformin by her treating physician reduced the frequency and severity of hypoglycaemic episodes but did not significantly improve the situation. Eventually, the patient was referred to our hospital. Her remaining personal history included a mild form of orthostatic dysregulation, migraine, and a multilocular nodular hepatic hyperplasia that required a left-sided hemihepatectomy 17 years ago. The clinical examination was unremarkable apart from irritation-free scars after hemihepatectomy (height, 168 cm; weight, 72 kg; BMI, 25.5 kg/m2; blood pressure, 127/67 mmHg; regular heartbeat, 80 bpm). Laboratory analysis including blood smear; biochemistry comprising electrolytes and kidney and liver parameters; glycated haemoglobin; blood lipids; iron; vitamins B1, B6, B12, and D; and zinc were within reference ranges. A continuous glucose flash monitoring system confirmed a typical pattern of postbariatric hypoglycaemia without any signs of fasting or nocturnal hypoglycaemia. A mixed-meal test (300 ml Ensure plus®) containing 60 g of carbohydrates after a 10-hour fasting period confirmed symptomatic postprandial hypoglycaemia (sweating, drowsiness, odd behaviour, and incoordination) at a glucose level of 2.5 mmol/l, and intravenous glucose administration was required for immediate remission of symptoms (). Due to the severe symptomatic presentation of the patient, a 68Ga-DOTA-Exendin-4 PET/CT was performed to exclude an atypical presentation of an insulinoma or focal nesidioblastosis, which might be a surgical target [–]. Therein, the pancreas showed a homogeneous signal distribution (SUV 5.7–8.3), but intensive uptake in the first and second part of the duodenum (SUVmax of 10.0) was observed (). To further differentiate this unexpectedly strong tracer accumulation, a double-balloon enteroscopy was performed, which revealed macroscopically unremarkable intraluminal structures in the duodenum. Histologically, there were no signs of malignancy or inflammation (). Representative biopsies of the pars 2 duodenii showed normal mucosa with hyperplastic Brunner's glands, which were strongly positive for the GLP-1 receptor on immunohistochemistry but negative for insulin (Figures and ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [72.0, 'kg']}",112,106.4,117.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 72.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (72.0 kg - 20 kg) = 112.0 mL/hr.
Hence, the patient's fluid maintenance is 112.0 mL/hr."
5267,22,Maintenance Fluids Calculations,physical,decimal,pmc-2852812-1,Extracted,"A 66-year-old, 160 cm, 48 kg man was scheduled to undergo a total knee arthroplasty. His medical history revealed a ten-year history of diabetes mellitus (DM), uncertain hypertension history, and previous knee surgery. The patient suffered from occasional dyspnea and chest discomfort. An ECG showed a sinus bradycardia of 57 bpm and a 99-m Tc-MIBI scan was normal. Laboratory tests showed glucose 4+ on urinalysis, HbA1c 10.0%, and serum glucose around 200-300 mg/dL.
At the pre-anesthesia preparation room, ECG and pulse oximetry were applied and blood pressure (BP) was measured non-invasively at 5-min intervals. The initial BP was 104/56 mmHg with a heart rate (HR) of 57 bpm. Combined spinal-epidural anesthesia was administered using a 17-gauge Tuohy needle and 27-gauge Whitacre spinal needle at the level of the L3-4 interspace under standard aseptic conditions. Upon the first attempt, the epidural space was found using a loss of resistance technique, and clear cerebrospinal fluid (CSF) was obtained after spinal needle insertion. There were no paresthesias. A total of 2.0 mL of 0.5% tetracaine, mixed with saline, the patient's CSF, and epinephrine 1 : 200,000, was administered slowly to the patient. An epidural catheter was inserted without resistance and advanced 5 cm upward (by having the bevel of the needle pointed cephalad) and a sensory block to T12 was achieved by a pin-prick test. Then, BP dropped to 87/46 mmHg, and the sensory block was checked at T6. Ephedrine hydrochloride 12 mg and 20 mg was administered intravenously and intramuscularly, respectively. BP raised to 120/65 mmHg, and the patient was transferred to the operating room. In the operating room, BP was 147/69 mmHg and rose to 153/79 mmHg after turning a tourniquet on. Then, the patient complained of a sudden onset of a severe headache and became restless. The BP recorded at the onset of the headache was 190/123 mmHg, and HR was 75 bpm. No ECG changes were noted. Labetalol hydrochloride (10 mg) was injected, and, to sedate the patient, midazolam (2 mg) was injected, but the patient was still irritable. Then, thiopental sodium (100 mg) was injected via IV. BP was maintained around 160/65 mmHg for an hour before a sudden tachycardia of 140 bpm and BP of 200/97 mmHg was observed. Lidocaine (80 mg) was injected and isosorbide dinitrate infusion began due to ST depression. The patient was semi-comatose with asymmetric pupils. BP gradually decreased and was maintained around 105/60 mmHg. After taking a brain CT scan, the patient was transferred to the ICU.
The brain CT showed a large amount of SAH and an intraventricular hemorrhage (IVH) (), and a CT brain angiogram showed a 6-mm ruptured intracranial aneurysm at the anterior communicating cerebral artery (ACOM) and a 4-mm unruptured cerebral aneurysm at the left middle cerebral artery bifurcation ( and ). GDC coil embolization at the ACOM was performed, and external ventricular drainage was carried out. The patient was transferred to the ICU for observation.
The patient was semi-comatous without light reflex, and pupils were asymmetric. BP was maintained by infusing dopamine, vasopressin, and levophad. The patient fell into a coma, unable to maintain stable vitals, and died 17 days after the surgery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [48.0, 'kg']}",88,83.6,92.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 48.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (48.0 kg - 20 kg) = 88.0 mL/hr.
Hence, the patient's fluid maintenance is 88.0 mL/hr."
5268,22,Maintenance Fluids Calculations,physical,decimal,pmc-6559969-1,Extracted,"A two-and-a-half-month-old male baby who had been hospitalized in the Pediatrics Ward for one month because of hypotonia, pneumonia, and respiratory distress was internalized in th PICU with the same symptoms. It was learned that he was born from the first pregnancy of a 28-year-old mother in the 38th gestational week by cesarean section because of polyhydramniosis and non-progressive labor with a birth weight of 2960 g. There was no consanguinity between the parents. It was stated that there was a considerable decrease in the baby’s movements during pregnancy. On physical examination, the height was found as 59 cm (50th percentile), the weight was found as 4550 g (3–10th percentile) and the head circumference was found as 38 cm (10–25th percentile). His consciousness was open and he was interested in the surroundings. The Glasgow Coma Score (GCS) was found as 15. His body temperature was measured as 37.2°C, apical heart beat was 145/min, respiratory rate was 62/min, and blood pressure was found 88/49 mm Hg. Marked hypotonia and dismorphic findings including small chin, long face, and highly arched palate were found. On examination of the respiratory system, bilateral crepitant rales were found. Examination of the other systems was found to be normal. Biochemical measurements were found to be normal except for a slight elevation in transaminases (AST: 82 IU/L, ALT: 84 IU/L) and respiratory acidosis was found (pH: 7.09, pCO2: 85 mm Hg, HCO3: 24 mmol/L). A complete bood count was found as normal. Among the infection markers, C-reactive protein was found as 0.53 mg/dL (0.01–0.5) and procalcitonin was found as 0.48 ng/mL (<0.5). On lung radiography, diffuse infiltration was observed in the right lung. The patient was intubated and mechanical ventilation was initiated. The antibiotics he was receiving (intravenous ampicillin and cefotaxim) were switched to intravenous vancomycin and meropenem.
In further investigations, the blood lactate, amino acid, carnitine, acylcarnitine, very-long-chain fatty acid levels, and urine organic acids were found as normal. Echocardiography, fundoscopic examination, and bone radiographs were found as normal. Mild laryngomalacia was found on bronchoscopy and a sweat test was within the normal limits. Upper gastrointestinal endoscopy was normal. No pathology was found on brain magnetic resonance imaging except for a choroid plexus cyst. Chromosomal analysis, spinal muscular atrophy gene examination, and fluoresence in-situ hybridization (FISH), which was performed in terms of Prader-Willi syndrome, were found to be normal. In the microscopic examination of the muscle biopsy, which was performed after all these results were obtained, a ‘nemaline body’ (rod body) was observed mostly in the sarcolemmal regions (–). A diagnosis of NM was made with these findings and further molecular examination was planned. NM_001100.3: c.1075A>C (p.I359L) (heterozygous) mutation was found in skeletal muscle α-actin” (ACTA1) gene whole genome sequencing, which was performed with the new-generation sequence analysis method (). The parents’ genetic tests directed to the disease were found to be normal.
Tracheostomy was performed on the 23rd day of hospitalization in the patient who failed extubation preparation tests because of hypotonia and insufficient respiratory effort. Subsequenly, the patient was discharged on the 45th day of hospitalization, education was given to his family, and he was followed up with a house ventilator. Our patient is aged 18 months at the present time, he is being connected to house ventilator at night and his respiration in room air is sufficent in the daytime. He can walk with assistance, he is being fed with a nasogastric tube because of swallowing difficulty, and gastrostomy is being planned. Written informed consent was received from the parents of this patient for this case presentation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4550.0, 'g']}",18.2,17.29,19.11,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4550.0 g so this converts to 4550.0 lbs * kg/1000 g = 4.55 kg. Hence, the patient's maintenance fluid is 4.55 kg * 4 mL/kg/hr = 18.2 mL/hr.
Hence, the patient's fluid maintenance is 18.2 mL/hr."
5269,22,Maintenance Fluids Calculations,physical,decimal,pmc-8161931-1,Extracted,"A 24-year-old, 165-lb male Caucasian patient with diabetes mellitus type 1 presented to the emergency department with a complaint of abdominal pain accompanied by nausea and vomiting. The patient stated that he was unable to self-administer basal insulin for two days after he ran out of insulin pen needles. His vital signs on presentation revealed blood pressure of 84/53 mmHg, heart rate of 103 beats per minute, respiratory rate of 18 breaths per minute, and temperature of 98.2 °F (36.7 °C). Physical examination at time of presentation showed that he was ill-looking, with dry oral mucosa and poor skin turgor. Initial diagnostic tests showed high anion gap, metabolic acidosis, ketonemia, and hyperglycemia, prompting the start of diabetic ketoacidosis management and subsequent intensive care unit (ICU) transfer (Table ). At this time, the patient only had a gauge-22 peripheral line placed at the dorsum of his left hand after multiple unsuccessful attempts at placing a larger peripheral line gauge.
In the ICU, efforts at internal jugular vein central line placement were unsuccessful as well due to the patient’s low volume status, making the target vein extremely difficult to cannulate even by increasing Trendelenburg tilt and doing venipuncture at end inspiration. Right subclavian vein catheterization using the infraclavicular approach was instead performed. However, the postprocedure chest X-ray showed that the catheter was somehow in the aorta (Fig. ). Blood gas obtained from the subclavian central line revealed arterial placement, prompting removal of the catheter with no serious consequences to the patient (Table ; Fig. ). A right femoral line was successfully placed, and continuous management of diabetic ketoacidosis was achieved with eventual normalization of the anion gap and clinical improvement of the patient. The patient stayed in the intensive care unit for 2 days and was then transferred to the medicine floors for continuation of glucose management with eventual discharge on the 4th day after case management; social work assisted in securing his insulin supplies, and diabetic education was performed.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [165.0, 'lbs']}",114.84268,109.10055,120.58481,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 165.0 lbs so this converts to 165.0 lbs * 0.453592 kg/lbs = 74.84268 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (74.84268 kg - 20 kg) = 114.84268 mL/hr.
Hence, the patient's fluid maintenance is 114.84268 mL/hr."
5270,22,Maintenance Fluids Calculations,physical,decimal,pmc-5437989-1,Extracted,"An 11-year-old girl was admitted to our hospital with microscopic hematuria and nephrotic-range proteinuria detected by school urinary screening. The patient did not have any characteristic features of Fabry’s disease such as angiokeratoma or neuralgia. On admission, her physical examination was unremarkable (body weight 47.4 kg, body height 157.3 cm), and her blood pressure normal (106/60 mmHg). Laboratory investigations revealed hypoproteinemia (serum total protein 5.6 g/dL, serum albumin 2.9 g/dL, serum IgG 318 mg/dL). All other biochemical investigations were within normal limits: blood urea nitrogen 8 mg/dL, serum creatinine 0.43 mg/dL, IgA 111 mg/dL, C3 140 mg/dL (normal 84 – 151 mg/dL), C4 26 mg/dL (normal 17 – 40 mg/dL). Anti-hepatitis B surface antigen, anti-hepatitis C antibody, and anti-nuclear antibody were negative. Urinalysis findings were 3+ for occult blood and 3+ for the dipstick protein reaction; her 24-hour urine protein excretion was 2.5 g. Light microscopy analysis of the initial renal biopsy specimen revealed diffuse mesangial proliferative glomerulonephritis with fibrocellular crescents in 4 of 13 glomeruli (a). Immunofluorescence revealed granular deposits of IgA (3+) and C3 (1+) in the mesangial areas (b), and electron microscopy revealed paramesangial electron-dense deposits. Based on these findings, a diagnosis of severe IgA nephropathy was made. The patient was treated intravenously with three courses of methylprednisolone (20 mg/kg/day) pulse therapy (MPT), followed by 2 years of alternate-day prednisolone (initially 1 mg/kg and then tapered gradually) combined with an angiotensin receptor blocker (telmisartan 1 mg/kg/day). In addition, a tonsillectomy was performed 3 months after MPT. However, microscopic hematuria and mild proteinuria persisted.
At the age of 13 years, the patient was re-admitted for a second renal biopsy to assess the therapeutic effect. All laboratory investigations were within normal limits: serum total protein 6.3 g/dL, serum albumin 4.0 g/dL, blood urea nitrogen 12 mg/dL, serum creatinine 0.44 mg/dL, IgA 108 mg/dL, C3 96 mg/dL, C4 26 mg/dL. Urinalysis revealed a 2+ value for occult blood and a dipstick protein reaction of 2+; the 24-hour urine protein excretion was 0.5 g. Light microscopy analysis of the second renal biopsy specimen revealed focal segmental mesangial proliferative glomerulonephritis. Immunofluorescence revealed granular deposits of IgA (2+) and C3 (1+) in the mesangial areas, and electron microscopy revealed paramesangial electron-dense deposits. After the second renal biopsy, the patient was additionally treated with three courses of MPT, and her microscopic hematuria disappeared within 6 months.
At the age of 15 years, she was admitted for a third renal biopsy. On admission, her physical examination was unremarkable (body weight 55.9 kg, body height 165 cm), and her blood pressure normal (102/70 mmHg). Laboratory investigations were all within normal limits: serum total protein 6.6 g/dL, serum albumin 4.2 g/dL, blood urea nitrogen 11 mg/dL, serum creatinine 0.48 mg/dL, IgA 135 mg/dL, C3 121 mg/dL, C4 25 mg/dL. Urinalysis was negative for occult blood and the dipstick protein reaction was 2+; her 24-hour urine protein excretion was 0.7 g. Light microscopy analysis of the third renal biopsy specimen revealed minor glomerular abnormalities (a). Immunofluorescence revealed granular deposits of IgA (2+) in the mesangial areas, and electron microscopy revealed paramesangial electron-dense deposits. In addition, numerous myelin-like bodies were first observed in podocytes (b). Low serum α-galactosidase A activity (13.8 Agal U, cut-off value < 20) and increased GL3 excretion in the urine (0.54 mg/mgCr, control 0.1 – 0.4) were also observed. On the basis of these findings, a final diagnosis of concomitant IgA nephropathy (healing stage) and subclinical Fabry’s disease was made.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [55.9, 'kg']}",95.9,91.105,100.695,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 55.9 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (55.9 kg - 20 kg) = 95.9 mL/hr.
Hence, the patient's fluid maintenance is 95.9 mL/hr."
5271,22,Maintenance Fluids Calculations,physical,decimal,pmc-4316416-1,Extracted,"A 7-year-old boy was admitted to the hospital for persistent symptoms of polydipsia and polyuria that started in early infancy. He drank an average of 3.9 L of water per day and urinated an average of 5.1 L per day, including at least three times during the night; on physical examination, he was otherwise healthy. His height and weight were 123.3 cm (39th percentile) and 20.7 kg (15th percentile), respectively. His medical history was unremarkable, and he did not have a history of head trauma or symptoms of neurological or pituitary dysfunction. An evaluation of the family history revealed seven family members, spanning four generations, who were suspected of having the same symptoms for an extended period of time (). His father reported an intake of 11 L of water per day and a urine output of 12 L per day. His grandmother reported an intake of 10 L of water per day and a urine output of 9 L per day. The pedigree was consistent with autosomal dominant inheritance.
The basal plasma levels of free thyroxine, total triiodothyronine, thyroid stimulating hormone, cortisol, adrenocorticotropic hormone, insulin like growth factor-I (IGF-I), IGF binding protein-3 were within the normal ranges. The basal plasma osmolarity was 278 mOsm/kg H2O, the urine osmolarity was 55 mOsm/kg H2O, the urine specific gravity was less than 1.005, the plasma sodium was 139 mEq/L, and the antidiuresis hormone (ADH) level was 8.66 pg/mL. He underwent a standard water deprivation test of sufficient duration to increase plasma osmolarity and plasma sodium above 300 mOsm/kg H2O and 145 mEq/L, respectively. After seven hours, the plasma osmolarity and sodium increased to 302 mOsm/kg H2O and 145 mEq/L, respectively; the urine osmolarity was 349 mOsm/kg H2O, and the ADH was 5.62 pg/mL. During the test, he continued to have inappropriately dilute urine and fluid diuresis. His body weight decreased by 9%. After a desmopressin challenge test of 20 µg, his urine osmolarity increased to 621 mOsm/kg H2O. These results confirmed a diagnosis of partial vasopressin-deficient DI (,).
The pituitary magnetic resonance imaging (MRI) showed a relatively small and hypointense neurohypophysis ().
After informed consent was obtained, peripheral blood specimens were collected from the his family members for molecular genetic analysis. Genomic DNA (gDNA) was extracted using the Wizard genomic DNA purification kit according to the manufacturer's instructions (Promega, Madison, WI, USA). All coding exons and their exon-intron boundaries of the AVP gene were amplified by polymerase chain reaction using primers designed by the authors (available by request). Cycle sequencing was performed with a Big Dye Terminator Cycle Sequencing Ready Reaction kit (Applied Biosystems, Foster City, CA, USA) on an ABI 3130xl Genetic Analyzer (Applied Biosystems). The sequencing results were compared to a reference sequence of the AVP gene, GenBank accession number NM 000490.4. The sequence variation was described according to the recommendations of the Human Genome Variation Society (). Direct sequencing analysis of the AVP-NPII gene revealed a heterozygous c. 286G>T mutation predicting an amino acid substitution (Gly96Cys) in exon 2. The AVP-NPII genes of the his father and grandmother were found to have the same mutation ().
After treatment with oral desmopressin 0.1 mg two times daily was started, the symptoms of polydipsia and polyuria were satisfactorily controlled, resulting in a dry bed throughout the night, and an improvement in food intake and growth. In three months, he gained 3 kg. Currently he drinks approximately 1.5 L of water daily and has a urine output of 1.5 L per day. His father and grandmother's water intake/diuresis per day are 1.8 L/1.8 L and 3.0 L/2.0 L, respectively, due to the effects of the medication.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [20.7, 'kg']}",60.7,57.665,63.735,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 20.7 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (20.7 kg - 20 kg) = 60.7 mL/hr.
Hence, the patient's fluid maintenance is 60.7 mL/hr."
5272,22,Maintenance Fluids Calculations,physical,decimal,pmc-4900332-1,Extracted,"A 58-year-old man presented with 3 weeks of dysphagia, which was experienced predominantly with solid foods. He had lost 3 kg in the last month. He had no past medical history. He had been a heavy drinker (1 L of beer per day) and a heavy smoker (20 cigarettes per day for 35 years). Laboratory tests showed the following: 162 U/L serum amylase (normal value <37–125 U/L), 160 IU/L serum lipase (normal value <6–53U/L), 172 mg/dl blood glucose, 8040/µL white blood cells, and 10.61 mg/dl C-reactive protein (CRP). Tumor markers (SCC, CEA, and CA19-9) were negative.
Upper gastrointestinal endoscopy showed mild narrowing of the lower esophagus. On chest and abdominal CT, cystic lesions extended from the abdomen into the mediastinum along with the esophagus and aorta, presumably via the esophageal and aortic hiatus. One of the mediastinal cysts also extended into the retrocrural space. Bilateral pleural effusions were seen. One of the abdominal cysts was connected to the pancreatic body. The main pancreatic duct (MPD) in the pancreatic tail was slightly dilated. A calcification was seen in the body of the pancreas (–). A laparoscopic lymph node biopsy was performed due to the possibility of necrotic lymph node metastases. There were no malignant cells in the specimens. Conservative antibiotic therapy was administered. Two months’ symptom after onset, repeat chest and abdominal CT images showed that the size of each cystic lesion had diminished. The patient was then diagnosed with pancreatic pseudocysts caused by chronic pancreatitis. Eight months after symptom onset, he returned with complaints of upper left abdominal pain. An abdominal CT indicated that the size of the cyst connected with the pancreatic body had increased (). CT-guided percutaneous drainage of the pancreatic cyst was performed and the size of the cyst was reduced. There was no increase in the size of the cyst upon further follow-up CT. He currently receives regular outpatient treatment.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.0, 'kg']}",12,11.4,12.6,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.0 kg. Hence, the patient's maintenance fluid is 3.0 kg * 4 mL/kg/hr = 12.0 mL/hr.
Hence, the patient's fluid maintenance is 12.0 mL/hr."
5273,22,Maintenance Fluids Calculations,physical,decimal,pmc-4058546-1,Extracted,"A 53-year-old woman, weighing 60 kg and with a body mass index of 23.4 kg/m2, was scheduled for an EGD during her routine medical exam. Ten years prior, she had visited the emergency medical center for allergic urticaria of unknown cause. The patient had no previous history of prescription use, smoking, or drinking. Further, no significant abnormalities were noted on her complete blood count (CBC) or blood chemistry analyses, except cholesterol and low density lipoprotein levels of 245 and 151 mg/dL, respectively. The patient's peripheral blood eosinophil count was 188 mm3 (normal range, 0 to 1,000).
The patient was fasted for ten hours, after which an intravenous cannula was secured in a peripheral vein, and a normal saline infusion was started at a rate of 40 mL/hr. Butylscopolamine (20 mg), an anticholinergic agent, was injected intravenously. After laryngo-tracheal application of 10% lidocaine spray, the patient's blood pressure, pulse, and oxygen saturation (SpO2) were monitored while in the left lateral decubitus position. Prior to anesthesia, the patient's blood pressure was 116/74 mm Hg, while her heart rate was 74 beats per minute, respiratory rate was 19 breaths per minute, and oxygen saturation was 99%. Midazolam (5 mg) was administered intravenously. Within 4 minutes after midazolam injection, the patient's pulse could not be palpated from her peripheral artery, and her SpO2 dropped 75%, after which she became cyanotic. The patient was immediately given 2 L of 100% oxygen using a nasal prong device, and 0.3 mg of flumazenil was injected intravenously. Within 5 minutes after midazolam injection, the patient showed decreased mentality, and nonspontaneous respiration. A second intravenous injection of flumazenil (0.2 mg) was administered to the patient to support her respiration, and a bag valve mask and cardiopulmonary resuscitation were used. The patient's blood pressure and peripheral pulse could not be assessed, but pupil size and pupil reflex were normal. At that time, sinus tachycardia was observed by electrocardiography (ECG) (). No wheezing or stridor was detected by auscultation. When tracheal intubation was performed, there was no secretion from the oral cavity or airway. The patient's SpO2 levels increased to greater than 90%, but her blood pressure remained below normal. Norepinephrine (8 µg/min) and epinephrine (1 mg) were administered intravenously. Cardiac massage was performed for 6 minutes. After norepinephrine and epinephrine administration, the patient's peripheral pulse rate was measured at 130 beats per minute, and the patient moved. The patient's blood pressure increased to 90/60 mm Hg and her respiratory rate was 24 breaths per minute. The tracheal tube was removed, and 5 L/min of oxygen was administered through a facial mask. The patient was then transferred to the intensive care unit (ICU). After rapid administration of 300 mL of normal saline, the infusion speed was adjusted to 140 mL/hr, and the patient was continually monitored. The patient developed a rash all over her body immediately. Dexamethasone (5 mg) and an antihistamine agent (3 mg) were subsequently administered via intravenous injection. The results of arterial blood gas analysis (ABGA) revealed a pH of 7.341, a blood carbon dioxide partial pressure (PaCO2) of 27.6%, a blood oxygen partial pressure (PaO2) of 97%, bicarbonate levels of 15 mmoL, and an SpO2 of 97%. No abnormal findings resulted from chemical analyses, except a lactate dehydrogenase level of 370 IU/L.
Absent stridor or wheezing on auscultation ruled out airway involvement due to the sedative effect of midazolam. There were no abnormal findings on a chest computed tomography (CT) scan performed the day following the event (). Among examinations performed after recovery from cardiac arrest, nonspecific findings with normal wall motion were detected by echocardiography, excepting depletion of the right ventricular volume (). Hematologic parameters including creatine kinase-MB and troponin I were also within the normal ranges, and thus cardiac arrest as a possible cause was also ruled out.
For one day, ABGA was repeated, and norepinephrine levels were reduced while the patient was in the ICU. The patient complained of general weakness. She was transferred to the general ward and stayed one additional day without exhibiting any abnormalities. After being discharged, the patient visited the hospital two times, but had no complaints or abnormal findings in her CBC or blood chemistry analyses. However, her blood tryptase level increased slightly during cardiac arrest to 14.8 µg/L (normal range, 1.9 to 13.5).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.0, 'kg']}",100,95,105,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.0 kg - 20 kg) = 100.0 mL/hr.
Hence, the patient's fluid maintenance is 100.0 mL/hr."
5274,22,Maintenance Fluids Calculations,physical,decimal,pmc-7972195-1,Extracted,"This female patient was admitted to hospital because of “short stature, hepatomegaly for 6 months” at the age of 3 years old. At admission, her height SDS was − 1.48 and weight was 15 kg (50th–75th centile). There were abnormalities in ANC (0.82 × 10^9 /L), TG (3.92 mmol/L), fasting glucose (3.48 mmol/L), lactic acid (9.61 mmol/L), and uric acid (519 μmol/L). The liver ultrasound suggested hepatomegaly. She also underwent liver biopsy and was tested for glucose response to epinephrine stimulation after overnight fasting and the results were positive. Therefore, she was clinically diagnosed as GSD. She was given oral uncooked cornstarch regularly. At the age of 10 years and a half, she was finally diagnosed with GSD type 1b through genetic testing. At the last visit, her triglycerides, lactic acid, pyruvic acid and uric acid were decreased than before. Her fasting hypoglycemia and metabolic acidosis have been significantly improved. She had a history of upper respiratory tract infections, about once a year.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [15.0, 'kg']}",50,47.5,52.5,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 15.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (15.0 kg - 10 kg) = 50.0 mL/hr.
Hence, the patient's fluid maintenance is 50.0 mL/hr."
5275,22,Maintenance Fluids Calculations,physical,decimal,pmc-4255050-1,Extracted,"A 35-year-old man diagnosed with type 2 diabetes (T2D) eight years ago and treated with intermittent metformin administration visited our clinic. He had a history of a spontaneously healed ureteral stones ten years ago. He was 169.3 cm tall, weighed 51.6 kg, and his body mass index (BMI) was 18 kg/m2. None of his family members had a known history of diabetes. He complained of a warm and painful lesion on his thigh for the last three weeks, but reported no recent history of trauma or injection. Initial physical examination of the painful lesion revealed tenderness and non-pitting edema of the anteromedial right thigh. His blood pressure and body temperature were 120/80 mmHg and 36.4℃, respectively. There was no leukocytosis (white blood cell count: 9,190/µL) and C-reactive protein was normal, but the erythrocyte sedimentation rate was elevated to 62 mm/hr. His glycemic control was very poor, with an HbA1c 14.5% and postprandial glucose of 446 mg/dL. Other biochemistry values were as follows: serum creatinine 0.4 mg/dL, blood urea nitrogen 24 mg/dL, potassium 4.6 mmol/L, sodium 132 mmol/L, calcium 9.1 mg/dL, phosphorus 3.6 mg/dL, alkaline phosphatase 86 U/L, albumin 4.1 g/dL, and creatinine kinase 436 mg/dL. He had proteinuria (trace) and glycosuria (4+) on urinalysis.
Serial blood culture showed no evidence of bacterial infection. As infectious causes were thought to be less likely, we conducted arterial and venous doppler ultrasonography of the extremity to exclude vascular problems such as deep vein thrombosis or peripheral artery disease. There was no evidence of vascular structural abnormality, but an ill-defined hyperechoic lesion and thick fluid collection in the right vastus medialis muscle was found. After four days, the amount of fluid increased, and thus fluid aspiration at the intermuscular fascial plane adjacent to the vastus lateralis was done (). The fluid was clear, watery and serous. Gram stain and culture of the fluid were negative. Magnetic resonance image (MRI) of the right thigh reflected diffuse edema around the vastus medialis with low signal intensity on T1 () and high signal intensity on T2 images (). The three-phase bone scan showed increased blood flow to the right thigh consistent with myonecrosis as shown on the thigh MRI (). The bone scan also revealed increased blood flow at the right medial tibial condyle consistent with an insufficiency fracture, which was subsequently confirmed by X-ray and MRI (). Since these clinical findings and images were highly suggestive of DMI of the right vastus medialis with insufficient fracture of the right tibial condyle, a muscle biopsy was not performed.
Due to the early onset of disease (age 27), no obesity and no family history of T2D, we needed to clearly identify the exact type of his diabetes. Baseline C-peptide level was very low (0.1 ng/mL) and did not sufficiently rise at 6 min after glucagon stimulation test (0.3 ng/mL). Antinuclear antibodies, and anti-IA2 antibody results were not significant, but antibodies to glutamic acid decarboxylase (anti-GAD Ab) were positive (2.0 U/mL). Other immunologic factors were negative. Considering his age, low BMI, positive anti-GAD Ab, and severely decreased C-peptide level, we diagnosed his diabetes as a case of latent autoimmune diabetes in adults (LADA). After we examined microvascular and macrovascular diabetic complications, he was diagnosed with peripheral neuropathy and non-proliferative retinopathy of both eyes as well as microalbuminuria based on spot urine analysis (152 µg/mg Creatinine).
When we evaluated the cause of the insufficiency fracture, we found that his bone mineral density (BMD) was reduced, with T-scores of -3.9 (Z-score -3.3) at L1-L4 and -2.7 (Z-score -2.3) at the femur neck. Due to the young age of the patient, we also evaluated possible etiologies of secondary osteoporosis, including hyperparathyroidism, hyperthyroidism, hypogonadism, and glucocorticoid excess. 25-hydroxy-vitamin D (25-[OH]D) level was also lower than the normal limits (<4 ng/mL, normal range 11.1 to 42.9) and osteocalcin level was slightly decreased (2.4 ng/mL, normal range 2.7 to 11.5). Thyroid function test was normal (free-T4 0.90 ng/dL, normal range 0.77 to 1.94 ng/dL; Thyroid stimulating hormone 2.24 µU/mL, normal range 0.30 to 4.00 µU/mL; T3 120 ng/dL, normal range 80 to 200 ng/dL), and there was no significant finding of thyroid autoantibodies. Parathyroid hormone (PTH) level was 19.6 pg/mL (normal range 13 to 54 pg/mL). C-telopeptide level was within normal limits (0.74 ng/mL, normal range 0.07 to 0.78 ng/mL). Testosterone and follicle stimulating hormone (FSH) levels were also within normal limits (Testosterone 2.19 ng/mL, normal range, 1.8 to 8.96 ng/mL; FSH 4.0 ng/mL, normal range, 2.8 to 9.6 ng/mL), with a slightly low luteinizing hormone level (1.3 ng/mL, normal range, 1.8 to 5.2 ng/mL).
Antibiotics were initially prescribed, but discontinued when bacterial infection was ruled out and DMI was thought to be the most likely clinical diagnosis. Instead, the patient was treated with analgesics such as acetaminophen, application of a long leg splint and bed rest, and multiple daily injections of insulin for strict glucose control. For his osteoporotic fracture, he was administered oral vitamin D and calcium agents. After about two weeks of supportive management, the tenderness and swelling of the right anteromedial thigh gradually reduced and the patient was able to walk without help, and so the splint was removed. 3 months later, when the hyperglycemia was controlled, we have done the oral glucose tolerance test and calculated the insulinogenic index (IGI, delta insulin 30 min-0 min/delta glucose 30 min-0 min). Calculated IGI was 0 (reference range >0.5), which reflects diminished beta-cell function on glucose stimulation. On follow-up ultrasonography after 6 months, the myonecrosis of the right vastus medialis muscle was dramatically resolved and his HbA1c had improved to 5.7%. In addition, his 25-(OH)D level had risen to 58.7 ng/mL after 6 months of treatment. Five months after treatment, the patient complained of frequent injections, so we changed his insulin regimen to a premixed combination insulin injection twice a day. He is currently under follow-up at the outpatient clinic without any evidence of recurrence.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [51.6, 'kg']}",91.6,87.02,96.18,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 51.6 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (51.6 kg - 20 kg) = 91.6 mL/hr.
Hence, the patient's fluid maintenance is 91.6 mL/hr."
5276,22,Maintenance Fluids Calculations,physical,decimal,pmc-4929385-1,Extracted,"A 59-year-old Japanese man who had liver dysfunction for over 1 year was referred to the former hospital with fatigue and jaundice. Prior to developing liver dysfunction, he had been diagnosed with hyperuricemia, hypertension, and dyslipidemia. Benzbromarone 50 mg daily, benidipine 4 mg daily, and pravastatin 5 mg daily were all prescribed. He also drank alcohol (∼60 g daily). After he had been diagnosed with liver dysfunction, ursodeoxycholic acid 400 mg daily was prescribed. The laboratory examinations on admission to the former hospital showed the following values: total bilirubin, 8.1 mg/dl; aspartate transaminase (AST), 1,457 IU/l; alanine transaminase (ALT), 1,696 IU/l; prothrombin time (PT), 69%, and PT international normalized ratio (PT-INR), 1.33. Eight days after admission to the former hospital, the laboratory examinations showed the following values: total bilirubin level, 21.6 mg/dl; AST, 340 IU/l; ALT, 529 IU/l; PT, 38%, and PT-INR, 1.82. Although he had received conservative treatment, disorientation, drowsiness, and incontinence appeared 14 days after his prior hospitalization, and he was diagnosed as having ALF with grade 2 hepatic encephalopathy [].
The patient was transferred to the Chiba University Hospital for treatment of the ALF. On admission, his body height and weight were 1.63 m and 60.2 kg, respectively. On physical examination, deep jaundice, abdominal distension, and leg edema were observed. His liver and spleen were not palpable. Flapping tremor and disorientation were also detected.
The patient's laboratory data on this admission are shown in table . The serologic and virologic markers were negative. Autoimmune hepatitis was also ruled out []. Based on his medical history, we suspected that the benzbromarone was responsible for his hepatic injury [, ]. CT imaging demonstrated heterogeneous hypoattentuation and atrophy of the liver with massive ascites (fig. ). The Model for End-Stage Liver Disease (MELD) score of the patient was 24 []. He fulfilled a number of the criteria for liver transplantation. He was registered as a potential liver recipient, and we continued medical treatment. Until liver transplantation, intermittent OLHDF was performed to improve the disturbances in his level of consciousness. Surgical construction of an arteriovenous fistula was performed in the right forearm 12 days after admission to our unit. After evaluating the condition of his blood vessels, the fistula was constructed in the right forearm. The deceased donor liver transplantation was successfully performed without any infectious complications 53 days after admission to our unit. The volume of his liver was 730 g, and histology of the liver revealed submassive necrosis in the right lobe and massive necrosis in the left lobe (fig. ). There was no evidence of liver cirrhosis, supporting the diagnosis of ALF rather than acute-on-chronic liver failure []. During his hospitalization, no symptoms of infectious complications were observed (fig. ). He remains well 1.5 years following transplantation. The fistula in his right forearm was closed 1 month after the liver transplantation.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [60.2, 'kg']}",100.2,95.19,105.21,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 60.2 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (60.2 kg - 20 kg) = 100.2 mL/hr.
Hence, the patient's fluid maintenance is 100.2 mL/hr."
5277,22,Maintenance Fluids Calculations,physical,decimal,pmc-6629596-1,Extracted,"A 15-year-old boy visited the emergency department presenting complaint of vomiting and lethargy. He was admitted to the general ward at Seoul National University Bundang Hospital. Two weeks before admission, he had experienced left thigh swelling after falling from a bed at a private rehabilitation center. Radiologic examination at the emergency department revealed a left femur shaft fracture. Two days later, he underwent orthopedic surgery for the femur fracture. He was discharged from the hospital without any complications seven days after surgery.Two days before the present admission, he suddenly began to have poor oral intake. The patient refused to eat solid foods. He only took in liquids. His body temperature was elevated to 38.0°C. One day before admission, bilious vomiting developed and the patient became lethargic. In addition, his urine output decreased. It became dark in appearance. As gastrointestinal symptoms persisted with features of dehydration, he was admitted to the general ward for supportive care and further evaluation of the bilious vomiting.
As the patient was an abandoned child residing in a private rehabilitation center, his perinatal history or family history was unknown. His past medical history in infancy was unclear either. He was initially diagnosed with cerebral palsy of unknown cause. Given his pain insensitivity with anhidrosis, he was later diagnosed with HSAN-IV at Seoul National University Bundang Hospital. He had suffered from recurrent orthopedic diseases such as femur fractures, septic arthritis, and osteomyelitis approximately 1–2 times per year. His fingertips were mutilated because of recurrent cellulitis and septic arthritis of fingers. He had recurrent trauma history due to an impulse control disorder and pain insensitivity as well as poor hygienic condition. His body temperature was unstable. It tended to change dramatically, ranging from abnormally low body temperature to high fevers along with unstable blood pressures indicative of autonomic dysregulation. He had been treated for severe dry skin, hyperkeratosis, fissuring, and xerotic eczema with topical ointments. He was wheelchair-bound and mentally retarded, although verbal communication with social workers was partially possible. During long-term follow-up at the Pediatric Nephrology Clinic of the same hospital, hypokalemia and hypomagnesemia were also detected, leading to suspicion of Gitelman syndrome. With regard to medications, he was taking anti-psychotics, psychostimulants, and spironolactone.
On physical examination, he was alert but cachectic. He was wearing a hip spica cast for the femur fracture. His height was 134 cm (<3rd percentile). His body weight was 29.1 kg (<3rd percentile). He had blood pressure of 130/88 mmHg, pulse rate of 97 beats/minute, respiratory rate of 21 times/minute, and body temperature of 37.3°C initially. Neither conjunctiva was anemic. Neither sclera was icteric. His lips and mucous membranes were slightly dehydrated. Both tympanic membranes were intact. His cervical lymph nodes were not palpable. The chest wall expanded symmetrically without retraction. Breath sounds were clear without crackles or wheezing. His heartbeat was regular without murmur. His abdomen was soft and flat. There was no tenderness or rebound tenderness in the abdomen. Bowel sounds were hyperactive. There was no shifting dullness on percussion. His liver or spleen was not palpable. There was no peripheral edema, digital clubbing, or cyanosis. However, all fingertips were mutilated (). His skin was dry. There was no rash or petechia.
On the day of admission, laboratory tests were done with the following results: sodium, 138 mmol/L; potassium, 3.2 mmol/L; aspartate transaminase (AST), 23 IU/L; alanine aminotransferase (ALT), 12 IU/L; total bilirubin, 1.0 mg/dL; blood urea nitrogen (BUN), 29 mg/dL; creatinine, 0.41 mg/dL; C-reactive protein (CRP) <0.03 mg/dL; and serum magnesium, 1.6 mg/dL. Supportive treatment was started to correct his dehydration and he was maintained in stable condition.
On the third day of hospitalization, a high fever developed suddenly and his temperature rose to 41.8°C. He had no response to antipyretic drugs. At the same time, his blood pressure suddenly dropped to 50/17 mmHg. He also had seizure-like movements, including upward eyeball deviation, loss of consciousness, and generalized clonic movement. Both pupils became fixed at 2 mm diameter. Results of laboratory tests were as follows: white blood cell (WBC) count of 19.4×103/µL, hemoglobin level of 9.6 g/dL, platelet count of 90×103/µL, sodium level of 137 mmol/L, potassium level of 2.6 mmol/L, AST level of 454 IU/L, ALT level of 258 IU/L, total bilirubin level of 4.3 mg/dL, direct bilirubin level of 2.6 mg/dL, amylase level of 228 IU/L, lipase level of 888 IU/L, creatinine phosphate kinase level of 1,258 IU/L, lactate dehydrogenase level of 985 IU/L, BUN level of 49 mg/dL, creatinine level of 1.62 mg/dL, and CRP level of 0.6 mg/dL. These results indicated acute liver failure, acute pancreatitis, disseminated intravascular coagulation, rhabdomyolysis, and acute kidney injury. Additional testing for anemia revealed plasma hemoglobin level of 27.5 mg/dL, serum ferritin level of 250 ng/mL, and weakly positive antinuclear antibody (1:40).
Repeated blood testing results on the same day revealed markedly worsened results as follows: AST, 492 IU/L; ALT, 545 IU/L; total bilirubin, 10.8 mg/dL; direct bilirubin, 5.1 mg/dL; amylase, 520 IU/L; lipase, 5,071 IU/L; prothrombin time international normalized ratio (PT INR), 3.1; activated partial thromboplastin time (aPTT), 52.7 seconds; fibrinogen, 160 mg/dL; D-dimer, 17.62 µg/mL; alkaline phosphatase, 126 IU/L; and γ-glutamyltranspeptidase, 98 IU/L. Aggressive management was performed, including fluid resuscitation, intravenous inotropes (dopamine and norepinephrine), antibiotics, and gabexatemesilate. He was transferred to the pediatric intensive care unit (PICU) and ventilator care was applied. In the PICU, he developed seizure-like movements. Lorazepam was injected once and mannitol was started to reduce intracranial pressure. Abdominal computed tomography revealed no definite radiological evidence of acute pancreatitis. However, multiple filling defects were noted in both kidneys. Findings of brain magnetic resonance imaging suggested hypoxic ischemic encephalopathy.
Further investigation of the etiology of fulminant hepatitis revealed a low serum level of ceruloplasmin (5.5 mg/dL) and increased 24-hour urine copper level (1,028 µg/dL). Liver biopsy was done under the suspicion of Wilson's disease. Liver pathology revealed centrilobular confluent necrosis with marked copper deposition in hepatocytes and Kupffer cells with extensive lobular disarray (). Liver copper deposit was 74 µg/g dry weight (reference range 10–35 µg/g). Ophthalmologic examination was negative for Kayser–Fleischer rings.
To confirm the diagnosis of suspected underlying genetic diseases based on his past medical history and present manifestations, gene studies for HSAN-IV, Gitelman syndrome, and Wilson disease were performed. HSAN-IV was confirmed based on results of NTRK1 gene sequencing for HSAN-IV which revealed c.2002G>T, p.Asp668Tyr heterozygote (American College of Medical Genetics and Genomics /Association for Molecular Pathology [ACMG/AMP] classification: pathogenic) and c.360-1G>A, (IVS3) heterozygote (ACMG/AMP classification: pathogenic), indicating a compound heterozygote mutation causing autosomal recessive disease (). In addition, SLC12A3 gene sequencing for Gitelman syndrome revealed a heterozygote c.1216A>C in exon 10 [p.Asn(AAT)406His(CAT)] (). However, ATP7B gene sequencing for Wilson disease showed negative results despite clinical manifestations, laboratory and liver pathologic findings, and a clinical course compatible with the diagnosis of this disease.
After initiating treatment with trientine (triethylenetetramine) 25 mg/kg/day via nasogastric tube as well as a low copper diet, clinical symptoms and laboratory findings began to improve markedly. Laboratory tests results on the 15th day in the hospital were as follows: WBC count of 8.66×103/µL, hemoglobin level of 12.9 g/dL, platelet count of 364×103/µL, sodium level of 137 mmol/L, potassium level of 4.0 mmol/L, AST level of 128 IU/L, ALT level of 127 IU/L, total bilirubin level of 1.3 mg/dL, BUN level of 25 mg/dL, creatinine level of 0.1 mg/dL, PT INR of 1.15, and aPTT of 52.3 seconds.
As the patient did not recover from brain damage caused by high fever and shock and his ability to breathe independently was not restored during hospitalization, he received a tracheostomy for long-term mechanical ventilator care and percutaneous endoscopic gastrostomy for enteral feeding. In a bed-ridden state on home ventilator care and gastrostomy feeding, trientine treatment and copper restriction diet were maintained without any problem after discharge from the hospital or during long-term follow-up at the outpatient clinic.
This study was approved by the Institutional Review Board (IRB) of Seoul National University Bundang Hospital (IRB no. B-1703-387-701). The need for informed consent was waived by the board.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [29.1, 'kg']}",69.1,65.645,72.555,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 29.1 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (29.1 kg - 20 kg) = 69.1 mL/hr.
Hence, the patient's fluid maintenance is 69.1 mL/hr."
5278,22,Maintenance Fluids Calculations,physical,decimal,pmc-5526772-1,Extracted,"A 41-year-old Japanese man was admitted to our hospital with liver damage, itchy skin, and pyrexia. His medical history was unremarkable, but one year previously his gamma-glutamyl transpeptidase levels had risen to 271 IU/L (normal: < 30 IU/L). Prior to this, the patient had consumed 540 mL of sake three times a week, and he had been reducing the amount of alcohol he consumed for about one year. He did not smoke or take any recreational drugs. He was single, was not homosexual, and he had not had sexual intercourse for over one year.
The patient had undergone treatment of his internal hemorrhoids as an outpatient at a nearby hospital that comprised an aluminum potassium sulfate and tannic acid (ALTA) injection. He developed a fever of 38 °C, dark colored urine, and itchy skin on postoperative day (POD) 1, and he took loxoprofen sodium, as required. He consulted another doctor on POD 7, because the symptoms had not improved, and his blood test results led to a diagnosis of liver dysfunction. His liver dysfunction had not improved by POD 14, and he was admitted to our hospital on POD 15.
The patient was 167 cm tall and weighed 52.5 kg. He presented with a blood pressure of 103/59 mmHg, a heart rate of 82 beats per minute, a temperature of 36.6 °C, and 99% oxygen saturation in room air. No specific physical findings were evident during the clinical examination on the day of hospitalization, but the patient had a rash, edema, hepatosplenomegaly, lymphadenopathy, and jaundice. The subjective symptoms, comprising the fever, dark colored urine, and itchy skin, had disappeared by POD 10.
The laboratory test results showed that the patient’s complete blood count was almost normal with a white blood cell count of 6900 cells/μL, a hemoglobin concentration of 14.7 g/dL, a hematocrit level of 43.1%, and a platelet count of 3.98 × 105 cells/μL, but a higher percentage of eosinophils was present (6.8%) (normal: 1.0%-5.0%), which peaked at 13.9% on POD 20. The patient’s serum liver enzyme and bilirubin levels were elevated at the time of admission. The aspartate aminotransferase (AST) level was 432 IU/L (normal: 10-40 IU/L), the alanine aminotransferase (ALT) level was 911 IU/L (normal: 10-40 IU/L), the alkaline phosphatase (ALP) level was 473 IU/L (normal: 115-359 IU/L), and the total bilirubin level was 1.3 mg/dL (normal: 0.2-1.2 mg/dL). Thus, compared with the ALP level, the AST and ALT levels showed greater magnitudes of elevation. The patient’s other blood test results were within the normal ranges, as follows: serum albumin: 4.0 g/dL (normal: 3.8-5.2 g/dL); serum creatinine: 0.86 mg/dL (normal: 0.65-1.09 mg/dL); C-reactive protein: 0.1 mg/dL (normal: 0-0.3 mg/dL); prothrombin time: 100% (normal: 80%-120 %); thyroid-stimulating hormone: 0.5 μIU/mL (normal: 0.34-4.04 μIU/mL); triiodothyronine: 2.98 pg/dL (normal: 2.36-5.00 pg/dL); and thyroxin: 1.18 ng/dL (normal: 0.88-1.67 ng/dL). The serological tests for autoantibodies generated weakly positive results (1:40) for anti-nuclear antibodies, and negative results for anti-smooth muscle and anti-mitochondrial antibodies. Negative results were obtained from the tests for the hepatitis B virus surface antigen, the hepatitis C virus antibody, rapid plasma reagin, the anti-Epstein-Barr virus immunoglobulin M (IgM) antibody, and the anti-cytomegalovirus IgM antibody, and from the Treponema pallidum hemagglutination test. The IgG level was within the normal range at 1415 mg/dL (normal: 800-1600 mg/dL) and the IgM level was within the normal range at 100 mg/dL (normal: 60-250 mg/dL). The IgE level was elevated at 1333 mg/dL (normal: < 250 mg/dL). Chest radiography did not reveal any abnormalities. No morphological changes were evident following abdominal ultrasonography, magnetic resonance cholangiopancreatography, and abdominal computed tomography (Figure ).
When the patient was hospitalized, we considered viral, alcohol-induced, autoimmune, drug-induced, biliary tract, and thyroid function-based diseases as frequent causes of acute liver dysfunction for the differential diagnosis, and, based on the patient’s medical history, and the serological and imaging results, we considered that alcohol and DILI were highly likely causes of the patient’s acute liver dysfunction. However, the patient had stopped drinking during the past year, so we thought that there was a high likelihood of DILI. Therefore, we began conservative treatment with a small amount of extracellular fluid replacement.
Figure presents the patient’s symptoms, laboratory test results, and treatment over the entire course. The liver transaminase and bilirubin levels decreased rapidly after admission, and the maximum levels were as follows: ALT: 950 IU/L on POD 15; AST: 470 IU/L on POD 17; and total bilirubin: 2.1 mg/dL on POD 17. The ALP and gamma-glutamyl transpeptidase levels showed consistent downward trends from POD 7. The patient's symptoms disappeared on POD 10, and no new symptoms appeared after hospitalization. We performed a liver biopsy on POD 25, and a drug-induced lymphocyte stimulation test (DLST) of the components of the ALTA injection and lidocaine on POD 28. The patient was discharged on POD 29, and he was managed as an outpatient without any prescriptions. At the time of the patient’s first outpatient appointment on POD 35, his liver transaminase and bilirubin levels had declined and were almost within the normal ranges.
Figure presents hematoxylin and eosin (H and E)-stained sections of the liver biopsy performed on POD 25. The H and E staining showed that the basic structure of the liver had been maintained without any hepatocyte dropout or disruption, and that the bile duct had not been disrupted. At a higher magnification, the H and E staining showed that the parenchymal cells were partially dilated and that a mild inflammatory cell infiltration was present in the area of the central vein. Neither eosinophil nor plasma cell infiltrations were detected within the liver tissue. Bile plugs were found at multiple sites within the parenchyma and sinusoids. Masson staining did not show the presence of liver tissue fibrosis.
The lymphocyte proliferation activity levels, which were determined from the DLST performed on POD 28, were 676 counts per minute (cpm) for the control and 871 cpm for the ALTA with lidocaine. The stimulation index, which was calculated as the ALTA with lidocaine cpm divided by the control cpm, was 1.29 (normal in Japanese people: < 1.8).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [52.5, 'kg']}",92.5,87.875,97.125,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 52.5 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (52.5 kg - 20 kg) = 92.5 mL/hr.
Hence, the patient's fluid maintenance is 92.5 mL/hr."
5279,22,Maintenance Fluids Calculations,physical,decimal,pmc-6939428-1,Extracted,"The patient is a 40-year-old man with a history of gastroesophageal reflux disease and a family history of colon cancer. He presented with severe abdominal pain, fecal urgency, and episodes of diarrhea. He had lost 22 lbs over two months. An abdominal CT and colonoscopy showed a severely lipomatous, bulbous, and protuberant ileo-cecal valve, with intussusception of the ileum into the cecum. Exploratory laparotomy revealed marked enlargement of the ileum due to massive fat deposition, and adhesions between the ascending colon and the right lateral lower abdominal wall. A dilated segment of the ileum and cecum was surgically resected, which demonstrated a bulbous, protuberant, abnormally smooth mucosal surface in the ileum, sharply demarcated from normal large intestinal mucosa at the ileo-cecal valve (). There was an 8 × 5 × 5 cm mass protruding through the ileo-cecal valve into the cecum (). At the proximal end of the resected specimen there was a short (4 cm) transition from normal small intestinal mucosa to the abnormal, smooth, bulbous mucosa. Microscopically, there was extensive infiltration of mature adipose throughout the submucosa ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [22.0, 'lbs']}",39.91608,37.92028,41.91188,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 22.0 lbs so this converts to 22.0 lbs * 0.453592 kg/lbs = 9.97902 kg. Hence, the patient's maintenance fluid is 9.97902 kg * 4 mL/kg/hr = 39.91608 mL/hr.
Hence, the patient's fluid maintenance is 39.91608 mL/hr."
5280,22,Maintenance Fluids Calculations,physical,decimal,pmc-7054073-1,Extracted,"A 14-year-old girl was scheduled for extractions of all third molars and remaining mandibular primary teeth #K, #S, and #T and surgical uprighting of the mandibular second molars (). Her medical history was significant for HoFH, anxiety, depression, and gastroesophageal reflux disease. She was diagnosed with HoFH at age 13 following an exploratory cardiac catheterization. Before the diagnosis, she had never experienced a cardiac event as is common with incidental diagnoses of HoFH. Her cardiovascular family history was unknown because of adoption at 33 weeks. Following the diagnosis of HoFH, an arteriovenous fistula was placed in her right forearm to allow for vascular access during lipid apheresis, which she underwent weekly.
Extra- and intraoral findings were normal, with no temporomandibular joint clicking, popping, or pain, lymphadenopathy, facial asymmetry, or xanthomas. Risks, benefits, complications, and alternative treatments were discussed. All surgical and anesthetic options were reviewed, and the patient elected to undergo total intravenous anesthesia (TIVA) because of her anxiety and phobia of dental procedures.
Anesthetic assessment to determine the patient's candidacy for TIVA was performed because of HoFH. Preoperative medical clearance from the patient's cardiologist was obtained with no perioperative cardiac recommendations. Per the patient's cardiologist, she never exhibited any positive cardiac risk factors or symptoms that would warrant cardiac monitoring before anesthesia. The appropriate time to perform the procedure was determined such that it was in succession to her therapeutic lipid apheresis and accounted for heparin drips in concert.
The physician overseeing the patient's apheresis recommended that the procedure be scheduled approximately for 4 days following apheresis treatment. Finally, the plan was formulated as follows: 1) The patient would receive her regular lipid apheresis treatment; 2) After 4 days, the activated partial thromboplastin time (aPTT) test would be performed to evaluate her clotting ability; 3) If the aPTT was within standard limits, the procedure would be scheduled for day 4 after her next lipid apheresis treatment ().
Four days after apheresis, the patient's reported aPTT value was 39.0 s, which was within a standard range of 25.9 to 39.5 s. The patient presented for surgery with a weight of 40 kg, height of 1.45 m, NPO ≥ 8 h, American Society of Anesthesiologists score III, Mallampati score III, and body mass index of 17.8 kg/m2. Monitors were placed on the patient, and intravenous access was established on the dorsum of the left hand to avoid complications associated with functioning of her arteriovenous fistula. The patient exhibited vasovagal syncope following intravenous access and was placed in the Trendelenburg position. Oxygen was delivered at 4 L/min via a nasal cannula, and a cold compress was placed on her forehead.
Baseline vitals before syncope were: blood pressure, 115/66 mmHg; heart rate, 83 beats/min; and oxygen saturation, 100%. After syncope, once vital signs returned to normal, intravenous doses of 1 mg midazolam, 50 µg fentanyl, 4 mg ondansetron, 4 mg dexamethasone, and 1 mg cefazolin were administered. Anesthesia was induced with an initial bolus of 40 mg of propofol, while sedation was maintained with an additional 220 mg of propofol hand-bolused in increments of 10 to 20 mg every 1 to 2 min and titrated to be effective throughout the procedure.
Local anesthesia was induced by infiltrating surgical sites with 8.5 ml of 2% lidocaine with 1 : 100,000 epinephrine. A bite block and throat pack were placed. Extractions of primary teeth and third molars were achieved with a #15 blade, followed by periosteal and straight elevators. Surgical dressings were placed at all surgical sites for hemostasis, and surgical sites were closed with a 3-0 gut suture to achieve primary closure. Surgical uprighting of both mandibular molars was achieved by introducing a small straight elevator to the mesial aspect of both teeth, without damaging the adjacent teeth or fully luxating the mandibular second molars.
The total procedure time was 22 min, and sedation lasted for 40 min. Vital signs were stable throughout the perioperative period (). Blood loss was minimal, and she was closely monitored postoperatively for excessive bleeding. The patient was arousable, and vital signs stabilized within 20% range of her initial baseline. She was awake, alert, and oriented to her surroundings, and was able to walk with minimal assistance. The patient returned to the clinic 1 week after the procedure and reported good wound healing at operative sites with minimal pain and swelling.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [40.0, 'kg']}",80,76,84,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 40.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (40.0 kg - 20 kg) = 80.0 mL/hr.
Hence, the patient's fluid maintenance is 80.0 mL/hr."
5281,22,Maintenance Fluids Calculations,physical,decimal,pmc-3558655-1,Extracted,"A 72-year-old woman (145 cm, 47 kg) who was diagnosed with ascending aortic dissection presented for ascending aorta and hemiarch replacement surgery. She visited the emergency department with chest discomfort, nausea, and vomiting which started the day before. Her past medical history included common bile duct stone and hypertension that was controlled with an angiotensin receptor blocker. On arrival, her vital signs were stable with a blood pressure of 147/100 mmHg and heart rate of 86 beats per minute (bpm). Physical examination revealed abdominal tenderness on her epigastric area. Her chest X-ray showed bilateral pleural effusion, while her electrocardiogram (ECG) was normal . A chest computed tomography (CT) revealed Stanford type A aortic dissection that started from the aortic root through the proximal descending aorta that resulted in a large amount of pericardial effusion. Immediate emergent operation was planned, and transthoracic echocardiography (TTE) could not be performed.
When she arrived in the operating room, electrocardiography, pulse oxymetry and invasive blood pressure monitoring was conducted. Her blood pressure was managed with continuous infusion of nicardipine 2 µg/kg/min, esmolol 100 µg/kg/min, nitroglycerin 2 µg/kg/min, and nitroprusside 0.5 µg/kg/min. The initial vital signs checked in the operating room were stable with blood pressure of 100/56 mmHg and heart rate of 86 bpm. Induction of anesthesia was performed with 7 mg of midazolam, 50 µg of sufentanil, and 10 mg of vecuronium. After the injection of the induction agents, her blood pressure decreased to 76/46 mmHg, and the maximum heart rate noted at the time was 100 bpm. The infusion of the hypotensive agents (nicardipine, esmolol, nitroglycerin and nitroprusside) was discontinued, and subsequently 10 mg of ephedrine, 30 µg of phenylephrine and rapid volume infusion using lactate Ringer's solution were administered. In response to persistent hypotension, 10 mg of ephedrine was administered again, but hypotension was exacerbated resulting in a blood pressure of 66/42 mmHg. After endotracheal intubation, transesophageal echocardiography (TEE) was performed to evaluate cardiac function and to guide the hemodynamic treatment. TEE showed a large amount of pericardial effusion (), septal hypertrophy, severe eccentric mitral regurgitation and systolic anterior motion (SAM) of mitral valve combined with dynamic left ventricular outflow tract (LVOT) obstruction (). To improve LVOT obstruction with SAM, 50 mg of esmolol and several 100 µg boluses of phenylephrine , and more rapid volume resuscitation (300 ml of lactate Ringer's solution and 300 ml of hydroxyethyl starch solution) were administered. Afterwards, the patient's blood pressure became stable at 102/56 mmHg and heart rate of 88 bpm. LVOT obstruction with SAM improved, and mitral regurgitation decreased to a mild level. A triple lumen catheter with introducer (Advanced Venous Access®) was placed in the right internal jugular vein and a pulmonary artery catheter was inserted to monitor the central venous and pulmonary artery pressure. Anesthesia was maintained with propofol (1.5-2.5 µg/ml), and remifentanil (8-20 ng/ml) by target controlled infusion system under bispectral index monitoring. Vecuronium was infused continuously (1 µg/kg/min) for muscle relaxation.
Following sternotomy and opening of pericardium, about 200 ml of bloody pericardial effusion was drained for evacuation. After the drainage, residual SAM and mitral regurgitation completely disappeared on TEE. An ascending aorta and hemiarch replacement was conducted under cardiopulmonary bypass (CPB). While attempting to wean from CPB, SAM with LVOT obstruction reappeared. Esmolol was administered with bolus (50 mg) and continuous infusion (50 µg/kg/min). Afterwards, SAM with LVOT obstruction improved, and patient was weaned from CPB successfully. Postoperative TTE was performed one week after surgery and revealed no evidence of SAM. She was discharged from the hospital 11 days following the operation without major complications.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [47.0, 'kg']}",87,82.65,91.35,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 47.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (47.0 kg - 20 kg) = 87.0 mL/hr.
Hence, the patient's fluid maintenance is 87.0 mL/hr."
5282,22,Maintenance Fluids Calculations,physical,decimal,usmle-6308,Extracted,"A 47-year-old man comes to the emergency department complaining of weight gain and abdominal discomfort. He states that over the past month he has gained 10 lbs. This week he began experiencing mild, diffuse abdominal discomfort. He denies nausea, vomiting, constipation, or diarrhea. The patient has not seen a physician in years and takes no medications. He is a truck driver. He states that he drinks a 6-pack of beer per night. On physical examination, there is jaundice, hepatomegaly, and a positive fluid wave. An abdominal ultrasound reveals cirrhosis, portal vein dilation, and moderate ascites. He undergoes a paracentesis that relieves his symptoms. Fluid analysis is shown below:

Serum:
Albumin: 4.0 g/dL

Ascitic fluid:
Color: Yellow
Leukocyte count: 100/mm^3 with 50% neutrophils
Protein: 2.3 g/dL
Albumin: 1.9 g/dL

A culture is pending. He is discharged and instructed to follow-up with a gastroenterologist for an upper endoscopy. Upper endoscopy reveals multiple, small non-bleeding esophageal varices.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.0, 'lbs']}",18.14368,17.2365,19.05086,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.0 lbs so this converts to 10.0 lbs * 0.453592 kg/lbs = 4.53592 kg. Hence, the patient's maintenance fluid is 4.53592 kg * 4 mL/kg/hr = 18.14368 mL/hr.
Hence, the patient's fluid maintenance is 18.14368 mL/hr."
5283,22,Maintenance Fluids Calculations,physical,decimal,pmc-5308436-1,Extracted,"A 10-kg, 1-year-old boy underwent craniofacial surgery at an Australian children’s hospital. Postoperatively, he had a number of issues in the post-anaesthesia care unit (PACU) (). The issues included difficulties in managing pain with variable pain scores using the Face, Legs, Activity, Cry, Consolability (FLACC) scale ranging from 0 to 6. During the postoperative period, the infant had an episode of over-sedation with a sedation score of 3, using the University of Michigan Sedation Scale (UMSS), which required opiate reversal with naloxone. In addition, he had decreased oxygen saturation, declining to 70% at one point and increased work of breathing. The infant was given continuous positive airway pressure (CPAP). A chest X-ray showed changes consistent with either atelectasis or aspiration, which required antibiotic treatment. The infant had a nasopharyngeal airway in situ.
Following these issues, the anaesthetist wrote progress notes, recommending that the intravenous (IV) morphine infusion should be maintained at the conservative dose of 10 µg/kg/h without bolus or halved if there were further sedation issues. However, he wrote an opioid infusion order in the range of 10–40 µg/kg/h, with a 10 µg/kg bolus (1 mL) of intervals no less than 10 min for pain. One ward nurse retrieved the patient from the PACU at 21:00, and a night duty nurse took over care at 21:30. Overnight, the infant was unsettled and breath-holding and was given a number of boluses of IV morphine and then the morphine infusion dose was doubled. The infant was reviewed by the paediatric intensive care unit (PICU) Outreach Team at 02:30, who made no changes to the treatment plan.
At 7:30, the same nurse who collected the infant from recovery was caring for him again. The specialist surgical team reviewed him shortly after. They suggested to the nurse that the nasopharyngeal airway could be ‘corked’ or spigotted and documented in the progress notes that the general medical team would review the infant regarding the changes on chest X-ray results, and that the pain management service would review analgesia. It was not documented whether these reviews were also verbally handed over to those teams. The infant was reviewed by the pain management service at 11:05 and at that time the infant appeared settled, with pain scores of 0–1. The pain management service documented a plan to continue the morphine infusion at 20 µg/kg/h but to wean it later in the day and to manage pain with regular oral paracetamol and ibuprofen. At 11:10, his distress escalated and his pain score was documented as 5/10 by the nurse. By 11:25, the infant remained unsettled and as no other analgesia was due, a 10 µg/kg (1 mL) bolus of IV morphine was given with some effect and the infant was asleep after 10 min. At 11:55, the nurse contacted the surgical team’s junior doctor regarding the updated medication recommendation. Still asleep, his nasopharyngeal airway was then corked, resulting in an increased work of breathing but no decrease in oxygen saturation. Upon awakening, the infant’s pain score was 1, and sedation score was 1. The nurse administered IV tramadol 2 mg/kg (20 mg dose) at 12:30; however, the work of breathing remained high and the nasopharyngeal airway was un-corked. His oxygen saturation began to drop to mid-80%, and increasing supplemental oxygen therapy had little effect. The nurse paged the surgical team twice at 13:03 and 13:18 with no response. The Associate Unit Manager (AUM) attempted to call the surgical team at 13:23, also to no avail. There was no attempt to contact the medical or pain teams.
At 13:25, a medical emergency team (MET) call was made. When the team arrived, the infant had increased work of breathing, an oxygen saturation of 70%, and an audible stridor. The team immediately ceased the morphine infusion and gave sodium chloride (0.9%) nebuliser via a mask. A stat. dose of 6 mg IV dexamethasone was administered. Oxygen saturation improved to around 90% with a respiratory rate of 36 breaths/min. An adrenaline nebuliser was given followed by 10 mg of IV parecoxib. The surgical team arrived during the MET call and when over-sedation was suggested, a senior doctor stated that he had explicitly asked that the morphine was to be ceased earlier in the day. This request had not been mentioned to the primary nurse and was not documented in the infant’s file.
A chest X-ray showed right lung changes, suggestive of aspiration. An arterial blood gas revealed respiratory and metabolic acidosis. At 13:50, 100 µg of IV naloxone was given (10 µg/kg), resulting in deeper breathing and large cough-clearing, thick secretions. Vital signs improved with an increased oxygen saturation of 95%. Following the MET intervention and management, the infant remained stable and pain was subsequently managed with paracetamol, ibuprofen and tramadol, along with deep suction every 30 min, humidified oxygen, and regular medical review. Two days after surgery, he was still noted to have an increased work of breathing with a nasopharyngeal airway in situ. His oxygen supplementation was gradually weaned and the nasopharyngeal airway was successfully removed 3 days following surgery, and he was discharged from hospital 4 days after surgery.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.0, 'kg']}",40,38,42,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.0 kg - 10 kg) = 40.0 mL/hr.
Hence, the patient's fluid maintenance is 40.0 mL/hr."
5284,22,Maintenance Fluids Calculations,physical,decimal,pmc-4958681-1,Extracted,"A 40-year-old para 1 woman without significant medical history was transferred to Chonnam National University Hospital. She had bilateral ovarian tumors detected by pelvic ultrasonography at a local gynecologic clinic for the evaluation of dysmenorrhea and hypermenorrhea. A pelvic ultrasonography revealed a 6.4×5.8×5.3-cm3 mass with irregular margin in the right ovary and a 6.3×5.2×4.2-cm3 multi-septated cystic mass in the left ovary. There was no obvious ascite in the abdominal cavity. Pulsed Doppler examination revealed low-resistant blood flow (resistance index 0.24). On physical examination, severe adhesion between these tumors and the cul-de-sac was noted. The patient's preoperative CA 125 level was 97.3 U/mL and other tumor markers (CA 19-9, CA 72-4, and CEA) were within normal ranges. Pelvic magnetic resonance imaging showed a 6.0×4.8×5.3-cm3 ill-defined, heterogenous signal intensity mass, including mixed cystic and solid portions in the right ovary. This mass was considered as a malignancy (i.e., clear cell carcinoma) likely arising from underlying endometriosis. Between the posterior portion of the right ovarian tumor and the cul-de-sac, there was a 5.5×5.0-cm2 enhanced solid mass with an irregular margin invading into the rectal serosa (). Additionally, there was a 7.2×5.9×6.1-cm3 multi-septated cystic mass in the left ovary () that was considered as a benign mucinous cystadenoma. Positron emission tomography-computed tomography revealed a high probability of ovarian malignancy involving both ovaries and possibly peritoneal carcinomatosis. The patient's preoperative body mass index was 30.84 kg/m2 (height 158-cm, weight 77 kg).
The patient underwent total abdominal hysterectomy, bilateral salpingo-oophorectomy, both pelvic lymph nodes dissection, omentectomy, and appendectomy through median incision at supine position. We performed operation for the basis of epithelial ovarian malignancy. A small number of ascites (500 mL) was present and peritoneal cytology was done. The right ovarian tumor measured at approximately 5.0×5.0-cm2 contained a 2.0×3.0-cm2 solid mass and chocolate-colored fluid. This mass was fixed in the cul-de-sac. It was hard indurated because of cancer infiltration. The left ovary mass measured at roughly 5.0×6.0-cm2 was an inflammatory cyst containing yellowish fluid. Multiple seeding lesions were found at rectal serosa, posterior uterine serosa, and appendix. Multiple whitish nodular lesions of up to 3.0×3.0-cm2 were detected at the omentum. These suspicious lesions were biopsied. No intrauterine tumor was found (). Intra-operative frozen biopsy analysis of the right ovarian tumor showed ESS with endometriosis because proliferative stromal cells with scant nuclear pleomorphism and mitosis were seen. Postoperative course was complicated by a disrupted vaginal stump. There was no other complication.
Final pathology was consistent with bilateral ovarian ESS arising from foci of endometriosis and involving the uterine serosa, rectal serosa, parametrium, peritoneum, omentum, and appendix (International Federation of Gynecology and Obstetrics [FIGO] stage IIIC). No evidence of tumor was found in the corpus of the uterus or the uterine cavity. Both pelvic lymph nodes were negative for tumor cells. The result of peritoneal cytology was negative for malignant cells. The mitotic activity in the spindle cells in the cellular area was limited to a maximum of two figures per 10 high-power fields. Stromal tissues had the characteristic tongue-like growth pattern (). Immunohistochemical staining revealed that neoplastic cells were immunopositive to antibodies specific for cluster of differentiation 10 (CD 10) (), Ki 67 (Ki index 3% to 5%) (), and progesterone receptor (). However, these neoplastic cells were immunonegative to estrogen receptor, desmin, alpha inhibin, calretinin, and actin.
The patient's CA 125 level was decreased from 97.3 U/mL before surgery to 38.8 U/mL after surgery. Adjuvant hormonal therapy was started one month after the operation in an effort to suppress the growth of any microscopic tumors. The patient had been taking oral megestrol acetate (Megesia, Dalimpharm, Seoul, Korea) at 160 mg daily for one month. She complained about weight gain. Therefore, the patient had been taking oral medroxyprogesterone acetate (Farlutal, Pfizer, New York, NY, USA) at 500 mg daily for four months. Six months after the beginning of treatment, her CA 125 level was decreased to 22.7 U/mL. Subsequent Positron emission tomography-computed tomography revealed no evidence of recurrence or metastases. However, she had complaints of generalized edema. Therefore, we decreased her drug dosages. She was taking oral medroxyprogesterone acetate (Provera, Pfizer) at 200 mg daily for three months. Three months later, she refused further hormonal therapy because of lasting side effects. At that time, an abdominopelvic computed tomography showed no evidence of recurrence. Therefore, we stopped the hormonal therapy and planned regular checkups with pelvic examination, tumor markers, and imaging studies. To date, she has shown no signs of recurrence.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [77.0, 'kg']}",117,111.15,122.85,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 77.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (77.0 kg - 20 kg) = 117.0 mL/hr.
Hence, the patient's fluid maintenance is 117.0 mL/hr."
5285,22,Maintenance Fluids Calculations,physical,decimal,usmle-7613,Extracted,"A 48-year-old woman with a history of osteoarthritis and hypertension presents to the office complaining of persistent abdominal pain for the last 2 months. She describes the pain as 'burning and achy' that is worse when she eats, which has lead to a weight loss of 4.5 kg (10.0 lb). The patient is currently taking lisinopril and atenolol for her blood pressure and ibuprofen as needed for her osteoarthritis. Her temperature is 37.1°C (98.7°F), heart rate is 75/min, and blood pressure is 120/80 mm Hg. An endoscopy is performed and a gastric ulcer is visualized and biopsied. The biopsy reveals H. pylori infection.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [4.5, 'kg']}",18,17.1,18.9,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 4.5 kg. Hence, the patient's maintenance fluid is 4.5 kg * 4 mL/kg/hr = 18.0 mL/hr.
Hence, the patient's fluid maintenance is 18.0 mL/hr."
5286,22,Maintenance Fluids Calculations,physical,decimal,pmc-8246657-1,Extracted,"The patient was an 18-year-old Japanese woman with no relevant medical history. Figure shows the course of her body weight, which had been around 44 kg until disease onset. Her weight loss started when she was 16 years old. She was diagnosed with an eating disorder and also presented with SMA syndrome, which seemed to be caused by weight loss due to the eating disorder because no other organic abnormality was present. The patient received conservative nutrition therapy at a hospital located in her residential area when she was 17 years old. The treatment initially improved her weight, but she ceased treatment due to dissatisfaction with the patient–doctor relationship, and her weight loss resumed.
The patient reported that abdominal symptoms due to SMA syndrome, such as abdominal distension and vomiting, resulted in weight loss. She desired to undergo surgery for SMA syndrome, and found on the internet a distant hospital that performed surgery for SMA syndrome. However, after undergoing laparoscopic duodenojejunostomy, her body weight did not improve during the six months after the surgery. When she was 18 years old, she arrived at our center, the University of Tokyo Hospital, with a chief complaint of weight loss. She was immediately hospitalized due to severe malnutrition.
At hospitalization, her height and weight were 159.1 cm and 27.5 kg, respectively (i.e., body mass index [BMI] of 10.9). She was diagnosed with anorexia nervosa binge-eating/purging type (ANBP) according to the Diagnostic Statistical Manual of Mental Disorders, Fifth Edition []. Notably, her vomiting, which had been considered a symptom of SMA syndrome before surgery, did not improve after surgery. Therefore, her vomiting could have been a symptom of ANBP, while she initially concealed her self-induced vomiting from us and only revealed it six months after the initial visit to our hospital.
After hospitalization, conservative treatment, including dietary nutrition and central venous nutrition, was performed while she was also monitored for refeeding syndrome. We further performed psychological work with the patient and her family, including psychoeducation, nutritional counseling with registered dietitians, and behavioral management based on operant conditioning [, ]. Her body weight gradually improved from 27.5 kg (BMI of 10.9) on day 0 to 34.1 kg (BMI of 13.5) on day 70.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [34.1, 'kg']}",74.1,70.395,77.805,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 34.1 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (34.1 kg - 20 kg) = 74.1 mL/hr.
Hence, the patient's fluid maintenance is 74.1 mL/hr."
5287,22,Maintenance Fluids Calculations,physical,decimal,pmc-3656526-1,Extracted,"One-and-a-half year old girl, born to non-consanguineous parents presented with sudden onset of protracted vomiting and unconsciousness of two days duration. She did not have fever. She was apparently asymptomatic till then. She had attained developmental milestones appropriately. She was able to walk independently, scribble, show few body parts and was able to speak a few meaningful words. Her growth was subnormal with both weight (7.4 kg) and length (76 cm) being less than third centile for age. On examination, her Glasgow Coma Scale score was five. She had hypotonia of all four limbs with brisk deep tendon reflexes. Bilateral plantar reflexes were extensors. There were no signs of meningeal irritation. She had a palpable liver 3 cm below costal margin with a span of 7 cm. Other systems were within normal limits. Her initial investigations revealed hemoglobin of 10.3 g%, total leucocyte count of 8300/mm3, platelet count of 2,79,000/mm3. Neutrophils comprised 84% and lymphocytes 14%. Her blood glucose concentration was 106 mg/dL (60-150 mg/dL), blood urea 42 mg/dl (8-32 mg/dL), serum creatinine 0.4 mg/dL (0.6-1.6 mg/dL), serum sodium 114 mEq/L (130-143 mEq/L), and serum potassium 5 mEq/dL (3.5-5 mEq/L). Liver enzymes were normal with aspartate transaminase of 37 U/L (5-40 U/L), alanine transaminase of 34 U/L (5-40 U/L), and alkaline phosphatase of 197 U/L (40-140 U/L). Cerebrospinal fluid analysis showed no cells on microscopy and gram stain and culture were negative for any organism. CSF glucose was 100 mg/dL (more than or equal to two thirds of blood sugar) and CSF protein was 54 mg/dL (10-20 mg/dL). Arterial blood gas analysis revealed a pH of 7.073 (7.35-7.45), PaO2 of 214 mmHg, PaCO2 of 8.2 mmHg (35-45 mmHg), HCO3- of 2.3 mmol/L (20-28 mmol/L) suggesting severe metabolic acidosis with a high anion gap. Serum ammonia was 2834 μg% (25-94 μg%) suggesting severe hyperammonemia. Serum lactate was 26 mg/dL (5-22 mg/dL). Thin layer chromatography of urine revealed moderate organic aciduria with significant ketonuria and excretion of valine and alanine. She was treated with intravenous sodium benzoate and fluids. Gradually her sensorium improved and she recovered from the acute illness. However she had residual left lower limb monoparesis. She was started on oral sodium benzoate, thiamine, biotin and carnitine and continued on the same.
Over next six months she gradually improved and achieved normal development except in gross motor domain. By two years of age she was speaking with two word sentences and achieved bowel control. She was able to walk with support. Over the next 4 to 4½ years period, she was regularly followed up for continuation of medications, development assessment, nutritional management and rehabilitation. She had three more acute episodes with vomiting and lethargy that required admissions and intravenous fluids. At 6.5 years of age, she was performing well at school and had good interaction with parents and peers. However she had weakness in the lower limbs and required assistance in walking. At this stage, her urine was subjected to gas chromatography and mass spectrometry, which revealed elevated methylmalonic acid. Tandem mass spectrometry showed significantly elevated propionyl carnitine and normal amino acid profile.
Genomic DNA was extracted from mother and proband. Direct sequencing of all the coding exons including flanking introns of MUT, MMAA and MMAB was carried out as described previously.[] Alignment of amino acid sequences of methylmalonic aciduria type A protein was carried out by Clustal W () as per the Entrez Protein database. SIFT and Polyphen are in silico tools which are used to predict the effect of amino acids substitutions. SIFT predicts whether an amino acid substitution affects protein function based on sequence homology and the physical properties of amino acids.[] Polyphen predicts the amino acid substitution based on the structure and function of a human protein using straightforward physical and comparative considerations.[] The missense mutation was submitted to SIFT () and PolyPhen ().
In exon 6 of MMAA, a G to A substitution at position 833 was found in a homozygous pattern (c.833G > A) []. This mutation leads to the substitution of glycine by aspartic acid at position 278 (p.G278D). The mother showed the same mutation in a heterozygous pattern.
Effects of missense mutation were predicted by SIFT and Polyphen. According to SIFT tool, the substitution at position 278 from G to D is predicted to affect protein function with a score of 0.02 (amino acids with probabilities <0.05 are predicted to be deleterious). According to the Polyphen, this variant is predicted to be probably damaging. Alignment of amino acids sequence of methylmalonic aciduria type A protein observed in the patient (resulting in a change of glycine to aspartic acid residue at position 278) showed it to be highly conserved across other species [].
Presently she is on daily oral supplementation of vitamin B12 one milligram and carnitine 500 mg. She is now 7 years and has normal intellectual functions and residual weakness in left lower limb.
During her mother's subsequent pregnancy, prenatal diagnosis was done at 12 weeks of gestation. Same mutation was confirmed in the fetus in homozygous state and she discontinued the pregnancy.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.4, 'kg']}",29.6,28.12,31.08,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.4 kg. Hence, the patient's maintenance fluid is 7.4 kg * 4 mL/kg/hr = 29.6 mL/hr.
Hence, the patient's fluid maintenance is 29.6 mL/hr."
5288,22,Maintenance Fluids Calculations,physical,decimal,pmc-4863518-1,Extracted,"A 52-year-old male patient was admitted in emergency in our clinic for acute abdomen and signs of peritonitis: diffuse abdominal pain and abdominal rigidity, ileus, nausea and chills. Anamnesis revealed no significant personal or family medical history, but the patient described a decreased appetite and weight loss of approximately 5 kg in the last 4 weeks.
Paraclinical exams supported the diagnoses of peritonitis, with leukocytosis (18000/ mmc), increased CRP and ESR (20mm/ h). The lab test also showed severe anemia (Hb 7 mg/ dl). As simple abdominal X-ray revealed pneumoperitoneum, an emergency surgery was mandatory.
After midline laparotomy, purulent generalized peritonitis, peritoneal carcinomatosis, ascitis and a giant malignant gastric perforation of 3,5-4 cm diameter were encountered. The surrounding gastric walls were rigid, infiltrated by the neoplastic process, with signs of gastric linitis plastica. The intent to mobilize the stomach was difficult and risky, so the classical techniques for repair could not be applied.
Due to the lack of the available gastric material, an atypical solution of gastric packing with greater omentum by means of transgastric traction had to be used. The intra-surgery images are relevant regarding this aspect.
The surgical technique had to be adapted to the local conditions. It includes highlighting the 3 distinct anatomical areas, individualized and personalized as operatory steps. The greater omentum became the efficient mobile part, which could be adapted for the creation of the contention effect. The gastric part is part of the technical criteria and the imposition carrying transduction becomes omentoplasty. The anatomic oro-gastric path represents the third distinct component reserved for supporting and handling the entire device and tissue-to-tissue fixation, whose biosynthesis is effective in time.
Materials, tools, and devices are specific and are part of the arsenal for transgastric omentoplasty kit.
A fragment of 4/3/1 cm of epiploic tissue was collected and sent to the histopathological examination for confirmation. The macroscopic examination showed whitish areas suggestive of mucinous carcinoma metastasis. The microscopic examination of hematoxylin and eosin-stained tissue sections from the formalin-fixed, paraffin-embedded surgical specimens revealed invasive mucinous carcinoma epiploic metastasis.
The postoperative follow up includes both drainage of subhepatic lodge, individualized in this case with two drain tubes (Pezzer and silicone) and a nasogastric probe. Loco-regional specific imagistics is imposed by the initiation of oral food intake.
The Barium radiograph 19 days post-surgery revealed: normal esophagus, increased fornix-diaphragm distance, giant malignant niche, with normal gastro-intestinal transit. Thoracic X-ray showed pleural liquid in both pulmonary bases.
The discharge diagnosis was perforated mucinous gastric carcinoma, gastric linitis, peritoneal carcinomatosis, neoplastic ascitis, generalized purulent peritonitis, gastric packing with epiploic material, severe secondary anemia, bilateral pleurisy.
The surgical solution proved successful for the immediate development of gastric perforation. Due to the extensive lesions and general risk factors, the two-stage surgery was chosen for the presented case. The underlying condition was not focused on in emergency, the patient being directed to the Oncology Department.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [5.0, 'kg']}",20,19,21,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 5.0 kg. Hence, the patient's maintenance fluid is 5.0 kg * 4 mL/kg/hr = 20.0 mL/hr.
Hence, the patient's fluid maintenance is 20.0 mL/hr."
5289,22,Maintenance Fluids Calculations,physical,decimal,pmc-5175041-1,Extracted,"Z.T. was a 11-month-old female baby. She was born at the 37th week of gestation weighing 2650 gr, and delivered by a cesarean section. She was followed in the neonatal intensive care unit for 2 weeks due to the respiratory insufficiency, cleft palate and feeding difficulty. At the first hospital visit after her discharge, pulmonary valvular stenosis and tetralogy of Fallot (TOF) were diagnosed on her echocardiograms. Balloon valvuloplasty was performed when she was 4 month- old. She was referred to our hospital for the surgical correction of her cardiac anomalies at the 11 months. On her physical examination in our clinic, her body weight was 6300 gr. (<3 percentile), height 62 cm. (<3 percentile) and head circumference, 41 cm. (<3 percentile). She had a wide forehead, low nasal bridge, cleft palate, micro/retrognathia, hypoplastic maxilla and hypertelorism (). Her heart rate was 130 bpm, respiratory rate was 32 breaths per minute with an oxygen saturation of 82% while breathing room air and her systemic blood pressure was 80/50 mmHg. She had bilateral sibilant rales and 2/6 systolic murmur at the pulmonic area on auscultation. Her liver was 3 cm. palpable below the subcostal margin and the spleen was nonpalpable. She had 3 hemangiomas with the diameters of 3 to 5 cm on her back. Her musculoskeletal and the genital examinations were within normal limits.
The mother of Z.T. was 26 and the father was 28 years old. There was no consanguinity between them and they had no dysmorphic facial appearance or any systemic illnesses. The mother had not received regular medical follow- ups during her pregnancy. She had never used tobacco or alcohol. There was no history of drug use or exposure to X-ray after she became pregnant. She had no history of infection, abortus or stillbirth, either. Their first degree relatives had not any congenital anomalies.
Biochemical and microbiological examinations of Z.T. showed mild infection with a white blood cell count of 13500/mm3, C reactive protein level of 2 mg/dl and 64% neutrophil dominancy (63%) on the peripheral blood smear, iron deficiency anemia and hypocalcemia with a serum calcium level of 7.3 mg/dl. Her 25 OH-D level was low (10 ng/ml), parathyroid and thyroid hormone levels were normal (15.2 pg/ml and 2.1 IU/ml, respectively). After treatment with calcium and vitamin D, her serum calcium levels have sustained within normal ranges. Serologic test results for toxoplasma, rubella and cytomegalovirus (TORCH) were negative. Her cardiothoracic ratio increased and the cardiac apex was elevated on the chest X-ray. On her echocardiogram, there was perimembranous ventricular septal defect, pulmonary stenosis, straddling tricuspid valve with a moderate degree of incompetence, patent ductus arteriosus, 50% dextroposition of aorta, tetralogy of Fallot and coronary arterial fistula on the ventricular septum. Abdominal ultrasonograms were normal except for a mild hepatomegaly.
As there were two afebrile seizure attacks in her neonatal history, electroencephalography (EEG) was performed. EEG reports indicated that there were sharp wave activities on the frontocentral, centrooccipital and temporooccipital regions of the left serebral hemisphere in relation with the centrooccipital region of the right cerebral hemisphere. Ophthalmic and audiological examinations of Z.T. were unremarkable. Cranial and spinal magnetic resonance examinations (MRI) showed mild dilatation of the lateral ventricules and a lipoma on the philum terminale.
The karyotype analysis of our case was reported as 46, XX. On her fluorescence in situ hybridization (FISH) analysis performed using DG (22q11) probe, deletion of band 11 on the long arm of chromosome 22 was detected.
After a successful total correction of TOF, tricuspid valvuloplasty and PDA ligation operations, she was discharged from our hospital on the twentieth postoperative day. We informed the family about the necessity of multidisciplinary approach for the children with VCFS to deal with their gastrointestinal, neurological, hematological, endocrinological, ophthalmic and the psychological problems in the future. We directed them for genetic counseling for the subsequent pregnancies. Z.T. underwent a plastic surgery for the correction of her cleft palate. She is 2 years old now and healthy.
The written consent of the family was taken for the publication of this case.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [6300.0, 'g']}",25.2,23.94,26.46,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 6300.0 g so this converts to 6300.0 lbs * kg/1000 g = 6.3 kg. Hence, the patient's maintenance fluid is 6.3 kg * 4 mL/kg/hr = 25.2 mL/hr.
Hence, the patient's fluid maintenance is 25.2 mL/hr."
5290,22,Maintenance Fluids Calculations,physical,decimal,pmc-5960510-1,Extracted,"A 33-year-old African American male patient was admitted to our hospital as a transfer from an outside hospital for further evaluation of the white blood cell (WBC) count of more than 100 K/mm []. He started experiencing fever, chills, poor appetite, and 10-pound weight loss over a month before admission. He visited an outside hospital with these symptoms. Basic laboratory investigations were done which revealed the WBC count of more than 100 K/mm []. His past medical history is significant for human immunodeficiency virus infection for the past 10 years. He has been noncompliant with his medications for HIV for more than 6 months. He had an appendectomy in 2003. He denied smoking cigarettes, drinking alcohol, and use of illicit drugs. He worked as a bus driver. He denied any exposure to pet animals or birds. He was afebrile on admission with blood pressure in the normal range. On examination, he had enlarged bilateral cervical, axillary, and inguinal lymph nodes. They were rubbery to touch and not tender on palpation. Absolute CD4 cell count was 847 cells/mm [] (reference range: 401–1532), and HIV viral load in serum was 101,591 copies/ml (reference range: not detected). Labs on admission showed that white blood cell count was 110.76 K/mm3 (reference range: 3.6–11.2 K/mm3) with 11% bands, 2% basophils, 29% blasts, 1% eosinophils, 3% lymphocytes, 7% metamyelocytes, 7% myelocytes, 9% promyelocytes, 8% monocytes, and 23% segmented neutrophils. Serum creatinine was 1.4 mg/dL (reference range: 0.7–1.3 mg/dL), alanine aminotransferase (ALT) was 14 U/L (reference range: 12–78 U/L), aspartate aminotransferase (AST) was 31 U/L (reference range: 15–37 U/L), and total bilirubin was 0.5 mg/dL (reference range: 0.2–1.0 mg/dL). He was started on intravenous fluids and allopurinol for mild acute kidney injury from tumor lysis. He was also started on a regimen of emtricitabine-tenofovir 200 mg–300 mg once daily with dolutegravir 50 mg daily for HIV. Bone marrow biopsy and aspiration were performed from the right iliac crest. Complete bone marrow evaluation with bone marrow aspiration, biopsy, and molecular and cytogenetic analysis was done, and it revealed chronic myeloid leukemia in blast crisis (35% bone marrow blasts). The cytogenetic analysis showed t(9:22) and inv(3). BCR-ABL FISH was positive. The RT-PCR was positive for coexpression of p210 and p190 fusion transcripts. He was started on intensive induction chemotherapy on hospital day 4 with cytarabine 100 mg/m [], continuous intravenous infusion (CIVI) for 7 days with idarubicin 12 mg/m [], and intravenous infusion (IV) for 3 days (also known as 7 + 3) along with dasatinib. At our institution, we use voriconazole for fungal prophylaxis during intensive induction chemotherapy. Due to drug interactions between dasatinib and voriconazole, the dose of dasatinib was reduced from 100 mg PO daily to 20 mg PO daily []. On hospital day 16, it was noted that his total bilirubin was elevated at 1.8 mg/dL (reference range: 0.2–1.0 mg/dL), AST was elevated at 60 (reference range: 15–37 U/L), and ALT was at 41 (reference range: 12–78 U/L). Since voriconazole is metabolized through the liver, it was stopped on hospital day 16. Ultrasonogram of the liver and biliary tree was normal. On hospital day 18, dasatinib dose was increased to its normal dose of 100 mg daily. Liver function tests done on hospital day 22 showed that total bilirubin trended down to 1.0 mg/dL, AST trended down to 19 mg/dL, and ALT trended down to 24 mg/dL. Then, on hospital day 29, the patient developed new-onset tea-colored urine, fever, chills, bilateral leg pain, and muscle cramps. Blood cultures and urine cultures were negative. Repeat liver function tests showed the following results: total bilirubin was 2.3 mg/dL, AST was 1254 mg/dL, and ALT was 290 mg/dL. Serum creatine kinase was >100,000 U/L (reference range: 26–308 U/L). shows the trend of CK and AST. Oral dasatinib and the patient's HIV medications emtricitabine-tenofovir 200 mg–300 mg once daily with dolutegravir 50 mg daily were discontinued.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.0, 'lbs']}",18.14368,17.2365,19.05086,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.0 lbs so this converts to 10.0 lbs * 0.453592 kg/lbs = 4.53592 kg. Hence, the patient's maintenance fluid is 4.53592 kg * 4 mL/kg/hr = 18.14368 mL/hr.
Hence, the patient's fluid maintenance is 18.14368 mL/hr."
5291,22,Maintenance Fluids Calculations,physical,decimal,pmc-3177414-1,Extracted,"A 19-year-old female (weight 66 kg, height 155 cm) with SLE was admitted to the intensive care unit (ICU) with dyspnea and hypoxemia despite therapy with high dose steroids and cyclophosphamide for 5 days. The decision was made to initiate plasmapheresis after an informed consent was secured for a hemodialysis catheter insertion. A size 11-French (3.7 mm) 20 cm long hemodialysis catheter (Quinton, Covidien, Mansfield, MA, USA) was inserted into the right femoral vein by an ICU “specialist”. No abdominal radiographs were obtained to ascertain the location of the catheter; however, a chest radiograph obtained later that day for follow-up on pulmonary infiltrates was reported to show a possible guide wire in the right side of the chest. The ICU physicians dismissed the radiologist report considering that the patient had not undergone attempts at internal jugular or the subclavian veins cannulations. Meanwhile, the patient underwent two plasmapheresis therapies through the catheter over two consecutive days without any symptoms. Another chest radiograph performed on the second day was reported to show an intact guide wire in the right hemothorax. A review of the radiographs by the ICU team confirmed the presence of an intact guide wire in the chest []. An abdominal radiograph confirmed that the wire was originating from the hemodialysis catheter [] inserted into the right femoral vein two days earlier for plasmapheresis. The guide wire was then extracted from the Quinton catheter by the intensivist. The patient underwent five additional plasmapheresis therapies uneventfully and was discharged home of the seventh day of hospitalization in good physical condition.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [66.0, 'kg']}",106,100.7,111.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 66.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (66.0 kg - 20 kg) = 106.0 mL/hr.
Hence, the patient's fluid maintenance is 106.0 mL/hr."
5292,22,Maintenance Fluids Calculations,physical,decimal,pmc-6521662-1,Extracted,"A 2-month-old (6 kg) boy was initially diagnosed with KD after 6 days of symptoms and treated with intravenous immunoglobulin (IVIG) (2 g/kg) and high-dose aspirin. Over the 1st month after his diagnosis, he had several readmissions for recurrent symptoms. Although his initial fever subsided with IVIG, he represented a week later with fever, rash, and conjunctivitis. He received a second dose of IVIG (2 g/kg) and remained on high-dose aspirin. Several days later, he developed a new fever, rash, and erythematous lips. He was readmitted and treated with methylprednisolone (30 mg/kg/day) for 3 days. He defervesced with this, but 4 days later, he again developed fever, conjunctivitis, and edema of his feet. He was ultimately treated with infliximab (5 mg/kg) intravenous for one dose and steroids (1 mg/kg/day tapered over 2 weeks). High-dose aspirin was continued from the time of his initial diagnosis through the 1st month. On echocardiogram, his coronary arteries had small aneurysms of the right and left main coronary artery which remained stable.
He remained well for the next 2 months without recurrent fever or symptoms. He then presented at 5 months (7.4 kg) with a 2-day history of intermittent left upper extremity pallor and coolness. He was afebrile with stable vital signs. The left lower arm was cool to touch and appeared pale when the infant was supine but pink when he sat up. There was fullness noted in the left axillary region on palpation. The left brachial pulse was unable to be palpated, while the pulses of the remaining extremities were easily appreciated and this was confirmed by Doppler. There were no signs of conjunctival injection, rash, edema, mucosal changes, or lymphadenopathy.
Computed tomography (CT) angiography of the left arm showed multiple aneurysms in the left axillary artery and a thrombosed aneurysm in the proximal left brachial artery. Angiogram of the left arm confirmed the CT findings [] with thrombosis of the brachial artery aneurysm. Collaterals along the upper arm were present bypassing the thrombosed region but were prone to compression when the infant was supine, thus leading to worsening symptoms when supine. Additional full-body imaging also revealed an aneurysm in the right brachial artery and small aneurysms in the axillary arteries bilaterally. No aneurysms were noted in the abdomen, pelvis, lower extremities, or the head and neck. Rheumatologic and hematologic evaluations were negative for any other etiology for peripheral aneurysms. Given concerns for limb ischemia, catheter-directed thrombolysis with tissue plasminogen activator (tPA) at the site of thrombosis was pursued in addition to systemic heparinization. The patient was started on tPA initially at 0.02 mg/kg/h and then increased to 0.04 mg/kg/h.
After 48 h of treatment with catheter-directed tPA, the patient had a brachial pulse auscultated with Doppler, and there were no further ischemic changes noted to the distal left arm. Intravenous heparin was continued and repeat angiogram still showed thrombus, but with some improvement in flow. The patient was transitioned to enoxaparin. After 6 months, repeat CT angiography of the left arm showed persistent large brachial artery aneurysm, but resolution of the thrombus []. No progressive or giant coronary aneurysms were seen during the disease course.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [7.4, 'kg']}",29.6,28.12,31.08,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 7.4 kg. Hence, the patient's maintenance fluid is 7.4 kg * 4 mL/kg/hr = 29.6 mL/hr.
Hence, the patient's fluid maintenance is 29.6 mL/hr."
5293,22,Maintenance Fluids Calculations,physical,decimal,pmc-4624354-1,Extracted,"A 70-year-old Japanese woman with a past history of bronchial asthma and paroxysmal atrial fibrillation was transferred to Kyushu University Hospital because of leg edema and insidious onset of proteinuria and microhematuria. She had presented with mild leg edema 8 months before, and was admitted to another hospital because of pneumonia. Then heavy proteinuria was identified. She had a history of polyarthralgia, although other symptoms such as skin rash, hair loss, oral ulcers, and Sicca syndrome were not evident.
On admission, the patient’s characteristics were: height 144 cm, body weight 38.7 kg, body temperature 36.9 °C, and blood pressure 120/46 mmHg. Physical examination revealed normal breath sounds, heart sounds, abdomen and nervous system, but signs of anemia in the palpebral conjunctiva and bilateral leg edema were found. Urinalysis revealed proteinuria (2+), and occult blood (2+). Urinary protein excretion was 2.3 g/day. Complete blood counts revealed: white blood cells 3050/μL, red blood cells 252 × 104/μL, hemoglobin 8.2 g/dL, hematocrit 24.3 %, and platelets, 12.9 × 104/μL, with no atypical leukocytes. Serum biochemical analyses revealed: total protein 6.9 g/dL, serum albumin 3.0 g/dL, blood urea nitrogen 33.0 mg/dL, serum creatinine 1.09 mg/dL (eGFR 43.2 mL/min/1.73 m2), sodium 141 mmol/L, potassium 5.1 mmol/L, chloride 115 mmol/L, calcium 8.3 mg/dL, phosphate 4.9 mg/dL, and C-reactive protein 0.21 mg/dL. Quantitative immunoglobulin analysis showed: IgG 2407 mg/dL (normal, 872–1815 mg/dL), IgA 114 mg/dL and IgM 53 mg/dL (59–269 mg/dL), and the additional measurement of IgG subclasses revealed IgG1 564 mg/dL (320–748 mg/dL), IgG2 1650 mg/dL (208–754 mg/dL), IgG3 214 mg/dL (6.6-88.3 mg/dL), and IgG4 1110 mg/dL (4.8–105 mg/dL). Serum levels of C3, C4 and total serum hemolytic activity (CH50) were 58 mg/dL (71–135 mg/dL), 9 mg/dL (11–34 mg/dL), and 32 U/mL (31.6–57.6 U/mL), respectively. Although rheumatoid factor was increased to 133 IU/mL (<15 IU/mL), antinuclear antibodies, anti-double-stranded DNA antibodies, anti-U1-ribonucleoprotein antibodies, myeloperoxidase anti-neutrophil cytoplasmic antibodies (ANCA), proteinase 3 ANCA, anti-glomerular basement membrane (GBM) antibodies, anti-Sjögren syndrome related antigen (SS)-A antibodies, anti-SS-B antibodies, circulating immune complexes, and cryoglobulins were all negative. Hepatitis B virus surface antigen, hepatitis C virus antibodies, and human T-lymphotropic virus 1 antibodies were negative. T-SPOT.TB assays for the diagnosis of latent tuberculosis was also negative. Abdominal ultrasonography and computed tomography scanning revealed the absence of systemic lymphadenopathy, and no abnormal findings in the pancreas, salivary glands, and thyroid gland, although ultrasonography showed mild enlargement of bilateral kidneys (right 10.3 × 4.4 cm, and left 10.8 × 4.1 cm).
Percutaneous kidney biopsy was performed on the 12th hospital day to determine the cause of the urinary abnormalities and kidney dysfunction. Light microscopic observation revealed global glomerulosclerosis in 1 of 13 glomeruli with mild interstitial edema and inflammation (Fig. ). The infiltrating cells were mainly mononuclear cells, but occasional eosinophils and a number of plasma cells were also noted. Storiform interstitial fibrosis was not evident (Fig. ). Twelve non-sclerotic glomeruli showed uniform changes; moderate to severe mesangial proliferation, increased mesangial matrix, and mild to moderate endocapillary hypercellularity. Subendothelial deposits (Fig. ), and double contours of the glomerular capillaries were also observed (Fig. ). No glomerular crescent was found. Immunofluorescence studies showed “full-house” staining for IgG (3+), IgA (1+), IgM (1+), C3 (2+), C1q (3+), and fibrinogen (1+) in the glomerular mesangium and the capillary wall (Fig. ). Ultrastructural examination showed focal foot process effacement of the glomerular epithelial cells, mesangial and subendothelial electron-dense deposits, and mesangial interposition (Fig. ). According to these findings, we confirmed the pathological diagnosis of MPGN type 1.
Because the patient showed extremely high serum IgG4, we performed a lip biopsy and found the diffuse infiltration of IgG4 positive plasma cell in the glandular area (Fig. ); thus, the diagnosis of IgG4-RD was confirmed. Kidney-infiltrating plasma cells also produced IgG4, suggesting focal and early stage IgG4-related kidney disease (IgG4-RKD) (Fig. ). However, additional immunofluorescence studies revealed predominant deposition of IgG2 and IgG3, negative IgG1, and minimal IgG4 deposition in the glomeruli (Fig. ).
Although we found discrepancies in IgG subclass among the glomeruli and kidney interstitium, we treated this patient as IgG4-RD. Oral prednisolone administration (initial dose 30 mg/day) was started. The patient showed decreased urinary protein, and increased serum albumin and complement levels. In examinations conducted in our outpatient clinic 8 months later, the patient showed proteinuria (±), hematuria (3+), white blood cell count 9690/μL, hemoglobin 11.4 g/dL, platelet count 32.5 × 104/μL, serum albumin 3.9 g/dL, serum creatinine 0.96 mg/dL, C3 99 mg/dL, C4 23 mg/dL, IgG 1002 mg/dL and IgG4 200 mg/dL (Fig. ).","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [38.7, 'kg']}",78.7,74.765,82.635,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 38.7 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (38.7 kg - 20 kg) = 78.7 mL/hr.
Hence, the patient's fluid maintenance is 78.7 mL/hr."
5294,22,Maintenance Fluids Calculations,physical,decimal,pmc-4969980-1,Extracted,"The three cases were diagnosed in the outpatient unit of the Nephrology Department at Strasbourg University Hospital, France.
Patient #1 was a 60-year-old man who underwent transplantation at the age of 52 for chronic renal failure due to polycystic kidney disease. He initially received immunosuppressive treatment, consisting of tacrolimus (4 mg/day), mycophenolate mofetil (MMF) (1 g x 2/day), and prednisone (7.5 mg/day). Eight years after renal transplantation, he presented with watery diarrhea, nausea and vomiting starting 15 days before consulting (September 25th, 2014). Physical examination revealed asthenia, weight loss (6Kg), hypotension, dry mouth, and acute renal failure (glomerular filtration rate [GFR]: 30 ml/min/1.73 m2). The patient reported no recent travel or contact with swimming pool water, non-drinking water or farm animals, but admitted to own a dog. No other family member experienced diarrhea.
Patient #2 was a 64-year-old man of Malian origin who had lived in France for 40 years and undergone transplantation at the age of 62 for chronic renal failure secondary to glomerulonephritis. Immunosuppressive treatment consisted of tacrolimus (7 mg x 2/day), MMF (750 mg x 2/day), and prednisone (10 mg/day). Two years and 4 months following renal transplantation, he presented with watery diarrhea and abdominal pain lasting for 15–20 days (starting September 26th, 2014). Physical examination revealed weight loss (13Kg), esophageal pain, and acute renal failure (GFR: 36 mL/min/1.73 m2). The patient also presented leucopenia and neutropenia, initially attributed to an overdose of tacrolimus. He reported no previous contact with non-drinking water, swimming pool water or farm animals, but had travelled to Mali for 2 months shortly before the onset of diarrhea. No other person of his family experienced diarrhea.
Patient #3 was a 34-year-old man of Kosovar origin who underwent transplantation aged 24-year-old for an undetermined reason. Acute transplant rejection 2 years later led to a second transplantation in September, 2014. Immunosuppressive treatment consisted of tacrolimus (6 mg x 2/day), MMF (750 mg x 2/day), and prednisone (25 mg/day). Ten days following the second renal transplantation (September 21th, 2014), the patient exhibited watery diarrhea and abdominal pain. Physical examination indicated weight loss (10Kg) and acute renal failure (GFR: 16 ml/min/1.73 m2). The patient, who reported no contact with non-drinking water, swimming pool water or farm animals, had travelled to Kosovo for 1 month before transplantation. His 2-year-old daughter also presented with diarrhea from an unknown cause that lasted for 3 days. No stool analyses were done for the daughter.
For all three patients, stool examinations performed at the first consultation revealed the presence of Cryptosporidium oocysts, using a modified Ziehl-Neelsen staining method (5–10 oocysts/slide, >100 oocysts/slide, and 1–5 oocysts/slide for cases #1, #2, and #3, respectively). All stool samples were negative for the bacteria Clostridium difficile, Salmonella, Shigella but also for rotavirus and norovirus, and for parasites Giardia and microsporidia.
DNA was extracted from the stool samples using a NucliSENS easyMAG device (bioMérieux, Marcy l’Etoile, France) []. Briefly, it consisted of adding 400 mg of stool samples to 1 mL of NucliSENS lysis buffer in a tube containing ceramic beads (lysing matrix D; MP Biomedicals, Illkirch, France), disrupted in a FastPrep-24 grinder (MP Biomedicals) at maximum power for 1 min. After 10 min of incubation at room temperature to ensure complete lysis, the tubes were centrifuged at 10,000 × g for 10 min and extraction was performed with 250 μL of supernatant. Elution was performed at 70 °C with 100 μL of elution buffer. An in-house real-time polymerase chain reaction (PCR) assay was set up to enable the detection and identification of the most common Cryptosporidium species/genotypes []. To this end, we used a single reaction tube with fluorescence-labelled probes for the real-time detection of Cryptosporidium, in addition to melting curve analyses of PCR products to differentiate between the Cryptosporidium species/genotypes. We conducted the amplification of a 258 bp DNA fragment located in the 18S ribosomal ribonucleic acid (rRNA) gene (GenBank accession n°L16996; positions 80 to 337) using the following primers: Cry80F: 5’-GTTAAACTGCRAATGGCT-3’; Cry337R: 5’-CGTCATTGCCACGGTA-3’. The CryAnch-labelled hybridization probe (5’-CCGTCTAAAGCTGATAGGTCAGAAACTTGAATG-fluorescein-3’) hybridizes in a region that is conserved among all Cryptosporidium species and the CrySens labelled hybridization probe (5’-LCRed640-GTCACATTAATTGTGATCCGTAAAG-3’) hybridizes in a polymorphic region (nucleotides 260 to 264) with various mismatches. Thermocycling and fluorescence detection were performed by means of a LightCycler 2.0 system (Roche Diagnostics) in a final volume of 20 μL, using a Roche LC Faststart DNA Master HYPROBE (Roche Diagnostics) with 0.5 μM of each primer, 0.2 μM of hybridization probe, 0.5U of UNG (Roche Diagnostics), and 5 μL of extracted DNA. After applying 95 °C for 10 min, amplification was commenced consisting of 50 cycles of 10-sec denaturation at 95 °C, 15 sec of annealing at 50 °C (with a touchdown protocol beginning at 60 °C), and 15 sec of elongation at 72 °C. The fluorescent signal (640 nm) was detected following the annealing step of each cycle. Species/genotypes differentiation was based on differences in the melting temperatures of the PCR-probe complexes, which were determined based on the extent of complementation of the probes to the target strand of the PCR product. For the melting curve analysis, a quick denaturation step was performed at 95 °C followed by a 30-sec annealing step from 45 °C to 80 °C (ramp-up rate: 0.1 °C/s), with continuous detection throughout the ramp up. The technique was validated using Cryptosporidium DNA of a stool collection already characterized at the genus level and positive controls for C. parvum and C. hominis [].
The five predominant human pathogenic Cryptosporidium species were identified based on their melting curve profiles (61.9 °C, 53.8 °C, 48.8 °C, 56.7 °C, and 51.8 °C for C. parvum, C. hominis, C. felis, C. meleagridis, and C. canis, respectively). Given that C. cuniculus, an emergent human species, possesses the same melting curve profile as that of C. hominis, with both species exhibiting the same DNA sequence at the hybridization probe locus, all isolates identified as C. hominis were then sequenced to differentiate C. hominis from C. cuniculus.
For sub-genotyping analysis, DNA samples were subjected to amplification of an 850-bp fragment of the gp60 gene using a nested PCR method []. The total volume of PCR mixture was 50 μL, containing 5 μL of DNA for the primary PCR or 5 μL of the primary PCR products, primers (outer primers: AL3531 and AL3535; inner primers: AL3432 and AL3534) at a concentration of 0.4 μM, 0.2 mM deoxyribonucleotide triphosphate mix, and 1.25U of DreamTaq DNA polymerase. Each PCR reaction was subjected to 40 cycles of 30s denaturation at 95 °C, 60s annealing at 55 °C, and 60s extension at 72 °C, with an initial 5 min denaturation at 95 °C and a final 10 min extension at 72 °C. PCR products were visualized by electrophoresis on an ethidium bromide stained 2 % agarose gel electrophoresis. Amplicons were purified and sequenced in both directions with the forward and reverse primers used in the secondary PCR at a concentration of 0.32 μM. Sequencing was performed using a BigDye Terminator v3.1 Cycle Sequencing Kit (Applied Biosystems, USA) and an ABI PRISM 3100 Genetic Analyzer® (Applied Biosystems, USA). We analyzed the quality of the generated electrophoregrams from each strand using 4Peaks software and compared them with those available in the GenBank database using the basic local alignment search tool. Subtype assignment was based on the number of trinucleotide repeats (TCA, TCG or TCT) in the coding for serine [].
For Patient #1, genotyping revealed a C. felis infection. For Patient #2, genotyping revealed C. hominis sub-genotype IaA13. For Patient #3, the C. parvum sub-genotype IIaA13G1R2 was identified.
All three patients were treated with nitazoxanide (500 mg x 2/day for 14 days). For Patient #1, the stools tested negative 2 weeks after treatment initiation, with no recurrence of diarrhea observed 4 months after the first episode. For Patient #2, a reduction of tacrolimus was initiated and the diarrhea regressed 8 days after treatment initiation, although 3 months after therapy was started, his stools still tested positive. A second administration of nitazoxanide was thus prescribed and we requested a stool sample from his daughter for testing. One month after the second treatment course, his stools were tested negative for Cryptosporidium oocysts. For Patient #3, tacrolimus was also reduced and his diarrhea was regressing 1 month after treatment initiation. Four months after the second treatment course, his stools were tested negative for Cryptosporidium oocysts.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [10.0, 'kg']}",40,38,42,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 10.0 kg. Hence, plugging into this formula, we get 40 mL/hr + 2 mL/kg/hr * (10.0 kg - 10 kg) = 40.0 mL/hr.
Hence, the patient's fluid maintenance is 40.0 mL/hr."
5295,22,Maintenance Fluids Calculations,physical,decimal,pmc-4478833-1,Extracted,"A 52-year-old, 88 kg man scheduled for sacral laminectomy and excision of the sacral mass for sacral chordoma, under general anesthesia. His past medical history revealed no specific findings. The preoperative results of biochemical studies, chest X-ray and electrocardiography, were normal. Physical examination revealed limitation of movement of the left thigh. General anesthesia was induced with intravenous propofol 2 mg/kg, morphine 0.1 mg/kg, atracurium 0.6 mg/kg and maintained with isoflurane/oxygen/nitrous oxide mixture under standard monitoring. After oral tracheal intubation, an endotracheal tube was fixed on the right side of the mouth and kept at 22 cm in depth. After intubation, the patient was placed in the prone position with the neck flexed at approximately 10°. The head was turned to the right side, and the left side of the face was placed on a soft gel rolling pad. The surgery proceeded for about 7 h. The total blood loss was about 1000 ml. After endotracheal extubation, patient was shifted to postanesthesia care unit, where swelling of the left parotid gland was noted. The swelling of the parotid gland increased in size and hardness. Painful sensations were complained of after the patient was sent to the room after 4 h stay at postanesthesia care unit.
ENT consulted, examination revealed firm, mildly erythematous swelling starting from the left per auricular face to the angle of the mandible, no parotid secretions noted. Patient was reassured, and pain was managed with nonsteroidal anti-inflammatory drugs. Patient was discharged to home at 7th postoperative day after complete recovery with a follow-up visit at ENT clinic.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [88.0, 'kg']}",128,121.6,134.4,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 88.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (88.0 kg - 20 kg) = 128.0 mL/hr.
Hence, the patient's fluid maintenance is 128.0 mL/hr."
5296,22,Maintenance Fluids Calculations,physical,decimal,pmc-8022529-1,Extracted,"The patient was a 70-year-old man with a history of cerebral infarction (no paralysis), hypertension, and duodenal ulcers; he had no history of allergies. On admission, he was independently ambulatory. The Eastern Cooperative Oncology Group Performance Status (ECOG PS; range, 0–4; with higher scores indicating worse disability) was 0 []. Serum transferrin, pre-albumin, and retinol-binding protein levels were 237 mg/dL (range: 190–300), 23.4 mg/dL (range: 22–40), and 1.90 mg/dL (range: 3.6–4.2), respectively, before the operation. He underwent resection of the right and caudate lobes of the liver, extrahepatic bile duct resection, choledochojejunostomy, and jejunostomy for perihilar cholangiocarcinoma.
During the first 3 months after the operation, the patient experienced hepatic failure, AKI, disseminated intravascular coagulation (DIC), and pneumonia. Hemodialysis was performed three times per week. The patient was bedridden for the entire day, and his ECOG PS was 3–4. The enteral tube was placed in the jejunum to administer medicine and nutrition; however, enteral nutrition was stopped repeatedly owing to the worsening of postoperative complications or gastrointestinal symptoms. Consequently, he received both parenteral and enteral nutrition with a total energy of 1200 kcal/day and 25.0 g/day protein. Physical findings and serum levels related to renal function are shown in Table . When his body composition was analyzed using the InBody® (Inbody S20; Biospace, Seoul, Korea) system, the skeletal muscle mass, skeletal muscle mass index (SMI), fat mass, body fat, and extracellular water (ECW) to total body water (TBW) ratio were 14.2 kg, 5.85 kg/m2, 19.4 kg, 39.0%, and 0.436, respectively. The patient had edema, ascites, and a pleural effusion. His dry weight estimated by subtracting the excess fluid from the actual body weight was 47.0 kg; the patient lost 10.0 kg in about 5 months. He met the diagnostic criteria for sarcopenia by the Asian Working Group for Sarcopenia (AWGS) [] and was classified as severely malnourished. He underwent repeated cycles of constipation and diarrhea.
The target energy intake was set at 35.0 kcal/kg/day (1700 kcal/day). The target protein intake was 1.20 g/kg/day (60.0 g/day) and 0.80 g/kg/day (40.0 g/day) when on and off dialysis, respectively, based on the consensus among the NST, the nephrologist, and the gastrointestinal surgeon, and consistent with the 2016 Clinical Practice Guideline for Acute Kidney Injury in Japan [] and recommendation of the third revision (2013) of the guidelines for parenteral and enteral nutrition in Japan []. The use of intravenous- and enteral-nutrition routes was evaluated continuously. The patient was assessed as having AKI which gradually improved but transitioned from acute to chronic kidney disease. The nephrologist assessed the need for weekly hemodialysis, which the patient received as needed. Priority was given to patient mobilization, balance of energy intake and expenditure, prevention of complications associated with bed rest, and prevention of the progression of generalized deconditioning.
The patient was fed via a combination of total parenteral nutrition, peripheral parenteral nutrition, and enteral nutrition; blood-glucose levels were monitored. We evaluated the patient’s physical findings, renal function test values (Table ) and adjusted laxative prescriptions to improve bowel movements. Dialysis was stopped on day 56. On day 112 of the NST intervention, the protein dose was 1.40 g/kg/day, and the energy and protein doses were stabilized. The intake of essential nutrients was sufficient with continuous enteral nutrition alone at a slow rate throughout the day (Table ).
The patient’s limbs were strong enough to perform activities of daily living (ADL) in bed, so upper body muscle training was started 5 days a week for 20 min. The aim of this training was to extend the sitting time on the bed and to acquire ADL-movement ability. Moreover, lower-limb muscle training was initiated to prevent the loss of skeletal muscle. As the patient’s nutritional status improved, the proportion of strength training in the regimen was gradually increased. The patient was able to stand unassisted on day 100 of the intervention; hence, walking training was started.
Renalen®MP was administered via an enteral route as an energy-dense nutrition formula to meet the target energy goals. Furthermore, we added branched-chain amino acids (BCAA)-enriched nutritional supplements (i.e., ENEVO® and Aminoleban®EN) because they are expected to promote protein synthesis []. Initially, Renalen®MP was administered during the daytime, and the patient frequently complained of gastroesophageal reflux and bloating during tube feeding, probably because of the high fat content in Renalen®MP. Because of these complaints, it was difficult for him to continue rehabilitation. Therefore, we changed the time of administration of Renalen®MP from daytime to nighttime (Table ). The patient was able to walk independently on day 150. He could also ingest a small amount of food orally. On day 200, the skeletal-muscle mass, SMI, fat mass, body fat, and ECW/TBW ratio were 19.1 kg, 7.95 kg/m2, 17.6 kg, 31.4%, and 0.436, respectively. The ECOG PS was 2. The rehabilitation was continued, so that the patient could be discharged.
The patient was able to receive daily nutrition both enterally and orally. The dynamic nutritional-assessment parameters and brachial muscle analysis increased over time (Figs. , ). Body weight and LBM slightly decreased by day 103 but increased after day 103. On day 200, they have improved to what it was almost before the surgery (Fig. ). He continued rehabilitation because his bowel movements were controlled.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [47.0, 'kg']}",87,82.65,91.35,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 47.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (47.0 kg - 20 kg) = 87.0 mL/hr.
Hence, the patient's fluid maintenance is 87.0 mL/hr."
5297,22,Maintenance Fluids Calculations,physical,decimal,pmc-3507110-1,Extracted,"A 2 day old male neonate presented with scalp swelling, weakness and whiteness of the body. The mother was Para 3+0 and she received antenatal care in a private hospital and kept all appointments and used only the prescribed drugs. She delivered vaginally in the same hospital but the process was prolonged and complicated by cervical dystocia and maternal exhaustion. The baby's condition at birth could not be assessed objectively because the Apgar Scores were not recorded at the site of delivery.
Physical examination revealed a mature neonate who looked ill, weak, and markedly pale. He was grunting and breathless but not jaundiced. The head showed a diffuse and extensive swelling of the scalp involving the parietal regions, the occiput and posterior aspect of the neck as well as the right peri orbital area. He was in obvious respiratory distress with flaring alae nasi and recession of the intercostals and sub costal areas.
He weighed 3.55kg and the head circumference and length were 37cm and 48cm respectively. He had a respiratory rate of 52 cycles per minute and peripheral pulse rate was 164 beat per minute. The breath sounds were vesicular with background-transmitted noise. The heart sounds were normal and soft systolic murmurs were heard. The abdomen and genitalia were normal but the Central Nervous System showed depressed primitive reflexes as well as high-pitched cry.
The clinical course was complicated by the development of subtle seizures and jaundice on the second and fourth days of hospitalization respectively.
The hemogram revealed marked anemia with Hematocrit of 19%; Leukocyte and Platelet Counts of 8 × 109/ L and 200 × 109/ L respectively. The serum Bilirubin level was 13mg / dl with the unconjugated component being 10.4 mg / dl. Radiograph of his skull showed massive scalp swelling overlying the entire skull, but worse over both parietal and occipital areas considered to be due to traumatic Cephalhematoma / edema in the presence of a displaced posterior parietal fracture. He was screened for sepsis and no organism was isolated.
Anemia was corrected with packed cell transfusion. Moreover, he received intra venous fluids, parenteral antibioticand dexamethasone as well as phototherapy. He responded to treatment and was discharged home in a satisfactory state after 10 days of hospitalization. The head circumference was 35.4 cm and he weighed 3.1 kg.
The child was seen at one year and achieved all developmental milestones appropriately. Neck control was at 14 weeks and he sat unaided at 7 months and walked at eleven months.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3.55, 'kg']}",14.2,13.49,14.91,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3.55 kg. Hence, the patient's maintenance fluid is 3.55 kg * 4 mL/kg/hr = 14.2 mL/hr.
Hence, the patient's fluid maintenance is 14.2 mL/hr."
5298,22,Maintenance Fluids Calculations,physical,decimal,pmc-3425292-1,Extracted,"A 22-year-old primigravida weighing 46 kg, known case of Eisenmenger's syndrome at 37 weeks of gestation, was scheduled for an elective caesarean section. At the age of 15 years, a cardiac catheterization was performed, which revealed a large mid-muscular VSD with severe pulmonary arterial hypertension (120/50 mmHg). She was explained about the existing cardiac condition and advised to avoid strenuous work.
Pre-operatively, apart from exertional dyspnoea (grade II), she was asymptomatic. Physical examination revealed grade II clubbing, pulse rate of 92/min, blood pressure of 130/90 mmHg and room air oxygen saturation (SpO2) of 90–92% with no rise in jugular venous pressure (JVP). No peripheral oedema or cyanosis was observed. Her lungs were clear to auscultate and cardiac examination showed regular rate and rhythm with loud P2 and pansystolic murmur over the lower left sternal border. Electrocardiography showed right axis deviation with right ventricular hypertrophy. Two-dimensional echocardiography (2D Echo) with colour Doppler revealed a large muscular VSD (19 mm × 20 mm) with a bidirectional shunt and a good left ventricular function with ejection fraction of 58% with severe pulmonary hypertension. Her haemoglobin was 12.6 g%, with a haematocrit of 40% and platelet count of 1,50,000/mm3. Arterial blood gas (ABG) on room air was pH-7.32, PaCO2-35 mmHg, PaO2-59 mmHg, and SaO2-91%. Cardiologist opinion was taken and she was advised to undergo elective caesarean section.
She was pre-medicated with Ranitidine 150 mg orally the night before surgery. Infective endocarditis prophylaxis was given. In the operation theatre, standard monitors, an arterial line and a central venous catheter were placed. Prophylactic dopamine infusion 10 μg/kg/min was started to maintain the systemic vascular resistance (SVR). After 3 min of pre-oxygenation, SpO2 increased to 100%. The pre-induction blood pressure (BP) and central venous pressure (CVP) were 130/90 mmHg and 10 mmHg, respectively. Intravenous induction was carried out with a low dose of thiopentone sodium 150 mg and fentanyl 50 μg titrated to anaesthetic and haemodynamic effects. The patient was intubated endotracheally with suxamethonium 50 mg. Anaesthesia was maintained with 50% oxygen and 0.5% halothane in air and neuromuscular blockade was achieved with vecuronium 5 mg. The end tidal carbon dioxide (EtCO2) was maintained between 32 and 35 mmHg.
A live female baby with Apgar score of 5 at 1 min and 8 at 5 min, weighing 1.9 kg, was extracted. Intravenous infusion of oxytocin 15 units was administered slowly over 30 min. Intraoperative analgesia was obtained with morphine 6 mg i.v. Blood loss was estimated to be about 500 mL. The patient remained haemodynamically stable throughout the procedure, which lasted for 45 min. Low-molecular weight heparin (LMWH) 5000 IU was given subcutaneously towards the end of the surgery. Neuromuscular blockade was reversed with neostigmine 2.5 mg and glycopyrrolate 0.5 mg and the patient was extubated and shifted to the post-operative ward with oxygen by mask for observation. Post-operatively, the patient was haemodynamically stable and dopamine was tapered off. Anticoagulation with heparin and analgesia with morphine 4 mg i.v. 8th hourly were continued for the next 1 week. Perioperatively, CVP was used as a guide to administer i.v. fluids and was maintained around 10 cm of H2O. Volume overload was avoided as it could easily precipitate right ventricular failure in these cases.[]
On the third post-operative day, she was found to have cyanosis with tachycardia, tachypnoea and hypotension (90/60 mmHg) with SpO2 of 75% despite supplemental oxygen. Her ABG revealed pH-7.42, PaCO2-32 mmHg, PaO2-45 mmHg and SaO2-72%. Dopamine was restarted at 10 μg/kg/min to maintain the systolic BP above 100 mmHg. SpO2 remained between 75% and 80% despite oxygen therapy. She improved gradually over a period of 3 days and dopamine was tapered off. She was discharged on the 15th post-operative day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [46.0, 'kg']}",86,81.7,90.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 46.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (46.0 kg - 20 kg) = 86.0 mL/hr.
Hence, the patient's fluid maintenance is 86.0 mL/hr."
5299,22,Maintenance Fluids Calculations,physical,decimal,pmc-7725136-1,Extracted,"A 57-year-old male with a 7-day history of fever and dyspnea was admitted to a local hospital and intubated for respiratory failure. COVID-19 was confirmed by a positive polymerase chain reaction (PCR) test result obtained via a nasopharyngeal swab. Thus, he was transferred as a severe COVID-19 pneumonia case in need of intensive care. He had a medical history of hypertension, dyslipidemia, and asthma. His height was 173 cm and his weight was 71.6 kg.
On arrival, the physical examination revealed body temperature of 38°C, blood pressure of 112/47 mmHg, pulse of 106 beats/min, and respiratory rate of 14 breaths/min. He was deeply sedated (Glasgow Coma Scale score: E1VtM4) and suffered severe respiratory failure; arterial blood gas analysis showed pH 7.283, partial pressure of carbon dioxide (PaCO2) 45 mmHg, partial pressure of oxygen (PaO2) 64 mmHg with invasive mechanical ventilation [pressure control ventilation with positive end-expiratory pressure (PEEP) of 12 cmH2O, peak inspiratory pressure (PIP) of 24 cmH2O, the fraction of inspired O2 (FiO2) of 0.75, inspiratory time of 1.6 s, frequency of 14/min, and the delivered tidal volume was about 470 mL]. The computed tomography scan revealed a bilateral consolidation with lower lung predominance; bulla or emphysema was not observed (Fig. ). Favipiravir, hydroxychloroquine, and tocilizumab were administered for the COVID-19 treatment. As mechanical ventilation, in accordance with the acute respiratory distress syndrome (ARDS) strategy, did not show sufficient improvement, prone position ventilation was also initiated. His oxygenation improved slightly but not enough; PaO2 was 78.4 mmHg with FiO2 of 0.6.
On the 15th day after admission, the chest X-ray suggested a giant bulla in the right lung (Fig. ). One day later, his respiratory condition deteriorated and the chest X-ray revealed the presence of severe right-sided pneumothorax (Fig. ). A 24-Fr chest drain was immediately inserted, covering the patient’s right chest with a plastic sheet and attaching an in-line filter to the suction tubing to minimize aerosolization. However, a significant air leak continued, and severe ventilator settings were still required (pressure control ventilation with PEEP of 12 cmH2O, PIP of 28 cmH2O, FiO2 of 0.6, inspiratory time of 0.9 s, frequency of 20/min, and the delivered tidal volume was about 320 mL) to compensate for the respiratory acidosis (pH 7.266, PaCO2 62.2 mmHg, PaO2 73.3 mmHg). The Murray score was 3. In addition, the pneumothorax was considered to be intractable and the continuous air leak increased the risk of medical staffs’ exposure. Thus, VV-ECMO treatment (MERA centrifugal blood pump system HCS-CFP; Senko Medical Instrument, Tokyo, Japan) was promptly initiated for lung protection at 5 h after performing the tube thoracotomy. The right internal jugular vein was cannulated with a 19-Fr heparin-coated cannula for blood return, and the right femoral vein was cannulated with a 24-Fr heparin-coated cannula for blood access. The blood flow was 4.5 L/min and sweep gas was 5.0 L/min. Heparin was given to maintain an activated partial thromboplastin time of about 50 s.
The PEEP was initially set to 0 cmH2O and the PIP was set to 5 cmH2O. After the air leak diminished, we gradually increased the pressure. On the 3rd day after starting ECMO, the PEEP was set to 5 cmH2O and the PIP was set to 10 cmH2O. On the 7th day, the PEEP was set to 8 cmH2O and the PIP was set to 12 cmH2O. On the 10th day, during the sweep gas off test, the arterial blood gas analysis showed pH 7.383, PaCO2 49.4 mmHg, PaO2 81.7 mmHg with PEEP of 10 cmH2O, PIP of 22 cmH2O, FiO2 of 0.4, inspiratory time of 1.1 s, frequency of 18/min, and the delivered tidal volume was about 480 mL. Thus, the patient was weaned from the ECMO and the chest drain was removed on the following day with no major comorbidities.
We performed the PCR test every other week. The PCR test result was negative on the 31st day after admission. The patient underwent tracheostomy on the 34th day. The ventilator management was completed on the 52nd day and he was transferred for rehabilitation on the 61st day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [71.6, 'kg']}",111.6,106.02,117.18,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 71.6 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (71.6 kg - 20 kg) = 111.6 mL/hr.
Hence, the patient's fluid maintenance is 111.6 mL/hr."
5300,22,Maintenance Fluids Calculations,physical,decimal,pmc-5692235-1,Extracted,"A 12 year old boy let go too soon from a rope swing over water, and fell onto rocks with his knees. He was taken to hospital with a deep wound under his left knee.
In the emergency room he was diagnosed with a penetrating wound of the left lower leg, exposing a part of the proximal tibia. The wound was sutured subcutaneously and cutaneously, and he was given amoxicillin-clavulanic acid (dosed 875/125 mg twice daily, for a weight of 45 kg).
The day afterwards (day 1), he returned to the emergency ward with photophobia, headache, nausea and fever (38.5 °C). Repeated history made clear that he had fallen about 2–3 m, but not directly on his head. There had been no loss of consciousness nor post-traumatic vomiting. Physical examination showed no signs of sepsis, a normal neurologic status, normal ear-nose-throat inspection, and the stitched wound had a normal aspect. Laboratory investigations showed a slight leukocytosis (12.600 µl−1) with neutrophilia (85 %), but a normal CRP (6.6 mg l−1) and sedimentation rate (2 mm u−1). He was hospitalized for observation and neurologic monitoring, the latter remaining normal. Amoxicillin-clavulanic acid was continued.
The day after admission (day 2), he remained febrile (up to 38.9 °C). Examination now showed evacuation of some pus from his leg wound, with a slight swelling, redness and local pain. The pus was sent for culture on two separately collected cotton-tipped swabs (supplementary data S1). Ultrasound of the leg showed a small (11×3 mm) subcutaneous collection, but could not differentiate between residual blood and abscess. Bone scintigraphy showed no signs of osteomyelitis nor septic arthritis, but did show increased blood flow in the cranial part of the left lower leg with global swelling, indicating an important soft tissue inflammation (). Amoxicillin-clavulanic acid was increased to 100/10 mg kg−1d−1.
On day 3, cultures of the pus showed growth of Aeromonas species (on both samples), but susceptibility testing was not yet known. Clinically, there was some improvement with diminishing redness, but tenderness, swelling and pus evacuation continued. Antibiotic treatment was not altered.
On day 5, there were no additional pathogens found on culture and susceptibility testing of the Aeromonas species showed resistance to amoxicillin-clavulanic acid. The finding of Aeromonas species came unexpectedly. Only after he was actively asked, did he admit to having fallen into the ditchwater (stagnant river) after having injured his knee. Taking this into account, the Aeromonas species was considered to be the pathogen of his wound infection. Clinically, he had become afebrile since day 3 (thus 24 h after initiation of antibiotic therapy) and the redness had disappeared, but there was still some pus evacuation and a tender fluctuating swelling near the wound. Therefore, antibiotic treatment was switched to ciprofloxacin based on the antibiogram. Evolution of inflammatory parameters showed a swift normalization. On day 6, a control culture of the wound only showed growth of Staphylococcus cohnii, a contaminant. A blood culture taken on day 3 remained sterile.
On day 7, the cutaneous stitches were removed, because there was continuing evacuation of pus. Hereafter, the wound started to heal slowly. To improve wound healing, therapy with Bioptron lamp (polarized, polychromatic, non-coherent light) was started on day 8. He received two sessions of 9 min daily. For the rest of the time, the wound was covered with povidone-iodine 10 % compresses.
On day 13, after 7 days of intravenous treatment with ciprofloxacin, he was released home with continuation of ciprofloxacin orally for a total treatment duration of 14 days. Therapy with Bioptron lamp was continued in ambulatory setting (Two times 9 min with a 20 min interval, once daily), until satisfying wound healing on day 26 ().","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [45.0, 'kg']}",85,80.75,89.25,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 45.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (45.0 kg - 20 kg) = 85.0 mL/hr.
Hence, the patient's fluid maintenance is 85.0 mL/hr."
5301,22,Maintenance Fluids Calculations,physical,decimal,pmc-8076427-2,Extracted,"A 17-year-old male who was referred to our endocrine clinic at the age of 15 years with an eight-year history of a poorly controlled T1DM. Upon referral, he was on insulin glargine and premeal insulin glulisine. He was noncompliant with his insulin therapy. His blood glucose was uncontrolled with hypo-and hyperglycemic levels. His baseline HbA1c ranged from 9% to 11%. There was no history of microvascular complications.
His physical examination revealed a height of 138 cm (<3rd percentile) and weight of 40 kg (<3rd percentile). He had abdominal distension with hepatomegaly, and liver span was 17 cm. His pubic hair and testicular size were Tanner stage 2.
His laboratory tests showed HbA1c of 9.8%, ALP of 200 U/L, aspartate transaminase (AST) of 169.2 U/L (normal range: 0-38 U/L), and alanine transaminase (ALT) of 310.6 U/L (normal range: 10-50 U/L). The cholesterol was 245 mg/dL, low-density lipoprotein (LDL) cholesterol was 144 mg/dL, and TG level was normal. The rest of his metabolic panel was normal. The IGF-1, LH, FSH, and testosterone were low. Thyroid function test was normal. Hepatic serology and autoimmune work-up were negative.
His bone age was about 14 years (chronological age of 15 years). Abdominal ultrasound revealed enlarged hyperechogenic liver with a size 19.2 cm, suggestive of liver steatosis (Figures , ).
Based on his clinical presentation and investigations, we diagnosed him with MS. He was put on an intensive insulin regimen. His blood glucose improved and liver enzymes normalized. Clinically, his liver size shrunk significantly. During his follow-up, he got his puberty, and his final height was 146 cm and weight was 46 kg.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [46.0, 'kg']}",86,81.7,90.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 46.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (46.0 kg - 20 kg) = 86.0 mL/hr.
Hence, the patient's fluid maintenance is 86.0 mL/hr."
5302,22,Maintenance Fluids Calculations,physical,decimal,pmc-3401773-1,Extracted,"The index case, a 21-year-old female came to gynecology OPD with complaint of primary amenorrhea (pubarche: 15 yrs and thelarche: 18 yrs). She weighed 69 kg and her height was 160 cm. General physical examination was within normal limits (no features suggestive of hypothyroidism, Cushing's syndrome, or Acromegaly). Her Tanner staging was B2P5A2. External genitalia examination revealed clitoromegaly (5 cm), separate vagina, and urethra openings. There was no labial fusion. Vagina was admitting one finger, but cervix could not be felt. No gonad was palpable in labia or inguinal regions. She was born out of non-consanguineous marriage and ante-natal history was not contributory. There was no similar complaint in the family.
In view of primary amenorrhea with clitoromegaly, serum total testosterone, LH, FSH, 17-OH Progesterone, DHEAS, thyroid profile, and prolactin were measured. All of the above hormone investigations were normal except raised serum total testosterone [4.78 ng/ml (0.15 to 0.81)], LH [20 mIU/ml (0.80 to 7.6)], and FSH [30 mIU/ml (0.7 to 11.1)]. Ultrasound pelvis revealed hypoplastic uterus (4.8 cm × 1.65 cm × 0.847 cm) and bilateral ill-defined gonad like structures high up in pelvis. At this point of time, mosaic Turner's syndrome (45 X/46 XY) was kept as the first possibility. But the Karyotype revealed 46 XY, so the clinical diagnosis was changed to partial gonadal dysgenesis. MRI abdomen and pelvis was advised to locate the gonads precisely. However, the patient was lost to follow up after that.
The patient came only after 3 years at the age of 24 years. This time, she was more concerned about clitoromegaly rather than primary amenorrhea. Anthropometry revealed: height: 168 cm, weight: 75 kg, BMI: 26.60 kg/ m2, upper segment: 74 cm, lower segment: 94cm, and arm span: 180 cm. Tanner staging was B2P4A1 and clitoromegaly had regressed from 5 to 4 cm. Hormone investigations revealed a decrease in serum total testosterone from 4.78 to 0.93 ng/ ml and a further increase in gonadotrophins (LH: 31.4 mIU/ml and FSH: 53.3 mIU/ ml). MRI showed hypoplastic uterus with thin endometrial cavity but could not localize gonads. So, diagnostic laparoscopy was planned. Intra-operatively, vaginal length was 10 cm, cervix and uterus were hypoplastic with B/L normal fallopian tubes in situ, left side showed tubular gonad and right side had spherical gonad. B/L gonadectomy and clitoral resection were carried out in the same sitting. Histopathology of left and right gonad revealed ovarian follicle with flattened cuboidal lining epithelium [] and hyalinized seminiferous tubules with Leydig cells [], respectively. Finally, she was diagnosed as true hermaphrodite. Post-operative period was uneventful. At discharge from hospital, she was started on estrogen replacement and the plan was to add progesterone after breakthrough bleeding.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [75.0, 'kg']}",115,109.25,120.75,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 75.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (75.0 kg - 20 kg) = 115.0 mL/hr.
Hence, the patient's fluid maintenance is 115.0 mL/hr."
5303,22,Maintenance Fluids Calculations,physical,decimal,pmc-7641057-1,Extracted,"A 60-year-old healthy male patient weighing 42 kg with squamous cell carcinoma of scalp was posted for excision and flap reconstruction. He gave a history of 5-6 beedi smoking per day and 3-4 times ganja inhalation/month for 30 years. His systemic examination and investigations including an electrocardiogram (ECG) were normal and viral markers were negative. Universal precautions were taken throughout the case. Anaesthesia was induced with fentanyl, propofol and atracurium. The trachea was intubated with an 8.0-mmID endotracheal tube and the patient was turned prone.
Surgeon infiltrated 10 ml of 2% lignocaine with 1:200,000 adrenaline around the incision site. During infiltration, a vessel was punctured, and further injection was stopped. Within 2-3 min of injection, ECG showed multiple atrial ectopic and missed beats []. Heart rate (HR) gradually increased from 100 to 140/min with blood pressure (BP) of 90/60 mmHg. Arterial cannula was inserted in the radial artery to monitor invasive blood pressure (IBP). During surgery, multifocal atrial tachycardia, junctional tachycardia and atrial fibrillation (AF) were noticed with irregularly irregular pulse. Diltiazem 10 mg was administered intravenously twice following which HR decreased to 90-110/min with BP: 90-100 / 65-70 mmHg but remained irregularly irregular. Arterial blood gas analysis was within normal limits. Morphine 3 mg and paracetamol 1 g were administered. Lignocaine 80 mg and esmolol 30 mg were administered prior to extubation. Postoperatively 12-lead ECG showed atrial fibrillation (AF) []. As advised by cardiologist, amiodarone 150 mg bolus followed by an infusion was started. The rhythm reverted to normal with normal vital parameters. Amiodarone infusion was stopped after 2 hours. ECG remained normal till his discharge from hospital on the fifth postoperative day.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [42.0, 'kg']}",82,77.9,86.1,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 42.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (42.0 kg - 20 kg) = 82.0 mL/hr.
Hence, the patient's fluid maintenance is 82.0 mL/hr."
5304,22,Maintenance Fluids Calculations,physical,decimal,pmc-8700017-1,Extracted,"A 20-day-old girl was admitted to the neonatal intensive care unit with a chief complaint of poor oral intake through the emergency room. She was lethargic and did not suck well with swallowing only 10 to 20 mL of formula at a time in the last two days. However, the amount of urine did not decrease, and diapers were changed 10 to 14 times per day. Vomiting and diarrhea were not observed. She was born at 38+2 weeks of gestation with 3380 g (50th–75th percentile) via cesarean section. No abnormal findings were noted during the prenatal and immediate postnatal periods. She was the first child of healthy, nonconsanguineous Korean parents, and her family history was unremarkable. At admission, her weight was 3100 g (25th–50th percentile), length was 53 cm (50th–75th percentile), and head circumference was 36 cm (50th–75th percentile). Although vital signs were appropriate for her age (heart rate 150 beats/min, blood pressure 78/50 mmHg, respiratory rate 48 breaths/min, and body temperature 36.5 °C), her lips were dry, and the capillary refill time was prolonged to 5–6 s. Physical examination revealed both thumbs in palms, frontal bossing, prominent upper lip, high arched palate, sparse frontal scalp hair, and bilateral 5th finger clinodactyly. An initial capillary blood gas analysis showed severe metabolic acidosis (pH 7.16, pCO2 28.3 mmHg, pO2 42 mmHg, HCO3−—17.3 mmol/L, base excess—17.3 mmol/L). With an impression of dehydration, 20 mL/kg normal saline was infused intravenously for over 1 h before other laboratory results were obtained.
The laboratory tests at admission were as follows: serum sodium 113.3 mEq/L, serum potassium 8.79 mEq/L, serum chloride 90.8 mEq/L, total CO2 8.1 mEq/L, serum lactic acid 1.0 mmol/L, serum ketone body 24 µmol/L, blood glucose level 83 mg/dL, blood urea nitrogen 55.1 mg/dL, and serum creatinine 0.65 mg/dL. Her urinalysis revealed a specific gravity of 1.014 and pH 5.0 and was negative for white blood cells and red blood cells. Her spot urine sodium and potassium levels were 74 and 27.7 mEq/L, respectively. The serum and urine osmolality values were 232 and 229 mOsm/kg, respectively. All the results of the neonatal screening test were normal, which included TSH (1.2 mIU/L), 17-hydroxyprogesterone (1.6 ng/mL), total galactose (1.0 mg/dL), and mass spectrometry for amino acid, organic acid, fatty acid, purine, peroxisome, and carbohydrate metabolic disorders. The plasma ammonia level was within the normal limit as 97 µg/dL. The plasma renin activity and serum aldosterone level were markedly elevated to 142.0 ng/mL/h (normal range, 0.32–1.84 ng/mL/h) and 4560 ng/dL (normal range, 4.2–20.9 ng/dL), respectively. Renal ultrasonography revealed no abnormalities except mild hydronephrosis in the right kidney (). No abnormal findings were found in cardiac echocardiography or brain magnetic resonance imaging.
To correct severe hyponatremia, 60 mL of 3% sodium chloride was initially intravenously administered over 8 h. Her urine output on the first day of admission was 8.45 mL/kg/h. Hyponatremia and hyperkalemia were improved with intravenous fluid and oral sodium chloride supplementation (8 mEq/kg/day). The patient consumed an adequate amount of milk (170–200 mL/kg/day), and weight gain was appropriate (40–80 g/day) after oral sodium chloride supplementation.
For the genetic diagnosis of the patient, targeted exome sequencing (TES) was performed. Genomic DNA was extracted from proband blood. All exon regions of all human genes (~22,000) were captured by a Twist Human Core Exome Kit (Twist Bioscience, South San Francisco, CA, USA). The captured regions of the genome were sequenced using a NovaSeq 6000 sequencing machine (Illumina, San Diego, CA, USA). In TES, no other pathogenic/likely pathogenic single-nucleotide variants (SNVs) or small insertion and deletion variants associated with the clinical phenotypes were identified. However, her clinical phenotypes and biochemical results indicated PHA1. Therefore, we performed a chromosomal microarray (CMA) to identify deletion-encompassing genes responsible for PHA1. CMA (CytoScan Dx, Affymetrix Cytogenetics, Santa Clara, CA, USA) revealed a 203 kb heterozygous deletion at 4q31.23: arr[GRCh37] 4q31.23(148865586_149069090)x1 (). This deletion spans exons 7–9 of NR3C2 and exons 15–23 of the ARHGAP10 gene. Haploinsufficiency of the NR3C2 gene, which encodes the mineralocorticoid receptor, is responsible for ADPHA1. However, the details of the functional role of the ARHGAP10 gene in human disease remain unclear. Parental testing showed that the deletion was paternally inherited. Her father had no history of clinical PHA1 manifestation and had normal plasma electrolytes and serum aldosterone values with only slightly elevated plasma renin activity at testing.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [3100.0, 'g']}",12.4,11.78,13.02,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 3100.0 g so this converts to 3100.0 lbs * kg/1000 g = 3.1 kg. Hence, the patient's maintenance fluid is 3.1 kg * 4 mL/kg/hr = 12.4 mL/hr.
Hence, the patient's fluid maintenance is 12.4 mL/hr."
5305,22,Maintenance Fluids Calculations,physical,decimal,pmc-3800393-1,Extracted,"The case involved a male infant 1 day old at the time of presentation. He was the first child of healthy parents. The infant was delivered normally at full term with a low birth weight of 1,750 g. There were no particularly notable points in the family history, medical history, or reproductive history.
On examination, the patient had a restricted mouth opening resulting from congenital oral synechia due to membranous adhesion between the free margin of the cleft palate and the floor of the mouth, lateral to the tongue on the left side. The cleft was of secondary palate with intact premaxilla. There were no other abnormalities found in the patient. No obvious auricular or nasal deformities were appreciated. Digits and extremities appeared normal, as did genitalia. Examination of the heart revealed no abnormalities.
The congenital oral synechia appeared as a thin membrane with a broad attachment at the floor of the mouth measuring approximately 2 cm in anteroposterior width. At the palatal margin the attachment narrowed to about 0.5 cm []. The membranous adhesion was pale pink in color and appeared to be avascular.
The infant faced feeding problems due to the restricted mouth opening, and therefore an immediate surgical excision of the synechia was decided on. Feeding was done using an infant feeding tube till anesthetic clearance was obtained for the procedure. At 1 week after birth, the congenital synechia was excised under sedation uneventfully restoring adequate mouth opening and allowing normal feeding []. A surgical closure of the cleft palate is planned for a later date.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1750.0, 'g']}",7,6.65,7.35,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1750.0 g so this converts to 1750.0 lbs * kg/1000 g = 1.75 kg. Hence, the patient's maintenance fluid is 1.75 kg * 4 mL/kg/hr = 7.0 mL/hr.
Hence, the patient's fluid maintenance is 7.0 mL/hr."
5306,22,Maintenance Fluids Calculations,physical,decimal,pmc-1805439-1,Extracted,"A 6-day-old Pakistani boy was admitted to hospital in June 2005 for bleeding from the left nipple. His parents are first cousins. He has two siblings aged 8 and 6 years. There was no family history of bleeding diathesis. The mother had a normal pregnancy with full antenatal care. Mode of delivery at term was an elective Caesarean section due to previous Caesarean sections. His birth weight was 2.7 kg. 1 mg of Vitamin K was given intramuscularly at delivery. His first neonatal check was normal. He had a small amount of self-limiting bleeding from the umbilical cord on day 3 of life. He went home on day 4.
On day 6 of life he had mild spontaneous left sided nipple bleeding, which presented as spots of blood stains on the left side of his baby dress.
Over the next 7 days he had two further episodes of a similar nature. Baseline biochemistry and full blood count were normal but a coagulation screen showed a prolonged prothrombin time of 41 s (control 14 s), a prolonged partial thromboplastin time of 132 s (control 33 s) and normal thrombin time of 15 s (control 14 s). In view of the mild nature of bleeding, the child was only treated with 1 mg of i.v. vitamin K. Subsequent coagulation assays revealed a plasma factor V activity of less than 0.01 IU/ml (normal range 0.50–1.50 IU/ml) determined by factor V clotting assay with all other coagulation factors in the normal range. Hence the diagnosis of congenital factor V deficiency was made. A cerebral ultrasound done at this stage was within normal limits. Oral transexamic acid at a dose of 15 mg/kg/dose 3 times daily was started.
Mother was found to have a plasma factor V activity of 0.44 IU/ml (normal range 0.5–1.50 IU/ml) and the father of 0.52 IU/ml by factor V clotting assay. Both levels are compatible with heterozygous factor V deficiency. The siblings had factor V activities of 0.61 and 1.1 IU/ml respectively. Genetic analysis at the St. Thomas Hospital hemophilia molecular genetics laboratory showed that the affected child is homozygous for a frame shift mutation resulting in a premature termination sequence at codon 2178 in exon 25 of the factor V gene and both parents are heterozygous for this mutation.
The infant presented at day 15 of age with a further episode of bleeding from the umbilical stump. The bleeding stopped promptly following administration of 20 ml/kg of fresh frozen plasma (FFP, methyleneblue sterilized, single donor and US sourced). Small bruises were noted around the venepuncture sites from the previous admission. A hematoma measuring 2 cm in diameter was noted on the anterolateral aspect of the left thigh. It was attributed to the injection of vitamin K at birth. His head circumference was increasing within normal range and a repeat cerebral ultrasound was normal.
The patient presented again at 5 weeks of age with pallor, irritability, lethargy and reduced feeding. His anterior fontanelle was bulging and tense. He was hemodynamically stable. His hemoglobin was 5.6 g/dl, which represented a significant drop from the previous estimation 3 weeks back. The cerebral ultrasound was repeated and showed a large intracerebral hemorrhage extending from the frontal lobe to the parieto-occipital region. There were a few cystic areas seen within this bleed, which suggested that the bleeding started at least a few weeks ago. The child was immediately transfused with 20 ml/kg of FFP and 15 ml/kg of packed red blood cells. He had a series of generalized fits within 5 hours of admission. The patient was transferred to the regional tertiary referral centre for specialised neurosurgical and haematological management. A cranial computed tomography (CT) scan showed a right, large, intracerebral bleed causing a shift of the midline to the left. The ventricles were not enlarged and the bleed did not extend into the ventricles (See Figure ). A Hickman line insertion was arranged to enable regular FFP infusions. Preoperatively he was transfused again with 20 ml/kg FFP and 10 ml/kg of platelet concentrate to achieve adequate hemostasis. Platelets are known to be a good source of factor V as it is stored in the platelet alpha granules. He was also given recombinant factor VIIa (Novoseven, NovoNordisk®) as an empirical adjunctive agent in the peri-operative period in view of the fact that reliably hemostatic levels of factor V (0.25–0.30 IU/ml) are difficult to achieve in this condition. Factor VIIa is unlikely to work in the absence of any factor V but can contribute to increased thrombin formation once factor V is present. Postoperatively a regime of FFP (15 ml/kg/dose) administration was set up: FFP twice a day for the first 10 days followed by once a day for the next 10 days. This was followed by at least alternate days (every 48 hours) of FFP at 20 ml/kg/day up to the present. Plasma factor V activity has been monitored: A maximum factor V level of 0.23 IU/ml was achieved within 20 minutes after transfusion. Trough levels were between <0.01 to 0.05 IU/ml. When undetectable factor V levels were noted inhibitor assays were performed. Inhibitors have not been detected so far. No further bleeding has been noted up to the present day. Immunisations including hepatitis B vaccination were given subcutaneously as is normal practice for children with severe bleeding disorders. Follow up until the present (21 months of age) revealed an appropriate increment in head circumference. Neurodevelopment has been within normal limits.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [2.7, 'kg']}",10.8,10.26,11.34,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 2.7 kg. Hence, the patient's maintenance fluid is 2.7 kg * 4 mL/kg/hr = 10.8 mL/hr.
Hence, the patient's fluid maintenance is 10.8 mL/hr."
5307,22,Maintenance Fluids Calculations,physical,decimal,pmc-5881287-1,Extracted,"A 16-day-old female baby presented to us with bilious vomiting and non-passage of meconium. Antenatal ultrasonography was not performed and there was no history of maternal drug intake during pregnancy. Baby was born by normal vaginal delivery at home and was 1.3 kg, sick and dehydrated at admission. Respiratory rate was 38/min, pulse 150/min and blood pressure was 80/60 mmHg. There was upper abdominal distention, but abdomen was soft without any rigidity. Anal opening was normally placed. Although haemogram was normal, serum urea and creatinine were moderately raised.
Erect abdominal X-ray revealed two gas-filled bowel loops in upper abdomen and paucity of gas in pelvis []. Clinical picture and plain X-ray abdomen suggested the diagnosis of proximal intestinal atresia. The baby was resuscitated with intravenous fluids, antibiotics and nasogastric (NG) tube was passed into the stomach. Laparotomy done by right supraumbilical transverse incision revealed grossly dilated stomach and duodenum. Duodenum was about 8 cm long and terminating blindly. There was total absence of jejunum and ileum. Cecum was about the size of a peanut and appendix very small. The microcolon was lying over the dilated duodenum [] and followed till rectum.
Cecum and appendix were excised. Saline was flushed into unused colon and milking of saline done in microcolon down to the rectum, confirming colonic patency. Duodenum was opened at distal dependent part, and single layer end-to-back anastomosis was done with ascending colon using 5-0 polyglactin suture. Baby had an uneventful post-operative recovery. NG aspiration gradually decreased and became non-bilious. NG tube was removed, and breastfeeding started on the 7th post-operative day. Baby tolerated breast milk and was discharged on the 10th post-operative day. Parents attended outpatient department with the baby for thefirst follow up after 1 week and were advised about future plans.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [1.3, 'kg']}",5.2,4.94,5.46,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 1.3 kg. Hence, the patient's maintenance fluid is 1.3 kg * 4 mL/kg/hr = 5.2 mL/hr.
Hence, the patient's fluid maintenance is 5.2 mL/hr."
5308,22,Maintenance Fluids Calculations,physical,decimal,pmc-6721255-1,Extracted,"A 15-year-old boy presented to the emergency department with acute bilious vomiting and epigastric pain. The patient appeared to suffer from considerable pain which occurred while participating in a basketball game, and gradually worsened after taking a meal and more than 2 L of water during the sports game. The patient reported that he received several forceful blows to his abdomen from other players. In addition, for the last one and a half years, the patient had early satiety and postprandial epigastric pain which was relieved when he was in a knee-chest position. One year prior to this admission, the patient had been brought to a different hospital for similar abdominal symptoms that had resolved without treatment within several hours.
His initial vital signs were normal. The patient had a strong, muscular and athletic build, a height of 185 cm and a weight of 66.0 kg. He reported a growth in height of 9 cm and no weight change for the past year. Palpation of his abdomen revealed generalised tenderness, but no guarding, and no abdominal masses were detected. Blood tests, including blood count (haemoglobin 154 g/L, white cell count 7.60×109/L and platelet count 22.9×109/L), chemistries (sodium 142 mmol/L, potassium 4.6 mmol/L, chloride 105 mmol/L, blood urea nitrogen 6.57 mmol/L and serum creatinine 59.3 μmol/L), liver function tests (albumin 56 g/L, bilirubin 21.2 μmol/L, aspartate aminotransferase 28 IU/L and alanine aminotransferase 18 IU/L) and inflammatory marker (C reactive protein 0.1 mg/L), were normal, with the exception of a slight elevation of amylase (163 U/L). The urinalysis was within normal limits. The abdominal ultrasound (US) showed no abnormalities other than a dilated stomach.
Despite the patient’s abdominal findings, his severe abdominal pain and history of forceful blows to the abdomen suggested the possibility of abdominal injuries, including intestinal perforation and abdominal haemorrhage. As a result, a contrasted CT of the abdomen and pelvis was performed. This CT was initially interpreted by a doctor on night duty as normal apart from a massively distended stomach (). After the CT scan, the patient lay in prone and knee-chest position for about an hour and then his symptoms resolved spontaneously. Therefore, gastric decompression with a nasogastric tube was not performed. The patient only underwent observation with intravenous hydration. No vomiting was found during the observation period. The next morning, the patient made a swift recovery. He had no abdominal symptoms, including postprandial pain. The follow-up abdominal US showed the volume of the stomach significantly decreased as normal and no other abnormalities were found. These suggested that there was a transient intestinal obstruction that was thought not to require emergency interventions. The patient was discharged, and a follow-up visit was arranged.
After his discharge, the CT review by an experienced radiologist revealed, however, a dilated proximal duodenum and an abrupt calibre change in the third portion of the duodenum (). The aortomesenteric angle and distance were 14° (normal range: 38°–65°) and 4 mm (normal range: 10–28 mm), respectively (). In addition, the abdominal fat was significantly low (). Furthermore, the third part of the duodenum passed anterior to the aorta in the retroperitoneal space. The position of the SMA and superior mesenteric vein was normal (). These suggested that there was no intestinal malrotation or volvulus in this patient. Based on these radiological findings and his clinical history, the patient was diagnosed with SMA syndrome.","Based on the patient's weight, what is the patient's maintenance fluid in mL/hr?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'weight': [66.0, 'kg']}",106,100.7,111.3,"For patient's with weight less than 10 kg, the rule for computing maintenance fluid is to multiply their weight by 4 mL/kg/hr to get the maintenance fluids per hour.
For patient's with weight between 10 kg and 20 kg, the formula for computing maintenance fluid is 40 mL/hr + 2 mL/kg/hr * (weight (in kilograms) - 10 kilograms).
For patient's with weight greater than 20 kg, the formula for computing the maintenance fluid is 60 mL/hr + 1 mL/kg/hr * (weight (in kilograms) - 20 kilograms).
The patient's weight is 66.0 kg. Hence, plugging into this formula, we get 60 mL/hr + 1 mL/kg/hr * (66.0 kg - 20 kg) = 106.0 mL/hr.
Hence, the patient's fluid maintenance is 106.0 mL/hr."
5309,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5034576-1,Extracted,"An 18-year-old Brazilian man developed dyspnea and fever of one week’s duration and was then diagnosed with right lower lobe pneumonia. Before this incident, he had not experienced any medical complications, lived in full sanitary conditions, denied previous symptoms related to disease, did not have any pets, and denied eating raw meat. He then began hospital inpatient treatment with intravenous antibiotics, and third-generation cephalosporin (Ceftriaxone) and a macrolide (Clarithromycin) were prescribed for 8 days. Laboratory tests from the patient’s admittance showed mild anemia with a hemoglobin (Hb) level of 11.7 g/dL, with normal mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH). Other biochemical results were as follows: creatinine 0.9 mg/dL, urea 32 mg/dL, total bilirubin 0.2 mg/dL, glucose 90 mg/dL, sodium 134 mEq/L, potassium 3.7 mEq/L, and C-reactive protein 138.2 mg/L. Leucocytes levels were a little low, with 2700 cells/μL. Blood and urine cultures were negative for infection and serological tests for human immunodeficiency virus (HIV), hepatitis B and C, and syphilis were all negative.
On the fourth day of this related treatment, our patient developed abdominal distension and pain in his lower right abdominal quadrant. Acute appendicitis was confirmed by ultrasound examination, and he underwent laparoscopic surgery the same day. Our patient was then taken to our intensive care unit for worsening of his clinical condition. On the fourth postoperative day, our patient developed fever associated with right pleural effusion, which was a lymphocytic exudate with an adenosine deaminase concentration of 17.99 U/L and negative culture (Fig. ). Thus, the attending physicians requested a bronchoscopy with bronchoalveolar lavage and transbronchial biopsy. The transbronchial fluid had negative cultures for infection. At that time, the antibiotic spectrum was extended for treatment of the sepsis, including piperacillin/tazobactam for 10 days.
Anatomopathological examination of the transbronchial biopsy specimen showed a small fragment of lung parenchyma with discrete septal thickening and a rounded structure suggestive of a pseudocyst containing Toxoplasma gondii bradyzoites (Fig. ).
Our patient showed progressive improvement after antibiotic therapy with piperacillin/tazobactam, and was discharged on the 14th day after surgery. A chest radiograph showed significant improvement in lung opacification (Fig. ) and serological tests for toxoplasmosis were negative for immunoglobulin G and immunoglobulin M.
Our patient was followed up on an outpatient basis for 2 years without any signs of recurrence of lung infections or other comorbidities. Serology for toxoplasmosis were repeated and remained negative.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [90.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",133.76,127.072,140.448,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 134.0 mEq/L. 
The concentration of glucose is 90.0 mg/dL. 
Plugging in these values into the formula gives us 134.0 mEq/L + 0.024 * (90.0 - 100) = 133.76 mEq/L.
Hence, the patient's corrected concentration of sodium is 133.76 mEq/L."
5310,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-4284,Extracted,"A 22-year-old woman with a history of type I diabetes mellitus presents to the emergency department with nausea, vomiting, and drowsiness for the past day. Her temperature is 98.3°F (36.8°C), blood pressure is 114/74 mmHg, pulse is 120/min, respirations are 27/min, and oxygen saturation is 100% on room air. Physical exam is notable for a confused and lethargic young woman. Initial laboratory values are notable for the findings below.

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 2.9 mEq/L
HCO3-: 9 mEq/L
BUN: 20 mg/dL
Glucose: 599 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.2 mg/dL
AST: 12 U/L
ALT: 10 U/L

An initial ECG is notable for sinus tachycardia.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [599.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",150.976,143.4272,158.5248,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 139.0 mEq/L. 
The concentration of glucose is 599.0 mg/dL. 
Plugging in these values into the formula gives us 139.0 mEq/L + 0.024 * (599.0 - 100) = 150.976 mEq/L.
Hence, the patient's corrected concentration of sodium is 150.976 mEq/L."
5311,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-5812,Extracted,"A 70-year-old male presents to the emergency department for increased sweating and epigastric pain that the patient has never felt before. The patient experienced these symptoms while he was eating. His symptoms did not improve so his wife brought him into the emergency department. The patient has a past medical history of diabetes mellitus, obesity, and anxiety. His current medications include simvastatin, hydrochlorothiazide, metformin, insulin, lisinopril and buspirone. His temperature is 99.5°F (37.5°C), pulse is 112/min, blood pressure is 110/70 mmHg, respirations are 18/min, and oxygen saturation is 94% on room air. The patient is currently short of breath. A lab panel is drawn and the results are below:

Serum:
Na+: 138 mEq/L
K+: 5.3 mEq/L
Cl-: 100 mEq/L
HCO3-: 24 mEq/L
BUN: 11 mg/dL
Ca2+: 9.7 mg/dL
Mg2+: 2.0 mEq/L
Creatinine: 1.2 mg/dL
Glucose: 180 mg/dL

An EKG is performed in the emergency department. A chest radiograph is performed and is seen in Figure A. A visit to the emergency department two days ago for indigestion resulted in radiography that was within normal limits.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [180.0, 'mg/dL'], 'Sodium': [138.0, 'mEq/L']}",139.92,132.924,146.916,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 138.0 mEq/L. 
The concentration of glucose is 180.0 mg/dL. 
Plugging in these values into the formula gives us 138.0 mEq/L + 0.024 * (180.0 - 100) = 139.92 mEq/L.
Hence, the patient's corrected concentration of sodium is 139.92 mEq/L."
5312,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6590859-2,Extracted,"Case 2 presentation
The patient is a 62-year-old African American male with an unknown past medical history who was brought by EMS after being found down at his home without heat by his neighbor.
On physical examination, his vital signs were: rectal temperature was 28.5 °C, heart rate 94 bpm, respiratory rate 22 breaths/min, and blood pressure 170/100 mmHg. On presentation, his Glasgow Coma Scale was 8 (E4 V1 M3). He was found to be non-responding verbally, pupils were reactive to light, lungs clear to auscultation, the heart had regular rate and rhythm. He was intubated in the emergency department.
Initial laboratory with blood gas analysis showed a metabolic and respiratory acidosis with the following pH 7.103; pCO2 65.6 mmHg; pO2 514.9 mmHg; HCO3 20.0 mmHg on the following ventilator settings: tidal volume 450 mL, respiratory rate 18 breaths/min, fraction of inspired oxygen (FiO2) 100% and positive end-expiratory pressure (PEEP) of 5 cmH2O. Other laboratory findings were the following: sodium 165 mmol/L, potassium 3.0 mmol/L, chloride 122 mmol/L, carbon dioxide (CO2) 18 mmol/L, glucose 182 mg/dL, blood urea nitrogen (BUN) 86 mg/dL, creatinine 1.83 mg/dL, AST 92 U/L, ALT 56 U/L, lipase 300 U/L, creatinine kinase 1,661 U/L, troponin 0.02 ng/mL, white blood cell count (WBC) 29.50 x 103 cmm, hemoglobin 5.4 g/dL, platelets 225 x 103 cmm, PT 17 sec, INR 1.5, APTT 36.4 sec, lactic acid 6.3 mmol/L. Urine drug screening was negative for any substances and alcohol level was <10 mg/dL. Initial EKG showed atrial fibrillation with premature ventricular complexes, left axis deviation, lateral injury pattern. Initial chest x-ray showed diffuse opacities on bilateral lung fields consistent with aspiration pneumonitis or infection.
The patient was admitted to the Intensive Care Unit (ICU) for rewarming with IV fluids and Bair Hugger (3M temperature management system). He developed multifactorial shock and was started on vasopressors, blood transfusion, and antibiotics. An echocardiogram was done 2 days after admission for shock investigation which demonstrated moderate left ventricular hypertrophy, anteroseptal and anterior akinesis with global hypokinesis, ejection fraction 25% with suspicion of apical thrombus and left atrial enlargement (Figure ).
Outcome and Follow-up
The patient was later started on anticoagulation after anemia resolved but anticoagulation was later held as he developed a psoas hematoma. He had 2 subsequent echocardiograms including a transesophageal echocardiogram during hospitalization that were concerning for apical thrombus. The patient was later discharged to a nursing home facility after 80 days of hospitalization with multiple complications.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [182.0, 'mg/dL'], 'Sodium': [165.0, 'mmol/L']}",166.968,158.6196,175.3164,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 165.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 165.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 165.0 mmol * 1 mEq/mmol = 165.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 165.0 mmol sodium/L converts to 165.0 mEq sodium/L. 
The concentration of glucose is 182.0 mg/dL. 
Plugging in these values into the formula gives us 165.0 mEq/L + 0.024 * (182.0 - 100) = 166.968 mEq/L.
Hence, the patient's corrected concentration of sodium is 166.968 mEq/L."
5313,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-8509,Extracted,"A 59-year-old Caucasian man with a history of hypertension and emphysema is brought to the hospital because of progressive lethargy and confusion. The patient has been experiencing poor appetite for the past 3 months and has unintentionally lost 9 kg (19.8 lb). He was a smoker for 35 years and smoked 1 pack daily, but he quit 5 years ago. He takes lisinopril and bisoprolol for hypertension and has no allergies. On examination, the patient appears cachectic. He responds to stimulation but is lethargic and unable to provide any significant history. His blood pressure is 138/90 mm Hg, heart rate is 100/min, and his oxygen saturation on room air is 90%. His mucous membranes are moist, heart rate is regular without murmurs or an S3/S4 gallop, and his extremities are without any edema. His pulmonary examination shows mildly diminished breath sounds in the right lower lobe with bilateral wheezing. His laboratory values are shown:
Sodium 110 mEq/L
Potassium 4.1 mEq/L
Chloride 102 mEq/L
CO2 41 mm Hg
BUN 18
Creatinine 1.3 mg/dL
Glucose 93 mg/dL
Urine osmolality 600 mOsm/kg H2O
Plasma osmolality 229 mEq/L
WBC 8,200 cells/mL
Hgb 15.5 g/dL
Arterial blood gas pH 7.36/pCO2 60/pO2 285
Chest X-ray demonstrates a mass in the right upper lobe.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [93.0, 'mg/dL'], 'Sodium': [110.0, 'mEq/L']}",109.832,104.3404,115.3236,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 110.0 mEq/L. 
The concentration of glucose is 93.0 mg/dL. 
Plugging in these values into the formula gives us 110.0 mEq/L + 0.024 * (93.0 - 100) = 109.832 mEq/L.
Hence, the patient's corrected concentration of sodium is 109.832 mEq/L."
5314,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7202579-1,Extracted,"A 69-year-old Hispanic male with a history of type 2 diabetes mellitus presented to our emergency department (ED) complaining of decreased urine output for two days along with intermittent nausea and vomiting for two weeks. His past medical history included hypertension and coronary artery disease. Three weeks prior to presenting to the ED, our patient had undergone routine lab studies, which had documented normal kidney function with a serum creatinine level (Cr) of 0.97 mg/dL and no microalbuminuria. He had been taking metformin 850 mg three times a day and lisinopril 10 mg per day for more than a year, which he continued to take during his presenting illness. He was not taking any non-steroidal anti-inflammatory agents or other over-the-counter (OTC) medications. On initial evaluation, the patient was alert and oriented and in no distress. He was afebrile with a blood pressure of 152/69 mmHg, heart rate of 84 beats per minute, respiratory rate of 14 breaths per minute, and oxygen saturation of 96% on room air. Except for mild abdominal tenderness, his exam was unremarkable.
Initial laboratory studies in the ED showed severe kidney injury with blood urea nitrogen (BUN) of 68 mg/dL and Cr of 12.2 mg/dL. Additionally, he was found to have a blood glucose level of 188 mg/dL, sodium level of 137 mmol/L, chloride level of 97 mmol/L, CO2 level of 8 mmol/L, potassium level of 6.2 mmol/L, and WBC count of 10,900 per uL with 83% neutrophils. Arterial blood gas revealed pH of 7.13 and partial pressure of carbon dioxide (PaCO2) of 21 mmHg. The anion gap (AG) was 32 mmol/L with a delta ratio of 1.3; lactate was 18.1 mmol/L. He had a pure high AG metabolic acidosis with high lactate levels. Renal ultrasound demonstrated kidneys of normal size and normal echogenicity without obstruction. Abdominal/pelvic CT was unremarkable. Supportive measures, including IV antibiotics, fluids, sodium bicarbonate as a drip infusion, and oral sodium polystyrene sulfonate were initiated. Bladder catheterization revealed less than 10 ml of urine. Urine microscopy was significant for brown muddy casts consistent with acute tubular necrosis (ATN). Electrocardiography results were normal.
He was transferred to our intensive care unit, where urgent conventional hemodialysis with a blood flow of 250 ml/min was initiated for MALA and oliguric renal failure. Sodium bicarbonate drip infusion was discontinued before the initiation of dialysis. During the initial dialysis, he became hypoxic with a decreased level of consciousness and hemodynamically instability. His mean arterial pressure decreased to 50 mm Hg with a pulse rate of 43 beats per minute. He was treated with epinephrine, followed by dopamine. Bilevel positive airway pressure (BPAP) oxygen delivery was instituted. Dialysis was discontinued after four hours, and management was guided by his wishes regarding resuscitation as conveyed by his family. Initially, the directive was that there should be no further escalation of care. Repeat laboratory studies obtained five hours after dialysis revealed a continued metabolic acidosis with an arterial pH of 7.14, lactic acid of 18.9 mmol/L, and AG of 42. Dopamine was continued; blood pressure stabilized, and the patient became considerably more responsive. After a discussion with the patient and family, a second, slow, and low-efficiency dialysis was performed with a blood flow of 200 ml/min, lasting for eight hours. During the first hospital day, a total of 12 hours of dialysis was delivered. Following the second dialysis, lactic acid decreased to 2.2 mmol/L and arterial pH was found to be 7.44. On the second hospital day, the patient’s urine output increased; blood pressure was found to be 111/57 mmHg, and dopamine was discontinued. Oxygenation improved, and he was transferred out of intensive care on the fifth hospital day. He was discharged from the hospital on day 12 with a Cr of 2.1 mg/dl and CO2 of 21 mmol/L. Metformin and lisinopril had been discontinued. At the two-month follow-up, the patient had a Cr of 1.1 mg/dL. A summary of his course is shown in Figure .","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [188.0, 'mg/dL'], 'Sodium': [137.0, 'mmol/L']}",139.112,132.1564,146.0676,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 137.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 137.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 137.0 mmol * 1 mEq/mmol = 137.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mmol sodium/L converts to 137.0 mEq sodium/L. 
The concentration of glucose is 188.0 mg/dL. 
Plugging in these values into the formula gives us 137.0 mEq/L + 0.024 * (188.0 - 100) = 139.112 mEq/L.
Hence, the patient's corrected concentration of sodium is 139.112 mEq/L."
5315,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7543146-1,Extracted,"A 5-week-old infant with CAH presented to the Emergency Room (ER) with fever and
fussiness.
He was born at 40 weeks gestation via C-section for failure to progress to a G1P1 mother
with negative prenatal serologies. APGAR scores were 8 and 9. Initial newborn course was
complicated by hypoglycemia, respiratory distress and tachypnea which resolved by day 2 of
life.
On day 3 of life, the newborn screening test was positive for congenital adrenal
hyperplasia. Pediatric endocrinology was consulted. Cortisol level obtained on day 2 of life
was 1.2 mcg/dL (2.9-19.4 mcg/dL) and 17-hydroxyprogesterone was 813 ng/dL (85-250 ng/dL). An
ACTH [CortrosynTM] stimulation test was performed and confirmed the diagnosis
with 1-hour post-stimulation 17 hydroxyprogesterone level of 17 836 ng/dl [85-250 ng/dL] and
cortisol level of 3.9 mcg/dl. The infant was initiated on hydrocortisone therapy at 30 mg/m²
per day, fludrocortisone 0.1 mg daily and Sodium chloride (table salt) 2 grams divided in
several feedings.
The infant presented to the ER at 5 weeks of age with fever and increased fussiness. There
was no respiratory distress, diarrhea, vomiting, rash, or decreased feeding. His father
reported symptoms of cough and a runny nose for a few days prior to this. On physical
examination, he was afebrile with oxygen saturation of 100%. He was noted to be irritable
and his skin was mottled ().
He did not have chest retractions, tachypnea, or nasal flaring. Laboratory results revealed
WBC 7.2 bil/L (5-19.5 bil/L), neutrophils 2.1 bil/L (1-9 bil/L), lymphocytes 2.5 bil/L
(2.5-16.5 bil/L), monocytes 2 bil/L (0.4-1.4 bil/L), Na 136 mmol/L (134-144 mmol/L),
potassium 5.9 mmol/L (4-6 mmol/L), HCO3 22 mmol/L (20-28 mmol/L), glucose of 110 mg/dL
(60-99 mg/dL), BUN 8 mg/dL (3-17 mg/dL), creatinine 0.33 mg/dL (0.1-0.36 mg/dL), and CRP
1.9 mg/L (0-7.9 mg/L). SARS-CoV-2 by Nucleic Acid Amplification (NAA) was detected on
nasopharyngeal swab. Pediatric infectious disease specialists were consulted. Blood culture,
urinalysis, and urine culture were negative. Chest x-ray demonstrated mild streaky bilateral
perihilar streaks with no focal consolidation or pleural effusions. Costophrenic angles were
clear with unremarkable lung apices and bronchoalveolar marking.
He was placed on triple maintenance hydrocortisone for stress dosing every 8 hours along
with fludrocortisone 0.15 mg daily. He received a normal saline bolus and was then placed on
maintenance IV fluids. He was transferred to the Pediatric Intensive Care Unit (PICU) and
Pediatric infectious disease specialists were consulted. Over the course of his admission,
he remained hemodynamically stable. He fed appropriately and did not require respiratory
support. He was discharged 2 days after admission and his stress hydrocortisone dose was
weaned down to his home regimen. At the time of this submission, he has been home for
4 weeks and doing well.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [110.0, 'mg/dL'], 'Sodium': [136.0, 'mmol/L']}",136.24,129.428,143.052,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 136.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 136.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 136.0 mmol * 1 mEq/mmol = 136.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mmol sodium/L converts to 136.0 mEq sodium/L. 
The concentration of glucose is 110.0 mg/dL. 
Plugging in these values into the formula gives us 136.0 mEq/L + 0.024 * (110.0 - 100) = 136.24 mEq/L.
Hence, the patient's corrected concentration of sodium is 136.24 mEq/L."
5316,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-1307,Extracted,"A 36-year-old man is brought to the emergency department by his neighbor because of altered mental status. He was found 6 hours ago stumbling through his neighbor's bushes and yelling obscenities. The neighbor helped him home but found him again 1 hour ago slumped over on his driveway in a puddle of vomit. He is oriented to self but not to place or time. His temperature is 36.9°C (98.5°F), pulse is 82/min, respirations are 28/min, and blood pressure is 122/80 mm Hg. Cardiopulmonary exam shows no abnormalities. He is unable to cooperate for a neurological examination. Muscle spasms are seen in his arms and jaw. Serum laboratory studies show:
Na+ 140 mEq/L
K+ 5.5 mEq/L
Cl- 101 mEq/L
HCO3- 9 mEq/L
Urea nitrogen 28 mg/dL
Creatinine 2.3 mg/dL
Glucose 75 mg/dL
Calcium 7.2 mg/dL
Osmolality 320 mOsm/kg
Calculated serum osmolality is 294 mOsm/kg. Arterial blood gas shows a pH of 7.25 and lactate level of 3.2 mmol/L (N=< 1 mmol/L). Examination of the urine shows oxalate crystals and no ketones.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [75.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",139.4,132.43,146.37,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.0 mEq/L. 
The concentration of glucose is 75.0 mg/dL. 
Plugging in these values into the formula gives us 140.0 mEq/L + 0.024 * (75.0 - 100) = 139.4 mEq/L.
Hence, the patient's corrected concentration of sodium is 139.4 mEq/L."
5317,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3411428-1,Extracted,"A 14-year-old Egyptian boy was referred to our institution for evaluation of recurrent hypoglycemic attacks which occurred especially in the mornings during the preceding two months. He had been diagnosed with T1DM at the age of five years and was treated with insulin in a dose of 0.7 to 1U/kg since that time. Recently, he started to develop recurrent attacks of hypoglycemia for which his insulin dose was decreased to 0.3U/kg. He had lost 2.5kg of weight and developed a craving for salt. He suffered from fatigue and dizziness. He was born and resided in a small village in Upper Egypt to unrelated Egyptian parents. He was the sixth child in his family with no history of diabetes or other auto immune diseases among family members. He had frequent hospital admissions for control of blood sugar. He was born at term with a birth weight of 3550 grams. Apart from post circumcision bleeding that was done at the age of two years by a barber, there was nothing significant in his past medical history. On physical examination, his body temperature was 36.1C, pulse rate was 92/min, blood pressure was 80/45mmHg, his height was in the 10th percentile while his weight was in the 25th percentile. He had no pallor, jaundice, or hyperpigmentation of either the skin or mucous membranes. His thyroid gland was not enlarged either on inspection or palpation. He was prepubertal: pubic and axillary hair Tanner stage 1 and testicular volume 3ml. He had slight abdominal distension, his liver and spleen were not enlarged and there was no evidence of ascities. Skin examination revealed vitiligo in the form of multiple hypopigmented areas located over the chest and abdomen. Serum biochemistry on admission showed an average blood glucose level of 77mg/dL (normal range: 82 to 110mg/dL), hemoglobin A1c 7.5% (normal range: 3.0 to 6.1), potassium: 5.9mmol/L (normal range 3.5 to 5), sodium 121mmol/L (normal range: 130 to 145) and calcium 9.7mg/dL (normal range: 8 to 10.5). Levels of blood urea nitrogen and creatinine were within the normal range. Liver function tests revealed bilirubin 11umol/L (normal <20umol/L), alanine aminotransferase (ALT) 186IU/L (normal <50IU/L), aspartate aminotransferase (AST) 123IUL (normal <50IU/L), alkaline phosphatase 108IU/L, (normal <350IU/L), and albumin 38g/L (normal range: 35 to 45g/L). Complete blood count, serum folate and vitamin B12 levels were normal. Viral hepatitis screens (HAV IgM, HBsAg, HBsIgM and IgG, Epstein-Barr virus, cytomegalovirus and herpes simplex virus) were negative. Anti-HCV and hepatitis C virus–polymerase chain reaction (HCV–PCR) were positive, with a viral load of 88,440IU/mL. Anti-endomysial antibodies were not detected. There were no serological features of autoimmune hepatitis (anti-smooth muscle antibody, antinuclear antibody, anti-liver/kidney microsomal antibody, and anti-parietal cell antibody were negative), anti-adrenal antibodies were positive and serum immunoglobulins were normal. Hormonal assays revealed cortisol <1.0ug/dL (normal range: 6 to 24), adrenocorticotropic hormone (ACTH) > 1250pg/mL (normal range: 20 to 100), a peak cortisol level below 0.2mcg/dL after intravenous ACTH stimulation test (250mcg). Thyroid stimulating hormone (TSH) was 6.11uIU/mL (normal range: 0.4 to 5.0). Anti-thyroglobulin (Tg autoantibodies) were 217.8IU/mL (normal: <120), anti-thyroid peroxidase (TPO autoantibodies) 5176IU/mL (normal 60), and free thyroxine 1.4ng/dL (normal range: 0.7 to 2.0). The serum luteinizing hormone was 0.1mIU/ml (normal range: 2.9 to 21.7), follicle-stimulating hormone 0.2mIU/ml (normal range: 5 to 30), testosterone 0.02ng/mL (normal range: 9.0 to 40.0), prolactin 13ng/mL (normal range: 3 to 30). Insulin C-peptide was <0.50ng/mL (normal range: 1.5 to 3.5). Parathormone (PTH) was 33.4pg/mL (normal range: 2 to 72). Thyroid ultrasonography revealed heterogeneous echogenicity without any nodules, while ultrasonography of the abdomen was normal. His immunogenetic study demonstrated that human leukocyte antigen (HLA) typing was HLA-DR3. Based on combinations of 1DM, subclinical hypothyroidism due to Hashimoto’s thyroiditis, adrenal insufficiency, vililligo and HLA-DR3, a diagnosis of APS2 was made. The presence of positivity for both anti-HCV and HCV-RNA with elevated ALT and AST levels even in the absence of hepatomegaly confirmed the diagnosis of chronic hepatitis C infection. His general condition improved gradually following the administration of hydrocortisone (10mg twice daily) and fludrocortisone (0.1mg twice daily). His diabetes was controlled with intensive multiple daily insulin injections. He was referred to the regional hepatology unit for further assessment including liver biopsy and consideration of hepatitis C eradication therapy but his father preferred to delay the treatment because he was worried about the side effects of the treatment.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [77.0, 'mg/dL'], 'Sodium': [121.0, 'mmol/L']}",120.448,114.4256,126.4704,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 121.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 121.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 121.0 mmol * 1 mEq/mmol = 121.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 121.0 mmol sodium/L converts to 121.0 mEq sodium/L. 
The concentration of glucose is 77.0 mg/dL. 
Plugging in these values into the formula gives us 121.0 mEq/L + 0.024 * (77.0 - 100) = 120.448 mEq/L.
Hence, the patient's corrected concentration of sodium is 120.448 mEq/L."
5318,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-5286,Extracted,"A 57-year-old woman presents to the emergency department for laboratory abnormalities detected by her primary care physician. The patient went to her appointment complaining of difficulty using her hands and swelling of her arms and lower extremities. The patient has notably smooth skin that seems to have not aged considerably. Upon seeing her lab values, her physician sent her to the ED. The patient has a past medical history of multiple suicide attempts, bipolar disorder, obesity, diabetes, and anxiety. Her current medications include lithium, insulin, captopril, and clonazepam. The patient's laboratory values are below.

Serum:
Na+: 140 mEq/L
K+: 5.2 mEq/L
Cl-: 100 mEq/L
HCO3-: 20 mEq/L
BUN: 39 mg/dL
Glucose: 127 mg/dL
Creatinine: 2.2 mg/dL
Ca2+: 8.4 mg/dL

The patient is restarted on her home medications. Her temperature is 99.5°F (37.5°C), pulse is 80/min, blood pressure is 155/90 mmHg, respirations are 11/min, and oxygen saturation is 97% on room air.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [127.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",140.648,133.6156,147.6804,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.0 mEq/L. 
The concentration of glucose is 127.0 mg/dL. 
Plugging in these values into the formula gives us 140.0 mEq/L + 0.024 * (127.0 - 100) = 140.648 mEq/L.
Hence, the patient's corrected concentration of sodium is 140.648 mEq/L."
5319,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3227318-1,Extracted,"A 12-year-old female, previously healthy, was admitted from the emergency department to the intensive care unit with a two weeks history of fever and multiple asymmetrical joint swelling and pain. Her admission temperature was 39.6°C, heart rate (HR) 130 beats/min, arterial blood pressure (BP) 127/57 mmHg, respiratory rate (RR) 35 breaths/min, and oxygen saturation (SpO2) 93% on air. On examination, the patient had hair lice with multiple scratch marks on her scalp, bilateral pleural effusion, ejection systolic murmur grade 2/6 over the aortic area, tender hepatomegaly (3 cm below the costal margin, liver span 10 cm), and multiple joint swelling, redness, and tenderness involving the right middle finger, right hip, and both knees and ankles. Admission laboratory results revealed a white blood cell (WBC) count of 6000 cells/mm3, lymphocytes 0.9×109cells/l, granulocytes 4.5×109·cells/l, monocytes 0.2×109cells/l, reticulocytes 28×109cells/l, platelets 156,000 cells/mm3, hemoglobin 107 g/l, serum sodium 125 mmol/l, serum potassium 4.8 mmol/l, serum glucose 4.3 mmol/l, serum urea 20.7 mmol/l, serum creatinine 90 mmol/l, lactate dehydrogenase (LDH) 1427 IU/L, aspartate aminotransferase (AST) 408 IU/L, alanine transaminase (ALT) 307 IU/L, alkaline phosphatase (ALP) 184 IU/L, albumin 19 g/l, gamma-glutamate transferase (GGT) 110 IU/L, creatine kinase (CK) 142 IU/L, total bilirubin 145 mmol/l, serum osmolality 289 mOsm/kg, and urine osmolality 647 mOsm/kg. The patient's international normalized ratio (INR) was 1.2, prothrombin time (PT) 14 (control 12), and activated partial thromboplastin time (aPTT) 36 (control 34). Screening tests for sickle cell disease, hepatitis A, hepatitis C, and human immunodeficiency virus were negative; however, she tested positive for anti-hepatitis B surface antigen (anti-HBs Ag) antibodies. Chest X-ray confirmed the presence of bilateral pleural effusion (right > left) and showed widened mediastinum with a pear-shaped heart suggestive of pericardial effusion. A twelve-lead electrocardiogram (ECG) demonstrated sinus tachycardia, diffuse ST-segment elevation with generalized T-wave inversion. Transthoracic echocardiogram revealed moderate size pericardial effusion and no evidence of endocarditis or valvular heart disease. Blood, sputum, and urine cultures were obtained in the emergency department and the patient was started empirically by the emergency department physician on ceftazidime 1.3 g intravenous (IV) every 8 hours and flucloxacillin 1.2 g IV every 6 hours. In addition, a right chest tube thoracostomy was inserted and placed to underwater seal; 800 ml of serous fluid was drained and there was no air leak. Analysis of pleural fluid showed lactate dehydrogenase (LDH) 5 IU/L, albumin 19 g/L, and pH 7.37. Gram-positive cocci in clusters were seen on Gram staining of the pleural fluid (admission sample). The patient's hair was shaved and she was started on anti-lice shampoo. Sputum microscopy was negative for acid-fast bacilli and a sample for mycobacterium tuberculosis culture and polymerase chain reaction test was sent off.
On the second day, the patient became more tachypneic (RR 40 breaths/min) and hypotensive (BP 90/40 mmHg). Her trachea was intubated, lungs were mechanically ventilated, antibiotics were changed to meropenem to broaden her coverage, and she was started on dopamine and norepinephrine infusions. After initiation of mechanical ventilation, air leak from the right chest tube was observed suggesting the presence of bronchopleural fistula, however, she maintained her SpO2 > 95% on FiO2 0.4. Echocardiography-guided pericardiocentesis was performed and 500 ml of pus was aspirated and a pig-tail catheter was inserted into the pericardium. Pericardial fluid analysis showed proteins 42 g/l, albumin 27 g/l, and Gram positive cocci in clusters on microscopy. Chest X-ray showed right minimal hydropneumothorax. Ultrasound examination of the abdomen revealed perinephric and subhepatic collections with free fluid in the abdomen and pelvis. Methicillin-sensitive Staphylococcus aureus was cultured from sputum, blood, pleural fluid, and pericardial aspirate. Urine cultures were negative. Rheumatoid factor levels were slightly above the upper range of normal at 48.8 IU/L. Cytomegalovirus IgM antibodies were negative, but the IgG titer was 1/21,000 IU/L.
On day 4, air started to leak continuously through the pericardial pig-tail catheter which was still draining pus and the air leak was most marked during mechanical inspiration. A broncho-pericardial or broncho-pleuropericardial fistula was suspected. The pig-tail catheter was inadvertently clamped and the patient's BP decreased to 80/50 mmHg and HR increased to 120 beats/min. BP and HR returned to baseline values after de-clamping the catheter. Computed tomography (CT) of the chest showed pneumopericardium [Figures and ] and hydropneumothorax []. The radiologist injected radio-opaque contrast material easily into the pericardial pig-tail catheter and the contrast material immediately spilled over into the right pleural cavity []. A CT fistulogram, thus, confirmed the presence of communication between the right pleural space and the pericardium []. The cardiothoracic surgeon recommended conservative management given the patient status at the time. On day 5, the abdominal collections were aspirated laparoscopically. On day 11, the patient developed disseminated intravascular coagulation and was bleeding from everywhere. On day 13, she died of multi-organ failure and her parents refused an autopsy.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [4.3, 'mmol/L'], 'Sodium': [125.0, 'mmol/L']}",124.45926,118.2363,130.68222,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 125.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 125.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 125.0 mmol * 1 mEq/mmol = 125.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 125.0 mmol sodium/L converts to 125.0 mEq sodium/L. 
The concentration of glucose is 4.3 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 4.3 mmol. To convert 4.3 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 4.3 mmol glucose * 0.001 mol/mmol = 0.0043 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0043 mol glucose * 180.16 g/mol = 0.77469 g glucose. To convert 0.77469 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 0.77469 g glucose * 1000.0 mg/g = 774.69 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 774.69 mg glucose/10.0 dL = 77.469 mg glucose/dL. The concentration value of 4.3 mmol glucose/L converts to 77.469 mg glucose/dL. 
Plugging in these values into the formula gives us 125.0 mEq/L + 0.024 * (77.469 - 100) = 124.45926 mEq/L.
Hence, the patient's corrected concentration of sodium is 124.45926 mEq/L."
5320,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3692154-1,Extracted,"A 57-year-old man with diabetes mellitus, systemic hypertension, and polycystic kidney disease presented with fever and left loin pain for 1 week. His medications included two oral anti-diabetic drugs (metformin and glimepiride) and two anti-hypertensive drugs. There was no history of dysuria or hematuria. Physical examination revealed pallor, bilateral pedal edema, pulse rate of 102/min, blood pressure of 160/100 mmHg, temperature of 39°C, and respiratory rate of 19/min. Abdomen examination revealed bilateral nodular enlarged kidneys with tenderness in the left renal angle. Respiratory system and cardiovascular system examinations were unremarkable. His hemoglobin (10.3 g/dL) was decreased and white blood cell count was increased to 13.8 × 109/L with neutrophils 84%, lymphocytes 12%, eosinophils 2%, and monocytes 2%. Platelet count was 364 × 109/L and 1.2% of reticulocyte count was normal. Blood sugar was 390 mg/dl, serum creatinine was 1.39 mg/dL, and the estimated four-variable MDRD GFR was 55 mL/min/1.73 m2. Blood gas analysis revealed high anion gap metabolic acidosis (pH, 7.26; pCO2, 25 mm Hg; HCO3, 19 meq/L; pO2, 128 mmHg; anion gap 16 meq/L; lactate, 1.5 meq/L; Na, 136 meq/L; K, 3.8 meq/L; and Cl 101 meq/L). Liver function tests, uric acid, calcium, inorganic phosphorus, and lipid profile were within normal limits. HBsAg, HIV, and anti-HCV antibody enzyme-linked immunosorbent assay were negative. Urine analysis showed 2+ ketone, 4+ glucose, and hematuria with 1+ proteinuria. Urine nitrite test was positive. There were 8–10 white blood cells per high-power field (hpf), 8–10 red blood cells per hpf, 12–15 pus cells per hpf, and no evidence of casts on microscopic examination of the urine sediment. Ultrasound revealed bilateral polycystic kidneys with features of thick wall and intracystic debris in one upper pole cyst of right kidney. Emergency non-contrast computerized tomogram of abdomen revealed features of bilateral emphysematous cyst infection [] with features of pyelonephritis. A provisional diagnosis of EPN with diabetic ketoacidosis was made. His initial management included intravenous antibiotics (piperacillin + tazobactum 4.5 gm q8h and levofloxacin 500 mg q24h), IV fluids, insulin infusion (regular insulin titrated to maintain capillary blood glucose range of 100–150 mg/dl), and supportive measures. Percutaneous aspiration of both the cysts was done under real-time ultrasound guidance on day 2. About 250 ml of purulent fluid was aspirated. Gram stain revealed multiple gram-negative bacilli. Urine and blood cultures showed no growth. Chest X-ray did not reveal any abnormality. Culture of pus revealed Escherichia coli (non-ESBL) sensitive to meropenem and pazufloxacin. Antibiotics were changed to meropenem, pazufloxacin from day 4. Patient became afebrile on day 6. Antibiotics were continued for a period of 3 weeks. Repeat ultrasound done after 3 weeks showed significant resolution of cyst collection on both sides. Patient was discharged on day 22 with oral antibiotics (faropenem and levofloxacin). Twelve weeks after discharge, patient is asymptomatic, with a serum creatinine of 1.04 mg/dL. He is presently on levofloxacin prophylaxis.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [390.0, 'mg/dL'], 'Sodium': [136.0, 'mEq/L']}",142.96,135.812,150.108,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 136.0 mEq/L. 
The concentration of glucose is 390.0 mg/dL. 
Plugging in these values into the formula gives us 136.0 mEq/L + 0.024 * (390.0 - 100) = 142.96 mEq/L.
Hence, the patient's corrected concentration of sodium is 142.96 mEq/L."
5321,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-1760,Extracted,"A 50-year-old man is brought to the emergency department by his wife because of lethargy and confusion for the past 24 hours. He has also had a productive cough for the past year and has had a 10-kg (22-lb) weight loss over the past 6 months. He has a history of multiple sclerosis and has not had an acute exacerbation in over 10 years. For the past 30 years, he has smoked 2 packs of cigarettes daily. He drinks 2 beers every day after work. His temperature is 37.0°C (98.6°F), pulse is 90/min, blood pressure is 130/90 mm Hg, and respirations are 22/min. On examination, the patient appears lethargic and cannot state his name or his location. Physical examination reveals scattered wheezing bilaterally. Deep tendon reflexes cannot be elicited. Laboratory studies show:
Serum
Na+ 115 mEq/L
K+ 4.5 mEq/L
HCO3- 22 mEq/L
Glucose 70 mg/dL
Blood urea nitrogen 8 mg/dL
Urine osmolality 450 mOsmol/kg H2O
Urine sodium 70 mEq/L
An x-ray of the chest reveals a central lung mass.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [70.0, 'mg/dL'], 'Sodium': [115.0, 'mEq/L']}",114.28,108.566,119.994,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 115.0 mEq/L. 
The concentration of glucose is 70.0 mg/dL. 
Plugging in these values into the formula gives us 115.0 mEq/L + 0.024 * (70.0 - 100) = 114.28 mEq/L.
Hence, the patient's corrected concentration of sodium is 114.28 mEq/L."
5322,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7816133-1,Extracted,"A 48-year-old man presented to the gastroenterologist with an episode of hiccups lasting at least 96 h. His past medical history only revealed an L5 surgical repair in 2005, and he denied allergies or recent travel. Aside from the hiccups, the patient recalled no other symptoms and denied abdominal pain, nausea, vomiting, diarrhea, chest pain, cough, dyspnea, or fever. He was started on ambulatory treatment with metoclopramide 10 mg every 8 h; however, the symptoms did not resolve.
He presented to the ER approximately 5 h later with the same complaint. His vitals showed a heart rate of 82 beats/min, respiratory rate 20 respirations/min, blood pressure 133/88 mmHg, oxygen saturation 93%, and temperature 36.7 °C. On the physical exam, the patient was alert and oriented with a normal affect and normal gait. The exam revealed no dermatological lesions and benign head, ear, nose, and throat exam. His chest showed a normal diameter. However, lung auscultation revealed the presence of crackles left lung base. The remainder exam was normal.
Initially, he was treated with IV metoclopramide, omeprazole 40 mg, ondansetron 8 mg, and oral frappe magaldrate/dimeticone (80/10 mg) without symptom improvement. Laboratory analysis revealed hyperglycemia (182 mg/dl), thrombocytopenia (81,000/mcl), leucopenia (4,000/mcl), and lymphopenia (700/mcl absolute count). The remaining results were normal (hemoglobin 16.2 g/l, hematocrit 48.3%, BUN 19.2, urea 41.1, serum creatinine 1.1 mg/dl, sodium 136.8 mEq/L, potassium 3.56 mEq/L). A chest X-ray (Fig. ) revealed bilateral infiltrates. The thoracic CT scan revealed multiple zones of diffuse alveolar infiltrate across all segments of both lungs (Fig. ).
SARS-CoV-2 PCR results were positive. The patient refused admission and was lost to follow-up.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [182.0, 'mg/dL'], 'Sodium': [136.8, 'mEq/L']}",138.768,131.8296,145.7064,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 136.8 mEq/L. 
The concentration of glucose is 182.0 mg/dL. 
Plugging in these values into the formula gives us 136.8 mEq/L + 0.024 * (182.0 - 100) = 138.768 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.768 mEq/L."
5323,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6865339-1,Extracted,"A 34-year-old previously healthy female presented with a mass on the left big toe that caused embarrassment and difficulty in wearing footwear. The mass was first noticed three years ago and has since started to grow in size. There was no associated discharge, skin changes or other masses elsewhere. The patient had no history of trauma, contact with an animal, and animal or human bite. She lived in an agricultural area and indulged in barefoot walking. The patient had neither history of any systemic illness or weight loss, fever, or easily fatigability nor any significant family history. However, the patient had a similar mass at the same site that was treated surgically 15 years ago and failed to provide any information regarding its diagnosis.
Upon examination, the patient was conscious, alert and oriented and not pale, jaundiced or cyanosed. Her vitals were normal, and the liver, spleen and lymph nodes were not palpable. Cardiovascular system, respiratory system and the central nervous system showed no abnormalities. Left big toe examination revealed 2 × 1 × 1 cm mass at the distal end. There were no changes in the overlying skin or the nail and no surrounding cellulitis. The distal neurovascular examination revealed normal findings. There was no palpable inguinal lymphadenopathy.
The laboratory data included a white blood cell count of 6000/μl, hemoglobin of 10.5 g/dl, platelet count of 233 × 10/μl, blood glucose 121 mg/dl, blood urine nitrogen 46 mg/dl, serum creatinine 69 mg/dl, sodium 138 mmol/L, potassium 3.8 mmol/L, serum albumin 3.4 g/dl, erythrocyte sedimentation rate 73 mm/h, and C-reactive protein 15.6 mg/dl. The X-ray of lower extremity revealed no significant abnormality ().
Incisional biopsy showed chronic inflammation with scattered granulomas mixed with neutrophils and actinomycetes.
MRI showed a 2-cm soft tissue focus at the tip and plantar aspect of big toe closely adherent to the tuft of distal phalanx but with no evidence of bony destruction ().
The mass was shaved off the bone with wide local excision, and the resultant defect was covered with Kutler bilateral V-Y advancement flaps ().
Final histopathology showed reactive epidermis with subepidermal multiple colonies of filamentous organisms with extensive mixed inflammatory reaction consistent with actinomycosis.
The patient was then referred to the infectious disease team, and a 6-week course of clindamycin was started to eradicate the infection. Follow up after 19 months shows no recurrence ( and ).","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [121.0, 'mg/dL'], 'Sodium': [138.0, 'mmol/L']}",138.504,131.5788,145.4292,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 138.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 138.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 138.0 mmol * 1 mEq/mmol = 138.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mmol sodium/L converts to 138.0 mEq sodium/L. 
The concentration of glucose is 121.0 mg/dL. 
Plugging in these values into the formula gives us 138.0 mEq/L + 0.024 * (121.0 - 100) = 138.504 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.504 mEq/L."
5324,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-4848,Extracted,"A 27-year-old woman presents to her primary care physician for a follow-up appointment. At her previous visit she had missed her previous two menses and also had a blood pressure of 147/100 mmHg. The patient has a past medical history of anxiety, depression, bulimia nervosa and irritable bowel syndrome. Her physician prescribed her an exercise program as well as started her on hydrochlorothiazide and ordered lab work. The results of the patient's lab work are below:

Serum:
Na+: 145 mEq/L
K+: 2.9 mEq/L
Cl-: 100 mEq/L
HCO3-: 30 mEq/L
BUN: 18 mg/dL
Ca2+: 10.9 mg/dL
Mg2+: 2.0 mEq/L
Creatinine: 1.2 mg/dL
Glucose: 110 mg/dL

The patient's blood pressure at this visit is 145/100 mmHg and she has still not experienced her menses. Her cardiac, abdominal, and pulmonary exams are within normal limits. Inspection of the patient's oropharynx is unremarkable as is inspection of her extremities. The patient is started on furosemide and sent home.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [110.0, 'mg/dL'], 'Sodium': [145.0, 'mEq/L']}",145.24,137.978,152.502,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 145.0 mEq/L. 
The concentration of glucose is 110.0 mg/dL. 
Plugging in these values into the formula gives us 145.0 mEq/L + 0.024 * (110.0 - 100) = 145.24 mEq/L.
Hence, the patient's corrected concentration of sodium is 145.24 mEq/L."
5325,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4859119-1,Extracted,"On October 11, 2011, a 23-year-old G3P2 (both alive) woman was referred to our department on a suspicion of a malignant ovarian disease. She had presented at the referring clinic 2 weeks earlier with abdominal distension, pain, dyspnea, nausea, and vomiting. She was 10 weeks pregnant; her last menstrual period was on August 1, 2011. The abdominal pain had increased 2 days prior to referral despite taking analgesics (paracetamol). She did not have any previous medical or surgical disease, and her gynecological history was unremarkable. Menarche was at the age of 12, and menstrual cycles were regular. She had two normal vaginal deliveries at term, in 2008 and 2010.
She was well-nourished and weighed 58 kg, in acute distress and mild dyspnea. Temperature, pulse rate, and blood pressure were within normal limits. Her physical examination revealed a moderately distended, tender, and tense abdomen with positive shifting dullness on percussion. The bowel sounds were normal. On pelvic examination, the uterine size and ovaries could not be made out because of the distention and tenderness, but bilateral irregular and mobile adnexal masses could be palpated with difficulty. Pelvic ultrasound revealed a single viable fetus at 11 weeks (crown-rump length 38 mm), with bilateral multilocular cystic ovarian masses, measuring 18.7 cm × 13.1 cm on the right and 14.6 cm × 12.6 cm on the left, associated with the moderate generalized peritoneal free fluid collection. The liver, gall bladder, spleen, and both kidneys were normal [].
Laboratory studies revealed: Hemoglobin; 12.1 g/dl, hematocrit (Hct); 35.5%, white blood cell; 8700, platelet; 406,000, Na; 133 mEq/L, K; 4.5 mEq/L, blood urea nitrogen; 23 mg/dl, creatinine; 0.5 mg/dl, fasting blood sugar; 90 mg/dl, aspartate aminotransferase; 44 U/l, alanine aminotransferase; 23 U/l, alkaline phosphatase; 105 U/l. Total protein; 5.6 g/dl, albumin 3.2 g/dl, liver function tests, prothrombin time, partial thromboplastin time, tests were also normal. Blood group was B rhesus positive and genotype AA.
A diagnosis of severe OHSS, with viable intrauterine pregnancy, was made. She was admitted for monitoring and supportive therapy. She had intravenous fluid (normal saline) at least 2000 ml per day, and liberal oral fluid intake encouraged. Medications included oral bromocriptine 2.5 mg daily for 5 days in addition to oral tramadol, piriton, metoclopramide, vasoprin, and ranitidine. During hospitalization, daily weighing, and abdominal girth measurements showed an increase from 58–63 kg to 89–92 cm, respectively, but there were no respiratory difficulties and her vital signs remained stable, the daily urine out-put was satisfactory. She responded well to treatment and at discharge, after 7 days; a full blood count, electrolytes, liver function, and coagulation profile gave results within normal limits. Hct was 34%; she weighed 63 kg, and abdominal girth was 88 cm.
She was seen weekly at the clinic. Resolution of the ascites and decrease in follicular size occurred gradually, demonstrated by clinical and ultrasonographic studies. On November 01, 2011; she had no complaints, she weighed 60 kg, abdominal girth was 84 cm and Hct; 32%, ultrasonography revealed a single active fetus of 13 weeks gestation, with regressed adnexal masses with no ascites []. She remained stable, and at 26 weeks gestation ultrasound showed normal sized ovaries and there was no free fluid in the abdomen and pelvis. The fetus was compatible with 27 weeks of gestation, and no gross anomaly noted, the placenta was posteriorly located. Amniotic fluid was also within normal limits [].
The pregnancy proceeded normally and at 39 weeks of gestation, the patient had spontaneous onset labor and underwent an uncomplicated vaginal delivery of male new born weighing 3.4 kg.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [90.0, 'mg/dL'], 'Sodium': [133.0, 'mEq/L']}",132.76,126.122,139.398,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 133.0 mEq/L. 
The concentration of glucose is 90.0 mg/dL. 
Plugging in these values into the formula gives us 133.0 mEq/L + 0.024 * (90.0 - 100) = 132.76 mEq/L.
Hence, the patient's corrected concentration of sodium is 132.76 mEq/L."
5326,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5586714-1,Extracted,"A 43-year-old woman with poorly controlled type 2 diabetes mellitus wpresented to our hospital in a confused state and fever. Clinically, she had an oral temperature of 39.6°C and was severely dehydrated, with a heart rate of 116 beats/min and a blood pressure of 100/60 mm Hg. On examination, she was lethargic with no focal neurological deficit or neck stiffness. Examination of the heart, chest and abdomen was unremarkable. Blood laboratory investigations showed: sugar 46 mmol/l, sodium 181 mmol/l (135–145 mmol/l), potassium 4.6 mmol/l (3.4–4.9 mmol/l), urea 11 mmol/l (2–6 mmol/l) and creatinine 80 µmol/l (60–80 µmol/l). Arterial blood gas analysis showed: Pao2 8.7 kPa, Paco2 4.2 kPa, pH 7.39, and bicarbonate 20 mmol/l (22–28 mmol/l). Urine showed marked pyuria and negative ketones. Blood and urine cultures were positive for Escherichia coli. Cerebrospinal fluid analysis showed normal biochemistry and cell count with negative microbiological workup. Brain CT was normal. The patient was managed as a case of HHS with Gram-negative sepsis. Immediate treatment with 0.45% saline and intravenous insulin infusions was started together with appropriate intravenous antibiotics. The saline infusion was started initially at 250 ml/h, with modification of rate and concentration so that the fall in serum sodium was not allowed to exceed 0.5 mmol/l per hour (table ). In the second week of the inpatient course, the patient's lethargy did not improve, in spite of fever subsidence, haemodynamic stabilization and proper correction of the biochemical parameters. She also developed behavioural changes with bouts of agitation and disorientation. Neurological evaluation revealed brisk deep tendon reflexes of the 4 limbs, but plantar responses were normal and there was no weakness. At the end of the second week, a brain MRI was made. It showed a high signal intensity lesion in the posterior central part of the pons in T2-weighted images (fig. ), consistent with CPM. The patient did not give any history of previous neurological disorder or trauma, and, consequently, she did not have any previous brain CT or MRI studies. A diagnosis of CPM in relation to hypernatraemia of HHS was concluded. No specific treatment was given, and the patient was closely observed. She fully recovered and was discharged in a normal mental and physical state by the end of the fourth week. We could not obtain a repeat brain MRI as the patient was lost to follow-up.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [46.0, 'mmol/L'], 'Sodium': [181.0, 'mmol/L']}",198.48966,188.56518,208.41414,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 181.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 181.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 181.0 mmol * 1 mEq/mmol = 181.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 181.0 mmol sodium/L converts to 181.0 mEq sodium/L. 
The concentration of glucose is 46.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 46.0 mmol. To convert 46.0 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 46.0 mmol glucose * 0.001 mol/mmol = 0.046 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.046 mol glucose * 180.16 g/mol = 8.28736 g glucose. To convert 8.28736 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 8.28736 g glucose * 1000.0 mg/g = 8287.36 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 8287.36 mg glucose/10.0 dL = 828.736 mg glucose/dL. The concentration value of 46.0 mmol glucose/L converts to 828.736 mg glucose/dL. 
Plugging in these values into the formula gives us 181.0 mEq/L + 0.024 * (828.736 - 100) = 198.48966 mEq/L.
Hence, the patient's corrected concentration of sodium is 198.48966 mEq/L."
5327,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-4924,Extracted,"A 25-year-old woman presents to her physician with a four month history of fatigue and weakness. The weakness has been progressive to the point where she cannot climb stairs and stand from a sitting position. She has only had one menstrual period in the last four months and has never been pregnant. She smokes a pack of cigarettes every day and does not take any medications. Her temperature is 98°F (36.7°C), blood pressure is 160/100 mmHg, pulse is 70/min, and respirations are 15/min. She is obese with a significant pannus. Abdominal striae are present. Her laboratory workup is notable for the following:

Serum:
Na+: 142 mEq/L
Cl-: 102 mEq/L
K+: 3.9 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 314 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.1 mg/dL
AST: 9 U/L
ALT: 8 U/L
24-hour urinary cortisol: 470 µg (< 300 µg)
Serum cortisol 30 µg/mL (5-23 µg/dL)
Serum adrenocorticotropin-releasing hormone (ACTH) 2 pg/mL (> 5 pg/mL)

A 48-hour high dose dexamethasone suppression trial shows that her serum cortisol levels do not decrease.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [314.0, 'mg/dL'], 'Sodium': [142.0, 'mEq/L']}",147.136,139.7792,154.4928,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 142.0 mEq/L. 
The concentration of glucose is 314.0 mg/dL. 
Plugging in these values into the formula gives us 142.0 mEq/L + 0.024 * (314.0 - 100) = 147.136 mEq/L.
Hence, the patient's corrected concentration of sodium is 147.136 mEq/L."
5328,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-1693,Extracted,"A 63-year-old man is brought to the emergency department after having 8–9 episodes of red watery stool. He has no abdominal pain or fever. He underwent an angioplasty 4 years ago and received 2 stents in his left main coronary artery. He has hypertension, hypercholesterolemia, coronary artery disease, and chronic constipation. Current medications include aspirin, metoprolol, and simvastatin. He drinks one beer daily. He is in distress. His temperature is 37.3°C (99.1°F), pulse is 110/min, respirations are 14/min, and blood pressure is 86/58 mm Hg. Examination shows pale conjunctivae. The abdomen is soft and nontender. Bowel sounds are increased. The lungs are clear to auscultation. Cardiac examination shows an S4 gallop. Rectal examination shows frank blood. Laboratory studies show:
Hemoglobin 9.8 g/dL
Leukocyte count 7,800/mm3
Platelet count 280,000/mm3
Prothrombin time 14 seconds (INR=0.9)
Serum
Na+ 135 mEq/L
K+ 4.1 mEq/L
Cl- 101 mEq/L
Urea nitrogen 16 mg/dL
Glucose 96 mg/dL
Creatinine 0.7 mg/dL
Two large bore intravenous catheters are inserted and 0.9% saline infusions are administered. A nasogastric tube is inserted. Aspiration shows clear gastric content containing bile. Directly afterwards, his pulse is 133/min and blood pressure is 80/54 mm Hg.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [96.0, 'mg/dL'], 'Sodium': [135.0, 'mEq/L']}",134.904,128.1588,141.6492,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 135.0 mEq/L. 
The concentration of glucose is 96.0 mg/dL. 
Plugging in these values into the formula gives us 135.0 mEq/L + 0.024 * (96.0 - 100) = 134.904 mEq/L.
Hence, the patient's corrected concentration of sodium is 134.904 mEq/L."
5329,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2848063-1,Extracted,"A 24-year-old Caucasian woman was admitted to the Accident and Emergency Department of our hospital with a sudden episode of nausea, vomiting and collapse, having become acutely unwell whilst at work. There was no past medical history and she was not taking any regular medication. On examination she was of normal body weight (weight 53 kg and body mass index 21 kg/m2), afebrile and her blood pressure was 103/56 with no postural change measured. Although she appeared drowsy and unwell, her systemic examination was unremarkable and no focal abnormalities were found on neurological examination of the central or peripheral nervous system. Initial biochemical analysis revealed sodium 127 mmol/l, potassium 3.2 mmol/l, urea 3.8 mmol/l, creatinine 77 and glucose 4.1 mmol/l. Inflammatory markers (white cell count and C-reactive protein) were normal. A computerised tomography (CT) and magnetic resonance (MR) of the brain demonstrated normal ventricles, no focal lesion or mass effect and normal sagittal sinus flow. Upon lumbar puncture, performed in the lateral decubitus position, an opening pressure of 40 mm of water was documented. Cerebrospinal fluid (CSF) microscopy revealed two white blood cells (WBCs) per mm3, <1 red blood cell (RBC) per mm3 and no organisms. CSF chemistry was unremarkable: protein 0.4 g/l and glucose 3.2 mmol/l. The patient had remained drowsy and she was managed in the Intensive Care Unit with a presumptive diagnosis of acute meningoencephalitis with a secondary syndrome of inappropriate anti-diuretic hormone (SIADH). No measurements of serum or urine osmolality were made. She was treated with antibiotics and acyclovir and was also supported with intravenous fluids and, within 24 hours, had improved such that she was transferred back to the ward.
During subsequent review she admitted to several months of generalised fatigue, sometimes falling asleep at work, and of intermittent headaches. With subsequent neurology specialist input to review the grossly elevated intracranial pressure, accompanied by normal imaging and CSF analysis, the patient was commenced on acetazolamide 250 mg daily for presumed idiopathic intracranial hypertension (IIH). Visual acuity and visual field (Goldman perimetry) testing was unremarkable. On endocrine review, generalised hyperpigmentation with facial melasma were noted and, although she had no buccal pigmentation, she did have marked pigmentation of a recent scar over her left shoulder (Figure ). A short synacthen (250 mcg) test (SST) was performed and demonstrated adrenal insufficiency with basal cortisol at 231 nmol/l, 30 minute cortisol 265 nmol/l and 60 minute at 200 nmol/l. A repeat SST showed basal cortisol at 138 nmol/l and 30 minute cortisol at 159 nmol/l and confirmed adrenal insufficiency. Adrenal antibodies were negative. Her plasma adrenocorticotropic hormone (ACTH) was raised at >278 pmol/l consistent with primary adrenal failure. She was commenced on glucocorticoid (hydrocortisone 10 mg bd) and mineralocorticoid (fludrocortisone 50 mcg) replacement therapy and discharged. On subsequent review two weeks later, she was feeling much better with CSF pressure reduced to 25 mm of water on repeat lumbar puncture. Acetazolamide was discontinued after three months and on subsequent reviews at six and 12 months, she continued to remain well on hydrocortisone and fludrocortisone replacement.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [4.1, 'mmol/L'], 'Sodium': [127.0, 'mmol/L']}",126.37278,120.05414,132.69142,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 127.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 127.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 127.0 mmol * 1 mEq/mmol = 127.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 127.0 mmol sodium/L converts to 127.0 mEq sodium/L. 
The concentration of glucose is 4.1 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 4.1 mmol. To convert 4.1 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 4.1 mmol glucose * 0.001 mol/mmol = 0.0041 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0041 mol glucose * 180.16 g/mol = 0.73866 g glucose. To convert 0.73866 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 0.73866 g glucose * 1000.0 mg/g = 738.66 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 738.66 mg glucose/10.0 dL = 73.866 mg glucose/dL. The concentration value of 4.1 mmol glucose/L converts to 73.866 mg glucose/dL. 
Plugging in these values into the formula gives us 127.0 mEq/L + 0.024 * (73.866 - 100) = 126.37278 mEq/L.
Hence, the patient's corrected concentration of sodium is 126.37278 mEq/L."
5330,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5434261-1,Extracted,"A 66-year-old man was transferred to our hospital because of confusion, severe general fatigue, and dyspnea of 1-week duration. The patient had chronic kidney disease related to diabetic nephropathy. Although we strongly recommended initiation of chronic HD, the patient refused the treatment.
The patient had a 15-year history of type 2 diabetes mellitus with triopathy. Other medical history included hypertension of unknown duration that was being treated with amlodipine besylate, losartan, and carvedilol. There was no prior history of seizures, neurological symptoms, loss of vision or other underlying illnesses, or use of any other drugs. Upon arrival at our outpatient department, the patient had severe dyspnea.
On admission (day 0), the patient had mild confusion and anasarca. His height was 168 cm; body weight, 74 kg; blood pressure, 124/43 mmHg; and body temperature, 35.7°C. Urinalysis showed 1+ proteinuria and 2+ occult blood, − glucose, and − ketone and urinary sediment revealed 1–4 erythrocytes, 1–4 leukocytes, 1–4 squamous cells, and 0-1 transitional cells per HPF, but no casts. Blood tests showed low hemoglobin (4.6 g/dL), white blood cell count of 5240/µL (82.3% neutrophils, 12.8% lymphocytes, 1.1% eosinophils, 3.6% monocytes, and 0.2% basophils), and thrombocytopenia (platelet count 84 × 103/µL). Blood chemistry showed blood urea nitrogen (BUN) of 222 mg/dL; serum creatinine, 25.4 mg/dL; total protein, 5.7 g/dL; albumin, 3.3 g/dL; lactate dehydrogenase, 403 IU/L; aspartate aminotransferase, 46 IU/L; alanine aminotransferase, 44 IU/L; serum sodium, 139 mmol/L; and serum potassium, 6.1 mmol/L, glucose 97 mg/dL. Serological tests showed C-reactive protein of 0.2 mg/dL. Coagulation parameters were normal. Chest X-ray showed congestion of the lung fields. The patient had pulmonary edema and uremic symptoms (vomiting and consciousness disorder). We performed brain MRI and electroencephalogram (EEG) to evaluate cerebral function.
T2-weighted fluid attenuated inversion recovery (FLAIR) MRI showed several old, small brain infarcts (Figures and ). Diffusion-weighted MR imaging (DWI) did not show increased apparent diffusion coefficient (ADC), which would be suggestive of vasogenic edema. EEG showed frequent slow waves, consistent with metabolic encephalopathy ().
The patient was placed on short-duration HD (2 hours) with smaller surface area (cellulose triacetate; membrane area: 0.7 m2) and low blood flow (100 mL/min) to avoid DDS (). His consciousness gradually improved and he did not develop symptoms of DDS.
On day 15, we repeated MRI and EEG. T2-weighted FLAIR MRI showed increased signal intensities bilaterally in the cortical and subcortical areas of the occipital lobe (Figures and ). DWI demonstrated no hyperintense signal alterations in these regions. He had no cerebral infarcts, but the ADC was elevated in bilateral occipital lesions (Figures and ). Thus, although the patient did not have clinical symptoms of DDS, we diagnosed that he had asymptomatic brain edema. EEG on day 15 had been compared with the findings on admission; namely, the slow waves on EEG had decreased, consistent with improving uremic encephalopathy. The patient underwent vascular access surgery for HD and continued maintenance HD. On day 29, a third MRI was performed and showed return to findings on admission ().
The patient was discharged on regular intermittent HD without any neurological deficits. No further neurological disturbances were noted during 1-year follow-up.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [97.0, 'mg/dL'], 'Sodium': [139.0, 'mmol/L']}",138.928,131.9816,145.8744,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 139.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 139.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 139.0 mmol * 1 mEq/mmol = 139.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mmol sodium/L converts to 139.0 mEq sodium/L. 
The concentration of glucose is 97.0 mg/dL. 
Plugging in these values into the formula gives us 139.0 mEq/L + 0.024 * (97.0 - 100) = 138.928 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.928 mEq/L."
5331,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-4289,Extracted,"A 19-year-old man with unknown medical history is found down on a subway platform and is brought to the hospital by ambulance. He experiences two episodes of emesis en route. In the emergency department, he appears confused and is complaining of abdominal pain. His temperature is 37.0° C (98.6° F), pulse is 94/min, blood pressure is 110/80 mmHg, respirations are 24/min, oxygen saturation is 99% on room air. His mucus membranes are dry and he is taking rapid, deep breathes. Laboratory work is presented below:

Serum:
Na+: 130 mEq/L
K+: 4.3 mEq/L
Cl-: 102 mEq/L
HCO3-: 12 mEq/L
BUN: 15 mg/dL
Glucose: 362 mg/dL
Creatinine: 1.2 mg/dL
Urine ketones: Positive


The patient is given a bolus of isotonic saline and started on intravenous insulin drip.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [362.0, 'mg/dL'], 'Sodium': [130.0, 'mEq/L']}",136.288,129.4736,143.1024,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 130.0 mEq/L. 
The concentration of glucose is 362.0 mg/dL. 
Plugging in these values into the formula gives us 130.0 mEq/L + 0.024 * (362.0 - 100) = 136.288 mEq/L.
Hence, the patient's corrected concentration of sodium is 136.288 mEq/L."
5332,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5010060-1,Extracted,"We report a case of 64-years-old female patient scheduled for replacement of severely stenosed aortic valve (AS) of degenerative etiology. Coronary angiogram was performed, in presurgery period, and revealed as follows: Left main, LAD, CX and RCA showed no signs of coronary disease. Trans thoracic echocardiogram (TTE) verified concentric hypertrophy of the left ventricle (IVS 1.45cm), normal dimension of heart chambers and good Ejection fraction (EF 55%), severe aortic stenosis (AVA less than 1cm2, Vmax5.04m/sec., PGmean62.5mmHg, PGmax102mmHg). In previous medical history patient had verified COPD and was suffering from chest pain and effort dyspnea. Laboratory findings at the day of surgery were as follows: Glucosis 7.10, Urea 9.20, Sodium 140, Potassium 3.8, WBC 6.54, RBC 4.08, Htc 0.367, PLT 202, Preoperative ECG: Regular sinus rithm, Heart rate 103bpm, depressed descending ST junction and R height 25mm in precordial leads V4-V6(signs of LV hypertrophy).","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [7.1, 'mmol/L'], 'Sodium': [140.0, 'mEq/L']}",140.66994,133.63644,147.70344,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.0 mEq/L. 
The concentration of glucose is 7.1 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 7.1 mmol. To convert 7.1 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 7.1 mmol glucose * 0.001 mol/mmol = 0.0071 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0071 mol glucose * 180.16 g/mol = 1.27914 g glucose. To convert 1.27914 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 1.27914 g glucose * 1000.0 mg/g = 1279.14 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1279.14 mg glucose/10.0 dL = 127.914 mg glucose/dL. The concentration value of 7.1 mmol glucose/L converts to 127.914 mg glucose/dL. 
Plugging in these values into the formula gives us 140.0 mEq/L + 0.024 * (127.914 - 100) = 140.66994 mEq/L.
Hence, the patient's corrected concentration of sodium is 140.66994 mEq/L."
5333,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2740289-1,Extracted,"A 54 year old Mexican mestizo man was admitted to the Internal Medicine department of the Regional Hospital Dr. “Valentín Gómez Farías” presenting with altered mental status, paresthesias, hypokalemia, and severe hypertension. The patient worked as a teacher. He was a 10 pack year smoker for 45 years and an occasional drinker. He also has a history of using cocaine and smoking marijuana. He lived a sedentary life, and was obese since childhood, being unable to lose weight with conventional diets. He had no family history of cancer or surgical interventions.
The patient was in good health until three months before admission when he presented with fatigue, intermittent paresthesias of all limbs, cold intolerance, polyuria, weight gain, and irritability. He consulted a primary care physician that made a diagnosis of diabetes mellitus, hypertension, and dyslipidemia and began treatment with Metformin 850 mg twice daily, Glargine insulin 16 units in the morning, Enalapril 10 mg twice daily, and Atorvastatin 20 mg at night. After one month, the patient discontinued the Enalapril on his own. During the next few months the patient presented with generalized edema, abdominal striae, and depressive symptoms. Also two days before admission he presented with confusion. On arrival, the physical exam found him to be obese, with plethoric facies, severe edema of the lower limbs, bruising and red-purple abdominal striae (). He was confused without any sign of focalization or lateralization. His vital signs showed a blood pressure of 210/140 mmHg, heart rate of 62 beats per minute, respiratory rate of 14 per minute, and temperature of 37.2 degree Celsius. Blood biochemistry results were as follows: hypokalemia of 1.8 mEq/L with severe metabolic alkalosis (ph 7.59, HCO3 50.7, pO2 50, Sat O2 90%), white cell count 5740/mmc, hemoglobin 13.1 g/dL, platelets 161,000/mmc, glucose 198 mg/dL, creatinine 0.74 mg/dL, sodium 141 mEq/L, chloride 99 mEq/L, lactic dehydrogenase 702 U/L, ALT 26.7 U/L, CPK 91 U/L, albumin 3.2 g/dL, PT 12 seconds (test 12.4 seconds) INR 0.95, urinary sodium 45.9 mmol/L, urinary potassium 48.2 mmol/L, urine glucose +++, urinary proteins +. The electrocardiogram showed a first degree AV block. The lungs where clear under auscultation. The chest X-ray showed an undefined nodular opacity in the hilar region of the right lung (). We started intravenous administration of large amount of potassium chloride (20 mEq per hour), intravenous insulin, and an intravenous antihypertensive (sodium nitroprusside). Following the treatment he experienced complete remission of mental confusion, and improvement, however his blood pressure did not normalize (150/100 mmHg). In view of these findings a protocol for detecting endocrine hypertension was followed, including tests for Cushing’s syndrome and primary hyperaldosteronism. Forty-eight hours later basal plasma renin activity and aldosterone were measured and determined as normal. The respective values were 0.53 ng/ml/h (normal values between 0.2-2.8 ng/ml/h) and 52.5 pg/mL (normal values between 10-160 pg/mL). The abdominal CT scan showed diffuse enlargement of the adrenal glands without focal lesions, without any abnormalities of the liver or spleen (). The 24 hour free cortisol urinary levels were 6600 μg (normal values 4-100 μg) using the immunoenzymatic method. The ACTH levels were 107 pg/mL (normal values are less than 46 pg/mL), by the quimioluminiscence method. High dose dexamethasone suppression test (8 mg) showed suppression of approximately 8% of the cortisol serum levels. A brain CT scan, including the sellar region was normal. These results, together with the clinical and radiological findings support the diagnostic hypothesis of ectopic ACTH-dependent Cushing’s syndrome. The patient persisted with hypokalemia and hypertension, both of which could not be controlled despite management with large dose of intravenous potassium (up to 240 mEq per day) for the hypokalemia, and Enalapril 20 mgs twice daily, Telmisartan 160 mg four times daily, Felodipine 10 mgs twice daily, and Spironolactone 200 mg four times daily (once primary hyperaldosteronism was excluded) for the hypertension. The concentration of tumor markers were as follows: alpha-fetoprotein of 3.8 ng/ml (normal values 0-15 ng/ml), carcinoembryonic antigen of 2.6 ng/ml (normal values 0-5 ng/ml), and serum glycoprotein CA 125 of 10.96 U/ml (normal values 0-35 U/ml). A chest CT scan showed a cavitated right lung mass localized in the medial lobe of the anterior medial segment and minimal pleural effusion (). We also observed some degree of pleural thickening. On day 24 a CT guided fine-needle lung biopsy was performed, () showing histopathological results of a small cell neoplasm (). The instability of the patient did not allow for the initiation of chemotherapy, therefore treatment with Ketoconazole 400 mgs was begun before initiating chemotherapy. While waiting for the patient’s basal situation to improve before starting chemotherapy, we started ketoconazole 400 mgs twice daily with a rapid normalization of blood pressure and potassium plasma levels. Seventy two hours later the patient presented with sepsis due to a right leg cellulitis that was treated with meropenem. Despite a partial response to the medical treatment the patient worsened and developed bilateral pleural effusions, and respiratory failure that required assisted mechanical ventilation dying a few days later.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [198.0, 'mg/dL'], 'Sodium': [141.0, 'mEq/L']}",143.352,136.1844,150.5196,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 141.0 mEq/L. 
The concentration of glucose is 198.0 mg/dL. 
Plugging in these values into the formula gives us 141.0 mEq/L + 0.024 * (198.0 - 100) = 143.352 mEq/L.
Hence, the patient's corrected concentration of sodium is 143.352 mEq/L."
5334,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-8561,Extracted,"A 60-year-old woman presents to the emergency department with her husband. He is concerned that she has had abnormal behavior and involuntary movements of her body for the last 3 weeks. She now has difficulty remembering names, dates, and events. She even fails to recognize pictures of her children. She was in her normal state of health 3 weeks ago. There is no history of fever, headache, head trauma, drug abuse, or change in medications. Past medical history is significant for type 2 diabetes mellitus. She takes metformin and a multivitamin. Family history is negative for psychiatric illness. Her blood pressure is 134/87 mm Hg, the heart rate is 70/min, and the temperature is 37.1°C (98.8°F). The exam is occasionally disrupted by sudden episodic jerking of her limbs. She is drowsy but arousable to voice, and is disoriented and confused. Extraocular movements are normal. Cranial nerves are intact. There is no neck stiffness. Her laboratory results are significant for:
Hemoglobin 14.3 g/dL
White blood cells 6,900/mm3
Platelets 347,000/mm3
Creatinine 1.0 mg/dL
Sodium 146 mmol/L
Potassium 4.1 mEq/L
Calcium 9.1 mg/dL
Glucose (random) 132 mg/dL
TSH 2.5 mU/L
She is admitted to the neurology service. A head MRI, lumbar puncture, and EEG are performed. The MRI is nondiagnostic. Electroencephalography (EEG) reveals periodic spike and slow waves at an interval of 1 second. Cerebrospinal fluid is positive for protein 14-3-3.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [132.0, 'mg/dL'], 'Sodium': [146.0, 'mmol/L']}",146.768,139.4296,154.1064,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 146.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 146.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 146.0 mmol * 1 mEq/mmol = 146.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 146.0 mmol sodium/L converts to 146.0 mEq sodium/L. 
The concentration of glucose is 132.0 mg/dL. 
Plugging in these values into the formula gives us 146.0 mEq/L + 0.024 * (132.0 - 100) = 146.768 mEq/L.
Hence, the patient's corrected concentration of sodium is 146.768 mEq/L."
5335,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5705885-1,Extracted,"A 20-year-old healthy female presented to the emergency room with confusion, vomiting, and generalized tonic-clonic seizure. She was last seen in her usual state of health 12 hours prior to arrival. Friends reported that she consumed an unknown amount of alcohol and ingested a quarter tablet of MDMA. The patient subsequently became paranoid, attempted to climb up walls, and drank ten bottles of water. She had a witnessed generalized tonic-clonic seizure with frothing at the mouth and recurrent seizure en route the Emergency Department. Both seizures broke spontaneously. Her initial vital signs were notable for a temperature of 38.0 degrees Celsius, heart rate of 88 beats/minute, blood pressure of 140/70 mm Hg, respiratory rate of 14 per minute, and oxygen saturation of 97% on room air. The patient was obtunded, and pupils were dilated, equal, and reactive to light bilaterally. Mucus membranes were moist. Neck was supple. Lung auscultation demonstrated good air entry with bilateral rhonchi. Cardiovascular examination was normal without any murmurs, rubs, or gallops. Abdominal exam was normal. Neurologic examination was limited but the patient had normal extremity tone, hyporeflexia was noted in biceps, triceps, knees, and ankles bilaterally, clonus was absent, and normal bilateral Babinski reflexes were noted. She received 10 mg of IV lorazepam for additional seizures and was intubated for airway protection. A summary of relevant laboratory findings is mentioned in . Her initial complete blood count had a white blood cell count of 20,600/μliter, hemoglobin of 12.8 g/dl, and platelet count of 233,000/μliter. Her chemistry panel was as follows: sodium 112 mmol/L, potassium 3.5 mmol/L, chloride 84 mmol/L, bicarbonate 16 mmol/L, blood urea nitrogen of 7 mg/dl, serum creatinine of 0.5 mg/dl, and serum glucose of 117 mg/dl. A liver function panel was normal.
Serum lactic acid was 2.8 and osmolality was 239 mmol/L. Urine chemistries were significant for a urine sodium 112 mmol/L and urine osmolality of 439 mmol/L. The urine electrolytes were checked prior to administration of any hypertonic saline. These electrolyte derangements suggested a state of syndrome of inappropriate antidiuretic hormone (SIADH). She received three doses of 3% hypertonic normal saline without a significant change in her serum sodium. A brain computed tomography (CT) scan showed cerebral edema.
Over the next couple of hours, she had increasing oxygen requirements on the ventilator of up to 100% FiO2 and a positive end-expiratory pressure of 20 mm Hg. The initial chest-radiograph was concerning for multifocal pneumonia; however a repeat chest-radiograph, twelve hours later, revealed diffuse bilateral hazy opacities concerning for acute respiratory distress syndrome (ARDS). Her blood gas analysis showed a pH of 7.28 with PaO2 of 53 mm Hg and an alveolar-arterial oxygen gradient of 492 mm Hg. Her PaO2 : FiO2 ratio was 53 suggesting severe ARDS. At that time, she was paralyzed with cis-atracurium and started on inhaled nitric oxide as salvage therapy. She subsequently developed hemodynamic compromise and was started on norepinephrine, ultimately requiring addition of vasopressin and dopamine to maintain stable hemodynamics. Finally, venovenous extracorporeal membrane oxygenation (ECMO) was started with immediate resolution of hypoxemia. Hyponatremia was corrected gradually with 3% hypertonic saline that led to resolution of altered mental status and improvement in hypoxemia. She was gradually weaned off of ECMO and extubated within three days.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [117.0, 'mg/dL'], 'Sodium': [112.0, 'mmol/L']}",112.408,106.7876,118.0284,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 112.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 112.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 112.0 mmol * 1 mEq/mmol = 112.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 112.0 mmol sodium/L converts to 112.0 mEq sodium/L. 
The concentration of glucose is 117.0 mg/dL. 
Plugging in these values into the formula gives us 112.0 mEq/L + 0.024 * (117.0 - 100) = 112.408 mEq/L.
Hence, the patient's corrected concentration of sodium is 112.408 mEq/L."
5336,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2767133-1,Extracted,"A 62-year-old Caucasian man was diagnosed with decompensated liver cirrhosis secondary to hepatitis C virus infection in 2002. He was hospitalized because of HE several times during 2004.
In November 2004, the patient was admitted to the emergency department because of personality changes that developed four hours after a lot of vomiting. After admission, loss of consciousness and respiratory distress occurred. He had a history of surgical operation to the right kidney due to nephrolithiasis approximately 29 years previously. Medications before admission included propranolol, aldactone, lactulose and ursodeoxycholic acid. Physical examination on admission indicated a blood pressure of 100/70 mmHg, heart rate 68 beats/minute and respiratory rate 24/min. There was mild jaundice, fetor hepaticus, splenomegaly (3 cm below costal margin) and a hernial sac about 20 cm in diameter at the right lumbar incision, reducible with difficulty (). After administering first aid, the patient was transferred to the internal medicine ward.
Admission laboratory tests were as follows: hemoglobin 11.6 g/dl, leukocytes 4,000/mm3, platelets 49,000/mm3, sodium 133 mEq/l, potassium 2.5 mEq/l, glucose 115 mg/dl, creatinine 0.7 mg/dl, alkaline phosphatase 220 U/L, aspartate aminotransferase (AST) 18 U/L, alanine aminotransferase (ALT) 30 U/l, γ-glutamyl transpeptidase 20 U/l, total bilirubin 4 mg/dl, direct bilirubin 2.1 mg/dl, total protein 5.7 g/dl, albumin 2.2 mg/dl, activated partial thromboplastin time 25 sec, prothrombin time: 15 sec, and international normalized ratio (INR) 1.2. The plasma ammonia level on admission was 422 μg/dl (normal range 25 to 94 μg/dl). His Child-Pugh score was 10 (Child’s class C). The model for end-stage liver disease (MELD) score was 14.
Nasogastric suction was performed and approximately 2,000 ml dark green bile aspirated. The patient received intravenous 40 mEq of potassium chloride (at a rate of 20 mEq/hour) over a period of 2 hours in the emergency department. Thereafter, intravenous potassium supplements in saline and in dextrose solution were given and an enema containing lactulose and ampicillin was given twice a day for 10 days. The patient recovered consciousness after the correction of the hypokalemia. Subsequently, the previous drug therapy was re-established.
Plain abdominal radiography taken in the upright position demonstrated no air-fluid levels, suggesting small bowel obstruction. Abdominal ultrasonography showed parenchymal inhomogeneity of the liver with irregular margins, splenomegaly (with a craniocaudal diameter of 157 mm), a large splenic vein, and a hernial sac sized 21 × 13 × 9.5 cm located in the right lumbar region. Magnetic resonance imaging revealed a 6.5 cm fascial defect and mesenteric fatty tissue and bowel as the content of the hernial sac but with no sign of incarceration (). A barium-contrast study of the small intestine showed that the hernial sac contained gastric antrum, duodenum and proximal jejunum (). Upper gastrointestinal endoscopy revealed straight, small-sized (F1) varices over the lower third of the esophagus and food retention, despite the patient fasting for at least 12 hours. Furthermore, a decentralization and deviation of the pylorus and antrum were observed.
The condition of the patient was discussed with the general surgeons. Repair of the hernia was not recommended because of the high risk of general anesthesia and operation and the high rate of postoperative mortality in patients with cirrhosis.
After two weeks, we observed a second episode of HE precipitated by a large volume of vomiting (approximately 2000 ml). Hypokalemia was again evident, and the patient lost consciousness, necessitating intravenous potassium administration. Three similar episodes were observed during the hospitalization period. During all of these episodes, his serum potassium concentration fell rapidly following a large volume of vomiting and the hernia sac collapsed. When the hernia sac was reduced, copious amount of bilious fluid flowed from the nasogastric tube.
shows the neurological and laboratory findings of all hepatic encephalopathy episodes observed during the hospital stay.
The patient was discharged 10 weeks after admission and he died 15 months later.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [115.0, 'mg/dL'], 'Sodium': [133.0, 'mEq/L']}",133.36,126.692,140.028,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 133.0 mEq/L. 
The concentration of glucose is 115.0 mg/dL. 
Plugging in these values into the formula gives us 133.0 mEq/L + 0.024 * (115.0 - 100) = 133.36 mEq/L.
Hence, the patient's corrected concentration of sodium is 133.36 mEq/L."
5337,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4766335-1,Extracted,"A twelve-year-old girl, with past medical history of Dravet syndrome and developmental delay, presented to our hospital emergency department with altered sensorium, one-day history of fever up to 105.6 F, decreased oral intake and urine output, fatigue, and intermittent cough. Seizure frequency was unchanged. Her home medications were valproic acid, clobazam, potassium bromide, and diazepam. On arrival to the emergency room she was found to be hypotensive (65/39 mmHg), tachycardic, and febrile. She received two normal saline boluses. Her laboratory results in emergency room included serum sodium 143 mEq/L, potassium 4.3 mEq/L, chloride 171 mEq/L, bicarbonate 24 mEq/L, Blood Urea Nitrogen (BUN) 12 mg/dL, serum creatinine 0.57 mg/dL, calcium 9.2 mg/dL, blood glucose of 60 mg/dL, and valproic acid level 23.7 mcg/L (therapeutic level 50–100 mcg/L), and normal liver function tests were performed. Her capillary blood gas revealed pH 7.40, PCO2 37.1 mmHg, bicarbonate 23.2 mEq/L, and base deficit −1 mEq/L. In the pediatric intensive care unit (PICU) patient remained stable, received intravenous fluids, was tested positive for influenza, and started on oseltamivir. Repeat electrolyte panel on multiple occasions, as shown in , had hyperchloremia (154–171 mEq/L) with negative anion gap (−40 to −52 mEq/L). Due to persistent hyperchloremia and as the patient takes potassium bromide for the past two years for refractory seizures possibility of bromide toxicity was considered. On day one of admission to PICU, potassium bromide therapy was stopped and serum bromide level was sent. The bromide level was 691 mcg/mL (normal therapeutic range 200–1000 mcg/mL). Despite normal bromide level in our patient potassium bromide was temporarily withheld and continued on IV hydration therapy. Over the next three days serum chloride and child's clinical condition improved.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [60.0, 'mg/dL'], 'Sodium': [143.0, 'mEq/L']}",142.04,134.938,149.142,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 143.0 mEq/L. 
The concentration of glucose is 60.0 mg/dL. 
Plugging in these values into the formula gives us 143.0 mEq/L + 0.024 * (60.0 - 100) = 142.04 mEq/L.
Hence, the patient's corrected concentration of sodium is 142.04 mEq/L."
5338,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3186895-1,Extracted,"Case : A 30-year-old male was admitted to our hospital with general weakness and drowsy mental status. He had eaten only 3-4 spoons of brown rice and fresh vegetable without salt for 3 months to treat his tic disorder, and he had been in bed-ridden state. He had taken propolis and enema by himself, and his past medical history was unremarkable except tic disorder since high school. His blood pressure was 100/70 mm Hg, pulse rate 72/min, and respiratory rate 18/min, body temperature 36℃. He had lost 14 kg in the past 3 months. Physical examination presented cracking over his skin around his neck and both shoulders.
Serum laboratory results were as follows; hemoglobin 16.2 g/dL, white blood cell (WBC) 4.9 × 103/µL, platelet 201 × 103/µL, total protein 5.6 g/dL, albumin 3.4 g/dL, aspartate aminotransferase (AST) 114 IU/L, alanine aminotransferase (ALT) 101 IU/L, alkaline phosphatase (ALP) 57 IU/L, γ-glutamyl transferase (GGT) 13 IU/L, bilirubin (total/direct) 3.22/0.8 mg/dL, glucose 166 mg/dL, amylase 98 IU/L, blood urea nitrogen (BUN) 33.6 mg/dL, creatinine 0.41 mg/dL, total CO2 20.2 mEq/L, sodium 101 mEq/L, potassium 4.0 mEq/L, chloride 68 mEq/L, calcium 6.8 mg/dL, inorganic phosphorus 2.7 mg/dL, magnesium 1.5 mEq/L, uric acid 1.0 mg/dL, C-reactive protein (CRP) 1.87 mg/dL, osmolality 213 mOsm/kg H2O, creatine phosphokinase (CPK) 1,472 IU/L (29-145), myoglobin 1,278 ng/mL, lactate dehydrogenase (LDH) 1,472 IU/L (0-500), total cholesterol 231 mg/dL, triglyceride 97 mg/dL, high density lipoprotein (HDL)-cholesterol 127 mg/dL, low density lipoprotein (LDL)-cholesterol 83 mg/dL, prealbumin 10.7 mg/dL, hemoglobin A1c 5.4%, thyroid stimulating hormone (TSH) 1.26 uIU/mL, free T4 0.75 ng/dL, and international normalized ratio (INR) 1.61. Urinalysis revealed a specific gravity of 1.012, pH 7.0, trace protein, glucose 2+, occult blood 3+, myoglobin 2,687 ng/m, urine sodium 62 mEq/L, potassium 34.4 mEq/L, chloride 43.1 mEq/L, and osmolality 484 mOsm/kg H2O.
Chest AP X-ray showed mediastinal emphysema and extensive soft tissue emphysema in his neck and chest wall. Abdominal ultrasonography revealed a small amount of ascites and small amount of fluid collection in his bilateral perinephric space. Chest CT showed extensive soft tissue emphysema in his neck and chest wall, extensive mediastinal emphysema, small right pneumothorax, and pericardial fluid (). To rule out esophageal perforation esophagography with gastrographin was performed and it showed no evidence of contrast leakage from his esophagus. The diagnosis of orthorexia nervosa with hyponatremia, rhabdomyolysis, pneumomediastinum, pneumothorax, and soft tissue emphysema was made. We started on intravenous fluid supplementation based on treatment of hyponatremia and refeeding syndrome, and oral feeding. He gradually improved, but his total protein and albumin decreased on the 5th hospital day to 4.4 g/dL and 2.5 g/dL, respectively. On the 7th hospital day, his platelet and WBC levels decreased to 27 × 103/µL and 1.2 × 103/µL, respectively. On the 12th hospital day his hemoglobin level decreased to 7.2 g/dL from his hospital 2nd day. Peripheral blood smear showed normochromic normocytic anemia with anisopoikilocytosis 2+, neutropenia, lymphocytopenia, relative monocytosis 14%, and thrombocytopenia. His iron level was 88 µg/dL, total iron binding capacity (TIBC) 168 µg/dL, ferritin 908.6 ng/mL, vitamin B12 988 pg/mL, folate 2.8 ng/mL, and his Coomb's test, plasma hemoglobin, haptoglobin, and serology were within normal limits. We transfused 6 units of platelet concentrate by his hospital 7th day and granulocyte colony-stimulating factor (G-CSF) 150 µg due to absolute neutrophil count (ANC) 560 and methicillin-susceptible Staphylococcus aureus (MSSA) bacteremia by his hospital 16th day. By his hospital 8th day, serum laboratory results were as follows; sodium 138 mEq/L, potassium 3.7 mEq/L, chloride 99 mEq/L, calcium 8.1 mg/dL, inorganic phosphorus 1.9 mg/dL, magnesium 1.4 mEq/L, total CO2 32.5 mEq/L, osmolality 271 mOsm/kg H2O, CPK 270 IU/L, myoglobin 57.8 ng/mL, LDH 1,011 IU/L, and total cholesterol 140 mg/dL. By hospital 18th day, his AST level was 25 IU/L, ALT 59 IU/L, ALP 89 IU/L, bilirubin (total/direct) 0.35/0.12 mg/dL, and by hospital 28th day, his LDH was 514 IU/L. Until his hospital 20th day, his platelet level steadily increased to 1,475 × 103/µL, and gradually decreased to 382 × 103/µL by the hospital 37th day. By his hospital 37th day, his hemoglobin increased to 12.1 g/dL and WBC also stabilized to 3.4 × 103/µL (neutrophil 48%).
He was discharged by his hospital 38th day in an improving state, and followed up at our rehabilitation department for physical therapy and psychological department for supportive therapy.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [166.0, 'mg/dL'], 'Sodium': [101.0, 'mEq/L']}",102.584,97.4548,107.7132,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 101.0 mEq/L. 
The concentration of glucose is 166.0 mg/dL. 
Plugging in these values into the formula gives us 101.0 mEq/L + 0.024 * (166.0 - 100) = 102.584 mEq/L.
Hence, the patient's corrected concentration of sodium is 102.584 mEq/L."
5339,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6037803-3,Extracted,"An 18-year-old girl presented with fatigue, anorexia, indigestion, constipation, and postprandial abdominal pain. She was diagnosed with cecal diverticulosis 5 years earlier, and Helicobacter pylori (HP)-positive gastric ulcer 1 year earlier. A previous UGI endoscopic examination showed no polyp in her stomach. On laboratory examination, WBC was 8,200/mm3, with polymorphonuclear cell 65%, hemoglobin 13.6 g/dL, and platelet count 205×103/mm3. Electrolytes levels showed sodium 142 mmol/L, potassium 4.4 mmol/L and chloride 106 mmol/L. The protein level was 7.4 g/dL, albumin 4.7 g/dL, calcium 9.3 mg/dL, phosphorus 4.7 mg/dL, cholesterol 167.9 mg/dL, glucose 99 mg/dL, BUN 10.1 mg/dL, creatinine 0.77 mg/dL, total bilirubin 0.35 mg/dL, AST 14 U/L, ALT 5 U/L, ESR 10 mm/hour, and CRP <0.3 mg/dL. UGI endoscopy revealed nodular gastritis in the antrum and a polyp of sessile type in the prepyloric area. Polypectomy was performed. The size of the polyp was 0.8×0.6×0.5 cm. She was negative to HP at the time of polypectomy. The pathological finding was HPP (). She was treated with medicines for her UGI mucosal lesions and the previous GI symptoms were resolved. Follow-up UGI endoscopy would be performed in one year.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [99.0, 'mg/dL'], 'Sodium': [142.0, 'mmol/L']}",141.976,134.8772,149.0748,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 142.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 142.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 142.0 mmol * 1 mEq/mmol = 142.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mmol sodium/L converts to 142.0 mEq sodium/L. 
The concentration of glucose is 99.0 mg/dL. 
Plugging in these values into the formula gives us 142.0 mEq/L + 0.024 * (99.0 - 100) = 141.976 mEq/L.
Hence, the patient's corrected concentration of sodium is 141.976 mEq/L."
5340,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4616927-1,Extracted,"A twenty-three-year-old man was admitted to the emergency room of an infectious disease hospital in Northeast Brazil with a one-month history of daily fever associated to diarrhea with mucus and weight loss of fifteen kilograms in six months. One week prior to admission, the patient's clinical picture worsened with headache, vomiting, disorientation and generalized tonic-clonic seizures. The patient also had a history of diabetes mellitus, tobacco smoking, alcoholism and drug addiction. He had no prior history of hospitalization. Upon physical examination the patient was pale, disoriented, and had periods of agitation. He had rhonchi on the pulmonary auscultation. Abdomen was tender on palpation of the upper right quadrant, liver and spleen were not palpable and no edema was seen in the lower extremities. Nuchal rigidity and meningeal irritation signs were present, however motor deficit was not identified.
Laboratory tests upon admission showed hemoglobin 10 g/dL, 3,440 leukocytes/mm, (4% bands, 45% neutrophils, 5% lymphocytes), 83,000 platelets/mm, urea was 19 mg/dL, creatinine 0.7 mg/dL, ionic calcium 1.23 mEq/L, sodium 130 mEq/L, potassium 4.2 mEq/L, and liver enzymes (ALT and AST) were within normal limits; lactic dehydrogenase was 494 IU/L. Cerebrospinal fluid (CSF) analysis revealed 10 white blood cells/mm (58% neutrophils, 31% lymphocytes, 11% monocytes) and 2 red blood cells/mm. CSF glucose was 122 mg/dL and protein 36 mg/ dL. India ink test revealed six Cryptococcus yeasts/mm. VDRL test was negative and anti-HIV test positive. CD4 count was 40/mm. Blood glucose was 344 mg/dL. Intravenous hydration, insulin, phenytoin, fluconazole, pyrimethamine, sulfadiazine, folinic acid, and amphotericin B were started. The patient did not improve and became obtunded and hypotensive. He was then intubated and put on mechanical ventilation. Arterial blood gases after intubation: pH 7.52, PaCO2 28.9 mmHg, HCO3 26.6 mmEq/L, PaO2 77.9 mmHg, SaO2 96.6% and FiO270%. Vasoactive drugs were added and the patient died less than 24 hours after admission. A post-mortem examination was performed and revealed disseminated cryptococcosis. The histopathology of the kidneys revealed severe renal involvement with Cryptococcus sp. in the glomerulus and interstitium ().","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [344.0, 'mg/dL'], 'Sodium': [130.0, 'mEq/L']}",135.856,129.0632,142.6488,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 130.0 mEq/L. 
The concentration of glucose is 344.0 mg/dL. 
Plugging in these values into the formula gives us 130.0 mEq/L + 0.024 * (344.0 - 100) = 135.856 mEq/L.
Hence, the patient's corrected concentration of sodium is 135.856 mEq/L."
5341,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4830054-1,Extracted,"A 33-year-old Nigerian man who presented with HIV infection was commenced on HAART (tenofovir 300 mg, emtricitabine 200 mg, and efavirenz 600 mg) for about 1 month and then developed generalized tonic-clonic seizures that occurred once in 3 months. He had no preceding history of seizures or family history of seizures, nor did he have any history suggestive of CNS infection or any use of psychotropic drugs or other form of drug treatment.
His clinical examination results were normal. His blood pressure was 120/80 mmHg; his baseline CD4 count was 130 cells/mm3; his blood sodium and glucose levels were normal at 137 mmol/L and 5.5 mmol/L, respectively; and his urea and creatinine were also within normal limits. Although his magnetic resonance imaging findings were unremarkable, an electroencephalogram showed intermittent bursts of high-voltage sharp waves and spikes bilaterally over frontotemporoparietal regions, consistent with complex partial seizures (Fig. ). The patient was initially administered sodium valproate with no appreciable control of seizures. His efavirenz plasma level was measured using high-performance liquid chromatography and was found to be 209.55 μg/ml. Efavirenz was subsequently replaced with nevirapine, resulting in instant resolution of his seizures. He has been seizure free for 3 years and has not required the use of any anticonvulsant. A repeat electroencephalogram showed no sign of seizure activity (Fig. ).","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [5.5, 'mmol/L'], 'Sodium': [137.0, 'mmol/L']}",136.97811,130.1292,143.82702,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 137.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 137.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 137.0 mmol * 1 mEq/mmol = 137.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mmol sodium/L converts to 137.0 mEq sodium/L. 
The concentration of glucose is 5.5 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 5.5 mmol. To convert 5.5 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 5.5 mmol glucose * 0.001 mol/mmol = 0.0055 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0055 mol glucose * 180.16 g/mol = 0.99088 g glucose. To convert 0.99088 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 0.99088 g glucose * 1000.0 mg/g = 990.88 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 990.88 mg glucose/10.0 dL = 99.088 mg glucose/dL. The concentration value of 5.5 mmol glucose/L converts to 99.088 mg glucose/dL. 
Plugging in these values into the formula gives us 137.0 mEq/L + 0.024 * (99.088 - 100) = 136.97811 mEq/L.
Hence, the patient's corrected concentration of sodium is 136.97811 mEq/L."
5342,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7769497-1,Extracted,"A 52-year-old Caucasian male with a significant past medical history of COPD, diabetes mellitus type 2, essential hypertension and chronic back pain presented to the emergency room with diffuse abdominal pain. The patient reported associated abdominal swelling with 3 episodes of nausea and vomiting in the past day. The patient also reports having felt lightheaded for the past couple weeks and reports falling 2 weeks ago. On arrival, the patient was afebrile with a blood pressure of 60/40, heart rate of 74, respiratory rate of 14 and saturating 98% on room air. Labs obtained were significant for a Na:130, Glucose: 115, BUN:46, Cr:4.3 (baseline:0.8), WBC:20.9, blood cultures grew gram + cocci. The patient denies drinking alcohol, smoking cigarettes or consuming anything corrosive. After not responding to fluids, a central line was placed and Norepinephrine started. CT of the abdomen demonstrated air within the wall of the stomach, portal veins and perigastric veins at which point surgery was consulted. After admission to the ICU, a follow-up EGD demonstrated Emphysematous gastritis secondary to gastric mucosal necrosis particularly in the proximal stomach just below the GE junction. The patient had already been placed on Piperacillin/Tazobactam and Metronidazole before admission to the ICU and after blood cultures came back positive for gram + cocci, Vancomycin was added. The following day the patient continued to complain of severe pain and follow up CT abdomen/pelvis demonstrated interval gastric perforation with mild free air within the upper abdomen and fluid within the posterior gastric wall representing gastric necrosis with perforation along with interval development of mild pneumoperitoneum (Figures , ).
He was taken to surgery and underwent a subtotal gastrectomy with splenectomy due to becoming hypotensive during the procedure and the fear that attaching his distal esophagus to the jejunum at that point would result in poor perfusion. The decision was made to close him up and go back in a few days. Things became even more interesting when wound cultures taken during surgery came back positive for both yeast and streptococcus parasanguinis. Follow-up blood cultures were also positive for yeast. Micafungin was started at that point. He went back to surgery where his esophagus was found to have retracted into his chest, as well as his abdominal mesh being covered with pus. As much pus was cleared out as possible and was closed back up. In order to attach his esophagus to his jejunum, a thoracic surgical approach would need to be done for which the patient was not stable enough to perform. Peritoneal fluid cultures taken during the procedure grew yeast. With fungemia in his bloodstream, TPN had to be stopped. ID recommended stopping zosyn and adding meropenem. He remained intubated in the ICU where his family made the decision to compassionately extubate and make him comfort care. Culture wound results that had been sent for identification of the fungal species came back positive for Candida Glabrata.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [115.0, 'mg/dL'], 'Sodium': [130.0, 'mEq/L']}",130.36,123.842,136.878,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 130.0 mEq/L. 
The concentration of glucose is 115.0 mg/dL. 
Plugging in these values into the formula gives us 130.0 mEq/L + 0.024 * (115.0 - 100) = 130.36 mEq/L.
Hence, the patient's corrected concentration of sodium is 130.36 mEq/L."
5343,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-3517,Extracted,"A 58-year-old man is brought to the emergency department after a witnessed tonic-clonic seizure. His wife says he has had a persistent dry cough for 6 months. During this time period, he has also had fatigue and a 4.5-kg (10-lb) weight loss. The patient has no history of serious illness and does not take any medications. He has smoked 1 pack of cigarettes daily for 35 years. He is confused and oriented only to person. Laboratory studies show a serum sodium concentration of 119 mEq/L and glucose concentration of 102 mg/dL. An x-ray of the chest shows an irregular, poorly demarcated density at the right hilum.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [119.0, 'mEq/L'], 'Glucose': [102.0, 'mg/dL']}",119.048,113.0956,125.0004,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 119.0 mEq/L. 
The concentration of glucose is 102.0 mg/dL. 
Plugging in these values into the formula gives us 119.0 mEq/L + 0.024 * (102.0 - 100) = 119.048 mEq/L.
Hence, the patient's corrected concentration of sodium is 119.048 mEq/L."
5344,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6232278-1,Extracted,"A 35-year-old male with a past medical history of diabetes mellitus type 2, hypercholesterolemia and recurrent boils from methicillin-resistant Staphylococcus aureus (MRSA) initially presented with a right axillary boil. The patient reported that 5 days prior he noticed a red, hot area under his right arm which then progressed to a boil that spontaneously ruptured. Over the course of the next several days the boil drained foul smelling fluid and became progressively more painful causing him to seek medical attention. He reported subjective fevers during the first 2 days of his symptoms, but the fevers resolved after the boil ruptured. He denied any other symptoms.
Upon examination the patient was alert and oriented and was noted to have an area of black necrotic skin in his right axilla, with surrounding erythema and associated induration on the right chest wall (Fig. ). On admission his heart rate was 132 beats per minute, blood pressure 116/80 mmHg, temperature 38.3°C, respirations 30 per minute and oxygen saturation 96% on room air. Laboratory studies revealed a white blood count of 26.2 K cells/dL, hemoglobin of 13.2 g/dL, sodium of 129 mEq/L, glucose of 289 mg/dL, serum creatinine of 0.9 mg/dL, C-reactive protein of 36.8 mg/dL, hemoglobin A1C of 13.5% and lactate of 3.3 mmol/L. The remaining laboratory values were within normal limits. The patient’s calculated Laboratory Risk Indicator for Necrotizing Fasciitis score was 10 points, supporting the clinical diagnosis of NSTI []. A computed tomography scan revealed a moderate amount of subcutaneous gas within the soft tissue of the right axilla and lateral chest wall along with surrounding edema.
The patient was started on linezolid and piperacillin–tazobactam for broad-spectrum coverage. He was taken emergently to the operating room for sharp debridement of skin, subcutaneous tissue, fascia and muscle of the right axilla and lateral chest wall. Intraoperatively a large amount of purulent and necrotic tissue was found. Fluid and tissue cultures were taken. The excised area measured 17 × 9 × 6 cm3 (Fig. ). The patient underwent a subsequent operation for further debridement and returned to the operating room 3 days after that for delayed primary closure over a drain (Fig. ). On hospital Day 6, the initial operative cultures returned with abundant growth of Kocuria rosea and rare growth of coagulase negative Staphylococcus. Although susceptibility studies were not performed, literature has shown Kocuria to be susceptible to commonly used antibiotics []. The patient’s antibiotics were narrowed to intravenous ampicillin–sulbactam and linezolid while he remained in the hospital. The patient was discharged on hospital Day 9 on oral amoxicillin–clavulanate and linezolid to complete a 14-day antibiotic course. Although the culture data did not support the use of linezolid, it was continued given his past history of recurrent MRSA boils. He returned to the outpatient clinic 27 days after wound closure for drain and suture removal. The patient had no follow-up complications and was released from the surgical service.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [289.0, 'mg/dL'], 'Sodium': [129.0, 'mEq/L']}",133.536,126.8592,140.2128,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 129.0 mEq/L. 
The concentration of glucose is 289.0 mg/dL. 
Plugging in these values into the formula gives us 129.0 mEq/L + 0.024 * (289.0 - 100) = 133.536 mEq/L.
Hence, the patient's corrected concentration of sodium is 133.536 mEq/L."
5345,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4286777-1,Extracted,"A 76-year-old woman came into our Emergency Department due to the loss of consciousness and a seizure. The patient was given an oral prescription of MC-SP complex (Picolight powder, Pharmbio Korea Co., Seoul, Korea) for the colonoscopy. She orally took one pack (10-mg sodium picosulfate, 3.5-g magnesium citrate) with 150 mL of water. Within 3 hours of her first dose of MC-SP, she suffered diarrhea, and about 11 hours after taking the first medicine, she suffered nausea, vomiting, and then symptoms of decreased energy and seizure accompanied by ocular deviation. Seizures lasted for 2-3 minutes. When she arrived at the Emergency Department, loss of consciousness was evident, but there were no signs of seizure. She had no history of seizures. About 5 years earlier, she had been taking levothyroxine sodium, 0.05 mg, (Synthroid, Bukwang Pharm, Seoul, Korea), atorvastatin calcium, 10 mg, (Lipinon, Dong-A Pharm, Seoul, Korea), hydrochlorothiazide, 12.5 mg (Dichlozid, Yuhan Pharm, Seoul, Korea), propranolol, 10 mg twice a day (Indenol, Dongkwang Pharm, Seoul, Korea), and diazepam, 2 mg (Myungin Diazepam, Myung In Pharm, Seoul, Korea) for hypothyroidism, hyperlipidemia, hypertension and depression, respectively. She had no family history of specific medical diseases. She had no history of alcohol consumption or smoking.
Upon arrival, her blood pressure was 150/90 mmHg, her pulse rate was 83 times per minute, her respiratory rate was 20 times per minute, her body temperature was 36℃, her blood glucose was 205 mg/dL, and her oxygen saturation level was 92%. The patient looked very sick and vomited continuously. On both sides, the pupil reflex was normal, and no signs of nystagmus manifested. The consciousness of the patient was vague. She couldn't respond to questions and could not even follow verbal instructions. According the Glasgow Coma Scale, her rating was 8 points, which is referred to as semicoma state. Auscultation of the abdomen produced no specific finding. During chest auscultation of both sides of the lower lung, rales were auscultated. Chest radiography showed a shadow increasing on both lower lung field, but there were no specific findings on the electrocardiogram.
Arterial blood gas analysis showed pH, 7.532, pCO2, 27.4 mmHg, pO2, 56.5 mmHg, HCO3, 22.5 mmol/L, base excess, 1.1 mmol/L, and oxygen saturation, 88.5%, indicating that she had acute respiratory alkalosis. In serum biochemical tests, the total calcium level was 8.2 mg/dL (reference value, 8.8-10.8 mg/dL), the ionized calcium level was 0.80 mmol/L (reference value, 1.0-1.2 mmol/L) and phosphate was 2.4 mg/dL (reference value, 2.4-5.1 mg/dL), indicating hypocalcemia and hypophosphatemia. Blood urea nitrogen was 9.6 mg/dL (reference value, 9-23 mg/dL), and the creatinine level was 0.6 mg/dL (reference value, 0.7-1.3 mg/dL), indicating no abnormality. The serum sodium level was 112 mEq/L (reference value, 132-146 mEq/L), and the potassium level was 2.4 mEq/L (reference value, 3.5-5.0 mEq/L), indicating hypokalemia and hyponatremia. The serum osmolality had decreased to 240 mOsmol/kg (reference value, 289-308 mOsmol/kg), and the urine osmolality was 370 mOsmol/kg (reference value, 300-900 mOsmol/kg). The fasting blood glucose level was 205 mg/dL, Hg A1C was 7.1% (reference value, 4.4%-6.4%), thyroid-stimulating hormone was 0.99 µIU/mL (reference value, 0.55-4.78 µIU/mL), free thyroxine (fT4) was 1.78 ng/dL (reference value, 0.89-1.8 ng/dL) at 8 AM. Cortisol was 46.88 µg/dL (reference value, 4.3-22.4 µg/dL), and at 8 AM. Aadrenocorticotropic hormone (ACTH) was 134.7 pg/dL (reference value, 5-50 pg/mL). The cortisol and ACTH levels had increased.
The brain computed tomography showed no acute brain lesions, such as bleeding (), and the brain magnetic resonance imaging showed no specific lesions. Magnetic resonance angiography showed no specific lesions associated with her current symptoms. She was diagnosed as having hyponatremia accompanied by vomiting and neurological symptoms, such as unconsciousness and seizures, and accompanied by aspiration pneumonia with respiratory alkalosis. To the treat pneumonia, we gave her antibiotics, and to treat the hyponatremia, we gave her an intravenous injection of 3% saline. We aimed to increase her sodium level to 124 mEq/L, so we injected 3% saline at a rate of 20 mL/hr for 24 hours, which corresponded to a corrected rate of 0.4 mEq/L. After 24 hours, she got had recovered to a 124-mEq/L level of serum sodium, and she was in a lethargy state. However, she was not completely oriented and could not questions. Symptoms, including vomiting and nausea, remained. After 48 hours, she had fully recovered to a 132-mEq/L level of serum sodium, her consciousness was normal, and even her symptoms of vomiting and nausea had disappeared. After that, she showed no neurological symptoms, such as seizures or unconsciousness.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [205.0, 'mg/dL'], 'Sodium': [112.0, 'mEq/L']}",114.52,108.794,120.246,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 112.0 mEq/L. 
The concentration of glucose is 205.0 mg/dL. 
Plugging in these values into the formula gives us 112.0 mEq/L + 0.024 * (205.0 - 100) = 114.52 mEq/L.
Hence, the patient's corrected concentration of sodium is 114.52 mEq/L."
5346,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4035763-1,Extracted,"A 66-year-old Caucasian woman with type 2 diabetes presented to our emergency department with a three-week history of generalized malaise, associated poor oral intake, and some diarrhea. Her enteric symptoms were vague and unquantifiable. She was obese and had a past medical history of poorly controlled type 2 diabetes for 15 years, hypertension, asthma, and depression. Her regular medication comprised metformin 3g daily, modified-release gliclazide 60mg daily, aspirin 100mg daily, atorvastatin 40mg daily, ramipril 10mg daily, and hydrochlorothiazide 25mg daily. Our patient was brought into hospital by ambulance; her pre-hospital observations were as follows: Glasgow Coma Scale score, 15; blood sugar level, 2.8mmol/L; blood pressure, 90/40mmHg; pulse, 54 beats per minute; respiratory rate, 32 breaths per minute; and peripheral oxygen saturation, 98% on 8L oxygen via a variable oxygen delivery mask. On arrival to our emergency department, she was confused with a Glasgow Coma Scale score of 14 out of 15 (E4V4M6), with the rest of her physiological parameters similar to her pre-hospital observations.
Her initial investigations were as follows: serum sodium, 140mmol/L (normal range: 137 to 145mmol/L); serum potassium, 7.3mmol/L (normal range: 3.5 to 4.9mmol/L); serum chloride, 91mmol/L (normal range: 100 to 109mmol/L); serum bicarbonate, 1mmol/L (normal range: 22 to 32mmol/L); anion gap, 55mmol/L (normal range: 7 to 17mmol/L); serum glucose, 2.3mmol/L; urea, 30.8mmol/L (normal range: 2.7 to 8.0mmol/L); and serum creatinine, 768umol/L (normal range: 50 to 100umol/L). Results from liver function tests were normal. Her troponin level was 50ng/L (normal range: <30ng/L). Venous blood gas measurements revealed a profound metabolic acidemia: pH, 6.58; partial pressure of CO2, 38.6mmHg; HCO3, 3.6mmol/L; glucose, 2.0mmol/L; and lactate, 16.7mmol/L. Her initial resuscitation strategy included 2000mL of 0.9% sodium chloride solution, 10mL of 10% calcium gluconate, 15 units insulin (Actrapid) in 50mL 50% dextrose, and 1mL/kg of 8.4% sodium bicarbonate solution.
Minutes after these initial investigations, our patient experienced a pulseless electrical activity cardiac arrest and was managed as per advanced life support protocol. She had a total downtime of 25 minutes. During cardiopulmonary resuscitation she was intubated and ventilated. Following return of spontaneous circulation, she required an infusion of adrenaline for blood pressure support. She had an unremarkable chest radiograph, electrocardiogram, and toxicology screen.
With a presumed diagnosis of ischemic bowel based on vague abdominal features and profound lactatemia, our patient was admitted to our intensive care unit (ICU) for preoperative optimization. In our ICU, she was sedated and ventilated on an inspired oxygen concentration of 40% and on modest ventilator paramters (peak inspiratory pressure <25cmH2O). To treat her severe circulatory shock, she was fluid-resuscitated with a total of 10,000mL crystalloid from a central venous pressure of 8cmH2O to 16cmH2O. In addition, she required very high doses of noradrenaline and adrenaline. Continuous veno-venous hemodiafiltration was commenced at exchange rates of 50mL/kg/h using Hemosol B0 solution. She was empirically started on vancomycin and piperacillin and tazobactam (Tazocin) as broad-spectrum antimicrobial cover.
Our patient went to theater 26 hours post admission for an exploratory laparotomy, which revealed no significant findings. We continued her broad-spectrum antimicrobial cover despite negative microbiological cultures. Renal replacement therapy continued and our patient’s acid-base balance slowly normalized over three days. Having excluded all causes of a high anion gap lactic acidosis, including negative red blood cell transketolase activity for thiamine deficiency, we presumed our patient to have had a severe MALA ‘triggered’ by an acute kidney injury from dehydration. This was supported by a serum metformin level of 4mg/L. Her renal function slowly improved with continuous veno-venous hemodiafiltration and she slowly recovered with a total of 35 days stay in ICU.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [2.3, 'mmol/L'], 'Sodium': [140.0, 'mmol/L']}",138.59449,131.66477,145.52421,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 140.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 140.0 mmol * 1 mEq/mmol = 140.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mmol sodium/L converts to 140.0 mEq sodium/L. 
The concentration of glucose is 2.3 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 2.3 mmol. To convert 2.3 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 2.3 mmol glucose * 0.001 mol/mmol = 0.0023 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0023 mol glucose * 180.16 g/mol = 0.41437 g glucose. To convert 0.41437 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 0.41437 g glucose * 1000.0 mg/g = 414.37 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 414.37 mg glucose/10.0 dL = 41.437 mg glucose/dL. The concentration value of 2.3 mmol glucose/L converts to 41.437 mg glucose/dL. 
Plugging in these values into the formula gives us 140.0 mEq/L + 0.024 * (41.437 - 100) = 138.59449 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.59449 mEq/L."
5347,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4992786-1,Extracted,"A fifty-seven-year-old female presented to emergency room with altered mental status, nausea, vomiting, and abdominal pain. The patient was in usual state of health 2 days before presentation, when she developed intermittent dull epigastric pain. The patient was able to tolerate the pain initially, but on day of presentation the pain became severe and persistent and she started having nonbilious vomiting. She also became somnolent and tachypneic and therefore the decision was made to bring her to the emergency room. Her past medical history was significant for diabetes mellitus and she was on insulin monotherapy. The family reported that for the last few weeks the patient was noncompliant with using insulin. On initial evaluation her vital signs were remarkable for temperature of 37 degree Celsius, pulse of 120/minutes, blood pressure (BP) of 134/78 mmHg, respiratory rate of 24 breath/minute, and oxygen saturation of 95% on 2-liter nasal cannula. Pertinent examination findings included obtunded patient who did not wake up to deep sternal rub, dry oral mucosa, and a weak gag reflex. Her pulmonary and cardiovascular examination was unremarkable. Admission labs indicated severe uncompensated metabolic acidosis with arterial blood gas showing pH of 7.02, PaCO2 of 14, PaO2 of 134, calculated bicarbonate of 4, and oxygen saturation of 97%. Serum chemistries indicated sodium 137 mEq/L (136–145 mEq/L), potassium 4.4 mEq/L (3.5–5.1 mEq/L), chloride 82 mEq/L (97–109 mEq/L), bicarbonate < 10 mEq/L (23–32 mEq/L), blood urea nitrogen (BUN) 32 mg/dL (7–17 mg/dL), serum creatinine 2.84 mg/dL (0.7–1.1 mg/dL), serum glucose 172 mg/dL (66–111 mg/dL), measured serum anion gap 46 (4–14), and measured serum osmolality 324 mOsm/kg (280–300 mOsm/kg). Her urine analysis was positive for ketones. Urine and serum drug screen was positive for cocaine. Other labs including complete blood count, lactic acid, serum Tylenol levels, and liver function tests were within normal limits. Admission chest roentgenogram was unremarkable ().
Given concern for severe uncompensated metabolic acidosis and decreased sensorium, the patient was intubated for airway protection. Initial differential diagnosis included toxic alcohol ingestion, euglycemic diabetic ketoacidosis, alcoholic ketoacidosis, and starvation ketoacidosis. The serum ethanol, methanol, ethylene glycol, and propylene glycol were undetectable on admission labs and serum beta-hydroxybutyrate (BHB) levels were significantly elevated 15.95 mmol/L (0.02–0.27 mmol/L) confirming the diagnosis of euglycemic diabetic ketoacidosis. As the patient's blood glucose was 172 mg/dL on admission, we initially administered 1 liter bolus of intravenous (IV) 5% Dextrose and 0.45% normal saline (D5-1/2 NS), followed by a maintenance rate of 250 cc/hour, supplemented with 20 mEq of potassium chloride IV per liter of D5-1/2 NS. Insulin drip was initiated at a rate of 0.1 units/kg/hour. Finger stick blood glucose was checked hourly to maintain blood glucose between 150 and 200 mg/dL. Basic metabolic panel and BHB levels were checked at four-hour interval. After initial 4 liters of volume resuscitation, the patient's anion gap started to close and in 18 hours period her gap closed completely as shown in .
The patient was subsequently transitioned to subcutaneous insulin. Her mentation improved and she was extubated. After extubation patient confirmed that she was on a cocaine binge for 2 days and missed her insulin doses during that time. The patient was transferred out of medical intensive care unit and was discharged from hospital subsequently.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [172.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",138.728,131.7916,145.6644,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 137.0 mEq/L. 
The concentration of glucose is 172.0 mg/dL. 
Plugging in these values into the formula gives us 137.0 mEq/L + 0.024 * (172.0 - 100) = 138.728 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.728 mEq/L."
5348,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3583052-1,Extracted,"A 21-day-old white male presented to the primary pediatrician for poor feeding, who noted that he had not regained his birth weight. Electrolytes were ordered as part of a failure to thrive workup, which revealed a sodium of 106 mmol/L, a potassium of 7.1 mmol/L, and a glucose of 1.8 mmol/L. After having a 17-OH progesterone level drawn, the infant was transferred to our tertiary referral hospital for electrolyte derangements with the presumptive diagnosis of salt-wasting congenital adrenal hyperplasia.
Birth history was significant for an uneventful pregnancy and delivery. Birth length was 51 cm (65th Percentile). Birth weight was 3.35 kg (37th percentile). Apgar scores were 8 and 9. Hyperpigmentation of the scrotum was noted at birth. Hypoglycemia was noted on the first day of life. He was discharged on the second day of life.
The past medical history was significant for two previous admissions for unconjugated hyperbilirubinemia with a maximum bilirubin of 367 μmol/L.He was treated with phototherapy on both occasions. His parents noted that his skin seemed to be progressively more pigmented over the first three weeks of life. This “bronzing” was attributed to phototherapy.
Physical exam upon arrival revealed normal vital signs and a blood pressure of 68/33 mmHg. His weight was 3.1 kg (7th Percentile). No dysmorphic features were noted. Genital exam revealed normal male genitalia with both testes descended. Phallus was normal in length and caliber with the urethral meatus at the tip. Physical exam was remarkable for marked bronzing of the skin.
Once in the pediatric intensive care unit, the patient was started on fludrocortisone and intravenous fluid support. He underwent a high-dose ACTH stimulation test and then was begun on glucocorticoid treatment at an initial dose of 28 mg/m2/day. Severe hyponatremia persisted despite the administration of 400 mcg/day of fludrocortisone in addition to 20 mEq/kg/day of sodium chloride. Diarrhea ensued. Escalating doses of glucocorticoid up to 54 mg/m2 were used. By the age of 5 months, he was weaned off of salt supplementation, and hydrocortisone doses were weaned to physiologic levels. Fludrocortisone doses have been gradually reduced.
The11-deoxycortisol values of theACTH stimulation became available early in this hospitalization and were consistent with 11β-hydroxylase deficiency with markedly elevated baseline and stimulated levels of 11-deoxycortisol (see ). The 17-hydroxyprogesterone obtained from his primary care physician returned at5.6 pmol/L (normal up to 2.9 pmol/L). As 11-deoxycorticosterone (DOC) and 11-deoxycortisol have been reported to be elevated in 21-hydroxylase deficiency and because salt wasting does not occur in 11-hydroxylase deficiency, 21-hydroxylase deficiency remained the presumptive diagnosis. The following day the baseline and stimulated 17-hydoxy progesterone levels returned to normal levels (4.5 nmol/L), arguing against 21-hydroxylase deficiency. He was evaluated for possible 11β-hydroxylase deficiency. A repeat 11-deoxycortisol after 12 days of hydrocortisone treatment returned to 1.49 nmol/L (normal range <.346–4.5).
Genetic testing was sent for CYP11B1 gene. The coding exons and the flanking intronic sequences were PCR amplified and sequenced in forward and reverse directions, using automated fluorescent dideoxy sequencing methods and the mRNA isoform NM_000497 as the reference sequence.
Genetic testing was also performed for the DAX1 (NROB1) gene associated with X-linked congenital adrenal hypoplasia. The coding exons and the flanking intronic sequences were PCR amplified and sequenced in forward and reverse directions, using automated fluorescent dideoxy sequencing methods and the NCBI reference files U31929.Gbk (DAX1, mRNA) and NM_000475.Gbk (NROB1, mRNA) as the reference sequences. This testing was positive for a new missense mutation not previously described. A T to C base change in the second exon was found, which substitutes proline for leucine at codon 447. His mother tested positive as a carrier for this gene. He has two older male siblings who have undergone genetic testing and have been found to be unaffected.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [1.8, 'mmol/L'], 'Sodium': [106.0, 'mmol/L']}",104.3783,99.15938,109.59722,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 106.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 106.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 106.0 mmol * 1 mEq/mmol = 106.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 106.0 mmol sodium/L converts to 106.0 mEq sodium/L. 
The concentration of glucose is 1.8 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 1.8 mmol. To convert 1.8 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 1.8 mmol glucose * 0.001 mol/mmol = 0.0018 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0018 mol glucose * 180.16 g/mol = 0.32429 g glucose. To convert 0.32429 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 0.32429 g glucose * 1000.0 mg/g = 324.29 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 324.29 mg glucose/10.0 dL = 32.429 mg glucose/dL. The concentration value of 1.8 mmol glucose/L converts to 32.429 mg glucose/dL. 
Plugging in these values into the formula gives us 106.0 mEq/L + 0.024 * (32.429 - 100) = 104.3783 mEq/L.
Hence, the patient's corrected concentration of sodium is 104.3783 mEq/L."
5349,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4519609-1,Extracted,"A 62-year-old woman who provided written and signed consent to publish this case report was admitted to our institution with a history of diabetes mellitus type II, hypertension, and chronic kidney disease secondary to diabetic nephropathy and a hysterectomy 15 years earlier. She presented with weakness, malaise, and loss of appetite. Complete blood count analysis revealed the following: white blood cell count 10.1 × 109/l; hemoglobin level 113 g/l; mean corpuscular volume 84 fl; mean corpuscular hemoglobin level 31 pg/cell, and platelet count 264. Further blood tests revealed the following: glucose level 7.8 mol/l; urea nitrogen level 28.1 mg/dl; creatinine 877 mol/l; sodium 134 mol/l, and potassium 3.5 mol/l. Four days after admission, the patient underwent hemodialysis with unfractionated heparin. Six days after the administration of heparin, she became febrile and was treated with the antibiotics vancomycin and amikacin. That was on day 6 after holding the heparin, which was promptly day 2 after vancomycin treatment had been initiated. Two days after commencing the vancomycin, her platelet count started to drop gradually, decreasing to 21 × 109/l over 8 days, which was day 16 since heparin was held. The HIT test was ordered by the nephrologists. Thereafter, a hematologist was consulted for the persistent thrombocytopenia, as heparin had already been stopped 16 days ago. Because her platelet count slightly regenerated (from 21 to 25 × 109/l), no additional steps were taken other than avoiding heparin, as the patient was scheduled to undergo permacath insertion for hemodialysis the next day. The following day, the platelet count dropped to 19 × 109/l. The patient was treated with steroids to increase the platelet level for the permacath insertion. Both platelet transfusion (owing to the possible HIT diagnosis) and heparinoid anticoagulants (owing to the urgency of the permacath insertion surgery) were avoided.
Because her platelet count continued to drop to 10 × 109/l over the next 24 h, methylprednisolone was given while waiting for the HIT test result. Because the platelet drop occurred following the fever and the vancomycin administration, a secondary ITP that could have been caused by DITP was considered. The next day, the patient developed a swollen, hot, and tender right leg. Doppler ultrasound revealed extensive progressive lower limb deep vein thrombosis. An inferior vena cava filter was inserted on the same day. The HIT test result was revealed positive result. Her platelet count rose to 23 × 109/l following the administration of methylprednisolone. She was labeled a HIT case, and the pretest probability 4Ts score was an intermediate score.
Bivalirudin (Angiomax) was started, but the deep vein thrombosis advanced to acute phlegmasia cerulea dolens requiring above-the-knee amputation. The leg had become gangrenous with continuous blood oozing caused by both the low platelet count and the anticoagulant drugs. Hemoglobin levels had also dropped to 8.6 g/dl because of the continuous bleeding, requiring the transfusion of 2 units of blood. Intravenous immunoglobulin (IVIG) was commenced to treat the DITP, and the platelet count started to increase. On the fourth day of IVIG treatment, the patient developed right thalamic lacunar infarction. The IVIG treatment was continued for 4 weeks along with bivalirudin. The platelet count responded well to the IVIG treatment, reaching 98 × 109/l after 6 days but dropping to 26 × 109/l over 4 weeks. The amputation site started to bleed again and developed an infection that required debridement. During her long-term admission, the patient received four different courses of vancomycin on days 13, 16, 34, and 75, at doses of 500–1,000 mg, along with 240 mg of amikacin, based on the findings from the blood and wound cultures. The patient was also treated with other antibiotics during the course of treatment, including ceftriaxone on day 26, marine, and linezolid on day 52. Romiplostim, which was the third and a U.S. Food and Drug Administration-approved ITP treatment, was administered promptly when IVIG was stopped. In response to romiplostim treatment, the platelet count increased promptly to the normal values, and the bleeding stopped. The patient, however, developed a third thrombosis in her right iliac vein. The next dose of romiplostim was administered on time, 1 week later, when the patient had been hematologically stabilized, i.e., no more bleeding occurred and a normal cell count was achieved. Bivalirudin was replaced by warfarin because of the normalized platelet count as well as the recurrent thrombosis events and the need for hemodialysis. The patient developed septicemia from the amputation site, which caused delayed healing and infection. The wound site was debrided several times, but no improvement was noted. The amputation site showed positive results on several swab cultures, but antibiotic treatment was ineffective. The patient was kept on conservative management strategies until her death after 3 months. Although vancomycin was suspected as the cause of her thrombocytopenia, no vancomycin antibody test was available in our laboratory to confirm the findings in this patient. No malignancy screening tests were conducted because she was not suspected to have a malignancy, and no postmortem autopsy was performed because it was considered unacceptable based on religious factors in her community.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [7.8, 'mmol/L'], 'Sodium': [134.0, 'mmol/L']}",134.9726,128.22397,141.72123,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 134.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 134.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 134.0 mmol * 1 mEq/mmol = 134.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mmol sodium/L converts to 134.0 mEq sodium/L. 
The concentration of glucose is 7.8 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 7.8 mmol. To convert 7.8 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 7.8 mmol glucose * 0.001 mol/mmol = 0.0078 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0078 mol glucose * 180.16 g/mol = 1.40525 g glucose. To convert 1.40525 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 1.40525 g glucose * 1000.0 mg/g = 1405.25 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1405.25 mg glucose/10.0 dL = 140.525 mg glucose/dL. The concentration value of 7.8 mmol glucose/L converts to 140.525 mg glucose/dL. 
Plugging in these values into the formula gives us 134.0 mEq/L + 0.024 * (140.525 - 100) = 134.9726 mEq/L.
Hence, the patient's corrected concentration of sodium is 134.9726 mEq/L."
5350,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2840971-1,Extracted,"A 70-year-old man, known only to have dyslipidemia, was admitted to our hospital because of fever associated with fatigue and nausea for 6 h. His medications were atorvastatin and omeprazole. He had no prior history of intravenous drug abuse. On examination, the patient was slightly drowsy but in no acute distress. His vital signs were: temperature 38.7°C, pulse 94 bpm, respiratory rate 20 per min, BP 123/59 mmHg and oxygen saturation 100% on room air. His overall exam was unremarkable. The patient did not have skin rash, signs of meningismus or a cardiac murmur. His laboratory findings were: WBC 7.0×106/L, hemoglobin 132 g/L, platelets 125×106/L, random glucose 16.9 mmol/L, sodium 132 mmol/L, potassium 3.6 mmol/L, bicarbonate 20 mmol/L, serum creatinine 88 micromol/L, ALT 69 U/L, AST 87 U/L and GTP 155 U/L. The rest of his laboratory work-up, including urinalysis, coagulation profile and hepatitis profile, were unremarkable. Chest X-ray was normal. Transthoracic echocardiogram did not show vegetations or valvular lesions. The patient was started on intravenous ceftriaxone and vancomycin. Two days later, two of his blood cultures grew MRSA. His intravenous antibiotic regimen was changed to linezolid and cefipime. The patient finished 2 weeks of this regimen with obvious clinical and laboratory improvement and was discharged home in good condition.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [16.9, 'mmol/L'], 'Sodium': [132.0, 'mmol/L']}",136.90728,130.06192,143.75264,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 132.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 132.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 132.0 mmol * 1 mEq/mmol = 132.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 132.0 mmol sodium/L converts to 132.0 mEq sodium/L. 
The concentration of glucose is 16.9 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 16.9 mmol. To convert 16.9 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 16.9 mmol glucose * 0.001 mol/mmol = 0.0169 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0169 mol glucose * 180.16 g/mol = 3.0447 g glucose. To convert 3.0447 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 3.0447 g glucose * 1000.0 mg/g = 3044.7 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 3044.7 mg glucose/10.0 dL = 304.47 mg glucose/dL. The concentration value of 16.9 mmol glucose/L converts to 304.47 mg glucose/dL. 
Plugging in these values into the formula gives us 132.0 mEq/L + 0.024 * (304.47 - 100) = 136.90728 mEq/L.
Hence, the patient's corrected concentration of sodium is 136.90728 mEq/L."
5351,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3318870-1,Extracted,"A 63-year-old man with history of hypertension and glucose intolerance since age 59 years was emergently admitted to our Institution from a peripheral Hospital for evaluation of a severe, constant posterior chest pain, radiating forward, and dyspnoea with a suspected diagnosis of acute aortic dissection.
On physical examination the patient was not shocked, his pulse was 87 beats/min, blood pressure 150/105 mmHg. He had truncal obesity, a ""moon face"" and proximal muscle weakness. An electrocardiogram showed left ventricular hypertrophy. His laboratory work-up revealed anaemia (Hb 10.7 g/dl), hypokaliemia (3.4 mEq/L), metabolic alkalosis (HCO3- 35 mmol/L) and hyperglycaemia (170 mg/dl). A CT scan of thorax and abdomen demonstrated a dissection starting just below left succlavian artery and extending downward to the left renal artery, involving the celiac tripod and superior mesenteric artery (). The dissection was classified as Stanford B, De Bakey III. Moreover CT scan of abdomen revealed incidentally a left adrenal tumour of 25 mm of diameter.
The patient was pharmacologically treated and was felt at risk for impending aortic rupture. Therefore, an emergent endograft positioning was planned. Our goal was to exclude the damaged segment of the aorta and to obliterate the entry of blood into the false lumen (both at the initial intimal tear and at the secondary tears along the vessel). Through an inguinal incision, the right common, superficial and profunda femoral artery were dissected free. A prosthetic graft (Valiant, Medtronic, Sunnyvale, CA, USA 42 mm x 198 mm) was placed just below the origin of the left succlavian artery up to the diaphragmatic hiatus. A postoperative control CT scan demonstrated the correct graft positioning, not endoleaks and the closure of all secondary tears ().
This patient was evaluated for hypercortisolism and the plasma cortisol was increased to 33.9 μg/dl (vn, value of normal, 5.6-23 μg/dl) without circadian rhythm and not suppressed by the administration of 1 mg of dexamethasone (overnight text: 9.8 μg/dl; vn <1.8 μg/dl ). The plasma adrenocorticotropic hormone (ACTH) was less than 10 pg/ml (vn 12-60 pg/ml) and 24h urinary free cortisol excretion (UFC) was elevated 465.6 μg/24 h (vn 26-135 μg/24h ).
A MRI of abdomen was performed to have a more accurate evaluation of the adrenal mass, it was of 2 cm of diameter, well capsulated, hyperintense in T1 sequences with a normal reduction of signal in T2 weighted sequences ().
A diagnosis of CS was made on basis of the endocrinological tests and for the presence of left adrenocortical lesion. Via laparotomic approach, a left adrenalectomy was performed during intravenous replacement of hydrocortisone, ACE-inhibitor, aspirin and insulin therapy.
Six months after adrenalectomy, blood pressure was controlled (135/75 mmHg) with anti-hypertensive therapy, laboratory analysis revealed glycaemia 102 mg/dl, glycated haemoglobin (HbA1c) 5.7%, potassium 4.26 mEq/l, sodium 139.7 mEq/L, plasma creatinine 1.05 g/dl, a.m. plasma cortiso l9.7 μg/dl, plasma ACTH 28 pg/ml and UFC 45 μg/24h.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [102.0, 'mg/dL'], 'Sodium': [139.7, 'mEq/L']}",139.748,132.7606,146.7354,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 139.7 mEq/L. 
The concentration of glucose is 102.0 mg/dL. 
Plugging in these values into the formula gives us 139.7 mEq/L + 0.024 * (102.0 - 100) = 139.748 mEq/L.
Hence, the patient's corrected concentration of sodium is 139.748 mEq/L."
5352,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-5660,Extracted,"A 45-year-old Spanish-speaking man with type I diabetes mellitus presents to the emergency department with nausea and abdominal pain. He has a past medical history of obesity, osteoarthritis, diabetes, diabetic nephropathy, and hypertension. His current medications include insulin, lisinopril, atorvastatin, and ibuprofen. His temperature is 100.5°F (38.1°C), blood pressure is 90/60 mmHg, pulse is 130/min, and respirations are 30/min. His pupils are equal and reactive to light bilaterally. He has poor skin turgor and capillary refill. Jugular venous distention is not detected. Bedside ultrasound reveals a collapsible inferior vena cava with light inspiration. His basic metabolic panel is displayed below:

Serum:
Na+: 119 mEq/L
Cl-: 95 mEq/L
K+: 5.0 mEq/L
HCO3-: not detectable
BUN: 50 mg/dL
Glucose: 960 mg/dL
Creatinine: 1.6 mg/dL
Ca2+: 8.9 mg/dL
PO4-: 3.5 mg/dL

He is admitted to the intensive care unit on a regular insulin drip and 0.9% isotonic saline. His basic metabolic panel four hours later is below:

Serum:
Na+: 120 mEq/L
Cl-: 90 mEq/L
K+: 4.2 mEq/L
HCO3-: 2 mEq/L
BUN: 50 mg/dL
Glucose: 680 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 8.5 mg/dL
PO4-: 3.0 mg/dL

Therapy remains unchanged. Three hours later, the patient is found to have the EKG in Figure A.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [960.0, 'mg/dL'], 'Sodium': [119.0, 'mEq/L']}",139.64,132.658,146.622,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 119.0 mEq/L. 
The concentration of glucose is 960.0 mg/dL. 
Plugging in these values into the formula gives us 119.0 mEq/L + 0.024 * (960.0 - 100) = 139.64 mEq/L.
Hence, the patient's corrected concentration of sodium is 139.64 mEq/L."
5353,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3917171-1,Extracted,"A 67-year-old woman presented to emergency department with complaints of episodes of inability to walk for the past 5 days, happening 4-5 times a day. Each episode lasted for 15-20 minutes and was associated with restlessness and breathlessness. Patient was apparently alright one month before, since then she started feeling generalized weakness on and off. However, for past 5 days symptoms were exaggerated and she started feeling sudden loss of power in both the lower limbs simultaneously and inability to walk. She could walk normally after the episode subsided. This episode was not associated with pain in the limbs. Patient was totally conscious during the entire episode. Her medical history was significant for diabetes and hypertension for the past 5 years. The patient's drug therapy consisted of insulin nova mixtard 30/70 (for the past 10 years), olmesartan 20 mg per day (for past 2 years), perindopril 4 mg per day (for past 16 months), and torsemide 10 mg per day (for past 6 months).
On examination she was found to be alert and fully oriented. Vital signs revealed a regular pulse rate of 93 beats per minute, blood pressure of 130/80 mmHg, temperature of 36.8°C, a respiratory rate of 14/min and oxygen saturation of 100% on room air by pulse oxymetry. Cardiac auscultation revealed normal heart sounds, respiratory examination revealed bilateral vesicular breath sounds with bilateral basal crepitations. Complete neurological examination did not reveal significant finding.
The results of laboratory examination were as follows: 10.6 g%, Total Leukocyte Count: 10,500, Differential Leukocyte Count: N70 L26 M3 E1 B0, ESR: 12 mm/hr, Random blood sugar: 98 mg/dl, Urea: 24 mg/dl, Creatinine: 1.2 mg/dl, Total Cholesterol: 198 mg/dl, Triglyceride: 112 mg/dl, HDL: 38 mg/dl, LDL: 138 mg/dl, Serum sodium: 134 mEq/L, Serum potassium: 8.6 mEq/L, Total calcium: 11 mg/dl, Ionized calcium: 1.30 mEq/L, Serum Magnesium: 2.5 mg/dl, Serum chloride: 104 mmol/L, Serum Bicarbonate: 24 mmol/l. ECG showed normal sinus rhythm, normal axis, and tall T waves. CT scan and EMG were not done.
Diabetic neuropathy, Gullian Barre Syndrome, metabolic cause of periodic paralysis.
The diagnosis of drug-induced hyperkalemia presenting as periodic paralysis was suggested by very high serum potassium concentration during the attack and also persistent hyperkalemia between attacks.
Patient was immediately admitted and the treatment for hyperkalemia was instituted. Drugs causing potassium retention were immediately stopped. Medical measures were started to lower down the level of serum K+ which included K+ bind sachet (calcium polystyrene sulfonate) thrice daily. Lactulose syrup and magnesium sulfate was given to avoid constipation. Her K+ started decreasing progressively and within 24 h K+ got reduced from 8.4 mEq/L to 6.8 mEq/L. In the next 24 h serum K+ further lowered from 6.8 to 5.4 mEq/L.
There was progressive fall of blood pressure during the course of the treatment and patient was overall drowsy and disoriented. Measures were taken to maintain her blood pressure.
Patient responded well to the treatment and was discharged in a stable state with serum K+ level of 5.1 mEq/L, and blood pressure of 120/80 mmHg on 5th day of admission.
The patient has been followed-up on an outpatient basis, her serum potassium has been stable with no further episodes of periodic paralysis.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [98.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",133.952,127.2544,140.6496,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 134.0 mEq/L. 
The concentration of glucose is 98.0 mg/dL. 
Plugging in these values into the formula gives us 134.0 mEq/L + 0.024 * (98.0 - 100) = 133.952 mEq/L.
Hence, the patient's corrected concentration of sodium is 133.952 mEq/L."
5354,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2900037-1,Extracted,"A 54-year-old male patient presented in emergency room with acute retention of urine. He was a known case of OI tarda (). Immediately foley's catheterization (no.-16fr.) was done to relieve retention. X-Ray KUB of the patient revealed a right side renal calculus and a vesicle calculus and was planned for cystolithotomy ().
On preanaesthetic evaluation, the patient weighed 22 kg, length 94 cm, head circumference 50 cm, chest circumference 65 cm, and was bedridden. He had undergone previously cystolithotomy at 6 months of age (details of that operation were not available). History revealed uneventful antenatal period and no delay in milestones. Patient developed normally upto 10yr of age and after that he started having skeletal fractures. There was no positive family history.
Investigation revealed Hb 12.6 g%, TLC 9300, platelet count 2.3 lacs, blood sugar 86 mg/dl, blood urea 40.4 mg/dl, serum creatinine 0.6 mg/dl, serum potassium 4.5meq/l, serum sodium 143meq/l, serum calcium 8.7meq/l.
Preoperative coagulation profile was normal. 2D echo revealed no valvular abnormalities and normal ejection fraction (64%). Pulmonary function tests revealed a moderate degree of restrictive lung disease.
The patient was accepted for surgery as ASA grade II. In view of anticipated difficult airway, it was planned to conduct the case under regional anaesthesia. In the operation theatre, i.v. line was secured using 18 G cannula. Monitoring included 5 lead ECG, manual blood pressure monitoring, SpO2, EtCO2, and temperature. Difficult airway cart was also kept standby. After preloading with 500ml of Ringer lactate i.v., caudal epidural anaesthesia was given in lateral position with 14ml of 0.25% of bupivacaine. Midazolam 1.0mg and butorphanol 1.0mg i.v. was given for sedation. During surgery, his vitals remained stable and no rescue medication was required. Operation lasted for about 40 min and patient had an uneventful recovery. He was discharged on 5th postoperative day.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [86.0, 'mg/dL'], 'Sodium': [143.0, 'mEq/L']}",142.664,135.5308,149.7972,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 143.0 mEq/L. 
The concentration of glucose is 86.0 mg/dL. 
Plugging in these values into the formula gives us 143.0 mEq/L + 0.024 * (86.0 - 100) = 142.664 mEq/L.
Hence, the patient's corrected concentration of sodium is 142.664 mEq/L."
5355,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3200049-1,Extracted,"A 67-year-old Indian man presented with two days history of acute onset generalized dyskinesia associated with mild confusional state. He had an 18 years history of type 2 diabetes mellitus causing ESRD, which was being treated with twice weekly hemodialysis for the last four years. There was no history of recent hypoglycemic or hypotensive episodes. He had no past or family history of movement disorders.
Physical examination revealed a blood pressure of 140/80 mm Hg. He was conscious but presented mild confusion. He had moderately severe generalized chorea, which dominantly affected the acral parts of the limbs and the oro-facial region. There was no evidence of parkinsonism, asterixis, or myoclonus. Laboratory investigations revealed evidence of uraemia and mild metabolic acidosis. Blood urea level was 141 mgm% (normal: 10.0 to 39.0 mgm%) while creatinine was 8.0 mgm% (normal: 0.5 to 1.4 mgm%). Serum bicarbonate was 19.2 mMol/L (normal: 24.0 to 36.0 mMol/L). Other variables included a haemoglobin level of 9.8 Gms% (normal: 12.0 to 14.0Gms%), blood sugar level of 140 mgm% (normal: 70 to 110 mgm%), serum calcium 7.9 mgm% (normal: 8.5 to 10.1 mgm%) and phosphorus 9.8 mgm% (normal: 2.5 to 4.5 mgm%). Serum pottasium was raised to 5.7 mEq/L (normal: 3.0 to 5.0 mEq/L) while serum sodium remained normal at 134 mEq/L (normal: 130 to 145 mEq/L). Serum venous lactate, serum iron and total iron binding capacity were normalSerum parathormone level was also normal.
Magnetic resonance imaging (MRI) scan of the brain was performed using a 1.5-Tesla machine. The T1-weighted images showed bilateral symmetrical low signal intensity in the basal ganglia, while the T2-weighted and fluid attenuation inversion recovey FLAIR images showed increased signal intensities in the same regions. The DW 1 images (b-values =500 s/mm2) showed increased signal intensities in bilateral basal ganglia along with decreased apparent diffusion coefficientADC values in the central portions of the basal ganglia surrounded by increased ADC values in their peripheral portions [].
The patient was advised oral clonazepam at a dose of 0.25 mgm thrice daily for symptomatic control of the movement disorder. However, he did not take the medication due to an apprehension that it is a “sleeping” tablet and may harm him. Concomitantly, the frequency of hemodialysis was increased to three times per week. The confusional state cleared off within four days and the movement disorder disappeared completely within 15 days. At this stage the blood urea had reduced to 82 mgm% and the serum creatinine was 5.2 mgm %. He was not administered any other drug like steroids. He has remained stable without the movement disorder during a six months follow-up. Repeat MRI scan of the brain performed three months after the first scan showed near total clearance of the basal ganglia BG lesions. No evidence of residual damage was seen [].","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [140.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",134.96,128.212,141.708,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 134.0 mEq/L. 
The concentration of glucose is 140.0 mg/dL. 
Plugging in these values into the formula gives us 134.0 mEq/L + 0.024 * (140.0 - 100) = 134.96 mEq/L.
Hence, the patient's corrected concentration of sodium is 134.96 mEq/L."
5356,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7661116-1,Extracted,"The patient in this case was a 40-year-old man with a history of uncontrolled diabetes mellitus and a hemoglobin A1c of 10.7. The patient had a history of uncontrolled blood sugar and diabetic ketoacidosis. The patient also had a history of using illicit drugs in previous years. Nevertheless, upon admission, he was found to be on daily sublingual buprenorphine. The patient was also a smoker, averaging one pack of cigarettes per day. Finally, it was noted that the patient had very poor dentation, and multiple caries were noted upon physical oral exam.
The patient was initially brought to hospital by Emergency Medical Services (EMS).
The patient's family found him to be lethargic with a distinct fruity smell from his mouth. Two weeks prior to admission, the patient was complaining of multiple symptoms, including increased leg swelling, shortness of breath, fatigue, nausea, vomiting, and poor appetite. There was no report of fever, chills, chest pain, or cough. He had history of penicillin allergy causing skin rash. The patient's history was obtained from the patient's mother.
The patient's vital signs on admission were temperature, 98.5 Fahrenheit (F); blood pressure, 98/64 millimeter of mercury (mm Hg); pulse, 101 beats per minute; and respiratory rate, 24 per minute. Cardiac exam showed tachycardia with III/VI systolic murmur. Lungs auscultation showed crackles at the bases, but no wheezing. Lower extremities had +2 pitting edema. Oral cavity showed very poor dentition, multiple caries, and necrotic teeth.
Other patient labs showed elevated blood sugar, up to 1000 milligrams per deciliter (mg/dl); white blood cell count, 29 thousand per cubic milliliter (K/µL); creatinine, 2.20 milligrams per deciliter (mg/dl); ALT, 15 units per liter (U/L); sodium, 141 millimoles per liter (mmol/L); and procalcitonin, 3.59 nanograms per milliliter (ng/mL). Troponin was less than 0.015 ng/mL. Blood gases showed pH, 6.9; lactic acid, 5.3 mmol/L; and blood glucose, 1060 mg/dl; urine drug screen was negative, and urine analysis showed no leukocytes.
A computed tomography (CT) of brain was performed and was negative for any acute finding.
However, magnetic resonance imaging (MRI) of brain without contrast showed small acute cortical infarct in the left cerebellar hemisphere with two another tiny acute embolic infarcts in the right parietal and occipital lobes ().
Chest X-ray showed bilateral lung congestion. Two sets of blood culture were obtained and sent to microbiology laboratory. He was started on broad-spectrum intravenous (IV) antibiotic vancomycin and cefepime. Two-dimensional transthoracic echocardiogram study was technically difficult and suboptimal in quality; thus, transesophageal echocardiogram (TEE) was performed, and it showed multiple echodensities compatible with vegetations, associated with moderate aortic valve insufficiency, and mild aortic stenosis. The largest vegetation measures 1.6 × 0.9 cm (Figures and ).The estimated left ventricular ejection fraction was approximately 30%.
Subsequently, the patient's blood cultures turned positive for Gram-positive rods, which were identified as Lactobacillus rhamnosus. Susceptibility tests were requested from microbiology laboratory, and it was manually performed using the broth dilution minimum inhibitory concentration (MIC) method. The results showed sensitivity to ampicillin with MIC equal to 1 microgram per milliliter (mg/ml), clindamycin with MIC equal to or less than 0.06 (mg/ml), erythromycin with MIC equal to or less than 0.06 (mg/ml), with penicillin MIC equal to 0.5 (mg/ml) and resistant to vancomycin with MIC higher than 32 (mg/ml). Due to the patient's history of penicillin allergy, the antibiotics were adjusted to IV meropenem. After 96 hours from admission, repeated blood culture became sterilized. Oral surgery was consulted, and the patient underwent full teeth extraction. Nevertheless, the identified source of the bacteremia was from the oral cavity. Due to the size of the vegetation and signs of congestive heart failure, the patient was evaluated by cardiothoracic surgeon and underwent surgery with aortic valve replacement using 23 mm Mosaic porcine tissue valve. Notes from surgery showed a large vegetation on the fused right and left coronary cusp, almost filling the aortic valve and also another vegetation on the noncoronary cusp. Tissue valve culture results showed the same organism isolated from the blood upon arrival to the hospital. Pathology of the excided aortic valve reported myxoid degeneration, focal acute inflammation with fibrinous exudate containing bacterial colonies.
The patient clinically responded well to antibiotic treatment and was discharged home to complete six weeks of IV meropenem. A follow-up and two-dimensional echocardiogram was scheduled after 3 months of end therapy, and it showed improvement in the ejection fraction up to 70%, and the bioprosthetic aortic valve was functioning normally with no signs of regurgitation.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [1060.0, 'mg/dL'], 'Sodium': [141.0, 'mmol/L']}",164.04,155.838,172.242,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 141.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 141.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 141.0 mmol * 1 mEq/mmol = 141.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mmol sodium/L converts to 141.0 mEq sodium/L. 
The concentration of glucose is 1060.0 mg/dL. 
Plugging in these values into the formula gives us 141.0 mEq/L + 0.024 * (1060.0 - 100) = 164.04 mEq/L.
Hence, the patient's corrected concentration of sodium is 164.04 mEq/L."
5357,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3970275-1,Extracted,"A 48-year-old male was referred to the endocrinology clinic complaining of generalized edema, increased blood pressure and blood glucose levels. The patient was on medication due to hypertension that was diagnosed 1 year ago. Recently, the blood pressure was not well-controlled, the blood glucose level was high and generalized edema developed.
The patient was diagnosed with MTC 14 years ago; total thyroidectomy with right cervical lymph node dissection was performed and I-131 metaiodobenzylguanidine (MIBG) 200 mCi was administered. He was treated with tumor resection for recurred MTC on a mediastinal lymph node 13 years ago. Nine years ago, MTC recurred on the left cervical and left parahilar lymph nodes and was treated with I-131 MIBG 200 mCi after surgery. Two years ago, MTC recurred thirdly on the cervical and mediastinal lymph nodes and lung and was treated with cervical and mediastinal lymph node dissection and the left upper lobe wedge resection of the lung. Since then, the patient has not shown any signs or symptoms of recurrence.
The patient's height was 172 cm and weight was 84 kg, 2 kg over his usual weight. His blood pressure was 185/110 mm Hg with a pulse rate of 90 beats per minute and a breathing rate of 18 breaths per minute. The patient's body temperature was 37℃. Moon face and facial flushing were observed. Buffalo hump and purple striae were absent. Mild pitting edema was observed on the anterior tibia and slight skin pigmentation was present.
Peripheral blood examination showed a white blood cell count of 14,450 cells/µL, hemoglobin of 15.3 g/dL, and platelet count of 358,000 cells/µL. On serum biochemical examination, total cholesterol was 252 mg/dL with total protein of 6.5 g/dL, albumin of 4.1 g/dL, total bilirubin of 1.1 mg/dL, alkaline phosphatase of 101 U/L, aspartate aminotransferase of 17 U/L, alanine aminotransferase of 62 U/L, blood urea nitrogen of 10.3 mg/dL, and creatinine of 0.6 mg/dL. On serum electrolyte examination, sodium was 145 mmol/L with potassium of 2.8 mmol/L, chloride of 94 mmol/L, and bicarbonate of 40.4 mmol/L. Fasting plasma glucose level was 168 mg/dL with glycated hemoglobin of 8.6%. Hormone examination showed total T4 of 12.75 µg/dL (range, 5 to 13) and thyroid stimulating hormone of 0.07 µIU/mL (range, 0.15 to 5.0). Serum calcitonin was 127.86 pg/mL (<10.0) and carcinoembryonic antigen was 29.46 ng/mL (<5). Plasma ACTH concentration was measured with immunoradiometric assay (ELSA-ACTH kit, CisBio, Belford, MA, USA), and was 203.9 pg/mL (range, 6.0 to 60.0). Serum cortisol concentration was 36.0 µg/dL (range, 5 to 25.0) with a 24-hour urine cortisol of 2,237.1 µg/day (range, 20 to 90). On the low dose dexamethasone suppression test, inhibited serum cortisol was 32.50 µg/dL. The 24-hour urine examination results were as follows: metanephrine 14.46 µg/day (range, 52 to 341), normetanephrine 28.21 µg/day (range, 88 to 444), epinephrine 6.57 µg/day (<40), norepinephrine 26.43 µg/day (<80), and vanillylmandelic acid 3.51 mg/day (<8). To validate the RET gene mutation, peripheral blood was collected from the patient and white blood cells were separated by centrifugation to extract genomic DNA. For polymerase chain reaction, BIGDYE version 3.1 cycles sequencing kit (Applied Biosystems, Foster, CA, USA) reagent was utilized and 3,730 automated sequencer (Applied Biosystems) was used to analyze DNA sequence. The DNA sequencing showed no RET gene mutation.
Chest and abdomen computed tomography revealed recurred lesions on the mediastinal lymph nodes, lungs, and liver (), but no abnormal findings in adrenal glands (). Sellar magnetic resonance imaging showed no abnormality in the pituitary gland (). Gastroscopy, colonoscopy, and positron emission tomography did not identify suspicious primary lesions in other regions.
Calcitonin and chromogranin A staining was positive on resected tissues on the third recurrence 2 years ago, which is indicative of MTC. ACTH immunohistochemistry staining was negative ().
Because curative resection of the MTC lesions was difficult on the fourth recurrence, close follow-up with further chemotherapy was considered. To control the ectopic ACTH syndrome, the patient was administered ketoconazole. The dosage was gradually increased over 3 months up to the maximum dosage (1,200 mg/day), but the serum cortisol concentration level did not decrease. Therefore, bilateral adrenalectomy was performed. After surgery, ACTH remained above 200 pg/mL, but plasma glucose and blood pressure levels were improved sufficiently and the oral antidiabetic agent and antihypertensive medication were discontinued. The patient has been living in good condition until 6 months after the surgery without any medication other than glucocorticoid and mineralocorticoid agents.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [168.0, 'mg/dL'], 'Sodium': [145.0, 'mmol/L']}",146.632,139.3004,153.9636,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 145.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 145.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 145.0 mmol * 1 mEq/mmol = 145.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 145.0 mmol sodium/L converts to 145.0 mEq sodium/L. 
The concentration of glucose is 168.0 mg/dL. 
Plugging in these values into the formula gives us 145.0 mEq/L + 0.024 * (168.0 - 100) = 146.632 mEq/L.
Hence, the patient's corrected concentration of sodium is 146.632 mEq/L."
5358,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-9627,Extracted,"A 32-year-old man presents with a history of diarrhea several days after eating a hot dog at a neighborhood barbeque. He notes that the diarrhea is visibly bloody, but he has not experienced a fever. He adds that several other people from his neighborhood had similar complaints, many of which required hospitalization after eating food at the same barbeque. His temperature is 37°C (98.6°F ), respiratory rate is 16/min, pulse is 77/min, and blood pressure is 100/88 mm Hg. A physical examination is performed and is within normal limits. Blood is drawn for laboratory testing. The results are as follows:
Hb%: 12 gm/dL
Total count (WBC): 13,100/mm3
Differential count:
Neutrophils: 80%
Lymphocytes: 15%
Monocytes: 5%
ESR: 10 mm/hr
Glucose, Serum: 90 mg/dL
BUN: 21 mg/dL
Creatinine, Serum: 1.96 mg/dL
Sodium, Serum: 138 mmol/L
Potassium, Serum: 5.2 mmol/L
Chloride, Serum: 103 mmol/L
Bilirubin, Total: 2.5 mg/dL
Alkaline Phosphatase, Serum: 66 IU/L
Aspartate aminotransferase (AST): 32 IU/L
Alanine aminotransferase (ALT): 34 IU/L
Urinalysis is normal except for RBC casts.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [90.0, 'mg/dL'], 'Sodium': [138.0, 'mmol/L']}",137.76,130.872,144.648,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 138.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 138.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 138.0 mmol * 1 mEq/mmol = 138.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mmol sodium/L converts to 138.0 mEq sodium/L. 
The concentration of glucose is 90.0 mg/dL. 
Plugging in these values into the formula gives us 138.0 mEq/L + 0.024 * (90.0 - 100) = 137.76 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.76 mEq/L."
5359,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4508971-1,Extracted,"A 38-year-old Turkish male was admitted to our outpatient clinic for hypercalcemia. Before entering our clinic, hypercalcemia has been detected in another medical center. History revealed, that he took ace inhibitor in combination with thiazide diuretic for hypertension. Due to the complications, like hypopotassemia this medicine was replaced with calcium channel blockers. In his family history, none of his first degree relatives had hypertension. His father died at 47 years of age due to biliary tract cancer. His three children were diagnosed with West Syndrome. One of them died at the age of 13 months, while the other 9 months of age. His third child is 2 years old and living with the respiratory support equipment. He also has a 13-year-old healthy son. There is no other significant clinical data in his medical history.
On his physical examination: blood pressure—150/90 mmHg, pulse −74 per minute, rhythmic. His general clinical appearance was good. The other systemic and laboratory findings were the following: complete blood count and thyroid function tests were normal: serum Ca level: 10.9 mg/dl (8.8–10.2), inorganic P: 2.4 mg/dl (2.7–4.5), Mg: 2.3(1.6–2.6), albumine: 3.9 g/dl, parathormone (PTH): 200 pg/ml (12–88), Na: 138 mmol/l, K+: 2.8 mmol/l, glucose: 85 mg/dl, creatinine: 0.84 mg/dl, alanine transaminase: 24 U/l, white blood cells 8 ML, hemoglobin 14 g/dl, platelet 219 C-reactive protein 0.4 mg/dl (0–0.8), alkaline phosphatase 61 U/l (38–126), 25-OH vitamin D3 22 ng/ml (14–66). Calcium level in 24-h urine: 251 mg/day, inorganic P: 88 mg/day, and K+ value in spot urine: 66 mmol/l. Aldosterone level was measured after normalization of his serum potassium level (result: 26.9 ng/dl). Plasma renin activity was <0.15 ng/ml/h. The patient was detected for multiple endocrine neoplasia syndromes. Levels of catecholamine and its metabolites in 24-h urine were normal. In the low dose (1 mg) dexamethasone suppression test, serum cortisol level was suppressed to the normal range. Serum prolactin, thyroid-stimulating hormone, adrenocorticotropic hormone, growth hormone, insulin-like growth factor 1 and calcitonin were normal.
Thyroid ultrasound revealed a 24 × 14 × 12.5 mm hypoechoic nodular lesion at the upper posterior part of the right thyroid lobe, within the thyroid capsule (intrathyroidal parathyroid adenoma?). MIBI (Technetium (99mTc) sestamibi) scintigraphy of parathyroid glands was consistent with the ultrasound finding. Abdominal magnetic resonance imaging revealed 1.6 cm adrenal gland mass consistent with adenoma, cystic lesions in both kidneys with the largest (3 cm in length) in the right kidney and also on this side 11 mm lesion which may be consistent with angiomyolipoma. Pituitary magnetic resonance imaging was normal.
The patient was operated for parathyroid adenoma. At the 3rd day after the operation, serum Ca level was found to be 9.5 mg/dl, inorganic P—3.6 mg/dl and parathyroid hormone—62 pg/ml. Pathological examination of the surgery material revealed parathyroid adenoma. The patient post operatively was followed during the 2 months with spironolactone therapy for his hypertension. This medication was stopped soon after, due to its side effects like erectile dysfunction. Post-surgery, which was conducted for the lesion (1.6 cm) identified on the left adrenal gland revealed adrenal aldosterone producing adenoma. Follow up the adrenal surgery, his blood pressure came to normal ranges and hypokalemia were improved. Blood potassium and calcium levels were within normal ranges. Genetic screening revealed negative mutation of MENIN gene.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [85.0, 'mg/dL'], 'Sodium': [138.0, 'mmol/L']}",137.64,130.758,144.522,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 138.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 138.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 138.0 mmol * 1 mEq/mmol = 138.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mmol sodium/L converts to 138.0 mEq sodium/L. 
The concentration of glucose is 85.0 mg/dL. 
Plugging in these values into the formula gives us 138.0 mEq/L + 0.024 * (85.0 - 100) = 137.64 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.64 mEq/L."
5360,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8493291-1,Extracted,"A 67-year-old woman with diabetes was admitted to the emergency department due to two generalized tonic-clonic seizures and loss of awareness in the interictal period. The patient had never experienced seizures before. Half a year ago she had surgical resection of pituitary tumor and did not get regular hormone replacement treatment. In the days leading up to the seizures, she did not have any signs of discomfort such as fever or headache. In the emergency room diazepam (5 mg, i.v.) and sodium valproate (50 mg, intravenous pumped at the rate of 160 mg/h) were given immediately as antiepileptic therapy, the seizures were terminated in several minutes and the patient fell in state of sedation shortly after, during which the patient could gradually open her eyes, answer simple questions and no more convulsions were observed. Routine blood tests in the emergency department showed hyperglycaemia (13.0 mmol/L), mild hypernatremia (151.7 mmol/L), and hyperchloremia (111.3 mmol/L). Then she was admitted to the neurology department and rescue measures including oxygen inhalation, antiepileptic therapy with sodium valproate (56 mg/h, 1 mg/kg/h), rehydration, maintaining water, and electrolyte balance were continued. About 3 h later, the patient passed into a lethargic state and she could only open her eyes on hearing our call but could not respond in words (GCS score of 8). The lethargic state continued for several hours and the patient fell in coma then (GCS score of 5), which lasted for the following 3 days. During this period the sodium valproate was pumped for 36 h continuously (56 mg/h for 24 h, 50 mg/h for 12 h, 24 mg/h for 12 h, total dose of 2,232 mg) and no remarkable facial or limb spasms or convulsions were recorded from admission. Tests of thyroid function, adrenocorticotropic hormone (ACTH), growth hormone (GH), cortisol, and sex hormone were conducted and the results supported the diagnosis of hypopituitarism (). MRI of the head was performed and no acute cerebral infarction, cerebral hemorrhage, and inflammatory changes were found (). A lumbar puncture was performed to the patient on the 2nd day of admission. The cerebrospinal fluid (CSF) showed elevated protein levels (0.60/L, reference range 0.15–0.45 g/L) and increased chloride (137.8 mmol/L, reference range 118–132 mmol/L) and normal glucose levels and CSF pressure (). Autoimmune encephalitis and viral encephalitis tests were both negative, and thus the diagnosis of encephalitis was ruled out. A 24-h electroencephalogram (EEG) revealed sharp waves, spike waves, sharp-slow waves, spike-slow waves in the bilateral frontal region on a continuous slow-wave background with a trend of evolution, and the EEG also recorded paroxysmal electrical activities in this region (). Combining the symptoms and examinations, the diagnosis of NCSE was considered. On the 3rd day of admission, diazepam (10 mg) was intravenously injected and the patient turned to a state of lethargy gradually and could open her eyes under painful stimulation, confirming the diagnosis of NCSE. Unfortunately, her family refused further treatment and she was discharged on the 3rd day, and she died of respiratory failure induced by epilepsy 5 days after her discharge from our hospital.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [13.0, 'mmol/L'], 'Sodium': [151.7, 'mmol/L']}",154.92099,147.17494,162.66704,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 151.7 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 151.7 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 151.7 mmol * 1 mEq/mmol = 151.7 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 151.7 mmol sodium/L converts to 151.7 mEq sodium/L. 
The concentration of glucose is 13.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 13.0 mmol. To convert 13.0 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 13.0 mmol glucose * 0.001 mol/mmol = 0.013 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.013 mol glucose * 180.16 g/mol = 2.34208 g glucose. To convert 2.34208 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 2.34208 g glucose * 1000.0 mg/g = 2342.08 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 2342.08 mg glucose/10.0 dL = 234.208 mg glucose/dL. The concentration value of 13.0 mmol glucose/L converts to 234.208 mg glucose/dL. 
Plugging in these values into the formula gives us 151.7 mEq/L + 0.024 * (234.208 - 100) = 154.92099 mEq/L.
Hence, the patient's corrected concentration of sodium is 154.92099 mEq/L."
5361,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3415193-1,Extracted,"A 28-day-old phenotypic female infant was admitted to pediatric endocrinology clinic of Al-Zahra Hospital, affiliated to Isfahan University of Medical Sciences, because of poor weight gain and lethargy.
She was a full-term infant with a birth weight of 3250 gr (50th percentile), length of 51 cm (50th percentile) and head circumference of 34 cm (50th percentile).The patient had no perinatal problem. She was the 1st child of nonconsanguineous parents.
At the time of admission, she was lethargic without history of vomiting or diarrhea.
There was not any familial history of similar presentation or features endocrine disease.
She had no history of drug consumption except vitamin A+D.
She was lethargic, had depressed fontanele. She had mild dehydration and decreased skin turgor.
In skin examination, she had mild hyperpigmentation, including oral cavity.
External genitalia seemed normal female type with no ambiguity. There was not any abdominal or inguinal mass in abdominal examination.
Her body weight, length and head circumference were 2900, 51 cm and 33.5 cm, all of them were beneath the 5th percentiles.
Her blood pressure was 60/40 mmHg, respiratory rate was 39/min, pulse rate was 112/min and body temperature was 37.1°C.
The initial biochemical examinations were as follows; serum sodium, 129 meq/lit(N:135-145) ; serum potassium, 6.1 meq/lit (N: 3.5-5.5);blood sugar, 45 mg/dl; blood urea nitrogen, 73 mg/dl; serum creatinine, 0.5 mg/dL; C-reactive protein ,negative; blood culture, negative. The results of venous blood gas were as follows; pH: 7.3 HCO3=11.9 mmol/L, PCO2= 35 mmHg which represented metabolic acidosis.
The results of hormonal tests were as follows; Cortisol: 0.2 μg/dl, ACTH: >1000 pg/ml, 17 OHP: 0.3 ng/ml.
Ultrasonographic examination revealed small hypoplastic uterus (6*7*3 ml) or atretic ovaries and adrenal glands had normal sizes.
Clinical Course and Follow-up
First, the patient hydrated with normal saline. Thereafter, considering hyponatremia, hyperkalemia, metabolic acidosis and decreased cortisol level and increased ACTH level, lipoid CAH was diagnosed and replacement therapy with standard doses of glucocorticoid (hydrocortisone) and mineralocorticoid (fludrocortisone) and sodium chloride was initiated.
After replacement therapy, electrolyte abnormalities were corrected during first week and the patient was discharged from hospital with good clinical condition.
She recommended referring for follow up. During follow-up, she had good clinical condition, with normal laboratory results except for 17 OHP which was lower during the period.
At 6-years old, the patient referred with high blood pressure and adrenal insufficiency because of arbitrary drug discontinuation by mother. Renal Doppler ultrasonography and scan was performed which was normal. Regarding the recommendation of pediatric nephrologist fludrocortisone and sodium chloride was discontinued and treatment continued with hydrocortisone . Ultrasonography revealed the testicles in the abdominal cavity and uterus was not detected in pelvis. Orchiectomy was performed. Chromosome study showed 46XY pattern.
On her most recent visit at the age of 6 years, the patient had no hyperpigmentation. Her height was 110 cm (10-25th percentile), weight 23 kg (75-90th percentile). Her last laboratory tests results were as follows; Na: 142 mmol/l, K: 4.5 mmol/l ,17OHP: 0.1 ng/ml, ACTH: 22 pg/ml, Renin:50.8 pg/ml, Aldosterone: 105 pg/ml.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [45.0, 'mg/dL'], 'Sodium': [129.0, 'mEq/L']}",127.68,121.296,134.064,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 129.0 mEq/L. 
The concentration of glucose is 45.0 mg/dL. 
Plugging in these values into the formula gives us 129.0 mEq/L + 0.024 * (45.0 - 100) = 127.68 mEq/L.
Hence, the patient's corrected concentration of sodium is 127.68 mEq/L."
5362,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5265797-1,Extracted,"A 45-year-old male patient visited the emergency room (ER) because of lower chest discomfort starting 6 hours earlier. He also complained of thirst and limb numbness. His medical history included diabetes mellitus, bronchial asthma, and unstable angina for 4 years, 2 years, and 1 year, respectively. He had been taking aspirin (100 mg/d), clopidogrel (75 mg/d), atorvastatin (10 mg/d), and candesartan (8 mg/d) for 1 year without changes. He took those medicines on the morning of his admission. He regularly used a Symbicort Turbuhaler® (AstraZeneca Korea, Seoul, Republic of Korea) (160/4.5 μg) for asthma management. One month before the present admission, he discontinued the oral hypoglycemic agents prescribed by his primary physician. He denied recent alcohol consumption and had quit smoking 1 year earlier. Except for these symptoms, he initially had no complaints, such as muscular pain, fever, upper respiratory symptoms, or signs, on visiting the ER. He had no history of excessive physical activity or recent trauma.
On initial physical examination in the ER, his vital signs were as follows: blood pressure, 100/60 mm Hg; heart rate, 71 beats/min; respiratory rate, 20 times/min; and body temperature, 36.6 °C. On chest auscultation, no abnormal sounds, such as rales or wheezing, were audible, and his heartbeat was regular without murmur. His general skin turgor was decreased, and his tongue was dry. His conjunctivae were not anemic and sclerae were not icteric. There were no palpable lymph nodes in the head or neck area. Organomegaly was not seen in the abdomen. No pretibial pitting edema, muscular swelling, or skin color changes were detected on either lower extremity. There was no tenderness in the upper or lower extremities. His muscle power was within normal limits.
Compared with a previous ECG, the rhythm and voltage were unchanged. His initial troponin-I was less than 0.1 ng/mL, creatinine kinase (CK) was 144 U/L (0–190 U/L), lactate dehydrogenase (LDH) was 220 U/L (135–225 U/L), and CK-MB, subunit of CK, was 3.5 ng/mL. Other initial laboratory data were hematocrit 45% (39%–52%), hemoglobin 14.5 g/dL (13–17 g/dL), white blood cell count 11,280/mm3 (4000–10,000/mm3, neutrophils: 68.2%, lymphoid cells: 25.6%, and monocytes: 4.5%), and platelet count 256,000/mm3 (130,000–400,000/mm3). Liver function tests were as follows: alkaline phosphatase 84 IU/L (35–130 IU/L), aspartate aminotransferase (AST) 21 IU/L (0–37 IU/L), alanine aminotransferase (ALT) 42 IU/L (0–41 IU/L), and glucose 696 mg/dL. Hemoglobin A1c (HbA1c) was 9.3% (4.2%–5.9%). Blood urea nitrogen (BUN) and creatinine were 19.9 mg/dL (6.0–20.0 mg/dL) and 1.11 mg/dL (0.6–1.2 mg/dL), respectively. Electrolyte results were sodium 123 mmol/L (135–145 mmol/L), potassium 4.7 mmol/L (3.3–5.1 mmol/L), and chloride 80 mmol/L (98–110 mmol/L). Serum osmolality was 296 mOsm/kg. Urinalysis with micro revealed no protein or blood on a dipstick and red blood cell 1 to 4/high-power field.
Continuous intravenous insulin and hydration with normal saline were started. In addition, 40 mg of esomeprazole was infused intravenously under a suspicion of GERD. Glucose levels, measured by a blood sugar meter, decreased to 240 mg/dL and chest discomfort improved 6 hours after this management. In the mean time, there were no other oral, intramuscular, and intravenous drug therapies except for oral lactulose for his constipation. He felt mild discomfort in the right buttock at that time but did not complain to the medical team. However, he complained of severe right buttock pain 12 hours after the esomeprazole infusion. Tender muscle swelling of 8 cm in diameter was seen in the right buttock area and a reddish skin color change was noted (Fig. ). Serum CK and LDH levels increased to 40,533 and 1326 U/L, respectively, and AST and ALT levels also increased to 320 and 83 IU/L, respectively. BUN and creatinine levels were 23.9 and 1.49 mg/dL, respectively. We started vigorous hydration through isotonic saline infusion and urine alkalinization by intravenous bicarbonate infusion. Another 40 mg of esomeprazole was administered because we did not regard esomeprazole as the causative agent of the rhabdomyolysis at that time. Serum CK, LDH, AST, and ALT levels were 84,226, 1943, 603, and 171 IU/L, respectively, 24 hours later. On the third day in hospital, he was admitted to the nephrology ward. Esomeprazole was ended, and hydration and alkalinization were continued. Serum CK and LDH levels decreased gradually (Fig. A and B), and his muscular symptoms and swelling in the buttock area improved gradually. A bone scan using 20 mCi of 99mTc-hydroxymethylene diphosphonate was performed on the seventh day in hospital and revealed multiple and diffuse uptake in the soft tissues of the right buttock and both lower legs (Fig. ). His clinical manifestations and laboratory findings improved, so he was discharged on the 12th day. We added oral hypoglycemic agents, linagliptin 5 mg and metformin 500 mg, to his previous drugs (aspirin, clopidogrel, candesartan, and atorvastatin). He is being followed in our outpatient department with no recurrence of rhabdomyolysis at 6 months.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [696.0, 'mg/dL'], 'Sodium': [123.0, 'mmol/L']}",137.304,130.4388,144.1692,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 123.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 123.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 123.0 mmol * 1 mEq/mmol = 123.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 123.0 mmol sodium/L converts to 123.0 mEq sodium/L. 
The concentration of glucose is 696.0 mg/dL. 
Plugging in these values into the formula gives us 123.0 mEq/L + 0.024 * (696.0 - 100) = 137.304 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.304 mEq/L."
5363,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6709832-1,Extracted,"A sixty years old male was admitted to our multidisciplinary ICU with complaints of aggression, altered sensorium, tremors, sweating, clonus in legs (myoclonus) and irrelevant talks. Initially he was managed in medicine emergency where a working diagnosis of gastroenteritis induced hyponatremia with sepsis was made. The patient received infusion of 3% NaCl, antibiotics and oxygen supplementation @ 6 L/min through venturi mask. In view of aggression and altered sensorium, CT brain was done, which was normal. An assessment by neurologist was done, who advised for MRI Brain for further evaluation. Patient was kept nil per oral in view of possibility of further deterioration and need for mechanical ventilation. Since there was no improvement, patient was shifted to ICU. In ICU, the intensivist took a detailed history from the attendants of the patient. His medical history included long standing hypertension, diabetes mellitus type 2, coronary artery disease with PTCA for triple vessel disease and a major depressive disorder. Relatives denied any allergies or illicit drug abuse. Patient was taking metoprolol 25 mg once daily, olmesartan 10 mg twice daily, ecospirin 75 mg once daily, atorvastatin 10 mg at night, metformin 1 g twice daily twice daily, pioglitazone 50 mg once daily, regular insulin 16 U and 20 U subcutaneous, pantoprazole 40 mg once daily along with some herbal powder for his comorbidities for the past 10 years. For last two years, patient's depression was controlled with escitalopram (SSRI) 10 mg and clonazepam (benzodiazepine) 0.5 mg. The patient had an acute episode of anxiety five days before admission to ICU, for which psychiatrist had prescribed another SSRI paroxetine 20 mg and alprazolam 0.5 mg. Symptoms did not subside, rather patient developed restlessness in his legs with current like sensation along with loose motions. His symptoms worsened over next 2 days, and he presented to the medical emergency with severe agitation and presenting complaints as described above.
In the ICU, patient was hemodynamically stable but severely agitated and restless and not responding to commands. Laboratory parameters measured included Hb 12.8 g%, TLC 10800/mm3, platelet count 2.7 lakh/mm3, INR 1.0, Na+ 117meq/L, K+ 4.5meq/L, serum creatinine 0.9 mg/dL and ABG pH 7.424/PaO2 109/PaCO2 28.9/HCO3 18.6/BD −4.3/SpO2 99%/lactate 0.7/Na+ 117/K+ 3.9/iCa+2 3.55/glucose 90 mg/dL/Cl− 83 mEq/L. In view of the recent escalation in the doses and addition of other antidepressants (SSRI) and benzodiazepines with concomitant intake of drugs like metoprolol, pantoprazole and some herbal medications associated with typical features, presumptive diagnosis of SS was made as per Hunters criteria. All antidepressants were stopped. Sedation using titrated doses of propofol (10 mg/hr) to maintain Ramsay score of 2–3 was started to alleviate the symptoms and allow the complete excretion of drugs. Patient received oxygen by face mask and was monitored continuously. Over the next 24 hours his agitation subsided and patient was awake and started responding to commands. Later propofol sedation was gradually tapered off. Thereafter, patient was discharged from ICU and referred back to psychiatrist for further management.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [90.0, 'mg/dL'], 'Sodium': [117.0, 'mEq/L']}",116.76,110.922,122.598,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 117.0 mEq/L. 
The concentration of glucose is 90.0 mg/dL. 
Plugging in these values into the formula gives us 117.0 mEq/L + 0.024 * (90.0 - 100) = 116.76 mEq/L.
Hence, the patient's corrected concentration of sodium is 116.76 mEq/L."
5364,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3313757-1,Extracted,"A 56-year-old woman was referred to our hospital with a 4–5 day history of nausea, two episodes of vomiting, and few episodes of loose motions, followed by oliguria at home. She denied any history of fever, dysentery, abdominal pain, trauma, muscle pain, or change in color of urine. She also denied history of any drug intake. On enquiring, the patient gave history of longstanding ill health in the form of generalized weakness, easy fatigability, cold intolerance, constipation, hair loss, and weight gain starting after her last child birth some 22 years back. Last delivery was a full-term normal delivery conducted by a local midwife at her home. She denied any history of profuse bleeding or blood transfusion during her last peripartum period. However, she had lactation failure and had menstrual cycles for a few months before complete cessation of menses after her last delivery. Physical examination revealed an ill-looking, dehydrated patient with pulse of 54 beats/ minute, blood pressure of 90/60 mm Hg without any postural drop, respiratory rate of 18/ minute, and oral temperature of 97.6°F (36.4°C). The patient had mild pallor, dry tongue, coarse and dry skin with non-pitting edema of the lower extremities. Hypopigmented area was seen around right nasal orifice and there was loss of lateral eyebrows. Thyroid gland was not palpable and there was no lymphadenopathy. Her breasts were atrophic and sparse axillary and pubic hair was noticed. Chest, cardiovascular, and abdominal examinations were non-contributory. Central nervous system examination revealed slow mentation in the form of delayed response to verbal commands. Examination of motor system did not reveal any focal neurodeficit, but deep tendon jerks were markedly delayed.
Laboratory evaluation revealed normochromic normocytic anemia. Liver function tests were normal except for low albumin. Kidney function test was deranged with initial urea of 71 mg/dl (normal value 20–40 mg/dl) and serum creatinine of 4.5 mg/dl (normal value 0.5–1.5 mg/dl). Muscle enzymes were slightly elevated with creatine phosphokinase (CPK) being 168 1U/l (normal value 10–70 IU/l) and lactate dehydrogenase (LDH) was 983 U/l (normal value 200–450 U/l). Arterial blood gas and electrolyte analysis revealed pH of 7.31, PCO2 of 27 mm Hg, bicarbonate of 13 mmol/l, serum sodium 130 mmol/l, and potassium of 3.6 mmol/l. Plasma glucose was only 38 mg/dl. Chest X-ray was normal and 12-lead ECG revealed sinus bradycardia with low-voltage QRS complex. Routine urine examination revealed pus cells 4–5, RBCs 2–3, absent albumin and casts. Renal ultrasound revealed relatively small-sized kidneys (right 8.5 × 3.2 cm, left 8.7 × 3.4 cm) with increased echogenicity, with maintained corticomedullary differentiation bilaterally. Her hormone profile revealed panhypopituitarism []. The diagnosis of panhypopituitarism most likely secondary to SS associated with acute renal failure was made on the basis of her past medical history of failure to lactate post her last child birth with gradual cessation of menses, peripheral signs and symptoms of hypothyroidism, and abnormal biochemical and hormone profile.
The patient was given intravenous fluids in the form of dextrose normal saline with close monitoring of urine output, replacement therapy in the form of intravenous hydrocortisone 50 mg intravenously 6 hourly, and levothyroxine given orally at a starting dose of 50 mcg/ day. The patient was also given intravenous antibiotics and antiemetics. Urine output began to improve on the 2nd day of admission. Her appetite also improved and there was complete cessation of vomiting. On repeating renal function tests and other biochemical tests, there was dramatic improvement in serial renal function parameters. With improvement in the general condition of the patient, intravenous antibiotics were stopped in view of absence of fever and negative septic screen. She was shifted to oral prednisolone 5 mg twice daily, while levothyroxine was continued at a dose of 50 mcg/day. The serial biochemical parameters of the patient are given in . She was discharged on the same medication on 10th day of admission and was advised to taper prednisolone to 5 mg/ day after 2 weeks. Four weeks after discharge, the patient had general sense of well-being with better appetite and renal function had normalized with creatinine 0.64 mg/ dl and serum urea 23 mg/dl. The patient was subjected to magnetic resonance imaging (MRI) brain with sellar and parasellar focus which revealed empty sella with normal rest of the brain parenchyma [].","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [38.0, 'mg/dL'], 'Sodium': [130.0, 'mmol/L']}",128.512,122.0864,134.9376,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 130.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 130.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 130.0 mmol * 1 mEq/mmol = 130.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mmol sodium/L converts to 130.0 mEq sodium/L. 
The concentration of glucose is 38.0 mg/dL. 
Plugging in these values into the formula gives us 130.0 mEq/L + 0.024 * (38.0 - 100) = 128.512 mEq/L.
Hence, the patient's corrected concentration of sodium is 128.512 mEq/L."
5365,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2621138-1,Extracted,"A 15 year old girl was brought to the emergency department with a history of sudden onset of paresthesia, involving initially the right leg, then, the right arm, the face and, subsequently the entire right side of the body, increasing during activity (walking) and ceasing during sleep, of two days duration. The patient described this as „the feeling of pins and needles“. There was no previous history of fever, headache, and neurological illnesses. She did not receive any medication. She was non-smoker. Clinical examination revealed a normal developed young girl, with normal memory, speech and orientation, with normal physical exam.
The preliminary impression of the emergency staff was of a functional disorder, and the patient was discharged home, with the recommendation to take calcium and magnesium supplements, being well known that the paresthesia of the mouth, hands, and feet is a common, transient symptom of the related conditions of hyperventilation syndrome and panic attacks. The patient was called back for a formal neurologic assessment scheduled for the next day. On the same day, the patient came back, with repeated involuntary movements involving her right side (foot, arm and face). She was admitted in the Intensive Care Unit and a diagnosis of Hemichorea-Hemiballismus (HC-HB) was made.
Hypotonia of muscles with normal power and normal deep tendon reflexes were present symmetrically. Her blood pressure was 110/55 mm Hg. Keyser Fleischer ring was absent at slit lamp examination.
This clinical symptom of spontaneous hemichorea was considered secondary to a poststreptococcal neurological disease, Sydenham's chorea, but was not associated with other clinical features of rheumatic fever (carditis, arthritis, erythema, rheumatic nodules) and neuropsychological features (dysarthria and emotional disorders). Also, the choreiform movements are rather more continuous in chorea Sydenham than paroxysmal as observed in the described case and the serum anti-streptolysin-O titre was < 200 IU.
Also, the possibility of continuous focal seizures (epilepsia partialis continua [EPC]) causing unilateral movements and CNS involvement (the contralateral basal ganglion, the thalamus and the subcortical areas) was considered. As a result, electroencephalography and brain CT and MRI scanning were scheduled.
Ischaemic and haemorrhagic strokes are the cause of chorea in most elderly patients, and these etiologies were excluded in our patient, based on the neuroimaging studies. Other differential diagnosis considered were: encephalitis, systemic lupus erythematosus, basal ganglia calcifications, Wilson's disease, thyroid disease and tuberous sclerosis. CSF was normal, anti-nuclear antibodies were negative, and serum ceruloplasmin and thyroxine levels were within the normal range. Also, the CT of the head did not reveal any lesion in the basal ganglia, as well as brain MRI exam. EEG was normal, even during the ictal recording, excluding the possibility of epilepsy [Fig. , Fig. ].
Multiple medications in different combinations were tried, including haloperidol, phenobarbital, clonazepam, diazepam, with minimal immediate benefit. Severe pain from the continuous right arm jerking was treated with perfalgan.
Other laboratory tests revealed: haemoglobin of 13 g%, total count of 8,800/mm3, differential count of N 60 E1 L29, and normal liver function tests. Her urea and serum creatinine were 20 mg% and 0.8 mg% respectively. Urine exam: glycosuria, without ketones. Blood glucose concentration was 367 mg% and glycosylated haemoglobin A1C was 13.9%. Estimated blood osmolality was 294 mosm/L and ketones were absent. Serum sodium: 132 mEq/L; potassium: 4.2 mEq/L; serum calcium and magnesium levels were normal. The diagnosis of diabetes was made and the patient was started on rapid analog insulin subcutaneous, until her blood sugar was brought below 250 mg%, following which long-acting insulin was started and continued for the first day. At the end of 24 hours, her blood sugar was 148 mg% and the involuntary movements had completely disappeared. She remained asymptomatic during her hospital stay and was discharged home on a combination of rapid-acting analog, before meals and long-acting analog insulin (subcutaneous) before dinner.
GAD antibodies were positive and C-peptide was low. Based on the presence of glutamic acid decarboxylase antibodies (9,000 U/ml; normal < 1. 4 U/ml), low C-peptide and high insulin requirements, we diagnosed type 1 diabetes mellitus.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [367.0, 'mg/dL'], 'Sodium': [132.0, 'mEq/L']}",138.408,131.4876,145.3284,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 132.0 mEq/L. 
The concentration of glucose is 367.0 mg/dL. 
Plugging in these values into the formula gives us 132.0 mEq/L + 0.024 * (367.0 - 100) = 138.408 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.408 mEq/L."
5366,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-6047,Extracted,"A 65-year-old man presents to the emergency department with shortness of breath and a sensation of anxiety. This started suddenly this afternoon and has persisted for the past several hours. The patient has a past medical history of obesity, diabetes, hypertension, and osteoarthritis. His current medications include atorvastatin, lisinopril, insulin, metformin, and ibuprofen. Laboratory values are ordered as seen below:

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.2 mEq/L
HCO3-: 24 mEq/L
BUN: 20 mg/dL
Glucose: 124 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.1 mg/dL
AST: 11 U/L
ALT: 11 U/L

An EKG is ordered as seen in Figure A. His temperature is 99.5°F (37.5°C), blood pressure is 147/92 mmHg, pulse is 177/min, respirations are 15/min, and oxygen saturation is 96% on room air. On physical exam you see a patient who is notably uncomfortable and appears anxious. Pulmonary exam is notable for minor bibasilar crackles. Cardiac exam is notable for tachycardia.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [124.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",139.576,132.5972,146.5548,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 139.0 mEq/L. 
The concentration of glucose is 124.0 mg/dL. 
Plugging in these values into the formula gives us 139.0 mEq/L + 0.024 * (124.0 - 100) = 139.576 mEq/L.
Hence, the patient's corrected concentration of sodium is 139.576 mEq/L."
5367,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-4772,Extracted,"A 55-year-old man with no significant medical history returns for follow-up of a fasting blood glucose (FBG) of 110 mg/dL. His mother had a myocardial infarction at age 52. He weighs 90 kg and his body mass index is 35 kg/m2. His repeat FBG is 160 mg/dL and hemoglobin A1c (HbA1c) is 7.0%. He is started on metformin but is lost to follow-up. Two years later, his HbA1c is 7.6% despite maximal metformin usage, so the patient is started on glyburide. Three months later, his HbA1c is 7.3% while on both medications, and subsequently prescribed glargine and aspart. Three months later, he is brought by his wife to the emergency department for evaluation of altered mental status. His electronic medical record notes that he was started on nitrofurantoin recently for an urinary tract infection. He is disoriented to place and time. His temperature is 99°F (37.2°C), blood pressure is 90/60 mmHg, pulse is 130/min, respirations are 26/min. His basic metabolic panel is shown below:

Serum:
Na+: 119 mEq/L
Cl-: 90 mEq/L
K+: 4.2 mEq/L
HCO3-: 24 mEq/L
BUN: 25 mg/dL
Glucose: 1,400 mg/dL
Creatinine: 1.9 mg/dL

His urine dipstick is negative for ketones. A peripheral intravenous line is established.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [1400.0, 'mg/dL'], 'Sodium': [119.0, 'mEq/L']}",150.2,142.69,157.71,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 119.0 mEq/L. 
The concentration of glucose is 1400.0 mg/dL. 
Plugging in these values into the formula gives us 119.0 mEq/L + 0.024 * (1400.0 - 100) = 150.2 mEq/L.
Hence, the patient's corrected concentration of sodium is 150.2 mEq/L."
5368,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7407036-1,Extracted,"A 22-year-old female (height 1.72 cm, weight 40 kg, and body mass index 13.5 kg/m2) was admitted to our emergency room while receiving cardiopulmonary resuscitation for 45 minutes. Rhythm upon arrival was ventricular fibrillation. Since return of spontaneous circulation could not be achieved by all medical measures provided, the patient was immediately transferred to the catheter laboratory. Extracorporeal cardiopulmonary resuscitation via venoarterial extracorporeal membrane oxygenation (va-ECMO) was established. Due to severe left ventricular (LV) dysfunction, an Impella® pump was added to ensure sufficient LV output. Subsequently, percutaneous coronary angiogram was performed and showed no coronary disease (). The patient's history was noticeable for anorexia nervosa (AN) with several hospitalizations for renutrition, at the last several months prior to emergency admission. During the last few days prior to sudden cardiac death and after excessive caloric restriction, our patient began to increase her caloric intake to improve her nutritional state to avoid complications at an upcoming doctor's appointment. Prior to admission, our patient was an outpatient; did not receive medical refeeding or preventive treatment with supplementation of vitamins, phosphorus, or micronutrients; and did not had a history of binge episodes.
Initial blood analysis showed a severe electrolyte disorder with potassium depletion (1.38 mmol), hypocalcemia (ionized calcium 1.75 mmol/l), hyponatremia (117 mmol/l), hypochloremia (54 mmol/l), hypophosphatemia (0.28 mmol/l), and hypoproteinemia (total protein 30.2 g/l; albumin 28.9 g/l). In addition, laboratory data indicated a high level of lactate (18 mmol/l) combined with a normal pH of 7.38. Initial sugar levels were elevated (blood glucose 430 mmol/l). The first performed echocardiogram confirmed severe LV dysfunction. In the electrocardiogram, a sinus tachycardia and prolongation of the corrected QT interval were detected (660 ms) (). Electrolytes were substituted. Transient anisocoria and simultaneous severe coagulopathy under va-ECMO therapy led to a cranial computed tomography (CT), showing small bilateral subdural hematoma (). Most likely, the patient had aspirated during resuscitation; therefore, calculated antibiotic therapy with ampicillin/sulbactam was given. After initiating inodilatative support with levosimendan, cardiac output significantly improved within the next 24 hours. The Impella® pump and va-ECMO were subsequently removed on day 3. After the patient's respiratory situation had stabilized, extubation took place on day 5. Neurological assessment 10 days after admittance showed a mild difference in reflexes such as vertical saccade. Cranial magnetic resonance imaging (MRI), performed on day 16, revealed unchanged small bilateral subdural hematoma (). Subsequent cardiac MRI performed after 2 weeks showed a recovered LV ejection fraction and no signs of myocarditis (). The patient was dismissed after 3 weeks of hospitalization without neurological deficit to a psychiatric care station for further treatment of AN.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [430.0, 'mmol/L'], 'Sodium': [117.0, 'mmol/L']}",300.52512,285.49886,315.55138,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 117.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 117.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 117.0 mmol * 1 mEq/mmol = 117.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 117.0 mmol sodium/L converts to 117.0 mEq sodium/L. 
The concentration of glucose is 430.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 430.0 mmol. To convert 430.0 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 430.0 mmol glucose * 0.001 mol/mmol = 0.43 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.43 mol glucose * 180.16 g/mol = 77.4688 g glucose. To convert 77.4688 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 77.4688 g glucose * 1000.0 mg/g = 77468.8 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 77468.8 mg glucose/10.0 dL = 7746.88 mg glucose/dL. The concentration value of 430.0 mmol glucose/L converts to 7746.88 mg glucose/dL. 
Plugging in these values into the formula gives us 117.0 mEq/L + 0.024 * (7746.88 - 100) = 300.52512 mEq/L.
Hence, the patient's corrected concentration of sodium is 300.52512 mEq/L."
5369,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2169248-1,Extracted,"A 77-year-old Caucasian female was admitted to the emergency department after two weeks of increasing abdominal pain associated with vomiting. Two days before admission, she developed psychomotor agitation. She had a past medical history of type 2 diabetes, arterial hypertension and cerebrovascular disease. She had had a stroke one month before with full recovery; at that time her creatinine was normal and she had been discharged from hospital with the following medications: metformin 3 g daily, perindopril 8 mg daily, and simvastatin 20 mg daily.
On admission examination revealed a Glasgow Coma Scale score of 12/15 (E4V3M5), blood pressure 136/87 mmHg, pulse 100 beats per minute, respiratory rate 20 breaths per minute and core body temperature 36.6°C. Despite being eupnoeic with oxygen saturation measured by pulse oximetry was 97% on room air, she presented with signs of poor perfusion.
Initial investigations revealed a creatinine of 6 mg/dL, sodium 142 mEq/L, potassium 4.7 mEq/L, chloride 103 mEq/L, glucose 216 mg/dL and C-reactive protein 3.14 mg/dl. Complete blood count (CBC) count showed 22.4 × 109/L white blood cells, with haemoglobin of 13.8 g/dL, and platelet count of 365 × 109/L. Arterial blood gas showed severe lactic acidosis (pH 6.87, PaCO2 8.2 mmHg, PaO2 146 mmHg, HCO3- 1.4 mEq/L, blood lactate 16 mmol/L). Chest X-rays and ECG were normal at the time of her admission. Serum toxicological results, namely benzodiazepines, tricyclic antidepressants, opiates and barbiturates, were negative.
The patient was admitted to the intensive care unit (ICU) with the diagnosis of metformin related lactic acidosis. Continuous venovenous haemodialysis (CVVHD) was initiated, with 2 L/h of dyalisate flow and 35 ml/kg/h of hemofiltration using the solutions from Fresenius HF BIC, with 2 and 4 mEq/L of potassium as needed, using a high-flux dyalizer membrane (ultraflux AV 600s). Elective endotracheal intubation and mechanical ventilation was performed.
Four hours after the initiation of CVVHD significant improvement of acid-base status was observed and blood lactate level had halved (table ). On the third day the patient was successfully weaned from the ventilator. On the 5th day a primary methicillin resistant Staphylococcus aureus bloodstream infection was diagnosed and the patient was started on vancomycin. The patient was discharged to the nephrology department ward on the seventh day.
Full recovery of renal function was observed after 30 days and the patient was discharged from hospital on the 60th day medicated with insulin and glycazide.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [216.0, 'mg/dL'], 'Sodium': [142.0, 'mEq/L']}",144.784,137.5448,152.0232,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 142.0 mEq/L. 
The concentration of glucose is 216.0 mg/dL. 
Plugging in these values into the formula gives us 142.0 mEq/L + 0.024 * (216.0 - 100) = 144.784 mEq/L.
Hence, the patient's corrected concentration of sodium is 144.784 mEq/L."
5370,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5827908-1,Extracted,"A 75-year-old woman living in a nursing home, with past medical history of multiple strokes, hypertension, hyperlipidemia, diabetes mellitus, osteoporosis, mental retardation, and PEG tube placement secondary to dysphagia from stroke 3 years earlier, presented to the emergency department with abdominal discomfort and six episodes of non-bloody, non-bilious vomiting over the preceding 24 h. Two days earlier, she had complained of itching around the location of the gastrostomy tube and was seen repeatedly pulling on the external component of the device. At presentation, the patient appeared clinically dehydrated. She was hemodynamically stable (heart rate 95 beats/min, blood pressure 105/70 mm Hg) and afebrile (temperature 36.3 °C). On physical exam, the abdomen was distended () with tenderness in the epigastric area and hypoactive bowel sounds. There was no guarding or rigidity. Aggressive intravenous hydration with normal saline was started.
Laboratory testing was performed and showed hemoglobin of 16.2 g/dL (13.5 - 17.5 g/dL), hematocrit of 47.2% (40 - 52%), white blood cell count of 11.5 × 109/L (4.0 - 11.0 × 109/L), platelet count of 418 × 109/L (150 - 450 × 109/L), sodium of 143 mEq/L (135 - 145 mEq/L), potassium of 3.7 mEq/L (3.5 - 5.0mEq/L), chloride of 95 mEq/L (96 - 110 mEq/L), blood urea nitrogen of 35 mg/dL (7 - 22 mg/dL), creatinine of 1.6 mg/dL (0.6 - 1.3 mg/dL), glucose of 135 mg/dL, and calcium of 10.2 mg/dL (8.5 - 10.5 mg/dL). The liver function tests were normal. Computed tomography (CT) scan of the abdomen was performed and showed that the internal inflated balloon of the gastrostomy tube had migrated distally and had become impacted in the pyloric channel, thus producing a functional gastric outlet obstruction.
The gastrostomy tube was pulled back, withdrawn into the stomach and secured to the abdominal wall with the help of the external bumper at 2.5 cm. Abdominal distention was improved after the PEG tube adjustment (). Enteral feeding was successfully resumed. Over the next several days, the patient’s clinical condition improved and the patient’s laboratory parameters normalized.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [135.0, 'mg/dL'], 'Sodium': [143.0, 'mEq/L']}",143.84,136.648,151.032,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 143.0 mEq/L. 
The concentration of glucose is 135.0 mg/dL. 
Plugging in these values into the formula gives us 143.0 mEq/L + 0.024 * (135.0 - 100) = 143.84 mEq/L.
Hence, the patient's corrected concentration of sodium is 143.84 mEq/L."
5371,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3858703-1,Extracted,"A 68-year-old male patient was admitted with complaints of pain in the left eye associated with redness for 3 days, nasal block with discharge for 5 days, breathlessness for 10 days, and cough with expectoration for 10 days. He was diagnosed to have fungal rhino sinusitis (mucormycosis), orbital cellulitis (mucormycosis), uncontrolled diabetes mellitus, ischemic heart disease, dilated cardiomyopathy with severe left ventricular systolic dysfunction with severe pulmonary artery hypertension, and nephropathy. He was on treatment with insulin for diabetes, tablet ecospirin for ischemic heart disease, and injection amphotericin for fungal rhino sinusitis. He was proposed for left orbital exenteration surgery. On examination, the patient was drowsy. His pulse rate was 86/min, irregular in rhythm, and blood pressure measured in right arm in supine position was 100/60 mm Hg. There was swelling of left eye with discharge. Cardiovascular system examination showed split in second heart sound. Respiratory system examination showed bilateral extensive rhonchi and rales. Oxygen saturation on room air was 91-92%. Airway examination showed modified Mallampati score of 3. His fasting blood glucose was 409 mg/dl and random glucose level was 329 mg/dl. His hemoglobin was 10.7 gm/dl, blood urea was 92 mg/dl, and serum creatinine was 2.0 mg/dl. Serum sodium level was 133 mEq/L and potassium level was 3.5 mEq/L. ECG showed right bundle branch block pattern and Q wave in leads V1–V3. Echocardiography showed global hypokinesia of left ventricle with left ventricular ejection fraction of 25%, severe pulmonary arterial hypertension, dilated cardiac chambers with apical clot in the right ventricle, and sclerosed aortic valve. Chest radiography showed features of cardiomegaly and congestive cardiac failure. Computed tomography (CT) scan of paranasal sinuses with orbit showed pan sinusitis and left orbital cellulitis with no intracranial extension. Considering the risk factors like congestive cardiac failure, sepsis, inadequate control of blood sugar, renal failure, and ischemic heart disease with poor left ventricular ejection fraction, grave risk consent was taken. All standard monitors like pulse oximetry, non-invasive blood pressure (NIBP) and ECG, were connected. Intravenous access was obtained with 18 G cannula. Oxygen was administered through nasal prongs.
The patient was placed in supine position with the head in neutral position and the eyes staring straight ahead. The anatomic landmark was marked at a point 3 cm lateral to the angle of the mouth on the left side. The skin over the cheek on the involved site was prepared with povidone-iodine and draped. A skin wheal was raised with a local anesthetic. A 22G, 10 cm-long spinal needle was inserted here [] and advanced upward toward the mandibular condyle in a plane lining with the patient's pupil as the patient's eyes stared ahead, and the trajectory was cephalad toward the external auditory meatus. At a depth of 5 cm, the greater wing of the sphenoid at the base of the skull was contacted. The needle was withdrawn and redirected more posteriorly to enter the foramen ovale. It was then advanced 1.5 cm. Paresthesia at the mandible was elicited, followed by paresthesia in the maxilla and orbit. Before injecting the local anesthetic, the needle was carefully aspirated to check for cerebrospinal fluid (CSF) and 2 ml of lignocaine 2% with 5 ml of bupivacaine 0.5% was given. Supraorbital and supratrochlear block was given with 0.5% bupivacaine 3 ml each. Intravenous sedation was given with midazolam 1 mg and morphine 3 mg. Patient was monitored all the time during surgery. Oxygen saturation was between 97% and 98%, blood pressure was ranging from 100/60 to 110/60 mm Hg, and heart rate was between 90/min and 106/min. The patient was specifically monitored for signs of an oculo-cardiac reflex. A standard exenteration was performed and the patient tolerated the procedure well with no episodes of hypoxia or bradycardia. The patient was comfortable during surgery. Blood sugar was controlled with insulin 5 U bolus and at an infusion rate of 2U/h. Blood sugar was between 170 and 220 mg/dl. Postoperatively pain was controlled with injection tramadol 50 mg tid.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [409.0, 'mg/dL'], 'Sodium': [133.0, 'mEq/L']}",140.416,133.3952,147.4368,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 133.0 mEq/L. 
The concentration of glucose is 409.0 mg/dL. 
Plugging in these values into the formula gives us 133.0 mEq/L + 0.024 * (409.0 - 100) = 140.416 mEq/L.
Hence, the patient's corrected concentration of sodium is 140.416 mEq/L."
5372,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-5824,Extracted,"A 57-year-old man presents to the emergency department with dizziness and an episode of fainting that occurred when he stood up from using the bathroom. Since then, he states he has felt generally uncomfortable and uneasy. The patient has a past medical history of obesity, and his current medications include atorvastatin, aspirin, and ibuprofen. He has not visited a physician in over three years and is notably non-compliant with his medications. The patient's lab values are ordered and return as below:

Serum:
Na+: 137 mEq/L
K+: 3.6 mEq/L
Cl-: 100 mEq/L
HCO3-: 24 mEq/L
Urea nitrogen: 15 mg/dL
Glucose: 110 mg/dL
Creatinine: 1.2 mg/dL
Ca2+: 9.9 mg/dL

An EKG is ordered as seen in Figure A. His temperature is 99.5°F (37.5°C), blood pressure is 100/65 mmHg, pulse is 80/min, respirations are 11/min, and oxygen saturation is 96% on room air. Physical exam reveals a middle-aged man who appears uncomfortable. Pulmonary exam is notable for mild bilateral crackles. Cardiac exam is notable for a rapid rate and thready distal pulses. Neurological exam is within normal limits.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [110.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",137.24,130.378,144.102,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 137.0 mEq/L. 
The concentration of glucose is 110.0 mg/dL. 
Plugging in these values into the formula gives us 137.0 mEq/L + 0.024 * (110.0 - 100) = 137.24 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.24 mEq/L."
5373,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6897349-1,Extracted,"A 75-year-old Caucasian female presented to the emergency room (ER) in January for a change in mental status and confusion after she was found wandering outside her home. The patient complained of generalized myalgias, nonproductive cough, and runny nose in the preceding few days for which she called her primary care physician and was given a script of oseltamivir, attributing the symptoms to influenza virus infection. Pertinent past medical history included hypertension, chronic kidney disease (CKD) stage III, with the baseline estimated glomerular filtration rate (eGFR) 45 milliequivalent/liter, and type II diabetes (DMT-2). Her medications included metformin, pioglitazone, amlodipine, atorvastatin, and ezetimibe. She used to live by herself and didn’t drink or smoke. Vitals in the ER were temperature: 93 F, pulse: 55/min, blood pressure: 96/54 mmHg, oxygen saturation: 98% on ambient air, and respiratory rate: 28/min.
Physical examination showed that she was lethargic and oriented only to self, with dry mucosal membranes and cold, clammy skin. The neck was supple; extraocular movements were intact. Lungs were clear to auscultation. The rest of the examination, including the cardiovascular and gastrointestinal systems, were unremarkable. Pertinent laboratory evaluation, including complete metabolic profile (CMP) showed serum glucose of 187 mg/dL, creatinine: 11.5 mg/dL (baseline 1.8 mg/dl), sodium: 131 meq/L, potassium: 7.9 meq/L, bicarbonate: 5 meq/L, anion gap: 35, and glycosylated hemoglobin (HbA1c) of 6.2 mg/dL. Complete blood count (CBC) showed hemoglobin of 10 g/dL, platelets 370,000/uL, and white blood cells (WBC): 9.3 k/uL. The coagulation profile was normal. The lactic acid level was eight (8) meq/L. Venous blood gas analysis showed pH: 7.009, pCO2: 18.2 mmHg, and bicarbonate level: 5.1 mmol/L. Serum osmolarity was 312 mOsm/kg, with an osmolar anion gap of 12 mOsm/kg. Urinalysis showed glucose of 500 mg/dL, proteinuria of 30 mg/dL. Electrocardiogram (EKG) showed a first-degree heart block and broad QRS complex, as shown in Figure .
Computerized tomographic scan (CT) head and chest X-ray were unremarkable.
She was aggressively resuscitated with intravenous (IV) fluids. Hyperkalemia was treated with IV insulin, dextrose, calcium gluconate, sodium bicarbonate, and inhaled albuterol. Urgent hemodialysis was also arranged. Attributing her acute severe metabolic acidosis to influenza complicated by bacterial superinfection, she was started on broad-spectrum antibiotics and oseltamivir, and workup for acute renal failure, including antinuclear antibody (ANA), antineutrophilic cytoplasmic antibody (ANCA), complement levels, urine eosinophils, and renal ultrasound, was ordered. After hemodialysis (HD), electrolytes improved to a bicarbonate level of 18 mmol/L, potassium of 3.8 meq/L, and a pH of 7.433. She remained hemodynamically stable at this point. Repeat metabolic profile (BMP) fours hour after the completion of HD showed the bicarbonate level dropping down to 13 meq/L again. Endocrinology was consulted due to persistent metabolic acidosis. At this point, the patient recalled that she was also taking dapagliflozin (an SGLT-2 inhibitor) up to two weeks before the presentation when she stopped taking it due to her improving HbA1c.
Her serum beta-hydroxybutyrate result came back at 92.5 mg/dl. She was started on IV insulin and dextrose. Serum beta-hydroxybutyrate started improving and resolved entirely within 15 hours of beginning IV insulin, and bicarbonate improved to 22 meq/l. Later on, her urine output improved and electrolytes stabilized without further need for HD. Creatinine trended down and stabilized at 2.5 meq/L.
She resumed a regular diet, and beta-hydroxybutyrate remained within the normal range. Her blood sugar levels remained in the range of 110-150 mg/dl without hypoglycemic agents. Workup for acute renal failure came back negative. She was discharged to a rehabilitation center with the plan to establish her diabetic regimen, depending on blood sugar levels on an outpatient basis.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [187.0, 'mg/dL'], 'Sodium': [131.0, 'mEq/L']}",133.088,126.4336,139.7424,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 131.0 mEq/L. 
The concentration of glucose is 187.0 mg/dL. 
Plugging in these values into the formula gives us 131.0 mEq/L + 0.024 * (187.0 - 100) = 133.088 mEq/L.
Hence, the patient's corrected concentration of sodium is 133.088 mEq/L."
5374,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7852477-1,Extracted,"A 53-year-old Asian male patient presented to the emergency department with a history of fever for 10 days with fatigue, myalgia, ageusia, hyposmia, and one episode of vomiting. The patient also complained of polydipsia, polyuria, and nocturia for 1 week with generalized weakness and mild breathlessness with non-productive cough for 2 days. He had a history of Hypertension and Diabetes mellitus but was not on medications. He was managing his blood glucose by lifestyle modification with diet and exercise.
On initial evaluation, the patient was dehydrated with a heart rate of 108 beats per minute, blood pressure of 126/76 mmHg, temperature of 36.8 °C, respiratory rate of 24 breaths per minute, and oxygen saturation of 91% in room air. His blood investigations showed plasma blood glucose of 1543 mg/dl, HbA1c 13.0%, blood urea 130 mg/dl, serum creatinine 2.9 mg/dl, serum sodium 145 mEq/L, serum potassium 5.3 mEq/L, and urine analysis was positive for ketones (Table ). His arterial blood gas analysis (ABG) revealed compensated metabolic acidosis with high anion gap. Chest x-ray revealed bilateral airspace consolidations, more prominent on the left side involving almost all zones (Fig. ). The patient was planned for ICU admission and as a part of routine COVID-19 testing in our hospital, rRT-PCR was done which was positive. Hence, he was shifted to our make-shift COVID hospital and admitted to the ICU.
The patient was started on empirical antibiotics, oxygen supplementation through nasal prongs, and DKA management was initiated mainly with cautious administration of intravenous fluids, insulin therapy, and potassium correction. All other possible community-acquired pathogens were excluded.
The patient’s DKA and acute kidney injury (AKI) improved gradually which was evident by the normalization of renal function and serum sodium levels. He also developed thrombocytopenia during the course of treatment which improved over a week. The patient also showed improvement in his breathing as his oxygen saturation rose to 97% in room air and his repeat chest x-ray revealed resolution of consolidations. On the 7th day of admission, he was shifted out of ICU to the general ward in stable condition.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [1543.0, 'mg/dL'], 'Sodium': [145.0, 'mEq/L']}",179.632,170.6504,188.6136,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 145.0 mEq/L. 
The concentration of glucose is 1543.0 mg/dL. 
Plugging in these values into the formula gives us 145.0 mEq/L + 0.024 * (1543.0 - 100) = 179.632 mEq/L.
Hence, the patient's corrected concentration of sodium is 179.632 mEq/L."
5375,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4421247-1,Extracted,"A 36-year-old 5-week postpartum woman presented to the emergency room with complaints of nausea and vomiting for 48 h. She also reported a 2-day history of general malaise and worsening dyspnoea. She denied chest pain, palpitations, diarrhoea or headaches. She reported eating; however, she limited herself to several small high-protein carbohydrate-free meals in an attempt to quickly return to her prepartum weight. Since her delivery, she had achieved an intentional weight loss of 30 lbs. Initial vital signs were: temperature 37 °C, blood pressure 140/63 mmHg, heart rate 84, respiratory rate 20 and a weight of 59.8 kg. She appeared unkempt and lethargic. Head and neck examinations were benign. Chest auscultation was clear with no adventitious sounds; heart examination was unremarkable. The abdomen was benign with a well-healed surgical C-section scar; there was no costovertebral angle tenderness. The extremities were without tenderness or oedema. She had no neurologic defects other than her blunted mentation.
Her past medical history was significant for a cesarean section, complicated by bladder damage, now resolved. Her only medication was percocet to manage post-surgical visceral pain. She denied alcohol or illicit substance use.
Initial laboratory data include sodium of 144 mEq/L, potassium 4.8 mEq/L, chloride 104 mEq/L and bicarbonate <5 mEq/L that is the lowest available determination possible at our institution. Her BUN was 3 mg/dL, creatinine was 1.1 mg/dL and glucose was 133 mg/dL. Serum lactate was 2.1 mmol/L, phosphate 1.0 mg/dL and magnesium 1.6 mg/dL. Arterial blood gas drawn on room air showed a pH of 6.9, PCO2 of 19 mmHg, PaO2 of 137 mmHg and SaO2 of 100%. White blood cell count was 17 600/mm3 with 88.2% segmented neutrophils, Hg 13.7 g/dL, haematocrit 43.1% and platelets of 340 000/mm3. Urinalysis had a pH of 5.5 with <80 mg/dL ketones. The serum osmolar gap was 7. A comprehensive drug screen was negative including salicylates and acetaminophen. Chest radiograph was normal. Blood and urine cultures were negative.
The patient was volume-depleted with a metabolic acidosis and a serum anion gap of 35. Fluid resuscitation with three ampules of sodium bicarbonate per litre of D5W at 100 cc/h was initiated for 24 h. Improvement in laboratory values occurred within 12 h with serum bicarbonate improving to 12 mEq/L. The serum bicarbonate improved to 20 mEq/L with normalization of the anion gap at 24 h. Symptomatic improvement occurred likewise. The patient was started on an 1800 kcal diet during her hospitalization, supplemented with a regular diet of home food provided by the husband. Breast feeding was stopped on advice from a lactation consultant and the acidosis did not reoccur. The patient's baby was reported to be in the 90th percentile for weight and height.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [133.0, 'mg/dL'], 'Sodium': [144.0, 'mEq/L']}",144.792,137.5524,152.0316,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 144.0 mEq/L. 
The concentration of glucose is 133.0 mg/dL. 
Plugging in these values into the formula gives us 144.0 mEq/L + 0.024 * (133.0 - 100) = 144.792 mEq/L.
Hence, the patient's corrected concentration of sodium is 144.792 mEq/L."
5376,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4091369-1,Extracted,"An 80-year-old woman presented with decreased mentality, a 3-day history of polyuria, general weakness, and poor oral intake. She had been diagnosed with type 2 diabetes mellitus more than 30 years before and was treated with an oral hypoglycemic agent.
At the current hospital admission, the patient's temperature was 38.0℃. Her blood pressure was 143/92 mmHg, heart rate was 123/min, respiratory rate was 28/min, and oxygen saturation was 99% in room air. She was dehydrated, and the rest of the physical examination findings were unremarkable. No definite abnormality was detected through neurologic examination. Her laboratory values were notable as follows: white blood cell (WBC) count of 16,540 cells/mm3, segmented neutrophil concentration of 88.4%, bicarbonate level of 17.3 mmol/L, C-reactive protein (CRP) level of over 34.1 mg/dL, glucose level of 648 mg/dL, hemoglobin A1c concentration of 8.4%, sodium level of 151 mEq/L, osmolality of 357 mOsm/Kg, and creatinine level of 1.19 mg/dL. Routine urinalysis showed WBC 30-49/HPF and some bacteria. Computer tomography (CT) scan of the abdomen showed multiple ill-defined nodular hypodense lesions in the left kidney that suggest acute pyelonephritis of the left kidney with multiple abscess formation (). No definite abnormality was observed on brain CT.
The patient was admitted to the hospital and treated with intravenous hydration and insulin and started treatment empirically on piperacillin/tazobactam (4.5 g q8hr, IV). We attempted percutaneous drainage of renal abscess, but did not succeed because of inadequate liquefaction. Cultures from peripheral blood and urine revealed K. pneumoniae, which was susceptible to most antibiotics including amikacin, cephalosporins, and ciprofloxacin. The string test was positive, showing a hypermucoviscosity phenotype. The patient was afebrile and in a stable condition on day 3 of hospitalization.
On day 6 of hospitalization, the patient developed a fever, her mental state deteriorated, and she developed stupor. At that time, her WBC count and CRP level decreased to 13,860 cells/mm3 and 5.99 mg/dL. The patient showed seizure-like activity, and neurologic examination revealed objective changes with positive pyramidal and Babinski signs. Magnetic resonance imaging (MRI) of the brain showed elevated signals in the lateral ventricles, Sylvian fissure, suprasellar, interpeduncular cistern, and posterior fossa, suggestive of ventriculitis (). Cerebrospinal fluid (CSF) showed a very turbid and milky appearance, and the WBC count was 7,200/mm3 segmented neutrophil concentration was 44%, protein level was 359.3 mg/dL, glucose level <10 mg/dL. The antibiotic regimen was changed from piperacillin/tazobactam to ceftriaxone (2 g q12hr, IV) and vancomycin (1 g q12hr, IV), and emergency extraventricular drainage (EVD) was performed. Although the blood culture at that time showed negative result, the CSF culture revealed K. pneumonia. We continued ceftraixone alone. K. pneumoniae isolated from the CSF was found to be of hypermucoviscosity phenotype and was shown same antibiotic susceptibility as those drawn from first blood culture. Abdomen CT scan was performed, and abscess of left kidney increased in size and protruded (), and other disseminated infection was not found. Percutaneous drainage for renal abscess was performed. Two weeks after admission, the EVD catheter and pig tail catheter of the left renal abscess were removed. The patient's general condition and laboratory data remained favorable. After 28 days of intravenous antibiotics, the patient was discharged to the long-term care facility with oral cefditoren (600 mg/day) of two weeks, showing improvement of neurologic state slowly, and after 1 month, could express in words.
We evaluated the serotyping and virulence genes of K. pneumoniae from blood and CSF including serotype K1, rmpA. For serotyping, we use PCR detection of serotype K1 specific alleles at the wzx loci, with the following primers, as previously described []. Consequently, serotype K1-specific alleles at the wzx were positive in the strains of the blood and CSF, indicating that the serotype of this K. pneumoniae was K1. The presence of genes encoding virulence factors was determined by polymerase chain reaction using primers documented previously [] and rmpA gene was confirmed in the microorganism from CSF and blood. We didn't analyze the presence of magA gene which was known as one of factor associated virulence.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [648.0, 'mg/dL'], 'Sodium': [151.0, 'mEq/L']}",164.152,155.9444,172.3596,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 151.0 mEq/L. 
The concentration of glucose is 648.0 mg/dL. 
Plugging in these values into the formula gives us 151.0 mEq/L + 0.024 * (648.0 - 100) = 164.152 mEq/L.
Hence, the patient's corrected concentration of sodium is 164.152 mEq/L."
5377,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3811690-1,Extracted,"A 53-year-old female presented to our hospital complaining of a 6-month history of backache. Judging from the blood testing results, she had hypercalcemia, and alkaline phosphatase (ALP) was increased to 1,253 U/L (normal range, 35 to 130); the patient was sent to the endocrinology department. Her past history was significant for a surgical procedure for fibrocystoma of her right humerus 20 years ago, and she had donated one of her kidneys to a relative 7 years previously. She had taken atorvastatin 10 mg, amlodipine 5 mg, and omega-3 fatty acid 1,000 mg daily for the past 3 years to treat high blood pressure and dyslipidemia. The patient had been misdiagnosed with a thyroid nodule and hypothyroidism at another hospital 4 years previously and had immediately been prescribed levothyroxine 50 µg/day. At that time, the thyroid ultrasonography revealed two nodules that were 0.3 and 0.5 cm in diameter on her right lobe and another nodule that was 2.3×1.3 cm in size that was projected backwards. She had fine needle aspiration cytology for the nodule on the left lobe, and this had revealed a benign nodule. She had been followed up every 6 months by neck ultrasonography. Two years later, when the nodule on the left lobe of the thyroid had increased in size to 2.9×1.7 cm, they carried out radiofrequency ablation. However, the thyroid nodule remained the same size even after the radiofrequency ablation, so they monitored its size every 6 months for 2 more years (). During that time, the patient began experiencing backache and visited the orthopedics department of our hospital where she was suspected of having metabolic bone disease due to the high serum ALP value.
The patient presented with generalized weakness and fatigue without other hypercalcemic symptoms. The peripheral blood examination was as follows: leukocyte count, 7,020/mm3; hemoglobin, 9.3 g/dL; platelet count, 249,000/mm3; prothrombin time (PT), 14.4 seconds (normal range, 11.9 to 14.3); activated partial thromboplastin time (aPTT), 31.3 seconds (normal range, 29.1 to 43.5); serum iron, 65 µg/dL (normal range, 40 to 160); total iron binding capacity (TIBC), 258 µg/dL (normal range, 230 to 430); transferrin saturation, 25%; and ferritin, 158.6 ng/mL (normal range, 13 to 150). Serum chemistry values were also obtained: blood urea nitrogen, 26.9 mg/dL; creatinine, 1.98 mg/dL; glucose, 110 mg/dL; ALP, 1,011 U/L; aspartate aminotransferase, 23 U/L; and alanine aminotransferase, 11 U/L. Serum calcium was 14.6 mg/dL, phosphate was 3.5 mg/dL, and ionized calcium was 7.2 mg/dL. Serum protein and serum albumin were 6.9 and 3.7 g/dL, respectively. The results of the serum electrolyte test revealed that sodium was 135.7 mmol/L, potassium was 4.3 mmol/L, chloride was 104.0 mmol/L, and serum osmotic pressure was 286 mOsm/kg. According to the serum lipid examination, the total cholesterol was 146 mg/dL, triglyceride was 95 mg/dL, high density lipoprotein was 33 mg/dL, and low density lipoprotein was 79 mg/dL. A thyroid function test found T3 was 108.9 ng/dL (normal range, 80 to 200), thyroid stimulating hormone was 0.40 mIU/L (normal range, 0.27 to 4.2), and free T4 was 0.74 ng/dL (normal range, 0.93 to 1.70). Under dual energy X-ray absorptiometry-based bone density examination, the T-score of the lumbar region was -1.4, while the T-scores of the neck were -1.2 on the left and -1.8 on the right. Except for the fifth lumbar vertebra, which had spondylolisthesis, nothing remarkable was found on magnetic resonance imaging.
According to further blood tests, 25-hydroxyvitamin D3 was 9.6 ng/mL (normal range, 4.8 to 52.8), and 1,25-dihydroxyvitamin D3 was 10.5 pg/mL (normal range, 19.6 to 54.3), while the intact parathyroid hormone (iPTH) was 1,911 pg/mL (normal range, 15 to 65). When we performed bone scanning with 99mTc, the amount of cortical bone radioactive isotope uptake increased very high (). Because we suspected hyperparathyroidism, we carried out a 99mTc sestamibi scan and suspected the lesion that had been previously diagnosed as a left thyroid nodule was likely a parathyroid adenoma (). Using thyroid Doppler ultrasonography, we discovered a hypervascular adenoma that was 5-cm-sized solid mass with similar echo of surrounding thyroid tissue in the center, and slightly low echo in outer part in the inferior site of left thyroid gland (), while on the right thyroid parenchyma we discovered two thyroid nodules, 0.3 and 0.5 cm each in diameter, that the patient had had 4 years before. We performed neck computed tomography and found there was no neck lymph node metastastasis and local invasion of other organs ().
The patient received both hydration and diuretic treatments until she underwent a surgical operation to control the hypercalcemia; she also had pamidronate 90 mg intravenous injections twice a week. On the 11th day after hydration and diuretic treatment, her condition had improved; serum calcium was reduced to 11.6 mg/dL, and creatinine improved to 1.11 mg/dL. On the 12th day, the patient had left parathyroid excision and was diagnosed with a parathyroid adenoma (). Following the surgical procedure, iPTH normalized to 42.5 pg/mL, but calcium and vitamin D were prescribed for 9 months to cure the hypocalcemia that had developed due to hungry bone syndrome. It has been a year since the surgical operation, and her calcium, phosphate, ALP, and iPTH all remain at normal levels.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [110.0, 'mg/dL'], 'Sodium': [135.7, 'mmol/L']}",135.94,129.143,142.737,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 135.7 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 135.7 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 135.7 mmol * 1 mEq/mmol = 135.7 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.7 mmol sodium/L converts to 135.7 mEq sodium/L. 
The concentration of glucose is 110.0 mg/dL. 
Plugging in these values into the formula gives us 135.7 mEq/L + 0.024 * (110.0 - 100) = 135.94 mEq/L.
Hence, the patient's corrected concentration of sodium is 135.94 mEq/L."
5378,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2858844-1,Extracted,"A 32-yr-old multipara with GDM was referred at 33 weeks and 2 days of her second pregnancy from a private clinic to the emergency room of our institute and presented with severe headache, blurred vision, dizziness, and vomiting for 2 days. She had never been diagnosed with overt DM in her medical history. Her first pregnancy was uneventful and she delivered by cesarean section due to failure to progress.
The referral note indicated that all antenatal screening tests, including the initial serum glucose level performed in the first trimester to the present pregnancy, were within normal range. However, at 25 weeks and 5 days, she was diagnosed with GDM based on 1-hr 50-g glucose tolerance test, the result of which was 240 mg/dL. The test result for a 100-g glucose tolerance test was unavailable. Since then, she was instructed to control blood glucose level by diet modification only. Two days prior to admission, severe headache, blurred vision, dizziness, and vomiting suddenly developed, and she went to a private clinic where she was admitted for conservative care. She was informed that her blood glucose levels ranged from 140 to 200 mg/dL and that she had polyhydramnios. Due to persistent vomiting and poor intake for 2 days, she was transferred to our emergency room for further diagnosis and care.
On physical examination, the patient was acute-ill looking with alert mental status. Blood pressure was 120/85 mmHg; pulse rate, 95 bpm; body temperature, 36.8℃ and respiratory rate, 20 times/min. Dry skin and dry tongue were present but neck stiffness was absent. No sign of focal neurologic deficit was noted. Hematology lab results were normal and high sensitivity C-reactive protein (CRP) was increased to 15.1 mg/dL (0-3.0). Other than a slight decrease in serum sodium to 133 mM/L (normal, 135-145 mM/L), serum electrolyte levels were normal. Kidney and liver function test results were within normal limits. Increased serum fasting glucose level of 164 mg/dL (normal, 70-110 mg/dL) was accompanied by HbA1c level of 7.7% suggesting poorly controlled diabetes. Random urine test results denoted increased specific gravity with ketone secretion and glucose and protein were absent. Arterial blood gas analysis showed a normal pH, however, the anion gap increased to 19 mM/L. Fetal sonogram showed a structurally normal fetus large for gestational age accompanied by polyhydramnios (amniotic fluid index=32.4 cm).
Due to her presenting symptoms, brain magnetic resonance (MR) imaging was scheduled to rule out intracranial pathology. However, tococardiogram performed prior to brain MR imaging demonstrated persistent severe variable decelerations (). Thus, emergency cesarean section was performed immediately. A female baby weighing 2,570 g was delivered at 1 min and 5 min with an APGAR score of 2 and 6, respectively. During surgery, maternal vital signs were stably maintained without massive bleeding. At postpartum, the uterus was firm without significant bleeding.
About 9 hr after surgery, brain MR imaging was performed because her symptoms persisted. The scan revealed an enlarged anterior pituitary gland with no area of enhancement in the center of the pituitary gland after contrast administration, suggesting pituitary necrosis (). The Synacthen test result was normal and other pituitary hormones were within normal range (adrenocorticotrophic hormone [ACTH] 16.1 pg/mL [10-60], growth hormone [GH] 0.8 ng/mL [0-9.5], prolactin 24.3 ng/mL [0-15], thyroid-stimulating hormone [TSH] 0.75 µIU/mL [0.35-5.50], free thyroxine [FT4] 0.99 ng/dL [0.89-1.76], luteinizing hormone [LH] 0.78 mIU/mL, and folliclestimulating hormone [FSH] 0.31 mIU/mL) on pituitary function investigation.
Postoperatively, elevated blood sugar was controlled with regular insulin for 2 days, and her initial presenting symptoms resolved over few days. She was discharged without medication after a week of uneventful postoperative recovery.
At 2 months follow up, although serum glucose level and pituitary function test results were unremarkable, follow-up brain MR imaging depicted progressive shrinkage of the pituitary gland; she failed to lactate and was amenorrheic (). She is under continuous surveillance without treatment.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [164.0, 'mg/dL'], 'Sodium': [133.0, 'mmol/L']}",134.536,127.8092,141.2628,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 133.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 133.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 133.0 mmol * 1 mEq/mmol = 133.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mmol sodium/L converts to 133.0 mEq sodium/L. 
The concentration of glucose is 164.0 mg/dL. 
Plugging in these values into the formula gives us 133.0 mEq/L + 0.024 * (164.0 - 100) = 134.536 mEq/L.
Hence, the patient's corrected concentration of sodium is 134.536 mEq/L."
5379,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7008170-1,Extracted,"A 60-year-old obese (BMI: 38.7 kg/m2) female patient from a rural area of North India presented with complaints of acute pain in the abdomen and abdominal distension for the last 7 days and an inability to pass stool for the last 3 days. She was a known case of type II diabetes mellitus for the last 6 years and was being treated with insulin for the same. There was no associated fever, jaundice, or any history suggestive of gastrointestinal bleeding. On examination, she was sick looking, with tachycardia (pulse of 100 beats/min), tachypnea (respiratory rate of 34 min−1), and hypotension (blood pressure 100/60 mmHg). Her abdomen was distended, with diffuse guarding and rigidity suggestive of peritonitis. Laboratory investigations demonstrated the following (values in parentheses indicate normal range): hemoglobin 9.2 g/dL (12–14 g/dL), white blood cell count 18 000/mm3 (4000–11 000/mm3), platelet count 32 000/mm3 (150 000–450 000/mm3), total bilirubin 0.9 mg/dL (0.3– 1.2 mg/dL), aspartate aminotransferase 722 IU/L (2–40 IU/L), alanine aminotransferase 169 IU/L (2–41 IU/L), alkaline phosphatase 249 IU/L (42–128 IU/L), albumin 2.13 g/dL (3.4–4.8 g/dL), sodium 142 meq/L (135–145 meq/L), potassium 3.6 meq/L (3.5–5 meq/L), urea 121 mg/dL (10–50 mg/dL), creatinine 1.0 mg/dL (0.5–1.2 mg/dL), and blood glucose (random) 170 mg/dL.
Chest X-ray was normal. X-ray abdomen in erect position showed no air under the diaphragm. Contrast-enhanced computed tomography (CECT) abdomen was performed, which demonstrated pneumoperitoneum and thickened duodenal wall, with decreased enhancement and intramural air foci (pneumatosis intestinalis) suggestive of gastric ischemia with necrosis (Fig. a). The visualized lungs appeared normal.
The patient was resuscitated with intravenous fluids and started on piperacillin-tazobactam. Inotropic support (noradrenaline) was required for hypotension. In view of severe sepsis and circulatory compromise that did not respond to initial fluid boluses, bilateral flank drains were placed to drain out the infected fluid and achieve partial source control. These yielded an output of around 500 mL of biliopurulent fluid in each drain. She responded favorably to resuscitation and drainage and was taken for emergency laparotomy around 10 h after the initial presentation. On exploration, there was gross peritoneal contamination with 700–800 mL of biliopurulent fluid. The liver was cirrhotic with a multinodular appearance. There was a solitary large perforation (6 cm × 6 cm) in the anterior wall of the distal stomach involving the pylorus and the first part of the duodenum (Fig. b). The tissue at the edges of the perforation site was necrotic with unhealthy blackish exudates covering it. Distal gastrectomy with Billroth II reconstruction was performed with hand-sewn closure of the duodenal stump. Cut section of the resected stomach showed multiple deep ulcers with punched out edges and blackish slough covering them (Fig. c,d). Histopathology demonstrated transmural necrotizing inflammation with the presence of multiple aggregates of fungal septate hyphae and acute branching pattern, confirming the morphology of Aspergillus spp (Fig. e,f).
Postoperatively, she was managed in the surgical intensive care unit. Liposomal amphotericin B was started in view of suspicion of fungal sepsis. However, despite optimal critical care and supportive management, she succumbed to septicemia with multiorgan dysfunction syndrome on postoperative day 2. Involvement of other organs could not be confirmed as consent for autopsy was not given.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [170.0, 'mg/dL'], 'Sodium': [142.0, 'mEq/L']}",143.68,136.496,150.864,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 142.0 mEq/L. 
The concentration of glucose is 170.0 mg/dL. 
Plugging in these values into the formula gives us 142.0 mEq/L + 0.024 * (170.0 - 100) = 143.68 mEq/L.
Hence, the patient's corrected concentration of sodium is 143.68 mEq/L."
5380,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3027455-1,Extracted,"A 29-year-old male presented to the emergency department (ED) after a suicide attempt by ingesting a large amount of rat poison, which according to emergency medical services (EMS) occurred just prior to arrival. Although EMS had been told that the patient had ingested a rat poison, the exact type of rodenticide was unknown.
Upon arrival to the ED, the patient was diaphoretic and in moderate respiratory distress. His vital signs were as follows: temperature 36.0 0C, blood pressure 113/99 mm Hg, heart rate 100 beats/minute, respiration rate 28 breaths/minute and oxygen saturation 88% on room air.
On arrival he was awake but appeared to be confused and was not answering questions. Excessive secretions were noted. His neck was supple. He had respiratory distress with harsh breath sounds and rhonchi throughout both lung fields. He was tachycardic but had a regular rhythm. The abdomen was soft and non-tender with increased bowel sounds. The patient had urinated on himself. He was moving all extremities but had some muscle fasciculations. His skin was diaphoretic, but no rash or track marks were evident. He was confused, uncooperative and not speaking. The pupils were 2 mm and non-reactive to light. Cranial nerves otherwise appeared to be intact. It was difficult to assess his motor, sensory and cerebellar function because he was very uncooperative. Initially he was moving all his extremities.
An initial bedside serum glucose analysis was 186 mg/dL. Other laboratory values were as follows: serum sodium 138 mmol/L, potassium 2.9 mmol/L, chloride 101 mmol/L, bicarbonate 17 mmol/L, glucose 247 mg/dL, blood urea nitrogen 16 mg/dL, and creatinine 1.0 mg/dL. Complete blood count showed a white blood count of 12.8 × 103/μL with 58% neutrophils and 33% lymphocytes, hemoglobin level of 17.2 g/dL and platelet count of 311,000 × 103/μL. Creatine kinase (CK) was 191 U/L (40–210) and CK-MB was 1.96 ng/ml (0.0–4.99) with a CK-MB index of 1% (0.0–2.49). Troponin I level was < 0.20 μg/L (0–2). His liver function tests showed that bilirubin, AST, ALT, and lipase were all within the normal range. Urine analysis was normal and the urine toxicology screen was negative. The coagulation profile was normal. His electrocardiogram showed sinus tachycardia without ischemic changes or QRS or QT prolongation. A plasma cholinesterase level was drawn and sent to the laboratory.
Fifteen minutes after being initially assessed, his condition rapidly deteriorated. He developed excessive salivation with large amounts of foamy white secretions, which continually spewed from his mouth, making it very difficult to keep his airway clear, even with mechanical suctioning. His oxygen saturation dropped into the low 80s, despite receiving high flow oxygen, and he was subsequently intubated. He was given 2 mg lorazepam intravenously (IV) prior to intubation to sedate him, and he was given another 2 mg of it after he was intubated.
Based on the history and physical examination findings, which were consistent with an overdose of a cholinergic agent – probably an organophosphate or carbamate – the patient was given 2 mg of atropine IV, without any effect. He was then given another 2 mg IV every five minutes until his secretions were dry. He received a total of 16 mg of atropine IV in the ED. He was also given 1 gram of pralidoxime as an IV infusion over 30 minutes. He was hydrated with intravenous normal saline and his hypokalemia was corrected with potassium chloride.
When the staff realized that he had possibly taken an organophosphate, they double gloved and donned gowns and masks. All of the patient’s clothes were removed and discarded in plastic bags. He was washed with soap and water. After he was intubated, a nasogastric tube was inserted. He was lavaged and 50 grams of activated charcoal was administered down the nasogastric tube. None of the EMS or ED personnel developed any signs or symptoms of cholinergic poisoning.
After intubation and treatment with atropine, pralidoxime and lorazepam, the patient’s respiratory status showed marked improvement. His oxygen saturation was 100%. He was admitted to the intensive care unit, where he did not require any further treatment with atropine or pralidoxime. He was weaned off the ventilator and extubated without difficulty on hospital day 4. He remained stable and was transferred to the medical floor where psychiatry was consulted. The patient was then admitted for attempting to suicide by ingesting a rat poison called “Tres Pasitos.” Its active ingredient is aldicarb, a very potent carbamate. His initial serum cholinesterase level was 103 units/ml (normal range 350–934), confirming the clinical diagnosis. This level was not repeated, because his clinical status greatly improved.
Eventually, he was cleared by psychiatry and discharged home with appointments for close follow up in the medical and psychiatry clinics. When the patient was seen in the medical clinic one week after discharge, he had no complaints, and no evidence of residual toxicity was found on examination. No further testing was performed.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [247.0, 'mg/dL'], 'Sodium': [138.0, 'mmol/L']}",141.528,134.4516,148.6044,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 138.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 138.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 138.0 mmol * 1 mEq/mmol = 138.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mmol sodium/L converts to 138.0 mEq sodium/L. 
The concentration of glucose is 247.0 mg/dL. 
Plugging in these values into the formula gives us 138.0 mEq/L + 0.024 * (247.0 - 100) = 141.528 mEq/L.
Hence, the patient's corrected concentration of sodium is 141.528 mEq/L."
5381,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6280328-1,Extracted,"A 7 years 4 months old girl presented with excessive weight gain. She was born at term with a birth weight of 2900 g [-0.96 standard deviation (SD)]. The parents reported that she began to gain weight rapidly at 1.5 years of age. There was no consanguinity between the parents. The patient had two healthy siblings (of ages 11 years and 9 months). Body weight was 61 kg (±3.9 SD) and height was 130 cm (±1.8 SD) with a body mass index (BMI) of 36 kg/m2 (±3.3 SD). She had a plethoric facial appearance, axillary acanthosis nigricans, pale/blue fingers and toes and stage 2 thelarche, bilaterally. The patient was admitted to hospital for further evaluation. During follow-up, it was observed that she had episodes of excessive sweating and a body temperature as low as 35.4 °C. Blood pressure was 95/60 mmHg (95 percentile: 120/80 mm/Hg). Laboratory evaluation showed the following results: sodium (Na), 156 mmol/L [normal range (NR): 135-145 mmol/L]; aspartate transaminase, 87 U/L (NR: 8-45 U/L); alanine aminotransferase, 57 U/L (NR: 7-55 U/L); urine density, 1024. The remaining liver function tests, serum electrolytes, lipids kidney function tests and complete blood count were normal. The patient had no polydipsia; thus, hypernatremia was considered to be due to insufficient intake. Oral fluid replacement was given and the hypernatremia was corrected (Na: 141 mmol/L). Impaired glucose tolerance (141 mg/dL at two hours) was detected in the oral glucose tolerance test performed due to morbid obesity and acanthosis nigricans; and the patient was started on metformin. An abdominal ultrasound was performed, due to the elevated transaminase levels, which revealed grade 3 hepatic steatosis.
In terms of hormonal problems that may present in the patient’s follow-up hormonal evaluation revealed the following results: free T4, 0.7 ng/mL (NR: 0.98-1.6 ng/mL; thyroid stimulating hormone (TSH), 4.8 µIU/mL (NR: 0.5-4.3 µIU/mL); adrenocorticotropic hormone (ACTH), 24 pg/mL (NR: 10-60 pg/mL); cortisol, 1.5 µg/mL (NR: 3-21 µg/mL); LH, 1.3 mIU/mL (prepubertal NR: <0.3 mIU/mL); estradiol, 12.9 pg/mL (prepubertal NR: <12 pg/mL); prolactin (PRL), 33 ng/mL (NR: 4.7-23.3 ng/mL). Insulin like growth factor-1 (IGF-1) was <25 ng/mL and IGF binding protein 3 (IGFBP3) 1870 ng/mL. Bone age was advanced at 10 years. Peak cortisol response to low dose ACTH stimulation test was low (9.9 µg/mL).
A diagnosis of secondary adrenal insufficiency, central hypothyroidism and central precocious puberty was made and treatment was initiated with hydrocortisone, thyroxine and leuprolide acetate. No further evaluation or treatment was considered for GH deficiency, due to the patient’s normal height. However, a predisposition to neural crest tumor was considered despite the low IGF-1 and IGFBP3 levels of the patient. Brain and pituitary magnetic resonance (MR) imaging studies were found to be normal. The IQ score was 65. The pale appearance of the fingers was considered to be due to Raynaud’s phenomenon (). Alterations in body temperature and Raynaud’s phenomenon were attributed to autonomic dysfunction. Pulmonary hypertension was detected on echocardiography and nifedipine was prescribed.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [141.0, 'mg/dL'], 'Sodium': [156.0, 'mmol/L']}",156.984,149.1348,164.8332,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 156.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 156.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 156.0 mmol * 1 mEq/mmol = 156.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 156.0 mmol sodium/L converts to 156.0 mEq sodium/L. 
The concentration of glucose is 141.0 mg/dL. 
Plugging in these values into the formula gives us 156.0 mEq/L + 0.024 * (141.0 - 100) = 156.984 mEq/L.
Hence, the patient's corrected concentration of sodium is 156.984 mEq/L."
5382,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-5833,Extracted,"A 72-year-old man is seen in the hospital for a sacral rash. The patient has been hospitalized for the past 3 weeks for a heart failure exacerbation. When the nurse went to bathe him this morning, she noticed a red rash over his sacrum. The patient reports mild discomfort and denies pruritus. The patient has chronic kidney disease, urinary incontinence, ischemic cardiomyopathy, gout, and poor mobility. His current medications include aspirin, furosemide, metoprolol, lisinopril, spironolactone, and prednisone that was started for a recent gout flare. The patient’s temperature is 97°F (37.2°C), blood pressure is 110/62 mmHg, pulse is 68/min, and respirations are 13/min with an oxygen saturation of 98% on room air. On physical examination, there is a 4 cm x 6 cm patch of non-blanchable erythema over the patient’s sacrum that is mildly tender to palpation. Labs are obtained, as shown below:

Leukocyte count: 10,000/mm^3 with normal differential
Hemoglobin: 15.2 g/dL
Platelet count: 400,000/mm^3

Serum:
Na: 138 mEq/L
K+: 4.3 mEq/L
Cl-: 104 mEq/L
HCO3-: 25 mEq/L
BUN: 26 mg/dL
Creatinine: 1.5 mg/dL
Glucose: 185 mg/dL

A hemoglobin A1c is pending.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [185.0, 'mg/dL'], 'Sodium': [138.0, 'mEq/L']}",140.04,133.038,147.042,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 138.0 mEq/L. 
The concentration of glucose is 185.0 mg/dL. 
Plugging in these values into the formula gives us 138.0 mEq/L + 0.024 * (185.0 - 100) = 140.04 mEq/L.
Hence, the patient's corrected concentration of sodium is 140.04 mEq/L."
5383,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2908655-1,Extracted,"An 84-year-old female with history of major depression and anxiety was evaluated by her psychiatrist for worsening anxiety and given a single dose of 3 mg of paliperidone. Eight hours later she became increasingly agitated and, according to her daughter, “looked like she was going to crawl out of her skin.” She then told her daughter “make it go away, make it go away,” and subsequently stopped speaking and responding to any physical or verbal stimuli, although she appeared awake and alert. She had no prior documented episodes of catatonia. Her daughter brought her into the local emergency department (ED).
In the ED, she had a temperature of 37.3°C, pulse 80 beats per minute, blood pressure 161/72 mm Hg, respiratory rate 20 breaths per minute and oxygen saturation of 98% on room air. Her medications were citalopram, trazodone, levothyroxine, and paliperidone. She lived with her daughter, who related no recent trauma. The patient previously took risperidone, but it had been discontinued after several months because of mild akathisia, with both restlessness and tremor.
Physical exam showed an alert, well appearing elderly female in no acute distress. Her pupils were equal round and reactive to light; she would not comply with extraocular muscle testing. She did open her mouth on request and stuck out her tongue midline; there was no erythema, and mucous membranes were moist. Cardiopulmonary exam was unremarkable; abdominal palpation did not cause any change in her facial expression and was soft without masses. While she complied with several requests for the cranial nerve exam she would not move her fingers or toes when asked, but was noted to turn her head in all directions and roll from side to side, moving all extremities equally. Her brachioradialis and achilles reflexes were equal and Babinski reflexes were downgoing. She exhibited stupor and mutism with fixed postures.
Finger-stick glucose was 114 mg/dL. Intravenous diphenhydramine, 25 mg and benztropine, 0.5 mg were given for dystonia without any change. Noncontrast head computed tomography (CT) was performed due to concern for stroke and was unremarkable. Laboratory tests showed white blood cell count of 7.4 K/mm3 with 60% neutrophils, her hematocrit was 37.6%, and platelets were 203 K/mm3. Electrolytes and renal function showed sodium 135 mmol/L, potassium 3.5 mmol/L, chloride 101 mmol/L, bicarbonate 20 mmol/L, calcium 9.8 mg/dL, blood urea nitrogen 12 mg/dL, and creatinine 1.0 mg/dL.
Due to the lack of inpatient psychiatric beds, she was observed in the ED for 12 hours. Psychiatric consultation had no specific recommendations. Sixteen hours after the dose of paliperidone, without other therapy, she began to talk and interact. More detailed neurological exam showed no focal deficits. Her mood and affect were appropriate. She did not recall the events of the previous evening but remembered her daughter talking, although she was unable to respond.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [114.0, 'mg/dL'], 'Sodium': [135.0, 'mmol/L']}",135.336,128.5692,142.1028,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 135.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 135.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 135.0 mmol * 1 mEq/mmol = 135.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mmol sodium/L converts to 135.0 mEq sodium/L. 
The concentration of glucose is 114.0 mg/dL. 
Plugging in these values into the formula gives us 135.0 mEq/L + 0.024 * (114.0 - 100) = 135.336 mEq/L.
Hence, the patient's corrected concentration of sodium is 135.336 mEq/L."
5384,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3537693-1,Extracted,"A 35-day-old male Egyptian baby was referred to our institution from a regional hospital for evaluation of a two-week history of recurrent vomiting associated with hyponatremia, hyperkalemia and failure to gain weight. He was the first child of related Egyptian parents. The pregnancy was uneventful and his mother had not been treated with any drugs. The existence of other children with this condition had not previously been mentioned. He was delivered at term by Caesarean section with a birth weight of 3.4kg, and cried immediately after delivery. He required admission to the special care baby unit shortly after birth for hypoglycemia; his blood sugar levels were easily maintained on 10% dextrose and then on milk feeds.
On examination, our patient’s weight was 3.5kg (below the third percentile), he was dehydrated, his blood pressure was 70/40mmHg, and he had no hyperpigmentation or dysmorphic features. A genital examination revealed distal penile hypospadias with chordee and normal testes (Figure ). Laboratory investigation results showed a serum sodium level of 119mmol/L, potassium 6.5mmol/L and glucose 55mg/dL. Blood gas analysis results showed a pH of 7.31, bicarbonate ion level of 16.9mmHg and a base excess of 6.3mmol/L. His cortisol level was 0.3μg/dL (normal range: 2.8 to 23μg/dL) and adrenocorticotropic hormone level, 512pg/mL (normal range: 6 to 48pg/mL). An adrenocorticotropic hormone stimulation test did not cause a rise in his cortisol level. His 17-hydroxyprogesterone level was 0.005ng/mL (normal range: 0.03 to 0.9ng/mL), androstenedione 0.012ng/mL (normal range: 0.1 to 0.17ng/mL), dehydroepiandrosterone 6ng/mL (normal range: 50 to 480ng/mL), plasma renin activity 90ng/mL/hour (normal range: 2.35 to 37ng/mL/hour) and aldosterone 31pg/mL (normal range: 50 to 900pg/mL). His triglyceride and creatine kinase levels were normal. His blood karyotype was 46,XY. A magnetic resonance imaging study of his abdomen revealed small adrenal glands and a normal genitourinary system.
Based on the clinical history and investigative findings, a provisional diagnosis of congenital adrenal hypoplasia associated with hypospadias was made. A molecular genetic study detected hemizygous mutations (p.Arg327Pro). A deoxyribonucleic acid (DNA) study of our patient’s mother confirmed her to be heterozygous for the same mutation. No mutation was found in his father. With the identification of a hemizygous mutation in the DAX-1 gene, a clinical diagnosis of X-linked congenital adrenal hypoplasia was confirmed. Further, mutation c.325delG in the MAMLD1 gene was detected, which may point to a possible etiology of hypospadias in our patient’s case. He was started on hydrocortisone at a dose of 10mg/m2/day and fludrocortisone 0.05mg/day. After three weeks of treatment the vomiting stopped, his weight was 4.1kg and his blood sugar, sodium, potassium and cortisol levels normalized. At the age of three months, a human chorionic gonadotropin (hCG) loading test was performed to evaluate his gonadal function. Basal values of luteinizing hormone and follicle-stimulating hormone were <0.5IU/L and 0.41IU/L, respectively, which is within normal prepubertal limits. The hCG loading test resulted in a normal testosterone response from <0.05ng/mL to 4.24ng/mL. The ratio of testosterone to DHT after hCG loading was 7.3:1.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [55.0, 'mg/dL'], 'Sodium': [119.0, 'mmol/L']}",117.92,112.024,123.816,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 119.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 119.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 119.0 mmol * 1 mEq/mmol = 119.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 119.0 mmol sodium/L converts to 119.0 mEq sodium/L. 
The concentration of glucose is 55.0 mg/dL. 
Plugging in these values into the formula gives us 119.0 mEq/L + 0.024 * (55.0 - 100) = 117.92 mEq/L.
Hence, the patient's corrected concentration of sodium is 117.92 mEq/L."
5385,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-1763,Extracted,"A 35-year-old African American woman comes to the physician because of intermittent palpitations over the past 2 weeks. During this period she has also had constipation and has felt more tired than usual. She was diagnosed with hypertension 4 weeks ago and treatment with chlorthalidone was begun. Her temperature is 36.5°C (97.7°F), pulse is 75/min, and blood pressure is 158/97 mm Hg. Physical examination shows a soft and nontender abdomen. There is mild weakness of the upper and lower extremities. Deep tendon reflexes are 1+ bilaterally. Laboratory studies show:
Hemoglobin 13.5 g/dL
Leukocyte count 5,000/mm3
Serum
Na+ 146 mEq/L
Cl− 100 mEq/L
K+ 2.8 mEq/L
HCO3− 30 mEq/L
Glucose 97 mg/dL
Urea nitrogen 10 mg/dL
Creatinine 0.8 mg/dL
Test of the stool for occult blood is negative. An ECG shows premature atrial complexes. Chlorthalidone is discontinued and oral potassium chloride therapy is begun. One week later, the patient's plasma aldosterone concentration is 26 ng/dL (N=3.6 to 24.0 ng/dL) and plasma renin activity is 0.8 ng/mL/h (N=0.3 to 4.2 ng/mL/h).","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [97.0, 'mg/dL'], 'Sodium': [146.0, 'mEq/L']}",145.928,138.6316,153.2244,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 146.0 mEq/L. 
The concentration of glucose is 97.0 mg/dL. 
Plugging in these values into the formula gives us 146.0 mEq/L + 0.024 * (97.0 - 100) = 145.928 mEq/L.
Hence, the patient's corrected concentration of sodium is 145.928 mEq/L."
5386,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7074520-1,Extracted,"An 11-year-old castrated male domestic shorthair cat was presented to the emergency service of the University of Missouri Veterinary Health Center (MU-VHC) for anorexia, lethargy and an apparent seizure in May 2019. Approximately 1 week prior to presentation, the cat had a suspected altercation with an unidentified animal. The owners cleaned a puncture wound to the neck and applied antibiotic ointment; the cat seemed relatively normal until 3 days prior to presentation.
Hyporexia prompted a visit to the primary care veterinarian, where there were no abnormalities on examination other than a temperature of 104oF (40oC). Point-of-care retroviral tests were negative, hematocrit was 40% and no parasites were identified on peripheral blood smear examination. The cat was discharged with pradofloxacin but re-presented the following day for complete anorexia and worsened lethargy. Fever was unchanged and mild icterus was now identified. A complete blood count (CBC) demonstrated a hematocrit of 31% with mild neutropenia (2.11 × 103/μl; reference interval [RI] 2.5–12.5 × 103/μl) and platelet aggregates; no parasites were identified. Subcutaneous crystalloid fluids were administered, but the cat was not hospitalized. The following morning, the cat experienced what the owners described as a seizure, prompting the emergency visit to MU-VHC. The cat, which had survived cytauxzoonosis 7 years prior, lived on several wooded acres adjacent to Mark Twain National Forest in Cherryville, MO, USA, and was treated regularly with a combination product containing fipronil, etofenprox and (S)-methoprene (Frontline Tritak; Merial).
On presentation at MU-VHC, the cat’s temperature was 104oF (40oC), pulse 180 beats per min, respiratory rate 24 breaths per min and was judged to be 6% dehydrated. There were no obvious wounds. Mucus membranes were pale and mildly icteric. Complete neurologic examination findings were not recorded, but the cat was reported to be dull and lethargic. Abnormalities on plasma chemistry profile included hyperglycemia (179 mg/dl; RI 80–155 mg/dl), hyponatremia (140 mEq/l; RI 148–154 mEq/l), hypochloremia (108 mEq/l; RI 112–123 mEq/l), hypokalemia (3.0 mEq/l; RI 3.1–4.6 mEq/l), hypocalcemia (8.4 mg/dl; RI 8.6–10.4 mg/dl) and hyperbilirubinemia (2.6 mg/dl; RI 0.1–0.2 mg/dl). Abnormalities on CBC included marked thrombocytopenia with few platelet clumps identified (10 × 103/μl; RI 166–466 × 103/μl), neutropenia (1.82 × 103/μl; RI 2.2.7–9.82 × 103/μl) and moderate numbers of intraerythrocytic signet ring-shaped inclusions compatible with C felis (). Hematocrit was again 31%.
Based on a suspected diagnosis of cytauxzoonosis and the associated costs for treatment, the owners opted against specific therapy and took the cat home. After their cat experienced several additional seizures later that same day, they arranged for an at-home euthanasia. Based on our discussions about the unique nature of repeat cytauxzoonosis, the owners requested that the veterinarian performing euthanasia harvest a small sample of liver and spleen to be shipped in formalin to the MU Veterinary Medical Diagnostic Laboratory for confirmation of the suspected diagnosis.
On hematoxylin and eosin stain of prepared tissues, portal tracts were infiltrated by small numbers of lymphocytes, macrophages and plasma cells. Marked lymphoid depletion of the splenic white pulp was noted. Mild extramedullary hematopoiesis was identified in the parenchyma of both the spleen and liver. Although modest in numbers, schizont structures typical of the protozoan C felis were recognized in hepatic arterioles and sinusoids, as well as in splenic sinusoids ( and ). Formalin-fixed paraffin-embedded tissues (from this case and a non-infected cat as a negative control) were sent to North Carolina State University for the molecular detection of C felis. Slides were heated to remove paraffin and total DNA was extracted. Partial C felis cytochrome oxidase C1, 18S rRNA and mitochondrial large ribosomal subunit-4 genes were amplified from the infected cat but not the control (see for methodologic detail).
In May of 2012, the same cat had been hospitalized at MU-VHC for treatment of acute cytauxzoonosis. Diagnosis was based on a typical presentation, including acute onset of anorexia and lethargy, high fever, pancytopenia, hyperbilirubinemia, hyperglycemia, panhypoproteinemia and multiple electrolyte abnormalities, as well as cytologic identification of numerous typical red blood cell (RBC) piroplasms. Engorged ticks were found on the cat at the time of diagnosis. Treatment included atovaquone and azithromycin, as well as intensive in-hospital supportive care, including multiple blood transfusions, thoracocentesis to relieve pleural effusion, and placement of an esophagostomy tube to facilitate feeding and medication administration. Despite a complicated clinical course, the cat was discharged after 9 days. It recovered completely, and a single CBC performed 2 weeks after hospital discharge failed to identify any parasites.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [179.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",141.896,134.8012,148.9908,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.0 mEq/L. 
The concentration of glucose is 179.0 mg/dL. 
Plugging in these values into the formula gives us 140.0 mEq/L + 0.024 * (179.0 - 100) = 141.896 mEq/L.
Hence, the patient's corrected concentration of sodium is 141.896 mEq/L."
5387,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-4395,Extracted,"A 72-year-old man presents to the emergency department for a change in his behavior. The patient's wife called 911 and he was brought in by emergency medical services. She noticed that he seemed somnolent and not very responsive. The patient has a past medical history of type II diabetes, obesity, osteoarthritis, and migraine headaches. His current medications include naproxen, insulin, atorvastatin, metformin, ibuprofen, omeprazole, and fish oil. His temperature is 99.5°F (37.5°C), blood pressure is 170/115 mmHg, pulse is 80/min, respirations are 19/min, and oxygen saturation is 98% on room air. On physical exam, the patient is somnolent and has a Glasgow Coma Scale of 11. Cardiac and pulmonary exams are notable for bibasilar crackles and a systolic murmur that radiates to the carotids. Neurological exam is deferred due to the patient's condition. Laboratory values are shown below.

Hemoglobin: 12 g/dL
Hematocrit: 36%
Leukocyte count: 9,500 cells/mm^3 with normal differential
Platelet count: 199,000/mm^3

Serum:
Na+: 144 mEq/L
Cl-: 98 mEq/L
K+: 4.0 mEq/L
HCO3-: 16 mEq/L
BUN: 44 mg/dL
Glucose: 202 mg/dL
Creatinine: 2.7 mg/dL
Ca2+: 9.2 mg/dL
AST: 12 U/L
ALT: 22 U/L

The patient is started on IV fluids.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [202.0, 'mg/dL'], 'Sodium': [144.0, 'mEq/L']}",146.448,139.1256,153.7704,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 144.0 mEq/L. 
The concentration of glucose is 202.0 mg/dL. 
Plugging in these values into the formula gives us 144.0 mEq/L + 0.024 * (202.0 - 100) = 146.448 mEq/L.
Hence, the patient's corrected concentration of sodium is 146.448 mEq/L."
5388,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7538038-1,Extracted,"A 3 year old boy, was admitted due to dyspnea in February, 2020. He presented with weakness, malaise, anorexia, severe dry cough, tachypnea and respiratory distress from 4 days prior to his admission.
In his past medical history the patient was premature and had liver cirrhosis due to biliary atresia. He underwent a living donor partial organ LT at 18 months old. Since then he received immunosuppressive medication which included prednisolone 5 mg daily and tacrolimus 2 mg daily.
At his last admission the patient’s mother mentioned a history of upper respiratory tract infection from 1 week ago that did not improve with regular medical therapies. On arrival, he had respiratory distress and decreased O2 saturation and tachypnea. He was admitted with impression of acute respiratory distress syndrome (ARDS) and was transferred to the pediatric intensive care unit immediately.
On examination, he was irritable, ill and toxic with a respiratory rate of 38–40/min, heart rate of 110/min, O2 saturation of 90–91% with a normal blood pressure and was afebrile. He was alert and orient with a Glasgow coma scale (GCS) of 15. His throat was congested without tonsillar exudation. In lung auscultation, harsh breath sounds were heard. Other physical examinations were normal.
His blood work results on admission were as follows: white blood cell (WBC) count of 12.8*103/μl (with a neutrophil count of 10,880 and a lymphocyte count of 1024); red blood cell count, 4.6*106/μl; platelet cell count, 187*103/μl; hemoglobin, 13.8 g/dl; C-reactive protein (CRP), 102 mg/dl; erythrocyte sedimentation rate (ESR), 56 mm/h; sodium, 141 meq/L; potassium, 4.5 meq/L; magnesium, 1.9 mg/dl; blood urea creatinine (BUN), 22.3 mg/dl; creatinine, 0.6 mg/dl; glucose, 88 mg/dl; lactate dehydrogenase, 1277 U/L. His liver function profile was as follows: alanine transaminase (ALT), 28 U/L; aspartate transaminase (AST), 50 U/L; alkaline phosphatase (Alk-ph), 162 U/L; albumin, 2.7 g/dl; prothrombin time (PT), 16 s; partial thromboplastin time (PTT), 28 s; international normalized ratio (INR), 1.7. Patient’s blood tacrolimus level at final visitation was 10 ng/mL.
Vancomycin (50 mg daily), meropenem (90 mg daily), azithromycin (15 mg daily), voriconazole (50 mg daily) and co-trimoxazole (60 mg daily) were started from the first day of admission. About 48 h after hospitalization, the patient became unresponsive to continuous positive airway pressure (CPAP) and he was intubated. After which prednisolone and tacrolimus were discontinued.
During the third day of admission, his liver enzymes started to rise (ALT, 337 U/L; AST, 377 U/L). He developed acute kidney injury and BUN and creatinine increased up to 98 mg/dl and 2.5 mg/dl, respectively. Blood cultures were negative for growth of any microorganisms.
Chest x-ray on admission showed bilateral infiltration and on day 4 of admission it became a white lung. With suspicion of COVID-19, hydroxychloroquine (15 mg daily), lopinavir/ritonavir (100 mg daily) and oseltamivir (30 mg daily) were added to the antibiotic regimen. Due to the outbreak of COVID-19, a nasopharyngeal swab was taken and sent for real time polymerase chain reaction (RT-PCR) which was positive.
During the hospital course, the patient developed multi organ failure which included renal failure, liver failure and heart failure. On day 6 of admission, the patient developed excessive bleeding from the nose and mouth. Following which, cardiorespiratory arrest occurred and after 45 min of CPR the patient died 6 days after hospital admission. His laboratory tests on day 5 were as follows: WBC count, 10.8 × 103/μl (with a neutrophil count of 9190 and a lymphocyte count of 702); RBC count, 4.6 × 106/μl; platelet cell count, 165 × 103/μl; hemoglobin, 10.8 g/dl; sodium, 146 meq/L; potassium, 5.1 meq/L; magnesium, 2.8 mg/dl; BUN, 92 mg/dl; creatinine, 2.3 mg/dl; glucose, 114 mg/dl; ALT, 4000 U/L; AST, 3000 U/L; Alk-Ph, 160 U/L; albumin, 3.3; total bilirubin, 0.2 mg/dl; direct bilirubin, 0.1 mg/dl; CRP, 109 mg/dl; ESR, 61 mm/h; PT, 16 s; PTT seconds, 28; INR, 1.7.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [114.0, 'mg/dL'], 'Sodium': [146.0, 'mEq/L']}",146.336,139.0192,153.6528,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 146.0 mEq/L. 
The concentration of glucose is 114.0 mg/dL. 
Plugging in these values into the formula gives us 146.0 mEq/L + 0.024 * (114.0 - 100) = 146.336 mEq/L.
Hence, the patient's corrected concentration of sodium is 146.336 mEq/L."
5389,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7593056-1,Extracted,"A 49-year-old male patient was admitted to our hospital with a 3-month history of general weakness and anorexia. The patient had been treated for stage 5 CKD secondary to diabetic nephropathy at the nephrology division for the last 3 years. The patient's blood urea nitrogen (BUN) level was 57.2 mg/dL and creatinine (Cr) level was 6 mg/dL at 3 months before admission, and he reported worsening of uremic symptoms, such as malaise, weight loss, anorexia, nausea, and vomiting. After his diagnosis of type 2 diabetes mellitus 20 years before admission, the patient was on combination therapy including oral hypoglycemic agents and insulin. He had no past history of pulmonary TB and viral hepatitis. At the time of admission, his blood pressure, pulse rate, respiration rate, and body temperature (BT) were 109/53 mm Hg, 80 beats/min, 20 breaths/min, and 37.3 °C, respectively. His consciousness was clear, and no murmur or crackles were detected on chest auscultation, although both conjunctivae were pale. No signs of a mass, organomegaly, and nearby tenderness were observed on the abdominal examination. A peripheral blood test on admission revealed the following: white blood cell (WBC) count, 7000/μL (neutrophils, 72%); hemoglobin, 5.2 g/dL; platelets, 374,000/μL; and erythrocyte sedimentation rate, 44 mm/h. Serum biochemical examination revealed the following: glucose, 267 mg/dL; total protein, 6.2 g/dL; albumin, 2.6 g/dL; BUN, 96.9 mg/dL; Cr, 8.1 mg/dL (estimated glomerular filtration rate, 8 mL/min); aspartate aminotransferase, 7 IU/L; alanine aminotransferase, 18 IU/L; Na+/K+/Cl−/total CO2, 130/6.0/100/14 mEq/L; calcium, 7.6 mg/dL; phosphorus, 6.2 mg/dL; uric acid, 13.4 mg/dL; and C-reactive protein, 14.6 mg/L. On urinalysis, 2+ was observed for albumin and 1+ for occult blood, and microscopic urinary sediment evaluation revealed 1 to 3 WBCs per high-power field (HPF) and 3 to 5 red blood cells per HPF. Serum immunological tests showed the following: iron, 14 μg/dL; total iron binding capacity, 199 μg/dL; ferritin, 172 ng/mL; and HbA1C, 8%. A 24-h urine examination revealed a urinary protein excretion level of 1156 mg/day and Cr clearance of 8.8 mL/min/1.73 m2. The patient's chest radiograph did not reveal pulmonary infiltrates in either lung field. On admission, hemodialysis was initiated after insertion of a dual-lumen temporary catheter for suspected exacerbation of uremia. Regular hemodialysis was conducted three times a week, and an autologous arteriovenous fistula was created on the 10th hospital day. During hemodialysis on the 14th day of hospitalization, high fever with a BT of 38.3°C was noted. With suspicion of catheter-related infection, we exchanged the catheter used for vascular access for hemodialysis and administered cefazolin (2.0 g, three times per week) after each hemodialysis. Methicillin-sensitive Staphylococcus epidermidis was isolated from blood cultures. On the 25th day of hospitalization, the patient presented with intermittent low-grade fever, abdominal pain, and watery diarrhea. Polymerase chain reaction (PCR) for Clostridium difficile toxins in stool specimens detected the toxin B-positive strain. On the diagnosis of pseudomembranous colitis (PMC), we discontinued the administration of cefazolin and administered oral metronidazole (1500 mg/day). However, the patient's abdominal discomfort, fever (BT, 37.5–38.3°C), and night sweats persisted. Because the origin of fever was not clear, abdominal computed tomography (CT) performed on the 28th hospital day revealed masses with irregular walls in the proximal portion of the ascending colon near the ileocecal valve and adjacent lymphadenopathy (Fig. A); an increase in 18F-Fluorodeoxyglucose (FDG) uptake was also noted in the corresponding region on whole-body positron emission tomography (PET)/CT scan (Fig. ). The radiologic diagnosis was colon cancer with lymph node metastases. Colonoscopy with biopsy for histopathologic diagnosis was performed. A fungating circumferential mass with hypertrophic ulcerations, which mimicked a colonic tumor, was found in the ascending colon (Fig. A). However, microscopic examination demonstrated chronic caseating granulomatous inflammation and positive Ziehl-Neelsen stain for acid-fast bacillus (AFB), consistent with colonic TB (Fig. A and B). PCR analysis of the colonic lesions was negative for M. tuberculosis. The patient's tuberculin skin test (TST) result was also negative, and tumor markers, such as carcinoembryonic antigen and carbohydrate antigen 19-9, were all normal. We recommended surgical intervention including hemi-colectomy in view of the morphologic characteristics of the colonic lesions, but the patient refused surgery. Accordingly, we initiated quadruple therapy (HRZE): isoniazid (INH; 300 mg/day), rifampicin (RIF; 600 mg/day), pyrazinamide (PZA; 30 mg/kg, three times per week), and ethambutol (EMB; 15 mg/kg, three times per week). The patient was discharged from the hospital on the 45th day of admission after complete resolution of systemic symptoms. Anti-TB quadruple therapy was applied for the first 2 months; thereafter, it was switched to dual combination therapy (HR) of INH and RIF. Three months after the administration of anti-TB medications, follow-up colonoscopy showed improvement in colonic lesions. However, 9 months after the initiation of quadruple therapy, a second follow-up abdominal CT and colonoscopy showed polypoid residual lesions in the ascending colon (Figs. B and 3B) and we conducted laparoscopy-assisted ileocecal resection. Anti-TB chemotherapy was maintained for a total of 12 months. Progression of lymphadenopathy in the abdominal cavity or recurrence of colonic TB was not noted on follow-up abdominal CT performed at 6 months after discontinuation of anti-TB medications.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [267.0, 'mg/dL'], 'Sodium': [130.0, 'mEq/L']}",134.008,127.3076,140.7084,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 130.0 mEq/L. 
The concentration of glucose is 267.0 mg/dL. 
Plugging in these values into the formula gives us 130.0 mEq/L + 0.024 * (267.0 - 100) = 134.008 mEq/L.
Hence, the patient's corrected concentration of sodium is 134.008 mEq/L."
5390,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4749773-1,Extracted,"A 25-year-old male with a family background of Alport disease was referred for an assessment of kidney involvement. Family history consisted of a mother-related uncle on dialysis with biopsy-proven Alport disease, another mother-related cousin with kidney involvement, and a grandfather who died due to sudden death at the age of 42. The patient was asymptomatic and normotensive (blood pressure 115/68 mmHg), with a body mass index of 24 and no tobacco consumption. Main laboratory results included hematocrit 44%, glycemia 78 mg/dL, serum creatinine 1.07 mg/dL, creatinine clearance of 74 mL/min, sodium 143 mEq/L, potassium 3.9 mEq/L, serum albumin 4.3 g/dL, and 24-hour urinary albumin excretion 250 mg/day. A renal ultrasound was normal.
Podocyturia was assessed as follows: fresh urine samples were centrifuged at 1500 rpm during 5 min and the supernatant was discarded; 10% formaldehyde in phosphate-buffered saline (PBS) pH 7.2–7.4 was added to the sediment to cover it. Smears were made from each sample on 2% silane-coated slides. The slides were stained with immunofluorescence technique and observed by epifluorescent microscopy. The slides were preincubated with no immune rabbit serum in phosphate-buffered saline 0.1 M, pH 7.4 (PBS, 1 : 100) at room temperature for 30 minutes, followed by incubation with a polyclonal anti-synaptopodin antibody (1 : 100, ab109560 Alexa Fluor®, Abcam, Cambridge, United Kingdom) overnight in a wet chamber at 4°C. After several rinses in PBS, the slides were incubated with anti-rabbit IgG secondary antibody (1 : 200 Alexa Fluor 488, Abcam, Cambridge, United Kingdom) for 2 hours at room temperature in a wet chamber. Finally, all the slides were mounted using Fluoroshield Mounting Medium with DAPI (Abcam, Cambridge, United Kingdom) and observed in an epifluorescent microscope (Nikon Eclipse E200, Nikon, Tokyo, Japan). Negative controls were performed without primary antibodies. Podocyte counting was assessed by counting in urinary smears the number of cells in 10 microscopy fields of ×20. The podocyte count was 1.07 cells per ×20 field; the number of podocytes per gram of urinary creatinine was 29.9, and the number of podocytes/100 mL of urine was 5.35 (). This result was compared with 5 controls (): 3 males and 2 females; mean age 22 ± 7.2 years with no past history of morbidities; creatinine clearance 108 mL/min; mean 24-hour urinary albumin excretion 88 ± 11 mg/day. The mean podocyte count was 0.12 ± 0.1 cells per ×20 field while the mean number of podocytes per gram of urinary creatinine was 10.7 and the mean number of podocytes/100 mL of urine was 1.1. The patient declined to undergo a kidney biopsy but accepted to receive amiloride 5 mg/day orally. After three months of therapy new podocyturia and laboratory results were obtained. The podocyte count was 0.2 cells per ×20 field; the number of podocytes per gram of urinary creatinine was 9, and the number of podocytes/100 mL of urine was 1 (). Blood pressure was 110/70 mmHg, serum creatinine 1.09 mg/dL, creatinine clearance 79 mL/min, sodium 143 mEq/L, potassium 3.9 mEq/L, and 24-hour urinary albumin excretion 19 mg/day.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [78.0, 'mg/dL'], 'Sodium': [143.0, 'mEq/L']}",142.472,135.3484,149.5956,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 143.0 mEq/L. 
The concentration of glucose is 78.0 mg/dL. 
Plugging in these values into the formula gives us 143.0 mEq/L + 0.024 * (78.0 - 100) = 142.472 mEq/L.
Hence, the patient's corrected concentration of sodium is 142.472 mEq/L."
5391,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6990560-1,Extracted,"A 34-year-old woman was admitted to the hospital due to abdominal pain, chills, fever, chest tightness, and shortness of breath after eating contaminated food 2 days earlier. After admission, she became nauseated and vomited; but without dysuria, urinary frequency, or urgency. She had a medical history of type I diabetes for 19 months, with poor control of blood glucose due to non-compliance with the insulin treatments. One month prior, she was found to have kidney stones. Physical examination revealed a temperature of 36.0 °C, pulse rate of 87 beats/minute, respiratory rate of 35 breaths/min, and a blood pressure of 105/66 mm of Hg. She had shortness of breath, dry skin, and dry mucous membranes and tongue; although her lungs sounded clear. There was an abdominal wall muscle strain in the epigastric area and right upper quadrant, with obvious tenderness. The right costovertebral angle also had tenderness.
Laboratory tests and imaging studies were as follows. Blood tests after admission showed a white blood cell count of 21.08 × 109/L, neutrophil count of 18.53 × 109/L, neutrophil percentage of 87.9%, platelet count of 107 × 109/L; and concentrations for albumin of 37.42 g/L, glucose of 35.95 mmol/L, urea of 10.54 mmol/L, creatinine of 145.1 μmol/L, bicarbonate of 2.2 mmol/L, potassium of 6.60 mmol/L, sodium of 122.10 mmol/L, β-hydroxybutyric acid of 10.08 mmol/L, lactic acid of 2.43 mmol/L, C-reactive protein of 448.39 mg/L, and procalcitonin > 100.000 ng/mL. Blood gas analysis showed a pH of 6.984, carbon dioxide partial pressure of 10.9 mm of Hg, oxygen partial pressure of 138.2 mm of Hg, measured bicarbonate of 2.5 mmol/L, calculated bicarbonate of 6.4 mmol/L, anion gap of 32.2 mmol/L, base excess of − 27.2 mmol/L, and carbon dioxide of 2.9 mmol/L. Urinalysis measurements were glucose, 4+; ketone body, 4+; leukocyte esterase, weakly positive; and white blood cell number, 41/μL; with negative results for urine culture. Blood culture identified Escherichia coli. Urinary CT scan revealed multiple stones in the right kidney and lower ureter, with right hydronephrosis; we therefore diagnosed EPN (Figs. , , and reflect the CT scans during hospital admission).
After being admitted to the hospital for definite diagnosis, our endocrinology department cooperated with urology, nephrology, infection department and imaging department to formulate a treatment plan, which suggested that the patients should undergo percutaneous drainage but the patient refused. Hospital management and outcomes after admission included intravenous infusion of small doses of insulin to correct ketoacidosis. Liver and renal functions returned to normal after albumin infusion and hydration. Based upon blood culture results, Cefoperazone sulbactam was upgraded to meropenem. Inflammatory indicators and body temperature gradually returned to normal, and abdominal pain was relieved. Repeated blood cultures were negative, and urine culture remained negative. Repeated urinary CT scans revealed multiple stones in the right kidney with worsening right hydronephrosis and pyelonephritis, but with reduced gas accumulation (Fig. ).
One month after discharge, the patient underwent percutaneous nephrolithotomy in the department of urology, and the urinary CT was reexamined after operation (Fig. ).Two months after discharge, the patient underwent the second percutaneous nephrolithotomy in the department of urology, and the urinary CT was reexamined after operation (Fig. ). Currently, three months after discharge, clinical follow-up checks detect normal renal function and stable blood glucose control.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [35.95, 'mmol/L'], 'Sodium': [122.1, 'mmol/L']}",135.2442,128.48199,142.00641,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 122.1 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 122.1 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 122.1 mmol * 1 mEq/mmol = 122.1 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 122.1 mmol sodium/L converts to 122.1 mEq sodium/L. 
The concentration of glucose is 35.95 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 35.95 mmol. To convert 35.95 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 35.95 mmol glucose * 0.001 mol/mmol = 0.03595 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.03595 mol glucose * 180.16 g/mol = 6.47675 g glucose. To convert 6.47675 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 6.47675 g glucose * 1000.0 mg/g = 6476.75 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 6476.75 mg glucose/10.0 dL = 647.675 mg glucose/dL. The concentration value of 35.95 mmol glucose/L converts to 647.675 mg glucose/dL. 
Plugging in these values into the formula gives us 122.1 mEq/L + 0.024 * (647.675 - 100) = 135.2442 mEq/L.
Hence, the patient's corrected concentration of sodium is 135.2442 mEq/L."
5392,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7417490-1,Extracted,"A 71 year old man with a medical history of alcohol abuse, diabetes mellitus, essential hypertension, and depression was admitted to the intensive care unit suffering from dyspnea, productive cough, hematemesis, and black colored stools. Physical examination revealed the patient in poor general condition; hypotensive with blood pressure 87/50 mm Hg, pulse 106 b.p.m, a temperature of 37.8 C and saturating 100% on 3 liters of oxygen. Laboratory tests showed hemoglobin 7.9 gram/deciliter (g/dl), leukocytes 7.9 kilo/microliter (k/uL), platelets 155 k/uL , sodium 129 mg/dL , potassium 3.4 millimole/liter (mmol/L) , BUN 22 mg/dL, creatinine 0.96 mg/dL, glucose 150 mg/dl, anion gap 25 mmol/L, lactic acid 5.3, ALT 44 units/liter (U/L), AST 74 U/L, total bilirubin 2.25 mg/dL, international normal ratio (INR) 1.6 and urine ketones negligible.
Blood pressure responded to intravenous (IV) hydration 30ml/kg. The patient was started on IV Rocephin,and azithromycin for pneumonia based on symptoms and chest XR showing right lower lung infiltrates. The patient has suspected bleeding from esophageal varices, an indication of heavy alcohol abuse. He was started on proton pump inhibitors and an octreotide drip was administered.
Esophagogastroduodenoscopy (EGD) revealed circumferential, diffuse, friable mucosa extending from the proximal esophagus to the distal esophagus with sharp demarcation at the esophagogastric junction (GEJ) ().
There were areas of black appearing esophageal mucosa in the distal esophagus. The gastric exam showed mild areas of erythema in the body but no Wischnewsky lesions, in other words gastric mucosal petechial hemorrhages. The duodenum revealed an area of semi-lunar ulceration in the bulb and several areas of ulceration/semi-circumferential with a black eschar-like appearance at the ulcerative base in the second and third part of the duodenum ().
Proton pump inhibitors continued, while octreotide drip was discontinued. Abdominal and pelvic CT with contrast was unremarkable for any thrombosis. It showed hepatic steatosis. The patient continued to improve on symptomatic management. One week later, a repeat EGD showed improving esophagitis and duodenum ulcers. Black discoloration of esophagus and duodenum was resolved. The patient continued to improve and was discharged.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [150.0, 'mg/dL'], 'Sodium': [129.0, 'mg/dL']}",57.3,54.435,60.165,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 129.0 mg/dL. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mg to mEq. The mass of sodium is 129.0 mg. To convert from 129.0 mg to mEq, first convert from mg to mmol.To convert 129.0 mg of sodium to g, multiply by the conversion factor 0.001, giving us 129.0 mg sodium * 0.001 g/mg = 0.129 g sodium. To convert from grams of sodium to moles, divide by the molar mass 22.99 g/mol, which will give 0.129 g/(22.99 g sodium/mol) = 0.00561 mol sodium. To convert 0.00561 mol of sodium to mmol, multiply by the conversion factor 1000.0, giving us 0.00561 mol sodium * 1000.0 mmol/mol = 5.61 mmol sodium. To convert from 5.61 mmol sodium to mEq, multiply the mmol amount by the valence, to get 5.61 mmol * 1 mEq/mmol = 5.61 mEq sodium. The current volume unit is dL and the target volume unit is L. The conversion factor is 0.1 L for every unit of dL. Our next step will be to divide the mass by the volume conversion factor of 0.1 to get the final concentration in terms of mEq/L. This will result to 5.61 mEq sodium/0.1 L = 56.1 mEq sodium/L. The concentration value of 129.0 mg sodium/dL converts to 56.1 mEq sodium/L. 
The concentration of glucose is 150.0 mg/dL. 
Plugging in these values into the formula gives us 56.1 mEq/L + 0.024 * (150.0 - 100) = 57.3 mEq/L.
Hence, the patient's corrected concentration of sodium is 57.3 mEq/L."
5393,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3249999-1,Extracted,"A 45-year-old female patient presented with abdominal pain and respiratory distress for the last 3 days. On general examination, the patient had a blood pressure of 110/80 mmHg and pulse rate of 100/minute. The patient was stable on the day of admission so the patient was empirically started on amikacin and ceftriaxone, managed conservatively and the investigations were sent for. The blood parameters were as follows: hemoglobin-10.8gm /dL, total leukocyte count- 23,700/mm3, platelet count-3,68,000/mm3. The biochemical investigations revealed the following: fasting blood sugar-129 mg/dL, urea-31 mg/dL, creatinine-0.89 mg/dL, bilirubin-1.3 mg/dL, conjugated bilirubin-0.8 mg/dL, alkaline phosphatase-541, AST-58 IU/mL, ALT-78 IU/mL, total protein-6.7 g/dL, albumin-2.8 g/dL, sodium-128meq/L, potassium-4.7meq/L, prothrombin time-20.8 seconds, INR:1.40, serum amylase-189 U/L, lipase-120 U/L. The patient was nonreactive for HIV and anti-HCV antibodies and was also hepatitis B surface antigen-negative.
On the second day of admission, the ultrasound of the abdomen showed an enlarged spleen, mild ascites and right-sided pleural effusion and features suggestive of pancreatitis. The plain and contrast CT scan of the whole abdomen performed on the second day of admission, showed that the pancreas were enlarged, with minimal area of necrosis seen in the tail region. Severe inflammatory changes were seen at peripancreatic fat extending into the lesser sac. There was inflammation extending into the paracolic gutters with thickening of the adjacent colonic walls, along Morrison's pouch, along both anterior pararenal spaces causing thickening of fascia of Gerota and lateroconal fascia. Inflammatory changes were also observed in the mesentery especially in the omentum []. Based on the CT scan findings of pancreatic necrosis, the patient was started on imipenem.
The pus from the pancreatic abscess was aspirated under CT guidance and sent for culture and sensitivity. The pus was inoculated on Blood agar, MacConkey agar, Sabouraud's dextrose agar (SDA) with and without antibiotics and thioglycollate broth. The culture of the pus yielded growth of E. coli and C. tropicalis. The bacterial isolate was found to be susceptible to piperacillin+ tazobactam and imipenem. The candidal isolate was identified to be C. tropicalis by growth on cornmeal Tween 80 agar []. The Candida isolate was found to be susceptible to amphotericin B. The initial culture report was conveyed to the clinician on the third day of admission.
Based on the preliminary culture findings the patient was continued on imipenem, and amphotericin B was added to the treatment regime, but the condition of the patient deteriorated on the fourth day of admission, for which the patient had to undergo necrosectomy of the infected pancreatic tissue. During the operation dense calcification was noted in the parieties and dense adhesion of the omentum was noted with the colon and stomach parieties and thick pus was drained from the lesser sac. The drained pus and the necrosectomy tissue sent for culture showed similar findings as that of the earlier aspirated pancreatic pus.
After the operation the patient was continued on imipenem and amphotericin B to which the patient showed a marked improvement with the subsidence of fever. The patient was discharged after 6 weeks of antifungal therapy. The patient was doing well at the time of discharge and later on follow-up.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [129.0, 'mg/dL'], 'Sodium': [128.0, 'mEq/L']}",128.696,122.2612,135.1308,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 128.0 mEq/L. 
The concentration of glucose is 129.0 mg/dL. 
Plugging in these values into the formula gives us 128.0 mEq/L + 0.024 * (129.0 - 100) = 128.696 mEq/L.
Hence, the patient's corrected concentration of sodium is 128.696 mEq/L."
5394,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8291511-1,Extracted,"We present the case of a 67-year-old female with a history significant for type II diabetes mellitus and obesity (body mass index of 43) who had been trying to lose weight with a combination of intermittent fasting and consumption of exogenous ketone supplements purchased online. Three months prior to hospitalization, the patient began a ketogenic diet that entailed intermittent fasting, whereby she would fast for upwards of 40 hours at a time with only drinking water and ingesting keto supplements; she reported drinking the ketone ester supplement three times a day on an empty stomach. The patient stated she had lost over 25 pounds since the beginning of her diet. After one of her fasting cycles, she ate half an avocado, some shrimp, and drank a ketone ester drink. Shortly after, the patient began feeling dizzy and started to vomit and ultimately presented to the hospital with severe fatigue, lower abdominal pain, nausea, and vomiting. She last took metformin (she was on a 750 mg twice daily home dose) on the morning of her presentation to the hospital and admitted to taking exogenous ketone supplements containing 30 g of beta-hydroxybutyrate (BHB) three times a day.
On evaluation, she was hemodynamically stable with baseline normal mental function but appeared dehydrated. Assessment of vitals showed the patient was tachycardic with a pulse rate of 120 beats per minute and borderline tachypnea with a respiratory rate of 20 breaths per minute. Her electrocardiogram did not show any arrhythmias or concerning changes in ST segments. On examination, she had dry mucous membranes and diffuse lower abdominal pain to palpation without guarding or rebound tenderness. Laboratory evaluation was notable for a white blood cell count of 30,100/mm3 (normal range: 4,500-11,000/mm3), creatinine 1.47 mg/dL (0.60-1.30 mg/dL), blood urea nitrogen 32 mg/dL (7-18 mg/dL), glucose 176 mg/dL (74-106 mg/dL), serum bicarbonate 8 mEq/L (21-32 mEq/L), anion gap 27.7 mEq/L (3-15 mEq/L), and a serum lactic acid of 2.9 mmol/L (0.4-2.0 mmol/L). The patient also had a moderately positive serum qualitative acetone level, plasma osmolality 312 mOsm/kg (275-301 mOsm/Kg), sodium 136 mEq/L (136-145 moml/L), and HbA1C of 8.4% (<5.7%). A urinalysis showed elevated urine ketones and was negative for glucose. Her pH from a venous blood gas analysis on admission was 6.81.
Differential diagnoses of diabetic ketoacidosis, alcoholic ketoacidosis, lactic acidosis, and salicylate toxicity were investigated. Serum and urine drug screens were negative for ethanol, acetaminophen, and salicylates. The patient was started on intravenous fluids with dextrose 5%-0.9% normal saline, sliding scale insulin, and 50 meq sodium bicarbonate 8.4%. After two days in the intensive care unit, the patient clinically felt much better. Her anion gap closed and her pH on a venous blood gas analysis was 7.38. The patient was transferred to the floors and was discharged the following day.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [176.0, 'mg/dL'], 'Sodium': [136.0, 'mEq/L']}",137.824,130.9328,144.7152,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 136.0 mEq/L. 
The concentration of glucose is 176.0 mg/dL. 
Plugging in these values into the formula gives us 136.0 mEq/L + 0.024 * (176.0 - 100) = 137.824 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.824 mEq/L."
5395,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4307707-1,Extracted,"A 71-year-old Filipino female with no known past medical history presented to an emergency department in Oakland, California, for neck swelling, fever, and difficulty breathing. She had been experiencing these symptoms for two weeks, with the neck swelling becoming progressively worse. On physical exam the patient appeared ill with a heart rate of 139, blood pressure of 87/36 and temperature 101.1, indicating septic shock. Physical exam revealed a large fluctuant mass over the left lateral neck. The center of this mass exhibited blackish discoloration and skin necrosis. Swelling and crepitus extended to the anterior and posterior neck, left shoulder and anterior chest wall.
Initial laboratory evaluation showed a white blood cell count of 22.9thou/mcL, Hemoglobin of 14.8g/dL, and platelets of 359thou/mcL. Notable chemistries were sodium of 125mmol/L, potassium 4.9mmol/L, chloride 110mmol/L, bicarbonate less than 5mmol/L, blood urea nitrogen 41mg/dL, creatinine 2.5mg/dL, glucose 917mg/dL, and lactic acid 3.5mmol/L. Urinalysis showed glucosuria and ketonuria. CT of chest and neck revealed extensive subcutaneous emphysema throughout the left lateral upper chest wall, left shoulder region, anterior mediastinum and throughout the superficial and deep spaces of the neck ().
The patient was taken to the operating room for debridement and was discovered to have necrotic deep muscle tissue and fascia. Intraoperative biopsies confirmed the diagnosis of necrotizing fasciitis, with necrotic and purulent material found in the dermis, subcutaneous tissues, and fascia.
During the patient’s hospital stay, she required numerous vasopressors and steroids for refractory hypotension, hemodialysis for refractory acidosis and uremia, and was taken to the operating room for debridement a total of three times. The patient expired on her seventh hospital day due to overwhelming sepsis and acidosis.
Cultures of blood, urine, and surgical specimens all grew K. pneumoniae. These isolates were string-test positive, indicating that this was the hypermucoviscous strain. All cultures were resistant to ampicillin, but otherwise were pan susceptible.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [917.0, 'mg/dL'], 'Sodium': [125.0, 'mmol/L']}",144.608,137.3776,151.8384,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 125.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 125.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 125.0 mmol * 1 mEq/mmol = 125.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 125.0 mmol sodium/L converts to 125.0 mEq sodium/L. 
The concentration of glucose is 917.0 mg/dL. 
Plugging in these values into the formula gives us 125.0 mEq/L + 0.024 * (917.0 - 100) = 144.608 mEq/L.
Hence, the patient's corrected concentration of sodium is 144.608 mEq/L."
5396,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4188770-1,Extracted,"A 75-year-old female patient (height 141 cm, weight 44 kg) visited the emergency room with low back pain and radiating pain, and was admitted for further evaluation. She was diagnosed with spinal stenosis and was scheduled to undergo L4-5-S1 PLIF. Ten days prior to the current admission, the patient presented abdominal pain accompanied by nausea and poor oral intake. A diagnostic workup including abdominal computed tomography (CT) and upper gastrointestinal endoscopy were normal. She was discharged after improving with conservative management.
She did not have underlying disease and family history of neuromuscular disease. The preoperative electrocardiogram revealed nonspecific ST and T wave change, and an echocardiogram was within normal limits. Chest radiograph and routine laboratory findings were normal. Upon arrival in the operating room, the patient's blood pressure was 130/80 mmHg, heart rate was 115 beats/min and pulse oxygen 92%. She was premedicated with intramuscular glycopyrrolate 0.2 mg before the surgery. After standard monitoring, general anesthesia was induced with pentothal sodium 175 mg, rocuronium 35 mg and remifentanil 0.05 µg/kg/min. Endotracheal intubation was performed using a light-wand. After induction of anesthesia, arterial cannulation was performed with a 20 G catheter in the right radial artery, and central venous cannulation was performed in the right internal jugular vein. Anesthesia was maintained with desflurane, a mixture of oxygen and air (FiO2 0.5) and intravenous infusion of remifentanil. The concentration of desflurane was controlled to maintain the bispectral index within 40-60. Warm forced air devices were used to maintain body temperature.
Throughout the operation, the patient showed no specific abnormalities of her vital signs. Phenylephrine 50 µg/min was infused to maintain the systolic blood pressure between 90 and 110 mmHg. The blood loss was about 1,000 ml and 2,150 ml of crystalloid solution, 500 ml of colloid solution and three pints of packed red blood cells were administered. The surgery was completed uneventfully and the anesthesia lasted 310 min. Core body temperature measured with esophageal stethoscope was around 36℃ during the operation. The neuromuscular blockade was reversed with glycopyrrolate 0.4 mg and neostigmine 1.5 mg at the end of the procedure. However, the patient presented with significantly delayed emergence from anesthesia. The patient was drowsy and needed assisted ventilation due to weak spontaneous respiratory efforts during the 40 min after surgery. At the time, arterial blood gas analysis revealed pH, 7.23; PaCO2, 41 mmHg; PaO2 284 mmHg; HCO3, 17.2 mEq/L and SaO2 100%. Other laboratory examinations revealed sodium 138 mmol/L, potassium 4.9 mmol/L, calcium 1.18 mmol/L, Hb 9.9 g/dl and glucose 112 mg/dl. No specific laboratory values to explain the-delayed emergence were noted. The patient was transferred to the intensive care unit in an intubated state. Although she was extubated at the intensive care unit after 30 min, she remained minimally arousable. Motor power was reduced from grade IV (mild weakness) to grade I (visible contraction but no movement) in bilateral upper and lower extremities, but no sensory loss was observed. Cervical spine magnetic resonance imaging (MRI), brain MRI and electroencephalography (EEG) were performed on the recommendation of a neurologist on postoperative day (POD) 1. Cervical spine MRI was normal. Brain lesions in bilateral post central gyrus, medial thalami, periventricular region, periaqueductal region and hypothalamus in brain MRI were suggestive of Wernicke's encephalopathy (WE). Accordingly, she was started on vitamin B1, but her motor functions and mental status did not recover. EEG showed diffuse cerebral dysfunction. On POD 10, nerve conduction study and electromyography demonstrated axonal dominant sensorimotor polyneuropathy. The neurologist then considered Guillain-Barre Syndrome (GBS) and treated with intravenous immunoglobulin. The patient was intubated due to the continuous respiratory muscle weakness and pulmonary infection led to respiratory failure requiring mechanical ventilation. On POD 12, hyponatremia (118 mmol/L) and clinical epileptic form discharge on EEG were detected. Symptomatic treatment was eventually with phenytoin and hypertonic saline.
The patient showed mental change and motor axonal peripheral neuropathy simultaneously, and presented abdominal pain, nausea and poor oral intake before the surgery. She also showed labile blood pressure (60-188/44-120 mmHg) and tachycardia (100-136 beats/min) suggestive of autonomic dysfunction, respiratory muscle weakness due to peripheral neuropathy and hyponatremia. These findings suggested AIP and the diagnosis was ascertained from detecting high urine porphobilinogen on POD 13. Glucose infusion was given to the patient, with a plan to administer heme arginate if the symptoms persisted.
Although her motor power was gradually improved, her general condition deteriorated rapidly with aggravating pneumonia and she expired on POD 35.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [112.0, 'mg/dL'], 'Sodium': [138.0, 'mmol/L']}",138.288,131.3736,145.2024,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 138.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 138.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 138.0 mmol * 1 mEq/mmol = 138.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mmol sodium/L converts to 138.0 mEq sodium/L. 
The concentration of glucose is 112.0 mg/dL. 
Plugging in these values into the formula gives us 138.0 mEq/L + 0.024 * (112.0 - 100) = 138.288 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.288 mEq/L."
5397,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-5468,Extracted,"A 33-year-old woman presents to the emergency department after she found out she had a blood pressure of 165/100 mmHg at a local pharmacy. The patient is not followed by a primary care physician and is not currently taking any medications. She has no other complaints at this time. A bedside ultrasound with Doppler of the abdomen is within normal limits. Laboratory values are ordered as seen below.

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
HCO3-: 33 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.2 mg/dL

The patient is given hydrochlorothiazide and sent home. An ECG performed at a subsequent follow up appointment is seen in Figure A.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [99.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",138.976,132.0272,145.9248,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 139.0 mEq/L. 
The concentration of glucose is 99.0 mg/dL. 
Plugging in these values into the formula gives us 139.0 mEq/L + 0.024 * (99.0 - 100) = 138.976 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.976 mEq/L."
5398,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-5230,Extracted,"A 35-year-old man is found unconscious outside his home by a passing neighbor and is brought to the emergency department by ambulance. Cardio-pulmonary resuscitation is performed and the patient awakens but remains somnolent and confused. He is unable to answer questions or provide any medical history. His temperature is 98.2°F (36.8°C), blood pressure is 108/62 mmHg, pulse is 110/min and respirations are 20/min. Physical exam shows decreased arousal. Pupils are round, symmetric, and reactive to light bilaterally. Fundoscopy is normal. The patient winces to palpation of the epigastric region and bilateral costovertebral angles. Initial labs are drawn and are shown below:

Serum:
Na+: 137 mEq/L
K+: 3.1 mEq/L
Cl-: 92 mEq/L
HCO3-: 6 mEq/L
BUN: 36 mg/dL
Glucose: 100 mg/dL
Creatinine: 1.7 mg/dL

Bladder catherization is notable for mildly bloody urine and microscopic analysis is shown in Figure A.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [100.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",137,130.15,143.85,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 137.0 mEq/L. 
The concentration of glucose is 100.0 mg/dL. 
Plugging in these values into the formula gives us 137.0 mEq/L + 0.024 * (100.0 - 100) = 137.0 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.0 mEq/L."
5399,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8202812-1,Extracted,"A 54-year-old diabetic gentleman presented with severe diffuse abdominal pain with abdominal distension for four days, followed by diarrhea and fever with chills for two days. He had undergone a right hemicolectomy for carcinoma cecum in a different hospital four years back. Postoperative biopsy reported well-differentiated adenocarcinoma with pathological staging - T4N2M0. He received eight cycles of adjuvant capecitabine and oxaliplatin, following which he was under six-monthly follow-up with no recurrence.
On examination, he was conscious, oriented, and dehydrated. He had tachycardia (110/min) with a blood pressure of 130/70 mm of Hg. The abdomen was distended, with diffuse tenderness and signs of peritonitis. His blood glucose at the time of presentation was 550 mg/dl with no ketoacidosis. Blood investigations showed hemoglobin of 13 gm/dl, total counts of 7600/mm3 with 81% neutrophils, platelet counts were 2.2 lacs/mm3, urea of 41 mg/dl, creatinine of 0.67 mg/dl, sodium of 138 mEq/dL, and potassium of 3.58 mEq/dL. An erect chest X-ray showed a thin rim of pneumoperitoneum under the right hemidiaphragm (Figure ).
A contrast-enhanced computed tomography (CECT) was done, which showed scattered foci of pneumoperitoneum, and edematous thickened ileal loop distal to the ileo-transverse anastomosis with a small collection with air foci within it, mesenteric fat stranding but no free fluid abdomen. The anastomotic site was healthy with no abnormal thickening suggestive of recurrence (Figure ).
After the initial resuscitation, he was taken up for an exploratory laparotomy. Intraoperatively, an unhealthy, thickened, distended ileal blind loop of length 8 cm with a sloughed-off portion of the bowel wall covered with pus flakes with a pinpoint micro-perforation, distal to the side-to-side ileo-transverse colon anastomosis (Figure ).
Resection of the previous anastomotic site and a redo functional end-to-end (anatomical side-to-side) ileo-transverse anastomosis was done using a linear stapler. The postoperative course was uneventful. The patient was discharged on a regular diet on the sixth postoperative day.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [550.0, 'mg/dL'], 'Sodium': [138.0, 'mEq/dL']}",1390.8,1321.26,1460.34,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 138.0 mEq/dL. We need to convert the concentration to mEq/L. The mass units of the source and target are the same so no conversion is needed. The current volume unit is dL and the target volume unit is L. The conversion factor is 0.1 L for every unit of dL. Our next step will be to divide the mass by the volume conversion factor of 0.1 to get the final concentration in terms of mEq/L. This will result to 138.0 mEq sodium/0.1 L = 1380.0 mEq sodium/L. The concentration value of 138.0 mEq sodium/dL converts to 1380.0 mEq sodium/L. 
The concentration of glucose is 550.0 mg/dL. 
Plugging in these values into the formula gives us 1380.0 mEq/L + 0.024 * (550.0 - 100) = 1390.8 mEq/L.
Hence, the patient's corrected concentration of sodium is 1390.8 mEq/L."
5400,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-191,Extracted,"A 39-year-old man comes to the physician for preoperative evaluation. He is scheduled for a right inguinal hernia repair the following day. He has a history of polycystic kidney disease and hypertension. His medications include lisinopril and vitamin D3 supplements. His father had the same kidney condition and died of an intracerebral aneurysm when the patient was 2 years old. His temperature is 37°C (98.6 F), pulse is 87/min, and blood pressure is 108/68 mm Hg. He has bilateral pitting edema. There is a right inguinal hernia; cough impulse is present. The remainder of the examination shows no abnormalities. Laboratory studies show:
Hemoglobin 9.0 g/dL
Serum
Na+ 132 mEq/L
K+ 6.5 mEq/L
Cl- 94 mEq/L
HCO3- 21 mEq/L
Glucose 86 mg/dL
Creatinine 2.9 mg/dL
Calcium 8.7 mg/dL
Phosphorus 4.9 mg/dL
An ECG shows tall T waves. Intravenous calcium gluconate is administered.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [86.0, 'mg/dL'], 'Sodium': [132.0, 'mEq/L']}",131.664,125.0808,138.2472,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 132.0 mEq/L. 
The concentration of glucose is 86.0 mg/dL. 
Plugging in these values into the formula gives us 132.0 mEq/L + 0.024 * (86.0 - 100) = 131.664 mEq/L.
Hence, the patient's corrected concentration of sodium is 131.664 mEq/L."
5401,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2173901-1,Extracted,"A 68 year-old woman with type 2 diabetes mellitus and intraductal breast carcinoma presented with a 2-day history of rapidly onset left groin pain and leg weakness. There were some discoloration and blisters on the medial aspect of the same thigh and she had felt warm but denied any rigors. She became unable to weight bear and began to vomit on the day of presentation. No history of trauma was noted to the area. Her past medical history included type 2 diabetes of eight years with reasonable control, requiring Metformin 1 gm twice daily. Her home daily glucose readings oscillated between ~5–7 mmol/L in the previous 6–8 weeks, with a HbAc1 of 6.5% two weeks prior. Serial levels had been between 6.2 and 7.1% in the previous 2 years. The only diabetes complication included mild background non-proliferative retinopathy which has been observed. Her breast cancer was diagnosed 6 months prior with grade 3 intraductal carcinoma with axillary metastasis requiring mastectomy with axillary clearance followed by systemic adjuvant chemotherapy with Adriamycin and Cyclophosphamide. Her last course of chemotherapy was 10 days prior with no mucositis or any other adverse effects. Past medical problems included hypertension and diverticular disease requiring partial sigmoid bowel resection 6 years ago.
Examination showed an ill-looking and obese woman with pyrexia of 38.8° Celsius, pulse rate of 110 beats per minute, regular and blood pressure of 100/70 supine. No standing blood pressure was possible. Her body mass index (BMI) was ~36 kg/m2 (weight 98.1 kg with height 1.64 m). The lower limb was markedly swollen with extensive ecchymosis extending from the left groin inferiorly to the mid thigh. The dorsalis pedis and posterior tibial arterial pulses were present. Crepitus was detected on the medial aspect of her thigh. Investigations showed a haemoglobin of 94 g/L (reference range [RR], 115–165), white cell count 4.0 × 109/L (RR, 4.0 – 11.0), neutrophils 3.4 × 109/L (RR, 4.0–7.0 × 109/L), platelet 197 × 109/L (RR, 150–450). Her sodium was 134 mmol/L (RR, 137 – 143), potassium 3.8 mmol/L (RR, 3.5 – 5.5), urea 8.1 mmol/L (RR, 2.6 – 6.4) and creatinine 142 umol/L (RR, 60 – 100), C-reactive protein 235 ug/L (RR, < 3), Creatine Kinase 1668 U/L (RR, < 125) and a random glucose of 22.4 mmol/L. Pelvic XR revealed diffuse gas formation extending inferiorly down the left leg (Figure ), further supported with computerized tomographic scans (Figure ).
Intravenous antibiotics including Penicillin, Gentamicin and Metronidazole were urgently administered together with crystalloid rehydration. Surgery was seriously considered but withheld due to the extensive nature of the infection. Not unexpectedly, the patient died of overwhelming sepsis in 12 hours despite rigorous and intensive medical therapy. Hyperbaric therapy was not available. Blood culture subsequently returned positive for Clostridium Septicum. Post mortem examination revealed extensive myofascial necrosis and subcutaneous gaseous formation (Figure ). Staining study revealed an abundance of gram-positive bacilli in the necrotic tissue supporting the blood culture finding. No bowel malignancy was detected.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [22.4, 'mmol/L'], 'Sodium': [134.0, 'mmol/L']}",141.28539,134.22112,148.34966,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 134.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 134.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 134.0 mmol * 1 mEq/mmol = 134.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mmol sodium/L converts to 134.0 mEq sodium/L. 
The concentration of glucose is 22.4 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 22.4 mmol. To convert 22.4 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 22.4 mmol glucose * 0.001 mol/mmol = 0.0224 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0224 mol glucose * 180.16 g/mol = 4.03558 g glucose. To convert 4.03558 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 4.03558 g glucose * 1000.0 mg/g = 4035.58 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 4035.58 mg glucose/10.0 dL = 403.558 mg glucose/dL. The concentration value of 22.4 mmol glucose/L converts to 403.558 mg glucose/dL. 
Plugging in these values into the formula gives us 134.0 mEq/L + 0.024 * (403.558 - 100) = 141.28539 mEq/L.
Hence, the patient's corrected concentration of sodium is 141.28539 mEq/L."
5402,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7478927-1,Extracted,"A 69-year-old female with a recent diagnosis of BCR/ABL+ CML, type 2 diabetes mellitus, hypertension, and coronary artery disease presented to the ED with complaints of shortness of breath (SOB). The patient reported her SOB started worsening over the last couple of days prior to admission. She denied any orthopnea or paroxysmal nocturnal dyspnea. She also reported dizziness (positional), palpitations, poor oral intake due to poor appetite, and nausea. The patient reported several episodes of coffee-ground emesis and black tarry stools for the last couple of days. She denied any hematemesis or bright red blood per rectum (BRBPR). She also endorsed easy bruising and episodes of blurry vision. Initial vital signs in the ED showed a heart rate of 105 beats per minute, blood pressure of 89/55, and 85% saturation on 4L nasal cannula. Lung exam revealed crackles with decreased breath sounds, muffled heart sounds, and no murmurs.
Lab results were as follows: hemoglobin of 7.9 g/dL, hematocrit of 25.6%, platelets of 379 K/mm3, WBCs of 105.2 K/mm3, and peripheral smear (Figure ) showed neutrophils of 46%, bands of 10%, lymphocytes of 10%, monocytes of 4%, metamyelocytes of 21%, myelocytes of 9%, and blasts of 1%.
Complete metabolic profile showed Na (sodium) of 134 mmol/L, K (potassium) of 7.3 mmol/L, bicarbonate of 19 mmol/L, BUN (blood urea nitrogen) of 103 mg/dL, creatinine of 3.4 mg/dL, glucose of 208 mg/dL, AST (aspartate aminotransferase) of 17 U/L, ALT (alanine aminotransferase) of 12 U/L, uric acid of 15.2 mg/dL, proBNP (pro b-type natriuretic peptide) of 1,135 pg/mL, troponin of <0.015 ng/mL, and procalcitonin of 1.3 ng/mL. COVID-19 screen was negative. Blood culture showed no growth after five days. Immunoglobulins were within normal limits. RF and ANA screen was negative. P-ANCA and C-ANCA were negative. C3 and C4 were within normal limits.
Chest X-ray (Figure ) showed air space disease, left side pleural effusion, and a boot-shaped heart concerning for pericardial effusion. Transthoracic echocardiography showed a large pericardial effusion of 2 cm circumferentially surrounding the heart with focal strands. There were no echo signs of frank tamponade (Figure ).
Bedside pericardiocentesis was performed and 900 cc of frank bloody fluid was removed. A drain was left in place for subsequent removal of 400 cc on day 2 and 250 cc on day 3. Pericardial fluid analysis revealed the following: negative gram stain/culture, bloody appearance, 2,300,000 RBCs, and 64,420 WBCs with polymorphonuclear neutrophils (PMNs) of 94%, lymphocytes of 2%, and monocytes of 2%. Pericardial cytology shows infiltration by CML (Figure ).
The patient was treated in the critical care unit for multifocal pneumonia, severe sepsis, and acute renal failure requiring hemodialysis (HD). The patient's hemodynamics improved after pericardiocentesis, and a total of 1,550 cc of bloody pericardial fluid was removed. WBCs decreased to 85k with hydroxyurea. Tyrosine kinase inhibitors (TKIs), such as nilotinib, were not started due to prolonged QTc (550 ms) and resistant atrial fibrillation. The patient was instructed to follow up with the outpatient hematology/oncology service to start chemotherapy once stable.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [208.0, 'mg/dL'], 'Sodium': [134.0, 'mmol/L']}",136.592,129.7624,143.4216,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 134.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 134.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 134.0 mmol * 1 mEq/mmol = 134.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mmol sodium/L converts to 134.0 mEq sodium/L. 
The concentration of glucose is 208.0 mg/dL. 
Plugging in these values into the formula gives us 134.0 mEq/L + 0.024 * (208.0 - 100) = 136.592 mEq/L.
Hence, the patient's corrected concentration of sodium is 136.592 mEq/L."
5403,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7760453-1,Extracted,"A 54-year-old obese female (body mass index, 28.4 kg/m2) presented to the Emergency Department of the West China Hospital with a 2-d history of intermittent abdominal pain, nausea, vomiting, and abdominal enlargement with an inability to pass stool and flatus.
She had undergone laparoscopic subtotal hysterectomy and bilateral adnexectomy in another institution 8 d prior because of uterine fibroids. During the operation, three trocars were applied: Two 10 mm trocars at the umbilicus and in the left lower quadrant, respectively, and a 5 mm trocar in the right lower quadrant, all of which were the bladed type. Additionally, a 24 FR soft silicon tube was drained through the 10 mm trocar port-site in the left lower quadrant. The fascial planes of the umbilical and right lower quadrant port sites were separately stitched with absorbable sutures, while the 10 mm port site in the left lower quadrant was left unclosed (only skin and subcutaneous tissue were sutured to fix the drain). The postoperative recovery was smooth, and gastrointestinal function recovered within 48 h. The drainage tube was removed 4 d after the operation under direct vision when the collected drainage liquid was less than 30 mL per day. One day later, she was discharged to home without discomfort. Six days after the operation, she felt dull pain at the site of the left drain accompanied with nausea, but she did not have difficulty passing stool or flatus. The patient thought the problem was probably due to the incision and did not pay much attention. From that day on, the abdominal pain and distension were gradually aggravated, with the onset of the inability to pass stool and flatus.
The patient had a history of uncontrolled diabetes mellitus and uterine fibroids.
The patient had no remarkable personal and family history.
The primary symptoms were a distended abdomen, strong sensitivity at the left lower quadrant with a rebound, a tender 8 cm in size palpable mass in the left lower quadrant just above the drainage site, and hyperactive bowel sounds.
All hematological parameters were within normal limits. The biochemical values were significant for Na+ (131 mmol/L), Cl- (89 mmol/L), glucose level (21.5 mmol/L), alanine aminotransferase (114 IU/L), and aspartate aminotransferase (120 IU/L).
The emergency computed tomography (CT) scan revealed the small bowel herniated through the 10 mm drain-site, with diffuse bowel distension and multiple air-fluid levels with gas in the small intestines (Figure ).","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [21.5, 'mmol/L'], 'Sodium': [131.0, 'mmol/L']}",137.89626,131.00145,144.79107,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 131.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 131.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 131.0 mmol * 1 mEq/mmol = 131.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 131.0 mmol sodium/L converts to 131.0 mEq sodium/L. 
The concentration of glucose is 21.5 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 21.5 mmol. To convert 21.5 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 21.5 mmol glucose * 0.001 mol/mmol = 0.0215 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0215 mol glucose * 180.16 g/mol = 3.87344 g glucose. To convert 3.87344 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 3.87344 g glucose * 1000.0 mg/g = 3873.44 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 3873.44 mg glucose/10.0 dL = 387.344 mg glucose/dL. The concentration value of 21.5 mmol glucose/L converts to 387.344 mg glucose/dL. 
Plugging in these values into the formula gives us 131.0 mEq/L + 0.024 * (387.344 - 100) = 137.89626 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.89626 mEq/L."
5404,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8684410-1,Extracted,"A 74-year-old male with a history of two transient ischemic attacks was brought into our facility for altered mental status after being found unconscious by a relative. His social history was significant for 55 pack-years of smoking. Due to his mentation on arrival, no further history was obtained. Vital signs were normal on admission. Physical examination on admission showed non-responsiveness to sternal rub, dry mucous membranes, decreased skin turgor, and thick white plaques around the corners of his mouth. Examination of the extremities showed 1+ bilateral lower leg edema, and pulmonary examination revealed right-sided wheezes and rales.
On admission, the patient had an elevated blood glucose of 662 mg/dL (normal: 70-110 mg/dL), an anion gap of 15, ß-hydroxybutyrate of 1.86 mmol/L (normal: 0.02-0.27 mmol/L), point-of-care (POC) lactate of 3.3 mmol/L (normal: 0.5-2.0 mmol/L), serum potassium of 3.8 mEq/L, urine volume of 850 mL, and no ketones on urinalysis. The arterial blood gas (ABG) showed a pH of 7.48, HCO3 of 24.6, and PCO2 of 33 meq/L. The slightly elevated anion gap on admission is likely multifactorial. It could have been caused by the increase in the negative charge for albumin and enhanced production of lactate seen in metabolic alkalosis []. Conversely, it is also possible that scant ketones, which are produced in a hyperosmolar hyperglycemic state, as seen by mildly elevated β-hydroxybutyrate and the absence of ketones in the urine, could have contributed to the elevated anion gap [].
Additionally, the patient had hypernatremia (sodium of 185 mEq/L corrected for hyperglycemia), acute kidney injury (blood urea nitrogen [BUN] of 49 mg/dL, creatinine [Cr] of 1.55 mg/dL, from a previous baseline Cr of 1.01 mg/dL), and hemoconcentration (hemoglobin [Hb] 17.1 g/dL, hematocrit [Hct] 51.6%). Chest X-ray indicated a potential right lower lung zone infiltrate. Computed tomography (CT) of the chest indicated right lower lobe mass or consolidation, with multiple mediastinal and hilar masses as well as enlarged left axillary nodes compatible with lymphadenopathy, suggestive of malignancy and metastatic disease (Figures , ). CT of the abdomen showed heterogeneous liver attenuation but could not differentiate between nonocclusive disease and metastatic disease. Adrenal nodules and kidney nodular densities were also present (Figure ). CT of the brain showed a suprasellar mass measuring 1.2 x 1.1 x 0.9 cm (Figure ). The patient was started on half normal saline and insulin, and the acute kidney injury significantly improved on day 3; however, no significant improvement in sodium level was noticed after correction for elevated glucose levels (Figure and Table ).
Additional investigations for the refractory hypernatremia showed a urine osmolarity of 699 (normal: 50-1,400), serum osmolarity of 360 (normal: 280-301), urine sodium of 10 mEq/L (normal: 20 mEq/L), serum AM cortisol of 61.3 ug/dL (normal AM: 6.2-19.4 ug/dL), 1-mg dexamethasone suppression test cortisol of 6.06 ug/dL (normal: <1.8ug/dL) and ACTH of 228 pg/mL (normal: 7.2-63.3 pg/mL) (Table ). MRI of the brain revealed a 1.1 x 1.2 x 1.1 cm enhancing lesion of the optic chiasm without evidence of mass effect (Figure ) and small lymph nodes in deep portions of the bilateral parotid glands that were potential metastasis. Throughout the admission, the patient’s arterial blood gas (ABG) showed a primary respiratory alkalosis with secondary metabolic alkalosis (pH of 7.48, HCO3 of 24.6, PCO2 of 33 meq/L), which was persistent until discharge (pH of 7.48, HCO3 of 27.6 meq/L, PCO2 of 37 mmHg). Additional endocrine investigations demonstrated an follicle-stimulating hormone (FSH) of 0.3 miU/L (normal: 1.5-12.4 miU/L), luteinizing hormone (LH) < 0.3 miU/L (normal: 1.7-8.6 miU/L), testosterone of 27 ng/dL (normal: 264-916 ng/dL), thyroid-stimulating hormone (TSH) of 0.01 u/iU/L (normal: 0.34-5.60 u/iU/L), and prolactin of 9.7 ng/mL (normal: 4.0-15.2 ng/mL). The plan was to obtain a lung biopsy to determine whether the mass was cancerous or not and to conduct a high dexamethasone suppression test for ectopic ACTH production. However, the patient declined further workup or treatment, opting for hospice instead.
Despite initial fluid resuscitation with half normal saline followed by dextrose water, the hypernatremia did not correct. The hypernatremia later resolved after the patient was started on desmopressin on day 7 of admission. The patient was sent home on hospice and was advised to increase his water intake.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [662.0, 'mg/dL'], 'Sodium': [185.0, 'mEq/L']}",198.488,188.5636,208.4124,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 185.0 mEq/L. 
The concentration of glucose is 662.0 mg/dL. 
Plugging in these values into the formula gives us 185.0 mEq/L + 0.024 * (662.0 - 100) = 198.488 mEq/L.
Hence, the patient's corrected concentration of sodium is 198.488 mEq/L."
5405,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3811799-1,Extracted,"A 29-year-old man presented at a emergency room in a stupor.
The patient had started psychiatric treatment after being diagnosed with personality disorder and hypochondriasis by the department of psychiatry in our hospital 4 years ago. After about 1 year of treatment, olanzapine was administered due to the patient's symptoms of social withdrawal and distrust of people. After the initiation of olanzapine, the patient's body weight increased by ≥30 kg, and hyperthermia occurred together with nausea and vomiting 1 week prior to the visit to our hospital. The patient received a prescription from a neighboring hospital and had taken antipyretics, but did not show any improvement. Then the patient showed mental deterioration and was admitted to our hospital via the emergency room.
Both parents were moderately built, and none of the family members, including siblings, had a metabolic disease such as diabetes.
The patient was on medication due to incidences of personality disorder, hypochondriasis, and psychotic tendency, taking olanzapine 10 mg, valproic acid 500 mg, clonazepam 0.5 mg, and lorazepam 1 mg on a daily basis. The aforementioned medication regimen was maintained for over 1 year without any dosage change, and the intake period of olanzapine was 32 months. There was no other underlying disease than the aforementioned, and there were no abnormal test results based on blood assay, including an assay for fasting plasma glucose, which was performed prior to administration of antipsychotics.
The patient had no history of smoking or alcohol drinking and was unemployed since completion of military service as social service personnel.
In physical examination, the patient showed acute signs of illness and was in a coma. His vital signs measured at the time of visit to our hospital were 110/70 mm Hg for blood pressure (BP), 120 beats per minute for pulse rate, 24 times per minute for respiratory rate, and 37.2℃ for body temperature. The patient's height was 181 cm, weight was 104 kg and body mass index (BMI) was 31.7 kg/m2. His consciousness state was stupor with normal light reflexes, and senses as well as spontaneous motions of extremities were maintained. Chest auscultation revealed that the heart rate was fast, but there was no murmur, and the patient had tachypnea, but had no crackles or wheezing sound auscultated. There was neither notable tenderness nor rebound tenderness from the abdomen. The patient's skin was dry overall.
Peripheral blood assay showed the following results: white blood cell 6,560/mm3 (neutrophil 72%), hemoglobin 20.2 g/dL, hematocrit 60.8%, and platelets 228,000/mm3. Taking the findings of physical examination into account, dehydration-induced hemoconcentration was suspected. The results of serum biochemical assay revealed that the plasma glucose level had increased to 1,216 mg/dL, the blood urea nitrogen level was 31 mg/dL, and creatinine level was 2.4 mg/dL. The result also showed the following: sodium, 149 mEq/L; potassium, 4.5 mEq/L; chloride, 96 mEq/L; total protein, 8.7 g/dL; albumin, 5.0 mg/dL; aspartate aminotransferase, 28 IU/L; alanine aminotransferase, 44 IU/L; total bilirubin, 0.6 mg/dL; calcium, 11.5 mg/dL; phosphate, 6.1 mg/dL; and creatine phosphokinase (CPK), 80 U/L (reference range, 30 to 170). Dipstick-utilized urine assay showed a positive reaction to ketone, and increases in amylase and lipase to 545 IU/L (reference range, 28 to 100) and 1,435 U/L (reference range, 13 to 60), respectively. Arterial blood gas analysis (ABGA) showed that the pH was 7.25, pCO2 was 18.9 mm Hg, pO2 was 86.1 mm Hg, HCO3- was 8.2 mEq/L, and oxygen saturation was 95.7%, presenting metabolic acidosis with 44.8 mEq/L of anion gap. The glycosylated hemoglobin level was 13.8%, while the serum C-peptide level tested during the administration of insulin were 0.38 ng/mL. So the patient was presumed to be in DKA and acute renal failure.
Electrocardiography findings showed sinus tachycardia with rate of 150 beats per minute.
There were no specific findings from the chest X-ray examination, and there was no evidence of ileus other than fecal impaction shown on abdominal X-ray examination. An abdominal computed tomography scan showed no findings of edema or necrosis or fluid retention in the pancreatic parenchyme and its periphery ().
Although there was no sign of BP reduction, the patient showed severe dehydration induced by extreme hyperglycemia and metabolic acidosis. We administered ≥4 L per day of fluid through intravenous infusion and immediately began insulin pump therapy. Within 24 hours of insulin therapy, the plasma glucose level was reduced to less than 300 mg/dL (), the anion gap level was reduced to normal range and ABGA showed that the patient was out of metabolic acidosis. But, in spite of fluid infusion of ≥2 L per day, hyperthermia occurred and the levels of CPK and creatinine began to increase rapidly to 16,161 U/L and 4.1 mg/dL, respectively, on the 3rd day of hospitalization. Also, the urinary myoglobin level was 1,879 ng/mL. In addition, the patient was in a confused mental state with severe muscle stiffness and rigidity, and increased uptake at upper and lower proximal limb was shown on bone scan (). Even with fluid treatment for acute renal failure, the level of creatinine continued to increase, so we started continuous renal replacement therapy (CRRT) on the 5th day of hospitalization (). After initiation of CRRT, the patient showed remarkable improvement in fever and consciousness, so we converted dialysis modality to intermittent hemodialysis 3 days later and maintained the treatment until the 12th day of hospitalization. The urine output was normalized and there was no additional elevation in creatinine and CPK concentrations, so we discontinued hemodialysis (). The patient presented consciousness deterioration, muscle stiffness, and high fever that did not respond to antipyretics and fluid infusion with history of taking antipsychotics, so we determined that the patient had NMS, and implemented supportive therapy including discontinuation of causative medication. We used the insulin pump for glycemic control in the early stage, and changed to multiple daily injections of insulin to manage the patient's condition. We could discontinue the administration of insulin on the 41st day after the first visit to our hospital as the insulin demand had gradually decreased. And we changed to metformin monotherapy. We stopped the administration of oral hypoglycemic agents on the 52nd day. On follow-up examination, we confirmed a notable reduction in glycosylated hemoglobin and a remarkable restoration of the serum C-peptide level (). Currently, the patient is maintaining very good glycemic control only by life style modification and is under prognostic observation as an outpatient.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [1216.0, 'mg/dL'], 'Sodium': [149.0, 'mEq/L']}",175.784,166.9948,184.5732,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 149.0 mEq/L. 
The concentration of glucose is 1216.0 mg/dL. 
Plugging in these values into the formula gives us 149.0 mEq/L + 0.024 * (1216.0 - 100) = 175.784 mEq/L.
Hence, the patient's corrected concentration of sodium is 175.784 mEq/L."
5406,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4348987-1,Extracted,"A 75-year-old female patient visited our hospital because of orthopnea, bilateral legs edema, and dyspnea on effort. The symptoms had been occurring since a month prior to admission. She had an 18-year history of hypothyroidism, for which levothyroxine had been prescribed. The physical findings on admission included bilateral pretibial edema and jugular venous distension without thyroid swelling. A third heart sound could be heard on auscultation, and a holoinspiratory crackle was detected at the base of both lungs. Her body temperature was 37.7°C; blood pressure, 116/91 mmHg; pulse rate, 160 beats/min and irregular; and oxygen saturation 95% when breathing room air. The remaining physical examination findings were unremarkable. Laboratory test results included the following: White blood cell count, 3400/mL (with a normal differential); red blood cell count, 340 × 104/mL; hemoglobin level, 11.3 g/dL (normal range: 12.0–16.0); platelet count, 11.0 × 104/mL (normal range: 15.0–45.0); and levels of sodium, 133 mEq/L (normal range: 135–147); potassium, 3.8 mEq/L; creatinine kinase, 356 IU/L (normal range: 43–146); glucose, 116 mg/dL; thyroid-stimulating hormone (TSH), 4.32 mIU/mL (normal range: 0.35–4.94); serum free thyroxine, 1.174 ng/dL (normal range: 0.70–1.48); antithyroid peroxidase antibody, 39.1 IU/mL (normal range: <10), antithyroglobulin antibody, 382.8 IU/mL (normal range: <50), brain natriuretic peptide 402.7 pg/mL (normal range: 0.0–18.4). An electrocardiogram revealed atrial fibrillation with a ventricular rate of 123 beats/min. A chest radiograph on admission revealed bilateral pleural effusion and pulmonary congestion []. An echocardiogram revealed diffuse hypokinesis of the left ventricle with a left ventricular ejection fraction (LVEF) of 24%. Moderate-to-severe tricuspid regurgitation with a peak flow velocity of 2.8 m/s was also detected. The estimated right ventricular systolic pressure was 46 mm Hg. These findings were consistent with those for congestive heart failure.
Intravenous infusion of isosorbide dinitrate, furosemide, and low-dose dopamine was immediately initiated. The patient's symptoms gradually improved, and the intravenous medications were gradually switched to carvedilol (10 mg/day), spironolactone (25 mg/day), and rivaroxaban (15 mg/day). Two weeks after admission, her dyspnea had resolved, and pulmonary congestion was almost absent on the follow-up chest radiograph []. However, her systolic blood pressure was approximately 60 − 80 mmHg, and she complained of dizziness and fainting. A coronary artery angiogram revealed normal artery status, and a repeat echocardiogram revealed an LVEF of 58%. We attempted to determine the cause of hypotension. cardiogenic, hypovolemic, septic, and neurogenic hypotension were ruled out.
Pituitary-adrenal axis reactivity test evaluation was then performed. Serum concentrations of cortisol and ACTH were low []. There was little plasma cortisol response after a bolus injection of 0.125 mg of ACTH []. ACTH-releasing hormone did not sufficiently increase the plasma ACTH concentration []. TSH, prolactin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and growth hormone levels were all increased by an infusion of TSH-releasing hormone, LH-releasing hormone, and rapid-acting insulin [-]. Although the LH and FSH levels were increased by LH-releasing hormone, their basal levels were high enough because of the patient's postmenopausal state, and we considered the LH- and FSH-releasing ability to be preserved. The TSH increase was excessive, which is consistent with the findings for primary hypothyroidism due to chronic thyroiditis. Plasma renin activity and aldosterone concentration were normal. Thus, a diagnosis of isolated ACTH deficiency was made. Magnetic resonance imaging revealed no pituitary lesions or adjacent lesions and antipituitary antibody testing was negative.
Oral administration of hydrocortisone (15 mg/day) was then initiated and the patient's clinical symptoms such as dizziness and fainting gradually improved. Her chest radiograph revealed no abnormalities []. Her systolic blood pressure was stable at 90 − 100 mmHg and she was discharged.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [116.0, 'mg/dL'], 'Sodium': [133.0, 'mEq/L']}",133.384,126.7148,140.0532,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 133.0 mEq/L. 
The concentration of glucose is 116.0 mg/dL. 
Plugging in these values into the formula gives us 133.0 mEq/L + 0.024 * (116.0 - 100) = 133.384 mEq/L.
Hence, the patient's corrected concentration of sodium is 133.384 mEq/L."
5407,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8369979-1,Extracted,"A 61-year-old male was referred to the hospital by his primary care physician for further evaluation of low potassium levels and elevated blood pressure. He initially went to his physician because he had experienced bilateral leg swelling for a week. Past medical history was significant for hypertension and fibromyalgia. Family history was significant for cardiovascular disease. He denied any alcohol, tobacco, or recreational drug consumption.
In the emergency department (ED), his vital signs were temperature 98.2 F, blood pressure 228/115 mmHg, pulse 80 beats per minute, respiratory rate 18 per minute, and SpO2 99%. On physical examination, abdomen was soft, bowel sounds were present with mild epigastric tenderness to palpation, and 1+ pitting edema on bilateral lower extremities. His laboratory result showed hemoglobin of 14.3 g/dL (13.2-17.5 g/dL), white blood cell count of 6.3 x 103/uL (4.5-11.0 x 103/uL), and platelet count of 201 x 103/uL (140-450 x 103/uL). Comprehensive metabolic panel showed a blood urea nitrogen of 18 mg/dL (5-25 mg/dL), serum creatinine of 0.96 mg/dL (0.61-1.24 mg/dL), sodium of 139 mmol/L (136-145 mmol/L), potassium of 2.1 mmol/L (3.5-5.2 mmol/L), chloride of 91 mmol/L (96-110 mmol/L), bicarbonate of 38 mmol/L (24-31 mmol/L), glucose of 89 mg/dL (70-99 mg/dL), alanine aminotransferase of 21 U/L (10-60 U/L), aspartate aminotransferase of 27 U/L (10-42 U/L), alkaline phosphatase of 89 U/L (38-126 U/L), and a total bilirubin of 1.1 mg/dL (0.2-1.3 mg/dL). EKG showed normal sinus rhythm with a rate of 60 beats per minute with flattened T-wave and presence of the U-wave complexes (Figure ). Labetolol HCl 20 mg IV and hydralazine 10 mg IV were given for blood pressure control in the ED as well as potassium 40 mEq PO and protonix 40 mg PO.
Once admitted and upon further questioning, the patient revealed that he was experiencing abdominal pain for the past 15 years. He describes himself as a ""naturalist"" and denies taking the proton-pump inhibitors that were initially prescribed to him. He wanted to resolve his abdominal pain with a natural remedy and resorted to over-the-counter deglycyrrhizinated licorice supplements for pain relief after multiple dietary variations had failed. Over the years, he had increased his daily dose for postprandial pain relief. He admitted that for the past 6-8 months he was consuming up to 20 licorice root 760 mg tablets a day, well exceeding the acceptable daily allowance (2280 mg). He further revealed he had a 10-pound weight loss in two months due to decreased oral intake. The last colonoscopy was over 10 years ago. The abdominal pain associated with oral intake was the reason he refused to take oral medications including home medication losartan-hydrochlorothiazide 100-12.5 mg and potassium PO repletion prescribed to him from the ED. Medication formulations were switched to IV.
A rapid response was called after the patient had a 10-second pause on telemetry. Repeated potassium levels showed potassium of 1.9 mmol/L and the patient was brought to the critical care unit for close observation. The patient was educated and was willing to receive potassium via oral solution in addition to the potassium he was receiving intravenously. The patient’s potassium levels were monitored every 4 hours as well as serial EKGs; he was unable to achieve a potassium level higher than 2.8 mmol/L in 24 hours. The potassium was eventually normalized to 3.5 mmol/L 48 hours post-admission via continued potassium IV infusion and oral intake equalling to 120 mEq daily.
Gastroenterology was consulted and an endoscopy was done, which showed gastritis and gastroesophageal reflux disease without evidence of Helicobacter pylori or other pathology. He was started on sucralfate 1 g suspension, reglan 10 mg, and continued on pantoprazole 40 mg IV. Psychiatry was also consulted; he was willing to take oral medications and was started on sertraline 25 mg QD and buspirone 10 mg TID. Carvedilol 12.5 BID, irbesartan 300 mg daily, and spironolactone 25 mg BID were all prescribed.
Systolic blood pressure remained above 200 despite several days on the antihypertensive medications including hydralazine 10 mg IV PRN. Despite dose adjustments of the antihypertensive medications, the patient’s blood pressure remained labile for over one week. Secondary causes of hypertension were investigated. Renin and aldosterone study showed plasma renin <0.1 ng/mL/h (0.2-1.6 ng/mL/h ), aldosterone level <3 ng/dL (<16 ng/dL), serum cortisol level 22 μg/dL (8.7-22.4 μg/dL), and 11 deoxy-cortisol <5 ng/dL (<19 ng/dL). Plasma metanephrines 0.22 nmol/L (0-0.49 nmol/L) and urine metanephrines of 122 μg/d (55-320 μg/d) were also unremarkable. Renal ultrasound and CT without contrast of the abdomen and pelvis were non-significant. Amlodipine 5 mg QD was added. Prior to discharge, the patient’s systolic blood pressure ranged between 120 and 160. He was sent home with a blood pressure cuff. The patient was thoroughly re-educated on the importance of medication compliance and the cessation of licorice supplement intake.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [89.0, 'mg/dL'], 'Sodium': [139.0, 'mmol/L']}",138.736,131.7992,145.6728,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 139.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 139.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 139.0 mmol * 1 mEq/mmol = 139.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mmol sodium/L converts to 139.0 mEq sodium/L. 
The concentration of glucose is 89.0 mg/dL. 
Plugging in these values into the formula gives us 139.0 mEq/L + 0.024 * (89.0 - 100) = 138.736 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.736 mEq/L."
5408,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-1270,Extracted,"A 54-year-old woman comes to the physician with abdominal distention and mild diffuse abdominal discomfort. She has not had nausea, vomiting, fever, or chills. She was diagnosed with alcoholic liver cirrhosis 2 years ago. Examination shows a protruding, distended abdomen that is dull to percussion with a positive fluid wave. Ultrasonography shows mild to moderate ascites. Appropriate treatment of the patient's condition is started. Four days later, the patient experiences palpitations and chest pain at home. She is brought to the emergency department, where her temperature is 37.3°C (99.1°F), pulse is 182/min, respirations are 18/min, and blood pressure is 82/50 mm Hg. An ECG shows ventricular tachycardia. Initial laboratory studies show:
Serum
Na+ 131 mEq/L
K+ 2.9 mEq/L
Cl- 92 mEq/L
Bicarbonate 34 mEq/L
Urea nitrogen 42 mg/dL
Creatinine 4.8 mg/dL
Glucose 90 mg/dL
Ca2+ 8.1 mg/dL
Mg2+ 1.5 mg/dL
Phosphate 4.7 mg/dL
Arterial Blood Gas
pH 7.52
pCO2 45 mm Hg
pO2 90.2 mm Hg
She is successfully cardioverted to normal sinus rhythm.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [90.0, 'mg/dL'], 'Sodium': [131.0, 'mEq/L']}",130.76,124.222,137.298,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 131.0 mEq/L. 
The concentration of glucose is 90.0 mg/dL. 
Plugging in these values into the formula gives us 131.0 mEq/L + 0.024 * (90.0 - 100) = 130.76 mEq/L.
Hence, the patient's corrected concentration of sodium is 130.76 mEq/L."
5409,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8572339-1,Extracted,"A previously healthy 35-month-old girl was brought to the emergency room of the Namazi hospital, Shiraz, Iran, due to reduced level of consciousness. She was well up to five days prior to her admission, after that she presented with dysuria and loss of appetite, and then developed polyuria, polydipsia, and weight loss (14 kg → 11 kg). There was no history of DM in her family.
On arrival, her height was measured 92 cm (25th−50th) percentile), she weighed 11 kg (5th–10th) percentile), and her Body Mass Index (BMI) (BMI-for-age) was at the 72nd percentile. Her vital signs were as follows: temperature: 38°C, heart rate (HR): 160, blood pressure (BP): 95/50, and her Glasgow coma scale (GCS) was 11/15. During her physical examination, capillary refilling time was more than 3 s with weak pulses. When checked with a capillary blood glucose meter, her glucose level was too high, so a serum glucose test was performed. Moreover, her first VBG was as follows: pH 7.26, PCO2: 32, PO2: 39, HCO3: 15.8, and BE: −12.6. Due to the decreased level of consciousness, brain CT scan was performed in which brain edema was reported.
As the first line of treatment, she was hydrated with normal saline (10 cc per kg), then the laboratory report revealed; blood sugar: 1124 mg/dl, BUN: 71 mg/dl, creatinine: 1.9 mg/dl, Na: 170 mEq/L (corrected Na: 186), and K: 5.1 mEq/L (effective osmolality was 402). Additionally, urine analysis was SG: 1.010, GLU: 3+, Ketone: trace. VBG after first hydration was as follows: pH: 7.27, PCO2: 34.8, and HCO3: 15.8. Based on the laboratory report; HHS was confirmed as diagnosis; hence, she was transferred to the Pediatric Intensive Care Unit (PICU).
On arrival at PICU, she developed generalized convulsion, and her GCS declined to less than 8; so she was intubated.
She was hydrated with normal saline again; then, the intravenous fluid was administered with 15 percent deficit and maintenance of fluid in addition to urine output replacement. Due to brain edema, deficit was given over 72 h, but according to urine output and serum sodium level, the amount of deficit increased up to 18 percent, and the sodium content of IV fluid decreased.
The first sodium level reported in PICU was 185 mEq/L, but it gradually decreased as hydration continued, and the amount of fluid increased (with the target level of 10 mEq/L decrease per day); then, it became stable around 145 mEq/L over the next five days. Our primary goal in her treatment was to correct sodium level maximum 10 mEq/L per day, to decrease osmolality maximum 3–5 mosm/L/h, and to reduce blood sugar maximum 75 mg/dl per hour.
On the 3rd day, HHS was resolved, but the patient became febrile, and the amount of endotracheal tube (ETT) secretion increased. The culture of ETT secretions revealed candida non-albicans and pseudomonas aeruginosa; hence, antibiotic was prescribed. Subsequently, the patient developed hypotension, so inotrope was initiated. On the same day, her blood creatine phosphokinase (CPK) increased to 6400 IU/L, and it reached 13,400 on the fifth day. Then, she developed hemoglobinuria; thereafter, hydration continued until the CPK level returned normal level on the 18th day (Table ).
Although enoxaparin was initiated for deep venous thrombosis (DVT) prophylaxis, she presented with the left forearm and hand swelling, on the 6th day. Doppler ultrasonography revealed thrombosis of the distal part of the brachial artery, so the therapeutic dose was initiated. Consequently, her conditions improved after 2 days, and a week later, Doppler sonography was normal.
On the 9th day, she was weaned off the ventilator, and on the 21st day, the patient was discharged from hospital without any sequela.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [1124.0, 'mg/dL'], 'Sodium': [170.0, 'mEq/L']}",194.576,184.8472,204.3048,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 170.0 mEq/L. 
The concentration of glucose is 1124.0 mg/dL. 
Plugging in these values into the formula gives us 170.0 mEq/L + 0.024 * (1124.0 - 100) = 194.576 mEq/L.
Hence, the patient's corrected concentration of sodium is 194.576 mEq/L."
5410,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5352960-1,Extracted,"A 69-year-old man was admitted to hospital with abdominal discomfort, tenderness, and dyspeptic complaints in August 2010. Abdominal ultrasonography revealed paraaortic lymphadenopathy and the patient was referred to the hematology department. He had no history of hypertension, diabetes mellitus, smoking, or alcohol use. The physical examination showed no sign of peripheral lymphadenopathy or hepatosplenomegaly. Laboratory results showed hypochromic microcytic anemia with a hemoglobin level of 11.9 g/dL, mean corpuscular volume (MCV) of 78 fl, erythrocyte sedimentation rate of 66 mm/h, and C-reactive protein level of 64 mg/L (normal range: 0-6 mg/L). The reticulocyte count was normal. There was no iron, folic acid, or vitamin B12 deficiency according to the laboratory results. All biochemical parameters were within normal range. Serologic tests for hepatitis, human immunodeficiency virus, Brucella, cytomegalovirus, Epstein-Barr virus, and HHV-8 were all negative. Serum immunoelectrophoresis demonstrated polyclonal hyperglobulinemia. Bone marrow aspiration and biopsy revealed normocellular findings. A computed tomography scan demonstrated a paraaortic lymphadenopathy (6 cm in diameter). Total lymph node excision was performed and the result of the pathologic specimen was reported as Castleman’s disease of the plasma cell type (Figure ). After operation, the patient was followed until July 2013, and he was in remission state according to laboratory and imaging studies. Follow-up laboratory results in 2011 showed that the erythrocyte sedimentation rate was 55 mm/h and the C-reactive protein was 25 mg/L. Follow-up laboratory results in 2012 showed that the erythrocyte sedimentation rate was 35 mm/h and the C-reactive protein level was 9.6 mg/L. During the patient’s last hematology visit in 2013, a physical examination revealed normal findings. Laboratory parameters showed that his hemoglobin level was 13.7 g/dL, the erythrocyte sedimentation rate was 33 mm/h, and the C-reactive protein level was 9.6 mg/L. All biochemical parameters were within normal range. Serum immunoelectrophoresis and protein electrophoresis were normal. Radiologically, there were millimetric lymph nodes in the paraaortic area. The patient stopped routine follow-up hematology visits after July 2013 and was not seen for three years due to the lack of complaints. In June 2016, the patient was admitted to the hematology department with complaints of nausea, vomiting, abdominal pain, and edema in the distal extremities. A physical examination revealed pale skin and conjunctiva without hepatosplenomegaly. Laboratory examinations revealed normochromic normocytic anemia (Hct, 25.7%; Hb, 9.6 g/dL; MCV, 87 fl) and elevated erythrocyte sedimentation rate (80 mm/h) and C-reactive protein (76 mg/L). The results of the laboratory findings were as follows: Glucose 95 mg/dL, BUN 75 mg/dL, creatinine 6.2 mg/dL, Na 139 mmol/L, K 5.0 mmol/L, Ca 8.2 mmol/L, phosphorus 5.2 mmol/L, uric acid 6.6 mg/dL, total cholesterol 223 mg/dL, LDL 126 mg/dL, GGT 15 U/L, ALP 97 U/L, AST 10 U/L, ALT 6 U/L, total protein 5.9 g/dL, albumin 2.4 g/dL, LDH 213 U/L, CPK 20 U/L, and serum iPTH level 151 pg/mL (15-65). The urine stick test revealed a positive result for protein (+++), but there were no erythrocyte or leukocyte casts in the microscopic evaluation of the urine sediment. The 24-h urine protein level was 10 g. ANA, anti-ds DNA, anti-GBM and ANCA profiles were all negative. The patient did not have any chronic inflammatory conditions such as tuberculosis, malaria, rheumatoid arthritis, or familial Mediterranean fever. The patient was referred to the nephrology department. An abdomen ultrasonography noted normal sized kidneys and a normal parenchymal thickness with increased grade 2 renal cortical echogenicity. All other findings were normal. A kidney biopsy was performed, which suggested AA-type amyloidosis (Figure ). Metabolic acidosis and uremic symptoms had occurred, oliguria developed, and creatinine clearance was decreased to 10 mL/dk. The patient was admitted for veno-venous hemodialysis intervention via a double-lumen dialysis catheter in the jugular vein. Hematologic assessment demonstrated that CD was in remission according to imaging studies. A PET-CT scan only reported multiple millimetric lymph nodes without FDG uptake in the paraaortic area. Hemodialysis intervention was continued three times a week due to progressive deterioration of kidney functions. The patient was discharged from hospital two weeks later with a hemodialysis catheter and followed weekly. Two months later, he was considered to have end stage renal disease and underwent routine hemodialysis intervention via a created arteriovenous fistula.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [95.0, 'mg/dL'], 'Sodium': [139.0, 'mmol/L']}",138.88,131.936,145.824,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 139.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 139.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 139.0 mmol * 1 mEq/mmol = 139.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mmol sodium/L converts to 139.0 mEq sodium/L. 
The concentration of glucose is 95.0 mg/dL. 
Plugging in these values into the formula gives us 139.0 mEq/L + 0.024 * (95.0 - 100) = 138.88 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.88 mEq/L."
5411,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-5483,Extracted,"A 69-year-old man presents to the emergency department with shortness of breath that has been worsening over the past month. The patient states that he has had worsening shortness of breath that has progressed to shortness of breath with simple activities and minor exertion. When he was unable to climb the stairs to his house today, he decided to come to the emergency department. The patient has a past medical history of poorly managed diabetes mellitus, hypertension, end stage renal disease, and obesity. His current medications include insulin, metformin, lisinopril, hydrochlorothiazide, and ibuprofen. The patient is notably non-compliant with his medications. An EKG and chest radiograph are normal. The patient had dialysis two days ago and attends most of his appointments. Laboratory values are ordered and are seen below:

Serum:
Na+: 135 mEq/L
K+: 4.5 mEq/L
Cl-: 100 mEq/L
HCO3-: 19 mEq/L
Urea nitrogen: 29 mg/dL
Glucose: 75 mg/dL
Creatinine: 2.5 mg/dL
Ca2+: 9.2 mg/dL
Mg2+: 1.7 mEq/L
AST: 11 U/L
ALT: 11 U/L

Leukocyte count and differential:
Leukocyte count: 4,500/mm^3
Platelet count: 150,000/mm^3
Neutrophil: 54%
Lymphocyte: 25%
Monocyte: 3%
Eosinophil: 1%
Basophil: 1%

Hemoglobin: 8.2 g/dL
Hematocrit: 22%
Mean corpuscular volume: 82 µm^3

The patient appears comfortable at rest but demonstrates notable shortness of breath when exerting himself. His temperature is 99.5°F (37.5°C), pulse is 89/min, blood pressure is 144/85 mmHg, respirations are 10/min, and oxygen saturation is 97% on room air. Pulmonary and cardiac exam are within normal limits.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [75.0, 'mg/dL'], 'Sodium': [135.0, 'mEq/L']}",134.4,127.68,141.12,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 135.0 mEq/L. 
The concentration of glucose is 75.0 mg/dL. 
Plugging in these values into the formula gives us 135.0 mEq/L + 0.024 * (75.0 - 100) = 134.4 mEq/L.
Hence, the patient's corrected concentration of sodium is 134.4 mEq/L."
5412,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5292295-1,Extracted,"A 77-year-old woman lost consciousness 6 hours before being admitting to a local clinic where she underwent brain CT. The patient was promptly referred to our department with suspected basal ganglion ICH based on the brain CT. The patient had no medical history other than diabetes. Her premorbid Eastern Cooperative Oncology Group score was 3 due to dementia but she had normal cognitive functioning. The patient had stopped taking her diabetic medication 2 months earlier, on her own volition, and had been suffering progressive debilitation. No other symptoms were present. The patient did not take any sedatives or tranquilizers. The initial vital signs were blood pressure 180/98 mmHg, pulse rate 110/min, respiratory rate 18/min, and body temperature 36.8°C. A neurological examination revealed stupor, intact brainstem signs, and greater than grade III motor strength in all four extremities without lateralizing signs. She did not exhibit any abnormal movements of the extremities. No specific abnormalities were found on a systemic physical examination. The initial serum laboratory test results were blood glucose 607 mg/dL, hemoglobin 12.8 g/dL, white blood cells 6,720/mm3, platelets 193,000/mm3, aspartate aminotransferase 32 IU/L, alanine aminotransferase 38 IU/L, blood urea nitrogen 17 mg/dL, serum creatinine 1.2 mg/dL, sodium 120 mEq/L, potassium 5.0 mEq/L, chloride 89 mEq/L, and lactate 12.5 mg/dL. No serum ethanol was detected, and an arterial blood gas analysis revealed the following: pH 7.454, pCO2 37.0 mmHg, pO2 78.1 mmHg, HCO3 25.4 mmol/L, and base excess 1.6 mmol/L. No ketones were detected in the urinalysis. Barbiturates, benzodiazepines, and tricyclic antidepressants were not found during a toxin-screening test. The initial brain CT showed a hyperdense lesion in the right basal ganglion (). On magnetic resonance imaging, T1-weighted images revealed high signal intensity indicative of changes due to nonketotic hyperglycemia; diffusion weighted imaging (DWI) and an apparent diffusion coefficient map showed restricted diffusion (). Blood glucose level was controlled with regular insulin, and conservative treatment and fluid resuscitation were provided. Electroencephalography revealed findings compatible with diffuse encephalopathy, but no signs of seizure were detected. After admission to the intensive care unit, the patient gradually recovered consciousness and was alert after 24 hours, as blood glucose and sodium were controlled. No abnormal movement disorder was noted after a return to consciousness. The patient was discharged 10 days after admission without any complications.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [607.0, 'mg/dL'], 'Sodium': [120.0, 'mEq/L']}",132.168,125.5596,138.7764,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 120.0 mEq/L. 
The concentration of glucose is 607.0 mg/dL. 
Plugging in these values into the formula gives us 120.0 mEq/L + 0.024 * (607.0 - 100) = 132.168 mEq/L.
Hence, the patient's corrected concentration of sodium is 132.168 mEq/L."
5413,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-8780,Extracted,"A 65-year-old diabetic man presents to the emergency department with severe retrosternal chest pain, vomiting, and diaphoresis for the last half hour. He has a history of diabetic chronic kidney disease. He is on insulin therapy. Oral medications include aspirin, losartan, and metformin. The vital signs include: temperature 36.8°C (98.2°F), pulse 88/min, respiration rate 14/min, and blood pressure 120/65 mm Hg. The weight is 78 kg (172.0 lb). The lungs are clear to auscultation. Cardiac examination shows no abnormalities. The electrocardiogram (ECG) shows ST-segment elevation in the precordial leads V-1–V-4. Left ventricular ejection fraction is estimated at 55%. The laboratory test results are as follows:
Laboratory test
Hemoglobin 15 g/dL
Leukocyte count 9,500/mm3
Serum
Glucose 215 mg/dL
Na+ 140 mEq/L
Cl− 102 mEq/L
K+ 4.1 mEq/L
Urea nitrogen 22 mg/dL
Creatinine 1.4 mg/dL
Cardiac troponin I 0.8 ng/mL
The patient is being considered for primary percutaneous coronary intervention.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [215.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",142.76,135.622,149.898,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.0 mEq/L. 
The concentration of glucose is 215.0 mg/dL. 
Plugging in these values into the formula gives us 140.0 mEq/L + 0.024 * (215.0 - 100) = 142.76 mEq/L.
Hence, the patient's corrected concentration of sodium is 142.76 mEq/L."
5414,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-8497,Extracted,"A 27-year-old diabetic male rushes to the emergency department after finding his blood glucose level to be 492 mg/dL which is reconfirmed in the ED. He currently does not have any complaints except for a mild colicky abdominal pain. His temperature is 37°C (98.6°F), respirations are 15/min, pulse is 67/min, and blood pressure is 122/88 mm Hg. Blood is drawn for labs the result of which is given below:
Serum:
pH 7.0
pCO2 32 mm Hg
HCO3- 15.2 mEq/L
Sodium 122 mEq/L
Potassium 4.8 mEq/L
Urinalysis is positive for ketone bodies. He is admitted to the hospital and given intravenous bicarbonate and then started on an insulin drip and normal saline. 7 hours later, he is found to be confused and complaining of a severe headache. His temperature is 37°C (98.6°F), pulse is 50/min, respirations are 13/min and irregular, and blood pressure is 137/95 mm Hg.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [492.0, 'mg/dL'], 'Sodium': [122.0, 'mEq/L']}",131.408,124.8376,137.9784,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 122.0 mEq/L. 
The concentration of glucose is 492.0 mg/dL. 
Plugging in these values into the formula gives us 122.0 mEq/L + 0.024 * (492.0 - 100) = 131.408 mEq/L.
Hence, the patient's corrected concentration of sodium is 131.408 mEq/L."
5415,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2275218-1,Extracted,"A 35 year old female with SCD, presented with pedal and periorbital edema, distension of abdomen, decreased urine output and dyspnoea on exertion since 1 month. On examination, she was pale, with pulse rate of 100/minute, normal temperature, and blood pressure was 160/100 mm Hg. Her abdomen was distended due to moderate ascites however there was no organomegaly/scars. Cardio-respiratory and neurological examination was unremarkable. Ultrasonography showed right kidney, 10.9 × 6.0 cm, left kidney of 11.4 × 5.8 cm, with increased echogenicity and maintained cortico-medullary differentiation. Moderate ascites was present.
On investigations, urine albumin was 500 mg/24 hours, microscopy showed 30–40 pus cells and 3–5 granular casts/high power field, urine culture was sterile, serum creatinine, 7.0 mg%, serum proteins, 4.5 gm/dL; serum albumin, 1.8 gm%, serum bilirubin was 0.5 mg/dL, serum alanine amino transferase was 16 units/L, random blood sugar was 87 mg/dL, serum uric acid was 7.5 mg/dL, serum sodium was 134 meq/L and serum potassium, 5.5 meq/L and positive sickling test was noted at 24 hours. Her hemoglobin was 7.1 gm/dL; total leucocyte count was 7,700/cmm with differential count showing neutrophils, 76%, lymphocytes, 20% and eosinophils and monocytes, each, 2%. Peripheral smear showed few crenated and sickled cells with mild hypochromia and anisopoikylocytosis.
She was dialyzed and 2 units of packed cells were transfused. Renal biopsy was performed and after paraffin embedding, 3 micrometer sections were taken and stained using Hematoxylin and eosin, Periodic Acid Schiff, Jone's silver methaneamine and Gomori's trichrome stains. Indirect immunofluorescence studies were performed using anti-human IgG, IgM, IgA, C1q, C3, albumin and fibrinogen anti-sera (DAKO, USA). Histopathology revealed one core with 13 glomeruli. All of them were moderately enlarged in size and 11 had exuberant and occasionally circumferential cellular (rarely fibrocellular) crescents occupying 70–90% urinary spaces, occasionally replacing capillary tufts and shrinking or pushing the capillary tufts towards vascular poles (Figure ). Capillary tufts had fairly open lumina lined by membranes with occasional reduplication, thickening/rupture. There was uniform moderate mesangial prominence. Capillaries and crescents were infiltrated by few sickle shaped, dysmorphic RBCs, platelet/fibrin thrombi. Afferent and efferent arterioles were filled with sickled RBCs. Bowman capsules were segmentally thickened and occasionally ruptured evoking periglomerular leucocytic reaction. Tubules were moderately degenerated and filled with cellular casts and rarely RBCs. Focal atrophy was also evident. Interstitium was moderately prominent for focal fibrosis and overlying focal mononuclear cellular infiltration with admixed neutrophils. Peri-tubular capillaries were dilated and filled with sickled RBCs (Figure ). At least one medium caliber and two small caliber arteries showed lumina filled with trapped dysmorphic RBCs.
Immunofluorescence studies showed fine granular fluorescence (+2) across 60–80% mesangial regions and adjacent capillaries of all glomeruli on staining with anti-human C3 and (trace/+1) with anti-human IgG, C1q and fibrinogen antisera (Figure ). Subsequently she was investigated for vasculitis and lupus nephritis. Indirect immunofluorescence and ELISA revealed anti-nuclear antibodies, (normal index: <1, test: 8.5), anti-dsDNA antibodies were >200 IU/mL (normal <25 IU/mL, Orgentec, Germany). Anti-neutrophil cytoplasmic antibodies were absent. Final diagnosis was made as SCN with DPLN, ISN/RPS class IV-G (A).
Hemoglobin variant study using High Performance Liquid Chromatography (d-10, Biorad, USA) was performed 5 days after transfusion which showed HbSA of 6.9% (Figure ).
She was treated with Methylprednisolone 500 mg, intravenously for 3 days and Cyclophosphamide, 500 mg intravenously immediately and dose was repeated after 21 days. Then she was switched over to oral Prednisolone, 40 mg/day. Hemodialysis was done on alternate days for 21 days. At follow-up of 2 months, she is on maintenance dialysis with urine output of less than 400 ml/day.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [87.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",133.688,127.0036,140.3724,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 134.0 mEq/L. 
The concentration of glucose is 87.0 mg/dL. 
Plugging in these values into the formula gives us 134.0 mEq/L + 0.024 * (87.0 - 100) = 133.688 mEq/L.
Hence, the patient's corrected concentration of sodium is 133.688 mEq/L."
5416,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4942506-1,Extracted,"A 36-year-old female smoker presented to the emergency department with epigastric abdominal pain, radiating to her back, of 1 week duration. Her past medical history was significant for type 2 diabetes for which she was on oral hypoglycemic agents and insulin; presumed secondary HTG for which she was on atorvastatin and gemfibrozil; furthermore, she used medroxyprogesterone acetate for contraception. She had stopped all these medications except the contraceptive 12 months prior to her presentation. The patient has no history of alcohol abuse, thyroid dysfunction, or family history of HTG. On admission, all vital signs were within normal limits. Physical examination was normal except for epigastric tenderness and a BMI of 31.4 kg/m2.
The initial relevant laboratory testing revealed sodium of 129 meq/l, potassium 3.7 meq/l, chloride 97 meq/l, BUN 10 mg/dl, creatinine 0.77 mg/dl (at baseline), bicarbonate 13.7 meq/l, anion gap 18 meq/l, glucose of 324 mg/dl, amylase 31 IU/l, lipase 206 IU/l, and TG 2,329 mg/dl with a previous baseline of around 2,000 mg/dl, serum calcium 9.0 mg/dl, TSH 1.182 µIU/ml, serum lactate 1.8 meq/l, negative urine ketones with serum beta-hydroxybutyrate 0.16 mmol/l, and negative urine pregnancy test. The abdominal computerized tomography scan showed no definite evidence of pancreatitis or any other pathology.
Despite unremarkable imaging, normal amylase, mild elevation of lipase, and a TG level that was mildly elevated from previous baseline, she was treated for possible HTGP with IV insulin based on the overall clinical picture. The differential diagnosis includes diabetic ketoacidosis (DKA); however, the patient lacked serum or urinary ketones. Regardless, IV insulin would treat both conditions of HTGP and DKA. The clinical impression of HTGP was further supported when her lipase increased to 370 IU/L and the TG levels on the initial sample was re-assayed resulting in a corrected reading of >10,000 mg/dl. The TG levels decreased to 6,069 mg/dl with IV insulin on day 5. However, given the worsening abdominal pain, plan for plasmapheresis to rapidly reduce the TG levels was taken. The TG levels decreased to 2,055 mg/dl after the first exchange and to 642 mg/dl after the second session, and her symptoms improved significantly.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [324.0, 'mg/dL'], 'Sodium': [129.0, 'mEq/L']}",134.376,127.6572,141.0948,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 129.0 mEq/L. 
The concentration of glucose is 324.0 mg/dL. 
Plugging in these values into the formula gives us 129.0 mEq/L + 0.024 * (324.0 - 100) = 134.376 mEq/L.
Hence, the patient's corrected concentration of sodium is 134.376 mEq/L."
5417,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5519313-1,Extracted,"The patient is a 63-year-old man with a past medical history of MALToma of the lung who presented with generalized weakness for the past one month associated with cough, fever, night sweats, and shortness of breath. The patient also had anorexia and weight loss of 15 pounds over one month. He denied a history of smoking. The patient was under treatment with isoniazid and pyridoxine for latent tuberculosis based on a positive skin tuberculin test.
On physical examination, his blood pressure was 110/59 mmHg, heart rate 118 beats per minute (bpm), respiratory rate 18/min, saturating 99% on room air with a temperature of 98.9oF. The patient was in no cardiopulmonary distress. A cardiovascular examination revealed no jugular venous distension, normal S1-S2, and no murmurs. On lung auscultation, the patient had rales at the left lung base.
Laboratory data showed sodium 134 mEq/L, potassium 4.2 mEq/L, chloride 103 mEq/L, bicarbonate 25 mEq/L, blood urea nitrogen 17 mg/dl, creatinine 0.9 mg/dl, glucose 96 mg/dl, hemoglobin 6.6 g/dl, hematocrit 20.1%, white blood cell count 5.5 x 103/microliter, and platelets 128 x 103/microliter. The coagulation profile showed prothrombin time (PT) 17.2 sec, partial thromboplastin time (PTT) 44.3 sec, and international normalized ratio (INR) 1.38.
Chest X-ray (CXR) and computed tomography (CT) scan showed right middle lobe opacity (Figures -). Repeat imaging after six months showed multiple masses in the lung and an osteoblastic bone lesion involving the left ilium (Figures -). Esophagogastroduodenoscopy showed a normal gastro-esophageal junction with erythematous mucosa in the stomach. The gastric biopsy was normal.
A lung biopsy done at initial presentation from the right middle lobe mass showed dense lymphoid infiltrate with proliferation of monocytoid B lymphocytes consistent with extranodal marginal zone lymphoma (BALToma/MALToma).
A CT-guided core needle biopsy from the left posterior pelvic mass that was noted six months after the initial presentation showed high grade diffuse large B-cell lymphoma involving skeletal muscles. The pathology report showed diffuse proliferation of lymphocytes, which were positive for cluster of differentiation (CD) 20 and B-cell lymphoma (BCL)-2 by immunohistochemistry tests. He was started on chemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) with subsequent complete clinical and radiologic remission (Figure ).","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [96.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",133.904,127.2088,140.5992,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 134.0 mEq/L. 
The concentration of glucose is 96.0 mg/dL. 
Plugging in these values into the formula gives us 134.0 mEq/L + 0.024 * (96.0 - 100) = 133.904 mEq/L.
Hence, the patient's corrected concentration of sodium is 133.904 mEq/L."
5418,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5966706-1,Extracted,"A 78-year-old African American man with past medical history of hypertension and alveolar emphysema presented to the emergency department with altered level of consciousness (LOC). He was found unresponsive and drooling on the couch by a family member. The patient's family had noted drooping of the right eyelid that had started the day before the incident. No headache, head injury, chest pain, palpitation, or decreased vision was reported but it was noted that he possibly could not see well in his peripheral visual field. The emergency medical services (EMS) reported an initial Glasgow Coma Score (GCS) of 7/15 (Eye 1, Verbal 1, and Motor 5) that began to improve on the way to the hospital. According to the EMS report, the patient's vital signs were normal at the scene including a blood pressure of 118/82 mmHg, heart rate of 92 per minute, and respiratory rate of 12 per minute. His blood glucose level was at 155 mg/dL.
He was a smoker, using a quarter of pack of cigarettes a day. His medications included amlodipine, ipratropium nebulizer, and albuterol nebulizer. He did not use alcohol or illicit drugs.
Upon arrival to the hospital, the patient was lethargic and had poor attention but was oriented to the time, place, and person. He denied headache, nausea, or vomiting. Physical examination revealed a GCS of 14/15 and normal vital signs, including blood pressure of 115/76 mmHg, body temperature of 37°C, respiratory rate of 20 per minute, and a regular pulse rate of 83 beats per minute. Pupils were equal in size and both had normal direct and consensual responses to light. Visual acuity appeared to be reduced but full evaluation was not possible. Complete ptosis of the right eye was noted. The right eye was deviated to the right with severe limitation in supraduction, infraduction, and adduction consistent with pupil-sparing third-cranial nerve (CN III) palsy. Fourth-cranial nerve (CN IV) palsy was also present in the right side. Extraocular eye movements were intact in the left eye. Sensation was intact over the face bilaterally. There were no other abnormal findings in the physical exam. Upon the admission, the plasma sodium level was slightly depressed at 130 mEq/L but the other initial lab findings were unremarkable ().
The patient was admitted to the internal medicine service for a stroke workup. Noncontrast computed tomography scan (CT scan) of the head showed only age related atrophic changes with no evidence of intracranial hemorrhage or mass effect. Brain magnetic resonance imaging (MRI) showed a sellar mass, and the pituitary MRI () revealed a large pituitary mass with extension to the right cavernous sinus. Intrinsic T1 hyperintensity suggested possible hemorrhage (pituitary apoplexy). Mild mass effect on the optic chiasm was noted. There were no evidence of extension of the mass beyond the lateral confines of the cavernous sinuses and no hydrocephalus or subarachnoid hemorrhage. The major intracranial flow voids were patent.
Lumbar puncture was performed and cerebrospinal fluid (CSF) analysis did not show any blood or xanthochromia. On his second hospital day, the patient developed an acute change in the mental status. He was noted to be lethargic and confused, not responding to his name, and having garbled speech. During that time, he had blood sugar of 98, blood pressure of 98/56 mmHg, and heart rate of 113 per minute. His acute confusional state resolved within an hour, but a clouding of consciousness continued to be present as was observed since admission. Electrocardiogram (EKG) and echocardiography were normal.
Based on the ophthalmoplegia, ptosis, altered mental status, visual symptom, and confirmatory findings in the MRI, the diagnosis of pituitary apoplexy was established. The hormonal profile () included a low serum cortisol at baseline (1.1 mcg/dL) and low concurrent adrenocorticotropin hormone (ACTH). Cosyntropin stimulation increased the cortisol to 11.6 mcg/dL after 60 minutes. Free thyroxine (T4) and thyroid stimulating hormone (TSH) were normal but prolactin was below the normal range. Insulin-like growth factor 1 (IGF-1), follicular stimulating hormone (FSH), and luteinizing hormone (LH) were normal.
After the blood was collected for the endocrine workup, intravenous hydrocortisone was administered with the dose of 100 mg every 8 hours for 36 hours and then transitioned to oral hydrocortisone 20 mg in the morning and 10 mg at noon. On the fourth hospital day, transnasal transsphenoidal resection of the sellar mass was performed which was successful with no complications. Two days after the surgery, the patient reported that his vision was improving. Post-op MRI showed postsurgical changes with no definite residue and no acute complication (). Histopathology exam showed pituitary gland tissue (most likely pituitary adenoma) with extensive necrosis and hemorrhage.
On the ophthalmologic exam 4 days after the surgery, visual acuity was 20/40 in both eyes which was at his baseline. There was no relative afferent pupillary defect. Extraocular movements were normal in both eyes. Ophthalmoscopy was bilaterally unremarkable with normal optic disc appearance. Visual field by confrontation technique was full in both eyes.
Postoperatively, the patient regained his normal mental status with no further episodes of confusion. Level of ACTH and endogenous cortisol remained low until the last follow-up, 9 months after the surgery (). The patient was found to be hypothyroid 9 months after the surgery. His testosterone level appeared to be low on 9 months, and his LH level dropped below the normal range, suggesting secondary hypogonadism. FSH and IGF-1 levels decreased to almost half while still being in the normal range (). The above-mentioned lab data indicates that the patient developed progressive hypopituitarism after the surgery.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [155.0, 'mg/dL'], 'Sodium': [130.0, 'mEq/L']}",131.32,124.754,137.886,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 130.0 mEq/L. 
The concentration of glucose is 155.0 mg/dL. 
Plugging in these values into the formula gives us 130.0 mEq/L + 0.024 * (155.0 - 100) = 131.32 mEq/L.
Hence, the patient's corrected concentration of sodium is 131.32 mEq/L."
5419,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5358194-1,Extracted,"A 55-year-old female presented to the casualty of our hospital on 13th March 2010 in a gasping condition. She was referred to our hospital from another hospital where she was admitted on 9th March with acute anterior wall myocardial infarction (AWMI). She was not thrombolysed but was treated with tab. clopidogrel + aspirin (75 and 150 mg) for 3 days followed by tab isosorbide dinitrate 5 mg tid, tab atorvastatin 10 mg h.s., and inj enoxiparin (Lupinox) 0.4 ml sc bid for 10 days. On March 15, 2010, she was shifted over to Isosorbide mononitrate (30 mg) OD. During her stay at the other hospital it was noticed that she could not maintain her O2 saturation without nasal oxygen supplementation. She was a known case of bronchial asthma on inhalational steroid for the last 12 years.
On examination the patient was tachypnoeic, cyanosed, drowsy, and disoriented. Her pulse rate was 124 beats per minute, regular. The B. P. was 130/80 mmHg. There was moderate bronchospasm and a few bibasal crackles. She was intubated and put on ventilatory support. An X-ray of chest showed Lt. lower zone consolidation.
The results of laboratory investigations on admission were Hb 12.69/dl, TLC 20,700/mm3 (P 84%, L 14%, E 1%, M 1%), platelets 189,000/mm3, S. creatinine 1.4 mg/dl, BUL 82 mg/dl, S. bilirubin 0.8 mg/dl, total proteins 6.6 g/dl, albumin 3.6 g/dl, globulin 3.0 g/dl, SGOT 57 U/L, SGPT 52 U/L, alk. phospatase, 98 U/L, S. sodium 149 mEq/L, and S. potassium 4.8 mEq/L. Two D Echo done on March 15, 2010, showed LVEF of 51% with apical hypokinesia. No clots, vegetations, or effusion were noted.BNP (19.310) was 784 pg/ml (N = 0 - 100 pg/ml). CPK (MB) 1st and 2nd readings were 19 IU/ml and 29 IU/ml respectively. D-dimer was 650 ng/ml, ANA (ELISA) borderline +ve, and ADA 5.0.ABG done on March 19, 2010 showed pH 7.398, PaO2 24.1 mmHg, PaCO2 72.6 mmHg, HCO3 43.8 mEq/L, O2 saturation 40.2%. Findings of serial ECGs are tabulated ().
Blood sugar on admission was 231 mg/dl. At discharge fasting and post prandial blood sugars were 135 mg/dl and 158 mg/dl respectively. S. creatinine was 1.6 mg/dl. US KUB showed bilateral increased echogenecity of cortex. A CT scan of brain was normal.
A diagnosis of acute left ventricular failure following AWMI with pneumonia and asthma was made. She was treated with inj augmentin 1.2 g iv bd, x 10d, moxifloxacin 400 mg iv od x 10 d, inj lasix 100 mg, stat followed by 40 mg od x 5 d, inj deriphylline 2 ml iv bd x 5 d followed by tab salbutamol 10 mg od, duolin and budecort nebulization 6 hourly, inj hydrocortisone 100 mg tid x 3 d, and then tapered off over the next 4 days. Tab isosorbide mononitrate 30 mg od was discontinued after 9 days.
Ventilatory support was withdrawn after 4 days (March 16, 2010) and she was put on nasal oxygen. On discontinuation of the nasal support on 17th March she desaturated within 10 - 15 minutes and was tachypnoeic, dyspnoeic and cyanosed. Her PaO2 dropped to 30% - 35%. This improved rapidly on reinstituting nasal O2. A repeat 2 D Echo (March 19, 2010) revealed mild LV dysfunction and pulmonary artery pressure of 62 mmHg. An HRCT of chest with CT angiogram revealed diffuse patchy infiltrates involving both the lungs including apices (). There was no evidence of pulmonary embolism. Possibility of interstitial lung disease was considered and she was started on tab methylprednisolone 16 mg bd. Over the next few days her tendency to and the rapidity of desaturation decreased progressively and after 4 weeks she could be totally weaned off oxygen support. A repeat HRCT scan done on 22nd April (5 weeks after admission) showed total resolution of the interstitial shadows (). During her hospital stay she had one episode of atrial fibrillation that responded to tab diltiazem (30 mg tid). Her thyroid function tests suggested hyperthyroidism (TSH 0.09 µIU/ml, T4 - 13.2 µg/dl, T3 2.2 ng/ml) and she was started on neomercazole 5 mg tid. The patient was discharged on 23rd April. She had no breathlessness or chest pain. Pulse and B.P. were normal. At follow up 10 days after discharge she was totally asymptomatic.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [231.0, 'mg/dL'], 'Sodium': [149.0, 'mEq/L']}",152.144,144.5368,159.7512,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 149.0 mEq/L. 
The concentration of glucose is 231.0 mg/dL. 
Plugging in these values into the formula gives us 149.0 mEq/L + 0.024 * (231.0 - 100) = 152.144 mEq/L.
Hence, the patient's corrected concentration of sodium is 152.144 mEq/L."
5420,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5661755-1,Extracted,"A 67-year-old male presented to the Beaumont Dearborn emergency department with the complaint of worsening left leg pain for 6 days. He was seen 2 days prior to this hospital visit at another facility after cutting his leg on his bed frame. He was discharged with Bactrim and Norco for presumed cellulitis. His medical history was significant for insulin-dependent type 2 diabetes mellitus, hypertension, and arthritis.
There was muscle weakness and loss of motion and sensation in his left leg. Extensive bullae and erythema were found along the anterior and posterior leg, from the medial malleolus to proximal thigh (). His vital signs were within normal limits: blood pressure 114/56, temperature 97.6, and pulse 77. Laboratory values were significant for hyponatremia (Na: 127), hypochloremia (Cl: 84), hypokalemia (2.7), hyperglycemia (Glu: 218), acute renal failure (blood urea nitrogen: 120; creatinine: 5.53; glomerular filtration rate: 10), and leukocytosis with bands (white blood cells: 23 000; bands: 8.7%).
In the emergency department, the patient was given vancomycin, clindamycin, and Zosyn. He was then brought to the operating room for emergent excisional debridement and placement of Quinton catheter for dialysis. Surgical findings included extensive necrosis of the skin, subcutaneous tissues, fascia, and underlying muscles. These findings extended from the medial thigh to the medial malleolus. Surgical debridement yielded 60 ’ 25 cm of necrotic tissue. A pulse lavage system was used to irrigate the wound and sterile dressing was applied. The patient was brought to the intensive care unit for further management, dialysis, and the plan to return for further debridement.
Patient was brought back to the operating room, hospital days 1 and 2, with continued debridement of necrotic tissue (). Wound cultures returned showing growth of Haemophilus influenza serotype a that was sensitive to ceftriaxone and resistant to Bactrim. His antibiotic therapy was changed to ceftriaxone monotherapy. Blood cultures were negative for growth.
On hospital day 7, there was an application of a skin substitute to promote wound healing. After debridement of residual necrotic tissue, portions of ACell MatriStem was applied to the 30 ’ 100 cm area of exposed wounds and tendons. Sterile dressing was applied.
On hospital day 17, wound exploration was performed. Extensive necrotic and desiccated tissue was found and debrided. Wet to dry dressing was applied.
On hospital day 22, the patient had another irrigation and debridement with the intension of a split-thickness skin graft. Approximately 720 cm2 of skin was harvested from the right calf and thigh and applied to the left leg.
On hospital day 27, the patient returned for another wound exploration. The wound was deemed unsuitable for further skin grafting, so approximately 2000 cm2 of VAC negative pressure dressing was applied over the exposed wound areas.
On hospital day 30, additional debridement and replacement of the VAC negative pressure wound took place.
On hospital day 37, VAC dressing replacement and wound exploration was performed. Intraoperatively, the left knee joint was found open with synovial fluid leakage with rupture of the quadriceps and adductor tendons. Orthopedics was consulted. They agreed that a complete limb salvage or below knee amputation (BKA) was no longer an option. The patient was scheduled for an above knee amputation (AKA).
On hospital day 42, the patient received a complete AKA of the left lower limb. Skin and cutaneous tissue from the left distal tibia was used as a full-thickness skin to complete closure of the AKA ().","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [218.0, 'mg/dL'], 'Sodium': [127.0, 'mEq/L']}",129.832,123.3404,136.3236,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 127.0 mEq/L. 
The concentration of glucose is 218.0 mg/dL. 
Plugging in these values into the formula gives us 127.0 mEq/L + 0.024 * (218.0 - 100) = 129.832 mEq/L.
Hence, the patient's corrected concentration of sodium is 129.832 mEq/L."
5421,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6726349-1,Extracted,"An 80-year-old male patient with a 4-year history of chronic NV-AF, type 2 diabetes mellitus and a history of dyslipidaemia presented to the emergency department with general weakness, nausea, vomiting of blood-tinged material, vague abdominal pain and black stool of 1 day’s duration. He denied fever or diarrhoea. His regular medications included dabigatran 110 mg twice daily for 4 years to prevent thromboembolic events, metformin 1,000 mg twice daily and insulin glargine 20 units at night. The last dose of dabigatran was on the morning of presentation. There were no previous episodes of bleeding or decreases in haemoglobin since dabigatran was started 4 years previously. No new medications had been administered recently. The patient denied alcohol or tobacco consumption. However, he mentioned the recent use, without physician counselling, of 200 ml of a boiled mixture of ginger and cinnamon twice daily for 3 days before presentation to hospital.
Physical examination was remarkable for overweight (body mass index 28 kg/m2), skin pallor, irregular tachycardia (115–125 bpm), tachypnoea (respiratory rate of 28/minute), low blood pressure (80/60 mmHg) and dry oral mucosa. His oxygen saturation was 94% on room air. Cardiovascular examination was remarkable for irregular tachycardia, chest examination was normal, and abdominal examination revealed mild tenderness all over the abdomen. His extremities were cold. Digital rectal examination showed melena. The remainder of the examination was unremarkable.
On presentation, the patient had a haemoglobin (Hb) of 8 g/dl (normal 13.5–17 g/dl), haematocrit (Hct) of 24% (normal 45–52%) microcytic hypochromic anaemia, reticulocyte index >2, platelet count of 600,000 (normal range 150,000–450,000/l), International Normalized Ratio (INR) of 1.9 (normal INR 1.1 or less), and activated partial thromboplastin time (aPTT) of 45 sec (normal 30–40 sec). His blood glucose level was 142 mg/dl (normal 70–140 mg/dl) and kidney function was normal (eGFR 90 ml/min/1.73 m2, estimated by CKD-EPI). Serum sodium was 140 mEq/l, serum potassium was 4.5 mEq/l, and a liver function test was normal.
As the history and clinical picture were suggestive of gastrointestinal bleeding with an element of haemorrhagic shock, resuscitation measures were started in the emergency department with administration of intravenous fluid and the patient was moved to the intensive care unit. He later developed severe haematemesis after which the trachea was intubated and the patient was mechanically ventilated. Packed red blood cell transfusion was started.
As the patient had taken his last dose of dabigatran 110 mg on the morning of admission, idarucizumab, a reversal agent of dabigatran, was administered (5 g intravenously according to protocol). Urgent upper endoscopy was performed and showed diffuse haemorrhage of the mucosal membrane with fresh blood and blood clots in the oesophagus, stomach and duodenum; no definite ulcers or oesophageal varices were identified. The resuscitation measures were continued with intravenous fluid (crystalloid and colloid) and blood products, but bleeding persisted with fresh blood from the nasogastric tube. Haemorrhagic shock continued despite volume replacement (fluid and blood) and vasopressor support, and the patient died within 24 hours.
The history of recent combination of herbal products (ginger and cinnamon) with DOACs (dabigatran) and the presence of diffuse haemorrhage of the mucosal membrane of the upper gastrointestinal tract raised the possibility of a herb–drug interaction leading to severe gastrointestinal bleeding.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [142.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",141.008,133.9576,148.0584,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.0 mEq/L. 
The concentration of glucose is 142.0 mg/dL. 
Plugging in these values into the formula gives us 140.0 mEq/L + 0.024 * (142.0 - 100) = 141.008 mEq/L.
Hence, the patient's corrected concentration of sodium is 141.008 mEq/L."
5422,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7098417-1,Extracted,"A 78-year-old man slipped and fell into a swamp and was found to be unconscious after hitting his head on a rock during the daytime in spring. His history included hypertension, atrial fibrillation and cerebral infarction requiring warfarin. A physician-staffed helicopter was dispatched at the request of the fire department. When the staff of the helicopter checked him at the rendezvous point, he was in a deep coma and shock state with subcutaneous emphysema at his left chest, so a venous route was secured, and tracheal intubation and left thoracostomy were performed before air evacuation. Left thoracostomy was made by the insertion of a chest drainage tube at the fourth intercostal space on the midaxillary line due to potential tension pneumothorax. During air transportation, he remained in a shock state due to minimum infusion based on permissive hypotension strategy, and the physician of the helicopter activated the massive transfusion protocol at the receiving emergency room [].
On arrival, his vital signs were as follows: Glasgow Coma Scale, E1VTM1 without sedation; blood pressure, 58/44 mmHg; heart rate, 120 beats per minute; percutaneous saturation, 90% (FiO2 1.0); body temperature, 33.7°C. The results of a venous gas analysis on arrival were as follows: pH, 7.353; PCO2, 41.7 mmHg; PO2, 38.9 mmHg; HCO3-, 22.6 mmol/L; base excess. -2.3 mmol/L; and lactate, 3.8 mmol/L. After receiving six units of blood type O transfusion and vitamin K, his systolic blood pressure temporarily increased to 100 mmHg, and he underwent traumatic pan scan.
Computed tomography (CT) revealed occipital fracture, cerebral contusion, cervical fracture (C2-C4), multiple left rib and sternal fractures with left-dominant bilateral hemothorax (Figure ).
He entered a shock state again after the CT examination and underwent transfusion again, but he then entered cardiac arrest. He underwent emergency bilateral thoracotomy with a normal surgical knife (no electrocautery) at the spine position. The initial bleeding amount in the bilateral thorax exceeded 1 L in addition to over 500 mL of blood that was drained via the chest drainage tube before thoracotomy. A bleeding tendency was also recognized at the skin incision sites. Gauze was packed into multiple bleeding sites, including venous hemorrhaging induced by the rib fractures, and the chest was closed. During damage surgery, he obtained spontaneous circulation after massive transfusion and the administration of fresh-frozen plasma, cryoprecipitate and human prothrombin complex.
The results of a biochemical blood analysis on arrival were as follows: white blood cell count, 15,000/μL; hemoglobin, 13.0 g/dL; platelet count, 6.0×104/μL; total protein, 4.1 g/dL; glucose, 357 mg/dL; HbA1C, 6.3%; total bilirubin, 0.7 mg/dL; aspartate aminotransferase, 38 IU/L; alanine aminotransferase, 20 IU/L; blood urea nitrogen, 23.1 mg/dL; creatinine, 1.13 mg/dL; sodium, 140 mEq/L; potassium, 4.8 mEq/L; chloride, 106 mEq/L; C-reactive protein, 0.04 mg/dL; prothrombin time international normalized ratio, 2.91; activated partial thromboplastin time, 85.0 (27.0) seconds; fibrinogen, 80 mg/dL; and fibrinogen fibrin degradation product, 960 μg/mL. He was transferred to the intensive care unit.
He received 36 units of packed red blood cells, 16 units of fresh-frozen plasma and 30 units of packed platelets to maintain circulation after admission. On the second hospital day, he received a second-look operation for the removal of the gauze, hemostasis, irrigation of thoracic cavity and placement of chest drainage tubes in the operation room. On the sixth hospital day, he became complicated with pneumonia and underwent tracheostomy. He also was complicated with thrombotic microangiopathy, resulting in multiple cerebral infarctions and foot necrosis. After these complications had improved, he regained consciousness and achieved spontaneous breathing without mechanical ventilation and stable circulation, resulting in his being able to walk with assistance, at least for a little while.
However, he became septic and developed hypoxia again, and CT and gastroscopy on the 28th hospital day revealed left pyothorax and emphysematous gastritis (Figure ). Cultures of both pyothorax and blood showed extended-spectrum β-lactamase (ESBL) Escherichia coli, which was treated by drainage and carbapenem administration.
Pyothorax and emphysematous gastritis improved, but he became complicated with repeated aspiration pneumonia after starting oral intake. CT on the 81st hospital day for evaluation of a recurrent fever revealed emphysematous cystitis (Figure ), which was treated by indwelling balloon and carbapenem administration again. The culture of the urine revealed ESBL E. coli.
After these treatments, his vital signs stabilized. He was transferred to another hospital for rehabilitation of dysphagia and disused muscle atrophy.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [357.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",146.168,138.8596,153.4764,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.0 mEq/L. 
The concentration of glucose is 357.0 mg/dL. 
Plugging in these values into the formula gives us 140.0 mEq/L + 0.024 * (357.0 - 100) = 146.168 mEq/L.
Hence, the patient's corrected concentration of sodium is 146.168 mEq/L."
5423,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6370124-1,Extracted,"A 72-year-old woman was referred to our emergency department from a dialysis clinic because of general discomfort and decreased blood pressure within 30 min after hemodialysis was initiated. Her status on arrival was as follows: blood pressure, 85/54 mmHg; heart rate, 122 bpm; and body temperature, 35.8°C. Her consciousness was clear. She complained of general discomfort, but no chest or abdominal pain was observed. Physical examination revealed a pale conjunctiva and soft abdomen. No bloody/tarry stool passage was observed. She had diabetes mellitus and uremia and underwent regular hemodialysis. She had undergone surgery for a left forearm arteriovenous pseudoaneurysm 15 days before, and a temporary hemodialysis catheter was inserted via the left femoral vein on the day after surgery. She had undergone hemodialysis via a left femoral catheter several times without any problems until this time. Blood examination revealed the following values: white blood cells, 27,580/μL; hemoglobin, 7.2 g/dL; platelets, 269,000/μL; glucose, 347 mg/dl; glutamic oxaloacetic transaminase/glutamic pyruvic transaminase, 29/10 IU/L; C-reactive protein, 13.36 mg/L; sodium, 136 mmol/L; potassium, 5.9 mmol/L; creatine phosphokinase, 78 IU/L; creatine kinase-muscle/brain, 5.3 ng/mL; troponin I, 0.039 ng/mL; pH, 7.114; and HCO3−, 13.8 mmol/L. Her blood pressure recovered after normal saline hydration and packed red blood cell transfusion. Owing to the incomplete regular hemodialysis and hyperkalemia, she was referred to the hemodialysis department to undergo hemodialysis again. Reduced blood pressure and change in consciousness developed soon after hemodialysis was initiated. She was intubated and referred back to the emergency department. Subsequently, central venous catheter insertion, fluid resuscitation, and vasopressor administration were performed. Blood examinations were repeated. Computed tomography was performed to exclude vascular emergency and revealed a double-lumen catheter tip protruding from the left iliac vein and hematoma in the left retroperitoneal space and pelvic cavity (Fig. ). Blood examination results revealed the following values: white blood cells, 26,840/μL; hemoglobin, 3.9 g/dL; platelets, 182,000/μL; pH, 7.018; HCO3−, 10.2 mmol/L; lipase 64 U/L; creatine phosphokinase, 152 IU/L; creatine kinase-muscle/brain, 9.6 ng/mL; troponin I, 0.106 ng/mL; and lactate, 11.5 mmol/L. She was then admitted to the intensive care unit for further care. The left femoral hemodialysis catheter was removed, and follow-up computed tomography revealed resolution of the retroperitoneal space hematoma. She was transferred to the ordinary ward 18 days later with stable hemodynamic status. Unfortunately, the patient developed hospital-acquired pneumonia and suspected arteriovenous shunt infection, and died from respiratory failure and sepsis on the 34th day after being transferred to our hospital.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [347.0, 'mg/dL'], 'Sodium': [136.0, 'mmol/L']}",141.928,134.8316,149.0244,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 136.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 136.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 136.0 mmol * 1 mEq/mmol = 136.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mmol sodium/L converts to 136.0 mEq sodium/L. 
The concentration of glucose is 347.0 mg/dL. 
Plugging in these values into the formula gives us 136.0 mEq/L + 0.024 * (347.0 - 100) = 141.928 mEq/L.
Hence, the patient's corrected concentration of sodium is 141.928 mEq/L."
5424,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8687798-1,Extracted,"A 40-year-old Caucasian man with a past medical history of uncontrolled type 2 diabetes mellitus with peripheral neuropathy, alcohol abuse, and chronic pancreatitis presented to the emergency department for a three-day history of profuse watery diarrhea, shortness of breath, and ataxia.
Diarrhea reportedly began soon after the patient had attended a group barbecue. Initially, the patient experienced two to three loose stools per day, which gradually occurred more and more frequently, up to one to two times per hour at the time of initial presentation. In addition to profuse diarrhea, the patient also became progressively short of breath and confused. The patient denied knowledge of any other guests experiencing similar symptoms, including his partner. He also denied any other sick contacts or consumption of undercooked food. He denied any melena or hematochezia. The patient’s vital signs were remarkable for tachypnea and tachycardia. On physical examination, he was in mild acute distress, covered in feces, with very dry mucous membranes and obvious tachypnea. He was initially alert and oriented to person, place, time, and situation.
In the ED, initial labs were notable for sodium of 114, creatinine of 1.44 (likely secondary to severe diarrhea and resultant dehydration), glucose of 379, elevated anion gap at 32, and arterial blood gas (ABG) showing pH of 7.006, PCO2 of 9, HCO3 of 2, and urinalysis positive for ketones, consistent with acute diabetic ketoacidosis (DKA).
A Clostridium difficile antigen test was performed and returned negative. Stool studies including stool Shiga toxin, Campylobacter antigen, and stool culture, as well as blood cultures were obtained. Due to the patient’s reported sexual exposures, a rapid HIV test was also done to assess the patient’s immune status, which returned negative. The patient was then admitted to the intensive care unit (ICU) for further management of acute DKA and hypovolemic hyponatremia secondary to severe diarrhea with unclear etiology.
Over the next 24 hours, the patient’s anion gap closed and DKA resolved, however, he became febrile, hypotensive (systolic blood pressures in the low 80’s and diastolic blood pressure in the low 50’s), and his mental status became increasingly altered (alert and oriented only to person) raising concern for septic shock. CT abdomen and pelvis with contrast was obtained to evaluate for a source of infection and was notable for diffuse colonic wall thickening which was concerning for infectious colitis (Figures , ).
The patient was started on broad-spectrum antibiotic therapy with vancomycin and Zosyn, without any decrease in stool output (max output within a 24-hour period was approximately 5200mL), resolution of fever, or improvement in mental status. Stool and blood culture results returned positive for Shigella flexneri on hospital day three and showed resistance to ampicillin, ampicillin/sulbactam, and trimethoprim/sulfamethoxazole. At this point, infectious disease was consulted for treatment recommendations, and the patient was started on ceftriaxone 2g IV every 24 hours to be continued for two weeks once negative blood cultures were obtained. Due to the unclear route of transmission (food-borne vs anal-oral), it was also recommended that a repeat HIV RNA test be performed three weeks after the initial test was completed to confirm HIV status. After ceftriaxone therapy was initiated, the patient’s vitals improved and stabilized, daily stool output steadily trended downward, and his mental status gradually returned to baseline.
The patient had a peripherally inserted central catheter (PICC)-line placed to allow him to be discharged home to complete the course of IV ceftriaxone. Prior to discharge he was advised to avoid sexual intercourse for at least one week after the cessation of diarrhea and was counseled on following safe sexual practices for several weeks after, as Shigella can remain in the stool for an extended period of time.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [379.0, 'mg/dL'], 'Sodium': [114.0, 'mEq/L']}",120.696,114.6612,126.7308,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 114.0 mEq/L. 
The concentration of glucose is 379.0 mg/dL. 
Plugging in these values into the formula gives us 114.0 mEq/L + 0.024 * (379.0 - 100) = 120.696 mEq/L.
Hence, the patient's corrected concentration of sodium is 120.696 mEq/L."
5425,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6230346-1,Extracted,"A 61-year-old man was transported to the ED by ambulance with a complaint of confusion. His past medical history was significant for recently diagnosed pemphigus vulgaris that was being treated with steroids. His family described gradual functional decline over the prior two weeks with no changes in his skin lesion. On the day of ED presentation, he was no longer responding verbally to his family members. He had no history of diabetes mellitus or peripheral vascular disease.
On assessment in the ED, he was found to have a waxing and waning level of consciousness and was alert to self only. His initial vital signs were heart rate of 134 beats per minute, blood pressure of 141/86 millimeters of mercury, respiration of 16 breaths per minute, temperature of 37.1°C (98.8°F), and oxygen saturation of 95% on room air. He was ill-appearing with dry mucous membranes and poor skin turgor. He was also found to have a cold, pulseless, right lower extremity. Laboratory evaluation revealed marked hyperclycemia (blood glucose, 1077 milligrams per deciliter [mg/dL]), hemoconcentration (hemoglobin, 20 grams/dL), sodium concentration of 172 millimoles/L, anion gap of 23, and acute kidney injury (creatinine, 2.47 mg/dL). Urinalysis revealed a urinary tract infection without ketones. His thyroid-stimulating hormone level and a noncontrast computed tomography of his head were unremarkable. Duplex ultrasound of the lower extremity demonstrated total occlusion of the right proximal common iliac and popliteal arteries.
Based on these results, we diagnosed HHS with limb ischemia and sepsis from urinary tract infection. The patient was treated with insulin, heparin, and broad-spectrum antibiotics in the ED. His free water deficit was calculated to be greater than 10 L. Fluid management included initial volume resuscitation with 3 L of Plasma-Lyte. He was then transitioned to slow sodium correction with normal saline over 24 hours. He was admitted to an intensive care unit (ICU) with vascular surgery consultation for management of the limb ischemia.
The patient underwent through-the-knee amputation due to irreversible tissue damage on hospital day three. During his ICU stay, his blood glucose and sodium levels were corrected gradually and the acute kidney injury resolved. The patient did well during hospitalization and was discharged to an inpatient rehabilitation facility on hospital day 11.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [1077.0, 'mg/dL'], 'Sodium': [172.0, 'mmol/L']}",195.448,185.6756,205.2204,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 172.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 172.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 172.0 mmol * 1 mEq/mmol = 172.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 172.0 mmol sodium/L converts to 172.0 mEq sodium/L. 
The concentration of glucose is 1077.0 mg/dL. 
Plugging in these values into the formula gives us 172.0 mEq/L + 0.024 * (1077.0 - 100) = 195.448 mEq/L.
Hence, the patient's corrected concentration of sodium is 195.448 mEq/L."
5426,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-292,Extracted,"A 37-year-old man comes to the physician for a follow-up examination. He is being evaluated for high blood pressure readings that were incidentally recorded at a routine health maintenance examination 1 month ago. He has no history of serious illness and takes no medications. His pulse is 88/min and blood pressure is 165/98 mm Hg. Physical examination shows no abnormalities. Serum studies show:
Na+ 146 mEq/L
K+ 3.0 mEq/L
Cl- 98 mEq/L
Glucose 77 mg/dL
Creatinine 0.8 mg/dL
His plasma aldosterone concentration (PAC) to plasma renin activity (PRA) ratio is 36 (N = < 10). A saline infusion test fails to suppress aldosterone secretion. A CT scan of the adrenal glands shows bilateral adrenal abnormalities. An adrenal venous sampling shows elevated PACs from bilateral adrenal veins.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [77.0, 'mg/dL'], 'Sodium': [146.0, 'mEq/L']}",145.448,138.1756,152.7204,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 146.0 mEq/L. 
The concentration of glucose is 77.0 mg/dL. 
Plugging in these values into the formula gives us 146.0 mEq/L + 0.024 * (77.0 - 100) = 145.448 mEq/L.
Hence, the patient's corrected concentration of sodium is 145.448 mEq/L."
5427,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6641835-1,Extracted,"A 39-year-old woman presented to our emergency department with severe continuous, involuntary flailing, violent, and undesired movements of the left limbs, which lasted for 3 days. Her family history was unremarkable, except for type 2 diabetes mellitus. She had history of type 2 diabetes mellitus with poor control and maintenance regular hemodialysis. Her body temperature was 35.9°C, blood pressure was 166/96 mmHg, and pulse rate was 106 beats/minute. Neurological examination demonstrated alert consciousness with good orientation, no facial droop, and score of Medical Research Council (MRC) for muscle strength was 5. Blood laboratory investigation revealed a white blood count of 5480 /μL (normal range, 4800–10800), serum glucose level of 765 mg/dL (normal range, 70–110), blood urea nitrogen level of 38.8 mg/dL (normal range, 6–24), serum creatinine level of 7.94 mg/dL (normal range, 0.5–1.4), sodium level of 125 mmol/L (normal range, 137–145), potassium level of 4.13 mmol/L (normal range, 3.1–5.3), magnesium level of 2.05 mg/dL (normal range, 1.8–2.55), phosphate level of 4.7 mg/dL (normal range, 2.6–4.4), calcium level of 8.3 mg/dL (normal range, 8.8–10.6), ketone body level of 0.1 mmol/L (normal range, 0.0–0.6), lactate level of 0.6 mmol/L (normal range, 0.5–2.2), and arterial blood gas level of pH: 7.465 (normal range, 7.35–7.45); PaO2, 115 mmHg (normal range, 75–100); PaCO2, 34.3 mmHg (normal range, 35–45); HCO3, 24.9 mmol/L (normal range, 22–26). An urgent brain CT showed hyperintensity within the right caudate nucleus and putamen (Fig. a), which we initially believed was acute hemorrhage. A follow-up brain magnetic resonance image (MRI) disclosed hyperintensity within the right caudate nucleus and putamen in the T1-weighted sequence (Fig. b) and hypointensity in the T2-weighted sequence (Fig. c). Acute cerebral hemorrhage was excluded, and the diagnosis of non-ketotic hyperglycemia-related hemichorea-hemiballism was established based upon the clinical and radiological manifestations. Intensive glycemic control via insulin injection was prescribed for the high glycated hemoglobin (HbA1c) level of 13.4% (normal range, 4–6). Medications including clonazepam and risperidone were also administered for symptomatic treatment. Four weeks later, the symptoms of unilateral involuntary violent and wide-amplitude movements of shoulder and hip had improved, apparently owing to tight serum glycemic control. The patient's hemichorea had resolved completely at the 3-month follow-up.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [765.0, 'mg/dL'], 'Sodium': [125.0, 'mmol/L']}",140.96,133.912,148.008,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 125.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 125.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 125.0 mmol * 1 mEq/mmol = 125.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 125.0 mmol sodium/L converts to 125.0 mEq sodium/L. 
The concentration of glucose is 765.0 mg/dL. 
Plugging in these values into the formula gives us 125.0 mEq/L + 0.024 * (765.0 - 100) = 140.96 mEq/L.
Hence, the patient's corrected concentration of sodium is 140.96 mEq/L."
5428,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2672256-1,Extracted,"A 59-year-old female presented to the ED with a chief complaint of abdominal pain. Her abdominal pain began three hours before presentation and had awoken her from sleep. This abdominal pain was described as “achy,” 5/10, intermittent, and located in the left lower quadrant without radiation. She denied nausea or vomiting and had no diarrhea or blood in her stools. Review of systems revealed that the patient had symptoms of dysuria for one day and left-sided flank pain along with her abdominal pain. She denied fevers or chills. She stated that, despite taking her prescribed insulin injections, her blood sugars have been persistently elevated above 400 with her personal glucometer. Her past medical history was significant for insulin-dependent diabetes mellitus (DM), hypertension, and prior cerebrovascular accident. She denied ever having any surgeries. She used regular insulin, Lantus (insulin glargine), and Ibuprofen. Her family history was noncontributory, and she denied alcohol, tobacco, or illicit drug use.
Physical exam revealed a temperature of 36.5° C, respiratory rate of 18 breaths per minute, heart rate of 93 beats per minute, blood pressure of 166/81 mm Hg, oxygen saturation of 99% on room air, and capillary blood glucose of 447 mg/dL. She was awake, alert, and interacting appropriately. Her pupils were equally round and reactive to light. The cardiac exam was normal and lungs were clear with breath sounds bilaterally. The abdomen was soft with minimal tenderness to palpation in the left periumbilical and left lower quadrant. There was no guarding or rebound. Extremities were warm and well-perfused. The neurological exam revealed no deficit.
The metabolic panel revealed sodium of 132 mEq/L (normal 135–145), BUN of 45 mg/dL (normal 8–22), Creatinine of 2.0 mg/dL (normal 0.5–1.3), glucose of 473 mg/dL, and an anion gap of 8.0. A CBC revealed a white blood cell count of 12.0 K/MM3 (normal 4.5–11.0) and a manual differential with 10.10 K/MM3 Neutrophils (normal 0.80–7.70). The hepatic panel was remarkable for an alkaline phosphatase of 189 U/L (normal 35–115). The urine was visibly clear and non-turbid. Urinalysis was leukocyte esterase and nitrate negative, but revealed large occult blood, glucosuria, protein of 300 mg/DL, and 3–6 WBC/HPF (normal 0–3).
While laboratory studies were pending, the patient received one liter IV normal saline, four mg of morphine sulfate IV for pain, and 10 units of regular insulin. Despite fluid administration and analgesia, the patient continued to have worsening 6/10 abdominal pain. Given the patient’s presentation of undifferentiated abdominal pain without clear etiology and her immunocompromised state, a non-contrast computed tomography (CT) scan of the abdomen was ordered. The CT scan revealed significant air in the bladder wall and lumen consistent with EC, severe left hydroureter and hydronephrosis without evidence of stones, and significant left perinephric stranding without gas in the renal parenchyma ().
A gram of Ceftriaxone and 500 mg of Gentamycin were started empirically along with a repeat fluid bolus and placement of a Foley catheter. While awaiting consultation and admission to the Urology service, the patient complained of increased abdominal pain and was increasingly tender in the left lower quadrant and suprapubic region. Her heart rate was persistently tachycardic (in the 130s), and she developed a fever to 39.4°C. In light of developing urosepsis and the potential for rapid progression to Emphysematous pyelonephritis, Interventional Radiology (IR) was consulted and placed a left nephrostomy tube to relieve the functional obstruction of the urinary tract just eight hours after the patient presented to the ED. After nephrostomy tube placement by IR, the patient was admitted to the ICU for close monitoring. The urine culture grew out Klebsiella pneumoniae and the patient was continued on IV antibiotics. Three days after admission, the nephrostomy tube was removed as the patient was able to void without use of a foley catheter and was able to control her pain. She was subsequently discharged and given a prescription for Levofloxacin 500 mg every day for fourteen days.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [473.0, 'mg/dL'], 'Sodium': [132.0, 'mEq/L']}",140.952,133.9044,147.9996,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 132.0 mEq/L. 
The concentration of glucose is 473.0 mg/dL. 
Plugging in these values into the formula gives us 132.0 mEq/L + 0.024 * (473.0 - 100) = 140.952 mEq/L.
Hence, the patient's corrected concentration of sodium is 140.952 mEq/L."
5429,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5649843-1,Extracted,"A 44-year-old African American female with history of peptic ulcer disease, mitral valve prolapse and anemia presented to the clinic for evaluation of epigastric abdominal pain, nausea and constipation. Review of systems was positive for weight loss of approximately 15 to 20 lbs and fatigue; negative for fever, hematochezia or melena. Medication consisted of dicyclomine, metoclopramide, sucralfate and ferrous sulfate recently prescribed by ER physician for abdominal symptoms. Past surgical history significant for total abdominal hysterectomy with bilateral salpingo-oophorectomy. Family history negative for colon cancer and her mother died from lung cancer at age 70. Physical examination revealed an obese female with blood pressue of 163/88 mmHg and epigastric tenderness to palpation. There were no palpable masses or lymphadenopathy detected. Stool guaic was negative. Laboratory investigation showed calcium level of 15.7 mg/dL, phosphorous 2.8 mg/dL, sodium 136 meq/L, potassium 3.5 meq/L, chloride 100 meq/L, bicarbonate 31 meq/L, BUN 30 mg/dL, creatinine 1.9 mg/dL, glucose 121 mg/dL, total protein 8.1 gm/dL, albumin 3.6 gm/dL, total bilirubin 0.4 mg/dL, SGOT 75 U/L, SGPT 50 U/L and alkaline phosphatase 227 U/L. White blood cell count was 11.3 K/mm3, HgB 8.6 gm/L, HCT 27.2 %, MCV 75.6 fL and platelet count 778 K/mm3, CEA 702 ng/mL. Intact PTH was not measured. Instead, the carboxy (C)-terminal PTH assay (includes C-terminal, intact PTH and midmolecule) was measured and found to be within normal limits at 48 ng/dL (reference range < 88 ng/dL; Specialty Laboratories, Valencia, CA).
She was admitted for evaluation and treatment of severe hypercalcemia. After administering IV pamidronate (Aredia) along with normal saline and IV furosemide, calcium level gradually declined from 15.7 to 10.1 mg/dL over a period of 7 days. CXR was normal and screening mammogram revealed BIRAD 2 benign findings. CT scan of abdomen with and without contrast showed multiple lesions within the liver (). Colonoscopy revealed a 3 cm ulcerated mass near the splenic flexure (biopsy showed moderately differentiated adenocarcinoma). EGD was normal. The following day after surgical consultation she was taken to the operating room for exploratory laparotomy undergoing segmental resection of the transverse colon, where the identified cancer was located (). Open core needle biopsy of a liver mass demonstrated adenocarcinoma compatible with metastasis from colon.
She was admitted on two additional occasions about 1 week apart, 6 days after initial hospital discharge, for refractory hypercalcemia associated with nausea, vomiting, lethargy and confusion. Temporary and partial response was observed to IV pamidronate, in addition to saline diuresis and IV furosemide, lowering calcium from 15.6 to 12.8 mg/dL over period of 10 days. On the second occasion, hypercalcemia was partially corrected with IV zoledronic acid (Zometa), along with saline diuresis and furosemide, dropping calcium from 16.2 to 13.1 mg/dL over 3 days. After being admitted to hospice, her condition continued to deteriorate and she died 7 weeks after initial hospital admission.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [121.0, 'mg/dL'], 'Sodium': [136.0, 'mEq/L']}",136.504,129.6788,143.3292,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 136.0 mEq/L. 
The concentration of glucose is 121.0 mg/dL. 
Plugging in these values into the formula gives us 136.0 mEq/L + 0.024 * (121.0 - 100) = 136.504 mEq/L.
Hence, the patient's corrected concentration of sodium is 136.504 mEq/L."
5430,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3890728-1,Extracted,"A 46-year-old woman presented with general weakness that had lasted for several weeks. She was diagnosed with type 2 diabetes mellitus (DM) 15 years ago and began continuous ambulatory peritoneal dialysis (CAPD) three years ago. An abdominal sonography obtained before CAPD began revealed a normal liver. The patient received CAPD with four daily exchanges of 2 L each time and switched to three exchanges with 2.5% glucose and one with 4.25% glucose solution; this was required because the ultrafiltration capacity was not sufficient and she became volume overloaded. A peritoneal equilibrium test was not performed. The patient had insulin administered subcutaneously when she started the CAPD but changed to intraperitoneal insulin treatment combined with subcutaneous treatment two years later. Hyperlipidemia treated with simvastatin and fenofibrate were started one year previously but stopped three months later because the drugs caused rhabdomyolysis. Lipid profiles began to worsen and she had to resume with atovastatin but did not develop rhabdomyolysis. Plasma glucose was poorly controlled despite the combination therapy of subcutaneous and intraperitoneal insulin injections. Insulin doses increased from 102 units daily up to 110 units daily during the previous month. The patient was 158 cm tall and weighed 58 kg. When she visited our clinic, her body mass index was 23 kg/m2. Vital signs were a blood pressure of 130/80 mmHg, pulse rate 68/min, respiratory rate 20/min, and body temperature 36.6℃. Her abdomen was soft and mildly distended. The initial complete blood count was white blood cells 8,000/mm3 (neutrophils 70.7%, lymphocytes 18.5%, eosinophils 3.2%), hemoglobin 11.5 g/dL, hematocrit 33.3%, and platelet 288,000/mm3. Her blood chemistry values were, fasting glucose 293 mg/dL, blood urea nitrogen 46.6 mg/dL, creatinine 10.3 mg/dL, sodium 134 mEq/L, potassium 4.4 mEq/L, chloride 90 mEq/L, AST 119 IU/L, ALT 192 IU/L, alkaline phosphatase 850 IU/L, amylase 110 U/L, total protein 6.8 g/dL, albumin 4.0 g/dL, calcium 11.1 mg/dL, phosphorus 6.2 mg/dL, CPK 43 IU/L, LDH 468 IU/L, total cholesterol 450 mg/dL, and triglyceride 1,096 mg/dL. Hepatitis B antigen and hepatitis C antibody were negative. ANCA, anti-liver kidney microsome antibody, and anti-smooth muscle antibody were all negative. Sonography of the abdomen revealed an increased echogenicity of the liver. A CT scan of the abdomen showed extensive low attenuated lesions in the liver capsule, the parenchyma of the left hepatic lobe and a small nodular lesion in the capsular area of the right lobe of the liver (). The MRI findings were consistent with the CT findings. The hepatic subcapsular area showed bright signals in the on-phase T1weighted images, but a marked signal decrease in the off-phase T1-weighed sequences; these findings suggested that the subcapsular area was composed of fat tissue. Hepatic subcapsular steatosis due to high dose intraperitoneal insulin was suspected; the patient was changed from CAPD to HD. Insulin was given only subcutaneously after changing to HD. A CT scan performed two months after starting HD showed complete resolution of the hepatic subcapsular steatosis (). Laboratory values were also improved: AST 34 IU/L, ALT 81 IU/L, alkaline phosphatase 733 IU/L, total cholesterol 259 mg/dL, and triglyceride 177 mg/dL. The blood sugar has been well controlled insulin therapy could be discontinued. Six months after changing from CAPD to HD, oral hypoglycemic agents have been sufficient to maintain adequate plasma glucose levels. Furthermore, liver enzyme levels are within normal range; the total cholesterol level was 206 mg/dL, and triglyceride level 157 mg/dL without requirement for lipid-lowering agents.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [293.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",138.632,131.7004,145.5636,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 134.0 mEq/L. 
The concentration of glucose is 293.0 mg/dL. 
Plugging in these values into the formula gives us 134.0 mEq/L + 0.024 * (293.0 - 100) = 138.632 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.632 mEq/L."
5431,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5757848-1,Extracted,"A 91-year-old female with a medical history of bilateral breast cancer, status post mastectomy and chemotherapy, iron deficiency anemia, hypertension, appendectomy, cholecystectomy, and dementia who lived in a long-term care facility. She had decreased appetite for several months, weight loss, intermittent nausea and vomiting, and was sedentary. Laboratory studies obtained at that time were significant for anemia, but with normal thyroid function studies. She had a 40 pack-year history of smoking, quit smoking over 27 years ago. Her home medications included: donepezil, metoprolol, hydralazine, Tylenol, colace, and cyanocobalamin.
The patient was admitted to our hospital with the diagnosis of FTT. Laboratory investigation revealed white blood cell (WBC) 16 K/uL, hemoglobin 8.4 g/dL, platelets 195 K/uL, international normalization ratio (INR) 1.24; complete metabolic panel shows serum sodium 135 mmol/L, potassium 3.7 mmol/L, chloride 103 mmol/L, bicarbonate 24 mmol/L, glucose 94 mg/dL, blood urea nitrogen 10 mg/dL, creatinine 0.6 mg/dL, calcium 7 mg/dL, total protein 4.7 g/dL, albumin 2 g/dL, alkaline phosphatase (ALP) 57 U/L, aspartate aminotransferase (AST) 10 U/L, alanine aminotransferase (ALT) 18 U/L, total bilirubin 0.2mg/dL. Evaluation with computed tomography (CT) scan of the chest and abdomen/pelvis revealed a right hepatic flexure mass invading the second portion of the duodenum and the right kidney (Figure ), with no clinical evidence of bowel obstruction. Carcinoembryonic antigen (CEA) 1090 ng/ml (reference- less than 3 ng/mL).
Surgical oncology team was consulted to evaluate the patient. On examination the patient had a nasogastric tube in place with bilious output, palpable non-tender mass in her right upper abdomen; the remainder the examination was unremarkable. The CT findings and management options were discussed with the patient, including a palliative care option. Patient opted for surgical intervention. After appropriate preoperative management, the patient was taken to the operating room for an exploratory laparotomy for en bloc resection of the mass for presumed colon cancer with invasion of duodenum and kidney. Intraoperatively, ascites was noted, the bowel was edematous, and the mass was fixed to the right retroperitoneum, kidney and duodenum; the overall findings suggested major resection would probably have a poor outcome. Therefore, gastrojejunostomy and ileocolic bypasses were created to prevent progression to clinical obstruction.
Postoperatively, the patient had an uneventful recovery. Operative findings were discussed with the patient and she decided to pursue palliative care management. She was discharged to her long-term care facility on postoperative day eight.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [94.0, 'mg/dL'], 'Sodium': [135.0, 'mmol/L']}",134.856,128.1132,141.5988,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 135.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 135.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 135.0 mmol * 1 mEq/mmol = 135.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mmol sodium/L converts to 135.0 mEq sodium/L. 
The concentration of glucose is 94.0 mg/dL. 
Plugging in these values into the formula gives us 135.0 mEq/L + 0.024 * (94.0 - 100) = 134.856 mEq/L.
Hence, the patient's corrected concentration of sodium is 134.856 mEq/L."
5432,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3470992-1,Extracted,"A 17-year-old South Asian man was referred to our department for recurrent episodes of generalized muscle weakness, fatigue and cramps from the age of two years. Hypokalemia was initially detected at the first episode and he was treated for periodic hypokalemic paralysis. Before the age of 12 years, these episodes were mild, readily improved with ringer lactate and potassium chloride by his treating physician and occurred only twice a year. Beyond the age of 12 years, these episodes gradually worsened in frequency and intensity to the point that they were refractory to previously administered therapies and sometimes required hospitalization.
His symptoms were aggravated by physical activity and hot weather, and were associated with polyuria, polydipsia, nocturia, paresthesias and occasional painless non-bloody diarrhea. He denied the use of any medication, including laxatives and diuretics. He also had a history of short stature and poor weight gain. His birth history was unremarkable but developmental landmarks were delayed. There was no family history of renal salt-wasting syndromes or delayed puberty. However, his parents were first cousins.
An examination revealed a thin and lean, but well-oriented adolescent with no acute distress. His height and weight were below the third percentile (weight 30kg; height 147cm). His blood pressure was 95/60mmHg with orthostatic changes. His sexual development was at Tanner Stage II.
Investigations at the admitting hospital revealed a normal leukocyte count, platelet count, hemoglobin level and erythrocyte sedimentation rate. His urea level was 34mg/dL, creatinine 0.9mg/dL and random blood glucose 105mg/dL. His estimated glomerular filtration rate based on the Modification of Diet in Renal Disease formula was 97.9ml/min per 1.73m2. His high blood urea nitrogen level was attributed to mild dehydration due to the hot weather. He was found to have metabolic alkalosis: pH 7.58, HCO3- 33.5, base excess +7.6. His serum electrolytes were as follows: sodium 124mmol/L, potassium 2.4mmol/L, calcium 6.5mmol/L and phosphate 3.4mg/dL. His serum magnesium level was not checked at that time. Serum albumin, creatine phosphokinase, free thyroxin, thyroid-stimulating hormone and parathyroid hormone levels were normal.
He was provisionally diagnosed with periodic hypokalemic paralysis and hypocalcemia. Treatment was started with potassium and calcium supplements. After one month, he showed little improvement and he was referred to our department for further evaluation.
Further laboratory tests revealed a low magnesium level (1.2mg/dl) and decreased 24-hour urinary excretion of calcium (25.9mg/24 h). Luteinizing hormone and follicle-stimulating hormone levels were also normal. His level of testosterone was low (0.85ng/mL, normal for his age 2.67 to 10.12ng/mL). Electrocardiography showed a normal sinus rhythm and prolonged QT interval. No abnormality was found on an abdominal X-ray, chest X-ray or brain magnetic resonance imaging. A renal ultrasound revealed a prominent pelvicalyceal system. An insulin tolerance test showed normal cortisol and growth hormone response.
Based on the findings of hypokalemic metabolic alkalosis without hypertension, severe hypomagnesemia and hypocalciuria, a diagnosis of GS was made. No organic cause of hypogonadism was established and the sex hormone findings were attributed to delayed puberty. Treatment was started with oral supplementation of potassium, magnesium and calcium along with spironolactone and liberal salt intake. Our patient and his parents were also counseled about delayed puberty.
A limitation to this case report was that the diagnosis could not be ascertained with sequencing of the implicated gene due to unavailability of genetic sequencing at the presenting hospital (Jinnah Hospital Lahore, Pakistan).","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [105.0, 'mg/dL'], 'Sodium': [124.0, 'mmol/L']}",124.12,117.914,130.326,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 124.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 124.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 124.0 mmol * 1 mEq/mmol = 124.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 124.0 mmol sodium/L converts to 124.0 mEq sodium/L. 
The concentration of glucose is 105.0 mg/dL. 
Plugging in these values into the formula gives us 124.0 mEq/L + 0.024 * (105.0 - 100) = 124.12 mEq/L.
Hence, the patient's corrected concentration of sodium is 124.12 mEq/L."
5433,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4488998-1,Extracted,"A 41-year-old female, with a past medical history of DM1 treated with insulin glargine and insulin aspart, presented with a 1-day history of diffuse abdominal pain and weakness. Her symptoms were associated with chills, nausea, and just one episode of emesis. Over the preceding 4 days, the patient had developed a Bartholin's gland cyst infection with abscess formation. She admitted to abstaining from any solid food intake in the previous 2 days; however, she maintained her liquid intake and continued taking her insulin glargine without insulin aspart. She denied any alcohol intake or drug abuse. Her vital signs were within normal limits. Physical examination was significant for diffuse abdominal tenderness without rigidity or guarding and a ruptured Bartholin's gland abscess with drainage to the skin. Blood work showed a white blood cell (WBC) count of 13,000 cells/mcL (normal range: 4,500-10,000/mcL), hemoglobin level 11.2 mg/dL (normal range: 12.3-15.3 g/dL), platelet count 448,000/mcL (normal range: 150,000-450,000/mcL), sodium 135 mmol/L (normal range: 136-145 mmol/L), potassium 3.6 mmol/L (normal range: 3.5-5.1 mmol/L), chloride 105 mmol/L (normal range: 98-107 mmol/L), carbon dioxide 6 mmol/L (normal range: 21-32 mmol/L), anion gap 24 mmol/L (normal range: 3-11 mmol/L), urea nitrogen 4 mg/dL (normal range: 7-18 mg/dL), creatinine 0.58 mg/dL (normal range: 0.6-1.3 mg/dL), glucose 191 mg/dL (normal range: 70-100 mg/dL), beta hydroxybutyrate >4.5 mg/dL (normal range: <0.4 mg/dL), magnesium 1.3 mg/dL (normal range: 1.6-2.3 mg/dL), phosphorus 1.3 mg/dL (normal range: 2.5-4.9 mg/dL), lactate 0.8 mmol/L (normal range: 0.4-2 mmol/L), and HBA1C 12.5% (normal range: 4-5.6%). Urinalysis was significant for +3 ketones and sugar. Arterial blood gas showed pH 7.07, pCO2 12. A urine drug screen was negative, and serum ethanol level was undetectable.
The patient was diagnosed with euglycemic DKA precipitated by an underlying infection. Intravenous fluid (IVF) resuscitation with normal saline was initially started at a rate of 1.0 L/h for a total of 2 L. The patient's hydration status, serum electrolytes, blood urea nitrogen (BUN), creatinine, glucose, and urine output were monitored closely. After 2 h, repeat blood work showed a serum sodium 141 mmol/L, carbon dioxide 8 mmol/L, potassium 3.5 mmol/L, and glucose 153 mg/dL. Subsequently, IVFs were switched to 5% dextrose and 0.45% NaCl at a rate of 250 cc/h, and an insulin drip at a rate of 5 units/h was started. Then, 30 mEq potassium was added to each liter of the IVF, excluding the first liter, targeting a serum potassium level of 4-5 mEq/L. After 11 h, blood work revealed a serum bicarbonate level of 16 mmol/L with a normal anion gap; hence, subcutaneous insulin and oral intake were initiated. Intravenous insulin was continued for another hour to ensure adequate plasma insulin levels. The Bartholin's gland abscess was treated, and the patient was discharged on the following day.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [191.0, 'mg/dL'], 'Sodium': [135.0, 'mmol/L']}",137.184,130.3248,144.0432,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 135.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 135.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 135.0 mmol * 1 mEq/mmol = 135.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mmol sodium/L converts to 135.0 mEq sodium/L. 
The concentration of glucose is 191.0 mg/dL. 
Plugging in these values into the formula gives us 135.0 mEq/L + 0.024 * (191.0 - 100) = 137.184 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.184 mEq/L."
5434,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3970334-1,Extracted,"A 15-year-old primigravid woman, at the 28th week of gestation, presented with a 3-day history of severe left thigh pain and high fever with chills to the emergency department. Physical examination revealed clinical signs of severe soft tissue infection with erythema, edema, and extreme tenderness of the skin over the medial aspect of the left upper thigh. The vital signs were temperature of 39.5°C; pulse rate 115 beats/min; blood pressure 90/60 mmHg; respiratory rate 30/min. The laboratory results on admission were as follows: white blood cell (WBC) count of 24,000/μL with 84 band forms, serum sodium 126 mmol/L, blood urea nitrogen (BUN) level of 23 mg/dL, C-reactive protein (CRP) of 29.5 mg/dL, and blood fasting glucose of 369 mg/dL.
She denied any recent trauma and her past medical history was unremarkable. She complained of an increase thirst and urination. Ultrasound obstetric exanimation performed at admission revealed a living, intrauterine fetus of 28 weeks gestational age. A venous Doppler examination of the lower extremities was normal without signs of deep venous thrombosis (DVT).
A skin abscess formation was suspected and she was initially treated with incision and drainage of pus exudates. She was started on empiric IV antibiotic coverage (amoxicillin-clavulanic acid 1.5 grams every 8 hours), IV fluids for correction of electrolytes, and rapid and long-action insulin for diabetes mellitus.
However, the patient had no clinical and laboratory improvement in the following 24 hours. Her temperature, WBC and count and CRP increased to 39.9 C, 27,000 μ/L and 31.8 mg/dL, respectively. Wound cultures grew Escherichia coli and Staphylococcus epidermidis. The patient was administered Vancomycin (1 gram every 12 hours) and Meropenem (1 gram every 8 hours). On the third hospital day, the patient was scanned at the MRI unit of the Department of Radiology, University Hospital of Patras, by means of a Philips Medical Systems 1T MRI scanner. Axial and coronal images were obtained. High signal areas at the soft tissues of the anteromedial part of left thigh, indicating inflammatory process, were visualized (Figures - and ). An emergency radical surgical debridement of infected necrotic tissue was performed involving skin, subcutaneous tissue, and fascia of the anterior-medial compartment of the anterior-medial compartment of the thigh up to the inguinal area (). The wound was packed open with gauze moistened with saline. She required four additional intraoperative debridement on daily basis until progression of disease had been halted and all necrotic tissue had been removed. On the fifth postoperative day, her WBC increased up to 31,000/μL with high fever of 39.5 C and an altered level of consciousness was noted. She was transferred to the intensive care unit for close monitoring and support of vital functions. She started to have preterm uterine contractions despite tocolytic therapy and delivered a viable male fetus weighing 1470 grams by normal labor. The baby died to neonatal intensive care unit due to septicaemia after 48 hours.
Intraoperative culture of infected tissue grew Enterococcus faecalis, Acinetobacter, and Candida albicans. Based on the sensitivity of the microorganisms from tissue cultures, we administered meropenem 2 gr × 3 daily, linezolid 600 mg × 2 daily, metronidazole 500 mg × 3 daily, and liposomal amphotericin B 300 mg once a day IV.
Finally, thirty-eight days after the initial debridement, the patient continued to improve clinically, and she was transferred to a plastic centre facility for reconstruction of the wound. The wound was covered with split-thickness skin graft. Ten days later, the patient was discharged and currently is well. The source of infection remains unclear.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [369.0, 'mg/dL'], 'Sodium': [126.0, 'mmol/L']}",132.456,125.8332,139.0788,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 126.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 126.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 126.0 mmol * 1 mEq/mmol = 126.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 126.0 mmol sodium/L converts to 126.0 mEq sodium/L. 
The concentration of glucose is 369.0 mg/dL. 
Plugging in these values into the formula gives us 126.0 mEq/L + 0.024 * (369.0 - 100) = 132.456 mEq/L.
Hence, the patient's corrected concentration of sodium is 132.456 mEq/L."
5435,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5580559-1,Extracted,"A 12-year-old boy was admitted to the Santa Maria Hospital of Terni on 27 September 2016, due to a three-day history of fever (38 °C) and vomiting with acute presentation. Approximately two weeks before, the child had suffered from an episode of mild fever associated with abdominal pain and diarrhea that spontaneously resolved in a few days. In addition, in the previous three months, the child had complained of fatigue and loss of appetite several times; the previous history was negative. A mild reduction in body weight, of approximately 2 kg, was noted. Finally, in the last year, the parents had noticed mild but significant hyperpigmentation of the skin and mucous membranes, without giving it any importance. The child was previously well, suffering no significant diseases. His physical and neurological development was always considered within the normal range. There was no family history of severe clinical problems, including autoimmune diseases.
shows a picture of the boy at the time of admission. Physical examination revealed a patient in mediocre general condition, with a body weight of 35 kg (28° centile), a height of 150 cm (50° centile), and a body mass index of 15 (10° centile). Marked darkening of the skin, particularly on the palms and areolae, was evident. Subcutaneous fat tissue was reduced. No pathological findings of the upper and lower respiratory tract, heart, abdomen, or central or peripheral central nervous system were detected. His blood pressure was 110/60 mmHg, which is within the normal range for his age. Laboratory evaluation revealed no abnormalities of white or red blood cell counts (5320/µL; normal values, 4000–10,000/µL and 4,390,000/µL, respectively), no anemia (Hb 12.8 g/dL; normal values, 12–16 g/dL), no increase in serum concentrations of acute phase reactants (C reactive protein, 0.20 mg/dL; normal values <0.65 mg/dL and procalcitonin <0.05 ng/mL), hyponatraemia (124 mEq/L; normal values, 135–145 mEq/L) and hypochloraemia (93 mEq/L; normal values 100–110 mEq/L), mild hyperkalaemia (5.2 mEq/L; normal values, 3.5–5 mEq/L), borderline hypoglycaemia (69 mg/dL; normal values 70–110 mg/dL), and slight increases in blood urea nitrogen (53 mg/dL, normal values 10–50 mg/dL), serum creatine phosphokinase (909 UI/L; normal values 0–171 UI/L), and serum uric acid (9.5 mg/dL; normal values, 4.8–8.7 mg/dL). His ammonia levels, arterial blood gas, and blood lactate were within the normal range.
Immunological evaluations revealed normal serum IgA (81 mg/dL; normal values, 70–400 mg/dL), IgG (716 mg/dL; normal values, 700–1600 mg/dL), and IgM levels (47 mg/dL; normal values, 40–280 mg/dL), as well as negative anti-nuclear antibodies, anti-neutrophil cytoplasmic antibodies, anti-mitochondrial antibodies, extractable nuclear antigen screening, anti-thyroglobulin antibodies, anti-thyroperoxidase antibodies, and anti-phospholipid antibodies. However, a marked increase in IgA anti-transglutaminase (129 U/mL; normal values, <4 U/mL) and anti-endomysium (positive with a titre of 1/80) antibodies was found. A genetic study with polymerase chain reaction (PCR) DNA amplification and inverse hybridization testing alleles DQA1*05, DQB1*02, and DQB1*03:01 revealed the presence of HLA haplotypes DQ2 and DQ8. Duodenal biopsy could be spared according to the 2012 ESPGHAN CD diagnostic guidelines as anti-tranglutaminase antibodies were elevated over 10 times the normal range (129 UI/mL; normal values, <4 UI/mL), confirmed by the positivity of anti-endomisium antibodies and by the compatible HLA aplotypes.
Beginning with the clinical and laboratory data [,], celiac disease was diagnosed. In addition, primary AD was suspected. The diagnosis of CD and AD occurred quite late because the previous history of this child was negative and the parents did not give much importance at the symptoms that occurred in the last year. This was confirmed by low values of morning cortisol (0.8 µg/dL) and dehydroepiandrosterone sulfate (16.2 µg/dL), with adrenocorticotropic hormone (ACTH) concentrations of 1250 pg/mL. No abnormalities in adrenal gland morphology were found in abdominal ultrasonography and magnetic resonance tomography images. The child was treated with intravenous saline solution starting with a bolus of 300 mL over 2 h, followed by a maintenance dose of 1600 mL every 24 h. Serum electrolyte concentrations were evaluated every hour in order to ensure the maintenance of normal values. Normalization of the child’s electrolyte values was established within 3 h and the infusion was discontinued after 48 h.
On the second day of observation, further evaluation of the patient’s adrenal function was planned. The basal aldosterone and renin concentrations were evaluated. The renin level was high (19.10 ng/mL/h), whereas the aldosterone level was low (3.30 pg/mL). The serum ACTH level was lower than the previous day, but higher than the normal values (from >1250 pg/mL on day 1 to 477 pg/mL on day 2; normal values, <46 pg/mL). In addition, ACTH administration only marginally increased the cortisol concentrations at 30 (0.8 µg/dL) and at 60 min (0.6 µg/dL; normal values, 4.3–23.0 µg/dL). A 5-h Synacthen stimulation test confirmed adrenal insufficiency, as serum cortisol values did not reach the minimum normal values at various times of evaluation. The basal cortisol level was undetectable (<50 nmol/L) and failed to rise following Synacthen administration: the 60-min value was <600 nmol/L and the 5-h value was <1000 nmol/L.
Considering the simultaneous co-existence of AD and CD, cortisone acetate was administered at 25 mg at 8 a.m. and 12.5 mg at 4 p.m., and a gluten-free diet was initiated, instructing the patient and his parents on how to follow it correctly. The child was discharged from the hospital after four days, and the follow-up was planned. Thirty days following discharge, the evaluation revealed that the skin hyperpigmentation had almost completely disappeared. The adrenal insufficiency was no longer present (serum sodium, 135 mEq/L, potassium 4.4 mEq/L, chloride 101 mEq/L, glucose 93 mg/dL) and only a small dose of cortisone acetate (37.5 mg/die) was required to maintain normal serum electrolyte and cortisol concentrations. The compliance to the gluten-free diet was confirmed by the patient and his family and was also associated with a significant increase in body weight, of 1.5 kg. The anti-transglutaminase antibodies were dosed at the one-month follow-up control, and were found to still be high (121 UI/mL).","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [69.0, 'mg/dL'], 'Sodium': [124.0, 'mEq/L']}",123.256,117.0932,129.4188,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 124.0 mEq/L. 
The concentration of glucose is 69.0 mg/dL. 
Plugging in these values into the formula gives us 124.0 mEq/L + 0.024 * (69.0 - 100) = 123.256 mEq/L.
Hence, the patient's corrected concentration of sodium is 123.256 mEq/L."
5436,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7160714-3,Extracted,"A 37-year-old male presenting with 2 weeks of polyuria, polydipsia, and epigastric pain and vomiting was admitted in an intensive care unit for consciousness alteration. Taking his medical history by interrogating his parents did not reveal any alcohol abuse or a prior history of biliary colic.
On admission, the initial assessment showed a Glasgow Coma Scale Score at 8/15, body temperature at 38.3°C, heart rate at 120 beats/min, blood pressure at 80/45 mmHg, respiratory rate at 30 breaths/min, and an oxygen saturation of 93% under room air. He needed intubation and mechanical ventilation.
The laboratory tests showed serum glucose at 32 mmol/l, pH = 7.31, bicarbonate = 10.7 mmol/l, serum sodium = 132 mmol/l, serum potassium = 3.9 mmol/l, lipase = 511 U/l, cholesterol = 12.8 mmol/l, serum triglyceride = 75 mmol/l, WBC count = 3900/mm3, platelet count = 101000/mm3, and CRP at 496 mg/l. Aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and bilirubin values were at the normal range.
An abdominal CT scan with contrast was obtained showing an acute pancreatitis grade E with two fluid collections in the pancreas. There was no evidence for gallstones. He was aggressively hydrated and received IV insulin.
A repeat abdomen CT scan, performed 7 days later, showed a necrotic fluid collection which was infected. An endoscopic drainage was performed. The patient's neurological status deteriorated with no sign of waking up and multiple episodes of seizures. A brain CT scan was performed, showing cortical and subcortical hypodense lesion in the right frontal area.
During his ICU stay, the patient developed septic shock with multiorgan failure. He died 45 days after ICU admission.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [32.0, 'mmol/L'], 'Sodium': [132.0, 'mmol/L']}",143.43629,136.26448,150.6081,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 132.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 132.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 132.0 mmol * 1 mEq/mmol = 132.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 132.0 mmol sodium/L converts to 132.0 mEq sodium/L. 
The concentration of glucose is 32.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 32.0 mmol. To convert 32.0 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 32.0 mmol glucose * 0.001 mol/mmol = 0.032 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.032 mol glucose * 180.16 g/mol = 5.76512 g glucose. To convert 5.76512 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 5.76512 g glucose * 1000.0 mg/g = 5765.12 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 5765.12 mg glucose/10.0 dL = 576.512 mg glucose/dL. The concentration value of 32.0 mmol glucose/L converts to 576.512 mg glucose/dL. 
Plugging in these values into the formula gives us 132.0 mEq/L + 0.024 * (576.512 - 100) = 143.43629 mEq/L.
Hence, the patient's corrected concentration of sodium is 143.43629 mEq/L."
5437,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-2021,Extracted,"A 66-year-old woman comes to the emergency department because of a 1-day history of severe abdominal pain, nausea, and vomiting. She has also had profuse watery diarrhea with streaks of blood for the past 5 days. She had a urinary tract infection 3 weeks ago and was treated with a 14-day course of ciprofloxacin. She appears in severe distress. Her temperature is 39.3°C (102.7°F), pulse is 110/min, and blood pressure is 100/60 mm Hg. Examination shows a distended abdomen, tenderness in the lower quadrants, and hypoactive bowel sounds; rebound tenderness and abdominal rigidity are absent. Cardiopulmonary examination shows no abnormalities. Test of the stool for occult blood is positive. Laboratory studies show:
Hemoglobin 10.2 g/dL
Leukocyte count 28,000/mm3
Serum
Na+ 133 mEq/L
K+ 3.3 mEq/L
Cl- 97 mEq/L
Glucose 98 mg/dL
Creatinine 1.3 mg/dL
Two wide bore needles are inserted and intravenous fluids are administered.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [98.0, 'mg/dL'], 'Sodium': [133.0, 'mEq/L']}",132.952,126.3044,139.5996,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 133.0 mEq/L. 
The concentration of glucose is 98.0 mg/dL. 
Plugging in these values into the formula gives us 133.0 mEq/L + 0.024 * (98.0 - 100) = 132.952 mEq/L.
Hence, the patient's corrected concentration of sodium is 132.952 mEq/L."
5438,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6935651-1,Extracted,"A 14-year-old girl, living in a refugee camp, was referred from a district hospital for the management of altered level of consciousness, fever, and hyperglycemia. Fever started 2 weeks prior to consultation for which she received empiric treatment for malaria in a district hospital. She was also diagnosed with severe acute on chronic malnutrition for which she received ready-to-use therapeutic food. The situation was worsened by polyuria, excessive thirst, uncontrolled hyperglycemia, persistent fever and progressive lethargy, necessitating her transfer to the endocrinology unit of the Mother and Child Center of Yaounde.
Past history was remarkable for diabetes which was diagnosed a year ago after 2 months of polyuria and excessive thirst. Insulin therapy was started at 0.5 IU/Kg/day with mixed insulin but patient's compliance was poor. She reported loss of sight 7 months ago (3 months after the diagnosis of diabetes). She is the 3rd child in a nonconsanguineous family of 10 children of whom three are alive. They fled the Central African Republic to Cameroon and for the past 4 years have been living in a refugee camp in the East region of Cameroon. Neither she nor the mother went to school.
On admission, she was lethargic (Glasgow coma scale was 13/15). Her weight was 19 kg (<3rd percentile), her height was 133 cm (<3rd percentile) for a BMI of 10.7 kg/m2, −5.5 SD for age. Vital signs were as follows: blood pressure: 100/80 mm Hg, pulse: 100 bpm, respiratory rate 34 cycles/min and temperature was 36.8°C. She had fine hair and poor dental hygiene. Her Tanner stage was B1P1. Her abdomen was distended with no palpable mass. She had vulvovaginal erythema. She had a dry mouth, sunken eyes, mixed signs of dehydration and severe malnutrition (skin pinch went back slowly) and bilateral leucocoria.
Her serum glucose level was 440 mg/dL (24.4 mmol/L), K + 3.3 mmol/L, corrected Na + 148.4 mmol/L, Cl-108 mmol/L. HbA1C was 12% (108 mmol/mol). Urinalysis revealed nitrites (3+), ketones (2+), glycosuria (3+), and culture later on showed growth of E coli. Her hemoglobin level was 12.3 g/dL, white blood cell count was 9500/mm3, and platelets count was 308 000/mm3. Aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) were in the upper limits (42 and 44 IU/L, respectively) and renal function was normal (blood urea nitrogen (BUN) 0.07 g/L, serum creatinine 3 mg/L). Blood proteins were 93 g/L. Blood gases were not available.
She was admitted to the intensive care unit. She received oral rehydration solution for the malnourished (10 mL/kg/hr for 2 hours) followed by 1.5 L/m2/day of normal saline intravenously (IV) and KCL 1.5 g/L (IV) for 24 hours. Rapid-acting insulin was started 2 hours later with an hourly subcutaneous dose of 0.1 IU/Kg. An antibiotic was also given (ceftriaxone at 50 mg/kg/day) as well as routine de-worming with a single dose of 400 mg of albendazole. Four hours following admission, she was more reactive; ketonuria was 1+, serum glucose level was 408 mg/dL (22.4 mmol/L). Rapid-acting insulin was replaced by multiple injections using neutral protamine Hagedorn insulin (NPH) and actrapid (1IU/kg/day). Ready-to-use therapeutic food F75 (75 kcal/100 mL) was started at 130 mL/kg/day divided into eight meals. Folic acid (5 mg once) and vitamin A (200 mg on days 1, 2, and 14) were added to the treatment.
The day after admission, she developed lower limb edema and abdominal distension without ascites and IV fluids were stopped. The oedema regressed on day 2. On day 3, the F75 was replaced with F100 (100 kcal/100 mL) 130 ml/kg/day and progressive introduction of Plumpy Nut® and normal food. Progression of her nutritional status is shown in Table .
Communication with and education of patient and her family was difficult because of unavailability of a translator trained in medical terminology and the fact that the patient was almost blind. This was partially improved following her cataract surgery performed 2 months later.
Upon discharge after 9 weeks spent in hospital, her weight was 29 kg, height 133 cm (BMI 16.4 kg/m2) and MUAC of 160 mm. She was discharged to her refugee camp on multiple insulin injections. Two months later, her weight was 32 kg, height 135 mm (BMI 17.56 kg/m2) and HbA1 C 10%.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [440.0, 'mg/dL'], 'Sodium': [148.4, 'mmol/L']}",156.56,148.732,164.388,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 148.4 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 148.4 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 148.4 mmol * 1 mEq/mmol = 148.4 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 148.4 mmol sodium/L converts to 148.4 mEq sodium/L. 
The concentration of glucose is 440.0 mg/dL. 
Plugging in these values into the formula gives us 148.4 mEq/L + 0.024 * (440.0 - 100) = 156.56 mEq/L.
Hence, the patient's corrected concentration of sodium is 156.56 mEq/L."
5439,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-931,Extracted,"A 32-year-old man comes to the physician for a follow-up examination. He has a 2-month history of increasing generalized fatigue and severe pruritus. He has hypertension and ulcerative colitis which was diagnosed via colonoscopy 5 years ago. Current medications include lisinopril and rectal mesalamine. He is sexually active with 2 female partners and uses condoms inconsistently. His temperature is 37.3°C (99.1°F), pulse is 86/min, and blood pressure is 130/84 mm Hg. Examination shows scleral icterus and multiple scratch marks on the trunk and extremities. The lungs are clear to auscultation. The abdomen is soft and nontender. The remainder of the examination shows no abnormalities. Laboratory studies show:
Hemoglobin 11.5 g/dL
Leukocyte count 7500/mm3
Platelet count 280,000/mm3
Serum
Na+ 138 mEq/L
Cl- 101 mEq/L
K+ 4.7 mEq/L
Urea nitrogen 18 mg/dL
Glucose 91 mg/dL
Creatinine 0.8 mg/dL
Bilirubin
Total 1.5 mg/dL
Direct 0.9 mg/dL
Alkaline phosphatase 460 U/L
AST 75 U/L
ALT 78 U/L
Anti-nuclear antibody negative
Antimitochondrial antibodies negative
Abdominal ultrasound shows thickening of the bile ducts and focal bile duct dilatation.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [91.0, 'mg/dL'], 'Sodium': [138.0, 'mEq/L']}",137.784,130.8948,144.6732,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 138.0 mEq/L. 
The concentration of glucose is 91.0 mg/dL. 
Plugging in these values into the formula gives us 138.0 mEq/L + 0.024 * (91.0 - 100) = 137.784 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.784 mEq/L."
5440,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6444668-1,Extracted,"A 10-year-old girl was admitted to our clinic due to ketoacidosis associated with newly diagnosed type 1 diabetes. Prior to admission, she had suffered from polyuria, polydipsia, and nycturia for about 2 weeks, and presented with fatigue, drowsiness and a lack of appetite for the last two days. Her history did not include any chronic diseases, and she had normal growth and development.
On admission, she was in a serious state, suffering from vomiting and dehydration, and displaying Kussmaul breathing, a respiratory rate of 45 breaths/min and tachycardia. The blood test revealed a blood glucose level of 26.8 mmol/L (482 mg/dl), pH 6.902, base excess (BE) of − 29.3 mmol/L, HbA1c of 12.9%, sodium level of 142 mEq/L, potassium level of 4.11 mEq/L and ketone level of 6.1 mmol/L. The patient was treated according to the recommendations of the International Society of Pediatric and Adolescent Diabetes and the Polish Diabetes Association [, ].
Initially the patient received 500 ml of 0.9% NaCl IV infusion. Next, a continuous IV infusion of short acting insulin was commenced with 2,5 U/ h dose, taking into consideration that the patient weight was 40 kg. IV Insulin infusion was sustained for 51 h with dosages ranging from 1,5 U/h to 4 U/h. Overall the patient received 81,75 units of IV insulin during the first 24 h of treatment. Moreover, potassium was supplemented intravenously accordingly to changes in electrolytes results. Although she remained in a serious condition during the first 24 h of treatment, she stopped vomiting and showed gradual improvement in blood test results, with pH normalization and a decrease in the level of ketones. The glucose level was maintained between 8.3 and 13.9 mmol/L (150–250 mg/dl) with intravenous insulin and glucose infusions. The neurological status was checked hourly, and was reported as stable. An ECG was performed within the first few hours of admission, which did not reveal any crucial abnormalities aside from tachycardia. The patient received 65 units of IV insulin during the second 24 h f treatment. During the whole continuous insulin infusion the patient fluid input was 7850 ml (4750 ml IV, 3100 ml orally) and diuresis was 3400 ml.
The patient’s overall condition improved during the second day of treatment, despite the fact that she was still receiving intravenous insulin. That day irregular heartbeats were noticed on auscultation during the physical examination and on the ECG monitor. A second ECG showed premature ventricular complexes (PVCs; also known as trigeminy) with LBBB (left bundle branch block) morphology and a normal axis (Fig. ). Continuous ECG monitoring was subsequently implemented, and the patient underwent a cardiac consultation. The echocardiogram showed no abnormalities in the structures of the heart and great vessels. The consultant cardiologist confirmed the diagnosis of ventricular arrhythmia (PVCs). The blood results revealed hypokalemia (nadir at 2.9 mmol/L) and hypophosphatemia (nadir at 0.45 mmol/L).
The ECG performed after the first recognition of the patient’s the irregular heart rhythm (Fig. ) showed: sinus rhythm at 100/min, normal cardiac axis, with premature ventricular complexes. Normal PQ interval (0,14 s), normal QRS duration (0,08 s), normal QT interval (0,31 s)and QTc 0,40 QTd 0,04 s. Normal T wave and repolarization. The biochemistry results at that moment were: Na 134 mmol/L Na 134 mmol/l [132–145]; K 3,56 mmol/l [4,1-5,3]; Ca 2,70 mmol/l [2,1-2,6]; Mg 0,83 mmol/l [0,53-1,11]; Phosphate 0,45 mmol/l [1,1-2,0] (assessed for the first time); pH 7,34 [7,35-7,45]; BE-11,5 mmol/l [− 2,0/+ 3,0]; HCO3 14,2 mmol/l [22,5-30,0]. CK level was not determined. The pattern visible in the ECG was not typical of hypokalemia, which is connected with initial T-wave decrease, followed by ST-segment depression, T-wave inversion, PR interval prolongation and increased P-wave amplitude, observed with further decreases in serum potassium levels. Severe hypokalemia may be associated with giant U-waves created by T- and U-wave fusion. Tachyarrhythmia and rarely atrioventricular block may evolve [–]. In our case we did not observe such abnormalities typical to low potassium level in the ECG. Moreover, the ECG was not typical of hypercalcaemia, which causes prolonged PQ interval and shortening of QT interval [, ]. Taking above into consideration we propose possible association between hypophosphatemia and premature ventricular complexes reported in the ECG.
Potassium was supplemented both orally and intravenously. Overall the patient received 123 mEq of potassium during the continuous insulin therapy. As far as phosphorus is concerned, the patient was fed with liquid dairy products that were rich in phosphate, as she was only able to swallow small amounts of non-solid foods due to odynophagia. She was also started on oral phosphate supplementation (phosphate mixture containing 17.8 g Na2HPO4 and 4.88 g NaH2PO4 in 100 ml of distilled water, containing 1.6 mmol of inorganic phosphate per 1 ml). As 1 mmol of inorganic phosphate weighs 31 mg, our patient was receiving 62 mg Pi/kg body weight every 24 h from the phosphate mixture. She continued to present an irregular heart rate, thus a 24-h ECG Holter monitor examination was performed. The results showed 38,000 monomorphic PVCs, 1615 occurrences of ventricular bigeminy, 1230 of ventricular trigeminy and 453 of ventricular quadrigeminy, which comprised 38% of all the heart electrical activity recorded.
The patient was started on intensive subcutaneous insulin regimen at the 3 day of treatment, after the biochemistry results improved. In the beginning she was receiving 15 units of ultra- long acting basal insulin and 27,5 units of rapid acting insulin for meals and correction doses.
The patient’s serum phosphate level normalized over the few next days of treatment (Table ), and ventricular arrhythmia ceased almost completely. Subsequent ECG Holter examination showed 1760 PVCs, 13 episodes of ventricular bigeminy and 79 episodes of ventricular trigeminy. Additionally, we noticed hypocalcaemia after 3 days of phosphate supplementation. Taking into consideration the patient’s severe vitamin D3 deficiency (25(OH)D3 level 9.83 ng/ml), we supplemented both calcium and vitamin D3.
Gradually the patient regained insulin sensivity and entered a partial remission phase. C- peptide level was 0,84 ng/ml.
The patient was discharged in an overall good condition receiving intensive functional insulin therapy. The regimen included 10 units of basal insulin administered once daily in the evening and rapid acting insulin with insulin: carbohydrate ratio set for each meal and also with recommended correction doses.
A cardiac check-up at the outpatient clinic following discharge revealed no signs of cardiac arrhythmia. The patient is currently on an insulin pump therapy regimen, and her growth and development are within the normal range.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [26.8, 'mmol/L'], 'Sodium': [142.0, 'mEq/L']}",151.1879,143.62851,158.7473,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 142.0 mEq/L. 
The concentration of glucose is 26.8 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 26.8 mmol. To convert 26.8 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 26.8 mmol glucose * 0.001 mol/mmol = 0.0268 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0268 mol glucose * 180.16 g/mol = 4.82829 g glucose. To convert 4.82829 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 4.82829 g glucose * 1000.0 mg/g = 4828.29 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 4828.29 mg glucose/10.0 dL = 482.829 mg glucose/dL. The concentration value of 26.8 mmol glucose/L converts to 482.829 mg glucose/dL. 
Plugging in these values into the formula gives us 142.0 mEq/L + 0.024 * (482.829 - 100) = 151.1879 mEq/L.
Hence, the patient's corrected concentration of sodium is 151.1879 mEq/L."
5441,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4290655-1,Extracted,"A 63-year-old female patient with a history of total hysterectomy for the treatment of uterine rupture 30 years previously presented with a fever of 38°C that had lasted for 3 days and swelling of the right cheek and lower jaw. Antimicrobial treatment prescribed by a general practitioner did not relieve the swelling. She was unable to eat solid food because of odynophagia and trismus and had repeated episodes of vomiting and diarrhea due to excessive water intake during hot days with the highest temperature of ≥35°C. Physical examination at presentation revealed swelling and warmth in the submandibular and buccal regions and mild airway narrowing. She complained of numbness of the extremities and cramps in the calves, hyperpnea, and restlessness. Blood pressure was 115/84 mmHg, pulse 72 bpm, arterial oxygen saturation 99%, and blood glucose 98 mg/dL. Since serum biochemistry and hematology examinations revealed abnormal electrolyte values, inflammatory response, and anemia, she was hospitalized for drainage and fluid therapy. Under local anesthesia, an incision was made in the gingiva on the buccal side of the mandibular premolars, and a gauze drain was inserted in the incision. Since spasm and numbness of the extremities continued, she was treated with diazepam 2.5 mg. Fluid therapy was initiated with 5% glucose solution 250 mL and a hypotonic electrolyte solution 1,000 mL/day. Laboratory findings on day 1 of hospitalization were Na 117 mEq/L, K 3.5 mEq/L, and Cl 83 mEq/L. Since abnormal electrolyte levels, nausea, vomiting, and diarrhea continued, she received metoclopramide 10 mg intravenously and also received infusions of a hypotonic electrolyte solution 1,500 mL/day and physiological saline 700 mL/day to correct serum sodium levels. On day 2 of hospitalization, numbness of the extremities disappeared and nausea and vomiting improved, but watery stools continued. Although the distance she was able to open the mouth improved to about two-finger width and she became able to eat meals, she still complained of anorexia. Fluid therapy was continued with a hypotonic electrolyte solution 1,000 mL, maltose-lactated Ringer's solution 500 mL/day, and physiological saline 1200 mL. In the evening of day 3, electrolyte levels returned to normal ranges although inflammatory reaction was still observed. Fluid therapy was switched to physiological saline 100 mL on day 4. Since severe vomiting and diarrhea recurred at night on day 4 of hospitalization, she received metoclopramide 10 mg intravenously, and electrolyte infusion of a hypotonic electrolyte solution 1,000 mL, maltose-lactated Ringer's solution 500 mL, and physiological saline 200 mL was restarted. On day 6, as swelling in the buccal and mandibular regions subsided, the gauze drain was removed. However, generalized malaise, vomiting, diarrhea, anorexia, and numbness of the extremities recurred, and serious hyponatremia with Na 111 mEq/L, K 3.7 mEq/L, and Cl 79 mEq/L developed. She was treated with water restriction and infusion of maltose-lactated Ringer's solution 500 mL/day, a hypotonic solution 500 mL/day, and physiological saline 600 mL/day. On day 7, sodium and potassium levels were further decreased. She received physiological saline 100 mL, 20% glucose solution 20 mL, 10% NaCl 20 mL, maltose-lactated Ringer's solution mixed with one ample of potassium aspartate, and a hypotonic solution to correct hyponatremia and received furosemide 20 mg to induce diuresis. The urinary sodium level was within the normal range at 66.8 mEq/L. On day 8, serum and urinary sodium concentrations were maintained within the normal range by slow infusion with physiological saline 500 mL, 10% NaCl solution 40 mL, and maltose-lactated Ringer's solution mixed with one ample of potassium aspartate and diuresis, and vomiting and diarrhea disappeared. On day 9, electrolyte levels had been corrected with a CRP level of 0.59; fluid therapy was discontinued. On day 10, patient was discharged from the hospital after a full recovery ().
We obtained patient consent for publication of personal information.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [98.0, 'mg/dL'], 'Sodium': [117.0, 'mEq/L']}",116.952,111.1044,122.7996,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 117.0 mEq/L. 
The concentration of glucose is 98.0 mg/dL. 
Plugging in these values into the formula gives us 117.0 mEq/L + 0.024 * (98.0 - 100) = 116.952 mEq/L.
Hence, the patient's corrected concentration of sodium is 116.952 mEq/L."
5442,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-5830,Extracted,"A 72-year-old man presents to the primary care clinic for evaluation of progressive fatigue and weight loss. His past medical history is significant for hypercholesterolemia, type 2 diabetes mellitus, aortic stenosis, and chronic renal insufficiency. He endorses being well-rested after waking from sleep but fatiguing rapidly during the day. In addition, he states that he has lost 15lbs over the previous month. His temperature is 98.3°F (36.8°C), pulse is 100/min, blood pressure is 110/85 mmHg, respirations are 16/min, and oxygen saturation is 96% on room air. Physical exam is notable for conjunctival pallor and scattered areas of ecchymoses. His laboratory results are shown below:

Serum:
Na+: 140 mEq/L
K+: 4.0 mEq/L
Cl-: 101 mEq/L
HCO3-: 22 mEq/L
BUN: 30 mg/dL
Glucose: 160 mg/dL
Creatinine: 1.9 mg/dL


Leukocyte count: 1,100/mm^3
Absolute neutrophil count 920/mm^3
Hemoglobin 8.4 g/dL
Platelet count: 45,000/mm^3
Mean corpuscular hemoglobin concentration: 34%
Red blood cell distribution width: 12.0%
Mean corpuscular volume: 92 µm^3
Lactate dehydrogenase: 456 IU/L
Haptoglobin 120 mg/dL
Fibrinogen 214 mg/dL

A bone marrow biopsy is performed which shows cells that are CD19+, CD20+, CD11c+, and stain with acid phosphatase 5 and tartrate-resistant.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [160.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",141.44,134.368,148.512,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.0 mEq/L. 
The concentration of glucose is 160.0 mg/dL. 
Plugging in these values into the formula gives us 140.0 mEq/L + 0.024 * (160.0 - 100) = 141.44 mEq/L.
Hence, the patient's corrected concentration of sodium is 141.44 mEq/L."
5443,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8232924-1,Extracted,"A 68-year-old, right-handed Caucasian female presented with sudden-onset word-finding difficulty, speech hesitation, and difficulty following commands upon awakening from a nap. No other neurological deficits were observed. Her only medical history was a recent diagnosis of mild hypertension two weeks prior. For this, she was started on and had inconsistently been taking amlodipine 5 mg. Her initial vital signs showed that she was afebrile (99.6°F) with a heart rate of 109 beats/minute and blood pressure of 129/94 mmHg. Physical examination revealed a National Institutes of Health Stroke Scale score of 4, which consisted of one point for answering the month incorrectly, one point for performing one task incorrectly when instructed to open and close eyes and then grip and release her hand, and two points for severe aphasia.
Basic metabolic panel showed sodium 133 mEq/L, potassium 3.6 mEq/L, chloride 99 mEq/L, CO2 21 mEq/L, glucose 234 mg/dL, blood urea nitrogen 18 mg/dL, creatinine 0.87 mg/dL, and calcium 8.7 mg/dL. Complete blood count showed white blood cell (WBC) 12.01 K/mcL, red blood cell (RBC) 4.29 mil/mcL, hemoglobin 14.0 g/dL, hematocrit 41.8%, and platelets 297 K/mcL.
Computed tomography (CT) without contrast revealed an area of hypoattenuation in the deep and subcortical white matter of the right parietal lobe, which could reflect an evolving infarct although nonspecific. Subsequent CT angiography and CT perfusion could not identify vascular territory ischemia or infarct. Because the patient was last known well more than 4.5 hours ago and based on imaging studies, she was not a candidate for receiving tissue plasminogen activator. Sixteen hours later, she still had hesitation producing words, although her word output had significantly improved. Magnetic resonance imaging (MRI) with and without contrast were performed. MRI of the brain without contrast showed a 5.1 × 2.6 cm area of hyperintensity in the left temporal lobe, while MRI with contrast showed a 1.8 × 1.6 cm area of hyperintensity in the left temporal lobe (Figure ).
The MRI findings were concerning for several etiologies, narrowing the differential diagnoses to infectious encephalitis, autoimmune limbic encephalitis, neoplasm, and postictal edema (Figure ). Acute herpes encephalitis had to be considered and was clinically excluded, although there was no involvement of other limbic structures, such as insula or cingulate gyrus, no hemorrhage, and only a small volume of mild diffusion restriction. Diffusion restriction smaller than the area of fluid-attenuated inversion recovery (FLAIR) signal abnormality made a recent infarct unlikely (Figures , ). Autoimmune/limbic encephalitis could have had this appearance but is often bilateral making this unlikely. Postictal edema was less likely given the degree of mass effect and the lack of involvement of additional limbic structures such as the hippocampal body/tail or cingulate gyrus. With the given differential, the patient was started on empiric acyclovir and levetiracetam, and a lumbar puncture was performed. A lumbar puncture and cerebrospinal fluid study revealed clear fluid, WBCs 6/mm³, RBCs 3/mm³, 70% neutrophils, 25% lymphocytes, glucose 77 mg/dL, protein 32 mg/dL, cryptococcal Ag negative, and non-reactive Venereal Disease Research Laboratory test. Herpes simplex virus polymerase chain reaction was negative. Hence, acyclovir was discontinued. Electroencephalogram (EEG) showed lateralized periodic discharge in the left frontotemporal region with a focal region of increased epileptic potential likely from the underlying structural abnormality (Figure ).
A brain biopsy was needed to further identify the FLAIR hyperintensity seen on MRI. The brain biopsy and resection revealed glioblastoma, isocitrate dehydrogenase-wildtype, World Health Organization grade IV with an O6-methylguanine-DNA-methyltransferase gene promoter methylation of 75.76%. At discharge, the patient was clinically doing well. Her treatment plan consisted of chemotherapy and radiation.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [234.0, 'mg/dL'], 'Sodium': [133.0, 'mEq/L']}",136.216,129.4052,143.0268,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 133.0 mEq/L. 
The concentration of glucose is 234.0 mg/dL. 
Plugging in these values into the formula gives us 133.0 mEq/L + 0.024 * (234.0 - 100) = 136.216 mEq/L.
Hence, the patient's corrected concentration of sodium is 136.216 mEq/L."
5444,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8010837-1,Extracted,"A 73-year-old Caucasian man was referred to our hospital for evaluation of a right PHEO, diagnosed two months before at another hospital, after the identification of a large retroperitoneal mass on abdominal computed tomography (CT). At that time, the patient experienced abdominal discomfort, unintentional weight loss of approximately 5 Kg within the previous 3 months, associated to sporadic episodes of watery diarrhea. At admission to our hospital, the patient was moderately dehydrated and tachypnoic. He denied any history of headache, palpitations, sweating, or hypertension. He reported episodes of watery diarrhea, up to 5-6 times a day and 2-3 times a week, without blood or mucus. He also had no relevant familial history of endocrine nor cancer diseases but only a paternal history of arterial hypertension. Physical examination showed blood pressure (BP) of 100/67 mmHg and heart rate of 88 beats/min; no significant orthostatic pressure gradient was measured. BP values, evaluated on several occasions, were 94/58 and 91/62 mm Hg. Laboratory tests showed a hypokalemia (3.3 mmol/L) with metabolic acidosis (pH 7.29, HCO3- 19 mmol/L), a serum magnesium level of 1.5 mg/dl and fasting blood glucose of 149 mg/dl. A 24-h urinary sample showed only a slight increase in normetanephrine excretion, 638 μg (normal values: 162-528/day), while metanephrine and methoxytyramine resulted within normal range. Serum chromogranin A was elevated (1028 ng/ml, normal values 20-100), as well as neuron-specific enolase level (NSE 35.7 nl/ml, normal values 1.0-13.5). Plasma cortisol, adrenocorticotropic hormone, thyroid-stimulating hormone, thyroxine, parathyroid hormone, and calcitonin were within the normal ranges. Contrast enhanced abdominal CT scan confirmed the presence of inhomogeneous right adrenal mass measuring 8.1 x 7.7 x 7.9 cm (). A 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) coupled with CT showed an area of high uptake (maximum standardized uptake value, SUV max 8.6) in the right adrenal gland, with a prevailing peripheral signal and central hypoactivity, and another area of high uptake (SUV max 9.6) in the lumbar region suspicious of lymph node localization (). In addition, 68GaDOTA-octreotate (DOTATATE) PET confirmed the peripheral high uptake (SUV max 6) in the right adrenal gland and the high uptake area (SUV max 3.7) in the lumbar region; a high uptake (SUV max 4.5) was also detected at the base of the left lung (). Based on these results, patient diagnosis was metastatic adrenal PHEO. Intravenous fluid infusion, sodium bicarbonate, potassium aspartate, magnesium sulphate supplementations were started allowing an improvement of clinical condition and blood pressure levels. Then, after 10-days pre-operative treatment with low dose alpha1-adrenergic antagonist doxazosin (given just before bed), he underwent surgical resection of the tumor. The patient had an uneventful postoperative course, except for sporadic watery diarrhea. Gross examination revealed a 10x8x6 cm brownish-yellow, friable adrenal mass. Histology showed a highly cellular tumor made up of monotonous medium-sized cells with discrete nuclear pleomorphism and mild hyperchromasia. Mitotic figures were above 3/10 high power fields, with some atypical mitoses. The cells were arranged in nests with areas of diffuse growth in more than 10% of the tumor. Confluent areas of necrosis were present. Foci of capsular and vascular invasion were noted as well as extension into periadrenal adipose tissue. The histological features were consistent with a malignant PHEO, with a PASS score (Pheochromocytoma of the Adrenal Gland Scaled Score) of 20 (), indicating a high risk of aggressive cellular behavior (PASS≥4). DNA genetic analysis of the patient with a next generation sequencing (NGS) approach using Trusight One Sequencing Panel by Illumina, revealed a synonymous single nucleotide variant of gene SDHA [rs6555055, NM_004168.2:c.619A>C, (p.Arg207=)] indicated by ClinVar database as associated to “probably benign” catecholamine-secreting PHEO (). The patient was discharged in satisfactory clinical condition. Therapy with lanreotide, a somatostatin analogue, at a dose of 60 mg once a month was initiated. At 2 months, multiple metastatic pulmonary and hepatic nodules were identified on CT scan (). The patient once again experienced abdominal discomfort, 4 kg weight loss, yet only sporadic watery diarrhea. Peptide receptor radionuclide therapy and sunitinib, a multi-targeted receptor tyrosine kinase inhibitor, were scheduled. In the meantime, lanreotide therapy was increased to 120 mg once a month. However, after about one month, the patient was re-admitted with a 10-day history of severe watery diarrhea, up to 20 times in 24 hrs, accompanied by nausea, vomiting and occasionally quick flushing. At presentation, he was suffering and markedly dehydrated. Physical examination showed BP of 90/67 mmHg, heart rate of 120 beats/min, the pulse was fast and weak, the breath was fast and short, the skin cold and clammy, and the urination was decreased. Laboratory tests were as follows: blood urea nitrogen 96 mg/dl; serum creatinine 3.5 mg/dl; Na+ 136 mmol/l; K+ 2.5 mmol/l; Cl- 115 mmol/l; pH 7.08; HCO3
- 5.5 mmol/l; Pa CO2 30 mm Hg; Pa O2 67 mm Hg; lactate 5 mmol/l (normal values 0.5-2.2); serum anion gap 15 mmol (corrected for serum albumin levels 16 mmol); urine anion gap was negative. Serum prealbumin was 29 mg/dl (normal values 15-35) and albumin 3.9 g/dl (normal values 3.5-5.0). At that time, serum chromogranin A was 2896 ng/ml and neuron-specific enolase 49.6 ng/ml. Twenty-four hours urinary normetanephrine excretion was 920.4 μg, while metanephrine resulted at 432.6 μg (normal values 64-302 μg/day). VIP plasma levels were measured, and circulating values were more than 10 times the upper normal limit (1285 pg/ml, normal values 18-100). Cardiac ultrasound showed a reduced left ventricular ejection fraction (35%). Due to the emerging clinical picture, histological sections were re-evaluated with additional immunostainings. Sections were stained with the following primary antibodies: anti-Chromogranin A (clone LK2H10 ready to use; Ventana-Roche), Anti-Vasoactive intestinal polypeptide -VIP (rabbit 1:500; Biogenex) and anti-Somatostatin Receptor 2A -SSTR2A (rabbit 1:100; Bio-Trend). The sections were immunostained with HRP Polymer (Optiview DAB IHC Detection kit; Roche) in accordance with the manufacturer’s specifications. Negative controls consisted of substituting normal mouse serum for the primary antibodies. A set of sections adjacent to these used for single labelling with VIP, was used for double labelling with Chromogranin A. The second antibody was immunostained with AP Polymer (Ultraview Universal Alcaline Phosphatase Red Detection Kit; Roche). Permanent red chromogen was used for staining development. Immunostaining revealed strong positivity for neuroendocrine marker chromogranin A and VIP (); a large number of cells co-expressed chromogranin A and VIP (). Weak was the positivity for SSTR2A (). A diagnosis of VIP-secreting PHEO was rendered. The patient was then transferred to the intensive care unit. He was managed with intensive intravenous fluid hydration, potassium salts and bicarbonates, as well as with octreotide (0.1 mg/8 h s.c.), sunitinib 50 mg/day and loperamide. However, his diarrhea worsened with further exacerbation of metabolic acidosis (pH 6.99, HCO3
- 4.3 mmol/l), leading to hemodynamic instability and shock. He died five days later.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [149.0, 'mg/dL'], 'Sodium': [136.0, 'mEq/L']}",137.176,130.3172,144.0348,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 136.0 mEq/L. 
The concentration of glucose is 149.0 mg/dL. 
Plugging in these values into the formula gives us 136.0 mEq/L + 0.024 * (149.0 - 100) = 137.176 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.176 mEq/L."
5445,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2876172-1,Extracted,"A 33-year-old Caucasian Greek woman presented to the emergency department of the Hospital with a continuous epigastric pain of four hours duration and intermittent vomiting. Her medical history included hypercholesterolemia and type 1 diabetes for 16 years treated with insulin injections twice daily. Our patient had omitted all insulin injections since 36 hours prior to presentation. Regarding coronary risk factors, apart from diabetes and hypercholesterolemia, she was a smoker of more than two packs of cigarettes daily.
On initial assessment she was drowsy with tachycardia (112 pulses/minute), tachypnoea (28 breaths/minute) and hypotension (85/44 mmHg). A physical examination of her abdomen had normal results. Her initial ECG revealed sinus tachycardia, ST segment elevation in the anteroseptal leads consistent with anterior myocardial infarction, and intraventricular conduction delay (Figure ). A urine dipstick test detected ketones, bedside capillary testing using a glucometer showed high glucose concentrations, and arterial blood gas analysis indicated metabolic acidosis (pH = 7.16, carbon dioxide partial pressure = 13 mmHg, oxygen partial pressure = 123 mmHg, bicarbonate concentration = 4 mmol/L, base excess = -24 mmol/L). We provisionally diagnosed diabetic ketoacidosis, possibly precipitated by an acute myocardial infarction.
We initially treated our patient with fluid replacement with normal saline, intravenous insulin at seven units/hour, sodium bicarbonate, aspirin, clopidogrel, and low molecular weight heparin. Biochemical results showed the following serum concentrations: potassium = 7.2 mEq/L, sodium = 127 mEq/L, urea = 97 mg/dl, creatinine = 2.26 mg/dl, and glucose = 676 mg/dl. A bedside cardiac ECG showed no segmental wall motion abnormality and a normal ejection fraction. As there were findings both for (epigastric pain, ECG pattern, presence of three coronary heart disease risk factors) and against the diagnosis of acute myocardial infarction (young age, normal ECG), we performed coronary angiography in order to exclude anterior acute myocardial infarction, which could lead to severe myocardial damage and possible severe complications (heart failure, among others) if treatment was delayed. During angiography, which revealed normal coronary arteries, ST segment elevation in the anteroseptal leads was still present in her ECG findings.
A repeat biochemical test after three hours showed the following values: sodium = 130 mEq/L, potassium = 4.9 mEq/L, and glucose = 255 mg/dl. A repeat ECG showed a complete resolution of the anteroseptal ST segment elevation and intraventricular conduction delay (Figure ). Her troponin I concentration 12 hours after admission was normal (0.1 μg/L). Our patient subsequently made an uneventful recovery. When she was discharged seven days after, both her ECG and biochemical results were normal.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [676.0, 'mg/dL'], 'Sodium': [127.0, 'mEq/L']}",140.824,133.7828,147.8652,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 127.0 mEq/L. 
The concentration of glucose is 676.0 mg/dL. 
Plugging in these values into the formula gives us 127.0 mEq/L + 0.024 * (676.0 - 100) = 140.824 mEq/L.
Hence, the patient's corrected concentration of sodium is 140.824 mEq/L."
5446,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4989056-1,Extracted,"A 53-year-old obese male presented due to a wound in his right thigh. He stated that the wound started as an itch and that it progressed to its current state in just 5 days. The wound started to smell bad. The patient had a history of diabetes, which he reports to be diet controlled. He is a truck driver by trade and says he does his best to do a good job with his diet. His past medical history was notable for testicular cancer status after radiation 9 years earlier. He states that his left groin skin has always been a little sensitive after the radiation and in that he often will itch it. He says this wound started out as an itch as well. Intense itching led to an open wound, at which point he applied povidone iodine and put a dressing on it. He was remarkably stoic, considering the extent of the wound.
Review of systems is negative except as noted above. The patient specifically denied fever, chills, chest pain, shortness of breath, abdominal pain, nausea, vomiting, diarrhea, urinary symptoms, or headache. His prescribed medications included atorvastatin for hyperlipidemia, Diltiazem and Lisinopril for hypertension, Metformin for diabetes, and Gabapentin for diabetic neuropathy. The patient had no allergies and his tetanus status was up to date.
Patient's vital signs were as follows: blood pressure 145/85 mmHg; respiratory rate 20/min; pulse 91/min, SpO2 99%, temperature 36.7°C; and pain 8/10. On physical exam, he was alert and oriented to person, time, and place and in no acute distress. Pertinent positive findings included a 4 cm × 10 cm elliptical wound on the left thigh with necrotic flesh within, which was exquisitely foul smelling (). The left leg appeared somewhat mottled and cellulitic compared to right leg. Both legs had intact dorsalis pedis and popliteal pulses.
Laboratory analysis revealed an elevated white blood cell (WBC) count of 17.1 k/cm with the remainder of the CBC within normal limits. The metabolic panel revealed blood sugar of 398 and corresponding hyponatremia of 128 mmol/L. The chloride and bicarbonate were also low at 89 mmol/L and 21 mmol/L, respectively, yielding an elevated anion gap of 18. The patient also has had hypoalbuminemia with a value of 2.5 g/dL. Lactate was elevated at 2.8 mmol/L. Coagulation studies were within normal limits. Blood cultures were sent. The urinalysis demonstrated clear glycosuria with >500 mg/dL of glucose, as well as pyuria with 17 WBC per high power field. There was no ketonuria, leukoesterase, or elevated nitrates.
AP and lateral radiographs of the left femur revealed mottled lucencies consistent with gas in the soft tissues of the medial thigh ().
A duplex Doppler exam with real time grey-scale imaging, spectral Doppler with wave form analysis, color Doppler, and physiologic maneuvers including compression were done to evaluate the venous system of the left leg from the groin down through the popliteal fossa. Subcutaneous edema was noted in left thigh, but there was no sonographic evidence of deep venous thrombosis.
The patient's presentation was most concerning for gas gangrene versus necrotizing fasciitis. Patient looked remarkably well, despite the differential diagnosis. He was resuscitated with 4 L of NSS, 10 U of intravenous regular insulin, 1 g of intravenous Vancomycin, and 3.375 g of intravenous Piperacillin-Tazobactam. He was given 2 oxycodone tablets for analgesia. Patient's mentation remained intact throughout. The patient was then transferred to the critical care unit where he underwent surgical debridement followed by hospitalization for intravenous antibiotics. He also received diabetes education, as he was not taking his Metformin, but rather under the impression that he was doing a good job controlling his diabetes with diet. His decompensated diabetes was likely a contributing cause to his necrotizing fasciitis. Following hospitalization, the patient was discharged with complete resolution of the infection and left with blood sugar well controlled.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [398.0, 'mg/dL'], 'Sodium': [128.0, 'mmol/L']}",135.152,128.3944,141.9096,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 128.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 128.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 128.0 mmol * 1 mEq/mmol = 128.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 128.0 mmol sodium/L converts to 128.0 mEq sodium/L. 
The concentration of glucose is 398.0 mg/dL. 
Plugging in these values into the formula gives us 128.0 mEq/L + 0.024 * (398.0 - 100) = 135.152 mEq/L.
Hence, the patient's corrected concentration of sodium is 135.152 mEq/L."
5447,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2652426-1,Extracted,"A 72-year-old man with known history of stage 3 chronic kidney disease, hypertension, coronary artery disease, hyperlipidemia presented with a 3-days history of low-grade fever, productive cough, dyspnea, night sweats and fatigue. Patient was a non-smoker and did not consume alcohol. His kidney disease was likely due to renovascular or/and chronic atheroembolic disease with baseline serum creatinine level of 1.7 mg/dl, giving him an estimated glomerular filtration rate of 50 mL/min/1.73 m2. His medications included metoprolol, isosorbide mononitrate, gabapentin, aspirin, candesartan, tamsulosin, atorvastatin. On examination, he was alert, and not in distress. His blood pressure was 140/80 mm Hg without orthostatic changes and temperature 100.3°F. The remainder of the examination was unremarkable except of few wheezes over both lung fields. He did not have pedal edema. Serum sodium was 145 mEq/L, potassium 4.8 mEq/L, urea nitrogen 34 mg/dl, creatinine 1.7 mg/dl and glucose 130 mg/dl. Hemoglobin was 12.1 g/dL, white blood cells 5.2 × 109/L and platelets 208 × 109/L. Treatment with 250 mg of azithromycin daily was given for six days without clinical improvement. A chest radiograph showed small left apical nodules and computed tomography (CT) scan of the chest demonstrated right lower lobe scarring and left upper lobe small nodules with focal pleural thickening (Figure ). Three weeks later, serum creatinine rose to 2.6 mg/dl and urea to 48 mg/dl. Urine volume never decreased; urinalysis showed trace proteinuria, without glucose or blood. Urine sediment did not show red blood cells, white blood cells or casts. Urine sodium was 35 mmol/L. Patient completed 2 weeks treatment with 500 mg of levofloxacin, with some clinical improvement. Six weeks after initial presentation, cultures of two sputum samples were reported to be positive for Mycobacterium gordonae and Mycobacterium avium complex (MAC) by DNA probe and subsequently the positive diagnosis of pulmonary nontuberculous mycobacterial infection was made. The patient rejected long-term triple therapy, given his mild symptoms and a concern about treatment adverse effects. The patient has remained well throughout a 2 months period of close clinical observation; he has been afebrile and his serum creatinine level returned to baseline of 1.7 mg/dl.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [130.0, 'mg/dL'], 'Sodium': [145.0, 'mEq/L']}",145.72,138.434,153.006,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 145.0 mEq/L. 
The concentration of glucose is 130.0 mg/dL. 
Plugging in these values into the formula gives us 145.0 mEq/L + 0.024 * (130.0 - 100) = 145.72 mEq/L.
Hence, the patient's corrected concentration of sodium is 145.72 mEq/L."
5448,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6755925-1,Extracted,"A 51-year-old gentleman, recently diagnosed to have type 2 diabetes mellitus and systemic hypertension, presented to the cardiology outpatient clinic on 28th July 2016 with history of pricking chest pain and shortness of breath for the past 7 years and recurrent attacks of syncope since the previous year. He weighed 49 kg and with a height of 157 cm; body mass index was 19.88 kg/m2. His blood pressure (BP) was 120/80 mmHg and pulse rate was 78/min and regular in rhythm. He was afebrile. Systemic examination was unremarkable.
Laboratory findings revealed hemoglobin of 15.1 g/dL, hematocrit of 47%, white blood cell count of 11,300/mm3 (differential count of neutrophils of 56%, lymphocytes 26%, eosinophils 11%, and monocytes of 7%), and platelet count of 293,000/mm3. Urine on routine examination showed a pH of 6.0, specific gravity of 1015, and was negative for albumin, glucose, red blood cells, and pus cells. Blood glucose fasting was 115 mg/dL and post-prandial was 219 mg/dL with an HbA1C of 7.1%. Blood urea was 27 mg/dL and creatinine was 1.0 mg/dL. Serum electrolytes were as follows: sodium 141 mEq/L, potassium 4.3 mEq/L, chloride 103 mEq/L, and bicarbonate 28 mEq/L. Serum cholesterol was 183 mg/dL, serum triglyceride 121 mg/dL, and serum uric acid 3.9 mg/dl. Two-dimensional (2D) echocardiogram showed normal left ventricular dimensions, no regional wall motion abnormality, and a left ventricular ejection fraction of 69%. Holter monitoring showed occasional supraventricular and ventricular premature complexes. On 2nd August, coronary angiography showed insignificant coronary artery disease with dominant right coronary system and he was discharged with medical advice.
On 3rd August, he attended emergency department with complaints of severe back pain, palpitation, and sweating. His back pain was sudden in onset, gradually progressive, throbbing type, rating 8/10 in pain scale, radiating to the left flank, aggravated by exertion, and partially relieved by rest. He had no other complaints. He was on metformin and calcium channel blocker. He looked anxious, agitated, and restless but was oriented and afebrile. His pulse rate was 112/min, respiratory rate was 28/min, and BP was 210/120 mmHg in the right upper limb and 210/100 mmHg over the left upper limb in supine position. There was no radio-femoral delay. Systemic examination was unremarkable except for a mild tenderness in the lumbar region.
On investigation, electrocardiography, chest X-ray, complete blood counts, liver function tests, 2D echocardiography, urine analysis, and toxicology screen were all within normal limits. Serum amylase and lipase were normal. Blood urea was 58 mg/dL and serum creatinine was 2 mg/dL. Venous blood gas (VBG) analysis showed a pH of 7.21, bicarbonate of 18 mmol/L, base excess of −9.4 mmol/L, and a lactate of 10.81 mmol/L. Serum electrolytes were sodium 138 mmol/L, potassium 3.8 mmol/L, and chloride 108 mmol/L, and anion gap was 12 mmol/L.
The following were considered in the differential diagnosis of this situation: (a) acute mesentric ischemia, (b) aortic dissection (c) hypertensive emergency, and (d) pancreatitis. Contrast-enhanced computed tomography abdomen showed a lesion in the left adrenal gland measuring about 3.5 × 3.2 cm with mild enhancement in the arterial phase, features consistent with pheochromocytoma [: Contrast enhanced CT scan of abdomen showing the mildly enhancing left adrenal mass]. No additional extra-adrenal tumors were seen. There was no evidence of mesenteric ischemia, aortic dissection, or pancreatitis. Upon further questioning his family members, it was known that he was unwell in the previous 6 months with on and off headache, palpitation, and anxiousness, which they attributed to the recently diagnosed diabetes mellitus.
His BP was managed with alpha adreno-receptor blocker and calcium channel blocker. Phenoxybenzamine was added at a dose of 10 mg twice a day and later increased to 20 mg three times daily. Persistent tachycardia and BP were stabilized with addition of beta blocker.
On 5th August 2016, the level of 24-h urine metanephrines was 14,536 mcg (reference range: less than 350 mcg/24 h) and nor-metanephrines was 7,607 mcg (reference range: less than 600 mcg/24 h).
Laparoscopic removal of pheochromocytoma was done under general anesthesia on 12th August 2016. After the surgery, there was a brief episode of hypoglycemia and hypotension, which was managed with 25% dextrose and normal saline, respectively. Azotemia resolved and blood gases were normalized. Pathological examination of the resected mass revealed a well-encapsulated tumor of size 5 cm × 4 cm × 3 cm, without hemorrhage. It showed polygonal and round cells with abundant cytoplasm and increased vasculature. There was no capsular or vascular invasion. Tumor cells were seen in the background of spindle cells with ganglion cells and Schwanian stroma. These features were reported as consistent with a CP–ganglioneuroma of the left adrenal gland []. Immunohistochemistry examination showed positivity for chromogranin, synaptophysin, and S-100 stains and negativity for calretinin in pheochromocytoma cells. Calretinin, chromogranin, synaptophysin, and S-100 stains were positive in the ganglioneuromatous component. Vimentin was positive and cytokeratin was negative. These staining characteristics confirmed the composite nature of the tumor.
At the time of discharge, his blood pressure and blood glucose were normal. Upon review on 28th February 2017, his BP was 130/80 mmHg without antihypertensive medicine. Blood glucose fasting was 90 mg/dL and post-prandial 66 mg/dL, with an HbA1C of 6.1% without any antidiabetic medicine. The levels of 24-h urinary metanephrines and normetanephrines were 62 and 604, mcg, respectively.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [115.0, 'mg/dL'], 'Sodium': [141.0, 'mEq/L']}",141.36,134.292,148.428,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 141.0 mEq/L. 
The concentration of glucose is 115.0 mg/dL. 
Plugging in these values into the formula gives us 141.0 mEq/L + 0.024 * (115.0 - 100) = 141.36 mEq/L.
Hence, the patient's corrected concentration of sodium is 141.36 mEq/L."
5449,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7396026-1,Extracted,"A previously healthy 44-year-old male with no prior comorbidities presented to emergency with a 2-day history of fever, worsening headache, and generalized weakness. He had no history of exposure to pool water. Examination revealed a Glasgow coma scale (GCS) of 14/15 with no focal deficit or neck stiffness. Laboratory workup was sent which showed leukocytosis 13.3 × 109/L. Rest of the investigations are summarized in . Computed tomography (CT) scan brain was performed which was reported normal. Lumbar puncture was performed which showed a raised opening pressure of 20 cm of water and had a raised leucocyte count of 1100/µL with predominant polymorphonuclear cells of 60% with a very high protein of 241 mg/dl and low glucose, i.e., 30 mg/dl (). The BioFire filmarray Polymerase chain reaction (PCR) was negative for bacteria and viruses, but wet mount prep for Naegleria fowleri was positive which was further confirmed with PCR.
The patient was started on Primary amebic meningoencephalitis (PAM) protocol which included Intravenous (IV) and intrathecal amphotericin-B, Per Oral (PO) miltefosine, IV rifampin, IV fluconazole, and IV dexamethasone. He was electively intubated and shifted to the intensive care unit (ICU). A repeat CT scan after 24 hours of hospital stay was performed which did not show any infarct or bleed but did show marked cerebral edema. He was started on mannitol 30 grams every 8 hours, which was stopped after 48 hours.
During the ICU stay, the patient remained on mechanical ventilation and was deeply sedated with agents, IV propofol and midazolam. Antiepileptic drug IV levetiracetam was added empirically, and an Electroencephalogram (EEG) was obtained which showed theta and delta slowing down with no epileptiform activity. He was kept well hydrated during the ICU stay, and continuous feeding was carried out through a nasogastric tube.
On the 3rd hospital day, the patient started producing urine at 300–500 ml/hour (he made a urine output of more than 7 liters in 24 hours). His sodium levels increased from 144 mmol/L to 175 mmol/L in 12 hours. His urea was 18 mg/dl, ionized calcium was 4.88 mg/dl, and blood sugar levels were 171 mg/dl. He was well hydrated with IV ringer lactate. Serum and urinary osmolality were performed which were 332 mosm/kg and 204 mosm/kg, respectively. Urine sodium was less than 10 mEq/L. He was started on PO desmopressin of 0.2 micrograms twice daily after which his urine output dropped to 60–80 ml/hour and sodium decreased from 175 to 162 and, later, 155 mmol/L. On the 4th hospital day, he went in asystole and died. His family had decided for Do Not Resuscitate (DNR) during the ICU admission keeping in view of the poor outcome of primary amoebic meningoencephalitis.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [171.0, 'mg/dL'], 'Sodium': [175.0, 'mmol/L']}",176.704,167.8688,185.5392,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 175.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 175.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 175.0 mmol * 1 mEq/mmol = 175.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 175.0 mmol sodium/L converts to 175.0 mEq sodium/L. 
The concentration of glucose is 171.0 mg/dL. 
Plugging in these values into the formula gives us 175.0 mEq/L + 0.024 * (171.0 - 100) = 176.704 mEq/L.
Hence, the patient's corrected concentration of sodium is 176.704 mEq/L."
5450,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3970048-1,Extracted,"A 28-year-old African American male with uncontrolled type II diabetes mellitus arrived at the emergency department with sudden pain in the right lower extremity and difficulty bearing weight. The patient described the pain as aching, 10 out of 10 during maximal intensity with no relation to movement and no alleviating factors. He denied any preceding trauma or similar episodes in the past. On admission, he was afebrile with a pulse rate of 124 and blood pressure of 113/78. Examination of the left inner thigh revealed erythema, warmth, and a nonhealing, circumferential wound with no evidence of discharge or induration. The right lower extremity was unremarkable. Laboratory values revealed an elevated leukocyte count of 14.82 cells/mcl, with neutrophils of 84%. Random glucose was 660 mg/dL, K+ 3.7 mmol/liter, and Na+ 129 mmol/liter with an anion gap of 20. Other laboratory findings included a serum lactate level of 4.7 with creatine kinase levels of 176/U/L. Hemoglobin A1c was 16%. Antinuclear antibody (Ab), jo-1 Ab, scl-70 Ab, proteinase 3a-Ab, and myeloperoxidase Ab were negative. Serology was negative for HIV and hepatitis A, B, and C and there was no bacterial or fungal growth on blood cultures.
Computerized tomography of the left thigh revealed irregular internal contrast enhancement and hypoattenuation of the vastus medialis. A complex suprapatellar joint effusion was also noted. Magnetic resonance imaging of the same area revealed generalized subcutaneous edema with diffuse signal abnormality involving the vastus medialis, lateralis, and intermedius muscles suggesting diffuse inflammatory changes. An ultrasound guided biopsy of the left thigh muscle was performed. Pathology showed necrotic and atrophic skeletal muscle infiltrated by necrotic neutrophils. A fragment of extensively fibrotic and atrophic skeletal muscle with mild mononuclear inflammation and hemosiderin deposition was noted. Gram stain was negative for bacteria. The patient received adequate pain control throughout the hospital course with management aimed towards achieving optimal glycemic control.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [660.0, 'mg/dL'], 'Sodium': [129.0, 'mmol/L']}",142.44,135.318,149.562,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 129.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 129.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 129.0 mmol * 1 mEq/mmol = 129.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 129.0 mmol sodium/L converts to 129.0 mEq sodium/L. 
The concentration of glucose is 660.0 mg/dL. 
Plugging in these values into the formula gives us 129.0 mEq/L + 0.024 * (660.0 - 100) = 142.44 mEq/L.
Hence, the patient's corrected concentration of sodium is 142.44 mEq/L."
5451,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7434292-1,Extracted,"Emergency medical services (EMS) were called to the home of a four-year-old female with a history of intermittent asthma and recent outpatient diagnosis of pneumonia after found to be cyanotic, surrounded by emesis, and without apparent respirations. Cardiopulmonary resuscitation was initiated by EMS upon arrival for pulseless electrical activity, and after eight minutes the patient achieved return of spontaneous circulation. She was subsequently intubated without the need for induction medications and transported to the emergency department (ED). Upon arrival to the ED, an initial physical exam revealed an intubated, unresponsive child with markedly diminished lung sounds bilaterally without wheezing, and an oxygen saturation of 60% on 100% fraction of inspired oxygen (FiO2). Additionally, respiratory therapy reported extreme difficulty with ventilation. Initial bedside chest radiographs (CXR) () were obtained and showed evidence suggestive of bilateral pneumothoraces, which in conjunction with the patient’s clinical picture prompted bilateral chest tube placement. Both returned large volumes of serous fluid, although no blood or air.
Continuation of the primary survey revealed tachycardia at 132 beats per minute with strong and regular peripheral pulses in all extremities. There was no jugular venous distention. The abdomen was soft without masses. A limited neurologic exam revealed bilateral sluggish pupils, with the right pupil at 6 millimeters (mm) and the left pupil at 3 mm. There were no obvious signs of trauma, and no dermatologic findings.
After initial stabilization, collateral history was obtained from the mother who stated the patient had been feeling tired with intermittent fevers over the prior few days, which led to a diagnosis of mild viral pneumonia by her outpatient pediatrician. Per her electronic health record, this was based on the patient’s age, gradual onset of symptoms with non-toxic appearance, and non-focal pulmonary findings on auscultation. Imaging and medications were therefore deferred, but return precautions were given should the patient’s clinical presentation worsen. With regard to her asthma, the patient had only occasionally used an inhaler for night-time coughing but otherwise had never been admitted, intubated, or prescribed oral steroids. She additionally denied any other known medical conditions, surgical history, allergies, or red flags to suggest the potential for non-accidental trauma.
Shortly thereafter, initial laboratory values resulted in a white blood cell count of 428,000 per milliliter (/mL) (4,400–12,900/mL) with a 96% blast differential, hemoglobin of 6.7 grams per deciliter (g/dL) (11.4–14.3 g/dL), and platelet count of 27,000/mL (187,000–445,000/mL). An electrolyte panel was significant for a sodium of 131 milliequivalents per liter (mEq/L) (135–145 mEq/L), potassium of 8.7 mEq/L (3.6–5.2 mEq/L), chloride of 102 mEq/L (102–112 mEq/L), bicarbonate of 10 mEq/L (19–26 mEq/L), blood urea nitrogen of 16 milligram per deciliter (mg/dL) (7–20 mg/dL), creatinine of 0.61 mg/dL (0.19–0.49 mg/dL), and a glucose of 461 mg/dL (70–140 mg/dL). An arterial blood gas resulted in a pH of 6.75 (7.35–7.45), PaCO2 of 60.6 mm/Hg (35–45 mmHg), PaO2 of 59.7 millimeters of mercury (mm Hg) (75–100 mm Hg), lactate of 12.14 mEq/L (0.2–1.8 mEq/L), HCO3 of 8.3 mEq/L (19–26 mEq/L), with the FiO2 at 100%. An alveolar-arterial gradient was calculated to be in excess of 577 mmHg (estimated normal gradient for the age of this patient is 5 mmHg).
Non-contrasted computed tomography (CT) of the head showed no evidence of intracranial abnormalities. Following the patient’s stabilization, the official read of the bedside CXR by pediatric radiology instead revealed a large mediastinal mass, manifesting features similar to that of bilateral pneumothoraces. Due to the patient’s age and concern for radiation, the patient did not receive CT of the chest as part of her initial workup. The patient was subsequently admitted for hyperleukocytosis with leukostasis and, in conjunction with hematology oncology, was started on leukapheresis and, later, induction chemotherapy. Over the course of the week, the patient’s clinical status continued to improve, and she was extubated and discharged home with a diagnosis of T-cell acute lymphoblastic leukemia.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [461.0, 'mg/dL'], 'Sodium': [131.0, 'mEq/L']}",139.664,132.6808,146.6472,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 131.0 mEq/L. 
The concentration of glucose is 461.0 mg/dL. 
Plugging in these values into the formula gives us 131.0 mEq/L + 0.024 * (461.0 - 100) = 139.664 mEq/L.
Hence, the patient's corrected concentration of sodium is 139.664 mEq/L."
5452,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6607589-1,Extracted,"A 26-year-old Sinhalese woman was transferred from a local hospital with a history of reduced urine output, shortness of breath, reduced level of consciousness, abdominal pain, vomiting, and mild degree fever of 2 days’ duration. Her bilateral lower limbs were edematous but she was not pale or icteric. Her pulse rate was 112 beats per minute and blood pressure was 140/70 mmHg. An abdominal examination did not reveal organomegaly. Bilateral lower zone crepitations were noted on lung auscultation. Her respiratory rate was 20 cycles per minute and oxygen saturation was 97% on air. She had right-sided lower motor type facial nerve palsy. Glasgow Coma Scale was 13/15. The rest of the neurological examination including other cranial nerves and ophthalmoscope examination was unremarkable.
Our initial working diagnosis was leptospirosis with acute kidney injury and treatment was initiated accordingly (intravenously administered antibiotic and hemodialysis via femoral vascular catheter), but we could not explain the cranial nerve involvement. The following day she came out with the history of a suicide attempt in which she had self-ingested brake oil (amount not clear) after a conflict with her husband.
On admission her renal functions were deranged with serum creatinine of 352 μmol/ L, blood urea of 14.1 mmol/l, Na+ 140 mmol/l, and K 5.2 mmol/l. Arterial blood gas showed pH 7.08, partial pressure of oxygen (PO2) 94, partial pressure of carbon dioxide (PCO2) 28, bicarbonate (HCO3) 13.8, and base excess − 18 mEq per liter. Her serum osmolality was 339 mosmols with an osmolar gap of 20 mOsm/kg and anion gap was 32 mEq/l. Although relevant, her urine was not examined for calcium oxalate crystals. Full blood count showed hemoglobin of 12.7 g/dl, platelet of 185 × 106/L, and white cell count of 15.2 × 106/L. Her C-reactive protein was 22 mg/dl. Her random blood sugar was 92 mg/dl. Her blood and urine cultures were negative. Her pro-calcitonin levels were within normal range. A chest X-ray did not reveal any abnormality such as consolidation or pleural effusion. A non-contrast computed tomography (CT) scan of her brain was normal. Leptospira antibody tested after 10 days of disease was negative. She was started on initial consecutive daily dialysis followed by every other day dialysis which yielded a considerable improvement in renal functions. After 10 days of hospital stay she was discharged with residual facial nerve palsy. Over the course of 3 months’ clinic follow-up she had complete renal and neurological improvement.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [92.0, 'mg/dL'], 'Sodium': [140.0, 'mmol/L']}",139.808,132.8176,146.7984,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 140.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 140.0 mmol * 1 mEq/mmol = 140.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mmol sodium/L converts to 140.0 mEq sodium/L. 
The concentration of glucose is 92.0 mg/dL. 
Plugging in these values into the formula gives us 140.0 mEq/L + 0.024 * (92.0 - 100) = 139.808 mEq/L.
Hence, the patient's corrected concentration of sodium is 139.808 mEq/L."
5453,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4445477-1,Extracted,"A 6-year-old girl was admitted to the hospital after three episodes of generalized, tonic seizures. Two days before admission, she developed watery diarrhoea and repeated vomiting.
Her perinatal history was complicated by premature birth (34th week) with weight 2200 g, Apgar scale −10. Her motor development was delayed in the first 2 years of life.
At admission, the girl complained about moderate abdominal pain and watery stools.
Physical examination showed a body temperature of 37.4 °C, pulse rate of 110 beats/min and blood pressure of 116/60 mmHg. The abdomen was soft, but painful. The bowel sounds were increased. Neurologic examination showed normal condition without pathological reflexes.
Laboratory findings presented the following: leukocyte count 4800/μL, erythrocyte count 4,920,000/μ, platelet count 253,000/μL, haemoglobin 13.3 g/dL and glucose 77 mg/dL. The serum electrolyte levels were as follows: sodium 137 mmol/L, potassium 4.89 mmol/L, calcium 2.49 mmol/L and magnesium 19.3 mmol/L. Aspartate aminotransferase was 49 U/L and alanine aminotransferase 26 U/L. C-reactive protein was elevated to 2.57 mg/dL. Serum samples showed an absence of antibodies against cytomegalovirus, Epstein-Barr, herpes simplex 1 and 2 viruses, Borrelia burgdorferi and Toxoplasma gondii. Lumbar puncture was not performed; cerebrospinal fluid could not be analysed for this patient.
Enzyme immunoassay detection of Rotavirus in the stool was positive. The stool culture and Adenovirus antigen were negative.
On the day of admission, the girl presented six episodes of generalized tonic seizures with lockjaw and flexion of the extremities. The first two episodes lasted up to 1 min and subsided after diazepam. The subsequent ones were shorter and disappeared spontaneously. Between these episodes, the patient’s consciousness was disturbed. During further hospitalization, no seizures were observed.
Brain magnetic resonance imagination (MRI) was performed on the third day after admission using a 3-T scanner (MAGNETOM Spectra, Siemens Healthcare, Erlangen, Germany). T1-weighted examination was performed before and after i.v. administration of gadobutrol (Bayer Vital, Leverkusen, Germany, 0.1 mmol/kg body weight). The imaging showed the hyperintense region in T2-weighted and fluid-attenuated inversion-recovery (FLAIR) MRI, a well-defined lesion in the splenium of the corpus callosum with restricted diffusion in diffusion-weighted MRI (DWI) and no enhancement in post contrast T1-weighted (Fig. ).
An electroencephalogram EEG was performed with a 42-channel DigiTrack system (Elmiko, PL), with electrodes placed in compliance with the international 20-electrode system. Her first EEG (the third day) showed slowed brain activity in the posterior occipitotemporal portion, consisting mainly of theta waves with a frequency of 4.5–5.5 Hz and amplitude of 40 uV.
She was treated with intravenous crystalloids without anticonvulsant control. After the MRI results, dexamethasone therapy (0.4 mg/kg/day for 5 days) was started.
An MRI performed 12 days after admission revealed no abnormal signal in the splenium of the corpus callosum (Fig. ). The EEG (awake and sleep) was completely normal.
The child was sent home without signs of neurological complications. At her follow-up examination 2.5 months later, she had age-appropriate motor skills and behaviour. Her EEG showed normal brain activity.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [77.0, 'mg/dL'], 'Sodium': [137.0, 'mmol/L']}",136.448,129.6256,143.2704,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 137.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 137.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 137.0 mmol * 1 mEq/mmol = 137.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mmol sodium/L converts to 137.0 mEq sodium/L. 
The concentration of glucose is 77.0 mg/dL. 
Plugging in these values into the formula gives us 137.0 mEq/L + 0.024 * (77.0 - 100) = 136.448 mEq/L.
Hence, the patient's corrected concentration of sodium is 136.448 mEq/L."
5454,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-10749,Extracted,"A 36-year-old obese African American female presents to her primary care physician complaining of blurry vision and increased fatigue. Aside from obesity, her past medical history includes multiple candidal infections in the past six months. Her physician sends her for laboratory testing, with the following results: hemoglobin 12.0 g/dL, glucose tolerance test of 212 mg/dL at 2 hours, sodium 137 mEq/L, potassium 4.1 mEq/L, and creatinine 0.9 mg/dL.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [212.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",139.688,132.7036,146.6724,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 137.0 mEq/L. 
The concentration of glucose is 212.0 mg/dL. 
Plugging in these values into the formula gives us 137.0 mEq/L + 0.024 * (212.0 - 100) = 139.688 mEq/L.
Hence, the patient's corrected concentration of sodium is 139.688 mEq/L."
5455,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4208431-1,Extracted,"A 24-year-old woman was admitted for severe malnutrition and dehydration in the context of anorexia nervosa that was diagnosed one year ago. During this time, she had been hospitalized during 4 months with a transitory gain of six kilograms. She was treated with serotonin reuptake inhibitor and denied taking illicit drug or potentially harmful products. On admission, she presented hypotension (90/50 mmHg), sinus bradycardia (40 bpm), slight hypoglycemia (3.9 mmol/L), and hypothermia (35.7°C). She measured 160 cm and her body weight was 36 kg, corresponding to a body mass index (BMI) of 14 kg/m2. At physical examination she was oriented but lethargic and slightly jaundiced. The abdomen was slightly tender without ascites. The liver was not enlarged.
Laboratory data at admission demonstrated the following: glycemia (3.5 mmol/L), Na+ 137 mmol/L (N: 136–144), K+ 3.7 mmol/L (3.6–4.6), total Ca2+ 2.34 mmol/L (N: 2.2–2.52), Mg2+ 1.10 mmol/L (N: 0.65–1.05), P2− 1.22 (N: 0.8–1.5), and osmolality 289 mOsm/kg. Platelets were at 144 G/L (N: 150–350), hemoglobin was at 133 g/L (N: 120–160), and leucocytes were at 6.6 G/L (N: 4–11). The liver function tests was abnormal with a factor V at 33% (N: >70%). Serum aminotransferase levels were increased as follow: AST 208 U/L (N: 11–42), ALT 341 (N: 9–42), and total bilirubin 65 μmol/L (N: 7–25). The vitamin C was normal at 78 umol/L (N: 17–85) as was the thiamine at 208 umol/L (N: 65–200).
She was treated with serotonin reuptake inhibitor and denied taking illicit drug or potentially harmful products. Her treatment was stopped, but laboratory tests continued to deteriorate.
After one week, the laboratory routine tests revealed abnormal hematological tests with hemoglobin at 114 g/L, leucopenia at 2.5 G/L, and thrombocytopenia at 52 G/L. Additional investigations included prealbumin: 121 mg/L (N: 223–380) and albumin: 36 g/L (N: 35–48). Electrolytes remained normal. Renal and thyroid functions were unremarkable. Liver tests were as follows: AST 1088 U/L, ALT 1868 U/L, GGT 138 U/L, PA 102 U/L, and total bilirubin 66 μmol/L. INR was at 1.02 and factor V at 85%. Additional laboratory tests were performed to exclude all possible causes of liver injury. Hepatitis A, B, C, and E, CMV, and HIV tests were negative. Autoantibodies were absent; iron studies and ceruloplasmin were normal. At abdominal ultrasound the liver appeared normal with no ascites. Portal and hepatic veins were unremarkable. Thus, a diagnosis of acute liver injury associated with anorexia nervosa was considered the most plausible diagnosis.
A careful and progressive refeeding was performed, but liver transaminases remained abnormal. Thus, 10 days after hospital admission, a liver biopsy was performed by the transjugular route.
At histology, architecture of the liver was normal without fibrosis. Portal tracts and biliary and vascular structures were normal. Cytoplasm of hepatocytes was clarified and some acidophil bodies were found predominant in the centrilobular region. In addition, ceroid pigments at the apical pole of the hepatocytes were observed ().
An electron microscopy study was also performed in a fragment of liver biopsy, which showed features that strongly suggested a phenomenon of autophagocytosis: the density of glycogen particles in the hepatocytes was very low, consistent with cytoplasm clarification on PAS staining at the optical microscopy. In addition, the number of both mitochondria and rough endoplasmic reticulum appeared to be reduced. This observation contrasts with an increased number of Golgi bodies and smooth endoplasmic reticulum as well as primary and secondary lysosomes containing digested material (). Eight weeks after admission, with progressive refeeding the test returned back to normal ().","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [3.5, 'mmol/L'], 'Sodium': [137.0, 'mmol/L']}",136.11334,129.30767,142.91901,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 137.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 137.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 137.0 mmol * 1 mEq/mmol = 137.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mmol sodium/L converts to 137.0 mEq sodium/L. 
The concentration of glucose is 3.5 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 3.5 mmol. To convert 3.5 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 3.5 mmol glucose * 0.001 mol/mmol = 0.0035 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0035 mol glucose * 180.16 g/mol = 0.63056 g glucose. To convert 0.63056 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 0.63056 g glucose * 1000.0 mg/g = 630.56 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 630.56 mg glucose/10.0 dL = 63.056 mg glucose/dL. The concentration value of 3.5 mmol glucose/L converts to 63.056 mg glucose/dL. 
Plugging in these values into the formula gives us 137.0 mEq/L + 0.024 * (63.056 - 100) = 136.11334 mEq/L.
Hence, the patient's corrected concentration of sodium is 136.11334 mEq/L."
5456,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8565698-1,Extracted,"A 44-year-old Hispanic woman with type II diabetes mellitus and no prior history of tobacco use was admitted to the hospital after being found unresponsive in her home. On arrival she had a temperature of 36.6 C degrees, heart rate of 126 bpm, respiratory rate of 26, blood pressure of 160/90, and an oxygen saturation of 78% on room air. Her physical exam was remarkable for a Glasgow coma score of 3, dry mucous membranes, and clear lung sounds to auscultation bilaterally. She was intubated upon arrival. Laboratory studies revealed a white blood cell count of 13000, CRP 412, blood glucose 997 mg/dl, serum sodium 160 mmol/L, serum creatinine of 3.72 mg/dL, and serum bicarbonate 11. Her arterial blood gas showed pH of 7.08, PaCO2 37.1, and PaO2 of 96 on 60% fraction of inspired O2 (FiO2) and she tested positive for SARS-CoV-2 by RT-PCR. COVID-19 specific labs were drawn and revealed elevated D-dimer to 1393 and normal values for troponin, BNP, procalcitonin, INR, AST/ALT, and ferritin. The patient was started on an insulin drip for her hyperglycemic syndrome. Her COVID-19 pneumonia was treated with 5 days of both remdesivir 100 mg IV daily and methylprednisolone 30 mg IV twice a day. Due to the critical presentation of the patient, empiric treatment for a possible superimposed bacterial pneumonia was also initiated on hospital day 1 with the broad-spectrum antibiotics cefepime and vancomycin.
The patient’s metabolic derangements improved during the first 3 days of her ICU stay, however her respiratory status worsened and she developed acute respiratory distress syndrome associated with her COVID-19 pneumonia. She required optimization of her ventilatory parameters along with rescue therapies including neuromuscular blockade and prone positioning by hospital day 4. Tracheal aspirate cultures were drawn at this time and revealed Pseudomonas aeruginosa and Aspergillus flavus. The patient was started on voriconazole 250 mg IV twice daily and switched to piperacillin/tazobactam 4.5 g IV every eight hours based on susceptibilities.
Computed tomography of the chest was obtained on hospital day 8 due to worsening hypoxemia and revealed diffuse ground glass opacities (GGO) and multiple cavitary lesions measuring up to 2.1 cm in the right middle and upper lobes ( and ). Micafungin 150 mg IV daily was added to the patient’s treatment regimen on hospital day 9 for invasive pulmonary aspergillosis given her poor response to treatment.
Bronchoscopy was performed on hospital day 13 due to worsening ventilation/perfusion ratio to less than 100 and lack of response to treatment. Multiple gray necrotic-appearing mucosal lesions were visualized bilaterally with near complete destruction of the left upper lobe and lingula. The lesions could be easily detached from the endobronchial wall and were non-friable. Endobronchial biopsy and bronchoalveolar lavage (BAL) were performed on the necrotic appearing lingula and Grocott’s methenamine silver stain on the sample revealed pauciseptated hyphae consistent with zygomycetes. Culture results were significant for isolated Candida albicans, glabrata, and krusei along with Aspergillus flavus and niger. The patient’s hemoglobin A1c was then checked and found to be 13. Given the endobronchial destruction on bronchoscopy, the histopathologic findings, and evidence of poorly controlled diabetes, a clinical diagnosis of pulmonary mucormycosis was made and the patient was then started on treatment with liposomal amphotericin B 5 mg/kg/day.
Despite aggressive therapy, the patient’s condition continued to decline. She required continuous renal replacement therapy and was deemed not to be a candidate for extracorporeal membrane oxygenation given her devastating pulmonary disease and multi-organ dysfunction. The patient expired on hospital day seventeen.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [997.0, 'mg/dL'], 'Sodium': [160.0, 'mmol/L']}",181.528,172.4516,190.6044,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 160.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 160.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 160.0 mmol * 1 mEq/mmol = 160.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 160.0 mmol sodium/L converts to 160.0 mEq sodium/L. 
The concentration of glucose is 997.0 mg/dL. 
Plugging in these values into the formula gives us 160.0 mEq/L + 0.024 * (997.0 - 100) = 181.528 mEq/L.
Hence, the patient's corrected concentration of sodium is 181.528 mEq/L."
5457,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3845239-1,Extracted,"A male patient aged 4 years and 3 months presented to the ER (emergency room) of our hospital with vomiting, diarrhea, and seizures. On day 1 of the illness, he had developed gastrointestinal symptoms, including vomiting and watery diarrhea that occurred 4-5 times per day. Four days later, bilateral generalized tonic-clonic seizures began, for which he was transported to our hospital. The seizures lasted up to 1 minute and subsided spontaneously. The patient was in a restless state of consciousness (level E3V4M5 according to the Glasgow Coma Scale and level II-10 according to the Japan Coma Scale). He stared, averted his gaze, continued to cry, and threw objects. This disturbance of consciousness persisted for 7 hours. The patient was sedated with midazolam, and MRI was performed. On awakening after 2 hours, the patient had regained a normal state of consciousness, after which there was no recurrence of disturbance of consciousness or seizures.
On admission, the patient's vital signs were as follows: temperature, 37.7°C; heart rate, 130 beats/minute; blood pressure, 100/60 mmHg; and SpO2, 98% (room air). No central nervous system abnormality, meningeal irritation, paralysis, or abnormalities in the thoracoabdominal region were observed. MRI revealed a hyperintense signal in the splenium of the corpus callosum on DWI and a hypointense signal in the ADC-map (). The patient's peripheral circulation was good.
The patient's medical history was unremarkable. He was born by spontaneous cephalic delivery after 39 weeks and 3 days of gestation (birth weight, 2664 g). No remarkable observations were noted during the pregnancy or perinatal period. The patient's growth and development were normal. The family medical history revealed that the father had febrile seizures.
The results of the patient's biochemical blood tests were as follows: WBCs, 3900/μL; Hb, 13.4 g/dL; Plt, 26.1 × 104/μL; BUN, 16 mg/dL; Cre, 0.3 mg/dL; Na, 132 mEq/L; K, 4.5 mEq/L; Cl, 101 mEq/L; AST, 41 IU/L; ALT, 21 IU/L; CRP, 2.59 mg/dL; Glu, 84 mg/dL; lactic acid, 7.8 mg/dL; pyruvic acid, 0.32 mg/dL; NH3, 49 μg/dL; pH, 7.424; PCO2, 39.6 mmHg; HCO3, 25.5 mmol/L; and BE, 1.6 mmol/L. No abnormality was detected on blood amino acid analysis or tandem mass screening. Cerebrospinal fluid (CSF) examination revealed a cell count of 4 cells (all mononuclear), a glucose concentration of 95 mg/dL, and a total protein concentration of 16 mg/dL.
On day 2 of admission, an electroencephalogram was obtained during sedated sleep. The spindle wave was appropriate for the patient's age. No bursts were observed. The patient's stool was positive for RV antigen. RT-PCR did not reveal RV RNA in the blood or CSF. RT-PCR analysis of RNA extracted from the stool revealed that the RV genotype was G5P[6].
On day 5 of admission, no recurrences were observed, and the patient was discharged. Eight days after admission, all abnormal signals had disappeared (). The clinical course was typical of MERS.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [84.0, 'mg/dL'], 'Sodium': [132.0, 'mEq/L']}",131.616,125.0352,138.1968,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 132.0 mEq/L. 
The concentration of glucose is 84.0 mg/dL. 
Plugging in these values into the formula gives us 132.0 mEq/L + 0.024 * (84.0 - 100) = 131.616 mEq/L.
Hence, the patient's corrected concentration of sodium is 131.616 mEq/L."
5458,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4572425-1,Extracted,"A 59-year-old Caucasian female with history of recurrent bilateral pleural effusions was admitted with worsening dyspnea and a nonproductive cough present over the course of one week. She had undergone outpatient right-sided thoracentesis on the day prior to admission, with drainage of 1500 mL of pleural fluid.
The recurrent pleural effusions had been occurring for three months prior to this presentation, and she had undergone thoracentesis twice for the right-sided pleural effusion and six times for the left-sided pleural effusion without any conclusive diagnosis. Results from all of thoracentesis procedures were suggestive of transudative effusions and cultures were negative.
On physical exam, this patient was mildly dyspneic but without retractions or accessory muscle use. There were decreased breath sounds at both lung bases. Temperature was 98.5°F, heart rate was 94/min, respiratory rate was 18/min, blood pressure was 97/55 mm Hg, and oxygen saturations were 99% on room air. Complete blood count and basic metabolic panel showed WBC 8.6 thou/μL, Hb 14.1 g/dL, Hct 44.2 g/dL, Plt 356 thou/μL, sodium of 140 mmol/L, potassium of 4 mmol/L, chloride of 101 mmol/L, bicarbonate 32 mmol/L, BUN 13 mg/dL, Creatinine 0.8 mg/dL, and glucose 112 mg/dL. Serum immunofixation electrophoresis showed small lambda monoclonal protein and no Bence-Jones proteinuria. Chest X-ray taken at the time of admission demonstrated a moderate to large left-sided pleural effusion as well as a right lower lobe consolidation. CT scan of chest showed bilateral pleural effusions, greater on the left side (). During her hospitalization, the patient underwent thoracentesis which showed WBC 484 mm3, RBC 38 mm3, lymphocyte count of 99%, monocyte count of 1%, glucose of 106 mg/dL, total bilirubin of 2.4 gm/dL, lactate dehydrogenase (LDH) of 80 U/L, amylase 19 U/L, cholesterol of 45 mg/dL, triglyceride 17 mg/dL, and adenosine deaminase of 2.3 U/L, and the cultures for routine, acid fast bacilli, and fungus were negative. Cytology demonstrated benign findings with numerous lymphocytes present. The patient underwent biopsy of the left upper lobe of the lung as well as chemical pleurodesis for her recurrent left-sided pleural effusion. Lung biopsy showed diffuse pulmonary amyloidosis, and Congo Red staining was positive confirming the diagnosis (Figures 
–). Biopsy of the pleura was negative for any pathologic findings.
The patient underwent hematology/oncology evaluation. Echocardiogram showed left concentric ventricular hypertrophy. Rheumatoid factor and thyroid stimulating hormone levels were normal. Follow-up immunoglobulin and electron microscopy as well as bone marrow biopsy were performed and favored plasma cell myeloma over primary amyloidosis. There were 6% plasma cells on aspirate smears and 15–20% on CD138 immunohistochemical staining of biopsy and clot sections. Flow cytometry showed 1.4% of monoclonal plasma cells typical of a plasma cell dyscrasia.
The patient was started on Cyclophosphamide, Dexamethasone, and Bortezomib (Velcade) therapy and was discharged in stable condition with outpatient follow-up. She had no recurrent pleural effusions at four-month follow-up.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [112.0, 'mg/dL'], 'Sodium': [140.0, 'mmol/L']}",140.288,133.2736,147.3024,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 140.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 140.0 mmol * 1 mEq/mmol = 140.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mmol sodium/L converts to 140.0 mEq sodium/L. 
The concentration of glucose is 112.0 mg/dL. 
Plugging in these values into the formula gives us 140.0 mEq/L + 0.024 * (112.0 - 100) = 140.288 mEq/L.
Hence, the patient's corrected concentration of sodium is 140.288 mEq/L."
5459,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4365329-1,Extracted,"A 54-year-old white female presented with abdominal pain, nausea, vomiting, and diarrhea (five watery bowel movements every day) for 2 days. The patient states that she has been eating a regular diet and denied eating outside the home and did not have fever, and no one in the family had similar symptoms. Past medical history was positive for hypothyroidism and bipolar disorder and family history was negative for diabetes. One year prior to this presentation the patient had routine blood work with fasting blood glucose of 95 mg/dL. The patient reported polyuria and polydipsia for one month prior to this presentation but did not seek any medical attention.
On physical examination her blood pressure was 127/65 mmHg, heart rate 80 beat/min, and temperature 37°C. Her body mass index was 35 kg/m2. She was in mild distress and had no thyromegaly, clear lungs, regular heart without murmurs, soft abdomen but with generalized tenderness, and hyperactive bowel sounds throughout. The remainder of the physical exam was normal.
WBC 14.8 × 109/L with neutrophils 89%, hemoglobin 18.2 g/L, and platelets 241 × 109/L. Her chemistry shows sodium 132 mmol/L, potassium 3.9 mmol/L, chloride 99 mmol/L, bicarbonate 12 mmol/L, BUN 5.71 mmol/L, creatinine 53.3 μmol/L, calcium 2.35 mmol/L, phosphorus 1.55 mmol/L, magnesium 1.1 mmol/L, and blood glucose 18.76 mmol/L. Arterial blood gases show PH 7.25, Pco2 3.72 kPa, and Po2 9.58 kPa on room air. Lactic acid was 1 mmol/L, amylase 1.1 μkat/L, and lipase 0.27 μkat/L, and serum ketones were positive. Her hemoglobin A1C was 13.7%. Urinalysis was positive for glucose and ketones.
It was obvious from the labs that the patient had diabetic ketoacidosis (high blood glucose, low bicarbonate, and positive ketones) with anion gap of 21. The patient was admitted to the medical intensive care unit. Intravenous normal saline fluid bolus was given with maintenance intravenous fluid after that. She was kept on nothing per mouth and started on insulin drip with hourly blood glucose check and every four hours serum electrolytes (sodium, potassium, chloride, magnesium, and phosphorus) check.
CT scan of the abdomen showed mild distension of the proximal small bowel and tiny amount of free fluids with wall thickening of distended small bowel loops. She was started on ampicillin/sulbactam after getting blood cultures. Stool sample was sent for analysis and the results were negative leukocytes and negative clostridium difficile toxin. Therefore, we decided to stop the antibiotics at this point and treat her as viral gastroenteritis. Later on, the patient's symptoms have improved and her anion gap closed, so we started her on liquid diet (which she was able to tolerate). She was switched to subcutaneous insulin injections (as insulin glargine at bedtime and sliding scale insulin before each meal) and transferred to medical floor. Her blood cultures did not grow any bacteria, and stool culture was negative. Insulin autoantibodies were negative, c-peptide was lower than normal (0.34 ng/mL), and her glutamic acid decarboxylase autoantibodies were highly positive (>30 U/mL).
After having diabetic education including a dietitian consult in the hospital, the patient was discharged home on subcutaneous insulin treatment with a diagnosis of latent autoimmune diabetes in adult. The patient was encouraged to do regular exercise.
The patient was concerned about her new diagnosis and its possible complications which required counseling about the importance of taking care of her diabetes and how this would help prevent future complications.
The patient was very compliant with the discharge plan and checked her blood sugar before each meal and at bedtime. She followed up in the diabetic clinic on a biweekly basis to adjust her insulin dose. Three months later her hemoglobin A1C was 7.7%. The patient has not experienced any adverse or unanticipated events.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [18.76, 'mmol/L'], 'Sodium': [132.0, 'mmol/L']}",137.71152,130.82594,144.5971,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 132.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 132.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 132.0 mmol * 1 mEq/mmol = 132.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 132.0 mmol sodium/L converts to 132.0 mEq sodium/L. 
The concentration of glucose is 18.76 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 18.76 mmol. To convert 18.76 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 18.76 mmol glucose * 0.001 mol/mmol = 0.01876 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.01876 mol glucose * 180.16 g/mol = 3.3798 g glucose. To convert 3.3798 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 3.3798 g glucose * 1000.0 mg/g = 3379.8 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 3379.8 mg glucose/10.0 dL = 337.98 mg glucose/dL. The concentration value of 18.76 mmol glucose/L converts to 337.98 mg glucose/dL. 
Plugging in these values into the formula gives us 132.0 mEq/L + 0.024 * (337.98 - 100) = 137.71152 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.71152 mEq/L."
5460,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6935333-1,Extracted,"A six-year-old girl was brought by her mother to the pediatric outpatient department of a tertiary care hospital in Karachi with a 15-day history of a persistent dull headache. The headache was more prominent on the left side of her face and was associated with nausea. Her mother also reported that since the past three days, she was unable to open her left eye. She had a swelling on the left side of the face, extending behind the ear up to the jawline.
The general physical examination was unremarkable. She was alert and oriented to time and place. Her vitals were taken which showed a heart rate of 96/min, respiratory rate of 30/min, afebrile and blood pressure of 100/70 mmHg. Her random blood sugar was 97 mg/dl. Pertinent examination finding included two palpable jugulodigastric nodes and the largest was more than 1 cm in size, soft in consistency, and neither was matted. Systemic examination revealed ptosis of the left eye with mild proptosis along with the presence of external and internal ophthalmoplegia. Her pupils were unequal, dilated, sluggishly reactive to light. The right pupil was reactive to light with intact direct and consensual reflexes, as compared to the absence of both reflexes in the left pupil. Systemic examination otherwise was unremarkable. Initially, the patient was managed with continuous observation for signs of raised intracranial pressure (ICP) and blood pressure was monitored periodically.
Her laboratory investigations were as follows: hemoglobin (Hb) 12.6 mg/dl (normal range: 12.0-15.5 mg/dl), total leukocyte count (TLC): 11200/mm3 (normal range: 3600-11,200/mm3), erythrocyte sedimentation rate (ESR): 5 mm 1st hour (normal: <20 mm/hr), blood urea nitrogen (BUN): 7 mg/dl (age-appropriate normal range: 7-10 mg/dl), creatinine: 0.2 mg/dl (age-appropriate normal range: 0.3-0.5 mg/dl), sodium: 135 mEq/L (normal range: 135-145 mEq/L), potassium: 3.9 mEq/L (normal range: 3.5-5.0 mEq/L), chloride: 98 mEq/L (normal range: 96-106 mEq/L), calcium: 9.8 mg/dl (normal range: 8.5-10.5 mg/dl), magnesium: 2 mEq/L (normal range: 1.5-2.3 mEq/L), uric acid: 2 mg/dl (normal range: 2.0-5.5 mg/dl), lactate dehydrogenase (LDH): 110 IU/L (normal range: 60-170 IU/L). During the course of her hospital stay, intravenous (IV) ceftriaxone, IV vancomycin and IV metronidazole were administered on suspicion of brain abscess.
A consultation for ophthalmology findings was taken, which showed normal visual acuity of 6/6 in both eyes. Her right eye appeared normal and the left eye had complete ptosis with a frozen eyeball, dilated pupil and mild proptosis. Vitreous media was clear and fundus was normal. The patient was suspected to have “orbital apex syndrome”, which is defined as the simultaneous dysfunction of the optic nerve and the cranial nerves (manifesting with vision loss, ptosis, and a complete internal and external ophthalmoplegia) as a result of a process occurring in the region of the optic canal and the superior orbital fissure. On neurological consultation, plain computed tomography (CT) scan of the brain was normal, while CT scan with contrast of the brain showed no space-occupying lesion. The patient was advised to undergo an urgent magnetic resonance imaging (MRI), which revealed a well-defined abnormal single intensity lesion in left masticator space involving the medial pterygoid, lateral pterygoid, masseter and temporalis muscles causing pressure remodeling of the pterygoid plate, and returning hypointense signals on T1-weighted images (T1WI), heterogeneously hyper-intense signals on T2-weighted images (T2WI), and fluid-attenuated inversion recovery (FLAIR) sequences without restriction on diffusion-weighted magnetic resonance imaging (DWI-MRI) and showed heterogeneous post-contrast enhancement with foci necrosis, which measured 5.9 x 4.2 x 4.1 cm (Figures ). Superiorly, it was extending into infratemporal fossa causing widening of pterygomaxillary fissures and also into extradural space of left middle cranial fossa through foramen ovale involving adjacent dura matter. It was also involving the left cavernous sinus encasing and displacing the internal carotid artery and blocking the left optic canal. Laterally, it was causing pressure remodeling of the left mandibular ramus. Inferiorly, it was extending up to the mandibular angle. There was no midline shift and ventricles were of the normal size. The findings were suggestive of an aggressive lesion in left masticator space with intracranial and cavernous sinus extension. The differential diagnosis that was considered included schwannoma, neurofibroma, and rhabdomyosarcoma; histopathology was recommended for confirmation.
On histopathology, the lower pole was undifferentiated and densely cellular with light and dark cell appearance with sheets of small, round, uniform cells with scant clear cytoplasm. These cells frequently contained amphophilic glycogen vacuoles that were divided into irregular lobules by fibrous strands. There was also the presence of large pleomorphic cells in an organoid pattern, with large areas of perivascular tumor necrosis. These findings were suggestive of ES. Immunohistochemistry was subsequently done and showed positive results for cluster of differentiation 99 (CD99) and friend leukemia integration 1 transcription factor (FLI-1) tumor markers, thus confirming the diagnosis of ES. Due to widespread metastasis (stage IV) of the tumor, the patient was kept on palliative care and the parents were counselled about the poor prognosis. The parents decided to leave against medical advice (AMA). Unfortunately, the patient died 10 days later.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [97.0, 'mg/dL'], 'Sodium': [135.0, 'mEq/L']}",134.928,128.1816,141.6744,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 135.0 mEq/L. 
The concentration of glucose is 97.0 mg/dL. 
Plugging in these values into the formula gives us 135.0 mEq/L + 0.024 * (97.0 - 100) = 134.928 mEq/L.
Hence, the patient's corrected concentration of sodium is 134.928 mEq/L."
5461,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3221905-1,Extracted,"A 35-year-old woman came to our emergency department complaining of severe general weakness and epigastric pain for the last 5 days. In her past medical history, she was diagnosed with AN and borderline personality disorder at a local psychiatric clinic 5 years ago. The only meals she used to have on a daily basis were milk and fruits for a period of 17 years, and even her daily meal intake rapidly decreased after her mother went abroad two weeks ago. This was because she appeared to be extremely dependent on her mother. She did not have any history of diabetes mellitus, hypertension, or hepatitis previously. However, she had taken psychiatric medications for 6 months approximately 5 years ago. In addition, she also intermittently took medications for amenorrhea and osteoporosis.
On admission, her vital signs were: blood pressure of 90/60 mm Hg, pulse rate of 60 beats/min, respiration rate of 20 breaths/min, and body temperature of 36.5℃. She was alert, but looked chronically ill and cachexic. Her body weight was 30 kg and body mass index was 11.71 kg/m2. She had a severely dehydrated tongue, but her chest and abdomen physical examination showed no abnormalities. Her laboratory examinations were as follows; white blood cell 8,940/mm3, hemoglobin 15.8 g/dL, hematocrit 43.8%, platelet 70,000/mm3, random blood glucose 132 mg/dL, blood urea nitrogen/creatinine 35.9/0.44 mg/dL, total protein/albumin 5.6/3.6 g/dL, aspartate aminotransferase/alanine aminotransferase 471/374 IU/L, total bilirubin 1.90 mg/dL, Na/K 127/2.6 mEq/L, Ca/P/Mg 8.5/5.3/1.6 mg/dL, total cholesterol 116 mg/dL, triglyceride 38 mg/dL, high density lipoprotein-cholesterol 74 mg/dL, low density lipoprotein-cholesterol <10 mg/dL, T3 0.43 ng/mL (0.78-1.82 ng/mL), free T4 0.94 ng/mL (0.85-1.86 ng/mL), thyroid stimulating hormone 1.71 mIU/L (0.17-4.05 mIU/L), adrenocoticotropic hormone 11.44 pg/mL (6.00-56.70 pg/mL), cortisol 17.40 ug/dL (9.41-26.06 ug/dL), and aldosterone 31.66 pg/mL (40-102 pg/mL). Initial cardiac biomarkers were elevated as follows; creatine kinase-MB 154.30 ng/mL (0-5 ng/mL), troponin-I 2.580 ng/mL (0-0.78 ng/mL) and N-terminal pro-B-type natriuretic peptide 8,963 pg/mL (0-155 pg/mL). Her chest X-ray and abdomen computed tomography showed no significant lesions associated with epigastic pain. Initial electrocardiogram showed sinus rhythm (60 beats/min), prolonged corrected QT interval (543 ms), pathologic Q waves in II, III, aVF and V1-V3, inverted T waves in II, III and aVF and poor R progression in precordial leads (). Echocardiogram revealed large akinetic areas around the apical, inferior, anterior and lateral sides with hypercontraction of the basal segments, linear echogenic mural thrombus, pericardial effusion, and a reduction of ejection fraction to 36% (). Therefore, we strongly suspected that she was SICMP because of her characteristic echocardiograhic findings.
Only standard medical treatment was given to the patient since she and her guardian refused to receive a coronary angiogram. Therefore, we started the treatment with low molecular weight heparin, and nutrition support with immediate multi-systemic interventions. Psychiatric consultation was also accompanied by medical therapy. After three days, we stopped anticoagulation therapy due to aggravated thrombocytopenia and prolonged prothrombin time (PT). Overall, her daily oral intake increased together with her body weight, 33 kg compared to 30 kg in the beginning. Electrolyte imbalance, liver dysfunction, and thrombocytopenia were also normalized. Two weeks later, the next follow-up echocardiogram indicated a significant improvement of the LV ejection fraction (42%) and wall motion abnormalities. On the other hand, apical mural thrombosis still remained and pericardial effusion increased (). On the next follow-up electrocardiogram, the corrected QT interval decreased to 453 ms. Furthermore, pathologic Q waves, inverted T waves and poor R progression observed in the initial ECG disappeared (). However, she and her guardian strongly insisted on discharging from the hospital against the clinician's recommendation. Although appointments with cardiology and psychiatry departments were arranged with continuing mental support and follow-up echocardiogram, she never came back to the hospital after her discharge.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [132.0, 'mg/dL'], 'Sodium': [127.0, 'mEq/L']}",127.768,121.3796,134.1564,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 127.0 mEq/L. 
The concentration of glucose is 132.0 mg/dL. 
Plugging in these values into the formula gives us 127.0 mEq/L + 0.024 * (132.0 - 100) = 127.768 mEq/L.
Hence, the patient's corrected concentration of sodium is 127.768 mEq/L."
5462,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5415487-1,Extracted,"The patient was a 27-year-old woman with panic disorder taking 20 mg olanzapine daily for 4 months. She was diagnosed with panic disorder at 25 years-of-age, when her random blood glucose (94 mg/dL) and glycated hemoglobin (4.9%) were normal. After starting paroxetine, her weight increased by 20 kg over 1.5 years as a result of hyperphagia and excessive drinking of soft drinks. Paroxetine was switched to olanzapine 4 months earlier. She was referred to Mito Kyodo General Hospital, Mito, Ibaraki, Japan, due to a 3-day history of excessive thirst and disturbed consciousness. She had impaired consciousness (Glasgow Coma Scale E3V3M5). Her blood pressure, pulse rate, and temperature were 154/84 mmHg, 125/min and 37.6°C, respectively, on admission. Laboratory data showed HHS with random blood glucose of 762 mg/dL, sodium of 182 mEq/L and serum osmolality of 430 mOsm/L, as shown in Table . Urine dipstick analysis showed ketones, proteins and glucose. A lumbar puncture showed clear cerebrospinal fluid with no evidence of infection (Table ). No bacteria were detected in blood, urine and cerebrospinal fluid cultures. Rapid antigen-detection assays from a nasopharyngeal swab were negative for influenza A and B. There were no increases of serum immunoglobulin M virus antibodies (Table ), and serum antinuclear antibody was negative. The patient was diagnosed with NMS, because her plasma creatine phosphokinase, white blood cell count and temperature were elevated to 8,530 IU/L, 11,400/μL and 39.5°C, respectively, and hypertension, tachycardia and altered consciousness developed. Furthermore, T2-weighted, diffusion-weighted and fluid-attenuated inversion recovery images of brain MRI carried out on the second hospital day showed high-intensity lesions in the SCC (Figure a), with decreased apparent diffusion coefficient values (Figure b), suggesting MERS.
The patient was treated with rehydration, continuous intravenous insulin infusion and subsequently with ventilator support for 5 days because of her impaired consciousness. Olanzapine was promptly withdrawn. Her body temperature and both the plasma creatine phosphokinase and sodium levels were normalized by the 14th day of admission. After continuous insulin infusion, blood glucose was controlled by multiple daily insulin injections, followed by oral therapy with vildagliptine. Serum C-peptide reactivity measured during multiple daily insulin injections was normal at 2.37 ng/mL (reference range 0.78–5.19 ng/mL). Her consciousness improved completely, and the abnormal SCC lesions were resolved on a follow-up MRI carried out on the 26th day of admission (Figure c).","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [762.0, 'mg/dL'], 'Sodium': [182.0, 'mEq/L']}",197.888,187.9936,207.7824,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 182.0 mEq/L. 
The concentration of glucose is 762.0 mg/dL. 
Plugging in these values into the formula gives us 182.0 mEq/L + 0.024 * (762.0 - 100) = 197.888 mEq/L.
Hence, the patient's corrected concentration of sodium is 197.888 mEq/L."
5463,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4531545-1,Extracted,"A 23-year-old Asian man with chronic renal allograft dysfunction was admitted to our hospital in May 2001 with a 10-day history of fever, intermittent chills, dry cough and progressive dyspnea. He underwent renal transplantation in 1994 for end-stage renal disease of unknown cause diagnosed in 1993. He had been on a medication of cyclosporine 200 mg/day and prednisolne 5–20 mg/day. His temperature was 40°C, blood pressure 120/70 mmHg supine, pulse rate 120/min and respiratory rate 20/min. Respiratory examination revealed mildly decreased breathing sounds on the right lower chest. We also noted several erythematous tender macules measuring 0.5 cm in diameter on both shins. He had no neurological signs of meningitis. Chest radiograph obtained on admission demonstrated increased opacity on the right lower lobe. Arterial blood gas analysis on room air revealed a pH of 7.38, PaCO2 22.1 mmHg, PaO2 49.4 mmHg, and SaO2 85.3%. A complete blood count yielded a leukocyte count of 5,600/mm (91.6% neutrophils), hemoglobin 5.6 g/dL, and platelet count 267,000/mm3. The renal allograft function was in acute exacerbation on chronic dysfunction; BUN 113 mg/dL, Cr 8.5 mg/dL, Na 125 mmol/L, K 6.4 mmol/L, protein 5.2 g/dL, albumin 2.9 g/dL, glucose 102 mg/dL. The patient had been treated with empirical antibiotics for the presumed diagnosis of severe community-acquired pneumonia. On the next day, his respiratory status deteriorated dramatically with a rapid development of hypotension. A repeat chest radiograph showed nearly complete opacification of both lung fields (). The patient was intubated and placed on mechanical ventilation. Dobutamine and dopamine were administered. Urgent anti-CMV IgM, CMV PCR and anti-HIV were negative. Anti-mycoplasma antibody titer was <1:20. Acid-fast bacillus smear and methenamine silver stain of sputum yielded negative results. The initial three sputum and blood cultures were sterile. On the eighth hospital day, tender macules on both shins coalesced to form erythematous patches. Skin biopsy showed granulomatous inflammation in the dermis and numerous yeast organisms with clear thick capsules (). The cerebrospinal fluid (CSF) exam was clear with normal glucose and slightly increased protein (95 mg/dL). The cryptococcal antigen titer was elevated in CSF at >1:256 and at >1:516 in serum. However, the microscopic examination of CSF preparations with India ink was negative for encapsulated yeasts and CSF cultures were negative. The culture of skin biopsy isolated a yeast organism, which was identified as Cryptococcus albidus by characteristic morphology, fermentation, and carbon assimilation tests using the API 20c AUX system (bioMérieu, Marcy-l’Etoile, France). The patient was treated intravenously with fluconazole immediately after the skin biopsy. After 10 days of fluconazole therapy, his chest radiograph and CT scan showed marked clearing with only one cavitary nodular lesion on the left upper lobe (). Percutaneous needle aspiration was performed for the left upper pulmonary nodule. Cytologic examination of the aspirates also revealed a typical morphology of the numerous cryptococci (). The patient was discharged on an oral regimen of fluconazole (200 mg/day). Fluconazole maintenance therapy was continued for 12 months on a long-term basis for prevention of cryptococcosis. At the time of the most recent follow-up, July 2002, his chest radiograph was stable and we detected no evidence of recurrent cryptococcal infection.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [102.0, 'mg/dL'], 'Sodium': [125.0, 'mmol/L']}",125.048,118.7956,131.3004,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 125.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 125.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 125.0 mmol * 1 mEq/mmol = 125.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 125.0 mmol sodium/L converts to 125.0 mEq sodium/L. 
The concentration of glucose is 102.0 mg/dL. 
Plugging in these values into the formula gives us 125.0 mEq/L + 0.024 * (102.0 - 100) = 125.048 mEq/L.
Hence, the patient's corrected concentration of sodium is 125.048 mEq/L."
5464,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4530922-1,Extracted,"A 56-year-old male was brought to the emergency department by paramedics for a syncopal episode and inability to move his lower extremities. He complained of abdominal pain and inability to move his legs beginning five hours prior to arrival. He awakened from a nap that afternoon and experienced numbness in both legs, which progressed to paralysis. At baseline, he was ambulatory without any history of weakness and was last ambulatory hours prior. He endorsed occasional pain in his legs when walking at baseline.
He also complained of abdominal pain with nausea and vomiting for two days. He had a history of alcohol use and reported dark-colored emesis and last bowel movement three days prior. On review of symptoms the patient denied any history of headache, dizziness, chest pain, back pain, trauma, fevers, or extremity weakness. He walked longer than a mile the day prior. History from the patient’s wife revealed that he had an episode of altered level of consciousness while on the couch and that finding combined with his abdominal pain and paralysis prompted her to call 911. The patient’s past medical history was significant for hypertension, peripheral arterial disease, and myocardial infarction 10 years prior. His past surgical history included “abdominal stents” and a left carotid stent. His social history was significant for a 25-pack/year history of smoking and daily alcohol. His medications included atenolol and ranitidine.
Physical exam showed an oral temperature of 36.7°C, blood pressure 107/65mmHg, heart rate 99 beats/minute and a respiratory rate of 30 breaths/min, with oxygen saturation on 15L non-rebreather mask of 94%. His weight was 72.5kg and he appeared older than his stated age. He was alert, cooperative and in moderate distress, primarily complaining of pain and cramping in his lower extremities and repeatedly asking staff to straighten out his legs although they were already lying straight and motionless on the gurney. His head exam was unremarkable with the exception of a dry oropharynx. Cervical spine, cardiac, and lung exams were unremarkable. His abdomen was firm and diffusely tender to palpation with generalized rebound and guarding. An irreducible left inguinal hernia was present. He had vomiting, and placement of a nasogastric tube revealed 1.5 liters of coffee-ground emesis. Lower extremities were thin, cool, and without any palpable or Dopplerable pulses in bilateral femoral, popliteal or pedal distribution. There was trace non-reproducible sensation to the mottled lower extremities, and no sensation distal to the ankles. Motor exam was significant for lower extremity paralysis.
Laboratory data consisted of sodium 121mEq/L (135–145), potassium 6.8mEq/L (3.3–4.8), chloride 89mEq/L (101–111), CO2 18mEq/L (25–34), BUN 31mg/dL (8–26), creatinine 1.5mg/dL (0.5–1.3), and blood glucose 367mg/dL (70–115). White blood cell 19.1thous/mcL (4.0–10.5), hemoglobin 12.8g/dL (13.5–16.9), lipase 107U/L (22–51), hematocrit 38.8% (39.5–50.0), and platelets 165thous/mcL (150–400). There was a left shift in the neutrophils 16.2thous/mcL (85%) (2.0–8.1). Alkaline phosphate 88IU/L (26–110), AST 84IU/L (8–40), ALT 38IU/L (0.0–60), total bilirubin 1mg/dL (0.0–1.4), total protein 5.4g/dL (6.1–8.2), albumin 2.6g/dL (3.2–5.5). Lactate 7.2mmol/L (0.7–2.1). ABG showed pH of 7.25 (7.38–7.42), pCO2 31.6mmHg (36–42), pO2 123.6mmHg (80–104), bicarbonate 13.5mmol/L (21–27). PT was 17.3sec (9.5–12.3), PTT 45.9sec (24.1–35.1), and INR 1.62 (0.87–1.14). B-type natriuretic peptide 1,950pg/mL (<100). Troponin 2.75ng/mL (<0.03).
Chest radiograph was unremarkable. Electrocardiogram (ECG) showed sinus rhythm at 95 beats/minute with ST elevation inferiorly, anteriorly and laterally (). Bedside ultrasound to evaluate the abdominal aorta was limited. Vascular surgery was consulted prior to CT for concern of a vascular catastrophe. Cardiology was consulted for the patient’s ECG findings consistent with myocardial infarction. The patient went for a non-contrast head CT that was unremarkable and a CT angiogram of the chest, abdomen and pelvis, which was significant for the abdominal aorta with no contrast opacification 2.2cm superior to the bifurcation (), high-grade stenosis of the right common iliac artery, complete occlusion of the left common iliac artery, stents in the celiac artery and superior mesenteric artery (SMA), evidence of occlusion of the proximal SMA and inferior mesenteric artery (IMA), hepatic, splenic, bilateral renal infarctions, left inguinal hernia, bowel obstruction, pneumatosis intestinalis with evidence of ischemic bowel, and aspiration in the right lower lung. General surgery was consulted.
The cardiology service stated that the patient was not a candidate for cardiac catheterization and to start anticoagulation and low-dose aspirin if there was no contraindication or planned surgery. They also recommended thrombolytics for the diffuse thrombotic disease. The patient did have an echocardiography study that revealed an ejection fraction of 35% and multiple regional wall motion abnormalities. General surgery recommended comfort measures as he was not a surgical candidate. Vascular surgery commented that bypass would be futile and if patient survived, would be a candidate for extra-anatomical axillo-bifemoral bypass in the future. The patient was admitted to the medical intensive care unit for broad-spectrum antibiotics and a heparin drip and succumbed to his illness the following day.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [367.0, 'mg/dL'], 'Sodium': [121.0, 'mEq/L']}",127.408,121.0376,133.7784,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 121.0 mEq/L. 
The concentration of glucose is 367.0 mg/dL. 
Plugging in these values into the formula gives us 121.0 mEq/L + 0.024 * (367.0 - 100) = 127.408 mEq/L.
Hence, the patient's corrected concentration of sodium is 127.408 mEq/L."
5465,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8123093-1,Extracted,"A 41-year old African-American woman with a history of type 2 diabetes for at least 2 years, obesity (body mass index (BMI), 44 kg/m2), hypertension, hyperlipidemia and sleep apnea presented to the emergency department at an outside hospital with acute worsening of shortness of breath which had begun one week prior to presentation. On presentation she was hypoxic with associated confusion and was emergently intubated and mechanically ventilated. Her diabetes history was notable for a worsening of glucose control over the past two years, with her hemoglobin A1c increasing from 8.4 % to 2018 to 12.8 % in August of 2019 in the setting of medication non-adherence and ongoing depression. At the time of admission, her hemoglobin A1c was 11.6 %. Chart review indicated that she was prescribed Lantus 60 units daily, metformin 1000 mg twice daily, glimepiride 4 mg twice daily with meals and 1.5 mg dulaglutide weekly as an outpatient. Physical exam was notable for acanthosis nigricans.
On admission, laboratory testing was notable for a sodium of 130 mEq/L, potassium 5.0 mEq/L, chloride 93 mmol/L, bicarbonate 16 mmol/L (anion gap 21), blood glucose 760 mg/dL, creatinine 1.65 mg/dL (eGFR 44), lactic acid of 8.33 mmol/L and serum β-hydroxybutyrate of 2.69 mmol/L. Arterial blood gas showed a pH of 7.36, pCO2 of 31 mmHg and pO2 of 55 mmHg, consistent with a mixed anion gap metabolic acidosis and respiratory alkalosis. SARS-CoV-2 PCR testing was positive. See Table for additional laboratory values, including inflammatory markers, which were initially elevated on admission.
Due to the elevated serum ketones and anion-gap metabolic acidosis, she was treated for diabetic ketoacidosis (DKA) with a continuous insulin infusion at 7 units/hr (0.05 units/kg/hr) along with a normal saline infusion. Her blood glucose levels remained elevated in the 400–500 mg/dL range while her anion gap decreased to 15 but did not resolve. Over the next 36 h her insulin infusion rate peaked at 34.5 units/hr (0.26 units/kg/hr) and she was started on 50 units of insulin glargine and 50 units of regular insulin every 6 h in addition to the insulin infusion to facilitate weaning off of the insulin drip. During the first 36 h following transfer to our hospital, she had an average insulin requirement of 5 units/kg/day. Her insulin infusion was weaned off within 48 h and her subcutaneous insulin requirements continued to be elevated at 3.24 units/kg/day. Following extubation on day 6, her insulin requirements dropped to 211 units per day (1.64 units/kg) and she continued to require over 200 units of subcutaneous insulin daily for the next 13 days (Fig. ). Her insulin requirements improved as she was weaned off of heated high flow nasal cannula and transitioned from tube feeds to a diabetic diet. Prior to discharge to a subacute rehabilitation center, she was transitioned to her home regimen of 60 units Lantus, metformin, glimepiride and dulaglutide. While in the hospital she had well-controlled blood sugars on this regimen. Two months after discharge, while still at the subacute rehabilitation center, her hemoglobin A1c was 6.0 %. Her kidney function had returned to her baseline (eGFR > 90).","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [760.0, 'mg/dL'], 'Sodium': [130.0, 'mEq/L']}",145.84,138.548,153.132,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 130.0 mEq/L. 
The concentration of glucose is 760.0 mg/dL. 
Plugging in these values into the formula gives us 130.0 mEq/L + 0.024 * (760.0 - 100) = 145.84 mEq/L.
Hence, the patient's corrected concentration of sodium is 145.84 mEq/L."
5466,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7410506-1,Extracted,"A 68-year-old male with a past medical history of prostate cancer post-radiation, on androgen suppression therapy, hypertension, dyslipidemia, St. Jude aortic valve (St. Jude Medical, Inc., St. Paul, MN) replacement in 2009, heart failure, and atrial fibrillation status post-Medtronic pacemaker (Medtronic plc, Minneapolis, MN) placement in 2014 was seen in the hospital after suffering from out-of-hospital cardiac arrest. The patient was in a casino with his wife when she noticed that he did not appear well; subsequently, he became unconscious. He was found to have pulseless electrical activity by the first responders. Chest compressions were initiated, and he received two rounds of epinephrine, after which he was successfully resuscitated. The patient was intubated in the field and transferred to the hospital. His initial blood laboratory workup showed the following values: blood sugar 238 mg/dL, blood urea nitrogen (BUN) 25, creatinine (Cr) 1.27 mg/dL, glomerular filtration rate (GFR) 56 mL/min, sodium 143 mmol/mL, potassium 3.8 mmol/mL, chloride 110 mmol/mL, bicarbonate 21 mmol/mL, calcium 8.5 mg/dL, magnesium 2.0 mg/dL, creatine phosphokinase (CPK) 641 U/L, creatine kinase MB (CK-MB) 18.38 ng/mL, and troponin 0.240 ng/mL. The ECG showed a ventricular paced rhythm with a prolonged QT interval. The corrected QT interval (QTc) on presentation was 601 ms (Figure ).
The patient was following simple commands off sedation, and therefore, the hypothermia protocol was not initiated. The patient was extubated overnight. He began suffering from multiple runs of sustained ventricular tachycardia (Figure ) and was started on amiodarone initially. The rhythm progressed to TdP (Figure ), and a lidocaine drip was started immediately. He received magnesium sulfate, and the cardiac electrophysiologist was consulted. The patient exhibited an ejection fraction of 40% on echo and was 100% right ventricular paced. Cardiac catheterization did not show significant coronary artery disease. The patient’s pacemaker was upgraded to a biventricular implantable cardioverter defibrillator. Thereafter, he suffered from another episode of TdP and was shocked with his implantable cardioverter defibrillator. The lidocaine drip was discontinued, and he was started on mexiletine and propranolol. The propranolol dose was increased to 40 mg BID with subsequent improvement in the rhythm. He was restarted on coumadin as per his preference and was discharged from the hospital with instructions to follow up with his cardiologist as an outpatient.
The patient was diagnosed with prostate cancer in June 2015. He had Gleason 8, T2a N0 prostate adenocarcinoma for which he declined any surgical intervention. He received radiation therapy along with adjunctive androgen suppression therapy. The patient was treated with lupron (leuprolide) depot (30 mg every four months). His ECG three months prior to the event showed a ventricular paced rhythm with a QTc of 498 ms and an ECG QSR duration of 177 ms (Figure ). The patient’s medications included flomax (tamsulosin; 0.4 mg), coumadin (7.5 mg), lipitor (10 mg), valsartan/hydrochlorothiazide (160 mg/12.5 mg), and lupron (leuprolide; 30 mg). He did not have any family history of long QT syndrome (LQTS) and had not previously suffered from ventricular tachycardia events.
After an extensive review of the patient’s medications, his prolonged QT was attributed to the rare side effect of androgen suppression therapy with lupron (leuprolide). The patient did not receive any further treatment with lupron (leuprolide) after this event. In the six-month follow-up visit, the patient revealed that he had not suffered from any further episodes of ventricular tachycardia or ventricular fibrillation. Moreover, his ECG showed an improvement in the QTc duration, which had reduced to 484 ms (Figure ). The patient continued follow-up with his outpatient cardiologist.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [238.0, 'mg/dL'], 'Sodium': [143.0, 'mmol/mL']}",143003.312,135853.1464,150153.4776,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 143.0 mmol/mL. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 143.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 143.0 mmol * 1 mEq/mmol = 143.0 mEq sodium. The current volume unit is mL and the target volume unit is L. The conversion factor is 0.001 L for every unit of mL. Our next step will be to divide the mass by the volume conversion factor of 0.001 to get the final concentration in terms of mEq/L. This will result to 143.0 mEq sodium/0.001 L = 143000.0 mEq sodium/L. The concentration value of 143.0 mmol sodium/mL converts to 143000.0 mEq sodium/L. 
The concentration of glucose is 238.0 mg/dL. 
Plugging in these values into the formula gives us 143000.0 mEq/L + 0.024 * (238.0 - 100) = 143003.312 mEq/L.
Hence, the patient's corrected concentration of sodium is 143003.312 mEq/L."
5467,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7769828-1,Extracted,"A 55-year-old man presented to our hospital’s emergency room on April 12, 2020, with complaints of anorexia, cough, and shortness of breath. The patient had a seven-day history of cough, fever, myalgia, and malaise before presentation. His medical history included diabetes, diverticulitis, and hyperlipidemia. Home medications included atorvastatin, clomiphene, insulin Humalog 16 units subcutaneous before meal and bedtime, canagliflozin, Levemir, 54 units subcutaneous daily, lisinopril, and metformin. Baseline serum creatinine was 1.24 mg/dl on routine laboratory testing prior to admission. He had no family history of kidney disease. He did not use tobacco or illicit drugs.
In the emergency department (ED), the patient was afebrile, oral temperature 97.6, blood pressure 105 mmHg systolic and 58 mmHg diastolic, tachycardic heart rate (HR) 128, tachypneic respiratory rate (RR) 28, blood glucose level 559 mg/dL, arterial blood gas (ABG) revealed pH arterial 7.11, partial pressure of carbon dioxide (PCO2) arterial 16, PCO2 total arterial 6, HCO3 arterial 5.1, PCO2 arterial 66. Arterial blood gas findings in the setting of hyperglycemia were consistent with DKA. Findings were further confirmed by positive ketonuria on urinalysis (UA). He was also found to have lactic acid level of 4.2 mmol/L in the setting of regular metformin use at home.
Initial blood and urinary examination are shown in Table . Renal function was abnormal (blood creatinine 2.96 mg/dL) and hematuria and proteinuria were detected. Complete metabolic panel also revealed serum sodium 124 mmol/L, potassium 7 mmol/L, bicarbonate 8 mmol/L, glucose 525 mg/dL, elevated anion gap of 31. Inflammatory markers were elevated (lactate dehydrogenase level 501 IU/L, C reactive protein 32.7 mg/L, ferritin level 2951 ng/mL, and procalcitonin level 4.31 mg/ml). The chest X-ray showed mild patchy bilateral pulmonary opacities. Patient was tested for COVID-19 and he tested positive.
Clinical course
In the ED, the patient was hypoxic O2 saturation 85% on room air. The patient was started on nasal cannula oxygen with minimal improvement in saturation after which he was put on 15 L of high flow nasal cannula oxygen without any improvement in O2 saturation. Then the patient was given etomidate 20 mg IV, succinylcholine 150 mg IV and was intubated and put on ventilator support. The patient was then admitted to intensive care unit. The patient was found hypotensive 90/52 mmHg after intubation and was started on norepinephrine for hemodynamic support. The patient was given 10 units of insulin as bolus with maintenance insulin drip. He was also administered azithromycin 500 mg IV and ceftriaxone 1 g IV and was continued on broad spectrum antibiotics.
Nephrology was consulted due to worsening kidney function, hyperkalemia, and decreased urine output. The patient was started on continuous renal replacement (CRRT) on hospital day two, about 27 hrs after admission. CRRT was provided as continuous venovenous hemodiafiltration using a Prismaflex CRRT machine (Baxter Inc, Deerfield, IL). The prescribed dose is 25 ml/kg/h. We used titratable anticoagulation with unfractionated heparin after CRRT was started. After a week on CRRT the patient continues to have hypoxia requiring prone positioning and mechanical ventilation. The patient was given convalescent plasma on hospital day six as an experimental treatment due to worsening respiratory status and multiorgan failure. On day nine, the patient continues to have minimal urine output, he was transfused convalescent plasma again, no remdesivir or tocilizumab was given during the hospitalization. The patient received dexamethasone since hospital day six for total eight days. The patient also had a thromboembolic event, he was found to have acute thrombosis of left common femoral vein, femoral and popliteal vein on hospital day 33, he remained on IV heparin which was later transitioned to coumadin.
On hospital day 19, the patient remained intubated, off pressor, CRRT was discontinued, serum creatinine was 3.44 mg/dL on CRRT that increased to 5.23 mg/dL the next day. On hospital day 20, he was started on hemodialysis. He was continued on hemodialysis on Monday, Wednesday, and Friday schedule. Patient underwent tracheostomy on day 24. The patient was weaned off ventilator on day 30 and placed on trach collar. Prior to day 42 the patient remained oliguric. The patient since then started to make good urine output gradually >30 cc/hr and received last hemodialysis on day 45. On day 48, serum creatinine level improved to 1.30 mg/dL after he stopped dialysis since hospital day 45 (Table ). He was tested for COVID 19 again on day 32 and test was repeated for next two days, all tests came back negative. The patient was eventually discharged to sub-acute rehabilitation after 48 days in hospital.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [559.0, 'mg/dL'], 'Sodium': [124.0, 'mmol/L']}",135.016,128.2652,141.7668,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 124.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 124.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 124.0 mmol * 1 mEq/mmol = 124.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 124.0 mmol sodium/L converts to 124.0 mEq sodium/L. 
The concentration of glucose is 559.0 mg/dL. 
Plugging in these values into the formula gives us 124.0 mEq/L + 0.024 * (559.0 - 100) = 135.016 mEq/L.
Hence, the patient's corrected concentration of sodium is 135.016 mEq/L."
5468,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-725,Extracted,"A 63-year-old man comes to the physician because of generalized fatigue and malaise for 2 months. He has been unable to engage in his daily activities. Three months ago, he was treated for a urinary tract infection with trimethoprim-sulfamethoxazole. He has hypertension, asthma, and chronic lower back pain. Current medications include hydrochlorothiazide, an albuterol inhaler, naproxen, and an aspirin-caffeine combination. Vital signs are within normal limits. Examination shows conjunctival pallor. The remainder of the examination shows no abnormalities. Laboratory studies show:
Hemoglobin 9.1 g/dL
Leukocyte count 8,900/mm3
Erythrocyte sedimentation rate 13 mm/h
Serum
Na+ 136 mEq/L
K+ 4.8 mEq/L
Cl- 102 mEq/L
Urea nitrogen 41 mg/dL
Glucose 70 mg/dL
Creatinine 2.4 mg/dL
Calcium 9.8 mg/dL
Urine
Protein 1+
Blood 1+
RBCs none
WBCs 8–9/hpf
Bacteria none
Urine cultures are negative. Ultrasound shows shrunken kidneys with irregular contours and papillary calcifications.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [70.0, 'mg/dL'], 'Sodium': [136.0, 'mEq/L']}",135.28,128.516,142.044,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 136.0 mEq/L. 
The concentration of glucose is 70.0 mg/dL. 
Plugging in these values into the formula gives us 136.0 mEq/L + 0.024 * (70.0 - 100) = 135.28 mEq/L.
Hence, the patient's corrected concentration of sodium is 135.28 mEq/L."
5469,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4010031-1,Extracted,"A 38-year-old woman presented to the emergency department with a two-day history of confusion, agitation, and “restless, swollen legs.” Her past medical history included gastric bypass surgery, depression, and previous alcohol abuse. Regular medications were fluoxetine, omeprazole, and cetirizine. On initial assessment in the emergency room she was tachycardic at 102 beats per minute, her blood pressure was 130/70 mmHg, and her chest was clear to auscultation with an SpO2 of 100% on room air. She was confused, with a GCS score of 10 (E3V2 M5), but with no focal neurological abnormalities or rash. Her temperature was 37.5°C and blood sugar was 5.6 mmol/L. Due to her confusion and agitation, sedation was given and a CT brain scan performed. This demonstrated no acute abnormality. A lumbar puncture was performed and treatment for CNS infection instituted with ceftriaxone and acyclovir. Her potassium was 1.9 mmol/L (3.6–5.0 mmol/L), sodium 146 mmol/L (136–145 mmol/L), phosphate 0.57 mmol/L (0.8–1.4 mmol/L), and chloride 122 mmol/L (96–106 mmol/L). Her renal function was otherwise normal with a urea of 2.7 mmol/L (2.5–6.6 mmol/L) and creatinine 56 μmol/L (60–120 μmol/L). An arterial blood gas (FiO2 0.40) demonstrated a compensated metabolic acidosis: H+ 38.6 nmol/L, PaCO2 3.5 kPa, PaO2 24.44 kPa, HCO3 18.8 mmol/L, BE 8.2 mmol/L, Lactate 1.13 mmol/L. An ECG showed ST segment depression and U-waves but no ectopic beats or arrhythmias.
On further questioning, the patient's family suggested that she may have been taking large amounts of Nurofen Plus, as this had been an issue previously.
Due to her confusion and profound biochemical abnormalities she was admitted to the intensive care unit for further management.
Her management on ITU involved invasive monitoring and correction of the biochemical abnormalities. During the initial 48 hours in hospital she received 509.5 mmol of intravenous potassium replacement, which increased the serum potassium to 4.8 mmol/L. Phosphate replacement was given and once the serum potassium level had improved, 1.26% sodium bicarbonate was used as maintenance intravenous fluid. With the correction of her biochemical abnormalities (), her neurological function improved to GCS 15 (E4V5 M6). The biochemical abnormalities in the serum and urine suggested a diagnosis of renal tubular acidosis with a serum anion gap of 9 mmol/L, urinary anion gap of 20 mmol/L, and transtubular potassium gradient of 11.37. On improvement of her symptoms and conscious level, the patient admitted to taking large amounts of Nurofen Plus tablets (20–40 per day) during the preceding weeks.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [5.6, 'mmol/L'], 'Sodium': [146.0, 'mmol/L']}",146.02136,138.72029,153.32243,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 146.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 146.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 146.0 mmol * 1 mEq/mmol = 146.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 146.0 mmol sodium/L converts to 146.0 mEq sodium/L. 
The concentration of glucose is 5.6 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 5.6 mmol. To convert 5.6 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 5.6 mmol glucose * 0.001 mol/mmol = 0.0056 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0056 mol glucose * 180.16 g/mol = 1.0089 g glucose. To convert 1.0089 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 1.0089 g glucose * 1000.0 mg/g = 1008.9 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1008.9 mg glucose/10.0 dL = 100.89 mg glucose/dL. The concentration value of 5.6 mmol glucose/L converts to 100.89 mg glucose/dL. 
Plugging in these values into the formula gives us 146.0 mEq/L + 0.024 * (100.89 - 100) = 146.02136 mEq/L.
Hence, the patient's corrected concentration of sodium is 146.02136 mEq/L."
5470,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3193049-1,Extracted,"An 84-year-old female was admitted for elective coronary angiography due to chest pain. Her height and body weight were 135 cm and 42.7 kg, respectively. She was healthy except for hypertension which was treated with amolodipine besilate (5 mg qd) and hydrochlorothiazide (12.5 mg qd). The blood creatinine was 0.9 mg/dL, the blood urea nitrogen (BUN) was 15.4 mg/dL, the glucose was 105 mg/dL, the sodium was 142 mmol/L, and the potassium was 3.8 mmol/L. Coronary angiography was performed from the left radial artery under local anesthesia. One hundred mL of Visipaque 320 (Iodixanol) contrast media was used. The coronary angiography showed minimal luminal narrowing of the mid-left anterior descending artery and was completed without complication. Twelve hours later, however, the patient had severe nausea and vomiting. Sixteen hours following coronary angiography, she was markedly confused, and was in a stuporous state with recurrent generalized tonic-clonic-type seizures. The neurologic examination was without focality. A brain MRI and electroencephalography were normal (). The diagnosis of hyponatremia was not entertained until blood was drawn and showed a sodium of 115 mmol/L, a potassium of 3.4 mmol/L, a glucose of 205 mg/dL, a creatinine of 0.6 mg/dL, a BUN of 7.3 mg/dL, a uric acid of 3.1 mg/dL, and an osmolarity of 241 mosm/L. A laboratory error was suspected until a second blood sample confirmed the initial results. With a differential diagnosis of hypo-osmolar hyponatremia, we measured the serum-free T4 and thyroid stimulating hormone, which were normal. A rapid Adenocorticotropic hormone stimulation test was performed and the results were within the normal range. The patient was treated with hypertonic saline (3% NaCl) at a rate of 2 mL/hr. She improved slowly over the following 26 hours. The serum and urine sodium levels returned to normal within 48 hours, together with a full clinical recovery ().","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [205.0, 'mg/dL'], 'Sodium': [115.0, 'mmol/L']}",117.52,111.644,123.396,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 115.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 115.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 115.0 mmol * 1 mEq/mmol = 115.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 115.0 mmol sodium/L converts to 115.0 mEq sodium/L. 
The concentration of glucose is 205.0 mg/dL. 
Plugging in these values into the formula gives us 115.0 mEq/L + 0.024 * (205.0 - 100) = 117.52 mEq/L.
Hence, the patient's corrected concentration of sodium is 117.52 mEq/L."
5471,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7050964-1,Extracted,"A 54-year-old man with a past history of hepatitis B and alcohol abuse in a Rehabilitation Centre was brought to our emergency department by his colleagues after being found in a comatose state. On admission, his Glasgow Coma Scale (GCS) score was 6 and physical examination disclosed Kussmaul’s respiration. A CT scan was normal. The patient was intubated for airway protection and was transferred to the intensive care unit (ICU). On ICU admission, his GCS score decreased to 4 with decerebrate posturing and generalized tonic-clonic seizures requiring 2 doses of intravenous diazepam. Auscultation of the lungs was normal. Blood pressure registered via a radial catheter was 60/30 mmHg with poor peripheral perfusion. Transthoracic echocardiography showed hyperkinetic ventricles with normal diastolic and valvular function. The initial 12-lead ECG demonstrated an irregular rhythm with no clearly visible P waves and coved-type rectilinear-sloping ST-segment elevation in leads V1 and V2 as well as an elevated J-point in leads V3 and V4 consistent with the Brugada type 1 pattern (). Laboratory results showed a severe metabolic acidosis with a HCO3- of 5.4 mmol/l and a pH of 6.60. The serum osmolality was 414 mOsm/kg, Na+ 144 mmol/l, K+ 6.7 mmol/l, urea 7.6 mmol/l, glucose 16.4 mmol/l, Cl- 103 mmol/l and lactate 12.9 mmol/l. The anion and osmolal gaps were calculated:
Anion gap: ([Na] + [K]) − ([Cl] + [HCO3]) = (144 + 6.7) − (103 + 5.4) = 42.3 mmol/l (normal value: 14±4 mmol/l)
Osmolal gap: Serum osmol − (1.86 (Na + K) + glucose + urea + 10) = 414 − 314.3 = 99.7 mOsm/kg (normal value: <10 mOsm/kg)
Due to the suspicious circumstances and severe metabolic acidosis with extremely enhanced anion and osmolal gaps, methanol (MeOH) or ethylene glycol intoxication was suspected and a serum toxicologic screen was ordered. Correction of acidosis was initiated with bicarbonate infusions and shortly after with continuous veno-venous haemodiafiltration (CVVH) and therapy with intravenous thiamine, pyridoxine, folic acid and ethanol was instituted. Fluid resuscitation and a noradrenaline infusion improved haemodynamic parameters. After amelioration of metabolic acidosis (pH 6.97, HCO3- 11 mmol/l) and correction of hyperkalaemia in 6 hours, the 12-lead ECG showed resolution of the Brugada type 1 pattern (). Unfortunately, the patient remained in a coma state evolving to brain death and died on the first day of the ICU stay. The serum MeOH concentration was 298.2 mg/dl (NV <5 mg/dl).","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [16.4, 'mmol/L'], 'Sodium': [144.0, 'mmol/L']}",148.69109,141.25654,156.12564,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 144.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 144.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 144.0 mmol * 1 mEq/mmol = 144.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 144.0 mmol sodium/L converts to 144.0 mEq sodium/L. 
The concentration of glucose is 16.4 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 16.4 mmol. To convert 16.4 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 16.4 mmol glucose * 0.001 mol/mmol = 0.0164 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0164 mol glucose * 180.16 g/mol = 2.95462 g glucose. To convert 2.95462 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 2.95462 g glucose * 1000.0 mg/g = 2954.62 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 2954.62 mg glucose/10.0 dL = 295.462 mg glucose/dL. The concentration value of 16.4 mmol glucose/L converts to 295.462 mg glucose/dL. 
Plugging in these values into the formula gives us 144.0 mEq/L + 0.024 * (295.462 - 100) = 148.69109 mEq/L.
Hence, the patient's corrected concentration of sodium is 148.69109 mEq/L."
5472,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7482009-1,Extracted,"An 11-year-old boy admitted with vomiting, generalized edema, and hyperglycemia, which was preceded by 5 days of coryzal symptoms, lethargy, and oral aft without fever. He was admitted to another hospital with hypotensive syncope and severe vomiting (20 times/day), and intravenous hydration was initiated. His blood glucose was 13.8 mmol/L and urine glucose was +++ at admission. Initially, he was diagnosed with stress hyperglycemia and acute gastroenteritis. After one day, he was referred to our hospital because of his persisting symptoms and hyperglycemia. There was no specific indicative feature in his personal or family history. His weight was 30 kg (−1.02 SDS), height was 147 cm (+0.75 SDS), heart rate was 118/minute, and blood pressure was 90/40 mm/Hg, and generalized nonitching systemic edema was present on his physical examination.
The laboratory tests showed that severe hemoconcentration was present. His biochemical findings were as follows: white blood cell count: 1.8 × 109 L; hemoglobin: 184 g/L; hematocrit: 51.3%; sodium: 130 mmol/L; potassium: 4.8 mmol/L; chloride: 105 mmol/L; urea: 20 mmol/L; creatinine: 45 µmol/L; and blood glucose: 11.1 mmol/L. On arterial blood gas analysis, pH was 7.33 and HCO3 was 13.6 mmol/L (). On sepsis work-up, CRP was 3 mg/L, and urine, stool, and blood culture were negative. Respiratory virus panel PCR was positive for respiratory syncytial virus (RSV) and enterovirus.
Aggressive fluid replacement was initiated at admission due to hypotension. Although urine output was normal during the first two days of hospitalization, his diuresis was inadequate on the third day (0.3 cc/kg/hr), and so 3000 cc/m2 5% dextrose and 0.45% NaCl were administered as maintenance fluid therapy. The patient's serum albumin levels, as well as his globulin levels, were highly reduced because of capillary leak (). There was severe hypogammaglobulinemia at admission. Additional laboratory examinations were performed in order to make the differential diagnoses of generalized edema, hyperglycemia, hyponatremia, prerenal acute renal failure, hypoalbuminemia, and hemoconcentration. The urine analysis showed that the urine density was 1033, and the 24-hour urine protein test, blood lipids, and renal tubular tests were within normal limits excluding renal diseases. To eliminate congestive heart failure, chest radiography, electrocardiography, cardiac enzymes test, and echocardiography were performed and were all proven to be within normal limits. The patient's feces alpha-1 antitrypsin level was negative, and protein-losing enteropathies were excluded. Complement studies and lymphocyte subset analysis by flow cytometry were within normal ranges when compared to his age references.
After initial stabilization with intravenous fluid boluses and insulin infusion the first two days, the patient's generalized edema increased, albumin values dropped to 1.9 g/dL, he had diarrhea, and he gained 3 kg of weight. Subcutaneous insulin treatment started with a dose of 0.3 IU/kg/day at the end of the second day. Intravenous human albumin treatment was given on the 2nd, 4th, and 7th day of admission. On the fourth day, the patient was given the ISCLS diagnosis by ruling out other causes. Following the diagnosis, intravenous immunoglobulin (IVIG) treatment was given on two consecutive days (). His edema decreased on the fifth day, and he was deemed clinically well on the 7th day, weighing 29 kg. As for the systemic effects of ISCLS, there was seldom amount of free fluid in the abdomen, the diameter of the appendix was increased, and minimal pleural effusion was found bilaterally. There was no compartment syndrome, rhabdomyolysis, or pulmonary edema during the recovery period.
For the differential diagnosis of DM, his fasting serum glucose was 13.8 mmol/L, simultaneous C-peptide was 0.44 nmol/L, HbA1c was 64 mmol/mol, and urine ketone was positive. Antiglutamic acid decarboxylase, anti-insulin antibody, and islet cell antibody were negative. The patient harbors type 1 DM predisposing HLA II haplotypes as follows: DRB1∗0301, DRB1∗0302, and DRB1∗0201. Although there was no family history for DM, since his autoantibodies were negative, next-generation gene sequencing for 14 MODY genes including GCK, HNF1A, HNF4A, HNF1B, PDX1, CEL, KLF11, NEUROD1, PAX4, INS, and BLK was analyzed, and they were all negative. Whole exome sequencing of the patient for candidate genes is ongoing. At the 6th and 12th month marks, as well as at the last outpatient visit, his insulin dose was still 0.4 IU/kg/day and HbA1c was 40 mmol/mol.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [13.8, 'mmol/L'], 'Sodium': [130.0, 'mmol/L']}",133.5669,126.88855,140.24525,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 130.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 130.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 130.0 mmol * 1 mEq/mmol = 130.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mmol sodium/L converts to 130.0 mEq sodium/L. 
The concentration of glucose is 13.8 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 13.8 mmol. To convert 13.8 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 13.8 mmol glucose * 0.001 mol/mmol = 0.0138 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0138 mol glucose * 180.16 g/mol = 2.48621 g glucose. To convert 2.48621 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 2.48621 g glucose * 1000.0 mg/g = 2486.21 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 2486.21 mg glucose/10.0 dL = 248.621 mg glucose/dL. The concentration value of 13.8 mmol glucose/L converts to 248.621 mg glucose/dL. 
Plugging in these values into the formula gives us 130.0 mEq/L + 0.024 * (248.621 - 100) = 133.5669 mEq/L.
Hence, the patient's corrected concentration of sodium is 133.5669 mEq/L."
5473,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-5020,Extracted,"A 54-year-old African American man presents to the emergency department with shortness of breath. He was at home watching television when his symptoms began. He has a past medical history of COPD, alcohol abuse, diabetes, asthma, obesity, pancreatitis, peripheral neuropathy, and hypertension. He has a 30 pack-year smoking history as well. His current medications include albuterol, insulin, nicotine patches, duloxetine, hydroxyurea, and lisinopril. Chest radiography confirms the diagnosis of a spontaneous pneumothorax. A chest tube is placed, and the patient is transferred to the medical floor. Laboratory results are ordered and are seen below:

Hemoglobin: 9 g/dL
Platelet count: 180,000/mm^3
Mean corpuscular volume: 125 µm^3
Reticulocyte count: 0.3%

Serum:
Na+: 139 mEq/L
Cl-: 102 mEq/L
K+: 4.2 mEq/L
HCO3-: 24 mEq/L
BUN: 20 mg/dL
Glucose: 133 mg/dL
Creatinine: 1.4 mg/dL
Ca2+: 10.2 mg/dL
Vitamin B12: 197 ng/L
AST: 22 U/L
ALT: 10 U/L
Troponins: undetectable

On the medical floor, the patient complains of continued fatigue and minor chest pain. A peripheral smear is ordered as seen in Figure A. An EKG is ordered and demonstrates a right bundle branch block which is unchanged from previous EKGs.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [133.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",139.792,132.8024,146.7816,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 139.0 mEq/L. 
The concentration of glucose is 133.0 mg/dL. 
Plugging in these values into the formula gives us 139.0 mEq/L + 0.024 * (133.0 - 100) = 139.792 mEq/L.
Hence, the patient's corrected concentration of sodium is 139.792 mEq/L."
5474,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3635627-1,Extracted,"A 62-year-old diabetic woman on chronic hemodialysis for 7 months was admitted to our hospital because of general weakness and constipation for 1 week. She was bed-ridden for 1 month because of a fracture of L3-L4 spine due to a pedestrian traffic accident. Her vital signs were within normal ranges, and she had no fever. Physical examination revealed soft but distended abdomen and hypoactive bowel sounds. Plain abdominal radiographs showed large bowel distension with stool impaction (). Laboratory data showed hemoglobin of 8.6 g/dL, hematocrit 25.8%, random glucose 258 mg/dL, blood urea nitrogen 24.8 mg/dL, serum creatinine 4.1 mg/dL, sodium 129 mEq/L, potassium 4.5 mEq/L, calcium 8.0 mg/dL, phosphorus 1.7 mg/dL, and C-reactive protein 48.1 mg/L. The serum magnesium level was 3.0 mg/dL, and was 2.2 mg/dL 1 week ago (normal range, 1.8-2.6 mg/dL). She had taken magnesium-containing laxative (magnesium hydroxide 1500 mg per day) for a month, which was prescribed by another clinic. Therefore, magnesium hydroxide was discontinued and other laxatives were given.
On the 3rd hospital day, the patient became lethargic and showed somnolence. Physical examination showed generally hypoactive deep tendon reflex, abdominal distension with no bowel sounds, and severe tenderness on the lower abdomen. Her vital signs were; blood pressure: 90/60 mm Hg, pulse rate: 90 beats/minute, and body temperature: 37.0℃. Electrocardiogram revealed normal sinus rhythm. The serum magnesium level was rapidly increased to 6.0 mg/dL. Plain abdominal radiographs showed more distended large bowel loops compared with those on admission. Computed tomography (CT) showed diffuse and marked dilatation of large bowel loops with fecal impaction, compatible with megacolon. The clinical course and the serum magnesium level are shown in . Calcium gluconate was infused for a temporary antagonizing effect of hypermagnesemia. Nasogastric tube and rectal tube were inserted for gastrointestinal decompression. Hemodialysis was performed daily for hypermagnesemia correction. After three consecutive hemodialyses, the serum magnesium decreased to 3.3 mg/dL and vital signs became normal. The patient started to have bowel movements, and abdominal distension subsided slightly with defecation. On the 11th hospital day, she complained of severe abdominal pain again. Diffuse abdominal tenderness and rebound tenderness were noticed. She was hypotensive (blood pressure 90/50 mm Hg) with a rapid pulse of 100/minute and febrile (37.5℃). The serum magnesium level was 3.1 mg/dL. Follow-up abdominal CT showed large air fluid levels in the upper pelvic cavity, representing gastrointestinal perforation (). Emergent Hartmann's operation was performed. Operative finding was necrosis of the transverse colon and rectum, and histologic findings were gangrenous colitis with microperforation and serosal abscess of the colon and rectum. After the operation, her abdominal pain was resolved and vital signs became normal.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [258.0, 'mg/dL'], 'Sodium': [129.0, 'mEq/L']}",132.792,126.1524,139.4316,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 129.0 mEq/L. 
The concentration of glucose is 258.0 mg/dL. 
Plugging in these values into the formula gives us 129.0 mEq/L + 0.024 * (258.0 - 100) = 132.792 mEq/L.
Hence, the patient's corrected concentration of sodium is 132.792 mEq/L."
5475,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8310435-1,Extracted,"A 68-year-old woman with a past medical history of metastatic melanoma, hypertension, deep vein thrombosis, and pulmonary embolism with inferior vena cava filter placement presented with altered mental status, hypotension, and fever. She had received her second dose of immunotherapy with ipilimumab+nivolumab shortly before presentation.
Initial vitals were significant for blood pressure of 75/40 mm Hg, heart rate of 110 beats per minute, respiratory rate 24 breaths per minute, oxygen saturation 95% on room air, and temperature 98.4 F. Physical exam was remarkable for altered mental status, moderate respiratory distress, and bilateral lower extremity edema. Initial blood work before fluid resuscitation showed Hg 10.3 g/dL; WBC 13.9 K/mcL; Platelets 164 K/mcL; Na 133 mEq/L; K 3.1 mEq/L; Cl 110 mEq/L; HCO3−1 mEq/L; BUN of 23 mg/dL; Cr 3.2 mg/dL; Plasma Glucose 103 mg/dL; Total Protein 5.0 g/dL; Albumin 2.6 g/dL; Aspartate Aminotransferase (AST) 737 U/L; Alanine Aminotransferase (ALA) 399 U/L; Alkaline Phosphatase (ALK) 99 U/L; Total Bilirubin 0.6 mg/dL; Direct Bilirubin 0.4 mg/dL; Calcium 7.3 mg/dL; Magnesium1.5 mg/dL; Inorganic Phosphorus 2.5 mg/dL; Procalcitonin 59.11 ng/mL; Lactic Acid 1.7 mmol/L; PT 17.7 SEC/INR 1.46; aPTT 49.2 SEC; COVID-19 PCR negative; SARS-CoV-2-IgG negative; Influenza Type A negative; Influenza Type B negative; Venous blood gas: pH 7.24, pCO2 of 24 mmHg ().
Additional diagnostic evaluations included the following:Electrocardiogram: normal sinus rhythm with premature ventricular contractions, heart rate of 94 beats per minute CXR: no focal consolidation or pleural effusion Computed tomography abdomen/pelvis w/o contrast: perinephric stranding and cholestasis Computed tomography head w/o contrast: no new acute intracranial abnormality or mass effect UA w/electrolytes: few white blood cells and red blood cells but no casts, urinary pH of 7.5, urine anion gap of 40, and fractional excretion of sodium of 0.6%
The patient underwent prophylactic right femur nailing with excision of a metastatic lesion and developed a fever of unknown origin, hypotension, acute blood loss, and acute tubular necrosis two weeks before presentation. At that time, she completed treatment with vancomycin, aztreonam, and metronidazole due to a penicillin allergy. However, the infectious workup remained negative throughout the admission. The patient remained afebrile, hemodynamically stable, and safely discharged to a subacute rehabilitation facility.
Four days after discharge, she presented to our emergency department for fever and hypotension. The team initiated the sepsis protocol, and the patient was adequately fluid resuscitated with an appropriate blood pressure response. Blood cultures were collected, and the patient received empiric antibiotic treatment and stress dose hydrocortisone with improvement in her mental status.
Throughout the hospital course, her functional status improved significantly. The patient again agreed to placement in a subacute rehab facility on day fourteen of hospitalization.
The clinical picture was suggestive of sepsis with multiorgan failure in the setting of a new RTA. The patient continued on antibiotics, maintenance fluids with lactated ringers, started on a sodium bicarbonate drip, and was admitted to the medical oncology service for further management. Working differential diagnoses included sepsis, adrenal insufficiency, antimicrobial toxicity, and immunotherapy adverse effects.
The patient completed a seven-day course of antibiotics. Infectious workup, including computed tomography abdominal and pelvis w/o contrast, urine culture, blood cultures, chest x-ray, and transthoracic echocardiogram (TTE), was unremarkable. While tapering the stress dose hydrocortisone, the patient developed transient hypotension, fever, and transaminitis episodes. Per discussion with the infectious disease team and primary oncologist, the thought was that the clinical presentation was likely related to immunotherapy.
Despite the acute renal failure resolution, the patient remained with a severe hyperchloremic non-anion gap metabolic acidosis (HCO3−1, the nadir of 9 mmol/L), along with persistent hypokalemia (the nadir of 2.4 mEq/L) indicating a distal (type-I) RTA.
Although possible, antimicrobial-induced RTA was unlikely due to the resolution of the renal failure and that none of the agents are known culprits to manifest acid/base disturbances []. Giving rise to a suspected immunotherapy-induced RTA, the patient was started on prednisone one mg/kg and transitioned to sodium bicarbonate tablets. Repeat blood work revealed an appropriate response with downtrending liver enzymes and increased serum sodium bicarbonate, indicating a resolving RTA.
Further workup revealed a negative autoimmune panel (anti-Ro (SS-A), anti-La (SS-B), ANA). SPEP, UPEP, free light chains, hepatitis serology, and thyroid function tests were unremarkable. Alkaline urine, a positive urinary anion gap, a nonanion gap metabolic acidosis with low serum bicarbonate, and persistent hypokalemia suggested a distal-type-1 RTA.
The patient followed up with nephrology and oncology as an outpatient. She completed a prednisone taper over four weeks and denied symptoms at the follow-up encounter.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [103.0, 'mg/dL'], 'Sodium': [133.0, 'mEq/L']}",133.072,126.4184,139.7256,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 133.0 mEq/L. 
The concentration of glucose is 103.0 mg/dL. 
Plugging in these values into the formula gives us 133.0 mEq/L + 0.024 * (103.0 - 100) = 133.072 mEq/L.
Hence, the patient's corrected concentration of sodium is 133.072 mEq/L."
5476,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7837787-1,Extracted,"A 74-year-old male was admitted to hospital with a chief complaint of general weakness since the last 3 months and increasingly burdensome. There was nausea, vomiting, but no heartburn, decreased appetite for the last 5 months, and weight loss of around 7 kg in the last 6 months. There is no fever, headaches are often felt since the last 6 months and usually do not improve even after taking analgetics, and patients also sometimes find it difficult to sleep. There is no cough and dyspnoea; the patient often feels pain in the right chest which only decreases after taking analgetics. Urination is smooth, but the volume of urine was less, irregular defecation as long as this complaint.
Previous medical history: the patient was treated at hospital with a diagnosis of moderate differentiation of invasive squamous cell esophageal carcinoma, suspected lung and brain metastases with electrolyte balance disorders. The patient received chemotherapy 13 times and radiotherapy 30 times during treatment at a hospital in another country six months ago. Laboratory results of the last serum sodium after chemotherapy is 124 mmol/L. One month before admission in our hospital, the patient received a total of 10 bottles of 3% sodium infusion in another hospital. The serum sodium levels after correction were 111 mmol/L, 112 mmol/L, and 117 mmol/L, respectively. There was no history of swelling, hypertension, diabetes mellitus, and thyroid disease.
Physical examination found vital signs within normal limits, good consciousness, and body mass index (BMI) 18.4 kg/m2. No signs of anemia and jaundice, no palpable tumor mass, and no lymphadenopathy were found. Thoracic, cardiac, and abdominal physical examinations were within normal limits. There was no extremity edema and abdominal ascites.
The results of laboratory tests are as follows: leukocytes 4,600/mm3, erythrocytes 3.35 × 106/mm3, hemoglobin 10.6 gr/dL, hematocrit 28.5%, platelets 99,000/mm3, MCV 85.1 pg, MCHC 37.0 gr/dL, neutrophils 76.9%, lymphocytes 20.1%, RBG 156 mg/dL, ALT 17 U/L, AST 14 U/L, creatinine 0.9 mg/dL, blood urea 26 mg/dL, sodium 117 mmol/L, potassium 3.2 mmol/L, clorida 83 mmol/L, and plasma osmolality 216 mMol/kg. Other examinations found normal electrocardiography and abdominal ultrasound within normal limit, except for cysts in the right kidney (6.5 × 5.7 mm). Histopathological examination of esophageal tumor tissue biopsy was moderate differentiation of invasive squamous cell esophageal carcinoma. Thoracic CT-scan impression was sicculer esophageal tumors as high as the middle third with a mark of adhesions with the posterior portion of the aorta, no metastasis to lymph nodes and lung. The impression of PET-CT scan results postradiotherapy was increased FDG uptake is seen at a long segment of the thoracic esophagus. In view of previous radiation, considerations include esophagitis versus residual tumor. No increase was seen at the right hilum. The previously seen coeliac axis node is much smaller and non-FDG-avid. There is no evidence of hypermetabolic hepatic metastasis. A tiny nodule in the lingula is nonspecific. Increased uptake is seen at the right parietal brain parenchyma. This may be related to recent fall versus metastasis.
Based on the history, physical examination, laboratory, and radiography investigation, the initial working diagnosis was esophageal carcinoma with SIADH. Management at that time was correction of hyponatremia with NaCl 3% based on the calculation of the patient's requirement. During treatment, the patient always complains of feelings of weakness, nausea but no vomiting, no appetite, headache, insomnia, and right chest pain that is temporarily improving by giving analgesics. There was no coughing and dyspnoea. Urine production per day was between 350 and 600 cc and irregularly defecating. On physical examination, blood pressure fluctuates within normal limits but once blood pressure reaches 160/100 mmHg, the patient has experienced a decrease in consciousness with laboratory results of sodium at that time: 108 mmol/L.
Laboratory results for four times electrolyte control tests after correction showed sodium levels of 108, 108, 122, and 112 mmol/L, respectively, never reached the normal levels although correction of sodium with 3% sodium based on the calculation of patient requirement was given repeatedly; low plasma osmolality and urine osmolality higher than the plasma osmolality were also found in this patient. Furthermore, the management of SIADH was given fluid restriction; hyponatremia was corrected with 3% sodium based on the calculation of the patient's requirement, injection of furosemide 40 mg intravenous daily, tetracycline 500 mg twice daily. We follow-up urine production daily, urine sodium, urine osmolality, and plasma osmolality.
The general condition of the patient improves; complaints often felt during hospitalization have diminished. Physical examination results: vital signs are within normal limits, and urine production increases around 1100 cc daily. Laboratory examination results: levels of sodium are 140 mmol/L. Results of urine examination are within normal limits (urine density: 1.010). The patient is permitted to outpatient with recommended continue oral therapy, calculate urine production daily, and electrolyte control.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [156.0, 'mg/dL'], 'Sodium': [140.0, 'mmol/L']}",141.344,134.2768,148.4112,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 140.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 140.0 mmol * 1 mEq/mmol = 140.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mmol sodium/L converts to 140.0 mEq sodium/L. 
The concentration of glucose is 156.0 mg/dL. 
Plugging in these values into the formula gives us 140.0 mEq/L + 0.024 * (156.0 - 100) = 141.344 mEq/L.
Hence, the patient's corrected concentration of sodium is 141.344 mEq/L."
5477,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-9412,Extracted,"A 45-year-old woman is brought to the Emergency Department by her husband due to increasing confusion. He reports that she has been urinating a lot for the past month or so, especially at night, and has also been constantly drinking water and tea. Lately, she has been more tired than usual as well. Her past medical history is significant for bipolar disorder. She takes lithium and a multivitamin. She has a levonorgestrel IUD. Her blood pressure is 140/90 mmHg, pulse rate is 95/min, respiratory rate is 16/min, and temperature is 36°C (96.8°F). At physical examination, she is drowsy and disoriented. Her capillary refill is delayed and her mucous membranes appear dry. The rest of the exam is nondiagnostic. Laboratory studies show:
Na+: 148 mEq/L
K+: 4.2 mEq/L
Serum calcium: 11.0 mg/dL
Creatinine: 1.0 mg/dL
Urine osmolality: 190 mOsm/kg
Serum osmolality: 280 mOsm/kg
Finger-stick glucose: 120 mg/dL
Fluid resuscitation is initiated.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [120.0, 'mg/dL'], 'Sodium': [148.0, 'mEq/L']}",148.48,141.056,155.904,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 148.0 mEq/L. 
The concentration of glucose is 120.0 mg/dL. 
Plugging in these values into the formula gives us 148.0 mEq/L + 0.024 * (120.0 - 100) = 148.48 mEq/L.
Hence, the patient's corrected concentration of sodium is 148.48 mEq/L."
5478,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6953132-1,Extracted,"A 32-year-old woman arrived at the emergency department with complaints of abdominal pain, nausea, and vomiting. Eight hours before arrival, with suicidal intent, she ingested 1500 mg of ipragliflozin, 800 mg of olmesartan medoxomil, and 640 mg of azelnidipine [a polypill of an angiotensin II receptor blocker/calcium channel blocker (ARB/CCB)], which was her mother’s medicine. She was treated with sodium valproate and chlorpromazine hydrochloride for her delusional disorder. She had previously experienced severe hypoglycemia in the event of an overdose of her mother’s medicine including an SGLT2 inhibitor along with a dipeptidyl peptidase-4 inhibitor and a sulphonylurea.
On admission, her vital signs were as follows: body temperature, 36.4 °C; heart rate, 47 beats/min; blood pressure, 66/26 mmHg; respiratory rate, 18 breaths/min and SpO2, 99% on room air. Except for slight drowsiness and hypotension, her physical examination was normal. Blood biochemistry showed the following: glucose, 126 mg/dL; urea nitrogen, 7.1 mmol/L; creatinine, 108 μmol/L; estimated glomerular filtration rate 42.3 mL/min/1.73 m2; sodium, 137 mmol/L; potassium, 4.8 mmol/L; calcium, 2.3 mmol/L; alanine aminotransferase, 32 IU/L; aspartate aminotransferase, 33 IU/L and creatine kinase, 50 IU/L. Urinalysis showed the following: specific gravity, 1.029; protein, negative; glucose > 1000 mg/dL; ketone, 0 mg/dL; bilirubin, 0 mg/dL; nitrite, negative and leukocytes, negative. An arterial blood gas analysis showed the following: pH, 7.40; pCO2, 43.0 Torr; HCO3−, 26.1 mmol/L; base excess, 1.6 mmol/L and anion gap, 8 mmol/L. A transthoracic echocardiogram revealed normal cardiac function and an inferior vena cava diameter > 20 mm.
The patient was admitted to the psychiatric ward because of her suicidal intent. Although she was treated with norepinephrine at 0.25 μg/kg/min, she still had hypotension. She was transferred to our intensive care unit (ICU) 20 h after ingestion.
After the treatment in the ICU, her blood pressure recovered, and we could discontinue norepinephrine as her blood concentration of ARB/CCB decreased 56 h after ingestion (Fig. ). The patient’s blood concentration of ipragliflozin was highest at the time of admission (9516.3 ng/mL), but her blood glucose level was normal. Thirty-six hours after ingestion, the blood concentration of ipragliflozin had decreased to 746.5 ng/mL, equivalent to the level of a therapeutic dose, and her renal function improved simultaneously. After improvement of renal function, the osmotic diuretic effect of the drug progressed and her blood glucose level declined. Her blood glucose level was at the lower end of the normal range, but continued to decline after 40 h of ingestion, so she was treated with glucose prophylactically. When glucose was added to maintain her blood glucose level, a marked increase in urine volume was observed (Fig. ). Crystalloid therapy was administered temporarily to treat the dehydration resulting from this diuretic effect. Unlike the previous admission due to overdose of SGLT2 inhibitors along with dipeptidyl peptidase-4 inhibitors and sulfonylureas, severe hypoglycemia was not observed during the clinical course. She was discharged from the ICU 64 h after ingestion and discharged from the hospital on day 17.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [126.0, 'mg/dL'], 'Sodium': [137.0, 'mmol/L']}",137.624,130.7428,144.5052,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 137.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 137.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 137.0 mmol * 1 mEq/mmol = 137.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mmol sodium/L converts to 137.0 mEq sodium/L. 
The concentration of glucose is 126.0 mg/dL. 
Plugging in these values into the formula gives us 137.0 mEq/L + 0.024 * (126.0 - 100) = 137.624 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.624 mEq/L."
5479,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-1081,Extracted,"A 55-year-old man comes to the emergency department because of headache, fever, chills, shortness of breath, and abdominal pain for 1 week. He also feels tired and nauseous. He returned from a trip to Botswana 2 weeks ago. He has type 2 diabetes mellitus. He has smoked one pack of cigarettes daily for the past 30 years and drinks a glass of beer daily. His only current medication is metformin. His temperature is 39.3°C (102.8°F), pulse is 122/min, respirations are 28/min, and blood pressure is 109/84 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 94%. Examination shows jaundice. A few scattered inspiratory crackles are heard in the thorax. The liver is palpated 2 cm below the right costal margin. Laboratory studies show:
Hemoglobin 9.2 g/dL
Leukocyte count 9,400/mm3
Platelet count 90,000/mm3
Serum
Na+ 137 mEq/L
Cl- 102 mEq/L
K+ 5.2 mEq/L
HCO3- 13 mEq/L
Glucose 69 mg/dL
Lactate dehydrogenase 360 U/L
Creatinine 0.9 mg/dL
Bilirubin
_ Total 4.2 mg/dL
_ Direct 0.8 mg/dL
AST 79 U/L
ALT 90 U/L
Urine
Blood 3+
Protein trace
RBC 0–1/hpf
WBC 1–2/hpf
Arterial blood gas analysis on room air shows a pH of 7.31.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [69.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",136.256,129.4432,143.0688,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 137.0 mEq/L. 
The concentration of glucose is 69.0 mg/dL. 
Plugging in these values into the formula gives us 137.0 mEq/L + 0.024 * (69.0 - 100) = 136.256 mEq/L.
Hence, the patient's corrected concentration of sodium is 136.256 mEq/L."
5480,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-1138,Extracted,"A 44-year-old woman is brought to the emergency department by her husband because of increasing confusion for 3 days. Her husband states that he noticed a yellowish discoloration of her eyes for the past 6 days. She has osteoarthritis. Current medications include acetaminophen and a vitamin supplement. She does not drink alcohol. She uses intravenous cocaine occasionally. She appears ill. Her temperature is 37.2 °C (99.0 °F), pulse is 102/min, respirations are 20/min, and blood pressure is 128/82 mm Hg. She is confused and oriented only to person. Examination shows scleral icterus and jaundice of her skin. Flapping tremors of the hand when the wrist is extended are present. The liver edge is palpated 4 cm below the right costal margin and is tender; there is no splenomegaly.
Hemoglobin 12.4 g/dL
Leukocyte count 13,500/mm3
Platelet count 100,000/mm3
Prothrombin time 68 sec (INR=4.58)
Serum
Na+ 133 mEq/L
Cl- 103 mEq/L
K+ 3.6 mEq/L
Urea nitrogen 37 mg/dL
Glucose 109 mg/dL
Creatinine 1.2 mg/dL
Total bilirubin 19.6 mg/dL
AST 1356 U/L
ALT 1853 U/L
Hepatitis B surface antigen positive
Hepatitis B surface antibody negative
Hepatitis C antibody negative
Anti-hepatitis A virus IgM negative
Acetaminophen level 12 mcg/mL (N < 20 mcg/mL)
The patient is transferred to the intensive care unit and treatment with tenofovir is begun.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [109.0, 'mg/dL'], 'Sodium': [133.0, 'mEq/L']}",133.216,126.5552,139.8768,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 133.0 mEq/L. 
The concentration of glucose is 109.0 mg/dL. 
Plugging in these values into the formula gives us 133.0 mEq/L + 0.024 * (109.0 - 100) = 133.216 mEq/L.
Hence, the patient's corrected concentration of sodium is 133.216 mEq/L."
5481,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7377653-1,Extracted,"A 44-year-old man felt generalized fatigue and took the day off from work. His son called him on the same day, but he did not respond. When the son visited his house, he found the patient unconscious and called an ambulance. He had no remarkable medical history. He was a never-smoker and drank 20 g of ethanol per day. He worked as a truck driver and lived with his only son after his divorce. His work zone was not located in any of the districts that were reported to have COVID-19 infections.
When the emergency medical technicians checked him, he had a tonic convulsive posture with severe hypoxia, and he was transported to our hospital under bag-valve-mask ventilation with high-concentration oxygen. On arrival, his Glasgow Coma Scale was E1V2M3. A physical examination revealed the following findings: blood pressure of 174/130 mmHg; heart rate of 140 beats per minute; a respiratory rate of 30 breaths per minute; SpO2 of 75% under room 15 L per minute of oxygen; and body temperature of 36.9 °C. A venous route was immediately secured, followed by endotracheal intubation.
An arterial gas analysis revealed the following findings: pH: 7.092; PCO2: 54.2 mmHg; PO2: 54.5 mmHg; base excess -15.0 mmol/L; and lactate: 6 mmol/L. Electrocardiography revealed sinus tachycardia. A chest X-ray revealed a bilateral ground-glass appearance (Figure ).
Cardiac echo showed hyper-dynamic left-ventricular wall motion. Whole-body CT revealed a bilateral ground-glass appearance in the ventral lung fields and bilateral consolidation in the dorsal lung fields (Figure ).
The pancreas was normal. The main results of a blood analysis were as follows: WBC count: 23,400/μL (neutrophil 87%, lymphocyte 6%, monocyte 6%); hemoglobin: 16.5 g/dL; platelet count: 22.0×104/μL; total protein: 7.0 g/dL; albumin: 4.3 g/dL; glucose: 177 mg/dL; HbA1C: 5.5%; total bilirubin: 1.5 mg/dL; aspartate aminotransferase: 322 IU/L; alanine aminotransferase: 79 IU/L; lactate dehydrogenase: 1,108 IU/L; blood urea nitrogen: 7.4 mg/dL; creatinine: 0.51 mg/dL; amylase: 413 (pancreas 76%) IU/L; creatine phosphokinase (CK): 44,139 IU/L; sodium: 110 mEq/L; potassium: 4.2 mEq/L; chloride: 79 mEq/L; brain natriuretic peptide: 760.1 pg/mL; C-reactive protein: 22.2 mg/dL: prothrombin time international normalized ratio: 1.02; activated partial thromboplastin time: 34.6 (26.6) seconds; fibrinogen: 242 mg/dL; D-dimer: 1.5 μg/mL; human immunodeficiency virus (HIV) antibody: negative; pneumococcal urinary antigen test: negative; legionella urinary antigen test: negative; rapid influenza diagnostic test: negative; microscopic finding of sputum: negative: and urine drug screening test: negative. Later, β-d glucan, rheumatoid factor, and anti-neutrophil cytoplasmic antibody were all found to be negative. He received a tentative diagnosis of pneumonia of unknown causes accompanying severe ARDS, rhabdomyolysis, and pancreatitis.
As he showed deterioration of PaO2 [PaO2/FiO2 (P/F) = 50] and a Murray score of 3.2, he underwent mechanical ventilation under 1.0 FiO2 and 10 cmH2O with positive end-expiratory pressure (PEEP) and received indwelling venovenous ECMO (MERA centrifugal blood pump system HAS-CFP; MERA NHP exelung NSH-R HPO-23WH-C; Senko Medical Instruments, Tokyo, Japan) with the right jugular vein (return side, 14 Fr) and right femoral vein (drainage side, 20 Fr) as the exit. As this event occurred during the night shift, we did not attempt supine therapy before introducing venovenous ECMO. He also showed hypotension and therefore underwent infusion of noradrenalin followed by vasopressin and 200 mg of hydrocortisone. Due to concerns of pneumonia, he received 1.5 g of meropenem and 500 mg of azithromycin in addition to an infusion of 5 g of γ-globulin and 40 ml of glycyrrhizin as antibacterial and antivirus treatments respectively.
After the induction of ECMO, the mode of mechanical ventilation was changed to a lung rest setting (0.25 FiO2 and 5 cmH2O with PEEP). Additional cardiac echo showed diffuse hypokinesis with a 30% ejection fraction, and troponin T became positive [207 pg/mL (normal range: <14 pg/mL)] on the first hospital day, and so he was diagnosed with myocarditis as a complication. On the second day, his blood pressure increased, resulting in a reduction in the vasopressor administration. His P/F remained under 100. On the third day, inflammatory data remained high, and hence azithromycin was replaced with levofloxacin. However, this led to skin reddening and he was switched back to azithromycin. A complication of anemia, thrombocytopenia, and coagulopathy required blood transfusion. A polymerase chain reaction (PCR) test for COVID-19 using sputum through the endotracheal tube without bronchoalveolar lavage (performed twice) and initial cultures of sputum, urine, and blood were all negative.
On the fifth day, the inflammatory data remained moderate, and hence meropenem was replaced with linezolid and piperacillin/tazobactam. On the same day, in an attempt to withdraw ECMO, the mechanical ventilation setting was changed from 5 to 10 cmH2O for PEEP and from 0.25 to 0.4 for FiO2. This resulted in the P/F increasing to over 100. After the circulation flow of ECMO was reduced from 3 to 1 L/minute, the P/F remained over 100; hence ECMO was ceased, and the cannulations were removed (Figure ).
As the patient was thought to require long-term mechanical ventilation, he underwent tracheostomy on the eighth hospital day. Sedative administration was ceased, and a negative water balance was targeted by limiting the infusion volume and the use of diuretics. He showed a transient decrease in his P/F by the formation of atelectasis due to bloody sputum; however, the average P/F improved day by day. On the 12th hospital day, his P/F exceeded 300 under 5 cmH2O for PEEP and 0.25 FiO2; hence mechanical ventilation was ceased (Figure ).
He recovered his ability to excrete sputum by himself, and tracheal cannulation was removed on the 13th hospital day. Even after ceasing all drugs for lung and inflammation, his pneumonia, rhabdomyolysis, and pancreatitis did not recur. He was discharged on the 22nd day on foot. The troponin T level remained high (334 pg/mL) even after the CK level normalized, so he was followed up as an outpatient. The serum virus neutralization assay performed as a serological test using pair serum samples with a more than two-week interval for Coxsackievirus B4 showed a four-fold increase in titer (from x64 to x256). Finally, the troponin T level returned to the normal range and showed no subsequent complications.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [177.0, 'mg/dL'], 'Sodium': [110.0, 'mEq/L']}",111.848,106.2556,117.4404,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 110.0 mEq/L. 
The concentration of glucose is 177.0 mg/dL. 
Plugging in these values into the formula gives us 110.0 mEq/L + 0.024 * (177.0 - 100) = 111.848 mEq/L.
Hence, the patient's corrected concentration of sodium is 111.848 mEq/L."
5482,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4901012-1,Extracted,"A 51-year old man had a breakfast cooked with wild mushrooms that he had gathered one day earlier during summer vacation in August, 2010 at the Jujak mountain located on the province of Jeollanam-do, the southern area of Korea. He was a bus driver. He had no particular past medical or social history other than the occasional ingestion of wild mushrooms during recreational hiking. He was healthy before this admission. He did not have a history of trauma, infection, other known underlying cause, or medication use that could explain the occurrence of rhabdomyolysis. He shared the meal with his wife and son who did not eat any more mushrooms due to nausea after ingesting a single piece of mushroom. However, he ate the mushrooms without immediate symptom. Six hours later, he began to complain of vomiting, diarrhea, and myalgia. He visited a local hospital where his general condition worsened and systolic BP fell to 60 mmHg requiring dopamine treatment and endotracheal intubation. Twenty-eight hours after ingestion of the mushrooms, he was transferred to the intensive care unit of our hospital. At the time of admission, he was alert, but acute ill-looking. He complained of generalized myalgia, chest discomfort, palpitations, and dyspnea. Blood pressure was 80/56 mmHg, heart rate 121/min, respiratory rate 25/min, and body temperature 36.3oC. Oliguria was noted with no response to intravenous fluid and furosemide. Systolic murmurs were present on auscultation. Laboratory tests showed the following: hemoglobin 15.9 g/dL, hematocrit 45.9%, leukocyte count 20,740/μL with neutrophil 89.6%, platelet 253,000/μL, C-reactive protein (CRP) 8.36 mg/dL, blood urea nitrogen (BUN) 38.5 mg/dL, serum creatinine 2.84 mg/dL, serum osmolarity 314 mOsm/kg, sodium 140 mEq/L, potassium 4.7 mEq/L, chloride 100 mEq/L, ionized calcium 0.75 mmol/L, glucose 187 mg/dL, cholesterol 221 mg/dL, albumin 4.0 g/dL, aspartate aminotransferase (AST) 1,214 U/L, alanine aminotransferase (ALT) 343 U/L, total bilirubin 0.51 mg/dL, alkaline phosphatase 92 IU/L, creatine kinase (CK) 69,121 U/L, CK-MB > 500 ng/mL, lactate dehydrogenase (LDH) 2,196 U/L, troponin I 1.86 ng/mL, N-terminal pro brain natriuretic peptide (NT-pro BNP) 7,414 pg/mL, amylase 1,930 U/L, lipase 18 U/L, prothrombin time (PT) 10.2 seconds. (INR 0.86), activated partial thromboplastin time (aPTT) 28.2 seconds, urine osmolarity 341 mOsm/kg, sodium 22 mEq/L, potassium 59.2 mEq/L, chloride 14 mEq/L, creatinine 123.8 mg/dL, myoglobin 51.7 ng/mL, and fractional excretion of sodium 0.36%. Urine analysis showed pH 5.0, specific gravity 1.020, protein 2+, ketone 2+, blood 4+, RBC 5-9/high-power field, and WBC 0-1/high-power field. Blood and urine cultures were all negative for microorganism. Arterial blood gas analysis was pH 7.04, PaCO2 69 mmHg, PaO2 172 mmHg, and HCO3
- 18.7 mmol/L. Chest radiographs revealed mild cardiomegaly without lung lesion. Electrocardiogram (ECG) showed sinus tachycardia with QT prolongation. The enlarged left ventricle (LV), severe LV systolic dysfunction (ejection fraction 30%), and akinesia of LV mid to apex wall suggesting stress induced cardiomyopathy were noted on echocardiography. He received ventilator support, hemodynamic monitoring, continuous venovenous hemodiafiltration, and conservative care including intravenous fluid and electrolyte repletion. Seventy hours after ingestion of the mushrooms, BUN 41.9 mg/dL, serum creatinine 3.46 mg/dL, AST 3,271 U/L, ALT 1,254 U/L, total bilirubin 1.55 mg/dL, CK 121,397 U/L, CK-MB >500 ng/mL, LDH 6,102 U/L, troponin I 11.77 ng/mL, amylase 2,779 U/L, lipase 601 U/L, PT 42.1 seconds. (INR 3.34), and aPTT > 150 seconds. Blood pressure continued to decrease despite intravenous fluid and inotropics. Ventricular tachycardia developed, and he died due to cardiogenic shock 72 hours after ingestion of the mushrooms.
The leftover samples of the mushrooms that he had ingested were sent to Agricultural Microbiology Division, National Academy of Agricultural Science, Rural Development Administration, Suwon, Korea. Those were identified as R. subnigricans by their gross morphology (). Further examination by microscopy also confirmed the presence of spores from R.
subnigricans.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [187.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",142.088,134.9836,149.1924,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.0 mEq/L. 
The concentration of glucose is 187.0 mg/dL. 
Plugging in these values into the formula gives us 140.0 mEq/L + 0.024 * (187.0 - 100) = 142.088 mEq/L.
Hence, the patient's corrected concentration of sodium is 142.088 mEq/L."
5483,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3542891-1,Extracted,"The patient is a 38-year-old male that was transferred to our emergency department (ED) from an outside hospital status post cardiac arrest. The patient was an inmate at a local prison who was found unresponsive in his prison cell. Emergency Medical Services (EMS) was called for medical support. Minimal health information was provided by the prison. The patient was found by EMS to be in ventricular tachycardia with a palpable pulse and was intubated on the scene. The patient was given 150 mg of amiodarone, and transportation to an outside facility was initiated. On laboratory evaluation at the outside hospital, the patient was noted to have a potassium level of 9. Treatment of the patient's hyperkalemia with insulin, beta-agonists, and calcium was initiated. After initial resuscitation, the patient was transported to our ED. While en route, the patient experienced an episode of pulseless ventricular tachycardia, requiring two episodes of cardioversion. Return of spontaneous circulation was achieved prior to ED arrival.
Upon arrival to our ED, vitals were as follows: blood pressure 91/48, heart rate 145 beats per minute, respiratory rate 14 breaths per minute, oxygen (O2) saturation 99%, temperature 35.3 Celsius (C). An electrocardiogram (ECG) was performed, which documented ventricular tachycardia at a rate of 140 without ST segment or T wave changes. On exam, the patient was noted to be intubated. Head, ears, eyes, nose, and throat (HEENT) exam revealed 3 millimeter (mm) pupils that were sluggishly reactive to light and equal bilaterally and an endotracheal tube at 25 centimeters (cm) at the teeth. The remainder of the HEENT exam was unremarkable. Neck exam revealed a cervical collar in place with no cervical spine step-off noted. Cardiovascular exam revealed a heart rate of 140 beats per minute with palpable distal pulses. Lungs were clear to auscultation bilaterally. Abdomen was soft with good bowel sounds and no evidence of distension. On neurological exam, the patient was noted to be sedated with a Glasgow coma scale (GCS) of 3T.
The patient had blood sent to the lab for multiple studies. The patient's complete blood count (CBC) revealed a white blood cell count of 23.6 thou/cu mm, a hemoglobin of 14.7 g/dL, a hematocrit of 45.5%, and a platelet count of 181 thou/cu mm. His basic metabolic panel revealed a sodium of 143 mmol/L, a potassium of 8.7 mmol/L, a chloride of 120 mmol/L, a bicarbonate of 16 mmol/L, a BUN of 22 mg/dL, a creatinine of 1.06 mg/dL, and a glucose of 191 mg/dL. Venous blood gas revealed a pH of 7.06, pCO2 of 58 mmHg, and pO2 of 77 mmHg. International normalized ratio (INR) was 1.4. Cardiac markers and urinalysis were both unremarkable. A urine drug screen was positive for benzodiazepines.
The patient's emergency department management began with initial stabilization. Due to his persistent ventricular tachycardia, the patient was given another bolus of amiodarone upon arrival and a subsequent amiodarone infusion was started. Due to low mean arterial pressures, two liter of normal saline was given intravenously, a right subclavian central venous line was placed, and a left radial arterial line was placed. A levophed drip was started at 0.1 mcg/kg/min and titrated to maintain a mean arterial pressure (MAP) of 65 for pressure support. Treatment for hyperkalemia was readministered concurrently, consisting of insulin, beta-agonists and kayexalate. Chest X-ray revealed clear lungs with radio paque capsules in the fundus of the stomach. Over the next thirty minutes, the patient's rhythm converted to normal sinus rhythm and slowed to around 70 beats per minute. Repeat potassium lab draw revealed persistently elevated potassium level of 8.3 mmol/L, and hyperkalemia treatment was repeated. At this point, nephrology was consulted for emergent dialysis, and the medical intensive care unit (MICU) was notified for admission. We later found out, from the MICU team, that the patient had an esophagogastroduodenoscopy (EGD) performed to remove the unknown pills from the patient's stomach, which were found to be potassium chloride pills. After removal of the pills and multiple episodes of dialysis, the patient stabilized and was weaned from pressure and ventilator support. The patient's leukocytosis was believed to be a stress response as the MICU team was never able to determine a source of infection; however, the patient remained on-broad spectrum intravenous antibiotics over the course of his stay.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [191.0, 'mg/dL'], 'Sodium': [143.0, 'mmol/L']}",145.184,137.9248,152.4432,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 143.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 143.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 143.0 mmol * 1 mEq/mmol = 143.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mmol sodium/L converts to 143.0 mEq sodium/L. 
The concentration of glucose is 191.0 mg/dL. 
Plugging in these values into the formula gives us 143.0 mEq/L + 0.024 * (191.0 - 100) = 145.184 mEq/L.
Hence, the patient's corrected concentration of sodium is 145.184 mEq/L."
5484,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6537048-1,Extracted,"A 78-year-old Hispanic female with a significant past medical history of type 2
diabetes mellitus, hypertension and hypothyroidism presented with altered mental
status. She was brought to the emergency department by her family members who
assisted with history gathering. According to her family, the patient had a cough
and worsening shortness of breath over 3 days prior to admission unrelieved by
over-the-counter antihistamine and antitussive medications. The family did not know
how long she had been diabetic or hypertensive. Nor could they list her medications.
Upon presentation she was lethargic, had labored breathing and was lying in bed
shaking. Her blood pressure was 142/67 mmHg in the supine position, heart rate
114 bpm, axillary temperature 36.7°C and she weighed 51.7 kg. On physical
examination, she was ill-appearing, obtunded, not following verbal commands and with
Glasgow coma scale of 9. She had decreased breath sounds over the left lung lower
field. The examination of the heart, abdomen and extremities was normal. On
neurological examination, she had hyperreflexia at the patellar and ankle joints, as
well as stimulated bilateral clonus and positive Babinski sign. The screening blood
tests performed upon her admission to the hospital were consistent with severe HHS.
Her initial laboratory findings revealed glucose 635 mg/dL (normal: 70–105), sodium
175 mEq/L (corrected Na: 188 mEq/L) (normal: 135–145 mEq/L), blood urea nitrogen
(BUN) 76 mg/dL (normal: 6–20 mg/dL), creatinine 1.61 mg/dL (normal: 0.5–1.2 mg/dL)
with a serum osmolality 410 mOsm/kg (normal: 280–300 mOsm/kg). Her urine ketones
were negative. On arterial blood gas her pH was 7.43, and HCO3 29 mEq/L
(normal: 22–29). Her initial hemoglobin (Hgb) was 16.8 g/dL, white blood cell count
(WBC) 18.3 × 103/µL and platelet count 194 × 103/µL. The
initial chest X-ray and noncontrast head computed tomogram (CT) were negative with
the head CT showing only mild diffuse cortical atrophy, proportional to the size of
the ventricular system. The calculated water deficit on admission was about 5.5 L.
In the emergency department, aggressive fluid resuscitation for volume replacement
was started using normal saline (NS), which initially caused worsening in sodium
values to 180 mEq/L (corrected Na: 193 mEq/L). After 2 L of NS, WBC was
23.2 × 103/µL, Hgb was 15.1 g/dL, platelet was
160 × 103/µL and her HCO3 was within normal limits in our
laboratory at 28 HCO3 mEq/L. She was admitted to the intensive care unit
(ICU), and nephrology was consulted. She was started on 0.45% NS and subsequently
switched to 5% dextrose in water. The sodium began to trend down, while maintaining
a mean steady decrease of 6 mEq/L of sodium daily, resulting in desired sodium range
within 5 days ().
An insulin drip was placed to control the severe hyperglycemia, which resolved
steadily over the first 48 h. The insulin drip was discontinued, and insulin
glargine with correctional insulin lispro was started. An abdominal pelvic CT was
negative. Due to her neurological findings, a continuous EEG (cEEG) was ordered,
which showed left frontocentral and temporal PLEDs on day 1. By day 2, the cEEG
showed only abnormal slowing without epileptiform discharges. During the
hospitalization, a nasogastric tube was placed and tube feeds were started due to
her poor mentation. Her kidney function improved and returned to baseline. She was
also found to have a left lower lobe infiltrate and was treated for community
acquired pneumonia. She was initially treated with ceftriaxone and azithromycin;
however, over the hospital course she clinically improved and was switched over to
oral cephalexin to finish the course. Her mental status improved and returned back
to baseline. In order to prevent potential aspiration, she underwent a successful
swallow study with modified barium and was started on regular diabetic diet. She
stayed in the hospital for 7 days and was diagnosed with severe hypernatremia
secondary to osmotic diuresis and dehydration from HHS. Her hemoglobin A1c was found
to be 9.9%, and upon discharge, she was placed on metformin, insulin glargine and
insulin lispro sliding scale. Due to her decline in functional status and
deconditioning, she was discharged to a skilled nursing facility. She received
diabetes teaching, which included lifestyle modifications, proper nutrition, insulin
administration and glucose checks. Unfortunately, there was no good follow-up with
the patient, because she returned to her home abroad.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [635.0, 'mg/dL'], 'Sodium': [175.0, 'mEq/L']}",187.84,178.448,197.232,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 175.0 mEq/L. 
The concentration of glucose is 635.0 mg/dL. 
Plugging in these values into the formula gives us 175.0 mEq/L + 0.024 * (635.0 - 100) = 187.84 mEq/L.
Hence, the patient's corrected concentration of sodium is 187.84 mEq/L."
5485,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3541550-1,Extracted,"An 84-year-old woman was brought to the emergency department with a complaint of acute onset, rapid, involuntary movements of the left upper limb and she was diagnosed with ketotic hyperglycemia with positive urine ketones. She had no significant past medical history except for essential hypertension. The patient was not exposed to newly onset medications, but was receiving angiotensin receptor blocker (valsartan 160 mg/d, orally) for hypertension. There was no family history of movement disorders, and she had no previous neurological and psychiatric symptoms either. On admission, the general physical examination was normal. Neurological examination showed an alert patient with acute onset involuntary, continuous, jerky movements of the left arm. The rest of the neurologic examination was unremarkable. The random blood glucose concentration was 309 mg/dL with (++) urine ketones and glycosuria. She had normal arterial blood gas analysis of pH, PCO and HCO3
− concentrations on room air and temperature. Blood count and liver function tests were normal. Her urea was 25 mg/dL and creatinine 1.21 mg/dL. Her glycosylated hemoglobin A1C (HbA1C) was 14.9%. Serum sodium: 130 mEq/L, potassium: 3.9 mEq/L, serum calcium: 8.6 mg/dL, phosphorus: 2.3 mg/dL, magnesium: 1.7 mg/dL, uric acid: 6.1 mg/dL, serum ceruloplasmin: 30.6 mg/dL (N: 20–60), and copper:135 μg/dL (N: 80–155). Estimated blood osmolality was 294 mosm/L (N: 285–295). Antinuclear antibody (ANA) profile, antineutrophilic cytoplasmic antibodies reactive to myeloperoxidase (p-ANCA), and proteinase-3 (c-ANCA), antiphospholipid antibodies (e.g., anticardiolipin antibodies), antismooth muscle antibody (ASMA), anti-liver-kidney-microsome antibody (LKM-1), antimitochondrial antibody (AMA), TSH receptor antibodies (TRab), antithyroid peroxidase (TPO), and antithyroglobulin (anti T) antibodies revealed negative. Chest radiograph and electrocardiograph were normal.
Brain magnetic resonance imaging (MRI) showed hyperintensity in the right striatum on T1-weighted () and low signal intensity on T2-weighted images ().
Management for diabetic ketosis was started on intravenous (IV) insulin infusion with hourly blood sugar monitoring. After the patient's glycemic control was achieved and urine ketones were negative, treatment with rapid-acting analog insulin of 8 unit before meals and long-acting analog insulin of 12 unit at night subcutaneously, and quetiapine fumarate 25 mg/d orally were commenced on the second day of her admission.
After achievement of blood glucose levels between 79 and 141 mg/dL, the involuntary movements declined and completely disappeared within 6 days, and quetiapine fumarate was discontinued without any recurrence of the described movements. The patient was discharged on a combination of rapid-and-long acting analog insulin (10 + 10 + 10 + 16 U SC) and advised regular follow up for glycemic profiles.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [309.0, 'mg/dL'], 'Sodium': [130.0, 'mEq/L']}",135.016,128.2652,141.7668,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 130.0 mEq/L. 
The concentration of glucose is 309.0 mg/dL. 
Plugging in these values into the formula gives us 130.0 mEq/L + 0.024 * (309.0 - 100) = 135.016 mEq/L.
Hence, the patient's corrected concentration of sodium is 135.016 mEq/L."
5486,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8396405-1,Extracted,"A 34-year-old female with a history of hypertension presented to the emergency department with a complaint of abdominal pain for two days. The pain started in the epigastrium then radiated to the right upper abdomen and her back. The pain was described as being sharp and associated with chills, nausea and vomiting. She denied any chest pain, shortness of breath, diarrhoea, bloody vomit, bloody stools, or urinary problems. She had prior episodes of biliary colic but had not seen a surgeon previously. Her blood pressure was 115/75 mmHg, pulse 82 beats per minute, temperature 37.10C, and respiration of 18 breaths per minute. Her physical examination showed no acute distress, normal mental status, and abdominal tenderness in the right upper quadrant.
Laboratory tests showed sodium 136mmol/L, potassium 3.6mmol/L, chloride 102mmol/L, carbon dioxide 28mmol/L, BUN 14mg/dl), creatinine 0.94mg/dl, glucose 82mg/dl, calcium 8.7mg/dl. Liver function tests and lipase were normal. Complete blood count revealed a white blood cell count (WBC) of 11.8K/mm3, haemoglobin of 14.7gm/dL, and platelets of 316K/mm3. Urinalysis revealed 2+ leukoesterase, WBC 11-20/high power field, and rare bacteria.
Abdominal ultrasonography and computed tomography (CT) scan showed cholelithiasis and acute cholecystitis, and hepatic steatosis. The patient was admitted to the hospital and resuscitated with intravenous crystalloid solution and antibiotics. On hospital day one, the patient was taken for laparoscopic cholecystectomy. An acutely inflamed distended gallbladder with adherent omentum was noted (Figure ). There was an unusually large blood vessel and medial aspect of the gallbladder coursing toward the inferior liver edge and heading into the falciform ligament. The gallbladder was removed using caution to preserve the unusual blood vessel, and a critical view of safety was obtained. The aberrant blood vessel had several small branches going into the gallbladder (Figure , ).
The patient tolerated the procedure well, was extubated and transferred to the recovery room. On postoperative day one, the patient tolerated diet, the pain was controlled, and abdominal examination was unremarkable. The Jackson Pratt drain was removed, and the patient was discharged home. The patient followed up in the clinic after two weeks, at which time no immediate issues were identified. A review of the histopathology revealed moderate acute and chronic cholecystitis and cholelithiasis. On further review of her CT scan due to the intraoperative finding of the unusual blood vessel, the hepatic falciform artery could readily be appreciated (figure ).","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [82.0, 'mg/dL'], 'Sodium': [136.0, 'mmol/L']}",135.568,128.7896,142.3464,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 136.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 136.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 136.0 mmol * 1 mEq/mmol = 136.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mmol sodium/L converts to 136.0 mEq sodium/L. 
The concentration of glucose is 82.0 mg/dL. 
Plugging in these values into the formula gives us 136.0 mEq/L + 0.024 * (82.0 - 100) = 135.568 mEq/L.
Hence, the patient's corrected concentration of sodium is 135.568 mEq/L."
5487,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8170122-1,Extracted,"An 81-year-old Caucasian man with a history of hypertension, type 2 diabetes mellitus, cardiovascular disease, hyperlipidemia, and benign prostate hypertrophy presented with a fall at home without witnessed syncope or seizures. His medications consisted of clopidogrel, enalapril, finasteride, gabapentin, glimepiride, sitagliptin, metformin, and tamsulosin.
At presentation at the Mount Sinai Medical Center, Brooklyn, New York, in September 2020, the patient complained of weakness, fatigue, and frequent urinations. His body temperature was 39.0 °C, and blood pressure was 150/95 mm Hg, with a pulse rate of 98 beats/minute and oxygen saturation rate of 98%. He was alert and oriented, with unremarkable lung and cardiovascular examination. Laboratory findings showed leukocytes, 6.6 × 103/µL; hemoglobin, 12.2 g/dL; thrombocytes, 89 × 103/µL; glucose, 235 mg/dL; sodium, 134 mEq/L; potassium 4.6 mEq/L; bicarbonate, 16 mEq/L; calcium, 8.5 mEq/L; serum creatinine (Scr) 1.1 mg/dL; blood urea nitrogen (BUN), 29 mg/dL; creatine phosphokinase (CPK), 9,128 IU/L; prothrombin time, 13.4 s; partial thromboplastin time, 25.3 s. Urinalysis and urinary microscopy demonstrated glucose, erythrocytes, and trace protein and no casts. A chest X-ray showed clear lungs. COVID-19 infection was diagnosed based on a reverse transcriptase-polymerase chain reaction test that detected acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in a throat swab sample. Initial treatment was supportive, with nasal cannula oxygen, doxycycline, and thrombosis prophylaxis with apixaban.
On day 5 after admission, the condition of the patient worsened. He became more tachypneic, with oxygen saturation decreased to 87% on nasal cannula. There were no episodes of hemodynamic instability. He developed non-oliguric deterioration of kidney function, with Scr and BUN increased to a maximum level of 5.8 mg/dL and 124 mg/dL, respectively. Arterial blood gas on non-rebreather mask showed pH 7.25, Pa O2 78 mmHg, Pa CO2 31 mmHg, and HCO3 13 meq/L. Chest X-ray showed diffuse patchy bilateral infiltrates. The patient was transferred to the Intensive Care Unit (ICU), started BiPAP therapy, intravenous steroids, and was given convalescent plasma. Over the next 48 hours, his respiratory status started improving, with Scr decreasing to 1.2 mg/dL, and CPK to 280 IU/L (). He was changed to high-flow oxygen therapy (HFOT) () and given 5 days of remdesivir treatment.
In the following period, the patient showed gradual respiratory improvement and diuresis. At 20 days after admission, he was discharged from the ICU, and after 43 days, when his throat swab test for coronavirus became negative, he was discharged home. At the time of discharge, Scr level was 0.9 mg/dL.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [235.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",137.24,130.378,144.102,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 134.0 mEq/L. 
The concentration of glucose is 235.0 mg/dL. 
Plugging in these values into the formula gives us 134.0 mEq/L + 0.024 * (235.0 - 100) = 137.24 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.24 mEq/L."
5488,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7160714-2,Extracted,"A 12-year-old female child with no medical history and no history of prior biliary colic or alcohol consumption was admitted in the pediatric unit for abdominal pain and fever. Questioning the parents' revealed that, for 4 weeks, she had been suffering from polyuria and polydipsia associated with a significant loss of weight. The patient's health status deteriorated gradually, with abdominal pain and fever. The physical exam showed diffuse abdominal tenderness with an important decrease of bowel sounds. Her blood pressure was at 60/30 mmHg, pulse at 160 beats/min, temperature at 39°C, and respiratory rate at 30/min. The laboratory exams showed serum glucose level at 21 mmol/l, hemoglobin A1c at 16.5%, pH = 7.24, bicarbonate at 5 mmol/l, anion gap at 36, serum sodium = 142 mmol/l, serum potassium = 2.7 mmol/l, lipase = 411 U/l, amylase = 361 U/l, cholesterol = 12.8 mmol/l, and serum triglyceride = 53 mmol/l with apparent lipema in the lab test tubes. The other biochemical values were at the normal range, particularly the aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase, and bilirubin values.
Computed tomography (CT) scan revealed gastric distension, changes in the interstitium of the pancreas, and intrahepatic bile duct dilatation. The imaging did not show any other anomaly causing acute pancreatitis, in particular, a gallstone disease or extrahepatic duct dilatation. The patient developed respiratory distress needing the use of mechanical ventilation, then she was transferred to the intensive care unit. In ICU, she underwent fluid infusion, catecholamine prescription, and insulin infusion. During her ICU stay, she developed septic shock, requiring large-spectrum antibiotics, and acute kidney injury (AKI) with refractory metabolic acidosis, requiring hemodialysis. Despite the intensive treatment, the patient developed a multiorgan failure. She died 12 days after ICU admission.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [21.0, 'mmol/L'], 'Sodium': [142.0, 'mmol/L']}",148.68006,141.24606,156.11406,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 142.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 142.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 142.0 mmol * 1 mEq/mmol = 142.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mmol sodium/L converts to 142.0 mEq sodium/L. 
The concentration of glucose is 21.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 21.0 mmol. To convert 21.0 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 21.0 mmol glucose * 0.001 mol/mmol = 0.021 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.021 mol glucose * 180.16 g/mol = 3.78336 g glucose. To convert 3.78336 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 3.78336 g glucose * 1000.0 mg/g = 3783.36 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 3783.36 mg glucose/10.0 dL = 378.336 mg glucose/dL. The concentration value of 21.0 mmol glucose/L converts to 378.336 mg glucose/dL. 
Plugging in these values into the formula gives us 142.0 mEq/L + 0.024 * (378.336 - 100) = 148.68006 mEq/L.
Hence, the patient's corrected concentration of sodium is 148.68006 mEq/L."
5489,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6709545-1,Extracted,"Our patient is a 61-year-old male with a recent diagnosis of metastatic non-small-cell lung carcinoma (NSCLC). Eight weeks after initiating treatment with pembrolizumab, he presented at the emergency department with a 5-day history of nausea, vomiting, diarrhea and generalized weakness. He had no personal or family history of endocrine or autoimmune disease. Physical examination revealed impaired consciousness, dry mouth, marbled skin and cold extremities. He was hypotensive (105/45 mmHg) and tachycardic (108/min). Blood analysis showed a marked hyperglycemia (1194 mg/dL = 66.3 mmol/L), pseudohyponatremia (117 mmol/L – corrected 143 mmol/L) (8) and acute renal insufficiency (CrCl 28 mL/min/1.73 m2). The positive reaction for urinary ketones and a blood gas analysis showing severe metabolic acidosis with respiratory compensation, established the diagnosis of diabetic ketoacidosis. The patient was hospitalized at our intensive care unit for monitoring, rehydration and intravenous insulin therapy. He recovered and was switched to a subcutaneous basal-prandial insulin regimen. An autoimmune etiology was probable, given the context and the presence of positive glutamic acid decarboxylase autoantibodies (GADAs) with low C-peptide levels (). The serum lipase level was also elevated at diagnosis (>3 times the upper reference limit). Abdominal computed tomography did not show signs of pancreatitis. The HLA class II genotype of our case was assessed by allele-specific oligonucleotide hybridization, as previously described (). HLA genotype analysis identified homozygosity for the haplotype DRB1*04-DQA1*03:01-DQB1*03:02 (DR4-DQ8). Subclinical hyperthyroidism was simultaneously detected (TSH 0.058 mIU/L, fT4 18.7 pmol/L) which evolved into manifest hypothyroidism (TSH 18.92 mIU/L, fT4 5.7 pmol/L) over the next weeks requiring levothyroxine substitution therapy. Ultrasonography of the thyroid did not demonstrate hypervascularity, and thyroid autoantibodies (TPOAb, TSI) were negative. This clinical pattern was suggestive of checkpoint blockade-induced thyroiditis (, , , ). We subsequently performed a systematic review to identify similar cases of diabetes mellitus associated with ICI.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [1194.0, 'mg/dL'], 'Sodium': [143.0, 'mmol/L']}",169.256,160.7932,177.7188,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 143.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 143.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 143.0 mmol * 1 mEq/mmol = 143.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mmol sodium/L converts to 143.0 mEq sodium/L. 
The concentration of glucose is 1194.0 mg/dL. 
Plugging in these values into the formula gives us 143.0 mEq/L + 0.024 * (1194.0 - 100) = 169.256 mEq/L.
Hence, the patient's corrected concentration of sodium is 169.256 mEq/L."
5490,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-595,Extracted,"A 48-year-old man comes to the physician because of severe joint pain and swelling involving different joints for 3 months. He has also been having loose stools and episodes of epigastric pain for 6 months. He reports a 10-kg (22-lb) weight loss during this period. He has type 2 diabetes mellitus. He does not smoke or drink alcohol. His medications include insulin and metformin. His vital signs are within normal limits. Examination shows pale conjunctivae, angular cheilitis, and glossitis. Axillary and cervical lymphadenopathy is present. A grade 2/6 pansystolic murmur is heard best at the apex. The right knee is swollen and tender; range of motion is limited. The sacroiliac joints are tender. Test of the stool for occult blood is negative. Laboratory studies show:
Hemoglobin 9.2 g/dL
Mean corpuscular volume 90 μm3
Leukocyte count 4,800/mm3
Serum
Na+ 134 mEq/L
Cl- 96 mEq/L
K+ 3.3 mEq/L
Glucose 143 mg/dL
Creatinine 1.2 mg/dL
A small intestine biopsy shows periodic acid-Schiff-positive (PAS-positive) macrophages in the lamina propria.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [143.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",135.032,128.2804,141.7836,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 134.0 mEq/L. 
The concentration of glucose is 143.0 mg/dL. 
Plugging in these values into the formula gives us 134.0 mEq/L + 0.024 * (143.0 - 100) = 135.032 mEq/L.
Hence, the patient's corrected concentration of sodium is 135.032 mEq/L."
5491,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8092952-1,Extracted,"A 40-year-old African American male patient, known to have homozygous sickle cell disease (SS genotype) and associated nephropathy, was admitted to our medical service in the summer of 2020 with a painful hemolytic crisis. He had presented with several weeks of progressive generalized weakness, generalized myalgias, and worsening dyspnea in the previous week. He had failed to take his prophylactic hydroxyurea for some time prior to presentation. Initial evaluation in the emergency department (ED) revealed lethargy and sedated level of consciousness with hypoxia and increased work of breathing. Following initial resuscitative measures in the ED, he improved. Pertinent admission laboratory data included sickle hemoglobin (HbS) 94.5%, hemoglobin A2 3.2%, mean corpuscular volume 103 fL, reticulocyte count 19.4% (baseline reticulocyte count of ~2.8%), white blood cell count 34.85×109/L with 85% neutrophils, platelet count 294×109/L, hemoglobin 4.6 g/dL, and hematocrit 13.1%. Peripheral smear revealed sickled red blood cells (RBCs). Chemistry revealed sodium 136 mmol/L, potassium 7.4 (3.5–5.0) mmol/L, glucose <20 mg/dL that quickly improved after 10% dextrose infusion, creatinine 7.20 mg/dL (baseline 1.5 mg/dL), bicarbonate <5 mmol/L, chloride 102 mmol/L, calcium 7.4 mg/dL, total bilirubin >40 mg/dL, phosphorus 11.6 mg/dL, conjugated bilirubin 38.7 mg/dL, unconjugated bilirubin 2.9 mg/dL, aspartate aminotransferase 374 IU/L, alanine aminotransferase 94 IU/L, alkaline phosphatase 418 IU/L, total protein 10.7 g/dL, albumin 3.6 g/dL, ferritin >6,000 ng/mL, creatine kinase 70 U/L, troponin I 0.042 (<0.034) ng/mL, ammonia 54 (<34) μmol/L, lactate dehydrogenase 3288 (313–618) U/L, N-terminal pro b-type natriuretic peptide 8940 (<125) pg/mL, partial thromboplastin time 31 s, prothrombin time 20.9 s, international normalized ratio 1.8, and lactic acid 11.6 mmol/L. The calculated MELD score was 40. Salicylate level was 1.7 mg/dL, and acetaminophen level was 14 μg/mL. Initial venous blood gas examination revealed pH 7.03, pCO2 38 mmHg, pO2 34 mmHg, TCO2 11 mmol/L, base deficit 19, and oxygen saturation was only 42%. Electrocardiogram (EKG) in the ED was abnormal and demonstrated sinus rhythm with prolonged QTc duration of 522 (<440) ms, together with inverted T waves in the lateral chest leads, V4–V6, consistent with true hyperkalemia (). He had promptly received emergency therapies for hyperkalemia including intravenous (IV) calcium gluconate infusion, IV sodium bicarbonate infusion, IV 10% dextrose infusion with insulin, and IV furosemide. In addition, he was started empirically on IV antibiotics, vancomycin, and meropenem.
He was transfused with two units of packed RBCs and was promptly transferred to the Medical ICU. He quickly underwent emergency RBC exchange with therapeutic apheresis via a right femoral vein cannula, utilizing 1,999 mL of packed RBCs with a net fluid balance of 270 mL. Sickle hemoglobin (HbS) quickly dropped to 26.3% post-apheresis exchange. Initial nephrology consultation on admission had recommended correction of metabolic acidosis and treatment of hyperkalemia with more isotonic sodium bicarbonate infusions, insulin/glucose infusions, and the initiation of oral sodium zirconium cyclosilicate (SZC). He received one hemodialysis treatment on day 3 following evidence of encephalopathy which was subsequently blamed on drug toxicity from IV ketamine that was used for pain management.
Despite observing significant improvement of the acute kidney injury on chronic kidney disease in the first two weeks of this admission with much improved serum creatinine 2–3 weeks into the admission, as well as normal urine output, and stabilization of serum bicarbonate level to 22–27 mmol/L, the patient had exhibited persistent hyperkalemia (5.2–6.7 mmol/L) even with continued administration of SZC at 10 mg 2 times daily. The simultaneous trajectories of serum creatinine, platelet count, and serum potassium concentrations during the admission are shown in . The patient had remained otherwise asymptomatic. Chlorthalidone, 25 mg daily, was added to manage the hyperkalemia without much success. Moreover, an EKG obtained in the 4th week of admission when the serum potassium that morning was 6.7 mmol/L was remarkably normal (). At this point, as demonstrated in , our patient had subsequently developed significantly progressive thrombocytosis, the result of previous treated sepsis. Admission leukocytosis of 34.85×109/L had decreased to 10.67×109/L in the 4th week of this admission. Nevertheless, usual therapies for hyperkalemia were again reinstituted in addition to the continued use of SZC and chlorthalidone.
From the foregoing observations and considerations, especially given the normal EKG shown in compared to the admission EKG in when he had true hyperkalemia with acute kidney injury and metabolic acidosis, for the very first time since this admission the possibility of pseudohyperkalemia was entertained. Consequently, later that same afternoon, following a conference call between the Nephrology and Internal Medicine Services, we repeated the simultaneous serum and plasma potassium measurements (after the emergency therapies for true hyperkalemia had been administered earlier that morning for a measured serum potassium level of 6.7 mmol/L). The measured simultaneous blood potassium levels were 5.8 mmol/L in serum versus 5.2 mmol/L in plasma. The reference range for blood potassium is 3.5–5.0 mmol/L. This confirmed the presence of pseudohyperkalemia secondary to the prevailing progressive thrombocytosis during this later part of the admission (). Pseudohyperkalemia is diagnosed when the serum potassium concentration exceeds that of plasma by at least 0.4 mmol/L. Subsequently, the new potassium binder SZC was discontinued.
Five weeks after discharge, the patient was re-admitted to the same medical service this time with symptomatic painful sickle cell anemia crisis, fevers, cough with green sputum production, leukocytosis of 31.98×109/L, bilirubin 8.4 mg/dL, and chest radiograph that demonstrated bilateral multifocal patchy infiltrates consistent with pneumonia. Both HIV 1 and 2 and repeated COVID-19 RT-PCR tests were negative. He was started empirically on IV ceftriaxone, IV azithromycin, and IV vancomycin. Blood cultures grew methicillin-resistant Staphylococcus aureus within 15 hours in two out of two bottles, and IV antibiotics were de-escalated to 6 weeks of IV vancomycin administration. Admission serum creatinine was only slightly increased at 1.48 mg/dL, potassium was 5.7 mmol/L, but bicarbonate was 23 mmol/L. The patient responded well to IV antibiotics with resolution of the fever, and WBC had quickly dropped to 14.99×109/L after 2 days. Despite this quick overall clinical improvement, persistent hyperkalemia was again recorded throughout this second admission despite a low-potassium diet, IV furosemide, and the addition of oral fludrocortisone, 0.2 mg daily. Admission platelet count of 546 ×109/L had decreased to 314–450×109/L following IV fluids and IV antibiotics. This time round, simultaneous serum and plasma potassium levels were checked multiple times, and serum and plasma potassium concentrations were similar, indicative of true hyperkalemia. Hyperkalemia in the past had been related to pseudohyperkalemia associated with thrombocytosis. Factors contributory to true hyperkalemia were suspected to include sepsis accompanying the sickle cell crisis and intravascular hemolysis, concurrent exposure to heparin (subcutaneous enoxaparin 40 mg daily for deep vein thrombosis prophylaxis), and underlying sickle cell nephropathy with chronic kidney disease. The patient was restarted on SZC 10 g b.i.d. for 48 hours, and continued at 10–15 g daily. Serum potassium was maintained in the 5.3–6.3 mmol/L range throughout the hospital stay. The administration of SZC was to be continued post-discharge for 6 weeks with monitoring of serum potassium levels. To our knowledge, the patient has remained stable since discharge from the hospital.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [20.0, 'mg/dL'], 'Sodium': [136.0, 'mmol/L']}",134.08,127.376,140.784,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 136.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 136.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 136.0 mmol * 1 mEq/mmol = 136.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mmol sodium/L converts to 136.0 mEq sodium/L. 
The concentration of glucose is 20.0 mg/dL. 
Plugging in these values into the formula gives us 136.0 mEq/L + 0.024 * (20.0 - 100) = 134.08 mEq/L.
Hence, the patient's corrected concentration of sodium is 134.08 mEq/L."
5492,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-524183-1,Extracted,"A 52-year-old male presented with fever, chills and blood in the urine. Four days prior to admission, he noted increased urinary frequency, urgency, occasional incontinence and burning sensation during micturition. His past medical history is significant for coronary artery disease, hyperlipidemia, hypertension and insulin dependent diabetes mellitus (most recent HgbA1c of 11.7 two weeks prior). He had 66-pack year history of smoking. Medications on admission included, aspirin, atenolol, cyclobenzaprine, gabapentin, gemfibrozil, glipizide, NPH insulin, hydrochlorthiazide/triamterene, nifedipine, nitroglycerin patch, omeprazole, and sertraline.
On physical examination, his temperature was 100.9°F, pulse 88, BP 123/71 mm/hg. Cardiac and pulmonary examinations were unremarkable. His abdomen was soft, nontender with positive bowel sounds and no organomegaly detected. The rectal examination was normal with a non-tender, smooth prostate. Neurological exam was exam was unremarkable.
Laboratory evaluation revealed white cell count 17,400 cells/mm3, hemoglobin 15.1 gm/dl, sodium 128 mmol/l, potassium 4.1 mmol/l, chloride 91 mmol/l, bicarbonate 24 mmol/L, glucose 273 mg/dl and an anion gap of 13. Urine analysis revealed red, cloudy urine with pH 5.0, nitrite positive and numerous white and red blood cells on microscopy. A pelvic X-ray (figure ) showed circumferential air in the bladder wall. CT scan of the pelvis (figure ) revealed gas in the bladder lumen and wall extending to the right ureter. He was empirically treated with gentamicin and piperacillin/tazobactam. He responded with defervescence and a decline in his white cell count. Urine cultures grew Escherichia coli and based on the sensitivities he was discharged home on ciprofloxacin.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [273.0, 'mg/dL'], 'Sodium': [128.0, 'mmol/L']}",132.152,125.5444,138.7596,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 128.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 128.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 128.0 mmol * 1 mEq/mmol = 128.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 128.0 mmol sodium/L converts to 128.0 mEq sodium/L. 
The concentration of glucose is 273.0 mg/dL. 
Plugging in these values into the formula gives us 128.0 mEq/L + 0.024 * (273.0 - 100) = 132.152 mEq/L.
Hence, the patient's corrected concentration of sodium is 132.152 mEq/L."
5493,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-6085,Extracted,"A 33-year-old woman presents to the emergency department with numbness and severe fatigue. She states that her symptoms started yesterday and have been gradually worsening. The patient is generally healthy, drinks alcohol on the weekends, and does not smoke. She was ill recently but recovered spontaneously. Her temperature is 102°F (38.9°C), blood pressure is 127/68 mmHg, pulse is 120/min, respirations are 17/min, and oxygen saturation is 98% on room air. Physical exam is notable for an anxious young woman who appears mildly confused. Neurological exam reveals she has decreased sensation to light touch bilaterally on her upper and lower extremities. Dermatologic exam reveals petechiae. Laboratory values are ordered as seen below.

Hemoglobin: 7.2 g/dL
Hematocrit: 25%
Leukocyte count: 6,500/mm^3 with normal differential

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 5.4 mEq/L
HCO3-: 22 mEq/L
BUN: 30 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.9 mg/dL
Ca2+: 10.2 mg/dL

A peripheral smear is performed as seen in Figure A.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [99.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",138.976,132.0272,145.9248,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 139.0 mEq/L. 
The concentration of glucose is 99.0 mg/dL. 
Plugging in these values into the formula gives us 139.0 mEq/L + 0.024 * (99.0 - 100) = 138.976 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.976 mEq/L."
5494,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7852477-2,Extracted,"A 78-year-old Asian male was brought to our make-shift COVID-19 hospital after being tested positive for rRT-PCR. The patient had a history of diabetes mellitus, hypertension, and recurrent ischemic stroke. He was on regular medications which included antiplatelets, statins, losartan, and oral hypoglycemic agents. On admission, the patient had a mild fever and dry cough for 2 days, and his examination revealed a pulse rate of 70 beats per minute, blood pressure of 150/70 mmHg, temperature of 37 °C, SaO2 of 96% in room air, and respiratory rate of 20 per minute. His blood glucose was 90 mg/dl and HbA1c 6.6%. On the 9th day of admission, the patient gradually became drowsy and less responsive to general commands. On examination, his GCS was 10/15, pulse rate of 124 beats per minute, blood pressure of 180/100 mmHg, respiratory rate of 26 per minute, and oxygen saturation of 95% at room air. On chest auscultation, there was wheeze bilaterally present and crepitations on right infrascapular area.
His blood investigation showed a blood glucose level of 626 mg/dl, blood urea 64 mg/dl, serum creatinine 1.77 mg/dl, serum sodium 167 mEq/L, serum potassium 4.2 mEq/L, serum osmolality 378 mOsm/kg, urine analysis was negative for ketones (Table ) and his arterial blood gas (ABG) analysis showed compensated metabolic acidosis. Chest x-ray revealed features of bilateral ill-defined airspace consolidations involving mostly lower zones with peripheral distribution (Fig. ). Hence patient was shifted to ICU with the diagnosis of HHS with AKI and management was initiated with careful fluid administration, insulin therapy, and empirical antibiotics. All other possible co-infections were excluded. The patient gradually improved over a period of 1 week and was shifted out of ICU in stable condition.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [626.0, 'mg/dL'], 'Sodium': [167.0, 'mEq/L']}",179.624,170.6428,188.6052,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 167.0 mEq/L. 
The concentration of glucose is 626.0 mg/dL. 
Plugging in these values into the formula gives us 167.0 mEq/L + 0.024 * (626.0 - 100) = 179.624 mEq/L.
Hence, the patient's corrected concentration of sodium is 179.624 mEq/L."
5495,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2883193-1,Extracted,"A 31-year-old Afghani female, living in Makkah Al Mukarrama was brought by her relatives during the Hajj season in 2009 to King Abdulaziz Hospital with a three-day history of high-grade fever, vomiting, cough, expectoration and increasing shortness of breath. The family denied previous history of any illnesses, though they had lately noticed that she always felt hot. No further information was available.
On examination in the emergency department, she was conscious but irritable. Recorded vitals in were as follows: temperature 39°C, HR 150 BPM, BP 100/55 mmHg and SaO2 98% with 4 L simple face oxygen mask. Chest examination revealed presence of few bilateral basal crackles, while neurological examination showed normal reactive pupils with no lateralization signs or neck stiffness. There was no documentation of neck stiffness on initial assessment.
Laboratory results were as follows: white blood cell count (WBC) 37.7 × 109/L (normal range [NR], 5.0–10.0 × 109/L); hemoglobin, 12.0 g/dL (NR, 12.0–16.0 g/dL); serum glutamic oxaloacetic transaminase (AST) 33 U/L (NR, 10–35 U/L); serum glutamic pyruvic transaminase (ALT) 23 U/L (NR, 0–40 U/L); blood urea nitrogen, 12.5 mg/dL (NR, 8–20 mg/dL); creatinine, 0.9 mg/dL (NR, 0.6–1.5 mg/dL); blood sugar, 430 mg/dL (NR, 50–110 mg/dL); serum sodium, 140.9 mEq/L and urine dipstick glucose +++ Ketones ++.
Her chest X-ray showed bilateral interstitial infiltrate. Lactic acid measurement test was not available. Blood, sputum and urine cultures were all obtained. Nasopharyngeal swab for H1N1 was also obtained.
The patient was diagnosed with diabetic ketoacidosis and community-acquired bronchopneumonia with possible influenza A (H1N1) viral pneumonia. She was admitted to the medical ward and was started on Ceftriaxone, Clindamycine and Oseltamivir (Tamiflu). She also received insulin infusion and was given IV hydration with normal saline (NS).
After 48 h of being in the medical ward, the medical team decided to intubate the patient because of tachypnea, hypoxia and restlessness. Her arterial blood gas (ABG) at that time was as follows: PH 7.2 PaO2 42 mmHg, pCO2 17.7 mmHg, HCO3 10.7 mEq/L. She remained in the medical ward for another 12 h until a bed could be arranged in the ICU.
In the ICU, the first set of vitals in ICU was as follows: temperature 39°C, HR 160 and BP 95/48 mm Hg. She was ventilated on Synchronized Intermittent Mandatory Ventilation (SIMV) mode with 60% FiO2, a tidal volume (Vt) of 450 and positive end-expiratory pressure (PEEP) of 5 mm Hg. On that setting, the pulse oximetry was showing a saturation of (SaO2) 100%. A right subclavian central line was inserted and central venous pressure (CVP) monitoring was started. Her initial CVP was 8 mm Hg, she was given 6–8 L of IV fluid boluses in the first 12-h of care in the ICU and a maintenance fluid of 150–200 cc/h of NS. Inotropic support was started with norepinephrine, which was titrated to maintain systolic BP above 90 mm Hg. She was sedated with midazolam and fentanyl. She was started on piperacillin/tazobactam, and ciprofloxacin, while Tamiflu was continued. Her H1N1 PCR was reported positive within 6 h of admission to the unit.
She remained critically ill, and after 48 h, she was still febrile with a high-grade temperature of 39.5°C despite around the clock on paracetamol. She also had sinus tachycardia with a heart rate of 130–160. Her blood pressure (BP) was fluctuating on high-dose norepinephrine, which was changed to phenylephrine and vasopressin. All cultures including sputum and blood did not grow any organisms, and despite that antibiotic was changed again in 48 h to imipenem and ciprofloxacin because of poor response to the initial regimen.
Her FiO2 requirement, however was progressively improving and in 48 h, she was on 40% FiO2, with ABG pH 7.4 PaO2 108 mm Hg, pCO2 28 mm Hg and HCO3 20 mEq/L. The bilateral chest x-ray infiltrate was resolving.
On the third day of admission, a thyroid function test was requested due to unexplained tachycardia. Thyroid function results were available in 24 h and were as follows Thyroid stimulating hormone TSH < 0.01 mIU/L (0.3–3.0 nmolIU/L), T3 50 nmol/L (1.1–3 nmol/L) T4 200 nmol/L (60–145 nmol/L).
The diagnosis of thyroid storm was considered and she was started on propylthiouracil, 150 mg every 6 h (the only available drug) and on esmolol infusion. No iodine preparation was available.
There was a significant improvement of tachycardia and hemodynamics after these measures but the patient was already progressing to multiorgan failure with progressively worsening renal and liver parameters as shown in . She was started on renal replacement therapy on the sixth day of admission. On the seventh day of admission, she suddenly became bradycardic and had a 6-min cardiac arrest. The patient's pupils were fixed and dilated after cardiopulmonary resuscitation. A CT of the brain was requested; it revealed a massive subarachnoid hemorrhage with severe brain edema. Despite aggressive measures that included Mannitol and hyperventilation, she progressed to brain death and was pronounced dead on the ninth day of admission to the hospital.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [430.0, 'mg/dL'], 'Sodium': [140.9, 'mEq/L']}",148.82,141.379,156.261,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.9 mEq/L. 
The concentration of glucose is 430.0 mg/dL. 
Plugging in these values into the formula gives us 140.9 mEq/L + 0.024 * (430.0 - 100) = 148.82 mEq/L.
Hence, the patient's corrected concentration of sodium is 148.82 mEq/L."
5496,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-4434,Extracted,"An 18-year-old G1P0 woman who is 10 weeks pregnant presents for her first prenatal visit. She reports nausea with occasional vomiting but denies bleeding, urinary symptoms, or abdominal pain. She just graduated high school and works at the local grocery store. She does not take any medications and has no known drug allergies. Physical examination is unremarkable. Initial laboratory studies reveal the following:

Serum:
Na+: 140 mEq/L
Cl-: 100 mEq/L
K+: 4.0 mEq/L
HCO3-: 24 mEq/L
BUN: 10 mg/dL
Glucose: 100 mg/dL
Creatinine: 1.0 mg/dL
Thyroid-stimulating hormone: 2.5 µU/mL
Ca2+: 9.5 mg/dL
AST: 25 U/L
ALT: 20 U/L

Leukocyte count: 10,000 cells/mm^3 with normal differential
Hemoglobin: 14 g/dL
Hematocrit: 42%
Platelet count: 200,000 /mm^3

Urine:
Epithelial cells: few
Glucose: negative
WBC: 20/hpf
Bacterial: > 100,000 cfu / E.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [100.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",140,133,147,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.0 mEq/L. 
The concentration of glucose is 100.0 mg/dL. 
Plugging in these values into the formula gives us 140.0 mEq/L + 0.024 * (100.0 - 100) = 140.0 mEq/L.
Hence, the patient's corrected concentration of sodium is 140.0 mEq/L."
5497,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7509571-1,Extracted,"A 56-year-old man presented to the emergency department with bleeding (>700 cc) around his colostomy site persisting for two days. The patient denied any pain with the bleeding, fever, chills, sweats, weakness, abdominal pain, nausea, vomiting, or diarrhea. The patient denied any history of smoking, alcohol, or any other substance abuse. The patient's surgical history included a remote colectomy with permanent colostomy for stage IV colon cancer and a subsequent colostomy revision and hernia repair (8 and 6 years, respectively, before this episode), after experiencing a massive bleed from a parastomal varices. The patient has a medical history of hypertension, hyperlipidemia, diabetes, hypothyroidism, colon cancer, obstructive sleep apnea, and obesity.
The patient's current medications upon presentation in the emergency department included pioglitazone, ipratropium bromide, insulin glargine, montelukast, levocetirizine, atorvastatin, azelastine, bisoprolol, levothyroxine, lisinopril, metformin, triamcinolone, and aspirin. The patient's blood pressure was 128/84 mmHg. The patient's white blood cell count was 3,970 cells/µL, platelet count was 119,000/µL, and red blood cell count was low at 4.080 million cells/uL. His hemoglobin and hematocrit levels were 13.7 g/dL and 39.2%, respectively. His sodium was below normal, and he was hypochloremic (135 mmol/L and 95 mmol/L, respectively), glucose was elevated at 313 mg/dL, and creatine was normal at 0.8 mg/dL. His liver function was normal, aside from slightly elevated alanine transaminase of 64 international units/L.
Given the recurrent bleeding over several days, surgery was consulted to evaluate the bleeding. No further bleeding was elicited, and the patient was discharged. However, the patient returned to the emergency department the next day reporting 50 cc of dark red blood while emptying his colostomy bag. Vascular surgery and gastroenterology were consulted. A right upper quadrant ultrasound demonstrated a gallstone, no pericholecystic fluid or wall thickening, and common bile duct diameter of 6 mm without intrahepatic biliary ductal dilatation. The liver measured 20 cm in length with the portal vein slightly dilated at 1.1 cm. Furthermore, the portal vein showed hepatopedal blood flow with a velocity of 14.6 cm/s. The liver echotexture was also hyperechogenic suggesting mild hepatic steatosis. Visualization of the pancreas was normal.
The colonoscopy performed through the stoma was without abnormality. EGD showed a normal esophagus without any esophageal varices and a normal duodenum; however, mild portal hypertensive gastropathy was found diffusely in the entire stomach. A CT scan of the abdomen showed the main portal vein to be slightly dilated measuring 14 mm. The superior mesenteric vein was also dilated measuring 15 mm. Mesenteric veins extending into the parastomal hernia were also dilated. As shown in , the CT scan demonstrated a parastomal hernia with accompanying dilated parastomal varices. Given the lack of further bleeding, the patient was released and given instructions on how to reduce the risk of further bleeding from the parastomal varices. The patient subsequently had another episode of massive bleeding (>700 cc) occurring two years after the incident described herein, which resolved sponstaneously after the patient aggressively debrided the vascular erosion and applied manual compression. No rebleeding has occurred in the year since the last incident.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [313.0, 'mg/dL'], 'Sodium': [135.0, 'mmol/L']}",140.112,133.1064,147.1176,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 135.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 135.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 135.0 mmol * 1 mEq/mmol = 135.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mmol sodium/L converts to 135.0 mEq sodium/L. 
The concentration of glucose is 313.0 mg/dL. 
Plugging in these values into the formula gives us 135.0 mEq/L + 0.024 * (313.0 - 100) = 140.112 mEq/L.
Hence, the patient's corrected concentration of sodium is 140.112 mEq/L."
5498,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-6080,Extracted,"A 67-year-old man presents to the emergency department with a fever and altered mental status. The patient has a history of Alzheimer dementia and is typically bed bound. His son found him confused with a warm and flushed complexion thus prompting his presentation. The patient has a past medical history of dementia, diabetes, and hypertension and typically has a visiting home nurse come to administer medications. Prior to examination, he is given haloperidol and diphenhydramine as he is combative and will not allow the nurses near him. His temperature is 102.9°F (39.4°C), blood pressure is 104/64 mmHg, pulse is 170/min, respirations are 22/min, and oxygen saturation is 100% on room air. Physical exam is notable for dry and flushed skin and a confused man. There is no skin breakdown, and flexion of the patient’s neck elicits no discomfort. Laboratory studies are drawn as seen below.

Hemoglobin: 15 g/dL
Hematocrit: 45%
Leukocyte count: 4,500/mm^3 with normal differential
Platelet count: 227,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 24 mEq/L
BUN: 30 mg/dL
Glucose: 97 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 10.2 mg/dL
AST: 12 U/L
ALT: 10 U/L

Urine:
Color: Yellow
Bacteria: Absent
Nitrites: Negative
Red blood cells: Negative

An initial chest radiograph is unremarkable. The patient is given 3 liters of Ringer's lactate and an electric fan to cool off. Two hours later, his temperature is 99°F (37.2°C), blood pressure is 154/94 mmHg, pulse is 100/min, respirations are 17/min, and oxygen saturation is 100% on room air. The patient’s mental status is at the patient’s baseline according to the son.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [97.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",138.928,131.9816,145.8744,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 139.0 mEq/L. 
The concentration of glucose is 97.0 mg/dL. 
Plugging in these values into the formula gives us 139.0 mEq/L + 0.024 * (97.0 - 100) = 138.928 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.928 mEq/L."
5499,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2760558-1,Extracted,"A 68 year-old Asian woman was admitted to our hospital presenting with a two-day history of high grade fever, diarrhea and nausea. The patient's symptoms began one day after eating grilled chicken and beef at a restaurant; however, she did not complain of abdominal pain, vomiting, or hematochezia. The patient was diagnosed with diabetes mellitus at the age of 50, had undergone haemodialysis due to diabetic nephropathy for the past 2 years, and was under three times weekly haemodialysis. She had also undergone an aortic mechanical valve replacement operation for aortic stenosis 7 months prior to the current admission.
Upon admission to our hospital, the patient's height was 149 cm and her body weight were 61.0 kg (dry weight). The patient's temperature was 106°F, blood pressure was 150/90 mmHg, heart rate was 152/min, and respiratory rate was 24/min. Cardiovascular examination revealed a Levine IV/VI systolic murmur at the right second intercostal space. Her bowel movements were slightly hypoactive and physical examination did not reveal any abdominal tenderness or rebound. No evidence of embolization including Osler node, Janeway lesion and petechiae was observed. No other abnormalities were noted on the systemic examination. Initial laboratory examinations revealed the following results: hemoglobin, 115 g/L [110-146 g/L]; total leukocyte counts, 10300/μL [3500-8200/μL] without left shift (Myelo 0.5%, Meta 0.5%, Stab 2.0%, Seg 90.0%, Lym 1.5%, Mono 5.5%); normal platelet counts, 1.42 × 103/μL [1.40-3.89 × 103/μL]; significantly elevated C-reactive protein, 18.54 mg/dL [<0.30 mg/dL]; Na 131 mEq/L, K 4.3 mEq/L, Cl 97 mEq/L, HCO3- 18.9 mmol/L; BUN 43.6 mg/dL, Cre 7.25 mg/dL (before haemodialysis); serum glucose, 173 mg/dL; and HbA1c, 7.3% [4.3-5.8%]. In addition, the patient was tested negative for HIV antibodies.
Salmonella enteritis or campylobacter enteritis was suspected due to the history of eating grilled chicken. Treatment was initiated with ciprofloxacin 300 mg q24hr, ceftriaxone 2 g q24hr, and clindamycin 600 mg q12hr intravenously, started on day of admission. Three days post-admission, a serial blood culture taken on admission revealed Salmonella enterica serotype Enteritidis (O9, H-g) that was sensitive to ceftriaxone (MIC <= 1) and ciprofloxacin (MIC <= 0.25) (Table ). After detection of the causable microorganism, ceftriaxone and clindamycin treatment was ceased, and the patient was treated with ciprofloxacin alone. Since the patient's aortic valve was a prosthetic, and Salmonella species have a high affinity for intravascular intima, there was a concern about prosthetic infective endocarditis. Therefore, the patient underwent transthoracic echocardiography (TTE) on day 7; however, no abnormalities were detected by TTE. On day 9, the patient showed a sudden disturbance in mental status, left conjugate deviation, and right hemiplegia. Diffusion-weighted imaging of the brain via MRI showed an acute cerebral infarction of the middle cerebral artery region (figure ). Following this discovery, the TTE was re-examined, followed by a transesophageal echocardiography (TEE) on day 13. The TEE revealed floppy vegetation on the mitral valve, which was 12 × 8 mm in size (figure ). We could not find any aberrance of the replaced aortic valve. Although surgery to remove the vegetation was considered, acute cerebral infarction contraindicated her from undergoing the operation. The ciprofloxacin dose was increased to 400 mg q24hr and was combined with ceftriaxone 2q q12hr, on day 12. Consequently, the patient was treated solely with ciprofloxacin for 8-day period (from day 4 to day 11). Although the patient's neurological deficit ameliorated gradually, she experienced another infarction at the left occipital lobe and the right cerebellar hemisphere on day 18. Conservative therapy with antibiotics was continued; however, her mental status progressively decreased and blood pressure deteriorated. Blood culture examinations were repeated, but they were all negative. haemodialysis ceased on day 35 due to the unstable haemodynamic status, although treatment with ciprofloxacin and ceftriaxone were continued. On day 39, the patient died of respiratory failure and cardiac arrest. Her clinical course is shown in figure . Autopsy revealed a rigid node on the mitral valve (figure ), associated with septic emboli (mass of gram-negative microorganisms) at the left occipital lobe (figure ).","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [173.0, 'mg/dL'], 'Sodium': [131.0, 'mEq/L']}",132.752,126.1144,139.3896,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 131.0 mEq/L. 
The concentration of glucose is 173.0 mg/dL. 
Plugging in these values into the formula gives us 131.0 mEq/L + 0.024 * (173.0 - 100) = 132.752 mEq/L.
Hence, the patient's corrected concentration of sodium is 132.752 mEq/L."
5500,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7713822-1,Extracted,"The present case report was published with the prior consent of the patient’s guardians.
A 23-year-old, 168 cm tall female patient, weighing 42 kg, visited the emergency room with a chief complaint of abdominal pain. The abdominal pain, accompanied by nausea and vomiting, kept increasing gradually for eight hours. The patient was diagnosed with major depression and bulimia nervosa nine years ago. The patient also had a history of frequent vomiting after episodes of binge eating, along with numerous suicide attempts. Ten hours before reporting to the hospital, the patient ate a very large quantity food, equivalent to approximately ten portions; however, the quantity of the vomit was much less, relative to the amount of food taken. The physical examination revealed abdominal pain and distension in the entire region, along with tenderness, but no rebound tenderness. Subsequent abdominal computed tomography (CT) revealed clear gastric distension. The results of various blood tests were normal. In the joint general surgery consultation that followed, it was decided that an immediate surgical treatment was not necessary; hence, the need for continuous observation of the condition was explained, and a gastroenterological or psychiatric hospitalization was advised, but both the patient and her guardians declined hospitalization. Afterward, they were warned of the possible complications, such as electrolyte imbalance, aspiration pneumonia, gastrointestinal perforation, ischemic changes, due to the pressure applied by gastrointestinal distension, and the possibility of death, in case the condition worsened. The self-discharge form was signed, and they returned home.
Seven hours after returning home, the patient re-visited the emergency room due to persistent abdominal pain, and mental confusion. At the time of the visit, the patient was unconscious. On physical examination, a more severe abdominal distension, and signs of abdominal rigidity were observed. Both legs of the patient had turned pale in color. No auscultation sounds were heard over the abdomen, and the dorsalis pedis pulse was not felt on either foot. Shock was suspected due to a 60/40 mmHg blood pressure, 160 beats/min heart rate, 22 times/minute aspiration rate, and 36.4℃ temperature. Other findings included pH 7.076, PaCO2 22.3 mmHg, PaO2 122 mmHg, HCO3- 6.3 mM/L, base excess (BE) 23.7 mM/L, and lactic acid 11.1 mM/L, which were measured in the arterial blood gas analysis and, thus, metabolic acidosis was confirmed. The electrolyte levels Na+ 157 mM/L, K+ 6.2 mM/L, and Cl- 130 mM/L, indicated that the electrolyte imbalance was severe (). In addition, the patient was in a severe hypoglycemic state with a blood sugar level of 15 mg/dl; because of an elevated creatinine level of 2.84 mg/dl, acute renal failure was suspected. First, to treat the metabolic acidosis, sodium bicarbonate was set at 80 mEq/h. In the abdominal X-ray, the gastrointestinal tract (GIT) was seen to be filled with a large amount of food but without any bowel gas (). Abdominal CT revealed a very large dilation of the stomach, esophagus, and the second part of the duodenum; it was suspected that the distended organs were pressing against the descending aorta, and the right kidney was pressed upwards (). One hour after the emergency room re-visit, the patient's mental state became lethargic—communication became impossible and spontaneous respiration decreased; as SpO2 was measured to be 88%, endotracheal intubation was performed. A Foley catheter was then inserted, but no urine was drained; an emergency hemodialysis was prepared, and for enough fluid supply, a central venous catheter was inserted into the right jugular vein. For continuous monitoring of changes in the vital signs, a conduit was placed in the right radial artery. An attempt was made to insert a nasogastric tube to relieve gastrointestinal pressure, but the food was not drained due to a blockage near the esophagus, which made further insertion impossible. An abdominal CT performed for follow-up observation revealed that the abdomen was still filled with food, and the nasogastric tube was twisted at the end of the esophagus (). It was also suspected that insertion was not possible due to gastroesophageal junction deviation or esophageal stenosis; however, no such sign was seen.
There was no decompression through the nasogastric tube, and as time passed, the mental state of the patient changed into a state of confusion. The patient’s vital signs became increasingly unstable. Since the symptoms and follow-up blood test results exacerbated, instead of performing a percutaneous drainage, it was decided to attempt a surgical decompression; subsequently, the patient was transferred to the operation room six hours after the re-visit. In the emergency room, a total of 3,170 ml of crystalloid fluid, in which a 5% glucose solution was included, was administered. Urine volume was not measured.
After reaching the operation room, the patient’s blood pressure was 70/46 mmHg and the heart rate was 128 beats/min. First, in order to improve the vital signs, crystalloid fluid was administered at the highest speed via the right arm’s peripheral venous catheter and via the central venous catheter of the right internal jugular vein. The instillation of norepinephrine was initiated with sustained dosing at an additional rate of 0.2 μg/kg/min, and continuous infusion of vasopressin at 4–8 unit/h was also initiated. Subsequently, general anesthesia was induced using sevoflurane 1–2 vol% and rocuronium 50 mg. In the arterial blood gas analysis conducted after entering the operating room, pH 7.45, PaCO2 20.8 mmHg, PaO2 335 mmHg, Na+ 161 mM/L, K+ 3.8 mM/L, glucose 205 mg/dl, lactate 13 mM/L, hemoglobin 6.8 g/dl, and HCO3- 14.4 mM/L were measured (). Four units of erythrocytes were prescribed to correct the reduced hemoglobin, and 20 mg of furosemide was injected due to a continuous lack of urination. Furthermore, for rapid transfusion, the rapid infusion system (RIS) was connected to the central venous catheter of the right internal jugular vein, and the transfusion of four erythrocyte units was initiated.
The operating surgeon planned and performed a gastrotomy, after making a skin incision of approximately 10 cm and within 20 min of beginning the surgery. The food and 5,000 ml of body fluid present in the stomach were drained via suction. Thirty minutes after the operation, blood pressure was maintained low at 60/40 mmHg and almost all food was drained; as a large amount of continuous gastric bleeding occurred after decompression, a total of 6,000 ml was drained into the suction bottle. In the follow-up arterial blood gas analysis, results showed: pH 6.75, PaCO2 46 mmHg, and lactate 20 mM/L. Acidosis had worsened, the blood sugar level had significantly increased to 469 mg/dl, electrolyte imbalance had exacerbated with K+ 7.5 mM/L, and hemoglobin had fallen to 4.3 g/dl, suggesting a large amount of bleeding. To correct this, 60 mEq of sodium bicarbonate, and two units of insulin were administered. Further, 1.2 g of calcium chloride was administered to treat hyperkalemia. Moreover, additional 20 μg of epinephrine was injected to correct persistent hypotension.
Bleeding in the stomach continued, and despite initiating erythrocyte transfusion via RIS, hemoglobin level decreased. As a result, a large amount of internal bleeding was suspected, and additional eight units of erythrocytes, and eight units of fresh frozen plasma were prescribed. The operating surgeon tried to determine the cause and area of bleeding, but as the surgical incision was only 10 cm, abdominal organs other than the stomach could not be identified with the naked eye. To reduce bleeding, the operating surgeon considered performing a total gastrectomy or extending the abdominal incision to confirm the bleeding areas from, other organs but concluded that the bleeding was due to ischemia-reperfusion injury after surgical decompression, and DIC. Since the patient’s vital signs steadily worsened, it was decided that the abdomen be closed urgently, and the patient moved to the intensive care unit (ICU).
One hour after the start of the operation, suturing after gastrectomy was completed. When the closing of the abdomen started, non-invasive blood pressure was not measured, and flat waveforms were observed in the catheter of the right radial artery. There was no pulse detected via palpation, and after confirming pulseless electrical activity through the observation of electrocardiogram, an additional 1 mg of epinephrine was injected, and cardiopulmonary resuscitation (CPR) was initiated.
A total of 3 mg of epinephrine was injected, with cardiac rhythm monitoring at 2 min intervals; afterward, 2 units of vasopressin were injected at 2 min intervals, totaling an injection of 4 units of vasopressin. After completing the abdominal closure while performing CPR, the patient was transferred to the intensive care unit, and no urine output was seen until the patient left the operation room.
The operation was conducted for 1 h 20 min, and the anesthesia time was 1 h 50 min. During the operation, a total of 800 ml, four erythrocyte units, were transfused, and 6,200 ml of crystalloid fluid were administered. A total of 6,000 ml was drained into the suction bottle—5,000 ml of food and body fluid through the suction unit via gastrectomy, and 1000 ml due to bleeding that had occurred after decompression from the start of the operation until finish; however, as mentioned earlier, the incision area was small, and bleeding occurring from other abdominal organs could not be confirmed, making it difficult to estimate the exact estimated blood loss. Additionally, prescribed erythrocytes and fresh frozen plasma were transfused through the RIS as the patient left the operation room.
After entering the ICU, CPR was stopped due to a return of spontaneous circulation, but the existing usage of epinephrine, norepinephrine, and vasopressin was preserved, and transfusion continued. However, blood pressure was still not measured, an additional 1,000 ml of bleeding was confirmed through the nasogastric tube, and bleeding from the closed abdominal area continued. Subsequently, as 3.5 g/dl hemoglobin was measured in the follow-up test, transfusion continued, and a 113.1-second prothrombin time, 180-s activated partial thromboplastin time, and platelet count of 22,000/μl were found, confirming that the patient was in a state of DIC. Despite continuous drug administration and transfusion, the hemoglobin level decreased to 1.8 g/dl, and after three hours in the ICU, the heartbeat disappeared, and the patient was declared dead.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [15.0, 'mg/dL'], 'Sodium': [157.0, 'mEq/L']}",154.96,147.212,162.708,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 157.0 mEq/L. 
The concentration of glucose is 15.0 mg/dL. 
Plugging in these values into the formula gives us 157.0 mEq/L + 0.024 * (15.0 - 100) = 154.96 mEq/L.
Hence, the patient's corrected concentration of sodium is 154.96 mEq/L."
5501,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3668109-1,Extracted,"A 53-yr old woman (body weight: 63 kg, height: 162 cm) was scheduled for living donor liver transplantation due to acuteon-chronic liver failure. Thirteen years ago, she was diagnosed with hepatitis B related liver cirrhosis. Two days ago, she was intubated due to rapidly developing grade 3-4 hepatic encephalopathy. In the preoperative evaluation, the chest X-ray, electrocardiography, and echocardiography were within normal range. Her laboratory examination showed Hb 7.9 g/dl, platelet count 27 × 109/L, prothrombin time 3.5 international normalized ratio, fibrinogen 52 mg/dl, antithrombin III 6%, sodium 136 mmol/L, potassium 3.9 mmol/L, creatinine 3.8 mg/dl, glucose 163 mg/dl, albumin 3.1 g/dl, total bilirubin 52.8 mg/dl, and ammonia 205 µmol/L. Her Child-Pugh and Model for End-Stage Liver Disease scores were 12 and 49, respectively. However, brain computerized tomography and invasive ICP monitoring could not be performed because the acute exacerbation of her clinical condition requires urgent liver transplantation.
Upon arrival at the operating room, she was still intubated and was in a comatose state. Dopamine of 10 µg/kg/min, dobutamine of 15 µg/kg/min, and norepinephrine of 0.1 µg/kg/min had been administered continuously. Her systolic/diastolic/mean arterial blood pressure and heart rate were 100/50/67 mmHg and 80 beats/min, respectively. After establishing the standard monitoring used in our institute, ultrasound ONSD measurements were done by a physician well-trained in ocular ultrasonography before anesthetic induction. Based on the method described in a previous report [], both eyes were scanned using a 7.5-MHz probe (ProSound SSD-4000, ALOKA, Tokyo, Japan) through closed eyelids with the patient in the supine position. Right and left eyes were scanned in both sagittal and transverse planes, and the ONSD value was calculated by estimating the average results of these measurements. The ONSD was measured 3 mm posterior to the globe in each eye. Her ONSD just before anesthesia induction was 6.4 mm (). Simultaneously, TCD was performed to assess cerebral blood flow velocity and ICP noninvasively. Transtemporal insonation of the left middle cerebral artery was done using a 2-MHz probe (Companion III, Viasys Healthcare, Warwick, UK). TCD measurements showed her systolic/diastolic/mean cerebral flow velocities were 100/7/37 cm/s (normal reference values of systolic/diastolic/mean velocities [mean ± SD]: 77.1 ± 12.23/37.4 ± 7.13/50.6 ± 8.42 cm/s). The resistance index was 0.93 (normal reference value: 0.52 ± 0.05) and the pulsatility index was 2.5 (normal reference value: 0.80 ± 0.13), and the second systolic peak (Windkessel effect) was lost, suggesting elevated ICP () [,]. The bispectral index and suppression ratio were 30 and 20, respectively, and right and left regional cerebral oxygen saturations were 15/15%.
Anesthesia was induced with thiopental and vecuronium, and was maintained using 0.5-1% isoflurane, a 50% O2/air mixture, and continuous infusion with fentanyl and vecuronium. The patient's lungs were ventilated with a tidal volume of 10-12 ml/kg at a respiratory rate of 10-12 breaths/min to maintain hypocarbia (PaCO2: 28-32 mmHg) throughout the procedure. Also, mild hypothermia (34-35℃) was induced, and mannitol of 40 g was administered every six hours for the management of ICP. After anesthesia induction, her arterial blood gas analysis showed a pH of 7.33, a PaCO2 of 28 mmHg, a PaO2 of 209 mmHg, bicarbonate of 14.8 mEq/L, and base excess of -10.0 mmEq/L. Intraoperative hemodynamics and laboratory data were shown .
After finishing surgery, she was transferred to the surgical intensive care unit. On the second postoperative day, right and left pupil size were 3/3 mm. According to Glasgow coma scale evaluation, eye opening score was 4, best motor response score was 4, best verbal response score was not evaluated due to endotracheal intubation. Bispectral index score ranged from 70 to 90. However, on the third postoperative day, she was developed septic shock, and the patient died by septic shock on the fourth postoperative day.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [163.0, 'mg/dL'], 'Sodium': [136.0, 'mmol/L']}",137.512,130.6364,144.3876,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 136.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 136.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 136.0 mmol * 1 mEq/mmol = 136.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mmol sodium/L converts to 136.0 mEq sodium/L. 
The concentration of glucose is 163.0 mg/dL. 
Plugging in these values into the formula gives us 136.0 mEq/L + 0.024 * (163.0 - 100) = 137.512 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.512 mEq/L."
5502,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-57,Extracted,"A 32-year-old man comes to the physician because of a 2-week history of diarrhea. During this period, he has had about 10 bowel movements per day. He states that his stools are light brown and watery, with no blood or mucus. He also reports mild abdominal pain and nausea. Over the past year, he has had 6 episodes of diarrhea that lasted several days and resolved spontaneously. Over this time, he also noticed frequent episodes of reddening in his face and neck. He returned from a 10-day trip to Nigeria 3 weeks ago. There is no personal or family history of serious illness. He has smoked a pack of cigarettes daily for the past 13 years. His temperature is 37°C (98.6°F), pulse is 110/min, and blood pressure is 100/60 mm Hg. Physical examination shows dry mucous membranes. The abdomen is tender with no rebound or guarding. The remainder of the examination shows no abnormalities. Serum studies show:
Na+ 136 mEq/L
Cl- 102 mEq/L
K+ 2.3 mEq/L
HCO3- 22 mEq/L
Mg2+ 1.7 mEq/L
Ca2+ 12.3 mg/dL
Glucose (fasting) 169 mg/dL
Nasogastric tube aspiration reveals significantly decreased gastric acid production.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [169.0, 'mg/dL'], 'Sodium': [136.0, 'mEq/L']}",137.656,130.7732,144.5388,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 136.0 mEq/L. 
The concentration of glucose is 169.0 mg/dL. 
Plugging in these values into the formula gives us 136.0 mEq/L + 0.024 * (169.0 - 100) = 137.656 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.656 mEq/L."
5503,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2740308-1,Extracted,"A 78-year-old Indian, non-smoker man, presented to out patient department with progressively increasing generalized weakness for two months. He gave history (on leading question) of weight loss (about 2 kg) during this period. There was no history of fever, cough, expectoration, hemoptysis or chest pain. Patient denied any history of joint pain, skin rash, photosensitivity, Raynaud's phenomenon or oral ulcers. There was no history high risk sexual behavior, intravenous drug abuse or blood transfusion. Patient had history of type-2 diabetes mellitus since last 10 years and was taking oral hypoglycemic agents (Metformin SR 850 mg twice daily and Glimiperide 2 mg once a day) with good control of blood sugars. He was also suffering from coronary artery disease for which he was taking his medications (Aspirin 75 mg once a day, Metoprolol SR 25 mg twice daily and Atorvastatin 10 mg once a day at night). There was no history of tuberculosis in the past. Family history was non contributory. Physical examination revealed well built and nourished elderly. He was afebrile with oral temperature of 98.2°F. His pulse was 82/minute and blood pressure was 126/72 mm of Hg. There was no pallor, icterus, peripheral lymphadenopathy, clubbing or bony tenderness. Chest examination revealed reduced expansion in infrascapular region on the right side with dull percussion note and reduced breath sounds in the same region. There was no hepatosplenomegaly. Examination of cardiovascular and nervous system did not reveal any abnormality.
Blood investigations revealed hemoglobin of 13.5 gm/dl, total leukocyte count 5,400/µl with differential counts showing mild eosinophilia (neutrophil 56%, lymphocyte 32%, monocyte 05%, and eosinophils 07%), platelets were 2,24,000/µl and ESR was 110 mm in 1st hour. Serum biochemistry including calcium (10 mg/dl), uric acid (4.0 mg/dl), sodium (141 mg/dl) and potassium (5.0 mg/dl) were normal. Liver function tests showed raised total protein (8.4 gm/dl) and reversed albumin (3.5 gm/dl) and globulins (4.9 gm/dl) ratio. Total bilirubin (0.4 mg/dl), alanine aminotransferase (39 U/L; reference value 30-65 U/L), aspartate aminotransferase (26 U/L; reference value 15-37 U/L) and alkaline phosphatase (51 U/L; reference value 50-136 U/L) were normal. Fasting blood sugar was 107 mg/dl. Renal functions tests showed normal blood urea (12 mg/dl) and creatinine (0.9 mg/dl). Lipid profile was also within normal limits. Patient tested for HIV infection by ELISA was negative.
Chest radiograph () showed mass lesion in right lower zone and multiple nodules in bilateral lung fields. For further characterization, CT of chest was done. It revealed a large mass with sharp margins in right lower lobe and multiple nodules in both lungs. Multiple nodules of varying sizes were seen in left upper lobe, lingula and apical segment of left lower lobe (, ). It also revealed mild right sided pleural effusion. On the basis of radiological findings, metastatic lung disease from extra thoracic origin, carcinoma lung with metastases were considered as differentials diagnoses. Patient was evaluated for extrathoracic primary site of malignancy. Stool samples for occult blood were negative for three times. Urine did not show any evidence of hematuria. Prostate specific antigen levels were normal. Urine examination was negative for Bence-Jones proteins. Serum electrophoresis revealed M-band and ß-2 microglobulins were raised (1952 µg/l; reference value 510-1470 µg/l) but other tests including bone marrow aspirate and biopsy did not reveal any evidence of plasma cell dyscrasia. Serum LDH was normal.
For the histological diagnosis, CT guided biopsy from the right lung mass was done. Histopathological examination () showed fibrocollagenous tissue infiltrated by monomorphic round cells with scanty cytoplasm, high nucleo-cytoplasmic ratio, large vesicular nucleus and prominent nucleoli in some of the cells. Frequent mitotic activity and apoptotic bodies were noted. Immunohistochemistry showed the cells to be positive for leukocyte common antigen (LCA) and CD20 (B-cell marker) while being negative for CD3 (T-cell marker), cytokeratin and neuroendocrine markers. Stains for acid fast bacilli and fungus were negative. Thus, a final pathological diagnosis of diffuse large cell B-cell lymphoma was rendered. Patient was evaluated for involvement of other sites by lymphoma. Contrast enhanced CT of abdomen did not revealed any mass lesion. Patient was referred to medical oncology for chemotherapy. However, family declined any treatment. Patient last seen a week back was stable.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [107.0, 'mg/dL'], 'Sodium': [141.0, 'mg/dL']}",61.468,58.3946,64.5414,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 141.0 mg/dL. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mg to mEq. The mass of sodium is 141.0 mg. To convert from 141.0 mg to mEq, first convert from mg to mmol.To convert 141.0 mg of sodium to g, multiply by the conversion factor 0.001, giving us 141.0 mg sodium * 0.001 g/mg = 0.141 g sodium. To convert from grams of sodium to moles, divide by the molar mass 22.99 g/mol, which will give 0.141 g/(22.99 g sodium/mol) = 0.00613 mol sodium. To convert 0.00613 mol of sodium to mmol, multiply by the conversion factor 1000.0, giving us 0.00613 mol sodium * 1000.0 mmol/mol = 6.13 mmol sodium. To convert from 6.13 mmol sodium to mEq, multiply the mmol amount by the valence, to get 6.13 mmol * 1 mEq/mmol = 6.13 mEq sodium. The current volume unit is dL and the target volume unit is L. The conversion factor is 0.1 L for every unit of dL. Our next step will be to divide the mass by the volume conversion factor of 0.1 to get the final concentration in terms of mEq/L. This will result to 6.13 mEq sodium/0.1 L = 61.3 mEq sodium/L. The concentration value of 141.0 mg sodium/dL converts to 61.3 mEq sodium/L. 
The concentration of glucose is 107.0 mg/dL. 
Plugging in these values into the formula gives us 61.3 mEq/L + 0.024 * (107.0 - 100) = 61.468 mEq/L.
Hence, the patient's corrected concentration of sodium is 61.468 mEq/L."
5504,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-5727,Extracted,"A 66-year-old woman presents to the emergency department with abdominal pain. Her symptoms began when she was eating dinner. She has a past medical history of obesity, constipation, intravenous drug use, and diabetes. The patient is instructed to be nil per os and is transferred to the surgical floor. Three days later she had a cholecystectomy and is recovering on the surgical floor. Her laboratory values are ordered as seen below.

Hemoglobin: 11 g/dL
Hematocrit: 33%
Leukocyte count: 8,500/mm^3 with normal differential
Platelet count: 197,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.5 mg/dL
Alkaline phosphatase: 533 U/L
GGT: 50 U/L
AST: 22 U/L
ALT: 20 U/L

The patient is currently asymptomatic and states that she feels well.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [99.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",138.976,132.0272,145.9248,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 139.0 mEq/L. 
The concentration of glucose is 99.0 mg/dL. 
Plugging in these values into the formula gives us 139.0 mEq/L + 0.024 * (99.0 - 100) = 138.976 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.976 mEq/L."
5505,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-6862,Extracted,"A 60-year-old woman presents to the emergency room with chest pain that started 20 minutes ago while watching television at home. The pain is substernal and squeezing in nature. She rates the pain as 6/10 and admits to having similar pain in the past with exertion. Her past medical history is significant for diabetes mellitus that is controlled with metformin. The physical examination is unremarkable. An electrocardiogram (ECG) shows ST-segment depression in the lateral leads. She is started on aspirin, nitroglycerin, metoprolol, unfractionated heparin, and insulin. She is asked not to take metformin while at the hospital. Three sets of cardiac enzymes are negative.
Lab results are given below:
Serum glucose 88 mg/dL
Sodium 142 mEq/L
Potassium 3.9 mEq/L
Chloride 101 mEq/L
Serum creatinine 1.2 mg/dL
Blood urea nitrogen 22 mg/dL
Cholesterol, total 170 mg/dL
HDL-cholesterol 40 mg/dL
LDL-cholesterol 80 mg/dL
Triglycerides 170 mg/dL
Hematocrit 38%
Hemoglobin 13 g/dL
Leucocyte count 7,500/mm3
Platelet count 185,000 /mm3
Activated partial thromboplastin time (aPTT) 30 seconds
Prothrombin time (PT) 12 seconds
    Urinalysis
Glucose negative
Ketones negative
Leucocytes negative
Nitrites negative
Red blood cells (RBC) negative
Casts negative
An echocardiogram reveals left ventricular wall motion abnormalities. With the pain subsiding, she was admitted and the medications were continued. A coronary angiography is planned in 4 days.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [88.0, 'mg/dL'], 'Sodium': [142.0, 'mEq/L']}",141.712,134.6264,148.7976,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 142.0 mEq/L. 
The concentration of glucose is 88.0 mg/dL. 
Plugging in these values into the formula gives us 142.0 mEq/L + 0.024 * (88.0 - 100) = 141.712 mEq/L.
Hence, the patient's corrected concentration of sodium is 141.712 mEq/L."
5506,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5984920-1,Extracted,"A 45-year-old Caucasian woman presented with abdominal pain, nausea, and vomiting for 17 h. At 22 h prior to admission, she went out to dinner and drank one glass of wine. A few hours after the meal, she developed epigastric and left upper quadrant abdominal pain that was moderate, persistent, cramping, and aching; the pain radiated to her left middle back and arm without exacerbating or alleviating factors. The pain was associated with nausea, vomiting, and she could not tolerate any oral intake. She felt thirsty and had polyuria and positional lightheadedness. She reported no fever, chills, chest pain, cough, sputum production, dysuria, hematuria, diarrhea, hematochezia, and melena.
On further questioning, the patient shared that she had a history of gestational glucose intolerance 6 years ago, and has had occasional impaired fasting glucose of 81–107 mg/dL for the past 6 years. She began following an American Diabetes Association (ADA) diet 2 years ago and lost 25 lb. Additionally, she had a past medical history of supraventricular tachycardia, irritable bowel syndrome, social alcohol use, cholecystectomy, and thyroid papillary adenocarcinoma status post partial thyroidectomy complicated by postsurgical hypothyroidism. Home medications included metoprolol tartrate, levothyroxine, and meloxicam. The patient reported no family history of diabetes.
Temperature 97.7 °F, pulse 130 bpm, respiratory rate 28 bpm, BP 134/71 mmHg, weight 87 kg, height 1.68 m, BMI 31 kg/m2, SpO2 99% on room air.
The patient was in moderate distress. There was no acanthosis nigricans. Cardiovascular system revealed tachycardia. A pulmonary exam revealed tachypnea, accessory muscle usage with moderate respiratory distress. Abdominal exam revealed central obesity, normoactive bowel sounds, left upper quadrant and epigastric tenderness to palpation, no rigidity or guarding. No costovertebral angle tenderness.
CBC: WBC 25.9 × 109/L, hemoglobin 14.7 g/dL, hematocrit 45.8%, platelet 386 × 109/L, MCV 100.2 µm3. BMP: sodium 135 mmol/L, potassium 7.4 mmol/L, chloride 89 mmol/L, bicarbonate 5 mmol/L, BUN 37 mg/dL, creatinine 1.27 mg/dL, glucose 931 mg/dL, eGFR 46 mL/min.
Liver chemistry: Total bilirubin 0.2 mg/dL, AST 23 U/L, ALT 54 U/L, ALP 138 U/L, total protein 7.5 g/dL, albumin 4.5 g/dL. Calcium 8.7 mg/dL, phosphate 1.4 mg/dL, magnesium 2.1 mg/dL. VBG: pH 6.92. Repeated ABG 2 h later: pH 7.21, pCO2 16 mmHg, pO2 129 mmHg, HCO3− 6.4 mmol/L, SaO2 98% on 2 L/min oxygen by nasal cannula. Beta-hydroxybutyrate 28 mmol/L, lactic acid 4.0 mmol/L. Urinalysis showed urine ketones 80 mg/dL, leukocyte esterase negative, urine culture no growth. HbA1c 6.4%. Lipid profile: triglycerides 89 mg/dL, total cholesterol 144 mg/dL, LDL 91 mg/dL, HDL 35 mg/dL. TSH 3.12 mIU/mL, free T4 1.26 ng/dL. Troponin I < 0.01 ng/mL.
Ultrasonography of the abdomen revealed mild hepatic steatosis, incidental mild to moderate right-sided hydronephrosis, status post cholecystectomy. ECG on admission: sinus rhythm, HR 126 bpm, peaked T waves at lead V2–V6 consistent with hyperkalemia, no ischemic changes.
All procedures performed in this study were in compliance with the ethical standards of the institutional and/or national research committee and with the 1964 Declaration of Helsinki and its later amendments or comparable ethical standards. Informed consent was obtained from the individual participant for being included in the study.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [931.0, 'mg/dL'], 'Sodium': [135.0, 'mmol/L']}",154.944,147.1968,162.6912,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 135.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 135.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 135.0 mmol * 1 mEq/mmol = 135.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mmol sodium/L converts to 135.0 mEq sodium/L. 
The concentration of glucose is 931.0 mg/dL. 
Plugging in these values into the formula gives us 135.0 mEq/L + 0.024 * (931.0 - 100) = 154.944 mEq/L.
Hence, the patient's corrected concentration of sodium is 154.944 mEq/L."
5507,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7683122-1,Extracted,"The patient is a 19-year-old female with a history of 6q24-related TNDM and Hashimoto's thyroiditis who was diagnosed with neonatal diabetes mellitus at birth.
She was born to a 25-year-old G3P2 mother, with a weight of 1927 grams, at 36 weeks of gestation via vaginal delivery after induction due to IUGR at an outside hospital. The pregnancy was significant for intrauterine growth restriction noted at 5 months of gestation. The pediatrician was at the delivery, and no resuscitation was needed. Apgar scores were 8 at 1 minute and 9 at 5 minutes. Macroglossia was noted. Umbilical hernia and hypotonia were not found. The infant was noted to have hypoglycemia on day of life one and was given intravenous glucose and went on to develop hyperglycemia. Glucose levels were the 400 mg/dl, and an insulin drip was started. The infant was transferred to the NICU from the outside hospital due to hyperglycemia and concerns for necrotizing enterocolitis (NEC). Due to concerns for NEC, oral feeds were discontinued and she was placed on TPN, providing a steady glucose load. No surgical intervention was necessary for the NEC. Glucose was difficult to control even while on TPN with blood sugar levels ranging from the 100s to >200 mg/dl. At about 1 month of age, glucose levels started dropping and insulin was weaned. During this time, due to an IV infiltrate, IV insulin was briefly discontinued and blood glucose was 268 mg/dl. Insulin infusion was restarted and was discontinued at about 1 month of age. Blood sugar levels ranged between 80 and 150 mg/dl. The infant was discharged shortly afterward, feeding ad lib and checking blood sugar before meals. She required intermittent subcutaneous insulin at home, which was finally discontinued at approximately 4 months of age. Since then, the patient did not require insulin or have diabetes symptoms. All developmental milestones were on time. At 15 years of age, she chipped her tooth and went to the dentist for evaluation. The dentist noted extensive tooth decay. Jaw X-rays showed bone loss of nearly 80% in the left mandible. Due to her history of TNDM, she was sent to her primary care provider for further workup and diabetes screening where blood glucose was 369 mg/dl and urinalysis showed positive ketones. She was sent to the emergency department, and laboratory examination showed blood glucose of 361 mg/dl, Na+ of 131 mEq/L, K+ of 3.4 mmol/L, bicarbonate of 19 mmol/L, 2+ urine ketones, anion gap of 16, and pH of 7.4. HbA1c was 15.4% during her admission. The diabetes autoimmune panel was negative (ICA-512, GAD-65, and Insulin Antibodies).
She endorsed long-standing polydipsia, polyphagia, and polyuria. She denied weight loss, nausea, vomiting, abdominal pain, confusion, blurry vision, fatigue, fever, and difficulty breathing. Family history was negative for autoimmune diseases except for hypothyroidism in the paternal grandmother and maternal great-grandmother. Physical exam showed a weight of 58.4 kg (70th percentile), height of 163 cm (55th percentile), and BMI of 21.98 kg/m2 (70th percentile). She was a well-appearing adolescent without thyromegaly and acanthosis nigricans and had Tanner Stage 5 breast. She was started on basal bolus insulin regimen consisting of 23 units of Glargine at bedtime and fast-acting insulin Lispro 1 unit per 10 grams of carbohydrates with meals.
She received the appropriate diabetes education. Laboratory examination also noted a TSH of 66 IU/ml (reference range: 0.35–5.5 uIU/ml); free T4 was 0.94 ng/dl (reference range: 0.8–1.8 ng/dl), and positive antibodies to thyroid peroxidase was 8580 IU/ml. She was treated with 75 mcg Levothyroxine that was titrated to a dose of 100 mcg. The 6q24 methylation-specific multiplex ligation-dependent probe amplification (MPLA) genetic test for transient neonatal diabetes identified hypomethylation within the 6q24 region. Deletion/duplication analysis ruled out paternal duplication of 6q24. Therefore, the hypomethylation could be the result of either paternal uniparental disomy of chromosome 6 (UPD6) or hypomethylation of the maternal allele. Via testing, UPD6 has been confirmed, meaning both copies of the 6q24 chromosome region in our patient were paternally inherited. This results in an epigenetic phenomena where both copies are still active. Typically, the paternal copy is active and the maternal copy is methylated and turned off. Epigenetic changes are typically de novo, as they depend on the parent of origin and are reset with each pregnancy, rather than DNA sequencing changes. Thus, risk of recurrence for parents, siblings, and offspring is unlikely. After diagnosis and her initial HbA1c of 15.4%, her HbA1c has ranged since then from 6.3% to 6.8%.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [361.0, 'mg/dL'], 'Sodium': [131.0, 'mEq/L']}",137.264,130.4008,144.1272,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 131.0 mEq/L. 
The concentration of glucose is 361.0 mg/dL. 
Plugging in these values into the formula gives us 131.0 mEq/L + 0.024 * (361.0 - 100) = 137.264 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.264 mEq/L."
5508,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3841495-1,Extracted,"A 48-year-old male, heavy alcohol consumer for the prior 6 years, presented with complaints of severe abdominal pain, vomiting and constipation for 3 days. There was no history of diabetes mellitus, hypertension, smoking, and previous abdominal pain. On admission to our hospital (on day 4 of illness), he was hemodynamically stable, had abdominal distention with diffuse tenderness and absent bowel sounds. Laboratory work up on day 4 revealed serum amylase: 898 U/l, lipase: 968 U/l, glucose: 116 mg/dl, Na+: 132 mEq/l, K+: 3.6 mEq/l, creatinine: 1.9 mg%, calcium: 8.6 mg/dl, bilirubin: 1.4 mg/dl, aspartate transaminase/alanine transaminase: 74/28 IU/l, alkaline phosphatase: 181 IU/l, serum proteins/albumin: 7.1/2.9 g/dl, serum cholesterol: 124 mg/dl, triglycerides: 130 mg/dl, Hb: 8.4 g/dl, leucocytes: 15,400/μl, platelets: 98,000/μl, prothrombin time: 18 s, activated partial thromboplastin time: 40 s. Computed tomography (CT) of abdomen [] carried out with intravenous contrast on day 4 revealed enlarged, diffusely enhancing pancreas, multiple peripancreatic fluid collections and bilateral pleural effusions, confirming grade E AP (CT severity index = 4). He was kept nil per orally. Continuous nasogastric aspiration, intravenous fluids, stress ulcer prophylaxis and subcutaneous unfractionated heparin 5000 units twice/day for venous thromboprophylaxis were started. On day 5, he developed right sided hemiplegia. CT of brain revealed large left MCA territory infarct [Figures and ]. Electrocardiogram (ECG) and echocardiography of the heart were normal. Work up for hyperhomocysteinemia, protein C and S deficiency, factor V Leiden, antithrombin III deficiency and antiphospholipid antibody syndrome was negative. Patient developed high grade fever and progressive acute renal failure from day 6. He was started on piperacillin + tazobactam and metronidazole. He was intubated on day 8 for progressive respiratory distress and hypoxia and was shifted to intensive care unit for mechanical ventilation. On day 9, he developed shock and was discharged against medical advice upon insistence of his relatives.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [116.0, 'mg/dL'], 'Sodium': [132.0, 'mEq/L']}",132.384,125.7648,139.0032,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 132.0 mEq/L. 
The concentration of glucose is 116.0 mg/dL. 
Plugging in these values into the formula gives us 132.0 mEq/L + 0.024 * (116.0 - 100) = 132.384 mEq/L.
Hence, the patient's corrected concentration of sodium is 132.384 mEq/L."
5509,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6971472-1,Extracted,"A 56-year-old woman was admitted to our emergency department (ED) with disturbance of consciousness and respiratory failure. She had influenza-like symptoms including cough and fatigue without fever 2 days prior to presentation. She did not have a medical history but took an over-the-counter drug that contains ibuprofen for headache.
The patient's height was 139 cm and weight was 29.0 kg. Her vital signs were: blood pressure, 131/78 mm Hg; heart rate, 78 b.p.m. and regular; axillary temperature, 35.1°C; respiratory rate, 30 breaths/min; SpO2, 85% with oxygen delivered through a face mask (3 L/min); and a Glasgow Coma Scale score of E3V3M5 on admission.
Rapid viral testing was positive for influenza A virus. Significant laboratory results included hypoglycemia (serum glucose, 48 mg/dL), transaminitis (aspartate aminotransferase [AST] 12,548 IU/L and alanine aminotransferase [ALT] 5,725 IU/L), hyperbilirubinemia (total bilirubin 3.5 mg/dL and direct bilirubin 1.6 mg/dL), elevated international normalized ratio (INR; 3.16), hyperammonemia (ammonia 102 μg/dL), lactic acidosis (7.0 mmol/L), azotemia (blood urea nitrogen 55 mg/dL), hypercreatinemia (serum creatinine 2.32 mg/dL), hyponatremia (134 mmol/L), hyperkalemia (6.7 mmol/L), hypolipidemia (total cholesterol 114 mg/dL and triglyceride 29 mg/dL). Carnitine was normal (223 μmol/L). Her liver function was normal 5 days before presentation.
The head computed tomography (CT) revealed no specific findings, although the head magnetic resonance imaging showed hyperintense signals at the bilateral globus pallidus in diffusion-weighted images and fluid attenuation inversion recovery (FLAIR)-weighted images and a hyperintense signal at the left front parietal lobe in FLAIR-weighted images (Fig. ). Abdominal CT revealed fatty and enlarged liver. Chest CT showed diffuse alveolar type infiltrates in the patient's right middle lobe with air bronchograms and respiratory muscle loss. Based on these findings, we diagnosed the patient with RS induced by influenza A virus and pneumonia. The clinical course of the patient is shown in Figure . She was intubated and placed on mechanical ventilation in the ED then transferred to the intensive care unit for supportive care. She was treated with prednisolone (500 mg/day for 3 days) and peramivir (100 mg/day for 5 days) for influenza encephalopathy. The patient's liver function gradually improved with supportive care, fresh frozen plasma, and vitamin K. Her transaminase trended down from AST 7,546 IU/L and ALT 4,127 IU/L on day 2, to AST 85 IU/L and ALT 704 IU/L on day 7, and to AST 23 IU/L and ALT 169 IU/L on day 14 of hospitalization. Her INR trended down from 3.16 on day 1, to 1.28 on day 7, and to 1.07 on day 14. A tracheostomy was carried out on day 12 because of respiratory insufficiency type II due to muscle atrophy with chronic malnutrition.
On 14 day, the patient's condition had dramatically improved, with no abnormal neurological findings. Her appetite returned to normal and anorexia resolved. Her total duration of hospital stay was 71 days, and she was transferred to a rehabilitation hospital without neurological deficits.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [48.0, 'mg/dL'], 'Sodium': [134.0, 'mmol/L']}",132.752,126.1144,139.3896,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 134.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 134.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 134.0 mmol * 1 mEq/mmol = 134.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mmol sodium/L converts to 134.0 mEq sodium/L. 
The concentration of glucose is 48.0 mg/dL. 
Plugging in these values into the formula gives us 134.0 mEq/L + 0.024 * (48.0 - 100) = 132.752 mEq/L.
Hence, the patient's corrected concentration of sodium is 132.752 mEq/L."
5510,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6016161-1,Extracted,"A 55-year-old woman with a history of type 2 diabetes mellitus, hyperlipidemia, obesity, and depression was referred to an endocrinologist with complaints of weight loss, palpitations, and diarrhea. The patient also had hypertension and was taking α-adrenergic receptor antagonists and a calcium channel blocker. She was found to have a thyroid-stimulating hormone (TSH) level of <0.10 (normal: 0.34 to 4.82) µlU/ml and a free T4 concentration of 4.28 (normal: 0.6 to 1.6) ng/dL. I123 thyroid scan revealed elevated, diffuse uptake bilaterally, without nodules, consistent with the diagnosis of Graves' disease. The patient was treated with 11.9 mCi of radioactive iodine. Ten days after the ablation treatment, the patient presented to a local hospital by ambulance after experiencing lightheadedness, diffuse abdominal pain, and one episode of bilious emesis.
Upon arrival, she was hypotensive (77/44 mm Hg), pale, bradycardic, and febrile (39.4°C). An electrocardiogram (ECG) revealed accelerated junctional rhythm at a rate of 53 beats/min. The patient was given atropine 0.5 mg intravenously without effect, followed by initiation of external cardiac pacing. Continuous intravenous infusions of dopamine and norepinephrine were started along with fluid resuscitation of 4 L of normal saline over a 2-hour period. She received one ampule of calcium gluconate with no change in her blood pressure, heart rate, or rhythm. Computed tomography of the abdomen was unrevealing. The patient was endotracheally intubated and transferred via helicopter to our facility.
Upon arrival to our facility, she was receiving intravenous infusions of dopamine at 20 µg/kg/min and norepinephrine at 10 µg/kg/min and remained hypotensive (92/55 mm Hg) and bradycardic (59 beats/min). ECG showed an accelerated junctional rhythm. Laboratory findings included serum sodium of 139 mEq/L, potassium of 5.3 mEq/L, chloride of 108 mEq/L, and total CO2 content of 15 mmol/L, serum glucose of 208 mg/dL, urea nitrogen of 38 mg/dL, creatinine of 1.5 mg/dL, ionized calcium of 1.15 mmol/L, total bilirubin of 0.4 mg/dL, serum alkaline phosphatase of 141 U/L, aspartate aminotransferase of 2196 U/L, and alanine aminotransferase of 2010 U/L. Plasma troponin I was repeatedly undetectable. The peripheral leukocyte count was 15.9 x 109 cells/L with no immature forms. There was evidence of an anion gap metabolic acidosis with a serum lactate concentration of 6.2 mmol/L. Blood cultures revealed no microbial growth. Thyroid function testing showed an undetectable TSH (<0.10 µlU/ml), a free T4 of 12.8 (normal: 0.6 to 1.6) ng/dL, total T4 of 21.9 (normal: 5.6 to 13.7) µg/dL, and a total T3 of 0.94 (normal: 0.8 to 1.8) ng/mL. The patient was treated for thyroid storm with 1000 mg of propylthiouracil by orogastric tube as a loading dose followed by 300 mg every 6 hours, 5 drops saturated solution of potassium iodide (SSKI) every 8 hours by orogastric tube, and 100 mg intravenously of hydrocortisone every 8 hours. The hypotension resolved, vasopressors were stopped, and the patient was extubated 25 hours after her initial presentation. During her stay in the intensive care unit, the patient exhibited fever (39.6°C maximum), tachycardia, and tremulousness. These manifestations resolved over a period of 22 hours. The patient was discharged in satisfactory condition on the fourth day of hospitalization on 100 mg of propylthiouracil orally every 8 hours. Outpatient testing days later demonstrated normalization of her thyroid function tests.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [208.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",141.592,134.5124,148.6716,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 139.0 mEq/L. 
The concentration of glucose is 208.0 mg/dL. 
Plugging in these values into the formula gives us 139.0 mEq/L + 0.024 * (208.0 - 100) = 141.592 mEq/L.
Hence, the patient's corrected concentration of sodium is 141.592 mEq/L."
5511,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3152516-1,Extracted,"A 56-year-old male with multiple co-morbidities, including a long-standing history of non-ischemic dilated cardiomyopathy, stage III chronic kidney disease, and congestive hepatopathy, underwent LVAD implantation two months prior to the most recent admission. He returned to the hospital due to persistent atrial fibrillation, progressively worsening dyspnea on exertion and rest, abdominal distension with ascites, and suspected ongoing hemolysis due to positioning of the inflow cannula at the apex of the LVAD.
It was decided that the patient should return to the operating room for placement of a new LVAD due to hemolysis and hypotension refractory to medical management. The night before the scheduled surgery, the patient was intubated due to worsening cardiopulmonary parameters, including increased work to breathe, and maintained on epinephrine 0.15 mcg/kg/min, norepinephrine 0.1 mcg/kg/min and dobutamine 3 mcg/kg/min. He was transferred to the operating room to replace the pump. Pre-op vitals included: temp 37.6 degrees Celsius, arterial blood pressure 64/50, mean arterial pressure 55, heart rate 118 and respiratory rate of 16. Prior to induction of anesthesia, labs included: white blood cells 15.2, hemoglobin 10, hematocrit 29.4, platelets 96, Na+ 130, K+ 3.1, Cl- 95, CO2 25, blood urea nitrogen 24, creatine 2.08, glucose 84, and international normalized ratio 3.5. Preoperative arterial blood gases were pH 7.48, pCO2 35.9, pO2 184.2, and HCO3 26.1. In the operating room, hemodynamic parameters were continuously monitored via radial arterial line and Swan-Ganz catheter. Induction was uneventful with etomidate 10 mg and cisatracurium 10 mg. The transesophageal echocardiography (TEE) probe was placed uneventfully. The surgeons entered the mediastinum using the previous sternal incision. Once they began dissecting out the mediastinum, the patient became severely hypotensive and asystolic, and the TEE did not detect any movement on both the left and right side of the heart.
The anesthesiologist alerted the surgeon that Advanced Cardiac Life Support (ACLS) protocol was needed and the surgeon communicated that chest compressions were contraindicated due to the position of the inflow cannula directly beneath the sternum. The anesthesiologist recommended AO-CPR with manual mid-abdominal compressions 1 to 2 inches left of midline (left paramedian) at a rate of 80 beats/min with maximal force while the surgeon cannulated the groin to provide long-term mechanical support in the form of ECMO. As instructed, two members of the team performed AO-CPR (Figure ). During ACLS, the patient continued to be mechanically ventilated and epinephrine, vasopressin, and sodium bicarbonate were given per ACLS protocol, and the hemodynamic parameters as a result of AO-CPR continued to be monitored (Figure ). The duration of the CPR was 15 minutes, during which time the surgeon was able to cannulate the femoral artery and vein and institute ECMO support. The chest was closed and the patient was transferred to the intensive care unit. The patient spent 24 hours in the intensive care unit on ECMO support and mechanical assist device. A decision was made to withdraw care after 24 hours and the patient expired.
Our case represents a difficult situation where the perioperative team faced a new challenge in the operating room: what are the alternatives to ECM when chest compressions are contraindicated due to position of the inflow cannula directly beneath the sternum? Neither the new guidelines published in the European Journal of Cardiothoracic Surgery in 2009 nor the American Heart Association in 2010 provided alternatives to ECM for patients with a mechanical assist device.
It became evident that there was a need for an alternative to ECM, such as AO-CPR, to protect the recent sternotomy until re-opening of the chest to provide internal cardiac massage. The Interactive Cardiovascular Thoracic Surgery e-community conducted a discussion to address whether AO-CPR could be used instead of ECM to either protect the recent sternotomy or while chest compressions are not possible during resternotomy []. After reviewing this evidence, Dunning et al. [] concluded that AO-CPR theoretically has the potential to provide adequate systemic perfusion while an emergency resternotomy is being performed, but further evidence is needed before it can be recommended for routine use.
In general, coronary perfusion pressure during cardiac arrest is the difference between pressure in the aorta (from which the coronary arteries arise) and the right atrium (into which the coronary arteries exit). Using a mathematical model to describe the biophysics of cardiopulmonary resuscitation with periodic z-axis acceleration or abdominal compression at aortic resonant frequencies, Babbs [] proposed that differences in wave mechanics, resulting from simultaneous compression of the abdominal aorta and the inferior vena cava, produced differences in pressure between the aorta and right atrium. During CPR, the minimal coronary perfusion pressure considered necessary for successful resuscitation with return of spontaneous circulation (ROSC) is 15 mmHg []. The values for mean aortic and central venous pressure for our patient were 77 and 62 mmHg, respectively, which provided a mean coronary perfusion pressure of 15 mmHg (77 to 62 mmHg). In a study of 100 patients, however, conventional CPR provided a mean CPP of only 12.5 mmHg []; thus, we propose that the abdominal only CPR in our patient could have served as an effective bridge between the arrest and initiation of ECMO.
In our case, AO-CPR was unplanned, but the surgeon refused chest compressions due to contraindications in this patient. Due to lack of alternatives for resuscitation other than ECMO in this patient, the anesthesiologist suggested that AO-CPR be performed as a temporary resuscitative effort until the surgeon could successfully cannulate the femoral artery and vein to provide long-term mechanical support. Two rescuers performed AO-CPR with generation of coronary perfusion pressure (CPP) of 15 mmHg for 15 minutes, the duration of resuscitation. Both achieved results that appeared to be identical. The evidence seems to suggest that AO-CPR in this particular situation may be comparable to ECM in generating adequate CPP, but at this point it is still too early to determine the true efficacy of AO-CPR compared to ECM with regards to ROSC and neurological outcome.
Other evidence of adequate CPP generated during AO-CPR includes that from Geddes and colleagues [] and Pargett et al. [] who compared AO-CPR with chest compressions in animal models, and showed that AO-CPR was equivalent or superior to standard chest compressions at providing coronary perfusion. Neither of these studies reported any visceral organ damage or contraindications to AO-CPR, nor did they comment on neurological outcome. At this time, we cannot comment on the efficacy of AO-CPR on neurological outcomes as neurological status could not be assessed in our patient because he was intubated, sedated and paralyzed until care was withdrawn.
This case report generates important concerns. In our patient, even though we generated a CPP of 15 mmHg, which has been shown in some patients to be adequate, we do not know whether it was adequate to allow ROSC or whether the ECMO was responsible for ROSC. Other concerns are: what is the optimal delivery (optimal rate, depth/force, duty cycle and location of hand position) of AO-CPR in achieving successful resuscitation with ROSC, what is the best strategy for ventilation during AO-CPR, and is there potential damage/injury to abdominal viscera during AO-CPR?","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [84.0, 'mg/dL'], 'Sodium': [130.0, 'mEq/L']}",129.616,123.1352,136.0968,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 130.0 mEq/L. 
The concentration of glucose is 84.0 mg/dL. 
Plugging in these values into the formula gives us 130.0 mEq/L + 0.024 * (84.0 - 100) = 129.616 mEq/L.
Hence, the patient's corrected concentration of sodium is 129.616 mEq/L."
5512,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8340512-1,Extracted,"On June 3rd, 2020, an 81-year-old French woman was admitted to the emergency department of a Paris hospital, for continuous fever and severe weakness for 5 days. On arrival, she had a mild fever (38.5 °C). She had a past medical history of chronic obstructive pulmonary disease (COPD) due to smoking (60 packs/year) and depression. Her past travel itinerary revealed her trips to Greece (2000), Dominican Republic (2002), Morocco (2010), Greece (2013 and 2015), and more recently to Tunisia (2019).
Cell blood count examination revealed moderate anaemia (10.8 g/dL, N = 12–16 g/dL), thrombocytopenia (65*109/L, N = 150–400*109/L), lymphocytopenia (0.3*109/L, N = 1–4*109/L), and normal leukocyte count (5.5*109/L, N = 4–10*109/L). The biochemical analyses of blood showed a normal creatinine (83µmol/L, 45–84 µmol/L) and glucose level (6.5mmol/L), a pH of 7.45, and an imbalance in electrolytes (Na = 126mmol/L, CL = 93mmol/L, K = 4mmol/L, and plasma lactate = 3.3mmol/L). A liver function test revealed ALT (38U/L) within normal range but an elevated AST (92U/L) with subsequent high C-reactive protein levels (84 mg/L, N < 5 mg/L). The blood tests were repeated a few days later, which showed a sudden decrease of thrombocytopenia (35*109/L, N = 150–400*109/L) and an elevated level of C-reactive protein (165 mg/L, N < 5 mg/L). Urine analysis showed Na < 20 mmol/L, K = 50 mmol/L; Urea = 323 mmol/L; Creatinine = 8.8 mmol/L. The clinical examination showed difficulty in swallowing and crepitations in the right lung. There were no abnormal respiratory, urinary, or digestive indications. Three days later, the thoraco-abdomino-pelvic computed tomography (CT) scan revealed a centrilobular emphysema probably related to the earlier history of COPD. No pulmonary edema or hepatosplenomegaly was seen. As inhalation pneumopathy was suspected, presumptive treatment with antibiotics Ceftriaxone (2 g/day) and Metronidazole (1.5 g/day) was given for 7 days. The patient was transferred to the ICU Department of Avicenne Hospital (Bobigny, France) on June 9th 2020, due to deterioration in her health condition along with hypoxemia (89 %). The patient was given supplemental oxygen at 2 L/minute. The clinical examination revealed a fever (39 °C), hypotension (90/50mmHg), confusion, somnolence (Glascow Coma Scale = 14) without sensory-motor deficits, cold peripheries, and diarrhoea. The history of frequent travels, sustained fever, along with thrombocytopenia suggested signs of malaria disease.
The LAMP-PCR (Alethia® Malaria, Meridian Bioscience) and lateral flow test (VIKIA® Malaria Ag Pf/Pan, Biomérieux, France) confirmed the presence of malaria parasite, Plasmodium sp. Microscopic examination (May-Grünwald Giemsa-stained thin blood smear) revealed the presence of trophozoites, schizonts, and gametocytes with 0.93 % parasitaemia. The particular band-form trophozoites, and other species-specific developmental stages of the parasite within RBC validated the presence of P. malariae (Fig. ). Conventional PCR amplification targeting 510 bp DNA fragment of small
subunit ribosomal RNA (ssrRNA) and bidirectional sequencing identified the parasite as P. malariae []. The patient was thus treated with chloroquine (10 mg/kg oral tablet in d1 and d2, and 5 mg/kg in d3) and 1 L/6 h IV perfusion of NaCl. The MGG-stained thick blood smears were examined on day 3 and day 7, after being shifted from ICU to a general ward, and a favourable evolution was observed within 5 days, with negative microscopy on d7.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [6.5, 'mmol/L'], 'Sodium': [126.0, 'mmol/L']}",126.4105,120.08997,132.73103,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 126.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 126.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 126.0 mmol * 1 mEq/mmol = 126.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 126.0 mmol sodium/L converts to 126.0 mEq sodium/L. 
The concentration of glucose is 6.5 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 6.5 mmol. To convert 6.5 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 6.5 mmol glucose * 0.001 mol/mmol = 0.0065 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0065 mol glucose * 180.16 g/mol = 1.17104 g glucose. To convert 1.17104 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 1.17104 g glucose * 1000.0 mg/g = 1171.04 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1171.04 mg glucose/10.0 dL = 117.104 mg glucose/dL. The concentration value of 6.5 mmol glucose/L converts to 117.104 mg glucose/dL. 
Plugging in these values into the formula gives us 126.0 mEq/L + 0.024 * (117.104 - 100) = 126.4105 mEq/L.
Hence, the patient's corrected concentration of sodium is 126.4105 mEq/L."
5513,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-4901,Extracted,"A 32-year-old man with a history of chronic alcoholism presents to the emergency department with vomiting and diarrhea for 1 week. He states he feels weak and has had poor oral intake during this time. The patient is a current smoker and has presented many times to the emergency department for alcohol intoxication. His temperature is 97.5°F (36.4°C), blood pressure is 102/62 mmHg, pulse is 135/min, respirations are 25/min, and oxygen saturation is 99% on room air. On physical exam, he is found to have orthostatic hypotension and dry mucus membranes. Laboratory studies are ordered as seen below.

Serum:
Na+: 139 mEq/L
Cl-: 101 mEq/L
K+: 3.9 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 9.8 mg/dL

The patient is given normal saline, oral potassium, dextrose, thiamine, and folic acid. The following day, the patient seems confused and complains of diffuse weakness and muscle/bone pain. An ECG and head CT are performed and are unremarkable.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [99.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",138.976,132.0272,145.9248,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 139.0 mEq/L. 
The concentration of glucose is 99.0 mg/dL. 
Plugging in these values into the formula gives us 139.0 mEq/L + 0.024 * (99.0 - 100) = 138.976 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.976 mEq/L."
5514,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-4420,Extracted,"A 32-year-old G1P0 woman presents to the emergency department at 34 weeks gestation. She complains of vague upper abdominal pain and nausea which has persisted for 2 weeks, as well as persistent headache over the past several days. Her temperature is 99.0°F (37.2°C), blood pressure is 164/89 mmHg, pulse is 88/min, respirations are 19/min, and oxygen saturation is 98% on room air.

Hemoglobin: 10 g/dL
Hematocrit: 30%
Leukocyte count: 7,800/mm^3 with normal differential
Platelet count: 25,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.2 mg/dL
AST: 199 U/L
ALT: 254 U/L

Urine:
Color: Yellow
Protein: Positive
Blood: Positive

The patient begins seizing.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [99.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",138.976,132.0272,145.9248,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 139.0 mEq/L. 
The concentration of glucose is 99.0 mg/dL. 
Plugging in these values into the formula gives us 139.0 mEq/L + 0.024 * (99.0 - 100) = 138.976 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.976 mEq/L."
5515,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-2296,Extracted,"A 38-year-old woman, gravida 2, para 2, is brought to the emergency department by her husband after an episode of unconsciousness. She delivered a healthy infant two weeks ago and the postpartum course was complicated by severe vaginal bleeding, for which she required 4 units of packed red blood cells. Since the blood transfusion, she has had decreased milk production and has felt fatigued. Her pulse is 118/min and blood pressure is 104/63 mm Hg. Her finger-stick glucose concentration is 34 mg/dL. Serum thyroid-stimulating hormone and thyroxine levels are low and the serum sodium level is 132 mEq/L.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [34.0, 'mg/dL'], 'Sodium': [132.0, 'mEq/L']}",130.416,123.8952,136.9368,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 132.0 mEq/L. 
The concentration of glucose is 34.0 mg/dL. 
Plugging in these values into the formula gives us 132.0 mEq/L + 0.024 * (34.0 - 100) = 130.416 mEq/L.
Hence, the patient's corrected concentration of sodium is 130.416 mEq/L."
5516,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3793492-1,Extracted,"The case was a 2-month-old male infant who had been referred to Namazee Hospital, Shiraz, Iran 7 days before the admission due to poor feeding, restlessness, and tachypnea. He was born through the cesarean section by a 31-year-old mother with the gestational age of 35 weeks, birth weight of 2450 g, and good APGAR (Appearance, Grimace, Activity, Respiration)1. The mother had undergone the cesarean section because of hypertension. The parents had non-consanguineous marriage and no history of specific diseases such as diabetes was there in the family.
The patient was hospitalized in Neonatal Intensive Care Unit(NICU)1 for 5 days with diagnosis of respiratory distress syndrome and then discharged with good general condition. He had desirable health status up to 1 week prior to admission. Then, he presented with poor feeding, restlessness, and respiratory distress and was referred to the hospital.
In the physical examination, the patient seemed dehydrated and lethargic and had kussmaul-respiration. Weight, length, and head circumference of the patient were 4200 g, 50 cm, and 37 cm, respectively and the rest of the physical examinations were normal. Moreover, the patient's laboratory findings revealed BS (Blood Sugar)2=410 mg/dl, BUN (Blood Urea Nitrogen)1=25 mg/dl, Na = 140 mEq/l, K = 3.9 mEq/l, pH = 7.12, HCO3= 8, PCO2= 21, and severe ketonemia.
The patient's treatment was started with intravenous fluid followed by insulin. During the hospital stay, he had two episodes of convulsion. After recovery from the acute phase of the disease, since the patient had permanent hyperglycemia, NPH3 insulin was started for him and finally he was discharged with 2.5 units NPH (Neutral Protamine Hagedorn) insulin in the morning and 1 unit in the evening.
Afterwards, blood sample was obtained from the patient and sent to the laboratory of doctors Henrik Thybo Christensen and Klaus Brusgaard in H. O. Andersen Children's Hospital and Department of Clinical Genetics in Denmark. Then, genetic mutation analysis of KCNJ11 was performed. In the analysis method, deoxyribonucleic acid was extracted and amplified by polymerase chain reaction followed by bi-directional sequencing of the entire coding region. The genetic variation c. 602G >T, p.R201 L was found in a heterozygous form. This genetic variation had been previously described as pathogenic by Codner in 2005.
After 2 months treatment with insulin, the treatment was switched from insulin to glibenclamide. At first, 0.1 mg/kg/day glibenclamide was given to the patient in the morning and at night. Then, based on the blood sugar level, glibenclamide was increased to 0.6 mg/kg/day. After treatment with glibenclamide, the patient's hyperglycemia was successfully controlled and he did not need insulin anymore. Now, the case is a 1-year-old infant with controlled hyperglycemia who only receives glibenclamide.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [410.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",147.44,140.068,154.812,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.0 mEq/L. 
The concentration of glucose is 410.0 mg/dL. 
Plugging in these values into the formula gives us 140.0 mEq/L + 0.024 * (410.0 - 100) = 147.44 mEq/L.
Hence, the patient's corrected concentration of sodium is 147.44 mEq/L."
5517,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7714420-2,Extracted,"A 49-year-old man with a history of severe alcohol abuse became unwell and was transported by emergency medical technicians to the ED at 3 pm. The family informed them that the patient was under treatment with DIS and had used 7 units of beer in the afternoon resulting in abdominal pain and thirst. Neither medication nor empty blisters were found at his home. Upon admission he showed a generalized erythema, decreased consciousness with a Glasgow Coma Score of 13/15 (Eye movement: 3, Verbal response: 4, Motor reaction: 6), tachycardia (125 beats/min) and a low blood pressure (70/30 mmHg). The first attending physician, a 1st year trainee in emergency medicine, tentatively diagnosed an anaphylactic shock but asked advice from the consultant in emergency medicine. The latter confirmed the presence of an erythema and found a diffusely painful abdomen on palpation. Auscultation of heart and lungs was normal. The patient was tachypneic with a peripheral oxygen saturation of 95% at room air. An arterial blood gas showed a pH of 7.50 (normal values 7.35–7.45), a bicarbonate of 20.8 mmol/L (normal values: 22–26 mmol/L), a base excess of -1.3 (normal values –3.5 to +3.5), a pCO2 of 27.1 mmHg (normal values: 35–45 mmHg), a pO2 of 83.8 mmHg (normal values: 83–108 mmHg), and a lactate of 4.1 mmol/L (normal values: 0.9–1.7 mmol/L). Further laboratory data showed a blood glucose of 179 mg/dl (normal values: 74–106 mg/dl), a sodium concentration of 133 mmol/L (normal values:136–145 mmol/L) and potassium concentration of 3.8 mmol/L (normal values: 3.6–4.8 mmol/L). The ethanolemia was 0.89 g/L and the consultant in emergency medicine diagnosed a DER. Because severe hypotension persisted even after a fast fluid bolus infusion of one liter of a balanced crystalloid solution, intravenous noradrenaline was started under invasive blood pressure monitoring. Administration of fomepizole was considered but not deemed necessary as the blood pressure rapidly recovered in the intensive care unit where noradrenaline could be discontinued, and the erythema disappeared. The patient could be discharged from the intensive care unit after 24 hrs.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [179.0, 'mg/dL'], 'Sodium': [133.0, 'mmol/L']}",134.896,128.1512,141.6408,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 133.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 133.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 133.0 mmol * 1 mEq/mmol = 133.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mmol sodium/L converts to 133.0 mEq sodium/L. 
The concentration of glucose is 179.0 mg/dL. 
Plugging in these values into the formula gives us 133.0 mEq/L + 0.024 * (179.0 - 100) = 134.896 mEq/L.
Hence, the patient's corrected concentration of sodium is 134.896 mEq/L."
5518,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2876707-1,Extracted,"A 62-year-old man presented with history of progressive breathlessness for the last eight years; and recently, low-grade fever, cough with purulent expectoration, and breathlessness at rest since the last three months. He was treated with various oral antibiotics, but his condition increasingly worsened. He had past history of appendicectomy 20 years back and fracture left humerus 15 years back. He is a known case of epilepsy since the last 15 years, which is controlled by oral diphenylhydantoin (phenytoin) 50 mg daily since the last 11 years. He is a shopkeeper, has never smoked, and has no significant family history. He also has no history of worm infestation; exposure to environmental, agricultural, and chemical pollutants; allergic diathesis or drug hypersensitivity reaction.
On examination, the patient was of average build, moderately nourished, with no anemia, icterus, clubbing, cyanosis, peripheral lymphadenopathy, skin rash, etc. There was nothing abnormal on general physical examination. His pulse rate was 110/min, respiration-38 breaths/min, blood pressure-110/70 mmHg, and temperature-99°F. Examination of respiratory system revealed bilateral diffuse, fine, late inspiratory crackles. Other systemic examinations were unremarkable.
His hemoglobin was 13 g%, total leukocyte count 12,800/ μL (polymorphs-62%, lymphocytes-20%, and eosinophils-18%), erythrocyte sedimentation rate - 19 mm in the first hour by Wintrobes method, blood sugar - 84 mg/ dL, blood urea - 24 mg/dL, serum creatinine - 0.7 mg/dL, SGOT - 28 IU, serum alkaline phosphatase - 95 IU/L, serum Na+ 142 mEq/L, serum K+ 4.1 mEq/L, serum Ca+ 10.5 mg/dL, with normal urine analysis, etc. Skiagram chest, PA view, revealed bilateral inhomogeneous infiltrates (more on the left side) with mild cardiomegaly []. His ECG was normal, but echocardiography revealed mild mitral regurgitation (MR), mild tricuspid regurgitation (TR), ejection fraction of 50%, normal left ventricle size and systolic function with reduced compliance. Results of serological tests for HIV, HBsAg, ANA, and ANCA were negative. The filarial and Aspergillus serological findings were also negative. Findings from sputum smears and culture examinations for pathogenic organisms, mycobacteria, and fungi were also negative. Stool examination gave a negative result for parasitic infestation. His arterial blood gas analysis revealed pH - 7.38, pO2 - 57.4, pCO2 - 41.1, HCO3 - 24.4, oxygen saturation- 89.1%, TCO2 - 25.7, base excess - 0.5, and shunt - 26.1. His spirometry revealed severe ventilatory abnormality, with FVC - 1.04 L (34% of the predicted), FEV1 - 0.91 L (37% of the predicted), FEV1/FVC ratio - 87%, PEF - 2.12 L/s (28% of the predictive value), and FEF25-75 - 0.65 L/s (19% of the predicted), etc. CT scan thorax revealed bilateral coarse interlobular septal thickening with perilymphatic nodularity and focal areas of reticular pattern more prominent at the lung periphery and bases []. There was mild pleural thickening at apex, but there was no evidence of pleural effusion, mediastinal lymphadenopathy, etc. Fiber-optic bronchoscopy revealed no endobronchial abnormalities, and bronchoalveolar lavage analysis revealed mixed inflammatory cells, including eosinophils, with no malignant cells, or cells with abnormal morphology, organisms (i.e., bacteria, acid-fast bacilli, fungi, and larva), or dust particles, etc. Transbronchial lung biopsy showed predominant chronic interstitial pneumonitis pattern with fibroblast proliferation, alveolar septal thickening, partial loss of alveolar architecture, and alveolar septal lympho-plasmocytic and eosinophilic infiltrates []. No granulomatous component or vasculitis or necrosis was evident.
The patient was initially managed with oxygen therapy, broad-spectrum antibiotics, and bronchodilators, along with supportive therapy. Fever and expectoration of sputum declined with the above-mentioned line of management, but breathlessness and peripheral eosinophilia persisted and even did not get corrected with a therapeutic trial of diethylcarbamizine therapy. The changes were felt to be related to DPH therapy. Lymphocyte stimulation test with phenytoin was done and found to be positive, with a stimulation index of 292%. Previous phenytoin therapy was stopped, and oral prednisolone (1 mg/Kg body wt/day) was added immediately, which resulted in improvements in both eosinophilia and, to some extent, breathlessness after two weeks. The patient was discharged after six weeks in a stable condition with partially improved lung functions but lost to follow-up for the next five months. Thereafter, he came for routine checkup, and this time he had breathlessness only on exertion with improvement in lung functions revealed on spirometry and marked clearance of radiographic abnormalities []. He also documented that he did not take any medications, including phenytoin or steroids, during that period.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [84.0, 'mg/dL'], 'Sodium': [142.0, 'mEq/L']}",141.616,134.5352,148.6968,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 142.0 mEq/L. 
The concentration of glucose is 84.0 mg/dL. 
Plugging in these values into the formula gives us 142.0 mEq/L + 0.024 * (84.0 - 100) = 141.616 mEq/L.
Hence, the patient's corrected concentration of sodium is 141.616 mEq/L."
5519,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8689433-1,Extracted,"A 5-year-old boy with type I diabetes mellitus was exposed by a classmate with COVID-19
illness. The patient's family was tested, and all members resulted positive. Over the next
few days, the young boy had minimal symptoms, described as rhinorrhea and decreased energy.
Besides the initial testing encounter, the family did not seek medical care as he was
relatively well, and they isolated at home as the COVID-19 pandemic continued in New York
City in March 2021.
Eight days later, the patient's parents noted he was off-balanced while walking. He also
reported “seeing double”; his hands were shaking, causing him to drop things like his glass
of milk. He had one low grade fever to 101 degrees F and mildly decreased appetite but
otherwise appeared well, so the family monitored him at home. His blood glucose was in the
normal range for him. Eleven days after the initial exposure to COVID-19, the mother
reported these symptoms to his endocrinologist who encouraged them to go to the emergency
room. By this time, he was unable to ambulate independently and needed to hold onto
something in order to walk. He had swaying truncal movements while sitting upright. His
hands would shake while he played with his toys. Otherwise, he was thinking clearly and was
his normal active self.
The family reported all medications were stored away in the house and the patient did not
have access to them. Of note, in addition to over-the-counter medications like acetaminophen
or ibuprofen, his father was on an immunosuppressant regimen for a kidney transplant. Family
denied any new foods or exposure at home. He did not receive any vaccinations during this
time. There was no family history of progressive or episodic ataxia.
He was diagnosed with type 1 diabetes mellitus one year earlier with serum testing positive
for glutamic acid decarboxylase (GAD) antibodies (value 47 IU/mL) and islet cell antibodies.
His home medications included basal and bolus insulin injections, and he wore a Dexcom G6
continuous glucose monitor. Despite treatment, he had variable glucose levels and a most
recent hemoglobin A1c value of 10%. He had an episode of gross hematuria in the past that
was attributed to nephrolithiasis. He had a family history of kidney disease.
On physical examination, his temperature was 36.6 °C, blood pressure 110/73 mm Hg, heart
rate 73 beats/min, respiratory rate 28 breaths/min, and oxygen saturation 99% on room air.
His initial glucose was 265 mg/dL. He was well appearing and playful. His mental status was
appropriate for his age. Neurologic examination showed mild dysarthria, truncal titubation,
irregular rapid alternating hand movements, bilateral dysmetria on finger-to-nose and
heel-to-shin testing. His gait was wide-based and ataxic. He was unable to tandem. The rest
of the neurologic examination was unremarkable. Notably, he had no nystagmus.
Laboratory workup revealed normal routine studies except for a decreased sodium of
129 mEq/L (normal 135-145 mEq/L), elevated creatinine 0.84 mg/dL (normal <0.6 mg/dL), and
elevated glucose 511 mg/dL (normal 70-140 mg/dL). SARS-CoV-2 IgG nucleocapsid antibody serum
testing was positive. Nasopharyngeal swab was positive for SARS-CoV-2 (COVID-19) by
polymerase chain reaction (PCR). Urinalysis showed elevated glucose to >1000 mg/dL and
ketones to 15 mg/dL, although this was close to his prior baseline studies. Otherwise,
complete blood count (CBC), basic metabolic panel (BMP), liver function test (LFT),
C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and venous blood gas (VBG)
were unrevealing. During hospitalization, his glucose levels had a wide range
(105-511 mg/dL) but the studies were never consistent with diabetic ketoacidosis.
Cerebrospinal fluid (CSF) was obtained. The opening pressure was elevated to 28 cm
H2O but he was moving during testing. CSF was clear and colorless with 8 WBC
(normal <5 cells/uL) and 0 RBC (normal 0 cells/uL). Manual differential showed 86%
lymphocytes and 14% monocytes. CSF total protein was 20 (normal 10-40 mg/dL) and glucose was
110 mg/dL. Other infectious testing sent from the CSF resulted negative. The CSF sample was
sent to the New York State Department of Health and tested negative for SARS-CoV-2. Brain
magnetic resonance imaging (MRI) with and without contrast was normal on hospital day 2
().
The patient remained admitted for 4 days, with some improvement in his ataxia. He was
discharged home with a rolling walker and outpatient physical therapy. Although he continued
to have some balance issues one month after discharge, by two months his symptoms had
completely resolved.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [511.0, 'mg/dL'], 'Sodium': [129.0, 'mEq/L']}",138.864,131.9208,145.8072,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 129.0 mEq/L. 
The concentration of glucose is 511.0 mg/dL. 
Plugging in these values into the formula gives us 129.0 mEq/L + 0.024 * (511.0 - 100) = 138.864 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.864 mEq/L."
5520,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2923795-1,Extracted,"A 74-yr-old woman was transferred to our emergency department from the local general hospital with an initial diagnosis of brain stem infarct on January 17, 2009. The patient was found unconscious and in a bed-ridden state during the early morning on the presenting day. The patient's breathing was shallow and irregular. The patient was unable to walk well due to a coccyx fracture two years ago, but she was able to perform daily life activities with minor help. One week ago, her facial edema started and she complained dry cough and general weakness three days ago. No other medical, familial, or social history was reported, and the patient had not taken any medication. There was also no evidence of intoxication.
According to the records of the local general hospital, the patient had an impending respiratory arrest and comatose mental status. Her blood pressure was 71/48 mmHg, her body temperature was 36.0℃, and her pulse rate was 99 beats/min with a sinus rhythm by electrocardiography (ECG). Neurologic examination revealed pinpoint pupils and a lack of brain stem reflexes, including the light reflex, corneal reflex, gag reflex, and doll's-eye phenomenon. She also showed decerebrated rigidity in response to painful external stimuli. The patient was assigned a score of 5 on the Glasgow Coma Scale, and the Babinski sign was detected at both feet. Brain computed tomography (CT) produced unremarkable results. Endotracheal intubation was performed for protection of the patient's airway, assisted ventilation was initiated, and an inotropic agent was injected to support the patient's state of shock, which did not respond to fluid therapy (1 L of normal saline). Prior to transfer, the patient's blood pressure was increased, but her neurologic findings were not improved. She was transferred to our hospital for further evaluation and treatment of a brain stem infarct.
On arrival, the patient's blood pressure was 70/40 mmHg, her pulse rate was 59 beats/min, and an intravenous infusion of premixed dopamine was administered (500 mL/800 mg, 20 µg/kg/min). The patient's body temperature was 34.8℃ according to a tympanic membrane thermometer, and her self-respiration was slow and shallow. The patient's lungs on auscultation were bilaterally clear, and cardiac examination showed a regular rate and rhythm without murmurs, gallops, or rubs. The patient's abdomen was soft without signs of guarding, tenderness, or rebound tenderness. A rectal examination revealed no masses, and the patient's stool was guaiac negative. No soiling due to urine or feces was noted on her undergarments.
The patient's face and extremities were edematous, and she presented with non-pitting edema. Her skin was dry, cool, pale, and slightly mottled and desquamated; however, there was no evidence of petechiae or purpura ().
The patient's level of consciousness was stupor to semi-coma. A neurologic examination revealed intact cranial nerves and she didn't show lateralizing signs. The patient's pupils were 3 mm across and briskly reactive. It was impossible to check for visual abnormalities and focal cerebellar findings. The results of the Babinski reflex test were negative.
The patient's laboratory values were as follows: WBC count 6,000/µL (86% neutrophils), hemoglobin 11.8 g/dL, sodium 121 mEq/L, potassium 4.2 mEq/L, chloride 87 mEq/L, BUN 1.3 mg/dL, creatinine 0.6 mg/dL, glucose 104 mg/dL, ALT 113 U/L, AST 74 U/L, albumin 3.3 g/dL, CK 499 IU/L, CK-MB 21.4 ng/mL, troponin-I <0.02 ng/mL, lactate 1.2 mM/L, urine RBCs 1-4/HPF, and urine WBCs 0-1.5/HPF. Arterial blood gas analysis (FiO2 1.0) revealed a pH of 7.486, a pCO2 of 30.6 mmHg, a pO2 of 36.4 mmHg, a HCO3- concentration of 22.9 mM/L, and an oxygen saturation of 77%.
A portable chest radiography revealed infiltration of the right lower lung zone and cardiomegaly. ECG revealed sinus bradycardia with no evidence of ischemia; the intervals and axis were normal except for a prolonged QTc interval. Echocardiography revealed a small amount of pericardial effusion, but it did not affect the patient's hemodynamic status.
During our resuscitative efforts, the patient's blood pressure didn't respond and additional laboratory test results confirmed hypothyroidism. The patient's free thyroxine was 0.05 ng/dL (0.93-1.7) and her TSH was 30.12 µIU/mL (0.27-5.0). A diagnosis of myxedema coma exacerbated by community-acquired pneumonia was thus assigned.
The patient was referred to the Department of Endocrinology and admitted to the intensive care unit for treatment and ventilatory support. The patient received 1,000 µg of levothyroxine orally for two days, followed by 300 µg/day for an additional three days and finally maintained on levothyroxine 0.1 mg orally each day. Following the administration of synthetic thyroid hormones for hypothyroidism and antibiotics for pneumonia, the patient regained consciousness and respiration. She was transferred to a general ward after two weeks in the intensive care unit and discharged from the hospital one week later.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [104.0, 'mg/dL'], 'Sodium': [121.0, 'mEq/L']}",121.096,115.0412,127.1508,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 121.0 mEq/L. 
The concentration of glucose is 104.0 mg/dL. 
Plugging in these values into the formula gives us 121.0 mEq/L + 0.024 * (104.0 - 100) = 121.096 mEq/L.
Hence, the patient's corrected concentration of sodium is 121.096 mEq/L."
5521,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7330196-1,Extracted,"A 64-year-old male visited a family medicine clinic due to lower extremity weakness lasting 1 month. The patient could not walk without assistance or walking aids. He was fully conscious and presented at the clinic in a wheelchair. He had numbness and a tingling sensation in his feet. There had been a 7 kg weight loss (from 60 to 53 kg) in a month. The patient had a past medical history of T2DM, diagnosed approximately 10 years previously. His medications were metformin 1000 mg daily and glipizide 10 mg daily; though he had irregularly attended his diabetes clinics, his adherence to medications was variable and he had had no recent follow-up or blood tests.
His vital signs were blood pressure, 141/93 mmHg; pulse, 108 beats per minute; respiratory rate, 20 breaths per minute; and temperature, 36.5°C. Physical examination of the nervous system revealed a decrease in motor power related to both hip flexion and elbow extension (grade 4). Pain sensation (tested by a pin prick test) was normal. Deep tendon reflexes of the knees and ankles indicated a slightly slow response (1+). The rest of his physical examination was normal.
Blood tests indicated a fasting plasma glucose (FPG) level of 650 mg/dL (36.1 mmol/L). Serum electrolytes were as follows: sodium, 135.3 mEq/L, potassium, 4.7 mEq/L, chloride, 97.3 mEq/L; and bicarbonate, 22.4 mEq/L. Serum creatinine was 1.4 mg/dL, and estimated glomerular filtration rate was 48.8 ml/min/1.73 m2. Thyroid function tests were normal. A glycated haemoglobin (HbA1c) was not taken at initial presentation.
The patient was referred to a district hospital because of symptomatic hyperglycaemia and poor mobility. During the patient’s 4-day hospital stay, the injectable insulin was prescribed to control his glucose level. The plasma glucose level was under control during the hospital stay and the weakness of the lower extremities improved. The patient could walk without assistance after hospital discharge. Subcutaneous insulin (30%/isophane 70% [mixtard 100 IU/ml] at 26 IU before breakfast and 14 IU before dinner) was prescribed after discharge from hospital. Six weeks later, the patient could walk to attend a follow-up visit at the family medicine clinic. Physical examination of the nervous system revealed normal muscle strength and normal muscle tone. The patient gained 5.9 kg of body weight (58.9 kg). The FPG was 281 mg/dL (15.6 mmol/L), and HbA1c was 10.9%. By the next follow-up visit (4 weeks later), the patient had made a full recovery from lower extremity weakness and could perform all activities of daily living. His body weight was 63 kg. His glycaemic test results were improved (FPG, 121 mg/dL [6.7 mmol/L]; HbA1c, 6.6%).","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [650.0, 'mg/dL'], 'Sodium': [135.3, 'mEq/L']}",148.5,141.075,155.925,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 135.3 mEq/L. 
The concentration of glucose is 650.0 mg/dL. 
Plugging in these values into the formula gives us 135.3 mEq/L + 0.024 * (650.0 - 100) = 148.5 mEq/L.
Hence, the patient's corrected concentration of sodium is 148.5 mEq/L."
5522,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8430448-1,Extracted,"A 59-year-old Asian housewife was referred to the emergency department (ED) of Dr. Soetomo General Hospital (SGH) with bluish coloration, numbness and progressive pain in her left leg. The patient had been hospitalized in another hospital for shortness of breath due to COVID-19 two days before the referral, but because of the limb coloration, she was referred to SGH. Similar pain was also felt in her right leg, which was reddish in color. The patient had complained about the pain for five years (initially sensed as frequent tingling), which worsened one week before her visit at the hospital. The pain was intermittent and was mostly felt while moving or walking, and worsened at night during sleep. Most of the time, the patient hanged her legs down to alleviate the pain. During initial assessment, fever, occasional coughing and intermittent dyspnea were observed. The patient also complained about pain during micturition five days before the hospitalization. There were no issues regarding appetite and defecation. The patient also had a four-year history of uncontrolled T2DM with a bad compliance to oral antidiabetic (glimepiride 2 mg 1 – 0 – 0) and untreated hypertension. No relevant family medical history was reported.
The physical examinations at the ED showed a lethargic condition with Glasgow Coma Scale (GCS) of E4M5V6. Her blood pressure was 150/90 mmHg with heart rate of 110 beats/minute (bpm). Her respiratory rate was 24 times/minute, and her temperature was 36.7°C with blood oxygen saturation (SpO
2) of 97%. Her pain was assessed using the Visual Analogue Scale (VAS) and resulted in a score of 6 out of 10. Her weight, height and body mass index (BMI) were 70 kg, 155 cm and 29.1, respectively. Head and neck examinations showed anemic conjunctivae with no icterus or cyanosis. Her cardiopulmonary examination was within a normal range (i.e., both sides of thorax were symmetrical and no retraction), as well as the abdominal examination (i.e., fluffy abdomen, bowel sounds were normal, liver and spleen were not palpable). Interestingly, her extremity assessment revealed a bluish coloration in her left leg with cold sensation during palpation and no pulse was detected (
). Detailed left leg examinations also discovered a necrotic region below her ankle, with a cold sensation up to one-third of her left lower extremity. Furthermore, the motoric and sensory functions of the left leg were poor. Meanwhile, her right leg was warm, had no necrosis, and exhibited normal sensory and motoric functions (
). Ankle Brachial Index (ABI) was negative on the left and 0.9 on the right.
The laboratory examinations showed hemoglobin (Hb) of 10.8 g/dl, hematocrit of 35%, leucocyte count of 24460 /μl and platelet count of 627000/μl. The differential blood count of leucocytes highlighted neutrophil domination (88.1%) followed by lymphocytes (5%). Hemostatic parameters, such as prothrombin time (PT), activated partial thromboplastin time (aPTT), and D-dimer were 14.6, 30.8 and 9740 ng/ml, respectively. Her liver functions of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were 70 U/l and 193 U/l respectively. Blood albumin was 2.89 g/dl, fasting blood glucose was 128 mg/dl, HbA1c was 9%. Renal functions test revealed a serum creatinine of 1.5 mg/dl and blood urea nitrogen (BUN) of 61 mg/dl (i.e., stage 3B with estimated Glomerular Filtration Rate [eGFR] of 38 ml/min/1.73 m
2). Her C-reactive protein (CRP) was 22.5 mg/l, sodium 132 mg/dl, potassium 4.7 mg/dl, chloride 96 mg/dl. HbsAg, anti-HCV and HIV were all negative. COVID-19 polymerase chain reaction (PCR) test was positive. The urinalysis showed following results: nitrite positive, leucocytes positive, glucose 4+, A/C< 30, P/C<0,15, while her arterial blood gas analysis (BGA) showed pH 7.42, pCO2 38, pO2 146, HCO3 23.4 and SpO
2 99%. Additionally, her chest X-ray showed bilateral pulmonary infiltrates (
).
Taking into account the patient’s complaints, history, physical, laboratory and radiological examinations, the patient was then diagnosed with COVID-19-associated pneumonia with left inferior extremity dead limb and bilateral inferior extremity ALI, as well as urinary tract infection, anemia, hypoalbuminemia, T2DM and chronic kidney disease (CKD) stage III. Subsequently, she was treated with oxygen via simple mask at 6 liters per minute (lpm), sodium chloride (NaCl) 0.9% infusion 1000 ml/24 hours, subcutaneous heparin injection (2×5000 unit), intravenous (iv) dexamethasone injection (6 mg 1×1), remdesivir 1×200 mg, ceftriaxone 2×1 g, metronidazole 3×500 mg, insulin aspart (novorapid) 14 – 16 – 16, insulin detemir (levemir) 0 – 0 – 10, albumin 20% transfusion 100 ml/4 hours, oral isoprinosine 3×500 mg, oral vitamin D 1×5000 IU and oral cilostazol 1×100 mg. Her diet was also maintained within 1900 kcal/day.
At day four, the dyspnea was improved but the leg started to feel burnt and the pain progressed. Blood pressure was 149/84 mmHg, heart rate 68 bpm, respiratory rate 20 times/minute, SpO
2 98%, VAS score 5, COVID-19 PCR negative, leucocyte count was 27540 /μl with the proportion of neutrophil 87.4%, serum creatinine 1.4 mg/dl, blood albumin 2.8 mg/dl, D-dimer 6540 ng/ml, ferritin 1602 ng/ml, fibrinogen 642.6 mg/dl and procalcitonin (PCT) of 1.08. At day 5, the patient only complained about her progressive leg pain, while her daily examinations revealed blood pressure of 127/74 mmHg, heart rate 86 bpm, respiratory rate 20 times/minute, SpO
2 99% and VAS score of 5. Meanwhile, the COVID-19 PCR was negative, leucocyte count was 31390/μl with neutrophil 86.6%, serum creatinine 1.3 mg/dl, blood albumin 3 mg/dl, D-dimer 5570 ng/ml, ferritin 1572 ng/ml, fibrinogen 542 mg/dl and PCT of 0.23. Additionally, an improvement of the bilateral pulmonary infiltrates on chest X-ray was also observed (
).
At day 7, the patient complained that the pain in her leg had increased significantly. Her blood pressure was 130/80 mmHg, heart rate 98 bpm, respiratory rate 20 times/minute and SpO
2 98%. The urine culture was positive for
Escherichia coli sensitive to cefoperazone sulbactam. Because of the progressive extremity pain, the patient was referred to the cardiothoracic and vascular surgery (CTS) division and, consistent with the first diagnosis, she was diagnosed with left dead limb and bilateral ALI (
), and was advised to perform computed tomography angiography (CTA) and undergo an above-knee amputation. At day 9, the right lower extremity CTA (
) discovered total occlusion due to 6 cm thrombus on right popliteal artery (from 1 cm above right femorotibial joint toward inferior). Right anterior tibial artery received contrast flow from collateral arteries and no contrast flow was seen in right posterior tibial, peroneal and dorsalis pedis arteries. Meanwhile, the left lower extremity CTA showed total occlusion due to 12.7 cm thrombus on left popliteal artery (from 6 cm above left femorotibial joint toward inferior). Moreover, no contrast flow was seen in left anterior tibial, posterior tibial, peroneal and dorsalis pedis arteries.
At day 11, the patient was still waiting for surgery and the pain increased. Her blood pressure was 130/80 mmHg, heart rate 88 bpm, respiratory rate 20 times/minute, SpO
2 98% and VAS equals 7. Laboratory parameters showed Hb 10.3, leucocyte count 22610/μl, platelet 509000/μL, D-dimer 3960 ng/ml and random blood glucose of 171. Subsequently, the patient received 8 lpm oxygen through a simple mask, diet type-B 1900 kcal/24 hours, iv fluid with NaCl 0.9% 1000 ml/24 hours, cefoperazone sulbactam 2×1 g iv, subcutaneous novorapid 14 – 16 – 16 unit, subcutaneous levemir 0 – 0 – 10 unit, subcutaneous heparin 2×5000 unit and oral cilostazol 1×100 mg. At day 13, her blood pressure was 127/70 mmHg, heart rate 90 bpm, respiratory rate 20 times/minute and SpO
2 98%. Laboratory results showed Hb 9, leucocyte count 11800/μL, platelet 410000/μL, BUN 20 mg/dl, serum creatinine 1.3 mg/dl and random blood glucose of 160. The eGFR was 45 ml/min/1.73 m
2 (stage 3A). At this point, the patient was assigned for antegrade right femoral artery thrombectomy and left above-knee amputation at the following day. At day 14, the surgeries (both amputation and thrombectomy) were performed (
) and 10 cm thrombus was retrieved in the right femoral artery. Lastly, as a follow-up, at day 17, no symptoms were observed, therefore the patient was discharged.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [128.0, 'mg/dL'], 'Sodium': [132.0, 'mEq/L']}",132.672,126.0384,139.3056,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 132.0 mEq/L. 
The concentration of glucose is 128.0 mg/dL. 
Plugging in these values into the formula gives us 132.0 mEq/L + 0.024 * (128.0 - 100) = 132.672 mEq/L.
Hence, the patient's corrected concentration of sodium is 132.672 mEq/L."
5523,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3170342-1,Extracted,"A 60-year-old Iranian woman presented to our hospital with pain and swelling in her right arm following a minor fall. Our initial physical examination revealed her to be in a good general condition. She was normotensive, with a pulse rate of 92 beats/minute. Her other laboratory values were as follows: body temperature 37°C, hemoglobin 12.2 g/dL, leukocytes 22 cells/mm3, platelets 200 U/L, sodium 141 mEq/L, potassium 4 mEq/L, glucose 11.6 mmol/L, blood urea nitrogen 15.1 mmol/L, and creatinine 250 mmol/L. A plain X-ray showed a pathologic fracture in the mid-shaft of her right humerus and a large, ill-defined soft tissue mass (Figure ). Magnetic resonance imaging (MRI) showed a huge lobulated mass destroying the shaft of the humerus and displacing the surrounding soft tissue. The mass was bright on serial T2-weighted MRI scans and dark on serial T1-weighted MRI scans, with marked enhancement after a gadolinium injection (Figure ). Four years ago she had been treated for a sacrococcygeal chordoma with surgical resection and post-operative radiotherapy. A local tumor recurrence developed after one year and required additional surgical procedures. A histological examination of the biopsy from the humeral lesion showed a lobulated mass composed of cuboidal to polygonal cells with eccentric nuclei, clear to eosinophilic cytoplasm, and pools of extracellular mucin (arrow in Figure ). Typically, few tumor cells have a ""physaliferous"" (bubble-bearing) appearance. On the basis of these findings, we considered differential diagnoses such as myxoid chondrosarcoma, myxoid liposarcoma, primary mixed tumor of the bone, metastasizing pleomorphic adenoma of the salivary gland, metastatic renal cell carcinoma (RCC), or metastatic carcinoma with intra-cytoplasmic mucin from the colon or lung [,]. Most metastatic carcinomas have more of the cytological features of malignancy than chordomas do. The tumor cells stained positive for AE1/3 (Figure ), ethidium monoazide (EMA), S100, and vimentin. Although both chordomas and chondrosarcomas stain with S100 protein, myxoid chondrosarcomas do not stain with keratin and EMA. Additional immunochemistry was performed for CD10, the results of which were negative in this case and usually expressed in RCC. Abdominal and pelvic ultrasonography and computed tomography (CT) of her chest and abdomen were normal. On the basis of this evidence and our review of the original histology following her previous chordoma excision (which was histologically identical to the humeral lesion), a diagnosis of metastatic chordoma was confirmed. She refused any active treatment.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [11.6, 'mmol/L'], 'Sodium': [141.0, 'mEq/L']}",143.61566,136.43488,150.79644,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 141.0 mEq/L. 
The concentration of glucose is 11.6 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 11.6 mmol. To convert 11.6 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 11.6 mmol glucose * 0.001 mol/mmol = 0.0116 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0116 mol glucose * 180.16 g/mol = 2.08986 g glucose. To convert 2.08986 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 2.08986 g glucose * 1000.0 mg/g = 2089.86 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 2089.86 mg glucose/10.0 dL = 208.986 mg glucose/dL. The concentration value of 11.6 mmol glucose/L converts to 208.986 mg glucose/dL. 
Plugging in these values into the formula gives us 141.0 mEq/L + 0.024 * (208.986 - 100) = 143.61566 mEq/L.
Hence, the patient's corrected concentration of sodium is 143.61566 mEq/L."
5524,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7869335-1,Extracted,"A 46-year-old woman (height: 162 cm, weight: 64 kg) underwent surgery for the treatment of a 16 × 13 mm, Koos stage 2 vestibular schwannoma at the cerebellopontine angle (Figure ). She had a current history of smoking but no other medical history and no tumor-related symptoms. Preoperative blood tests and electrocardiogram findings were normal. Her American Society of Anaesthesiologists Physical Status classification (ASA-PS) was class 2.
The patient received no premedication. Anesthesia was induced with a target-controlled infusion (TCI) of propofol (effect compartment concentration 3.0 µg/mL) and remifentanil 0.5 µg/kg/min. Tracheal intubation was performed with the aid of rocuronium 50 mg, and a radial artery line was placed. She was placed in the prone position in pinions and head-holders.
Anesthesia was maintained uneventfully with TCI of propofol (effect compartment concentration 2.0-2.5 µg/mL) in oxygen (FIO2 0.4) and remifentanil (0.2-0.3 µg/kg/min). Fentanyl (300 µg) and rocuronium (20 mg) were added during surgery. The surgery was uneventful and the tumor was removed completely; she was placed in the supine position with the pinions removed, and all anesthetics discontinued. The total operation time was 440 minutes. During surgery, her systolic blood pressure (BP) ranged between 100 and 120 mm Hg, heart rate (HR) was between 60 and 70 beats per min (bpm), and SpO2 was 99%-100%.
For the next 30 minutes, she remained unconscious and unresponsive to painful stimuli and did not cough. Both pupils were 2 mm in diameter. Her temperature was 38.4°C, BP was 145/75 mm Hg, and HR was 90 bpm. Arterial blood gas analysis revealed a pH of 7.415, PaCO2 of 44.3 mm Hg, PaO2 of 139.2 mm Hg, serum sodium of 137 mmol/L, serum potassium of 3.5 mmol/L, glucose of 164 mg/dL, and ionized calcium of 1.06 mmol/L. Doxapram (40 mg) and sugammadex (200 mg) were administered intravenously, since we assumed that the prolonged anesthetics were possibly the cause for delayed emergence. However, the patient's consciousness did not improve and she was transferred for CT scanning 60 minutes after surgery completion. CT scans revealed a cerebellar hemorrhage (30 × 37 mm) (Figure ). Immediately after the diagnosis, she was transferred back to the operating room to remove the hematoma. Anesthesia was maintained with a TCI level of propofol (effect compartment concentration 1.0) in oxygen (FIO2 0.4) and remifentanil (0.2-0.3 µg/kg/min). Fentanyl (300 µg) and rocuronium (20 mg) were added. The cause of the hematoma was not detected, and the total operation time for removal was 143 minutes. Fifteen minutes after termination of surgery and discontinuation of anesthetics, the tracheal tube was removed because spontaneous breathing and effective laryngeal reflex had resumed although the patient was still unconscious (Glasgow Coma Scale score [GCS] of E1 VT M4). Her total time under anesthesia for both surgeries was 804 minutes and total blood loss, urine output, and volume of crystalloid were 530 g, 2325 mL, and 3200 mL, respectively.
The patient gradually recovered consciousness following ventricle drainage for hydrocephalus the next day. She was discharged 58 days after the original surgery.
Written informed patient consent was obtained for the publication of this manuscript and accompanying figures. This manuscript adheres to the appropriate EQUATOR guidelines.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [164.0, 'mg/dL'], 'Sodium': [137.0, 'mmol/L']}",138.536,131.6092,145.4628,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 137.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 137.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 137.0 mmol * 1 mEq/mmol = 137.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mmol sodium/L converts to 137.0 mEq sodium/L. 
The concentration of glucose is 164.0 mg/dL. 
Plugging in these values into the formula gives us 137.0 mEq/L + 0.024 * (164.0 - 100) = 138.536 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.536 mEq/L."
5525,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6620230-1,Extracted,"We report a case of a 37-year-old male with PWS who suffered from ESKD. At 3 years of age, he started overeating and developed obesity. At 5 years of age, PWS was suspected based on the patient’s body type, facial expression, and overeating. Dietary restriction was instructed; however, at 17 years of age, he was diagnosed with type 2 DM (T2DM). At 30 years of age, a diagnosis of PWS was confirmed by genetic testing. At age 32 years, he suffered from nephrotic syndrome, and diabetic retinopathy was diagnosed at the same time.
By June 2015, renal function had continuously deteriorated and his serum creatinine reached 8.9 mg/dL (eGFR at 5.0 mL/min/1.73 m2). Therefore, the patient was admitted to the hospital for initiating RRT. At admission, physical examination revealed: 150.8 cm height, 80.3 kg BW, BP 112/64 mmHg, HR 110/min, SO2 99% (room air). He showed systemic edema and urine volume decreased to 800 mL/24 h. The patient’s IQ was inferred 40–60. Blood chemistry showed: TP 6.4 g/dL, albumin 2.4 g/dL, CRP 10.9 mg/dL, BUN 83 mg/dL, UA 6.4 mg/dL, Na 136 mEq/L, K 5.4 mEq/L, Cl 110 mEq/L, Ca 7.1 mg/dL, P 12.7 mg/dL and HCO3− 14.7 mEq/L. Complete blood count was: WBC 16,770/μL, RBC 354 × 104/μl, Hgb 8.1 g/dL, Ht 27.6%, MCV 78 fl, MCH 22.9 pg, MCHC 29.3% and Plt 54.2 × 104/μl. Urinalysis showed massive proteinuria (4839 mg/24 h) without hematuria or pyuria. He had been receiving insulin injection 4 times a day. Random blood glucose level was 156 mg/dL and HbA1c was 6.8%.
After admission, restricted fluid intake, nutritional management, and temporary HD was performed 6 times for 2 weeks since massive edema prevented insertion of PD catheter. The reasons for choosing PD were as follows: vessels in his both forearms looked premature for creating A-V fistula at that time, suspecting intolerance in hemodialysis session for long hours and difficult cessation of fluid and food intake which are necessary for hemodialysis. Negative aspect of PD was specifically considered as a difficulty in maintaining sanitary in inlet of PD catheter. In either modality, family burden for supporting his dialysis was also considered.
Substantially his body weight decreased to 64 kg (− 16 kg from admission; BMI 28.4 kg/m2) and a catheter for PD was inserted using the non-stylet method under general anesthesia combined with epidural anesthesia at the 14th day of admission. We selected the JBS-2 semi-long PD Catheter with the exit site placed in the left upper abdomen (Fig. ). The catheter position was not ideally located initially but it functioned well for the following PD session after the surgery (Fig. ). From the third postoperative day, nocturnal intermittent PD (NIPD) was started. Since he could not sufficiently understand the procedure of PD, instructions for PD as well as insulin self-injection were provided to his father. He was discharged at the day 35 of hospitalization.
At the 2nd, 5th, 7th, and 13th month after NIPD introduction, a subcutaneous tunnel infection occurred (Fig. ). Since additional antibiotic therapy could not terminate infection, he underwent subcutaneous pathway diversion and PD catheter replacement for three times consequently. However, that was the last infection episode and infection-free PD was observed until the present time for next 27 months. With regard to the dialysis modality, NIPD was chosen first because he desired to continue his daytime job for handicapped person. At the 7th month after NIPD introduction, the treatment was switched to continuous cycling PD (CCPD) and 7.5% icodextrin solution (Extraneal™, Baxter, Tokyo, Japan) was added daytime because urine output gradually decreased, and ultrafiltration volume became insufficient. At the 10th month after NIPD introduction, glucose concentration in peritoneal dialysate increased from 1.5 to 2.5% (Reguneal™, Baxter, Tokyo, Japan). “Hybrid dialysis”, which combined daily PD with once-a-week HD, was started by creating A-V fistula at the 16th month after NIPD introduction. Owing to this “hybrid dialysis”, adequate ultrafiltration volume was maintained for following 17 months. Dialysis efficiency has been checked by blood tests and chest X-ray once a month and revealed adequate dialysis without major problems; accordingly, BUN level was below 50 mg/dL and serum potassium level below 5 mEq/L. Blood sugar was well maintained by daily intensive insulin therapy with oral dulaglutide initially and then this regimen was successfully replaced with once-weekly GLP-1 agonist associated with once a day ultralong-acting insulin finally. HbA1c had been maintained under 7% since NIPD introduction. His maximum body weight without overhydration reached to 71 kg (BMI 31.6 kg/m2) during this period. Finally, he lost his A-V fistula twice and returned to PD (CCPD) alone at the 38th month of NIPD introduction because of difficulty in creating another vascular access. For evaluating efficacy of PD, serum β2-microglobulin level was monitored every 2 months and revealed between 34 and 40 mg/L during the latest CCPD alone period.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [156.0, 'mg/dL'], 'Sodium': [136.0, 'mEq/L']}",137.344,130.4768,144.2112,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 136.0 mEq/L. 
The concentration of glucose is 156.0 mg/dL. 
Plugging in these values into the formula gives us 136.0 mEq/L + 0.024 * (156.0 - 100) = 137.344 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.344 mEq/L."
5526,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6176125-1,Extracted,"A 68-year-old Japanese female was transferred to the ED by ambulance because she had fainted after dizziness. Her past medical history was hypertension, diabetes mellitus and chronic kidney disease, and she was on multiple medications. She had been anorexic for ~1 month. She was an ex-smoker and a social drinker.
On admission, her mental status was recovered and her conscious levels were E4V5M6 (Glasgow Coma Scale (GCS)). Her physical findings and vital signs were as follows: height 139.0 cm, body weight 52.3 kg, body mass index 27.1 kg/m2, blood pressure 128/75 mmHg, heart rate 152 beats/min with irregularity, body temperature 36.8°C, oxygen saturation on room air 98% and respiratory rate 18 breaths/min. Her physical examinations, which included her conjunctiva, cervical lymph nodes, chest, heart and abdomen, revealed normal findings.
Baseline laboratory results were as follows: white blood cell count (WBC) 10 300/μL↑, hemoglobin 12.8 g/dL, blood urea nitrogen 34 mg/dL↑, creatinine 4.09 mg/dL↑, sodium 128 mEq/L↓, potassium 2.6 mEq/L↓, chlorides 87 mEq/L↓, total protein 7.1 g/dL, albumin 4.2 g/dL, C-reactive protein (CRP) 0.07 mg/dL, glucose 262 mg/dL↑ and β-glycated hemoglobin 5.9%. Urinalysis revealed protein (1+), sugar (4+) and ketones (+) with no blood cells or casts. Electrocardiogram revealed atrial fibrillation, but there were no abnormal findings on chest radiograph or on brain or thoracicoabdominal computed tomography (CT).
These findings suggested that her AMS might be caused by one or more conditions, namely, hyponatremia, ketonuria, hyperglycemia and acute kidney injury (uremia), which were presumably due to dehydration, diabetic ketosis and chronic kidney disease. She was hospitalized and treated with electrolytes, including sodium chloride and potassium chloride, and insulin.
Although her blood electrolytes, serum glucose and renal function gradually improved, general conditions, including her consciousness, deteriorated. On the third day after hospitalization, her cognitive function became impaired with reduced conscious levels to E4V3M4 (GCS). Abnormal breaths with apnea and tachypnea accompanied by a fever (37.8°C) appeared, and glossoptosis was found (Fig. ). Both an oropharyngeal airway and bite block were placed in order to maintain her airway, which is we realized that she suffered from multiple, painful dental caries, but no findings of within the oropharynx.
Laboratory results on the hospital Day 3 were as follows: WBC 14 800/μL with 94.1% neutrophils↑ and CRP 0.08 mg/dL. There were no abnormal findings on chest radiograph, brain or thoracicoabdominal CT, brain magnetic resonance imaging, or spinal fluid examination.
Because no abnormalities were detected in the central nervous system, empiric treatment was initiated with 2.25 g q6hr of piperacillin/tazobactam for fever of unknown origin presumably caused by bacterial infection(s).
On hospital Day 6, a dentist examined her teeth and found 15 dental caries, then dental extractions were performed on four teeth. In particular, pus was discharged from the left upper canine with gingival swelling, which was diagnosed with acute apical abscess.
On hospital Day 7, her mental status was completely normal (Fig. ), indicating that apical abscess was acute, severe inflammation of the dental pulp with minimal chance of spontaneous recovery [–] and may have caused her AMS and abnormal breathing. Although two sets of blood cultures sampled on hospital Day 3 were negative, bacterial culture from the dental pus sampled on hospital Day 6 yielded methicillin-sensitive Staphylococcus aureus. Antibiotic treatment was de-escalated to 1 g q8hr of cefazolin on hospital Day 13 and was completed on hospital Day 20. The patient fully recovered and was discharged on hospital Day 23.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [128.0, 'mEq/L'], 'Glucose': [262.0, 'mg/dL']}",131.888,125.2936,138.4824,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 128.0 mEq/L. 
The concentration of glucose is 262.0 mg/dL. 
Plugging in these values into the formula gives us 128.0 mEq/L + 0.024 * (262.0 - 100) = 131.888 mEq/L.
Hence, the patient's corrected concentration of sodium is 131.888 mEq/L."
5527,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-8498,Extracted,"A 60-year-old man with a long-standing history of type 2 diabetes and hypertension managed with lisinopril and metformin presents with itchy skin. He also describes moderate nausea, vomiting, muscle weakness, and fatigue. The vital signs include: temperature 36.8°C (98.2°F), heart rate 98/min, respiratory rate 15/min, blood pressure 135/85 mm Hg, oxygen saturation 100% on room air. Physical exam is notable for pale conjunctivae, pitting edema, and ascites. Laboratory findings are shown below:
BUN 78 mg/dL
pCO2 25 mm Hg
Creatinine 7.2 mg/dL
Glucose 125 mg/dL
Serum chloride 102 mmol/L
Serum potassium 6.3 mEq/L
Serum sodium 130 mEq/L
Total calcium 1.3 mmol/L
Magnesium 1.2 mEq/L
Phosphate 1.9 mmol/L
Hemoglobin 9.5 g/dL
MCV 86 μm3
Bicarbonate (HCO3) 10 mmol/L
Shrunken kidneys are identified on renal ultrasound. The doctor explains to the patient that he will likely need dialysis due to his significant renal failure until a renal transplant can be performed. The patient is concerned because he is very busy and traveling a lot for work.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [130.0, 'mEq/L'], 'Glucose': [125.0, 'mg/dL']}",130.6,124.07,137.13,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 130.0 mEq/L. 
The concentration of glucose is 125.0 mg/dL. 
Plugging in these values into the formula gives us 130.0 mEq/L + 0.024 * (125.0 - 100) = 130.6 mEq/L.
Hence, the patient's corrected concentration of sodium is 130.6 mEq/L."
5528,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2760916-1,Extracted,"A 60-year-old gentleman was admitted with the presenting complaint of acute onset weakness of both the lower limbs (started as inability to stand up after squatting), inability to move both the lower limbs and breathlessness. He had no other presenting complaints including history of back pain, trauma, chest pain, palpitations or syncope. He had bilateral cystic bronchiectasis of the lungs of unknown etiology, cor pulmonale and he was a diabetic on oral hypoglycemic agents (glibenclamide, glimepiride) and a hypertensive on atenolol and spironolactone. His other medications were frusemide and theophylline + etofylline.
On admission, he was conscious oriented and his vitals were: Temperature - 99°F, pulse-110/min, BP-130/80 mm Hg, RR-26/min reg and O2 saturation-95% with 10litres/min of oxygen flow. He had clubbing, bilateral pitting pedal edema and bilateral symmetrical areflexic motor weakness of the lower limbs (Power 1/5) and absent bilateral plantar response. Lung examination showed bilateral coarse crepitations. All peripheral pulses were equally felt and the rest of the system examination was unremarkable. His average urine output was > 1000 ml/day. His previous renal function tests were normal, with a normal serum potassium level. Magnetic resonance imaging (MRI) spine was advised by the neurologist.
Arterial blood gas analysis showed pH 7.28, pCO2 60, pO2 159 and bicarbonate 27.8. ECG showed normal sinus rhythm, right axis deviation, PR interval of 0.20 ms, right bundle branch block (RBBB), right ventricular hypertrophy (RVH) and ST depression/T inversion in leads III, aVF and V1-V3.
Laboratory investigations revealed blood sugar of 493 mg/dL, blood urea nitrogen (BUN) of 88 mg/dL, serum creatinine of 1.6 mg/dL, serum sodium of 119 mEq/L, serum potassium of 8.9 mEq/L, Hb-19.4g/dL, hematocrit-67% and WBC-8,200/cu.mm, creatine phosphokinase, was 95 IU L and thyroid profile was normal. Daily measurements of hemoglobin and PCV level did not show any evidence of ongoing hemolysis.
Chest X-ray and computed tomography chest showed bilateral cystic bronchiectasis of the lungs. Echocardiography showed dilated right atrium and ventricle, severe pulmonary artery hypertension, normal left ventricle size and systolic function and EF of 68%. Arterial Doppler of both lower limbs revealed thin plaques along the arteries with normal flow velocity.
Immediate treatment for hyperkalemia included intravenous calcium gluconate, nebulised salbutamol, insulin infusion and potassium binding resin and potassium free diet. Repeat serum potassium after one hour of conservative management was still 8.7 mg/dL. The Nephrologist started him on immediate hemodialysis, as the serum potassium did not respond adequately to medical therapy and as he was still at high risk of life-threatening cardiac events. Salbutamol nebulization and insulin infusion were continued. After one cycle of hemodialysis, medications and potassium restriction, his serum potassium was 7.1 mg/dL but his motor power improved to 4/5 in both the lower limbs (he was able to lift both his legs against gravity and mild resistance). Repeat ECG post-hemodialysis was the same. Imaging was not performed initially as he required urgent treatment for the hyperkalemia. Subsequently there was remarkable improvement in motor power, MRI spine was withheld.
He was kept on non-invasive ventilation which was discontinued the next day. He required three cycles of hemodialysis before his serum potassium reached the normal range. Throughout the course of the illness, he had no episode of arrhythmia, heart block or cardiac arrest. At discharge, his serum potassium and renal function were within the normal range. He was able to walk normally without any disturbances in posture or balance and his motor power was 5/5 in all the 4 limbs.
Follow-up was done after two weeks of discharge when he had normal motor power (able to walk and ride motorcycle) and normal potassium and renal function tests.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [119.0, 'mEq/L'], 'Glucose': [493.0, 'mg/dL']}",128.432,122.0104,134.8536,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 119.0 mEq/L. 
The concentration of glucose is 493.0 mg/dL. 
Plugging in these values into the formula gives us 119.0 mEq/L + 0.024 * (493.0 - 100) = 128.432 mEq/L.
Hence, the patient's corrected concentration of sodium is 128.432 mEq/L."
5529,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4129213-1,Extracted,"A 51-yr-old Korean male visited the emergency room with complaints of high fever, chills, and abdominal pain in August 2013. He described the pain as increasing progressively in intensity, worsening after meals, and accompanied by nausea. He also suffered from diarrhea twice. He was diagnosed with Graves' disease 2 weeks ago, and was being treated with MMI (20 mg per day). His other medications included bisoprolol and 100 mg aspirin for atrial fibrillation. He did not have any history of drug or food allergies. He denied the use of tobacco, alcohol, and any dietary supplements. His family history was unremarkable, and did not include thyroid disease or gastrointestinal disorders.
Upon admission, his vital signs were as follows: blood pressure of 100/70 mmHg, heart rate of 121 beats per minute, a respiratory rate of 21 times per minute, and a body temperature of 39.0℃. He had a slightly enlarged thyroid gland, but there was no pharyngeal injection. Physical examination revealed tenderness in the epigastric and upper abdomen without rebound tenderness, guarding, or rigidity.
The results of blood tests were as follows: white blood cell count of 5,460/µL, hemoglobin of 16.3 g/dL, and platelet count of 103,000/µL. Biochemical parameters were glucose of 222 mg/dL, triglycerides of 113 mg/dL, blood urea nitrogen of 30.3 mg/dL, creatinine of 1.45 mg/dL, sodium of 133.8 mM/L, potassium of 3.9 mM/L, chloride of 97.3 mM/L, aspartate transaminase of 34 IU/L, alanine transaminase of 46 IU/L, alkaline phosphatase of 46 U/L, total bilirubin of 2.60 mg/dL, C-reactive protein (CRP) of 46.7 mg/L, amylase of 86 IU/L (normal range: 29-110), and lipase of 86 IU/L (normal range: 14-60).
A thyroid function test at the first visit revealed TSH of 0.01 mIU/L (normal range: 0.27-4.20), free T4 of 3.89 ng/dL (normal range: 0.93-1.70), total T3 of 199.8 ng/dL (normal range: 80-200), anti-TPO antibody of 17.84 (normal range: 0-34), and TSH-receptor antibody of 8.8 IU/L (normal range: 0.00-1.75). In Tc-99m thyroid scan, the uptake ratio was 4.8%. There was no elevation of serum antibodies for respiratory viruses including adenovirus, influenza, parainfluenza, and rhinovirus. He also tested negative for serum antibodies against tsutsugamushi, leptospira, and hantavirus.
The following day, MMI therapy was restarted after holding 42 hr because his fever had subsided and there was no evidence of agranulocytosis. However, 5 hr after he took the second dose of MMI (10 mg), abdominal pain and fever (39.2℃) developed again. At that time, laboratory studies showed a white blood cell count of 5,580/µL (72.7% neutrophils and 1.9% eosinophils), total bilirubin of 1.84 mg/dL, and CRP of 26.0 mg/L. His serum amylase and lipase levels increased to 265 IU/L and 682 IU/L, respectively. Electrophoresis revealed that his pancreatic amylase isoenzyme levels were elevated. An abdominal CT revealed a swollen pancreas with peripancreatic inflammatory fat stranding, suggestive of acute pancreatitis (). An abdominal ultrasound was then performed, which showed no evidence of cholelithiasis or biliary duct dilatation ().
After the withdrawal of MMI, his fever and abdominal pain improved, and pancreatic enzyme levels began to decrease and finally normalized (). We measured IgG and IgG4 to exclude autoimmune pancreatitis. The serum levels of IgG and IgG subclass-4 were in the normal range (901.5 mg/dL, normal range: 700-1,600; and 349 mg/L, normal range: 30-2,010, respectively). The serologic typing of HLA alleles revealed DRB1*0803 and DQB1*0601. After discharge, PTU (50 mg t.i.d) was prescribed for treatment of Graves' disease and his hyperthyroidism was gradually controlled without any side-effects.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [133.8, 'mmol/L'], 'Glucose': [222.0, 'mg/dL']}",136.728,129.8916,143.5644,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 133.8 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 133.8 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 133.8 mmol * 1 mEq/mmol = 133.8 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.8 mmol sodium/L converts to 133.8 mEq sodium/L. 
The concentration of glucose is 222.0 mg/dL. 
Plugging in these values into the formula gives us 133.8 mEq/L + 0.024 * (222.0 - 100) = 136.728 mEq/L.
Hence, the patient's corrected concentration of sodium is 136.728 mEq/L."
5530,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6732200-1,Extracted,"A 92-year-old man with hypertension, chronic obstructive pulmonary disease (COPD), peptic ulcer disease and dementia presented to the emergency department with a 2-day history of abdominal pain in the left upper quadrant, distention, dry cough and intractable vomiting. On physical examination, the patient had epigastric tenderness and bowel sounds were reduced. The patient’s vital signs included blood pressure of 168/84 mmHg, heart rate of 99 beats/minutes, respiratory rate of 24 beats/minutes, and oxygen saturation of 95% in room air. His temperature was 37.9 °C. The rest of physical examination findings were unremarkable. Complete blood cell count showed the following results: leukocyte count 10100/mm3 with 85% segmented neutrophils, hemoglobin 12 g/dl, platelet 350000/microliter, and international normalized ratio (INR) of 0.97. Other laboratory findings included: glucose 167 mg/dl, blood urea nitrogen (BUN) 28 mg/dl, serum creatinine 2.0 mg/dl, sodium 135 mEq/L, potassium 3.3 mEq/L, serum glutamic oxaloacetic transaminase (SGOT) 15 U/L, total bilirubin 0.5 mg/dl, and lipase 25 U/L. The patient underwent chest X-ray and abdominal computed tomography (CT) scan without contrast material, the results of which are shown in and Figure 2.
What is your diagnosis?
Diagnosis:
Chest X-ray showed left lower lung interstitial opacities and air bubble below the left hemi diaphragm ( (left), arrows). Abdominal CT scan revealed intramural gas within a dilated stomach ( (right), arrow). A diagnosis of gastric emphysema was made.
Case fate:
The patient was not toxically ill and recovered with conservative management of nasogastric decompression, intravenous fluids, total parenteral nutrition and intravenous antibiotics. The patient was discharged from the hospital 7 days after presentation.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [135.0, 'mEq/L'], 'Glucose': [167.0, 'mg/dL']}",136.608,129.7776,143.4384,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 135.0 mEq/L. 
The concentration of glucose is 167.0 mg/dL. 
Plugging in these values into the formula gives us 135.0 mEq/L + 0.024 * (167.0 - 100) = 136.608 mEq/L.
Hence, the patient's corrected concentration of sodium is 136.608 mEq/L."
5531,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3350077-1,Extracted,"A nine-year-old girl who had complaint of vomiting following eating and growth retardation after birth had been diagnosed with achalasia at the age of one. Endoscopic balloon dilation for achalasia had been performed for three times. The patient was one year old when she underwent the first endoscopic trial. No complications emerged during the endoscopic procedures. Allgrove syndrome was diagnosed in the patient due to adrenal insufficiency, developed nearly a year ago; consequently, hydrocortisone therapy was initiated.
The typical facial appearance of Allgrove syndrome including long philtrum, narrow upper lip, and fish mouth was observed during the preoperative assessment. At the same time retardation of growth and development, hyper-nasal speech, alacrima and adrenal insufficiency were observed. Her weight are only fifteen kilograms, hypernasal speech, alacrima, and adrenal insufficiency were observed. Oral hydrocortisone was also used due to adrenal insufficiency. Physical examination and interpretation of laboratory tests were defined normal (fasting blood glucose: 6,6 mmol/L, Na: 143 mEq/L, and K: 3,5 mEq/L). Postural tests were performed to assess autonomic dysfunction. We observed a decrease of approximately 15 mmHg in systolic artery pressure and an increase about 10 mm Hg in diastolic artery pressure. We concluded that autonomic dysfunction did not exist. The doses of steroids to be applied during the postoperative and preoperative periods were determined in the pediatric clinic. The patient, assessed in ASA risk group III, was given no premedication before anesthesia. Prednisolone 18 mg was administered intravenously on the night before surgery. The preoperative blood glucose level was recorded as 11 mmol/L.
The ECG, noninvasive blood pressure and SpO2 of the patient who was transferred onto the operating table, were monitored; infusion fluid which includes NaCl (4,5 g/l) and glucose (25 g/l) was started at the speed of 125 mL/h, because preoperative fluid deficit was given before. The patient was intubated with a 4 mm ID cuffed endotracheal tube after the anesthesia was induced by 75 mg of thiopental sodium, 1 mg of vecuronium, and 20 μcg fentanyl. For protective purposes topical polymyxin ophthalmic ointment was used an the eyes before they were covered. Anesthesia was maintained with 2% sevoflurane in concentration of 50% O2 and 50% N2O. Mechanical ventilation was continued to be ETCO2 30–40 mmHg. Prednisolone 25 mg was infused preoperatively. Monitoring of blood glucose was performed hourly.
In perioperative and postoperative period, we did not observe a condition that requires the intervention at HR, SAP and SpO2 ().
In intraoperative period, blood glucose was measured 12 mmol/L was at the first hour and 18 mmol/L at the second hour. Then, vascular access was opened and 0.9% NaCl infusion was started at 100 mL/h. 50 U regular insulin in 50 mL of 0.9% NaCl solution was prepared and it started infusion at 1,5 mL/h. Fluid infusion rate was reduced from 125 mL/h to 50 mL/h, and 15 mEq KCl was added. The operation is completed at 135 minutes in other words 15 minutes after the start of insulin infusion. Blood glucose was measured 13 mmol/L at postoperative 30th minute and insulin infusion rate was reduced to 0.7 mL/h. Because blood glucose decreased to 10 at postoperative first hour, insulin infusion was stopped.
Tramadol 30 mg is administrated by intravenous route as postoperative analgesic. There were no problems at extubation nor recovery from anesthesia. Consciousness, HR, SAP, SpO2, and respiration rate and pattern were normal. Blood glucose, Na, and K levels were measured 200, 148, and 3.2, respectively, at postoperative twelve hour, respectively.
The patient did not have any preoperative or postoperative anesthetic problems except a rise in the blood glucose level. The patient was discharged from the hospital on postoperative day 5.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [143.0, 'mEq/L'], 'Glucose': [6.6, 'mmol/L']}",143.45374,136.28105,150.62643,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 143.0 mEq/L. 
The concentration of glucose is 6.6 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 6.6 mmol. To convert 6.6 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 6.6 mmol glucose * 0.001 mol/mmol = 0.0066 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0066 mol glucose * 180.16 g/mol = 1.18906 g glucose. To convert 1.18906 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 1.18906 g glucose * 1000.0 mg/g = 1189.06 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1189.06 mg glucose/10.0 dL = 118.906 mg glucose/dL. The concentration value of 6.6 mmol glucose/L converts to 118.906 mg glucose/dL. 
Plugging in these values into the formula gives us 143.0 mEq/L + 0.024 * (118.906 - 100) = 143.45374 mEq/L.
Hence, the patient's corrected concentration of sodium is 143.45374 mEq/L."
5532,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5830024-1,Extracted,"A 61-year-old male with a history of melanoma metastatic to the chest wall and lungs presents to the emergency department with a three-day history of malaise, nausea, vomiting, polyuria, decreased PO intake, and dizziness. He has no other history of chronic diseases. He was recently started on nivolumab and ipilimumab, a combination of anti-PD-1 and anti-CTLA-4 immunotherapy. After the third dose, he developed a generalized maculopapular rash, a known side effect of his immunotherapy regimen, for which he was started on high-dose prednisone three days prior to presentation. The patient reports antecedent fatigue and nausea that profoundly worsened after starting high-dose prednisone. On presentation, he appeared in distress. He was tachycardic with a heart rate of 126 beats per minute, tachypneic with a respiratory rate of 24 breaths per minute, and hypotensive with a blood pressure of 90/50 mmHg. His oral mucosa was dry. His labs revealed potassium 9.5 mmol/L, sodium 127 mmol/L, bicarbonate <10 mmol/L, blood glucose 1211 mg/dL, anion gap >31 mmol, arterial blood pH 7.14, beta-hydroxybutyrate 13.7 mmol/L, lactic acid 2.4 mmol/L, serum creatinine 4.55, positive urine ketones, urine glucose >1000 mg/dL, and serum lipase 414 IU/L. The patient was admitted to the intensive care unit for management of diabetic ketoacidosis (DKA). He has no prior history of diabetes. He was managed with IV hydration and insulin drip and later transitioned to subcutaneous insulin after the anion gap closed. He required daily insulin adjustments, and it was hard to achieve optimal glycemic control. During his hospitalization, workup revealed a hemoglobin A1C of 6.9%. His serum C-peptide was undetectable <0.1 ng/ml. Glutamic acid decarboxylase autoantibodies (GADA) and zinc transporter 8 autoantibodies (ZnT8A) analyzed by ELISA, insulin autoantibodies (IAA) analyzed by radioimmunoassay, islet antigen 2 autoantibodies (IA-2A) analyzed by radiobinding assay, and islet cell antibodies (ICA) analyzed by immunofluorescence assay were all negative. To date, the patient is on subcutaneous basal-bolus insulin regimen with glargine and lispro, respectively. Our patient did not carry the high-risk HLA haplotype of FD identified in Japanese populations.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [127.0, 'mmol/L'], 'Glucose': [1211.0, 'mg/dL']}",153.664,145.9808,161.3472,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 127.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 127.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 127.0 mmol * 1 mEq/mmol = 127.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 127.0 mmol sodium/L converts to 127.0 mEq sodium/L. 
The concentration of glucose is 1211.0 mg/dL. 
Plugging in these values into the formula gives us 127.0 mEq/L + 0.024 * (1211.0 - 100) = 153.664 mEq/L.
Hence, the patient's corrected concentration of sodium is 153.664 mEq/L."
5533,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-6934,Extracted,"A 24-year-old woman is brought to the emergency room (ER) by her co-workers after they found her unconscious in her cubicle when they returned from lunch. They tell you that she has diabetes but do not know anything more about her condition. The woman’s vital signs include: pulse 110/min, respiratory rate 24/min, temperature 36.7°C (98.0°F), and blood pressure 90/60 mm Hg. On physical examination, the patient is breathing heavily and gives irrelevant responses to questions. The skin and mucous membranes appear dry. Examination of the abdomen reveals mild diffuse tenderness to palpation. Deep tendon reflexes in the extremities are 1+ bilaterally. Laboratory studies show:
Finger stick glucose 630 mg/dL
Arterial blood gas analysis:
pH 7.1
PO2 90 mm Hg
PCO2 33 mm Hg
HCO3 8 mEq/L
Serum:
Sodium 135 mEq/L
Potassium 3.1 mEq/L
Chloride 136 mEq/L
Blood urea nitrogen 20 mg/dL
Serum creatinine 1.2 mg/dL
Urine examination shows:
Glucose Positive
Ketones Positive
Leukocytes Negative
Nitrite Negative
RBCs Negative
Casts Negative
The patient is immediately started on a bolus of intravenous (IV) 0.9% sodium chloride (NaCl).","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [135.0, 'mEq/L'], 'Glucose': [630.0, 'mg/dL']}",147.72,140.334,155.106,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 135.0 mEq/L. 
The concentration of glucose is 630.0 mg/dL. 
Plugging in these values into the formula gives us 135.0 mEq/L + 0.024 * (630.0 - 100) = 147.72 mEq/L.
Hence, the patient's corrected concentration of sodium is 147.72 mEq/L."
5534,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7494222-1,Extracted,"A 53 year-old African-American male with past medical history of essential hypertension presented to emergency room for acute onset of visual floaters and left visual field deficits upon awakening in the morning. Patient reported red white and blue puzzle-shaped particles in the far left vision of both eyes. Five days prior to admission patient was seen at the dermatology office for chronic contact dermatitis and furunculosis and he was started on prednisone 20 mg daily. Patient endorsed having large amount of sugary drinks in the days leading to his admission. Patient denied any headache, dizziness, speech and swallowing problem, limb weakness, numbness or tingling, gait abnormalities, difficulty hearing, urinary/bowel incontinence, previous similar complaints, history of stroke or head trauma. Furthermore, the patient denied any illicit drug use. At presentation, he was hypertensive at 150/84 mm-of-Hg, with otherwise normal vital signs. Triage finger-stick glucose (FSG) was 630 mg/dl.
On exam, he was awake, alert, oriented to time, place and person. Neurological exam was notable for subtle left sided ptosis and left sided homonymous hemianopia (HH), with otherwise normal cranial nerve exam. Visual acuity was 20/70 OS and 20/30 OD. Motor strength, sensory, reflexes, coordination exams were normal. Gait was assessed with caution due to left sided deficit, otherwise with intact heel to toe walking and tandem. Stroke code was initially called due to focal neurological deficits, but no tPA was administered as he was outside the treatment window. His NIHSS score was 3 (L homonymous hemianopia; subtle Left upper extremity pronator drift).
Labs were significant for Sodium of 129mEq/L, Anion gap of 14, bicarbonate of 26, pH 7.324 on >ABG, Glucose 630 mg/dL, beta-hydroxybutyrate 1.0mmol/L, , creatinine 1.25 mg/dL, HbA1C 14.2% and serum osmolality 322mmol/kg. Urinalysis showed trace ketones (5 mg/dl) and Glucose of >1000 mg/dL. EKG and Chest X-ray were normal.
CT head as substantiated by MRI brain showed no acute but chronic microvascular ischemic changes and mild cerebral atrophy. CT angiography of head showed no large vessel occlusion, high-grade stenosis, aneurysm or vascular malformation. Fetal origin of left PCA with hypoplastic P1 segment was noted. CTA of neck showed no significant stenosis according to NASCET criteria. Routine EEG was performed in the waking, drowsy and sleeping states and it was normal with no epileptiform discharges, and transthoracic echocardiogram showed normal LVEF, valves and chambers with no evidence of thrombi. Orbital MRI with contrast did not show any abnormality.
Our patient was admitted for HHS management from newly diagnosed diabetes and managed with aggressive hydration and insulin therapy. Ophthalmology was consulted and followed the patient throughout his stay. Initial exam by ophthalmology showed a congruent left homonymous hemianopia, suggestive of occipital lobe lesions. Final result showed scattered nonspecific superior visual field defects, dramatically improved from prior. Our patient's visual fields improved with glycemic improvement, and he was discharged with close neurology and ophthalmology follow up and primary care for new onset Diabetes. During ophthalmology follow up, on the same week of discharge, he reported near resolution of visual field defects.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [129.0, 'mEq/L'], 'Glucose': [630.0, 'mg/dL']}",141.72,134.634,148.806,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 129.0 mEq/L. 
The concentration of glucose is 630.0 mg/dL. 
Plugging in these values into the formula gives us 129.0 mEq/L + 0.024 * (630.0 - 100) = 141.72 mEq/L.
Hence, the patient's corrected concentration of sodium is 141.72 mEq/L."
5535,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8337150-1,Extracted,"A 62 year-old-African American male patient presented to the emergency department with a 3-day history of general feeling of malaise, poor appetite, decreased urine output, and blood in his urine. His comorbidities include hypertension, morbid obesity (BMI of 39.6), and suboptimally controlled type II diabetes. He was socially distancing alone at home and reported no known sick contacts. He denied taking any anticoagulation medication and had no symptoms of urinary urgency or dysuria. He also denied recent strenuous activity, alcohol ingestion, or taking any over-the-counter supplements. Home medications included aspirin 81 mg, glargine 25 units daily, hydrochlorothiazide-lisinopril 12.5mg–20 mg daily, pioglitazone 30 mg, and simvastatin 20 mg daily.
On presentation, he was febrile to 38.1°C with a heart rate of 103, respiratory rate of 20, blood pressure of 91/58 mmHg, and saturating well on room air. Physical examination yielded a patient with a large body habitus and mild respiratory distress. Pertinent initial laboratory findings revealed a sodium of 132 mmol/L, potassium 4.5 mmol/L, magnesium 2.0 mg/dL, phosphorus 8.9 mg/dL, corrected calcium 4.4 mg/dL, BUN 54 mg/dL, creatinine 4.90 mg/dL (baseline of 1.1 mg/dL), glucose 372 mg/dL, aspartate aminotransferase (AST) 1077 units/L (baseline of 16 units/L), alanine aminotransferase (ALT) of 158 units/L (baseline of 24 units/L), alkaline phosphatase 45 units/L, total bilirubin 0.4 mg/dL, glomerular filtration rate (GFR) 14 mL/min, and lactic acid of 2.1 mmol/L. Urine albumin-to-creatinine ratio one month prior to presentation was 30 mg/g. Creatinine kinase was 327, 629 units/L, and peaked on presentation. Hemoglobin A1C glycosylated was 12.9%. D-dimer was 2.01 mcg/mL FEU. Arterial blood gas showed a pH of 7.35, CO2 of 31 mmHg, and bicarbonate of 17.1 mmol/L. C-reactive protein (CRP) was 136.39 mg/L, and thyroid-stimulating hormone (TSH) was 1.397 uIU/mL. Hepatitis viral panel was obtained and negative. Urine toxicology was negative. Urine analysis showed a moderate amount of blood and 19/hpf red blood cells. The progression of creatinine and creatinine kinase is depicted in , respectively.
Point-of-care ultrasound of the bladder showed <100 mL of urine. Ultrasound of the abdomen showed hepatomegaly with fatty infiltration and no acute cholecystitis or choledocholithiasis, as well as no hydronephrosis. The initial chest radiograph was significant for multifocal patchy airspace disease suggestive of atypical pneumonia or viral infection including COVID-19 ().
Initial COVID-19 RNA PCR was negative. Respiratory viral panel for influenza and respiratory syncytial virus (RSV) was also negative. He was given a bolus of 2 L lactated ringer (LR) and started on maintenance LR at 200 mL/hour as well as sevelamer 2400 mg three times a day. For the first 48 hours, he was anuric. He also received ceftriaxone and azithromycin for community-acquired pneumonia coverage. His anion gap and metabolic acidosis resolved shortly after administration of IV fluids. Following the first 48 hours, his urine output increased to 600 mL over 24 hours on the third day and was red tinged. Urine output decreased to 210 mL and 150 mL per 24 hours on hospitalization days four and five, respectively. On the third day of his hospitalization, given the elevated D-dimer and concerning chest radiograph findings, COVID-19 PCR was repeated and found to be positive.
Despite his positive test, the patient did not have respiratory symptoms and continued to oxygenate well on room air. On day 3, continuous renal replacement therapy (CRRT) was initiated due to persistent low urine output, worsening kidney indices, and volume overload. He received 3 consecutive days of CRRT while maintenance fluids were continued at 100 mL per hour. His urine output gradually increased, and CRRT was interrupted. By day 5, his creatine kinase downtrended to 57, 074 units/L with improved serum creatinine to 5.46 mg/dL. At the end of the first week of his hospitalization, his urine appeared clear and total 24-hour output was 700 mL. Given his improvement in urine output and downward trend in creatinine, CRRT was stopped.
On day 8 of his hospitalization, his oxygen levels desaturated to 87% while walking to the bathroom and he was placed on 2 L supplemental oxygen via a nasal cannula. Maintenance fluids were also discontinued at this time, and he developed a fever to 38.1°C. Chest X-ray showed worsening bilateral infiltrates ().
At this point in his clinical course, his blood pressures remained elevated, ranging from 170/80 to 200/90, and antihypertensive medication doses were progressively increased up to amlodipine 10 mg daily and hydralazine 100 mg thrice a day. On day 12, the patient went into acute hypoxic respiratory failure, developed tachycardia with a heart rate of 120s beats per minute and tachypnea with a respiratory rate of 30. An arterial blood gas (ABG) was obtained which showed a pH of 7.41, CO2 29 mmHg, bicarbonate 18.4 mmol/L, and PaO2 of 82 mmHg. He was placed on BiPAP at 60% FiO2, broad-spectrum antibiotics for pneumonia coverage, and heparin drip for suspected pulmonary embolism and was transferred to the intensive care unit (ICU).
In the ICU, he was started on a 10-day course of dexamethasone and weaned to a high-flow nasal cannula after 2 days. Remdesevir was never given due to kidney dysfunction. He was also intermittently treated with diuretics. By day 14 of his hospitalization, his daily urine output was 2.9 L and clear in color. He received an echocardiogram which showed an ejection fraction of 65–70% with no valvular or diastolic dysfunction. Ultrasound of the lower extremities was negative for deep vein thrombosis. As his respiratory status improved, he was weaned to 6 L supplemental oxygen via a nasal cannula and was transferred out of the ICU. The patient gradually improved as he completed the 10-day course of dexamethasone, and at the time of discharge, 26 days after his presentation, his creatinine gradually decreased to 1.16 mg/dL and he was sent home, on room air.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [132.0, 'mmol/L'], 'Glucose': [372.0, 'mg/dL']}",138.528,131.6016,145.4544,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 132.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 132.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 132.0 mmol * 1 mEq/mmol = 132.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 132.0 mmol sodium/L converts to 132.0 mEq sodium/L. 
The concentration of glucose is 372.0 mg/dL. 
Plugging in these values into the formula gives us 132.0 mEq/L + 0.024 * (372.0 - 100) = 138.528 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.528 mEq/L."
5536,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-8169,Extracted,"A 23-year-old man presents with severe right lower quadrant abdominal pain for the past 2 hours. He says the pain started in the periumbilical region and has now shifted to the lower right quadrant. He describes the pain as spasmodic. Past medical history is insignificant, and the patient denies any history of smoking, alcohol, or drug use. The patient’s vital signs show: pulse 88/min, respiratory rate 18/min, blood pressure 126/84 mm Hg, and temperature 38.4°C (101.0°F). On physical examination, there is severe tenderness to palpation in the right lower quadrant with rebound and guarding. The patient is rushed to the operating room for a laparoscopic appendectomy. The following preoperative laboratory tests are obtained:
Serum glucose (random) 123 mg/dL
  Serum electrolytes
Sodium 143 mEq/L
Potassium 4.7 mEq/L
Chloride 102 mEq/L
    Serum creatinine 1.7 mg/dL
Blood urea nitrogen 32 mg/dL
    Hemoglobin (Hb%) 12.5 g/dL
Mean corpuscular volume (MCV)  80 fl
Reticulocyte count 1%
Erythrocyte count 5.1 million/mm³
Leukocyte count 14,000/mm³
Neutrophils 80%
During the induction of anesthesia, isoflurane and a second compound are administered. About 25 minutes after induction, the patient develops significant muscle rigidity and his temperature increases to 40.8°C (105.4°F). The patient’s blood pressure is now 158/94 mm Hg.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [143.0, 'mEq/L'], 'Glucose': [123.0, 'mg/dL']}",143.552,136.3744,150.7296,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 143.0 mEq/L. 
The concentration of glucose is 123.0 mg/dL. 
Plugging in these values into the formula gives us 143.0 mEq/L + 0.024 * (123.0 - 100) = 143.552 mEq/L.
Hence, the patient's corrected concentration of sodium is 143.552 mEq/L."
5537,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6781379-1,Extracted,"A 52-year-old Cameroonian man, married and a car driver, was admitted to our nephrology inpatient ward for acute kidney injury. He had no relevant past history regarding disease or toxic exposure. He occasionally consumed alcohol and was not a smoker. He had been well until 8 weeks prior to admission, when he developed progressive fatigue, anorexia, involuntary weight loss (~ 12% of his usual body weight), and intermittent nocturnal fever that had been treated twice as malaria and typhoid fever. The malaria and typhoid fever treatments received were parenteral quinine and ofloxacin (doses and duration of treatment not described for both), and both were unsuccessful. A few days before consultation in our hospital, he developed polyuria, polydipsia, constipation, and diffuse abdominal pain that rapidly worsened, prompting consultation at the emergency service of our hospital. The findings of a serum creatinine level of 36.7 mg/L (normal range, < 15 mg/L) and a blood urea nitrogen level of 1.23 g/L (normal range, 0.15–0.45) led to his transfer to the nephrology unit. Upon admission, further questioning revealed that a few days prior to consultation, the patient had inconsistent verbalizations and hallucinations. He was very ill-looking, severely dehydrated, with nontender fixed bilateral inguinal lymph node enlargement (4 cm for the largest), nonreactive urine dipstick, and a fecaloma. His Glasgow Coma Scale score was E4V2M6, blood pressure was 170/88 mmHg, pulse rate was 102/minute, respiratory rate was 17/minute, temperature was 37.7 °C, body surface area was 1.66 m2, and random capillary glucose was 0.91 g/L. Apart from the impaired verbal response (in the Glasgow Coma Scale) that limited cognitive function examination, no cranial palsy, meningeal signs, motility abnormalities, sensitivity abnormalities, or coordination abnormalities were found on neurological examination. Cardiac auscultation revealed regular tachycardia. Abdominal examination revealed diffuse tenderness and increased bowel sounds but no defense, contracture, abdominal distention, or visceral enlargement. The result of the rest of the physical examination was normal. Laboratory tests revealed red blood cells 5.4 × 1012/L, hemoglobin 14.3 g/dl, white blood cells 6.2 × 109/L, neutrophils 2.6 × 109/L, eosinophils 0, basophils 0, lymphocytes 2.7 × 109/L, monocytes 6.2 × 109/L, platelets 137 × 109/L, total calcium 199.5 mg/L (normal range, 84–105), ionized Ca2+ 101.75 mg/L (normal range, 46–54), serum phosphorus 40.20 mg/L (normal range, 25–50), plasma sodium 152 mmol/L (normal range, 135–145), serum potassium 3.1 mmol/L (normal range, 3.5–5), serum chloride 110 mmol/L (normal range, 96–107), and serum magnesium 19.80 mg/L (normal range, 18–26).
A provisional diagnosis of a lymphoproliferative disorder or a granulomatous disease causing acute kidney injury was made. Further laboratory tests showed parathyroid hormone (PTH) level 9.70 pg/ml (normal range, 17–73), PTH-related peptide (PTH-rp) level < 8.5 pg/ml (normal range, < 13.0), 1.25(OH)2D3 level 32 ng/ml (normal range, 18–71 ng/ml for nondialysis subjects), erythrocyte sedimentation rate 50 mm (normal range, < 20 mm), C-reactive protein (CRP) 148.72 mg/L (normal range, < 6 mg/L), and prostate-specific antigen 0.21 ng/ml (normal range, < 4 ng/ml). Figure shows the curve of concurrent serum protein electrophoresis. Plain x-rays of the skull and chest radiographs (Fig. a and b) revealed an osteolytic lesion in the skull and mediastinal lymph nodes. A resting electrocardiogram (Fig. ) confirmed sinus tachycardia as the lone abnormality. Twenty-four hours following admission to the nephrology unit, specific hypercalcemia management was initiated with 4-mg zoledronate once and hydration using intravenous liquids (isotonic saline, 2 L/24 hours and 5% dextrose, 1 L/24 hours) for 3 consecutive days before introduction of oral furosemide 40 mg once daily to correct consequential fluid overload. A symmetric purpura limited to the lower limbs (Fig. ) progressively developed from the fourth to sixth days of hospitalization, with temperatures reaching a plateau at 40–40.5 °C. On evaluation 9 days after initiation of specific hypercalcemia management, serum calcium and sodium returned to normal values, with complete recovery of related symptoms and signs, as well as renal function (Fig. a–c). On the 14th day of hospitalization, although the purpura completely regressed, fever persisted, and lymph node enlargement extended beyond the groins to the cervical region. At this time, results of bacteriological cultures, including urine culture and three serial hemocultures, were all negative, and CRP was 115.61 mg/L. Complete blood count showed red blood cells 2.5 × 1012/L, hemoglobin 6.6 g/dl, white blood cells 2 × 109/L, neutrophils 0.6 × 109/L, eosinophils 0.06 × 109/μl, basophils 0, lymphocytes 1.3 × 109/L, monocytes 0.4 × 109/L, and platelets 44 × 109/L. Peripheral blood smear confirmed a low platelet count but showed neither blasts nor flower cells. The reticulocyte count was 22,640/mm3. The bone marrow aspirate showed 8.3% normal cellularity with no abnormal infiltrate (including blast cells) or fibrosis. This marrow hypocellularity together with pancytopenia led to the diagnosis of nonsevere aplastic anemia according to the revised Camitta criteria []. Inguinal lymph node biopsy showed large cells with distinct nucleoli, dispersed chromatin, and scant cytoplasm with intracytoplasmic CD3 and Ki67 markers, all suggestive of aggressive precursor T-cell lymphoma (Fig. a–d). Because lymphoblasts were not observed either in bone marrow analysis or in the peripheral blood smear, and considering histopathologic findings of the lymph node biopsy, T-ALL was ruled out, and the diagnosis of T-LBL was retained [, ]. An abdominal ultrasound obtained to assess T-LBL extension showed no organ (spleen, liver, kidney) enlargement. Additional examinations evaluating disease prognosis showed serum lactate dehydrogenase 1145.2 IU/L (normal range, 200–400), uric acid 148 mg/L (normal range, < 70 mg/L), serum glutamic oxaloacetic transaminase 72.3 IU/L (normal range, < 37), and serum glutamic pyruvic transaminase 27.6 IU/L (normal range, < 45). The patient was then transferred to the oncology unit, where he immediately received transfusion of 3 U of whole blood within 2 days prior to chemotherapy. The chemotherapy, which was based on the standard cyclophosphamide-doxorubicin-vincristine-prednisolone (CHOP) protocol for NHL [], consisted of a 15-minute intravenous infusion of 1250 mg of cyclophosphamide on day 1, a 2-minute intravenous bolus of 80 mg doxorubicin on day 1, a 2-minute intravenous bolus of 2 mg vincristine on day 1, and 100 mg of oral prednisolone once daily on days 1 to 5 of the cycle. Following this CHOP cycle, 1 ml of filgrastim was administered subcutaneously once daily for 3 consecutive days as supportive treatment for aplastic anemia. Resolution of fever and recovery from fatigue and anorexia were noted from the third day of the CHOP cycle. The patient was discharged at the end of the cycle. One week following hospital discharge, he died at home a few hours after fever recurrence.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [152.0, 'mmol/L'], 'Glucose': [0.91, 'g/L']}",151.784,144.1948,159.3732,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 152.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 152.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 152.0 mmol * 1 mEq/mmol = 152.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 152.0 mmol sodium/L converts to 152.0 mEq sodium/L. 
The concentration of glucose is 0.91 g/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from g to mg. The mass of glucose is 0.91 g. To convert 0.91 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 0.91 g glucose * 1000.0 mg/g = 910.0 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 910.0 mg glucose/10.0 dL = 91.0 mg glucose/dL. The concentration value of 0.91 g glucose/L converts to 91.0 mg glucose/dL. 
Plugging in these values into the formula gives us 152.0 mEq/L + 0.024 * (91.0 - 100) = 151.784 mEq/L.
Hence, the patient's corrected concentration of sodium is 151.784 mEq/L."
5538,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-9635,Extracted,"A 55-year-old woman visits the clinic after experiencing what she describes as an odd episode of tingling in her fingers and the sensation of smelling sour milk. She denies loss of consciousness, confusion, or incontinence. She also denies a history of head trauma or the ingestion of toxic substances. Past medical history is significant for type 2 diabetes mellitus, which is well controlled with metformin. Her temperature is 36.8°C (98.2°F), the heart rate is 98/min, the respiratory rate is 15/min, the blood pressure is 100/75 mm Hg, and the O2 saturation is 100% on room air. The physical exam, including a full neurologic and cardiac assessment, demonstrates no abnormal findings. Laboratory findings are shown. Brain MRI does not indicate any areas of infarction or hemorrhage. ECG is normal, and EEG is pending.
BUN 15 mg/dL
pCO2 40 mmHg
Creatinine 0.8 mg/dL
Glucose 95 mg/dL
Serum chloride  103 mmol/L
Serum potassium 3.9 mEq/L
Serum sodium 140 mEq/L
Total calcium 2.3 mmol/L
Magnesium 1.7 mEq/L
Phosphate 0.9 mmol/L
Hemoglobin 14 g/dL
Glycosylated hemoglobin 5.5%
Total cholesterol 4 mmol/L
Bicarbonate (HCO3) 19 mmol/L
Urine toxicology screen is negative.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [140.0, 'mEq/L'], 'Glucose': [95.0, 'mg/dL']}",139.88,132.886,146.874,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 140.0 mEq/L. 
The concentration of glucose is 95.0 mg/dL. 
Plugging in these values into the formula gives us 140.0 mEq/L + 0.024 * (95.0 - 100) = 139.88 mEq/L.
Hence, the patient's corrected concentration of sodium is 139.88 mEq/L."
5539,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4703168-1,Extracted,"A 34-year-old male with a past medical history of MS was brought into the emergency department by Emergency Medical Services after being found unresponsive by his mother with three pill bottles at his side. The bottles were an empty bottle of valacyclovir, an empty bottle of temazepam and a bottle of dalfampridine still containing some pills. His mother gave the history that the patient was under multiple social stressors of late. Other than MS, the patient was diagnosed with insomnia and had no other pertinent past medical history. His current medications were valacyclovir, temazepam, dalfampridine (4-AP) and a tysabri IV infusion (all part of his MS treatment regimen).
The initial vital signs were as follows: Blood pressure: 155/82mmHg; Heart rate: 106/min; Respiratory rate: 24/min; Temperature: 97.4ºF; O2 sat: 97% 2L NC. The bedside glucose was 144mg/dl. The patient appeared extremely tremulous, was awake, but not responding to questioning nor following simple commands. He responded to tactile stimulation by localizing to the pain. He did not appear to have any focal deficits. His pupils were 4 mm, equal and reactive and his mucous membranes were moist. His heart sounds were tachycardic, with no murmurs. The patient had clear breath sounds bilaterally and no retractions. The abdomen had normoactive bowel sounds. The skin was diaphoretic with piloerection.
Intravenous access was established, labs were drawn and the patient was given two liters of normal saline. Soon after arrival, the patient lost consciousness, his oxygen saturation decreased to below 90% and he began to have a tonic-clonic seizure. The patient was administered boluses of lorazepam, to a total of 8 mg, without effect in seizure resolution. He was intubated and subsequently placed on a lorazepam and propofol infusion for sedation. He was loaded with one gram of phenytoin and 300mg phenobarbital and then placed on a phenobarbital infusion. Clinically the patient continued to have frequent, recurrent seizures.
The patients lab values on arrival were significant for a white blood cell count of 31.1×103/mcL, a sodium of 143mEq/L, potassium 3.1mEq/L, chloride 107mEq/L, bicarbonate of 24mEq/L, a blood urea nitrogen of 15mg/dL and a creatinine of 1.2mg/dL. The anion gap was 12. The lactic acid was 3.4mg/dl. Total creatinine kinase was 99 units/L. Liver function tests and coagulation studies were all within normal limits. Ethanol, acetaminophen and salicylate levels were all negative. A urine toxicology screen was positive for benzodiazepines. An arterial blood gas showed pH 7.22, pCO2 65, pO2 127 and HCO3 26.6 (performed immediately after intubation). Computerized tomography of the brain and chest x-ray were both normal. The electrocardiogram showed a sinus rhythm at 88 beats per minute with normal QRS and QT intervals. Drug levels were sent for 4-AP and valacyclovir. The 4-AP level resulted at 530ng/mL (therapeutic: 25 to 49ng/mL). The valacyclovir level was 7.5mcg/mL (therapeutic 2.0–4.0mcg/mL).
The patient was admitted to the intensive care unit (ICU) and while he was there he continued to have seizures. While in the ICU the patient had two electroencephalographs (EEGs) performed. The EEG on hospital day 2 showed epileptiform activity and the other EEG was performed on hospital day 7 and was indicative of epileptiform encephalopathy.
The patient stopped seizing on hospital day 3. The patient was extubated on hospital day 12. He was discharged, with normal mental status and neurologic exam to an inpatient psychiatric facility.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [143.0, 'mEq/L'], 'Glucose': [144.0, 'mg/dL']}",144.056,136.8532,151.2588,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 143.0 mEq/L. 
The concentration of glucose is 144.0 mg/dL. 
Plugging in these values into the formula gives us 143.0 mEq/L + 0.024 * (144.0 - 100) = 144.056 mEq/L.
Hence, the patient's corrected concentration of sodium is 144.056 mEq/L."
5540,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4590547-1,Extracted,"A 55-year-old nonsmoking unmedicated black woman without past surgical or medical history apart from mild untreated hypertension presented with deteriorated general condition, lethargy, and confusion. There was no personal or family history of thrombosis. A few weeks prior to admission, she had polyuria, polydipsia, and polyphagia. Laboratory findings mainly showed diabetic ketoacidosis (DKA) in the context of a new-onset diabetes with a pH of 7.22, partial pressure of carbon dioxide (pCO2) 12 mmHg, bicarbonates 5 mmol/L, random glucose 56.8 mmol/L, urinary ketones 7.8 mmol/L, sodium 158 mmol/L, chloride 111 mmol/L, potassium 7.9 mmol/L, urea 24.0 mmol/L, creatinine 302 µmol/L, international normalized ratio (INR) 1.16, partial thromboplastin time 25.5 s, and fibrinogen 5.92 g/L. The calculated osmolarity of 396.8 mOsm and intensity of the hyperglycemia evoked mixed features of hyperglycemic hyperosmolar state (HHS). A DKA protocol composed of intravenous insulin and normal saline fluid was started, and the latter rapidly changed to a quarter-normal saline and then dextrose 5% in water due to initial hypernatremia. Cerebral computed tomography scan showed no intracranial hemorrhage or other acute problems. No thromboprophylaxis was given. One of the two blood cultures returned positive for Gram-positive cocci in clusters 29.8 hours after admission for which vancomycin was started. Institutional Review Board approval as well as informed, written consent was not deemed necessary for the following retrospective review. All principles outlined in the Declaration of Helsinki were followed.
A peripherally inserted central catheter (PICC) line was installed on the left side on day 3 to facilitate fluid administration. The patient’s level of consciousness improved, as she was no longer confused. With regard to thromboprophylaxis, compression stockings were preferred to heparin because of thrombocytopenia (platelets at 199×109/L at arrival to 49 on day 4) with a normal coagulogram. Thrombotic thrombocytopenic purpura was contemplated, but no schistocyte was seen that day or on the two subsequent blood films. On day 4, the INR was slightly elevated at 1.33 (prothrombin time of 16.2 s) with a normal activated partial thromboplastin time of 27.5 s, a marginally low fibrinogen of 1.98 g/L, elevated D-dimers at >2 mg/L, and lactate dehydrogenase (LDH) of 334 U/L, revealing some extent of disseminated intravascular coagulation. On day 5, those values were stable, and the patient reported mild catheter-related discomfort that was relieved by acetaminophen. On day 6, platelet count was at 29×109/L and LDH was 848 U/L, and the patient was found to have dyspnea and tachypnea without chest pain, and left arm pain from shoulder to wrist as well as erythema without induration or edema. The patient had a blood pressure of 115/81 mmHg, heart rate 104/min, oxygen saturation 97%, respiratory rate 40/min, and temperature 36.7°C. On the left arm, no exudate was seen at the PICC line site. Radial pulse was nearly absent, and capillary refill was prolonged. There was hand numbness and motor function impairment from the elbow to the distal hand extremity. Arterial thrombosis and pulmonary emboli were suspected.
The vascular surgery team was contacted, and the patient immediately underwent a Doppler ultrasonography and angioscan which showed bilateral deep vein thrombosis (DVT) in legs, bilateral multiple pulmonary embolisms, and left subclavian artery thrombosis with significant extension in descending aorta. The concomitant events raised suspicions of paradoxical embolus through a patent foramen ovale (PFO). There was no evidence of cerebral involvement. A left subclavian thrombectomy was performed. The venous aspect of the clot clinically heightened the probability of a PFO. This was confirmed by transesophageal echocardiography (TOE) which showed left-to-right and spontaneous right-to-left shunts through a PFO but no thrombus. Unfractionated heparin was given as treatment for pulmonary embolisms as the patient was hemodynamically stable. Platelet transfusions were given as platelets count reached 25×109/L. Bacteria in the previously positive blood culture was identified as Micrococcus sp., a commensal organism considered nonpathogenic, so vancomycin was discontinued. Over 2 days, creatine kinase went from a high of 25,367 U/L to 6,331 U/L. Factor V (506) Leiden mutation and prothrombin 20210A mutation were ruled out. At discharge, the patient had regained most of her left arm’s motricity and had scheduled physiotherapy appointments. Warfarin bridging was done using tinzaparin until therapeutic INRs of 2–3 were reached. Long-term – possibly lifelong – anticoagulation was discussed, while PFO closure was not promoted.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [158.0, 'mmol/L'], 'Glucose': [56.8, 'mmol/L']}",180.15942,171.15145,189.16739,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 158.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 158.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 158.0 mmol * 1 mEq/mmol = 158.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 158.0 mmol sodium/L converts to 158.0 mEq sodium/L. 
The concentration of glucose is 56.8 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 56.8 mmol. To convert 56.8 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 56.8 mmol glucose * 0.001 mol/mmol = 0.0568 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0568 mol glucose * 180.16 g/mol = 10.23309 g glucose. To convert 10.23309 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 10.23309 g glucose * 1000.0 mg/g = 10233.09 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 10233.09 mg glucose/10.0 dL = 1023.309 mg glucose/dL. The concentration value of 56.8 mmol glucose/L converts to 1023.309 mg glucose/dL. 
Plugging in these values into the formula gives us 158.0 mEq/L + 0.024 * (1023.309 - 100) = 180.15942 mEq/L.
Hence, the patient's corrected concentration of sodium is 180.15942 mEq/L."
5541,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6507253-1,Extracted,"An 11-year-old, 6.6 kg, female spayed Maltese, presented comatose to the University of Queensland Veterinary Teaching Hospital within 30 minutes of blunt force trauma after being hit by a car. The dog was previously well with no current medications. Initial physical examination revealed the dog to be laterally recumbent and comatose, with bilateral pin-point pupils and an absent menace response. The oral mucous membranes were cyanotic and the dog rapidly progressed to respiratory arrest. The heart rate was initially 60 beats per minute (bpm). Unfortunately, a blood pressure reading was not recorded at this time. There was haemorrhage from the mouth with trauma evident to the oral mucosa.
A venous blood gas performed at presentation showed a mixed acidosis (pH 6.97 [reference interval: 7.35-7.44], lactate 12.4 mmol/L [reference: <2 mmol/L], pCO2 44 mmHg [reference interval: 33.6-41.2 mmHg]), and hyperglycaemia of 24.8 mmol/L [reference interval: 3.3-6.8 mmnol/L]. The sNa was in the normal range at 138 mmol/L [reference interval: 135-153 mmol/L].
An intravenous (IV) catheter was placed and 3 mg alphaxalone was given IV to permit intubation and manual intermittent positive pressure ventilation with 100% oxygen. A 20 ml/kg IV bolus of lactated Ringer's solution (LRS) was administered, followed by a 4 ml/kg bolus of 7% hypertonic saline (HTS) and an infusion of 0.5g/kg of mannitol over 20 minutes. LRS was subsequently continued at approximately 10 ml/kg/hr for one hour and then reduced to 5 ml/kg/hr. Analgesia was provided with fentanyl at 2 ug/kg IV bolus for three sequential boluses, followed by a constant rate infusion (CRI) at 4 ug/kg/hr.
Once spontaneous ventilation was noted, extubation was achieved and treatment continued in an oxygen cage. Neurological status at this time was improving, however, the dog was still obtunded with ongoing bilaterally miotic pupils and an absent menace response. The heart rate had increased to 116 bpm with strong femoral pulses and a systolic blood pressure of 180 mm Hg as measured by doppler. The respiratory rate was 60 breaths per minute with bilaterally harsh lung sounds in all fields. Chest radiographs were performed which demonstrated changes consistent with pulmonary contusions in the right cranial and left caudal lung fields. The dog was assessed as having a TBI with pulmonary contusions.
Approximately two hours after presentation and following initial treatment, a repeat venous blood gas showed the lactate had decreased to near normal at 2.8 mmol/L, with a pH of 7.34, and the hyperglycaemia had resolved (glucose 6.4 mmol/L). The dog's neurological status improved slightly, though some agitation was subsequently noted. A 0.01 mg/kg IV bolus of acepromazine was administered to address this. Five and a half hours after presentation, a venous gas showed a markedly increased sNa of 159 mmol/L (). Other blood work remained unremarkable.
The following morning, fourteen hours following presentation the sNa was measured to be 162 mmol/L. A free water deficit of 480 ml was calculated, and her IV fluids were changed to five percent dextrose in water (D5W) at 40 ml/hr, concurrently with LRS at 25 ml/hr. The goal was to replace the free water deficit over 12 to 24 hours with a decrease of sNa of 0.5 mmol/L/hour. Despite this, 24 hours after presentation and 12 hours following free water commencement, the sNa had only decreased by 4 mmol/L to 158 mmol/L. The urine specific gravity (USG) was 1.012 concomitantly ().
The dog was noted to have improved consciousness, but was intermittently vocalising. A head tilt to the right and rolling to the left when handled was also noted. The menace response remained bilaterally absent and there was absent conscious proprioception in both forelimbs and delayed in the hindlimbs. Withdrawal was present in all limbs. The dog was noted to be urinating large volumes frequently and refused to eat or drink. Harsh lung sounds were evident bilaterally, with an SpO2 of 94% on room air and 98% whilst receiving cage oxygen. Due to ongoing vocalisation, phenobarbitone at 2 mg/kg slow IV was commenced every 12 hours for sedation.
Approximately forty hours after presentation, the dog's mentation had markedly improved as evidenced by reduced anxiety and vocalisation. The dog was responsive to sound and was able to ambulate with assistance. Oxygen supplementation was discontinued as pulmonary function had normalised, and the fentanyl CRI was reduced to 2 ug/kg/hr. Nutritional support was initiated at this time in the form of Hills a/d slurry via syringe with a total volume of 10 ml given on this day.
Despite ongoing parenteral free water supplementation, the sNa remained elevated at 157 mmol/L, with a USG of 1.005. This poor response to free water supplementation prompted desmopressin (DDAVP) administration, one drop of 4 μg/ml solution into the conjunctival sac. Free water administration continued unaltered. Measurement of sNa 12 hours later revealed no change, remaining steady at 157 mmol/L. Therefore, a second dose of one drop DDAVP was administered conjunctivally. Almost no effect was noted as six hours later; the sNa was 156 mmol/L. At this time the desmopressin dose was increased to two drops every 12 hours. Three hours later, sNa was 151 mmol/L with concurrent D5W at 40 ml/hr and LRS at 25 ml/hr.
The dog's neurological status continued to improve. By the third day the menace response had returned in the left eye; there was reduced rolling and circling, and return of conscious proprioception in both forelimbs was noted. Despite the improvement in neurological status the dog developed intermittent head pressing, displayed ongoing subjective polyuria, and was also noted to be lame in the left foreleg, which continued throughout her hospital stay. A transient increase in rectal temperature was also noted (40.2°C); however, this normalised following active cooling with a fan and was thought most likely secondary to anxiety. Maropitant was administered at 1 mg/kg subcutaneously every 24 hours for suspected nausea (ptyalism) and ongoing inappetence. The dog subsequently began to eat 20 mls of Hills a/d slurry every four to six hours. Water was offered every four hours. LRS and fentanyl were discontinued, and D5W was increased to 50 ml/hr. She was continued on two drops of DDAVP in the conjunctival sac every 12 hours.
Despite this increase in D5W and DDAVP, during the fourth day the dog's sNa had increased again to 156 mmol/L and DDAVP was subsequently increased to three drops every 12 hours. Urine specific gravity was recorded to be 1.010 at the commencement of day 4. A mild hypokalaemia of 3.3 mmol/L (reference range: 3.4–4.9 mmol/L) was noted and LRS with 40 mmol/L KCl was recommenced at 10 ml/hr and the D5W was reduced to 40mls/hr. Four hours after the increase in DDAVP the sNa dropped to 151 mmol/L.
By the fifth day the sNa was between 151 and 153 mmol/L and frequent urination continued. The DDAVP was decreased to two drops every 12 hours, and the fluids remained unchanged.
On the sixth day sNa was 148 mmol/L. The dog became more alert and aggressive, which was consistent with her temperament prior to the TBI. She was starting to lick slurry from a bowl in addition to the syringe feeding commenced earlier. Over the following two days, her sNa remained between 148 and 150 mmol/L with a K of 4.4-4.8 mmol/L and a USG of 1.008. The clinical status remained unchanged and treatment was continued with 2 drops of DDAVP every 12 hours, and the D5W was reduced to 10 ml/hr. The USG increased slightly to 1.012 by day 8.
In the morning of day 9, the dog was ambulatory, although bumping into objects. The sNa was 144 mmol/L, and the DDAVP was therefore discontinued. The following day, the sNa was 140 mmol/L with a K of 6.2 mmol/L. The blood pH was 7.21, bicarbonate 11.2 mmol/L, pCO2 28 mm Hg, and base excess -15.2 mmol/L. The urea was 12.40 (reference interval: 3.40–10.80 mmol/L). She was given sodium bicarbonate (8.4%), 10 mmol, diluted in 50 ml of saline IV over three hours. A urine sample collected by cystocentesis showed cocci on sediment exam and amoxicillin clavulanic acid (12.5 mg/kg) was initiated subcutaneously once daily. The sNa for that day was 146 mmol/L and the K dropped to 5.1 mmol/L.
The dog had improved mentation with no head pressing or circling. Although she was ambulatory without ataxia, she would follow walls when walking. Her vision appeared reduced. The USG was 1.022 with a sNa of 148 mmol/L. She was discharged home on day 13 with oral amoxicillin clavulanic acid.
The dog returned two days later for a recheck, at which time her owner reported almost normal mentation. A repeat sNa was 152 mmol/L with a K of 4.8 mmol/L. She had an ongoing lameness of 4/5 in her left foreleg with no distinct foci of pain on palpation of the limb. Her aggressive behaviour limited the musculoskeletal examination.
During a final recheck 10 days later, the owner reported that her personality and behaviour had returned to what they had been before the accident. Given her ongoing left forelimb lameness, she was anaesthetised the following day after a preanaesthetic blood screen, in which her sNa was 143 mmol/L. Radiographs were taken of both forelimbs and showed bilateral severe osteoarthritis of her elbows, with the left being more severe than the right. The persistent lameness was likely from osteoarthritis exacerbated by trauma.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [143.0, 'mmol/L'], 'Glucose': [6.4, 'mmol/L']}",143.36725,136.19889,150.53561,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 143.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 143.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 143.0 mmol * 1 mEq/mmol = 143.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mmol sodium/L converts to 143.0 mEq sodium/L. 
The concentration of glucose is 6.4 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 6.4 mmol. To convert 6.4 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 6.4 mmol glucose * 0.001 mol/mmol = 0.0064 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0064 mol glucose * 180.16 g/mol = 1.15302 g glucose. To convert 1.15302 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 1.15302 g glucose * 1000.0 mg/g = 1153.02 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1153.02 mg glucose/10.0 dL = 115.302 mg glucose/dL. The concentration value of 6.4 mmol glucose/L converts to 115.302 mg glucose/dL. 
Plugging in these values into the formula gives us 143.0 mEq/L + 0.024 * (115.302 - 100) = 143.36725 mEq/L.
Hence, the patient's corrected concentration of sodium is 143.36725 mEq/L."
5542,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4411813-1,Extracted,"A 48-year-old male from West Bengal, in eastern part of India, presented to the emergency department with complaints of sudden onset of pain and distension of abdomen for 2 h. The patient was having low-grade fever and cough with scanty expectoration for last 1-month along with weight loss of 3 kg during this period. With this clinical picture and bilateral upper zone opacities in X-ray chest [], the patient was put on anti-tubercular therapy in another center (Directly Observed Treatment Shortcourse-Category I) though the sputum was negative for acid fast bacilli on Ziehl–Neelson stain on two occasions. On admission, his general examination revealed pulse rate was 112/min and regular, blood pressure was 134/86 mm of Hg, respiratory rate was 36/min and temperature was 100°F. Abdomen was distended, tender with rigidity and guarding. Tenderness was aggravated by movement and cough. Percussion note was tympanitic all throughout the abdomen. On examination of the respiratory system, there was vesicular breath sounds of diminished intensity with coarse crackles bilaterally over infraclavicular areas. Cardiovascular system and central nervous system examination did not reveal any significant abnormality. A diagnosis of perforated hollow viscous abdomen was made provisionally. Routine hematological investigations revealed hemoglobin 110 g/L, total leukocyte count -11.2 × 109/L, neutrophil 68% and lymphocytes 27%. Peripheral smear showed the polymorphonuclear leukocytosis without any parasite or premature cell. Liver enzymes were mildly elevated; aspartate transaminase -64 U/L, alanine transaminase-78 U/L, and alkaline phosphatase -156 U/L. Random plasma glucose was 98 mg/dL, blood urea nitrogen -12 mmol/L and creatinine -1.1 μmol/L. Sodium - 134 mEq/L and potassium -3.4 mEq/L. Serum amylase and lipase study was normal. Routine urine examination was normal. HbSAg, anti-hepatitis C virus and HIV tests were negative. Review of old chest radiograph showed infiltrations in bilateral upper zones with increased broncho vascular markings. X-ray abdomen in an erect posture showed free gas under the diaphragm. Ultrasonography of the abdomen revealed intraperitoneal gaseous distension with intraperitoneal free fluids having internal echogenicity. Patient was urgently shifted to the operation theater for exploratory laparotomy. A midline incision was given. On opening the abdomen, we found around 500 ml of purulent fluid and two small perforations 1cm apart about 20 cm proximal to the ileocaecal junction. After collecting pus sample for microbiological study thorough peritoneal lavage was done, and the perforations were sealed with omental fat. A pelvic drain was given and the incision was closed in a single layer. Postoperative period was eventful as the patient's tidal volume remained low and there was respiratory distress. The patient was shifted to intensive care unit and ventilated mechanically. Patient was treated with intravenous (I/V) piperacillin-tazobactam and amikacin. Gram staining of the pus showed Gram-negative bacilli with bipolar staining. The pus culture showed lactose fermenting pink colonies in MacConkey's agar on 2nd day which turned dry and wrinkled on day 4. The blood agar showed dry and wrinkled colonies on day 4 suspicious of B. pseudomallei []. The antibiotic was changed over to ceftazidime 2 g 8 h along with Amikacin. On 6th postoperative day, the organism was confirmed to be B. pseudomallei by the above-mentioned culture characteristics and standard biochemical methods (positive oxidase and nitrate reduction test, arginine dihydrolase activity, oxidation of glucose and lactose). The organism was sensitive to imipenem, doxycyclin, and cotrimoxazole. Antibiotic was switched over to imipenem 1 g 8 h along with doxycyclin 100 mg twice daily. On 9th postoperative day, we could wean off the ventilator and the patient was put on T-piece ventilation with oxygen. On 12th postoperative day, T-piece was removed, and the oxygen saturation was maintained in room air. Imipenem and doxycyclin were continued for a period of 14 days and then the patient was put on cotrimoxazole (160 + 800 mg). The patient was discharged from the hospital on 24th postoperative day with advice to continue cotrimoxazole for 4 months. On the follow-up of the patient after 6 months, the patient was doing fine, and there was no relapse.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [134.0, 'mEq/L'], 'Glucose': [98.0, 'mg/dL']}",133.952,127.2544,140.6496,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 134.0 mEq/L. 
The concentration of glucose is 98.0 mg/dL. 
Plugging in these values into the formula gives us 134.0 mEq/L + 0.024 * (98.0 - 100) = 133.952 mEq/L.
Hence, the patient's corrected concentration of sodium is 133.952 mEq/L."
5543,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6115549-1,Extracted,"A 47-year-old man presented with a 10-day history of right scrotal pain, swelling and erythema. He had malodorous drainage from right scrotum for two days. He had no diabetes mellitus (DM), hypertension or any other co-morbid diseases; also there were no any risk factors including drug-use, immunodeficiency, genito-urinary or anorectal trauma and infection in his medical history. Massive edema in both of two hemiscrotum and black necrotizing area with malodorous pus drainage in the bottom of the right hemiscrotum was detected in his physical examination (). His anorectal examination was normal. Laboratory analysis revealed as a serum creatinin 0.9 mg/dl, hemoglobin 14.9 g/dl, glucose 486 mg/dL, CRP 156 mg/L, WBC14.5x106 cells/mL, sodium 132 mmol/L. There was no infection sign in bilateral testis, but their sizes were found smaller in scrotal ultrasound (right testis 25x20 mm, left testis 20x20 mm). Intravenous crystallized insulin therapy was given for decreasing serum glucose levels and intravenous imipenem 4x500 mg and Clindamycin 4x600 mg were started prophylactically to the patient according to the infectious disease consultation. All necrotizing tissues were debrided in right scrotum. Right hemiscrotectomy was performed and right testis had a normal blood supply appearance in operation (). Open wound dressing with the nitrofurazone and rifamycin was performed in first three days after operation. The vacuum-assisted closure technique (VAC) (a technique that keeps the wound environment under sterile condition and decreases the frequency of changing protective covers of wound) was performed to the patient in postoperative 3rd day to postoperative 15th day. VAC dressing makes its function by creating mechanical stress with negative pressure of the vacuum system; wound edges diminish, granulation formation accelerates, cellular proliferation and neoangiogenesis increases.
Pathological result revealed as Fournier gangrene and Rhizobium radiobacter was isolated from both of the tissue and abscess cultures. Rhizobium radiobacter was only resistant to trimethoprim sulfamethoxazole and sensitive to ceftazidime, cefepime, imipenem, meropenem, ertapenem, amikacin, gentamycin and tetracycline; therefore same antibiotics were continued to the patient. Control tissue culture was done at postoperative 13th day and by the results revealed as negative wound site was sutured primarily at postoperative 15th day. Patient was discharged at postoperative 18th day with the suggestion of endocrinology consultation for a new diagnosed diabetes mellitus. Patient had come to third month control, he had no symptoms and his scrotum was normal.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [132.0, 'mmol/L'], 'Glucose': [486.0, 'mg/dL']}",141.264,134.2008,148.3272,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 132.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 132.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 132.0 mmol * 1 mEq/mmol = 132.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 132.0 mmol sodium/L converts to 132.0 mEq sodium/L. 
The concentration of glucose is 486.0 mg/dL. 
Plugging in these values into the formula gives us 132.0 mEq/L + 0.024 * (486.0 - 100) = 141.264 mEq/L.
Hence, the patient's corrected concentration of sodium is 141.264 mEq/L."
5544,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3878513-2,Extracted,"A 22-year-old female was admitted to the Intensive Care Unit (ICU) of our hospital with a history of high fever lasting 1 week and severe upper abdominal pain with nausea, vomiting, and diarrhea. The vomitus contained a small amount of red fluid and her stools were often dark. On admission to the ICU, physical examination revealed a normal temperature (36.6°C), normal blood pressure (115/70 mmHg), high pulse rate (115/min), and respiration rates on the upper end of normal (20/min). The patient showed signs of confusion, conjunctival injection, and sclera xanthochromia.
All of the patient’s abdominal muscles were tense with apparent tenderness, and the bowel sounds were decreased. There was also a significant amount of dark red fluid coming from the vagina, but the patient was not currently menstruating. The patient had no history of alcohol abuse, medication, or biliary tract disease.
Laboratory tests performed upon ICU admission provided the following results.
Hemocyte analysis indicated a systemic inflammatory state, with leukocytosis (20.9 × 109/L vs. 4-10 × 109/L) and elevated neutrophils (14.2 × 109/L vs. 2.0-8.0 × 109/L). The platelet count was low (12 × 109/L vs. 100-300 × 109/L) and the hemoglobin was low (76 g/L vs. 110-170 g/L), but serum amylase was slightly elevated (120 U/L vs. 0-103 U/L). Tests of renal function indicated impairment, as shown by elevated serum creatinine (362 μmol/L vs. 44-106 μmol/L) and BUN (29.9 mmol/L vs. 2.3-7.8 mmol/L). In addition, liver function tests indicated impairment, with substantially elevated levels of ALT (262 U/L vs. 0-40 U/L) and AST (1359 U/L vs. 0-40 U/L). Total bilirubin was also high (37.8 μmol/L vs. 0-20 μmol/L), as was direct bilirubin (21.8 μmol/L vs. 0-7 μmol/L), but albumin was low (31.5 g/L vs. 35-55 g/L). Creatine kinase was elevated (353 U/L vs. 20-170 U/L), as was the creatine kinase myocardium isozyme (75 U/L vs. 0-20 U/L). In addition, the patient was hyperglycemic (blood glucose: 7.5 mmol/L vs. 3.8-6.1 mmol/L). Both the prothrombin time (22.2 s vs. 10-13 s) and activated coagulation time of whole blood (74.4 s vs. 23.7-36.4 s) were increased. Urine analysis showed proteinuria, hematuria, and occult blood positivity. While the serum sodium level was normal (125 mmol/L vs. 135-145 mmol/L), the serum calcium level was slightly low (1.72 mmol/L vs. 2.0-2.6 mmol/L). All other routine laboratory values were within the normal range.
CT images of the thoraco–abdominal region revealed bilateral pleural effusions, seroperitoneum, pancreatic edema, peripancreatic fat stranding, and a slightly enlarged spleen (Figure ).
Based on the above findings, the initial diagnosis was multiorgan dysfunction syndrome with SAP and uterine hemorrhage. The patient was treated in the ICU with blood transfusion including erythrocyte suspension, and was given platelets, fresh frozen plasma, etamsylate, antibiotics, somatostatin, omeprazole, and reduced glutathione. On the third day of ICU hospitalization, the patient’s condition had improved and her symptoms of high fever, abdominal pain, and uterine hemorrhage had become significantly relieved or completely resolved. The patient was transferred to the Department of Gastroenterology for further treatment to address the SAP. On the third day of hospitalization in the Department of Gastroenterology, the patient developed polyuria and her serum amylase level had become substantially elevated (416 U/L vs. 0-103 U/L). The treating physician considered alternative causes of SAP since the patient lacked signs of the common causative factors, including gallstones, alcohol abuse, and hyperlipidemia. The physician ordered an ELISA test of the IgM and IgG antibodies of Hantavirus and the result was positive. The patient’s diagnosis was corrected to HFRS complicated with SAP.
On the seventh day of hospitalization, a fine-bore naso-jejunal tube was inserted to provide enteral nutrition. All of the patient’s laboratory values gradually returned to within the normal ranges over the following 3 days. On the tenth day, the patient was discharged with full recovery. At the 1-year follow-up, the patient showed no signs or symptoms of HFRS or SAP.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [125.0, 'mmol/L'], 'Glucose': [7.5, 'mmol/L']}",125.84288,119.55074,132.13502,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 125.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 125.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 125.0 mmol * 1 mEq/mmol = 125.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 125.0 mmol sodium/L converts to 125.0 mEq sodium/L. 
The concentration of glucose is 7.5 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 7.5 mmol. To convert 7.5 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 7.5 mmol glucose * 0.001 mol/mmol = 0.0075 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0075 mol glucose * 180.16 g/mol = 1.3512 g glucose. To convert 1.3512 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 1.3512 g glucose * 1000.0 mg/g = 1351.2 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1351.2 mg glucose/10.0 dL = 135.12 mg glucose/dL. The concentration value of 7.5 mmol glucose/L converts to 135.12 mg glucose/dL. 
Plugging in these values into the formula gives us 125.0 mEq/L + 0.024 * (135.12 - 100) = 125.84288 mEq/L.
Hence, the patient's corrected concentration of sodium is 125.84288 mEq/L."
5545,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6796695-1,Extracted,"A 62-year-old man of Jehovah’s Witness faith developed a life threatening rapid progressive necrotizing fasciitis of his right lower extremity. His comorbidities consisted of type 2 diabetes mellitus, alcohol use disorder, nicotine use, and depression. He was non-compliant with his long-acting nocturnal insulin. The patient developed a non-healing right heel ulcer which began in the fall of the preceding year. He initially presented with his wound to the first health care institution 3 months later and was admitted for approximately 7 weeks. The patient subsequently underwent 4 surgical debridements and received IV antibiotics. Since that recent hospital admission, he had been following up at a local Wound Clinic.
Three weeks after discharge the patient subsequently developed increasing severe lightheadedness, generalized weakness, and dizziness which prompted patient to be evaluated in the Emergency Department (ED) of the second institution. In the ED the patient vitals were: temperature 37 °C, pulse 86 beats/min, respiratory rate 25 breaths/min, oxygen saturation of 98%, and a blood pressure of 98/59 mmHg. Physical examination was significant for right heel ulcer with purulent drainage. Initial laboratory results were significant for: WBC 32,700/mm3, hemoglobin 7.3 g/dL, MCV 83.4 fL, sodium 128 mmol/L, Creatinine 3.38 mg/dL, BUN 45 mg/dL, lactate 3.8 mmol/L and blood glucose level of 606 mg/dL. The patient was then admitted with septic shock, a heel ulcer with suspected osteomyelitis, and acute kidney injury. He was treated with IV antibiotics and epoetin alfa and iron sucrose parenterally. In-patient MRI of the right foot showed osteomyelitis of the calcaneus with a ruptured Achilles tendon and surrounding edema indicating infectious tenosynovitis. Subsequently during inpatient course, he developed severe right lower extremity pain and fever which prompted an emergent X-Ray of the right lower extremity. Imaging results showed prominent areas of subcutaneous emphysema throughout the soft tissue extending to the distal right femur suspicious for NF. The patient immediately underwent right-sided above the knee guillotine amputation with lateral thigh debridement. He was in critical condition post-op and a facility transfer was deemed necessary.
On arrival via ambulance to the intensive care unit trauma service at the 3rd institution (our hospital) the patient was in critical condition, with waxing and waning mentation, he was only oriented to self and examination revealed foul smelling AKA amputation wound which had crepitus to palpation. Significant laboratory results were: WBC of 24,800/mm3, hemoglobin 4.7 g/dL, MCV 75.4 fL, sodium 142 mmol/L, Creatinine 1.0, BUN 55 mg/dl, lactate 1.9 and serum glucose 300 mg/dL. The patient was resuscitated with IV fluids, IV antibiotic therapy, and pain management. He subsequently went for CT scan of the right residual limb to assess the extent of subcutaneous tissue involvement. Imaging showed subcutaneous emphysema extending to the neck of the femur (). Subsequently he had emergent operative wound debridement using a micro debridement tool to enhance bloodless surgery. Intraoperative discussion of a possible hip disarticulation and hemipelvectomy occurred with determination of a poor prognosis of survival. The patient therefore underwent 6 debridement surgeries over the next 14 days with the 1st surgery consisting of a revision amputation ().
Post operatively he improved significantly to a regular diet, stabilized vital signs, and normal mental status. The patient was discharged one month after initial admission to our institution to a rehabilitation facility. His wound at the time of discharge had healthy granulation tissue with a wound vac in place (). He was subsequently seen 2 weeks after at trauma surgeon’s office for his first outpatient follow up.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [142.0, 'mmol/L'], 'Glucose': [300.0, 'mg/dL']}",146.8,139.46,154.14,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 142.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 142.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 142.0 mmol * 1 mEq/mmol = 142.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mmol sodium/L converts to 142.0 mEq sodium/L. 
The concentration of glucose is 300.0 mg/dL. 
Plugging in these values into the formula gives us 142.0 mEq/L + 0.024 * (300.0 - 100) = 146.8 mEq/L.
Hence, the patient's corrected concentration of sodium is 146.8 mEq/L."
5546,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6323657-1,Extracted,"A 58-year-old Japanese man with an 8-year history of T2DM had a symptom of pain in his right lower leg and visited the emergency room in Kawasaki Medical School. Previously, he had felt the same pain in the same region when his blood glucose was very high and thereby he was diagnosed as having T2DM 8 years before.
He had acute osteomyelitis in his right lower leg when he was a baby. Except for this, he had no past history. He had no remarkable family history. He was a barber; he smoked tobacco (pack-years = 0.75 pack/day × 40 years) and he drank alcohol every day. After the episode of acute osteomyelitis when he was a baby, there was no problem in his legs until he had general fatigue and felt pain in his right lower leg at the age of 50. He visited the emergency room. His vital signs were as follows: heart rate 76 beats/minute, blood pressure 116/70 mmHg, and body temperature 36.4 °C. He had a symptom of slight local swelling and heat sensation in the same area with pain in his right lower leg, but there were no findings in physical and neurological examinations. In addition, there was no ulcer or injury on his skin surface. Laboratory data (Table ) were as follows: white blood cell count, 7400/μL (neutrophil 64.7%); C-reactive protein (CRP), 2.50 mg/dl; plasma glucose, 382 mg/dL; hemoglobin A1c (HbA1c), 11.7%. He was diagnosed as having T2DM, but he had no diabetic complications. Magnetic resonance imaging (MRI) of his lower limbs showed an abscess and inflammatory change in his right lower leg (Fig. ). An axial T1-weighted (T1W) image of his right lower leg showed a slightly lower intensity, and an axial T2-weighted (T2W) image showed a markedly higher intensity (Fig. , upper panels). Based on these findings, we made a diagnosis of acute exacerbation of chronic osteomyelitis and T2DM. We thought that it would be better to hospitalize him and start administering antibiotics via a drip, but he did not agree to the hospitalization. Therefore, as an alternative, we started 300 mg/day of cefcapene pivoxil hydrochloride hydrate and insulin therapy (18 units of aspart) on an out-patient basis. After starting insulin therapy, his blood glucose level gradually decreased, and his leg pain was also gradually mitigated. Finally, his leg pain disappeared 2 weeks later. His CRP became within normal range, and 3 months later the focus in his right lower leg was markedly reduced on MRI. In addition, the focus was not detected in ultrasonography of the right tibia site. Just in case, however, we continued antibiotics therapy for 4 months. Since his glycemic control was improved 2 months later, we stopped insulin therapy and started orally administered anti-diabetic drugs.
He was then followed up as an out-patient with T2DM for approximately 8 years. The medication at that time was 1000 mg/day of metformin, 25 mg/day of alogliptin, 15 mg/day of pioglitazone, and 50 mg/day of ipragliflozin. However, he did not take the medicine for approximately 8 months on his own judgement at the age of 58. After his interruption of therapy for 8 months, he felt the same pain in the same right lower leg again. He immediately visited our hospital. He had symptoms of slight local swelling and heat sensation together with pain in the same area in his right lower leg, but again there were no findings in physical and neurological examinations at this time. His vital signs were as follows: heart rate 99 beats/minute, blood pressure 130/70 mmHg, and body temperature 37.0 °C. He had a symptom of slight local swelling and heat sensation in the same area with pain in his right lower leg, but there was no ulcer or injury on his skin surface. Laboratory data were as follows: white blood cell count, 6680/μL (neutrophil 63.4%); CRP, 0.32 mg/dl; erythrocyte sedimentation rate (ESR), 31 mm/hour; plasma glucose, 652 mg/dL; HbA1c, 6.9%; glycoalbumin 46.1%. Other laboratory data were as follows: red blood cell, 476 × 104/μL; hemoglobin (Hb), 15.9 g/dL; platelet, 25.1/μL; total protein (TP), 7.6 g/dL; albumin (Alb), 4.4 g/dL. Liver and renal function were within normal range as follows: aspartate aminotransferase (AST), 39 U/L; alanine aminotransferase (ALT), 50 U/L; γ-glutamyl transpeptidase (γ-GTP), 51 U/L; lactate dehydrogenase (LDH), 172 U/L; creatinine (Cre), 0.54 mg/dL; blood urea nitrogen (BUN), 13 mg/dL; Na, 131 mEq/L; K, 4.4 mEq/L; Cl, 96 mEq/L. Pathogenic bacteria were not detected. He had no diabetic complications, probably because his glycemic control was relatively good before the interruption of therapy. His leg MRI showed a spreading of the abscess and inflammatory change in his right lower leg (Fig. , lower panels). We hospitalized him in our institution but he did not agree to undergo surgery for remission. Therefore, we started 3.0 g/day of sulbactam sodium/ampicillin sodium and insulin therapy (24 units of aspart and 20 units of glargine). After starting insulin therapy, his blood glucose level gradually decreased, and his leg pain was also gradually mitigated. Local swelling and heat sensation disappeared approximately 5 days later. Finally, his leg pain disappeared approximately 2 weeks later, and he was discharged from our hospital. Just in case, however, we continued antibiotics therapy (450 mg/day of rifampicin and 4 g/day of trimethoprim) for approximately 2 months. After a total of 3-month antibiotics therapy during hospitalization and after discharge, we stopped antibiotics therapy. He was then followed up for approximately 6 months, and his leg MRI showed a reduction of the abscess and inflammatory change in his right lower leg. He had no symptoms and/or problems, and his inflammation markers remained within normal levels for at least 6 months.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [131.0, 'mEq/L'], 'Glucose': [652.0, 'mg/dL']}",144.248,137.0356,151.4604,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 131.0 mEq/L. 
The concentration of glucose is 652.0 mg/dL. 
Plugging in these values into the formula gives us 131.0 mEq/L + 0.024 * (652.0 - 100) = 144.248 mEq/L.
Hence, the patient's corrected concentration of sodium is 144.248 mEq/L."
5547,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7379011-2,Extracted,"A 16.8 kg, 10-year-old female spayed Beagle (dog 2) was evaluated for a 3-day history of hematochezia after a prophylactic rattlesnake vaccine administered 4 days before onset of clinical signs. Initial physical examination disclosed obtundation, tachycardia (170 beats per minute), tachypnea (36 breaths per minute), and a grade II/VI left apical systolic heart murmur. Gingival hemorrhage, cutaneous petechiae, and ecchymoses and melena were present.
The initial CBC showed regenerative anemia (HCT, 11.7%; reticulocytes, 134 600/μL), neutrophilia (11 448/μL) with left shift (bands, 322/μL), monocytosis (3225/μL; RR, 150-1200/μL), and thrombocytopenia (8000/μL). No spherocytes were present. A biochemistry profile disclosed increased blood urea nitrogen (BUN) concentration (47 mg/dL), hypoalbuminemia (1.9 g/dL; RR, 3.4-4.3 g/dL), hyperglycemia (193 mg/dL), hypocholesterolemia (84 mg/dL; RR, 139-353 mg/dL), hypokalemia (2.1 mmol/L), and hyponatremia (136 mmol/L; RR, 143-151 mmol/L). Serum bilirubin concentration was normal (0.2 mg/dL). Urinalysis on a voided sample disclosed hematuria (50-100 RBC/hpf). An echocardiogram showed no evidence of endocarditis. An electrocardiogram identified a frequent accelerated idioventricular rhythm and occasional ventricular premature beats. The dog was diagnosed with IMT, suspected to be primary or possibly triggered by the prophylactic rattlesnake vaccine. Disseminated intravascular coagulation was considered less likely because there was no evidence of thrombosis, schistocytosis, and plasma fibrinogen concentration was normal in this dog.
Therapeutic plasma exchange was initiated 4 days after starting immunosuppressive medications (dexSP [0.2 mg/kg q24h] and cyclosporine [5 mg/kg q24h] IV). Three platelet transfusions were administered 2 days before initiating TPE because of ongoing severe hemorrhage.
Dog 2 received 3 TPE treatments over 4 days, providing a total of 4.0 plasma volumes exchanged over all treatments.
Clinical signs suggestive of hypovolemia and responsive to bolus infusions of FFP occurred during the first TPE session. The third TPE session was temporarily discontinued while the extracorporeal circuit was replaced because of severe clotting in the extracorporeal catheter and inlet line before ACD-A infusion that obstructed the downstream inlet blood filter.
Dog 2 was hospitalized for 8 days and euthanized 2 days after the third TPE treatment because of persistent thrombocytopenia (11 000/μL) and hemorrhage requiring ongoing blood transfusions; there was no response to treatment. This dog required 22 pRBC units during hospitalization.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [136.0, 'mmol/L'], 'Glucose': [193.0, 'mg/dL']}",138.232,131.3204,145.1436,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 136.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 136.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 136.0 mmol * 1 mEq/mmol = 136.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mmol sodium/L converts to 136.0 mEq sodium/L. 
The concentration of glucose is 193.0 mg/dL. 
Plugging in these values into the formula gives us 136.0 mEq/L + 0.024 * (193.0 - 100) = 138.232 mEq/L.
Hence, the patient's corrected concentration of sodium is 138.232 mEq/L."
5548,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-5452558-1,Extracted,"A 62-year-old African-American male with diabetes (hemoglobin A1c 10.1% in 07/2016, +2.3% from 10/2015) with sarcoidosis and stage 3b chronic kidney disease (baseline creatinine 1.8–2.0 mg/dL) was admitted with right lower lobe (RLL) pneumonia and bacteremia. He drank wine socially but never used tobacco products or illicit drugs and lived on a rural property with private well water.
The week before admission, he was working on this property and drank lots of well water. He developed congestion and muscle soreness, followed by a productive cough with blood-streaked sputum, wheezing, and shortness of breath. He went to the closest emergency department. His temperature was 37.8°C, heart rate 104/min, respirations 20/min, blood pressure 167/78 mmHg, and oxygen saturation 93% on room air. Peripheral white blood cell (WBC) count was 2.9 K/μL with 80% polymorphonuclear leukocytes (PMNs). Basic metabolic profile revealed sodium 133 mmol/L, blood urea nitrogen (BUN) 39 mg/dL, creatinine 1.8 mg/dL, estimated glomerular filtration rate (eGFR) 38 mL/min/SA, and glucose 319 mg/dL. Chest X-ray [] read airspace disease with right lung base consolidation suggestive of acute lobar pneumonia. The patient left against medical advice and received a 10-day course of oral cefdinir 300 mg twice a day and methylprednisolone 4 mg 6-day taper. The following week, blood cultures taken from his recent ED visit grew nonlactose fermenting Gram-negative rods in the aerobic bottle; VITEK® MS identified A. salmonicida sensitive to ampicillin, ampicillin/sulbactam, cefepime, ceftazidime, ceftriaxone, gentamicin, levofloxacin, meropenem, piperacillin/tazobactam, tobramycin, and trimethoprim-sulfamethoxazole and intermediate to cefazolin. He was admitted to our service for treatment of bacteremia and pneumonia.
On admission, his temperature was 36.2°C, heart rate 72/min, respirations 18/min, blood pressure 158/56 mmHg, and oxygen saturation 95% on room air. He had rales in the RLL lobe with egophony and expiratory wheezing throughout lower lung lobes bilaterally, remainder of examination unremarkable. Peripheral WBC count was 12.8 K/μL with 89% PMNs. Complete metabolic profile remarkable for sodium 133 mmol/L, BUN 54 mg/dL, creatinine 2.28 mg/dL, eGFR 34 mL/min/SA, and glucose 648 mg/dL.
Given the unusual bacteria, we asked the patient about exposure to fish or other bodies of water: he had not been swimming, fishing, or boating for several decades; he ate store-bought fish 2 days after he went to the emergency department; and he drank well water at his property. We asked the laboratory at the referring hospital to repeat the patient's blood culture manually; using matrix-assisted laser desorption ionization time-of-flight technology, it grew the same A. salmonicida pathogen, reporting >98% accuracy. Sputum cultures grew normal flora; bronchoscopy did not reveal other organisms or malignancy. Workup for an intra-abdominal source was negative: Patient's last colonoscopy in 2010 did not reveal masses, hepatitis panel was nonreactive, computed tomography of the chest/abdomen/pelvis [] was unremarkable, and barium swallow did not reveal aspiration. We began intravenous cefepime 2.0 g every 12 h. Two days after initiation of therapy, the patient's coughing improved without additional episodes of hemoptysis. Repeat blood cultures were negative, chest X-ray [] demonstrated resolution of RLL pneumonia. His acute-on-chronic kidney disease and hyperglycemia returned to baseline following fluid resuscitation and insulin. After 5 days of antibiotic therapy, his respiratory symptoms resolved completely, and he was discharged to home on a 10-day course of intravenous ceftriaxone 2.0 g/day.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [133.0, 'mmol/L'], 'Glucose': [648.0, 'mg/dL']}",146.152,138.8444,153.4596,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 133.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 133.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 133.0 mmol * 1 mEq/mmol = 133.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mmol sodium/L converts to 133.0 mEq sodium/L. 
The concentration of glucose is 648.0 mg/dL. 
Plugging in these values into the formula gives us 133.0 mEq/L + 0.024 * (648.0 - 100) = 146.152 mEq/L.
Hence, the patient's corrected concentration of sodium is 146.152 mEq/L."
5549,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3811692-1,Extracted,"32-year-old female.
General weakness.
She was receiving insulin injections for type 1 diabetes, but her symptoms had not been improved at all, which prompted her decision to come to our hospital.
She had been using 32 U insulin every day for type 1 diabetes for 11 years before her visit to our hospital.
All family members, including both parents and all siblings, had diabetes.
When she appeared, her blood pressure was 130/80 mm Hg, pulse rate was 74 beats per minute, and body temperature was 36.6℃. She had no other symptoms, except for general weakness and central obesity (body mass index 23.4 kg/m2). No tumor-like mass was checked at her head and neck, nothing was discovered in chest auscultation. When we checked her abdomen, neither any pain nor hepatosplenomegaly was observed. No skin or oral mucosa pigmentation was found. There was no edema in lower leg. The neurological examination results were also normal. She weighed 51.5 kg and was 148.2 cm tall, and she was somewhat short woman with a short neck and round face, similar to a clinical features of AHO, but there was no pathognomonic brachydactyly.
The result of complete blood count was the hemoglobin 9.3 g/dL, the erythrocyte average volume 96 fL, leukocyte 5,720/mm3, and platelets 310,000/mm. The results of anemia work up were the total iron binding capacity 447.5 µg/dL, serum ferritin 35.11 ng/mL, reticulocyte count 2.89%, average erythrocyte hemoglobin density 32.6 g/dL, and vitamin B12 839.65 pg/mL. Her blood glucose level was 212 mg/dL, the level of hemoglobin A1c was 7.3%, and the simultaneous measurement of serum level of C-peptide showed decreased level of 0.13 ng/mL. Serum concentration of total calcium were 5.5 mg/dL (range, 8.7 to 1.4); ionized Ca 1.56 mg/dL (range, 2.3 to 2.58); phosphorus 6.7 mg/dL (range, 2.5 to 4.5); total protein 6.7 g/dL; albumin 3.3 g/dL; alkaline phosphatase 329 IU/L; aspartate aminotransferase 119 IU; alanine aminotransferase 65 IU/L. Intact PTH level was 13.32 pg/mL (range, 13 to 54). Serum adrenocorticotropic hormone (ACTH) and cortisol levels were 11.92 pg/mL (range, 10 to 60) and 0.94 (range, 9.4 to 26.1). The results of rapid ACTH stimulation test for adrenal function were normal. The results of thyroid function test were T3 99.01 ng/mL, free T4 0.85 µg/dL, and thyroid stimulating hormone 7.99 µIU/mL. The results for antimicrosomal and antithyroglobulin antibody were positive (52.91 IU/mL, 132.57 IU/mL), and, both islet cell antibody and antiglutamic acid decarboxylase antibody tested negative. In the Ellsworth-Howard examination, urinary phosphoric acid was slightly increased (12.3 mg/dL) and the increase of cyclic adenosine monophosphate (cAMP) was sufficient (4,400 µmol/mL). There was no GNAS mutation. Serum levels of sodium, potassium, blood urea nitrogen, and creatinine were within normal limits at 144 mmol/L, 5.3 mmol/L, 8.2 mg/dL, and 1.0 mg/dL.
The chest X-ray showed no abnormal lesion. An brain computed tomography scan showed prominent calcifications in both basal ganglion and hypothalamus (). The thyroid sonogram discovered several nodules, sized 4.5×3.7 mm and 3.9×2.9 mm on each side that were suspected to be thyroid papillary cancer.
The patient came to the hospital experiencing general weakness, and she was diagnosed with hypocalcaemia on laboratory examination. At that time, both the levels of PTH and vitamin D were within normal range, but she had previously experienced spasm symptoms and the levels of previous intact PTH were low (4.38 to 10.66 pg/mL) 7 years ago. She has taken oral calcium medicine for treatment of idiopathic hypoparathyroidism because she had no underlying secondary disorders for hypocalcemia and low PTH level. Although she has no pathognomonic brachydactyly, her appearance was similar to AHO in clinical features including short stature, intelligence decline, round face, calcification on basal ganglion and hypothalamus, or obesity. Furthermore, she had a lower normal PTH level and hypocalemia on admission, and we decided to investigate the PTH resistance to identify PHP Ia or PPHP with AHO. In the Ellsworth-Howard examination for investigation of the PTH resistance, it was confirmed that there was no PTH resistance at the kidney and there was no sign of GNAS mutation. We diagnosed this case as hypocalcemia due to idiopathic hypoparathyroidism for lower serum calcium and traced intact PTH levels and began calcium and calcitriol medicine to treat the hypocalcaemia. Subsequently, her symptoms were improved with normalization of ionized Ca at 2.32 mg/dL (range, 2.3 to 2.53). The results of fine needle aspiration on two nodules of thyroid were suggestive malignancy and she underwent a total thyroidectomy. The biopsy results were papillary microcarcinoma with lymphocytic thyroiditis for two suspicious nodules (sized 1.5×1.0 cm on the left and 2.0×1.0 cm on the right). Among the four parathyroid glands, the left inferior parathyroid gland was not discovered, and the remaining three parathyroid glands were remained during surgery. We used levothyroxine 0.05 mg medication for Hashimoto thyroiditis and insulin determir 12 U and aspart 16 U for glucose control.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [144.0, 'mmol/L'], 'Glucose': [212.0, 'mg/dL']}",146.688,139.3536,154.0224,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 144.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 144.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 144.0 mmol * 1 mEq/mmol = 144.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 144.0 mmol sodium/L converts to 144.0 mEq sodium/L. 
The concentration of glucose is 212.0 mg/dL. 
Plugging in these values into the formula gives us 144.0 mEq/L + 0.024 * (212.0 - 100) = 146.688 mEq/L.
Hence, the patient's corrected concentration of sodium is 146.688 mEq/L."
5550,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3981268-1,Extracted,"A 50-year old man was admitted to our hospital because of a 1-week history of jaundice, fatigue and malaise. On physical examination, the patient was obese, with a body mass index of 37 kg/m, and a waist circumference of 136 cm. His temperature was 36.6°C, blood pressure 160/90 mmHg, and heart rate 107 bpm. Hepatomegaly was detected. The liver was soft, and nontender, with a smooth edge palpable 5 cm below the right costal margin. No xanthomas were found.
The patient’s medical history included type II diabetes mellitus, diagnosed 7 years ago, dyslipidemia (elevated triglycerides, mildly increased cholesterol, and reduced high density lipoprotein - cholesterol), two-vessel coronary artery disease, treated with percutaneous transluminal coronary angioplasty plus stenting 7 months before this admission, and an episode of acute pancreatitis 4 years ago. His family history was notable for gastric cancer in his father.
The patient was an unmarried chandler, who lived with his parents and brother in a working-class suburb of Athens. He had been a heavy smoker (approximately 115 pack-years), but consumed only small quantities of alcohol during social events (<100 g per week). He reported no use of illicit drugs or anabolic steroids, no ingestion of mushrooms, herbal preparations or nutritional supplements, and no exposure to environmental toxins. He was following an extremely unhealthy dietary pattern, characterized by exorbitant calorie intake (estimated amount of 8000 kcal per day), and excessive consumption of saturated animal fats and simple carbohydrates, combined with a sedentary lifestyle and lack of physical activity. His daily medication regimen included aspirin, nebivolol, enalapril, metformin, vildagliptin, and omega-3 fatty acids [eicosapentaenoic (EPA), and docosahexaenoic acid (DHA)].
The most prominent laboratory abnormalities were conjugated hyperbilirubinemia (total bilirubin 10 mg/dL, direct bilirubin 6.6 mg/dL), elevation of liver enzymes, with a disproportionate rise of aminotransferases in comparison to alkaline phosphatase (aspartate transaminase 474 U/L, alanine transaminase 647 U/L, gamma-glutamyltransferase >1453 U/L, alkaline phosphatase 409 U/L), and striking hypertriglyceridemia (triglycerides >1420 mg/dL). The glycosylated hemoglobin value of 11.1% indicated poor diabetic control. Additional abnormal test results were as follows: hematocrit 39%, hemoglobin 13g/dL, mean corpuscular volume 84 fl, lactate dehydrogenase 512 U/L, serum sodium 112 meq/L, glucose 431 mg/dL, total cholesterol >705 mg/dL, high density lipoprotein - cholesterol (HDL-C) 26 mg/dL, erythrocyte sedimentation rate 103 mm/h, C-reactive protein 43 mg/L. The patient’s plasma had a turbid appearance. Urinalysis showed marked glycosuria and bilirubinuria.
Hepatitis A immunoglobulin M (IgM) antibody, hepatitis B surface antigen and core IgM antibody, a polymerase chain reaction assay for hepatitis C viral RNA, and serologic tests for Epstein-Barr virus, human immunodeficiency virus, and cytomegalovirus were negative. Tests for anti-nuclear, anti-smooth-muscle, anti-liver-kidney microsomal type 1, antimitochondrial, and anti-neutrophil cytoplasmic antibodies were also negative. Levels of α1-antitrypsine and ceruloplasmin were normal, and transferrin saturation was less than 40%.
Abdominal ultrasound examination revealed hepatic enlargement and a diffuse increase in echogenicity of the liver as compared with that of the kidneys (bright liver). No other organ abnormality was observed. An abdominal computed tomography scan (), obtained after oral and intravenous administration of contrast material, demonstrated a low-density hepatic parenchyma, which appeared darker than the spleen. Both imaging studies were consistent with fatty infiltration of the liver.
Given the patient’s history, physical examination, laboratory results and imaging findings, we concluded the following clinical diagnoses: first, type IV hyperlipoproteinemia, according to Fredrickson’s classification (familial hypertriglyceridemia), exacerbated by excessive intake of simple carbohydrates, obesity, and insulin resistance, all of which increase very-low-density lipoprotein synthesis; second, acute form of NASH. Moreover, the patient met Adult Treatment Panel III criteria for metabolic syndrome.
The patient was then started on a low calorie diet, with complete exclusion of carbohydrates and fats, and pure intake of high quality protein (chicken breast). He was also treated with isophane insulin (40-30 IU), and omega-3 fatty acids (EPA/DHA 920/760 mg bid). During the next 10 days, the patient showed dramatic improvement of his clinical and laboratory status (), and was discharged from the hospital. He was advised to keep on the medication received during his hospitalization, reduce calorie intake, eat plenty of vegetables and fruits, rich in fiber and complex carbohydrates with a low glycemic index, avoid saturated fats and simple carbohydrates, walk 30 min every day, quit smoking, and abstain completely from alcohol.
Eight weeks later, the patient was invited for a follow-up appointment. Having strictly implemented medical recommendations, he had lost 20 kg of body weight. His signs and symptoms were entirely resolved. Further, impressive amelioration of laboratory values was noted (). Continuation of lifestyle modification was emphasized, and isophane insulin dose was reduced by 20% (32-24 IU). Aspirin 100 mg qd, metformin 850 mg bid, pioglitazone 30 mg qd, atorvastatin 20 mg qd, and EPA/DHA 920/760 mg bid were prescribed.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [112.0, 'mEq/L'], 'Glucose': [431.0, 'mg/dL']}",119.944,113.9468,125.9412,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 112.0 mEq/L. 
The concentration of glucose is 431.0 mg/dL. 
Plugging in these values into the formula gives us 112.0 mEq/L + 0.024 * (431.0 - 100) = 119.944 mEq/L.
Hence, the patient's corrected concentration of sodium is 119.944 mEq/L."
5551,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-5910,Extracted,"A 63-year-old man presents to the emergency department with periorbital swelling. He states that he was gardening, came inside, looked in the mirror, and then noticed his eyelids were swollen. He denies pain, pruritus, or visual disturbances. He states that he was drinking “a lot of water"" to prevent dehydration, because it was hot outside this morning. His medical history is significant for rheumatoid arthritis. He takes methotrexate and acetaminophen as needed. The patient’s temperature is 98°F (36.7°C), blood pressure is 168/108 mmHg, and pulse is 75/min. Physical examination is notable for periorbital edema, hepatomegaly, and bilateral 1+ pitting lower extremity edema. Labs and a urinalysis are obtained, as shown below:

Leukocyte count: 11,000/mm^3
Hemoglobin: 14 g/dL

Serum:
Na: 138 mEq/L
K+: 4.3 mEq/L
Cl-: 104 mEq/L
HCO3-: 25 mEq/L
Urea nitrogen: 26 mg/dL
Creatinine: 1.4 mg/dL
Glucose: 85 mg/dL
Aspartate aminotransferase (AST, GOT): 15 U/L
Alanine aminotransferase (ALT, GPT): 19 U/L
Albumin: 2.0 g/dL

Urine:
Protein: 150 mg/dL
Creatinine: 35 mg/dL

An abdominal ultrasound reveals an enlarged liver with heterogeneous echogenicity and enlarged kidneys with increased echogenicity in the renal parenchyma. A biopsy of the kidney is obtained.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [138.0, 'mEq/L'], 'Glucose': [85.0, 'mg/dL']}",137.64,130.758,144.522,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 138.0 mEq/L. 
The concentration of glucose is 85.0 mg/dL. 
Plugging in these values into the formula gives us 138.0 mEq/L + 0.024 * (85.0 - 100) = 137.64 mEq/L.
Hence, the patient's corrected concentration of sodium is 137.64 mEq/L."
5552,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6402858-1,Extracted,"A 40-year-old man with no past medical history presented to the emergency department with weakness, generalized abdominal pain, nausea, and intractable vomiting of one-week duration. He also endorsed multiple episodes of loose, non-bloody bowel movements. He denied any fevers/chills, hematochezia, melena, voiding difficulty, dysuria, hematuria, or flank pain. Of note, the patient denied any prior history of abdominal pain, changes in bowel habits, or underlying family history of gastrointestinal or renal disease. The patient, however, stated that he had not seen a physician in the past 18 years.
On physical examination, his temperature was 36.8°C, heart rate 69 bpm, respiratory rate 16 br/min, blood pressure 147/102 mmHg, and oxygen saturation 100% on room air. The patient appeared diaphoretic and in moderate distress. The abdomen was soft, diffusely tender, no distension/guarding /rigidity, and normoactive bowel sounds, costovertebral angle (CVA) tenderness, and Murphy sign negative.
Laboratory data revealed a white blood cell count of 6100 K/mcl, hemoglobin 5.9 g/dL, hematocrit 18%, and platelet count 240,000 K/mcl. The basic metabolic panel revealed sodium of 130 mmol/L, potassium 4.7 mmol/L, chloride 95 mmol/L, CO2 24 mmol/L, blood urea nitrogen (BUN) >150 mg/dL, creatinine 26.9 mg/dL, anion gap 21, glucose 87 mg/dL, and serum calcium 6.5 mg/dL. Liver function studies and lipase were within normal limits. The fecal occult blood test (FOBT) was negative. Anemia workup showed normal iron, low total iron binding capacity (TIBC), high ferritin, normal B12, and low reticulocyte count. Arterial blood gas showed pH 7.35, pCO2 18, pO2 149. Lactic acid was 0.4 mmol/L, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) were normal. Urinalysis showed microscopic hematuria, proteinuria, and a urine protein to creatinine ratio of 2.5.
Imaging revealed renal ultrasound with an increased echogenicity of both kidneys without atrophy or hydronephrosis. Computed tomography (CT) abdomen/pelvis revealed diffuse bowel wall thickening from the terminal ileum throughout the entire colon with thumbprinting noted, surrounding mesenteric inflammatory changes extending to the rectum, and 9 cm kidneys (Figures -). There was no visualized lymphadenopathy or retroperitoneal mass on CT.
Subsequently, the patient was transfused two units of packed red blood cells, given analgesics, and placed on intravenous fluids at 100 cc/hour. Nephrology and gastroenterology were consulted. On hospital Day 2, the patient was noted to have persistent anion gap metabolic acidosis, uremia, and hyperkalemia with hyperphosphatemia. The electrocardiogram obtained showed a sinus rhythm with no acute ST wave changes. The patient was given D50 with insulin administration. He subsequently underwent hemodialysis with ultrafiltration. On hospital Day 3, the patient endorsed a significant improvement in his abdominal pain with the ability to pass formed stool. He was placed on oral amlodipine, sevelamer, and sodium bicarbonate.
Further laboratory testing showed that parathyroid hormone was elevated, consistent with secondary hyperparathyroidism. Hepatitis B, C, and HIV were negative. Serum complement studies demonstrated a low level of C3 but normal C4. Double-stranded deoxyribonucleic acid (DNA), immunoglobulin G (IgG), rheumatoid factor, cytoplasmic antineutrophil cytoplasmic antibodies (c-ANCA), perinuclear-ANCA (p-ANCA), and glomerular basement antibody were negative. There was no monoclonal gammopathy on serum protein electrophoresis (SPEP)/urine protein electrophoresis (UPEP). Fecal leukocyte, stool culture, ova/parasite, Clostridium difficile (C. diff) toxin assay, and Escherichia coli (E. coli) O157:H7 Ag testing were negative. The peripheral smear was unremarkable and demonstrated no schistocytes.
Throughout subsequent days, the patient had complete resolution of abdominal complaints, however, despite providing supportive therapies with intravenous fluids, red blood cell transfusions, and hemodialysis, the patient continued to have a worsening of his BUN and creatinine. A renal biopsy was obtained to evaluate for underlying glomerular disease, which revealed several glomeruli with fibrous-fibrocellular crescents, widespread prominent interstitial fibrosis, and tubular atrophy, with 90% glomerulosclerosis consistent with IgAN (Figures -).
Electron microscopy revealed scattered mesangial and intramembranous dense deposits (Figure ).
Immunofluorescence performed showed mesangial IgA deposits seen in a glomerulus with open capillaries, and IgA staining in a sclerotic glomerular with bright enhancements indicating casts (Figures -).
It was determined by nephrology that he would need long-term dialysis. He underwent left upper extremity radiocephalic arteriovenous (AV) fistula creation and right internal jugular tunneled catheter placement for outpatient hemodialysis access. He was discharged with instructions to follow up in the outpatient department with dialysis.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [130.0, 'mmol/L'], 'Glucose': [87.0, 'mg/dL']}",129.688,123.2036,136.1724,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 130.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 130.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 130.0 mmol * 1 mEq/mmol = 130.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mmol sodium/L converts to 130.0 mEq sodium/L. 
The concentration of glucose is 87.0 mg/dL. 
Plugging in these values into the formula gives us 130.0 mEq/L + 0.024 * (87.0 - 100) = 129.688 mEq/L.
Hence, the patient's corrected concentration of sodium is 129.688 mEq/L."
5553,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-1432,Extracted,"A 35-year-old woman with type 1 diabetes mellitus comes to the emergency department for evaluation of a 1-month history of fever, fatigue, loss of appetite, and a 3.6-kg (8-lb) weight loss. She has also had a cough for the last 2 months. She reports recent loss of pubic hair. The patient immigrated from the Philippines 7 weeks ago. Her mother has systemic lupus erythematosus. She has never smoked and does not drink alcohol. Her only medication is insulin, but she sometimes misses doses. She is 165 cm (5 ft 5 in) tall and weighs 49 kg (108 lb); BMI is 18 kg/m2. She appears lethargic. Her temperature is 38.9°C (102°F), pulse is 58/min, and blood pressure is 90/60 mm Hg. Examination shows decreased sensation to touch and vibration over both feet. The remainder of the examination shows no abnormalities. Serum studies show:
Na+ 122 mEq/L
Cl- 100 mEq/L
K+ 5.8 mEq/L
Glucose 172 mg/dL
Albumin 2.8 g/dL
Cortisol 2.5 μg/dL
ACTH 531.2 pg/mL (N=5–27 pg/mL)
CT scan of the abdomen with contrast shows bilateral adrenal enlargement.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [122.0, 'mEq/L'], 'Glucose': [172.0, 'mg/dL']}",123.728,117.5416,129.9144,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 122.0 mEq/L. 
The concentration of glucose is 172.0 mg/dL. 
Plugging in these values into the formula gives us 122.0 mEq/L + 0.024 * (172.0 - 100) = 123.728 mEq/L.
Hence, the patient's corrected concentration of sodium is 123.728 mEq/L."
5554,26,Sodium Correction for Hyperglycemia,lab test,decimal,usmle-1580,Extracted,"A 36-year-old woman comes to the physician because of a 4-day history of fever, malaise, chills, and a cough productive of moderate amounts of yellow-colored sputum. Over the past 2 days, she has also had right-sided chest pain that is exacerbated by deep inspiration. Four months ago, she was diagnosed with a urinary tract infection and was treated with trimethoprim/sulfamethoxazole. She appears pale. Her temperature is 38.8°C (101.8°F), pulse is 92/min, respirations are 20/min, and blood pressure is 128/74 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 99%. Examination shows pale conjunctivae. Crackles are heard at the right lung base. Cardiac examination shows no abnormalities. Laboratory studies show:
Hemoglobin 12.6 g/dL
Leukocyte count 13,300/mm3
Platelet count 230,000/mm3
Serum
Na+ 137 mEq/L
Cl- 104 mEq/L
K+ 3.9 mEq/L
Urea nitrogen 16 mg/dL
Glucose 89 mg/dL
Creatinine 0.8 mg/dL
An x-ray of the chest shows an infiltrate at the right lung base.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [137.0, 'mEq/L'], 'Glucose': [89.0, 'mg/dL']}",136.736,129.8992,143.5728,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 137.0 mEq/L. 
The concentration of glucose is 89.0 mg/dL. 
Plugging in these values into the formula gives us 137.0 mEq/L + 0.024 * (89.0 - 100) = 136.736 mEq/L.
Hence, the patient's corrected concentration of sodium is 136.736 mEq/L."
5555,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4309303-1,Extracted,"A 26-year-old male expatriate was brought to the emergency of Sultan Qaboos University Hospital, Muscat, Oman, in severe respiratory distress. He was having vomiting, shortness of breath, productive cough, and mild fever for almost a week. There was no history of any previous illness.
On arrival he was in severe distress with a respiratory rate of 44/minute, heart rate of 103/minute, and blood pressure of 148/97 mmHg. Arterial blood gas analysis while on oxygen showed severe metabolic acidosis {pH—6.9, PCO2—12 mmHg, PO2—600 mmHg, and HCO3—4.4 mmol/L}. Creatinine and urea were very high and the hemoglobin was very low. The basic blood test results were as follows: fasting blood sugar—4.9 mmol/L; creatinine—1327 μmol/L; urea—46.8 mmol/L; bicarbonate—2 mmol/L; sodium—119 mmol/L; potassium—5.8 mmol/L; glomerular filtration rate—4 mL/min/1.73 m2; anion gap—22 mmol/L; calcium—2.18 mmol/L; phosphate—3.98 mmol/L; lactate—0.7 mmol/L; hemoglobin—5.4 g/dL; white cell count—52 × 109/L; lactate dehydrogenase—378 U/L; creatine kinase—2548 U/L; INR—1.29; activated partial thromboplastin time—69.2 seconds. Urine dipstick showed the presence of proteins, glucose, and red blood cells. Chest radiograph showed consolidation in the right mid zone and slight blunting of the right costophrenic angle ().
The grossly elevated creatinine and urea, low hemoglobin, severe metabolic acidosis, bilateral small kidneys in ultrasound scan of the abdomen, and a high white cell count suggested a primary renal involvement complicated by a pneumonic illness and possibly sepsis. He deteriorated rapidly and was electively intubated and mechanical ventilation was initiated. He received supportive care, fluids, measures to reduce potassium, and broad spectrum antibiotics. Since the acidosis and the renal function did not show any improvement, he was taken up for dialysis later on the same day. Bronchoscopy showed inflamed right bronchi and the subdivisions lined by a thick layer of yellow secretions (). The bronchial washings and brushings showed broad aseptate hyphae with right angled branching consistent with Mucor species ().
Amphotericin (liposomal amphotericin B, 7 mg/kg/day) was added along with the broad spectrum antibiotics which he was receiving since admission. He continued to have dialysis on a regular schedule. Though there was mild improvement in the clinical and metabolic parameters, he continued to be critically ill. He was extubated on the seventh day of admission and was shifted to the ward once the vitals and the level of consciousness were stable. Two days later during dialysis he suddenly developed hypotension. The patient was conscious and communicating and the blood pressure picked up with inotropes. However, he suddenly developed massive hemoptysis. Though he was reintubated and cardiopulmonary resuscitation was initiated he could not be resuscitated.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [119.0, 'mmol/L'], 'Glucose': [4.9, 'mmol/L']}",118.71867,112.78274,124.6546,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 119.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 119.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 119.0 mmol * 1 mEq/mmol = 119.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 119.0 mmol sodium/L converts to 119.0 mEq sodium/L. 
The concentration of glucose is 4.9 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 4.9 mmol. To convert 4.9 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 4.9 mmol glucose * 0.001 mol/mmol = 0.0049 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0049 mol glucose * 180.16 g/mol = 0.88278 g glucose. To convert 0.88278 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 0.88278 g glucose * 1000.0 mg/g = 882.78 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 882.78 mg glucose/10.0 dL = 88.278 mg glucose/dL. The concentration value of 4.9 mmol glucose/L converts to 88.278 mg glucose/dL. 
Plugging in these values into the formula gives us 119.0 mEq/L + 0.024 * (88.278 - 100) = 118.71867 mEq/L.
Hence, the patient's corrected concentration of sodium is 118.71867 mEq/L."
5556,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6601186-1,Extracted,"A 20-year-old male patient presented to internal medicine clinic with weakness and polyuria. His past medical history was unremarkable. On initial assessment, the patient had no chest pain or shortness of breath, and he was afebrile, with blood pressure of 107/69 mmHg, and heart rate of 62 b.p.m. Cardiac and pulmonary auscultation were normal and further physical examination showed no other abnormalities. The electrocardiogram (ECG) showed a normal sinus rhythm and a heart rate of 59 b.p.m. without ischaemic changes. Laboratory results revealed hyperglycaemia (glucose 1104 mg/dL, reference range: 74–106 mg/dL), hyponatraemia (Na 121 mmol/L, corrected Na 145 mmol/L, reference range: 135–145 mmol/L), hypertriglyceridaemia (triglyceride 1306 mg/dL, reference range: 0–150 mg/dL), haemoglobin A1c 17.7% (reference range: 4.5–6.0%), negative high-sensitive troponin (reference range <1.5 ng/L), N-terminal pro-brain natriuretic peptide 1220 pg/mL (reference range: 0–100 pg/mL), C-reactive protein 0.82 mg/dL (reference range: 0–0.5 mg/dL), and effective osmolality 361 mOsm/L. Arterial blood gas analysis revealed pH 7.44 (reference range: 7.35–7.45), pO2 78 mmHg (reference range: 80–100 mmHg), pCO2 37.4 mmHg (reference range: 35–45 mmHg), and bicarbonate 25.2 mmol/L (reference range: 22–26 mmol/L) (). The patient was admitted to intensive care unit (ICU) with HHS as a first presentation of unknown DM. After hospitalization, intravenous fluid and insulin infusion therapy were started. Baseline transthoracic echocardiography (TTE) revealed normal valvular functions and global left ventricular hypokinesis with an ejection fraction (EF) of 36% (left ventricular end-diastolic and end-systolic volumes were 109 and 70 mL, respectively and left ventricular end-diastolic and end-systolic diameters were 50 and 40 mm, respectively), which was determined by the Simpson’s method (, , Movie S1–S3). After TTE, metoprolol 25 mg/day, ramipril 2.5 mg/day, and fenofibrate 267 mg/day were also started. The patient’s clinical condition improved after blood glucose level normalization. During ICU follow-up, troponin levels were within normal reference range and ECG showed normal sinus rhythm without ischaemic changes. Transthoracic echocardiography revealed progressive improvement in the left ventricular systolic function with an EF of 54% at the 5-day follow-up and an EF of 69% (left ventricular end-diastolic and end-systolic volumes were 102 and 32 mL, respectively and left ventricular end-diastolic and end-systolic diameters were 49 and 31 mm, respectively) at the 15-day follow-up after blood glucose control (, , Movie S1–S3). The patient was discharged with intensive insulin, metoprolol 50 mg/day, ramipril 5 mg/day, and fenofibrate 267 mg/day therapy and a programme of intensive follow-up for blood glucose regulation.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [121.0, 'mmol/L'], 'Glucose': [1104.0, 'mg/dL']}",145.096,137.8412,152.3508,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 121.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 121.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 121.0 mmol * 1 mEq/mmol = 121.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 121.0 mmol sodium/L converts to 121.0 mEq sodium/L. 
The concentration of glucose is 1104.0 mg/dL. 
Plugging in these values into the formula gives us 121.0 mEq/L + 0.024 * (1104.0 - 100) = 145.096 mEq/L.
Hence, the patient's corrected concentration of sodium is 145.096 mEq/L."
5557,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2923793-1,Extracted,"A 20-yr-old female visited the emergency department because of a 1-day history of vomiting (10 times) and was experiencing epigastric pain with diarrhea on March 23, 2009. The upper gastric pain was continuous without radiation. The patient had been drinking almost daily alcoholic beverages soju (alcohol concentration in the range of 19-22%) for 5 days prior to admission. The patient had a smoking history of one pack-year. Two years previously, the patient experienced DKA accompanied by acute pancreatitis. At that time, the patient had been diagnosed with type 1 diabetes mellitus. Insulin treatment began at that time. However, 7 months prior to the current admission, the patient ceased taking insulin.
Upon admission, the patient was determined to be 161 cm in height, 55 kg in weight with a body mass index of 21.2. On admission, the patient was alert but appeared acutely ill. Initial vital signs were blood pressure 90/60 mmHg, pulse rate of 88 beats/min, respiratory rate of 20/min and body temperature of 36.5℃. Physical examination revealed a dehydrated tongue and skin turgor. There was no evidence of xanthoma, xanthelasma or eruptive xanthoma. No palpable lymph node enlargement was apparent on head and neck examination, and no abdominal tenderness on abdominal examination. Bowel sound was normoactive.
Initial laboratory findings were ABGA (pH 7.148, pCO2 12.9 mmHg, pO2 126 mmHg, HCO3- 8.4 mM/L, SaO2 98.0%), glucose level 281 mg/dL, hemoglobin A1c 13.8% , C-peptide (premeal) 0.441 ng/mL (normal reference: 1.1-4.4 ng/mL), total cholesterol 1,640 mg/dL, TG 15,240 mg/dL, measured low density lipoprotein cholesterol (LDL-C) 246 mg/dL (determined by homogeneous enzymatic colorimetry method assay), high density lipoprotein cholesterol (HDL-C) 69 mg/dL, serum ketone body 3.1 mM/L (normal reference 0-0.05 mM/L), total bilirubin 1.2 mg/dL, AST 19 IU/L, ALT 14 IU/L, total protein 8.4 g/dL, serum albumin 4.1 g/dL, alkaline phosphatase 147 IU/L, serum amylase 81 U/L, serum lipase 108 U/L, WBC 13,310/µL, hemoglobin 13.9 g/dL, hsCRP 5.616 mg/dL, BUN 14.0 mg/dL, creatinine 0.6 mg/dL, sodium 125 mEq/L, potassium 4.4 mEq/L and chloride 95 mEq/L. There were no abnormalities in the coagulation test. Serum sample was milky and turbid, which suggested a lipemic state (). Anti-glutamic acid decarboxylase (GAD) antibody was 0.12 U/mL (normal reference 0-0.9 U/mL), and anti-islet antibody-2 (IA-2) antibody was <0.4 U/mL (normal reference 0-0.4 U/mL). Apolipoprotein E genotyping assessed by polymerase chain reaction revealed ε2/ε3.
The patient was aggressively hydrated and treated with intravenous insulin in the intensive care unit. On admission, serum sodium was 125 mEq/L and serum osmolality was 317 mOsm/kg. We suspected pseudohyponatremia caused by hyperlipidemia and hyperglycemia, and tried normal saline infusion. In spite of significant improvement in glucose level for the first 12 hr, sodium level dropped to 115 mEq/L. After correcting the hyponatremia with 3% NaCl solution, continuous insulin infusion and hydration for next 12 hr, serum sodium level rose to 121 mEq/L.
On the second day of hospitalization, the patient complained of aggravated epigastric pain. Follow-up laboratory analyses revealed a serum amylase level of 443 U/L and a serum lipase level of 615 U/L. On abdominal computed tomography (CT) scan, the pancreas was diffusely swollen with peripancreatic fat infiltration and fluid collection, which suggested acute pancreatitis grade D, according to the Balthazar CT severity index (). The Ranson's score was 4 at this point. There was no lipidemia retinalis on an ophthalmologic exam.
On the third day of hospitalization, the TG was 506 mg/dL, total cholesterol 281 mg/dL, LDL-C 101 mg/dL and HDL-C 36 mg/dL. The epigastric pain had diminished. The patient commenced oral intake, multiple subcutaneous insulin injection and fibrate medication.
On the fourth day of hospitalization, the serum amylase level was 50 U/L and lipase level was 36 U/L. The patient was discharged without any complication on post-admission day 8. Fourteen days after discharge, analyses revealed total cholesterol 308 mg/dL, TG 309 mg/dL, LDL-C 184 mg/dL, HDL-C 66 mg/dL, serum amylase level 107 U/L and serum lipase level 48 U/L. Lipoprotein electrophoresis performed after recovery showed a normal pattern.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [125.0, 'mEq/L'], 'Glucose': [281.0, 'mg/dL']}",129.344,122.8768,135.8112,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 125.0 mEq/L. 
The concentration of glucose is 281.0 mg/dL. 
Plugging in these values into the formula gives us 125.0 mEq/L + 0.024 * (281.0 - 100) = 129.344 mEq/L.
Hence, the patient's corrected concentration of sodium is 129.344 mEq/L."
5558,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7294477-1,Extracted,"A 60-year-old man presented with fever and productive cough for 2 days. He had a history of type 2 diabetes for 12 years and received peritoneal dialysis for diabetic nephropathy for 5 years. He also received antihypertensive drugs for hypertension for 10 years. There was no personal or family history of coagulopathy or stroke, trauma, chest pain, or illicit intravenous drug use.
Admission physical examination revealed the patient to be febrile (39.1°C), tachycardic with a pulse of 112/min, a respiratory rate of 22/min, and hypertensive with a blood pressure of 170/80 mm Hg. Bibasilar crackles were heard on auscultation. The peritoneal dialysis catheter was correctly positioned in the right lower abdomen, with no local erythema. There was no exudate buildup in catheter dressings. His systemic examination was otherwise unremarkable, with no tenderness, ecchymosis, or other external signs of trauma.
Initial blood workup showed neutrophilic leukocytosis with a white blood cell count of 12.8 × 109/L (normal reference: 4.0–10 × 109/L) and 82.6% neutrophils (normal reference: 50%–70%). The patient was anemic (hemoglobin 95 g/L; normal reference: 120–160 g/L), with a normal platelet count (181 × 109/L; normal reference: 100–300 × 109/L). Both his prothrombin time (PT; 12.1 s, normal reference: 10–14 s) and activated partial thromboplastin time (aPTT; 34.1 s, normal reference: 20–40 s) were normal. Blood chemistry showed elevated blood urea nitrogen (20.5 mmol/L; normal reference: 3.2–7.1 mmol) and creatinine (1125 µmol/L; normal reference: 53–106 µmol/L). Blood glucose was 6.4 mmol/L (normal reference: 3.9–6.1 mmol/L), K+ 4.14 mmol/L (normal reference: 3.5–5.5 mmol/L), Na+ 145 mmol/L (normal reference: 135–145 mmol/L), Cl+ 108 mmol/L (normal reference: 95–105 mmol/L), and Ca++ 2.1 mmol/L (normal reference: 2.25–2.58 mmol/L). Liver function test was normal. Arterial blood gas analysis showed pH 7.40 (normal reference: 7.35–7.45), PaO2 60.1 mm Hg (normal reference: 95–100 mm Hg), PaCO2 44.8 mm Hg (normal reference: 35–45 mm Hg), and HCO3– 29.6 mmol/L (normal reference: 22–27 mmol/L). Chest X ray revealed patchy opacities in the right lower lung. The right diaphragmatic surface and costophrenic angle were also blurred. Furthermore, the cardiac silhouette was enlarged.
Treatment for pulmonary infection with cefoperazone-sulbactam (1.5 g every 12 h) was initiated. The patient also received subcutaneous insulin (30 units/day) and oral nifedipine sustained release tablet (30 mg daily). Peritoneal dialysis continued with 2.5% low calcium peritoneal dialysate.
At day 3 post admission, the patient became disoriented. He was still febrile (40.3°C). SPO2 declined to 88% despite of 5 L/min oxygen via a nasal cannula. Blood gas analysis showed pH 7.30, PaO2 53.10 mm Hg, PaCO2 58.50 mm Hg, and HCO3– 29.3 mol/L. Blood chemistry revealed that blood urea nitrogen (22.7 mmol/L) and serum creatinine (1345 µmol/L) continued to rise, and his plasma glucose also increased (8.4 mmol/L). K+, Na+, Cl+, and Ca++ were within normal range. His C-Reactive Protein (CRP) was 183 mg/L (normal reference: <8 mg/L), and procalcitonin 66.06 ng/mL (normal reference: <0.5 ng/mL). The liver function, platelet count, aPTT, and PT were normal. Thromboelastogram showed normal coagulation factor reaction time (9.9 min; normal reference: 5–10), fibrinogen reaction time (1.9 min; normal reference: 1–3), α (alpha) angle (64.9°; normal reference: 53°–72°), shear stress coefficient strength (19,233 d/s; normal reference: 4500–11,000 d/s), and hyperfibrinolysis (0.0%; normal reference: <8%) with increased platelet function (79.4 mm; normal reference: 50–70).
The patient was diagnosed with respiratory failure (type II) and pulmonoencephalopathy, and transferred to the intensive care unit (ICU) and placed on mechanical ventilation. Imipenem (0.5 g every 6 h) was added, and low-molecular-weight heparin (enoxaparin, 3500–5500 Da, 5–10 IU/kg/h) and insulin were delivered continuously by pumps. Peritoneal dialysis was discontinued and CVVH was undertaken at 32 mL/kg/h for renal insufficiency. The patient became oriented. Arterial blood gases showed normal pH (7.43), improved PaO2 (88.6 mm Hg), normal PaCO2 (36.5 mm Hg), and HCO3– (23.5 mmol/L). However, fever persisted (39.5°C), and the patient had difficulty weaning off mechanical ventilation.
Abdominal computed tomography (CT) at day 5 showed a hypointense shadow in the left hepatic lobe (61 mm × 56 mm) with an indistinct border (). Liver abscess was confirmed upon ultrasound-guided drainage. The culture revealed Klebsiella pneumonia that was sensitive to third-generation cephalosporin and imipenem. Imipenem (1.0 g every 8 h) and metronidazole (0.5 g every 8 h) were given, and mechanical ventilation and CVVH continued.
At day 12, the patient complained left back pain, which improved the next day without treatment. Platelet count (243 × 109/L) was normal, but both aPTT (67.5 s) and PT (17.3 s) were prolonged; his thromboelastogram (heparin cup) was normal. No cutaneous and mucosal bleeding was observed. The patient had no hemoptysis and his fecal occult blood test was negative. Abdominal CT scan at day 16 revealed left iliopsoas swelling, about 61.7 mm × 64.1 mm, with inhomogeneous densities, and occasional hyperintense opacities and an indistinct border (). A diagnosis of iliopsoas hematoma was made. Anticoagulation therapy with low-molecular-weight heparin was discontinued and switched to ex vivo anticoagulation with citrate. Mechanical ventilation and anti-infection therapy (imipenem 1.0 g every 8 h, metronidazole 0.5 g every 8 h) continued. No improvement was seen, and 3 days later, the patient died after his family decided to terminate therapy.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [145.0, 'mmol/L'], 'Glucose': [8.4, 'mmol/L']}",146.23202,138.92042,153.54362,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 145.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 145.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 145.0 mmol * 1 mEq/mmol = 145.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 145.0 mmol sodium/L converts to 145.0 mEq sodium/L. 
The concentration of glucose is 8.4 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 8.4 mmol. To convert 8.4 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 8.4 mmol glucose * 0.001 mol/mmol = 0.0084 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0084 mol glucose * 180.16 g/mol = 1.51334 g glucose. To convert 1.51334 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 1.51334 g glucose * 1000.0 mg/g = 1513.34 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1513.34 mg glucose/10.0 dL = 151.334 mg glucose/dL. The concentration value of 8.4 mmol glucose/L converts to 151.334 mg glucose/dL. 
Plugging in these values into the formula gives us 145.0 mEq/L + 0.024 * (151.334 - 100) = 146.23202 mEq/L.
Hence, the patient's corrected concentration of sodium is 146.23202 mEq/L."
5559,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2876866-1,Extracted,"A 23 year-old female patient, 160 cm tall and 48 kg, was diagnosed with acute appendicitis and admitted for a laparoscopic appendectomy. She had no abnormalities in her pediatric medical history, but from the age 18, she had slowly begun experiencing headaches in her left temporal lobe, nausea, and vomiting. In June of that year, she experienced generalized convulsions and aphasia. In a brain MRI and MRA, an infarction in the posterior divisions of the left mesencephalic arteries was found. Also, in a blood test, an increase in lactic acid was discovered (7.54 mM/L [normal level: 0.5-2.254 mM/L]). The patient was suspected to have MELAS syndrome. She was diagnosed with MELAS after testing (adenosine-to-guanine transition at t-RNA nucleotide 3243 in PCR sequencing). After she turned 21, she was diagnosed with Type I DM. The patient had to orally ingest 200 mg of carbamazepine and 100 mg of aspirin per day and subcutaneously inject 30 units of insulin in the morning and 20 units in the evening. She had no history of total anesthesia.
In a physical examination before the anesthesia, the patient was able to read but had auditory aphasia such that she could not understand spoken words. In the physical examination, there were no signs of hypotonia or amyotrophy of the limbs. The laboratory results showed hyponatremia (126 mEq/L), hyperglycemia (257 mg/dl), and light metabolic acidosis (pH 7.346, PaCO2 36.3 mmHg, HCO3 20.1 mM/L, BE -5.3 mM/L). There were no abnormal findings in the chest X-ray and electrocardiogram. One year prior to her admission to the hospital, she had an ECG that revealed a cardiac index of 67% and no abnormal findings. For sugar control, 4 units of shortacting insulin were injected, and 0.9% normal saline was administered to control hyponatremia. No other pre-operative measures were performed.
After the patient was taken to the operating room, we attached ECG standard leads II, noninvasive monitors for blood pressure, heart rate, arterial oxygen saturation, capnogram, and bispectral index (BIS), and a nerve stimulator to the patient using the Multi Channel Anesthesia Monitor S/5™ (Datex-Ohmeda, USA). Preliminary vital signs were as follows: blood pressure 115/65 mmHg, heart rate 100 beats/min, oxygen saturation rate 97%, and the ECG results appeared normal. The patient underwent 3 minutes of denitrogenation with 100% oxygen through a face mask. Afterwards, we administered lidocaine (40 mg) with the Master TCI (Fresenius Vial S.A., France); we then injected 2% propofol (Fresofol®, Fresenius Kabi, Austria) and remifentanil (Ultiva™, GlaxoSmithKline, UK) at target concentrations of 4 µg/ml (Marsh-model) and 5 ng/ml (Minto-model), respectively. After roughly 90 seconds had passed, we checked lid reflexes and found that the patient had lost consciousness. We administered atracurium (0.5 mg/kg), the BIS was 50, and we saw that there was no response to TOF stimulation with the nerve stimulator placed on the ulnar nerve. Endotracheal intubation was then performed without complications. We started mechanical respiration with air (1.5 L/min), oxygen (1.5 L/min), respiratory volume of 450 ml, and respiratory rate of 12 breaths per minute. To control ventilation, the capnogram was kept at 35-40 mmHg. We used spirometry to measure the respiratory volume and pulmonary compliance. We started invasive blood pressure monitoring through the radial artery and measured the esophageal temperature with a body temperature monitor. During the operation, we used a forced-air warming blanket (Bair Hugger™, Austine Medical, USA) to stabilize the patient's body temperature. For fluid maintenance, we administered 0.9% normal saline at 200 ml per hour. During the operation, the patient's vitals were kept stable with blood pressure at 120-140/60-80 mmHg, heart rate 80-100 beats/min, oxygen saturation 100%, body temperature 37.0-37.4℃, and BIS 40-60. Thirty minutes after inducing anesthesia, the arterial blood gas study showed pH 7.44, PaCO2 32 mmHg, PaO2 299 mmHg, HCO3 23.3 mM/L, BE -2.1 mM/L; her electrolytes were Na+ 125 mEq/L, K+ 3.8 mEq/L, Cl- 88 mEq/L; and her blood sugar was 176 mg/dl. Twenty minutes prior to the end of the operation, we administered ondansetron (4 mg) to prevent post-operative nausea and vomiting. After suturing the peritoneum, we stopped injecting remifentanil, kept the level of propofol in the target effect site at 2 µg/ml, and restored spontaneous breathing. After the operation was over, we stopped injecting propofol and stabilized spontaneous breathing at 300 ml per breath on the spirometer. On the nerve stimulator, the TOF rate was kept at 0.95. To reverse the muscle relaxant effects, we administered glycopyrrolate (0.4 mg) and pyridostigmine (15 mg). Afterwards, the patient responded to voice commands and opened her eyes. With stabilized spontaneous breathing, she was extubated. The operation lasted around 1 hour, and during the operation, 350 ml of 0.9% normal saline were used. We then moved the patient to the recovery room and kept her under observation with blood pressure, electrogram, and oxygen saturation monitors. In the recovery room, we gave her oxygen at 5 L/min through the facial mask. The arterial blood gas study showed pH 7.32, PaCO2 43 mmHg, PaO2 219 mmHg, HCO3 21.2 mM/L, and BE -3.6 mM/L; her electrolyte levels were Na+ 128 mEq/L, K+ 4.1 mEq/L, and Cl- 90 mEq/L; and her blood sugar level was 120 mg/dl. We then moved the patient to the ward where we performed a lactic acid test, which measured 3.6 mM/L. Three days after the operation, the patient showed no complications from the operation or anesthesia, so she was released from the hospital.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [126.0, 'mEq/L'], 'Glucose': [257.0, 'mg/dL']}",129.768,123.2796,136.2564,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 126.0 mEq/L. 
The concentration of glucose is 257.0 mg/dL. 
Plugging in these values into the formula gives us 126.0 mEq/L + 0.024 * (257.0 - 100) = 129.768 mEq/L.
Hence, the patient's corrected concentration of sodium is 129.768 mEq/L."
5560,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-4208257-1,Extracted,"A 16-year-old male was referred to our institute Asan Medical Center Children's Hospital for evaluation of rapid weight gain and stunted growth velocity over 4 years. On admission, the patient's systolic and diastolic blood pressure was 108 and 72 mmHg, respectively. Body weight and height were 61.1 kg (-0.18 SDS) and 138.5 cm (-5.44 SDS), respectively. The BMI was 31.1 kg/m2 (+2.16 SDS). He displayed a moon-shaped face, buffalo hump, truncal obesity, acanthosis nigricans, and abdominal striae. The volume of each testis was 1 mL, while the Tanner stage of pubic hair was 2.
The serum cholesterol level was 173 mg/dL, and serum sodium and potassium levels were 144 mmol/L and 4.5 mmol/L, respectively. The serum insulin and glucose levels were 24.7 µU/mL and 74 mg/dL, respectively. Hemoglobin A1c was 5.8%. The serum cortisol levels in the morning and evening were 23.1 µg/dL and 26.2 µg/dL, respectively, suggesting loss of circadian rhythm. The 24-hour urine free cortisol level was elevated to 160 µg/day (<50 µg/day). The serum cortisol level after overnight dexamethasone suppression was 16.1 µg/dL (<5 µg/dL). A low-dose dexamethasone-suppression test was performed according to the standard protocol (oral dexamethasone 20 µg/kg/day for 2 days). The plasma ACTH, serum cortisol and 24-hour urine free cortisol levels were 40.6 pg/mL (<20 pg/mL), 29.4 µg/day (<5 µg/dL), and 73.5 µg/day (<10 µg/day), respectively, indicating a definitive diagnosis of Cushing syndrome. Subsequently, a high-dose dexamethasone test with an oral dexamethasone dose of 80 µg/kg/day demonstrated suppressed plasma ACTH (16.6 pg/mL) and serum cortisol (2.0 µg/dL) levels, indicating that the Cushing disease had been caused by pituitary ACTH secretion.
The patient's bone age, as determined by the Greulich-Pyle method), was 11 years. A simple x-ray of the thoracolumbar spine showed osteopenia (), and bone mineral density (BMD) z-scores of the lumbar spine and femur neck were -6.127 and -4.518, respectively, as determined by dual-energy x-ray absorptiometry (Lunar Co., Madison, WI, USA). Sellar magnetic resonance imaging (MRI) did not show any evidence of pituitary tumor. As this result suggested a pituitary source of ACTH secretion, BIPSS was performed to determine the laterality of the ACTH secretion. The peak ACTH level measured from the right inferior petrosal sinus (IPS) after injection of corticotropin-releasing hormone (CRH) was remarkably higher than that measured from the left IPS, suggesting right lateralization of ACTH secretion ().
Subsequently, a right hemihypophysectomy was performed by the endonasal transsphenoidal approach. Examination of the biopsied tissue suggested pituitary microadenoma. However, the 24-hour urine free cortisol was persistently elevated to 85.8 µg/day. Repeated BIPSS, moreover, did not show lateralization of ACTH secretion. The peak ACTH levels, though, were markedly increased after CRH loading from both the left and the right petrosal sinus (). Fourteen days after the right hemihypophysectomy, a total hypophysectomy was performed by the transsphenoidal approach. The histological findings were suggestive of nonneoplastic pituitary tissue. Postoperatively, the 24-hour urine free cortisol was 22.5 µg/day, and the plasma ACTH and serum cortisol levels were 6.9 pg/mL and 1.2 µg/dL, respectively. Owing to symptoms of adrenal insufficiency, hydrocortisone were given at a stress dose of 100 mg/m2/day intravenously after surgery and subsequently tapered to the physiologic oral dose of 15 mg/m2/day.
An L-dopa test and combined anterior pituitary function test after 2 weeks of the total hypophysectomy revealed growth hormone (GH) deficiency, central hypothyroidism, hypogonadotropic hypogonadism, and ACTH deficiency (). Levothyroxine sodium was added at a dose of 100 µg/day.
Two days after total hypophysectomy, desmopressin was started because he showed polyuria, hypernatremia (serum Na, 157 mmol/L), and high serum osmolality (330 mosm/kg) without concentrated urine (urine osmolarity, 96 mosm/kg).
Within a month of the total hypophysectomy, recombinant human GH therapy was initiated at a dose of 0.02 mg/kg/day for 6 days a week subcutaneously. Two months after the total hypophysectomy, intravenous pamidronate was administered at a dose of 1 mg/kg/day over 4 hours for three days every 4 months for three years. Testosterone enanthate was initiated at a dose of 250 mg monthly at age 19 years.
The growth rate of the patient increased to 6 cm over the initial one-year follow-up. At age 21, recombinant human GH therapy was discontinued (). After another six months, the peak growth hormone level, as determined by insulin tolerance test, was 0.1 ng/mL, indicating adult GH deficiency. GH therapy subsequently was restarted at a dose of 0.4 mg/day. At his current age of 26, the patient's final height has attained the target range (172.2 cm, -0.20 SDS); weight (58.7 kg, -0.85 SDS). His BMD of femur neck and lumbar spine were 0.679 g/cm2 (z-score= -4.3 ) and 0.555 g/cm2 (z-score= -3.0), respectively.
At age 26 years, the patient's testis volume was 1 mL and sexual maturity rating of pubic hair is Tanner stage 4. He has been under treatment with testosterone enanthate, desmopressin acetate, prednisolone, levothyroxine sodium, and recombinant human GH for combined pituitary hormone deficiency and adult GH deficiency.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [157.0, 'mmol/L'], 'Glucose': [74.0, 'mg/dL']}",156.376,148.5572,164.1948,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 157.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 157.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 157.0 mmol * 1 mEq/mmol = 157.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 157.0 mmol sodium/L converts to 157.0 mEq sodium/L. 
The concentration of glucose is 74.0 mg/dL. 
Plugging in these values into the formula gives us 157.0 mEq/L + 0.024 * (74.0 - 100) = 156.376 mEq/L.
Hence, the patient's corrected concentration of sodium is 156.376 mEq/L."
5561,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3856144-1,Extracted,"An 18-year-old man was brought to the emergency department (ED) because of altered mental status. Family reported that he had nausea and vomiting before presenting to the ED. Past medical history was significant for diabetes, diabetic ketoacidosis (DKA), and hypothyroidism. Past surgical and social histories were unremarkable. Home medication was insulin glargine.
Physical exam revealed a lethargic patient. Vitals were blood pressure 130/70 mmHg, pulse 96/minute, respiration 28/minute, temperature was normal. Lung auscultation showed left basal crackles.
Chest radiograph (CXR) showed lower lobe infiltrates and pneumomediastinum (PM). Laboratory results: Arterial blood gas: PH 6.930 (7.350–7.450), PCO2 16 mmHg (35–45), PO2 138 mmHg (81–110), and serum bicarbonate 3 mmol/L (22–26); serum electrolytes: sodium 129 mmol/L (136–144), potassium 6.4 mmol/L (3.3–5.1), and chloride 100 mmol/L (101–111); glucose 1087 mg/dL (60–250), blood urea nitrogen 40 mg/dL (8–26), and creatine 2.68 mg/dL (0.70–1.20). Blood counts were normal.
The patient was intubated for airway protection because of altered mental status. A postintubation CXR showed PM, lower lobe infiltrates, and an air-filled distended stomach. An oral-gastric (OG) tube was placed easily, to decompress the air-filled distended stomach after bagging prior to intubation and in view of nausea and vomiting. A chest computed tomography scan showed multilobar infiltrates suggestive of aspiration pneumonia, PM, and the tip of the OG tube to be in the right hemithorax. The patient underwent a right thoracotomy with the intention to repair the esophageal rupture. Intraoperatively, the tip of the OG tube was found to be retracted into the esophageal lumen. Inspection of the esophagus did not reveal a clear rupture. An OG tube was placed intraoperatively, and a chest tube was placed into the right pleural space.
The patient was given intravenous (IV) fluid for hydration, IV insulin drip, IV metronidazole, and IV levofloxacin. Serial CXRs showed clearing of pneumonic infiltrates and PM. The chest tube was discontinued, and the patient was successfully extubated. After extubation, an esophagogram was performed and showed no extravasation of contrast.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [129.0, 'mmol/L'], 'Glucose': [1087.0, 'mg/dL']}",152.688,145.0536,160.3224,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 129.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 129.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 129.0 mmol * 1 mEq/mmol = 129.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 129.0 mmol sodium/L converts to 129.0 mEq sodium/L. 
The concentration of glucose is 1087.0 mg/dL. 
Plugging in these values into the formula gives us 129.0 mEq/L + 0.024 * (1087.0 - 100) = 152.688 mEq/L.
Hence, the patient's corrected concentration of sodium is 152.688 mEq/L."
5562,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-3461311-1,Extracted,"The patient, a 55-year-old woman, was admitted to our hospital on February 3rd, 2012. Her chief complaint was repeated consciousness obstacle over two years. She had been in good health with normal menstrual cycles until her third delivery in 1988. She started to get mild hypofunction of gonad, thyroid, and adrenal cortex after severe postpartum hemorrhage. Unfortunately, owing to the limited medical resources in her hometown, she was not diagnosed as Sheehan's syndrome and did not receive enough professional treatment. Her menstrual periods prolonged (about 40–50 days) with little volume and short duration. In 1990, she conceived naturally for the fourth time but the symptoms got worse after delivery, especially in recent years. From 2000, she had unconsciousness for three times. She gradually had serious hypoglycemia, progressive fatigue, loss of cutaneous pigment, dryness, and furfuration of the skin, loss of muscle strength, and a decrease in libido after the fourth delivery. Nevertheless, she had no symptoms of vomiting, nausea, abdominal pain, or orthostatic dizziness. The family history of similar symptoms and previous history of hypertension or diabetes were not found.
The general physical examination showed that the blood pressure, heart rate, and temperature were within normal limits. She was in a coma and appeared chronically ill and pale with dryness and furfuration of the skin. Her eyebrows (), glandebalaes and pubes fell off. There was no remarkable abnormality in lung, heart, and neurological examinations.
Routine laboratory findings demonstrated a red blood cell count of 3.32 × 1012/L, a hemoglobin of 101 g/L, a hematocrit of 30.3%, the random blood glucose 2.89 mmol/L, the serum sodium 121.0 mmol/L, the chloride 94.5 mmol/L, carbon dioxide combining power (CO2CP) 17.2 mmol/L, the uric acid 63 μmol/L, the aspartate transaminase (AST) 72 U/L, the total protein (TP) 51.3 g/L, the albumin (ALB) 28.6 g/L, the globulin (GLB) 22.7 g/L, the triglyceride (TG) 2.83 mmol/L, the total cholesterol 7.62 mmol/L, the low-density lipoprotein cholesterol (LDL-C) 6.43 mmol/L, and the high-density lipoprotein cholesterol (HDL-CH) 0.67 mmol/L. The urine routine and stool routine were normal.
As the clinical manifestations suggested Sheehan's syndrome, related endocrinological tests were finished as follows. The thyroid function test revealed a serum triiodothyronine (T3) of 0.31 ng/mL (normal 0.6 to 1.81), a thyroxine (T4) of 0 μg/dL (normal 4.5 to 12.5), a free triiodothyronine (FT3) of 0.88 pg/mL (normal 1.8 to 4.2), a free thyroxine (FT4) of 0.16 ng/mL (normal 0.8 to 1.76), a thyroid-stimulating hormone (TSH) level of 1.547 μIU/mL (normal 0.35 to 5.5), and a thyroglobulin autoantibody of 83.6 U/mL (normal 0 to 60). The plasma adrenocorticotropic hormone (ACTH) level was 4.8 pg/mL (normal 0 to 46). The plasma crotisol level was 0.75 μg/dL (normal 3.9 to 22.4). The growth hormone (GH) level was 0.049 ng/mL (normal 0 to 10). The follicle-stimulating hormone (FSH) was 4.30 mIU/mL, the luteinizing hormone (LH) was 1.78 mIU/mL and the estradiol (E2) was 10.52 pg/mL.
The brain magnetic resonance imaging (MRI) showed a diminutive pituitary and an empty sella turcica (). There was no evidence of hemorrhage, intracranial mass, or aneurysm ().
She was diagnosed as Sheehan's syndrome and pituitary crisis. Replacement therapy was instituted with hydrocortisone and levothyroxine sodium.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [121.0, 'mmol/L'], 'Glucose': [2.89, 'mmol/L']}",119.84958,113.8571,125.84206,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 121.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 121.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 121.0 mmol * 1 mEq/mmol = 121.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 121.0 mmol sodium/L converts to 121.0 mEq sodium/L. 
The concentration of glucose is 2.89 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 2.89 mmol. To convert 2.89 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 2.89 mmol glucose * 0.001 mol/mmol = 0.00289 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.00289 mol glucose * 180.16 g/mol = 0.52066 g glucose. To convert 0.52066 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 0.52066 g glucose * 1000.0 mg/g = 520.66 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 520.66 mg glucose/10.0 dL = 52.066 mg glucose/dL. The concentration value of 2.89 mmol glucose/L converts to 52.066 mg glucose/dL. 
Plugging in these values into the formula gives us 121.0 mEq/L + 0.024 * (52.066 - 100) = 119.84958 mEq/L.
Hence, the patient's corrected concentration of sodium is 119.84958 mEq/L."
5563,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-6476073-1,Extracted,"69-year-old female with no significant past medical history with the exception of anxiety presented as a transfer from an outside hospital with acute onset of hypersomnolence and aphasia. She was last seen normal the night before by her family. Her vitals on arrival were within normal limits; blood pressure was 134/64 mmHg, heart rate was 88 per minute, respiratory rate was of 22 breaths per minutes, and she was afebrile. On exam she appeared drowsy, nonverbal, and intermittently following one-step commands. Her cranial nerves were intact and on motor exam she had mild generalized weakness but was able to move all extremities against gravity. Sensory exam was confounded by her decreased mental status. Bilateral plantar reflexes were equivocal. National Institute of Health Stroke Scale (NIHSS) was 10. She was out of the 4.5-hour time window to consider IV thrombolysis therapy and on exam her presenting symptoms did not localize to one cerebral vascular territory.
Initial diagnostic work-up: serum white blood cell count 11000/uL, hemoglobin 14.2g/dL, platelets 190000/uL, sodium 143mmol/L, potassium 5.7mmol/ (repeat 4.4mmol/L), blood urea nitrogen 34mg/dL, creatinine 1.05mg/dL, glucose 323mg/dL, troponins <7ng/L, aspartate aminotransferase 46 U/L, and alanine aminotransferase 45 U/L. Urinary analysis was positive for moderate leukocytes and negative nitrites, and her toxicology screen was negative.
Noncontrasted CT brain demonstrated bilateral thalamic hypodensities. A CT angiogram (CTA) demonstrated focal areas of basilar artery narrowing, an Artery of Percheron (AOP) arising from the right PCA (Figures , , and ) and no large vessel occlusions. MRI brain demonstrated bilateral paramedian thalamic infarcts (Figures and ) extending into the midbrain on diffusion weighted imaging (DWI). Her ejection fraction was 65% with no atrial septum shunt on transthoracic echocardiogram.
Her serum low density lipoprotein was 130mg/dL and her glycosylated hemoglobin was 13.8%. She was diagnosed with diabetes mellitus type 2. Her stroke etiology was thought to be secondary to small vessel disease given the arterial bed involved and her uncovered lipohyalinosis risk factors. Patient was discharged on atorvastatin 40 mg, aspirin 81 mg, and an insulin regimen. On discharge to rehab her NIHSS improved to four.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [143.0, 'mmol/L'], 'Glucose': [323.0, 'mg/dL']}",148.352,140.9344,155.7696,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 143.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 143.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 143.0 mmol * 1 mEq/mmol = 143.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mmol sodium/L converts to 143.0 mEq sodium/L. 
The concentration of glucose is 323.0 mg/dL. 
Plugging in these values into the formula gives us 143.0 mEq/L + 0.024 * (323.0 - 100) = 148.352 mEq/L.
Hence, the patient's corrected concentration of sodium is 148.352 mEq/L."
5564,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2559825-1,Extracted,"A 2 year and 11-month-old mestizo boy was admitted to the Hospital Infantil del Estado de Sonora (Children Hospital of Sonora State, Mexico) with muscle cramps, fine tremors on hands and feet for the last 2 days. His mother reported chronic diarrhea for the last year with 6 hospitalizations because of diarrhea and dehydration. During physical examination, upper abdominal distention was observed (Figure ), in addition to hypotrophic arms and legs and positive Chvostek's and Trousseau's signs. His weight and height were less than the fifth percentile for his age.
Blood count showed hemoglobin 101 g/L, white blood cells 8500/mmc, platelets 472,000/mmc, GVS 26 mm/h and reticulocytes 3%. Microcytic and hypochromic anemia was evident, with hematocrit 30%, mean globular volume 73 fL, serum iron 41 μg/dL and ferritin under 5 μg/L. Serum laboratory tests revealed hypocalcemia with total calcium of 5.7 mg/dL, sodium 133 mEq/L, potassium 3.2 mEq/L, chloride 103 mEq/L, glucose 82 mg/dL, AST 71 U/L, ALT 44 U/L, albumin 2.5 g/L, and C-reactive protein 0.5 mg/L. Billirubins, urine examination, and serial stool analyses for infectious etiologies, were negative.
The patient's tetany resolved after replacement of calcium and additional analyses were performed. IgA and IgG anti-gliadin antibodies as well as IgA anti-transglutaminase were positive, with index values of 3.5, 35.7 and 26.8, respectively. Index value was defined as the ratio of the absorbance of the test serum divided by the cut-off value []. Additionally, there was IgA reactivity to maize prolamins (zeins). The diagnosis of CD was confirmed by inflammatory cells infiltrate in the small intestinal mucosa and lymphocytes in the surface epithelium on duodenal biopsy, in a Marsh IIa/IIb classification (Figure ). After initiation of a gluten-free diet and lactose-free milk (at the beginning), mineral and vitamins supplements, the patient's symptoms completely resolved within 6 weeks. The clinical and nutritional response to the gluten-free diet was excellent. In a 2-month follow-up period, he presented normal blood counts and serum biochemical analyses. Additionally, his weight and height were in the 75 percentile for his age, antibodies titers were normal and there were no further episodes of tetany or diarrhea over 4 years follow up period.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Sodium': [133.0, 'mEq/L'], 'Glucose': [82.0, 'mg/dL']}",132.568,125.9396,139.1964,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 133.0 mEq/L. 
The concentration of glucose is 82.0 mg/dL. 
Plugging in these values into the formula gives us 133.0 mEq/L + 0.024 * (82.0 - 100) = 132.568 mEq/L.
Hence, the patient's corrected concentration of sodium is 132.568 mEq/L."
5565,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-7519975-1,Extracted,"A 33-year-old Hispanic, blind, and aphasic female with a history of diabetes mellitus on insulin at home, craniotomy for meningioma status post ventriculoperitoneal (VP) shunt placement, presented to the hospital with a one-day history of drowsiness and emesis. Computed tomography (CT) of the abdomen revealed several loops of small bowel in the right side of the abdomen with thickening immediately adjacent to the VP shunt concerning for inflammation of the bowel (). CT head revealed areas of acute infarct seen involving the brain stem as well as the cerebellar hemispheres and moderate enlargement of the ventricular system with left-sided intraventricular hemorrhage (Figures and ). Due to the acute nature of her abdomen and the concern for a seeded VP shunt from this intra-abdominal infection, neurosurgery was consulted. The patient subsequently underwent externalization of her VP shunt at the neck. Concurrently, general surgery was consulted who decided to perform an explorative laparotomy for her acute abdomen. Preoperative records showed that her mean arterial blood pressure was ranging from 60 to 65 mmHg, heart rate was ranging from 70 to 82 normal sinus rhythm, the temperature was 98.4 F, and oxygen saturation was 96-98 on room air. Her preoperative electrocardiogram (ECG) showed normal sinus rhythm with no acute ST-T wave changes (). Her preoperative laboratory values were as follows: white blood cell count 5300 per microliter of blood, hemoglobin 8.2 grams/deciliter, platelet 98000 per microliter of blood, prothrombin time 16.1 seconds, international normalized ratio 1.2, serum sodium 148 meq/liter, serum potassium 3.7 meq/liter, chloride 112 meq/liter, BUN 17 mg/deciliter, creatinine 0.4 mg/deciliter, serum glucose 125 mg/deciliter, serum calcium 8.2 mg/deciliter, magnesium 2.4 gm/deciliter, aspartate transaminase 32 units per liter, and alanine transaminase 43 units per liter. The patient was deemed to be at high risk for the major cardiac event after the surgery defined as death, myocardial infarction, or cardiac arrest within 30 days after noncardiac surgery. The Revised Cardiac Risk Index (RCRI) for preoperative risk was 3 points (class IV risk) based on the proposed intraperitoneal surgery, cerebrovascular disease, and preoperative treatment with insulin. Due to the emergent nature of the required surgery, an extensive discussion was done with the patient's next of kin who agreed to proceed with the surgery. The patient was well monitored intraoperatively in the standard manner under the direct supervision of the attending anesthesiologist. Intraoperatively, the patient suddenly started becoming bradycardic and went into asystole. Immediate cardiopulmonary resuscitative (CPR) efforts were initiated as per the standard advanced cardiovascular life support (ACLS) algorithm. High-quality chest compressions and epinephrine injection were administered every 3 minutes. Appropriate rhythm checks in between the chest compression were done. The patient already had an advanced airway in place for surgery. There were appropriate peripheral intravenous lines, triple lumen central venous catheter, and arterial line that was placed preoperatively for access and hemodynamic monitoring. The patient did not have a shockable rhythm throughout the cardiac arrest. After 30 minutes of CPR, the patient did not have any signs of the return of spontaneous circulation (ROSC). Thus, the patient was pronounced dead and all resuscitation efforts were ceased. The abdominal cavity was closed. The patient was disconnected from the ventilator with a plan to move to the mortuary. After 20 minutes of declaring the patient dead, spontaneous circulation and breathing were noted by the operating room (OR) staff. The patient's mean arterial blood pressure was noted to be 60 mmHg without any vasopressor agents and heart rate was 62 bpm, sinus rhythm with spontaneous respiration at a rate of 12 breaths per minute. She had an oxygen saturation of 88-90% on room air with a temperature of 98.2 Fahrenheit. Surgery was immediately resumed, and the patient underwent reexploration. The patient was found to have infarcted distal ileum and right colon secondary to scarred adhesion and inflammatory response involving VP shunt.
Surgery was concluded, and the patient was transferred to the intensive care unit. Postoperatively, the patient was on 3 vasopressors. By postoperative day 2, the patient was off the vasopressor, and by postoperative day 3, the patient was extubated. On postoperative day 4, the patient was transferred to a regular room on the 2 L nasal cannula. Considering the patient's poor prognosis, the patient was provided comfort care and died on postoperative day 7.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [125.0, 'mg/dL'], 'Sodium': [148.0, 'mEq/L']}",148.6,141.17,156.03,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 148.0 mEq/L. 
The concentration of glucose is 125.0 mg/dL. 
Plugging in these values into the formula gives us 148.0 mEq/L + 0.024 * (125.0 - 100) = 148.6 mEq/L.
Hence, the patient's corrected concentration of sodium is 148.6 mEq/L."
5566,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-2693864-1,Extracted,"A 50-yr-old man with a history of alcohol abuse presented with increasing fatigue, generalized weakness, decreased appetite, and abdominal distension and discomfort for the past 2 weeks. He was admitted to the Department of Internal Medicine under the impression of acute pancreatitis, and he was referred to the Department of Dermatology for the multiple painful subcutaneous nodules on his legs, which had suddenly developed 3 weeks before ().
On admission, his hemoglobin value was 11.4 g/dL (reference range: 13-18 g/dL), the total count of white blood cells was 31,300/µL (reference range: 4,000-10,000/µL) with 90.7% segment neutrophils, but the coagulation profiles and platelet counts were normal. The serum amylase was 1,909 U/L (reference range: 20-120 U/L), and the lipase was 2,306 U/L (reference range: 5-51 U/L). Liver function testing revealed an aspartate aminotrans terase level of 104 U/L (reference range: 13-40 U/L), an alanine aminotransferase level of 24 U/L (reference range: 7-40 U/L), and a lactate dehydrogenase level of 665 U/L (reference range: 200-400 U/L). The fasting glucose level was 133.9 mg/dL (reference range of 70-110 mg/dL) and the electrolytes were unbalanced. The calcium level was 7 mg/dL (reference range: 8.6-10 mg/dL), and the sodium level was 125 mEq/L (reference range: 136-145 mEq/L). The blood urea nitrogen and creatinine were 40.1 mg/dL and 2.1 mg/dL, respectively. After 48 hr, the blood urea nitrogen was increased to 62.7 mg/dL after intravenous fluid administration. As his leukocytosis, elevated serum LDH at admission, and hypocalcemia, hypoalbuminemia, increase in blood urea nitrogen during initial 48 hr were poor prognostic factors in Ranson criteria, increased risk of complications was predicted. The chest radiograpy showed mild pleural effusion. On the abdominal computed tomography scan and magnetic resonance (MR) imaging taken on the second day of admission, a swollen pancreas with an dilated pancreatic duct, a loculated fluid collection in the left anterior perirenal space, multiple hepatic cysts, and massive ascites were noted (). On abdominal paracentesis, the amylase level was 14,696 U/L, the serum-ascites albumin gradient was calculated to be 1.07, and there was no evidence of malignancy.
A skin biopsy performed on the 4th day of admission from the nodule on the left lower leg showed a diffuse subcutaneous fat necrosis and ghost-like cells with thick shadowy walls and no nuclei. There was a fine granular basophilic material deposited within and around the necrotic fat cells (). These findings were consistent with pancreatic panniculitis. After 10 days of intensive medical care for the pancreatic disease, the patient's condition began to worsen; he and his family began to refuse any further treatment. Despite a strong warning by physicians, he insisted on the discharge and died at home 1 week later.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [133.9, 'mg/dL'], 'Sodium': [125.0, 'mEq/L']}",125.8136,119.52292,132.10428,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 125.0 mEq/L. 
The concentration of glucose is 133.9 mg/dL. 
Plugging in these values into the formula gives us 125.0 mEq/L + 0.024 * (133.9 - 100) = 125.8136 mEq/L.
Hence, the patient's corrected concentration of sodium is 125.8136 mEq/L."
5567,26,Sodium Correction for Hyperglycemia,lab test,decimal,pmc-8407674-2,Extracted,"An 18-year-old female, newly diagnosed Diabetic (unknown type) 2 months back, presented with a day’s history of altered sensorium and fast breathing. This was preceded by generalized malaise, joint pains, and heartburn for 4 days, and progressive weight loss. She was partially treated for 2 days from a clinic with subcutaneous Actrapid 15 IU stat; then, Metformin 500 mg once daily, received Normal Saline 500 mL twice daily, Folate, Ceftriaxone, Metronidazole, Omeprazole, TRAP. A month before the presentation, the patient had stopped taking her medication and was reportedly drinking plenty of drinks that contained processed sugar.
At admission, she was restless and disoriented with a Glasgow Coma Scale (GCS) of 11/15 (E4V2M5). She was afebrile at 36.4°C, had severe dehydration, Kussmaul breathing, mild distress, tachypnea at 30 breaths per minute, and pulse oximetry at 98% on ambient air. She had tachycardia at 112 beats per minute with a blood pressure of 146/75 mmHg.
On investigation, her random blood sugar was 21.2 mmol/L, serum ketones were 3.4 mmol/L, the admission serum: Sodium (Na+) 121 mmol/L, potassium (K+) 4.6 mmol/L, HBA1C 12.1%, CRP 1.69 mg/L, marked Leukocytosis of 16,480 cells/microliter, predominant neutrophilia of 12,840 cells/microliter, Thrombocytosis 419,000 cells/microliter. A respiratory exam revealed coarse crepitations in the right axillary region. The patient received initial fluid resuscitation, and, later admitted to the Highly Dependent Unit (HDU) on the medical ward requiring additional administration of 0.9% normal saline, ceftriaxone, initiation of intravenous rapid-acting insulin infusion, and intravenous KCl at 40 mmol twice a day. With a corrected Na+ level of 128 mmol/L hypertonic saline 150 mmol in 500 mL of Normal saline was initiated to run slowly over 24 hours.
On day 2 of admission, she had Na+ 153 mmol/, K+ 3.7 mmol/L, and serum ketones 2.8 mmol/L. She was switched to half strength Darrow’s and hypertonic saline stopped due to hypernatremia. Given the improving levels of consciousness and gradual reduction in RBS and Serum Ketones, she started on subcutaneous rapid-acting insulin. However, on day 4, Na+ continued to rise to 176 mmol/L and by day 5, Na+ was 162 mmol/L.
The patient was discharged on day 8 on mixtard 15 IU pre-breakfast, 10 IU pre-supper, and soluble insulin Actrapid at 6 IU pre-lunch in a stable condition.","What is the patient's corrected sodium concentration for hyperglycemia in terms of mEq/L? Use the sodium correction equation based on the one derived in Hillier, 1999. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.","{'Glucose': [21.2, 'mmol/L'], 'Sodium': [121.0, 'mmol/L']}",127.76654,121.37821,134.15487,"The formula for Sodium Correction for Hyperglycemia based on Hiller, 1999 is Measured sodium + 0.024 * (Serum glucose - 100), where Measured Sodium is the sodium concentration in mEq/L and the Serum glucose is the concentration of glucose in mg/dL.
The concentration of sodium is 121.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 121.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 121.0 mmol * 1 mEq/mmol = 121.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 121.0 mmol sodium/L converts to 121.0 mEq sodium/L. 
The concentration of glucose is 21.2 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 21.2 mmol. To convert 21.2 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 21.2 mmol glucose * 0.001 mol/mmol = 0.0212 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0212 mol glucose * 180.16 g/mol = 3.81939 g glucose. To convert 3.81939 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 3.81939 g glucose * 1000.0 mg/g = 3819.39 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 3819.39 mg glucose/10.0 dL = 381.939 mg glucose/dL. The concentration value of 21.2 mmol glucose/L converts to 381.939 mg glucose/dL. 
Plugging in these values into the formula gives us 121.0 mEq/L + 0.024 * (381.939 - 100) = 127.76654 mEq/L.
Hence, the patient's corrected concentration of sodium is 127.76654 mEq/L."
5568,30,Serum Osmolality,lab test,decimal,usmle-4284,Extracted,"A 22-year-old woman with a history of type I diabetes mellitus presents to the emergency department with nausea, vomiting, and drowsiness for the past day. Her temperature is 98.3°F (36.8°C), blood pressure is 114/74 mmHg, pulse is 120/min, respirations are 27/min, and oxygen saturation is 100% on room air. Physical exam is notable for a confused and lethargic young woman. Initial laboratory values are notable for the findings below.

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 2.9 mEq/L
HCO3-: 9 mEq/L
BUN: 20 mg/dL
Glucose: 599 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.2 mg/dL
AST: 12 U/L
ALT: 10 U/L

An initial ECG is notable for sinus tachycardia.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [599.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",318.42063,302.4996,334.34166,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 599.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (20.0 / 2.8) + (20.0 / 18) = 318.42063 mmol/L.The patient's calculated serum osmolality concentration is 318.42063 mmol/L. This is equalivalent to 318.42063 mOsm/kg."
5569,30,Serum Osmolality,lab test,decimal,pmc-3519780-1,Extracted,"A 43 year-old male was referred to the Emergency Department (ED) of our hospital after his workplace colleagues noted increasingly strange behavior for three days. The patient arrived complaining of generalized fatigue, lethargy, fevers, severe band-like headache, slurred speech, and increasing confusion. Though it was felt that the patient’s history was not completely reliable secondary to confusion, he was able to deny throat pain, chest pain, diarrhea, abdominal pain, recent sick contacts, or recent travel. Review of systems was limited secondary to altered mental status, but he did admit to mild dry cough.
Though initially denying immune compromise in the ED, the patient later disclosed he was HIV+. He could not recall his CD4 count but stated that his last viral load was undetectable. Past medical history was significant for hypertension and hypercholesterolemia. Outpatient medications included Atripla, spironolactone, and gemfibrozil. He had a history of unprotected anal sex with men but denied new partners. He had no recent contact with animals. He smoked a pack of cigarettes per day but did not drink or use drugs.
In the ED, the patient’s temperature was 103.9°F (39.9°C). Heart rate was 121 beats per minute, and respiratory rate was 30 breaths per minute. Oxygen saturation was 94% on room air. Blood pressure was 142/90. The patient appeared unwell. He was somnolent but easily aroused. Pertinent findings on general physical exam included a supple neck and decreased breath sounds diffusely. On neurologic exam, he was noted to be dysarthric. He had general slowness of thought and processing. He was slightly confused, though he was oriented and able to name the days of the week forwards and backwards if given sufficient time.
Initial laboratory evaluation was notable for a white blood cell (WBC) count of 10.1 × 103 cells/mm3, [lab reference range 4.0–10.8], hemoglobin of 15.7 g/dL [lab range 14.0–18.0], platelet count of 135 × 103/mm3 [lab range 150–350]. Automated differential showed 87.5% segmented cells (lab range 30-85%), 9.3% lymphocytes (lab range 15-55%), 2.4% monocytes (lab range 0-10%), 0.8% eosinophils (lab range 0-5%), and 0% basophils. No manual differential was performed. A basic metabolic panel showed serum sodium of 134 mmol/L [lab range 137–145], serum potassium of 4.2 mmol/L (lab range 3.5-5.1), serum chloride of 100 mmol/L (lab range 98–107), and CO2 of 19 mmol/L [lab range 22.0–30.0]. Blood urea nitrogen, serum creatinine, and serum glucose were elevated at 33 mg/dL [lab range 9–20], 1.8 mg/dL [lab range 0.7–1.3] and 159 mg/dL [lab range 70–99], respectively. C-reactive protein (CRP) was high at 581 mg/dL [lab range 0–10]. Liver function studies showed an albumin level of 4.4 g/dL (lab range 3.5-5.0), total protein of 7.6 g/dL (lab range 6.3-8.2), total bilirubin of 0.7 mg/dL (lab range 0.2-1.3), direct bilirubin of 0.5 mg/dL (lab range 0–0.3), alkaline phosphatase of 62 U/L (lab range 38–126), alanine aminotransferase (ALT) of 49 U/L (lab range 13–69), and aspartate aminotransferase (AST) of 89 U/L (lab range 15–46). Urinalysis showed 2+ albumin, 3+ blood, trace WBC esterase, negative nitrite, 5–10 WBC, 0–5 red blood cells (RBC), 5–10 epithelial cells, 5–10 hyaline casts, 3+ amorphous cells, and 1+ mucous. A non-contrast computed tomography (CT) scan of the head did not reveal any abnormalities. Nasopharyngeal influenza assay was negative.
Due to the combination of altered mental status, headache, and fever, a lumbar puncture was performed. The results demonstrated an elevated cerebrospinal fluid (CSF) glucose of 97 mg/dL [normal 40–70], CSF protein of 37 mg/dL [normal 12–60], and normal cell count and gram stain. Blood cultures were sent.
A chest x-ray was done and was read as a left hilar mass extending down towards the left lower lobe (see Figure 
). A chest CT was obtained to better characterize the hilar mass (see Figure 
). This chest CT demonstrated a left lower lobe consolidation with air bronchograms suggesting a diagnosis of pneumonia. Based upon the aforementioned findings, the patient was started on azithromycin and ceftriaxone for community-acquired pneumonia, as well as empiric acyclovir for herpes encephalitis.
Given the findings of dysarthria and altered mental status in an HIV + individual with unknown CD4+ count, a brain MRI was obtained. No contrast was administered secondary to acute renal injury. The diffusion-weighted coronal cut can be seen in Figure 
, demonstrating abnormal restricted diffusion and swelling of the splenium of the corpus callosum without other significant abnormalities. Abnormal T2-weighted signal in the SCC can be seen in Figure 
. These MRI findings in an HIV + individual raised concern for CNS opportunistic infection. However, since the patient was hemodynamically stable, was on antiretroviral therapy, and had a negative lumbar puncture, it was decided to treat the pneumonia initially and closely monitor the patient’s mental status.
Over the first two to three days of hospitalization, the patient continued to have high fevers, confusion, and dysarthria. His laboratory markers improved on antibiotics. His serum CRP trended down from 581 mg/L at admission to 200 mg/L on day three. After day three the patient began to demonstrate significant clinical improvement. The patient’s admission CD4+ count returned on day three at 156 cells/mm3, and an HIV viral load came back on day four at <20 copies/mL. On day four, urine antigens for Streptococcus pneumoniae and Legionella pneumophila serogroup 1 were sent. By day five the patient’s neurologic symptoms had resolved, as had his acute renal insufficiency. This same day his Legionella pneumophila urinary antigen returned positive.
On hospital day six a repeat MRI was obtained to monitor radiologic progression of the SCC lesion. This repeat study showed partial interval clearing of the previously noted abnormalities: restricted diffusion, abnormal increased flair, and abnormal T2 signally in the SCC. On hospital day seven the patient was discharged home on oral azithromycin. He had no residual deficits. Initial CSF viral studies including herpes simplex virus 1 and 2, varicella, cytomegalovirus, enterovirus, and JC virus all returned negative, as did the syphilis, hepatitis B, and hepatitis C serologies. Sputum for acid fast bacilli and routine culture were negative. Legionella antibody IgG titers sent on day four later came back at 1:64.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [33.0, 'mg/dL'], 'Glucose': [159.0, 'mg/dL'], 'Sodium': [134.0, 'mmol/L']}",288.61905,274.1881,303.05,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mmol/L. 
The concentration of bun is 33.0 mg/dL. 
The concentration of glucose is 159.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (33.0 / 2.8) + (33.0 / 18) = 288.61905 mmol/L.The patient's calculated serum osmolality concentration is 288.61905 mmol/L. This is equalivalent to 288.61905 mOsm/kg."
5570,30,Serum Osmolality,lab test,decimal,pmc-7780870-1,Extracted,"Case 1: A 52-year-old male was admitted for community-acquired pneumonia with fever, cough and dyspnea to Shahid Yahyanejad Hospital, Babol, Iran. He had neither a recent travel history of China nor close contact with a COVID-19 patient. He was an otherwise healthy and non-smoker individual with no drug history.
Clinical examination revealed vital signs including temperature of 38 °C, a pulse rate of 110 beats per minute, a blood pressure of 130/80 mm Hg, a respiratory rate of 20 breaths per minute, and Oxygen saturation (SpO2) of 89% while breathing ambient air. Lung CT scan revealed bilateral multilobar peripheral ground-glass opacities (GGOs) along with interlobular septal thickening indicative of COVID-19 (). In the other words, axial non-contrast CT image showed widespread bilateral GGOs and some areas of consolidative pulmonary opacities with thickened interlobular and interlobular lines called crazy paving pattern. Also in this patient, RT-PCR assay of nasal and pharyngeal samples were positive for COVID-19. According to his laboratory data and imaging findings, he received inpatient medical and supportive treatment including supplemental oxygen for COVID-19 and his status improved thus his SpO2 reached 99% in room air, but soon after with the patient's personal consent; he was discharged.
A few hours later, the patient returned to the emergency department with worsening dyspnea and two episodes of generalized tonic–clonic seizures. His vital signs at admission included a temperature of 38.5 °C, pulse rate of 120 beats per minute, blood pressure of 140/80 mm Hg, respiratory rate of 22 breaths per minute, and SpO2 of 98% while breathing ambient air. On neurological examination, the patient was conscious and oriented.
The cranial nerves examination was normal and his pupils were midsize and reactive to light and accommodation. His serum glucose level at the time of unconsciousness was 110 mg/dL. Other laboratory data were as follows: white blood cell (WBC), 13.00×109/L with 10% lymphocytes; hemoglobin (Hb), 12.2 g/dL; platelet, 268,000/µL; C-reactive protein (CRP), 63 mg/L; interleukin-6 (IL-6), 2 pg/mL; pro-B-type natriuretic peptide (proBNP) <20 pg/mL; procalcitonin (PCT), 0.05 ng/mL; blood urea nitrogen (BUN), 11 mg/dL; creatinine (Serum), 0.6 mg/dL; sodium, 139 mEq/L; potassium, 3.8 mEq/L; magnesium, 2.2 mg/dL; phosphors, 4 mg/dL; calcium, 7.5 mg/dL; alkaline phosphatase (ALP), 170 U/L; aspartate aminotransferase (AST), 56 U/L; alanine aminotransferase (ALT), 87 U/L, and negative troponin. A brain CT scan was normal. Patients received anticonvulsant medications. A single 500 mg oral dose of chloroquine phosphate, Kaletra (lopinavir/ ritonavir) two 200 mg tablets twice daily, and azithromycin 500 mg PO daily were administered. With his condition improved and his inflammatory markers decreased, the patient was discharged.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [11.0, 'mg/dL'], 'Glucose': [110.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",288.03968,273.6377,302.44166,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 11.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (11.0 / 2.8) + (11.0 / 18) = 288.03968 mmol/L.The patient's calculated serum osmolality concentration is 288.03968 mmol/L. This is equalivalent to 288.03968 mOsm/kg."
5571,30,Serum Osmolality,lab test,decimal,pmc-7232043-1,Extracted,"A 37-year-old man with a past medical history of pancreatitis, type 2 diabetes
mellitus on insulin, and ulcerative colitis was brought to the emergency department
with complaints of nausea, vomiting, and diarrhea for a 1-week duration followed by
anuria for 48 hours prior to this presentation. Vital signs on presentation include
a temperature of 36.3°C, blood pressure of 103/60 mm Hg, heart rate of 79 beats per
minute, and respiratory rate of 16 breaths per minute, saturating at 100% on room
air. On examination, the patient appeared somnolent with dry mucous membranes and
loss of skin turgor. Limited neurologic examination was unremarkable. Comprehensive
serum drug screen was negative. Laboratory data are relevant for serum blood urea
nitrogen 160 mg/dL, creatinine 8.4 mg/dL, Na 107 mEq/L, potassium 6.1 mEq/L,
bicarbonate 7 mEq/L, anion gap of 33, glucose 169 mg/dL, and measured serum
osmolality of 297 mOsm/L. Electrocardiogram showed normal sinus rhythm with peak
T-waves. Urine studies revealed Na <10 mEq/L, creatinine 286 mg/dL, and
osmolality of 311 mOsm/L, with hyaline casts and fractional excretion of sodium of
0.6%. No prior history of renal disease noted, and renal ultrasound was
unremarkable. Given refractory and worsening hyperkalemia, worsening uremia, and
acidosis, emergent dialysis was planned. However, the lowest sodium bath available
for dialysis being 130 mEq, 0.45% normal saline was infused during the dialysis
session to prevent rapid sodium correction. He received one session of hemodialysis
and serum Na increased to 124 mEq/L and blood urea nitrogen decreased to 87 mg/dL
during the 5-hour dialysis session. The patient’s mentation gradually improved,
fully alert, awake, and oriented without any immediate neurological deficits.
Detailed neurological examination performed prior to discharge was also
unremarkable, including normal cranial nerve examination, muscle strength, and deep
tendon reflexes, sensory function, gait, and coordination. Both T1- and T2-weighted
imaging sequences on magnetic resonance imaging (MRI) scan performed 7 days after
the rapid correction event was unremarkable. The patient’s neurological examination
remained unremarkable on his 4-week posthospital clinic follow-up.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [160.0, 'mg/dL'], 'Glucose': [169.0, 'mg/dL'], 'Sodium': [107.0, 'mEq/L']}",280.53175,266.50516,294.55834,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 107.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 107.0 mEq. To convert from 107.0 mEq to mmol, convert from mEq to mmol. The compound 107.0 has a valence of 1, and so divide the valence by the value of mEq to get, 107.0 mEq/(1 mEq/mmol) = 107.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 107.0 mEq sodium/L converts to 107.0 mmol sodium/L. 
The concentration of bun is 160.0 mg/dL. 
The concentration of glucose is 169.0 mg/dL. 
Plugging these values into the equation, we get 2 * 107.0 + (160.0 / 2.8) + (160.0 / 18) = 280.53175 mmol/L.The patient's calculated serum osmolality concentration is 280.53175 mmol/L. This is equalivalent to 280.53175 mOsm/kg."
5572,30,Serum Osmolality,lab test,decimal,pmc-7519979-1,Extracted,"A 7-day-old female infant was brought to the emergency department with decreased responsiveness and poor feeding. She was born at 384/7 weeks' gestation, with a birthweight of 2770 g (10th–25th percentile) to a 38-year-old primiparous woman with adequate prenatal care. The pregnancy was complicated by gestational thrombocytopenia diagnosed in the third trimester, which required treatment with hydrocortisone. Her prenatal laboratory findings, including syphilis rapid plasma reagin, hepatitis Bs antigen, HIV, gonorrhea, and chlamydia, were negative. The result of her group B Streptococcus screening test was positive. An urgent cesarean delivery was performed because of her nonreactive nonstress test at the obstetric clinic. Rupture of amniotic membranes occurred at delivery. The postdelivery course of infant was uncomplicated; the Apgar scores were 7 and 9 at 1 and 5 minutes, respectively. In the postnatal ward, the neonate fed poorly, with low maternal milk supply. The mother was seen by a lactation consultant who advised her to continue breastfeeding. The neonate was discharged from the hospital 48 hours after birth with a weight of 2,665 g (4% loss from birthweight), and the family advised to arrange follow-up with the primary care physician. The infant's platelet count, obtained before discharge because of the maternal history of gestational thrombocytopenia, was noted to be 180,000/μL (180 × 109/L). At the primary care physician visit on day 3 of age, the infant's weight was 2,475 g (∼11% lower than birthweight). She was noted to be otherwise well appearing though the mother continued to report difficulty with latching and breast milk supply. She received lactation consultation again in the office.
On day 6, the infant became increasingly lethargic and uninterested in feeding. She was taken to the emergency department (ED) where it was recorded that she had an average of 3 wet diapers/day and less than 1 stool/day over the past 2 days. In addition, the mother endorsed a history of right-sided gaze and head deviation for a few seconds while the infant was being placed in the car seat on the way to the ED. On initial physical examination at the ED, the infant was lethargic and minimally responsive, with a prolonged capillary refill time and appeared grossly dehydrated with standing skinfolds. Her vital signs were as follows: temperature, 34.2°C (93.5°F); heart rate, 184 beats/min; respiratory rate, 64 breaths/min; and oxygen saturation, 100% in room air. Her weight was 2,220 g (∼20% below birthweight). Multiple short self-limiting brief episodes of right gaze deviation and left arm tonic-clonic movements were also noted. Laboratory testing in the ED revealed the following.
Sodium 173 mEq/L (reference range 135–145 mEq/L) Potassium 6.8 mEq/L (reference range 3.8–6.0 mEq/L) Chloride 130 mEq/L (reference range 95–110 mEq/L) BUN 165 mg/dL (reference range 7–25 mg/dL) Creatinine 1.92 mg/dL (reference range 0.2–0.4 mg/dL) Bicarbonate 10 mEq/L (reference range 18–24 mEq/L) Glucose 111 mg/dL (reference range 75–105 mg/dl)
Capillary pH 7.29 (reference range 7.35–7.45) PaCO2 32 mm Hg (reference range 35–45 mm·Hg) Base excess −10 mEq/L
White blood cells (WBC) of 18,700/μL reference range (5,000–20,000/μL) Hemoglobin of 16.7 g/dL (167 g/L) (reference 14.3–24.5 g/dl) Hematocrit of 53%, (reference 44–64%) Platelet count of 74,000/μL (reference 130–450/μL)
There was no left shift on the CBC. In the ED, the infant received 2 normal saline boluses and was started on intravenous fluids and antibiotics and was transferred to a level IV neonatal intensive care unit for further care, where her vital signs improved. On examination, the infant was hypoactive but responsive to stimulation. She continued to have intermittent episodes of seizures (tonic-clonic seizures of both upper and lower extremity and right gaze deviation) on admission. Respirations were not labored, and heart sounds were normal on auscultation. Rest of the examination findings were within normal limits. Serum sodium concentration was 174 mEq/L, potassium 6.5 mEq/L, chloride 134 mEq/L, blood urea nitrogen 158 mg/dL, creatinine 1.61 mg/dL, and bicarbonate 15 mEq/L. Another normal saline bolus was given, and intravenous fluids continued. The WBC count was 11,800/μL, and the hemoglobin and hematocrit dropped to 13.3 g/dL and 41%, respectively. The platelet count dropped significantly to 9,000/μL. The infant continued to receive treatment for dehydration and sepsis. In addition, she was evaluated and treated for herpes simplex virus (HSV) infection, disseminated intravascular coagulation, and metabolic diseases. Head ultrasonography and computed tomography were performed to rule out intracranial hemorrhage because of the suspected seizure and acute drop in hemoglobin, hematocrit, and platelet count. The scans revealed significant bilateral intraventricular hemorrhage (IVH) involving the lateral, third, and fourth ventricles and basal cistern (Figures and ). In addition, a parenchymal hemorrhage was noted mainly in the ventral medial aspect of the thalamus and basal ganglia on the left side. A bedside ventricular tap was performed to relieve elevated intracranial pressure. She was given a loading dose of phenobarbital and video electroencephalography was performed, which showed that the patient continued to have electrographic seizures requiring multiple antiepileptic drug boluses of phenobarbital, levetiracetam, and fosphenytoin to stop the seizure. Further treatment included fluid rehydration with age-appropriate fluids aimed at correcting the hypernatremia by no more than 0.5 mmol/L per hour. The infant received several platelet and plasma transfusions. Electrolytes were checked every 4 to 6 hours, showing gradual improvement of levels. Also, treatment with broad-spectrum antibiotics and acyclovir was continued until sepsis and herpes simplex virus infection were ruled out. Hematologic, genetic, and metabolic testing was negative for any increased risk for bleeding or thrombosis.
The infant's neurologic state continued to deteriorate with the cessation of spontaneous movements, absent reaction to painful stimuli, and fixed and dilated pupils. She became apneic and was intubated to support respiration. Further brain imaging with magnetic resonance imaging, including venous and arterial angiography, showed stable IVH within the lateral, third, and fourth ventricles. It also showed previously known parenchymal hemorrhages in the bilateral thalami and basal ganglia, which was more prominent on the left side. Arterial angiography showed no flow in the intracranial arteries, and venous angiography showed no flow in dural venous sinuses suggestive of cerebral venous sinus thrombosis (Figures –). The infant continued to remain apneic and was unable to wean off the ventilator. After extensive counseling, the parents decided against comfort care for the infant. As per their request, tracheostomy and gastrostomy tubes were placed and the infant was discharged from the hospital.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [173.0, 'mEq/L'], 'Glucose': [111.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [165.0, 'mg/dL']}",411.09524,390.54048,431.65,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 173.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 173.0 mEq. To convert from 173.0 mEq to mmol, convert from mEq to mmol. The compound 173.0 has a valence of 1, and so divide the valence by the value of mEq to get, 173.0 mEq/(1 mEq/mmol) = 173.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 173.0 mEq sodium/L converts to 173.0 mmol sodium/L. 
The concentration of bun is 165.0 mg/dL. 
The concentration of glucose is 111.0 mg/dL. 
Plugging these values into the equation, we get 2 * 173.0 + (165.0 / 2.8) + (165.0 / 18) = 411.09524 mmol/L.The patient's calculated serum osmolality concentration is 411.09524 mmol/L. This is equalivalent to 411.09524 mOsm/kg."
5573,30,Serum Osmolality,lab test,decimal,pmc-6476048-1,Extracted,"A 24-year-old female with a history of HIV/AIDS, nonischemic cardiomyopathy, and methamphetamine and marijuana abuse presented with acute onset lower extremity pain. The patient reported to have snorted methamphetamine overnight and woke up with severe lower extremity pain as well as inability to move. Surgical history was significant for excision of sublingual glands. Family history: mother was HIV positive; both mother and father had significant history of substance abuse. She drank one to two alcoholic drinks per week and was an everyday smoker, between 1/4 pack and 1/2 pack per day. Her vital signs were significant for tachycardia, tachypnea, and hypotension. Lower extremity examination was positive for tender lower extremities with no palpable dorsalis pedis, posterior tibial, and popliteal pulses bilaterally. Initial lab tests were significant for lactic acidosis, acute kidney injury, EKG with nonspecific ST-T wave changes (), elevated troponin, 1.08 ng/ml, peaked at 3.5 ng/ml and urine drug screen was positive for methamphetamine and marijuana. Hemoglobin 11.9 gm/dl, white blood cells 10.4, platelets 178, sodium 139 mmol/liter, potassium 4.1 mmol/liter, chloride 104 mmol/liter, bicarbonate 20 mmol/liter, BUN 11 mg/dl, creatinine 1.3 mg/liter, blood glucose 141 mg/dl, AST 68 units/liter, ALT 41 units/liter, total bilirubin 0.9 grams/dl, alkaline phosphatase 107 IU/liter, and INR 1.8. Arterial and venous duplex of the lower extremities revealed no blood flow. CT angiogram showed large segment aortic occlusion (4 cm) just beyond the renal arteries and partial occlusive thrombus in the superior mesenteric artery with early ischemia (Figures and ). There were also multiple areas of bilateral renal infarcts left greater than right with the main renal arteries patent bilaterally. Transthoracic echocardiogram showed an echo dense mass, 2.4 cm × 2.8 cm, 1.2 cm × 2.0 cm in size, in the left ventricle with defined margins that are distinct from the endocardium seen throughout systole and diastole, consistent with left ventricular thrombus (Figures –). Ejection fraction was estimated to be 15 %, with increased wall thickness and grade 3 diastolic dysfunction. There was mild to moderate mitral and tricuspid regurgitation with normal valve structure. CT head was obtained due to an altered mental status which was negative for acute bleeding. The patient became profoundly hypotensive which was likely due to cardiogenic shock despite being on maximum vasopressors. She developed limb ischemia due to compartment syndrome requiring fasciotomy. Interventional radiology and vascular surgery were consulted, surgical thrombectomy was done. The patient's status worsened developing rhabdomyolysis, shock liver, and acute kidney injury with severe metabolic acidosis. She could not tolerate continuous renal replacement therapy. The patient had an episode of ventricular fibrillation and expired after three days of being hospitalized.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [11.0, 'mg/dL'], 'Glucose': [141.0, 'mg/dL'], 'Sodium': [139.0, 'mmol/L']}",289.7619,275.27381,304.25,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mmol/L. 
The concentration of bun is 11.0 mg/dL. 
The concentration of glucose is 141.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (11.0 / 2.8) + (11.0 / 18) = 289.7619 mmol/L.The patient's calculated serum osmolality concentration is 289.7619 mmol/L. This is equalivalent to 289.7619 mOsm/kg."
5574,30,Serum Osmolality,lab test,decimal,usmle-5812,Extracted,"A 70-year-old male presents to the emergency department for increased sweating and epigastric pain that the patient has never felt before. The patient experienced these symptoms while he was eating. His symptoms did not improve so his wife brought him into the emergency department. The patient has a past medical history of diabetes mellitus, obesity, and anxiety. His current medications include simvastatin, hydrochlorothiazide, metformin, insulin, lisinopril and buspirone. His temperature is 99.5°F (37.5°C), pulse is 112/min, blood pressure is 110/70 mmHg, respirations are 18/min, and oxygen saturation is 94% on room air. The patient is currently short of breath. A lab panel is drawn and the results are below:

Serum:
Na+: 138 mEq/L
K+: 5.3 mEq/L
Cl-: 100 mEq/L
HCO3-: 24 mEq/L
BUN: 11 mg/dL
Ca2+: 9.7 mg/dL
Mg2+: 2.0 mEq/L
Creatinine: 1.2 mg/dL
Glucose: 180 mg/dL

An EKG is performed in the emergency department. A chest radiograph is performed and is seen in Figure A. A visit to the emergency department two days ago for indigestion resulted in radiography that was within normal limits.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [11.0, 'mg/dL'], 'Glucose': [180.0, 'mg/dL'], 'Sodium': [138.0, 'mEq/L']}",289.92857,275.43214,304.425,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 11.0 mg/dL. 
The concentration of glucose is 180.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (11.0 / 2.8) + (11.0 / 18) = 289.92857 mmol/L.The patient's calculated serum osmolality concentration is 289.92857 mmol/L. This is equalivalent to 289.92857 mOsm/kg."
5575,30,Serum Osmolality,lab test,decimal,pmc-2760916-1,Extracted,"A 60-year-old gentleman was admitted with the presenting complaint of acute onset weakness of both the lower limbs (started as inability to stand up after squatting), inability to move both the lower limbs and breathlessness. He had no other presenting complaints including history of back pain, trauma, chest pain, palpitations or syncope. He had bilateral cystic bronchiectasis of the lungs of unknown etiology, cor pulmonale and he was a diabetic on oral hypoglycemic agents (glibenclamide, glimepiride) and a hypertensive on atenolol and spironolactone. His other medications were frusemide and theophylline + etofylline.
On admission, he was conscious oriented and his vitals were: Temperature - 99°F, pulse-110/min, BP-130/80 mm Hg, RR-26/min reg and O2 saturation-95% with 10litres/min of oxygen flow. He had clubbing, bilateral pitting pedal edema and bilateral symmetrical areflexic motor weakness of the lower limbs (Power 1/5) and absent bilateral plantar response. Lung examination showed bilateral coarse crepitations. All peripheral pulses were equally felt and the rest of the system examination was unremarkable. His average urine output was > 1000 ml/day. His previous renal function tests were normal, with a normal serum potassium level. Magnetic resonance imaging (MRI) spine was advised by the neurologist.
Arterial blood gas analysis showed pH 7.28, pCO2 60, pO2 159 and bicarbonate 27.8. ECG showed normal sinus rhythm, right axis deviation, PR interval of 0.20 ms, right bundle branch block (RBBB), right ventricular hypertrophy (RVH) and ST depression/T inversion in leads III, aVF and V1-V3.
Laboratory investigations revealed blood sugar of 493 mg/dL, blood urea nitrogen (BUN) of 88 mg/dL, serum creatinine of 1.6 mg/dL, serum sodium of 119 mEq/L, serum potassium of 8.9 mEq/L, Hb-19.4g/dL, hematocrit-67% and WBC-8,200/cu.mm, creatine phosphokinase, was 95 IU L and thyroid profile was normal. Daily measurements of hemoglobin and PCV level did not show any evidence of ongoing hemolysis.
Chest X-ray and computed tomography chest showed bilateral cystic bronchiectasis of the lungs. Echocardiography showed dilated right atrium and ventricle, severe pulmonary artery hypertension, normal left ventricle size and systolic function and EF of 68%. Arterial Doppler of both lower limbs revealed thin plaques along the arteries with normal flow velocity.
Immediate treatment for hyperkalemia included intravenous calcium gluconate, nebulised salbutamol, insulin infusion and potassium binding resin and potassium free diet. Repeat serum potassium after one hour of conservative management was still 8.7 mg/dL. The Nephrologist started him on immediate hemodialysis, as the serum potassium did not respond adequately to medical therapy and as he was still at high risk of life-threatening cardiac events. Salbutamol nebulization and insulin infusion were continued. After one cycle of hemodialysis, medications and potassium restriction, his serum potassium was 7.1 mg/dL but his motor power improved to 4/5 in both the lower limbs (he was able to lift both his legs against gravity and mild resistance). Repeat ECG post-hemodialysis was the same. Imaging was not performed initially as he required urgent treatment for the hyperkalemia. Subsequently there was remarkable improvement in motor power, MRI spine was withheld.
He was kept on non-invasive ventilation which was discontinued the next day. He required three cycles of hemodialysis before his serum potassium reached the normal range. Throughout the course of the illness, he had no episode of arrhythmia, heart block or cardiac arrest. At discharge, his serum potassium and renal function were within the normal range. He was able to walk normally without any disturbances in posture or balance and his motor power was 5/5 in all the 4 limbs.
Follow-up was done after two weeks of discharge when he had normal motor power (able to walk and ride motorcycle) and normal potassium and renal function tests.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [88.0, 'mg/dL'], 'Glucose': [493.0, 'mg/dL'], 'Sodium': [119.0, 'mEq/L']}",296.81746,281.97659,311.65833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 119.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 119.0 mEq. To convert from 119.0 mEq to mmol, convert from mEq to mmol. The compound 119.0 has a valence of 1, and so divide the valence by the value of mEq to get, 119.0 mEq/(1 mEq/mmol) = 119.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 119.0 mEq sodium/L converts to 119.0 mmol sodium/L. 
The concentration of bun is 88.0 mg/dL. 
The concentration of glucose is 493.0 mg/dL. 
Plugging these values into the equation, we get 2 * 119.0 + (88.0 / 2.8) + (88.0 / 18) = 296.81746 mmol/L.The patient's calculated serum osmolality concentration is 296.81746 mmol/L. This is equalivalent to 296.81746 mOsm/kg."
5576,30,Serum Osmolality,lab test,decimal,pmc-6590859-2,Extracted,"Case 2 presentation
The patient is a 62-year-old African American male with an unknown past medical history who was brought by EMS after being found down at his home without heat by his neighbor.
On physical examination, his vital signs were: rectal temperature was 28.5 °C, heart rate 94 bpm, respiratory rate 22 breaths/min, and blood pressure 170/100 mmHg. On presentation, his Glasgow Coma Scale was 8 (E4 V1 M3). He was found to be non-responding verbally, pupils were reactive to light, lungs clear to auscultation, the heart had regular rate and rhythm. He was intubated in the emergency department.
Initial laboratory with blood gas analysis showed a metabolic and respiratory acidosis with the following pH 7.103; pCO2 65.6 mmHg; pO2 514.9 mmHg; HCO3 20.0 mmHg on the following ventilator settings: tidal volume 450 mL, respiratory rate 18 breaths/min, fraction of inspired oxygen (FiO2) 100% and positive end-expiratory pressure (PEEP) of 5 cmH2O. Other laboratory findings were the following: sodium 165 mmol/L, potassium 3.0 mmol/L, chloride 122 mmol/L, carbon dioxide (CO2) 18 mmol/L, glucose 182 mg/dL, blood urea nitrogen (BUN) 86 mg/dL, creatinine 1.83 mg/dL, AST 92 U/L, ALT 56 U/L, lipase 300 U/L, creatinine kinase 1,661 U/L, troponin 0.02 ng/mL, white blood cell count (WBC) 29.50 x 103 cmm, hemoglobin 5.4 g/dL, platelets 225 x 103 cmm, PT 17 sec, INR 1.5, APTT 36.4 sec, lactic acid 6.3 mmol/L. Urine drug screening was negative for any substances and alcohol level was <10 mg/dL. Initial EKG showed atrial fibrillation with premature ventricular complexes, left axis deviation, lateral injury pattern. Initial chest x-ray showed diffuse opacities on bilateral lung fields consistent with aspiration pneumonitis or infection.
The patient was admitted to the Intensive Care Unit (ICU) for rewarming with IV fluids and Bair Hugger (3M temperature management system). He developed multifactorial shock and was started on vasopressors, blood transfusion, and antibiotics. An echocardiogram was done 2 days after admission for shock investigation which demonstrated moderate left ventricular hypertrophy, anteroseptal and anterior akinesis with global hypokinesis, ejection fraction 25% with suspicion of apical thrombus and left atrial enlargement (Figure ).
Outcome and Follow-up
The patient was later started on anticoagulation after anemia resolved but anticoagulation was later held as he developed a psoas hematoma. He had 2 subsequent echocardiograms including a transesophageal echocardiogram during hospitalization that were concerning for apical thrombus. The patient was later discharged to a nursing home facility after 80 days of hospitalization with multiple complications.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [86.0, 'mg/dL'], 'Glucose': [182.0, 'mg/dL'], 'Sodium': [165.0, 'mmol/L']}",370.8254,352.28413,389.36667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 165.0 mmol/L. 
The concentration of bun is 86.0 mg/dL. 
The concentration of glucose is 182.0 mg/dL. 
Plugging these values into the equation, we get 2 * 165.0 + (86.0 / 2.8) + (86.0 / 18) = 370.8254 mmol/L.The patient's calculated serum osmolality concentration is 370.8254 mmol/L. This is equalivalent to 370.8254 mOsm/kg."
5577,30,Serum Osmolality,lab test,decimal,pmc-2811977-1,Extracted,"The patient was a 40-year-old unmarried male who was symptomatic since last 7 years for progressive ataxia. He also complained of clumsiness in fine activities including writing. There was a history of slurring of speech for the past 2 years. In addition, he had also noted a paucity of facial, axillary and pubic hair and impotence including absence of early morning erections. Many indigenous medications were consumed for the same. Past history was significant for bouts of diarrhea since his early twenties.
Clinical examination revealed a well nourished, moderately built adult with a BMI of 21 kg/sq.m. His arm span was 182 cm with a height of 170 cm. Hypoandrogenism was seen with reduced facial, axillary and pubic hair []. Gynecomastia was present. General physical examination was normal. Higher mental functions were normal with an MMSE of 30/30. Speech revealed scanning dysarthria. Cranial nerve examination revealed bilateral gaze evoked nystagmus with fast phase in direction of gaze. Saccades and pursuit were normal. Fundus examination was unremarkable. No pyramidal or sensory findings were noted. Romberg's test was negative. Ankle reflexes were bilaterally hypoactive. Bilaterally symmetric dysmetria, dyssynergia, incoordination, and truncal ataxia were noted. Stance was broad based with gait ataxia. In summary, this man had a progressive pan-cerebellar syndrome with evidence of hypogonadism. In view of the history of recurrent diarrhea, a possibility of gluten ataxia was considered.
Hb = 11.3 gm% with a normocytic normochromic picture. Total leukocyte counts = 8,700/ cu.mm; platelets adequate. Fasting blood sugar level = 84 mg/dl; 2 hour post lunch sugar = 106 mg/dl. Blood urea nitrogen = 13 mg/dl; serum creatinine = 0.6 mg/dl; sodium = 142 mEq/L; potassium = 4.1 mEq/L Serum calcium = 8.9 mg/dl; phosphorus = 4.2 mg/dl. Total proteins = 7.5 g/dl; serum albumin level = 3.9 g/dl. AST levels = 22 IU; ALT levels= 23 IU; Alkaline phosphatase = 110 IU. Total cholesterol = 119 mg%; serum triglyceride= 206 mg%. HIV ELISA and other viral markers were negative. Stool routine and microscopy revealed minimal fat globules; no occult blood or parasites. Serum vitamin B12 levels = 795.7pg/ml; vitamin E levels = 7.60 mg/L (6–19 mg/L). Serum FSH levels = 1.11 mIU/ml (1.4–18.1 mIU/ml); LH levels = 0.30 mIU/ml (1.5–9.3 mIU/ml). Serum testosterone levels = 0.33 ng/ml (2.7–10.7 ng/ml) T3=125 ng/dl; T4= 9.5 μg/dl; TSH=4.46 μU/ml. Testicular volume – Right = 9 cc and Left = 10.5 cc (normal = 13–19 cc). Nerve conduction studies revealed bilaterally attenuated H reflexes with normal Sensory Nerve Action Potentials (SNAPs) and Compound motor action potentials (CMAPs). Magnetic Resonance Imaging (MRI) of the brain revealed gross cerebellar atrophy []. On gastroscopy there was mild gastric atrophy with mild duodenitis in the D1 segment. Histopathology of biopsy specimens from both areas revealed features which were consistent with celiac sprue (short flattened villi, intra-epithelial lymphocytic infiltrates, increased villous-crypt ratio) [].
Serum IgA Anti-Gliadin Antibodies (AGA) = 31.2 U/ml (n = ≤11 U/ml) Serum IgG Anti-gliadin Antibodies= 17.4 U/ml (n = 11–17 U/ml). Serum IgA Anti-tissue Transglutaminase (TTG) = 168.90 U/ml (0–20 U/ml) Serum IgA Anti-endomysial Antibodies (EMA) = 243.40 U/ml (0–20 U/ml)
On the basis of the above findings, patient was diagnosed to have gluten ataxia and enteropathy with additional hypogonadotropic hypogonadism. He has been initiated on a gluten-free diet and is under evaluation for hormonal replacement therapy.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [13.0, 'mg/dL'], 'Glucose': [84.0, 'mg/dL'], 'Sodium': [142.0, 'mEq/L']}",293.30952,278.64404,307.975,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. 
The concentration of bun is 13.0 mg/dL. 
The concentration of glucose is 84.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (13.0 / 2.8) + (13.0 / 18) = 293.30952 mmol/L.The patient's calculated serum osmolality concentration is 293.30952 mmol/L. This is equalivalent to 293.30952 mOsm/kg."
5578,30,Serum Osmolality,lab test,decimal,usmle-8509,Extracted,"A 59-year-old Caucasian man with a history of hypertension and emphysema is brought to the hospital because of progressive lethargy and confusion. The patient has been experiencing poor appetite for the past 3 months and has unintentionally lost 9 kg (19.8 lb). He was a smoker for 35 years and smoked 1 pack daily, but he quit 5 years ago. He takes lisinopril and bisoprolol for hypertension and has no allergies. On examination, the patient appears cachectic. He responds to stimulation but is lethargic and unable to provide any significant history. His blood pressure is 138/90 mm Hg, heart rate is 100/min, and his oxygen saturation on room air is 90%. His mucous membranes are moist, heart rate is regular without murmurs or an S3/S4 gallop, and his extremities are without any edema. His pulmonary examination shows mildly diminished breath sounds in the right lower lobe with bilateral wheezing. His laboratory values are shown:
Sodium 110 mEq/L
Potassium 4.1 mEq/L
Chloride 102 mEq/L
CO2 41 mm Hg
BUN 18
Creatinine 1.3 mg/dL
Glucose 93 mg/dL
Urine osmolality 600 mOsm/kg H2O
Plasma osmolality 229 mEq/L
WBC 8,200 cells/mL
Hgb 15.5 g/dL
Arterial blood gas pH 7.36/pCO2 60/pO2 285
Chest X-ray demonstrates a mass in the right upper lobe.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [110.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [18.0, 'mg/dL'], 'Glucose': [93.0, 'mg/dL']}",231.59524,220.01548,243.175,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 110.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 110.0 mEq. To convert from 110.0 mEq to mmol, convert from mEq to mmol. The compound 110.0 has a valence of 1, and so divide the valence by the value of mEq to get, 110.0 mEq/(1 mEq/mmol) = 110.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 110.0 mEq sodium/L converts to 110.0 mmol sodium/L. 
The concentration of bun is 18.0 mg/dL. 
The concentration of glucose is 93.0 mg/dL. 
Plugging these values into the equation, we get 2 * 110.0 + (18.0 / 2.8) + (18.0 / 18) = 231.59524 mmol/L.The patient's calculated serum osmolality concentration is 231.59524 mmol/L. This is equalivalent to 231.59524 mOsm/kg."
5579,30,Serum Osmolality,lab test,decimal,pmc-7455384-1,Extracted,"A 57-year-old man was admitted to the ED with complaints of syncope and weakness. We noticed that in his medical history, leeches were applied to treat the diabetic wounds on his feet two hours before he attended our clinic. After this, the leeches spontaneously detached but he observed bleeding from his bites and bleeding did not stop in spite of compression with tight bandages. A review of the patient’s past medical history revealed hypertension, diabetes mellitus, diabetic foot, ischemic heart disease and coronary artery bypass surgery.
Vital signs were as follows; fever: 36.6°C, blood pressure: 85/50 mmHg, heart rate: 112/min and respiratory rate: 28/min. Physical examination revealed tenderness in the whole abdomen. Ampulla was empty with rectal examination. There was an ulcerative lesion with size 5x3 cm on the site of the amputated first toe. Additionally, there were multiple bites due to leech therapy on both feet (Figure ).
Laboratory tests indicated the following: hemoglobin: 7.6 g/dL, white blood cells: 9370/mm3, platelets: 147000/mL, blood urea nitrogen: 29.1 mg/dL, creatinine: 1.98 mg/dL, glucose: 527 mg/dL, Na: 127 mmol/L, K: 6 mmol/L, CL: 94.5 mmol/L, C-reactive protein: 1.27 mg/dL and other routine blood tests and coagulation functions were all normal. Blood gas analysis revealed pH: 7.26, pO2: 86 mmHg, and bicarbonate: 20.2 mmol/L. Abdominal ultrasonography (USG) showed gas in the intrahepatic biliary ducts. No obstructive pathology was found to mesenteric blood flow on Doppler USG. CT without intravenous contrast was performed because of abnormal renal function tests. CT revealed gas near the stomach, among colon segments (pneumatosis cystoides intestinalis, PSI) and intrahepatic biliary ducts in central and left hepatic lobe (hepatic portal venous gas, HPVG) (Figure , Figure , respectively).
The patient was referred to another hospital that had an intensive care unit and started conservative treatment with antibiotics and intravenous fluid. Twelve hours after treatment, his general condition did not improve and signs of diffused peritonitis were observed on abdominal examination. The patient underwent exploratory laparotomy. Necrosis was found in the terminal ileum and the entire colon during laparotomy. Doppler USG detected low flow in the vessels supplying these necrotic segments. However, resection was decided due to necrosis of these segments. These necrotic intestinal segments were resected and an end-ileostomy was performed. He had an uneventful recovery and was discharged on the 17th postoperative day.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [29.1, 'mg/dL'], 'Glucose': [527.0, 'mg/dL'], 'Sodium': [127.0, 'mmol/L']}",293.67063,278.9871,308.35416,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 127.0 mmol/L. 
The concentration of bun is 29.1 mg/dL. 
The concentration of glucose is 527.0 mg/dL. 
Plugging these values into the equation, we get 2 * 127.0 + (29.1 / 2.8) + (29.1 / 18) = 293.67063 mmol/L.The patient's calculated serum osmolality concentration is 293.67063 mmol/L. This is equalivalent to 293.67063 mOsm/kg."
5580,30,Serum Osmolality,lab test,decimal,pmc-6311974-1,Extracted,"A 38-year-old man presented to an emergency department with progressive weakness and decreased urine output after having vomited up to 20 times per day over a period of 7 days. The patient was referred to our intensive care unit. Before medical consultation, he was healthy, and no other symptoms were reported. Diarrhea, fever, chills, or abdominal pain was absent.
Clinical examination revealed a patient of normal weight (height: 180 cm, weight: 70 kg). Blood pressure and heart rate were elevated (150/80 mmHg, 105/min); the respiratory rate was normal (13/min), but oxygen saturation was low (89%). During blood pressure measurement, a positive Trousseau sign was noted. The mucous membranes were dry, and the physical examination was otherwise unremarkable.
Arterial blood gas analysis revealed a metabolic alkalosis with partial respiratory compensation (pH: 7.71 [7.35–7.45], base excess: 40.5 mmol/l [-2-3 mmol/l], pCO2: 56.1 mmHg [32–45 mmHg], pO2: 43.5 mmHg [83–108 mmHg], bicarbonate: 72.2 mmol/l [21–26 mmol/l], lactate: 2.8 mmol/l [0.5–1.6 mmol/l], chloride: 52 mmol/l [98–106 mmol/l], sodium: 130 mmol/l [136–146 mmol/l], potassium: 2.4 mmol/l [3.5–5.1 mmol/l], ionized calcium: 0.77 mmol/l [1.15–1.29 mmol/l] and glucose: 165 mg/dl [70–105 mg/dl]).
Ultrasound revealed a distended and full stomach; the inferior vena cava was collapsing on inspiration. Otherwise, the ultrasound was unremarkable. The electrocardiography [] showed a prolonged QT interval (QTc 547 ms).
Laboratory tests were consistent with acute kidney injury (creatinine: 5.2 mg/dl, urea: 176 mg/dl); liver function tests, coagulation tests, albumin, lipase, procalcitonin, total calcium, hemoglobin, and thyroid-stimulating hormone were normal. Leukocytes were minimally elevated (11500/μl).
We suspected a prerenal acute kidney injury and a hypochloremic metabolic alkalosis due to gastric losses of HCl and fluids. Initial management consisted of oxygen therapy to correct hypoxemia and intravenous fluid therapy with normal saline and potassium chloride. Initially, a balanced crystalloid solution was infused, and later normal saline with KCl (40 mmol/l) was used because of the higher chloride content. Metoclopramide was administered to promote gastric emptying. To prevent further gastric losses of HCl, a proton-pump inhibitor was given. The patient was put on nihil per os for 24 h.
After 24 h, a total of 4.5 l of crystalloid fluid was infused. There was no further vomiting. A repeated bedside ultrasound revealed an empty stomach. The pH was corrected to 7.49, bicarbonate was reduced to 48.6 mmol/l, base excess was 23.4, chloride was 69 mmol/l, and potassium was still low at 2.8 mmol/l. There was hypoventilation with a pCO2 of 68.4 mmHg. We noted onset of diuresis. After 72 h of fluid therapy, the acid-base and electrolyte status was normal. Creatinine had decreased to 3.5 mg/dl. Small meals were tolerated.
Since there was no evidence of an infectious etiology for the excessive vomiting and the ultrasound had shown a distended stomach, an upper gastrointestinal endoscopy was performed []. A significant stenosis of the duodenum was diagnosed. Although there was no ulcer visible, an occult ulcer was deemed to be possible. A portal hypertensive gastropathy was diagnosed while esophageal varices were absent. Helicobacter pylori testing was positive, so an eradication therapy was initiated. A repeated endoscopy confirmed the stenosis, but again, no ulcer was seen. Since a focused abdominal ultrasound did not reveal the reason for the stenosis, a magnetic resonance imaging scan was performed to rule out malignancy such as pancreatic or gallbladder cancer or a thrombosis of the mesenteric vein. There was no evidence of malignancy or cirrhosis. An endosonography was done without evidence of malignancy or mesenteric vein thrombosis. At that point, the stenosis had partly resolved, and endoscopic passage was possible. We concluded that the temporary duodenal stenosis was caused most likely by portal hypertension of unknown etiology, and our differential diagnosis included idiopathic noncirrhotic portal hypertension after exclusion of cirrhosis and portal vein obstruction.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [130.0, 'mmol/L'], 'Glucose': [165.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [176.0, 'mg/dL']}",332.02381,315.42262,348.625,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 130.0 mmol/L. 
The concentration of bun is 176.0 mg/dL. 
The concentration of glucose is 165.0 mg/dL. 
Plugging these values into the equation, we get 2 * 130.0 + (176.0 / 2.8) + (176.0 / 18) = 332.02381 mmol/L.The patient's calculated serum osmolality concentration is 332.02381 mmol/L. This is equalivalent to 332.02381 mOsm/kg."
5581,30,Serum Osmolality,lab test,decimal,pmc-6197028-1,Extracted,"The patient is a 73-year-old female with past medical history of sero-positive ocular Myasthenia Gravis (with anti-acetylcholine receptor antibody) and COPD who presented by helicopter with altered mental status and weakness. On presentation the patient was hypotensive and afebrile with a heart rate in the 20s. She received atropine en route and was started on a dopamine drip along with aggressive fluid resuscitation. Blood pressure improved to 111/54 with HR increasing to the low 30’s. Lab work at outside hospital showed sodium 145 mmol/L, potassium 6.0 mmol/L, chloride 107 mmol/L, with a BUN of 41 mg/dL and creatinine 2.32 mg/dL. POC glucose was 191 and AST 55 U/L with ALT 37 U/L. Her hyperkalemia was treated with insulin and dextrose and had returned to normal limits by time of presentation. Repeat kidney, liver function tests, and serum electrolytes were within normal limits. Troponins were drawn and found to be 0.062 ng/mL with a Brain Natriuretic Peptide of 60 pg/ml. ECG was performed and showed patient had a complete heart block. The patient was admitted to Medical Intensive Care Unit where transcutaneous pacing was attempted but found to be ineffective. The patient was brought to the cardiac cath lab for transvenous pacing. Review of prior to admission medications showed that the patient had taken her PO pyridostigmine prior to developing bradycardia with altered mental status. She denied taking any of her COPD medication prior to presentation including any short or long acting beta agonists. Neurology was consulted for further evaluation of causes of heart block in a patient with MG. Pyridostigmine was held for concern of its affect in leading to complete heart block. With pyridostigmine held, the patient reverted back to sinus rhythm and transvenous pacing was removed. Using the Naranjo scale for adverse drug reaction patient received a score of 6 for a probable adverse drug reaction. Given the patient’s lack of infectious etiology, including negative Lyme serology, alternative pharmacological causes of heart block and reversion to sinus rhythm after removal of the offending agent, pyridostigmine was diagnosed as the causative agent. When the patient was stabilized she was discharged home with pyridostigmine held with close follow-up with her neurologist for further management of her MG.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [41.0, 'mg/dL'], 'Glucose': [191.0, 'mg/dL'], 'Sodium': [145.0, 'mmol/L']}",315.25397,299.49127,331.01667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 145.0 mmol/L. 
The concentration of bun is 41.0 mg/dL. 
The concentration of glucose is 191.0 mg/dL. 
Plugging these values into the equation, we get 2 * 145.0 + (41.0 / 2.8) + (41.0 / 18) = 315.25397 mmol/L.The patient's calculated serum osmolality concentration is 315.25397 mmol/L. This is equalivalent to 315.25397 mOsm/kg."
5582,30,Serum Osmolality,lab test,decimal,usmle-5071,Extracted,"A 68-year-old man presents to the emergency department with confusion. The patient lives in a nursing home and has Alzheimer dementia at baseline. His nurse noticed that he was more confused than usual and was somnolent for the past 12 hours. The patient’s nurse also noticed that he was soiling his diapers more frequently with copious amounts of urine. The patient has lost 15 pounds since his last physician appointment 3 weeks ago. Laboratory values are ordered as seen below.

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 12.2 mg/dL
PTH: 8 pg/mL

The patient is referred to another physician for a more thorough workup including laboratory work and CT imaging.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [99.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",290.64286,276.11072,305.175,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (20.0 / 2.8) + (20.0 / 18) = 290.64286 mmol/L.The patient's calculated serum osmolality concentration is 290.64286 mmol/L. This is equalivalent to 290.64286 mOsm/kg."
5583,30,Serum Osmolality,lab test,decimal,pmc-2808564-1,Extracted,"A 49-yr-old man presented to the emergency room with mental confusion and vomiting in December 2003. Two days earlier he had abrupt onset of abdominal pain, vomiting, and constipation. Since then, he had exhibited slurred speech. A search of his home found no prescription medication. He had liver cirrhosis with hepatitis B. He had two episodes of hepatic encephalopathy since 2002, and had been on oral lactulose therapy.
His blood pressure was 130/90 mmHg, and pulse rate was 64 beats/min. On physical examination, he was neurologically in a disoriented and drowsy mental state. His abdomen was distended, and bowel sound was absent. Ascites were noted. Laboratory investigations revealed a white blood cell count of 3,000/µL; hemoglobin 8.1 g/dL; platelet count 22,000/µL; serum aspartate transaminase 65 U/L; alanine transaminase 32 U/L; albumin 1.9 g/dL; total bilirubin 3.5 mg/dL; ammonia 185 µg/dL; blood urea nitrogen 22.3 mg/dL; creatinine 1.2 mg/dL; sodium 143 mEq/L; potassium 4.5 mEq/L; glucose 110 mg/dL; prothrombin time 25.1 sec (2.2 in international normalized ratio); partial thromboplastin time 73.2 sec (vs. a control of 35 sec); alpha-fetoprotein 3.14 ng/mL.
Plain abdomen (upright film) revealed multiple air-fluid levels, distention of bowel loops, and presence of bowel gas in the left lower quadrant of the abdomen (). Initially, we gave him lactulose enemas every 6 hr for one day. Oral lactulose was not used because of frequent vomiting and ileus. However, there was no improvement in his mental state. Furthermore, he became to a state of coma, and there was an elevation of his venous ammonia level (298 µg/dL). Computed tomography of the head revealed no evidence of intracranial hemorrhage or cerebrovascular injury. Therefore, with the consent of his family, we gave him 0.5 mg of neostigmine subcutaneously to improve his peristaltic movement. Three minutes after this treatment, there was a prompt evacuation of stool with a reduction in abdominal distention and an increase in bowel sound on physical examination. Then we gave him 2 L of polyethylene glycol electrolyte solution through a nasogastric tube for 4 hr. After these treatments, his venous ammonia level decreased to the normal range (19.0-60.0 µg/dL) within 12 hr, and the coma disappeared after 2 days. Plain abdomen (upright film) also revealed no air-fluid level (). Then, oral lactulose therapy was restarted, and his condition remained stable. After 5 days, he was discharged from the hospital.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [22.3, 'mg/dL'], 'Glucose': [110.0, 'mg/dL'], 'Sodium': [143.0, 'mEq/L']}",300.0754,285.07163,315.07917,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 143.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 143.0 mEq. To convert from 143.0 mEq to mmol, convert from mEq to mmol. The compound 143.0 has a valence of 1, and so divide the valence by the value of mEq to get, 143.0 mEq/(1 mEq/mmol) = 143.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mEq sodium/L converts to 143.0 mmol sodium/L. 
The concentration of bun is 22.3 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 143.0 + (22.3 / 2.8) + (22.3 / 18) = 300.0754 mmol/L.The patient's calculated serum osmolality concentration is 300.0754 mmol/L. This is equalivalent to 300.0754 mOsm/kg."
5584,30,Serum Osmolality,lab test,decimal,pmc-3481032-1,Extracted,"A 47-year-old man who visited our department of family medicine, complained that he was experiencing chronic fatigue. His fatigue started about 1 year ago, and worsened with stress or after a day of work. His fatigue had previously improved after resting and sleeping but not for the last 6 months. He did not have a remarkable medical history, with the exception of treatment for reflux esophagitis. His dietary history included multivitamins and 4 weeks' consumption of red ginseng, 6 months ago. He did not smoke and consumed alcohol approximately twice a week. Additionally, he did not have any sleeping disorder of symptoms related to the digestive, nervous and circulatory systems, the results of a depression test were also normal, confirming that he was not suffering from any depressive disorder. Our patient's body temperature, heartbeat, and blood pressure were normal. No unusual signs were noted during simple neurologic testing or physical examination of the heart, lungs, abdomen, and muscle-bone system. There were no palpable lymph nodes in his neck, axilla, and perineum. The results of a peripheral blood test conducted to diagnose chronic fatigue were also normal as follows: hemoglobin, 15.6 mm Hg; platelets, 267/el; white blood cells, 7,390/bl; and erythrocyte sedimentation rate, 3 mm/h. In serum chemistry testing, the following levels were noted: aspartate aminotransferase, 34 IU/L; alanine aminotransferase, 35 IU/L; total protein/albumin, 7.5/4.8 g/dL; globulin, 2.6 g/dL; alkaline phosphatase, 182 IU/L; Ca/P, 9.9/3.9 mg/dL; fasting plasma glucose, 71 mg/dL; blood urea nitrogen, 11.8 mg/dL; creatinine, 0.65 mg/dL; sodium, 150 mEq/L; potassium, 4.1 mEq/L; and thyroid-stimulating hormone, 3.6 id. The routine urine analysis results were also normal. Antinuclear antibody and acquired immune deficiency syndrome test results were negative, and no specific signs were observed on abdomen ultrasonography and colonoscopy. However, we observed chronic gastritis and reflux esophagitis during gastroscopy. We recommended aerobic exercise, provided supportive psychotherapy, and prescribed medication for reflux esophagitis. We also asked the patient to submit a dietary diary and visit us again after 1 month. One month later, the patient said he had experienced no improvement in his fatigue and that he was extremely fatigued after these workouts as well. His dietary diary revealed that he ate slices of raw tuna more than twice per week. We eventually learned that raw tuna was his favorite food and that he has been consuming it for the past 5 years, partly because of his occupation. Suspecting methyl-mercury exposure, we conducted a blood test. We also conducted the hair toxic mineral assay (HTMA), after confirming that he had not permed, dyed, or coated his hair or used any functional shampoos. Mercury levels from blood and urine tests were within normal limits. We subsequently administered the patient a dietary medication designed to remove heavy metals. Each capsule contains zinc oxide, magnesium oxide, calcium, and L-cysteine.
After administering a dietary medication designed to remove heavy metals for 3 months, we found that the mercury concentration in our patient had decreased to 1.972. Using the fatigue severity scale (FSS) and visual analogue scale (VAS) (), we measured the patient's degree of fatigue before and after proem intake for 3 consecutive months. His FSS score was 49, and his VAS was 9 before Proem intake. One month after Proem administration, his FSS score was 48 and VAS was 8. After 3 months of intake, his FSS score reduced to 17 and his VAS reduced to 2 ().",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [11.8, 'mg/dL'], 'Glucose': [71.0, 'mg/dL'], 'Sodium': [150.0, 'mEq/L']}",308.15873,292.75079,323.56667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 150.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 150.0 mEq. To convert from 150.0 mEq to mmol, convert from mEq to mmol. The compound 150.0 has a valence of 1, and so divide the valence by the value of mEq to get, 150.0 mEq/(1 mEq/mmol) = 150.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 150.0 mEq sodium/L converts to 150.0 mmol sodium/L. 
The concentration of bun is 11.8 mg/dL. 
The concentration of glucose is 71.0 mg/dL. 
Plugging these values into the equation, we get 2 * 150.0 + (11.8 / 2.8) + (11.8 / 18) = 308.15873 mmol/L.The patient's calculated serum osmolality concentration is 308.15873 mmol/L. This is equalivalent to 308.15873 mOsm/kg."
5585,30,Serum Osmolality,lab test,decimal,pmc-7362642-1,Extracted,"A 76-year-old man with a past medical history of prostate cancer, paroxysmal atrial fibrillation, and recurring pneumonia was found to have a 10-mm nodule in the left lower lung without hilar or mediastinal lymphadenopathy on CT of the chest with IV contrast (Figure ). CT/PET scan showed abnormal uptake in the lung nodule (Figure ) and grade II cervical lymphadenopathy. CT-guided biopsy of the left lower lung was performed. Histopathology showed a malignant neoplasm of plasmacytoid cells (Figure ). A panel of immunohistochemical stains was performed to further evaluate the lesion. The tumor cells were strongly and diffusely immunoreactive for the melanocytic marker MART-1 (Figure ). However, stains for AE1/AE3, CK7, TIF-1, Napsin, P63, PSA, and PASP were negative. The immunohistochemical results confirmed a diagnosis of metastatic melanoma of unknown primary origin (MUP) to the cervical lymph nodes (LNs) and lungs. The patient had just finished four cycles of ipilimumab when he presented to our clinic complaining of fatigue, generalized weakness, dizziness, nausea, abdominal pain, and a 10-pound weight loss. The patient denied any fever, chills, chest pain, shortness of breath, or diarrhea. He denied any smoking or drug-use history. Vital signs included a blood pressure of 98/60 mmHg, heart rate of 92 bpm, respiratory rate of 20 bpm, and oxygen saturation of 92% on room air. The physical exam was unremarkable except for a slightly enlarged left cervical LN, dark pigmentation of the lips and gingiva, and sinus tachycardia without abnormal heart sounds or murmurs. The complete blood count was within normal limits.
The labs before starting ipilimumab were as follows - sodium (Na): 140 mEq/L (normal range: 135-145 mEq/L), potassium: (K) 3.6 mEq/L (normal range: 3.5-5.2 mEq/L), chloride (Cl): 105 mEq/L (normal range: 96-106 mEq/L), carbon dioxide (CO2): 28 mEq/L (normal range: 23-29 mEq/L), blood urea nitrogen (BUN): 19 mg/dL (normal range: 6-20 mg/dL); creatinine (Cr): 1.3 mg/dL (normal range: 0.8-1.2 mg/dL); albumin: 3.9 g/dL, and glucose: 110 mg/dL (normal range: 64-100 mg/dL); morning cortisol: 17 μg/dL (normal range: 5-25 μg/dL), adrenocorticotropic hormone (ACTH): 14 pg/mL (normal range: <80 pg/mL), thyroid-stimulating hormone (TSH): 2.4 μU/mL (normal range: 0.4-5 μU/mL), and free thyroxin: 1.2 ng/dL (normal range: 0.8-2.8 ng/dL).
The labs after four cycles of ipilimumab were as follows - Na: 131 mEq/L, K: 4.1 mEq/L, Cl: 87 mEq/L, CO2: 27 mEq/L, BUN: 6 mg/dL, Cr: 1.1 mg/dL, albumin: 3.7 g/dL, and glucose: 89 mg/dL; morning cortisol: 5 μg/dL, ACTH: 120 pg/mL, TSH: 5 μU/mL, free thyroxin: 0.9 ng/dL, testosterone: 437 ng/dL (normal range: 270-1,070 ng/dL), follicle-stimulating hormone (FSH): 3.5 mIU/mL (normal range: 1.5-12.4 mIU/mL), luteinizing hormone (LH): 6.8 mIU/mL (normal range: 1.24-7.8 mIU/mL), prolactin: 11 ng/mL (normal range: 2-18 ng/mL). Aldosterone was undetectable, and renin was 31 ng/mL/h (normal range for normal sodium diet: 0.6-4.3 ng/mL/h). The patient's HbA1C was 5.7%, and blood culture showed no growth. Urinalysis showed no abnormality and procalcitonin was negative. After the administration of 250 μg intravenous (IV) cosyntropin, cortisol was found to be 6.8 μg/dL at 30 mins, and 10.2 μg/dL at 60 mins, confirming the diagnosis of PAI.
He was diagnosed with grade 3 toxicity of ipilimumab and, given his severe symptoms limiting his daily activities, was hospitalized. The patient was immediately started on IV fluid resuscitation and hydrocortisone 100 mg IV bolus, followed by 50 mg IV every six hours. A CT of the abdomen and pelvis with and without IV contrast revealed no evidence of intraabdominal or pelvic pathology. MRI of the brain with and without contrast revealed no evidence of hypophysitis and no evidence of intracranial metastatic disease. Symptomatic improvement was seen at 24 hours. He was discharged with a four-day taper of hydrocortisone as per the recommendations of the endocrinologist. On his follow-up at the endocrinology clinic, his symptoms continued to improve. A repeat cosyntropin stimulation test showed cortisol levels within normal limits. The patient was started on a second checkpoint inhibitor, nivolumab, for 16 cycles of treatment while being followed up by an endocrinologist to monitor any side effects. A repeat CT/PET FDG 12 months later showed complete disappearance of the left lung nodule, indicating tumor remission (Figure ).",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [19.0, 'mg/dL'], 'Glucose': [110.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",292.89683,278.25199,307.54167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 19.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (19.0 / 2.8) + (19.0 / 18) = 292.89683 mmol/L.The patient's calculated serum osmolality concentration is 292.89683 mmol/L. This is equalivalent to 292.89683 mOsm/kg."
5586,30,Serum Osmolality,lab test,decimal,usmle-4848,Extracted,"A 27-year-old woman presents to her primary care physician for a follow-up appointment. At her previous visit she had missed her previous two menses and also had a blood pressure of 147/100 mmHg. The patient has a past medical history of anxiety, depression, bulimia nervosa and irritable bowel syndrome. Her physician prescribed her an exercise program as well as started her on hydrochlorothiazide and ordered lab work. The results of the patient's lab work are below:

Serum:
Na+: 145 mEq/L
K+: 2.9 mEq/L
Cl-: 100 mEq/L
HCO3-: 30 mEq/L
BUN: 18 mg/dL
Ca2+: 10.9 mg/dL
Mg2+: 2.0 mEq/L
Creatinine: 1.2 mg/dL
Glucose: 110 mg/dL

The patient's blood pressure at this visit is 145/100 mmHg and she has still not experienced her menses. Her cardiac, abdominal, and pulmonary exams are within normal limits. Inspection of the patient's oropharynx is unremarkable as is inspection of her extremities. The patient is started on furosemide and sent home.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [18.0, 'mg/dL'], 'Glucose': [110.0, 'mg/dL'], 'Sodium': [145.0, 'mEq/L']}",302.53968,287.4127,317.66666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 145.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 145.0 mEq. To convert from 145.0 mEq to mmol, convert from mEq to mmol. The compound 145.0 has a valence of 1, and so divide the valence by the value of mEq to get, 145.0 mEq/(1 mEq/mmol) = 145.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 145.0 mEq sodium/L converts to 145.0 mmol sodium/L. 
The concentration of bun is 18.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 145.0 + (18.0 / 2.8) + (18.0 / 18) = 302.53968 mmol/L.The patient's calculated serum osmolality concentration is 302.53968 mmol/L. This is equalivalent to 302.53968 mOsm/kg."
5587,30,Serum Osmolality,lab test,decimal,pmc-7543146-1,Extracted,"A 5-week-old infant with CAH presented to the Emergency Room (ER) with fever and
fussiness.
He was born at 40 weeks gestation via C-section for failure to progress to a G1P1 mother
with negative prenatal serologies. APGAR scores were 8 and 9. Initial newborn course was
complicated by hypoglycemia, respiratory distress and tachypnea which resolved by day 2 of
life.
On day 3 of life, the newborn screening test was positive for congenital adrenal
hyperplasia. Pediatric endocrinology was consulted. Cortisol level obtained on day 2 of life
was 1.2 mcg/dL (2.9-19.4 mcg/dL) and 17-hydroxyprogesterone was 813 ng/dL (85-250 ng/dL). An
ACTH [CortrosynTM] stimulation test was performed and confirmed the diagnosis
with 1-hour post-stimulation 17 hydroxyprogesterone level of 17 836 ng/dl [85-250 ng/dL] and
cortisol level of 3.9 mcg/dl. The infant was initiated on hydrocortisone therapy at 30 mg/m²
per day, fludrocortisone 0.1 mg daily and Sodium chloride (table salt) 2 grams divided in
several feedings.
The infant presented to the ER at 5 weeks of age with fever and increased fussiness. There
was no respiratory distress, diarrhea, vomiting, rash, or decreased feeding. His father
reported symptoms of cough and a runny nose for a few days prior to this. On physical
examination, he was afebrile with oxygen saturation of 100%. He was noted to be irritable
and his skin was mottled ().
He did not have chest retractions, tachypnea, or nasal flaring. Laboratory results revealed
WBC 7.2 bil/L (5-19.5 bil/L), neutrophils 2.1 bil/L (1-9 bil/L), lymphocytes 2.5 bil/L
(2.5-16.5 bil/L), monocytes 2 bil/L (0.4-1.4 bil/L), Na 136 mmol/L (134-144 mmol/L),
potassium 5.9 mmol/L (4-6 mmol/L), HCO3 22 mmol/L (20-28 mmol/L), glucose of 110 mg/dL
(60-99 mg/dL), BUN 8 mg/dL (3-17 mg/dL), creatinine 0.33 mg/dL (0.1-0.36 mg/dL), and CRP
1.9 mg/L (0-7.9 mg/L). SARS-CoV-2 by Nucleic Acid Amplification (NAA) was detected on
nasopharyngeal swab. Pediatric infectious disease specialists were consulted. Blood culture,
urinalysis, and urine culture were negative. Chest x-ray demonstrated mild streaky bilateral
perihilar streaks with no focal consolidation or pleural effusions. Costophrenic angles were
clear with unremarkable lung apices and bronchoalveolar marking.
He was placed on triple maintenance hydrocortisone for stress dosing every 8 hours along
with fludrocortisone 0.15 mg daily. He received a normal saline bolus and was then placed on
maintenance IV fluids. He was transferred to the Pediatric Intensive Care Unit (PICU) and
Pediatric infectious disease specialists were consulted. Over the course of his admission,
he remained hemodynamically stable. He fed appropriately and did not require respiratory
support. He was discharged 2 days after admission and his stress hydrocortisone dose was
weaned down to his home regimen. At the time of this submission, he has been home for
4 weeks and doing well.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [8.0, 'mg/dL'], 'Glucose': [110.0, 'mg/dL'], 'Sodium': [136.0, 'mmol/L']}",280.96825,266.91984,295.01666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.0 mmol/L. 
The concentration of bun is 8.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 136.0 + (8.0 / 2.8) + (8.0 / 18) = 280.96825 mmol/L.The patient's calculated serum osmolality concentration is 280.96825 mmol/L. This is equalivalent to 280.96825 mOsm/kg."
5588,30,Serum Osmolality,lab test,decimal,pmc-2803921-1,Extracted,"A 31-year-old Caucasian Brazilian woman was admitted to the hospital with a 6-month history of chest pain and progressive dyspnea on exertion. She had angiofibromas on the malar regions of the face, which were present since her childhood. During her pregnancy, 11 years ago, she was diagnosed with polycystic kidney disease associated with tuberous sclerosis. She had repetitive urinary tract infections, which resulted in progressive loss of renal function. Both her grandfather and child had polycystic kidneys, and her son also presented seizures. The patient also had a history of hemorrhoidal disease causing intermittent bleeding.
On examination, the patient appeared pale, and her vital signs included a blood pressure of 120/80 mmHg and a heart rate of 110 bpm. Auscultation revealed the presence of fine crackles in both lungs, and a loud systolic heart murmur was heard on the precordium. Her abdomen was tense and painful to palpation, but there were no signs of peritoneal irritation. There was a palpable mass occupying the upper abdomen and both flanks; Traube's space was obliterated. Laboratory evaluation revealed a red blood cell (RBC) count of 2.81 × 106/mm3, hemoglobin level of 9.0 g/dL, hematocrit of 27% and platelet count of 130 × 103/mm3. Her WBC count was normal. Serum creatinine was 3.3 mg/dL; urea, 87 mg/dL; glucose, 85 mg/dL; sodium, 135 mEq/L; potassium, 4.2 mEq/L; uric acid 4.5 mg/dL; albumin, 2.8 g/dL; calcium, 7.9 mg/dL; phosphorus, 5.2 mg/dL; and magnesium, 2.4 mg/dL.
Chest computed tomography (CT) revealed cystic formations throughout the lungs, consistent with lymphangioleiomyomatosis (Figure ), and the presence of a pericardial effusion. The echocardiogram showed a small pericardial effusion, and moderate left ventricular hypertrophy, and a normal systolic function. An abdominal CT scan demonstrated enlarged, heterogeneous kidneys, with multiple fat-density formations (negative densities, ranging from -15 to -148 Hounsfield units), which corresponded to angiomyolipomas (Figure ). Pulmonary function tests showed a severe obstructive pulmonary disorder with reduced forced vital capacity, and a positive response to bronchodilator. She started treatment with medroxyprogesterone, and her respiratory status remained stable. An echocardiogram performed three years later revealed worsening of cardiac condition, enlargement of right cavities and left atrium, and thickening of the aortic valve leaflets; systolic function was preserved. Follow-up CT scans did not show significant changes.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [87.0, 'mg/dL'], 'Glucose': [85.0, 'mg/dL'], 'Sodium': [135.0, 'mEq/L']}",305.79365,290.50397,321.08333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 135.0 mEq. To convert from 135.0 mEq to mmol, convert from mEq to mmol. The compound 135.0 has a valence of 1, and so divide the valence by the value of mEq to get, 135.0 mEq/(1 mEq/mmol) = 135.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mEq sodium/L converts to 135.0 mmol sodium/L. 
The concentration of bun is 87.0 mg/dL. 
The concentration of glucose is 85.0 mg/dL. 
Plugging these values into the equation, we get 2 * 135.0 + (87.0 / 2.8) + (87.0 / 18) = 305.79365 mmol/L.The patient's calculated serum osmolality concentration is 305.79365 mmol/L. This is equalivalent to 305.79365 mOsm/kg."
5589,30,Serum Osmolality,lab test,decimal,pmc-4154918-1,Extracted,"A 58 year old female was admitted to the hospital with a long standing history of dyspepsia and abdominal pain. The pain character changed in the last month prior to admission. She described the pain as cramping in the lower abdomen starting 1-1.5 hours after food accompanied by bloating and nausea but no vomiting and without radiation to other locations. It usually subsided after 4-5 hours with no treatment. She also complained of constipation. She was reluctant to eat because of the pain and as a result lost 3 kg weight in one month. From two days prior to admission, she started to feel an intensified and generalized abdominal pain associated with belching, nausea and vomiting. She also gave a history of decreased gas passing during this period.
On physical examination at admission, she was not in acute distress. The abdomen was slightly distended with mild generalized tenderness on palpation. Bowel sounds were present. The rectal examination was normal. There were no other positive physical findings noted. Laboratory results were normal and included Hb: 13 gr/dl; WBC: 9000/mm3; platelets: 220000/mm3; ESR: 25 mm/h; FBS: 99 mg/dl; BUN: 26 mg/dl; Cr: 1.1 mg/dl; Na: 138 meq/l; and K: 3.8 meq/l.
CT scan of the abdomen and pelvis revealed an intraluminal space occupying lesion in the terminal ileum. There was no lymphadenopathy. The lesion was also demonstrated in the small bowel barium study and noted to have a maximum diameter of 5.5 cm ().
Colonoscopy did not show any gross pathology in the colon. The patient underwent laparoscopic exploration that showed a pedunculated mass in the terminal ileum accompanied by intussusception ().
Thirty cm from the ileo cecal vaive including the mass, was surgically removed. The ileocecal valve was preserved. In gross examination the mass was found to be creamy-white in color with a rubbery consistency, measuring 5.5 x 4.5 x 4.0 cm with smooth surface and patchy erythema of the covering mucosa.
Cut sections showed homogenous tan cut surfaces. Histological examination of the submucosal mass showed a rather cellular lesion composed principally of bland-looking spindle cells with a collagenous and myxoid background accompanied by various diffusely scattered inflammatory cells, including plasma cells, lymphocytes and eosinophils ().
No mitosis, necrosis or hemorrhage was present. Immunohistochemical studies showed positive reactions of the spindle cells for smooth muscle actin, human muscle actin, vimentin and calponin and was negative for ALK-1, desmin, CD34, CD117 (C-kit) and P63. Ki-67 was positive in 5% of the tumor cell nuclei. The final pathologic diagnosis was IMT.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [26.0, 'mg/dL'], 'Glucose': [99.0, 'mg/dL'], 'Sodium': [138.0, 'mEq/L']}",290.78571,276.24642,305.325,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 26.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (26.0 / 2.8) + (26.0 / 18) = 290.78571 mmol/L.The patient's calculated serum osmolality concentration is 290.78571 mmol/L. This is equalivalent to 290.78571 mOsm/kg."
5590,30,Serum Osmolality,lab test,decimal,pmc-3125360-1,Extracted,"A 27-year-old Iranian woman, recipient of a living, unrelated renal transplant five years earlier, presented with a productive cough, weight loss and fever. The cause of her end-stage renal disease was chronic pyelonephritis. Six weeks prior to her admission, her immunosuppressant regimen was switched from oral cyclosporine (100 mg, twice daily) to oral sirolimus (1 mg, twice daily) with a diagnosis of chronic allograft nephropathy (serum creatinine level of 2 mg/dL). Her mycophenolate mofetil dose was decreased from 2000 to 1000 mg/day and prednisolone was continued with the previous dose (5 mg, daily). Four weeks later, she developed a mild cough, weakness and anorexia. Her condition progressed to a more constant cough and weight loss until she was hospitalized.
Physical examination revealed her blood pressure to be 110/60 mm/Hg, respiratory rate 20/min, pulse rate 92/min and body temperature 38°C. A chest examination revealed fine crackles mainly on her lower lung fields. On admission, the laboratory findings were as follows: white blood cell count 5.1 × 109/L, hemoglobin 7.2 g/dL, hematocrit 22.4%, mean corpuscular volume 75 fL (normal range, 77-97 fL), mean corpuscular hemoglobin 24 pgm (normal range, 26-32 pgm), mean corpuscular hemoglobin concentration 32% (normal, 32-36%), platelet count 213 × 109/L, fasting blood glucose 105 mg/dL, blood urea 62 mg/dL, serum creatinine 1.9 mg/dL, sodium 135 mEq/L, potassium 4.5 mEq/L, aspartate aminotransferase 37 IU/L, alanine aminotransferase 45 IU/L, alkaline phosphatase 1106 IU/L and total bilirubin 1 mg/dL. A urine analysis was unremarkable.
On the first day of admission, sirolimus and mycophenolate mofetil were discontinued and cyclosporine (200 mg/day) was started. The dose of prednisolone was not altered (5 mg, daily). A chest X-ray showed fine miliary nodules throughout the entire lung fields. Echocardiography revealed normal pericardium and cardiac chambers. Her left ventricular ejection fraction was 65%. An ultrasound examination of her renal allograft did not reveal any pathologic finding. A 6 mm induration was observed on a TB skin test. Sputum and bronchial aspirate examination was positive for acid-fast bacilli, suggestive of Mycobacterium tuberculosis infection. A chest computed tomography (CT) scan illustrated widespread miliary nodules throughout the lung fields, compatible with miliary TB (Figure ).
In the evening of her fourth day of admission, our patient developed an increasing right lower quadrant abdominal pain spreading to her entire abdomen. Physical examination revealed widespread abdominal tenderness and rebound. An ultrasonographic study of her abdomen disclosed a small fluid collection in the right lower quadrant. Two cysts were detected in her left ovary (54 × 32 mm and 33 × 31 mm). An abdominal CT scan with oral contrast revealed that her pancreas and spleen were normal. Her colonic wall thickness was measured as 4 mm and free fluid was visible in dependent parts of her abdominal cavity. Her peritoneal cavity was then opened with a midline incision and widespread peritonitis was found. Her inflamed appendix (9 × 6 cm) was perforated at its tip. Her ileocecal area and cecum were inflamed with fragile tissues. A cecostomy was performed and a drain was placed. Histopathological examination of the resected appendix revealed caseating epithelioid granulomas, epithelioid histiocytes and Langhans giant cells in the sub-mucosa and sub-serosa of her appendix (Figure ). The histological picture, along with positive mycobacterial cultures from the sputum and bronchial aspirate, was suggestive of tuberculous appendicitis. After surgery, chemotherapy for TB was started and continued for nine months. An immunosuppressive regimen was continued with cyclosporine, mycophenolate mofetil and prednisolone. During follow-up visits, the pulmonary and abdominal signs and symptoms were resolved.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [62.0, 'mg/dL'], 'Glucose': [105.0, 'mg/dL'], 'Sodium': [135.0, 'mEq/L']}",297.97619,283.07738,312.875,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 135.0 mEq. To convert from 135.0 mEq to mmol, convert from mEq to mmol. The compound 135.0 has a valence of 1, and so divide the valence by the value of mEq to get, 135.0 mEq/(1 mEq/mmol) = 135.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mEq sodium/L converts to 135.0 mmol sodium/L. 
The concentration of bun is 62.0 mg/dL. 
The concentration of glucose is 105.0 mg/dL. 
Plugging these values into the equation, we get 2 * 135.0 + (62.0 / 2.8) + (62.0 / 18) = 297.97619 mmol/L.The patient's calculated serum osmolality concentration is 297.97619 mmol/L. This is equalivalent to 297.97619 mOsm/kg."
5591,30,Serum Osmolality,lab test,decimal,pmc-6215343-1,Extracted,"We present the case of a 52-year-old Mexican man who worked as an office employee and lived in a suburban area of the city of Colima, Mexico. He and his wife denied recent trips outside the city. Zoonosis was absent. He was not physically active and did not have an adequate diet. Pathological antecedents revealed liver cirrhosis, diagnosed 12 years ago, alongside esophageal varices that had been treated with sclerotherapy 7 years prior. He also had a diagnosis of essential hypertension, diagnosed 20 years ago. His treatment prior to hospitalization included 20 mg of propranolol every 12 hours, which was used to treat his essential hypertension, esophageal varices, and to reduce his portal hypertension.
He arrived at our institution “IMSS General Hospital Zone 1, Colima” in the early afternoon (day 1, see Table ). He began to experience extreme pain localized in his right foot, 16 to 18 hours prior to admission, with a local pain scale of 10/10. He denied any recent forms of punctures to the overlying skin (including animal and insect bites).
On physical examination during admission, he was somnolent, oriented in person and space, but not oriented to time. His vital signs were: arterial pressure (AP, systolic/diastolic) 67/49, mean AP (MAP) 55, heart rate (HR) 88, respiratory rate (RR) 16, and body temperature 36 °C. He presented hepatopathy facies and spontaneous eyelid opening, his oral mucosa was dry, and his neck showed jugular engorgement grade I. Both hemithorax were slightly hypoventilated with no adventitious sounds. Precordial was rhythmic with low intensity sounds and no murmurs were heard. Peristalsis was present in his abdomen but low in intensity and there was no hepatosplenomegaly. His upper extremities were symmetrical, eutrophic, with no signs of edema; he moved his upper extremities freely without any limitation, no asterixis was present, and a force scale of 4/5 was seen. During exploration of inferior extremities, there was a clear asymmetric pattern. His right lower extremity was volume augmented with signs of edema ++ including large and small bullae formation with serohematogenous liquid inside involving most of his right foot and ankle (Fig. ). The pedal pulse was present but weak and had a local elevated temperature on palpation. His movements were markedly limited due to extreme pain. Deep vein thrombosis maneuvers were performed and were not present. Plantar reflexes were also not seen.
A peripheral intravenously administered high-dose double scheme of antibiotics (clindamycin plus ceftriaxone), crystalloid fluids, and corticosteroids was initiated. Laboratory studies were performed soon after admission: hemoglobin (Hb) 12.6 g/dl, hematocrit (Htc) 40.3%, mean corpuscular volume (MCV) 103.9 fL, white blood cells (WBC) 39,400/mm3, neutrophils 37,460/mm3, platelets 104,000/mm3, thrombin time (TT) 26.7 seconds, international normalized ratio (INR) 2.15, partial thromboplastin time (PTT) 42.8 seconds, glucose 61 g/dL, urea 102.72 mg/dL, creatinine 1.8 mg/dL, total bilirubin (TB) 3.4 mg/dL, direct bilirubin (DB) 2.6 mg/dL, indirect bilirubin 0.8 mg/dL, albumin 1.5 g/dL, alanine aminotransferase (ALT) 35 U/L, aspartate aminotransferase (AST) 58 U/L, P 7.1 mEq/L, Ca 8.4 mEq/L, Cl 106 mEq/L, K 6.4 mEq/L, Na 129 mEq/L, Mg 1.72 mEq/L, lactate dehydrogenase (LDH) 420 U/L, and C-reactive protein (CRP) 16.07 mg/L. Correction of hypoglycemia and electrolyte imbalance was initiated. Deep vein thrombosis was ruled out by clinical assessment and Doppler ultrasound. Aspiration of bulla liquid was obtained and sent to a laboratory for cultivation (positive to Cedecea lapagei, results returned on day 2). Interdisciplinary consultation with angiology was carried out (no indications were added). He was classified with a Sequential Organ Failure Assessment (SOFA) score of 11, Acute Physiology and Chronic Health Evaluation (APACHE) II of 22 points (42.4% mortality rate), and a Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score of 11 points (high risk > 75% of having necrotizing fasciitis) [].
In the late afternoon (day 1) his somnolence and disorientation persisted, he was hypotensive with an AP of 80/40 with a MAP of 55, and he was unresponsive to fluid resuscitation. His hypoglycemia persisted despite vigorous treatment. No fever was present and his skin was pale. His left lower limb had ascending progression of serohematogenous bullae proximal to the patella. His extreme pain continued. Since our patient’s MAP was persistently below 65 mmHg despite intravenously administered fluid therapy, an anterior jugular central venous catheter was placed and we decided to include norepinephrine 8 mg in 0.9% 1000 cc physiological solution passing at a rate of 8 ml/hour, categorizing the case as septic shock []. Concomitantly he had developed acute kidney injury (AKI) “Kidney Disease: Improving Global Outcomes” (KDIGO) stage II.
During the night (day 1), abundant large fetid serohematogenous bullae and edema continued to advance up his right thigh with persistent generalized hypoperfusion. Because of previous mentioned conditions, it was decided to change antibacterial therapy to intravenously administered imipenem and clindamycin. Bullae fluid culture results and antibiogram were not available at that time. Norepinephrine was boosted to maintain MAP above 65 mmHg. Intensive care unit (ICU) was called in for valorization to admit our patient. Unfortunately, due to the lack of space in the ICU, this idea was dismissed. Since rapid deterioration was evident, new laboratory studies were ordered (approximately 10 hours after initial blood test): Hb 10.1 g/dL, Htc 32.7%, MCV 107.5 fL, WBC 11.6/mm3, platelets 35,000/mm3, TT “Does not coagulate”, PTT “Does not coagulate”, glucose 30 g/dL, urea 115.5 mg/dL, creatinine 2.4 mg/dL, K 6.4 mEq/L, Na 130 mEq/L, LDH 406 U/L, and CRP 220 mg/L. His SOFA score was 16.
Necrotizing fasciitis was our primary diagnosis due to clinical and laboratory findings (LRINEC score of 12 points). Even though the diagnosis was very likely, the lack of a biopsy study meant that we could not confirm such a diagnosis. Multiple organ dysfunction secondary to septic shock was also diagnosed. The differential diagnosis of animal or insect bite was dismissed due to lack of exposure history and lack of puncture wound.
During the next morning (day 2) he maintained the same general conditions. Norepinephrine was boosted up again (MAP 50). Soon after, he entered cardiopulmonary arrest and cardiopulmonary resuscitation was performed. Unfortunately he died later that morning.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [102.72, 'mg/dL'], 'Glucose': [61.0, 'g/dL'], 'Sodium': [129.0, 'mEq/L']}",3683.5746,3499.39587,3867.75333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 129.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 129.0 mEq. To convert from 129.0 mEq to mmol, convert from mEq to mmol. The compound 129.0 has a valence of 1, and so divide the valence by the value of mEq to get, 129.0 mEq/(1 mEq/mmol) = 129.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 129.0 mEq sodium/L converts to 129.0 mmol sodium/L. 
The concentration of bun is 102.72 mg/dL. 
The concentration of glucose is 61.0 g/dL. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from g to mg. The mass of glucose is 61.0 g. To convert 61.0 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 61.0 g glucose * 1000.0 mg/g = 61000.0 mg glucose. The volume units is dL so no volume conversion is needed. Hence, the concentration value of 61.0 g glucose/dL converts to 61000.0 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 129.0 + (102.72 / 2.8) + (102.72 / 18) = 3683.5746 mmol/L.The patient's calculated serum osmolality concentration is 3683.5746 mmol/L. This is equalivalent to 3683.5746 mOsm/kg."
5592,30,Serum Osmolality,lab test,decimal,pmc-3830317-1,Extracted,"A 42-year-old woman presented with acute onset lower limb paralysis associated with severe proximal muscle pain. These symptoms were not associated with respiratory difficulty, dysphagia, dysarthria or sensory symptoms and there was no associated backache, fever, rash or constitutional symptoms. She had a 2 year history of hypertension, which was poorly controlled despite treatment with a combination of nifedipine, atenolol and losartan. She was treated by a general practitioner and at initial diagnosis of hypertension had undergone biochemical evaluation including serum electrolyes, which had been within normal limits. She experienced two similar, but short lasting episodes of weakness in the preceding year, but had not been investigated. Three days prior to admission she had been given Frusemide as add on therapy by her general practitioner due to uncontrolled hypertension. Her blood pressure on admission was 160/100 mmHg. Clinical examination favored an acute onset myopathy with symmetric flaccid paralysis of lower limbs (muscle power - 3/5) with normal muscle power (5/5) in the upper limbs.
Initial work-up revealed severe hypokalemia (potassium - 2.0 mmol/l) with an elevated creatine kinase (CK) of 11347 IU (16-190) and increased lactic dehydrogenase of 856 IU/l (240-480). Patient's urine was positive for myoglobin with a high urinary myoglobin 4,170 μg/l. Serum creatinine was 130 μmol/l. In addition, patient had high urinary potassium of 19.45 mmol/24 h with metabolic alkalosis (pH - 7.540, HCO3-38 mmol/l, base excess - 15 mmol/l and PCO2-44 mmHg).
The other biochemical values on initial evaluation were as follows; serum aspartate aminotransferase - 244 IU/l (up to 35 IU/l); alanine aminotransferase - 193 IU/l (2-40); Sodium - 145 mmol/l; blood urea - 45 mg/dl; calcium - 0.9 mmol/l (1.12-1-32); phosphorus - 2.7 mg/dl (2.7-4.5); magnesium - 1.4 mg/dl (1.58-2.55); fasting blood glucose 110 mg/dl and the total protein was 7.6 g/dl with albumin 3.2 g/dl. Thyroid function tests were normal with a free T4 level of 1.02 ng/dl and thyroid-stimulating hormone 3.2 μIU/ml.
Based on the above findings, patient was diagnosed as having hypokalemic paralysis and rhabdomyolysis. Treatment was initiated by oral and intravenous supplementation of potassium and after 10 days, muscular strength and CK levels had returned to normal. Conduction studies and electromyography, which were performed after the correction of hypokalemia, were normal.
The coexistence of hypertension, hypokalemia with high urinary potassium loss in association with metabolic alkalosis raised the possibility of primary aldosteronism (PA), which lead to further hormonal evaluation. Aldosterone levels were 22,600 ng/dl (normal, 3.6-24.0 ng/dl) and the plasma renin activity (PRA) value was below the detection limit of our method (0.2 ng/ml/h). Aldosterone/renin ratio (ARR) was 113,000 ng/ml per ng/ml/h (<10). Abdominal ultrasound did not reveal adrenal lesions, but abdominal computed tomography scan showed a 20 mm × 16 mm hypodense mass in the medial limb of the right suprarenal gland []. She underwent right sided adrenalectomy and pathological examination of the gland confirmed a 20 mm adrenal adenoma. Post-operatively the patient was normokalemic without spiranolactone and the PRA was 0.52 ng/ml/h; aldosterone was 1.3 ng/dl with a reduced ARR of 2.5 (<20) ng/ml per ng/ml/h. After 4 weeks of discharge, her BP was normal without any antihypertensives and she was normokalemic with normal muscle strength.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [45.0, 'mg/dL'], 'Glucose': [110.0, 'mg/dL'], 'Sodium': [145.0, 'mmol/L']}",312.18254,296.57341,327.79167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 145.0 mmol/L. 
The concentration of bun is 45.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 145.0 + (45.0 / 2.8) + (45.0 / 18) = 312.18254 mmol/L.The patient's calculated serum osmolality concentration is 312.18254 mmol/L. This is equalivalent to 312.18254 mOsm/kg."
5593,30,Serum Osmolality,lab test,decimal,usmle-5217,Extracted,"A 55-year-old man presents to the emergency department for fever and altered mental status. The patient was found by his wife in his chair at home. She noticed he responded incoherently to her questions. He has a past medical history of pancreatitis and alcohol abuse and is currently in a rehabilitation program. His temperature is 103°F (39.4°C), blood pressure is 127/68 mmHg, pulse is 120/min, respirations are 12/min, and oxygen saturation is 98% on room air. Laboratory values are obtained and shown below.

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 25 mEq/L
BUN: 29 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 5.2 mg/dL
AST: 12 U/L
ALT: 10 U/L
1,25 dihydroxycholecalciferol: 50 nmol/L

Physical exam notes a diffusely distended and tender abdomen.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [139.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [29.0, 'mg/dL'], 'Glucose': [99.0, 'mg/dL']}",293.85714,279.16428,308.55,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 29.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (29.0 / 2.8) + (29.0 / 18) = 293.85714 mmol/L.The patient's calculated serum osmolality concentration is 293.85714 mmol/L. This is equalivalent to 293.85714 mOsm/kg."
5594,30,Serum Osmolality,lab test,decimal,usmle-5823,Extracted,"A 77-year-old man presents to the emergency department for shortness of breath. The patient states that over the past month he has felt short of breath when doing everyday tasks, and today he even felt short of breath while taking a nap. The patient has a past medical history of obesity, diabetes, hypertension, and asthma. His current medications include lisinopril, insulin, metformin, and an albuterol inhaler. His temperature is 99.5°F (37.5°C), blood pressure is 130/90 mmHg, pulse is 85/min, respirations are 11/min, and oxygen saturation is 96% on room air. An EKG is ordered as seen in Figure A. A chest radiograph is ordered as seen in Figure B. Laboratory studies are ordered as seen below:

Serum:
Na+: 137 mEq/L
K+: 3.9 mEq/L
Cl-: 100 mEq/L
HCO3-: 24 mEq/L
Urea nitrogen: 9 mg/dL
Glucose: 122 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 10.2 mg/dL
Mg2+: 1.5 mEq/L
AST: 15 U/L
ALT: 9 U/L
Alkaline phosphatase: 32 U/L
Glutamyltransferase (GGT): 12 U/L
Albumin: 3.9 g/dL
Total protein: 6.9 g/dL
Total bilirubin: 0.9 mg/dL
Direct bilirubin: 0.2 mg/dL

On physical exam the patient appears obese and in distress. He has bilateral lower extremity pitting edema and yellowing of his toenails. Pulmonary exam is notable for bilateral crackles. Cardiac exam demonstrates a normal rate and rhythm with a displaced cardiac apex. There is JVD to the angle of the mandible.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [9.0, 'mg/dL'], 'Glucose': [122.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",283.99206,269.79246,298.19166,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 9.0 mg/dL. 
The concentration of glucose is 122.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (9.0 / 2.8) + (9.0 / 18) = 283.99206 mmol/L.The patient's calculated serum osmolality concentration is 283.99206 mmol/L. This is equalivalent to 283.99206 mOsm/kg."
5595,30,Serum Osmolality,lab test,decimal,pmc-4805229-1,Extracted,"This 8-year-old male patient had been suffering from recurrent cough, breathlessness, and malaise since he was 5 years old. He had been administered antibiotics orally for tonsillitis almost every 1-2 months for his complaints. These episodes had been usually associated with fever. He also had a history of five episodes of afebrile convulsions with temporary vision loss. Although laboratory results were negative for tuberculosis, he was administered antituberculosis therapy for one year because of the opacity noted in his chest roentgenogram (). However, he did not respond to the therapy. Also, he had been suffering from polyuria and polydipsia for almost three years. He has been drinking water (6 L/m2/day) and waking up approximately three times to drink and urinate each night.
At the time of admission, the patient’s vital functions were within normal ranges. Physical examination revealed a thin child who weighed 23 kg (15th percentile) and measured 115 cm in height (30th percentile) but appeared to be healthy. His oral mucosa was dry and breath sounds were reduced on the left side. Other physical findings were normal including the neurological system.
Laboratory results showed a hemoglobin level of 11.7 g/dL, a total leucocyte count of 10.800/mm3, and a differential count within normal ranges. While the erythrocyte sedimentation rate (82 mm/h) and C-reactive protein (38 mg/L) were elevated, the electrolytes, serum calcium, uric acid, as well as renal and liver functions were within normal ranges. Basal serum sodium, urea, and glucose levels were also within normal ranges (142 meq/L, 11 mg/dL, and 96 mg/dL, respectively). Before the water deprivation test, urine specific gravity, serum and urine osmolarity values were 1,000, 293 mOsm/kg, and 133 mOsm/kg, respectively. Following a 14-hour period of water deprivation, the serum sodium level increased to 155 meq/L and urine specific gravity, serum and urine osmolality were found as 1,007, 323 mOsm/kg and 240 mOsm/kg, respectively. Serum antidiuretic hormone was <0.5 pg/mL both before and after the water deprivation test and these levels were consistent with cDI. Polyuria and polydipsia symptoms were relieved with desmopressin. The pituitary hormone profile was in normal ranges except for a low level of insulin-like growth factor of 79 ng/dL (-2/-3 SDS) and antidiuretic hormone. CNS investigation revealed presence of two 10- and 14-mm lesions on the left parietal and temporo-occipital lobes and a small adenohypophysis (2 mm in diameter). The infundibulum was normal in appearance, but neurohypophysis intensity was decreased (, ).
Contrast-enhanced computed tomography of the chest showed a large lobulated calcified mass (, ). The lung biopsy gave no morphological clues of malignancy, such as increased and/or abnormal mitotic activity, conspicuous cellular atypia, or necrosis (). Immunohistochemically, the proliferating cells were highlighted with vimentin, smooth muscle actin, and muscle-specific actin. Focal and weak immunoreactivity against desmin was also noted in some areas. There was no nuclear staining with anaplastic lymphoma kinase (ALK). These morphological findings were interpreted to be in favor of IMT. Later, a thorough examination of the resection material also confirmed the diagnosis of IMT.
Clinical and pathological findings suggested IMT. The mass was excised with an incision extending from the diaphragm to the pericardium, and the invaded part in the atrium was trimmed. After an uneventful pneumonectomy, the patient was discharged. Corticosteroid or chemotherapy was not considered because of the unclear benefits. Three months after pneumonectomy, the patient’s acute phase reactants decreased to normal levels and the febrile episodes diminished, due to resection of the inflammatory focus. A contrast-enhanced magnetic resonance scan performed three months after the pneumonectomy showed findings similar to the former magnetic resonance image, with two well-defined round lesions with perifocal edema.
Currently, the patient is being followed with regard to his growth velocity, potential adenohypophysis hormone deficiency, as well as with regard to cerebral lesions.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [142.0, 'mEq/L'], 'Glucose': [96.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [11.0, 'mg/dL']}",293.2619,278.59881,307.925,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. 
The concentration of bun is 11.0 mg/dL. 
The concentration of glucose is 96.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (11.0 / 2.8) + (11.0 / 18) = 293.2619 mmol/L.The patient's calculated serum osmolality concentration is 293.2619 mmol/L. This is equalivalent to 293.2619 mOsm/kg."
5596,30,Serum Osmolality,lab test,decimal,usmle-8498,Extracted,"A 60-year-old man with a long-standing history of type 2 diabetes and hypertension managed with lisinopril and metformin presents with itchy skin. He also describes moderate nausea, vomiting, muscle weakness, and fatigue. The vital signs include: temperature 36.8°C (98.2°F), heart rate 98/min, respiratory rate 15/min, blood pressure 135/85 mm Hg, oxygen saturation 100% on room air. Physical exam is notable for pale conjunctivae, pitting edema, and ascites. Laboratory findings are shown below:
BUN 78 mg/dL
pCO2 25 mm Hg
Creatinine 7.2 mg/dL
Glucose 125 mg/dL
Serum chloride 102 mmol/L
Serum potassium 6.3 mEq/L
Serum sodium 130 mEq/L
Total calcium 1.3 mmol/L
Magnesium 1.2 mEq/L
Phosphate 1.9 mmol/L
Hemoglobin 9.5 g/dL
MCV 86 μm3
Bicarbonate (HCO3) 10 mmol/L
Shrunken kidneys are identified on renal ultrasound. The doctor explains to the patient that he will likely need dialysis due to his significant renal failure until a renal transplant can be performed. The patient is concerned because he is very busy and traveling a lot for work.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [78.0, 'mg/dL'], 'Glucose': [125.0, 'mg/dL'], 'Sodium': [130.0, 'mEq/L']}",294.80159,280.06151,309.54167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. 
The concentration of bun is 78.0 mg/dL. 
The concentration of glucose is 125.0 mg/dL. 
Plugging these values into the equation, we get 2 * 130.0 + (78.0 / 2.8) + (78.0 / 18) = 294.80159 mmol/L.The patient's calculated serum osmolality concentration is 294.80159 mmol/L. This is equalivalent to 294.80159 mOsm/kg."
5597,30,Serum Osmolality,lab test,decimal,usmle-5286,Extracted,"A 57-year-old woman presents to the emergency department for laboratory abnormalities detected by her primary care physician. The patient went to her appointment complaining of difficulty using her hands and swelling of her arms and lower extremities. The patient has notably smooth skin that seems to have not aged considerably. Upon seeing her lab values, her physician sent her to the ED. The patient has a past medical history of multiple suicide attempts, bipolar disorder, obesity, diabetes, and anxiety. Her current medications include lithium, insulin, captopril, and clonazepam. The patient's laboratory values are below.

Serum:
Na+: 140 mEq/L
K+: 5.2 mEq/L
Cl-: 100 mEq/L
HCO3-: 20 mEq/L
BUN: 39 mg/dL
Glucose: 127 mg/dL
Creatinine: 2.2 mg/dL
Ca2+: 8.4 mg/dL

The patient is restarted on her home medications. Her temperature is 99.5°F (37.5°C), pulse is 80/min, blood pressure is 155/90 mmHg, respirations are 11/min, and oxygen saturation is 97% on room air.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [39.0, 'mg/dL'], 'Glucose': [127.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",300.98413,285.93492,316.03334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 39.0 mg/dL. 
The concentration of glucose is 127.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (39.0 / 2.8) + (39.0 / 18) = 300.98413 mmol/L.The patient's calculated serum osmolality concentration is 300.98413 mmol/L. This is equalivalent to 300.98413 mOsm/kg."
5598,30,Serum Osmolality,lab test,decimal,pmc-6174808-1,Extracted,"A morbidly obese 43-year-old female with a history of hypertension, dyslipidemia, and diabetes mellitus presented with severe abdominal pain. She had an episode of acute pancreatitis one year ago. She complained of right upper quadrant pain radiating to the back over 6-hour duration alongside six episodes of vomitus. A review of systems was only notable for a headache and dizziness. She reported no family history of dyslipidemia or acute pancreatitis. She denied tobacco, alcohol, or illicit substance use. There was no history of gallstones, appendectomy, new medications, procedures (including ERCP), or any complications related to her diabetes.
Admission vitals revealed afebrile patient with a heart rate of 103/min, respiratory rate of 20/min, BP 116/62 mmHg, and oxygen saturation of 96% on a nasal cannula at 5 liter/min. The patient was alert and orientated but was in moderate distress. The abdomen was obese and soft and with tenderness in the epigastric region. There was no guarding, rigidity, or Murphy's sign. Her body mass index (BMI) was 47.1. Other systemic signs of elevated triglycerides including xanthelasma, corneal arcus, and tendon xanthoma were absent.
Initial laboratory investigations showed an elevated white cell count of 16.9 μ/L (4.5 -11 μ/L), haemoglobin 12.2 g/dL (12-16 g/dL), platelet count 368000 mm3 (130,000-400,000mm3), sodium 129 mEq/L (136-144 mEq/L), potassium 3.8 mEq/L (3.5-5mEq/L), anion gap of 2 (8-16), BUN 45 mg/dL ( 7-20 mg/dL), creatinine 0.6 (0.4-1.3), glucose 206 mg/dL (74-117 mg/dL), and serum calcium 7.9 mg/dL (8.5-10.2 mg/dL). Liver function tests showed total bilirubin 0.5 mg/dL (0.1-1.2mg/dL), aspartate aminotransferase 16 IU/L (8-46 IU/L), alanine aminotransferase 11 U/L (7-55 IU/L), total protein 8.5 g/dL (6.1-7.9 g/dL), albumin 4 g/dL (3.5-5.5 g/dL), and PT 11.6 seconds (9.8-13.4 seconds). Initial arterial blood gas (ABG) analysis showed pH 7.5, pCO2 37.5, and pO2 67 at FiO2 of 40%.
The patient had an elevated lipase of 4143 U/L (reference 22-51 U/L), total cholesterol of 694 mg/dL (100-199 mg/dL), and a triglyceride level of 600 mg/dL (reference 0-149 mg/dL). Computed tomography (CT) of the abdomen showed diffuse enlargement of the pancreas consistent with pancreatitis (). There was no evidence of gallstones or biliary sludge which was also confirmed by an ultrasound abdomen. Other competing etiologies including alcohol, autoimmune pancreatitis, abdominal trauma, pancreatic divisum, sphincter of Oddi dysfunction (SOD), viral infection, drugs, and toxins were all ruled out, making the most likely diagnosis hypertriglyceridemia-induced AP (HTG AP).
The patient was treated with boluses of intravenous (IV) normal saline and supportive care. On the second day of admission, the patient developed hypotension and had persistent tachycardia. She likely developed acute respiratory distress syndrome (ARDS) from complications of acute pancreatitis. Fluid overload was ruled out with a sonogram of the inferior vena cava (diameter of 1.5 cm), a central venous pressure of 6 cm of H2O, and echocardiography indicating left ventricular ejection fraction of 55% with no left ventricular diastolic dysfunction. The patient was subsequently transferred to the intensive care unit for hypovolemic shock and respiratory distress requiring intubation and mechanical ventilation. As per revised Atlanta classification, she was categorized as severe acute pancreatitis based on Marshall scoring system for organ failure with a score of 3, with a score of 1 from respiratory failure (PaO2/FiO2 of 240) and two from cardiovascular (systolic BP <90, not fluid responsive). Patient's fasting blood glucose was 288 mg/dL (74-117 mg/dl), and diabetic ketoacidosis (DKA) was ruled out with the absence of serum or urine ketones, no elevated anion gap, and no acidosis. ABG analysis showed pH of 7.5, bicarbonate of 23, and an anion gap of 2.
Following the patients decline into shock, an ABG indicated an acidic pH of 6.99, PCO2 9.4, PO2 134, and HCO3 of 5.4. The serum bicarbonate level was low at 15mmol/L and the calculated anion gap was elevated at 22 (normal 8–16). Lactic acid level was 3.8 mmol/L (0.5-1.9 mmol/L).
Repeat abdominal contrast-enhanced CT on the third day showed marked pancreatic and peripancreatic infiltration consistent with AP and no signs of necrosis. Continuous insulin infusion was started for HTG from day 1, lowering her triglyceride levels down to 247 mg/dL over five days as shown in . She was also started on a liquid diet via nasogastric tube from day 5. After nine days in the ICU, the patient was successfully extubated and was switched to oral diet on day 11, which was gradually advanced as tolerated. She was downgraded to the floor on the same day and discharged on day 17. The patient required nasal oxygen to maintain saturation as she was recovering from ARDS. She was discharged on gemfibrozil 600mg twice daily to prevent further episodes of HTG AP. Patient has been followed upon discharge and remains compliant with gemfibrozil, leading to a controlled triglyceride level of 123 mg/dL and no further episodes of AP.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [129.0, 'mEq/L'], 'Glucose': [206.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [45.0, 'mg/dL']}",285.51587,271.24008,299.79166,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 129.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 129.0 mEq. To convert from 129.0 mEq to mmol, convert from mEq to mmol. The compound 129.0 has a valence of 1, and so divide the valence by the value of mEq to get, 129.0 mEq/(1 mEq/mmol) = 129.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 129.0 mEq sodium/L converts to 129.0 mmol sodium/L. 
The concentration of bun is 45.0 mg/dL. 
The concentration of glucose is 206.0 mg/dL. 
Plugging these values into the equation, we get 2 * 129.0 + (45.0 / 2.8) + (45.0 / 18) = 285.51587 mmol/L.The patient's calculated serum osmolality concentration is 285.51587 mmol/L. This is equalivalent to 285.51587 mOsm/kg."
5599,30,Serum Osmolality,lab test,decimal,pmc-2672257-1,Extracted,"A 37-year-old woman with a history of bulimia nervosa and depression ingested approximately seventy 20 mg fluoxetine capsules and 4–5 cans of beer in a self-professed suicide attempt. Shortly thereafter, she telephoned a friend who activated the EMS system. The patient’s prescribed medications were fluoxetine 20 mg daily and buspirone 15 mg twice daily. The patient stated that she had taken her buspirone only as directed, with the last dose on the morning of the fluoxetine overdose, about six hours earlier. She specifically denied ingesting any additional buspirone or any other medications. She admitted to “purging” herself daily for the last week. Other than some orthopedic surgical procedures, she denied any other significant past medical history, including seizures.
The paramedics arrived approximately 90 minutes post-ingestion and found the patient to be awake, alert, sitting up, and emotionally upset. The initial blood pressure was 142/palp and cardiac monitoring showed a sinus tachycardia at 120/minute. In the emergency department (ED) her vital signs were: temperature 37.2°C, pulse 91/min, blood pressure 132/72 mmHg, respirations 20/min, O2 saturation 99% on room air. The emergency physician noted the patient to be alert and oriented, but with slurred speech and slow verbal response time. The patient had a non-focal neurologic exam without tremor, rigidity, or hyperreflexia, and the remainder of the physical examination was without noted abnormalities. The patient was given 50 g of activated charcoal, and blood and urine samples were obtained for baseline values and for quantitative serum acetaminophen and salicylate measurements. Serum chemistries showed sodium 138 mmol/L, potassium 4.2 mmol/L, chloride 105 mmol/L, bicarbonate 23 mmol/L, BUN 11 mg/dL, creatinine 0.6 mg/dL, glucose 81 mg/dL, salicylate 3.9 mg/dL, acetaminophen <1μg/mL, and ethanol 48 mg/dL. A qualitative urine pregnancy test was negative. An electrocardiogram revealed a normal sinus rhythm of 97 beats per minute with normal intervals (QRS 88 msec, QTc 461 msec).
Approximately three hours after the ingestion, the patient cried out and then experienced a generalized tonic-clonic seizure lasting 30 seconds witnessed by the ED personnel. The seizure resolved spontaneously, and the patient had a post-ictal period lasting five minutes. The patient received an intravenous loading dose of phenobarbital (620 mg [10mg/kg]) and was then transported without incident to a regional toxicology referral center.
On arrival to the intensive care unit, the patient was somnolent but easily arousable. Vital signs were: temperature 36.9°C, pulse 82/min, blood pressure 112/78 mmHg, respirations 24/min. A repeat physical examination was unremarkable including the neurologic exam. Additional laboratory data obtained upon admission included serum creatinine kinase (140 IU/L), calcium (8.8 mg/dL), and a comprehensive urine drug screen (which combines the enzyme-multiplied immunoassay technique, thin layer chromatography, and gas chromatography/mass spectroscopy to detect over 1500 drugs and metabolites) that showed the presence of only phenobarbital, fluoxetine, ethanol, and caffeine. The laboratory verified that buspirone can be detected by this analysis. Quantitative serum levels of fluoxetine, norfluoxetine, and buspirone were ordered on admission. The fluoxetine level six hours after the ingestion was 922 ng/mL (therapeutic = 50–480 ng/mL) and the norfluoxetine level was 379 ng/mL (therapeutic = 50–450 ng/mL). The quantitative buspirone level could not be determined due to laboratory handling error. The patient was observed overnight without any further seizure activity or other unusual events. The psychiatry consultation and liaison service evaluated the patient the following morning and arranged for outpatient therapy. The patient was then discharged home in stable condition.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [138.0, 'mmol/L'], 'Blood Urea Nitrogen (BUN)': [11.0, 'mg/dL'], 'Glucose': [81.0, 'mg/dL']}",284.42857,270.20714,298.65,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mmol/L. 
The concentration of bun is 11.0 mg/dL. 
The concentration of glucose is 81.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (11.0 / 2.8) + (11.0 / 18) = 284.42857 mmol/L.The patient's calculated serum osmolality concentration is 284.42857 mmol/L. This is equalivalent to 284.42857 mOsm/kg."
5600,30,Serum Osmolality,lab test,decimal,usmle-12712,Extracted,"A 25-year-old man presents to the emergency department after fainting at his investment banking office. He states that he has experienced intermittent headaches since high school, but has never fainted. He reports eating multiple small meals regularly throughout the day. He further notes that multiple family members have frequently complained about headaches. Physical exam reveals a well-nourished, well-built, afebrile man with BP 170/80, HR 55, RR 10. Chemistries reveal Na 147, K 3, Cl 110, HCO3 30, BUN 25, Cr 1.1, glucose 120.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [25.0, 'mg/dL'], 'Glucose': [120.0, 'mg/dL'], 'Sodium': [147.0, 'mEq/L']}",309.59524,294.11548,325.075,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 147.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 147.0 mEq. To convert from 147.0 mEq to mmol, convert from mEq to mmol. The compound 147.0 has a valence of 1, and so divide the valence by the value of mEq to get, 147.0 mEq/(1 mEq/mmol) = 147.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 147.0 mEq sodium/L converts to 147.0 mmol sodium/L. 
The concentration of bun is 25.0 mg/dL. 
The concentration of glucose is 120.0 mg/dL. 
Plugging these values into the equation, we get 2 * 147.0 + (25.0 / 2.8) + (25.0 / 18) = 309.59524 mmol/L.The patient's calculated serum osmolality concentration is 309.59524 mmol/L. This is equalivalent to 309.59524 mOsm/kg."
5601,30,Serum Osmolality,lab test,decimal,pmc-8383553-1,Extracted,"A 13-year-old previously healthy female presented to a local hospital with a 1-month history of polydipsia and polyphagia and a 1-day history of fatigue, pallor, and Kussmaul breathing. Her initial blood glucose level was unobtainable due to serum appearing “milky” and the resultant turbidity interfering with the lab assay. Triglycerides were measured at 3,540 mg/dL (40.0 mmol/L). Urinalysis showed glycosuria and ketonuria. After the patient received appropriate fluid resuscitation, she was started on an insulin drip at 0.05 U/kg/h and transferred to our pediatric intensive care unit (PICU) for management of DKA, severe lipemia, and concern for possible cerebral edema.
On arrival to the PICU, the patient was tachycardic (heart rate of 166), tachypneic (respiratory rate of 41) with Kussmaul breathing, and disoriented. Her capillary blood gas revealed metabolic acidosis with respiratory compensation with a pH 7.10, pCO2 11.1 mm Hg, and HCO3 3.5 mmol/L. Her metabolic panel was remarkable for hyponatremia (sodium 121 mmol/L, uncorrected for hyperglycemia and hyperlipidemia), hypochloremia (chloride 85 mmol/L), acidosis (bicarbonate 6 mmol/L) with an anion gap of 30 mmol/L, hyperglycemia (glucose 533 mg/dL), and acute kidney injury with a blood urea nitrogen 25 mg/dL and creatinine 1.51 mg/dL. Potassium level was normal (4.5 mmol/L). Triglycerides were 7,556 mg/dL (85.4 mmol/L). Due to concern for cerebral edema, an intravenous dose of mannitol (0.5 g/kg) was given that resulted in improvement in her neurological status. She became more alert, oriented, and interactive and quickly returned to her neurological baseline.
The patient was treated with appropriate fluid replacement and insulin infusion of 0.1 U/kg/h. She had an uneventful resolution of her electrolyte abnormalities and hyperglycemia and successfully transitioned to subcutaneous insulin after 24 h. Her triglyceride levels initially increased to 22,228 mg/dL (251.2 mmol/L) but then trended down to 4,876 mg/dL (55.1 mmol/L). She was allowed to have a low-fat diet and her triglyceride levels rebounded to 14,443 mg/dL (163.2 mmol/L). She was noted to have scattered yellow-tinged papules on her upper and lower extremities, which were diagnosed by dermatology as eruptive xanthomas in the setting of hypertriglyceridemia (). She was also found to have mild pancreatitis with a lipase level of 272 U/L (normal 11 - 82 U/L). Liver transaminase levels were normal. An abdominal ultrasound revealed hepatosplenomegaly that was thought to be resulting from acute systemic metabolic abnormalities.
Due to severe and worsening hypertriglyceridemia, she was placed back on insulin and glucose infusions with restricted oral intake. Lipid-lowering treatment was started with oral fenofibrate 54 mg daily and omega-3-acid ethyl esters 4 g daily. After 7 days her triglyceride level had decreased to 1,337 mg/dL (15.1 mmol/L) and she transitioned back to subcutaneous insulin and a low-fat diet. Her triglyceride levels remained stable for 2 days on that regimen. The fenofibrate was increased to 145 mg daily and the omega-3-acid ethyl esters were discontinued. She was discharged to home with a triglyceride level of 1,187 mg/dL (13.4 mmol/L). Her treatment course and triglyceride levels are presented in .
At follow-up in diabetes clinic one month later, her triglycerides were normal at 65 mg/dL (0.73 mmol/L). She was complaining of vague musculoskeletal and abdominal discomfort intermittently and, therefore, the fenofibrate treatment was discontinued with close follow-up with a lipid specialist.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [25.0, 'mg/dL'], 'Glucose': [533.0, 'mg/dL'], 'Sodium': [121.0, 'mmol/L']}",280.53968,266.5127,294.56666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 121.0 mmol/L. 
The concentration of bun is 25.0 mg/dL. 
The concentration of glucose is 533.0 mg/dL. 
Plugging these values into the equation, we get 2 * 121.0 + (25.0 / 2.8) + (25.0 / 18) = 280.53968 mmol/L.The patient's calculated serum osmolality concentration is 280.53968 mmol/L. This is equalivalent to 280.53968 mOsm/kg."
5602,30,Serum Osmolality,lab test,decimal,pmc-3208579-1,Extracted,"A 63-year-old G2P2 female presented ambulatory to the ED with the chief complaint of abdominal pain, described further to the triage nurse as abdominal cramping and a mass in her vagina. The patient described that she had had a ""bulge"" in her vagina for the past 2 years and was currently being treated by her gynecologist for an enterocele with estrogen cream. Elective surgical repair of an enterocele was planned. She complained to the triage nurse of abdominal pain intermittently for the preceding 1 week. She stated that when she coughed something protruded from her vagina and she believed that her rectum had prolapsed. She was initially triaged to the lower acuity area of the emergency department, but due to worsening pain, she was brought back to a room on the acute care side approximately 30 min after her arrival. She described working in her garden when she coughed, experiencing a ""bulge"" extending through and out of her vagina. According to the patient, this ""bulge"" had been worsening for 2 months but had never extended past her labia. The patient complained of severe cramping in the left lower quadrant of her abdomen, but denied any diffuse abdominal pain. Her past medical history was significant for hypertension and breast cancer treated with surgery and chemotherapy without radiation. The patient did not have a history of vaginal or vulvar cancer. Her surgical history was significant for mastectomy and breast reconstruction, laparoscopic-assisted vaginal hysterectomy and bilateral oopherectomy (5 years previously), and pubovaginal sling (4 years previously).
On examination she was pleasant, appearing well and in no acute distress, with a temperature of 36.8 C°, pulse of 70, and blood pressure of 142/97 mmHg. Initial abdominal examination demonstrated no tenderness to palpation and no peritoneal signs. On genitourinary exam approximately 15 cm of small bowel protruded through the vaginal introitus (see Figure ). The bowel exhibited peristaltic waves and was dark red in color. Manual reduction was attempted to reduce strangulation, but was unsuccessful because of the large amount of bowel present and to the patient's discomfort during the attempt. Intravenous morphine was administered for pain control. Sterile moist gauze was placed over the eviscerated bowel, and the gynecology department was immediately consulted for surgical management of the patient. The patient was given a bolus of 1 l normal saline and intravenous ertapenam and metronidazole to cover enteric organisms.
Laboratory data results included white blood cell count, 5.9 k/ul; hemoglobin, 13.1 g/dl; hematocrit, 38.6%; platelets, 287 k/ul; prothrombin time and partial thromboplastin time were normal. Sodium was 142 mEq/l; chloride, 109 mEq/l; potassium, 3.8 mEq/l; bicarbonate 23 mEq/l; glucose, 123 mg/dl; blood urea nitrogen, 17 mg/dl; creatinine, 0.7 mg/dl; calcium 9.3 mg/dl. The electrocardiogram showed normal sinus rhythm, with left atrial enlargement.
While awaiting surgical consultation and 45 min after being placed in a room, the patient developed relative hypotension; her blood pressure decreased from 183/108 to 107/63 mmHg. She became less responsive and experienced rigors. Repeat abdominal exam showed diffuse abdominal tenderness with peritoneal signs that rapidly progressed to frank peritonitis. The herniated bowel had become dark and dusky. A second large bore IV was placed, and aggressive fluid resuscitation with 2 l normal saline was initiated. Her bed was placed in the Trendelenburg position to reduce tension on the eviscerated bowel, and preparations were made to intubate the patient because of her rapid decline. The fluid resuscitation was successful in improving her mental status and blood pressure, and she did not require intubation. She was transported quickly to the operating room for repair by both gynecology and general surgery physicians. General surgery resected approximately 20 cm of the distal ileum, which they noted to be inflamed and thickened with two areas of ischemia. This was followed by resection and repair of the vaginal cuff by gynecologic surgery. The patient was discharged from the hospital 6 days later in improved condition.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [142.0, 'mEq/L'], 'Glucose': [123.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [17.0, 'mg/dL']}",296.90476,282.05952,311.75,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. 
The concentration of bun is 17.0 mg/dL. 
The concentration of glucose is 123.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (17.0 / 2.8) + (17.0 / 18) = 296.90476 mmol/L.The patient's calculated serum osmolality concentration is 296.90476 mmol/L. This is equalivalent to 296.90476 mOsm/kg."
5603,30,Serum Osmolality,lab test,decimal,usmle-5711,Extracted,"A 32-year-old man is brought into the emergency department by his friends. The patient was playing soccer when he suddenly became short of breath. The patient used his albuterol inhaler with minimal improvement in his symptoms. He is currently struggling to breathe. The patient has a past medical history of asthma and a 25 pack-year smoking history. His current medications include albuterol, fluticasone, and oral prednisone. His temperature is 99.5°F (37.5°C), blood pressure is 137/78 mmHg, pulse is 120/min, respirations are 27/min, and oxygen saturation is 88% on room air. On pulmonary exam, the patient exhibits no wheezing with bilateral minimal air movement. The patient’s laboratory values are ordered as seen below.

Hemoglobin: 15 g/dL
Hematocrit: 43%
Leukocyte count: 5,500/mm^3 with normal differential
Platelet count: 194,000/mm^3

Serum:
Na+: 138 mEq/L
Cl-: 102 mEq/L
K+: 4.4 mEq/L
HCO3-: 24 mEq/L
BUN: 20 mg/dL
Glucose: 120 mg/dL
Creatinine: 1.0 mg/dL
Ca2+: 10.2 mg/dL
pH: 7.44
PaCO2: 10 mmHg
PaO2: 60 mmHg
AST: 12 U/L
ALT: 10 U/L

The patient is started on an albuterol nebulizer, magnesium sulfate, and tiotropium bromide. Repeat vitals reveal an oxygen saturation of 90% with a pulse of 115/min.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [120.0, 'mg/dL'], 'Sodium': [138.0, 'mEq/L']}",289.80952,275.31904,304.3,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 120.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (20.0 / 2.8) + (20.0 / 18) = 289.80952 mmol/L.The patient's calculated serum osmolality concentration is 289.80952 mmol/L. This is equalivalent to 289.80952 mOsm/kg."
5604,30,Serum Osmolality,lab test,decimal,pmc-3825672-1,Extracted,"A 21-year-old woman was admitted to the emergency department 4 hours after taking 20 tablets of CBS in a suicide attempt. Each tablet included 300 mg of CBS, which is equivalent to 120 mg of Bi2O3. There was no alcohol or another intravenous drug usage. In the emergency service, the patient underwent gastric lavage and received intravenous fluid therapy, after which she was admitted to the internal medicine intensive care unit.
Physical examination upon admission was unremarkable: blood pressure, 100/60 mm Hg; pulse, 76 beats/minute; respiration rate, 12 breaths/minute; and body temperature, 36.5°C. Laboratory tests were as follows: white blood cell count, 7860/mm3; hemoglobin, 10.8 g/dL; platelet count, 445,000/mm3; serum sodium, 141 mEq/L; potassium, 4.3 mEq/L; chloride, 104 mEq/L; glucose, 108 mg/dL; amylase, 85 U/L; aspartate aminotransferase (AST), 35 U/L; alanine aminotransferase (ALT), 14 U/L; lactate dehydrogenase (LDH), 150 U/L; hepatitis B surface antigen, nonreactive; and anti-hepatitis C virus, nonreactive. Her INR was reported to be normal at 1.1. Thyroid function tests were normal. Chest radiography also showed no abnormalities. Abdominal ultrasonography demonstrated slightly increased echogenicity in the renal parenchyma. Electrocardiography and echocardiography findings were normal. The patient rapidly became oliguric (<500 mL/day) and thereafter was anuric (0 mL/day). Blood creatinine increased to 2.6 mg/dL (blood urine nitrogen [BUN], 8 mg/dL) during the first 24 hours and to 3.1 mg/dL (BUN, 11 mg/dL) the next day. The baseline creatinine value was normal. Nevertheless, levels of LDH, ALT, and AST were elevated at 1,129 U/L, 62 U/L, and 139 U/L, respectively. Her scleraes were anicteric. The abdomen was soft, flat, and without palpable organomegaly. There was no edema. Arterial blood gases showed metabolic acidosis with a pH of 7.28, PaCO2 of 30 mmHg, PaO2 of 80 mmHg, BE of −11 mmol/L, and HCO3 of 14 mmol/L. Blood chemistry and urine sediment showed signs of proximal tubular dysfunction (Fanconi’s syndrome) with hypophosphatemia, hypouricemia, metabolic acidosis, and renal glycosuria despite normal plasma glucose concentration.
After consultation with personnel at Turkey’s National Poison Information Center, we started oral treatment with the chelating agent sodium-2,3-dimercapto-1-propanesulfonate (DMPS), which is related structurally to 2,3-dimercapto-1-propanol (dimercaprol, also known as British anti-Lewisite), using the following regimen: DMPS, 600 mg orally every 8 hours for 14 days. Hemodialysis was performed because of anuria and severe metabolic acidosis. Hemodialysis was conducted daily for the first 4 days and then three times weekly. Arterial blood gases returned to normal. Afterwards, the patient’s urine output progressively increased. Levels of LDH, ALT, and AST also returned to normal. The patient recovered clinically and was discharged after 15 days in hospital. Her serum creatinine and BUN levels upon discharge were 5.2 mg/dL and 20.0 mg/dL, respectively. Eight weeks after discharge, the patient’s renal function (serum creatinine and BUN) test results remained high. The patient is still on hemodialysis approximately 1 year later.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [108.0, 'mg/dL'], 'Sodium': [141.0, 'mEq/L']}",295.14286,280.38572,309.9,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 108.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (20.0 / 2.8) + (20.0 / 18) = 295.14286 mmol/L.The patient's calculated serum osmolality concentration is 295.14286 mmol/L. This is equalivalent to 295.14286 mOsm/kg."
5605,30,Serum Osmolality,lab test,decimal,usmle-672,Extracted,"A 9-year-old girl is admitted to the hospital with a one-day history of acute abdominal pain and vomiting. She also has a two-day history of fever, headache, and neck pain. Her immunizations are up-to-date. She is confused and oriented only to place and person. Her temperature is 39.7°C (103.5°F), pulse is 148/min, blood pressure is 90/50 mm Hg, and respiratory rate is 28/min. Cervical range of motion is limited by pain. The remainder of the neurologic examination shows no abnormalities. Laboratory studies show:
Hemoglobin 10.9 g/dL
Leukocyte count 44,000/mm3
Serum
pH 7.33
Na+ 130 mEq/L
Cl- 108 mEq/L
K+ 6.1 mEq/L
HCO3- 20 mEq/L
Urea nitrogen 34 mg/dL
Glucose 180 mg/dL
Creatinine 2.4 mg/dL
Urine ketones negative
A CT scan of the head shows enhancement of the arachnoid and pia mater. Cerebrospinal fluid analysis shows a leukocyte count of 3,400/μL (90% neutrophils), a glucose concentration of 50 mg/dL, protein concentration of 81 mg/dL, and no erythrocytes. Gram stain of the CSF shows gram-negative diplococci.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [130.0, 'mEq/L'], 'Glucose': [180.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [34.0, 'mg/dL']}",282.14286,268.03572,296.25,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. 
The concentration of bun is 34.0 mg/dL. 
The concentration of glucose is 180.0 mg/dL. 
Plugging these values into the equation, we get 2 * 130.0 + (34.0 / 2.8) + (34.0 / 18) = 282.14286 mmol/L.The patient's calculated serum osmolality concentration is 282.14286 mmol/L. This is equalivalent to 282.14286 mOsm/kg."
5606,30,Serum Osmolality,lab test,decimal,usmle-7444,Extracted,"A 66-year-old man presents to your office for a regular checkup. His only current complaint is periodic difficulty falling asleep at night. He takes captopril and hydrochlorothiazide for hypertension, atorvastatin for hyperlipidemia, and aspirin for cardiovascular disease prevention. His past medical history is significant for tympanoplasty performed 8 years ago for tympanic membrane rupture after an episode of purulent otitis media and intussusception that required surgical intervention 10 years ago. He also had a severe anaphylactic reaction after his 2nd Tdap administration 3 years ago. His blood pressure is 145/90 mm Hg, heart rate is 88/min, respiratory rate is 12/min, and temperature is 36.4°C (97.5°F). Physical examination only reveals a laterally displaced point of maximum impulse. Blood analysis shows the following findings:
Sodium
139 mEq/L (139 mmol/L)
Potassium
5.0 mEq/L (5.0 mmol/L)
Chloride
100 mEq/L (100 mmol/L)
Bicarbonate
22 mEq/L (22 mmol/L)
Albumin
3.8 mg/dL (38 g/L)
Urea nitrogen
8 mg/dL (2.86 mmol/L)
Creatinine
2.1 mg/dL (0.185 mmol/l)
Uric acid
5.8 mg/ dL (0.34 mmol/L)
Calcium
8.9 mg/ dL (2.22 mmol/L)
Glucose
106 mg/ dL (5.89 mmol/L)
Total cholesterol
254 mg/dL (5.57 mmol/L)
Low-density lipoprotein
58 mg/dL (1.5 mmol/L)
High-density lipoprotein
77 mg/dL (2.0 mmol/L)
Triglycerides
159 mg/dL (1.8 mmol/L)
The patient is concerned about pneumococcal infection. He has never been vaccinated against pneumococcus, and he would like to get the appropriate vaccination. You advise him that he should not be vaccinated with PCV13 (pneumococcal conjugate vaccine) and should instead be administered PPSV23 (pneumococcal polysaccharide vaccine).",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [139.0, 'mEq/L'], 'Glucose': [106.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [8.0, 'mg/dL']}",286.74603,272.40873,301.08333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 8.0 mg/dL. 
The concentration of glucose is 106.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (8.0 / 2.8) + (8.0 / 18) = 286.74603 mmol/L.The patient's calculated serum osmolality concentration is 286.74603 mmol/L. This is equalivalent to 286.74603 mOsm/kg."
5607,30,Serum Osmolality,lab test,decimal,pmc-7605961-1,Extracted,"A five-hour-old female baby was referred to our centre due to non-progressive abdominal distension since birth. This baby was born by caesarean section at term. The reason for C/section is unknown as the mother was unavailable at the time of admission. Birth weight at delivery was 2.4 kilograms and the APGAR score was 8 and 9 in the 1st and 5th minutes respectively. Antenatal history was uneventful and ultrasound done during pregnancy was normal. This is the first-born child to both parents. There are no reported cases of renal or malformations in the family.
Examination on admission showed the baby was sick looking, in respiratory distress and pink on oxygen therapy saturating at 97%. Her temperature was 36.9 °C, respiratory rate was 58 breaths/minute and Silverman Anderson score was 7. Her random blood glucose on admission was 5.8 mmol/L. In her respiratory system examination she had marked lower chest indrawing, nasal flaring and grunting with coarse crepitations throughout. Her abdomen was distended, soft with palpable kidneys bilaterally and the digital rectal exam was normal. On her central nervous system examination, she had a wide anterior fontanelle communicating with the posterior fontanelle with present reflexes. She had rocker bottom feet on musculo-skeletal examination.
Her abdominal pelvic ultrasound showed bilaterally enlarged echogenic kidneys with loss of cortico-medullary differentiation and multiple tiny cystic spaces. The right kidney was 8 х 3.3 cm and the left kidney was 7.4 х 3 cm. The rest of the findings were unremarkable. An echocardiogram showed patent ductus arteriosus and moderate tricuspid regurgitation with mild pulmonary regurgitation. Her blood workup showed a normal serum sodium level of 136.8 mmol/L, potassium of 5.6 mmol/L, urea of 3.74 mmol/L, serum creatinine of 133 µmol/L, AST of 28.3 U/L and ALT of 154.0 U/L, total protein of 58.0 g/L and albumin of 33.93 g/L. Serology for HIV was negative. We reached a diagnosis of polycystic kidney disease, early onset neonatal sepsis and acyanotic congenital heart disease. We started the baby on IV fluids of 10% dextrose 140 mL in 24 hours (we gave 75% of the maintenance fluid due to the underlying cardiac lesion), IV ampicillin 240 mg twice daily and kept the baby on CPAP.
The next day after admission during morning rounds this baby was still very sick looking, with coarse crepitations all over the chest and had passed only 10 mL of urine in the catheter. We gave intravenous furosemide 2 mg once daily. Unfortunately, seven hours later the baby changed condition and stopped breathing. She was resuscitated but it was unsuccessful and death was certified.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [136.8, 'mmol/L'], 'Glucose': [5.8, 'mmol/L'], 'Blood Urea Nitrogen (BUN)': [3.74, 'mmol/L']}",283.14767,268.99029,297.30505,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.8 mmol/L. 
The concentration of bun is 3.74 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 3.74 mmol. To convert 3.74 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 3.74 mmol bun * 0.001 mol/mmol = 0.00374 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.00374 mol bun * 28.02 g/mol = 0.10479 g bun. To convert 0.10479 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.10479 g bun * 1000.0 mg/g = 104.79 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 104.79 mg bun/10.0 dL = 10.479 mg bun/dL. The concentration value of 3.74 mmol bun/L converts to 10.479 mg bun/dL. 
The concentration of glucose is 5.8 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 5.8 mmol. To convert 5.8 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 5.8 mmol glucose * 0.001 mol/mmol = 0.0058 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0058 mol glucose * 180.16 g/mol = 1.04493 g glucose. To convert 1.04493 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 1.04493 g glucose * 1000.0 mg/g = 1044.93 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1044.93 mg glucose/10.0 dL = 104.493 mg glucose/dL. The concentration value of 5.8 mmol glucose/L converts to 104.493 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 136.8 + (10.479 / 2.8) + (10.479 / 18) = 283.14767 mmol/L.The patient's calculated serum osmolality concentration is 283.14767 mmol/L. This is equalivalent to 283.14767 mOsm/kg."
5608,30,Serum Osmolality,lab test,decimal,pmc-8702392-1,Extracted,"A 50-year-old woman with a medical history of chronic neck and back pain secondary to a motor vehicle accident (MVA) in 2016, who had been receiving outpatient epidural injections for pain control, presented to the emergency room with complaints of severe headache. She reported that she had a cervical epidural injection roughly 30-45 minutes prior to this event.
She described the headache as sharp in character, constant, at the base of her skull, and 10/10 in severity with radiation to the neck and upper back. It was not relieved by lying down. Her headache was also associated with nausea, vomiting, and photophobia. She denied having a history of fever or neck rigidity.
On presentation, her vital signs were as follows: systolic blood pressure (SBP): 190 mmHg; diastolic blood pressure (DBP): 97 mmHg; pulse rate: 62 beats/min; respiratory rate: 18/min; and temperature: 37.8° Celsius (100° Fahrenheit). On examination, the patient was alert, oriented to time, place, and person, and was able to follow commands. Cranial nerves and visual field examination was negative for any focal deficits; extra-ocular muscles were intact without nystagmus; pupils were symmetrical, round, and reactive to light; the facial sensation was intact to light touch, and facial movements were full and symmetric with no dysarthria; the soft palate was elevated symmetrically; shoulder shrug strength was full bilaterally; and tongue protrusion in the midline with full side-to-side movement. On motor examination, the tone was normal in passive range of motion in the four limbs, power was normal and equal bilaterally, deep tendon reflexes were symmetric bilaterally, Babinski’s sign was negative with toes going downward bilaterally, no dysmetria in finger-nose testing, and she was able to stand without assistance. Sensory examination showed intact sensation to light touch in the bilateral upper and lower extremities.
Blood work showed the following findings: sodium: 136 mEq/L; potassium: 4.1 mEq/L; blood urea nitrogen (BUN)/creatinine: 10/0.66; glucose: 182 mg/dL; white blood cell (WBC) count: 21.2/L; hemoglobin: 14.5 g/dL; and platelets: 289/L.
A head computed tomography (CT) scan was performed, which showed newly evident pneumocephalus in the ventricular system and the extra-axial subarachnoid space within the sulci of the right frontal lobe (Figures , ).
The patient was then admitted with a working diagnosis of pneumocephalus most likely in the setting of traumatic cervical epidural injection.
Pain control was done with butalbital (50 mg)/acetaminophen (325 mg)/caffeine (40 mg) oral tablet, with Dilaudid and ketorolac as needed. Oxygen supplementation was done with the help of a non-rebreather mask connected to 15 liters of oxygen, which was gradually tapered down to 6 liters via a high-flow nasal cannula after 24 hours.
Cervical and thoracic spine magnetic resonance imaging was performed with and without contrast to rule out epidural abscesses that showed multiple levels of spondylosis mainly prevalent in C4-C7 without evidence of epidural fluid collection.
A repeat CT scan of the head was done after 48 hours, which showed complete resolution of the intracranial pneumocephalus (Figure ).
Her headache gradually improved and oxygen supplementation was then discontinued.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [136.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [10.0, 'mg/dL'], 'Glucose': [182.0, 'mg/dL']}",285.68254,271.39841,299.96667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.0 mEq. To convert from 136.0 mEq to mmol, convert from mEq to mmol. The compound 136.0 has a valence of 1, and so divide the valence by the value of mEq to get, 136.0 mEq/(1 mEq/mmol) = 136.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mEq sodium/L converts to 136.0 mmol sodium/L. 
The concentration of bun is 10.0 mg/dL. 
The concentration of glucose is 182.0 mg/dL. 
Plugging these values into the equation, we get 2 * 136.0 + (10.0 / 2.8) + (10.0 / 18) = 285.68254 mmol/L.The patient's calculated serum osmolality concentration is 285.68254 mmol/L. This is equalivalent to 285.68254 mOsm/kg."
5609,30,Serum Osmolality,lab test,decimal,pmc-4541682-1,Extracted,"A 47-year-old man visited the emergency room because of decreased mentality. He was diagnosed with diabetes mellitus (DM), but had not received regular treatment. His blood pressure was 60/30 mm Hg and body temperature was 38.5℃. Laboratory data showed white blood cell of 13.150×109/L, with a differential count of 90.7% neutrophils and 8.5% lymphocytes, hemoglobin of 14.3 g/dL, platelet count of 507×109/L, glucose levels of 443 mg/dL, blood urea nitrogen of 52.5 mg/dL, serum creatinine concentrations of 1.9 mg/dL, aspartate aminotransferase of 69 IU/L, alanine transaminase of 38 IU/L, sodium of 125.7 mmol/L, potassium of 5.4 mmol/L, C-reactive protein (CRP) levels of 19.42 mg/dL, ketone bodies in the blood 3 positive and HbA1c of 18.20%. Arterial blood gas analysis revealed a pH of 7.032, pCO2 of 21.8 mm Hg, pO2 of 83.3 mm Hg, and HCO3 of 5.8 mmol/L. Chest X-ray and computed tomography (CT) scans showed multiple consolidation and ground glass opacities in both lung fields (). The patient was initially diagnosed with diabetic ketoacidosis as a result of severe pneumonia. An immediate hydration and insulin therapy were started, and dose-adjusted piperacillin and tazobactam sodium were also administered for pneumonia. The patient was admitted to the intensive care unit (ICU) for mechanical ventilator therapy. The ketoacidosis had improved with hydration and insulin therapy, but on the second day of hospitalization, diuretic-resistant pulmonary edema developed and continuous renal replacement therapy was started. Klebsiella pneumonia was identified in sputum cultures. After 8 days of treatment, the lung lesions had regressed (). The patient was finally moved to the general ward. However, on the 5th day in the general ward, he started complaining of vague abdominal pain. His pain had aggravated with severe tenderness. An erect abdominal X-ray showed gaseous distention of small bowel loops with suspicious stepladder sign, suggesting mechanical obstruction (). Subsequent abdominal CT suggested multiple perforation of the transverse colon with panperitonitis ().
An emergency laparotomy was performed. Necrotic intestines were observed from the distal ascending colon to the proximal transverse colon. Necrotic portions were resected and the Periodic Acid Schiff and Grocott's methenamine silver staining of the resected specimen showed septated fungal hyphae with acute angle branching, suggesting aspergillus species (). The patient was finally diagnosed with colonic IA. Intravenous liposomal amphotericin-B (3 mg/kg/day) was additionally administered for 35 days. He was discharged with oral voriconazole to treat his reported remaining, abdominal discomfort and mildly elevated CRP levels. Voriconazole was discontinued at a follow-up visit to the outpatient department 2 weeks after discharge when his abdominal discomfort had relieved and CRP levels normalized.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [52.5, 'mg/dL'], 'Glucose': [443.0, 'mg/dL'], 'Sodium': [125.7, 'mmol/L']}",294.76111,280.02305,309.49917,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 125.7 mmol/L. 
The concentration of bun is 52.5 mg/dL. 
The concentration of glucose is 443.0 mg/dL. 
Plugging these values into the equation, we get 2 * 125.7 + (52.5 / 2.8) + (52.5 / 18) = 294.76111 mmol/L.The patient's calculated serum osmolality concentration is 294.76111 mmol/L. This is equalivalent to 294.76111 mOsm/kg."
5610,30,Serum Osmolality,lab test,decimal,usmle-6934,Extracted,"A 24-year-old woman is brought to the emergency room (ER) by her co-workers after they found her unconscious in her cubicle when they returned from lunch. They tell you that she has diabetes but do not know anything more about her condition. The woman’s vital signs include: pulse 110/min, respiratory rate 24/min, temperature 36.7°C (98.0°F), and blood pressure 90/60 mm Hg. On physical examination, the patient is breathing heavily and gives irrelevant responses to questions. The skin and mucous membranes appear dry. Examination of the abdomen reveals mild diffuse tenderness to palpation. Deep tendon reflexes in the extremities are 1+ bilaterally. Laboratory studies show:
Finger stick glucose 630 mg/dL
Arterial blood gas analysis:
pH 7.1
PO2 90 mm Hg
PCO2 33 mm Hg
HCO3 8 mEq/L
Serum:
Sodium 135 mEq/L
Potassium 3.1 mEq/L
Chloride 136 mEq/L
Blood urea nitrogen 20 mg/dL
Serum creatinine 1.2 mg/dL
Urine examination shows:
Glucose Positive
Ketones Positive
Leukocytes Negative
Nitrite Negative
RBCs Negative
Casts Negative
The patient is immediately started on a bolus of intravenous (IV) 0.9% sodium chloride (NaCl).",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [630.0, 'mg/dL'], 'Sodium': [135.0, 'mEq/L']}",312.14286,296.53572,327.75,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 135.0 mEq. To convert from 135.0 mEq to mmol, convert from mEq to mmol. The compound 135.0 has a valence of 1, and so divide the valence by the value of mEq to get, 135.0 mEq/(1 mEq/mmol) = 135.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mEq sodium/L converts to 135.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 630.0 mg/dL. 
Plugging these values into the equation, we get 2 * 135.0 + (20.0 / 2.8) + (20.0 / 18) = 312.14286 mmol/L.The patient's calculated serum osmolality concentration is 312.14286 mmol/L. This is equalivalent to 312.14286 mOsm/kg."
5611,30,Serum Osmolality,lab test,decimal,usmle-7982,Extracted,"A 32-year-old woman is admitted to the hospital after undergoing an open cholecystectomy under general anesthesia. Preoperatively, the patient was administered a single dose of intravenous ceftriaxone. Now, the anesthetic effects have worn off, and her pain is well managed. The patient has a prior medical history of hypertension which has been well-controlled by captopril for 2 years. Her vitals currently show: blood pressure 134/82 mm Hg, heart rate 84/min, and respiratory rate 16/min. Postoperative laboratory findings are significant for the following:
Serum glucose (random) 174 mg/dL
    Serum electrolytes
Sodium 142 mEq/L
Potassium 3.9 mEq/L
Chloride 101 mEq/L
    Serum creatinine 0.9 mg/dL
Blood urea nitrogen 10 mg/dL
    Alanine aminotransferase (ALT) 150 U/L
Aspartate aminotransferase (AST) 172 U/L
Serum bilirubin (total) 0.9 mg/dL
Preoperative labs were all within normal limits.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [10.0, 'mg/dL'], 'Glucose': [174.0, 'mg/dL'], 'Sodium': [142.0, 'mEq/L']}",297.2381,282.37619,312.10001,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. 
The concentration of bun is 10.0 mg/dL. 
The concentration of glucose is 174.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (10.0 / 2.8) + (10.0 / 18) = 297.2381 mmol/L.The patient's calculated serum osmolality concentration is 297.2381 mmol/L. This is equalivalent to 297.2381 mOsm/kg."
5612,30,Serum Osmolality,lab test,decimal,usmle-6070,Extracted,"A 27-year-old college student presents to his physician for constant fatigue. The patient states that for the past several weeks he has felt oddly fatigued and has struggled to complete his work. He is a foreign exchange student and is concerned he will fail out of his academic program. He has experienced some occasional nausea and vomiting which has caused him to lose weight. The patient is a first year college student, drinks alcohol regularly, smokes marijuana, and has unprotected sex with multiple partners. His temperature is 99.5°F (37.5°C), blood pressure is 127/68 mmHg, pulse is 90/min, respirations are 17/min, and oxygen saturation is 98% on room air. Laboratory values are ordered as seen below.

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.2 mg/dL
Total bilirubin: 2.0 mg/dL
AST: 85 U/L
ALT: 92 U/L

Urine
Color: Amber/brown
Marijuana: Positive
Amphetamines: Positive
Cocaine: Positive

The patient refuses an examination of his genitals.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [99.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",290.64286,276.11072,305.175,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (20.0 / 2.8) + (20.0 / 18) = 290.64286 mmol/L.The patient's calculated serum osmolality concentration is 290.64286 mmol/L. This is equalivalent to 290.64286 mOsm/kg."
5613,30,Serum Osmolality,lab test,decimal,usmle-5351,Extracted,"A 30-year-old man presents to his primary care physician complaining of headaches. He states that over the past month he has been trying to study for an accounting exam, but he finds it increasingly more difficult to focus due to his headaches. He also complains of lower extremity muscle cramping. He has no significant past medical history and takes ibuprofen and acetaminophen as needed. The patient’s temperature is 98°F (36.7°C), blood pressure is 168/108 mmHg, and pulse is 75/min. Labs are obtained, as shown below:

Serum:
pH (VBG): 7.50
Na: 146 mEq/L
K+: 3.2 mEq/L
Cl-: 104 mEq/L
HCO3-: 32 mEq/L
Urea nitrogen: 20 mg/dL
Creatinine: 1.1 mg/dL
Glucose: 85 mg/dL

An ultrasound reveals a hypoechoic lesion within the right adrenal gland. A 2 cm right-sided homogeneous adrenal mass is confirmed with computed tomography.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [85.0, 'mg/dL'], 'Sodium': [146.0, 'mEq/L']}",303.86508,288.67183,319.05833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 146.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 146.0 mEq. To convert from 146.0 mEq to mmol, convert from mEq to mmol. The compound 146.0 has a valence of 1, and so divide the valence by the value of mEq to get, 146.0 mEq/(1 mEq/mmol) = 146.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 146.0 mEq sodium/L converts to 146.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 85.0 mg/dL. 
Plugging these values into the equation, we get 2 * 146.0 + (20.0 / 2.8) + (20.0 / 18) = 303.86508 mmol/L.The patient's calculated serum osmolality concentration is 303.86508 mmol/L. This is equalivalent to 303.86508 mOsm/kg."
5614,30,Serum Osmolality,lab test,decimal,pmc-4766335-1,Extracted,"A twelve-year-old girl, with past medical history of Dravet syndrome and developmental delay, presented to our hospital emergency department with altered sensorium, one-day history of fever up to 105.6 F, decreased oral intake and urine output, fatigue, and intermittent cough. Seizure frequency was unchanged. Her home medications were valproic acid, clobazam, potassium bromide, and diazepam. On arrival to the emergency room she was found to be hypotensive (65/39 mmHg), tachycardic, and febrile. She received two normal saline boluses. Her laboratory results in emergency room included serum sodium 143 mEq/L, potassium 4.3 mEq/L, chloride 171 mEq/L, bicarbonate 24 mEq/L, Blood Urea Nitrogen (BUN) 12 mg/dL, serum creatinine 0.57 mg/dL, calcium 9.2 mg/dL, blood glucose of 60 mg/dL, and valproic acid level 23.7 mcg/L (therapeutic level 50–100 mcg/L), and normal liver function tests were performed. Her capillary blood gas revealed pH 7.40, PCO2 37.1 mmHg, bicarbonate 23.2 mEq/L, and base deficit −1 mEq/L. In the pediatric intensive care unit (PICU) patient remained stable, received intravenous fluids, was tested positive for influenza, and started on oseltamivir. Repeat electrolyte panel on multiple occasions, as shown in , had hyperchloremia (154–171 mEq/L) with negative anion gap (−40 to −52 mEq/L). Due to persistent hyperchloremia and as the patient takes potassium bromide for the past two years for refractory seizures possibility of bromide toxicity was considered. On day one of admission to PICU, potassium bromide therapy was stopped and serum bromide level was sent. The bromide level was 691 mcg/mL (normal therapeutic range 200–1000 mcg/mL). Despite normal bromide level in our patient potassium bromide was temporarily withheld and continued on IV hydration therapy. Over the next three days serum chloride and child's clinical condition improved.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [12.0, 'mg/dL'], 'Glucose': [60.0, 'mg/dL'], 'Sodium': [143.0, 'mEq/L']}",293.61905,278.9381,308.3,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 143.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 143.0 mEq. To convert from 143.0 mEq to mmol, convert from mEq to mmol. The compound 143.0 has a valence of 1, and so divide the valence by the value of mEq to get, 143.0 mEq/(1 mEq/mmol) = 143.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mEq sodium/L converts to 143.0 mmol sodium/L. 
The concentration of bun is 12.0 mg/dL. 
The concentration of glucose is 60.0 mg/dL. 
Plugging these values into the equation, we get 2 * 143.0 + (12.0 / 2.8) + (12.0 / 18) = 293.61905 mmol/L.The patient's calculated serum osmolality concentration is 293.61905 mmol/L. This is equalivalent to 293.61905 mOsm/kg."
5615,30,Serum Osmolality,lab test,decimal,pmc-4421245-1,Extracted,"A 49-year-old male presented with severe nephrotic syndrome (proteinuria 16.8 g/day, serum albumin 1 g/dL, 3+ lower extremity oedema, severe dyslipidaemia resistant to statins), gastrointestinal bleeding and weight loss. His past medical history was notable for a coronary artery disease and myocardial infarction. Renal function tests were within normal limits, with blood urea of 13 mg/dL and serum creatinine of 0.9 mg/dL. Serum glucose (71 mg/dL), potassium (4.7 mmol/L) and sodium (140 mmol/L) were within normal limits. Tests for hepatitis B surface antigen and antibodies against hepatitis C virus and human immunodeficiency virus were negative. Tests for antinuclear antibody and anti-double stranded DNA antibody were also negative. Serum complement (C) levels were within normal range (C3: 159 mg/dL, C4: 29 mg/dL) and the serum protein electrophoresis showed no M-spike. Renal sonogram revealed normal size kidneys and an unusual mass in the left flank region. Abdominal magnetic resonance imaging showed a large (12.6 cm × 11.2 cm × 10.1 cm) heterogeneous mass of the proximal jejunum. Biopsies of both the tumour and the kidney were performed. The tumour biopsy confirmed spindle cell neoplasm, composed of uniform cells arranged in poorly formed fascicles and exhibiting scattered mitotic figures. Immunoperoxidase stains for CD34 and CD117 (c-kit) were positive in the tumour cells, while stains for smooth muscle actin, desmin and pancreatin were negative. Given the histological immunostaining properties and size of the mass, the diagnosis of gastrointestinal stromal tumour (GIST) of high malignant potential was made.
Renal biopsy was performed to investigate the cause of proteinuria. On light microscopy, the biopsy showed 71 glomeruli of normal size and cellularity. Endocapillary or extracapillary proliferative changes were not present in the glomeruli. Periodic acid-Schiff and Jones’ methenamine silver-stained sections demonstrated uniform thickening of the glomerular capillary walls with ‘crater’ and fine ‘spike’-like projections. Immunoperoxidase stain for c-kit was performed and it was negative. Immunofluorescence studies showed fine granular deposition of IgG (3+), C3 (2+) and C4 (1+) along the peripheral capillary loops. Trace deposition of IgA, IgM and C1q was also noted in the same distribution. Ultrastructural analysis revealed numerous fine granular subepithelial electron-dense deposits, separated from each other by basement membrane ‘spikes’ (Figure ). Small subendothelial electron-dense deposits were also seen in several places. The mesangium revealed normal cellular elements and a mildly expanded extracellular matrix with scattered, in some places large, electron-dense deposits (Figure ). The diagnosis of MN was made. Because of the presence of subendothelial and mesangial deposits, a secondary form of MN was suggested.
Following the biopsy results, the patient was placed on oral imatinib mesylate (400 mg/day) for 8 months, and the surgical excision of the tumour was performed when the tumour became resectable. Imatinib mesylate has been administrated continuously. The patient had never received any specific immunosuppressive therapy for MN, but his proteinuria slowly decreased to 3.0 g/day at the time of surgery, and completely resolved at 8 months after surgery (Figure ). At that time the patient had no oedema, his serum albumin was 4.6 g/dL, serum creatinine was 1.0 mg/dL and the dyslipidaemia had resolved as well.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [13.0, 'mg/dL'], 'Glucose': [71.0, 'mg/dL'], 'Sodium': [140.0, 'mmol/L']}",288.5873,274.15794,303.01667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mmol/L. 
The concentration of bun is 13.0 mg/dL. 
The concentration of glucose is 71.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (13.0 / 2.8) + (13.0 / 18) = 288.5873 mmol/L.The patient's calculated serum osmolality concentration is 288.5873 mmol/L. This is equalivalent to 288.5873 mOsm/kg."
5616,30,Serum Osmolality,lab test,decimal,pmc-4109115-1,Extracted,"In December 2012, a 39-year-old Chinese woman complaining of anuria with lower abdominal pain visited our hospital. She had not received unremarkable medical treatments before except for the right lateral allogeneic renal transplantation in 2009 at another hospital (hereafter referred to as Hospital A) owing to uremia. Initially, she had a good postoperative recovery via routinely taking the antirejection immunosuppressants cyclosporin A and prednisone. Simultaneously, she took calcitriol to manage commonly encountered HPT and osteoporosis after renal transplantation []. However, she had undergone anuria with lower abdominal pain 6 months ago, which was diagnosed as acute unilateral ureteral obstruction. Subsequently, the patient had been receiving retrograde internal 6F ureteral double J stenting provided by Bard-InLay and discharged from Hospital A. Unfortunately, she had been harassed by the identical symptoms 2 months later. Although Bard-InLay stent was the most commonly used auxiliary implement in urological interventions for its tapered tip and lubricious coating to facilitate smooth insertion and effective negotiation around obstructions, clinicians in Hospital A had substituted domestic ureteral stent brand of YZB/Jiangsu-0038-2004 for Bard-InLay, in view of different adaptabilities to the stents caused by racial diversity and personality. Surprisingly, only 3 weeks later, it is necessary for the patient to receive the third double J stent placement to solve the extremely same problem of anuria and abdominal symptoms. Even so, this last try in Hospital A was still invalid after one month.
After viewing the medical history, we began to make a physical examination for her. She had unremarkable physical signs except for a suffering moon face and slight abdominal bulge and pain. Routine blood investigation file revealed red blood cells, white blood cells, and platelet counts of 4.11 × 1012/L, 10.38 × 109/L, and 322 × 109/L, respectively. Besides, the following data were obtained: total protein, 54.8 g/L; albumin, 29.0 g/L; glucose, 4.69 mmol/L; urea nitrogen, 2.84 mmol/L; creatinine, 61 μmol/L; potassium, 3.30 mmol/L; sodium, 135.5 mmol/L; chlorinum, 103.1 mmol/L; magnesium, 0.63 mmol/L; phosphonium, 1.00 mmol/L; intact PTH, 32.1 pg/mL; 24-hour urine calcium, 4.42 mmol/L; and calcium, 2.19 mmol/L. For the imaging diagnosis, type-B ultrasound revealed moderate hydronephrosis of the transplanted kidney in the right lateral of pelvic cavity. Kidney-ureter-bladder (KUB) radiography clearly showed the stent modified by cutting a length of 9 cm from one end of the classical 25 cm full-length double J ureteral stent to improve its clinical acceptability (as the donor kidney is usually placed in a lower position in the pelvic cavity) (, red arrows, and ). After careful and detailed examinations, we conducted the operation to substitute a new Bard-InLay internal 6F double J stent for the originally blocked one. Subsequently, infrared spectrum analysis elucidated that the calculi in the completely blocked stent consisted of whewellite, weddellite, and carbonated apatite (Figures and , red arrows and dashed lines). The patient's urine volume reached 4300 mL the next whole day after operation. Besides, her kidney function tests and multiple urine cytologies were absolutely normal. After discontinuing calcitriol, the patient was found to be calculi-free and the 9-month follow-up showed a good recovery without stent obstruction or anuria with lower abdominal pain, which she had been confronting several times before receiving the appropriate management in our hospital.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [2.84, 'mmol/L'], 'Glucose': [4.69, 'mmol/L'], 'Sodium': [135.5, 'mmol/L']}",278.53631,264.60949,292.46313,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.5 mmol/L. 
The concentration of bun is 2.84 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 2.84 mmol. To convert 2.84 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 2.84 mmol bun * 0.001 mol/mmol = 0.00284 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.00284 mol bun * 28.02 g/mol = 0.07958 g bun. To convert 0.07958 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.07958 g bun * 1000.0 mg/g = 79.58 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 79.58 mg bun/10.0 dL = 7.958 mg bun/dL. The concentration value of 2.84 mmol bun/L converts to 7.958 mg bun/dL. 
The concentration of glucose is 4.69 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 4.69 mmol. To convert 4.69 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 4.69 mmol glucose * 0.001 mol/mmol = 0.00469 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.00469 mol glucose * 180.16 g/mol = 0.84495 g glucose. To convert 0.84495 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 0.84495 g glucose * 1000.0 mg/g = 844.95 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 844.95 mg glucose/10.0 dL = 84.495 mg glucose/dL. The concentration value of 4.69 mmol glucose/L converts to 84.495 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 135.5 + (7.958 / 2.8) + (7.958 / 18) = 278.53631 mmol/L.The patient's calculated serum osmolality concentration is 278.53631 mmol/L. This is equalivalent to 278.53631 mOsm/kg."
5617,30,Serum Osmolality,lab test,decimal,pmc-4025155-1,Extracted,"An 8-year-old boy was admitted with a history of abdominal bloating associated with rectal tenesmus and increased flatus. These symptoms recurred especially during the afternoon and evening. No associated gastrointestinal symptoms were reported. His clinical history was characterized by rumination in the first years of life with associated non-organic feeding disorders as a picky eater. Radioallergosorbent test for alimentary and inhalant allergens, skin prick tests and celiac screening was negative. Ultrasonography did not reveal any organomegaly or fluid presence in the abdomen. Abdominal radiographs showed a distended colon with increased gas in the rectum and coprostasis, without signs of obstruction. On physical examination, weight was 22 kg and height 129 cm, with a mild degree of malnutrition according to the Waterloo classification. Cardiorespiratory objectivity was normal. A significantly non-tender, hypertympanitic abdominal distension was present. No hepatomegaly nor splenomegaly were noted. Rectal examination revealed a sensation of hypertonic anus sphincter without perineal erythema and stool. Neurologic examination was normal. The following laboratory investigations were performed: complete blood count (red blood cell count 5.1 × 106/mm3, Hb 13.8 g/dl, HCT 43%, MCV 84 fl, white blood cell count 5 × 103/mm3, neutrophils 34%, lymphocytes 60%, monocytes 4%, eosinophils 2%, basophils 0%, platelets 297 × 103/mm3), C-reactive protein was 0.10 mg/dl (normal 0–0.50 mg/dl), erythrocyte sedimentation rate 5 mm within the first hour, glycemia 68 mg/dl, serum glutamic oxaloacetic transaminase 26 IU/l, serum glutamic pyruvate transaminase 14 IU/l, serum gamma-GT 7 IU/l, amylase 67 U/l, lipase 27 U/l, BUN 26 mg/dl, creatine 0.5 mg/dl, iron 54 μg/dl, sodium 140 mmol/l, potassium 4.3 mmol/l, calcium 9.78 mg/dl, total proteins 7.1 g/dl, and albumin 48 g/l; coagulation parameters and urinalysis were normal. Also, lactate dehydrogenase (395 U/l), muscle enzymes (creatine phosphate kinase 75 IU/l, CK-MB 10 IU/l), thyroid hormones (free thyroxine 10.98 pmol/l, thyroid-stimulating hormone 1.925 μIU/ml), celiac serology, cytomegalovirus, Epstein-Barr virus, herpesvirus serology and autoantibodies (ANA, nDNA, ANCA) were normal, and megacolon was excluded using barium enema. After ruling out primary pathologic causes, a neuropsychiatric consultation was requested with the disclosure of continuous aerophagia and anxiety disorder with obsessive compulsive notes and game-playing dependency. It was possible to reassure the family on the absence of an organic gastrointestinal disease with indications to neuropsychiatric and cognitive follow-up.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [26.0, 'mg/dL'], 'Glucose': [68.0, 'mg/dL'], 'Sodium': [140.0, 'mmol/L']}",293.06349,278.41032,307.71666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mmol/L. 
The concentration of bun is 26.0 mg/dL. 
The concentration of glucose is 68.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (26.0 / 2.8) + (26.0 / 18) = 293.06349 mmol/L.The patient's calculated serum osmolality concentration is 293.06349 mmol/L. This is equalivalent to 293.06349 mOsm/kg."
5618,30,Serum Osmolality,lab test,decimal,pmc-7026865-1,Extracted,"An 82-year-old man with the past medical history of congestive heart failure (ejection fraction 30-35%), non-ischemic cardiomyopathy and history of a permanent pacemaker for sick sinus syndrome and normal functional and mental status at baseline was brought to our hospital for acute onset of lethargy and confusion for two days. On examination, his blood pressure was 150/77 mmHg, heart rate 64 beats/minute, respiratory rate 16/minute, temperature 36.9 degree Celsius, saturation 100% on room air. His Glasgow Coma Score was 9. He had no signs of meningeal irritation; no focal motor deficit was noted, no facial droop, no tremor of extremities, normal flexor plantar response with normal deep tendon reflexes. We were unable to completely assess the sensory system and all 12 cranial nerves due to encephalopathy. His cardiovascular, respiratory and abdominal examination did not reveal any abnormalities. There were no skin rashes and no significant lymphadenopathy. The family denied any head trauma, fever, chills, sick contacts, and recent travel. No new medications were prescribed to the patient before this presentation. His total leucocyte count was 6.26 x 103/µL, blood urea nitrogen 8 mg/dl (reference range: 6-20), serum creatinine 0.82 mg/dl (reference range: 0.6-1.00), serum sodium 138 mmol/L (reference range: 133-145), serum potassium 3.8 mmol/L (reference range: 3.5-5.5), magnesium 2.1 mg/dl (reference range: 1.7-2.2), phosphorus 4.1 mg/dl (reference range: 2.5-4.5), serum glucose 134 mg/dl (reference range: 70-130), aspartate aminotransferase 20 units/L (reference range: 15-37), alanine aminotransferase 31 units/L (reference range: 30-65), serum lactic acid 1.8 mmol/L (reference range: 0.5-2.2). His vitamin B12 and serum folic acid level were normal. Urinalysis and urine culture ruled out urinary tract infection. His computed tomography (CT) of the head without contrast did not reveal any acute intracranial pathology (Figure ).
A urine drug screen was non-revealing; serum alcohol level was 3 mg/dL (reference: 0-10). Electrocardiogram showed normal sinus rhythm without any ST-T wave changes and chest X-ray did not show any evidence of acute radiographic abnormality (Figure ).
Arterial blood gas showed ph 7.44, pCO2 35.2 mmHg, pO2 98 mmHg, bicarbonate 23.2 mmol/L on room air. Blood cultures did not show any growth. We did not perform a lumbar puncture, as there was no suspicion for acute meningoencephalitis based on history and examination. Electroencephalogram showed mild to moderate slowing with theta frequency predominantly consistent with mild to moderate encephalopathy.
His serum ammonia level was elevated to 274 μmol/L (reference range: 11-35). CT of the abdomen without contrast did not reveal cirrhotic changes of the liver (Figure ).
A liver ultrasound with Doppler showed the normal size and echo texture of the liver and mildly dilated main portal vein. It also showed patent hepatic and portal veins with normal directional flow seen through the portal vein (Figure ).
Hepatitis A IgM antibody, hepatitis B surface antigen, hepatitis B core IgM antibody were non-reactive while hepatitis C antibody titer was less than 0.1 signal to cut off ratio (reference range <0.8). Esophagogastroduodenoscopy did not reveal esophageal varices or any source of active bleeding. Serum and urine amino acid concentration obtained by liquid chromatography-mass spectrometry did not reveal aminoacidopathy. On careful review of the patient’s history before hospital admission, it was revealed that he was severely constipated for at least a week before the onset of encephalopathy. The cause of severe constipation could not be exactly determined. There was no new medication prescribed or use of sodium valproate at home. We treated the patient with lactulose through nasogastric tube 20 gm every six hours to maintain 3-4 loose stools per day. The patient’s serum ammonia level trended down to 46 and thereafter to 30 μmol/L after four days. Mental status improved significantly with a decrease in hyperammonemia and relief of constipation. He was subsequently transferred out of ICU and strongly recommended to avoid constipation with as-needed use of lactulose.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [8.0, 'mg/dL'], 'Glucose': [134.0, 'mg/dL'], 'Sodium': [138.0, 'mmol/L']}",286.30159,271.98651,300.61667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mmol/L. 
The concentration of bun is 8.0 mg/dL. 
The concentration of glucose is 134.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (8.0 / 2.8) + (8.0 / 18) = 286.30159 mmol/L.The patient's calculated serum osmolality concentration is 286.30159 mmol/L. This is equalivalent to 286.30159 mOsm/kg."
5619,30,Serum Osmolality,lab test,decimal,pmc-6037803-3,Extracted,"An 18-year-old girl presented with fatigue, anorexia, indigestion, constipation, and postprandial abdominal pain. She was diagnosed with cecal diverticulosis 5 years earlier, and Helicobacter pylori (HP)-positive gastric ulcer 1 year earlier. A previous UGI endoscopic examination showed no polyp in her stomach. On laboratory examination, WBC was 8,200/mm3, with polymorphonuclear cell 65%, hemoglobin 13.6 g/dL, and platelet count 205×103/mm3. Electrolytes levels showed sodium 142 mmol/L, potassium 4.4 mmol/L and chloride 106 mmol/L. The protein level was 7.4 g/dL, albumin 4.7 g/dL, calcium 9.3 mg/dL, phosphorus 4.7 mg/dL, cholesterol 167.9 mg/dL, glucose 99 mg/dL, BUN 10.1 mg/dL, creatinine 0.77 mg/dL, total bilirubin 0.35 mg/dL, AST 14 U/L, ALT 5 U/L, ESR 10 mm/hour, and CRP <0.3 mg/dL. UGI endoscopy revealed nodular gastritis in the antrum and a polyp of sessile type in the prepyloric area. Polypectomy was performed. The size of the polyp was 0.8×0.6×0.5 cm. She was negative to HP at the time of polypectomy. The pathological finding was HPP (). She was treated with medicines for her UGI mucosal lesions and the previous GI symptoms were resolved. Follow-up UGI endoscopy would be performed in one year.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [10.1, 'mg/dL'], 'Glucose': [99.0, 'mg/dL'], 'Sodium': [142.0, 'mmol/L']}",293.10714,278.45178,307.7625,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mmol/L. 
The concentration of bun is 10.1 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (10.1 / 2.8) + (10.1 / 18) = 293.10714 mmol/L.The patient's calculated serum osmolality concentration is 293.10714 mmol/L. This is equalivalent to 293.10714 mOsm/kg."
5620,30,Serum Osmolality,lab test,decimal,pmc-5705885-1,Extracted,"A 20-year-old healthy female presented to the emergency room with confusion, vomiting, and generalized tonic-clonic seizure. She was last seen in her usual state of health 12 hours prior to arrival. Friends reported that she consumed an unknown amount of alcohol and ingested a quarter tablet of MDMA. The patient subsequently became paranoid, attempted to climb up walls, and drank ten bottles of water. She had a witnessed generalized tonic-clonic seizure with frothing at the mouth and recurrent seizure en route the Emergency Department. Both seizures broke spontaneously. Her initial vital signs were notable for a temperature of 38.0 degrees Celsius, heart rate of 88 beats/minute, blood pressure of 140/70 mm Hg, respiratory rate of 14 per minute, and oxygen saturation of 97% on room air. The patient was obtunded, and pupils were dilated, equal, and reactive to light bilaterally. Mucus membranes were moist. Neck was supple. Lung auscultation demonstrated good air entry with bilateral rhonchi. Cardiovascular examination was normal without any murmurs, rubs, or gallops. Abdominal exam was normal. Neurologic examination was limited but the patient had normal extremity tone, hyporeflexia was noted in biceps, triceps, knees, and ankles bilaterally, clonus was absent, and normal bilateral Babinski reflexes were noted. She received 10 mg of IV lorazepam for additional seizures and was intubated for airway protection. A summary of relevant laboratory findings is mentioned in . Her initial complete blood count had a white blood cell count of 20,600/μliter, hemoglobin of 12.8 g/dl, and platelet count of 233,000/μliter. Her chemistry panel was as follows: sodium 112 mmol/L, potassium 3.5 mmol/L, chloride 84 mmol/L, bicarbonate 16 mmol/L, blood urea nitrogen of 7 mg/dl, serum creatinine of 0.5 mg/dl, and serum glucose of 117 mg/dl. A liver function panel was normal.
Serum lactic acid was 2.8 and osmolality was 239 mmol/L. Urine chemistries were significant for a urine sodium 112 mmol/L and urine osmolality of 439 mmol/L. The urine electrolytes were checked prior to administration of any hypertonic saline. These electrolyte derangements suggested a state of syndrome of inappropriate antidiuretic hormone (SIADH). She received three doses of 3% hypertonic normal saline without a significant change in her serum sodium. A brain computed tomography (CT) scan showed cerebral edema.
Over the next couple of hours, she had increasing oxygen requirements on the ventilator of up to 100% FiO2 and a positive end-expiratory pressure of 20 mm Hg. The initial chest-radiograph was concerning for multifocal pneumonia; however a repeat chest-radiograph, twelve hours later, revealed diffuse bilateral hazy opacities concerning for acute respiratory distress syndrome (ARDS). Her blood gas analysis showed a pH of 7.28 with PaO2 of 53 mm Hg and an alveolar-arterial oxygen gradient of 492 mm Hg. Her PaO2 : FiO2 ratio was 53 suggesting severe ARDS. At that time, she was paralyzed with cis-atracurium and started on inhaled nitric oxide as salvage therapy. She subsequently developed hemodynamic compromise and was started on norepinephrine, ultimately requiring addition of vasopressin and dopamine to maintain stable hemodynamics. Finally, venovenous extracorporeal membrane oxygenation (ECMO) was started with immediate resolution of hypoxemia. Hyponatremia was corrected gradually with 3% hypertonic saline that led to resolution of altered mental status and improvement in hypoxemia. She was gradually weaned off of ECMO and extubated within three days.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [7.0, 'mg/dL'], 'Glucose': [117.0, 'mg/dL'], 'Sodium': [112.0, 'mmol/L']}",233,221.35,244.65,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 112.0 mmol/L. 
The concentration of bun is 7.0 mg/dL. 
The concentration of glucose is 117.0 mg/dL. 
Plugging these values into the equation, we get 2 * 112.0 + (7.0 / 2.8) + (7.0 / 18) = 233.0 mmol/L.The patient's calculated serum osmolality concentration is 233.0 mmol/L. This is equalivalent to 233.0 mOsm/kg."
5621,30,Serum Osmolality,lab test,decimal,pmc-3236148-1,Extracted,"A 64-year-old man with a history of hypertension, chronic kidney disease, and liver failure secondary to hepatitis C, with status post liver transplant 13 years priorly, was brought in by ambulance to the emergency department for acutely altered mental status. The patient had been in his usual state of health, until he told his family 3 hours before that he “felt sick.” The family incidentally found him on the floor, confused and lethargic, and immediately called the ambulance.
Upon arrival, the patient had a temperature of 96.4°F; pulse, 117 beats per minute; blood pressure, 151/93 mmHg; respiratory rate, 22 breaths per minute; and oxygen saturation of 100% on nonrebreather. The patient was known to have a history of recurrent episodes of hepatic encephalopathy, and his last episode of hepatic encephalopathy was in the prior 3 months, which was treated and controlled with lactulose. The patient's family stated that the patient had run out of lactulose 4 days before presentation. Other than lactulose, the patient was compliant with all of his home medications, including amlodipine, buproprion, cyclosporine, hydrocodone, lasix, methocarbamol, and ramipril. The patient had no known history of seizure, recent illness, brain trauma, or recent surgical procedures.
Physical examination showed a male in no acute distress with a Glasgow Coma Scale of 12 (eyes, 4; verbal, 3; motor, 5). There were no signs of trauma found on his body. His pupils were equally round and reactive to light, and his neck was supple and soft with a cervical collar in place. Cardiopulmonary examination was unremarkable except for tachycardia. Abdominal examination was unremarkable. Because he was not following commands, the neurologic examination was limited. However, the patient was able to move all extremities equally and pulses were distally equal to all extremities. There was no posturing or clonus noted, and Babinski was downgoing in both feet.
Fingerstick glucose level was 210 mg/dL and bedside hemoglobin level was 13.1 g/dL. Noncontrast head and cervical spine computed tomography revealed no acute pathologic lesion. Chest radiography also showed no acute pathologic lesion. Laboratory tests showed white blood cell counts of 5.5 K/mm3 with 60% neutrophils, hematocrit of 36.5%, and platelets of 115 K/mm3. Electrolyte and liver function results were as follows: sodium, 141 mmol/L; potassium, 3.5 mmol/L; chloride, 104 mmol/L; bicarbonate, 22 mmol/L; calcium, 9.3 mg/dL; blood urea nitrogen, 71 mmol/L; creatinine, 1.9 mg/dL; total bilirubin, 2.1 mg/dL; aspartate aminotransferase, 128 U/L; alanine aminotransferase, 124 U/L; alkaline phosphatase, 231 U/L; albumin, 4.0 g/dL; lipase, 30 U/L; prothrombin time, 14.5 seconds; INR, 1.09; and ammonia, 501 μmol/L (reference range, 15–55 μmol/L). Toxicology serum screen results were negative for acetaminophen, salicylate, and ethanol. Urine toxicology screen results were positive only for opiates. Venous blood gas was pH 7.44.
Owing to the patient's obtunded condition and inability to protect his airway, the patient was electively intubated and given midazolam drip for sedation. The patient was admitted to the intensive care unit (ICU) for monitoring with a presumed diagnosis of hepatic encephalopathy. While administration of empiric antibiotics was started in the emergency department, it was discontinued after an infectious etiology was deemed unlikely and culture results were negative. Results of a magnetic resonance imaging brain scan were also negative, including no evidence of infarct.
During the ICU stay, the patient was readministered lactulose, and ammonia levels decreased to117 μmol/L by hospital day 2 and to 78 μmol/L by hospital day 4. Despite discontinuation of sedation, the patient remained unresponsive. A neurologist was consulted and a bedside electroencephalogram (EEG) revealed findings consistent with status epilepticus. However, the patient had no clinical manifestations of status epilepticus, leading to a diagnosis of nonconvulsive status epilepticus. A phenytoin load was immediately administered, while a midazolam infusion was restarted, ultimately leading to EEG resolution of the status epilepticus. The patient did not immediately improve neurologically during the hospitalization stay and was ultimately transferred to another facility for continued treatment and rehabilitation.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [71.0, 'mmol/L'], 'Glucose': [210.0, 'mg/dL'], 'Sodium': [141.0, 'mmol/L']}",364.71738,346.48151,382.95325,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mmol/L. 
The concentration of bun is 71.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 71.0 mmol. To convert 71.0 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 71.0 mmol bun * 0.001 mol/mmol = 0.071 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.071 mol bun * 28.02 g/mol = 1.98942 g bun. To convert 1.98942 g of bun to mg, multiply by the conversion factor 1000.0, giving us 1.98942 g bun * 1000.0 mg/g = 1989.42 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1989.42 mg bun/10.0 dL = 198.942 mg bun/dL. The concentration value of 71.0 mmol bun/L converts to 198.942 mg bun/dL. 
The concentration of glucose is 210.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (198.942 / 2.8) + (198.942 / 18) = 364.71738 mmol/L.The patient's calculated serum osmolality concentration is 364.71738 mmol/L. This is equalivalent to 364.71738 mOsm/kg."
5622,30,Serum Osmolality,lab test,decimal,pmc-8500255-1,Extracted,"A 77-year-old woman with anemia, CKD stage V, and hypertension was transferred from a medical clinic to the emergency department of Wangaya General Hospital, Bali. The patient had nausea and vomiting with a frequency of more than ten times a day for the past ten days. Fatigue and a decrease in appetite were also found. The patient had hypertension for five years with uncontrolled blood pressure and did not consume any drugs. There was no previous history of seizure and hemodialysis.
On arrival, she had a Glasgow Coma Scale (GCS) of E4V5M6, blood pressure was 160/70 mmHg, heart rate was 69 beats per minute, respiratory rate was 20 breaths per minute, body temperature was 36.5ºC, and oxygen saturation was 99% in room air. The other examinations including respiratory, cardiovascular, abdominal, and neurological were normal. The result of laboratory blood test revealed haemoglobin 10.7 g/dL (12-16 g/dL), blood glucose 120 mg/dL (80-200 mg/dL), blood urea nitrogen (BUN) 179 mg/dL (10-50 mg/dL), serum creatinine 11.6 mg/dL (0.3-1.2 mg/dL), serum sodium 116 mmol/L (130-145 mmol/L), potassium 6.3 mmol/L (3.5-5.5 mmol/L), and chloride 103 mmol/L (95-108 mmol/L). According to the Cockcroft-Gault equation, the calculated glomerular filtration rate (GFR) was less than 15 mL/minute/1.73 m².
The patient was admitted for the management of CKD stage V, anemia, hypertension, and electrolyte imbalance. Her initial ECG showed normal sinus rhythm with peaked T waves (Figure ). During hospitalization, no seizure episodes were reported. Subsequently, hemodialysis was planned for the next two days as the patient were on the waiting list. The first hemodialysis was performed after two days, which lasted for three hours with a blood flow rate of 300 mL/ per minute, and 1000ml of total body fluid was removed. The patient suffered an episode of first witnessed tonic-clonic seizure approximately seven hours following hemodialysis. This seizure episode was resolved by itself, and the patient was back to baseline with minor complaints of headache following dialysis.
After a neurologic consult, a non-contrast CT brain (Figure ) was obtained, which did not show any hemorrhage, infarct, or space-occupying lesion (SOL) intracranially. Neurology also recommended diazepam 10 mg IV (as needed) for any future breakthrough seizure episodes. Blood chemistry after initial hemodialysis revealed serum sodium at 134 mmol/L, potassium at 4.5 mmol/L, chloride at 98 mmol/L, BUN at 132 mg/dL, and serum creatinine at 11.1 mg/dL. The second hemodialysis was completed three days after the first session with a similar blood flow rate of 300 mL/min, removal of 1000 ml total body fluid in four hours duration. The patient suffered another tonic-clonic seizure eight hours after the hemodialysis lasting thirty seconds and resolved by itself before diazepam was injected. A re-evaluation of blood chemistry was done. Blood electrolyte was normal, BUN was 95 mg/dL, and serum creatinine was 3 mg/dL. In the next four days, the patient had received the third session of hemodialysis with adjusted duration and blood flow rate (two hours; 150 mL/min). This time, the patient did not experience any seizure activity at all. She was diagnosed with dialysis disequilibrium syndrome.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [179.0, 'mg/dL'], 'Glucose': [120.0, 'mg/dL'], 'Sodium': [116.0, 'mmol/L']}",302.59524,287.46548,317.725,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 116.0 mmol/L. 
The concentration of bun is 179.0 mg/dL. 
The concentration of glucose is 120.0 mg/dL. 
Plugging these values into the equation, we get 2 * 116.0 + (179.0 / 2.8) + (179.0 / 18) = 302.59524 mmol/L.The patient's calculated serum osmolality concentration is 302.59524 mmol/L. This is equalivalent to 302.59524 mOsm/kg."
5623,30,Serum Osmolality,lab test,decimal,usmle-1490,Extracted,"A 62-year-old man comes to the physician because of fatigue and swelling of the lower legs for 3 weeks. One year ago, he had an 85% stenosis in the left anterior descending artery, for which he received 2 stents. He was diagnosed with hepatitis C 5 years ago. He has type 2 diabetes mellitus and arterial hypertension. Current medications include aspirin, metformin, and ramipril. He does not smoke or drink alcohol. His temperature is 37°C (98.6°F), pulse is 92/min, and blood pressure is 142/95 mm Hg. Examination shows 2+ pretibial edema bilaterally. The remainder of the examination shows no abnormalities. Laboratory studies show:
Hemoglobin 10.2 g/dL
Leukocyte count 6500/mm3
Platelet count 188,000/mm3
Serum
Na+ 137 mEq/L
Cl− 105 mEq/L
K+ 5.2 mEq/L
Urea nitrogen 60 mg/dL
Glucose 110 mg/dL
Creatinine 3.9 mg/dL
Albumin 3.6 mg/dL
HbA1C 6.8%
Urine
Blood negative
Glucose 1+
Protein 3+
WBC 0–1/hpf
A renal biopsy shows sclerosis in the capillary tufts and arterial hyalinosis.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [60.0, 'mg/dL'], 'Glucose': [110.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",301.53968,286.4627,316.61666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 60.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (60.0 / 2.8) + (60.0 / 18) = 301.53968 mmol/L.The patient's calculated serum osmolality concentration is 301.53968 mmol/L. This is equalivalent to 301.53968 mOsm/kg."
5624,30,Serum Osmolality,lab test,decimal,pmc-3042401-1,Extracted,"A 80-year-old Caucasian man presented to our hospital with acute right lower quadrant and periumbilical abdominal pain. He had no history of previous alcohol abuse, cholelithiasis, abdominal trauma or surgery, nor ingestion of raw food or medications. On admission, hematological tests revealed normal hematocrit and platelet counts, and an increased white blood cell count of 23,800 mm-3 (reference range: 4,000 to 10,000 mm-3) with 37.8% lymphocytes. The biochemical test results were within the reference range: ALT: 11 U/L (0 to 35), AST: 12 (0 to 35), glucose: 123, urea: 49, and creatinine: 1,1, Na: 142, K: 4.9, and serum amylase: 3157 UI/L (10 to 110). A computed tomographic (CT) abdominal scan was performed revealing necrosis over 30% of the pancreas and the presence of liquid in the peripancreatic cavity (Figure ). With this finding, it was decided to perform an endoscopic ultrasound. The pancreatic parenchyma showed a slightly abnormally structured and irregular mass-like aspect on the head, compatible with an inflammatory process. The pancreatic body reflected a homogeneous pattern with an irregular and slightly dilated main pancreatic duct. In the neck of the pancreas, a cystic lesion with a dense aspect of 42.2 × 35.1 mm was revealed, probably related to a pseudocystic versus postnecrotic cavity. A gallbladder with hyperechogenic foci without an acoustic shadow floating inside, which is compatible with microlithiasis, was described. Endoscopy ultrasound fine needle aspiration (EUS-FNA; by using lineal equipment and a 22G needle puncture) was performed over the injury in the pancreatic head (Figure ). Samples obtained were submitted for cytohistological and microbiological evaluation. Pathology results showed small fragments of pancreatic parenchyma without evidence of malignancy surrounded by areas of necrosis and inflammation. Microbiological analysis reveals a monoculture isolating Citrobacter freundii by biochemical testing with an API 20E system (API Biomerieux SA, Marcy I'Etoile, France yielded the numerical code 1604572 for the isolate. According to the API 20E database, this represented a ""very good identification"" for C. freundii. An analysis using 16SrRNA gene by PCR-Sequencing method was performed to confirm the pathogen identity. 16SrRNA gene of strain and Citrobacter freundii (FN997639) has the nearest kinship and are located in the same phylogenetic tree.
Experiments with this bacterium in cell lines (cytopathic effect) and rats (i.p. injection) were performed and showed vacuolization of the cells as well as development of acute pancreatitis in the rats, demonstrating high levels of virulence of the strain. Susceptibility testing showed intermediate susceptibility to cefuroxim, although it was completely susceptible to ciprofloxacin. Oral ciprofloxacine (500 mg × 2) was administrated over six weeks. During treatment our patient progressed satisfactorily. A week after starting the treatment, he felt well and the abdominal pain gradually decreased. With the diagnosis of an acute necrotizing pancreatitis complicated with a pseudocystic percutaneous, he was discharged and referred to our Pancreatobiliary Unit. An abdominal ultrasound (Figure ) performed six months later revealed a complete resolution of the previous inflammatory process.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [49.0, 'mg/dL'], 'Glucose': [123.0, 'mg/dL'], 'Sodium': [142.0, 'mEq/L']}",308.33333,292.91666,323.75,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. 
The concentration of bun is 49.0 mg/dL. 
The concentration of glucose is 123.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (49.0 / 2.8) + (49.0 / 18) = 308.33333 mmol/L.The patient's calculated serum osmolality concentration is 308.33333 mmol/L. This is equalivalent to 308.33333 mOsm/kg."
5625,30,Serum Osmolality,lab test,decimal,pmc-4877837-1,Extracted,"The 5 year old female child enjoyed good health in the past until three days before the admission when she began to have high fever, vomiting and diarrhea. The child was treated by the mother with different formulation of acetaminophen as suppositories 250 mg and tablets 500 mg every 3 hours for three consecutive days. The used dose of acetaminophen was calculated by the physician at the admission time to Pediatric Intensive Care Unit of UHC, being approximately 90 mg/kg/24h for the last 72 hours. No other concomitant medication was administered.
At the admission the child presented with high fever, vomiting, confusion, drowsiness alternated with agitation especially to external stimuli. On examination, absent neck stiffness, Babinski response was negative, pupils were slightly midriatic, corneal reflex was present, sensible only to pain according to AVPU evaluation and was classified as grade II to III of encephalopathy, dehydrated and icteric. The arterial pressure was 90/50 mmHg, heart rate was 160/min, the respiratory rate was 45/min the temperature was 39°C, the pulsoximeter 97% saturation in room air. Abdominal palpation revealed liver enlargement 2-3 cm under the costal arch, and a soft palpable abdomen. The bedside blood sugar was 45 mg/dl, ALT 5794 UI/L, AST 6000 UI/L, Total Bilirubine 3.5 mg/dl, INR 3.86, blood urea 80 mg/dl, blood creatinine 1.3 mg/dl, 8GT 60 UI/l, Na+ 111 mmol/l, K+3.5 mmol/l. The blood albumin level 3 g/dl, Red blood cells 4.4*1012/L, Hemoglobine 12.3 g/dl, Platelets 332*109/L, White blood cell 25*109/L C reactive Protein 70 mg/dl. A careful disease history was taken and acetaminophen poisoning was strongly suspected. The blood acetaminophen obtained 10 hours after the last administered dose, was sent abroad having the positive result 32.9 mg/l. The viral serologic profile includes HIV, HEV, HAV, HCV, HBV, Coksaxie Virus, influenza A, B, Adeno Virus, was negative. The chest radiograph was normal. Blood culture failed to isolate any microorganism. NAC was immediately given by nasogastric tube as the only drug formulation the hospital could provide according to the standard oral guideline with 140 mg/kg loading dose followed by 70 mg/kg every 4 hours for a total of 18 doses over 72 hours. Oral feeding was stopped and the hydration was maintained by electrolytic solution.
After administration of 18 oral recommended NAC doses of hepatic failure treatment protocol, the renal indicators as blood creatinine, blood urea and the liver enzymes were improved but without INR. The coagulopathy aggravated with clinical manifestations of melena and hematemesis despite the therapy with fresh frozen plasma, Vitamin K, Human Albumin, Acid tranexamic, Lactulose. Abdomen became painful and the blood sugar 340 mg/dl, hypernatremia 160 meq/l, hypokalemia 2.7 meq/l. Acute pancreatitis was suspected and confirmed by hyperamylasaemia 255 UI/l, hyperlypasaemia 514 UI/l, and ultrasound examination which revealed a swollen pancreas and minimal peritoneal liquid at Douglas space. Accordingly the therapy was modified to parenteral hydration, fluid and electrolytes correction and reduces enteral stimulation. A further 24 hours of NCA treatment was added until the INR and pancreatic enzyme decline.
As the patient condition improved in terms of hepatic failure and clinical acute pancreatitis, the fever remained high with chills and high spikes. The patient developed left leg pain with thrombophlebitis and coccygofemoral arthritis.
The repeated blood culture finally isolated Klebsiella pneumoniae despite the extendum spectrum antibiotics (Cefuroxime 150 mg/kg/day and gentamicin 5 mg/kg/day) and the therapy was adopted according to antibiotic susceptibility (Piperacillin-Tazobactam and Amikacin) supported with Pentaglobine. This situation required also the use of anticoagulant (Fraxiparin 2850 UI s/c) and Ibuprofen. Despite the long progress of the disease the child recovered totally within 29 days with a complete resolution of all clinical and laboratory abnormalities. The liver function tests remained in normal range during the following up of 1st, 3rd, 6th and 12th month.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [111.0, 'mmol/L'], 'Glucose': [340.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [80.0, 'mg/dL']}",269.46032,255.9873,282.93334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 111.0 mmol/L. 
The concentration of bun is 80.0 mg/dL. 
The concentration of glucose is 340.0 mg/dL. 
Plugging these values into the equation, we get 2 * 111.0 + (80.0 / 2.8) + (80.0 / 18) = 269.46032 mmol/L.The patient's calculated serum osmolality concentration is 269.46032 mmol/L. This is equalivalent to 269.46032 mOsm/kg."
5626,30,Serum Osmolality,lab test,decimal,pmc-3505931-1,Extracted,"A 74-year-old female patient was admitted to the Internal Medicine Department of the public Kozani General Hospital with extended skin detachment of 24-hour duration. For the past 7 days she had received trimethoprim-sulfamethoxazole (960 mg twice daily) for a lower urinary tract infection.
On admission confluent erythema and widespread epidermal necroses (~25% body surface) were present that affected face, trunk, and extremities including palms and soles, with a positive Nikolsky's sign (). Mouth erosions and enema of conjunctivae were also present. Her vitals included 140/65 mmHg blood pressure, 78 pulses/min, and temperature 38.5°C. Her medical history was remarkable for arterial hypertension on perindopril/indapamide, nephrolithiasis treated with citric acid/monosodium citrate per os and anxiety on bromazepam and alprazolam. She was on these medications without any alterations for the previous 6 months. The laboratory workout () revealed white blood count 3.72 × 103 cells/mL (75% neutrophils, 20% lymphocytes, 3% monocytes); hemoglobin: 10.7 g/dL; hematocrit: 32.7%; platelets: 221 × 103 cells/mL; C-reactive protein: 10.6 mg/dL; blood urea nitrogen: 107 mg/dL; serum creatinin: 1.91 mg/dL; alkaline phosphatase: 40 ng/mL; serum glucose: 208 mg/dL; aspartate aminotransferase: 92 U/L; alanine aminotransferase: 177 U/L; bicarbonates: 20.1 mEq/L; Na+: 131 mEq/L; K+: 4.08 mEq/L; total serum protein: 6.3 g/dL. The constellation of clinical and laboratory data sets the diagnosis of TEN. Her SCORTEN index2 was 3 (age > 40 years old, blood urea nitrogen > 28 mg/dL, body surface involvement > 10%) which corresponds to an expected mortality risk of 35.8%.
Immediately after the establishment of diagnosis, treatment was initiated in loco according to a recent therapeutic proposal []. She was not transferred to a reference center as she strongly wished to be nursed nearby her residence. Additionally her unstable condition was considered as a relative hindrance for this. The patient received 500 mg methylprednisolone bolus i.v. followed by 5 mg/kg i.v. infliximab. High-dose intravenous immunoglobulin (2 g/kg) was initiated the same day and was given over the next 5 days. She was also treated with appropriate supportive measures, including careful monitoring of liquid and electrolytes equilibrium and wound care. Already from the second day of hospitalization the skin condition markedly stabilized and the patient's status improved rapidly thereafter (). The patient was discharged after 19 days in stationary care in excellent general condition and remained without any sequels 9 months afterwards.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [107.0, 'mg/dL'], 'Glucose': [208.0, 'mg/dL'], 'Sodium': [131.0, 'mEq/L']}",311.76984,296.18135,327.35833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 131.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 131.0 mEq. To convert from 131.0 mEq to mmol, convert from mEq to mmol. The compound 131.0 has a valence of 1, and so divide the valence by the value of mEq to get, 131.0 mEq/(1 mEq/mmol) = 131.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 131.0 mEq sodium/L converts to 131.0 mmol sodium/L. 
The concentration of bun is 107.0 mg/dL. 
The concentration of glucose is 208.0 mg/dL. 
Plugging these values into the equation, we get 2 * 131.0 + (107.0 / 2.8) + (107.0 / 18) = 311.76984 mmol/L.The patient's calculated serum osmolality concentration is 311.76984 mmol/L. This is equalivalent to 311.76984 mOsm/kg."
5627,30,Serum Osmolality,lab test,decimal,pmc-4035763-1,Extracted,"A 66-year-old Caucasian woman with type 2 diabetes presented to our emergency department with a three-week history of generalized malaise, associated poor oral intake, and some diarrhea. Her enteric symptoms were vague and unquantifiable. She was obese and had a past medical history of poorly controlled type 2 diabetes for 15 years, hypertension, asthma, and depression. Her regular medication comprised metformin 3g daily, modified-release gliclazide 60mg daily, aspirin 100mg daily, atorvastatin 40mg daily, ramipril 10mg daily, and hydrochlorothiazide 25mg daily. Our patient was brought into hospital by ambulance; her pre-hospital observations were as follows: Glasgow Coma Scale score, 15; blood sugar level, 2.8mmol/L; blood pressure, 90/40mmHg; pulse, 54 beats per minute; respiratory rate, 32 breaths per minute; and peripheral oxygen saturation, 98% on 8L oxygen via a variable oxygen delivery mask. On arrival to our emergency department, she was confused with a Glasgow Coma Scale score of 14 out of 15 (E4V4M6), with the rest of her physiological parameters similar to her pre-hospital observations.
Her initial investigations were as follows: serum sodium, 140mmol/L (normal range: 137 to 145mmol/L); serum potassium, 7.3mmol/L (normal range: 3.5 to 4.9mmol/L); serum chloride, 91mmol/L (normal range: 100 to 109mmol/L); serum bicarbonate, 1mmol/L (normal range: 22 to 32mmol/L); anion gap, 55mmol/L (normal range: 7 to 17mmol/L); serum glucose, 2.3mmol/L; urea, 30.8mmol/L (normal range: 2.7 to 8.0mmol/L); and serum creatinine, 768umol/L (normal range: 50 to 100umol/L). Results from liver function tests were normal. Her troponin level was 50ng/L (normal range: <30ng/L). Venous blood gas measurements revealed a profound metabolic acidemia: pH, 6.58; partial pressure of CO2, 38.6mmHg; HCO3, 3.6mmol/L; glucose, 2.0mmol/L; and lactate, 16.7mmol/L. Her initial resuscitation strategy included 2000mL of 0.9% sodium chloride solution, 10mL of 10% calcium gluconate, 15 units insulin (Actrapid) in 50mL 50% dextrose, and 1mL/kg of 8.4% sodium bicarbonate solution.
Minutes after these initial investigations, our patient experienced a pulseless electrical activity cardiac arrest and was managed as per advanced life support protocol. She had a total downtime of 25 minutes. During cardiopulmonary resuscitation she was intubated and ventilated. Following return of spontaneous circulation, she required an infusion of adrenaline for blood pressure support. She had an unremarkable chest radiograph, electrocardiogram, and toxicology screen.
With a presumed diagnosis of ischemic bowel based on vague abdominal features and profound lactatemia, our patient was admitted to our intensive care unit (ICU) for preoperative optimization. In our ICU, she was sedated and ventilated on an inspired oxygen concentration of 40% and on modest ventilator paramters (peak inspiratory pressure <25cmH2O). To treat her severe circulatory shock, she was fluid-resuscitated with a total of 10,000mL crystalloid from a central venous pressure of 8cmH2O to 16cmH2O. In addition, she required very high doses of noradrenaline and adrenaline. Continuous veno-venous hemodiafiltration was commenced at exchange rates of 50mL/kg/h using Hemosol B0 solution. She was empirically started on vancomycin and piperacillin and tazobactam (Tazocin) as broad-spectrum antimicrobial cover.
Our patient went to theater 26 hours post admission for an exploratory laparotomy, which revealed no significant findings. We continued her broad-spectrum antimicrobial cover despite negative microbiological cultures. Renal replacement therapy continued and our patient’s acid-base balance slowly normalized over three days. Having excluded all causes of a high anion gap lactic acidosis, including negative red blood cell transketolase activity for thiamine deficiency, we presumed our patient to have had a severe MALA ‘triggered’ by an acute kidney injury from dehydration. This was supported by a serum metformin level of 4mg/L. Her renal function slowly improved with continuous veno-venous hemodiafiltration and she slowly recovered with a total of 35 days stay in ICU.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mmol/L'], 'Glucose': [2.3, 'mmol/L'], 'Blood Urea Nitrogen (BUN)': [30.8, 'mmol/L']}",313.1242,297.46799,328.78041,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mmol/L. 
The concentration of bun is 30.8 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 30.8 mmol. To convert 30.8 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 30.8 mmol bun * 0.001 mol/mmol = 0.0308 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0308 mol bun * 28.02 g/mol = 0.86302 g bun. To convert 0.86302 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.86302 g bun * 1000.0 mg/g = 863.02 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 863.02 mg bun/10.0 dL = 86.302 mg bun/dL. The concentration value of 30.8 mmol bun/L converts to 86.302 mg bun/dL. 
The concentration of glucose is 2.3 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 2.3 mmol. To convert 2.3 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 2.3 mmol glucose * 0.001 mol/mmol = 0.0023 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0023 mol glucose * 180.16 g/mol = 0.41437 g glucose. To convert 0.41437 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 0.41437 g glucose * 1000.0 mg/g = 414.37 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 414.37 mg glucose/10.0 dL = 41.437 mg glucose/dL. The concentration value of 2.3 mmol glucose/L converts to 41.437 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (86.302 / 2.8) + (86.302 / 18) = 313.1242 mmol/L.The patient's calculated serum osmolality concentration is 313.1242 mmol/L. This is equalivalent to 313.1242 mOsm/kg."
5628,30,Serum Osmolality,lab test,decimal,pmc-3593508-1,Extracted,"A 70-year-old male was brought to the emergency department with complaints of increasing difficulty in breathing, cough with expectoration and fever of about one-week duration. The patient was suffering from cough with expectoration, breathlessness on and off for the past two years and vague abdominal discomfort for the past six months. The patient was not a diabetic or hypertensive but smoker for the past 40 years. On examination, the patient was thin built, ill-looking and pale. His pulse rate was 86/min and blood pressure was 140/80 mm of Hg. On palpation, the abdomen was tender in the epigastric and right hypochondriac region. There was no evidence of lymphadenopathy. Papules and excoriations were seen over the perianal region. The patient was conscious and coherent. No abnormality of central nervous system (CNS) was noted. Normal vesicular breathing with rales and course crackles were found in both the lung fields. Examination of cardiovascular system (CVS) was unremarkable.
At the time of admission, random blood sugar was 85 mg/dl, blood urea - 44 mg/dl, creatinine - 4 mg/ dl, hemoglobin - 9.3 g/dl, total count - 7200 cells/cmm, differential count- P67%, L29%, E04%, absolute esinophil count - 480 cells/cmm, erythrocyte sedimentation rate -10 mm and 24 mm at half an hour and one hour respectively. Serum sodium was 123 mmol/l, serum potassium - 3.3 meq/l, chloride - 89 meq/l and bicarbonates- 26 meq/l. Mantoux test and test for anti-human immunodeficiency virus (HIV) antibodies were negative. Electrocardiogram showed sinus tachycardia. Chest X-ray was suggestive of multiple fluid-filled cavities in the left lung and pending the results of sputum examination, the patient was empirically put on injection deriphylline, amoxycillin-clavulanic acid, gentamicin, ranitidine and metronidazole with a provisional diagnosis of acute exacerbation of chronic obstructive pulmonary disease (COPD)/lung abscess.
On day three of admission, the patient continued to have difficulty in breathing. Physical examination showed bilateral wheeze and no other abnormality. Electrocardiogram (ECG) showed sinus tachycardia. The patient was put on increasing dose of bronchodilators following which he appeared to be relieved temporarily. SPO2 was 96% without O2 Sputum for acid fast bacilli (AFB) was negative on three consecutive days. Wet mount of the sputum showed plenty of actively motile larvae of S. stercoralis [, ]. Routine culture of sputum yielded a moderate growth of Escherichia coli which was susceptible to gentamicin and amikacin. Examination of stool and repeat sputum was requested by our laboratory following the detection of larvae in the sputum. Stool sample and sputum sample collected on two consecutive days showed plenty of motile larvae of S. stercoralis []. The patient was put on albendazole 400 mg bid for three days. Repeat chest X-ray showed persistence of lung abscess on the left side. Ivermectin 12 mg OD was subsequently added to the treatment regimen and albendazole continued for further three days. Repeat stool examination done on the two consecutive days did not show any larvae of S. stercoralis. Sputum could not be examined as the patient could not submit the sample as there was no expectoration. Repeat chest X-ray showed clearance of fluid in the lung abscess with only thick fibroid wall of the cavity. He became afebrile and appetite improved. The patient was feeling better and was discharged at request with advice to report after two weeks. Follow-up of the patient four weeks later showed the patient was asymptomatic and stool examination did not show any parasites.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [123.0, 'mmol/L'], 'Glucose': [85.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [44.0, 'mg/dL']}",266.43651,253.11468,279.75834,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 123.0 mmol/L. 
The concentration of bun is 44.0 mg/dL. 
The concentration of glucose is 85.0 mg/dL. 
Plugging these values into the equation, we get 2 * 123.0 + (44.0 / 2.8) + (44.0 / 18) = 266.43651 mmol/L.The patient's calculated serum osmolality concentration is 266.43651 mmol/L. This is equalivalent to 266.43651 mOsm/kg."
5629,30,Serum Osmolality,lab test,decimal,pmc-3350132-1,Extracted,"A 69-year-old man was admitted to a hospital in the South of Brazil, with weight loss, weakness, and difficulty to swallow. In the last 4 months, he had anorexia, asthenia, and difficulty to swallow any food. When he tried to eat, he felt nausea and sometimes vomited. He had lost 7 kg. He denied fever or other symptoms. He was an active smoker that had smoked 100 pack-years. He did not abuse alcohol or other drugs. He had arterial hypertension, type 2 diabetes mellitus with HbA1c: 6.5% one month earlier and mild chronic obstructive pulmonary disease. He had presented three no disabling ischemic strokes. He was taking hydrochlorothiazide 25 mg, simvastatin 20 mg, and acetylsalicylic acid 100 mg, once a day; and captopril 50 mg TID. His father died of sudden death at 83 years old, and his mother died of stroke at 80 years old. His brother died of esophageal cancer with 55 years old. He lived with his wife. His physical examination revealed an alert, oriented man, with blood pressure: 120/70 mmHg; heart rate: 72 bpm; respiratory rate: 20 rpm; axillary temperature: 36°C; pulse oximetry: 95%; weight: 33.5 kg; height: 1.53 m; BMI: 14.3 kg/m2. There were several lymph nodes the cervical region, the larger one with 1.5 cm, and digital clubbing. Other aspects of his physical examination were normal. Two months before admission, chest radiography showed signs of chronic obstructive pulmonary disease, micronodules and linear opacities in the upper lobes, and a small consolidation in the lower left lobe. The initial laboratory evaluation revealed hemoglobin = 8.6 g/dL (normal range: 13–14.2 g/dL); VCM = 88.9 fL (80–100 fL); leukocytes = 7220/μL (4000–10000/μL); neutrophils = 2758/μL (1800–7500/μL); eosinophils = 606/μL (40–500/μL); basophils = 87/μL (<100/μL); monocytes = 477/μL (120–1000/μL); lymphocytes = 3292/μL (1000–4000/μL); platelets: 409000/μL (150–400 × 103/μL); serum sodium: 134 mEq/L (135–145 mEq/L); potassium: 5.2 mEq/L (3.5–5.1 mEq/L); creatinine: 0.64 mg/dL (0.5–1.2 mg/dL); ureic nitrogen: 21 mg/dL (5–20 mg/dL); calcium: 7.8 mg/dL (8.5–10.4 mg/dL); albumin: 3.0 g/dL (3.5–5.0 g/dL); ALT: 17 U/L (<31U/L); glucose: 94/mg/dL (70–99 mg/dL). An upper gastrointestinal endoscopy was normal, and a nasojejunal tube was inserted. The patient remained with the same symptoms, receiving food and liquids through a nasojejunal tube. In the sixth day after admission, after being submitted to chest and abdomen computerized tomography, he developed fever (39.5°C), confusion, blood pressure 160/110 mmHg, heart rate: 120 bpm, pulse oximetry: 95%. He received intravenous dipyrone. A few moments later, his blood pressure dropped to 80/40 mmHg, and intravenous saline solution was infused. A blood sample to measure serum ACTH and cortisol was drawn. In the next two days, he had no fever, and two samples of blood culture were negative. In the following days, the patient developed severe hyponatremia (sodium = 122 mEq/L and 119 mEq/L), and postural hypotension was identified (supine resting = 122/60 mmHg and standing = 100/60 mmHg). The results of computed tomography of chest and abdomen are shown in Figures and . Serum cortisol and ACTH were, respectively, 1.03 μg/dL (4.3–22.4 μg/dL) and 626 pg/mL (12–46 pg/mL), and serum TSH was 8.06 μU/mL (0.35–5.5 μU/mL). The patient received intravenous hydrocortisone, and hydrochlorothiazide was discontinued. Electrolyte abnormalities, anorexia, and difficulty to swallow are resolved. A biopsy of the left adrenal gland showed signet-ring cell adenocarcinoma with areas of necrosis. In the immunohistochemical study, the cells were positive for CK7, TTF-1, and CEA, and negative for CK20, vimentin, CA19.9, CD10, prostatic specific antigen, and thyroglobulin. Therefore, the diagnosis of adenocarcinoma of pulmonary origin was made. Bone and brain metastases were not evident in bone scintigraphy and brain computerized tomography. A few days later, the patient was switched to 5 mg oral prednisone and 0.1 mg of fludrocortisone and was discharged to his home. One month after initiating glucocorticoids, he came to the outpatient oncology division. He was eating normally, his weight increased to 40.1 kg, but he refused the palliative chemotherapy offered.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [134.0, 'mEq/L'], 'Glucose': [94.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [21.0, 'mg/dL']}",280.72222,266.68611,294.75833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. 
The concentration of bun is 21.0 mg/dL. 
The concentration of glucose is 94.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (21.0 / 2.8) + (21.0 / 18) = 280.72222 mmol/L.The patient's calculated serum osmolality concentration is 280.72222 mmol/L. This is equalivalent to 280.72222 mOsm/kg."
5630,30,Serum Osmolality,lab test,decimal,pmc-4322508-1,Extracted,"A 10-year-old girl was admitted to our hospital with 4-day history of consciousness disturbance and decreased activity. She had a 10-day history of fever and bizarre behavior such as junk feeding and abusiveness on the 2nd day of illness. Then, she had decreased activity with a gate disturbance and urine incontinency as well as a suspected history of seizure.
On admission, she was lethargic and an examination revealed normal vital signs. There was no lymphadenopathy or hepatosplenomegaly. In the neurological examinations, she was drowsy and unresponsive to verbal commands. Her pupils were normal sized and reactive to light. Other examinations were unremarkable except for an unsteady gait and neck stiffness.
The laboratory findings included a leukocyte count of 5900/μl (segmental neutrophil 80%, lymphocyte 18%, and monocyte 2%), hemoglobin 12.8 gr/dl, platelet count 264000/μl, serum potassium 4.4 mEq/dl, sodium 141 mEq/dl, total calcium 9.5 mg/dl, urea 28 mg/dl, creatinine 0.6 mg/dl, glucose 132 mg/dl, cerebrospinal fluid(CSF) analysis revealed white blood cell 200/ mm3( lymphocyte 35 %, neutrophil 65%), red blood cell 100/mm3, protein 18 mg/dl, and sugar 89 mg/dl.
The serum PCR was negative for herpes simplex virus 1, 2 (HSV 1, 2). Blood culture, urine culture, and CSF culture were all negative as well as a negative PPD test. An electroencephalogram (EEG) showed generalized slow waves. In brain CT scan, we found nonspecific evidence of brain edema.
A brain MRI revealed high signal intensities in the basal ganglia in FLAIR image () and there was no restrictions in the lesion in the diffusion-weighted image (DWI) and the apparent diffusion coefficient map image (ADC-MAP), which ruled out vascular problems or stroke in our case (-3). With the brain MRI findings, we thought about EBV encephalitis and checked the serologic tests. Serologic testing was compatible with acute EBV infection, positive for viral capsid antigen (VCA) IgM and negative for VCA IgG. Encephalitis was confirmed by clinical and radiological findings.
Empirical intravenous antibiotics and Acyclovir were administered, but stopped after the final negative CSF results for microorganisms were obtained. She gradually recovered and discharged after the 14th day of admission. At 6 weeks after the onset of illness, she could walk and speak well but could not go back to school.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [141.0, 'mEq/dL'], 'Glucose': [132.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [28.0, 'mg/dL']}",2837.33333,2695.46666,2979.2,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mEq/dL. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The current volume unit is dL and the target volume unit is L. The conversion factor is 0.1 L for every unit of dL. Our next step will be to divide the mass by the volume conversion factor of 0.1 to get the final concentration in terms of mmol/L. This will result to 141.0 mmol sodium/0.1 L = 1410.0 mmol sodium/L. The concentration value of 141.0 mEq sodium/dL converts to 1410.0 mmol sodium/L. 
The concentration of bun is 28.0 mg/dL. 
The concentration of glucose is 132.0 mg/dL. 
Plugging these values into the equation, we get 2 * 1410.0 + (28.0 / 2.8) + (28.0 / 18) = 2837.33333 mmol/L.The patient's calculated serum osmolality concentration is 2837.33333 mmol/L. This is equalivalent to 2837.33333 mOsm/kg."
5631,30,Serum Osmolality,lab test,decimal,pmc-5965442-1,Extracted,"A three-month-old full term male was brought to the pediatric ED by his grandmother for evaluation of “jerking” activity worsening in frequency and severity for approximately three weeks. The grandmother described the “jerking” activity as intermittent upper body stiffening with associated eye blinking and drooling with a change in level of alertness just following the event. She reported that the episodes had increased in frequency over the few days prior to ED arrival but claimed the episodes had been present for the approximately one month. The grandmother stated that initially the jerking occurred approximately once per day; however, there were three episodes noted on the day of presentation. She described these episodes as lasting seconds to minutes and were not associated with color change, respiratory distress, or spitting up. They occurred at any time of the day, with no predilection for early morning or sleep arousal, and there was no association with feeding. She denied any recent history of falls, head trauma, fever, cough, congestion, diarrhea or rash. The remainder of the review of systems was negative. The infant was formula-fed every four hours and had been producing a normal amount of wet diapers and stool. When questioned about the pregnancy, the grandmother was unsure if the mother had been using drugs or alcohol, but stated that the infant was the product of an uncomplicated labor and delivery with a normal newborn screening. His birth weight was reported as 2.86 kg. The infant attended daycare, but there were no known sick contacts. The grandmother stated that the baby had been healthy, meeting his development milestones, and gaining weight appropriately according to his last well-child visit. There was a maternal history of multiple sclerosis reported by the grandmother.
On physical exam, the infant appeared well and was noted to make eye contact with the grandmother. Initial weight and vital signs reported at triage were as follows: weight: 5.51 kg, temperature 98.0° F, respiratory rate 22 breaths/min, heart rate 143 beats/min, oxygen saturation of 97% on room air. The pertinent positives of his exam included a full anterior fontanelle but no bulging. Extraocular movements were equal with no nystagmus appreciated. There was a mild left ocular prominence noted but no proptosis. He had no facial deformity or external signs of trauma with tears present and moist mucous membranes. His neck was supple, and appropriate head control was appreciated when he was seated in his grandmother’s lap. An overall slight increase in his tone was noted. All movements were observed to be symmetrical with no obvious motor deficit or weakness.
Moments after the initial assessment, the ED staff was called to the bedside by the grandmother. The infant was observed to have left eye blinking followed by asynchronous right eye blinking with drooling at the mouth. He was unresponsive to direct confrontation. No other jerking motions were observed. The episode lasted less than two minutes during which time he was placed on a cardiac monitor and vital signs were stable. Immediately following the episode, the infant was not responding normally to the grandmother but became increasingly more alert and returned back to baseline within several minutes.
Given his initial presentation and witnessed seizure activity, laboratory tests and imaging were ordered. The results of his lab work were as follows: WBC 10.4 × 103, Hgb 12.4 g/dL, Hct 36.3%, platelets 302 × 103/mm; Differential: lymphocytes 77%, neutrophils 14%, eosinophils 9%. Sodium 136 mEq/L, potassium 5.5 mEq/L, chloride 106 mEq/L, bicarbonate 20 mEq/L, BUN 5 mg/dL, creatinine 0.22 mg/dL, glucose 100 mg/dL, magnesium 2.1 mEq/L, phosphorus 5.5 mg/dL, anion gap 10.
In an attempt to spare exposure to ionizing radiation, the decision was made to perform a stat non-contrast magnetic resonance imaging (MRI) of the brain. After review of the scout images from MRI, a magnetic resonance angiogram protocol was added. Imaging revealed a large supratentorial cystic and solid mass in the left temporal region measuring 8.6cm × 7.9cm × 5.1cm. A plan was then made to transfer the patient to a pediatric intensive care unit, which could afford a higher level of care. A loading dose of levetiracetam (55 mg) intravenously was administered and D10 NS was run at maintenance.
The infant had five seizures on the day of admission, two of them witnessed. He was given an additional dose of levetiracetam 20 mg/kg IV and then continued on a maintenance dose of 10 mg/kg. The patient was also started on a dexamethasone 0.5 mg/kg. No subsequent seizure activity was reported following medication titration. Operative management was conducted by pediatric neurosurgery on hospital day 6. The patient underwent a left craniotomy with gross tumor resection. Pathology report indicated the tumor was consistent with DIG. In the post-operative period, the patient was observed to have a left lateral gaze palsy, and repeat imaging revealed a new acute infarct of the right thalamus. Due to the acute infarct, a neurology consult was obtained and the infant underwent a full work-up for a new-onset hypercoaguable state. The infant was found to have a slightly elevated anti-thrombin III level, and the infarct was not attributed to surgical management. Echocardiography was found to be normal and the patient was subsequently started on aspirin. The infant’s subgaleal Jackson-Pratt drain remained in place until post-operative day 3. No respiratory or gastrointestinal complications arose and the patient was tolerating full feeds within several days post-operatively.
Despite the right thalamic infarct, the patient had an excellent post-operative course in the months following discharge. At his last well-child visit, no neurological deficits were appreciated and the infant was meeting expected milestones for his age.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [5.0, 'mg/dL'], 'Glucose': [100.0, 'mg/dL'], 'Sodium': [136.0, 'mEq/L']}",279.34127,265.37421,293.30833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.0 mEq. To convert from 136.0 mEq to mmol, convert from mEq to mmol. The compound 136.0 has a valence of 1, and so divide the valence by the value of mEq to get, 136.0 mEq/(1 mEq/mmol) = 136.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mEq sodium/L converts to 136.0 mmol sodium/L. 
The concentration of bun is 5.0 mg/dL. 
The concentration of glucose is 100.0 mg/dL. 
Plugging these values into the equation, we get 2 * 136.0 + (5.0 / 2.8) + (5.0 / 18) = 279.34127 mmol/L.The patient's calculated serum osmolality concentration is 279.34127 mmol/L. This is equalivalent to 279.34127 mOsm/kg."
5632,30,Serum Osmolality,lab test,decimal,pmc-3665245-1,Extracted,"A 37-year-old woman was admitted to our hospital because of amenorrhea and infertility. She also suffered from fatigue, numbness, and swelling in hands and foot. Her systolic blood pressure was found to be <90 mmHg. She had mild myxedema without acromegalic phenotype. No galactorrhea was described. Her past history was remarkable. She had a traffic accident at 14 years of age. She had regular menstrual cycles until 20 years of age. After 20 years of age, no menstrual bleedings have yet occurred nowadays. She also complained from mild headache around eyes. Polydipsia and polyuria were not defined.
Laboratory tests include serum biochemistry, and hormones revealed glucose: 86 mg/dL (70–105 mg/dL), urea: 17.1 mg/dL (18–45 mg/dL), creatinine: 0.7 mg/dL (0.57–1.11 mg/dL), calcium: 8.8 mg/dL (8.4–10.2 mg/dL), phosphorus: 3.3 mg/dL (2.5–4.5 mg/dL), magnesium: 2.1 mg/dL (1.7–3.1 mg/dL) Na: 141 mmol/L (136–145 mmol/L), K: 4.7 mmol/L (3.5–5.1 mmol/L), fT3: 2.12 pmol/L (2.63–5.70 pmol/L), fT4: 5.81 pmol/L (9.01–19.04 pmol/L), TSH: 1.28 IU/mL (0.35–4.94 IU/mL), LH: 0.02 mIU/mL, FSH: 0.06 mIU/mL, PRL: 1.81 ng/mL (5.18–26.53 ng/mL), oestrogen: 24 pg/mL, progesterone: 0.1 ng/mL, cortisol: 0.01 μg/dL (3–19 μg/dL), and ACTH: 10.9 pg/mL (22.5–95.3 pg/mL). She was hypotensive without any electrolyte imbalance. We administered stress-dose steroid and then reduced to replacement dose by titration. At followup, hypotension was improved. Thyroid function tests displayed lower fT3 and fT4 and normal TSH levels which was thought to be secondary hypothyroidism. We gave her levothyroxine (LT4) replacement. Urine-specific gravity was 1011 and fluid intake and urine output were normal. She had no menstrual bleedings for seventeen years, and also serum progesterone level, was low so called hypogonadism. She was consulted with gynecologist and endometrial wall thickness was lower, so she was offered to take estrogen progesterone replacement treatment. With all these findings, we suspected panhypopituitarism. Hypophyseal magnetic resonance imaging (MRI) was taken and was shown as hypophyseal hypoplasia with dimensions of 4.6 mm height and 8.5 mm width. And also posterior pituitary bright spot was seen on MRI. Twelve-lead electrocardiogram was taken ().
At cardiac auscultation murmur was heard. Patient was consulted with a cardiologist. A two-dimensional transthoracic echocardiography was taken it showed normal left ventricular systolic function with 65% ejection fraction, left atrium enlargement, and mild mitral and tricuspid regurgitation. A 24-hour rhythm holter electrocardiography (ECG) was taken (); it showed that basic rhythm was sinusal rhythm, minimal heart rate was 44/min, mean heart rate was 62/min, maximal heart rate was 107/min, and no ventricular/supraventricular tachycardia or pause was detected. Maximal QT/QTc interval was 549 ms.
We considered that QT prolongation may be caused by hypopituitarism. Steroid replacement therapy was started on the 5th hospital day and thyroid replacement therapy on the 11th hospital day. Three weeks after starting steroid replacement therapy, the levels of cortisol and thyroid hormone were normalized. Two-dimensional echocardiography showed normal cardiac wall and valve motions. Also, an ECG showed QT normalization (). QT/QTC interval was measured 364/392 ms.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [17.1, 'mg/dL'], 'Glucose': [86.0, 'mg/dL'], 'Sodium': [141.0, 'mmol/L']}",292.88492,278.24067,307.52917,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mmol/L. 
The concentration of bun is 17.1 mg/dL. 
The concentration of glucose is 86.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (17.1 / 2.8) + (17.1 / 18) = 292.88492 mmol/L.The patient's calculated serum osmolality concentration is 292.88492 mmol/L. This is equalivalent to 292.88492 mOsm/kg."
5633,30,Serum Osmolality,lab test,decimal,pmc-5295522-1,Extracted,"A 27-year-old African American female presented to the hospital after a sudden onset of severe retrosternal chest pain. Past medical history was insignificant for hypertension or diabetes mellitus. Patient has a history of smoking cigarettes, beginning at age 9, and frequent marijuana use. The patient was treated with morphine and Percocet for pain. Lab data and urine toxicology screen were negative for troponins and significant for marijuana, respectively. Urine drug screen was negative for cocaine and amphetamines. Drug screen was positive for opiates, but this result is most likely an artifact of morphine and Percocet treatment for chest pain. Initial laboratory findings included hemoglobin 12 g/dL, hematocrit 12.6%, platelets 223 × 103/μL, glucose 156 mg/dL, BUN 9 mg/dL, creatinine 0.8 mg/dL, sodium 135 mEq/L, potassium 4 mEq/L, chloride 101 mEq/L, and bicarbonate 18 mEq/L. In the emergency room, vital signs demonstrated a pulse rate of 98 beats/min, respiratory rate 22 breaths/min, blood pressure 132/89 mm Hg, temperature 98.1 °F, and oxygen saturation 100% on room air. The remainder of the physical examination was unremarkable. Initial electrocardiogram (ECG) demonstrated normal sinus rhythm, and the patient was admitted to telemetry for observation. The subsequent morning, the patient actively experienced chest pain and ECG changes. ECG demonstrated ST segment elevations in leads II and III, and T-wave inversions in V1-V3. Stat troponin level was found to be elevated at 11.07 ng/mL (< 0.30 ng/mL). The patient immediately underwent cardiac catheterization which demonstrated a 99% blockage of the left anterior descending artery and revascularization was performed (, ). Two-dimensional echocardiogram demonstrated a left ventricular ejection fraction of 40% with anterior wall akinesis. Transesophageal echocardiogram ruled out an apical mural thrombus, but confirmed the ejection fraction and wall akinesis from the previous echocardiogram. The patient was also found to have hyperlipidemia after the conduction of a lipid panel. Hypercoaguable state and vasculitis workup was negative.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [9.0, 'mg/dL'], 'Glucose': [156.0, 'mg/dL'], 'Sodium': [135.0, 'mEq/L']}",281.88095,267.7869,295.975,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 135.0 mEq. To convert from 135.0 mEq to mmol, convert from mEq to mmol. The compound 135.0 has a valence of 1, and so divide the valence by the value of mEq to get, 135.0 mEq/(1 mEq/mmol) = 135.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mEq sodium/L converts to 135.0 mmol sodium/L. 
The concentration of bun is 9.0 mg/dL. 
The concentration of glucose is 156.0 mg/dL. 
Plugging these values into the equation, we get 2 * 135.0 + (9.0 / 2.8) + (9.0 / 18) = 281.88095 mmol/L.The patient's calculated serum osmolality concentration is 281.88095 mmol/L. This is equalivalent to 281.88095 mOsm/kg."
5634,30,Serum Osmolality,lab test,decimal,pmc-7769497-1,Extracted,"A 52-year-old Caucasian male with a significant past medical history of COPD, diabetes mellitus type 2, essential hypertension and chronic back pain presented to the emergency room with diffuse abdominal pain. The patient reported associated abdominal swelling with 3 episodes of nausea and vomiting in the past day. The patient also reports having felt lightheaded for the past couple weeks and reports falling 2 weeks ago. On arrival, the patient was afebrile with a blood pressure of 60/40, heart rate of 74, respiratory rate of 14 and saturating 98% on room air. Labs obtained were significant for a Na:130, Glucose: 115, BUN:46, Cr:4.3 (baseline:0.8), WBC:20.9, blood cultures grew gram + cocci. The patient denies drinking alcohol, smoking cigarettes or consuming anything corrosive. After not responding to fluids, a central line was placed and Norepinephrine started. CT of the abdomen demonstrated air within the wall of the stomach, portal veins and perigastric veins at which point surgery was consulted. After admission to the ICU, a follow-up EGD demonstrated Emphysematous gastritis secondary to gastric mucosal necrosis particularly in the proximal stomach just below the GE junction. The patient had already been placed on Piperacillin/Tazobactam and Metronidazole before admission to the ICU and after blood cultures came back positive for gram + cocci, Vancomycin was added. The following day the patient continued to complain of severe pain and follow up CT abdomen/pelvis demonstrated interval gastric perforation with mild free air within the upper abdomen and fluid within the posterior gastric wall representing gastric necrosis with perforation along with interval development of mild pneumoperitoneum (Figures , ).
He was taken to surgery and underwent a subtotal gastrectomy with splenectomy due to becoming hypotensive during the procedure and the fear that attaching his distal esophagus to the jejunum at that point would result in poor perfusion. The decision was made to close him up and go back in a few days. Things became even more interesting when wound cultures taken during surgery came back positive for both yeast and streptococcus parasanguinis. Follow-up blood cultures were also positive for yeast. Micafungin was started at that point. He went back to surgery where his esophagus was found to have retracted into his chest, as well as his abdominal mesh being covered with pus. As much pus was cleared out as possible and was closed back up. In order to attach his esophagus to his jejunum, a thoracic surgical approach would need to be done for which the patient was not stable enough to perform. Peritoneal fluid cultures taken during the procedure grew yeast. With fungemia in his bloodstream, TPN had to be stopped. ID recommended stopping zosyn and adding meropenem. He remained intubated in the ICU where his family made the decision to compassionately extubate and make him comfort care. Culture wound results that had been sent for identification of the fungal species came back positive for Candida Glabrata.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [46.0, 'mg/dL'], 'Glucose': [115.0, 'mg/dL'], 'Sodium': [130.0, 'mEq/L']}",282.81746,268.67659,296.95833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. 
The concentration of bun is 46.0 mg/dL. 
The concentration of glucose is 115.0 mg/dL. 
Plugging these values into the equation, we get 2 * 130.0 + (46.0 / 2.8) + (46.0 / 18) = 282.81746 mmol/L.The patient's calculated serum osmolality concentration is 282.81746 mmol/L. This is equalivalent to 282.81746 mOsm/kg."
5635,30,Serum Osmolality,lab test,decimal,pmc-4119326-1,Extracted,"We report a case of 49-years-old male who received a kidney from a live unrelated donor since 7 years ago. During these seven years multiple low grade fevers was being appeared every year that healed without a diagnosis. On 29 May 2013, he presented with 39 °C fever associated with dysuria, oliguria, right lower quadrant abdominal pain, anorexia, cough and dyspnea. The patient had also history of diabetes mellitus, hypertension and gout. Blood pressure measured 130/90 mmHg, pulse rate 96 per minute, and respiratory rate 18 per minute. Laboratory tests were as follow: BUN= 19 mg/dl, Cr= 2 mg/dl, Na= 133 mEq/l, K=4.5 mEq/l, FBS=130 mg/dl, ESR= 50 mm/hour, CRP= 44.1 mg/dl, WBC= 5.8 ×106/µL, RBC= 4.02 × 106/µL, Hg= 11.3 g/dl, hematocrit= 33.6%, MCV 83.58 fl, and platelet= 171 × 106/µL. In sonography investigation, his kidney graft was 123×55 mm with normal parenchymal echo. The test for cytomegalovirus (CMV Ag-pp65) was negative and enterobacter growth was seen in the blood culture. In high resolution computed tomography (HRCT), an increase in heart size, mediastinum vascular swelling, reticular densities, septal thickness, bronchial wall thickness, mild bronchiectasis, patchy and nodular alveolar densities on the inferior lobe of both lungs were seen. Spiral CT scan showed micro-consolidation patchy lesions on the inferior lobe of both lungs (). Bronchoscopy showed hyper-vascularity in the trachea, and in broncho-alveolar lavage (BAL) growth of non-A, non-D streptococci were detected with no growth of acid fast bacilli or mycobacterium tuberculosis. After 17 days of antibiotic and antifungal therapy, his fever did not corrupt. Spirometry results, showed a decreased FEV1 to 75%. On June 23th, inferior lobe wedge resection of the left lung was performed. In macroscopic pathologic examinations, fragments of lung tissue measuring 5×2×2 cm and gray brown and soft tissue in serial cross sections were observed.Moreover, microscopic evaluations conducted on issue removed during a procedure (). Finally, the diagnosis of BOOP was reported with no evidence of malignancy. Sirolimus was withdrawn and cyclosporine was started and dosage of prednisolone was increased. His fever was discontinued and general condition as well as pulmonary symptoms were gradually improved.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [19.0, 'mg/dL'], 'Glucose': [130.0, 'mg/dL'], 'Sodium': [133.0, 'mEq/L']}",280.00794,266.00754,294.00834,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 133.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 133.0 mEq. To convert from 133.0 mEq to mmol, convert from mEq to mmol. The compound 133.0 has a valence of 1, and so divide the valence by the value of mEq to get, 133.0 mEq/(1 mEq/mmol) = 133.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mEq sodium/L converts to 133.0 mmol sodium/L. 
The concentration of bun is 19.0 mg/dL. 
The concentration of glucose is 130.0 mg/dL. 
Plugging these values into the equation, we get 2 * 133.0 + (19.0 / 2.8) + (19.0 / 18) = 280.00794 mmol/L.The patient's calculated serum osmolality concentration is 280.00794 mmol/L. This is equalivalent to 280.00794 mOsm/kg."
5636,30,Serum Osmolality,lab test,decimal,pmc-5477883-1,Extracted,"A 37-year-old woman presented with recent constitutional upset and a year-long history of swelling of her face and hands. Her past medical history included pre-eclampsia. Her father had suffered from focal segmental glomerulosclerosis and her brother underwent renal transplantation for reflux nephropathy. Examination revealed peri-orbital oedema and hypertension (140/100 mmHg). Her pulse rate was 58 beats/min.
Investigations included haemoglobin 11.6 g/l, white cell count 6.2 × 109/l, sodium 137 mmol/l, potassium 3.6 mmol/l, creatinine 148 μmol/l, estimated glomerular filtration rate (GFR) 37 ml/min/1.73 m2, urea 7.6 mmol/l, cholesterol 9.8 mmol/l, alkaline transferase 97 IU/l, alanine transaminase 45 IU/l, alkaline phosphatase 89 IU/l, albumin 45 g/l, calcium 2.37 mmol/l and glucose 4.9 mmol/l. Hepatitis, Epstein-Barr and cytomegalovirus serologies were negative.
Urinalysis was normal. A 24-h urine collection identified 0.30 g of protein and a creatinine clearance of 58 ml/min. Ultrasonography revealed her kidneys to measure 11 cm on the left and 10 cm on the right. A small pericardial effusion was evident on echocardiography, with no left ventricular hypertrophy. Magnetic resonance angiography revealed patent renal arteries.
A renal biopsy was undertaken. Twenty-two glomeruli were available for analysis, with no evidence of focal lesion or glomerulonephritis. Further, light microscopy, immunohistochemistry and electron microscopy were unremarkable.
At this point the patient described myalgias. Thyroid function tests showed a free thyroxine (FT4) concentration of <3 pmol/l and a thyroid stimulating hormone (TSH) concentration of >75 mu/l, consistent with severe hypothyroidism. Creatine kinase was elevated to 3454 IU/l, but urinary myoglobin was not detected. She was commenced on levothyroxine 100 mcg. Her blood pressure (110/70 mmHg), serum creatinine (94 μmol/l), creatine kinase and cholesterol (4.2 mmol/l) all normalized.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [137.0, 'mmol/L'], 'Glucose': [4.9, 'mmol/L'], 'Blood Urea Nitrogen (BUN)': [7.6, 'mmol/L']}",286.50969,272.18421,300.83517,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mmol/L. 
The concentration of bun is 7.6 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 7.6 mmol. To convert 7.6 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 7.6 mmol bun * 0.001 mol/mmol = 0.0076 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0076 mol bun * 28.02 g/mol = 0.21295 g bun. To convert 0.21295 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.21295 g bun * 1000.0 mg/g = 212.95 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 212.95 mg bun/10.0 dL = 21.295 mg bun/dL. The concentration value of 7.6 mmol bun/L converts to 21.295 mg bun/dL. 
The concentration of glucose is 4.9 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 4.9 mmol. To convert 4.9 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 4.9 mmol glucose * 0.001 mol/mmol = 0.0049 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0049 mol glucose * 180.16 g/mol = 0.88278 g glucose. To convert 0.88278 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 0.88278 g glucose * 1000.0 mg/g = 882.78 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 882.78 mg glucose/10.0 dL = 88.278 mg glucose/dL. The concentration value of 4.9 mmol glucose/L converts to 88.278 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (21.295 / 2.8) + (21.295 / 18) = 286.50969 mmol/L.The patient's calculated serum osmolality concentration is 286.50969 mmol/L. This is equalivalent to 286.50969 mOsm/kg."
5637,30,Serum Osmolality,lab test,decimal,pmc-6379930-1,Extracted,"A 44-year-old Caucasian man, a construction worker in an urban area, married and with two children, with no past medical history, previous treatment, or toxic habits, presented 1 week before entering the hospital with general weakness and respiratory difficulty that gradually increased in intensity, accompanied by cough without expectoration. He had also experienced recent fever (38.9 °C, 102.0 °F) and some episodes of vomiting and diarrhea. He was admitted to the ICU with a diagnosis of community-acquired pneumonia and respiratory failure. At the time of admission to the ICU, the patient was conscious, oriented, and collaborative, without presenting any neurological alteration. The patient was febrile (38 °C, 100.4 °F) and tachycardic (heart rate 110 beats/min), his blood pressure was 120/80 mmHg, and he was tachypneic (28 breaths/min), without intercostal print, with an oxygen saturation of 88% with a Ventimask (Flexicare Medical, Mountain Ash, UK) at 50%. Lung auscultation showed conserved vesicular murmur and basal and midfields bilateral crackles. His heart sounds were regular, rhythmic, and without murmurs. No heart failure data were recorded. We observed a soft and depressible abdomen with peristalsis present, without visceromegalies. The patient’s lower limbs were without edema and had symmetric palpable peripheral pulses. Empiric antibiotic treatment was started with ceftriaxone (2 g/24 h, 7 days), levofloxacin (500 mg/24 h, 7 days), and oseltamivir (150 mg/12 h, 5 days), and 24 h after the admission, the patient was diagnosed with influenza A(H1N1) pneumonia after the virus was isolated in the nasopharyngeal swab samples taken at admission by PCR (DNA isolation). In the patient’s medical history, he did not highlight any history of toxic habits; information on medication taken regularly or any drug allergies was not recorded.
The patient required mechanical ventilation, and his initial evaluation was favorable with stable hemodynamics. On day 12 of the admission, he developed acute severe hypotension (systolic blood pressure < 80 mmHg) with tachycardia (heart rate > 140 beats/min) and a markedly worsening respiratory status. Arterial acid-base balance at that time showed fraction of inspired oxygen 60%, pH 7.39, partial pressure of carbon dioxide 26.7 mmHg, partial pressure of oxygen 55.9 mmHg, bicarbonate 15.9 mmol/L, base excess − 8.1, lactic acid 0.9 mmol/L, and oxygen saturation 91.2%. The patient’s respiratory status failed to respond to high-dose vasopressors and ventilatory support. The laboratory findings at that time showed the following: red blood cells 3.4 × 106/mm3, hemoglobin 9.7 g/dl, mean corpuscular volume 96.5 fl (normal reference value 80–100), average corpuscular hemoglobin 28.5, leukocytes 14.8 × 103/mm3 (normal reference value 4.5–11.1 × 103), 74.9% neutrophils, 14.8% lymphocytes, international normalized ratio 1.29, basal glucose 155 mg/dl (normal reference value 65–110), blood urea nitrogen 33 mg/dl (normal reference value 5–20), creatinine 1.10 mg/dl, sodium 145 mEq/L, potassium 3.9 mEq/L, troponin I 0.022 ng/dl, (normal reference value < 0.034), D-dimer > 10,000 ng/ml (normal reference value < 500), and C-reactive protein > 90 mg/L (normal reference value 0–12).
The cultures of the bronchial secretion (sputum of the patient) and of urine and blood (direct puncture of a peripheral artery) were negative for both aerobic and anaerobic bacteria, as were urine antigens for Pneumococcus and Legionella. An anteroposterior chest radiograph showed right basal infiltrate (Fig. a). To determine the cause of this acute hemodynamic instability and facilitate patient management, TTE was performed for a differential diagnosis of hypovolemia, acute LV or RV dysfunction, cardiac tamponade, aortic dissection, severe valvular regurgitation, dynamic LV outflow tract obstruction, or PE. Poor-quality images were obtained, necessitating the completion of the study with TEE.
TEE demonstrated a small and hyperdynamic LV and a severely dilated and dysfunctional RV. In the midesophageal four chambers view with TEE, the RV end-diastolic area to LV end-diastolic area ratio was 1.7 (normal reference value < 0.6), and the RV end-diastolic diameter to LV end-diastolic diameter ratio was 1.4 (normal reference value < 0.9). TEE also showed McConnell’s sign, normokinesia of the RV apical segment, and akinesia of the RV mid-free wall (Fig. a, Additional file 1) and a systolic flattening of the interventricular septum (Fig. b, Additional file 2), suggesting RV pressure overload. There was no evidence of a thrombus either on the right side of the heart or in the pulmonary arteries. These findings of acute RV failure due to pressure overload raised the possibility of a PE or RV myocardial infarction []. A 12-lead electrocardiogram showed T-wave inversion in leads V1 to V4 and an S1Q3T3 pattern without abnormalities in the ST segment (Fig. c). The combined use of electrocardiography and TEE in this clinical setting suggested a high probability of PE. The unfavorable hemodynamic situation of the patient prevented transfer to carry out other complementary tests that could confirm the diagnosis of PE. Fibrinolytic and anticoagulant therapies were administered immediately, achieving a favorable clinical outcome.
Twenty-four hours later, with the patient stable from a hemodynamic and respiratory point of view, computed tomography (CT) pulmonary angiography showed multiple filling defects in both the pulmonary artery and bilateral lobar arteries; this outcome is consistent with PE and peripheral pulmonary consolidations that were more extensive on the right side with hypodense zones compatible with areas of hypoperfusion (Fig. a). The diagnosis of PE was confirmed. The patient continued with anticoagulant and antibiotic treatment during admission, progressing favorably from both a hemodynamic and respiratory point of view. Mechanical ventilation was removed on the 27th day. After 11 days of admission, he showed acute renal failure secondary to the nephrotoxic effects of tobramycin, with subsequent normalization of renal function on the 31st day of admission. After completing approximately 2 weeks of rehabilitation, on the 45th day after admission, the patient was discharged without complications. He achieved normalization of the chest x-ray (Fig. b) and normalization of RV morphology (Fig. b, Additional file 3) and functionality (Fig. c). Three years and five months after discharge, the patient remained free of symptoms and was living a normal life.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [33.0, 'mg/dL'], 'Glucose': [155.0, 'mg/dL'], 'Sodium': [145.0, 'mEq/L']}",310.39683,294.87699,325.91667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 145.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 145.0 mEq. To convert from 145.0 mEq to mmol, convert from mEq to mmol. The compound 145.0 has a valence of 1, and so divide the valence by the value of mEq to get, 145.0 mEq/(1 mEq/mmol) = 145.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 145.0 mEq sodium/L converts to 145.0 mmol sodium/L. 
The concentration of bun is 33.0 mg/dL. 
The concentration of glucose is 155.0 mg/dL. 
Plugging these values into the equation, we get 2 * 145.0 + (33.0 / 2.8) + (33.0 / 18) = 310.39683 mmol/L.The patient's calculated serum osmolality concentration is 310.39683 mmol/L. This is equalivalent to 310.39683 mOsm/kg."
5638,30,Serum Osmolality,lab test,decimal,usmle-5660,Extracted,"A 45-year-old Spanish-speaking man with type I diabetes mellitus presents to the emergency department with nausea and abdominal pain. He has a past medical history of obesity, osteoarthritis, diabetes, diabetic nephropathy, and hypertension. His current medications include insulin, lisinopril, atorvastatin, and ibuprofen. His temperature is 100.5°F (38.1°C), blood pressure is 90/60 mmHg, pulse is 130/min, and respirations are 30/min. His pupils are equal and reactive to light bilaterally. He has poor skin turgor and capillary refill. Jugular venous distention is not detected. Bedside ultrasound reveals a collapsible inferior vena cava with light inspiration. His basic metabolic panel is displayed below:

Serum:
Na+: 119 mEq/L
Cl-: 95 mEq/L
K+: 5.0 mEq/L
HCO3-: not detectable
BUN: 50 mg/dL
Glucose: 960 mg/dL
Creatinine: 1.6 mg/dL
Ca2+: 8.9 mg/dL
PO4-: 3.5 mg/dL

He is admitted to the intensive care unit on a regular insulin drip and 0.9% isotonic saline. His basic metabolic panel four hours later is below:

Serum:
Na+: 120 mEq/L
Cl-: 90 mEq/L
K+: 4.2 mEq/L
HCO3-: 2 mEq/L
BUN: 50 mg/dL
Glucose: 680 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 8.5 mg/dL
PO4-: 3.0 mg/dL

Therapy remains unchanged. Three hours later, the patient is found to have the EKG in Figure A.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [50.0, 'mg/dL'], 'Glucose': [960.0, 'mg/dL'], 'Sodium': [119.0, 'mEq/L']}",309.19048,293.73096,324.65,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 119.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 119.0 mEq. To convert from 119.0 mEq to mmol, convert from mEq to mmol. The compound 119.0 has a valence of 1, and so divide the valence by the value of mEq to get, 119.0 mEq/(1 mEq/mmol) = 119.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 119.0 mEq sodium/L converts to 119.0 mmol sodium/L. 
The concentration of bun is 50.0 mg/dL. 
The concentration of glucose is 960.0 mg/dL. 
Plugging these values into the equation, we get 2 * 119.0 + (50.0 / 2.8) + (50.0 / 18) = 309.19048 mmol/L.The patient's calculated serum osmolality concentration is 309.19048 mmol/L. This is equalivalent to 309.19048 mOsm/kg."
5639,30,Serum Osmolality,lab test,decimal,usmle-1002,Extracted,"A 42-year-old woman comes to the physician for a routine health maintenance examination. She has generalized fatigue and has had difficulties doing her household duties for the past 3 months. She has eczema and gastroesophageal reflux disease. She has a history of using intravenous methamphetamine in her youth but has not used illicit drugs in 23 years. Her medications include topical clobetasol and pantoprazole. She is 160 cm (5 ft 3 in) tall and weighs 105 kg (231 lb); BMI is 42 kg/m2. Her temperature is 37°C (98.6°F), pulse is 95/min, and blood pressure is 145/90 mm Hg. The lungs are clear to auscultation. Cardiac examination shows no abnormalities. Pelvic examination shows a normal vagina and cervix. Laboratory studies show:
Hemoglobin 13.1 g/dL
Leukocyte count 7,800/mm3
Platelet count 312,000/mm3
Serum
Na+ 141 mEq/L
K+ 4.6 mEq/L
Cl- 98 mEq/L
Urea nitrogen 12 mg/dL
Fasting glucose 110 mg/dL
Creatinine 0.8 mg/dL
Total cholesterol 269 mg/dL
HDL-cholesterol 55 mg/dL
LDL-cholesterol 160 mg/dL
Triglycerides 320 mg/dL
Urinalysis is within normal limits. An x-ray of the chest shows no abnormalities. She has not lost any weight over the past year despite following supervised weight loss programs, including various diets and exercise regimens.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [141.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [12.0, 'mg/dL'], 'Glucose': [110.0, 'mg/dL']}",292.39683,277.77699,307.01667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. 
The concentration of bun is 12.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (12.0 / 2.8) + (12.0 / 18) = 292.39683 mmol/L.The patient's calculated serum osmolality concentration is 292.39683 mmol/L. This is equalivalent to 292.39683 mOsm/kg."
5640,30,Serum Osmolality,lab test,decimal,pmc-2827066-1,Extracted,"A 21-year-old patient Caucasian Turkish male presented to the emergency department with the complaint of weakness. He had played football one day before and noticed that he had difficulty in moving his extremities when he woke up at night. He had similar complaints a week ago while taking a shower and his complaint sustained for a few days. In his history of illness, he had double vision complaints and was evaluated for multiple sclerosis, but no diagnosis could be established four years ago.
On physical examination, his blood pressure was 140/80 mmHg, heart rate 86 beat/min, respiratory rate 18/min, and body temperature 36.7°C. The patient was alert, cooperative, and oriented. There was generalized paralysis in over all four limbs (power grade 3/5). There was no sensory deficit. Other systemic and neurologic examinations were normal.
The results of the laboratory evaluation were as follows: potassium (K+) 2.8 mEq/L and sodium (Na+) 141 mEq/L, urea 14 mg/dl, random blood glucose 110 mg/dl and creatinine 0.8 mg/dl. Blood gases showed pH 7.4, bicarbonate 22 mmol/L, pCO2 31.3 mmHg, pO2 97 mmHg and oxygen saturation 99%. Biochemical analyses of urine and thyroid function tests were normal. There was no specific finding at electrocardiogram.
The prediagnosis was thought to be a pseudo attack because of suspicion of multiple sclerosis related with double vision complaints in the past. Neurology department was consulted. However, cranial magnetic resonance imaging (MRI) did not confirm the prediagnosis. MRI and MRI angiography were normal.
During investigation period, initial therapy included 10 mmol of potassium chloride (KCL) per hour given by the intravenous route. Within two days, serum levels of potassium normalized and all clinical symptoms improved.
He was then asked for further history, it was recorded that about 2 months ago, the patient had used a powderized over-the-counter product named 'tekumut' for 2 weeks to quit smoking. He continued to use the same product at various intervals as he felt the desire to smoke. The patient was asked to bring a sample of the product and refrain from using it. The granulated product was studied and determined to contain 'licorice' containing glycyrrhizic acid.
The patient was discharged with recommendations of taking 1 tablet of oral potassium per day and applying to endocrinology and neurology clinics for follow up. The serum K+ level was normal after one week when he applied to the endocrinology outpatient clinic and he was asymptomatic. In the follow-up visit after 2.5 months, the serum potassium level of the patient was completely normalized and the patient was asymptomatic.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [14.0, 'mg/dL'], 'Glucose': [110.0, 'mg/dL'], 'Sodium': [141.0, 'mEq/L']}",293.11111,278.45555,307.76667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. 
The concentration of bun is 14.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (14.0 / 2.8) + (14.0 / 18) = 293.11111 mmol/L.The patient's calculated serum osmolality concentration is 293.11111 mmol/L. This is equalivalent to 293.11111 mOsm/kg."
5641,30,Serum Osmolality,lab test,decimal,pmc-4616927-1,Extracted,"A twenty-three-year-old man was admitted to the emergency room of an infectious disease hospital in Northeast Brazil with a one-month history of daily fever associated to diarrhea with mucus and weight loss of fifteen kilograms in six months. One week prior to admission, the patient's clinical picture worsened with headache, vomiting, disorientation and generalized tonic-clonic seizures. The patient also had a history of diabetes mellitus, tobacco smoking, alcoholism and drug addiction. He had no prior history of hospitalization. Upon physical examination the patient was pale, disoriented, and had periods of agitation. He had rhonchi on the pulmonary auscultation. Abdomen was tender on palpation of the upper right quadrant, liver and spleen were not palpable and no edema was seen in the lower extremities. Nuchal rigidity and meningeal irritation signs were present, however motor deficit was not identified.
Laboratory tests upon admission showed hemoglobin 10 g/dL, 3,440 leukocytes/mm, (4% bands, 45% neutrophils, 5% lymphocytes), 83,000 platelets/mm, urea was 19 mg/dL, creatinine 0.7 mg/dL, ionic calcium 1.23 mEq/L, sodium 130 mEq/L, potassium 4.2 mEq/L, and liver enzymes (ALT and AST) were within normal limits; lactic dehydrogenase was 494 IU/L. Cerebrospinal fluid (CSF) analysis revealed 10 white blood cells/mm (58% neutrophils, 31% lymphocytes, 11% monocytes) and 2 red blood cells/mm. CSF glucose was 122 mg/dL and protein 36 mg/ dL. India ink test revealed six Cryptococcus yeasts/mm. VDRL test was negative and anti-HIV test positive. CD4 count was 40/mm. Blood glucose was 344 mg/dL. Intravenous hydration, insulin, phenytoin, fluconazole, pyrimethamine, sulfadiazine, folinic acid, and amphotericin B were started. The patient did not improve and became obtunded and hypotensive. He was then intubated and put on mechanical ventilation. Arterial blood gases after intubation: pH 7.52, PaCO2 28.9 mmHg, HCO3 26.6 mmEq/L, PaO2 77.9 mmHg, SaO2 96.6% and FiO270%. Vasoactive drugs were added and the patient died less than 24 hours after admission. A post-mortem examination was performed and revealed disseminated cryptococcosis. The histopathology of the kidneys revealed severe renal involvement with Cryptococcus sp. in the glomerulus and interstitium ().",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [19.0, 'mg/dL'], 'Glucose': [344.0, 'mg/dL'], 'Sodium': [130.0, 'mEq/L']}",285.89683,271.60199,300.19167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. 
The concentration of bun is 19.0 mg/dL. 
The concentration of glucose is 344.0 mg/dL. 
Plugging these values into the equation, we get 2 * 130.0 + (19.0 / 2.8) + (19.0 / 18) = 285.89683 mmol/L.The patient's calculated serum osmolality concentration is 285.89683 mmol/L. This is equalivalent to 285.89683 mOsm/kg."
5642,30,Serum Osmolality,lab test,decimal,pmc-4095999-1,Extracted,"A 22-year-old man was referred to our hospital after falling from height. He has no feature in his history and family history. He was conscious and cooperative. Vital signs and laboratory tests were within normal limits. Abdominal ultrasonography revealed free fluid in perisplenic and perihepatic areas and Morrison pouch. It is more prominent in the perisplenic area. Abdominal computed tomogram (CT) revealed laceration of liver, grade 5 splenic laceration, fracture of the left acetabulum, and dislocation of the left hip; brain CT revealed air-fluid level in right maxillary sinus and both sphenoid sinuses, upper and medial wall fracture of right orbita; thorax CT revealed parenchymal laceration and contusional changes. He was optimized for emergency splenectomy and close left hip reduction.
Preoperative laboratory findings were as follows: WBC: 23600/mm3, Hb: 12.6 g/dL, Htc: % 44, platelets: 292000/mm3, glucose: 141 mg/dL, BUN: 22 mg/dL, Cr: 0.99 mg/dL, Na+: 140 mEq/L, K+: 2.37 mEq/L, and Cl−: 105 mEq/L. Postoperatively the patient was admitted to the intensive care unit. On the 2nd day of the operation, he was extubated without any problem. Right pleural fluid was detected in control chest X-ray after extubation (). The patient was examined by thoracic surgeon and chest tube was placed on the right side. The appearance of the fluid was chylous which was later confirmed on biochemical analysis (triglyceride level: 90 mg/dL; cholesterol level: 7 mg/dL). Conservative treatment for chylothorax with nothing by mouth and total parenteral nutrition (TPN) was instituted. On the 3rd day of the operation, thorax CT showed right pleural fluid and chest tube was 2 placed on the right side. The appearance of the fluid was chylous which was later confirmed on biochemical analysis (triglyceride level: 245 mg/dL; cholesterol level: 15 mg/dL). On the 4th day of the operation chest X-ray showed left pleural fluid and chest tube was placed on the left side. on the 10th day of the operation, the patient was discharged to the ward. On the 11th day of the operation, although left basal tube was inserted, left total pneumothorax () was developed and left apical tube thoracostomy was performed. Left apical chest tube was removed 6 days after insertion and left basal chest tube was removed 13 days after insertion. On the 18th day of the operation, although right basal tube was inserted, control chest X-ray showed right total pneumothorax and right apical tube thoracostomy was performed. After right apical tube thoracostomy was performed, right basal chest tube was removed 16 days after insertion. Right apical chest tube removed 6 days after insertion. The patient was discharged from hospital on the 28th day of operation without any complication.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [22.0, 'mg/dL'], 'Glucose': [141.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",295.69048,280.90596,310.475,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 22.0 mg/dL. 
The concentration of glucose is 141.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (22.0 / 2.8) + (22.0 / 18) = 295.69048 mmol/L.The patient's calculated serum osmolality concentration is 295.69048 mmol/L. This is equalivalent to 295.69048 mOsm/kg."
5643,30,Serum Osmolality,lab test,decimal,pmc-4532066-1,Extracted,"A 33 year old man was admitted to the hospital with fever and decreased urine output. Thirty six days prior to admission, renal transplantation was performed in this hospital. He was placed on intravenous solumedrol pulse followed by maintenance oral prednisone and intravenous cyclosporin for 2 weeks. He complained of mild epigastric discomfort and nausea. His blood pressure was 140/90 mmHg, body temperature 37.5 °C, pulse 88, and respirations 22. On physical examination the lungs were clear with a normal regular heart beats with out murmur. There was no organo-megaly, but mild tenderness and swelling of the operation site was noted.
Laboratory analysis revealed hemoglobin 9.9 gm/dl, hematocrit 29.4%, white blood cell 10,500/mm3 with normal differential and platelets 207,000/mm3. Blood chemistry showed FBS 125mg/dl, BUN 79.9mg/dl, Cr 7.1mg/dl, Na 129mM/L, K6.2mM/L, Ca 8.1 mg/dl, P 2.7mg/dl, Cl 92mM/L, total protein 5.0gm/dl, albumin 3.0gm/dl, total bilirubin 0.2gm/dl, AST 10 IU/L, ALT 22IU/L, alkaline phosphatase 77IU/L, total cholesterol 188mg/dl, and prothrombin time 11 sec. Urinalysis revealed protein+4 with many red blood cells under microscopy.
An endoscopic examination was performed on the 11th hospital day. There were multiple dark red, grouped and discrete vesicles of 3 to 5mm in diameter along the entire esophagus (,). The stomach showed several flat erosions confined to the antrum, but the duodenum was normal. All vesicular lesions were easily removed from the esophagus with biopsy forceps. Light microscopy showed characteristic intranuclear inclusions and multi-nucleated giant cells (). The patient was placed on acyclovir from the 14th hospital day. Follow up endoscopy 11 days later revealed a complete absence of vesicles and the presence of faint scars in the esophagus. Renal impairment was also improved. For the confirmation of herpes esophagitis, in situ hybridization of herpes viral DNA was performed, resulting in a positive test for type 1 herpes simplex ().",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [79.9, 'mg/dL'], 'Glucose': [125.0, 'mg/dL'], 'Sodium': [129.0, 'mmol/L']}",293.48016,278.80615,308.15417,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 129.0 mmol/L. 
The concentration of bun is 79.9 mg/dL. 
The concentration of glucose is 125.0 mg/dL. 
Plugging these values into the equation, we get 2 * 129.0 + (79.9 / 2.8) + (79.9 / 18) = 293.48016 mmol/L.The patient's calculated serum osmolality concentration is 293.48016 mmol/L. This is equalivalent to 293.48016 mOsm/kg."
5644,30,Serum Osmolality,lab test,decimal,usmle-6147,Extracted,"A 47–year-old man presents to the emergency department with worsening weakness in the setting of persistent abdominal pain. The man arrived to the United States 6 months ago and has been working in a restaurant as a cook. His abdominal pain started 4 months ago, but he could not find time away from work to see a doctor. He reports nausea but denies any vomiting. His temperature is 98.6°F (37°C), blood pressure is 98/61 mmHg, pulse is 110/min, and respirations are 18/min. He has no cardiac murmurs but does have tenderness in his epigastric region. His heme-occult test is positive. His laboratory workup notes the following:

Hemoglobin: 7.2 g/dL
Hematocrit: 23%
Leukocyte count: 11,000/mm^3 with normal differential
Platelet count: 470,000/mm^3

Serum:
Na+: 137 mEq/L
Cl-: 109 mEq/L
K+: 3.1 mEq/L
HCO3-: 23 mEq/L
BUN: 52 mg/dL
Glucose: 89 mg/dL
Creatinine: 0.9 mg/dL

An esophagogastroduodenoscopy reveals the presence of a mass surrounded by bleeding ulcers. On initial shave biopsy, the preliminary diagnosis is mucosa-associated lymphatic tissue lymphoma (MALToma).",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [137.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [52.0, 'mg/dL'], 'Glucose': [89.0, 'mg/dL']}",297.51587,282.64008,312.39166,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 52.0 mg/dL. 
The concentration of glucose is 89.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (52.0 / 2.8) + (52.0 / 18) = 297.51587 mmol/L.The patient's calculated serum osmolality concentration is 297.51587 mmol/L. This is equalivalent to 297.51587 mOsm/kg."
5645,30,Serum Osmolality,lab test,decimal,pmc-6800504-1,Extracted,"A 43-year-old Iranian (Persian) woman was admitted to the Shahid Madani Hospital with palpitations and dyspnea. She had been experiencing palpitations for 2 years and recently (since about 10 days before admission) had developed dyspnea with New York Heart Association functional class II. Her past medical history was unremarkable, including usual childhood illnesses and no history of rheumatic fever. She never experienced atrial fibrillation and was receiving a low dosage of propranolol (10-mg tablet daily), fluoxetine (10-mg capsule daily), and alprazolam (0.5-mg tablet daily) for her palpitations. She was not receiving oral contraceptive medications. She was the mother of two healthy children, who were both delivered through normal vaginal delivery. She did not have any history of abortion. Her familial history was also unremarkable. She was a housewife who lived with her husband and her two children, never had a job, and was financially supported by her husband. She had never smoked or consumed alcohol or opiates, and she did not follow any special diet.
At the time of admission, her vital signs were within normal ranges (blood pressure 110/70 mmHg, pulse rate 95 beats/minute, respiratory rate 23/minute, oxygen saturation 95%), and her physical examinations revealed nothing considerable. Her extraocular motions full, her gross visual fields were full to confrontation, and her conjunctiva were clear. Her scleras were nonicteric, her pupils equal round and reactive to light and accommodation, and her fundi were also normal. Her hearing was normal. Her tympanic membrane landmark was well visualized. Pharyngeal injection with exudates was not noted. Her uvula moved up in midline. She had a normal gag reflex. Her jugular venous pressure was 8 cm, and her thyroid was not palpable. She had no masses and no adenopathy. Her lung auscultation was normal. She had no rales, rhonchi, wheezes, or rubs. No dullness to percussion was detected. Her diaphragm moved well with respiration. She had no heaves or thrills. She had a normal S1 heart sound, and her S2 sound was narrowly split. No murmur or abnormal heart sound was detected by auscultation. Her pulses were notable for sharp carotid upstrokes. Distal pulses of her extremities were 2+ and symmetric. Her neurologic examination revealed that she was awake, alert, and fully oriented. Her cranial nerves I–XII were intact. Her strength was normal. Her sensory examination revealed normal responses to touch and pinprick. No edema of her arms or head was noticeable. She had no tremor or dysmetria.
Her basic laboratory test results and cardiac enzyme findings were normal, except for mild leukocytosis (white blood cell count 14,400), which remained in the same range until discharge. The results of some other laboratory tests were as follows: hemoglobin, 12.5 g/dl; hematocrit, 41.0%; mean corpuscular volume, 89.0 fl; platelets, 256,000; reticulocyte index, 1.6%; Na+, 140 mEq/L; K+, 4.2 mEq/L; blood glucose, 102 mg/dl; blood urea nitrogen, 19 mg/dl; serum creatinine 1.0 mg/dl; total bilirubin, 0.5 mg/dl; direct bilirubin, 0.1 mg/dl; alkaline phosphatase, 135 mg/dl; aspartate aminotransferase, 45 IU/L; alanine aminotransferase, 27 IU/L; lactate dehydrogenase, 413 IU/L; erythrocyte sedimentation rate in first hour, 27 mm; creatine phosphokinase, 21 IU/L; creatine kinase-MB, 12%; cardiac troponin I, 0.1 ng/ml; hepatitis B surface antigen, negative; C-reactive protein, negative; and rheumatoid factor, negative. Urine analysis revealed specific gravity, 1.003; pH, 6.5; protein, negative; blood, negative; white blood cell count, 2–3; red blood cell count, negative; and bacteria, negative. Arterial blood gas tests revealed pH, 7.43; pCO2, 38 mmHg; PO2, 88 mmHg; HCO3−, 23 mEq/L; and oxygen saturation, 98% on room air.
Electrocardiography demonstrated tachycardia (rate about 100 beats/minute) without any cardiac arrhythmia. No sign of RV overload was noticeable. Primary transthoracic echocardiography revealed a mass in the RA; therefore, transesophageal echocardiography (TEE) was performed. TEE revealed RA enlargement and a huge, dense, multilobulated, hypermobile mass in the RA (1.4 cm × 7.4 cm) and extending into the right RV, which appeared to be emanating from the SVC (Fig. ). Furthermore, the mass was noted in the upper part of the SVC (20 mm from the mouth); however, the left ventricle (LV) and right ventricle (RV) had normal size, and their normal systolic functions were preserved (LV ejection fraction, 55%). Although the RA area was enlarged (23cm2), its systolic pressure was 43 mmHg, displaying moderate pulmonary hypertension. The main pulmonary artery and its branches were also dilated. The valvular evaluation demonstrated mild mitral regurgitation and mild tricuspid regurgitation, but no septal defect or patent foramen ovale was seen.
Systemic anticoagulation was immediately instituted with intravenous heparin, and the patient was transferred to the cardiac intensive care unit. Likewise, computed tomographic (CT) angiography demonstrated a partial filling defect in the SVC that was connected to another filling defect in the RA (46 mm × 26 mm) (Figs. and ). Moreover, partial filling defects were visible in the distal part of the right and left pulmonary arteries, extending to their branches, proposing massive pulmonary emboli (Fig. ). Atelectatic bundles were seen in the middle and lingual lobes, but the size of the heart was normal, and no pleural effusions were detectable.
The contrast-enhanced CT scans and ultrasonographic findings for the chest and abdomen did not show any evidence of tumor or malignancy. Also, there was no evidence of venous filling defects below the diaphragm or deep vein thrombosis (DVT) of the lower extremities. Because of the hypermobile huge mass in the RA and following a cardiac surgeon’s consultation, the patient was indicated for surgery and later was prepared for cardiac surgery. Anticoagulation therapy was continued until the patient was transferred to the operating room. Coagulation test results prior to the surgery were prothrombin time 12 seconds (international normalized ratio [INR] 1) and partial thromboplastin time 60 seconds.
At the time of surgery, following a median sternotomy, cardiopulmonary bypass (CPB) was instituted following cannulation of the ascending aorta and the inferior vena cava. The RA and SVC were opened, and the long-standing “white clots” were extracted. Afterward, the heart was arrested with St. Thomas’ Hospital cardioplegic solution, and circulatory arrest with antegrade cerebral perfusion was initiated. Clots were also removed from the branches of both the right and left pulmonary arteries (Fig. ). All the suture lines were closed, and the patient was weaned from CPB following 152 minutes with cross-clamping and circulatory arrest times of 112 and 20 minutes, respectively. Intraoperative TEE after clot removal revealed normal LV size and systolic function, and there were not any signs of clots in the SVC, RA, or other parts. The patient tolerated the procedure well and had an uncomplicated postoperative course. The final TTE did not show any signs of recurrence of the masses or pulmonary hypertension. The pathologic evaluations confirmed that all the surgically removed specimens were thromboses. A complete coagulation workup revealed heterozygosity in the following genes: factor V Leiden HR2 (4070 A/G), methylenetetrahydrofolate reductase (MTHFR) (1298 A/C), β-fibrinogen (− 455 G/A), glycoprotein Ia (807 C/A), plasminogen activator inhibitor 1 (PAI-1; 5G/4G), tissue plasminogen activator (intron 8 del/ins), and apolipoprotein E (E2/E3).
The patient’s symptoms, including palpitation and dyspnea, dissolved completely after the surgery, and she was discharged on warfarin to maintain an INR of 2–3. Finally, she was followed for 1 year after her discharge for any symptoms and signs of the clots, but the follow-up results were all negative. No pulmonary hypertension was detected by TTE in follow-up.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [19.0, 'mg/dL'], 'Glucose': [102.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",292.45238,277.82976,307.075,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 19.0 mg/dL. 
The concentration of glucose is 102.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (19.0 / 2.8) + (19.0 / 18) = 292.45238 mmol/L.The patient's calculated serum osmolality concentration is 292.45238 mmol/L. This is equalivalent to 292.45238 mOsm/kg."
5646,30,Serum Osmolality,lab test,decimal,pmc-5383592-1,Extracted,"A 38-year-old Hispanic woman with a past medical history of pulmonary embolism, DVT, and asthma was seen for an evaluation of her recurrent episodes of thrombosis. She had experienced three episodes of DVT and one episode of pulmonary embolism. The first episode of DVT occurred 5 years ago, and the second episode happened 3 years ago. The pulmonary embolism occurred 1 year ago, following her third episode of DVT. Each DVT episode presented with lower leg edema and pain, and was confirmed by lower extremity ultrasound. The pulmonary embolism episodes presented as shortness of breath and low oxygen saturation.
She was given the following medications to take at home: Ipratropium-Albuterol (Duoneb Neb), 3 mL by inhalation every 4 hours as needed, and warfarin sodium (Coumadin), 12 mg orally once daily. However, she was non-adherent to the use of warfarin. The notable aspects of her family history were that her mother had diabetes mellitus and hypertension, while her father had colon cancer at age of 42. She was a current smoker and had been smoking 2 packs of cigarettes daily for 20 years. She denied alcohol and drug use. A review of systems was non-contributory.
A recent complete blood cell count revealed the following: white blood count 11.1×109/L, hemoglobin level 14.9 g/dL, hematocrit 45.4%, mean corpuscular volume (MCV) 81.6 fL, mean corpuscular hemoglobin (MCH) level 30.7 pg, mean corpuscular hemoglobin concentration (MCHC) 32.8 g/dL, platelet count 555×109/L, neutrophil 46%, lymphocyte 41%, monocyte 4.6%, eosinophil 3.9%, and basophil 0.1%. A basic metabolic profile (BMP) showed the following levels: sodium 139 mmol/L, potassium 4.1 mmol/L, chloride 109 mmol/L, carbon dioxide 29 mmol/L, blood urea nitrogen (BUN) 6 mg/dL, creatinine 0.6 mg/dL, glucose 86 mg/dL, calcium 9.1 mg/dL, phosphorus 3.8 mg/dL, magnesium 2.2 mg/dL, total protein 7.8 g/dL, albumin 3.7 g/dL, aspartate amino-transferase (AST) 16 U/L, alanine amino-transferase (AST) 20 U/L, and alkaline phosphatase 119 U/L.
Her latest chest computed tomography showed a small incomplete filling defect in the right upper lobe, suggesting a chronic non-occluding pulmonary embolism. A coagulation workup, including lupus anticoagulant, protein C and S level/activity, antithrombin III level/activity, factor V level/activity, anti-cardiolipin IgG antibody, anti-cardiolipin IgM antibody, beta 2-GPI antibody (IgG,IgA, and IgM), Von Willebrand factor (VWF), factor VIII, methylenetetrahydrofolate reductase (MTHFR) gene mutation, homocysteine level, and prothrombin mutation analysis showed normal findings. For evaluation of high-normal platelet level, JAK2 mutation was analyzed; no other cause of thrombocytosis had been identified in the patient's history or laboratory findings. The result showed G571S mutation in JAK2 exon 12, and negative for CALR mutation. Total nucleic acid from plasma was used to sequence exons 12 and 13 using the polymerase chain reaction technique. The patient refused to undergo a bone marrow study.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [6.0, 'mg/dL'], 'Glucose': [86.0, 'mg/dL'], 'Sodium': [139.0, 'mmol/L']}",284.92063,270.6746,299.16666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mmol/L. 
The concentration of bun is 6.0 mg/dL. 
The concentration of glucose is 86.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (6.0 / 2.8) + (6.0 / 18) = 284.92063 mmol/L.The patient's calculated serum osmolality concentration is 284.92063 mmol/L. This is equalivalent to 284.92063 mOsm/kg."
5647,30,Serum Osmolality,lab test,decimal,pmc-6858266-1,Extracted,"A 27-year-old man arrived at the emergency department (ED) after an episode of syncope. The patient was lifting off the floor a family member who had just experienced a fall, when he suddenly lost consciousness. He denied any presyncopal symptoms including nausea, vomiting, diaphoresis, dizziness, visual disturbances, chest pain, palpitations, abdominal discomfort, fever, and chills. Per his mother, who witnessed the event, the patient did not experience abnormal body movements or tongue biting or urinary incontinence during syncope. He was unconscious for several minutes but regained consciousness promptly and was not confused. After the syncopal event, the patient’s only complaint was tooth pain likely caused by local trauma during the fall. The patient did not recollect any head trauma and had no headaches prior to or after the incident. He had never had a similar event in the past.
The patient’s past medical and surgical history included unrepaired unilateral cryptorchidism and surgically corrected intussusception during infancy, both attributable to history of premature birth. He reported episodes of self-limited palpitations unrelated to exertion. He drank alcohol occasionally but had not had a drink for a week prior to admission. The patient never smoked or used drugs. He denied taking any medications or herbal supplements. He had no known family history of early-onset coronary artery disease, heart failure, valvular disease, arrhythmias, congenital heart disease, or sudden deaths.
On physical examination, the patient appeared to be in no distress and was alert and oriented to person, place, time, and situation. Blood pressure was 140/90 mm Hg, pulse was 86 beats/minute (bpm), respirations were 12 breaths/minute, and the temperature was 97.8 °F. Weight was 106.6 kg and the body mass index was 39.11 kg/m². Orthostatic vital signs were not obtained upon arrival and were negative after fluid resuscitation received in the ED. The head was atraumatic. The neck was obese with normal carotid pulses and no bruits. Jugular venous distention and hepatojugular reflux were absent. The heart examination revealed an irregularly irregular rhythm and normal heart sounds. There was no right ventricular heave, murmur, nor friction rub noted. A right mid-abdominal well-healed scar was observed. There was no abdominal distention and the abdomen was non-tender. Bowel sounds were normal. Radial, dorsalis pedis, and posterior tibial pulses were normal bilaterally.
Initial laboratory results revealed white blood cells 8.8 k/uL (normal range, 4.0-10.5), 79% (25% to 62%) of which were segmented neutrophils, hemoglobin 17.4 g/dL (12.5-16.0), platelets 329 K/uL (150-450), sodium 144 (136-145 mEq/l), potassium 4.5 (3.5-5.1 mEq/L), glucose 106 (70-105 mg/dL), troponin <0.03 ng/mL (<0.03), D-dimer ˂150 (0-230 DU ng/ml), creatinine 0.9 (0.7-1.3 mg/dl), blood urea nitrogen 14 (7-25 mg/dl), and TSH was 3.2 (0.45-5.33 uIU/mL). Urine toxicology was negative.
The electrocardiogram (ECG) revealed atrial fibrillation (AF), with a ventricular rate of 83 bpm and an S1Q3T3 pattern along with an incomplete right bundle branch block. A repeat ECG completed four hours later demonstrated a return to normal sinus rhythm but with the persistence of the S1Q3T3 pattern and incomplete right bundle branch block. Broad differential diagnosis of right ventricular dysfunction in young adults was entertained, including pulmonary embolism, pulmonary hypertension from obstructive sleep apnea, congenital heart disease, and right ventricular dysplasia leading to ventricular arrhythmias. Computed tomography angiography (CTA) of the chest was performed in the ED. The test was negative for pulmonary embolism but described a 4.9-cm irregular low-density anterior mediastinal mass.
TTE revealed normal left ventricular ejection fraction estimated at 55% to 65% with abnormal septal motion suggestive of severely dilated right ventricle and right atrium. The left atrium had a normal cavity size with normal volume index. Rheumatic mitral valve disease with trace regurgitation and mild stenosis were noted. The tricuspid valve was thickened with trace regurgitation but no stenosis. Pulmonary artery systolic pressure was 24.4 mmHg, which was likely underestimated in the presence of trivial tricuspid regurgitation. Agitated saline contrast was given to evaluate for intracardiac shunt which was negative for the right to left anomalous inter-atrial connection. Unexplained right heart enlargement was further explored with TEE, which was performed the next day.
TEE revealed a large superior SVASD (arrow; Figure ).
Left-to-right shunting (arrow) was indicated by color flow Doppler (Figure ).
The CTA completed earlier (Figure ) was reviewed with the radiologist who appreciated the right superior pulmonary vein connection to the superior vena cava (SVC).
The patient was started on anticoagulation in the setting of AF with an ASD and was referred to cardiothoracic surgery. He underwent a successful ASD repair. During operation, it was confirmed that the right superior pulmonary vein drained into the SVC and it was noticed that the left superior vena cava crossed the hilum and joined the coronary sinus, which was dilated. The surgical technique performed was intra-atrial baffle repair of SVASD, which corrected the congenital defect. A patch method was used to augment SVC-right atrial confluence to achieve an unobstructed SVC connection to the right heart system.
During the procedure, the thymic mass was resected, and the pathology results were consistent with nodular lymphoid tissues with Hassall’s corpuscles and epithelial cells within a fatty stroma, recapitulating normal histology, consistent with hyperplasia. No atypia or malignancy was recognized.
The patient made a good clinical recovery. The patient was discharged from the hospital five days postoperatively on oral aspirin 325 mg daily, metoprolol tartrate 50 mg twice daily and Tramadol 50 mg every six hours as needed for pain control. At the follow-up visit in the cardiology office, he reported very good exercise tolerance during daily activities and cardiac rehabilitation sessions.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [14.0, 'mg/dL'], 'Glucose': [106.0, 'mg/dL'], 'Sodium': [144.0, 'mEq/L']}",298.88889,283.94445,313.83333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 144.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 144.0 mEq. To convert from 144.0 mEq to mmol, convert from mEq to mmol. The compound 144.0 has a valence of 1, and so divide the valence by the value of mEq to get, 144.0 mEq/(1 mEq/mmol) = 144.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 144.0 mEq sodium/L converts to 144.0 mmol sodium/L. 
The concentration of bun is 14.0 mg/dL. 
The concentration of glucose is 106.0 mg/dL. 
Plugging these values into the equation, we get 2 * 144.0 + (14.0 / 2.8) + (14.0 / 18) = 298.88889 mmol/L.The patient's calculated serum osmolality concentration is 298.88889 mmol/L. This is equalivalent to 298.88889 mOsm/kg."
5648,30,Serum Osmolality,lab test,decimal,pmc-3917171-1,Extracted,"A 67-year-old woman presented to emergency department with complaints of episodes of inability to walk for the past 5 days, happening 4-5 times a day. Each episode lasted for 15-20 minutes and was associated with restlessness and breathlessness. Patient was apparently alright one month before, since then she started feeling generalized weakness on and off. However, for past 5 days symptoms were exaggerated and she started feeling sudden loss of power in both the lower limbs simultaneously and inability to walk. She could walk normally after the episode subsided. This episode was not associated with pain in the limbs. Patient was totally conscious during the entire episode. Her medical history was significant for diabetes and hypertension for the past 5 years. The patient's drug therapy consisted of insulin nova mixtard 30/70 (for the past 10 years), olmesartan 20 mg per day (for past 2 years), perindopril 4 mg per day (for past 16 months), and torsemide 10 mg per day (for past 6 months).
On examination she was found to be alert and fully oriented. Vital signs revealed a regular pulse rate of 93 beats per minute, blood pressure of 130/80 mmHg, temperature of 36.8°C, a respiratory rate of 14/min and oxygen saturation of 100% on room air by pulse oxymetry. Cardiac auscultation revealed normal heart sounds, respiratory examination revealed bilateral vesicular breath sounds with bilateral basal crepitations. Complete neurological examination did not reveal significant finding.
The results of laboratory examination were as follows: 10.6 g%, Total Leukocyte Count: 10,500, Differential Leukocyte Count: N70 L26 M3 E1 B0, ESR: 12 mm/hr, Random blood sugar: 98 mg/dl, Urea: 24 mg/dl, Creatinine: 1.2 mg/dl, Total Cholesterol: 198 mg/dl, Triglyceride: 112 mg/dl, HDL: 38 mg/dl, LDL: 138 mg/dl, Serum sodium: 134 mEq/L, Serum potassium: 8.6 mEq/L, Total calcium: 11 mg/dl, Ionized calcium: 1.30 mEq/L, Serum Magnesium: 2.5 mg/dl, Serum chloride: 104 mmol/L, Serum Bicarbonate: 24 mmol/l. ECG showed normal sinus rhythm, normal axis, and tall T waves. CT scan and EMG were not done.
Diabetic neuropathy, Gullian Barre Syndrome, metabolic cause of periodic paralysis.
The diagnosis of drug-induced hyperkalemia presenting as periodic paralysis was suggested by very high serum potassium concentration during the attack and also persistent hyperkalemia between attacks.
Patient was immediately admitted and the treatment for hyperkalemia was instituted. Drugs causing potassium retention were immediately stopped. Medical measures were started to lower down the level of serum K+ which included K+ bind sachet (calcium polystyrene sulfonate) thrice daily. Lactulose syrup and magnesium sulfate was given to avoid constipation. Her K+ started decreasing progressively and within 24 h K+ got reduced from 8.4 mEq/L to 6.8 mEq/L. In the next 24 h serum K+ further lowered from 6.8 to 5.4 mEq/L.
There was progressive fall of blood pressure during the course of the treatment and patient was overall drowsy and disoriented. Measures were taken to maintain her blood pressure.
Patient responded well to the treatment and was discharged in a stable state with serum K+ level of 5.1 mEq/L, and blood pressure of 120/80 mmHg on 5th day of admission.
The patient has been followed-up on an outpatient basis, her serum potassium has been stable with no further episodes of periodic paralysis.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [24.0, 'mg/dL'], 'Glucose': [98.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",282.01587,267.91508,296.11666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. 
The concentration of bun is 24.0 mg/dL. 
The concentration of glucose is 98.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (24.0 / 2.8) + (24.0 / 18) = 282.01587 mmol/L.The patient's calculated serum osmolality concentration is 282.01587 mmol/L. This is equalivalent to 282.01587 mOsm/kg."
5649,30,Serum Osmolality,lab test,decimal,pmc-3608317-1,Extracted,"A 91-year-old Puerto Rican man presented for evaluation of progressively worsening shortness of breath over the past six months associated with two weeks of productive cough of yellowish sputum. The patient also had complaints of fatigue, palpitations and dyspnea with minimal exertion. His past medical history was significant for pulmonary tuberculosis in 1969 for which he received approximately 24 months of medical treatment. The patient also had a history of coronary artery disease, bronchiectasis, moderate pulmonary hypertension, moderate chronic obstructive pulmonary disease (COPD), and has had multiple exacerbations of his bronchiectasis and COPD which did not require hospitalization. He had a history of smoking 30 cigarette packs per year but discontinued cigarette smoking 45 years prior to his admission. He denied alcohol or drug use and had no history of prior surgeries. He had been followed by a pulmonologist for over seven years, and spirometry testing done four months before his presentation showed an forced expiratory volume1 (FEV1) to forced vital capacity (FVC) ratio of 64%, FEV1 of 71%, and FVC of 84%. One year prior to presentation, an echocardiographic assessment demonstrated left ventricular hypertrophy with moderate pulmonary hypertension, and a dobutamine stress echocardiogram demonstrated a defect in the inferior wall consistent with a previous infarction.
On physical examination, the patient was tachycardic at a heart rate of 140 beats per minute, tachypneic with a respiratory rate of 18 breaths per minute and saturating oxygen at 94% on atmospheric air. The patient was awake, alert, and oriented to person, time, and place and able to speak in full sentences. He did not demonstrate jugular venous distention, but his trachea was deviated towards his right side. There was no evidence of stridor. The patient’s breath sounds were diminished bilaterally with more prominently diminished sounds over his right lung fields. Coarse rhonchi were notable over his right lower lung. No wheezing or rales were appreciated. Heart sounds were more prominent on the right side of the chest and were characterized as an irregular tachycardia, with no murmurs, gallops or accentuated heart sounds appreciated. Laboratory studies demonstrated a white blood cell count of 7100/mm3, hemoglobin level 9.1g/dL, hematocrit 28.0%, sodium 137mEq/L, potassium 4.0mEq/L, chlorine 101mEq/L, bicarbonate 30mEq/L, blood urea nitrogen 16mg/dL, serum creatinine 0.6mg/dL, glucose 140mg/dL, troponin I: 0.03ng/mL, B-type natriuretic peptide 320ng/L, and normal liver and kidney function. Arterial blood gas showed a pH of 7.480, partial pressure of carbon dioxide of 46, partial pressure of oxygen of 116 and an oxygen saturation of 99% on two L of oxygen. An electrocardiogram showed a multifocal atrial tachycardia without T wave or ST segment changes (Figure ). A chest X-ray demonstrated opacification of the right hemithorax with a marked mediastinal shift to the right and hyperinflation of the left lung (Figure ). A computed tomography scan of the patient’s chest showed hyperinflation of his left lung, cystic bronchiectasis, mediastinal shifting to the right with clockwise rotation of his trachea and marked absence of normal lung parenchyma in his right lung (Figures , ). Venous Doppler ultrasound of his lower extremities was negative for venous thrombosis. The patient’s presentation was attributed to a cardiac arrhythmia secondary to his extensive lung disease and was treated with calcium channel blockers to control his heart rate. However, four days into his hospital course, he became lethargic with a three gram drop of his hemoglobin and subsequently went into cardiac arrest. The patient was immediately intubated and was resuscitated according to Advanced Cardiac Life Support protocol. During the arrest he was noticed to have profound coffee ground emesis. Despite resuscitation efforts, the patient remained pulseless and subsequently died.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [16.0, 'mg/dL'], 'Glucose': [140.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",287.49206,273.11746,301.86666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 16.0 mg/dL. 
The concentration of glucose is 140.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (16.0 / 2.8) + (16.0 / 18) = 287.49206 mmol/L.The patient's calculated serum osmolality concentration is 287.49206 mmol/L. This is equalivalent to 287.49206 mOsm/kg."
5650,30,Serum Osmolality,lab test,decimal,pmc-2900037-1,Extracted,"A 54-year-old male patient presented in emergency room with acute retention of urine. He was a known case of OI tarda (). Immediately foley's catheterization (no.-16fr.) was done to relieve retention. X-Ray KUB of the patient revealed a right side renal calculus and a vesicle calculus and was planned for cystolithotomy ().
On preanaesthetic evaluation, the patient weighed 22 kg, length 94 cm, head circumference 50 cm, chest circumference 65 cm, and was bedridden. He had undergone previously cystolithotomy at 6 months of age (details of that operation were not available). History revealed uneventful antenatal period and no delay in milestones. Patient developed normally upto 10yr of age and after that he started having skeletal fractures. There was no positive family history.
Investigation revealed Hb 12.6 g%, TLC 9300, platelet count 2.3 lacs, blood sugar 86 mg/dl, blood urea 40.4 mg/dl, serum creatinine 0.6 mg/dl, serum potassium 4.5meq/l, serum sodium 143meq/l, serum calcium 8.7meq/l.
Preoperative coagulation profile was normal. 2D echo revealed no valvular abnormalities and normal ejection fraction (64%). Pulmonary function tests revealed a moderate degree of restrictive lung disease.
The patient was accepted for surgery as ASA grade II. In view of anticipated difficult airway, it was planned to conduct the case under regional anaesthesia. In the operation theatre, i.v. line was secured using 18 G cannula. Monitoring included 5 lead ECG, manual blood pressure monitoring, SpO2, EtCO2, and temperature. Difficult airway cart was also kept standby. After preloading with 500ml of Ringer lactate i.v., caudal epidural anaesthesia was given in lateral position with 14ml of 0.25% of bupivacaine. Midazolam 1.0mg and butorphanol 1.0mg i.v. was given for sedation. During surgery, his vitals remained stable and no rescue medication was required. Operation lasted for about 40 min and patient had an uneventful recovery. He was discharged on 5th postoperative day.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [40.4, 'mg/dL'], 'Glucose': [86.0, 'mg/dL'], 'Sodium': [143.0, 'mEq/L']}",305.20635,289.94603,320.46667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 143.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 143.0 mEq. To convert from 143.0 mEq to mmol, convert from mEq to mmol. The compound 143.0 has a valence of 1, and so divide the valence by the value of mEq to get, 143.0 mEq/(1 mEq/mmol) = 143.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mEq sodium/L converts to 143.0 mmol sodium/L. 
The concentration of bun is 40.4 mg/dL. 
The concentration of glucose is 86.0 mg/dL. 
Plugging these values into the equation, we get 2 * 143.0 + (40.4 / 2.8) + (40.4 / 18) = 305.20635 mmol/L.The patient's calculated serum osmolality concentration is 305.20635 mmol/L. This is equalivalent to 305.20635 mOsm/kg."
5651,30,Serum Osmolality,lab test,decimal,pmc-7031711-1,Extracted,"An 84-year-old female presented to the emergency department with complaints of constipation, vomiting, decreased appetite, and excessive urination for the last 10 days and altered sensorium for the last 2 days. There was a history of generalised bone pain for last 3 months for which she was prescribed calcium. Except Bell's palsy 5 months back with complete recovery, past and family history was unremarkable. On examination, the patient was drowsy but arousable. She was dehydrated, and blood pressure was 146/90 mm Hg. Her systemic examination including neurological did not reveal any localisation. Investigations revealed anemia (Hb—6.5 g/dl), deranged renal function (urea—118 mg/dl, creatinine 5.62 mg/dl), increased total protein (9.27 g/dl) and globulin (7.34 g/dl), low albumin (1.93 g/dl), and hypercalcemia (total calcium-15.07 mg/dl). Random plasma glucose (131 mg/dl) and serum electrolytes (sodium/potassium—141/3.92 meq/L) were in the normal range. Serum PTH levels were normal. In addition, serum ammonia levels were also normal (39.4 mmol/L, normal 17–90 mmol/L). Noncontrast computerised tomography of brain showed age-related changes in the bilateral cerebral hemisphere with multiple lytic lesions of varying sizes noticed in the cranial vault and base of the skull. The patient was diagnosed as hypercalcaemic encephalopathy with suspicion of multiple myeloma. To confirm the diagnosis of multiple myeloma, serum protein electrophoresis was performed, which showed M protein (in the beta region) 4.9 g/dL with increased beta 2 microglobulin (9284 ng/ml, normal 609–2366 ng/ml). Bone marrow aspiration showed 60% plasma cells. The final diagnosis of multiple myeloma with hypercalcaemic encephalopathy was made. The patient was treated with iv. fluids (0.9% normal saline, 200 ml/hr with the rate adjusted to maintain urine output 100–150 ml/hr). The patient was also treated with loop diuretics and calcitonin. The next day, zolendronic acid (at modified dose according to GFR) was added. On day 9 of hospitalisation, the patient was put on dexamethasone, lenalidomide, and bortezomib. At the end of 2nd week patient's sensorium was improved, with normalization of serum calcium and renal function ().",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [118.0, 'mg/dL'], 'Glucose': [131.0, 'mg/dL'], 'Sodium': [141.0, 'mEq/L']}",331.42063,314.8496,347.99166,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. 
The concentration of bun is 118.0 mg/dL. 
The concentration of glucose is 131.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (118.0 / 2.8) + (118.0 / 18) = 331.42063 mmol/L.The patient's calculated serum osmolality concentration is 331.42063 mmol/L. This is equalivalent to 331.42063 mOsm/kg."
5652,30,Serum Osmolality,lab test,decimal,pmc-4251025-1,Extracted,"A 69-year-old lady diabetic and hypertensive on treatment presented with sudden onset of vertigo followed by weakness of left upper and lower limbs of 1.5 hours duration. She had associated dysarthria and deviation of angle of mouth to the right side. There was no history of loss of consciousness, visual symptoms, seizures, headache, hiccoughs, and dysphagia. No previous history suggestive of transient ischemic attacks, stroke, intracerebral hemorrhage, neck pain, trauma. She was diagnosed to have left atrial myxoma (LAM; based on cardiac magnetic resonance imaging, MRI [], and echocardiogram) 13 months prior to the presentation and was not on any therapy. She had declined the surgical treatment of the tumor when it was diagnosed. At presentation, her vitals were stable, all peripheral pulses were felt, and no bruits were heard. Auscultation over chest revealed no murmurs. Neurologically, the patient was conscious, oriented, had severe dysarthria, no nystagmus, pupils were 2-mm reactive to light; she had gaze preference to right, left upper motor neuron facial palsy with 0/5 power in left sided limbs. Sensory system and right-sided limbs (motor, cerebellar) were normal. Deep tendon reflexes were normal except ankle jerks, which were sluggish bilaterally. Right plantar reflex was flexor while left was extensor. National Institutes of Health Stroke Scale (NIHSS) score at admission was 14, and modified Rankin score (mRS) was 4.
Investigations revealed hemoglobin -10.9 gm/dl, total count -6000/cmm, platelet count -2,37,000/cmm, prothrombin time - normal, blood glucose -255 mg/dl, urea -39 mg/dl, creatinine -1.2 mg/dl, Na -141 meq/l. A non-contrast computerized tomographic (CT) scan done at presentation [] was normal. A clinical diagnosis stroke was made; the site of lesion being on right side above the nucleus of the facial nerve, may be in subcortical or brainstem region with no additional localizing signs. Patient and relatives were explained about the treatment options available and the risk and benefit of thrombolysis, and consent was obtained for intravenous thrombolytic therapy (IVT). Patient was shifted to the stroke unit. As there were no contraindications for IVT and she being in the window period, 0.9 mg/kg of rt-PA was started according to the standard guidelines. About 15 minutes after starting the treatment, the patient started improving, and by the end of procedure, the patient had only minimal left-sided limb weakness, slight dysarthria, and facial weakness. The NIHSS score at the end of thrombolysis was 5, with mRS being 1. Patient was closely monitored during the procedure and later, in the stroke unit as per the protocol. There were no complications and the blood pressure was normal throughout the procedure.
Five hours after the completion of the thrombolysis, she developed vomiting and became drowsy and then lapsed into altered sensorium. Examination revealed blood pressure of 184/100 mm of Hg, and pulse rate of 86/min. Neurologically, she was in altered sensorium, not opening eyes to stimuli, responding to commands, or verbalizing. Her right pupil was 3 mm not reacting, left 2 mm reacting to light. There was vertical dysconjugation (right eye lower than the left), and dolls eye movements restricted in vertical directions. She was moving her right upper and lower limb minimally to pain, not moving left upper and lower limb even to deep painful stimuli; NIHSS score was 31 and mRS was 5. She worsened in sensorium and developed respiratory difficulty so she was intubated and connected to mechanical ventilator. Clinical possibility of post IVT bleed was considered localizing to the right side above midbrain. Patient underwent plain CT scan which revealed [] hemorrhage in the right thalamus and upper midbrain (right more than left) with intraventricular extension and mild hydrocephalus.
Patient was treated with anti-edema measures and other supportive measures as per the guidelines for the management of post thrombolysis bleed. Cardiac echocardiogram showed well-defined heterogeneous mobile mass in the left atrium measuring 2.3 × 2.7 × 1.8 cm, attached to the roof of left atrium and prolapsing across the mitral valve with attached thrombus suggestive of LAM with thrombus. Troponin I was negative, lipid profile — normal, serum homocysteine - normal, glycosylated hemoglobin was (HbA1C): 9.8% suggestive of poor control of her diabetes. Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) of the brain done 30 days after the event showed resolving late sub-acute hematoma in right thalamus with extension to right upper midbrain with hypointense rim with vessles being normal [].
She was on ventilator for 25 days, then gradually improved in neurological status and was weaned off from the ventilator. At the time of discharge (70 days post stroke), the patient has residual deficits in the form of moderate weakness of left upper limb and mild weakness of left lower limb, with pupil of 3 mm, bilateral equal and reactive to light. The NIHSS score was 8, and mRS was 4. Subsequently, she has been on regular follow-up from last two years. Except for mild distal left hand weakness, she is leading a normal life. She has been under care of a cardiologist for LAM and has declined surgery.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [39.0, 'mg/dL'], 'Glucose': [255.0, 'mg/dL'], 'Sodium': [141.0, 'mEq/L']}",310.09524,294.59048,325.6,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. 
The concentration of bun is 39.0 mg/dL. 
The concentration of glucose is 255.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (39.0 / 2.8) + (39.0 / 18) = 310.09524 mmol/L.The patient's calculated serum osmolality concentration is 310.09524 mmol/L. This is equalivalent to 310.09524 mOsm/kg."
5653,30,Serum Osmolality,lab test,decimal,pmc-2803816-1,Extracted,"A 70-year-old woman presented with headache, weakness, fatigue, right palpebral ptosis and diplopia. Magnetic resonance imaging (MRI) of the sella revealed a sellar mass involving the pituitary gland and infundibular stalk, which also extended into the right cavernous sinus and the sphenoid sinus. The neurologists demonstrated infiltrations of the right II, III, IV, V and VI cranial nerves (figure , figure and figure ).
A week after occurrence of right palpebral ptosis, the patient received immediate transsphenoidal decompression surgery. The histological examination revealed that the mass was the infiltration of a high-grade B-cell non-Hodgkin's lymphoma involving respiratory system epithelial cells.
After the transsphenoidal operation, the patient was transported to our endocrinology clinic. Her skin was pale and she had right palpebral ptosis. No lymphadenopathy or goiter was found. She did not have galactorrhea. Her axillary and pubic hair was scant. Her blood pressure was 120/70 mmHg with a pulse rate of 80 beats/per minute (hypertension and bradycardia existing before the operation, were improved postoperatively). Examination of the chest, abdomen and cardiovascular system was normal.
As per whole blood count, hemoglobin was 12.3 g/dl, hematocrit was 38%, white blood cell count (WBC) was 11,760/mm3, lymphocytes were 1400/mm3, neutrophils were 9660/mm3 and platelet count was 123,000/mm3. The biochemical analysis results of the blood were as follows: glucose: 90 mg/dl, blood urea nitrogen (BUN): 22 mg/dl, creatinine: 0.7 mg/dl, sodium: 141 mEq/L, potassium: 4 mEq/L, serum osmolarity: 295 mOsm/kg H2O, with a paired urine osmolality of 173 mOsm/kg, free T4: 20.4 pmol/L, thyroid stimulating hormone (TSH): 0.705 mIU/L, cortisol at 8 am, 16.7 mcg/dl, adrenocorticotrophic hormone (ACTH) at 8 am, 41 ng/L, luteinizing hormone (LH): 0.1 mIU/ml, follicle-stimulating hormone (FSH): 1.8 mIU/ml, estradiol: 8.1 pg/ml, prolactin (PRL): 102.4 ng/dl. Low levels of urine osmolality after overnight water deprivation along with normal plasma osmolality suggested DI. Desmopressin treatment was not administered because the daily urine volume did not exceed 4 liters (her weight was 56 kg).
Hyperprolactinemia was attributed to the stalk compression which interrupted dopamine transport to lactotrophs. The low levels of FSH and LH observed in this post-menopausal woman suggested infiltration of the anterior pituitary by lymphoma. Because primary sellar lymphoma is very rare and histological examination of our patient revealed that the mass was due to infiltration of a high-grade B-cell non-Hodgkin's lymphoma involving respiratory system epithelial cells, computed tomography (CT) of the paranasal sinus and MRI of the thorax and abdomen were performed.
Although MRI of the thorax and abdomen did not show any abnormalities, when the paranasal sinus CT scan was performed, we concluded that the primary lymphoma originated from the sphenoid sinus and infiltrated the pituitary gland. When bone marrow aspiration was performed, lymphoma infiltration to the bone marrow was detected and the thrombocytopenia was thought to be resulting from lymphoma infiltration of the bone marrow. Chemotherapy and radiotherapy to the sellar area were planned, but the patient died and her family did not permit an autopsy.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [22.0, 'mg/dL'], 'Glucose': [90.0, 'mg/dL'], 'Sodium': [141.0, 'mEq/L']}",294.85714,280.11428,309.6,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. 
The concentration of bun is 22.0 mg/dL. 
The concentration of glucose is 90.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (22.0 / 2.8) + (22.0 / 18) = 294.85714 mmol/L.The patient's calculated serum osmolality concentration is 294.85714 mmol/L. This is equalivalent to 294.85714 mOsm/kg."
5654,30,Serum Osmolality,lab test,decimal,pmc-5502936-1,Extracted,"A 13-month-old boy with a history of a small ventricular septal defect was brought to the emergency department (ED) for an acute onset of respiratory distress after FB aspiration. The child grabbed a granola bar with nuts from his mother and ate it while walking and laughing. Suddenly, he started choking and developed breathing difficulty. His father and a neighbor administered back blows, but he did not cough up any nuts. His father immediately called 911. When the emergency medical service (EMS) arrived within a few minutes, the child was still responsive and breathing on his own, but developed worsening respiratory distress. EMS found him cyanotic, but did not see any visible FB in the oral airway or oropharynx. EMS initiated bag mask ventilation with 100% oxygen and brought him to the ED. In the ED, he was noted to be in moderate respiratory distress with respiratory rate of 52/min, heart rate of 171/min and oxygen saturation of 90% on non-rebreather mask with 100% oxygen. He had noisy breathing, but was able to phonate intermittently and made a weak cry. He was pale and had mottled skin with cold extremities. Chest auscultation revealed decreased air entry in both lung fields without wheezing or crackles.
The ED attending physician performed direct laryngoscopy, but did not find any FB. The anesthesiologist intubated the child with a 4.0 uncuffed endotracheal tube for the progressively worsening respiratory distress with oxygen desaturation. A peripheral intravenous line and an intraosseous line were placed and normal saline bolus was started. Initial chest X-ray (CXR) showed patchy opacity in the right middle lobe (). A repeat CXR to confirm the position of endotracheal tube showed interval development of bilateral, diffuse, hazy ground glass opacities suggestive of pulmonary edema (). The patient received dexamethasone, nebulized racemic epinephrine and Unasyn. Venous blood gas showed pH of 7.20, PvCO2 of 50 mmHg, PvO2 of 28.6 mmHg, HCO3 of 10.9 mmol/L, base deficit of 15.8, oxygen saturation of 63.8% on mechanical ventilation with inspired oxygen of 100%, respiratory rate of 25/min and pressure support (PS) of 18 cm H2O with positive end-expiratory pressure (PEEP) of 10 cm H2O. The basic metabolic panel revealed Na 134 mmol/L, K 4 mmol/L, Cl 110 mmol/L, CO2 of 14 mmol/L, glucose 418 mg/dL, blood urea nitrogen (BUN) 17 mg/dL and creatinine 0.4 mg/dL. CO2 of 14 mmol/L suggested metabolic acidosis, most likely a lactic acidosis either from hypoxemia or systemic circulatory impairment from hemodynamic changes of Muller’s maneuver in response to FB obstruction of trachea.
The otolaryngologist performed bedside flexible laryngoscopy, which also did not show a FB in the larynx or hypopharynx. The child was taken emergently to the operating room (OR) for direct laryngoscopy and rigid bronchoscopy. Multiple pieces of nuts were found in the distal trachea at the level of carina (), occluding the airway completely. All the pieces of nuts were removed. During the procedure, a significant amount of pink, frothy fluid suggestive of pulmonary edema fluid was suctioned from the airway. Tracheal aspirate and blood culture for bacteria were taken and he was started on intravenous Unasyn. He received another dose of dexamethasone, two doses of furosemide 20 mg each and nebulized albuterol. After complete removal of the FB from the airway, he was re-intubated with a 4.0-mm endotracheal tube and was placed on mechanical ventilation with inspired oxygen of 100%. His respiratory status continued to worsen. A repeat CXR () 2½ h after initial CXR showed worsening pulmonary edema. The ventilator settings were readjusted to PS of 24 cm H2O and PEEP of 10 cm H2O to achieve oxygen saturation greater than 94%. He was transferred to the pediatric intensive care unit for further management of pulmonary edema and close monitoring of respiratory status. Pediatric pulmonary was notified late and was not involved in the bronchoscopy for FB removal.
He was extubated 15 h later when his oxygen saturation improved and was placed on bilevel positive airway pressure (BiPAP) mask. Arterial blood gas showed pH of 7.37, PaCO2 of 40 mmHg, PaO2 of 65 mmHg, HCO3 of 23 mmol/L, base deficit of −2 and oxygen saturation of 92% on BiPAP of 10/5 cm H2O with inspired oxygen of 35%. By this time, HCO3 had increased to 23 mmol/L reflecting reversal of metabolic acidosis when oxygenation improved and systemic circulation was normalized. A CXR taken 36 h after initiation of mechanical ventilation showed a marked resolution of the bilateral pulmonary edema. Unasyn was discontinued 3 days later when cultures from the tracheal aspirate and blood were negative. He was weaned to room air on hospital day 3 and discharged to home on hospital day 4. On multiple follow-up visits to clinic, the child was doing well with no long-term respiratory complications.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [17.0, 'mg/dL'], 'Glucose': [418.0, 'mg/dL'], 'Sodium': [134.0, 'mmol/L']}",297.29365,282.42897,312.15833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mmol/L. 
The concentration of bun is 17.0 mg/dL. 
The concentration of glucose is 418.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (17.0 / 2.8) + (17.0 / 18) = 297.29365 mmol/L.The patient's calculated serum osmolality concentration is 297.29365 mmol/L. This is equalivalent to 297.29365 mOsm/kg."
5655,30,Serum Osmolality,lab test,decimal,usmle-10445,Extracted,"A 50-year-old female with a past medical history of hypertension comes to your clinic for a refill of her lisinopril medication. She is also taking lovastatin and hydrochlorothiazide. The patient's vital signs are as follows: HR 80, BP 150/100, and BMI 40. Physical exam is remarkable for a waist-to-hip ratio of 1.0 and the presence of diffuse dark patches on her skin (Figure A). Her fasting lab results are as follows: Sodium: 145 mmol/L, Potassium: 5.0 mmol/L, Chloride: 105 mmol/L, Bicarbonate: 25 mmol/L, BUN: 10 mg/dL, Creatinine: 1.0 mg/dL, Glucose: 200 mg/dL, Triglyceride: 200 mg/dL, LDL: 250 mg/dL, Total cholesterol: 300 mg/dL, HDL: 30 mg/dL, and Hemoglobin A1C: 7.0%.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [10.0, 'mg/dL'], 'Glucose': [200.0, 'mg/dL'], 'Sodium': [145.0, 'mmol/L']}",304.68254,289.44841,319.91667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 145.0 mmol/L. 
The concentration of bun is 10.0 mg/dL. 
The concentration of glucose is 200.0 mg/dL. 
Plugging these values into the equation, we get 2 * 145.0 + (10.0 / 2.8) + (10.0 / 18) = 304.68254 mmol/L.The patient's calculated serum osmolality concentration is 304.68254 mmol/L. This is equalivalent to 304.68254 mOsm/kg."
5656,30,Serum Osmolality,lab test,decimal,usmle-9627,Extracted,"A 32-year-old man presents with a history of diarrhea several days after eating a hot dog at a neighborhood barbeque. He notes that the diarrhea is visibly bloody, but he has not experienced a fever. He adds that several other people from his neighborhood had similar complaints, many of which required hospitalization after eating food at the same barbeque. His temperature is 37°C (98.6°F ), respiratory rate is 16/min, pulse is 77/min, and blood pressure is 100/88 mm Hg. A physical examination is performed and is within normal limits. Blood is drawn for laboratory testing. The results are as follows:
Hb%: 12 gm/dL
Total count (WBC): 13,100/mm3
Differential count:
Neutrophils: 80%
Lymphocytes: 15%
Monocytes: 5%
ESR: 10 mm/hr
Glucose, Serum: 90 mg/dL
BUN: 21 mg/dL
Creatinine, Serum: 1.96 mg/dL
Sodium, Serum: 138 mmol/L
Potassium, Serum: 5.2 mmol/L
Chloride, Serum: 103 mmol/L
Bilirubin, Total: 2.5 mg/dL
Alkaline Phosphatase, Serum: 66 IU/L
Aspartate aminotransferase (AST): 32 IU/L
Alanine aminotransferase (ALT): 34 IU/L
Urinalysis is normal except for RBC casts.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [21.0, 'mg/dL'], 'Glucose': [90.0, 'mg/dL'], 'Sodium': [138.0, 'mmol/L']}",288.5,274.075,302.925,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mmol/L. 
The concentration of bun is 21.0 mg/dL. 
The concentration of glucose is 90.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (21.0 / 2.8) + (21.0 / 18) = 288.5 mmol/L.The patient's calculated serum osmolality concentration is 288.5 mmol/L. This is equalivalent to 288.5 mOsm/kg."
5657,30,Serum Osmolality,lab test,decimal,pmc-5788815-1,Extracted,"A 28-year-old male patient was admitted to the emergency room with impaired consciousness after ingesting antifreeze for suicide purpose about 5 h earlier. At the time of admission, his guardians brought the container of the antifreeze that he had ingested, which was then checked accordingly. The patient had an elevated blood pressure of 130/79 mmHg, pulse rate of 98 beats/min, and respiration rate of 30 breaths/min at the time of admission; his body temperature was 35.4℃. He showed signs of acute illness and presented with lethargic consciousness and restlessness. No other specific findings were found. The venous blood gas analysis results showed pH 6.90, PaCO2 34 mmHg, PaO2 25 mmHg, bicarbonate 6.7 mmol/L, base excess −26.1 mmol/L, and oxygen saturation 15%. Serum biochemical analysis showed sodium 136.4 mEq/L, potassium 7.80 mEq/L, chloride 110 mEq/L, calcium 9.9 mg/dL, phosphorus 3.2 mg/dL, glucose 125 mg/dL, osmolality 375 mOsmol/kg, blood urea nitrogen (BUN) 11 mg/dL, and creatinine 1.67 mg/dL. The patient also showed signs of high anion gap metabolic acidosis with an anion gap of 19.7 mmol/L and osmolar gap of 91.34 mOsm/kg H20. Urinalysis showed proteinuria and microscopic hematuria. Electrocardiogram findings showed sinus tachycardia with a heart rate of 134 beats/min, whereas chest radiography showed mild pulmonary edema. Fluid replacement, sodium bicarbonate, and thiamine were administered as the initial treatment, and fomepizole was loaded at 15 mg/kg intravenously and administered four times, each at 10 mg/kg in 12-h intervals. One hour after admission, the patient's consciousness deteriorated from lethargy to stupor, necessitating tracheal intubation. Two hours after admission, overall condition deteriorated and acidosis was not corrected. Consequently, he was transferred to the intensive care unit, where continuous renal replacement therapy was initiated. Thirty hours after dialysis, metabolic acidosis was controlled, as indicated by pH 7.46, PaCO2 36 mmHg, PaO2 106 mmHg, HCO3 25.6 mEq/L, and anion gap 5.9 mmol/L (). His vital signs stabilized on the 6th day of admission, and consequently, he was extubated. However, the patient's levels of BUN and creatinine remained elevated at 39 and 4.28 mg/dL, respectively, and his hourly urine output was only 10–30 mL, and calcium oxalate crystals were detected on urine microscopy (). The patient's acute renal failure persisted, and therefore the treatment was switched to routine hemodialysis, maintained at three rounds every other day. Starting from the 12th day of admission and the start of dialysis, daily urine output increased to >1,000 mL; thus, dialysis was discontinued. On the 23rd day of admission, the serum BUN/creatinine level decreased to 18.4/1.73 mg/dL, and the daily urine output was being maintained at 3000–4000 mL. The patient was discharged and monitored through Follow-ups. During the outpatient follow-up visit at 3 months after discharge, the levels of BUN and creatinine were 17 and 0.95 mg/dL, respectively, with no proteinuria or hematuria ().",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [11.0, 'mg/dL'], 'Glucose': [125.0, 'mg/dL'], 'Sodium': [136.4, 'mEq/L']}",283.67302,269.48937,297.85667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.4 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.4 mEq. To convert from 136.4 mEq to mmol, convert from mEq to mmol. The compound 136.4 has a valence of 1, and so divide the valence by the value of mEq to get, 136.4 mEq/(1 mEq/mmol) = 136.4 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.4 mEq sodium/L converts to 136.4 mmol sodium/L. 
The concentration of bun is 11.0 mg/dL. 
The concentration of glucose is 125.0 mg/dL. 
Plugging these values into the equation, we get 2 * 136.4 + (11.0 / 2.8) + (11.0 / 18) = 283.67302 mmol/L.The patient's calculated serum osmolality concentration is 283.67302 mmol/L. This is equalivalent to 283.67302 mOsm/kg."
5658,30,Serum Osmolality,lab test,decimal,pmc-4162725-1,Extracted,"An otherwise healthy 34-year-old white female presented to the emergency department (ED) with one-hour history of back pain. The pain began gradually in the center of her thoracic spine at the level of T7–T8 and progressively became worse. She described the pain as a severe dull pain, constant, radiating through to the chest, up the back into the neck and down the back into both buttocks. She attempted to relieve the pain by soaking in warm water; when that was unsuccessful her family member brought her to the ED. She denied history of back pain, trauma, fever, abdominal pain, paresis, paralysis, urinary retention, or paresthesias.
On initial examination, the patient was uncomfortable and moaning. Vital signs were blood pressure 155/90 mm Hg, pulse rate 82 beats/min, respiratory rate 20 breaths/min, and temperature 36.2 degrees C (97.1 F). She was mildly tender over the mid thoracic spine. Heart sounds were regular, pulses were equal in both extremities and bilaterally in the groin, and no other abnormalities of the physical exam were found.
Electrocardiogram performed upon arrival was interpreted as normal sinus bradycardia, rate of 58 bpm, with nonspecific ST segment and T-wave changes. Laboratory evaluation revealed hemoglobin 13.6 g/dL (12.0 to 15.3 g/dL), WBC 11.0 × 103/μL (4.0 to 11.0), platelet count 286 × 103 /μL (150 to 450 × 103 μ/L), sodium 141 mmol/L (135–145 mmol/L), potassium 3.3 mmol/L (3.5–5.1 mmol/L), chloride 106 mmol/L (98 – 109 mmol/L), bicarbonate 29 mmol/L (23 to 31 mmol/L), blood urea nitrogen 13 mg/dL (6 to 26 mg/dL), creatinine 0.83 mg/dL (0.5 to 1.20 mg/dL), and glucose 120 mg/dL (70 – 99 mg/dL). Troponin level was <0.01 ng/mL (<0.01 ng/mL = Expected range for 99% population), myoglobin was 7534 ng/mL (28 – 72 mg/mL) and creatine kinase 2336 IU/L (24 – 170 IU/L). Urinalysis revealed large blood by dipstick with 31 to 50 RBCs (patient was menstruating), negative results for nitrite and leukocyte esterase. Urine toxicology was negative for illicit drugs, and the urine pregnancy test was negative. Chest radiograph was negative for any lung pathology, mediastinum was normal width and no pathology was seen on the thoracic vertebrae. Computed tomography angiogram of the chest was normal; no aortic dissection was found.
An intravenous catheter was inserted when blood was drawn for laboratory evaluation. Hydromorphone 0.5 mg and diazepam 2.5 mg was intravenously given for pain relief and normal saline was begun at 150 ml/hour. Approximately one hour after arrival the patient complained of aching all over and then began to vomit, undigested food with no blood. She mentioned to the staff that a friend with whom she had had dinner had called her and told her that she was also ill. The patient explained that they had eaten fish that her friend had purchased at a local market and cooked for dinner. It was buffalo fish (Ictiobus).
After reviewing the laboratory values, the rate of intravenous normal saline was increased to 300 ml/hour. The patient was further questioned for an etiology of the rhabdomyolysis and an ingestion of a toxin was considered. An Internet search was performed looking at buffalo fish and rhabdomyolysis, and information on Haff disease was identified. The Illinois Poison Control Center was notified. The Illinois Poison Control Center subsequently contacted the Cook County Board of Health and all buffalo fish were removed from the local market.
The patient was admitted to the hospital for continued hydration. On day two the creatine kinase peaked at 30,549 IU/L, approximately 19 hours after arrival. Blood urea nitrogen and creatinine remained normal. Creatine kinase levels began to decline, and the patient was discharged on day three.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [13.0, 'mg/dL'], 'Glucose': [120.0, 'mg/dL'], 'Sodium': [141.0, 'mmol/L']}",293.30952,278.64404,307.975,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mmol/L. 
The concentration of bun is 13.0 mg/dL. 
The concentration of glucose is 120.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (13.0 / 2.8) + (13.0 / 18) = 293.30952 mmol/L.The patient's calculated serum osmolality concentration is 293.30952 mmol/L. This is equalivalent to 293.30952 mOsm/kg."
5659,30,Serum Osmolality,lab test,decimal,pmc-8504876-1,Extracted,"A 57-year-old man with a history of intellectual disability and cognitive impairment was admitted to the Emergency Department (ED) from an extended care facility with a one-week history of generalized, morbilliform erythematous rash associated with a fever of 100.3 °F (39.4 °C) and moderate dysphagia followed by eosinophilia, thrombocytopenia, elevated transaminase enzymes and proteus bacteremia of the presumed urinary source. On admission, the patient was extremely agitated and he was unable to provide any history. Hence, it was unsure whether the patient had any associated pruritus or not. According to the ED documentation, the patient received a second dose of the Moderna vaccine the day before admission.
About two weeks prior, the patient was treated with hydroxyzine pamoate (Vistaril) 50 mg and diphenhydramine 25 mg at an outpatient department for chronic infestation of scabies. The patient had a past medical history of seizures for which he had been taking divalproex sodium (Depakote) 500 mg and levetiracetam (Keppra) 500 mg. We were unable to get any documents for the course of anticonvulsant treatment.
On physical examination, the patient was alert but febrile, tachycardic, and tachypneic. He had diffuse non-elevated erythematous patches on the face, chest, abdomen, lower extremities, and buttock (Figure , ) without the involvement of oral mucosa, palms, and soles. No vesicles, pustules, bulla, or wheals were noted. On review of the systems, no lymphadenopathy was noted, chest examination showed bilateral clear breath sound without wheezing in auscultation with a normal rate, and regular rhythm of pulse in the cardiovascular examination was found.
Laboratory results (Table ) revealed a normal WBC count of 10.4 with a high neutrophil 83.4% and 5.6% eosinophils/ absolute eosinophil .6K/uL (normal 0-3%) followed by 25% after restarting the Depakote, platelet 128,000, hemoglobin 14.1, total bilirubin 4 mg/dl, AST 485 U/L, ALT 657 U/L, ALP 147 U/L, albumin 2.9 g/dl, lactic acid 3.9 mmol/L, Na 148 meq/l, glucose 225 mg/dl, BUN 45 mg/dl, Cr 1.3 mg/dl, urine protein 100 mg/dl, urine nitrite 2+, urine WBC 10-20/HPF, urine bacteria 4+/hpf and blood/urine culture was positive for Proteus. Therefore, the patient was treated with IV Zosyn followed by oral amoxicillin 875 mg for 7 days. The CT abdomen demonstrated mild wall thickening in the urinary bladder with mild hepatomegaly.
Additional work-up with an acute hepatitis panel, HIV, and syphilis were negative. ANA test, Mono test, HHV-6, and HHV-7 were negative as well. The patient was held off all the home medications to identify the causative one and subsequently significant improvement of rash was noted followed by a down-trending of the liver function test (LFT) panel.
On the fourth day, anticonvulsant Depakote was started again and a subsequent increase in transaminase was noted (Table ). In consensus with the GI consultant, Depakote was discontinued after which LFT began improving. Skin lesions started fading followed by improvement in eosinophilia, and thrombocytopenia. The transaminase continued to improve to 156 and 504 for AST and ALT respectively. At the time of discharge, the patient was on levetiracetam and advised for follow-up with the primary care provider and GI specialist on an outpatient basis.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [45.0, 'mg/dL'], 'Glucose': [225.0, 'mg/dL'], 'Sodium': [148.0, 'mEq/L']}",324.57143,308.34286,340.8,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 148.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 148.0 mEq. To convert from 148.0 mEq to mmol, convert from mEq to mmol. The compound 148.0 has a valence of 1, and so divide the valence by the value of mEq to get, 148.0 mEq/(1 mEq/mmol) = 148.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 148.0 mEq sodium/L converts to 148.0 mmol sodium/L. 
The concentration of bun is 45.0 mg/dL. 
The concentration of glucose is 225.0 mg/dL. 
Plugging these values into the equation, we get 2 * 148.0 + (45.0 / 2.8) + (45.0 / 18) = 324.57143 mmol/L.The patient's calculated serum osmolality concentration is 324.57143 mmol/L. This is equalivalent to 324.57143 mOsm/kg."
5660,30,Serum Osmolality,lab test,decimal,pmc-4446924-1,Extracted,"A 38-year-old man presented with nausea, vomiting and loose stools of 2 days duration. Patient gave history of consumption of a tuber taken from the nearby forest with the intent of deliberate self-harm. Patient has consumed the tuber 6 days prior to the presentation. It was followed by nausea, vomiting, loose stools and haematochezia on 4th day. He also complained haematuria and bleeding from gums and rectum on 5th day. On 6th day he observed scalp hair fall, and easy pluckability of beard, moustache and body hair. He also complained oliguria on day 6. Patient's wife has brought the tuber. It was identified as G. superba. Patient revealed that he had consumed 250 g of the tuber along with water.
Patient had no history of any illness. He was apprehensive, with pulse rate of 120 bpm, blood pressure 70/40 mmHg, febrile, with congestion of conjunctivae. The pillow and bed were full of his hair. Patient himself demonstrated easy pluckability of hair. His investigations were, haemoglobin 6.0 g/dl, total leucocyte count 14,000/mm3, differential count: polymorphs: 60, lymphocytes 30, monocytes 5, eosinophils 5%, erythrocyte sedimentation rate 40 mm after first hour, platelet counts 0.24 lakhs/mm3, peripheral smear showed no abnormal cells and no features of haemolysis, there was thrombocytopenia, random blood glucose 120 mg/dl, serum creatinine 5.4 mg/dl, blood urea 188 mg/dl, serum sodium 127 mEq/L, serum potassium 3.9 mEq/L, serum chloride 88 mEq/L, serum bicarbonate 12.0 mmol/L, serum bilirubin 1.0 mg/dl, serum glutamic oxaloacetic transaminase 45 U/L, serum glutamic pyruvic transaminase: 65 U/L, serum alkaline phosphatase 125 U/L, serum proteins 6.9 g/dl, serum albumin 4.3 g/dl, serum creatinine kinase 65 IU/L (reference range: 40–200 IU/L), fractional excretion of sodium <1%, urine microscopy showed plenty of red blood cells and urine myoglobin was negative. Ultrasound abdomen revealed normal sized kidneys. Electrocardiogram showed T inversion in V4, V5, and V6. Chest radiograph was normal.
He was initiated on intravenous fluids, sodium bicarbonate supplementation and ionopressors. He was transfused with two units of whole blood. Blood pressure improved after 24 h. The bleeding manifestations subsided over next 72 h. Serum creatinine fell over next 6 days. Hair loss continued for next 10 days. He lost entire scalp hair. Patient regained scalp hair after 4 months.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [188.0, 'mg/dL'], 'Glucose': [120.0, 'mg/dL'], 'Sodium': [127.0, 'mEq/L']}",327.80952,311.41904,344.2,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 127.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 127.0 mEq. To convert from 127.0 mEq to mmol, convert from mEq to mmol. The compound 127.0 has a valence of 1, and so divide the valence by the value of mEq to get, 127.0 mEq/(1 mEq/mmol) = 127.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 127.0 mEq sodium/L converts to 127.0 mmol sodium/L. 
The concentration of bun is 188.0 mg/dL. 
The concentration of glucose is 120.0 mg/dL. 
Plugging these values into the equation, we get 2 * 127.0 + (188.0 / 2.8) + (188.0 / 18) = 327.80952 mmol/L.The patient's calculated serum osmolality concentration is 327.80952 mmol/L. This is equalivalent to 327.80952 mOsm/kg."
5661,30,Serum Osmolality,lab test,decimal,usmle-9949,Extracted,"A 30-year-old man who was recently placed on TMP-SMX for a urinary tract infection presents to urgent care with a new rash. The vital signs include: blood pressure 121/80 mm Hg, pulse 91/min, respiratory rate 18/min, and temperature 36.7°C (98.2°F). Physical examination reveals a desquamative skin covering both of his lower extremities. A basic chemistry panel reveal sodium 139 mmol/L, potassium 3.8 mmol/L, chloride 110 mmol/L, carbon dioxide 47, blood urea nitrogen 23 mg/dL, creatinine 0.9 mg/dL, and glucose 103 mg/dL.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [23.0, 'mg/dL'], 'Glucose': [103.0, 'mg/dL'], 'Sodium': [139.0, 'mmol/L']}",291.93651,277.33968,306.53334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mmol/L. 
The concentration of bun is 23.0 mg/dL. 
The concentration of glucose is 103.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (23.0 / 2.8) + (23.0 / 18) = 291.93651 mmol/L.The patient's calculated serum osmolality concentration is 291.93651 mmol/L. This is equalivalent to 291.93651 mOsm/kg."
5662,30,Serum Osmolality,lab test,decimal,usmle-6047,Extracted,"A 65-year-old man presents to the emergency department with shortness of breath and a sensation of anxiety. This started suddenly this afternoon and has persisted for the past several hours. The patient has a past medical history of obesity, diabetes, hypertension, and osteoarthritis. His current medications include atorvastatin, lisinopril, insulin, metformin, and ibuprofen. Laboratory values are ordered as seen below:

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.2 mEq/L
HCO3-: 24 mEq/L
BUN: 20 mg/dL
Glucose: 124 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.1 mg/dL
AST: 11 U/L
ALT: 11 U/L

An EKG is ordered as seen in Figure A. His temperature is 99.5°F (37.5°C), blood pressure is 147/92 mmHg, pulse is 177/min, respirations are 15/min, and oxygen saturation is 96% on room air. On physical exam you see a patient who is notably uncomfortable and appears anxious. Pulmonary exam is notable for minor bibasilar crackles. Cardiac exam is notable for tachycardia.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [124.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",292.03175,277.43016,306.63334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 124.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (20.0 / 2.8) + (20.0 / 18) = 292.03175 mmol/L.The patient's calculated serum osmolality concentration is 292.03175 mmol/L. This is equalivalent to 292.03175 mOsm/kg."
5663,30,Serum Osmolality,lab test,decimal,usmle-4766,Extracted,"A 37-year-old woman with a history of a kidney transplant presents with a cough, fever, and fatigue. Her symptoms started 1 week ago and have been steadily worsening. She has a history of IV drug use and worked in the past as a commercial sex work in her 20's. She recently traveled to Malasia 1 month ago. Her temperature is 101°F (38.3°C), blood pressure is 114/64 mmHg, pulse is 110/min, respirations are 19/min, and oxygen saturation is 93% on room air. Her physical exam is notable for bilateral coarse breath sounds. Laboratory values are ordered as seen below.

Serum:
Na+: 140 mEq/L
Cl-: 102 mEq/L
K+: 4.7 mEq/L
HCO3-: 22 mEq/L
BUN: 30 mg/dL
Glucose: 96 mg/dL
Creatinine: 1.5 mg/dL (baseline 1.4 mg/dL)
Ca2+: 9.1 mg/dL

A chest radiograph is obtained as seen in Figure A and a CT scan of the chest is obtained as seen in Figure B.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [30.0, 'mg/dL'], 'Glucose': [96.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",296.04762,281.24524,310.85,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 30.0 mg/dL. 
The concentration of glucose is 96.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (30.0 / 2.8) + (30.0 / 18) = 296.04762 mmol/L.The patient's calculated serum osmolality concentration is 296.04762 mmol/L. This is equalivalent to 296.04762 mOsm/kg."
5664,30,Serum Osmolality,lab test,decimal,pmc-5667281-1,Extracted,"The patient was an 82-year-old woman who had a history of non-ruptured brain aneurysm, mitral valve regurgitation, which was replaced with a biological valve, atrial fibrillation (Af), and right cerebellar infarction. Her son found her lying unconscious by her bed in the morning and called an ambulance. Her Glasgow Coma Scale score was 3 on arrival at the emergency department of our hospital. Her vital signs showed a blood pressure of 139/85 mmHg, heart rate of 100 b.p.m., body temperature of 36.4°C, and respiratory rate of 30 breaths/min. Her oxygen saturation was 85% on receiving 10 L/min and assisted ventilation with a bag valve mask. Her pupils were 2 mm in diameter, equally rounded, and reactive to light bilaterally. There was a subcutaneous hemorrhage in her forehead. Breathing sounds were clear bilaterally and systolic murmur was heard at the apex. Even though her right arm was warm, her left arm and both feet were cold. Pulses of the right carotid artery and right radial artery were normal, but pulses of the left radial artery and bilateral femoral arteries were weak. Muscle tonus was weak in all of the extremities. The patient's prescribed medications included warfarin 2.5 mg, aspirin 100 mg, spironolactone 25 mg, tolvaptan 7.5 mg, furosemide 80 mg, rabeprazole 10 mg, and iron sulfate 105 mg.
An electrocardiogram carried out on arrival showed Af, an inverted T wave in V1 to V3, an abnormal Q wave in V1 to V4, and ST elevation in V3 and V4 (Fig. ). A chest X-ray showed prominent cardiomegaly, pulmonary congestion, and dilation of the upper mediastinum. Cardiac ultrasound, performed by an ultrasound technician, showed decreased wall contraction in the anterior wall, septum, and apex. Color Doppler ultrasound imaging did not detect blood flow in the abdominal aorta.
Laboratory data showed the following: creatine kinase (CK), 133 IU/L; CK-MB, 17 IU/L; aspartate aminotransferase, 37 IU/L; alanine aminotransferase, 19 IU/L; blood urea nitrogen, 37.3 mg/dL; creatinine, 0.93 mg/dL; sodium, 141 mEq/L; potassium, 5.1 mEq/L; chloride, 109 mEq/L; glucose, 145 mg/dL; troponin I, 0.65 ng/mL; brain natriuretic peptide, 291.8 pg/mL; and prothrombin international normalized ratio, 1.29.
We undertook head computed tomography (CT) to rule out intracranial hemorrhage, but there were no abnormalities, besides a previous right cerebellar infarction. Therefore, we performed contrast CT to examine dissection of the aorta. Contrast CT did not show dissection of the aorta, but we found emboli in bilateral common carotid arteries, the left subclavian artery, the celiac artery, and the distal abdominal aorta. Poor contrast in the left ventricle, spleen, and both kidneys was also observed. Some clots were recognized in the left atrium (Fig. ). Brain magnetic resonance imaging was carried out and showed a diffuse high-intensity area (Fig. ). This finding suggested acute ischemic stroke in almost all of the patient's brain.
The patient's prognosis was so poor that cerebrovascular catheter intervention or any other embolectomy could not be undertaken. Intravenous heparin was given, but she died within 24 h.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [37.3, 'mg/dL'], 'Glucose': [145.0, 'mg/dL'], 'Sodium': [141.0, 'mEq/L']}",303.37698,288.20813,318.54583,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. 
The concentration of bun is 37.3 mg/dL. 
The concentration of glucose is 145.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (37.3 / 2.8) + (37.3 / 18) = 303.37698 mmol/L.The patient's calculated serum osmolality concentration is 303.37698 mmol/L. This is equalivalent to 303.37698 mOsm/kg."
5665,30,Serum Osmolality,lab test,decimal,pmc-3970045-1,Extracted,"A 33-year-old male presented with bilateral thigh pain after regular squatting. The patient often squatted for exercise and never developed rhabdomyolysis. On the following day, the patient developed severe bilateral pain and stiffness in both thighs. He took Tylenol for pain and denied using any steroid or illicit drugs. He noticed dark brown-colored urine which urged him to come to the hospital. There was no history of fever, cough, sore throat, headache, blurred vision, palpitations, diarrhea, or abdominal pain. The patient also had a past medical history of hyperthyroidism and was taking methimazole which he stopped 2 months prior to admission. On physical examination, the patient was alert and oriented in no acute distress. His blood pressure was 137/77 mmHg and pulse was 100 beats per minute, and he was afebrile. His eyes showed no lid lag or exophthalmos. An examination of neck revealed mild thyroid enlargement on swallowing but not tender. No thyroid bruit was heard. Heart and chest examinations were normal. Examination of thighs showed mild swelling and tenderness. Neurological examination showed no hand tremor, normal muscle power, and deep tendon reflex 2+ all. The remainder of the physical examination was unremarkable. A chest X-ray and an ECG were normal.
The laboratory findings revealed the following values: blood urea nitrogen 10 mg/dL (8–22 mg/dL), creatinine 0.8 mg/dL (0.4–1.6 mg/dL), sodium 140 mg/dL (136–146 mg/dL), potassium 4.4 mg/dL (3.5–5.3 mg/dL), carbon dioxide 29 mg/dL (23–32 mg/dL), chloride 103 mg/dL (98–110 mg/dL), phosphate 4.6 (2.4–4.1 mg/dL), magnesium 1.97 (1.7–2.2 mg/dL), glucose 83 mg/dL (74–115 mg/dL), a hemoglobin 16.2 g/dL (13.5–17.5 g/dL), a white blood cell count 9.3 K/mcL (4.5–11 K/mcL) with a differential of 72.9 percent neutrophil, 17.7 percent lymphocyte, and 8.2 percent monocyte, platelet 217 K/mcL (130–400 K/mcL), CK 98407 IU/L (26–189 IU/L), thyroid stimulating hormone 0.01 mIU/mL (0.34–5.6 mIU/mL), free T4 1.98 ng/dL (0.58–1.64 ng/dL), T3 176.5 ng/dL (87–178 ng/dL), alkaline phosphatase 66 U/L (30–115 U/L), AST 993 U/L (2–40 U/L), ALT 228 U/L (2–50 U/L), LDH 2330 U/L (90–225 U/L), albumin 2.8 g/dL (3.5–5 g/dL), total bilirubin 1.63 mg/dL (normal < 1.5 mg/dL), and direct bilirubin 0.39 mg/dL (normal < 0.3 mg/dL). Urinalysis showed a specific gravity of 1.021, blood large, ketone trace, protein 300 mg/gL, red blood cell 0–4, white blood cell 0–4, urine myoglobin 36 mcg/L (normal < 28), and serum myoglobin 2250 mcg/L (normal 0–60). Urine toxicology was negative. TSH receptor antibody 48% (normal < 10%), antithyroglobulin antibody, and anti-thyroid peroxidase antibody were negative.
The patient was diagnosed with rhabdomyolysis and was treated with aggressive intravenous fluid and sodium bicarbonate drip. Urine output and electrolyte were closely monitored. He was started on methimazole for hyperthyroidism. His symptom significantly improved and serum creatinine kinase level also gradually decreased without electrolyte imbalance or acute kidney injury. The patient was discharged home with stable condition and had a radioactive iodine uptake done which showed high radioactive iodine uptake with homogenous activity consistent with Graves' disease.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [10.0, 'mg/dL'], 'Glucose': [83.0, 'mg/dL'], 'Sodium': [140.0, 'mg/dL']}",129.98254,123.48341,136.48167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mg/dL. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mg to mmol. The mass of sodium is 140.0 mg. To convert 140.0 mg of sodium to g, multiply by the conversion factor 0.001, giving us 140.0 mg sodium * 0.001 g/mg = 0.14 g sodium. To convert from grams of sodium to moles, divide by the molar mass 22.99 g/mol, which will give 0.14 g/(22.99 g sodium/mol) = 0.00609 mol sodium. To convert 0.00609 mol of sodium to mmol, multiply by the conversion factor 1000.0, giving us 0.00609 mol sodium * 1000.0 mmol/mol = 6.09 mmol sodium. The current volume unit is dL and the target volume unit is L. The conversion factor is 0.1 L for every unit of dL. Our next step will be to divide the mass by the volume conversion factor of 0.1 to get the final concentration in terms of mmol/L. This will result to 6.09 mmol sodium/0.1 L = 60.9 mmol sodium/L. The concentration value of 140.0 mg sodium/dL converts to 60.9 mmol sodium/L. 
The concentration of bun is 10.0 mg/dL. 
The concentration of glucose is 83.0 mg/dL. 
Plugging these values into the equation, we get 2 * 60.9 + (10.0 / 2.8) + (10.0 / 18) = 129.98254 mmol/L.The patient's calculated serum osmolality concentration is 129.98254 mmol/L. This is equalivalent to 129.98254 mOsm/kg."
5666,30,Serum Osmolality,lab test,decimal,pmc-7890937-1,Extracted,"A 64-year-old man with a history of chronic obstructive pulmonary disease and ethanol abuse use presented to the emergency department with altered mentation. He was obtunded on arrival, unable to provide any additional history. Presenting vitals were notable for blood pressure of 150/93, pulse of 69 beats per minute, temperature of 97.3 °F (36.3 °C), respiratory rate of 18 BPM, and SpO2 95%. Physical exam revealed bilateral upper extremity tremors and obtundation. Pupils were symmetric and reactive to light, and he periodically tracked with his eyes. Neurological exam, including reflexes, was limited due to altered mental status. Cardiopulmonary exam was benign. Chest X-ray was notable for a normal cardiopulmonary silhouette. Electrocardiogram revealed normal sinus rhythm with a QTc interval of 409 ms. Computed tomography of the brain without contrast showed normal gray-white matter differentiation.
Laboratory evaluation revealed a sodium 143 mEq/L (135 – 145 mEq/L), potassium 3.0 mEq/L (3.6 – 5.1 mEq/L), chloride 105 mEq/L (98 – 110 mEq/L), bicarbonate 27 mEq/L (22 – 32 mEq/L), blood urea nitrogen 14 mg/dL (6 – 24 mg/dL), creatinine 1.11 mg/dL (0.64 – 1.27 mg/dL), undetectable blood ethanol level, blood glucose 95 mg/dL (67 – 99 mg/dL), calcium 12.8 mg/dL (8.5 – 10.5 mg/dL), ionized calcium 6.3 mg/dL (4.2 – 5.2 mg/dL), phosphorus of 2.2 mg/dL (2.4 – 4.8 mg/dL), and albumin 4.0 g/dL (3.5 – 5.0 g/dL). Initial management consisted of volume expansion with 3 L normal saline without improvement in mentation. Calcitonin was given on hospital day 2 and zoledronic acid was given on hospital day 3, but hypercalcemia persisted. Further labwork returned with intact parathyroid hormone (iPTH) 17 pg/mL (18 – 80 pg/mL), parathyroid hormone related peptide (PTHrP) 9 pg/mL (pg/mL 14 – 27), serum protein electrophoresis (SPEP) and immunofixation (IFE) without evidence of monoclonal protein, κ light chains 85.4 mg/L (3.3 – 19.4 mg/L), λ light chains 40.8 mg/L (5.7 – 26.3 mg/L), and β-2 microglobulin 3.75 mg/L (0.97 – 2.64 mg/L). The elevation of κ/λ ratio in the setting of a normal glomerular filtration rate prompted evaluation for a monoclonal gammopathy. Skeletal survey was negative for lytic lesions and bone marrow biopsy was negative for plasma cell dyscrasia. Finally, the following labs resulted: 25-hydroxy vitamin D > 150 ng/mL (30.0 – 100.0 ng/mL), 1,25-hydroxy vitamin D 36 pg/mL (18 – 72 pg/mL). The patient remained agitated and confused for the first 10 days of hospitalization, but mentation improved thereafter with calcium normalizing after 18 days. Upon recovery, he reported misunderstanding medication instructions and had been consuming 4 vitamin D 50,000 IU tablets daily.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [143.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [14.0, 'mg/dL'], 'Glucose': [95.0, 'mg/dL']}",296.27778,281.46389,311.09167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 143.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 143.0 mEq. To convert from 143.0 mEq to mmol, convert from mEq to mmol. The compound 143.0 has a valence of 1, and so divide the valence by the value of mEq to get, 143.0 mEq/(1 mEq/mmol) = 143.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mEq sodium/L converts to 143.0 mmol sodium/L. 
The concentration of bun is 14.0 mg/dL. 
The concentration of glucose is 95.0 mg/dL. 
Plugging these values into the equation, we get 2 * 143.0 + (14.0 / 2.8) + (14.0 / 18) = 296.27778 mmol/L.The patient's calculated serum osmolality concentration is 296.27778 mmol/L. This is equalivalent to 296.27778 mOsm/kg."
5667,30,Serum Osmolality,lab test,decimal,usmle-6186,Extracted,"A 70-year-old man with history of asthma and chronic obstructive pulmonary disease presents to the emergency department with resting dyspnea for the past 2 hours after watching his granddaughter play soccer. Despite albuterol, ipratropium, magnesium, methylprednisolone, and high flow nasal cannula, the patient agrees to elective intubation and is transferred to the intensive care unit. His hospital course is prolonged by pneumonia, which is managed with vancomycin, pipercillin-tazobactam, and gentamicin to cover for ventilator-associated etiologies. He is maintained on nasogastric tube feeds, lactated ringer fluid boluses, and subcutaneous heparin for deep vein thrombosis prophylaxis. On hospital day 7, the patient proves difficult to wean from his ventilator due to labored tachypnea. As the nurse rotates the patient to change his sacral pressure ulcer dressing, the patient's peak airway pressure increases sharply to 55 cm H2O. The nurse noted that the patient was wincing at the time. His temperature is 100.1°F (38.1°C), blood pressure is 100/50 mmHg, and pulse is 100/min. His respirations are 22/min on the ventilator despite a set respiratory rate of 14/min. His laboratory results are shown below:

Leukocyte count and differential:
Leukocyte count: 18,000/mm^3
Segmented neutrophils: 90%
Bands: 10%
Eosinophils: 5%
Basophils: 2%
Lymphocytes: 2%
Monocytes: 1%

Serum:
Na+: 135 mEq/L
Cl-: 107 mEq/L
K+: 3.2 mEq/L
HCO3-: 18 mEq/L
Urea nitrogen: 45 mg/dL
Glucose: 89 mg/dL
Creatinine: 1.3 mg/dL
Alkaline phosphatase: 100 U/L
Aspartate aminotransferase (AST, GOT): 250 U/L
Alanine aminotransferase (ALT, GPT): 300 U/L
Gamma-Glutamyltransferase (GGT): 2 U/L
Amylase: 10 IU/dL
Lipase: 5 IU/dL

Bedside ultrasound imaging is shown in Figure A.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [45.0, 'mg/dL'], 'Glucose': [89.0, 'mg/dL'], 'Sodium': [135.0, 'mEq/L']}",291.01587,276.46508,305.56666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 135.0 mEq. To convert from 135.0 mEq to mmol, convert from mEq to mmol. The compound 135.0 has a valence of 1, and so divide the valence by the value of mEq to get, 135.0 mEq/(1 mEq/mmol) = 135.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mEq sodium/L converts to 135.0 mmol sodium/L. 
The concentration of bun is 45.0 mg/dL. 
The concentration of glucose is 89.0 mg/dL. 
Plugging these values into the equation, we get 2 * 135.0 + (45.0 / 2.8) + (45.0 / 18) = 291.01587 mmol/L.The patient's calculated serum osmolality concentration is 291.01587 mmol/L. This is equalivalent to 291.01587 mOsm/kg."
5668,30,Serum Osmolality,lab test,decimal,usmle-5439,Extracted,"A 55-year-old man presents to the emergency department for abdominal pain. The patient states that he has had abdominal pain for a while, but it became unbearable today and he is concerned. He also endorses a weight loss of 20 pounds this past month and complains of bulky and foul-smelling stools. The patient is homeless and is currently living by a local wash where he obtains his drinking water and cleans his clothes. He admits to recently eating raw meat that he found. The patient has a past medical history of alcohol abuse, malnutrition, Wernicke-Korsakoff psychosis, IV drug use, and a recent hospitalization for intoxication of unknown etiology. The patient is not taking any medications currently. His temperature is 99.1°F (37.3°C), blood pressure is 100/67 mmHg, pulse is 120/min, respirations are 11/min, and oxygen saturation is 98% on room air. On physical exam, the patient complains of epigastric tenderness. Cardiopulmonary exam is within normal limits. The patient is started on IV fluids, thiamine, folate, magnesium, and dextrose. Laboratory values are ordered as seen below:

Hemoglobin: 9.0 g/dL
Hematocrit: 25%
Leukocyte count: 5,500 cells/mm^3 with normal differential
Platelet count: 222,000/mm^3

Serum:
Na+: 137 mEq/L
Cl-: 102 mEq/L
K+: 4.1 mEq/L
HCO3-: 24 mEq/L
BUN: 24 mg/dL
Glucose: 68 mg/dL
Creatinine: 1.4 mg/dL
Ca2+: 9.8 mg/dL
Amylase: 22 U/L
Lipase: 22 U/L
Aspartate aminotransferase (AST): 58 U/L
Alanine aminotransferase (ALT): 18 U/L

A computed tomography (CT) scan is obtained as seen in Figure A.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [24.0, 'mg/dL'], 'Glucose': [68.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",286.34921,272.03175,300.66667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 24.0 mg/dL. 
The concentration of glucose is 68.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (24.0 / 2.8) + (24.0 / 18) = 286.34921 mmol/L.The patient's calculated serum osmolality concentration is 286.34921 mmol/L. This is equalivalent to 286.34921 mOsm/kg."
5669,30,Serum Osmolality,lab test,decimal,usmle-5603,Extracted,"A 23-year-old woman is brought to the emergency department by emergency medical services. She was found trying to hang herself in her kitchen. The patient has a past medical history of drug abuse, alcoholism, anxiety, mania, irritable bowel syndrome, and hypertension. Her current medications include naltrexone, sodium docusate, and clonazepam as needed. Her temperature is 99.5°F (37.5°C), blood pressure is 100/65 mmHg, pulse is 90/min, respirations are 15/min, and oxygen saturation is 99% on room air. On physical exam, you note a teary young woman. There are multiple bilateral superficial cuts along her wrists. The patient's cardiac and pulmonary exams are within normal limits. Neurological exam reveals a patient who is alert and oriented. The patient claims that you cannot send her home because if you do she will kill herself. Laboratory values are ordered and return as below.

Hemoglobin: 15 g/dL
Hematocrit: 40%
Leukocyte count: 4,500 cells/mm^3 with normal differential
Platelet count: 197,500/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 102 mEq/L
K+: 4.4 mEq/L
HCO3-: 24 mEq/L
BUN: 20 mg/dL
Glucose: 90 mg/dL
Creatinine: 1.0 mg/dL
Ca2+: 10.2 mg/dL
AST: 12 U/L
ALT: 10 U/L

The patient is transferred to the crisis intervention unit.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [90.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",290.14286,275.63572,304.65,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 90.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (20.0 / 2.8) + (20.0 / 18) = 290.14286 mmol/L.The patient's calculated serum osmolality concentration is 290.14286 mmol/L. This is equalivalent to 290.14286 mOsm/kg."
5670,30,Serum Osmolality,lab test,decimal,pmc-3147132-1,Extracted,"A 28-year-old man was admitted to our hospital because of reduced livido and increased fatigability. He had been in good health until 1 year earlier, when he noticed reduced livido. Four months before admission, he noticed frequent headaches, thirst, polydipsia, and polyuria. Because he was voiding urine every hour, he visited his family doctor. Magnetic resonance imaging (MRI) revealed a suprasellar mass, and he was thus referred to our hospital for further evaluation and treatment. Although polydipsia and polyuria had been gradually relieved by the time of admission, he became aware of increased fatigability.
At the time of admission, he was 176 cm tall and weighed 72 kg. His temperature was 37.6°C, pulse rate was 60/min, and blood pressure was 110/60 mmHg. No goiter or enlargement of lymph nodes was noted. Axillar and pubic hair were lost and there was palpable erythematous rush on his forehead (). The remainder of the physical examination was unremarkable.
Laboratory results revealed the following results: blood urea nitrogen 9.6 mg/dL, creatinine 0.79 mg/dL, serum sodium 141 mEq/l, potassium 4.0 mEq/l, chloride 100 mEq/l, calcium 9.4 mg/dL, phosphate 3.7 mg/dL, fasting plasma glucose 80 mg/dL, and C-reactive protein 0.07 mg/dL. Endocrinologic data revealed a mild decrease in free T4 level (0.6 ng/dL) with normal thyroid-stimulating hormone (TSH) level (0.9106 μU/mL) and decreased cortisol (4.7 μg/mL), adrenocorticotropic hormone (ACTH; 6 pg/mL), luteinizing hormone (LH; 0.2 mIU/mL), follicle stimulating hormone (FSH; 1.3 mIU/mL), and testosterone (0.05 ng/mL) levels. Urinary cortisol was undetectable. Plasma osmolality was 288 mOsm/kgH2O, with a urinary osmolality of 239 mOsm/kgH2O, and arginine vasopressin (AVP) was undetectable (<0.15 pg/mL). Urinary output was from 1.5 to 2.2 L/day.
His clinical course and laboratory findings led us to suspect CDI with anterior pituitary dysfunction. We thus performed hormonal provocative tests. The patient was given an infusion of 5% saline at a rate of 0.05 mL/kg for 120 min. Although plasma AVP was undetectable before and after administration of hypertonic saline, urine osmolality (391 mOsm/kgH2O) increased above the plasma levels (296 mOsm/kgH2O) (). Hormonal provocative tests revealed that growth hormone (GH) response to GH-releasing hormone was normal, TSH response to TSH-releasing hormone was low and blunted, and FSH and LH response to LH-releasing hormone were low and blunted (). Although ACTH response to corticotrophin-releasing hormone (CRH) was normal, cortisol response to CRH was low (maximum 13.0 μg/mL). Cortisol response to rapid ACTH stimulation test was low (maximum 15.9 μg/mL). Results of these hormonal tests were compatible with the diagnosis of CDI with partial GC deficiency.
MRI revealed enhancing lesion centrally in the pituitary stalk, which spread continuously to the bottom of the third ventricle, and the high intensity of the posterior lobe was lost, compatible with the diagnosis of CDI (). Considering the patient's age, we first suspected of neurohypophysial germinoma. However, this was unlikely because cerebrospinal fluid was negative for malignant cells, and β-human chorionic gonadotropin (HCG) levels were normal. Next, we suspected sarcoidosis because chest X-ray revealed hilar enlargement. A biopsy from the skin of the forehead was performed, which revealed noncaseating granuloma composed of epithelioid cells (). Multinucleated giant cells were also present. Thus, the diagnosis of sarcoidosis was made.
While waiting for histologic confirmation of biopsy results, hydrocortisone replacement was begun with a dose of 20 mg daily. Soon after the replacement therapy was begun, moderate polyuria (3.5–4.0 liters daily) occurred (). After the diagnosis of sarcoidosis was confirmed, he was treated with 40 mg of prednisolone and his general condition improved. The hypertonic saline test was repeated while he was taking 40 mg of prednisolone. Plasma AVP was undetectable during the hypertonic saline test and urine osmolality was consistently below plasma levels, which was compatible with a diagnosis of CDI (). He was treated with 1-desamino-8-D-arginine vasopressin (dDAVP).
MRI following prednisolone therapy revealed a reduction in the size of the affected lesion. However, his pituitary function remained unchanged, and he is currently being treated with prednisolone, levothyroxine natrium, HCG, and dDAVP.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [9.6, 'mg/dL'], 'Glucose': [80.0, 'mg/dL'], 'Sodium': [141.0, 'mEq/L']}",289.87302,275.37937,304.36667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. 
The concentration of bun is 9.6 mg/dL. 
The concentration of glucose is 80.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (9.6 / 2.8) + (9.6 / 18) = 289.87302 mmol/L.The patient's calculated serum osmolality concentration is 289.87302 mmol/L. This is equalivalent to 289.87302 mOsm/kg."
5671,30,Serum Osmolality,lab test,decimal,pmc-6781379-1,Extracted,"A 52-year-old Cameroonian man, married and a car driver, was admitted to our nephrology inpatient ward for acute kidney injury. He had no relevant past history regarding disease or toxic exposure. He occasionally consumed alcohol and was not a smoker. He had been well until 8 weeks prior to admission, when he developed progressive fatigue, anorexia, involuntary weight loss (~ 12% of his usual body weight), and intermittent nocturnal fever that had been treated twice as malaria and typhoid fever. The malaria and typhoid fever treatments received were parenteral quinine and ofloxacin (doses and duration of treatment not described for both), and both were unsuccessful. A few days before consultation in our hospital, he developed polyuria, polydipsia, constipation, and diffuse abdominal pain that rapidly worsened, prompting consultation at the emergency service of our hospital. The findings of a serum creatinine level of 36.7 mg/L (normal range, < 15 mg/L) and a blood urea nitrogen level of 1.23 g/L (normal range, 0.15–0.45) led to his transfer to the nephrology unit. Upon admission, further questioning revealed that a few days prior to consultation, the patient had inconsistent verbalizations and hallucinations. He was very ill-looking, severely dehydrated, with nontender fixed bilateral inguinal lymph node enlargement (4 cm for the largest), nonreactive urine dipstick, and a fecaloma. His Glasgow Coma Scale score was E4V2M6, blood pressure was 170/88 mmHg, pulse rate was 102/minute, respiratory rate was 17/minute, temperature was 37.7 °C, body surface area was 1.66 m2, and random capillary glucose was 0.91 g/L. Apart from the impaired verbal response (in the Glasgow Coma Scale) that limited cognitive function examination, no cranial palsy, meningeal signs, motility abnormalities, sensitivity abnormalities, or coordination abnormalities were found on neurological examination. Cardiac auscultation revealed regular tachycardia. Abdominal examination revealed diffuse tenderness and increased bowel sounds but no defense, contracture, abdominal distention, or visceral enlargement. The result of the rest of the physical examination was normal. Laboratory tests revealed red blood cells 5.4 × 1012/L, hemoglobin 14.3 g/dl, white blood cells 6.2 × 109/L, neutrophils 2.6 × 109/L, eosinophils 0, basophils 0, lymphocytes 2.7 × 109/L, monocytes 6.2 × 109/L, platelets 137 × 109/L, total calcium 199.5 mg/L (normal range, 84–105), ionized Ca2+ 101.75 mg/L (normal range, 46–54), serum phosphorus 40.20 mg/L (normal range, 25–50), plasma sodium 152 mmol/L (normal range, 135–145), serum potassium 3.1 mmol/L (normal range, 3.5–5), serum chloride 110 mmol/L (normal range, 96–107), and serum magnesium 19.80 mg/L (normal range, 18–26).
A provisional diagnosis of a lymphoproliferative disorder or a granulomatous disease causing acute kidney injury was made. Further laboratory tests showed parathyroid hormone (PTH) level 9.70 pg/ml (normal range, 17–73), PTH-related peptide (PTH-rp) level < 8.5 pg/ml (normal range, < 13.0), 1.25(OH)2D3 level 32 ng/ml (normal range, 18–71 ng/ml for nondialysis subjects), erythrocyte sedimentation rate 50 mm (normal range, < 20 mm), C-reactive protein (CRP) 148.72 mg/L (normal range, < 6 mg/L), and prostate-specific antigen 0.21 ng/ml (normal range, < 4 ng/ml). Figure shows the curve of concurrent serum protein electrophoresis. Plain x-rays of the skull and chest radiographs (Fig. a and b) revealed an osteolytic lesion in the skull and mediastinal lymph nodes. A resting electrocardiogram (Fig. ) confirmed sinus tachycardia as the lone abnormality. Twenty-four hours following admission to the nephrology unit, specific hypercalcemia management was initiated with 4-mg zoledronate once and hydration using intravenous liquids (isotonic saline, 2 L/24 hours and 5% dextrose, 1 L/24 hours) for 3 consecutive days before introduction of oral furosemide 40 mg once daily to correct consequential fluid overload. A symmetric purpura limited to the lower limbs (Fig. ) progressively developed from the fourth to sixth days of hospitalization, with temperatures reaching a plateau at 40–40.5 °C. On evaluation 9 days after initiation of specific hypercalcemia management, serum calcium and sodium returned to normal values, with complete recovery of related symptoms and signs, as well as renal function (Fig. a–c). On the 14th day of hospitalization, although the purpura completely regressed, fever persisted, and lymph node enlargement extended beyond the groins to the cervical region. At this time, results of bacteriological cultures, including urine culture and three serial hemocultures, were all negative, and CRP was 115.61 mg/L. Complete blood count showed red blood cells 2.5 × 1012/L, hemoglobin 6.6 g/dl, white blood cells 2 × 109/L, neutrophils 0.6 × 109/L, eosinophils 0.06 × 109/μl, basophils 0, lymphocytes 1.3 × 109/L, monocytes 0.4 × 109/L, and platelets 44 × 109/L. Peripheral blood smear confirmed a low platelet count but showed neither blasts nor flower cells. The reticulocyte count was 22,640/mm3. The bone marrow aspirate showed 8.3% normal cellularity with no abnormal infiltrate (including blast cells) or fibrosis. This marrow hypocellularity together with pancytopenia led to the diagnosis of nonsevere aplastic anemia according to the revised Camitta criteria []. Inguinal lymph node biopsy showed large cells with distinct nucleoli, dispersed chromatin, and scant cytoplasm with intracytoplasmic CD3 and Ki67 markers, all suggestive of aggressive precursor T-cell lymphoma (Fig. a–d). Because lymphoblasts were not observed either in bone marrow analysis or in the peripheral blood smear, and considering histopathologic findings of the lymph node biopsy, T-ALL was ruled out, and the diagnosis of T-LBL was retained [, ]. An abdominal ultrasound obtained to assess T-LBL extension showed no organ (spleen, liver, kidney) enlargement. Additional examinations evaluating disease prognosis showed serum lactate dehydrogenase 1145.2 IU/L (normal range, 200–400), uric acid 148 mg/L (normal range, < 70 mg/L), serum glutamic oxaloacetic transaminase 72.3 IU/L (normal range, < 37), and serum glutamic pyruvic transaminase 27.6 IU/L (normal range, < 45). The patient was then transferred to the oncology unit, where he immediately received transfusion of 3 U of whole blood within 2 days prior to chemotherapy. The chemotherapy, which was based on the standard cyclophosphamide-doxorubicin-vincristine-prednisolone (CHOP) protocol for NHL [], consisted of a 15-minute intravenous infusion of 1250 mg of cyclophosphamide on day 1, a 2-minute intravenous bolus of 80 mg doxorubicin on day 1, a 2-minute intravenous bolus of 2 mg vincristine on day 1, and 100 mg of oral prednisolone once daily on days 1 to 5 of the cycle. Following this CHOP cycle, 1 ml of filgrastim was administered subcutaneously once daily for 3 consecutive days as supportive treatment for aplastic anemia. Resolution of fever and recovery from fatigue and anorexia were noted from the third day of the CHOP cycle. The patient was discharged at the end of the cycle. One week following hospital discharge, he died at home a few hours after fever recurrence.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [1.23, 'g/L'], 'Glucose': [0.91, 'g/L'], 'Sodium': [152.0, 'mmol/L']}",352.98413,335.33492,370.63334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 152.0 mmol/L. 
The concentration of bun is 1.23 g/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from g to mg. The mass of bun is 1.23 g. To convert 1.23 g of bun to mg, multiply by the conversion factor 1000.0, giving us 1.23 g bun * 1000.0 mg/g = 1230.0 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1230.0 mg bun/10.0 dL = 123.0 mg bun/dL. The concentration value of 1.23 g bun/L converts to 123.0 mg bun/dL. 
The concentration of glucose is 0.91 g/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from g to mg. The mass of glucose is 0.91 g. To convert 0.91 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 0.91 g glucose * 1000.0 mg/g = 910.0 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 910.0 mg glucose/10.0 dL = 91.0 mg glucose/dL. The concentration value of 0.91 g glucose/L converts to 91.0 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 152.0 + (123.0 / 2.8) + (123.0 / 18) = 352.98413 mmol/L.The patient's calculated serum osmolality concentration is 352.98413 mmol/L. This is equalivalent to 352.98413 mOsm/kg."
5672,30,Serum Osmolality,lab test,decimal,pmc-6600853-1,Extracted,"A 50 years old Aryan female from Lalitpur district, Nepal, presented to Patan Hospital Emergency Department in December 2018 with complaints of abdominal pain that had persisted for two days. She had multiple episodes of vomiting. In terms of the patient’s history, she had been treated with amlodipine and atenolol for hypertension and undergone a total abdominal hysterectomy 5 years prior for fibroids. She was a farmer living in suburban area of Lalitpur and involved in growing of vegetables and rearing of cows and poultry. On assessment, her blood pressure was 170/100 mmHg and her pulse rate was 88 beats per minute. Temperature was 98 degree Fahrenheit. Abdominal examination showed tenderness in the right upper quadrant.
Below are the laboratory parameters with normal range in parentheses:
Complete blood count : white cell count 8.4 (4-10) X 10^9/L ; neutrophils 60 % ; lymphocytes 37 % ; monocyte 1 % ; eosinophil 2 % ; red blood cells 4.8 (4.2–5.4) × 10^12/L; hemoglobin 12.5 ( 12-15) g/dL ; platelets 145 ( 150-400) X 10^9/L
Biochemistry: random blood sugar 124 (79-160) mg/dL; urea 28 (17-45) mg/dL; creatinine 0.7 (0.8-1.3) mg/dL; sodium 135 (135-145) mmol/L; potassium 3.8 (3.5 – 5) mmol/L; calcium 8.5 (8.4-10.2) mg/dL; albumin 3.4 (3.5-4) gm/dL; magnesium 1.8 (1.6-2.3 mg/dL); amylase 45 (30-125) U/L; lipase 56 (10-150) U/L.
Hepatic panel: bilirubin total 2 (0.1-1.2) mg/dL and direct 0.5 (0-0.4) mg/dL; alanine transaminase 53 (5-30) units/L; aspartate transaminase 47 (5-30) units/L; alkaline phosphatase 76 (50-100) IU/L
Ultrasound of the abdomen revealed a gallstone with a thickened gall bladder wall. She was admitted to the surgical ward with a provisional diagnosis of biliary colic, and managed conservatively with intravenous fluids, anti-emetics and analgesics. Her pain subsided. and her blood pressure also fell down to normal range with analgesia. But she developed a headache from 2
nd day and fever of 101 degrees Fahrenheit on the 4
th day. Injection ceftriaxone 1 gram twice daily was started empirically. The next day, she developed altered sensorium. Neurological examination revealed disorientation to time, place and person with neck stiffness but no papilledema or any focal neurological deficit. Plantar reflex was normal bilaterally.
Plain computed tomography (CT) of the head was normal. Cerebrospinal fluid (CSF) analysis revealed the following (with normal range in parentheses): Red blood cells= 6 (0–10)/mm^3; white blood cells = absent (0–5/mm^3); protein= 45 (20–45) mg/dL; sugar= 71 (45–80) mg/dL; lactate= 2 (1.1–2.8) mmol/L; adenosine deaminase (ADA) = 6.2 U/L; GeneXpert was negative for Mycobacterium Tuberculosis; CSF India ink staining was negative; Bacterial culture showed no growth over 48 hours. However, CSF cryptococcal antigen was positive by latex agglutination (Latex-Cryptococcus Antigen Detection System; IMMY). Serological test for HIV were negative.
With the diagnosis of cryptococcal meningitis, she was transferred to the intensive care unit (ICU) and liposomal amphotericin B (4 mg/kg/day) and Fluconazole (800 mg daily) were prescribed while ceftriaxone was continued. Unfortunately her family members could not afford the expensive liposomal amphotericin B. The government of Nepal provides liposomal amphotericin B (single dose of 10 mg/kg) free of cost to patients with visceral leishmaniasis (VL)
. We wrote an application letter to the relevant authority to request liposomal amphotericin B for the patient. We asked for a total of 56 vials of the medicine (each vial contained 50 mg of liposomal amphotericin B) that would be sufficient for a two-week course. The relevant government authority refused to provide liposomal amphotericin B to our patient stating that the drug is to be dispensed to patients with VL only, as per the government policy. She was then started on fluconazole alone, but her status deteriorated. In addition, she also developed right sided hemiparesis 3 days following the diagnosis. Magnetic resonance imaging (MRI) of the brain was performed that revealed an acute infarct involving the left parietal lobe and basal ganglia, with multiple acute lacunar infarcts in the bilateral frontal and parietal lobes and bilateral cerebellum. She was in sinus rhythm. Echocardiography was normal. Aspirin 75 mg and atorvastatin 40 mg daily were administered as a result.
In a few days, her family members provided the liposomal amphotericin B. They revealed that they had connections with influential politicians who helped them acquire the medicine from the same government center who had previously refused them. She then received the two-week course of liposomal amphotericin B along with fluconazole. The patient improved gradually. She had hypokalemia during treatment with Amphotericin B which was managed with a potassium chloride infusion at 5 mEq/hour. She started showing improvement in her higher mental functions after the 5th day of amphotericin B administration.
After completion of 2 weeks of Amphotericin B, her higher mental function had returned to normal, and she could walk on her own with some residual weakness in her right upper limbs. She was then discharged from hospital and daily fluconazole 800 mg was continued for 8 more weeks.
On first follow up 1 week following discharge she was doing well. She was last seen in February 2019 after completing 8 weeks of fluconazole 800 mg daily. She was asymptomatic and was prescribed a daily tablet of fluconazole 400 mg for 1 year.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [28.0, 'mg/dL'], 'Glucose': [124.0, 'mg/dL'], 'Sodium': [135.0, 'mmol/L']}",286.88889,272.54445,301.23333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.0 mmol/L. 
The concentration of bun is 28.0 mg/dL. 
The concentration of glucose is 124.0 mg/dL. 
Plugging these values into the equation, we get 2 * 135.0 + (28.0 / 2.8) + (28.0 / 18) = 286.88889 mmol/L.The patient's calculated serum osmolality concentration is 286.88889 mmol/L. This is equalivalent to 286.88889 mOsm/kg."
5673,30,Serum Osmolality,lab test,decimal,usmle-5016,Extracted,"An 87-year-old man presents to the emergency department with decreased hearing. The patient states that for the past week he has had decreased hearing that is predominantly affecting his left ear. He denies any fever, chills, nausea, vomiting, or changes in his vision. The patient has a past medical history of asthma, HIV, and anxiety. His current medications include HAART, albuterol, and clonazepam. The patient states his last CD4 count taken 2 weeks ago was 650. His temperature is 99.5°F (37.5°C), blood pressure is 127/68 mmHg, pulse is 100/min, respirations are 11/min, and oxygen saturation is 98% on room air. Laboratory values are obtained and shown below:

Hemoglobin: 11 g/dL
Hematocrit: 33%
Leukocyte count: 2,500/mm^3 with normal differential
Platelet count: 197,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 24 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.2 mg/dL
AST: 12 U/L
ALT: 10 U/L

On physical exam, you note an elderly man in no current distress. Cardiopulmonary exam is within normal limits. HEENT exam reveals the finding in Figure A but is otherwise unremarkable. Neurological exam reveals decreased hearing in the patient's left ear but is otherwise non-focal. On otoscopy, the tympanic membrane is hypomobile.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [99.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",290.64286,276.11072,305.175,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (20.0 / 2.8) + (20.0 / 18) = 290.64286 mmol/L.The patient's calculated serum osmolality concentration is 290.64286 mmol/L. This is equalivalent to 290.64286 mOsm/kg."
5674,30,Serum Osmolality,lab test,decimal,usmle-4818,Extracted,"A 29-year-old woman presents to the emergency department with joint pain and a notable rash. She has had joint pain for the past 12 months but noticed the rash recently as well as generalized malaise. She states her joint pain is symmetric, in her upper extremities, and is worse in the morning. Her temperature is 97.6°F (36.4°C), blood pressure is 111/74 mmHg, pulse is 83/min, respirations are 14/min, and oxygen saturation is 98% on room air. Laboratory studies are ordered as seen below.

Hemoglobin: 10 g/dL
Hematocrit: 30%
Leukocyte count: 6,800/mm^3 with normal differential
Platelet count: 207,000/mm^3

Serum:
Na+: 140 mEq/L
Cl-: 101 mEq/L
K+: 4.9 mEq/L
HCO3-: 21 mEq/L
BUN: 30 mg/dL
Glucose: 120 mg/dL
Creatinine: 1.8 mg/dL

The patient is ultimately admitted to the hospital.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [30.0, 'mg/dL'], 'Glucose': [120.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",297.38095,282.5119,312.25,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 30.0 mg/dL. 
The concentration of glucose is 120.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (30.0 / 2.8) + (30.0 / 18) = 297.38095 mmol/L.The patient's calculated serum osmolality concentration is 297.38095 mmol/L. This is equalivalent to 297.38095 mOsm/kg."
5675,30,Serum Osmolality,lab test,decimal,pmc-3471405-1,Extracted,"The patient was a 33-year-old Caucasian male with advanced AIDS (CD4+ cell count: 59 cells/mm3, HIV-1 RNA level of 308,000 copies/mL) and an extensive history of opportunistic infections including prior disseminated histoplasmosis, disseminated Mycobacterium avium complex (MAC), Pneumocystis jirovecii (PCP) pneumonia, cutaneous varicella-zoster infection, and cytomegalovirus (CMV) gastric ulcer. He had been placed on combination antiretroviral therapy (cART) with emtricitabine/tenofovir and raltegravir as well as opportunistic infection prophylaxis with itraconazole, azithromycin, trimethoprim/sulfamethoxazole (TMP/SMX), and valganciclovir, although the patient reported being poorly adherent to all prescribed medications. He presented to the hospital with a two-week history of worsening cough, shortness of breath, intermittent fever and chills, and black tarry stools. On admission, he appeared cachectic, chronically ill, and in obvious distress. Vital signs were notable for tachycardia and mild tachypnea. Physical examination revealed facial Molluscum contagiosum, ulcerations on the right lateral tongue, oropharyngeal thrush, mild diffuse abdominal pain, and moderate hepatosplenomegaly. A complete blood count was significant for pancytopenia with a leukocyte count of 2,800 cells/μL (93% neutrophils, 4% lymphocytes, and 1% monocytes), hematocrit of 20% (down from the patient's baseline of 30%), and platelet count of 28,000/mL. The results of a comprehensive metabolic panel were as follows: sodium 133 mmol/L, potassium 4.1 mmol/L, chloride 102 mmol/L, bicarbonate 22 mmol/L, blood urea nitrogen 16 mg/dL, creatinine 0.76 mg/dL, glucose 103 mg/dL, calcium 7.7 mg/dL, AST 113 units/L, ALT 25 units/L, and alkaline phosphatase 450 units/L.
On the evening of admission, the patient became febrile to 39.5°C and increasingly tachycardic, tachypneic, and hypoxic requiring supplemental oxygen, several liters of intravenous fluids, and two units of packed red blood cells. A chest radiograph was obtained which showed a diffuse miliary pattern concerning for PCP pneumonia and/or disseminated opportunistic infectious process such as tuberculosis, MAC, or fungal infection. He was started on empiric treatment with vancomycin, piperacillin/tazobactam, high dose TMP/SMX, prednisone, ethambutol, azithromycin, and liposomal amphotericin B. He responded well to broad-spectrum treatment over the next few days and subsequently underwent diagnostic bronchoscopy with bronchoalveolar lavage (BAL). BAL cultures returned positive for H. capsulatum. The patient also underwent esophagogastroduodenoscopy (EGD) given his persistent melanotic stools and progressively declining hematocrit (nadir of 18%) requiring multiple blood transfusions. EGD was significant for a well-healed scar on the greater curvature of the stomach from prior CMV gastric ulcer and new diffuse erosions throughout the second, third, and fourth segments of the duodenum (). Multiple biopsies were taken which showed duodenal mucosa with granulomatous inflammation. Gomori's methenamine silver (GMS) stain identified macrophages with small intracellular yeasts consistent with disseminated histoplasmosis (). Bone marrow involvement was also suspected in light of the patient's significant pancytopenia, but he had previously refused bone marrow biopsy. Urine Histoplasma antigen came back markedly elevated at >39 ng/mL (above the upper limit of detection for this particular assay) confirming the diagnosis, and the patient was treated with a two-week course of intravenous liposomal amphotericin B followed by indefinite oral itraconazole.
Following a two-week inpatient hospitalization, the patient demonstrated excellent improvement. All major presenting symptoms were resolved, including the melanotic stools, and his hematocrit was stable at his baseline. By the time of discharge, the patient had regained his prior level of functioning including full ambulatory capacity. Several weeks after discharge, sputum acid-fast culture returned positive for MAC for which he was continued on ethambutol and azithromycin.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [16.0, 'mg/dL'], 'Glucose': [103.0, 'mg/dL'], 'Sodium': [133.0, 'mmol/L']}",277.43651,263.56468,291.30834,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 133.0 mmol/L. 
The concentration of bun is 16.0 mg/dL. 
The concentration of glucose is 103.0 mg/dL. 
Plugging these values into the equation, we get 2 * 133.0 + (16.0 / 2.8) + (16.0 / 18) = 277.43651 mmol/L.The patient's calculated serum osmolality concentration is 277.43651 mmol/L. This is equalivalent to 277.43651 mOsm/kg."
5676,30,Serum Osmolality,lab test,decimal,pmc-4830367-1,Extracted,"A 3-year-old boy, who was intubated, was admitted to the emergency care unit. His parents had found him unconscious and cyanotic in the garden and there was a mark of his rain-hood on his neck, which suggested suffocation. He was resuscitated twice before his admission to our hospital. On admission his Glasgow coma score (GCS) was 3. Electrocardiogram and chest radiograph were normal. An emergency brain magnetic resonance imaging (MRI) was performed. Although there was no apparent lesion in the brain stem, bilateral diffuse thalamic, putaminal and globus palllideal lesions were detected on MRI ( and ). Examination revealed tachypnea (respiratory rate, 42/min), but other findings were normal. Arterial blood gases (ABGs) were pH, 7.52; PaCO2, 29 mmHg; and PaO2, 142 mmHg. The chest radiograph, electrocardiogram, and echocardiogram were normal. Laboratory studies disclosed the following values: hematocrit, 33.7%, white blood cell count, 10.6×109/L; sodium, 140 mEq/L; potassium, 3.7 mEq/L; serum urea nitrogen; 6 mg/dL; creatinine, 0.21 mg/ dL; and glucose, 110 mg/dL. Liver transaminases levels were normal. Serum lactate level was 1.97 mmol/L (normal range 0.5-2.2). His electroencephalogram was normal. His tachypnea could not be treated with analgesia (fentanyl infusion) and sedation (midazolam infusion). On the 16th day of admission hyperventilation resolved spontaneously. Tracheostomy was performed and he was discharged from the intensive care unit in vegetative state with normal ventilation.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [6.0, 'mg/dL'], 'Glucose': [110.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",288.25397,273.84127,302.66667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 6.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (6.0 / 2.8) + (6.0 / 18) = 288.25397 mmol/L.The patient's calculated serum osmolality concentration is 288.25397 mmol/L. This is equalivalent to 288.25397 mOsm/kg."
5677,30,Serum Osmolality,lab test,decimal,pmc-8104150-1,Extracted,"A 42-year-old Japanese man with a history of type 2 diabetes mellitus was admitted to our hospital with a 3-day history of fever and claimed to have had insect bites for the past three weeks. Two days before admission, the patient noticed a macule with swelling on his right anterior forearm. The patient developed fever the next day, and the area of swelling on his right forearm expanded, with blisters in the center. He visited a local clinic and was prescribed cefcapene pivoxil for the diagnosis of cellulitis. However, on the day of admission, the patient developed fever, chills, and general fatigue, and the swelling on his forearm worsened. The patient returned to the local clinic and was transferred to our hospital with a diagnosis of tick bite disease.
He denied having sore throat, cough, dyspnea, chest pain, abdominal pain, back pain, and muscle pain. He had a history of diabetes, smoked 1 pack of cigarettes per day, and drank socially. He denied recent animal exposure, recent travel, or any history of allergies. On physical examination, his blood pressure was 149/82 mmHg, pulse rate was 101 beats per minute, body temperature was 39.4°C, respiratory rate was 22 breaths per minute, and oxygen saturation was 98% on room air. His physical examination results were unremarkable, except for tenderness and swelling on his right forearm, with a blister in the center measuring 20 mm × 20 mm (Fig. ). Initial laboratory tests revealed a white blood cell count of 810 cells/μL with 33% neutrophils, 54% lymphocytes, 2% atypical lymphocytes, and 1% promyelocytes; hemoglobin level of 12.4 mg/dL; and platelet count of 56,000 cells/μL.
Serum chemistry evaluation revealed the following results: blood urea nitrogen 11.6 mg/dL, creatinine 0.8 mg/dL, sodium 138 mEq/L, potassium 3.7 mEq/L, chloride 92 mEq/L, albumin 4.1 g/dL, total protein 7.4 g/dL, aspartate aminotransferase 14 IU/L, alanine aminotransferase 12 IU/L, lactate dehydrogenase 189 IU/L, alkaline phosphatase 233 U/L, total bilirubin 0.5 mg/dL, glucose 208 mg/dL, C-reactive protein 23.5 mg/dL, HbA1c 6.8%, prothrombin time 16.7 seconds, activated partial thromboplastin time 36.1 seconds, fibrinogen 180 mg/dL, fibrin degradation product 416 μg/mL, and d-dimer 157 ng/mL. Urine analysis revealed normal findings, and chest radiography revealed no pneumonia.
Initial workups in the emergency room raised suspicion for a tick bite infection with cellulitis; hence, intravenous cefazolin (1 g every 8 hours) and minocycline (100 mg every 12 hours) were initiated.
On day 2, subcutaneous bleeding appeared on his left forearm, which was on the sphygmomanometer attachment site on the right upper arm. Given that his platelet count was decreased to 35,000 cells/μL, platelet transfusion (100,000 U) was performed. On day 3, his platelet count, and additional examination revealed the following results: ferritin level 2045 ng/mL (normal range, 39–340 ng/dL), and human immunodeficiency virus antibody negative. Blood culture on admission revealed P aeruginosa, and the lesion culture grew non-fermenters, such as gram-negative rods and Staphylococcus-like gram-positive cocci. Infectious diseases consultation was performed, and within 5 days the lesion developed from a macule, into a papule, and then to a hemorrhagic bulla with P aeruginosa bacteremia, suggestive of ecthyma gangrenosum. After repeated blood cultures, his treatment regimen was switched to cefepime (2 g every 8 hours), vancomycin (1 g every 12 hours), and minocycline (100 mg every 12 hours).
On day 4, microscopic examination of the peripheral blood smear revealed that 50% leukocytes were abnormal lymphocytes, mostly promyelocytes. Bone marrow aspirate examination and immunophenotyping confirmed the diagnosis of APL with PML-retinoic acid alpha receptor (RARA). The patient received induction chemotherapy with all-trans retinoic acid, cytarabine, and idarubicin.
On day 5, blood cultures from day 3 also revealed P aeruginosa, whereas pus culture grew Pseudomonas aeruginosa and methicillin-susceptible Staphylococcus aureus. The patient was continued on cefepime based on the findings of the susceptibility test, and 8 successfully treated with a 14-day course of antibiotics. IgM and IgG antibodies for Rickettsia japonica and severe fever with thrombocytopenia syndrome tested negative. The patient achieved complete remission after treatment for APL with PML-RARA, and no evidence of APL relapse has been noted at the 3-year follow-up. The patient is currently being monitored at our hospital.
This study was approved by the institutional review board of St. Mary's Hospital (No. 17-0203). Written consent from the patient was obtained for the purpose of publication of the case details.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [138.0, 'mEq/L'], 'Glucose': [208.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [11.6, 'mg/dL']}",291.69841,277.11349,306.28333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 11.6 mg/dL. 
The concentration of glucose is 208.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (11.6 / 2.8) + (11.6 / 18) = 291.69841 mmol/L.The patient's calculated serum osmolality concentration is 291.69841 mmol/L. This is equalivalent to 291.69841 mOsm/kg."
5678,30,Serum Osmolality,lab test,decimal,pmc-6003792-1,Extracted,"An 87-year-old man was conveyed to the emergency department after being found to be drowsy by his helper. He was watching television before he was found slumped in a chair, staring into space with saliva drooling. There was no history of recent fever, headache, fall, or trauma, and no recent hospitalization. Past medical history was significant for hypertension, stage 5 chronic kidney disease, a cerebrovascular accident, pacemaker insertion for sick sinus syndrome, a transurethral resection of the prostate for benign prostatic hyperplasia and pulmonary tuberculosis. His long-term medications were aspirin, omeprazole, amlodipine, and furosemide.
On examination, his Glasgow coma scale was 7 (M4E2V1), and his pupils were equal and reactive. His vital signs were stable, with a temperature of 36.7 degree Celsius, pulse rate of 66 beats per minute, respiratory rate of 18 breaths per minute, oxygen saturation of 99% on room air, and blood pressure of 144/84 mmHg. He had a new onset right hemiparesis and normal reflexes. There was no evidence of any head injury or cerebrospinal fluid otorrhea or rhinorrhea. Stat capillary blood glucose was 8.7 mmol/L. Infective markers were normal, white blood count was 5.6 x103/µL, C-reactive protein was 0.3 mg/L, urea was 17.7 mmol/L (stable), sodium was 137 mmol/L, potassium was 5.1 mmol/L, creatinine was 331 µmol/L (stable), and corrected calcium was 2.29 mmol/L. The liver function test was normal. Electrocardiogram (ECG) did not show any evidence of acute myocardial ischemia. An urgent CT brain revealed air bubbles within the dural venous sinuses (bilateral cavernous, superior sagittal, straight, and left sigmoid sinuses) (Figure ). There was no definite evidence of ischemic changes on CT brain. Pneumocephalus was initially thought to be the cause of his drowsiness and right hemiparesis. The neurosurgery team suggested conservative management of the pneumocephalus.
A facial bone CT was ordered to rule out trauma, as it is the commonest cause of pneumocephalus. The CT scan, done two days later, demonstrated a minimally displaced fracture of the lateral wall of the right maxillary sinus. Of note, there was an acute left middle cerebral artery territory infarct with hemorrhagic conversion, a mass effect on the left ventricle, and a resultant midline shift (Figure ). The pneumocephalus had resolved.
In view of a poor premorbid state, the severity of the stroke, and a lapse in the diagnosis of stroke, the patient was conservatively managed. He was started on statins; antiplatelets were held off in view of significant hemorrhagic conversion causing the midline shift. He underwent physiotherapy but remained bed-ridden.
A repeat CT brain one month later showed improvement in hemorrhagic transformation and a resolution of midline shift. He was then started on dual antiplatelet therapy. Despite the medical management, he demised one month after the initial presentation.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [17.7, 'mmol/L'], 'Glucose': [8.7, 'mmol/L'], 'Sodium': [137.0, 'mmol/L']}",300.42022,285.39921,315.44123,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mmol/L. 
The concentration of bun is 17.7 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 17.7 mmol. To convert 17.7 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 17.7 mmol bun * 0.001 mol/mmol = 0.0177 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0177 mol bun * 28.02 g/mol = 0.49595 g bun. To convert 0.49595 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.49595 g bun * 1000.0 mg/g = 495.95 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 495.95 mg bun/10.0 dL = 49.595 mg bun/dL. The concentration value of 17.7 mmol bun/L converts to 49.595 mg bun/dL. 
The concentration of glucose is 8.7 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 8.7 mmol. To convert 8.7 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 8.7 mmol glucose * 0.001 mol/mmol = 0.0087 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0087 mol glucose * 180.16 g/mol = 1.56739 g glucose. To convert 1.56739 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 1.56739 g glucose * 1000.0 mg/g = 1567.39 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1567.39 mg glucose/10.0 dL = 156.739 mg glucose/dL. The concentration value of 8.7 mmol glucose/L converts to 156.739 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (49.595 / 2.8) + (49.595 / 18) = 300.42022 mmol/L.The patient's calculated serum osmolality concentration is 300.42022 mmol/L. This is equalivalent to 300.42022 mOsm/kg."
5679,30,Serum Osmolality,lab test,decimal,pmc-6803752-1,Extracted,"This is a 73-year-old Caucasian female with history of hypertension and irritable bowel syndrome who presented to the hospital due to sudden onset retrosternal, squeezing, nonradiating chest heaviness during an episode of diarrhea. The pain was associated with minimal shortness of breath. She received aspirin 325 mg by EMS along with sublingual nitroglycerin. On examination in the emergency room, she had a blood pressure of 115/64 mm Hg, a regular heart rate of 67 beats per minute, a respiratory rate of 18 breaths per minute, and saturating 97% on room air. She had normal breath sounds and heart sounds on examination. She was started on nitroglycerin infusion, after which her chest heaviness partially improved but persisted. Initial EKG showed no acute changes but prolonged PR interval of 324 milliseconds ().
The patient was known to have a history of prolonged PR interval noted on prior EKGs. Initial labs showed serum sodium 136 mmol/L, potassium 4.1 mmol/L, bicarbonate 22 mmol/L, chloride 102 mmol/L, BUN 42 mg/dL, creatinine 1 mg/dL, glucose 118 mg/dL, calcium 8.7 mg/dL, white cell count 7.3/nL, hemoglobin 12.1 g/dL, and platelet count 219/nL. Coagulation profile and hepatic function panel were also within normal limits. Initial troponin was 0.46 ng/dL which increased to 3.06 ng/dL after five hours. An initial diagnosis of NSTEMI was made, and the patient was started on a heparin infusion. Urgent coronary catheterization was organized.
Coronary angiogram demonstrated a nonobstructive coronary artery disease (Figures and ) with a ventriculogram showing apical ballooning and ejection fraction of 40% suggestive of takotsubo cardiomyopathy (Figures and ). The patient was admitted to the CCU, and a transthoracic echo was done and consistent with the findings of coronary catheterization: it showed an ejection fraction of 45% with hyperdynamic inferobasal and anterior basal walls with apical ballooning indicative of takotsubo cardiomyopathy (). She was diagnosed as having takotsubo syndrome, and her heparin infusion was discontinued. Her hospitalization was complicated by Mobitz 1 AV block (), wide complex escape rhythms, and subsequent complete heart block (). Because of her baseline prolonged PR interval and very high projected pacing burden, biventricular pacer was inserted. The patient remained hemodynamically stable and was discharged home after a couple of days.
A repeat echocardiogram was done outpatient, two months after hospitalization, and showed improvement: she had an ejection fraction of 55-60% with resolution of the apical ballooning and hyperdynamic wall motion changes, which were initially noted during hospitalization (). Pacemaker interrogation revealed 100% ventricular pacing and continues to show 100% ventricular pacing even twenty months after hospital discharge. This signifies the persistence and chronicity of the AV block even after her hospitalization and after the resolution of her cardiomyopathy.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [136.0, 'mmol/L'], 'Blood Urea Nitrogen (BUN)': [42.0, 'mg/dL'], 'Glucose': [118.0, 'mg/dL']}",293.55556,278.87778,308.23334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.0 mmol/L. 
The concentration of bun is 42.0 mg/dL. 
The concentration of glucose is 118.0 mg/dL. 
Plugging these values into the equation, we get 2 * 136.0 + (42.0 / 2.8) + (42.0 / 18) = 293.55556 mmol/L.The patient's calculated serum osmolality concentration is 293.55556 mmol/L. This is equalivalent to 293.55556 mOsm/kg."
5680,30,Serum Osmolality,lab test,decimal,pmc-5827908-1,Extracted,"A 75-year-old woman living in a nursing home, with past medical history of multiple strokes, hypertension, hyperlipidemia, diabetes mellitus, osteoporosis, mental retardation, and PEG tube placement secondary to dysphagia from stroke 3 years earlier, presented to the emergency department with abdominal discomfort and six episodes of non-bloody, non-bilious vomiting over the preceding 24 h. Two days earlier, she had complained of itching around the location of the gastrostomy tube and was seen repeatedly pulling on the external component of the device. At presentation, the patient appeared clinically dehydrated. She was hemodynamically stable (heart rate 95 beats/min, blood pressure 105/70 mm Hg) and afebrile (temperature 36.3 °C). On physical exam, the abdomen was distended () with tenderness in the epigastric area and hypoactive bowel sounds. There was no guarding or rigidity. Aggressive intravenous hydration with normal saline was started.
Laboratory testing was performed and showed hemoglobin of 16.2 g/dL (13.5 - 17.5 g/dL), hematocrit of 47.2% (40 - 52%), white blood cell count of 11.5 × 109/L (4.0 - 11.0 × 109/L), platelet count of 418 × 109/L (150 - 450 × 109/L), sodium of 143 mEq/L (135 - 145 mEq/L), potassium of 3.7 mEq/L (3.5 - 5.0mEq/L), chloride of 95 mEq/L (96 - 110 mEq/L), blood urea nitrogen of 35 mg/dL (7 - 22 mg/dL), creatinine of 1.6 mg/dL (0.6 - 1.3 mg/dL), glucose of 135 mg/dL, and calcium of 10.2 mg/dL (8.5 - 10.5 mg/dL). The liver function tests were normal. Computed tomography (CT) scan of the abdomen was performed and showed that the internal inflated balloon of the gastrostomy tube had migrated distally and had become impacted in the pyloric channel, thus producing a functional gastric outlet obstruction.
The gastrostomy tube was pulled back, withdrawn into the stomach and secured to the abdominal wall with the help of the external bumper at 2.5 cm. Abdominal distention was improved after the PEG tube adjustment (). Enteral feeding was successfully resumed. Over the next several days, the patient’s clinical condition improved and the patient’s laboratory parameters normalized.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [143.0, 'mEq/L'], 'Glucose': [135.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [35.0, 'mg/dL']}",306,290.7,321.3,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 143.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 143.0 mEq. To convert from 143.0 mEq to mmol, convert from mEq to mmol. The compound 143.0 has a valence of 1, and so divide the valence by the value of mEq to get, 143.0 mEq/(1 mEq/mmol) = 143.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mEq sodium/L converts to 143.0 mmol sodium/L. 
The concentration of bun is 35.0 mg/dL. 
The concentration of glucose is 135.0 mg/dL. 
Plugging these values into the equation, we get 2 * 143.0 + (35.0 / 2.8) + (35.0 / 18) = 306.0 mmol/L.The patient's calculated serum osmolality concentration is 306.0 mmol/L. This is equalivalent to 306.0 mOsm/kg."
5681,30,Serum Osmolality,lab test,decimal,usmle-8169,Extracted,"A 23-year-old man presents with severe right lower quadrant abdominal pain for the past 2 hours. He says the pain started in the periumbilical region and has now shifted to the lower right quadrant. He describes the pain as spasmodic. Past medical history is insignificant, and the patient denies any history of smoking, alcohol, or drug use. The patient’s vital signs show: pulse 88/min, respiratory rate 18/min, blood pressure 126/84 mm Hg, and temperature 38.4°C (101.0°F). On physical examination, there is severe tenderness to palpation in the right lower quadrant with rebound and guarding. The patient is rushed to the operating room for a laparoscopic appendectomy. The following preoperative laboratory tests are obtained:
Serum glucose (random) 123 mg/dL
  Serum electrolytes
Sodium 143 mEq/L
Potassium 4.7 mEq/L
Chloride 102 mEq/L
    Serum creatinine 1.7 mg/dL
Blood urea nitrogen 32 mg/dL
    Hemoglobin (Hb%) 12.5 g/dL
Mean corpuscular volume (MCV)  80 fl
Reticulocyte count 1%
Erythrocyte count 5.1 million/mm³
Leukocyte count 14,000/mm³
Neutrophils 80%
During the induction of anesthesia, isoflurane and a second compound are administered. About 25 minutes after induction, the patient develops significant muscle rigidity and his temperature increases to 40.8°C (105.4°F). The patient’s blood pressure is now 158/94 mm Hg.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [143.0, 'mEq/L'], 'Glucose': [123.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [32.0, 'mg/dL']}",304.2619,289.04881,319.475,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 143.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 143.0 mEq. To convert from 143.0 mEq to mmol, convert from mEq to mmol. The compound 143.0 has a valence of 1, and so divide the valence by the value of mEq to get, 143.0 mEq/(1 mEq/mmol) = 143.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mEq sodium/L converts to 143.0 mmol sodium/L. 
The concentration of bun is 32.0 mg/dL. 
The concentration of glucose is 123.0 mg/dL. 
Plugging these values into the equation, we get 2 * 143.0 + (32.0 / 2.8) + (32.0 / 18) = 304.2619 mmol/L.The patient's calculated serum osmolality concentration is 304.2619 mmol/L. This is equalivalent to 304.2619 mOsm/kg."
5682,30,Serum Osmolality,lab test,decimal,pmc-4944805-1,Extracted,"A 76-year-old woman with multiple sclerosis and diabetes mellitus was transported to the ED by ambulance from her private residence. Her family had called 9-1-1 because they had perceived a change in her mental status. Over the course of two days, the patient had become non-verbal and the family had noticed intermittent episodes of “arm spasms” followed by prolonged periods of unresponsiveness. At baseline, the patient was fully alert and oriented and capable of coherently communicating. She had been chronically bed-bound because of paralysis of her lower extremities. During the past three months, a large bed sore had developed on her sacral area.
The patient’s vital signs were significant for hypothermia (95.7F rectal) and tachycardia (109 beats/min). Her blood pressure, respiratory rate and pulse oximetry were within normal limits. Her bedside serum glucose concentration was elevated (327mg/dL).
Physical examination revealed an elderly woman mumbling incoherently. She did not follow any commands. Her mucus membranes were dry. Her neck was supple. Her heart and lung exams were unremarkable beyond the tachycardia. She had diffuse abdominal discomfort with palpation, indicated by facial grimacing. Her lower extremities were atrophied and contracted. Examination of her back revealed a large stage 4 decubitus ulcer extending from her sacrum to her lower lumbar spine. There was purulent and malodorous discharge with surrounding cellulitis of the wound edges.
The patient was assessed to be septic and was started on broad-spectrum antibiotics (piperacillin/tazobactam and vancomycin). She was hydrated with two liters of normal saline.
Initial laboratory tests included two sets of blood cultures, a complete blood count and a basic metabolic panel. Results showed a white blood cell count of 34.6K/cm2, hemoglobin of 10.7gm/dL, and platelet count of 540K/cm2. Her basic metabolic panel showed the following concentrations: sodium 137mEq/L; chloride 88mEq/L; potassium 4.1mEq/L; bicarbonate 26mEq/L; blood urea nitrogen 23mg/dL; creatinine 0.80mg/dL; and glucose 298mg/dL. A chest radiograph was unremarkable.
Within one hour after her arrival in the ED, the patient had another episode of “arm spasm” that lasted less than one minute. It was reported by the family members who were with the patient at the time but was not witnessed by medical personnel. This event was presumed to be a seizure, so the patient was intubated to protect her from possible aspiration and prevent hypoxia. Given her apparent abdominal tenderness on physical examination, the presumed seizure, and her altered mental status, CTs of her abdomen and brain were ordered. The abdominal CT ( and ) showed diffuse gas extending throughout the thoracolumbar spinal canal. A small amount of subcutaneous emphysema was noted near the sacrum, and the radiologist was concerned about sacral bone osteomyelitis. Her brain CT showed gas within the right frontal horn and the subarachnoid spaces of the craniocervical junction.
Levetiracetam was administered for seizure prophylaxis, and the initial empiric antibiotic coverage was augmented with cefepime and metronidazole for improved cerebrospinal fluid (CSF) penetration and anaerobic bacterial coverage. Her family refused a lumbar puncture. The patient was admitted to the intensive care unit (ICU) with a diagnosis of sepsis, meningitis, and infected sacral ulcer.
Blood cultures were negative for growth, but a sacral wound culture grew fecal flora. After 36 hours in the ICU, the patient’s condition had not improved, and the family requested comfort measures for her. She died six days after initial presentation.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [137.0, 'mEq/L'], 'Glucose': [298.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [23.0, 'mg/dL']}",298.76984,283.83135,313.70833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 23.0 mg/dL. 
The concentration of glucose is 298.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (23.0 / 2.8) + (23.0 / 18) = 298.76984 mmol/L.The patient's calculated serum osmolality concentration is 298.76984 mmol/L. This is equalivalent to 298.76984 mOsm/kg."
5683,30,Serum Osmolality,lab test,decimal,pmc-4360732-1,Extracted,"A 69-year-old African American male with a past medical history of hypertension, seizure disorder, but no underlying psychiatric diagnoses, presented to the emergency department with confusion and urinary incontinence. He had had recurrent episodes of hyponatremia of unclear etiology associated with weakness and a fluctuating mental status. Previous records did not exist in our hospital system, and the patient was not able to provide any information regarding the severity, diagnostic workup, treatment and the number of prior episodes. On arrival, his blood pressure was 162/62 mm Hg, the heart rate 70 beats per minute, the respiratory rate 16 breaths per minute and the temperature 98.7 F. Cardiovascular, respiratory and abdominal examinations were unremarkable. He had normal skin turgor with no peripheral edema and no focal motor deficits. Computed tomography of the head was unremarkable for any intracranial findings. In the emergency department, his serum sodium concentration was 117 mEq/l, BUN was 6 mg/dl, creatinine was 0.7 mg/dl and glucose was 96 mg/dl. The urine osmolality was 132 mosm/kg, and plasma osmolality was 250 mOsm/kg. Urine sodium was not checked initially. He received 1 liter bolus of normal saline. A second serum sodium concentration was obtained at 12 h after the bolus, and the level was 127 mEq/l. The patient produced 8 liters of urine in his first 12 h after arrival. Five percent dextrose water (D5W) was then started at 100 ml per hour to relower the serum sodium concentration and to prevent rebound increase. Fifteen hours after the initial normal saline bolus, his serum sodium concentration decreased to 123 mEq/l. His urine osmolality and urine sodium were now 315 mosm/kg and 128 mEq/l, respectively. Additional history obtained after he regained consciousness revealed an inability to maintain oral intake due to poor appetite for 3 months. However, he continued to drink fluids. He was adamant that he only drank occasionally, 2–3 drinks per month, and he denied a history of liver disease. His home medications included amlodipine, lisinopril and phenytoin. His serum sodium concentration was monitored, and the rate of D5W was adjusted to control the rate of increase in serum sodium concentration to no more than 10–12 mEq/l in 24 h and 18 mEq/l in 48 h. The patient was finally discharged at a serum sodium concentration of 130 mEq/l without any neurological sequelae.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [117.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [6.0, 'mg/dL'], 'Glucose': [96.0, 'mg/dL']}",241.47619,229.40238,253.55,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 117.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 117.0 mEq. To convert from 117.0 mEq to mmol, convert from mEq to mmol. The compound 117.0 has a valence of 1, and so divide the valence by the value of mEq to get, 117.0 mEq/(1 mEq/mmol) = 117.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 117.0 mEq sodium/L converts to 117.0 mmol sodium/L. 
The concentration of bun is 6.0 mg/dL. 
The concentration of glucose is 96.0 mg/dL. 
Plugging these values into the equation, we get 2 * 117.0 + (6.0 / 2.8) + (6.0 / 18) = 241.47619 mmol/L.The patient's calculated serum osmolality concentration is 241.47619 mmol/L. This is equalivalent to 241.47619 mOsm/kg."
5684,30,Serum Osmolality,lab test,decimal,pmc-4595366-1,Extracted,"A 47-year-old female visited our cardiology clinic due to dyspnea that had been progressive over the previous few months. The patient complained of resting dyspnea and peripheral pitting edema. She had no prior medical history or family history of cardiovascular disease. On physical examination, her height was 160 cm and body weight was 70 kg. Her blood pressure was 230/145 mm Hg, and her heart rate was 100 beats per minute. Auscultation of the chest revealed a coarse breathing sound with crackling and regular heart beats with no murmur. The liver and spleen were not palpable, and her bowel sounds were normal.
A blood examination revealed a 7,200/mm3 leukocyte count, 16.5 g/dL hemoglobin, a 274,000/mm3 platelet count, 296 mg/dL random glucose, 8.3% hemoglobin A1c (HbA1c), 28 mg/dL blood urea nitrogen, 1.5 mg/dL creatinine, 7.0 g/dL protein, 3.6 g/dL albumin, 33 IU/L aspartate aminotransferase, 24 IU/L alanine aminotransferase, 292 IU/L alkaline phosphatase, 2.58 mg/L high-sensitivity C-reactive protein, 248 mg/dL total cholesterol, 111 mg/dL triglycerides, 41 mg/dL high density lipoprotein, 181 mg/dL low density lipoprotein, 136 mmol/L sodium, and 4.2 mmol/L potassium. The results of a routine urinalysis were as follows: proteinuria, 2+; glycosuria, 2+; red blood cell, 0 to 1/high power field (HPF) and white blood cell, 5 to 9/HPF; and spot urine protein to creatinine ratio, 428 mg/g. A thyroid function test (TFT) revealed 88 ng/dL T3 (normal range, 78 to 182), 1.44 ng/dL free T4 (normal range, 0.8 to 1.78), and 9.86 mIU/L thyroid stimulating hormone (normal range, 0.17 to 4.05). The TFT results showed subclinical hypothyroidism, but thyroid autoantibodies were negative.
Cardiomegaly was detected on a chest radiograph, and the cardiothoracic ratio was 66% (). The electrocardiogram showed inverted T waves in the lateral and inferior leads, with no significant ST changes. A transthoracic echocardiogram revealed LV hypertrophy and severe systolic dysfunction (). The interventricular septal diameter was 1.3 cm, the LV posterior wall diameter was 1.8 cm, the LV internal diameter in diastole was 5.8 cm (normal range, 3.9 to 5.3), the LV internal diameter in systole was 5.1 cm (normal range, 2.1 to 4.0), and the left ventricular ejection fraction (LVEF) was 25% (). Coronary angiography was performed, and the results were normal.
The patient was treated with multiple antihypertensive drugs, including calcium channel blockers, diuretics, angiotensin converting enzyme inhibitors, and β-blockers to control a hypertensive crisis, but her blood pressure remained >160/100 mm Hg. Abdominal computed tomography was performed to evaluate secondary hypertension, which revealed no abnormalities in either the renal arteries or adrenal glands.
To manage diabetes mellitus, she was referred to Department of Endocrinology and Metabolism at Kyung Hee University Hospital at Gangdong. Because the patient had uncontrolled hypertension, newly diagnosed diabetes mellitus, and soft tissue and bone overgrowth, a diagnosis of acromegaly was suspected. Rough and thick skin was observed, and skin tags were noted around the neck. An enlarged jaw and protruded frontal bones were observed, and soft tissue overgrowth of the heel was noted on a lateral view of a foot X-ray (). The basal IGF-1 level was measured as 183.8 ng/mL, which was within the normal range (90 to 360). Acromegaly was diagnosed after performing a 75-g glucose-loading GH suppression test (). In a thyrotropin-releasing hormone stimulation test, GH levels were found to be increased (). MRI of the sella revealed a 5-mm microadenoma on the left side of the pituitary gland (). A combined pituitary stimulation test performed before surgery revealed that both basal and stimulated hormone levels were normal.
Hyperglycemia was treated with 500 mg metformin twice a day and 12 U insulin glargine once a day via subcutaneous injection. We performed a diabetic complication test, and fundoscopy showed severe nonproliferative diabetic retinopathy ().
Three weeks after admission, combination antihypertensive therapy caused a reduction in blood pressure to <140/80 mm Hg. A follow-up echocardiogram showed no significant difference in LV hypertrophy, but LVEF was improved to 66% ().
After transsphenoidal resection of the pituitary tumor, the tumor was identified as a GH-secreting adenoma () that showed strong staining with anti-GH antibodies in immunohistochemical analysis ().
We performed a follow-up 75-g glucose-loading GH suppression test 2 weeks after surgery, and GH levels were suppressed to 0.15 ng/mL, which means cure state (). The levels of GH and IGF-1 were 0.57, 243.7 ng/mL on postoperative day (POD) 3, 0.38, 295.4 ng/mL on POD 50, and 0.4, 249.5 ng/mL 6 months after surgery (). A follow-up transthoracic echocardiography 6 months after surgery revealed improved LV hypertrophy and LVEF compared with preoperative values.
The patient was prescribed calcium channel blockers and angiotensin-receptor blockers. Her blood pressure was maintained at 120/70 mm Hg 1 year after surgery. Her blood glucose levels were well controlled, with an HbA1c of 5.4%, using only 500 mg/day metformin without insulin. The degree of diabetic retinopathy was improved somewhat, and the patient was followed-up at the outpatient clinic.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [28.0, 'mg/dL'], 'Glucose': [296.0, 'mg/dL'], 'Sodium': [136.0, 'mmol/L']}",298.44444,283.52222,313.36666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.0 mmol/L. 
The concentration of bun is 28.0 mg/dL. 
The concentration of glucose is 296.0 mg/dL. 
Plugging these values into the equation, we get 2 * 136.0 + (28.0 / 2.8) + (28.0 / 18) = 298.44444 mmol/L.The patient's calculated serum osmolality concentration is 298.44444 mmol/L. This is equalivalent to 298.44444 mOsm/kg."
5685,30,Serum Osmolality,lab test,decimal,pmc-4411813-1,Extracted,"A 48-year-old male from West Bengal, in eastern part of India, presented to the emergency department with complaints of sudden onset of pain and distension of abdomen for 2 h. The patient was having low-grade fever and cough with scanty expectoration for last 1-month along with weight loss of 3 kg during this period. With this clinical picture and bilateral upper zone opacities in X-ray chest [], the patient was put on anti-tubercular therapy in another center (Directly Observed Treatment Shortcourse-Category I) though the sputum was negative for acid fast bacilli on Ziehl–Neelson stain on two occasions. On admission, his general examination revealed pulse rate was 112/min and regular, blood pressure was 134/86 mm of Hg, respiratory rate was 36/min and temperature was 100°F. Abdomen was distended, tender with rigidity and guarding. Tenderness was aggravated by movement and cough. Percussion note was tympanitic all throughout the abdomen. On examination of the respiratory system, there was vesicular breath sounds of diminished intensity with coarse crackles bilaterally over infraclavicular areas. Cardiovascular system and central nervous system examination did not reveal any significant abnormality. A diagnosis of perforated hollow viscous abdomen was made provisionally. Routine hematological investigations revealed hemoglobin 110 g/L, total leukocyte count -11.2 × 109/L, neutrophil 68% and lymphocytes 27%. Peripheral smear showed the polymorphonuclear leukocytosis without any parasite or premature cell. Liver enzymes were mildly elevated; aspartate transaminase -64 U/L, alanine transaminase-78 U/L, and alkaline phosphatase -156 U/L. Random plasma glucose was 98 mg/dL, blood urea nitrogen -12 mmol/L and creatinine -1.1 μmol/L. Sodium - 134 mEq/L and potassium -3.4 mEq/L. Serum amylase and lipase study was normal. Routine urine examination was normal. HbSAg, anti-hepatitis C virus and HIV tests were negative. Review of old chest radiograph showed infiltrations in bilateral upper zones with increased broncho vascular markings. X-ray abdomen in an erect posture showed free gas under the diaphragm. Ultrasonography of the abdomen revealed intraperitoneal gaseous distension with intraperitoneal free fluids having internal echogenicity. Patient was urgently shifted to the operation theater for exploratory laparotomy. A midline incision was given. On opening the abdomen, we found around 500 ml of purulent fluid and two small perforations 1cm apart about 20 cm proximal to the ileocaecal junction. After collecting pus sample for microbiological study thorough peritoneal lavage was done, and the perforations were sealed with omental fat. A pelvic drain was given and the incision was closed in a single layer. Postoperative period was eventful as the patient's tidal volume remained low and there was respiratory distress. The patient was shifted to intensive care unit and ventilated mechanically. Patient was treated with intravenous (I/V) piperacillin-tazobactam and amikacin. Gram staining of the pus showed Gram-negative bacilli with bipolar staining. The pus culture showed lactose fermenting pink colonies in MacConkey's agar on 2nd day which turned dry and wrinkled on day 4. The blood agar showed dry and wrinkled colonies on day 4 suspicious of B. pseudomallei []. The antibiotic was changed over to ceftazidime 2 g 8 h along with Amikacin. On 6th postoperative day, the organism was confirmed to be B. pseudomallei by the above-mentioned culture characteristics and standard biochemical methods (positive oxidase and nitrate reduction test, arginine dihydrolase activity, oxidation of glucose and lactose). The organism was sensitive to imipenem, doxycyclin, and cotrimoxazole. Antibiotic was switched over to imipenem 1 g 8 h along with doxycyclin 100 mg twice daily. On 9th postoperative day, we could wean off the ventilator and the patient was put on T-piece ventilation with oxygen. On 12th postoperative day, T-piece was removed, and the oxygen saturation was maintained in room air. Imipenem and doxycyclin were continued for a period of 14 days and then the patient was put on cotrimoxazole (160 + 800 mg). The patient was discharged from the hospital on 24th postoperative day with advice to continue cotrimoxazole for 4 months. On the follow-up of the patient after 6 months, the patient was doing fine, and there was no relapse.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [12.0, 'mmol/L'], 'Glucose': [98.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",285.45302,271.18037,299.72567,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. 
The concentration of bun is 12.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 12.0 mmol. To convert 12.0 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 12.0 mmol bun * 0.001 mol/mmol = 0.012 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.012 mol bun * 28.02 g/mol = 0.33624 g bun. To convert 0.33624 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.33624 g bun * 1000.0 mg/g = 336.24 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 336.24 mg bun/10.0 dL = 33.624 mg bun/dL. The concentration value of 12.0 mmol bun/L converts to 33.624 mg bun/dL. 
The concentration of glucose is 98.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (33.624 / 2.8) + (33.624 / 18) = 285.45302 mmol/L.The patient's calculated serum osmolality concentration is 285.45302 mmol/L. This is equalivalent to 285.45302 mOsm/kg."
5686,30,Serum Osmolality,lab test,decimal,usmle-6354,Extracted,"A 27-year-old man presents to the emergency department with a chief concern of abdominal pain and diarrhea. The patient states that for the past 4 days he has experienced abdominal pain, diarrhea, weakness and a subjective fever. He also endorses a weight loss of 11 pounds during this time. The patient has a past medical history of celiac disease, constipation, and depression. His current medications include fish oil, a multivitamin, sodium docusate, and fluoxetine. His temperature is 98.5°F (36.9°C), blood pressure is 110/75 mmHg, pulse is 90/min, respirations are 13/min, and oxygen saturation is 98% on room air. Physical exam is notable for a young man in mild distress. Cardiac and pulmonary exams are within normal limits. Abdominal exam is notable for generalized tenderness and increased bowel sounds. Oral exam is notable for multiple shallow painful ulcers. Laboratory values are ordered as seen below:

Hemoglobin: 12 g/dL
Hematocrit: 36%
Leukocyte count: 8,000 cells/mm^3 with normal differential
Platelet count: 227,500/mm^3

Serum:
Na+: 141 mEq/L
Cl-: 101 mEq/L
K+: 4.5 mEq/L
HCO3-: 24 mEq/L
BUN: 17 mg/dL
Glucose: 82 mg/dL
Creatinine: 1.0 mg/dL
Ca2+: 10.1 mg/dL
AST: 12 U/L
ALT: 11 U/L

A stool guaiac test is performed which returns positive. The patient is started on IV fluids and morphine.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [17.0, 'mg/dL'], 'Glucose': [82.0, 'mg/dL'], 'Sodium': [141.0, 'mEq/L']}",292.62698,277.99563,307.25833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. 
The concentration of bun is 17.0 mg/dL. 
The concentration of glucose is 82.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (17.0 / 2.8) + (17.0 / 18) = 292.62698 mmol/L.The patient's calculated serum osmolality concentration is 292.62698 mmol/L. This is equalivalent to 292.62698 mOsm/kg."
5687,30,Serum Osmolality,lab test,decimal,pmc-7703305-1,Extracted,"This 74-year-old woman was admitted to a community hospital in a rural area of the Mideast USA with the sudden onset of progressive symmetrical weakness of hands and feet, and numbness in a stocking glove distribution. Two weeks prior, she had an episode of abdominal pain and fecal incontinence that resolved. The patient had a 25-year history of hypertension. She also had a history of asthma, chronic obstructive pulmonary disease, mild depression, urinary tract infections, appendectomy, cholecystectomy, hysterectomy, thyroid lobectomy, cosmetic leg vein stripping, and repair of a ventral hernia. She had a remote history of smoking and did not drink alcohol. Her medications included enalapril, furosemide, potassium, montelukast, and amitriptyline plus perphenazine.
Computed tomography (CT) of the head and spine showed no acute processes. CT of the abdomen showed diverticulosis. The patient was started on empiric ciprofloxacin and metronidazole for presumptive urinary tract infection. Four days later, she was transferred to a nursing home for rehabilitation. Two days after that, she was brought back to the community hospital emergency room with profound weakness of her arms and inability to grasp with either hand. She also had increasing paresthesia of her feet. Her serum sodium was 127 mEq/L (reference range [RR]: 135-145 mEq/L). She was admitted with suspected Guillain Barré syndrome. A few days later, she was transferred to a referral hospital for further neurological evaluation.
On admission to the referral hospital, the patient was afebrile, with pulse 125/minute, blood pressure 140/90 mm Hg, respirations 18/minute and oxygen saturation 97% on supplemental oxygen at 3 L/min. She had distal extremity weakness, worse on the right (0/5) than the left (1-2/5). Sensory examination revealed numbness up to the ankles and wrists. Distal tendon reflexes were absent. Her sodium was 122 mEq/L, potassium 4.2 mEq/L (RR: 3.6-5 mEq/L), chloride 91 mEq/L (RR: 98-108 mEq/L), bicarbonate 26 mEq/L (RR: 22-26 mEq/L), glucose 98 mg/dL (RR: 65-100 mg/dL), blood urea nitrogen (BUN) 8 mg/dL (RR: 7-21 mg/dL), creatinine 0.4 mg/dL (RR: 0.5-1.4), hemoglobin 14.3 g/dL (RR: 12.0-15.2 g/dL), mean corpuscular volume 81.8 fL (RR: 78-101 fL), platelets 243,000/mm3 (RR: 140,000-450,000/mm3), white blood cell (WBC) count 13,500/mm3 (RR: 4,100-10,900/mm3) (83% neutrophils, 12% bands, 2% lymphocytes, 2% monocytes), erythrocyte sedimentation rate (ESR) 42 mm/hr (RR: <30 mm/hr), rheumatoid factor 226 IU/dL (RR: 40-60 IU/dL), C-reactive protein 16.8 mg/L (“high risk” >3 mg/L) and anti-nuclear antibody <40 IU/L (RR: <40 IU/L). Lumbar puncture showed cerebrospinal fluid with 1 WBC/mm3 and protein 73 mg/dL (RR: 15-60 mg/dL).
The next day, electromyography showed evidence of a severe axonal and demyelinating sensorimotor peripheral neuropathy. Magnetic resonance imaging of the brain showed age-related volume loss with chronic microangiopathic disease. Blood and urine testing for lead and mercury poisoning returned negative. Intravenous immunoglobulin therapy was started.
The next day, the patient was pleasant and conversant despite persistent sodium levels between 120 and 129 mEq/L. Her upper and lower extremities showed 2+ edema. CT showed marked elevation of the left hemidiaphragm, a small left pleural effusion and left basilar atelectasis. CT of the abdomen and pelvis was negative. Serology for human immunodeficiency virus, hepatitis B, hepatitis C, and Lyme disease IgM returned negative. The syndrome of inappropriate antidiuretic hormone was suspected and fluid restriction commenced.
The next day, a rheumatologist elicited a history of 2 episodes in the past 9 months of frontal headache, dry mouth, anorexia and early satiety; also, the patient had been told by an optometrist that she had dry eyes, but this was asymptomatic. The patient had remained afebrile in the hospital, with blood pressure 117-142 / 50-70 mm Hg. On examination by the rheumatologist, the patient had a non-blanching erythematous skin rash over her feet, palpable purpura over her left breast, loss of sensation from her feet up to her knees and from her fingertips to her elbows, inability to move her legs and right arm, areflexia, and glossitis, but no salivary or parotid gland enlargement. The WBC count was 13,700/mm3, hemoglobin 12.7 g/dL, BUN 8 mg/dL, and creatinine 0.3 mg/dL. The rheumatologist suspected vasculitis and prednisone (50 mg daily) was started. C3 complement was later reported 110 mg/dL (RR: 79-152 mg/dL), C4 complement <10 mg/dL (RR: 13-75 mg/dL), and serum protein electrophoresis and cryoglobulin test negative. Over the next few days, there was no neurological improvement, but the patient's serum sodium rose to 132 mEq/L.
The next day, the patient reported feeling much better, but that night began having episodes of confusion and delirium. Immunoglobulin therapy was discontinued and trazodone was started. The following day, she remained afebrile and hemodynamically stable. Her oxygen saturation was 98-100%. She appeared comfortable. Her lungs were clear. Her neurological status remained unchanged. The next day, serology for anti-Ro/SSA and anti-La/SSB was negative. The following day, open biopsies of the peroneus brevis muscle and peroneal and sural nerves were performed, which revealed necrotizing vasculitis of vessels in muscle and sural nerve, active and chronic neurogenic muscular changes, epineural fibrosis and chronic axonal loss.
The next day, the patient developed a large hematoma of unclear etiology in her upper right arm. Her platelet count dropped from 230,000/mm3 to 136,000/mm3. Chest radiograph showed unchanged left basilar atelectasis. The patient was receiving stress-ulcer prophylaxis as well as deep venous thrombosis prophylaxis. Bilateral venous duplex examination of her upper extremities showed no evidence of deep venous thrombosis. Immunofluorescence for anti-neutrophilic cytoplasmic antibodies was reported negative at a dilution of 1:20 (normal <1:40).
The following day, the patient exhibited acute mental status changes. Her hemoglobin dropped from 11.7 g/dL to 9.2 g/dL over 12 hours. CT showed a large left parietotemporal intraparenchymal hematoma with surrounding vasogenic edema; this compressed the posterior aspect of the left lateral ventricle and induced a small amount of midline shift. A decompressive craniotomy was performed. Follow-up CT showed a decrease in compression of the left ventricle and decreased midline shift. Electroencephalogram showed severely abnormal diffuse slowing, periodic lateralized epileptiform discharges, bi-hemispheric epileptiform discharges, and an electrographic seizure. Intravenous phenytoin (100 mg) was given.
The patient’s family was informed that she was not likely to make a meaningful recovery. A decision was reached with the family to provide comfort measures only and the patient died several days later.
Postmortem examination revealed necrotizing vasculitis in skeletal muscle, ( and ), peripheral nerves, esophagus, stomach, small intestine, pancreas, liver, adrenals, kidneys, lungs and pericardium, involving predominantly medium-sized arteries, but also some large parenchymal arteries in the liver, associated with multifocal thromboses in liver (up to 2 cm), myocardium, thoracic lymph nodes and left adrenal gland, and hemorrhages in left parietal-occipital cerebrum (7 × 6 × 5 cm), upper right arm (29 × 18 cm), stomach, intestines, bladder, pericardium, trachea, mesentery, omentum, right ovary and right breast. In addition to and , a virtual (digital) slide of skeletal muscle is available for viewing at the Larry Nichols collection. It is case 003.
Autopsy also revealed leukocytoclastic vasculitis involving arterioles, capillaries and venules in the skin ().
Autopsy also revealed a small, 0.6 cm, moderately differentiated, invasive adenocarcinoma in the cecum. The cerebral blood vessels had severe hypertensive vasculopathy and moderate atherosclerosis in those of the circle of Willis, but no vasculitis. There was severe acute transmural ischemic colitis of the rectum, a microscopic acute infarct of the left adrenal, and moderate coronary atherosclerosis, with up to 60% stenosis of the left anterior descending coronary artery. The myocardium had a microscopic area of necrosis adjacent to a thrombosed arteriole. The aorta had moderate atherosclerosis and mild cystic medial degeneration, but no aortitis. The pulmonary arteries contained a branched, recently formed (4 × 0.5 × 0.3 cm) thrombus in the left lower lobe, a branched, recently formed (6 × 1 × 0.5 cm) thrombus in the right middle lobe, microscopic non-occlusive thrombi, and multifocal fibrous intimal thickening suggestive of previous organized thromboemboli, but no vasculitis. The skin had petechiae and ecchymoses on the trunk and limbs. The kidneys had arteriolar nephrosclerosis, but no vasculitis or glomerulonephritis.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [132.0, 'mEq/L'], 'Glucose': [98.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [8.0, 'mg/dL']}",272.30159,258.68651,285.91667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 132.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 132.0 mEq. To convert from 132.0 mEq to mmol, convert from mEq to mmol. The compound 132.0 has a valence of 1, and so divide the valence by the value of mEq to get, 132.0 mEq/(1 mEq/mmol) = 132.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 132.0 mEq sodium/L converts to 132.0 mmol sodium/L. 
The concentration of bun is 8.0 mg/dL. 
The concentration of glucose is 98.0 mg/dL. 
Plugging these values into the equation, we get 2 * 132.0 + (8.0 / 2.8) + (8.0 / 18) = 272.30159 mmol/L.The patient's calculated serum osmolality concentration is 272.30159 mmol/L. This is equalivalent to 272.30159 mOsm/kg."
5688,30,Serum Osmolality,lab test,decimal,pmc-4703168-1,Extracted,"A 34-year-old male with a past medical history of MS was brought into the emergency department by Emergency Medical Services after being found unresponsive by his mother with three pill bottles at his side. The bottles were an empty bottle of valacyclovir, an empty bottle of temazepam and a bottle of dalfampridine still containing some pills. His mother gave the history that the patient was under multiple social stressors of late. Other than MS, the patient was diagnosed with insomnia and had no other pertinent past medical history. His current medications were valacyclovir, temazepam, dalfampridine (4-AP) and a tysabri IV infusion (all part of his MS treatment regimen).
The initial vital signs were as follows: Blood pressure: 155/82mmHg; Heart rate: 106/min; Respiratory rate: 24/min; Temperature: 97.4ºF; O2 sat: 97% 2L NC. The bedside glucose was 144mg/dl. The patient appeared extremely tremulous, was awake, but not responding to questioning nor following simple commands. He responded to tactile stimulation by localizing to the pain. He did not appear to have any focal deficits. His pupils were 4 mm, equal and reactive and his mucous membranes were moist. His heart sounds were tachycardic, with no murmurs. The patient had clear breath sounds bilaterally and no retractions. The abdomen had normoactive bowel sounds. The skin was diaphoretic with piloerection.
Intravenous access was established, labs were drawn and the patient was given two liters of normal saline. Soon after arrival, the patient lost consciousness, his oxygen saturation decreased to below 90% and he began to have a tonic-clonic seizure. The patient was administered boluses of lorazepam, to a total of 8 mg, without effect in seizure resolution. He was intubated and subsequently placed on a lorazepam and propofol infusion for sedation. He was loaded with one gram of phenytoin and 300mg phenobarbital and then placed on a phenobarbital infusion. Clinically the patient continued to have frequent, recurrent seizures.
The patients lab values on arrival were significant for a white blood cell count of 31.1×103/mcL, a sodium of 143mEq/L, potassium 3.1mEq/L, chloride 107mEq/L, bicarbonate of 24mEq/L, a blood urea nitrogen of 15mg/dL and a creatinine of 1.2mg/dL. The anion gap was 12. The lactic acid was 3.4mg/dl. Total creatinine kinase was 99 units/L. Liver function tests and coagulation studies were all within normal limits. Ethanol, acetaminophen and salicylate levels were all negative. A urine toxicology screen was positive for benzodiazepines. An arterial blood gas showed pH 7.22, pCO2 65, pO2 127 and HCO3 26.6 (performed immediately after intubation). Computerized tomography of the brain and chest x-ray were both normal. The electrocardiogram showed a sinus rhythm at 88 beats per minute with normal QRS and QT intervals. Drug levels were sent for 4-AP and valacyclovir. The 4-AP level resulted at 530ng/mL (therapeutic: 25 to 49ng/mL). The valacyclovir level was 7.5mcg/mL (therapeutic 2.0–4.0mcg/mL).
The patient was admitted to the intensive care unit (ICU) and while he was there he continued to have seizures. While in the ICU the patient had two electroencephalographs (EEGs) performed. The EEG on hospital day 2 showed epileptiform activity and the other EEG was performed on hospital day 7 and was indicative of epileptiform encephalopathy.
The patient stopped seizing on hospital day 3. The patient was extubated on hospital day 12. He was discharged, with normal mental status and neurologic exam to an inpatient psychiatric facility.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [143.0, 'mEq/L'], 'Glucose': [144.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [15.0, 'mg/dL']}",299.35714,284.38928,314.325,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 143.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 143.0 mEq. To convert from 143.0 mEq to mmol, convert from mEq to mmol. The compound 143.0 has a valence of 1, and so divide the valence by the value of mEq to get, 143.0 mEq/(1 mEq/mmol) = 143.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mEq sodium/L converts to 143.0 mmol sodium/L. 
The concentration of bun is 15.0 mg/dL. 
The concentration of glucose is 144.0 mg/dL. 
Plugging these values into the equation, we get 2 * 143.0 + (15.0 / 2.8) + (15.0 / 18) = 299.35714 mmol/L.The patient's calculated serum osmolality concentration is 299.35714 mmol/L. This is equalivalent to 299.35714 mOsm/kg."
5689,30,Serum Osmolality,lab test,decimal,pmc-7008170-1,Extracted,"A 60-year-old obese (BMI: 38.7 kg/m2) female patient from a rural area of North India presented with complaints of acute pain in the abdomen and abdominal distension for the last 7 days and an inability to pass stool for the last 3 days. She was a known case of type II diabetes mellitus for the last 6 years and was being treated with insulin for the same. There was no associated fever, jaundice, or any history suggestive of gastrointestinal bleeding. On examination, she was sick looking, with tachycardia (pulse of 100 beats/min), tachypnea (respiratory rate of 34 min−1), and hypotension (blood pressure 100/60 mmHg). Her abdomen was distended, with diffuse guarding and rigidity suggestive of peritonitis. Laboratory investigations demonstrated the following (values in parentheses indicate normal range): hemoglobin 9.2 g/dL (12–14 g/dL), white blood cell count 18 000/mm3 (4000–11 000/mm3), platelet count 32 000/mm3 (150 000–450 000/mm3), total bilirubin 0.9 mg/dL (0.3– 1.2 mg/dL), aspartate aminotransferase 722 IU/L (2–40 IU/L), alanine aminotransferase 169 IU/L (2–41 IU/L), alkaline phosphatase 249 IU/L (42–128 IU/L), albumin 2.13 g/dL (3.4–4.8 g/dL), sodium 142 meq/L (135–145 meq/L), potassium 3.6 meq/L (3.5–5 meq/L), urea 121 mg/dL (10–50 mg/dL), creatinine 1.0 mg/dL (0.5–1.2 mg/dL), and blood glucose (random) 170 mg/dL.
Chest X-ray was normal. X-ray abdomen in erect position showed no air under the diaphragm. Contrast-enhanced computed tomography (CECT) abdomen was performed, which demonstrated pneumoperitoneum and thickened duodenal wall, with decreased enhancement and intramural air foci (pneumatosis intestinalis) suggestive of gastric ischemia with necrosis (Fig. a). The visualized lungs appeared normal.
The patient was resuscitated with intravenous fluids and started on piperacillin-tazobactam. Inotropic support (noradrenaline) was required for hypotension. In view of severe sepsis and circulatory compromise that did not respond to initial fluid boluses, bilateral flank drains were placed to drain out the infected fluid and achieve partial source control. These yielded an output of around 500 mL of biliopurulent fluid in each drain. She responded favorably to resuscitation and drainage and was taken for emergency laparotomy around 10 h after the initial presentation. On exploration, there was gross peritoneal contamination with 700–800 mL of biliopurulent fluid. The liver was cirrhotic with a multinodular appearance. There was a solitary large perforation (6 cm × 6 cm) in the anterior wall of the distal stomach involving the pylorus and the first part of the duodenum (Fig. b). The tissue at the edges of the perforation site was necrotic with unhealthy blackish exudates covering it. Distal gastrectomy with Billroth II reconstruction was performed with hand-sewn closure of the duodenal stump. Cut section of the resected stomach showed multiple deep ulcers with punched out edges and blackish slough covering them (Fig. c,d). Histopathology demonstrated transmural necrotizing inflammation with the presence of multiple aggregates of fungal septate hyphae and acute branching pattern, confirming the morphology of Aspergillus spp (Fig. e,f).
Postoperatively, she was managed in the surgical intensive care unit. Liposomal amphotericin B was started in view of suspicion of fungal sepsis. However, despite optimal critical care and supportive management, she succumbed to septicemia with multiorgan dysfunction syndrome on postoperative day 2. Involvement of other organs could not be confirmed as consent for autopsy was not given.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [142.0, 'mEq/L'], 'Glucose': [170.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [121.0, 'mg/dL']}",336.65873,319.82579,353.49167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. 
The concentration of bun is 121.0 mg/dL. 
The concentration of glucose is 170.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (121.0 / 2.8) + (121.0 / 18) = 336.65873 mmol/L.The patient's calculated serum osmolality concentration is 336.65873 mmol/L. This is equalivalent to 336.65873 mOsm/kg."
5690,30,Serum Osmolality,lab test,decimal,pmc-4421247-1,Extracted,"A 36-year-old 5-week postpartum woman presented to the emergency room with complaints of nausea and vomiting for 48 h. She also reported a 2-day history of general malaise and worsening dyspnoea. She denied chest pain, palpitations, diarrhoea or headaches. She reported eating; however, she limited herself to several small high-protein carbohydrate-free meals in an attempt to quickly return to her prepartum weight. Since her delivery, she had achieved an intentional weight loss of 30 lbs. Initial vital signs were: temperature 37 °C, blood pressure 140/63 mmHg, heart rate 84, respiratory rate 20 and a weight of 59.8 kg. She appeared unkempt and lethargic. Head and neck examinations were benign. Chest auscultation was clear with no adventitious sounds; heart examination was unremarkable. The abdomen was benign with a well-healed surgical C-section scar; there was no costovertebral angle tenderness. The extremities were without tenderness or oedema. She had no neurologic defects other than her blunted mentation.
Her past medical history was significant for a cesarean section, complicated by bladder damage, now resolved. Her only medication was percocet to manage post-surgical visceral pain. She denied alcohol or illicit substance use.
Initial laboratory data include sodium of 144 mEq/L, potassium 4.8 mEq/L, chloride 104 mEq/L and bicarbonate <5 mEq/L that is the lowest available determination possible at our institution. Her BUN was 3 mg/dL, creatinine was 1.1 mg/dL and glucose was 133 mg/dL. Serum lactate was 2.1 mmol/L, phosphate 1.0 mg/dL and magnesium 1.6 mg/dL. Arterial blood gas drawn on room air showed a pH of 6.9, PCO2 of 19 mmHg, PaO2 of 137 mmHg and SaO2 of 100%. White blood cell count was 17 600/mm3 with 88.2% segmented neutrophils, Hg 13.7 g/dL, haematocrit 43.1% and platelets of 340 000/mm3. Urinalysis had a pH of 5.5 with <80 mg/dL ketones. The serum osmolar gap was 7. A comprehensive drug screen was negative including salicylates and acetaminophen. Chest radiograph was normal. Blood and urine cultures were negative.
The patient was volume-depleted with a metabolic acidosis and a serum anion gap of 35. Fluid resuscitation with three ampules of sodium bicarbonate per litre of D5W at 100 cc/h was initiated for 24 h. Improvement in laboratory values occurred within 12 h with serum bicarbonate improving to 12 mEq/L. The serum bicarbonate improved to 20 mEq/L with normalization of the anion gap at 24 h. Symptomatic improvement occurred likewise. The patient was started on an 1800 kcal diet during her hospitalization, supplemented with a regular diet of home food provided by the husband. Breast feeding was stopped on advice from a lactation consultant and the acidosis did not reoccur. The patient's baby was reported to be in the 90th percentile for weight and height.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [3.0, 'mg/dL'], 'Glucose': [133.0, 'mg/dL'], 'Sodium': [144.0, 'mEq/L']}",296.46032,281.6373,311.28334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 144.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 144.0 mEq. To convert from 144.0 mEq to mmol, convert from mEq to mmol. The compound 144.0 has a valence of 1, and so divide the valence by the value of mEq to get, 144.0 mEq/(1 mEq/mmol) = 144.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 144.0 mEq sodium/L converts to 144.0 mmol sodium/L. 
The concentration of bun is 3.0 mg/dL. 
The concentration of glucose is 133.0 mg/dL. 
Plugging these values into the equation, we get 2 * 144.0 + (3.0 / 2.8) + (3.0 / 18) = 296.46032 mmol/L.The patient's calculated serum osmolality concentration is 296.46032 mmol/L. This is equalivalent to 296.46032 mOsm/kg."
5691,30,Serum Osmolality,lab test,decimal,pmc-5889268-1,Extracted,"A 64-year-old male was transferred to our emergency department due to incontinence and impaired consciousness. His airway was patent, but his Glasgow Coma Scale at the time of the presentation was deteriorated (E3V2M4). He had no history of diabetes or hypertension, did not drink alcohol regularly, and had ceased smoking several years prior. The patient was not constipated before admission. His wife stated that he played golf the day before visit, and he presented dry mouth and felt thirsty the night before admission. He had undergone left hemicolectomy for pT3N1M0 stage IIIa colon cancer 3 years earlier. His postoperative course was uneventful and was subsequently given 5-FU/folinic acid and oxaliplatin at doses of 1.5 g/m2, 75 mg/m2, and 85 mg/m2, respectively.
Arterial blood gas levels were abnormal: pH, 7.432; pCO2, 27 Torr; pO2, 127.0 Torr; glucose, 172 mg/dL; base excess −5.5, indicating lactic acidosis with respiratory compensation. His lactic acid level was 5.1 mmol/L (0.44–1.78 mmol/L). An emergent serum biochemistry evaluation indicated normal liver and kidney function: total bilirubin, 0.53 mg/dL; aspartate aminotransferase, 19 IU/L; alanine aminotransferase, 6 IU/L; blood urea nitrogen, 10.0 mg/dL; and creatinine, 0.76 mg/dL. His serum ammonia level was 338 μg/dL (30–86 μg/dL). Serum sodium and potassium levels were of 151.1 and 4.8 mEq/L, respectively. Computed tomography did not reveal any intracranial pathology such as hematoma, stroke, or metastasis. Magnetic resonance imaging revealed lacunar infarctions close to the cerebral ventricle. However, we did not observe any symptoms associated with these lesions. The patient was diagnosed with disturbance of consciousness caused by hyperammonemia. We stopped chemotherapy and started intravenous glycerol infusion, diuretics, and fluid replacement. The patient became fully conscious with a serum ammonia level of 31 μg/dL by the next day.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [10.0, 'mg/dL'], 'Glucose': [172.0, 'mg/dL'], 'Sodium': [151.1, 'mEq/L']}",315.32698,299.56063,331.09333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 151.1 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 151.1 mEq. To convert from 151.1 mEq to mmol, convert from mEq to mmol. The compound 151.1 has a valence of 1, and so divide the valence by the value of mEq to get, 151.1 mEq/(1 mEq/mmol) = 151.1 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 151.1 mEq sodium/L converts to 151.1 mmol sodium/L. 
The concentration of bun is 10.0 mg/dL. 
The concentration of glucose is 172.0 mg/dL. 
Plugging these values into the equation, we get 2 * 151.1 + (10.0 / 2.8) + (10.0 / 18) = 315.32698 mmol/L.The patient's calculated serum osmolality concentration is 315.32698 mmol/L. This is equalivalent to 315.32698 mOsm/kg."
5692,30,Serum Osmolality,lab test,decimal,usmle-5709,Extracted,"A 68-year-old man presents to the emergency department with a chief complaint of cough and fever. The patient states that he has been feeling progressively worse these past few days and decided to come into the emergency department when he felt short of breath and febrile. Prior to his symptoms he was at a barbecue. He has a medical history of obesity, asthma, diabetes, and heart disease. He states that he had a recent surgery for his ""heart problems."" His current medications include albuterol, salmeterol, insulin, metformin, warfarin, aspirin, and ibuprofen. He lives in a nursing home where he is well taken care of. Physical exam is significant for pulmonary crackles and a cardiac murmur. A chest radiograph is ordered as seen in Figure A. Laboratory results are shown:

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.7 mEq/L
HCO3-: 23 mEq/L
BUN: 20 mg/dL
Glucose: 145 mg/dL
Creatinine: 1.3 mg/dL
Ca2+: 10.1 mg/dL
AST: 11 U/L
ALT: 11 U/L

Hemoglobin: 11.1 g/dL
Hematocrit: 38%
Leukocyte count: 15,000/mm^3 with normal differential
Platelet count: 255,000/mm^3
INR: 2.9

A peripheral smear is ordered and is seen in Figure B. The patient is started on IV ceftriaxone.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [145.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",293.19841,278.53849,307.85833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 145.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (20.0 / 2.8) + (20.0 / 18) = 293.19841 mmol/L.The patient's calculated serum osmolality concentration is 293.19841 mmol/L. This is equalivalent to 293.19841 mOsm/kg."
5693,30,Serum Osmolality,lab test,decimal,usmle-6209,Extracted,"A 27-year-old woman presents to the emergency department with weakness of her legs which has progressed to an inability for her to stand. The patient works as a school teacher in Alaska and regularly goes hiking and camping. She recently returned from a camping trip where she hiked through tall brush and drank from mountain streams. The patient was also involved in a motor vehicle accident 2 days ago but did not seek treatment. The patient has a medical history that is unremarkable and is currently taking multivitamins and other than a recent bout of diarrhea is generally healthy. Her temperature is 99.5°F (37.5°C), blood pressure is 120/68 mmHg, pulse is 120/min, respirations are 17/min, and oxygen saturation is 98% on room air. Physical exam is notable for a very anxious woman with 1/5 strength of the patient’s lower extremities and 2/5 strength of her trunk muscles with diminished sensation. Laboratory studies are ordered as seen below.

Hemoglobin: 15 g/dL
Hematocrit: 43%
Leukocyte count: 6,500/mm^3 with normal differential
Platelet count: 194,000/mm^3

Serum:
Na+: 138 mEq/L
Cl-: 102 mEq/L
K+: 4.4 mEq/L
HCO3-: 24 mEq/L
BUN: 20 mg/dL
Glucose: 120 mg/dL
Creatinine: 1.0 mg/dL
Ca2+: 10.2 mg/dL
pH: 7.44
PaCO2: 10 mmHg
PaO2: 90 mmHg
AST: 12 U/L
ALT: 10 U/L

The patient complains about difficulty breathing. Repeat laboratory values are notable for the findings below.

pH: 7.35
PaCO2: 30 mmHg
PaO2: 80 mmHg

The patient is intubated and sent to the MICU.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [120.0, 'mg/dL'], 'Sodium': [138.0, 'mEq/L']}",289.80952,275.31904,304.3,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 120.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (20.0 / 2.8) + (20.0 / 18) = 289.80952 mmol/L.The patient's calculated serum osmolality concentration is 289.80952 mmol/L. This is equalivalent to 289.80952 mOsm/kg."
5694,30,Serum Osmolality,lab test,decimal,pmc-7580480-1,Extracted,"A 35-day old male infant presented to our hospital with a history of 3-day diarrhea and vomiting for multiple episodes which were projectile, non-bilious, non blood stained and associated with decreased urinary output. Neither fever nor irritability was noted. He was born at 41+4 weeks of gestation by elective cesarean section due to postdated pregnancy with a birth weight of 3.1kg. He cried immediately after birth and was exclusively on breastfeeding till date.
Antenatal scans were normal, maternal serology was non reactive, had no genetic diseases in the family and had no risk factors for sepsis.
On general examination, he was lethargic with sunken eyes, dry oral mucosa, and depressed anterior fontanelle. Vitals were normal. Examinations of the respiratory system, cardiovascular and abdomen were within normal limits. His blood pressure was recorded as 90/50 mm Hg (above 50th centile). His weight was 3.0 kg (z score -2.78), length 55cm (z score -0.67) and head circumference 37 cm (z score 1.78).
On physical examination, normal male genitalia but with pigmentation was noted which was darker than the infant's skin tone ().
Investigations showed a negative septic screening with deranged electrolytes. His serum Na+ was 116 meq/l, K+ was 6.1meq/l, urea was 33 mg/dl and creatinine was 0.5 mg/dl. Random blood sugar was 75mg/dl. His initial blood gas analysis showed: pH- 7.42 (7.35-7.45), Pco2 23.5 (35-45), HCO3 15.6 mmol/L (22-28 mmol/L), Base excess -9 mmol/L (-4.0 to +4.0 mmol/L), lactate of 2.8 mmol/L (<2 mmol/L). Liver Function Test was within the normal limit.
Both ECG and Ultrasonography findings were normal. Hence, pyloric stenosis was excluded.
A probable diagnosis of CAH with the salt-wasting crisis was made according to examination and investigation and treatment was commenced.
He was given 20ml/kg of 0.9% saline bolus, continuous nebulized Salbutamol (2.5 mg) and Hydrocortisone intravenously (2mg/kg 6 hourly). Blood was drawn and sent for 17-hydroxyprogesterone (17-OHP) which later came to be positive 405ng/ml (<22.0 ng/ml) and confirmed our diagnosis. His glucose and electrolytes have been monitored daily while in the hospital, and they gradually improved by 7th day.
He was discharged home with oral Prednisolone at 15mg/m2/day and Fludrocortisone Acetate at 0.3mg/ day. He was followed-up after 8 days in the outpatient department. His weight was 3.5 kg. Electrolytes were normal and medications had been adjusted accordingly based on his weight.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [33.0, 'mg/dL'], 'Glucose': [75.0, 'mg/dL'], 'Sodium': [116.0, 'mEq/L']}",247.95238,235.55476,260.35,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 116.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 116.0 mEq. To convert from 116.0 mEq to mmol, convert from mEq to mmol. The compound 116.0 has a valence of 1, and so divide the valence by the value of mEq to get, 116.0 mEq/(1 mEq/mmol) = 116.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 116.0 mEq sodium/L converts to 116.0 mmol sodium/L. 
The concentration of bun is 33.0 mg/dL. 
The concentration of glucose is 75.0 mg/dL. 
Plugging these values into the equation, we get 2 * 116.0 + (33.0 / 2.8) + (33.0 / 18) = 247.95238 mmol/L.The patient's calculated serum osmolality concentration is 247.95238 mmol/L. This is equalivalent to 247.95238 mOsm/kg."
5695,30,Serum Osmolality,lab test,decimal,usmle-5833,Extracted,"A 72-year-old man is seen in the hospital for a sacral rash. The patient has been hospitalized for the past 3 weeks for a heart failure exacerbation. When the nurse went to bathe him this morning, she noticed a red rash over his sacrum. The patient reports mild discomfort and denies pruritus. The patient has chronic kidney disease, urinary incontinence, ischemic cardiomyopathy, gout, and poor mobility. His current medications include aspirin, furosemide, metoprolol, lisinopril, spironolactone, and prednisone that was started for a recent gout flare. The patient’s temperature is 97°F (37.2°C), blood pressure is 110/62 mmHg, pulse is 68/min, and respirations are 13/min with an oxygen saturation of 98% on room air. On physical examination, there is a 4 cm x 6 cm patch of non-blanchable erythema over the patient’s sacrum that is mildly tender to palpation. Labs are obtained, as shown below:

Leukocyte count: 10,000/mm^3 with normal differential
Hemoglobin: 15.2 g/dL
Platelet count: 400,000/mm^3

Serum:
Na: 138 mEq/L
K+: 4.3 mEq/L
Cl-: 104 mEq/L
HCO3-: 25 mEq/L
BUN: 26 mg/dL
Creatinine: 1.5 mg/dL
Glucose: 185 mg/dL

A hemoglobin A1c is pending.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [26.0, 'mg/dL'], 'Glucose': [185.0, 'mg/dL'], 'Sodium': [138.0, 'mEq/L']}",295.56349,280.78532,310.34166,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 26.0 mg/dL. 
The concentration of glucose is 185.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (26.0 / 2.8) + (26.0 / 18) = 295.56349 mmol/L.The patient's calculated serum osmolality concentration is 295.56349 mmol/L. This is equalivalent to 295.56349 mOsm/kg."
5696,30,Serum Osmolality,lab test,decimal,pmc-3716036-1,Extracted,"A 54-year-old female with a medical history of hypertension, hepatitis C, and cirrhosis presented with nausea, vomiting and dysphagia of 1-day duration following surveillance esophagogastroduodenoscopy (EGD) and banding from an outside hospital. She reported that her symptoms started immediately post-procedure and that she continued to have multiple episodes of mostly clear vomit with streaks of blood. She also reported throat, chest, and epigastric pain and was unable to eat anything since the procedure due to her symptoms.
Her past medical history included hypertension, hepatitis C, cirrhosis, gastroesophageal reflux disease, variceal hemorrhage, gall stones and Graves disease. She was on propranolol, lactulose, alprazolam and amlodipine at home. Social history was significant for heavy alcohol use for over 30 years, which she quit following an episode of variceal bleeding. She had no episodes of recurrent gastrointestinal bleeding since her last EGD and banding. On physical examination, she was an ill-appearing female, had dry oral mucosa, tachycardic, had epigastric and RUQ tenderness with negative Murphy's sign, and no rebound or guarding. During the interview, she vomited small amounts of non-bloody white material several times.
On presentation, her laboratory tests were as follows: WBC 13.1, Hb/Hct 14/39.7, platelets 260; Na 152, K 3.6, Cl 112, CO2 22, BUN 30, Cr 0.87, glc 146; lipase 93, Alk Phos 113, AST/ALT 48/75, lactic acid 2.0 and drug screen was positive for propofol.
The patient was admitted for dehydration due to nausea and vomiting. She was started on IV fluids, anti-emetics, pain control and kept NPO (nothing by mouth). Her dyselectrolytemia improved following hydration and her diet was advanced on the following day. She could not tolerate oral intake and reported worsening dysphagia, nausea and vomiting. Over the course of next 2 days, the patient continued to have worsening dysphagia with no relief from anti-emetics. A barium swallow was administered which showed a complete obstruction of the distal esophagus (). The differential for obstruction was thought to be either from local edema from the banding procedure, impacted food or a hematoma from the procedure. An EGD was performed; the scope was advanced to 34 cm to the level of obstruction and it was noted to have a band with entrapped varix in the center of the lumen surrounded by fibrotic material closing off the rest of the lumen (). Several attempts were made with biopsy forceps to reopen the lumen that resulted in a small amount of bleeding and the scope was removed at this point. Conservative management of the patient continued, i.e., NPO with intravenous hydration and pain control. Her symptoms improved over the course of the next 3–4 days and she started tolerating diet advancement and was subsequently discharged.
She presented the next day with a recurrence of similar symptoms, i.e., dysphagia, abdominal pain and vomiting. A repeat barium swallow showed patency of the esophagus with a parallel channel that retained contrast much later than the initial swallow, suggestive of an esophageal tear with an intramural dissection of 6 cm to the level of gastro-esophageal junction ().
The patient was kept NPO with peripheral parenteral nutrition and close monitoring for possible esopheageal perforation. Over the course of the next several days, the diet was carefully advanced with inputs from gastroenterologist and surgical consultants. After 5 days, the patient reported much improvement in her symptoms and was able to tolerate a full diet for the first time.
A repeat barium swallow was obtained prior to discharge that showed no obstruction or dissection. A small stricture was noted at the proximal margin at the origin of the prior dissection (). She was discharged with subsequent follow-up appointment at the GI clinic.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [30.0, 'mg/dL'], 'Glucose': [146.0, 'mg/dL'], 'Sodium': [152.0, 'mEq/L']}",322.8254,306.68413,338.96667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 152.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 152.0 mEq. To convert from 152.0 mEq to mmol, convert from mEq to mmol. The compound 152.0 has a valence of 1, and so divide the valence by the value of mEq to get, 152.0 mEq/(1 mEq/mmol) = 152.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 152.0 mEq sodium/L converts to 152.0 mmol sodium/L. 
The concentration of bun is 30.0 mg/dL. 
The concentration of glucose is 146.0 mg/dL. 
Plugging these values into the equation, we get 2 * 152.0 + (30.0 / 2.8) + (30.0 / 18) = 322.8254 mmol/L.The patient's calculated serum osmolality concentration is 322.8254 mmol/L. This is equalivalent to 322.8254 mOsm/kg."
5697,30,Serum Osmolality,lab test,decimal,pmc-7538038-1,Extracted,"A 3 year old boy, was admitted due to dyspnea in February, 2020. He presented with weakness, malaise, anorexia, severe dry cough, tachypnea and respiratory distress from 4 days prior to his admission.
In his past medical history the patient was premature and had liver cirrhosis due to biliary atresia. He underwent a living donor partial organ LT at 18 months old. Since then he received immunosuppressive medication which included prednisolone 5 mg daily and tacrolimus 2 mg daily.
At his last admission the patient’s mother mentioned a history of upper respiratory tract infection from 1 week ago that did not improve with regular medical therapies. On arrival, he had respiratory distress and decreased O2 saturation and tachypnea. He was admitted with impression of acute respiratory distress syndrome (ARDS) and was transferred to the pediatric intensive care unit immediately.
On examination, he was irritable, ill and toxic with a respiratory rate of 38–40/min, heart rate of 110/min, O2 saturation of 90–91% with a normal blood pressure and was afebrile. He was alert and orient with a Glasgow coma scale (GCS) of 15. His throat was congested without tonsillar exudation. In lung auscultation, harsh breath sounds were heard. Other physical examinations were normal.
His blood work results on admission were as follows: white blood cell (WBC) count of 12.8*103/μl (with a neutrophil count of 10,880 and a lymphocyte count of 1024); red blood cell count, 4.6*106/μl; platelet cell count, 187*103/μl; hemoglobin, 13.8 g/dl; C-reactive protein (CRP), 102 mg/dl; erythrocyte sedimentation rate (ESR), 56 mm/h; sodium, 141 meq/L; potassium, 4.5 meq/L; magnesium, 1.9 mg/dl; blood urea creatinine (BUN), 22.3 mg/dl; creatinine, 0.6 mg/dl; glucose, 88 mg/dl; lactate dehydrogenase, 1277 U/L. His liver function profile was as follows: alanine transaminase (ALT), 28 U/L; aspartate transaminase (AST), 50 U/L; alkaline phosphatase (Alk-ph), 162 U/L; albumin, 2.7 g/dl; prothrombin time (PT), 16 s; partial thromboplastin time (PTT), 28 s; international normalized ratio (INR), 1.7. Patient’s blood tacrolimus level at final visitation was 10 ng/mL.
Vancomycin (50 mg daily), meropenem (90 mg daily), azithromycin (15 mg daily), voriconazole (50 mg daily) and co-trimoxazole (60 mg daily) were started from the first day of admission. About 48 h after hospitalization, the patient became unresponsive to continuous positive airway pressure (CPAP) and he was intubated. After which prednisolone and tacrolimus were discontinued.
During the third day of admission, his liver enzymes started to rise (ALT, 337 U/L; AST, 377 U/L). He developed acute kidney injury and BUN and creatinine increased up to 98 mg/dl and 2.5 mg/dl, respectively. Blood cultures were negative for growth of any microorganisms.
Chest x-ray on admission showed bilateral infiltration and on day 4 of admission it became a white lung. With suspicion of COVID-19, hydroxychloroquine (15 mg daily), lopinavir/ritonavir (100 mg daily) and oseltamivir (30 mg daily) were added to the antibiotic regimen. Due to the outbreak of COVID-19, a nasopharyngeal swab was taken and sent for real time polymerase chain reaction (RT-PCR) which was positive.
During the hospital course, the patient developed multi organ failure which included renal failure, liver failure and heart failure. On day 6 of admission, the patient developed excessive bleeding from the nose and mouth. Following which, cardiorespiratory arrest occurred and after 45 min of CPR the patient died 6 days after hospital admission. His laboratory tests on day 5 were as follows: WBC count, 10.8 × 103/μl (with a neutrophil count of 9190 and a lymphocyte count of 702); RBC count, 4.6 × 106/μl; platelet cell count, 165 × 103/μl; hemoglobin, 10.8 g/dl; sodium, 146 meq/L; potassium, 5.1 meq/L; magnesium, 2.8 mg/dl; BUN, 92 mg/dl; creatinine, 2.3 mg/dl; glucose, 114 mg/dl; ALT, 4000 U/L; AST, 3000 U/L; Alk-Ph, 160 U/L; albumin, 3.3; total bilirubin, 0.2 mg/dl; direct bilirubin, 0.1 mg/dl; CRP, 109 mg/dl; ESR, 61 mm/h; PT, 16 s; PTT seconds, 28; INR, 1.7.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [22.3, 'mg/dL'], 'Glucose': [88.0, 'mg/dL'], 'Sodium': [141.0, 'mEq/L']}",294.85317,280.11051,309.59583,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. 
The concentration of bun is 22.3 mg/dL. 
The concentration of glucose is 88.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (22.3 / 2.8) + (22.3 / 18) = 294.85317 mmol/L.The patient's calculated serum osmolality concentration is 294.85317 mmol/L. This is equalivalent to 294.85317 mOsm/kg."
5698,30,Serum Osmolality,lab test,decimal,pmc-7781561-1,Extracted,"A 44-year-old homeless male patient with unclear past medical history at admission was brought in by ambulance for sudden onset of intractable non-bilious, non-bloody vomiting associated with altered mental status. A fingerstick glucose screening upon admission revealed a blood glucose of >600 mg/dL. His blood pressure was 163/83 mmHg, heart rate of 92 beats per minute, respiratory rate of 18 breaths per minute, and oxygen saturation of 99% on room air. Physical examination was remarkable for a thin physique, altered sensorium, but responsive to verbal and tactile stimuli and incoherent speech. The rest of the physical examination was benign except for pinpoint pupils.
Initial laboratory data revealed a blood sugar of 875 mg/dL, pH of 7.27, lactate of 3.8 mmol/L, bicarbonate of 13 mEq/L, partial pressure of CO2 of 43 mmHg, sodium of 147 mEq/L (corrected sodium of 159 mEq/L), potassium of 5.1 mEq/L, chloride of 93 mEq/L, anion gap of 41 and large blood and urine ketones were detected. Additionally, the patient had an elevated BUN/creatinine of 56/2.0 mg/dL suggestive of acute kidney injury from likely pre-renal cause and urine toxicology positive for opiates, cocaine, and methadone. Due to the acuity of his altered sensorium, a head CT was ordered and revealed an old left middle cerebral artery infarction. The initial acid-base analysis revealed a high anion gap metabolic acidosis, mild respiratory acidosis from possible lack of optimal respiratory compensation due to suppression of the respiratory drive caused by opioid intoxication, and a delta-delta gap more than two suggestive of metabolic alkalosis from the recurrent vomiting (Table ).
The patient initially received 2 liters of 0.9% saline solution. Electrolytes repeated after three hours, revealed an increase of corrected sodium from 159 mEq/L to 162 mEq/L. The fluid choice was changed to Ringer’s Lactate (LR) infusion at 200 mL/hour, and 10 units bolus of regular insulin was given and continued with insulin intravenous infusion at 5.5 units/hours adjusted at his weight (55 kg). Subsequent evaluation of electrolytes revealed a steady-state of the corrected serum sodium at 156-158 mEq/L between hour 6 to hour 20 since the first serum sodium obtained at admission.
Once the blood glucose was close to 200 mg/dL, we decided to change the fluids from LR to dextrose 5% (D5W) to initiate the correction of sodium at a rate of approximately 0.5 mEq/L/hour. After 24 hours, the corrected sodium was 151 mEq/L compared to 159 mEq/L at admission with a noticeable change of his mental status that slowly improved when the serum sodium decreased and not when the blood sugar decreased, revealing that the altered mental status was likely from the hypernatremia and not the DKA. The patient was bridged 24 hours after the initial encounter with long-acting insulin and short-acting insulin at 0.2 Units/Kg was started once the patient was able to tolerate oral intake, his mental status improved, and the anion gap resolved.
Once the patient was fully alert, he expressed that suffered from Type 1 Diabetes and had an opioid and cocaine use disorder. The patient was later downgraded to general ward and discharged after counseling regarding risks of opioid and cocaine use, especially in the context of Type 1 diabetes.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [56.0, 'mg/dL'], 'Glucose': [875.0, 'mg/dL'], 'Sodium': [147.0, 'mEq/L']}",362.61111,344.48055,380.74167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 147.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 147.0 mEq. To convert from 147.0 mEq to mmol, convert from mEq to mmol. The compound 147.0 has a valence of 1, and so divide the valence by the value of mEq to get, 147.0 mEq/(1 mEq/mmol) = 147.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 147.0 mEq sodium/L converts to 147.0 mmol sodium/L. 
The concentration of bun is 56.0 mg/dL. 
The concentration of glucose is 875.0 mg/dL. 
Plugging these values into the equation, we get 2 * 147.0 + (56.0 / 2.8) + (56.0 / 18) = 362.61111 mmol/L.The patient's calculated serum osmolality concentration is 362.61111 mmol/L. This is equalivalent to 362.61111 mOsm/kg."
5699,30,Serum Osmolality,lab test,decimal,pmc-6541993-1,Extracted,"A 28-year-old male patient was admitted to endocrinology outpatient clinic with complaints of impaired balance, hearing loss, and numbness in the hands for a long time. There were type 1 diabetes mellitus, hypopituitarism, and short-term myoclonic jerks after head trauma in his medical history. The drugs he used were insulin aspart, insulin glargine, and carbamazepine. In the family history there was a consanguineous marriage between the parents. His family did not have any history of HDR syndrome. Vital signs upon admission found a blood pressure of 100/70 mmHg, heart rate of 84 beats/min, and body temperature of 36.6°C. He was not mentally retarded. In the neurological examination, the patient was awake, oriented, and cooperative with exam; cranial nerves, motor strength, sensory testing, and proprioception were all intact; only ataxic gait was present. Hair in the face and axillary and inguinal regions was decreased, bilateral testes were small, and gynecomastia was present. All other examinations were normal.
In laboratory examination, the following are found: leukocyte: 8.6 103/ml (4-10), hemoglobin: 10.8 gr/dl (12.1-17.2), MCV: 99.7 fL (82.2-99), platelet: 119 103/ml (150-400), glucose: 386 mg/dL (70-100), urea: 80 mg/dL (16.6-48.5), creatinine: 1.9 mg/dL (0.70-1.2), sodium: 161 mmol/L (136-145), potassium: 4.48 mmol/L (3.5-5.1), calcium: 5.68 mg/dL (8.4-10.2), phosphorus: 5.7 mg/dL (2.5-4.5), albumin: 4.02 g/dL (3.5-5.2), HbA1c: 7.6% (4-6), TSH: 1.42 mU/L (0.27-4.2), free T4: 0.546 ng/dL (0.93-1.7), free T3: 1.53 ng/L (2-4.4), iPTH: 19.90 ng/dL (12-88), FSH: 1.3 U/L (1.7 -12), LH: 7.67 IU/L (1.24-8.62), total testosterone: 8.88 ng/dL (249-836), cortisol: 10.15 mcg/dL (6.02-18.4), prolactin: 8.19 mcg/L (4.4- 15.2), B12: 273.2 ng/L (197-771), folic acid: 1.9 mcg/dL (3.89-20), urine analysis Ph: 5.5, density: 1014, microalbumin in spot urine: 0.34 mg/dl (0-2), microprotein in spot urine: 36.3 mg/dl (0-15), creatinine in spot urine: 227.61 (39-259) mg/dl, serum osmolarity: 394 mOsm/KgH2O (285-295), and urine osmolarity: 590 mOsm/KgH2O (50-1200). On abdominal ultrasonography, the size of left kidney was preserved, long axis of right kidney was 8.5 cm, and there was a minimal reduction in cortex thickness and a grade 1 increase in right kidney parenchyma echogenicity. As a result of laboratory and imaging findings, in addition to the diagnosis of type 1 diabetes mellitus and hypopituitarism, chronic kidney disease, primary hypoparathyroidism, and megaloblastic anemia due to folic acid deficiency were detected.
The audiogram showed a moderate mix type sensorineural hearing loss in the left ear and mild sensorineural hearing loss at increased frequencies in the right ear []. There were no pathological findings on eye examination. Bilateral symmetrical calcifications were detected in the basal ganglia, vermis, and cerebellum in brain CT []. There were no pathological findings in the pituitary MRI.
HDR syndrome was considered because of the diagnosis of primary hypoparathyroidism, hearing loss, and nondiabetic chronic kidney disease in addition to type 1 diabetes mellitus, hypopituitarism, and epilepsy. The patient's electrolyte and hormone replacement therapies were held. The symptoms and signs improved and the patient was taken to regular follow-up program.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [80.0, 'mg/dL'], 'Glucose': [386.0, 'mg/dL'], 'Sodium': [161.0, 'mmol/L']}",372.01587,353.41508,390.61666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 161.0 mmol/L. 
The concentration of bun is 80.0 mg/dL. 
The concentration of glucose is 386.0 mg/dL. 
Plugging these values into the equation, we get 2 * 161.0 + (80.0 / 2.8) + (80.0 / 18) = 372.01587 mmol/L.The patient's calculated serum osmolality concentration is 372.01587 mmol/L. This is equalivalent to 372.01587 mOsm/kg."
5700,30,Serum Osmolality,lab test,decimal,pmc-8136440-1,Extracted,"A 30-year-old female who was 31 weeks pregnant was transferred to our emergency department complaining of nausea and headache. The patient and her husband had been living in a camping tent and had dinner in front of a fireplace with three other family members. While asleep, the patient noticed nausea and headache symptoms and visited the local clinic. The patient was a nonsmoker with no significant medical history.
Upon arrival at the local clinic's emergency department, the patient was well oriented with a Glasgow Coma Scale score of 15 (E4V5M6). The patient had no local neurological deficits. Her vital signs included blood pressure of 110/80 mm Hg, respiration rate of 15 breaths/min, heart rate of 70 beats/min, body temperature of 36.9°C, and oxygen saturation 98%. Arterial blood gas test results on ambient air on arrival were as follows: pH 7.440, PaCO2 31.6 mm Hg; PaO2, 97.0 mm Hg; HCO3
− 22.9 mEq/L, lactate 1.6 mmol/L, and COHb 28.6%. Her laboratory data were unremarkable, as follows: white blood cells, 7100/µL; hemoglobin, 11.5 g/dL; serum creatine kinase, 60 IU/L; sodium 133 mmol/L; potassium, 3.4 mmol/L; blood glucose 84 mg/dL; blood urea nitrogen 9.6 mg/dL; creatinine 0.41 mg/dL; total bilirubin 0.3 mg/dL; aspartate aminotransferase 13 IU/L; alanine aminotransferase 10 IU/L; and lactate dehydrogenase 156 IU/L. Urine drug screening tests (Triage®, Biosite) were negative.
As the patient was diagnosed with CO intoxication based on her interview, physical examination, and high blood COHb concentration, high-flow oxygen (15 L/min) was given during transportation by ambulance, followed by a decrease in COHb levels of up to 3.9%. Fetal wellbeing was confirmed with normal heart rate, normal umbilical cord blood flow, and an estimated fetal weight of 2019 g.
After arrival to our hospital, HBO2 therapy was initiated 5 hours after exposure to CO. The patient underwent additional HBO2 therapy. In accordance with our protocol, which was decided by referring to the report of Weaver et al and consulting with our team, the patient's HBO2 therapy (100% oxygen at two atmospheres for 60 minutes) was administered three times for 2 days. After the treatment, the COHb level improved to 0.7%, and no abnormalities were observed in the patient and the fetal, so she was discharged.
At 41 weeks, she delivered a healthy infant weighing 2862 g with 1- and 5-minute Apgar scores of 7 and 9, respectively. Currently, after 3-month follow-up, both the infant and mother are doing well.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [9.6, 'mg/dL'], 'Glucose': [84.0, 'mg/dL'], 'Sodium': [133.0, 'mmol/L']}",274.09524,260.39048,287.8,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 133.0 mmol/L. 
The concentration of bun is 9.6 mg/dL. 
The concentration of glucose is 84.0 mg/dL. 
Plugging these values into the equation, we get 2 * 133.0 + (9.6 / 2.8) + (9.6 / 18) = 274.09524 mmol/L.The patient's calculated serum osmolality concentration is 274.09524 mmol/L. This is equalivalent to 274.09524 mOsm/kg."
5701,30,Serum Osmolality,lab test,decimal,usmle-4395,Extracted,"A 72-year-old man presents to the emergency department for a change in his behavior. The patient's wife called 911 and he was brought in by emergency medical services. She noticed that he seemed somnolent and not very responsive. The patient has a past medical history of type II diabetes, obesity, osteoarthritis, and migraine headaches. His current medications include naproxen, insulin, atorvastatin, metformin, ibuprofen, omeprazole, and fish oil. His temperature is 99.5°F (37.5°C), blood pressure is 170/115 mmHg, pulse is 80/min, respirations are 19/min, and oxygen saturation is 98% on room air. On physical exam, the patient is somnolent and has a Glasgow Coma Scale of 11. Cardiac and pulmonary exams are notable for bibasilar crackles and a systolic murmur that radiates to the carotids. Neurological exam is deferred due to the patient's condition. Laboratory values are shown below.

Hemoglobin: 12 g/dL
Hematocrit: 36%
Leukocyte count: 9,500 cells/mm^3 with normal differential
Platelet count: 199,000/mm^3

Serum:
Na+: 144 mEq/L
Cl-: 98 mEq/L
K+: 4.0 mEq/L
HCO3-: 16 mEq/L
BUN: 44 mg/dL
Glucose: 202 mg/dL
Creatinine: 2.7 mg/dL
Ca2+: 9.2 mg/dL
AST: 12 U/L
ALT: 22 U/L

The patient is started on IV fluids.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [44.0, 'mg/dL'], 'Glucose': [202.0, 'mg/dL'], 'Sodium': [144.0, 'mEq/L']}",314.93651,299.18968,330.68334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 144.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 144.0 mEq. To convert from 144.0 mEq to mmol, convert from mEq to mmol. The compound 144.0 has a valence of 1, and so divide the valence by the value of mEq to get, 144.0 mEq/(1 mEq/mmol) = 144.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 144.0 mEq sodium/L converts to 144.0 mmol sodium/L. 
The concentration of bun is 44.0 mg/dL. 
The concentration of glucose is 202.0 mg/dL. 
Plugging these values into the equation, we get 2 * 144.0 + (44.0 / 2.8) + (44.0 / 18) = 314.93651 mmol/L.The patient's calculated serum osmolality concentration is 314.93651 mmol/L. This is equalivalent to 314.93651 mOsm/kg."
5702,30,Serum Osmolality,lab test,decimal,pmc-8571488-1,Extracted,"A 32-year-old man presented to the emergency department of the hospital with the complaint of severe acute abdominal pain. The patient felt completely healthy until the afternoon of the day before the presentation when he was eating two plates of uncooked vegetables such as parsley, basil, and coriander; that were ingested without enough mastication, and after about ten minutes, he developed sudden onset, severe abdominal pain located at the epigastric and left upper quadrant (LUQ) region. Then, about ten minutes later he noticed an abdominal distention feeling a mass at the LUQ area and acute dyspnea ensued. His abdominal pain was sharp in quality and he rated the intensity of the pain at 10 of 10 (on a scale from 1 to 10, with 0 representing “no pain” and 10 “very much pain”), but no radiation. It was partially alleviated by the knee-chest position and was exacerbated by the supine position. He also reported having nausea and retching but no emesis. The patient's medical history was mild dyspepsia from 20 years ago which was under treatment by Ranitidine consumed as needed and surgical history of appendectomy 4 years ago. There was no significant and relevant family, allergic, social, or habitual history. Upon physical examination; the patient was terrifically ill and was crying and urging for help desperately while he had a knee-chest position on the ground. In vital signs, he had a blood pressure of 110/85 mmHg, pulse rate of 96 beats per minute, a temperature of 36.5 centigrade, and respiratory rate of 28 breaths per minute. On abdominal examination, upon inspection, there was a local distention at the LUQ and epigastric region. The patient refused deep palpation and had a voluntary guarding abdomen but on light palpation, a severely tender mass was found at the LUQ. Other systemic examinations were unremarkable. In laboratory data, the white-cell count was 8400 per cubic millimeter, with 77.2 % neutrophils, 16.4 % lymphocytes. The hemoglobin level was 15 g per deciliter, and the platelet count was 169,000 per cubic millimeter. The serum level of sodium was 139 mmol per liter, potassium level 4.7 mmol per liter, Blood urea nitrogen level 23 mg per deciliter, creatinine level 1 mg per deciliter, and blood glucose 111 milligrams per deciliter. Venous blood gas analysis showed a pH of 7.33, partial pressure of carbon dioxide of 43.9 mm Hg, and a bicarbonate level of 23.1 mmol per liter. The liver function test, amylase, lipase, erythrocyte sedimentation rate, C-reactive protein, prothrombin time, partial thromboplastin time, and the international normalized ratio were within the normal range. Abdominal X-ray (supine and upright) showed a massively dilated stomach in an expected intraabdominal location with collapsed small bowel loops ( and ). Abnormal position of gastric cardia and double bubble gastric air-fluid levels were also found (). Upright chest X-ray demonstrated no evidence of pneumoperitoneum but the distended stomach was obvious (). These findings were in favor of gastric outlet obstruction (G.O.O). In spite, there was no classic appearance of complete gastric volvulus, due to clinical history of acute onset of severe epigastric pain, these findings were suggestive of G.O.O due to acute gastric volvulus. According to the aforementioned findings, a nasogastric tube was tried to assist gastric decompression but failed to pass through which was further in favor of gastric volvulus. Ceftriaxone and metronidazole were administered; thereafter, the patient underwent laparotomy (). During the operation, the diagnosis of acute mesenteroaxial volvulus was confirmed and its reduction was done. Subsequently, partial gastrectomy of the gangrenous part and then gastropexy was performed. The postoperative course was uncomplicated and the patient was discharged in generally good condition. At outpatient follow-up after 2 weeks of discharge, he was doing well.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [23.0, 'mg/dL'], 'Glucose': [111.0, 'mg/dL'], 'Sodium': [139.0, 'mmol/L']}",292.38095,277.7619,307,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mmol/L. 
The concentration of bun is 23.0 mg/dL. 
The concentration of glucose is 111.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (23.0 / 2.8) + (23.0 / 18) = 292.38095 mmol/L.The patient's calculated serum osmolality concentration is 292.38095 mmol/L. This is equalivalent to 292.38095 mOsm/kg."
5703,30,Serum Osmolality,lab test,decimal,pmc-6990560-1,Extracted,"A 34-year-old woman was admitted to the hospital due to abdominal pain, chills, fever, chest tightness, and shortness of breath after eating contaminated food 2 days earlier. After admission, she became nauseated and vomited; but without dysuria, urinary frequency, or urgency. She had a medical history of type I diabetes for 19 months, with poor control of blood glucose due to non-compliance with the insulin treatments. One month prior, she was found to have kidney stones. Physical examination revealed a temperature of 36.0 °C, pulse rate of 87 beats/minute, respiratory rate of 35 breaths/min, and a blood pressure of 105/66 mm of Hg. She had shortness of breath, dry skin, and dry mucous membranes and tongue; although her lungs sounded clear. There was an abdominal wall muscle strain in the epigastric area and right upper quadrant, with obvious tenderness. The right costovertebral angle also had tenderness.
Laboratory tests and imaging studies were as follows. Blood tests after admission showed a white blood cell count of 21.08 × 109/L, neutrophil count of 18.53 × 109/L, neutrophil percentage of 87.9%, platelet count of 107 × 109/L; and concentrations for albumin of 37.42 g/L, glucose of 35.95 mmol/L, urea of 10.54 mmol/L, creatinine of 145.1 μmol/L, bicarbonate of 2.2 mmol/L, potassium of 6.60 mmol/L, sodium of 122.10 mmol/L, β-hydroxybutyric acid of 10.08 mmol/L, lactic acid of 2.43 mmol/L, C-reactive protein of 448.39 mg/L, and procalcitonin > 100.000 ng/mL. Blood gas analysis showed a pH of 6.984, carbon dioxide partial pressure of 10.9 mm of Hg, oxygen partial pressure of 138.2 mm of Hg, measured bicarbonate of 2.5 mmol/L, calculated bicarbonate of 6.4 mmol/L, anion gap of 32.2 mmol/L, base excess of − 27.2 mmol/L, and carbon dioxide of 2.9 mmol/L. Urinalysis measurements were glucose, 4+; ketone body, 4+; leukocyte esterase, weakly positive; and white blood cell number, 41/μL; with negative results for urine culture. Blood culture identified Escherichia coli. Urinary CT scan revealed multiple stones in the right kidney and lower ureter, with right hydronephrosis; we therefore diagnosed EPN (Figs. , , and reflect the CT scans during hospital admission).
After being admitted to the hospital for definite diagnosis, our endocrinology department cooperated with urology, nephrology, infection department and imaging department to formulate a treatment plan, which suggested that the patients should undergo percutaneous drainage but the patient refused. Hospital management and outcomes after admission included intravenous infusion of small doses of insulin to correct ketoacidosis. Liver and renal functions returned to normal after albumin infusion and hydration. Based upon blood culture results, Cefoperazone sulbactam was upgraded to meropenem. Inflammatory indicators and body temperature gradually returned to normal, and abdominal pain was relieved. Repeated blood cultures were negative, and urine culture remained negative. Repeated urinary CT scans revealed multiple stones in the right kidney with worsening right hydronephrosis and pyelonephritis, but with reduced gas accumulation (Fig. ).
One month after discharge, the patient underwent percutaneous nephrolithotomy in the department of urology, and the urinary CT was reexamined after operation (Fig. ).Two months after discharge, the patient underwent the second percutaneous nephrolithotomy in the department of urology, and the urinary CT was reexamined after operation (Fig. ). Currently, three months after discharge, clinical follow-up checks detect normal renal function and stable blood glucose control.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [10.54, 'mmol/L'], 'Glucose': [35.95, 'mmol/L'], 'Sodium': [122.1, 'mmol/L']}",290.72944,276.19297,305.26591,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 122.1 mmol/L. 
The concentration of bun is 10.54 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 10.54 mmol. To convert 10.54 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 10.54 mmol bun * 0.001 mol/mmol = 0.01054 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.01054 mol bun * 28.02 g/mol = 0.29533 g bun. To convert 0.29533 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.29533 g bun * 1000.0 mg/g = 295.33 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 295.33 mg bun/10.0 dL = 29.533 mg bun/dL. The concentration value of 10.54 mmol bun/L converts to 29.533 mg bun/dL. 
The concentration of glucose is 35.95 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 35.95 mmol. To convert 35.95 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 35.95 mmol glucose * 0.001 mol/mmol = 0.03595 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.03595 mol glucose * 180.16 g/mol = 6.47675 g glucose. To convert 6.47675 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 6.47675 g glucose * 1000.0 mg/g = 6476.75 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 6476.75 mg glucose/10.0 dL = 647.675 mg glucose/dL. The concentration value of 35.95 mmol glucose/L converts to 647.675 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 122.1 + (29.533 / 2.8) + (29.533 / 18) = 290.72944 mmol/L.The patient's calculated serum osmolality concentration is 290.72944 mmol/L. This is equalivalent to 290.72944 mOsm/kg."
5704,30,Serum Osmolality,lab test,decimal,usmle-4719,Extracted,"A 16-year-old female presents to her primary care physician due to lack of menstruation. She has never had a period and is anxious that she is not “keeping up” with her friends. She states that her breasts began developing when she was 13, and she had a growth spurt around the same time. Review of systems reveals that she has also been getting headaches every few months over the last year with some photosensitivity and nausea each time. Ibuprofen relieves her symptoms. The patient is a competitive ice skater and has never been sexually active. Her mother has a history of migraine headaches, and her older sister has a history of bipolar disorder. Both underwent menarche at age 15. At this visit, the patient’s temperature is 98.6°F (37.0°C), pulse is 70/min, blood pressure is 118/65 mmHg, and respirations are 13/min. Her body mass index is 23.8 kg/m^2. Cardiopulmonary and abdominal exams are unremarkable. Both breasts are Tanner IV with no expressable discharge. Pelvic and axillary hair growth is also Tanner IV. The patient is unable to tolerate a full pelvic exam, but the part of the vaginal canal that is examined is unremarkable. Laboratory studies are ordered and are below:

Serum:
Na+: 139 mEq/L
K+: 4.1 mEq/L
Cl-: 100 mEq/L
HCO3-: 24 mEq/L
Urea nitrogen: 12 mg/dL
Glucose: 73 mg/dL
Creatinine: 0.9 mg/dL
Ca2+: 9.7 mg/dL
Mg2+: 1.7 mEq/L
AST: 11 U/L
ALT: 11 U/L
Follicle Stimulating Hormone (FSH): 16.2 mIU/mL (4.7-21.5 mIU/ml)
Estrogen: 240 pg/mL (64-357 pg/mL)

Abdominal ultrasound is performed and shows a normal uterus and ovaries.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [12.0, 'mg/dL'], 'Glucose': [73.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",286.34127,272.02421,300.65833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 12.0 mg/dL. 
The concentration of glucose is 73.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (12.0 / 2.8) + (12.0 / 18) = 286.34127 mmol/L.The patient's calculated serum osmolality concentration is 286.34127 mmol/L. This is equalivalent to 286.34127 mOsm/kg."
5705,30,Serum Osmolality,lab test,decimal,pmc-7417490-1,Extracted,"A 71 year old man with a medical history of alcohol abuse, diabetes mellitus, essential hypertension, and depression was admitted to the intensive care unit suffering from dyspnea, productive cough, hematemesis, and black colored stools. Physical examination revealed the patient in poor general condition; hypotensive with blood pressure 87/50 mm Hg, pulse 106 b.p.m, a temperature of 37.8 C and saturating 100% on 3 liters of oxygen. Laboratory tests showed hemoglobin 7.9 gram/deciliter (g/dl), leukocytes 7.9 kilo/microliter (k/uL), platelets 155 k/uL , sodium 129 mg/dL , potassium 3.4 millimole/liter (mmol/L) , BUN 22 mg/dL, creatinine 0.96 mg/dL, glucose 150 mg/dl, anion gap 25 mmol/L, lactic acid 5.3, ALT 44 units/liter (U/L), AST 74 U/L, total bilirubin 2.25 mg/dL, international normal ratio (INR) 1.6 and urine ketones negligible.
Blood pressure responded to intravenous (IV) hydration 30ml/kg. The patient was started on IV Rocephin,and azithromycin for pneumonia based on symptoms and chest XR showing right lower lung infiltrates. The patient has suspected bleeding from esophageal varices, an indication of heavy alcohol abuse. He was started on proton pump inhibitors and an octreotide drip was administered.
Esophagogastroduodenoscopy (EGD) revealed circumferential, diffuse, friable mucosa extending from the proximal esophagus to the distal esophagus with sharp demarcation at the esophagogastric junction (GEJ) ().
There were areas of black appearing esophageal mucosa in the distal esophagus. The gastric exam showed mild areas of erythema in the body but no Wischnewsky lesions, in other words gastric mucosal petechial hemorrhages. The duodenum revealed an area of semi-lunar ulceration in the bulb and several areas of ulceration/semi-circumferential with a black eschar-like appearance at the ulcerative base in the second and third part of the duodenum ().
Proton pump inhibitors continued, while octreotide drip was discontinued. Abdominal and pelvic CT with contrast was unremarkable for any thrombosis. It showed hepatic steatosis. The patient continued to improve on symptomatic management. One week later, a repeat EGD showed improving esophagitis and duodenum ulcers. Black discoloration of esophagus and duodenum was resolved. The patient continued to improve and was discharged.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [22.0, 'mg/dL'], 'Glucose': [150.0, 'mg/dL'], 'Sodium': [129.0, 'mg/dL']}",128.39048,121.97096,134.81,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 129.0 mg/dL. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mg to mmol. The mass of sodium is 129.0 mg. To convert 129.0 mg of sodium to g, multiply by the conversion factor 0.001, giving us 129.0 mg sodium * 0.001 g/mg = 0.129 g sodium. To convert from grams of sodium to moles, divide by the molar mass 22.99 g/mol, which will give 0.129 g/(22.99 g sodium/mol) = 0.00561 mol sodium. To convert 0.00561 mol of sodium to mmol, multiply by the conversion factor 1000.0, giving us 0.00561 mol sodium * 1000.0 mmol/mol = 5.61 mmol sodium. The current volume unit is dL and the target volume unit is L. The conversion factor is 0.1 L for every unit of dL. Our next step will be to divide the mass by the volume conversion factor of 0.1 to get the final concentration in terms of mmol/L. This will result to 5.61 mmol sodium/0.1 L = 56.1 mmol sodium/L. The concentration value of 129.0 mg sodium/dL converts to 56.1 mmol sodium/L. 
The concentration of bun is 22.0 mg/dL. 
The concentration of glucose is 150.0 mg/dL. 
Plugging these values into the equation, we get 2 * 56.1 + (22.0 / 2.8) + (22.0 / 18) = 128.39048 mmol/L.The patient's calculated serum osmolality concentration is 128.39048 mmol/L. This is equalivalent to 128.39048 mOsm/kg."
5706,30,Serum Osmolality,lab test,decimal,pmc-3853607-1,Extracted,"A 35-year-old male patient was admitted in surgery out-patient department with complains of fever for 2 weeks, abdominal pain and vomiting for 4 days, abdominal distension for 2 days, and constipation for 2 days. He did not receive any treatment during 2 weeks. There was no history of chronic abdominal pain or analgesic abuse, but patient was a smoker and alcoholic. There was no any history suggestive of previous typhoid infection. On physical examination, abdomen was tense, tender, and distended with absent bowel sound. Both guarding and rigidity were present all over the abdomen. On digital rectal examination, there was empty rectum. An upright abdominal radiograph showed free gas under both domes of diaphragm. Laboratory examinations gave the following results: Hematocrit 30%, white blood cell count 14500/cm3, platelets 268 000/cm3, sodium 138 mEq/L, potassium 3.2 mEq/L, blood urea 32 mg/dl, S. Creatinine 1.6 mg/dl, blood glucose 110 mg/dl, and total bilirubin of 2.5 mg/dl. Diagnostic test for hepatitis B, hepatitis C and HIV were negative. The patient was Widal positive (Titer of > 1:160). An abdominal ultrasound showed features consistent with intestinal perforation showing both free fluid and free air with fine floating echoes in peritoneal cavity. However, blood culture was negative for Salmonella typhi in the patient. No bile culture was performed pre-operatively. Hence, the diagnosis of acute peritonitis due to intestinal perforation was made pre-operatively.
The patient was resuscitated with intravenous fluid and commenced on antibiotics ceftriaxone and metronidazole pre-operatively. Nasogastric tube insertion for decompression and urethral catheterization was carried out for monitoring urine output. Exploratory laparotomy was performed through midline incision and fecal peritonitis with exudative flakes all over the intestine was found. Thorough peritoneal lavage was carried out with normal saline. There were 24 perforations (21 in terminal ileum and 3 in cecum) present in distal 35-40 cm of terminal ileum reaching up to ileocecal junction and the Cecum on anti-mesenteric border as shown in Figures and . Resection of the perforated intestinal segment with ileo-transverse anastomosis (side-to-side) with proximal loop ileostomy was performed. Abdominal tube drain Fr. 30 was put in pelvis after thorough peritoneal lavage using the normal saline and abdomen was closed in layers. Patient was kept on i.v. fluids and nil orally for 3 days. Broad spectrum antibiotic in the form of 3rd generation cephalosporin with metronidazole and fluoroquinolone were given for 7 days. Nasogastric tube and abdominal drain tube were removed on 3rd post -operative day (POD). Ileostomy started functioning on 4th POD. Patient was discharged on 7th POD with oral fluoroquinolone for 7 days. Histopathological examination revealed evidence of severe acute inflammation, with fibrinopurulent exudates extending along the serosal surface of intestine and acute and chronic inflammation was observed immediately adjacent to the site of perforation. Evidence of villous blunting and elongation of the crypts was observed, which suggests chronic mucosal injury. We were unable to isolate S. typhi from resected bowel specimen; however, stool culture was positive for S. typhi. We were unable to perform Polymerase chain reaction for isolation of S. typhi and other serotypes responsible for TIP due to scarcity of resources at our center. These findings are consistent with TIP. On the basis of these findings, the diagnosis of typhoid enteric perforation was confirmed. Patient came regularly for follow-up, gained weight, and managed ileostomy properly. We closed ileostomy after 12 weeks.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [32.0, 'mg/dL'], 'Glucose': [110.0, 'mg/dL'], 'Sodium': [138.0, 'mEq/L']}",293.53968,278.8627,308.21666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 32.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (32.0 / 2.8) + (32.0 / 18) = 293.53968 mmol/L.The patient's calculated serum osmolality concentration is 293.53968 mmol/L. This is equalivalent to 293.53968 mOsm/kg."
5707,30,Serum Osmolality,lab test,decimal,pmc-2615353-1,Extracted,"A 40-year-old man was admitted to our emergency department with abdominal pain and bloody diarrhea. The patient had watery diarrhea for 3 days, but 3 hours prior to presentation, it became bloody. He had neither a history of symptoms suggestive of an inflammatory bowel disease nor a recent history of antibiotic use. In addition, he had neither a history of recent travel nor a diet change. His medical history was unremarkable for risk factors of bowel ischemia, except for hypertension that was well controlled with angiotensin receptor blockers. He smoked 1 pack of cigarette per day for 10 years, and there was no family history of cerebrovascular or cardivascular disease. Notably, he had been taking an herbal food supplement, Ephedra sinica or ma huang (total 1,000 mg; 3 times/day) throughout the previous month for weight loss.
His blood pressure was 110/70 mmHg, pulse rate 73/min, respiratory rate 20/min, and body temperature 36.5℃. His body mass index was 25.7 kg/m2. The patient appeared acutely ill but otherwise was a healthy, well-nourished man. His abdomen was soft and obese with mild tenderness in the periumbilical area, and his bowel sounds were normoactive. Laboratory data on admission showed hemoglobin 15.6 g/dL, hematocrit 44.4%, white blood cell count 7,500/mm3, and platelet 214,000/mm3. His serum sodium level was 138 mmol/L, potassium 4.1 mmol/L, chloride 103 mmol/L, fasting glucose 98 mg/dL, serum albumin 3.9 g/dL, total cholesterol 145 mg/dL, triglyceride 75 mg/dL, LDL cholesterol 81 mg/dL, blood urea nitrogen 10 mg/dL, and creatinine 1.2 mg/dL. The patient's coagulation profiles were normal. The stool white blood cell test was negative, while the stool occult blood test was positive. Stool specimens were negative for enteric pathogens.
Abdominal and pelvic CT scans showed a patent superior mesenteric artery and circumferential wall thickening of the ascending, transverse, and descending colon sparing the rectosigmoid junction (). Colonoscopy performed on admission showed findings compatible with segmental colitis extending from the ascending to the descending colon. The involved areas were edematous and hyperemic, with areas of frank hemorrhage (). Three days after intravenous hydration and nutritional support, the bloody diarrhea resolved. At an 8-day follow-up, colonoscopy showed markedly improved mucosa without any complications (). The colonoscopic biopsy specimen of the affected area showed focal mucosal erosion and chronic inflammatory cell infiltration consistent with ischemic colitis ().
The patient completely recovered without complications and with only conservative management. On discharge, he was advised to discontinue the use of herbal medications and to avoid any ephedrine- or pseudoephedrine-containing cold remedies.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [10.0, 'mg/dL'], 'Glucose': [98.0, 'mg/dL'], 'Sodium': [138.0, 'mmol/L']}",285.01587,270.76508,299.26666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mmol/L. 
The concentration of bun is 10.0 mg/dL. 
The concentration of glucose is 98.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (10.0 / 2.8) + (10.0 / 18) = 285.01587 mmol/L.The patient's calculated serum osmolality concentration is 285.01587 mmol/L. This is equalivalent to 285.01587 mOsm/kg."
5708,30,Serum Osmolality,lab test,decimal,pmc-8291511-1,Extracted,"We present the case of a 67-year-old female with a history significant for type II diabetes mellitus and obesity (body mass index of 43) who had been trying to lose weight with a combination of intermittent fasting and consumption of exogenous ketone supplements purchased online. Three months prior to hospitalization, the patient began a ketogenic diet that entailed intermittent fasting, whereby she would fast for upwards of 40 hours at a time with only drinking water and ingesting keto supplements; she reported drinking the ketone ester supplement three times a day on an empty stomach. The patient stated she had lost over 25 pounds since the beginning of her diet. After one of her fasting cycles, she ate half an avocado, some shrimp, and drank a ketone ester drink. Shortly after, the patient began feeling dizzy and started to vomit and ultimately presented to the hospital with severe fatigue, lower abdominal pain, nausea, and vomiting. She last took metformin (she was on a 750 mg twice daily home dose) on the morning of her presentation to the hospital and admitted to taking exogenous ketone supplements containing 30 g of beta-hydroxybutyrate (BHB) three times a day.
On evaluation, she was hemodynamically stable with baseline normal mental function but appeared dehydrated. Assessment of vitals showed the patient was tachycardic with a pulse rate of 120 beats per minute and borderline tachypnea with a respiratory rate of 20 breaths per minute. Her electrocardiogram did not show any arrhythmias or concerning changes in ST segments. On examination, she had dry mucous membranes and diffuse lower abdominal pain to palpation without guarding or rebound tenderness. Laboratory evaluation was notable for a white blood cell count of 30,100/mm3 (normal range: 4,500-11,000/mm3), creatinine 1.47 mg/dL (0.60-1.30 mg/dL), blood urea nitrogen 32 mg/dL (7-18 mg/dL), glucose 176 mg/dL (74-106 mg/dL), serum bicarbonate 8 mEq/L (21-32 mEq/L), anion gap 27.7 mEq/L (3-15 mEq/L), and a serum lactic acid of 2.9 mmol/L (0.4-2.0 mmol/L). The patient also had a moderately positive serum qualitative acetone level, plasma osmolality 312 mOsm/kg (275-301 mOsm/Kg), sodium 136 mEq/L (136-145 moml/L), and HbA1C of 8.4% (<5.7%). A urinalysis showed elevated urine ketones and was negative for glucose. Her pH from a venous blood gas analysis on admission was 6.81.
Differential diagnoses of diabetic ketoacidosis, alcoholic ketoacidosis, lactic acidosis, and salicylate toxicity were investigated. Serum and urine drug screens were negative for ethanol, acetaminophen, and salicylates. The patient was started on intravenous fluids with dextrose 5%-0.9% normal saline, sliding scale insulin, and 50 meq sodium bicarbonate 8.4%. After two days in the intensive care unit, the patient clinically felt much better. Her anion gap closed and her pH on a venous blood gas analysis was 7.38. The patient was transferred to the floors and was discharged the following day.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [32.0, 'mg/dL'], 'Glucose': [176.0, 'mg/dL'], 'Sodium': [136.0, 'mEq/L']}",293.20635,278.54603,307.86667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.0 mEq. To convert from 136.0 mEq to mmol, convert from mEq to mmol. The compound 136.0 has a valence of 1, and so divide the valence by the value of mEq to get, 136.0 mEq/(1 mEq/mmol) = 136.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mEq sodium/L converts to 136.0 mmol sodium/L. 
The concentration of bun is 32.0 mg/dL. 
The concentration of glucose is 176.0 mg/dL. 
Plugging these values into the equation, we get 2 * 136.0 + (32.0 / 2.8) + (32.0 / 18) = 293.20635 mmol/L.The patient's calculated serum osmolality concentration is 293.20635 mmol/L. This is equalivalent to 293.20635 mOsm/kg."
5709,30,Serum Osmolality,lab test,decimal,pmc-3830277-1,Extracted,"A 68-year-old Indian male patient presented with the complaints of generalized malaise, poor appetite, weight loss, headache and polyuria for last 2 months. He had a chronic ill-looking appearance, a dehydrated tongue and dry skin. Urine output was 5000-5500 mL/day with a history of nocturia and craving for cold fluids. No history of head injury, tubercular meningitis, central nervous system infections or chronic drug intake.
His physical findings on admission were height 156 cm; body weight, 44.5 kg and body mass index, 18.3. Blood pressure was 100/64 mmHg without postural change and pulse rate, 68/min with a regular rhythm. No edema was noted in his legs or feet. He had scant axillary and pubichair. Neurologic examination including visual field was found to be normal.
Laboratory findings were as follows: White blood cell count 6400/mm3 (neutrophils 51%, lymphocyte 42%, monocyte 5%, eosinophils 2%, basophils 0%); hemoglobin, 13.4 g/dL; hematocrit, 35.5%; red blood cell count, 3.4 × 106/mm3; and platelets, 3.3 × 105/mm3 Serum sodium was 137 mmol/L; potassium, 3.9 mmol/L; and chloride, 103 mmol/L. Blood urea nitrogen was 12 mg/dL; serum creatinine, 0.8 mg/dL; and uric acid, 6.1 mg/dL. Fasting plasma glucose was74 mg/dL; hemoglobin A1c, 4.9% and serum calcium of 9.4 mg/dL.
Anterior pituitary function tests revealed panhypopituitarism (serum cortisol 1.8 μg/dL, Adrenocorticotrophic hormone 15.6 pg/mL, total T3 56 ng/mL, total T4 4.2 μg/dL, thyroid stimulating hormone 1.86 mIU/mL, luteinizing hormone 0.8 mIU/mL, follicle stimulating hormone 1.67 mIU/mL, serum testosterone of 122 ng/dL and serum prolactin of 12 ng/mL. Water deprivation test revealed central diabetes insipidus [].
Magnetic resonance imaging (MRI) revealed [Figures and ] a well-defined sellar-suprasellar lesion, which was heterogenous and mildly hyperintense on T1-weighted images and brightly hyperintense on T2-weighted (T2W) images. Internal well-defined hypointense nodule was also seen on T2W images. No obvious post contrast enhancement was seen. Pituitary tissue was compressed and stalk was central. The mass was abutting chiasma, but no obvious mass effect/compression seen. Findings were highly suggestive of RCC.
Transsphenoidal surgery with complete excision of the mass was carried out and histopathological examination revealed cyst wall with columnar lining suggestive of RCC. Patient was started on replacement doses of levothyroxine, hydrocortisone tablets and testosterone injections. His symptoms improved and he was doing well in follow-up. Surprisingly his polyuria improved in postsurgical period without vasopressin replacement.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [12.0, 'mg/dL'], 'Glucose': [74.0, 'mg/dL'], 'Sodium': [137.0, 'mmol/L']}",282.39683,268.27699,296.51667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mmol/L. 
The concentration of bun is 12.0 mg/dL. 
The concentration of glucose is 74.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (12.0 / 2.8) + (12.0 / 18) = 282.39683 mmol/L.The patient's calculated serum osmolality concentration is 282.39683 mmol/L. This is equalivalent to 282.39683 mOsm/kg."
5710,30,Serum Osmolality,lab test,decimal,pmc-2908655-1,Extracted,"An 84-year-old female with history of major depression and anxiety was evaluated by her psychiatrist for worsening anxiety and given a single dose of 3 mg of paliperidone. Eight hours later she became increasingly agitated and, according to her daughter, “looked like she was going to crawl out of her skin.” She then told her daughter “make it go away, make it go away,” and subsequently stopped speaking and responding to any physical or verbal stimuli, although she appeared awake and alert. She had no prior documented episodes of catatonia. Her daughter brought her into the local emergency department (ED).
In the ED, she had a temperature of 37.3°C, pulse 80 beats per minute, blood pressure 161/72 mm Hg, respiratory rate 20 breaths per minute and oxygen saturation of 98% on room air. Her medications were citalopram, trazodone, levothyroxine, and paliperidone. She lived with her daughter, who related no recent trauma. The patient previously took risperidone, but it had been discontinued after several months because of mild akathisia, with both restlessness and tremor.
Physical exam showed an alert, well appearing elderly female in no acute distress. Her pupils were equal round and reactive to light; she would not comply with extraocular muscle testing. She did open her mouth on request and stuck out her tongue midline; there was no erythema, and mucous membranes were moist. Cardiopulmonary exam was unremarkable; abdominal palpation did not cause any change in her facial expression and was soft without masses. While she complied with several requests for the cranial nerve exam she would not move her fingers or toes when asked, but was noted to turn her head in all directions and roll from side to side, moving all extremities equally. Her brachioradialis and achilles reflexes were equal and Babinski reflexes were downgoing. She exhibited stupor and mutism with fixed postures.
Finger-stick glucose was 114 mg/dL. Intravenous diphenhydramine, 25 mg and benztropine, 0.5 mg were given for dystonia without any change. Noncontrast head computed tomography (CT) was performed due to concern for stroke and was unremarkable. Laboratory tests showed white blood cell count of 7.4 K/mm3 with 60% neutrophils, her hematocrit was 37.6%, and platelets were 203 K/mm3. Electrolytes and renal function showed sodium 135 mmol/L, potassium 3.5 mmol/L, chloride 101 mmol/L, bicarbonate 20 mmol/L, calcium 9.8 mg/dL, blood urea nitrogen 12 mg/dL, and creatinine 1.0 mg/dL.
Due to the lack of inpatient psychiatric beds, she was observed in the ED for 12 hours. Psychiatric consultation had no specific recommendations. Sixteen hours after the dose of paliperidone, without other therapy, she began to talk and interact. More detailed neurological exam showed no focal deficits. Her mood and affect were appropriate. She did not recall the events of the previous evening but remembered her daughter talking, although she was unable to respond.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [12.0, 'mg/dL'], 'Glucose': [114.0, 'mg/dL'], 'Sodium': [135.0, 'mmol/L']}",280.61905,266.5881,294.65,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.0 mmol/L. 
The concentration of bun is 12.0 mg/dL. 
The concentration of glucose is 114.0 mg/dL. 
Plugging these values into the equation, we get 2 * 135.0 + (12.0 / 2.8) + (12.0 / 18) = 280.61905 mmol/L.The patient's calculated serum osmolality concentration is 280.61905 mmol/L. This is equalivalent to 280.61905 mOsm/kg."
5711,30,Serum Osmolality,lab test,decimal,pmc-5051109-1,Extracted,"A 53-year-old male presented with 1 day duration of acute severe right lower quadrant abdominal pain, sharp, non-radiating associated with fever, chills and nausea but no vomiting or weight loss. On physical exam, his vital signs were blood pressure 126/68 mm Hg, pulse 90/min, respiratory rate 14/min, and temperature 99.4 °F. Abdominal exam revealed distension tenderness to Mcburney’s point, with guarding and rigidity but bowel sounds were normal. Laboratory data showed hemoglobin 13.4 g/dL, hematocrit 40.1%, white count 8.1 × 103/µL, platelets 172 × 103/µL, sodium 133 mmol/L, potassium 4.6 mmol/L, chloride 99 mmol/L, bicarbonate 20 mmol/L, BUN 24 mg/dL, creatinine 2.1 mg/dL and glucose 181 mg/dL. Computed tomography (CT) scan of abdomen showed the perforated appendicitis with two appendicoliths seen in the right lower quadrant (). Laparoscopic appendectomy with drainage of periappendiceal abscess was performed. Surgical pathology of appendix showed moderately differentiated adenocarcinoma with signet-ring cell (< 50% signet ring component) and carcinoid features involving muscular wall (). Tumor was penetrating and perforating the visceral serosa and diffusely infiltrating > 4/5 wall of the proximal portion of appendix with lymphovascular invasion. Special studies showed that the tumor is immunoreactive to CK20 (), focal to CD56, chromogranin (), synaptophysin; negative to CK7 (), TTF-1, PSA and CDx2. Mucin stain is positive (). The immunostains support the diagnosis. Patient was started on chemotherapy and after 3 months, patient complained of abdominal pain for which CT abdomen was performed which showed findings suspicious for spreading cancer. Patient failed chemotherapy and underwent hemicolectomy and peritonectomy as there were seedings on the peritoneum.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [24.0, 'mg/dL'], 'Glucose': [181.0, 'mg/dL'], 'Sodium': [133.0, 'mmol/L']}",284.62698,270.39563,298.85833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 133.0 mmol/L. 
The concentration of bun is 24.0 mg/dL. 
The concentration of glucose is 181.0 mg/dL. 
Plugging these values into the equation, we get 2 * 133.0 + (24.0 / 2.8) + (24.0 / 18) = 284.62698 mmol/L.The patient's calculated serum osmolality concentration is 284.62698 mmol/L. This is equalivalent to 284.62698 mOsm/kg."
5712,30,Serum Osmolality,lab test,decimal,pmc-4007782-1,Extracted,"A 27-year-old woman with no known illnesses or history of psychiatric disorders was admitted approximately 6 hours after attempting suicide by ingesting 150 mg of amlodipine. She was newly married and had a conjugal conflict.
On admission, the patient was conscious but lethargic with cold extremities. Her blood pressure was 75/49 mmHg and the pulse rate was 105 bpm. She received gastric lavage and still complained of nausea.
The patient was started on intravenous fluids and transferred to the intensive care unit. On physical examination, the patient was slightly lethargic and had the following vital signs: systolic blood pressure, 80 mmHg; pulse, 125 bpm; respiratory rate, 26 breaths/min; and temperature, 36.5°C, pulse oximetry displayed 98% oxygen saturation under oxygen supplement. The head and neck exams were unremarkable. The cardiac examination found normal heart sounds without any murmurs. The lungs were clear to auscultation. The extremities were cold, with neither edema nor cyanosis.
The laboratory investigations showed a white blood cell count of 12,400/mm3 with 75% neutrophils, hemoglobin of 10.3 g/dL, and platelet count of 282,000/mm3. The electrolyte rates were sodium, 134 mEq/L; potassium, 3.8 mEq/L; bicarbonate, 16 mEq/L; blood urea, 18 mg/dL; creatinine, 2.3 mg/dL; and glucose, 85 mg/dL. The initial electrocardiogram showed a sinus tachycardia at 120 bpm with normal QRS, nonspecific ST segment, and T wave abnormalities. The chest radiograph was normal.
Despite the intravenous fluid infusion, 2000 mL crystalloids, the mean arterial blood pressure remained below 55 mmHg. Simultaneously, two grams of calcium gluconate were administered, without the improvement of arterial blood pressure. Dobutamine infusion was also started in an effort to increase the patient's inotropy. However, the patient's status remained unchanged at 15 μg/kg/min. Moreover, an insulin infusion was initiated at 0.5 IU/kg/h. Blood sugar levels were measured every hour and glucose administrated whenever they reached rates lower than 100 mg/dL. Two hours later, the patient's blood pressure increased to 90/45 mmHg. Over the next four hours, there was a sustained increase in blood pressure to 100/50 mmHg. Dobutamine dose was progressively reduced, and then suspended over the next day. The mean blood pressure remained above 90 mmHg. Twenty four hours later, the insulin infusion was stopped. Seven days later the patient was discharged from the hospital after psychiatric consultation.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [18.0, 'mg/dL'], 'Glucose': [85.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",279.15079,265.19325,293.10833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. 
The concentration of bun is 18.0 mg/dL. 
The concentration of glucose is 85.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (18.0 / 2.8) + (18.0 / 18) = 279.15079 mmol/L.The patient's calculated serum osmolality concentration is 279.15079 mmol/L. This is equalivalent to 279.15079 mOsm/kg."
5713,30,Serum Osmolality,lab test,decimal,pmc-7450474-1,Extracted,"A 40-year-old Asian woman, non-smoker, housewife, presented in December, 2018 with progressive shortness of breath, initially only during physical exertion (i.e, walking upstairs) which later started occurring even at rest and a non-productive cough of three years duration which worsened in the ten days preceding presentation. She also complained of chest tightness during this presentation. She did not have a history suggestive of orthopnea or paroxysmal nocturnal dyspnea, swelling of her legs and/or body, fever, blood mixed sputum, chest pain or joints pain. She did not have exposure to patients with pulmonary tuberculosis. She had presented to an ophthalmologist 3 years back due to pain and redness of both eyes and was later diagnosed with bilateral granulomatous uveitis. She was treated with topical steroid for the same duration with intermittent intervals of as long as 2–3 months.
On examination, she was afebrile with a blood pressure of 130/80 mmHg in the right arm and heart rate was 80/minute. She had clubbing of her digits. Examination of peripheral pulses revealed absent pulse over the left radial and brachial arteries and feeble pulse over the right radial and brachial arteries, and bilateral carotid arteries. Carotid bruit was heard on the left side. Her oxygen saturation at room air was only 76% and required 4 liters/minute of oxygen to maintain 92% saturation (Normal >95%). Her jugular venous pressure was not raised and there was no pedal or sacral edema.
Laboratory parameters with normal ranges in parenthesis, are as follows:
Complete blood count: white cell count 4.2 (4–10) × 10^9/L; neutrophils 78%; lymphocytes 20%; red blood cells 4.6 (4.2–5.4) × 10^12/L; haemoglobin 13.3 (12–15) g/dL; platelets 244 (150–400) × 10^9/L.
Biochemistry: random blood sugar 126 (65–110) mg/dL; urea 29 (17–45) mg/dL; creatinine 0.9 (0.8–1.3) mg/dL; sodium 139 (135–145) mmol/L and potassium 4.3 (3.5–5) mmol/L.
Hepatic panel: bilirubin total 0.8 (0.1–1.2) mg/dL and direct 0.5 (0–0.4) mg/dL; alanine transaminase 39 (5–30) units/L; aspartate transaminase 45 (5–30) units/L; alkaline phosphatase 103 (50–100) IU/L; albumin 2.6 (3.5–5) g/dL
Erythrocyte sedimentation rate (ESR) was elevated at 45 mm/hr and c-reactive protein (CRP) was 4 mg/L (Normal < 10 mg/L). Angiotensin converting enzyme (ACE) levels were elevated at 186 u/L (Normal < 52 u/L); rheumatoid factor and anti-nuclear antibodies by indirect immunofluorescence were negative. Sputum examination did not reveal any organisms including acid fast bacilli. Sputum analysed by gene Xpert also did not detect
Mycobacterium tuberculosis. The electrocardiogram was normal. Echocardiography showed moderate tricuspid regurgitation with moderate pulmonary arterial hypertension with a normal systolic function.
Chest X-ray (
) revealed bilateral reticulo-nodular infiltrates involving the middle and lower zones and some parts of the upper zones. No changes were noted compared to a radiograph done three years ago. The pulmonary function test showed a restrictive pattern. High resolution computed tomography (CT) of the chest (
) showed diffuse ground glass changes with interlobular septal thickening with mosaic attenuation and multiple enlarged calcified mediastinal and hilar lymph nodes (separate image of mediastinal section could not be retrieved). Bronchoscopy with trans-bronchial lung biopsy revealed non- caseating granulomatous inflammation with characteristic ‘asteroid bodies’ (
 and
), and was negative for malignancy and tuberculosis. Hence the diagnosis of sarcoidosis (pulmonary and ocular) was made.
The findings of abnormal pulse led us to do a CT angiogram of aorta and its branches.
 shows stenosis of the left subclavian artery with almost complete block at the distal part as well as the proximal left axillary artery. Though images not available for the report, there was stenosis of right axillary, brachial artery and its branches, with sparing of abdominal aorta up to the lower extremities. This was suggestive of large vessel vasculitis in the upper extremities, Takayasu arteritis (Type I).
With the diagnosis of sarcoidosis with coexisting Takayasu arteritis, she was treated with prednisolone 60 mg once daily (1 mg/kg/day) along with supportive treatment including oxygen, chest physiotherapy, bone protection with calcium and vitamin D, and thromboembolism prophylaxis with daily 60 mg of subcutaneous enoxaparin. Ophthalmology examination showed bilateral granulomatous uveitis and was treated with topical prednisolone drops. She dramatically improved over 3–4 days and required only 1 liter/minute of oxygen support. Pneumococcal vaccination was administered. She was later discharged on domiciliary oxygen with a tapering prednisolone dosage.
After four weeks of discharge, while she was still on 30 mg of prednisolone, she developed blurring of vision. Ophthalmologic examination showed increased intraocular pressure with findings suggestive of Secondary glaucoma, probably steroid induced. Topical steroid was stopped and since oral steroid was to be tapered off quickly, azathioprine 50 mg/day was started as a steroid sparing immunosuppressant. Glaucoma was treated with topical timolol (0.25% twice daily) and oral acetazolamide (500 mg followed by 250 mg twice daily), and she responded well over the course of 2 weeks.
The patient is still on regular follow up (after 15 months of diagnosis) and is currently asymptomatic. She does not require oxygen and does not have symptoms of vasculitis (carotidynia, headache, lightheadedness, vertigo, tingling, numbness, limb claudication, cyanosis, arthralgias and skin lesions like erythema nodosum). She is currently taking azathioprine 50 mg/day, prednisolone 10 mg/day with calcium and vitamin D supplements. She is also on regular follow up every 3 months with a pulmonologist.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [139.0, 'mmol/L'], 'Glucose': [126.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [29.0, 'mg/dL']}",295.35714,280.58928,310.125,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mmol/L. 
The concentration of bun is 29.0 mg/dL. 
The concentration of glucose is 126.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (29.0 / 2.8) + (29.0 / 18) = 295.35714 mmol/L.The patient's calculated serum osmolality concentration is 295.35714 mmol/L. This is equalivalent to 295.35714 mOsm/kg."
5714,30,Serum Osmolality,lab test,decimal,pmc-2884456-1,Extracted,"This 22-year-old right-handed male, a known case of schizophrenia who had attempted suicide four times earlier, was brought to this hospital as a case of alleged self-inflected injury. As told by the parents, this young man had inflicted self-injury by a nail driven inside his skull with the help of a wooden plank []. It takes about 1.5 h before reaching hospital. At the time of admission in emergency department, on examination this right-handed patient was fully conscious and oriented, talkative with no history of headache, vomiting, seizures, visual disturbances, and with a Glassgow Coma Scale (GCS) of 15\15. There were no focal signs (with intact higher functions, no limbs weakness, sensory loss, bladder bowel involvement, facial asymmetry, and cranial nerves involvement) and a nail was protruding out of his skull in midline approximately 2 cm out near coronal suture. The vitals were as follows: blood pressure 110\66 mmHg, pulse 88\min of normal character, respiratory rate 18\min, pallor +, JVP normal, hydration was adequate, pupil normal size normal reaction, and plantar B\L flexor. This patient had a history of such suicidal attempts four times in the past; last one was almost 4 months back and he was on and off taking anti-psychotic treatment, details of which was not available. Patient was put on conservative treatment along with antibiotics (injection cefurexime BD, amikacin 500 BD, metrogyl 100 ml TDS), antiepileptic drugs (injection eptoin TDS), and antipsychotic treatment sodium valproate, escitalopram, olanzipine, and alprazolam. An urgent plain X-ray of head and neck AP and lateral view [Figures and ] and non-contract CT scan (NCCT) head [] was performed.
Patient was planned for emergency frontal craniotomy. After relevant investigation (hemogram like Hb 12 g%, TLC 8400, DLC P84L14E0M2, platelet 2.2 lakhs, PT 11.2\11\,APTT 24\22, serum electrolytes (Na 142,K 4.2), urea 14 mg\dl, creatinine 0.9 mg\dl, blood glucose (R) 140 mg%, and arranging blood products, after written informed consent and proper counseling patient was taken inside the operation theatre. Inj ranitidine 25 mg and inj metoclopramide 10 mg had already been given intramuscularly 45 min earlier, and nasal Ryle's tube was put at the time of admission before operation as prophylaxis for full stomach to prevent aspiration. In operation theatre, invasive arterial and central venous line was put after local anesthetic infiltration to measure beat to beat variability in blood pressure and large volume fluid shift intraoperatively with two large bore intravenous cannula after that craniotomy done under balanced general anesthesia with rapid sequence induction. Intraoperatively colloids, blood products, and inotropes were kept ready with monitoring SPO2, ETCO2, ECG, urine output, and temperature. Under full aseptic precaution, frontal craniotomy was done. Bone chips were removed around nail without disturbing nail for proper exposure .Then the nail was removed very slowly in line of its original axis to avoid bleeding. Wound site was decontaminated and drain was put, and then aseptically flap was reposited. Vitals were maintained within normal limit during entire intraoperative period. There occurred a small rent in superior sagittal sinus during removal of nail. The bleeding was controlled by the surgeon with the help of gel foams, surgicell, suction, and bipolar cautery. After surgery, the patient was successfully extubated with stable vitals and shifted to intensive care unit. Rest of the postoperative phase was uneventful. Treatment with antibiotic and anti-psychotic drugs was continued similarly to the preoperative phase.
The wound was on the left side of the scalp with the nail directing toward right frontal lobe, which is an eminent center and involved in motor function, memory, language, social, and sexual function. The patient was discharged after 8 days along with psychiatric and psychological counseling. He was conscious and oriented without any neurological deficit.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [14.0, 'mg/dL'], 'Glucose': [140.0, 'mg/dL'], 'Sodium': [142.0, 'mEq/L']}",296.77778,281.93889,311.61667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. 
The concentration of bun is 14.0 mg/dL. 
The concentration of glucose is 140.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (14.0 / 2.8) + (14.0 / 18) = 296.77778 mmol/L.The patient's calculated serum osmolality concentration is 296.77778 mmol/L. This is equalivalent to 296.77778 mOsm/kg."
5715,30,Serum Osmolality,lab test,decimal,pmc-8572339-1,Extracted,"A previously healthy 35-month-old girl was brought to the emergency room of the Namazi hospital, Shiraz, Iran, due to reduced level of consciousness. She was well up to five days prior to her admission, after that she presented with dysuria and loss of appetite, and then developed polyuria, polydipsia, and weight loss (14 kg → 11 kg). There was no history of DM in her family.
On arrival, her height was measured 92 cm (25th−50th) percentile), she weighed 11 kg (5th–10th) percentile), and her Body Mass Index (BMI) (BMI-for-age) was at the 72nd percentile. Her vital signs were as follows: temperature: 38°C, heart rate (HR): 160, blood pressure (BP): 95/50, and her Glasgow coma scale (GCS) was 11/15. During her physical examination, capillary refilling time was more than 3 s with weak pulses. When checked with a capillary blood glucose meter, her glucose level was too high, so a serum glucose test was performed. Moreover, her first VBG was as follows: pH 7.26, PCO2: 32, PO2: 39, HCO3: 15.8, and BE: −12.6. Due to the decreased level of consciousness, brain CT scan was performed in which brain edema was reported.
As the first line of treatment, she was hydrated with normal saline (10 cc per kg), then the laboratory report revealed; blood sugar: 1124 mg/dl, BUN: 71 mg/dl, creatinine: 1.9 mg/dl, Na: 170 mEq/L (corrected Na: 186), and K: 5.1 mEq/L (effective osmolality was 402). Additionally, urine analysis was SG: 1.010, GLU: 3+, Ketone: trace. VBG after first hydration was as follows: pH: 7.27, PCO2: 34.8, and HCO3: 15.8. Based on the laboratory report; HHS was confirmed as diagnosis; hence, she was transferred to the Pediatric Intensive Care Unit (PICU).
On arrival at PICU, she developed generalized convulsion, and her GCS declined to less than 8; so she was intubated.
She was hydrated with normal saline again; then, the intravenous fluid was administered with 15 percent deficit and maintenance of fluid in addition to urine output replacement. Due to brain edema, deficit was given over 72 h, but according to urine output and serum sodium level, the amount of deficit increased up to 18 percent, and the sodium content of IV fluid decreased.
The first sodium level reported in PICU was 185 mEq/L, but it gradually decreased as hydration continued, and the amount of fluid increased (with the target level of 10 mEq/L decrease per day); then, it became stable around 145 mEq/L over the next five days. Our primary goal in her treatment was to correct sodium level maximum 10 mEq/L per day, to decrease osmolality maximum 3–5 mosm/L/h, and to reduce blood sugar maximum 75 mg/dl per hour.
On the 3rd day, HHS was resolved, but the patient became febrile, and the amount of endotracheal tube (ETT) secretion increased. The culture of ETT secretions revealed candida non-albicans and pseudomonas aeruginosa; hence, antibiotic was prescribed. Subsequently, the patient developed hypotension, so inotrope was initiated. On the same day, her blood creatine phosphokinase (CPK) increased to 6400 IU/L, and it reached 13,400 on the fifth day. Then, she developed hemoglobinuria; thereafter, hydration continued until the CPK level returned normal level on the 18th day (Table ).
Although enoxaparin was initiated for deep venous thrombosis (DVT) prophylaxis, she presented with the left forearm and hand swelling, on the 6th day. Doppler ultrasonography revealed thrombosis of the distal part of the brachial artery, so the therapeutic dose was initiated. Consequently, her conditions improved after 2 days, and a week later, Doppler sonography was normal.
On the 9th day, she was weaned off the ventilator, and on the 21st day, the patient was discharged from hospital without any sequela.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [71.0, 'mg/dL'], 'Glucose': [1124.0, 'mg/dL'], 'Sodium': [170.0, 'mEq/L']}",427.80159,406.41151,449.19167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 170.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 170.0 mEq. To convert from 170.0 mEq to mmol, convert from mEq to mmol. The compound 170.0 has a valence of 1, and so divide the valence by the value of mEq to get, 170.0 mEq/(1 mEq/mmol) = 170.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 170.0 mEq sodium/L converts to 170.0 mmol sodium/L. 
The concentration of bun is 71.0 mg/dL. 
The concentration of glucose is 1124.0 mg/dL. 
Plugging these values into the equation, we get 2 * 170.0 + (71.0 / 2.8) + (71.0 / 18) = 427.80159 mmol/L.The patient's calculated serum osmolality concentration is 427.80159 mmol/L. This is equalivalent to 427.80159 mOsm/kg."
5716,30,Serum Osmolality,lab test,decimal,pmc-4614597-1,Extracted,"A 94-year old woman was presented to the emergency department (ED) because of general weakness, abdominal pain, and dyspepsia for 4 days. She had diabetes mellitus, chronic atrial fibrillation, hypertension, and coronary artery disease with multi-vessel stenting in her medical history. The patient’s vital sign at the admission time included blood pressure of 182/86 mmHg, heart rate of 78 beats/minute, respiratory rate of 22 beats/minute, and oxygen saturation of 97% on room air. She was afebrile and physical examination showed the abdominal right upper quadrant tenderness without peritoneal signs. The rest of physical examinations were unremarkable. Abdominal ultrasonography demonstrated on a small gallbladder without gallstone as well as dilatation of the main bile duct and bilateral intra-hepatic ducts. The complete blood cell count showed the following results: leukocyte count 5100/mm3 with 77.8% of segmented neutrophils, hemoglobin 12 gram/deciliter, and platelet 180000/microliter. Other laboratory findings included: glucose 134 milligram/deciliter, blood urea nitrogen (BUN) 24 milligram/deciliter, serum creatinine 1.8 milligram/deciliter, sodium 134 milliequivalent/liter, potassium 3.8 milliequivalent/liter, serum glutamic oxaloacetic transaminase (SGOT) 26 unit/liter, albumin 3.5 gram/deciliter, total bilirubin 1.0 milligram/deciliter, lipase 31 unit/liter, and with an International Normalized Ratio (INR) of 1.52.
With assumption of obstructive biliary tract process, the patient underwent ERCP. During cannulation of the bile duct, a guidewire was applied to enter via the ampulla of Vater. In spite of iatrogenic penetrating of a periampular diverticulum in the first try (), the guidewire was inserted into the bile duct for sphincterotomy, intraductal ultrasonography, biopsy, and stenting. The final diagnosis was distal common bile duct stenosis. Due to old age and comorbidities of the patient, she was shifted to the ED for more observation. After 2 hours, patient became symptomatic with dyspnea and abdominal pain. Repeated physical examination revealed generalized subcutaneous emphysema with extensive puffiness and palpable crepitation in all over the body from head to the extremities. She had mild fever and abdominal distention without any peritoneal signs. Her oxygen saturation was 94% on room air. Laboratory test results showed leukocyte count of 18400/mm3 with left shift. The whole body computed tomography (CT) scan revealed extensive subcutaneous emphysema (). Since there was no evidence of either contrast leakage from the biliary tract or fluid collections in the peritoneal and retroperitoneal cavity, she was conservatively managed with oxygen supplement, nasogastric tubing, parenteral nutrition, and broad-spectrum antibiotics. The patient responded well and gradual resolution of the subcutaneous emphysema was happened after 9 days.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [24.0, 'mg/dL'], 'Glucose': [134.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",284.01587,269.81508,298.21666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. 
The concentration of bun is 24.0 mg/dL. 
The concentration of glucose is 134.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (24.0 / 2.8) + (24.0 / 18) = 284.01587 mmol/L.The patient's calculated serum osmolality concentration is 284.01587 mmol/L. This is equalivalent to 284.01587 mOsm/kg."
5717,30,Serum Osmolality,lab test,decimal,pmc-3420417-1,Extracted,"Mr. B is a 59-year-old African American male with a long history of bipolar disorder, maintained on fluphenazine decanoate, and lithium carbonate for over 30 years without any incidence of toxicity. His past medical history is significant for hypertension, Type II diabetes, and morbid obesity. He presented with a 1-week history of increasing confusion and lethargy, slurred speech, urinary incontinence, worsening tremor, and gait difficulties. He was found lying on the floor beside his bed on the day of presentation. The family was unaware of how long the patient had been lying there but found him awake and alert, unable to lift himself off the floor. About 2 weeks before presentation, his antihypertensive regimen was modified with a doubling of the dose of Valsartan to 320 mg/day, in addition to his regular lisinopril 20 mg/day. His other medications were lithium carbonate 450 mg twice daily and fluphenazine decanoate 37.5 mg every 3 weeks (last administered 3 weeks before admission). His last recorded lithium level was 0.7 just prior to the above medication changes. Other relevant baseline laboratory results a few weeks before onset of symptoms included Na-134 mEq/L, K-4.1, BUN, 23, and Cr. 2.4 mg/dL.
Collateral history from his outpatient psychiatrists revealed that patient had been stable on the above regimen of lithium and fluphenazine decanoate with no medication changes made within the past 6 months.
On examination in the ER, the patient was in moderate distress, dehydrated asking for water to drink. His vital signs were fluctuating with temperature ranging from 99.3 to 100.1, heart rate from 75 to 102, and BP from 123/69 to 223/112 all over a period of 6 hours. Cardiovascular and respiratory exams were unremarkable. Neurological exam revealed slurred speech, hand tremors, and rigidity in the extremities with decreased motor strength in the upper extremities and lower extremities. Patient was oriented to place and person but not to time.
Admission labs showed a leukocytosis of WBC-22.6, neutrophil count of 87.9%; sodium was 142 mEq/L; potassium was 3.5 mEq/L, bicarbonate 20.1 mmol/L; BUN 35 mg/dL; creatinine 4.1 mg/dL; blood glucose 145, troponin I 5.64; CPK 6008; CK (MB) isoenzyme 36.7 and a lithium level of 1.20 mEq/L. Blood, urine and sputum cultures yielded no growth. CT/MRI brain showed old frontoparietal infarct, and EEG was reported as within normal limits for drowsiness and briefly aroused state with no epileptiform discharges. CSF from spinal tap was unremarkable.
Patient was commenced on IV fluid hydration and broad-spectrum antibiotics. Lithium was discontinued and fluphenazine decanoate was not administered. Repeated blood cultures yielded no growth, and thus antibiotics were discontinued. Patient showed gradual improvement in his mental status, he had no problems with articulation, and he was fully orientated within a week of admission. His lithium levels had decreased to 0.89 on day 5 and 0.55 on day 7, and his renal function was back to baseline. Patient's vital signs stabilized, and there was minimal rigidity at the time of discharge.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [35.0, 'mg/dL'], 'Glucose': [145.0, 'mg/dL'], 'Sodium': [142.0, 'mEq/L']}",304.55556,289.32778,319.78334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. 
The concentration of bun is 35.0 mg/dL. 
The concentration of glucose is 145.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (35.0 / 2.8) + (35.0 / 18) = 304.55556 mmol/L.The patient's calculated serum osmolality concentration is 304.55556 mmol/L. This is equalivalent to 304.55556 mOsm/kg."
5718,30,Serum Osmolality,lab test,decimal,pmc-7478927-1,Extracted,"A 69-year-old female with a recent diagnosis of BCR/ABL+ CML, type 2 diabetes mellitus, hypertension, and coronary artery disease presented to the ED with complaints of shortness of breath (SOB). The patient reported her SOB started worsening over the last couple of days prior to admission. She denied any orthopnea or paroxysmal nocturnal dyspnea. She also reported dizziness (positional), palpitations, poor oral intake due to poor appetite, and nausea. The patient reported several episodes of coffee-ground emesis and black tarry stools for the last couple of days. She denied any hematemesis or bright red blood per rectum (BRBPR). She also endorsed easy bruising and episodes of blurry vision. Initial vital signs in the ED showed a heart rate of 105 beats per minute, blood pressure of 89/55, and 85% saturation on 4L nasal cannula. Lung exam revealed crackles with decreased breath sounds, muffled heart sounds, and no murmurs.
Lab results were as follows: hemoglobin of 7.9 g/dL, hematocrit of 25.6%, platelets of 379 K/mm3, WBCs of 105.2 K/mm3, and peripheral smear (Figure ) showed neutrophils of 46%, bands of 10%, lymphocytes of 10%, monocytes of 4%, metamyelocytes of 21%, myelocytes of 9%, and blasts of 1%.
Complete metabolic profile showed Na (sodium) of 134 mmol/L, K (potassium) of 7.3 mmol/L, bicarbonate of 19 mmol/L, BUN (blood urea nitrogen) of 103 mg/dL, creatinine of 3.4 mg/dL, glucose of 208 mg/dL, AST (aspartate aminotransferase) of 17 U/L, ALT (alanine aminotransferase) of 12 U/L, uric acid of 15.2 mg/dL, proBNP (pro b-type natriuretic peptide) of 1,135 pg/mL, troponin of <0.015 ng/mL, and procalcitonin of 1.3 ng/mL. COVID-19 screen was negative. Blood culture showed no growth after five days. Immunoglobulins were within normal limits. RF and ANA screen was negative. P-ANCA and C-ANCA were negative. C3 and C4 were within normal limits.
Chest X-ray (Figure ) showed air space disease, left side pleural effusion, and a boot-shaped heart concerning for pericardial effusion. Transthoracic echocardiography showed a large pericardial effusion of 2 cm circumferentially surrounding the heart with focal strands. There were no echo signs of frank tamponade (Figure ).
Bedside pericardiocentesis was performed and 900 cc of frank bloody fluid was removed. A drain was left in place for subsequent removal of 400 cc on day 2 and 250 cc on day 3. Pericardial fluid analysis revealed the following: negative gram stain/culture, bloody appearance, 2,300,000 RBCs, and 64,420 WBCs with polymorphonuclear neutrophils (PMNs) of 94%, lymphocytes of 2%, and monocytes of 2%. Pericardial cytology shows infiltration by CML (Figure ).
The patient was treated in the critical care unit for multifocal pneumonia, severe sepsis, and acute renal failure requiring hemodialysis (HD). The patient's hemodynamics improved after pericardiocentesis, and a total of 1,550 cc of bloody pericardial fluid was removed. WBCs decreased to 85k with hydroxyurea. Tyrosine kinase inhibitors (TKIs), such as nilotinib, were not started due to prolonged QTc (550 ms) and resistant atrial fibrillation. The patient was instructed to follow up with the outpatient hematology/oncology service to start chemotherapy once stable.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [103.0, 'mg/dL'], 'Glucose': [208.0, 'mg/dL'], 'Sodium': [134.0, 'mmol/L']}",316.34127,300.52421,332.15833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mmol/L. 
The concentration of bun is 103.0 mg/dL. 
The concentration of glucose is 208.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (103.0 / 2.8) + (103.0 / 18) = 316.34127 mmol/L.The patient's calculated serum osmolality concentration is 316.34127 mmol/L. This is equalivalent to 316.34127 mOsm/kg."
5719,30,Serum Osmolality,lab test,decimal,usmle-5230,Extracted,"A 35-year-old man is found unconscious outside his home by a passing neighbor and is brought to the emergency department by ambulance. Cardio-pulmonary resuscitation is performed and the patient awakens but remains somnolent and confused. He is unable to answer questions or provide any medical history. His temperature is 98.2°F (36.8°C), blood pressure is 108/62 mmHg, pulse is 110/min and respirations are 20/min. Physical exam shows decreased arousal. Pupils are round, symmetric, and reactive to light bilaterally. Fundoscopy is normal. The patient winces to palpation of the epigastric region and bilateral costovertebral angles. Initial labs are drawn and are shown below:

Serum:
Na+: 137 mEq/L
K+: 3.1 mEq/L
Cl-: 92 mEq/L
HCO3-: 6 mEq/L
BUN: 36 mg/dL
Glucose: 100 mg/dL
Creatinine: 1.7 mg/dL

Bladder catherization is notable for mildly bloody urine and microscopic analysis is shown in Figure A.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [36.0, 'mg/dL'], 'Glucose': [100.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",292.4127,277.79206,307.03333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 36.0 mg/dL. 
The concentration of glucose is 100.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (36.0 / 2.8) + (36.0 / 18) = 292.4127 mmol/L.The patient's calculated serum osmolality concentration is 292.4127 mmol/L. This is equalivalent to 292.4127 mOsm/kg."
5720,30,Serum Osmolality,lab test,decimal,pmc-6969475-1,Extracted,"Our patient was a 29-year-old unemployed white man with no significant past medical history. He was a current smoker with a one-pack-per-day habit and a family history of coronary artery disease on his father’s side. He presented to the emergency room of our hospital with a 1-month history of intermittent chest pain. His chest pain was localized to the right side and was pressure-like, of moderate intensity 4–6/10, nonradiating, and relieved by standing up and worsened by lying flat, but otherwise it was not changed with increase or decrease in activity level. He had no associated palpitations, shortness of breath, dizziness, or lower extremity edema. He had been taking ibuprofen 500 mg orally as needed at home in an attempt to relieve his pain. Two days prior to this presentation, his chest pain became more constant with the same quality. On the day of admission, he developed difficulty in swallowing food. He experienced dysphagia (food stuck in the lower part of his esophagus); however, he had no associated nausea or vomiting. His physical examination revealed the following vital signs: blood pressure 144/75 mmHg and heart rate 72 beats per minute. Pulse oximetry showed his oxygenation was 99% on room air. Examination of his head, eyes, ears, nose, and throat revealed that his condition was normocephalic and atraumatic. His extraocular movements were intact. His pharynx was clear. His neck was supple without jugular vein distention. His chest wall was nontender. His lungs had clear breath sounds bilaterally without any evidence of wheezing, rales, or rhonchi. His cardiac examination revealed a regular rate and rhythm. His abdomen was soft and nontender with positive bowel sounds. His neurological examination revealed that he was alert and oriented to time, place, and person. His sensation was intact; he had no facial droop; and his pupils were equal and reactive to light and accommodation. His cranial nerves were intact. His power was 5/5 in all four extremities. His reflexes were intact. His complete blood count findings were as follows: white blood cell count 8300/μl (normal range 4500–11,000/μl), hemoglobin 14.4 mg/dl (12–16 mg/dl), hematocrit 41% (35–48%; 12–17.5 g/dl), and platelet count 273,000 (140,000–450,000/μl). His blood chemistry findings were as follows: sodium 139 mmol/ (normal range 135–145 mmol/L), potassium 4.1 mmol/dl (3.5–5.2 mmol/dl), chloride 106 mmol/L (96–110 mmol/L), CO2 27 mmol/L (24–31 mmol/L), glucose 105 mg/dl (70–99 mg/dl), blood urea nitrogen 7 mg/dl (5–25 mg/dl), creatinine 0.72 mg/dl (0.44–1.0 mg/dl), aspartate aminotransferase 16 IU/L (10–42 IU/L), alanine aminotransferase 21 IU/L (10–60 IU/L), calcium 9.6 mg/dl (8.5–10.5 mg/dl), bilirubin 0.5 mg/dl (0.2–1.3 mg/dl), and lactate 1.0 mmol/dl (0.5–2.0 mmol/dl). His international normalized ratio was 1.14 (normal range 2–3 with conventional anticoagulation). The finding of his electrocardiogram (ECG) was negative for any ST changes. The patient’s chest x-ray showed a suspected loop of bowel on the right side of the chest (Fig. ). Subsequently, the patient underwent CT of the chest, which showed a 7-cm defect in the right hemidiaphragm anteriorly with a large amount of intra-abdominal fat and a loop of proximal transverse colon within the hernial sac (diaphragmatic hernia of Morgagni). The herniated contents were located in the right pericardial location (Figs. , , and ). A nasogastric tube was inserted to decompress the bowel. The patient was evaluated by a surgeon. Eventually, the patient underwent laparoscopic repair of his diaphragmatic hernia (Figs. , , and ) with a successful outcome. His chest pain and dysphagia resolved completely. When he was seen 6 months later for follow-up, he was completely asymptomatic without any complications.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [139.0, 'mmol/L'], 'Glucose': [105.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [7.0, 'mg/dL']}",286.33333,272.01666,300.65,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mmol/L. 
The concentration of bun is 7.0 mg/dL. 
The concentration of glucose is 105.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (7.0 / 2.8) + (7.0 / 18) = 286.33333 mmol/L.The patient's calculated serum osmolality concentration is 286.33333 mmol/L. This is equalivalent to 286.33333 mOsm/kg."
5721,30,Serum Osmolality,lab test,decimal,pmc-8369979-1,Extracted,"A 61-year-old male was referred to the hospital by his primary care physician for further evaluation of low potassium levels and elevated blood pressure. He initially went to his physician because he had experienced bilateral leg swelling for a week. Past medical history was significant for hypertension and fibromyalgia. Family history was significant for cardiovascular disease. He denied any alcohol, tobacco, or recreational drug consumption.
In the emergency department (ED), his vital signs were temperature 98.2 F, blood pressure 228/115 mmHg, pulse 80 beats per minute, respiratory rate 18 per minute, and SpO2 99%. On physical examination, abdomen was soft, bowel sounds were present with mild epigastric tenderness to palpation, and 1+ pitting edema on bilateral lower extremities. His laboratory result showed hemoglobin of 14.3 g/dL (13.2-17.5 g/dL), white blood cell count of 6.3 x 103/uL (4.5-11.0 x 103/uL), and platelet count of 201 x 103/uL (140-450 x 103/uL). Comprehensive metabolic panel showed a blood urea nitrogen of 18 mg/dL (5-25 mg/dL), serum creatinine of 0.96 mg/dL (0.61-1.24 mg/dL), sodium of 139 mmol/L (136-145 mmol/L), potassium of 2.1 mmol/L (3.5-5.2 mmol/L), chloride of 91 mmol/L (96-110 mmol/L), bicarbonate of 38 mmol/L (24-31 mmol/L), glucose of 89 mg/dL (70-99 mg/dL), alanine aminotransferase of 21 U/L (10-60 U/L), aspartate aminotransferase of 27 U/L (10-42 U/L), alkaline phosphatase of 89 U/L (38-126 U/L), and a total bilirubin of 1.1 mg/dL (0.2-1.3 mg/dL). EKG showed normal sinus rhythm with a rate of 60 beats per minute with flattened T-wave and presence of the U-wave complexes (Figure ). Labetolol HCl 20 mg IV and hydralazine 10 mg IV were given for blood pressure control in the ED as well as potassium 40 mEq PO and protonix 40 mg PO.
Once admitted and upon further questioning, the patient revealed that he was experiencing abdominal pain for the past 15 years. He describes himself as a ""naturalist"" and denies taking the proton-pump inhibitors that were initially prescribed to him. He wanted to resolve his abdominal pain with a natural remedy and resorted to over-the-counter deglycyrrhizinated licorice supplements for pain relief after multiple dietary variations had failed. Over the years, he had increased his daily dose for postprandial pain relief. He admitted that for the past 6-8 months he was consuming up to 20 licorice root 760 mg tablets a day, well exceeding the acceptable daily allowance (2280 mg). He further revealed he had a 10-pound weight loss in two months due to decreased oral intake. The last colonoscopy was over 10 years ago. The abdominal pain associated with oral intake was the reason he refused to take oral medications including home medication losartan-hydrochlorothiazide 100-12.5 mg and potassium PO repletion prescribed to him from the ED. Medication formulations were switched to IV.
A rapid response was called after the patient had a 10-second pause on telemetry. Repeated potassium levels showed potassium of 1.9 mmol/L and the patient was brought to the critical care unit for close observation. The patient was educated and was willing to receive potassium via oral solution in addition to the potassium he was receiving intravenously. The patient’s potassium levels were monitored every 4 hours as well as serial EKGs; he was unable to achieve a potassium level higher than 2.8 mmol/L in 24 hours. The potassium was eventually normalized to 3.5 mmol/L 48 hours post-admission via continued potassium IV infusion and oral intake equalling to 120 mEq daily.
Gastroenterology was consulted and an endoscopy was done, which showed gastritis and gastroesophageal reflux disease without evidence of Helicobacter pylori or other pathology. He was started on sucralfate 1 g suspension, reglan 10 mg, and continued on pantoprazole 40 mg IV. Psychiatry was also consulted; he was willing to take oral medications and was started on sertraline 25 mg QD and buspirone 10 mg TID. Carvedilol 12.5 BID, irbesartan 300 mg daily, and spironolactone 25 mg BID were all prescribed.
Systolic blood pressure remained above 200 despite several days on the antihypertensive medications including hydralazine 10 mg IV PRN. Despite dose adjustments of the antihypertensive medications, the patient’s blood pressure remained labile for over one week. Secondary causes of hypertension were investigated. Renin and aldosterone study showed plasma renin <0.1 ng/mL/h (0.2-1.6 ng/mL/h ), aldosterone level <3 ng/dL (<16 ng/dL), serum cortisol level 22 μg/dL (8.7-22.4 μg/dL), and 11 deoxy-cortisol <5 ng/dL (<19 ng/dL). Plasma metanephrines 0.22 nmol/L (0-0.49 nmol/L) and urine metanephrines of 122 μg/d (55-320 μg/d) were also unremarkable. Renal ultrasound and CT without contrast of the abdomen and pelvis were non-significant. Amlodipine 5 mg QD was added. Prior to discharge, the patient’s systolic blood pressure ranged between 120 and 160. He was sent home with a blood pressure cuff. The patient was thoroughly re-educated on the importance of medication compliance and the cessation of licorice supplement intake.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [18.0, 'mg/dL'], 'Glucose': [89.0, 'mg/dL'], 'Sodium': [139.0, 'mmol/L']}",289.37302,274.90437,303.84167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mmol/L. 
The concentration of bun is 18.0 mg/dL. 
The concentration of glucose is 89.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (18.0 / 2.8) + (18.0 / 18) = 289.37302 mmol/L.The patient's calculated serum osmolality concentration is 289.37302 mmol/L. This is equalivalent to 289.37302 mOsm/kg."
5722,30,Serum Osmolality,lab test,decimal,pmc-2693865-1,Extracted,"A 39-yr-old female presented with recurrent oro-genital ulcers, erythema nodosum, and arthralgia. She was diagnosed as having Behcet's disease. She had taken the maintenance therapy with colchicines. Two years later, she was admitted to our hospital because of oral and genital ulcer, lower abdominal pain, and frequent diarrhea for 15 days. She had suffered from intermittent hematochezia and cramping abdominal pain for the previous two years. Further history taking revealed she had a post-traumatic epilepsy by traffic accident 13 yr before and had taken anti-epilepsy drugs, carbamazepine and sodium valproate.
On admission, her blood pressure was 90/60 mmHg, her pulse rate was 70/min, body temperature was 36.5℃, and respiration rate was 20/min. Her abdominal pain was located in the bilateral lower quadrants without rebound tenderness. She felt cramping pain intermittently. She appeared chronically ill and reported that her stools were maroon, followed by mucoid. On examination of external genitalia, a linear to ovoid shaped ulcerating wound was observed ().
Laboratory values showed a white blood cell count of 8,600/µL, hemoglobin of 9.1 g/dL, and a platelet count of 172,000/µL. Her liver function test showed aspartate transaminase of 13 IU/L, alanine transaminase of 6 IU/L, albumin of 2.3 g/dL, alkaline phosphatase of 357 U/L, and total bilirubin of 0.2 mg/dL. The other laboratory findings showed fast blood sugar of 119 mg/dL, blood urea nitrogen of 5.2 mg/dL, creatinine of 0.8 mg/dL, sodium of 136 mEq/L, and potassium of 3.3 mEq/L.
An esophagogastroduodenoscopy (EGD) was performed to rule out the presence of a massively bleeding upper gastrointestinal lesion. The EGD was normal. Colonoscopic examination revealed grossly normal-appearing mucosa in the rectum and the sigmoid colon. However, descending, transverse, and ascending colon, including the cecum, showed multiple longitudinal ulcers and inflammatory pseudopolyps with a cobblestone appearance. The ileocecal valve and terminal ileum were preserved from the inflammation. A suspicious fistular opening just above the anus was observed (). Microscopically, specimens from ulcers of the colon showed shallow ulcerations with inflammatory infiltration consisting of lymphocytes and plasma cells. There were no granulmas ().
Further studies during her hospitalization showed that the patient was negative for HIV. She was negative for antinulear antibody and HLA-B51. Under sterile condition, intradermal injection of the skin with a 20-guage needle was done. Within 48 hr, an erythematous papule developed. The pathergy test was positive. Histological examination of the perineal lesion revealed chronic ulcer with acute and chronic inflammatory cell infiltration and increased small blood vessels (). On ophthalmologic examination, there was no ocular manifestation of Behcet's disease.
Total parenteral nutrition with nothing per oral and intravenous administration of methylprednisolone, 62.5 mg were started. In addition, metronidazole was injected for anal fistula. After 1 week, the patient responded well clinically and was tolerable with diet. Treatment with prednisone, 40 mg and 5-aminosalicylate (mesalazine), 4.0 g by mouth was started. The abdominal symptoms and vulva ulcer improved gradually, and she was discharged 2 months after admission. The dose of prednisone was tapered and discontinued. One year later, she was doing well without recurrence of symptoms.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [5.2, 'mg/dL'], 'Glucose': [119.0, 'mg/dL'], 'Sodium': [136.0, 'mEq/L']}",280.46825,266.44484,294.49166,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.0 mEq. To convert from 136.0 mEq to mmol, convert from mEq to mmol. The compound 136.0 has a valence of 1, and so divide the valence by the value of mEq to get, 136.0 mEq/(1 mEq/mmol) = 136.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mEq sodium/L converts to 136.0 mmol sodium/L. 
The concentration of bun is 5.2 mg/dL. 
The concentration of glucose is 119.0 mg/dL. 
Plugging these values into the equation, we get 2 * 136.0 + (5.2 / 2.8) + (5.2 / 18) = 280.46825 mmol/L.The patient's calculated serum osmolality concentration is 280.46825 mmol/L. This is equalivalent to 280.46825 mOsm/kg."
5723,30,Serum Osmolality,lab test,decimal,pmc-8015483-1,Extracted,"A young 29-year-old healthy man who came to the Neurology Clinics, United Clinics in Madinah Al-Munawarah, at day three with a persistent positional headache after microscopic varicocelectomy for primary infertility. It was associated with nausea and low back pain at the site of spinal puncture. The headache was global type and improved temporarily with hydration and oral caffeine intake. During follow-up, he presented to the Emergency Department with still recurrent headache and new onset of vomiting and blurred vision at day 10. There was neither history of trauma nor relevant past or family medical history for thromboembolic disorders; he had not been on any medical therapy before. On examination, he was conscious and oriented with a GCS of 15/15. His body temperature was 37.1°C, with a heart rate of 86 beats/min. His blood pressure was 133/85 mmHg, and his respiratory rate was 17 breaths/min. Fundoscopic examination showed bilateral papilledema, and no focal neurological deficits were recognized ().
Laboratory investigations revealed a sodium level of 131 mEq/L, blood urea and nitrogen levels of 4.5 mg/dL, a creatinine level of 55 micromole/L, and a level of glucose was 109 mg/dL. A complete blood count revealed a normal white blood cell count of 8×109/L, a hemoglobin level of 12.9 g/dL, and a platelet level of 356×109/L. The liver function test was normal, with an alanine aminotransferase (ALT) level of 33 U/L, an aspartate aminotransferase (AST) level of 16 U/L, a bilirubin value of 2 mg/dL, and an alkaline phosphatase (ALP) level of 103 U/L. Further hematological workup revealed normal levels of protein C and S. His D-dimer level was 2.1 nmol/L, with a fibrinogen level of 3.1 g/L. His partial thromboplastin time was 35 seconds and high prothrombin time was 11.1 seconds. Anticardiolipin and anti-lupus antibodies were negative. Fasting plasma homocysteine level is within normal range (13.4 µmol/L). Antithrombin III activity level is 114% which is within normal limit. The sickle cell screening is negative. The total cholesterol is 6.4 mmol/l, triglyceride 1.85 mmol/l, high density lipoprotein is 1.14 mmol/l, and low-density lipoprotein is 5.1 mmol/l. Further genetic tests that include factor V Leiden and prothrombin gene mutation were negative.
Magnetic resonance (MR) imaging showed increase signal intensity in both T1 weighted images (WI) and T2WI as well as bilateral superficial cortical veins with filling defect as seen in the magnetic resonance venography (MRV); there was no diffusion restriction suggesting venous infarction (Figure 1). Findings are consistent with superior sagittal sinus thrombosis.
He required admission to the hospital to observe and stabilize him. He was started on heparin infusion and warfarin until the target INR level reached 2-3. On day 8 after admission, the patient showed complete resolution of headache and vomiting. He still had a blurred vision and he was started on acetazolamide 250 mg daily dose for 3 months only. His symptoms gradually improving over time until complete recovery by the end of the second month after discharge.
His last follow-up was 4 months after surgery and was asymptomatic and his further genetic tests were unremarkable. His INR was maintained between 2 to 3 through all visits to coagulation clinic. He is going to undergo MR imaging follow-up by the end of the 6th month prior to stop anticoagulation.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [4.5, 'mg/dL'], 'Glucose': [109.0, 'mg/dL'], 'Sodium': [131.0, 'mEq/L']}",269.6627,256.17956,283.14583,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 131.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 131.0 mEq. To convert from 131.0 mEq to mmol, convert from mEq to mmol. The compound 131.0 has a valence of 1, and so divide the valence by the value of mEq to get, 131.0 mEq/(1 mEq/mmol) = 131.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 131.0 mEq sodium/L converts to 131.0 mmol sodium/L. 
The concentration of bun is 4.5 mg/dL. 
The concentration of glucose is 109.0 mg/dL. 
Plugging these values into the equation, we get 2 * 131.0 + (4.5 / 2.8) + (4.5 / 18) = 269.6627 mmol/L.The patient's calculated serum osmolality concentration is 269.6627 mmol/L. This is equalivalent to 269.6627 mOsm/kg."
5724,30,Serum Osmolality,lab test,decimal,pmc-6855657-1,Extracted,"A 66-year-old Taiwanese man had a history of hypertension, rheumatoid arthritis on quinine, methotrexate, and methylprednisolone, and cement injection for compression fracture of osteoporotic vertebrae. He underwent an endovascular stent graft of abdominal aortic aneurysm 18 months ago at an urban hospital. According the clinical course, he had been suffering from recurrent episodes of fever, chills, and abdominal fullness 6 months ago, but no definite diagnosis could be confirmed. One month ago, his C-reactive protein (CRP) was 20 mg/dL and the contrast-enhanced abdominal computed tomography (CT) revealed an endoleak (Fig. ), yet no fluid accumulation within the psoas muscle was detected. After a 4-day course of intravenous (IV) amoxicillin/clavulanic acid, fever subsided and he was discharged.
This time, he presented to our emergency department with fever, chills, and watery diarrhea for 1 day. On examinations, he was febrile with a body temperature of 37.6°C, a blood pressure of 117/68 mmHg, and a heart rate of 95 beats/min. Laboratory tests revealed white blood cell count of 5700 cells/mm3 with segmented neutrophils of 85.5%, hemoglobin of 11.4 g/dL, platelet counts of 271 × 103 cells/mm3, blood urea nitrogen of 17 mg/dL, keratinize of 1.1 mg/dL, sodium of 132 mEq/L, potassium of 3.7 mEq/L, albumin of 3.4 g/dL, glutamic-pyruvic transaminase of 63 U/L, alkaline phosphates of 77 U/L, lactate dehydrogenase of 381 U/L, lactate 18.5 mg/dL, CRP of 9.73 mg/dL, blood glucose of 105 mg/dL, and erythrocyte sedimentation rate (ESR) 113 mm/h. Stool analysis showed no pus cell. Abdominal CT uncovered the presence of an irregular enhancement within left psoas muscle, connecting with contiguous thromboses aneurysmal sac, which was suggestive of left psoas abscess associated with an infected endograft (Fig. ).
After admission, cardiovascular surgeon suggested initiating cautious trial of antimicrobial therapy alone instead of concomitant radical debridement with graft removal, considering patient's frailty with immunosuppressant's and the radiological absence of endoleak and connecting fistula. CT-guided drainage was not feasible in radiologist's opinion owing to a high risk of close proximity to great vessels. The blood culture yielded growth of Listeria monocytogenes, susceptible to ampicillin, penicillin, and sulfamethoxazole/trimethoprim (SMX/TMP). IV ampicillin (2 g, 6 times daily) with 8 days of synergistic gentamicin (80 mg, twice daily) was chosen as the initial regiment and it created satisfactory response. Ampicillin was continued for 30 days and then shifted to IV co-trimoxazole (80/400 mg, 4 times daily) for 12 days. He remained asymptomatic with a decline of CRP to 0.36 mg/dL and ESR to 39 mm/h. He was discharged on the 44th hospital day.
Three months later, abdominal CT illustrated nearly complete resolution of bilateral psoas abscess. Orally SMX/TMP 400 mg/80 mg was prescribed for 13.5 months at outpatient follow-up. Until now, he kept regular outpatient surveillance and made an uneventful recovery.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [17.0, 'mg/dL'], 'Glucose': [105.0, 'mg/dL'], 'Sodium': [132.0, 'mEq/L']}",275.90476,262.10952,289.7,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 132.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 132.0 mEq. To convert from 132.0 mEq to mmol, convert from mEq to mmol. The compound 132.0 has a valence of 1, and so divide the valence by the value of mEq to get, 132.0 mEq/(1 mEq/mmol) = 132.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 132.0 mEq sodium/L converts to 132.0 mmol sodium/L. 
The concentration of bun is 17.0 mg/dL. 
The concentration of glucose is 105.0 mg/dL. 
Plugging these values into the equation, we get 2 * 132.0 + (17.0 / 2.8) + (17.0 / 18) = 275.90476 mmol/L.The patient's calculated serum osmolality concentration is 275.90476 mmol/L. This is equalivalent to 275.90476 mOsm/kg."
5725,30,Serum Osmolality,lab test,decimal,usmle-4639,Extracted,"A 12-year-old boy is brought in by his parents as they are concerned about his behavior. He is constantly arguing with his parents and blatantly defying their every request. In school, he is known for being intentionally tardy and for defying his teachers. Upon further questioning of the patient you learn about some of his recent behaviors such as beginning smoking to bother his parents. You also notice that he is disrespectful towards you. You then learn that he has also gotten into weekly fights with his peers at school with no apparent cause. In addition, last week he was seen hitting one of the local neighborhood cats with a baseball bat trying to kill it. The patient lives at home with his two parents in a pre-World War II house that was recently renovated. Physical exam is unremarkable.

Laboratory values are as follows:

Na: 140 mmol/L
K: 4.5 mmol/L
Cl: 100 mmol/L
Glucose: 80 mg/dL
Ca: 10 mmol/L
Mg: 3 mEq/L
Cr: 0.8 mg/dL
BUN: 10 mg/dL
Serum lead: < .01 µg/dL
Hb: 15 g/dL
Hct: 45%
MCV: 95
Urine toxicology: negative

As the patient leaves the office you notice him stealing all of the candy from the office candy bowl. The patient seems unconcerned about his behavior overall.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mmol/L'], 'Glucose': [80.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [10.0, 'mg/dL']}",288.01587,273.61508,302.41666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mmol/L. 
The concentration of bun is 10.0 mg/dL. 
The concentration of glucose is 80.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (10.0 / 2.8) + (10.0 / 18) = 288.01587 mmol/L.The patient's calculated serum osmolality concentration is 288.01587 mmol/L. This is equalivalent to 288.01587 mOsm/kg."
5726,30,Serum Osmolality,lab test,decimal,pmc-7944606-1,Extracted,"A 20-month-old healthy Asian girl weighing 10.3 kg without any medical history, in a coma, and with progressive generalized weakness was admitted to our emergency department. She had complained of constipation, and 200 mg of MgO in divided doses daily had been prescribed earlier for 4 days by her family physician. According to the family, there was no stool discharge for 5 days, and the patient had episodes of vomiting twice in the morning in addition to a reduced level of consciousness. No remarkable findings were observed regarding her birth history, growth rate, or family history. She was not taking any medication, except for MgO as a laxative.
The vital signs on admission were as follows: temperature of 97.1 °F (36.2 C°), heart rate of 104 beats per minute, systolic and diastolic pressures of 110 and 60 mmHg, respectively, respiratory rate of 28 breaths per minute, and oxygen saturation of 98% in room air. The physical examination revealed that the state of consciousness was E2V1M1 on the Glasgow Coma Scale. Her extremities did not respond to pain stimulus; however, her facial expression was set and showed little display of feeling. The neurological examination showed a symmetric decrease in muscle tone. The deep tendon reflexes were also decreased, and the pupillary reflexes were sluggish. No abnormalities were observed in her respiratory status or heart sounds. The abdomen was distended with diminished bowel sounds, and a mass of stool was palpable.
The laboratory findings showed that the patient had fatal hypermagnesemia (11.0 mg/dL) and hyperglycemia (377 mg/dL). The hemogram showed leukocytosis (white blood cell count 26,760/μL) with bands accounting for 82.6% and no anemia (hemoglobin 13.9 mg/mL). Other results included the following: serum calcium, 9.3 mg/dL; serum sodium, 130 mEq/L; serum potassium, 4.0 mEq/L; serum chloride, 100 mEq/L; serum creatine, 0.17 mg/dL; blood urine nitrogen, 30.4 mg/dL; total bilirubin, 0.2 mg/dL; venous blood pH, 7.33; partial pressure of carbon dioxide (PaCO2), 36.5 mmHg; and partial pressure of oxygen (PO2), 60.6 mmHg. An electrocardiogram showed normal and no block patterns. The blood cultures were negative. The patient was diagnosed with fatal hypermagnesemia caused by intoxication from a laxative containing MgO. She was instantly administered calcium gluconate infusion at 3.9 mEq for over 10 min. She was then continuously infused with calcium gluconate at 0.23 mEq/hour as a Mg antagonist to reverse the neuromuscular and cardiac effects of hypermagnesemia. She was kept hydrated with 0.9% sodium chloride to maintain good urine output to excrete the Mg, and a total of 720 mL was administered over the next 12 hours. An enema was performed, which expelled a large mass of stool and a large amount of muddy stool. After 2 hours, her serum Mg level was decreased to 5.9 mg/dL, and she regained consciousness to a level of being verbally responsive. Over the next 12 hours, her neurologic status continued to improve. Her serum Mg and glucose levels decreased to 2.4 mg/dL and 116 mg/dL, respectively. The patient recovered, and was discharged without recurrence of hypermagnesemia. At the follow-up visit 3 days later, her serum Mg level was 1.9 mg/dL. Five years after discharge, during a follow-up evaluation, she was neurologically well and had returned to her baseline status without a recurrence of hypermagnesemia and hyperglycemia.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [30.4, 'mg/dL'], 'Glucose': [377.0, 'mg/dL'], 'Sodium': [130.0, 'mEq/L']}",291.80159,277.21151,306.39167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. 
The concentration of bun is 30.4 mg/dL. 
The concentration of glucose is 377.0 mg/dL. 
Plugging these values into the equation, we get 2 * 130.0 + (30.4 / 2.8) + (30.4 / 18) = 291.80159 mmol/L.The patient's calculated serum osmolality concentration is 291.80159 mmol/L. This is equalivalent to 291.80159 mOsm/kg."
5727,30,Serum Osmolality,lab test,decimal,usmle-1270,Extracted,"A 54-year-old woman comes to the physician with abdominal distention and mild diffuse abdominal discomfort. She has not had nausea, vomiting, fever, or chills. She was diagnosed with alcoholic liver cirrhosis 2 years ago. Examination shows a protruding, distended abdomen that is dull to percussion with a positive fluid wave. Ultrasonography shows mild to moderate ascites. Appropriate treatment of the patient's condition is started. Four days later, the patient experiences palpitations and chest pain at home. She is brought to the emergency department, where her temperature is 37.3°C (99.1°F), pulse is 182/min, respirations are 18/min, and blood pressure is 82/50 mm Hg. An ECG shows ventricular tachycardia. Initial laboratory studies show:
Serum
Na+ 131 mEq/L
K+ 2.9 mEq/L
Cl- 92 mEq/L
Bicarbonate 34 mEq/L
Urea nitrogen 42 mg/dL
Creatinine 4.8 mg/dL
Glucose 90 mg/dL
Ca2+ 8.1 mg/dL
Mg2+ 1.5 mg/dL
Phosphate 4.7 mg/dL
Arterial Blood Gas
pH 7.52
pCO2 45 mm Hg
pO2 90.2 mm Hg
She is successfully cardioverted to normal sinus rhythm.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [131.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [42.0, 'mg/dL'], 'Glucose': [90.0, 'mg/dL']}",282,267.9,296.1,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 131.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 131.0 mEq. To convert from 131.0 mEq to mmol, convert from mEq to mmol. The compound 131.0 has a valence of 1, and so divide the valence by the value of mEq to get, 131.0 mEq/(1 mEq/mmol) = 131.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 131.0 mEq sodium/L converts to 131.0 mmol sodium/L. 
The concentration of bun is 42.0 mg/dL. 
The concentration of glucose is 90.0 mg/dL. 
Plugging these values into the equation, we get 2 * 131.0 + (42.0 / 2.8) + (42.0 / 18) = 282.0 mmol/L.The patient's calculated serum osmolality concentration is 282.0 mmol/L. This is equalivalent to 282.0 mOsm/kg."
5728,30,Serum Osmolality,lab test,decimal,pmc-6683832-1,Extracted,"An 89-year-old male smoker patient presented at the emergency department of our hospital with left, deep purplish cervical swelling with draining sinuses. The patient reported that three months ago, painless erythematous nodular swellings appeared in the left lateral neck area. No respiratory symptoms, fever, or weight loss were reported except for occasional dry cough and mucous expectoration since he had been a lifelong smoker of 70 pack-years. The patient was a taxi and bus driver. His past medical history included surgery for benign prostate hypertrophy 15 years ago, as well as an unscheduled visit to the emergency department of our hospital, 6 months ago, due to an acute hypertensive episode associated with pulmonary edema, being treated by intravenous diuretics. Since then, he had been on valsartan-hydrochlorothiazide therapy (16 mg + 12.5 mg), once daily. On examination, the patient, a tall and thin man, (BMI = 19.6 Kg/m2), with normal skin color, had a normal physical appearance except for his left lateral neck lesion including draining tract sinuses with purulent material () and scarce low-pitched expiratory wheezes. The cardiovascular examination showed a mild systolic murmur in the right second intercostal space compatible with moderate aortic valve regurgitation. On admission, the blood pressure (BP) and heart rate (HR) were 145/70 mmHg and 86 beats per minute, respectively, while blood and biochemistry tests were as follows: Hct = 37.3%; Hb = 13.8 g/dL; MCV = 81.7 fL; MCH = 29.6 pg; PLT = 214 × 103/μL; WBC = 6.3 × 103/μL (leukocyte type: NEU% = 70%, LYM% = 20%, MON% = 7%, and EOS = 3%); INR = 1.22; serum glucose = 101 mg/dL; urea = 39 mg/dL; creatinine = 1.02 mg/dL; Na+ = 139 mmol/L; K+ = 4.2 mmol/L; and erythrocyte sedimentation rate (ESR) = 52 mm/1st hour. The Mantoux test showed 10 mm induration, and his chest X-ray had no significant findings. The computed tomography (CT scan) showed minimal fibrous bands in the upper zone area of the right upper lobe, while a small calcified nodule (3 mm diameter) was also found in the periphery of the apical-posterior segment of the left upper lobe (). Fiberoptic bronchoscopy revealed a diffusely red and hyperemic bronchial mucosa, particularly intense in the segments of the right upper lobe, with the presence of some small anthracotic areas (). Bronchoalveolar lavage fluid (BAL) obtained from the apical-posterior segment of the left upper lobe showed increased (>70%) lymphocytes, 15% neutrophils, few (<8%) macrophages, and scarcity of bronchial epithelial cells with no evidence of malignancy. Direct smear for acid-fast bacilli was also negative. The surgical biopsy and the microscopic examination of the cervical lymph node showed epithelial granuloma with central coagulative (caseous) necrosis and the presence of M. tuberculosis complex, respectively. In addition, the microscopic examination of the purulent content of draining sinuses in the patient's neck also revealed the presence of M. tuberculosis complex. Final diagnosis for TL was established by histopathologic examination (Figures and ).
The patient was started on a four- (4-) drug antituberculous regimen. One month after the initiation of the antituberculous regimen, and after an initial remission regarding the magnitude of the patient's neck growth, he experienced an enlargement of his lymph nodes with reappearance of draining sinuses. It was then decided to add oral steroids (20 mg prednisolone daily). Four weeks after steroid administration, there was a spectacular, almost complete remission, of his neck growth. The antituberculous treatment was continued for 6 months, and the patient was free of disease after its completion.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [39.0, 'mg/dL'], 'Glucose': [101.0, 'mg/dL'], 'Sodium': [139.0, 'mmol/L']}",297.53968,282.6627,312.41666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mmol/L. 
The concentration of bun is 39.0 mg/dL. 
The concentration of glucose is 101.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (39.0 / 2.8) + (39.0 / 18) = 297.53968 mmol/L.The patient's calculated serum osmolality concentration is 297.53968 mmol/L. This is equalivalent to 297.53968 mOsm/kg."
5729,30,Serum Osmolality,lab test,decimal,pmc-5139857-1,Extracted,"A 33 years old Caucasian male presented to the emergency room of St.Vincent Mercy Medical Center at Toledo, Ohio with a history of intermittent hemetemesis for last couple of weeks which has increased in severity during the last 24 hours, progressing to 4 episodes of a cup full of blood. He also had complaints of light headedness and dizziness. He had no history of hemetochezia, melena, fever, chills, constipation, diarrhea, abdominal pain or nausea. He had no recent NSAIDs use, headache, chest pain, shortness of breath or palpitation.
Patient had past history of Diabetes Mellitus type 1 and is on Insulin. Patient had history significant for Gallstone pancreatitis which resulted in Pseudocyst formation. Patient had undergone Cholecystectomy and Cystojejunostomy in 2007. He had history of Spinal Stenosis, right knee surgery and Tonsillectomy. Patient was allergic to Avandia, Fentanyl, and Metfromin. Patient was on Tramadol, Neurontin, Insulin, Zolpidem and Omeprazole. Patient had no history of Gastrointestinal (GI) disease in family. His father had diabetes and mother had COPD and pernicious anemia. Patient was a non smoker, non alcoholic and denied using any illicit drugs. His bowel and bladder functions were unaltered.
On presentation his vitals were Temp: 36.3 °C, Pulse: 114/min, Blood pressure: 102/54 mm of Hg, Oxygen saturation: 99% on room air and Respiratory rate: 16/min. On physical examination he was conscious, coherent, pale looking and weak with warm and moist skin without dermatosis. No signs of Jaundice or generalized Lymphadenopathy were found. He had no obvious spinal or limb deformities. He had normal pulses in all extremities without any signs of cyanosis. His oral cavity was normal without ulcerations. His chest was symmetrically expanding with good breath sounds and without labored breathing. He had adynamic precordium with apex beat located in 5th intercostal space at midclavicular line. He had normal heart sounds without any murmur. His abdomen was soft and flat. He had tenderness in epigastric region. No organomegaly or masses were found and bowel sounds were normal. Patient had normal neurological examination with grossly intact cranial nerves and normal reflexes. Pupils were equal and reacting to light normally.
His initial investigations were Hemoglobin 6.3 gm/dl, Hematocrit of 18.7%, MCV: 88.8 fL, White cell count 8.4 k/ul (Neutrophils 84, Lymphocytes 10, Monocytes 6, Eosinophils 0, Basophils 0), Platelet count: 327 k/ul, Sodium: 137 meq/l, Potassium: 4.7 mEq/l, Bicarbonate: 24.5 mEq/l, Chloride: 103 mEq/l, Blood Urea Nitrogen: 35 mg/dl, Creatinine: 0.59 mg/dl, Glucose: 231 mg/dl, Bilirubin: Direct: 0.12 and total 0.28 mg/dl, Proteins total: 4.4 g/dl, Albumin: 2.7 g/dl, AST: 31 units/L, ALT: 44 units/l, Calcium: 7.9 mEq/l, Alkaline phosphatase: 53 units/l, Lipase: 23 units/l, pCO2 46, pO2 84, pH 7.34, PTT: 23.4 (20.3-30.9 sec), Prothrombin time: 12.5 (9.7-12 sec), INR: 1.2, Fibrinogen: 420(140-420 mg/dl). Hepatitis serology and ANA screen were negative. He had undergone Liver biopsy was performed during surgery which was found normal without any changes of cirrhosis of liver ().
On upper GI endoscopy (EGD) esophageal and stomach mucosa were found normal without any active sites of bleeding. Fundus was clearly seen without varices. Pylorus was patent and the duodenal bulb was normal. The major papilla was identified in the descending duodenum and had normal appearance. Just distal to the major papilla in the 2nd portion of duodenum, there was a large submucosal bulge suspicious for an ectopic duodenal varix (). On withdrawal of the scope findings were confirmed.
Abdominal and pelvic CT scan with contrast showed massive gastric distention. Gastric outlet obstruction was suspected. Pancreatic Pseudocyst in the tail of the pancreas had significantly increased in size from the previous study. Changes of chronic pancreatitis were present.
Mesenteric Arteriogram showed slow contrast filling of the superior mesenteric vein with significant limiting of flow. Superior Mesenteric Vein obstruction was suspected. Multiple venous varicosities around the distal stomach and the pancreatic head region were found (). Possibility of at least partial thrombosis of the Superior Mesenteric Vein (SMV) near the pancreatic head region was suspected secondary to pancreatitis. Splenic vein was found of normal caliber without any varicosities.
Patient had undergone end to side Mesocaval Anastomosis with a Dacron 10 mm graft between the Superior Mesenteric Vein and the Inferior Vena Cava along with adhesionolysis and liver biopsy. During surgery no varicosities found in the gastric and esophageal region or no dilation found in the splenic or inferior mesenteric venous system. There were multiple adhesions found in the tail region of pancreas possibly because of previous Cystojejunostomy in that area. Similarly many adhesions found in the peripancreatic region most likely due to changes of chronic pancreatitis. Patient was discharged without any complications and found asymptomatic in the follow up visits with normal hemoglobin level and without any evidence of bleeding. Considering the young age of the patient and relatively absent varices at other sites Mesocaval shunt surgery was chosen as a treatment over Transjugular Intrahepatic Portosystemic Shunt (TIPS) and duodenal resection.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [35.0, 'mg/dL'], 'Glucose': [231.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",299.33333,284.36666,314.3,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 35.0 mg/dL. 
The concentration of glucose is 231.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (35.0 / 2.8) + (35.0 / 18) = 299.33333 mmol/L.The patient's calculated serum osmolality concentration is 299.33333 mmol/L. This is equalivalent to 299.33333 mOsm/kg."
5730,30,Serum Osmolality,lab test,decimal,pmc-5358194-1,Extracted,"A 55-year-old female presented to the casualty of our hospital on 13th March 2010 in a gasping condition. She was referred to our hospital from another hospital where she was admitted on 9th March with acute anterior wall myocardial infarction (AWMI). She was not thrombolysed but was treated with tab. clopidogrel + aspirin (75 and 150 mg) for 3 days followed by tab isosorbide dinitrate 5 mg tid, tab atorvastatin 10 mg h.s., and inj enoxiparin (Lupinox) 0.4 ml sc bid for 10 days. On March 15, 2010, she was shifted over to Isosorbide mononitrate (30 mg) OD. During her stay at the other hospital it was noticed that she could not maintain her O2 saturation without nasal oxygen supplementation. She was a known case of bronchial asthma on inhalational steroid for the last 12 years.
On examination the patient was tachypnoeic, cyanosed, drowsy, and disoriented. Her pulse rate was 124 beats per minute, regular. The B. P. was 130/80 mmHg. There was moderate bronchospasm and a few bibasal crackles. She was intubated and put on ventilatory support. An X-ray of chest showed Lt. lower zone consolidation.
The results of laboratory investigations on admission were Hb 12.69/dl, TLC 20,700/mm3 (P 84%, L 14%, E 1%, M 1%), platelets 189,000/mm3, S. creatinine 1.4 mg/dl, BUL 82 mg/dl, S. bilirubin 0.8 mg/dl, total proteins 6.6 g/dl, albumin 3.6 g/dl, globulin 3.0 g/dl, SGOT 57 U/L, SGPT 52 U/L, alk. phospatase, 98 U/L, S. sodium 149 mEq/L, and S. potassium 4.8 mEq/L. Two D Echo done on March 15, 2010, showed LVEF of 51% with apical hypokinesia. No clots, vegetations, or effusion were noted.BNP (19.310) was 784 pg/ml (N = 0 - 100 pg/ml). CPK (MB) 1st and 2nd readings were 19 IU/ml and 29 IU/ml respectively. D-dimer was 650 ng/ml, ANA (ELISA) borderline +ve, and ADA 5.0.ABG done on March 19, 2010 showed pH 7.398, PaO2 24.1 mmHg, PaCO2 72.6 mmHg, HCO3 43.8 mEq/L, O2 saturation 40.2%. Findings of serial ECGs are tabulated ().
Blood sugar on admission was 231 mg/dl. At discharge fasting and post prandial blood sugars were 135 mg/dl and 158 mg/dl respectively. S. creatinine was 1.6 mg/dl. US KUB showed bilateral increased echogenecity of cortex. A CT scan of brain was normal.
A diagnosis of acute left ventricular failure following AWMI with pneumonia and asthma was made. She was treated with inj augmentin 1.2 g iv bd, x 10d, moxifloxacin 400 mg iv od x 10 d, inj lasix 100 mg, stat followed by 40 mg od x 5 d, inj deriphylline 2 ml iv bd x 5 d followed by tab salbutamol 10 mg od, duolin and budecort nebulization 6 hourly, inj hydrocortisone 100 mg tid x 3 d, and then tapered off over the next 4 days. Tab isosorbide mononitrate 30 mg od was discontinued after 9 days.
Ventilatory support was withdrawn after 4 days (March 16, 2010) and she was put on nasal oxygen. On discontinuation of the nasal support on 17th March she desaturated within 10 - 15 minutes and was tachypnoeic, dyspnoeic and cyanosed. Her PaO2 dropped to 30% - 35%. This improved rapidly on reinstituting nasal O2. A repeat 2 D Echo (March 19, 2010) revealed mild LV dysfunction and pulmonary artery pressure of 62 mmHg. An HRCT of chest with CT angiogram revealed diffuse patchy infiltrates involving both the lungs including apices (). There was no evidence of pulmonary embolism. Possibility of interstitial lung disease was considered and she was started on tab methylprednisolone 16 mg bd. Over the next few days her tendency to and the rapidity of desaturation decreased progressively and after 4 weeks she could be totally weaned off oxygen support. A repeat HRCT scan done on 22nd April (5 weeks after admission) showed total resolution of the interstitial shadows (). During her hospital stay she had one episode of atrial fibrillation that responded to tab diltiazem (30 mg tid). Her thyroid function tests suggested hyperthyroidism (TSH 0.09 µIU/ml, T4 - 13.2 µg/dl, T3 2.2 ng/ml) and she was started on neomercazole 5 mg tid. The patient was discharged on 23rd April. She had no breathlessness or chest pain. Pulse and B.P. were normal. At follow up 10 days after discharge she was totally asymptomatic.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [82.0, 'mg/dL'], 'Glucose': [231.0, 'mg/dL'], 'Sodium': [149.0, 'mEq/L']}",340.11905,323.1131,357.125,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 149.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 149.0 mEq. To convert from 149.0 mEq to mmol, convert from mEq to mmol. The compound 149.0 has a valence of 1, and so divide the valence by the value of mEq to get, 149.0 mEq/(1 mEq/mmol) = 149.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 149.0 mEq sodium/L converts to 149.0 mmol sodium/L. 
The concentration of bun is 82.0 mg/dL. 
The concentration of glucose is 231.0 mg/dL. 
Plugging these values into the equation, we get 2 * 149.0 + (82.0 / 2.8) + (82.0 / 18) = 340.11905 mmol/L.The patient's calculated serum osmolality concentration is 340.11905 mmol/L. This is equalivalent to 340.11905 mOsm/kg."
5731,30,Serum Osmolality,lab test,decimal,pmc-5519313-1,Extracted,"The patient is a 63-year-old man with a past medical history of MALToma of the lung who presented with generalized weakness for the past one month associated with cough, fever, night sweats, and shortness of breath. The patient also had anorexia and weight loss of 15 pounds over one month. He denied a history of smoking. The patient was under treatment with isoniazid and pyridoxine for latent tuberculosis based on a positive skin tuberculin test.
On physical examination, his blood pressure was 110/59 mmHg, heart rate 118 beats per minute (bpm), respiratory rate 18/min, saturating 99% on room air with a temperature of 98.9oF. The patient was in no cardiopulmonary distress. A cardiovascular examination revealed no jugular venous distension, normal S1-S2, and no murmurs. On lung auscultation, the patient had rales at the left lung base.
Laboratory data showed sodium 134 mEq/L, potassium 4.2 mEq/L, chloride 103 mEq/L, bicarbonate 25 mEq/L, blood urea nitrogen 17 mg/dl, creatinine 0.9 mg/dl, glucose 96 mg/dl, hemoglobin 6.6 g/dl, hematocrit 20.1%, white blood cell count 5.5 x 103/microliter, and platelets 128 x 103/microliter. The coagulation profile showed prothrombin time (PT) 17.2 sec, partial thromboplastin time (PTT) 44.3 sec, and international normalized ratio (INR) 1.38.
Chest X-ray (CXR) and computed tomography (CT) scan showed right middle lobe opacity (Figures -). Repeat imaging after six months showed multiple masses in the lung and an osteoblastic bone lesion involving the left ilium (Figures -). Esophagogastroduodenoscopy showed a normal gastro-esophageal junction with erythematous mucosa in the stomach. The gastric biopsy was normal.
A lung biopsy done at initial presentation from the right middle lobe mass showed dense lymphoid infiltrate with proliferation of monocytoid B lymphocytes consistent with extranodal marginal zone lymphoma (BALToma/MALToma).
A CT-guided core needle biopsy from the left posterior pelvic mass that was noted six months after the initial presentation showed high grade diffuse large B-cell lymphoma involving skeletal muscles. The pathology report showed diffuse proliferation of lymphocytes, which were positive for cluster of differentiation (CD) 20 and B-cell lymphoma (BCL)-2 by immunohistochemistry tests. He was started on chemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) with subsequent complete clinical and radiologic remission (Figure ).",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [17.0, 'mg/dL'], 'Glucose': [96.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",279.40476,265.43452,293.375,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. 
The concentration of bun is 17.0 mg/dL. 
The concentration of glucose is 96.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (17.0 / 2.8) + (17.0 / 18) = 279.40476 mmol/L.The patient's calculated serum osmolality concentration is 279.40476 mmol/L. This is equalivalent to 279.40476 mOsm/kg."
5732,30,Serum Osmolality,lab test,decimal,usmle-8780,Extracted,"A 65-year-old diabetic man presents to the emergency department with severe retrosternal chest pain, vomiting, and diaphoresis for the last half hour. He has a history of diabetic chronic kidney disease. He is on insulin therapy. Oral medications include aspirin, losartan, and metformin. The vital signs include: temperature 36.8°C (98.2°F), pulse 88/min, respiration rate 14/min, and blood pressure 120/65 mm Hg. The weight is 78 kg (172.0 lb). The lungs are clear to auscultation. Cardiac examination shows no abnormalities. The electrocardiogram (ECG) shows ST-segment elevation in the precordial leads V-1–V-4. Left ventricular ejection fraction is estimated at 55%. The laboratory test results are as follows:
Laboratory test
Hemoglobin 15 g/dL
Leukocyte count 9,500/mm3
Serum
Glucose 215 mg/dL
Na+ 140 mEq/L
Cl− 102 mEq/L
K+ 4.1 mEq/L
Urea nitrogen 22 mg/dL
Creatinine 1.4 mg/dL
Cardiac troponin I 0.8 ng/mL
The patient is being considered for primary percutaneous coronary intervention.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [22.0, 'mg/dL'], 'Glucose': [215.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",299.80159,284.81151,314.79167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 22.0 mg/dL. 
The concentration of glucose is 215.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (22.0 / 2.8) + (22.0 / 18) = 299.80159 mmol/L.The patient's calculated serum osmolality concentration is 299.80159 mmol/L. This is equalivalent to 299.80159 mOsm/kg."
5733,30,Serum Osmolality,lab test,decimal,pmc-7098417-1,Extracted,"A 78-year-old man slipped and fell into a swamp and was found to be unconscious after hitting his head on a rock during the daytime in spring. His history included hypertension, atrial fibrillation and cerebral infarction requiring warfarin. A physician-staffed helicopter was dispatched at the request of the fire department. When the staff of the helicopter checked him at the rendezvous point, he was in a deep coma and shock state with subcutaneous emphysema at his left chest, so a venous route was secured, and tracheal intubation and left thoracostomy were performed before air evacuation. Left thoracostomy was made by the insertion of a chest drainage tube at the fourth intercostal space on the midaxillary line due to potential tension pneumothorax. During air transportation, he remained in a shock state due to minimum infusion based on permissive hypotension strategy, and the physician of the helicopter activated the massive transfusion protocol at the receiving emergency room [].
On arrival, his vital signs were as follows: Glasgow Coma Scale, E1VTM1 without sedation; blood pressure, 58/44 mmHg; heart rate, 120 beats per minute; percutaneous saturation, 90% (FiO2 1.0); body temperature, 33.7°C. The results of a venous gas analysis on arrival were as follows: pH, 7.353; PCO2, 41.7 mmHg; PO2, 38.9 mmHg; HCO3-, 22.6 mmol/L; base excess. -2.3 mmol/L; and lactate, 3.8 mmol/L. After receiving six units of blood type O transfusion and vitamin K, his systolic blood pressure temporarily increased to 100 mmHg, and he underwent traumatic pan scan.
Computed tomography (CT) revealed occipital fracture, cerebral contusion, cervical fracture (C2-C4), multiple left rib and sternal fractures with left-dominant bilateral hemothorax (Figure ).
He entered a shock state again after the CT examination and underwent transfusion again, but he then entered cardiac arrest. He underwent emergency bilateral thoracotomy with a normal surgical knife (no electrocautery) at the spine position. The initial bleeding amount in the bilateral thorax exceeded 1 L in addition to over 500 mL of blood that was drained via the chest drainage tube before thoracotomy. A bleeding tendency was also recognized at the skin incision sites. Gauze was packed into multiple bleeding sites, including venous hemorrhaging induced by the rib fractures, and the chest was closed. During damage surgery, he obtained spontaneous circulation after massive transfusion and the administration of fresh-frozen plasma, cryoprecipitate and human prothrombin complex.
The results of a biochemical blood analysis on arrival were as follows: white blood cell count, 15,000/μL; hemoglobin, 13.0 g/dL; platelet count, 6.0×104/μL; total protein, 4.1 g/dL; glucose, 357 mg/dL; HbA1C, 6.3%; total bilirubin, 0.7 mg/dL; aspartate aminotransferase, 38 IU/L; alanine aminotransferase, 20 IU/L; blood urea nitrogen, 23.1 mg/dL; creatinine, 1.13 mg/dL; sodium, 140 mEq/L; potassium, 4.8 mEq/L; chloride, 106 mEq/L; C-reactive protein, 0.04 mg/dL; prothrombin time international normalized ratio, 2.91; activated partial thromboplastin time, 85.0 (27.0) seconds; fibrinogen, 80 mg/dL; and fibrinogen fibrin degradation product, 960 μg/mL. He was transferred to the intensive care unit.
He received 36 units of packed red blood cells, 16 units of fresh-frozen plasma and 30 units of packed platelets to maintain circulation after admission. On the second hospital day, he received a second-look operation for the removal of the gauze, hemostasis, irrigation of thoracic cavity and placement of chest drainage tubes in the operation room. On the sixth hospital day, he became complicated with pneumonia and underwent tracheostomy. He also was complicated with thrombotic microangiopathy, resulting in multiple cerebral infarctions and foot necrosis. After these complications had improved, he regained consciousness and achieved spontaneous breathing without mechanical ventilation and stable circulation, resulting in his being able to walk with assistance, at least for a little while.
However, he became septic and developed hypoxia again, and CT and gastroscopy on the 28th hospital day revealed left pyothorax and emphysematous gastritis (Figure ). Cultures of both pyothorax and blood showed extended-spectrum β-lactamase (ESBL) Escherichia coli, which was treated by drainage and carbapenem administration.
Pyothorax and emphysematous gastritis improved, but he became complicated with repeated aspiration pneumonia after starting oral intake. CT on the 81st hospital day for evaluation of a recurrent fever revealed emphysematous cystitis (Figure ), which was treated by indwelling balloon and carbapenem administration again. The culture of the urine revealed ESBL E. coli.
After these treatments, his vital signs stabilized. He was transferred to another hospital for rehabilitation of dysphagia and disused muscle atrophy.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [23.1, 'mg/dL'], 'Glucose': [357.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",308.08333,292.67916,323.4875,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 23.1 mg/dL. 
The concentration of glucose is 357.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (23.1 / 2.8) + (23.1 / 18) = 308.08333 mmol/L.The patient's calculated serum osmolality concentration is 308.08333 mmol/L. This is equalivalent to 308.08333 mOsm/kg."
5734,30,Serum Osmolality,lab test,decimal,pmc-2804727-1,Extracted,"27 years old married Indian female with Indoaryan ethinicity presented to the hospital with a history of sudden onset palpitation, sweating with cold hands and feet, since the last 3 months. These symptoms were intermittent and usually used to last for 1-5 minutes. There was no history of syncope, chest pain, breathlessness, hemoptysis, fever, history suggestive of rheumatic heart disease or any substance abuse. 1 year back patient had fever which lasted for 2 weeks along with enlarged preauricular lymph node.
FNAC of the node had revealed it to be a non-caseating granulomatous pathology. Patient was put on anti-tubercular therapy by family physician that she continued for 9 months. There is also history of anterior uveitis 6 months back and 4 months back she had infra-nuclear type of facial palsy. She had complete recovery from these symptoms. She was put on proton pump inhibitors since last 3 months by her treating physician attributing her complaints of palpitation and uneasiness to some epigastric discomfort.
On examination patient was conscious, oriented, had mild pallor but no icterus, cyanosis, edema or clubbing. She had a small non-tender lymph node palpable, in her left submandibular region. Her blood pressure was 100/70 mmHg with no postural drop, Pulse; 80/mt, regular. She was afebrile and had no features of respiratory distress.
Investigations revealed Hb-9 g/dl, W.B.C count- 8000/μL, Platelet count- 2 lakh/μL, E.S.R- 30 mm, Peripheral blood film- mild hypochromic picture, Blood sugar- 60 mg/dl, Urea-21 mg/dl, creatinine- 1 g/dl, Albumin- 3.5 g/dL, SGOT- 137 U/L, SGPT- 101 U/L, Alkaline Phosphatase- 111 U/L, Serum Calcium- 1.0 mmol/l, Serum Sodium- 137 meq/l, Serum Potassium- 3.7 mEq/l. Serum amylase- 72 U/L. Her X-Ray chest showed bilateral hilar prominence. Angiotensin converting enzyme levels were 209.7 (Normal = 65 to 114.4). An electrocardiogram showed ventricular ectopics (Trigeminy) during the episode of palpitation (Figure ). She was put on beta-blocker and a holter cardiac study was done. Patient was managed in cardiac care unit for continuous ECG monitoring. On continuous cardiac monitoring it was found that she was having recurrent sustained ventricular tachycardias completely coinciding with her feeling of palpitation and sweating (Figure ). Each Ventricular tacvhycardia lasted for 30 sec to 2 minutes. Her blood pressure remained stable during the arrhythmias. After a loading dose of continuous infusion of amiodarone, frequency of stable Ventricular tacvhycardias decreased but persisted and a she was then chemically cardioverted with continuous infusion both amiodarone and lidocaine. Echocardiography was done which showed only trivial Mitral Regurgitation, with no evidence of Congestive heart failure with preserved ejection fraction.
CECT chest showed significant anterior mediastinal and bilateral hilar lymphadenopathy with FNAC of hilar nodes showing features of non-caseating granuloma. Endomyocardial biopsy was performed at the interventricular septum. Cardiac biopsy showed non-caseating granulomata, highly suggestive of a diagnosis of cardiac sarcoidosis (Figure ). A diagnosis of cardiac sarcoid was made on the basis of these CECT findings, histology, and the clinical picture.
Patient was simultaneously put on prednisolone 60 mg/day and shifted to oral amiodarone 200 mg tid. Due to poor financial status of the patient, implantation of intracardiac defibrillator was not possible in our case. Patient was discharged in a good clinical condition after 7 days of hospital stay.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [21.0, 'mg/dL'], 'Glucose': [60.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",284.83333,270.59166,299.075,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 21.0 mg/dL. 
The concentration of glucose is 60.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (21.0 / 2.8) + (21.0 / 18) = 284.83333 mmol/L.The patient's calculated serum osmolality concentration is 284.83333 mmol/L. This is equalivalent to 284.83333 mOsm/kg."
5735,30,Serum Osmolality,lab test,decimal,pmc-8415682-1,Extracted,"A 27-year-old unmarried female with premorbid history of generalized anxiety disorder (GAD) presented to us with first the episode of generalized tonic-clonic seizure on the previous day. About one week prior to ictus, she was discharged from another hospital with the diagnosis of SARS-CoV-2 infection. According to the eye witness, she had a sudden up-rolling of eyes along with tonic-clonic movements of all limbs followed by lateral tongue bite and fall with injuries of forehead and black eye (left side). The seizure lasted for about 2 minutes. After convulsion, she had post-ictal confusion and lethargy which persisted for about an hour. She was continuing SSRI (Escitalopram 10 mg) for her anxiety disorder. There was no family history of seizure, stress, sleep deprivation, and substance abuse. It was also not associated with fever, headache, neck stiffness, photophobia, nausea, and vomiting. No history of previous traumatic head injury, paresis, visual impairment, speech impairment, and involuntary movements. Her menstrual cycle was normal and regular. She had no additional systemic disease. She received Favipiravir (11600 mg), during her SARS-CoV-2 infection. She was hemodynamically stable with normal sensorium. Neurological and other clinical examinations were normal except blackeye on left side. The cause of the seizure was undetermined at that moment.
Her laboratory analysis includes Hb-10.2 g/dL (n = 12–15.0 g/dL), TLC-8700/cu.mm (n = 4000–11000/cu.mm), ESR-16 (n = <30), FBS-106 mg/dL (n = 80–120 mg/dL), Na+-138 mEQ/L (n = 130–145 mEQ/L), K+-4.2 mEQ/L (n = 3.4–5.5 mEQ/L), Urea-22 mg/dL (n = 7–20 mg/dL), creatinine-0.7 mg/dL (n = 0.7–1.3 mg/dL), Ca++-9.2 mg/dL (8.5–10.2 mg/dL), and Mg++-1.7 mg/dL (n = 1.7–2.2 mg/dL). Other common infections like malaria and dengue were excluded. A chest X-ray and ECG were normal. MRI Brain showed [] bi-frontal FLAIR hyper-intense areas suggesting focal cerebritis. Inter-ictal EEG [] showed no epileptiform discharges, but theta background (possibly post-ictal changes) CSF study showed mild elevation of protein 62 mg/dL (normal: 20–40) with cell count of 10 (all lymphocytes). CSF viral screening was negative. Serum autoimmune profile, antinuclear antibody, anti-TPO antibody, and para-neoplastic antibody panel were negative.
She was started with Levetiracetam 500 mg twice daily. She was also prescribed Midazolam Nasal spray as SOS basis. SSRI was advised to continue as earlier. She was well counseled about the provoking and risk factors of seizure and also advised not to miss dose.
After 6-week follow-up in OPD, she was clinically stable and had no side effects of Levetiracetam. Repeat MRI Brain and EEG were normal []. No further episode of seizure was occurred. In addition, she was doing her regular day-to-day activities.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [138.0, 'mEq/L'], 'Glucose': [106.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [22.0, 'mg/dL']}",289.74603,275.25873,304.23333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 22.0 mg/dL. 
The concentration of glucose is 106.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (22.0 / 2.8) + (22.0 / 18) = 289.74603 mmol/L.The patient's calculated serum osmolality concentration is 289.74603 mmol/L. This is equalivalent to 289.74603 mOsm/kg."
5736,30,Serum Osmolality,lab test,decimal,usmle-5196,Extracted,"A 28-year-old woman presents to the emergency department with shortness of breath. She immigrated from Uganda two months ago. She reports cough with occasional blood-tinged sputum and night sweats for the past week. She denies any chest pain or discomfort currently. The patient denies any sexual activity or intravenous drug use. She denies any history of cancer in her family. She currently lives in an apartment with several other female migrant workers. She received a vaccination against tuberculosis when she lived in Uganda. Her temperature is 99°F (37.2°C), blood pressure is 110/70 mmHg, pulse is 100/min, respirations are 20/min, and oxygen saturation is 94% on room air. Breath sounds are decreased in the left posterior lower and middle lung fields; egophony is present on the left middle lung field. The remainder of the physical exam is unremarkable. A complete blood count and basic metabolic panel are obtained:

Serum:
Na+: 135 mEq/L
Cl-: 100 mEq/L
K+: 3.5 mEq/L
HCO3-: 26 mEq/L
BUN: 10 mg/dL
Glucose: 105 mg/dL
Creatinine: 0.6 mg/dL

Leukocyte count: 20,000/mm^3
Segmented neutrophils: 69 %
Bands: 10 %
Eosinophils: 2 %
Basophils: 1 %
Lymphocytes: 25 %
Monocytes: 3 %

Hemoglobin: 11 g/dL
Hematocrit: 33 %
Platelet count: 400,000/mm^3

An electrocardiogram reveals sinus tachycardia without acute ST-T wave changes. Chest radiography is obtained in Figure A.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [135.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [10.0, 'mg/dL'], 'Glucose': [105.0, 'mg/dL']}",279.40476,265.43452,293.375,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 135.0 mEq. To convert from 135.0 mEq to mmol, convert from mEq to mmol. The compound 135.0 has a valence of 1, and so divide the valence by the value of mEq to get, 135.0 mEq/(1 mEq/mmol) = 135.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mEq sodium/L converts to 135.0 mmol sodium/L. 
The concentration of bun is 10.0 mg/dL. 
The concentration of glucose is 105.0 mg/dL. 
Plugging these values into the equation, we get 2 * 135.0 + (10.0 / 2.8) + (10.0 / 18) = 279.40476 mmol/L.The patient's calculated serum osmolality concentration is 279.40476 mmol/L. This is equalivalent to 279.40476 mOsm/kg."
5737,30,Serum Osmolality,lab test,decimal,pmc-4078418-1,Extracted,"A 52-year-old Asian Indian man was brought by family members to the nephrology department of our hospital with complaints of sudden onset of generalized involuntary limb movements associated with mildly altered mental status, gait imbalance, and slurred speech that began 2 days earlier. Patient's relatives noticed in him recent onset of confusion, frequent amnesia, loss of alertness, disorientation, defects in judgment, poor regulation of emotions, and alterations in his perception ability, psychomotor skills, and behavior. Patient complained of recent onset of inability to walk straight. He was a known case of ESRD secondary to Type 2 diabetes mellitus for many years. He was being treated with regular hemodialysis thrice a week for 4 years. There was no recent history indicating episodes of hypoglycemia or hypotension. There was no previous history of movement disorders. Family history was unremarkable.
Clinical examination revealed him to be normotensive with a blood pressure of 120/80 mm Hg. He was conscious, but mildly confused. Generalized chorea was noted mainly involving the limbs and the face. No signs of myoclonus, asterixis, or Parkinsonism were noted. Laboratory investigations indicated raised blood urea and serum creatinine levels and slight metabolic acidosis. Blood urea nitrogen level was 30.7 (normal 1.7-8.3) mmol/L and serum creatinine level was 1073 (normal 62-124) μmol/L. The other findings were as follows: serum bicarbonate level 16 (normal 21–28) mmol/L, hemoglobin level 10.1 (normal 13-17) g/dL, random blood glucose level 10.7 (normal 3.3-5.5) mmol/L, corrected serum calcium 1.98 (normal 2.1–2.6) mmol/L, serum phosphorus 1.39 (normal 0.87-1.45) mmol/L, serum potassium 4.1 (normal 3.6-5.1) mmol/L, and serum sodium 135 (normal 135-145) mmol/L. Serum parathormone, blood iron and blood lactate levels, and total iron binding capacity were normal.
Magnetic resonance imaging (MRI) of the brain was performed on the day of the visit. The diffusion-weighted (DW) images revealed hyperintense/bright signal in the basal ganglia bilaterally. Reduced apparent diffusion coefficient (ADC) values were demonstrated in the central parts of the bilateral basal ganglia and increased ADC values were demonstrated in the periphery [Figure and ].
Symmetrical hypointense areas were noted on T1-weighted images involving the basal ganglia bilaterally []. T2-weighted, fluid attenuation inversion recovery (FLAIR), and T2*-weighted images showed symmetrical hyperintense areas involving the basal ganglia bilaterally [Figure –].
Diagnosis of reversible and symmetrical lesions of the basal ganglia bilaterally related to diabetic nephropathy and chronic renal failure was made and frequency of hemodialysis was increased from three to five sessions per week. The increased frequency of hemodialysis was continued for 2 weeks. The altered mental status, behavioral changes, and slurred speech resolved within 3 days. The generalized chorea resolved completely within 6 days. After a week, the blood urea level regressed to 8 mmol/L and the serum creatinine level reduced to 308 μmol/L. He was not prescribed any particular medicine including steroids or clonazepam. Follow-up MRI of brain was performed 4 weeks after the first one, which showed complete resolution of the basal ganglial lesions bilaterally []. No evidence of any residual lesions was seen. Regular thrice-weekly hemodialysis was continued. He remained free of chorea and slurred speech and maintained normal mental status during a 4-month follow-up.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [30.7, 'mmol/L'], 'Glucose': [10.7, 'mmol/L'], 'Sodium': [135.0, 'mmol/L']}",311.43129,295.85973,327.00285,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.0 mmol/L. 
The concentration of bun is 30.7 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 30.7 mmol. To convert 30.7 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 30.7 mmol bun * 0.001 mol/mmol = 0.0307 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0307 mol bun * 28.02 g/mol = 0.86021 g bun. To convert 0.86021 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.86021 g bun * 1000.0 mg/g = 860.21 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 860.21 mg bun/10.0 dL = 86.021 mg bun/dL. The concentration value of 30.7 mmol bun/L converts to 86.021 mg bun/dL. 
The concentration of glucose is 10.7 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 10.7 mmol. To convert 10.7 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 10.7 mmol glucose * 0.001 mol/mmol = 0.0107 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0107 mol glucose * 180.16 g/mol = 1.92771 g glucose. To convert 1.92771 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 1.92771 g glucose * 1000.0 mg/g = 1927.71 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1927.71 mg glucose/10.0 dL = 192.771 mg glucose/dL. The concentration value of 10.7 mmol glucose/L converts to 192.771 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 135.0 + (86.021 / 2.8) + (86.021 / 18) = 311.43129 mmol/L.The patient's calculated serum osmolality concentration is 311.43129 mmol/L. This is equalivalent to 311.43129 mOsm/kg."
5738,30,Serum Osmolality,lab test,decimal,pmc-6323657-1,Extracted,"A 58-year-old Japanese man with an 8-year history of T2DM had a symptom of pain in his right lower leg and visited the emergency room in Kawasaki Medical School. Previously, he had felt the same pain in the same region when his blood glucose was very high and thereby he was diagnosed as having T2DM 8 years before.
He had acute osteomyelitis in his right lower leg when he was a baby. Except for this, he had no past history. He had no remarkable family history. He was a barber; he smoked tobacco (pack-years = 0.75 pack/day × 40 years) and he drank alcohol every day. After the episode of acute osteomyelitis when he was a baby, there was no problem in his legs until he had general fatigue and felt pain in his right lower leg at the age of 50. He visited the emergency room. His vital signs were as follows: heart rate 76 beats/minute, blood pressure 116/70 mmHg, and body temperature 36.4 °C. He had a symptom of slight local swelling and heat sensation in the same area with pain in his right lower leg, but there were no findings in physical and neurological examinations. In addition, there was no ulcer or injury on his skin surface. Laboratory data (Table ) were as follows: white blood cell count, 7400/μL (neutrophil 64.7%); C-reactive protein (CRP), 2.50 mg/dl; plasma glucose, 382 mg/dL; hemoglobin A1c (HbA1c), 11.7%. He was diagnosed as having T2DM, but he had no diabetic complications. Magnetic resonance imaging (MRI) of his lower limbs showed an abscess and inflammatory change in his right lower leg (Fig. ). An axial T1-weighted (T1W) image of his right lower leg showed a slightly lower intensity, and an axial T2-weighted (T2W) image showed a markedly higher intensity (Fig. , upper panels). Based on these findings, we made a diagnosis of acute exacerbation of chronic osteomyelitis and T2DM. We thought that it would be better to hospitalize him and start administering antibiotics via a drip, but he did not agree to the hospitalization. Therefore, as an alternative, we started 300 mg/day of cefcapene pivoxil hydrochloride hydrate and insulin therapy (18 units of aspart) on an out-patient basis. After starting insulin therapy, his blood glucose level gradually decreased, and his leg pain was also gradually mitigated. Finally, his leg pain disappeared 2 weeks later. His CRP became within normal range, and 3 months later the focus in his right lower leg was markedly reduced on MRI. In addition, the focus was not detected in ultrasonography of the right tibia site. Just in case, however, we continued antibiotics therapy for 4 months. Since his glycemic control was improved 2 months later, we stopped insulin therapy and started orally administered anti-diabetic drugs.
He was then followed up as an out-patient with T2DM for approximately 8 years. The medication at that time was 1000 mg/day of metformin, 25 mg/day of alogliptin, 15 mg/day of pioglitazone, and 50 mg/day of ipragliflozin. However, he did not take the medicine for approximately 8 months on his own judgement at the age of 58. After his interruption of therapy for 8 months, he felt the same pain in the same right lower leg again. He immediately visited our hospital. He had symptoms of slight local swelling and heat sensation together with pain in the same area in his right lower leg, but again there were no findings in physical and neurological examinations at this time. His vital signs were as follows: heart rate 99 beats/minute, blood pressure 130/70 mmHg, and body temperature 37.0 °C. He had a symptom of slight local swelling and heat sensation in the same area with pain in his right lower leg, but there was no ulcer or injury on his skin surface. Laboratory data were as follows: white blood cell count, 6680/μL (neutrophil 63.4%); CRP, 0.32 mg/dl; erythrocyte sedimentation rate (ESR), 31 mm/hour; plasma glucose, 652 mg/dL; HbA1c, 6.9%; glycoalbumin 46.1%. Other laboratory data were as follows: red blood cell, 476 × 104/μL; hemoglobin (Hb), 15.9 g/dL; platelet, 25.1/μL; total protein (TP), 7.6 g/dL; albumin (Alb), 4.4 g/dL. Liver and renal function were within normal range as follows: aspartate aminotransferase (AST), 39 U/L; alanine aminotransferase (ALT), 50 U/L; γ-glutamyl transpeptidase (γ-GTP), 51 U/L; lactate dehydrogenase (LDH), 172 U/L; creatinine (Cre), 0.54 mg/dL; blood urea nitrogen (BUN), 13 mg/dL; Na, 131 mEq/L; K, 4.4 mEq/L; Cl, 96 mEq/L. Pathogenic bacteria were not detected. He had no diabetic complications, probably because his glycemic control was relatively good before the interruption of therapy. His leg MRI showed a spreading of the abscess and inflammatory change in his right lower leg (Fig. , lower panels). We hospitalized him in our institution but he did not agree to undergo surgery for remission. Therefore, we started 3.0 g/day of sulbactam sodium/ampicillin sodium and insulin therapy (24 units of aspart and 20 units of glargine). After starting insulin therapy, his blood glucose level gradually decreased, and his leg pain was also gradually mitigated. Local swelling and heat sensation disappeared approximately 5 days later. Finally, his leg pain disappeared approximately 2 weeks later, and he was discharged from our hospital. Just in case, however, we continued antibiotics therapy (450 mg/day of rifampicin and 4 g/day of trimethoprim) for approximately 2 months. After a total of 3-month antibiotics therapy during hospitalization and after discharge, we stopped antibiotics therapy. He was then followed up for approximately 6 months, and his leg MRI showed a reduction of the abscess and inflammatory change in his right lower leg. He had no symptoms and/or problems, and his inflammation markers remained within normal levels for at least 6 months.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [13.0, 'mg/dL'], 'Glucose': [652.0, 'mg/dL'], 'Sodium': [131.0, 'mEq/L']}",302.86508,287.72183,318.00833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 131.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 131.0 mEq. To convert from 131.0 mEq to mmol, convert from mEq to mmol. The compound 131.0 has a valence of 1, and so divide the valence by the value of mEq to get, 131.0 mEq/(1 mEq/mmol) = 131.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 131.0 mEq sodium/L converts to 131.0 mmol sodium/L. 
The concentration of bun is 13.0 mg/dL. 
The concentration of glucose is 652.0 mg/dL. 
Plugging these values into the equation, we get 2 * 131.0 + (13.0 / 2.8) + (13.0 / 18) = 302.86508 mmol/L.The patient's calculated serum osmolality concentration is 302.86508 mmol/L. This is equalivalent to 302.86508 mOsm/kg."
5739,30,Serum Osmolality,lab test,decimal,usmle-6059,Extracted,"A 45-year-old African American man presents to his primary care physician with a chief concern of constant fatigue. He states that it started a few days ago and has been steadily worsening. The patient has a past medical history of constipation and depression and is currently taking TMP-SMX for a urinary tract infection. He went to the emergency department for an episode of severe and diffuse pain 2 months ago. The patient is a vegan and lives with his wife. His temperature is 98.3°F (36.8°C), blood pressure is 129/68 mmHg, pulse is 100/min, respirations are 15/min, and oxygen saturation is 98% on room air. Laboratory values are obtained and shown below.

Hemoglobin: 9 g/dL
Hematocrit: 30%
Leukocyte count: 6,500/mm^3 with normal differential
Platelet count: 197,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 5.3 mEq/L
HCO3-: 25 mEq/L
BUN: 27 mg/dL
LDH: 544 U/L
Coombs test: Positive
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 9.9 mg/dL
AST: 12 U/L
ALT: 10 U/L

A peripheral smear is ordered as seen in Figure A.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [27.0, 'mg/dL'], 'Glucose': [99.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",293.14286,278.48572,307.8,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 27.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (27.0 / 2.8) + (27.0 / 18) = 293.14286 mmol/L.The patient's calculated serum osmolality concentration is 293.14286 mmol/L. This is equalivalent to 293.14286 mOsm/kg."
5740,30,Serum Osmolality,lab test,decimal,pmc-7034958-1,Extracted,"A 17-year-old female patient with complaints of “chest tightness, shortness of breath for 4 days and blurred consciousness for 5 hrs” was admitted to our hospital in July 2017. The patient had symptoms of nausea, vomiting, drinking and polyuria one week prior. At that time, she was given symptomatic treatment for gastroenteritis, and no improvement was observed. The symptoms of chest tightness and shortness of breath appeared 4 days prior and were not considered in the treatment. One day ago, chest tightness and shortness of breath were obviously aggravated. Mediastinal gas was found by a chest CT examination in the local hospital, so she was sent to our hospital through the emergency channel. On the way to the hospital, she exhibited a gradual vagueness of consciousness and a slow response. The patient denied that she had a previous history of diabetes or other diseases, we learned that the patient had a habit of drinking sweet drinks (such as Coca Cola, Sprite), and the patient did not smoke or drink alcohol.
According to the physical examination, her temperature was 36.6°C, pulse was 130 bpm, respiratory rate was 35 per minute, and blood pressure was 108/61 mmHg. She had poor spirits, lethargy, mild dehydration, and a small amount of crepitation at the entrance to the anterior thoracic neck, her breathing was deep and rapid (Kussmaul breathing), she were smelled the smell of rotten apple, and both lungs were auscultated and exhibited clear sounds without dry or wet sounds. Her heart rate was 130 bpm (normal rhythm), the precordial auscultation heart sound was remote, the friction sound was synchronized with the heart rhythm (Hamman sign, the unique sign of pneumopericardium), and pathological noises were not heard.
According to the assistant examinations, the chest CT showed extensive air in the neck subcutaneously and mediastinum, which had spread along the bronchovascular bundle, and no pneumothorax was found in the bilateral chest (). The arterial blood gas analysis results were as follows (oxygen inhalation 3 L/min): pH of 6.90 (reference range: 7.35 to 7.45), partial pressure of oxygen of 144 mmHg (83~108 mmHg), partial pressure of carbon dioxide of 10 mmHg (35~48 mmHg), residual alkali could not be detected, and bicarbonate concentration of 9.0 mmol/L. Her white blood cell count was 22.45 × 109/L (4–10×109/L), neutrophil level was 79.1% (50–70%), blood glucose concentration was 40.62 mmol/L (3.5–6.1 mmol/L), HbA1C1 level was 3.5% (4.0–6.0%), creatinine concentration was 123.6 μmol/L (40–97 μmol/L), urea nitrogen concentration was 7.2 mmol/L (1.7–8.3 mmol/L), serum potassium concentration was 3.24 mmol/L (3.5–5.5 mmol/L), serum sodium concentration was 119.0 mmol/L (135–155 mmol/L), serum chlorine concentration was 89 mmol/L (90–110 mmol/L), glutamic pyruvic transaminase concentration was 13.2 U/L (0–40 U/L), glutamic oxaloacetic transaminase concentration was 19.9U/L (0–40U/L), and total protein concentration was 72.4g/L (60.0–85.0g/L). Her urine glucose level was 3+, urinary ketone body level was 3+, urinary protein level was 2+, and urinary pH level was 5.0 (6.0–7.0).
After admission, she underwent oxygen inhalation, mediastinal gas drainage through the neck, massive fluid replacement, and correction of acidosis, regulating her blood glucose level and other symptomatic support treatment was provided. The symptoms of nausea and vomiting were gradually relieved, the breathing gradually became stable, and the heart rhythm dropped to the normal range after 24 hrs. Three days later, when the patient’s condition was stable, the oesophageal barium meal examination excluded oesophageal rupture. The accumulation of gas in the mediastinum of the patient evident in the chest CT had completely disappeared after 10 days. Standard hypoglycaemic therapy was continued after discharge. To date, which is after approximately 2 years, the patient has not exhibited recurrence.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [7.2, 'mmol/L'], 'Glucose': [40.62, 'mmol/L'], 'Sodium': [119.0, 'mmol/L']}",285.86111,271.56805,300.15417,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 119.0 mmol/L. 
The concentration of bun is 7.2 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 7.2 mmol. To convert 7.2 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 7.2 mmol bun * 0.001 mol/mmol = 0.0072 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0072 mol bun * 28.02 g/mol = 0.20174 g bun. To convert 0.20174 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.20174 g bun * 1000.0 mg/g = 201.74 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 201.74 mg bun/10.0 dL = 20.174 mg bun/dL. The concentration value of 7.2 mmol bun/L converts to 20.174 mg bun/dL. 
The concentration of glucose is 40.62 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 40.62 mmol. To convert 40.62 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 40.62 mmol glucose * 0.001 mol/mmol = 0.04062 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.04062 mol glucose * 180.16 g/mol = 7.3181 g glucose. To convert 7.3181 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 7.3181 g glucose * 1000.0 mg/g = 7318.1 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 7318.1 mg glucose/10.0 dL = 731.81 mg glucose/dL. The concentration value of 40.62 mmol glucose/L converts to 731.81 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 119.0 + (20.174 / 2.8) + (20.174 / 18) = 285.86111 mmol/L.The patient's calculated serum osmolality concentration is 285.86111 mmol/L. This is equalivalent to 285.86111 mOsm/kg."
5741,30,Serum Osmolality,lab test,decimal,pmc-3342550-1,Extracted,"A 59-yr-old man was admitted to our hospital because he had exhibited progressive lethargy and confusion since the early morning. He had often complained of fatigue over the previous 3 months. Three days prior to presentation, he had eaten a large amount of dog meat at a party, become nauseated, and vomited. The next day, he had eaten chicken and freshwater snails, had again become nauseated, and developed severe vomiting. On the day of admission, he failed to arise at his normal time and exhibited inappropriate behavior and drowsiness.
During his childhood, the patient had suffered recurrent abdominal pain and periodic episodes of convulsions, but he had not experienced any seizures in adulthood. On examination, the patient was in a semi-coma; his Glasgow Coma Scale score was 10/15, and he was disoriented in time, place, and person. His vital signs were stable, with a blood pressure of 150/80 mmHg, pulse rate of 84/min, respiratory rate of 24/min, and body temperature of 36℃. Laboratory investigations showed that he had hyperammonemia (143.8 mM), elevated liver enzymes (alanine aminotransferase, 179 U/L; aspartate aminotransferase, 91 U/L), a total bilirubin level of 1.91 mg/dL, and a blood glucose level of 106 mg/dL. His blood urea nitrogen and serum creatinine levels were 17.7 mg/dL and 1.01 mg/dL, respectively. Blood analysis revealed mild leukocytosis (10.41 × 103 leukocytes/µL) and a normal hemoglobin level, platelet count, and clotting profile. Serum electrolyte analysis showed mild hypernatremia (149 mEq sodium/L), but serum potassium and chloride levels were within normal range. Results of a toxicology screen were normal.
Further investigations revealed no evidence of gastrointestinal bleeding, and computed tomography (CT) and diffusion-weighted magnetic resonance imaging revealed no brain lesions. Abdominal CT imaging did not show any abnormality. The cerebrospinal fluid was normal upon examination.
Although hyperammonemia was suspected as the cause of the patient's mental changes, there was no evidence of chronic liver disease. Despite the administration of a lactulose enema, the patient's serum ammonia level increased to 370 mM and he remained confused, leading us to initiate acute hemodialysis. During the procedure, the patient had a generalized tonic-clonic seizure, for which 1 mg of lorazepam was administered intravenously. The seizure subsided, but the patient continued to move convulsively, leading to several additional injections of intravenous lorazepam. A diagnosis of nonconvulsive status epilepticus was made, and the antiepileptic drug levetiracetam was administered.
After the initial session of hemodialysis, the patient's serum ammonia level had decreased to 170 mM, but it soon rose to 228 mM. Plasma and urine amino acid analysis and urine organic acid quantitation were performed. Under suspicion of a urea cycle disorder, arginine (3 g) and sodium benzoate (3 g) were administered via nasogastric tube every 4-6 hr. Dextrose solution (10%) was supplied intravenously, and a protein-free formula was supplied via a feeding tube.
By the morning of the next day, the patient's serum ammonia level had decreased to 36 mM. However, because it rose to 107 mM by the afternoon, and the patient was still semi-comatose, hemodialysis was performed one more time. At that time, an electroencephalogram did not show any signs of epileptic discharge.
After the second hemodialysis session, the patient's serum ammonia level stabilized at less than 30 mM. A plasma amino acids analysis revealed elevated ornithine (196 µM; normal 19-81 µM), decreased citrulline (3 µM; normal 19-62 µM), and elevated glutamine and lysine. Urine organic acids analysis revealed highly elevated urinary orotic acid (603.5 mg/mg creatinine) and a mild urinary uracil peak. No liver biopsy or genetic analysis was performed.
The accumulated evidence led to a diagnosis of late-onset ornithine carbamoyltransferase deficiency. After 5 days, the patient's mental status returned to normal. He continued to receive sodium benzoate (3 g) and arginine (3 g) three times daily. The protein-free formula, which was administered continuously, was gradually changed to increase the dietary protein without a significant rise in serum ammonia levels (). The patient was discharged home after 2 weeks with instructions to continue the medication and formula. His family received special counseling on diet and emergency management before his discharge.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [149.0, 'mEq/L'], 'Glucose': [106.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [17.7, 'mg/dL']}",310.21032,294.6998,325.72084,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 149.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 149.0 mEq. To convert from 149.0 mEq to mmol, convert from mEq to mmol. The compound 149.0 has a valence of 1, and so divide the valence by the value of mEq to get, 149.0 mEq/(1 mEq/mmol) = 149.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 149.0 mEq sodium/L converts to 149.0 mmol sodium/L. 
The concentration of bun is 17.7 mg/dL. 
The concentration of glucose is 106.0 mg/dL. 
Plugging these values into the equation, we get 2 * 149.0 + (17.7 / 2.8) + (17.7 / 18) = 310.21032 mmol/L.The patient's calculated serum osmolality concentration is 310.21032 mmol/L. This is equalivalent to 310.21032 mOsm/kg."
5742,30,Serum Osmolality,lab test,decimal,pmc-6796695-1,Extracted,"A 62-year-old man of Jehovah’s Witness faith developed a life threatening rapid progressive necrotizing fasciitis of his right lower extremity. His comorbidities consisted of type 2 diabetes mellitus, alcohol use disorder, nicotine use, and depression. He was non-compliant with his long-acting nocturnal insulin. The patient developed a non-healing right heel ulcer which began in the fall of the preceding year. He initially presented with his wound to the first health care institution 3 months later and was admitted for approximately 7 weeks. The patient subsequently underwent 4 surgical debridements and received IV antibiotics. Since that recent hospital admission, he had been following up at a local Wound Clinic.
Three weeks after discharge the patient subsequently developed increasing severe lightheadedness, generalized weakness, and dizziness which prompted patient to be evaluated in the Emergency Department (ED) of the second institution. In the ED the patient vitals were: temperature 37 °C, pulse 86 beats/min, respiratory rate 25 breaths/min, oxygen saturation of 98%, and a blood pressure of 98/59 mmHg. Physical examination was significant for right heel ulcer with purulent drainage. Initial laboratory results were significant for: WBC 32,700/mm3, hemoglobin 7.3 g/dL, MCV 83.4 fL, sodium 128 mmol/L, Creatinine 3.38 mg/dL, BUN 45 mg/dL, lactate 3.8 mmol/L and blood glucose level of 606 mg/dL. The patient was then admitted with septic shock, a heel ulcer with suspected osteomyelitis, and acute kidney injury. He was treated with IV antibiotics and epoetin alfa and iron sucrose parenterally. In-patient MRI of the right foot showed osteomyelitis of the calcaneus with a ruptured Achilles tendon and surrounding edema indicating infectious tenosynovitis. Subsequently during inpatient course, he developed severe right lower extremity pain and fever which prompted an emergent X-Ray of the right lower extremity. Imaging results showed prominent areas of subcutaneous emphysema throughout the soft tissue extending to the distal right femur suspicious for NF. The patient immediately underwent right-sided above the knee guillotine amputation with lateral thigh debridement. He was in critical condition post-op and a facility transfer was deemed necessary.
On arrival via ambulance to the intensive care unit trauma service at the 3rd institution (our hospital) the patient was in critical condition, with waxing and waning mentation, he was only oriented to self and examination revealed foul smelling AKA amputation wound which had crepitus to palpation. Significant laboratory results were: WBC of 24,800/mm3, hemoglobin 4.7 g/dL, MCV 75.4 fL, sodium 142 mmol/L, Creatinine 1.0, BUN 55 mg/dl, lactate 1.9 and serum glucose 300 mg/dL. The patient was resuscitated with IV fluids, IV antibiotic therapy, and pain management. He subsequently went for CT scan of the right residual limb to assess the extent of subcutaneous tissue involvement. Imaging showed subcutaneous emphysema extending to the neck of the femur (). Subsequently he had emergent operative wound debridement using a micro debridement tool to enhance bloodless surgery. Intraoperative discussion of a possible hip disarticulation and hemipelvectomy occurred with determination of a poor prognosis of survival. The patient therefore underwent 6 debridement surgeries over the next 14 days with the 1st surgery consisting of a revision amputation ().
Post operatively he improved significantly to a regular diet, stabilized vital signs, and normal mental status. The patient was discharged one month after initial admission to our institution to a rehabilitation facility. His wound at the time of discharge had healthy granulation tissue with a wound vac in place (). He was subsequently seen 2 weeks after at trauma surgeon’s office for his first outpatient follow up.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [55.0, 'mg/dL'], 'Glucose': [300.0, 'mg/dL'], 'Sodium': [142.0, 'mmol/L']}",320.30952,304.29404,336.325,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mmol/L. 
The concentration of bun is 55.0 mg/dL. 
The concentration of glucose is 300.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (55.0 / 2.8) + (55.0 / 18) = 320.30952 mmol/L.The patient's calculated serum osmolality concentration is 320.30952 mmol/L. This is equalivalent to 320.30952 mOsm/kg."
5743,30,Serum Osmolality,lab test,decimal,pmc-3470992-1,Extracted,"A 17-year-old South Asian man was referred to our department for recurrent episodes of generalized muscle weakness, fatigue and cramps from the age of two years. Hypokalemia was initially detected at the first episode and he was treated for periodic hypokalemic paralysis. Before the age of 12 years, these episodes were mild, readily improved with ringer lactate and potassium chloride by his treating physician and occurred only twice a year. Beyond the age of 12 years, these episodes gradually worsened in frequency and intensity to the point that they were refractory to previously administered therapies and sometimes required hospitalization.
His symptoms were aggravated by physical activity and hot weather, and were associated with polyuria, polydipsia, nocturia, paresthesias and occasional painless non-bloody diarrhea. He denied the use of any medication, including laxatives and diuretics. He also had a history of short stature and poor weight gain. His birth history was unremarkable but developmental landmarks were delayed. There was no family history of renal salt-wasting syndromes or delayed puberty. However, his parents were first cousins.
An examination revealed a thin and lean, but well-oriented adolescent with no acute distress. His height and weight were below the third percentile (weight 30kg; height 147cm). His blood pressure was 95/60mmHg with orthostatic changes. His sexual development was at Tanner Stage II.
Investigations at the admitting hospital revealed a normal leukocyte count, platelet count, hemoglobin level and erythrocyte sedimentation rate. His urea level was 34mg/dL, creatinine 0.9mg/dL and random blood glucose 105mg/dL. His estimated glomerular filtration rate based on the Modification of Diet in Renal Disease formula was 97.9ml/min per 1.73m2. His high blood urea nitrogen level was attributed to mild dehydration due to the hot weather. He was found to have metabolic alkalosis: pH 7.58, HCO3- 33.5, base excess +7.6. His serum electrolytes were as follows: sodium 124mmol/L, potassium 2.4mmol/L, calcium 6.5mmol/L and phosphate 3.4mg/dL. His serum magnesium level was not checked at that time. Serum albumin, creatine phosphokinase, free thyroxin, thyroid-stimulating hormone and parathyroid hormone levels were normal.
He was provisionally diagnosed with periodic hypokalemic paralysis and hypocalcemia. Treatment was started with potassium and calcium supplements. After one month, he showed little improvement and he was referred to our department for further evaluation.
Further laboratory tests revealed a low magnesium level (1.2mg/dl) and decreased 24-hour urinary excretion of calcium (25.9mg/24 h). Luteinizing hormone and follicle-stimulating hormone levels were also normal. His level of testosterone was low (0.85ng/mL, normal for his age 2.67 to 10.12ng/mL). Electrocardiography showed a normal sinus rhythm and prolonged QT interval. No abnormality was found on an abdominal X-ray, chest X-ray or brain magnetic resonance imaging. A renal ultrasound revealed a prominent pelvicalyceal system. An insulin tolerance test showed normal cortisol and growth hormone response.
Based on the findings of hypokalemic metabolic alkalosis without hypertension, severe hypomagnesemia and hypocalciuria, a diagnosis of GS was made. No organic cause of hypogonadism was established and the sex hormone findings were attributed to delayed puberty. Treatment was started with oral supplementation of potassium, magnesium and calcium along with spironolactone and liberal salt intake. Our patient and his parents were also counseled about delayed puberty.
A limitation to this case report was that the diagnosis could not be ascertained with sequencing of the implicated gene due to unavailability of genetic sequencing at the presenting hospital (Jinnah Hospital Lahore, Pakistan).",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [34.0, 'mg/dL'], 'Glucose': [105.0, 'mg/dL'], 'Sodium': [124.0, 'mmol/L']}",265.97619,252.67738,279.275,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 124.0 mmol/L. 
The concentration of bun is 34.0 mg/dL. 
The concentration of glucose is 105.0 mg/dL. 
Plugging these values into the equation, we get 2 * 124.0 + (34.0 / 2.8) + (34.0 / 18) = 265.97619 mmol/L.The patient's calculated serum osmolality concentration is 265.97619 mmol/L. This is equalivalent to 265.97619 mOsm/kg."
5744,30,Serum Osmolality,lab test,decimal,pmc-4731484-1,Extracted,"A 22-year-old Nepali male came to the Emergency Department of a teaching-hospital in central Nepal with chief complaint of sudden appearance of blisters on oral mucosa after taking Ibuprofen 400-mg tablets 8 hourly for 2 days for eye pain. He developed multiple maculae initially over trunk, then chest, face, lower limbs on the third day. He was admitted to the Emergency and upon examination, had extensive erythema (), necrosis, and exfoliating bullous detachment of the epidermis () and mucous membranes (conjunctival, oral, and genital), with a positive Nikolsky's sign. The body temperature was 38℃, respiratory rate being 24 breaths/min, pulse rate 110 beats/min, blood pressure 130/90 mm Hg, SPO2 98%, and glucose random blood sugar 91 mg/dL.
The laboratory analyses are as follows: Na+, 138.8 mmol/L; K+, 4.02 mmol/L; urea, 41.0 mg/dL; creatinine, 1.0 mg/dL; platelet count, 60,000 mm3, white blood cell, 3,600×106/L; hemoglobin, 11.8 g/dL; prothombin (test), 17.5 seconds; prothombin (control), 13.0 seconds; international normalized ratio, 1.37; packed cell volume, 32.05%; bleeding time, 3 minutes; clotting time, 9 minutes; immunodeficiency virus I&II, nonreactive; hepatitis B surface antigen, nonreactive; urine routine examination, pus cells (8–10); C-reactive protein level, 340 mg/L; aspartate aminotransferase, 85 IU/L; alanine aminotransferase, 150 IU/L; total proteins concentration, 50 g/L; and albumin, 20 g/L.
Skin biopsy revealed prominent cell death with basal vacuolar changes and lymphocyte infiltrates with haziness in the dermo-epidermal junction which corroborated the clinical diagnosis of SJS-TEN.
Ibuprofen was immediately withdrawn and the patient was transferred to the intensive care unit (ICU). On admission to ICU, arterial blood gas analyses are as follows: pH, –7.442; pCO2, 28.5; pO2, 95.5; HCO3, 19.7; blood urea nitrogen, 17.0 mg/dL; blood-sugar random, 162.0; antinuclear antibody enzyme linked immune sorbant assay method, negative.
Patient had extensive sloughing off the face () painful oral erosions with severe crusting of the lips and increased salivation. The plaques with vesicles, sloughed off more than 50% of body surface area which rendered difficulty to access vein on patients limbs. So, central venous pressure line insertion was done and enteral-nutrition was provided via a nasogastric tube. The patient's specific treatment with plasma exchange and fluid resuscitation with crystalloid infusions (1 mL/kg of body weight per hour) fine-tuned on the bases of the arterial blood pressure (>65 mm Hg), central venous pressure (≤10 mm Hg) and diuresis rate [] was done. The basis for early plasma exchange was to remove/reduce the level of residual ibuprofen and its metabolites, critical cytokines (tumor necrosis factor-alpha [TNF-α], interferon-gamma [IFN-γ]), and drug-induced inflammatory mediators (perforin, granzyme-B released from cytotoxic T-lymphocytes and granulysin secreted by cytotoxic T-lymphocytes and natural killer cells) from the circulation []. However, the plasma exchange remain unsupported by controlled studies []. Subsequent systemic treatment included intravenous Ceftriaxone 1.0 gm 12 hourly (microbial findings on skin: Staphylococcus aureus and Pseudomonas aeruginosa; the symptoms and signs being warm, tender, erythematous, and edematous plaque over lower extremities with ill-defined borders), intravenous immunoglobulins (IVIG) 1.0-g/kg body weight/day infused over 6 hours for 3 successive days and corticosteroids 0.5-mg/kg body weight. Intravenous tramadol 25 mg was given for analgesia as per the patient's condition. The patient recovered completely after 5 weeks of intensive systemic and topical treatment.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [138.8, 'mmol/L'], 'Glucose': [91.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [17.0, 'mg/dL']}",288.72698,274.29063,303.16333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.8 mmol/L. 
The concentration of bun is 17.0 mg/dL. 
The concentration of glucose is 91.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.8 + (17.0 / 2.8) + (17.0 / 18) = 288.72698 mmol/L.The patient's calculated serum osmolality concentration is 288.72698 mmol/L. This is equalivalent to 288.72698 mOsm/kg."
5745,30,Serum Osmolality,lab test,decimal,pmc-5649843-1,Extracted,"A 44-year-old African American female with history of peptic ulcer disease, mitral valve prolapse and anemia presented to the clinic for evaluation of epigastric abdominal pain, nausea and constipation. Review of systems was positive for weight loss of approximately 15 to 20 lbs and fatigue; negative for fever, hematochezia or melena. Medication consisted of dicyclomine, metoclopramide, sucralfate and ferrous sulfate recently prescribed by ER physician for abdominal symptoms. Past surgical history significant for total abdominal hysterectomy with bilateral salpingo-oophorectomy. Family history negative for colon cancer and her mother died from lung cancer at age 70. Physical examination revealed an obese female with blood pressue of 163/88 mmHg and epigastric tenderness to palpation. There were no palpable masses or lymphadenopathy detected. Stool guaic was negative. Laboratory investigation showed calcium level of 15.7 mg/dL, phosphorous 2.8 mg/dL, sodium 136 meq/L, potassium 3.5 meq/L, chloride 100 meq/L, bicarbonate 31 meq/L, BUN 30 mg/dL, creatinine 1.9 mg/dL, glucose 121 mg/dL, total protein 8.1 gm/dL, albumin 3.6 gm/dL, total bilirubin 0.4 mg/dL, SGOT 75 U/L, SGPT 50 U/L and alkaline phosphatase 227 U/L. White blood cell count was 11.3 K/mm3, HgB 8.6 gm/L, HCT 27.2 %, MCV 75.6 fL and platelet count 778 K/mm3, CEA 702 ng/mL. Intact PTH was not measured. Instead, the carboxy (C)-terminal PTH assay (includes C-terminal, intact PTH and midmolecule) was measured and found to be within normal limits at 48 ng/dL (reference range < 88 ng/dL; Specialty Laboratories, Valencia, CA).
She was admitted for evaluation and treatment of severe hypercalcemia. After administering IV pamidronate (Aredia) along with normal saline and IV furosemide, calcium level gradually declined from 15.7 to 10.1 mg/dL over a period of 7 days. CXR was normal and screening mammogram revealed BIRAD 2 benign findings. CT scan of abdomen with and without contrast showed multiple lesions within the liver (). Colonoscopy revealed a 3 cm ulcerated mass near the splenic flexure (biopsy showed moderately differentiated adenocarcinoma). EGD was normal. The following day after surgical consultation she was taken to the operating room for exploratory laparotomy undergoing segmental resection of the transverse colon, where the identified cancer was located (). Open core needle biopsy of a liver mass demonstrated adenocarcinoma compatible with metastasis from colon.
She was admitted on two additional occasions about 1 week apart, 6 days after initial hospital discharge, for refractory hypercalcemia associated with nausea, vomiting, lethargy and confusion. Temporary and partial response was observed to IV pamidronate, in addition to saline diuresis and IV furosemide, lowering calcium from 15.6 to 12.8 mg/dL over period of 10 days. On the second occasion, hypercalcemia was partially corrected with IV zoledronic acid (Zometa), along with saline diuresis and furosemide, dropping calcium from 16.2 to 13.1 mg/dL over 3 days. After being admitted to hospice, her condition continued to deteriorate and she died 7 weeks after initial hospital admission.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [30.0, 'mg/dL'], 'Glucose': [121.0, 'mg/dL'], 'Sodium': [136.0, 'mEq/L']}",289.43651,274.96468,303.90834,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.0 mEq. To convert from 136.0 mEq to mmol, convert from mEq to mmol. The compound 136.0 has a valence of 1, and so divide the valence by the value of mEq to get, 136.0 mEq/(1 mEq/mmol) = 136.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mEq sodium/L converts to 136.0 mmol sodium/L. 
The concentration of bun is 30.0 mg/dL. 
The concentration of glucose is 121.0 mg/dL. 
Plugging these values into the equation, we get 2 * 136.0 + (30.0 / 2.8) + (30.0 / 18) = 289.43651 mmol/L.The patient's calculated serum osmolality concentration is 289.43651 mmol/L. This is equalivalent to 289.43651 mOsm/kg."
5746,30,Serum Osmolality,lab test,decimal,pmc-3890728-1,Extracted,"A 46-year-old woman presented with general weakness that had lasted for several weeks. She was diagnosed with type 2 diabetes mellitus (DM) 15 years ago and began continuous ambulatory peritoneal dialysis (CAPD) three years ago. An abdominal sonography obtained before CAPD began revealed a normal liver. The patient received CAPD with four daily exchanges of 2 L each time and switched to three exchanges with 2.5% glucose and one with 4.25% glucose solution; this was required because the ultrafiltration capacity was not sufficient and she became volume overloaded. A peritoneal equilibrium test was not performed. The patient had insulin administered subcutaneously when she started the CAPD but changed to intraperitoneal insulin treatment combined with subcutaneous treatment two years later. Hyperlipidemia treated with simvastatin and fenofibrate were started one year previously but stopped three months later because the drugs caused rhabdomyolysis. Lipid profiles began to worsen and she had to resume with atovastatin but did not develop rhabdomyolysis. Plasma glucose was poorly controlled despite the combination therapy of subcutaneous and intraperitoneal insulin injections. Insulin doses increased from 102 units daily up to 110 units daily during the previous month. The patient was 158 cm tall and weighed 58 kg. When she visited our clinic, her body mass index was 23 kg/m2. Vital signs were a blood pressure of 130/80 mmHg, pulse rate 68/min, respiratory rate 20/min, and body temperature 36.6℃. Her abdomen was soft and mildly distended. The initial complete blood count was white blood cells 8,000/mm3 (neutrophils 70.7%, lymphocytes 18.5%, eosinophils 3.2%), hemoglobin 11.5 g/dL, hematocrit 33.3%, and platelet 288,000/mm3. Her blood chemistry values were, fasting glucose 293 mg/dL, blood urea nitrogen 46.6 mg/dL, creatinine 10.3 mg/dL, sodium 134 mEq/L, potassium 4.4 mEq/L, chloride 90 mEq/L, AST 119 IU/L, ALT 192 IU/L, alkaline phosphatase 850 IU/L, amylase 110 U/L, total protein 6.8 g/dL, albumin 4.0 g/dL, calcium 11.1 mg/dL, phosphorus 6.2 mg/dL, CPK 43 IU/L, LDH 468 IU/L, total cholesterol 450 mg/dL, and triglyceride 1,096 mg/dL. Hepatitis B antigen and hepatitis C antibody were negative. ANCA, anti-liver kidney microsome antibody, and anti-smooth muscle antibody were all negative. Sonography of the abdomen revealed an increased echogenicity of the liver. A CT scan of the abdomen showed extensive low attenuated lesions in the liver capsule, the parenchyma of the left hepatic lobe and a small nodular lesion in the capsular area of the right lobe of the liver (). The MRI findings were consistent with the CT findings. The hepatic subcapsular area showed bright signals in the on-phase T1weighted images, but a marked signal decrease in the off-phase T1-weighed sequences; these findings suggested that the subcapsular area was composed of fat tissue. Hepatic subcapsular steatosis due to high dose intraperitoneal insulin was suspected; the patient was changed from CAPD to HD. Insulin was given only subcutaneously after changing to HD. A CT scan performed two months after starting HD showed complete resolution of the hepatic subcapsular steatosis (). Laboratory values were also improved: AST 34 IU/L, ALT 81 IU/L, alkaline phosphatase 733 IU/L, total cholesterol 259 mg/dL, and triglyceride 177 mg/dL. The blood sugar has been well controlled insulin therapy could be discontinued. Six months after changing from CAPD to HD, oral hypoglycemic agents have been sufficient to maintain adequate plasma glucose levels. Furthermore, liver enzyme levels are within normal range; the total cholesterol level was 206 mg/dL, and triglyceride level 157 mg/dL without requirement for lipid-lowering agents.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [46.6, 'mg/dL'], 'Glucose': [293.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",300.92063,285.8746,315.96666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. 
The concentration of bun is 46.6 mg/dL. 
The concentration of glucose is 293.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (46.6 / 2.8) + (46.6 / 18) = 300.92063 mmol/L.The patient's calculated serum osmolality concentration is 300.92063 mmol/L. This is equalivalent to 300.92063 mOsm/kg."
5747,30,Serum Osmolality,lab test,decimal,pmc-7263001-1,Extracted,"A 61-year-old man presented to the ED after having black stools for 24 hours. This episode was preceded by the spontaneous onset of abdominal cramps, followed by dyspnea, fatigue, and light-headedness. His prior medical history included multiple hospital admissions for upper GI bleeding. There was no history of smoking, alcohol intake, or illicit drug use. On initial examination, he appeared lethargic, with a blood pressure of 101/55 mmHg, a pulse of 83 beats/minute, a respiratory rate of 16 breaths/minute, and oxygen saturation of 100% while breathing room air. He had conjunctival pallor. Cardiovascular examination revealed a systolic ejection murmur with late systolic peaking and soft second heart sounds. Laboratory tests showed a blood glucose concentration of 101 mg/dL, a white blood cell count of 4.6 x 109/L, a hemoglobin concentration of 8 g/dL, and a platelet count of 207 x 109/L. Other laboratory tests showed sodium 138 mEq/L, potassium 3.9 mmol/L, chloride 105 mmol/L, carbon dioxide 22 mEq/L, blood urea nitrogen 21 mg/dL, and creatinine 0.9 mg/dL. He was deficient in high molecular weight multimers of von Willebrand factor (vWF). Abdominal CT and upper GI endoscopy yielded negative results. A previous capsule examination of the small bowel had been negative. Two-dimensional transthoracic echocardiogram revealed a severely sclerotic aortic valve with area of 0.65 cm2 and left ventricular ejection fraction 65% (Figure ).
The patient was treated with intravenous administration of the proton pump inhibitor octreotide as well as two units of packed red blood cells. Because of his history of chronic GI bleeding, anemia, and AS, he was diagnosed with Heyde syndrome, a diagnosis supported by the deficiency in high molecular weight multimers of vWF.
The patient underwent a minimally invasive aortic valve replacement, with the insertion of a 27-mm tissue valve. At the present writing, three years after the procedure, the patient has been asymptomatic with no further episodes of bleeding.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Glucose': [101.0, 'mg/dL'], 'Sodium': [138.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [21.0, 'mg/dL']}",289.11111,274.65555,303.56667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 21.0 mg/dL. 
The concentration of glucose is 101.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (21.0 / 2.8) + (21.0 / 18) = 289.11111 mmol/L.The patient's calculated serum osmolality concentration is 289.11111 mmol/L. This is equalivalent to 289.11111 mOsm/kg."
5748,30,Serum Osmolality,lab test,decimal,usmle-1384,Extracted,"A 30-year-old man comes to the physician after receiving a high blood pressure reading of 160/90 mm Hg at an annual employee health check-up. During the past few months, the patient has had occasional headaches and mild abdominal pain, both of which were relieved with ibuprofen. He has also had several episodes of heart palpitations. He has no history of serious illness. His mother and father both have hypertension. He has smoked one pack of cigarettes daily for the past 10 years and drinks one glass of wine daily. He occasionally smokes marijuana. He appears pale. His temperature is 36.8°C (98.2°F), pulse is 103/min, and blood pressure is 164/102 mm Hg. Physical examination shows no abnormalities. Laboratory studies show:
Hemoglobin 15.3 g/dL
Leukocyte count 7,900/mm3
Platelet count 223,000/mm3
Serum
Na+ 138 mEq/L
K+ 4.6 mEq/L
Cl- 103 mEq/L
Urea nitrogen 14 mg/dL
Glucose 90 mg/dL
Creatinine 0.9 mg/dL
Plasma metanephrines 1.2 nmol/L (N < 0.5 nmol/L)
Urine toxicology screening is positive for tetrahydrocannabinol (THC). Renal doppler shows no abnormalities. A CT scan of the abdomen shows a mass in the left adrenal gland.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [138.0, 'mEq/L'], 'Glucose': [90.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [14.0, 'mg/dL']}",286,271.7,300.3,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 14.0 mg/dL. 
The concentration of glucose is 90.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (14.0 / 2.8) + (14.0 / 18) = 286.0 mmol/L.The patient's calculated serum osmolality concentration is 286.0 mmol/L. This is equalivalent to 286.0 mOsm/kg."
5749,30,Serum Osmolality,lab test,decimal,pmc-4943902-1,Extracted,"A 59-year-old man presented to the Emergency Department (ED) with acute progressive dyspnea preceded by expectoration of a cup of ""blood-tinged"" sputum. The ""hemoptysis"" had started 3 hours prior after sudden coughing and was described by his wife as very dark in color. Our electronic medical record indicated that he had attended our outpatient hepatology clinic regularly for hepatitis B virus–related HCC with a huge 20-cm mass in the right hemiliver, which was diagnosed 5 years ago; he received transarterial chemoembolization (TACE) twice for the mass at the time of diagnosis and no further invasive procedure was performed for the past years; follow-up abdominal imaging regularly at 6-month interval showed no evidence of tumor rupture and no change of necrotic mass until recently (). Current medications included sorafenib and entecavir, which he had taken for the past 5 years. He denied any history of aspiration, vomiting, hematemesis, or melena; the last esophagogastroduodenoscopy did not show presence of varix a year ago. Recently, he had intermittent right flank discomfort and a low-grade fever without chills for a year. He was a never-smoker and denied history of asthma.
On arrival, he was in acute respiratory distress with a respiratory rate of 28 breaths per minute and was receiving oxygen at the rate of 10 L/min via a facial mask in the ambulance. Other vital signs were as follows: blood pressure 138/91 mm Hg, pulse rate 111 beats per minute, temperature 36.4℃, and oxygen saturation 90% using the full facial oxygen mask. Bilateral whole-lung wheezing was dominant and right-sided crackles were heard upon auscultation. There was no visible blood in the oral cavity. The results of the initial arterial blood gas analyses during full facial oxygen mask administration were pH 7.4, pCO2 30 mm Hg, pO2 79 mm Hg, and HCO3 20.4 mmol/L. After administering an inhaled bronchodilator with a systemic steroid, intravenous methylprednisolone 40 mg, his oxygen demand gradually decreased to 3 L/min administered via a nasal cannula.
In order to find the possible source of the ""hemoptysis,"" computed tomography (CT) of the chest with angiography was performed, which showed a new area of consolidation in the right basal lung suggesting necrotizing pneumonia (). Otherwise, no definite hypertrophied bronchial artery was seen and there was no possible bleeding focus.
Blood tests showed marked leukocytosis (28,690/mL, 78% segmented neutrophils) with significantly elevated C-reactive protein (CRP, 28.11 mg/dL) and lactic acid (4.3 mmol/L).
There was no change in the hemoglobin level from his baseline (12.8 g/dL). His hematocrit was 38.3% and the platelet count was normal (252×103/µL). The blood urea nitrogen was not elevated (15 mg/dL); serum sodium was 134 mmol/L and the serum glucose level was 158 mg/dL. Liver function tests were also within the usual range (aspartate aminotransferase, 35 IU/L; alanine aminotransferase, 40 IU/L; total bilirubin, 1.1 mg/dL; albumin, 3.3 g/dL; and prothrombin time, 64% [patient's baseline, 69%]).
Treatment with intravenous piperacillin/tazobactam 4.5 g every 6 hours and levofloxacin 750 mg daily was initiated immediately and the patient was admitted to the general ward. Given the relatively mild pneumonia severity index (risk class III, 89 points) and radiologic extent of pneumonia, inflammatory markers including leukocyte count and CRP were persistently highly elevated. There were no improvements in his clinical signs (respiratory symptoms, cough, dark-colored sputum, and wheezing) or X-ray while continuing antibiotics. There was no bacterial growth on the initial blood and sputum cultures. A sputum acid fast stain for tuberculosis was negative. The urinary pneumococcal antigen test was also negative. On hospitalization day 5, his dyspnea worsened and the oxygen demand increased up to 6 L/min via nasal cannula.
On hospital day 7, the patient developed type 2 respiratory failure (pH, 7.13; pCO2, 105 mm Hg; pO2, 123 mm Hg; HCO3, 25.2 mmol/L) despite the use of noninvasive ventilator support overnight. Intubation was performed, and immediately afterwards, a massive volume of dark-brown secretions with a consistency like anchovy-paste was expectorated via the endotracheal tube. We thought that it was very strange because his mental status had been alert and there was no preceding aspiration event. Since the huge hepatic mass had been compressing the right lung, we considered the possibility of a connection and reviewed the initial CT scan with the Division of Thoracic Imaging, Department of Radiology. Indeed, a possible communication tract between the hepatic mass and the right middle bronchus was discovered (). A sputum smear was performed which showed numerous neutrophils and dyskeratotic cells.
The patient was admitted to the intensive care unit to receive mechanical ventilation and the antibiotic therapy was changed to intravenous meropenem 1 g every 8 hours. Bronchoscopy performed the next day showed obstruction of the right middle bronchus with a large amount of thick brown secretions. No overt defect was seen. After toileting, the patient was successfully extubated.
In the ward, he continued to expectorate dark brown sputum despite improvement in the pneumonic consolidation, laboratory findings, and oxygen demand. After 12 days of intravenous antibiotics to cover necrotizing pneumonia and continued administration of sorafenib and entecavir, the chest X-ray showed slightly improved consolidation and a sign of an air-fluid level under the right diaphragm.
On the 25th hospital day, a repeat CT scan was taken, which showed simultaneous disappearance of the pneumonic consolidation and the necrotic fluid within the hepatic mass (). A fistula connecting the two sides was seen (). The patient's history was carefully recorded again and the patient and his wife confirmed that there had not been any blood in the sputum at any time; it had always been brown and like the anchovy-paste (). It turned out that an intern in the ED had initially recorded it as ""hemoptysis."" A sputum smear was performed again and showed numerous bilirubin castlike objects ().
Considering the short life expectancy due to HCC, he and his family did not want to receive further invasive procedures or surgery. While continuing antibiotics and tapering the steroid, the patient received inpatient rehabilitation and was successful discharged. We decided to continue antibiotics, sorafenib, and entecavir in the outpatient clinic. He is now followed-up by both respiratory physicians and hepatologists for 1 month without recurrence of pneumonia.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [15.0, 'mg/dL'], 'Glucose': [158.0, 'mg/dL'], 'Sodium': [134.0, 'mmol/L']}",282.13492,268.02817,296.24167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mmol/L. 
The concentration of bun is 15.0 mg/dL. 
The concentration of glucose is 158.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (15.0 / 2.8) + (15.0 / 18) = 282.13492 mmol/L.The patient's calculated serum osmolality concentration is 282.13492 mmol/L. This is equalivalent to 282.13492 mOsm/kg."
5750,30,Serum Osmolality,lab test,decimal,pmc-2672256-1,Extracted,"A 59-year-old female presented to the ED with a chief complaint of abdominal pain. Her abdominal pain began three hours before presentation and had awoken her from sleep. This abdominal pain was described as “achy,” 5/10, intermittent, and located in the left lower quadrant without radiation. She denied nausea or vomiting and had no diarrhea or blood in her stools. Review of systems revealed that the patient had symptoms of dysuria for one day and left-sided flank pain along with her abdominal pain. She denied fevers or chills. She stated that, despite taking her prescribed insulin injections, her blood sugars have been persistently elevated above 400 with her personal glucometer. Her past medical history was significant for insulin-dependent diabetes mellitus (DM), hypertension, and prior cerebrovascular accident. She denied ever having any surgeries. She used regular insulin, Lantus (insulin glargine), and Ibuprofen. Her family history was noncontributory, and she denied alcohol, tobacco, or illicit drug use.
Physical exam revealed a temperature of 36.5° C, respiratory rate of 18 breaths per minute, heart rate of 93 beats per minute, blood pressure of 166/81 mm Hg, oxygen saturation of 99% on room air, and capillary blood glucose of 447 mg/dL. She was awake, alert, and interacting appropriately. Her pupils were equally round and reactive to light. The cardiac exam was normal and lungs were clear with breath sounds bilaterally. The abdomen was soft with minimal tenderness to palpation in the left periumbilical and left lower quadrant. There was no guarding or rebound. Extremities were warm and well-perfused. The neurological exam revealed no deficit.
The metabolic panel revealed sodium of 132 mEq/L (normal 135–145), BUN of 45 mg/dL (normal 8–22), Creatinine of 2.0 mg/dL (normal 0.5–1.3), glucose of 473 mg/dL, and an anion gap of 8.0. A CBC revealed a white blood cell count of 12.0 K/MM3 (normal 4.5–11.0) and a manual differential with 10.10 K/MM3 Neutrophils (normal 0.80–7.70). The hepatic panel was remarkable for an alkaline phosphatase of 189 U/L (normal 35–115). The urine was visibly clear and non-turbid. Urinalysis was leukocyte esterase and nitrate negative, but revealed large occult blood, glucosuria, protein of 300 mg/DL, and 3–6 WBC/HPF (normal 0–3).
While laboratory studies were pending, the patient received one liter IV normal saline, four mg of morphine sulfate IV for pain, and 10 units of regular insulin. Despite fluid administration and analgesia, the patient continued to have worsening 6/10 abdominal pain. Given the patient’s presentation of undifferentiated abdominal pain without clear etiology and her immunocompromised state, a non-contrast computed tomography (CT) scan of the abdomen was ordered. The CT scan revealed significant air in the bladder wall and lumen consistent with EC, severe left hydroureter and hydronephrosis without evidence of stones, and significant left perinephric stranding without gas in the renal parenchyma ().
A gram of Ceftriaxone and 500 mg of Gentamycin were started empirically along with a repeat fluid bolus and placement of a Foley catheter. While awaiting consultation and admission to the Urology service, the patient complained of increased abdominal pain and was increasingly tender in the left lower quadrant and suprapubic region. Her heart rate was persistently tachycardic (in the 130s), and she developed a fever to 39.4°C. In light of developing urosepsis and the potential for rapid progression to Emphysematous pyelonephritis, Interventional Radiology (IR) was consulted and placed a left nephrostomy tube to relieve the functional obstruction of the urinary tract just eight hours after the patient presented to the ED. After nephrostomy tube placement by IR, the patient was admitted to the ICU for close monitoring. The urine culture grew out Klebsiella pneumoniae and the patient was continued on IV antibiotics. Three days after admission, the nephrostomy tube was removed as the patient was able to void without use of a foley catheter and was able to control her pain. She was subsequently discharged and given a prescription for Levofloxacin 500 mg every day for fourteen days.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [132.0, 'mEq/L'], 'Glucose': [473.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [45.0, 'mg/dL']}",306.34921,291.03175,321.66667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 132.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 132.0 mEq. To convert from 132.0 mEq to mmol, convert from mEq to mmol. The compound 132.0 has a valence of 1, and so divide the valence by the value of mEq to get, 132.0 mEq/(1 mEq/mmol) = 132.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 132.0 mEq sodium/L converts to 132.0 mmol sodium/L. 
The concentration of bun is 45.0 mg/dL. 
The concentration of glucose is 473.0 mg/dL. 
Plugging these values into the equation, we get 2 * 132.0 + (45.0 / 2.8) + (45.0 / 18) = 306.34921 mmol/L.The patient's calculated serum osmolality concentration is 306.34921 mmol/L. This is equalivalent to 306.34921 mOsm/kg."
5751,30,Serum Osmolality,lab test,decimal,pmc-2672144-1,Extracted,"A 59-yr-old man visited outpatient clinic for evaluation of progressive dyspnea on exertion and chest discomfort for 4 months. He had no remarkable medical and family history.
On the physical examination, his height was 170 cm, weight 77 kg, the blood pressure 104/66 mmHg, the heart rate 76/min, the respiratory rate 20/min, and the body temperature 36℃. He had clear mentality, chronic ill-looking appearance and clear sclerae. Jugular venous distension was noted, but no cervical and axial lymphadenopathy was observed. The heart sounds were regular without murmur, but presystolic gallop (S4) was checked. The breath sounds were clear without rales or wheezing. Abdominal examination revealed normal bowel sounds without any palpable mass. There was no definite pitting edema. Otherwise the physical findings were unremarkable.
The blood cell counts were as follows: the hemoglobin 13.0 gm/dL, the white blood cell count 6,700/µL, and the platelet count 198,000/µL. According to the serological biochemical assay, fasting blood sugar was 107 mg/dL, Na+ 142 mEq/L, K+ 4.0 mEq/L, Ca2+ 9.6 mg/dL, P- 3.7 mg/dL, blood urea nitrogen 12 mg/dL, creatinine 0.9 mg/dL, total protein 7.0 g/dL, albumin 4.3 g/dL, aspartate transaminase 20 IU/L, alanine transaminase 22 IU/L, alkaline phosphatase 188 IU/L, lactate dehydrogenase 285 IU/L, and beta-2 microglobulin 1.7 mg/L (normal; 0.8-2.2). Urinalysis showed trace amount of proteinuria, and the urine Bence-Jones protein was suspected. Serum protein electrophoresis study was normal. On the immunochemistry findings, IgG was 1,052 mg/dL (normal; 700-1,600), IgA 105 mg/dL (normal; 70-400), IgM 49 mg/dL (normal; 40-230), and IgE was elevated as 385 IU/mL (normal; 10-180). In serum and urine immunoelectrophoresis study, lambda type MG was shown ().
The chest radiography film showed a slightly enlarged cardiac silhouette and there was no pulmonary congestion. There was no bony lesion on plain skull radiography. Electrocardiography (ECG) showed regular sinus rhythm, intermittent atrial premature beats, poor R wave progression, and Q wave in precordial leads ().
The echocardiography revealed dilated both atria, concentric left ventricular (LV) hypertrophy (end-diastolic interventricular septum thickness=13 mm and end-diastolic posterior wall thickness=13 mm, respectively). Both LV dimension and LV ejection fraction were within normal limits. On the Doppler study, ratio of early mitral inflow (E) to late filling velocity (A) (E/A) was 3.0, deceleration time was 135 msec. Tissue Doppler showed 4.03 cm/sec of early diastolic mitral annular velocity (E') with E/E' ratio of 21.6, suggesting restrictive physiology of diastolic dysfunction with elevated LV filling pressure (). There was scanty amount of pericardial effusion without definite evidence of constriction.
Bone marrow (BM) aspirate smears showed normocellular marrow particle, and estimated M:E ratio was 1.71:1. The granulocyte series were normal in number and showed good maturation sequences. Plasma cells were increased and counted up to 6.8% of absolute neutrophil count compatible with monoclonal gammopathy of undetermined significance (MGUS) (). There were no amorphous eosinophilic amyloid material in both H&E and Congo-red staining for ruling out amyloidosis for endomyocardial (), BM, and enteral biopsies. However, immunostaining for lambda light chain in myocardium showed positive result ().
The presentation was clinically consistent with non-amyloidotic light chain deposition cardiomyopathy (). He was managed conservatively with low-dose vasodilators and diuretics, and his symptom mildly resolved. After 9 months follow up, he readmitted for aggravated heart failure, and died due to intractable heart failure and ventricular arrhythmia in the end.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [12.0, 'mg/dL'], 'Glucose': [107.0, 'mg/dL'], 'Sodium': [142.0, 'mEq/L']}",294.23016,279.51865,308.94167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. 
The concentration of bun is 12.0 mg/dL. 
The concentration of glucose is 107.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (12.0 / 2.8) + (12.0 / 18) = 294.23016 mmol/L.The patient's calculated serum osmolality concentration is 294.23016 mmol/L. This is equalivalent to 294.23016 mOsm/kg."
5752,30,Serum Osmolality,lab test,decimal,pmc-8675570-1,Extracted,"We describe the case of a 55-year-old male who presented to the emergency department via emergency medical services for the chief complaint of sudden onset shortness of breath that woke him from his sleep just prior to arrival. He reported three days of non-radiating lumbar back pain and two episodes of non-bloody emesis leading up to this event. His medical history included hypertension and type 2 diabetes mellitus. His current medications were metformin, amlodipine, losartan, and atenolol. Initial vital signs revealed heart rate (HR) 75, respiratory rate (RR) 29, blood pressure (BP) 119/62, and oxygen saturation 99% on 2L nasal cannula. Temperature was 36.3°C.
Physical examination was significant for an ill-appearing male patient who was anxious and tachypneic. He also had significant work of breathing with retractions and abdominal breathing. Lungs were clear to auscultation, with no wheezing, rhonchi, or rales. Abdominal exam revealed mild epigastric tenderness with no rebound, guarding, or palpable pulsatile mass. No costovertebral angle (CVA) tenderness or midline tenderness was elicited. Neurological exam revealed no focal deficits.
Due to his presentation and multiple comorbidities we had significant concern for the possible acute coronary syndrome, dissection, sepsis, or pulmonary embolism. Blood work including complete blood count (CBC), comprehensive metabolic panel (CMP), lactic acid, troponin, urine analysis (UA) was ordered. CT-angiogram of his chest, abdomen, and pelvis was also ordered.
Complete blood count revealed a white blood cell count of 20.4 x 103/uL, hemoglobin of 11.2 g/dL, and platelet count of 376 x 103/uL. Comprehensive metabolic panel was significant for a sodium of 145 mmol/L, potassium 6.1 mmol/L, chloride 100 mmol/l, bicarbonate <7 mmol, blood urea nitrogen (BUN) 67 mg/dl, creatinine 14.7 mg/dL, calcium 9.1 mg/dL, and glucose of 165. Troponin I was <0.012 ng/mL. Initial lactic acid was recorded at 13.9 mmol/L. An arterial blood gas revealed severe anion gap metabolic acidosis with a pH of 6.9, pCO2 of 22.3 mmHg, pO2 of 105.5 mmHg, HCO3 of 5.3 meq/L, and a Base Excess of -24.8 mmol/l. The patient was anuric at this time. Initial EKG showed normal sinus rhythm (NSR), nonspecific ST abnormalities, vent rate 73, QTC 471. The CT scan revealed an obstructing stone at the left proximal ureteropelvic junction (Figures , ) and at the right ureterovesical junction (Figure ), with resultant bilateral hydronephrosis (Figure ).
While in the ED the patient progressively became hypotensive and was given broad-spectrum antibiotics, Vancomycin and Cefepime, due to concern for sepsis and aggressive fluid resuscitation was initiated. The patient did not respond to fluid resuscitation and was started initially on Levophed. In addition, the patient received 100 mL of 8.4% sodium bicarbonate and 2 grams of calcium gluconate for severe metabolic acidosis and hyperkalemia. Due to the expected clinical decline, the patient was intubated in the emergency department. Critical Care, Nephrology, and Urology were consulted emergently in the ED. After initial stabilization, the patient was taken for immediate bilateral percutaneous nephrostomy (PCN) placement by Interventional Radiology (IR) and placement of a trialysis catheter for initiation of hemodialysis afterward. Urinalysis from the PCN revealed hematuria, but no evidence of infection.
After successful placement of bilateral PCN, the patient was transferred to the intensive care unit (ICU) in critical condition. He was maintained on multiple vasopressors consisting of combinations of norepinephrine, vasopressin, epinephrine, and phenylephrine along with stress dose hydrocortisone. Repeat blood gas and labs revealed a worsening metabolic and lactic acidosis with a repeat pH of 6.7 and a lactic acid of 15.9. The patient was started on hemodialysis with a high bicarbonate dialysate for emergent clearance of hyperkalemia and refractory acidosis. After hemodialysis, the patient’s pH was 7.1, despite a worsening lactic acidosis of 17.0 mmol/L. Overnight the patient was converted to continuous venous-venous hemodialysis, a form of continuous renal replacement therapy (CRRT). Within 24 hours the patient’s acidemia corrected and blood pressure stabilized allowing for a de-escalation of vasopressors. A repeat chemistry revealed recovering renal function along with urine production in the nephrostomy tubes. On hospital day 3, the patient was successfully extubated, weaned off all vasopressors, and CRRT was stopped. Blood and urine cultures taken prior to dialysis were negative after five days. On hospital day 6, Urology performed a cystoscopy with bilateral ureteral stent placement and removal of bilateral percutaneous nephrostomy tubes. On hospital day 8, the patient had made a remarkable recovery from being critically ill. His creatinine was 1.5, BUN 27, and he was discharged home with urology follow-up in 1-2 weeks.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [145.0, 'mmol/L'], 'Blood Urea Nitrogen (BUN)': [67.0, 'mg/dL'], 'Glucose': [165.0, 'mg/dL']}",323.09524,306.94048,339.25,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 145.0 mmol/L. 
The concentration of bun is 67.0 mg/dL. 
The concentration of glucose is 165.0 mg/dL. 
Plugging these values into the equation, we get 2 * 145.0 + (67.0 / 2.8) + (67.0 / 18) = 323.09524 mmol/L.The patient's calculated serum osmolality concentration is 323.09524 mmol/L. This is equalivalent to 323.09524 mOsm/kg."
5753,30,Serum Osmolality,lab test,decimal,pmc-5464381-1,Extracted,"A 50-year-old Filipino woman with a history of type II diabetes mellitus and hypertension presented to the emergency department with three days of generalised weakness and abdominal discomfort. She also described decreased oral intake for several days prior to presentation due to persistent nausea and intermittent facial flushing since the onset of her symptoms. She denied fevers, chest pain, dyspnoea, cough, headache, and dysuria. Her last bowel movement was four days prior to presentation. She took metformin daily and glipizide only when her blood glucose was higher than 140 mg/dL. Her only other medication was lisinopril. She denied alcohol, tobacco, or illicit drug use.
The patient’s vital signs on presentation were a temperature of 37.1℃, heart rate of 152 beats/min, respiratory rate of 16 breaths/min, blood pressure of 175/79 mmHg, and oxygen saturation of 100% on ambient air. She had facial and neck flushing. Other pertinent findings on physical examination included dry mucous membranes, tachycardia, a regular heart rhythm, and a normal S1 and S2 without murmurs. She had hypoactive bowel sounds with a moderately distended and diffusely tender abdomen.
Laboratory tests demonstrated a serum sodium of 120 mmol/L, potassium of 5.3 mmol/L, chloride of 76 mmol/L, carbon dioxide of 25 mmol/L, urea nitrogen of 30 mg/dL, creatinine of 0.94 mg/dL, glucose of 612 mg/dL, and lactate of 2.1 mmol/L. Her anion gap was 19 (24 if corrected for an albumin of 2.1 g/dL). Her white blood cell count was 19.3 × 109 cells/L. Her haemoglobin and platelet counts were normal. Her initial troponin I was 0.07 µg/L (reference range: <0.04 µg/L). Urinalysis demonstrated a glucose >500 mg/dL and ketones of 20 mg/dL. The serum beta-hydroxybutyrate was 3.67 mmol/L. A haemoglobin A1c was 9.2%. Her serum lipase was within normal limits. Her chest radiograph was normal. An acute abdominal series demonstrated dilation of the large bowel measuring up to 7 cm within the region of the transverse colon ().
The patient was aggressively resuscitated with isotonic crystalloid solution and was started on an insulin infusion. Her hyponatremia and anion gap resolved over the ensuing 24–48 h. Despite resuscitative efforts, the patient remained persistently tachycardic with a heart rate ranging 140–160 beats/min. She was treated empirically for sepsis with broad-spectrum antibiotics. Her serum troponin I peaked at 0.10 µg/L. Serial electrocardiograms demonstrated sinus tachycardia and Q waves in the inferior and anteroseptal leads suggestive of prior infarct, but there were no acute ST segment or dynamic T wave changes. A trans-thoracic echocardiogram demonstrated preserved left ventricular systolic function with an estimated ejection fraction of 60%–65% without wall motion abnormalities. Two sets of blood cultures drawn at the time of presentation remained negative.
A CT scan of the abdomen and pelvis, which was ordered to further assess the X-ray findings, confirmed diffuse massive dilation of the colon with an abrupt transition point at the splenic flexure and decompression of the distal colon. No anatomic obstruction was identified. The combination of the hypoactive bowel sounds and CT imaging pointed to acute colonic pseudo-obstruction. Her CT scan also demonstrated a 6.9- × 7.0-cm heterogeneous, partially necrotic mass within the right adrenal gland (). In the context of hypertension, tachycardia, nausea, and acute-onset facial flushing, pheochromocytoma was suspected. Plasma total free metanephrines and 24-h urine total metanephrines were markedly elevated (21,282 pg/mL and 42,638 mcg/24 h, respectively).
The patient’s blood pressure and heart rate remained persistently elevated. She was started on phenoxybenzamine and a nicardipine infusion and had marked improvement of her vital signs. Her acute colonic pseudo-obstruction was reversed with the administration of phenoxybenzamine and an aggressive bowel regimen. She underwent a right adrenalectomy, which confirmed the diagnosis of pheochromocytoma. Since surgery, she has had no recurrence of abdominal symptoms. In addition, her diabetes and hypertension have improved dramatically.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [30.0, 'mg/dL'], 'Glucose': [612.0, 'mg/dL'], 'Sodium': [120.0, 'mmol/L']}",284.71429,270.47858,298.95,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 120.0 mmol/L. 
The concentration of bun is 30.0 mg/dL. 
The concentration of glucose is 612.0 mg/dL. 
Plugging these values into the equation, we get 2 * 120.0 + (30.0 / 2.8) + (30.0 / 18) = 284.71429 mmol/L.The patient's calculated serum osmolality concentration is 284.71429 mmol/L. This is equalivalent to 284.71429 mOsm/kg."
5754,30,Serum Osmolality,lab test,decimal,pmc-7336193-1,Extracted,"A 60-year-old female visited our emergency department complaining of epigastric pain and hematemesis. She ate sliced raw fish one day ago. She had hypertension. There was no noteworthy fact in her social and family history. She did not take any antiplatelet drug and anticoagulation drug. On her initial visit, blood pressure was 105/91 mmHg, pulse rate was 72 beats per minute, respiratory rate was 24 breaths per minute, and body temperature was 37.2°C. In abdominal physical examination, there was pain and tenderness in the epigastric area. But there was no rebound tenderness and muscle rigidity. The bowel sound was normal. In laboratory test, the white blood cell count was 14,900/mm3, hemoglobin was 10 g/dL, and platelet count was 199,000/mm3. The result of coagulation test was PT 1.13 (INR) and aPTT 24.4 sec. The result of blood chemistry was total protein 5.9 g/dL, albumin 3.5 g/dL, AST 27 IU/L, ALT 11 IU/L, ALP 118 IU/L, total bilirubin 0.6 mg/dL, BUN 21.2 mg/dL, creatinine 0.8 mg/dL, Na 142 mEq/L, K 3.8 mEq/L, Cl 106 mmol/L, CRP 0.08 mg/dL, and blood sugar 145 mg/dL.
Abdominal computed tomography scan showed about 8 × 3 cm nonenhancing mass in the stomach antrum and lower body. The Hounsfield unit of mass was 50∼60 units (). It suggested submucosal hematoma in stomach.
Emergent esophagogastroduodenoscopy was performed. A pool of blood was on the greater curvature side of body in the stomach. Greater than 5 cm-sized mass was noted on the anterior wall of body and antrum. The mass was round, dark brownish. But surrounding mucosa was normal. The overlying mucosa of mass was ruptured. Dark red hematoma was noted inside the mass (). Removal of hematoma and hemostasis could not be performed owing to noncooperation of the patient.
She was diagnosed with ruptured intramural hematoma. We decided to treat conservatively because further bleeding was not occurred. We treated with intravenous proton pump inhibitor and fluids. In addition, we made her fasting for one week.
On hospital day 8, the gastric intramural hematoma has disappeared in the follow-up abdominal CT scan (). On follow-up EGD, the gastric intramural hematoma on anterior wall of low body and proximal antrum has disappeared. EGD showed active ulcer on the same site (). At that time, EGD showed a whitish worm resembling a short thread. The worm moved at the gastroesophageal junction. The worm was removed out of the body by using a biopsy forcep. The worm was a 2 cm-sized nematode. It was confirmed as anisakis (Figures –).
Then, the meal was served. Further bleeding was not occurred. The patient was recovered and discharged without other complications.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [21.2, 'mg/dL'], 'Glucose': [145.0, 'mg/dL'], 'Sodium': [142.0, 'mEq/L']}",299.62698,284.64563,314.60833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. 
The concentration of bun is 21.2 mg/dL. 
The concentration of glucose is 145.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (21.2 / 2.8) + (21.2 / 18) = 299.62698 mmol/L.The patient's calculated serum osmolality concentration is 299.62698 mmol/L. This is equalivalent to 299.62698 mOsm/kg."
5755,30,Serum Osmolality,lab test,decimal,pmc-6641835-1,Extracted,"A 39-year-old woman presented to our emergency department with severe continuous, involuntary flailing, violent, and undesired movements of the left limbs, which lasted for 3 days. Her family history was unremarkable, except for type 2 diabetes mellitus. She had history of type 2 diabetes mellitus with poor control and maintenance regular hemodialysis. Her body temperature was 35.9°C, blood pressure was 166/96 mmHg, and pulse rate was 106 beats/minute. Neurological examination demonstrated alert consciousness with good orientation, no facial droop, and score of Medical Research Council (MRC) for muscle strength was 5. Blood laboratory investigation revealed a white blood count of 5480 /μL (normal range, 4800–10800), serum glucose level of 765 mg/dL (normal range, 70–110), blood urea nitrogen level of 38.8 mg/dL (normal range, 6–24), serum creatinine level of 7.94 mg/dL (normal range, 0.5–1.4), sodium level of 125 mmol/L (normal range, 137–145), potassium level of 4.13 mmol/L (normal range, 3.1–5.3), magnesium level of 2.05 mg/dL (normal range, 1.8–2.55), phosphate level of 4.7 mg/dL (normal range, 2.6–4.4), calcium level of 8.3 mg/dL (normal range, 8.8–10.6), ketone body level of 0.1 mmol/L (normal range, 0.0–0.6), lactate level of 0.6 mmol/L (normal range, 0.5–2.2), and arterial blood gas level of pH: 7.465 (normal range, 7.35–7.45); PaO2, 115 mmHg (normal range, 75–100); PaCO2, 34.3 mmHg (normal range, 35–45); HCO3, 24.9 mmol/L (normal range, 22–26). An urgent brain CT showed hyperintensity within the right caudate nucleus and putamen (Fig. a), which we initially believed was acute hemorrhage. A follow-up brain magnetic resonance image (MRI) disclosed hyperintensity within the right caudate nucleus and putamen in the T1-weighted sequence (Fig. b) and hypointensity in the T2-weighted sequence (Fig. c). Acute cerebral hemorrhage was excluded, and the diagnosis of non-ketotic hyperglycemia-related hemichorea-hemiballism was established based upon the clinical and radiological manifestations. Intensive glycemic control via insulin injection was prescribed for the high glycated hemoglobin (HbA1c) level of 13.4% (normal range, 4–6). Medications including clonazepam and risperidone were also administered for symptomatic treatment. Four weeks later, the symptoms of unilateral involuntary violent and wide-amplitude movements of shoulder and hip had improved, apparently owing to tight serum glycemic control. The patient's hemichorea had resolved completely at the 3-month follow-up.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [38.8, 'mg/dL'], 'Glucose': [765.0, 'mg/dL'], 'Sodium': [125.0, 'mmol/L']}",306.35714,291.03928,321.675,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 125.0 mmol/L. 
The concentration of bun is 38.8 mg/dL. 
The concentration of glucose is 765.0 mg/dL. 
Plugging these values into the equation, we get 2 * 125.0 + (38.8 / 2.8) + (38.8 / 18) = 306.35714 mmol/L.The patient's calculated serum osmolality concentration is 306.35714 mmol/L. This is equalivalent to 306.35714 mOsm/kg."
5756,30,Serum Osmolality,lab test,decimal,pmc-6935651-1,Extracted,"A 14-year-old girl, living in a refugee camp, was referred from a district hospital for the management of altered level of consciousness, fever, and hyperglycemia. Fever started 2 weeks prior to consultation for which she received empiric treatment for malaria in a district hospital. She was also diagnosed with severe acute on chronic malnutrition for which she received ready-to-use therapeutic food. The situation was worsened by polyuria, excessive thirst, uncontrolled hyperglycemia, persistent fever and progressive lethargy, necessitating her transfer to the endocrinology unit of the Mother and Child Center of Yaounde.
Past history was remarkable for diabetes which was diagnosed a year ago after 2 months of polyuria and excessive thirst. Insulin therapy was started at 0.5 IU/Kg/day with mixed insulin but patient's compliance was poor. She reported loss of sight 7 months ago (3 months after the diagnosis of diabetes). She is the 3rd child in a nonconsanguineous family of 10 children of whom three are alive. They fled the Central African Republic to Cameroon and for the past 4 years have been living in a refugee camp in the East region of Cameroon. Neither she nor the mother went to school.
On admission, she was lethargic (Glasgow coma scale was 13/15). Her weight was 19 kg (<3rd percentile), her height was 133 cm (<3rd percentile) for a BMI of 10.7 kg/m2, −5.5 SD for age. Vital signs were as follows: blood pressure: 100/80 mm Hg, pulse: 100 bpm, respiratory rate 34 cycles/min and temperature was 36.8°C. She had fine hair and poor dental hygiene. Her Tanner stage was B1P1. Her abdomen was distended with no palpable mass. She had vulvovaginal erythema. She had a dry mouth, sunken eyes, mixed signs of dehydration and severe malnutrition (skin pinch went back slowly) and bilateral leucocoria.
Her serum glucose level was 440 mg/dL (24.4 mmol/L), K + 3.3 mmol/L, corrected Na + 148.4 mmol/L, Cl-108 mmol/L. HbA1C was 12% (108 mmol/mol). Urinalysis revealed nitrites (3+), ketones (2+), glycosuria (3+), and culture later on showed growth of E coli. Her hemoglobin level was 12.3 g/dL, white blood cell count was 9500/mm3, and platelets count was 308 000/mm3. Aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) were in the upper limits (42 and 44 IU/L, respectively) and renal function was normal (blood urea nitrogen (BUN) 0.07 g/L, serum creatinine 3 mg/L). Blood proteins were 93 g/L. Blood gases were not available.
She was admitted to the intensive care unit. She received oral rehydration solution for the malnourished (10 mL/kg/hr for 2 hours) followed by 1.5 L/m2/day of normal saline intravenously (IV) and KCL 1.5 g/L (IV) for 24 hours. Rapid-acting insulin was started 2 hours later with an hourly subcutaneous dose of 0.1 IU/Kg. An antibiotic was also given (ceftriaxone at 50 mg/kg/day) as well as routine de-worming with a single dose of 400 mg of albendazole. Four hours following admission, she was more reactive; ketonuria was 1+, serum glucose level was 408 mg/dL (22.4 mmol/L). Rapid-acting insulin was replaced by multiple injections using neutral protamine Hagedorn insulin (NPH) and actrapid (1IU/kg/day). Ready-to-use therapeutic food F75 (75 kcal/100 mL) was started at 130 mL/kg/day divided into eight meals. Folic acid (5 mg once) and vitamin A (200 mg on days 1, 2, and 14) were added to the treatment.
The day after admission, she developed lower limb edema and abdominal distension without ascites and IV fluids were stopped. The oedema regressed on day 2. On day 3, the F75 was replaced with F100 (100 kcal/100 mL) 130 ml/kg/day and progressive introduction of Plumpy Nut® and normal food. Progression of her nutritional status is shown in Table .
Communication with and education of patient and her family was difficult because of unavailability of a translator trained in medical terminology and the fact that the patient was almost blind. This was partially improved following her cataract surgery performed 2 months later.
Upon discharge after 9 weeks spent in hospital, her weight was 29 kg, height 133 cm (BMI 16.4 kg/m2) and MUAC of 160 mm. She was discharged to her refugee camp on multiple insulin injections. Two months later, her weight was 32 kg, height 135 mm (BMI 17.56 kg/m2) and HbA1 C 10%.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [0.07, 'g/L'], 'Glucose': [440.0, 'mg/dL'], 'Sodium': [148.4, 'mmol/L']}",323.74444,307.55722,339.93166,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 148.4 mmol/L. 
The concentration of bun is 0.07 g/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from g to mg. The mass of bun is 0.07 g. To convert 0.07 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.07 g bun * 1000.0 mg/g = 70.0 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 70.0 mg bun/10.0 dL = 7.0 mg bun/dL. The concentration value of 0.07 g bun/L converts to 7.0 mg bun/dL. 
The concentration of glucose is 440.0 mg/dL. 
Plugging these values into the equation, we get 2 * 148.4 + (7.0 / 2.8) + (7.0 / 18) = 323.74444 mmol/L.The patient's calculated serum osmolality concentration is 323.74444 mmol/L. This is equalivalent to 323.74444 mOsm/kg."
5757,30,Serum Osmolality,lab test,decimal,pmc-5437990-1,Extracted,"A 2-year-old previously healthy male of Albanian decent presented to the emergency room with cough. He was diagnosed with a viral upper respiratory tract infection and discharged home. Two days later, he returned to the emergency room with a worsening cough, productive of white sputum, shortness of breath, and fever. On review of systems, he was also noted to have decreased oral intake and several episodes of emesis. There were no known sick contacts. On exam, he was febrile, tachycardic, and tachypneic. He was noted to be pale and mildly dehydrated. Decreased breath sounds were appreciated over the right lung field. Initial labs were as follows: hemoglobin of 8.7 g/dL, hematocrit 28.7%, platelet count 474,000 g/dL, sodium 134 meq/L, potassium 3.8 meq/L, chloride 98 meq/L, HCO3 15 meq/L, BUN 21 mg/dL, creatinine 0.5 mg/dL, glucose 67 mg/dL, calcium 9.3 mg/dL. His urinalysis showed specific gravity 1.016, trace ketones, 30 mg/dL protein, trace blood, and urine microscopy showed 4 WBCs and 2 RBCs. Initial chest X-ray showed a right sided middle and lower lobe pneumonia and a small right sided pleural effusion. In the emergency room, the patient was given a dose of ceftriaxone, started on oxygen for increased work of breathing, given an IV fluid bolus of normal saline and admitted to the general pediatric floor.
His past medical history was significant for iron deficiency anemia diagnosed at 11 months of age; he had a normal hemoglobin electrophoresis at that time. Family history and social history was non-contributory. The patient has no known drug allergies. He was noted to have normal growth and development.
On hospital day 3, the patient was noted to have increasing respiratory distress. Repeat chest X-ray and a chest sonogram showed a large right sided pleural effusion with multiple thick septations. He was treated with vancomycin and ceftriaxone for management of empyema. Concurrently, his BUN and creatinine increased to 67 mg/dL and 1.6 mg/dL, respectively, and his hemoglobin and platelet counts both decreased to 3.2 g/dL and 23 × 103/µL, respectively. Lactic dehydrogenase (LDH) was 5,850 U/L, total bilirubin 2.1 mg/dL and direct bilirubin 0.8 mg/dL. The partial thromboplastin time (PTT) was prolonged to 60.7 seconds. The patient was transferred to the PICU for further care.
Pediatric hematology, nephrology, and transfusion medicine were consulted. The peripheral smear was notable for toxic granulation in the neutrophils, large platelets, burr cells, target cells, microspherocytes, and schistocytes. Antibody screen was negative but the direct antiglobulin test was positive with both IgG and polyspecific antisera. Anti-I was identified at 4 °C. The patient’s RBCs mixed with 5 randomly selected, AB0-identical, antibody screen negative, normal adult serum samples showed strong agglutination (4+). This is consistent with T-antigen activation. Lectin agglutination was not done. Analysis for other etiologies of atypical HUS, including testing for Factor H and CH50, were not sent as these studies are not readily available at our institution. ADAMST13 testing was not performed as there was a low clinical suspicion for thrombotic thrombocytopenic purpura.
Due to urgent transfusion need, washed RBCs were not initially available and the patient was given a RBC transfusion with a resultant increase in the hemoglobin from 3.2 g/dL to 5.5 g/dL. Forced-air warming was initiated in an attempt to keep the patient warm.
On hospital day 4, he became oliguric. This coincided with a peak in his BUN and creatinine to 103 mg/dL and 2.8 mg/dL, respectively. A temporary hemodialysis catheter was placed and continuous veno venous hemodiafiltration (CVVHDF) was initiated. A right sided chest tube was placed. Blood cultures and pleural fluid cultures taken at two separate times during the hospitalization were negative, but the urine Streptococcus pneumoniae antigen was positive. His hemoglobin again dropped to 3.7 g/dL. At this time, he was transfused with washed RBCs. The hemoglobin was noted to increase to 8.4 g/dL and the platelet count to 22 × 103/µL. Despite this increase, the patient had persistent hemolysis, and the hemoglobin again decreased to a low of 5.6 g/dL by hospital day 5. He was given an additional washed RBC transfusion with an increase in hemoglobin to 10.1 g/dL and an increase in platelet count from 18 × 103/µL to 32 × 103/µL.
On hospital day 6, it was decided to initiate plasmapheresis secondary to pHUS disease progression. The patient weighed 14 kg and was 101 cm tall. The total blood volume was calculated as 1,442 mL. Because of the patient’s size, washed RBCs were used to prime the COBE® Spectra for the PE procedure. The apheresis machine was primed according to the manufacturer’s instructions with normal saline and anticoagulant citrate dextrose A (ACD-A) and subsequently primed a second time with 0.5 U of RBCs. 5% albumin (~ 1 L per procedure) was used as replacement fluid. The ACD-A to whole blood ratio was 1 : 15. The access was a right internal jugular Shiley catheter. After the first PE, the hemoglobin increased to a high of 12.1 g/dL and then gradually decreased to 7.6 g/dL by hospital day 9. The platelet count gradually increased from 32 × 103/µL immediately following PE, to 68 × 103/µL by hospital day 9. At this time, it was decided to perform a second PE using the same prime and replacement fluid. The following day, the hemoglobin rose to 9 g/dL, and by hospital day 11, the platelet count increased to 166 × 103/µL.
The hemoglobin gradually decreased following the second PE to 5 g/dL on hospital day 16. The patient was transfused with washed RBCs, after which the hemoglobin remained greater than 9 g/dL until discharge on hospital day 24. The platelet count remained stable from hospital day 11 until discharge. On the day of discharge, the hemoglobin and platelet count were 10 g/dL and 429 × 103/µL, respectively. The two values remained normal on follow-up ().
With respect to his renal course, the patient was transitioned to intermittent hemodialysis on hospital day 6. He received a total of five hemodialysis treatments, his last treatment on hospital day 12. His creatinine on hospital day 12 was 3.3 mg/dL and declined to 0.4 mg/dL on hospital day 24. He went home on amlodipine for hypertension.
The chest tube was removed on hospital day 11. On hospital day 15, the patient had significant desaturations with a new oxygen requirement. A chest CT revealed a large air cavity representing a pneumatocele of the right lung base. His antibiotic regimen was changed to zosyn and vancomycin. On hospital day 16 he had a right thoracotomy and decortication and placement of two chest tubes. Chest tubes were removed by hospital day 18. The patient was discharged from the hospital 5 days later on augmentin to complete a 3 week course.
Three months following initial diagnosis of pHUS, the patient developed cholelithiasis and chronic cholecystitis and underwent a laparoscopic cholecystectomy. He has, otherwise, had no complications during a 10 month follow-up period.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [21.0, 'mg/dL'], 'Glucose': [67.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",279.22222,265.26111,293.18333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. 
The concentration of bun is 21.0 mg/dL. 
The concentration of glucose is 67.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (21.0 / 2.8) + (21.0 / 18) = 279.22222 mmol/L.The patient's calculated serum osmolality concentration is 279.22222 mmol/L. This is equalivalent to 279.22222 mOsm/kg."
5758,30,Serum Osmolality,lab test,decimal,pmc-8387066-1,Extracted,"This 34-year-old gravida 3 para 2 woman had a 9-year-old and a 7-year-old from uncomplicated pregnancies. On a prenatal visit 6 weeks prior, her hemoglobin was 12 g/dL and platelets 254,000/mm3. The patient was admitted to a rural community hospital in the Midwest USA in labor at 38 6/7 weeks gestation at 15:00, with temperature 36.8o C, blood pressure 132/81 mm Hg and oxygen saturation 96%. She was given epidural anesthesia and started on low-dose oxytocin.
Shortly after midnight, at 00:20, the patient abruptly complained of dyspnea, blurred vision and a headache. She then developed chest pain. Her eyes rolled back and she became marginally responsive to verbal stimuli. The fetal heart rate became labile and varied from 90 to 150/minute. The patient’s oxygen saturation dropped to 89%. She was given supplemental oxygen. Epidural anesthesia and oxytocin were discontinued. Her saturation increased to 95% and her blood pressure was 120/84 mm Hg.
The patient’s oxygen saturation, heart rate and blood pressure became labile, and she became unresponsive. At 00:36, her saturation decreased to 74%. At 00:48, the fetal heart rate dropped to 60-70/minute. The baby was delivered with forceps at 01:00, with Apgar scores of 5 at one minute, 6 at 5 minutes and 9 at 10 minutes. The placenta was delivered at 01:08, apparently complete and intact.
Following delivery of the baby and placenta, at 01:16, the patient’s heart rate increased to 174/minute and blood pressure decreased to 57/37 mm Hg, with saturation 94%. She was given ephedrine. Her heart rate decreased to 53/minute, with blood pressure 58/37 mm Hg and saturation 78% at 01:24. She then became tachycardic and hypertensive, with heart rate 187/minute, blood pressure 145/109 mm Hg and saturation 99% at 01:35. Her saturation fell to 82%, with heart rate 170/minute and blood pressure 93/79 mm Hg at 01:40. Her fundus was boggy and bleeding. A second intravenous line was placed in right femoral vein and the patient was transferred to an intensive care unit (ICU).
On arrival in the ICU at 02:00, the patient’s saturation was 99%. Blood drawn at 02:10 showed hemoglobin 7.1 g/dL, white blood cell count 34,500/mm3 (38% neutrophils, 46% bands, 14% lymphocytes, 1% monocytes, 1% metamyelocytes), platelets 145,000/mm3, partial thromboplastin time (PTT) 87.3 seconds (RR: 25.3-35 seconds) and fibrinogen <15 mg/dL (RR: 267-484 mg/dL). The patient’s saturation was labile, soon dropping to 79% and then increasing to 99%. Her heart rate ranged from 133/minute to 187/minute. She had hypotension treated with infusions of dopamine, dobutamine and phenylephrine. At 03:15, the patient’s hemoglobin was 3.3 g/dL, platelets 95,000/mm3 and white blood cell count 29,200/mm3. She was transfused red blood cells, platelets, fresh frozen plasma and cryoprecipitate. The patient was intubated and mechanically ventilated. At 03:59, arterial blood showed pH 6.81, PCO2 17 mm Hg and PO2 432 mm Hg. At 05:17, glucose was 334 mg/dL (RR: 70-110 mg/dL), blood urea nitrogen 10 mg/dL (RR: 5-20 mg/dL), creatinine 1.4 mg/dL (RR: 0.5-1.4 mg/dL), sodium 142 mEq/L, potassium 5.4 mEq/L, chloride 110 mEq/L, bicarbonate 7 mEq/L, calcium 6.7 mg/dL (RR: 8.5-10.5 mg/dL), bilirubin 3 mg/dL (RR: 0.1-1.2 mg/dL), alkaline phosphatase 124 U/L (RR: 40-125 U/L), alanine aminotransferase 77 U/L (RR: <40 U/L), aspartate aminotransferase 125 U/L (RR: <40 U/L), and albumin 2.5 g/dL (RR: 3.5-5.5 g/dL).
The patient’s urine output dropped until, by 10:00, she was anuric. Line placement for dialysis was unsuccessful. The patient became hypoxemic; arterial blood, drawn at 10:05, on mechanical ventilation with 100% oxygen, showed pH 7.33, PCO2 22 mm Hg and PO2 36 mm Hg. The patient had severe bleeding from the uterus. The uterus was packed, but the bleeding overwhelmed the packing within 10 minutes. At 11:00, an emergency hysterectomy was performed for uncontrollable uterine bleeding. Vaginal tears were sutured. At 11:25, the patient’s hemoglobin was 13 g/dL, white blood cell count 14,200/mm3 (26% neutrophils, 51% bands, 16% lymphocytes, 4% monocytes, 3% metamyelocytes) and platelets 78,000/mm3.
Twenty minutes following surgery, the patient suffered a severe deterioration in clinical status. She began developing cardiac arrhythmias including bigeminy, junctional rhythms and ventricular tachycardia. The patient was eventually transfused 18 units of red blood cells, 12 units of platelets, 7 units of fresh frozen plasma and 24 units of cryoprecipitate. At 13:19, her hemoglobin was 14.8 g/dL, white blood cell count 16,600/mm3, platelets 88,000/mm3, international normalized ratio (INR) 2.1 (RR: 0.9-1.1), PTT 61.3 seconds and fibrinogen 150 mg/dL. At 13:24, arterial blood showed pH 7.09, PCO2 48 mm Hg and PO2 30 mm Hg, on 100% oxygen and 15 cm H2O of positive end-expiratory pressure. The patient’s clinical condition continued to deteriorate despite heroic efforts and she died at 13:55, 13 hours and 35 minutes after the onset of dyspnea.
Autopsy revealed numerous small pulmonary blood vessels containing squamous cells (), many surrounded by cleared space in the luminal blood, and some accompanied by small calcifications (). The squamous cells were positive on immunohistochemical stain for cytokeratin AE3 (). Mucinous material was identified in scattered small pulmonary blood vessels on mucicarmine stain. Autopsy revealed many sites of hemorrhage in heart, stomach, duodenum, kidneys, bladder, vagina and pelvis, and 1000 mL of partially clotted blood in the abdominal cavity. The pleural cavities contained serous fluid, 210 mL on the left and 550 mL on the right. There was pulmonary congestion and edema, with a combined lung weight of 1080 grams. There were occasional fibrin thrombi in renal glomeruli.
Examination of the placenta showed an intact complete 496-gram placenta with no significant abnormalities. Examination of the uterus from the hysterectomy showed decidualized endometrium and cervical foci of hemorrhage with blood vessels containing anucleate squames.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [10.0, 'mg/dL'], 'Glucose': [334.0, 'mg/dL'], 'Sodium': [142.0, 'mEq/L']}",306.12698,290.82063,321.43333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. 
The concentration of bun is 10.0 mg/dL. 
The concentration of glucose is 334.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (10.0 / 2.8) + (10.0 / 18) = 306.12698 mmol/L.The patient's calculated serum osmolality concentration is 306.12698 mmol/L. This is equalivalent to 306.12698 mOsm/kg."
5759,30,Serum Osmolality,lab test,decimal,usmle-10,Extracted,"A 45-year-old woman comes to the physician because of fatigue and irregular menstrual cycles for the past year. She also complains of recurrent sinus infections. During the past 6 months, she has had increased urinary frequency and swelling of her feet. She has also had difficulty lifting her 3-year-old niece for the past 3 weeks. She was recently diagnosed with depression. She works as a medical assistant. The patient has smoked one half-pack of cigarettes daily for 25 years and drinks four beers on the weekends. Her only medication is escitalopram. She is 160 cm (5 ft 3 in) tall and weighs 79 kg (175 lb); BMI is 31 kg/m2. She appears tired. Her temperature is 37°C (98.6°F), pulse is 80/min, respirations are 18/min, and blood pressure is 140/82 mm Hg. Physical examinations shows neck obesity and an enlarged abdomen. Examination of the skin shows multiple bruises on her arms and legs. There is generalized weakness and atrophy of the proximal muscles. Laboratory studies show:
Serum
Na+ 150 mEq/L
K+ 3.0 mEq/L
Cl- 103 mEq/L
HCO3- 30 mEq/L
Urea nitrogen 19 mg/dL
Creatinine 0.9 mg/dL
Glucose 136 mg/dL
A 1 mg overnight dexamethasone suppression test shows a serum cortisol of 167 nmol/L (N < 50) and a 24-hour urinary cortisol is 425 μg (N < 300 μg). Serum ACTH is 169 pg/mL (N = 7–50). Subsequently, a high-dose dexamethasone suppression test shows a serum cortisol level of 164 nmol/L (N < 50).",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [19.0, 'mg/dL'], 'Glucose': [136.0, 'mg/dL'], 'Sodium': [150.0, 'mEq/L']}",314.34127,298.62421,330.05833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 150.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 150.0 mEq. To convert from 150.0 mEq to mmol, convert from mEq to mmol. The compound 150.0 has a valence of 1, and so divide the valence by the value of mEq to get, 150.0 mEq/(1 mEq/mmol) = 150.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 150.0 mEq sodium/L converts to 150.0 mmol sodium/L. 
The concentration of bun is 19.0 mg/dL. 
The concentration of glucose is 136.0 mg/dL. 
Plugging these values into the equation, we get 2 * 150.0 + (19.0 / 2.8) + (19.0 / 18) = 314.34127 mmol/L.The patient's calculated serum osmolality concentration is 314.34127 mmol/L. This is equalivalent to 314.34127 mOsm/kg."
5760,30,Serum Osmolality,lab test,decimal,usmle-5128,Extracted,"A 57-year-old man presents to the emergency department for shortness of breath. He was riding the train home from a business conference when his symptoms began. The patient has a past medical history of obesity, diabetes, diabetic nephropathy, hypertension, and a 40 pack-year smoking history. His current medications include atorvastatin, lisinopril, insulin, metformin, and nicotine gum. His temperature is 99.5°F (37.5°C), blood pressure is 130/87 mmHg, pulse is 120/min, respirations are 15/min, and oxygen saturation is 93% on room air. An EKG is ordered as seen in Figure A. A chest radiograph is ordered as seen in Figure B. Laboratory values are ordered as seen below:

Serum:
Na+: 137 mEq/L
Cl-: 105 mEq/L
K+: 4.1 mEq/L
HCO3-: 24 mEq/L
BUN: 22 mg/dL
Glucose: 129 mg/dL
Creatinine: 1.2 mg/dL
Ca2+: 10.1 mg/dL
AST: 11 U/L
ALT: 12 U/L

On physical exam you note a patient who seems in distress. His cardiac exam is notable for tachycardia. Pulmonary exam reveals bilateral air movement without any wheezes or crackles. The patient's right lower extremity appears mildly inflamed, and palpation of the calf elicits pain.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [22.0, 'mg/dL'], 'Glucose': [129.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",289.02381,274.57262,303.475,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 22.0 mg/dL. 
The concentration of glucose is 129.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (22.0 / 2.8) + (22.0 / 18) = 289.02381 mmol/L.The patient's calculated serum osmolality concentration is 289.02381 mmol/L. This is equalivalent to 289.02381 mOsm/kg."
5761,30,Serum Osmolality,lab test,decimal,pmc-7780870-2,Extracted,"Case 2: A 74-year-old male with a 3-day history of fever, anorexia, vomiting, and shortness of breath was admitted to our hospital. The patient had no history of drug and alcohol abuse and was a non-smoker. His vital signs at admission were as follows: temperature of 38.2 °C, pulse rate of 110 beats per minute, blood pressure of 130/80 mm Hg, respiratory rate of 20 breaths per minute, and SpO2 of 90% in ambient air. After a thorough workup including routine tests and computerized tomography, he received a treatment for COVID-19 and was discharged with good condition and reduced inflammatory markers. Twelve days later, he was readmitted with worsening dyspnea, palpitation, lethargy, confusion, drowsiness, blurring of vision, and generalized weakness. The initial vital signs included body temperature of 38 °C, pulse rate of 120 beats per minute, blood pressure of 140/80 mm Hg, respiratory rate of 22 breaths per minute, and SpO2 of 85% while breathing ambient air. Cranial nerves examination was normal and his pupils were midsize and reactive to light and accommodation.
Laboratory data were as follows: blood glucose level, 102 mg/dL; BUN, 29.6 mg/dL; creatinine (Serum), 0.9 mg/dL; sodium, 138 mEq/L; potassium, 4.6mEq/L; magnesium: 1.7 mg/dL; phosphures, 4 mg/dL; calcium, 8.9mg/dL; ALP, 706 U/L; AST: 66 U/L, ALT: 53 U/L, and troponin level, 4 ng/mL. The blood sample revealed the following results: WBC count 10.4×109/L with 7% lymphocytes and 91% neutrophils; CRP and erythrocyte sedimentation rate (ESR) of 128 mg/L and 57 mm/h, respectively. Chest CT scan showed bilateral GGOs which was expected due to the underlying COVID-19 infection (). The axial unenhanced CT image of the brain showed a hypodense lesion in the superior and lateral aspects of the left cerebellar hemisphere without significant mass effect (). Due to his atrial fibrillation (AF) pattern in the electrocardiogram (ECG), along with his fluctuating SpO2, the patient was admitted to the intensive care unit (ICU). Patient received heparin-based prophylaxis. A single 500 mg oral dose of chloroquine phosphate, Kaletra (lopinavir/ ritonavir) two 200 mg tablets twice daily, meropenem 1 g IV q8hr and vancomycin 1 gram q12hr were administered. After 3 days, his drowsiness diminished and he was able to tolerate oral diets. Also, his CRP level decreased to 63 mg/L. Therefore, he was transferred to the infectious diseases ward. Four days later, he developed arrhythmia, confusion and new-onset hemiplegia. At the time, WBC count was 10.00×109/L with 9.5% lymphocytes; pro BNP, 8930 pg/mL; D-dimer, 7500 μg/L; CRP, 203 mg/L and PCT, 0.2 ng/mL. Anticoagulant was started for him and he was readmitted to ICU. Nine days later, his condition improved and he was discharged with an SpO2 of 95% and CRP of 30 mg/L.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [29.6, 'mg/dL'], 'Glucose': [102.0, 'mg/dL'], 'Sodium': [138.0, 'mEq/L']}",292.2381,277.62619,306.85001,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 29.6 mg/dL. 
The concentration of glucose is 102.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (29.6 / 2.8) + (29.6 / 18) = 292.2381 mmol/L.The patient's calculated serum osmolality concentration is 292.2381 mmol/L. This is equalivalent to 292.2381 mOsm/kg."
5762,30,Serum Osmolality,lab test,decimal,usmle-6150,Extracted,"A 27-year-old immigrant from Bolivia presents to the emergency department with cough and shortness of breath. She immigrated to the United States five months ago and does not present with any medical records. The patient also complains of nausea and vomiting. Her temperature is 99.5°F (37.5°C), blood pressure is 90/65 mmHg, pulse is 140/min, respirations are 18/min, and oxygen saturation is 98% on room air. Cardiac exam reveals an apical murmur. Pulmonary exam reveals mild bibasilar crackles. On abdominal exam, you note increased abdominal girth without any tenderness. Neurological and musculoskeletal exams are within normal limits. Laboratory values are ordered as seen below.

Hemoglobin: 12 g/dL
Hematocrit: 36%
Leukocyte count: 4,500/mm^3 with normal differential
Platelet count: 100,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.4 mEq/L
HCO3-: 24 mEq/L
BUN: 20 mg/dL
Glucose: 220 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.2 mg/dL
ß-hCG: 175,000 mIU/mL
AST: 12 U/L
ALT: 10 U/L

An EKG is performed as seen in Figure A. The patient is started on IV fluids.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [220.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",297.36508,282.49683,312.23333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 220.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (20.0 / 2.8) + (20.0 / 18) = 297.36508 mmol/L.The patient's calculated serum osmolality concentration is 297.36508 mmol/L. This is equalivalent to 297.36508 mOsm/kg."
5763,30,Serum Osmolality,lab test,decimal,usmle-5250,Extracted,"A 55-year-old male comes to the emergency department complaining of blood in his urine and severe back pain. He reports that the pain is left-sided, colicky, and began acutely this morning. The pain occasional radiates to his left groin. He also reports increased urinary frequency and an episode of blood-tinged urine. According to the patient, this has happened multiple times before. His medical history is also notable for hypertension, type II diabetes mellitus, and obstructive sleep apnea. His current medications include aspirin, metformin, and lisinopril. The patient’s temperature is 100.4°F (38°C), blood pressure is 148/85 mmHg, pulse is 71/min, and respirations are 14/min with an oxygen saturation of 98% on room air. Physical examination is significant for left-sided costovertebral angle tenderness. A urine dipstick is heme-positive. A urinalysis is pending. Labs are drawn, as shown below:

Serum:
Na+: 144 mEq/L
Cl-: 95 mEq/L
K+: 4.3 mEq/L
HCO3-: 23 mEq/L
Urea nitrogen: 18 mg/dL
Glucose: 142 mg/dL
Creatinine: 1.0 mg/dL
Calcium: 7.8 mg/dL

A radiograph is obtained, as shown in Figure A.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [144.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [18.0, 'mg/dL'], 'Glucose': [142.0, 'mg/dL']}",302.31746,287.20159,317.43333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 144.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 144.0 mEq. To convert from 144.0 mEq to mmol, convert from mEq to mmol. The compound 144.0 has a valence of 1, and so divide the valence by the value of mEq to get, 144.0 mEq/(1 mEq/mmol) = 144.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 144.0 mEq sodium/L converts to 144.0 mmol sodium/L. 
The concentration of bun is 18.0 mg/dL. 
The concentration of glucose is 142.0 mg/dL. 
Plugging these values into the equation, we get 2 * 144.0 + (18.0 / 2.8) + (18.0 / 18) = 302.31746 mmol/L.The patient's calculated serum osmolality concentration is 302.31746 mmol/L. This is equalivalent to 302.31746 mOsm/kg."
5764,30,Serum Osmolality,lab test,decimal,pmc-4852186-1,Extracted,"A 52-year-old African-American male presented to the emergency department with a one-week history of dark urine and abdominal pain. His past medical history was significant for spastic partial quadriplegia (C5-C7, incomplete) secondary to trauma six years prior, neurogenic bladder with suprapubic catheter placement five years prior, recurrent urinary tract infections (UTI), depression, and chronic constipation. He complained of pain and could localize it in the right lower quadrant of the abdomen with no radiation to any other part of the abdomen. He described the pain as constant, burning in nature, and 8 out of 10 in severity. The pain was associated with fever, chills, and nausea. On query, he denied hematuria, urostomy site discharge, flank pain, vomiting, diarrhea, or bloody stools. The patient had been afflicted by multiple UTIs in the last six months, the causal organisms for which included the Morganella species, Vancomycin-resistant enterococci, and Escherichia coli. His symptoms during this admission were consistent with those of his previous infections. Surgical history included two herniated cervical disc repairs and suprapubic catheter placement. He was not allergic to any drug in particular. His domiciliary medications included baclofen, gabapentin, docusate sodium, glycerin suppository, mirtazapine, and sertraline. He did not report any significant medical diseases running in his family. He did not report any alcohol, tobacco, or illicit drug use. His ambulation was restricted, necessitating bed confinement and the use of a wheelchair due to paraplegia and spastic deforming contractures. On physical exam, his blood pressure was 124/74, he had a pulse rate of 77, and his oral body temperature was 98.4 degrees Fahrenheit. His body mass index was 17.63 kg/m. The remainder of his physical examination was significant for lower extremity contractures. There was no abdominal tenderness and rigidity.
Initial lab work revealed a hemoglobin of 12.4 g/dl, a white blood count of 11.39 Th/uL, and a platelet count of 286 Th/uL. A basic metabolic panel (BMP) showed a sodium at 143 meq/L, potassium at 4.4 meq/L, chloride at 108 meq/L, bicarbonate at 27 meq/L, BUN at 17 mg/dl, and creatinine at 0.7 mg/dl. Blood sugars were at 97 mg/dl. Urinalysis with microscopy revealed purple urine, leukocytes at 21 40/HPF, RBCs at 15 cells/HPF, leukocyte esterase positive, and nitrates positive. Urine was alkalotic with a pH of 8.5 and a specific gravity of 1.010. Empirically intravenous ceftriaxone was initiated on a daily basis.
The patient’s catheter tubing and bag contained bright purple urine with small amounts of pale colored sediment. Figures - demonstrate purple-colored urine in the urine bag and catheter tubing, respectively. The patient denied any episodes of purple urine in the past. A urine culture grew Proteus vulgaris resistant to Cefazolin and sensitive to other cephalosporins, trimethoprim/sulfamethoxazole (TMP­ /SMX), and piperacillin/tazobactam. He was started empirically on ceftriaxone that was continued after culture results, and the following day clear yellow urine had accumulated in his urine bag. The blood cultures remained negative, and his leukocytosis resolved. After being given four doses of intravenous ceftriaxone and a discernible improvement in symptoms, he was discharged from the hospital on a three-day course of TMP /SMX to complete the prescribed seven-day course of antibiotics.
Informed patient consent was obtained for treatment of this patient.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [17.0, 'mg/dL'], 'Glucose': [97.0, 'mg/dL'], 'Sodium': [143.0, 'mEq/L']}",297.46032,282.5873,312.33334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 143.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 143.0 mEq. To convert from 143.0 mEq to mmol, convert from mEq to mmol. The compound 143.0 has a valence of 1, and so divide the valence by the value of mEq to get, 143.0 mEq/(1 mEq/mmol) = 143.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mEq sodium/L converts to 143.0 mmol sodium/L. 
The concentration of bun is 17.0 mg/dL. 
The concentration of glucose is 97.0 mg/dL. 
Plugging these values into the equation, we get 2 * 143.0 + (17.0 / 2.8) + (17.0 / 18) = 297.46032 mmol/L.The patient's calculated serum osmolality concentration is 297.46032 mmol/L. This is equalivalent to 297.46032 mOsm/kg."
5765,30,Serum Osmolality,lab test,decimal,pmc-4300485-1,Extracted,"A 45-year-old female was admitted in our hospital with a one-year history of generalized weakness, easy fatigability, loss of appetite, generalized body aches and pains, malaise and chronic ill health.
She had consulted several practitioners and been diagnosed as a case of major depressive disorder and hypothyroidism. She had been prescribed a number of antidepressants and Thyroxine. Detailed history revealed that the onset of symptoms had been 8 years earlier when she had her last child. It was a full term vaginal delivery at home. The patient denied any history of profuse bleeding postpartum. However, she had lactation failure and cessation of her menstrual cycles after the delivery.
Physical examination at the time of admission revealed an ill-looking patient with cold extremities and torso, feeble pulse with a rate of 54 bpm, blood pressure 80/60 mmHg in lying down and 68/ 50 mmHg in sitting posture; with postural drop (+), respiratory rate of 16/min, temperature (oral) 36.9ºF. The patient had pallor, coarse dry skin, non-pitting edema of lower limbs, sparse eyebrows and eyelashes, atrophied breasts, very scanty body hair and a hoarse voice. Chest and cardiovascular examinations were normal. Abdominal examination revealed diffuse tenderness. The patient was conscious, mentation, however, was slow. CNS examination revealed sluggish Deep Tendon Reflexes and a typical hung-up reflex was observed in the ankles.
Laboratory parameters showed anemia (normocytic, normochromic), blood sugar (random) 40 mg/dl, urea 26 mg/dl, serum creatinine 1.0 mg/dl, serum sodium 144 mEq /L, serum potassium 3.6 mEq/L, serum calcium 8.0 mg/dl. Liver function tests, chest roentgenogram, and USG abdomen were normal. ECG showed low voltage QRS complexes, sinus bradycardia, and prolonged QT interval (QTc=0.48 seconds). Routine urine examination revealed 8 to 10 pus cells without any evidence for the presence of sugar or albumin. The hormone profile showed serum cortisol (8.00 AM) 3.17 ug/dL (normal range 4.30-22.40), serum TSH 3.12 mIU/ml (normal range 0.5-6.5), serum FSH 3.00 mIU/l (normal range 2.0-6.6), serum LH 0.42 mIU/l (normal range 3.0-12.0), serum PRL 0.86 ng/ml (normal range >2.0) and serum GH 0.22 ng/ml (normal range >3.0). An impression of hypopituitarism was made based on history, physical examination and laboratory parameters (biochemical and hormonal).
The patient was managed with I.V. fluids (dextrose/normal saline) and hormone replacement therapy in the form of injection Hydrocortisone (50 mg I.V. 6 hourly) and Thyroxine at a dose of 50 mcg/day. The patient was also put on antibiotics (for UTI) and calcium supplements. Her general condition showed a dramatic improvement; appetite improved, blood pressure showed an upward trend and body and extremities became warm. Blood glucose levels increased from baseline 40 mg/dl to 165 mg/dl (random). The patient was switched to orals, and hydrocortisone was changed to tablets. Prednisolone 5 mg (morning), and 2.5 mg (evening), while Thyroxine continued at the same dose. The patient was discharged on the 7th day of admission and advised to continue the same medication at home.
MRI brain of the patient was done on follow up, which revealed an empty sella (). The rest of the scan was normal.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [26.0, 'mg/dL'], 'Glucose': [40.0, 'mg/dL'], 'Sodium': [144.0, 'mEq/L']}",299.50794,284.53254,314.48334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 144.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 144.0 mEq. To convert from 144.0 mEq to mmol, convert from mEq to mmol. The compound 144.0 has a valence of 1, and so divide the valence by the value of mEq to get, 144.0 mEq/(1 mEq/mmol) = 144.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 144.0 mEq sodium/L converts to 144.0 mmol sodium/L. 
The concentration of bun is 26.0 mg/dL. 
The concentration of glucose is 40.0 mg/dL. 
Plugging these values into the equation, we get 2 * 144.0 + (26.0 / 2.8) + (26.0 / 18) = 299.50794 mmol/L.The patient's calculated serum osmolality concentration is 299.50794 mmol/L. This is equalivalent to 299.50794 mOsm/kg."
5766,30,Serum Osmolality,lab test,decimal,pmc-7396026-1,Extracted,"A previously healthy 44-year-old male with no prior comorbidities presented to emergency with a 2-day history of fever, worsening headache, and generalized weakness. He had no history of exposure to pool water. Examination revealed a Glasgow coma scale (GCS) of 14/15 with no focal deficit or neck stiffness. Laboratory workup was sent which showed leukocytosis 13.3 × 109/L. Rest of the investigations are summarized in . Computed tomography (CT) scan brain was performed which was reported normal. Lumbar puncture was performed which showed a raised opening pressure of 20 cm of water and had a raised leucocyte count of 1100/µL with predominant polymorphonuclear cells of 60% with a very high protein of 241 mg/dl and low glucose, i.e., 30 mg/dl (). The BioFire filmarray Polymerase chain reaction (PCR) was negative for bacteria and viruses, but wet mount prep for Naegleria fowleri was positive which was further confirmed with PCR.
The patient was started on Primary amebic meningoencephalitis (PAM) protocol which included Intravenous (IV) and intrathecal amphotericin-B, Per Oral (PO) miltefosine, IV rifampin, IV fluconazole, and IV dexamethasone. He was electively intubated and shifted to the intensive care unit (ICU). A repeat CT scan after 24 hours of hospital stay was performed which did not show any infarct or bleed but did show marked cerebral edema. He was started on mannitol 30 grams every 8 hours, which was stopped after 48 hours.
During the ICU stay, the patient remained on mechanical ventilation and was deeply sedated with agents, IV propofol and midazolam. Antiepileptic drug IV levetiracetam was added empirically, and an Electroencephalogram (EEG) was obtained which showed theta and delta slowing down with no epileptiform activity. He was kept well hydrated during the ICU stay, and continuous feeding was carried out through a nasogastric tube.
On the 3rd hospital day, the patient started producing urine at 300–500 ml/hour (he made a urine output of more than 7 liters in 24 hours). His sodium levels increased from 144 mmol/L to 175 mmol/L in 12 hours. His urea was 18 mg/dl, ionized calcium was 4.88 mg/dl, and blood sugar levels were 171 mg/dl. He was well hydrated with IV ringer lactate. Serum and urinary osmolality were performed which were 332 mosm/kg and 204 mosm/kg, respectively. Urine sodium was less than 10 mEq/L. He was started on PO desmopressin of 0.2 micrograms twice daily after which his urine output dropped to 60–80 ml/hour and sodium decreased from 175 to 162 and, later, 155 mmol/L. On the 4th hospital day, he went in asystole and died. His family had decided for Do Not Resuscitate (DNR) during the ICU admission keeping in view of the poor outcome of primary amoebic meningoencephalitis.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [18.0, 'mg/dL'], 'Glucose': [171.0, 'mg/dL'], 'Sodium': [175.0, 'mmol/L']}",365.92857,347.63214,384.225,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 175.0 mmol/L. 
The concentration of bun is 18.0 mg/dL. 
The concentration of glucose is 171.0 mg/dL. 
Plugging these values into the equation, we get 2 * 175.0 + (18.0 / 2.8) + (18.0 / 18) = 365.92857 mmol/L.The patient's calculated serum osmolality concentration is 365.92857 mmol/L. This is equalivalent to 365.92857 mOsm/kg."
5767,30,Serum Osmolality,lab test,decimal,pmc-4528787-1,Extracted,"A 57-year-old man with a history of hypertension and right hip fracture called emergency medical services and complained of severe leg pain. When the emergency medical services team arrived on scene, the patient was found down on the floor with right leg weakness; he was confused and aphasic. No fumes or smoke was evident. His initial laboratory investigation at a local hospital showed potassium 6.1 mEq/L, blood urea nitrogen 26 mg/dL, creatinine 2.3 mg/dL, D-dimer 2240 µg/L, lactic acid 15 mmol/L, and glucose 166 mg/dL. Arterial blood gas analysis disclosed pH 6.60, PCO2 50 mm Hg, Po2 176 mm Hg, and HCO3 4.9 mEq/L on a Fio2 100%. Due to altered mental status, he was intubated and was subsequently transferred to our medical facility. On route, for the treatment of hyperkalemia, he was given 3 ampoules of sodium bicarbonate, calcium gluconate, kayexalate, and insulin with dextrose water.
Six hours after the incident, the patient was more alert and oriented and his leg pain had subsided. Details of smoking history could not be obtained due to the intubation. On physical examination, temperature was 35.8°C, heart rate 107 bpm, blood pressure 137/94 mm Hg, and respiratory rate 14 breaths/minute. He had regular heart rhythm, no murmur or pericardial rub. His abdomen was soft with active bowel sound. There were no symptoms and signs of limb ischemia on admission. He had no leg pain, pallor, poikilothermia, pulselessness, paresthesia, or paralysis. Motor power was at least grade 4 in all 4 extremities. His dorsalis pedis pulse was 2+ bilaterally. Initial investigations at our medical facility showed white blood cell 11400/µL, neutrophils 89%, hemoglobin 13.1 g/dL, hematocrit 38.6%, platelet 159000/µL, blood urea nitrogen 29 mg/dL, creatinine 2.0 mg/dL, sodium 142 mEq/L, potassium 3.9 mEq/L, chloride 102 mEq/L, bicarbonate 19 mEq/L, lactic acid 4.25 mmol/L, troponin T 0.1 ng/mL, and negative for acetone. Electrocardiogram showed sinus tachycardia and no ST-T change. The liver function test demonstrated aspartate aminotransferase 1697 IU/L, alanine aminotransferase 1263 IU/L, alkaline phosphatase 138 IU/L, total bilirubin 0.7 mg/dL, total protein 6.2 gm/dL, and albumin 3.5 mg/dL. Urinalysis showed white blood cell 5 to 10/high-power field, red blood cell 0 to 3/high-power field, moderate blood but negative for urine myoglobin. Coagulogram showed prothrombin time 17.5 seconds, partial thromboplastin time 25.8 seconds, and international normalized ratio 1.59. Calculated fractional excretion of sodium and urea were 2.11% and 43.67%, respectively, consistent with acute tubular necrosis. The viral hepatitis panel was negative except for a positive AntiHBc IgG antibody. Arterial blood gas analysis on admission depicted pH 7.319, PO2 130.3 mm Hg, PCO2 40.8 mm Hg, HCO3 20.5 mEq/L, and Sao2 100%, carboxyhemoglobin 0.2%, and methemoglobin 0.1% while on assist-control mode of mechanical ventilation with Fio
2 100%. Computed tomography of head was performed and showed chronic right basal ganglion infarct. Transthoracic echocardiography was performed and showed severely depressed left ventricular function with ejection fraction of less than 20%, grade II/IV diastolic dysfunction with mild TR, mild MR, and mild PR. Akinesis of the septal wall and hypokinesis of the anterolateral wall were present. Moreover, computed tomography of abdomen, pelvis, and chest without contrast revealed right lower lung consolidation with small right pleural effusion, moderately bilateral nonspecific perinephric fat stranding, submucosal fatty infiltration, and mild wall thickening of the descending colon down to the rectum. Subtle perirectal fat stranding was also visualized. Initially, he was treated with empiric antibiotics for possible pneumonia with severe sepsis with piperacillin-tazobactam, levofloxacin, and vancomycin. Aspirin and full-dose enoxaparin were started to cover possible acute coronary syndrome. Surgery was consulted due to a concern of bowel ischemia. Proctoscopy was done and showed normal pink rectal mucosa without blood in the vault. Because the patient was hemodynamically stable, had no abdominal pain, and lactic acid level had returned to normal, the surgery service recommended continued fluid replacement for volume expansion.
His lactate levels decreased spontaneously from 15 mmol/L to 3.39, 2.52, and 1.28 mmol/L at 0, 10, 14, and 33 hours, respectively, after his initial symptoms, along with an improvement of arterial pH and anion gap (). After 24 hours of admission, he improved dramatically and was extubated on day 2 of admission. Five hours after extubation (42 hours after admission), he started to have left leg pain. His left leg turned bluish and became paler with prominent livedo reticularis throughout his left leg (). Therefore, a heparin drip was initiated promptly and vascular surgery was consulted. Soon after that, the patient developed sudden cardiac arrest with pulseless electrical activity. He had return of spontaneous circulation after 15 minutes of cardiopulmonary resuscitation. At that moment, his lactate level rebounded to 8.13 mmol/L. To rule out acute aortic dissection and acute massive pulmonary embolism as well as acute left limb gangrene from embolism, computed tomography of pulmonary artery with contrast and computed tomography angiogram of aorta were performed. He had no pulmonary emboli or abdominal aortic dissection. He did have high-grade stenosis of the infrarenal abdominal aorta just above the bifurcation, near total occlusion of the right common iliac artery, severe luminal narrowing of the left common iliac artery, bilateral external iliac arteries, and bilateral common femoral arteries by calcified and noncalcified plaques ( and ). Emergent revascularization was planned but the patient developed pulseless electrical activity/asystole again and passed away.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [29.0, 'mg/dL'], 'Glucose': [166.0, 'mg/dL'], 'Sodium': [142.0, 'mEq/L']}",303.57937,288.4004,318.75834,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. 
The concentration of bun is 29.0 mg/dL. 
The concentration of glucose is 166.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (29.0 / 2.8) + (29.0 / 18) = 303.57937 mmol/L.The patient's calculated serum osmolality concentration is 303.57937 mmol/L. This is equalivalent to 303.57937 mOsm/kg."
5768,30,Serum Osmolality,lab test,decimal,pmc-8382603-1,Extracted,"A previously healthy 70-year-old man (without hypertension or diabetes) presented (on the June 25, 2020) at the Emergency Department with complaints of lower limb weakness with an acute onset of numbness and the feeling of dead lower limbs preceded by a cough, which was dry and paroxysmal, accompanied by mild chest discomfort and a high-grade fever without sweating or rigors. The fever and cough lasted for 7 days before the occurrence of weakness. His condition progressed over a day involving the upper limbs, neck, and facial muscles, and the patient was unable to turn in bed, stand, walk independently, move his upper limbs, or close his eyes. Difficulty swallowing, nasal regurgitation, or choking was not seen, and he had normal sensations and sphincters. Additionally, no convulsions, loss of consciousness, or other symptoms related to cranial nerves or higher functions were seen.
On examination, the patient was conscious, alert, and orientated to time, place, and person. A mini-mental status examination (MMSE) was at 30. A cranial nerve examination revealed bilateral facial nerve palsy on the right side with facial deviation to the left, and the inability to close both eyes and blow his cheeks to whistle. Nystagmus, ophthalmoplegia, diplopia, cerebellar symptoms, and bulbar palsy were not detected. He had a normal jaw jerk with weak neck flexion. Furthermore, an upper limb examination showed hypotonia with absent reflexes and a muscle power assessment (MRC) was at grade 3 proximally and grade 2 distally, with normal sensations and absent tendon reflexes. A lower limb examination also revealed hypotonia with an MRC of grade 2 proximally and distally, absent reflexes, normal sensations, a flexor plantar response with normal coordination, and the patient was unable to walk.
General investigations were conducted with complete blood counts showing hemoglobin (Hb) 11 g, total white blood cells 6, lymphocytes 12%, C-reactive protein (CRP) 110, erythrocyte sedimentation rate 70, platelets 396, serum ferritin 1000 ng/ml, blood urea 40 mg/dl, serum creatinine 0.9 mg/dl, serum potassium 3.5 mmol/L, sodium 135 mmol/L, alanine transferase 40, aspartate transaminase 20, alkaline phosphatase 150, random blood sugar 120 mg/dl, and a positive COVID-19 test. A computerized tomography (CT) chest scan showed a ground-glass appearance (Figures and ), and a nerve conduction study (NCS) reported demyelinating neuropathy consistent with acute inflammatory demyelinating polyradiculoneuropathy. Although it is a rare finding, a cerebrospinal fluid (CSF) examination was positive for both COVID-19 and supporting the diagnosis of Guillain-Barre syndrome.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [40.0, 'mg/dL'], 'Glucose': [120.0, 'mg/dL'], 'Sodium': [135.0, 'mmol/L']}",290.95238,276.40476,305.5,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.0 mmol/L. 
The concentration of bun is 40.0 mg/dL. 
The concentration of glucose is 120.0 mg/dL. 
Plugging these values into the equation, we get 2 * 135.0 + (40.0 / 2.8) + (40.0 / 18) = 290.95238 mmol/L.The patient's calculated serum osmolality concentration is 290.95238 mmol/L. This is equalivalent to 290.95238 mOsm/kg."
5769,30,Serum Osmolality,lab test,decimal,pmc-7427655-1,Extracted,"An apparently healthy 13-year-old male was admitted in the emergency department with symptoms of palpitations, muscle pain, tremors, and headache of 3-h duration. He denied fever, diarrhea, vomiting, or ingestion of any kind of drug. On physical examination, the patient had a good general condition, with height and weight on the 50th percentiles for age and gender. He was euvolemic, pale, and sweating. Cardiac auscultation revealed the presence of rhythmic tachycardia without murmurs or friction, and there was tachypnea without added bruises. He also presented weakness of the lower limbs and distal hand tremor. There were no skin lesions or edema.
Multiple medical results and 16 discharge reports from different hospitals were provided by the parents. The current clinical symptoms started when he was 10 years old and since that time he had had many recurrent episodes of severe hypokalemia that had led to frequent hospital admissions, one of them in the intensive care unit due to long QT syndrome (LQTS). Many diagnoses had been ruled out, e.g. familial hypokalemic periodic paralysis, by specific genetic testing.
The patient had a medical history of previous episodes of allergic asthma with sporadic use of terbutaline, gastritis due to H. pylori, sinus tachycardia, surgical correction of strabismus, appendicectomy, and a high-flow priapism secondary to arteriovenous fistula that had been treated with selective arterial embolization when he was 6 years old. Importantly, the medical team was informed that some years previously, as a consequence of unexplained detection of benzodiazepines in the patient’s blood, custody of the child had been temporarily withdrawn from the mother.
Amazingly, the minor behaved as an adult. He had the role of interlocutor with the medical team and his comments were full of medical vocabulary that showed technical knowledge that did not correlate well with his age.
Blood analysis at admission showed the following values: hemoglobin 12.3 g/dL, leukocytes 11.68×109/L, sodium 142 mmol/L, potassium 2.4 mmol/L, chloride 101 mmol/L, urea 4 mmol/L, creatinine 53 µmol/L, glomerular filtration rate (Schwartz formula) 112 mL/min/1.73 m2, glucose 5.6 mmol/L, transtubular potassium gradient 4.9, venous blood acid-base equilibrium pH 7.33, and HCO3
- 24.5 mmol/L. Urinalysis showed pH 6.5, sodium 162 mmol/L, potassium 38 mmol/L, urea 388 mmol/L, creatinine 22.8 mmol/L, urine osmolality 982 mOsm/kg, and fractional potassium excretion 36.8%. Proteinuria and hematuria were not observed. Hormone analysis revealed aldosterone after 30 min rest of 0.06 nmol/L and urinary aldosterone of 7.0 nmol/24 h. ECG showed sinus tachycardia of 120 bpm and a QT interval of 460 ms (max 440 ms). Renal ultrasound was normal and did not show lithiasis or nephrocalcinosis.
The treatment strategy consisted in intravenous potassium replacement, reaching normal potassium plasma levels after 12 h of parenteral infusion, with no need for further potassium supplements to maintain stable potassium levels in blood after discontinuation of parenteral infusion.
Two days after admission the patient was not receiving any potassium supplement or pharmacological treatment. He was asymptomatic and had potassium levels of 4.4 mmol/L in his 8:45 a.m. blood test. Suddenly he complained of intense headache, distal tremor, and tachycardia, and a second blood test performed at 2:15 p.m. revealed that the serum potassium level had decreased to 3.4 mmol/L. Thereafter, over a 2-h interval and without any specific treatment, the symptoms gradually disappeared and the patient was then discharged with oral potassium supplements.
Given the combination of transient and recurrent severe hypokalemia and rapid response to first-line treatment, as well as the presence of clinical signs suggestive of adrenergic crisis, a possible overdose of β-adrenergic agonist drugs was suspected. The two blood samples obtained on the day of discharge were analyzed at the Catalonian Antidoping Laboratory. Plasma salbutamol levels of 3 ng/mL and 65 ng/mL were present in the 8:45 a.m. and 14:15 p.m. blood samples, respectively [reference range for peak plasma concentration after 0.04-0.1 mg inhaler dose = 0.6-1.4 ng/mL. These findings confirmed the diagnosis of hidden abuse of β-adrenergic agonists in the context of a possible factitious syndrome.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [4.0, 'mmol/L'], 'Glucose': [5.6, 'mmol/L'], 'Sodium': [142.0, 'mmol/L']}",293.60786,278.92747,308.28825,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mmol/L. 
The concentration of bun is 4.0 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 4.0 mmol. To convert 4.0 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 4.0 mmol bun * 0.001 mol/mmol = 0.004 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.004 mol bun * 28.02 g/mol = 0.11208 g bun. To convert 0.11208 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.11208 g bun * 1000.0 mg/g = 112.08 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 112.08 mg bun/10.0 dL = 11.208 mg bun/dL. The concentration value of 4.0 mmol bun/L converts to 11.208 mg bun/dL. 
The concentration of glucose is 5.6 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 5.6 mmol. To convert 5.6 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 5.6 mmol glucose * 0.001 mol/mmol = 0.0056 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0056 mol glucose * 180.16 g/mol = 1.0089 g glucose. To convert 1.0089 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 1.0089 g glucose * 1000.0 mg/g = 1008.9 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1008.9 mg glucose/10.0 dL = 100.89 mg glucose/dL. The concentration value of 5.6 mmol glucose/L converts to 100.89 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (11.208 / 2.8) + (11.208 / 18) = 293.60786 mmol/L.The patient's calculated serum osmolality concentration is 293.60786 mmol/L. This is equalivalent to 293.60786 mOsm/kg."
5770,30,Serum Osmolality,lab test,decimal,pmc-3190515-1,Extracted,"A 48-year-old morbidly obese African-American male with a medical history of congestive heart failure, hypertension, obstructive sleep apnea on 2 l of home oxygen and non-complaint with continuous positive airway pressure at night presented to the emergency department (ED) with worsening shortness of breath and lower extremity oedema over one week. Vital signs in the ED were temperature, 98.7 degrees Fahrenheit; blood pressure, 116/66 mmHg; heart rate, 130 beats per minute; respiratory rate, 30; oxygen saturation, 85% on 2 l nasal cannula; weight, 162 kg and body mass index, 47. Physical examination revealed a morbidly obese male in acute respiratory distress with an irregularly irregular pulse and one plus lower extremity pitting oedema. Laboratory values in the ED include white blood cell count, 9 800/μl; haemoglobin, 14.2 g/dl; platelet count, 230 000/μl; sodium, 140 mEq/l; potassium, 4.5 mEq/l; chloride, 104 mEq/l; bicarbonate, 29 mEq/l; blood urea nitrogen (BUN), 38 mg/dl; creatinine, 1.4 mg/dl; glucose, 105 mg/dl; aspartate aminotransferase (AST), 51 U/l; alanine aminotransferase (ALT), 40 U/l; alkaline phosphatase, 68 U/l; total bilirubin, 1.5 mg/dl; albumin, 3.4 g/dl; total protein, 7.1 g/dl; international normalised ratio (INR), 1.2; myoglobin, 97 μg/l; troponin, 0.07 ng/ml and B-type natriuretic peptide, 934 pg/ml. Urine toxicology screen was positive for cocaine. Arterial blood gas showed a pH 7.33, paCO2 68.5 and paO2 88.6 on FiO2 of 40%. Electrocardiogram confirmed atrial fibrillation with a rapid ventricular response. Echocardiogram revealed a myopathic severely enlarged left ventricular chamber with moderate concentric left ventricular hypertrophy and severe global hypokinesis with an ejection fraction of 8 to 10%. The patient's work of breathing and oxygenation improved with Bipap. He was started on diltiazem and diuresis was initiated. The patient was admitted to the step-down unit with a new diagnosis of atrial fibrillation.
On hospital day number eight, the overnight nurse found the patient unresponsive. A code blue was called. His initial rhythm was ventricular fibrillation and he was shocked with 200 J twice before regaining pulses. When stabilised, he was transferred to the intensive care unit (ICU) where he regained consciousness and full neurologic function within one hour of the event. The following day, an automatic implantable cardioverter defibrillator (AICD) was placed. Intraoperatively, the patient had runs of ventricular tachycardia with hypotension to 80 mmHg systolic. Postoperatively, the patient was found to have a right fixed mid-dilated pupil, flaccid paralysis of the left arm and leg with hyperreflexia throughout the left side. Computed tomography (CT) of the head revealed a right midbrain and thalamic stroke thought to be secondary to transient arrhythmia-induced hypoperfusion, intraoperatively.
On postoperative day number three, after AICD placement and stroke, the patient acutely developed a rigid distended board-like abdomen with dullness to percussion. Vitals at that time were temperature, 98.4 degrees Fahrenheit; blood pressure, 112/67 mmHg; heart rate range, 55 beats per minute, and respiratory rate 26 on ventilator settings of assist control volume control with a rate of 26; tidal volume, 500 ml; FiO2, 40% and positive end-expiratory pressure of 5. His peak inspiratory pressure on the ventilator had risen from 26 to 72 mmHg; his plateau had risen from 15 to 48 mmHg with oxygen desaturation from 93 to 85%. The patient had received 1.5 l in and urinated 4.5 l over the 24 hours, leading up to this event. His laboratory values from that morning were unchanged from previous (white blood count, 10 400/μl; haemoglobin, 12.6 g/dl; platelets, 200 000/μl; sodium, 139 mEq/l; potassium, 4.7 mEq/l; chloride, 100 mEq/l; bicarbonate, 34 mEq/l; BUN, 36 mg/dl; creatinine, 1.41 mg/dl; glucose, 78 mg/dl; calcium, 8.3 mg/dl; magnesium, 2.0 mEq/l; phosphorus, 3.0 mg/dl; AST, 77 U/l; ALT, 94 U/l; alkaline phosphatase, 186 U/l; total bilirubin, 1.3 mg/dl). This constellation of findings prompted the team to measure an abdominal compartment pressure which was elevated to 53 cm H2O (40 mmHg) with an abdominal perfusion pressure (APP) of 42 mmHg. A CT scan of the abdomen and pelvis was performed which showed no dilated loops of bowel, no ileus, no evidence of free air, abscess or obstruction and minimal free fluid []. Pertinent labs from the event revealed a lactate of 1.0 mg/dl; lipase, 159 U/l; amylase, 76 U/l; creatinine, 1.53 mg/dl. Surgery was consulted and the FiO2 was increased to 100%, which improved his oxygen saturation to 96% despite his elevated peak inspiratory pressures.
Surgical recommendations were for an emergent bedside surgical abdominal decompression. The patient was administered 10 mg of intravenous cisatracurium besylate by anaesthesia in preparation for surgical management. Shortly following paralytic administration, his peak inspiratory pressure corrected from 72 to 23 mmHg, his plateau pressure from 48 to 16 mmHg and his oxygenation status tolerated a decrease in FiO2 down to 40% with his oxygen saturation returning to baseline. Measurement of his abdominal compartment pressure revealed a drop from 53 (40 mmHg) to 23 cm H2O (17 mmHg) and then normalised to 15 cm H20 (11 mmHg) over a three-hour period. During this entire event, the patient averaged 100 to 200 cc/hr of urine output and laboratory values from the following day showed a drop in creatinine from 1.53 to 1.29 mg/dl. Given this correction, surgical management was postponed and the patient was monitored. The patient remained hospitalised for an additional 73 days. He was ultimately transferred to a skilled nursing facility without return of symptoms.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [36.0, 'mg/dL'], 'Glucose': [78.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",295.19048,280.43096,309.95,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 36.0 mg/dL. 
The concentration of glucose is 78.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (36.0 / 2.8) + (36.0 / 18) = 295.19048 mmol/L.The patient's calculated serum osmolality concentration is 295.19048 mmol/L. This is equalivalent to 295.19048 mOsm/kg."
5771,30,Serum Osmolality,lab test,decimal,pmc-6007257-1,Extracted,"A 55-year-old female patient was examined in the emergency department with abdominal pain that had been persistent for ~10 days and having been aggravated for the last 3–4 days. Her past history was notable for diabetes mellitus (DM) for ~25 years. Additionally, she had undergone a coronary by-pass operation 10 years ago and a left infrapatellar amputation 4 years ago. Chronic renal failure had been diagnosed 2 years ago and she had been receiving hemodialysis treatment three times a week for the last 1 year. She had no history of abdominal trauma. Laboratory tests resulted with; White Blood Cell: 15 100/mm3, Hemoglobin: 8.5 g/dL, C-reactive protein: 40 mg/dL, Urea: 37.9 mg/dL, Creatinine: 2.25 mg/dL, Albumin: 2.4 g/dL, Sodium: 134 mmol/L, Potassium: 3.1 mmol/L, Calcium: 7.9 mg/dL, Glucose: 329 mg/dL and other biochemical parameters were normal. The abdomen was diffusely tender, and she also had guarding and rebound tenderness during the physical examination. Blood temperature was 38.7°C. An abdominal ultrasonography (US) showed diffuse intraabdominal free fluid collection. On an abdominal computed tomography (CT) there were free fluid collections in all abdominal quadrants; there also existed intraabdominal minimal free air images. There were air-fluid images in the splenic parenchyma (abscess?, perforation?) (Fig. a). The radiology department reported that it may be a gastrointestinal perforation. Based on the current findings, the patient was urgently operated according for a preliminary diagnosis of acute abdomen. Intraabdominal seropurulent fluid of ~2000 ml was aspirated perioperatively. There were diffuse fibrin matrixes in the entire peritoneum. No intestinal perforation was noted during exploration. There was a perforated abscess pouch with a size of ~8 × 6 cm2, which expanded posteriorly from splenic hilus and partly contained necrotic foci (Fig. b). Splenectomy and drainage were performed and the abdominal cavity was irrigated with abundant isotonic saline. Patient was postoperatively monitored in intubated state at intensive care unit. No proliferation occurred in her blood culture. Escherichia coli was isolated from the abscess culture, however, and Meropenem 500 mg I.V. (three times a day) and Metronidazole 500 mg I.V. (three times a day) treatment was commenced as recommended by the infectious diseases department. Her dialysis program was maintained according to blood parameters. The patient died on postoperative Day 25 due to septic shock and multiple organ failure. Histopathologic examination revealed suppurative inflammation and abscess formation of the splenic tissue (Fig. ). Informed consent was obtained from her son who participated in this case.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [37.9, 'mg/dL'], 'Glucose': [329.0, 'mg/dL'], 'Sodium': [134.0, 'mmol/L']}",299.81349,284.82282,314.80416,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mmol/L. 
The concentration of bun is 37.9 mg/dL. 
The concentration of glucose is 329.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (37.9 / 2.8) + (37.9 / 18) = 299.81349 mmol/L.The patient's calculated serum osmolality concentration is 299.81349 mmol/L. This is equalivalent to 299.81349 mOsm/kg."
5772,30,Serum Osmolality,lab test,decimal,usmle-5830,Extracted,"A 72-year-old man presents to the primary care clinic for evaluation of progressive fatigue and weight loss. His past medical history is significant for hypercholesterolemia, type 2 diabetes mellitus, aortic stenosis, and chronic renal insufficiency. He endorses being well-rested after waking from sleep but fatiguing rapidly during the day. In addition, he states that he has lost 15lbs over the previous month. His temperature is 98.3°F (36.8°C), pulse is 100/min, blood pressure is 110/85 mmHg, respirations are 16/min, and oxygen saturation is 96% on room air. Physical exam is notable for conjunctival pallor and scattered areas of ecchymoses. His laboratory results are shown below:

Serum:
Na+: 140 mEq/L
K+: 4.0 mEq/L
Cl-: 101 mEq/L
HCO3-: 22 mEq/L
BUN: 30 mg/dL
Glucose: 160 mg/dL
Creatinine: 1.9 mg/dL


Leukocyte count: 1,100/mm^3
Absolute neutrophil count 920/mm^3
Hemoglobin 8.4 g/dL
Platelet count: 45,000/mm^3
Mean corpuscular hemoglobin concentration: 34%
Red blood cell distribution width: 12.0%
Mean corpuscular volume: 92 µm^3
Lactate dehydrogenase: 456 IU/L
Haptoglobin 120 mg/dL
Fibrinogen 214 mg/dL

A bone marrow biopsy is performed which shows cells that are CD19+, CD20+, CD11c+, and stain with acid phosphatase 5 and tartrate-resistant.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [30.0, 'mg/dL'], 'Glucose': [160.0, 'mg/dL']}",299.60317,284.62301,314.58333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 30.0 mg/dL. 
The concentration of glucose is 160.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (30.0 / 2.8) + (30.0 / 18) = 299.60317 mmol/L.The patient's calculated serum osmolality concentration is 299.60317 mmol/L. This is equalivalent to 299.60317 mOsm/kg."
5773,30,Serum Osmolality,lab test,decimal,pmc-3475921-1,Extracted,"A 41-year-old female presented with insidious onset headache of 6-month duration, which was diffuse, dull aching, at times exacerbated to severe throbbing headache. There were no aggravating and relieving factors, no association with visual symptoms, vomiting, fever or any other neurologic symptoms. During evaluation by her neurologist, computerized tomography (CT) of brain was performed, which showed a sellar mass. She was further evaluated by neurosurgeon and a magnetic resonant imaging (MRI) was performed which confirmed a sellar mass with a probable diagnosis of pituitary adenoma. She was referred to us for endocrinological work-up. On further questioning she did not have any symptoms related to pituitary dysfunction. Her past history was significant for being empirically treated for tubercular pericardial effusion 10 years back. She had two children, with the second delivery 8 years back. She had an uneventful postpartum period. General and physical examination was essentially normal. Visual perimetry showed normal visual fields in both eyes.
Her hematological and biochemical work-up was normal barring erythrocyte sedimentation rate (ESR) which was 54 mm at the end of first hour. Her hemoglobin was 14 g/ dl; total leucocyte count was 6700/μl, neutrophil count of 64%, lymphocyte count of 30%, monocyte 4%, eosinophil 2%; fasting plasma glucose 92 mg/dl, blood urea 22 mg/ dl, serum creatinine 0.6 mg/dl, serum bilirubin 0.5 mg/dl, ALT-6IU/l, ALP 32 IU/l, serum alkaline phosphatase 86 U/l, serum calcium 8.5 mg/dl, serum phosphates 3.4 mg/dl. She had normal hormonal work-up (fT3 – 3.4 pg/ ml [2.4-4.2], fT4 – 1.4 ng/ ml [0.8-1.7], TSH – 3.56 [0.5- 6.5] μIU/ml; LH/FSH – 7.8/9.4 IU/l; S. estradiol– 75 pg/ml; S. prolactin – 14 ng/ml [< 25]; S. Cortisol basal/ACTH stimulated – 14 /23.6 μg/dl). The Mantoux test was strongly positive (20×55mm). Chest radiography, 2D echocardiogram, ultrasound abdomen were normal. Serum angiotensin convertase enzyme was 39.0 U/l (8-65). Autoimmune workup did not reveal any abnormality with CRP – 1.2 mg/l (normal < 7 mg/l); antinuclear antibodies (< 1:40), and antineutrophilic cytoplasmic antibodies (< 1:16), anti-TPO Ab - 4 IU/l (< 9), RA factor 4 IU/l (< 20), and anti-TTG Ab- 3.54 IU/ ml (< 15). CT scan of chest and abdomen was normal. A review of MRI brain favored hypophysitis more than pituitary adenoma in view of homogeneity of the mass, thickened and midline pituitary stalk, strong and diffuse enhancement after contrast, and loss of posterior pituitary hyper intensity and maintenance of sellar floor []. The possibility was discussed with the patient and close observation with steroid therapy was contemplated.
However, before initiation of steroids she had an episode of severe headache with vomiting without any neurological deficits. The episode made the patient apprehensive of her underlying sellar mass and she favored surgery. She underwent successful transnasal transsphenoidal excision of the mass. Postoperatively she had transient diabetes insipidus on the second and third postoperative days, revealed by marked polyuria and raised serum sodium [154 meq/l (135-145 meq/l)]. It was managed with subcutaneous injection vasopressin, followed by no further requirement of vasopressin from the fourth postoperative day onward. The histopathological examination of the tissue showed the lesion to be filled with well-defined epitheloid granulomas, lymphocytic infiltration, and histiocytes []. Immunohistochemistry stained positive for CD3 (T-lymphocytes), CD20 (B-lymphocytes), and CD68 (histiocytes) []. In view of these findings a diagnosis of combined granulomatous and lymphocytic hypophysitis was made. There were no acid-fast bacilli seen. Tissue PCR could not be done due to financial constraints. Postoperatively she was asymptomatic, had normal pituitary functions, and there was no residual lesion on MRI.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [22.0, 'mg/dL'], 'Glucose': [92.0, 'mg/dL'], 'Sodium': [154.0, 'mEq/L']}",320.96825,304.91984,337.01666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 154.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 154.0 mEq. To convert from 154.0 mEq to mmol, convert from mEq to mmol. The compound 154.0 has a valence of 1, and so divide the valence by the value of mEq to get, 154.0 mEq/(1 mEq/mmol) = 154.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 154.0 mEq sodium/L converts to 154.0 mmol sodium/L. 
The concentration of bun is 22.0 mg/dL. 
The concentration of glucose is 92.0 mg/dL. 
Plugging these values into the equation, we get 2 * 154.0 + (22.0 / 2.8) + (22.0 / 18) = 320.96825 mmol/L.The patient's calculated serum osmolality concentration is 320.96825 mmol/L. This is equalivalent to 320.96825 mOsm/kg."
5774,30,Serum Osmolality,lab test,decimal,pmc-4488998-1,Extracted,"A 41-year-old female, with a past medical history of DM1 treated with insulin glargine and insulin aspart, presented with a 1-day history of diffuse abdominal pain and weakness. Her symptoms were associated with chills, nausea, and just one episode of emesis. Over the preceding 4 days, the patient had developed a Bartholin's gland cyst infection with abscess formation. She admitted to abstaining from any solid food intake in the previous 2 days; however, she maintained her liquid intake and continued taking her insulin glargine without insulin aspart. She denied any alcohol intake or drug abuse. Her vital signs were within normal limits. Physical examination was significant for diffuse abdominal tenderness without rigidity or guarding and a ruptured Bartholin's gland abscess with drainage to the skin. Blood work showed a white blood cell (WBC) count of 13,000 cells/mcL (normal range: 4,500-10,000/mcL), hemoglobin level 11.2 mg/dL (normal range: 12.3-15.3 g/dL), platelet count 448,000/mcL (normal range: 150,000-450,000/mcL), sodium 135 mmol/L (normal range: 136-145 mmol/L), potassium 3.6 mmol/L (normal range: 3.5-5.1 mmol/L), chloride 105 mmol/L (normal range: 98-107 mmol/L), carbon dioxide 6 mmol/L (normal range: 21-32 mmol/L), anion gap 24 mmol/L (normal range: 3-11 mmol/L), urea nitrogen 4 mg/dL (normal range: 7-18 mg/dL), creatinine 0.58 mg/dL (normal range: 0.6-1.3 mg/dL), glucose 191 mg/dL (normal range: 70-100 mg/dL), beta hydroxybutyrate >4.5 mg/dL (normal range: <0.4 mg/dL), magnesium 1.3 mg/dL (normal range: 1.6-2.3 mg/dL), phosphorus 1.3 mg/dL (normal range: 2.5-4.9 mg/dL), lactate 0.8 mmol/L (normal range: 0.4-2 mmol/L), and HBA1C 12.5% (normal range: 4-5.6%). Urinalysis was significant for +3 ketones and sugar. Arterial blood gas showed pH 7.07, pCO2 12. A urine drug screen was negative, and serum ethanol level was undetectable.
The patient was diagnosed with euglycemic DKA precipitated by an underlying infection. Intravenous fluid (IVF) resuscitation with normal saline was initially started at a rate of 1.0 L/h for a total of 2 L. The patient's hydration status, serum electrolytes, blood urea nitrogen (BUN), creatinine, glucose, and urine output were monitored closely. After 2 h, repeat blood work showed a serum sodium 141 mmol/L, carbon dioxide 8 mmol/L, potassium 3.5 mmol/L, and glucose 153 mg/dL. Subsequently, IVFs were switched to 5% dextrose and 0.45% NaCl at a rate of 250 cc/h, and an insulin drip at a rate of 5 units/h was started. Then, 30 mEq potassium was added to each liter of the IVF, excluding the first liter, targeting a serum potassium level of 4-5 mEq/L. After 11 h, blood work revealed a serum bicarbonate level of 16 mmol/L with a normal anion gap; hence, subcutaneous insulin and oral intake were initiated. Intravenous insulin was continued for another hour to ensure adequate plasma insulin levels. The Bartholin's gland abscess was treated, and the patient was discharged on the following day.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [141.0, 'mmol/L'], 'Glucose': [153.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [4.0, 'mg/dL']}",291.92857,277.33214,306.525,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mmol/L. 
The concentration of bun is 4.0 mg/dL. 
The concentration of glucose is 153.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (4.0 / 2.8) + (4.0 / 18) = 291.92857 mmol/L.The patient's calculated serum osmolality concentration is 291.92857 mmol/L. This is equalivalent to 291.92857 mOsm/kg."
5775,30,Serum Osmolality,lab test,decimal,pmc-3980927-1,Extracted,"A 53-year-old African American female presented to the emergency department with a one-day history of upper and lower extremity weakness and paresthesias. She reported waking up with lower extremity weakness and became progressively weak and unable to ambulate throughout the course of the morning. After sustaining a fall, she was able to crawl to the nearest phone to call a friend to transport her to the emergency department.
The patient's past medical history consisted of hypertension, diabetes mellitus, pulmonary hypertension, nonischemic cardiomyopathy, and systolic heart failure. Home medications included simvastatin 40 mg daily, digoxin 0.125 mg daily, furosemide 40 mg daily, carvedilol 25 mg twice daily, lisinopril 10 mg daily, spironolactone 25 mg twice daily, insulin 70/30 (40 units every AM, 25 units every PM), ferrous sulfate 325 mg daily, and potassium chloride 20 mEq twice daily. The patient reported taking two potassium chloride tablets twice daily for approximately the past week.
Vital signs on admission were as follows: temperature 36.5°C, blood pressure 139/77 mmHg, pulse 95 beats/min, respiratory rate 13 breaths/min, and oxygen saturation 98% on room air. Physical examination revealed flaccid paralysis in both upper and lower extremities. Cranial nerves and sensation were intact with no focal motor deficits. Pertinent laboratory values on admission were as follows: sodium 127 mEq/L, potassium greater than 8 mEq/L, carbon dioxide 15 mEq/L, blood urea nitrogen 114 mg/dL, glucose 316 mg/dL, creatinine 3.5 mg/dL, and digoxin 1.8 ng/mL. Electrocardiogram (ECG) showed first-degree atrioventricular block (PR interval 246 ms) with peaked T waves. The patient was determined to be in acute renal failure with her baseline creatinine being 1.3 mg/dL four months prior to admission; history also revealed radiocontrast administration with no timing specified in relation to this admission for acute renal failure.
Upon receiving laboratory results, therapy was immediately initiated with one gram of calcium gluconate, 10 units of regular insulin plus 25 grams of dextrose, and 50 mEq of sodium bicarbonate intravenously. Repeat labs two hours after treatment revealed a serum potassium concentration of 8 mEq/L. Serum potassium was decreased to 6.5 mEq/L three hours after additional sodium bicarbonate and insulin plus a 30 gram dose of sodium polystyrene sulfonate. Repeat serum creatinine at this time was 2.8 mg/dL. The patient was admitted for further workup and management of nonoliguric renal failure and hyperkalemia. Neuromuscular symptoms and ECG returned to baseline within 24 hours of presentation and serum potassium returned to 4.2 mEq/L at approximately 36 hours. Lisinopril, spironolactone, and potassium chloride therapies were discontinued and hydralazine and isosorbide mononitrate were initiated prior to discharge.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [127.0, 'mEq/L'], 'Glucose': [316.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [114.0, 'mg/dL']}",312.26984,296.65635,327.88333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 127.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 127.0 mEq. To convert from 127.0 mEq to mmol, convert from mEq to mmol. The compound 127.0 has a valence of 1, and so divide the valence by the value of mEq to get, 127.0 mEq/(1 mEq/mmol) = 127.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 127.0 mEq sodium/L converts to 127.0 mmol sodium/L. 
The concentration of bun is 114.0 mg/dL. 
The concentration of glucose is 316.0 mg/dL. 
Plugging these values into the equation, we get 2 * 127.0 + (114.0 / 2.8) + (114.0 / 18) = 312.26984 mmol/L.The patient's calculated serum osmolality concentration is 312.26984 mmol/L. This is equalivalent to 312.26984 mOsm/kg."
5776,30,Serum Osmolality,lab test,decimal,pmc-4365329-1,Extracted,"A 54-year-old white female presented with abdominal pain, nausea, vomiting, and diarrhea (five watery bowel movements every day) for 2 days. The patient states that she has been eating a regular diet and denied eating outside the home and did not have fever, and no one in the family had similar symptoms. Past medical history was positive for hypothyroidism and bipolar disorder and family history was negative for diabetes. One year prior to this presentation the patient had routine blood work with fasting blood glucose of 95 mg/dL. The patient reported polyuria and polydipsia for one month prior to this presentation but did not seek any medical attention.
On physical examination her blood pressure was 127/65 mmHg, heart rate 80 beat/min, and temperature 37°C. Her body mass index was 35 kg/m2. She was in mild distress and had no thyromegaly, clear lungs, regular heart without murmurs, soft abdomen but with generalized tenderness, and hyperactive bowel sounds throughout. The remainder of the physical exam was normal.
WBC 14.8 × 109/L with neutrophils 89%, hemoglobin 18.2 g/L, and platelets 241 × 109/L. Her chemistry shows sodium 132 mmol/L, potassium 3.9 mmol/L, chloride 99 mmol/L, bicarbonate 12 mmol/L, BUN 5.71 mmol/L, creatinine 53.3 μmol/L, calcium 2.35 mmol/L, phosphorus 1.55 mmol/L, magnesium 1.1 mmol/L, and blood glucose 18.76 mmol/L. Arterial blood gases show PH 7.25, Pco2 3.72 kPa, and Po2 9.58 kPa on room air. Lactic acid was 1 mmol/L, amylase 1.1 μkat/L, and lipase 0.27 μkat/L, and serum ketones were positive. Her hemoglobin A1C was 13.7%. Urinalysis was positive for glucose and ketones.
It was obvious from the labs that the patient had diabetic ketoacidosis (high blood glucose, low bicarbonate, and positive ketones) with anion gap of 21. The patient was admitted to the medical intensive care unit. Intravenous normal saline fluid bolus was given with maintenance intravenous fluid after that. She was kept on nothing per mouth and started on insulin drip with hourly blood glucose check and every four hours serum electrolytes (sodium, potassium, chloride, magnesium, and phosphorus) check.
CT scan of the abdomen showed mild distension of the proximal small bowel and tiny amount of free fluids with wall thickening of distended small bowel loops. She was started on ampicillin/sulbactam after getting blood cultures. Stool sample was sent for analysis and the results were negative leukocytes and negative clostridium difficile toxin. Therefore, we decided to stop the antibiotics at this point and treat her as viral gastroenteritis. Later on, the patient's symptoms have improved and her anion gap closed, so we started her on liquid diet (which she was able to tolerate). She was switched to subcutaneous insulin injections (as insulin glargine at bedtime and sliding scale insulin before each meal) and transferred to medical floor. Her blood cultures did not grow any bacteria, and stool culture was negative. Insulin autoantibodies were negative, c-peptide was lower than normal (0.34 ng/mL), and her glutamic acid decarboxylase autoantibodies were highly positive (>30 U/mL).
After having diabetic education including a dietitian consult in the hospital, the patient was discharged home on subcutaneous insulin treatment with a diagnosis of latent autoimmune diabetes in adult. The patient was encouraged to do regular exercise.
The patient was concerned about her new diagnosis and its possible complications which required counseling about the importance of taking care of her diabetes and how this would help prevent future complications.
The patient was very compliant with the discharge plan and checked her blood sugar before each meal and at bedtime. She followed up in the diabetic clinic on a biweekly basis to adjust her insulin dose. Three months later her hemoglobin A1C was 7.7%. The patient has not experienced any adverse or unanticipated events.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [5.71, 'mmol/L'], 'Glucose': [18.76, 'mmol/L'], 'Sodium': [132.0, 'mmol/L']}",288.4906,274.06607,302.91513,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 132.0 mmol/L. 
The concentration of bun is 5.71 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 5.71 mmol. To convert 5.71 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 5.71 mmol bun * 0.001 mol/mmol = 0.00571 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.00571 mol bun * 28.02 g/mol = 0.15999 g bun. To convert 0.15999 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.15999 g bun * 1000.0 mg/g = 159.99 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 159.99 mg bun/10.0 dL = 15.999 mg bun/dL. The concentration value of 5.71 mmol bun/L converts to 15.999 mg bun/dL. 
The concentration of glucose is 18.76 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 18.76 mmol. To convert 18.76 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 18.76 mmol glucose * 0.001 mol/mmol = 0.01876 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.01876 mol glucose * 180.16 g/mol = 3.3798 g glucose. To convert 3.3798 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 3.3798 g glucose * 1000.0 mg/g = 3379.8 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 3379.8 mg glucose/10.0 dL = 337.98 mg glucose/dL. The concentration value of 18.76 mmol glucose/L converts to 337.98 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 132.0 + (15.999 / 2.8) + (15.999 / 18) = 288.4906 mmol/L.The patient's calculated serum osmolality concentration is 288.4906 mmol/L. This is equalivalent to 288.4906 mOsm/kg."
5777,30,Serum Osmolality,lab test,decimal,usmle-6158,Extracted,"A 25-year-old man presents to the emergency department for severe abdominal pain. The patient states that for the past week he has felt fatigued and had a fever. He states that he has had crampy lower abdominal pain and has experienced several bouts of diarrhea. The patient states that his pain is somewhat relieved by defecation. The patient returned from a camping trip 2 weeks ago in the Rocky Mountains. He is concerned that consuming undercooked meats on his trip may have caused this. He admits to consuming beef and chicken cooked over a fire pit. The patient is started on IV fluids and morphine. His temperature is 99.5°F (37.5°C), blood pressure is 130/77 mmHg, pulse is 90/min, respirations are 12/min, and oxygen saturation is 98% on room air. Laboratory studies are ordered and are seen below.

Hemoglobin: 10 g/dL
Hematocrit: 28%
Leukocyte count: 11,500 cells/mm^3 with normal differential
Platelet count: 445,000/mm^3

Serum:
Na+: 140 mEq/L
Cl-: 102 mEq/L
K+: 4.1 mEq/L
HCO3-: 24 mEq/L
BUN: 24 mg/dL
Glucose: 145 mg/dL
Creatinine: 1.4 mg/dL
Ca2+: 9.6 mg/dL
Erythrocyte sedimentation rate (ESR): 75 mm/hour

Physical exam is notable for a patient who appears to be uncomfortable. Gastrointestinal (GI) exam is notable for abdominal pain upon palpation. Ear, nose, and throad exam is notable for multiple painful shallow ulcers in the patient’s mouth. Inspection of the patient’s lower extremities reveals a pruritic ring-like lesion. Cardiac and pulmonary exams are within normal limits.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [24.0, 'mg/dL'], 'Glucose': [145.0, 'mg/dL']}",296.62698,281.79563,311.45833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 24.0 mg/dL. 
The concentration of glucose is 145.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (24.0 / 2.8) + (24.0 / 18) = 296.62698 mmol/L.The patient's calculated serum osmolality concentration is 296.62698 mmol/L. This is equalivalent to 296.62698 mOsm/kg."
5778,30,Serum Osmolality,lab test,decimal,pmc-3845239-1,Extracted,"A male patient aged 4 years and 3 months presented to the ER (emergency room) of our hospital with vomiting, diarrhea, and seizures. On day 1 of the illness, he had developed gastrointestinal symptoms, including vomiting and watery diarrhea that occurred 4-5 times per day. Four days later, bilateral generalized tonic-clonic seizures began, for which he was transported to our hospital. The seizures lasted up to 1 minute and subsided spontaneously. The patient was in a restless state of consciousness (level E3V4M5 according to the Glasgow Coma Scale and level II-10 according to the Japan Coma Scale). He stared, averted his gaze, continued to cry, and threw objects. This disturbance of consciousness persisted for 7 hours. The patient was sedated with midazolam, and MRI was performed. On awakening after 2 hours, the patient had regained a normal state of consciousness, after which there was no recurrence of disturbance of consciousness or seizures.
On admission, the patient's vital signs were as follows: temperature, 37.7°C; heart rate, 130 beats/minute; blood pressure, 100/60 mmHg; and SpO2, 98% (room air). No central nervous system abnormality, meningeal irritation, paralysis, or abnormalities in the thoracoabdominal region were observed. MRI revealed a hyperintense signal in the splenium of the corpus callosum on DWI and a hypointense signal in the ADC-map (). The patient's peripheral circulation was good.
The patient's medical history was unremarkable. He was born by spontaneous cephalic delivery after 39 weeks and 3 days of gestation (birth weight, 2664 g). No remarkable observations were noted during the pregnancy or perinatal period. The patient's growth and development were normal. The family medical history revealed that the father had febrile seizures.
The results of the patient's biochemical blood tests were as follows: WBCs, 3900/μL; Hb, 13.4 g/dL; Plt, 26.1 × 104/μL; BUN, 16 mg/dL; Cre, 0.3 mg/dL; Na, 132 mEq/L; K, 4.5 mEq/L; Cl, 101 mEq/L; AST, 41 IU/L; ALT, 21 IU/L; CRP, 2.59 mg/dL; Glu, 84 mg/dL; lactic acid, 7.8 mg/dL; pyruvic acid, 0.32 mg/dL; NH3, 49 μg/dL; pH, 7.424; PCO2, 39.6 mmHg; HCO3, 25.5 mmol/L; and BE, 1.6 mmol/L. No abnormality was detected on blood amino acid analysis or tandem mass screening. Cerebrospinal fluid (CSF) examination revealed a cell count of 4 cells (all mononuclear), a glucose concentration of 95 mg/dL, and a total protein concentration of 16 mg/dL.
On day 2 of admission, an electroencephalogram was obtained during sedated sleep. The spindle wave was appropriate for the patient's age. No bursts were observed. The patient's stool was positive for RV antigen. RT-PCR did not reveal RV RNA in the blood or CSF. RT-PCR analysis of RNA extracted from the stool revealed that the RV genotype was G5P[6].
On day 5 of admission, no recurrences were observed, and the patient was discharged. Eight days after admission, all abnormal signals had disappeared (). The clinical course was typical of MERS.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [16.0, 'mg/dL'], 'Glucose': [84.0, 'mg/dL'], 'Sodium': [132.0, 'mEq/L']}",274.38095,260.6619,288.1,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 132.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 132.0 mEq. To convert from 132.0 mEq to mmol, convert from mEq to mmol. The compound 132.0 has a valence of 1, and so divide the valence by the value of mEq to get, 132.0 mEq/(1 mEq/mmol) = 132.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 132.0 mEq sodium/L converts to 132.0 mmol sodium/L. 
The concentration of bun is 16.0 mg/dL. 
The concentration of glucose is 84.0 mg/dL. 
Plugging these values into the equation, we get 2 * 132.0 + (16.0 / 2.8) + (16.0 / 18) = 274.38095 mmol/L.The patient's calculated serum osmolality concentration is 274.38095 mmol/L. This is equalivalent to 274.38095 mOsm/kg."
5779,30,Serum Osmolality,lab test,decimal,pmc-4902214-1,Extracted,"A 33-year-old man presented to the emergency department ED) with complaint of 2-day history of abdominal pain. His pain developed with gradual onset prominently in epigastric area after eating dried mushrooms. The pain was diffuse, persistent, radiating to the back and aggravated by meal. He had been tolerating only liquids and had complaints of nausea and vomiting. He had no history of diabetes mellitus, hypertension, alcohol consumption, malignancy, or prior surgery. On arrival his blood pressure was 128/72 mmHg, with a heart rate of 101 beats/minute and a respiratory rate of 20 breaths/minute. He was afebrile. Physical examination revealed diffuse abdominal distention, hyper-pitched bowel sounds, and tenderness more marked over the umbilicus with no guarding or rebound tenderness. A complete blood cell count showed the following: leukocyte count 12600 /mm3; segmented neutrophils 90%; hemoglobin level of 14 mg/dl; hematocrit 30%; and platelet 420000/µL. Other laboratory studies included: glucose 101 mg/dL; serum urea nitrogen 45 mg/dL; serum creatinine 2.0 mg/dL; sodium 148 mEq/L; potassium 3.1 mEq/L; serum glutamic oxaloacetic transaminase (SGOT) 38 U/L and lipase 30 U/L. shows patient’s plain upright abdominal X-ray as well as coronal and axial cuts of abdominal CT scan.
What is your diagnosis?
Diagnosis:
Abdominal CT scan showed multiple masses with peculiar shape (, arrows) in stomach and ileum. Post contrast CT scan showed peculiar shape masses impacting the bowel on the middle side of the abdomen with dilated small intestine above that level. The CT scan finding was consistent with evidence of a mechanical obstruction.
Case fate:
The patient underwent conservative treatment such as nasogastric suction, decompression, aggressive intravenous fluids, bowel rest and antibiotics for 3 days. The undigested mushrooms had passed through later. He had an uneventful recovery with no complications.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [45.0, 'mg/dL'], 'Glucose': [101.0, 'mg/dL'], 'Sodium': [148.0, 'mEq/L']}",317.68254,301.79841,333.56667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 148.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 148.0 mEq. To convert from 148.0 mEq to mmol, convert from mEq to mmol. The compound 148.0 has a valence of 1, and so divide the valence by the value of mEq to get, 148.0 mEq/(1 mEq/mmol) = 148.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 148.0 mEq sodium/L converts to 148.0 mmol sodium/L. 
The concentration of bun is 45.0 mg/dL. 
The concentration of glucose is 101.0 mg/dL. 
Plugging these values into the equation, we get 2 * 148.0 + (45.0 / 2.8) + (45.0 / 18) = 317.68254 mmol/L.The patient's calculated serum osmolality concentration is 317.68254 mmol/L. This is equalivalent to 317.68254 mOsm/kg."
5780,30,Serum Osmolality,lab test,decimal,pmc-5471576-1,Extracted,"A 33-year-old female presented to the emergency room complaining of painful lesions on her right upper extremity that began approximately two days prior to presentation. She also noted generalized malaise, chills, subjective fever, nausea, vomiting, abdominal pain, and dyspnea on exertion. She became short of breath with minimal activity. Past medical history was significant for hepatitis C, polysubstance abuse, and nicotine dependence. Approximately six months prior to current illness, she was hospitalized and treated for staphylococcal left knee septic arthritis.
Initial vital signs were BP 144/71 mmHg, pulse 107 beats/min, temperature 98.1°F (36.7°C), respiratory rate 20 breaths/min, and oxygen saturation 99% breathing ambient air. Physical examination demonstrated petechiae and ecchymosis on all four extremities along with several tender erythematous nodules. She also had jugular venous distention to the angle of the mandible. There were bibasilar rales on pulmonary examination and a 2/6 intensity holodiastolic murmur was present at the 2nd right interspace on cardiac examination. There was mild bilateral lower extremity pitting edema. The remainder of the physical exam was unremarkable. Laboratory data demonstrated serum sodium 131 mEq/L, potassium 3.0 mEq/L, chloride 97 mEq/L, bicarbonate 24 mEq/L, BUN 21 mg/dl, creatinine 1.01 mg/dl, and glucose of 110 mg/dL. Cardiac troponin was undetectable. White blood cell count was 9.3 k/μl, hemoglobin 14.3 g/dl, hematocrit 41.5%, and platelet count 99 k/μl. Blood cultures grew Methicillin Sensitive Staphylococcus aureus (MSSA). Electrocardiogram demonstrated accelerated junctional rhythm at 99 beats/minute with retrograde P waves ().
Transthoracic echocardiogram revealed normal LV chamber dimension, wall motion, and left ventricular ejection fraction estimated at 60–65%. The aortic valve was not clearly visualized but aortic regurgitation was noted with continuous wave and color flow Doppler. Transesophageal echocardiogram revealed severe aortic regurgitation; pressure half-time of the regurgitant jet was 320 ms. A large mobile mass measuring 1.3 cm by 1.0 cm was attached to the septal wall of the left ventricular outflow tract (LVOT) (Figures and ). The mass was attached at the site of a jet lesion where the aortic valve regurgitant jet contacted the LVOT wall ().
She was treated with intravenous antibiotics. Due to the size and location of the vegetation, she was referred for aortic valve replacement and resection of the LVOT vegetation. Pathologic analysis of the native aortic valve revealed a 0.6 × 0.4 cm ovoid perforation of the noncoronary leaflet likely due to prior endocarditis with acute vegetation on the septal surface of the LVOT under the right coronary leaflet. The patient did well postoperatively and was treated adequately with a six-week course of intravenous antibiotics.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [131.0, 'mEq/L'], 'Glucose': [110.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [21.0, 'mg/dL']}",275.61111,261.83055,289.39167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 131.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 131.0 mEq. To convert from 131.0 mEq to mmol, convert from mEq to mmol. The compound 131.0 has a valence of 1, and so divide the valence by the value of mEq to get, 131.0 mEq/(1 mEq/mmol) = 131.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 131.0 mEq sodium/L converts to 131.0 mmol sodium/L. 
The concentration of bun is 21.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 131.0 + (21.0 / 2.8) + (21.0 / 18) = 275.61111 mmol/L.The patient's calculated serum osmolality concentration is 275.61111 mmol/L. This is equalivalent to 275.61111 mOsm/kg."
5781,30,Serum Osmolality,lab test,decimal,pmc-7029460-1,Extracted,"A 76-year-old white man presented to our emergency department (ED) with recent onset of unsteady gait, poor oral intake, dysarthria, and dizziness for 1 week prior to presentation. His wife called an ambulance and had him brought to our ED as she noticed he was short of breath for the prior 12 hours. He did not have any symptoms suggestive of a recent upper respiratory tract infection or gastroenteritis. He denied exposure to sick contacts, recent immunizations, or consumption of canned foods or beverages. He did have a past medical history significant for esophageal stricture (diagnosed 2 years before) for which he had been undergoing routine endoscopic balloon dilation (last attempt was 3 months before). He lived in a rural upstate New York county and had retired as a meat-cutter 15 years before. His only medications at the time were ferrous sulfate (324 mg daily), pantoprazole (40 mg twice daily), and a multivitamin. He did not have a history of tobacco smoking. He consumed approximately two standard drinks in a week. He had no known allergies. While in our ED, his vital signs were: temperature, 37 ºC (98.6 ºF); heart rate, 100–110 beats per minute; blood pressure, 141/82 mmHg; and oxygen saturation 82% on room air and requiring 100% fraction of inspired oxygen (FiO2) via facemask to maintain saturations above 96%. On physical examination, he was in marked respiratory distress but not toxic-appearing. He was awake but drowsy, oriented only to self. His pupils were equal and symmetrical with appropriate response to light. His extra-ocular movements were intact. There was no facial droop; there was no deviation of tongue or uvula. His gag reflex was impaired. He could move all four extremities spontaneously and on command. However, motor strength appeared to be symmetrically and mildly diminished in all extremities and accompanied by decreased tone. Diminished knee and ankle reflexes were noted bilaterally. He had a diminished flexor plantar response bilaterally. Sensation was grossly intact in his face, trunk, and extremities. Coordination was impaired in upper and lower extremities with dysmetria and dysdiadochokinesia. Gait was not assessed. He had no visible involuntary movements. His neck was supple without signs of meningismus. A cardiovascular examination was unremarkable, with normal heart sounds and equal symmetrical pulses in bilateral extremities. His abdominal, musculoskeletal, and skin examinations were unremarkable. Although he was hemodynamically stable, he became lethargic with stridor and progressive hypoxia. Given concern for airway protection, he was emergently intubated with a 7.5 mm endotracheal tube on first attempt and placed on mechanical ventilatory support. For intubation, he was administered 1.5 mg/kg of succinylcholine and 0.3 mg/kg of etomidate intravenously. Maintenance fluids (normal saline at 125 cc/hour) and empiric intravenous administration of ceftriaxone at a dose of 2 g every 24 hours (to cover for possible aspiration pneumonia) was initiated. He was transferred to our intensive care unit for further management. A nasopharyngolaryngoscopy revealed bilateral true vocal cord paralysis. After stabilization on a ventilator, he underwent a tracheostomy on day 3 of admission and was transitioned successfully to a tracheostomy collar. Following extubation, he had consistent and gradual recovery of mental status. This was not, however, accompanied by any progressive improvement in motor function. He continued to have vocal cord immobility and flaccid weakness of his extremities.
On presentation, laboratory testing revealed a white blood cell (WBC) count, 13,800 cells/μL; hemoglobin, 14.7 g/dl; platelet count, 235,000 cells/μL; sodium, of 143 mmol/L; potassium, 4.2 mmol/L; chloride, 105 mmol/L; glucose, 176 mg/dL; bicarbonate, 27 mmol/L; creatinine, 0.53 mg/dL; blood urea nitrogen (BUN), 15 mg/dL; and calcium, 8.0 mg/dL. A hepatic function panel revealed a total protein level, 5.2 g/dL; serum albumin, 3.5 g/dL; total bilirubin, 0.5 mg/dl; aspartate aminotransferase (AST), 18 U/L; alanine aminotransferase (ALT), 21 U/L; international normalized ratio (INR), 1.08; creatine kinase, 127 U/L; and troponin I less than 0.015 ng/mL. Urine analysis demonstrated cloudy urine with specific gravity 1.018, pH 4.8, with 116 red blood cells (RBCs) and 4 white blood cells (WBCs), negative leukocyte esterase and nitrite. An electrocardiogram and chest X-ray were unremarkable. A urine drug screen and serum alcohol levels were negative. Serum thyroid-stimulating hormone (TSH) and cortisol levels were within normal limits. Thiamine, vitamin B6, and B12 levels were normal. Serological tests were negative for Lyme disease, human immunodeficiency virus (HIV), syphilis, hepatitis B, and hepatitis C. Blood and urine cultures obtained at presentation showed no growth. Non-contrast computed tomography (CT) of his head and magnetic resonance imaging (MRI) of his brain were normal except for mild ventriculomegaly (Fig. ). CT angiography of his head and neck revealed patent intracranial vasculature. A repetitive nerve stimulation electromyographic (EMG) study demonstrated patchy, moderate to severe, peripheral motor nerve denervation consistent with AIDP. A lumbar puncture was performed and analysis of the obtained cerebrospinal fluid (CSF) showed albuminocytologic dissociation with less than 3 nucleated cells per mL of fluid, elevated CSF protein of 62 mg/dl, and normal glucose levels (88 mg/dl). CSF cultures did not demonstrate any growth. Anti-GQ1B antibody and anti-acetylcholine receptor (AChR) antibody levels were negative.
A subacute presentation with ataxia, stridor with respiratory distress, and areflexia with weakness of bilateral upper and lower extremity offers a challenging differential (Table ).
It is prudent to first rule out an acute vascular cause such as stroke, especially involving the cerebellum and brainstem; for example, for example, an absence of any lateralizing neurological signs and disturbed consciousness would rule out stroke, especially one with brainstem involvement. Next, metabolic abnormalities due to alcoholism, vitamin deficiencies, or electrolyte deficiencies would be evident on a metabolic panel and on serum vitamin and ethyl alcohol levels. An absence of a suggestive history of exposure to Clostridium botulinum, such as consumption of canned or tinned foods, cosmetic use of botulinum toxin injection, or intravenous drug use, significantly lowers the possibility of botulism. An absence of fever and meningeal signs, and analysis of CSF obtained on lumbar puncture, can rule out meningitis and encephalitis. Spinal cord trauma and spinal shock in the initial stages would result in flaccid paralysis of extremities aside from obvious signs of trauma. Also, concomitant bulbar paralysis is highly unlikely. Overlapping autoimmune demyelinating syndromes such as Guillain–Barré syndrome (GBS) and Bickerstaff’s brainstem encephalitis (BBE) must be considered. GBS is more likely to have a characteristic pattern of ascending paralysis. BBE is considered to lie on the same spectrum as MFS as it may present with ataxia and ophthalmoplegia and can have positive anti-GQ1b antibodies. However, BBE is characterized more by hyperreflexia and somnolence. New-onset MG can be suspected but, in our patient, motor involvement was patchy, the anti-AChR antibody test result was negative, and EMG was not suggestive of MG.
Based on the above, a diagnosis of MFS involving the bulbar muscles was made and our patient was started on a 5-day course of intravenous immunoglobulin at a daily dose of 0.4 mg/kg body weight per day. Following completion of this course, he showed clinical improvement in phonation, overall muscle strength, as well as tone. Although he initially did require overnight ventilatory support through his tracheostomy, the need for this gradually diminished and he was weaned off the ventilator altogether.
Subsequent follow-up laryngoscopies after 1, 2, and 4 weeks showed improvement in vocal cord abduction. His overall respiratory status also improved with decreasing oxygen requirement and decreased need for tracheostomy suctioning. He continued to have moderate pharyngeal dysphagia and required placement of a jejunostomy tube for feeding. His hospitalization was also complicated with development of aspiration pneumonia. He was eventually discharged to a skilled nursing facility on a tracheostomy collar and jejunostomy tube after a total of 6 weeks of hospitalization and subsequently discharged home after making suitable progress in physical rehabilitation. He continued to follow-up with the physical medicine and rehabilitation (PMR) out-patient clinic and remained tracheostomy-dependent at 6 months following hospitalization. He was able to ambulate with a walker at that time.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [15.0, 'mg/dL'], 'Glucose': [176.0, 'mg/dL'], 'Sodium': [143.0, 'mmol/L']}",301.13492,286.07817,316.19167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 143.0 mmol/L. 
The concentration of bun is 15.0 mg/dL. 
The concentration of glucose is 176.0 mg/dL. 
Plugging these values into the equation, we get 2 * 143.0 + (15.0 / 2.8) + (15.0 / 18) = 301.13492 mmol/L.The patient's calculated serum osmolality concentration is 301.13492 mmol/L. This is equalivalent to 301.13492 mOsm/kg."
5782,30,Serum Osmolality,lab test,decimal,pmc-4020898-1,Extracted,"The subject was a 23-year-old Japanese man with no abnormalities identified on examination and no particular medical history. Two weeks prior to onset of cardiac arrest, he noticed slight fever, coughing, loss of appetite, and weight loss of 3 kg. He did not have symptoms such as nausea, vomiting, or diarrhea. While jogging, the patient became aware of back pain and lost consciousness. A bystander immediately administered basic life support. Then, emergency medical technician-paramedics continuously administered cardiac pulmonary resuscitation using an automated external defibrillator to the subject, who was thereafter transported by ambulance to our hospital, Yamaguchi Grand Medical Center.
At the time of transfer to the hospital, the blood pressure of the subject could not be measured. An electrocardiogram (ECG) monitor indicated that his heart rate was 30 bpm (pulseless electrical activity) (). In addition, his body temperature was 37.3°C and he had a Glasgow coma scale score of E1M1V1 (no eye opening, no verbal response, no motor response). Physical examination revealed swelling of the thyroid gland on the anterior side of the neck; however, there were no signs of jaundice or peripheral edema. In addition, there were no signs of exophthalmos, finger tremor, loss of hair, or nail lesions. Because of pulseless electrical activity, cardiac arrest was diagnosed using an ECG, and administration of medication (epinephrine and atropine) led to ventricular fibrillation ( and ). As a result, defibrillation was administered using a direct current (DC) type 360-J monophasic defibrillator (Nihon Kohden Corporation, Tokyo, Japan) and the sinus rhythm was restored. Nonetheless, heart rate and breathing sounds were normal.
The laboratory findings were as follows: a white blood cell count of 13,800/μL; hemoglobin, 12.0 g/dL; platelets, 434,000/μL; C-reactive protein, 0.2 mg/dL; aspartate aminotransferase, 51 IU/L; alanine aminotransferase, 74 IU/L; lactic dehydrogenase, 217 IU/L; creatine kinase 61 IU/L; creatine kinase MB 46 IU/L; troponin T, <0.05 ng/mL; blood urea nitrogen, 16.4 mg/dL; creatinine, 0.81 mg/dL; blood glucose, 77 mg/dL; sodium, 143 mmol/L; potassium, 5.8 mmol/L; chloride, 97 mmol/L; calcium, 9.2 mg/dL; arterial blood gases (FiO2:100%, timing of return of spontaneous circulation and post-tracheal intubation); pH 7.53; PaCO2 30.8 mmHg; PaO2 184 mmHg; and HCO3 11.4 mEq/L.
Chest radiography revealed no congestion or pneumothorax in the lung field. After the sinus rhythm improved, an ECG revealed no significant changes in ST-T or QT interval prolongation (). In the echocardiography results, there was no cardiac wall motion dyssynchrony suggestive of ischemic heart disease, and the ejection fraction was 70%. There were no right side of the heart findings indicative of cardiac tamponade and thromboembolism. Thyroid ultrasound imaging showed that the parenchyma was marginally irregular and heterogeneous with rich blood flow.
On examination of thyroid function, the following findings were obtained: thyroid-stimulating hormone (TSH) level: <0.005 (reference range: 0.24–3.72), free thyroxine (T4) level: 5.03 (reference range: 0.94–1.52), free triiodothyronine (T3) level: >30.00 (reference range: 2.01–3.72), TSH receptor antibody: 30.2% (reference values: <15), and TSH-stimulating receptor antibody: 146% (reference values: <180).
After spontaneous circulation was returned, the reduced level of consciousness persisted and artificial respiration and cerebral hypothermia were administered. Hyperthyroidism-induced thyroid storm was strongly suspected and the patient was treated with thiamazole 60 mg/day, inorganic iodine (iodine solution 150 mg/day), hydrocortisone 300 mg/day, and metoprolol tartrate (beta-blocker) 120 mg/day for 2 weeks. After the initial 2 weeks, thiamazole 60 mg/day and metoprolol tartrate (beta-blocker) 120 mg/day were taken.
On day 22 of hospitalization, the subject was weaned from the artificial respirator; however, hypoxic encephalopathy- induced higher cerebral dysfunction persisted.
On day 30 of hospitalization, follow-up testing revealed that free T4 and free T3 levels had returned to normal (free T4 level: 1.46 and free T3 level: 3.43), but TSH suppression persisted (TSH <0.005). Because of higher cerebral dysfunction, coronary angiogram and magnetic resonance imaging (MRI) of the heart were not performed in accordance with the wishes of his family. On day 55, the subject was transferred to another hospital for long-term medical care. TSH level was 0.14 at the time.
At the present 1-year follow-up, no signs of recurrent ventricular fibrillation or other cardiac arrest rhythms have been observed in the other hospital in which the patient is receiving long-term medical care.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [16.4, 'mg/dL'], 'Glucose': [77.0, 'mg/dL'], 'Sodium': [143.0, 'mmol/L']}",296.13492,281.32817,310.94167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 143.0 mmol/L. 
The concentration of bun is 16.4 mg/dL. 
The concentration of glucose is 77.0 mg/dL. 
Plugging these values into the equation, we get 2 * 143.0 + (16.4 / 2.8) + (16.4 / 18) = 296.13492 mmol/L.The patient's calculated serum osmolality concentration is 296.13492 mmol/L. This is equalivalent to 296.13492 mOsm/kg."
5783,30,Serum Osmolality,lab test,decimal,pmc-6962441-1,Extracted,"A 43-year-old woman visited the emergency room for oliguria. She was followed up in the hospital for type I diabetes mellitus, chronic kidney disease due to diabetic nephropathy, hypertension and heart failure with dilated cardiomyopathy. She had a history of volume depletion due to diarrhea and a decrease in urine volume. At the time of arrival, level of consciousness was drowsy and the Glasgow coma scale was 14. Physical examination revealed dehydration, including decrease in skin turgor, and tongue dehydration. The vital signs were blood pressure 110/60mmHg, pulse rate 104 beats/min, respiratory rate 20 breaths/min, and body temperature 36.2℃. In the chest auscultation the cardiac sound was normal without murmur and the breath sound was normal. Abdominal examination revealed no specific findings such as tenderness, and no pitting edema was observed in the lower extremities. Complete blood cell count examination revealed hemoglobin 8.3 g/dL; hematocrit 27.7%; WBC 12,070/mm3; and platelet count 195,000/mm3. The initial laboratory values were: serum sodium 134mEq/L; potassium 4.2mEq/L; calcium 8.71mg/dL; phosphorus 4.28mg/dL; magnesium 1.89mg/dL; serum urea nitrogen 46.7mg/dL; creatinine 6.86mg/dL; albumin 2.49 g/dL; total bilirubin 0.12mg/dL; AST/ALT 6.7/3.8 IU/L; glucose 235mg/dL; lactic acid 8.21mg/dL; alkaline phosphatase 68 IU/L; NGAL 739 ng/mL; ammonia 77 ug/dL; Pro-BNP >35,000 pg/mL; and CRP 3.95mg/dL. Arterial blood gas analysis revealed pH 7.14; pCO2 24mmHg; pO2 121mmHg, and tCO2 8.3mL/dL. The serum IgA was 109 mg/dL; ASO 32U; C3 92mg/dL; C4 35mg/dL; FANA negative; and ANCA negative. In the urine analysis, the specific gravity of urine was 1.007; pH 5.0; urine protein 2+; blood 3+; RBC 1–4/HPF; and WBC 5–9/HPF. Urine creatinine level was 14.9mg/dL, and urine protein was 6.78mg/dL. In the immune serum test, the HBs Ag/Ab, Anti-HCV Ab, Anti-HIV Ab, and VDRL results were all negative. Due to persistence of oliguria, continuous RRT was started. On the ninth hospital day, her mentation changed from alert to stupor mentation. The Glasgow coma scale (GCS) changed from 15 to 5. Brain images showed normal findings (). The following laboratory values were obtained: serum sodium 138mEq/L; potassium 4.5 mEq/L; calcium 8.26mg/dL; phosphorus <0.41mg/dL; magnesium 1.96 mg/dL; serum urea nitrogen 21.4mg/dL; creatinine 1.45 mg/dL; albumin 2.32 g/dL; glucose 209 mg/dL; and CRP 2.75mg/dL. After phosphate intravenous replacement, 0.25–0.5mmol/kg monobasic potassium phosphate (Phosten, JW, Korea) for 6 days, and administration of phosphate-containing replacement solution Phoxilium(containing phosphate at 1.2 mmol/L; Baxter Gambro, Deerfield, IL, USA) use, the phosphate level increased to 2.97mEq/L and mental state returned to alert (). On the 29th day of continuous RRT, normal urine volume was recovered with decrease in serum creatinine level. On the 33rd day, serum creatinine level decreased to 2.08mg/dL, subsequently RRT was stopped. At the time of discharge, serum creatinine and phosphorus level were 1.82mg/dL and 2.75mg/dL, respectively with alert mentation. The patient is still on outpatient follow-up.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [46.7, 'mg/dL'], 'Glucose': [235.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",297.73413,282.84742,312.62084,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. 
The concentration of bun is 46.7 mg/dL. 
The concentration of glucose is 235.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (46.7 / 2.8) + (46.7 / 18) = 297.73413 mmol/L.The patient's calculated serum osmolality concentration is 297.73413 mmol/L. This is equalivalent to 297.73413 mOsm/kg."
5784,30,Serum Osmolality,lab test,decimal,usmle-1292,Extracted,"Two days after admission to the hospital, a 74-year-old man develops confusion and headache. He has also been vomiting over the past hour. His temperature is 36.7°C (98°F), pulse is 98/min, respirations are 22/min, and blood pressure is 140/80 mm Hg. He is lethargic and oriented only to person. Examination shows flushed skin. Fundoscopic examination shows bright red retinal veins. Serum studies show:
Na+ 138 mEq/L
K+ 3.5 mEq/L
Cl- 100 mEq/L
HCO3- 17 mEq/L
Creatinine 1.2 mg/dL
Urea nitrogen 19 mg/dL
Lactate 8.0 mEq/L (N = 0.5 - 2.2 mEq/L)
Glucose 75 mg/dL
Arterial blood gas analysis on room air shows a pH of 7.13.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [19.0, 'mg/dL'], 'Glucose': [75.0, 'mg/dL'], 'Sodium': [138.0, 'mEq/L']}",286.95238,272.60476,301.3,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 19.0 mg/dL. 
The concentration of glucose is 75.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (19.0 / 2.8) + (19.0 / 18) = 286.95238 mmol/L.The patient's calculated serum osmolality concentration is 286.95238 mmol/L. This is equalivalent to 286.95238 mOsm/kg."
5785,30,Serum Osmolality,lab test,decimal,pmc-2652426-1,Extracted,"A 72-year-old man with known history of stage 3 chronic kidney disease, hypertension, coronary artery disease, hyperlipidemia presented with a 3-days history of low-grade fever, productive cough, dyspnea, night sweats and fatigue. Patient was a non-smoker and did not consume alcohol. His kidney disease was likely due to renovascular or/and chronic atheroembolic disease with baseline serum creatinine level of 1.7 mg/dl, giving him an estimated glomerular filtration rate of 50 mL/min/1.73 m2. His medications included metoprolol, isosorbide mononitrate, gabapentin, aspirin, candesartan, tamsulosin, atorvastatin. On examination, he was alert, and not in distress. His blood pressure was 140/80 mm Hg without orthostatic changes and temperature 100.3°F. The remainder of the examination was unremarkable except of few wheezes over both lung fields. He did not have pedal edema. Serum sodium was 145 mEq/L, potassium 4.8 mEq/L, urea nitrogen 34 mg/dl, creatinine 1.7 mg/dl and glucose 130 mg/dl. Hemoglobin was 12.1 g/dL, white blood cells 5.2 × 109/L and platelets 208 × 109/L. Treatment with 250 mg of azithromycin daily was given for six days without clinical improvement. A chest radiograph showed small left apical nodules and computed tomography (CT) scan of the chest demonstrated right lower lobe scarring and left upper lobe small nodules with focal pleural thickening (Figure ). Three weeks later, serum creatinine rose to 2.6 mg/dl and urea to 48 mg/dl. Urine volume never decreased; urinalysis showed trace proteinuria, without glucose or blood. Urine sediment did not show red blood cells, white blood cells or casts. Urine sodium was 35 mmol/L. Patient completed 2 weeks treatment with 500 mg of levofloxacin, with some clinical improvement. Six weeks after initial presentation, cultures of two sputum samples were reported to be positive for Mycobacterium gordonae and Mycobacterium avium complex (MAC) by DNA probe and subsequently the positive diagnosis of pulmonary nontuberculous mycobacterial infection was made. The patient rejected long-term triple therapy, given his mild symptoms and a concern about treatment adverse effects. The patient has remained well throughout a 2 months period of close clinical observation; he has been afebrile and his serum creatinine level returned to baseline of 1.7 mg/dl.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [34.0, 'mg/dL'], 'Glucose': [130.0, 'mg/dL'], 'Sodium': [145.0, 'mEq/L']}",309.36508,293.89683,324.83333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 145.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 145.0 mEq. To convert from 145.0 mEq to mmol, convert from mEq to mmol. The compound 145.0 has a valence of 1, and so divide the valence by the value of mEq to get, 145.0 mEq/(1 mEq/mmol) = 145.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 145.0 mEq sodium/L converts to 145.0 mmol sodium/L. 
The concentration of bun is 34.0 mg/dL. 
The concentration of glucose is 130.0 mg/dL. 
Plugging these values into the equation, we get 2 * 145.0 + (34.0 / 2.8) + (34.0 / 18) = 309.36508 mmol/L.The patient's calculated serum osmolality concentration is 309.36508 mmol/L. This is equalivalent to 309.36508 mOsm/kg."
5786,30,Serum Osmolality,lab test,decimal,usmle-8125,Extracted,"A 59-year-old man presents with intense, sharp pain in his toe for the past hour. He reports similar symptoms in the past and this is his 2nd visit to the emergency department this year with the same complaint. The patient is afebrile and the vital signs are within normal limits. On physical examination, there is significant erythema, swelling, warmth, and moderate pain on palpation of the right 1st toe. The remainder of the examination is unremarkable. A plain radiograph of the right foot reveals no abnormalities. Joint arthrocentesis of the inflamed toe reveals urate crystals. Laboratory studies show:
Serum glucose (random) 170 mg/dL
Sodium 140 mEq/L
Potassium 4.1 mEq/L
Chloride 100 mEq/L
Uric acid 7.2 mg/dL
Serum creatinine 0.8 mg/dL
Blood urea nitrogen 9 mg/dL
Cholesterol, total 170 mg/dL
HDL-cholesterol 43 mg/dL
LDL-cholesterol 73 mg/dL
Triglycerides 135 mg/dL
HDL: high-density lipoprotein; LDL: low-density lipoprotein
Ibuprofen is prescribed for the acute treatment of this patient's symptoms. He is also put on chronic therapy to prevent the recurrence of future attacks.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [9.0, 'mg/dL'], 'Glucose': [170.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",292.65873,278.02579,307.29167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 9.0 mg/dL. 
The concentration of glucose is 170.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (9.0 / 2.8) + (9.0 / 18) = 292.65873 mmol/L.The patient's calculated serum osmolality concentration is 292.65873 mmol/L. This is equalivalent to 292.65873 mOsm/kg."
5787,30,Serum Osmolality,lab test,decimal,pmc-3656526-1,Extracted,"One-and-a-half year old girl, born to non-consanguineous parents presented with sudden onset of protracted vomiting and unconsciousness of two days duration. She did not have fever. She was apparently asymptomatic till then. She had attained developmental milestones appropriately. She was able to walk independently, scribble, show few body parts and was able to speak a few meaningful words. Her growth was subnormal with both weight (7.4 kg) and length (76 cm) being less than third centile for age. On examination, her Glasgow Coma Scale score was five. She had hypotonia of all four limbs with brisk deep tendon reflexes. Bilateral plantar reflexes were extensors. There were no signs of meningeal irritation. She had a palpable liver 3 cm below costal margin with a span of 7 cm. Other systems were within normal limits. Her initial investigations revealed hemoglobin of 10.3 g%, total leucocyte count of 8300/mm3, platelet count of 2,79,000/mm3. Neutrophils comprised 84% and lymphocytes 14%. Her blood glucose concentration was 106 mg/dL (60-150 mg/dL), blood urea 42 mg/dl (8-32 mg/dL), serum creatinine 0.4 mg/dL (0.6-1.6 mg/dL), serum sodium 114 mEq/L (130-143 mEq/L), and serum potassium 5 mEq/dL (3.5-5 mEq/L). Liver enzymes were normal with aspartate transaminase of 37 U/L (5-40 U/L), alanine transaminase of 34 U/L (5-40 U/L), and alkaline phosphatase of 197 U/L (40-140 U/L). Cerebrospinal fluid analysis showed no cells on microscopy and gram stain and culture were negative for any organism. CSF glucose was 100 mg/dL (more than or equal to two thirds of blood sugar) and CSF protein was 54 mg/dL (10-20 mg/dL). Arterial blood gas analysis revealed a pH of 7.073 (7.35-7.45), PaO2 of 214 mmHg, PaCO2 of 8.2 mmHg (35-45 mmHg), HCO3- of 2.3 mmol/L (20-28 mmol/L) suggesting severe metabolic acidosis with a high anion gap. Serum ammonia was 2834 μg% (25-94 μg%) suggesting severe hyperammonemia. Serum lactate was 26 mg/dL (5-22 mg/dL). Thin layer chromatography of urine revealed moderate organic aciduria with significant ketonuria and excretion of valine and alanine. She was treated with intravenous sodium benzoate and fluids. Gradually her sensorium improved and she recovered from the acute illness. However she had residual left lower limb monoparesis. She was started on oral sodium benzoate, thiamine, biotin and carnitine and continued on the same.
Over next six months she gradually improved and achieved normal development except in gross motor domain. By two years of age she was speaking with two word sentences and achieved bowel control. She was able to walk with support. Over the next 4 to 4½ years period, she was regularly followed up for continuation of medications, development assessment, nutritional management and rehabilitation. She had three more acute episodes with vomiting and lethargy that required admissions and intravenous fluids. At 6.5 years of age, she was performing well at school and had good interaction with parents and peers. However she had weakness in the lower limbs and required assistance in walking. At this stage, her urine was subjected to gas chromatography and mass spectrometry, which revealed elevated methylmalonic acid. Tandem mass spectrometry showed significantly elevated propionyl carnitine and normal amino acid profile.
Genomic DNA was extracted from mother and proband. Direct sequencing of all the coding exons including flanking introns of MUT, MMAA and MMAB was carried out as described previously.[] Alignment of amino acid sequences of methylmalonic aciduria type A protein was carried out by Clustal W () as per the Entrez Protein database. SIFT and Polyphen are in silico tools which are used to predict the effect of amino acids substitutions. SIFT predicts whether an amino acid substitution affects protein function based on sequence homology and the physical properties of amino acids.[] Polyphen predicts the amino acid substitution based on the structure and function of a human protein using straightforward physical and comparative considerations.[] The missense mutation was submitted to SIFT () and PolyPhen ().
In exon 6 of MMAA, a G to A substitution at position 833 was found in a homozygous pattern (c.833G > A) []. This mutation leads to the substitution of glycine by aspartic acid at position 278 (p.G278D). The mother showed the same mutation in a heterozygous pattern.
Effects of missense mutation were predicted by SIFT and Polyphen. According to SIFT tool, the substitution at position 278 from G to D is predicted to affect protein function with a score of 0.02 (amino acids with probabilities <0.05 are predicted to be deleterious). According to the Polyphen, this variant is predicted to be probably damaging. Alignment of amino acids sequence of methylmalonic aciduria type A protein observed in the patient (resulting in a change of glycine to aspartic acid residue at position 278) showed it to be highly conserved across other species [].
Presently she is on daily oral supplementation of vitamin B12 one milligram and carnitine 500 mg. She is now 7 years and has normal intellectual functions and residual weakness in left lower limb.
During her mother's subsequent pregnancy, prenatal diagnosis was done at 12 weeks of gestation. Same mutation was confirmed in the fetus in homozygous state and she discontinued the pregnancy.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [42.0, 'mg/dL'], 'Glucose': [106.0, 'mg/dL'], 'Sodium': [114.0, 'mEq/L']}",248.88889,236.44445,261.33333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 114.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 114.0 mEq. To convert from 114.0 mEq to mmol, convert from mEq to mmol. The compound 114.0 has a valence of 1, and so divide the valence by the value of mEq to get, 114.0 mEq/(1 mEq/mmol) = 114.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 114.0 mEq sodium/L converts to 114.0 mmol sodium/L. 
The concentration of bun is 42.0 mg/dL. 
The concentration of glucose is 106.0 mg/dL. 
Plugging these values into the equation, we get 2 * 114.0 + (42.0 / 2.8) + (42.0 / 18) = 248.88889 mmol/L.The patient's calculated serum osmolality concentration is 248.88889 mmol/L. This is equalivalent to 248.88889 mOsm/kg."
5788,30,Serum Osmolality,lab test,decimal,pmc-4711209-1,Extracted,"A 40-year-old female presented to emergency department with alleged history of consumption of one tablet of celphos (3 g) in the morning. The time interval between consumption of poison and presentation to hospital was approximately 1 h. On arrival, the patient was conscious, irritable with pulse rate of 100/min, blood pressure (BP) of 80/60 mm Hg, respiratory rate of 30/min and temperature of 98°F []. Per abdominal examination revealed tenderness. Arterial blood gas (ABG) findings on room air were PaO2 82.6, PaCO2 19.6, pH 7.326, HCO3 9.9 with base excess-4, and oxygen saturation of 97%. Intravenous (IV) access was secured and resuscitated with 1 L of Ringer's lactate. The patient was given gastric lavage and was shifted to Intensive Care Unit (ICU) for further management. Routine investigation revealed hemoglobin of 11 g/dl, blood sugar of 96 mg/dl, total leukocyte count (TLC) of 10,000/mm3, platelet count of 1.09 L/mm3, blood urea of 20 mg/dl, serum creatinine of 0.6 mg/dl, serum sodium of 138 milliequivalent/L, and serum potassium of 4.6 milliequivalent/L. Coagulation profile, liver function test (LFT), chest X-ray, and electrocardiogram (ECG) were within normal limits. The patient was started on intralipid emulsion 20% at 10 ml/h and gradually tapered with monitoring of serum triglyceride level. Time interval between ingestion of poison and starting of lipid emulsion was 12 h. She also received IV magnesium sulfate (MgSO4) 1 g over 20 min followed by 1 g/h for first 24 h and then 1 g every 6 h. Close monitoring of vitals and serum magnesium level [] was performed.
She improved clinically on day 5 and intralipid and MgSO4 were stopped. The patient did not require any ionotropic and ventilatory support during ICU stay. She was discharged on 9th day in a stable condition.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [96.0, 'mg/dL'], 'Sodium': [138.0, 'mEq/L']}",288.47619,274.05238,302.9,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 96.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (20.0 / 2.8) + (20.0 / 18) = 288.47619 mmol/L.The patient's calculated serum osmolality concentration is 288.47619 mmol/L. This is equalivalent to 288.47619 mOsm/kg."
5789,30,Serum Osmolality,lab test,decimal,usmle-4195,Extracted,"A 65-year-old obese man presents to his primary care clinic feeling weak. He was in the military and stationed in Vietnam in his youth. His current weakness gradually worsened to the point that he had to call his son to help him stand to get on the ambulance. He smokes a pack of cigarettes every day and drinks a bottle of vodka a week. He has been admitted for alcohol withdrawal multiple times and has been occasionally taking thiamine, folic acid, and naltrexone. He denies taking steroids. His temperature is 98°F (36.7°C), blood pressure is 170/90 mmHg, pulse is 75/min, and respirations are 20/min. He is obese with a significant pannus. Hepatomegaly is not appreciable. Abdominal striae are present. His workup is notable for the following:

Serum:
Na+: 142 mEq/L
Cl-: 102 mEq/L
K+: 3.9 mEq/L
HCO3-: 25 mEq/L
BUN: 24 mg/dL
Glucose: 292 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 10.1 mg/dL
AST: 7 U/L
ALT: 14 U/L
24-hour urinary cortisol: 400 µg (reference range < 300 µg)
Serum cortisol: 45 pg/mL (reference range < 15 pg/mL)

A 48-hour high dose dexamethasone suppression trial shows that his serum cortisol levels partially decrease to 25 pg/mL and his adrenocorticotropin-releasing hormone (ACTH) level decreases from 10 to 6 pg/mL (reference range > 5 pg/mL).",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [142.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [24.0, 'mg/dL'], 'Glucose': [292.0, 'mg/dL']}",308.79365,293.35397,324.23333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. 
The concentration of bun is 24.0 mg/dL. 
The concentration of glucose is 292.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (24.0 / 2.8) + (24.0 / 18) = 308.79365 mmol/L.The patient's calculated serum osmolality concentration is 308.79365 mmol/L. This is equalivalent to 308.79365 mOsm/kg."
5790,30,Serum Osmolality,lab test,decimal,usmle-5910,Extracted,"A 63-year-old man presents to the emergency department with periorbital swelling. He states that he was gardening, came inside, looked in the mirror, and then noticed his eyelids were swollen. He denies pain, pruritus, or visual disturbances. He states that he was drinking “a lot of water"" to prevent dehydration, because it was hot outside this morning. His medical history is significant for rheumatoid arthritis. He takes methotrexate and acetaminophen as needed. The patient’s temperature is 98°F (36.7°C), blood pressure is 168/108 mmHg, and pulse is 75/min. Physical examination is notable for periorbital edema, hepatomegaly, and bilateral 1+ pitting lower extremity edema. Labs and a urinalysis are obtained, as shown below:

Leukocyte count: 11,000/mm^3
Hemoglobin: 14 g/dL

Serum:
Na: 138 mEq/L
K+: 4.3 mEq/L
Cl-: 104 mEq/L
HCO3-: 25 mEq/L
Urea nitrogen: 26 mg/dL
Creatinine: 1.4 mg/dL
Glucose: 85 mg/dL
Aspartate aminotransferase (AST, GOT): 15 U/L
Alanine aminotransferase (ALT, GPT): 19 U/L
Albumin: 2.0 g/dL

Urine:
Protein: 150 mg/dL
Creatinine: 35 mg/dL

An abdominal ultrasound reveals an enlarged liver with heterogeneous echogenicity and enlarged kidneys with increased echogenicity in the renal parenchyma. A biopsy of the kidney is obtained.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [26.0, 'mg/dL'], 'Glucose': [85.0, 'mg/dL'], 'Sodium': [138.0, 'mEq/L']}",290.00794,275.50754,304.50834,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 26.0 mg/dL. 
The concentration of glucose is 85.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (26.0 / 2.8) + (26.0 / 18) = 290.00794 mmol/L.The patient's calculated serum osmolality concentration is 290.00794 mmol/L. This is equalivalent to 290.00794 mOsm/kg."
5791,30,Serum Osmolality,lab test,decimal,pmc-6178251-1,Extracted,"A 19-year-old Pakistani/Asian man with a low socioeconomic background was brought to the emergency department of our hospital with a 15-h history of altered behavior, acute confusion, and disturbed gait. His family did not report any fever, recent fall, accident, or substance abuse. His parents had died at a young age, and he was living with his paternal uncle. He used to work in a generator shop, and he had a history of occasional alcohol and cannabis intake and benzodiazepine abuse 6 months earlier.
On presentation, his blood pressures was 148/65 mmHg with a regular heart rate 96 beats/min. His oxygen saturation was normal, but his breathing was rapid and deep at a rate of 32/min. His temperature was recorded at 36.8 °C. On examination, he was found to be very agitated and was not comprehending. His neck was supple, and his examination result was negative for Kernig’s and Brudzinski’s signs. He was moving all four limbs symmetrically and withdrawing from painful stimuli. His tendon reflexes were normal bilaterally, and his plantar responses were downward. His pupils were normal in size and equally reactive to light. The results of his chest, abdominal, and cardiac examinations were within normal limits.
Laboratory investigations showed serum anion gap 28 mmol/L, osmolal gap 22.5 mOsmol/kg, arterial pH 7.23, lactate 15 mmol/L, potassium 5.6 mmol/L, sodium 140 mmol/L, bicarbonate 5.8 mmol/L, random blood sugar 108 mg/dl, serum blood urea nitrogen (BUN) 7 mg/dl, serum creatinine 1.3 mg/dl, hemoglobin 17 g/dl, white blood cell count 24.4 × 109 (neutrophils 82%), platelets 447 × 109, negative urine toxicology screen (amphetamine, cannabinoids, barbiturates, benzodiazepines, opiates, and cocaine), and negative serum ethanol. Serum methanol levels were not measured, because the assay was not available. urinalysis demonstrated 2+ proteins, 1 white blood cell, 10 red blood cells, 5+ hemoglobin, no cast, and no crystals. The results of amylase, lipase, creatinine phosphokinase, and liver function tests, including alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase, were within normal ranges. Blood and urine culture results were negative.
The patient’s chest radiography result was normal. His electrocardiogram showed sinus tachycardia. Ultrasound of his kidneys revealed bilateral swollen kidneys. Computed tomography (CT) of his head showed cerebral edema.
At that point, our differential diagnosis included acute methanol or ethylene glycol poisoning (on the basis of high anion gap metabolic acidosis; elevated osmolal gap; and history of substance abuse in the past, though there was no history of intake) and septic encephalopathy (acute confusional state with raised white blood cell count).
In the presence of severe metabolic acidosis and acute kidney injury, the patient was started on an intravenous diluted sodium bicarbonate infusion along with intravenous crystalloids. Empiric intravenous ceftriaxone was initiated.
During the first 24 hours of admission, the patient showed remarkable improvement in his consciousness level; however, he was still delirious but started following commands. His serum bicarbonate improved to 18 mEq/L, and his white blood cell count decreased. Although his urine output was adequate at approximately 1.2–1.5 L/d, his serum creatinine worsened. The family and the patient were questioned again regarding intake of methanol or ethylene glycol, but denied it completely.
On day 3 of admission, the patient confessed taking transformer oil in order to commit suicide. The transformer oil had been kept in their home for more than 1 year and was collected from a burst transformer. On subsequent days, after an initial improvement, the patient’s consciousness level deteriorated rapidly, and he started complaining of continuous headache with episodes of increased agitation alternating with acute delirium. Despite an adequate urine output and normal electrolytes, his serum creatinine kept on worsening.
At that time, his consciousness level was not explained by uremia, because his BUN was only 50 mEq/L, though his creatinine had risen to 8.5 mg/dl. Hemodialysis was considered at that point, but our suspicion was intake of some lipophilic substance that could not be dialyzed. Because of the patient’s unexplained delirious state, CT of the head was repeated, which revealed abnormal low-density areas in bilateral temporal, parietal, and occipital lobes; genu of corpus callosum; and right cerebellar peduncle along with cerebral edema.
On day 7, the patient’s urine output declined, and his BUN and creatinine increased to 80 mg/dl and 12.5 mg/dl, respectively. He had two episodes of generalized tonic-clonic seizures and was dialyzed immediately for 4 hours. After the first hemodialysis session, although the patient’s BUN fell only slightly from 80 to 60 mg/dl, he showed a remarkable improvement in his consciousness level. He became calm and alert, his agitation was almost alleviated, and his complaints of headache became less frequent. He was again dialyzed consecutively for the next 2 days.
After three consecutive sessions of hemodialysis, no further dialysis was needed. The patient’s headache subsided completely, and his consciousness level improved significantly, which further pointed to removal of certain substances via dialysis as the cause of altered sensorium and kidney injury. He was discharged on day 12 with stable serum creatinine, which was completely normalized 10 days after discharge. The patient is under regular follow-up, and his renal function is normal. The trend of the patient’s renal function is shown in Table .",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [80.0, 'mg/dL'], 'Glucose': [108.0, 'mg/dL'], 'Sodium': [140.0, 'mmol/L']}",314.57143,298.84286,330.3,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mmol/L. 
The concentration of bun is 80.0 mg/dL. 
The concentration of glucose is 108.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (80.0 / 2.8) + (80.0 / 18) = 314.57143 mmol/L.The patient's calculated serum osmolality concentration is 314.57143 mmol/L. This is equalivalent to 314.57143 mOsm/kg."
5792,30,Serum Osmolality,lab test,decimal,pmc-4531545-1,Extracted,"A 23-year-old Asian man with chronic renal allograft dysfunction was admitted to our hospital in May 2001 with a 10-day history of fever, intermittent chills, dry cough and progressive dyspnea. He underwent renal transplantation in 1994 for end-stage renal disease of unknown cause diagnosed in 1993. He had been on a medication of cyclosporine 200 mg/day and prednisolne 5–20 mg/day. His temperature was 40°C, blood pressure 120/70 mmHg supine, pulse rate 120/min and respiratory rate 20/min. Respiratory examination revealed mildly decreased breathing sounds on the right lower chest. We also noted several erythematous tender macules measuring 0.5 cm in diameter on both shins. He had no neurological signs of meningitis. Chest radiograph obtained on admission demonstrated increased opacity on the right lower lobe. Arterial blood gas analysis on room air revealed a pH of 7.38, PaCO2 22.1 mmHg, PaO2 49.4 mmHg, and SaO2 85.3%. A complete blood count yielded a leukocyte count of 5,600/mm (91.6% neutrophils), hemoglobin 5.6 g/dL, and platelet count 267,000/mm3. The renal allograft function was in acute exacerbation on chronic dysfunction; BUN 113 mg/dL, Cr 8.5 mg/dL, Na 125 mmol/L, K 6.4 mmol/L, protein 5.2 g/dL, albumin 2.9 g/dL, glucose 102 mg/dL. The patient had been treated with empirical antibiotics for the presumed diagnosis of severe community-acquired pneumonia. On the next day, his respiratory status deteriorated dramatically with a rapid development of hypotension. A repeat chest radiograph showed nearly complete opacification of both lung fields (). The patient was intubated and placed on mechanical ventilation. Dobutamine and dopamine were administered. Urgent anti-CMV IgM, CMV PCR and anti-HIV were negative. Anti-mycoplasma antibody titer was <1:20. Acid-fast bacillus smear and methenamine silver stain of sputum yielded negative results. The initial three sputum and blood cultures were sterile. On the eighth hospital day, tender macules on both shins coalesced to form erythematous patches. Skin biopsy showed granulomatous inflammation in the dermis and numerous yeast organisms with clear thick capsules (). The cerebrospinal fluid (CSF) exam was clear with normal glucose and slightly increased protein (95 mg/dL). The cryptococcal antigen titer was elevated in CSF at >1:256 and at >1:516 in serum. However, the microscopic examination of CSF preparations with India ink was negative for encapsulated yeasts and CSF cultures were negative. The culture of skin biopsy isolated a yeast organism, which was identified as Cryptococcus albidus by characteristic morphology, fermentation, and carbon assimilation tests using the API 20c AUX system (bioMérieu, Marcy-l’Etoile, France). The patient was treated intravenously with fluconazole immediately after the skin biopsy. After 10 days of fluconazole therapy, his chest radiograph and CT scan showed marked clearing with only one cavitary nodular lesion on the left upper lobe (). Percutaneous needle aspiration was performed for the left upper pulmonary nodule. Cytologic examination of the aspirates also revealed a typical morphology of the numerous cryptococci (). The patient was discharged on an oral regimen of fluconazole (200 mg/day). Fluconazole maintenance therapy was continued for 12 months on a long-term basis for prevention of cryptococcosis. At the time of the most recent follow-up, July 2002, his chest radiograph was stable and we detected no evidence of recurrent cryptococcal infection.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [113.0, 'mg/dL'], 'Glucose': [102.0, 'mg/dL'], 'Sodium': [125.0, 'mmol/L']}",296.02381,281.22262,310.825,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 125.0 mmol/L. 
The concentration of bun is 113.0 mg/dL. 
The concentration of glucose is 102.0 mg/dL. 
Plugging these values into the equation, we get 2 * 125.0 + (113.0 / 2.8) + (113.0 / 18) = 296.02381 mmol/L.The patient's calculated serum osmolality concentration is 296.02381 mmol/L. This is equalivalent to 296.02381 mOsm/kg."
5793,30,Serum Osmolality,lab test,decimal,pmc-4691631-1,Extracted,"A 27-year-old woman, living in the central region of Thailand, gravida 1, presented at 37 weeks and 5 days' gestation with complaints of both arm and leg weakness and painful muscle cramps. Her symptoms had begun 5 days earlier. She had myalgia and showed progressive difficulty of proximal muscle activities more than distal muscle activities, without signs of muscle wasting. The patient had no ptosis, and her respiration was normal. A dermatologic exam was unremarkable. She had no history of diarrhea or toxin exposure. Her daily medication consisted of a tablet of ferrous fumarate and a single supplement containing iron, iodine, and folic acid (Triferdine). She had no significant prior antenatal history, no hearing problem, no sign of autoimmune disease, no history of dry eyes or dry mouth, no history of diuretic intake, no history of chronic alcohol intake, and no family history of weakness and hypokalemia.
In the initial assessment, the patient was afebrile, and her blood pressure was 109/65 mmHg. A neurological examination revealed the following motor power: grade 3/5 in both arms, grade 4/5 in both forearms, grade 4/5 in both thighs, and grade 5/5 in both legs. All the deep tendon reflexes were 2+. The well-being of the fetus was assured by a nonstress test. Normal fetal bone development and mineralization were observed by ultrasound.
Investigations showed a total leukocyte count of 8,310/mm3 (5000–10000), with a neutrophil count of 68% (40–75), a lymphocyte count of 24% (20–50), a monocyte count of 6% (2–10), and eosinophil count of 2% (1–6). The hemoglobin was 11.7 g (11–15), platelets were 261,000 cells/mm3 (140,000–400,000), serum potassium was 2.0 mmol/L (3.5–5.0), sodium was 139.5 mmol/L (135–145), and chloride was 108 mmol/L (97–110). Bicarbonate was 19.9 mmol/L (22–32), and it decreased over the next few days to 16.0 mmol/L. In addition, albumin was 3.2 g/dL (3.4–5.0), calcium was 9.7 mg/dL (8.4–10.4), corrected serum calcium was 10.34 mg/dL, magnesium was 1.8 mg/dL (1.8–2.4), phosphorus was 3.8 mg/dL (2.5–4.5), blood sugar was 114 mg%, BUN was 4.1 mg/dL (7–18), creatinine was 0.52 mg/dL (0.55–1.02), aspartate aminotransferase (AST) was 194 U/L (15–37), alanine aminotransferase (ALT) was 124 U/L (0–65), globulin was 2.7 g/dL (2.8–3.3), total bilirubin was 0.43 g/dL (0.0–10.0), direct bilirubin was 0.22 mg/dL (0–0.50), and alkaline phosphatase was 137 U/L (40–150). Urine analysis was negative for blood and urinary tract infections. The urinary pH was 7.0 (5.0–7.5) on a pH meter, and the urinary ketone level was 2+. CPK was 5,338 IU/L (<145). Thyroid function tests were in the normal limit for a third-trimester pregnancy, and serum morning cortisol was mildly increased. Urine was collected after 24 h. The 24 h urine potassium level was elevated at 77 mmol, suggesting hypokalemia from renal losses. Serum anion gap was 13.6 mmol/L. The reduction in bicarbonate and normal anion gap pointed to normal anion gap metabolic acidosis. The patient had no history of extrarenal causes of normal anion gap metabolic acidosis such as vomiting, diarrhea, gastrointestinal fistula, and laxative abuse. These data suggest renal tubular acidosis as a cause. Urine pH of 7.0 pointed out that kidneys could not acidify urine compatible with distal tubular dysfunction. Her serum phosphate was normal and she had no glucosuria. Serum bicarbonate easily increased to 20.9 mmol/L after 0.36 mEq/kg administration. So, all data suggest that she had distal RTA. Then she had no history and no clinical suggestion of anemia and autoimmune disease and had no history of deafness, and besides the fact that screening tests for the underlying causes of the distal RTA were normal the etiology in this case was indeterminate. The serum uric acid was 4.1 mg/dL, antinuclear antibody was negative, and a whole abdomen ultrasound showed mild hydronephrosis, without any detectable renal mass or stones.
Treatments included hydration, correction of the metabolic acidosis with alkali therapy, and potassium supplementation. The patient's clinical and laboratory test results gradually improved. One week after starting the treatments, all the laboratory test results were negative. The patient was discharged.
At 412/7 weeks of gestation, the patient was diagnosed with failure to progress and was taken to the operating room for a cesarean section. A healthy male newborn was delivered. The newborn weighted 3,360 g at birth, and he had an Apgar score of 9 and 10 at 1 and 5 min, respectively. Thin meconium-stained amniotic fluid was found. The operation and postpartum period were uneventful. On follow-up, serum electrolytes, CPK, and creatinine were within normal limits. At the 6-week postpartum check-up, the patient was in good health. She received an injection of depot medroxyprogesterone acetate (DMPA) for contraception.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [4.1, 'mg/dL'], 'Glucose': [114.0, 'mg/dL'], 'Sodium': [139.5, 'mmol/L']}",286.79762,272.45774,301.1375,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.5 mmol/L. 
The concentration of bun is 4.1 mg/dL. 
The concentration of glucose is 114.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.5 + (4.1 / 2.8) + (4.1 / 18) = 286.79762 mmol/L.The patient's calculated serum osmolality concentration is 286.79762 mmol/L. This is equalivalent to 286.79762 mOsm/kg."
5794,30,Serum Osmolality,lab test,decimal,usmle-5791,Extracted,"A 33-year-old man presents to the emergency department with back pain. He is currently intoxicated but states that he is having severe back pain and is requesting morphine and lorazepam. The patient has a past medical history of alcohol abuse, drug seeking behavior, and IV drug abuse and does not routinely see a physician. His temperature is 102°F (38.9°C), blood pressure is 127/68 mmHg, pulse is 120/min, respirations are 17/min, and oxygen saturation is 98% on room air. Physical exam is notable for tenderness over the thoracic and lumbar spine. The pain is exacerbated with flexion of the spine. The patient’s laboratory values are notable for the findings below.

Hemoglobin: 12 g/dL
Hematocrit: 36%
Leukocyte count: 16,500/mm^3 with normal differential
Platelet count: 197,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.2 mg/dL
CRP: 5.2 mg/L

Further imaging is currently pending.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [99.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",290.64286,276.11072,305.175,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (20.0 / 2.8) + (20.0 / 18) = 290.64286 mmol/L.The patient's calculated serum osmolality concentration is 290.64286 mmol/L. This is equalivalent to 290.64286 mOsm/kg."
5795,30,Serum Osmolality,lab test,decimal,pmc-6278222-1,Extracted,"A 50-year-old married male presented with complaints of excessive water intake (7–8 L/day) and repetitive, intrusive ideas about the same, for the last 1 year which is further increased for the last 2 months. One year back, he had an episode of HSV encephalitis which was resolved within 1 month; however, he started having repeated thoughts of taking water and sexual obsessions (about having incestuous relationship). Although he recognized it as his own thought and tried hard to resist it, he did not succeed. For this, he additionally used to perform various compulsive rituals such as touching the head or praying, etc., however, those would only aggravate the symptoms. Over and above, for the last 8 months, he used to feel that some foul smell was coming from his mouth for which, as he reported, he started drinking excessively.
His physical examination (including examination of oral cavity) revealed no abnormality. Blood pressure was 110/70 mm of Hg, PR 76/min. Mental status examination showed that he was well kempt, tidy and was having obsessive thoughts of taking water, and an anxious affect. The obsessions were egodystonic, repetitive, intrusive, and involved minimum 6 h in a day. His routine investigation reports were within normal limits: Na: 133 mEq/L; K: 3.6 mEq/L; urea: 13 mg/dL, creatinine: 0.6 mg/dL, fasting blood sugar: 90 mmol/dL, and postprandial blood sugar: 132 mmol/dL. Urine routine examination and ultrasonography of urinary system showed no specific abnormality.
A provisional diagnosis of “Polydipsia under investigation” was made, and he was admitted to our department for observation and diagnostic clarification. On admission, his daily water intake was quantified, and it was nearly 10–12 L/day, body weight was 55 kg, and he was passing 1200 ml of urine daily. Just after the admission, the urine osmolality was documented to be 246 mOsm/kg (normal is above 300 mOsm/kg). The endocrinologist worked up for diabetes insipidus (DI) and primary polydipsia. Normal renal function tests ruled out nephrogenic causes of DI. Later, the patient was subjected to 7-hour water deprivation test and was administered vasopressin. The results ruled out pituitary DI. Further, average serum cortisol after corticotrophin stimulation test ruled out hypothalamic–pituitary–adrenal axis dysfunction.
The magnetic resonance imaging report showed nonenhancing signal intensities in the right uncus, hippocampus, and right cingulate cortex. We treated him on tablet fluoxetine, 20 mg/day, along with behavioral management and psychoeducation, and advised to add sugar and salt to his water bottle. The patient improved within 1 month and is maintaining in remission at 3 months follow-up with a Y-BOCS[] score of 7/40.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [13.0, 'mg/dL'], 'Glucose': [90.0, 'mmol/dL'], 'Sodium': [133.0, 'mEq/L']}",1171.44286,1112.87072,1230.015,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 133.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 133.0 mEq. To convert from 133.0 mEq to mmol, convert from mEq to mmol. The compound 133.0 has a valence of 1, and so divide the valence by the value of mEq to get, 133.0 mEq/(1 mEq/mmol) = 133.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mEq sodium/L converts to 133.0 mmol sodium/L. 
The concentration of bun is 13.0 mg/dL. 
The concentration of glucose is 90.0 mmol/dL. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 90.0 mmol. To convert 90.0 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 90.0 mmol glucose * 0.001 mol/mmol = 0.09 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.09 mol glucose * 180.16 g/mol = 16.2144 g glucose. To convert 16.2144 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 16.2144 g glucose * 1000.0 mg/g = 16214.4 mg glucose. The volume units is dL so no volume conversion is needed. Hence, the concentration value of 90.0 mmol glucose/dL converts to 16214.4 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 133.0 + (13.0 / 2.8) + (13.0 / 18) = 1171.44286 mmol/L.The patient's calculated serum osmolality concentration is 1171.44286 mmol/L. This is equalivalent to 1171.44286 mOsm/kg."
5796,30,Serum Osmolality,lab test,decimal,usmle-5401,Extracted,"A 32-year-old woman presents to her primary care physician for constant fatigue. The patient states that she is always tired. She claims she is too tired to exercise and has gained 7 pounds recently. She complains of constipation and a decrease in libido as well. She states that she hasn't felt herself lately and is struggling with her relationships. The patient has a past medical history of obesity and diabetes. Her current medications include insulin, lisinopril, metformin, and sodium docusate. Her temperature is 99.5°F (37.5°C), blood pressure is 147/98 mmHg, pulse is 90/min, respirations are 17/min, and oxygen saturation is 98% on room air. Laboratory values are obtained and shown below.

Hemoglobin: 10.0 g/dL
Hematocrit: 30%
MCV: 88 fL
Leukocyte count: 7,500/mm^3 with normal differential
Platelet count: 192,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 129 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.2 mg/dL
AST: 12 U/L
ALT: 10 U/L

A peripheral blood smear is performed as seen in Figure A.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [129.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",292.30952,277.69404,306.925,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 129.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (20.0 / 2.8) + (20.0 / 18) = 292.30952 mmol/L.The patient's calculated serum osmolality concentration is 292.30952 mmol/L. This is equalivalent to 292.30952 mOsm/kg."
5797,30,Serum Osmolality,lab test,decimal,pmc-6068752-1,Extracted,"A 49-year-old male patient presented with acute-onset progressive abdominal cramping pain that had started 1 day previously. He had a medical history of poorly controlled diabetes mellitus and hypertension, as well as renal stone formation after percutaneous nephrolithotomy with double J replacement. There was no history of trauma. Dysuria and mild urgency were noted. He denied having any fever, chills, cough, chest pain, nausea, vomiting, and diarrhea. His temperature was 36.8 °C, blood pressure was 162/89 mmHg, and heart rate was 131/min. On physical examination, a hyperactive bowel sound was noted, accompanied by whole abdominal tenderness, especially at the left quadrant. The Murphy sign was negative, and no tenderness was noted at McBurney’s point. There was no bilateral knocking pain. The laboratory results were as follows: white blood cell count 40,250/µL (band-form neutrophils 2.0%, segment-form neutrophils 86.0%, lymphocytes 5.0%, eosinophils 0.0%, and monocytes 6.0%), hemoglobin 6.7 g/dL, platelet count 645,000/mL, blood urine nitrogen 51 mg/dL, creatinine 1.9 mg/dL, sodium 124 mmol/L, potassium 5.5 mmol/L, glucose 790 mg/dL, alanine aminotransferase 19 U/L, lipase 768 IU/L, total bilirubin 1.00 mg/dL, troponin I <0.01 μg/L, ketone bodies 4.5 mmol/L, and serum osmolarity 336 mOsm/kg. The urinalysis results were as follows: Red blood cell count 10–19/high-power field (HPF), white blood cell count 10–19/HPF, glucose 4+, ketone bodies 1+, bacteria 1+/HPF, and yeast 3+/HPF. The venous blood gas analysis revealed the following results: pH 7.390, pCO2 29.2 mmHg, pO2 44.5 mmHg, HCO3 17.3 mmol/L, actual base excess −6.3 mmol/L, base excess in extracellular fluid −7.6 mmol/L, and O2 saturation 78.9%. The detailed results of laboratory evaluations are listed in . The plain film showed diffuse bilateral opacities over the lung field (A). The kidney, ureter, and bladder (KUB) study revealed gallbladder stone, double J catheter placement from the pelvic cavity to the right renal region, and a heterogeneous mass with air density at the left side (B).
Contrast-enhanced abdominal CT was performed, which revealed several cavitary nodules in both lower lung fields (A,B). A perirenal heterogeneous mass with gas density was found inside the left renal capsule (C). According to the above-mentioned clinical symptoms and images, EPN and multiple septic pulmonary emboli were suspected. The broad-spectrum antibiotics meropenem and teicoplanin were administrated for sepsis. Meropenem was administered for 13 days and teicoplanin was used for 9 days; then, the patient was shifted to ceftriaxone for 3 days. In addition, the patient’s hyperkalemia was treated with insulin in 5% glucose solution and calcium polystyrene sulfonate powder (Kalimate). Transfusion of 2 U packed red blood cells was done for anemia. Famotidine was administered to prevent stress ulcer. Emergency percutaneous nephrostomy was done (D), and pus and urine were collected for culture. The cultures showed E. coli growth in urine and pus. No growth of significant aerobic or anaerobic pathogens in blood was noted. After timely treatment, the sepsis was controlled. The follow-up plain film and abdominal CT revealed a few cavitary nodules and less accumulation of perirenal abscess. The patient was discharged and followed up at the urologic and chest outpatient departments. The follow-up serum creatinine level is summarized in . This study was approved by the Institutional Review Board (IRB) of Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation (IRB no. 07-CR-059).",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [51.0, 'mg/dL'], 'Glucose': [790.0, 'mg/dL'], 'Sodium': [124.0, 'mmol/L']}",310.10317,294.59801,325.60833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 124.0 mmol/L. 
The concentration of bun is 51.0 mg/dL. 
The concentration of glucose is 790.0 mg/dL. 
Plugging these values into the equation, we get 2 * 124.0 + (51.0 / 2.8) + (51.0 / 18) = 310.10317 mmol/L.The patient's calculated serum osmolality concentration is 310.10317 mmol/L. This is equalivalent to 310.10317 mOsm/kg."
5798,30,Serum Osmolality,lab test,decimal,usmle-5561,Extracted,"A 40-year-old woman with body mass index of 38 kg/m^2 presents to the emergency department with persistent bouts of epigastric pain for the past 2 hours with worsening nausea and vomiting. She has a history of polycystic ovarian syndrome and gastroesophageal reflux disease diagnosed by endoscopy, for which she takes omeprazole. She had a laparoscopic appendectomy 2 years ago. Her temperature is 98.3°F (36.8°C), blood pressure is 130/70 mmHg, pulse is 95/min, and respirations are 18/min. Her pulse oximeter reads 99% on room air. Abdominal tenderness is reproducible on physical exam without radiation in the upper abdomen. Her laboratory results are notable for the following:

Leukocyte count and differential:
Leukocyte count: 20,000/mm^3
Segmented neutrophils: 95%
Bands: 15%
Eosinophils: 2%
Basophils: 1%
Lymphocytes: 1%
Monocytes: 1%

Serum:
Na+: 135 mEq/L
Cl-: 100 mEq/L
K+: 4.2 mEq/L
HCO3-: 22 mEq/L
Urea nitrogen: 30 mg/dL
Glucose: 110 mg/dL
Creatinine: 1.1 mg/dL
Alkaline phosphatase: 50 U/L
Aspartate aminotransferase (AST, GOT): 25 U/L
Alanine aminotransferase (ALT, GPT): 15 U/L
Gamma-Glutamyltransferase (GGT): 1 U/L
Lipase: 250 IU/dL
Amylase: 300 IU/dL

She is admitted to the medical floor after being started on lactated ringer's solution and oxycodone as needed. Overnight, the patient complains that her pain is inadequately controlled. Her temperature is 98.3°F (36.8°C), blood pressure is 110/70 mmHg, pulse is 110/min, and respirations are 25/min. Her pulse oximeter reads 90% on room air. Her breathing is audible and labored with crackles heard on auscultation of her lungs bilaterally. After the patient is started on 10 liters of oxygen via nasal cannula, her SpO2 improves to 95%. An arterial blood gas is obtained:

pH 7.41
pCO2 30 mm Hg
pO2 125 mm Hg
HCO3 21 mEq/L
Base Excess +2

A chest radiograph is shown in Figure A.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [30.0, 'mg/dL'], 'Glucose': [110.0, 'mg/dL'], 'Sodium': [135.0, 'mEq/L']}",286.8254,272.48413,301.16667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 135.0 mEq. To convert from 135.0 mEq to mmol, convert from mEq to mmol. The compound 135.0 has a valence of 1, and so divide the valence by the value of mEq to get, 135.0 mEq/(1 mEq/mmol) = 135.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mEq sodium/L converts to 135.0 mmol sodium/L. 
The concentration of bun is 30.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 135.0 + (30.0 / 2.8) + (30.0 / 18) = 286.8254 mmol/L.The patient's calculated serum osmolality concentration is 286.8254 mmol/L. This is equalivalent to 286.8254 mOsm/kg."
5799,30,Serum Osmolality,lab test,decimal,usmle-725,Extracted,"A 63-year-old man comes to the physician because of generalized fatigue and malaise for 2 months. He has been unable to engage in his daily activities. Three months ago, he was treated for a urinary tract infection with trimethoprim-sulfamethoxazole. He has hypertension, asthma, and chronic lower back pain. Current medications include hydrochlorothiazide, an albuterol inhaler, naproxen, and an aspirin-caffeine combination. Vital signs are within normal limits. Examination shows conjunctival pallor. The remainder of the examination shows no abnormalities. Laboratory studies show:
Hemoglobin 9.1 g/dL
Leukocyte count 8,900/mm3
Erythrocyte sedimentation rate 13 mm/h
Serum
Na+ 136 mEq/L
K+ 4.8 mEq/L
Cl- 102 mEq/L
Urea nitrogen 41 mg/dL
Glucose 70 mg/dL
Creatinine 2.4 mg/dL
Calcium 9.8 mg/dL
Urine
Protein 1+
Blood 1+
RBCs none
WBCs 8–9/hpf
Bacteria none
Urine cultures are negative. Ultrasound shows shrunken kidneys with irregular contours and papillary calcifications.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [41.0, 'mg/dL'], 'Glucose': [70.0, 'mg/dL'], 'Sodium': [136.0, 'mEq/L']}",290.53175,276.00516,305.05834,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.0 mEq. To convert from 136.0 mEq to mmol, convert from mEq to mmol. The compound 136.0 has a valence of 1, and so divide the valence by the value of mEq to get, 136.0 mEq/(1 mEq/mmol) = 136.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mEq sodium/L converts to 136.0 mmol sodium/L. 
The concentration of bun is 41.0 mg/dL. 
The concentration of glucose is 70.0 mg/dL. 
Plugging these values into the equation, we get 2 * 136.0 + (41.0 / 2.8) + (41.0 / 18) = 290.53175 mmol/L.The patient's calculated serum osmolality concentration is 290.53175 mmol/L. This is equalivalent to 290.53175 mOsm/kg."
5800,30,Serum Osmolality,lab test,decimal,usmle-5124,Extracted,"A 45-year-old homeless man is brought to the emergency department by the police. He was found intoxicated and passed out in a library. The patient has a past medical history of IV drug abuse, diabetes, alcohol abuse, and malnutrition. The patient has been hospitalized previously for multiple episodes of pancreatitis and sepsis. Currently, the patient is minimally responsive and only withdraws his extremities in response to painful stimuli. His temperature is 99.5°F (37.5°C), blood pressure is 90/48 mmHg, pulse is 150/min, respirations are 17/min, and oxygen saturation is 95% on room air. Physical exam is notable for tachycardia, a diastolic murmur at the left lower sternal border, and bilateral crackles on pulmonary exam. The patient is started on IV fluids, vancomycin, and piperacillin-tazobactam. Laboratory values are ordered as seen below.

Hemoglobin: 9 g/dL
Hematocrit: 30%
Leukocyte count: 11,500/mm^3 with normal differential
Platelet count: 297,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.0 mEq/L
HCO3-: 28 mEq/L
BUN: 33 mg/dL
Glucose: 60 mg/dL
Creatinine: 1.7 mg/dL
Ca2+: 9.7 mg/dL
PT: 20 seconds
aPTT: 60 seconds
AST: 1,010 U/L
ALT: 950 U/L

The patient is admitted to the medical floor. Five days later, the patient's neurological status has improved. His temperature is 99.5°F (37.5°C), blood pressure is 130/90 mmHg, pulse is 90/min, respirations are 11/min, and oxygen saturation is 99% on room air.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [33.0, 'mg/dL'], 'Glucose': [60.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",293.11905,278.4631,307.775,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 33.0 mg/dL. 
The concentration of glucose is 60.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (33.0 / 2.8) + (33.0 / 18) = 293.11905 mmol/L.The patient's calculated serum osmolality concentration is 293.11905 mmol/L. This is equalivalent to 293.11905 mOsm/kg."
5801,30,Serum Osmolality,lab test,decimal,pmc-3069581-1,Extracted,"The patient was a 51-yr-old woman with swelling of the extremities and bilateral ptosis on March 8, 2010. She complained of exertional dyspnea and weakness. She married at the age of 25. After that time, she developed drooping of her eyes, with the left eye drooping more than the right eye. Her symptoms persisted and they had gradually increased during about the last 10 yr. About 8 yr ago, she underwent a ptosis repair operation at a local clinic, but her symptoms were not improved. She denied a history of loss of consciousness, headache, dysphagia, dysarthria and myalgia. There was no family history of similar symptoms and no history of trauma. There was no previous history of diabetes and hypertension.
On examination, she was determined to be 151 cm in height and 48 kg in weight. The initial vital signs were a blood pressure of 140/80 mmHg, a pulse rate of 68 beats/min and a respiratory rate of 20/min. She was lethargic and had facial puffiness and no goiter. The lung and heart examinations were unremarkable. All the extremities showed pitting. She had marked bilateral ptosis, while the external ocular movements were normal (). The other cranial nerve examinations were unremarkable.
The laboratory findings were a total leucocyte count 4.75 × 103/µL with 61.6% polymorphs, a hemoglobin level of 9.0 g/dL, the random blood glucose was 124 mg/dL, the serum sodium was 130 mM/L, the potassium was 3.7 mM/L, the blood urea nitrogen (BUN) was 13 mg/dL, the creatinine was 0.8 mg/dL, the aspartate transaminase (AST) was 81 IU/L, the alanine transaminase (ALT) was 29 IU/L, the total bilirubin was 0.93 mg/dL, the creatine kinase (CK) was 1,195 IU/L (normal reference: 20-180 IU/L ), the lactate dehydrogenase (LDH) was 517 IU/L (normal reference: 101-218 IU/L), the total cholesterol was 256 mg/dL, the triglyceride was 121 mg/dL, the high density lipoprotein cholesterol (HDL-C) was 40 mg/dL and the low density lipoprotein cholesterol (LDL-C) was 196 mg/dL. The urinary analysis was negative for blood and protein with using a dipstick. As the clinical findings suggested hypothyroidism and myasthenia gravis, a thyroid function test and acetylcholine receptor binding antibody test were done. The serum T3 was 0.195 ng/mL (normal reference: 0.86-2.02 ng/mL), the free T4 was 0.08 ng/dL (normal reference: 0.93-1.705 ng/dL), the thyroid-stimulating hormone (TSH) was 2.08 µIU/mL (normal reference: 0.27-4.2 µIU/mL), the antimicrosomal antibody was 17 IU/mL (normal reference: 0-34 IU/mL), the antithyroglobulin antibody was 20.1 IU/mL (normal reference: 0-114 IU/mL) and the acetylcholine receptor binding antibody was negative.
Secondary hypothyroidism was suspected. We performed a careful history taking and other pituitary hormone evaluations. At the age of 26 the patient delivered her daughter and she had a history of massive postpartum vaginal bleeding. Thereafter she not resumed menses. The basal levels of other hormones were a serum cortisol of 4.03 µg/dL, the adrenocorticotropic hormone (ACTH) was 29.64 pg/mL, the growth hormone (GH) was 0.06 ng/mL, the IGF-1 was 25 ng/mL (normal reference: 71-263 ng/mL), the prolactin was 1.59 ng/mL, the luteinizing hormone (LH) was 1.49 IU/L, the follicle-stimulating hormone (FSH) was 4.91 IU/L, the E2 was 17.29 pg/mL and the testosterone was 0.02 ng/mL. The combined pituitary stimulation test, including the insulin tolerance test, the thyrotropin-releasing hormone (TRH) stimulation test and the gonadotropin-releasing hormone (GnRH) stimulation test showed panhypopituitarism (). Brain magnetic resonance imaging (MRI) showed a finding of an empty sella turcica and there was no evidence of an intracranial mass, hemorrhage and aneurysm ().
Nerve conduction study (NCS) and electromyography (EMG) of the limbs reveled normal results with the exception of incidentally detected carpal tunnel syndrome. Needle EMG of the orbicularis oculi showed no evidence of dysfunction of the neuromuscular junction.
We diagnosed her as having Sheehan's syndrome, bilateral ptosis and subclinical myopathy caused by secondary hypothyroidism. Replacement with prednisolone of 10 mg/day and thyroxine (T4) 100 µg/day was started. The dose of prednisolone was decreased to 5 mg/day after 4 weeks. At 3 months follow-up, she had become euthyroid with normalized muscle enzymes. She recovered from her presenting symptoms and the bilateral ptosis was much improved ().",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [13.0, 'mg/dL'], 'Glucose': [124.0, 'mg/dL'], 'Sodium': [130.0, 'mmol/L']}",271.53175,257.95516,285.10834,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 130.0 mmol/L. 
The concentration of bun is 13.0 mg/dL. 
The concentration of glucose is 124.0 mg/dL. 
Plugging these values into the equation, we get 2 * 130.0 + (13.0 / 2.8) + (13.0 / 18) = 271.53175 mmol/L.The patient's calculated serum osmolality concentration is 271.53175 mmol/L. This is equalivalent to 271.53175 mOsm/kg."
5802,30,Serum Osmolality,lab test,decimal,pmc-8310435-1,Extracted,"A 68-year-old woman with a past medical history of metastatic melanoma, hypertension, deep vein thrombosis, and pulmonary embolism with inferior vena cava filter placement presented with altered mental status, hypotension, and fever. She had received her second dose of immunotherapy with ipilimumab+nivolumab shortly before presentation.
Initial vitals were significant for blood pressure of 75/40 mm Hg, heart rate of 110 beats per minute, respiratory rate 24 breaths per minute, oxygen saturation 95% on room air, and temperature 98.4 F. Physical exam was remarkable for altered mental status, moderate respiratory distress, and bilateral lower extremity edema. Initial blood work before fluid resuscitation showed Hg 10.3 g/dL; WBC 13.9 K/mcL; Platelets 164 K/mcL; Na 133 mEq/L; K 3.1 mEq/L; Cl 110 mEq/L; HCO3−1 mEq/L; BUN of 23 mg/dL; Cr 3.2 mg/dL; Plasma Glucose 103 mg/dL; Total Protein 5.0 g/dL; Albumin 2.6 g/dL; Aspartate Aminotransferase (AST) 737 U/L; Alanine Aminotransferase (ALA) 399 U/L; Alkaline Phosphatase (ALK) 99 U/L; Total Bilirubin 0.6 mg/dL; Direct Bilirubin 0.4 mg/dL; Calcium 7.3 mg/dL; Magnesium1.5 mg/dL; Inorganic Phosphorus 2.5 mg/dL; Procalcitonin 59.11 ng/mL; Lactic Acid 1.7 mmol/L; PT 17.7 SEC/INR 1.46; aPTT 49.2 SEC; COVID-19 PCR negative; SARS-CoV-2-IgG negative; Influenza Type A negative; Influenza Type B negative; Venous blood gas: pH 7.24, pCO2 of 24 mmHg ().
Additional diagnostic evaluations included the following:Electrocardiogram: normal sinus rhythm with premature ventricular contractions, heart rate of 94 beats per minute CXR: no focal consolidation or pleural effusion Computed tomography abdomen/pelvis w/o contrast: perinephric stranding and cholestasis Computed tomography head w/o contrast: no new acute intracranial abnormality or mass effect UA w/electrolytes: few white blood cells and red blood cells but no casts, urinary pH of 7.5, urine anion gap of 40, and fractional excretion of sodium of 0.6%
The patient underwent prophylactic right femur nailing with excision of a metastatic lesion and developed a fever of unknown origin, hypotension, acute blood loss, and acute tubular necrosis two weeks before presentation. At that time, she completed treatment with vancomycin, aztreonam, and metronidazole due to a penicillin allergy. However, the infectious workup remained negative throughout the admission. The patient remained afebrile, hemodynamically stable, and safely discharged to a subacute rehabilitation facility.
Four days after discharge, she presented to our emergency department for fever and hypotension. The team initiated the sepsis protocol, and the patient was adequately fluid resuscitated with an appropriate blood pressure response. Blood cultures were collected, and the patient received empiric antibiotic treatment and stress dose hydrocortisone with improvement in her mental status.
Throughout the hospital course, her functional status improved significantly. The patient again agreed to placement in a subacute rehab facility on day fourteen of hospitalization.
The clinical picture was suggestive of sepsis with multiorgan failure in the setting of a new RTA. The patient continued on antibiotics, maintenance fluids with lactated ringers, started on a sodium bicarbonate drip, and was admitted to the medical oncology service for further management. Working differential diagnoses included sepsis, adrenal insufficiency, antimicrobial toxicity, and immunotherapy adverse effects.
The patient completed a seven-day course of antibiotics. Infectious workup, including computed tomography abdominal and pelvis w/o contrast, urine culture, blood cultures, chest x-ray, and transthoracic echocardiogram (TTE), was unremarkable. While tapering the stress dose hydrocortisone, the patient developed transient hypotension, fever, and transaminitis episodes. Per discussion with the infectious disease team and primary oncologist, the thought was that the clinical presentation was likely related to immunotherapy.
Despite the acute renal failure resolution, the patient remained with a severe hyperchloremic non-anion gap metabolic acidosis (HCO3−1, the nadir of 9 mmol/L), along with persistent hypokalemia (the nadir of 2.4 mEq/L) indicating a distal (type-I) RTA.
Although possible, antimicrobial-induced RTA was unlikely due to the resolution of the renal failure and that none of the agents are known culprits to manifest acid/base disturbances []. Giving rise to a suspected immunotherapy-induced RTA, the patient was started on prednisone one mg/kg and transitioned to sodium bicarbonate tablets. Repeat blood work revealed an appropriate response with downtrending liver enzymes and increased serum sodium bicarbonate, indicating a resolving RTA.
Further workup revealed a negative autoimmune panel (anti-Ro (SS-A), anti-La (SS-B), ANA). SPEP, UPEP, free light chains, hepatitis serology, and thyroid function tests were unremarkable. Alkaline urine, a positive urinary anion gap, a nonanion gap metabolic acidosis with low serum bicarbonate, and persistent hypokalemia suggested a distal-type-1 RTA.
The patient followed up with nephrology and oncology as an outpatient. She completed a prednisone taper over four weeks and denied symptoms at the follow-up encounter.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [133.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [23.0, 'mg/dL'], 'Glucose': [103.0, 'mg/dL']}",279.93651,265.93968,293.93334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 133.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 133.0 mEq. To convert from 133.0 mEq to mmol, convert from mEq to mmol. The compound 133.0 has a valence of 1, and so divide the valence by the value of mEq to get, 133.0 mEq/(1 mEq/mmol) = 133.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mEq sodium/L converts to 133.0 mmol sodium/L. 
The concentration of bun is 23.0 mg/dL. 
The concentration of glucose is 103.0 mg/dL. 
Plugging these values into the equation, we get 2 * 133.0 + (23.0 / 2.8) + (23.0 / 18) = 279.93651 mmol/L.The patient's calculated serum osmolality concentration is 279.93651 mmol/L. This is equalivalent to 279.93651 mOsm/kg."
5803,30,Serum Osmolality,lab test,decimal,pmc-7837787-1,Extracted,"A 74-year-old male was admitted to hospital with a chief complaint of general weakness since the last 3 months and increasingly burdensome. There was nausea, vomiting, but no heartburn, decreased appetite for the last 5 months, and weight loss of around 7 kg in the last 6 months. There is no fever, headaches are often felt since the last 6 months and usually do not improve even after taking analgetics, and patients also sometimes find it difficult to sleep. There is no cough and dyspnoea; the patient often feels pain in the right chest which only decreases after taking analgetics. Urination is smooth, but the volume of urine was less, irregular defecation as long as this complaint.
Previous medical history: the patient was treated at hospital with a diagnosis of moderate differentiation of invasive squamous cell esophageal carcinoma, suspected lung and brain metastases with electrolyte balance disorders. The patient received chemotherapy 13 times and radiotherapy 30 times during treatment at a hospital in another country six months ago. Laboratory results of the last serum sodium after chemotherapy is 124 mmol/L. One month before admission in our hospital, the patient received a total of 10 bottles of 3% sodium infusion in another hospital. The serum sodium levels after correction were 111 mmol/L, 112 mmol/L, and 117 mmol/L, respectively. There was no history of swelling, hypertension, diabetes mellitus, and thyroid disease.
Physical examination found vital signs within normal limits, good consciousness, and body mass index (BMI) 18.4 kg/m2. No signs of anemia and jaundice, no palpable tumor mass, and no lymphadenopathy were found. Thoracic, cardiac, and abdominal physical examinations were within normal limits. There was no extremity edema and abdominal ascites.
The results of laboratory tests are as follows: leukocytes 4,600/mm3, erythrocytes 3.35 × 106/mm3, hemoglobin 10.6 gr/dL, hematocrit 28.5%, platelets 99,000/mm3, MCV 85.1 pg, MCHC 37.0 gr/dL, neutrophils 76.9%, lymphocytes 20.1%, RBG 156 mg/dL, ALT 17 U/L, AST 14 U/L, creatinine 0.9 mg/dL, blood urea 26 mg/dL, sodium 117 mmol/L, potassium 3.2 mmol/L, clorida 83 mmol/L, and plasma osmolality 216 mMol/kg. Other examinations found normal electrocardiography and abdominal ultrasound within normal limit, except for cysts in the right kidney (6.5 × 5.7 mm). Histopathological examination of esophageal tumor tissue biopsy was moderate differentiation of invasive squamous cell esophageal carcinoma. Thoracic CT-scan impression was sicculer esophageal tumors as high as the middle third with a mark of adhesions with the posterior portion of the aorta, no metastasis to lymph nodes and lung. The impression of PET-CT scan results postradiotherapy was increased FDG uptake is seen at a long segment of the thoracic esophagus. In view of previous radiation, considerations include esophagitis versus residual tumor. No increase was seen at the right hilum. The previously seen coeliac axis node is much smaller and non-FDG-avid. There is no evidence of hypermetabolic hepatic metastasis. A tiny nodule in the lingula is nonspecific. Increased uptake is seen at the right parietal brain parenchyma. This may be related to recent fall versus metastasis.
Based on the history, physical examination, laboratory, and radiography investigation, the initial working diagnosis was esophageal carcinoma with SIADH. Management at that time was correction of hyponatremia with NaCl 3% based on the calculation of the patient's requirement. During treatment, the patient always complains of feelings of weakness, nausea but no vomiting, no appetite, headache, insomnia, and right chest pain that is temporarily improving by giving analgesics. There was no coughing and dyspnoea. Urine production per day was between 350 and 600 cc and irregularly defecating. On physical examination, blood pressure fluctuates within normal limits but once blood pressure reaches 160/100 mmHg, the patient has experienced a decrease in consciousness with laboratory results of sodium at that time: 108 mmol/L.
Laboratory results for four times electrolyte control tests after correction showed sodium levels of 108, 108, 122, and 112 mmol/L, respectively, never reached the normal levels although correction of sodium with 3% sodium based on the calculation of patient requirement was given repeatedly; low plasma osmolality and urine osmolality higher than the plasma osmolality were also found in this patient. Furthermore, the management of SIADH was given fluid restriction; hyponatremia was corrected with 3% sodium based on the calculation of the patient's requirement, injection of furosemide 40 mg intravenous daily, tetracycline 500 mg twice daily. We follow-up urine production daily, urine sodium, urine osmolality, and plasma osmolality.
The general condition of the patient improves; complaints often felt during hospitalization have diminished. Physical examination results: vital signs are within normal limits, and urine production increases around 1100 cc daily. Laboratory examination results: levels of sodium are 140 mmol/L. Results of urine examination are within normal limits (urine density: 1.010). The patient is permitted to outpatient with recommended continue oral therapy, calculate urine production daily, and electrolyte control.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mmol/L'], 'Glucose': [156.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [26.0, 'mg/dL']}",297.95238,283.05476,312.85,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mmol/L. 
The concentration of bun is 26.0 mg/dL. 
The concentration of glucose is 156.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (26.0 / 2.8) + (26.0 / 18) = 297.95238 mmol/L.The patient's calculated serum osmolality concentration is 297.95238 mmol/L. This is equalivalent to 297.95238 mOsm/kg."
5804,30,Serum Osmolality,lab test,decimal,pmc-3928834-1,Extracted,"Twenty-eight-year-old female, G4 P3 0 1 3, presented with a progressive decline in urine output for one month, fever, nausea and vomiting for two weeks. Detailed questionnaire revealed that she underwent medical termination of pregnancy by dilatation and curettage by quack, three months ago followed by profuse urethro-vaginal bleeding, urinary ascites and shock for which she was managed conservatively with parenteral fluid, blood component therapy, per cutaneous abdominal tube drainage in a local nursing home. After recovery from shock, the patient noticed a continuous leakage of urine per vaginam for two months followed by progressive decline in urine output for which she consulted various nursing homes with no relief and then she was referred to us. Since first surgery was done by untrained para-medical person, details of which was not available. Available records and frequent questionnaire from attendants could reveal that she had incurred massive vesico-urethral trauma during MTP.
On examination, the patient was pale, no pedal edema. Bilateral kidneys were palpable with mild tenderness and the bladder was not palpable. Locally, only vaginal opening with scarred area at the site of urethral orifice seen, anterior vaginal wall was lacerated. Cystoscopy, even with pediatric scope was not feasible.
Her hemoglobin was 7.2 gm%, TLC-8800/cmm, P67%, L27%, M4% E2%, blood sugar-84 mg%, blood urea-108 mg%, serum creatine-3.9 mg%, serum Na-134 mEq/l and K-5.8 mEq/l. USG-abdomen showed bilateral kidneys enlarged with gross hydronephrosis and both ureters dilated till lower end and a small fibrotic bladder. Plain X-ray of KUB Kidney,Ureter,Bladder region and Electrocardiogram showed no abnormality. Bilateral Percutaneous nephrostomy (PCN were done under local anesthesia. Urine from bilateral PCN was cloudy, sent for culture sensitivity and the patient was put on antibiotic accordingly. When PCN urine culture report revealed no growth, 24 hour urine creatinine clearance from right kidney was 42 mg/ml/minute and from left kidney was 49 mg/ml/minute. After improving the general condition of the patient and when serum creatinine had returned to 1.2 mg%, bilateral antegrade pyelogram was done which showed the blind ending of ureters at lower end and no contrast in the bladder. Repeat sonography of KUB region showed that right kidney measures 10.2 × 4.5 cm in size and parenchymal thickness- 14 mm while left kidney measures 10.5 × 4.8 cm and parenchymal thickness- 15 mm. Both kidneys showed normal cortico-medullary differentiation. Moreover, there was good creatinine clearance from both kidneys, so intravenous urography IVU was omitted. Since there was no urethral opening, only scarring was present and further, bladder was a fibrotic remnant and non distensible on sonography, so voiding cysto-urethrography VCUG was not feasible. The patient was counselled for urinary diversion. She was neither willing to accept any kind of stoma, nor willing to perform clean intermittent catheterization CIC. She was planned for MAINZ II pouch. Pre-operatively, colonoscopy was done to exclude any bowel disease. She was given 300 cc saline enema to check for integrity of anal sphincter and one day prior to surgery, she received poly-ethylene glycol lavage. Under general anesthesia, she received single dose third generation cephalosporin just before induction and was explored through infraumbilical midline approach. Intra-operatively, both ureters were dilated and a fibrotic remnant of the bladder was present and anterior wall uterus was partially injured []. After identifying the rectosigmoid junction, colon was folded on itself, tagged with stay suture, detubularized by making inverted U-shaped incision (20 cm long) along antimesenteric border using cutting diathermy and posterior wall of the pouch was formed by closing in two layers. After making an incision in posterior peritoneum, right ureter was mobilized almost up to its midpoint. Left ureter was mobilized by incising along the line of toldt. Both ureters were reimplanted on posterior wall lateral to midline, via a 4 cm long submucosal tunnel using 5-0 Vicryl suture and were anchored on the posterior wall of the pouch. Both ureters were stented over 10F infant feeding tubes and brought out through anus by side of 30F flatus tube. After closing anterior walls of reservoir, pouch was fixed to periosteum of sacral promontory. Abdominal tube drain was inserted in pelvis. Flatus tube and infant feeding tubes were sutured to perianal skin. Post-op period remained uneventful. Abdominal tube drain and flatus tubes were removed on 4th post-op day. Infant feeding tubes were removed on 10th post-op day. Initially, she used to pass urine every 2-4 h, gradually day time frequency improved and she developed no nocturnal incontinence. At 3-year follow-up, serum electrolytes are normal and USG-KUB showed no dilatation of upper tract.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [134.0, 'mEq/L'], 'Glucose': [84.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [108.0, 'mg/dL']}",311.2381,295.67619,326.8,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. 
The concentration of bun is 108.0 mg/dL. 
The concentration of glucose is 84.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (108.0 / 2.8) + (108.0 / 18) = 311.2381 mmol/L.The patient's calculated serum osmolality concentration is 311.2381 mmol/L. This is equalivalent to 311.2381 mOsm/kg."
5805,30,Serum Osmolality,lab test,decimal,pmc-3250606-1,Extracted,"A 2-year-old-boy was admitted to our hospital with a 2-day history of decreased activity with gait disturbance. He had an 11-day history of coughing, rhinorrhea and 8-day history of fever prior to admission. He had no significant past medical history. On admission, he was lethargic and his body temperature was 36.9℃. Physical examination showed enlarged tonsils bilaterally with exudates. Neurologic examination was unremarkable except for an unsteady gait. Laboratory findings included a leukocyte count of 15,200/µL (segmented neutrophil 28.1%, lymphocyte 58.8%, and monocyte 11.5%), hemoglobin 11.3 g/dL, platelet count 439,000/µL, serum sodium 139 mEq/L, potassium 4.4 mEq/L, chlorine 99 mEq/L, blood urea nitrogen 8.0 mg/dL, creatinine 0.6 mg/dL, glucose 91 mg/dL, ammonia 34 µmol/L, and plasma lactate/pyruvic acid 2.44/0.55 mmol/L. Cerebrospinal fluid (CSF) analysis was contaminated with blood due to a traumatic tap. CSF analysis revealed red blood cell 330,000/µL, white blood cell 100/µL (lymphocyte 75%), protein >300 mg/dL, glucose 71 mg/dL, CSF immunoglobulin (Ig) G index 1.12 (<0.85), with a negative results for oligoclonal band. Brain MRI revealed multiple high signal intensities in both basal ganglia and thalami (). CSF for EBV polymerase chain reaction (PCR) was positive and serologic testing was compatible with an acute EBV infection: positive for viral capsid antigen (VCA)-IgM, negative for VCA-IgG, EBV early antigen (EA)-IgG, and EBV nuclear antigen (EBNA)-IgG. CSF PCR for herpes simplex type I, II, Mycoplasma pneumoniae, and Mycobacterium tuberculosis were all negative. CSF viral cultures for influenza type A, B, and enteroviruses were negative. No bacterial organism was isolated from patient's blood, stool, and urine. An electroencephalogram showed abnormal localized slowing over the left hemisphere and right posterior head. Encephalitis was diagnosed by clinical and radiologic findings, and empirical intravenous antibiotics and acyclovir were administered, but stopped after the final negative CSF results for microorganisms were obtained. He recovered gradually without neurologic deficits and was discharged after the 7th day of admission. At 5 weeks after the onset of illness, he revealed no neurological symptoms or deficits on examination. However, follow-up brain MRI demonstrated new multiple high signal intensities in both periventricular white matter with interval disappearance of previous lesions on T2-weighted and fluid attenuated inversion recovery (FLAIR) images (). Since he remained clinically silent during the follow-up period, no additional studies were performed and no treatments were initiated. Serologic testing for EBV was compatible with recent past infection: positive for VCA-IgG, negative for VCA-IgM, EA-IgG, and EBNA-IgG. Brain MRI performed at 1 year after onset of the disease showed complete disappearance of previous white matter abnormal signal intensities with no newly developed lesions (). During the 1-year follow-up, the patient continued to remain healthy with no neurological deficits.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [8.0, 'mg/dL'], 'Glucose': [91.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",285.9127,271.61706,300.20833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 8.0 mg/dL. 
The concentration of glucose is 91.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (8.0 / 2.8) + (8.0 / 18) = 285.9127 mmol/L.The patient's calculated serum osmolality concentration is 285.9127 mmol/L. This is equalivalent to 285.9127 mOsm/kg."
5806,30,Serum Osmolality,lab test,decimal,pmc-4005209-1,Extracted,"A 53-year-old man, nonalcoholic, nonsmoker, presented with complaints of persistent vomiting, burning micturation, increased frequency of urine since last 10 days, and pain and swelling in both feet and ankle since 15 days. There was history of similar pain in leg which started at the age of 17 years and later occurred frequently at varied intervals. There was history of loss of all hair from the body at the age of 17 year. He had been treated for left ureteric stone a year back and his family including his mother, two younger brothers, and one of his sons had renal stones. His son also lost his hair all over the body at the age of 10 years. On examination his pulse was 122 beats per min, blood pressure (BP) 70 mmHg systolic, respiratory rate (RR) 26/min, and he was afebrile. His anthropometric measurements were: Waist circumference 106 cm, height 170 cm, and weight 85 kg. He had bilateral tender swelling involving both feet and ankle. There were no hair on his body [] and multiple skin tags around neck, axilla were found [Figures and ]. Systemic examination including cardiovascular, respiratory, and per abdomen were unremarkable. A probable diagnosis of alopecia universalis with urinary tract infection with systemic inflammatory response syndrome (SIRS) was made and patient was investigated. The investigations revealed: Hemoglobin (Hb) 12.2 g%, erythrocyte sedimentation rate (ESR) 74 mm in 1st h, total leukocyte count (TLC) 7,800/mm3, blood urea 125 mg/dl (17-43), serum creatinine 2.27 mg/dl (0.67-1.17), serum uric acid 21.7 mg/dl, total bilirubin 0.5 mg/dl, direct 0.2 mg/dl, total serum protein 6.0 mg/dl, albumin 3.9 mg/dl, serum glutamic-oxaloacetic transaminase (SGOT) 18 U/l, serum glutamic-pyruvic transaminase (SGPT) 15 U/l, alkaline phosphatase (ALP) 174 U/l, sodium 140 mEq/l, potassium 2.97 mEq/l, chloride 88 mEq/L, calcium 9.6 mg/dl, phosphorus 4.6 mg/dl, vitamin D 53.94 nmol/l, serum total cholesterol 287 mg/dl, triglyceride 404 mg/dl, high density lipoprotein (HDL) 36 mg/dl, low density lipoprotein (LDL) 170.2 mg/dl, very low density lipoprotein (VLDL) 80 mg/dl, prostate specific antigen (PSA) 1.04 ng/ml (<4), blood sugar (fasting (F)) 108 mg/dl, and HbA1c 5.7%. Urine examination showed presence of albumin, pus cells 20-25/high power field (HPF), red blood cell (RBC) 2-4/HPF, and no growth in urine culture. The 24 h urine protein was in nephrotic range with 7.07 g excretion/day. Thyroid stimulating hormone (TSH) was 14.51 μIU/ml (0.35-5.50), triiodothyronine (T3) 0.8 ng/dl (2-4.4), thyroxine (T4) 0.01 pg/dl (0.6-2.2), and C-reactive protein (CRP) was positive. Other investigation including arterial blood gas (ABG), human immunodeficiency virus (HIV), hepatitis C virus (HCV), hepatitis B surface anitgen (HBsAg), complement levels (C3, C4), antinuclear antibody (ANA), rheumatoid arthritis factor (RA), and anti-thyroid peroxidase (TPO) antibodies were not significant. Computed tomography (CT) scan of abdomen showed multiple crystals in both kidneys. Patient was treated with intravenous crystalloids, antiemetic (ondansetron/promethazine), antibiotic (levofloxacin), oral hypouricemic drug (fabuxostat), rozuvastatin, thyroxin, and tramadol. Patient started improving gradually and his uric acid level decreased from 21.7 to 10.4 mg/dl over a period of 2 weeks.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [125.0, 'mg/dL'], 'Glucose': [108.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",330.64286,314.11072,347.175,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 125.0 mg/dL. 
The concentration of glucose is 108.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (125.0 / 2.8) + (125.0 / 18) = 330.64286 mmol/L.The patient's calculated serum osmolality concentration is 330.64286 mmol/L. This is equalivalent to 330.64286 mOsm/kg."
5807,30,Serum Osmolality,lab test,decimal,usmle-1670,Extracted,"A 43-year-old woman comes to the physician because of a fever, nausea, and a nonproductive cough for 7 days. During this period, she has had headaches, generalized fatigue, and muscle and joint pain. She has also had increasing shortness of breath for 2 days. She has type 2 diabetes mellitus and osteoarthritis of her left knee. Current medications include insulin and ibuprofen. She had smoked two packs of cigarettes daily for 20 years but stopped 10 years ago. Her temperature is 38.1°C (100.6°F), pulse is 94/min, respirations are 18/min, and blood pressure is 132/86 mm Hg. The lungs are clear to auscultation. There are multiple skin lesions with a blue livid center, pale intermediate zone, and a dark red peripheral rim on the upper and lower extremities. Laboratory studies show:
Hemoglobin 14.6 g/dL
Leukocyte count 11,100/mm3
Serum
Na+ 137 mEq/L
K+ 4.1 mEq/L
Cl- 99 mEq/L
Urea nitrogen 17 mg/dL
Glucose 123 mg/dL
Creatinine 0.9 mg/dL
An x-ray of the chest is shown.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [17.0, 'mg/dL'], 'Glucose': [123.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",286.90476,272.55952,301.25,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 17.0 mg/dL. 
The concentration of glucose is 123.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (17.0 / 2.8) + (17.0 / 18) = 286.90476 mmol/L.The patient's calculated serum osmolality concentration is 286.90476 mmol/L. This is equalivalent to 286.90476 mOsm/kg."
5808,30,Serum Osmolality,lab test,decimal,usmle-5714,Extracted,"A 60-year-old man presents to the emergency department for fatigue and feeling off for the past week. He has not had any sick contacts and states that he can’t think of any potential preceding symptoms or occurrence to explain his presentation. The patient has a past medical history of diabetes, hypertension, and congestive heart failure with preserved ejection fraction. His temperature is 98°F (36.7°C), blood pressure is 125/65 mmHg, pulse is 90/min, respirations are 14/min, and oxygen saturation is 100% on room air. Laboratory values are obtained and shown below.

Hemoglobin: 12 g/dL
Hematocrit: 36%
Leukocyte count: 6,500/mm^3 with normal differential
Platelet count: 197,000/mm^3

Serum:
Na+: 147 mEq/L
Cl-: 105 mEq/L
K+: 4.1 mEq/L
HCO3-: 26 mEq/L
BUN: 21 mg/dL
Glucose: 100 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.1 mg/dL
AST: 12 U/L
ALT: 10 U/L

Urine:
Appearance: clear
Specific gravity: 1.003

The patient is admitted to the floor, a water deprivation test is performed, and his urine studies are repeated yet unchanged.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [147.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [21.0, 'mg/dL'], 'Glucose': [100.0, 'mg/dL']}",307.05556,291.70278,322.40834,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 147.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 147.0 mEq. To convert from 147.0 mEq to mmol, convert from mEq to mmol. The compound 147.0 has a valence of 1, and so divide the valence by the value of mEq to get, 147.0 mEq/(1 mEq/mmol) = 147.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 147.0 mEq sodium/L converts to 147.0 mmol sodium/L. 
The concentration of bun is 21.0 mg/dL. 
The concentration of glucose is 100.0 mg/dL. 
Plugging these values into the equation, we get 2 * 147.0 + (21.0 / 2.8) + (21.0 / 18) = 307.05556 mmol/L.The patient's calculated serum osmolality concentration is 307.05556 mmol/L. This is equalivalent to 307.05556 mOsm/kg."
5809,30,Serum Osmolality,lab test,decimal,pmc-8396405-1,Extracted,"A 34-year-old female with a history of hypertension presented to the emergency department with a complaint of abdominal pain for two days. The pain started in the epigastrium then radiated to the right upper abdomen and her back. The pain was described as being sharp and associated with chills, nausea and vomiting. She denied any chest pain, shortness of breath, diarrhoea, bloody vomit, bloody stools, or urinary problems. She had prior episodes of biliary colic but had not seen a surgeon previously. Her blood pressure was 115/75 mmHg, pulse 82 beats per minute, temperature 37.10C, and respiration of 18 breaths per minute. Her physical examination showed no acute distress, normal mental status, and abdominal tenderness in the right upper quadrant.
Laboratory tests showed sodium 136mmol/L, potassium 3.6mmol/L, chloride 102mmol/L, carbon dioxide 28mmol/L, BUN 14mg/dl), creatinine 0.94mg/dl, glucose 82mg/dl, calcium 8.7mg/dl. Liver function tests and lipase were normal. Complete blood count revealed a white blood cell count (WBC) of 11.8K/mm3, haemoglobin of 14.7gm/dL, and platelets of 316K/mm3. Urinalysis revealed 2+ leukoesterase, WBC 11-20/high power field, and rare bacteria.
Abdominal ultrasonography and computed tomography (CT) scan showed cholelithiasis and acute cholecystitis, and hepatic steatosis. The patient was admitted to the hospital and resuscitated with intravenous crystalloid solution and antibiotics. On hospital day one, the patient was taken for laparoscopic cholecystectomy. An acutely inflamed distended gallbladder with adherent omentum was noted (Figure ). There was an unusually large blood vessel and medial aspect of the gallbladder coursing toward the inferior liver edge and heading into the falciform ligament. The gallbladder was removed using caution to preserve the unusual blood vessel, and a critical view of safety was obtained. The aberrant blood vessel had several small branches going into the gallbladder (Figure , ).
The patient tolerated the procedure well, was extubated and transferred to the recovery room. On postoperative day one, the patient tolerated diet, the pain was controlled, and abdominal examination was unremarkable. The Jackson Pratt drain was removed, and the patient was discharged home. The patient followed up in the clinic after two weeks, at which time no immediate issues were identified. A review of the histopathology revealed moderate acute and chronic cholecystitis and cholelithiasis. On further review of her CT scan due to the intraoperative finding of the unusual blood vessel, the hepatic falciform artery could readily be appreciated (figure ).",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [14.0, 'mg/dL'], 'Glucose': [82.0, 'mg/dL'], 'Sodium': [136.0, 'mmol/L']}",281.55556,267.47778,295.63334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.0 mmol/L. 
The concentration of bun is 14.0 mg/dL. 
The concentration of glucose is 82.0 mg/dL. 
Plugging these values into the equation, we get 2 * 136.0 + (14.0 / 2.8) + (14.0 / 18) = 281.55556 mmol/L.The patient's calculated serum osmolality concentration is 281.55556 mmol/L. This is equalivalent to 281.55556 mOsm/kg."
5810,30,Serum Osmolality,lab test,decimal,pmc-6988660-1,Extracted,"A 36-year old male presented to the ED with generalized weakness, confusion, and fatigue starting one week prior. The symptoms were associated with some episodes of nausea, vomiting, and loose semisolid stools. The patient reported shortness of breath that had progressed to rest over the past weeks. He denied any fever but reported some chills. He denied any chest pain, palpitations, lower extremity swelling, abdominal pain, or other complaints. The patient has routine weekly labs which showed hyponatremia (sodium = 122 mmol/dL, baseline 130 mmol/dL) so he was sent for evaluation to the emergency room by his cardiologist. The patient has a past medical history of nonischemic cardiomyopathy diagnosed at age 16. A transthoracic echocardiogram done about 9 months prior showed a left ventricular ejection fraction of less than 20% and severe concentric left ventricular hypertrophy. The patient had an automatic implantable cardioverter-defibrillator (AICD) placement 8 years prior for primary prevention of sudden cardiac death. The patient had been on a chronic milrinone infusion delivered through a peripherally inserted central catheter (PICC) line for the past 3 years. This was initiated as a bridge to transplant. However, during transplant evaluation, he was noted to have secondary pulmonary hypertension and would need a combined heart and lung transplant, and no transplant center in the state would accept his insurance for a combined transplant. Besides cardiomyopathy, he also has a history of chronic atrial fibrillation, congenital hydrocephalus with ventriculoperitoneal shunt (since the age of 2), and spinal stenosis. Of note, the patient was taking apixaban, bumetanide, magnesium oxide, allopurinol, digoxin, metolazone, eplerenone, and carvedilol.
On exam, the patient had a red, swollen left upper extremity at the site of his PICC and white nail beds on the left hand and cool extremities, but no lower extremity edema. The patient was afebrile, had an elevated heart rate of 109 beats per minute (bpm), an elevated respiratory rate of 26 breaths per minute, and SpO2 was 96% on 2 L nasal cannula. All other vitals were within normal limits.
Labs on admission are as follows: WBC: 10.9 × 103/mcL; sodium: 123 mmol/L; potassium: 4.7 mmol/L; chloride: 90 mmol/L; bicarbonate: 22; BUN: 27 mg/dL; creatinine: 0.9 mg/dL; glucose: 102 mg/dL; INR: 1.56; total bilirubin: 4.12 mg/dL; alkaline phosphatase: 166 units/L; AST: 44 units/L; and ALT: 27 units/L. The patient was initially diagnosed with viral gastroenteritis and his symptoms of nausea, vomiting, and diarrhea resolved within 2 days. As the team was preparing to discharge the patient, 2 sets of blood cultures taken at admission came back positive for Candida dubliniensis. The patient's WBC count increased from 11.0 to 15.2 with continued stability in his vital signs other than an increase in his heart rate to 120 s bpm. A chest X-ray on admission showed no acute abnormalities, stable cardiomegaly, and an AICD in place. An electrocardiogram (EKG) showed atrial flutter. CT scan of the head showed a left VP shunt with mild ventriculomegaly of the lateral and third ventricles unchanged since 2017. No evidence of intracranial hemorrhage was found. A lumbar puncture obtained clear CSF that was sent to microbiology. The CSF cultures had no growth. The patient was started on empiric micafungin 100 mg IV daily and vancomycin.
A blood culture of the PICC line and a culture of the catheter tip was positive for Candida dubliniensis as determined by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry. Minimum inhibitory concentrations (MICs) for antifungals are listed in .
The PICC line was removed and a right-sided internal jugular vein (IJV) central line was placed. Vancomycin was discontinued after one day once the culture grew yeast. A negative blood culture of C. dubliniensis was drawn 4 weeks after the first positive culture. Micafungin was continued for a total of 6 weeks after the initial positive culture.
Transesophageal echocardiogram (TEE) () showed a new finding of echogenicity of one of the three leads consistent with lead vegetation. Consistent with a TEE done 8 months ago, there was minimal thickening of the aortic valve, mild thickening of the mitral valve with moderate to severe mitral regurgitation, and moderate to severe tricuspid regurgitation. One of the leads had a mobile echodensity measuring 0.4 × 1.3 cm, consistent with lead vegetation. No valvular vegetations were identified on TEE. The findings of the TEE were consistent with AICD fungal septicemia. An AICD lead extraction was done one week after admission at an outside facility with a temporary transcutaneous pacer placed, after which the patient returned to our inpatient facility for placement of a replacement AICD two weeks later. Blood cultures done at the outside facility were negative. Blood cultures from the right and left arms done at our facility after AICD implantation returned Staphylococcus aureus on 2/2 sets sensitive to cefazolin, oxacillin, tetracycline, and trimethoprim/sulfamethoxazole. The right-side IJV central line was removed and a left-side IJV central line was placed with negative blood cultures after placement. The micafungin was recommended to be continued for four weeks after new AICD placement and cefazolin was started for two weeks due to the right-sided IJV central line MSSA infection. A vascular surgeon was consulted for optimal line access with the least infectious risk. The vascular surgeon recommended a PICC line. A replacement PICC line was placed three weeks later and the patient was discharged the next day with a PICC line for milrinone, cefazolin, and micafungin infusion.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [123.0, 'mmol/L'], 'Blood Urea Nitrogen (BUN)': [27.0, 'mg/dL'], 'Glucose': [102.0, 'mg/dL']}",261.30952,248.24404,274.375,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 123.0 mmol/L. 
The concentration of bun is 27.0 mg/dL. 
The concentration of glucose is 102.0 mg/dL. 
Plugging these values into the equation, we get 2 * 123.0 + (27.0 / 2.8) + (27.0 / 18) = 261.30952 mmol/L.The patient's calculated serum osmolality concentration is 261.30952 mmol/L. This is equalivalent to 261.30952 mOsm/kg."
5811,30,Serum Osmolality,lab test,decimal,usmle-5151,Extracted,"A 52-year-old homeless man presents to the emergency department intoxicated. He was found passed out in a park and brought in by police. The patient's past medical history and medications are not known. He was brought in 1 week ago for intravenous drug overdose which was treated appropriately at the time. His temperature is 99.5°F (37.5°C), blood pressure is 92/58 mmHg, pulse is 120/min, respirations are 8/min, and oxygen saturation is 98% on room air. The patient is started on IV fluids and given a dose of naloxone. Basic laboratory values are ordered as seen below.

Hemoglobin: 10 g/dL
Hematocrit: 32%
Leukocyte count: 7,500/mm^3 with normal differential
Platelet count: 167,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 5.1 mEq/L
HCO3-: 25 mEq/L
BUN: 52 mg/dL
Glucose: 99 mg/dL
Creatinine: 2.1 mg/dL
Ca2+: 10.2 mg/dL
AST: 62 U/L
ALT: 50 U/L

The patient is clinically sober 4 hours later and history and physical exam is able to be performed. The patient complains of joint pain and pain/tingling in his extremities. Cardiopulmonary exam is notable for a murmur along the left sternal border. The patient has decreased sensation in his legs bilaterally. Dermatologic exam reveals the finding in Figure A.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [52.0, 'mg/dL'], 'Glucose': [99.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",302.07143,286.96786,317.175,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 52.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (52.0 / 2.8) + (52.0 / 18) = 302.07143 mmol/L.The patient's calculated serum osmolality concentration is 302.07143 mmol/L. This is equalivalent to 302.07143 mOsm/kg."
5812,30,Serum Osmolality,lab test,decimal,usmle-4987,Extracted,"A 27-year-old woman was found unconscious by one of her roommates. When the roommate was unable to arouse the patient, she immediately brought her into the emergency department. The roommate states that the night before, they had held a party at their house. The roommate admits that there was considerable alcohol and substance use at the event. The patient is currently minimally responsive. The patient has a past medical history of asthma, severe anxiety, alcohol dependence, marijuana use, and occasional IV drug use. An EKG is obtained as seen in Figure A, a head CT is obtained as seen in Figure B, and a chest radiograph is seen in Figure C. Lab results are ordered and are below:

Serum:
Na+: 142 mEq/L
Cl-: 105 mEq/L
K+: 4.2 mEq/L
HCO3-: 24 mEq/L
BUN: 11 mg/dL
Glucose: 69 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 9.8 mg/dL
AST: 14 U/L
ALT: 15 U/L

Hemoglobin: 13 g/dL
Hematocrit: 39 %
Leukocyte count: 6,000 cells/mm^3 with normal differential
Platelet count: 150,000/mm^3

Her temperature is 99.5°F (37.5°C), pulse is 112/min, blood pressure is 100/70 mmHg, respirations are 13/min, and oxygen saturation is 97% on room air. The patient is not responsive enough for a full physical exam. The patient’s pupils are responsive to light, and her skin is warm and moist.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [11.0, 'mg/dL'], 'Glucose': [69.0, 'mg/dL'], 'Sodium': [142.0, 'mEq/L']}",291.7619,277.17381,306.35,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. 
The concentration of bun is 11.0 mg/dL. 
The concentration of glucose is 69.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (11.0 / 2.8) + (11.0 / 18) = 291.7619 mmol/L.The patient's calculated serum osmolality concentration is 291.7619 mmol/L. This is equalivalent to 291.7619 mOsm/kg."
5813,30,Serum Osmolality,lab test,decimal,pmc-7480889-1,Extracted,"A 37-year-old Saudi female, who is not known to have any medical illness, presented to the emergency department with chest pain, cough, shortness of breath, hemoptysis and generalized joint pain. Her symptoms progressed over the last four days. There was no history of fever, skin rashes, sicca symptoms, no uveitis, no oral or genital ulcers. She denied any history of drug abuse and alcohol intake. She is not a smoker. There was no history of previous miscarriages and thrombovenous embolism.
The patient was admitted to isolation section in the emergency department (ER). Her Glasgow coma scale (GCS) was 15, temperature 37 C, blood pressure 110/65, respiratory rate 20, heart rate 120 bpm. Oxygen saturation on room air was 90% improved to 96% on high flow oxygen. Heart sounds were normal, no murmurs, jugular venous pressure (JVP) not raised, bilateral lower limb pedal pitting edema, bilateral equal breathing sound with audible crackles in both lungs and no tenderness or guarding in the abdomen. Musculoskeletal exam showed active arthritis in the 2nd, 3rd and 4th proximal interphalangeal joints of the right hand.
Initial hematological examination revealed white blood cells (WBC) 13,000 cells/µL, hemoglobin 5.2 g/dL, platelets 414,000 u/L, normal coagulation profile, glucose 9.1 mmol, creatinine 284 µmmol/L, blood urea nitrogen (BUN) 10.9 mmol/L, sodium (Na) 134 mmol/L, potassium (K) 3.8 mmol/L, chloride (Cl) 96 mmol/L, lactic acid 1.8 mmol, albumin 35 g/L; liver function tests were normal, cardiac enzymes and electrocardiogram were normal, C-reactive protein (CRP) 252 mg/L; urine analysis and microscopy revealed no red blood cells casts. Chest X-ray revealed bilateral pulmonary infiltration (Figure ). COVID-19 polymerase chain reaction (PCR) test was negative. CT brain showed no acute brain insults. Chest CT showed a widespread lung patchy consolidation with a central and peripheral distribution, permeated by ground glass areas and crazy paving pattern. The apices lower zones were relatively spared. Findings were likely suggestive of diffuse alveolar hemorrhage (Figures -).
Patient's blood, urine and wound cultures were taken. Toxicology screen was negative. The patient was stabilized, received proper hydration, 2 units packed red blood cells and broad-spectrum antibiotics initiated. Her serology showed that C-ANCA (PR3) 94.79 AU/mL (strong positive), P-ANCA 7.88 AU/mL (negative), antinuclear antibody (ANA) mild positive 1/80. Her complement C3 and C4 levels were within normal, the rest of rheumatological workup was unremarkable. At this point intravenous pulse methyl prednisone was initiated for three days.
The patient was shifted to the intensive care unit (ICU), as she had ongoing hemoptysis and her oxygen saturation dropped to 84% on BiPAP with FiO2 75%. After she completed the pulse steroids, prednisone 60 mg daily was initiated; linezolid was added to the antibiotic regimen. Twenty-four hours later, her GCS dropped to 9/15; she was intubated, and she was initiated on six sessions of plasmapheresis.
After she completed the plasmapheresis, the second COVID-19 swab test was positive. At this point, ritonavir/lopinavir was added and antibiotics was changed to imipenem based on infectious disease recommendations. Prednisone was reduced to 30 mg and intravenous immunoglobulin was initiated for a total of five doses.
To confirm the diagnosis of COVID-19 infection, a third sample was taken and it came positive. She was having continuous fever; antifungal treatment was added. Her hemoptysis decreased significantly after the intravenous immunoglobulin (IVIG). After 20 days of ICU admission, she had increased oxygen demands and required more vasopressors, and eventually passed away.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [10.9, 'mmol/L'], 'Glucose': [9.1, 'mmol/L'], 'Sodium': [134.0, 'mmol/L']}",288.01597,273.61517,302.41677,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mmol/L. 
The concentration of bun is 10.9 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 10.9 mmol. To convert 10.9 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 10.9 mmol bun * 0.001 mol/mmol = 0.0109 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0109 mol bun * 28.02 g/mol = 0.30542 g bun. To convert 0.30542 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.30542 g bun * 1000.0 mg/g = 305.42 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 305.42 mg bun/10.0 dL = 30.542 mg bun/dL. The concentration value of 10.9 mmol bun/L converts to 30.542 mg bun/dL. 
The concentration of glucose is 9.1 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 9.1 mmol. To convert 9.1 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 9.1 mmol glucose * 0.001 mol/mmol = 0.0091 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0091 mol glucose * 180.16 g/mol = 1.63946 g glucose. To convert 1.63946 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 1.63946 g glucose * 1000.0 mg/g = 1639.46 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1639.46 mg glucose/10.0 dL = 163.946 mg glucose/dL. The concentration value of 9.1 mmol glucose/L converts to 163.946 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (30.542 / 2.8) + (30.542 / 18) = 288.01597 mmol/L.The patient's calculated serum osmolality concentration is 288.01597 mmol/L. This is equalivalent to 288.01597 mOsm/kg."
5814,30,Serum Osmolality,lab test,decimal,pmc-5836266-1,Extracted,"A 47-year-old, previously healthy woman was admitted to the emergency room because of acute-onset confusion occurring in the morning of the admission day. Her blood pressure at presentation was 270/220 mm Hg, her heart rate was 112 beats per minute, and her body temperature was 38.1°C. Neurological examination revealed disorientation to time, place, and person, and bilateral positive Babinski responses, but there was no other focal sign. Routine laboratory tests showed a peripheral blood pleocytosis (leukocytes 14,010/uL), azotemia (blood urea nitrogen 48.7 mg/dL, creatinine 3.0 mg/dL), and hyperglycemia (fasting blood sugar 282 mg/dL; HbA1c 7.3%). Serum sodium was 134 mmol/L. The high-sensitivity C-reactive protein level was slightly increased (0.83 mg/dL [range 0–0.5 mg/dL]). Other laboratory findings including immunologic tests were normal: ammonia 36 ug/dL (range 15–45 ug/dL), anti-nuclear antibody (–), anti-phospholipid antibody immunoglobulin G/immunoglobulin M (•/•), rheumatoid factor 5 IU/mL (range, 0–18 IU/mL), and lupus anticoagulant (–).
Brain magnetic resonance imaging (MRI) revealed a lesion of vasogenic edema without enhancement involving nearly the whole area of pons, the left side of the midbrain, and the bilateral medial thalami (Fig. ). Diffusion-weighted and gradient-echo MRI were unremarkable. Electroencephalogram showed continuous attenuation of background activity with loss of posterior dominant rhythm. Spinal tap was conducted. Opening pressure was slightly increased (21 cm H2O). The levels of CSF protein (102.6 mg/dL) and albumin (64.8 mg/dL) were high (range 15–45 mg/dL). However, other CSF profiles were normal: red blood cells were absent, leukocyte count 4/mm3, glucose 159.3 mg/dL (serum glucose 267 mg/dL), and oligoclonal band negative.
Fever subsided spontaneously without a specific treatment within 1 day. No bacterial species were recovered from cultures of 3 blood samples. Urinalysis did not show bacteriuria or pyuria, and urine culture was negative for bacteria. CSF polymerase chain reaction tests for herpes simplex virus type I and II, varicella zoster virus, cytomegalovirus, Epstein-Barr virus, and Japanese encephalitis virus were all negative. In addition, sputum gram stain, bacterial culture, and smear for acid-fast bacilli were negative. Therefore, the patient was treated only conservatively for hypertension, azotemia, and hyperglycemia. The patient's symptoms completely resolved 3 days after symptom onset, and the edema was confirmed to have disappeared almost completely on the MRI conducted on the ninth hospital day (Fig. ).",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [48.7, 'mg/dL'], 'Glucose': [282.0, 'mg/dL'], 'Sodium': [134.0, 'mmol/L']}",301.05952,286.00654,316.1125,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mmol/L. 
The concentration of bun is 48.7 mg/dL. 
The concentration of glucose is 282.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (48.7 / 2.8) + (48.7 / 18) = 301.05952 mmol/L.The patient's calculated serum osmolality concentration is 301.05952 mmol/L. This is equalivalent to 301.05952 mOsm/kg."
5815,30,Serum Osmolality,lab test,decimal,pmc-3286780-1,Extracted,"A 50-yr-old man, who had been healthy except a history of prostatic cancer two years ago, was admitted to Samsung Medical Center, Seoul, Korea, on November 21, 2009, with high fever and productive cough for three days. He complained of hemoptysis with right pleuritic chest pain. His family members and he had not traveled to other countries in the previous year. On admission, he had fever (38.9℃), pulse rate of 65 beats/min, blood pressure of 184/154 mmHg, and respiratory rate of 20 breaths/min. Physical examination showed decreased breath sounds at the right lower lung field. Laboratory tests showed 6,860 leukocytes/µL (78.6% neutrophils and 15.2% lymphocytes), hemoglobin 14.8 g/dL, and platelet 154,000/µL. Other laboratory values included serum sodium 131 mM/L, blood urea nitrogen 14.1 mg/dL, creatinine 1.2 mg/dL, glucose 138 mg/dL, and lactic acid 2.3 mM/L. Arterial blood gas analysis showed pH 7.483, pCO2 29.9 mmHg, pO2 59.9 mmHg, HCO3 21.9 mM/L and SaO2 91.5% on room air. His chest radiograph showed pneumonic consolidation at the right lower lung zone. Real-time reverse transcription PCR in nasopharyngeal swab was positive for pandemic influenza A (H1N1). Gram stain of sputum showed many Gram-positive cocci and urinary antigen test for Streptococcus pneumoniae was negative. He was given ceftriaxone and levofloxacin empirically as well as oseltamivir. On the same day of admission, his condition rapidly deteriorated and he was transferred to the intensive care unit. He received a ventilator support after intubation because of respiratory failure. A computed tomography scan of the chest showed necrotizing pneumonia involving the right lower lobe (). Culture of sputum and endotracheal aspirate grew MRSA, and it was susceptible to gentamicin, clindamycin, rifampicin, and trimethoprim/sulfamethoxazole, however, resistant to ciprofloxacin, erythromycin, and tetracycline. The D-test for inducible clindamycin resistance was negative. The patient suffered from hemoptysis and substantial amount of purulent sputum over 2 weeks. He was fully recovered after vancomycin treatment for 2 weeks followed by oral rifampicin and trimethoprim/sulfamethoxazole for 3 weeks.
For genotyping of the bacterial isolate, multilocus sequence typing (MLST) was carried out by PCR amplification and sequencing of seven housekeeping genes (arcC, aroE, glpF, gmk, pta, tpi, and yqiL) as previously described (). The allelic profiles and sequence types (STs) were assigned by the MLST web site (). SCCmec types were determined by the multiplex PCR method. Staphylococcal protein A (spa) typing was performed as previously described (). The spa types were determined by using Ridom SpaServer (). Isolates were screened for the lukF-PV and lukS-PV genes encoding the components of the PVL toxin by PCR amplification of a portion of both the lukS-PV and lukF-PV ORFs by using the primer pair luk-PV-1 and luk-PV-2 designed by Lina et al. (). Pulsed field gel electrophoresis (PFGE) was performed as described previously (). The PFGE patterns were analysed using GelCompar II software (Applied Maths, Belgium). Typing of the MRSA isolate from the patient revealed that the isolate belonged to MLST ST8, carried SCCmec type IV, and was positive for PVL. The spa type was t008 (Ridom Staph Type). The analysis of the PFGE patterns showed that this isolate was the same pulsotype as the USA300 strain, which was obtained from the Network on Antimicrobial Resistance in Staphylococcus aureus (NARSA), supported under NIAID/NIH contract #HHSN2722 0070 0055C (). The arcA gene in the arginine catabolic mobile element (ACME) which is characteristic for the USA300 strain was also positive.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [14.1, 'mg/dL'], 'Glucose': [138.0, 'mg/dL'], 'Sodium': [131.0, 'mmol/L']}",274.70238,260.96726,288.4375,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 131.0 mmol/L. 
The concentration of bun is 14.1 mg/dL. 
The concentration of glucose is 138.0 mg/dL. 
Plugging these values into the equation, we get 2 * 131.0 + (14.1 / 2.8) + (14.1 / 18) = 274.70238 mmol/L.The patient's calculated serum osmolality concentration is 274.70238 mmol/L. This is equalivalent to 274.70238 mOsm/kg."
5816,30,Serum Osmolality,lab test,decimal,usmle-5268,Extracted,"A 55-year-old woman presents to the emergency department with chest pain, shortness of breath, and weakness. She has no known past medical history and generally refuses to see a physician for health issues. Review of systems is notable for chronic, severe gastroesophageal reflux disease and chronic diarrhea. Her temperature is 98.3°F (36.8°C), blood pressure is 177/105 mmHg, pulse is 88/min, respirations are 14/min, and oxygen saturation is 97% on room air. Laboratory values are ordered as seen below.

Hemoglobin: 10 g/dL
Hematocrit: 30%
Leukocyte count: 4,500/mm^3 with normal differential
Platelet count: 192,400/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 101 mEq/L
K+: 6.3 mEq/L
BUN: 65 mg/dL
Glucose: 99 mg/dL
Creatinine: 3.1 mg/dL

Notably, the patient requires nursing to help her with most tasks such as putting on her gown and manipulating a cup of water given poor mobility of her hands. She also has recurrent episodes of severe hand pain, which self resolve. The patient is given calcium, insulin, and dextrose and started on dialysis.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [65.0, 'mg/dL'], 'Glucose': [99.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",306.71429,291.37858,322.05,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 65.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (65.0 / 2.8) + (65.0 / 18) = 306.71429 mmol/L.The patient's calculated serum osmolality concentration is 306.71429 mmol/L. This is equalivalent to 306.71429 mOsm/kg."
5817,30,Serum Osmolality,lab test,decimal,pmc-2827067-1,Extracted,"A 28-year-old Indian male, with Indoaryan ethnicity non-smoker, non-alcoholic patient, laborer by occupation presented to hospital with a history of gradually increasing painful swelling in the neck of 3 months duration associated with difficulty in swallowing and palpitations. It was not associated with hoarseness of voice, difficulty in breathing. Patient also complained of low grade fever of 3 months duration, continuous, associated with chills but no rigors or any diurnal variations. There was also history of generalized weakness, diplopia on downward gaze, drooping of eyelids on both sides. Patient had no such complaint in past or no such history was found in family or first degree relatives. On examination patient was conscious, oriented, with nasal twang speech. Look was lethargic and had proptosis and ptosis. Large thyroid swelling was visible, bilaterally symmetrical and tender, smooth, firm in consistency, non-fluctuant, with audible bruit present. B.P-100/60 mmHg, Pulse- 98/min, Temp- 100 0F and respiratory rate of 18/min. Examination also revealed bilateral weakness of superior recti, inferior oblique, lateral recti and left medial rectus.
Investigations revealed Hb-12 g/dl, TLC-9,000/cmm, DLC- N68 E3 L27 M2 B0, Platelets - 2.25 lacs/cmm, ESR - 35 mm, P.B.F - Normocytic normochromic picture, Urea-13 mg/dL, Bl. Glucose (R)- 92 mg/dL, Sr. Creatinine-0.5 mg/dL, Sr. total protein- 6.9 g/dL, Sr. albumin- 3.1, SGOT- 56 U/L, SGPT -20 U/L, ALP- 116 U/L, Sr.Ca++= 1.01 mmol/L, Phosphate-4.0 mg/dl, S.sodium-136 meq/l, Sr. K+-2.9 meq/l, Chest X-ray-Normal, X-ray neck- soft tissue swelling anterior to trachea, routine urine exam- normal, ECG- PR interval prolonged, flattened T waves, TSH- 0.005 µIU/ml, Free T4- 6.89 ng/dL, Free T3- 16.19 pg/ml. FNAC thyroid- thyroid follicular cells, colloid, Hurthle cells and lymphocytes (features suggestive of Hashimoto's thyroiditis), and Neostigmine test for myasthenia gravis- Positive (Figures and ).
In addition to Neomercazole 10 mg three times daily, Pyridostigmine 30 mg three times daily was added for the treatment of ptosis and increased to 60 mg t.i.d., with patient showing dramatic improvement both in symptoms and signs after the start of therapy.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [13.0, 'mg/dL'], 'Glucose': [92.0, 'mg/dL'], 'Sodium': [136.0, 'mEq/L']}",281.75397,267.66627,295.84167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.0 mEq. To convert from 136.0 mEq to mmol, convert from mEq to mmol. The compound 136.0 has a valence of 1, and so divide the valence by the value of mEq to get, 136.0 mEq/(1 mEq/mmol) = 136.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mEq sodium/L converts to 136.0 mmol sodium/L. 
The concentration of bun is 13.0 mg/dL. 
The concentration of glucose is 92.0 mg/dL. 
Plugging these values into the equation, we get 2 * 136.0 + (13.0 / 2.8) + (13.0 / 18) = 281.75397 mmol/L.The patient's calculated serum osmolality concentration is 281.75397 mmol/L. This is equalivalent to 281.75397 mOsm/kg."
5818,30,Serum Osmolality,lab test,decimal,pmc-8285755-1,Extracted,"History of present illness
A 25-year-old African American female with no known past medical history or psychiatric history was brought to the hospital by her mother due to changes in her behavior (nervousness, sweating, lack of sleep) and palpitation. The patient experienced auditory and visual hallucinations (yelled at people she alone could see to keep them away from her). The patient's mother stated that she thought the patient was suicidal when she heard her saying, ""I am going to die,"" prompting her to call 911. However, there was no evidence of suicidality at this time. The patient's mother reported the patient's occasional use of cannabis and alcohol. At the emergency room (ER), a diagnosis of anxiety was made, and she was treated and discharged home on hydroxyzine 25 mg every six hours. However, her symptoms persisted and even worsened despite compliance with medications. She spent the next two days in her room, unable to sleep, anxious, and repeating the exact words, ""you are going to be okay."" Her anxiety worsened and became more agitated warranting readmission and an extensive workup that included anti-NMDA receptor antibodies showing an NMDA titer of 1:320 in her CSF and confirming anti-NMDA receptor encephalitis. IV steroids, plasma exchange, and rituximab were then administered during this patient's long hospital stay. She completed numerous lab tests, including brain magnetic resonance imaging (MRI) and electroencephalogram (EEG), which were negative. She was then discharged home for later follow-up visits.
After two days, she returned to the hospital with a report of worsening combativeness, confusion, and aggression at home. She exhibited suicidal behaviors, including possessing a razor blade to hurt herself and overdosing on a handful of unspecified medications. NMDA titers were repeated and showed increased levels of 1:1280. IV immunoglobulins (IVIG) and intravenous methylprednisolone and rituximab were repeated. She was later transferred to a higher level care center due to the concern of no improvement in her aggression and combativeness with new features of catatonia, including mutism, sitting abnormally still, staring, catalepsy, waxy flexibility, occasional impulsivity, and occasional aggression. At this center, she received lorazepam for 10 days with no significant improvement in her symptoms and was then commenced on emergency ECT treatment. Catatonia due to another medical condition was considered during the patient's treatment course. The differential diagnoses considered during her treatment were hepatitis B virus, primary central nervous system vasculitis, neuroleptic malignant syndrome, and hypersensitivity to first-generation antipsychotics such as haloperidol. The possibility of neuropsychiatric systemic lupus erythematosus (SLE) was considered in this patient given the sociodemographic and symptomatic profile but the physicians who managed this patient did not consider her as having SLE.
Examination
During the assessment, the patient was alert and mute but followed simple commands and nodded yes/no in response to questions. Pupils were equal and reactive to light; she blinked to threat in all visual fields. Intact extraocular movements without nystagmus or ptosis were observed. Her facial sensations were intact and symmetric to light touch on the V1-V3 distribution. Her face was symmetric with a smile and tight eye closure. Uvula and palate rose midline. Shoulder shrug/head turns were symmetric with 5/5 strength. The tongue was midline with no protrusion. There was an increased tone in all her four extremities but no abnormal movements. Strength in all extremities was ⅗, and reflexes of 2+ were present symmetrically in her biceps, brachioradialis, patellar, and Achilles. However, she exhibited catatonic features, which lasted from minutes to hours. Her Bush-Francis Catatonia Rating Scale (BFCRS) was 13 (1 for mobility, 3 for mutism, 2 for staring, 1 for posturing, 3 for waxy flexibility, 1 for impulsivity, 1 for combativeness).
Mental status examination revealed a young lady, well-groomed, with casual wear. She was cooperative and calm. She exhibited minimal psychomotor retardation with a lack of movement. Her speech was slow, with a latency of about 5 seconds. Her affect was flat and mood dysphoric. She was awake, alert, and oriented to time, place, person, and event. Her thought process was linear and concrete. Her judgment and insight were fair.
Investigation
The following investigations were completed during her latest hospital stay. Complete metabolic panel showed; sodium 137 meq/l (normal range: 135 - 148 meq/l), potassium 4.4 meq/l (normal range: 3.5 - 5.3 meq/l), chloride 102 meq/l (normal range: 98 - 107 meq/l), Co2 28 meq/l (normal range: 22 - 29 meq/l), blood urea nitrogen (BUN) 16 mg/dl (normal range: 6 - 20 mg/dl), serum glucose 100 mg/dl (normal range: 70 - 110 mg/dl), blood creatinine 0.9 mg/dl (normal range: 0.57 - 1.11 mg/dl), calcium 9.1 mg/dl (normal range: 8.5 - 10.5 mg/dl), anion gap 7 meq/l (normal range: 5 - 13 meq/l), BUN/creatinine ratio 18 (normal range: 10 - 20). Complete blood count (CBC) showed white blood cell (WBC) 17.55 103/ul (normal range: 4.6 - 10.2 103/ul), RBC 4.77 106/ul (normal range: 4.04 - 5.48 106/ul), hemoglobin 11.9 g/dl (normal range: 12.2 - 16.2 g/dl), hematocrit 37.6% (normal range: 37.7 - 47.9%), mean corpuscular volume (MCV) 78.8 fl (normal range: 80 - 97 fl), mean corpuscular hemoglobin (MCH) 24.9 pg (normal range: 27.0 - 31.2 pg), mean corpuscular hemoglobin concentration (MCHC) 31.6 g/dl (normal range: 31.8 - 35.4 g/dl), platelet count 508 X 103/ul (normal range: 142.0 - 424.0 X 103/ul), mean platelet volume (MPV) 10.2 fl (normal range: 9.4 - 12.4 fl), red cell distribution width (RDW) 17.3% (normal range: 11.6 - 14.6%). Thyriod stimulating hormone (TSH) was 1.03 mIU/L (0.5 to 5.0 mIU/L). The hepatitis B viral panel showed a negative hepatitis B surface antigen and positive hepatitis B core antibody. Malignancy work-up, including transvarginal ultrasound and pelvic MRI, was negative for any malignancy ruling out ovarian teratoma. There were no suspicious adnexal masses.
Anti-NMDAR antibodies were positive at the most recent visit with a serum NMDA titer increase to 1:1280 from the previous 1:320 at the initial diagnosis of NMDAR encephalitis. A brain MRI showed no mass lesion, hemorrhage, or acute infarct. There was no leptomeningeal or intraparenchymal enhancement (Figure ). The ventricular system, cisterns, and sulci were of normal size, shape, and contour. EEG showed normal findings. Other imaging investigations done were CT chest, abdomen, and pelvis, all of which showed no primary malignancy or metastatic lesion.
Treatment
At her initial visit, after the diagnosis of anti-NMDAR encephalitis, she received intravenous immunoglobulins (IVIG) and intravenous methylprednisolone. However, when the NMDA titer was found to be elevated, the decision was made to repeat IVIG, intravenous methylprednisolone, and add rituximab. She received IVIG 2 g/kg over five days, was continued on rituximab and IVIG 1 g. Haloperidol 5 mg three times daily, memantine 5 mg daily, clonazepam 1 mg three times daily, and gabapentin. During her hospitalization, she had extensive long-term electroencephalographic monitoring that did not disclose any seizure activity.
Further immunotherapies were considered. The patient received a third dose of rituximab and was started on prednisone 60 mg daily. Due to concerns for catatonia, lorazepam 2 mg every six hours was commenced and titrated to a high dose. Because she had only a minimal response, amantadine 100 mg twice a day was added. Nonetheless, these treatments proved to be of limited benefit, as the patient remained symptomatic while on admission for about 10 days. An emergent ECT was performed, and she subsequently had 12 ECT sessions, after which her BFCRS score decreased to 0 with significant improvement in her catatonia, cognitive function, and overall mental status. The patient was started on a prolonged prednisone taper and was later discharged on 40 mg four times daily, with instructions on tapering it down. She was recommended for follow-up with psychiatry and neurology.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [137.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [16.0, 'mg/dL'], 'Glucose': [100.0, 'mg/dL']}",285.26984,271.00635,299.53333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 16.0 mg/dL. 
The concentration of glucose is 100.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (16.0 / 2.8) + (16.0 / 18) = 285.26984 mmol/L.The patient's calculated serum osmolality concentration is 285.26984 mmol/L. This is equalivalent to 285.26984 mOsm/kg."
5819,30,Serum Osmolality,lab test,decimal,usmle-6214,Extracted,"A 27-year-old man presents to the emergency department due to a change in his skin color. The patient went on a long hike this morning, and his girlfriend noticed that his skin had changed color when they were driving home. The patient has a past medical history of marijuana use, IV drug use, alcohol use, and asthma. His current medications include albuterol, fluticasone, and ibuprofen. His temperature is 97.5°F (36.4°C), blood pressure is 120/75 mmHg, pulse is 60/min, respirations are 10/min, and oxygen saturation is 98% on room air. Laboratory studies are ordered and are seen below.

Hemoglobin: 10 g/dL
Hematocrit: 32%
Leukocyte count: 5,500 cells/mm^3 with normal differential
Platelet count: 207,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 99 mEq/L
K+: 4.3 mEq/L
HCO3-: 24 mEq/L
BUN: 17 mg/dL
Glucose: 89 mg/dL
Creatinine: 1.0 mg/dL
Ca2+: 10.1 mg/dL
Bilirubin, total: 11.3 mg/dL
Bilirubin, direct: 7.8 mg/dL

Physical exam is notable for a patient with skin that appears yellow/orange. Cardiac, pulmonary, abdominal, and neurological exams are within normal limits.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [17.0, 'mg/dL'], 'Glucose': [89.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",289.01587,274.56508,303.46666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 17.0 mg/dL. 
The concentration of glucose is 89.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (17.0 / 2.8) + (17.0 / 18) = 289.01587 mmol/L.The patient's calculated serum osmolality concentration is 289.01587 mmol/L. This is equalivalent to 289.01587 mOsm/kg."
5820,30,Serum Osmolality,lab test,decimal,pmc-7081570-1,Extracted,"On Aug. 9th, 2019, a 75-year-old man with end-stage renal disease (ESRD) on continuous ambulatory peritoneal dialysis (CAPD) for 5 years, which was 1.5% low-calcium dialysate in a 4-to-5-h dwell three times every day and 2.5% low-calcium dialysate in an 8-to-10-h dwell once every night, was admitted to the nephrology department with an 1-week history of abdominal pain and a cloudy peritoneal dialysis effluent (Fig. a). The patient had a past medical history of hypertension. For the reason that his pressure was lower than before, the antihypertensive drugs were stopped on admission.
Physical examination revealed an emaciated man with a blood pressure of 110/75 mmHg, a breath of 16 beats/min, a pulse of 76 beats/min and a temperature of 36.8 °C. A head examination revealed no face edema. The cardiopulmonary exam was unremarkable. Abdominal examination revealed a soft abdomen, with moderate tenderness to palpation throughout particularly at the lower abdomen, moderate guarding with no rebound and normative bowel sounds. There was no discharge or erythema at the peritoneal dialysis catheter exit site. The tubing of the peritoneal dialysis catheter was intact and there was no macroscopic evidence of the peritoneal dialysis catheter damage.
Laboratory tests on the admitted day were available. The blood routine examination was as follows: white blood cell (WBC) count of 5.00 × 109/L, a neutrophil ratio of 78.2%, lymphocyte ratio of 14.1%, red blood cell (RBC) count of 3.43 × 1012/L, hemoglobin of 83.10 g/L and platelet count of 110 × 109/L. The biochemical routine examination was as follows: sodium 137.00 mmol/L, potassium 2.97 mmol/L, chloride 95.0 mmol/L, glucose 7.4 mmol/L, blood urea nitrogen 21.76 mmol/L and creatinine 878.2 μmol/L. BNP (natriuretic peptide B) was 135 pg/ml and myoglobin was 402.4 ng/ml. The initial peritoneal effluent analysis further revealed as follows: WBC count of 1537.0 × 106/L, chloride 105.8 mmol/L, glucose 20.8 mmol/L, total protein 2.59 g/L, lactic dehydrogenase (LDH) 54.8 U/L, adenosine deaminase (ADA) 0.9 U/L. The changes of important laboratory results were being detected during the admitted period (Fig. c).
Based on the history, physical examination and laboratory results with the findings in the peritoneal dialysis fluid, a diagnosis of peritoneal dialysis-related peritonitis was confirmed. Besides related symptomatic treatments, the empiric antibiotic treatment was initiated with levofloxacin (0.5 g intravenously) every day, ceftazidime (0.25 g intraperitoneally) in a 3-h dwell four times every day and vancomycin (1.0 g intraperitoneally) in an 8-h dwell once at night every 5 days. Final culture of initial peritoneal effluent results indicated the organism was P. multocida, which was found to be sensitive to ampicillin/sulbactam, cefazolin, cefotaxime, cefoxitin, levofloxacin, ampicillin, cefuroxime, imipenem, ciprofloxacin, ceftazidime, meropenem, and cefoperazone/sulbactam, while in the blood there were no bacterial infections were having been found. According to the drug-sensitive test, the intravenously antibiotic treatment was switched to meropenem (0.5 g intravenously) every 12 h, with peritoneal antibiotic treatment still. After one-day treatment, the symptoms disappeared but the WBC count of peritoneal effluent was still above the normal level of the WBC counts, which reminded the infection remained existed. Therefore, Cefazidime was switched to amikacin (200 mg intraperitoneally) in a 3-h dwell four times every day and on Aug. 18th, intravenously meropenem was switched to cefoperazone/sulbactam (1.5 g intravenously) every 12 h. And for the reason that the CAPD was noneffective and the peritoneal infection was not controlled, the patient was undergone temporary hemodialysis four times every week with imipenem/cilastatin (500 mg intraperitoneally) in a 6-h dwell every day for continuing peritoneal antibiotic treatment. After 12-day antibiotic treatment, the WBC count of peritoneal effluent was not significantly improved and the peritoneal effluent was still cloudy. When it was the deadline of the ISPD guideline recommending to hemodialysis, the patient firmly refused the lasting hemodialysis and asked for a further treatment. According to the drug-sensitive results and reviewed case reports (Table ), the patient was switched to ampicillin/sulbactam (3 g intravenously) twice every day. The WBC count of peritoneal effluent was markedly improved and the antibiotic treatment was continued until the WBC count of the peritoneal effluent was below 100 × 106/L and the PD effluent was clear, which revealed the infection was controlled (Fig. b, c). During the treatment, the patient was undergone temporary hemodialysis 12 times to maintain the function of excretion. When the infection was controlled and the function of CAPD recovered, the temporary hemodialysis was stopped and the patient was returned to CAPD. The patient discharged after using ampicillin/sulbactam for 17 days and continued amoxicillin (0.25 g orally) three times a day for another 6 days. The detail key dates of altering antibiotics and methods have been listed (Table ).
The patient and his family were thankful to us and cooperated the further inquiry with us. On further inquiring, the patient reported that he had had a cat at home and when the patient did CAPD, the cat was usually playing with the tubing or contacting the patient during CAPD. However, during his peritoneal dialysis exchange, every step of peritoneal dialysis went all right, without noticing any abnormalities. The patient has suffered from peritoneal dialysis-related peritonitis once in the near 2 years but the causes were not P. multocida. He did not report this incident in admission. After treatment, he continues CAPD to do well.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [21.76, 'mmol/L'], 'Glucose': [7.4, 'mmol/L'], 'Sodium': [137.0, 'mmol/L']}",303.18227,288.02316,318.34138,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mmol/L. 
The concentration of bun is 21.76 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 21.76 mmol. To convert 21.76 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 21.76 mmol bun * 0.001 mol/mmol = 0.02176 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.02176 mol bun * 28.02 g/mol = 0.60972 g bun. To convert 0.60972 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.60972 g bun * 1000.0 mg/g = 609.72 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 609.72 mg bun/10.0 dL = 60.972 mg bun/dL. The concentration value of 21.76 mmol bun/L converts to 60.972 mg bun/dL. 
The concentration of glucose is 7.4 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 7.4 mmol. To convert 7.4 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 7.4 mmol glucose * 0.001 mol/mmol = 0.0074 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0074 mol glucose * 180.16 g/mol = 1.33318 g glucose. To convert 1.33318 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 1.33318 g glucose * 1000.0 mg/g = 1333.18 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1333.18 mg glucose/10.0 dL = 133.318 mg glucose/dL. The concentration value of 7.4 mmol glucose/L converts to 133.318 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (60.972 / 2.8) + (60.972 / 18) = 303.18227 mmol/L.The patient's calculated serum osmolality concentration is 303.18227 mmol/L. This is equalivalent to 303.18227 mOsm/kg."
5821,30,Serum Osmolality,lab test,decimal,pmc-6476073-1,Extracted,"69-year-old female with no significant past medical history with the exception of anxiety presented as a transfer from an outside hospital with acute onset of hypersomnolence and aphasia. She was last seen normal the night before by her family. Her vitals on arrival were within normal limits; blood pressure was 134/64 mmHg, heart rate was 88 per minute, respiratory rate was of 22 breaths per minutes, and she was afebrile. On exam she appeared drowsy, nonverbal, and intermittently following one-step commands. Her cranial nerves were intact and on motor exam she had mild generalized weakness but was able to move all extremities against gravity. Sensory exam was confounded by her decreased mental status. Bilateral plantar reflexes were equivocal. National Institute of Health Stroke Scale (NIHSS) was 10. She was out of the 4.5-hour time window to consider IV thrombolysis therapy and on exam her presenting symptoms did not localize to one cerebral vascular territory.
Initial diagnostic work-up: serum white blood cell count 11000/uL, hemoglobin 14.2g/dL, platelets 190000/uL, sodium 143mmol/L, potassium 5.7mmol/ (repeat 4.4mmol/L), blood urea nitrogen 34mg/dL, creatinine 1.05mg/dL, glucose 323mg/dL, troponins <7ng/L, aspartate aminotransferase 46 U/L, and alanine aminotransferase 45 U/L. Urinary analysis was positive for moderate leukocytes and negative nitrites, and her toxicology screen was negative.
Noncontrasted CT brain demonstrated bilateral thalamic hypodensities. A CT angiogram (CTA) demonstrated focal areas of basilar artery narrowing, an Artery of Percheron (AOP) arising from the right PCA (Figures , , and ) and no large vessel occlusions. MRI brain demonstrated bilateral paramedian thalamic infarcts (Figures and ) extending into the midbrain on diffusion weighted imaging (DWI). Her ejection fraction was 65% with no atrial septum shunt on transthoracic echocardiogram.
Her serum low density lipoprotein was 130mg/dL and her glycosylated hemoglobin was 13.8%. She was diagnosed with diabetes mellitus type 2. Her stroke etiology was thought to be secondary to small vessel disease given the arterial bed involved and her uncovered lipohyalinosis risk factors. Patient was discharged on atorvastatin 40 mg, aspirin 81 mg, and an insulin regimen. On discharge to rehab her NIHSS improved to four.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [143.0, 'mmol/L'], 'Glucose': [323.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [34.0, 'mg/dL']}",316.0873,300.28294,331.89167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 143.0 mmol/L. 
The concentration of bun is 34.0 mg/dL. 
The concentration of glucose is 323.0 mg/dL. 
Plugging these values into the equation, we get 2 * 143.0 + (34.0 / 2.8) + (34.0 / 18) = 316.0873 mmol/L.The patient's calculated serum osmolality concentration is 316.0873 mmol/L. This is equalivalent to 316.0873 mOsm/kg."
5822,30,Serum Osmolality,lab test,decimal,pmc-7734887-1,Extracted,"Initial presentation
A 27-year-old male presented to a community emergency department in summer of 2016 in western Washington State complaining of lightheadedness and ""almost passing out."" The patient reported that he had been feeling generally fatigued over the past 48 hours. He was normally very active, hiking and rock climbing frequently, however he felt as though he had not been able to hike at his normal brisk pace. The day before his presentation, while finishing a long hike, he had become lightheaded and nearly lost consciousness, stating that he rapidly lowered himself to the ground. His girlfriend, who accompanied him, confirms that he did not fully lose consciousness. The patient cannot recall any preceding symptoms; he specifically denies having chest pain, palpitations, shortness of breath, headache, or any focal neurological deficits. Several seconds after the episode, the patient felt completely back to his recent baseline. He had no persistent lightheadedness.
Upon returning from the hike that day, the patient visited a local urgent care. He had no symptoms at the time and was noted to have dry mucus membranes on physical exam. His work-up there included complete blood count, comprehensive metabolic panel, and electrocardiogram, which were normal. The patient was diagnosed with dehydration and presyncope and was discharged to home.
At home, the patient rehydrated orally and went to bed. He awoke at 02:00 with recurrent symptoms so he drove to the emergency department.
Upon arrival, the patient was placed on a monitor in the triage room and was noted by the triage nurse to be in complete atrioventricular dissociation. During triage, the patient briefly lost consciousness, during which time the triage nurse noted an eight-second ventricular pause on the cardiac monitor. External pacer/defibrillator pads were placed and the patient was brought back to a trauma room. On initial physician interview, the patient noted continued lightheadedness but denied chest pain, palpitations, jaw or arm pain, nausea, edema, or shortness of breath. He also denied headache, focal weakness, and speech or coordination changes. He reported no fever or respiratory symptoms in the past week.
The patient had no past medical or surgical history. He received all routine pediatric vaccinations and screening studies. He was not prescribed any medications and denied using any supplements or alternative medical treatments. He had no known drug allergies. He had a family history of hypertension in his mother and coronary artery disease in his father, diagnosed in his 60s. There was also a family history of colorectal cancer in his father. He denied any known family history of sudden cardiac death or cardiac arrhythmias, although he admitted to not being well informed about his family history. The patient was a non-smoker, drank one to two alcoholic drinks per week, and denied recreational or intravenous drug use.
During the travel history, the patient did report having traveled extensively throughout the United States over the past year to participate in outdoor recreational activities. He recalled camping in the Northeast region two months ago, after which he had some low grade fever and a red rash on his right shoulder. He described the rash as circular and gradually enlarging. He did not recall any central clearing. The fever and rash spontaneously resolved and he did not seek medical attention for these. He had no further symptoms after that, up until 48 hours prior to his presentation to the emergency department.
A complete review of systems was obtained and was negative. Vital signs were blood pressure: 112/65; heart rate: 62; respiratory rate: 12; temperature: 98.5.
Physical exam revealed a fit-appearing young male who was mildly diaphoretic but was alert and fully oriented and in no acute medical distress. Cardiac exam demonstrated a borderline bradycardic rate. There were no murmurs, rubs, or gallops. There was no extremity edema and peripheral pulses were symmetric. There was no jugular venous distention. Breath sounds were clear to auscultation and symmetric. His abdomen was soft and non-tender. The remainder of the physical examination was without noted abnormalities. Notably, there was no rash, focal weakness, or joint tenderness or effusion. He had a normal neurologic exam.
An electrocardiogram was obtained rapidly after the patient’s admission to the emergency department. This showed atrioventricular (AV) dissociation with accelerated junctional rhythm. Axis was normal. There were no acute ST elevation or depression and no T wave abnormalities. See Figure for the ECG.
Complete blood count in the emergency department showed a white blood cell count of 8,500 per microliter (reference range 3,800-11,000 per microliter), hematocrit of 41.2% (reference range 39-50%), and a platelet count of 248,000 per microliter (150,000-400,000 per microliter). White blood cell differential was within the hospital laboratory’s established normal limits.
A comprehensive metabolic panel revealed a glucose of 97 mg/dL (reference range 65-99 mg/dL), creatinine of 0.80 mg/dL (reference range 0.7-1.30 mg/dL), blood urea nitrogen (BUN) of 15 mg/dL (reference range 7-18 mg/dL), sodium of 140 mmol/L (reference range 136-145 mmol/L), and potassium of 3.6 mmol/L (reference range 3.5-5.1). Transaminases and alkaline phosphatase were within normal laboratory reference ranges.
Urine toxicology screen was negative for any drugs of abuse.
A point-of-care troponin was not elevated outside of the reference range. A repeat troponin was checked 4.5 hours later and was also within normal limits.
Subsequent serial ECGs demonstrated periods of junctional rhythm slower than atrial rhythm, confirming third-degree heart block.
Intervention
The patient was given a 1-liter bolus of intravenous normal saline and was admitted to a cardiac telemetry floor. A transvenous pacemaker was placed. Blood was sent for serologic testing for Borrelia burgdorferi antibodies. He was started on empiric therapy with 2 grams of IV ceftriaxone given once daily on the presumption of Lyme carditis as well as maintenance IV normal saline.
Serial laboratory evaluation each morning consisted of a complete blood count and comprehensive metabolic panel. These laboratory studies did not fall significantly outside of reference ranges throughout the course of the patient’s hospitalization. Serial electrogardiograms were obtained and showed persistent complete atrioventricular block in the first three days of his hospitalization. Additional diagnostic studies that were ordered during the patient’s hospital stay included an echocardiogram, which revealed a normal left ventricular wall thickness, normal left ventricular ejection fraction of 55-60% (reference range 55-60%), and no significant valvular regurgitation or stenosis. There was no evidence of diastolic dysfunction to suggest infiltrative cardiomyopathy. There was no pericardial effusion. A thyroid stimulating hormone level was checked and was 1.210 microIU/mL (reference range 0.358- 3.740 microIU/mL).
Outcomes
The patient’s enzyme-linked immunosorbent assay (ELISA) and subsequent Western blot serology testing returned positive for Borrelia burgdorferi antibodies, suggesting active infection. He remained in the hospital for 10 days during which time his cardiac telemetry monitoring showed gradually lengthening intervals of Mobitz I second-degree heart block. Following seven days of treatment, there were no further intervals of third-degree heart block. Upon discharge from the hospital, pacemaker wire was removed. The patient followed up with a family medicine physician one week following his discharge. ECG done at that time showed normal sinus rhythm.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [15.0, 'mg/dL'], 'Glucose': [97.0, 'mg/dL'], 'Sodium': [140.0, 'mmol/L']}",290.74603,276.20873,305.28333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mmol/L. 
The concentration of bun is 15.0 mg/dL. 
The concentration of glucose is 97.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (15.0 / 2.8) + (15.0 / 18) = 290.74603 mmol/L.The patient's calculated serum osmolality concentration is 290.74603 mmol/L. This is equalivalent to 290.74603 mOsm/kg."
5823,30,Serum Osmolality,lab test,decimal,pmc-6789384-1,Extracted,"A 38-year-old man arrived at our emergency department with acutely altered mental status.
The patient suffered from alcoholism and had a known history of recurrent episodes of hepatic encephalopathy; the most recent episode had happened 5 mo earlier. He had stopped drinking alcohol for 5 mo and had started drinking again 1 wk prior to this presentation. On the morning of admission, the family had incidentally found him lying in bed, confused and lethargic, and immediately called an ambulance.
The patient did not have any history of disease and did not have a history of seizures or brain trauma, and he had not recently undergone surgery.
The patient has been drinking alcohol everyday for 16 years. Family history was not contributory.
Upon arrival, the patient had a blood pressure of 96/56 mm Hg, pulse rate of 132 beats per minute, body temperature of 37.5 °C, respiratory rate of 22 breaths per min, and oxygen saturation of 96% in room air. Physical examination revealed no acute distress and a Glasgow Coma Scale score of 5 (eyes, 1; verbal, 3; and motor, 1). No signs of trauma were observed on his body. His pupils were equal in size, round, and nonreactive to light. Cardiopulmonary and abdominal examination findings were unremarkable. Bilateral Babinski signs were absent, but the neurological examination otherwise was limited because the patient could not follow commands.
Laboratory studies showed a white blood cell count of 9900/μL with 75.8% of neutrophils, hemoglobin level of 17.6 g/dL, hematocrit of 50.6%, and platelet count of 117000/μL. Electrolyte, liver function, and blood chemistry results were as follows: Sodium, 132 mmol/L; potassium, 3.5 mmol/L; calcium, 8.2 mg/dL; magnesium, 2.4 mg/dL; blood urea nitrogen, 34 mg/dL; creatinine, 2.72 mg/dL; total bilirubin, 6.7 mg/dL; direct bilirubin, 3.8 mg/dL; alanine aminotransferase, 496 IU/L; alkaline phosphatase, 163 IU/L; albumin, 3.9 g/dL; lipase, 73 IU/L; prothrombin time (international normalized ratio), 1.17; and ammonia, 277.7 μmol/L (reference range, 6-47 μmol/L). The fasting blood glucose level was 168 mg/dL; the lactate level was 71.5 mg/dL. The arterial blood gas pH was 7.29 (partial pressure of carbon dioxide, 56 mm Hg; partial pressure of oxygen, 71 mm Hg; and actual bicarbonate level, 26.9 mmol/L).
Electrocardiograms and chest radiographs revealed no acute pathological finding. Brain computed tomography without contrast enhancement revealed no hemorrhage or acute ischemic stroke. Abdominal computed tomography showed atelectasis in both lower lung zones, fatty liver, and ileus.
In the emergency department, one episode of generalized seizure with frothing at the mouth and both eyes deviated to the left side lasting for several minutes was noted. An intravenous injection of lorazepam (1 ampoule of 2 mg) was immediately administered for seizure control; at that time, the patient’s Glasgow Coma Scale score was 3 (eyes, 1; verbal, 1; and motor, 1). The patient was intubated and admitted to an ICU for monitoring with a diagnosis of hepatic encephalopathy. Lorazepam and vitamin B infusion were administered to prevent alcohol withdrawal syndrome; lactulose (30 mL) via a nasogastric tube was administered three times per day for management of hepatic encephalopathy, and broad-spectrum empirical antibiotics were administered for control of any infection. On the second day of his hospitalization, several episodes of involuntary bilateral feet dorsiflexion were noted. His ammonia level decreased to 88.1 μmol/L by the third day of hospitalization, but intermittent involuntary movement in the lower face was still noted.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [132.0, 'mmol/L'], 'Blood Urea Nitrogen (BUN)': [34.0, 'mg/dL'], 'Glucose': [168.0, 'mg/dL']}",285.47619,271.20238,299.75,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 132.0 mmol/L. 
The concentration of bun is 34.0 mg/dL. 
The concentration of glucose is 168.0 mg/dL. 
Plugging these values into the equation, we get 2 * 132.0 + (34.0 / 2.8) + (34.0 / 18) = 285.47619 mmol/L.The patient's calculated serum osmolality concentration is 285.47619 mmol/L. This is equalivalent to 285.47619 mOsm/kg."
5824,30,Serum Osmolality,lab test,decimal,pmc-3965927-1,Extracted,"An 83-year-old woman was admitted to the emergency department of our hospital on May 5 with a clinical history of abdominal pain, nausea, vomiting, and diarrhea which started three days previously. Her past medical history was characterized by chronic atrial fibrillation, cardiomegaly, and a not-further-specified adnexal mass asportation. The patient denied being a smoker and referred to chronic assumption of digitalis, furosemide, and oral anticoagulant therapy. She also referred to a previous hospitalization in January in another hospital with similar but milder symptoms, resolved in few hours. At that time a plain abdominal X-ray was performed and the radiologist's report was negative. We could not examine the X-ray film prior to performance of CT as it was brought later. At physical examination, she had no fever, with a painful and tender abdomen at superficial and deep palpation on the mid-lower quadrants. Blumberg's, Murphy's, and McBurney's signs were negative. Peristalsis was torpid. Digital rectal exploration showed fecal traces and blood streaks. Blood gas analysis showed a pH of 7.38, pCO2 of 29 mmHg, pO2 of 84 mmHg, Na+ of 139 mmol/L, K+ of 3.5 mmol/L, Cl− of 104 mmol/L, and Lactates of 3.0 mmol/L and SpO2 of 94.7%. Blood test results were as follows: Hb 17.60 g/dL, hematocrit 51.90%, white blood cell count 22.710 μL (neutrophilia 83.3%), PT-INR 1.78, glucose 158 mg/dL, blood urea 54.00 mg/dL, and creatinine 1.50 mg/dL. Upon clinical suspicion of bowel obstruction or infarction, the patient underwent contrast-enhanced CT examination (LightSpeed VCT 64 Slice GE; slice thickness: 1.25; contrast media: Iomeron 350 mg/mL Bracco) which showed the presence of a significant parietal thickening of the transverse and descending colon, a mesenteric loose tissue imbibition, venous engorgement, no filling defect of visceral arteries, and the presence of fluid collections in the Douglas pouch and perihepatic space. As a collateral finding, a hyperdense sharp-pointed curvilinear foreign body was identified in the sigma and was associated with a perifocal persistent contrast-enhancement (CE) within a pseudotumoral mass (Figures , , and ). It was not possible to differentiate whether it was lying in the bowel lumen or in the context of the intestinal wall. No free abdominal air was discovered. Having previously evaluated the CT scan and examining the X-ray that the patient's family had brought in the meantime, our radiologist concluded that the FB was already present in January (). Due to worsening of the clinical condition and on the basis of imaging findings, it was decided to perform an emergency surgical intervention. After laparotomy was performed, 100 mL of citrine fluid was collected and sent to our laboratory to be analyzed. Macroscopically small bowel loops and in particular the colon were pale, suggesting a condition of hypoperfusion, although no marked areas of ischemia and infarction were found. Pulsation of the superior mesenteric artery was present. The distal portion of the sigmoid colon resulted tenaciously adherent to the pelvic wall, with a wooden consistency. An intraoperative endoscopy was performed, but it was not possible to pass beyond the rectal-sigmoid junction due to a stenotic condition related to the rigidity and angle of the sigma wall. Dissection of the sigma from the pelvic wall revealed an ingested chicken bone perforating the sigma and lying within an inflammatory pseudotumour originating from the colonic wall (). A Hartmann's intervention was performed, consisting of the resection of the rectosigmoid colon with closure of the rectal stump and an end colostomy. This surgical procedure was decided in order to avoid the risk of dehiscence of a colocolic anastomosis due to the evident intestinal hypoperfusion. A control CT, performed 8 days after surgery, did not show any complication or fluid collection. Histological examination showed extensive hemorrhagic ulceration of the colonic mucosa, complicated by the perforation of the colonic wall and associated serositis. Surrounding areas presented ischemic aspects with reactive locoregional lymphnodes. Collected peritoneal fluid analysis revealed the presence of reactive mesothelial cells, blood cells, and amorphous proteinaceous material (). The patient was dismissed 12 days after the operation in good status. Regular checks have been carried out in the outpatient setting.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [139.0, 'mmol/L'], 'Glucose': [158.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [54.0, 'mg/dL']}",306.06349,290.76032,321.36666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mmol/L. 
The concentration of bun is 54.0 mg/dL. 
The concentration of glucose is 158.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (54.0 / 2.8) + (54.0 / 18) = 306.06349 mmol/L.The patient's calculated serum osmolality concentration is 306.06349 mmol/L. This is equalivalent to 306.06349 mOsm/kg."
5825,30,Serum Osmolality,lab test,decimal,pmc-3170342-1,Extracted,"A 60-year-old Iranian woman presented to our hospital with pain and swelling in her right arm following a minor fall. Our initial physical examination revealed her to be in a good general condition. She was normotensive, with a pulse rate of 92 beats/minute. Her other laboratory values were as follows: body temperature 37°C, hemoglobin 12.2 g/dL, leukocytes 22 cells/mm3, platelets 200 U/L, sodium 141 mEq/L, potassium 4 mEq/L, glucose 11.6 mmol/L, blood urea nitrogen 15.1 mmol/L, and creatinine 250 mmol/L. A plain X-ray showed a pathologic fracture in the mid-shaft of her right humerus and a large, ill-defined soft tissue mass (Figure ). Magnetic resonance imaging (MRI) showed a huge lobulated mass destroying the shaft of the humerus and displacing the surrounding soft tissue. The mass was bright on serial T2-weighted MRI scans and dark on serial T1-weighted MRI scans, with marked enhancement after a gadolinium injection (Figure ). Four years ago she had been treated for a sacrococcygeal chordoma with surgical resection and post-operative radiotherapy. A local tumor recurrence developed after one year and required additional surgical procedures. A histological examination of the biopsy from the humeral lesion showed a lobulated mass composed of cuboidal to polygonal cells with eccentric nuclei, clear to eosinophilic cytoplasm, and pools of extracellular mucin (arrow in Figure ). Typically, few tumor cells have a ""physaliferous"" (bubble-bearing) appearance. On the basis of these findings, we considered differential diagnoses such as myxoid chondrosarcoma, myxoid liposarcoma, primary mixed tumor of the bone, metastasizing pleomorphic adenoma of the salivary gland, metastatic renal cell carcinoma (RCC), or metastatic carcinoma with intra-cytoplasmic mucin from the colon or lung [,]. Most metastatic carcinomas have more of the cytological features of malignancy than chordomas do. The tumor cells stained positive for AE1/3 (Figure ), ethidium monoazide (EMA), S100, and vimentin. Although both chordomas and chondrosarcomas stain with S100 protein, myxoid chondrosarcomas do not stain with keratin and EMA. Additional immunochemistry was performed for CD10, the results of which were negative in this case and usually expressed in RCC. Abdominal and pelvic ultrasonography and computed tomography (CT) of her chest and abdomen were normal. On the basis of this evidence and our review of the original histology following her previous chordoma excision (which was histologically identical to the humeral lesion), a diagnosis of metastatic chordoma was confirmed. She refused any active treatment.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [15.1, 'mmol/L'], 'Glucose': [11.6, 'mmol/L'], 'Sodium': [141.0, 'mEq/L']}",308.72105,293.285,324.1571,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. 
The concentration of bun is 15.1 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 15.1 mmol. To convert 15.1 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 15.1 mmol bun * 0.001 mol/mmol = 0.0151 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0151 mol bun * 28.02 g/mol = 0.4231 g bun. To convert 0.4231 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.4231 g bun * 1000.0 mg/g = 423.1 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 423.1 mg bun/10.0 dL = 42.31 mg bun/dL. The concentration value of 15.1 mmol bun/L converts to 42.31 mg bun/dL. 
The concentration of glucose is 11.6 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 11.6 mmol. To convert 11.6 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 11.6 mmol glucose * 0.001 mol/mmol = 0.0116 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0116 mol glucose * 180.16 g/mol = 2.08986 g glucose. To convert 2.08986 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 2.08986 g glucose * 1000.0 mg/g = 2089.86 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 2089.86 mg glucose/10.0 dL = 208.986 mg glucose/dL. The concentration value of 11.6 mmol glucose/L converts to 208.986 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (42.31 / 2.8) + (42.31 / 18) = 308.72105 mmol/L.The patient's calculated serum osmolality concentration is 308.72105 mmol/L. This is equalivalent to 308.72105 mOsm/kg."
5826,30,Serum Osmolality,lab test,decimal,usmle-4681,Extracted,"A 47-year-old female with a history of hypertension presents to your outpatient clinic for numbness, tingling in her right hand that has been slowly worsening over the last several months. She has tried using a splint but receives minimal relief. She is an analyst for a large consulting firm and spends most of her workday in front of a computer. Upon examination, you noticed that the patient has a prominent jaw and her hands appear disproportionately large. Her temperature is 99 deg F (37.2 deg C), blood pressure is 154/72 mmHg, pulse is 87/min, respirations are 12/min. A fasting basic metabolic panel shows: Na: 138 mEq/L, K: 4.1 mEq/L, Cl: 103 mEq/L, CO2: 24 mEq/L, BUN: 12 mg/dL, Cr: 0.8 mg/dL, Glucose: 163 mg/dL.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [12.0, 'mg/dL'], 'Glucose': [163.0, 'mg/dL'], 'Sodium': [138.0, 'mEq/L']}",289.34127,274.87421,303.80833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 12.0 mg/dL. 
The concentration of glucose is 163.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (12.0 / 2.8) + (12.0 / 18) = 289.34127 mmol/L.The patient's calculated serum osmolality concentration is 289.34127 mmol/L. This is equalivalent to 289.34127 mOsm/kg."
5827,30,Serum Osmolality,lab test,decimal,pmc-2827435-1,Extracted,"A 25-year-old Turkish woman was admitted to our hospital in October 2008. She was suffering from abdominal pain, weakness, anorexia, and a 7-kg to 8-kg weight loss. It was discovered that she had a palpable abdominal mass three years prior to presentation. Physical examination revealed a 15 × 20-cm mass with regular contours in the her periumbilical region (Figure ). Four years prior to presentation, during her second pregnancy, she was admitted to a hospital because of abdominal pain, and an ultrasonographic examination then revealed an abdominal mass. As she did not want to terminate her pregnancy, she declined to undergo further examinations. After her pregnancy, she was told by her doctor that the mass had grown markedly. Because she was afraid of regularly visiting a doctor, she treated herself using alternative medicines such as eucalyptus tea, bay leaves and oleander. She claimed that drinking this tea made the mass shrink.
Her laboratory results at the time of presentation were as follows: hemoglobin, 13 g/dl; white blood cell count, 10,500/cm3; platelets, 302,000/cm3; sodium, 135 mEq/L; potassium, 4.1 mEq/L; blood urea nitrogen, 28 mg/dl; creatinine, 1.1 mg/dl; glucose, 110 mg/dl; aspartate aminotransferase (AST), 36 IU/L; and alanine aminotransferase (ALT), 41 IU/L. On abdominal X-rays, all of her intestines were seen shifted to the right. An intravenous pyleogram (IVP) showed a mass associated with her left kidney. Abdominal computed tomography (CT) and magnetic resonance imaging (MRI) revealed an 18 × 11 × 12-cm mass located in the middle of her left kidney and extending inferiorly, with diffuse contrast enhancement (Figures to ). The mass was consistent with renal cell carcinoma on CT. Owing to the mass, she develped left hydroureteronephrosis (Figure ). Her right kidney appeared to be within normal limits on the IVP and CT examinations. A laparotomy was performed via a midline incision. A 25 × 16 × 12 cm, 3380 g mass, arising from the left kidney and shifting the ureter proximally, was excised together with the left kidney (Figures , , ). Our patient was discharged on the sixth postoperative day, with no signs of complications.
Meanwhile, microscopic examination of hematoxylin and eosin (H&E)-stained sections at low power showed a neoplasm with a pseudocapsule and a tubulocystic pattern divided by thin fibrous septa. At higher magnification, the cells appeared to be round to polygonal with abundant granular eosinophilic cytoplasm, a regular round nucleus, and a central nucleolus. There were no foci of clear cell changes, necrosis, or mitotic figures.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [28.0, 'mg/dL'], 'Glucose': [110.0, 'mg/dL'], 'Sodium': [135.0, 'mEq/L']}",286.11111,271.80555,300.41667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 135.0 mEq. To convert from 135.0 mEq to mmol, convert from mEq to mmol. The compound 135.0 has a valence of 1, and so divide the valence by the value of mEq to get, 135.0 mEq/(1 mEq/mmol) = 135.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mEq sodium/L converts to 135.0 mmol sodium/L. 
The concentration of bun is 28.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 135.0 + (28.0 / 2.8) + (28.0 / 18) = 286.11111 mmol/L.The patient's calculated serum osmolality concentration is 286.11111 mmol/L. This is equalivalent to 286.11111 mOsm/kg."
5828,30,Serum Osmolality,lab test,decimal,pmc-6942743-1,Extracted,"A 59-year-old Caucasian man with ESRD due to glomerulonephritis and failed kidney transplant who was undergoing CCPD for 7 months presented to the emergency department with periumbilical pain for several days. This was the first time the patient had experienced these symptoms since the initiation of CCPD. His medical history additionally included hypertension, valvular heart disease, degenerative arthritis, parathyroidectomy, and tobacco use. He had discontinued all of his immunosuppressive medications because his kidney transplant had been nonfunctional for several years.
Physical examination revealed a well-built, seemingly healthy man weighing 157 pounds with a blood pressure of 144/92 mmHg and a heart rate of 85 beats/min, without distress, and without jaundiced sclerae. He had clear lungs and systolic heart murmur. Abdominal examination revealed a soft abdomen with some fullness on the right lower quadrant proximal to his previous renal transplant, periumbilical tenderness, and intact exit site with no tunnel tenderness. He had active bowel sounds.
Laboratory testing revealed a white blood cell (WBC) count of 9.1 × 103/μL with 70% neutrophils, hemoglobin level of 12.9 g/dL, hematocrit count of 38.5%, and platelet count of 263 × 103/μL. Serum chemistry analysis showed the following levels: sodium 139 mmol/L, potassium 3.4 mmol/L, chloride 95 mmol/L, total carbon dioxide 28 mmol/L, glucose 127 mg/dL, blood urea nitrogen 31 mg/dL, and creatinine 12.46 mg/dL. The peritoneal fluid was colorless and appeared hazy. Initial analysis showed a WBC count of 4,470 cells/μL with 85% polymorphonuclear cells and 15% mononuclear cells. Gram staining of the peritoneal fluid was negative for any organisms, only showing WBCs.
Based on the available information, the patient was diagnosed with PD-peritonitis, and empiric treatment with 1 g of vancomycin and 1 g of ceftazidime was administered intravenously and daily infusions initiated. The final diagnosis was made through peritoneal fluid culture that showed light growth of P. multocida after 3 days. The isolate was sensitive to ampicillin, ceftriaxone, ceftazidime, gentamicin, and ciprofloxacin. Therefore, antibiotics were adjusted according to the bacterial cultures, where intravenous ampicillin-sulbactam was started and then switched to oral amoxicillin-clavulanate for a total of 3 weeks. Patient had subsequent improvement in symptoms and laboratory results. He was able to continue PD successfully without any interruption or the need for catheter removal.
Upon taking further history, the patient reported having several cats at home, none of which were kittens. At night, he would begin his PD treatment and go into a different room to watch television. Therefore, the cats were assumed to play with the dialysis equipment or chew on the tubing, possibly leading to infection, although the patient did not recall noticing any fluid leakage from the tubing. Prior to discharge, the patient's dialysis technique was confirmed by direct observation, and aseptic technique was ensured. The patient additionally decided to place his cats outside the home at night before starting PD treatment. He did not have any more episodes of PD-peritonitis caused by P. multocida after changing his routine.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [139.0, 'mmol/L'], 'Glucose': [127.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [31.0, 'mg/dL']}",296.12698,281.32063,310.93333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mmol/L. 
The concentration of bun is 31.0 mg/dL. 
The concentration of glucose is 127.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (31.0 / 2.8) + (31.0 / 18) = 296.12698 mmol/L.The patient's calculated serum osmolality concentration is 296.12698 mmol/L. This is equalivalent to 296.12698 mOsm/kg."
5829,30,Serum Osmolality,lab test,decimal,pmc-2760558-1,Extracted,"A 68 year-old Asian woman was admitted to our hospital presenting with a two-day history of high grade fever, diarrhea and nausea. The patient's symptoms began one day after eating grilled chicken and beef at a restaurant; however, she did not complain of abdominal pain, vomiting, or hematochezia. The patient was diagnosed with diabetes mellitus at the age of 50, had undergone haemodialysis due to diabetic nephropathy for the past 2 years, and was under three times weekly haemodialysis. She had also undergone an aortic mechanical valve replacement operation for aortic stenosis 7 months prior to the current admission.
Upon admission to our hospital, the patient's height was 149 cm and her body weight were 61.0 kg (dry weight). The patient's temperature was 106°F, blood pressure was 150/90 mmHg, heart rate was 152/min, and respiratory rate was 24/min. Cardiovascular examination revealed a Levine IV/VI systolic murmur at the right second intercostal space. Her bowel movements were slightly hypoactive and physical examination did not reveal any abdominal tenderness or rebound. No evidence of embolization including Osler node, Janeway lesion and petechiae was observed. No other abnormalities were noted on the systemic examination. Initial laboratory examinations revealed the following results: hemoglobin, 115 g/L [110-146 g/L]; total leukocyte counts, 10300/μL [3500-8200/μL] without left shift (Myelo 0.5%, Meta 0.5%, Stab 2.0%, Seg 90.0%, Lym 1.5%, Mono 5.5%); normal platelet counts, 1.42 × 103/μL [1.40-3.89 × 103/μL]; significantly elevated C-reactive protein, 18.54 mg/dL [<0.30 mg/dL]; Na 131 mEq/L, K 4.3 mEq/L, Cl 97 mEq/L, HCO3- 18.9 mmol/L; BUN 43.6 mg/dL, Cre 7.25 mg/dL (before haemodialysis); serum glucose, 173 mg/dL; and HbA1c, 7.3% [4.3-5.8%]. In addition, the patient was tested negative for HIV antibodies.
Salmonella enteritis or campylobacter enteritis was suspected due to the history of eating grilled chicken. Treatment was initiated with ciprofloxacin 300 mg q24hr, ceftriaxone 2 g q24hr, and clindamycin 600 mg q12hr intravenously, started on day of admission. Three days post-admission, a serial blood culture taken on admission revealed Salmonella enterica serotype Enteritidis (O9, H-g) that was sensitive to ceftriaxone (MIC <= 1) and ciprofloxacin (MIC <= 0.25) (Table ). After detection of the causable microorganism, ceftriaxone and clindamycin treatment was ceased, and the patient was treated with ciprofloxacin alone. Since the patient's aortic valve was a prosthetic, and Salmonella species have a high affinity for intravascular intima, there was a concern about prosthetic infective endocarditis. Therefore, the patient underwent transthoracic echocardiography (TTE) on day 7; however, no abnormalities were detected by TTE. On day 9, the patient showed a sudden disturbance in mental status, left conjugate deviation, and right hemiplegia. Diffusion-weighted imaging of the brain via MRI showed an acute cerebral infarction of the middle cerebral artery region (figure ). Following this discovery, the TTE was re-examined, followed by a transesophageal echocardiography (TEE) on day 13. The TEE revealed floppy vegetation on the mitral valve, which was 12 × 8 mm in size (figure ). We could not find any aberrance of the replaced aortic valve. Although surgery to remove the vegetation was considered, acute cerebral infarction contraindicated her from undergoing the operation. The ciprofloxacin dose was increased to 400 mg q24hr and was combined with ceftriaxone 2q q12hr, on day 12. Consequently, the patient was treated solely with ciprofloxacin for 8-day period (from day 4 to day 11). Although the patient's neurological deficit ameliorated gradually, she experienced another infarction at the left occipital lobe and the right cerebellar hemisphere on day 18. Conservative therapy with antibiotics was continued; however, her mental status progressively decreased and blood pressure deteriorated. Blood culture examinations were repeated, but they were all negative. haemodialysis ceased on day 35 due to the unstable haemodynamic status, although treatment with ciprofloxacin and ceftriaxone were continued. On day 39, the patient died of respiratory failure and cardiac arrest. Her clinical course is shown in figure . Autopsy revealed a rigid node on the mitral valve (figure ), associated with septic emboli (mass of gram-negative microorganisms) at the left occipital lobe (figure ).",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [43.6, 'mg/dL'], 'Glucose': [173.0, 'mg/dL'], 'Sodium': [131.0, 'mEq/L']}",287.18254,272.82341,301.54167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 131.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 131.0 mEq. To convert from 131.0 mEq to mmol, convert from mEq to mmol. The compound 131.0 has a valence of 1, and so divide the valence by the value of mEq to get, 131.0 mEq/(1 mEq/mmol) = 131.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 131.0 mEq sodium/L converts to 131.0 mmol sodium/L. 
The concentration of bun is 43.6 mg/dL. 
The concentration of glucose is 173.0 mg/dL. 
Plugging these values into the equation, we get 2 * 131.0 + (43.6 / 2.8) + (43.6 / 18) = 287.18254 mmol/L.The patient's calculated serum osmolality concentration is 287.18254 mmol/L. This is equalivalent to 287.18254 mOsm/kg."
5830,30,Serum Osmolality,lab test,decimal,pmc-8038922-1,Extracted,"A 47-year-old Caucasian female with a past medical history of major depressive disorder, chronic alcohol abuse, and an unspecified eating disorder was brought to the hospital by emergency medical services under the Florida Mental Health Act due to new-onset altered mental status. The patient had been found to be too weak to stand and her only reported oral intake had been alcohol with no food for an undefinable amount of time. Examination in the emergency room revealed a tangential thought process and poor responses to questioning. She believed she was in her home and the hospital staff were friends and family. She was found to be tachycardic with a heart rate of 131 beats per minute (bpm), blood pressure 105/75 mm Hg, respirations 16 breaths per minute with a 99% pulse oxygen level, and afebrile 37.3⁰C (99.1⁰F). On physical exam, the patient was noted to be cachexic and tremulous with a body mass index (BMI) of 15.9kg/m2. Horizontal nystagmus was noted. The rest of the physical exam was unremarkable. Laboratory analysis abnormalities showed leukocytosis 19.04 x 103/uL, hypokalemia with potassium 3.2 mmol/L, slight hypernatremia 146 mmol/L, creatinine 2.2 mg/dL, blood urea nitrogen (BUN) 59 mg/dL, glucose 144 mg/dL, and mild hypercalcemia 10.5mmol/L. Liver function was normal as well as albumin levels. Urine toxicology was negative and alcohol level was < 3 mg/dL. Patient met criteria for sepsis as she was tachycardic with acute kidney injury with elevated creatinine, leukocytosis, and an elevated lactic acid level of 4.97 mmol/L (normal 0.90-1.70 mmol/L) with altered mental status. Lipase levels were found to be elevated at 1234 unit/L. Chest x-ray and computed tomography (CT) head were unremarkable. She was admitted to the intensive care unit (ICU) with severe sepsis, altered mental status, acute kidney injury, and failure to thrive.
The patient was started on high-dose thiamine supplementation with close monitoring of electrolytes. She experienced persistent encephalopathy, ataxia, and nystagmus. The patient was retaining urine on bladder scan and a Foley catheter was placed with a urine sample sent for urinalysis. She was started on intravenous ceftriaxone. Magnetic resonance imaging (MRI) of the brain without contrast also showed no acute intracranial processes. The initial urinalysis returned positive and urine cultures were sent out. The urine culture was positive for Escherichia coli and antibiotics were adjusted according to the sensitivity panel. The patient did not show any improvement in mental status following completion of the antibiotic course. The patient continued to display fluctuating mental status, believing she was at home with her parents and, on rare occasions, understood that she was in the hospital. The patient also showed increased agitation in the late evenings where she was found to be combative and tearful. These episodes required extra nursing support with frequent reorientation. After discussion with Neurology and Psychiatry, it was determined the patient’s cognitive status was likely permanent and was classified as Korsakoff syndrome. As the primary team, multiple antipsychotics were attempted to stabilize her moods and agitation, including varying doses of haloperidol, ziprasidone, and quetiapine. Eventually we settled on a scheduled low dose of quetiapine, which showed only minimal improvement in patient’s mental status.
By this point, the patient had been hospitalized for over two months. There were multiple barriers making a safe discharge plan difficult to establish. We conversed with the patient’s sister and power of attorney (POA) regarding possible alternative treatments, including initiation of memantine. After discussing the risks and benefits, we agreed to initiate memantine. Notably, the patient’s sister reported a family history of alcoholism in both parents and a prodrome of altered mental status for a month-long period prior to their father’s death. The patient’s mother’s cause of death was unknown. The patient and her sister had last spoken one month prior to admission and her sister reported the patient was alert and oriented x4 at that time with no prior history of Wernicke’s or memory deficits.
A Folstein mini-mental state exam (MMSE) was first performed prior to initiation of the medication on which the patient scored an 18/30. Her primary deficits were in cognition and recall. She showed no deficits in attention, calculation, or language skills. She was started on a low dose of memantine 5 mg twice a day and observed. After one week of treatment, she appeared to have more frequent, intermittent episodes of clarity during which she was oriented to place and was able to recall she was in the hospital, however, she could not recall reasons for hospitalizations despite daily reorienting. She was consistently disoriented to time and self. Long-term memory including details regarding childhood and early adult life remained preserved. Nursing staff noticed she appeared to be calmer in the evenings and her mood appeared less labile. Her MMSE after one week of treatment with memantine was 19/30. During the remainder of her admission, we avoided making any changes to her quetiapine. Her memantine was increased to a maintenance dose of 10 mg twice a day with continued observation of her cognitive function and weekly MMSEs. Her mental status continuously fluctuated over the next few weeks, ranging between 18-22/30. After 119 days, she was deemed medically optimized for discharge to a long-term memory care facility.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [59.0, 'mg/dL'], 'Glucose': [144.0, 'mg/dL'], 'Sodium': [146.0, 'mmol/L']}",321.07143,305.01786,337.125,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 146.0 mmol/L. 
The concentration of bun is 59.0 mg/dL. 
The concentration of glucose is 144.0 mg/dL. 
Plugging these values into the equation, we get 2 * 146.0 + (59.0 / 2.8) + (59.0 / 18) = 321.07143 mmol/L.The patient's calculated serum osmolality concentration is 321.07143 mmol/L. This is equalivalent to 321.07143 mOsm/kg."
5831,30,Serum Osmolality,lab test,decimal,pmc-7061730-1,Extracted,"This 20-year-old woman from the Northeast USA had type I (von Gierke) glycogen storage disease and was transferred to a referral hospital for liver transplant evaluation. The patient had received a living-related renal transplant at age 15 for renal failure attributed to her glycogen storage disease. She had had a laparoscopic cholecystectomy at age 18. She had developed chronic rejection of her renal transplant and hemodialysis had to be resumed approximately 10 months prior, at which point immunosuppression was presumably stopped. One week prior to transfer, she received a second living-related renal transplant. Three days postoperatively, the transplant renal vein thrombosed. Five days postoperatively, the new allograft was removed. Following the allograft nephrectomy, the patient had increasing transaminases, prothrombin time, partial thromboplastin time and lactate. Her platelet count and hemoglobin fell. She became obtunded and hypotensive. The patient was intubated and mechanically ventilated. An infusion of dopamine was started for blood pressure support. She was given platelets, packed red blood cells, fresh frozen plasma, cryoprecipitate and desmopressin. She was transferred to a referral hospital on postoperative day 7 for liver transplant evaluation.
On admission to the referral hospital, the patient's temperature was 36 degrees C, pulse 100/minute, respirations 16/minute (on ventilator) and blood pressure 110/60 mm Hg. Her abdomen was diffusely tender with serous drainage from her surgical drain. She was incontinent of stool and had pedal edema. Neurologic examination showed a grade III hepatic coma, with grimacing to pain. She was mildly hyperreflexic. Blood testing showed multi-organ biochemical derangement with ammonia 108 uMol/L (reference range [RR]: 5-50 uMol/L), lactate 21.7 mEq/L (RR: 0.7-1.8 mEq/L), and bilirubin 12.7 mg/dL (RR: 0.3-1.5 mg/dL). Tissue injury was manifested by elevated serum aspartate aminotransferase (AST) 18,895 U/L (RR: <40 U/L), alanine aminotransferase (ALT) 2659 U/L (RR: <40 U/L), and amylase 1570 U/L (RR: 25-125 U/L). Additional metabolic testing revealed serum sodium 136 mEq/L (RR: 136-145 mEq/L), potassium 6.2 mEq/L (RR: 3.5-5.1 mEq/L), chloride 89 mEq/L (RR: 95-110 mEq/L), bicarbonate 11 mEq/L (RR: 21-31 mEq/L), calcium 7.3 mg/dL (RR: 8.5-10.5 mg/dL), phosphorus 14.3 mg/dL (RR: 2.5-4.5 mg/dL), magnesium 1.7 mEq/L (RR: 1.6-2.5 mEq/L), glucose 331 mg/dL (RR: 70-110 mg/dL), blood urea nitrogen 8 mg/dL (RR: 9-20 mg/dL), and creatinine 3.7 mg/dL (RR: 0.8-1.5 mg/dL). The patient’s hemoglobin was 7.4 g/dL (RR: 11.7-15.7 g/dL), and white blood cell count 10,100/mm3 (RR: 4,000-10,000/mm3). She was coagulopathic with platelets 52,000/mm3 (RR: 140,000-440,000/mm3), prothrombin time (PT) 21.8 seconds (RR: 10.5-13 seconds), and partial thromboplastin time (PTT) 57.8 seconds (RR: 25-33 seconds). Arterial blood showed pH 7.12, PCO2 32 mm Hg and PO2 134 mm Hg. Chest x-ray showed no pulmonary edema.
The patient was admitted with diagnoses of fulminant hepatic failure, coagulopathy, metabolic acidosis, renal failure and anemia. Computed tomography (CT) scan of the head showed no intracranial bleeding. Transcranial Doppler examination showed slightly increased cerebral blood flow. CT scan of the abdomen showed an enlarged liver, and an ultrasound examination of the abdomen had findings that suggested the possibility of hepatic vein thrombosis, but was not definitive. The patient was given red blood cells, platelets, fresh frozen plasma, cryoprecipitate, bicarbonate, and started on slow continuous ultrafiltration dialysis. Cefotetan and vancomycin therapy were started.
The following day, the patient was weaned from dopamine. Her transaminase values decreased and her lactate decreased to 19.1 mEq/L. Abdominal CT scan showed a lower chest infiltrate consistent with infection or posttransplant lymphoproliferative disorder. Her amylase rose to 3113 U/L. Blood cultures drawn on admission were reported positive for gram positive cocci in pairs and chains. Later that day, the patient developed an unstable heart rhythm. She was started on esmolol.
On the third day at the referral hospital, the patient remained unresponsive. Her lactate and transaminases continued to fall, but lipase increased above 4000 U/L and bilirubin climbed to 22 mg/dL. The admission blood culture isolate was identified as Enterococcus faecalis. Arterial line catheter tip culture from admission yielded Enterococcus faecium and Enterococcus faecalis.
On the fourth day, the patient continued in hepatic coma and shock, with metabolic acidosis (lactate 27.9 mEq/L). She had diffuse 2+ edema and bilateral rhonchi. Blood and sputum cultures from the third day were positive for Enterococcus faecalis. At 13:30, the patient's Swan Ganz right heart catheter was changed and culture of the catheter tip subsequently yielded 100 colonies of Enterococcus faecalis. At 18:28, the patient's bilirubin was 25.8 mg/dL, ALT 619 U/L, AST 5224 U/L, PT 20.4 seconds, PTT 34.8 seconds, sodium 129 mEq/L, potassium 3.3 mEq/L, chloride 81 mEq/L, bicarbonate 19 mEq/L, blood urea nitrogen 3 mg/dL, creatinine 1.7 mg/dL, glucose 504 mg/dL, white blood cell count 8,100/mm3 (83% segmented neutrophils, 8% bands, 2% lymphocytes, 7% monocytes), hemoglobin 10.5 g/dL, and platelets 24,000/mm3.
Considering that the patient's liver might be the anatomic source of her life-threatening enterococcal sepsis and was non-functional, a decision was reached to perform an emergency hepatectomy with a portocaval shunt and hope of soon finding a suitable liver for transplantation. During the procedure, the patient needed 91 units of blood, 30 units of platelets, and 24 units of cryoprecipitate and fresh frozen plasma. As the surgeons were closing the abdomen, the patient became bradycardic and started bleeding through her endotracheal tube. Arterial blood showed pH 7.15, PCO2 27 mm Hg and PO2 59 mm Hg. Cardiopulmonary resuscitation including pericardiocentesis with removal of 200 ml of fluid was to no avail.
The explanted liver weighed 3700 grams (RR: <1800 grams) and showed near-total necrosis with massive hemorrhage, but no significant inflammation and no organisms on special stains. Neither the surgical pathology examination of the explanted liver nor the autopsy showed hepatic vein thrombosis.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [8.0, 'mg/dL'], 'Glucose': [331.0, 'mg/dL'], 'Sodium': [136.0, 'mEq/L']}",293.24603,278.58373,307.90833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.0 mEq. To convert from 136.0 mEq to mmol, convert from mEq to mmol. The compound 136.0 has a valence of 1, and so divide the valence by the value of mEq to get, 136.0 mEq/(1 mEq/mmol) = 136.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mEq sodium/L converts to 136.0 mmol sodium/L. 
The concentration of bun is 8.0 mg/dL. 
The concentration of glucose is 331.0 mg/dL. 
Plugging these values into the equation, we get 2 * 136.0 + (8.0 / 2.8) + (8.0 / 18) = 293.24603 mmol/L.The patient's calculated serum osmolality concentration is 293.24603 mmol/L. This is equalivalent to 293.24603 mOsm/kg."
5832,30,Serum Osmolality,lab test,decimal,pmc-2799424-1,Extracted,"The patient, a 7 years and 6 months old boy, was the second child of unrelated healthy parents. He was born by cesarean section after a full term pregnancy. His birth weight was 3,250 kg (50 percentile), length 50 cm (50 percentile) and head circumference (HC) 35.5 cm (50 percentile). His perinatal period was without problems. The motor development was normal as he sat independently at the age of 7 months and walked unassisted at the age of 11 months. His language development was delayed; first words were spoken later than aged 2 years and 6 months, and at 5 years he was referred to logotherapy. His parents described him as a healthy, sociable and smart boy with low linguistic skills. When the patient attended 1st grade in the mainstream school he was referred by his schoolteacher for full developmental assessment because of learning difficulties and speech developmental delay.
On physical examination he was quite a sociable child, with mild dysmorphic facial features such as ocular hypertelorism, downward slanting palpebral fissures, epicanthal folds, flat nasal bridge, short nose with flat philtrum, and thin upper lip. Additionally, his neck was short and the feet were stubby and flat. His weight was 27 kg (50th percentile), height 122 cm (25th percentile) and his HC 52 cm (25th percentile). On developmental examination: his nonverbal skills were equivalent to a 5 years 9 months level with good language understanding, being able to spell, read and write small words, but his oral speech development was very poor. His expressive language was limited to small words and phrases with many phonological difficulties. According to Griffiths Mental Development Scales and Bayley Scales of Infant Development (2nd edition) his General Developmental Quotient (GDQ) was 78 with performance DQ of 86 and language DQ of 61. His behavior was normal for developmental age.
On neurological examination he was slightly hypotonic but without asymmetry. Heart auscultation revealed a mild systolic murmur. Audiological examination showed a mild bilateral selective high frequency hearing loss (4000-8000 Hz). Heart ultrasound (triplex) showed a single papillary muscle resulting in mild mitral valve regurgitation but without hemodynamic changes. The echocardiogram was normal. Full ophthalmologic examination was normal. Hematological tests revealed anemia with Hb of 9.3 g/100 ml, Ht of 30%, MCV of 57.9, MCH of 18, and MCHC of 31 g/100 ml, with normal blood cell and platelet counts 269,000/μl (140,000/μl-300,000/μl). Bleeding time was very elongated >17 min (2-4 min) and platelet aggregation test (PSA) was abnormal 196 sec (<142 sec).
Results of further biochemical tests were the following: urea: 34 mg/dl, blood sugar: 86 mg/dl, creatinine: 0.35 mg/dl, calcium: 9.4 mg/dl, Mg: 2.5 mg/dl, K: 4.8 mEq/l, Na: 140 mEq/l, Cl:106 mEq/l, SGOT: 40 U/l, SGPT: 30 U/l, GT: 8 U/l, cholesterol: 132 mg/dl, HD: 61 mg/dl, LDL: 59 mg/dl, CPK: 65 u/l, and ammonia: 0.69 μg/dl. Thyroid function and kidney-liver-spleen ultrasound were also normal.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [34.0, 'mg/dL'], 'Glucose': [86.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",296.92063,282.0746,311.76666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 34.0 mg/dL. 
The concentration of glucose is 86.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (34.0 / 2.8) + (34.0 / 18) = 296.92063 mmol/L.The patient's calculated serum osmolality concentration is 296.92063 mmol/L. This is equalivalent to 296.92063 mOsm/kg."
5833,30,Serum Osmolality,lab test,decimal,usmle-6085,Extracted,"A 33-year-old woman presents to the emergency department with numbness and severe fatigue. She states that her symptoms started yesterday and have been gradually worsening. The patient is generally healthy, drinks alcohol on the weekends, and does not smoke. She was ill recently but recovered spontaneously. Her temperature is 102°F (38.9°C), blood pressure is 127/68 mmHg, pulse is 120/min, respirations are 17/min, and oxygen saturation is 98% on room air. Physical exam is notable for an anxious young woman who appears mildly confused. Neurological exam reveals she has decreased sensation to light touch bilaterally on her upper and lower extremities. Dermatologic exam reveals petechiae. Laboratory values are ordered as seen below.

Hemoglobin: 7.2 g/dL
Hematocrit: 25%
Leukocyte count: 6,500/mm^3 with normal differential

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 5.4 mEq/L
HCO3-: 22 mEq/L
BUN: 30 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.9 mg/dL
Ca2+: 10.2 mg/dL

A peripheral smear is performed as seen in Figure A.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [30.0, 'mg/dL'], 'Glucose': [99.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",294.21429,279.50358,308.925,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 30.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (30.0 / 2.8) + (30.0 / 18) = 294.21429 mmol/L.The patient's calculated serum osmolality concentration is 294.21429 mmol/L. This is equalivalent to 294.21429 mOsm/kg."
5834,30,Serum Osmolality,lab test,decimal,usmle-8725,Extracted,"A 68-year-old man presents with shortness of breath, particularly when walking up stairs and when lying down to go to sleep at night. He also complains of a chronic cough and states that he now uses 2 extra pillows at night. The patient has a history of type 2 diabetes that is well-managed with metformin. He also takes Prozac for a long-standing history of depression. The patient has a 60-pack-year smoking history. He also has a history significant for alcohol abuse, but he quit cold turkey 15 years ago when his brother was killed in a drunk driving accident. Both he and his brother were adopted, and he does not know other members of his biological family. Despite repeated efforts of patient counseling, the patient is not interested in quitting smoking. The physical exam is significant for an obese male using accessory muscles of aspiration. The vital signs include: temperature 36.8°C (98.2°F), heart rate 95/min, respiratory rate 16/min, and blood pressure 130/85 mm Hg. The oxygen saturation is 90% on room air. Additional physical exam findings include cyanotic lips, peripheral edema, hepatomegaly, and ascites. The cardiovascular exam is significant for an S3 heart sound and elevated JVP. The pulmonary exam is significant for expiratory wheezing, diffuse rhonchi, and hyperresonance on percussion. The laboratory test results are as follows:
BUN 15 mg/dL
pCO2 60 mm Hg
Bicarbonate (HCO3) 32 mmol/L
Creatinine 0.8 mg/dL
Glucose 95 mg/dL
Serum chloride 103 mmol/L
Serum potassium 3.9 mEq/L
Serum sodium 140 mEq/L
Total calcium 2.3 mmol/L
Hemoglobin 26 g/dL
Bilirubin total 0.9 mg/dL
Bilirubin indirect 0.4 mg/dL
Iron 100
Ferritin 70
TIBC 300
The l posterior-anterior chest X-ray is shown in the image.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [15.0, 'mg/dL'], 'Glucose': [95.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",290.63492,276.10317,305.16667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 15.0 mg/dL. 
The concentration of glucose is 95.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (15.0 / 2.8) + (15.0 / 18) = 290.63492 mmol/L.The patient's calculated serum osmolality concentration is 290.63492 mmol/L. This is equalivalent to 290.63492 mOsm/kg."
5835,30,Serum Osmolality,lab test,decimal,pmc-4402468-1,Extracted,"While playing cricket, a 26-year-old Indian Asian male without any significant past medical history experienced a two-week history of intermittent, retrosternal stabbing chest pain that radiated to his left arm and shoulder. The pain was pleuritic, positional, and associated with diaphoresis and nausea. The patient was diagnosed with costochondritis by his primary care physician. Seven days prior to admission, the patient had an upper respiratory tract infection with fever and chills. He denied smoking, drinking alcohol, or to using drugs; however, he reported that he had been drinking protein shakes for 3 years for muscle building. Upon physical exam, the patient was afebrile with a BP of 118/86 mmHg, PR of 111/min, and RR of 22/min. The remainder of the physical exam was completely unremarkable. Laboratory data showed Hb 15.6 g/dL, Hct 44.6, WBC 19.9 K/μL, platelet count 675 K/μL, glucose 157 mg/dL, BUN 21 mg/dL, Cr 1.2 mg/dL, Ca 9.7 mg/dL, albumin 4.7 g/dL, total protein 7.8 g/dL, sodium 137 mmol/L, potassium 3.3 mmol/L, chloride 98 mmol/L, and bicarbonate 20 mmol/L. Urine drug screen was negative. ECG showed ST elevation in the anterolateral leads (). After consulting cardiology, the patient was taken to the cardiac catheterization lab for rescue angioplasty. A 95% mid-spiral right coronary artery dissection with total left anterior descending spontaneous dissection was demonstrated (Figures and ). Both the dissections were classified as type 1. The remaining vessels were normal. Left ventricular ejection fraction was measured at 15–20%. Percutaneous coronary intervention (PCI) to LAD and mid-RCA was performed. Vasculitis work-up was subsequently negative.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [21.0, 'mg/dL'], 'Glucose': [157.0, 'mg/dL'], 'Sodium': [137.0, 'mmol/L']}",290.22222,275.71111,304.73333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mmol/L. 
The concentration of bun is 21.0 mg/dL. 
The concentration of glucose is 157.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (21.0 / 2.8) + (21.0 / 18) = 290.22222 mmol/L.The patient's calculated serum osmolality concentration is 290.22222 mmol/L. This is equalivalent to 290.22222 mOsm/kg."
5836,30,Serum Osmolality,lab test,decimal,pmc-6521491-1,Extracted,"An 8-year-old boy was admitted to the Emergency Room of Santa Maria della Misericordia hospital, Perugia, Italy, on February 10, 2018 because he had suffered from severe diarrhoea (> 6 stools per day), vomiting (3 episodes per day) and high fever (> 39.0 °C) over the previous two days. He did not have unusual travel, dietary, or animal contact and did not receive any doses of the RV vaccine. In the Emergency Room, the child was drowsy, body temperature was 38.7 °C, heart rate 170 beats/min, respiratory rate 50 breaths/min, and blood pressure 85/45 mmHg. Severe dehydration was evident. The weight was 2.5 kg lower than that evaluated several days before disease onset, revealing a 10% loss. The oral mucosa was very dry, eyes sunken and skin liftable in persistent folds. Moreover, no urine was found in the bladder after catheterization. Laboratory tests revealed low serum concentrations of both potassium (2.7 mEq/L) and sodium (128 mEq/L), confirming hypo electrolytic gastroenteritis. Glycaemia was lower than the normal (47 mg/dL). Kidney function tests showed a relevant pre-renal failure, with creatinine at 2.48 mg/dL and urea at 133 mg/dL. Severe acute gastroenteritis was diagnosed according to the Ruuska and Vesikari criteria for the definition of severity of RV diarrhoeal episodes [], and the child was hospitalized.
After hospitalization, faecal samples for bacteria and virus identification were collected. Cultures for all the bacterial pathogens usually associated with acute severe gastroenteritis were negative, while an enzyme immunoassay for the detection of RVA (Ridascreen® Rotavirus, R-Biopharm AG, Germany) was positive. A sample of faeces was used for reverse transcription-polymerase chain reaction and nucleotide sequencing of the infecting RV. Moreover, tests were performed to evaluate host immune system function, including total immunoglobulin concentration, neutrophil function and lymphocyte immunophenotyping; however, no abnormalities were revealed.
Intravenous fluids were immediately administered according to the World Health Organization recommendation [], and the response was rapid. Diarrhoea progressively reduced, vomiting disappeared, and oral feeding was resumed the day after admission. Blood pressure, heart rate, and respiratory rate returned to normal values within 24 h as it was for diuresis. Pre-renal failure disappeared after 48 h. Weight returned to initial values within one week.
Management of the case was approved by the Ethics Committee of Umbria Region, Perugia, Italy (2018-PED-03), and parents provided informed written consent. The patient’s parents also provided informed consent for the publication of this case report.
Total RNA was extracted from 140 μL of 10% faecal suspensions in distilled water using the Viral RNeasy Mini Kit (Qiagen/Westburg, Segrate, Italy), according to the manufacturer’s instructions. RNA was eluted in 60 μL of RNase-free water and stored at − 80 °C until use. After an initial step of denaturation, the viral RNA was subjected to retro-transcription (RT) using the Invitrogen Superscript III reverse transcriptase kit (Life Technologies, Monza, Italy) with a single cycle at 37 °C for 60 min and 95 °C for 5 min. The obtained DNA was then used as a template for PCR amplification of VP7 (primers Beg9-End9) and VP4 (primers Con3-Con2) segments [, ]. The reactions were performed with the Invitrogen Platinum Taq kit (Life Technologies, Monza, Italy), following the manufacturer’s instructions. RVA genotyping was carried out by a multiple semi-nested PCR using a mixture of primers specific for G- and P-types, as previously described for genotype assignment []. Retro-transcription and all PCR reactions were performed following slightly modified EuroRota-Net protocols [].
Since the low amount of DNA obtained after the first round PCR, for nucleotide sequence analysis, a second nested PCR was carried out using VP7-F, VP7-R, VP4-F, and VP4-R primers, resulting in a 881 bp product for VP7 and a 663 bp product for VP4 [, ]. Nucleotide sequencing of amplified genes was performed at Eurofins Genomics (Ebersberg, Germany) using primers used for the second PCR. In addition, the amplification and nucleotide sequencing of all the RVA genomic segments was performed. Briefly, the RT-PCR was conducted by using specific primers for each gene segment, and nucleotide sequencing was performed at Eurofins Genomics using the same primers included in the RT-PCR reactions. The nucleotide sequences obtained were analysed and corrected with ChromasPro2.23 software (Technelysium, Queensland, Australia). Nucleotide and amino acid sequence similarity searches were performed using the BLAST (Basic Local Alignment Search Tool) server on the GenBank database of the NCBI (National Center for Biotechnology Information, National Institute of Health, Bethesda, MD).
The assignment of genotypes for all the 11 gene segments was performed with the “RotaC v2.0 - classification tool for rotaviruses group A”. Multiple sequence alignments and phylogenetic tree construction were performed with MEGA6 software [], applying the maximum-likelihood method and using the Tamura3 + G substitution model. The sequences obtained in this study are available in GenBank () under the accession numbers listed in Table .
The phylogenetic trees revealed relatedness between the VP7 and VP4 genes of the PG2 G3P[8] RVA Italian strain and those belonging to recent G3P[8] RVAs detected worldwide. The G3 VP7 belonged to the equine-like G3 lineage and shared the highest nucleotide sequence identity (99.8%) with the previously identified equine-like G3 (Fig. ). Moreover, it was significantly different from the G3 strains detected previously in Italy and included in the phylogenetic tree within the G3-3c and 3d lineages. The P[8] VP4 revealed a similar clustering pattern as that observed for the VP7. Strain PG2 was closely related to the same strains highlighted by the VP7 analysis, with the P[8] Italian strains previously detected in the same sampling area (in combination with G1 and G4 VP7) grouped separately, despite sharing the same lineage 3 in this case (Fig. ).
Finally, the PG2 RVA strain clustered in a branch different from that of the VP7 gene of Rotateq® (18.5% nucleotide difference and 7.2% amino acid difference) and in a lineage different from those of the VP4 specificities included in the Rotateq® and Rotarix® vaccines (6.3 and 9.6% nucleotide difference and 5.8 and 10.3% amino acid difference, respectively). The comparison of the deduced amino acid sequences revealed only 4 substitutions (T87A, N213 T, K238D, D242A) across the VP7 epitopes (Fig. ).
Strain PG2 showed the G3-P[8]-I2-R2-C2-M2-A2-N2-T2-E2-H2 genotype, revealing a complete genotype 2 (DS-1 like) genomic backbone []. All the gene segments investigated revealed the highest nucleotide sequence identities (98.5 to 99.8%) with equine-like G3P[8] RVA strains detected in Brazil in 2015 (Table ).",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [128.0, 'mEq/L'], 'Glucose': [47.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [133.0, 'mg/dL']}",306.11111,290.80555,321.41667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 128.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 128.0 mEq. To convert from 128.0 mEq to mmol, convert from mEq to mmol. The compound 128.0 has a valence of 1, and so divide the valence by the value of mEq to get, 128.0 mEq/(1 mEq/mmol) = 128.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 128.0 mEq sodium/L converts to 128.0 mmol sodium/L. 
The concentration of bun is 133.0 mg/dL. 
The concentration of glucose is 47.0 mg/dL. 
Plugging these values into the equation, we get 2 * 128.0 + (133.0 / 2.8) + (133.0 / 18) = 306.11111 mmol/L.The patient's calculated serum osmolality concentration is 306.11111 mmol/L. This is equalivalent to 306.11111 mOsm/kg."
5837,30,Serum Osmolality,lab test,decimal,usmle-1910,Extracted,"A 25-year-old man is brought to the physician because of fatigue, lethargy, and lower leg swelling for 2 weeks. He also noticed that his urine appeared darker than usual and for the last 2 days he has passed only small amounts of urine. His temperature is 37.5°C (98.6°F), pulse is 88/min, respirations are 15/min, and blood pressure is 154/98 mm Hg. Examination shows 2+ pretibial edema bilaterally. Laboratory studies show:
Hemoglobin 10.9 g/dL
Leukocyte count 8200/mm3
Platelet count 220,000/mm3
Serum
Na+ 137 mEq/L
Cl- 102 mEq/L
K+ 4.8 mEq/L
HCO3- 22 mEq/L
Glucose 85 mg/dL
Urea nitrogen 34 mg/dL
Creatinine 1.4 mg/dL
Urine
Blood 2+
Protein 3+
Glucose negative
RBC 10–12/HPF with dysmorphic features
RBC casts numerous
Renal biopsy specimen shows a crescent formation in the glomeruli with extracapillary cell proliferation.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [34.0, 'mg/dL'], 'Glucose': [85.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",290.86508,276.32183,305.40833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 34.0 mg/dL. 
The concentration of glucose is 85.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (34.0 / 2.8) + (34.0 / 18) = 290.86508 mmol/L.The patient's calculated serum osmolality concentration is 290.86508 mmol/L. This is equalivalent to 290.86508 mOsm/kg."
5838,30,Serum Osmolality,lab test,decimal,pmc-3731624-1,Extracted,"A 10-month-old boy with a body weight of 9.6 kg presented with progressive lethargy. His past medical history was unremarkable. He had suffered from gastritis 2 weeks before and started vomiting again 2 days before admission. The patient had no fever, excessive sweating or diarrhea, and his urine output was normal. Physical examination revealed a sleepy but easily arousable infant with a heart rate of 160 per minute, a respiration rate of 32 per minute and a body temperature of 37.7°C. On all four extremities, a blood pressure of 135/95 mm Hg was measured, a value above the 99th percentile (P) by age and height (e.g. P 95th is 103/56 mm Hg). There were no signs of meningitis or intracranial hypertension, no abnormalities in sensibility and strength, and reflexes were normal. Cardiopulmonary examination revealed no heart murmurs, and breath sounds were normal. The abdomen was not painful to palpation and there were no masses. No edema was found, and the skin was unremarkable. Based on the combination of hypertensive crisis and the neurological findings, the diagnosis of malignant hypertension was made and the patient was admitted to our pediatric intensive care unit for evaluation and intravenous antihypertensive therapy [, , ]. Nicardipine at 1 mcg/kg/min lowered his blood pressure to an acceptable level of 105/55 mm Hg (P 95th) within a few hours.
Laboratory results showed a normal complete blood cell count, serum electrolytes (Na 137 mmol/l, K 4.1 mmol/l, Cl 104 mmol/l), creatinine 13 µmol/l, urea 3.6 mmol/l and glucose 5.6 mmol/l. Glomerular filtration rate was 118 ml/min, and blood lactate as well as ammonia levels were normal. An arterial blood gas analysis revealed a mild meta-bolic acidosis with respiratory compensation (pH 7.40, bicarbonate 17.7 mmol/l, pCO2 29 mm Hg).
A computed tomography of the brain revealed no intracranial bleeding, no tumor and no signs of elevated intracranial pressure. An abdominal ultrasound showed normal kidneys without hydronephrosis, and Doppler studies were unremarkable. On the ultrasound, an abdominal mass with the characteristic ‘target sign’ of an ileocecal intussusception was visualized in the right lower quadrant (fig. ). Radiographically guided hydrostatic reduction with water-soluble contrast failed. Laparotomy was performed, which confirmed the diagnosis of intussusception. After repositioning, intestinal perfusion was adequate and bowel resection was not necessary. The anesthetics used during the surgery had no major influence on the blood pressure. Following surgery, the mental status returned to normal and antihypertensive medication could be discontinued. His blood pressure decreased to a normal level (P 50th 90/40 mm Hg).",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [3.6, 'mmol/L'], 'Glucose': [5.6, 'mmol/L'], 'Sodium': [137.0, 'mmol/L']}",283.2075,269.04712,297.36787,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mmol/L. 
The concentration of bun is 3.6 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 3.6 mmol. To convert 3.6 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 3.6 mmol bun * 0.001 mol/mmol = 0.0036 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0036 mol bun * 28.02 g/mol = 0.10087 g bun. To convert 0.10087 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.10087 g bun * 1000.0 mg/g = 100.87 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 100.87 mg bun/10.0 dL = 10.087 mg bun/dL. The concentration value of 3.6 mmol bun/L converts to 10.087 mg bun/dL. 
The concentration of glucose is 5.6 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 5.6 mmol. To convert 5.6 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 5.6 mmol glucose * 0.001 mol/mmol = 0.0056 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0056 mol glucose * 180.16 g/mol = 1.0089 g glucose. To convert 1.0089 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 1.0089 g glucose * 1000.0 mg/g = 1008.9 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1008.9 mg glucose/10.0 dL = 100.89 mg glucose/dL. The concentration value of 5.6 mmol glucose/L converts to 100.89 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (10.087 / 2.8) + (10.087 / 18) = 283.2075 mmol/L.The patient's calculated serum osmolality concentration is 283.2075 mmol/L. This is equalivalent to 283.2075 mOsm/kg."
5839,30,Serum Osmolality,lab test,decimal,pmc-6230352-1,Extracted,"A 39-year-old man with no known health issues prior to ED presentation,was brought to the ED by family members with concerns for fever, generalized weakness, and abdominal pain of one week’s duration. He had been evaluated at an urgent care facility and referred to the ED after treatment with acetaminophen for temperature of 39.2 °C and ondansetron for nausea; rapid antigen testing for influenza and streptococcus were negative. He reported one week of fevers, night sweats, and anorexia with non-radiating, right upper quadrant pain, as well as multiple episodes of vomiting and the development of loose, gray-colored stools. He denied back pain or urinary symptoms. He had taken a small number of acetaminophen tablets of unknown dosage over the preceding week for fever, but denied regular or excessive use. He denied recent travel, unusual foods, herb or mushroom ingestion, ethanol use, or intravenous (IV) drug abuse. Socially, he admitted to daily marijuana and tobacco use.
Physical examination revealed an acutely ill man with scleral icterus, who was diaphoretic and moaning, complaining of pain. Vital signs on presentation included an oral temperature of 37.3 °C, heart rate of 78 beats per minute, blood pressure of 132/70 millimeters of mercury, and respiratory rate of 20 breaths per minute. Mucous membranes were dry, lungs were clear, and the heart sounds were regular without murmurs or gallops. The abdomen was soft with moderate tenderness in the right upper quadrant without guarding. The liver edge was palpable two centimeters (cm) inferior to the costal margin in the midclavicular line. He was slow to answer but oriented to person, place and time.
Laboratory findings were notable for significantly elevated white blood cell count of 22,300 / millimeters cubed (mm3), hemoglobin of 18.7 grams per deciliter (g/dL), platelets of 171,000 /mm.3 Liver function studies were remarkable for total bilirubin of 16.4 milligrams per deciliter (mg/dL), direct bilirubin of 10.6 mg/dL, aspartate aminotransferase of 2,682 international units per liter (IU/L), alanine aminotransferase of 7,521 IU/L, and alkaline phosphatase of 288 IU/L. Lipase was markedly elevated at 16,879 IU/L. Serum bicarbonate was 24 milliequivalents per liter (mEq/L), blood urea nitrogen was 26 mg/dL, and creatinine 1.53 mg/dL. Glucose was 61 mg/dL, and the remainder of electrolyte panel was normal. Coagulation studies revealed prothrombin time of 41.1 seconds and international normalized ratio (INR) of 4.3. Venous blood gas was notable for pH of 7.38 with lactate significantly elevated at 12.7 mEq/L. Toxicology workup was negative: ethanol less than 3 mg/dL and acetaminophen less than 2 micrograms per liter (μg/mL). Urine screen for drugs of abuse was positive for cannabinoids but negative for benzodiazepines, phencyclidine, opiates, and amphetamines.
Initial imaging included a right upper quadrant ultrasound (US) that revealed gallbladder distension with sludge, peri-cholecystic fluid and anterior wall thickening, but no gallstones. The common bile duct was measured at five millimeters (mm). Computerized tomography (CT) of the abdomen and pelvis obtained without contrast confirmed abnormal gallbladder findings from US and also demonstrated an edematous pancreas with peri-pancreatic fat stranding, without obstructing mass, as well as trace ascites. Initial management included a bolus of two L of IV crystalloids as well as broad-spectrum antibiotic coverage for possible biliary sepsis (1.5 grams [g] vancomycin and 3.375g piperacillin-tazobactam). A repeat bedside glucose of 53 mg/dL was treated with IV dextrose.
The patient was admitted to the medical intensive care unit with consults from the surgical and gastroenterology services. Primary admission diagnoses included acute hepatitis, acalculous cholecystitis and acute pancreatitis of unclear etiology. Lipid panel, including triglycerides, returned normal and the pattern of liver function abnormality did not point to an obstructive picture. Hepatitis serologies subsequently returned positive and suggestive of acute infection: hepatitis B core immunoglobulin M (IgM) reactive, hepatitis B surface antigen reactive, hepatitis B e-antigen and antibody reactive, and hepatitis B deoxyribonucleic acid level significantly elevated at 51,416 IU/mL, indicating highly active viral replication. Testing for cytomegalovirus, hepatitis C virus, hepatitis A virus, hepatitis D virus, hepatitis E virus, Epstein-Barr virus, and human immunodeficiency virus 1 and 2 were all negative.
The patient was questioned regarding risk factors for viral hepatitis; he stated he was sexually active with male and female partners and admitted to unprotected oral intercourse three weeks prior to his acute illness and barrier-protected anal intercourse six months prior to presentation. There was no history of tattoos or blood transfusions and no known prior history of hepatitis infection.
Antiviral treatment was initiated with IV entecavir; IV N-acetylcysteine therapy was given for hepatoprotective effects. Antimicrobial therapy was continued with piperacillin-tazobactam, although cultures of blood and urine showed no growth on hospital day 2, and remained negative. Consultation with transplant surgery placed the patient on emergent status for priority liver transplantation.
The patient developed acute mental status changes with drowsiness alternating with agitation; he could no longer speak in full sentences, and was not oriented to time or situation. Serum glucose was 153 mg/dL and CT of the brain did not reveal structural abnormalities. Progressive decline in level of consciousness with asterixis was associated with ammonia level of 228 micromoles per liter (μmol/L); hepatic encephalopathy was treated with lactulose and rifaximin, given orally. IV vitamin K1 and fresh frozen plasma were given for treatment of worsening coagulopathy, with INR increased to 9.0. He was intubated for airway protection after a vomiting episode with possible aspiration.
The patient’s mental status continued to worsen, and repeat unenhanced head CT demonstrated interval development of cerebral edema with early signs of brainstem herniation. After neurosurgery consultation, hyperosmolar therapy was initiated with IV mannitol and hypertonic saline infusions. Decline in renal function with a fall in serum sodium to 131 mmol/L and minimal urine output was treated with continuous veno-venous hemofiltration. The patient’s neurologic status continued to decline with loss of brainstem reflexes. Given the patient’s likelihood of severe irreversible neurological disability, the possibility for successful liver transplantation was deemed unlikely and the patient’s family elected to withdraw care. After compassionate extubation, the patient expired on hospital day 3, less than 60 hours after his initial ED presentation.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [26.0, 'mg/dL'], 'Glucose': [61.0, 'mg/dL'], 'Sodium': [131.0, 'mmol/L']}",274.6746,260.94087,288.40833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 131.0 mmol/L. 
The concentration of bun is 26.0 mg/dL. 
The concentration of glucose is 61.0 mg/dL. 
Plugging these values into the equation, we get 2 * 131.0 + (26.0 / 2.8) + (26.0 / 18) = 274.6746 mmol/L.The patient's calculated serum osmolality concentration is 274.6746 mmol/L. This is equalivalent to 274.6746 mOsm/kg."
5840,30,Serum Osmolality,lab test,decimal,pmc-8700017-1,Extracted,"A 20-day-old girl was admitted to the neonatal intensive care unit with a chief complaint of poor oral intake through the emergency room. She was lethargic and did not suck well with swallowing only 10 to 20 mL of formula at a time in the last two days. However, the amount of urine did not decrease, and diapers were changed 10 to 14 times per day. Vomiting and diarrhea were not observed. She was born at 38+2 weeks of gestation with 3380 g (50th–75th percentile) via cesarean section. No abnormal findings were noted during the prenatal and immediate postnatal periods. She was the first child of healthy, nonconsanguineous Korean parents, and her family history was unremarkable. At admission, her weight was 3100 g (25th–50th percentile), length was 53 cm (50th–75th percentile), and head circumference was 36 cm (50th–75th percentile). Although vital signs were appropriate for her age (heart rate 150 beats/min, blood pressure 78/50 mmHg, respiratory rate 48 breaths/min, and body temperature 36.5 °C), her lips were dry, and the capillary refill time was prolonged to 5–6 s. Physical examination revealed both thumbs in palms, frontal bossing, prominent upper lip, high arched palate, sparse frontal scalp hair, and bilateral 5th finger clinodactyly. An initial capillary blood gas analysis showed severe metabolic acidosis (pH 7.16, pCO2 28.3 mmHg, pO2 42 mmHg, HCO3−—17.3 mmol/L, base excess—17.3 mmol/L). With an impression of dehydration, 20 mL/kg normal saline was infused intravenously for over 1 h before other laboratory results were obtained.
The laboratory tests at admission were as follows: serum sodium 113.3 mEq/L, serum potassium 8.79 mEq/L, serum chloride 90.8 mEq/L, total CO2 8.1 mEq/L, serum lactic acid 1.0 mmol/L, serum ketone body 24 µmol/L, blood glucose level 83 mg/dL, blood urea nitrogen 55.1 mg/dL, and serum creatinine 0.65 mg/dL. Her urinalysis revealed a specific gravity of 1.014 and pH 5.0 and was negative for white blood cells and red blood cells. Her spot urine sodium and potassium levels were 74 and 27.7 mEq/L, respectively. The serum and urine osmolality values were 232 and 229 mOsm/kg, respectively. All the results of the neonatal screening test were normal, which included TSH (1.2 mIU/L), 17-hydroxyprogesterone (1.6 ng/mL), total galactose (1.0 mg/dL), and mass spectrometry for amino acid, organic acid, fatty acid, purine, peroxisome, and carbohydrate metabolic disorders. The plasma ammonia level was within the normal limit as 97 µg/dL. The plasma renin activity and serum aldosterone level were markedly elevated to 142.0 ng/mL/h (normal range, 0.32–1.84 ng/mL/h) and 4560 ng/dL (normal range, 4.2–20.9 ng/dL), respectively. Renal ultrasonography revealed no abnormalities except mild hydronephrosis in the right kidney (). No abnormal findings were found in cardiac echocardiography or brain magnetic resonance imaging.
To correct severe hyponatremia, 60 mL of 3% sodium chloride was initially intravenously administered over 8 h. Her urine output on the first day of admission was 8.45 mL/kg/h. Hyponatremia and hyperkalemia were improved with intravenous fluid and oral sodium chloride supplementation (8 mEq/kg/day). The patient consumed an adequate amount of milk (170–200 mL/kg/day), and weight gain was appropriate (40–80 g/day) after oral sodium chloride supplementation.
For the genetic diagnosis of the patient, targeted exome sequencing (TES) was performed. Genomic DNA was extracted from proband blood. All exon regions of all human genes (~22,000) were captured by a Twist Human Core Exome Kit (Twist Bioscience, South San Francisco, CA, USA). The captured regions of the genome were sequenced using a NovaSeq 6000 sequencing machine (Illumina, San Diego, CA, USA). In TES, no other pathogenic/likely pathogenic single-nucleotide variants (SNVs) or small insertion and deletion variants associated with the clinical phenotypes were identified. However, her clinical phenotypes and biochemical results indicated PHA1. Therefore, we performed a chromosomal microarray (CMA) to identify deletion-encompassing genes responsible for PHA1. CMA (CytoScan Dx, Affymetrix Cytogenetics, Santa Clara, CA, USA) revealed a 203 kb heterozygous deletion at 4q31.23: arr[GRCh37] 4q31.23(148865586_149069090)x1 (). This deletion spans exons 7–9 of NR3C2 and exons 15–23 of the ARHGAP10 gene. Haploinsufficiency of the NR3C2 gene, which encodes the mineralocorticoid receptor, is responsible for ADPHA1. However, the details of the functional role of the ARHGAP10 gene in human disease remain unclear. Parental testing showed that the deletion was paternally inherited. Her father had no history of clinical PHA1 manifestation and had normal plasma electrolytes and serum aldosterone values with only slightly elevated plasma renin activity at testing.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [55.1, 'mg/dL'], 'Glucose': [83.0, 'mg/dL'], 'Sodium': [113.3, 'mEq/L']}",250.88968,238.3452,263.43416,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 113.3 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 113.3 mEq. To convert from 113.3 mEq to mmol, convert from mEq to mmol. The compound 113.3 has a valence of 1, and so divide the valence by the value of mEq to get, 113.3 mEq/(1 mEq/mmol) = 113.3 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 113.3 mEq sodium/L converts to 113.3 mmol sodium/L. 
The concentration of bun is 55.1 mg/dL. 
The concentration of glucose is 83.0 mg/dL. 
Plugging these values into the equation, we get 2 * 113.3 + (55.1 / 2.8) + (55.1 / 18) = 250.88968 mmol/L.The patient's calculated serum osmolality concentration is 250.88968 mmol/L. This is equalivalent to 250.88968 mOsm/kg."
5841,30,Serum Osmolality,lab test,decimal,usmle-6290,Extracted,"A 45-year-old man is brought to the emergency department by police. He was found passed out in a store. The patient is dressed in soiled clothing that smells of urine and his pants are soaked in vomit. The patient has a past medical history of IV drug use, alcohol use, and multiple fractures secondary to scurvy. He is not currently taking any medications. His temperature is 99.5°F (37.5°C), blood pressure is 90/63 mmHg, pulse is 130/min, respirations are 15/min, and oxygen saturation is 95% on room air. The patient is started on IV fluids, thiamine, and dextrose. The patient becomes arousable at this point and begins vomiting into a basin. On physical exam, the patient appears poorly kempt and uncomfortable. His epigastric region is tender upon palpation. Cardiac exam reveals a normal rate and rhythm. Pulmonary exam is clear to auscultation bilaterally. A CT scan of the abdomen is ordered as seen in Figure A. Laboratory values are ordered as seen below:

Serum:
Na+: 139 mEq/L
Cl-: 102 mEq/L
K+: 4.0 mEq/L
HCO3-: 26 mEq/L
BUN: 20 mg/dL
Glucose: 73 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.2 mg/dL
Lipase: 295 U/L
AST: 57 U/L
ALT: 39 U/L

Hemoglobin: 9 g/dL
Hematocrit: 30%
Mean corpuscular volume: 120 µm^3
Leukocyte count: 8,500/mm^3 with normal differential
Platelet count: 199,000/mm^3

The patient continues to vomit and is observed in the emergency department. Several hours later his temperature is 99.5°F (37.5°C), blood pressure is 110/72 mmHg, pulse is 97/min, respirations are 15/min, and oxygen saturation is 95% on room air. Physical exam reveals a cardiac and pulmonary exam that are within normal limits. HEENT exam reveals suprasternal crepitus, an oropharynx that is blood-stained, and no signs of lymphadenopathy. Inspection of the patient’s lower extremities is within normal limits.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [73.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",289.19841,274.73849,303.65833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 73.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (20.0 / 2.8) + (20.0 / 18) = 289.19841 mmol/L.The patient's calculated serum osmolality concentration is 289.19841 mmol/L. This is equalivalent to 289.19841 mOsm/kg."
5842,30,Serum Osmolality,lab test,decimal,usmle-4459,Extracted,"A 4-year-old girl presents to the emergency department after persistent vomiting and complaints that her abdomen hurts. Her parents came home to their daughter like this while she was at home being watched by the babysitter. The child is otherwise healthy. Family history is notable for depression, suicide, neuropathic pain, diabetes, hypertension, cancer, and angina. The child is now minimally responsive and confused. Her temperature is 100°F (37.8°C), blood pressure is 100/60 mmHg, pulse is 140/min, respirations are 22/min, and oxygen saturation is 100% on room air. Physical exam is notable for a confused girl who is vomiting bloody emesis into a basin. Laboratory studies are ordered as seen below.

Serum:
Na+: 140 mEq/L
Cl-: 101 mEq/L
K+: 3.9 mEq/L
HCO3-: 11 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.0 mg/dL

Radiography is notable for a few radiopaque objects in the stomach. Urine and serum toxicology are pending.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [99.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",292.64286,278.01072,307.275,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (20.0 / 2.8) + (20.0 / 18) = 292.64286 mmol/L.The patient's calculated serum osmolality concentration is 292.64286 mmol/L. This is equalivalent to 292.64286 mOsm/kg."
5843,30,Serum Osmolality,lab test,decimal,usmle-4379,Extracted,"A 75-year-old man with coronary artery disease and mitral valve stenosis status-post coronary artery bypass graft and mitral bioprosthetic valve replacement is evaluated in the intensive care unit. His postsurgical course was complicated by ventilator-associated pneumonia and bilateral postoperative pleural effusions requiring chest tubes. He has been weaned from the ventilator and has had his chest tubes removed but has required frequent suctioning to minimize aspirations. He has been dependent on a percutaneous gastrostomy tube for enteral nutrition for the past four weeks. He is currently on aspirin, carvedilol, atorvastatin, ceftazidime, and pantoprazole. He has a history of prostate cancer status post radical prostatectomy. His temperature is 96°F (35.6°C), blood pressure is 95/55 mmHg, pulse is 50/min, and respirations are 20/min. On physical exam, he is not alert and oriented but responds with moans when stimulated. His laboratory data are listed below:

Serum:
Na+: 145 mEq/L
Cl-: 110 mEq/L
K+: 3.4 mEq/L
HCO3-: 26 mEq/L
BUN: 10 mg/dL
Glucose: 112 mg/dL
Creatinine: 1.4 mg/dL
Thyroid-stimulating hormone: 10 µU/mL
Ca2+: 11.1 mg/dL
PO4-: 1.0 mg/dL
AST: 6 U/L
ALT: 10 U/L
Albumin: 2.5 mg/dL
Lactate dehydrogenase: 200 U/L (140-280 U/L)
Haptoglobin: 150 mg/dL (30-200 mg/dL)
1,25-(OH)2 D3: 10 pg/mL (15-75 pg/mL)
Parathyroid hormone: 9 pg/mL (10-60 pg/mL)

Leukocyte count: 10,000 cells/mm^3 with normal differential
Hemoglobin: 9 g/dL
Hematocrit: 30 %
Platelet count: 165,000 /mm^3

His electrocardiogram and chest radiograph are shown in Figures A and B.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [10.0, 'mg/dL'], 'Glucose': [112.0, 'mg/dL'], 'Sodium': [145.0, 'mEq/L']}",299.79365,284.80397,314.78333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 145.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 145.0 mEq. To convert from 145.0 mEq to mmol, convert from mEq to mmol. The compound 145.0 has a valence of 1, and so divide the valence by the value of mEq to get, 145.0 mEq/(1 mEq/mmol) = 145.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 145.0 mEq sodium/L converts to 145.0 mmol sodium/L. 
The concentration of bun is 10.0 mg/dL. 
The concentration of glucose is 112.0 mg/dL. 
Plugging these values into the equation, we get 2 * 145.0 + (10.0 / 2.8) + (10.0 / 18) = 299.79365 mmol/L.The patient's calculated serum osmolality concentration is 299.79365 mmol/L. This is equalivalent to 299.79365 mOsm/kg."
5844,30,Serum Osmolality,lab test,decimal,pmc-4411570-1,Extracted,"A 73-year-old woman arrived to the emergency department after an attempt suicide by taking five zolpidem pills and bittern of unknown amounts. She complained of dizziness and general weakness. There was no other past history other than hypertension. Her GCS was 13/15(E3/V4/M6). The patient was oriented to time, place and person and normal muscle power and sensory in the extremities. Her initial blood pressure was 149/94 mmHg, pulse rate 82 beats/min, respiratory rate 28 breaths/min and body temperature 36.0 °C. Electrocardiograph showed QT prolongation of 0.482 s [].
Complete blood counts showed white blood cell (WBC) counts 1,249/mL, hemoglobin (Hb) 16.9 g/dL and platelet counts 265,000/mL. In addition, the arterial blood gas analysis (ABGA) showed pH 7.36, PCO2 35.0 mmHg, PO2 68.6 mmHg, HCO32− 19.2 mmol/L, O2 saturation 92.4%, glucose 145 mg/dL, blood urea nitrogen (BUN) 13.6 mg/dL, creatinine 0.77 mg/dL, aspartate aminotransferase (AST) 49 IU/L, alanine aminotransferase (ALT) 27 IU/L, albumin 5.5 g/dL, C-reactive protein (CRP) 0.09 mg/dL, [Na+] 149 mEq/L, [K+] 4.5 mEq/L, [Cl−] 120 mEq/L and [Mg2+] 7.8 mEq/L. Zolpidem was measured as 0.12 mg/L on urinalysis and 0.94 mg/L on serum biochemistry. Brain CT taken right after the visit revealed no evidences of acute brain hemorrhage and following MRI showed no evidences of acute infarction.
Altered mentality of patient might have been due to zolpidem (0.94 mg/L) ingestion. The patient also had electrolyte imbalance. Hypernatremia and hyperchloremia were corrected by infusion of half-saline and hypermagnesemia was corrected by injection of 10% calcium gluconate 20 mL. A repeat blood test 12 h later showed decreasing levels of [Na+], [K+], [Cl−], and [Mg2+] to 144, 4.3, 120, and 3.2 mEq/L, respectively. The mental status of patient returned to normal without any sequelae.
Following further improvement of the electrolyte measurements, the patient was transferred to the general ward for conservative treatment. All electrolyte measurements returned to normal 4 days after the incident ([Na+] 138 mEq/L, [K+] 3.8 mEq/L, [Cl−] 109 mEq/L, and [Mg2+] 2.4 mEq/L). Electrocardiograph returned to normal after correcting electrolyte imbalances. The patient was transferred to the psychiatric ward for further evaluation and management of suicide attempt. The patient was discharged home 1 week after the incident.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [13.6, 'mg/dL'], 'Glucose': [145.0, 'mg/dL'], 'Sodium': [149.0, 'mEq/L']}",310.9127,295.36706,326.45833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 149.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 149.0 mEq. To convert from 149.0 mEq to mmol, convert from mEq to mmol. The compound 149.0 has a valence of 1, and so divide the valence by the value of mEq to get, 149.0 mEq/(1 mEq/mmol) = 149.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 149.0 mEq sodium/L converts to 149.0 mmol sodium/L. 
The concentration of bun is 13.6 mg/dL. 
The concentration of glucose is 145.0 mg/dL. 
Plugging these values into the equation, we get 2 * 149.0 + (13.6 / 2.8) + (13.6 / 18) = 310.9127 mmol/L.The patient's calculated serum osmolality concentration is 310.9127 mmol/L. This is equalivalent to 310.9127 mOsm/kg."
5845,30,Serum Osmolality,lab test,decimal,usmle-4434,Extracted,"An 18-year-old G1P0 woman who is 10 weeks pregnant presents for her first prenatal visit. She reports nausea with occasional vomiting but denies bleeding, urinary symptoms, or abdominal pain. She just graduated high school and works at the local grocery store. She does not take any medications and has no known drug allergies. Physical examination is unremarkable. Initial laboratory studies reveal the following:

Serum:
Na+: 140 mEq/L
Cl-: 100 mEq/L
K+: 4.0 mEq/L
HCO3-: 24 mEq/L
BUN: 10 mg/dL
Glucose: 100 mg/dL
Creatinine: 1.0 mg/dL
Thyroid-stimulating hormone: 2.5 µU/mL
Ca2+: 9.5 mg/dL
AST: 25 U/L
ALT: 20 U/L

Leukocyte count: 10,000 cells/mm^3 with normal differential
Hemoglobin: 14 g/dL
Hematocrit: 42%
Platelet count: 200,000 /mm^3

Urine:
Epithelial cells: few
Glucose: negative
WBC: 20/hpf
Bacterial: > 100,000 cfu / E.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [10.0, 'mg/dL'], 'Glucose': [100.0, 'mg/dL']}",289.12698,274.67063,303.58333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 10.0 mg/dL. 
The concentration of glucose is 100.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (10.0 / 2.8) + (10.0 / 18) = 289.12698 mmol/L.The patient's calculated serum osmolality concentration is 289.12698 mmol/L. This is equalivalent to 289.12698 mOsm/kg."
5846,30,Serum Osmolality,lab test,decimal,pmc-7748582-1,Extracted,"The patient discussed in this case report is a 53-year-old male with a past medical history of hypertension, hyperlipidemia, and diabetes mellitus type 2, managed on metformin and canagliflozin. After undergoing a routine laparoscopic appendectomy, his postoperative course remained uneventful. He started tolerating oral feeds, having bowel movements and remained hemodynamically stable. Therefore, he was discharged two days after the surgery. However, a few hours later, on the day of discharge, he presented to the emergency department with sudden onset generalized abdominal pain, non-exertional shortness of breath, and fever.
On presentation, he was febrile (temperature: 100.7°F), tachycardia (heart rate: 114 bpm), tachypneic (respiratory rate: 30/min), and hypoxic with an oxygen saturation of 87% on room air. His physical examination was benign; lungs were clear to auscultation bilaterally and soft, non-tender abdomen. The surgical site looked clean, without any discharge, and was non-tender to touch.
The patient’s initial laboratory measurements were all within normal limits: blood glucose 126 mg/dL, sodium 134 mmol/L, potassium 4.5 mmol/L, chloride 105 mmol/L, bicarbonate 17 mEq/L, blood urea nitrogen (BUN) 11 mg/dL, and creatinine 0.9 mg/dL. The exception was a high anion gap of 20.8 mEq/L and a pH of 7.21. The patient was started on four liters nasal cannula, switched to non-rebreather as he remained hypoxic, and was subsequently admitted to the hospital for further management. A septic workup was initiated, and the patient was placed on empiric antibiotics.
Further laboratory results revealed positive serum ketones (beta-hydroxybutyrate 2.69 mmol/L), whereas the urinalysis revealed glucosuria (urine glucose > 1500 mg/dL) and ketonuria and no proteins. A urine culture was negative for any infectious growth. Serum lactate was 13 mg/dL. A computerized axial tomography (CAT) scan of the patient’s chest showed bilateral lower lobe consolidations suggestive of probable pneumonia. A CAT scan of his abdomen showed probable postoperative ileus with no obstruction or abscess. On further questioning, the patient reported having resumed canagliflozin and his regular diet as instructed upon being discharged.
Due to a high anion gap and positive ketones in the blood with normal blood glucose levels, the patient was diagnosed with euglycemic diabetic ketoacidosis secondary to his SGLT2-inhibitor use. Thus, canagliflozin was stopped, and the patient was started on an insulin drip with 10% dextrose. Subsequently, he was transferred to the intensive care unit (ICU) for closer monitoring. The patient’s condition started improving after the treatment with insulin and dextrose. On day two, following admission, his symptoms improved, and subsequent laboratory results also looked better with a lower anion gap of 16.2 mEq/L. On day three following admission, he was switched from an insulin drip to subcutaneous insulin and sliding scale as his laboratory results approached normal, with an anion gap of 13.2 mEq/L and beta-hydroxybutyrate of 0.81 mmol/L. With symptom resolution, the patient was then returned to the floor. However, his urine glucose remained high (>1500 mg/dL).
Discharged the next day and advised to continue subcutaneous insulin for a week, the patient was asked to consult his endocrinologist for further management. He was also recommended against resuming canagliflozin.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [11.0, 'mg/dL'], 'Glucose': [126.0, 'mg/dL'], 'Sodium': [134.0, 'mmol/L']}",278.92857,264.98214,292.875,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mmol/L. 
The concentration of bun is 11.0 mg/dL. 
The concentration of glucose is 126.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (11.0 / 2.8) + (11.0 / 18) = 278.92857 mmol/L.The patient's calculated serum osmolality concentration is 278.92857 mmol/L. This is equalivalent to 278.92857 mOsm/kg."
5847,30,Serum Osmolality,lab test,decimal,usmle-6080,Extracted,"A 67-year-old man presents to the emergency department with a fever and altered mental status. The patient has a history of Alzheimer dementia and is typically bed bound. His son found him confused with a warm and flushed complexion thus prompting his presentation. The patient has a past medical history of dementia, diabetes, and hypertension and typically has a visiting home nurse come to administer medications. Prior to examination, he is given haloperidol and diphenhydramine as he is combative and will not allow the nurses near him. His temperature is 102.9°F (39.4°C), blood pressure is 104/64 mmHg, pulse is 170/min, respirations are 22/min, and oxygen saturation is 100% on room air. Physical exam is notable for dry and flushed skin and a confused man. There is no skin breakdown, and flexion of the patient’s neck elicits no discomfort. Laboratory studies are drawn as seen below.

Hemoglobin: 15 g/dL
Hematocrit: 45%
Leukocyte count: 4,500/mm^3 with normal differential
Platelet count: 227,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 24 mEq/L
BUN: 30 mg/dL
Glucose: 97 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 10.2 mg/dL
AST: 12 U/L
ALT: 10 U/L

Urine:
Color: Yellow
Bacteria: Absent
Nitrites: Negative
Red blood cells: Negative

An initial chest radiograph is unremarkable. The patient is given 3 liters of Ringer's lactate and an electric fan to cool off. Two hours later, his temperature is 99°F (37.2°C), blood pressure is 154/94 mmHg, pulse is 100/min, respirations are 17/min, and oxygen saturation is 100% on room air. The patient’s mental status is at the patient’s baseline according to the son.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [30.0, 'mg/dL'], 'Glucose': [97.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",294.10317,279.39801,308.80833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 30.0 mg/dL. 
The concentration of glucose is 97.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (30.0 / 2.8) + (30.0 / 18) = 294.10317 mmol/L.The patient's calculated serum osmolality concentration is 294.10317 mmol/L. This is equalivalent to 294.10317 mOsm/kg."
5848,30,Serum Osmolality,lab test,decimal,pmc-2615294-1,Extracted,"A 50-year-old female presented with chronic fatigue. The patient was diagnosed with osteoporosis five years prior and was taking alendronate. Hypercalcemia was diagnosed two years following the osteoporosis diagnosis, and the patient visited the hospital for a comprehensive check-up. The patient did not have any history of diabetes, hypertension, tuberculosis, or hepatitis. She was the first daughter of two sons and two daughters. Concurrently, her 81-year-old mother, who was bedridden for unknown reasons, was also undergoing tests for hypercalcemia, and was subsequently diagnosed with multiple parathyroid adenomas and pancreatic tumors, based on the test results. Her father had a history of sudden death by an acute cardiac event.
In the neck examination, the thyroid was not enlarged, and palpable tumors were absent. Heart and lung sounds were normal, and no abnormalities were detected in the abdomen, all extremities, or neurological tests. The axillary hair and the pubic hair were normal, hirsutism was absent, and galactorrhea was not observed.
In blood electrolyte tests, sodium was 144 mmol/L, potassium was 4.0 mmol/L, chloride was 107 mmol/L, blood calcium was 12.6 mg/mL, ionized calcium was 5.4 mg/dL, and inorganic phosphate was 3.3 mg/dL. In general biochemical tests, fasting blood glucose was 93 mg/dL, blood urea nitrogen was 8.9 mg/dL, creatinine was 0.8 mg/dL, and the hepatic function test was normal. Her 24-hour urinary calcium excretion was 326 mg/day, the amount of phosphate excretion was 460 mg/day, and the creatinine clearance rate was 64 mL/min. Thyroid hormone tests were within normal range, and intact-PTH was increased to 99.8 pg/mL. Prolactin was also mildly increased to 27.63 ng/mL. Plasma insulin was 9.2 uIU/mL (4.2 - 48), gastrin was 21 pg/mL (0 - 90), glucagon was 40 pg/mL (40 - 130), pancreatic polypeptide was 79 pmol/L (< 100), and vasoactive intestinal polypeptide was 32 pg/mL (< 100). In dual X-ray absorptiometry (DXA), the T score of the femur was decreased to - 2.0, confirming the osteopenia finding.
In the neck ultrasound, in the posterior area of the left thyroid, a tumor suspected to be a parathyroid adenoma 10 mm in size was detected, and in the parathyroid scan, uptake was detected in two glands (). In the neck computed tomography (CT), parathyroid tumors, 10 mm in the left side and 8 mm in the right side, were detected. In the chest CT, abnormal findings in the lung and the mediastinum were not detected. On the brain magnetic resonance imaging (MRI), a tumor 7 mm in size in the pituitary was detected (). On the abdominal MRI, a 2.3 cm left adrenal tumor and a pancreatic tumor were observed, and a 7 cm uterine myoma and a bladder wall myoma were detected (). Esophagogastroduodenoscopy (EGD) and endoscopic ultrasonography (EUS) revealed an esophageal leiomyoma 20 mm in size in the area 20 cm away from the incisor, and in the pancreatic head, a tumor 6 mm in size was detected (). In general positron emission tomography (PET), increased fluorodeoxyglucose (FDG) uptake in the pituitary was seen. Nonetheless, the increase of the uptake by other lesions was not detected, and thus indicated the benign nature of the multiple tumors.
From the peripheral blood of the patient and her mother, genomic DNA was extracted, and sequencing of the MEN1 gene was performed. Sequencing analysis revealed a transition of GAG to GTG at codon 350 of exon 7, causing an amino acid change from aspartic acid to valine, D350V ().
Because of the detection of double parathyroid adenoma, pituitary adenoma, pancreatic tumor, and adrenal cortical tumor, as well as accompanying multiple leiomyomas in the bladder, the uterus, and the esophagus, MEN1 was diagnosed. For parathyroid adenoma, a subtotal parathyroidectomy was performed, leaving half of the left inferior parathyroid gland, and a prophylactic thymectomy was performed as well. In postsurgical histological tests, the diagnosis of parathyroid adenoma was confirmed (). After surgery, the intact-PTH level was decreased to 5.79 pg/mL. The remaining tumors are under follow up observation.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [144.0, 'mmol/L'], 'Glucose': [93.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [8.9, 'mg/dL']}",296.34524,281.52798,311.1625,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 144.0 mmol/L. 
The concentration of bun is 8.9 mg/dL. 
The concentration of glucose is 93.0 mg/dL. 
Plugging these values into the equation, we get 2 * 144.0 + (8.9 / 2.8) + (8.9 / 18) = 296.34524 mmol/L.The patient's calculated serum osmolality concentration is 296.34524 mmol/L. This is equalivalent to 296.34524 mOsm/kg."
5849,30,Serum Osmolality,lab test,decimal,usmle-5892,Extracted,"A 67-year-old man is brought to the emergency department when he was found obtunded at the homeless shelter. The patient is currently not responsive and smells of alcohol. The patient has a past medical history of alcohol use, IV drug use, and hepatitis C. His temperature is 99°F (37.2°C), blood pressure is 95/65 mmHg, pulse is 95/min, respirations are 13/min, and oxygen saturation is 95% on room air. The patient is started on IV fluids, and his pulse decreases to 70/min. On physical exam, the patient has an abdominal exam notable for distension and a positive fluid wave. The patient displays mild yellow discoloration of his skin. The patient has notable poor dentition and poor hygiene overall. A systolic murmur is heard along the left sternal border on cardiac exam. Pulmonary exam is notable for mild bibasilar crackles. Laboratory values are ordered, and return as below:

Hemoglobin: 10 g/dL
Hematocrit: 32%
Leukocyte count: 7,500 cells/mm^3 with normal differential
Platelet count: 227,000/mm^3

Serum:
Na+: 125 mEq/L
Cl-: 100 mEq/L
K+: 5.0 mEq/L
HCO3-: 24 mEq/L
BUN: 51 mg/dL
Glucose: 89 mg/dL
Creatinine: 2.2 mg/dL
Ca2+: 10.0 mg/dL
AST: 22 U/L
ALT: 19 U/L

Urine:
Color: Amber
Nitrites: Negative
Sodium: 12 mmol/24 hours
Red blood cells: 0/hpf

Over the next 24 hours, the patient produces very little urine.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [51.0, 'mg/dL'], 'Glucose': [89.0, 'mg/dL'], 'Sodium': [125.0, 'mEq/L']}",273.15873,259.50079,286.81667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 125.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 125.0 mEq. To convert from 125.0 mEq to mmol, convert from mEq to mmol. The compound 125.0 has a valence of 1, and so divide the valence by the value of mEq to get, 125.0 mEq/(1 mEq/mmol) = 125.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 125.0 mEq sodium/L converts to 125.0 mmol sodium/L. 
The concentration of bun is 51.0 mg/dL. 
The concentration of glucose is 89.0 mg/dL. 
Plugging these values into the equation, we get 2 * 125.0 + (51.0 / 2.8) + (51.0 / 18) = 273.15873 mmol/L.The patient's calculated serum osmolality concentration is 273.15873 mmol/L. This is equalivalent to 273.15873 mOsm/kg."
5850,30,Serum Osmolality,lab test,decimal,pmc-5011300-1,Extracted,"A 62-year-old woman with type 2 diabetes mellitus, hypertension, gastroesophageal reflux disease, and depression presented with 4 days of nausea, vomiting, and generalized weakness. Her symptoms became progressively worse such that by the day of admission she had decreased appetite, polydipsia, polyuria, and could not walk. The patient denied fever, chills, abdominal pain, diarrhea, or sick contacts. Home medications were atorvastatin, metformin, sucralfate, pioglitazone, canagliflozin, exenatide, omeprazole, fluoxetine, ranitidine, lisinopril, and alprazolam.
On physical examination, the patient’s vital signs included a temperature of 38.3°C, blood pressure 134/61, heart rate 107, respiratory rate 24, and oxygen saturation of 100% on 2 liters nasal cannula oxygen. The patient appeared ill and distressed. She had dry mucous membranes, clear lung sounds bilaterally, and her heart was regular without murmurs, gallops, or rubs. Her abdomen was soft and nontender with present bowel sounds. Extremities showed no edema, and she had no focal neurological findings. Laboratory revealed a metabolic acidosis with a pH of 7.08 and anion gap >17. Chemistry panel indicated sodium 134 mEq/L, potassium 5.2 mEq/L, chloride 112 mEq/L, CO2 <5 mEq/L, blood urea nitrogen 22 mg/dL, and creatinine 1.3 mg/dL. Blood glucose was 213 mg/dL, and urinalysis revealed glucose 2+ and ketones 3+. Serum ketones were present at 1:8 dilution, with a lactic acid of 0.8 mmol/L. The patient’s hemoglobin A1C (HbA1c) was 11.1.
The patient was admitted to the intensive care unit for severe metabolic acidosis secondary to DKA. Aggressive fluid resuscitation was undertaken and an insulin drip initiated. Within 6 hours, the anion gap metabolic acidosis improved. On further review of her medication history, it was discovered that canagliflozin had been started several months prior. Further study of that medication and its uncommon side effects led to the etiology of the DKA. The patient required 5 days of hospitalization for complete resolution of her symptoms. She was sent home with a regimen of long- and short-acting insulins, as well as instructions to avoid canagliflozin. Her endocrinologist was advised of this adverse reaction.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [22.0, 'mg/dL'], 'Glucose': [213.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",287.69048,273.30596,302.075,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. 
The concentration of bun is 22.0 mg/dL. 
The concentration of glucose is 213.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (22.0 / 2.8) + (22.0 / 18) = 287.69048 mmol/L.The patient's calculated serum osmolality concentration is 287.69048 mmol/L. This is equalivalent to 287.69048 mOsm/kg."
5851,30,Serum Osmolality,lab test,decimal,pmc-5984920-1,Extracted,"A 45-year-old Caucasian woman presented with abdominal pain, nausea, and vomiting for 17 h. At 22 h prior to admission, she went out to dinner and drank one glass of wine. A few hours after the meal, she developed epigastric and left upper quadrant abdominal pain that was moderate, persistent, cramping, and aching; the pain radiated to her left middle back and arm without exacerbating or alleviating factors. The pain was associated with nausea, vomiting, and she could not tolerate any oral intake. She felt thirsty and had polyuria and positional lightheadedness. She reported no fever, chills, chest pain, cough, sputum production, dysuria, hematuria, diarrhea, hematochezia, and melena.
On further questioning, the patient shared that she had a history of gestational glucose intolerance 6 years ago, and has had occasional impaired fasting glucose of 81–107 mg/dL for the past 6 years. She began following an American Diabetes Association (ADA) diet 2 years ago and lost 25 lb. Additionally, she had a past medical history of supraventricular tachycardia, irritable bowel syndrome, social alcohol use, cholecystectomy, and thyroid papillary adenocarcinoma status post partial thyroidectomy complicated by postsurgical hypothyroidism. Home medications included metoprolol tartrate, levothyroxine, and meloxicam. The patient reported no family history of diabetes.
Temperature 97.7 °F, pulse 130 bpm, respiratory rate 28 bpm, BP 134/71 mmHg, weight 87 kg, height 1.68 m, BMI 31 kg/m2, SpO2 99% on room air.
The patient was in moderate distress. There was no acanthosis nigricans. Cardiovascular system revealed tachycardia. A pulmonary exam revealed tachypnea, accessory muscle usage with moderate respiratory distress. Abdominal exam revealed central obesity, normoactive bowel sounds, left upper quadrant and epigastric tenderness to palpation, no rigidity or guarding. No costovertebral angle tenderness.
CBC: WBC 25.9 × 109/L, hemoglobin 14.7 g/dL, hematocrit 45.8%, platelet 386 × 109/L, MCV 100.2 µm3. BMP: sodium 135 mmol/L, potassium 7.4 mmol/L, chloride 89 mmol/L, bicarbonate 5 mmol/L, BUN 37 mg/dL, creatinine 1.27 mg/dL, glucose 931 mg/dL, eGFR 46 mL/min.
Liver chemistry: Total bilirubin 0.2 mg/dL, AST 23 U/L, ALT 54 U/L, ALP 138 U/L, total protein 7.5 g/dL, albumin 4.5 g/dL. Calcium 8.7 mg/dL, phosphate 1.4 mg/dL, magnesium 2.1 mg/dL. VBG: pH 6.92. Repeated ABG 2 h later: pH 7.21, pCO2 16 mmHg, pO2 129 mmHg, HCO3− 6.4 mmol/L, SaO2 98% on 2 L/min oxygen by nasal cannula. Beta-hydroxybutyrate 28 mmol/L, lactic acid 4.0 mmol/L. Urinalysis showed urine ketones 80 mg/dL, leukocyte esterase negative, urine culture no growth. HbA1c 6.4%. Lipid profile: triglycerides 89 mg/dL, total cholesterol 144 mg/dL, LDL 91 mg/dL, HDL 35 mg/dL. TSH 3.12 mIU/mL, free T4 1.26 ng/dL. Troponin I < 0.01 ng/mL.
Ultrasonography of the abdomen revealed mild hepatic steatosis, incidental mild to moderate right-sided hydronephrosis, status post cholecystectomy. ECG on admission: sinus rhythm, HR 126 bpm, peaked T waves at lead V2–V6 consistent with hyperkalemia, no ischemic changes.
All procedures performed in this study were in compliance with the ethical standards of the institutional and/or national research committee and with the 1964 Declaration of Helsinki and its later amendments or comparable ethical standards. Informed consent was obtained from the individual participant for being included in the study.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [37.0, 'mg/dL'], 'Glucose': [931.0, 'mg/dL'], 'Sodium': [135.0, 'mmol/L']}",334.93651,318.18968,351.68334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.0 mmol/L. 
The concentration of bun is 37.0 mg/dL. 
The concentration of glucose is 931.0 mg/dL. 
Plugging these values into the equation, we get 2 * 135.0 + (37.0 / 2.8) + (37.0 / 18) = 334.93651 mmol/L.The patient's calculated serum osmolality concentration is 334.93651 mmol/L. This is equalivalent to 334.93651 mOsm/kg."
5852,30,Serum Osmolality,lab test,decimal,pmc-8531789-1,Extracted,"We report a 23-year-old African American male with a medical history of pediatric DDRT secondary to left-sided dysplastic kidney and right-sided obstructive uropathy. He presented to the emergency department with a one-week history of decreasing urine output, increased shortness of breath, generalized weakness, and nausea. He initially received his DDKT in 2010, which has been complicated by multiple episodes of both acute T cell-mediated and acute antibody-mediated rejection. The patient admitted to a two-month history of immunosuppressive medication nonadherence with tacrolimus, mycophenolate, and prednisone.
Physical examination revealed a young male, in no distress, weighing 142 pounds. He had a blood pressure of 153/102 mmHg and a heart rate of 77 beats/min. Exam findings are as follows: pale conjunctiva, lungs clear to auscultation, regular heart rate and rhythm, active bowel sounds, no abdominal tenderness, and no focal neurological deficit. Admission labs included a serum creatinine of 64.6 mg/dL (0.67–1.17 mg/dL) with a blood urea nitrogen (BUN) of 212 mg/dL (6–20 mg/dL), which increased to a serum creatinine of 73.8 mg/dL and BUN of 244 mg/dL prior to initiation of emergent dialysis. Serum chemistry included sodium 137 mmol/L (136–145 mmol/L), potassium 6.0 mmol/L (3.5–5.1 mmol/L), chloride 98 mmol/L (98–107 mmol/L), total carbon dioxide 7 mmol/L (22–29 mmol/L), glucose 68 mg/dL (74–106 mg/dL), and phosphorus 14.7 mg/dL (2.7–4.5 mg/dL).
The patient was initiated on emergent dialysis via a temporary dialysis catheter. Dialysis was complicated by new onset of seizures, initially thought to be secondary to dialysis disequilibrium syndrome. An electroencephalogram (EEG) was performed showing right temporal spikes epileptiform discharges with intermittent slow waves lateralized to the right hemisphere. Patient was thought to have epilepsy with initial seizure exacerbation secondary to severe metabolic derangements in setting of acute renal failure and severe azotemia. He was initiated on daily levetiracetam with resolution of seizures.
Patient received continuous renal replacement therapy (CRRT) while in the intensive care unit. After stabilization of his acute medical issues, a tunneled dialysis catheter was placed in his right internal jugular vein prior to discharge. Ultimately, the patient was diagnosed with renal allograft failure secondary to medication nonadherence and was discharged home on intermittent hemodialysis with improvement in serum creatinine to 23.8 mg/dL and BUN of 76 mg/dL at time of discharge, after completion of four hemodialysis sessions.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [76.0, 'mg/dL'], 'Glucose': [68.0, 'mg/dL'], 'Sodium': [137.0, 'mmol/L']}",304.92063,289.6746,320.16666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mmol/L. 
The concentration of bun is 76.0 mg/dL. 
The concentration of glucose is 68.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (76.0 / 2.8) + (76.0 / 18) = 304.92063 mmol/L.The patient's calculated serum osmolality concentration is 304.92063 mmol/L. This is equalivalent to 304.92063 mOsm/kg."
5853,30,Serum Osmolality,lab test,decimal,usmle-6106,Extracted,"A 30-year-old man with history of intravenous drug use and methamphetamine-associated chronic thromboembolic pulmonary hypertension (CTEPH) is brought to the emergency department by his girlfriend for worsening abdominal pain and fevers. The patient said the pain was initially around his umbilicus, but he is now experiencing intense tenderness near his groin. He was initially prescribed rivaroxaban, but due to insurance issues, he was switched to warfarin for management of CTEPH two weeks ago. His temperature is 102°F (38.9°C), blood pressure is 95/60 mmHg, pulse is 95/min, respirations are 22/min. He states that his blood pressure usually runs low. His physical exam is notable for an unremarkable cardiac exam, bibasilar crackles, and RLQ tenderness with rebound tenderness when the LLQ is palpated. Laboratory results are shown below:

Hemoglobin: 11 g/dL
Hematocrit: 35 %
Leukocyte count: 16,000/mm^3 with normal differential
Platelet count: 190,000/mm^3

Serum:
Na+: 137 mEq/L
Cl-: 100 mEq/L
K+: 3.7 mEq/L
HCO3-: 23 mEq/L
BUN: 40 mg/dL
Glucose: 110 mg/dL
Creatinine: 0.8 mg/dL
Ca2+: 9.1 mg/dL
AST: 34 U/L
ALT: 45 U/L

International normalized ratio (INR): 6.2
Prothrombin time (PT): 40 seconds
Partial thromboplastin time: 70 seconds

Blood type: O
Rhesus: Positive
Antibody screen: Negative

A clinical diagnosis is made and supported by the surgical consult team in lieu of imaging. The next operating room for an add-on procedure will not be available for another 5 hours. Appropriate medical therapy is initiated.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [40.0, 'mg/dL'], 'Glucose': [110.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",294.39683,279.67699,309.11667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 40.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (40.0 / 2.8) + (40.0 / 18) = 294.39683 mmol/L.The patient's calculated serum osmolality concentration is 294.39683 mmol/L. This is equalivalent to 294.39683 mOsm/kg."
5854,30,Serum Osmolality,lab test,decimal,pmc-6031976-1,Extracted,"An 18-year-old male (height 155 cm and weight 51 kg) was accidentally hit by an unfastened crane hook and suffered serious injuries to the right side of his neck and jaw. He presented to the hospital emergency room with severe neck pain, bleeding from the mouth, and a deep lacerated injury on the right side of his jaw and upper part of the neck, with surgical emphysema (). His Glasgow Coma Scale (GCS) score was E4V5M5, and his pupils were bilaterally equal and 2 mm in size. His initial recorded vital signs were: blood pressure of 96/60 mmHg, heart rate of 100 beats/min, respiratory rate of 18/min, and SpO2 of 93% in room air. A computerized tomography (CT) scan of his facial bones and upper cervical spine revealed a comminuted displaced fracture, which involved the angle and body of the right hemimandible, with adjacent soft tissue laceration, hematoma, and air pockets (). There was a displaced comminuted fracture of the right transverse process of the atlas that extended into the right lateral mass, and a fracture of the right occipital condyle that extended to the foramen transversarium margin (). The atlas was rotated, with displacement of the atlanto-occipital and atlanto axial joints. A magnetic resonance image (MRI) scan of neck showed the absence of right vertebral artery flow void and a thrombus in the right vertebral artery (). Bilateral vertebral artery Doppler was performed, which showed right vertebral artery flow stasis, indicating a thrombus. The nasal bones, nasal cavity, nasopharynx, and laryngeal cartilages were normal. There was no intracranial injury and no involvement of the spinal cord; hence, no sensory motor deficits or bladder or bowel involvement were identified. A thin pre-vertebral hematoma was seen extending from level C1 to C4, and the rest of the cervical vertebrae were normal. Since the inner cortex of the mandible was comminuted and shattered, the right inferior alveolar artery was cut completely, with bleeding into the oral cavity. Mouth opening was restricted, and the inter incisor distance was 1 cm.
After the neck wound was covered with dressing, a cervical collar was applied. The patient was admitted to the high dependency unit (HDU); and after proper explanation of the anesthetic and surgical plan to the patient and his guardian, he underwent an open reduction and internal fixation of the mandible and exploration of the neck injury the next day. His basal oxygen saturation was at 95%, and an arterial blood gas analysis in room air revealed a pH of 7.36, PaCO2 of 40 mmHg, PaO2 of 110 mmHg, bicarbonate level of 22 mmol/L, and arterial oxygen saturation of 98%. His blood investigations revealed hemoglobin levels of 11.9 gm%, platelets of 2.04 lakhs/mm3, serum urea of 22.0 mg/dL, serum creatinine of 0.6 mg/dL, serum glucose of 93 mg/dL, sodium of 140 meq/dL, and potassium of 3.9 meq/dL. A large bore intravenous cannula was inserted into the dorsum of the left hand, and ringer lactate was started. He was connected to a multipara monitor that displayed his electrocardiogram (ECG), noninvasive arterial pressure, pulse oximetry, endtidal carbon dioxide (ETCO2) and core temperature. The ECG showed a sinus rhythm, with a heart rate of 92/min and a normal axis, blood pressure of 110/65 mmHg and respiratory rate of 14/min. Glycopyrrolate (0.2 mg) was given intravenously. An awake fiber-optic nasotracheal intubation was planned, with a backup emergency surgical airway kit in case the first method failed. The nasal cavity was anesthetized by packing with cotton tape gauze soaked in 2% lidocaine and 0.05% oxymetazoline hydrochloride, and the oropharynx was nebulized with 2% lidocaine spray. The larynx and trachea were anaesthetized by nebulization with lignocaine, and supplemental oxygen was administered via a nasal catheter. A 5.5 mm fiber-optic bronchoscope was taken, and a 7.0 mm size cuffed reinforced endotracheal tube was slid up the full length of the shaft and gently secured to the beveled end of the bronchoscope.
The oral cavity was full of clots as the right inferior alveolar artery was cut. The oral cavity was intermittently cleared, to enable clear visualization. The fiber-optic bronchoscope was introduced into the left nasal cavity and gently advanced through the glottis into the trachea to just above the carina. Then, the endotracheal tube was gently railroaded and advanced into the trachea. Successful placement of the tube in the trachea was verified by capnography and bilateral equal air entry. The cuff was inflated to seal the airway, and the tube was securely fixed. Fentanyl (50 µg, 1 µg/kg), propofol (80 mg), and atracurium (25 mg) were given intravenously. A throat pack was inserted gently through the available inter incisor space. Anesthesia was maintained using a mixture of 50% oxygen, 50% nitrous oxide, and 1–1.5% isoflurane, with intermittent doses of atracurium. Intermittent positive pressure ventilation was instituted, and ETCO2 was maintained at 35 mm Hg. The perioperative period was uneventful, without significant changes in blood pressure or heart rate (systolic pressure 110–130 mmHg, diastolic pressure 70–86 mmHg, heart rate 85–108 beats/min). The mean arterial pressure (MAP) was maintained between 90 to 100 mmHg to maintain perfusion and reduce the risk of posterior circulation ischemia. A total of 1000 mL of crystalloids was given perioperatively. At the end of the procedure, which lasted 90 minutes, neuromuscular blockade was reversed with neostigmine (2.5 mg) and glycopyrrolate (0.4 mg), which were given intravenously. The throat pack was removed and the trachea was extubated when the patient was awake with protective airway reflexes, and the neuromuscular transmission recovered to a train of four (TOF) ratio of 0.9. Paracetamol (1,000 mg) was given intravenously for postoperative analgesia, and ondansetron (4 mg) was given intravenously for antiemetic prophylaxis. The patient was transferred to the HDU for observation, and he made an uneventful recovery and was started on IV antibiotics and enoxaparin for anticoagulation, 48 hours following surgery for one week, to establish vertebral artery flow. This was later replaced with oral aspirin. The neurosurgical intervention included cervical immobilization using a cervical collar brace for 12 weeks, to achieve spinal stabilization and prevent further nerve damage, including injury to the brain stem.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [22.0, 'mg/dL'], 'Glucose': [93.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/dL']}",2813.02381,2672.37262,2953.675,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/dL. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The current volume unit is dL and the target volume unit is L. The conversion factor is 0.1 L for every unit of dL. Our next step will be to divide the mass by the volume conversion factor of 0.1 to get the final concentration in terms of mmol/L. This will result to 140.0 mmol sodium/0.1 L = 1400.0 mmol sodium/L. The concentration value of 140.0 mEq sodium/dL converts to 1400.0 mmol sodium/L. 
The concentration of bun is 22.0 mg/dL. 
The concentration of glucose is 93.0 mg/dL. 
Plugging these values into the equation, we get 2 * 1400.0 + (22.0 / 2.8) + (22.0 / 18) = 2813.02381 mmol/L.The patient's calculated serum osmolality concentration is 2813.02381 mmol/L. This is equalivalent to 2813.02381 mOsm/kg."
5855,30,Serum Osmolality,lab test,decimal,usmle-1580,Extracted,"A 36-year-old woman comes to the physician because of a 4-day history of fever, malaise, chills, and a cough productive of moderate amounts of yellow-colored sputum. Over the past 2 days, she has also had right-sided chest pain that is exacerbated by deep inspiration. Four months ago, she was diagnosed with a urinary tract infection and was treated with trimethoprim/sulfamethoxazole. She appears pale. Her temperature is 38.8°C (101.8°F), pulse is 92/min, respirations are 20/min, and blood pressure is 128/74 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 99%. Examination shows pale conjunctivae. Crackles are heard at the right lung base. Cardiac examination shows no abnormalities. Laboratory studies show:
Hemoglobin 12.6 g/dL
Leukocyte count 13,300/mm3
Platelet count 230,000/mm3
Serum
Na+ 137 mEq/L
Cl- 104 mEq/L
K+ 3.9 mEq/L
Urea nitrogen 16 mg/dL
Glucose 89 mg/dL
Creatinine 0.8 mg/dL
An x-ray of the chest shows an infiltrate at the right lung base.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [16.0, 'mg/dL'], 'Glucose': [89.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",284.65873,270.42579,298.89167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 16.0 mg/dL. 
The concentration of glucose is 89.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (16.0 / 2.8) + (16.0 / 18) = 284.65873 mmol/L.The patient's calculated serum osmolality concentration is 284.65873 mmol/L. This is equalivalent to 284.65873 mOsm/kg."
5856,30,Serum Osmolality,lab test,decimal,pmc-4270706-1,Extracted,"The health of a 7-year-old male child with type I diabetes was maintained on a daily regimen of insulin. One day, however, the child developed sudden onset of cold-like symptoms such as runny and stuffy nose with a mild fever. He was diagnosed with acute sinusitis by a local general practitioner and prescribed three different medications namely paracetamol, chlorpheniramine, and a combination of amoxicillin and clavulanate at their regular doses in syrup form. On the third day of his treatment, the child was brought to a local hospital's emergency department with symptoms of nausea, vomiting, weak and rapid pulse, deep sighing breaths, drowsiness, and unsteady gait. On examination, his blood sugar was extremely high and showed an arterial blood gas pH of 7.12 with base excess of −7 mmol/L, and a bicarbonate of 12.6 mEq/L. The WBC count was 15.2 × 103/μL, hemoglobin of 12.6 mg/dL, and hematocrit of 40.1%. His chemistry panel demonstrated a serum sodium of 134 mEq/L, potassium 4.5 mEq/L, chloride 91 mEq/L, BUN 11.6 mg/dL, creatinine 1.2 mg/dL, and a blood sugar of 440 mg/dL. The serum ketones were positive on urine dipstick. He was admitted as a medical emergency and treated for diabetic ketoacidosis with fluid replacement and insulin therapy to prevent further complications and achieve a normal health state.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [11.6, 'mg/dL'], 'Glucose': [440.0, 'mg/dL'], 'Sodium': [134.0, 'mEq/L']}",296.5873,281.75794,311.41667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. 
The concentration of bun is 11.6 mg/dL. 
The concentration of glucose is 440.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (11.6 / 2.8) + (11.6 / 18) = 296.5873 mmol/L.The patient's calculated serum osmolality concentration is 296.5873 mmol/L. This is equalivalent to 296.5873 mOsm/kg."
5857,30,Serum Osmolality,lab test,decimal,pmc-6016161-1,Extracted,"A 55-year-old woman with a history of type 2 diabetes mellitus, hyperlipidemia, obesity, and depression was referred to an endocrinologist with complaints of weight loss, palpitations, and diarrhea. The patient also had hypertension and was taking α-adrenergic receptor antagonists and a calcium channel blocker. She was found to have a thyroid-stimulating hormone (TSH) level of <0.10 (normal: 0.34 to 4.82) µlU/ml and a free T4 concentration of 4.28 (normal: 0.6 to 1.6) ng/dL. I123 thyroid scan revealed elevated, diffuse uptake bilaterally, without nodules, consistent with the diagnosis of Graves' disease. The patient was treated with 11.9 mCi of radioactive iodine. Ten days after the ablation treatment, the patient presented to a local hospital by ambulance after experiencing lightheadedness, diffuse abdominal pain, and one episode of bilious emesis.
Upon arrival, she was hypotensive (77/44 mm Hg), pale, bradycardic, and febrile (39.4°C). An electrocardiogram (ECG) revealed accelerated junctional rhythm at a rate of 53 beats/min. The patient was given atropine 0.5 mg intravenously without effect, followed by initiation of external cardiac pacing. Continuous intravenous infusions of dopamine and norepinephrine were started along with fluid resuscitation of 4 L of normal saline over a 2-hour period. She received one ampule of calcium gluconate with no change in her blood pressure, heart rate, or rhythm. Computed tomography of the abdomen was unrevealing. The patient was endotracheally intubated and transferred via helicopter to our facility.
Upon arrival to our facility, she was receiving intravenous infusions of dopamine at 20 µg/kg/min and norepinephrine at 10 µg/kg/min and remained hypotensive (92/55 mm Hg) and bradycardic (59 beats/min). ECG showed an accelerated junctional rhythm. Laboratory findings included serum sodium of 139 mEq/L, potassium of 5.3 mEq/L, chloride of 108 mEq/L, and total CO2 content of 15 mmol/L, serum glucose of 208 mg/dL, urea nitrogen of 38 mg/dL, creatinine of 1.5 mg/dL, ionized calcium of 1.15 mmol/L, total bilirubin of 0.4 mg/dL, serum alkaline phosphatase of 141 U/L, aspartate aminotransferase of 2196 U/L, and alanine aminotransferase of 2010 U/L. Plasma troponin I was repeatedly undetectable. The peripheral leukocyte count was 15.9 x 109 cells/L with no immature forms. There was evidence of an anion gap metabolic acidosis with a serum lactate concentration of 6.2 mmol/L. Blood cultures revealed no microbial growth. Thyroid function testing showed an undetectable TSH (<0.10 µlU/ml), a free T4 of 12.8 (normal: 0.6 to 1.6) ng/dL, total T4 of 21.9 (normal: 5.6 to 13.7) µg/dL, and a total T3 of 0.94 (normal: 0.8 to 1.8) ng/mL. The patient was treated for thyroid storm with 1000 mg of propylthiouracil by orogastric tube as a loading dose followed by 300 mg every 6 hours, 5 drops saturated solution of potassium iodide (SSKI) every 8 hours by orogastric tube, and 100 mg intravenously of hydrocortisone every 8 hours. The hypotension resolved, vasopressors were stopped, and the patient was extubated 25 hours after her initial presentation. During her stay in the intensive care unit, the patient exhibited fever (39.6°C maximum), tachycardia, and tremulousness. These manifestations resolved over a period of 22 hours. The patient was discharged in satisfactory condition on the fourth day of hospitalization on 100 mg of propylthiouracil orally every 8 hours. Outpatient testing days later demonstrated normalization of her thyroid function tests.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [139.0, 'mEq/L'], 'Glucose': [208.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [38.0, 'mg/dL']}",303.12698,287.97063,318.28333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 38.0 mg/dL. 
The concentration of glucose is 208.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (38.0 / 2.8) + (38.0 / 18) = 303.12698 mmol/L.The patient's calculated serum osmolality concentration is 303.12698 mmol/L. This is equalivalent to 303.12698 mOsm/kg."
5858,30,Serum Osmolality,lab test,decimal,pmc-7502416-1,Extracted,"The patient was a 68-year-old male nursing home resident, with a past medical history of diabetes mellitus, hypertension, and stage IV chronic kidney disease. He denied any history of tobacco, alcohol, or substance use. After an outbreak of COVID-19 at his residence, a routine polymerase chain reaction (PCR) test was done, which confirmed COVID-19 infection two days prior to presenting to the emergency department (ED). The patient complained of loss of appetite and nausea for one week while denying any respiratory symptoms. In the ED, he was afebrile and saturating 97% on room air. On examination, he appeared dehydrated and lethargic, while his lung sounds were clear and his abdomen was soft and non-tender. Laboratory workup on admission revealed white blood cell (WBC) 8900 ug/L without lymphopenia, sodium 136 mmol/L, blood urea nitrogen (BUN) 77 mg/dl, creatinine 6.6 mg/dl, glucose 46 mg/dl, procalcitonin 6.04 ng/ml, C-reactive protein (CRP) 158 mg/L, aspartate aminotransferase (AST) 27 U/L, alanine aminotransferase (ALT) 20 U/L, alkaline phosphatase (ALP) 123 U/L and total bilirubin of 0.5 mg/dl. The chest radiograph showed a faint patchy opacity in the left perihilar region (Figure ). He was admitted for acute on chronic kidney injury and hypoglycemia due to poor oral intake. He was also empirically covered with antibiotics for possible superimposed bacterial pneumonia.
Over the next few days, the patient's kidney function improved with hydration. He had persistent nausea, vomiting, and anorexia, but no abdominal pain. A non-contrast abdominal computed tomography (CT) scan revealed peripancreatic fat stranding, greatest around the tail, with mild duodenal wall thickening and adjacent fat stranding, likely from pancreatitis. The gallbladder appeared normal, without wall thickening or surrounding inflammatory changes, and the common bile duct was not dilated (Figure ). Amylase and lipase levels were elevated at 1030 U/L and 2035 U/L, respectively, but the triglyceride and calcium levels were normal. The patient was kept on bowel rest, and given continuous intravenous fluids and antiemetics. Throughout the admission, he did not have any respiratory signs or symptoms, nor did he require oxygen supplementation. Repeat chest radiograph did not show any focal consolidations. The patient's appetite eventually improved, and his diet was advanced. He was discharged seven days later back to his nursing home with a follow-up appointment.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [77.0, 'mg/dL'], 'Glucose': [46.0, 'mg/dL'], 'Sodium': [136.0, 'mmol/L']}",302.05556,286.95278,317.15834,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.0 mmol/L. 
The concentration of bun is 77.0 mg/dL. 
The concentration of glucose is 46.0 mg/dL. 
Plugging these values into the equation, we get 2 * 136.0 + (77.0 / 2.8) + (77.0 / 18) = 302.05556 mmol/L.The patient's calculated serum osmolality concentration is 302.05556 mmol/L. This is equalivalent to 302.05556 mOsm/kg."
5859,30,Serum Osmolality,lab test,decimal,usmle-4901,Extracted,"A 32-year-old man with a history of chronic alcoholism presents to the emergency department with vomiting and diarrhea for 1 week. He states he feels weak and has had poor oral intake during this time. The patient is a current smoker and has presented many times to the emergency department for alcohol intoxication. His temperature is 97.5°F (36.4°C), blood pressure is 102/62 mmHg, pulse is 135/min, respirations are 25/min, and oxygen saturation is 99% on room air. On physical exam, he is found to have orthostatic hypotension and dry mucus membranes. Laboratory studies are ordered as seen below.

Serum:
Na+: 139 mEq/L
Cl-: 101 mEq/L
K+: 3.9 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 9.8 mg/dL

The patient is given normal saline, oral potassium, dextrose, thiamine, and folic acid. The following day, the patient seems confused and complains of diffuse weakness and muscle/bone pain. An ECG and head CT are performed and are unremarkable.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [139.0, 'mEq/L'], 'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [99.0, 'mg/dL']}",290.64286,276.11072,305.175,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (20.0 / 2.8) + (20.0 / 18) = 290.64286 mmol/L.The patient's calculated serum osmolality concentration is 290.64286 mmol/L. This is equalivalent to 290.64286 mOsm/kg."
5860,30,Serum Osmolality,lab test,decimal,pmc-3152516-1,Extracted,"A 56-year-old male with multiple co-morbidities, including a long-standing history of non-ischemic dilated cardiomyopathy, stage III chronic kidney disease, and congestive hepatopathy, underwent LVAD implantation two months prior to the most recent admission. He returned to the hospital due to persistent atrial fibrillation, progressively worsening dyspnea on exertion and rest, abdominal distension with ascites, and suspected ongoing hemolysis due to positioning of the inflow cannula at the apex of the LVAD.
It was decided that the patient should return to the operating room for placement of a new LVAD due to hemolysis and hypotension refractory to medical management. The night before the scheduled surgery, the patient was intubated due to worsening cardiopulmonary parameters, including increased work to breathe, and maintained on epinephrine 0.15 mcg/kg/min, norepinephrine 0.1 mcg/kg/min and dobutamine 3 mcg/kg/min. He was transferred to the operating room to replace the pump. Pre-op vitals included: temp 37.6 degrees Celsius, arterial blood pressure 64/50, mean arterial pressure 55, heart rate 118 and respiratory rate of 16. Prior to induction of anesthesia, labs included: white blood cells 15.2, hemoglobin 10, hematocrit 29.4, platelets 96, Na+ 130, K+ 3.1, Cl- 95, CO2 25, blood urea nitrogen 24, creatine 2.08, glucose 84, and international normalized ratio 3.5. Preoperative arterial blood gases were pH 7.48, pCO2 35.9, pO2 184.2, and HCO3 26.1. In the operating room, hemodynamic parameters were continuously monitored via radial arterial line and Swan-Ganz catheter. Induction was uneventful with etomidate 10 mg and cisatracurium 10 mg. The transesophageal echocardiography (TEE) probe was placed uneventfully. The surgeons entered the mediastinum using the previous sternal incision. Once they began dissecting out the mediastinum, the patient became severely hypotensive and asystolic, and the TEE did not detect any movement on both the left and right side of the heart.
The anesthesiologist alerted the surgeon that Advanced Cardiac Life Support (ACLS) protocol was needed and the surgeon communicated that chest compressions were contraindicated due to the position of the inflow cannula directly beneath the sternum. The anesthesiologist recommended AO-CPR with manual mid-abdominal compressions 1 to 2 inches left of midline (left paramedian) at a rate of 80 beats/min with maximal force while the surgeon cannulated the groin to provide long-term mechanical support in the form of ECMO. As instructed, two members of the team performed AO-CPR (Figure ). During ACLS, the patient continued to be mechanically ventilated and epinephrine, vasopressin, and sodium bicarbonate were given per ACLS protocol, and the hemodynamic parameters as a result of AO-CPR continued to be monitored (Figure ). The duration of the CPR was 15 minutes, during which time the surgeon was able to cannulate the femoral artery and vein and institute ECMO support. The chest was closed and the patient was transferred to the intensive care unit. The patient spent 24 hours in the intensive care unit on ECMO support and mechanical assist device. A decision was made to withdraw care after 24 hours and the patient expired.
Our case represents a difficult situation where the perioperative team faced a new challenge in the operating room: what are the alternatives to ECM when chest compressions are contraindicated due to position of the inflow cannula directly beneath the sternum? Neither the new guidelines published in the European Journal of Cardiothoracic Surgery in 2009 nor the American Heart Association in 2010 provided alternatives to ECM for patients with a mechanical assist device.
It became evident that there was a need for an alternative to ECM, such as AO-CPR, to protect the recent sternotomy until re-opening of the chest to provide internal cardiac massage. The Interactive Cardiovascular Thoracic Surgery e-community conducted a discussion to address whether AO-CPR could be used instead of ECM to either protect the recent sternotomy or while chest compressions are not possible during resternotomy []. After reviewing this evidence, Dunning et al. [] concluded that AO-CPR theoretically has the potential to provide adequate systemic perfusion while an emergency resternotomy is being performed, but further evidence is needed before it can be recommended for routine use.
In general, coronary perfusion pressure during cardiac arrest is the difference between pressure in the aorta (from which the coronary arteries arise) and the right atrium (into which the coronary arteries exit). Using a mathematical model to describe the biophysics of cardiopulmonary resuscitation with periodic z-axis acceleration or abdominal compression at aortic resonant frequencies, Babbs [] proposed that differences in wave mechanics, resulting from simultaneous compression of the abdominal aorta and the inferior vena cava, produced differences in pressure between the aorta and right atrium. During CPR, the minimal coronary perfusion pressure considered necessary for successful resuscitation with return of spontaneous circulation (ROSC) is 15 mmHg []. The values for mean aortic and central venous pressure for our patient were 77 and 62 mmHg, respectively, which provided a mean coronary perfusion pressure of 15 mmHg (77 to 62 mmHg). In a study of 100 patients, however, conventional CPR provided a mean CPP of only 12.5 mmHg []; thus, we propose that the abdominal only CPR in our patient could have served as an effective bridge between the arrest and initiation of ECMO.
In our case, AO-CPR was unplanned, but the surgeon refused chest compressions due to contraindications in this patient. Due to lack of alternatives for resuscitation other than ECMO in this patient, the anesthesiologist suggested that AO-CPR be performed as a temporary resuscitative effort until the surgeon could successfully cannulate the femoral artery and vein to provide long-term mechanical support. Two rescuers performed AO-CPR with generation of coronary perfusion pressure (CPP) of 15 mmHg for 15 minutes, the duration of resuscitation. Both achieved results that appeared to be identical. The evidence seems to suggest that AO-CPR in this particular situation may be comparable to ECM in generating adequate CPP, but at this point it is still too early to determine the true efficacy of AO-CPR compared to ECM with regards to ROSC and neurological outcome.
Other evidence of adequate CPP generated during AO-CPR includes that from Geddes and colleagues [] and Pargett et al. [] who compared AO-CPR with chest compressions in animal models, and showed that AO-CPR was equivalent or superior to standard chest compressions at providing coronary perfusion. Neither of these studies reported any visceral organ damage or contraindications to AO-CPR, nor did they comment on neurological outcome. At this time, we cannot comment on the efficacy of AO-CPR on neurological outcomes as neurological status could not be assessed in our patient because he was intubated, sedated and paralyzed until care was withdrawn.
This case report generates important concerns. In our patient, even though we generated a CPP of 15 mmHg, which has been shown in some patients to be adequate, we do not know whether it was adequate to allow ROSC or whether the ECMO was responsible for ROSC. Other concerns are: what is the optimal delivery (optimal rate, depth/force, duty cycle and location of hand position) of AO-CPR in achieving successful resuscitation with ROSC, what is the best strategy for ventilation during AO-CPR, and is there potential damage/injury to abdominal viscera during AO-CPR?",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [24.0, 'mg/dL'], 'Glucose': [84.0, 'mg/dL'], 'Sodium': [130.0, 'mEq/L']}",273.2381,259.57619,286.9,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. 
The concentration of bun is 24.0 mg/dL. 
The concentration of glucose is 84.0 mg/dL. 
Plugging these values into the equation, we get 2 * 130.0 + (24.0 / 2.8) + (24.0 / 18) = 273.2381 mmol/L.The patient's calculated serum osmolality concentration is 273.2381 mmol/L. This is equalivalent to 273.2381 mOsm/kg."
5861,30,Serum Osmolality,lab test,decimal,pmc-4842364-1,Extracted,"A 71-year-old male with past medical history significant for bladder cancer status after radical cystectomy on chemotherapy, diabetes, coronary artery disease, and hypertension presented to the emergency room with complaints of fever and shivering. Three days prior to admission, his oncologist diagnosed him with anemia. He had complaints of cough with white sputum consisting of up to half a cup per day. He denied any shortness of breath, diarrhea, hematuria and dysuria, or weight loss.
Upon physical examination patient was febrile with a temperature of 100.7 F, blood pressure of 110/62 mmHg, heart rate of 114/min, and respiratory rate of 20/min and had O2 saturation of 100% on two liters' nasal cannula. Pertinent findings revealed irregular rate and rhythm with distant heart sounds. The remainder of the physical exam was otherwise unremarkable. Laboratory data demonstrated hemoglobin of 7.0 g/dL, hematocrit of 21.7%, white blood cell count of 5.7 K/μL with absolute neutrophil count 5.0 K/μL, and platelet count 37 K/μL. Basic metabolic panel revealed glucose of 100 mg/dL, blood urea nitrogen of 27 mg/dL, creatinine of 0.7 mg/dL, calcium 8.0 mg/dL, albumin 2.9 g/dL, sodium 134 mmol/L, potassium 4.4 mmol/L, chloride 103 mmol/L, and bicarbonate 20 mmol/L. Electrocardiogram showed atrial fibrillation with low voltage. Chest X-ray showed marked enlargement of the cardiac silhouette with a possibility of large pericardial effusion ().
The patient was admitted to the intensive care unit for sepsis and large pericardial effusion. He was started on empiric antibiotics. Computed tomography scan of the chest was ordered to rule out any metastasis which revealed a large pericardial effusion that was 2.2-cm in thickness (). Echocardiography demonstrated large circumferential pericardial effusion.
A cardiothoracic surgeon was called on consult and the patient underwent a pericardial window where 800 mL of hemorrhagic pericardial effusion was drained. Pericardial biopsy illustrated metastatic urothelial carcinoma (). Immunostains were performed which were positive for pancytokeratin, CK7, CK20, and uroplakin and negative for PSA. Patient remained critical and, despite all the efforts, the patient deteriorated and expired over the course of a few days due to his relatively poor prognosis.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [27.0, 'mg/dL'], 'Glucose': [100.0, 'mg/dL'], 'Sodium': [134.0, 'mmol/L']}",283.19841,269.03849,297.35833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mmol/L. 
The concentration of bun is 27.0 mg/dL. 
The concentration of glucose is 100.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (27.0 / 2.8) + (27.0 / 18) = 283.19841 mmol/L.The patient's calculated serum osmolality concentration is 283.19841 mmol/L. This is equalivalent to 283.19841 mOsm/kg."
5862,30,Serum Osmolality,lab test,decimal,usmle-5727,Extracted,"A 66-year-old woman presents to the emergency department with abdominal pain. Her symptoms began when she was eating dinner. She has a past medical history of obesity, constipation, intravenous drug use, and diabetes. The patient is instructed to be nil per os and is transferred to the surgical floor. Three days later she had a cholecystectomy and is recovering on the surgical floor. Her laboratory values are ordered as seen below.

Hemoglobin: 11 g/dL
Hematocrit: 33%
Leukocyte count: 8,500/mm^3 with normal differential
Platelet count: 197,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.5 mg/dL
Alkaline phosphatase: 533 U/L
GGT: 50 U/L
AST: 22 U/L
ALT: 20 U/L

The patient is currently asymptomatic and states that she feels well.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [99.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",290.64286,276.11072,305.175,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (20.0 / 2.8) + (20.0 / 18) = 290.64286 mmol/L.The patient's calculated serum osmolality concentration is 290.64286 mmol/L. This is equalivalent to 290.64286 mOsm/kg."
5863,30,Serum Osmolality,lab test,decimal,usmle-5954,Extracted,"A 25-year-old male presents to his primary care physician for fatigue, abdominal pain, diarrhea, and weight loss. He states that this issue has occurred throughout his life but seems to “flare up” on occasion. He states that his GI pain is relieved with defecation, and his stools are frequent, large, and particularly foul-smelling. The patient has a past medical history of an ACL tear, as well as a car accident that resulted in the patient needing a transfusion and epinephrine to treat transfusion anaphylaxis. His current medications include vitamin D and ibuprofen. He recently returned from a camping trip in the eastern United States. He states that on the trip they cooked packed meats over an open fire and obtained water from local streams. His temperature is 99.5°F (37.5°C), blood pressure is 120/77 mmHg, pulse is 70/min, respirations are 11/min, and oxygen saturation is 98% on room air. Physical exam reveals poor motor control and an ataxic gait on neurologic exam. Cardiac and pulmonary exams are within normal limits. Laboratory studies are ordered and return as below:

Hemoglobin: 9.0 g/dL
Hematocrit: 25%
Haptoglobin: 12 mg/dL
Leukocyte count: 7,500 cells/mm^3 with normal differential
Platelet count: 255,000/mm^3

Serum:
Na+: 140 mEq/L
Cl-: 102 mEq/L
K+: 5.0 mEq/L
HCO3-: 24 mEq/L
BUN: 24 mg/dL
Glucose: 82 mg/dL
Creatinine: 1.0 mg/dL
Ca2+: 9.0 mg/dL
LDH: 457 U/L
AST: 11 U/L
ALT: 11 U/L

Radiography is ordered which reveals a stress fracture in the patient’s left tibia.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [24.0, 'mg/dL'], 'Glucose': [82.0, 'mg/dL'], 'Sodium': [140.0, 'mEq/L']}",293.12698,278.47063,307.78333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 24.0 mg/dL. 
The concentration of glucose is 82.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (24.0 / 2.8) + (24.0 / 18) = 293.12698 mmol/L.The patient's calculated serum osmolality concentration is 293.12698 mmol/L. This is equalivalent to 293.12698 mOsm/kg."
5864,30,Serum Osmolality,lab test,decimal,usmle-4287,Extracted,"A 52-year-old man is brought to the emergency department by police. The patient was found harassing patrons at a local pub. The patient has a past medical history of substance abuse. He is not currently taking any medications. His temperature is 99.5°F (37.5°C), blood pressure is 140/95 mmHg, pulse is 95/min, respirations are 15/min, and oxygen saturation is 99% on room air. On physical exam, the patient demonstrates poor grooming and poor dentition. He is currently resting. Cardiac exam demonstrates a normal rate and rhythm. Pulmonary exam reveals minor bibasilar crackles. Laboratory values are ordered as seen below.

Hemoglobin: 9 g/dL
Hematocrit: 30%
Leukocyte count: 7,500 cells/mm^3 with normal differential
Platelet count: 199,000/mm^3

Serum:
Na+: 137 mEq/L
Cl-: 100 mEq/L
K+: 4.4 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.0 mg/dL
AST: 33 U/L
ALT: 24 U/L

An alcohol breath test reveals a value of .48. A peripheral smear is ordered as seen in Figure A.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [99.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",286.64286,272.31072,300.975,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (20.0 / 2.8) + (20.0 / 18) = 286.64286 mmol/L.The patient's calculated serum osmolality concentration is 286.64286 mmol/L. This is equalivalent to 286.64286 mOsm/kg."
5865,30,Serum Osmolality,lab test,decimal,usmle-6189,Extracted,"A 45-year-old woman presents to the emergency department with hematemesis. Her son said that the patient had complained of gnawing abdominal pain that worsened before and improved after meals for the past 3 weeks. She frequently travels for work and is often stressed. She drinks alcohol socially and does not smoke tobacco or marijuana. She has not had anything to eat or drink for the past 24 hours due to the pain, but coughed up ""several cup of"" frank red blood before arrival. Her temperature is 98°F (37°C), blood pressure is 80/50 mmHg, pulse is 140/min, respirations are 23/min, and oxygen saturation is 96% on room air. Gastric ultrasound reveals high gastric residual volume. The patient is empirically started on 3 units of uncrossmatched O-negative blood transfusion and pantoprazole. The patient's initial laboratory data return in the meantime:

Hemoglobin: 5 g/dL
Hematocrit: 18 %
Leukocyte count: 8,000/mm^3 with normal differential
Platelet count: 400,000/mm^3

Serum:
Na+: 140 mEq/L
Cl-: 115 mEq/L
K+: 3.2 mEq/L
HCO3-: 26 mEq/L
BUN: 60 mg/dL
Glucose: 104 mg/dL
Creatinine: 1.1 mg/dL

Blood type: AB
Rhesus status: negative

After bedside esophageogastroduodenoscopy with stapling of several peptic ulcers, repeat labs are obtained in 2 hours. The patient now complains of feeling hot with intermittent shivering. She denies any other symptoms. Her temperature is 101°F (38.3°C), blood pressure is 100/55 mmHg, pulse is 100/min, respirations are 20/min, and oxygen saturation is 99% on room air. Her lungs are clear to auscultation bilaterally, and no accessory respiratory muscle use is observed. No rash is seen.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mEq/L'], 'Glucose': [104.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [60.0, 'mg/dL']}",307.20635,291.84603,322.56667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 60.0 mg/dL. 
The concentration of glucose is 104.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (60.0 / 2.8) + (60.0 / 18) = 307.20635 mmol/L.The patient's calculated serum osmolality concentration is 307.20635 mmol/L. This is equalivalent to 307.20635 mOsm/kg."
5866,30,Serum Osmolality,lab test,decimal,pmc-4594448-1,Extracted,"A thirteen-year-old Caucasian male presented to the Penn State Hershey Emergency Department (PA, USA) with severe fecal impaction for three weeks. He had an episode of encopresis at school while taking 8.5 g of polyethylene glycol 3350 per day infrequently – his pediatrician had prescribed 17 g by mouth once daily on a regular basis, but the encopresis experienced on this dose caused significant embarrassment to the patient resulting in noncompliance. Two days prior to admission, he developed severe abdominal pain with cramping, vomiting, decreased oral intake, and diminished urine output. He also complained of pallor, diaphoresis, insomnia, and restlessness. He was treated with magnesium citrate 10 ounces orally and a saline enema at an outside hospital without relief and eventual worsening of his symptoms. He had a significant history of chronic functional constipation beginning at the age of two years consisting of large, hard, painful stools that led to a pattern of withholding for upwards of eight days. He struggled to become toilet trained and was seen in our Pediatric Gastroenterology clinic for a first visit at three years of age. He had passed meconium shortly after birth, and his medical history only included a repair of a penile hypospadias. His diet contained less than sixteen ounces of milk per day, and he was growing well with weight and height in the 85th percentile and 50th percentile, respectively. A rectal examination demonstrated normal sphincter tone and a posterior shelf. Daily oral mineral oil was prescribed; however, he was lost to follow-up thereafter. He was seen by his pediatrician for annual health visits since 10 years of age and concerns of constipation with encopresis were addressed appropriately – including regular daily osmotic laxative therapy, letters to school teachers to facilitate the patient’s use of the restroom as needed, and high fiber diet. His parents reportedly attempted to manage his constipation with intermittent doses of oral mineral oil, senna, naturopathic therapy, and glycerin or bisacodyl suppositories as needed primarily to manage acute distress as they were wary of long term dependence on medications. With increasing age, the patient was given more responsibility for adhering to his therapy. To his parents, he appeared to be in control of his constipation for the most part, till onset of the current illness. His diet was predominantly low fiber with very limited intake of vegetables or fruits.
Upon arrival to our hospital, he was in constant, severe discomfort and restless, but preferentially lying on his sides. His temperature was 36.4°C, heart rate 116 beats per minute, and blood pressure 126/93 mmHg. His weight was 68 kg (93rd percentile) and height was 168 cm (76th percentile). He had dry mucosal membranes and skin. His abdomen was moderately distended, firm to palpation with diffuse tenderness, and had palpable hard fecal masses in the suprapubic area and bilateral lower quadrants. He had mild bilateral non-pitting pedal edema. Perianal inspection revealed oozing, liquid brown stool with no skin tags. A digital rectal examination revealed a large, hard ball of stool impacted in the distal rectum. Inguinal lymphadenopathy and scrotal edema were absent. An abdominal radiograph demonstrated a large stool burden causing rectal dilation of 10 cm with distention of the sigmoid colon extending upwards to the level of the umbilicus (). Laboratory testing revealed the following results which were all within normal limits: sodium 140 mmol/L, potassium 4.1 mmol/L, chloride 100 mmol/L, bicarbonate 24 mmol/L, blood urea nitrogen 11 mg/dL, creatinine 0.61 mg/dL, and glucose 91 mg/dL. His complete blood cell count, thyroid function studies, tissue transglutaminase IgA and total IgA were normal. He was given a parenteral normal saline bolus for rehydration. Within thirty minutes of the fluid bolus, he developed worsening pedal edema and overlying erythema spreading upwards from his feet to his knees. Due to a concern for deep venous thrombosis, a Duplex Ultrasound was performed; it did not reveal a thrombus, but showed changes in the waveforms in his common femoral and external iliac veins bilaterally, indicating pelvic venous compression (). D-dimer and coagulation studies were obtained and were within normal limits. The pediatric surgeons performed a manual disimpaction under general anesthesia due to his worsening clinical status. A three-digit rectal examination encountered perineal edema and a large fecal impaction, which was manually removed with abdominal compression and transanal disruption. Nine liters of crystalloid solution were given in serial irrigations and resulted in multiple stool masses being removed. Over the next three days, his bowel was sufficiently cleaned out with sixteen liters of polyethylene glycol 3350 with electrolytes infused via a nasogastric tube. A repeat abdominal radiograph confirmed a significant reduction in the stool burden and decompression of his entire colon. His pedal and perineal edema resolved, and he was discharged on maintenance polyethylene glycol 3350 solution 17 gm twice daily and Bisacodyl 10 mg tablet once daily.
One week later he had a barium enema which showed a posterior rectal shelf along with a change in caliber of the distal rectum with spiculations. These findings created concern for decreased colonic motility. Four months after discharge, he continued to have soft daily bowel movements with compliance to maintenance laxative therapy. The pedal and perineal edema had resolved. He had a good appetite and denied abdominal discomfort. Serial clinical examinations at two follow up visits did not reveal recurrence of palpable mass per abdomen. An abdominal radiograph one month later demonstrated minimal residual stool, and a repeat Doppler ultrasound showed normal venous waveforms (). Hence, imaging studies for evaluating other causes of extrinsic venous compression were not pursued. Further investigation of the etiology of the constipation, including a rectal biopsy and anorectal and colonic manometry, were deferred at this time due to the resolution of the constipation. Subsequent annual visits to his pediatrician’s office found him to be adhering to a higher fiber diet, daily laxative as prescribed, with no reported difficulty in stooling and steady growth. His weight had gone up to 70.5 kg at 14 years of age and to 81.4 kg at 15 years of age.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mmol/L'], 'Blood Urea Nitrogen (BUN)': [11.0, 'mg/dL'], 'Glucose': [91.0, 'mg/dL']}",288.98413,274.53492,303.43334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mmol/L. 
The concentration of bun is 11.0 mg/dL. 
The concentration of glucose is 91.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (11.0 / 2.8) + (11.0 / 18) = 288.98413 mmol/L.The patient's calculated serum osmolality concentration is 288.98413 mmol/L. This is equalivalent to 288.98413 mOsm/kg."
5867,30,Serum Osmolality,lab test,decimal,usmle-5117,Extracted,"A 32-year-old woman presents to her primary care physician for recent onset headaches, weight loss, and restlessness. Her symptoms started yesterday, and since then she has felt sweaty and generally uncomfortable. The patient’s past medical history is unremarkable except for a recent viral respiratory infection which resolved on its own. The patient is not currently on any medications. Her temperature is 99.5°F (37.5°C), blood pressure is 127/68 mmHg, pulse is 110/min, respirations are 14/min, and oxygen saturation is 98% on room air. On physical exam, you see a sweaty and uncomfortable woman who has a rapid pulse. The patient demonstrates no abnormalities on HEENT exam. The patient’s laboratory values are ordered as seen below.

Hemoglobin: 12 g/dL
Hematocrit: 36%
Leukocyte count: 8,500/mm^3 with normal differential
Platelet count: 195,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 102 mEq/L
K+: 4.4 mEq/L
HCO3-: 24 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.0 mg/dL
Ca2+: 10.2 mg/dL
TSH: .03 mIU/L
AST: 12 U/L
ALT: 10 U/L

The patient is prescribed propranolol and proplythiouracil. She returns 1 week later complaining of severe fatigue.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [99.0, 'mg/dL'], 'Sodium': [139.0, 'mEq/L']}",290.64286,276.11072,305.175,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (20.0 / 2.8) + (20.0 / 18) = 290.64286 mmol/L.The patient's calculated serum osmolality concentration is 290.64286 mmol/L. This is equalivalent to 290.64286 mOsm/kg."
5868,30,Serum Osmolality,lab test,decimal,usmle-4384,Extracted,"A 27-year-old male presents to the emergency department after a motor vehicle collision. The patient was an unrestrained driver in a head-on collision. The patient appears intoxicated and is complaining of severe pain. He has a past medical history of cocaine, heroin, and MDMA use, and he is not currently taking any medications. His temperature is 99.5°F (37.5°C), blood pressure is 80/50 mmHg, pulse is 160/min, respirations are 15/min, and oxygen saturation is 95% on room air. An EKG is obtained as seen in Figure A. Laboratory values are ordered as below:

Serum:
Na+: 140 mEq/L
Cl-: 100 mEq/L
K+: 4.1 mEq/L
HCO3-: 24 mEq/L
BUN: 20 mg/dL
Glucose: 110 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.1 mg/dL

Hemoglobin: 10 g/dL
Hematocrit: 23%
Leukocyte count: 5,000 cells/mm^3 with normal differential
Platelet count: 150,000/mm^3

On physical exam the patient is notably short of breath. Cardiac exam is notable for a rapid rate and thready pulses as well as jugular venous distention (JVD). Pulmonary exam reveals unilateral breath sounds. A neurological exam is deferred due to patient non-compliance.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mEq/L'], 'Glucose': [110.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL']}",293.25397,278.59127,307.91667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (20.0 / 2.8) + (20.0 / 18) = 293.25397 mmol/L.The patient's calculated serum osmolality concentration is 293.25397 mmol/L. This is equalivalent to 293.25397 mOsm/kg."
5869,30,Serum Osmolality,lab test,decimal,pmc-4950766-1,Extracted,"A 69 year old Hispanic female with a past medical history significant for hypertension, diabetes mellitus, coronary artery disease status post revascularization, ischemic cardiomyopathy and chronic kidney disease had presented to our hospital for further evaluation and care. For the past few months the patient had suffered weight loss (approximately 30–35 lb), generalized malaise, low grade fevers (99.9 F), non-productive cough, myalgias and arthralgias. She did not endorse any night sweats or recent travel history, and there were no sick contacts at home. Prior to admission to our institution the patient was at an outside hospital and was being treated for sepsis with combinations of antibiotics including intravenous vancomycin, meropenem, echinocandin, metronidazole, and piperacillin tazobactam for 2 to 3 weeks duration as she was developing fevers and productive cough.
The physical exam yielded a thin and chronically ill appearing female patient.
Vital signs at the time of admission were notable for hypertension (186/79 mmHg). Her eyes did not show any conjunctival hemorrhaging or icterus, however there was conjunctival pallor. Oropharynx did not show any active exudates or ulcerative lesions. Her cardiac exam did not reveal any murmurs and her airways were clear to auscultation. Abdominal exam revealed palpable splenomegaly. Examination of the extremities did not show nail deformities including splinter hemorrhages or nail pitting. Her skin had no evidence of skin nodularities or other lesions. There was a 1 cm non tender, movable left axillary lymph node. The rest of the physical examination was unremarkable.
Initial laboratory work revealed that the patient had pancytopenia. White blood cell count (WBC) was stated at 2.4 K/uL, absolute neutrophil count (ANC) 1.92 K/uL, hemoglobin (Hgb) of 11.6, and platelet count of 39,000/uL. B2-microglobulin was seen elevated at 9.2 mg/L. Basic metabolic panel obtained showed sodium 134 mEq/L, Potassium 3.5 mEq/L, Chloride 103 mEq/L, Bicarbonate 26 mEq/L, Blood urea nitrogen 30 mg/dl, Creatinine 0.90 mg/dl, glucose 220 mg/dl. Liver function panel showed Albumin 2.2 g/dl, normal transaminases, total bilirubin 0.8 mg/dl, direct bilirubin 0.4 mg/dl. Urine analysis showed 200 mg/dl of protein and occasional amorphous crystals.
Initial computed tomography (CT) scan of the abdomen and pelvis during hospital admission showed a 15 cm spleen which was heterogenous and micronodular, as well as scattered abdominal and pelvic lymphadenopathy (Fig. ). No imaging signs of portal hypertension were noted.
During the hospitalization our patient was noted to become more confused and agitated, and there was concern that the patient was having seizures as she was seen numerous times to lose consciousness and awaken, with occasional loss of bladder function. A brain magnetic resonance imaging (MRI) showed subcortical non enhancing FLAIR hyper intense foci in the bilateral posterior occipital lobes.
Lumbar puncture and cerebral spinal fluid (CSF) studies were further performed for further analysis, and showed: WBC 1; no red blood cells; protein 62 mg/dL; glucose 35 mg/dL; and, lactate dehydrogenase 234 mIU/mL. Most notable negative findings in the CSF included no detectable viral cultures for cytomegalovirus, adenovirus, herpes virus, and varicella zoster virus, negative cryptococcal antigen serology and negative bacterial and fungal cultures.
Electroencephalogram studies showed triphasic morphology waves with and without sharp negative component at 2–3 hertz. These were seen in continuum mostly with subtle waxing and waning features. To 0.5 mg intravenous alprazolam, above discharges had slowly resolved, replaced by organized background that consists of 6 hertz rhythms. Importantly, there was a clinical improvement after alprazolam; suggesting a nonconvulsive seizures responding to benzodiazepine.
Two weeks later after the initial CT imaging and after the patient was more stable from the neurological perspective in order to attempt a lymph node excisional biopsy, a PET-CT imaging was performed and showed complete resolution of the previously detected lymphadenopathy and splenomegaly. (Fig. ).
Additional serologies for viral hepatitis and autoimmune etiology work up were performed. A bone marrow biopsy was performed and additional serum erythropoietin level, iron profile; cobalamin and folate level were determined.
The patient returned to the benign hematology clinic after discharged from the hospital. During her follow up appointment she appeared in better spirits and recovering well. Physical examination was notable for an absence of lymphadenopathy particularly in the cervical and axillary region, as well as no palpable organomegaly in the abdomen. It was further revealed that her antinuclear antibody (ANA) titer was highly positive (1:640), ESR 108 mm/hr with a CRP 6.74 mg/L. Negative viral hepatitis B, C and Human Immunodeficiency virus serologies.
Serum quantitative immunoglobulin showed a mildly elevated Ig A and Ig G level, without other abnormalities. Serum and urine protein electrophoresis did not reveal a monoclonal gammopathy. Serum free light chain levels showed kappa 96.3 mg/L and lambda 60.06 mg/dL with a normal ratio 1.6 in a patient with chronic kidney disease.
Complement C3 level was normal with a slightly elevated C4 at 46 mg/dL.
Bone marrow aspirate yielded a predominance of CD3 positive polytypical small T cells and a population of polyclonal B-cells by flow cytometry and negative for lymphoma or other malignant process. A focal lymphohistiocytic aggregate with granuloma formation was noted; occasional larger cells with prominent nucleolus identified; eosinophils were increased mildly in the vicinity of this aggregate. Acid fast bacilli and fungal stains were attempted; however the focal granuloma could not be appreciated at subsequent sections.
The patient’s pancytopenia was thought to be likely secondary to systemic lupus erythematosus and she was thus referred to rheumatology for further work up, and further testing included anti-double-stranded DNA, anti-RNP, anti-CCP antibody, ANCA vasculitis panel, direct antiglobulin test, lupus anticoagulant, anticardiolipin antibody, anti-double-stranded DNA antibody, and anti-SSA and anti-SSB. All these tests were negative, thus ruling out systemic erythematous lupus, rheumatoid arthritis, and other connective tissue disorders.
The interval improvement and self-limited clinical course in our case led us to believe that her elevated ANA titers, her bone marrow granuloma were secondary to an EBV infection-related syndrome. Monospot test was not performed and at that point we evaluated for EBV PCR and EBER staining in the bone marrow. Initial EBV PCR results were positive (960 copies/mL), while Epstein–Barr virus-encoded small RNAs staining in the bone marrow was negative. Our in situ hybridization stain is validated to work on decalcified bone marrow trephine biopsies and all stains include an on-slide positive control. As such, the likelihood of a false negative result is low. A possible explanation includes a sampling factor with lack of infected B-cells in the bone marrow despite the presence of viremia.
Her follow up labs during subsequent clinic visits showed WBC 5.3 K/uL, ANC 3.15 K/uL, Hgb 7.4 g/dL, calculated reticulocyte index of 1.1 and platelets 172 K/uL. Iron was 68 ug/dL, transferrin 124.1 mg/dL, ferritin 2952 ng/mL and serum erythropoietin levels were 31.7 mIU/mL. Serum cobalamin was 394 pg/mL and serum folate 12.3 ng/mL. Since there was spontaneous interval resolution of her neutropenia and her thrombocytopenia our diagnosis at that point was cytopenias secondary to infectious mononucleosis and anemia of chronic kidney disease related to diabetes.
Our patient presented 7 weeks later at the emergency room with a recurrent febrile syndrome with diffuse cervical and axillary lymphadenopathy and splenomegaly (Fig. ) and worsening cytopenias: WBC 1800/uL, ANC 1480/uL, Hgb 8.3 gr/dL, platelet count 20,000/uL; a repeat EBV titer revealed 6580 copies/mL. CT imaging with contrast found bilateral axillary, mediastinal and hilar lymphadenopathy. Low volume retroperitoneal and pelvic lymphadenopathy, hepatosplenomegaly with numerous small ill-defined hypodense lesions was in the spleen and probably also within the liver (Fig. ). At this time a repeat bone marrow biopsy and an excisional lymph node biopsy were performed and reviewed. The bone marrow specimen showed a solitary large cell positive for CD30 identified in the clot. No atypical cells are identified in core biopsy as assessed by IHC for CD30 and Pax-5. EBER was positive in few and scattered cells. The lymph node sections demonstrated near-total effacement of the lymph node architecture by a neoplasm comprised of neoplastic cells with Hodgkin-Reed-Sternberg morphology. The neoplastic cells were positive for CD15, CD30, PAX5 (weak), and MUM1. They were negative for CD3, CD20, CD45, ALK, and EMA. The findings were diagnostic of classical Hodgkin lymphoma, best subtyped as lymphocyte-depleted. (Fig. ). The expression of PAX5 with weak intensity coupled with MUM1 expression by the neoplastic cells is diagnostic of classical Hodgkin lymphoma. The expression of PAX5, a gene encoding a B-cell-specific transcription factor, excluded T-cell lymphoma as a diagnostic consideration. It is worth noting also that flow cytometry done on a bone marrow sample with involvement by lymphoma showed no evidence of T-cell or B-cell immunophenotypic aberrancies.
The patient was started on ABVD chemotherapy regime, bleomycin was held secondary to patient’s history of cardiomyopathy. She received three cycles of chemotherapy with complete clinical remission. Additional cycles of chemotherapy were not completed given prolonged and severe chemotherapy-induced cytopenias that eventually recovered over the following months. A bone marrow biopsy at completion of treatment revealed no morphologic evidence of residual Hodgkin lymphoma. Her most recent surveillance PET-CT imaging, nine months from completion of treatment, showed no hypermetabolic lymphoma and continuing complete metabolic response to therapy.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [134.0, 'mEq/L'], 'Glucose': [220.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [30.0, 'mg/dL']}",290.93651,276.38968,305.48334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. 
The concentration of bun is 30.0 mg/dL. 
The concentration of glucose is 220.0 mg/dL. 
Plugging these values into the equation, we get 2 * 134.0 + (30.0 / 2.8) + (30.0 / 18) = 290.93651 mmol/L.The patient's calculated serum osmolality concentration is 290.93651 mmol/L. This is equalivalent to 290.93651 mOsm/kg."
5870,30,Serum Osmolality,lab test,decimal,usmle-4289,Extracted,"A 19-year-old man with unknown medical history is found down on a subway platform and is brought to the hospital by ambulance. He experiences two episodes of emesis en route. In the emergency department, he appears confused and is complaining of abdominal pain. His temperature is 37.0° C (98.6° F), pulse is 94/min, blood pressure is 110/80 mmHg, respirations are 24/min, oxygen saturation is 99% on room air. His mucus membranes are dry and he is taking rapid, deep breathes. Laboratory work is presented below:

Serum:
Na+: 130 mEq/L
K+: 4.3 mEq/L
Cl-: 102 mEq/L
HCO3-: 12 mEq/L
BUN: 15 mg/dL
Glucose: 362 mg/dL
Creatinine: 1.2 mg/dL
Urine ketones: Positive


The patient is given a bolus of isotonic saline and started on intravenous insulin drip.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [130.0, 'mEq/L'], 'Glucose': [362.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [15.0, 'mg/dL']}",285.46825,271.19484,299.74166,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. 
The concentration of bun is 15.0 mg/dL. 
The concentration of glucose is 362.0 mg/dL. 
Plugging these values into the equation, we get 2 * 130.0 + (15.0 / 2.8) + (15.0 / 18) = 285.46825 mmol/L.The patient's calculated serum osmolality concentration is 285.46825 mmol/L. This is equalivalent to 285.46825 mOsm/kg."
5871,30,Serum Osmolality,lab test,decimal,usmle-9635,Extracted,"A 55-year-old woman visits the clinic after experiencing what she describes as an odd episode of tingling in her fingers and the sensation of smelling sour milk. She denies loss of consciousness, confusion, or incontinence. She also denies a history of head trauma or the ingestion of toxic substances. Past medical history is significant for type 2 diabetes mellitus, which is well controlled with metformin. Her temperature is 36.8°C (98.2°F), the heart rate is 98/min, the respiratory rate is 15/min, the blood pressure is 100/75 mm Hg, and the O2 saturation is 100% on room air. The physical exam, including a full neurologic and cardiac assessment, demonstrates no abnormal findings. Laboratory findings are shown. Brain MRI does not indicate any areas of infarction or hemorrhage. ECG is normal, and EEG is pending.
BUN 15 mg/dL
pCO2 40 mmHg
Creatinine 0.8 mg/dL
Glucose 95 mg/dL
Serum chloride  103 mmol/L
Serum potassium 3.9 mEq/L
Serum sodium 140 mEq/L
Total calcium 2.3 mmol/L
Magnesium 1.7 mEq/L
Phosphate 0.9 mmol/L
Hemoglobin 14 g/dL
Glycosylated hemoglobin 5.5%
Total cholesterol 4 mmol/L
Bicarbonate (HCO3) 19 mmol/L
Urine toxicology screen is negative.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mEq/L'], 'Glucose': [95.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [15.0, 'mg/dL']}",290.63492,276.10317,305.16667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 15.0 mg/dL. 
The concentration of glucose is 95.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (15.0 / 2.8) + (15.0 / 18) = 290.63492 mmol/L.The patient's calculated serum osmolality concentration is 290.63492 mmol/L. This is equalivalent to 290.63492 mOsm/kg."
5872,30,Serum Osmolality,lab test,decimal,pmc-3338240-1,Extracted,"A 26 year old male was admitted to the emergency with alleged history of accidental ingestion of thinner. He had consumed about 200–250 ml of thinner, mistaking it for water in the darkness of the night. He was brought within half an hour of thinner ingestion with complaints of vomiting, headache, weakness and dizziness. On examination, the patient was conscious, with a dusky discoloration of tongue and nails along with tachycardia and mild tachypnoea. Other vital parameters and systemic examination were within normal limits. Blood withdrawn for investigations was found to be chocolate brown in color. Because of the color of the blood, severe unexplained cyanosis and alleged history of thinner consumption, a clinical diagnosis of methemoglobinemia was made. Blood investigations revealed Hb = 15.5 gm%, platelet count = 2.1 lac/mm3, blood sugar = 112 mg%, blood urea = 18 mg%, serum creatinine = 1.0 mg%, serum bilirubin = 1.1 mg%, S. Na+ = 143 mEq/L and S. K+ = 3.6 mEq/L. Chest X-ray was normal and arterial blood gas (ABG) analysis revealed mild hypoxemia and metabolic acidosis (pH = 7.23, pO2 = 91 mmHg, pCO2 = 31.5 mmHg, HCO3 = 14.3 mEq/L, BE = 13.2 mEq/L). Oxygen therapy was given and vitals monitoring was carried out. Methemoglobin levels in blood using the absorption spectrophotometry method were performed, which were 32.61% of total hemoglobin. He was given supplemental oxygen and a gastric lavage was done. Inj. methylene blue (MB) 100 mg along with vitamin C 1 g and dextrose containing fluids were administered intravenously. As there was no improvement in the cyanosis, another dose of MB 100 mg IV was repeated after 1 h. An ABG performed at this point showed pH = 7.32, pO2 = 117 mmHg, pCO2 = 30.7 mmHg, HCO3 = 17.4 mEq/L, BE = 8.7 mEq/L. Methemoglobin levels continued to increase and were 49.7% after 6 h and 71.7% after 8 h. ABG revealed pH = 7.32, pO2 = 60.2 mmHg, pCO2 = 37.4 mmHg, HCO3 = 19.3 meq/L, BE = 7.0 mEq/L. Patient's trachea was intubated and he was mechanically ventilated with 100% oxygen. He became hemodynamically unstable and was put on vasopressor support with inj. dopamine 15 μgkg/1min/1. Even after 12 h, his methemoglobin levels remained significantly high (74.9%) and, therefore, an exchange transfusion was planned. After the exchange transfusion, the methemoglobin levels decreased to 40.2% (ABG revealed pH = 7.40, pO2 = 98.4 mmHg, pCO2 = 32.8 mmHg, HCO3 = 21.1 mEq/L, BE = 4.8 mEq/L). The patient had two episodes of bradycardia in the next couple of hours and about 6 h later; he had a cardiac arrest, but was successfully revived. Vasopressor support had to be increased (inj. noradrenalin 2-3 μgmin-1) and mechanical ventilation was continued. The next day, he was given another dose of MB (100 mg) and the methemoglobin levels decreased to 8.60%. Supportive therapy was continued, and the patient was gradually weaned off ventilatory support after 4 days. The SpO 
2increased to 95% on day 3 and to 96–97% on day 5. The patient's trachea was subsequently extubated on day 5 and continued to maintain a good gas exchange on face mask oxygen (5L/min). The patient was discharged from the intensive care unit on day 7.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [143.0, 'mEq/L'], 'Glucose': [112.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [18.0, 'mg/dL']}",298.65079,283.71825,313.58333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 143.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 143.0 mEq. To convert from 143.0 mEq to mmol, convert from mEq to mmol. The compound 143.0 has a valence of 1, and so divide the valence by the value of mEq to get, 143.0 mEq/(1 mEq/mmol) = 143.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mEq sodium/L converts to 143.0 mmol sodium/L. 
The concentration of bun is 18.0 mg/dL. 
The concentration of glucose is 112.0 mg/dL. 
Plugging these values into the equation, we get 2 * 143.0 + (18.0 / 2.8) + (18.0 / 18) = 298.65079 mmol/L.The patient's calculated serum osmolality concentration is 298.65079 mmol/L. This is equalivalent to 298.65079 mOsm/kg."
5873,30,Serum Osmolality,lab test,decimal,usmle-7682,Extracted,"A 61-year-old woman visits the clinic with a complaint of new-onset episodic abnormal body movements. She says her husband noticed it twice in the past week. There were jerky movements for roughly 15 seconds during her last episode. She denies any recent trauma or fever. Her vital signs include: blood pressure 114/74 mm Hg, pulse 81/min, temperature 36.7°C (98.1°F) and respiratory rate 10/min. On physical examination, there is no evidence of focal neurological deficits. A basic metabolic panel is ordered which shows:
Sodium 141 mEq/L
Potassium 5.1 mEq/L
Chloride 101 mEq/L
Bicarbonate 24 mEq/L
Albumin 4.3 mg/dL
Urea nitrogen 11 mg/dL
Creatinine 1.0 mg/dL
Uric Acid 6.8 mg/dL
Calcium 8.9 mg/dL
Glucose 111 mg/dL
A contrast magnetic resonance imaging (MRI) of the head is shown in the provided image.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [141.0, 'mEq/L'], 'Glucose': [111.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [11.0, 'mg/dL']}",292.09524,277.49048,306.7,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. 
The concentration of bun is 11.0 mg/dL. 
The concentration of glucose is 111.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (11.0 / 2.8) + (11.0 / 18) = 292.09524 mmol/L.The patient's calculated serum osmolality concentration is 292.09524 mmol/L. This is equalivalent to 292.09524 mOsm/kg."
5874,30,Serum Osmolality,lab test,decimal,pmc-3968599-1,Extracted,"A 52-year-old female patient was admitted in March 2012 with fever, cough, breathlessness and progressive dyspnea with respiratory distress and decrease urine output of 10 days duration. There was no history of abdominal pain, dysuria or trauma and no recent use of non-steroidal anti-inflammatory medication.
On examination, she was breathless with blood pressure of 150/90 mmHg, temperature 40°C, respiratory rate of 30 breaths/min, heart rate of 100 bpm. Laboratory investigations revealed hemoglobin, 10.3 g/l; total white cell count, 9.88 × 103/μl (differential count: 74% neutrophils, 20% lymphocytes, 4% monocytes and 2% eosinophils); platelet count, 211 × 103/μl; serum creatinine (SCr), 10.8 mg/dl sodium, 138 mEq/l; potassium, 5.3 mEq/l; blood urea, 76 mg/dl; and blood glucose, 72 mg/dl.
Renal ultrasound showed normal sized kidneys with hyper reflective cortex. Serological tests for malaria, leptospirosis, dengue and viral hepatitis were negative. The initial blood, urine and sputum cultures were sterile. Urinalysis showed proteinuria, hematuria and two to five fine granular casts. SCr phosphokinase levels and liver function test chest radiograph were unremarkable while tests for antinuclear antibody, anti-double-stranded deoxyribonucleic acid, anti-neutrophil cytoplasmic antibody, anti-glomerular basement membrane antibody, coombs’ test, cryoglobulins and C-reactive protein were all negative and complement components (C3 and C4) were low. Enzyme-linked immunosorbent assays test for human immunodeficiency virus (HIV), hepatitis B surface antigen and hepatitis C virus were negative. Patients had influenza H1N1 virus subtype specific ribonucleic acid detected in a nasopharyngeal swab using reverse transcriptase-polymerase chain reaction. She had a history of exposure to swine flu positive patient and was managed using oseltamivir, antibiotic, fluid replacement and dialysis. Patients received oseltamivir, 75 mg within 48 h of presumed diagnosis for 5 days and supportive measures as needed. Initially, she was treated with peritoneal dialysis and she remained oliguric and required intermittent hemodialysis for a total of 5 times through temporary jugular dialysis catheter for 4 h each.
Renal biopsy [] revealed two fragment of renal tissue containing 11 glomeruli with associated tubules and vessels. All the glomeruli show uniform mesangial prominence. Capillary lumina were open, and membranes were of normal thickness. Tubules showed mild to moderate degeneration. Interstitium was mildly prominent for uniform edema and diffuse infiltration with leucocytes. Immunofluorescence microscopy did not reveal staining with anti-human sera tested (IgG, IgM, IgA and C1q). Influenza nucleoprotein (InfA-NP) antigen-positive cells were not detected in kidney tissue. A diagnosis of mesangial proliferative glomerulonephritis with acute tubule interstitial nephritis was made. The patient was treated with methyl prednisolone 500 mg for 3 days followed by oral prednisolone 1 mg/kg/day. Her condition also improved rapidly and she was discharged with SCr of 1.5 mg/dl. Her SCr was 1 mg/dl at 1 month follow-up.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [138.0, 'mEq/L'], 'Glucose': [72.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [76.0, 'mg/dL']}",307.14286,291.78572,322.5,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 76.0 mg/dL. 
The concentration of glucose is 72.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (76.0 / 2.8) + (76.0 / 18) = 307.14286 mmol/L.The patient's calculated serum osmolality concentration is 307.14286 mmol/L. This is equalivalent to 307.14286 mOsm/kg."
5875,30,Serum Osmolality,lab test,decimal,usmle-5686,Extracted,"A 14-year-old male presents to the emergency department with altered mental status. His friends who accompanied him said that he complained of abdominal pain while camping. They denied his consumption of anything unusual from the wilderness, or any vomiting or diarrhea. His temperature is 100.5°F (38.1°C), blood pressure is 95/55 mmHg, pulse is 130/min, and respirations are 30/min. His pupils are equal and reactive to light bilaterally. The remainder of the physical exam is unremarkable. His basic metabolic panel is displayed below:

Serum:
Na+: 116 mEq/L
Cl-: 70 mEq/L
K+: 4.0 mEq/L
HCO3-: 2 mEq/L
BUN: 50 mg/dL
Glucose: 1010 mg/dL
Creatinine: 1.2 mg/dL

While the remainder of his labs are pending, the patient becomes bradypneic and is intubated. His ventilator is adjusted to volume control assist-control with a respiratory rate (RR) of 14/min, tidal volume (Vt) of 350 mL, positive end-expiratory pressure (PEEP) of 5 cm H2O, and fractional inspired oxygen (FiO2) of 40%. His height is 5 feet 5 inches. Intravenous fluids and additional medical therapy are administered.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [116.0, 'mEq/L'], 'Glucose': [1010.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [50.0, 'mg/dL']}",305.96825,290.66984,321.26666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 116.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 116.0 mEq. To convert from 116.0 mEq to mmol, convert from mEq to mmol. The compound 116.0 has a valence of 1, and so divide the valence by the value of mEq to get, 116.0 mEq/(1 mEq/mmol) = 116.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 116.0 mEq sodium/L converts to 116.0 mmol sodium/L. 
The concentration of bun is 50.0 mg/dL. 
The concentration of glucose is 1010.0 mg/dL. 
Plugging these values into the equation, we get 2 * 116.0 + (50.0 / 2.8) + (50.0 / 18) = 305.96825 mmol/L.The patient's calculated serum osmolality concentration is 305.96825 mmol/L. This is equalivalent to 305.96825 mOsm/kg."
5876,30,Serum Osmolality,lab test,decimal,pmc-7550932-1,Extracted,"A 49-year-old male smoker presented to the emergency department complaining of chest pain
and progressive dyspnea for the past 4 days. The chest pain was constant, sharp,
nonradiating in nature noticed over both sides of the chest. The pain progressively worsened
over time and with deep inspiration. The patient has a 10 pack-year smoking history.
On arrival his heart rate was 119 beats/minute, respiratory rate 23 breaths/minute, blood
pressure 109/59 mm Hg, and peripheral capillary oxygen saturation of 84% on room air. Chest
examination revealed diminished breath sounds and increased resonance on the left thorax.
His jugular venous pressure measured up to 12 cm of H2O.
Laboratory results were significant for white blood cell count of 12 200/µL, absolute
neutrophil count of 10 300/µL, bands 8%, hemoglobin 16.1 g/dL, hematocrit 47%, platelets
247 000/µL, sodium 125 mEq/L, potassium 4.3 mEq/L, chloride 91 mEq/L, bicarbonate 24 mEq/L,
blood urea nitrogen 18 mg/dL, creatinine 0.99 mg/dL, glucose 114 mg/dL, albumin 2.7 g/dL,
and calcium of 8.1 mg/dL. Troponins were negative. Lactic acid was 1.7 mmol/L. A stat chest
X-ray revealed the entire left lung occupied by thin-walled bullae, left-to-right
mediastinal shift, heterogeneous opacification of the right upper lobe, and a 1-cm nodule in
the right mid-zone ().
Subsequently, computed tomography (CT) with contrast of the chest was obtained which
revealed giant bullae in the hemithorax, atelectasis of the left lower lobe, peripheral
pneumothorax in posterior medial sulcus as well as the anterolateral base of the hemithorax,
marked mediastinal shift to the right, and consolidation with bronchiectasis in the right
upper/middle/lower lobes ().
Thoracic Surgery was consulted for a video-assisted thoracoscopy for distinguishing the
etiology of tension from giant bullae versus undiagnosed chronic tension pneumothorax and
possible bullectomy. The patient was found to have tension giant bullae and underwent
bullectomy.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [125.0, 'mEq/L'], 'Glucose': [114.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [18.0, 'mg/dL']}",262.7619,249.62381,275.9,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 125.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 125.0 mEq. To convert from 125.0 mEq to mmol, convert from mEq to mmol. The compound 125.0 has a valence of 1, and so divide the valence by the value of mEq to get, 125.0 mEq/(1 mEq/mmol) = 125.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 125.0 mEq sodium/L converts to 125.0 mmol sodium/L. 
The concentration of bun is 18.0 mg/dL. 
The concentration of glucose is 114.0 mg/dL. 
Plugging these values into the equation, we get 2 * 125.0 + (18.0 / 2.8) + (18.0 / 18) = 262.7619 mmol/L.The patient's calculated serum osmolality concentration is 262.7619 mmol/L. This is equalivalent to 262.7619 mOsm/kg."
5877,30,Serum Osmolality,lab test,decimal,pmc-7660023-1,Extracted,"Our case was an eight-month-old boy with mild diarrhea and abnormal movement. He was taken to Erfan Niayesh Hospital. Diarrhea started three days before hospitalization, and the patient had a mild cough with diarrhea. One day after the beginning of diarrhea, the patient had a seizure several times. The seizures were on waking state and in the form of tilting of the lips and blinking and clonic movements of the limbs for a few seconds. During the four hours, the seizures were similarly repeated seven times. The patient did not lose consciousness during the seizure attacks, but, at the end of the seizures, he fell asleep. I would like to inform you that the patient did not have a fever and a runny nose. He was born from nonrelative parents, with birth
weight 3250 gr., weight 9500gr, head circumference equal to 37cm, cesarean section. Parents have had three pregnancies and one abortion, and one healthy baby. He had no major or important problem at birth. Also, he did not have icter at birth. In family history, his father had a seizure at the age of eighteen years. old without any other problem. Meanwhile, the patient’s mother had a scattered cough about three weeks ago. He had normal physical examination and development. The infant could roll over and move forward slightly. The environmental connection was appropriate with age.
First analytical studies showed WBC=8700 (neutrophil=27% and lymphocyte=68%),
Hb=12.7, MCV=80.04 plt=346000, ESR=29, Ca=11.5, Mg=2, Blood sugar=82 , CRP=2,
ALT=30, AST=46, Na=138, K=4.7, BUN=8, Cr=0.5, TSH=5.4, NH3=83, Lactate=15, Urine
Reducing Substance=Negative, CT scan of the lungs were normal
And finally: COVID19 PCR=Target detected Seizures did not recur after phenobarbital was started. The patient was treated for coronavirus infection.
The patient was scheduled to be discharged on an outpatient basis for a brain MRI and EEG(after the quarantine period is over). The patient had no significant problems at the time of discharge.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [138.0, 'mEq/L'], 'Glucose': [82.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [8.0, 'mg/dL']}",283.4127,269.24206,297.58333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 8.0 mg/dL. 
The concentration of glucose is 82.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (8.0 / 2.8) + (8.0 / 18) = 283.4127 mmol/L.The patient's calculated serum osmolality concentration is 283.4127 mmol/L. This is equalivalent to 283.4127 mOsm/kg."
5878,30,Serum Osmolality,lab test,decimal,pmc-2526386-1,Extracted,"A 42-yr-old man who had been in and out of psychiatric hospitals repeatedly since having been diagnosed with schizophrenia in his late teens, according to DSM-IV criteria, presented to the emergency room (E.R.) with an immediate history of vomiting, rigidity, and tremor. The patient had been treated with chlorpromazine 600 mg and benztropine 1 mg daily on an outpatient basis before coming to the E.R. Several months before visiting the E.R., the patient had a cough, felt chilled, and experienced a cold sweat. He visited the internal medicine department of another hospital for these symptoms and he was diagnosed with active pulmonary tuberculosis. Six days before visiting the E.R., he started taking antituberculotic drugs (rifampin 600 mg, isoniazid 400 mg, and pyrazinamide 1,500 mg, daily). Four days before visiting the E.R., his sleep became disturbed, and his speech became limited. Rigidity in all four extremities and tremor in both arms were observed at this time. He also vomited twice before being taken to the E.R. of the university hospital.
His arterial blood pressure was 126/76 mmHg, heart rate was 120 beats/min, and body temperature was 37℃. The patient was delirious, and his verbal output was sparse. He showed severe ""lead pipe"" rigidity and frequent hand tremor. Abnormal laboratory findings included elevated serum creatine kinase (CK 2296.9 IU/L and CK-MB 11.2 ng/mL), uric acid (16.4 mg/dL), aspartate aminotransferase (AST 57 IU/L), glucose (158 mg/dL), myoglobin (557.4 ng/mL), and decreased serum blood urea nitrogen (BUN 6 mg/dL). The serum electrolyte panel (sodium 140 mM/L, potassium 3.7 mM/L, chloride 107 mM/L, carbon dioxide 25 mM/L) and calcium (8.9 mg/dL) were within normal ranges. Leukocytosis was not present, and the pre- and postcontrast brain CT scan did not reveal any abnormal findings.
On the first day in the E.R., chlorpromazine, benztropine, and antituberculotic drugs were discontinued simultaneously, and vigorous intravenous hydration and Foley catheter insertion were carried out to prevent acute renal failure. On the third day in the E.R., the patient was alert and oriented, and subjective improvement was reported. The serum myoglobin level was also normal (46.0 ng/mL). On the fourth day in the E.R., the rigidity in all four extremities improved, but he was still unable to sit up in bed without assistance. The Foley catheter was removed, but hydration was maintained. On the fifth day in the E.R., the serum CK level decreased to 403 IU/L. The patient was alert, ambulatory with help, and was discharged with a psychiatric appointment 1 week later, but without an antipsychotic prescription. One week after discharge, he was rechallenged with an antipsychotic, risperidone 1 mg daily, because of aggravated psychotic symptoms. About 3 months after discharge, he has not shown any specific neuropsychiatric sequelae of NMS and has taken antipsychotics and antituberculotic drugs regularly without any serious adverse events.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mmol/L'], 'Glucose': [158.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [6.0, 'mg/dL']}",290.92063,276.3746,305.46666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mmol/L. 
The concentration of bun is 6.0 mg/dL. 
The concentration of glucose is 158.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (6.0 / 2.8) + (6.0 / 18) = 290.92063 mmol/L.The patient's calculated serum osmolality concentration is 290.92063 mmol/L. This is equalivalent to 290.92063 mOsm/kg."
5879,30,Serum Osmolality,lab test,decimal,pmc-6097298-1,Extracted,"A 62-year-old Sri Lankan Sinhalese man from the North Central Province of Sri Lanka presented with generalized malaise and body weakness. He had type 2 diabetes and had been on Mixtard (human insulin) for 10 years. He had been hypertensive for 5 years and was on losartan potassium. His anti-hypertensive drugs were withheld 2 months previously because he had low-normal blood pressure. He described proximal muscle weakness of the body of 1 month’s duration with difficulty in getting up from a squatting position and raising his hands above his head. He noticed polyuria and nocturia with recent worsening of glycemic control. There was no history of fever, vomiting, diarrhea, or any drug abuse prior to the onset of the symptoms. He denied a suggestive family history of diabetes mellitus, hypertension, or renal disease.
On examination, he was conscious and rational. His blood pressure was 110/64 mm Hg and his pulse was 76/minute. The rest of the cardiovascular system and respiratory system examination was normal. His abdomen was soft and non-tender. A neurological examination revealed normal higher functions and cranial nerves. A motor system examination showed hypotonia of all four limbs and a power of 4/5 in both lower limbs and 5/5 in both upper limbs. All reflexes were present, but diminished. His plantar reflex was bilaterally unresponsive. There was no sensory or autonomic involvement.
Initial blood investigations showed sodium ion (Na+) 146 mEq/L, potassium ion (K+) 1.95 mEq/L, urea 4.3 mmol/L, creatinine 0.7 mg/dl, and random blood glucose 300 mg/dl. His hemoglobin was 13.2 g/dL with white count of 5.7 × 106 and platelets 240 × 106. Transaminases were normal. His serum albumin was 34 g/L. Severe hypokalemia was confirmed in the repeat blood sample. Arterial blood gas revealed severe metabolic alkalosis with pH of 7.6, partial pressure of carbon dioxide (CO2) of 41 mmHg, and bicarbonate of 40.3 mmol/L.
Further investigations revealed the following (Table ). The results of an X-ray of his kidney-ureter-bladder and an ultrasound scan of his kidneys were normal with no evidence of nephrocalcinosis.
He was treated aggressively with intravenously administered potassium chloride, and calcium and magnesium supplements. But he was noted to have persistent hypokalemia with pottasium wasting in urine. Spironolactone was added to the treatment regime. On day 4 while receiving potassium chloride and spironolactone, his serum potassium was 2.6 mmol/L. In this clinical context BS was suspected in our patient. Unfortunately, he could not afford plasma rennin and serum aldosterone levels. He was started on indomethacin 50 mg thrice a day. On day 7 he was noted to have a marked improvement in proximal muscle weakness and his serum potassium reached 3 mmol/L; with the correction of potassium, our patient’s glycemic controlled improved. He was discharged with the advice of liberal salt intake, K+ and magnesium cation (Mg2+) supplements, spironolactone, and indomethacin. He is currently doing well with low normal potassium value with the above treatment.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [146.0, 'mEq/L'], 'Glucose': [300.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [4.3, 'mmol/L']}",312.96988,297.32139,328.61837,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 146.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 146.0 mEq. To convert from 146.0 mEq to mmol, convert from mEq to mmol. The compound 146.0 has a valence of 1, and so divide the valence by the value of mEq to get, 146.0 mEq/(1 mEq/mmol) = 146.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 146.0 mEq sodium/L converts to 146.0 mmol sodium/L. 
The concentration of bun is 4.3 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 4.3 mmol. To convert 4.3 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 4.3 mmol bun * 0.001 mol/mmol = 0.0043 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0043 mol bun * 28.02 g/mol = 0.12049 g bun. To convert 0.12049 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.12049 g bun * 1000.0 mg/g = 120.49 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 120.49 mg bun/10.0 dL = 12.049 mg bun/dL. The concentration value of 4.3 mmol bun/L converts to 12.049 mg bun/dL. 
The concentration of glucose is 300.0 mg/dL. 
Plugging these values into the equation, we get 2 * 146.0 + (12.049 / 2.8) + (12.049 / 18) = 312.96988 mmol/L.The patient's calculated serum osmolality concentration is 312.96988 mmol/L. This is equalivalent to 312.96988 mOsm/kg."
5880,30,Serum Osmolality,lab test,decimal,pmc-3313757-1,Extracted,"A 56-year-old woman was referred to our hospital with a 4–5 day history of nausea, two episodes of vomiting, and few episodes of loose motions, followed by oliguria at home. She denied any history of fever, dysentery, abdominal pain, trauma, muscle pain, or change in color of urine. She also denied history of any drug intake. On enquiring, the patient gave history of longstanding ill health in the form of generalized weakness, easy fatigability, cold intolerance, constipation, hair loss, and weight gain starting after her last child birth some 22 years back. Last delivery was a full-term normal delivery conducted by a local midwife at her home. She denied any history of profuse bleeding or blood transfusion during her last peripartum period. However, she had lactation failure and had menstrual cycles for a few months before complete cessation of menses after her last delivery. Physical examination revealed an ill-looking, dehydrated patient with pulse of 54 beats/ minute, blood pressure of 90/60 mm Hg without any postural drop, respiratory rate of 18/ minute, and oral temperature of 97.6°F (36.4°C). The patient had mild pallor, dry tongue, coarse and dry skin with non-pitting edema of the lower extremities. Hypopigmented area was seen around right nasal orifice and there was loss of lateral eyebrows. Thyroid gland was not palpable and there was no lymphadenopathy. Her breasts were atrophic and sparse axillary and pubic hair was noticed. Chest, cardiovascular, and abdominal examinations were non-contributory. Central nervous system examination revealed slow mentation in the form of delayed response to verbal commands. Examination of motor system did not reveal any focal neurodeficit, but deep tendon jerks were markedly delayed.
Laboratory evaluation revealed normochromic normocytic anemia. Liver function tests were normal except for low albumin. Kidney function test was deranged with initial urea of 71 mg/dl (normal value 20–40 mg/dl) and serum creatinine of 4.5 mg/dl (normal value 0.5–1.5 mg/dl). Muscle enzymes were slightly elevated with creatine phosphokinase (CPK) being 168 1U/l (normal value 10–70 IU/l) and lactate dehydrogenase (LDH) was 983 U/l (normal value 200–450 U/l). Arterial blood gas and electrolyte analysis revealed pH of 7.31, PCO2 of 27 mm Hg, bicarbonate of 13 mmol/l, serum sodium 130 mmol/l, and potassium of 3.6 mmol/l. Plasma glucose was only 38 mg/dl. Chest X-ray was normal and 12-lead ECG revealed sinus bradycardia with low-voltage QRS complex. Routine urine examination revealed pus cells 4–5, RBCs 2–3, absent albumin and casts. Renal ultrasound revealed relatively small-sized kidneys (right 8.5 × 3.2 cm, left 8.7 × 3.4 cm) with increased echogenicity, with maintained corticomedullary differentiation bilaterally. Her hormone profile revealed panhypopituitarism []. The diagnosis of panhypopituitarism most likely secondary to SS associated with acute renal failure was made on the basis of her past medical history of failure to lactate post her last child birth with gradual cessation of menses, peripheral signs and symptoms of hypothyroidism, and abnormal biochemical and hormone profile.
The patient was given intravenous fluids in the form of dextrose normal saline with close monitoring of urine output, replacement therapy in the form of intravenous hydrocortisone 50 mg intravenously 6 hourly, and levothyroxine given orally at a starting dose of 50 mcg/ day. The patient was also given intravenous antibiotics and antiemetics. Urine output began to improve on the 2nd day of admission. Her appetite also improved and there was complete cessation of vomiting. On repeating renal function tests and other biochemical tests, there was dramatic improvement in serial renal function parameters. With improvement in the general condition of the patient, intravenous antibiotics were stopped in view of absence of fever and negative septic screen. She was shifted to oral prednisolone 5 mg twice daily, while levothyroxine was continued at a dose of 50 mcg/day. The serial biochemical parameters of the patient are given in . She was discharged on the same medication on 10th day of admission and was advised to taper prednisolone to 5 mg/ day after 2 weeks. Four weeks after discharge, the patient had general sense of well-being with better appetite and renal function had normalized with creatinine 0.64 mg/ dl and serum urea 23 mg/dl. The patient was subjected to magnetic resonance imaging (MRI) brain with sellar and parasellar focus which revealed empty sella with normal rest of the brain parenchyma [].",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [130.0, 'mmol/L'], 'Glucose': [38.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [71.0, 'mg/dL']}",287.46825,273.09484,301.84166,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 130.0 mmol/L. 
The concentration of bun is 71.0 mg/dL. 
The concentration of glucose is 38.0 mg/dL. 
Plugging these values into the equation, we get 2 * 130.0 + (71.0 / 2.8) + (71.0 / 18) = 287.46825 mmol/L.The patient's calculated serum osmolality concentration is 287.46825 mmol/L. This is equalivalent to 287.46825 mOsm/kg."
5881,30,Serum Osmolality,lab test,decimal,usmle-5824,Extracted,"A 57-year-old man presents to the emergency department with dizziness and an episode of fainting that occurred when he stood up from using the bathroom. Since then, he states he has felt generally uncomfortable and uneasy. The patient has a past medical history of obesity, and his current medications include atorvastatin, aspirin, and ibuprofen. He has not visited a physician in over three years and is notably non-compliant with his medications. The patient's lab values are ordered and return as below:

Serum:
Na+: 137 mEq/L
K+: 3.6 mEq/L
Cl-: 100 mEq/L
HCO3-: 24 mEq/L
Urea nitrogen: 15 mg/dL
Glucose: 110 mg/dL
Creatinine: 1.2 mg/dL
Ca2+: 9.9 mg/dL

An EKG is ordered as seen in Figure A. His temperature is 99.5°F (37.5°C), blood pressure is 100/65 mmHg, pulse is 80/min, respirations are 11/min, and oxygen saturation is 96% on room air. Physical exam reveals a middle-aged man who appears uncomfortable. Pulmonary exam is notable for mild bilateral crackles. Cardiac exam is notable for a rapid rate and thready distal pulses. Neurological exam is within normal limits.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [137.0, 'mEq/L'], 'Glucose': [110.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [15.0, 'mg/dL']}",285.46825,271.19484,299.74166,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 15.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (15.0 / 2.8) + (15.0 / 18) = 285.46825 mmol/L.The patient's calculated serum osmolality concentration is 285.46825 mmol/L. This is equalivalent to 285.46825 mOsm/kg."
5882,30,Serum Osmolality,lab test,decimal,pmc-7313116-1,Extracted,"We present a 32-year-old transgender female with a past medical history most significant for depression with suicidal ideation who presented to our hospital due to an acute onset of nausea and lethargy with one episode of nonbloody emesis. Symptoms were not alleviated or exacerbated by any specific factors. The patient had purchased a Cerbera odollam plant on the internet a week prior. She ingested one seed of this plant, as this was suggested to be the lethal dose, with the intent of ending her life. The exact time between ingestion and presentation was unknown. On transportation to the hospital, the patient had a documented heart rate in the 30s with a junctional rhythm and therefore received a total of 10 vials of Digibind (digoxin immune fab). She denied any headache, visual disturbances, chest pain, palpitations, shortness of breath, abdominal tenderness, diarrhea, or constipation.
On presentation, the patient's vital signs were blood pressure of 105/74 mmHg, heart rate of 106 beats per minute, respiratory rate of 18 breaths per minute, body temperature at 98.6 degrees F, and oxygen level of 98% on room air. Physical examination was noted as within normal limits. Labs performed included urine toxicology which was positive for cannabis, digoxin level 0.2 ng/mL, salicylate level less than 1.7 mg/dL, acetaminophen level less than 2 mcg/mL, blood alcohol content of 0, lactic acid 1.2 mmol/L, white blood cell count 8,100/μL, hemoglobin 13.9 g/dL, hematocrit 40.8%, platelets 165/μL, sodium 138 mmol/L, potassium 4.3 mmol/L, chloride 103 mmol/L, bicarbonate 29 mmol/L, blood urea nitrogen 10 mg/dL, creatinine 0.84 mg/dL, glucose 107 mg/dL, total bilirubin 0.5 mg/dL, AST 37 U/L, ALT 61 U/L, and alkaline phosphatase 48 U/L.
Electrocardiogram (ECG) was performed shortly after arrival. This demonstrated a significant decrease in heart rate as compared to presenting vital signs. The heart rate had decreased from 106 beats per minute to 36 beats per minute (). Therefore, the patient was monitored on telemetry, and repeat ECGs were ordered. Her heart rate remained in the 30s to 40s, and the rhythm was sinus bradycardia. Upon consultation, the toxicology team recommended to monitor electrolytes and heart rate closely while continuing intravenous fluids. If there were any conduction blocks or further slowing of heart rate, 5 more vials of Digibind could be given. She had a hypoglycemic episode with blood glucose of 60 mg/dL. She was administered dextrose and responded appropriately.
The following day, the psychiatry team was consulted, and the patient was diagnosed with gender dysphoria and depressive disorder and noted to have narcissistic and borderline personality traits. The patient met the criteria for inpatient psychiatric hospitalization once medically cleared.
The toxicology team continued to follow the patient during her hospitalization. Being that her digoxin level was only 0.2 ng/mL and she had normalized potassium levels, her likelihood for toxicity was low. Given her lab work and improving heart rate on ECGs (Figures and ), the team was reassured that the patient's clinical status was improving. The patient's home hormonal therapy was started, and she was admitted to the psychiatry unit.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [138.0, 'mmol/L'], 'Glucose': [107.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [10.0, 'mg/dL']}",285.51587,271.24008,299.79166,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mmol/L. 
The concentration of bun is 10.0 mg/dL. 
The concentration of glucose is 107.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (10.0 / 2.8) + (10.0 / 18) = 285.51587 mmol/L.The patient's calculated serum osmolality concentration is 285.51587 mmol/L. This is equalivalent to 285.51587 mOsm/kg."
5883,30,Serum Osmolality,lab test,decimal,pmc-2943688-1,Extracted,"Patient: 63-year-old male
Major complaint: Fever
Pre-existing history: Mitral valve insufficiency
Family history/lifestyle history: Nothing particularly relevant
A slight fever had persisted from about June 2008 until 10 days before surgey. In July 2008, the patient underwent a TUR-P for prostatic hyperplasia using 3 days of cefotiam (CTM) i.v. 0.5g ×2/day and was discharged from the hospital on Day 10 after surgery without fever. On about Day 40 after surgery, a fever of 38–39°C was observed, so the patient was suspected of having a urinary-tract infection and was admitted to the hospital.
Body height: 166.3 cm; Body weight: 59.5 kg; Body temperature: 37.8°C; Pulse rate: stable at 84/min; Blood pressure: 116/76 mmHg. Respiratory sound: resonant; Cardiac sound: clear/no noise; Abdomen: flat/soft; Neurological findings: nothing in particular. Laboratory data at the time of admission:
Hematological values: WBC 9000/µL, RBC 4.01 × 106/µL, Hb 10.3 g/dL, Ht 30.5 %, Plt 36.6 × 104/µL , PT 78 %, PT-INR 1.14, APTT 29.4 sec, Fib 628 mg/dL
Biochemistry: TP 6.8 g/dL, Alb 3.2 g/dL, T-bil 0.5 mg/dL, D-bil 0.0 mg/dL, AST 24 IU/L, ALT 35 IU/L, ALP 631 IU/L, γ-GTP 102 IU/L, Ch.E 198 IU/L, LDH 203 IU/L, CK 18 IU/L, Amy 71 IU/L, T-chol 193 mg/dL, TG 80 mg/dL, LDL 122 mg/dL, BUN 9 mg/dL, Cre 0.7 mg/dL, UA 2.4 mg/dL, Na 139 mEq/L, K 4.2mEq/L, Cl 103 mEq/L, Ca 9.4 mg/dL, IP 3.5 mg/dL, Glu 95 mg/dL, HbA1c 5.4%, CRP 5.6 mg/dL
Urinalysis: pH 7.5, RBC many/hpf, WBC many/hpf
After admission, CTM 0.5 g × 2/day was administered for 3 days, but the CRP did not become negative, so Meropenem (MEPM) 0.5 g × 2/day was administered instead. A tendency for pyretolysis was observed, but because recovery from the urinary-tract infection was slow, echocardiography was performed for the purpose of eliminating endocarditis. In the echocardiogram findings, vegetation was observed, so Ampicillin (ABPC) 2 g × 4/day and Gentamicin (GM) 60 mg × 2/day were administered for four weeks. Pyretolysis and decreased CRP were observed, but the CRP did not become negative. Even after the 4-week administration of antibiotics, the vegetation persisted in the echocardiogram and a possibility of valve failure was suspected, so a valve replacement was performed. Furthermore, the head and chest to pelvic CT did not show any obvious abscess formation.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [139.0, 'mEq/L'], 'Glucose': [95.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [9.0, 'mg/dL']}",286.49206,272.16746,300.81666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 9.0 mg/dL. 
The concentration of glucose is 95.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (9.0 / 2.8) + (9.0 / 18) = 286.49206 mmol/L.The patient's calculated serum osmolality concentration is 286.49206 mmol/L. This is equalivalent to 286.49206 mOsm/kg."
5884,30,Serum Osmolality,lab test,decimal,pmc-2633322-1,Extracted,"We are presenting a case with acute abdomen, i.e. ileum perforation, caused by accidentally ingesting a chicken wishbone.
A fifty-year-old male was presented in the surgical emergency clinic with abdominal pain, nausea, and vomiting. The symptoms had started two days earlier. He used tobacco, but denied having consumed alcohol. The patient's height was 170 cm and his weight was 120 kg. His vital signs were: blood pressure 120/80 mmHg; pulse rate 90 beats/min.; respiration rate 19/min.; body temperature 38.5°C. His past medical history consisted of surgery for a thrombophlebitis in his right arm one year earlier.
Upon physical examination, a distended and diffusely tender abdomen with right lower abdomen rebound was revealed. The patient's skin and mucosa were pale.
The emergent laboratory tests revealed as follow: white blood cells (WBC): 12.6 × 109/liter; serum creatinine: 126 mol/L; blood urea nitrogen: 8.6 mmol/L; blood sugar: 11.6 mmol/L; Na: 141 mmol/L; K: 4.0 mmol/L; Ca++: 1.08 mmol/L; urinalysis: a lot of mucus, 4–6 Leucocytes; some epithelial cells. Plain abdominal radiography showed mechanical obstruction. Urgent abdominal ultrasound revealed mechanical obstruction, dilated small bowels and free liquid in the peritoneal cavity.
Laparotomy was performed in general anesthesia on the day the patient was admitted. Intra operative findings revealed diffuse fibro purulent peritonitis with adhesions between small bowels; and about 40 cm from Bauchini valve the presence of a sharp chicken wishbone perforated the ileum at the ante mesenteric site (Figure ). The wall of that part of the ileum was thick and succulent. The patient was treated after the adhesiolisis with resection of the perforated distal ileum and ileum stoma. The postoperative treatment went well; the wound healed per secundum. Clebsiela spp. was isolated in the stained abdominal liquid and treated with the proper antibiotics. Four months after the first operation and losing 25 kg, the patient underwent reconstruction of bowel continuity, and discharged on the tenth postoperative day with normal bowel movements.
Retrospectively, after the first operation the patient admitted that four days earlier he had rapidly eaten and swallowed several mouthfuls of chicken meat without chewing and accidentally ingested a chicken bone.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [141.0, 'mmol/L'], 'Glucose': [11.6, 'mmol/L'], 'Blood Urea Nitrogen (BUN)': [8.6, 'mmol/L']}",302.2164,287.10558,317.32722,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mmol/L. 
The concentration of bun is 8.6 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 8.6 mmol. To convert 8.6 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 8.6 mmol bun * 0.001 mol/mmol = 0.0086 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0086 mol bun * 28.02 g/mol = 0.24097 g bun. To convert 0.24097 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.24097 g bun * 1000.0 mg/g = 240.97 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 240.97 mg bun/10.0 dL = 24.097 mg bun/dL. The concentration value of 8.6 mmol bun/L converts to 24.097 mg bun/dL. 
The concentration of glucose is 11.6 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 11.6 mmol. To convert 11.6 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 11.6 mmol glucose * 0.001 mol/mmol = 0.0116 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0116 mol glucose * 180.16 g/mol = 2.08986 g glucose. To convert 2.08986 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 2.08986 g glucose * 1000.0 mg/g = 2089.86 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 2089.86 mg glucose/10.0 dL = 208.986 mg glucose/dL. The concentration value of 11.6 mmol glucose/L converts to 208.986 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (24.097 / 2.8) + (24.097 / 18) = 302.2164 mmol/L.The patient's calculated serum osmolality concentration is 302.2164 mmol/L. This is equalivalent to 302.2164 mOsm/kg."
5885,30,Serum Osmolality,lab test,decimal,pmc-5010060-1,Extracted,"We report a case of 64-years-old female patient scheduled for replacement of severely stenosed aortic valve (AS) of degenerative etiology. Coronary angiogram was performed, in presurgery period, and revealed as follows: Left main, LAD, CX and RCA showed no signs of coronary disease. Trans thoracic echocardiogram (TTE) verified concentric hypertrophy of the left ventricle (IVS 1.45cm), normal dimension of heart chambers and good Ejection fraction (EF 55%), severe aortic stenosis (AVA less than 1cm2, Vmax5.04m/sec., PGmean62.5mmHg, PGmax102mmHg). In previous medical history patient had verified COPD and was suffering from chest pain and effort dyspnea. Laboratory findings at the day of surgery were as follows: Glucosis 7.10, Urea 9.20, Sodium 140, Potassium 3.8, WBC 6.54, RBC 4.08, Htc 0.367, PLT 202, Preoperative ECG: Regular sinus rithm, Heart rate 103bpm, depressed descending ST junction and R height 25mm in precordial leads V4-V6(signs of LV hypertrophy).",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mEq/L'], 'Glucose': [7.1, 'mmol/L'], 'Blood Urea Nitrogen (BUN)': [9.2, 'mmol/L']}",296.31276,281.49712,311.1284,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 9.2 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of bun from mmol to mg. The mass of bun is 9.2 mmol. To convert 9.2 mmol of bun to mol, multiply by the conversion factor 0.001, giving us 9.2 mmol bun * 0.001 mol/mmol = 0.0092 mol bun. To convert from mol bun to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0092 mol bun * 28.02 g/mol = 0.25778 g bun. To convert 0.25778 g of bun to mg, multiply by the conversion factor 1000.0, giving us 0.25778 g bun * 1000.0 mg/g = 257.78 mg bun. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 257.78 mg bun/10.0 dL = 25.778 mg bun/dL. The concentration value of 9.2 mmol bun/L converts to 25.778 mg bun/dL. 
The concentration of glucose is 7.1 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of glucose from mmol to mg. The mass of glucose is 7.1 mmol. To convert 7.1 mmol of glucose to mol, multiply by the conversion factor 0.001, giving us 7.1 mmol glucose * 0.001 mol/mmol = 0.0071 mol glucose. To convert from mol glucose to grams, multiply by the molar mass 180.16 g/mol, which will give 0.0071 mol glucose * 180.16 g/mol = 1.27914 g glucose. To convert 1.27914 g of glucose to mg, multiply by the conversion factor 1000.0, giving us 1.27914 g glucose * 1000.0 mg/g = 1279.14 mg glucose. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1279.14 mg glucose/10.0 dL = 127.914 mg glucose/dL. The concentration value of 7.1 mmol glucose/L converts to 127.914 mg glucose/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (25.778 / 2.8) + (25.778 / 18) = 296.31276 mmol/L.The patient's calculated serum osmolality concentration is 296.31276 mmol/L. This is equalivalent to 296.31276 mOsm/kg."
5886,30,Serum Osmolality,lab test,decimal,pmc-4705711-1,Extracted,"A 2.5-year-old-male child was brought with a chief complaint of acute onset drooping of the right upper eyelid that persisted without improvement for 5 days. There was a preceding history of fever of 8 days duration followed by a vesicular eruption on the right scalp and forehead extending to the tip of the nose. Prior to the presentation at our institution, he had received oral paracetamol 5 ml t.i.d and Neosporin eye ointment applied locally. There was no improvement of condition with the treatment. Review of systems was negative for a history of seizures, throat pain, and no similar rashes in any other part of the body. The child was afebrile and quiet with the pulse rate of 88/min and respiratory rate of 28/min.
Ocular examination revealed right eye axial proptosis with restriction of extraocular movements in dextroversion. There was a moderate blepharoptosis on the right side. Visual acuity was grossly normal. The anterior segment and fundus examination revealed no abnormalities. The left eye was normal [].
The remainder of the physical examinations was normal except for right submandibular and cervical lymphadenopathy. There were multiple healed hyperpigmented lesions on the right side of the scalp, forehead, and nose, suggestive of herpes zoster infection. There were no signs of meningitis.
Hematological examination showed a total leukocyte count - 12,700 cells/mm cu, neutrophils - 59%, lymphocytes - 49%, hemoglobin - 10.8 g/dl, platelet count - 411,000 cells/mm cu, random blood sugar - 95 mg/dl, Na/K - 138/4.8 mg/dl, urea/creatinine - 10/0.2 mg/dl, prothrombin time - 16 s, international normalized ratio - 1.26, HIV/hepatitis B surface antigen/hepatitis C virus test - negative, and amylase - 27 IU/L (25–200). Microbiological examination of the urine was normal. Blood and urine cultures revealed no organism. Ultrasonography of parotid region showed bulky right parotid gland, heterogeneous with multiple intraparotid lymph nodes, the largest measuring 9.5 mm. The left parotid gland was normal. There were multiple enlarged bilateral upper, mid, and lower cervical lymph nodes, the largest measuring 15 mm. X-ray of the chest and paranasal sinuses were normal. Computed tomography (CT) scan of the orbit and head showed orbital abscess in the right retrobulbar space and right cavernous sinus enlargement with filling defect suggestive of thrombosis. Maxillary and ethmoidal sinuses had features suggestive of sinusitis [Fig. and ]. The child was commenced on intravenous injection vancomycin 60 mg/kg/day in two divided doses, amikacin 20 mg/kg 3 times daily and oral acyclovir 30 mg/day for 14 days. In a view of stable general condition, we continued with oral acyclovir. Intravenous antibiotics were added to treat intraorbital abscess with maxillary and ethmoidal sinusitis.
With treatment, ptosis and proptosis improved, and the patient regained full extraocular movements. Visual acuity was grossly normal. The patient was discharged after 2 weeks on oral Augmentin for further 2 weeks. At 5 months follow-up, the condition was improved [].",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [138.0, 'mEq/L'], 'Glucose': [95.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [10.0, 'mg/dL']}",284.84921,270.60675,299.09167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. 
The concentration of bun is 10.0 mg/dL. 
The concentration of glucose is 95.0 mg/dL. 
Plugging these values into the equation, we get 2 * 138.0 + (10.0 / 2.8) + (10.0 / 18) = 284.84921 mmol/L.The patient's calculated serum osmolality concentration is 284.84921 mmol/L. This is equalivalent to 284.84921 mOsm/kg."
5887,30,Serum Osmolality,lab test,decimal,usmle-5962,Extracted,"A 59-year-old African American woman presents to the emergency department for fever and back pain that has persisted for 2 days. The patient states that the pain is episodic and intense. Her symptoms have not responded to acetaminophen. The patient endorses having lost 7 pounds recently without trying to lose weight. She also states that she has had abdominal pain and trouble focusing at work as well as a recent cough and fever which she attributes to allergies. The patient’s past medical history is notable for a recent distal radius fracture and a 50 pack-year smoking history. Her temperature is 99.5°F (37.5°C), blood pressure is 127/67 mmHg, pulse is 99/min, respirations are 14/min, and oxygen saturation is 98% on room air. Physical exam is notable for left-sided flank tenderness. The patient assumes an antalgic position in the stretcher. Chest radiography is performed as seen in Figure A. Laboratory studies are ordered as seen below.

Hemoglobin: 14 g/dL
Hematocrit: 44%
Leukocyte count: 10,500/mm^3 with normal differential
Platelet count: 195,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Phosphate: 1.5 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 12.2 mg/dL
AST: 12 U/L
ALT: 10 U/L

Ultrasound reveals unilateral hydronephrosis.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [139.0, 'mEq/L'], 'Glucose': [99.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL']}",290.64286,276.11072,305.175,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (20.0 / 2.8) + (20.0 / 18) = 290.64286 mmol/L.The patient's calculated serum osmolality concentration is 290.64286 mmol/L. This is equalivalent to 290.64286 mOsm/kg."
5888,30,Serum Osmolality,lab test,decimal,usmle-8023,Extracted,"A 75-year-old man presents to the emergency department with a racing heart and lightheadedness for 3 hours. He has had similar episodes in the past, but the symptoms never lasted this long. He denies chest pain, shortness of breath, headaches, and fevers. He had a myocardial infarction 4 years ago and currently takes captopril, metoprolol, and atorvastatin. His pulse is irregular and cardiac auscultation reveals an irregular heart rhythm. Laboratory reports show:
Serum glucose 88 mg/dL
Sodium 142 mEq/L
Potassium 3.9 mEq/L
Chloride 101 mEq/L
Serum creatinine 0.8 mg/dL
Blood urea nitrogen 10 mg/dL
Cholesterol, total 170 mg/dL
HDL-cholesterol 40 mg/dL
LDL-cholesterol 80 mg/dL
Triglycerides 170 mg/dL
Hematocrit 38%
Hemoglobin 13 g/dL
Leucocyte count 7,500/mm3
Platelet count 185,000 /mm3
Activated partial thromboplastin time (aPTT) 30 seconds
Prothrombin time (PT) 12 seconds
Cardiac enzymes Negative
An ECG shows the absence of P-waves with an irregular RR complex. A few hours later, his symptoms subside and he is discharged with an additional anticoagulation drug.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [142.0, 'mEq/L'], 'Glucose': [88.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [10.0, 'mg/dL']}",292.46032,277.8373,307.08334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. 
The concentration of bun is 10.0 mg/dL. 
The concentration of glucose is 88.0 mg/dL. 
Plugging these values into the equation, we get 2 * 142.0 + (10.0 / 2.8) + (10.0 / 18) = 292.46032 mmol/L.The patient's calculated serum osmolality concentration is 292.46032 mmol/L. This is equalivalent to 292.46032 mOsm/kg."
5889,30,Serum Osmolality,lab test,decimal,pmc-4530922-1,Extracted,"A 56-year-old male was brought to the emergency department by paramedics for a syncopal episode and inability to move his lower extremities. He complained of abdominal pain and inability to move his legs beginning five hours prior to arrival. He awakened from a nap that afternoon and experienced numbness in both legs, which progressed to paralysis. At baseline, he was ambulatory without any history of weakness and was last ambulatory hours prior. He endorsed occasional pain in his legs when walking at baseline.
He also complained of abdominal pain with nausea and vomiting for two days. He had a history of alcohol use and reported dark-colored emesis and last bowel movement three days prior. On review of symptoms the patient denied any history of headache, dizziness, chest pain, back pain, trauma, fevers, or extremity weakness. He walked longer than a mile the day prior. History from the patient’s wife revealed that he had an episode of altered level of consciousness while on the couch and that finding combined with his abdominal pain and paralysis prompted her to call 911. The patient’s past medical history was significant for hypertension, peripheral arterial disease, and myocardial infarction 10 years prior. His past surgical history included “abdominal stents” and a left carotid stent. His social history was significant for a 25-pack/year history of smoking and daily alcohol. His medications included atenolol and ranitidine.
Physical exam showed an oral temperature of 36.7°C, blood pressure 107/65mmHg, heart rate 99 beats/minute and a respiratory rate of 30 breaths/min, with oxygen saturation on 15L non-rebreather mask of 94%. His weight was 72.5kg and he appeared older than his stated age. He was alert, cooperative and in moderate distress, primarily complaining of pain and cramping in his lower extremities and repeatedly asking staff to straighten out his legs although they were already lying straight and motionless on the gurney. His head exam was unremarkable with the exception of a dry oropharynx. Cervical spine, cardiac, and lung exams were unremarkable. His abdomen was firm and diffusely tender to palpation with generalized rebound and guarding. An irreducible left inguinal hernia was present. He had vomiting, and placement of a nasogastric tube revealed 1.5 liters of coffee-ground emesis. Lower extremities were thin, cool, and without any palpable or Dopplerable pulses in bilateral femoral, popliteal or pedal distribution. There was trace non-reproducible sensation to the mottled lower extremities, and no sensation distal to the ankles. Motor exam was significant for lower extremity paralysis.
Laboratory data consisted of sodium 121mEq/L (135–145), potassium 6.8mEq/L (3.3–4.8), chloride 89mEq/L (101–111), CO2 18mEq/L (25–34), BUN 31mg/dL (8–26), creatinine 1.5mg/dL (0.5–1.3), and blood glucose 367mg/dL (70–115). White blood cell 19.1thous/mcL (4.0–10.5), hemoglobin 12.8g/dL (13.5–16.9), lipase 107U/L (22–51), hematocrit 38.8% (39.5–50.0), and platelets 165thous/mcL (150–400). There was a left shift in the neutrophils 16.2thous/mcL (85%) (2.0–8.1). Alkaline phosphate 88IU/L (26–110), AST 84IU/L (8–40), ALT 38IU/L (0.0–60), total bilirubin 1mg/dL (0.0–1.4), total protein 5.4g/dL (6.1–8.2), albumin 2.6g/dL (3.2–5.5). Lactate 7.2mmol/L (0.7–2.1). ABG showed pH of 7.25 (7.38–7.42), pCO2 31.6mmHg (36–42), pO2 123.6mmHg (80–104), bicarbonate 13.5mmol/L (21–27). PT was 17.3sec (9.5–12.3), PTT 45.9sec (24.1–35.1), and INR 1.62 (0.87–1.14). B-type natriuretic peptide 1,950pg/mL (<100). Troponin 2.75ng/mL (<0.03).
Chest radiograph was unremarkable. Electrocardiogram (ECG) showed sinus rhythm at 95 beats/minute with ST elevation inferiorly, anteriorly and laterally (). Bedside ultrasound to evaluate the abdominal aorta was limited. Vascular surgery was consulted prior to CT for concern of a vascular catastrophe. Cardiology was consulted for the patient’s ECG findings consistent with myocardial infarction. The patient went for a non-contrast head CT that was unremarkable and a CT angiogram of the chest, abdomen and pelvis, which was significant for the abdominal aorta with no contrast opacification 2.2cm superior to the bifurcation (), high-grade stenosis of the right common iliac artery, complete occlusion of the left common iliac artery, stents in the celiac artery and superior mesenteric artery (SMA), evidence of occlusion of the proximal SMA and inferior mesenteric artery (IMA), hepatic, splenic, bilateral renal infarctions, left inguinal hernia, bowel obstruction, pneumatosis intestinalis with evidence of ischemic bowel, and aspiration in the right lower lung. General surgery was consulted.
The cardiology service stated that the patient was not a candidate for cardiac catheterization and to start anticoagulation and low-dose aspirin if there was no contraindication or planned surgery. They also recommended thrombolytics for the diffuse thrombotic disease. The patient did have an echocardiography study that revealed an ejection fraction of 35% and multiple regional wall motion abnormalities. General surgery recommended comfort measures as he was not a surgical candidate. Vascular surgery commented that bypass would be futile and if patient survived, would be a candidate for extra-anatomical axillo-bifemoral bypass in the future. The patient was admitted to the medical intensive care unit for broad-spectrum antibiotics and a heparin drip and succumbed to his illness the following day.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [121.0, 'mEq/L'], 'Glucose': [367.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [31.0, 'mg/dL']}",273.46032,259.7873,287.13334,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 121.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 121.0 mEq. To convert from 121.0 mEq to mmol, convert from mEq to mmol. The compound 121.0 has a valence of 1, and so divide the valence by the value of mEq to get, 121.0 mEq/(1 mEq/mmol) = 121.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 121.0 mEq sodium/L converts to 121.0 mmol sodium/L. 
The concentration of bun is 31.0 mg/dL. 
The concentration of glucose is 367.0 mg/dL. 
Plugging these values into the equation, we get 2 * 121.0 + (31.0 / 2.8) + (31.0 / 18) = 273.46032 mmol/L.The patient's calculated serum osmolality concentration is 273.46032 mmol/L. This is equalivalent to 273.46032 mOsm/kg."
5890,30,Serum Osmolality,lab test,decimal,pmc-7500016-1,Extracted,"A 68-year-old Hispanic man with ESRD initially presented to an outside urgent care clinic with a 3-day history of a painful rash over the right thorax. His examination revealed a dermatomal, vesicular eruption at the T9 dermatome consistent with zoster reactivation. He was started on oral acyclovir 800 mg five times daily. The recommended renal dosing for a patient receiving dialysis would have been 200 mg twice daily. Over the following 4 days, his family noted progressively worsening confusion. On the day of admission, the patient’s son called emergency medical services due to the patient’s confusion, agitation, and auditory hallucinations. Prior to this presentation, the patient had lived independently and was able to complete all activities of daily living without assistance. His past medical history included ESRD, hypertension, type 2 diabetes mellitus, anemia due to chronic renal disease, and secondary hyperparathyroidism. Prior to arrival at our hospital, his medications included amlodipine 5 mg oral once daily, aspirin 81 mg oral once daily, metoprolol succinate 150 mg oral once daily, and 20 units of insulin NPH-regular 70–30% twice daily. Oral acyclovir 800 mg five times daily was the only new medication, started 4 days prior to arrival. He received outpatient dialysis three times weekly. Per the report of his family, he did not smoke or drink alcohol. His family was unaware of any family history of neurologic disorders. He was unemployed and had no recent travel exposures. He had not been previously vaccinated against VZV.
Upon physical examination, he was agitated and oriented only to self. His vital signs upon presentation included a body temperature of 37.3 °C, heart rate of 100 beats per minute, blood pressure of 177/90 mmHg, respirations of 20 breaths per minute, and oxygen saturation of 93% on 2 L by nasal cannula. Examination of the patient’s head and neck revealed no signs of trauma. His pupils were equal, round, and reactive to light. His oropharyngeal examination revealed dry mucous membranes but no lesions or ulcers. His pulmonary examination result was clear to auscultation bilaterally. His cardiovascular examination revealed normal heart sounds without murmurs, rubs, or gallops. His abdomen was nontender and without signs of guarding. His extremities were warm, and no lower extremity edema was present. His musculoskeletal examination revealed normal range of motion and no joint erythema or effusions. His skin examination revealed a right-sided rash with erythematous papules with vesicles along the T9 dermatome (see Fig. ). Upon neurologic examination, he was unable to follow commands for testing cranial nerves, strength, or coordination. His speech was dysarthric but not aphasic. He moved all extremities spontaneously and withdrew to pain. His reflexes were 3+ bilaterally in the upper and lower extremities with no clonus and a negative Babinski sign. His muscle tone was normal.
His laboratory studies were notable for a serum glucose level of 170 mg/dl, sodium level of 133 mEq/L, blood urea nitrogen level of 43 mg/dl, creatinine level of 5.90 mg/dl, calcium level of 8.5 mg/dl, white blood cell count of 6.8 × 109 cells/L, hemoglobin level of 11.5 g/dl, and platelet count of 239 × 109 cells/L. His thyroid-stimulating hormone level was 2.95 mIU/L. The result of his urine drug screen was negative, and his ethanol level was <10 mg/dl. The result of his urinalysis was negative for leukocyte esterase or nitrites.
MRI of the patient’s brain did not reveal large-territory infarct or evidence of vasculopathy. His electroencephalogram demonstrated diffuse slowing and disorganization consistent with a toxic-metabolic encephalopathy, but he had no epileptic discharges. His chest x-ray did not reveal any pulmonary infiltrates or evidence of pneumonia. CSF studies showed a protein level of 85 mg/dl, glucose level of 76 mg/dl, no red blood cells, no white blood cells, and no organisms on Gram staining. His CSF PCR result was positive for VZV and negative for other common etiologies of bacterial or viral encephalitis.
The emergency department did not initially have access to his prior urgent care pharmacy records. Upon receiving the positive VZV CSF PCR result, he was started on intravenous acyclovir renally dosed at 5 mg/kg and was admitted to the medicine service for his acute encephalopathy. With common toxic and metabolic causes of encephalopathy ruled out in the emergency department, our primary differential diagnosis was between VZV encephalitis and AIN. Uremic encephalopathy was also included in our differential diagnosis. However, review of the outpatient dialysis records revealed adequately dosed dialysis, as evident by achieving target dialysis clearance parameters and no missed dialysis sessions, making this diagnosis unlikely. When the outside pharmacy records arrived, revealing inappropriate acyclovir dosing, AIN became the favored diagnosis. Acyclovir was stopped, and serum drug levels were sent to a reference laboratory. CSF titers for anti-VZV immunoglobulin M (IgM) and IgG were also pending at this time.
Nephrology was consulted, and the patient underwent two 4-hour dialysis sessions on consecutive days, after which his neurologic status improved significantly. His hospital course was not complicated by other evidence of infection, electrolyte abnormalities, or hypoglycemia that could have contributed to his acute encephalopathy. By hospital day 4, he had returned to his baseline neurologic status. On hospital day 5, he had a normal neurologic examination result and was discharged to home. At follow-up 6 months later, the patient had experienced no further episodes of confusion, dysarthria, or hallucinations and was living independently. The temporal onset of hallucinations, dysarthria, and confusion after initiating acyclovir therapy combined with the rapid improvement after discontinuation of acyclovir and initiating hemodialysis made AIN the likely diagnosis.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [133.0, 'mEq/L'], 'Glucose': [170.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [43.0, 'mg/dL']}",290.80159,276.26151,305.34167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 133.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 133.0 mEq. To convert from 133.0 mEq to mmol, convert from mEq to mmol. The compound 133.0 has a valence of 1, and so divide the valence by the value of mEq to get, 133.0 mEq/(1 mEq/mmol) = 133.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mEq sodium/L converts to 133.0 mmol sodium/L. 
The concentration of bun is 43.0 mg/dL. 
The concentration of glucose is 170.0 mg/dL. 
Plugging these values into the equation, we get 2 * 133.0 + (43.0 / 2.8) + (43.0 / 18) = 290.80159 mmol/L.The patient's calculated serum osmolality concentration is 290.80159 mmol/L. This is equalivalent to 290.80159 mOsm/kg."
5891,30,Serum Osmolality,lab test,decimal,pmc-3245397-1,Extracted,"A 16-year-old female was referred to our hospital for management of bromate intoxication. She had been in good health until she ingested 75 mL of cold wave neutralizer in a suicide attempt. Within one hour of ingestion she developed nausea, vomiting, and diffuse abdominal pain. Upon arrival to the emergency room of another hospital, she received gastric lavage. During a second hospital admission, her urinary output decreased and she was referred to our hospital. Physical examination upon admission revealed the following: blood pressure, 100/60 mmHg; pulse, 92 beats/min; respiration, 16/min; and body temperature, 36.5℃. Laboratory tests showed the following: white blood cell count, 6,470/µL; hemoglobin, 10.2 g/dL; platelet count, 245,000/µL; serum sodium, 141 mEq/L; potassium, 3.7 mEq/L; chloride, 108 mEq/L; blood urea nitrogen, 39 mg/dL; creatinine, 9.4 mg/dL; bicarbonate, 24 mmol/L; glucose, 101 mg/dL; and amylase, 374 U/L. Liver transaminase levels were normal.
Urinalysis showed a specific gravity of 1.05, a pH of 6.0, and scores of 1+ for urine protein, and 3+ for blood. No casts or crystals were observed. On the second day of hospitalization, her daily urinary volume decreased to 600 mL. Hemodialysis was initiated and repeated every other day. On the seventh day, a percutaneous kidney biopsy was performed, which revealed no glomerular abnormality, but some renal tubules displayed degeneration and atrophy (). On the eleventh day, the patient's daily urinary volume increased to 1,300 mL and her serum creatinine level decreased to 2.3 mg/dL. Hemodialysis was halted, and the patient was discharged on hospital day 14 without hearing loss or other sequelae.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [141.0, 'mEq/L'], 'Glucose': [101.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [39.0, 'mg/dL']}",301.53968,286.4627,316.61666,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. 
The concentration of bun is 39.0 mg/dL. 
The concentration of glucose is 101.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (39.0 / 2.8) + (39.0 / 18) = 301.53968 mmol/L.The patient's calculated serum osmolality concentration is 301.53968 mmol/L. This is equalivalent to 301.53968 mOsm/kg."
5892,30,Serum Osmolality,lab test,decimal,pmc-6037803-4,Extracted,"A 14-year-old girl presented with intermittent abdominal pain for 3 to 4 years, which had recently aggravated. Her parents had a history of HP-induced gastric ulcer and had been treated a few years ago. However, medical evaluation of the child had not been performed. Routine laboratory examination revealed WBC 7,200/mm3, with polymorphonuclear cell 55.5%, hemoglobin level 14.0 g/dL, and platelet count 213×103/mm3. Electrolytes showed sodium levels 140 mmol/L, potassium 3.4 mmol/L and chloride 105 mmol/L. The total protein level was 8.0 g/dL, albumin 4.8 g/dL, calcium 9.8 mg/dL, phosphorus 4.0 mg/dL, cholesterol 163 mg/dL, glucose 83 mg/dL, BUN 6.4 mg/dL, creatinine 0.62 mg/dL, total bilirubin 0.97 mg/dL, AST 17 U/L, ALT 9 U/L, and CRP <0.8 mg/dL. UGI endoscopy showed chronic superficial gastritis of the stomach body, marked hyperemia and a short mucosal breakage in the distal esophagus. A longitudinal sessile polyp was noted in the GEJ area. The polyp was markedly congested and appeared like a hemangioma. She was negative for HP in the rapid urea test, stool HP antigen, and serum HP-specific immunoglobulin G tests. The pathological finding was sentinel polyp (). Polypectomy has not been performed yet. He is taking anti-reflux medicine, and no specific GI symptom presents. Follow-up UGI endoscopy would be performed in one year.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mmol/L'], 'Glucose': [83.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [6.4, 'mg/dL']}",286.89683,272.55199,301.24167,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mmol/L. 
The concentration of bun is 6.4 mg/dL. 
The concentration of glucose is 83.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (6.4 / 2.8) + (6.4 / 18) = 286.89683 mmol/L.The patient's calculated serum osmolality concentration is 286.89683 mmol/L. This is equalivalent to 286.89683 mOsm/kg."
5893,30,Serum Osmolality,lab test,decimal,pmc-8457406-1,Extracted,"A 21-year-old man from Sinnar, Central Sudan, referred to Wad-Medani Teaching Hospital for the management of snake bite. He initially treated at Singa Teaching Hospital after snake bite to his left foot where he was admitted and received two units of blood, one unit of fresh frozen plasma and injectable antibiotics. The patient was referred to our hospital after 6 days without improvement for further workup and treatment.
On admission, there was localized abdominal pain at the umbilicus, hemoptysis, and hematuria associated with a decrease in urine amount and frequency, but there were no history of bleeding gums, epistaxis, hematemesis, and melena. There was no breathlessness, vomiting, headache, dizziness, focal neurological deficit, or paresthesia to the affected limb. The personal and past histories were insignificant.
On examination, he was oriented and conscious, not pale or jaundiced. His pulse rate was 112 beat/min, respiratory rate was 25 cycle/min, blood pressure was 100/70 mm of Hg, and his temperature was 39.3℃. The affected limb was swollen up to the knee with tenderness on palpation. There was ecchymosis around the affected area. Examination of the other systems was unremarkable.
The investigations were as follows: Complete blood count showed leukocytosis (14,000/mm3), and platelet count was 157/mm3 with low hemoglobin (8.6 g/dL). Urine, in general, showed uncountable RBCs and 2–4 pus cells. Blood urea was 44 mg/dL, serum creatinine was 0.5 mg/dL, serum sodium was 130 mEq/L, and serum potassium was 5.5 mmol/L. Random blood glucose was 88 mg/dL. The patient's prothrombin time (PT) was 20 seconds, activated partial thromboplastin time (aPTT) was prolonged 43 seconds, and the international normalization ratio (INR) was 1.6. On the first day of admission, the patient received one unit of blood, one unit of fresh-frozen plasma every 6 h, antivenom, vitamin K, injectable antibiotics, and antipyretics.
On the fourth day of admission, the patient became pale and distressed. Chest examination showed that the right side of the chest moves less with percussive dullness and no air entry. Posterior-anterior chest radiograph showed massive right-side hemothorax. Immediately, 550 mL of blood was drained through needle inserted posteriorly in the second intercostal space midscapular line lateral to the spine and patient transfused with one unit of blood. Hours later, chest tube with under water seal was inserted and kept for further drainage and collection. On the following days, the tube drained about 3 L of blood. The patient's general condition improved gradually in the subsequent days and chest radiograph showed complete resolution of the hemothorax as shown in Figures and . After which, chest tube with under water seal system was removed and the patient discharged in a good condition.
During hospitalization, the patient received six units of blood and thirty units of fresh-frozen plasma, antivenom, vitamin K, injectable ceftriaxone, vancomycin, metronidazole, and antipyretics. On discharge, the patient's coagulation profile returns to normal limit.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [130.0, 'mEq/L'], 'Glucose': [88.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [44.0, 'mg/dL']}",280.60317,266.57301,294.63333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. 
The concentration of bun is 44.0 mg/dL. 
The concentration of glucose is 88.0 mg/dL. 
Plugging these values into the equation, we get 2 * 130.0 + (44.0 / 2.8) + (44.0 / 18) = 280.60317 mmol/L.The patient's calculated serum osmolality concentration is 280.60317 mmol/L. This is equalivalent to 280.60317 mOsm/kg."
5894,30,Serum Osmolality,lab test,decimal,pmc-3811690-1,Extracted,"A 53-year-old female presented to our hospital complaining of a 6-month history of backache. Judging from the blood testing results, she had hypercalcemia, and alkaline phosphatase (ALP) was increased to 1,253 U/L (normal range, 35 to 130); the patient was sent to the endocrinology department. Her past history was significant for a surgical procedure for fibrocystoma of her right humerus 20 years ago, and she had donated one of her kidneys to a relative 7 years previously. She had taken atorvastatin 10 mg, amlodipine 5 mg, and omega-3 fatty acid 1,000 mg daily for the past 3 years to treat high blood pressure and dyslipidemia. The patient had been misdiagnosed with a thyroid nodule and hypothyroidism at another hospital 4 years previously and had immediately been prescribed levothyroxine 50 µg/day. At that time, the thyroid ultrasonography revealed two nodules that were 0.3 and 0.5 cm in diameter on her right lobe and another nodule that was 2.3×1.3 cm in size that was projected backwards. She had fine needle aspiration cytology for the nodule on the left lobe, and this had revealed a benign nodule. She had been followed up every 6 months by neck ultrasonography. Two years later, when the nodule on the left lobe of the thyroid had increased in size to 2.9×1.7 cm, they carried out radiofrequency ablation. However, the thyroid nodule remained the same size even after the radiofrequency ablation, so they monitored its size every 6 months for 2 more years (). During that time, the patient began experiencing backache and visited the orthopedics department of our hospital where she was suspected of having metabolic bone disease due to the high serum ALP value.
The patient presented with generalized weakness and fatigue without other hypercalcemic symptoms. The peripheral blood examination was as follows: leukocyte count, 7,020/mm3; hemoglobin, 9.3 g/dL; platelet count, 249,000/mm3; prothrombin time (PT), 14.4 seconds (normal range, 11.9 to 14.3); activated partial thromboplastin time (aPTT), 31.3 seconds (normal range, 29.1 to 43.5); serum iron, 65 µg/dL (normal range, 40 to 160); total iron binding capacity (TIBC), 258 µg/dL (normal range, 230 to 430); transferrin saturation, 25%; and ferritin, 158.6 ng/mL (normal range, 13 to 150). Serum chemistry values were also obtained: blood urea nitrogen, 26.9 mg/dL; creatinine, 1.98 mg/dL; glucose, 110 mg/dL; ALP, 1,011 U/L; aspartate aminotransferase, 23 U/L; and alanine aminotransferase, 11 U/L. Serum calcium was 14.6 mg/dL, phosphate was 3.5 mg/dL, and ionized calcium was 7.2 mg/dL. Serum protein and serum albumin were 6.9 and 3.7 g/dL, respectively. The results of the serum electrolyte test revealed that sodium was 135.7 mmol/L, potassium was 4.3 mmol/L, chloride was 104.0 mmol/L, and serum osmotic pressure was 286 mOsm/kg. According to the serum lipid examination, the total cholesterol was 146 mg/dL, triglyceride was 95 mg/dL, high density lipoprotein was 33 mg/dL, and low density lipoprotein was 79 mg/dL. A thyroid function test found T3 was 108.9 ng/dL (normal range, 80 to 200), thyroid stimulating hormone was 0.40 mIU/L (normal range, 0.27 to 4.2), and free T4 was 0.74 ng/dL (normal range, 0.93 to 1.70). Under dual energy X-ray absorptiometry-based bone density examination, the T-score of the lumbar region was -1.4, while the T-scores of the neck were -1.2 on the left and -1.8 on the right. Except for the fifth lumbar vertebra, which had spondylolisthesis, nothing remarkable was found on magnetic resonance imaging.
According to further blood tests, 25-hydroxyvitamin D3 was 9.6 ng/mL (normal range, 4.8 to 52.8), and 1,25-dihydroxyvitamin D3 was 10.5 pg/mL (normal range, 19.6 to 54.3), while the intact parathyroid hormone (iPTH) was 1,911 pg/mL (normal range, 15 to 65). When we performed bone scanning with 99mTc, the amount of cortical bone radioactive isotope uptake increased very high (). Because we suspected hyperparathyroidism, we carried out a 99mTc sestamibi scan and suspected the lesion that had been previously diagnosed as a left thyroid nodule was likely a parathyroid adenoma (). Using thyroid Doppler ultrasonography, we discovered a hypervascular adenoma that was 5-cm-sized solid mass with similar echo of surrounding thyroid tissue in the center, and slightly low echo in outer part in the inferior site of left thyroid gland (), while on the right thyroid parenchyma we discovered two thyroid nodules, 0.3 and 0.5 cm each in diameter, that the patient had had 4 years before. We performed neck computed tomography and found there was no neck lymph node metastastasis and local invasion of other organs ().
The patient received both hydration and diuretic treatments until she underwent a surgical operation to control the hypercalcemia; she also had pamidronate 90 mg intravenous injections twice a week. On the 11th day after hydration and diuretic treatment, her condition had improved; serum calcium was reduced to 11.6 mg/dL, and creatinine improved to 1.11 mg/dL. On the 12th day, the patient had left parathyroid excision and was diagnosed with a parathyroid adenoma (). Following the surgical procedure, iPTH normalized to 42.5 pg/mL, but calcium and vitamin D were prescribed for 9 months to cure the hypocalcemia that had developed due to hungry bone syndrome. It has been a year since the surgical operation, and her calcium, phosphate, ALP, and iPTH all remain at normal levels.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [135.7, 'mmol/L'], 'Glucose': [110.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [26.9, 'mg/dL']}",287.11825,272.76234,301.47416,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.7 mmol/L. 
The concentration of bun is 26.9 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 135.7 + (26.9 / 2.8) + (26.9 / 18) = 287.11825 mmol/L.The patient's calculated serum osmolality concentration is 287.11825 mmol/L. This is equalivalent to 287.11825 mOsm/kg."
5895,30,Serum Osmolality,lab test,decimal,usmle-5916,Extracted,"A 33-year-old woman presents to the emergency department at 37 weeks gestation. She states that she has had a headache for the past day and generally does not feel well. Her past medical history is unremarkable, and she is currently taking prenatal vitamins. Her temperature is 99°F (37.2°C), blood pressure is 177/108 mmHg, pulse is 100/min, respirations are 16/min, and oxygen saturation is 97% on room air. Physical exam is notable for diffuse discomfort to abdominal palpation. A spot urine protein to creatinine ratio is 37. Laboratory values are ordered as seen below.

Hemoglobin: 9 g/dL
Hematocrit: 30%
Leukocyte count: 6,500/mm^3 with normal differential
Platelet count: 47,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 5.3 mEq/L
HCO3-: 25 mEq/L
BUN: 40 mg/dL
Glucose: 99 mg/dL
Creatinine: 2.3 mg/dL
Ca2+: 10.2 mg/dL
AST: 112 U/L
ALT: 150 U/L

A peripheral smear is performed as seen in Figure A.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [139.0, 'mEq/L'], 'Glucose': [99.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [40.0, 'mg/dL']}",297.78571,282.89642,312.675,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. 
The concentration of bun is 40.0 mg/dL. 
The concentration of glucose is 99.0 mg/dL. 
Plugging these values into the equation, we get 2 * 139.0 + (40.0 / 2.8) + (40.0 / 18) = 297.78571 mmol/L.The patient's calculated serum osmolality concentration is 297.78571 mmol/L. This is equalivalent to 297.78571 mOsm/kg."
5896,30,Serum Osmolality,lab test,decimal,usmle-5629,Extracted,"A 65-year-old man presents to the emergency department with confusion and chest pain. He states his symptoms started after he landed on a return flight from Brazil. Since then, the patient states that he feels anxious, short of breath, and has pleuritic chest pain. The patient has a past medical history of diabetes and chronic kidney disease. His medications include insulin, lisinopril, aspirin, and atorvastatin. His temperature is 101°F (38.3°C), blood pressure is 154/94 mmHg, pulse is 90/min, respirations are 17/min, and oxygen saturation is 96% on room air. Physical exam is notable for a confused man. The patient’s laboratory studies are ordered as seen below.

Serum:
Na+: 140 mEq/L
Cl-: 103 mEq/L
K+: 5.3 mEq/L
HCO3-: 25 mEq/L
BUN: 33 mg/dL
Glucose: 168 mg/dL
Creatinine: 1.8 mg/dL
Ca2+: 10.0 mg/dL
Troponin: < 0.05 mcg/L

A chest CT angiogram, an echocardiogram (ECG), and a second troponin are ordered and are all unremarkable. The patient’s chest pain resolves with diazepam. A lumbar puncture is performed and based on the results the patient is subsequently started on acyclovir.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mEq/L'], 'Glucose': [168.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [33.0, 'mg/dL']}",301.11905,286.0631,316.175,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. 
The concentration of bun is 33.0 mg/dL. 
The concentration of glucose is 168.0 mg/dL. 
Plugging these values into the equation, we get 2 * 140.0 + (33.0 / 2.8) + (33.0 / 18) = 301.11905 mmol/L.The patient's calculated serum osmolality concentration is 301.11905 mmol/L. This is equalivalent to 301.11905 mOsm/kg."
5897,30,Serum Osmolality,lab test,decimal,usmle-4753,Extracted,"A 69-year-old male presents to the emergency department for slurred speech and an inability to use his right arm which occurred while he was eating dinner. The patient arrived at the emergency department within one hour. A CT scan was performed of the head and did not reveal any signs of hemorrhage. The patient is given thrombolytics and is then managed on the neurology floor. Three days later, the patient is recovering and is stable. He seems depressed but is doing well with his symptoms gradually improving as compared to his initial presentation. The patient complains of neck pain that has worsened slowly over the past few days for which he is being given ibuprofen. Laboratory values are ordered and return as indicated below:

Serum:
Na+: 130 mEq/L
K+: 3.7 mEq/L
Cl-: 100 mEq/L
HCO3-: 24 mEq/L
Urea nitrogen: 7 mg/dL
Glucose: 70 mg/dL
Creatinine: 0.9 mg/dL
Ca2+: 9.7 mg/dL

Urine:
Appearance: dark
Glucose: negative
WBC: 0/hpf
Bacterial: none
Na+: 320 mEq/L/24 hours

His temperature is 99.5°F (37.5°C), pulse is 95/min, blood pressure is 129/70 mmHg, respirations are 10/min, and oxygen saturation is 98% on room air.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [130.0, 'mEq/L'], 'Glucose': [70.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [7.0, 'mg/dL']}",266.38889,253.06945,279.70833,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. 
The concentration of bun is 7.0 mg/dL. 
The concentration of glucose is 70.0 mg/dL. 
Plugging these values into the equation, we get 2 * 130.0 + (7.0 / 2.8) + (7.0 / 18) = 266.38889 mmol/L.The patient's calculated serum osmolality concentration is 266.38889 mmol/L. This is equalivalent to 266.38889 mOsm/kg."
5898,30,Serum Osmolality,lab test,decimal,pmc-5767490-1,Extracted,"A 42-year-old man presented with repetitive generalized tonic-clonic seizures. He was found unconscious following approximately 4 hours of heavy physical labor at an outdoor construction site under extremely hot and humid weather conditions, with ambient temperatures of about 35°C and humidity of more than 70%. During transportation by ambulance, the patient experienced 3–4 tonic-clonic seizures lasting several minutes, without recovering consciousness. After arriving at the emergency department, the patient experienced 2 convulsions that lasted several minutes and ceased following intravenous infusion of 5 mg of lorazepam and 800 mg of fosphenytoin. Prior to the episode of HS, the patient had been receiving treatment for bipolar disorder for 5 years with lithium, amitriptyline, and escitalopram. He had no other medical history and was not a smoker or consumer of alcohol. Vital signs during initial evaluation were: blood pressure 110/80 mmHg, heart rate 140 beats per minute, respiratory rate 40 breaths per minute, and tympanic temperature 40.8°C. During neurological examination, the patient was observed to be in a state of deep drowsiness with Glasgow Coma Scale (E1V1M3) score 5. Pupils were bilaterally equal, 3 mm in size, and reactive to light. No focal neurological deficits such as nystagmus, gaze palsy, weakness, muscular rigidity, or cerebellar signs were observed. A complete blood count showed white blood cell count of 10,870/μL, hemoglobin level of 13.3 g/dL, hematocrit of 39.9%, and platelet count of 240,000/μL. Blood chemistry revealed a blood urea nitrogen level of 23.9 mg/dL, creatinine level of 1.51 mg/dL, sodium level of 137.4 meq/L, potassium level of 4.7 meq/L, chloride level of 107.5 meq/L, calcium level of 9.4 mg/dL, alanine aminotransferase level of 234 IU/L, aspartate aminotransferase level of 381 IU/L, total bilirubin level of 2.03 mg/dL, direct bilirubin level of 0.57 mg/dL, lactate de-hydrogenase level of 1,360 IU/L, glucose level of 124 mg/dL, creatine phosphokinase level of 3,789 IU/L, and ammonia level of 41 μmol/L. Additional laboratory tests showed a serum prolactin level of 57.56 ng/mL, high sensitivity-C reactive protein level of 0.095 mg/dL, and erythrocyte sedimentation rate of 2 mm/h. Blood gas analysis showed pH of 7.56, PaO2 of 74.2 mmHg, PaCO2 of 16.2 mmHg, HCO3− level of 14.1 mmol/L, and O2 saturation of 95%. Urinalysis demonstrated absence of myoglobinuria, proteinuria, hematuria, and pyuria. No abnormalities were detected in the cerebrospinal fluid except for mildly elevated protein contents of 66 mg/dL. The electrocardiogram revealed sinus tachycardia at the rate of 146 beats/min without ST segment changes. Brain magnetic resonance imaging results were normal (). The electroencephalography (EEG) revealed a generalized attenuation of background activity after the administration of 5 mg of intravenous lorazepam to control repetitive convulsions (). The patient was therefore diagnosed with HS accompanied by status epilepticus. He was promptly transferred to the intensive care unit and treated with surface cooling and infusion of intravenous cold saline. The seizures were also well controlled. By day 5 following admission, the patient’s level of consciousness gradually improved to alert, and abnormal laboratory parameters returned to the normal values. Continuous EEG monitoring during fosphenytoin infusion showed absence of epileptiform activity (). On day 14, the patient was discharged in a healthy state, with no complications. At 4 months following the episode of HS, he showed no neurological abnormalities.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [137.4, 'mEq/L'], 'Glucose': [124.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [23.9, 'mg/dL']}",290.2246,275.71337,304.73583,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.4 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.4 mEq. To convert from 137.4 mEq to mmol, convert from mEq to mmol. The compound 137.4 has a valence of 1, and so divide the valence by the value of mEq to get, 137.4 mEq/(1 mEq/mmol) = 137.4 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.4 mEq sodium/L converts to 137.4 mmol sodium/L. 
The concentration of bun is 23.9 mg/dL. 
The concentration of glucose is 124.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.4 + (23.9 / 2.8) + (23.9 / 18) = 290.2246 mmol/L.The patient's calculated serum osmolality concentration is 290.2246 mmol/L. This is equalivalent to 290.2246 mOsm/kg."
5899,30,Serum Osmolality,lab test,decimal,pmc-2923795-1,Extracted,"A 74-yr-old woman was transferred to our emergency department from the local general hospital with an initial diagnosis of brain stem infarct on January 17, 2009. The patient was found unconscious and in a bed-ridden state during the early morning on the presenting day. The patient's breathing was shallow and irregular. The patient was unable to walk well due to a coccyx fracture two years ago, but she was able to perform daily life activities with minor help. One week ago, her facial edema started and she complained dry cough and general weakness three days ago. No other medical, familial, or social history was reported, and the patient had not taken any medication. There was also no evidence of intoxication.
According to the records of the local general hospital, the patient had an impending respiratory arrest and comatose mental status. Her blood pressure was 71/48 mmHg, her body temperature was 36.0℃, and her pulse rate was 99 beats/min with a sinus rhythm by electrocardiography (ECG). Neurologic examination revealed pinpoint pupils and a lack of brain stem reflexes, including the light reflex, corneal reflex, gag reflex, and doll's-eye phenomenon. She also showed decerebrated rigidity in response to painful external stimuli. The patient was assigned a score of 5 on the Glasgow Coma Scale, and the Babinski sign was detected at both feet. Brain computed tomography (CT) produced unremarkable results. Endotracheal intubation was performed for protection of the patient's airway, assisted ventilation was initiated, and an inotropic agent was injected to support the patient's state of shock, which did not respond to fluid therapy (1 L of normal saline). Prior to transfer, the patient's blood pressure was increased, but her neurologic findings were not improved. She was transferred to our hospital for further evaluation and treatment of a brain stem infarct.
On arrival, the patient's blood pressure was 70/40 mmHg, her pulse rate was 59 beats/min, and an intravenous infusion of premixed dopamine was administered (500 mL/800 mg, 20 µg/kg/min). The patient's body temperature was 34.8℃ according to a tympanic membrane thermometer, and her self-respiration was slow and shallow. The patient's lungs on auscultation were bilaterally clear, and cardiac examination showed a regular rate and rhythm without murmurs, gallops, or rubs. The patient's abdomen was soft without signs of guarding, tenderness, or rebound tenderness. A rectal examination revealed no masses, and the patient's stool was guaiac negative. No soiling due to urine or feces was noted on her undergarments.
The patient's face and extremities were edematous, and she presented with non-pitting edema. Her skin was dry, cool, pale, and slightly mottled and desquamated; however, there was no evidence of petechiae or purpura ().
The patient's level of consciousness was stupor to semi-coma. A neurologic examination revealed intact cranial nerves and she didn't show lateralizing signs. The patient's pupils were 3 mm across and briskly reactive. It was impossible to check for visual abnormalities and focal cerebellar findings. The results of the Babinski reflex test were negative.
The patient's laboratory values were as follows: WBC count 6,000/µL (86% neutrophils), hemoglobin 11.8 g/dL, sodium 121 mEq/L, potassium 4.2 mEq/L, chloride 87 mEq/L, BUN 1.3 mg/dL, creatinine 0.6 mg/dL, glucose 104 mg/dL, ALT 113 U/L, AST 74 U/L, albumin 3.3 g/dL, CK 499 IU/L, CK-MB 21.4 ng/mL, troponin-I <0.02 ng/mL, lactate 1.2 mM/L, urine RBCs 1-4/HPF, and urine WBCs 0-1.5/HPF. Arterial blood gas analysis (FiO2 1.0) revealed a pH of 7.486, a pCO2 of 30.6 mmHg, a pO2 of 36.4 mmHg, a HCO3- concentration of 22.9 mM/L, and an oxygen saturation of 77%.
A portable chest radiography revealed infiltration of the right lower lung zone and cardiomegaly. ECG revealed sinus bradycardia with no evidence of ischemia; the intervals and axis were normal except for a prolonged QTc interval. Echocardiography revealed a small amount of pericardial effusion, but it did not affect the patient's hemodynamic status.
During our resuscitative efforts, the patient's blood pressure didn't respond and additional laboratory test results confirmed hypothyroidism. The patient's free thyroxine was 0.05 ng/dL (0.93-1.7) and her TSH was 30.12 µIU/mL (0.27-5.0). A diagnosis of myxedema coma exacerbated by community-acquired pneumonia was thus assigned.
The patient was referred to the Department of Endocrinology and admitted to the intensive care unit for treatment and ventilatory support. The patient received 1,000 µg of levothyroxine orally for two days, followed by 300 µg/day for an additional three days and finally maintained on levothyroxine 0.1 mg orally each day. Following the administration of synthetic thyroid hormones for hypothyroidism and antibiotics for pneumonia, the patient regained consciousness and respiration. She was transferred to a general ward after two weeks in the intensive care unit and discharged from the hospital one week later.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [121.0, 'mEq/L'], 'Glucose': [104.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [1.3, 'mg/dL']}",248.24206,235.82996,260.65416,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 121.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 121.0 mEq. To convert from 121.0 mEq to mmol, convert from mEq to mmol. The compound 121.0 has a valence of 1, and so divide the valence by the value of mEq to get, 121.0 mEq/(1 mEq/mmol) = 121.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 121.0 mEq sodium/L converts to 121.0 mmol sodium/L. 
The concentration of bun is 1.3 mg/dL. 
The concentration of glucose is 104.0 mg/dL. 
Plugging these values into the equation, we get 2 * 121.0 + (1.3 / 2.8) + (1.3 / 18) = 248.24206 mmol/L.The patient's calculated serum osmolality concentration is 248.24206 mmol/L. This is equalivalent to 248.24206 mOsm/kg."
5900,30,Serum Osmolality,lab test,decimal,pmc-3277472-1,Extracted,"MR was a 14-year-old Muslim Kurdish student living in Sulimania, northeast of Iraq. His parents were of an educated middle class family who enjoyed good health and stable relationships. He was brought by his mother to the hospital on 18th July 2010 for refusing to eat, which had led to severe weight loss and generalized weakness. His condition began seven months prior when his friends teased him about his plumpness and greedy appetite. Consequently, he started restricting his food intake, avoiding high-calorie foods and indulging routinely in extensive exercise. His parents tried to convince him to eat regular meals, but he refused. He was obsessed about his body shape and measured his waist and thigh circumferences regularly. His food intake decreased rapidly until his daily meal became no more than a cup of yogurt and pieces of cucumber. A few weeks before his visit to the hospital, he experienced severe fatigue, headaches, joints aches and attacks of epigastric pain followed by vomiting. He was treated by the local doctor with multivitamins, anti-emetics and anti-spasmodics, but without improvement.
The patient seemed to be overprotected by his mother. He was the youngest of seven siblings and a clever boy. She described him as being a graceful and obedient child, but somewhat of a perfectionist. There was neither a history of physical or mental illness nor sexual abuse during childhood.
On admission to the hospital, he appeared to be severely ill. He was pale, emaciated and dehydrated. He had lost about 20 kg during the past four months, according to his mother, who reported episodes of irritability and depressed mood with the decrease in weight. His body weight was 28 kg and height 147 cm, which is below the 2nd percentile for his age according to the growth chart. His BMI was 13.0, reflecting a 37% deficit in weight for his height [].
Upon examination, he showed generalized muscle wasting, and his skin was dry and covered by lanugo hair. His chest was clear, and he had a scaphoid soft abdomen. His blood pressure was 90/60 mmHg, heart rate 55 bpm and body temperature 37.8°C. Laboratory tests were as follows: blood glucose: 60 mg/dl, blood urea: 18 mg/d, serum sodium: 136 mg/dl, serum creatinine: 0.6 mg/dl, serum cholesterol: 147 mg/dl, WBC: 2200, platelet count: 150000, ESR: 1, and HB: 12 mg/dl. Blood proteins were low with slightly elevated liver enzymes. The blood culture was negative. Thyroid functions tests and steroid hormones were normal. General urine examination and culture revealed an acute bacterial infection, which accounted for his fever. Skull, spine and chest x-ray, brain scan and abdominal ultrasound were all normal. A previous gastroscopy at another hospital showed mild mucosal atrophy. An ECG revealed sinus bradycardia. The patient was smaller and shorter than his matching peers. He looked attentive but indifferent to his serious condition. His speech was rational and did not reveal delusions or hallucinations. However, he expressed strong denial of his body appearance and insisted he had a normal body shape. His mood was depressed, but he denied suicidal ideation.
The patient was admitted on 18th July 2010 to Sulimania General Hospital and was referred later for psychiatric consultation. A liaison treatment plan was designed by the attending physician, psychiatrist and dietitian focusing on scheduled feeding under the dietitian's advice, which was to be achieved through a nasogastric tube. Caloric intake was measured to reach 2000 calories per day, and he was instructed to rest in bed under a nurse's supervision. This ameliorated his previous hypoglycemic attacks. He was prescribed oral cephalosporin 250 mg qds to treat his urinary infection. On the second day of his admission, the psychiatrist prescribed a 20 mg daily dose of fluoxetine to treat his depressed mood and food-related obsessions. A 5 mg nightly dose of olanzapine was prescribed to resolve the distorted thoughts about his body image and promote sedation. Nasogastric refeeding was continued for the first week in the hospital until oral feeding was established. The tube was removed on the 6th day. In addition, a few sessions of cognitive psychotherapy were conducted with the patient.
At the end of the third week, he became more realistic and rational about his body weight and was more compliant with eating normal meals. His mood and irritability improved. He was discharged after 24 days in the hospital, advised to abide by the regulations of the dietitian and continue his medication for three months. He was to report to the psychiatry clinic on alternate weeks. His body weight had increased to 30 kg.
He did not keep his appointments and appeared six months later at the clinic weighing 38 kg. He was enjoying better health, although he was still having eating peculiarities. He had maintained his daily exercise but was reluctant to gain more weight. After consultation, he was advised to continue on fluoxetine for another three months. The family was advised to escort him regularly for psychotherapy sessions and watch his dietary intake.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [136.0, 'mEq/L'], 'Glucose': [60.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [18.0, 'mg/dL']}",281.7619,267.67381,295.85,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.0 mEq. To convert from 136.0 mEq to mmol, convert from mEq to mmol. The compound 136.0 has a valence of 1, and so divide the valence by the value of mEq to get, 136.0 mEq/(1 mEq/mmol) = 136.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mEq sodium/L converts to 136.0 mmol sodium/L. 
The concentration of bun is 18.0 mg/dL. 
The concentration of glucose is 60.0 mg/dL. 
Plugging these values into the equation, we get 2 * 136.0 + (18.0 / 2.8) + (18.0 / 18) = 281.7619 mmol/L.The patient's calculated serum osmolality concentration is 281.7619 mmol/L. This is equalivalent to 281.7619 mOsm/kg."
5901,30,Serum Osmolality,lab test,decimal,usmle-1760,Extracted,"A 50-year-old man is brought to the emergency department by his wife because of lethargy and confusion for the past 24 hours. He has also had a productive cough for the past year and has had a 10-kg (22-lb) weight loss over the past 6 months. He has a history of multiple sclerosis and has not had an acute exacerbation in over 10 years. For the past 30 years, he has smoked 2 packs of cigarettes daily. He drinks 2 beers every day after work. His temperature is 37.0°C (98.6°F), pulse is 90/min, blood pressure is 130/90 mm Hg, and respirations are 22/min. On examination, the patient appears lethargic and cannot state his name or his location. Physical examination reveals scattered wheezing bilaterally. Deep tendon reflexes cannot be elicited. Laboratory studies show:
Serum
Na+ 115 mEq/L
K+ 4.5 mEq/L
HCO3- 22 mEq/L
Glucose 70 mg/dL
Blood urea nitrogen 8 mg/dL
Urine osmolality 450 mOsmol/kg H2O
Urine sodium 70 mEq/L
An x-ray of the chest reveals a central lung mass.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [115.0, 'mEq/L'], 'Glucose': [70.0, 'mg/dL'], 'Blood Urea Nitrogen (BUN)': [8.0, 'mg/dL']}",236.74603,224.90873,248.58333,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 115.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 115.0 mEq. To convert from 115.0 mEq to mmol, convert from mEq to mmol. The compound 115.0 has a valence of 1, and so divide the valence by the value of mEq to get, 115.0 mEq/(1 mEq/mmol) = 115.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 115.0 mEq sodium/L converts to 115.0 mmol sodium/L. 
The concentration of bun is 8.0 mg/dL. 
The concentration of glucose is 70.0 mg/dL. 
Plugging these values into the equation, we get 2 * 115.0 + (8.0 / 2.8) + (8.0 / 18) = 236.74603 mmol/L.The patient's calculated serum osmolality concentration is 236.74603 mmol/L. This is equalivalent to 236.74603 mOsm/kg."
5902,30,Serum Osmolality,lab test,decimal,pmc-3840624-1,Extracted,"A 72-year-old woman was admitted to hospital reporting dizziness and gait disturbance. She had been under maintenance hemodialysis for three years because of advanced diabetic nephropathy. At 70 years of age, she was diagnosed with stage IIIc ovarian cancer with carcinomatous peritonitis. Poorly differentiated adenocarcinoma cells were detected in the ascites. She received a simple total hysterectomy and bilateral oophorectomy after nine cycles of chemotherapy with paclitaxel and carboplatin, followed by an additional six cycles of chemotherapy.
When she admitted to hospital, her blood pressure was 113/54 mmHg, and body temperature was 36.6°C. She was conscious and a physical examination of the nervous system revealed only positive Babinski reflex sign without any other neurologic abnormality including nystagmus. We could not evaluate her gait disturbance because her II-IV metatarsal bone was fractured during a fall that occurred several days before admission. In addition to the chief complaints, transient hypertension, headache, and nausea appeared during each hemodialysis session. Her symptoms appeared about one hour after the beginning of hemodialysis, and moreover, they lasted during treatment, and subsided gradually after the session. Thus, a diagnosis of DDS was made.
Findings from laboratory examinations were as follows; hemoglobin, 11.7 g/dL; hematocrit 35.9%; white blood cells (WBCs), 3,990 WBC/μL; sodium, 141 mmol/L; potassium 4.9 mmol/L; chloride, 101 mmol/L; blood urea nitrogen, 56.3 mg/dL; creatinine, 6.24 mg/dL; C-reactive protein, 0.18 mg/dL; B-type natriuretic peptide, 276.38 pg/mL; blood glucose, 137 mg/dL; hemoglobin A1c, 6.7%; and normal liver function tests.
Both contrast-enhanced cranial computed tomography and non-enhancement cranial magnetic resonance imaging did not demonstrate any intracranial pathological abnormalities including mass lesions, bleeding, and metastatic disease. Five days after the admission, she presented with consciousness disturbance and short-term memory loss, which gradually worsened especially during hemodialysis. Cranial computed tomography images showed mild exacerbation of hydrocephalus (Figure ). Intracranial pressure at that time was 180 cmH2O (normal intracranial pressure: 60 to 150 cmH2O), and poorly differentiated adenocarcinoma cells, which were compatible with the metastasis of ovarian cancer cells, were detected in cerebrospinal fluid (CSF). NM had a negative effect on the patient’s general health. She died 42 days after admission.
Postmortem pathological examinations revealed cancer cells covering the surface of the brain and spinal cord (Figure ); however, no other apparent metastatic lesions were detected.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [56.3, 'mg/dL'], 'Glucose': [137.0, 'mg/dL'], 'Sodium': [141.0, 'mmol/L']}",309.71825,294.23234,325.20416,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 141.0 mmol/L. 
The concentration of bun is 56.3 mg/dL. 
The concentration of glucose is 137.0 mg/dL. 
Plugging these values into the equation, we get 2 * 141.0 + (56.3 / 2.8) + (56.3 / 18) = 309.71825 mmol/L.The patient's calculated serum osmolality concentration is 309.71825 mmol/L. This is equalivalent to 309.71825 mOsm/kg."
5903,30,Serum Osmolality,lab test,decimal,usmle-4731,Extracted,"A 29-year-old man presents to the emergency department after experiencing a motor vehicle accident. The patient was the front seat passenger in a head on collision. The patient is responsive only to painful stimuli. His temperature is 99.5°F (37.5°C), blood pressure is 90/60 mmHg, pulse is 150/min, respirations are 17/min, and oxygen saturation is 95% on room air. The patient is started on IV fluids and is given blood products. A FAST exam reveals no signs of intra-abdominal bleeding. A chest radiograph is ordered as seen in Figure A. A pelvic binder is placed and fluid and blood resuscitation is continued. Fifteen minutes later his temperature is 99.5°F (37.5°C), blood pressure is 110/70 mmHg, pulse is 100/min, respirations are 13/min, and oxygen saturation is 97% on room air. The patient is now able to respond to questions. The patient's lab values are ordered and are as below:

Serum:
Na+: 137 mEq/L
Cl-: 102 mEq/L
K+: 4.2 mEq/L
HCO3-: 24 mEq/L
BUN: 20 mg/dL
Glucose: 110 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 9.6 mg/dL
AST: 12 U/L
ALT: 14 U/L

Hemoglobin: 11 g/dL
Hematocrit: 30%
Leukocyte count: 6,500 cells/mm^3 with normal differential
Platelet count: 255,000/mm^3

The patient suddenly becomes short of breath. A chest radiograph is ordered as seen in Figure B. A FAST exam is repeated and is within normal limits.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Glucose': [110.0, 'mg/dL'], 'Sodium': [137.0, 'mEq/L']}",287.25397,272.89127,301.61667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. 
The concentration of bun is 20.0 mg/dL. 
The concentration of glucose is 110.0 mg/dL. 
Plugging these values into the equation, we get 2 * 137.0 + (20.0 / 2.8) + (20.0 / 18) = 287.25397 mmol/L.The patient's calculated serum osmolality concentration is 287.25397 mmol/L. This is equalivalent to 287.25397 mOsm/kg."
5904,30,Serum Osmolality,lab test,decimal,usmle-1693,Extracted,"A 63-year-old man is brought to the emergency department after having 8–9 episodes of red watery stool. He has no abdominal pain or fever. He underwent an angioplasty 4 years ago and received 2 stents in his left main coronary artery. He has hypertension, hypercholesterolemia, coronary artery disease, and chronic constipation. Current medications include aspirin, metoprolol, and simvastatin. He drinks one beer daily. He is in distress. His temperature is 37.3°C (99.1°F), pulse is 110/min, respirations are 14/min, and blood pressure is 86/58 mm Hg. Examination shows pale conjunctivae. The abdomen is soft and nontender. Bowel sounds are increased. The lungs are clear to auscultation. Cardiac examination shows an S4 gallop. Rectal examination shows frank blood. Laboratory studies show:
Hemoglobin 9.8 g/dL
Leukocyte count 7,800/mm3
Platelet count 280,000/mm3
Prothrombin time 14 seconds (INR=0.9)
Serum
Na+ 135 mEq/L
K+ 4.1 mEq/L
Cl- 101 mEq/L
Urea nitrogen 16 mg/dL
Glucose 96 mg/dL
Creatinine 0.7 mg/dL
Two large bore intravenous catheters are inserted and 0.9% saline infusions are administered. A nasogastric tube is inserted. Aspiration shows clear gastric content containing bile. Directly afterwards, his pulse is 133/min and blood pressure is 80/54 mm Hg.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [16.0, 'mg/dL'], 'Glucose': [96.0, 'mg/dL'], 'Sodium': [135.0, 'mEq/L']}",281.04762,266.99524,295.1,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 135.0 mEq. To convert from 135.0 mEq to mmol, convert from mEq to mmol. The compound 135.0 has a valence of 1, and so divide the valence by the value of mEq to get, 135.0 mEq/(1 mEq/mmol) = 135.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mEq sodium/L converts to 135.0 mmol sodium/L. 
The concentration of bun is 16.0 mg/dL. 
The concentration of glucose is 96.0 mg/dL. 
Plugging these values into the equation, we get 2 * 135.0 + (16.0 / 2.8) + (16.0 / 18) = 281.04762 mmol/L.The patient's calculated serum osmolality concentration is 281.04762 mmol/L. This is equalivalent to 281.04762 mOsm/kg."
5905,30,Serum Osmolality,lab test,decimal,pmc-3317255-1,Extracted,"A 38-year-old white male with alcoholic cirrhosis diagnosed 3 years prior was admitted to the University Hospital with a 30-day history of anorexia, asthenia, ascites, and edema of the legs. He also complained of fever, diarrhea (3-4 episodes per day), and a productive cough over the last two days. The patient was taking 100 mg of spironolactone/day. At the time of the physical examination, the patient did not have a fever (axillary temperature: 37°C) and was cachectic, pale (+++), with rales in both lungs, which were more intense on the left side. The patient had tense ascites, spider angiomas, and caput medusae, in addition to palmar erythema, and leg and scrotal edema. His skin was dry, with ecchymosis around both knees, and he had thinning hair and lesions resembling pellagra. Neurologic examination revealed that the patient was alert without intellectual or motor impairments (West-Haven hepatic encephalopathy criteria: 0).
The laboratory data at admission were as follows: blood hemoglobin: 6.2 g/dL; hematocrit: 20.3%; red blood cells: 2,160,000/mm3; mean corpuscular volume: 94 fL; red cell distribution width: 16%; white blood cells: 18,080, with a neutrophil count of 16,091/mm3, and 1,446 band forms/mm3; platelets: 265,000/mm3; C-reactive protein: 128 mg/dL; aspartate aminotransferase: 34 IU/L; alanine aminotransferase: 25 IU/L; lactate dehydrogenase: 435 IU/L; serum total protein: 4.1 g/dL; albumin 1.07 g/dL; international normalized ratio: 1.35; prothrombin activity: 68%; serum total bilirubin: 1.1 mg/dL; serum sodium: 136 mEq/L; potassium: 4.3 mEq/L; calcium: 7.2 mg/dL; phosphorus: 3.8 mg/dL; magnesium: 1.9 mg/dL; urea: 36 mg/dL; creatinine: 0.54 mg/dL; fasting blood glucose: 86 mg/dL; serum iron: 15.5 µg/dL, total iron-binding capacity: 74.5 µg/dL; folic acid: 5.5 ng/mL; vitamin B12: >1,000 pg/mL. Ascitic fluid analysis revealed the following: pH 8.0; density: 1,010; cells: 950/mm3, with a neutrophil count of 646/mm3; glucose: 95 mg/dL; lactate dehydrogenase: 931 IU/L; albumin: 0.16 g/dL (serum/ascitic liquid albumin gradient: 0.91, suggestive of exudate). Cytopathological examination revealed no neoplastic cells, and the bacterial culture was negative. The abdominal ultrasound revealed a normal gallbladder and biliary tract and a homogeneous atrophic liver. Abdominal computed tomography revealed a calcified pancreas, voluminous ascites, and mild left pleural effusion. Esophagogastroduodenoscopy revealed esophageal varices and mild gastritis.
After the diagnosis of liver cirrhosis (Child-Pugh class B) and spontaneous bacterial peritonitis, the patient was treated with IV ceftriaxone (1 g b.i.d.), oral spironolactone (100 mg/day), IV albumin (1.5 g/kg on the 1st day and 1.0 g/kg on the 3rd day), furosemide (20 mg IV, b.i.d.), intramuscular phytomenadione (10 mg), oral vitamin B complex, and packed blood cells.
The Nutrology Support Team was consulted and found signs of chronic malnutrition, including a low body mass index, 17.9 kg/m2 (body weight: 48.8 kg) and signs of reduced corporal fat and muscle reserves (arm circumference: 15.5 cm; triceps skin fold: 3 mm). In addition to atrophic musculature in both thighs and lower legs, extensive bilateral subcutaneous edema with the presence of ecchymosis, corkscrew hairs, and perifollicular hemorrhage, mainly around the knees, were noted (). A diagnosis of kwashiorkor (acute protein malnutrition) and scurvy was made, and because the patient was anorectic and consumed a diet that was low in energy and nutrients, enteral tube feeding was initiated. A skin biopsy and a blood sample to measure plasma ascorbic acid were obtained from the patient before the continuous IV infusion of 1.5 g of vitamin C/day was started.
The patient maintained a daily positive body water balance, experienced diarrhea, and developed serum electrolyte abnormalities, including hyponatremia (sodium: 130 mEq/L), hypokalemia (potassium: 2.99 mEq/L), hypomagnesemia (magnesium: 1.1 mg/dL), and hypophosphatemia (phosphorus: 1.98 mg/dL). A diagnosis of refeeding syndrome was made based on these electrolyte imbalances; the enteral nutrition that the patient was receiving (containing 1600 kcal (32 kcal/body weight) was tapered, and the electrolyte abnormalities were treated.
Despite hemodynamic support and medication treatment, the patient had a poor clinical evolution and died of septic shock 10 days after admission to the hospital. His initial serum level of vitamin C was <0.2 mg/dL, which increased to normal values (1.3 mg/dL) on the 4th day of IV vitamin C supplementation. The skin biopsy showed atrophic, hyperkeratosis epidermis. On the dermis, there were several hair follicles plugged with keratin, hemorrhage, and dermal atrophy, which are suggestive of scurvy ().",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [36.0, 'mg/dL'], 'Glucose': [86.0, 'mg/dL'], 'Sodium': [136.0, 'mEq/L']}",289.63492,275.15317,304.11667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 136.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.0 mEq. To convert from 136.0 mEq to mmol, convert from mEq to mmol. The compound 136.0 has a valence of 1, and so divide the valence by the value of mEq to get, 136.0 mEq/(1 mEq/mmol) = 136.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mEq sodium/L converts to 136.0 mmol sodium/L. 
The concentration of bun is 36.0 mg/dL. 
The concentration of glucose is 86.0 mg/dL. 
Plugging these values into the equation, we get 2 * 136.0 + (36.0 / 2.8) + (36.0 / 18) = 289.63492 mmol/L.The patient's calculated serum osmolality concentration is 289.63492 mmol/L. This is equalivalent to 289.63492 mOsm/kg."
5906,30,Serum Osmolality,lab test,decimal,pmc-5175055-1,Extracted,"A 68-year-old female patient presented to our emergency service with inability to pass gas and feces for 2 days, abdominal distension, and vomiting. Her personal medical history was unremarkable, without any previous disease or operation. This multipara patient was 155 cm tall, and weighed 40 kg. Her vital signs were as follows: ABP: 120/70 mmHg, pulse rate: 78/min, respiratory rate: 23/min, body temperature: 36.7°C. Physical examination revealed abdominal distension without abdominal guarding, and rebound tenderness. The rectal ampulla was empty on digital rectal examination. Other system examinations were unremarkable. Results of laboratory tests were as follows: Htc: 43.1%; WBC: 11700/mm3, glucose: 125 mg/dL, BUN: 61mg/dL, creatinine: 1.21 mg/dL, sodium: 135 mEq/L, potassium: 4.3 mEq/L. Standing KUB revealed air-fluid level of intestines (). On whole abdominal ultrasound, dilated intestinal loops, and free fluid between intestinal loops were detected. Computed tomography (CT) demonstrated obstructive obturator hernia on the left side (Figures , ). The patient was operated urgently with the diagnosis of intestinal obstruction caused by strangulated obturator hernia. On exploration, a strangulated intestinal loop was detected within the left obturator channel, and reduced. Intestinal ischemia, necrosis or perforation were not detected, so additional intervention was not performed. The defect was repaired using a polypropylene mesh placed in the preperitoneal region. The patient was lost on postoperative 3rd day because of acute respiratory failure.",What is the patient's serum osmolality in terms of mOsm/kg? You may take the alcohol content as 0 mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Blood Urea Nitrogen (BUN)': [61.0, 'mg/dL'], 'Glucose': [125.0, 'mg/dL'], 'Sodium': [135.0, 'mEq/L']}",298.73016,283.79365,313.66667,"The formula for computing serum osmolality is 2 * Na + (BUN / 2.8) + (glucose / 18), where Na is the concentration of sodium in mmol/L, the concentration of BUN is in mg/dL, and the concentration of glucose is in mg/dL.
The concentration of sodium is 135.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 135.0 mEq. To convert from 135.0 mEq to mmol, convert from mEq to mmol. The compound 135.0 has a valence of 1, and so divide the valence by the value of mEq to get, 135.0 mEq/(1 mEq/mmol) = 135.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mEq sodium/L converts to 135.0 mmol sodium/L. 
The concentration of bun is 61.0 mg/dL. 
The concentration of glucose is 125.0 mg/dL. 
Plugging these values into the equation, we get 2 * 135.0 + (61.0 / 2.8) + (61.0 / 18) = 298.73016 mmol/L.The patient's calculated serum osmolality concentration is 298.73016 mmol/L. This is equalivalent to 298.73016 mOsm/kg."
5907,31,HOMA-IR (Homeostatic Model Assessment for Insulin Resistance),lab test,decimal,pmc-3114100-1,Extracted,"In the 1998 report on the treatment of B, he was 20 years old. B had been a child with a classical gender dysphoric development and fulfilled the current criteria for GnRH analog treatment eligibility. He was interviewed shortly after his legal gender change. This meant that he had had puberty suppression, cross-sex hormone treatment, a mastectomy, ovariectomy, and uterus extirpation. From his assessment during the diagnostic phase, he appeared to be an intelligent person (IQ = 128) with excellent problem-solving capabilities with respect to emotional matters. Vulnerable aspects of his psychological functioning were his insecurity about himself and moderately depressed feelings. In all other areas, his scores on a broad range of measures were in the average range, as compared to Dutch normative samples. Shame concerning his transsexualism made him highly selective in his friendships and guarded in his contacts with new people. At the assessment, 1 year after his ovariectomy but prior to his metaidoioplasty, he no longer reported feelings of gender dysphoria. He had adjusted easily to the male role and expressed no doubts on the adequacy of his masculine behavior. After the development of his secondary male sex characteristics, nobody had ever approached him as a woman. He never felt any regrets about his decision and had never contemplated living as a girl again. Knowing what gender reassignment implied, he would do it all over again. B was happy with his life and did not feel lonely. He showed a significant pre-post treatment decrease in his feelings of inadequacy. At the time, he was attending medical school.
B attended the pediatric endocrinology clinic for the first time when he was age 13.7 years. His medical history was uneventful. Puberty had started 1–2 years previously, but menarche had not occurred. On physical examination, a healthy girl was seen with a height of 157.3 cm and a Tanner pubertal stage of B3, P3. Bone age according to Tanner and Whitehouse was 13.5 years. Target height, as a female, was estimated at 171 cm, based on the parental height. Puberty suppression was induced by the GnRH analog Triptorelin, in a dose of 3.75 mg every 4 weeks intramuscularly. On this dosage, B steadily kept on growing.
At age 18.6 years, his height was 165.8 cm. Induction of male puberty and accompanying secondary male sex characteristics was initiated by administration of 100 mg testosterone-ester mixture intramuscularly every 2 weeks. This was, after 6 months, increased to 250 mg testosterone-ester mixture, every 2–3 weeks intramuscularly. At the start of the androgen treatment, the Triptorelin treatment was discontinued.
When B was 20 years old, he had a subcutaneous mastectomy by way of an infra-areolar approach, a few months later followed by a hysterectomy and gonadectomy. Two years later, metaidoioplasty and testes implantation were performed.
Fifteen years after the first interview and testing session, at age 35, B was seen again at the clinic. He lived on his own and he worked as a family doctor in private practice with two colleagues. All family members knew about his transitioning as did some of his friends. He was very satisfied about his circle of friends and had never been treated negatively because of his transsexualism.
B was still satisfied about his (minor) breast surgery, his ovariectomy, and his hysterectomy, but no longer about the metaidoioplasty he underwent one year after the first follow-up session. He did not like its size and shape and he could hardly urinate in a standing position. He was able to have orgasms, but he could not have sexual intercourse. Because of his desire to have more convincingly male appearing external genitals and his wish to be able urinate in a standing position, he considered having a phalloplasty. Despite his good looks and very masculine appearance, he had not had many steady girlfriends, which may have resulted from the guardedness he already had as an adolescent. At age 29, he had a serious relationship with a woman, which lasted for 5 years. However, he chose not to live together when the opportunity to do so arose. After his choice to continue living apart, his girlfriend ended the relationship, a few months before his interview at the clinic. This made him very much regret his lack of commitment. B considered it likely that his need to distance himself from her had been related to his shame about his genital appearance and his feelings of inadequacy in sexual matters. Additional factors, such as serious illness of his father and a suicide among his sisters’ in-laws, made him rather sad at the time of the interview. Although his psychoneuroticism score on the Symptom Checklist-90 (Arrindell & Ettema, ) was in the normal range, his depression subscore was high, indicating depressed feelings. However, on the Beck Depression Inventory, he scored in the “minimal range” (van der Does, ), indicating that he did not fulfill criteria for clinical depression. On the Adult Self-Report, assessing adaptive functioning and problems in adults aged 18-59 years (Achenbach & Rescorla, ), all his scores were in the normal range.
It seems, therefore, that B functioned well in most aspects of life, but that he was still struggling with the question, how to handle the dissatisfaction and shame about his genital appearance.
At age 35, on physical examination, we saw a healthy and well virilized person. Blood pressure was 120/85 mmHg, final height was 169.5 cm and weight was 73 kg, which resulted in a body mass index (BMI) of 25.4 kg/m2. Sitting height was 88 cm. Skull circumference was 55.5 cm. For a comparison of his anthropometrical measurements to the normal reference values of Dutch males and females, see Table .
A fasting venous blood sample was drawn. General health markers, like hematological parameters (Hb, ht, erythrocytes), renal function, and liver enzymes, were all within the normal reference value ranges. His lipid profile showed a total cholesterol level of 228.3 mg/dl (<251.5 mg/dl), LDL-cholesterol 154.8 mg/dl (<193.5 mg/dl), HDL-cholesterol 55.0 mg/dl (>34.8 mg/dl), and triglycerides 97.4 mg/dl (<177 mg/dl). His glucose value was 97.3 mg/dl (<144.1 mmol/l) with an insulin level of 21 pmol/l (12–96 pmol/l for a fasting sample). His HbA1c was 5.4% (4.3–6.1%). These values were in the normal range.
With respect to the gonadal axis, a normal-low serum testosterone level of 236.6 ng/dl (231–866 ng/dl) was found. This relatively low level was probably due to the fact that the blood sample was taken just before the next testosterone-ester mixture injection. Gonadotropins were elevated as a consequence of the gonadectomy. LH and FSH were 16 U/l and 50 U/l, respectively. Additionally determined endocrine parameters, such as thyroid and adrenal function, were all within normal reference ranges.
With respect to bone mineral density (BMD), a dual energy X-ray absorptiometry (DEXA) scan was performed to determine B’s BMD in the lumbar spine, the non-dominant hip, and (further) total body. The observed values were related to the bone peak mass for white females and for white males, resulting in T-scores. For all values, the z-score was determined as well (see Table ).",What is the patient's HOMA-IR score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Insulin': [756.0, 'pmol/L'], 'Glucose': [97.3, 'mg/dL']}",1089.76,1035.272,1144.248,"The formula for computing HOMA-IR score is (insulin (µIU/mL) * glucose mg/dL)/405.
The concentration of insulin is 4536.0 pmol/L. We to need convert the concentration of insulin to pmol/L, by multiplying by the conversion factor of 6.0 µIU/mL/pmol/L. This makes the insulin concentration 756.0 * 6 µIU/mL/pmol/L = 4536.0 µIU/mL.
The concentration of glucose is 97.3 mg/dL. 
Plugging into the formula will give us 4536.0 * 97.3/405 = 1089.76. Hence, the patient's HOMA-IR score is 1089.76."
5908,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,pmc-5403165-2,Extracted,"A 17-year-old young man presented to the pediatric emergency department with intermittent high-grade fever for two days in August 2015. This was associated with myalgia, headache, rhinorrhea, sore throat, productive cough and abdominal pain. Physical examination showed a congested oropharynx and soft abdomen with hyperactive bowel sounds. Laboratory tests showed a WBC of 3.06×109/L, a HCT of 38.6% and a platelet count of 151×109/L. Throat swab tested negative for influenza quick test and negative for beta-hemolytic streptococcus and nasopharyngeal swab was positive for DENV-2. His stool was negative for adenovirus (Adenolex test, Orion Diagnostica, Finland, as text in S1). He was treated for acute bacterial tonsillitis with oral amoxicillin and followed up in the pediatric clinic 2 days after, with marked improvement of symptoms.",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Symptom onset <=3 days': True, 'Purulent tonsils': False, 'Fever in past 24 hours': True, 'Severe tonsil inflammation': False, 'Absence of cough or coryza': False}",2,2,2,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
The patient is reported to have a fever in the past 24 hours and so we increment the score by 1, making the current total 0 + 1 = 1.
The patient is determined to have a cough or corzyea at the time of admission. Because of this, we do not add any points to the current total, keeping the current total at 1.
The patient is reported to have a symptom onset ≤3 days and so we increment the score by 1, making the current total 1 + 1 = 2.
The patient is reported to not have purulent tonsils and so we do not increment the score, keeping the current total at 2.
The patient is reported to not have severe tonsil inflammation and so we do not increment the score, keeping the current total at 2.
The patient's FeverPain score is 2 points."
5909,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,usmle-395,Extracted,"An 11-year-old boy is brought to the emergency department 30 minutes after he was found screaming and clutching his head. He has had nausea and occasional episodes of vomiting for 1 week, fever and left-sided headaches for 2 weeks, and increasing tooth pain over the past 3 weeks. He has no history of ear or sinus infections. He is in moderate distress. His temperature is 38.7°C (101.7°F), pulse is 170/min, respirations are 19/min, and blood pressure is 122/85 mmHg. He is confused and only oriented to person. The pupils react sluggishly to light. Fundoscopic examination shows papilledema bilaterally. Extraocular movements are normal. Flexion of the neck causes hip flexion.",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Symptom onset <=3 days': True, 'Fever in past 24 hours': True, 'Absence of cough or coryza': True}",3,3,3,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
The patient is reported to have a fever in the past 24 hours and so we increment the score by 1, making the current total 0 + 1 = 1.
The patient is determined to have an absence of cough or coryza. Because of this, we add one point to the score, making the current total 1 + 1 =  2.
The patient is reported to have a symptom onset ≤3 days and so we increment the score by 1, making the current total 2 + 1 = 3.
Whether the patient has purulent tonsils is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 3.
Whether the patient has severe tonsil inflammation is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 3.
The patient's FeverPain score is 3 points."
5910,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,pmc-5965193-1,Extracted,"A six-year-old female presented to a small rural ED with her mother for a four-day history of sore throat and fever. Fever at home was reported as high as 102 degrees Fahrenheit. The mother had been treating her child’s symptoms with over-the-counter acetaminophen and cold medicine. There was additional report of ear pain and a mild cough. There were no complaints of abdominal pain, urinary symptoms, or rash. Immunizations were reported as up to date. The patient had recently been seen by her pediatrician and had a rapid strep screen that was negative. There was no significant past medical history, surgical history, or allergies. The child took no scheduled medications at home. Reviews of systems were negative.
On initial presentation, triaged vitals were temperature 102.7 degrees Fahrenheit, heart rate 112 beats per minute (bpm) and blood pressure 97/72 mmHg. The child was awake, alert, and interactive. On exam, no significant posterior pharyngeal erythema or tonsillar exudates were noted. Bilateral ear canals were patent with no tympanic membrane abnormalities. There were no other noteworthy physical exam findings. Based on the history and physical exam, the patient’s pharynx was re-swabbed for rapid strep and she was given ibuprofen for her fever. The rapid strep throat screen resulted negative. She was diagnosed with viral pharyngitis and was discharged home with follow-up with her pediatrician in two days.
Six days later the patient presented a second time. This time the chief complaint was worsening sore throat and swollen hard neck. Temperature on arrival was 101.6 degrees Fahrenheit, heart rate 156 bpm, blood pressure 112/83 mmHg, and respiratory rate 20 breaths per minute. Pertinent exam findings were anterior neck that was firm and with fullness with palpation. Diffuse cervical lymphadenopathy was present. Patient was able to flex and extend her neck normally. No tonsillar exudates or erythema noted. Tympanic membranes were clear with patent canals bilaterally. Another rapid strep screen and culture were collected and recorded as negative. Radiographs of the chest and soft tissue of the neck were read by radiology as no acute findings. A mono-spot test resulted negative. Complete blood count (CBC) showed white blood cells (WBC) 19.1 K/uL; high end of assay was 11,000 K/uL. The patient was diagnosed with pharyngitis and was administered dexamethasone and amoxicillin/clavulanate. She was discharged to home with a prescription for amoxicillin/clavulanate and prednisolone and directed to follow up with her pediatrician.
Several hours later the attending emergency physician contacted the family to inquire how the child was doing post discharge. When the mother reported that her child was vomiting, she was told to return to the ED. A third time to the ED, seven hours after recent discharge, the patient presented clammy and diaphoretic. Heart rate was 58bpm, blood pressure 123/61 mmHg, temperature 97.9, and respiratory rate 16 breaths per minute. CBC showed WBC 21.1 K/uL. Basic metabolic panel was within normal limits of assay, as was a urinalysis. Anti-streptolysin-O blood test was reported as negative. Thyroid-stimulating hormone was ordered and reported as undetectable and free T4 2.29 NG/DL elevated for this assay.
Computed tomography (CT) of the soft tissue of the neck was completed and read by radiology as multiloculated heterogeneous fluid and presence of a soft tissue lesion in the left thyroid lobe measuring 2.8 × 3.5cm in axial cross-section and about five centimeters in craniocaudal dimension ( and ). Findings were most compatible with acute suppurative thyroiditis.",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Symptom onset <=3 days': False, 'Purulent tonsils': False, 'Fever in past 24 hours': True, 'Severe tonsil inflammation': False, 'Absence of cough or coryza': False}",1,1,1,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
The patient is reported to have a fever in the past 24 hours and so we increment the score by 1, making the current total 0 + 1 = 1.
The patient is determined to have a cough or corzyea at the time of admission. Because of this, we do not add any points to the current total, keeping the current total at 1.
The patient is reported to not have a symptom onset ≤3 days and so we do not increment the score, keeping the current total at 1.
The patient is reported to not have purulent tonsils and so we do not increment the score, keeping the current total at 1.
The patient is reported to not have severe tonsil inflammation and so we do not increment the score, keeping the current total at 1.
The patient's FeverPain score is 1 points."
5911,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,pmc-6396525-1,Extracted,"An 81-year-old Asian man presented to our department complaining of fever since the preceding day. The patient had been under treatment for the previous 3 years for chronic heart failure and chronic renal failure. He did not have a history of malignancy, diabetes mellitus, cytotoxic therapy, or corticosteroid use, and no foreign bodies had been implanted. The patient’s family history was unremarkable. Physical examination revealed a heart rate of 101 beats/min, blood pressure of 87/48 mmHg, respiratory rate of 20 breaths/min, temperature of 37.0 °C, and oxygen saturation of 87% on room air. He had no caries or periodontitis. Results of respiratory, cardiac, and abdominal examinations were unremarkable. Limb examination demonstrated mild edema of both legs. Abdominal computed tomography (CT) showed a low-density mass in the right iliopsoas muscle indicative of an iliopsoas abscess (Fig. ). The patient’s white blood cell count, C-reactive protein (CRP), and procalcitonin levels were 19,400/μl, 13.35 mg/dl, and 3.950 ng/ml, respectively. Serum blood urea nitrogen and creatinine were elevated at 77.2 mg/dl and 3.69 mg/dl, respectively. A CT-guided percutaneous drainage of the psoas abscess was performed, and an indwelling catheter was placed. Gram staining of the drained fluid revealed many neutrophils and Gram-positive streptococci. On the basis of these findings, a presumptive diagnosis of iliopsoas abscess caused by Streptococcus species was made, and treatment with ampicillin/sulbactam (ABPC/SBT) 1.5 g, administered intravenously every 8 h, was initiated. Results of organism cultures of the abscess and blood were positive, and P. micra was identified by using the API ZYM system (Sysmex-bioMérieux Co. Ltd., Tokyo, Japan), with the organism exhibiting susceptibility to penicillin G, ampicillin, clindamycin, and meropenem. By day 7, the patient’s white blood cell count normalized. By day 20, his CRP level was decreased to 0.35 mg/dl. Therefore, the pigtail catheter was removed. The patient died of peritonitis due to colon diverticulum perforation after 5 weeks of treatment. An autopsy revealed no right iliopsoas abscess at the time of death.",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Fever in past 24 hours': True, 'Symptom onset <=3 days': False, 'Absence of cough or coryza': True}",2,2,2,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
The patient is reported to have a fever in the past 24 hours and so we increment the score by 1, making the current total 0 + 1 = 1.
The patient is determined to have an absence of cough or coryza. Because of this, we add one point to the score, making the current total 1 + 1 =  2.
The patient is reported to not have a symptom onset ≤3 days and so we do not increment the score, keeping the current total at 2.
Whether the patient has purulent tonsils is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 2.
Whether the patient has severe tonsil inflammation is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 2.
The patient's FeverPain score is 2 points."
5912,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,pmc-7257222-1,Extracted,"A 29-years-old female experienced an episode of mild upper respiratory tract infection followed by a slowly developing dysphagia and dyspnea. This led to impaired exercise tolerance lasting several months, with recent subacute exacerbation. There was no significant history of travel or exposure to infectious agents. She had not suffered from fever or other acute or chronic infectious symptoms. Her palatine tonsils had been removed in childhood. She was diagnosed with epilepsy at age 17 and had been free of epileptic symptoms for over 5 years with levetiracetam (500 mg two times per day) and lamotrigine (150 mg two times per day). Her family history was unremarkable.
She spoke with hoarse voice, without signs or findings that would have suggested systemic involvement. There were no signs of generalized mucosal disease. Fiberoptic examination showed swelling of the lingual tonsil, epiglottic and arytenoid mucosa, causing airway obstruction (Fig. a). C-reactive protein concentration and blood sedimentation rate were low, and anti-nuclear, anti-neutrophil, anti-glomerular basement membrane, anti-myeloperoxidase, anti-proteinase 3, tissue transglutaminase and cyclic citrullinated peptide antibodies were negative. Thyroid function was normal and thyroid peroxidase antibodies were 34 IU/ml (normal value < 60 IU/ml). Plasma parathyroid hormone (39 ng/l; normal 18–80 ng/l) and serum vitamin D-25 (77 nmol/l; normal > 50 nmol/l) were normal. No evidence for acute or chronic viral, bacterial, mycobacterial or fungal infections, including hepatitis B and C, human immunodeficiency virus and tularemia, was found.
Due to her swollen lingual tonsil and laryngeal mucosa causing airway obstruction, she was hospitalized and received empiric cefuroxime (1.5 g thrice daily) and methylprednisolone (75 mg once daily, height 173 cm, weight 63 kg, prednisolone dose 1.2 mg/kg) intravenously. After a transient positive response, she was discharged from the hospital after 6 days. Soon after, she was readmitted to due to a rapid reoccurrence of the symptoms. A modest positive response was seen after per oral clindamycin and oral prednisolone (60 mg/days) with dose reduction for 14 days. Lingual tonsil and epiglottis were biopsied. Histology showed granulomatous reaction in lingual tonsil with CD68+ (Kp-1) epithelioid histiocytes (Fig. ). The CD20+ B lymphocyte count was increased while Pax-5+ positive B lymphocyte count was normal. CD138+ plasma cells were scarce, and they showed polytypic kappa- and lambda light chain expression. The number of CD3+ T cells was normal, and most T cells were CD4+. Eosinophils were practically absent and well-formed follicles were not seen. Epstein–Barr virus in situ hybridization (EBER), p16, cytomegalovirus and mycobacteria were negative. Morphology, immunohistochemical staining, serum electrophoresis and bone marrow aspirate did not raise suspicion of lymphoid neoplasia, thus, no clonality studies were done.
Due to granulomas, sarcoidosis was considered. However, chest X-ray, computerized tomography of chest and ultrasound of neck and abdomen were unremarkable. Positron emission tomography/computed tomography (PET/CT) showed increased fluorodeoxyglucose (FDG) uptake in the lingual tonsil, without evidence of widespread sarcoidosis (Fig. ). No other pathological FDG foci were found. Focal physiological FDG accumulation was seen in ureters on both sides of the spinal column. This is a common finding due to ureteral peristalsis and pooling of radiotracer in the recumbent patient. The patient had no neurological symptoms and brain magnetic resonance imaging was normal. Serum angiotensin converting enzyme (ACE) was within normal range (11–20 U/l; reference range 9–65 U/l) while daily urine calcium output was normal or slightly elevated (5.0–6.31 mmol; reference range 1.2–5.5 mmol).
Subsequently, an unusual presentation of primary or secondary immunodeficiency was considered. There was no consanguinity; the patient or her family had no history of repeated infections or autoimmunity. White cell, lymphocyte, and B, T and NK lymphocyte subset counts were within normal limits. CD19+ B cell count was 153 × 109/l (normal range 80–616 × 109/l). Proportions of memory CD27+ B-cells (30.3%) and IgD−IgM−CD27+ switched memory B cells 7.2%; (normal range 6.5–29.2%) were normal and the percentage of activated CD21low B cells was high (6.6%; normal range 0.6–3.5%). Percentages of various CD3+CD4+ and CD3+CD8+ T cell subsets appeared normal. Serum total IgG (3.5 g/l; normal range 6.77–15.0 g/l) and all IgG subclass concentrations were low: IgG1 2.45 g/l (normal range 4.9–11.4 g/l), IgG2 0.91 g/l (normal range 1.5–6.4 g/l), IgG3 0.18 g/l (normal range 0.2–1.1 g/l) and IgG4 0.02 g/L (normal range 0.08–1.4 g/l). Anti-polysaccharide response to Pneumovax® were impaired, with only 3/10 serotypes reaching a level of 0.35 µg/ml after immunization. However, serum IgA (0.90 g/l; normal range 0.52–4.02 g/l) and IgM concentrations (0.57 g/l; normal range 0.47–2.84 g/l) were normal. Dihydrorhodamine test excluded chronic granulomatous disease. These findings were thus consistent with either granulomatous CVID or most likely secondary drug-induced hypogammaglobulinemia with a novel clinical presentation [–]. Genetic analysis (Blueprint Genetics, Primary Immunodeficiency Plus panel. ) did not find known mutations causative of CVID-like or other primary immunodeficiencies.
Due to symptomatic upper airway obstruction, dysphagia, lack of evident infection and unsatisfactory response to prednisolone treatment and possible granulomatous CVID, the patient received immunoglobulin replacement and rituximab therapy (Mabthera® 100 mg, 200 mg and 500 mg on three consecutive days combined with 100 mg hydrocortisone and 1 g paracetamol), with a favorable response within 2 weeks accompanied by significant improvement in dysphagia and respiratory symptoms. Seven months later, her exercise capacity was good. She has remained asymptomatic for over 16 months after rituximab treatment. Her fiberoptic pharyngeal findings improved (Fig. ). She continues to receive subcutaneous immunoglobulin replacement with serum IgG levels in the range of 10 to 12 g/l.",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Purulent tonsils': True, 'Symptom onset <=3 days': False, 'Severe tonsil inflammation': False}",2,2,2,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
Whether the patient has a fever in the past 24 hours is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 0.
Whether the patient has an absence of cough or coryza is not reported and so we assume that it is absent for the patient. Because of this, we add one point to the score, making the current total 0 + 1 =  1.
The patient is reported to not have a symptom onset ≤3 days and so we do not increment the score, keeping the current total at 1.
The patient is reported to have purulent tonsils and so we increment the score by 1, making the current total 1 + 1 = 2.
The patient is reported to not have severe tonsil inflammation and so we do not increment the score, keeping the current total at 2.
The patient's FeverPain score is 2 points."
5913,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,pmc-7850324-1,Extracted,"A 22-year-old man with bipolar disorder and anxiety presented with fevers, chills, nausea, vomiting, and a non-productive cough for four days. He reported a fever up to 40°C at home and an inability to tolerate oral intake for approximately two days. His cough was dry and not associated with sputum production or hemoptysis. He endorsed headaches and diarrhea as associated symptoms. He reported a significant tetrahydrocannabinol (THC) and nicotine vaping history, which included the use of two nicotine cartridges and one THC cartridge daily. His last use was approximately 1 week prior to presentation. He denied neck pain and stiffness, leg swelling, dysuria, and abdominal pain. There was no personal or family history of thromboembolism. His home medications, taken daily, included lamotrigine and escitalopram. He had no recent travel history or sick contacts. The patient lived in a college dormitory in a major U.S. city. He had no pets or recent contact with birds. He denied any known exposure to heavy metals, agricultural chemicals, or any dyes, foams, and resins. The patient had also never been exposed to toxic gases such as chlorine. It should be noted that this patient presented to the hospital for care approximately four months before the first U.S. case of COVID-19, and as such, this is not investigated as part of the work-up.",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Purulent tonsils': False, 'Symptom onset <=3 days': True, 'Severe tonsil inflammation': False}",2,2,2,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
Whether the patient has a fever in the past 24 hours is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 0.
Whether the patient has an absence of cough or coryza is not reported and so we assume that it is absent for the patient. Because of this, we add one point to the score, making the current total 0 + 1 =  1.
The patient is reported to have a symptom onset ≤3 days and so we increment the score by 1, making the current total 1 + 1 = 2.
The patient is reported to not have purulent tonsils and so we do not increment the score, keeping the current total at 2.
The patient is reported to not have severe tonsil inflammation and so we do not increment the score, keeping the current total at 2.
The patient's FeverPain score is 2 points."
5914,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,pmc-6727329-1,Extracted,"A 63-year-old Caucasian man presented to our hospital with 2 weeks of progressive generalized weakness, vague abdominal discomfort, and dyspnea on exertion requiring more frequent use of his inhaler. He did not report similar symptoms in the past, and he denied any associated chest pain, cough, changes in bowel habits, fevers, chills, weight loss, recent travel, tick bites, or sick contacts. His past medical history was relevant for chronic bronchitis diagnosed 10 years ago. He was a former one-pack-per-day smoker for 20 years. His family history was noncontributory.
The patient’s vital signs at presentation showed a blood pressure of 128/84 mmHg, heart rate of 75 beats/minute, respiratory rate of 18 breaths/minute, oxygen saturation of 99% on room air, and body temperature of 97.7 °F. On physical examination, the patient was in no apparent distress and was awake, alert, and oriented to person, place, and time. His heart and lung examination revealed sinus tachycardia and diffuse expiratory wheezes throughout the lung fields. The patient’s abdominal examination was pertinent for a nonperitonitic tenderness to palpation in the left upper quadrant. His neurological examination was remarkable for weakness in the right upper extremity. His laboratory data are summarized in Table .
See Fig. for the timeline of the patient’s kidney function and absolute eosinophil count while receiving steroid treatment.
Findings of computed tomography (CT) of the patient’s brain were unremarkable. Magnetic resonance imaging (MRI) of his brain revealed subacute infarcts involving the left frontal white matter and left cerebellum; in addition, an evolving subacute infarct was seen in the left corona radiata. CT of the chest demonstrated diffuse ground-glass opacity, and CT of the abdomen was remarkable for a wedge-shaped area of low attenuation in the spleen consistent with splenic infarct. His transthoracic echocardiogram revealed a mural apical thrombus in the left ventricular (LV) apex with reduced ejection fraction (31–35%). Cardiac MRI performed 7 days after anticoagulation therapy was initiated showed a diffuse subendocardial scarring of the middle to apical LV segments and the right ventricular side of the septum. It also revealed evidence of edema of the middle anteroseptum and apical septum, consistent with endomyocardial fibrosis. However, no mural thrombus was visualized.
A presumptive diagnosis of HES was made on the basis of presenting symptoms, laboratory data, and imaging studies. Investigation for secondary causes, including immunological testing (Table ), blood and urine cultures, ova and parasites, and infectious serology (Table ), were unrevealing, and results of urine drug screening were negative. Bone marrow biopsy demonstrated a normocellular bone marrow population with eosinophilia comprising 60–70%, without evidence of lymphoproliferative disorder or metastatic neoplasm. Cytogenetic analysis was unrevealing: negative for breakpoint cluster region-Abelson murine leukemia viral oncogene homolog 1 (BCR-ABL1) fusion, eosinophilia-associated platelet-derived growth factor receptor alpha (PDGFRA), platelet-derived growth factor receptor beta (PDGFRB), fibroblast growth factor receptor 1 (FGFR1), Janus kinase 2 (JAK2) mutation, and JAK2 pericentriolar material 1 (PCM1) fusion.
Due to the stigma of hemolysis (normocytic acute anemia, elevated lactate dehydrogenase and bilirubin, positive schistocytes with relative thrombocytopenia), further investigation was pursued. The result of the Coombs test (direct and indirect) was negative. A disintegrin-like and metalloprotease with thrombospondin type 1 motif 13 (ADAMTS13) activity level was greater than 50%, and the expression of complement regulatory proteins CD59 and CD55 on erythrocytes was within normal limits as determined by flow cytometry.
Due to a further decline in the estimated glomerular filtration rate (GFR) early in the patient’s hospital course, a kidney biopsy was pursued. Renal biopsy revealed a glomerular and vascular TMA, interstitial fibrosis, and inflammation with focal eosinophils (Fig. ). IHC staining for eosinophil granule major basic protein 1 (MBP1) was not performed.
Our patient was started on prednisone 1 mg/kg daily and a heparin protocol at 18 U/kg/hour with an activated partial thromboplastin time goal of 60–100 seconds. Simultaneously, warfarin was initiated. Once the patient’s international normalized ratio was within therapeutic range (2.0–3.0), he was anticoagulated with heparin and warfarin for an additional 48 hours. His eosinophil count and estimated GFR were monitored on an outpatient basis, and his prednisone dose was gradually tapered. After the eighth week, the patient was maintained on 5 mg of prednisone daily.
By the time the renal biopsy report was available, the patient’s kidney function had started to recover; hence, no further intervention was required. After initiation of treatment with steroids, the patient achieved resolution of pulmonary, cardiac, neurologic, and abdominal symptoms. Repeat echocardiography after 5 weeks showed improvement of LV ejection fraction to 50–55%. Complete normalization of eosinophil count and renal function was observed after 4 and 8 weeks of therapy, respectively (Fig. ). At his 10-week follow-up, the patient continued to do well under close surveillance for renal and cardiac complications. At 12-month follow-up, he continued to have a normal eosinophil count and renal function. However, cardiac MRI showed persistent endocardial fibrosis.",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Purulent tonsils': True, 'Symptom onset <=3 days': False, 'Severe tonsil inflammation': False}",2,2,2,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
Whether the patient has a fever in the past 24 hours is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 0.
Whether the patient has an absence of cough or coryza is not reported and so we assume that it is absent for the patient. Because of this, we add one point to the score, making the current total 0 + 1 =  1.
The patient is reported to not have a symptom onset ≤3 days and so we do not increment the score, keeping the current total at 1.
The patient is reported to have purulent tonsils and so we increment the score by 1, making the current total 1 + 1 = 2.
The patient is reported to not have severe tonsil inflammation and so we do not increment the score, keeping the current total at 2.
The patient's FeverPain score is 2 points."
5915,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,pmc-6449525-1,Extracted,"A 72-year-old male attended the otorhinolaryngology outpatient department with complaints of right ear discharge over 2 years. He had no other constitutional symptoms. The patient had undergone left side myringoplasty 5 years previously for chronic suppurative otitis media. His chronic ear discharge was not resolved after ear surgery. The ear discharge was sent for bacterial culture which showed no growth. The patient was taking topical ciprofloxacin ear drops, without any resolution of the symptoms.
On examination of the ear, it revealed mild myringitis, thickening of the posterior ear canal, and active purulent discharge. There was some pinkish-to-pale colored granulation tissue at the posterosuperior quadrant of the tympanic membrane ().
The tympanic membrane was intact. The patient was concerned about malignancy and we took tissue from the granulations at the ear canal and sent it for histopathological examination. Histopathological examination showed squamous epithelium with granulo- matous inflammation. The acid-fast bacilli stain was positive for acid-fast bacilli ().
There were no fungal hyphae on Grocott’s methenamine silver stain and no evidence of any malignancy. Real-time polymerase chain reaction (PCR) of the formalin-fixed paraffin-embedded tissue was positive for Myco-bacterium tuberculosis, which was surprising.
The patient was then properly evaluated by chest physicians, and denied any fever, cough, weight loss, or hemoptysis. He had no past history of exposure to tuberculosis. The patient’s routine laboratory findings including complete blood count, liver function tests, erythrocyte sedimentation rate (ESR), and serum creatinine were normal. However, QuantiFERON-TB Gold was positive. A computed tomography (CT) scan of the both sides of the temporal bone was performed, which showed narrowing of the left external auditory canal ().
This lesion was treated for extrapulmonary tuberculosis, including rifampicin (600 mg daily), isoniazid (300 mg daily), pyrazinamide (2,000 mg) daily, and ethambutol (1600 mg) daily for 2 months. The isoniazid and rifampicin were continued for the next 8 months. The patient’s otorrhea was resolved within 1 month after starting the antitubercular therapy (ATT). Examination of the external auditory canal and tympanic membrane were normal after 6 months of treatment.",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Purulent tonsils': True, 'Symptom onset <=3 days': False}",2,2,2,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
Whether the patient has a fever in the past 24 hours is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 0.
Whether the patient has an absence of cough or coryza is not reported and so we assume that it is absent for the patient. Because of this, we add one point to the score, making the current total 0 + 1 =  1.
The patient is reported to not have a symptom onset ≤3 days and so we do not increment the score, keeping the current total at 1.
The patient is reported to have purulent tonsils and so we increment the score by 1, making the current total 1 + 1 = 2.
Whether the patient has severe tonsil inflammation is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 2.
The patient's FeverPain score is 2 points."
5916,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,pmc-6821478-1,Extracted,"Three-month-old female infant, admitted for social reasons. Fourth daughter of
non-consanguineous parents; mother with cognitive deficit. Born of 36-week pregnancy
complicated by gestational diabetes in the third trimester. Caesarean delivery due
to dystocia. Apgar Index=8/9; birth weight of 2,650 g (Percentile3-15),
length of 45.5 cm (Percentile3), head circumference of 33.2 cm
(Percentile15). Admitted in the first five weeks of life to the
neonatal intermediate care unit due to respiratory failure, asymptomatic
hypoglycemia, feeding difficulty and by social reason. Second admission to hospital
at two months old, lasting 48 hours, for acute bronchiolitis caused by respiratory
syncytial virus (RSV). Adequate weight-bearing growth and psychomotor
development.
The infant was taken to the pediatric emergency room for a clinical picture of 48
hours of fever (maximum axillary temperature 38.5°C), prostration and groaning, in
the context of varicella, with the first skin lesions identified for about ten days.
Upon examination at the emergency room, the infant had fever, was groaning, normal
fontanel, blood pressure of 94/54 mmHg, heart rate at 150 bpm, good perfusion,
eupneic. Numerous skin lesions in crust throughout the body, with signs of secondary
bacterial infection on the scalp. Remaining examinations showed no alterations.
Laboratorial results were ():
hemoglobin 76 g/L, leukocytes 45,7×109/L (neutrophils 51%), platelets
588×109/L, C-reactive protein (CRP) 18.8 mg/dL, glycemia, serum
transaminases and blood gas analysis were normal, two negative blood cultures,
urinalysis without abnormal findings, sterile urine culture, normal chest
radiography.
The patient was admitted with diagnostic hypothesis of sepsis, probably secondary to
impetiginized varicella. Intravenous antibiotic therapy with ceftriaxone (100
mg/kg/day) and topical (fusidic acid) was initiated.
On the third day of hospitalization, a swelling was identified in the left 7th rib,
at the nipple line, with hard consistency and poorly defined limits, apparently
painful to palpation and no other local signs of inflammation.
On the following day, laboratorial tests were repeated (): hemoglobin 79 g/L, leukocytes 13.4×109/L
(neutrophils 15%), CRP 4.8 mg/dL, sedimentation rate of 80 mm/1st hour. Chest
radiography did not show changes in costal arches. Ultrasound of soft tissues () showed volumetric increase of the
costochondral joint with free intra-articular fluid and irregularity of the costal
arch’s anterior end. Three-phase 99mTc-HMDP bone scintigraphy () showed focal hyperemia in the left anterior mid-arch
of the left costal arch and, in late images, high uptake of the radiopharmaceutical
in topography corresponding to the focus of hyperemia identified in blood diffusion
phase and area of hypo fixation of the radiopharmaceutical upon respective
costochondral joint topography, aspects compatible with inflammatory/infectious
pathology. The distribution of the radiopharmaceutical was normal in the rest of the
skeleton.
During hospitalization, the infant was always hemodynamically stable, with apirexia
from the third day and progressive improvement of general condition and cutaneous
lesions. Ten-day therapy with ceftriaxone was completed, at which time the infant
was submitted to laboratory reassessment (): hemoglobin 86 g/L, leucocytes 14.8×109/L (neutrophils
19%), CRP 0.3 mg/dL and sedimentation rate at 35 mm/1st hour. Oral
amoxicillin-clavulanic acid (70 mg/kg/day) was initiated, completing six weeks of
antibiotic therapy, presenting at the time of resolution of the palpable swelling
sedimentation rate at 10 mm/1st hour, CRP lower than 0.1 mg/dL () and control ecography showing
irregularity of the costal arch’s anterior extremity, although sclerotic borders of
apparently continuous form and aspects suggestive of consolidation were seen ().
Follow-up was maintained with appointments in Pediatrics, and immunity was then
tested with determination of immunoglobulins, resulting normal. There were no
intercurrences in the following year after hospital admission.",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Purulent tonsils': True, 'Symptom onset <=3 days': True, 'Severe tonsil inflammation': False}",3,3,3,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
Whether the patient has a fever in the past 24 hours is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 0.
Whether the patient has an absence of cough or coryza is not reported and so we assume that it is absent for the patient. Because of this, we add one point to the score, making the current total 0 + 1 =  1.
The patient is reported to have a symptom onset ≤3 days and so we increment the score by 1, making the current total 1 + 1 = 2.
The patient is reported to have purulent tonsils and so we increment the score by 1, making the current total 2 + 1 = 3.
The patient is reported to not have severe tonsil inflammation and so we do not increment the score, keeping the current total at 3.
The patient's FeverPain score is 3 points."
5917,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,usmle-585,Extracted,"A 43-year-old man comes to the physician because of nasal congestion and fatigue for 12 days. During this period, he has had fevers and severe pain over his cheeks. His nasal discharge was initially clear, but it has turned yellowish over the last couple of days. He has no visual complaints. He has been taking an over-the-counter nasal decongestant and acetaminophen without much relief. He has type 2 diabetes mellitus and hypertension. He underwent an appendectomy 23 years ago. He does not smoke or drink alcohol. His current medications include metformin, sitagliptin, and enalapril. He appears tired. His temperature is 38.5°C (101.3°F), pulse is 96/min, and blood pressure is 138/86 mm Hg. Examination shows purulent discharge in the nose and pharynx and normal appearing ears. The left maxillary sinus is tender to palpation.",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Purulent tonsils': False, 'Symptom onset <=3 days': True, 'Severe tonsil inflammation': False}",2,2,2,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
Whether the patient has a fever in the past 24 hours is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 0.
Whether the patient has an absence of cough or coryza is not reported and so we assume that it is absent for the patient. Because of this, we add one point to the score, making the current total 0 + 1 =  1.
The patient is reported to have a symptom onset ≤3 days and so we increment the score by 1, making the current total 1 + 1 = 2.
The patient is reported to not have purulent tonsils and so we do not increment the score, keeping the current total at 2.
The patient is reported to not have severe tonsil inflammation and so we do not increment the score, keeping the current total at 2.
The patient's FeverPain score is 2 points."
5918,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,pmc-7296882-1,Extracted,"A 73-year-old male presented to the ED with fever and lethargy for one day. His past medical history is significant for hyperlipidemia, hypertension, gout, and chronic ITP. His past surgical history included a recent dental procedure with a dental implant placement.
On examination, his temperature was 39.3 degree Celsius, blood pressure was 137/89 mmHg, heart rate was 99 beats/min. Cardiovascular system and respiratory system were unremarkable. Laboratory findings showed a white blood cell (WBC) count of 3600/mm3, hemoglobin of 12.2 g/dL with a hematocrit of 36.3%, and platelet count of 45000/mm3. The baseline platelet count of the patient was 90000/mm3. Chest X-ray (as shown in Figure ), respiratory panel, and urinalysis were negative for infection. Blood cultures did not show any growth. CT maxillofacial without contrast showed metallic implant in the left maxillary tooth and moderate to severe paranasal sinusitis (as shown in Figure ). The patient was diagnosed with sepsis secondary to transient bacteremia secondary to dental procedure versus sinusitis and was started on broad-spectrum antibiotics.
The patient improved clinically with antibiotics and the signs of active infection resolved. However, his platelet count continued to worsen with a nadir of 25000/mm3. Hematology was consulted and the peripheral blood smear was reviewed which was unremarkable with no hemolysis. Other causes of thrombocytopenia such as infection with HIV, hepatitis C, autoimmune panel, thyroid stimulating hormone (TSH) were ruled out. Of note, the patient had a bone marrow biopsy nine months before presentation which showed 5.6% plasma cells without evidence of clonality and high-normal number of megakaryocytes with thrombocytopenia consistent with peripheral destruction or sequestration confirming his previous diagnosis of chronic ITP. A presumptive diagnosis of acute on chronic ITP was made. He was started on IV immunoglobulins 1 mg/kg of ideal body weight before considering an immunosuppressant in a patient with infection and there was an improvement in platelet counts from 25000/mm3 to 41000/mm3. He was subsequently started on prednisone 100 mg and his platelets drastically improved to 120000/mm3. He was discharged on prednisone 100 mg PO daily for 7 days with an outpatient hematology follow up.",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Symptom onset <=3 days': True, 'Purulent tonsils': True, 'Severe tonsil inflammation': True}",4,4,4,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
Whether the patient has a fever in the past 24 hours is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 0.
Whether the patient has an absence of cough or coryza is not reported and so we assume that it is absent for the patient. Because of this, we add one point to the score, making the current total 0 + 1 =  1.
The patient is reported to have a symptom onset ≤3 days and so we increment the score by 1, making the current total 1 + 1 = 2.
The patient is reported to have purulent tonsils and so we increment the score by 1, making the current total 2 + 1 = 3.
The patient is reported to have severe tonsil inflammation and so we increment the score by 1, making the current total 3 + 1 = 4.
The patient's FeverPain score is 4 points."
5919,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,pmc-6701271-1,Extracted,"The patient was an 82-year-old female who is a nursing home resident presented to an outside hospital with a two-week history of jaundice that had progressively worsened. She was brought to the emergency department and found to have hyperbilirubinemia with a total bilirubin of 10.7 and a direct bilirubin of 8.7. She was afebrile, and white blood cell count was 8.9. A CT scan of her abdomen and a MRCP were diagnostic for Mirizzi syndrome, revealing large stones compressing the common bile duct (CBD) with proximal dilation. She was transferred to our hospital for a higher level of care with hepato-pancreatico-biliary surgeons. Of note, her past medical history was significant for morbid obesity with a BMI of 42, dementia, diabetes mellitus, hypothyroidism, deep vein thrombosis (DVT), depression, anemia, tobacco use, and congestive heart failure (CHF). Her surgical history consisted of an appendectomy.
Upon arrival at our hospital, the patient underwent an endoscopic retrograde cholangiopancreatography (ERCP) with the removal of small stones in the common bile duct, sphincterotomy, and two stent placements with ends terminating in the distal right and left hepatic ducts. However, despite this, there was still tapering in the common hepatic and common bile ducts noted from extrinsic compression from the large stones in the gallbladder and a significant filling defect through the cystic duct (). Additionally, the patient developed a fever and leukocytosis and persistently elevated bilirubin, with the most likely cause being an obstruction of the biliary stents causing persistent cholangitis and cholecystitis. The ERCP was repeated, and a third stent was placed. The patient's fever was controlled, and the bilirubin began to trend down.
Once the patient was stabilized, she was taken to the operating room for a cholecystectomy. The procedure began laparoscopically, but dense adhesions in the right upper quadrant involving the liver, gall bladder, omentum, and transverse colon prevented the development of adequate and safe dissection planes, and thus, the procedure was converted to open. The lysis of adhesions continued to be difficult, but once the gallbladder was dissected out, two large, firm masses were palpated within the fundus and the neck of the gallbladder. Given the difficulty with the anatomy to safely do a cholecystectomy with the gallstones en bloc, the decision was made at this time to do a partial cholecystectomy with the removal of the stones. The anterior gallbladder wall was first opened near the fundus, and the gallbladder wall was first dissected off the stone and then the stone from the posterior wall. When removed, the stone measured approximately 3.5 centimeters (), and pus and necrotic tissue were found within the gallbladder.
Attention was then turned to the neck of the gallbladder where the anterior wall of the gallbladder was again incised, revealing another a large 4-centimeter stone () that was dissected off the posterior wall and removed. It was noted at this time that there was significant arterial bleeding with a loss of approximately 300 cc of blood and the development of mild hypotension and tachycardia. Given the new symptoms and the patient's baseline hemoglobin of 8.4, the patient received two units of red blood cells intraoperatively. The arterial bleeding was controlled with sutures, and attention was turned to the biliary tree upon which a defect in the common hepatic duct and the common bile duct was noted, presumably where the cystic duct previously entered and from the cholecystocholedochal fistula formation. The defect measured approximately three centimeters in length and eight millimeters in width after debridement of necrotic tissue.
Given the fragility of the tissue and the size of CBD defect, it was not closed primarily. However, the patient's hemodynamic instability and overall health status made a biliary-enteric anastomosis a very high-risk operation with significant morbidity and mortality for the patient. Thus, the decision was made to use a dissected, viable gallbladder wall piece to form a free flap to repair the defect in the biliary tree (). The mucosal surface of the gall bladder wall was juxtaposed to the lumen of the common ducts and secured in place with a running 5-0 PDS suture. The remnant gallbladder stump was closed and oversewn in a continuous fashion. The area was extensively irrigated given the pus and necrosis that was discovered during the cholecystectomy. One drain was placed within the closed gallbladder remnant and the second one outside the closed gallbladder remnant. The abdomen was then closed in the usual manner.
Immediately, postoperatively, the patient was managed in the intensive care unit given her instability during the operation but was transferred to a step down unit shortly after on postoperative day two. She was observed off of antibiotics with normalization of leukocytosis, remained afebrile and hemodynamically stable, and had continuously down trending bilirubin levels throughout the remainder of her hospital stay. Clinically, she recovered well and was stable for discharge on postoperative day seven with drains remaining in place and to be removed on a follow-up as an outpatient. On a subsequent follow-up, the patient was noted to remain clinically stable and follow-up CT scans revealed no intrahepatic biliary duct dilation, a normal caliber common bile duct, no intraluminal filling defect, a patent stent, and no biliary leak (). Laboratory evaluation revealed no leukocytosis and normalization of liver enzymes and total bilirubin levels. Given these results, her surgical drains were removed, but her biliary stents remained in place, and despite multiple contact points and counseling to have a follow-up with the gastroenterologists for ERCP and removal, she was noncompliant and the stents remain in place to date. She however remains stable and healthy during her one follow-up appointment as of this writing and continues to be monitored closely with phone check-ins with no evidence of further hepatobiliary symptoms or complaints of incisional hernias.",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Purulent tonsils': True, 'Symptom onset <=3 days': True, 'Severe tonsil inflammation': False}",3,3,3,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
Whether the patient has a fever in the past 24 hours is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 0.
Whether the patient has an absence of cough or coryza is not reported and so we assume that it is absent for the patient. Because of this, we add one point to the score, making the current total 0 + 1 =  1.
The patient is reported to have a symptom onset ≤3 days and so we increment the score by 1, making the current total 1 + 1 = 2.
The patient is reported to have purulent tonsils and so we increment the score by 1, making the current total 2 + 1 = 3.
The patient is reported to not have severe tonsil inflammation and so we do not increment the score, keeping the current total at 3.
The patient's FeverPain score is 3 points."
5920,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,pmc-2740255-1,Extracted,"A 37-year-old Indian woman presented to our university based, academic emergency department, with a chief complaint of fever of one-week duration. The patient reported the fever was persistent and fluctuated between 102 and 103 degrees Fahrenheit. The elevated temperatures were associated with shaking chills and diffuse myalgias. Review of systems was otherwise unremarkable. She denied any recent change in her appetite or weight.
The patient had a past medical history significant for Systemic Lupus Erythematosis (SLE) that was diagnosed at age 16. She received a cadaveric renal transplant ten years prior to admission secondary to Lupus nephropathy. Over the past year, the patient had suffered from chronic rejection and was on the renal transplant list for a second time. Additional past medical history includes hypertension, chronic Molluscum contagiosum on the lower extremities, thyroid cancer status post total thyroidectomy, and renal cell carcinoma status post right native nephrectomy.
Medications included tacrolimus 2 milligrams twice daily, prednisone 5 milligrams daily, darbepoetin alfa 60 milligrams subcutaneously weekly, atenolol 25 milligrams daily, amlodipine 5 milligrams daily, calcitriol 0.25 micrograms daily, levothyroxine 100 micrograms daily, iron supplementation, and a daily multivitamin. Mycophenolate mofetil was recently stopped secondary to epistaxis and gingival bleeding. The patient denied any known drug allergies and was not taking any over the counter medications.
The patient denied any recent travel history but did report spending fourteen days in Nicaragua approximately nine months prior to presentation. While in Nicaragua, the patient recalled a transient diarrheal illness that resolved without incident. The patient denied a history of smoking, alcohol use, illegal drug use, or high-risk sexual behavior.
On physical examination, the patient was awake, alert, and oriented to person, place, and time and in no acute distress. The patient’s vital signs were as follows: blood pressure 112/81, heart rate 115, respiratory rate 16, oral temperature 101.6 degrees Fahrenheit, oxygen saturation on room air 97 percent. The remainder of the patient’s physical examination was unremarkable except for the skin, which was warm, dry, and with numerous 2-5 millimeter pearly, flesh-colored, umbilicated papules on the lower extremities consistent with Molluscum contagiosum.
Initial laboratory studies () were significant for a relative monocytosis, normochromic normocytic anemia, increased lactate dehydrogenase with normal Coombs test, thrombocytopenia, high indirect bilirubin, hyponatremia, metabolic acidemia, and renal failure. The patient reported her creatinine was recently measured to be approximately 2.4. It was 3.7 in the emergency department at presentation. A urine analysis was performed and found to contain 1+ blood; however, microscopic analysis failed to reveal any erythrocytes. The patient’s initial chest radiograph was negative for any acute disease process. A blood smear was obtained (). Numerous ring trophozites measuring approximately 2.0 microns were seen and estimated to involve 3.8 percent of the erythrocytes. The infected erythrocytes appeared the same size as the surrounding, non-infected cells. No other inclusions, with the exception of the pyroplasms, were seen in the erythrocytes. A rapid malaria antigen test was performed and found to be negative.
At this point, the patient was admitted with a presumptive diagnosis of Babesiosis. The patient was started on azithromycin 250 milligrams daily, doxycycline 100 milligrams twice daily, and atovaquone 750 milligrams twice daily. On hospital day two, additional data was obtained about the patient’s hematologic status. The patient was found to have a reticulocyte count of 1.32 (an inadequate bone marrow response most likely secondary to chronic renal failure), a haptoglobin level less than 7, and a falling hemoglobin level. In the setting of increased red cell destruction and decreased red cell production, the patient was transfused two units of packed red blood cells. The patient responded well to the transfusions and her hemoglobin subsequently stabilized while her lactate dehydrogenase and haptoglobin improved only marginally.
While the patient’s hemoglobin initially dropped, the patient’s renal function steadily improved with treatment of her underlying infection. By the end of the patient’s one-week hospital stay, her creatinine had returned to baseline. In addition, her bilirubin, electrolytes, white blood cell count, and platelet count improved over the week.
The diagnosis of Babesiosis was eventually confirmed by polymerase chain reaction (PCR) performed by Focus Diagnostics Incorporated in Cypress, California. In addition, a diagnosis of Lyme disease was presumed secondary to elevated Lyme titers and high rate of concurrent infection of Babesiosis with Lyme disease. Our patient did extremely well and was discharged home with no residual symptoms.",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Purulent tonsils': True, 'Symptom onset <=3 days': True, 'Severe tonsil inflammation': False}",3,3,3,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
Whether the patient has a fever in the past 24 hours is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 0.
Whether the patient has an absence of cough or coryza is not reported and so we assume that it is absent for the patient. Because of this, we add one point to the score, making the current total 0 + 1 =  1.
The patient is reported to have a symptom onset ≤3 days and so we increment the score by 1, making the current total 1 + 1 = 2.
The patient is reported to have purulent tonsils and so we increment the score by 1, making the current total 2 + 1 = 3.
The patient is reported to not have severe tonsil inflammation and so we do not increment the score, keeping the current total at 3.
The patient's FeverPain score is 3 points."
5921,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,usmle-11883,Extracted,"A 31-year-old woman presents to your office with one week of recurrent fevers. The highest temperature she recorded was 101°F (38.3°C). She recently returned from a trip to Nigeria to visit family and recalls a painful bite on her right forearm at that time. Her medical history is significant for two malarial infections as a child. She is not taking any medications. On physical examination, her temperature is 102.2°F (39°C), blood pressure is 122/80 mmHg, pulse is 80/min, respirations are 18/min, and pulse oximetry is 99% on room air. She has bilateral cervical lymphadenopathy and a visible, enlarged, mobile posterior cervical node. Cardiopulmonary and abdominal examinations are unremarkable. She has an erythematous induration on her right forearm.",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Symptom onset <=3 days': True, 'Severe tonsil inflammation': False}",2,2,2,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
Whether the patient has a fever in the past 24 hours is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 0.
Whether the patient has an absence of cough or coryza is not reported and so we assume that it is absent for the patient. Because of this, we add one point to the score, making the current total 0 + 1 =  1.
The patient is reported to have a symptom onset ≤3 days and so we increment the score by 1, making the current total 1 + 1 = 2.
Whether the patient has purulent tonsils is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 2.
The patient is reported to not have severe tonsil inflammation and so we do not increment the score, keeping the current total at 2.
The patient's FeverPain score is 2 points."
5922,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,pmc-4381573-1,Extracted,"A 65-year-old male marathon runner presented to a primary care physician with abrupt onset of posterior left knee pain that began two days before. There had been no injury associated with the pain. He denied systemic symptoms, including fever, chills, night sweats, or malaise. Past medical history included asymptomatic severe mitral valve regurgitation secondary to bileaflet mitral valve prolapse, for which he underwent robot-assisted minimally invasive mitral valve repair and prosthetic ring placement approximately 6 months prior to presentation. There was also a history of hypertension and hyperlipidemia. He lived in the central United States with his wife and was employed as an attorney. He consumed approximately two alcoholic drinks per night, was a never smoker, and had no history of intravenous drug use. There were no other significant exposures or travel documented.
The patient recovered from his mitral valve repair, had stopped anticoagulation after 6 weeks, and had returned to walking and/or running 3–5 miles per day. A transthoracic echocardiogram that was done approximately 2 months postoperatively demonstrated a normal functioning valve, with only trace regurgitation.
He was initially treated with symptomatic pain relief with hydrocodone-acetaminophen but had no improvement in the left popliteal fossa pain and was therefore referred to an orthopedic provider. A plain radiograph demonstrated Baker's cyst and he was treated with a cortisone injection. Due to persistence of symptoms, he was subsequently evaluated for possible deep venous thrombosis via venous ultrasound which indicated a left popliteal thrombus and aneurysm. As a result of this finding, he was admitted to an outside hospital for further evaluation.
At the outside facility, he underwent MRI of the left knee, CT angiogram with bilateral extremity runoff, and transthoracic echocardiogram. These studies revealed left popliteal aneurysm with occlusive eccentric thrombus and incomplete clot of a right renal artery branch. The following day, a transthoracic echocardiogram was done and showed a highly mobile mass attached to the anterior mitral valve leaflet, measuring approximately 1.5 cm.
Due to the abnormal findings, he was transferred to our facility for further evaluation and management. On admission, the patient appeared well. Temperature was 36.8°C, blood pressure was 123/48, heart rate was 85 beats per minute, respiratory rate was 16 breaths per minute, and peripheral oxygen saturations were 98% on room air. A 1/6 holosystolic murmur heard best over the mitral valve was auscultated; the remainder of the physical examination was normal. There was no mention of onychomycosis. His laboratory evaluation demonstrated mild anemia (11.4 g/dL; reference 13.5–17.5 g/dL), elevated erythrocyte sedimentation rate (60 mm/1 hour; reference 0–22 mm/1 hour), and elevated C-reactive protein (75.9 mg/L; reference < 8.0 mg/L). The peripheral white blood cell count and differential, platelet count, INR, and prothrombin time were all normal.
The patient underwent transesophageal echocardiogram (TEE) which revealed two highly mobile masses attached to the mitral valve with the largest mass measuring approximately 1 cm by 3 cm. The patient underwent surgery the following day. Intraoperatively, the mitral valve had firm, white vegetations with destruction of both anterior and posterior leaflets. Samples were taken and sent immediately to pathology for review. The preliminary frozen pathology demonstrated fungal elements (Figures and ). He underwent aggressive debridement and mitral valve replacement with a porcine valve. The patient was started on intravenous liposomal amphotericin B 5 mg/kg/day intraoperatively and caspofungin 50 mg daily was added the next day for empiric treatment while waiting identification of the organism. Final pathology described active native valve endocarditis with fungal organisms involving the myxomatous mitral valve. The mitral valve tissue was cultured on inhibitory mold agar and ultimately grew a Scopulariopsis species with no other microbial growth, including negative bacterial and mycobacterial cultures. Fungal blood cultures were obtained but were negative for growth. Due to the severity of the disease and highly resistant nature of the organism, oral voriconazole dosed at 300 mg twice daily was also added to the antifungal regimen.
The day following mitral valve debridement and replacement, vascular medicine and vascular surgery were consulted regarding the suspected mycotic aneurysm and thrombus of the left popliteal artery. CT angiogram with lower extremity runoff was repeated and showed the left popliteal artery mycotic aneurysm and thrombus, as well as bilateral renal infarcts. Ten days after mitral valve surgery, he underwent resection of the popliteal artery and peroneal artery bypass. The pathologic examination revealed GMS-positive staining hyphae, and inhibitory mold agar cultures again grew a pure culture of Scopulariopsis species.
The Scopulariopsis species from the cultures was ultimately identified by combined phenotypic characterization and DNA sequencing as Scopulariopsis brevicaulis. Phenotypically, the organism was a tan powdery colony and microscopically demonstrated branching annellides with chaining, round conidia with a truncated base consistent with Scopulariopsis brevicaulis. From a sequencing standpoint, D2 ribosomal sequencing was utilized with the top 3 matches being a greater than 95% match (100%, 99.31%, and 95.45%) to Scopulariopsis species in the Mayo Fungal Library. Antifungal susceptibilities were completed utilizing broth dilution as per recommended guidelines from the Clinical and Laboratory Standards Institute and were consistent with those reported in the literature: amphotericin 2 µg/mL, caspofungin 1 µg/mL, micafungin 0.125 µg/mL, anidulafungin 4 µg/mL, posaconazole 2 µg/mL, voriconazole 8 µg/mL, itraconazole 2 µg/mL, and terbinafine 0.5 µg/mL [].
Liposomal amphotericin was discontinued after 18 days due to acute renal injury, and caspofungin and oral voriconazole therapy were continued. He completed 8 weeks of combination therapy and was continued on oral voriconazole for chronic suppression. Voriconazole was chosen despite susceptibility data given reported clinical efficacy combined with lack of correlation between the susceptibility data and patient outcomes []. He unfortunately developed peripheral neuropathy, suspected by his local neurologist to be secondary to the voriconazole, and he was transitioned to delayed-release oral posaconazole dosed at 100 mg daily for chronic suppression [, ]. Posaconazole levels were followed and remained therapeutic with levels >1.0 mcg/mL. The inflammatory markers normalized at 6 months. Follow-up TEEs at 3 months and 7 months postoperatively did not show recurrence of endocarditis. Further, after cessation of the voriconazole he reported improvement, but not full resolution, of his neuropathy symptoms.",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Purulent tonsils': True, 'Symptom onset <=3 days': False, 'Severe tonsil inflammation': False}",2,2,2,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
Whether the patient has a fever in the past 24 hours is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 0.
Whether the patient has an absence of cough or coryza is not reported and so we assume that it is absent for the patient. Because of this, we add one point to the score, making the current total 0 + 1 =  1.
The patient is reported to not have a symptom onset ≤3 days and so we do not increment the score, keeping the current total at 1.
The patient is reported to have purulent tonsils and so we increment the score by 1, making the current total 1 + 1 = 2.
The patient is reported to not have severe tonsil inflammation and so we do not increment the score, keeping the current total at 2.
The patient's FeverPain score is 2 points."
5923,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,pmc-8237919-1,Extracted,"A 45-year-old male patient arrived at our otorhinolaryngology department for an emergency examination. Owing to the policy of his employing company, he was obliged to self-test for SARS-CoV-2 twice a week. Four hours before his arrival, the patient had attempted to perform a SARS-CoV-2 rapid antigen test (GenBody Inc, Cheonan, KR) at home by taking an OPS. Upon specimen collection, he felt a mild resistance and had a gag reflex, which resulted in the ingestion of the swab applicator.
The patient showed no signs of respiratory distress and had stable vital signs. He showed no apparent regurgitation of saliva. We performed a SARS-CoV-2 rapid antigen test (Hangzhou Clungene Biotech, CN) by taking an NPS and obtained a negative result.
During routine ear, nose, and throat examination, including flexible rhinopharyngolaryngoscopy, we found no foreign body in the upper respiratory tract or at the pharyngeal level.
We performed thoracic and abdominal computed tomography (CT) scans in the supine and right lateral recumbent positions. Swab applicators are usually made of nylon. Thus, their radiopacity is not guaranteed without a documented radiopaque marking. In our case, we did not have the manufacturer’s description in hand. To overcome this problem, we asked the patient to drink water to fill the stomach with fluid. After proper windowing, a radiolucent band was visible in the stomach, suggestive of a foreign body (Figure ). No other abnormalities were observable in the imaged regions.
In collaboration with the department of gastroenterology, we performed an urgent gastroscopy with a flexible endoscope (Olympus, JP). Despite four hours having elapsed since the incident, we still identified the swab stick intact in the stomach. After firmly catching the object with a polypectomy loop, it was withdrawn and removed safely (Figure ). A second look showed no signs of mucosal damage or any residual foreign bodies along the esophagus and stomach. We examined the foreign body and confirmed that it had been removed without missing parts (Figure ). After eventless observation, the patient was discharged on the same day.
Informed consent was obtained from the patient for all the procedures and for the publication of information on his clinical course. All actions were made in accordance with the World Medical Association’s Declaration of Helsinki.",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Purulent tonsils': True, 'Symptom onset <=3 days': False}",2,2,2,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
Whether the patient has a fever in the past 24 hours is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 0.
Whether the patient has an absence of cough or coryza is not reported and so we assume that it is absent for the patient. Because of this, we add one point to the score, making the current total 0 + 1 =  1.
The patient is reported to not have a symptom onset ≤3 days and so we do not increment the score, keeping the current total at 1.
The patient is reported to have purulent tonsils and so we increment the score by 1, making the current total 1 + 1 = 2.
Whether the patient has severe tonsil inflammation is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 2.
The patient's FeverPain score is 2 points."
5924,33,FeverPAIN Score for Strep Pharyngitis,diagnosis,integer,pmc-8710718-1,Extracted,"We present a case of a 1-year-old Caucasian girl, whose past medical history was unremarkable. Two and a half months before the initial presentation, the first tooth (lower incisor) erupted and soon after 11 more teeth erupted in the upper and lower jaw.
Two months before admission, the girl traveled abroad with her family. The family negated symptoms of SARS-CoV-2 infection.
The girl initially developed an itchy skin rash. Two weeks later, she developed diarrhea which lasted for 6 days. A pediatrician also noticed acute otitis media and signs of acute stomatitis. Laboratory results showed elevated C-reactive protein (CRP, 60 mg/l) and leukocytosis.
One month after the initial presentation and one week after the resolution of diarrhea, her medical condition worsened, she became irritable, refused to eat solid food, and suddenly lost three deciduous incisors from the lower jaw. The rest of her teeth in the lower jaw were mobile. There was no report of injury or elevated temperature.
Family history was unremarkable.
At admission to our hospital, she was hemodynamically stable, afebrile, and irritable. Her heart rate was 176 beats/min. She presented with extensive necrosis of the frontal region of the mandibular alveolar ridge extending to deciduous molars and was missing three incisors (). The affected area was swollen and exposed, with extensive fibrin coating. Maxillary gingiva showed no signs of gingival or periodontal inflammation. There were some aphthous changes on the tongue and buccally. On the skin, there was a generalized erythematous maculopapular rash with petechiae and scratches on the trunk and buttock. Desquamation of the skin on the fingers and edema of the wrists and ankles was also seen. There was redness of the perigenital region. Peripheral lymph nodes were not enlarged. Neurologic examination was normal.
During hospitalization, the second left incisor in the mandible fell out, the girl had cold limbs, and occasionally a reticular pattern was seen on the skin. Transiently, a wound between the second and third toes on the left foot was present.
The girl had just one peak temperature of 38.2°C; otherwise, she was afebrile and cardiovascularly compensated. On the third day after admission, she developed hypertension with systolic blood pressure between 125 and 140 mmHg and diastolic blood pressure between 60 and 90 mmHg (above the 95th percentile for age and height, which is 105/60 mmHg). She also had a persistent tachycardia with a pulse rate between 150 and 180 beats/min.
In blood laboratory test results, there was a mild elevation of CRP (20 mg/l), negative procalcitonin, leukocytosis, and thrombocytosis. Lactate dehydrogenase (LDH), liver transaminases, and fibrinogen were elevated as well. Thyroid hormones (T3 and T4) were slightly elevated.
Nasopharyngeal swab was positive for rhinovirus and enterovirus infections but was negative for other viruses including SARS-CoV-2. The swabs of the oral cavity and mandible were negative for pathogenic bacteria and herpesviruses. Skin swabs from several places showed S. aureus and Candida albicans superinfection and a vaginal swab showed the presence of Candida albicans.
The serology for SARS-CoV-2 was found positive for both IgG and IgA antibodies (IgG: 1.88; IgA: 2.17). Blood culture was negative. Her immune status was unremarkable, and primary immunodeficiencies were ruled out with laboratory tests. The girl had normal lymphocyte subpopulations, at presentation minimally elevated IgG levels, and normal IgM and IgA, normal test of phagocytosis, and normal values of complement. Immunoserology testing revealed positive IgG anticardiolipin antibodies (aCL) (12 AUG) and IgG anti-beta2-glycoprotein I antibodies (anti-ß2GPI) [16 AUG]). Vitamin A deficiency, herpes simplex virus 1 and 2, varicella zoster virus, HIV, rubella, and measles infections were ruled out. The urine sample was unremarkable. The plasma renin level was normal for the girl's age [7.3 μg/l/h (ref.: 0–3 years: <16.6 μg/l/h)]. The heart breakdown enzymes were normal.
CT and MR imaging of the lower jaw showed diffusely altered bone with edema and necrosis of the mandibular corpus and the above alveolar ridge in the region extending from tooth 84 to tooth 74 (). It showed severe inflammation of the surrounding soft tissues and muscles as well. There was loss of teeth 71, 81, and 82.
Ultrasound of the abdomen showed slightly enlarged liver. Doppler ultrasound of renal arteries was normal, and thyroid ultrasound was normal as well. Chest X-ray was normal. Electrocardiogram and echocardiogram showed no abnormalities.
Biopsy of the mucosa of the lower jaw, tooth, mandible (twice), and skin was performed. During biopsy, teeth 83 and 73 were removed due to total loss of supporting alveolar bone. Histopathologically (), biopsy of the mucosa of the lower jaw showed necrosis, granulation tissue, and changes compatible with epulis, corresponding partly to pyogenic granuloma and partly to peripheral ossifying fibroma. No diagnostic changes for lymphoma or Langerhans cell histiocytosis were present. Immunohistochemistry for SARS-CoV-2 was negative. Necrosis and endothelial damage with individual mural thrombi and in some cases the appearance of recanalization of thrombotic changes along small vessels were seen ().
Biopsy of the mandible showed vital reactive bone with fibrosis without suppurative inflammation indicative of active infection.
Biopsy of the tooth showed normal structures of the tooth with adjacent structures of the alveolar ridge.
The second biopsy of the soft tissue of the mandible showed minimally reactive bone, and reactive spindle-cell proliferation with individual multinucleated giants of the osteoclast type. Compared with the previous biopsy, the changes were more chronic in appearance with reparative inflammation, without granulation tissue or necrosis.
The samples of skin changes in the sacral area were taken and sent for analysis and possible bacterial and fungal infections. Histopathologically, sacral focal necrosis of the epidermis and swelling of endothelial cells of the dermis were seen (). There was no thrombosis and no visible changes typical for malignancy, histiocytosis, or active infection. Stevens–Johnson syndrome (SJS) was also excluded based on the skin-biopsy result. Swollen endothelial cells of small veins in the upper dermis that almost or completely close the lumen were confirmed by electronic microscopy (). There were no fibrins or platelets in the lumen of the examined vessels and on the endothelium. Endothelial cell organelles were unremarkable. No viral particles were detected. Immunofluorescence examination was unspecific.
The results of molecular genetic testing by the next-generation sequencing (NGS) method showed no changes in the 4,813 analyzed genes, including 304 genes associated with primary immunodeficiencies, genes associated with COVID-19 vasculitis (TREX1), type I interferonopathies (STING1, COPA), and monogenic vasculitis (DADA2) (, ).
The patient was treated with combined antibiotic therapy with amoxicillin and clavulanic acid intravenously. On the 13th day of hospitalization, we also introduced metronidazole 100 mg q 8 h orally and clindamycin 100 mg q 8 h intravenously and later orally. Because of the suspicion for hypercoagulability, she received antiplatelet therapy with 50 mg of acetylsalicylic acid daily. For the skin, she received ointment with a combination of corticosteroid, antibiotic, and antifungal active substance due to proven superinfection with S. aureus and Candida albicans. Against itching, she received loratadine twice daily. Against oral pain, we applied 1% lidocaine chloride locally three times a day. She needed analgesia (paracetamol 100 mg/6 h) and, due to food refusal, parenteral hydration. Due to tachycardia and arterial hypertension, she received 1 mg of antihypertensive drug amlodipine (0.1 mg/kg) twice daily.
Two weeks after the beginning of antimicrobial and antiplatelet therapy, the girl showed clinical improvement. The changes in the mandible and skin were no longer so pronounced, and blood pressure gradually decreased. Skin therapy slowly helped to reduce the intensity of the rash. Normalization in inflammatory parameters and decrease of D-dimer value were recorded. Thrombocytosis and slightly elevated LDH and AST persisted. Control thyroid hormones were in the normal range.
A week after discharge, the girl was better, except for her blood pressure, which was still high, so we adjusted the therapy of amlodipine to 2 mg (0.2 mg/kg) twice daily.
Three weeks after the discharge, she stopped antibiotic therapy, and after 1 month she also stopped taking antihypertensive drug amlodipine. Follow-up echocardiography was normal. One month after discharge, the serology for SARS-CoV-2 was negative.
At the last follow-up, almost 1 year after the first admission, the girl was in a better mood, no rash was present, and there was no inflammation in her oral cavity, but six teeth in the lower jaw (73, 72, 71, 81, 82, and 83) were missing, and other teeth showed caries. Her laboratory results were normal, except for persistently positive IgG aCL (11 AUG) and IgG anti-ß2GPI antibodies (16 AUG).",What is the patient's FeverPAIN score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Symptom onset <=3 days': False, 'Purulent tonsils': False}",1,1,1,"The criteria for the FeverPAIN score are listed below:
    
1. Fever in past 24 hours: No = 0 points, Yes = +1 point
2. Absence of cough or coryza: No = 0 points, Yes = +1 point
3. Symptom onset ≤3 days: No = 0 points, Yes = +1 point
4. Purulent tonsils: No = 0 points, Yes = +1 point
5. Severe tonsil inflammation: No = 0 points, Yes = +1 point

The FeverPAIN score is calculated by summing the points for each criterion.
    
The patient's current FeverPain score is 0.
Whether the patient has a fever in the past 24 hours is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 0.
Whether the patient has an absence of cough or coryza is not reported and so we assume that it is absent for the patient. Because of this, we add one point to the score, making the current total 0 + 1 =  1.
The patient is reported to not have a symptom onset ≤3 days and so we do not increment the score, keeping the current total at 1.
The patient is reported to not have purulent tonsils and so we do not increment the score, keeping the current total at 1.
Whether the patient has severe tonsil inflammation is not reported and so we assume that it is absent for the patient. Because of this, we do not increment the score, keeping the current total at 1.
The patient's FeverPain score is 1 points."
5925,38,Free Water Deficit,lab test,decimal,pmc-6175253-1,Extracted,"A 32-year-old female with history of diabetes mellitus type one and a successful RYGB for morbid obesity three years ago presented to our clinic with the complaints of cough, greenish yellow sputum production, chills and night sweats for the last three months. She was feeling more fatigued, generalized weakness and unintentionally lost 33 pounds during that time. She denied recent history of travel out of state. The patient was in the United States and had never been to a country with endemic tuberculosis. She denied recent remote history of incarceration. She also denied hemoptysis, shortness of breath, headache or fever. She had no history of being diagnosed with TB or history of recent sick contacts. On physical examination, her temperature was 36.9°C, blood pressure was 116/60 mm Hg, pulse was 84 per minute and respiratory rate was 16 per minute. On chest auscultation, few rhonchi were present in the right upper lung and the rest of the physical examination was unremarkable. The Initial blood work showed sodium of 134 mmol/L (136–145 mmol/L), potassium of 4.2 mmol/L (3.5–5.1 mmol/L), bicarbonate of 28 mEq/L (23–31 mEq/L), blood urea nitrogen (BUN) of 6 mg/dL (9–21 mg/dL), creatinine of 0.33 mg/dL (0.6–1.1 mg/dL), glucose of 150 mg/dL (80–115 mg/dL) and liver function tests were within normal range. Her white blood cell count was 14,500/µL (4500–11000/µL) with 81% neutrophils. Her chest X-ray showed multiple small nodular opacities throughout the right lung with a probable cavity in the right lung apex (Figure ). Suspicion was raised for possible active TB and she was admitted in airborne isolation. Two peripheral blood cultures, sputum culture along with acid-fast bacilli (AFB) were ordered. Computed tomography (CT) chest without contrast showed multiple thick-walled cavities in the right upper lobe. The largest cavity was 7 cm. There were innumerable centrilobular nodules and tree in bud opacities throughout the right lung (Figures , ). Mycobacterium tuberculosis bacillus was detected by sputum AFB staining and later confirmed by culture and polymerase chain reaction (PCR) assay. She also had a positive QuantiFERON test. She was started on anti-tuberculosis treatment (ATT) medications including Isoniazid 300 mg daily, Rifampin 300 mg twice daily, Ethambutol 800 mg daily, Pyrazinamide 1000 mg daily and Pyridoxine 50 mg daily for the first two months and then two drugs Isoniazid and Rifampin for the next four months. After three days of hospital stay, she started showing some improvement in her symptoms such as cough and night sweats. She understood the isolation precautions, especially respiratory precautions and use of mask in the presence of other individuals. She was later discharged in stable condition with the above-mentioned medications. She had complete resolution of her symptoms in two months and completed six months course of ATT.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [32, 'years'], 'weight': [33.0, 'lbs'], 'Sodium': [134.0, 'mmol/L']}",-0.32075,-0.30471,-0.33679,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 32 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 33.0 lbs so this converts to 33.0 lbs * 0.453592 kg/lbs = 14.96854 kg. The concentration of sodium is 134.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 14.96854 * (134.0/140 - 1) = -0.32075 L. The patient's free body water deficit is -0.32075 L."
5926,38,Free Water Deficit,lab test,decimal,pmc-3180982-1,Extracted,"A 17-year-old female patient weighing 35 Kg presented to emergency department with history of chronic intermittent abdominal pain, vomiting, and anorexia for three months, history of recurrent generalized tonic clonic seizures for 2 days and history of rapidly progressive ascending type of limb weakness with respiratory distress for one day. She had no history of snakebite, pain chest, poison intake, or blunt injury to neck or abdomen.
She initially presented to a private nursing home where she was intubated and transferred to our hospital on portable ventilator. On examination she was conscious (E4VTM1) with power of 1/5 in all limbs, plantars were mute, and deep tendon reflexes were absent. Her heart rate was 120/min and blood pressure was 100/60 mm Hg. She was breathing at a set rate given by ventilator. Systemic examination was insignificant. She was transferred to intensive care unit with a diagnosis of acute inflammatory demyelinating polyneuropathy. She also had features suggestive of autonomic neuropathy in the form of postural hypotension, tachycardia, and sweating.
Routine baseline workups including hemogram, blood sugars, liver and kidney function, chest X-ray, electrocardiography, electroencephalography were normal. Cerebrospinal fluid analysis was normal. Urine Watson–Schwartz test[] was positive for porphobilinogen. Electrolyte screening showed mild hyponatremia (serum sodium 126 mmol/L). Serum phosphates and serum potassium were within normal limits. Ultrasonography of abdomen was unremarkable and serum lead levels were within normal limits. Nerve conduction study showed axonal motor neuropathy.
She was treated as a case of AIP with high dose of carbohydrate (300–400gm/day), heme arginate (3 mg/kg/day for 4 days) and gabapentin for seizures control. Precautions were taken not to prescribe any porphyrogenic drugs. At 60th day of her ICU stay ST segment elevation was noticed on the cardiac monitor and 12 lead ECG was ordered which showed [] ST segment elevation in lead II. Cardiac enzyme markers were not elevated. Transthoracic echocardiography was done to rule out any cardiac pathology. It showed posterior pericardial calcification with anterior mitral leaflet and papillary muscle calcification [Figures and ] and relaxation abnormality around mitral valve suggestive of early pericardial constriction. Serum calcium (10.8 mg/dl) and phosphorus levels (5 mg/dl) were within normal limits. Tracheal tube aspirate for acid-fast bacilli was negative for 3 days in continuation. Patient required prolonged ventilator support and was finally discharged with the advise to follow up.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [17, 'years'], 'sex': 'Female', 'weight': [35.0, 'kg'], 'Sodium': [126.0, 'mmol/L']}",-2.1,-1.995,-2.205,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 17 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 35.0 kg. The concentration of sodium is 126.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 35.0 * (126.0/140 - 1) = -2.1 L. The patient's free body water deficit is -2.1 L."
5927,38,Free Water Deficit,lab test,decimal,pmc-3094288-1,Extracted,"A 17-year-old Caucasian female presented to local hospital with a history of acute alcohol intoxication and ingestion of large quantities of acetaminophen. The patient complained of nausea for 2 days and subjective increase in thirst and urine output for a day. She did not notice any dysuria, abdominal pain or change in the colour of her urine. She did however report a remarkable increase in lower back pain that she had attributed to strenuous exercise.
Two days prior to her presentation to the emergency department, the young lady had attended a party where she consumed over 300 mL of vodka and ingested twenty 500 mg tablets of acetaminophen later that night.
Past medical history revealed that she had experienced an episode of rash after having taken liquid acetaminophen as a child. She had not taken acetaminophen since infancy and also denied regular use of any other analgesic. Family history was non-contributory for relevant physiological and psychological illness. The patient reported feeling stressed due to a recent slip in school grades, however denied any suicidal ideation.
Physical examination in the emergency department revealed blood pressure of 140/92 mmHg, pulse 80 bpm, temperature 36.9°C, respiratory rate of 16 breaths per minute and oxygen saturation of 100% at room air. Height and weight were recorded at 170 cm and 63 kg. Physical examination was otherwise unremarkable. No rash, joint swelling or sign of dehydration was detected.
Initial renal function tests at the local hospital revealed serum creatinine and BUN levels of 1.6 mg/dL and 19.3 mg/dL, respectively. Other laboratory results included: glucose 112 mg/dL, sodium 141 mEq/L, potassium 4.3 mEq/L, chloride 104 mEq/L, bicarbonate 29 mEq/L, albumin 43 g/L, aspartate transaminase 20 IU/L, alkaline phosphate 66 IU/L and total bilirubin 1.11 mg/dL. Her INR was reported to be normal at 0.9. Toxicity screens on admission showed acetaminophen level at 9.06 μg/mL. Urine dipstick showed trace amount of blood and 2 plus protein. Microscopy revealed 25 red blood cells per high power field and was otherwise non-contributory. Abdominal ultrasound revealed increased hepatic echogenicity and the kidneys were normal in appearance.
At the outside hospital, she was given morphine, ondansetron and lansoprazole for her back pain and gastrointestinal symptoms. Acetylcysteine was not administered as the patient presented more than 24 hours after the ingestion of acetaminophen.
Renal function tests were repeated later that evening and monitored frequently thereafter. Over the course of 36 hours, the patient's serum creatinine and BUN levels elevated from 1.6 mg/dL and 19.3 mg/dL to 5.7 mg/dL and 49.6 mg/dL, respectively. Urine output was reported to be 2.7 mL/kg/hour. At this time, the patient was transferred to our Children's Hospital for rapidly progressive renal insufficiency.
Physical examination upon admission showed normal vital signs: blood pressure 115/74 mmHg, pulse 60 bpm, temperature 36.6°C, respiratory rate 16 breaths per minute and 100% oxygen saturation at room air. Serum creatinine and BUN levels were measured at 6.3 mg/dL and 52.4 mg/dL, respectively. Furthermore, her electrolytes were recorded as follows: random glucose 86 mg/dL, sodium 134 mEq/L, potassium 5.7 mEq/L, chloride 104 mEq/L and bicarbonate 22 mEq/L. Coagulation study revealed an INR of 1.0 and an APTT of 28 seconds. Other investigations including blood counts and liver functions tests were within normal range. The patient's daily urine output was 3.3 mL/kg/hour at this time. Urinalysis revealed small amounts of protein and blood in her urine. Staining for eosinophils on the random urine sample was positive.
Renal biopsy was performed to further delineate the underlying cause of rapidly progressive renal insufficiency. Figure depicts the histological findings. The biopsy showed no evidence of glomerulonephritis. The interstitium was mildly edematous with small aggregates of inflammatory cells, mainly lymphocytes and eosinophils. Immunofluorescence and electron microscopy were both negative for immune deposits. The histological findings were compatible with acute interstitial nephritis.
The patient was managed supportively by careful monitoring of fluid intake and output. Corticosteroids therapy was considered if no improvement of her renal function was observed. However, her serum creatinine and BUN levels peaked at 7.0 mg/dL and 60 mg/dL two days after admission then began to improve without further medical intervention. Her serum creatinine and BUN levels upon discharge were 4.7 mg/dL and 48 mg/dL respectively. Outpatient follow-up at two weeks after discharge showed that she had completely recovered; her creatinine was 1 mg/dL and BUN was 18 mg/dL.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [17, 'years'], 'weight': [63.0, 'kg'], 'Sodium': [141.0, 'mEq/L']}",0.27,0.2565,0.2835,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 17 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 63.0 kg. The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 63.0 * (141.0/140 - 1) = 0.27 L. The patient's free body water deficit is 0.27 L."
5928,38,Free Water Deficit,lab test,decimal,pmc-7772166-1,Extracted,"This is a case of a 15-month-old male who was referred to King Saud Medical Complex in Riyadh, Saudi Arabia, for a multidisciplinary follow-up plan and genetic testing. Regarding his history, the patient was delivered at the 39th gestational week of a 23-year-old mother by cesarean section due to the failure of progression, weighing 2.4 kg, and was reported to have developed respiratory distress upon birth. Regarding the mother, she is medically free and was on multivitamins while there were no reports of any radiation or teratogenic exposure that was reported during her pregnancy. After birth, the patient was placed in the neonatal intensive care unit (NICU) for six months due to his abnormal respiration. There is no family history of any genetic disorders, consanguinity, or congenital anomalies.
Initially, the patient was suffering from developmental delay and extensor muscle weakness of the upper and lower limbs. Moreover, an epiglottopexy procedure was performed due to choanal atresia and a high arched palate. Afterward, he was breathing on room air through a nasal cannula. Ever since the epiglottopexy, the patient has been on continuous positive airway pressure (CPAP) with no attempt to wean him off the ventilation due to poor response. Even though the patient did not present any gastrointestinal abnormalities, there was a difficulty in feeding, which led to nasogastric tube insertion for oral nutrition and supplementation. The patient also developed hypogonadotropic hypogonadism, which was confirmed by testing; an abnormal facial shape, which was a dysmorphic triangular face; coloboma; and bilateral low-set ears. A shallow acetabular roof, micropenis, small bilateral kidney, high arched palate, and hypo-plastic left thumb was also noted (Figure ). Regarding the cardiovascular system, the patient had a moderate to large ventricular septal defect (VSD), dilated left atrium and left ventricle, and mild pulmonary stenosis. Furthermore, the patient did not develop any seizures or loss of consciousness, but he was hypotonic. However, his gastrointestinal system showed no abnormalities.
Regarding the investigation, his blood work was within normal limits except for a low serum creatinine of 13 µmol/L (normal range: 71-133 µmol/L) and hyponatremia of 130 mEq/L. Meanwhile, his brain magnetic resonance imaging (MRI) showed mild periventricular leukomalacia, benign external hydrocephalus, with the suggestion of Blake's pouch cyst (Figure ). The genetic investigation was performed for the patient, and he was found to have chromodomain helicase DNA-binding protein 7 (CHD7), c.2572C˃T p(Arg858), and the diagnosis of CHARGE syndrome was confirmed based on the physical examination and the gene sequencing report. The patient is in hospital and is followed up by a multidisciplinary team consisting of a cardiologist, neurologist, nephrologist, general pediatrician, gastroenterologist, otolaryngologist, ophthalmologist, pulmonologist, and physiotherapist with a plan to try and increase and improve his life expectancy and quality of life moving forward.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [15, 'months'], 'weight': [2.4, 'kg'], 'sex': 'Male', 'Sodium': [130.0, 'mEq/L']}",-0.10286,-0.09772,-0.108,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
This means that the patient is 1 year and 3 oldThe patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 2.4 kg. The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 2.4 * (130.0/140 - 1) = -0.10286 L. The patient's free body water deficit is -0.10286 L."
5929,38,Free Water Deficit,lab test,decimal,pmc-6311974-1,Extracted,"A 38-year-old man presented to an emergency department with progressive weakness and decreased urine output after having vomited up to 20 times per day over a period of 7 days. The patient was referred to our intensive care unit. Before medical consultation, he was healthy, and no other symptoms were reported. Diarrhea, fever, chills, or abdominal pain was absent.
Clinical examination revealed a patient of normal weight (height: 180 cm, weight: 70 kg). Blood pressure and heart rate were elevated (150/80 mmHg, 105/min); the respiratory rate was normal (13/min), but oxygen saturation was low (89%). During blood pressure measurement, a positive Trousseau sign was noted. The mucous membranes were dry, and the physical examination was otherwise unremarkable.
Arterial blood gas analysis revealed a metabolic alkalosis with partial respiratory compensation (pH: 7.71 [7.35–7.45], base excess: 40.5 mmol/l [-2-3 mmol/l], pCO2: 56.1 mmHg [32–45 mmHg], pO2: 43.5 mmHg [83–108 mmHg], bicarbonate: 72.2 mmol/l [21–26 mmol/l], lactate: 2.8 mmol/l [0.5–1.6 mmol/l], chloride: 52 mmol/l [98–106 mmol/l], sodium: 130 mmol/l [136–146 mmol/l], potassium: 2.4 mmol/l [3.5–5.1 mmol/l], ionized calcium: 0.77 mmol/l [1.15–1.29 mmol/l] and glucose: 165 mg/dl [70–105 mg/dl]).
Ultrasound revealed a distended and full stomach; the inferior vena cava was collapsing on inspiration. Otherwise, the ultrasound was unremarkable. The electrocardiography [] showed a prolonged QT interval (QTc 547 ms).
Laboratory tests were consistent with acute kidney injury (creatinine: 5.2 mg/dl, urea: 176 mg/dl); liver function tests, coagulation tests, albumin, lipase, procalcitonin, total calcium, hemoglobin, and thyroid-stimulating hormone were normal. Leukocytes were minimally elevated (11500/μl).
We suspected a prerenal acute kidney injury and a hypochloremic metabolic alkalosis due to gastric losses of HCl and fluids. Initial management consisted of oxygen therapy to correct hypoxemia and intravenous fluid therapy with normal saline and potassium chloride. Initially, a balanced crystalloid solution was infused, and later normal saline with KCl (40 mmol/l) was used because of the higher chloride content. Metoclopramide was administered to promote gastric emptying. To prevent further gastric losses of HCl, a proton-pump inhibitor was given. The patient was put on nihil per os for 24 h.
After 24 h, a total of 4.5 l of crystalloid fluid was infused. There was no further vomiting. A repeated bedside ultrasound revealed an empty stomach. The pH was corrected to 7.49, bicarbonate was reduced to 48.6 mmol/l, base excess was 23.4, chloride was 69 mmol/l, and potassium was still low at 2.8 mmol/l. There was hypoventilation with a pCO2 of 68.4 mmHg. We noted onset of diuresis. After 72 h of fluid therapy, the acid-base and electrolyte status was normal. Creatinine had decreased to 3.5 mg/dl. Small meals were tolerated.
Since there was no evidence of an infectious etiology for the excessive vomiting and the ultrasound had shown a distended stomach, an upper gastrointestinal endoscopy was performed []. A significant stenosis of the duodenum was diagnosed. Although there was no ulcer visible, an occult ulcer was deemed to be possible. A portal hypertensive gastropathy was diagnosed while esophageal varices were absent. Helicobacter pylori testing was positive, so an eradication therapy was initiated. A repeated endoscopy confirmed the stenosis, but again, no ulcer was seen. Since a focused abdominal ultrasound did not reveal the reason for the stenosis, a magnetic resonance imaging scan was performed to rule out malignancy such as pancreatic or gallbladder cancer or a thrombosis of the mesenteric vein. There was no evidence of malignancy or cirrhosis. An endosonography was done without evidence of malignancy or mesenteric vein thrombosis. At that point, the stenosis had partly resolved, and endoscopic passage was possible. We concluded that the temporary duodenal stenosis was caused most likely by portal hypertension of unknown etiology, and our differential diagnosis included idiopathic noncirrhotic portal hypertension after exclusion of cirrhosis and portal vein obstruction.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [38, 'years'], 'weight': [70.0, 'kg'], 'sex': 'Male', 'Sodium': [130.0, 'mmol/L']}",-3,-2.85,-3.15,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 38 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 70.0 kg. The concentration of sodium is 130.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 70.0 * (130.0/140 - 1) = -3.0 L. The patient's free body water deficit is -3.0 L."
5930,38,Free Water Deficit,lab test,decimal,pmc-3597915-1,Extracted,"A 56-year-old man was admitted to the renal unit of the tertiary university hospital with symptoms of polyuria with nocturia, and polydipsia with severe thirst for the past 2 months. Initially, the patient visited a local clinic and was diagnosed as type 2 DM with a fasting blood sugar, 150mg/dL. Despite being controlled hyperglycemia with an oral hypoglycemic agent, he continued drinking daily more than 8 L of cold water (about 10 bottles of refrigerated water, 750 ml capacity) and passed large amounts of urine frequently. He had no specific history including head trauma or mental disorder, and denied any pertinent family history. The patient showed no signs of systemic illness such as fever or arthralgia, or neurologic symptoms involving the central nervous system. He has been working as a gardener with 176 cm in height and 68 kg in weight (71 kg before this event). The physical examination was unremarkable with blood pressure of 132/70 mmHg, pulse rate of 80/min, respiratory rate of 16/min, and temperature of 36.8℃. In the laboratory findings, his white blood cell count was 9,700/mm3; hemoglobin, 13.4 g/dL; platelet, 376×103/mm3; sodium, 140 mEq/L; potassium, 3.8 mEq/L; blood urea nitrogen (BUN), 12 mg/dL; creatinine, 1.0 mg/dL and osmolality 295 mOsm/kg water. HbA1c was 7.2% and post-prandial glucose was checked around 180mg/dl with fasting blood sugar of 140 mg/dL. In urine analysis, the urine pH was 6.0; specific gravity 1.006; albumin (-); glucose (-); WBC 0-4/HPF; RBC 0-2/HPF, and osmolality 140mOsm/kg water. Fluid intake and output in 24 hours recorded 9 L in oral water intake from water containers and 11.7 L in urine output. In hormone assays, ACTH was 25.2 pg/mL (reference value, 6.0-76.0 pg/mL), prolactin 8 µg/L (reference value, 0-15 µg/L), cortisol 9.8 µg/dL (referencel value, 5-25 µg/dL), hGH 2.26 ng/mL (reference value, 0.5-17 ng/mL), and TSH 0.99 µU/mL (reference value, 0.5-4.7 µU/mL). Also, angiotensin converting enzyme (ACE) activity was within normal range (reference value, <40 U/L).
On hospital day 5, the patient underwent a water deprivation test according to the method of Miller-Moses test because of persistent polydipsia and polyuria despite blood glucose control. The results are shown in . During dehydration, the patient lost 3kg (4.4% of body weight), and urine osmolality remained hypotonic below 130 mOsm/kg. Basal ADH level was 5.18 pg/dL, and the repeat ADH level following the stimulation by water deprivation was 3.95 pg/dL, which revealed no increment despite the increased serum osmolality up to 300 mOsm/kg from the baseline levels of 285 to 295 mOsm/kg. One puff (5 µg) of desmopressin nasal spray resulted in the increase of urine osmolality to 266 mOsm/kg (>100% increase from the baseline level, 126 mOsm/kg) and in the marked reduction of urine output from 200-410 ml/hr to 44-60 ml/hr. These results were compatible with CDI,, whose causes would be mostly idiopathic because of normal findings in hypothalamus and hypophysis in magnetic resonance imaging (MRI) scan of sella ().
On discharge (hospital day 9), the dose of desmopressin nasal spray (minirin nasal spray®) was adjusted to 1 puff per 12 hrs (10 µg/day), and urine output was markedly reduced to below 2-3 L/day with no more intense thirst. Also, DM was controlled with fasting blood sugar below 115 mg/dL by metformin (novamet GR® 500mg bid) and American Diabetes Association (ADA) recommended diet.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [56, 'years'], 'weight': [68.0, 'kg'], 'Sodium': [140.0, 'mEq/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 56 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 68.0 kg. The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 68.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
5931,38,Free Water Deficit,lab test,decimal,pmc-7779137-1,Extracted,"The patient was a 10-day-old boy with no known family history. He was delivered vaginally at another facility on the fourth day of gestational week 39. His birth weight was 2734 g and he had an Apgar score of 8/9. At 10 days of age, the patient was seen by a physician at the same facility for his two-week checkup, during which he was found to be not gaining weight at a healthy rate (+9 g/day). On the same day, a newborn mass screening test found that he may have 21-OHD. The patient was then taken to our hospital’s emergency department.
The physical findings at admission were as follows: body weight, 2634 g; body temperature, 38.2 °C; heart rate, 147 bpm; blood pressure, 74/45 mmHg; respiratory rate, 40 breaths per minute; SpO2, 100% (room air); sunken anterior fontanelle; no conjunctival congestion; mild conjunctival jaundice; and no pharyngeal redness. Regarding the chest, there were regular heart sounds with no murmurs and clear breath sounds. The abdomen was soft and flat with normal peristaltic sounds. Pigmentation of the genital area was observed (Figure ).
Peripheral body areas were not cold to the touch. Dry skin was present.
Laboratory tests were performed after admission. A mass screening test performed on day four found a very high concentration of 17-hydroxyprogesterone (17-OHP; direct method) of 279.5 ng/mL. A markedly low sodium level (125 mEq/L) and markedly high potassium level (8.5 mEq/L) were also observed. At a later date, endocrine testing results showed that the levels of the following items were elevated: testosterone, 514.8 ng/dL; aldosterone, 103.9 ng/dL; adrenocorticotropic hormone (ACTH), 323.0 pg/mL; and renin, >45 ng/(mL·h). The levels of the following parameters were within the normal ranges: cortisol, 14.9 μg/dL; and estradiol, 28.4 pg/mL. Additionally, urinary steroid profile using gas chromatography-mass spectrometry showed that urinary 3α, 17α, 20α-pregnanetriolone (Ptl) (21.818 mg/g Cre), pregnanediol (PD5) (0.230 mg/g Cre) and 11β-hydroxyandorosterone (11-OHAn) (4.894 mg/g Cre) (Table ).
At the beginning of hospitalization, based on the results of mass screening testing and clinical symptoms, the patient was diagnosed with classic 21-OHD. The patient was considered to have acute adrenal failure due to hyperkalemia and hyponatremia. Intravenous HC was administered rapidly at 100 mg/m2. Thereafter, a 100 mg/(m2·day) dose of HC and saline were administered by continuous infusion. Glucose-insulin therapy was initiated to treat the hyperkalemia. On Hospitalization Day 3, his body temperature reached 39.2 °C. His urinalysis revealed leukocytes and bacteriuria (Streptococcus agalactiae 100,000 CFU/mL collected by catheterization), and renal ultrasonography found grade 1 hydronephrosis of the left kidney (Figure ).
As sepsis workup, we also performed bacterial cultures in blood and spinal fluid; no bacteria were detected in these samples. Therefore, an intravenous antibiotics treatment for UTI was started. The patient was able to keep his body temperature below 37.5℃ on Hospitalization Day 5, but the hyperkalemia persisted. At that time, we considered pseudohyperkalemia by blood sampling, acute renal failure, urinary obstruction, hemolysis, and drug-induced as the differential diagnosis of hyperkalemia, but all of them were denied. The doses of HC and FC are dependent on the individual patient and managed based on the severity of clinical symptoms []. Consequently, using serum potassium levels as an indicator, the dose of HC was increased to 120 mg/(m2·day) on Hospitalization Day 7 and then further increased to 144 mg/(m2·day) on Hospitalization Day 9. Despite these dose increases, serum potassium levels could not be controlled; therefore, oral administration of 0.18 mg/day FC and 0.1 g/(kg·day) sodium chloride was initiated. On Hospitalization Day 18, the serum potassium level was 7.5 mEq/L, and the transtubular potassium gradient (TTKG) and fractional excretion of sodium were 2.5 and 9.29 %, respectively. Since these findings suggested low aldosterone bio-activity, the dose of FC was increased to 0.36 mg/day. Thereafter, serum potassium levels gradually decreased. In addition, a mass screening test was again performed again on Hospitalization Day 14, revealing that the 17-OHP concentration (direct method) decreased to 4.9 ng/mL. On Hospitalization Day 18, the serum renin activity had reduced to 17.7 ng/(mL·h). Thereafter, the dose of HC was gradually reduced to 35 mg/(m2·day). The patient was discharged on Hospitalization Day 38 (Figure ).
Following discharge, the doses of HC and FC were reduced to maintenance doses of 12 mg/(m2·day) and 0.2 mg/day, respectively. The administration of sodium chloride was discontinued. The patient has received regular follow-up care, but no notable findings and no electrolyte abnormalities have been observed to date, and the low TTKG improved to 7.4.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [10, 'days'], 'weight': [2634.0, 'g'], 'Sodium': [125.0, 'mEq/L']}",-0.16933,-0.16086,-0.1778,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 10 days old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 2634.0 g so this converts to 2634.0 lbs * kg/1000 g = 2.634 kg. The concentration of sodium is 125.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 125.0 mEq. To convert from 125.0 mEq to mmol, convert from mEq to mmol. The compound 125.0 has a valence of 1, and so divide the valence by the value of mEq to get, 125.0 mEq/(1 mEq/mmol) = 125.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 125.0 mEq sodium/L converts to 125.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 2.634 * (125.0/140 - 1) = -0.16933 L. The patient's free body water deficit is -0.16933 L."
5932,38,Free Water Deficit,lab test,decimal,pmc-4003442-1,Extracted,"The patient is a 6-year-old boy who is referred to our hospital with complaints of fever, malaise, anorexia, nausea, and vomiting from 4 weeks ago. During this period, the patient had lost 7 kg and his nausea, vomiting, and anorexia had gradually worsened. Before referral to us, he had several referrals as outpatients and two hospitalizations with no definite diagnosis of his illness. The physical examination showed only lethargy and pallor and no other signs including lymphadenopathy and hepatosplenomegaly.
Initial laboratory studies were as follows: Na: 141 mmol/L, K: 3.6mmol/L, BUN: 18, Cr: 0.8mg/dl, Ca: 15.8mg/dl, P: 2.8mg/dl, uric acid: 5.8 mg/dl, LDH: 587 U/L, Mg: 1.4mg/dl, Alkaline phosphatase: 305U/L, Alb: 4gr/dl. Complete blood count included: WBC: 7.4×109 /L (lymphocyte: 72%, PMN: 26%), HB: 7.1gr/dl, PLT: 90×109 /L. Arterial blood gas analysis was as follows: PH: 7.47, PCO2: 31mmHg, HCO3: 22 mEq/L.
Blood count was normal 16 days prior to our visit. In peripheral blood smear no other abnormal point was seen except microcytic anemia, and mild thrombocytopenia. Chest X-ray was normal. In abdominal ultrasound, liver and spleen size were normal and there was sand in inferior pole of right kidney. Despite severe hypercalcemia, there were no significant electrocardiographic changes. The corrected QT interval (QTc) was in the normal range and echocardiography was normal. Serum levels of PTH and 1,25-(OH)2 Vitamin D were 7 pg/ml (10-65 pg/ml) and 15 pg/ml (20-70 pg/ml), respectively, but it was impossible to measure PTHrP. Bone marrow aspiration was performed for the patient due to anemia, thrombocytopenia, prolonged fever, and weight loss. Bone marrow smears showed ALL with L1 morphology. Flowcytometry of bone marrow was also consistent with early pre B-ALL phenotype. Cytogenetic analysis of bone marrow was normal and showed 46, XY karyotype. Bone marrow samples analysis for t (9; 22), t (12; 21), t (1; 19), and t (4; 11) using PCR method were negative.
Patient was hospitalized in pediatric intensive care unit for treatment and close monitoring of severe hypercalcemia. Aggressive hydration with normal saline was started with two times of the maintenance. Pamidronate 1 mg/kg IV infusion over 4 hours and furosemide 1 mg/kg IV every 6 hours was started. After 12 hours of treatment onset, regarding the serum calcium level increment from 15.8 to 17 mg/dl, dexamethasone (2 mg every 12 hours) was added to the previous treatment. Since serum calcium level was 16 mg/dl, 36 hours after treatment, the patient underwent emergency hemodialysis, and then calcium level became normal. Pamidronate and furosemide were discontinued and regarding the diagnosis of ALL, the patient was undergone chemotherapy protocol ALL IC-BFM 2002. Dexamethasone was continued and calcium remained within normal limits and the patient's clinical symptoms, including nausea, vomiting, weakness and lethargy resolved. Bone marrow aspiration on day 15 showed complete remission with less than 5% blasts (M1 marrow). Chemotherapy was continued for 24 months and the patient is now in complete remission, 25 months after treatment discontinuation.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [6, 'years'], 'weight': [7.0, 'kg'], 'Sodium': [141.0, 'mmol/L']}",0.03,0.0285,0.0315,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 6 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 7.0 kg. The concentration of sodium is 141.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 7.0 * (141.0/140 - 1) = 0.03 L. The patient's free body water deficit is 0.03 L."
5933,38,Free Water Deficit,lab test,decimal,usmle-5071,Extracted,"A 68-year-old man presents to the emergency department with confusion. The patient lives in a nursing home and has Alzheimer dementia at baseline. His nurse noticed that he was more confused than usual and was somnolent for the past 12 hours. The patient’s nurse also noticed that he was soiling his diapers more frequently with copious amounts of urine. The patient has lost 15 pounds since his last physician appointment 3 weeks ago. Laboratory values are ordered as seen below.

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 12.2 mg/dL
PTH: 8 pg/mL

The patient is referred to another physician for a more thorough workup including laboratory work and CT imaging.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [68, 'years'], 'weight': [15.0, 'lbs'], 'Sodium': [139.0, 'mEq/L']}",-0.0243,-0.02308,-0.02551,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 68 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 15.0 lbs so this converts to 15.0 lbs * 0.453592 kg/lbs = 6.80388 kg. The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 6.80388 * (139.0/140 - 1) = -0.0243 L. The patient's free body water deficit is -0.0243 L."
5934,38,Free Water Deficit,lab test,decimal,pmc-4496647-1,Extracted,"A 17-year-old African American male who was previously healthy with the exception of high blood pressure presented to a referring hospital with a 4-day history of coughing, vomiting, headache, facial edema, and lower extremity cramping. One day prior to admission, he also had noticed decreased urine output. At the referring hospital, he was found to be hypertensive with a serum creatinine of 52 mg/dL (4597 µmol/L) and was transferred to our pediatric intensive care unit for further evaluation and treatment.
Patient was born at term gestation and there were no significant health problems. Patient during his routine clinic visits was noted to have high blood pressure by his primary care physician but no further evaluation was done as the blood pressure was attributed to his obesity. Patient did not have any prior surgeries and was not taking any medications. There was no significant history of renal disease, dialysis, or kidney transplant in any of the family members.
On admission, patient was noted to be afebrile, hypertensive with blood pressure of 179/93 mm Hg and heart rate of 88 beats per minute, and tachypneic with respiratory rate in the 40s but saturating at 100% on room air. His anthropometric measurements showed his height to be 180 cm, his weight to be 115 kg, and body mass index to be >99%. Pertinent positives in physical exam include obesity, respiratory distress with nasal flaring, bilateral periorbital edema, and bilateral lower extremity edema. Laboratory results showed the patient to have azotemia with blood urea nitrogen (BUN) of 203 mg/dL and serum creatinine of 52 mg/dL, measured by enzymatic method. He had severe metabolic acidosis with bicarbonate of 10 mmol/L. Patient also had severe electrolyte imbalances including hyponatremia (126 mmol/L), hyperkalemia (6.3 mmol/L), hyperphosphatemia (10.5 mg/dL), hypocalcemia (5.3 mg/dL), and severe anemia with hemoglobin at 5.1 g/dL. Parathyroid hormone levels were elevated at 682 pg/mL (normal 11–80 pg/mL). Urine dipstick showed 3+ protein and 2+ blood and a urine protein to creatinine ratio was elevated at 14 (normal <0.2). Serological workup including complement levels, antinuclear antibodies, antinuclear cytoplasmic antibodies, and antiphospholipid antibodies was negative. Chest X-ray was significant for cardiomegaly and pulmonary edema. Echocardiogram showed severe left ventricular hypertrophy. Renal ultrasound revealed bilateral small, echogenic kidneys (right kidney 7.7 × 5.2 × 4.8 cm; left kidney 8.7 × 4.3 × 4.1 cm) consistent with dysplastic kidneys. Patient emergently underwent hemodialysis for fluid overload and to correct electrolyte imbalance. His anemia and electrolyte imbalances were slowly corrected. He is currently transitioned to peritoneal dialysis awaiting kidney transplant.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [17, 'years'], 'weight': [115.0, 'kg'], 'sex': 'Male', 'Sodium': [126.0, 'mmol/L']}",-6.9,-6.555,-7.245,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 17 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 115.0 kg. The concentration of sodium is 126.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 115.0 * (126.0/140 - 1) = -6.9 L. The patient's free body water deficit is -6.9 L."
5935,38,Free Water Deficit,lab test,decimal,pmc-7360221-1,Extracted,"A 39-year-old male patient (173 cm, 135 kgm, body mass index: 45.1) was a case of morbid obesity. He had undergone laparoscopic SG for morbid obesity on August 21, 2018, which led to his poor appetite, nausea and vomiting. In following 3 weeks, he lost 17 kilograms of body weight. On September 16, 2018, he was sent to our hospital due to persistent watery diarrhea, dehydration, and general weakness for 3 days. Upon the arrival at our hospital, his vital signs were blood pressure 117/57 mm Hg, pulse rate 108/min, respiratory rate 18/min, body temperature 37.1°C. Electrocardiography showed sinus tachycardia. The laboratory data revealed severe hypokalemia (K 2.6 mmol/L [3.6–5.1]), acute kidney injury (Bun 29 mg/dL [8–20], Cr 4.36 mg/dL [0.44–1.03] estimated Glomerular filtration rate 16 [mL/min]), and normal liver, pancreas, cardiac enzymes as well as other electrolytes (Na 137 mmol/L [136–144], Cl 111 mmol/L [100–111], bicarbonate 26 mmol/L [22–26]) (Table ). Other positive findings were mild anemia and leukocytosis (white blood cell 10.1^103/uL [3.8–10.0], Hemoglobin 10.6 g/dL [12–16]), elevated C-Reactive protein 2.3 mg/dL (<1.0) and lactic acid 3.1 mmol/L (0.5–2.2).
He was admitted for aggressive intravenous hydration. On the third day of admission, the patient's potassium level (3.2 mmol/L) and kidney function (Bun 23 mg/dL, Cr 2.57 mg/dL, eGFR 30 mL/min) were getting better, but he was getting deteriorated with drowsy consciousness. The brain computed tomography revealed no significant findings. Tracing his medical history, he was diagnosed as a bipolar affective disorder for 20 years. He was under regular follow-up in the psychiatric clinic with lithium carbonate 600 mg twice daily, risperidone 2 mg twice daily, and flurazepam 60 mg once daily. He was still taking the same dosage during these days after surgery. Lithium level was found to be 3.42 mEq/L and lithium toxicity was diagnosed. Lithium carbonate was discontinued immediately, and urgent hemodialysis was suggested by nephrologist.
After 3 courses of hemodialysis, his serum lithium level subsequently declined to 0.63 mEq/L and creatinine level to 1.58 mg/dL, while his consciousness returned normal. In the following days, neurologic sequelae were noted by muscle weakness (muscle power 2 points over bilateral dorsi-flexors and plantar-flexors) and pain sensation in both feet. The nerve conduction test revealed sensorimotor polyneuropathy with conduction block. The patient was discharged thirty-five days after admission, while his serum lithium and creatinine level declined to 0.06 mEq/L and 1.05 mg/dl, respectively. He was advised to keep a passive range of motion exercise until the nerve function recovers. Lithium carbonate was replaced by lamotrigine now.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [39, 'years'], 'weight': [135.0, 'kg'], 'Sodium': [137.0, 'mmol/L']}",-1.73571,-1.64892,-1.8225,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 39 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 135.0 kg. The concentration of sodium is 137.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 135.0 * (137.0/140 - 1) = -1.73571 L. The patient's free body water deficit is -1.73571 L."
5936,38,Free Water Deficit,lab test,decimal,pmc-3030014-1,Extracted,"A 32-year-old, 173 cm, 79 kg male patient was admitted to the emergency room (ER) for the treatment of facial pain due to an automobile accident. On arrival, he was fully conscious with an Glasgow Coma Scale score of 15/15 and stable vital signs: blood pressure (BP) 115/76 mmHg, heart rate (HR) 58 beats/min, and body temperature 37℃. Frontal skull fracture was suspected, and an X-ray skull and computed tomography (CT) were taken which demonstrated a fracture of the zygomatic bone on the right side. Under general anesthesia, an open reduction of the right sided zygomatic bone fracture was planned. Patient's medical history, neurological and physical examinations were normal. Preoperative blood test findings were normal: Na+ 143 mEq/L, K+ 3.9 mEq/L, Cl- 106 mEq/L, Ca2+ 9.3 mg/dl. The electrocardiogram (ECG) and chest X-ray results were also normal (). No premedication was provided, and the patient's vital signs were measured immediately after entering the operating room (OR); BP was 120/80 mmHg, HR was 50 beats/min, and pulse oximetry (SpO2) was 99%. Due to the facial injury, facemask ventilation was thought to be difficult to perform and hence, manual assisted ventilation, using rapid-sequence induction, with O2 of 5 L/min was performed and, 450 mg of thiopental and 80 mg of succinylcholine were injected intravenously one after another. After tracheal intubation, manual assisted ventilation was performed with 2.0 vol% of sevoflurane.
Immediately after tracheal intubation, BP increased from 120/80 to 160/90 mmHg and HR rose from 50 to 120 beats/min, and premature ventricular complexes (PVC) were detected on ECG. Therapy for ventricular arrthymias was intitated with a 70 mg of lidocaine intravenous injection, but the ventricular arrhythmias changed into patterns of ventricular bigeminy, ventricular tachycardia (VT), and torsades de pointes subsequently; BP measured at that time was 60/30 mmHg. Immediately, the administration of sevoflurane was discontinued and manual assisted ventilation was performed with 100% O2, while an external cardiac defibrillator was being prepared for attempting defibrillation. As an intravenous injection of esmolol was being prepared, ventricular fibrillation (VF) without measurable BP was detected. Instantly, cardiopulmonary resuscitation (CPR) by chest compression was performed. As early defibrillation was attempted using 360 J, chest compression was resumed and 1 mg of epinephrine was administered intravenously. Thereafter, VF on ECG disappeared, and the heart rhythm returned to its normal sinus rhythm (NSR). Considering it difficult to proceed with the operation, the patient was transferred to the intensive care unit (ICU) as soon as the patient's vital signs stabilized and normal spontaneous respiration was confirmed.
After the patient was transferred to the ICU, arterial blood gas analysis (ABGA) and electrolyte studies were conducted and the results showed a pH of 7.334, PaCO2 of 44.8 mmHg, PaO2 of 70.1 mmHg, base excess -2.7 mmol/L, HCO3- 23.3 mmol/L, SaO2 of 93%, Na+ 142 mmol/L, K+ 4.2 mmol/L, Cl- 103 mmol/L, Ca2+ 1.16 mmol/L, and Mg2+ 1.7 mg/dl; which were within their normal limits. However, chest X-ray revealed cardiomegaly and mild pulmonary edema, while ECG detected a T-wave inversion in leads II, III, aVF, and V2-6, and QTc prolongation to 547 ms (). On ultrasound, akinesia of the anteroseptum & inferoposterolateral wall of the left ventricle was detected, and in coronary angiography, the left ventricular ejection fraction was 38% demonstrating hyposystole, and an increase in the left ventricular cavity size to 60 mm were detected, while there were no other abnormalities seen. Thereafter, ECG was recorded daily on a continous basis with Holter monitor. Epinephrine provocation test was positive and hence the patient was diagnosed with LQTS. On the fifth day of admission, implantable cardioverter-defibrillator (ICD) was implanted. Afterwards, the patient's vital signs improved and were within their normal ranges and the QTc intervals on ECG also showed normalization. Hence on the twelfth day of admission, open reduction of the fractured zygomatic bone on the right side was performed under general anesthesia.
In the preoperative evaluation, blood tests showed findings within their normal ranges. On ECG, T-wave inversion persisted in leads II, III, and aVF. Normal T-waves were seen in V2-6 and the QTc of 406 ms was also within its normal limits (). As a premedication, 2.5 mg of midazolam was injected intravenously at the entrance of the OR. On arrival in the OR, vital signs were measured: BP 110/75 mmHg; HR 85 beats/min; SpO2 95%. Before induction of anesthesia, preoxygenation was performed with 6 L/min of O2, and propofol administration was initiated with an effect-site concentration of 4.0 µg/ml using a target-controlled infusion device (Orchestra™, Fresenius Vial S.A, France). Afterwards, 0.15 µg/kg/min of remifentanil, a useful opioid, was continuously injected intravenously, loss of consciousness was confirmed. Following complete muscle relaxation by an intravenous injection of 70 mg of rocuronium, tracheal intubation was performed. BP recorded immediately after intubation was 100/60 mmHg, and HR was 75 beats/min. After the patient's vital signs stabilized, propofol was infused with an effect-site concentration of 2.5-3.0 µg/ml, and continuous remifentanil infusion was given at a rate of 0.05 µg/kg/min to 0.10 µg/kg/min. During anesthesia, no particular changes were noted in BP and on ECG. The left radial artery was catheterized to monitor the arterial pressure. Similarly, HR, ECG, SpO2, end-tidal CO2, etc. were monitored, but they did not reveal any particular changes. After completion of the operation, muscle relaxation was reversed immediately with an infusion of glycopyrrolate 0.2 mg and pyridostigmine 10 mg. After confirming normal spontaneous respiration and consciousness, the patient was extubated and when his vital signs were found to be stable, he was transferred to the recovery room (RR). The total time exposed to anesthesia was 3 hours and 45 minutes. In the RR, the patient was in a stable condition and after he fully recovered from the anesthesia, he was transferred to the general ward. On the nineth postoperative day, the patient was discharged without any complications.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [32, 'years'], 'weight': [79.0, 'kg'], 'Sodium': [143.0, 'mEq/L']}",1.01571,0.96492,1.0665,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 32 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 79.0 kg. The concentration of sodium is 143.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 143.0 mEq. To convert from 143.0 mEq to mmol, convert from mEq to mmol. The compound 143.0 has a valence of 1, and so divide the valence by the value of mEq to get, 143.0 mEq/(1 mEq/mmol) = 143.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mEq sodium/L converts to 143.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 79.0 * (143.0/140 - 1) = 1.01571 L. The patient's free body water deficit is 1.01571 L."
5937,38,Free Water Deficit,lab test,decimal,pmc-4400448-1,Extracted,"A 17-year-old girl presented herself in our emergency department in the morning after suicidal ingestion of 250–300, 325 mg acetylsalicylic acid (Aspirin®). She announced that she had ingested the tablets on the previous evening. She developed vomiting and tinnitus prior to admission. She was 167 cm tall and weighed 52 kg. Her blood pressure was 132/74 mmHg, heart rate 110/min and the respiratory rate 26/min. She was alert, her pupillary response slightly delayed, she had mild epigastric tenderness and the bowel sounds were diminished. Her blood values were as following: pH 7.51, pO2 121 mmHg (16.1 kPa), pCO2 18 mmHg (2.38 kPa), HCO3
− 14 mmol/L, lactate 0.8 mmol/L, sodium 142 mmol/L, potassium 3.2 mmol/L, chloride 123 mmol/L, ionized calcium 0.98 mmol/L, creatinine 72 μmol/L (0.81 mg/dL). The serum salicylate concentration was 6.4 mmol/L (88 mg/dL).
We administered 100 mL sodium bicarbonate 8.4%, 40 mmol potassium, 2 mg tropisetron and 80 mg esomeprazole intravenously. Furthermore, a central venous catheter was introduced into the internal jugular vein and haemodialysis was begun. Haemodialysis was continued until the salicylate levels decreased sufficiently. The clinical course was uneventful and we transferred her to our psychiatric department.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [17, 'years'], 'weight': [52.0, 'kg'], 'sex': 'Female', 'Sodium': [142.0, 'mmol/L']}",0.44571,0.42342,0.468,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 17 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 52.0 kg. The concentration of sodium is 142.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 52.0 * (142.0/140 - 1) = 0.44571 L. The patient's free body water deficit is 0.44571 L."
5938,38,Free Water Deficit,lab test,decimal,usmle-1298,Extracted,"A 53-year-old woman is brought to the emergency department because of an episode of lightheadedness and left arm weakness for the last hour. Her symptoms were preceded by tremors, palpitations, and diaphoresis. During the past 3 months, she has had increased appetite and has gained 6.8 kg (15 lbs). She has hypertension, hyperlipidemia, anxiety disorder, and gastroesophageal reflux. She works as a nurse in an ICU and has been under more stress than usual. She does not smoke. She drinks 5 glasses of wine every week. Current medications include enalapril, atorvastatin, fluoxetine, and omeprazole. She is 168 cm (5 ft 6 in) tall and weighs 100 kg (220 lb); BMI is 36 kg/m2. Her temperature is 37°C (98.8°F), pulse is 78/min, and blood pressure is 130/80 mm Hg. Cardiopulmonary examination shows no abnormalities. The abdomen is soft and nontender. Fasting serum studies show:
Na+ 140 mEq/L
K+ 3.5 mEq/L
HCO3- 22 mEq/L
Creatinine 0.8 mg/dL
Glucose 37 mg/dL
Insulin 280 μU/mL (N=11–240)
Thyroid-stimulating hormone 2.8 μU/mL
C-peptide 4.9 ng/mL (N=0.8–3.1)
Urine screen for sulfonylurea is negative.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [53, 'years'], 'weight': [100.0, 'kg'], 'sex': 'Female', 'Sodium': [140.0, 'mEq/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 53 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 100.0 kg. The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 100.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
5939,38,Free Water Deficit,lab test,decimal,pmc-6477550-1,Extracted,"A 16-year-old female adolescent was referred to our hospital with severe hypertension (systolic pressure 178 mmHg), which was first detected 7 months prior to presentation during a routine annual physical examination. She complained of intermittent headache for about 1 year, and her previous blood pressure, measured 1 month prior to her detection of hypertension, had been normal. She showed mild hypokalemia (3.4 mmol/L) in a routine blood test, and an additional workup considering secondary hypertension was planned. Despite taking amlodipine (0.1 mg/kg twice a day), her blood pressure remained uncontrolled.
Upon admission to our hospital, her systolic and diastolic blood pressures were 155 mmHg (>99th percentile) and 111 mmHg (>99th percentile) respectively. She was 162.8 cm tall (50th–75th percentile) and weighed 55 kg (50th–75th percentile). Physical examination including ophthalmological examination revealed no abnormality other than hypertension, and her family history was negative for hypertension or renal diseases. Laboratory examination revealed normal levels of hemoglobin (14.4 g/dL), serum creatinine (0.57 mg/dL), serum total cholesterol (144 mg/dL), and normal urinalysis. Serum sodium, potassium, chloride, and total carbon dioxide levels were 134 mmol/L, 3.4 mmol/L, 102 mmol/L, and 27 mmol/L, respectively. Plasma renin activity was 9.83 ng/mL/hr (normal, 0.5–3.3 ng/mL/hr), and serum aldosterone level was 77.3 ng/dL (normal, 4–48 ng/dL). Urinary levels of vanillylmandelic acid, epinephrine, norepinephrine, dopamine, metanephrine, and normetanephrine were normal, and plasma levels of epinephrine, norepinephrine, and dopamine were also normal. Chest radiography, electrocardiography, and echocardiography showed normal findings. Renal Doppler ultrasonography revealed an avascular bilobed cyst in the lower pole of the right kidney (). Abdominal computed tomography (CT) angiography showed bilaterally normal renal arteries and an eccentric soft tissue component at the peripheral aspect of the cystic lesion (). The mass remained unenhanced during the arterial phase, and its margin was indistinguishable from the surrounding tissue (). During the delayed phase, its eccentric capsule showed enhancement, and an intact mass could be observed (), consistent with CT findings of JGC tumors.
A right partial nephrectomy was performed, and a clear resection margin was identified. The well-encapsulated mass measured 2.5 cm ×2.2 cm×2.0 cm in size with a partially cystic-appearing cut surface. Microscopic examination revealed sheets of polygonal tumor cells with amphophilic cytoplasm. Immunohistochemical examination showed that the tumor cells stained positive for CD34 and focally positive for CD117 (C-Kit) and smooth muscle actin. ()
Postoperatively, her blood pressure returned to normal (105/63 mmHg) without using any antihypertensive medication. On the 3rd postoperative day, the plasma renin activity (0.52 ng/mL/hr), serum aldosterone (3.9 ng/dL), and serum potassium (3.6 mmol/L) levels returned to normal. Her blood pressure and laboratory findings remained within the reference range over the next 3 years postoperatively until her last follow-up.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [16, 'years'], 'weight': [55.0, 'kg'], 'sex': 'Female', 'Sodium': [134.0, 'mmol/L']}",-1.41429,-1.34358,-1.485,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 16 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 55.0 kg. The concentration of sodium is 134.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 55.0 * (134.0/140 - 1) = -1.41429 L. The patient's free body water deficit is -1.41429 L."
5940,38,Free Water Deficit,lab test,decimal,pmc-5411553-1,Extracted,"A 76-year-old woman with a history of bronchial asthma complained of edema. She had been diagnosed with thrombocytosis due to ET 3 years earlier. Her condition was stable at diagnosis, but edema occurred 2 months later, upon which administration of hydroxyurea was initiated.
The patient’s height, weight, and blood pressure were 150 cm, 50 kg, and 180/80 mmHg, respectively. She was alert and appeared healthy. She did not have any remarkable heart, lung, or abdominal abnormalities. Pitting edema was demonstrated in her lower extremity.
The laboratory data were as follows: hemoglobin, 15.8 g/dl; hematocrit, 47.3 %; platelets, 490,000/μl; white blood cells, 8,100/μl, C-reactive protein, <0.2 mg/dl; blood urea nitrogen, 25.7 mg/dl; serum creatinine, 1.2 mg/dl; total cholesterol, 182 mg/dl; total protein, 5.9 g/dl; albumin, 3.1 g/dl; globulin, 2.8 g/dl; lactate dehydrogenase, 241 IU/l; aspartate aminotransferase, 18 IU/l; alanine aminotransferase, 12 IU/l; total bilirubin, 0.3 mg/dl; γ-glutamyl transpeptidase, 25 IU/l; alkaline phosphatase, 284 IU/l; Na, 141 mmol/l; K, 4.8 mmol/l; and Cl, 109 mmol/l. Urinalysis showed 3+ proteinuria and 2+ hematuria.
Renal biopsy was performed (Fig. ); 13 glomeruli could be evaluated, 2 of which exhibited global sclerosis. Moderate mesangial proliferation with several crescents and arteriolosclerotic changes were observed. Immunohistological staining was positive for IgG and IgA with a granular pattern and negative for IgM, C1q, C3, and fibrinogen. Electron microscopy showed electron-dense deposits in the mesangium. The patient was diagnosed with IgA nephropathy with an active lesion, and treatment consisting of 30 mg prednisolone, 50 mg cyclophosphamide, and 80 mg telmisartan per day was started. Although treatment improved the proteinuria and hematuria, the patient’s serum creatinine level remained unchanged. Telmisartan decreased her blood pressure, but her hematocrit level could not be normalized. The patient experienced a complicated acute myocardial infarction 3 years later. She died 5 years later from ischemic bowel disorder and heart failure.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [76, 'years'], 'weight': [50.0, 'kg'], 'sex': 'Female', 'Sodium': [141.0, 'mmol/L']}",0.16071,0.15267,0.16875,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 76 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 50.0 kg. The concentration of sodium is 141.0 mmol/L. Plugging in these values into the equation, we get 0.45 * 50.0 * (141.0/140 - 1) = 0.16071 L. The patient's free body water deficit is 0.16071 L."
5941,38,Free Water Deficit,lab test,decimal,pmc-7985187-1,Extracted,"A 12-day-old female infant presented with a history of poor sucking and was hospitalized for further examination of hyperkalemia and hyponatremia. She had been born at full term with a birth weight of 3,326 g and had shown no symptoms at birth. When she was brought to our hospital, her weight was 3,339 g. As the skin turgor and capillary refill time were normal, no obvious dehydration was observed. Neither hyperpigmentation of the skin nor virilization of the external genitalia was observed. Laboratory test results were as follows: serum sodium: 134 mEq/L; serum potassium: 6.2 mEq/L; serum glucose: 72 mg/dL; blood urea nitrogen (BUN): 12 mg/dL; and creatinine: 0.49 mg/dL. Metabolic acidosis was not noted. Urinalysis results were normal. Urinary sodium and potassium levels were 12 mmol/L [fractional excretion of sodium (FeNa) was 0.68%] and 16 mmol/L [fractional excretion of potassium (FeK) was 1.98%], respectively (Table ). Abdominal ultrasonography revealed mild hydronephrosis [Society for Fetal Urology (SFU) grade 1] in the left kidney (Figure ). The infant’s feeding was dramatically improved by administering intravenous saline. The serum sodium level increased to 137 mEq/L; however, the serum potassium level was still above 6.0 mEq/L. Hormone evaluation results were as follows: adrenocorticotropic hormone (ACTH): 50.3 pg/mL; cortisol: 25.4 μg/dL; plasma renin activity (PRA): 36.7 ng/mL/h; and aldosterone: 1,678.2 pg/mL (Table ). PRA and aldosterone levels were markedly elevated, suggesting profound tubular resistance to aldosterone. Hence, we suspected the presence of S-PHA with hydronephrosis.
On day four of her admission (16 days since birth), oral sodium chloride supplementation, as well as calcium polystyrene sulfonate, was started. However, the serum potassium level increased to 6.7 mEq/L, and an electrocardiogram revealed the peaking of T waves. Hydrocortisone (50 mg/m2) was intravenously administered, and the serum potassium level rapidly decreased to 5.4 mEq/L on the following day. With a presumptive diagnosis of CAH, we continued treatment with hydrocortisone. The infant’s electrolytes remained normal on follow-up. However, a mass screening test performed on day four showed a very low concentration of 17-hydroxyprogesterone (17-OHP; direct method) of 2.0 ng/mL. To exclude a diagnosis of adrenal insufficiency, we performed a urine steroid profile analysis for further consideration. During that time, we continued steroid administration along with oral hydrocortisone. The patient was temporarily discharged on day 22 of admission (34 days since birth) and was prescribed oral hydrocortisone of 6 mg/day, sodium chloride supplementation of 1.0 g/day, and calcium polystyrene sulfonate of 2.0 g/day (Figure ). We confirmed that the urine steroid profile was normal, and steroid administration was gradually decreased. At six months of age, we discontinued all drugs after confirming that there had been no recurrence of electrolyte abnormalities and that there were no symptoms induced by high renin or high aldosterone levels. The patient is currently one year old. She has been followed up with no problems noted other than the continued but mild hydronephrosis.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [12, 'days'], 'weight': [3339.0, 'g'], 'sex': 'Female', 'Sodium': [134.0, 'mEq/L']}",-0.08586,-0.08157,-0.09015,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 12 days old. This means the patient is 0 years old.
The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 3339.0 g so this converts to 3339.0 lbs * kg/1000 g = 3.339 kg. The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 3.339 * (134.0/140 - 1) = -0.08586 L. The patient's free body water deficit is -0.08586 L."
5942,38,Free Water Deficit,lab test,decimal,pmc-6663053-1,Extracted,"A 63-year-old male patient was admitted through the emergency department with a 2-month history of watery diarrhoea of 6–10 stools a day, abdominal pain that woke him up at night, anorexia and weight loss of 10 kg. No fever or other symptoms were reported. He had been previously medicated with ciprofloxacin and sulfamethoxazole/trimethoprim for possible small bowel bacterial overgrowth without improvement. The patient had also undergone a colonoscopy and upper gastrointestinal endoscopy which were both normal.
The patient had history of arterial hypertension and dyslipidaemia and had been medicated with olmesartan/hydrochlorothiazide 20/12.5 mg once daily for 10 years, atenolol 100 mg once daily, lercanidipine 20 mg once daily, clonidine 0.15 mg three times daily, and simvastatin 20 mg once daily. He lived in the countryside and drank well water that was not submitted to microbiological tests. He had no history of allergies, alcohol intake, contact with animals or recent travels abroad.
At admission the patient was conscious with normal vital signs. His weight was 99 kg with a body mass index of 29.89 kg/m2. Abdominal examination was unremarkable and no peripheral oedema or adenopathies were present.
Blood tests revealed a haemoglobin of 14.4 g/l, white blood cells of 10.04×109/l, C-reactive protein of 0.16 mg/dl, erythrocyte sedimentation rate of 18 mm, albumin of 4.4 g/dl, sodium of 137 mmol/l, potassium of 3.7 mmol/l, low folic acid (2.5 mg/dl) and normal liver enzymes (). Abdominal ultrasound was normal. The patient was discharged to the outpatient clinic and was treated with metronidazole on the assumption he had a protozoal infection, without improvement. He lost another 5 kg, developed hypoalbuminaemia of 2.9 mg/dl and hypokalaemia with a need for oral supplementation. An extended study was then performed.
Laboratory evaluation revealed thyroid function, cortisol level, protein electrophoresis, antinuclear antibodies and coeliac auto-antibodies were all normal. HIV and viral hepatitis tests were negative. Fasciola, Entamoeba and Giardia serological tests were negative, and gastrin and VIP levels were normal ().
Bacteriological, mycobacteriological, parasitological and clostridium stool tests were negative. Stool osmolarity was normal, and tests for reducing sugars and fat were negative.
Upper gastrointestinal endoscopy was macroscopically normal with histology of duodenum (D3) biopsies showing moderate villous atrophy (). Lower gastrointestinal endoscopy including biopsies was normal. Thoracic, abdominal and pelvic CT scans were normal.
At this point the patient had lost a total of 20 kg and his blood pressure had dropped, so atenolol and clonidine were suspended. Simvastatin was also suspended. A gluten-free diet was initiated with no improvement, and fasting and a cholestyramine trial were attempted, also without improvement.
Following a literature review, olmesartan-induced enteropathy was suspected and the drug was halted. Two days later the diarrhoea stopped, the patient gradually gained weight, and the hypoalbuminaemia and hypokalaemia resolved. After 2 months, the patient had regained his normal weight. Interestingly, the patient restarted olmesartan autonomously due to his disbelief in the presumed aetiology, only for the symptoms to recur with diarrhoea restarting after 2 days of therapy and ceasing again 1 day after its discontinuation.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [63, 'years'], 'weight': [99.0, 'kg'], 'sex': 'Male', 'Sodium': [137.0, 'mmol/L']}",-1.27286,-1.20922,-1.3365,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 63 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 99.0 kg. The concentration of sodium is 137.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 99.0 * (137.0/140 - 1) = -1.27286 L. The patient's free body water deficit is -1.27286 L."
5943,38,Free Water Deficit,lab test,decimal,pmc-7223027-1,Extracted,"A 34-year-old woman was admitted to the emergency unit complaining of limb numbness and watery diarrhoea (8–10 bowel movements/day) which started 2 weeks earlier. The patient reported a weight loss of about 10 kg in the last 2 months in the absence of hyporexia. Her clinical history unravelled microcytic anaemia treated with oral iron replacement. Physical examination showed severe weakness of the limbs with a bilaterally positive Trousseau’s sign without cardiorespiratory abnormalities. Vital parameters were within the normal range. The abdomen was flat, without tenderness, while auscultation disclosed increased intestinal sounds. Her ECG showed a sinus rhythm with type 1 atrioventricular block, flat T waves associated with U waves and an elongated QTc interval (570 ms). Laboratory tests revealed severe electrolyte imbalance, with hyponatraemia (133 mmol/L), hypokalaemia (1.6 mmol/L), hypocalcaemia (ionised calcium of 0.9 mmol/L), hypophosphataemia (1.6 mg/dL) and hypomagnesaemia (1.4 mmol/L). Furthermore, the patient had hypochromic microcytic anaemia (haemoglobin of 85 g/L, with a mean cell volume of 68 fL and a mean cell haemoglobin of 20.6 pg), normal platelet count (297×10ˆ9/L), iron (serum iron 18 µg/dL; ferritin 2 ng/mL) and folate deficiency (2 ng/mL), as well as hypoproteinaemia and hypoalbuminaemia (total serum protein 4.4 g/dL; albumin 2.6 g/dL). Due to severe electrolyte imbalance, a conspicuous electrolyte replacement was rapidly administered, leading to a slight improvement in electrocardiographic abnormalities. The patient was then admitted to the internal medicine ward for adequate investigation and treatment. During the hospitalisation, the common causes of infectious diarrhoea were excluded by stool cultures, and the faecal occult blood test resulted negative. Both ultrasound and abdominal X-ray examinations were unremarkable. Liver function tests revealed a slight increase of transaminases, with alanine transaminase and aspartate transaminase values of 47 U/L and 60 U/L (n.v. 5-35 for both parameters), respectively. Based on the lack of fever, normal C reactive protein and the presence of non-bloody, watery diarrhoea, the patient was further evaluated with an upper endoscopy. The examination revealed stigmata of villous atrophy at the duodenal level (), where biopsies were taken from the bulb and the second portion. Histopathological analysis showed the presence of a severe villous atrophy (Marsh-Oberhüber grade 3c) () without any evidence of aberrant intraepithelial lymphocytes. Based on the histopathological result, we used enzyme-linked immunoassay to test IgA anti-TG2, which turned to be positive at low titre (23 U/mL, n.v. <10 U/mL). This result was associated with the positivity of IgA antiendomysial antibodies (1:80) revealed by indirect immunofluorescence. The genetic test showed human leucocyte antigen (HLA)-DQ2 positivity. Therefore, a firm diagnosis of CD was established and the patient started a gluten-free diet (GFD). Due to rapid improvement after gluten withdrawal, a course with steroid treatment was deemed not necessary. Since diarrhoea and paraesthesia showed significant improvement with complete regression in about a week, the patient was discharged in good health.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [34, 'years'], 'weight': [10.0, 'kg'], 'sex': 'Female', 'Sodium': [133.0, 'mmol/L']}",-0.25,-0.2375,-0.2625,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 34 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 10.0 kg. The concentration of sodium is 133.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 10.0 * (133.0/140 - 1) = -0.25 L. The patient's free body water deficit is -0.25 L."
5944,38,Free Water Deficit,lab test,decimal,usmle-7931,Extracted,"A 53-year-old woman presents to a physician for a regular check-up. She has no complaints, but notes that she has been anxious and easily irritable for no particular reason over the past year. Six months ago, she was diagnosed with grade I arterial hypertension and prescribed lifestyle modification and weight loss to control her blood pressure. She currently takes aspirin (81 mg) and rosuvastatin (10 mg) daily. The vital signs are as follows: blood pressure 145/80 mm Hg, heart rate 81/min, respiratory rate 14/min, and temperature 36.6℃ (97.9℉). She weighs 91 kg (213.8 lb), the height is 167 cm (5.5 ft), and the BMI is 32.6 kg/m2. The physical examination is unremarkable. Blood testing was performed, and the results are shown below.
Plasma glucose 109.9 mg/dL (6.1 mmol/L)
Plasma triglycerides  185.8 mg/dL (2.1 mmol/L)
Na+ 141 mEq/L
K+ 4.2 mEq/L
The patient was prescribed atenolol.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [53, 'years'], 'weight': [91.0, 'kg'], 'sex': 'Female', 'Sodium': [141.0, 'mEq/L']}",0.325,0.30875,0.34125,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 53 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 91.0 kg. The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 91.0 * (141.0/140 - 1) = 0.325 L. The patient's free body water deficit is 0.325 L."
5945,38,Free Water Deficit,lab test,decimal,pmc-3121001-1,Extracted,"A 2-month old boy was admitted to our primary clinic because of poor weight gain, hyponatremia, and hyperkalemia. Initially, he was thought to have electrolyte abnormalities caused by dehydration and discharged without an exact diagnosis. When he was 6 years old, he manifested voice change, acne, testicular enlargement, and premature pubarche. His height and weight were 124 cm (2.31 SDS) and 27 kg (2.63 SDS), respectively. The volume of each testis was 7 mL, the stretched penile length was 7 cm, and his bone age was 13 years by Greulich and Pyle's method, which was remarkably advanced for his chronological age. His serum 17-hydroxypregnenolone (17-OHP) and testosterone levels were elevated to 480 ng/mL (normal range: 0.32-3 ng/mL) and 2.0 ng/mL (normal range: 0.03-0.1 ng/mL), respectively. He was diagnosed with precocious puberty caused by CAH. He was treated with hydrocortisone (15 mg/m2/day) and 9α-fludrocortisone (0.1 mg/day). However, he did not take medicine after 11 months of treatment. At age 17 years, he visited our outpatient clinic because of bilateral testicular enlargement and short stature. He was scheduled to be treated by surgical resection of testicular tumors because testicular biopsy demonstrated large, polygonal, and eosinophilic cells with round nuclei and prominent nucleoli, which are consistent findings with Leydig cell tumors (). His height and weight were 155.1 cm (-2.90 SDS) and 68 kg (0.49 SDS), respectively, and body mass index (BMI) was 30.2 (>97th percentile). He was normotensive (110/70 mmHg). His right and left testicles measured 10×6 cm, 7.5×4.5 cm, respectively (), with both being of firm consistency. His pubic hair Tanner stage was grade V. Gynecomastia and skin hyperpigmentation were noted. Radiography of left hand and wrist showed a closed epiphyseal plate. His serum 17-OHP concentration was 506.20 ng/mL (normal range: 0.32-3 ng/mL), ACTH level was 187.6 pg/mL (normal range: 2-49 pg/mL), plasma renin activity was 20.0 ng/mL/h (normal range: 0.4-8.8 ng/mL/h), and dehydroepiandrosterone sulfate (DHEA-S) level was 270.6 µg/dL (normal range: 30-555 µg/dL). He had an androstenedione level of 18.0 ng/mL (normal range: 0.57-1.5 ng/mL), a luteinizing hormone (LH) concentration of 0.23 mIU/mL (normal range: 1.54-7.0 mIU/mL), a follicle-stimulating hormone (FSH) level of 1.6 mIU/mL (normal range: 1.54-7.0 mIU/mL) and a testosterone level of 6.13 ng/mL (normal range: 3.5-9.7 ng/mL). His serum sodium and potassium concentrations were 141 mmol/L and 4.1 mmol/L, respectively, and serum α-fetoprotein and β-hCG levels were 1.4 ng/mL (normal range <20 ng/mL) and 1.0 mIU/mL (normal range <5 mIU/mL), respectively. Abdominal computerized tomography revealed a 1.5 cm-sized adrenal adenoma on the left side and focal adrenal hyperplasia on the right side. Mutation analysis of CYP21A2 revealed a compound heterozygote, c.293-13A>G and c.1066C>T (p.R356W). To reduce the size of his tumors and to improve his hormonal profile, he was prescribed ACTH suppressive therapy with dexamethasone (0.25 mg tid). After 3 weeks, the tumors markedly regressed. The volume of each testis estimated using a Prader orchidometer was 25 mL (). His serum 17-OHP and ACTH concentrations had decreased to 1.0 ng/mL and 9.4 pg/mL, respectively, and serum testosterone concentration was reduced to 0.05 ng/mL (normal range: 3.5-9.7 ng/mL). He was switched from dexamethasone to prednisolone (5 mg twice a day) for maintenance, which had no effect on the volume of his testes. Following the switch, 17-OHP concentration was 19.8 ng/mL, ACTH concentration was 45.3 pg/mL, plasma renin activity was 20.0 ng/mL/h, and testosterone level was 3.0 ng/mL.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [17, 'years'], 'weight': [68.0, 'kg'], 'sex': 'Male', 'Sodium': [141.0, 'mmol/L']}",0.29143,0.27686,0.306,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 17 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 68.0 kg. The concentration of sodium is 141.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 68.0 * (141.0/140 - 1) = 0.29143 L. The patient's free body water deficit is 0.29143 L."
5946,38,Free Water Deficit,lab test,decimal,usmle-1360,Extracted,"A 35-year-old man comes to the emergency department with fever, chills, dyspnea, and a productive cough. His symptoms began suddenly 2 days ago. He was diagnosed with HIV 4 years ago and has been on triple antiretroviral therapy since then. He smokes one pack of cigarettes daily. He is 181 cm (5 ft 11 in) tall and weighs 70 kg (154 lb); BMI is 21.4 kg/m2. He lives in Illinois and works as a carpenter. His temperature is 38.8°C (101.8°F), pulse is 110/min, respirations are 24/min, and blood pressure is 105/74 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 92%. Examinations reveals crackles over the right lower lung base. The remainder of the examination shows no abnormalities. Laboratory studies show:
Hemoglobin 11.5 g/dL
Leukocyte count 12,800/mm3
Segmented neutrophils 80%
Eosinophils 1%
Lymphocytes 17%
Monocytes 2%
CD4+ T-lymphocytes 520/mm3(N ≥ 500)
Platelet count 258,000/mm3
Serum
Na+ 137 mEq/L
Cl- 102 mEq/L
K+ 5.0 mEq/L
HCO3- 22 mEq/L
Glucose 92 mg/dL
An x-ray of the chest shows a right lower-lobe infiltrate of the lung.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [35, 'years'], 'weight': [70.0, 'kg'], 'sex': 'Male', 'Sodium': [137.0, 'mEq/L']}",-0.9,-0.855,-0.945,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 35 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 70.0 kg. The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 70.0 * (137.0/140 - 1) = -0.9 L. The patient's free body water deficit is -0.9 L."
5947,38,Free Water Deficit,lab test,decimal,pmc-2827053-1,Extracted,"A 36-year-old, previously healthy Hispanic female with no significant past medical history and no prior history of hypertension presented to the emergency room with sharp retrosternal chest pain radiating to the back. She was 165 centimeter tall and weighed 70 kilogram. She was a housewife and mother of two living children. She smoked one pack of cigarettes a day for more than ten years. For 3 months prior to presentation, she had been taking 18-20 tablets of caffeine-based weight loss pills daily, which was higher than the recommended daily dose. Each tablet contains 60-100 mg of caffeine and she was taking 1080 mg to 2000 mg of caffeine daily. She denied the use of other medications, stimulants, herbal, alcohol and illicit drugs. She said that she had lost approximately 20-25 kilograms in last 3 months. No family history of hypertension, diabetes or coronary artery disease. She denied palpitation, chest pain, insomnia, headache, abdominal pain or increase in urination.
On presentation, her blood pressure was found to be 220/110 mm Hg in right arm and 230/118 mm Hg in left arm. Her initial work-up included an electrocardiogram which showed T-wave inversion in leads III, aVF and V6. A complete blood count showed hemoglobin 12.9 g/dl (normal: 12.0-16.0 g/dl), white blood cell count 15.1 k/ul (normal: 4.0-11.0 k/ul) and platelet count 231 k/ul (normal: 150-450 k/ul). Serum basic metabolic panel showed sodium 132 mmol/L (normal: 135-145 mmol/L), potassium 3.3 mmol/L (normal: 3.5-5.3 mmol/L), chloride 103 mmol/L (normal: 95/105 mmol/L), bicarbonate 23 mmol/L (normal: 22-31 mmol/L), creatinine 1.3 mg/dl (normal: 0.6-1.3 mg/dl), calcium 8.3 mg/dl (normal: 8.6-10.3 mg/dl), and anion gap 6 mmol/L (normal: 7-17 mmol/L). Liver function test showed normal aspartate transaminase (15 U/L; normal: 0-55 U/L), alanine transaminase (23 U/L; normal: <45 U/L), alkaline phosphatase (55 U/L; normal: 34-104 U/L) and albumin (3.5 g/dl,normal:3.0-5.1 g/dl). Urinalysis showed only elevated specific gravity of 1.031(normal: 1.005-1.03). There were no crystals, protein and glucose in the urinalysis. Troponin I level was less than 0.030 ng/ml (normal: 0.0-0.049 ng/ml). Urine and serum toxicology screens were negative for cocaine, amphetamine, marijuana, benzodiazepines, barbiturates and phencyclidine. A chest X-ray did not show any infiltrate, consolidation, effusion or mediastinal widening. A computed tomography aortogram showed aortic dissection involving the posterior aspect of the arch extending into the common iliac arteries and right proximal external iliac artery. The dissection extended into the left subclavian and axillary arteries. There was narrowing of the origin of the right renal artery due to dissection (Stanford type B dissection) (Figure ,Figure , & Figure .)
She was started on intravenous esmolol and nitroprusside for blood pressure control and was admitted to the medical intensive care unit. During hospitalization, her blood pressure remained well controlled with amlodipine. All other investigations for a secondary cause of hypertension were negative.Patient was discharged home and upon follow-up 2 week later, her blood pressure remained well controlled with low dose amlodipine.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [36, 'years'], 'weight': [70.0, 'kg'], 'sex': 'Female', 'Sodium': [132.0, 'mmol/L']}",-2,-1.9,-2.1,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 36 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 70.0 kg. The concentration of sodium is 132.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 70.0 * (132.0/140 - 1) = -2.0 L. The patient's free body water deficit is -2.0 L."
5948,38,Free Water Deficit,lab test,decimal,pmc-8272273-1,Extracted,"This was a 2-month-old male patient who was born at term with a birth weight of 3450 g. He was the second child of non-consanguineous Chinese parents. Since 2 weeks old he was admitted to local hospital due to recurrent vomiting, diarrhea, poor feeding, dehydration, hyponatremia, and hyperkalemia. Prompt therapy with sodium chloride (NaCl) and 5% dextrose as well as sodium bicarbonate infusion were initiated, then the patient was transferred to our unit for further investigation.
Physical examination (PE) on admission showed: weight of 4 kg (−1SD), length of 55 cm (0 SD), no dehydration, no hyperpigmentation, and normal external genitalia. The laboratory findings were as follows: Plasma Na 130 mmol/L (Normal Range [NR] 135 ~ 145 mmol/L), K 6.86 mmol/L (NR 3.5 ~ 5.0 mmol/L), Cl 104 mmol/L (NR 96 ~ 106 mmol/L), Adrenocorticotropic hormone (ACTH) 3.37 pmol/L (NR 1.6 ~ 13.9 pmol/L), cortisol < 5μg/dl (NR 5 ~ 20μg/dl), plasma renin activity (PRA) 1019.2 pg/ml (NR adult 4 ~ 24 pg/ml, neonatal renin 2.5–20 times higher than adult []), and plasma Ald 117.0 pg/ml (NR infants 1-12 months 50-900 pg/ml []). Further analysis showed plasma testosterone (T), progesterone (P), Androstenedione (A4), and 17-hydroxyprogesterone (17-OHP) levels were in the normal range. Urinalysis and CT scan for adrenal and renal were also normal. Patient was treated with fludrocortisone (Fc) 0.1 mg/day along with sodium supplementation 2-3 g/day. Since 6-month-old his mother had stopped sodium supplementation. FC dose had been reduced from 1.5 years old till 1.67 years old and was then fully discontinued by his parents. Currently, he is 5.17 years old with height of 104 cm (− 1.93SD). He is asymptomatic with normal serum electrolyte levels.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [2, 'months'], 'weight': [4.0, 'kg'], 'sex': 'Male', 'Sodium': [130.0, 'mmol/L']}",-0.17143,-0.16286,-0.18,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 2 months old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 4.0 kg. The concentration of sodium is 130.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 4.0 * (130.0/140 - 1) = -0.17143 L. The patient's free body water deficit is -0.17143 L."
5949,38,Free Water Deficit,lab test,decimal,pmc-4528876-1,Extracted,"A 78-year-old man presented with 1-day history of nausea and vomiting. His symptoms started suddenly the night prior to presentation. The nausea was constant, to the point where he could no longer tolerate oral intake. Vomiting occurred 5 to 6 times throughout the evening, but there were no further episodes as of the morning of presentation. He endorsed very minimal epigastric burning, which he described as a “gas pain,” but he had no other abdominal symptoms. His bowel movements were normal. The patient was discharged from the hospital 10 days prior; during that hospitalization, he had symptomatic bradycardia felt to be secondary to his β-blocker. His dosage was reduced, his bradycardia improved, and he was discharged home. Since discharge, he noted persistent exertional dyspnea and bilateral lower extremity edema.
The past medical history was remarkable for type 2 diabetes mellitus, hyperlipidemia, paroxysmal atrial fibrillation, nonischemic cardiomyopathy (ejection fraction of approximately 40%) with stage III diastolic dysfunction, and chronic kidney disease (baseline creatinine 2.2). He smoked 4 cigarettes daily for 25 years, but not the last 20 years. His medications included aspirin, simvastatin, furosemide, metoprolol tartrate, and glipizide.
On examination, his blood pressure was 136/71 mmHg, heart rate 77 bpm, respiratory rate 16, temperature 36.1°C, oxygen saturation 100% (room air), weight 82 kg, and no orthostasis. In general, he was not in acute distress. There were no skin lesions. Mucous membranes were moist. Lung fields were clear to auscultation bilaterally. Heart was regular without murmurs, rubs, or gallops. He had jugular venous distention 4 cm above the sternal angle. His abdomen was benign. He had no tenderness over his liver and no hepatomegaly was present. He had minimal bilateral lower extremity edema.
The patient’s white blood cell count was 15 200/mm3. The hemoglobin was 13 g/dL, and the platelet count was 97 000/mm3. The total bilirubin was 3.3 mg/dL, direct bilirubin 1.3 µg/dL, aspartate aminotransferase (AST) 4725 IU/L (normal value = 12-38 IU/L), alanine aminotransferase (ALT) 3240 IU/L (normal value = 10-45 IU/L), alkaline phosphatase 110 IU/L (normal value = 25-100 IU/L), total protein 6.6 g/dL, and albumin 3.7 g/dL. The international normalized ratio (INR) was 2.6. His sodium was 134 mmol/L, potassium 5.6 mmol/L, bicarbonate 21 mmol/L, blood urea nitrogen 54 mg/dL, and creatinine 3.5 mg/dL. His brain-natriuretic peptide was 1040 pg/mL (normal = <100 pg/mL), and troponin was 0.50 ng/mL (normal = <0.09 mg/mL). His lipase was 49.0 IU/L (normal = 10-50 IU/L).
An abdominal ultrasound revealed increased echogenicity of the liver parenchyma, patent hepatic vasculature, and no dilated intrahepatic or extrahepatic ducts. The acetaminophen level was zero and the urine drug screen negative. Hepatitis A to C serologies were negative, and antinuclear antibody, antimitochondrial antibody, F-actin antibody, and liver-kidney microsome-1 antibody titers were all normal. Further review of his past records indicated that his liver tests were AST 47 IU/L and ALT 53 IU/L during his hospitalization 10 days ago.
The patient’s electrocardiogram (ECG; ) revealed multiple conduction defects including a right bundle branch block, left anterior fascicular block, and a first-degree atrioventricular block. He also had inferior Q waves and T wave inversions in leads I, aVL, and V3. These findings along with the conduction defects were all seen on previous ECGs. Review of prior records indicated that he had a left heart catheterization about 18 months prior to this admission. At that time was found to have nonobstructive coronary disease.
His most recent echocardiogram (), which was performed 2 weeks prior to this admission, showed a reduced ejection fraction (40%), biatrial enlargement (, RA and LA), and biventricular hypertrophy (, VS and PW; , arrows). There was also a granular or “speckled” appearance of the myocardium (, asterisk). The estimated peak right ventricular systolic pressure was 34 mm Hg based on an estimated right atrial pressure of 13 mm Hg, without primary valvular abnormalities. Mitral valve inflow Doppler and mitral annulus tissue Doppler () were consistent with severe left ventricular diastolic dysfunction. The E/e ratio was >15, consistent with an elevated left ventricular filling pressure. There was hypokinesis to akinesis of the inferior and septal walls.
The patient was monitored overnight and his symptoms resolved without intervention. His blood pressure remained within normal limits and he had normal urine output. The aminotransferases declined dramatically, to a level of 1070 IU/L within 48 hours. He was discharged home in baseline condition. One month later, he was seen in cardiology clinic during which time he had further evaluation with cardiac magnetic resonance imaging (MRI; ). This revealed diffuse myocardial thickening of both left and right ventricles with delayed hyperenhancement in a pattern consistent with amyloidosis ( and , asterisks). Both atria were dilated in size, with evidence of patchy subendocardial scar ( and , arrows). The patient declined endomyocardial biopsy and further invasive investigation or therapy.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [78, 'years'], 'weight': [82.0, 'kg'], 'sex': 'Male', 'Sodium': [134.0, 'mmol/L']}",-1.75714,-1.66928,-1.845,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 78 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 82.0 kg. The concentration of sodium is 134.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 82.0 * (134.0/140 - 1) = -1.75714 L. The patient's free body water deficit is -1.75714 L."
5950,38,Free Water Deficit,lab test,decimal,usmle-1339,Extracted,"A 36-year-old man is brought to the emergency department for right upper quadrant abdominal pain that began 3 days ago. The pain is nonradiating and has no alleviating or exacerbating factors. He denies any nausea or vomiting. He immigrated from Mexico 6 months ago and currently works at a pet shop. He has been healthy except for 1 week of bloody diarrhea 5 months ago. He is 182 cm (5 ft 11 in) tall and weighs 120 kg (264 lb); BMI is 36 kg/m2. His temperature is 101.8°F (38.8°C), pulse is 85/min, respirations are 14/min, and blood pressure is 120/75 mm Hg. Lungs are clear to auscultation. He has tenderness to palpation in the right upper quadrant. Laboratory studies show:
Hemoglobin 11.7 g/dL3
Leukocyte Count 14,000/mm
Segmented neutrophils 74%
Eosinophils 2%
Lymphocytes 17%
Monocytes 7%
Platelet count 140,000/mm3
Serum
Na+ 139 mEq/L
Cl- 101 mEq/L
K+ 4.4 mEq/L
HCO3- 25 mEq/L
Urea nitrogen 8 mg/dL
Creatinine 1.6 mg/dL
Total bilirubin 0.4 mg/dL
AST 76 U/L
ALT 80 U/L
Alkaline phosphatase 103 U/L
Ultrasonography of the abdomen shows a 4-cm round, hypoechoic lesion in the right lobe of the liver with low-level internal echoes.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [36, 'years'], 'weight': [120.0, 'kg'], 'sex': 'Male', 'Sodium': [139.0, 'mEq/L']}",-0.51429,-0.48858,-0.54,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 36 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 120.0 kg. The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 120.0 * (139.0/140 - 1) = -0.51429 L. The patient's free body water deficit is -0.51429 L."
5951,38,Free Water Deficit,lab test,decimal,pmc-6755931-1,Extracted,"A 16-year-old male, presented with five days history of progressively worsening dry cough with exertional dyspnoea, three days after the onset of these symptoms he developed edema and oliguira. There was no history of hematuria, headache, seizures, rashes, joint pain, hearing or visual abnormalities. He did not give any history of repeated urinary tract infection, and had a good scholastic performance. There was no family history of any renal disease. Past medical history was uneventful except for burning sensation in hand and feet on and off for past two years. Clinically he was under nourished, weight: 39 kgs (<3rd centile); Height: 160 cms (3rd centile). On examination there was mild pallor, facial puffiness, ascites and limb edema. He had stage II hypertension, with raised JVP, tender hepatomegaly, basal crepitation, tachycardia and gallop cardiac rhythm. Fundus examination was normal. There was no renal bruit. Neurolog ical and musculoskeletal examination was normal.
Investigations showed hemoglobin of 9.1 gm/dl and total leucocyte count of 14200/cu.mm with normal differentials and platelet count. Complete urine examination revealed 2+ protein with no RBC/WBC or casts. Along with elevated blood urea (303 mg/dl) and serum creatinine (9.3 mg/dl), there was hyponatremia (129 mmol/L) and hyperkalemia (6.0 mEq/L). The liver enzyme were also abnormal with raised AST (265U/l) and ALT (686U/l). Renal ultrasound showed right kidney (8 × 4.4) cms and left kidney (9.6 × 5.2) cms with both showing increased cortical echogenicity and loss of cortico-medullary differentiation.
Bone chemistry showed Calcium, Phosphorus and ALP of 5.1 mg/dl, 8.9 mg/dl and 170 IU/L respectively. Parathormone (30.55 ng/ml) and 25-OH D3 level (68.43 ng/ml) were normal. Echocardiogram demonstrated dilated cardiomyopathy with, global left ventricle hypokinesia and pulmonary arterial hypertension. Work up for autoimmune and vasculitis (C3, C4, ANCA and ANA) was normal. Micturating cystourethorgram done in view of discrepancy in renal sizes ruled out reflux. Following the detailed clinical evaluation and investigations, a possibility of chronic kidney disease (CKD) stage-V probably due to nephronophthisis or chronic glomerulopathy or chronic interstitial nephritis with uremic neuropathy or vitamin B 12 deficiency (421 pg/ml) were considered.
In view of ESRD with fluid overload, uraemia and hyperkalemia, regular hemodialysis along with supportive measures were initiated. Hypertension was controlled on four anti-hypertensive medications. He also required oral digoxin and sildenafil in renal corrected doses in view of poor cardiac status and severe pulmonary hypertension. However, he continued to have episodes of severe burning and pain sensation over both lower limbs not relieved with adequate hemodialysis, analgesics or vitamin B12 supplementation. A possibility of Fabry's disease was kept in view of cardiac involvement, renal failure and acroparasthesias. Electroneuromyography was suggestive of bilateral common peroneal motor and sensory axonal neuropathy in the lower limbs and bilateral sural sensorial axonal neuropathy.
A renal biopsy was performed which showed visceral epithelial proliferation in two of the viable glomeruli with prominent cytoplasmic vacuolization in all the visceral epithelial cells. There was extensive interstitial fibrosis and tubular atrophy, involving more than 75% of the core. Marked fibrous intimal proliferations of arteries wereseen. The electron microscopy revealed podocytes stuffed with myeloid bodies []. Hence a possibility of Fabrys disease was considered and was confirmed by absence ofalpha galactosidase activity in blood. Genetic testing for a molecular diagnosis was not performed in view of cost constraints. In addition, Enzyme replacement therapy (ERT) was not started as parents could not afford the therapy. The child continues to be on thrice weekly hemodialysis.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [16, 'years'], 'weight': [39.0, 'kg'], 'Sodium': [129.0, 'mmol/L']}",-1.83857,-1.74664,-1.9305,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 16 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 39.0 kg. The concentration of sodium is 129.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 39.0 * (129.0/140 - 1) = -1.83857 L. The patient's free body water deficit is -1.83857 L."
5952,38,Free Water Deficit,lab test,decimal,pmc-4950766-1,Extracted,"A 69 year old Hispanic female with a past medical history significant for hypertension, diabetes mellitus, coronary artery disease status post revascularization, ischemic cardiomyopathy and chronic kidney disease had presented to our hospital for further evaluation and care. For the past few months the patient had suffered weight loss (approximately 30–35 lb), generalized malaise, low grade fevers (99.9 F), non-productive cough, myalgias and arthralgias. She did not endorse any night sweats or recent travel history, and there were no sick contacts at home. Prior to admission to our institution the patient was at an outside hospital and was being treated for sepsis with combinations of antibiotics including intravenous vancomycin, meropenem, echinocandin, metronidazole, and piperacillin tazobactam for 2 to 3 weeks duration as she was developing fevers and productive cough.
The physical exam yielded a thin and chronically ill appearing female patient.
Vital signs at the time of admission were notable for hypertension (186/79 mmHg). Her eyes did not show any conjunctival hemorrhaging or icterus, however there was conjunctival pallor. Oropharynx did not show any active exudates or ulcerative lesions. Her cardiac exam did not reveal any murmurs and her airways were clear to auscultation. Abdominal exam revealed palpable splenomegaly. Examination of the extremities did not show nail deformities including splinter hemorrhages or nail pitting. Her skin had no evidence of skin nodularities or other lesions. There was a 1 cm non tender, movable left axillary lymph node. The rest of the physical examination was unremarkable.
Initial laboratory work revealed that the patient had pancytopenia. White blood cell count (WBC) was stated at 2.4 K/uL, absolute neutrophil count (ANC) 1.92 K/uL, hemoglobin (Hgb) of 11.6, and platelet count of 39,000/uL. B2-microglobulin was seen elevated at 9.2 mg/L. Basic metabolic panel obtained showed sodium 134 mEq/L, Potassium 3.5 mEq/L, Chloride 103 mEq/L, Bicarbonate 26 mEq/L, Blood urea nitrogen 30 mg/dl, Creatinine 0.90 mg/dl, glucose 220 mg/dl. Liver function panel showed Albumin 2.2 g/dl, normal transaminases, total bilirubin 0.8 mg/dl, direct bilirubin 0.4 mg/dl. Urine analysis showed 200 mg/dl of protein and occasional amorphous crystals.
Initial computed tomography (CT) scan of the abdomen and pelvis during hospital admission showed a 15 cm spleen which was heterogenous and micronodular, as well as scattered abdominal and pelvic lymphadenopathy (Fig. ). No imaging signs of portal hypertension were noted.
During the hospitalization our patient was noted to become more confused and agitated, and there was concern that the patient was having seizures as she was seen numerous times to lose consciousness and awaken, with occasional loss of bladder function. A brain magnetic resonance imaging (MRI) showed subcortical non enhancing FLAIR hyper intense foci in the bilateral posterior occipital lobes.
Lumbar puncture and cerebral spinal fluid (CSF) studies were further performed for further analysis, and showed: WBC 1; no red blood cells; protein 62 mg/dL; glucose 35 mg/dL; and, lactate dehydrogenase 234 mIU/mL. Most notable negative findings in the CSF included no detectable viral cultures for cytomegalovirus, adenovirus, herpes virus, and varicella zoster virus, negative cryptococcal antigen serology and negative bacterial and fungal cultures.
Electroencephalogram studies showed triphasic morphology waves with and without sharp negative component at 2–3 hertz. These were seen in continuum mostly with subtle waxing and waning features. To 0.5 mg intravenous alprazolam, above discharges had slowly resolved, replaced by organized background that consists of 6 hertz rhythms. Importantly, there was a clinical improvement after alprazolam; suggesting a nonconvulsive seizures responding to benzodiazepine.
Two weeks later after the initial CT imaging and after the patient was more stable from the neurological perspective in order to attempt a lymph node excisional biopsy, a PET-CT imaging was performed and showed complete resolution of the previously detected lymphadenopathy and splenomegaly. (Fig. ).
Additional serologies for viral hepatitis and autoimmune etiology work up were performed. A bone marrow biopsy was performed and additional serum erythropoietin level, iron profile; cobalamin and folate level were determined.
The patient returned to the benign hematology clinic after discharged from the hospital. During her follow up appointment she appeared in better spirits and recovering well. Physical examination was notable for an absence of lymphadenopathy particularly in the cervical and axillary region, as well as no palpable organomegaly in the abdomen. It was further revealed that her antinuclear antibody (ANA) titer was highly positive (1:640), ESR 108 mm/hr with a CRP 6.74 mg/L. Negative viral hepatitis B, C and Human Immunodeficiency virus serologies.
Serum quantitative immunoglobulin showed a mildly elevated Ig A and Ig G level, without other abnormalities. Serum and urine protein electrophoresis did not reveal a monoclonal gammopathy. Serum free light chain levels showed kappa 96.3 mg/L and lambda 60.06 mg/dL with a normal ratio 1.6 in a patient with chronic kidney disease.
Complement C3 level was normal with a slightly elevated C4 at 46 mg/dL.
Bone marrow aspirate yielded a predominance of CD3 positive polytypical small T cells and a population of polyclonal B-cells by flow cytometry and negative for lymphoma or other malignant process. A focal lymphohistiocytic aggregate with granuloma formation was noted; occasional larger cells with prominent nucleolus identified; eosinophils were increased mildly in the vicinity of this aggregate. Acid fast bacilli and fungal stains were attempted; however the focal granuloma could not be appreciated at subsequent sections.
The patient’s pancytopenia was thought to be likely secondary to systemic lupus erythematosus and she was thus referred to rheumatology for further work up, and further testing included anti-double-stranded DNA, anti-RNP, anti-CCP antibody, ANCA vasculitis panel, direct antiglobulin test, lupus anticoagulant, anticardiolipin antibody, anti-double-stranded DNA antibody, and anti-SSA and anti-SSB. All these tests were negative, thus ruling out systemic erythematous lupus, rheumatoid arthritis, and other connective tissue disorders.
The interval improvement and self-limited clinical course in our case led us to believe that her elevated ANA titers, her bone marrow granuloma were secondary to an EBV infection-related syndrome. Monospot test was not performed and at that point we evaluated for EBV PCR and EBER staining in the bone marrow. Initial EBV PCR results were positive (960 copies/mL), while Epstein–Barr virus-encoded small RNAs staining in the bone marrow was negative. Our in situ hybridization stain is validated to work on decalcified bone marrow trephine biopsies and all stains include an on-slide positive control. As such, the likelihood of a false negative result is low. A possible explanation includes a sampling factor with lack of infected B-cells in the bone marrow despite the presence of viremia.
Her follow up labs during subsequent clinic visits showed WBC 5.3 K/uL, ANC 3.15 K/uL, Hgb 7.4 g/dL, calculated reticulocyte index of 1.1 and platelets 172 K/uL. Iron was 68 ug/dL, transferrin 124.1 mg/dL, ferritin 2952 ng/mL and serum erythropoietin levels were 31.7 mIU/mL. Serum cobalamin was 394 pg/mL and serum folate 12.3 ng/mL. Since there was spontaneous interval resolution of her neutropenia and her thrombocytopenia our diagnosis at that point was cytopenias secondary to infectious mononucleosis and anemia of chronic kidney disease related to diabetes.
Our patient presented 7 weeks later at the emergency room with a recurrent febrile syndrome with diffuse cervical and axillary lymphadenopathy and splenomegaly (Fig. ) and worsening cytopenias: WBC 1800/uL, ANC 1480/uL, Hgb 8.3 gr/dL, platelet count 20,000/uL; a repeat EBV titer revealed 6580 copies/mL. CT imaging with contrast found bilateral axillary, mediastinal and hilar lymphadenopathy. Low volume retroperitoneal and pelvic lymphadenopathy, hepatosplenomegaly with numerous small ill-defined hypodense lesions was in the spleen and probably also within the liver (Fig. ). At this time a repeat bone marrow biopsy and an excisional lymph node biopsy were performed and reviewed. The bone marrow specimen showed a solitary large cell positive for CD30 identified in the clot. No atypical cells are identified in core biopsy as assessed by IHC for CD30 and Pax-5. EBER was positive in few and scattered cells. The lymph node sections demonstrated near-total effacement of the lymph node architecture by a neoplasm comprised of neoplastic cells with Hodgkin-Reed-Sternberg morphology. The neoplastic cells were positive for CD15, CD30, PAX5 (weak), and MUM1. They were negative for CD3, CD20, CD45, ALK, and EMA. The findings were diagnostic of classical Hodgkin lymphoma, best subtyped as lymphocyte-depleted. (Fig. ). The expression of PAX5 with weak intensity coupled with MUM1 expression by the neoplastic cells is diagnostic of classical Hodgkin lymphoma. The expression of PAX5, a gene encoding a B-cell-specific transcription factor, excluded T-cell lymphoma as a diagnostic consideration. It is worth noting also that flow cytometry done on a bone marrow sample with involvement by lymphoma showed no evidence of T-cell or B-cell immunophenotypic aberrancies.
The patient was started on ABVD chemotherapy regime, bleomycin was held secondary to patient’s history of cardiomyopathy. She received three cycles of chemotherapy with complete clinical remission. Additional cycles of chemotherapy were not completed given prolonged and severe chemotherapy-induced cytopenias that eventually recovered over the following months. A bone marrow biopsy at completion of treatment revealed no morphologic evidence of residual Hodgkin lymphoma. Her most recent surveillance PET-CT imaging, nine months from completion of treatment, showed no hypermetabolic lymphoma and continuing complete metabolic response to therapy.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [69, 'years'], 'weight': [3035.0, 'lbs'], 'Sodium': [134.0, 'mEq/L']}",-26.54971,-25.22222,-27.8772,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 69 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 3035.0 lbs so this converts to 3035.0 lbs * 0.453592 kg/lbs = 1376.65172 kg. The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. Plugging in these values into the equation, we get 0.45 * 1376.65172 * (134.0/140 - 1) = -26.54971 L. The patient's free body water deficit is -26.54971 L."
5953,38,Free Water Deficit,lab test,decimal,pmc-3127313-1,Extracted,"A 2-month-old 4.3 kg male child was diagnosed as extrahepatic biliary atresia and was scheduled for laparotomy. The child was brought to the pediatrics clinics 2 weeks earlier with complaints of rapid breathing since 12 days, vomiting (non bilious) since 8 days, and decreased oral intake since 1 day. The child was passing clay colored stools and dark colored urine. There was yellow discoloration of skin since 2 weeks, which was progressively increasing. The mother revealed the presence of recurrent rhinorrhoea from the first day of life.
Examination revealed icterus. Abdomen examination showed hepatospenomegaly (liver on left side and spleen on right side) and umbilical hernia. Electrocardiogram (ECG) displayed inverted P waves in I, aVL and aVR, which were suggestive of situs inversus. Chest X-ray revealed evidence of bronchopneumonia and the cardiac shadow was on the right side. Ultrasonography abdomen also indicated situs inversus. Echocardiography was suggestive of situs inversus with dextrocardia with normal cardiac anatomy. Hepatobiliary iminodiacetic acid (HIDA) scan was indicative of extra hepatic biliary atresia (EHBA) with the liver in left upper abdomen. Child was diagnosed as situs inversus with dextrocardia, bronchopneumonia, and extrahepatic biliary atresia.
Bronchopneumonia was managed with intravenous antibiotics, paracetamol, and steam inhalation. The child was placed on therapy with oral phenoparbitone 10 mg twice a day and intravenous Vitamin K 5 mg once a day for 10 days. Investigations revealed hemoglobin 9.5 g/dL, total leucocyte count (TLC) 17400/mm3, platelet count 4.5 lac/mm3, serum sodium 131 meq/L, serum potassium 4.4 meq/L, random blood sugar 70 mg/dL, serum bilirubin 19.2 mg/dL (normal 0.2-1.2) (direct-12, indirect 7.2), SGOT 148IU/L (normal 15-50) , SGPT 93 IU/L (normal 15-50), alkaline phosphatase 1232 IU/L (normal 50-300), blood urea 18 mg/dL (15-45), serum creatinine 0.6 mg/dL (0.6-1.2), prothrombin time (PT) 11.3 sec (test), 12 sec (control), and aPTT test 38.7 sec Control 29 sec (normal 20-40 sec). The child was listed for corrective biliary surgery.
The operating room was kept warm prior to shifting of the child. In the operating room, routine monitors (electrocardiogram, pulse oximeter, non invasive blood pressure) were attached. Left-sided ECG leads were attached on the right side and vice versa. Anesthesia was induced with intravenous fentanyl (9 μg) and thiopentone (25 mg), and lungs were ventilated with isoflurane in oxygen and nitrous oxide (50:50) (MAC 1.2) using Jackson Rees modification of Ayre's T piece. After achieving neuromuscular blockade with atracurium (2.5 mg), trachea was intubated with endotracheal tube size 3.5 mm ID. Capnography and temperature monitoring was also initiated. Urethra was catheterized and urinary output was monitored. Anesthesia was maintained with desflurane in oxygen and nitrous oxide (50:50) (MAC 1) using paediatric close circuit along with boluses of atracurium (0.5 mg) and fentanyl (1 μg) as required. The child was kept warm using warm fluids, warming mattress and by adequately covering the child with cotton.
The surgeon found the liver on left side with right lobe on the left side, malrotated gut (caecum, appendix on the left side), two atretic gall bladders, annular pancreas with preduodenal portal vein, cirrhotic enlarged liver, and a multi-lobulated spleen. Hepatic roux-en-y portoenterostomy with Ladd's procedure was done. The surgical incision site was infiltrated with 6 mL of 0.125% bupivacaine. The hydration was maintained using normal saline. The surgery lasted 5 hours, and blood loss of 100 mL was replaced with packed red blood cells.
At the end of surgery, the airway resistance increased. The airway pressures increased from 18 cm H2O to 28 cm H2O. Endotracheal tube suctioning was done. On auscultation, breath sound was reduced on the right lung fields. Repeat suction was done. We suspected a mucus plug to be obstructing the endotracheal tube and changed the tube after repeat laryngoscopy. A mucus plug was seen at the tip of the tube. The ventilation became better. Residual neuromuscular blockade was reversed and trachea was extubated. The child had good respiratory efforts with bilateral equal air entry. The child was shifted to the pediatric intensive care unit for further management. The child was nursed in the incubator and ECG and pulse oximeter monitoring were continued. The vitals and urinary output were within normal limits. The humidified oxygen was supplemented using an oxygen hood. The postoperative hemoglobin was 9.9 g/dL. The serum electrolytes were normal. The analgesia was provided with rectal paracetamol suppository. The child had an uneventful recovery and was discharged on the 18th postoperative day.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [2, 'months'], 'weight': [4.3, 'kg'], 'sex': 'Male', 'Sodium': [131.0, 'mEq/L']}",-0.16586,-0.15757,-0.17415,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 2 months old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 4.3 kg. The concentration of sodium is 131.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 131.0 mEq. To convert from 131.0 mEq to mmol, convert from mEq to mmol. The compound 131.0 has a valence of 1, and so divide the valence by the value of mEq to get, 131.0 mEq/(1 mEq/mmol) = 131.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 131.0 mEq sodium/L converts to 131.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 4.3 * (131.0/140 - 1) = -0.16586 L. The patient's free body water deficit is -0.16586 L."
5954,38,Free Water Deficit,lab test,decimal,pmc-8330443-1,Extracted,"A 3-month-old, previously well Chinese girl, presented with one-week history of diarrhoea followed by one episode of afebrile seizure. She was referred from a district hospital for further work up and management. Her birth history was also unremarkable. She was delivered at term with birth weight of 3.72 kg (75th centile) and length of 55 cm (97th centile) (). She had been on exclusive breastfeeding for 1 month and then changed to infant formula. She was on multiple different brands of cow’s milk formula in view of recurrent episodes of loose stool and excessive flatulence.
On examination, she was moderately dehydrated and tachycardic. Her weight was 6.2 kg (above 75th centile) and length of 61 cm (75th centile). Examination revealed ballotable right kidney. Initial laboratory investigations showed hyponatremia (117 mmol/L), hypochloremia (90 mmol/l), hyperkalemia (9 mmol/L) with metabolic acidosis. She required intravenous (IV) normal saline bolus (10 ml/kg) given at the district hospital and IV hydration with 5% correction over 12 hours. She was given one cycle of lytic cocktail with calcium resonium 6 hourly to correct the hyperkalemia. Her electrolytes normalized after 4 days of treatment. Stool culture for rotavirus and reducing sugar were negative. In view of the possibility of cow’s milk protein allergy, she was commenced on extensive hydrolysed milk formula and subsequently responded well with resolution of diarrhoea. She had no recurrent episode of seizure and her neurological examination was unremarkable with normal ultrasound scan of the brain.
Her urine culture grew Enterobacter and therefore, she was treated with 7 days course of cefuroxime. Ultrasound of kidney, ureter, and bladder (USG KUB) showed right duplex kidney with gross hydronephrosis and hydroureter, while a micturating cystourethrogram (MCUG) showed grade 5 vesicoureteric reflux on the right side.
Routine screening for CAH is not done in our country. The diagnosis of transient PHA became apparent when the serum aldosterone level obtained on admission was elevated at 3700 pmol/l (normal range <1109 pmol/L) with normal 17-hydroxyprogesterone (17-OHP) level (0.8 nmol/L, reference range 1.0-14.12 nmol/L). Adrenocorticotropic hormone (ACTH) stimulation test was also normal. She was commenced on oral trimethoprim for urinary tract prophylaxis prior to discharge. She has no subsequent recurrent episode of electrolyte disturbances nor urinary tract infection as evidenced by negative urine culture post treatment. She is now two years old and currently under our follow up. Her growth is satisfactory with weight 12.4 kg (above 50th centile) and height 90 cm (90th centile). Her developmental milestones are appropriate and she is currently awaiting urethral implantation.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [3, 'months'], 'weight': [6.2, 'kg'], 'sex': 'Female', 'Sodium': [117.0, 'mmol/L']}",-0.61114,-0.58058,-0.6417,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 3 months old. This means the patient is 0 years old.
The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 6.2 kg. The concentration of sodium is 117.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 6.2 * (117.0/140 - 1) = -0.61114 L. The patient's free body water deficit is -0.61114 L."
5955,38,Free Water Deficit,lab test,decimal,pmc-6712280-1,Extracted,"A 41-year-old, 65-kg, female smoker (15 pack-year history) patient was admitted for an endoscopic resection of a submucous uterine myoma under general anesthesia. This was the second surgery for the same myoma. Preoperative examination and laboratory test results were normal. Baseline blood pressure and heart rate were 120/70 mmHg and 80 beats per minute, respectively. An intravenous catheter was placed and normal saline was administered. General anesthesia was induced with fentanyl and propofol. The I-gel® laryngeal mask No. 4 was inserted. Anesthesia was maintained with desflurane in 40% of oxygen. The patient was placed in lithotomy position and a hysteroscopy with a bipolar 9-mm resectoscope, utilizing 0.9% saline as the distention/irrigation medium was conducted.
In the 50th minute of the procedure, end-tidal CO2 dropped from 35 to 25 mmHg and pulse oximetry (SpO2) from 100% to 90%. Other vital signals including blood pressure and heart rate were stable. Crackling sounds were heard from the base of the lungs. As a pulmonary oedema was suspected, the volume of irrigated saline was checked. A total of 9000 mL of saline was used and only 4000 mL was collected. The surgery was stopped. At that point the patient was uncovered and a generalized oedema was noticed, with a marked distended abdomen and cervical oedema with tissue tension. The inspired fraction of oxygen was increased to 100% and an arterial blood analysis was performed, which showed pH 7.09, PaCO2 41 mmHg, PO2 70 mmHg, HCO3+ 12.4 mEq/L, Na+ 145 mEq/L, K+ 2.3 mEq/L, Ca2+ 0.76 mEq/L, hemoglobin 5.9 g/dL, O2 sat 89%, and blood glucose level of 50 mg/dL.
Therefore, 100 mL of sodium bicarbonate 8.4% and 20 mg of furosemide were administered. Laryngeal mask was replaced by a tracheal tube to improve oxygenation and ventilation. Using a video laryngoscope C-MAC®, the airway oedema could be observed, especially in the arytenoid region, which restricted the observation of the vocal cords and only let the intubation of a 6.5-mm tracheal tube. The arterial and central lines were put and 10 mEq of potassium chloride, 2 g of calcium chloride, 2 g of magnesium sulfate, and 20 mL of dextrose 30% were administered through the central line. The patient was placed in supine position and surgeons performed a laparoscopy to exclude uterus perforation. There was no uterine rupture, but a prominent oedema of the intestinal loops and a small amount of peritoneal free fluid were observed. A bladder catheter was inserted. The patient`s auricular temperature was 33°C.
The patient was admitted to ICU. Her postoperative chest X-ray showed bilateral pulmonary oedema ().
During her ICU stay, the serious electrolyte disturbances (hypokalemia, hypocalcaemia, and hypomagnesaemia) and acidosis were corrected. Hemoglobin increased to 9.3 g/dL (Her pre-procedure hemoglobin level was 11.9 g/dL). There were no coagulation abnormalities. Temperature returned to the normal state. Generalized oedema was resolved with a urine output of 3000 mL in total, which made extubation possible six hours after ICU admission. She received oxygen supplementation for 12 hours with a nasal cannula and was transferred to the general ward approximately 24 hours after ICU admission, where she stayed for another day, after which she was discharged.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [41, 'years'], 'weight': [65.0, 'kg'], 'Sodium': [145.0, 'mEq/L']}",1.16071,1.10267,1.21875,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 41 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 65.0 kg. The concentration of sodium is 145.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 145.0 mEq. To convert from 145.0 mEq to mmol, convert from mEq to mmol. The compound 145.0 has a valence of 1, and so divide the valence by the value of mEq to get, 145.0 mEq/(1 mEq/mmol) = 145.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 145.0 mEq sodium/L converts to 145.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 65.0 * (145.0/140 - 1) = 1.16071 L. The patient's free body water deficit is 1.16071 L."
5956,38,Free Water Deficit,lab test,decimal,pmc-6642719-1,Extracted,"A 33-year-old previously healthy woman weighing 70 kg was brought to the emergency department (ED) by Emergency Medical Services (EMS) in cardiac arrest. The patient was undergoing liposuction of her thighs in a physician’s clinic with no intraoperative complications a few minutes before the event. The surgeon reported harvesting 1.5 L of fat from the patient’s thigh and mid-back during the procedure, which lasted 45 minutes.
A few minutes following the procedure, the surgeon noticed that the patient was becoming more somnolent. Her vital signs were stable, including a blood pressure of 170/90 mmHg. The doctor suspected a possible clinical manifestation of hypoglycemia and subsequently administered oral dextrose solution without any improvement.
Two hours after the procedure, the patient started feeling dizzy with a rapid decline of her mental status leading to tonic-clonic seizure followed by a complete loss of consciousness. EMS arrived on the scene after five to 10 minutes. EMS personnel reported the patient was gasping, cyanotic, and drooling. During transport to the ED, she had a cardiopulmonary arrest, so the EMS team immediately initiated resuscitation using Basic Life Support guidelines.
Upon arrival to the ED, the cardiac monitor showed asystole, so the patient was intubated and resuscitation resumed using the advanced cardiac life support algorithm. Return of spontaneous circulation was achieved after 12 minutes of resuscitation in the ED (22 minutes post-arrest).
The plastic surgeon who performed the procedure was asked for details about the procedure technique and the anesthesia modality. He reported using the power-assisted liposuction technique in his private clinic. As for anesthesia, he reported the use of five vials of 50 mL lidocaine 2% (20 mg/mL) subcutaneously during the operation; making the total dose of lidocaine equal to 5000 mg. He also pointed to prior use of the same procedure and anesthesia three months earlier while performing an uncomplicated abdominal liposuction on the same patient.
Following the return of spontaneous circulation, electrocardiogram showed normal sinus rhythm, no QT prolongation with a corrected QT interval (QTc) of 466 ms and a normal QRS interval of 100 ms with no ST- or T-wave abnormalities [].
Neurological examination revealed no response to verbal or painful stimuli (Glasgow Coma Scale of 3T), pupils equal in size bilaterally and reactive to light, preserved corneal and oculocephalic reflexes, and a downward Babinski reflex bilaterally.
Arterial blood gas analysis on mechanical ventilation on 100% fraction of inspired oxygen (FiO2) showed a pH of 7.34, a CO2 pressure of 39.9 mmHg, an O2 pressure of 131 mmHg, and a bicarbonate concentration of 20.8 mmol/L.
Laboratory workup included a complete blood count, and measurement of serum electrolytes, lactate, cardiac and liver enzyme levels. The results were the following: white blood cell count 9.8 × 109/L with 41% polymorphonuclear cells; a hemoglobin level 10.4 g/dL; platelet count 336 × 106/L; troponin 0.003 ng/mL; sodium concentration 144 mmol/L; potassium 3.5 mmol/L; chloride 99 mmol/L; bicarbonate 16 mmol/L; glucose 346 mg/dL; blood urea nitrogen 13 mg/dL; creatinine 1.0 mg/dL; aspartate aminotransferase 225 IU/L; alanine aminotransferase 238 IU/L; γ-glutamyl transpeptidase 12 IU/L; alkaline phosphatase 55 IU/L; and lactate 17.55 mmol/L. Her serum lidocaine level upon presentation to the ED was 5.30 µg/mL (therapeutic range = 1.50–5.00 µg/mL).
Imaging included a computerized tomography (CT) scan of the brain without contrast material as well as CT angiography of the chest to rule out intracranial bleed and massive pulmonary embolism, respectively, which could be a reason for the patient’s arrest. Positive findings included bilateral consolidations consistent with aspiration pneumonitis without any signs of intracranial bleeding, pulmonary embolism, or aortic dissection. The patient was started on antibiotic therapy.
The patient developed generalized myoclonic jerks that were attributed to possible anoxic brain injury following her cardiac arrest so she was started on valproic acid.
The patient was admitted to the intensive care unit. Magnetic resonance imaging of the brain was done three days later and showed signs of severe hypoxic-ischemic brain injury, which was confirmed by electroencephalogram (EEG) (electrocerebral silence on EEG).
The patient’s hospital stay was complicated by an increase in brain edema and pressure, electrolytes disturbances, multiple nosocomial infections with end-organ damage leading to the patient’s death secondary to septic shock two months later.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [33, 'years'], 'weight': [70.0, 'kg'], 'sex': 'Female', 'Sodium': [144.0, 'mmol/L']}",1,0.95,1.05,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 33 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 70.0 kg. The concentration of sodium is 144.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 70.0 * (144.0/140 - 1) = 1.0 L. The patient's free body water deficit is 1.0 L."
5957,38,Free Water Deficit,lab test,decimal,pmc-3431052-1,Extracted,"A 44-year-old Sudanese-American female was transferred to our hospital from another facility with the chief complaint of chronic diarrhea. She had emigrated from Sudan to the United States ten years previously and had never revisited her home country. She was relatively healthy until nine months prior to admission when she experienced the insidious onset of cramping epigastric pain and diarrhea. The diarrhea was in large volume, with 10–20 bowel movements daily. Her stools were watery, with very little formed stool and no blood or mucus. Her condition led to profound weakness and debility, and she was essentially bed-bound. She reported intermittent nausea, vomiting, severe loss of appetite, and a 100-pound weight loss in the preceding nine months. She denied any fever, sick contacts, history of foreign travel, hiking, camping, exposure to animals, or drinking well water. Past medical history was significant for a positive tuberculin test ten years ago. She was breast feeding at that time and therefore did not receive isoniazid. She denied smoking but admitted drinking 6 beers per day until just prior to her presentation.
Over the preceding nine months, the patient had been admitted to a community hospital several times and extensively investigated for the cause of her diarrhea. Stool ova and parasite examination, as well as Giardia and Cryptosporidium antigen tests, was negative. A workup for malabsorption and colonoscopy was normal; upper GI endoscopy showed mild gastritis and blunting of small intestinal villi. The patient was started on a celiac diet with no improvement in her symptoms. HIV and hepatitis serologies were negative. Her thyroid function tests were normal. A CT scan of the abdomen showed fatty liver.
Upon transfer to our hospital, the patient was found to be severely dehydrated with multiple electrolyte abnormalities: sodium 133 mmol/L, potassium 4.0 mmol/L, chloride 105 mmol/L, bicarbonate 14 mmol/L, BUN 2.85 mmol/L, creatinine 30.50 mmol/L, magnesium 0.6 mmol/L, and phosphorus 1.13 mmol/L. She was anemic with a hemoglobin of 94 g/L and hematocrit of 31%. Her leukocyte count was 10.3 × 109/L with 64% neutrophils and an increased absolute lymphocyte count of 2.16 × 109/L; the rest of the differential was normal. Erythrocyte sedimentation rate was more than 120 mm/hr. Albumin was 25 g/L, AST 64 U/L, ALT 104 U/L, alkaline phosphatase 187 U/L, total bilirubin 5.13 μmol/L, and direct bilirubin 3.42 μmol/L. Diarrhea was again evaluated, and tests for ova and parasites, including microsporidia, stool cultures, polymerase chain reaction (PCR) for Clostridium difficile, fat and reducing substances, osmolar gap, fecal leukocytes, and occult blood, were all negative. Anti-tissue transglutaminase IgA and anti-gliadin IgA antibodies were negative. Vasoactive intestinal peptide and urine 5-HIAA levels were normal. Consultation with gastroenterology led to an additional stool culture for Salmonella, Shigella, Campylobacter, Aeromonas, Plesiomonas, and E. coli O157, repeat ova and parasite exam, and tests for Cryptosporidium antigen, Cyclospora, and Isospora. All testing was negative with the exception of a modified acid-fast stain which was positive for Isospora (Cystoisospora) belli ().
An infectious disease consult suggested investigating for potential causes of immunocompromise as the degree of diarrhea was too severe for a simple I. belli infection. A repeat HIV 1, 2, and HIV group O test was negative by serology. There was no evidence of immunoglobulin deficiency; serum IgA was normal, while IgG and IgM were mildly elevated. The patient was treated with trimethoprim 160 mg (TMP)-sulfamethoxazole 800 mg (SMZ) four times a day for two weeks with resolution of diarrhea.
Unfortunately, the abdominal pain and loss of appetite persisted and a subsequent HTLV-1 and 2 antibody screen was reported positive. HTLV-1 infection was confirmed by western blot. At followup one month later, the patient was found to have new bilateral inguinal lymphadenopathy. A CT scan of the chest showed axillary, mediastinal, and right hilar lymphadenopathy. Likewise, a CT scan of the abdomen showed new extensive retroperitoneal lymphadenopathy which was enclosing and displacing the vasculature. There was a lytic lesion in the right femoral neck with significant fragility of the cortex as well as sclerotic abnormality of the L3 transverse process and L3 vertebral body. Skeletal survey and bone scan showed multiple lytic lesions. A right inguinal lymph node biopsy showed partial effacement by an interfollicular T-cell infiltrate with residual B-cell nodules mimicking follicular lymphoma. Immunohistochemistry showed the abnormal cells to express CD2, CD3, and CD4 with absence of CD5 and CD7. Flow cytometry confirmed the immunophenotype and PCR for T-cell receptor gamma gene showed a monoclonal rearrangement. B-cell gene rearrangement assay was polyclonal. Biopsy of the right hip and femur curettings showed involvement by peripheral T-cell lymphoma with expression of CD3, CD25, and partial CD30 ().
A diagnosis of ATLL was rendered as per WHO guidelines []. Her diarrhea returned in the interim, and repeat stool examination was positive for I. belli, prompting a repeat course of TMP-SMZ.
The patient was transferred to the oncology service and started on the cyclophosphamide, hydroxydaunorubicin hydrochloride (doxorubicin hydrochloride), vincristine, and prednisone (CHOP) regimen. An orthopedics consult for right hip pain led to prophylactic stabilization of the right femur for an impending pathologic fracture. Femoral shavings revealed a focal atypical lymphoid infiltrate consistent with lymphoma. The patient then underwent two cycles of treatment with CHOP for stage 4 T-cell lymphoma. She did not tolerate chemotherapy well. Abdominal pain and diarrhea continued despite TMP-SMZ; nausea and vomiting did not improve significantly. She returned to the hospital several times over the next three months with dehydration, severe electrolyte imbalances, and complications secondary to chemotherapy and concomitant loss of weight and strength. After discussion with the patient and her family, a mutual decision was taken to send her to a nursing home with hospice care. The patient died a few weeks after discharge.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [44, 'years'], 'weight': [100.0, 'lbs'], 'sex': 'Female', 'Sodium': [133.0, 'mmol/L']}",-1.13398,-1.07728,-1.19068,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 44 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 100.0 lbs so this converts to 100.0 lbs * 0.453592 kg/lbs = 45.3592 kg. The concentration of sodium is 133.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 45.3592 * (133.0/140 - 1) = -1.13398 L. The patient's free body water deficit is -1.13398 L."
5958,38,Free Water Deficit,lab test,decimal,pmc-4025155-1,Extracted,"An 8-year-old boy was admitted with a history of abdominal bloating associated with rectal tenesmus and increased flatus. These symptoms recurred especially during the afternoon and evening. No associated gastrointestinal symptoms were reported. His clinical history was characterized by rumination in the first years of life with associated non-organic feeding disorders as a picky eater. Radioallergosorbent test for alimentary and inhalant allergens, skin prick tests and celiac screening was negative. Ultrasonography did not reveal any organomegaly or fluid presence in the abdomen. Abdominal radiographs showed a distended colon with increased gas in the rectum and coprostasis, without signs of obstruction. On physical examination, weight was 22 kg and height 129 cm, with a mild degree of malnutrition according to the Waterloo classification. Cardiorespiratory objectivity was normal. A significantly non-tender, hypertympanitic abdominal distension was present. No hepatomegaly nor splenomegaly were noted. Rectal examination revealed a sensation of hypertonic anus sphincter without perineal erythema and stool. Neurologic examination was normal. The following laboratory investigations were performed: complete blood count (red blood cell count 5.1 × 106/mm3, Hb 13.8 g/dl, HCT 43%, MCV 84 fl, white blood cell count 5 × 103/mm3, neutrophils 34%, lymphocytes 60%, monocytes 4%, eosinophils 2%, basophils 0%, platelets 297 × 103/mm3), C-reactive protein was 0.10 mg/dl (normal 0–0.50 mg/dl), erythrocyte sedimentation rate 5 mm within the first hour, glycemia 68 mg/dl, serum glutamic oxaloacetic transaminase 26 IU/l, serum glutamic pyruvate transaminase 14 IU/l, serum gamma-GT 7 IU/l, amylase 67 U/l, lipase 27 U/l, BUN 26 mg/dl, creatine 0.5 mg/dl, iron 54 μg/dl, sodium 140 mmol/l, potassium 4.3 mmol/l, calcium 9.78 mg/dl, total proteins 7.1 g/dl, and albumin 48 g/l; coagulation parameters and urinalysis were normal. Also, lactate dehydrogenase (395 U/l), muscle enzymes (creatine phosphate kinase 75 IU/l, CK-MB 10 IU/l), thyroid hormones (free thyroxine 10.98 pmol/l, thyroid-stimulating hormone 1.925 μIU/ml), celiac serology, cytomegalovirus, Epstein-Barr virus, herpesvirus serology and autoantibodies (ANA, nDNA, ANCA) were normal, and megacolon was excluded using barium enema. After ruling out primary pathologic causes, a neuropsychiatric consultation was requested with the disclosure of continuous aerophagia and anxiety disorder with obsessive compulsive notes and game-playing dependency. It was possible to reassure the family on the absence of an organic gastrointestinal disease with indications to neuropsychiatric and cognitive follow-up.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [8, 'years'], 'weight': [22.0, 'kg'], 'sex': 'Male', 'Sodium': [140.0, 'mmol/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 8 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 22.0 kg. The concentration of sodium is 140.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 22.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
5959,38,Free Water Deficit,lab test,decimal,pmc-8191249-1,Extracted,"A 35-year-old, 79 kg female developed left sided ptosis with ipsilateral facial pain and numbness during third trimester of pregnancy but was not investigated. Following uneventful cesarean delivery in a peripheral hospital, her symptoms improved only to worsen subsequently. Her brain magnetic resonance imaging (MRI) revealed sphenoid sinus meningioma invading suprasellar, left cavernous sinus and left orbital areas. During the third postpartum week she presented to emergency department of our hospital with increasing headache. Neurosurgeon administered her dexamethasone and planned for combined endonasal and left pterional craniotomy in collaboration with ENT surgeon. Her investigations revealed normal liver functions and blood glucose, Na 140 mEq/L and K 3.6 mEq/L. Following anesthesia induction and tracheal intubation, 8 mg of dexamethasone was administered. Anesthesia was maintained with 50% oxygen and infusion of fentanyl and propofol. Intrarterial blood pressure, neurophysiology monitoring beside routine monitoring was instituted. Approximately 30 min into endonasal phase, her Na was 144 mEq/L and K was 3.7 mEq/L with normal glucose. Urine output (UO) at that time was 200 ml, which increased to 250 ml in the next hour. She was receiving 5 ml/kg/h of crystalloids. No diuretic or mannitol was administered during the procedure. Nearly 30 min before the completion of nasal procedure, Na was 146 mEq/L with 300 ml UO. ENT surgeon handed over the patient to neurosurgeon after 90 min. Serum Na kept on worsening and reached 156 mEq/L after 3 h with increasing UO. Therefore, a presumptive diagnosis of CDI was made in consultation with endocrinologist and 1 mcg of desmopressin was given IV. UO during the remaining surgical period got reduced to 70–100 ml/h with decline in Na to 149 mEq/L at the end of nine hours of procedure. Total UO was 3,000 cc (most of which was in pre-desmopressin phase). Owing to the stormy intraoperative course she was ventilated overnight in the neurocritical care unit (NCCU) and was extubated next day after her check MRI which was normal. In NCCU, discontinuation of desmopressin resulted in recurrence of polyuria, hypernatremia, and high serum osmolality (309 mOsm/kg). Desmopressin was restarted 1 mcg twice daily IV and later on changed to oral route 60 mcg morning and evening with 30 mcg in the afternoon. In addition, she was advised hydrocortisone and levothyroxine. She was discharged home after 2 weeks, with normal Na and normal UO. On her last visit to the clinic after 3.5 months, her Na and UO were controlled on desmopressin.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [35, 'years'], 'weight': [79.0, 'kg'], 'sex': 'Female', 'Sodium': [156.0, 'mEq/L']}",4.51429,4.28858,4.74,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 35 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 79.0 kg. The concentration of sodium is 156.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 156.0 mEq. To convert from 156.0 mEq to mmol, convert from mEq to mmol. The compound 156.0 has a valence of 1, and so divide the valence by the value of mEq to get, 156.0 mEq/(1 mEq/mmol) = 156.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 156.0 mEq sodium/L converts to 156.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 79.0 * (156.0/140 - 1) = 4.51429 L. The patient's free body water deficit is 4.51429 L."
5960,38,Free Water Deficit,lab test,decimal,pmc-5965442-1,Extracted,"A three-month-old full term male was brought to the pediatric ED by his grandmother for evaluation of “jerking” activity worsening in frequency and severity for approximately three weeks. The grandmother described the “jerking” activity as intermittent upper body stiffening with associated eye blinking and drooling with a change in level of alertness just following the event. She reported that the episodes had increased in frequency over the few days prior to ED arrival but claimed the episodes had been present for the approximately one month. The grandmother stated that initially the jerking occurred approximately once per day; however, there were three episodes noted on the day of presentation. She described these episodes as lasting seconds to minutes and were not associated with color change, respiratory distress, or spitting up. They occurred at any time of the day, with no predilection for early morning or sleep arousal, and there was no association with feeding. She denied any recent history of falls, head trauma, fever, cough, congestion, diarrhea or rash. The remainder of the review of systems was negative. The infant was formula-fed every four hours and had been producing a normal amount of wet diapers and stool. When questioned about the pregnancy, the grandmother was unsure if the mother had been using drugs or alcohol, but stated that the infant was the product of an uncomplicated labor and delivery with a normal newborn screening. His birth weight was reported as 2.86 kg. The infant attended daycare, but there were no known sick contacts. The grandmother stated that the baby had been healthy, meeting his development milestones, and gaining weight appropriately according to his last well-child visit. There was a maternal history of multiple sclerosis reported by the grandmother.
On physical exam, the infant appeared well and was noted to make eye contact with the grandmother. Initial weight and vital signs reported at triage were as follows: weight: 5.51 kg, temperature 98.0° F, respiratory rate 22 breaths/min, heart rate 143 beats/min, oxygen saturation of 97% on room air. The pertinent positives of his exam included a full anterior fontanelle but no bulging. Extraocular movements were equal with no nystagmus appreciated. There was a mild left ocular prominence noted but no proptosis. He had no facial deformity or external signs of trauma with tears present and moist mucous membranes. His neck was supple, and appropriate head control was appreciated when he was seated in his grandmother’s lap. An overall slight increase in his tone was noted. All movements were observed to be symmetrical with no obvious motor deficit or weakness.
Moments after the initial assessment, the ED staff was called to the bedside by the grandmother. The infant was observed to have left eye blinking followed by asynchronous right eye blinking with drooling at the mouth. He was unresponsive to direct confrontation. No other jerking motions were observed. The episode lasted less than two minutes during which time he was placed on a cardiac monitor and vital signs were stable. Immediately following the episode, the infant was not responding normally to the grandmother but became increasingly more alert and returned back to baseline within several minutes.
Given his initial presentation and witnessed seizure activity, laboratory tests and imaging were ordered. The results of his lab work were as follows: WBC 10.4 × 103, Hgb 12.4 g/dL, Hct 36.3%, platelets 302 × 103/mm; Differential: lymphocytes 77%, neutrophils 14%, eosinophils 9%. Sodium 136 mEq/L, potassium 5.5 mEq/L, chloride 106 mEq/L, bicarbonate 20 mEq/L, BUN 5 mg/dL, creatinine 0.22 mg/dL, glucose 100 mg/dL, magnesium 2.1 mEq/L, phosphorus 5.5 mg/dL, anion gap 10.
In an attempt to spare exposure to ionizing radiation, the decision was made to perform a stat non-contrast magnetic resonance imaging (MRI) of the brain. After review of the scout images from MRI, a magnetic resonance angiogram protocol was added. Imaging revealed a large supratentorial cystic and solid mass in the left temporal region measuring 8.6cm × 7.9cm × 5.1cm. A plan was then made to transfer the patient to a pediatric intensive care unit, which could afford a higher level of care. A loading dose of levetiracetam (55 mg) intravenously was administered and D10 NS was run at maintenance.
The infant had five seizures on the day of admission, two of them witnessed. He was given an additional dose of levetiracetam 20 mg/kg IV and then continued on a maintenance dose of 10 mg/kg. The patient was also started on a dexamethasone 0.5 mg/kg. No subsequent seizure activity was reported following medication titration. Operative management was conducted by pediatric neurosurgery on hospital day 6. The patient underwent a left craniotomy with gross tumor resection. Pathology report indicated the tumor was consistent with DIG. In the post-operative period, the patient was observed to have a left lateral gaze palsy, and repeat imaging revealed a new acute infarct of the right thalamus. Due to the acute infarct, a neurology consult was obtained and the infant underwent a full work-up for a new-onset hypercoaguable state. The infant was found to have a slightly elevated anti-thrombin III level, and the infarct was not attributed to surgical management. Echocardiography was found to be normal and the patient was subsequently started on aspirin. The infant’s subgaleal Jackson-Pratt drain remained in place until post-operative day 3. No respiratory or gastrointestinal complications arose and the patient was tolerating full feeds within several days post-operatively.
Despite the right thalamic infarct, the patient had an excellent post-operative course in the months following discharge. At his last well-child visit, no neurological deficits were appreciated and the infant was meeting expected milestones for his age.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [3, 'months'], 'weight': [5.51, 'kg'], 'Sodium': [136.0, 'mEq/L']}",-0.09446,-0.08974,-0.09918,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 3 months old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 5.51 kg. The concentration of sodium is 136.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.0 mEq. To convert from 136.0 mEq to mmol, convert from mEq to mmol. The compound 136.0 has a valence of 1, and so divide the valence by the value of mEq to get, 136.0 mEq/(1 mEq/mmol) = 136.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mEq sodium/L converts to 136.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 5.51 * (136.0/140 - 1) = -0.09446 L. The patient's free body water deficit is -0.09446 L."
5961,38,Free Water Deficit,lab test,decimal,pmc-3230026-1,Extracted,"A 56-yr-old man with liver cirrhosis caused by the hepatitis B virus visited our hospital on December 30, 2008 for evaluation of weakness in his lower legs of 1-week duration. He first experienced discomfort and myalgia in his lower legs, which worsened over time and made him unable to walk. He had undergone a percutaneous coronary intervention 10 yr previously at the local hospital and had taken simvastatin (20 mg/day) regularly since then. He was diagnosed with Child-Pugh C cirrhosis due to hepatitis B virus a year ago and followed-up at the same hospital with stable liver function in a compensated state. Ten days before visiting our hospital, he was switched from simvastatin to fluvastatin (20 mg/day) by his doctor, as the patient was concerned about his liver disease. In addition to fluvastatin (20 mg/day), his medications included aspirin (100 mg/day), betaxolol (10 mg/day), candesartan (16 mg/day), lactulose (30 mL/day), and entecavir (0.5 mg/day) without diuretics or fibrates. His medical history was significant for no alcohol use and 10 pack-years of smoking, but he had quit smoking 10 yr previously.
The patient's blood pressure was 122/76 mmHg, his temperature was 36.8℃, his pulse was 63 beats/min, weight was 98 kg, and his body mass index was 29.8 kg/m2. He had mild tenderness of the lower extremities but all other assessments were unremarkable. Laboratory findings included sodium 125 mM/L, potassium 5.1 mM/L, chloride 97 mM/L, phosphorus 3.1 mg/dL, CO2 24.4 mM/L, serum creatinine 1.0 mg/dL, blood urea nitrogen 21 mg/dL, glucose 176 mg/dL, calcium 8.3 mg/dL, phosphorus 3.1 mg/dL, aspartate transaminase 1,303 IU/L (normal < 40), alanine transaminase 354 IU/L (normal < 40), alkaline phosphatase 145 IU/L (normal 40 to 120), total bilirubin 4.6 mg/dL, direct bilirubin 1.4 mg/dL, protein 8.0 g/dL, albumin 2.7 g/dL, and uric acid 3.5 mg/dL. His hematocrit was 38.5%, platelet count was 80,000/µL, and white blood cell count was 11,100/µL, with 18.5% lymphocytes, 69.7% polymorphonuclear leukocytes, 10.% monocytes, 1.4% eosinophils, and 0.2% basophils. His prothrombin time (PT) was 1.78 INR (40.7%) and activated partial thromboplastin time (aPTT) was 36.5 seconds. His total serum creatine kinase (CK) was 36,804 IU/L (normal 50 to 250 IU/L) and his CK-MB was 157.0 ng/mL (normal < 5 ng/mL). Thyroid function test was within normal limits. Urinalysis revealed no red or white blood cells, positive dipsticks for protein, occult blood, bilirubin and urobilinogen, but negative for glucose. A 99mTc-diphosphonate scintigram bone scan showed increased uptake over all extremities and muscles of the thorax and abdomen ().
The patient was diagnosed with fluvastatin-induced rhabdomyolysis. Treatment with fluvastatin, betaxolol and candesartan was discontinued, and he received massive hydration and urine alkalization. He was treated with intravenous sodium bicarbonate (100 mEq in 1,000 mL of half-normal saline at a rate of up to 500 mL/h or 50 mEq/h) titrated to a urine pH > 6.5. He was administered a 20-80 mg dose of intravenous furosemide to maintain diuresis. The extent of rhabdomyolysis progressed despite supportive treatment. His CK concentration was increased to 166,160 IU/L, and renal failure occurred. He underwent continuous renal replacement therapy on day 7, but his renal function did not recover and hepatic function worsened, with PT prolonged to 3.8 INR (18%) and total bilirubin increased to 24.5 mg/dL (). He died due to rhabdomyolysis complicated by hepatic failure on day 15.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [56, 'years'], 'weight': [98.0, 'kg'], 'sex': 'Male', 'Sodium': [125.0, 'mEq/L']}",-6.3,-5.985,-6.615,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 56 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 98.0 kg. The concentration of sodium is 125.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 125.0 mEq. To convert from 125.0 mEq to mmol, convert from mEq to mmol. The compound 125.0 has a valence of 1, and so divide the valence by the value of mEq to get, 125.0 mEq/(1 mEq/mmol) = 125.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 125.0 mEq sodium/L converts to 125.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 98.0 * (125.0/140 - 1) = -6.3 L. The patient's free body water deficit is -6.3 L."
5962,38,Free Water Deficit,lab test,decimal,pmc-8642045-1,Extracted,"A 62-year-old male patient with a history of kidney failure secondary to amyloidosis
presented with chills, rigors, epigastric tenderness, and diarrhea. A tiny granuloma with
scanty discharge at the exit site and a turbid peritoneal dialysate were observed the day
before admission.
He was anuric and had been on PD for 13 years, with a CAPD dialysis regimen as follows:
2.5% 2.5 L glucose dialysate with three exchanges in the daytime, plus an additional
exchange with 7.5% 2 L icodextrin dialysate overnight. He performed CAPD bag exchanges
himself and was known to have a history of glucose-6-phosphate dehydrogenase deficiency
and hypertension. His CAPD regimen showed 600 mL/day of ultrafiltration, which was mainly
attributable to icodextrin use. The International Society for PD released guidelines in
2000 regarding ultrafiltration failure (UF failure), which defined UF failure using the
3 × 4 rule (), which declares that ultrafiltration failure exists if net ultrafiltration
is <400 mL following drainage of a 4% (3.86% or 4.25%, dependent on pharmacopeia)
dialysis solution that has stayed intraperitoneally for 4 h. Thus, in this instance,
ultrafiltration failure has not occurred.
A review of his home records indicated blood pressure readings ranging from 100/70 to
140/90 mmHg. Daily net ultrafiltration ranged from −400 to −900 mL, while the daily fluid
intake was ∼500 mL.
Upon admission, he had a fever of 38.5 °C and elevated blood pressure (150/83 mmHg). His
heart rate was 78 bpm. His oxygen saturation (SpO2) was 95% in ambient air. His
body weight (without PD) was 57.8 kg, and his body mass index was 19.3 kg/m2.
No edema was noted. He had reduced appetite but good compliance with drug and fluid
intake. On physical examination, there was guarding and abdominal rigidity, but bowel
sounds were present. He had good knowledge of peritonitis, including probable entry
routes, symptoms, and interventions for a suspected occurrence. Thus far, the overall
clinical manifestations of this patient receiving PD (e.g., the new onset of abdominal
pain as evidenced by the presence of abdominal guarding, fever, and appearance of cloudy
effluent) strongly suggested the presence of CAPD-associated peritonitis ().
Laboratory testing data are shown in . Hematologic investigations revealed
anemia (hemoglobin 10.8 g/dL; hematocrit 31.5%), while a blood chemistry panel showed
hyponatremia (132 mmol/L), hypocalcemia (2.09 mmol/L), hypokalemia (3.2 mmol/L),
hypoalbuminemia (30 g/L), and significantly elevated creatinine (1,089 µmol/L), with an
estimated glomerular filtration rate of 4.5 mL/min/1.73 m2, signifying stage-5
chronic kidney disease.
The PD adequacy, as reflected by Kt/Vurea, was 1.78 weekly, which indicated
borderline adequacy. Dialysis adequacy is a broad concept and includes fluid balance,
small solute clearance, removal of uremic toxins of medium or large molecular weight, and
maintenance of nutritional status. Kt/Vurea is a consistent predictor of
survival in PD patients () and is, therefore, an important
monitoring parameter. The total (peritoneal and kidney) small-solute clearance should be a
total Kt/Vurea of ≥1.7 per week (). The peritoneal equilibration
test (PET) classified the patient as an average transporter (4 h dialysate to plasma ratio
of creatinine [D/P creatinine], 0.791; 4 to 0 h dialysate glucose ratio [D/D0 glucose],
0.334). PET is used to characterize the capacity for transportation of the patient’s
peritoneal membrane (). Transport capacity assists in deciding on the dwell time and is also a
central factor in determining the morbidity and mortality of PD patients (). Generally,
patients with a high peritoneal transport status will find it beneficial to receive APD
treatment employing lower dwell time, whereas patients with low peritoneal transport
status may find treatments with longer dwell times, e.g., CAPD, more beneficial ().
PD effluent showed the following cell counts: white blood cell (WBC),
3,157/mm3; polymorphonuclear neutrophilic cell (PMN), 97%; lymphocytes, 3%;
and eosinophils, 2%. A small amount of Pseudomonas aeruginosa, sensitive
to gentamicin, was cultured from the exit site, and the PD effluent culture revealed a
small amount of Streptococcus mitis, which was sensitive to penicillin G.
Apart from these clinical elements, the provisional diagnosis of CAPD-associated
peritonitis was confirmed by the presence of a dialysis effluent WBC count >100
cells/mm3 (following a 120 min minimum dwell time) with PMNs >50% and
positive effluent culture (; ).
The patient was able to complete the activities of daily living independently. There was
a strong bond among family members, who provided physical and emotional support to the
patient with his daily PD care. He lived with his wife and son, both of whom were
incredibly supportive of the patient and provided constant assistance in delivering
high-quality PD care at home.
The patient accepted that his kidney failure was a chronic illness. He remained the
primary source of income for his family and was employed as an engineer at a construction
company, which enabled him to be financially independent. He needed to perform one CAPD
bag exchange at work daily. However, his work environment was not an ideal place for bag
exchange because of the narrow space, dust, poor hygiene status, and central
air-conditioning systems. During the patient interview, details regarding the hygiene
status at work that may lead to CAPD-associated peritonitis were assessed. However, he
could not leave his job and admitted that he did not turn off the fan or close doors and
windows during CAPD bag exchanges because of the stuffy summer weather. Many researchers
have demonstrated that airborne bacteria concentrations are correlated with airborne
particulate matter (PM) concentrations () and that airborne PM can carry
microorganisms (). PD catheters represent a potential channel that allows pathogens to enter
the peritoneal cavity from the atmosphere. When the PD catheters and dialysate bags are
connected and/or disconnected, or the exit site is cleaned, the risk of infection with
airborne microorganisms increases. Thus, PD patients performing exchanges in areas with
high levels of environmental PM2.5 (PM2.5 relates to airborne droplets or particles with a
diameter of <2.5 µm) experienced a higher rate of infection from PD within 12 months
than those performing exchanges in areas with low exposure to environmental PM2.5 ().
This case report was written retrospectively. No interventional protocol was administered
to the patient concerned. Ethical approval from the author’s affiliated institution was
not required under the condition that confidentiality and anonymity of the patient were
maintained in the final report and analysis. The patient provided written consent for the
publication of his data.
There were three prioritized health problems in the present case: peritonitis and the
exit-site infection, imbalanced nutrition (insufficient intake of nutrients required to
meet the increased metabolic demands due to CAPD-associated peritonitis), and
psychosocial concerns (workplace hygiene and inability to change jobs).
For immediate nursing management of the present case, the PD effluent was drained by
the dialysis nurse after a dwell time of ∼2 h and carefully inspected before laboratory
tests were performed (cell counts, differential, gram stain, and cultures). Peritoneal
lavage was then performed as prescribed by the physician, with three rapid exchanges of
PD fluid bags to remove inflammatory cells and microorganisms from the peritoneal cavity
and to provide symptomatic relief ().
Empiric antibiotic therapy for PD-associated peritonitis was started as prescribed by
the physician as soon as a cloudy effluent was noted (which can indicate peritonitis),
without waiting for cell count and culture results from the laboratory. shows a list of
prescribed medications administered to the patient. Intraperitoneal administration of
antibiotics is preferred over intravenous (IV) or per os routes to reduce the chances of
treatment failure unless there is clinical evidence of systemic sepsis, in which case IV
antibiotics are administered (). An effluent cell analysis with a WBC > 100/µL
(3,157/µL in the present case) with at least 50% PMN cells (97% in the present case)
indicated that peritonitis was the most probable cause of the cloudy effluent. The
dialysis nurse recommended that heparin was also indicated in the present case; with
prescription, the addition of heparin at a dose of 500 IU in every 1 L of dialysate may
assist in preventing catheter occlusion by inhibiting fibrin formation ().
For the exit-site infection, the initial nursing management involved the collection of
a swab by the dialysis nurse for culture and sensitivity tests. The swab was taken at
the first instance of exit-site inspection on admission. An appropriate antimicrobial
therapy was then administered as prescribed. Antimicrobial therapy should cover both
Gram-negative and Gram-positive bacteria (including Staphylococcus
aureus which tends to cause relatively poor clinical outcomes such as the
need for PD-catheter removal) (; ). Because this patient had a history of P.
aeruginosa infection, an antibiotic covering this microorganism was
recommended by the dialysis nurse. In the present case, 0.1% gentamicin cream was
prescribed by the physician, as purulence, tenderness, and edema were absent at the exit
site. Once culture results were available, therapy was modified based on the specific
sensitivity patterns. In the present case, since gentamicin cream was effective against
P. aeruginosa, it was continued as the drug of choice as recommended
by the dialysis nurse.
The frequency of exit-site care with 0.5% chlorhexidine gluconate also needed to be
increased (). The clinical response was reviewed by the dialysis nurse after the
initiation of antibiotic treatment, and clinical improvement was expected during the
first 72 h. Once the culture and sensitivity results were known, the antibiotic therapy
was appropriately adjusted by the physician, and continuous treatment was provided by
the dialysis nurse. In the present case, the bacterial culture of the PD effluent
revealed Streptococcus mitis that was sensitive to penicillin G.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [62, 'years'], 'weight': [57.8, 'kg'], 'sex': 'Male', 'Sodium': [132.0, 'mmol/L']}",-1.98171,-1.88262,-2.0808,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 62 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 57.8 kg. The concentration of sodium is 132.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 57.8 * (132.0/140 - 1) = -1.98171 L. The patient's free body water deficit is -1.98171 L."
5963,38,Free Water Deficit,lab test,decimal,pmc-8383592-1,Extracted,"A 45-year-old woman presented to our hospital with a failure to thrive. She was in her usual state of health until 6 years prior to admission. She developed a poor appetite and severe food aversion, and her weight declined from 54.5 kg to her admission weight of 34.2 kg. The patient reported chronic constipation and intolerance of many foods, including oil, fats and meats. She denied dysphagia, odynophagia, abdominal bloating, pain, or diarrhea. The personal and family medical histories were unremarkable. She was not on any prior medications or supplements. She denied tobacco, alcohol, or illicit drug use.
On physical examination, the patient was afebrile with normal vital signs. She measured 5 feet 1 inch tall and weighed 34.2 kg, with a body mass index (BMI) of 14.2 kg/m2. There was profound cachexia. There was no hepatosplenomegaly, abdominal tenderness, or distention. A comprehensive gastrointestinal workup including computed tomography of the abdomen and pelvis, videofluoroscopic swallowing study, esophagogastroduodenoscopy, colonoscopy, gastric emptying study, and small bowel series, was unremarkable. Complete blood count was normal. Notable abnormalities on the metabolic panel were the sodium at 129 mEq/L (normal 135 - 148), chloride at 88 mEq/L (normal 96 - 109), and creatinine at 0.4 mg/dL (normal 0.5 - 1.2). The aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were 154 U/L (normal 0 - 31) and 136 U/L (normal 0 - 31), respectively. The serum bicarbonate, urea nitrogen, glucose, total bilirubin, alkaline phosphatase (ALP), albumin and prealbumin were normal. Psychiatry was consulted, and she was diagnosed with anorexia nervosa.
The patient was started on a regular diet on day 1 of hospitalization, with estimated needs of 1,345 - 1,598 calories per day and 40 - 47 g of protein per day. However, given her gastrointestinal symptoms and laboratory abnormalities, several tests were pursued which required alterations in her diet during the initial week of hospitalization. For the most part, she was nil per os (NPO) status or ordered for a clear liquid diet while workup was pending until day 8 of hospitalization. Thus, refeeding was determined to have started on day 8 of hospitalization. She was initially ordered a vegan diet per her request, with subsequent liberalization to a regular diet. A calorie count performed on days 14 - 16 of hospitalization revealed she was consuming almost 100% of all food trays. Total parenteral nutrition was discussed early during her hospitalization, given food intolerance and disruptions in oral nutrition; however, it was not pursued. Notably, her weight initially decreased from her admission weight of 34.2 kg to a nadir around 30.8 - 31.0 kg on days 10 - 13 of hospitalization. Her weight began to increase starting day 14 of hospitalization or day 7 of refeeding.
On hospitalization day 6 (i.e., before refeeding), the patient’s AST and ALT rose steeply to 671 and 362 U/L, respectively. They peaked at 750 and 638 U/L, respectively, on hospitalization day 10, 2 days after refeeding was initiated (). Additional laboratory workup for the etiology of liver injury (LI) included hepatitis A, B, and C serologies, which were negative. Serum ceruloplasmin and copper were normal. Ferritin and serum iron were mildly elevated. Anti-mitochondrial antibody titers were slightly elevated at 1:20 dilution, but this was considered a false positive with negative anti-nuclear and anti-smooth muscle antibodies. The immunoglobulin profile was also normal. Acetaminophen levels were undetectable. A right upper quadrant ultrasound was normal. A percutaneous liver biopsy was performed on hospitalization day 11, 3 days after refeeding; histology revealed mild glycogen depletion, marked ceroid pigment around the central veins, and scattered hepatocellular atrophy (). There was no histologic evidence of hepatic steatosis, inflammation, or significant fibrosis.
The patient continued to tolerate a regular diet and gain weight during her hospital course. She was eventually transferred to an Eating Disorders Unit for monitoring and treatment. She then started on the nutrition protocol for eating disorders with a slow increase in daily nutrition from 1,500 calories per day to 4,000 calories per day by day 40 of hospitalization. Over the subsequent 2 months, the patient’s weight increased from 34.2 kg (BMI 14.2 kg/m2) to 38.4 kg (BMI 16.0 kg/m2), and her transaminases normalized.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [45, 'years'], 'weight': [34.2, 'kg'], 'Sodium': [129.0, 'mEq/L']}",-1.34357,-1.27639,-1.41075,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 45 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 34.2 kg. The concentration of sodium is 129.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 129.0 mEq. To convert from 129.0 mEq to mmol, convert from mEq to mmol. The compound 129.0 has a valence of 1, and so divide the valence by the value of mEq to get, 129.0 mEq/(1 mEq/mmol) = 129.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 129.0 mEq sodium/L converts to 129.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 34.2 * (129.0/140 - 1) = -1.34357 L. The patient's free body water deficit is -1.34357 L."
5964,38,Free Water Deficit,lab test,decimal,pmc-3350132-1,Extracted,"A 69-year-old man was admitted to a hospital in the South of Brazil, with weight loss, weakness, and difficulty to swallow. In the last 4 months, he had anorexia, asthenia, and difficulty to swallow any food. When he tried to eat, he felt nausea and sometimes vomited. He had lost 7 kg. He denied fever or other symptoms. He was an active smoker that had smoked 100 pack-years. He did not abuse alcohol or other drugs. He had arterial hypertension, type 2 diabetes mellitus with HbA1c: 6.5% one month earlier and mild chronic obstructive pulmonary disease. He had presented three no disabling ischemic strokes. He was taking hydrochlorothiazide 25 mg, simvastatin 20 mg, and acetylsalicylic acid 100 mg, once a day; and captopril 50 mg TID. His father died of sudden death at 83 years old, and his mother died of stroke at 80 years old. His brother died of esophageal cancer with 55 years old. He lived with his wife. His physical examination revealed an alert, oriented man, with blood pressure: 120/70 mmHg; heart rate: 72 bpm; respiratory rate: 20 rpm; axillary temperature: 36°C; pulse oximetry: 95%; weight: 33.5 kg; height: 1.53 m; BMI: 14.3 kg/m2. There were several lymph nodes the cervical region, the larger one with 1.5 cm, and digital clubbing. Other aspects of his physical examination were normal. Two months before admission, chest radiography showed signs of chronic obstructive pulmonary disease, micronodules and linear opacities in the upper lobes, and a small consolidation in the lower left lobe. The initial laboratory evaluation revealed hemoglobin = 8.6 g/dL (normal range: 13–14.2 g/dL); VCM = 88.9 fL (80–100 fL); leukocytes = 7220/μL (4000–10000/μL); neutrophils = 2758/μL (1800–7500/μL); eosinophils = 606/μL (40–500/μL); basophils = 87/μL (<100/μL); monocytes = 477/μL (120–1000/μL); lymphocytes = 3292/μL (1000–4000/μL); platelets: 409000/μL (150–400 × 103/μL); serum sodium: 134 mEq/L (135–145 mEq/L); potassium: 5.2 mEq/L (3.5–5.1 mEq/L); creatinine: 0.64 mg/dL (0.5–1.2 mg/dL); ureic nitrogen: 21 mg/dL (5–20 mg/dL); calcium: 7.8 mg/dL (8.5–10.4 mg/dL); albumin: 3.0 g/dL (3.5–5.0 g/dL); ALT: 17 U/L (<31U/L); glucose: 94/mg/dL (70–99 mg/dL). An upper gastrointestinal endoscopy was normal, and a nasojejunal tube was inserted. The patient remained with the same symptoms, receiving food and liquids through a nasojejunal tube. In the sixth day after admission, after being submitted to chest and abdomen computerized tomography, he developed fever (39.5°C), confusion, blood pressure 160/110 mmHg, heart rate: 120 bpm, pulse oximetry: 95%. He received intravenous dipyrone. A few moments later, his blood pressure dropped to 80/40 mmHg, and intravenous saline solution was infused. A blood sample to measure serum ACTH and cortisol was drawn. In the next two days, he had no fever, and two samples of blood culture were negative. In the following days, the patient developed severe hyponatremia (sodium = 122 mEq/L and 119 mEq/L), and postural hypotension was identified (supine resting = 122/60 mmHg and standing = 100/60 mmHg). The results of computed tomography of chest and abdomen are shown in Figures and . Serum cortisol and ACTH were, respectively, 1.03 μg/dL (4.3–22.4 μg/dL) and 626 pg/mL (12–46 pg/mL), and serum TSH was 8.06 μU/mL (0.35–5.5 μU/mL). The patient received intravenous hydrocortisone, and hydrochlorothiazide was discontinued. Electrolyte abnormalities, anorexia, and difficulty to swallow are resolved. A biopsy of the left adrenal gland showed signet-ring cell adenocarcinoma with areas of necrosis. In the immunohistochemical study, the cells were positive for CK7, TTF-1, and CEA, and negative for CK20, vimentin, CA19.9, CD10, prostatic specific antigen, and thyroglobulin. Therefore, the diagnosis of adenocarcinoma of pulmonary origin was made. Bone and brain metastases were not evident in bone scintigraphy and brain computerized tomography. A few days later, the patient was switched to 5 mg oral prednisone and 0.1 mg of fludrocortisone and was discharged to his home. One month after initiating glucocorticoids, he came to the outpatient oncology division. He was eating normally, his weight increased to 40.1 kg, but he refused the palliative chemotherapy offered.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [69, 'years'], 'weight': [33.5, 'kg'], 'Sodium': [134.0, 'mEq/L']}",-0.71786,-0.68197,-0.75375,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 69 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 33.5 kg. The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 33.5 * (134.0/140 - 1) = -0.71786 L. The patient's free body water deficit is -0.71786 L."
5965,38,Free Water Deficit,lab test,decimal,pmc-7246398-1,Extracted,"A 59-year-old woman with no family history of kidney disease was receiving treatment for hypertension and dyslipidemia. The patient was taking oral olmesartan medoxomil (20 mg once daily), oral amlodipinebesylate (10 mg once daily), and oral rosuvastatin calcium (2.5 mg once daily). She had been experiencing symptoms of a common cold for approximately one month and developed a night fever 14 days before admission. Oral antipyretics and similar drugs did not improve her symptoms. Her serum creatinine level reached 2.4 mg/dL 14 days before admission and increased to 3.6 mg/dL on the day of admission, which was the day when she was referred to our hospital for an investigation of her worsening renal function. Findings on her arrival were as follows: body height, 160 cm; body weight, 60 kg; blood pressure, 138/80 mmHg; pulse, 80 beats/min; body temperature, 37.3°C; no anemia in the palpebral conjunctiva; breathing sounds were clear/no secondary noises; no heart murmurs; no edema in the legs; no joint pain or eruption; and no oral enanthem.
Blood test results on admission were as follows: white blood cell count, 12,900 cells/μL; lymphocytes, 800 cells/μL; monocytes, 11,000 cells/μL; neutrocytes, 10,800 cells/μL; eosinophils, 100 cells/μL; basophils, 0 cells/μL; red blood cell count, 3.57 × 10⁶ cells/μL; hemoglobin, 10.9 g/dL; hematocrit, 31.7%; platelets, 350 × 10³ cells/μL; aspartate transaminase, 62 IU/L; alanine transaminase, 119 IU/L; lactate dehydrogenase, 289 IU/L; total protein, 6.3 g/dL; albumin, 2.3 g/dL; urea nitrogen, 35 mg/dL; creatinine, 3.73 mg/dL; sodium, 136 mmol/L; potassium, 3.8 mmol/L; calcium, 8.0 mg/dL; phosphate, 4.8 mg/dL; C-reactive protein, 14.25 mg/dL; immunoglobulin G, 1,169 mg/dL; immunoglobulin A, 413 mg/dL; immunoglobulin M, 98 mg/dL; complement component, 3 132 mg/dL; complement component, 4 30.3 mg/dL; and 50% hemolytic complement, 98.8 U/mL. Furthermore, serine proteinase 3 antineutrophil cytoplasmic antibody, <0.51 IU/mL; myeloperoxidase antineutrophil cytoplasmic antibody (MPO-ANCA), 8.2 IU/mL; anti-double-strand (ds)-DNA antibody IgG, 54.9 IU/mL; anti-Smith antibody, negative; anticardiolipin immunoglobulin, 1 U/mL; and lupus anticoagulant, negative. Antinuclear antibody homogeneous pattern 160-fold and nucleolar pattern 80-fold were identified.
Urine testing revealed proteinuria (2081 mg/day) and hematuria (red blood cells ≥ 100/high-power field (poikilocytes 0–10%)). Plain thoracoabdominal computed tomography indicated reticular shadows in both inferior lobes. Renal size was preserved.
We suspected SLE because four items from the diagnostic criteria of the American College of Rheumatology (ACR) were satisfied: presence of antinuclear antibodies, positivity for anti-ds-DNA antibody, serum lymphocytopenia, and urine protein of 2.0 g/day. Treatment with mycophenolate mofetil (MMF) (1000 mg/day, orally) and prednisolone (PSL) (40 mg/day, orally) was started for SLE/lupus nephritis. On the 32nd hospital day, results of the renal biopsy that was taken on the 7th hospital day were confirmed. The disease course after admission is shown in .
Global sclerosis was observed in two of a total 17 glomeruli. Cellular crescents and fibrinoid necrosis with rupture of Bowman capsule were observed in 14 of the remaining 15 glomeruli ().
The degree of tubulointerstitial injury was 85%. Immunofluorescence showed pauci-immune type crescentic glomerulonephritis (1+ deposition in a granular manner in the mesangial area of C3 only) ().
She was diagnosed as AAV according to the Chapel Hill Consensus Conference (CHCC) 2012 definitions [] and the classification algorithm of AAV by Watts et al. []. She was suspected of SLE/AAV OS with serological features of SLE, and the treatment was changed to PSL monotherapy on day 8. Thereafter, the dosage of PSL was gradually decreased, and serum creatinine levels improved from a maximum of 7.06 mg/dL to 3.39 mg/dL on day 56.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [59, 'years'], 'weight': [60.0, 'kg'], 'Sodium': [136.0, 'mmol/L']}",-0.85714,-0.81428,-0.9,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 59 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 60.0 kg. The concentration of sodium is 136.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 60.0 * (136.0/140 - 1) = -0.85714 L. The patient's free body water deficit is -0.85714 L."
5966,38,Free Water Deficit,lab test,decimal,pmc-3303746-1,Extracted,"A 78-year-old retired male mechanical engineer from Arkansas presented with 3-month history of low-grade fever, rigors, and confusion, associated with poor appetite, 15-pound unintentional weight loss, abdominal discomfort, and increased frequency of urination. He denied having nausea, vomiting, or changes in bowel habits. The patient had no significant past medical history, and had no history of sick contacts, recent travel, ingestion of raw food or milk, or known exposures to animals. Urinalysis showed microscopic hematuria, but no pyuria. Although urine culture was negative, he was treated for presumed urinary tract infection with a 7-day course of oral ciprofloxacin without significant improvement, followed by a 14-day course of doxycycline for presumed prostatitis. He was afebrile while taking doxycycline, but fever recurred 3 days after completion of the antibiotic. He was noted by his wife to be confused and found to have blood pressure (90/60 mmHg) on the day of admission.
On admission, he had a temperature of 37.3°C, a heart rate of 130 beats/minute, and a blood pressure of 118/72 mmHg. A complete physical examination, including neurological evaluation, was within normal limit. Laboratory results were notable for neutrophilic leukocytosis (white blood cell count of 28.0 × 109/L, absolute neutrophil count of 26 × 109/L), anemia (hemoglobin of 111 g/L), elevated C-reactive protein (31.1 mg/L), and mild hyponatremia (128 mmol/L). His liver and kidney functions were normal, and chest X-ray was unremarkable. Computed tomography (CT) of the head showed mild cerebral degenerative changes. Abdominal CT was significant for three large thick-walled low-density lesions in the right hepatic lobe, with the largest measuring 75 × 55 × 58 mm and multiple smaller low-attenuation lesions within the liver, likely representing multiple hepatic abscesses (). Ultrasound-guided aspiration yielded 25 mL of purulent fluid with subsequent placement of two drainage catheters. Gram stain of the purulent fluid showed many white blood cells but no organisms. Fungal and acid-fast smear were negative as well. Intravenous meropenem and vancomycin were empirically begun while awaiting culture results.
Although the patient responded promptly to antimicrobial therapy with resolving confusion, fever, and leukocytosis, his cultures, including blood cultures remained negative. The negative cultures were possibly attributed to the demeclocycline, a tetracycline with some antibacterial properties [], that the patient received for the treatment of hyponatremia. The patient underwent transesophageal echocardiography to evaluate for endocarditis given concern for septic hepatic emboli from occult source, and it was negative for signs of endocarditis. Due to good clinical response, the patient was discharged on hospital day 7 on ertapenem administered via a peripherally inserted central catheter line, despite negative cultures. Following discharge, the liver aspirate was later reported to be growing a gram-positive bacillus in the anaerobic plate (CDC blood sheep agar) after 6 days of incubation. Identification via PCR-amplified 16S rRNA sequencing technique revealed Eggerthella lenta (Eggerthella lenta strain SECO-Mt75m2 16S ribosome RNA gene sequence: GGATGAACGCTGGCGGCGTGCCTAACACATGCAAGTCGAACGATGAAACCGCCCTCGGGCGGACATGAAGTGGCGAACGGGTGAGTAACACGTGACCAACCTGCCCCCCTCTCCGGGACAACCTTGGGAAACCGAGGCTAATACCGGATACTCCCTCCCCTGCTCCTGCAGGGGTCGGGAAAGCCCAGGCGGAGGGGGATGGGGTCGCGGCCCATTAGGTAGTAGGCGGGGTAACGGCCCACCTAGCCCGCGATGGGTAGCCGGGTTGAGAGACCGACCGGCCACATTGGGACTGAGATACGGCCCAGACTCCTACGGGAGGCAGCAGTGGGGAATTTTGCGCAATGGGGGCAACCCTGACGCAGCAACGCCGCGTGCGGGACGACGGCCTTCGGGTTGTAAACCGCTTTCAGCAGGGAAGAAATTCGACGGTACCTGCAGAAGAAGCTCCGGCTAACTACGT, GenBank # AY937380.1, National Center for Biotechnology Information, U.S. National Library of Medicine). Antimicrobial susceptibility testing was not performed because of inadequate growth. At followup, the patient was doing well clinically with radiographic resolution of the hepatic abscesses after a 6-week course of ertapenem (). Colonoscopy after resolution of infection showed extensive diverticulosis distal to the hepatic flexure.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [78, 'years'], 'weight': [15.0, 'lbs'], 'sex': 'Male', 'Sodium': [128.0, 'mmol/L']}",-0.29159,-0.27701,-0.30617,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 78 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 15.0 lbs so this converts to 15.0 lbs * 0.453592 kg/lbs = 6.80388 kg. The concentration of sodium is 128.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 6.80388 * (128.0/140 - 1) = -0.29159 L. The patient's free body water deficit is -0.29159 L."
5967,38,Free Water Deficit,lab test,decimal,pmc-3542890-1,Extracted,"A 58-year-old male presents to the Emergency Department via EMS as a possible stroke. Per spouse, he woke up from sleep with left-sided facial droop, slurred speech, and left arm weakness. He had gone to sleep at approximately 10 pm and awoke with the left-sided complaints at approximately 4 am the morning of arrival. He had a past medical history of adrenal adenoma, chronic gastritis, and a vasectomy in 1993. The patient's medications prior to admission were alprazolam, esomeprazole, probiotics, and a daily multivitamin. The patient is aware of his left-sided weakness and complains of heaviness on his left side. He reports no history of alcohol, tobacco, or illicit drug use. The patient's spouse reported that he had been unwell for three months with unexplained weight loss, fever, chills, and loss of appetite. At the time of presentation, various specialists including gastroenterology failed to determine an underlying cause for the patient's complaints besides “anemia of chronic disease.” Furthermore, he was scheduled for an upper and lower endoscopy the day of presentation and was in the process of preparation (cathartics) for that. He has been on a gluten-free diet for elevated tissue transglutaminase and gliadin antibody titers by his endocrinologist. Upon arrival at patient's residence, EMS reported a positive stroke screen with a Cincinnati score of 2, positive for left arm weakness, and left-sided facial droop. Vital signs upon arrival to the Emergency Department were temperature 36.4 degrees Celsius by tympanic reading, pulse 105 beats per minute, blood pressure 116/56 mmHg, respirations 18 breaths per minute, and pulse oximetry 98% on room air. His weight was recorded as 68 kilograms. He was not in any distress but appeared pale and cachectic. His neurologic exam was positive for a left facial droop with weakness of cranial nerves 3, 5, and 7. There was no uvular deviation, and pupils were equal and reactive bilaterally with intact extraocular movements. The upper extremities had symmetric sensation to fine touch with a left pronator drift and 3/5 strength in the proximal and distal muscle groups in comparison to the right. There was no dysmetria. The lower extremities had 5/5 strength bilaterally and absent Babinski reflexes. His NIH stroke scale score was 6. The rest of his physical exam was unremarkable.
Initial labs included a metabolic panel with measured sodium of 131 mmol/L and blood glucose of 125 mg/dL but were otherwise normal. The complete blood count showed a hemoglobin of 9.6 g/dL and a hematocrit of 29.9%. The white blood cell count was 12.5 thou/cu mm with 78.8% neutrophils and no bands. Cardiac enzymes and urinalysis were both normal. The point-of-care INR was 1.5. Stroke alert protocol imaging included a CT angiogram of the head and neck with and without contrast and postprocedure multiplanar reconstructions. These revealed acute/subacute CVA in the right insula cortex and right basal ganglia () as well as significant narrowing of the proximal M1 branch of the right middle cerebral artery (MCA) secondary to either embolus or atherosclerotic disease (). Perfusion images demonstrate elevated time to peak in the posterior right MCA distribution with normal capillary transit time and normal cerebral blood volume consistent with compensated collateral blood flow ().
The patient received 300 mg aspirin per rectum and IV fluids prior to admission to the neuro-ICU. The patient was deemed an unsuitable candidate for thrombolysis as onset was estimated approximately 6 hours prior to ED arrival. Neurosurgery was consulted and decided that the risks of endovascular therapy did not outweigh the benefits for the patient.
Followup the next day revealed that the patient had an echocardiogram that showed a mass on the posterior leaflet of the mitral valve with mitral regurgitation. Following echocardiogram, the patient had an acute sudden deterioration in his mental status and displayed respiratory compromise. On examination, his pupils were “blown” (enlarged) bilaterally and he was emergently intubated for airway protection. His emergent noncontrast CT of the head () showed a subcortical hemorrhage with intraventricular extension and subfalcine herniation. Neurosurgery emergently brought the patient to the operating room with a postoperative diagnosis of right intracranial hemorrhage secondary to ruptured mycotic MCA aneurysm. On postoperative day one, the family decided to withdraw care and the patient expired.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [58, 'years'], 'weight': [68.0, 'kg'], 'sex': 'Male', 'Sodium': [131.0, 'mmol/L']}",-2.62286,-2.49172,-2.754,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 58 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 68.0 kg. The concentration of sodium is 131.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 68.0 * (131.0/140 - 1) = -2.62286 L. The patient's free body water deficit is -2.62286 L."
5968,38,Free Water Deficit,lab test,decimal,pmc-6925778-1,Extracted,"An 8-month-old outdoor neutered male European domestic short-hair (DSH) cat was referred to our clinic with a 3-week history of diarrhea, anorexia, and lethargy. Physical examination revealed pyrexia (40.1°C). The mucous membranes were moderately pale and the cat was estimated to be 6-7% dehydrated. The body weight was 3.3 kg on initial presentation with a body condition score of 6/9. The peripheral lymph nodes were normal. Abdominal palpation revealed small bowel distention with fluid. The heart rate was 250 bpm with a moderate grade III/VI left parasternal systolic murmur with no thrill; the femoral pulses were weak and synchronous with the heart beats. The respiratory rate was 30 breaths/min, without abnormal lung sounds. No respiratory distress was detected. An electrocardiogram showed sinus tachycardia. Hematological abnormalities included: moderate to severe non regenerative anemia (packed cell volume 20.8%, reference range 30.3–52.3%), absolute aggregate reticulocyte count was 38 × 109/L (regenerative response > 80 × 109/L), neutrophilia 13.2 × 109/L (reference range 4.8–10.29 × 109/L) with a left shift, monocytosis 0.70 × 109/L (reference range 0.05–0.67 × 109/L) and pseudothrombocytopenia 88 × 109/L (reference range 151–600 × 109/L) due to platelet clumping. Biochemical abnormalities included elevation of: creatine kinase 515 U/L (reference range 91–326 U/L), blood urea nitrogen 67 mg/dl (reference range 18–41 mg/dl), aspartate aminotransferase 46 U/L (reference range 21–44 U/L), total protein 8.71 g/dl (reference range 5.5–7.7 g/dl).
Concurrent hypoalbuminemia was found to be 2.78 g/dl (reference range 3–4.6 g/dl). The electrolyte levels were low: total calcium 2.07 mmol/L (reference range 2.1–2.87 mmol/L), sodium 142.8 mmol/L (reference range 150–165 mmol/L), and potassium 3.13 mmol/L (reference range 3.5–5 mmol/L). The iron level was 7.16 mol/L (reference range 10.7–37.6 mol/L). Thoracic radiography (3 views) showed no abnormalities in the cardiac silhouette, lung fields, and the pulmonary vessels. An echocardiogram (2-dimensional, M-mode, and Doppler) was performed in our clinic by V. A. using a 4–8 MHz phased-array transducer; the patient was not sedated. The 2-dimensional study revealed a large hyperechoic vegetation of the aortic valve leaflets (9 mm, on the right parasternal long axes, 5 chamber view) ().
The mitral, tricuspid and pulmonic valves were normal, M-mode the left ventricular internal dimension at end-diastole was 18.4 mm [15.1 mm ± 2.1] [] and the left ventricle internal diameter at the end-systole was 12.9 mm [6.9 mm ± 2.2] []. The interventricular septum at end-diastole and end-systole showed remarkable thinning: 3.3 mm [5 mm ± 0.7] [] and 6.1 mm [7.6 ± 1.2] [], respectively (M-mode study). The left ventricle caudal wall thickness was normal at end-diastole and end-systole: 4.6 mm [4.6 mm ± 0.5] [] and 7.1 mm [7.8 mm ± 1] [], respectively (2-dimensional study). Global left ventricular contractility was mildly depressed and fractional shortening was 29.6% [40% ± 10%] [] (M-mode study). The left atrial diameter at 9 mm was below the reference range [12.1 mm ± 1.8] [] and the ratio of the left atrial dimension to the aortic annulus dimension was 0.9 [1.29 ± 0.23] [] (2-dimensional study). There was a significant Doppler increase of the aortic flow velocity on subcostal view: aortic velocity 4.79 m/s [1.1 ± 0.2] [] equivalent to an aortic pressure gradient of 91.9 mmHg. After performing an echocardiogram, the differential diagnosis of valve vegetation included infectious endocarditis, sterile granuloma, fungal granuloma, tumor, and thrombus. Other clinical signs, such as fever and gastrointestinal signs, suggested that the patient was much more likely to have endocarditis than a thrombus. Abdominal ultrasonography revealed enlarged mesenteric lymph nodes and moderate dilatation of small bowel loops. The patient was hospitalized and antibiotic treatment was started with metronidazole (10 mg/kg IV every 12 hours), cefazoline (20 mg/kg SC every 12 hours), and marbofloxacin (2 mg/Kg IM every 24 hours).
Atenolol (0.5 mg/kg PO every 12 hours) was administered in view of the severity of aortic valve stenosis and to prevent fatal ventricular arrhythmias, but considering the concurrent mild systolic dysfunction, arterial blood pressure and fractional shortening were assessed twice daily. Clopidogrel (18.75 mg PO every 12 hours) was administered for the prevention of cardiogenic embolism. During hospitalization the patient was rehydrated by intravenous infusion of isotonic crystalloid solution (Ringer's acetate, 2.5 ml/kg/h). After 48 hours lactate was increased to 3.8 mmol/L (<1.46 mmol/L) and after 72 hours the patient developed hypothermia, bradycardia, low systolic blood pressure 85 mmHg (>120 mmHg), and, finally, cardiac arrest. Blood polymerase chain reaction for Bartonella henselae and a urine culture test were performed.
The urine culture test showed growth on MacConckey Agar and BrillianceTM Salmonella Agar base (Oxoid®, UK) between 105 and 106 UFC/ml. The organism was biochemically identified as Salmonella typhimurium with the use of API 20E® and API 50CHL® (bioMerieux®, France). The serotype was assessed using polyvalent Salmonella Antisera (Oxoid, UK) for somatic (O) and flagella antigens (H). Antibiotic susceptibility testing was assessed with Kirby–Bauer method (CLSI), and it showed that Salmonella typhimurium was sensitive to third generation but not to fluoroquinolones, blood polymerase chain reaction for Bartonella henselae was negative, serology for FIV/FeLV was not performed for lack of owner's consent.
A necropsy confirmed the presence of a large vegetation (9 mm in diameter) on the aortic valve leaflets ().
Histology of the aortic valve leaflets and myocardium was consistent with neutrophilic endocarditis and suppurative localized myocarditis caused by Salmonella typhimurium ().
Postmortem culture of the aortic valve was positive for Salmonella typhimurium at more than 105 CFU/ml; bacterial taxonomy was evaluated by conventional biochemical test (bioMerieux, France) and using polyvalent Salmonella antisera (Oxoid, UK) for somatic (O) and flagella (H) antigens.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [8, 'months'], 'weight': [3.3, 'kg'], 'Sodium': [142.8, 'mmol/L']}",0.0396,0.03762,0.04158,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 8 months old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 3.3 kg. The concentration of sodium is 142.8 mmol/L. Plugging in these values into the equation, we get 0.6 * 3.3 * (142.8/140 - 1) = 0.0396 L. The patient's free body water deficit is 0.0396 L."
5969,38,Free Water Deficit,lab test,decimal,pmc-2481241-1,Extracted,"A 52-year-old white male with O2-dependent COPD, hypertension, GERD, idiopathic gastroparesis, and chronic low back pain was noted to have persistent hypokalemia in the 2.7–3.3 meq/L range over more than 2 years. He complained also of chronic generalized weakness and fatigue. He denied nausea or vomiting, but did have occasional loose stools. The hypokalemia persisted despite discontinuation of diuretic treatment for hypertension and fludrocortisone that had been prescribed briefly for orthostatic hypotension. There was no improvement with aggressive oral potassium supplementation in amounts up to 120 meq per day. The patient's serum potassium level normalized on three occasions when he was hospitalized and given supplemental potassium (COPD exacerbations in 7/06 and 1/07, pseudoseizures in 7/07), but the hypokalemia promptly recurred after discharge from the hospital (Figure ). His medications were paroxetine, trazodone, pregabalin, sustained-release morphine, loratadine, isosorbide mononitrate, lisinopril, metoprolol, simvastatin, omeprazole, metoclopramide, potassium chloride, calcium/vitamin D tablets, alendronate, and mometasone, tiotropium, and albuterol inhalers. He smoked one-half pack of cigarettes per day and did not drink alcohol.
On physical examination, he was a chronically ill-appearing man wearing a nasal cannula. Height was 69 inches, weight 205 pounds. There were no cushingoid facies, buffalo hump, or abdominal striae. Vital signs were temperature 98.6 degrees, pulse 95, respiratory rate 14, blood pressure 128/73. There was no thyromegaly or lymphadenopathy. Lungs showed decreased breath sounds and mild expiratory wheezes bilaterally. Heart sounds were regular with no murmurs, rubs, or gallops. The abdomen was soft and non-tender, with no masses or organomegaly. Extremities showed no edema, clubbing or cyanosis. The neurologic examination revealed mild generalized muscular weakness (4+/5) and normal deep tendon reflexes.
Laboratory results include serum sodium 137 mg/dL, potassium 3.0 mg/dL, chloride 95 mmol/L, CO2 30.0 mmol/L, blood urea nitrogen 5 mg/dL, creatinine 0.8 mg/dL, calcium 9.3 mg/dL, phosphorus 4.1 mg/dL, albumin 3.6 g/dL, ferritin 126 ng/mL, hemoglobin 12.7 g/dL, white blood cell count 10.6 K/cmm, and platelet count 160 K/cmm. Serum aldosterone was 4.8 ng/dL (normal 4–31 ng/dL) and the plasma renin activity was 0.33 ng/mL/hr (normal 1.31–3.96 ng/mL/hr upright, 0.15–2.33 ng/mL/hr supine). Spot urine potassium was 8.6 mEq/L, urine sodium was < 10 mEq/L, and urine chloride was 16 mmol/L.
In the absence of a clear explanation for this patient's chronic hypokalemia, he was asked to give the details of his diet. He admitted to drinking 4 liters of Pepsi-Cola per day for the past several years. It was his habit to sip cola slowly but almost continuously, throughout the day. When hospitalized, he had stopped drinking cola and his potassium levels had temporarily normalized. In early May 2008, he decreased his cola intake to 2 liters per day, with a resultant increase in the serum potassium from 3.0 to 3.5 mg/dL (Figure ).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [52, 'years'], 'weight': [205.0, 'lbs'], 'sex': 'Male', 'Sodium': [137.0, 'mmol/L']}",-1.19554,-1.13576,-1.25532,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 52 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 205.0 lbs so this converts to 205.0 lbs * 0.453592 kg/lbs = 92.98636 kg. The concentration of sodium is 137.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 92.98636 * (137.0/140 - 1) = -1.19554 L. The patient's free body water deficit is -1.19554 L."
5970,38,Free Water Deficit,lab test,decimal,pmc-6186097-1,Extracted,"A 59-year-old black male with type 2 diabetes mellitus progressed to end stage renal failure; he received a kidney from his wife 11 years prior to presentation. He came to the outpatient clinic for routine screening and was asymptomatic. Maintenance immunosuppression therapy included tacrolimus, prednisone, and azathioprine. He was also taking medications for hypertension (atenolol and enalapril), dyslipidemia (atorvastatin), hypothyroidism (levothyroxine), and diabetes (insulin NPH). Surprisingly, he was found to have a blood creatinine level of 7.2 mg/dL and blood urea of 81 mg/dL. His previously blood creatinine levels were 2.0 mg/dL 2 months prior and in the range of 2.0 to 2.5 mg/dL 4 months prior, estimated glomerular filtration rate (GFR) by MDRD (Modification of Diet in Renal Disease Study equation): 39.6 mL/min/1.73 m2). Other laboratory results were as follows: hemoglobin (Hb), 12.0 g/L; sodium (Na), 145 mEq/L; potassium (K), 4.3 mEq/L; uric acid, 10.5 mg/dL; aspartate aminotransferase (AST), 14 U/L; alanine transaminase (ALT), 13 U/L; total calcium, 8.3 mg/dL; bicarbonate, 16.6 mE/L; albumin, 3.4 g/dL. The patient did not smoke or drink alcohol and denied any type of surgery. He also denied recent episodes of diarrhea or antibiotic use. On physical examination, he had a blood pressure of 130/80 mmHg, pulse rate of 68 beats/min, respiratory rate of 16/min, and weight of 54 kg. He had no signs of edema or dehydration. The patient was admitted to the hospital and underwent hemodialysis. A kidney biopsy was performed. Histologic analysis showed cortical and medullary areas with nine glomeruli, one of which was sclerotic, and two arteries. The pathology report of the kidney biopsy was compatible with oxalate nephropathy and severe acute tubular necrosis associated with intense calcium oxalate deposition (Fig. ). There were no signs of rejection and C4d immunohistochemistry was negative. Fibrosis of the interstitium was moderate. Two days after the biopsy, urine sample was collected and centrifuged; calcium oxalate crystals could be seen under polarized light. The patient denied ingestion of products containing ethylene glycol, any other medication such as orlistat, and any other drugs different from what was prescribed to him. However, he reported that in the last month he had been eating 5 cashew pseudofruit (“cashew apple”) every day and drinking a large amount of cashew pseudofruit juice (about 1000 mL) every day instead drinking water. The fruits were picked up from a tree in the patient’s backyard. He did not eat cashew nuts. We could deduce that the patient was ingesting every day, for at least 1 month, approximately 2 to 3 g of ascorbic acid in his diet. This calculation was based on an ascorbic acid concentration of 219.3 mg/100 mL in the pseudofruit. The patient underwent five hemodialysis sessions and was discharged with a creatinine of 3.9 mg/dL and no further requirement for dialysis. Three months after hospital discharge, his creatinine was 3.4 mg/dL (MDRD GFR: 24 mL/min/1.732).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [59, 'years'], 'weight': [54.0, 'kg'], 'Sodium': [145.0, 'mEq/L']}",1.15714,1.09928,1.215,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 59 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 54.0 kg. The concentration of sodium is 145.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 145.0 mEq. To convert from 145.0 mEq to mmol, convert from mEq to mmol. The compound 145.0 has a valence of 1, and so divide the valence by the value of mEq to get, 145.0 mEq/(1 mEq/mmol) = 145.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 145.0 mEq sodium/L converts to 145.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 54.0 * (145.0/140 - 1) = 1.15714 L. The patient's free body water deficit is 1.15714 L."
5971,38,Free Water Deficit,lab test,decimal,pmc-3583052-1,Extracted,"A 21-day-old white male presented to the primary pediatrician for poor feeding, who noted that he had not regained his birth weight. Electrolytes were ordered as part of a failure to thrive workup, which revealed a sodium of 106 mmol/L, a potassium of 7.1 mmol/L, and a glucose of 1.8 mmol/L. After having a 17-OH progesterone level drawn, the infant was transferred to our tertiary referral hospital for electrolyte derangements with the presumptive diagnosis of salt-wasting congenital adrenal hyperplasia.
Birth history was significant for an uneventful pregnancy and delivery. Birth length was 51 cm (65th Percentile). Birth weight was 3.35 kg (37th percentile). Apgar scores were 8 and 9. Hyperpigmentation of the scrotum was noted at birth. Hypoglycemia was noted on the first day of life. He was discharged on the second day of life.
The past medical history was significant for two previous admissions for unconjugated hyperbilirubinemia with a maximum bilirubin of 367 μmol/L.He was treated with phototherapy on both occasions. His parents noted that his skin seemed to be progressively more pigmented over the first three weeks of life. This “bronzing” was attributed to phototherapy.
Physical exam upon arrival revealed normal vital signs and a blood pressure of 68/33 mmHg. His weight was 3.1 kg (7th Percentile). No dysmorphic features were noted. Genital exam revealed normal male genitalia with both testes descended. Phallus was normal in length and caliber with the urethral meatus at the tip. Physical exam was remarkable for marked bronzing of the skin.
Once in the pediatric intensive care unit, the patient was started on fludrocortisone and intravenous fluid support. He underwent a high-dose ACTH stimulation test and then was begun on glucocorticoid treatment at an initial dose of 28 mg/m2/day. Severe hyponatremia persisted despite the administration of 400 mcg/day of fludrocortisone in addition to 20 mEq/kg/day of sodium chloride. Diarrhea ensued. Escalating doses of glucocorticoid up to 54 mg/m2 were used. By the age of 5 months, he was weaned off of salt supplementation, and hydrocortisone doses were weaned to physiologic levels. Fludrocortisone doses have been gradually reduced.
The11-deoxycortisol values of theACTH stimulation became available early in this hospitalization and were consistent with 11β-hydroxylase deficiency with markedly elevated baseline and stimulated levels of 11-deoxycortisol (see ). The 17-hydroxyprogesterone obtained from his primary care physician returned at5.6 pmol/L (normal up to 2.9 pmol/L). As 11-deoxycorticosterone (DOC) and 11-deoxycortisol have been reported to be elevated in 21-hydroxylase deficiency and because salt wasting does not occur in 11-hydroxylase deficiency, 21-hydroxylase deficiency remained the presumptive diagnosis. The following day the baseline and stimulated 17-hydoxy progesterone levels returned to normal levels (4.5 nmol/L), arguing against 21-hydroxylase deficiency. He was evaluated for possible 11β-hydroxylase deficiency. A repeat 11-deoxycortisol after 12 days of hydrocortisone treatment returned to 1.49 nmol/L (normal range <.346–4.5).
Genetic testing was sent for CYP11B1 gene. The coding exons and the flanking intronic sequences were PCR amplified and sequenced in forward and reverse directions, using automated fluorescent dideoxy sequencing methods and the mRNA isoform NM_000497 as the reference sequence.
Genetic testing was also performed for the DAX1 (NROB1) gene associated with X-linked congenital adrenal hypoplasia. The coding exons and the flanking intronic sequences were PCR amplified and sequenced in forward and reverse directions, using automated fluorescent dideoxy sequencing methods and the NCBI reference files U31929.Gbk (DAX1, mRNA) and NM_000475.Gbk (NROB1, mRNA) as the reference sequences. This testing was positive for a new missense mutation not previously described. A T to C base change in the second exon was found, which substitutes proline for leucine at codon 447. His mother tested positive as a carrier for this gene. He has two older male siblings who have undergone genetic testing and have been found to be unaffected.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [21, 'days'], 'weight': [3.1, 'kg'], 'Sodium': [106.0, 'mmol/L']}",-0.45171,-0.42912,-0.4743,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 21 days old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 3.1 kg. The concentration of sodium is 106.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 3.1 * (106.0/140 - 1) = -0.45171 L. The patient's free body water deficit is -0.45171 L."
5972,38,Free Water Deficit,lab test,decimal,pmc-4421539-1,Extracted,"A 69-year-old Japanese woman visited our emergency room complaining of sudden headache, nausea and left haemiplegia. She had been undergoing chronic haemodialysis therapy for 17 years due to the advancement of chronic glomerulonephritis. A subtotal parathyroidectomy had been performed due to medical therapy-resistant secondary hyperparathyroidism 15 years previously. The secondary hyperparathyroidism had relapsed in the residual parathyroid gland 2 years previously, and since then 10 μm of maxacalcitol three times a week had been administered. Ticlopidine chloride 100 mg and aspirin 100 mg had also been applied since the symptoms of arterial sclerotic obliterans at her left femoral artery had become overt. Simple X-ray and X-ray computed tomographic examinations revealed obvious calcification around the thoracic aorta, abdominal aorta, bronchial wall and bilateral femoral arteries. No remarkable events had been noticed before the onset of her current symptoms.
Her height was 145 cm and body weight was 35.8 kg. Her blood pressure was 169/76 mmHg. Despite the left haemiplegia, her consciousness was clear and sensation was intact. The red-eye finding was absent. No remarkable findings were noted at her chest or abdomen. The laboratory results were as follows: haemoglobin 9.6 g/dL, serum creatinine 5.65 mg/dL, urea nitrogen 40.7 mg/dL, sodium 137 mEq/L, potassium 4.0 mEq/L, chloride 108 mEq/L, calcium 10.7 mg/dL, inorganic phosphate 4.1 mg/dL, magnesium 2.0 mg/dL and intact parathyroid hormone 1458 pg/mL. An ultrasonic examination detected a swollen parathyroid gland at her left frontal neck. Cranial computed tomography demonstrated a right subdural haematoma (Figure A) in addition to the calcification at the tentorium cerebella and falx cerebri (Figure B).
An emergency operation for the subdural haematoma was performed. Sclerotic lesions that looked like many rock barnacles sticking to sea rocks were found in the dura mater (Figure A). Adhesions of those sclerotic lesions and cerebral superficial arteries were observed (Figure B). Although the artery responsible for the subdural haematoma was not confirmed, the haemorrhage was likely to have been caused in part by such an adhesion. No obvious brain damage was observed.
By histological observation, calcified tissues were found in such sclerotic lesions with a rock barnacle-like appearance, and cells forming a single layer were found on the surface of this tissue (Figure A). An obvious lamellar structure was demonstrated in the calcified tissue by a polarization microscopic observation (Figure B and C). Osteopontin immunoreactivity was found around the calcified tissue (Figure A). Multinucleated giant cells infiltrated near the tissue, and a tartrate-resistant acid phosphatase immunoreactivity was demonstrated in those cells (Figure B).
The patient recovered after the emergency operation and was discharged a few days later only presenting lower limb muscle weakness.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [69, 'years'], 'weight': [35.8, 'kg'], 'sex': 'Female', 'Sodium': [137.0, 'mEq/L']}",-0.34521,-0.32795,-0.36247,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 69 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 35.8 kg. The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. Plugging in these values into the equation, we get 0.45 * 35.8 * (137.0/140 - 1) = -0.34521 L. The patient's free body water deficit is -0.34521 L."
5973,38,Free Water Deficit,lab test,decimal,pmc-3436703-1,Extracted,"A 28-day-old baby boy, born at term from an uneventful pregnancy and vaginal delivery (Apgar score: 9/10), was referred from a nearby town to our hospital after a week of irritability and feeding difficulties. He was a 3200 g. (cephalic perimeter: 38.5 cm), phenotypically normal infant, seriously lethargic, hypertonic, with intermittent lower right limb clonic seizures. His breath was superficial, and suck, grasp and Moro reflexes were absent. His anterior fontanel was bulging, and his cerebrospinal fluid was xanthochromic. Although serum electrolytes, creatinine, C-protein and blood cell count were normal, the child presented metabolic acidosis (pH: 7.18; HCO3: 15.5 mmol/L). Brain MRI (Figure ) confirmed a massive IVH with periventricular infiltration and hydrocephalus. Moreover, an II/VI systolic murmur, with upper arm blood pressure up to 178/94 mm Hg, and 57/49 mm in his leg, led to the diagnosis of aortic coarctation.
The patient’s initial course, under mechanical ventilation, captopril and phenobarbital, was favorable. Five days later, however, sudden polyuria (9 ml/kg/h), clinical signs of dehydration with unexpected weight loss (6%), and hyposthenuria (124 mOsm/kg), despite high serum sodium (156 mmol/L), chloride (126 mmol/L) and osmolality (326 mOsm/kg), led to the diagnosis of CDI. Subcutaneous (sc) desmopressin (0.02 μg. b.i.d.) achieved a rapid recovery (average serum sodium, 138 mmol/L; osmolality, 290 mOsm/kg). Surgical correction of his severe juxtaductal coarctation was performed 6 days after his metabolic stabilization. A ventriculoperitoneal shunt was performed shortly thereafter. Due to the child’s severe deglutory handicap, sc desmopressin therapy was still recommended at discharge. The family was instructed to perform subcutaneous injection and daily diuresis and body weight control at home, and the patient was scheduled for periodic clinical and analytical (serum sodium) check-ups.
Four months later, the infant maintained a proper fluid balance. However, his delayed growth and neurodevelopment was progressively more evident, and his swallowing disability had almost led to malnourishment (Table ). He was scheduled for quarterly monitoring and nutritional support at his local hospital, under whose control he remained until two years of age. Throughout this period, his scant oral intake was supported by means of continuous debit enteral nutrition and he received desmopressin (0.1 μg bid, sc), phenobarbital (15 mg bid) and captopril (1 mg tid).
When he returned at two years of age, he had had no seizures, his ventriculoperitoneal shunt was working properly and, due to the fact that his food intake had been stable (though low), with no significant vomiting or diarrhoea, he maintained almost perfect fluid control. However, we saw a small, thin, microcephalic child (Table ), with very small developmental progress and whose deglutition had just improved. His serum sodium (146 mmol/L), osmolality (294 mOsm/kg), glucose (4.0 mmol/L), a.m. cortisol (292.6 mmol/L), free thyroxin (19.6 pmol/L), insulin (2.2 μU/mL) and IGF-1 (78 ng/mL) were within normal range, but his vasopressin was lesser than 1.1 pmol/L. His urinary osmolality ranged from 758 mOsm/kg (3 hours after desmopressin) to 226 mOsm/kg prior to the following dose. Given his unfavourable nutritional evolution, with insufficient deglutition, a gastrostomy was advised to provide nutritional support.
At the three-year check-up, the patient was under nasal desmopressin treatment (10 μg bid). This was recommended at his local hospital some four months before, when he underwent a gastrostomy, which unfortunately soon failed because of septic complications. Subsequently, the undernourished (Table ) and seriously delayed child (developmental age of about 9–10 months) got progressively worse: His fluid balance became quite unstable and, on at least two occasions, he suffered weight loss and clinical deterioration for several days related to a common cold. The family was informed about the risk posed by the probable dehydration episodes suffered by the child. The sc route for the desmopressin therapy and a new attempt at gastrostomy were once again recommended.
This advice was not followed, and at the age of 3 years and 5 months, the child was admitted to his local hospital after five days of a new nasal cold. His medical report registered a Glasgow Score of 8, body weight loss of 12%, and 189 mmol/L of serum sodium. After a few hours of saline infusion, he achieved a certain degree of clinical recovery. However, the next day he worsened again, and forty hours after his admittance, he entered into status epilepticus and was transferred to our hospital.
We received a sedated, malnourished child, with an irregular breathing rate and whose serum sodium was 147 mmol/L. Electroencephalogram and brain CT confirmed the suspected cerebral edema. After two weeks of intensive care, he was fully awake, but was quadriplegic, with hyperreflexic, spastic limbs, wrists in palmar flexion, bilateral Babinski sign, and a severely hypotonic neck. Central pontine myelinolysis was diagnosed; however, MRI were not those expected for this diagnosis, but rather of old hemorrhagic infarcts (Figure ). On discharge, desmopressin (0.13 μg bid, sc) was once again recommended and phenobarbital was replaced by levetiracetam (200 mg bid). Gastrostomy was uneventfully restored two weeks later.
Six months later (four years of age), sc desmopressin did maintain a fair balance. The deglutition ability of our quadriplegic patient had progressed admirably and his nutrition was greatly improved (Table ). His facial expression and babbling likewise evidenced some developmental improvement.
Despite his severe cognitive impairment, over the following year our patient improved significantly in terms of his cervical control, a useful ability to push with his left hand likewise being perceived. Poor, but increasingly disyllabic verbal expression and a significant capacity to understand simple verbal messages were also appreciated. As he had achieved an almost normal swallowing ability, his gastrostomy was closed and desmopressin was returned to the oral route (0.3 -0.35 μg bid).
At the check-up some days before his fifth birthday, he was an overweight boy (Table ).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [28, 'days'], 'weight': [3200.0, 'g'], 'Sodium': [156.0, 'mmol/L']}",0.21943,0.20846,0.2304,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 28 days old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 3200.0 g so this converts to 3200.0 lbs * kg/1000 g = 3.2 kg. The concentration of sodium is 156.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 3.2 * (156.0/140 - 1) = 0.21943 L. The patient's free body water deficit is 0.21943 L."
5974,38,Free Water Deficit,lab test,decimal,pmc-5423745-1,Extracted,"A 9-month-old boy, who was born from a non-consanguineous marriage, presented to our clinic with complaints of continuous high grade fever for the past 15 days. His body temperature was over 39.5°C in spite of ibuprofen/acetaminophen and anti-infection therapy. The development of his body frame was normal, weighing 10 kg. Clinical examination revealed mild pallor, gray hair and patchy hypopigmentation of the skin (), red rashes on the trunk, submandibular lymphadenopathy and protuberant abdomen with massive hepatosplenomegaly. The boy had no mucocutaneous bleeding and iris pigmentation, and cardiovascular and nervous systems were normal. His history since birth was negative for frequent chest infections, draining bilateral ears and fever. There was no family history of the disease.
Routine blood examination revealed pancytopenia with febrile neutropenia (hemoglobin of 72 g/L, white blood cell count of 9.05×109/L, neutrophil count of 0.9×109/L, and platelet count of 43×109/L). Blood biochemical examination revealed elevated C-reactive protein (69.4 mg/L), high ferritin levels (>2000 ng/mL), low fibrinogen levels (0.66 g/L), hyponatremia (129.5 mmol/L), hypoalbuminemia (20.1 g/L), and hypertriglyceridemia (4.99 mmol/L). Relevant hematological findings were LDH 1062 U/L, ALT 92.8 U/L, AST 339.1 U/L, GGT 350 U/L, and TBA 241.4 μmol/L. Routine urine and cerebrospinal fluid examination were normal. Blood cultures were negative. Epstein-Barr virus (EBV) DNA detection was 1.34×106 IU. Abdominal ultrasound revealed hepatosplenomegaly. Lung CT images revealed double pneumonia with multiple patchy lesions ().
Peripheral blood smear revealed several abnormal giant granules in most leukocytes. Bone marrow aspirate revealed prominent granules within the lymphocytes and myeloid cells (). Furthermore, hemophagocytosis was observed on the bone marrow aspiration smear. Light microscopic images of the boy’s hair revealed abnormal clumping of melanin. Pigment clumps were small and uniformly distributed along the hair shaft ().
HLH-related genes (including AP3B1, FASLG, PRF1, TNFRSF1A, BIRC4, ITK, RAB27A, UNC13D, CASP10, ITPKC, SH2D1A, CD27, LYST, STX11, FAS, MAGT1 and STXBP2) were detected with high-throughput sequencing. It was found that LYST gene mutations at c.11183delA, p.N3728fs and c.9453delA, p.K3151fs were separate from his mother and father. Based on HGMD (Human Gene Mutation Database) analysis, these were novel frameshift mutations, validated by Sanger sequencing ( and ).
The boy was diagnosed with CHS in the accelerated phase due to his typical clinical characteristics, laboratory examinations and the detected LYST gene. According to the 2004 revised guidelines of the Histiocyte Society (), the patient fulfilled the diagnostic criteria for HLH (five out of eight criteria). The HLH-2004 treatment protocol, including cyclosporine A (5 mg·kg-1·day-1), dexamethasone (10 mg·(m2)-1·day-1, half dose every 2 weeks), and etoposide (150 mg/m2, twice a week for the first 2 weeks and once a week during the following 6 weeks), was administrated (). Maximal supportive care was provided, such as antibacterial and antiviral treatment (meropenem and ganciclovir), liver and cardiac protective agent, high doses of intravenous gamma globulin (2 g/kg), multiple transfusions, including platelets and packed red blood cells for anemia and fresh frozen plasma to improve the function of blood coagulation, prophylactic oral cotrimoxazole, and antimycotic voriconazole (). After the initial 8 weeks of therapy, all blood parameters returned to normal, pneumonia was cured (), and the disease was in temporary remission. Continuation therapy of the HLH regimen was then started. To date, the boy is in good condition. Stem cell transplantation has been planned.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [9, 'months'], 'weight': [10.0, 'kg'], 'sex': 'Male', 'Sodium': [129.5, 'mmol/L']}",-0.45,-0.4275,-0.4725,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 9 months old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 10.0 kg. The concentration of sodium is 129.5 mmol/L. Plugging in these values into the equation, we get 0.6 * 10.0 * (129.5/140 - 1) = -0.45 L. The patient's free body water deficit is -0.45 L."
5975,38,Free Water Deficit,lab test,decimal,usmle-1002,Extracted,"A 42-year-old woman comes to the physician for a routine health maintenance examination. She has generalized fatigue and has had difficulties doing her household duties for the past 3 months. She has eczema and gastroesophageal reflux disease. She has a history of using intravenous methamphetamine in her youth but has not used illicit drugs in 23 years. Her medications include topical clobetasol and pantoprazole. She is 160 cm (5 ft 3 in) tall and weighs 105 kg (231 lb); BMI is 42 kg/m2. Her temperature is 37°C (98.6°F), pulse is 95/min, and blood pressure is 145/90 mm Hg. The lungs are clear to auscultation. Cardiac examination shows no abnormalities. Pelvic examination shows a normal vagina and cervix. Laboratory studies show:
Hemoglobin 13.1 g/dL
Leukocyte count 7,800/mm3
Platelet count 312,000/mm3
Serum
Na+ 141 mEq/L
K+ 4.6 mEq/L
Cl- 98 mEq/L
Urea nitrogen 12 mg/dL
Fasting glucose 110 mg/dL
Creatinine 0.8 mg/dL
Total cholesterol 269 mg/dL
HDL-cholesterol 55 mg/dL
LDL-cholesterol 160 mg/dL
Triglycerides 320 mg/dL
Urinalysis is within normal limits. An x-ray of the chest shows no abnormalities. She has not lost any weight over the past year despite following supervised weight loss programs, including various diets and exercise regimens.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [42, 'years'], 'weight': [105.0, 'kg'], 'sex': 'Female', 'Sodium': [141.0, 'mEq/L']}",0.375,0.35625,0.39375,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 42 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 105.0 kg. The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 105.0 * (141.0/140 - 1) = 0.375 L. The patient's free body water deficit is 0.375 L."
5976,38,Free Water Deficit,lab test,decimal,pmc-8418704-1,Extracted,"We present a case involving a 37-year-old Japanese female with eating disorders. Eighteen years earlier, she described episodes of binging and purging and weight loss (42 kg; BMI, 16.4) with amenorrhea, intense fear of gaining weight and a distorted view of her body weight and shape. She was diagnosed with anorexia nervosa, binge-purging type according to the DSM-5, and she was admitted to the Department of Psychiatry 5 times because of abnormal weight loss. At the sixth admission, she was admitted because of emaciation with shortness of breath and tiredness, and her weight was 30.0 kg (BMI, 10.5 kg/m2). Laboratory tests at admission revealed the following: aspartate aminotransferase, 1731 IU/L; alanine transaminase, 1210 IU/L; gamma-glutamyltransferase, 277 U/L; creatinine, 0.43 mg/dL; urea nitrogen, 29 mg/dL; phosphorus, 3.1 mEq/L; sodium, 137 mEq/L; potassium, 4.5 mEq/L; chlorine, 99 mEq/L; white blood cell count, 2800/µL; red blood cell count, 40.7 × 109/µL; hemoglobin, 14.1 g/dL; platelets, 9.3 × 104/µL; and troponin I (sensitive assay), 0.006 ng/mL. Her ECG showed a heart rate of 57 beats/min, P-R interval of 0.247 s, and corrected QT interval of 0.464 s. On the afternoon of the first day of hospitalization, a simple measurement caused hypoglycemia (20 mg/dL), and she lost consciousness. This loss of consciousness was improved by administration of 50% glucose solution, which was coinjected with the maintenance infusion. On the night of the second day of hospitalization, the electrocardiogram monitor revealed tachycardia, and a 12-lead electrocardiogram was performed. Sinus rhythm was observed, but negative T waves were observed in II, III, aVf, and V1–6 (Fig. ). Ultrasound echo showed hypokinesia at the apex of the heart and hypercontraction at the base of the heart, suggesting Takotsubo cardiomyopathy. The left ventricular ejection fraction was 20%. Refeeding syndrome was also present and became hypophosphatemia, and we administered phosphorus. Rest and oxygen administration gradually improved her cardiac function; the left ventricular ejection fraction also improved to 50% based on echocardiography. Her amount of food intake gradually increased, and we provided psychotherapy. On the 12th day, treatment for eating disorders was continued, as her general condition was improving. Finally, her weight increased to 43 kg (BMI, 15.2 kg/m2) with psychiatric treatment, and she was discharged.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [37, 'years'], 'weight': [43.0, 'kg'], 'Sodium': [137.0, 'mEq/L']}",-0.46071,-0.43767,-0.48375,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 37 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 43.0 kg. The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 43.0 * (137.0/140 - 1) = -0.46071 L. The patient's free body water deficit is -0.46071 L."
5977,38,Free Water Deficit,lab test,decimal,usmle-3517,Extracted,"A 58-year-old man is brought to the emergency department after a witnessed tonic-clonic seizure. His wife says he has had a persistent dry cough for 6 months. During this time period, he has also had fatigue and a 4.5-kg (10-lb) weight loss. The patient has no history of serious illness and does not take any medications. He has smoked 1 pack of cigarettes daily for 35 years. He is confused and oriented only to person. Laboratory studies show a serum sodium concentration of 119 mEq/L and glucose concentration of 102 mg/dL. An x-ray of the chest shows an irregular, poorly demarcated density at the right hilum.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [58, 'years'], 'weight': [4.5, 'kg'], 'sex': 'Male', 'Sodium': [119.0, 'mEq/L']}",-0.405,-0.38475,-0.42525,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 58 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 4.5 kg. The concentration of sodium is 119.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 119.0 mEq. To convert from 119.0 mEq to mmol, convert from mEq to mmol. The compound 119.0 has a valence of 1, and so divide the valence by the value of mEq to get, 119.0 mEq/(1 mEq/mmol) = 119.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 119.0 mEq sodium/L converts to 119.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 4.5 * (119.0/140 - 1) = -0.405 L. The patient's free body water deficit is -0.405 L."
5978,38,Free Water Deficit,lab test,decimal,pmc-3763621-2,Extracted,"A 12-month old male infant, with weight 4.8 kg, height 68.9 cm (weight-for-height z-score −6.21, weight-for-age z-score −5.61, length-for-age z-score −2.88) was admitted to icddr,b's, Dhaka Hospital. He had a history of watery stool for five days and high-grade intermittent fever with cough for four days. On admission, physical examination revealed a temperature of 38.7 ºC, heart rate 120/min with normal rhythm, and respiration rate 48/min. In addition, the patient was lethargic, hypotonic, and severely dehydrated. On auscultation of the chest, coarse crackles were found in both lungs, and the heart sounds were normal. The abdomen was soft and non-tender. On admission, biochemical data showed Na 139.1 mmol/L, K 1.82 mmol/L, and P 2.4 mg/dL. The chest x-ray showed bilateral hilar consolidation. Based on the physical examination and laboratory data, the initial diagnosis was pneumonia complicated by sepsis, severe malnutrition, hypokalaemia, and hypophosphataemia. Initial treatment was given with intravenous antibiotics and fluid therapy. In addition, zinc, folic acid, multivitamin, potassium and magnesium supplements were given according to icddr,b's standardized management protocol for severely-malnourished children. On the second day, tetanic spasm was developed as secondary complication due to hypocalcaemia (Ca 1.68 mmol/L). Repeated biochemical results showed continued hypophosphataemia (P 0.9 mg/dL) while sodium and potassium levels were almost normal (Na 133.8 mmol/L, K 3.80 mmol/L). The tetanic spasm was treated with intravenous calcium gluconate and vitamin D. By the 6th day, the patient recovered from fever and was discharged on the 9th day with normal plasma electrolyte levels (Na 136.8 mmol/L, K 4.30 mmol/L, Ca 2.35 mmol/L, P 5.2 mg/dL).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [12, 'months'], 'weight': [4.8, 'kg'], 'sex': 'Male', 'Sodium': [139.1, 'mmol/L']}",-0.01851,-0.01758,-0.01944,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
This means that the patient is 1 year and 0 oldThe patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 4.8 kg. The concentration of sodium is 139.1 mmol/L. Plugging in these values into the equation, we get 0.6 * 4.8 * (139.1/140 - 1) = -0.01851 L. The patient's free body water deficit is -0.01851 L."
5979,38,Free Water Deficit,lab test,decimal,pmc-2719188-1,Extracted,"A 46-yr-old woman was diagnosed with nasopharyngeal cancer 5 months before being admitted to our hospital for a course of chemotherapy. She had no history of chronic alcohol consumption or benzodiazepine addiction, or any other significant medical history including malnutrition, surgery or herbal medications. There were no laboratory abnormalities. Concurrent chemoradiation therapy was performed with cisplatin (100 mg/m2 at 3-week intervals). One month after the completion of concurrent chemoradiation therapy, we gave her chemotherapy consisting of a continuous infusion of 5-FU 1,000 mg/m2/day for 4 days and cisplatin 75 mg/m2 for 1 hr on the first day of each chemotherapy cycle at 3-week intervals. She experienced NCI CTC (v. 3.0) grade 2 stomatitis and grade 3 neutropenia during the first cycle, which resolved after supportive therapy. There was no diarrhea or vomiting of significant grade.
On the 20th day of the second round of chemotherapy with 5-FU and cisplatin, she experienced dizziness with nystagmus, but these symptoms resolved with conservative management. Fifteen days after the dizziness episode, she showed acute onset disorientation, headache, and lethargy. Her mental status showed confusion, but neither focal neurological signs nor pathological reflexes were noted. Her blood pressure was 110/70 mmHg, pulse rate 110/min, respiratory rate 14/min, and body temperature 36.4℃. Her myelosuppression status after chemotherapy was a white blood cell count of 1,300/µL (neutrophils 74.4%, lymphocytes 14.3%), hemoglobin concentration of 8.1 g/dL, and platelet count of 62,000/µL. At that time, the level of serum BUN and creatinine were 10 mg/dL and 0.6 mg/dL. Her serum sodium and potassium were 133 and 3.5 mM/L, respectively. The total protein was 5.8 g/dL (reference range, 6.5-8.4 g/dL), serum albumin 3.6 g/dL (reference range, 3.5-5.1 g/ dL), triglyceride 67 mg/dL (reference range, 28-150 mg/dL), cholesterol 68 mg/dL (reference range, 130-240 mg/dL), and magnesium 1.9 mg/dL (reference range, 1.9-3.1 mg/dL). The body weight of the patient at diagnosis was 52 kg and was 54 kg at the time of this event. Her serum folic acid concentration was 2 ng/mL (reference range, 3-17 ng/mL), vitamin B12 concentration 1,259 pg/mL (reference range, 253-1,090 pg/mL), and thiamine concentration 138.1 ng/dL (reference range, 21.3-81.9 ng/dL). The ammonia concentration was normal. Brain magnetic resonance imaging (MRI) showed symmetrical high signal intensities in the posterior aspect of the medulla and periaqueductal area of the midbrain that were consistent with Wernicke's encephalopathy. A small amount of subdural hematoma in the right posterior occipital area was noted (). She was given intravenous thiamine, 500 mg for 5 days, and then oral thiamine, 60 mg/day, even though the initial serum thiamine level was normal. Her confused mental state resolved after several hours, and her dizziness and nystagmus gradually improved over the next 5 days.
The brain MRI was repeated in the outpatient clinic 1 month after the episode. The MRI showed nearly complete resolution of the previous abnormal signal intensities in the posterior aspect of the medulla and the periaqueductal area of the midbrain, including the subdural hematoma ().",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [46, 'years'], 'weight': [54.0, 'kg'], 'Sodium': [133.0, 'mEq/L']}",-1.35,-1.2825,-1.4175,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 46 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 54.0 kg. The concentration of sodium is 133.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 133.0 mEq. To convert from 133.0 mEq to mmol, convert from mEq to mmol. The compound 133.0 has a valence of 1, and so divide the valence by the value of mEq to get, 133.0 mEq/(1 mEq/mmol) = 133.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mEq sodium/L converts to 133.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 54.0 * (133.0/140 - 1) = -1.35 L. The patient's free body water deficit is -1.35 L."
5980,38,Free Water Deficit,lab test,decimal,pmc-3784883-1,Extracted,"A 22-year old woman was referred to endocrine clinic because of three episodes of generalized tonic-clonic seizure from one month ago. She was the product of consanguineous marriage. She was newly married and had no children. As far as she knew, family history was negative for similar disorder or other endocrine problems. She had normal regular menses. She was an oriented female with normal face appearance and short body stature (her height was 153 cm; her weight and BMI were 60 kg and 25.6 kg/ m2 respectively).
She had normal vital signs:
BP: 100/70 mm Hg, Temperature: 37°C, Pulse rate: 80/ min and regular, Respiratory rate: 16/min.
Physical exam revealed shortening of fourth and fifth metacarpal in both hands with greater degree of fourth metacarpal involvement in right hand. The knuckles of her ring and little fingers looked depressed during clinching fist position [Figures and ]. Hands movements and function were normal. Radiograph study of hands showed short fourth and fifth metacarpal in both hands []. Deep tendon reflexes were normal and plantar reflexes were flexor. Chvostek's and Trousseau's signs were negative at the time of admission to endocrine ward.
Laboratory results showing the following results: WBC: 7700/μl, hemoglobin (Hb):11.7g/dl, mean cell volume (MCV): 84 (fl), platelet (Plt):255,000/μl), blood urea: 19mg/dl, Cr: 0.8 mg/dl, blood sugar: 73 mg/dl, Potassium: 3.6 mEq/L, Sodium: 141 mEq/L, calcium:5.3-7.1 mg/ dl (8.5-10.4), Ionized calcium: 3.88 mg/dl (4.6-5.3), serum phosphorus:6.4-7.3 mg/dl (2.8-4.5), serum Mg (magnesium): 2.20 mg/dl (1.8-2.6), serum ALP (serum Alkaline phosphatase):162 IU/L (64-306), Intact PTH: 17.91pg/ml (15-65), serum Albumin: 4.2 gr/dl (3.5-5.2). Liver function, urine analysis and thyroid function tests were all normal. Erythrocyte sedimentation rate (ESR) was 17 mm/hour and RF (Rheumatoid factor) was negative.
There were transient sharp epileptiform discharges in both frontocentral regions predominantly in right side in Electroencephalography (EEG) study.
CXR and ECG results were normal.
Brain magnetic resonance imaging (MRI) revealed multiple abnormal signal foci at subcortical white matter and there was no space occupying lesion.
There were nonspecific nonenhancing T2 and FLAIR high signal foci at left forceps major area in brain magnetic resonance imaging (MRI) with and without contrast.
We made the diagnosis of IPH and she was initiated on intravenous calcium infusion along with oral calcium tablets, calcitriol and also sodium valproate and after controlling of her hypocalcemia she was discharged to home and she was advised to return to the clinic for periodic monitoring with serum calcium and phosphorous levels and 24 hours urinary calcium collection.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [22, 'years'], 'weight': [60.0, 'kg'], 'sex': 'Female', 'Sodium': [141.0, 'mEq/L']}",0.21429,0.20358,0.225,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 22 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 60.0 kg. The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 60.0 * (141.0/140 - 1) = 0.21429 L. The patient's free body water deficit is 0.21429 L."
5981,38,Free Water Deficit,lab test,decimal,pmc-3943037-1,Extracted,"A previously healthy, 12-kg, 22-month-old female toddler was referred to us with high fever, non-bloody and non-xanthic jumpy vomiting, and non-bloody watery diarrhea following a trip. Her height was 80 cm (below the percentile 25%) and head circumference was 47 cm (percentile 50%). Several hours later, her level of consciousness decreased (Glasgow coma scale=7), she developed generalized tonic-clonic seizures, and was transferred to PICU. Quadripelagic spasms with greater intensity in the right upper and lower limbs as well as spasity and severe dystonia were then noted. In the course of the disease, she was transferred to Amirkola Children Hospital in Babol. On the first examination after admission to this center, her complete blood count, PT, PTT, and urine analysis were normal. C reactive protein, erythrocyte sedimentation rate, blood sugar, blood urea nitrogen, creatinine, calcium, sodium, potassium, aspartate transaminase, alanine transaminase, alkaline phosphatase, total bilirubin, and direct bilirubin were reported to be 2 mg/dL, 7 mm/hr, 94 mg/dL, 9.2 mg/dL, 0.6 mg/dL, 9.4 mg/dL, 140 mEq/L, 5.2 mEq/L, 100 U/L, 119 U/L, 247U/L, 1.1 mg/dL, and 0.5 mg/dL, respectively. Evaluation of the cerebrospinal fluid (CSF), blood ammonia, lactate, and pyruvate were also normal. Urine reducing substances, amino acids chromatography and blood gas were normal. Anticonvulsant therapy with phenytoin, Phenobarbital, and midazolam drip was begun. Respiratory support by mechanical ventilation was also initiated. Acyclovir (Zovirax), dexamethasone, intravenous immunoglobulin (IVIG), amikacin (for UTI), and imipenem were prescribed.
Diazepam (0.2 mgr /kgr q6h), levodopa(10mgr/day), and trihexifenidilo(2mgr/6h) were used to treat dystonia. Although dystonia and spasity gradually declined, mental and physical sequelae developed. She therefore became a candidate for percutaneous endoscopic gastrostomy (PEG). MRI revealed increased T2 signal intensity in the thalami, basal ganglia (putamen and globus pallidus), and periventricular white matter presenting hemorrhage accompanied with necrosis in those regions ().
The patient underwent supportive care including physiotherapy, speech therapy, and outpatient supports.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [22, 'months'], 'weight': [12.0, 'kg'], 'sex': 'Female', 'Sodium': [140.0, 'mEq/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
This means that the patient is 1 year and 10 oldThe patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 12.0 kg. The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 12.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
5982,38,Free Water Deficit,lab test,decimal,pmc-6552952-1,Extracted,"A 4.5-month-old boy, presenting dry cough since two weeks that did not respond to antibiotics (amoxicillin-clavulanic acid), was admitted to the pediatric intensive care unit due to tachycardia and respiratory distress. He also presented anorexia and weight loss, without any episode of diarrhea and vomiting. The vital signs were as follows: RR = 30, HR = 90, BP = 80/60, and T = 37°C.
He was the first child of the family (no serious medical history of the mothers) and his birth weight was 3.5 kg, whereas at the time of admission he weighed 4.5 kg. The patient was calm during the examination and appeared normal with no sign of dehydration. Sodium electrolytes, blood gas analysis, and CBC were performed, and the patient was treated with fluid therapy and intravenous antibiotics.
The test results of patient tests were as follows: PH = 7.60/ PCO2 = 48/HCO3 = 46.1/ BE = 24; Na = 122 mEq/L/ K = 2.1 mEq/L/CL = 60 mEq/L/ Mg = 1.2 mEq/L.
The patient had hypocalcemia metabolic alkalosis, hypokalemia, and hyponatremia. Urine electrolytes measured were as follows: Na = 67 mEq/L, CL = 63 mEq/L, and K = 14 mEq/L. Transtubular K gradient (TTKG) was found to be 2.5.
Sodium and potassium concentrations were measured after every six hours. Liquid therapy with half saline and 60 mEq/L potassium was prescribed to the patient. Since K urine excretion was <15 mEq/L, the cause of hypokalemia was nonrenal excretion. Barter syndrome was thus not the diagnosis.
Twelve hours after the initiation of the treatment with liquid therapy, Na and K were 136 mEq/L and 3.9 mEq/L, respectively.
The patient responded appropriately to Na and K administration. Serum potassium and chloride levels decreased to 40 mEq/L, and therefore, oral potassium was also administered. Sonography did not show any positive signs of nephrocalcinosis and hypertrophic pyloric stenosis.
In response to respiratory symptoms and underweightness and metabolic alkalosis presented by the patient, sweat test was performed twice. Initially, the sweat chlorine and sodium were 58 mEq/L and 60 mEq/L, respectively, whereas, later, the levels of chlorine and sodium were increased to 65 mEq/L and 68 mEq/L, respectively.
Two weeks later, tests were repeated: Urine Na = 28 mmol/L/ Urine K = 11 mmol/L/ Urine CL = 16 mmol/L.
Liver enzymes were seen to be increased; however, urea, creatinine, glucose, albumin, potassium, sodium, and magnesium were normal in serum. During first examination, fat drop stool was not seen, but in the next test, fesses were seen with many fat drops, and the Sudan III test showed more than 100 fat drop.
The activity of trypsin was decreased by 1/24, where its normal rate is 1/96. Fecal elastase activity was 20 μg/g (normal > 200), seen as severe decrease in stool elastase.
Due to clinical and laboratory findings, such as positive sweat tests and other signs of metabolic alkalosis in infants, cystic fibrosis (CF) was diagnosed.
The patient was treated with fat-soluble vitamins, chest physiotherapy, antibiotics, MCT oil and pancreatic enzymes (due to gastrointestinal involvement and absorption of the patient), and amniotic nerve fibrosis and was discharged with good general condition.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [5, 'months'], 'weight': [4.5, 'kg'], 'Sodium': [122.0, 'mEq/L']}",-0.34714,-0.32978,-0.3645,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 5 months old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 4.5 kg. The concentration of sodium is 122.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 122.0 mEq. To convert from 122.0 mEq to mmol, convert from mEq to mmol. The compound 122.0 has a valence of 1, and so divide the valence by the value of mEq to get, 122.0 mEq/(1 mEq/mmol) = 122.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 122.0 mEq sodium/L converts to 122.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 4.5 * (122.0/140 - 1) = -0.34714 L. The patient's free body water deficit is -0.34714 L."
5983,38,Free Water Deficit,lab test,decimal,pmc-5996444-1,Extracted,"A 78-year-old Sri Lankan man presented to the emergency department with acute onset upper and lower limb weakness for several-hour duration. The patient denied any limb weakness on the night prior to admission and was otherwise healthy. Upon waking up in the morning he found difficulty in getting up with weakness involving all four limbs. He was able to lift limbs but was unable to walk or dress himself. The weakness persisted and remained the same until the time of admission five hours later. Weakness was symmetrical and nonprogressive and involved all four limbs. There was no pain, numbness, or abnormal movements in limbs. Swallowing and breathing were not impaired. Urinary and faecal incontinence were absent.
Patient's past medical history consisted of type 2 diabetes, hypertension, ischemic heart disease, and systolic heart failure. Home medications included Mixtard 18 U mane and 8 U vesper, Losartan 50 mg twice daily, Nifedipine 20 mg twice daily, Spironolactone 50 mg daily, Frusemide 40 mg daily, Atorvastatin 20 mg daily, and Amiodarone 100 mg daily. Dietary history revealed that he was drinking king coconut water 2–4 servings almost every day for past one week.
He was overweight (height: 166 cm, weight: 70 kg, BMI: 25.4 kg/m2). Xanthelasma and arcus senilis were present. He had elevated blood pressure (140/90) with cardiac apex lying in 6th intercostal space. Examination of limbs revealed symmetrical weakness with more distal involvement (proximal 4/5, distal 3/5). Limb reflexes were not impaired except for absent bilateral ankle jerks. Impaired sensation of pain and temperature was present in a glove and stocking type distribution. Joint position sensation was diminished in both upper and lower limbs. Examination of central nervous, respiratory, and gastrointestinal systems was normal.
Investigations revealed renal dysfunction (serum creatinine: 3.66 mg/dl-, eGFR: 15 ml/min, blood urea: 20.32 mmol/l, and arterial blood HCO3−: 12.7 meq/l). He had severe hyperkalemia (serum potassium: 7.02 mmol/l) with electrocardiogram showing tall, tented T waves and sine waves. Serum sodium was 129 meq/l. Renal ultrasound showed increased cortical echogenicity and impaired corticomedullary demarcation. Noncontrast computerized tomography of brain revealed normal findings. Electromyogram did not reveal acute radiculopathy, plexopathy, or myopathy. Nerve conduction studies revealed distal segmental axonal neuropathy suggestive of diabetic polyneuropathy.
Standard ward protocol for managing hyperkalemia was followed. Patient was initially given IV 10% calcium gluconate 10 ml over 10 minutes followed by a repeat dose. Spironolactone and Losartan were immediately withheld. He was given IV 50% Dextrose 50 ml with 10 U of Soluble Insulin. Patient was nebulized with Salbutamol 5 ml over 10 minutes and it was repeated twice. The interventions showed biochemical and electrocardiographic improvement in two hours (serum potassium: 6.1 meq/l). He was commenced on calcium resonium 15 g three times daily. Limb weakness showed rapid clinical improvement within 24 hours.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [78, 'years'], 'weight': [70.0, 'kg'], 'sex': 'Male', 'Sodium': [129.0, 'mEq/L']}",-2.75,-2.6125,-2.8875,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 78 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 70.0 kg. The concentration of sodium is 129.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 129.0 mEq. To convert from 129.0 mEq to mmol, convert from mEq to mmol. The compound 129.0 has a valence of 1, and so divide the valence by the value of mEq to get, 129.0 mEq/(1 mEq/mmol) = 129.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 129.0 mEq sodium/L converts to 129.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 70.0 * (129.0/140 - 1) = -2.75 L. The patient's free body water deficit is -2.75 L."
5984,38,Free Water Deficit,lab test,decimal,pmc-4421357-1,Extracted,"A 6-month-old male infant was admitted to our hospital for diagnostic workup of failure to thrive. The pregnancy, delivery and postnatal adaptation had been normal. At the age of 8 weeks marked failure to thrive was noticed. Initial treatment included various dietary regimens. The mother supplemented the daily fluid intake with water at the infant's demand. At 6 months of age, despite formula intake of 140–160 ml/kg/day, adequate weight gain was not achieved. Since birth, the body weight had dropped from the 90th to the 3rd percentile.
On admission, the patient's weight was 5710 g (3rd percentile), height was 64.5 cm (3rd percentile) and head circumference was 43 cm (20th percentile). Psychomotor development appeared normal for age. The infant's mother described recurrent episodes of constipation, a persistent moderate increase of body temperature and reported that the child had always been feeding well. During hospitalization with feeds on demand we observed an elevated fluid intake of 260 ml/kg/day and a maximum urine output of 8.9 ml/kg/h.
Laboratory data demonstrated hypernatraemia (Na 160 mmol/L), hyperchloraemia (Cl 127 mmol/L) and a high total serum protein. The serum osmolality was elevated (339 mOsm/kg) while urine analysis showed a low to normal osmolality of 209 mOsm/kg with a low sodium concentration (<20 mmol/L). Clinical and laboratory investigations did not disclose any other abnormalities.
An intravenous challenge test with 0.6 μg 1-deamino-8-D-arginine-vasopressin (dDAVP) was performed. Urine was collected for 6 h. The patient hourly received a fluid volume equal to that of the previous hour's urine production. The patient did not reveal a decrease in urinary volume (hourly urine production remained at ≥7.5 ml/kg), and urine osmolality remained <160 mmol/L despite mild hypernatraemia (153 mmol/L) and hyperosmolality (339 mosmol/L). During the course of the test, serum osmolality and serum sodium concentration remained unchanged. Based on the lack of response to dDAVP, central diabetes insipidus was excluded. An increased serum ADH level of >30 ng/L before the dDAVP test supported the diagnosis of CNDI. Coagulation factor VIII and von Willebrand factor did not rise within 4 h after dDAVP administration, indicating impaired functional integrity of AVPR2.
Oral treatment with indomethacin (1.2 mg/kg/day), hydrochlorothiazide (1.6 mg/kg/day) and amiloride (0.15 mg/kg/day) was started as soon as the diagnosis was established. Urine volume and laboratory parameters normalized and a normal weight gain was achieved.
At 2 and a half years of age, the patient has been treated with a low sodium diet (maximum sodium administration 2 mmol/kg/day), hydrochlorothiazide (1.3 mg/kg/day), amiloride (0.1 mg/kg/day) and indomethacin (1.2 mg/kg/day). A normal constant weight gain and a favourable psychomotor development have been observed.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [6, 'months'], 'weight': [5710.0, 'g'], 'sex': 'Male', 'Sodium': [160.0, 'mmol/L']}",0.48943,0.46496,0.5139,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 6 months old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 5710.0 g so this converts to 5710.0 lbs * kg/1000 g = 5.71 kg. The concentration of sodium is 160.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 5.71 * (160.0/140 - 1) = 0.48943 L. The patient's free body water deficit is 0.48943 L."
5985,38,Free Water Deficit,lab test,decimal,pmc-6174724-1,Extracted,"A 38-year-old male was referred to our clinic with symptoms of abdominal pain, nausea, vomiting, and fever for a month. During this period, the patient's weight had reduced by 10 kg. An ultrasound study was requested reporting a bilateral mass corresponding to the adrenal region. In the next step, an abdominopelvic CT scan with and without oral and intravenous contrast was performed, which revealed two adrenal masses of 115 mm × 66 mm and 65 mm × 43 mm in the right and left adrenal glands, respectively. There was no retroperitoneal lymphadenopathy [].
At the time of admission, primary physical examination and basic laboratory tests were normal. Blood pressure and temperature were within normal limits and no peripheral lymphadenopathy was detected. On physical examination, the thyroid gland was normal on palpation and no skin hyperpigmentation was seen. Laboratory tests revealed the following results: white blood cell (WBC) count = 7.5 × 109/L, hemoglobin (Hb) level = 10.8 g/dL, platelet (PLT) count = 179 × 109/L, erythrocyte sedimentation rate (ESR) =6 mm/h, serum creatinine = 1.2 mg/dL, serum sodium = 144 mEq/L, and serum potassium = 4.7 mEq/L; a urine analysis was normal.
Around 10 days after the initial tests, additional tests were performed for the patient; their results were as follows: WBC = 2.4 109/L, Hb = 7.6 g/dL, PLT = 60 × 109/L, serum sodium = 125 mEq/L, and potassium = 5.5 mEq/L. Cortisol, metanephrine, normetanephrine, and vanillylmandelic acid of the 24-h urine output were 39 μg, 46 μg, 60 μg, and 1.6 μg, respectively. Morning serum cortisol was normal (13.5 μg/dL) whereas the adrenocorticotropic hormone level was elevated (90 pg/mL).
Furthermore, lactate dehydrogenase level was 893 U/L and ESR had risen to 63 mm/h, which demonstrated the rapid progression of the disease and indicated the onset of adrenal insufficiency. aA biopsy sample was taken from the aforementioned masses under the guide of CT scan. This CT scan, done 20 days after the first CT scan showed rapid progression of the disease with further enlargement of the adrenal masses along with retroperitoneal lymphadenopathy [].
The Pathological examination of the biopsy reported high-grade B-cell lymphoma with immunohistochemistry positive for CD20 and negative for CK and CD3. Therefore, we decided to perform bone marrow biopsy and chest CT scan. The bone marrow biopsy was negative for malignancy, but the chest CT scan revealed a few lymph nodes. During this evaluation study, the patient's condition deteriorated significantly, so after the pathological diagnosis, chemotherapy was immediately initiated for the patient by an oncologist; the patient was treated with six cycles of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) chemotherapy. The CT scan performed 2 months after the end of R-CHOP chemotherapy showed regression of the bilateral adrenal mass [], and subsequently, the patient's general condition improved significantly.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [38, 'years'], 'weight': [10.0, 'kg'], 'sex': 'Male', 'Sodium': [125.0, 'mEq/L']}",-0.64286,-0.61072,-0.675,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 38 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 10.0 kg. The concentration of sodium is 125.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 125.0 mEq. To convert from 125.0 mEq to mmol, convert from mEq to mmol. The compound 125.0 has a valence of 1, and so divide the valence by the value of mEq to get, 125.0 mEq/(1 mEq/mmol) = 125.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 125.0 mEq sodium/L converts to 125.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 10.0 * (125.0/140 - 1) = -0.64286 L. The patient's free body water deficit is -0.64286 L."
5986,38,Free Water Deficit,lab test,decimal,pmc-5348859-1,Extracted,"A 9-day-old breastfed boy infant was admitted to the emergency department with chief complaints of poor feeding, decreased urine output, and lethargy. In general appearance, the infant was lethargic with sunken eyes, dried mucosa, and reduced skin turgor. He had no urine output within previous 12 h. Laboratory studies disclosed the following serum values: Na: 195 mEq/L, potassium (K): 5.3 mEq/L, calcium (Ca): 8.5 mEq/L, blood urea nitrogen: 184 mg/dL, serum creatinine (Cr): 1.8 mg/dL, birth weight: 3140 g, and current weight: 2340 g (25% weight reduction within 9 days). During admission, the infant was given two bolus of 15 mL/kg N/S solution during 1 hour. After emergent phase, the serum Na became 193 mEq/L. Then, 200 ml of half saline was infused over 10 h which resulted in convulsion. At the time of the convulsion, his Na concentration was 178 (it means 17 mEq/L reductions in Na concentration during 10 h).
Treatment of hypernatremic dehydration consists of emergent and rehydration phases. In this case, both were corrected faster than standard rate. Subsequently, the infant experienced the complications of fast correction of hypernatremia. We assessed this case again and found a novel equation. This equation can be used in similar situations. In the following section, we discussed on the treatment of hypernatremia in general and in the mentioned case.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [9, 'days'], 'weight': [2340.0, 'g'], 'sex': 'Male', 'Sodium': [195.0, 'mEq/L']}",0.55157,0.52399,0.57915,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 9 days old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 2340.0 g so this converts to 2340.0 lbs * kg/1000 g = 2.34 kg. The concentration of sodium is 195.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 195.0 mEq. To convert from 195.0 mEq to mmol, convert from mEq to mmol. The compound 195.0 has a valence of 1, and so divide the valence by the value of mEq to get, 195.0 mEq/(1 mEq/mmol) = 195.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 195.0 mEq sodium/L converts to 195.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 2.34 * (195.0/140 - 1) = 0.55157 L. The patient's free body water deficit is 0.55157 L."
5987,38,Free Water Deficit,lab test,decimal,pmc-5004031-1,Extracted,"A previously healthy 74-year-old Japanese female was hospitalized with unknown fever and high C-reactive protein (CRP) values in December 2015. On admission, she was 155 cm in height and 59.2 kg in weight and had temperature of 37.6°C, blood pressure of 118/64 mmHg, pulse rate of 71/min, respiration rate of 18/min, and SpO2 of 94% at room temperature. Physical examination revealed no specific findings. After admission, she developed herpangina-like aphthous ulcers at the palate, when significant monocytosis (absolute monocyte counts >5,000/μL) was first noted; however, monocytosis fluctuated (). Thereafter, a CT scan of the abdomen showed localized thickening of the intestinal wall () and colonofiberscopy (CF) revealed the presence of multiple ovoid punched-out ulcers at the terminal ileum and aphthous lesions at the ascending colon (). In addition, the patient also developed multiple erythematous rashes on her right thigh (). Given the diagnostic criteria of BD [], the rash was not typical erythema nodosum but was thought rather to be acneiform eruption. Ophthalmological studies showed no evidence of BD signs. Taken together, BD was suspected in this patient from fulfilling 2 major and 1 minor clinical features required in the diagnosis of BD []. Thereafter, from the second week of admission, the patient again developed a significant monocytosis (from 15% to >70% in PB, with absolute monocyte counts to a maximum of 23,900/μL) associated with urinary infection at the 5th week of admission (). These findings with subsequent bone marrow study confirmed a diagnosis of AMoL (Figures and ).
Blood results at the 5th week of admission, when AMoL was diagnosed, were as follows: white blood cells (33,200/μL) containing 15% blasts, 21% promonocytes, 19% mature monocytes, 1% myelocytes, 10% neutrophils, and 33% lymphocytes (). Flow cytometric data of a major cell population in PB were as follows: CD13+ (86.4%), CD14+ (80.0%), CD33+ (97.4%), CD34+ (0.8%), CD41+ (44.8%), CD56+ (32.4%), and HLA-DR+ (97.0%). Mature lymphocytes in PB consisted of mostly T cells (approximately 90%), whose markers were CD4+ (59.2%) and CD8+ (27.4%), respectively. By contrast, the hypercellular BM consisted of 33.2% blasts, 15.0% promonocytes, 33.6% mature monocytes, 6.8% granulocytes, 1.4% lymphocytes, 2.0% plasma cells, and 8.0% erythroblasts with an M/E ratio of 0.85 (). No significant abnormalities indicating MDS were noted. Flow cytometric results of the major cell population in BM were as follows: CD13+ (38.3%), CD14+ (26.0%), CD33+ (97.5%), CD41+ (45.5%), CD34+ (2.3%), CD56+ (38.0%), and HLADR+ (80.9%). Mature lymphocytes in BM were mostly T cells (approximately 90%) with a CD4/CD8 ratio of 0.54. Myeloperoxidase positive cells accounted for 10% of the mononuclear cells present in both the PB and BM, while alpha-naphthyl butyrate esterase (inhibited by sodium fluoride) positive cells comprised more than 60% of cells in both the PB and BM. These findings were compatible with the diagnostic criteria of AMoL (FAB M5b) []. In addition, the karyotypes of PB and BM cells were both 46, XX [20/20]. The other blood chemistry was uneventful except for high levels of CRP (15.75 mg/dL), with aspartate aminotransferase 13 U/L, alanine aminotransferase 14 U/L, lactate dehydrogenase 205 U/L, total bilirubin 0.76 mg/dL, total protein 6.9 g/dL, albumin 2.9 g/dL, blood urea nitrogen 23.4 mg/dL, creatinine 1.61 mg/dL, sodium 135 mmol/L, potassium 3.6 mmol/L, chlorine 97 mmol/L, and calcium 8.0 mg/dL.
Since the diagnosis of AMoL (FAB M5b) was confirmed, the biopsied tissues showing BD-like illness were reevaluated with immunostaining except for stomatitis lesions and were proved to have leukemic cell infiltrations. The intestinal ulcer-associated granulation tissues with vascularization and infiltration of cells were positive for lysozyme, CD13, CD14, and CD33 (Figures and ). Also the histopathology of skin rash showed that the infiltrating cells were positive for lysozyme, CD13, CD14, and CD33 (Figures and ). These findings confirmed that the lesions primarily thought due to BD-like illness were in fact AMoL-related. In addition, HLA-typing, performed to ascertain whether the patient had BD-related HLA types, detected the presence of A2/A24 and B52/B55 but not the BD-related HLA-B51 or B5 alleles [, ]. As shown in , the patient was initially treated with adalimumab for BD-like illness, following the successful report for a case of intestinal BD with trisomy 8 MDS by Kimura et al. []; however, after AMoL was confirmed, she was transferred to another hospital for intensive chemotherapy as a very high-risk patient.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [74, 'years'], 'weight': [59.2, 'kg'], 'Sodium': [135.0, 'mmol/L']}",-0.95143,-0.90386,-0.999,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 74 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 59.2 kg. The concentration of sodium is 135.0 mmol/L. Plugging in these values into the equation, we get 0.45 * 59.2 * (135.0/140 - 1) = -0.95143 L. The patient's free body water deficit is -0.95143 L."
5988,38,Free Water Deficit,lab test,decimal,pmc-6369598-1,Extracted,"An 8-month-old boy, human immunodeficiency virus (HIV) exposed but HIV deoxyribonucleic acid polymerase chain reaction negative at 6 weeks, presented to Princess Mar ina Hospital (the main public referral hospital in Gaborone, Botswana) with a 3 weeks’ history of vomiting after feeds. Vomiting was projectile, nonbilious, and nonbloody. It was not associated with diarrhea, but there was a 1-month history of intermittent episodes of passing small amounts of very hard stools every three or more days. There was no history of fever, shortness of breath, or cough.
He was born at term by uncomplicated spontaneous vaginal delivery with a birth weight of 3355 g and Apgar scores 9, 10, and 10 at 1, 5, and 10 min, respectively. He was not dysmorphic. His mother's Venereal Disease Research Laboratory result was negative at antenatal booking, and he had never received antibiotics.
His mother was HIV infected, and hence, he received single-dose nevirapine after birth followed by zidovudine for 4 weeks. Postnatally, he was a well baby and was discharged from hospital on day 2 of life. He was exclusively formula fed. His child vaccine card showed suboptimal growth between −2 and −3 Z-scores on the World Health Organization weight-for-age growth chart. At 7 months, he had a bout of acute gastroenteritis followed by weight loss, and he then plotted below −3 Z-scores for weight-for-age. This weight decline coincided with developmental regression in language and gross motor milestones. At 6 months, he was reported to have been attempting single words and sitting without support, but from 7-month onward, he could no longer sit or speak any words. His immunizations were up-to-date.
On physical examination, he was emaciated and irritable. He had no pallor, jaundice, or lymphadenopathy. He had no dysmorphic features or any signs of respiratory distress. His vital signs were axillary temperature 36.5° C, respiratory rate 40/min, and pulse rate 148/min. His anthropometric measurements revealed weight 3.7 kg, length 59 cm, head circumference 39 cm, weight for age −3 Z-score, weight for length −3 Z-score, and length for age −3 Z-score.
He had a soft, grossly distended abdomen. There were no distended veins, scars, or hepatosplenomegaly. Bowel sounds were present but reduced. There was no palpable mass in the epigastrium. Repeated abdominal examination after feeding revealed a mass in the left upper quadrant that appeared to move to the right in a peristaltic fashion. It measured about 4 cm in diameter approximately. Examination of other systems was unremarkable.
Arterial blood gas showed a metabolic alkalosis with PH 7.49, pCO2 37 mmHg, pO2 89 mmHg, standard bicarbonate 28 mmol/L, and base excess +4.6. Serum urea and electrolytes were essentially normal with sodium 135 mmol/L, potassium 4.5 mmol/L, chloride 94.4 mmol/L, creatinine 20 mmol/L, and urea 4.6 mmol/L. The full blood count was normal with white blood cells 6.9 × 103/mL, hemoglobin 11.3 g/dL, mean cell volume 80 fL, and platelets 218 × 103/mL.
Erect and supine abdominal X-rays showed a distended gastric bubble with dilated loops of bowel, and a granular pattern suggestive of fecal impaction in the colon. Abdominal ultrasound scan showed a gaseous abdomen with feces in the colon. No other abdominal masses were appreciated.
A barium swallow and meal showed the unrestricted passage of contrast in the esophagus but delayed and restricted passage through the pylorus into the duodenum, suggestive of a partial but significant gastric outlet obstruction [Figures and ]. We thus entertained the diagnosis of infantile hypertrophic pyloric stenosis (IHPS).
The child underwent a laparotomy. There was a soft band of tissue crossing from the porta hepatis to the transverse colon which was constricting the pylorus. The pylorus was so severely stenosed that a size 8 feeding tube could not pass through the pyloric sphincter. The band of tissue was so tight that the gastric antrum was partly incorporated into the inferior surface of the left lobe of the liver [Figures and ]. The pylorus and gastric antrum were freed after ligating the constricting band of tissue.
Postoperatively, his recovery was uneventful. He was later successfully followed up in our nutritional rehabilitation unit until the malnutrition resolved.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [8, 'months'], 'weight': [3.7, 'kg'], 'Sodium': [135.0, 'mmol/L']}",-0.07929,-0.07533,-0.08325,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 8 months old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 3.7 kg. The concentration of sodium is 135.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 3.7 * (135.0/140 - 1) = -0.07929 L. The patient's free body water deficit is -0.07929 L."
5989,38,Free Water Deficit,lab test,decimal,pmc-7407036-1,Extracted,"A 22-year-old female (height 1.72 cm, weight 40 kg, and body mass index 13.5 kg/m2) was admitted to our emergency room while receiving cardiopulmonary resuscitation for 45 minutes. Rhythm upon arrival was ventricular fibrillation. Since return of spontaneous circulation could not be achieved by all medical measures provided, the patient was immediately transferred to the catheter laboratory. Extracorporeal cardiopulmonary resuscitation via venoarterial extracorporeal membrane oxygenation (va-ECMO) was established. Due to severe left ventricular (LV) dysfunction, an Impella® pump was added to ensure sufficient LV output. Subsequently, percutaneous coronary angiogram was performed and showed no coronary disease (). The patient's history was noticeable for anorexia nervosa (AN) with several hospitalizations for renutrition, at the last several months prior to emergency admission. During the last few days prior to sudden cardiac death and after excessive caloric restriction, our patient began to increase her caloric intake to improve her nutritional state to avoid complications at an upcoming doctor's appointment. Prior to admission, our patient was an outpatient; did not receive medical refeeding or preventive treatment with supplementation of vitamins, phosphorus, or micronutrients; and did not had a history of binge episodes.
Initial blood analysis showed a severe electrolyte disorder with potassium depletion (1.38 mmol), hypocalcemia (ionized calcium 1.75 mmol/l), hyponatremia (117 mmol/l), hypochloremia (54 mmol/l), hypophosphatemia (0.28 mmol/l), and hypoproteinemia (total protein 30.2 g/l; albumin 28.9 g/l). In addition, laboratory data indicated a high level of lactate (18 mmol/l) combined with a normal pH of 7.38. Initial sugar levels were elevated (blood glucose 430 mmol/l). The first performed echocardiogram confirmed severe LV dysfunction. In the electrocardiogram, a sinus tachycardia and prolongation of the corrected QT interval were detected (660 ms) (). Electrolytes were substituted. Transient anisocoria and simultaneous severe coagulopathy under va-ECMO therapy led to a cranial computed tomography (CT), showing small bilateral subdural hematoma (). Most likely, the patient had aspirated during resuscitation; therefore, calculated antibiotic therapy with ampicillin/sulbactam was given. After initiating inodilatative support with levosimendan, cardiac output significantly improved within the next 24 hours. The Impella® pump and va-ECMO were subsequently removed on day 3. After the patient's respiratory situation had stabilized, extubation took place on day 5. Neurological assessment 10 days after admittance showed a mild difference in reflexes such as vertical saccade. Cranial magnetic resonance imaging (MRI), performed on day 16, revealed unchanged small bilateral subdural hematoma (). Subsequent cardiac MRI performed after 2 weeks showed a recovered LV ejection fraction and no signs of myocarditis (). The patient was dismissed after 3 weeks of hospitalization without neurological deficit to a psychiatric care station for further treatment of AN.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [22, 'years'], 'weight': [40.0, 'kg'], 'Sodium': [117.0, 'mmol/L']}",-3.28571,-3.12142,-3.45,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 22 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 40.0 kg. The concentration of sodium is 117.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 40.0 * (117.0/140 - 1) = -3.28571 L. The patient's free body water deficit is -3.28571 L."
5990,38,Free Water Deficit,lab test,decimal,usmle-973,Extracted,"A 54-year-old man comes to the emergency department because of a 2-day history of increasingly severe abdominal pain, nausea, and bilious vomiting. His last bowel movement was yesterday and he has not passed flatus since then. He underwent appendectomy at the age of 39. He has psoriasis, hypertension, type 2 diabetes mellitus, and chronic back pain. He drinks two beers daily. He takes a topical corticosteroid, ramipril, metformin, and ibuprofen daily. He is 176 cm (5 ft 9 in) tall and weighs 108 kg (240 lb); BMI is 35.4 kg/m2. His temperature is 36.8°C (98.4°F), respirations are 15/min, pulse is 90/min, and blood pressure is 112/67 mm Hg. Examination shows thick, scaly, plaques over both elbows and knees. Abdominal examination shows three well-healed laparoscopic scars. The abdomen is distended and there are frequent, high-pitched bowel sounds on auscultation. Digital rectal examination shows an empty rectum. Laboratory studies show:
Hematocrit 44%
Leukocyte count 9,000/mm3
Platelet count 225,000/mm3
Serum
Na+ 139 mEq/L
K+ 4.1 mEq/L
Cl− 101 mEq/L
HCO3− 26 mEq/L
Glucose 95 mg/dL
Creatinine 1.1 mg/dL
Alkaline phosphatase 78 U/L
Aspartate aminotransferase (AST, GOT) 19 U/L
Alanine aminotransferase (ALT, GPT) 14 U/L
γ-Glutamyltransferase (GGT) 52 U/L (N=5–50 U/L)
Hemoglobin A1C 6.4%
Abdominal ultrasound shows nonpropulsive peristalsis of the small bowel.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'weight': [108.0, 'kg'], 'sex': 'Male', 'Sodium': [139.0, 'mEq/L']}",-0.46286,-0.43972,-0.486,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 54 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 108.0 kg. The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 108.0 * (139.0/140 - 1) = -0.46286 L. The patient's free body water deficit is -0.46286 L."
5991,38,Free Water Deficit,lab test,decimal,pmc-5361634-4,Extracted,"A 3-month-old Mestizo boy was admitted for a 2 day history of diarrhoea and vomiting, with a mean of nine watery stools and one episode of vomiting over the previous 24 h. He had not received any medications. On examination, the child was irritable, with sunken eyes and no tears, with dry oral mucosa and intense thirst. The patient had decreased skin turgor and presented abdominal distension with decreased peristalsis. Capillary refill was 4 s. Vitals signs were as follows: temperature, 37 °C; pulse, 145 beats min−1; respiration, 30 breaths min−1. His weight was 3.4 kg and length 55 cm. His weight-for-age, length-for-age and weight-for-length were less than the −3 z score and he was classified as severely wasted. The CBC reported: haemoglobin, 11.5 g dl−1; leukocytes, 23.9×103 µl−1; neutrophils, 16.8×103 µl−1; platelets, 622×103 µl−1. Electrolyte determination reported: Na, 130 mEq l−1; K, 2.5 mEq l−1. The patient was classified as having a fluid deficit of 5–10 % with moderate dehydration, and was assigned to receive plan B rehydration. He was administered two courses of ORS (WHO low-osmolarity ORS, same as Case 2), each at 100 mgkg−1 for 4 h and was discharged in good condition after 24 h. He was also given racecadotril (5 mg, three times daily) for 3 days and ampicillin (150 mg, four times daily) for 5 days. The antibiogram revealed that the E. coli strain was pansusceptible. The stool pattern was reported normal after 6 days from onset.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [3, 'months'], 'weight': [3.4, 'kg'], 'sex': 'Male', 'Sodium': [130.0, 'mEq/L']}",-0.14571,-0.13842,-0.153,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 3 months old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 3.4 kg. The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 3.4 * (130.0/140 - 1) = -0.14571 L. The patient's free body water deficit is -0.14571 L."
5992,38,Free Water Deficit,lab test,decimal,pmc-7042143-3,Extracted,"Patient 3 is a 66-year-old man with a history of catheter ablation of atrial fibrillation in January 2016, status post two electrical cardioversions in 2014 and 2015; coronary artery disease with percutaneous coronary angioplasty of the left anterior descendent artery in 2008; and hypertension and dyslipidaemia, but normal left ventricular function and no valvular abnormality as per the most recent echocardiogram. He was presented to the emergency room with palpitations. His height and weight were 185 cm and 77 kg, respectively. His blood pressure was 125/77 mmHg. His electrolytes were as follows: sodium 139 mmol/L, potassium 3.6 mmol/L, and calcium 2.06 mmol/l. His list of medications included bisoprolol 2.5 mg o.d., amlodipine 5 mg o.d., pantoprazole 20 mg o.d., ramipril 5 mg o.d., rivaroxaban 20 mg o.d., and atorvastatin 10 mg o.d. Electrocardiogram on admission revealed atrial fibrillation. He received 300 mg of amiodarone intravenously before cardioversion. shows his ECG prior to cardioversion. He received one DC shock at 200 J and was reverted back to sinus rhythm. shows his ECG during cardioversion. shows his ECG after electrical cardioversion. The patient had a recurrence of atrial fibrillation 5 months after cardioversion and a redo catheter ablation for atrial fibrillation afterwards. Since then, no documented recurrence of atrial fibrillation but at least one episode of palpitation lasting 1 h was noted. He is currently on long acting flecainide 200 mg o.d., bisoprolol 2.5 mg o.d., and rivaroxaban 20 mg o.d.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [66, 'years'], 'weight': [77.0, 'kg'], 'sex': 'Male', 'Sodium': [139.0, 'mmol/L']}",-0.275,-0.26125,-0.28875,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 66 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 77.0 kg. The concentration of sodium is 139.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 77.0 * (139.0/140 - 1) = -0.275 L. The patient's free body water deficit is -0.275 L."
5993,38,Free Water Deficit,lab test,decimal,pmc-7970398-1,Extracted,"A 78-year-old man (weight 76 Kg) with a history of chronic kidney disease, arterial hypertension and recurrent deep vein thrombosis was admitted to our hospital for acute respiratory and renal failure. He was on therapy with warfarin, amlodipine 5 mg once a day, atorvastatin 20 mg once a day, cinacalcet 30 mg three times a week, calcium and vit D supplementation. He described generalized malaise, muscle ache and fever the week before. In the emergency department, the patient’s temperature was 37.8 °C, he had sinus tachycardia with 108 beats per minute, blood pressure was 190/90 mm Hg, respiratory rate 18 breaths per minute, and oxygen saturation 97% on room air. Laboratory findings showed a hypocapnic hypoxemia with metabolic acidosis, serum creatinine was 9 mg/dL, sodium 126 mmol/L, kalium 5.7 mmol/L, INR was 8.37. Warfarin was stopped and he received intravenous Vit K. A diagnosis of viral pneumonia was based on computed tomographic (CT) scan and the patient was transferred to ICU. A nasopharyngeal swab for SARS-CoV-2 was performed but was negative, nevertheless a treatment based on hydroxychloroquine, azithromycin, steroids, tocilizumab was started given to the high COVID-19 suspicion. During the following two days, INR decreased from 3.04 to 1.5, renal function did not improve and hemodialysis was started three days after admission with the insertion of a catheter in the right femoral vein. One bolus dose of 5000IU sodium UFH was used during the first dialysis treatment (Day 0, platelet count: 305×103/μL). The trend of platelet count is shown in Figure. 1 On day 1 he received one dose of 40 mg enoxaparin. On day 2, haemoglobin started to decrease and heparin was stopped. On day 4 hemoglobin was 8.5 g/dL and melena were observed. On day 5, hemoglobin was 7.8 g/dL, platelet count was 219×103/μL and he underwent a transfusion of packed red blood cells. From day 5 to day 9, no bleeding was observed and haemoglobin values were stable. On day 10, platelet count was 153×103/μL, the femoral catheter was removed, and 5000IU calcium heparin subcutaneously twice a day was started. As shown in the figure, the platelet count further decreased: on day 17 platelet count was 49×103/μL, calcium heparin was stopped and HIT was suspected. The pretest clinical score (4 T’s) for the diagnosis of HIT was 4 (viral pneumonia and tocilizumab as a possible cause for thrombocytopenia) and the patient was investigated for a diagnosis of HIT. An IgG specific chemiluminescence test for heparin-PF4 antibodies (AcuStar; HIT-IgGPF4-H) was positive (9.44 U/ml). The presence of HIT could not be confirmed by a platelet aggregation test because the platelet aggregation test is no longer available in the Bologna area. On day 18 (platelet count 41×103/μL), he complained of right lower extremity pain, a whole leg ultrasound showed a right common femoral DVT (4T’s score 6) and argatroban was started. During argatroban treatment, platelet increased: from 51×103/μL on day 19 to 267×103/μL on day 31 and no recurrent thrombotic event or bleeding complication was observed. The patient was discharged on warfarin. In ICU, the patient required 48 hours of non-invasive ventilation, a nasopharyngeal swab for SARS-CoV-2 was repeated and the RT-PCR for SARS-CoV-2 was positive; on day 14, serological test showed positive IgG and IgM against SARS-CoV-2. Thus, the diagnosis of acute renal failure and pneumonia due to SARS-CoV-2 infection was confirmed. When he was discharged, serum creatinine was 6.14 mg/dL, sodium 137 mmol/L, kalium 5 mmol/L, INR 2.7. During the 12-week follow-up by our anticoagulation clinic, there were neither thrombotic nor bleeding events.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [78, 'years'], 'weight': [76.0, 'kg'], 'sex': 'Male', 'Sodium': [126.0, 'mmol/L']}",-3.8,-3.61,-3.99,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 78 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 76.0 kg. The concentration of sodium is 126.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 76.0 * (126.0/140 - 1) = -3.8 L. The patient's free body water deficit is -3.8 L."
5994,38,Free Water Deficit,lab test,decimal,pmc-7811210-1,Extracted,"An 18-year-old healthy non-smoking Japanese male ingested 60 tablets of sleepiness-prevention medicine (containing a total of approximately 6.0 g caffeine) in a suicide attempt. Eighty minutes later he was transferred to the emergency department of our hospital because of complaints of nausea and headache. In his past social history, he got maladjustment to high school since he hit his friend and was suspended from school for ten days by principal. Although no personal and family history of psychiatric illness was noted, a scar of wrist cutting was observed. On arrival, his vital signs included Glasgow Coma Scale of 15, his blood pressure of 152/82 mmHg, pulse rate of 139 beats/min, respiratory rate of 22/min, oximetry of 100% on room air, and body temperature of 36.8 °C. Pertinent findings on physical examination included body weight of 58.8 kg, clear breath sounds and a regular, rapid heart rhythm with systolic ejection murmur on auscultation. Electrocardiogram showed sinus tachycardia at a rate of 139 beats/min with QT prolongation (QTc 617 ms) (Fig. a). Arterial blood gas analysis showed lactic acidosis (lactate 3.8 mmol/L). The other laboratory data were as follows: white blood cells 11,120/mcL; hemoglobin 17.4 g/dL; platelets 24.5×104/mcL; blood urea nitrogen 13 mg/dL (4.6 mmol/L); serum creatinine 0.73 mg/dL (64.5 mcmol/L); sodium 142 mmol/L; potassium 2.6 mmol/L; chloride 103 mmol/L; creatinine phosphokinase 126 IU/L (Table ). We observed nothing special on systemic computed tomography (CT) scan. After arrival, we performed gastric lavage of 1600 mL and administered 30 g of activated charcoal through a nasogastric tube. We administered total amount of 20 mmol potassium at the rate of 20 mmol/hour, and the patient was admitted to an intensive care unit. As he was agitated, with a Richmond Agitation-Sedation Scale score of + 2 as a symptom of acute caffeine poisoning, we immediately started administration of dexmedetomidine (maximum 0.7 µg/kg/hour) (Fig. ). Seven hours later, serum potassium and lactate normalized to 3.7 mmol/L and 1 mmol/L, respectively, and QTc also normalized (Fig. b). Administration of dexmedetomidine was stopped at 12 hours after dexmedetomidine infusion because he got quiet. Because he still had suicide ideation, he was hospitalized in psychiatric ward for medical protection. He said he just has been thinking of dying since high school and did not talk anymore. He was gradually free from suicide ideation and was discharged on his third day in hospital.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [18, 'years'], 'weight': [58.8, 'kg'], 'sex': 'Male', 'Sodium': [142.0, 'mmol/L']}",0.504,0.4788,0.5292,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 18 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 58.8 kg. The concentration of sodium is 142.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 58.8 * (142.0/140 - 1) = 0.504 L. The patient's free body water deficit is 0.504 L."
5995,38,Free Water Deficit,lab test,decimal,pmc-4421258-1,Extracted,"A 47-year-old woman was evaluated at the emergency department for a lithium overdose. Four hours before admission she had deliberately ingested for suicidal purposes 40 tablets of lithium carbonate (300 mg of lithium carbonate in each tablet corresponding to 8.12 mEq of lithium) and 20 ml of a 0.25% clonazepam solution. She had started lithium treatment for a bipolar disorder 2 days before, as prescribed by her psychiatrist.
On arrival the patient was alert with psychomotor slowing. A neurological examination showed alternating bouts of agitation and lethargy, along with fine tremors and hyperreflexia, but no focal deficits. The EKG documented sinus bradycardia with 50 bpm but no ST segment or T-wave abnormalities, blood pressure was 95/50 mmHg and arterial oxygen saturation 92%. Serum creatinine was 0.8 mg/l, sodium 138 mEq/l and potassium 4.8 mEq/l; liver function tests and blood count were normal. Diuresis was <30 ml/h. Initially, serum lithium levels were 1.62 mEq/l but increased up to 2.77 mEq/l 8 h later, despite initial treatment with intravenous crystalloids and gastric lavage. The patient remained oliguric and became more confused while being affected by nausea and vomiting; she was then transferred to the renal ICU for evaluation and monitoring.
At ICU admission the patient was lethargic and complained of intense nausea; pulse was 52 bpm (sinus bradycardia), blood pressure 98/50 mmHg; during the preceding 12 h she had passed 360 ml of urine only. Body weight was 74 kg (usual BW 76 kg). Blood gas analysis showed pH 7.40, PaCO2 36 mmHg, PaO2 74 mmHg and bicarbonate 21 mEq/l; serum sodium was 137 mEq/l, potassium 4.5 mEq/l, chloride 105 mEq/l and creatinine 1.2 mg/dl.
We started SLED using a double lumen 12 F, 16 cm central venous catheter positioned in the right jugular vein, the dialysis machine AK 200S Ultra (Gambro, Italy) and the F8HPS polysulfone filter (KUf 18 ml/h/mmHg, KoA urea 848 ml/min, Fresenius, Italy) with a blood flow of 200 ml/ min and countercurrent dialysate flow of 300 ml/min []. A BW increase of 1.5 kg was programmed during the 8-h treatment. Blood samples were collected every 2 h during SLED for serum lithium level measurement; urine was also collected.
Lithium levels during and after SLED are shown in Figure . During SLED the urea serum level decreased by 65% and lithium serum levels by 86%. Diuresis increased sharply during treatment; nonetheless, the lithium amount recovered in the urine was 5.8 mEq only. SLED was completed safely within the prescribed time without anticoagulants. The patient fully awoke recovering a normal mental status within the first 4 h of treatment. Having completely recovered from the intoxication the patient was transferred into a psychiatric facility 3 days after admission.
For the purpose of data analysis, differential equations describing a two-compartment open pharmacokinetic model were fit to lithium serum concentration-time data. SLED clearance and renal clearance were modelled using indicator variables. With the aim of modelling the transient oliguria at admission, the indicator variable for renal clearance was arbitrarily set to 0 at the start of the observation period and to 1 at the time when lithium decreased to levels <1.6 mEq/l (i.e. after ∼2 h of SLED). The pharmacokinetic model was fit to the data using the iterative non-linear weighted least-squares estimator in the Adapt II software package (Biomedical Simulations Resource, University of Southern California, Los Angeles, CA, USA) [].
Observed and predicted lithium concentrations by the pharmacokinetic model are shown in Figure . The results of the analysis can be interpreted as follows: the progressive increase in lithium levels over the first 24 h, up to 4 mEq/l, can be accounted for by the transient oliguria detected after the admission; the high lithium clearance, achieved over the course of SLED treatment, caused a dramatic drop in lithium serum concentration. The rebound of lithium detected after the end of SLED, which can be explained by redistribution from the peripheral compartment, was only mild, being dampened by the recovery of renal function.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [47, 'years'], 'weight': [74.0, 'kg'], 'sex': 'Female', 'Sodium': [137.0, 'mEq/L']}",-0.79286,-0.75322,-0.8325,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 47 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 74.0 kg. The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 74.0 * (137.0/140 - 1) = -0.79286 L. The patient's free body water deficit is -0.79286 L."
5996,38,Free Water Deficit,lab test,decimal,pmc-6452601-1,Extracted,"He was born on 13th February 2006, at 37 weeks of gestation to a 39-year-old gravida 6 para 6 mother after uncomplicated twin pregnancy. The parents were second degree cousins of Saudi origins. He has 2 elder brothers and 3 sisters, all are alive and healthy. His birth weight was 2.0 kg, body length was 46 cm, and head circumference was 32 cm. He was discharged with his mother in good condition after 3 days of admission to the nursery for observation.
At the age of 18 days, he was presented to the emergency department with history of vomiting, poor feeding, and decreased activity with failure to thrive. On physical examination, his weight was 1.66 kg, blood pressure (BP) was 67/51 mmHg, heart rate was 160/min, temperature was 36.2°C, and respiratory rate (RR) was 58/min. He was dehydrated, not dysmorphic with no evidence of hyperpigmentation. Normal systemic examination, with normal male genitalia ().
He was admitted to neonatal intensive care unit with impression of sepsis. Laboratory tests showed hyponatremia 128 mmol/L with hyperkalemia 6.2 mmol/L. Septic workup was carried out and were awaited. He was managed with intravenous fluids and antibiotics. He was noticed to have persisted hyponatremia and hyperkalemia, therefore endocrine consultation was requested. A provisional diagnosis of congenital adrenal hyperplasia was made as it is the most common cause of salt wasting at this age group. His endocrinological data revealed unelevated adrenocorticotropic hormone (ACTH), serum aldosterone low-normal while plasma renin was very high. Adrenocorticotropic hormone stimulation test was carried out with 0.25 mg synthectin which showed normal cortisol response at 60 minutes. Seventeen hydroxyprogesterone, dehydroepiandrosterone sulfate (DHEAS), and testosterone were normal. Chromosomal study showed 46 XY ().
These results ruled out CAH. He was diagnosed to have isolated aldosterone deficiency, and managed with fludrocortisone and sodium chloride orally with excellent response. He was followed up in outpatient clinic regularly and was maintaining normal serum sodium and potassium. He was thriving well ().
At 18 months of age, he was noticed to have increased pigmentation specially the lips and gum, but was thriving well. Glucocorticoid deficiency was suspected. Urgent ACTH stimulation test was carried out with 0.25 mg synthectin. Basal ACTH >2000 pg/ml. Serum cortisol failed to rise in response to ACTH at 60 min. Seventeen hydroxyprogesterone was normal. Testosterone and DHEAS were normal (). He was diagnosed to have primary adrenal insufficiency managed with hydrocortisone and fludrocortisone orally. At 18 months of age ultrasound done, showed right testis at the right inguinal area. He underwent orchidopexy for right undescended testis ().
He was followed up regularly in outpatient department showing normal ACTH and serum electrolytes, and was thriving well. His last visit was at the age of 12 years and 3 months (). His height was 134 cm (just below 3rd centile), his weight was 29 kilograms (below 10th centile).
He is now 12 years and 3 months old boy, his birth weight was 1.8 kg. He was discharged with his mother in good condition. He was growing normally and was not having any significant illness.
At the age of 9 years and 6 months, his mother brought him to endocrine clinic accompanying his twin-A brother. The mother complained that she noticed him to have progressive weight loss, fatigue, decreased activity, and progressively increasing generalized body pigmentation, which was noticed for 3 months. There was no history of vomiting, abdominal pain, or change in bowel habit. There was no history of preceding infection. On examination, he was alert and conscious. The Glasgow Coma Scale is 15/15, lethargic, dehydrated with generalized marked hyperpigmentation. The body weight was 18 kg (below 3rd centile), the height was 122 cm (below 5th centile). His temperature was 36.5°C, heart rate was 109/min, BP was 104/59 mmHg, RR was 36/min, and oxygen saturation was 100%. Systemic examination was normal except for right undescended testis (). He was admitted to Pediatric Intensive Care Unit with the impression of adrenal crisis due to adrenal insufficiency. He was managed with intravenous hydrocortisone, intravenous normal saline, kayexalate, and fludrocortisone. Orchidopexy was carried out later ().
As his twin-A brother was diagnosed to have primary adrenal insufficiency, AHC was suspected and blood samples for gene study were sent for both of them which proved DAX-1 mutation. After 2 months of hydrocortisone replacement the ACTH was 45.37 pg/mL. At 12 years and 3 months of age his wight was 32 kg (above 10th centile), and his height was 135 cm (3rd centile) ().
Both brothers are now on oral hydrocortisone and fludrocortisone replacement therapy.
They are thriving well, repeated hormonal evaluation, particularly serum ACTH was performed and is maintained within the normal reference range. Both of them have normal penile length, and Tanner stage 1 for testis and pubic hair.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [12, 'years'], 'weight': [32.0, 'kg'], 'sex': 'Male', 'Sodium': [128.0, 'mmol/L']}",-1.64571,-1.56342,-1.728,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 12 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 32.0 kg. The concentration of sodium is 128.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 32.0 * (128.0/140 - 1) = -1.64571 L. The patient's free body water deficit is -1.64571 L."
5997,38,Free Water Deficit,lab test,decimal,pmc-3008953-1,Extracted,"A 23-year-old female was referred from the Urology clinic as a case of solitary pelvic kidney and azotemia. She had history of primary amenorrhea, recurrent urinary tract infections and recent onset hypertension. Examination revealed her to be of average built (body weight of 62 kg and height of 168cms), euvolemic, with no pallor, BP- 110/70 mm of Hg (on medication), and no gross skeletal abnormality or hearing defects. Her cardiovascular, abdominal and respiratory examination was normal. She had feminine body features. Her gynecological examination showed a small vaginal pouch of about 2.5 cm ending blindly. There was no family history of any gynecological or renal abnormalities.
Investigations showed hemoglobin 117g/dL, WBC count- 7.5×103/dmm3, platelets - 3.55×109/mm3, urea-4.3 mmol/L, Creatinine 2mg/dl, albumin - 3.5g/dL, Calcium 9mg/dl, phosphorus- 6.5 mg/dL, sodium - 140 mmol/L, potassium- 4.8 mmol/L, PTH- 29 pmol/L. Urine examination showed 2+ proteins, leucocytes 4-6/HPF, no RBCs, 24-hour urinary protein of 1.2 gram and a creatinine clearance of 38ml/min (24-hour urinary creatinine estimation). Her hormonal profile was within normal limits. Detailed ultrasound revealed left kidney not localized, a 9.5 cm right pelvic kidney, with increased echotexture, loss of cortico-medullary differentiation, few cortical cysts and mild hydronephrosis Uterus was not seen but both ovaries were present []. A Magnetic Resonance Imaging (MRI) scan revealed solitary pelvic kidney in relation to right internal iliac vessels and gynecological abnormalities were confirmed [Figures –]. Tc 99 DMSA scan showed a poorly outlined right pelvic kidney showing nonhomogenous tracer uptake by functional parenchymal tissue. Left kidney was not visualized. A cystoscopy done by urologists prior to her referral had shown only right ureteric orifice and absent left ureteric orifice. Genetic study revealed 46 XX karyotype.
The features are consistent with type 2 MRKH syndrome with chronic kidney disease (CKD)-stage 3. Her CKD is likely because of chronic pyelonephritis secondary to anomalies of her urinary tract. She was counseled and is on regular follow-up in renal and gynecological clinics. Because of the social stigma she refused to be assessed by a plastic surgeon as was advised by her gynecologist. She is on conservative measures for her CKD but her follow-up in renal clinic is erratic.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [23, 'years'], 'weight': [62.0, 'kg'], 'sex': 'Female', 'Sodium': [140.0, 'mmol/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 23 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 62.0 kg. The concentration of sodium is 140.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 62.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
5998,38,Free Water Deficit,lab test,decimal,pmc-3415193-1,Extracted,"A 28-day-old phenotypic female infant was admitted to pediatric endocrinology clinic of Al-Zahra Hospital, affiliated to Isfahan University of Medical Sciences, because of poor weight gain and lethargy.
She was a full-term infant with a birth weight of 3250 gr (50th percentile), length of 51 cm (50th percentile) and head circumference of 34 cm (50th percentile).The patient had no perinatal problem. She was the 1st child of nonconsanguineous parents.
At the time of admission, she was lethargic without history of vomiting or diarrhea.
There was not any familial history of similar presentation or features endocrine disease.
She had no history of drug consumption except vitamin A+D.
She was lethargic, had depressed fontanele. She had mild dehydration and decreased skin turgor.
In skin examination, she had mild hyperpigmentation, including oral cavity.
External genitalia seemed normal female type with no ambiguity. There was not any abdominal or inguinal mass in abdominal examination.
Her body weight, length and head circumference were 2900, 51 cm and 33.5 cm, all of them were beneath the 5th percentiles.
Her blood pressure was 60/40 mmHg, respiratory rate was 39/min, pulse rate was 112/min and body temperature was 37.1°C.
The initial biochemical examinations were as follows; serum sodium, 129 meq/lit(N:135-145) ; serum potassium, 6.1 meq/lit (N: 3.5-5.5);blood sugar, 45 mg/dl; blood urea nitrogen, 73 mg/dl; serum creatinine, 0.5 mg/dL; C-reactive protein ,negative; blood culture, negative. The results of venous blood gas were as follows; pH: 7.3 HCO3=11.9 mmol/L, PCO2= 35 mmHg which represented metabolic acidosis.
The results of hormonal tests were as follows; Cortisol: 0.2 μg/dl, ACTH: >1000 pg/ml, 17 OHP: 0.3 ng/ml.
Ultrasonographic examination revealed small hypoplastic uterus (6*7*3 ml) or atretic ovaries and adrenal glands had normal sizes.
Clinical Course and Follow-up
First, the patient hydrated with normal saline. Thereafter, considering hyponatremia, hyperkalemia, metabolic acidosis and decreased cortisol level and increased ACTH level, lipoid CAH was diagnosed and replacement therapy with standard doses of glucocorticoid (hydrocortisone) and mineralocorticoid (fludrocortisone) and sodium chloride was initiated.
After replacement therapy, electrolyte abnormalities were corrected during first week and the patient was discharged from hospital with good clinical condition.
She recommended referring for follow up. During follow-up, she had good clinical condition, with normal laboratory results except for 17 OHP which was lower during the period.
At 6-years old, the patient referred with high blood pressure and adrenal insufficiency because of arbitrary drug discontinuation by mother. Renal Doppler ultrasonography and scan was performed which was normal. Regarding the recommendation of pediatric nephrologist fludrocortisone and sodium chloride was discontinued and treatment continued with hydrocortisone . Ultrasonography revealed the testicles in the abdominal cavity and uterus was not detected in pelvis. Orchiectomy was performed. Chromosome study showed 46XY pattern.
On her most recent visit at the age of 6 years, the patient had no hyperpigmentation. Her height was 110 cm (10-25th percentile), weight 23 kg (75-90th percentile). Her last laboratory tests results were as follows; Na: 142 mmol/l, K: 4.5 mmol/l ,17OHP: 0.1 ng/ml, ACTH: 22 pg/ml, Renin:50.8 pg/ml, Aldosterone: 105 pg/ml.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [28, 'days'], 'weight': [2900.0, 'g'], 'sex': 'Female', 'Sodium': [129.0, 'mEq/L']}",-0.13671,-0.12987,-0.14355,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 28 days old. This means the patient is 0 years old.
The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 2900.0 g so this converts to 2900.0 lbs * kg/1000 g = 2.9 kg. The concentration of sodium is 129.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 129.0 mEq. To convert from 129.0 mEq to mmol, convert from mEq to mmol. The compound 129.0 has a valence of 1, and so divide the valence by the value of mEq to get, 129.0 mEq/(1 mEq/mmol) = 129.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 129.0 mEq sodium/L converts to 129.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 2.9 * (129.0/140 - 1) = -0.13671 L. The patient's free body water deficit is -0.13671 L."
5999,38,Free Water Deficit,lab test,decimal,pmc-3579059-1,Extracted,"An 8-year-old boy, previously diagnosed as cerebral palsy with developmental delay, microcephaly and mental retardation, presented with sudden onset of huge swelling of the tongue for last 24 hours. Two weeks back, he developed generalized tonic clonic convulsion with status epilepticus for the first time. He was then admitted to a nursing home and managed with intravenous diazepam followed by loading dose of phenytoin as per standard protocol. He was discharged with instruction to get intravenous phenytoin (300 mg/day) once daily at home for the next 15 days. There was no history of headache or vomiting. There was no history of respiratory distress, swelling of face, itching, and loose stool. No history of atopy or similar type of episodes seen in other family members.
On examination, the child was conscious but irritable. There was swelling of whole dorsum of tongue, which was protruding outside the mouth with oozing of blood over both the edges of tongue following superadded infection []. The oral cavity was so blocked by edematous tongue that the child could not speak or swallow anything. Face, lips, and gums were normal. His body weight was 24.5 kg, height was 123 cm and head circumference was 45.5 cm. His pulse rate was 144/min, regular, normal volume, respiratory rate 32/min, blood pressure 120/70 mm of Hg, temperature 99.8°F. The child had mild pallor without any pedal edema or cyanosis. Abdomen was soft without any visceromegaly. There was mild respiratory distress due to oro-pharyngeal obstruction. Auscultation of his chest including cardiovascular system was otherwise normal. There was no ataxia, nystagmus, or altered sensorium. However, he had neurologic manifestation of spastic diplegic cerebral palsy with associated complication.
Investigation revealed hemoglobin of 12.8 g/dL. Total leukocyte count of 16900/cmm, polymorphs 86%, lymphocytes 12%, platelet counts 2.2 lakhs/cmm, ESR 22/1st hour. Biochemistry showed serum sodium 138 meq/L, potassium 5.2 meq/L, calcium 8.6 mg/dL. Renal function and liver function tests were normal. Chest X-ray and sonography of abdomen did not reveal any abnormality.
Serum C1 esterase inhibitor was 0.62 mg/L (normal: 0.21-0.39 mg/L), which excludes hereditary angioedema. Serum phenytoin level (37.20 μg/ml, toxic range > 20 μg/ml) was elevated.
The child responded to supportive management along with parenteral empirical antibiotics and with intravenous steroids (hydrocortisone), antihistamines, and epinephrine within 2 days. Macroglossia due to edema was reduced and the tongue could be repositioned within the oral cavity []. He was discharged with valproate sodium and other advice like physiatric management, etc.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [8, 'years'], 'weight': [24.5, 'kg'], 'Sodium': [138.0, 'mEq/L']}",-0.21,-0.1995,-0.2205,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 8 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 24.5 kg. The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 24.5 * (138.0/140 - 1) = -0.21 L. The patient's free body water deficit is -0.21 L."
6000,38,Free Water Deficit,lab test,decimal,pmc-7476800-1,Extracted,"A 65-year-old man was referred to the hospital in 5th July 2019 because of refractory edema in both legs.
The patient had a history of CKD stage 3a, a hypotrophic left kidney, and hypertension. He had been prescribed amlodipine 2.5 mg for hypertensive medication. He also underwent radical prostatectomy for prostate cancer two years earlier. He underwent pelvic MRI using gadoterate meglumine (15 mL), immediately after iodide contrast-enhanced chest and abdomen computed tomography (CT) for cancer surveillance. Thirty days before CT scan, his creatinine level was 1.28 mg/dL and his estimated glomerular filtration rate (eGFR) was 58 mL/min/1.73 m2. After 185 days, he visited a local clinic because of edematous changes in both lower extremities. CT angiography of the lower extremities was performed; no stenosis or occlusion of vessels was observed. Although diuretics were administered for 2 weeks, the edema worsened and was accompanied by pruritus and pain (). Eventually, he was referred to our hospital for further evaluation.
Upon admission, his body temperature was 36.8°C and his blood pressure was 110/60 mmHg. His height was 161.3 cm, weight was 53.2 kg and body mass index was 20.4 kg/m2. Physical examination revealed grade 2+ pretibial pitting edema with redness, mild heat, and tenderness in both lower extremities. Both inguinal lymph nodes were not enlarged.
Initial laboratory findings at admission (about 210 days after MRI scan) were as follows: white blood cell count, 6,200 /μL (neutrophil 66%, lymphocyte 22%, monocyte 10.3%, eosinophil 0.5%); hemoglobin, 10.7 g/dL; platelet, 253,000 /μL; blood urea nitrogen, 41 mg/dL; serum creatinine, 2.07 mg/dL; eGFR, 32 mL/min/1.73 m2; serum sodium, 134 mmol/L; potassium, 3.4 mmol/L; chloride, 102 mmol/L; total CO2, 20 mmol/L; calcium, 9.3 mg/dL; phosphate, 1.5 mg/dL; total protein, 6.9 g/dL; albumin, 4.0 g/dL; aspartate transaminase, 43 U/L; alanine aminotransferase, 15 U/L; and C-reactive protein, 0.96 mg/dL. Routine urine analysis revealed a pH of 6.0 and trace proteins. Red and white blood cells were absent in the urine. The spot urine protein/creatinine ratio was 209 mg/g and the spot urine albumin/creatinine ratio was 60 mg/g. Thyroid function tests were normal: thyroid stimulating hormone, 2.47 μIU/mL and free T4, 0.98 ng/dL. Fractional excretion of Na 0.1% and Fractional excretion of urea on admission was 17.6%, which suggested the patient was prerenal AKI.
Chest radiography and echocardiogram findings were normal. During doppler sonography of both lower extremities, the venous velocity was normal and there was no evidence of thrombosis. None of the aforementioned findings were suggestive of refractory edema.
Fluid therapy was administered to treat the AKI, which was probably caused by the diuretics he was given during his two-week stay in the local clinic. Subsequently, his renal function improved: serum creatinine, 1.18 mg/dL; and eGFR, 63.9 mL/min/1.73 m2. Since the redness and tenderness of both legs were suggestive of cellulitis-associated edema, intravenous cefazolin was administered for two weeks. However, the lesion gradually spread from his ankle to his thigh and changed into fibrotic induration. Contracture of the ankle and knee joints also occurred ().
To detect diffuse or localized systemic sclerosis, antinuclear antibody, anti-Scl 70 antibody, and anti-centromere antibody tests were performed, but the results were all negative. Also, eosinophilia and paraproteinemia was not seen, which is commonly accompanied in scleromyxedema or eosinophilic fasciitis. Although approximately 50 weeks had passed since he was exposed to the gadolinium, the characteristic clinical features led to the suspicion of NSF. A biopsy of the right anterior tibial skin lesion was performed to examine tissue for disease. This revealed unique features of the NSF such as dermal thickening with collagen fibers extending into the subcutaneous septa and a large number of spindle-shaped fibrocytes (). Neither eosinophilic tissue infiltration nor fat necrosis with calcification of adipocytes was found.
Systemic methylprednisolone (20 mg/day) was administered for two weeks to treat the NSF. Additionally, UV-A1 topical phototherapy of 1.5 joule (J)/cm2 was administered to the lower leg lesion twice a week. The patient underwent intensive physical therapy including stretching, pneumatic compression, and Transcutaneous Electric Nerve Stimulation . We administered MTX 15 mg weekly while reducing the methylprednisolone dose weekly by half until a dose of 2 mg/day was administered. Simultaneously, the UV-A1 intensity was gradually increased to 3.0 J/cm2. After 6 months of treatment, the reddish edema improved and the skin induration decreased. Although the contracture of the ankles was still present (), there was no further disease progression. Currently, the patient receives MTX (10 mg) weekly and methylprednisolone (2 mg) daily.
Informed consent for publication of clinical data was submitted by the patient and the images are published with the consent of the patient.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [65, 'years'], 'weight': [53.2, 'kg'], 'sex': 'Male', 'Sodium': [134.0, 'mmol/L']}",-1.14,-1.083,-1.197,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 65 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 53.2 kg. The concentration of sodium is 134.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 53.2 * (134.0/140 - 1) = -1.14 L. The patient's free body water deficit is -1.14 L."
6001,38,Free Water Deficit,lab test,decimal,pmc-6819601-1,Extracted,"A 72-year-old woman with a 5-pack-year smoking history presented with drowsiness after esophagogastroduodenoscopy (EGD). Her past medical history was remarkable for community-acquired pneumonia at right middle lung (Fig. a) 3 months prior, from which she made a full recovery following antibiotic therapy. She had a 2-month history of polyuria, polydipsia, nocturia, lightheadedness upon standing up quickly, fatigue, loss of appetite, and 15 kg of weight loss from a baseline weight of 60 kg. She had no fever, cough, dyspnea, hemoptysis, chest pain, or night sweats. She presented to the outpatient unit, and the investigation at that time showed a fasting plasma glucose level of 100 mg/dL (5.5 mmol/L) and an HbA1c of 4.8%. Thyroid function tests revealed a normal serum triiodothyronine (T3) level of 2 nmol/L (reference range 1.23–3.07 nmol/L), a low free thyroxine (FT4) level of 3.86 pmol/L (reference range 11.97–21.88 pmol/L), and a suppressed thyroid stimulating hormone (TSH) level of 0.06 mIU/L (reference range 0.27–4.0 mIU/L). A chest x-ray showed minimal infiltration at medial aspect of right lower lung, which had decreased compared with a previous chest x-ray (Fig. b).
The patient underwent EGD 2 months after the outpatient visit. She was kept nil
per os for 10 h prior to the procedure. The EGD findings were mild non-erosive antral gastritis. After EGD, she developed nausea, vomiting, and drowsiness. Physical examination revealed a body temperature of 37 °C, a blood pressure of 100/57 mmHg, a pulse rate of 90/min, and a respiratory rate of 16/min. She was 44.5 kg in body weight, was 148 cm in height, and had a body mass index of 20.3 kg/m2. She had flat neck veins, a normal thyroid gland without nodules, normal breath sounds, no abnormal palpable masses, no hepatosplenomegaly, no breast masses, and no superficial lymphadenopathy. Neurological examination was remarkable for bitemporal hemianopia evaluated by confrontation test.
She was immediately admitted to the hospital because of the altered mental status. At the first hour after admission, she had polyuria with a urine output of 300 mL/hour (6.7 mL/kg/hour). Laboratory tests showed a serum sodium level of 160 mmol/L; a potassium level of 3.9 mmol/L; a chloride level of 125 mmol/L; a bicarbonate level of 24 mmol/L; a creatinine level of 1.4 mg/dL. Serum osmolality was 325 mOsm/kg. Her urine specific gravity was 1.002 without proteinuria or glucosuria. Urine osmolality was 62 mOsm/kg. Diabetes insipidus was diagnosed based on evidence of polyuria along with hypernatremia and low urine osmolality. Desmopressin acetate (DDAVP) 1 microgram was given by subcutaneous injection. One hour later, her urine output decreased to 70 mL/hour, and urine osmolarity increased to 570 mOsm/kg. Based on decreasing urine output and a more than 50% increase in urine osmolality in response to DDAVP, a diagnosis of central diabetes insipidus was made.
Given the diagnosis of central diabetes insipidus, further investigations including magnetic resonance imaging (MRI) of the pituitary gland and evaluation of the anterior pituitary hormones were performed. Pituitary MRI demonstrated a heterogeneous high signal intensity (SI) lesion in T1-weighted (T1W) imaging, which also appeared as a low SI lesion in T2-weighted (T2W) imaging with heterogeneous gadolinium enhancement at the sellar and suprasellar region, measuring 2.4 × 2.6 × 3.9 cm. The lesion was compressing the hypothalamus bilaterally and the inferior aspect of optic chiasm with increased SI in T2W imaging at the right optic nerve and bilateral optic tracts. It was also anteriorly displacing the residual pituitary gland. The pituitary stalk could not be identified, and the bright spot of posterior lobe was absent. These MRI findings suggested pituitary macroadenoma with hemorrhage (Fig. ). The bony skull showed a normal appearance without lytic lesion. There were also multiple small gadolinium-enhancing lesions up to 0.7 cm in size with adjacent vasogenic brain edema at subcortical and subpial regions of the left frontal and parietal areas; therefore, multiple stages of cysticercosis and brain metastases were included in the differential diagnosis (Fig. ).
Pituitary hormonal profiles (Table ) showed inappropriately low gonadotropins levels, a low plasma adrenocorticotropic hormone (ACTH) level, and a low morning serum cortisol level that did not respond to cosyntropin stimulation, indicating secondary adrenal insufficiency. Serum prolactin level was mildly elevated, but no further increase was seen in a diluted sample. Hyperprolactinemia was suspected to be caused by stalk interruption. Thyroid function tests performed 2 months prior to admission showed a low free T4 level of 3.86 pmol/L and a low TSH level of 0.06 mIU/L, suggesting central hypothyroidism. On admission, serum free T4 level had decreased to 2.32 pmol/L with an unexpectedly elevated TSH level of 19.07 mIU/L. A low IGF-1 level in combination with deficiency of more than two pituitary hormones was highly indicative of growth hormone deficiency.
The patient underwent craniotomy for tumor removal. Intraoperative findings showed one grey-purplish firm mass at the sellar and retrochiasmatic regions with some necrosis and hemorrhage. The tumor was partially removed. A histopathological study revealed adenocarcinoma with the immunohistochemical staining positive for cytokeratin-7 and thyroid transcription factor-1 (TTF-1) but negative for cytokeratin-20, CDX-2 and GFAP (Fig. ). These findings were consistent with metastatic adenocarcinoma originating from the lung.
To identify the primary adenocarcinoma of the lung, a CT scan of the chest was performed which revealed a 2.2 × 2.2 cm enhancing soft tissue mass at the proximal part of the right bronchus that supplies the medial segment of the right middle lung. This was causing atelectasis of the distal part of the medial segment of the right middle lung and diffuse centrilobular emphysema at both upper lobes without pleural effusion. The liver, spleen, kidneys, and adrenal glands appeared unremarkable. No osteolytic lesion of the ribs, spine, and other bony structures were seen (Fig. ). The final diagnosis was advanced adenocarcinoma of the lung with pituitary metastasis associated with panhypopituitarism and central diabetes insipidus.
Palliative care for the advanced-stage lung cancer was offered to the patient. She received hormone replacement including desmopressin acetate 10 mcg intranasal solution daily, oral prednisolone 5 mg daily, and levothyroxine 75 mcg daily for central diabetes insipidus, secondary adrenal insufficiency, and central hypothyroidism, respectively. Two months later, she developed bilateral ophthalmoplegia and died 4 months after the diagnosis.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [72, 'years'], 'weight': [44.5, 'kg'], 'sex': 'Female', 'Sodium': [160.0, 'mmol/L']}",2.86071,2.71767,3.00375,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 72 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 44.5 kg. The concentration of sodium is 160.0 mmol/L. Plugging in these values into the equation, we get 0.45 * 44.5 * (160.0/140 - 1) = 2.86071 L. The patient's free body water deficit is 2.86071 L."
6002,38,Free Water Deficit,lab test,decimal,pmc-5965161-1,Extracted,"An 11-month-old male with no known past medical history presented to the ED with central nervous system (CNS) depression and then went into cardiac arrest. The patient was lethargic for two hours after awakening that morning and then had a seizure. During the prior 24–48 hours, he was irritable with decreased activity and was later retching. He was noted to be healthy before developing these symptoms. Upon arrival in the ED, he was unresponsive with no gag reflex. Vital signs were temperature 36.1° Celsius, heart rate 156 beats per minute, respiratory rate 8 breaths per minute, oxygen saturation 80% on room air. Physical exam revealed a well-nourished, 20.5 lb., 11-month-old male, with normal development, no trauma, normal oropharynx, normal tympanic membranes, no lymphadenopathy, tachycardia, clear lungs, normal abdomen and Glasgow Coma Scale rating of 4. He was intubated for significant CNS depression and required no medications for induction or paralysis. Post-intubation chest radiograph is shown in . He subsequently became bradycardic with a heart rate in the 40s with a wide complex rhythm. Initial electrocardiogram (ECG) was performed and is shown in . He then became pulseless, and cardiopulmonary resuscitation was initiated. Laboratory analysis revealed sodium 136 mmol/L, potassium 7.7 mmol/L, chloride 115 mmol/L, bicarbonate 8.0 mmol/L, blood urea nitrogen 24 mg/dL, creatinine 0.9 mg/dL, and glucose 175 mg/dL Venous blood gas pH was 6.77. An ECG was repeated (). He received intravenous fluid resuscitation, sodium bicarbonate infusion, calcium chloride, insulin, glucose, ceftriaxone and four doses of epinephrine. Resuscitation continued for approximately one hour but the patient ultimately died.
Further laboratory findings in the ED included a complete blood count (CBC) with differential, liver function tests (LFTs), one blood culture and toxicology screen. CBC demonstrated white blood cell count 13.8 K/mcL with absolute neutrophil count of 2.5 K/mcL and absolute lymphocyte count of 10.7 K/mcL, hemoglobin 10.0 gm/dL, hematocrit 34.7%, and platelet count 321 K/mcL. LFTs showed total bilirubin 0.6 mg/dL, aspartate aminotransferase 77 IU/L, and alanine transferase 97 IU/U. A single blood culture from the right external jugular vein revealed aerobic gram-positive rods that were reported two days later as Bacillus species (not Bacillus anthracis). Toxicology screening revealed urine enzyme-linked immunosorbent assay positive for tetrahydrocannabinol-carboxylic acid (THC-COOH) and undetectable serum acetaminophen and salicylate concentrations. Route and timing of exposure to cannabis were unknown.
Autopsy revealed a non-dilated heart with normal coronary arteries. Microscopic examination showed a severe, diffuse, primarily lymphocytic myocarditis, with a mixed cellular infiltrate in some areas consisting of histiocytes, plasma cells, and eosinophils. Myocyte necrosis was also observed. There was no evidence of concomitant bacterial or viral infection based on post-mortem cultures obtained from cardiac and peripheral blood, lung pleura, nasopharynx and cerebrospinal fluid. Post-mortem cardiac blood analysis confirmed the presence of Δ-9-carboxy-tetrahydrocannabinol (Δ-9-carboxy-THC) at a concentration of 7.8 ng/mL. Additional history disclosed an unstable motel-living situation and parental admission of drug possession, including cannabis.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [11, 'months'], 'weight': [20.5, 'lbs'], 'sex': 'Male', 'Sodium': [136.0, 'mmol/L']}",-0.15941,-0.15144,-0.16738,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 11 months old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 20.5 lbs so this converts to 20.5 lbs * 0.453592 kg/lbs = 9.29864 kg. The concentration of sodium is 136.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 9.29864 * (136.0/140 - 1) = -0.15941 L. The patient's free body water deficit is -0.15941 L."
6003,38,Free Water Deficit,lab test,decimal,pmc-8131661-2,Extracted,"A 2-month-old girl presented with the first episode of UTI. She had high-grade fever for 3 days associated with foul-smelling urine. She had no vomiting, and her oral intake was normal. She was born full term with birth weight of 3.2 kg. Both antenatal and immediate postnatal periods were uneventful. Her growth had been along the 50th centile. On arrival at the hospital, her BP was 116/66 mmHg. Her anterior fontanelle was normotensive, and she had moist mucous membrane. Apart from a soft systolic murmur, no other abnormalities were detected. Her electrolytes were severely deranged: serum sodium of 116 mmol/L, potassium of 7 mmol/L, and presence of metabolic acidosis. Urine culture grew Pseudomonas aeruginosa. Intravenous fluid and antibiotics were instituted. Hyperkalemia and acidosis were resolved within 48 h of therapy, but she needed oral sodium replacement for a further 24 h. Evaluation post-UTI showed right hydronephrosis with an anteroposterior renal pelvic diameter of 1.7 cm and an abnormal connection between the bladder and vagina on micturition cystourethrography (MCUG). She was then referred to the surgical team for corrective surgery. While waiting for the surgery, she suffered another two episodes of UTI despite started on antibiotic prophylaxis. In both episodes, the electrolytes were deranged in the same fashion. After the correction of the vesico-vaginal fistula, no recurrence of UTI was observed, and her electrolytes remained normal. She was planned for a DMSA to assess the degree of her kidney scarring.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [2, 'months'], 'weight': [3.2, 'kg'], 'sex': 'Female', 'Sodium': [116.0, 'mmol/L']}",-0.32914,-0.31268,-0.3456,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 2 months old. This means the patient is 0 years old.
The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 3.2 kg. The concentration of sodium is 116.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 3.2 * (116.0/140 - 1) = -0.32914 L. The patient's free body water deficit is -0.32914 L."
6004,38,Free Water Deficit,lab test,decimal,pmc-4421247-1,Extracted,"A 36-year-old 5-week postpartum woman presented to the emergency room with complaints of nausea and vomiting for 48 h. She also reported a 2-day history of general malaise and worsening dyspnoea. She denied chest pain, palpitations, diarrhoea or headaches. She reported eating; however, she limited herself to several small high-protein carbohydrate-free meals in an attempt to quickly return to her prepartum weight. Since her delivery, she had achieved an intentional weight loss of 30 lbs. Initial vital signs were: temperature 37 °C, blood pressure 140/63 mmHg, heart rate 84, respiratory rate 20 and a weight of 59.8 kg. She appeared unkempt and lethargic. Head and neck examinations were benign. Chest auscultation was clear with no adventitious sounds; heart examination was unremarkable. The abdomen was benign with a well-healed surgical C-section scar; there was no costovertebral angle tenderness. The extremities were without tenderness or oedema. She had no neurologic defects other than her blunted mentation.
Her past medical history was significant for a cesarean section, complicated by bladder damage, now resolved. Her only medication was percocet to manage post-surgical visceral pain. She denied alcohol or illicit substance use.
Initial laboratory data include sodium of 144 mEq/L, potassium 4.8 mEq/L, chloride 104 mEq/L and bicarbonate <5 mEq/L that is the lowest available determination possible at our institution. Her BUN was 3 mg/dL, creatinine was 1.1 mg/dL and glucose was 133 mg/dL. Serum lactate was 2.1 mmol/L, phosphate 1.0 mg/dL and magnesium 1.6 mg/dL. Arterial blood gas drawn on room air showed a pH of 6.9, PCO2 of 19 mmHg, PaO2 of 137 mmHg and SaO2 of 100%. White blood cell count was 17 600/mm3 with 88.2% segmented neutrophils, Hg 13.7 g/dL, haematocrit 43.1% and platelets of 340 000/mm3. Urinalysis had a pH of 5.5 with <80 mg/dL ketones. The serum osmolar gap was 7. A comprehensive drug screen was negative including salicylates and acetaminophen. Chest radiograph was normal. Blood and urine cultures were negative.
The patient was volume-depleted with a metabolic acidosis and a serum anion gap of 35. Fluid resuscitation with three ampules of sodium bicarbonate per litre of D5W at 100 cc/h was initiated for 24 h. Improvement in laboratory values occurred within 12 h with serum bicarbonate improving to 12 mEq/L. The serum bicarbonate improved to 20 mEq/L with normalization of the anion gap at 24 h. Symptomatic improvement occurred likewise. The patient was started on an 1800 kcal diet during her hospitalization, supplemented with a regular diet of home food provided by the husband. Breast feeding was stopped on advice from a lactation consultant and the acidosis did not reoccur. The patient's baby was reported to be in the 90th percentile for weight and height.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [36, 'years'], 'weight': [59.8, 'kg'], 'sex': 'Female', 'Sodium': [144.0, 'mEq/L']}",0.85429,0.81158,0.897,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 36 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 59.8 kg. The concentration of sodium is 144.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 144.0 mEq. To convert from 144.0 mEq to mmol, convert from mEq to mmol. The compound 144.0 has a valence of 1, and so divide the valence by the value of mEq to get, 144.0 mEq/(1 mEq/mmol) = 144.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 144.0 mEq sodium/L converts to 144.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 59.8 * (144.0/140 - 1) = 0.85429 L. The patient's free body water deficit is 0.85429 L."
6005,38,Free Water Deficit,lab test,decimal,pmc-5278593-1,Extracted,"A 3-year-old healthy male child weighing 15 kg was posted for Duhamel procedure for Hirschsprung disease. His preoperative hemoglobin was 11 g/dl, serum sodium (Na) 140 mmol/L, and chloride (Cl) 100 mmol/L. An evening before surgery, TGI was started through nasogastric tube and 4.5 L of NS was used over a period of 10 h. On the morning of surgery, the child was found to be lethargic. He vomited once before induction of general anesthesia. The surgery was uneventful. On completion of surgery, the patient was reversed with intravenous (IV) neostigmine 50 mcg/kg and 10 mcg/kg glycopyrrolate. After reversal though the child had adequate tidal volume, but he was not responding to commands or moving his limbs. An arterial blood gas sample (ABG) which was sent to rule out electrolyte imbalance showed pH 7.05, PaO2 92.4 mmHg, PaCO2 40 mmHg, Na 132 mmol, K 3.5 mmol/L, Cl 117 mmol/L, bicarbonate (HCO3) 11 mmol/L, and base excess (BE)-18.9.
An IV infusion of 5% dextrose in water with 50% of the calculated amount of sodium bicarbonate (NaHCO3) was started. The child showed improvement and started responding to commands and was extubated. His ABG after NaHCO3 infusion was pH 7.35, Na 134 mmol/L, K 3.4 mmol/L, Cl 104 mmol/L, HCO3 15.8 and BE 8, PaO2 90 mmHg, and PaCO2 37 mmHg. Thereafter his recovery was uneventful, and the child was discharged from the hospital on the 7th postoperative day.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [3, 'years'], 'weight': [15.0, 'kg'], 'sex': 'Male', 'Sodium': [134.0, 'mmol/L']}",-0.38571,-0.36642,-0.405,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 3 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 15.0 kg. The concentration of sodium is 134.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 15.0 * (134.0/140 - 1) = -0.38571 L. The patient's free body water deficit is -0.38571 L."
6006,38,Free Water Deficit,lab test,decimal,pmc-8500762-1,Extracted,"A 56-year-old Caucasian female presented with a 3-day history of fever, vomiting for 2 days, and altered sensorium since the morning of presentation to our emergency department. On examination, the weight was 52 kg and the height was 168 cm. She suffered from complete paraplegia due to spinal cord injury 30 years ago with absence of motor and sensory function below Th1 and from chronic hepatitis C infection. She was drowsy but arousable. At the time of admission, body temperature was 101.8 F, with otherwise normal vital signs. Except for preexisting paraplegia, there were no further symptoms or signs of neurological deficit, in particular, no nuchal rigidity. Laboratory chemistry revealed normal hepatic and altered inflammatory parameters (total bilirubin of 0.68 mg/dl, alkaline phosphatase of 102 U/l, aspartate aminotransferase of 87 U/l, alanine aminotransferase of 24 U/l, leukocyte level of 19 G/l, glucose of 147 mg/dl, and high-sensitivity C-reactive protein of 153 mg/l), as well as reduced levels of natrium (131 mmol/l). Initial computed tomography scan of the brain showed diffuse cerebral edema (). The patient was admitted to our intensive care unit, where due to suspected meningoencephalitis intravenous administration of ceftriaxone, ampicillin, dexamethasone, and aciclovir was started. Cerebrospinal fluid (CSF) examination was performed shortly after first doses of antibiotic therapy. The CSF was turbid, with increased protein of 889.6 mg/dl, reduced glucose of 19 mg/dl, and elevated neutrophil granulocytes of 3478 cells/μl. CSF real-time PCR assay for common CSF pathogens (Streptococcus agalactiae, Escherichia coli K1, Haemophilus influenzae, Listeria monocytogenes, Neisseria meningitides, Streptococcus pneumoniae, HSV 1/2, VZV, CMV, and Cryptococcus neoformans/gattii) was negative. Blood cultures taken on admission were negative. CSF cultures confirmed β-hemolytic, gram-positive streptococci () which were positive for Lancefield group C that could subsequently be identified as S. equi subsp. zooepidemicus by mass spectrometry due to MALDI-TOF MS (Bruker®) using the MBT IVD Library 9.0 giving a score value of 2.49. In addition, the cerebrospinal fluid was examined by a commercial PCR targeting the 16S ribosomal DNA (SepsiTest™-UMD; Molzym, Bremen, Germany). DNA was extracted by MolYsis™ complete kit (Molzym). Both kits were used according to the manufacturer's instructions. The PCR product of 430 base pairs was sequenced and used for Blast® search in GenBank® (NCBI, NIH, Bethesda MD, USA). The sequence obtained from the CSF was identical to S. equi, but subspecies could not be identified by this molecular tool.
The S. equi subsp. zooepidemicus isolates were tested susceptible for ceftriaxone as well as for penicillin and ampicillin. Resistance determination was carried out according to the current EUCAST Standard Version 11.0 of 2021 using agar diffusion methods. Searching for a possible path of infection, a small chronic wound on the left leg was observed. However, multiple cultures of the skin lesions were tested negative. The patient confirmed close contact to horses before onset of symptoms and recovered completely after a two-week course of ceftriaxone.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [56, 'years'], 'weight': [52.0, 'kg'], 'Sodium': [131.0, 'mmol/L']}",-1.67143,-1.58786,-1.755,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 56 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 52.0 kg. The concentration of sodium is 131.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 52.0 * (131.0/140 - 1) = -1.67143 L. The patient's free body water deficit is -1.67143 L."
6007,38,Free Water Deficit,lab test,decimal,pmc-5348144-1,Extracted,"A 26-year-old Chinese male was admitted to our hospital with recurrent vomiting and elevated serum creatinine (Scr) lasting 9 months without any clear inducement factors (Fig. ).
He was examined to have left ventricular hypertrophy in a physical examination 2 years ago. Due to no symptom, he did not go to hospital for further treatment. Eleven months ago, he went to hospital because of gross hematuria. After 2 months, he felt fatigability, nausea, and vomited several times suddenly. He had normal blood pressure (BP), temperature, regular heartbeat, and rhythm. Physical examination revealed normal vital signs. No abnormity was observed in routine urine test and blood test, but blood biochemical test revealed his Scr increased to 150 μmol/L (Chronic Kidney Disease Epidemiology Collaboration [CKD-EPI] equation estimated glomerular filtration rate [eGFR]: 55 mL/min/1.73 m2). After receiving proper treatment, fatigability, nausea, and vomit were obviously relieved. But 5 months later, these symptoms reoccurred and he felt abdominal pain with urine protein 0.183 g/24 h (urinary volume: 1.8 L). Gastroscope and enteroscopy checking were normal. Besides, no abnormality was detected by abdomen computed tomography (CT) except thicken ascending colon. The echocardiography showed thickening of the left ventricular wall and normal wall motion, suggesting nonobstructive hypertrophic cardiomyopathy. Moreover, cardiac magnetic resonance image (MRI) revealed left ventricular hypertrophy, suggesting hypertrophic cardiomyopathy. Over the past 9 months, he lost weight obviously, BMI 17.58 kg/m2 (height: 171 cm, weight: 51.4 kg), occasionally with blurred vision and conjunctival congestions. In addition, his mother had similar medical history. His mother was diagnosed gastrointestinal dysfunction with sudden emergence of repeating nausea and vomiting symptoms at the age of 36. After 12 years’ treatment, she had no remission and felt depressed. Finally, she died at the age of 48.
No obvious abnormality was found in examination findings on admission: BP 98/60 mm Hg, temperature 37°C, heart rate (HR) 85 bpm with order rhythm, except systolic rumor between the third and fourth rib of left margin of heart. He had no edema and any discomfort in abdomen and nervous system. The electrocardiogram revealed sinus rhythm with extreme clockwise translocation.
No abnormality was observed in routine test, such as urine, blood, and stool. And the specific gravity of urine and urine pH was within normal limits. Quantification of proteinuria showed 0.126 g/24 h (urinary volume: 1.8 L). Tests of renal function showed Scr136 μmol/L (CKD-EPI eGFR: 61 mL/min/1.73 m2), urea nitrogen 7.9 mmol/L, uric acid 449 μmol/L. Hemoglobin was 11.3 g/dL, leucocyte count 7.9∗109/L (normal differential), and platelets 173∗109/L. Serum electrolyte analysis showed sodium 138 mmol/L, potassium 3.75 mmol/L, serum carbon dioxide 31.7 mmol/L, calcium 2.29 mmol/L, and phosphate 1.24 mmol/L. Liver function laboratory tests were normal, with alanine aminotransferase 22 IU/L, aspartate transaminase 23 IU/L, alkaline phosphatase 56 IU/L, and albumin 42 g/L. Blood lipid, glucose, thyroid function, and myocardial enzyme were normal. ANA, ENA, anti-GBM, and ANCA were negative. ANCA were tested by enzyme-linked immunosorbent assays for anti-PR-3 and anti-MPO antibodies. Immunoglobin (Ig) A 164 mg/dL, IgG 1270 mg/dL, IgM 194 mg/dL, C3 was 63 mg/dL, and C4 17 mg/dL. Urine and serum protein immunofixation electrophoresis were both normal, with IgA, G, M, light chain κ, and λ all negative. Serologic tests for hepatitis B virus, hepatitis C virus, and HIV were negative. Tumor markers such as AFP, carcinoembryonic antigen, CA 199, and CA 125 were all negative. Moreover, urine ACR was less than 2.5 mg/mol and 24 h urine electrolyte excretion (urinary volume: 1.3 L) was decreased with sodium 37.7 mmol/24 h, potassium 13.13 mmol/24 h, chloridion 39 mmol/24 h, calcium 0.42 mmol/24 h, and phosphate 3.35 mmol/24 h. In addition, bone marrow aspiration was performed and no abnormal plasmocyte was found, which ruled myeloma out.
Ultrasound revealed normal kidneys, with left kidney 98∗41 mm and right kidney 100∗32 mm. To investigate the reason of the elevated serum creatinine, a renal biopsy was performed on January 13, 2015. The biopsy showed global sclerosis in 9 of 28 glomeruli. For light microscopy (LM), the serial sections were stained with H&E, periodic acid-Schiff, Masson's trichrome and Jones’ methenamine silver stains, and Congo red. LM (Fig. A periodic acid-Schiff stain [PAS] staining) showed that most capillary loops were open and expansion of individual mesangium by a few weak PAS-positive, homogeneous, and amorphous substances without proliferation of mesangial cells. Renal amyloid deposits stained with Congo red stain and confirmed by the appearance of apple green birefringence from Congo red stain under polarized light (Fig. B, C). They predominated in interstitial tissue, and mainly in renal medulla. Immunofluorescence staining was negative, including IgA, IgG, IgM, C3, C4, C1q, and fibrinogen. Immunoreactivity of renal tissue AA amyloid deposition and light chain κ or λ were all negative. But immunofluorescence staining showed the presence of TTR fixation in amyloid deposited (Fig. D). Characteristic amyloid fibers in renal intertsitium were confirmed by tranmission electron microscopy (Fig. E). The renal biopsy was jointly reviewed by 2 pathologists (XP and JX).
After assessing the family history over 3 generations, genomic DNA of all family members (except his mother) was extracted from peripheral blood by using the standard phenol-chloroform extraction method. Polymerase chain reaction was used to amplify the coding region of TTR gene (the oligonucleotide primers in Table ) and TTR mutations were screened by direct sequencing using an ABI Prism 3100 Genetic Analyzer (Applied Biosystems). The sample sequences were compared with the genomic DNA sequence of TTR [Ensembl: ENSG00000118271; Assembly: GRCh38.p2 (GCF_000001405.28)]. Direct DNA sequencing of all family members’ TTR gene revealed a mutation at position 3 of codon 75 (c.224T>C, p.Leu75Pro) (previously reported as p.Leu55Pro) in the proband (Fig. ).
Finally, combining clinical, laboratory examination, renal biopsy, and gene diagnosis, this patient was diagnosed as ATTR amyloidosis that was caused by TTR p.Leu75Pro mutation. To relieve gastrointestinal symptoms, he was treated by mosapride 5 mg three times a day (tid) and lactulose oral solution 15 mL tid. After 5 months, he received allograft liver transplantation (LT). Now he felt symptom relief, but his Scr increased to 180 μmol/L.
This study was approved by the Institutional Review Board of Ruijin Hospital, Shanghai Jiao Tong University School of Medicine. It was in accordance with the principle of the Helsinki Declaration II. The written informed consent was obtained from each participant.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [26, 'years'], 'weight': [51.4, 'kg'], 'sex': 'Male', 'Sodium': [138.0, 'mmol/L']}",-0.44057,-0.41854,-0.4626,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 26 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 51.4 kg. The concentration of sodium is 138.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 51.4 * (138.0/140 - 1) = -0.44057 L. The patient's free body water deficit is -0.44057 L."
6008,38,Free Water Deficit,lab test,decimal,pmc-2729907-1,Extracted,"A 23-yr-old woman with type 2 DM and Graves' disease has revisited to the Department of Emergency of Gyeongsang National University Hospital due to nausea, generalized weakness, polyuria and weight loss of 5 kg for 7 days in October 2003 since she was discharged from our hospital three weeks before. She was previously diagnosed as type 2 DM in 1996, and recently started insulin treatment to improve glycemic control due to persistently elevated HbA1c irrespective of oral administration of hypoglycemic agents. Three years before, she had taken propylthiouracil for hyperthyroid Graves' disease for 2 yr. In May 2003, she was diagnosed as relapse of hyperthyroidism at a local clinic and referred to our hospital for management of thyrotoxicosis refractory to usual dosage of propylthiouracil, 300 mg/day and proliferative diabetic retinopathy and nephropathy. She had 7.9 mM/L fasting blood glucose, 1.07 nM/L C-peptide (reference range [RR], 0.1-0.83), 222 mM/L fructosamine (RR, 205-285), 8.3% HbA1c (RR, 4.5-5.6) and 0.01 mU/L TSH and 2.02 pM/L free T3 on thryoid function tests. At that time, Her weight was 54 kg and height was 147 cm (body mass index, 25.0 kg/m2). Her thyroid had the volume of about 40 g and it looked diffusely enlarged and rubbery consistency on palpation. The technetium-99m (Tc-99m) thyroid scan revealed marginally increased and somewhat irregular uptake (3.8%). As from hospitalization, the patient had oral administration of relatively high dose of methimazole (60 mg daily), propranolol (160 mg daily) and 12 drops of Lugol's solution (three times a day) for 14 days, and consecutively lithium carbonate (900 mg daily) for 14 days because of persisting tachycardia (>110/ min), dyspnea on exertion and still high concentration of free T3 (4.44 pM/L). She was discharged with receiving methimazole (60 mg daily) and beta-blocker ().
She had no family history of thyroid disease, but both parents have been suffering from type 2 DM. She denied ingestion of any drugs including alcohol or excessive consumption of fizzy drinks these days. She also has been adhering to administration of antithyroid drug, beta-blocker and insulin (0.5 units/kg/day) since being discharged. On physical examination, the patient had 143/89 mmHg blood pressure, 36.8℃ body temperature, 22/min respiration rate, and 121/min pulse rate. She looked acutely ill, and had slightly tremulous, warmhands, and decreased skin turgor and dried tongue. She was 48 kg weight and body mass index 22.2 kg/m2. Exophthalmos was not present. The abdomen was soft and flat, and liver and spleen were not palpable.
On admission, her laboratory findings were as follows; hemoglobin 12.3 g/dL, WBC 8.65×109/L (segmented neutrophil 58%, lymphocyte 29%), platelet 398×109/L, total protein 65 g/L, albumin 32 g/L, ALP 3.47 ukat/L, AST 0.42 ukat/L, ALT 0.6 ukat/L, BUN 9.2 mM/L and creatinine 88.7 µM/L. Levels of blood glucose (32.7 mM/L) and fructosamine (396 mM/L) were elevated. Her serum electrolytes and blood gas parameters were as follows: sodium 144.1 mM/L, potassium 5.4 mM/L, chloride 102 mM/L, calcium 2.5 mM/L, phosphorus 1.0 mM/L, pH 7.32, pCO2 35 mmHg, pO2 98 mmHg, and bicarbonate 16 mM/L. The fasting serum C-peptide was 0.44 nM/L. Serum anion gap was 20.9 and osmolarity was calculated as 321 mosm/kg. Amylase and lipase levels were normal and anti-GAD antibody was negative. Thyroid function tests revealed that the patient had more aggravated hyperthyroid state; 0.01 mU/L TSH, 2.78 pM/L free T3 and 45.38 pM/L free T4 (RR, 11.41-23.08) than when she was hospitalized two weeks before (0.12 mU/L TSH, 1.41 pM/L free T3 and 30.26 pM/L free T4). TSH-receptor antibody level was 26.3 IU/L (RR, <1) and antimicrosomal antibody was 29.3 U/mL (RR, <60). The Tc-99m scan showed still enlarged thyroid with more increased uptake 6.5% than previous uptake scan (3.8%) performed taking propylthiouracil two months before. Based on above results, the patient was diagnosed as HHS accompanying mild ketosis on type 2 DM and aggravated Graves' hyperthyroidism. We treated her with intravenous insulin injection and large volume of intravenous fluid administration. And also, she took high dose of methimazole (90 mg daily, six times a day) and beta-blockers. On the second day, nausea and generalized weakness have been improved.
At two months after acute presentation, we measured levels of C-peptide after 75 g glucose loading; 0 min (0.12 nM/L), 30 min (0.74 nM/L), 60 min (1.02 nM/L), 90 min (1.49 nM/L) and 120 min (1.32 nML). Throughout follow-ups for 2 months, she took insulin (0.9 units/kg/day), metformin (1,500 mg daily) and methimazole (45 mg daily). The mean fasting capillary blood glucose level on self monitoring was rather elevated than the target, but free T3 level became normalized ().",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [23, 'years'], 'weight': [48.0, 'kg'], 'sex': 'Female', 'Sodium': [144.1, 'mmol/L']}",0.70286,0.66772,0.738,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 23 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 48.0 kg. The concentration of sodium is 144.1 mmol/L. Plugging in these values into the equation, we get 0.5 * 48.0 * (144.1/140 - 1) = 0.70286 L. The patient's free body water deficit is 0.70286 L."
6009,38,Free Water Deficit,lab test,decimal,pmc-8424402-1,Extracted,"A 79-year-old female presented to the department of acute geriatric medicine due to unintended weight loss of 6 kg in the last 6 months, loss of appetite and fatigue. The medical history was remarkable: exactly 2 years before admission she was admitted to the department of internal medicine in the same hospital because of thoracic pain on the right side with an intensity of 10 in the visual analog scale. In the computed tomography a spiculated pulmonary lesion of 30 mm diameter was detected in the right anterolateral upper lobe of the lung. The radiologist classified the lesion highly suspicious for cancer. A positron emission tomography confirmed the suspicion for cancer due to high activity in the fluorodeoxyglucose metabolism. A newly detected pleural effusion was drained and amber fluid with bloody spots was analyzed. It revealed a mass of neutrophilic granulocytes, histiocytes and mesothelial cells, findings that were classified as reactive for inflammation. No tumor cells were found. Cultures for the detection of tuberculosis and anaerobic or aerobic germs were negative. Aminopenicillin was given parenterally and an appointment was made for bioptic clarification of the lesion for outpatients, an appointment that was not perceived because of negative attitudes of the patient against an invasive procedure. Therefore, no exact diagnosis of the tumor could be made. No further decision making process between physician and patient`s relatives were documented.
Two years later, on admission to the department of acute geriatric medicine, she had a reduced general condition. On her right upper field, the respiratory sound was attenuated. Her skin was pale, and she was emaciated. The body mass index was 16 (ideal value 24–29, age and sex adjusted).
In the comprehensive geriatric assessment, we found 18.5 score points in the Mini Nutritional Assessment (range 0–30 points, lower points indicating malnutrition), indicating malnutrition and 95 score points (range 0–100 points, higher points indicating higher performance status) in the Barthel index, indicating the self-care uncompromised. The cognitive tests (Mini Mental test and Clock Performance Test) were unremarkable.
A repeated thoracic computer tomography indicated an enlargement of the lesion in the right upper lobe of the lung to 9 × 9 × 7.5 cm diameter with a similar lesion in the right lower field of the lung being highly suspicious for metastasis. The lesion was spiculated, with an unshaped border and lobulated. The draining bronchus stopped abruptly in front of the lesion. The lymph nodes were normal; we noted no destruction of the adjacent ribs.
Laboratory findings of the peripheral venous blood sample were as following: leucocytes 11,300/mm3 (86.6% neutrophils); hemoglobin count 9.9 g/dl; platelet count 3,34,000/mm3.
Her serum chemistry results were as follows: [Na+], 135 mmol/l; [K+], 4.3 mmol/l; estimated glomerular filtration rate (MDRD formula) 51 ml/minute; C-reactive protein 115 mg/l. The results of liver metabolism were unremarkable. The test for COVID-19 virus (polymerase chain reaction test) was negative as well as the test for Mycobacterium tuberculosis (QuantiFERON®-TB Gold Test).
After drawing samples for blood cultures, a calculated therapy for suspected popped up pneumonia was started with ampicillin plus sulbactam parenterally due to the diagnostic workup.
One set of blood cultures were sent to our microbiological laboratory and incubated in the Beckton and Dickinson (BD) Bactec™ Instrument, which provided a positive result for the aerobic bottle after an incubation period of 15 h and 30 min. A Gram staining performed with the positive blood culture and the specimen was plated and incubated accordingly to the manufacturer’s protocol. The Gram staining showed short Gram-negative rods (Fig. ). After 24 h of incubation at 35 °C under aerobic conditions growth could be seen on PolyViteX Agar, Columbia Blood Agar and MacConckey media (BD) (Fig. ), showing a mucoid morphology as previously described by Chavez et al. []. Cultivated bacteria were further analyzed with a Bruker Microflex MALDI-TOF (Matrix assisted laser desorption ionization–time of flight) mass spectrometer setup. Data which were obtained from the Bruker Microflex setup showed a strong result for Wohlfahrtiimonas chitiniclastica according to the score of 2.56 and a consistency rating of A +++ due to the manufacturer`s protocol, using the research version 4.1 model-based testing compass database from Bruker Daltonics. Since the MALDI TOF analysis provided a solid result of > 2, which secures identification at species level. Therefore, no further diagnostic procedures were necessary to provide the clinician with a feasible result.
To provide guidance for adequate therapy in this case, our laboratory conducted an elipsometer-tests (BD) and interpreted the results according to EUCAST (European Committee on antimicrobial susceptibility testing) PK/PD (pharmacokinetic/pharmacodynamic) non-species related breakpoints (Table ), since species specific breakpoints were absent [, ]. The strain of Wohlfahrtiimonas chitiniclastica showed very low minimum inhibitory concentrations for all antibiotics indicating antibiotic treatment could be taken into account.
Along with the blood culture results an additional exposure history was performed. The results showed that the patient lived with a dog and was a cigarette smoker with an exposure of 30 pack years and denied drug use. The patient remained afebrile and without pain. Her chief complaints were fatigue and exhaustion. Blood cell counts and parameters of inflammation remained unchanged despite the advanced oncologic situation. We initiated nutritional support using supplements and a diet adjusted to the recommendations of the dietologist. Detailed consultation on further diagnostic and therapeutic options followed on several occasions and clinical visits were accompanied by the patient’s cohabitant. For personal reasons, the patient refused further diagnostic or therapeutic measures. In accordance with the patient’s wishes, we constituted a palliative care and finalised the antibiotic course after 8 days without consecutive laboratory controls. The further clinical course after discharge from hospital was unremarkable according to the report of her family doctor. Due to the increased need of care, the patient`s cohabitant established home nursing. The patient died 19 days after the discharge from hospital; no autopsy was performed due to the order of the family.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [79, 'years'], 'weight': [6.0, 'kg'], 'sex': 'Female', 'Sodium': [135.0, 'mmol/L']}",-0.09643,-0.09161,-0.10125,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 79 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 6.0 kg. The concentration of sodium is 135.0 mmol/L. Plugging in these values into the equation, we get 0.45 * 6.0 * (135.0/140 - 1) = -0.09643 L. The patient's free body water deficit is -0.09643 L."
6010,38,Free Water Deficit,lab test,decimal,pmc-2803985-1,Extracted,"We are presenting a case with acute abdomen, i.e. ileoileal intusussception, caused by Burkitt lymphoma. A sixteen-year-old Caucasian Kosovar boy, presented in the surgical emergency clinic as acute abdomen, with abdominal pain, nausea, vomiting, and problems with defecation and flatulence. The symptoms started three days ago, worsening on admission day.
The patient's height was 178 cm, and his weight was 70 kg. His vital signs were: blood pressure 120/80 mmHg; pulse rate: 76 beats/min; respiratory rate 20/min; body temperature 37.1°C.
During physical examination, a distended, diffusely tender and painful abdomen with lower abdomen rebound was revealed. The patient's skin was pale with sweats.
Plane abdominal radiography showed mechanical obstruction. (Fig. )
The emergency laboratory tests presented as follows: Red blood cells (RBC): 4.61 × 109/L; white blood cells (WBC): 7.3 × 109/L; Hemoglobin (Hgb): 128 g/L; Hematocrit (Htc): 0.42; blood sugar: 5.42 mmol/L; blood urea nitrogen (BUN): 2.6 mmol/L; serum creatinine: 88 μmol/L; BUN/Creat ratio: 8.5; total protein: 72 g/L; albumin: 36 g/l; ALP: 60 IU/L; ALT: 26 IU/L; AST:40 IU/L; direct bilirubin: 5.8 μmol/L; total bilirubin: 20.5 μmol/L; indirect bilirubin: 14.7 μmol/L; Gama GT: 26 IU/L; C-reactive protein: 15.6 mg/L; serum amylase: 30 U/L: electrolytes: Na: 138 mmol/L; K: 3.75 mmol/L; Cl: 102 mmol/L; urinalysis: 2-4 Leucocytes, some bacteria and some uric acid crystals. Blood group: O Rh(D) poz.
Three weeks prior he had been surgically treated as acute abdomen caused by acute appendicitis and Mckelly Diverticulitis. Appendectomy and short resection of the ileum with diverticulum, and end-to-end anastomosis was performed. The immediate post operative period went well. After his discharge, his second hospital admission was two weeks after operation with abdominal pain and constipation problems which released spontaneously after two days.
At his third admission as acute abdomen, urgent laparotomy was performed in general endo tracheal anesthesia on the day after admission. Intra operative findings revealed small bowel dilatation, with intussusceptions of the terminal ileum, 2 cm from ileocecac valve. There were multiple enlarged mesenteric lymph nodes at the meso of the terminal ileum, ascending and the transverse colon, without palpable liver metastases.
We have done des intussusceptions caused by tumor from the wall of the ileum. (Fig. , , )
Adhesions at the anastomosis, and 60 cm above that, were released. The right extended haemicolectomy with end to end ileum-transverse anastomosis was performed. Post operative period went well; blood pressure was 120/80 mmHg, pulse rate beats: 65/min; temp.: 36.7°C. The wound healed per primam. He was treated with frozen fresh plasma (several doses-seven), red blood cells (one dose); antibiotic, analgesics, H2 blockers, vitamins, amino acids, human albumins. He was discharged on the 10th postoperative days, with good bowel movements. He was oriented to the Hematology Department for further treatment, for Burkitt Lymphoma with chemotherapy.
HP opinion: Giemsa staining demonstrated neoplastic lymphocytes infiltration. Immunochemical testing was positive for Burkitt lymphoma (CD10, CD20, CD34, Bcl-2, Ki67, IgM, MIB-1 with a proliferation index of over 90% of neoplastic cells) and c-myc translocation determined by FISH analysis (fusion and split). (Fig. , , , , )",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [16, 'years'], 'weight': [70.0, 'kg'], 'sex': 'Male', 'Sodium': [138.0, 'mmol/L']}",-0.6,-0.57,-0.63,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 16 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 70.0 kg. The concentration of sodium is 138.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 70.0 * (138.0/140 - 1) = -0.6 L. The patient's free body water deficit is -0.6 L."
6011,38,Free Water Deficit,lab test,decimal,pmc-5484263-1,Extracted,"A 7-year-old girl visited the emergency department with severe polyuria. She had a 3-day history of frequent urination (3–4 times every hour), polydipsia, and lethargy. Although she drank more beverage than usual, she felt excessive thirst and lost weight from 22 to 19.6 kg in 7 days. She had recently moved to a new house and was having a hard time fitting in at the new school. She was previously healthy with no past admissions or serious illness. She had no change of eating habits and lifestyle recently. No history or family history of endocrine disease including diabetes mellitus was reported. At admission, her height was 127.4 cm (50th–75th percentile), weight was 19.6 kg (5th–10th percentile), and body mass index (BMI) was 12.08 kg/m2 (<first percentile). Her temperature was 37.2°C, heart rate was 88 beats/min, respiratory rate was 18 beats/min, blood pressure was 100/60 mm Hg, and pulse oximetry was 100% on room air. Her mental status was alert, sensation was intact, and motor strength was quite good considering her condition. However, she looked cachectic and lethargic. Her glucose level was too high to check with a capillary blood glucose meter, so a blood test was performed and rehydration therapy with intravenous fluid (isotonic saline 10 mL/kg loading dose for 1 hour) was started immediately (Table ). Initial biochemistry results demonstrated severe hyperglycemia (1167 mg/dL), hyperosmolality of 350 mOsm/kg (effective osmolality 311 mOsm/kg), mild acidosis (venous pH 7.34), hyponatremia (sodium 123 mmol/L; corrected for blood glucose: 140 mmol/L), severe glycosuria, and mild ketonuria.
On the basis of the laboratory results, intensive intravenous fluid and regular insulin were administered and laboratory examinations were performed every 2 hours to check and modulate electrolyte changes. Serum glucose level decreased approximately 60 mg/dL/h and normalized to 115 mg/dL 17 hours after treatment started, which led a gradual decrease in serum osmolality (Fig. ). No evidence of acidosis or severe ketosis confirmed the diagnosis of HHS. A neurological examination and brain computed tomography scan were performed to check for complications of HHS, but no cerebral edema was found.
The laboratory results that confirmed the diagnosis of T1DM were as follows: glycated hemoglobin (HbA1c), 15.6% (reference, <5.6%); C-peptide, 0.12 ng/mL (reference, 1.10–4.40 ng/ml); anti-GAD antibody, 2.4 U/mL (reference, ≤9.0 U/mL); anti-insulin antibody, 4.9% (reference, ≤7.0%); anti-islet cell antibody, negative; and 24-hour urine c-peptide, 4.5 μg/day (reference, 17.2–181.0 μg/day). All parameters of other hormone group were within normal range; triiodothyronine, 86.23 ng/dL (reference, 80.00–200.00 ng/dL); free thyroxine, 1.40 ng/dL (reference, 0.70–2.00 ng/dL); thyroid-stimulating hormone (TSH), 2.78 μIU/mL (reference, 0.5–4.5 μIU/mL); anti-thyroglobulin, 25.30 IU/mL (reference, ≤115.00 IU/mL); anti-microsome, 5.19 IU/mL (reference, ≤34.0 IU/mL); anti-TSH receptor 0.40 IU/L (reference, ≤1.75 IU/L).
After a 13-day hospital stay that included blood glucose control and T1DM education, she was discharged without any symptoms. Anthropometric measurements at discharge were height, 127.0 cm (50th–75th percentile); weight, 24.0 kg (25th–50th percentile); and BMI, 14.88 (29th percentile). She is being followed-up in the outpatient clinic regularly with split insulin therapy (Neutral protamine Hagedorn and regular insulins) and self-glucose monitoring. At recent visits (4 months after discharge), her HbA1c level was 7.1%, and she was maintaining blood glucose within the target range.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [7, 'years'], 'weight': [19.6, 'kg'], 'Sodium': [123.0, 'mmol/L']}",-1.428,-1.3566,-1.4994,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 7 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 19.6 kg. The concentration of sodium is 123.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 19.6 * (123.0/140 - 1) = -1.428 L. The patient's free body water deficit is -1.428 L."
6012,38,Free Water Deficit,lab test,decimal,pmc-6984147-1,Extracted,"A 51-year-old man was admitted to our hospital in mid-April with a history of edema in the lower extremities since the beginning of April. Medical history included FRNS at 15 years of age that had been treated using PSL at an initial dosage of 1.0 mg/kg/day at the time of relapse. Steroid therapy had finished by 42 years of age, after which time complete remission was maintained. Since he had developed depression as a part of SIPS at 16 years of age, he had been regularly seeing a psychiatrist and had maintained control of psychiatric symptoms under a stable condition using fluvoxamine maleate acid at 300 mg/day.
On admission, body weight was 68.1 kg, representing a gain of about 10 kg to a higher than usual weight over the preceding 2 weeks. Blood pressure was also high, at 159/103 mm Hg. Major laboratory examinations on admission showed: white blood cells, 7,340/μL; blood hemoglobin, 13.7 g/dL; platelet count, 36.1 ×104/μL; partial thromboplastin time, 10.3 s; activated partial thromboplastin time, 23.0 s; D-dimer, 3.4 µg/mL; total protein, 4.3 g/dL; serum albumin, 1.5 g/dL; lactate dehydrogenase, 240 U/L; aspartate aminotransferase, 17 U/L; alanine aminotransferase, 7 U/L; low-density lipoprotein cholesterol, 326 mg/dL; triglyceride, 278 mg/dL; blood urea nitrogen, 12.9 mg/dL; serum creatinine, 0.85 mg/dL; sodium, 142 mEq/L; potassium, 4.2 mEq/L; chloride, 104 mEq/L; C-reactive protein, 0.03 mg/dL; glycated hemoglobin (HbA1c), 5.6%; C3, 167 mg/dL; C4, 40.3 mg/dL; hemolytic complement activity (CH50), 58 mg/dL; immunoglobulin (Ig)G, 949 mg/dL; IgA, 398 mg/dL; IgM, 52 mg/dL; antinuclear antibody, (–); and antineutrophil cytoplasmic antibodies, (–). Urinalysis revealed: proteinuria, 7.8 g/day; glycosuria, (–); occult blood, (–); and urinary protein selectivity, 0.20. Immunoelectrophoretic study showed no myeloma protein. Chest X-ray disclosed mild bilateral pleural effusion.
These findings suggested relapse of MCNS because of the high selective glomerular proteinuria, hypoalbuminemia, hyperlipidemia, and peripheral edema. We therefore performed percutaneous renal biopsy and obtained the following findings. Light microscopy revealed 29 glomeruli, none of which were globally or segmentally sclerotic. Glomeruli were nearly normal but showed up to mild mesangial proliferation (Fig. ). Immunofluorescent staining showed normal findings. However, electron microscopy showed diffuse effacement of the foot processes (Fig. ). Finally, we reached a definitive diagnosis of recurrent FRNS.
We started immunosuppressive therapy with PSL at an initial dosage of 0.3 mg/kg/day (20 mg/day) in combination with CsA at an initial dosage of 1.5 mg/kg/day (Fig. ). Standard immunosuppressive therapy for recurrent FRNS is PSL alone at an initial dosage of 1.0 mg/kg/day for a minimum of 4 weeks, but the history of depression as a part of SIPS necessitated a reduction in the dosage and duration of steroid therapy. On the other hand, CsA requires cautious use to avoid CsA-induced nephrotoxicity. To prevent CsA-induced nephropathy, maintaining the appropriate blood CsA concentration within a narrow therapeutic window appears essential. Monitoring of CsA was thus performed using concentrations at 2-h post-dose, with a target window of 600–900 ng/mL []. Complete remission of FRNS was achieved by 2 weeks after starting treatment, but SIPS recurred the day after remission. We thus promptly reduced the dosage of PSL (weekly reduction by 2.5–5 mg/day), and SIPS quickly showed improvements. The dosage of PSL was 5 mg/day as a maintenance dose at 5 weeks after the start of treatment, and complete remission was further maintained without relapse.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [51, 'years'], 'weight': [68.1, 'kg'], 'sex': 'Male', 'Sodium': [142.0, 'mEq/L']}",0.58371,0.55452,0.6129,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 51 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 68.1 kg. The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 68.1 * (142.0/140 - 1) = 0.58371 L. The patient's free body water deficit is 0.58371 L."
6013,38,Free Water Deficit,lab test,decimal,pmc-4329376-1,Extracted,"A 68-year-old female was admitted to the hospital because of a 5-day history of left pleuritic chest pain. She had no other relevant medical history except for a ten-year history of hypertension. On admission, her blood pressure was 146/70 mm Hg and her body temperature was 36.9℃. Physical examination was unremarkable, and urinalysis did not reveal any abnormal findings. Laboratory findings were as follows: hemoglobin 11.7 g/dL, hematocrit 32.7%, blood urea nitrogen (BUN) 6.9 mg/dL, serum creatinine 0.74 mg/dL, sodium 130 mEq/L, potassium 3.9 mEq/L, total protein 5.6 g/dL, albumin 3.9 g/dL, and total cholesterol 167 mg/dL. According to chest X-ray, a pleural effusion was present in the left lower lobe. The pleural fluid (PF) was exudative, and PF analysis showed a pH of 7.4, total protein of 5800 mg/dL, albumin of 3200 mg/dL, lactate dehydrogenase of 679 IU/L, and glucose of 92 mg/dL. In addition, the white blood cell (WBC) count was 3879/mm3 with 99% mononuclear cells, and adenosine deaminase (ADA) was shown to be 104.0 IU/L in the PF. Pleural biopsy and pleural cytology were negative for malignancy. Based on the exudative characteristics and the high ADA level in the PF, pleural tuberculosis was suspected and anti-tuberculosis treatment was started. Treatment comprised rifampicin 600 mg/day, isoniazid 300 mg/day, ethambutol hydrochloride 1200 mg/day, and pyrazinamide 1500 mg/day.
During the 4-week anti-tuberculosis therapy regimen, the patient developed nausea, vomiting, general weakness, and edema. Urinalysis revealed 4+proteinuria with a few transitional epithelial cells, some coarse granular casts, and many mucous threads. According to a 24-h urine collection, protein and albumin values were 9.2 and 6.2 g/day, respectively. Laboratory findings were as follows: hemoglobin 12.1 g/dL, WBC 5490/mm3, BUN 33.2 mg/dL, serum creatinine 1.36 mg/dL, creatinine clearance 39 mL/min, total protein 5.6 g/dL, albumin 2.4 g/dL, serum aspartate aminotransferase 282 IU/L, alanine aminotransferase 282 IU/L, normal total bilirubin, and a total cholesterol of 283 mg/dL. Antinuclear antibody and P-anti-neutrophil cytoplasmic antibody (ANCA) and C-ANCA were all negative with normal serum complement levels.
According to a renal biopsy, MCD was present with focal thinning of the glomerular basement membrane (). Non-sclerotic glomeruli were normocellular without mesangial expansion, and the tubules showed minimal atrophy and mild focal tubular injury. Additionally, the interstitium was widened by minimal fibrosis, and no depositions of immunoglobulins or complement components were observed in the glomeruli. Electron microscopy showed the podocyte foot processes to be diffusely effaced ().
Due to toxic hepatitis, rifampicin and isoniazid were discontinued, but ethambutol hydrochloride and pyrazinamide were maintained. Moxifloxacin was added after 1 week, and isoniazid was added after 2 weeks. The pleural tuberculosis was well controlled with isoniazid, ethambutol hydrochloride, and moxifloxacin thereafter.
When her diagnosis was confirmed to be MCD, we determined to use steroid therapy at first. However, she was afraid of adverse effects of steroid treatment and asked us to observe closely. Moreover, we found out that heavy proteinuria was developed after using anti-tuberculosis agents. In addition, hepatitis also occurred after anti-tuberculosis agents started, and then we had to stop rifampicin and isoniazid agents. Fortunately, she improved spontaneously without steroid use only after quitting rifampicin. Therefore, we observed and followed up continuously. Her nausea, vomiting, and general edema improved and her body weight recovered from 68 kg to 63 kg at 3 weeks after rifampicin discontinuation, and a random urine protein-to-creatinine ratio was 0.14 at 8 weeks (). Furthermore, her serum albumin and cholesterol levels were shown to be 3.9 g/dL and 180 mg/dL, respectively, 8 weeks after stopping rifampicin.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [68, 'years'], 'weight': [63.0, 'kg'], 'sex': 'Female', 'Sodium': [130.0, 'mEq/L']}",-2.025,-1.92375,-2.12625,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 68 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 63.0 kg. The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. Plugging in these values into the equation, we get 0.45 * 63.0 * (130.0/140 - 1) = -2.025 L. The patient's free body water deficit is -2.025 L."
6014,38,Free Water Deficit,lab test,decimal,pmc-2728609-1,Extracted,"A 51-year-old male, with a five-year history of a progressive unexplained 50 pound weight loss, presented with one week of worsening generalized weakness and diminished ability to perform activities of daily living. Physical exam was notable for a temperature of 35.9°C with orthostatic hypotension. He was cachectic with extensive muscle wasting, kyphosis, and 2+ bilateral pitting edema in the lower extremities. BMI was 14.8 kg/m2.
His medical history was remarkable for prior extensive negative evaluations for infection, neoplasm, malabsorption, or metabolic disease. He had received care from his primary medical doctor as well as a gastroenterologist, endocrinologist, hematologist, and several complementary and alternative care providers. Laboratory results, imaging studies, and multiple GI endoscopies had not demonstrated a medical cause for the patient's persistent malnourishment and continued weight loss. Bone marrow biopsy four years earlier was remarkable for a hypocellular marrow with gelatinous transformation. Complete blood count at that time revealed a normocytic anemia (Hgb: 11.1 g/dl, MCV: 97.9 fL), leukopenia (2.9 × 109/L), and severe lymphopenia (0.6 × 109/L). Two DEXA bone scans (in 2005 and 2006) demonstrated worsening osteoporosis, with lumbar T-scores of −3.4 and −3.6, and femoral T-scores of −3.4 and −3.6, respectively.
At the current admission, blood work was notable for a normocytic anemia (Hgb: 12.0 g/dl, MCV: 94.8 fL), as well as a mildly increased white blood cell count (11.9 × 109/L) with profound lymphopenia (0.0 × 109/L) and 45% band neutrophils. Platelets were 160 × 109/L. Reticulocyte index was 0.36 and iron studies were consistent with anemia of chronic disease (iron: 71 ug/dl, ferritin: 676 ng/mL, TIBC: 151 ug/dl, transferrin saturation: 47%). The patient was hypovolemic (BUN/Cr: 72.0) and hyponatremic (Na: 122 mEq/L) with low serum protein (5.4 g/dl), albumin (2.6 g/dl), and prealbumin (7.8 mg/dl). TSH was normal, aminotransferases were mildly elevated, and HIV and viral hepatitis serologies were negative.
Psychiatric evaluation, which had not been previously done, revealed a cognitively-intact man with poor insight and judgment regarding his condition. Depressive symptoms were noted, but he denied any history of suicidal ideation or self-injurious behaviors. No signs of psychosis were found. Ritualistic food preparation and restricting dietary habits were noted, although he did not endorse typical anorexia nervosa obsessions about body image or weight, nor did these appear to be consistent with obsessive-compulsive disorder. He expressed feelings of guilt and confusion with regards to sexual orientation and religious beliefs.
Following extensive negative testing for other etiologies of cachexia, the patient was diagnosed with an eating disorder, not otherwise specified (ED-NOS) and a mood disorder, NOS. He was placed in a skilled nursing facility for physical rehabilitation, pending placement in a day hospital program for eating disorder-related psychotherapy.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [51, 'years'], 'weight': [50.0, 'lbs'], 'sex': 'Male', 'Sodium': [122.0, 'mEq/L']}",-1.74957,-1.66209,-1.83705,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 51 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 50.0 lbs so this converts to 50.0 lbs * 0.453592 kg/lbs = 22.6796 kg. The concentration of sodium is 122.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 122.0 mEq. To convert from 122.0 mEq to mmol, convert from mEq to mmol. The compound 122.0 has a valence of 1, and so divide the valence by the value of mEq to get, 122.0 mEq/(1 mEq/mmol) = 122.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 122.0 mEq sodium/L converts to 122.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 22.6796 * (122.0/140 - 1) = -1.74957 L. The patient's free body water deficit is -1.74957 L."
6015,38,Free Water Deficit,lab test,decimal,pmc-4595366-1,Extracted,"A 47-year-old female visited our cardiology clinic due to dyspnea that had been progressive over the previous few months. The patient complained of resting dyspnea and peripheral pitting edema. She had no prior medical history or family history of cardiovascular disease. On physical examination, her height was 160 cm and body weight was 70 kg. Her blood pressure was 230/145 mm Hg, and her heart rate was 100 beats per minute. Auscultation of the chest revealed a coarse breathing sound with crackling and regular heart beats with no murmur. The liver and spleen were not palpable, and her bowel sounds were normal.
A blood examination revealed a 7,200/mm3 leukocyte count, 16.5 g/dL hemoglobin, a 274,000/mm3 platelet count, 296 mg/dL random glucose, 8.3% hemoglobin A1c (HbA1c), 28 mg/dL blood urea nitrogen, 1.5 mg/dL creatinine, 7.0 g/dL protein, 3.6 g/dL albumin, 33 IU/L aspartate aminotransferase, 24 IU/L alanine aminotransferase, 292 IU/L alkaline phosphatase, 2.58 mg/L high-sensitivity C-reactive protein, 248 mg/dL total cholesterol, 111 mg/dL triglycerides, 41 mg/dL high density lipoprotein, 181 mg/dL low density lipoprotein, 136 mmol/L sodium, and 4.2 mmol/L potassium. The results of a routine urinalysis were as follows: proteinuria, 2+; glycosuria, 2+; red blood cell, 0 to 1/high power field (HPF) and white blood cell, 5 to 9/HPF; and spot urine protein to creatinine ratio, 428 mg/g. A thyroid function test (TFT) revealed 88 ng/dL T3 (normal range, 78 to 182), 1.44 ng/dL free T4 (normal range, 0.8 to 1.78), and 9.86 mIU/L thyroid stimulating hormone (normal range, 0.17 to 4.05). The TFT results showed subclinical hypothyroidism, but thyroid autoantibodies were negative.
Cardiomegaly was detected on a chest radiograph, and the cardiothoracic ratio was 66% (). The electrocardiogram showed inverted T waves in the lateral and inferior leads, with no significant ST changes. A transthoracic echocardiogram revealed LV hypertrophy and severe systolic dysfunction (). The interventricular septal diameter was 1.3 cm, the LV posterior wall diameter was 1.8 cm, the LV internal diameter in diastole was 5.8 cm (normal range, 3.9 to 5.3), the LV internal diameter in systole was 5.1 cm (normal range, 2.1 to 4.0), and the left ventricular ejection fraction (LVEF) was 25% (). Coronary angiography was performed, and the results were normal.
The patient was treated with multiple antihypertensive drugs, including calcium channel blockers, diuretics, angiotensin converting enzyme inhibitors, and β-blockers to control a hypertensive crisis, but her blood pressure remained >160/100 mm Hg. Abdominal computed tomography was performed to evaluate secondary hypertension, which revealed no abnormalities in either the renal arteries or adrenal glands.
To manage diabetes mellitus, she was referred to Department of Endocrinology and Metabolism at Kyung Hee University Hospital at Gangdong. Because the patient had uncontrolled hypertension, newly diagnosed diabetes mellitus, and soft tissue and bone overgrowth, a diagnosis of acromegaly was suspected. Rough and thick skin was observed, and skin tags were noted around the neck. An enlarged jaw and protruded frontal bones were observed, and soft tissue overgrowth of the heel was noted on a lateral view of a foot X-ray (). The basal IGF-1 level was measured as 183.8 ng/mL, which was within the normal range (90 to 360). Acromegaly was diagnosed after performing a 75-g glucose-loading GH suppression test (). In a thyrotropin-releasing hormone stimulation test, GH levels were found to be increased (). MRI of the sella revealed a 5-mm microadenoma on the left side of the pituitary gland (). A combined pituitary stimulation test performed before surgery revealed that both basal and stimulated hormone levels were normal.
Hyperglycemia was treated with 500 mg metformin twice a day and 12 U insulin glargine once a day via subcutaneous injection. We performed a diabetic complication test, and fundoscopy showed severe nonproliferative diabetic retinopathy ().
Three weeks after admission, combination antihypertensive therapy caused a reduction in blood pressure to <140/80 mm Hg. A follow-up echocardiogram showed no significant difference in LV hypertrophy, but LVEF was improved to 66% ().
After transsphenoidal resection of the pituitary tumor, the tumor was identified as a GH-secreting adenoma () that showed strong staining with anti-GH antibodies in immunohistochemical analysis ().
We performed a follow-up 75-g glucose-loading GH suppression test 2 weeks after surgery, and GH levels were suppressed to 0.15 ng/mL, which means cure state (). The levels of GH and IGF-1 were 0.57, 243.7 ng/mL on postoperative day (POD) 3, 0.38, 295.4 ng/mL on POD 50, and 0.4, 249.5 ng/mL 6 months after surgery (). A follow-up transthoracic echocardiography 6 months after surgery revealed improved LV hypertrophy and LVEF compared with preoperative values.
The patient was prescribed calcium channel blockers and angiotensin-receptor blockers. Her blood pressure was maintained at 120/70 mm Hg 1 year after surgery. Her blood glucose levels were well controlled, with an HbA1c of 5.4%, using only 500 mg/day metformin without insulin. The degree of diabetic retinopathy was improved somewhat, and the patient was followed-up at the outpatient clinic.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [47, 'years'], 'weight': [70.0, 'kg'], 'sex': 'Female', 'Sodium': [136.0, 'mmol/L']}",-1,-0.95,-1.05,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 47 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 70.0 kg. The concentration of sodium is 136.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 70.0 * (136.0/140 - 1) = -1.0 L. The patient's free body water deficit is -1.0 L."
6016,38,Free Water Deficit,lab test,decimal,pmc-4170087-1,Extracted,"A 52-years-old female was visited to our hospital emergency department due to abrupt onset of headache, fever, and vomiting. On her past history she suffered from chronic sinusitis 10 years ago. Two years ago, she received right total maxillectomy for treatment of right maxillary sinus infection with necrosis. Since one year ago, she experienced orthopedic surgery of open reduction and internal fixation of both femur due to slip down injury (). She had no history of hypertension, diabetes, hepatitis, and tuberculosis. Family history of other family members could not obtained except her elder sister because she did not wanted disclose her disease further to her family members. Her elder sister diagnosed osteopetrosis 12 years ago during dental procedure and had past history of femur fracture since 22 years ago. On her social history, she took intermittent alcohol consumption without smoking.
On arrival at the emergency department, she had a systolic blood pressure of 110 mmHg, diastolic pressure of 70 mmHg, pulse rate of 133 per minute, breathing rate of 22 per minute, body temperature of 38.3℃. She had 153 cm of height, 40.1 kg of body weight, and 17.1 kg/m2 of body mass index (BMI). On physical and neurological examination, she showed right eye proptosis and lateral gaze palsy, left hearing disturbance, and left facial nerve area sensory deficit.
Laboratory examinations were performed at the time of visiting; leukocyte was 14,000/mm3 (reference range 4,000-10,000), hemoglobin was 10.6 g/dL (reference range 12.0-16.0), platelet count was 354,000/mm3 (reference range 140,000-400,000), erythrocyte sedimentation rate was 81 mm/hr (reference range 0-20), and C-reactive protein was 18.12 mg/dL (reference range 0-0.50). Blood chemistry showed serum albumin 3.7 g/dL (reference range 3.5-5.0), total calcium 7.8 mg/dL (reference range 7.8-10.0), phosphorus 1.6 mg/dL (reference range 2.9-4.3), ionized calcium 0.89 mM/L (reference range 0.96-1.40), sodium 125 mM/L (reference range 137-150), potassium 4.1 mM/L (reference range 3.5-5.3), chloride 87 mmol/L (reference range 99-110), bicarbonate 28 mmol/L (reference range 22-34).
Radiographs of chest and PNS showed diffuse sclerotic change in bony structures (). Brain magnetic resonance imaging (MRI) showed leptomeningitis with abscess formation along right Meckel's cave and right cavernous sinus wall ().
Empirical parenteral antibiotics were started with ceftriaxone, metronidazole, and vancomycin for cavernous sinus thrombophlebitis and meningitis. Antibiotics were changed to ceftriaxone alone after obtained blood culture results with streptococcus constellatus, milleri infection.
Ten days after admission, she showed symptoms of febrile sensation, vomiting, whirling type vertigo, and generalized tonic chronic seizure attack. Mental status changed from alert to deep drowsy. On brain MRI scan, epidural empyema along right frontotemporal convexity and aggravation of meningeal enhancement were seen (). She was moved to intensive care unit and antibiotics were changed to vancomycin and metronidazole because antibiotics therapy with ceftriaxone alone caused aggravation of patient's symptom. Intravenous (IV) steroid and mannitol were administered to control increased intracranial pressure. Prompt neurosurgical decompression was indicated, but neurosurgery was not done due to refusal of operation by family members, patient's poor nutritional status like extremely low BMI and sclerotic bone disease with possibility of nonunion after operation. On cerebrospinal fluid (CSF) examination, red blood cell 0/mm3, leukocyte 800/mm3 on fluid analysis, but micro-organism was not grown.
Thirteen days after admission, she was transferred to general ward because her mental status changed to alert again with no further seizure attack. Seventeen days after admission, fever was developed again, so metronidazole was changed to meropenem to cover broader spectrum of infection. Vancomycin was stopped for 2 weeks later because fever was developed during previous vancomycin usage, and maintained meropenem alone for further 10 weeks. On endoscopic examination, sphenoid sinus was suspected to focus of infection. Five weeks after admission, she got a right sphenoidotomy under local anesthesia. Complete resolution of infection was obtained after broad spectrum antibiotic therapy for 12 weeks.
For etiologic evaluation, we tested further examination for diffuse sclerosing bony structure. Laboratory data revealed elevated serum levels of tartrate resistant acid phosphatase (TRAP) without carbonic anhydrase II DNA mutation, the intact parathyroid hormone (PTH) was elevated by 144.04 pg/mL (reference range 15-65), the 1,25-dihydroxy-vitamin D (1,25-[OH]2D) was elevated by 91.0 pg/mL (reference range 20.0-60.0), and the 25-hydroxy-vitamin D3 (25-[OH]D3) was decreased by 11.43 ng/mL (reference range 20-30). Results of bone formation and resorption marker were various with the value of bone alkaline phosphatase isoenzyme 34.2 g/L (age and gender specific reference range below 22), osteocalcin 10.4 ng/mL (age and gender specific reference range 4.0-12.0), and deoxypyridinoline 9.5 nM deoxypyridinoline (DPD)/mM (reference range 3.0-7.4), respectively. A plain radiograph of the spine showed end-plate thickening and sclerosis producing the classic ""sandwich vertebra"" appearance (). Bone mineral densitometry showed increased lumbar spine vertebral bone density and bone mineral content values (bone mineral density 2.713 g/cm2 with T-score +14.84, bone mineral content of lumbar spine 173.28 g). For evaluation of chloride channel 7 (CLCN7) deficiency osteopetrosis, we performed a CLCN7 gene mutation analysis using genomic DNA which was extracted from peripheral blood using genomic DNA prep kit (Solgent Co. Ltd., Daejeon, Korea). But we could not found any mutations on 24 and 25 exon of CLCN7 gene. And her older sister's spine X-ray also showed sandwich vertebra appearance () and the CLCN7 gene mutation was not found, too.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [52, 'years'], 'weight': [40.1, 'kg'], 'sex': 'Female', 'Sodium': [125.0, 'mmol/L']}",-2.14821,-2.0408,-2.25562,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 52 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 40.1 kg. The concentration of sodium is 125.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 40.1 * (125.0/140 - 1) = -2.14821 L. The patient's free body water deficit is -2.14821 L."
6017,38,Free Water Deficit,lab test,decimal,pmc-6555724-1,Extracted,"The patient was a 45-year-old male who was admitted to our institution due to uremia. He had no diabetes and biliary tract disease history, and his BMI (body mass index) was 22.99 kg/m2 (183cm, 77 kg). He underwent kidney transplantation in our institution on 9th August, 2017. The donor was from donation after cardiac death (DCD). Before surgery, he received antilymphocyte therapy of basiliximab (20 mg i.v.). The surgery was successful and the initial immunosuppressive regimen consisted of tacrolimus (6 mg/day, 0.078 mg/kg/day), mycophenolate mofetil (1500 mg/day) and corticosteroids (initial dose 35 mg/day). The patient recovered well after surgery and was discharged on day 26+ with blood creatine level 156.6umol/L and trough concentration of tacrolimus 10.6 ng/ml then. After discharged, He reexamined in our institution once a week. From day 26+ to day 60+, the reexamine results showed his blood creatine level continued to decline to 101.7umol/L (day 60+), the dosage of corticosteroids was gradually tapered from 35 mg/day to 5 mg/day, and the dosage of tacrolimus was maintained at 6 mg/d with trough concentration ranged from 9.5–11.2 ng/ml. In addition, the recipient neither had a history of high fat diet nor presented hyperlipidemia from day 1+ to 67+ posttransplant, the laboratory analysis results showed the serum triglyceride (TG) level was in the range of 0.71–1.43 mmol/L while the cholesterol (CHOL) level was 3.3–4.5 mmol/L during the period.
On day 67+, he presented with acute abdominal pain in middle and left area of abdomen accompanied with nausea and vomiting. Physical examination showed diffuse abdominal tenderness with diminish bowel sound. Laboratory analysis showed WBC 9.16 × 109/L, neutrophils 7.98 × 109/L, hemoglobin 73 g/L, platelets 78 × 109/L, blood creatinine 147.4umol/L, blood urea nitrogen (BUN) 17.79 mmol/L, calcium 2.52 mmol/L, potassium 4.72 mmol/L, sodium 138 mmol/L, serum amylase 679.3 IU/L (normal 15–115), lipase 755 U/L (normal 6–51), trough concentration tacrolimus> 30 ng/ml (dosage was 6 mg/day) accompanied with elevated fasting blood glucose (29.49 mmol/L) and diabetic ketoacidosis (DKA) tendercy (blood ketone body test +). Abdominal computed tomography scan showed enlarged pancreatic head with peripancreatic inflammation and inflammatory exudate without dilatation of biliary tract (Fig. ). Pancreatitis diagnosis was made on the basis of the information all above.
Tacrolimus treatment was discontinued, somatostatin (3 mg, q12h, i.v.) was administrated to treat pancreatitis, other treatments included fluid replacement, insulin (i.v.) and imipenem (1 g, q12h, i.v.). Three days after somatostatin using (day 70+), patient’s condition improved significantly, abdomen symptoms relieved, blood amylase level were normalized (72 IU/L) and lipase level deceased to 69 U/L, blood glucose level maintained around 10–15 mmol/L. Cyclosporine (4 mg/kg/day) was administrated as an alternative for tacrolimus on day 75+, and the patient was discharged on day 80 + .
There was no recurrence of pancreatitis in 7 months follow up.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'years'], 'weight': [77.0, 'kg'], 'sex': 'Male', 'Sodium': [138.0, 'mmol/L']}",-0.66,-0.627,-0.693,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 45 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 77.0 kg. The concentration of sodium is 138.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 77.0 * (138.0/140 - 1) = -0.66 L. The patient's free body water deficit is -0.66 L."
6018,38,Free Water Deficit,lab test,decimal,pmc-8142406-1,Extracted,"An 82-year-old Japanese man was transferred to the emergency unit of Shimada Municipal Hospital, Shimada, Shizuoka, Japan, with complaints of severe watery diarrhea and hematochezia. The patient had suffered from hypertension and hyperlipidemia since the age of 50. He had undergone total hip replacement for right femoral head fracture caused by a traffic accident at the age of 71, and he received a surgical procedure for lumber spinal stenosis at the age of 74. Borderline diabetes mellitus with HbA1c levels ranging from 6.0% to 6.6% was pointed out since the age of 72, while the blood glucose level remained within a normal range. At the age of 76, the diagnosis of hypertensive and diabetic chronic kidney disease was made. The patient suffered from pneumonia when he was 78 years old. One year before admission, an infected cyst (abscess) around the right femoral prosthesis was indicated by fluorodeoxyglucose-positron emission tomography. Staphylococcus aureus was cultured, and the first and third-generation Cefem plus new quinolone were continuously administered. Three months before admission, continuous drainage from the infected lesion was conducted. No gastrointestinal complaints were recorded prior to the final admission.
His watery diarrhea was severe, more than 10 times a day, and hematochezia was associated. The body temperature was 37.5°C, blood pressure 138/90 mm Hg, heart rate 100 beats per minute, and oxygen saturation 96% while breathing ambient air. The body weight was 57.0 kg with a body mass index at 22.0. Systolic heart murmur was auscultated. The abdomen was soft with weak bowel sounds. There was tenderness of the whole abdomen on palpation, without guarding, rigidity, distention, or mass formation. Main results of laboratory tests on admission included the following: white blood cells 4400/μL, hemoglobin 13.3 g/dL, platelets 305 000/μL, Na 135 mmol/L, K 3.6 mmol/L, Cl 102 mmol/L, Ca 6.4 mg/dL, Pi 4.6 mg/dL, albumin 1.8 g/dL, blood urea nitrogen 49.9 mg/dL, creatinine 5.3 mg/dL, and C-reactive protein 26.1 mg/dL. The electrocardiogram showed a normal sinus rhythm with long PR and QT intervals. Deterioration of renal functions for the last 10-year period is illustrated in Figure . For the last 3 months, hemodialysis was needed.
Plain and contrast-enhanced computed tomography scans, performed on the first and eighth days of hospitalization, respectively, indicated significant ischemic changes of the sigmoid colon through the rectum with wall thickening of the sigmoid colon, ascites retention, bilateral pleural effusions, and mild renal atrophy. Colonofiberscopy indicated diverticulosis in the sigmoid colon and ischemic changes and erosions of the stenotic sigmoid colon through rectum (Figure ). Microbiologically, the stool proved normal flora, and fecal Clostridium difficile toxin test and blood microbial culture were negative. The clinical diagnosis of ischemic and infectious colitis secondary to the long-term usage of antibiotics was made. Intravenous infusion of ceftriaxone for 5 days was chosen empirically because it is metabolized in the liver. However, it was ineffective for relieving diarrhea and colitis, and then meropenem was chosen for controlling the intractable colonic symptoms. Inflammation peaked out 14 days after the treatment, but soon, the inflammatory reaction and diarrhea re-exacerbated. The patient expired 26 days after admission. No free air was observed in the abdominal cavity on the contrast-enhanced computed tomography scan 3 days before death.
The autopsy was conducted 6 hours after death. In the sigmoid colon, fibrosing and adhesive diverticulitis with mucosal ischemic changes and erosions were grossly observed. Microscopically, eosinophilic hyaline material was deposited throughout the gut wall. The deposits were congophilic. Immunohistochemically, amyloid A, visualized by the monoclonal antibody mc-1 against serum amyloid A1 (SAA1), was identified in the lamina propria mucosae through the subserosa, including diverticular and vascular walls (Figure ). In the prepylorus of the stomach, a large perforating ulcer measuring 12 mm was found, and purulent peritonitis with turbid ascites was associated (Figure ). Candida infection was microscopically demonstrated on the involved mucosa and serosa at the site of gastric perforation (Figure ). Candida albicans were cultured from turbid ascitic fluid containing a total of 1150 mL. Candidal esophagitis was also noted. Deposition of amyloid A was evident in the gastric mucosa through the subserosa, and the amyloid deposition was especially prominent and seen in the full-thickness of the mucosa at the site of gastric perforation (Figure ). Amyloid A was also diffusely deposited in the wall of the esophagus through the rectum. Pleural effusion was associated (left: 150 mL, right: 300 mL).
Systemic congophilic deposition of amyloid A was further demonstrated in the tongue, salivary gland, thyroid gland, lung, heart, pancreas, splenic white pulp, adrenal glands, kidney, urinary bladder, and ureter. The deposition was especially pronounced in the thyroid gland (38 g) and urinary tract.
Atrophic kidneys weighed 72 g (left) and 73 g (right). Microscopically, amyloid A deposits caused amyloid glomerulopathy in association with vascular wall involvement. Features of diabetic glomerulosclerosis were indistinct because of marked amyloid deposition, while arteriolosclerosis was observed. Pancreatic islets focally showed diabetes-related localized hyaline (amyloid) deposition. Characteristically, co-deposition of amyloid A and IgM in the renal glomerulus was demonstrated by immunostaining using formalin-fixed, paraffin-embedded sections after prolonged protease-1 digestion (Figure ). IgG and IgA were undetectable. The co-deposition of amyloid A and IgM was scarcely observed in the systemic amyloid A deposits outside the kidney (Figure ).
Most of the hepatocytes were immunostained with the anti-SAA1 monoclonal antibody mc-1. Cytoplasmic granular positivity was evident. The acinar cells of the pancreas and salivary gland were also positively stained. These findings indicated accelerated production of SAA1 protein by these cells as a prolonged inflammatory response (Figure ).
Another incidental finding included aortic stenosis caused by dystrophic calcification in the cusps of the aortic valve. Left ventricular hypertrophy (heart weight 415 g) was caused by both aortic stenosis and amyloid deposition. The aorta revealed severe atherosclerosis. The abscess lesion around the right femoral prosthesis was not evaluated.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [82, 'years'], 'weight': [57.0, 'kg'], 'Sodium': [135.0, 'mmol/L']}",-1.01786,-0.96697,-1.06875,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 82 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 57.0 kg. The concentration of sodium is 135.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 57.0 * (135.0/140 - 1) = -1.01786 L. The patient's free body water deficit is -1.01786 L."
6019,38,Free Water Deficit,lab test,decimal,pmc-3537693-1,Extracted,"A 35-day-old male Egyptian baby was referred to our institution from a regional hospital for evaluation of a two-week history of recurrent vomiting associated with hyponatremia, hyperkalemia and failure to gain weight. He was the first child of related Egyptian parents. The pregnancy was uneventful and his mother had not been treated with any drugs. The existence of other children with this condition had not previously been mentioned. He was delivered at term by Caesarean section with a birth weight of 3.4kg, and cried immediately after delivery. He required admission to the special care baby unit shortly after birth for hypoglycemia; his blood sugar levels were easily maintained on 10% dextrose and then on milk feeds.
On examination, our patient’s weight was 3.5kg (below the third percentile), he was dehydrated, his blood pressure was 70/40mmHg, and he had no hyperpigmentation or dysmorphic features. A genital examination revealed distal penile hypospadias with chordee and normal testes (Figure ). Laboratory investigation results showed a serum sodium level of 119mmol/L, potassium 6.5mmol/L and glucose 55mg/dL. Blood gas analysis results showed a pH of 7.31, bicarbonate ion level of 16.9mmHg and a base excess of 6.3mmol/L. His cortisol level was 0.3μg/dL (normal range: 2.8 to 23μg/dL) and adrenocorticotropic hormone level, 512pg/mL (normal range: 6 to 48pg/mL). An adrenocorticotropic hormone stimulation test did not cause a rise in his cortisol level. His 17-hydroxyprogesterone level was 0.005ng/mL (normal range: 0.03 to 0.9ng/mL), androstenedione 0.012ng/mL (normal range: 0.1 to 0.17ng/mL), dehydroepiandrosterone 6ng/mL (normal range: 50 to 480ng/mL), plasma renin activity 90ng/mL/hour (normal range: 2.35 to 37ng/mL/hour) and aldosterone 31pg/mL (normal range: 50 to 900pg/mL). His triglyceride and creatine kinase levels were normal. His blood karyotype was 46,XY. A magnetic resonance imaging study of his abdomen revealed small adrenal glands and a normal genitourinary system.
Based on the clinical history and investigative findings, a provisional diagnosis of congenital adrenal hypoplasia associated with hypospadias was made. A molecular genetic study detected hemizygous mutations (p.Arg327Pro). A deoxyribonucleic acid (DNA) study of our patient’s mother confirmed her to be heterozygous for the same mutation. No mutation was found in his father. With the identification of a hemizygous mutation in the DAX-1 gene, a clinical diagnosis of X-linked congenital adrenal hypoplasia was confirmed. Further, mutation c.325delG in the MAMLD1 gene was detected, which may point to a possible etiology of hypospadias in our patient’s case. He was started on hydrocortisone at a dose of 10mg/m2/day and fludrocortisone 0.05mg/day. After three weeks of treatment the vomiting stopped, his weight was 4.1kg and his blood sugar, sodium, potassium and cortisol levels normalized. At the age of three months, a human chorionic gonadotropin (hCG) loading test was performed to evaluate his gonadal function. Basal values of luteinizing hormone and follicle-stimulating hormone were <0.5IU/L and 0.41IU/L, respectively, which is within normal prepubertal limits. The hCG loading test resulted in a normal testosterone response from <0.05ng/mL to 4.24ng/mL. The ratio of testosterone to DHT after hCG loading was 7.3:1.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [35, 'days'], 'weight': [3.5, 'kg'], 'sex': 'Male', 'Sodium': [119.0, 'mmol/L']}",-0.315,-0.29925,-0.33075,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 35 days old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 3.5 kg. The concentration of sodium is 119.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 3.5 * (119.0/140 - 1) = -0.315 L. The patient's free body water deficit is -0.315 L."
6020,38,Free Water Deficit,lab test,decimal,pmc-6922534-1,Extracted,"A 78-year-old female presented to the surgical emergency unit at the University Hospital with abdominal pain and nausea. Symptoms had begun 48 hours prior to hospital admission. She had lost over 10 kg of body weight in the previous couple of months, hence a diagnosis of gastrointestinal malignancy was suspected. Her vital signs were: RR, 140/90 mmHg; pulse rate, 90 beats/min; respiration rate, 15/min; and body temperature, 38.1°C. Her past medical history revealed only arterial hypertension. She did not mention having ingested the foreign body.
Physical examination pointed to a distended and diffusely tender abdomen with right lower abdomen rebound. Laboratory tests were as follows: white blood cell count, 11.6 × 109/L; serum creatinine level, 58 μmol/L; blood urea nitrogen level, 2.5 mmol/L; blood glucose level, 6.1 mmol/L; sodium 137 mmol/L; potassium 4.4 mmol/L; CRP 76.6 mg/L. An urgent abdominal X-ray did not show any sign of ileus or perforation.
A multidetector-row computed tomography (MDCT) examination of the abdomen was performed using a 64-detector-row CT scanner (Siemens Somatom Definition AS, Erlangen, Germany). Scans were performed before and after the administration of intravenous contrast, with prior peroral diluted iodine contrast uptake, and images were analyzed in axial and reconstructed coronal and sagittal planes. MDCT revealed mural thickening and enhancement of the cecum with haziness and linear areas of high attenuation in the pericecal fat tissue (Fig. ). The terminal ileum and ileocecal valve had a normal appearance. The wall thickness and outer diameter of the appendix were normal, having neither air nor appendicolith in the lumen. There was no periappendiceal abscess, phlegmon, extra-luminal air, or enlarged lymph nodes. Additionally, a foreign body in the lumen of the colon was not seen. Due to MDCT signs of mural thickening and enhancement of the cecum with haziness and linear areas of high attenuation in the pericecal fat tissue as well as due to increased inflammatory laboratory parameters, the patient was hospitalized and treated with broad-spectrum antibiotics (ciprofloxacin and metronidazole) and crystalloid fluids.
The day after admission, colonoscopy under conscious sedation was performed following oral bowel preparation. Close to the Bauchini valve, the clear presence of a sharp 5.5-cm-long chicken bone perforating the cecal wall at the antemesenteric site was seen. The mucosa of the remainder of the cecum had a normal appearance (Fig. A). A quarter of the bone that had penetrated the cecal wall was pulled out using a polypectomy snare (Fig. B). Due to the form and length of the bone, we continued withdrawing it through the entire colon, using pointed end trailing. During the entire removal process, we insufflated air in the bowel (maintaining a wide lumen) and positioned the bone to the center of the visual field to avoid mucosal injury. The slight curvature of the bone was helpful for passing the splenic and hepatic flexures without any damage (Fig. ). Post-procedure treatment with fluid resuscitation and broad-spectrum antibiotics (ciprofloxacin and metronidazole) was successful, and the patient was discharged three days after colonoscopy with normal laboratory results and without any pain.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [78, 'years'], 'weight': [10.0, 'kg'], 'sex': 'Female', 'Sodium': [137.0, 'mmol/L']}",-0.09643,-0.09161,-0.10125,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 78 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 10.0 kg. The concentration of sodium is 137.0 mmol/L. Plugging in these values into the equation, we get 0.45 * 10.0 * (137.0/140 - 1) = -0.09643 L. The patient's free body water deficit is -0.09643 L."
6021,38,Free Water Deficit,lab test,decimal,pmc-5217592-1,Extracted,"A 30 year old G2P1001 sub-Saharan African female teacher at 11 weeks amenorrhea, presented to the Nkwen Baptist Health Center (Bamenda, North West Region of Cameroon) on the 15th of May 2016 with bilateral lower limb swelling and pain of 5 days duration. She had no known chronic illness and denied having a family history of VTE.
She reported being well till 2 weeks prior to presentation when she started experiencing abdominal pains; the pain was mainly in her lower abdomen, dull in nature, non-radiating, mild in intensity, was initially intermittent then became constant. It was associated with intermittent low grade fever. This prompted her to consult at a remote health center, where a urinalysis and malaria parasite test was done but their results were inconclusive. She was then cautioned to be having early pregnancy symptoms and placed on acetaminophen 3 g per day in three divided doses which she took for a week with no regression of symptoms. The persistent and progressively worsening pain now localized at the right lower quadrant prompted a second consultation at another health facility. This pain was still associated with low grade fever and now included; loss of appetite and intermittent postprandial vomiting. The attending physician on examination remarked right iliac fossa tenderness and rebound tenderness with a positive Rovsing’s sign. Presumptive diagnosis of acute appendicitis and differential of ovarian cyst in pregnancy were retained. An emergency surgery was booked. However, intra-operative findings revealed a normal appendix and ovaries.
Following surgery, lower abdominal pains persisted and she complained of a sudden onset of crampy constant pains in her right thigh. She was told to be having post surgery pain, for which she was then given analgesics. On day 3 post hospitalization she was discharged on analgesics, antibiotics and progesterone suppository. While at home, the pains persisted and 2 days later involved her left calf area. This was associated with bilateral lower limb swelling that was more on the right lower limb. The pain increased in severity making it difficult for her to walk. This prompted consultation at our health facility.
On arrival she was ill-looking and in painful distress. Her blood pressure was 122/76 mmHg, heart rate 94 beats/min, respiratory rate of 22 breaths/min, temperature 37 °C, O2 saturation at 97% and weight 58 kg. Her conjunctivae were pink and sclera anicteric, heart sounds were normal and lung fields clear. On examining the abdomen, a clean midline incision was seen and there was tenderness on deep palpation of the lower abdominal quadrants marked on the right. There was bilateral lower limb pitting oedema extending to the thighs with right lower limb more swollen than left. The limbs were mildly erythematous but there was no area of cracked skin or wound on both limbs that could have served as portal of entry for skin infection. Both lower limbs were warm tender.
Based on these we made a tentative diagnosis of bilateral lower limb deep venous thrombosis in early pregnancy with a possible pelvic vein thrombosis that was misdiagnosed for acute appendicitis. Our health facility was not equipped with the necessary tools and personnel to confirm our diagnosis and manage the patient. She was therefore referred to a tertiary care center about 40 km from our facility.
At the tertiary center compressive doppler ultrasound of the pelvis and lower limbs revealed pelvic and bilateral lower extremity veins seen with echoes in the right common iliac vein (Fig. ), right femoral vein, left femoral vein and left popliteal vein. There was decreased colour flow in these veins and decreased compressibility. These suggested DVT of the right common iliac vein, right femoral vein, left femoral vein and left popliteal vein and thus confirmed our diagnosis of bilateral lower limb and pelvic DVT.
Further laboratory testing showed the following: normal white cell count of 8100/µl, mild anaemia with haemoglobin of 9.8 g/dl, thrombocytosis of 532,000/µl, normal kidney function test (serum creatinine of 0.64 mg/dl and urea of 12.7 mg/dl), glycaemia of 85.9 mg/dl and normal serum electrolytes of: (Sodium 134 mmol/l, Potassium of 4.17 mmol/l and Chloride of 103 mmol/l). Cardiac echography and electrocardiogram done were all normal.
The patient was immediately started on low molecular weight heparin (LMWH) 80 mg subcutaneous route daily. After 5 days of treatment the patient’s symptoms had subsided and she was discharge and counter referred for continuation of care. We continued her daily LMWH injections and scheduled her for a repeat of the pelvic and lower limb ultrasound. Six weeks later there were no more echoes in the pelvic and lower limb veins (Fig. ). She continued daily LMWH till 12 weeks postpartum.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [30, 'years'], 'weight': [58.0, 'kg'], 'Sodium': [134.0, 'mmol/L']}",-1.24286,-1.18072,-1.305,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 30 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 58.0 kg. The concentration of sodium is 134.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 58.0 * (134.0/140 - 1) = -1.24286 L. The patient's free body water deficit is -1.24286 L."
6022,38,Free Water Deficit,lab test,decimal,pmc-2943688-1,Extracted,"Patient: 63-year-old male
Major complaint: Fever
Pre-existing history: Mitral valve insufficiency
Family history/lifestyle history: Nothing particularly relevant
A slight fever had persisted from about June 2008 until 10 days before surgey. In July 2008, the patient underwent a TUR-P for prostatic hyperplasia using 3 days of cefotiam (CTM) i.v. 0.5g ×2/day and was discharged from the hospital on Day 10 after surgery without fever. On about Day 40 after surgery, a fever of 38–39°C was observed, so the patient was suspected of having a urinary-tract infection and was admitted to the hospital.
Body height: 166.3 cm; Body weight: 59.5 kg; Body temperature: 37.8°C; Pulse rate: stable at 84/min; Blood pressure: 116/76 mmHg. Respiratory sound: resonant; Cardiac sound: clear/no noise; Abdomen: flat/soft; Neurological findings: nothing in particular. Laboratory data at the time of admission:
Hematological values: WBC 9000/µL, RBC 4.01 × 106/µL, Hb 10.3 g/dL, Ht 30.5 %, Plt 36.6 × 104/µL , PT 78 %, PT-INR 1.14, APTT 29.4 sec, Fib 628 mg/dL
Biochemistry: TP 6.8 g/dL, Alb 3.2 g/dL, T-bil 0.5 mg/dL, D-bil 0.0 mg/dL, AST 24 IU/L, ALT 35 IU/L, ALP 631 IU/L, γ-GTP 102 IU/L, Ch.E 198 IU/L, LDH 203 IU/L, CK 18 IU/L, Amy 71 IU/L, T-chol 193 mg/dL, TG 80 mg/dL, LDL 122 mg/dL, BUN 9 mg/dL, Cre 0.7 mg/dL, UA 2.4 mg/dL, Na 139 mEq/L, K 4.2mEq/L, Cl 103 mEq/L, Ca 9.4 mg/dL, IP 3.5 mg/dL, Glu 95 mg/dL, HbA1c 5.4%, CRP 5.6 mg/dL
Urinalysis: pH 7.5, RBC many/hpf, WBC many/hpf
After admission, CTM 0.5 g × 2/day was administered for 3 days, but the CRP did not become negative, so Meropenem (MEPM) 0.5 g × 2/day was administered instead. A tendency for pyretolysis was observed, but because recovery from the urinary-tract infection was slow, echocardiography was performed for the purpose of eliminating endocarditis. In the echocardiogram findings, vegetation was observed, so Ampicillin (ABPC) 2 g × 4/day and Gentamicin (GM) 60 mg × 2/day were administered for four weeks. Pyretolysis and decreased CRP were observed, but the CRP did not become negative. Even after the 4-week administration of antibiotics, the vegetation persisted in the echocardiogram and a possibility of valve failure was suspected, so a valve replacement was performed. Furthermore, the head and chest to pelvic CT did not show any obvious abscess formation.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [63, 'years'], 'weight': [59.5, 'kg'], 'Sodium': [139.0, 'mEq/L']}",-0.255,-0.24225,-0.26775,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 63 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 59.5 kg. The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 59.5 * (139.0/140 - 1) = -0.255 L. The patient's free body water deficit is -0.255 L."
6023,38,Free Water Deficit,lab test,decimal,pmc-8084696-1,Extracted,"A 15-year-old male patient visited our outpatient clinic for a second opinion on symptoms of generalized edema in January 2020. He had been previously diagnosed with primary IL in the duodenum a few years earlier at another hospital where supportive therapies, including albumin replacement and parenteral nutritional support, were applied to relieve the edema. In November 2018, the patient reported worsening symptoms to which everolimus and later sirolimus were applied; however, both treatments failed to have a positive impact on symptom progression. The patient had no other prior medical reports or any prior surgeries. Octreotide had never been tried.
On admission, his symptoms were general weakness, weight loss, and vomiting. His laboratory tests revealed hypoalbuminemia (albumin 1.9 g/dL), electrolyte imbalance (Na 132 mmol/L, K 2.7 mmol/L, Cl 104 mmol/L), hypomagnesemia (Mg 1.2 mg/dL), and hypocalcemia (ionized calcium 0.92 mmol/L). Alpha-1 antitrypsin levels in stool were estimated at 167.66 mg/mL (normal range <100 mg/mL). Echocardiography and abdomen computed tomography indicated nothing of particular interest, whereas contrast-enhanced magnetic resonance lymphangiography () revealed abnormal lymphatic flow toward the second portion of the duodenum. Esophagogastroduodenography and capsule endoscopy revealed focal IL around the minor papilla in the second portion of the duodenum. Results did not show any fluid collections in the other third spaces (e.g., pleural space and retroperitoneum space).
Two treatment options, surgery or lymphatic embolization, were extensively discussed in multi-departmental conferences. Surgical resection required pylorus-preserving pancreatoduodenectomy as focal changes were located near the minor papilla. From a surgeon's point of view, this kind of major resection is rarely performed in this age group due to the risk of poor surgical outcomes. Therefore, a less invasive lymphatic intervention was chosen.
To investigate the anatomic details and lymphatic flow dynamics, lymphangiography was first performed through the inguinal lymph node, and hepatic lymphatics were depicted using ultrasound guidance. The intra-nodal lymphangiogram showed leakage of Lipiodol into the second portion of the duodenum. Liver lymphangiography was performed using a 23-G needle placed in the periportal space and revealed contrast agent leakage into the same locations identified by intranodal lymphangiography ().
The first embolization was attempted via the liver lymphatics based on the short distance between the needle tip and the leakage site (). This procedure was partially successful. The patient's diarrhea decreased, and his albumin level elevated from 1.5 to 2.2 g/dL. However, hypoalbuminemia with generalized edema persisted.
After another multidisciplinary discussion, we decided to attempt a second round of lymphatic embolization. The thoracic duct was accessed via a retrograde approach from the left subclavian vein using a 5-Fr catheter and a 1.7-Fr microcatheter, advancing down to one of the lumbar lymphatic channels past the cisterna chyli. Lymphangiography was then performed using an iodine contrast agent to evaluate lymphatic drainage. The lymphangiogram demonstrated leakage from an engorged, tortuous lymphatic channel originating from the cisterna chyli into the duodenal lumen around the endoscopic clip previously deployed for guidance (). Embolization was successfully performed using diluted glue (1:3) and coils.
After the second treatment, the patients' albumin level increased, remaining stable at 3.7 g/dL. He could tolerate fat-rich foods without experiencing generalized edema. Eight months later, he visited our outpatient clinic for a regular checkup at which point his albumin level had further increased to 5.0 g/dL (, only online). His nutritional status had also improved. His hemoglobin level had increased from the initial 8.8 to 15.2 g/dL, and his body weight had increased from 46 to 56.5 kg. His alpha-1 antitrypsin level was also normalized at 26 mg/mL.
The medical records of the patients were reviewed retrospectively with the approval of the Clinical Research Ethics Committee, and informed consent was obtained from the patient regarding the reporting and publication of this case report (IRB File No. SMC 2020-05-166-01).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [15, 'years'], 'weight': [56.5, 'kg'], 'sex': 'Male', 'Sodium': [132.0, 'mmol/L']}",-1.93714,-1.84028,-2.034,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 15 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 56.5 kg. The concentration of sodium is 132.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 56.5 * (132.0/140 - 1) = -1.93714 L. The patient's free body water deficit is -1.93714 L."
6024,38,Free Water Deficit,lab test,decimal,pmc-6230595-1,Extracted,"A 45-year-old male with no past medical history was transferred to our tertiary care facility after presenting to a community hospital with a one-week history of generalized abdominal pain, jaundice, dark urine, and lower extremity edema. His initial evaluation revealed severe hyperbilirubinemia and elevated transaminases, prompting his transfer. He denied any alcohol consumption for the previous twenty years or intravenous drug use. He had no medical history, was taking no medications prior to presentation, except a multivitamin. He denied taking any herbal supplements and his family history was unremarkable. He was married and employed as an auto mechanic.
On examination, he was notably jaundiced and cachectic in appearance with a height of 1.7 m, weight of 82.5 kg, and body mass index (BMI) of 28.3 kg/m2. He was afebrile with a pulse of 95 beats per minute, respiratory rate of 16 breaths per minute, and pulse oxygen saturation of 95% while on room air. He had marked scleral icterus; proptosis was noted. On thyroid examination, he had a large symmetrical, non-tender goiter with audible bruit. Heartbeat was irregularly irregular. His abdomen was mildly tender diffusely without ascites or organomegaly. Mild bilateral lower extremity edema was present. Skin was warm to the touch. A fine tremor was noted; asterixis of hands was intermittently present.
Initial laboratory evaluation revealed a hemoglobin of 12.1 g/dL (13.5-16.5), platelet count of 115 k/µL (150-400), and white blood cell count of 11.8 k/µL (4.5-11). His international normalized ratio (INR) was 2.4. His serum sodium was 128 mmol/L (137-147), potassium of 4.3 mmol/L (3.5-5.1) with creatinine of 1.77 mg/dL (0.4-1.24), blood urea nitrogen (BUN) of 57 mg/dL (7-25) and serum glucose 159 mg/dL (70-100). Notably, his total bilirubin was 19.8 mg/dL (0.3-1.2), direct bilirubin 13.8 mg/dL (<0.4), alkaline phosphatase 332 U/L (25-110), aspartate aminotransferase (AST) 86 U/L (7-40), and alanine aminotransferase (ALT) 50 U/L (7-56). His gamma-glutamyltransferase was 20 U/L (9-64). Total iron was 32 mcg/dL (50-185), percent iron saturation 11% (28%-42%), total iron binding capacity (TIBC) was 283 mcg/dL (270-380), and ferritin 121 ng/mL (30-300). The patient also had negative serology for hepatitis A, B, and C.
A workup for thyroid dysfunction demonstrated a thyroid-stimulating hormone (TSH) of 0.026 mcg/mL (0.35-5.00) with a free T4 of 4.3 ng/dL (0.6-1.6), free T3 4.6 pg/mL (2.1-3.9), and total T3 125 ng/dL (87-180). TSH receptor antibody was>40 IU/L (0.00 −1.75) and thyroid peroxidase (TPO) antibody was >1000 IU/mL (<5.61). An ultrasound of the patient's thyroid was notable for a mildly enlarged heterogeneous and hypervascular thyroid without nodularity. Based on these findings along with his presenting symptoms and signs, the patient was diagnosed with Graves’ disease.
In light of worsening cholestatic jaundice (Figure ), a thorough hepatology evaluation was undertaken for potential autoimmune, infectious, and primary hepatobiliary causes of cholestasis. The laboratory testing were all negative. Cardiac evaluation was notable for an ejection fraction of 55%-60% with right ventricular dilation and moderate mitral regurgitation. Moderate left atrial and severe right atrial enlargement was found with elevated central venous pressure as well as pulmonary artery pressure. Abdominal ultrasound demonstrated increase echogenicity of the liver and revealed trace abdominal and pelvic ascites. Further workup for cholestatic jaundice included a computed tomography scan of the abdomen and pelvis, which was notable for fatty liver, cardiomegaly, and diffuse irregular appearance of bones with prominent trabecula. Endoscopic retrograde cholangiopancreatography (ERCP) showed normal caliber common bile duct and common hepatic duct with normal intrahepatic ducts, without filling defects, strictures, or stenosis. Endoscopic ultrasound (EUS) was notable for normal pancreatic parenchyma as well as normal pancreatic and common bile ducts. The patient subsequently underwent transjugular liver biopsy with unremarkable hepatic vein pressures and a corrected sinusoidal pressure gradient of 5-6 mm Hg (normal). Pathology showed cholestasis and mild ductal proliferation with focal pericholangitis but no hepatic steatosis, fibrosis, hepatocellular injury, or necrosis. Periodic acid-Schiff (PAS) diastase digestion showed normal glycogen content without unusual intrahepatic inclusions; hepatic iron stores were normal.
Prior to transfer to our facility, he was initially stabilized with intravenous diltiazem drip 5 mg per hour titrated for rate control of his atrial fibrillation with rapid ventricular response, in combination with hydrocortisone 50 mg every eight hours and propylthiouracil (PTU) 150 mg every six hours for management of thyrotoxicosis. Due to concern for fulminant liver failure, urgent transfer was pursued to our facility. Upon arrival, the patient's thyrotoxicosis and resultant atrial fibrillation and diastolic heart failure were managed aggressively given his calculated Burch-Wartofsky score of 45. PTU was stopped in light of FDA black box warning, and methimazole was initiated at a dose of 20 mg every 8 hours; corticosteroids were continued for management of thyroid storm until normalization of total T3. The patient experienced gradual improvement in his free T4 (Figure ). His atrial fibrillation was managed with oral digoxin 125 µg after digitalizing doses and metoprolol 100 mg oral twice daily.
While the index of concern for acute liver failure prompted a swift and extensive investigation, it was entirely negative for primary hepatobiliary causes of his cholestasis including ERCP, EUS, and transjugular liver biopsy. Based on negative rheumatologic, autoimmune, and infectious causes workup, it was concluded that his cholestatic jaundice was related to Graves’ disease related thyrotoxicosis. This clinical hunch was further solidified with his clinical and metabolic improvement (Table ). Total bilirubin was 13.9 mg/dL on admission to the outside facility, peaking 17 days later at 39.1 mg/dL and improving to 14.0 mg/dL two weeks following discharge. An important point that needs to be made was his high bone-specific alkaline phosphatase, which was markedly elevated at 103 mcg/L (0-20), demonstrating a high bone turnover state related to his hyperthyroidism. The patient was discharged two weeks after his hospitalization with plans for definitive outpatient management of Graves’ disease.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'years'], 'weight': [82.5, 'kg'], 'sex': 'Male', 'Sodium': [128.0, 'mmol/L']}",-4.24286,-4.03072,-4.455,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 45 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 82.5 kg. The concentration of sodium is 128.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 82.5 * (128.0/140 - 1) = -4.24286 L. The patient's free body water deficit is -4.24286 L."
6025,38,Free Water Deficit,lab test,decimal,pmc-6385391-1,Extracted,"A 4-year-old boy, who had no systemic or inherited disease, presented with a 3-week history of intermittent vomiting without diarrhea or abdominal pain. In the past year, he experienced polydipsia and polyuria. Physical examination revealed body weight 17.5 kg (50th percentile), body height 100 cm (15~50th percentile), blood pressure 230/120 mmHg, heart rate 138 /min, and decreased skin turgor. There was no focal neurological deficit, blood pressure discrepancy between upper and lower extremities, palpable mass, nor any appreciation of an abdominal thrill. Laboratory studies revealed serum Na+ 124 mmol/L, K+ 2.4 mmol/L, Cl− 87 mmol/L, Ca2+ 8.5 mg/dL, HCO3− 34.5 mEq/L, creatinine 0.41 mg/dL, albumin 3.4 g/dL, IgG 247 mg/dL, and osmolality 290 mOsm/KgH2O. Urine analysis was significant for creatinine 11.2 mg/dL, Na+ 24 mEq/L, K+ 18 mEq/L, Cl− 24 mEq/L, osmolality 232 mOsm/KgH2O, RBC 168/μL, FENa 6%, and nephrotic-range proteinuria (55 mg/m2/hour). Survey for possible glomerulonephritis demonstrated the absence of anti-streptolysin O, p-ANCA, c-ANCA, ANA, and normal immunoglobulin A, C3, and C4 levels. In addition, work-up for secondary hypertension included: free T4 1.51 (normal range 0.8–2.0 ng/dL), TSH 5.7 (normal range 0.25–5.00 μIU/mL), cortisol 40.18 (normal range 4.3–25 μg/dL), ACTH 9.32 (normal range < 46 pg/mL), renin 1745 (normal range 2–15 ng/L), aldosterone 92.6 (normal range 4–25 ng/dL), and urine vanillylmandelic acid 3.8 (normal range 1.9–9.9 g/day). Renal ultrasonography revealed hyperechoic right kidney (7.6 cm in length) and small left kidney (5.3 cm in length). Due to the presence of hyperreninemic hypertension, natriuretic-hyponatremia, hypokalemia, and nephrotic range proteinuria, HHS was highly suspected. Computed tomography angiography confirmed high-grade renal artery stenosis with hypoplasia of the left kidney (Fig. ).
In terms of management for this case, we began with volume repletion by normal saline administration. Subsequently, his blood pressure declined from 210/120 mmHg to 180/90 mmHg. Intravenous calcium channel blocker was used to treat his hypertensive emergency, while oral captopril was prescribed for RAA axis blockage after diagnosis of unilateral renal artery stenosis. The systolic blood pressure gradually declined to 150~160 mmHg on the 3rd day. Potassium supplement was infused for his profound hypokalemia and generalized muscle weakness. Due to the severity of left renal artery stenosis, he was not a candidate for angiographic intervention, and decision was made to proceed with left nephrectomy. Overall, electrolyte abnormalities such as hyponatremia and hypokalemia were corrected within 1 week after admission, and resolution of polyuria, polydipsia, proteinuria, and hypertension were achieved 2 weeks after nephrectomy (Additional file : Table S1).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [4, 'years'], 'weight': [17.5, 'kg'], 'Sodium': [124.0, 'mmol/L']}",-1.2,-1.14,-1.26,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 4 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 17.5 kg. The concentration of sodium is 124.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 17.5 * (124.0/140 - 1) = -1.2 L. The patient's free body water deficit is -1.2 L."
6026,38,Free Water Deficit,lab test,decimal,usmle-6742,Extracted,"A 62-year-old man presents with multiple episodes of hemoptysis for a week. It is associated with generalized weakness, decreased appetite, and a 5.4 kg (12 lb) weight loss in 2 months. He has a smoking history of a pack a day for the last 47 years. Physical examination reveals pallor, while the rest of the results are within normal limits. Laboratory studies reveal decreased hemoglobin and a serum sodium value of 130 mEq/L. Chest X-ray shows a 3 cm rounded opaque shadow.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [62, 'years'], 'weight': [5.4, 'kg'], 'sex': 'Male', 'Sodium': [130.0, 'mEq/L']}",-0.23143,-0.21986,-0.243,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 62 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 5.4 kg. The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 5.4 * (130.0/140 - 1) = -0.23143 L. The patient's free body water deficit is -0.23143 L."
6027,38,Free Water Deficit,lab test,decimal,pmc-8572339-1,Extracted,"A previously healthy 35-month-old girl was brought to the emergency room of the Namazi hospital, Shiraz, Iran, due to reduced level of consciousness. She was well up to five days prior to her admission, after that she presented with dysuria and loss of appetite, and then developed polyuria, polydipsia, and weight loss (14 kg → 11 kg). There was no history of DM in her family.
On arrival, her height was measured 92 cm (25th−50th) percentile), she weighed 11 kg (5th–10th) percentile), and her Body Mass Index (BMI) (BMI-for-age) was at the 72nd percentile. Her vital signs were as follows: temperature: 38°C, heart rate (HR): 160, blood pressure (BP): 95/50, and her Glasgow coma scale (GCS) was 11/15. During her physical examination, capillary refilling time was more than 3 s with weak pulses. When checked with a capillary blood glucose meter, her glucose level was too high, so a serum glucose test was performed. Moreover, her first VBG was as follows: pH 7.26, PCO2: 32, PO2: 39, HCO3: 15.8, and BE: −12.6. Due to the decreased level of consciousness, brain CT scan was performed in which brain edema was reported.
As the first line of treatment, she was hydrated with normal saline (10 cc per kg), then the laboratory report revealed; blood sugar: 1124 mg/dl, BUN: 71 mg/dl, creatinine: 1.9 mg/dl, Na: 170 mEq/L (corrected Na: 186), and K: 5.1 mEq/L (effective osmolality was 402). Additionally, urine analysis was SG: 1.010, GLU: 3+, Ketone: trace. VBG after first hydration was as follows: pH: 7.27, PCO2: 34.8, and HCO3: 15.8. Based on the laboratory report; HHS was confirmed as diagnosis; hence, she was transferred to the Pediatric Intensive Care Unit (PICU).
On arrival at PICU, she developed generalized convulsion, and her GCS declined to less than 8; so she was intubated.
She was hydrated with normal saline again; then, the intravenous fluid was administered with 15 percent deficit and maintenance of fluid in addition to urine output replacement. Due to brain edema, deficit was given over 72 h, but according to urine output and serum sodium level, the amount of deficit increased up to 18 percent, and the sodium content of IV fluid decreased.
The first sodium level reported in PICU was 185 mEq/L, but it gradually decreased as hydration continued, and the amount of fluid increased (with the target level of 10 mEq/L decrease per day); then, it became stable around 145 mEq/L over the next five days. Our primary goal in her treatment was to correct sodium level maximum 10 mEq/L per day, to decrease osmolality maximum 3–5 mosm/L/h, and to reduce blood sugar maximum 75 mg/dl per hour.
On the 3rd day, HHS was resolved, but the patient became febrile, and the amount of endotracheal tube (ETT) secretion increased. The culture of ETT secretions revealed candida non-albicans and pseudomonas aeruginosa; hence, antibiotic was prescribed. Subsequently, the patient developed hypotension, so inotrope was initiated. On the same day, her blood creatine phosphokinase (CPK) increased to 6400 IU/L, and it reached 13,400 on the fifth day. Then, she developed hemoglobinuria; thereafter, hydration continued until the CPK level returned normal level on the 18th day (Table ).
Although enoxaparin was initiated for deep venous thrombosis (DVT) prophylaxis, she presented with the left forearm and hand swelling, on the 6th day. Doppler ultrasonography revealed thrombosis of the distal part of the brachial artery, so the therapeutic dose was initiated. Consequently, her conditions improved after 2 days, and a week later, Doppler sonography was normal.
On the 9th day, she was weaned off the ventilator, and on the 21st day, the patient was discharged from hospital without any sequela.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [35, 'months'], 'weight': [11.0, 'kg'], 'sex': 'Female', 'Sodium': [185.0, 'mEq/L']}",2.12143,2.01536,2.2275,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
This means that the patient is 2 years and 11 oldThe patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 11.0 kg. The concentration of sodium is 185.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 185.0 mEq. To convert from 185.0 mEq to mmol, convert from mEq to mmol. The compound 185.0 has a valence of 1, and so divide the valence by the value of mEq to get, 185.0 mEq/(1 mEq/mmol) = 185.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 185.0 mEq sodium/L converts to 185.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 11.0 * (185.0/140 - 1) = 2.12143 L. The patient's free body water deficit is 2.12143 L."
6028,38,Free Water Deficit,lab test,decimal,pmc-5290178-1,Extracted,"A previously healthy 3-year-old girl was admitted to the Emergency Department (ER) because of seizures and drowsiness. Three days before the ER visit, she had respiratory symptoms and her oral intake had been poor. The day before the visit, she had a fever and had taken medicines including Cefcapene Pivoxil HCl Hydrate (FLOMOX Fine granules for children 100 g, Ildong, Seoul, Korea) 2 doses. Her mother said that she had been relatively good in daytime and went to bed supperless. About 5 o'clock in the morning, one hour before the ER visit, she woke up with cold sweating and became irritable and drowsy. Generalized tonic-clonic type seizures developed en route to the hospital. She was born by Caesarean at full-term age and a weight of 3.8 kg. She was the first-born to nonconsanguineous parents. Her growth and developmental status was appropriate for the same age. Her mother said that newborn screening test and past medical history was unremarkable. She has a younger sister with normal growth development and no other symptoms or signs.
At the ER, physical examination findings included her height 104 cm (75th–90th percentile), weight 16.5 kg (75th percentile), body mass index 15.26 kg/m2 (50th percentile), heart rate 110/min, respiratory rate 24/min, body temperature was 37.7℃. She was in a state of tonic-clonic seizures and conscious level was deeply drowsy. Head and neck examination showed slight dried tongue, normal tympanic membrane and no palpable neck lymph nodes. On examination of the chest, breath and heart sounds were normal. Abdominal examination showed normal bowel sounds, without tenderness on palpation, and not apparent hepatosplenomegaly. There was no edema on extremity or rashes on the skin. Laboratory finding showed the following results: white blood cell 30.5 ×103/µL (reference range [RR], 5.5–15.5 ×103/µL), hemoglobin 11.8 g/dL (RR, 11.5–13.5 g/dL), platelet count 459 109/L (RR, 150–450 109/L), erythrocyte sedimentation rate 25 mm/hr (RR, 0–20 mm/hr), C-reactive protein 4.23 mg/dL (RR, 0.0–0.5 mg/dL), aspartate aminotransferase 47 U/L (RR, 13–35 U/L), alanine aminotransferase 16U/L (RR, 7–35 U/L), total cholesterol 156 mg/dL (RR, 150–250 mg/dL), triglyceride 48 mg/dL (RR, 50–130 mg/dL), free fatty acid 740 µEq/L (RR, 300–480 µEq/L), sodium 135 mEq/L (RR, 136–142 mEq/L), potassium 3.4 mEq/L (RR, 3.8–5.0 mEq/L), phosphorus 6.6 mg/dL (RR, 4.0–7.0 mg/dL), calcium 9.8 mg/dL (RR, 9.0–11.0 mg/dL), magnesium 3.1 mg/dL (RR, 1.3–2.1 mg/dL), blood glucose 14 mg/dL (RR, 70–110 mg/dL), blood ketone negative. Arterial blood gas analysis showed that pH 7.42, pCO2 29.0 mmHg, HCO3- 18.5 mmol/L. The level of insulin was 0.2 µIU/mL (RR, 4–24 µIU/mL), cortisol >62.80 µg/dL (RR, 6.7–22.6 µg/dL), ACTH 1,777.0 pg/mL (RR, 7.2–63.3 pg/mL). Blood ammonia was 136 µmol/L (RR, 9–35 µmol/L). Urine organic acid analysis showed that 4-Hydroxypheylacetic acid 73.3 mmol/mol ceatinine (RR, 0.0–69.9 mmol/mol ceatinine). Plasma amino acid analysis revealed no prominent abnormality. Urinalysis showed that ketone 2 positive but no proteinuria or hematuria. Urine microscopy revealed 0–2 /mm3 white cells and 0–2 /mm3 red cells. Chest radiography showed no cardiomegaly and no other significant abnormalities. The cerebral spinal fluid (CSF) study showed that white blood cell 0/µL, red blood cell 0–2 /high power field, glucose 27 mg/dL, protein 17.9 mg/dL (RR, 12–60 mg/dL), Herpes simplex type I polymerase chain reaction negative, enterovirus culture negative. The CSF pressure could not be accurately measured. Brain magnetic resonance imaging done on second hospital day showed bilateral symmetrical areas of hyperintensity on diffusion weighted imaging with a low apparent diffusion coefficient value in the thalami, parietal, and temporal lobes, and it was consistent with cytotoxic edema, which can be seen in hypoglycemic encephalopathy ().
For all the anticonvulsants treatment such as midazolam, phenobarbital and phenytoin, her mentality was stupor and seizures were continued. Intubation and mechanical ventilation was conducted. Despite 10% glucose bolus and continuous infusion at a rate of 15 mg/kg/min with hydrocortisone at a dose of 5 mg/kg/day injection, blood glucose was stabilized above 70 mg/dL after 6 hours from initiation. Empirical L-carnitine solution 55 mg/kg/day divided 3 times was started on the second day. She could be extubated on the third day, but focal seizures developed and progressed. On the fifth day, she was reintubated and midazolam continuous infusion was done. She was seizures-free state on the ninth day, so the anticonvulsants could be tapered but she was kept on phenytoin, phenobarbital, topiramate and oxacarbazepine. Her visual fixation and tracking were disabled. The locomotion and transitional movements such as supine to sit were severely impaired. She was transferred to rehabilitation medicine on the 35th day.
We wonder the etiology of her hypoglycemia because the hospital course was extraordinarily severe and a negative serum ketone was also unusual. A few weeks later, we confirmed the initial serum carnitine level done on the third day was very low (<0.01 µmol/L). We consider primary or secondary carnitine deficiency by other metabolic disorders. The association of exposures to antibiotics containing pivalic acid and hypoglycemia was reported on CDSP. So we conducted gene analysis to confirm CDSP.
Analysis of SLC22A5, the gene that encodes the OCTN2 transporter, identified the c.396G>A(p.W132X) and c.539A>C(p.Q180P) variations. The c.396G>A(p.W132X) is a known mutation identified within more than 1 family, but c.539A>C(p.Q180P) is a novel variation. Her mother's DNA study showed she was a c.396G>A(p.W132X) heterozygote without c.539A>C(p.Q180P). Her younger sister's DNA study shows no variations. Her father refused to participate in the DNA study ().
Follow-up of serum carnitine levels showed a low level even after administering L-carnitine solution. After changing medication to L-carnitine tablets 60mg/kg/day divided 3 times, serum carnitine level is improving ().",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [3, 'years'], 'weight': [16.5, 'kg'], 'sex': 'Female', 'Sodium': [135.0, 'mEq/L']}",-0.35357,-0.33589,-0.37125,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 3 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 16.5 kg. The concentration of sodium is 135.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 135.0 mEq. To convert from 135.0 mEq to mmol, convert from mEq to mmol. The compound 135.0 has a valence of 1, and so divide the valence by the value of mEq to get, 135.0 mEq/(1 mEq/mmol) = 135.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mEq sodium/L converts to 135.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 16.5 * (135.0/140 - 1) = -0.35357 L. The patient's free body water deficit is -0.35357 L."
6029,38,Free Water Deficit,lab test,decimal,pmc-8371619-1,Extracted,"We present an 11-year-old female with complex medical history consisting of developmental delay, septo-optic dysplasia, central DI, panhypopituitarism including central adrenal insufficiency, hypothyroidism, and epilepsy. Her weight at presentation was 49.5 kg. She presented to the emergency department (ED) of a tertiary care academic medical center with impending respiratory failure (approximately two months after the first confirmed case of SARS-CoV-2 within the United States). She became ill eight days before presenting to the ED with fever. At that time, she was taken to a local urgent care facility where she was diagnosed with an acute otitis media. She was started on PO amoxicillin for an anticipated 10-day course of therapy. She was also given stress-dosed hydrocortisone (30 mg PO, twice daily) given her underlying panhypopituitarism. During the subsequent days, there was no reported change in oral intake or urine output (UOP). Her fevers initially improved; however, they never fully resolved. Three days prior to presentation, the patient experienced increased frequency and temperature of fevers. She again presented to a local urgent care facility where a nasopharyngeal swab was positive for the SARS-CoV-2 virus (via the PCR test). Within a few days, she developed a persistent, nonproductive cough, increased work of breathing, and shortness of breath, prompting the evaluation in the ED. Initial vital signs were remarkable for rectal temperature of 40.8°C, heart rate of 163 beats per minute, respiratory rate of 34 breaths per minute, and oxygen saturation of 89%. Physical exam revealed an alert female in a moderate amount of respiratory distress as evidenced by tachypnea and intermittent grunting. Dry oral mucosa was noted indicating a mild amount of dehydration. The remainder of the physical exam was unremarkable. Laboratory results were remarkable for hyperosmolar hypernatremia (serum sodium of 156 mmol/L and serum osmolality of 321 mOsm), mild hyperglycemia (serum glucose of 146 mg/dL), and elevated ESR (21 mm/hr), CRP (2.3 mg/dL), and procalcitonin (6.9 ng/dL). Her respiratory distress acutely worsened within hours of her ED arrival, and she was intubated for acute hypoxic and hypercarbic respiratory failure (immediate postintubation arterial blood gas with pH 7.20, PCO2 78, PO2 132, HCO3 30, and BD 1.7).
The patient was admitted to the pediatric intensive care unit (PICU). She was transitioned from her home regimen of subcutaneous desmopressin to a 0.5 mU/kg/hr Vasopressin infusion. Review of her baseline condition revealed that her DI was well controlled on her home regimen. She was continued on stress-dosed steroids (methylprednisolone 20 mg q6h IV). The patient had acute lung injury (SaO2/FiO2 = 120). Mechanical ventilator settings were adjusted to minimize ventilator-induced lung injury. Arterial and central venous lines were placed to promote more accurate determination of oxygenation (PaO2/FiO2 ratios) and venous monitoring. She was started on ceftriaxone, azithromycin, and hydroxychloroquine in addition to receiving one dose of tocilizumab. Ceftriaxone was used to treat presumed bacterial superinfection based on the severity of the patient's clinical status. At the time of the patient's presentation, our institutional protocol for the treatment of severe COVID-19 infection was based on current literature suggesting that the combination of azithromycin and hydroxychloroquine may achieve antiviral and anti-inflammatory effects against SARS-CoV-2 []. Additionally, at this time, tocilizumab was suggested to have beneficial effects against “cytokine storming” in SARS-CoV-2 patients []. The patient had hypotension that was unresponsive to fluid resuscitation. An epinephrine infusion was started to maintain adequate blood pressures. Given the patient's underlying conditions and critical state, chemistry panels were drawn every six hours on day one of admission. These panels quickly revealed a steady worsening of hypernatremia to a maximum value of 171 mmol/L associated with increasingly abundant UOP of more than 4 L on the first day of hospitalization (Figures and ). These changes occurred despite a maximum Vasopressin infusion rate of 8 mU/kg/hr along with appropriate, simultaneous adjustments in both the sodium concentration and rate of administered IV fluids.
By the second day of hospitalization, a net positive fluid balance of 2.8 L was noted and severe hypernatremia persisted (serum sodium of 160 mmol/L). Her moderate ARDS continued (PaO2/FiO2 = 132) []. When the hypernatremia persisted into the third day of hospitalization, a trial of Furosemide (10 mg IV) in addition to decreasing the Vasopressin dose from 8 mU/kg/hr to 6 mU/kg/hr was attempted. After five doses of IV Furosemide over a 48-hour period along with reduction in the Vasopressin dose, successful diuresis along with resolution of hypernatremia was achieved (net balanced fluid balance of -497 mL and reduction in serum sodium to 138 mmol/L, respectively) (Figures and ). Her ARDS gradually improved. The patient was extubated on hospital day 10. She remained hospitalized in the PICU for a total of 29 days during which time she was weaned from supplemental oxygen and was gradually weaned from sedative medications. She had normal serum sodium levels and UOP throughout the remainder of her PICU stay. She was discharged to her home with an outpatient subspecialist follow-up.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [11, 'years'], 'weight': [49.5, 'kg'], 'sex': 'Female', 'Sodium': [156.0, 'mmol/L']}",3.39429,3.22458,3.564,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 11 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 49.5 kg. The concentration of sodium is 156.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 49.5 * (156.0/140 - 1) = 3.39429 L. The patient's free body water deficit is 3.39429 L."
6030,38,Free Water Deficit,lab test,decimal,pmc-5894559-1,Extracted,"A 11-year and 2-month-old girl came to the hospital because of bifrontal headache, nausea, and vomiting. She was suspected to have craniopharyngioma on brain magnetic resonance imaging (MRI) and underwent surgical resection with a ventriculoperitoneal shunt. At the age of 11 years and 2 months, she weighed 60 kg (2.15 standard deviation score [SDS]) and was 152 cm (1.03 SDS) tall with a body mass index (BMI) of 26 kg/m2 (>97th percentile) and Tanner stage I. After resection, she was treated using a cyber gamma-knife (3 cycle) due to the presence of residual tumor. She developed multiple pituitary hormone deficiencies, which were treated with hormone replacement therapy including levothyroxine 100 μg daily, hydrocortisone 6 mg/m2/day, oral desmopressin 0.1 mg 3 times per day, and conjugated estrogen 0.625 mg daily. During her regular hospital follow-up, laboratory findings demonstrated an elevated aspartate aminotransferase (AST) level of 144 IU/L, an alanine aminotransferase (ALT) level of 65 IU/L, a total cholesterol level of 281 mg/dL, and a triglyceride level of 425 mg/dL, with increased echogenicity on her liver ultrasound, indicating NAFLD.
After 2 years of tumor resection, increased size of residual tumor was found, suggesting recurred craniopharyngioma. She was referred to our hospital. At the age of 13 years and 3 months, her height, weight, and BMI were 155.5 cm (-0.08 SDS), 65.7 kg (1.81 SDS), and 27 kg/m2 (97th percentile), respectively. Her sexual maturity rating was Tanner stage I. Laboratory findings showed an AST of 103 IU/L, an ALT of 104 IU/L, a total cholesterol of 230 mg/dL, a triglyceride level of 359 mg/dL, total protein of 7.0 g/dL, serum albumin level of 4.3 g/dL, sodium 140 mmol/L, potassium 3.7 mmol/L, and chloride of 106 mmol/L. Serum insulin-like growth factor-1 (IGF-1) and IGF-1 binding protein were 67.2 ng/mL and 3,596 ng/mL, respectively. She underwent a second tumor resection at our hospital. Two months later, she was diagnosed with multiple pituitary hormone deficiency on a combined anterior pituitary function test () with Tanner stage I, and was kept on hormone replacement therapy. Three years after the second resection, her fasting blood glucose and hemoglobin A1c levels were 126 mg/dL and 6.7%, respectively. She was diagnosed with type 2 DM associated with hypothalamic obesity, and was started on metformin. During the follow-up period, the NAFLD, dyslipidemia, and type 2 DM laboratory findings improved.
She was lost to follow up for 2 years and then showed up at the outpatient clinic at the age of 18 years and 9 months, with a weight loss of 25.8 kg that had occurred over 21 months. At this time, her height, weight, and BMI were 168.3 cm (1.44 SDS), 54.3 kg (0.03 SDS), and 19.2 kg/m2 (25th percentile), respectively showing Tanner stage of III (). One month later, she presented to the Emergency Department with dyspnea, orthopnea, anorexia, and general weakness. She had been not taking any medications for about 2 weeks. Her lips were cyanotic, her fingers clubbed, and her oxygen saturation was 88%. Laboratory findings revealed thrombocytopenia (a platelet count of 59,000/mm3) and a prolonged prothrombin time (17 seconds; reference range, 10–13 seconds), indicating liver dysfunction. She was severely dehydrated with hypernatremia (164 mmol/L) and increased serum and urine osmolarity (346 mosm/kg and 160 mosm/kg, respectively). She was treated with intravenous fluids, oral desmopressin, and a stress dose of intravenous hydrocortisone. Mesenteric hepatic Doppler ultrasonography and dynamic computed tomography of the liver demonstrated a reduced liver volume with an engorged portal vein and splenomegaly. Her hepatic vein wedge pressure was 21 mmHg (normal range, 1–5 mmHg) measured during transjugular liver biopsy, indicating portal hypertension. The liver biopsy identified micronodular cirrhosis (). In room air, oxygen saturation was 88% and 94% in sitting and lying positions, respectively. Her alveolar arterial oxygen gradient was 77, which was increased for her age (normal range, 5–10 mmHg). A bubble contrast echocardiography and lung perfusion scan suggested diffusely increased activity in the brain, kidneys, and spleen, which were consistent with a right to left shunt (). She was finally diagnosed with hepatopulmonary syndrome grade 3 due to liver cirrhosis induced by NAFLD, which was attributed to hypothalamic obesity after craniopharyngioma resection.
The patient was subsequently hospitalized three times because of aggravated dyspnea, revealing worsened grade 4 hepatopulmonary syndrome, dizziness with hypotension due to menorrhagia induced by thrombocytopenia, and hematemesis due to duodenal ulcer. She was followed up every 3 months with her prescribed hormone medications, including levothyroxine, prednisolone, desmopressin, recombinant human growth hormone, estrogen, and medroxyprogesterone acetate. At the age of 19 years, her height is 169.8 cm (1.72 SDS) and weight is 60.6 kg (0.86 SDS) with a BMI of 21.0 kg/m2 (25th–50th percentile) With metformin treatment, her hemoglobin A1c level has decreased to 5.0%, and her lipid profile has been normalized: total cholesterol 95 mg/dL and triglyceride 84 mg/dL (). Her AST and ALT levels have also been normalized, however, her prothrombin time is continuously prolonged, which is a sign of severe chronic cirrhosis of the liver. She has been registered as a candidate for cadaveric liver transplantation.
The study was waived from approval of the Institutional Review Board of Asan Medical Center has been waived, but informed consent was obtained from the patient.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [19, 'years'], 'weight': [60.6, 'kg'], 'Sodium': [164.0, 'mmol/L']}",5.19429,4.93458,5.454,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 19 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 60.6 kg. The concentration of sodium is 164.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 60.6 * (164.0/140 - 1) = 5.19429 L. The patient's free body water deficit is 5.19429 L."
6031,38,Free Water Deficit,lab test,decimal,pmc-5637643-1,Extracted,"A 76-years-old Caucasian female with CLL (diagnosed five years ago with stable high lymphocyte count) and non-ischemic cardiomyopathy presented with worsening dyspnea on exertion. One year earlier she presented with dyspnea on exertion and mild bilateral lower extremity edema. Her initial EF was 50% by echocardiogram and her left heart catheterization did not show any evidence of coronary artery disease. A month prior to admission she developed progressive dyspnea with exertion and worsening lower extremity edema. At that time she also was found to have an EF of 25% (decreased from 50%) and hyponatremia. Her regimes of diuretics, beta-blocker, and ACEI were further optimized.
On admission, she was found to have borderline blood pressure (103/60 mmHg), and bilateral lower extremity edema. Upon further previous chart review, she had a persistent elevated serum free lambda light chain of about 870–1000 mg/L and faint lambda light chain monoclonal protein on SPEP (54–118 mg/dL) over the last 18 months. At this admission, the white blood cell count was 27.4 × 109/L with 70% lymphocytes (same range as her baseline). The red blood cell count was 3.90 × 1012/L, and the platelet count was 188 × 109/L. She also had worsening hyponatremia (sodium of 123 meq/L, baseline 130–133 meq/L). Creatinine was 1.2 mg/dL (baseline 1.0–1.2) and urine analysis was negative for protein.
SPEP and immunofixation analysis revealed lambda free light chain (Bence Jones) proteinemia and hypogammaglobulinemia involving IgG and IgA. Serum free lambda light chain was 724 mg/L, and kappa/lambda ratio was 0.01, indicating overproduction of lambda light chain. UPEP showed a spike in the beta region, 888.7 mg/24h. EKG was low voltage and CXR revealed bilateral small pleural effusion. Trans-thoracic echocardiogram (TTE) revealed normal left ventricular wall thickness, severe global systolic hypokinesis of the left ventricle, EF 25%, an inter-ventricular diastolic septal thickness of 8.0 mm, moderate right atria dilation and moderate low gradient aortic stenosis.
A right heart catheterization was performed revealing elevated right and left heart filling pressures (RA17 mmHg, PA 55/28 mmHg (mean 38 mmHg), PCW 28 mmHg). Cardiac index was low at 1.53 L/min/m2. Endo-myocardial biopsy showed focal patchy infiltration of the myocardium and fibrous tissue with Congo red stain positive for amyloid ().
Bone marrow biopsy revealed hypercellular marrow that was replaced by nodules of small lymphocytes and patchy sheets of plasma cells. Plasma cells comprise approximately 50% of the cellularity. Immunohistochemistry stains highlighted the plasma cells that were lambda light chain-restricted. Flow cytometry showed 63% monoclonal B-cells that express CD5 and kappa light chain-restricted as well as clonal plasma cells that express lambda light chain, demonstrating that she had two separate clones. A Congo red stain did not show definitive amyloid deposition ().
Patient’s home medications of beta-blocker and ACE inhibitor were discontinued. She was treated with furosemide intravenously and her weight decreased to 48.4 kg from 50.5 kg. Patient was maintained on furosemide and spironolactone with plans for chemotherapy. However, she was readmitted for refractory heart failure symptoms requiring inotropic support. Ultimately, she chose a palliative approach.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [76, 'years'], 'weight': [48.4, 'kg'], 'sex': 'Female', 'Sodium': [123.0, 'mEq/L']}",-2.64471,-2.51247,-2.77695,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 76 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 48.4 kg. The concentration of sodium is 123.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 123.0 mEq. To convert from 123.0 mEq to mmol, convert from mEq to mmol. The compound 123.0 has a valence of 1, and so divide the valence by the value of mEq to get, 123.0 mEq/(1 mEq/mmol) = 123.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 123.0 mEq sodium/L converts to 123.0 mmol sodium/L. Plugging in these values into the equation, we get 0.45 * 48.4 * (123.0/140 - 1) = -2.64471 L. The patient's free body water deficit is -2.64471 L."
6032,38,Free Water Deficit,lab test,decimal,pmc-5303805-1,Extracted,"A 7.5 year old female presented with a progressive fatigue, bluish discoloration of the skin and fever for few days. There were no symptoms of cough, chest pain, headache or upper respiratory tract infection. Patient’s past history was significant to recurrent episodes of shortness of breath, interrupted breathing, fever, and bluish skin discoloration, which seems to have approximately 2 months prior to this hospitalization. The patient’s mother reports a rapid weight gain, which started around the age of 5 years. Breasts enlargement at the age of 4 years and acne development was also noticed 2 months prior to this hospitalization. In addition, there has been a history of slow mental function and weak memory with very poor school performance. This has been accompanied with history of worsening fatigue, sleepiness, cold intolerance, and excessive sweating. Also, her pain threshold seems to be altered. She does not complain or cry when she get needle phlebotomy. The father and mother are not related. The patient has 3 sisters and one brother and none has similar symptoms.
On physical examination, she looked well with no apparent respiratory distress despite bluish discoloration of lips and her SpO2 of 75% on room air. She was obese with weight of 45 kilogram (kg), height of 126 centimeter (cm) and body mass index (BMI) of 28. Tanner stage was 3 with early puberty signs. Rest of physical exam was unremarkable with normal muscle power and neurological exam.
Her initial laboratory investigations showed normal complete blood count (CBC), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and Chest x ray (CXR). However, she had a marked hypernatremia with serum sodium (Na) of 186 millimole/liter (mmol/l). In addition, arterial blood gas (ABG) was consistent with chronic hypoventilation as noted of elevated arterial partial pressure carbon dioxide. (PCO2) of 50 millimeter mercury (mm hg), normal acidity (pH) of 7.36 and bicarbonate (HCO3) of 29 mmol/l. Renal and pelvic ultrasound, electrocardiogram, echocardiogram and contrasted brain magnetic resonance imaging (MRI) were normal. She had a very high prolactin level (197 nanogram per liter (ng/l), normal range 3.3-24) and normal thyroid and cortisol levels. Overnight polysomnogram was carried out later and showed severe hypoventilation with mean end tidal CO2 (EtCO2) of 56 mmhg, maximum EtCO2 of 68 mm hg and patient spent 100% of total sleep time with EtCO2 >50 mm hg ().
Lowest oxygen (O2) saturation was 65% especially during Rapid eye movement sleep and patient had intermittent hypopneas. All these events of sleep disordered-breathing were corrected using bi-level positive airway pressure (BiPAP) in spontaneous/timed (S/T) mode with inspiratory positive airway pressure (IPAP) of 16 centimeter of water pressure (CWP), expiratory positive airway pressure (EPAP) of 6 CWP, back up respiratory rate of 15/minute and inspiratory time (I-time) of 1 second. This was delivered through small nasal mask with minimal leak and patient tolerated it well. She continued to tolerate being on BiPAP therapy during a year of follow up.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [5, 'years'], 'weight': [45.0, 'kg'], 'sex': 'Female', 'Sodium': [186.0, 'mmol/L']}",8.87143,8.42786,9.315,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 5 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 45.0 kg. The concentration of sodium is 186.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 45.0 * (186.0/140 - 1) = 8.87143 L. The patient's free body water deficit is 8.87143 L."
6033,38,Free Water Deficit,lab test,decimal,pmc-6218756-1,Extracted,"A 64-year-old African American man, resident of a correctional facility, was transferred from an outside hospital for further management of liver failure. He was initially admitted at an outside hospital when routine blood tests showed leukocyte count 24,000/µL, platelet count 123,000/µL, serum sodium level 127 meq/L, aspartate aminotransferase (AST) 169 U/L, alanine aminotransferase (ALT) 116 U/L, alkaline phosphatase (ALP) 230 U/L, total bilirubin 17.7 mg/dL, and direct bilirubin 13 mg/dL. His past medical and surgical history was significant for decompensated alcohol-induced cirrhosis with untreated chronic hepatitis C; recurrent ascites; hypertension; schizophrenia; cholecystectomy; and appendectomy. He is a current smoker (40 pack-year) but quit drinking alcohol and using intravenous drugs 6 years ago. The patient complained of mild diffuse abdominal pain with several episodes of watery, nonbloody, nonfoul-smelling diarrhea. He denied fevers, chills, vomiting, melena, or hematochezia. He also reported an unintentional weight loss of 18 pounds over the last 6 months. The rest of the review of the system was negative.
On examination, he was alert and oriented, with temperature 37.3 degrees Celsius, pulse 113/min, blood pressure 103/71 mmHg, respiratory rate 18/min, and saturation 96% on room air. He had icteric sclera. Heart and lung exam was normal. Abdomen was mildly distended, nontender, and tympanic with no shifting dullness. Extremities were warm, with left foot and leg-pitting edema and severe tenderness without erythema. On direct questioning, the patient recalled hurting his left leg 8 days prior to admission while removing his boots, followed 3 days later by swelling, pain in the left foot and ankle that progressed to the leg. No skin lesions or wounds were noted.
His admission labs were significant for a leukocyte count of 14,700/µL, hemoglobin 12.1 g/dL, platelet count 137,000/µL, sedimentation rate 20 mm/hr, C-reactive protein 16mg/dL (normal range 0–0.5 mg/dl), AST 161 U/L, ALT 99 U/L, ALP 177 U/L, total bilirubin 15 mg/dL, direct bilirubin 10.7 mg/dL, albumin 1.5 g/dL, and INR 1.54. HIV antibodies were negative. Hepatitis C virus (HCV) RNA was 184,000 copies/mL.
Six hours after admission, the patient developed worsening tachycardia (125/min) with hypotension. He was given 2 liters of intravenous normal saline boluses and started on vancomycin and cefepime empirically. Blood cultures grew a mucoid strain of K. pneumoniae, in both aerobic and anaerobic cultures within 8 hours of collection, resistant only to ampicillin. Vancomycin was discontinued, and further serotype testing was not performed at that time.
A diagnostic paracentesis revealed ascites leukocyte count 358/mL with 66% neutrophils, and peritoneal fluid cultures were negative. A transthoracic echocardiogram was normal. A CT scan of the chest was done showing mild lower lung atelectasis. A triple-phase CT scan of the liver showed an enlarged left hepatic lobe with a shrunken right lobe with cirrhotic morphology, a small right hepatic lobe cyst, and moderate ascites. Magnetic resonance imaging of the left foot and leg without contrast revealed intraosseous abscess in the second metatarsal and marrow edema within the cuneiforms and second through fourth metatarsal bases suggestive of osteomyelitis (Figures –). There was extensive edema within the subcutaneous soft tissues of the leg and dorsum of the foot, with infiltration of subcutaneous fat compatible with cellulitis (Figures and ).
The patient's hospital course was complicated by encephalopathy requiring transient intubation for airway protection and acute kidney injury secondary to sepsis and hepatorenal syndrome requiring hemodialysis. The patient sepsis and bacteremia resolved; his mental status improved but remained in renal failure. He was discharged to a correctional facility to complete 8 weeks of intravenous ceftazidime.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [64, 'years'], 'weight': [18.0, 'lbs'], 'Sodium': [127.0, 'mEq/L']}",-0.45489,-0.43215,-0.47763,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 64 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 18.0 lbs so this converts to 18.0 lbs * 0.453592 kg/lbs = 8.16466 kg. The concentration of sodium is 127.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 127.0 mEq. To convert from 127.0 mEq to mmol, convert from mEq to mmol. The compound 127.0 has a valence of 1, and so divide the valence by the value of mEq to get, 127.0 mEq/(1 mEq/mmol) = 127.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 127.0 mEq sodium/L converts to 127.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 8.16466 * (127.0/140 - 1) = -0.45489 L. The patient's free body water deficit is -0.45489 L."
6034,38,Free Water Deficit,lab test,decimal,pmc-8101516-1,Extracted,"An 81-year-old man presented to the gastroenterology clinic complaining of progressive dysphagia to solid food for 6 months. He had poor appetite and weight loss of 22 kg. He denied chest pain, regurgitation, cough, abdominal pain, nausea, vomiting, diarrhea, hematochezia, or melena. His past medical history was significant for essential hypertension, coronary artery disease, chronic hepatitis B infection, hypothyroidism, and sarcoidosis. The patient’s past surgical history was significant for coronary artery bypass grafting (CABG) surgery, bilateral cataract surgery, and multiple tooth extractions. Family history was noncontributory. Home medications included aspirin, quinapril, atenolol, levothyroxine, and entecavir. He denied using tobacco, alcohol, or illicit drugs.
On physical examination, the patient appeared chronically ill and cachectic. Vital signs demonstrated a temperature of 36.8 °C, blood pressure of 128/60 mmHg, heart rate of 65 beats per minute, and respiratory rate of 12 breaths per minute. Cardiovascular and lung exams were unremarkable. Abdominal exam showed a soft and non-tender abdomen with normal bowel sounds. Complete blood count (CBC) revealed a low hemoglobin of 11.6 g/dL and a mean corpuscular volume (MCV) of 63 fL consistent with microcytic anemia. Otherwise, the patient had a normal white blood cell (WBC) of 6.6 × 109/L and platelets of 167 × 109/L. Comprehensive metabolic panel (CMP) was within normal limits: Sodium 143 mmol/L, potassium 3.8 mmol/L, chloride 106 mmol/L, CO2 25 mmol/L, glucose 121 mg/dL, creatinine 0.81 mg/dL, BUN 12 mg/dL, calcium 9.4 mg/dL, total protein 6.5 g/dL, albumin 4.2 g/dL, total bilirubin 1.0 mg/dL, AST 12 U/L, ALT 12 U/L, and alkaline phosphatase 100 U/L.
An esophagogastroduodenoscopy (EGD) was performed to investigate the cause of dysphagia. EGD revealed a normal appearing esophagus, patchy erythema in the gastric antrum, normal appearing gastric body, and normal appearing duodenum (). A gastric biopsy was obtained, and histologic examination revealed glandular atrophy with acellular, eosinophilic deposits in the lamina propria and submucosa. Congo red stain revealed apple-green birefringence on polarized light consistent with gastric amyloidosis.
Further workup followed to evaluate the etiology of amyloidosis. Serum protein electrophoresis (SPEP) did not show a monoclonal (M) band. Urine protein electrophoresis (UPEP) did reveal the presence of proteinuria, but also failed to show an M band. Immunofixation showed elevated free kappa light chains of 104.90 mg/dL and an elevated free Kappa/Lambda ratio of 156.57. At this point, the patient was referred to a hematology/oncology specialist for a bone marrow biopsy. Bone marrow biopsy showed that plasma cells constituted 28.5% of the bone marrow consistent with multiple myeloma. The patient was started on lenalidomide, bortezomib, and dexamethasone. One month later, he was seen for a follow-up visit at the oncologist’s office. He reported improvement in dysphagia and weight gain of 1 kg. Unfortunately, the patient’s malignancy progressed, and his condition continued to deteriorate over the next 5 months. He eventually developed pneumonia complicated by septic shock, respiratory failure, and acute kidney injury. He was admitted to the intensive care unit where he suffered a sudden cardiac arrest and expired.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [81, 'years'], 'weight': [22.0, 'kg'], 'Sodium': [143.0, 'mmol/L']}",0.23571,0.22392,0.2475,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 81 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 22.0 kg. The concentration of sodium is 143.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 22.0 * (143.0/140 - 1) = 0.23571 L. The patient's free body water deficit is 0.23571 L."
6035,38,Free Water Deficit,lab test,decimal,pmc-3446141-1,Extracted,"A 45 days old infant with female appearing genitalia was admitted because of recurrent vomiting, poor feeding and cholestasis. It was a product of consanguineous parents with birth weight of 3300 grams. Problems started from third day of life with recurrent vomiting and poor intake which led to poor weight gain.
Intermittent clay colored stool was reported by parents, with changing to completely acholic type a few days before admission. No similar presentation or family history of other features of liver or edocrine disease was reported. On Physical examination length measured 50 cm (<5th percentile), weight 3000 g (<5th percentile), and head circumference 36.5 cm (5–10th percentile). She had a weak pulse, with a heart rate of about 130 beats per minute. Blood pressure was 50/40 mmHg at admission. She had pallor and decreased subcutaneous fat and ill appearance with severe dehydration. Patient's sclerae and skin were obviously jaundiced. External genitalia seemed normal female type. The patient was admitted to PICU and blood drawn for necessary laboratory tests. Initial resuscitation including; rehydration therapy and correction of blood glucose and electrolyte abnormalities started. Broad spectrum antibiotic also was administered due to patient's ill appearance.
Sepsis workups including blood culture and urine culture were performed, which later results showed both negative. Cosidering cholestasis presentation, other investigation including tyrosine level, laboratory assessment for metabolic disorders including serum and urine amino acid chromatography, urinary organic acid profile and NH3 and lactate levels were evaluated with all in normal range but serum alpha1 antitrypsin concentration was mildly increased. The markers for hepatitis and TORCH infections were also negative.
The laboratory tests were as follows: serum sodium 102 meq/lit and serum k+ level 9 meq/lit. Total and direct bilirubin was 13.9 mg/dl and 5.4 mg/dl retrospectively. Erythrocyte sedimentation rate was 7. Thyroid function test was normal and serum glucose level by either glucose oxidas or orthotoloidas method were lower than normal but with no significant difference. Other laboratory findings are shown in . Buccal smear was negative for bar body. Abdominal sonography showed both adrenals hypertrophic but otherwise normal. Pelvic sonography revealed the testicles in the inguinal canal, moreover, a uterus was not detected in pelvis. Ophthalmic fundoscopy in view of corioretinitis, cataract was not conclusive; chromosome study showed 46XY pattern.
Severe electrolytes abnormalities guided us to possible diagnosis of CAH, and further evaluation including findings in proved this diagnosis. Fludrocortisones and hydrocortisone replacement therapy was instituted and resulted in dramatic improvement. Electrolyte abnormalities and blood sugar was corrected during first week of treatment (Na=130 and K=4.5 Meq/lit). One week later, the total and direct bilirubin declined to 5 and 2.5 mg/dl respectively. After one month, bilirubin levels and all of the liver function tests returned to normal, jaundice disappeared and acholic stools changed to normal pattern. In the following 6 months no history of acholic stool or hypoglycemic attacks were noticed.
On her most recent visit at the age of 15 months, the patient had no obvious problem. Her height was 75 cm (25th percentile), weight 9.5 kg (10–25th percentile) and head circumference 46 cm (25th percentile); her neurodevelopment was appropriate for age.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'days'], 'weight': [3000.0, 'g'], 'sex': 'Female', 'Sodium': [102.0, 'mEq/L']}",-0.48857,-0.46414,-0.513,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 45 days old. This means the patient is 0 years old.
The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 3000.0 g so this converts to 3000.0 lbs * kg/1000 g = 3.0 kg. The concentration of sodium is 102.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 102.0 mEq. To convert from 102.0 mEq to mmol, convert from mEq to mmol. The compound 102.0 has a valence of 1, and so divide the valence by the value of mEq to get, 102.0 mEq/(1 mEq/mmol) = 102.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 102.0 mEq sodium/L converts to 102.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 3.0 * (102.0/140 - 1) = -0.48857 L. The patient's free body water deficit is -0.48857 L."
6036,38,Free Water Deficit,lab test,decimal,usmle-8188,Extracted,"A 55-year-old female comes to see her doctor for a rapidly enlarging abdomen and swelling of both legs. She was hospitalized 2 weeks ago for an upper gastrointestinal bleeding episode. On that occasion, her esophagogastroduodenoscopy showed grade 1 esophageal varices and a 1 cm clean-based antral ulcer. The patient was discharged on omeprazole. Review of symptoms shows that the patient is forgetful, does not sleep well, and is drowsy and fatigued during the day which prevents her from working full-time. She denies abdominal pain. The patient has a 10-year history of type 2 diabetes mellitus, hypertension, and hypercholesterolemia but no history of angina or coronary heart disease. She drank alcohol moderately heavy in her twenties and currently drinks less than 3 drinks per week and does not smoke. Her family history is unremarkable. On physical examination, her blood pressure is 132/82 mm Hg, pulse is 88/min, and her temperature is 37.0°C (98.6°F). She weighs 106.6 kg (235 lb) and her BMI is 33. She is alert, oriented to person, place, year, and month but not to the day. Her sclerae are nonicteric. Her pulmonary and cardiovascular exam are normal but her abdomen is distended with a fluid wave and mild tenderness to palpation. There is no hepatosplenomegaly. There is a 2+ edema to mid-calf and pedal pulses are barely palpable. Her neurological exam is without motor or sensory deficits but she demonstrates flapping tremor of her hands while asked to hold them in front of her for a few seconds and her skin exam shows a few spider telangiectasias on her face and upper chest. After an initial evaluation, lab tests were obtained:
Serum sodium 133 mEq/L
Serum potassium 3.8 mEq/L
BUN 8 mg/dL
Serum creatinine 1.0 mg/dL
Serum albumin 2.5 mg/dL
Aspartate aminotransferase 68 IU/ml
Alanine aminotransferase  46 IU/ml
Alkaline phosphatase  130 IU/ml
Total bilirubin  1.8 mg/dL
 WBC count 4,200/mm3
Platelets 94,000/mm3
Hematocrit 35.5%
Prothrombin time (INR) 1.5
A liver biopsy is performed and the results are pending.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'weight': [106.6, 'kg'], 'sex': 'Female', 'Sodium': [133.0, 'mEq/L']}",-2.665,-2.53175,-2.79825,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 55 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 106.6 kg. The concentration of sodium is 133.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 133.0 mEq. To convert from 133.0 mEq to mmol, convert from mEq to mmol. The compound 133.0 has a valence of 1, and so divide the valence by the value of mEq to get, 133.0 mEq/(1 mEq/mmol) = 133.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mEq sodium/L converts to 133.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 106.6 * (133.0/140 - 1) = -2.665 L. The patient's free body water deficit is -2.665 L."
6037,38,Free Water Deficit,lab test,decimal,pmc-6223070-1,Extracted,"A 53-year old white male was referred to University Hospital Limerick with a macular rash on extensor aspects of upper limb and torso, bilateral loin pain, arthralgia, fatigue, active urinary sediment and acute kidney injury in August 2015. The current presentation was preceded by two previous episodes of illness in which he had reported similar symptoms along with haemoptysis in April and July 2014. Past medical history revealed the presence of a peripapilary melanoma of the left eye treated with radiotherapy in 2010 and a basal cell carcinoma of the mid-back excised in 2000. The patient denied tobacco use and drank occasionally and denied any family history off kidney disease. He worked on a farm and was married with two children. On presentation his blood pressure was 124/70 mmHg, weight 91 kg, and there was evidence of macular rash on his back but no lower limb oedema. Urine evaluation demonstrated activity with 3+ protein and 3+ blood, and his serum creatinine was elevated at 128 μmol/L compared to a baseline of 116 μmol/L recorded in April 2014. Serology was positive for P-ANCA with a titre of 160 and he had an anti-MPO titre of over 200 units/mL; apart from this ANA was positive with a titre of 1600 with negative Anti-dsDNA, Anti-Sm, Anti-Sm/RNP and Anti-SSB/RO/LA; Serology for HIV 1 + 2 Ag/Ab and Hepatitis BsAg & Hepatitis C antibody were negative; complement levels were within normal range C3 of 0.82 g/L and C4 of 0.24 g/L. ESR was 30 mm/h and Hs-CRP was 48 mg/L; rest of his routine bloods were unremarkable (White cell count 5.8 × 109/L, haemoglobin 13.5 g/dL, neutrophils 4.00 × 109/L, platelet 210 × 109/L, sodium 141 mmol/L, potassium 4.2 mmol/L, total protein 69 g/L, albumin 39 g/L, serum calcium 2.31 mmol/L, serum phosphate 1.09 mmol/L, bilirubin 7.3 µmol/L, alkaline phosphatase 81 IU/L, gamma-glutamyl transferase 25 IU/L, alanine-aminotransferase 39 IU/L, prothrombin time 12.0 s, activated partial thromboplastin time 32.0 s). Chest X-ray was normal. A recent ultrasound of his kidneys demonstrated normal size and shape with normal cortex. A native kidney biopsy revealed evidence of moderate arteriosclerosis with 30–35% fibrosis, areas of thrombotic microangiopathy but without evidence of fibrinoid necrosis or epithelial crescents. Immunofluorescence was negative and electron microscopy revealed thin glomerular basement membranes with mean measurements less than 250 nM and many measurements less than 200 nM, consistent with thin basement membrane disease (TBMD).
Based on the presence of an AKI with active urine sediment, associated skin rash, and positive serology with high titres of P-ANCA and anti-MPO along with an antecedent history of haemoptysis, we diagnosed an ANCA-associated vasculitis likely microscopic polyangiitis (MPA) based on the European Medicines Agency Algorithm, although the kidney biopsy sample failed to demonstrate classical features of renal vasculitis []. Treatment was initiated with corticosteroids and intravenous rituximab infusions (at day 0 and day 18) with prophylaxis for pneumocystis (co-trimoxazole), osteoporosis (oral Vitamin D3 and bisphosphonates), and gastritis (proton pump inhibitor). Four weeks later his urine sediment normalised with no detectable blood or protein; his CRP fell to < 5 mg/L and his ANCA titres fell to 40 but his anti-MPO level remained remarkably high 198 IU/mL. Two months later, he developed severe depression attributed to steroids requiring taper and the initiation of anti-psychotic therapy.
Six months following initial presentation, his vasculitis remained clinically quiescent and the patient was commenced on azathioprine (AZA) as a steroid sparing agent for maintenance immunosuppression. Two weeks after AZA commencement, the patient presented to the emergency department with acute painful disseminated morbilliform rash along with fever and myalgia. On examination temp was 39.7 °C and a widespread indurated erythematous papular rash was noted (Fig. a, b). An extensive viral and immunologic work up was negative including virology for herpes zoster, and simplex. Considering his history of immunosuppression he was empirically started on acyclovir. Full blood count revealed neutrophilic leucocytosis with neutrophil count of 12.2 × 109/L, Hs-CRP 259 and ESR 59, and a stable serum creatinine concentration of 115 μmol/L. A full septic work up was negative including negative serology for HIV, hepatitis A, B, C, and CMV. A skin biopsy was diagnostic of Sweet’s syndrome, in which the affected lesions revealed extensive neutrophilic infiltrate in the dermis but without evidence of leukocytoclastic vasculitis, herpes, zoster, or erythema multiform. Azathioprine was stopped and the patient was treated with oral prednisolone (30 mg once daily followed by a steroid taper) and colchicine (500 mcg twice daily) []. Within 4 weeks, the rash had completely resolved (Fig. c, d) and his inflammatory markers normalised. As the onset of symptoms were temporally related to initiation of AZA, a diagnosis of drug-induced Sweet syndrome. His steroid dose was tapered gradually to zero and treatment with colchicine was continued. As of August 2017, his vasculitis remains quiescent and there has been no recurrence of Sweet syndrome, however his ANCA titres remain elevated with anti-MPO levels 170 RU/mL.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [53, 'years'], 'weight': [91.0, 'kg'], 'sex': 'Male', 'Sodium': [141.0, 'mmol/L']}",0.39,0.3705,0.4095,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 53 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 91.0 kg. The concentration of sodium is 141.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 91.0 * (141.0/140 - 1) = 0.39 L. The patient's free body water deficit is 0.39 L."
6038,38,Free Water Deficit,lab test,decimal,pmc-6043912-1,Extracted,"A 66-year-old woman with a history of hypertension and hyperlipidemia was referred and admitted to our hospital in the middle of November 2015 due to coma accompanied by AKI. Six years earlier, she had been found to have these diseases and had been treated with atorvastatin as well as antihypertensive agents, including amlodipine, olmesartan medoxomil, and carvedilol. Although the renal parameters had not been monitored on a regular basis, her serum creatinine (sCr) level slightly increased from 0.58 mg/dL in July 2013 to 0.69 mg/dL in September 2015, indicating declines in the estimated Cr clearance (eCrCL) determined by Cockcroft-Gault formula and the estimated glomerular filtration rate (eGFR) based on the revised Japanese equation from 72.7 to 59.5 mL/min and 78.9 to 64.7 mL/min/1.73 m2, respectively. Eight days before this admission, she had noticed a maculopapular rash over the left ear and been empirically treated with oral cefcapene pivoxil hydrochloride 300 mg/day combined with topical gentamicin by her general practitioner. Three days later, the rash had progressed to clusters of clear vesicles. She was then diagnosed with left trigeminal HZ and subjected to oral valacyclovir 1 g three times a day. On the fifth day of the valacyclovir treatment, the patient started to exhibit mild dysarthria characterized by slurred speech followed by a progressive deterioration of consciousness. The next day, she was brought to another emergency hospital by her son. A physical examination revealed her to be stuporous and afebrile without any facial drooping, tongue deviation, hemiparesis, or quadriparesis. Diagnostic brain computed tomography and magnetic resonance imaging revealed no remarkable abnormalities, whereas a laboratory analysis revealed the elevated levels of sCr of 7.44 mg/dL and serum potassium of 6.2 mmol/L. She was empirically given 10 mg of furosemide as well as 10 mL of 8.5% calcium gluconate intravenously and then transferred and admitted to our hospital for further work-up.
On admission, the patient had a blood pressure of 191/105 mm Hg with a pulse of 101 beats/min. She was a well-nourished woman of 152 cm in height and 47.4 kg in weight. Her consciousness level was E3V4M6 on the Glasgow Coma Scale (GCS). Renal sonography on both kidneys revealed preservation of the size with normal renal cortex echogenicity. A laboratory examination revealed the following results: hemoglobin, 11.9 g/dL; hematocrit, 36.9%; platelet count, 15.9 × 104/μL; blood urea nitrogen, 53 mg/dL; sCr, 7.27 mg/dL; uric acid, 8.8 mg/dL; total protein, 6.4 g/dL; serum albumin, 3.3 g/dL; sodium, 122 mmol/L; potassium, 5.9 mmol/L; chloride, 92 mmol/L; Ca, 8.3 mg/dL; phosphorus, 5.0 mg/dL; C3, 112 mg/dL; C4, 25 mg/dL; immunoglobulin (Ig) G, 1246 mg/dL; IgA, 239 mg/dL; and IgM, 73 mg/dL. A serological study revealed an increased level of C-reactive protein of 3.55 mg/dL, whereas the patient was negative for antimyeloperoxidase antineutrophil cytoplasmic antibody (ANCA), antiproteinase 3-ANCA, anti-glomerular basement membrane antibodies, and anti–double-stranded DNA antibodies. No serum thyroid-stimulating hormone abnormalities were found. A lumbar puncture revealed a protein concentration of 54 mg/dL and glucose concentration of 91 mg/dL, whereas Gram staining failed to show microorganisms, and cultures of blood and cerebrospinal fluid (CSF) were also negative. Although we did not perform a polymerase chain reaction to screen the patient’s CSF for HZ virus DNA, the serum and CSF acyclovir levels at this point were 26.9 and 6.25 μg/mL, respectively; as such, valacyclovir-related pathologies were strongly suspected to be implicated in the patient’s neuropsychiatric manifestations. All medications were discontinued, and she was subjected to a single session of hemofiltration (HF) for the management of anuric AKI accompanied by hyperkalemia and hyponatremia when her neurological status further worsened (E1V1M4 on GCS).
A temporary dialysis catheter was placed in the right jugular vein and a Foley catheter was inserted in the bladder to monitor the urine output. Then, HF was initiated with a high-flux hemodialyzer (FB-70U, cellulose triacetate membrane, 0.7 m2; Nipro Co., Osaka, Japan). The rates of blood flow and ultrafiltration were set at 120 mL/min and 1000 mL/h, respectively. The HF replacement fluid was the standard formulation of Sublood®-BSG (Fuso Pharmaceutical Industries Ltd., Osaka, Japan) administered after filter at 1000 mL/h. After 3 hours, the patient developed respiratory distress due to aspiration and was intubated for airway protection, and then she was placed on mechanical ventilation when an urgent laboratory analysis revealed that her serum levels of potassium and sodium were 4.1 and 124 mmol/L, respectively. HF was ceased, and she was then started on intravenous 3% hypertonic saline of varying doses to correct the reduced serum sodium level at a recommended rate according to the therapeutic guidance. On the following day, there was a slight improvement in the patient’s neurological status (E2VTM4), and the serum sodium level increased to 131 mmol/L when the patient underwent a 3-hour session of hemoperfusion (HP) using an activated charcoal cartridge (Hemosorba CHS-350®; Asahi Medical Co., Tokyo, Japan), and it further increased to 139 mmol/L at 14 hours later. After an initial hemodialysis (HD) session, her urine output began to increase () along with gradual improvements in her consciousness from E3VTM6 on hospital day 3 to E4VTM6 on hospital day 5, whereas the serum levels of acyclovir steadily decreased during the observation period (). The patient was eventually extubated on hospital day 7 with a favorable neurological recovery (E4V5M6), and medications including statins and antihypertensive agents were resumed thereafter. She was discharged on hospital day 16, having fully returned to her normal baseline mental status with a recovered sCr level of 0.68 mg/dL corresponding to an eCrCL of 60.4 mL/min and eGFR of 65.7 mL/min/1.73 m2 At the time, the results of a urine sediment examination were unremarkable, and a urine dipstick analysis was negative for protein and occult blood.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [66, 'years'], 'weight': [47.4, 'kg'], 'Sodium': [122.0, 'mmol/L']}",-2.74243,-2.60531,-2.87955,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 66 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 47.4 kg. The concentration of sodium is 122.0 mmol/L. Plugging in these values into the equation, we get 0.45 * 47.4 * (122.0/140 - 1) = -2.74243 L. The patient's free body water deficit is -2.74243 L."
6039,38,Free Water Deficit,lab test,decimal,pmc-3470992-1,Extracted,"A 17-year-old South Asian man was referred to our department for recurrent episodes of generalized muscle weakness, fatigue and cramps from the age of two years. Hypokalemia was initially detected at the first episode and he was treated for periodic hypokalemic paralysis. Before the age of 12 years, these episodes were mild, readily improved with ringer lactate and potassium chloride by his treating physician and occurred only twice a year. Beyond the age of 12 years, these episodes gradually worsened in frequency and intensity to the point that they were refractory to previously administered therapies and sometimes required hospitalization.
His symptoms were aggravated by physical activity and hot weather, and were associated with polyuria, polydipsia, nocturia, paresthesias and occasional painless non-bloody diarrhea. He denied the use of any medication, including laxatives and diuretics. He also had a history of short stature and poor weight gain. His birth history was unremarkable but developmental landmarks were delayed. There was no family history of renal salt-wasting syndromes or delayed puberty. However, his parents were first cousins.
An examination revealed a thin and lean, but well-oriented adolescent with no acute distress. His height and weight were below the third percentile (weight 30kg; height 147cm). His blood pressure was 95/60mmHg with orthostatic changes. His sexual development was at Tanner Stage II.
Investigations at the admitting hospital revealed a normal leukocyte count, platelet count, hemoglobin level and erythrocyte sedimentation rate. His urea level was 34mg/dL, creatinine 0.9mg/dL and random blood glucose 105mg/dL. His estimated glomerular filtration rate based on the Modification of Diet in Renal Disease formula was 97.9ml/min per 1.73m2. His high blood urea nitrogen level was attributed to mild dehydration due to the hot weather. He was found to have metabolic alkalosis: pH 7.58, HCO3- 33.5, base excess +7.6. His serum electrolytes were as follows: sodium 124mmol/L, potassium 2.4mmol/L, calcium 6.5mmol/L and phosphate 3.4mg/dL. His serum magnesium level was not checked at that time. Serum albumin, creatine phosphokinase, free thyroxin, thyroid-stimulating hormone and parathyroid hormone levels were normal.
He was provisionally diagnosed with periodic hypokalemic paralysis and hypocalcemia. Treatment was started with potassium and calcium supplements. After one month, he showed little improvement and he was referred to our department for further evaluation.
Further laboratory tests revealed a low magnesium level (1.2mg/dl) and decreased 24-hour urinary excretion of calcium (25.9mg/24 h). Luteinizing hormone and follicle-stimulating hormone levels were also normal. His level of testosterone was low (0.85ng/mL, normal for his age 2.67 to 10.12ng/mL). Electrocardiography showed a normal sinus rhythm and prolonged QT interval. No abnormality was found on an abdominal X-ray, chest X-ray or brain magnetic resonance imaging. A renal ultrasound revealed a prominent pelvicalyceal system. An insulin tolerance test showed normal cortisol and growth hormone response.
Based on the findings of hypokalemic metabolic alkalosis without hypertension, severe hypomagnesemia and hypocalciuria, a diagnosis of GS was made. No organic cause of hypogonadism was established and the sex hormone findings were attributed to delayed puberty. Treatment was started with oral supplementation of potassium, magnesium and calcium along with spironolactone and liberal salt intake. Our patient and his parents were also counseled about delayed puberty.
A limitation to this case report was that the diagnosis could not be ascertained with sequencing of the implicated gene due to unavailability of genetic sequencing at the presenting hospital (Jinnah Hospital Lahore, Pakistan).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [17, 'years'], 'weight': [30.0, 'kg'], 'Sodium': [124.0, 'mmol/L']}",-2.05714,-1.95428,-2.16,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 17 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 30.0 kg. The concentration of sodium is 124.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 30.0 * (124.0/140 - 1) = -2.05714 L. The patient's free body water deficit is -2.05714 L."
6040,38,Free Water Deficit,lab test,decimal,pmc-5925609-1,Extracted,"A 68-year-old gentleman was admitted with fever, productive cough, and left-sided pleuritic chest pain and diagnosed with left lower lobe pneumonia accompanied by a complicated parapneumonic effusion. A pigtail catheter was placed for effusion drainage, which further required intrapleural DNase and tPA to facilitate clearance. Of note, the patient also attested to a 30 pound weight loss over the previous year and notably had a remote history of gastrointestinal stromal tumor in remission after medical therapy. Physical examination at the time of consultation was unremarkable except for cachexia and a weight of 52 kg (body mass index of 16.4 kg/m2). Over the course of the 10-day hospitalization, plasma [Na+] had declined from 137 to 128 mEq/L despite a 1–1.5 L fluid restriction. Plasma chemistries were also notable for a [K+] of 4 mEq/L, BUN of 8 mg/dL, and a creatinine of 0.4 mg/dL. Thyroid studies and ACTH stimulation test were normal. Urine chemistries were as follows: [Na+] = 75 mEq/L, [K+] = 64 mEq/L, osmolality = 546 mOsm/kg, urine urea nitrogen 644 mg/dL, urine creatinine 86 mg/dL. Urine output was about 800 mL/day.
To use the stepwise approach, we estimated TBW at 31.2 L (0.6*52 kg) using 60% as the percent water weight to reflect the increase in TBW relative to weight due to cachexia and SIADH-associated overhydration in spite of the patient’s advanced age. fECF was estimated at 0.4 which is near normal, reflecting a balance between cachexia with reduced muscle mass and ICF, and SIADH hyponatremia which tends to expand ICF more than ECF. With P[Na+K] = 132 mEq/L and P[Na+K]pw = 142 (assumes normal plasma water fraction of 93%), a modest target for rise in plasma [Na+] of 3 mEq/L/day was chosen.
The patient was eating about half his diet so we assumed insensible losses exceeded food water content by 0.25 L/day. He was also receiving 150 mL of IV piperacillin–tazobactam dissolved in NS. Based on this, one could use the following estimates:
In light of these calculations, the patient was placed on a fluid restriction of two 8 ounce cups a day (about 480 mL) and prescribed 1 g po bid of NaCl (~34 mEq Na+) to provide the approximate Na+ for the required positive balance above and beyond what was already being provided by dietary intake and antibiotic-associated IV fluids (assumed from the pre-treatment urinary Na+ excretion rate).
To compare strategies, we next designed a therapeutic regimen utilizing a classic approach based on TBW excess. The TBW excess associated with the desired 3 mEq/L change in plasma [Na+] from 128 to 131 mEq/L is calculated as follows:
Thus, to achieve the desired change in plasma [Na+] from 128 to 131 mEq/L, we would plan on a negative fluid balance of 0.73 L to target the calculated TBW excess:
The TBW excess approach calculates a fluid restriction of 170 mL/day, even more onerous than the fluid restriction prescribed by our proposed approach. The reason for the difference is that the TBW excess approach assumes that cation balance (dMCB/dt) is equal to zero. That is, volume balance accounts wholly for EFWB. In fact, positive Na+ balance during the correction of SIADH-associated hyponatremia with fluid restriction is well described and may contribute to the rise in plasma [Na+] (, –). In essence, negative fluid balance created with fluid restriction leads to clinically unnoticed ECF volume depletion engendering positive Na+ balance for correction. Thus, in our case, a loss of 0.71 L/day of EFW raises plasma [Na+] by 3 mEq/L/day, but also depletes the ECF by 0.28 L/day (0.4*0.71 L/day). This ECFV deficit is “added back” to restore ECF volume as isotonic NaCl, which does not affect plasma [Na+].
In this case, as in many cases, the two 8 ounce cups per day beverage restriction proved to be difficult. The plasma [Na+] the following day was unchanged at 128 mEq/L and the patient admitted to drinking 4 or more cups of fluid. Given the challenging fluid restriction, we wanted to examine additional therapies to liberalize the fluid restriction in this case. NaCl supplementation is often used as an adjunct to fluid restriction for the treatment of SIADH. But how does NaCl supplementation affect EFWB? Since total solute excretion rate and urine osmolality determine urine flow rate (), we can alternatively express urinary EFWC as:
where OERurine is the total urinary osmole excretion rate and (Na + K)urine is the daily urinary monovalent cation excretion rate (equals Vu*U[Na+K]). The change in urinary EFWC with NaCl supplementation can be approximated as:
where Na+supp is the amount of NaCl supplementation provided in mEq Na+ per day. Thus, when U[osm] is greater than 2*P[Na+K]pw as in this case (546 mOsm/kg vs. 284 mEq/L), increasing the osmolar excretion rate (OERurine) through NaCl supplementation paradoxically decreases urinary EFWC, an effect which would tend to increase EFWB and worsen hyponatremia. So why does salt supplementation work in many cases of SIADH? Luckily, pure NaCl ingestion decreases EFWI more than the fall in EFWC resulting in a net overall decrease in EFWB and rise in plasma [Na+]. Since humans cannot urinate salt crystals, a pure NaCl load sans water obligates some degree of urinary volume loss which underlies the rise in plasma [Na+]. Thus, in our patient, if we wanted to increase the fluid restriction to 1 L/day, we would need to increase urine volume by about 0.5 L/day requiring an extra 273 mosm (546 mOsm/kg*0.5 L) of solute or 136.5 mEq NaCl per day. If we add to this value the requisite 40 mEq/day positive Na+ balance, we must provide 176.5 mEq of NaCl per day (about ten 1 g NaCl tablets).
Disadvantages of NaCl supplementation include a potential for excessive ECF volume expansion or increased thirst which may counteract compliance with the relaxed fluid restriction. Thus, another approach is to utilize loop diuretics to block urinary concentration and increase urinary EFWC (). Previous reports utilize 40 mg oral furosemide once daily to create a daily urine volume of about 1.5–2 L per day. In the case of SIADH, where we want to maintain euvolemia, high Na+ intake and the post-diuretic, rebound Na+ retention is leveraged to create a slightly positive Na+ balance (), which we assume to be the previously calculated requirement of 40 mEq/day. While the exact amount of Na+ intake required to accomplish this is uncertain, a daily Na+ intake of about 150 mEq is reasonable and would require about 90 mEq of supplemental Na+ (five to six 1 g NaCl tablets) assuming the patient’s pre-treatment intake is in balance with urinary excretion at about 60 mEq/day. Thus, in our patient, assuming a diuretic induced daily urine output of 1.5 L, we can now liberalize the fluid intake to 1.2 L per day, since urine output has now increased by 0.7 L.
Urea supplementation is an alternative to liberalize fluid intake in the treatment of SIADH (). In contrast to NaCl supplementation, addition of urea increases non-electrolyte excretion rate, and thus effectively raises urinary EFWC to counterbalance the increase in oral EFWI due to liberalization of the fluid restriction. Thus, adding 273 mosm of urea (about 16 g urea) increases urinary volume by 0.5 L (273 ÷ 546 mOsm/kg) and allows us to liberalize the fluid restriction to 1 L.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [68, 'years'], 'weight': [52.0, 'kg'], 'sex': 'Male', 'Sodium': [128.0, 'mEq/L']}",-2.22857,-2.11714,-2.34,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 68 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 52.0 kg. The concentration of sodium is 128.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 128.0 mEq. To convert from 128.0 mEq to mmol, convert from mEq to mmol. The compound 128.0 has a valence of 1, and so divide the valence by the value of mEq to get, 128.0 mEq/(1 mEq/mmol) = 128.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 128.0 mEq sodium/L converts to 128.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 52.0 * (128.0/140 - 1) = -2.22857 L. The patient's free body water deficit is -2.22857 L."
6041,38,Free Water Deficit,lab test,decimal,pmc-4517638-1,Extracted,"A 4-month-old baby girl was admitted to our pediatric intensive care unit with acute renal failure and respiratory distress.
She was a fifth-born to consanguineous parents, born full term after an unremarkable pregnancy. Her birth weight was 4kg, and meconium was passed on the first day of life. She had a 14-year-old sister diagnosed with CF at 1 year of age. The parents were concerned regarding the salty taste of their daughter’s skin and an offensive stool odor since birth. They also noticed her stools becoming oily and bulky by 3 months of age, but she was not investigated for CF.
The patient had a persistent paroxysmal cough for 3 weeks that progressed as she developed shortness of breath and tachypnea. She also had a 1 week history of vomiting, lethargy and decreased oral intake. Her parents sought medical advice at private clinics, and bronchodilators and antibiotics were prescribed, without improvement. Three days prior to admission, the patient’s sister fell on the patient’s neck and chest; the next day, swelling was noticed on the patient’s neck.
During the initial examination, the patient was found to be irritable in severe distress, tachypneic, tachycardic with normal blood pressure, and severely dehydrated. She had palpable subcutaneous crepitation over her neck, extending to the anterior chest wall. There was intercostal and subcostal retraction; on auscultation, air entry was decreased with the bilateral presence of crepitation.
A basic workup revealed metabolic alkalosis in capillary blood gas (pH 7.48; partial pressure of oxygen in arterial blood, PaO2, 88mmol/L; partial pressure of carbon dioxide, PCO2, 48mmol/L; bicarbonate, HCO3, 35mmol/L), hypokalemia (potassium 3mmol/L), hyponatremia (sodium 125mmol/L), hypochloremia (chloride 61mmol/L) and renal impairment with high urea (15.9mmol/L) and creatinine (155mmol/L) and low urine chloride (<20mmol/L). In addition, a normal calcium/creatinine ratio was detected in her urine (0.107mol/1mol), and a septic workup was negative. A chest X-ray (Fig. ) showed pneumomediastinum and subcutaneous emphysema. In addition to oxygen provided by a face mask, she was given two intravenous boluses of 0.9% saline (20ml/kg each), followed by maintenance intravenous infusion of 0.45% saline with potassium chloride supplementation. Ceftriaxone and clindamycin were started intravenously. A computed tomography (CT) scan of her neck (Fig. ) showed a tracheal tear with pneumomediastinum.
During admission, she significantly improved regarding hydration, activity, and oral intake. Electrolyte abnormalities were corrected. Her tracheal tear was managed conservatively. The neck swelling disappeared, and a subsequent X-ray and CT scan 1 week later showed complete resolution of the air leak. A sweat chloride test had high results (95mmol/L) (conductance method), and a cystic fibrosis transmembrane conductance regulator (CFTR) gene mutation test was performed. She was started on pancreatic enzymes, a vitamin supplement, a salt supplement, and regular chest physiotherapy. After completing a course of antibiotics, she was discharged in stable condition. The CF gene was later reported to contain a homozygous mutation (c.2988 + 1G > A; IVS18 + 1G > A).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [4, 'months'], 'weight': [4.0, 'kg'], 'sex': 'Female', 'Sodium': [125.0, 'mmol/L']}",-0.25714,-0.24428,-0.27,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 4 months old. This means the patient is 0 years old.
The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 4.0 kg. The concentration of sodium is 125.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 4.0 * (125.0/140 - 1) = -0.25714 L. The patient's free body water deficit is -0.25714 L."
6042,38,Free Water Deficit,lab test,decimal,pmc-4300583-1,Extracted,"We report the case of a 17-year-old Pakistani young man who presented with short stature and underdeveloped secondary sexual characters. He had been operated on for patent foramen ovale five years previously and the procedure was uneventful. His birth history was found to be significant due to breech presentation. He has experienced no delay in achieving developmental milestones, his intelligence level was within the normal range, and his school records reflected good performance. He had six siblings, all of which were healthy, with normal height. His mother and father had a height of 165cm and 154cm, respectively. An examination showed that his pulse was 109/min, his blood pressure was 90/60mmHg, his height was 142cm, his weight was 34.5kg, his body mass index was 17.10kg/m2, and his calculated mid-parental height (MPH) was 166.5cm, with an MPH range of 156.5 to 176.5cm. His Standard Deviation Score (SDS) was - 4.3. He had no hair growth on his face, axilla, and pubis (Tanner stage 1). Both of his testes were between 1 and 2mL in volume, and his stretch penile length was 4cm. A systemic examination was unremarkable.
His lab investigations showed a fasting blood glucose level of 85mg/dL, sodium at 141mmol/L, potassium at 3.8mmol/L, serum calcium at 9.4mg/dL, phosphorus at 6.2mg/dL (normal, 2.5 to 4.5mg/dL), albumin at 4.5gm/dL, hemoglobin at 11.4g/dL, thyroid stimulating hormone (TSH) at 8.58uIU/mL, free thyroxine at (FT4) 0.46ng/dL (normal, 0.89 to 1.76ng/dL), an anti-thyroid peroxidase antibody (anti-TPO) level of 17.8IU/mL (normal, less than 35IU/mL), and an anti-thyroglobulin antibodies level of under 20IU/mL (normal, less than 40IU/mL), prolactin at 21.1ng/mL (normal, 3.0 to 14.7ng/mL). A short synacthen test revealed a morning baseline cortisol level of 0.30ug/dL (normal, 4.3 to 22.4ug/dL), and cortisol after 60 minutes of 250mcg cosyntropin injection was 3.5ug/dL. His insulin like growth factor-1 (IGF-1) level was 31.56ng/mL (normal, 247.3 to 481.7ng/mL), his morning testosterone level was under 2.5ng/dL (normal, 280 to 800ng/dL), his follicle stimulating hormone level (FSH) was 0.41uIU/mL (normal, 0.0 to 10.0), and his luteinizing hormone level (LH) was under 0.1uIU/mL (normal 1.2 to 7.8).
A biochemical picture favored an anterior pituitary hormones deficiency. Symptoms of diabetes insipidus such as polyuria, polydipsia, nocturia, and nocturnal enuresis were absent. His 24-hour urinary volume was 1800ml and his serum osmolarity was 285mosm/kg.
His bone age was 10 years according to the Greulich and Pyle method as was shown by his X-rays. A magnetic resonance imaging (MRI) scan of his pituitary showed T1 hyperintense focus in the midline at the median eminence with non-visualization of pituitary stalk. Posterior pituitary was not seen in relation to the anterior pituitary in the pituitary fossa. Anterior pituitary was seen in pituitary fossa at its normal location and was returning a normal signal. This represented ectopic posterior pituitary with absent pituitary stalk (Figure ).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [17, 'years'], 'weight': [34.5, 'kg'], 'Sodium': [141.0, 'mmol/L']}",0.14786,0.14047,0.15525,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 17 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 34.5 kg. The concentration of sodium is 141.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 34.5 * (141.0/140 - 1) = 0.14786 L. The patient's free body water deficit is 0.14786 L."
6043,38,Free Water Deficit,lab test,decimal,pmc-4594352-1,Extracted,"We present the case of a 34-year-old male with a past medical history of hypertension, hypercholesteremia, anxiety, acid reflux, and irritable bowel syndrome who presented with the complaints of severe cramping abdominal pain associated with nausea, vomiting, bright red blood per rectum, and constipation. The patient denied having similar symptoms in the past or any history of abdominal surgery. He had an upper gastrointestinal series 10 years ago, which was unremarkable except for a hiatal hernia. He is a body builder and admitted to the use of AAS. He was 1500 mg of testosterone/nandrolone, via intramuscular injection, per week for 3 months. 3 weeks prior to the presentation, he abruptly decreased the dose to 500 mg/week.
On presentation, he was found to be diaphoretic, in mild distress, with tachycardia at 100 beats/min and tenderness in the suprapubic region with no guarding, rebound tenderness or palpable masses. Laboratory studies were normal apart from an increased white blood cell count at 15.0, increased hemoglobin at 17.9 and increased hematocrit at 51.2%. He had mild changes in sodium (134), as well as blood urea nitrogen (24). He weighed 265 pounds, with a body mass index of 40.3. A computer tomography (CT) scan of the abdomen demonstrated mild diffuse nonspecific colonic wall thickening, with two separate areas of apparent short segment small bowel intussusception without evidence of obstruction [Figures –]. In addition, a small umbilical hernia containing fat was visualized. Our patient was subsequently medically managed, with pain control and hydration. A colonoscopy completed the day after admission demonstrated edema and erythema in the distal ileum and colon, most densely starting in the distal transverse colon and increasing within the rectum. There were no ulcers, polyps, tumors or sites of hemorrhage noted. Biopsies were taken from each section of the colon. The subsequent pathological evaluation indicated acute and chronic colitis from the descending colon forward and changes suggesting ischemic colitis in the rectum [Figures –].
A follow-up CT scan was completed on the third day of admission but demonstrated no definitive intussusceptions []. There was no longer any overt colitis evidenced though there may have been an underlying inflammatory process based on submucosal lucency in the transverse colon. With the apparent resolution of the small bowel intussusceptions with conservative medical management, accompanied by a resolution of the patient's pain, he was discharged home.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [34, 'years'], 'weight': [265.0, 'lbs'], 'sex': 'Male', 'Sodium': [134.0, 'mEq/L']}",-3.09091,-2.93636,-3.24546,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 34 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 265.0 lbs so this converts to 265.0 lbs * 0.453592 kg/lbs = 120.20188 kg. The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 120.20188 * (134.0/140 - 1) = -3.09091 L. The patient's free body water deficit is -3.09091 L."
6044,38,Free Water Deficit,lab test,decimal,pmc-3811692-1,Extracted,"32-year-old female.
General weakness.
She was receiving insulin injections for type 1 diabetes, but her symptoms had not been improved at all, which prompted her decision to come to our hospital.
She had been using 32 U insulin every day for type 1 diabetes for 11 years before her visit to our hospital.
All family members, including both parents and all siblings, had diabetes.
When she appeared, her blood pressure was 130/80 mm Hg, pulse rate was 74 beats per minute, and body temperature was 36.6℃. She had no other symptoms, except for general weakness and central obesity (body mass index 23.4 kg/m2). No tumor-like mass was checked at her head and neck, nothing was discovered in chest auscultation. When we checked her abdomen, neither any pain nor hepatosplenomegaly was observed. No skin or oral mucosa pigmentation was found. There was no edema in lower leg. The neurological examination results were also normal. She weighed 51.5 kg and was 148.2 cm tall, and she was somewhat short woman with a short neck and round face, similar to a clinical features of AHO, but there was no pathognomonic brachydactyly.
The result of complete blood count was the hemoglobin 9.3 g/dL, the erythrocyte average volume 96 fL, leukocyte 5,720/mm3, and platelets 310,000/mm. The results of anemia work up were the total iron binding capacity 447.5 µg/dL, serum ferritin 35.11 ng/mL, reticulocyte count 2.89%, average erythrocyte hemoglobin density 32.6 g/dL, and vitamin B12 839.65 pg/mL. Her blood glucose level was 212 mg/dL, the level of hemoglobin A1c was 7.3%, and the simultaneous measurement of serum level of C-peptide showed decreased level of 0.13 ng/mL. Serum concentration of total calcium were 5.5 mg/dL (range, 8.7 to 1.4); ionized Ca 1.56 mg/dL (range, 2.3 to 2.58); phosphorus 6.7 mg/dL (range, 2.5 to 4.5); total protein 6.7 g/dL; albumin 3.3 g/dL; alkaline phosphatase 329 IU/L; aspartate aminotransferase 119 IU; alanine aminotransferase 65 IU/L. Intact PTH level was 13.32 pg/mL (range, 13 to 54). Serum adrenocorticotropic hormone (ACTH) and cortisol levels were 11.92 pg/mL (range, 10 to 60) and 0.94 (range, 9.4 to 26.1). The results of rapid ACTH stimulation test for adrenal function were normal. The results of thyroid function test were T3 99.01 ng/mL, free T4 0.85 µg/dL, and thyroid stimulating hormone 7.99 µIU/mL. The results for antimicrosomal and antithyroglobulin antibody were positive (52.91 IU/mL, 132.57 IU/mL), and, both islet cell antibody and antiglutamic acid decarboxylase antibody tested negative. In the Ellsworth-Howard examination, urinary phosphoric acid was slightly increased (12.3 mg/dL) and the increase of cyclic adenosine monophosphate (cAMP) was sufficient (4,400 µmol/mL). There was no GNAS mutation. Serum levels of sodium, potassium, blood urea nitrogen, and creatinine were within normal limits at 144 mmol/L, 5.3 mmol/L, 8.2 mg/dL, and 1.0 mg/dL.
The chest X-ray showed no abnormal lesion. An brain computed tomography scan showed prominent calcifications in both basal ganglion and hypothalamus (). The thyroid sonogram discovered several nodules, sized 4.5×3.7 mm and 3.9×2.9 mm on each side that were suspected to be thyroid papillary cancer.
The patient came to the hospital experiencing general weakness, and she was diagnosed with hypocalcaemia on laboratory examination. At that time, both the levels of PTH and vitamin D were within normal range, but she had previously experienced spasm symptoms and the levels of previous intact PTH were low (4.38 to 10.66 pg/mL) 7 years ago. She has taken oral calcium medicine for treatment of idiopathic hypoparathyroidism because she had no underlying secondary disorders for hypocalcemia and low PTH level. Although she has no pathognomonic brachydactyly, her appearance was similar to AHO in clinical features including short stature, intelligence decline, round face, calcification on basal ganglion and hypothalamus, or obesity. Furthermore, she had a lower normal PTH level and hypocalemia on admission, and we decided to investigate the PTH resistance to identify PHP Ia or PPHP with AHO. In the Ellsworth-Howard examination for investigation of the PTH resistance, it was confirmed that there was no PTH resistance at the kidney and there was no sign of GNAS mutation. We diagnosed this case as hypocalcemia due to idiopathic hypoparathyroidism for lower serum calcium and traced intact PTH levels and began calcium and calcitriol medicine to treat the hypocalcaemia. Subsequently, her symptoms were improved with normalization of ionized Ca at 2.32 mg/dL (range, 2.3 to 2.53). The results of fine needle aspiration on two nodules of thyroid were suggestive malignancy and she underwent a total thyroidectomy. The biopsy results were papillary microcarcinoma with lymphocytic thyroiditis for two suspicious nodules (sized 1.5×1.0 cm on the left and 2.0×1.0 cm on the right). Among the four parathyroid glands, the left inferior parathyroid gland was not discovered, and the remaining three parathyroid glands were remained during surgery. We used levothyroxine 0.05 mg medication for Hashimoto thyroiditis and insulin determir 12 U and aspart 16 U for glucose control.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [32, 'years'], 'weight': [51.5, 'kg'], 'Sodium': [144.0, 'mmol/L']}",0.73571,0.69892,0.7725,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 32 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 51.5 kg. The concentration of sodium is 144.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 51.5 * (144.0/140 - 1) = 0.73571 L. The patient's free body water deficit is 0.73571 L."
6045,38,Free Water Deficit,lab test,decimal,pmc-4027064-1,Extracted,"A 12.9-year-old girl visited our department of pediatrics complaining of chronic abdominal pain and diarrhea. She had also experienced tetany of the hand and foot for several months. At her full-term birth, her weight was 2.75 kg. Her family history had no history of renal, endocrinologic, or cardiovascular disease. Her father's height was 170 cm, her mother's 155 cm, and the midparental height, 156 cm. She had no history of diuretics use. Her height was 138.4 cm (<3rd percentile, -2.33 standard deviation score [SDS]); her weight was 43.3 kg (25th-50th percentile, -0.23 SDS); her body mass index was 22.7 kg/m2 (85th-90th percentile). The puberal stage was breast II and pubic hair I, and her bone age, according to the Greulich-Pyle method, was 11 years. Her blood pressure was 100/60 mmHg. Initial biochemical analysis revealed, on the basis of the following values, metabolic alkalosis with hypokalemia: sodium 139 mEq/L, potassium 2.4 mEq/L, chloride 98 mEq/L, blood urea nitrogen 5.8 mg/dL, creatinine 0.4 mg/dL, aspartate aminotransferase 48 U/L, alanine aminotransferase 67 U/L, pH 7.467, PCO2 47.4 mmHg, HCO3- 34.5 mmol/L (normal range, 22 to 26 mmol/L), base excess 9.6 mmol/L (-4 to 2 mmol/L), total calcium 9.9 mg/dL, phosphorus 4.7 mg/dL. Further laboratory investigation showed the following: magnesium 1.48 mg/dL (1.5 to 2.3 mg/dL), serum osmolality 218 mOsmol/kg (275 to 295 mOsmol/kg), renin 32.66 ng/mL/hr (<4.2 ng/mL/hr), and aldosterone 361.28 pg/mL (20 to 220pg/mL). Urine test results were as follows: Na+ 61 mEq/L, K+ 29.0 mEq/L, Cl- 57 mEq/L, osmolality 641 mOsmol/kg (50 to 1400 mOsmol/kg), spot urine calcium/creatinine ratio <0.02 mg/mg (0.03 to 0.2 mg/mg), 24 hours urine calcium 0.62 mg/kg (1.0 to 4.0 mg/kg/day), 24 hours urine magnesium 0.74 mg/kg (2.82±0.79 mg/kg/day). The calculated transtubular potassium gradient (TTKG) had increased to 8.078.
The patient had normal thyroid and parathyroid function. Abdominal ultrasound showed normal kidneys and diffuse mild fatty infiltration of the liver. GH stimulation tests for short stature revealed complete deficiency (). Magnetic resonance imaging of the brain revealed no remarkable findings. Her intelligence quotient as measured by the Korean Wechsler Intelligence Scale for Children III test was 67. Whole-blood DNA sequencing showed heterozygous mutation in the SLC12A3 gene (). Although her sister and brother were not genetically evaluated, they showed normal electrolyte and blood gas readings.
The patient was treated with 0.7 IU/kg/wk of GH and administered oral replacement of magnesium oxide (MgO, 1 g) and potassium chloride (KCl, 1.8 g). Serum photassium and magnesium level increased to 3.0 mEq/L and 1.85 mg/dL. She showed a 5.6 cm height gain over seven months. The frequency of abdominal pain and diarrhea markedly decreased, and the tetany and muscle-cramping symptoms were eliminated.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [9, 'years'], 'weight': [43.3, 'kg'], 'sex': 'Female', 'Sodium': [139.0, 'mEq/L']}",-0.18557,-0.17629,-0.19485,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 9 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 43.3 kg. The concentration of sodium is 139.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 139.0 mEq. To convert from 139.0 mEq to mmol, convert from mEq to mmol. The compound 139.0 has a valence of 1, and so divide the valence by the value of mEq to get, 139.0 mEq/(1 mEq/mmol) = 139.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mEq sodium/L converts to 139.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 43.3 * (139.0/140 - 1) = -0.18557 L. The patient's free body water deficit is -0.18557 L."
6046,38,Free Water Deficit,lab test,decimal,pmc-4479744-1,Extracted,"A 43-year-old woman suddenly developed fever at a body temperature of 39.1℃ and leukopenia. Fever spontaneously subsided after 3 days. She gradually developed nausea and could not eat due to severe vomiting. She had no spontaneous bowel movement and did not notice passage of flatus for nearly a week. She had weight loss of 4-5 kg in 2 weeks.
She had no prior history of cancer, metabolic or neurological diseases, trauma, or abdominal or pelvic surgery. She was taking no medications. At admission, vital signs were blood pressure of 106/72 mm Hg, pulse rate of 75 beats/min, respiratory rate of 20 breaths/min, and body temperature of 39.1℃. She had normal hair distribution, no skin rash, and no palpable superficial lymph nodes. Headache, photosensitivity, oral ulceration, and arthralgia were not evident. The abdomen was soft and markedly distended, with no audible bowel sounds. She had focal tenderness in the epigastrium.
Laboratory test results showed a hemoglobin level of 11.0 g/dL, white blood cell count of 2,710/mm3 (absolute neutrophil count: 1,951/mm3 and lymphocytes: 216/mm3) and platelet count of 118,000/mm3. Creatinine level was 0.44 mg/dL; sodium level, 138 mmol/L; potassium level, 2.7 mmol/L; and chloride level, 109 mmol/L. She had normal thyroid function. Her fasting glucose level and high sensitivity CRP values were normal. Antinuclear antibody (titer of 1:1280 with speckled pattern) was positive. Anti-Ro antibody, anti-La antibody, and anti-Ro52 antibody (3+, 1+, 3+, respectively) were positive. Anti-Smith antibody, rheumatoid factor, anti-cardiolipin antibody, anti-β2-glycoprotein I (β2-GPI) antibody, and the direct Coombs test result were negative.
The urinalysis result was normal. The stool white blood cell count was 0-1/low-power field. Stool bacterial culture, and tests results for adenovirus, astrovirus, norovirus, enterovirus, and rotavirus by PCR were all negative. Marked gaseous dilatation and air-fluid levels were observed on plain abdominal radiography (). An abdominal and pelvic CT scan showed a small amount of ascites, mild intrahepatic duct dilatation, and marked distension of the small bowel without a definite obstructive lesion. No evidence of ureterohydronephrosis or peritonitis was observed (). She had no notable findings on esophagogastroduodenoscopy and colonoscopy. Capsule endoscopy was performed. No mucosal lesion in the small bowel was observed. Small bowel transit time was nearly 10 hours, and passage of the capsule occurred after 3 days. Despite several positive autoimmune serologic markers, clinical manifestations did not meet the diagnostic criteria for autoimmune diseases, such as systemic sclerosis, SLE, or Sjögren syndrome.
She had slight improvement with conservative care, including hydration and intravenous metoclopramide, throughout the 18-day hospitalization course. On the 14th day following discharge, she presented with recurrent nausea and abdominal distension. Severe small bowel dilatation and air-fluid levels were present on a plain abdominal radiography. Because we could not completely rule out the possibility of secondary IPO due to autoimmune diseases such as SLE, she was given oral prednisolone 40 mg/day (about 1 mg/kg) for 7 days. She stopped oral prednisolone because of adverse effects including suicidal ideation and hair loss. The oral steroid trial failed to improve the symptoms, as demonstrated on radiography (), and was discontinued. Oral pyridostigmine 60 mg/day was administered, but the radiographic finding did not improve. With oral prokinetics only, the ileus gradually improved on radiography ().
Forty-five days following discharge, she came to the hospital due to oral ulcers. Four months later, she developed arthralgias of the knees, elbows, wrists, and shoulders. She was finally diagnosed with SLE according to positive serology and overall clinical manifestations. Oral steroids were recommended but refused. She did take oral prokinetics and non-steroidal anti-inflammatory drugs ().",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [43, 'years'], 'weight': [4.0, 'kg'], 'sex': 'Female', 'Sodium': [138.0, 'mmol/L']}",-0.02857,-0.02714,-0.03,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 43 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 4.0 kg. The concentration of sodium is 138.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 4.0 * (138.0/140 - 1) = -0.02857 L. The patient's free body water deficit is -0.02857 L."
6047,38,Free Water Deficit,lab test,decimal,usmle-10,Extracted,"A 45-year-old woman comes to the physician because of fatigue and irregular menstrual cycles for the past year. She also complains of recurrent sinus infections. During the past 6 months, she has had increased urinary frequency and swelling of her feet. She has also had difficulty lifting her 3-year-old niece for the past 3 weeks. She was recently diagnosed with depression. She works as a medical assistant. The patient has smoked one half-pack of cigarettes daily for 25 years and drinks four beers on the weekends. Her only medication is escitalopram. She is 160 cm (5 ft 3 in) tall and weighs 79 kg (175 lb); BMI is 31 kg/m2. She appears tired. Her temperature is 37°C (98.6°F), pulse is 80/min, respirations are 18/min, and blood pressure is 140/82 mm Hg. Physical examinations shows neck obesity and an enlarged abdomen. Examination of the skin shows multiple bruises on her arms and legs. There is generalized weakness and atrophy of the proximal muscles. Laboratory studies show:
Serum
Na+ 150 mEq/L
K+ 3.0 mEq/L
Cl- 103 mEq/L
HCO3- 30 mEq/L
Urea nitrogen 19 mg/dL
Creatinine 0.9 mg/dL
Glucose 136 mg/dL
A 1 mg overnight dexamethasone suppression test shows a serum cortisol of 167 nmol/L (N < 50) and a 24-hour urinary cortisol is 425 μg (N < 300 μg). Serum ACTH is 169 pg/mL (N = 7–50). Subsequently, a high-dose dexamethasone suppression test shows a serum cortisol level of 164 nmol/L (N < 50).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'years'], 'weight': [79.0, 'kg'], 'sex': 'Female', 'Sodium': [150.0, 'mEq/L']}",2.82143,2.68036,2.9625,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 45 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 79.0 kg. The concentration of sodium is 150.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 150.0 mEq. To convert from 150.0 mEq to mmol, convert from mEq to mmol. The compound 150.0 has a valence of 1, and so divide the valence by the value of mEq to get, 150.0 mEq/(1 mEq/mmol) = 150.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 150.0 mEq sodium/L converts to 150.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 79.0 * (150.0/140 - 1) = 2.82143 L. The patient's free body water deficit is 2.82143 L."
6048,38,Free Water Deficit,lab test,decimal,pmc-5385993-1,Extracted,"A 14-year-old girl was admitted to our emergency department with a four-day history
of generalized myalgia, muscular weakness and dark urine. On the day of admission,
she noted much-reduced diuresis and had difficulty walking. During the previous
days, the patient had been participating in a dance festival in hot conditions.
There was no past history of muscle cramps or hospital admissions due to
rhabdomyolysis. She was the only child of non-consanguineous parents.
At presentation, she was dehydrated. Her blood pressure was 120/60 (90th
percentile). Her muscle strengths in the proximal and distal muscles of the upper
and lower extremities were 4/5. Deep tendon reflexes were normal, and there was no
neurologic deficit. The remainder of her physical examination was normal. Her weight
was 57kg, and her height was 165cm.
The laboratory evaluation revealed ARF with a blood urea nitrogen of 263mg/dL (range
19.3 - 44.9mg/dL), a blood creatinine of 9.59mg/dL (range 0.60 - 1.30mg/dL) and a
glomerular filtration rate calculated according to the original Schwartz formula of
11.6mL/min/1.73m2. The blood gases showed metabolic acidosis (pH
7.30; HCO3 17.7mmol/L; base excess - 7.9; lactate 1.4mmol/L). Blood
biochemistries were as follows: sodium 129mmol/L (range 136 - 145mmol/L), potassium
6.12 (range 3.4 - 5.1mmol/L), ionized calcium 1.03mmol/L (range 1.13 - 1.32mmol/L),
phosphorus 9.3mg/dL (3.1 - 5.5mg/dL), magnesium 1.8mg/dL (range 1.6 - 2.3mg/dL),
myoglobin 28173mg/dL (range 9 - 82mg/dL), creatine kinase > 400,000UI/L (range 28
- 142UI/L), aspartate aminotransferase 3266UI/L (range 0 - 26), alanine
aminotransferase 1310UI/L (range 19 - 44UI/L).
Because of massive rhabdomyolysis, the patient was admitted to our pediatric
intensive care unit and was given intravenous fluid combined with diuretic therapy
to reverse ARF, glucose and insulin therapy to correct hyperkalemia and calcium
gluconate to prevent cardiac arrhythmias secondary to ion changes. During the first
hours of admission, she presented anuria that was unresponsive to medical therapy.
After eight hours of receiving supportive therapy, she was started on continuous
veno-venous hemodiafiltration (Gambro Prismaflex® System, Lisbon;
Portugal).
A hemodialysis catheter (12F; triple lumen) was inserted in the right femoral vein.
Hemodiafltration was performed using the hemofilter ST 60, and heparin was the
anticoagulant chosen. The following initial settings were used: blood-pump
150mL/min, dialysate (Prismasol 4®) 1000mL/hr, pre-filter
replacement solution (Prismasol 4®) 500mL/hr, post-filter
replacement solution (Prismasol 4®) 500mL/hr and fluid removal
50mL/hr. During the first two days of therapy, the main problem with
hemodiafiltration was easy coagulability of the hemofilter due to high levels of
myoglobin in circulation. To overcome this problem, higher pre-dilution flow rates
were used (maximum 1500mL/h). After 48 hours, she had asymptomatic hypophosphatemia
of 2.7mg/dL that was corrected after adding phosphorous to the replacement
solutions. On day 5, intermittent hemodialysis was started, and three sessions on
alternate days were performed. A calcium antagonist was prescribed on day six due to
worsening hypertension.
Signs and symptoms were controlled with medical treatment and renal replacement
therapy. Creatinine kinase and myoglobin returned to normal values in two weeks. Her
diuresis started to recover after the second day of therapy. At discharge, her renal
function was recovering, and she had a glomerular filtration rate of
88.9mL/min/1.73m2.
Regarding the investigation of the underlying insult, an acylcarnitine analysis by
tandem mass spectrometry of the patient's dried blood spot revealed a deficiency of
very long-chain acyl-CoA dehydrogenase (VLCAD). A genetic study revealed the
following mutations in compound heterozygosity of the VLCAD gene: p.P65Tfs*7 (c.
187_192insA) and p.R336H (c.1097G > A).
Frequent meals with carbohydrate-rich intake before exercise and restriction of
long-chain fatty acids intake along with medium-chain fatty acid supplementation
were recommended to prevent further attacks.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [14, 'years'], 'weight': [57.0, 'kg'], 'sex': 'Female', 'Sodium': [129.0, 'mmol/L']}",-2.68714,-2.55278,-2.8215,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 14 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 57.0 kg. The concentration of sodium is 129.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 57.0 * (129.0/140 - 1) = -2.68714 L. The patient's free body water deficit is -2.68714 L."
6049,38,Free Water Deficit,lab test,decimal,pmc-4800764-1,Extracted,"The patient was a 39-year-old woman who was referred to the renal division because of repeated glucosuria. She had no polyuria, polydipsia, or weight loss. Her blood pressure was 120/70 mmHg, and her body weight was 55 kg. Routine urinary analysis showed 2+ to 3+ glucose with no other abnormalities. A quantitative test for urine glucose was 7.56 g/24 h. Her medical history and clinical examination revealed no significant findings. Fasting plasma glucose (4.92 mmol/l), albumin (42.8 g/l), creatinine (97 μmol/l), sodium (139.80 mmol/l), chloride (138.5 mmol/l), potassium (3.92 mmol/l), calcium (2.10 mmol/l), phosphate (1.04 mmol/l), magnesium (1.08 mmol/l), bicarbonate (19.4 mmol/l), uric acid (79 μmol/l), and hemoglobin A1C (5.3 %) were all within normal ranges. One hundred healthy Chinese volunteers (200 chromosomes) were included as controls. Informed written consent was obtained from all participants prior to participation in the study.
Genomic DNA was extracted by salting out from peripheral white blood cells. The entire coding region and adjacent intronic segments of SLC5A2 were screened for mutations by the direct sequencing of PCR products. The genomic DNA reference sequences of SLC5A2 (NG_012892.1, Gene ID: 6524, MIM: 182381, GEO Profiles ID: 62739973 and 65974292) and protein reference sequences of SGLT2 (NP_003032, UniProtKB - P31639) were acquired from the Entrez gene and protein database, respectively. To exclude the possibility that the identified mutations represented common polymorphisms, control chromosomes were tested by PCR-restriction-fragment length polymorphism. A novel missense SLC5A2 mutation was found in the patient (c.1891G > A/p.E631K, Fig. ). The amino acid residue (631E) was found to be highly conserved among human SGLT subtypes and across SGLT2 homologs in multiple species. The mutation was not detected in any of the control 200 chromosomes, indicating that it does not represent a common polymorphism.
Human SGLT2 cDNA from normal kidney, generated by reverse transcription (RT)-PCR, was cloned into the pGEM-T easy vector (Promega, Madison, WI). Wild-type and c.1891A mutagenized SLC5A2 generated by site-directed mutagenesis were subcloned into the PEXL-GFP vector [], and verified by sequencing. Human HEK293 cells (obtained from central laboratories of Peking Union Medical College Hospital, and originally from the American Type Culture Collection) were seeded into 24-well plates 24 h before transfection. Plasmid constructs (0.5 μg) were transfected into cultured cells at 70–80 % confluency using X-tremeGENE HP DNA transfection reagent according to the manufacturer’s instructions (Roche, Mannheim, Germany). After 24 h of incubation, expression of SGLT2 wild type–GFP and mutant–GFP fusion proteins was detected by western blotting, confocal laser microscopy, and transport assays as we have done in previous studies [, ].
Western blotting analysis (Fig. ) demonstrated that 631 K SGLT2 expression was significantly lower than that of wild-type SGLT2–GFP (0.24 ± 0.14 vs. 1, P = 0.002, n = 4, Fig. ). Confocal imaging revealed that both the wild-type and mutant fusion proteins were expressed in a punctate pattern in the cell membrane, which merged well with the cell membrane marker 1,10-dioctadecyl-3,3,3’,3’-tetramethyl-indocarbocyanine perchlorate (DiIC18(3), Fig. ).
The function of wild-type SGLT2–GFP and 631 K SGLT2–GFP fusion proteins in cultured HEK293 cells was confirmed by transport of the glucose analog 2-(N-(7-nitrobenz-2-oxa-1,3- diazol-4-yl)amino)-2-deoxyglucose (2-NBDG), evaluated by fluorescence intensity using flow cytometry. 2-NBDG uptake in HEK293 cells transfected with wild-type SGLT2–GFP was increased about 3.5-fold compared with those transfected with GFP-only control vector (7926 ± 1153 vs. 2314 ± 791, P < 0.001, n = 4, Fig. ). The uptake activity of the mutant SGLT2 631 K-GFP fusion protein was significantly decreased compared with wild-type SGLT2–GFP (3629 ± 1082 vs. 7926 ± 1153, P < 0.001, n = 4, Fig. ).
The Medical Ethics Committee of the Inner Mongolia People’s Hospital and Peking University approved the protocol. Data were compared with the t-test or analysis of variance followed by Fisher’s least significant difference methods for multiple comparisons. Data are shown as the mean ± SD, and significant differences were declared at P < 0.05.
Kidney proximal tubules reabsorb almost 180 g glucose daily, which is filtered through the glomeruli. SGLT2 accounts for most glucose reabsorption. It is responsible for the active transport of glucose across the brush border membrane, and is expressed almost exclusively in the kidney []. Recent studies have reported that SLC5A2 mutations are causative of FRG [, , –]. The long-term outcome of FRG patients is excellent, so SGLT2 inhibitors have been the subject of particular attention for the treatment of diabetes [, ]. Although research into FRG may help with a breakthrough for diabetes treatment, expression and functional studies of SLC5A2 mutations in FRG are rare, and the role of SGLT2 C-terminal mutations needs further clarification.
A previous study [] suggested that overt glucosuria requires the individual to be homozygous or compound heterozygous for SLC5A2 mutations. Consistent with this, our patient with a heterozygous mutation had “mild” glucosuria (urine glucose excretion, 7.56 g/day). However, our findings still imply that the mutation causes a clinically relevant SGLT2 dysfunction. Our in vitro study of 293 cells showed that the transport activity of the mutant SGLT2 631 K-GFP fusion proteins was significantly lower than that of wild-type. SLC5A2 mutations may reduce or abolish transporter activity by impairing protein synthesis, processing, or insertion into the plasma membrane. Furthermore, transporter activity may be reduced or abolished by accelerating protein removal or degradation, altering functional regulation, or impairing intrinsic activity. The mutant SGLT2 631 K–GFP in our study had a similar punctate membrane expression pattern to wild-type, but a decreased expression intensity. Thus, the mutation (c.1891G > A/p.E631K) is likely to impair protein synthesis or accelerate protein removal or degradation. Our results also suggest that the SGLT2 C-terminal is very important for protein expression levels. We speculate that the reduced expression of the SGLT2 mutant is responsible for the decreased transport activity of mutant SGLT2.
Although it was not possible to perform a family study in the present case, identification of mutations that cause glucosuria will enable the establishment of a genotypic FRG diagnosis, providing important information for families and physicians. In general, renal biopsies are unnecessary for FRG patients, so the effect of the 631 K mutation on SGLT2 expression in the kidney is still unknown. We were restricted to an in vitro study of the expression and function of SGLT2 using GFP as a fluorescent label because we previously found that the SGLT2 antibody was unsuited to use in 293 cells, COS-7 cells, and Xenopus laevis oocytes.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [39, 'years'], 'weight': [55.0, 'kg'], 'Sodium': [139.8, 'mmol/L']}",-0.03929,-0.03733,-0.04125,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 39 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 55.0 kg. The concentration of sodium is 139.8 mmol/L. Plugging in these values into the equation, we get 0.5 * 55.0 * (139.8/140 - 1) = -0.03929 L. The patient's free body water deficit is -0.03929 L."
6050,38,Free Water Deficit,lab test,decimal,pmc-3479936-2,Extracted,"O. J. is a 47-year-old lady admitted on account of a two-week history of bilateral foot ulcer which started as a swelling on the dorsum of the foot following a 6-hour journey in a tightlypacked bus. Swelling was painless and spontaneously ruptured one week later with clear fluid discharge which became purulent later. There is history of feeling of numbness in both feet for the previous 6 months and no history of intermittent claudication. Feeling of numbness and then progressive darkening of the right 2nd, 3rd, 4th, and 5th toes develop few hours following the return journey, 2 weeks post-bullae formation. The patient is a known diabetic for 8 years but not regular on medications or clinic visit. She was diagnosed hypertensive in the course of the present illness. Her elder sister is diabetic hypertensive, while her mother is hypertensive. She has one child alive; last child 15 years ago was macrosomic and macerated stillbirth. She has never smoked a cigarette and there is no significant alcohol intake.
Anthropometry showed that weight = 98 kg, BMI = 35 kgm−2 (central obesity) waist-hip ratio = 0.9. Healing ulcer 4 cm × 6 cm on the lateral aspect of the dorsum of both feet, dry gangrene of 2nd, 3rd, 4th and 5th right toes (), dorsalis pedis and posterior tibial pulsation full volume on both left and right foot with sensory loss in stocking distribution.
Pulse rate = 96 bpm, regular, full volume; blood pressure = 160/90 mmHg, apex beat not displaced, heart sounds were normal S1 S2.
Spot blood glucose = 16.9 mmol/L; urinalysis showed glucose +++, erythrocyte +++; Serum urea & electrolytes showed, urea = 2.1 mmol/L, sodium = 130 mmol/L, potassium = 4.6 mmol/L, chloride = 92 mmol/L, bicarbonate = 002028 mmol/L.
She was placed on insulin, empirical antibiotic (ceftriazone, and clindamycin), amlodipine, lisinopril, vasoprin.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [47, 'years'], 'weight': [98.0, 'kg'], 'Sodium': [130.0, 'mmol/L']}",-3.5,-3.325,-3.675,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 47 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 98.0 kg. The concentration of sodium is 130.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 98.0 * (130.0/140 - 1) = -3.5 L. The patient's free body water deficit is -3.5 L."
6051,38,Free Water Deficit,lab test,decimal,pmc-5615275-1,Extracted,"In early March 2017, the Nephrology service was consulted to see an overweight 83-year-old female patient admitted to the Hospitalist service a week earlier with dyspnea and volume overload from symptomatic heart failure complicated by rapid ventricular response atrial fibrillation, against a background history of hypertension and stage 3 CKD. Other pertinent past medical history include hypertension, sarcoidosis, COPD, atrial fibrillation and type 2 diabetes mellitus. A month earlier, she was discharged after 5 days with symptomatic hypotension and dizziness associated acute kidney injury with peak creatinine of 2.21 mg/dL, and then associated with UTI that was treated with Bactrim. At the time she was also on Lisinopril, which was then discontinued. Subsequently following conservative management in the hospital, kidney function as measured by the serum creatinine had returned to near baseline of 0.96 mg/dL at discharge.
This time in March 2017, she had become increasingly short of breath and hypotensive as well and serum creatinine had risen back up again to as high as 1.79 mg/dL at the time of the Nephrology consultation. Temperature was 36.9 °C, heart rate 67 per/min, respiratory rate 18 per/min, oxygen saturation 90% on room air, and blood pressure was 106/60. She weighed up to 75.4 kg, height was 163 cm, with a BMI of 28.4 kg/m2. She was dyspneic, JVD was elevated, with 2+ bilateral extremity edema and reduced breath sounds in both lung bases bilaterally, with bibasilar inspiratory rales evident posteriorly. Admission chest radiograph showed cardiomegaly, new bilateral pleural effusions, pulmonary vascular congestion and hypoventilation. Echocardiogram revealed normal left ventricular systolic function with ejection fraction of 64%, mild mitral valve regurgitation, bi-atrial enlargement, normal right ventricular function with right ventricular systolic pressure of 29 mmHg. At the time of this consultation, serum albumin was 2.8 g/dL, sodium was 134 mmol/L, potassium 3.6 mmol/L, chloride 94 mmol/L, bicarbonate 24 mmol/L, calcium 8.9 g/dL, hematocrit 24.9%, WBC, platelets, TSH, Free T4, AST, ALT and total bilirubin were all normal. Pro Pro B Naturetic Peptide level that was elevated at 581 pg/mL on 2 February 2017 had rapidly escalated to 4907 pg/mL by 23 February 2017, three weeks later, just prior to this admission (Pro Pro B Naturetic Peptide reference range ≤ 450 pg/mL).
Earlier in the admission, she was started on intravenous amiodarone for rate control of atrial fibrillation. Furthermore, oral Diltiazem, 120 mg three times a day, was subsequently discontinued when she became hypotensive. She had been started on continuous intravenous Furosemide infusion at 10 mg/h but the previous 24-h urine output was only 1500 cc.
We doubled the dose of intravenous continuous infusion of Furosemide to 20 mg/h and added intravenous Chlorothiazide 500 mg every 12 h. The chlorothiazide was discontinued after one dose when the patient raised concerns for a history of drug-induced pancreatitis. We then increased the dose of intravenous Furosemide to 25 mg/h, added daily intravenous Albumin 25 gm infusion to run concurrently with the continuous Furosemide infusion because of severe hypoalbuminemia. The edematous legs and feet were elevated and wrapped with ACE wraps. Overnight, urine output had more than doubled to 3450 cc (). Subsequently, twenty-four urine output increased to over 3–4 L (). After 5 days of the Furosemide infusion, she was switched to oral Bumetanide 2 mg twice daily. She continued to make urine in excess of 2.5 L an day and was discharged after another two days, much improved with edema, dyspnea and orthopnea resolved, together with significant weight loss (). She had achieved a weight loss of 12 kg during the last nine days of the admission. Her serum creatinine trajectory also improved during the second half of this admission and serum creatinine at discharge was 1.29 mg/dL ( and ).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [83, 'years'], 'weight': [75.4, 'kg'], 'Sodium': [134.0, 'mmol/L']}",-1.45414,-1.38143,-1.52685,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 83 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 75.4 kg. The concentration of sodium is 134.0 mmol/L. Plugging in these values into the equation, we get 0.45 * 75.4 * (134.0/140 - 1) = -1.45414 L. The patient's free body water deficit is -1.45414 L."
6052,38,Free Water Deficit,lab test,decimal,pmc-8559641-1,Extracted,"A 44-year-old male patient diagnosed with vitiligo at 10 years old, came to the emergency department due to excessive thirst and polyuria of 8 to 10 L/day. The patient had a family history (father and 3 siblings) of type 2 diabetes mellitus and autoimmune hypothyroidism.
He was subsequently hospitalized in the endocrinology service with diagnosis of polydipsia-polyuria syndrome and high suspicion of diabetes insipidus. On physical examination the following were noted: Blood pressure, 110/70 mmHg; heart rate, 65 bpm; respiratory rate, 16 breaths per minute; body weight, 81 kg (178.5 lb); height, 170 cm; and BMI, 28 kg/m2.
In the preferential examination multiple irregular hypopigmented maculas were found in different parts of the body, compatible with vitiligo ().
Also decreased the baresthesia and pallesthesia sensitivity in feet. The remainder of the examination was unremarkable. Biochemical and hormonal examinations revealed the following: serum Na, 141 mEq/l; serum K, 3.84 mEq/l; fasting blood glucose, 110 mg/dl; serum creatinine, 0.81 mg/dl; thyroid profile with free t4, 1.25 µg/dl (normal range: 0.8–1.7 µg/dl); TSH, 2,248 µUI/ml (normal range: 0.4–4 µUI/ml); antimicrosomal antibodies, 32.9 U/ml (normal range: <60 U/ml); and HbA1c at 6.2%.
Given the presumptive diagnosis of diabetes insipidus, the patient underwent a water deprivation test (Miller test), and after the subcutaneous administration of 5U vasopressin (desmopressin phase), he was subsequently diagnosed with partial central diabetes insipidus ().
To identify the etiology, we requested a magnetic resonance imaging (MRI) of the pituitary with gadolinium (), which revealed the presence of two microadenomas (4×2 mm and 2×3 mm) in the posterolateral region of the adenohypophysis, a filiform neurohypophysis with decreased signal intensity, and normal thickness of the pituitary stalk. Likewise, due to blood glucose and HbA1c values, he was diagnosed with prediabetes.
The patient received initially pharmacological treatment based on chlorpropamide 100 mg QD, carbamazepine 200 mg TID and hydrochlorothiazide 25 mg QD, because desmopressin was not available at that time. In addition, it was recommended to limit the intake of foods rich in sodium and simple sugars, as well as to undertake regular physical activity and maintain an adequate state of hydration.
The patient had favorable response to the treatment, and was discharged with good tolerance and adherence to the medication. Ophthalmological and auditory evaluation was performed, and showed no abnormalities. However, during the outpatient controls, he had multiple episodes of polyuria requiring hospitalization, that were attributed to the decompensation of the underlying disease, the last being 13 years after diagnosis with polyuria of up to 15 L, which was associated with a weight loss of 10 kg, and strikingly, random blood sugar of 310 mg/dl. This was the last cause of hospitalization for glycemic management.
Because the patient had a family history of autoimmune hypothyroidism, as well as a personal history of vitiligo and idiopathic central diabetes insipidus by probable autoimmune etiology, we suspected a presentation pattern of latent autoimmune diabetes in adults (LADA 2). In line with this, we requested antibodies to glutamic acid decarboxylase 65 (GAD-65) and islet antigen 2 (IA-2) antibody, both of which were negative.
Consequently, type 2 diabetes mellitus was diagnosed considering that the patient was overweight and had a family history. The results of the blood tests were obtained as follows: HbA1c was 8.2% and basal C-peptide was 0.32 nmol/l.
Glycemia was controlled by administration of metformin 850 mg QD and progressive titration of the insulin dose until a schedule of insulin NPH 20 units in the morning and 10 units at night was established. During hospitalization, the drugs used for the management of diabetes insipidus were replaced by intranasal desmopressin 10 µg at night because this medication was already available in our country, with no adverse reactions.
One month later during his out-patient control, he reported two episodes of hypoglycemia and a result of fasting blood glucose of 83mg/dl, so we decided to withdraw insulin therapy. The next control in six months revealed serum sodium of 139 mEq/l, fasting blood glucose of 133 mg/dl, and HbA1c of 6.9%. Currently, the patient is asymptomatic and follows his out-patient controls by our service.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [44, 'years'], 'weight': [81.0, 'kg'], 'Sodium': [141.0, 'mEq/L']}",0.34714,0.32978,0.3645,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 44 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 81.0 kg. The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 81.0 * (141.0/140 - 1) = 0.34714 L. The patient's free body water deficit is 0.34714 L."
6053,38,Free Water Deficit,lab test,decimal,pmc-6935651-1,Extracted,"A 14-year-old girl, living in a refugee camp, was referred from a district hospital for the management of altered level of consciousness, fever, and hyperglycemia. Fever started 2 weeks prior to consultation for which she received empiric treatment for malaria in a district hospital. She was also diagnosed with severe acute on chronic malnutrition for which she received ready-to-use therapeutic food. The situation was worsened by polyuria, excessive thirst, uncontrolled hyperglycemia, persistent fever and progressive lethargy, necessitating her transfer to the endocrinology unit of the Mother and Child Center of Yaounde.
Past history was remarkable for diabetes which was diagnosed a year ago after 2 months of polyuria and excessive thirst. Insulin therapy was started at 0.5 IU/Kg/day with mixed insulin but patient's compliance was poor. She reported loss of sight 7 months ago (3 months after the diagnosis of diabetes). She is the 3rd child in a nonconsanguineous family of 10 children of whom three are alive. They fled the Central African Republic to Cameroon and for the past 4 years have been living in a refugee camp in the East region of Cameroon. Neither she nor the mother went to school.
On admission, she was lethargic (Glasgow coma scale was 13/15). Her weight was 19 kg (<3rd percentile), her height was 133 cm (<3rd percentile) for a BMI of 10.7 kg/m2, −5.5 SD for age. Vital signs were as follows: blood pressure: 100/80 mm Hg, pulse: 100 bpm, respiratory rate 34 cycles/min and temperature was 36.8°C. She had fine hair and poor dental hygiene. Her Tanner stage was B1P1. Her abdomen was distended with no palpable mass. She had vulvovaginal erythema. She had a dry mouth, sunken eyes, mixed signs of dehydration and severe malnutrition (skin pinch went back slowly) and bilateral leucocoria.
Her serum glucose level was 440 mg/dL (24.4 mmol/L), K + 3.3 mmol/L, corrected Na + 148.4 mmol/L, Cl-108 mmol/L. HbA1C was 12% (108 mmol/mol). Urinalysis revealed nitrites (3+), ketones (2+), glycosuria (3+), and culture later on showed growth of E coli. Her hemoglobin level was 12.3 g/dL, white blood cell count was 9500/mm3, and platelets count was 308 000/mm3. Aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) were in the upper limits (42 and 44 IU/L, respectively) and renal function was normal (blood urea nitrogen (BUN) 0.07 g/L, serum creatinine 3 mg/L). Blood proteins were 93 g/L. Blood gases were not available.
She was admitted to the intensive care unit. She received oral rehydration solution for the malnourished (10 mL/kg/hr for 2 hours) followed by 1.5 L/m2/day of normal saline intravenously (IV) and KCL 1.5 g/L (IV) for 24 hours. Rapid-acting insulin was started 2 hours later with an hourly subcutaneous dose of 0.1 IU/Kg. An antibiotic was also given (ceftriaxone at 50 mg/kg/day) as well as routine de-worming with a single dose of 400 mg of albendazole. Four hours following admission, she was more reactive; ketonuria was 1+, serum glucose level was 408 mg/dL (22.4 mmol/L). Rapid-acting insulin was replaced by multiple injections using neutral protamine Hagedorn insulin (NPH) and actrapid (1IU/kg/day). Ready-to-use therapeutic food F75 (75 kcal/100 mL) was started at 130 mL/kg/day divided into eight meals. Folic acid (5 mg once) and vitamin A (200 mg on days 1, 2, and 14) were added to the treatment.
The day after admission, she developed lower limb edema and abdominal distension without ascites and IV fluids were stopped. The oedema regressed on day 2. On day 3, the F75 was replaced with F100 (100 kcal/100 mL) 130 ml/kg/day and progressive introduction of Plumpy Nut® and normal food. Progression of her nutritional status is shown in Table .
Communication with and education of patient and her family was difficult because of unavailability of a translator trained in medical terminology and the fact that the patient was almost blind. This was partially improved following her cataract surgery performed 2 months later.
Upon discharge after 9 weeks spent in hospital, her weight was 29 kg, height 133 cm (BMI 16.4 kg/m2) and MUAC of 160 mm. She was discharged to her refugee camp on multiple insulin injections. Two months later, her weight was 32 kg, height 135 mm (BMI 17.56 kg/m2) and HbA1 C 10%.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [14, 'years'], 'weight': [19.0, 'kg'], 'sex': 'Female', 'Sodium': [148.4, 'mEq/L']}",0.684,0.6498,0.7182,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 14 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 19.0 kg. The concentration of sodium is 148.4 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 148.4 mEq. To convert from 148.4 mEq to mmol, convert from mEq to mmol. The compound 148.4 has a valence of 1, and so divide the valence by the value of mEq to get, 148.4 mEq/(1 mEq/mmol) = 148.4 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 148.4 mEq sodium/L converts to 148.4 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 19.0 * (148.4/140 - 1) = 0.684 L. The patient's free body water deficit is 0.684 L."
6054,38,Free Water Deficit,lab test,decimal,pmc-5757850-1,Extracted,"An 86-year-old woman presented with the chief complaint of difficulty walking. She lived with her daughter who agreed that she was moving more slowly than usual. At her baseline, the patient had memory lapses with regards to recent events but was able to complete most of her activities of daily living. The patient had a past medical history of hypertension, a right-sided thalamic infarct, and dyslipidemia. Her home medications included metoprolol, 50 mg daily, hydrochlorothiazide, 25 mg daily, lisinopril, 40 mg daily, aspirin, 81 mg daily, and simvastatin, 20 mg daily.
The patient was 4 foot 9 inches and weighed 88 pounds, which was 24 pounds below her previous weight documented five years prior. Her blood pressure was 233/122 mmHg, while the rest of her vital signs were within normal limits. She was alert, oriented to person and place but not time, and was able to provide most of her history. Her gait was slow, she had difficulty sitting up on her own, had decreased skin turgor, and did not have peripheral edema. The rest of her exam was unremarkable.
The initial workup done in the emergency department revealed a serum sodium of 99 mEq/L, a serum potassium of 3.7 mEq/L, serum chloride of 69 mEq/L, serum blood urea nitrogen (BUN) of 10 mg/dL, serum creatinine of 0.67 mg/dL, urine osmolality of 354 mOsm/kg, and urine sodium of 105 mEq/L. Her serum thyroid-stimulating hormone (TSH) and AM cortisol, which were measured later in the course of her hospital admission, were 0.66 uIU/mL and 21.5 mcg/dL, respectively. The patient was given 0.9% sodium chloride and was admitted to the intensive care unit. Five hours later, the patient’s neurological exam and laboratory studies were unchanged from admission (Table ). At this point, the decision was made to switch from 0.9% sodium chloride to 3% sodium chloride.
Within 24 hours of switching to 3% sodium chloride, the patient’s serum sodium increased to 109 mEq/L, and she did not have any changes in her neurological exam. The patient received hypertonic saline for a total of two days. At the end of the two-day period, her serum sodium increased to 120 mEq/L, her mental status remained intact, and her neurological exam remained unchanged.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [86, 'years'], 'weight': [88.0, 'lbs'], 'sex': 'Female', 'Sodium': [99.0, 'mEq/L']}",-5.26037,-4.99735,-5.52339,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 86 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 88.0 lbs so this converts to 88.0 lbs * 0.453592 kg/lbs = 39.9161 kg. The concentration of sodium is 99.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 99.0 mEq. To convert from 99.0 mEq to mmol, convert from mEq to mmol. The compound 99.0 has a valence of 1, and so divide the valence by the value of mEq to get, 99.0 mEq/(1 mEq/mmol) = 99.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 99.0 mEq sodium/L converts to 99.0 mmol sodium/L. Plugging in these values into the equation, we get 0.45 * 39.9161 * (99.0/140 - 1) = -5.26037 L. The patient's free body water deficit is -5.26037 L."
6055,38,Free Water Deficit,lab test,decimal,pmc-2672144-1,Extracted,"A 59-yr-old man visited outpatient clinic for evaluation of progressive dyspnea on exertion and chest discomfort for 4 months. He had no remarkable medical and family history.
On the physical examination, his height was 170 cm, weight 77 kg, the blood pressure 104/66 mmHg, the heart rate 76/min, the respiratory rate 20/min, and the body temperature 36℃. He had clear mentality, chronic ill-looking appearance and clear sclerae. Jugular venous distension was noted, but no cervical and axial lymphadenopathy was observed. The heart sounds were regular without murmur, but presystolic gallop (S4) was checked. The breath sounds were clear without rales or wheezing. Abdominal examination revealed normal bowel sounds without any palpable mass. There was no definite pitting edema. Otherwise the physical findings were unremarkable.
The blood cell counts were as follows: the hemoglobin 13.0 gm/dL, the white blood cell count 6,700/µL, and the platelet count 198,000/µL. According to the serological biochemical assay, fasting blood sugar was 107 mg/dL, Na+ 142 mEq/L, K+ 4.0 mEq/L, Ca2+ 9.6 mg/dL, P- 3.7 mg/dL, blood urea nitrogen 12 mg/dL, creatinine 0.9 mg/dL, total protein 7.0 g/dL, albumin 4.3 g/dL, aspartate transaminase 20 IU/L, alanine transaminase 22 IU/L, alkaline phosphatase 188 IU/L, lactate dehydrogenase 285 IU/L, and beta-2 microglobulin 1.7 mg/L (normal; 0.8-2.2). Urinalysis showed trace amount of proteinuria, and the urine Bence-Jones protein was suspected. Serum protein electrophoresis study was normal. On the immunochemistry findings, IgG was 1,052 mg/dL (normal; 700-1,600), IgA 105 mg/dL (normal; 70-400), IgM 49 mg/dL (normal; 40-230), and IgE was elevated as 385 IU/mL (normal; 10-180). In serum and urine immunoelectrophoresis study, lambda type MG was shown ().
The chest radiography film showed a slightly enlarged cardiac silhouette and there was no pulmonary congestion. There was no bony lesion on plain skull radiography. Electrocardiography (ECG) showed regular sinus rhythm, intermittent atrial premature beats, poor R wave progression, and Q wave in precordial leads ().
The echocardiography revealed dilated both atria, concentric left ventricular (LV) hypertrophy (end-diastolic interventricular septum thickness=13 mm and end-diastolic posterior wall thickness=13 mm, respectively). Both LV dimension and LV ejection fraction were within normal limits. On the Doppler study, ratio of early mitral inflow (E) to late filling velocity (A) (E/A) was 3.0, deceleration time was 135 msec. Tissue Doppler showed 4.03 cm/sec of early diastolic mitral annular velocity (E') with E/E' ratio of 21.6, suggesting restrictive physiology of diastolic dysfunction with elevated LV filling pressure (). There was scanty amount of pericardial effusion without definite evidence of constriction.
Bone marrow (BM) aspirate smears showed normocellular marrow particle, and estimated M:E ratio was 1.71:1. The granulocyte series were normal in number and showed good maturation sequences. Plasma cells were increased and counted up to 6.8% of absolute neutrophil count compatible with monoclonal gammopathy of undetermined significance (MGUS) (). There were no amorphous eosinophilic amyloid material in both H&E and Congo-red staining for ruling out amyloidosis for endomyocardial (), BM, and enteral biopsies. However, immunostaining for lambda light chain in myocardium showed positive result ().
The presentation was clinically consistent with non-amyloidotic light chain deposition cardiomyopathy (). He was managed conservatively with low-dose vasodilators and diuretics, and his symptom mildly resolved. After 9 months follow up, he readmitted for aggravated heart failure, and died due to intractable heart failure and ventricular arrhythmia in the end.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [59, 'years'], 'weight': [77.0, 'kg'], 'Sodium': [142.0, 'mEq/L']}",0.66,0.627,0.693,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 59 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 77.0 kg. The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 77.0 * (142.0/140 - 1) = 0.66 L. The patient's free body water deficit is 0.66 L."
6056,38,Free Water Deficit,lab test,decimal,pmc-4421632-1,Extracted,"A heretofore healthy 18-year-old man presented with a 2-day history of nausea, vomiting and stomach ache while consuming induction (20 g/day for 5 days) and maintenance (1 g/day for the next 6 weeks) dosages of creatine monohydrate for bodybuilding purposes. He did not have any significant past medical or family history. At physical examination, he weighed 74 kg, and his BMI was 24.18 kg/m2. His blood pressure was 150/90 mmHg, and he had abdominal tenderness. The initial laboratory studies were as follows: serum urea 39.98 mmol/L (normal 0–36 mmol/L), serum creatinine 201.55 mmol/L (normal 44.2–106 mmol/L), uric acid 0.37 mmol/L (normal 0–0.33 mmol/L), potassium 3.56 mmol/L (normal 3.5–5.0 mmol/L), sodium 148 mmol/L (normal 136–145 mmol/L), pH 7.36 (normal 7.35–7.45), Hct 36.8 (normal 37–52) and total protein 64.87 g/L (normal 64–87 g/L). Urinalysis revealed only proteinuria, and daily protein excretion was 284 mg. The other biochemical parameters and blood count were normal.
The patient was hospitalized, and the creatine supplements were discontinued. Intravenous fluids were administered. During hospitalization, his serum creatinine level increased to 403.10 mmol/L (). Serology revealed negative antinuclear, anti-double-stranded DNA and anti-neutrophil cytoplasmic antibodies. The spiral computed tomographic scan and ultrasonography revealed no abnormalities in the kidneys.
The renal biopsy revealed focal tubular injury with dilatation of tubular lumina and flattening of the tubular epithelial cells. Some of them had hyperchromatic nuclei and prominent nucleoli with occasional mitotic figures. There were sloughed epithelial cells, leucocytes and cellular debris in the tubular lumina; however, there were no pigmented casts. The glomeruli appeared to be normal. Immune complex deposition was not identified with immunoflourescence staining. With these features, the renal biopsy diagnosed acute tubular necrosis ().
Twenty-five days after stopping the creatine supplements, the patient's blood pressure (120/70 mmHg), serum creatinine (88.4 mmol/L) and proteinuria (82 mg/day) normalized, and the patient was discharged from the hospital with a weight of 72 kg.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [18, 'years'], 'weight': [74.0, 'kg'], 'Sodium': [148.0, 'mmol/L']}",2.53714,2.41028,2.664,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 18 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 74.0 kg. The concentration of sodium is 148.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 74.0 * (148.0/140 - 1) = 2.53714 L. The patient's free body water deficit is 2.53714 L."
6057,38,Free Water Deficit,lab test,decimal,pmc-3871037-1,Extracted,"A 67-year-old female visited the outpatient clinic of our institution complaining of numbness and coldness in both feet. She has been diagnosed with type 2 diabetes 5 years prior and was being treated with a sulfonylurea (gliclazide 30 mg). Based on the examination results, she was diagnosed with diabetic peripheral neuropathy, and thioctacid (600 mg) was prescribed. She experienced repeated occurrences of hunger, hand tremor, cold sweat, and dizziness 3 to 4 hours after a meal since having taken the drug, but symptoms consistently improved after eating snacks. Her past history was insignificant except an appendectomy 40 years prior. On physical examination, her height was 165 cm and body weight 60 kg. Blood pressure was 130/90 mm Hg. There was no thyroid goiter or skin pigmentation.
Blood examination showed leukocyte count 4,700/mm3, hemoglobin 13.0 g/dL, platelet 202,000/mm3, blood urea nitrogen 17.0 mg/dL, Cr 0.7 mg/dL, total protein 7.1 g/dL, albumin 4.6 g/dL, aspartate aminotransferase 26 IU/L, alanine aminotransferase 36 IU/L, alkaline phosphatase 116 IU/L, total cholesterol 166 mg/dL, triglyceride 115 mg/dL, high density lipoprotein 39 mg/dL, calcium 8.8 mg/dL, phosphate 3.3 mg/dL, sodium 135 mEq/L, and potassium 4.2 mEq/L. Thyroid and adrenal cortical function tests were performed. Free T4 was 1.12 ng/dL (normal range, 0.93 to 1.7), thyroid stimulating hormone 2.25 µIU/L (normal range, 0.27 to 4.2), adrenocorticotropic hormone 16.5 pg/mL (normal range, 6 to 56.7), and cortisol 13.4 µg/dL.
On admission, hemoglobin A1c (HbA1c) was 6.6%, fasting blood glucose 208 mg/dL, and postprandial blood glucose 195 mg/dL. Serum insulin, when measured by radioimmunoassay (RIA, immunoradiometric assay, INSULIN-IRMA, Biosource Europe, Nivelles, Belgium) was normal at 15.33 and 19.41 µIU/mL on fasting and postmeal, respectively (normal range, 2 to 25). However, C-peptide (immunoradiometric assay, C-Peptide IRMA, IZOTOP, Budapest, Hungary) was increased to 13.96 ng/mL on fasting and 18.24 ng/mL after meals (normal range, 1.07 to 3.51).
Sulfonylurea administration was discontinued, but the hypoglycemic symptoms persisted. After eating carbohydrate snacks between meals, daytime frequency of hypoglycemia decreased, but hypoglycemia with a level less than 50 mg/dL persisted at dawn with prolonged fasting. A 72-hour fasting test was attempted but was ended after 6 hours because the patient complained of severe hypoglycemia with a blood sugar level of 44 mg/dL. During a 6-hour examination, the blood sugar levels were 90, 70, and 44 mg/dL at baseline, 4 and 6 hours, and the serum insulin values measured by RIA were within the normal range at 22.92, 22.16, and 27.47 µIU/mL, respectively. The C-peptide values were increased to 15.60, 20.31, and 15.65 ng/mL, respectively. The antinuclear antibody was negative, while the insulin autoantibody value (RIA, Cobra 5010, Biosource Europe) was very high at 53% (normal range, <7). The human leukocyte antigen (HLA) class II result was DRB1*0406/1454. Abdominal computed tomography revealed no abnormalities in the pancreas ().
Because the patient continued to suffer from fasting hypoglycemia after suspending sulfonylurea administration, and serum C-peptide and insulin autoantibody levels increased, she was diagnosed with IAS. As the sulfhydryl-containing thioctacid first administered 2 weeks before the occurrence of hypoglycemia, it was regarded as the causal factor and discontinued. The patient continued to eat complex carbohydrates between meals, but hypoglycemia persisted. Prednisolone (10 mg) administration reduced the frequency of hypoglycemia and was able to be discontinued after 2 months because recovery was observed. At 4 months after diagnosis, the insulin autoantibodies were still high at 80.4%, but no signs of hypoglycemia were evident. At the 2-year follow-up, insulin autoantibody titer was reduced to 50.9%, and hypoglycemia was no longer detected.
The patient visited the rehabilitation department of another hospital to treat diabetic peripheral neuropathy 2 years after the initial occurrence and was prescribed thioctacid. Hypoglycemia recurred 10 days later, for which she visited our hospital. At that time, the patient was treated with voglibose (0.6 mg). HbA1c was 5.7% and insulin autoantibody was 77.2%. We performed a 75 g oral glucose tolerance test. The fasting plasma glucose was 98 mg/dL and the 2-hour plasma glucose after glucose load was 135 mg/dL, but serum insulin levels measured by enzyme-linked immunosorbent assay (ELISA, Roche Elecsys insulin test, Roche Diagnostics, Mannheim, Germany) were increased to more than 1,000 µU/mL for both fasting and 2 hours posttest. Fasting and 2-hour posttest C-peptide values were 10.91 and 16.92 ng/mL, respectively. After taking prednisolone (10 mg), she recovered from hypoglycemia. The dose of prednisolone was tapered by 5 mg and was discontinued 2 months later. Before discharge, the patient was instructed to avoid thioctacid. Six months after discharge, most of the values were normalized, i.e., HbA1c 5.7%, serum insulin 267 µU/mL, and C-peptide 3.71 ng/mL, but insulin autoantibodies remained high at 78% without hypoglycemia.
The patient was again prescribed thioctacid 2 years after the second occurrence, for which she revisited our hospital due to the recurrence of hypoglycemia. At that time, she was taking voglibose (0.6 mg) as a hypoglycemic agent. Her serum insulin level based on ELISA was abnormal, measuring higher than 1,000 µU/mL, while C-peptide was 21.06 ng/mL and insulin autoantibodies were 96%. According to the test results, the patient was prescribed prednisolone (5 mg), and after 4 months, serum insulin (measured by ELISA) and C-peptide were reduced to 210 µU/mL and 2.81 ng/mL, respectively, but the insulin autoantibodies remained high (88.9%). However, there was no sign of hypoglycemia ().",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [67, 'years'], 'weight': [60.0, 'kg'], 'sex': 'Female', 'Sodium': [135.0, 'mEq/L']}",-0.96429,-0.91608,-1.0125,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 67 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 60.0 kg. The concentration of sodium is 135.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 135.0 mEq. To convert from 135.0 mEq to mmol, convert from mEq to mmol. The compound 135.0 has a valence of 1, and so divide the valence by the value of mEq to get, 135.0 mEq/(1 mEq/mmol) = 135.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mEq sodium/L converts to 135.0 mmol sodium/L. Plugging in these values into the equation, we get 0.45 * 60.0 * (135.0/140 - 1) = -0.96429 L. The patient's free body water deficit is -0.96429 L."
6058,38,Free Water Deficit,lab test,decimal,pmc-2612654-1,Extracted,"Presenting complain – A 5 yr old Indian girl presented at the hospital with the chief complain of pain and distension of the abdomen. She complained of pain for last 4 days, the pain was continuous in nature and diffusely involved the whole abdomen but was more so in the umbilical and the hypo-gastric regions, pain was non-radiating, was relieved on lying still and aggravated on movement. No predisposing cause of the pain could be found and the girl's mother said that she complained of stomach pain suddenly. The pain had gradually increased in intensity over time. Abdominal distension developed about 2 days after she complained of pain. She also complained of multiple episodes of vomiting (about 15 per day), the vomitus was greenish yellow in colour, non bloody, odourless and copious in amount. She complained of burning micturation as well and described an increase in pain during urination. She also complained of loss of appetite and mild constipation but denied any fever or cough. Past history – Her mother described that she had developed similar kind of features 4 yrs back when a ceiling fan had fallen on her stomach, she was hospitalized and was diagnosed as a case of intrauterine rupture of urinary bladder. Exploratory laparotomy was performed and bladder rupture was repaired. The post operative recovery was uneventful with no further complains.
Birth history – She was a full term normal spontaneous vaginal delivery, her development milestones and vaccination status are up to date.
The girl was conscious and alert and was in pain.
Height-103 cms, Weight-28 kgs
Vital signs as follows: temp-98.8^F, pulse-126/min, RR-28/min, BP-100/70 mm Hg.
Abdominal exam-previous operative scar, abdomen distended, diffuse tenderness over whole abdomen, no rigidity, no guarding, liver and spleen impalpable, shifting dullness and fluid thrill were found to be present, bowel sounds were absent.
Examination of rest of the systems was uneventful.
Hb-12.5 gm%, TLC-14000, Na-130 mEq/L, K-6.5, Urea-210 mg/dl, creatinine-2.4 mg/dl, bilirubin-0.6(direct-0.3)mg/dl, AST-85 iu, ALT-49 iu.
X-ray abdomen erect showed diffuse ground glass appearance in the abdomen (Fig. ). No air fluid levels no gas under diaphragm was seen.
Abdominal ultrasound showed intraperitoneal fluid collection.
Diagnostic peritoneal tapping revealed a non bloody straw colour fluid which was found to be urine. The collected urine was found to be sterile.
IVP or cystogram were not undertaken as the peritoneal tap and ultrasound confirmed the presence of urine in the abdomen, in case of doubt i definetely recommend these tests.
The patient was catherized and put on intravenous ceftriaxone and metronidazole pre-operatively and was continued on the same for a period of 5 days. Emergent exploratory laparatomy was performed; intraperitoneal rupture of the bladder as a result of scar dehiscence of the previous bladder rupture repair was found located on the dome of the bladder and was repaired in layers. About two litres of urine was drained out of the peritoneal cavity. The rest of the bladder was found to be absolutely normal. The girl's recovery was fast and uncomplicated; her blood urea and creatinine levels were in the normal range in just two days after the operation. Subsequently she was discharged on oral antibiotics and dietary supplements with advice for regular follow up.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [5, 'years'], 'weight': [28.0, 'kg'], 'sex': 'Female', 'Sodium': [130.0, 'mEq/L']}",-1.2,-1.14,-1.26,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 5 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 28.0 kg. The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 28.0 * (130.0/140 - 1) = -1.2 L. The patient's free body water deficit is -1.2 L."
6059,38,Free Water Deficit,lab test,decimal,pmc-4124770-1,Extracted,"A 79-year-old Japanese woman with a past medical history of hypertension and arrhythmia suddenly developed left hemiparesis and drowsy state, and was sent to our emergency room. A neurological examination showed mild consciousness disturbance, conjugate deviation to right, mild dysarthria, left unilateral spatial neglect, left facial and motor weakness, and left sensory disturbance. Magnetic resonance imaging depicted a large high intensity lesion in right middle and posterior cerebral arterial territory on diffusion weighted images, and her right internal carotid artery was obstructed on magnetic resonance arteriography (MRA). Atrial fibrillation was observed on electrocardiogram. No other vascular lesion which may have caused the disease was noted, suggesting cardiogenic cerebral embolism. Her blood analysis showed almost normal findings including hemoglobin 13.0g/dL, hematocrit 39.8%, sodium (Na) 142mEq/L, blood urea nitrogen (BUN) 16mg/dL, and creatinine, 0.69mg/dL. In addition to anti-edema therapy, the continuous intravenous infusion of heparin was initiated on the following day because no apparent hemorrhage was identified on computed tomography (CT). No marked change was noted in neurological signs, and her brain edema tended to improve on CT. On day 14, her right internal carotid artery became patent on MRA, and hemorrhage occurred in the infarct region of her right middle cerebral artery. Thus, heparin administration was discontinued on the same day.
However, hemorrhage and brain edema expanded on day 15 (Figure ), and consciousness disturbance deteriorated. Concurrently, in addition to polyuria and hyponatremia (Figure and Table ), features of dehydration appeared, such as reduction of skin turgor, collapse of the inferior vena cava (IVC), and weight loss. Fluid replacement induced only an increase of urine volume and failed to correct dehydration tendency (input of 3410mL compared to a total urinary output of 3710mL on day 20). Considering the possibility of diabetes insipidus, a water deprivation antidiuretic hormone stimulation test (by inserting 10mcg of desmopressin into a nostril by using the spray once) was performed on day 28, however, her urine volume did not decrease. Despite adequate fluid replacement, she was in negative fluid balance and her weight had decreased by 4.6%, from 39.2kg to 37.4kg. An endocrinological examination excluded SIADH because of hydration features. CSWS was assumed to be a more probable pathological state, and salt supply was added to fluid replacement on day 29. Following the alleviation of hemorrhagic transformation, her excessive urine volume slowly decreased, and her hyponatremia and dehydration improved. She was transferred to another rehabilitation hospital about 2 months after admission.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [79, 'years'], 'weight': [39.2, 'kg'], 'sex': 'Female', 'Sodium': [142.0, 'mEq/L']}",0.252,0.2394,0.2646,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 79 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 39.2 kg. The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. Plugging in these values into the equation, we get 0.45 * 39.2 * (142.0/140 - 1) = 0.252 L. The patient's free body water deficit is 0.252 L."
6060,38,Free Water Deficit,lab test,decimal,pmc-3950226-1,Extracted,"The patient was a 20-year-old previously healthy woman. She was a university student. Her height and body weight were 168.1 cm and 52.2 kg, respectively. She ingested bamboo salt (about 150 grams ) in a day for the purpose of digestion and weight reduction. After that, she had more than ten episodes of vomiting and diarrhea for 2-3 hours. On arrival at our emergency department, vital signs were blood pressure of 128/81mmHg, heart rate of 75 beat/min, respiration rate of 20/min, and body temperature of 37.3℃. Her consciousness was clear but she complained of generalized weakness. The complete blood counts showed hemoglobin 11.3 g/dL, WBC 10,000 cells/µL, and platelet 196,000/µL. The results of her blood chemistry were as follows: Aspartate transaminase 11 IU/L, Alanine transaminase 9 IU/L, total protein 6.4 g/dL, albumin 4.5 g/dL, blood urea nitrogen 5.2mg/dL, and creatinine 0.57mg/dL. Serum sodium, potassium and chloride were 174mEql/L, 3.6mEq/L and 135mEq/L respectively. Urine sodium, potassium, chloride and osmolarity were 440mEq/L, 125.7 mEq/L, 314mEq/L and 841mosm/kg, respectively. On arterial blood gas analysis, pH was 7.32, PaCO2 36mmHg, bicarbonate 18.5mEq/L, PaO2 93mmHg and O2 saturation 97%. On the 1st day, total input and urine output was 3,700ml and 2,100ml, respectively. Her symptoms such as nausea, vomiting and diarrhea improved rapidly with 0.45% saline infusion and supportive care. On the 2nd day, her serum sodium concentration dropped to 152 mEq/L and urine output was 2,200ml/day. On the 3rd day, serum sodium concentration returned to normal range (). She recovered completely without any sequelae in 3 days.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [20, 'years'], 'weight': [52.2, 'kg'], 'sex': 'Female', 'Sodium': [174.0, 'mEq/L']}",6.33857,6.02164,6.6555,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 20 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 52.2 kg. The concentration of sodium is 174.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 174.0 mEq. To convert from 174.0 mEq to mmol, convert from mEq to mmol. The compound 174.0 has a valence of 1, and so divide the valence by the value of mEq to get, 174.0 mEq/(1 mEq/mmol) = 174.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 174.0 mEq sodium/L converts to 174.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 52.2 * (174.0/140 - 1) = 6.33857 L. The patient's free body water deficit is 6.33857 L."
6061,38,Free Water Deficit,lab test,decimal,pmc-5580559-1,Extracted,"A 12-year-old boy was admitted to the Santa Maria Hospital of Terni on 27 September 2016, due to a three-day history of fever (38 °C) and vomiting with acute presentation. Approximately two weeks before, the child had suffered from an episode of mild fever associated with abdominal pain and diarrhea that spontaneously resolved in a few days. In addition, in the previous three months, the child had complained of fatigue and loss of appetite several times; the previous history was negative. A mild reduction in body weight, of approximately 2 kg, was noted. Finally, in the last year, the parents had noticed mild but significant hyperpigmentation of the skin and mucous membranes, without giving it any importance. The child was previously well, suffering no significant diseases. His physical and neurological development was always considered within the normal range. There was no family history of severe clinical problems, including autoimmune diseases.
shows a picture of the boy at the time of admission. Physical examination revealed a patient in mediocre general condition, with a body weight of 35 kg (28° centile), a height of 150 cm (50° centile), and a body mass index of 15 (10° centile). Marked darkening of the skin, particularly on the palms and areolae, was evident. Subcutaneous fat tissue was reduced. No pathological findings of the upper and lower respiratory tract, heart, abdomen, or central or peripheral central nervous system were detected. His blood pressure was 110/60 mmHg, which is within the normal range for his age. Laboratory evaluation revealed no abnormalities of white or red blood cell counts (5320/µL; normal values, 4000–10,000/µL and 4,390,000/µL, respectively), no anemia (Hb 12.8 g/dL; normal values, 12–16 g/dL), no increase in serum concentrations of acute phase reactants (C reactive protein, 0.20 mg/dL; normal values <0.65 mg/dL and procalcitonin <0.05 ng/mL), hyponatraemia (124 mEq/L; normal values, 135–145 mEq/L) and hypochloraemia (93 mEq/L; normal values 100–110 mEq/L), mild hyperkalaemia (5.2 mEq/L; normal values, 3.5–5 mEq/L), borderline hypoglycaemia (69 mg/dL; normal values 70–110 mg/dL), and slight increases in blood urea nitrogen (53 mg/dL, normal values 10–50 mg/dL), serum creatine phosphokinase (909 UI/L; normal values 0–171 UI/L), and serum uric acid (9.5 mg/dL; normal values, 4.8–8.7 mg/dL). His ammonia levels, arterial blood gas, and blood lactate were within the normal range.
Immunological evaluations revealed normal serum IgA (81 mg/dL; normal values, 70–400 mg/dL), IgG (716 mg/dL; normal values, 700–1600 mg/dL), and IgM levels (47 mg/dL; normal values, 40–280 mg/dL), as well as negative anti-nuclear antibodies, anti-neutrophil cytoplasmic antibodies, anti-mitochondrial antibodies, extractable nuclear antigen screening, anti-thyroglobulin antibodies, anti-thyroperoxidase antibodies, and anti-phospholipid antibodies. However, a marked increase in IgA anti-transglutaminase (129 U/mL; normal values, <4 U/mL) and anti-endomysium (positive with a titre of 1/80) antibodies was found. A genetic study with polymerase chain reaction (PCR) DNA amplification and inverse hybridization testing alleles DQA1*05, DQB1*02, and DQB1*03:01 revealed the presence of HLA haplotypes DQ2 and DQ8. Duodenal biopsy could be spared according to the 2012 ESPGHAN CD diagnostic guidelines as anti-tranglutaminase antibodies were elevated over 10 times the normal range (129 UI/mL; normal values, <4 UI/mL), confirmed by the positivity of anti-endomisium antibodies and by the compatible HLA aplotypes.
Beginning with the clinical and laboratory data [,], celiac disease was diagnosed. In addition, primary AD was suspected. The diagnosis of CD and AD occurred quite late because the previous history of this child was negative and the parents did not give much importance at the symptoms that occurred in the last year. This was confirmed by low values of morning cortisol (0.8 µg/dL) and dehydroepiandrosterone sulfate (16.2 µg/dL), with adrenocorticotropic hormone (ACTH) concentrations of 1250 pg/mL. No abnormalities in adrenal gland morphology were found in abdominal ultrasonography and magnetic resonance tomography images. The child was treated with intravenous saline solution starting with a bolus of 300 mL over 2 h, followed by a maintenance dose of 1600 mL every 24 h. Serum electrolyte concentrations were evaluated every hour in order to ensure the maintenance of normal values. Normalization of the child’s electrolyte values was established within 3 h and the infusion was discontinued after 48 h.
On the second day of observation, further evaluation of the patient’s adrenal function was planned. The basal aldosterone and renin concentrations were evaluated. The renin level was high (19.10 ng/mL/h), whereas the aldosterone level was low (3.30 pg/mL). The serum ACTH level was lower than the previous day, but higher than the normal values (from >1250 pg/mL on day 1 to 477 pg/mL on day 2; normal values, <46 pg/mL). In addition, ACTH administration only marginally increased the cortisol concentrations at 30 (0.8 µg/dL) and at 60 min (0.6 µg/dL; normal values, 4.3–23.0 µg/dL). A 5-h Synacthen stimulation test confirmed adrenal insufficiency, as serum cortisol values did not reach the minimum normal values at various times of evaluation. The basal cortisol level was undetectable (<50 nmol/L) and failed to rise following Synacthen administration: the 60-min value was <600 nmol/L and the 5-h value was <1000 nmol/L.
Considering the simultaneous co-existence of AD and CD, cortisone acetate was administered at 25 mg at 8 a.m. and 12.5 mg at 4 p.m., and a gluten-free diet was initiated, instructing the patient and his parents on how to follow it correctly. The child was discharged from the hospital after four days, and the follow-up was planned. Thirty days following discharge, the evaluation revealed that the skin hyperpigmentation had almost completely disappeared. The adrenal insufficiency was no longer present (serum sodium, 135 mEq/L, potassium 4.4 mEq/L, chloride 101 mEq/L, glucose 93 mg/dL) and only a small dose of cortisone acetate (37.5 mg/die) was required to maintain normal serum electrolyte and cortisol concentrations. The compliance to the gluten-free diet was confirmed by the patient and his family and was also associated with a significant increase in body weight, of 1.5 kg. The anti-transglutaminase antibodies were dosed at the one-month follow-up control, and were found to still be high (121 UI/mL).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [12, 'years'], 'weight': [35.0, 'kg'], 'sex': 'Male', 'Sodium': [124.0, 'mEq/L']}",-2.4,-2.28,-2.52,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 12 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 35.0 kg. The concentration of sodium is 124.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 124.0 mEq. To convert from 124.0 mEq to mmol, convert from mEq to mmol. The compound 124.0 has a valence of 1, and so divide the valence by the value of mEq to get, 124.0 mEq/(1 mEq/mmol) = 124.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 124.0 mEq sodium/L converts to 124.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 35.0 * (124.0/140 - 1) = -2.4 L. The patient's free body water deficit is -2.4 L."
6062,38,Free Water Deficit,lab test,decimal,pmc-3573489-2,Extracted,"A 6-year-old girl, resident of Pauri Garhwal, Uttarakhand (India), was evaluated for recurrent abdominal pain, seizures and hypertension. Past history was significant for left percutaneous nephrolithotomy when she was 5 years old. At evaluation, undernutrition (weight, 14.5 kg; height, 112 cm) and hypertension (blood pressure 113/82 mmHg) were noted. Evaluation revealed renal dysfunction (blood urea 102 mg/dl; creatinine 5.49 mg/dl), hemoglobin 10.4 g/dl; sodium 138 mEq/l; potassium 3.4 mEq/l; calcium 8.6 mg/dl; phosphate 3.8 mg/dl; alkaline phosphatase 568 IU/l, pH 7.39; bicarbonate 21.9 mEq/l; and PTH 347 pg/ml. Ultrasonography demonstrated bilateral multiple renal pelvicalyceal stones. A diagnosis of PH1 was considered, prompting a mutational testing. As disease progressed, chronic ambulatory peritoneal dialysis was initiated.
The median urinary oxalate level in the three cases was 283.5 mg/1.73 m2/day (normal, <40 mg/1.73 m2/day).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [6, 'years'], 'weight': [14.5, 'kg'], 'sex': 'Female', 'Sodium': [138.0, 'mEq/L']}",-0.12429,-0.11808,-0.1305,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 6 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 14.5 kg. The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 14.5 * (138.0/140 - 1) = -0.12429 L. The patient's free body water deficit is -0.12429 L."
6063,38,Free Water Deficit,lab test,decimal,pmc-8175418-1,Extracted,"A 63-year-old man presented with abdominal distension, worsening jaundice and lower extremity swelling over the previous 48 hours. Past medical history included Hepatitis C cirrhosis, upper gastrointestinal (GI) bleed secondary to esophageal varices and hepatocellular carcinoma (HCC). HCC, with metastasis to the hilar lymph nodes and lungs, was found to be unresectable and the patient was not a candidate for a liver transplant. He had been treated with lenvatinib as first-line, then transitioned to sorafenib and trans-catheter arterial chemo-embolization (TACE). Home medications included furosemide and spironolactone. He had no previous history of SBP and was not on prophylactic antibiotics. Social history was positive for previous tobacco use 15 years prior. There was no history of chronic liver disease or GI malignancies in the family.
On exam, vital signs were within normal limits. The patient's weight was 78 kg and BMI was 27 kg/m2. Physical exam revealed scleral icterus, tense ascites and bilateral pitting edema in the lower extremities. No asterixis was noted. Exam of other organ systems was nonrevealing. Laboratory testing showed an elevated white blood cell count of 18.8 x 109/L, low hemoglobin of 11.3 g/dL, a platelet count of 200 x 109/L, elevated International normalized ratio of 1.9, low sodium of 123 mmol/L, elevated potassium of 5.5 mmol/L, low albumin of 1.6 g/dL, and elevated C- reactive protein level of 70 mg/L. Liver function enzymes were elevated: aspartate transaminase 129 U/L, alanine aminotransferase 71 U/L, and bilirubin 6.3 mg/dL. Ammonia level was elevated at 58 mg/L. Model for end-stage liver disease sodium (MELD-Na) score was 29, corresponding to 90-day mortality of 20%. Ultrasound of the abdomen demonstrated features of a cirrhotic liver and a large volume of ascites. The portal vein was occluded and measured 1.63 cm. There was cavernous transformation seen with color flow Doppler in the region of the portal vein (Figure ). The patient underwent an ultrasound-guided, large-volume paracentesis and a total of 5.0 L of clear straw-colored fluid was removed. Peritoneal fluid cytology was negative for malignant cells. Ascitic fluid analysis revealed albumin less than 0.6 g/dL, total protein of 1.6 g/dL, lactate dehydrogenase of 182 U/L, and glucose of 43 mg/dL. Ascitic fluid polymorphonuclear neutrophil (PMN) count was 2,983, prompting empiric IV ceftriaxone therapy for SBP. Serum ascitic albumin gradient was >1.1 g/dL, consistent with ascites secondary to portal hypertension in the setting of cirrhosis and portal vein thrombosis.
Peritoneal fluid cultures were obtained. The culture was grown on a MacConkey agar plate and then confirmed with an API-20E test (BioMerieux, Inc., France). The test was positive for S. enterica, susceptible to ceftriaxone, levofloxacin and trimethoprim/sulfamethoxazole. Therefore, IV ceftriaxone was continued, with a good clinical response. The patient received IV albumin 25% infusion on day 1 and day 3 post paracentesis. The patient needed repeat paracentesis on day 3 and day 6, with the removal of another 5.0 L and 3.1 L of fluid, respectively. Repeat peritoneal cultures were negative, confirming response to antibiotic treatment. The patient had an uneventful course during hospitalization and completely recovered from the SBP, with the resolution of abdominal pain. He was transitioned to oral SBP prophylaxis therapy (trimethoprim/sulfamethoxazole daily) upon discharge.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [63, 'years'], 'weight': [78.0, 'kg'], 'Sodium': [123.0, 'mmol/L']}",-5.68286,-5.39872,-5.967,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 63 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 78.0 kg. The concentration of sodium is 123.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 78.0 * (123.0/140 - 1) = -5.68286 L. The patient's free body water deficit is -5.68286 L."
6064,38,Free Water Deficit,lab test,decimal,pmc-4154290-1,Extracted,"An eighteen year old boy, born out of non-consangious marriage, first in birth order, born at term by vaginal delivery with normal perinatal history and normal motor and mental mile stones, was admitted in accident and emergency department with history of progressively worsening crampy leg pain from one month, increased frequency of micturation and increased thirst for last three weeks. There was history of inability to move his limbs from last 3 days. There was no history of rash, headache, fever, vomiting, diarrhea, and weight loss and bladder or bowel incontinence. There was no history of any drug or herbal medicine intake. On examination, patient was conscious, cooperative and well oriented in time, place and person. General physical examination revealed pulse 92 per minute, blood pressure 110/70mmHg and respiratory rate of 16 per minute. There were bony deformities in the form of widening of bilateral wrists and bilateral knock-knees. Chest, cardiovascular and abdominal examinations were unremarkable. Nervous system examination revealed normal higher mental functions and no cranial nerve deficit. Motor examination revealed hypotonia and a power grade of 3/5 in both arms and 2/5 in both lower limbs. Deep tendon reflexes were depressed all over and bilateral planter response was flexor. Differential diagnosis in our patient included hypokalemic periodic paralysis, myositis and renal tubular acidosis. Laboratory investigation revealed random blood glucose of 112 mg/dl, serum sodium 144 mmol/liter, serum potassium 1.3 mmol/liter, pH 7.30, serum bicarbonate 20.3 mmol/liter, serum chloride 112 mmol/liter, partial pressure oxygen 83 mmHg, oxygen saturation of 93% and partial pressure carbon dioxide 34 mmHg. Haemogram, kidney function and liver function tests at presentation are depicted in (). Muscle enzymes in the form of Creatine phosphokinase (CPK) were 1823 U/liter (0-195) and Lactate dehydrogenase (LDH) 886 U/liter (100-235). In view of severe hpokalemia, patient was immediately started on intravenous potassium chloride infusion at a rate of 30 meq/hour and oral potassium was started simultaneously in a dose of 20 meq 6 hourly. There was a predictable improvement in muscle weakness after initiation of potassium therapy and patient became ambulatory after 24 hours of treatment. In view of severe hypokalemia, systemic acidosis and skeletal deformities, a strong possibility of renal tubular acidosis was made. Subsequently, patient was subjected to anthropometric examination which revealed severe disproportionate short stature () with height of 144 cm (<3rd centile, standard deviation score (SDS)=-4.30), upper segment (74 cm), lower segment (70 cm), upper segment to lower segment ratio (1.05), arm span (142 cm), head circumference (52 cm) and mid parental height of 162 cm. Patient´s weight was 33 kg with a body mass index (BMI) of 15.9 kg/m² (<3rd centile, SDS=-2.85). Patient had well developed secondary sexual characters in the form of pubic hair stage 5, stretched penile length (SPL 10 cm), bilateral testicular volume >15ml. Hearing tests in the form of Rinne and Weber and ophthalmic tests including Schirmer’s test were unrevealing. 24 hour urinary calcium was 472 mg per day, urinary creatinine 702 mg per day, urinary phosphorus 824 mg per day and urinary protein of <50mg per day and no glycosuria. After correcting hypokalemia, there was further fall in serum pH to 7.27 with serum bicarbonate of 16.5 mmol/litre. Urinary pH at this time was 7.0.Abdominal ultrasonography (USG) revealed bilateral medullary nephrocalcinosis. Digital abdominal X- ray revealed fine calcified foci in bilateral renal area (). Skeletal survey revealed widening of both wrists and bilateral knock knees (). In view of severe hypokalemia and normal anion gap (12 mmol/litre) hyperchloremic metabolic acidosis and inability to acidify urine with associated hypercalciurea and no apparent secondary cause, a diagnosis of primary distal renal tubular acidosis was made. However exact etiological diagnosis could not be established because of unavailibity of genetic testing in our Centre.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [18, 'years'], 'weight': [33.0, 'kg'], 'sex': 'Male', 'Sodium': [144.0, 'mmol/L']}",0.56571,0.53742,0.594,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 18 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 33.0 kg. The concentration of sodium is 144.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 33.0 * (144.0/140 - 1) = 0.56571 L. The patient's free body water deficit is 0.56571 L."
6065,38,Free Water Deficit,lab test,decimal,usmle-123,Extracted,"A 54-year-old man comes to the physician because of diarrhea that has become progressively worse over the past 4 months. He currently has 4–6 episodes of foul-smelling stools per day. Over the past 3 months, he has had fatigue and a 5-kg (11-lb) weight loss. He returned from Bangladesh 6 months ago after a year-long business assignment. He has osteoarthritis and hypertension. Current medications include amlodipine and naproxen. He appears pale and malnourished. His temperature is 37.3°C (99.1°F), pulse is 76/min, and blood pressure is 140/86 mm Hg. Examination shows pale conjunctivae and dry mucous membranes. Angular stomatitis and glossitis are present. The abdomen is distended but soft and nontender. Rectal examination shows no abnormalities. Laboratory studies show:
Hemoglobin 8.9 g/dL
Leukocyte count 4100/mm3
Platelet count 160,000/mm3
Mean corpuscular volume 110 μm3
Serum
Na+ 133 mEq/L
Cl- 98 mEq/l
K+ 3.3 mEq/L
Creatinine 1.1 mg/dL
IgA 250 mg/dL
Anti-tissue transglutaminase, IgA negative
Stool culture and studies for ova and parasites are negative. Test of the stool for occult blood is negative. Fecal fat content is 22 g/day (N < 7). Fecal lactoferrin is negative and elastase is within normal limits.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'weight': [5.0, 'kg'], 'sex': 'Male', 'Sodium': [133.0, 'mEq/L']}",-0.15,-0.1425,-0.1575,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 54 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 5.0 kg. The concentration of sodium is 133.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 133.0 mEq. To convert from 133.0 mEq to mmol, convert from mEq to mmol. The compound 133.0 has a valence of 1, and so divide the valence by the value of mEq to get, 133.0 mEq/(1 mEq/mmol) = 133.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mEq sodium/L converts to 133.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 5.0 * (133.0/140 - 1) = -0.15 L. The patient's free body water deficit is -0.15 L."
6066,38,Free Water Deficit,lab test,decimal,pmc-3190515-1,Extracted,"A 48-year-old morbidly obese African-American male with a medical history of congestive heart failure, hypertension, obstructive sleep apnea on 2 l of home oxygen and non-complaint with continuous positive airway pressure at night presented to the emergency department (ED) with worsening shortness of breath and lower extremity oedema over one week. Vital signs in the ED were temperature, 98.7 degrees Fahrenheit; blood pressure, 116/66 mmHg; heart rate, 130 beats per minute; respiratory rate, 30; oxygen saturation, 85% on 2 l nasal cannula; weight, 162 kg and body mass index, 47. Physical examination revealed a morbidly obese male in acute respiratory distress with an irregularly irregular pulse and one plus lower extremity pitting oedema. Laboratory values in the ED include white blood cell count, 9 800/μl; haemoglobin, 14.2 g/dl; platelet count, 230 000/μl; sodium, 140 mEq/l; potassium, 4.5 mEq/l; chloride, 104 mEq/l; bicarbonate, 29 mEq/l; blood urea nitrogen (BUN), 38 mg/dl; creatinine, 1.4 mg/dl; glucose, 105 mg/dl; aspartate aminotransferase (AST), 51 U/l; alanine aminotransferase (ALT), 40 U/l; alkaline phosphatase, 68 U/l; total bilirubin, 1.5 mg/dl; albumin, 3.4 g/dl; total protein, 7.1 g/dl; international normalised ratio (INR), 1.2; myoglobin, 97 μg/l; troponin, 0.07 ng/ml and B-type natriuretic peptide, 934 pg/ml. Urine toxicology screen was positive for cocaine. Arterial blood gas showed a pH 7.33, paCO2 68.5 and paO2 88.6 on FiO2 of 40%. Electrocardiogram confirmed atrial fibrillation with a rapid ventricular response. Echocardiogram revealed a myopathic severely enlarged left ventricular chamber with moderate concentric left ventricular hypertrophy and severe global hypokinesis with an ejection fraction of 8 to 10%. The patient's work of breathing and oxygenation improved with Bipap. He was started on diltiazem and diuresis was initiated. The patient was admitted to the step-down unit with a new diagnosis of atrial fibrillation.
On hospital day number eight, the overnight nurse found the patient unresponsive. A code blue was called. His initial rhythm was ventricular fibrillation and he was shocked with 200 J twice before regaining pulses. When stabilised, he was transferred to the intensive care unit (ICU) where he regained consciousness and full neurologic function within one hour of the event. The following day, an automatic implantable cardioverter defibrillator (AICD) was placed. Intraoperatively, the patient had runs of ventricular tachycardia with hypotension to 80 mmHg systolic. Postoperatively, the patient was found to have a right fixed mid-dilated pupil, flaccid paralysis of the left arm and leg with hyperreflexia throughout the left side. Computed tomography (CT) of the head revealed a right midbrain and thalamic stroke thought to be secondary to transient arrhythmia-induced hypoperfusion, intraoperatively.
On postoperative day number three, after AICD placement and stroke, the patient acutely developed a rigid distended board-like abdomen with dullness to percussion. Vitals at that time were temperature, 98.4 degrees Fahrenheit; blood pressure, 112/67 mmHg; heart rate range, 55 beats per minute, and respiratory rate 26 on ventilator settings of assist control volume control with a rate of 26; tidal volume, 500 ml; FiO2, 40% and positive end-expiratory pressure of 5. His peak inspiratory pressure on the ventilator had risen from 26 to 72 mmHg; his plateau had risen from 15 to 48 mmHg with oxygen desaturation from 93 to 85%. The patient had received 1.5 l in and urinated 4.5 l over the 24 hours, leading up to this event. His laboratory values from that morning were unchanged from previous (white blood count, 10 400/μl; haemoglobin, 12.6 g/dl; platelets, 200 000/μl; sodium, 139 mEq/l; potassium, 4.7 mEq/l; chloride, 100 mEq/l; bicarbonate, 34 mEq/l; BUN, 36 mg/dl; creatinine, 1.41 mg/dl; glucose, 78 mg/dl; calcium, 8.3 mg/dl; magnesium, 2.0 mEq/l; phosphorus, 3.0 mg/dl; AST, 77 U/l; ALT, 94 U/l; alkaline phosphatase, 186 U/l; total bilirubin, 1.3 mg/dl). This constellation of findings prompted the team to measure an abdominal compartment pressure which was elevated to 53 cm H2O (40 mmHg) with an abdominal perfusion pressure (APP) of 42 mmHg. A CT scan of the abdomen and pelvis was performed which showed no dilated loops of bowel, no ileus, no evidence of free air, abscess or obstruction and minimal free fluid []. Pertinent labs from the event revealed a lactate of 1.0 mg/dl; lipase, 159 U/l; amylase, 76 U/l; creatinine, 1.53 mg/dl. Surgery was consulted and the FiO2 was increased to 100%, which improved his oxygen saturation to 96% despite his elevated peak inspiratory pressures.
Surgical recommendations were for an emergent bedside surgical abdominal decompression. The patient was administered 10 mg of intravenous cisatracurium besylate by anaesthesia in preparation for surgical management. Shortly following paralytic administration, his peak inspiratory pressure corrected from 72 to 23 mmHg, his plateau pressure from 48 to 16 mmHg and his oxygenation status tolerated a decrease in FiO2 down to 40% with his oxygen saturation returning to baseline. Measurement of his abdominal compartment pressure revealed a drop from 53 (40 mmHg) to 23 cm H2O (17 mmHg) and then normalised to 15 cm H20 (11 mmHg) over a three-hour period. During this entire event, the patient averaged 100 to 200 cc/hr of urine output and laboratory values from the following day showed a drop in creatinine from 1.53 to 1.29 mg/dl. Given this correction, surgical management was postponed and the patient was monitored. The patient remained hospitalised for an additional 73 days. He was ultimately transferred to a skilled nursing facility without return of symptoms.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [48, 'years'], 'weight': [162.0, 'kg'], 'sex': 'Male', 'Sodium': [140.0, 'mEq/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 48 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 162.0 kg. The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 162.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
6067,38,Free Water Deficit,lab test,decimal,pmc-4676380-1,Extracted,"Man of 54 years old had for four months diarrhea, watery stools, often in every three
hours lasting 15 days; had 14 kg weight loss during this period, with asthenia,
anorexia, malaise, muscle weakness and cramps. Laboratory tests showed VIP (intestinal
polypeptide active vessel) 242 pg/ml (<75); Na=138; K=1.6; and creatinine=1.53.
Ultrasonography showed hypoechoic image on segment IV of 4.2 cm, confirmed by CT with
the presence of several hypervascular images in liver segments IV, III, II (). Ultrasonography guided biopsy was
performed in one liver nodule that revealed metastatic neuroendocrine carcinoma by
immunohistochemistry. Laparotomy confirmed multiple liver metastases (). Intraoperative ultrasonography showed
nodule in pancreatic body. Bodycaudal pancreatectomy with splenectomy () and left hepatic trisegmentectomy were
performed (). No tumor was found in the
pancreatic parenchyma. Histopathology showed acinar atrophy and hyperplasia of islets in
the caudal region. In peri-pancreatic adipose tissue was confirmed the presence of five
nodes with well-differentiated neuroendocrine carcinoma infiltrating the adipose tissue
adjacent the neoplastic infiltration beyond perineural and angiolymphatic (). Hepatic lesions confirmed the diagnosis of
metastatic well-differentiated neuroendocrine carcinoma. Immunohistochemical analysis
showed positivity for sinaftofisin, chromogranin and intestinal polypeptide active
vessel (VIP). Ki-67 was positive in 10%. Patient had no major complications. There was
immediate regression of diarrhea and electrolyte abnormalities. After 12 months,
returned again with the same initial clinical picture. Liver CT images showed multiple
metastatic nodulation diffusely distributed. Therapy with somatostatin analogue with
prolonged action (LAR) and chemotherapy with inhibitors of mTOR (everolimus) was started
with regression of liver lesions and clinical symptoms. At the third year
postoperatively he was without clinical signs of disease recurrence.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'weight': [14.0, 'kg'], 'sex': 'Male', 'Sodium': [138.0, 'mEq/L']}",-0.12,-0.114,-0.126,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 54 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 14.0 kg. The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 14.0 * (138.0/140 - 1) = -0.12 L. The patient's free body water deficit is -0.12 L."
6068,38,Free Water Deficit,lab test,decimal,usmle-9396,Extracted,"A 58-year-old man presents to the Emergency Department after 3 hours of intense suprapubic pain associated with inability to urinate for the past day or two. His medical history is relevant for benign prostatic hyperplasia (BPH) that has been under treatment with prazosin and tadalafil. Upon admission, he is found to have a blood pressure of 180/100 mm Hg, a pulse of 80/min, a respiratory rate of 23/min, and a temperature of 36.5°C (97.7°F). He weighs 84 kg (185.1 lb) and is 175 cm (5 ft 7 in) tall. Physical exam, he has suprapubic tenderness. A bladder scan reveals 700 ml of urine. A Foley catheter is inserted and the urine is drained.  Initial laboratory tests and their follow up 8 hours after admission are shown below.
Admission 8 hours after admission
Serum potassium 4.2 mmol/L Serum potassium 4.0 mmol/L
Serum sodium 140 mmol/L Serum sodium 142 mmol/L
Serum chloride 102 mmol/L Serum chloride 110 mmol/L
Serum creatinine 1.4 mg/dL Serum creatinine 1.6 mg/dL
Serum blood urea nitrogen 64 mg/dL Serum blood urea nitrogen 62 mg/dL
Urine output 250 mL Urine output 260 mL
A senior attending suggests a consultation with Nephrology.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [58, 'years'], 'weight': [84.0, 'kg'], 'sex': 'Male', 'Sodium': [140.0, 'mmol/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 58 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 84.0 kg. The concentration of sodium is 140.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 84.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
6069,38,Free Water Deficit,lab test,decimal,pmc-6556792-1,Extracted,"An Asian male infant was born by vaginal delivery at 39 weeks of gestation, with a birth weight of 3410 g, to a 34-year-old mother (gravida: 3; parity: 1; preterm: 0; miscarriage: 1; liveborn: 1) with pregnancy notable for fetal diagnosis of left-sided CDH. Maternal obstetrical history was significant for an ectopic pregnancy and an uncomplicated birth of a healthy, term male infant. Family history was significant for a maternal uncle who died at 21 years of age and another maternal uncle and two maternal male cousins who died in early childhood, all due reportedly to adrenal issues. Given prenatal diagnosis and family history, both parents underwent Sema4 expanded carrier screening with no significant findings. Both parents screened negative for congenital adrenal hyperplasia. Amniocentesis revealed karyotype as 46,XY.
Physical examination at birth was notable for decreased breath sounds on the left side of the chest consistent with CDH, scaphoid abdomen, upslanting palpebral fissure, high-arched palate, smooth philtrum, and mild ankyloglossia. Skin exam was normal with no hyperpigmentation. Testes were descended bilaterally with a normal phallus.
Preoperative renal ultrasound was significant for mild bilateral hydronephrosis. Echocardiogram on day of life 2 revealed moderate pulmonary hypertension. He underwent uncomplicated repair of CDH on day of life 3. He remained hemodynamically stable before, during, and in the immediate postoperative period. He was extubated on day of life 8, successfully transitioned to room air by day of life 10, and reached full oral feeds by day of life 14. On day of life 17, he was noted to have decreased oral feeding and a brief episode of self-resolved bradycardia. A rule-out-sepsis workup was initiated. Soon after, the patient developed a prolonged generalized seizure, unresponsive to intravenous phenobarbital, and required emergent intubation.
Initial laboratory results were notable for severe hyponatremia (Na+: 111 mmol/L) and hyperkalemia (K+: 9.2 mmol/L), a glucose level of 51 mg/dL, an arterial pH of 7.49, and a bicarbonate level of 16 mmol/L (reference range: 25–32 mmol/L) (Figures and ). He was treated with intravenous hypertonic saline, calcium gluconate, furosemide, an insulin infusion, dextrose 12.5% infusion, and albuterol nebulization. He was started on dopamine infusion secondary to systemic hypotension. Given this compilation of symptoms, adrenal insufficiency was suspected and hydrocortisone was initiated.
Over the next 48 hours, electrolyte derangements resolved. Blood, urine, and cerebrospinal fluid cultures were negative, and antibiotics were discontinued. Magnetic resonance imaging of the brain was normal. Initial video electroencephalogram was significant for epileptiform discharges but no seizures. An extensive endocrine evaluation was conducted. Some initial diagnostic labs were unable to be sent before the patient received hydrocortisone and hypertonic saline. Available labs were notable for low aldosterone (5.4 ng/dL, reference range: 7–99 ng/dL), normal dehydroepiandrosterone sulfate (87 μg/dL, reference range: 32–431 μg/dL), and normal 17-hydroxyprogesterone (159 ng/dL, reference range: <199 ng/dL). The sample for plasma renin was of insufficient quantity. The cortisol level was sent after starting hydrocortisone and thus deemed inconclusive.
Renal sonogram revealed a normal right adrenal and nonvisualized left adrenal gland. In view of the unconfirmed etiology and unrevealing testing by then, the baby was trialed off hydrocortisone on day of life 22, but hyponatremia and hyperkalemia recurred the following day with Na+ of 116 mmol/L and K+ of 9.9 mmol/L. The repeat cortisol level at this time was normal at 10.1 μg/dL, and renin and aldosterone levels could not be obtained because of insufficient sample. Hydrocortisone was restarted, along with fludrocortisone and sodium chloride (NaCl) supplements. Enteral feeds were restarted with low mineral formula, Similac® PM 60/40. He had an additional episode of electrolyte derangement on day of life 43, which was managed by adjusting the dosage of hydrocortisone, fludrocortisone, and NaCl supplementation. Prior to discharge at 10 weeks of age, aldosterone remained low (3.8 ng/dL, reference range: 7–99 ng/dL), with normal renin levels (20.5 ng/ml/hr, reference range: 2.4–37 ng/mL/hr) on treatment. Newborn screening and microarray sent during admission were normal. He was subsequently discharged home on hydrocortisone, fludrocortisone, and NaCl supplements.
We considered the diagnosis of congenital adrenal hypoplasia (AHC) and requested DNA test of the NR0B1 gene that is associated with AHC. Single gene sequencing and deletion/duplication analysis of the NR0B1 gene (NM_000475.4) identified a variant of uncertain significance (VUS): c.1142T>C (p.Leu381Pro). This variant has never been reported before and is not present in population databases []. Different missense variants at this codon have been reported in individuals affected with X-linked AHC []. Missense pathogenic variants in NR0B1 and the variant seen in our patient are located in the same protein domain []. These publications suggest that the leucine residue and the structural domain it resides may be critical for the NR0B1 protein (DAX1) function [, ]. The mother was found to carry the same variant, which was absent in the 14-year-old unaffected brother. Therefore, this variant is likely clinically significant and is consistent with a diagnosis of X-linked AHC in our patient.
At 15 months of age, the patient is receiving physical and feeding therapy for oropharyngeal dysphagia. He is walking, has words, and is increasing his solid intake. He is currently on physiologic hydrocortisone, fludrocortisone, and NaCl supplementation. He has not had any electrolyte abnormalities since discharge from the hospital. He is followed every 2-3 months and will be monitored closely during adolescence for pubertal signs, as most children with AHC do not go into spontaneous puberty.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [15, 'months'], 'weight': [3410.0, 'g'], 'Sodium': [111.0, 'mmol/L']}",-0.42381,-0.40262,-0.445,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
This means that the patient is 1 year and 3 oldThe patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 3410.0 g so this converts to 3410.0 lbs * kg/1000 g = 3.41 kg. The concentration of sodium is 111.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 3.41 * (111.0/140 - 1) = -0.42381 L. The patient's free body water deficit is -0.42381 L."
6070,38,Free Water Deficit,lab test,decimal,pmc-8010837-1,Extracted,"A 73-year-old Caucasian man was referred to our hospital for evaluation of a right PHEO, diagnosed two months before at another hospital, after the identification of a large retroperitoneal mass on abdominal computed tomography (CT). At that time, the patient experienced abdominal discomfort, unintentional weight loss of approximately 5 Kg within the previous 3 months, associated to sporadic episodes of watery diarrhea. At admission to our hospital, the patient was moderately dehydrated and tachypnoic. He denied any history of headache, palpitations, sweating, or hypertension. He reported episodes of watery diarrhea, up to 5-6 times a day and 2-3 times a week, without blood or mucus. He also had no relevant familial history of endocrine nor cancer diseases but only a paternal history of arterial hypertension. Physical examination showed blood pressure (BP) of 100/67 mmHg and heart rate of 88 beats/min; no significant orthostatic pressure gradient was measured. BP values, evaluated on several occasions, were 94/58 and 91/62 mm Hg. Laboratory tests showed a hypokalemia (3.3 mmol/L) with metabolic acidosis (pH 7.29, HCO3- 19 mmol/L), a serum magnesium level of 1.5 mg/dl and fasting blood glucose of 149 mg/dl. A 24-h urinary sample showed only a slight increase in normetanephrine excretion, 638 μg (normal values: 162-528/day), while metanephrine and methoxytyramine resulted within normal range. Serum chromogranin A was elevated (1028 ng/ml, normal values 20-100), as well as neuron-specific enolase level (NSE 35.7 nl/ml, normal values 1.0-13.5). Plasma cortisol, adrenocorticotropic hormone, thyroid-stimulating hormone, thyroxine, parathyroid hormone, and calcitonin were within the normal ranges. Contrast enhanced abdominal CT scan confirmed the presence of inhomogeneous right adrenal mass measuring 8.1 x 7.7 x 7.9 cm (). A 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) coupled with CT showed an area of high uptake (maximum standardized uptake value, SUV max 8.6) in the right adrenal gland, with a prevailing peripheral signal and central hypoactivity, and another area of high uptake (SUV max 9.6) in the lumbar region suspicious of lymph node localization (). In addition, 68GaDOTA-octreotate (DOTATATE) PET confirmed the peripheral high uptake (SUV max 6) in the right adrenal gland and the high uptake area (SUV max 3.7) in the lumbar region; a high uptake (SUV max 4.5) was also detected at the base of the left lung (). Based on these results, patient diagnosis was metastatic adrenal PHEO. Intravenous fluid infusion, sodium bicarbonate, potassium aspartate, magnesium sulphate supplementations were started allowing an improvement of clinical condition and blood pressure levels. Then, after 10-days pre-operative treatment with low dose alpha1-adrenergic antagonist doxazosin (given just before bed), he underwent surgical resection of the tumor. The patient had an uneventful postoperative course, except for sporadic watery diarrhea. Gross examination revealed a 10x8x6 cm brownish-yellow, friable adrenal mass. Histology showed a highly cellular tumor made up of monotonous medium-sized cells with discrete nuclear pleomorphism and mild hyperchromasia. Mitotic figures were above 3/10 high power fields, with some atypical mitoses. The cells were arranged in nests with areas of diffuse growth in more than 10% of the tumor. Confluent areas of necrosis were present. Foci of capsular and vascular invasion were noted as well as extension into periadrenal adipose tissue. The histological features were consistent with a malignant PHEO, with a PASS score (Pheochromocytoma of the Adrenal Gland Scaled Score) of 20 (), indicating a high risk of aggressive cellular behavior (PASS≥4). DNA genetic analysis of the patient with a next generation sequencing (NGS) approach using Trusight One Sequencing Panel by Illumina, revealed a synonymous single nucleotide variant of gene SDHA [rs6555055, NM_004168.2:c.619A>C, (p.Arg207=)] indicated by ClinVar database as associated to “probably benign” catecholamine-secreting PHEO (). The patient was discharged in satisfactory clinical condition. Therapy with lanreotide, a somatostatin analogue, at a dose of 60 mg once a month was initiated. At 2 months, multiple metastatic pulmonary and hepatic nodules were identified on CT scan (). The patient once again experienced abdominal discomfort, 4 kg weight loss, yet only sporadic watery diarrhea. Peptide receptor radionuclide therapy and sunitinib, a multi-targeted receptor tyrosine kinase inhibitor, were scheduled. In the meantime, lanreotide therapy was increased to 120 mg once a month. However, after about one month, the patient was re-admitted with a 10-day history of severe watery diarrhea, up to 20 times in 24 hrs, accompanied by nausea, vomiting and occasionally quick flushing. At presentation, he was suffering and markedly dehydrated. Physical examination showed BP of 90/67 mmHg, heart rate of 120 beats/min, the pulse was fast and weak, the breath was fast and short, the skin cold and clammy, and the urination was decreased. Laboratory tests were as follows: blood urea nitrogen 96 mg/dl; serum creatinine 3.5 mg/dl; Na+ 136 mmol/l; K+ 2.5 mmol/l; Cl- 115 mmol/l; pH 7.08; HCO3
- 5.5 mmol/l; Pa CO2 30 mm Hg; Pa O2 67 mm Hg; lactate 5 mmol/l (normal values 0.5-2.2); serum anion gap 15 mmol (corrected for serum albumin levels 16 mmol); urine anion gap was negative. Serum prealbumin was 29 mg/dl (normal values 15-35) and albumin 3.9 g/dl (normal values 3.5-5.0). At that time, serum chromogranin A was 2896 ng/ml and neuron-specific enolase 49.6 ng/ml. Twenty-four hours urinary normetanephrine excretion was 920.4 μg, while metanephrine resulted at 432.6 μg (normal values 64-302 μg/day). VIP plasma levels were measured, and circulating values were more than 10 times the upper normal limit (1285 pg/ml, normal values 18-100). Cardiac ultrasound showed a reduced left ventricular ejection fraction (35%). Due to the emerging clinical picture, histological sections were re-evaluated with additional immunostainings. Sections were stained with the following primary antibodies: anti-Chromogranin A (clone LK2H10 ready to use; Ventana-Roche), Anti-Vasoactive intestinal polypeptide -VIP (rabbit 1:500; Biogenex) and anti-Somatostatin Receptor 2A -SSTR2A (rabbit 1:100; Bio-Trend). The sections were immunostained with HRP Polymer (Optiview DAB IHC Detection kit; Roche) in accordance with the manufacturer’s specifications. Negative controls consisted of substituting normal mouse serum for the primary antibodies. A set of sections adjacent to these used for single labelling with VIP, was used for double labelling with Chromogranin A. The second antibody was immunostained with AP Polymer (Ultraview Universal Alcaline Phosphatase Red Detection Kit; Roche). Permanent red chromogen was used for staining development. Immunostaining revealed strong positivity for neuroendocrine marker chromogranin A and VIP (); a large number of cells co-expressed chromogranin A and VIP (). Weak was the positivity for SSTR2A (). A diagnosis of VIP-secreting PHEO was rendered. The patient was then transferred to the intensive care unit. He was managed with intensive intravenous fluid hydration, potassium salts and bicarbonates, as well as with octreotide (0.1 mg/8 h s.c.), sunitinib 50 mg/day and loperamide. However, his diarrhea worsened with further exacerbation of metabolic acidosis (pH 6.99, HCO3
- 4.3 mmol/l), leading to hemodynamic instability and shock. He died five days later.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [73, 'years'], 'weight': [5.0, 'kg'], 'Sodium': [136.0, 'mEq/L']}",-0.07143,-0.06786,-0.075,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 73 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 5.0 kg. The concentration of sodium is 136.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.0 mEq. To convert from 136.0 mEq to mmol, convert from mEq to mmol. The compound 136.0 has a valence of 1, and so divide the valence by the value of mEq to get, 136.0 mEq/(1 mEq/mmol) = 136.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mEq sodium/L converts to 136.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 5.0 * (136.0/140 - 1) = -0.07143 L. The patient's free body water deficit is -0.07143 L."
6071,38,Free Water Deficit,lab test,decimal,pmc-3751282-1,Extracted,"A 69-year-old male was admitted to our institution because of a sudden onset of vomiting and abdominal distention in April 2012. His general history did not include smoking or alcohol consumption; however, his medical history included a femoral head fracture, which was treated with an artificial femoral head when he was 60 years old, and congestive heart failure, which improved with diuretic administration in November 2011.
His past history also included an episode of ischaemic colitis which presented with severe left-sided abdominal pain. Abdominal radiography and computed tomography revealed no abnormal findings, although colonoscopy revealed longitudinal ulcers in the descending colon (Fig. a). These findings led to a diagnosis of ischaemic colitis. Capsule endoscopy revealed circumferential ulcers in the distal small intestine (Fig. b) and single-balloon enteroscopy confirmed the same in the distal ileum (Fig. c). Ischaemic enteritis was suspected and the patient was prescribed a treatment that included fasting and blood transfusion. Thereafter, his symptom improved rapidly.
On admission, the patient’s blood pressure was 103/54 mmHg, heart rate was 72 beats/min, body temperature was 36.3 °C and oxygen saturation was 97 % in room air. On clinical examination, his weight was 51 kg, height was 166 cm and body mass index was 18.5 kg/m2. Inspection of the palpebral conjunctiva revealed evidence of mild anaemia, whereas a chest auscultation revealed no abnormal findings and physical examination revealed no oedema or cyanosis. The patient’s abdomen was markedly distended and reduced peristalsis was evident with mild tenderness over abdominal region. There were no palpable masses or signs of peritoneal irritation.
Blood chemistry revealed a normal white blood cell count (7000 cells/μL), mild anaemia (red blood cell count, 321 × 104/μL; haemoglobin, 9.2 g/dL), elevated C-reactive protein level (4.8 mg/dL), mild hypoproteinaemia (5.5 g/dL), mild hypoalbuminaemia (2.4 g/dL), mildly elevated serum creatine level (1.36 mg/dL), mildly elevated blood urea nitrogen level (25.6 mg/dL), hyponatraemia (128 mEq/L) and an elevated glucose level (144 mg/dL; Table ). Tuberculin and several stool culture tests were negative. On admission, plain abdominal radiography revealed dilated small intestinal loops (Fig. a). Plain abdominal computed tomography revealed extensively dilated small intestinal loops, a calibre change around the ileal end and an absence of ascites (Fig. b, c). Therefore, small intestinal obstruction was diagnosed and a transnasal ileus tube was placed (Fig. a). During decompression of the small intestinal obstruction using the ileus tube, the patient was fasting and was treated with total parenteral nutrition. The ileus tube was progressively moved along the small intestine until it reached the distal ileum on post-admission day 4. The injected contrast medium revealed a stricture in the distal ileum (Fig. b). Transanal single-balloon enteroscopy performed to inspect the stricture revealed a circumferential and afferent tubular ulcer in the distal ileum, 5 cm from the ileocecal valve (Fig. a); gastrofluorography confirmed the stricture (Fig. b), which was dilated using balloon catheters on several occasions but could not be improved.
Despite treatment, the patient’s nutritional status deteriorated and his anaemia progressed, with the latter necessitating a blood transfusion. Consequently, we decided to perform surgery on post-admission day 37.
Operative findings revealed several strictures in the distal ileum (Fig. a). In total, 42 cm of the ileum, including the known stricture, was resected. Several circumferential ulcers with clear margins were detected in the ileum at 5–28 cm from the ileocecal valve (Fig. b). Histological findings revealed the following (Fig. a–c): stenotic portions of the ileum formed ulcers of grade Ul-II with an intact muscularis mucosa, the ileal lumen was covered with fibrin and fibrous connective tissue, an inflammatory cell infiltrate was present in all layers, particularly lymphocytes and eosinophils, dilatation and congestion of capillary vessels was observed in the submucosa and haemosiderin staining revealed sideroferous cells in the submucosal layers. Considering these findings, ischaemic enteritis was confirmed in the resected specimen.
The patient’s post-operative course was uneventful. Oral intake was initiated and the patient experienced no recurrence of small intestinal obstruction or symptom of abdominal pain.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [69, 'years'], 'weight': [51.0, 'kg'], 'sex': 'Male', 'Sodium': [128.0, 'mEq/L']}",-2.18571,-2.07642,-2.295,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 69 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 51.0 kg. The concentration of sodium is 128.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 128.0 mEq. To convert from 128.0 mEq to mmol, convert from mEq to mmol. The compound 128.0 has a valence of 1, and so divide the valence by the value of mEq to get, 128.0 mEq/(1 mEq/mmol) = 128.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 128.0 mEq sodium/L converts to 128.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 51.0 * (128.0/140 - 1) = -2.18571 L. The patient's free body water deficit is -2.18571 L."
6072,38,Free Water Deficit,lab test,decimal,pmc-5115207-1,Extracted,"A 15-year-old female patient weighing 50 kg with a height of 143 cm was admitted for abnormal uterine bleeding that persisted for two years. The patient was diagnosed with Rubinstein-Taybi syndrome when she was one year old. She displayed strabismus, preauricular fistula, and grade II mental retardation. She had a history of thoraco-lumbar spinal fusion to correct scoliosis (); there were no limitations to neck flexion or extension after the fusion. The patient experienced uterine bleeding that persisted for about 20 days every month for 2 years. Ultrasonography findings of the left ovary showed a polycystic ovary (). To treat her symptoms, hormonal treatment, including contraception pills and progesterone therapy, was administered, but there was no improvement in the control of the abnormal bleeding. As there were no other means to control this bleeding, we decided to perform a hysterectomy.
A preoperative ECG showed a premature atrial complex with prolonged QT. The CBC findings showed a hemoglobin level of 13.5 mg/dL and a hematocrit of 38.5%. Electrolyte levels showed a sodium level of 144 mEq and a potassium level of 4.5 mEq. The patient’s nasal septum was deflected but there was no abnormality in the oral cavity, and her preoperative airway examination was classified as Mallampati class II. Upon arrival at the operating room, the patient was attached to an electrocardiogram, noninvasive blood pressure monitoring, and pulse oximetry monitoring. Before induction, her vital signs were 120/60 mmHg (blood pressure), SpO2 100%, and 120 beats/min (heart rate). She was preoxygenated for three minutes with 100% O2; then, 200 mg of pentothal sodium and 40 mg of rocuronium were administered via intravenous injection. After the intubation, sevoflurane was maintained at a rate of 2.5% and remifentanyl was infused at a rate of 0.2–0.5 μg/kg/min. During the operation, vital signs were stable with no specific incidents. Laparoscopic hysterectomy along with fistulectomy of the preauricular fistula was performed; total operation time was one hour and forty five minutes. The patient was discharged 5 days later without further complications.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [15, 'years'], 'weight': [50.0, 'kg'], 'sex': 'Female', 'Sodium': [144.0, 'mEq/L']}",0.85714,0.81428,0.9,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 15 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 50.0 kg. The concentration of sodium is 144.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 144.0 mEq. To convert from 144.0 mEq to mmol, convert from mEq to mmol. The compound 144.0 has a valence of 1, and so divide the valence by the value of mEq to get, 144.0 mEq/(1 mEq/mmol) = 144.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 144.0 mEq sodium/L converts to 144.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 50.0 * (144.0/140 - 1) = 0.85714 L. The patient's free body water deficit is 0.85714 L."
6073,38,Free Water Deficit,lab test,decimal,pmc-4722162-2,Extracted,"A 16-year-old female who was diagnosed with Philadelphia chromosome-positive acute lymphoblastic leukemia presented intermittent fever immediately after transplantation. Fungal pneumonia was developed on PTD 7 and cytomegalovirus (CMV) viremia was diagnosed on PTD 18. The following day, she developed intermittent short-term memory loss, drowsiness and tremor in both hands. Serum Na level was 130 mEq/L and brain MRI was unremarkable. Mild hyponatremia of approximately 130 mEq/L was persisted for next 4 days, urine output dramatically increased to 5,528 mL (4,035 mL/m2), with 1 L of negative fluid balance on PTD 22. Serum Na decreased to 124 mEq/L and she developed seizures. Following conservative fluid treatment using 3% and 0.9% saline for 24 hours, serum Na was normalized. However, the serum Na decreased again to 129 mEq/L on PTD 45, but did not respond to conservative treatment including fluid restriction. Therefore, pediatric hemato-oncologist was consulted on PTD 53.
On the past medical history, The pretransplantation conditioning regimen comprised cyclophosphamide (260 mg/kg), ATG (2.5 mg/kg), methylprednisolone (1 mg/kg), and total body irradiation (total dose, 1,320 cGy/8 fx). Short course methotrexate and cyclosporine were used for the GVHD prophylaxis. Emperical antibiotics with teicoplanin (10 mg/kg) and meropenem (60 mg/kg) were given to her due to fever. On PTD 7, voriconazole (loading dose of 6 mg/kg/dose every 12 hours for 2 doses on day 1, followed by maintenance dose at 4 mg/kg/dose every 12 hours) was initiated due to fungal pneumonia. Leukocyte engraftment was obtained on PTD 12. Six days later, CMV real-time quantitative polymerase chain reaction was positive with 21,000 copies/mL (reference range, <500 copies/mL) and ganciclovir (10 mg/kg) was initiated.
At the time of consultation (PTD 53), her body weight was 36 kg (<3rd percentile), a 15% reduction since admission. Urine output was 2,424 mL (1,924 mL/m2) with approximately 1.6 L of negative fluid balance. She developed NCs such as disorientation and short-term memory loss. Her serum Na was 126 mEq/L, BUN 21 mg/dL, and Osm 266 mOsm/kg, urine Na 121 mEq/L, and urine Osm 311 mOsm/kg. Thyroid hormones, cortisol and ADH levels were within normal ranges, while BNP was increased to 154 pg/mL (reference range, <100 pg/mL). The clinical pictures and laboratory profiles was highly suggestive of CSW. Her urine volume was replaced by an intravenous fluid with isotonic saline. Two days later, serum Na levels became normal and her vital findings stabilized. Despite stabilized vital signs, appropriate water balance with normal electrolyte levels, her abnormal neurological symptoms such as amnesia, disorientation and tremor persisted until PTD 64. Brain MRI was reperformed and the result showed chemotherapy-related leukoencephalopathy (). On PTD 100, the patient was discharged without neurologic sequelae or electrolyte imbalance.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [16, 'years'], 'weight': [36.0, 'kg'], 'sex': 'Female', 'Sodium': [126.0, 'mEq/L']}",-2.16,-2.052,-2.268,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 16 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 36.0 kg. The concentration of sodium is 126.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 126.0 mEq. To convert from 126.0 mEq to mmol, convert from mEq to mmol. The compound 126.0 has a valence of 1, and so divide the valence by the value of mEq to get, 126.0 mEq/(1 mEq/mmol) = 126.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 126.0 mEq sodium/L converts to 126.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 36.0 * (126.0/140 - 1) = -2.16 L. The patient's free body water deficit is -2.16 L."
6074,38,Free Water Deficit,lab test,decimal,pmc-4912772-1,Extracted,"The patients were siblings from a non-consanguineous Uzbekistan family. Patient 1 was a 3-yr-old 46,XX female with ambiguous genitalia. She was previously evaluated for her abnormal genital development and underwent first genital surgery in Turkey. On an initial evaluation at age 2 y 8 m, her height was 100 cm (+2.1 SD), her weight was 15.8 kg, (+1.4 SD), blood pressure (BP) was 110/70 mmHg (94th/96th percentiles). The physical examination revealed that the phallus was 5 cm long and 2 cm wide (Prader grade IV); no gonads were palpable in the inguinal region. The areola and palmar creases were pigmented bilaterally. An ACTH stimulation test (250 μg) showed grossly elevated baseline ACTH (238 pg/mL) and basal cortisol of 4.7 μg/dL with non-response to ACTH and moderately elevated progesterone and 17OHP after 60 min; 11-deoxycortisol and androstenedione concentrations were markedly high (Table ). The serum sodium was 136 mmol/L, potassium 3.1 mmol/L, plasma renin activity (PRA) was very low at 15 ng/dL/h (nl, 171–1115), and aldosterone 2 ng/dL (nl, 3–35). Her total testosterone levels were 132 ng/dL (nl, <3–10) and dehydroepiandrosterone sulfate (DHEAS) 165.2 μg/dL (nl, <5-57). She was followed up at the King Chulalongkorn Memorial Hospital (Bangkok, Thailand) due to the family relocation at age 3 yr for further management. After receiving the results of an ACTH stimulation test, she was started treatment with hydrocortisone, 5 mg thrice daily (10 mg/m2/d) which improved BP into the normal range (90/60 mmHg), suppressed testosterone, and PRA became measurable (200–496 ng/dL/h).
Patient 2 is the younger brother of Patient 1. He presented at 2 years of age with acne and masculinization (isosexual precocious puberty). Physical examination revealed an advanced maturation of external genitalia as well as a low-pitched voice. His Tanner stages were G3 and PH1, and each of his testes was 3 mL in volume. His height was 97 cm (+3.2 SD) and weight was 17 kg (+2.9 SD). Height gain was accelerated from 12-month-old on the growth chart (from +2.6 SD to +3.2 SD). Skin pigmentation appeared consistent with his ethnicity, but no evident mucosal pigmentation. His BP was 110/65 mmHg (92th/95th percentiles). Labs revealed serum Na 136 mmol/L, K 4.3 mmol/L, bicarbonate 24 mmol/L, BUN 12 and Cr 0.3 mg/dL, respectively. An ACTH stimulation test showed elevated baseline ACTH, a low basal cortisol (2.3 μg/dL) with non-response to ACTH and moderately elevated 17OHP after 60 min (Table ). 11-deoxycortisol concentrations were not measured. PRA was low at 106 ng/dL/h (nl, 171–1115), and low aldosterone 0.2 ng/dL (nl, 3–35). He was then treated with hydrocortisone 2.5 mg thrice daily (11 mg/m2/d). His blood pressure was well controlled, and PRA was increased up to 738 ng/dL/h.
Genomic DNA from peripheral blood leucocytes of the patients and their parents was extracted by using the QIAamp® DNA Blood Mini Kit (Qiagen, Valencia, CA) after taking informed consent. The coding sequence of CYP11B1 gene including exon-intron boundaries was amplified in eight fragments using specific primers (Table ). PCR products were treated with ExoSAP-IT (USP Corporation, Cleveland, OH), and sent for direct sequencing at Macrogen Inc. (Seoul, Korea). Analyses were performed by Sequencher 4.2 (Gene Codes Corporation, Ann Arbor, MI).
We performed a minigene in vitro experiment of the CYP11B1 splicing mutation. A segment of the wild-type (WT) and mutant (IVS7 + 1G > A) genomic DNA (gDNA) of CYP11B1 gene consisting of exons 6 to 9 and their in-between introns was amplified by PCR using the oligonucleotides listed in Table . We used the gDNA of a normal control and the patient with IVS7 + 1G > A CYP11B1 mutation as a template of minigene constructs. PCR reactions were carried out in a 20 μl volume containing 50 ng gDNA, 10xPCR buffer, 25 mM MgCl2, 10 μM dNTPs, 5 U/μl Taq polymerase and 10 μM of each primer, using the following parameters: 30s at 94 °C, 30s at 60 °C and 1.30 min at 72 °C. The PCR product was cleaved with BamHI-HF and XbaI enzymes and cloned into the corresponding sites of pcDNA™3.1/myc-His B mammalian expression vector (Invitrogen, Carlsbad, CA) using T4 DNA ligase (New England BioLabs, UK). The wild-type and mutant vectors were confirmed by direct sequencing using NCBI Reference Sequences (RefSeq) NG_007954.1 as the genomic reference and NM_000497.3 as the mRNA reference.
COS-7 cells were cultured in Dulbecco’s Modified Eagles Medium, High Glucose (HyClone Laboratories, Logan, UT) supplemented with 10 % fetal bovine serum (Sigma-Aldrich, Singapore) and 0.01 % penicillin/streptomycin (HyClone Laboratories) at 37 °C in a humidified 5 % CO2 incubator. Cells were grown on 6-well plates and transiently transfected with the wild-type and mutant minigene constructs (1 μg) using Effectene® Transfection Reagent (Qiagen). Cells incubated for 48 h after transfection and then were washed 3 times with PBS and kept frozen at − 20 °C. Total cellular RNA was extracted using QIAamp® RNA Blood Mini Kit (Qiagen) and treated with DNaseI (Qiagen). The RNAs were then used as template for cDNA synthesis using ImProm-II™ Reverse Transcription System (Promega Corporation, Madison, WI). Finally, both the WT and mutant cDNAs were amplified by PCR using the same primers and conditions as used for the minigene construction. The PCR products were analyzed by electrophoresis on a 1 % agarose gel followed by staining with ethidium bromide. Each PCR product was confirmed by Sanger sequencing after subcloning into pGEM®-T Easy vectors (Promega).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [3, 'years'], 'weight': [15.8, 'kg'], 'Sodium': [136.0, 'mmol/L']}",-0.27086,-0.25732,-0.2844,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 3 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 15.8 kg. The concentration of sodium is 136.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 15.8 * (136.0/140 - 1) = -0.27086 L. The patient's free body water deficit is -0.27086 L."
6075,38,Free Water Deficit,lab test,decimal,pmc-7716385-1,Extracted,"A previously healthy 77-year-old female, a nonsmoker, was admitted to the hospital after a month of malaise, tiredness, dizziness, dyspnea, severe headache, and anorexia.
Recently, her general practitioner diagnosed her with arterial hypertension and started administering the diuretic bendroflumethiazide. She received no other medications, no corticosteroids, and no anticoagulants. Her chest X-ray revealed emphysematous lungs without apical bullae.
Upon arrival at the hospital, her blood pressure was 190/50 mmHg, pulse 40-50 bpm, serum-Na 114, and serum-K 3.2 mmol/L. Electrocardiogram (ECG) showed third-degree atrioventricular block and narrow, nodal escape rhythm. CT cerebrum was without any acute changes. Echocardiography was normal. Height was 165 cm, weight 55 kg, and BMI 20 kg/m2.
Bendroflumethiazide was withdrawn, the Na-deficit slowly corrected, and electrolyte derangements were abolished, but the atrioventricular (AV)-block persisted. After implantation of a pacemaker, the blood pressure fell to 160/70 mmHg, she was administered amlodipine, the blood pressure normalized, and the symptoms disappeared. This supported the theory that arterial hypertension with a very high systolic pressure and a wide amplitude was due to initially unnoticed bradycardia and the electrolyte derangements to treatment with the thiazide, conjointly causing the symptoms of the patient.
A dual-chamber (DDD) pacemaker was implanted without immediate complications. Two screw-in electrodes (helical active fixation leads) were inserted via the left subclavian vein. Puncture of the subclavian vein was guided by venography and fluoroscopy, the needle pointing towards the intersection of the clavicle and the first costa (Figure ).
The vein was punctured in the second attempt, with no aspiration of air, Seldinger technique using two peel-away-sheaths with a diameter of 9 and 7 French to introduce a guidewire into the right atrium and two pacemaker electrodes.
The atrial lead was repositioned a couple of times before good values were obtained on the lateral wall of the right atrium, where it was secured. The ventricular electrode was placed in the apex of the right ventricle. During the implantation, severe problems were not encountered, neither when searching for venous access, nor when fixing the leads.
Later the same day, her chest X-ray showed bilateral apical pneumothorax; it measured 15 mm on the left side, 10 mm on the right side (Figure ).
She was administered high flow oxygen on a nasal cannula. The patient stayed clinically stable and experienced no breathing problems, no pleuritic chest pain, and no pericardial signs or symptoms.
The following day, the left pneumothorax had diminished to 7 mm, the right pneumothorax was unchanged, but there was a small effusion in the right costophrenic angle (Figure ).
This was confirmed by fluoroscopy (Figures -). The atrial electrode seemed to respect the atrial wall (Figure ).
Repeated chest X-ray, fluoroscopy, and echocardiography did not show perforation of the right atrium, and there was no pericardial effusion, no ECG changes, and the pacemaker values remained fine with nonconclusive falls in sense and impedance. The atrial lead parameters at implantation and the following day were: capture 0.8/1 V (duration 0.4 ms); sense 4/2.4 mV, and impedance 400/342 Ohms.
The following day the left pneumothorax had diminished to 5 mm, but the changes on the right side were the same (Figures -). This led to the decision to replace the atrial electrode, even though the position was unchanged (Figure ).
The atrial electrode was repositioned; the tip was moved to the right atrial appendage without complications. Echocardiography remained normal.
Two weeks later, the chest X-ray had normalized (Figure ). The pacemaker was functioning well, and the patient felt fine under the circumstances.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [77, 'years'], 'weight': [55.0, 'kg'], 'Sodium': [114.0, 'mEq/L']}",-4.59643,-4.36661,-4.82625,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 77 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 55.0 kg. The concentration of sodium is 114.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 114.0 mEq. To convert from 114.0 mEq to mmol, convert from mEq to mmol. The compound 114.0 has a valence of 1, and so divide the valence by the value of mEq to get, 114.0 mEq/(1 mEq/mmol) = 114.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 114.0 mEq sodium/L converts to 114.0 mmol sodium/L. Plugging in these values into the equation, we get 0.45 * 55.0 * (114.0/140 - 1) = -4.59643 L. The patient's free body water deficit is -4.59643 L."
6076,38,Free Water Deficit,lab test,decimal,pmc-3069581-1,Extracted,"The patient was a 51-yr-old woman with swelling of the extremities and bilateral ptosis on March 8, 2010. She complained of exertional dyspnea and weakness. She married at the age of 25. After that time, she developed drooping of her eyes, with the left eye drooping more than the right eye. Her symptoms persisted and they had gradually increased during about the last 10 yr. About 8 yr ago, she underwent a ptosis repair operation at a local clinic, but her symptoms were not improved. She denied a history of loss of consciousness, headache, dysphagia, dysarthria and myalgia. There was no family history of similar symptoms and no history of trauma. There was no previous history of diabetes and hypertension.
On examination, she was determined to be 151 cm in height and 48 kg in weight. The initial vital signs were a blood pressure of 140/80 mmHg, a pulse rate of 68 beats/min and a respiratory rate of 20/min. She was lethargic and had facial puffiness and no goiter. The lung and heart examinations were unremarkable. All the extremities showed pitting. She had marked bilateral ptosis, while the external ocular movements were normal (). The other cranial nerve examinations were unremarkable.
The laboratory findings were a total leucocyte count 4.75 × 103/µL with 61.6% polymorphs, a hemoglobin level of 9.0 g/dL, the random blood glucose was 124 mg/dL, the serum sodium was 130 mM/L, the potassium was 3.7 mM/L, the blood urea nitrogen (BUN) was 13 mg/dL, the creatinine was 0.8 mg/dL, the aspartate transaminase (AST) was 81 IU/L, the alanine transaminase (ALT) was 29 IU/L, the total bilirubin was 0.93 mg/dL, the creatine kinase (CK) was 1,195 IU/L (normal reference: 20-180 IU/L ), the lactate dehydrogenase (LDH) was 517 IU/L (normal reference: 101-218 IU/L), the total cholesterol was 256 mg/dL, the triglyceride was 121 mg/dL, the high density lipoprotein cholesterol (HDL-C) was 40 mg/dL and the low density lipoprotein cholesterol (LDL-C) was 196 mg/dL. The urinary analysis was negative for blood and protein with using a dipstick. As the clinical findings suggested hypothyroidism and myasthenia gravis, a thyroid function test and acetylcholine receptor binding antibody test were done. The serum T3 was 0.195 ng/mL (normal reference: 0.86-2.02 ng/mL), the free T4 was 0.08 ng/dL (normal reference: 0.93-1.705 ng/dL), the thyroid-stimulating hormone (TSH) was 2.08 µIU/mL (normal reference: 0.27-4.2 µIU/mL), the antimicrosomal antibody was 17 IU/mL (normal reference: 0-34 IU/mL), the antithyroglobulin antibody was 20.1 IU/mL (normal reference: 0-114 IU/mL) and the acetylcholine receptor binding antibody was negative.
Secondary hypothyroidism was suspected. We performed a careful history taking and other pituitary hormone evaluations. At the age of 26 the patient delivered her daughter and she had a history of massive postpartum vaginal bleeding. Thereafter she not resumed menses. The basal levels of other hormones were a serum cortisol of 4.03 µg/dL, the adrenocorticotropic hormone (ACTH) was 29.64 pg/mL, the growth hormone (GH) was 0.06 ng/mL, the IGF-1 was 25 ng/mL (normal reference: 71-263 ng/mL), the prolactin was 1.59 ng/mL, the luteinizing hormone (LH) was 1.49 IU/L, the follicle-stimulating hormone (FSH) was 4.91 IU/L, the E2 was 17.29 pg/mL and the testosterone was 0.02 ng/mL. The combined pituitary stimulation test, including the insulin tolerance test, the thyrotropin-releasing hormone (TRH) stimulation test and the gonadotropin-releasing hormone (GnRH) stimulation test showed panhypopituitarism (). Brain magnetic resonance imaging (MRI) showed a finding of an empty sella turcica and there was no evidence of an intracranial mass, hemorrhage and aneurysm ().
Nerve conduction study (NCS) and electromyography (EMG) of the limbs reveled normal results with the exception of incidentally detected carpal tunnel syndrome. Needle EMG of the orbicularis oculi showed no evidence of dysfunction of the neuromuscular junction.
We diagnosed her as having Sheehan's syndrome, bilateral ptosis and subclinical myopathy caused by secondary hypothyroidism. Replacement with prednisolone of 10 mg/day and thyroxine (T4) 100 µg/day was started. The dose of prednisolone was decreased to 5 mg/day after 4 weeks. At 3 months follow-up, she had become euthyroid with normalized muscle enzymes. She recovered from her presenting symptoms and the bilateral ptosis was much improved ().",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [51, 'years'], 'weight': [48.0, 'kg'], 'Sodium': [130.0, 'mmol/L']}",-1.71429,-1.62858,-1.8,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 51 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 48.0 kg. The concentration of sodium is 130.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 48.0 * (130.0/140 - 1) = -1.71429 L. The patient's free body water deficit is -1.71429 L."
6077,38,Free Water Deficit,lab test,decimal,pmc-3681292-1,Extracted,"A 35-year-old male, not known to have any chronic illness, presented with a 4-month history of mild, dull, and intermittent abdominal pain, associated with jaundice, loss of appetite, and weight loss of 10 kilograms, as well as a one-month history of abdominal swelling.
On examination, he had normal vital signs, but he was pale and jaundiced. There were no palpable lymph nodes. There was central intra-abdominal mass 15 cm in diameter, firm, and tender with smooth surface. He had single right testicle in the scrotum. Laboratory investigations () showed white blood cells: 14.7 × 1000/mm3 (normal: 4 × 1000–10 × 1000/mm3), hemoglobin: 7.4 g/dL (normal: 13–17 g/dL), and platelets: 480 × 1000/mm3 (normal: 150 × 1000–400 × 1000/mm3). Blood chemistry and renal function were within normal limits. Aspartate aminotransferase: 53 u/L (normal: 12–39 u/L), alanine aminotransferase: 16 u/L (normal: 0–40 u/L), alkaline phosphatase: 472 u/L (normal: 40–129 u/L), gamma glutamyl transpeptidase: 155 U/L (normal: 11–50 U/L), bilirubin: 115 umol/L then 330 umol/L (normal: 3.5–24 umol/L), and direct bilirubin: 306 umol/L (normal: up to 7 umol/L). Tumor markers: β-HCG: 1131379 IU/L (normal: 0–5 IU/L), LDH: 2331 U/L (normal: 240–480 U/L), AFP: 1.4 IU/mL (normal: 0–5 IU/mL), CA19-9: 9 U/mL (normal: 0–37 U/mL) CEA: 1.2 Ug/L (normal: 0–3 Ug/L). FT4: 49.4 pmol/L (normal up to 20 pmol/L) and TSH: 0.01 μ/L (normal 0.45–4.5 μ/L). CT scans of chest, abdomen, and pelvis with contrast showed huge pelvic-abdominal mass measuring 19 × 14.7 × 22 cm with extensive retroperitoneal lymphadenopathy, and liver and lung metastases (). CT-guided Tru-Cut biopsy of the mass showed a mixed germ cell tumor (Figures and ) with predominantly seminomatous component (CD117 positive, ) and foci consistent with choriocarcinoma (β-HCG positive, ). Despite a high risk of intratumor bleeding attributed to tumor size and the oncologist's recommendation for immediate chemotherapy, the patient and his family refused chemotherapy as they planned to travel abroad for a second opinion. On the following days, his condition deteriorated and his level of consciousness decreased; his BP was 70/40 mmHg, pulse rate 140/min, respiratory rate 35/min, and oxygen saturation 91% with nonrebreathing mask on 15 liters oxygen/min. So, he was transferred immediately to the medical intensive care unit (MICU) where he was intubated. Laboratory investigations () showed white blood cells: 8.4 × 1000/mm3, hemoglobin: 2.5 g/dL, and platelets: 113 × 1000/mm3. Bun: 11.5 mmol/L (normal: 1.7–8.3 mmol/L), creatinine: 222 umol/L (normal: 62–124 umol/L), K: 5.2 mmol/L (normal: 3.6–5.1 mmol/L), Na: 134 mmol/L (normal: 135–145 mmol/L), bicarbonate: 9 mmol/L (normal: 24–30 mmol/L), Cl: 98 mmol/L (normal: 96–110 mmol/L), bilirubin: 722 umol/L, and lactate: 5 mmol/L (normal: 0.5–2.2 mmol/L). INR: 1.4, APTT: 31 seconds (normal: 26–38.5 seconds). ABG: PH: 7.128, PO2: 270, PCO2: 22, HCO3: 8, and oxygen saturation: 99%. The patient was given intravenous fluids, packed red blood cells, fresh frozen plasma and cryopricepitate transfusions, and vasopressors. CT angiogram showed multiple enhancing hepatic metastasis with extensive blood leaking and pooling in the liver and to a lesser extent in the pelvic mass with large amount of intraperitoneal fluid (most likely hemoperitoneum) (). So, angiography and embolization of the right Hepatic artery with gelfoam were done.
Despite these interventions, the bleeding continued. Hemoglobin and blood pressure continued dropping, and hepatic surgeon advised for conservative treatment as the patient was at high risk for bleeding (INR 2.3 and aPTT 49.20 seconds). Moreover, the patient developed DIC, evidenced by prolonged INR, aPTT, and low platelets, and activated factor seven was given.
The patient developed anuria as his intra-abdominal pressure reached 50–55 mmHg. Surgery team was consulted for decompression laparotomy, but they thought it was useless and would not help the patient. At the end, the patient died secondary to hemorrhagic shock, DIC, and abdominal compartment syndrome with renal shutdown.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [35, 'years'], 'weight': [10.0, 'kg'], 'sex': 'Male', 'Sodium': [134.0, 'mmol/L']}",-0.25714,-0.24428,-0.27,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 35 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 10.0 kg. The concentration of sodium is 134.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 10.0 * (134.0/140 - 1) = -0.25714 L. The patient's free body water deficit is -0.25714 L."
6078,38,Free Water Deficit,lab test,decimal,pmc-3819695-1,Extracted,"A 47-month-old female
Voiding difficulty and urinary incontinence
The patient was born fullterm with a birth weight of 2.4 kg. At the age of 2 weeks, she was diagnosed with Hirschsprung disease and underwent the Duhamel operation. At that time, a ganglion cell was noted at the proximal sigmoid. After the operation, she was able to evacuate the bowels well until 6 months of age and she stopped visiting the outpatient clinic. She has a history of constipation of over 1 year. Constipation had been managed with oral lactulose and enema using glycerin at a nearby hospital over 1 year when she complained abdominal pain, agitation and holding her stools with 3- or 4-day interval. After enema, sausage-shaped stools were frequently observed. Her mother could not remember the exact characters of stool. There was no abnormal and unusual feeding history or urinary pattern before admission.
The patient was transferred to our hospital due to acute urinary obstruction. One week ago, diffuse lower abdominal pain developed which was managed at a local clinic with medicine for constipation. However, abdominal pain persisted. One day before admission, abdominal distension and voiding difficulty developed.
On initial evaluation the patient had a blood pressure of 110/70 mmHg, a pulse rate of 96 beats/min, a respiratory rate of 24 breaths/min, a body temperature of 36.5℃ with a body weight of 14.5 kg (the 50-75 percentile) and a height 99.9 cm (>the 97 percentile). She was irritable because she could not pass urine despite the feeling of micturition. Her abdomen was distended, and focal tenderness was present at the lower quadrant. Auscultation revealed lower than normal bowel sounds. The location of the anal orifice on the perineal area and anal tone were both physiologic. No abnormal dimple or skin lesion on her sacral area was observed and her neurologic examination was physiologic and normal. Fecal materials were palpable on digital rectal examination.
Abundant fecal materials were observed on abdominal X-ray (), and ultrasonography (USG) of the abdomen revealed a distended bladder with a thin bladder wall and both hydronephrosis of grade III (). Hematological examinations and blood chemistries were as follows: a hemoglobin level of 13.0 g/dL, a total white cell count of 5.9×109/L, a platelet count of 357×109/L and granulocyte and lymphocyte levels of 41.5% and 46.1%, respectively; A serum calcium level of 9.7 mg/dL (8.6-10.2), a magnesium level of 1.2 mg/dL (1.5-2.3), a sodium level of 144.1 mmol/L (135-145), a potassium level of 3.6 mmol/L (3.3-5.1) and a chloride level of 104.6 mmol/L (98-110). Her blood urea nitrogen, creatinine, hepatic transaminase and C-reactive protein levels were normal. Urinalysis collected via a catheter was normal. Thyroid function test was not checked. Sigmoidoscopy could not be performed to her because of a large amount of feces in her distal colon despite repeated glycerin enema and digital evacuation.
After urinary catheterization, 720 mL of urine was drained and abdominal pain and distension was improved. However, urinary obstruction persisted and urinary catheterization was kept continuously. On day 3 after admission, voiding difficulty persisted despite loose stool passage after repeated glycerine enema. For ruled out the abdominal mass, whole-abdominal computed tomography (CT) was performed and showed a large fecaloma in the sigmoid colon and a displaced bladder (). The coronal image of the CT showed that the distal part of the colon was markedly dilated and contained heterogeneous materials consisting of impacted feces. The markedly dilated distal colon was suspected as Duhamel pouch. The bladder neck was displaced into the upper abdomen because of the large fecaloma-filled pouch. After repeated glycerin enemas and digital evacuations, spontaneous urination was noted on day 5. USG revealed a normal sized bladder and improved both hydronephrosis. However, she could not evacuate bowels sufficiently by herself. We could palpate a membranous tissue in her rectum at the time of digital evacuation. On day 7, a colon study revealed a giant Duhamel pouch filled with fecal materials without a definitive the membranous tissue in her rectum (). We decided to perform an operation because she had a giant Duhamel pouch, an unidentified membranous tissue and to perform a full-thickness rectal biopsy. Two weeks later, operation was done after sufficient evacuation of the feces in her rectum. A septum was noted in Duhamel pouch, which ran transverse direction in her rectum on the operative findings. Post-Duhamel septum revision was performed. Histopathologic findings of the full-thickness rectal biopsies showed a ganglion cell in the rectum. Since the operation, she has been visiting our outpatient clinic regularly. She has been free of defecation and urination difficulties without the need for medicine.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [47, 'months'], 'weight': [14.5, 'kg'], 'sex': 'Female', 'Sodium': [144.1, 'mmol/L']}",0.25479,0.24205,0.26753,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
This means that the patient is 3 years and 11 oldThe patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 14.5 kg. The concentration of sodium is 144.1 mmol/L. Plugging in these values into the equation, we get 0.6 * 14.5 * (144.1/140 - 1) = 0.25479 L. The patient's free body water deficit is 0.25479 L."
6079,38,Free Water Deficit,lab test,decimal,pmc-4337925-1,Extracted,"On October 21, 2013, a 61-year-old man was admitted to the gastroenterology ward. To measure the patient's nutritional condition, medical history, physical measurements, biochemical data, medical examinations and treatments, nutritional physical examination data, and food/nutrition-related diet history were examined. Based on the medical history, the principal diagnosis and symptom was general weakness. The patient was diagnosed with diabetes mellitus 10 years ago, hypertension (10 years ago), and rectal cancer 3 years ago, for which the patient underwent an ileostomy on November 14, 2011 and received leucovorin plus fluorouracil (LV5FU2) as preop #1 and postop #8 chemotherapy. Afterward, the patient underwent ileostomy repair on December 3, 2012, and then a liver wedge resection on July 18, 2013 for liver S4 metastasis during the follow-up (f/u). Afterward the patient received chemotherapy #4 from September 2 through October 14, 2013 using oxaliplatin, folinic acid, and 5-fluorouracil (FLOFOX4). The patient's current drug prescriptions include Lantus 10 U/day, Apidra 6 U #3/day, and Nutriflex lipid peri [+ Humulin-R (regular insulin) 15 U] every other day (EOD), and chemotherapy was paused due to general weakness.
The first screening visit was conducted on October 22, 2013. At the time of hospital admission (October 21, 2013), the physical measurements were: height, 167 cm; body weight, 53.2 kg; ideal body weight (IBW), 61.4 kg; %IBW, 86.6%; body mass index (BMI), 19.1 kg/m2; usual weight, 64.8 kg (July 18, 2013); and weight change of -11.6 kg (17.9% loss) over the most recent 3 months. Examinations upon admission showed the following: total protein/albumin, 5.6/3.2 g/dL; hemoglobin/hematocrit (Hgb/Hct), 8.4 g/dL/25.4%; total lymphocyte count (TLC), 741.2 cells/mm3; cholesterol, 162 mg/dL; blood urea nitrogen/creatinine (BUN/Cr), 20/1.0 mg/dL; Ca/P, 8.3/2.3 mg/dL; Na/K/Cl, 132/4.2/98 mEq/L; C-reactive protein, 6.28 mg/dL; hemoglobin A1c, 9.7%; and casual glucose, 470 mg/dL.
The nutritional and physical examination data showed that the patient had stomatitis, nausea, and vomiting as side effects of chemotherapy and the blood pressure was 142/83 mmHg. In terms of food/nutrition-related diet history, the dietary prescription and diet-related experiences were such that the patient experienced a loss of appetite after chemotherapy, did not receive education intended for cancer patients (due to being too tired). The patient's food and beverage consumption over the most recent week (after the fourth round of chemotherapy) includes six glasses of cola (480 kcal/day; 120 g of sugar) due to stomatitis, nausea, and vomiting. At the hospital, the administration of other foods was not attempted since the patient experienced pain and vomiting after consuming soft foods, particularly gruel (not eaten) and intravenous alimentation (Nutriflex lipid peri EOD; energy, 465 kcal; C:P:F ratio, 34.4:17.2:48.4; carbohydrate, 40 g; protein, 20 g; fat, 25 g). No liquid or solid food supplements or biologically active substances were consumed. The patient stayed in the bed whole day.
In the Patient-Generated Subjective Global Assessment [] conducted for nutritional assessment, the patient scored 15 points, indicating the need for improved symptom and focused nutrition management. Approximately 1600-1860 kcal of energy (baseline weight, 53.2 kg; based on calculation, 30-35 kcal/kg needed) and 64-85 g of protein (baseline weight, 53.2 kg; based on calculation, 1.2-1.6 g/kg needed) were set as the required nutritional intake.
Two nutritional diagnoses were made: frist, malnutrition arising from a decrease in food intake related to the side effects of chemotherapy (stomatitis, nausea, vomiting) as well as a lack of food/nutrition-related knowledge regarding food types and quantities. The evidence for this diagnosis being that the patient experienced a 17.9% weight loss over the most recent 3 months and consumed only 28% of the required nutrients during the most recent week (after the fourth round of chemotherapy); second, the patient's lack of knowledge with regard to foods and nutrients which is possibly attributable to fear for food intake and this was observed through refusal to ingest food and tendency to ingest only cola after chemotherapy.
As a nutritional intervention for the first diagnosis, the medical team was advised to change the patient's diet to diabetic thin rice gruel () (1,700 kcal and 72 g of protein) and supply any intravenous aliments according to the amount of oral intake, which would provide ≥ 30% of the hospital food and the intravenous aliment maintenance to the patients. The hospital-supplied food consisted of soft and non-irradiated foods considering the patient's stomatitis, and in the case of this particular patient, it was decided that close monitoring after dietary changes would be required. As a nutritional intervention for the second diagnosis, the patient was consulted for the need to consume a diverse range of foods and the hospital diet (diabetic thin rice gruel and consider the patient's preferences and lactose intolerance). This intervention would stop for the patient consuming cola, which could worsen the nausea, and try the hospital-supplied foods.
The second screening visit was conducted on October 24, 2013, and physical measurements, biochemical data, medical examinations and treatments, nutritional physical examination data, and food/nutrition-related diet history were examined. On follow-up, there was no change in physical measurements, and examinations revealed the following: total protein/albumin, 5.1/3.1 g/dL; Hgb/Hct, 8.5 g/dL/25.7%; TLC, 712 cells/mm3; cholesterol, 135 mg/dL; BUN/Cr, 19/1.0 mg/dL; Ca/P, 7.8/1.6 mg/dL; Na/K/Cl, 138/50/107 mEq/L; blood glucose (fasting, postprandial 2 hour glucose #3), 177/208/363/309 mg/dL (10/22), 270/206/206/120 mg/dL (10/23), and 126/133/260/246 mg/dL (10/24). Nutritional and physical examination data, included gastroenterological symptoms such as nausea and vomiting after consuming certain foods. For example, the patient had a vomit after drinking orange juice while apple juice did not cause any gastrointestinal trouble. Vital signs were 135/80 mmHg. In terms of food/nutrition-related diet history, the patient's dietary prescription and diet-related experiences were such that he was informed about diabetic thin rice gruels, non-irritating foods, and nutrient supplement drinks.
The patient's food and beverage consumption consisted of the supplied hospital diet: 20% of rice gruel, 50% of the steamed eggs and nutritious beverages, and 100% of the soup and apple juice (energy, 1,050 kcal; C:P:F ratio, 56.0: 14.4: 29.6; carbohydrate, 147 g; protein, 37.2 g; fat, 34.5 g) along with intravenous aliments (Hepasol inj 500 mL/day; 200 kcal, 50 g protein). After the first screening, the patient tried various foods and started learning to move in a wheelchair. The patient's nutrient requirements were the same as at the first screening. Upon nutrition monitoring and assessment, the goal set after the first screening with regard to nutritional intervention was partially achieved considering that the hospital food consumption was at 62% of the overall consumption and the intravenous aliment had changed (Nutriflex lipid peri EOD to Hepasol/d). After the second nutritional intervention, the patient stopped consuming cola and began to consume a diverse range of hospital foods; thus, the goal of the intervention was reached.
After the second screening, the patient again had two nutritional diagnoses: first, excessive protein supplementation, because extra protein was administered via the intravenous aliments outside oral intake, and the patient was consuming 125% the required protein quantity; second, the patient's lack of knowledge regarding food and nutrition due to absence of education about chemotherapy and food preparation. With regard to nutritional interventions, that for the first nutritional diagnosis involved advising the medical team to stop supplying protein via the intravenous aliments. For the second nutritional diagnosis, advising the medical team educate the patient about food choices and preparation which are appropriate for managing side effects of chemotherapy. The goal of the intervention was consumption of energy and protein > 70% of the requirement and maintenance or increase of body weight. Continuous monitoring was required, and even after discharged, the patient required proper outpatient care.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [61, 'years'], 'weight': [53.2, 'kg'], 'Sodium': [132.0, 'mEq/L']}",-1.824,-1.7328,-1.9152,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 61 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 53.2 kg. The concentration of sodium is 132.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 132.0 mEq. To convert from 132.0 mEq to mmol, convert from mEq to mmol. The compound 132.0 has a valence of 1, and so divide the valence by the value of mEq to get, 132.0 mEq/(1 mEq/mmol) = 132.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 132.0 mEq sodium/L converts to 132.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 53.2 * (132.0/140 - 1) = -1.824 L. The patient's free body water deficit is -1.824 L."
6080,38,Free Water Deficit,lab test,decimal,pmc-4158427-1,Extracted,"A 62-year-old Hispanic man presented to the hospital with generalized weakness, near syncope, and weight loss of 25 lbs over the past four months. He complained of early satiety and lack of appetite. He denied any fever, rash, nasal congestion, myalgia, arthralgia, shortness of breath, cough, hemoptysis, urinary symptoms, or gastrointestinal bleeding. Upon arrival he was found to have severe anemia. He had a history of hypertension, stroke, and hyperlipidemia and was being treated with lisinopril 20 mg daily, metoprolol 100 mg twice a day, aspirin 325 mg daily, simvastatin 40 mg daily, and hydralazine 100 mg three times a day. He had been on hydralazine for the last four and half years. He had no history of renal or lung disease. He quit smoking 20 years ago. Physical exam was unremarkable with stable vital signs. Oxygen saturation was maintained on room air. Upon arrival, he received blood transfusion and his symptoms improved.
Initial labs showed hemoglobin of 4.1 g/dL, hematocrit of 14.6%, MCV of 64 fl, and platelet count of 557,000/µL. Serum chemistries revealed sodium of 140 mmol/L, potassium of 3.3 mmol/L, chloride of 106 mmol/L, bicarbonate of 24 mmol/L, blood urea nitrogen of 32 mg/dL, and creatinine of 2.13 mg/dL. Urinalysis showed 2+ blood and 2+ protein. He was found to have acute kidney injury with proteinuria of 1742 mg per 24 hours. Examination of the urine sediment showed >50 RBCs per high power field with >50% dysmorphic RBCs and rare RBC cast. Anti-neutrophil cytoplasmic antibody (ANCA) serology showed a predominant increase in proteinase 3 (PR3) titer (55.94 units; normal: 0–21 units) and, to a lesser extent, myeloperoxidase (MPO) titer (23.07 units; normal: 0–21 units). In addition, anti-histone antibody was positive and antinuclear antibody (ANA) titer was elevated at 1 : 640 with a homogenous pattern. Anti-GBM antibody, anti-dsDNA antibody, Smith antibody, SSA, SSB, and ribonucleoprotein antibody were all negative. Hepatitis B surface antigen, hepatitis C antibody, and HIV 1 and 2 antibody were also negative. C3 levels were slightly low (94 mg/dL; normal: 98–162 mg/dL) and C4 levels were within normal range (25 mg/dL). Renal ultrasound was unremarkable. CT scan of the chest revealed bilateral ground-glass infiltrates. Due to unexplained severe anemia, the patient underwent colonoscopy which revealed diverticulosis with one actively bleeding pedunculated polyp in the rectum. There was no evidence of vasculitis involving the colon. EGD revealed blood surrounding the upper esophageal sphincter, which appeared to be emanating from the upper airway. This prompted serial bronchopulmonary lavages and bronchoscopy which were negative for hemorrhage. Subsequently, a transbronchial biopsy was performed and showed intra-alveolar blood and hemosiderin-laden macrophages consistent with pulmonary hemorrhage; there was no evidence of malignancy or granulomas. Kidney biopsy was performed promptly and revealed focal segmental necrotizing glomerulonephritis with 2 of 11 glomeruli showing cellular crescents. Seven glomeruli showed segmental necrosis with disruption of the basement membrane, nuclear fragments, fibrin deposition, a few neutrophils, and obliteration of capillary lumens (). Immunofluorescence and electron microscopy were negative for antigen antibody immune complexes. The interstitium showed minimal interstitial fibrosis and tubular atrophy and the vessels were unremarkable.
Hydralazine was discontinued and the patient was treated with three doses of pulse intravenous methylprednisolone 1 gm per dose followed by prednisone 60 mg daily and biweekly taper to 10 mg by 3 months. Concomitantly, he received three monthly pulse doses of intravenous cyclophosphamide at 500 mg per m2 of body surface area. The patient was continued on prednisone 5 mg daily for 18 months. His renal function began to improve immediately with resolution of microscopic hematuria. After one month of therapy, MPO and PR3 ANCA became negative and anemia resolved. Six months later, his MPO ANCA became positive with low titer of 27 units. At that time, there was no microscopic hematuria, renal function remained stable, and there was no evidence of recurrent disease. At one-year follow-up, he had no symptoms related to vasculitis and hemoglobin was normal (15.4 g/dL). His kidney function continued to be stable with serum creatinine of 1.1 mg/dL and estimated glomerular filtration rate of 72 mL/min/1.73 m2 (MDRD-4). The urine protein creatinine ratio decreased from initial value of 1.7 mg/mg to 0.6 mg/mg. The PR3 ANCA and anti-histone antibody remained undetectable. He continued to have a positive ANA (1 : 160 titer) and low titer MPO ANCA of 32 units. At one and a half years of follow-up, there was no evidence of recurrent renal or pulmonary disease. Overall, this case demonstrates clinicopathologic features consistent with hydralazine-induced pauci-immune ANCA positive glomerulonephritis and provides the first evidence that MPO as well as PR3 ANCAs may be associated with this disease.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [62, 'years'], 'weight': [25.0, 'lbs'], 'sex': 'Male', 'Sodium': [140.0, 'mmol/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 62 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 25.0 lbs so this converts to 25.0 lbs * 0.453592 kg/lbs = 11.3398 kg. The concentration of sodium is 140.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 11.3398 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
6081,38,Free Water Deficit,lab test,decimal,pmc-6799647-2,Extracted,"The second case describes the girl's little brother, a 5-year-old boy admitted in our clinic for the same symptoms as his sister due to wild mushroom ingestion, but approximately 24 hours later. His family and personal history were also negative.
The clinical examination at the time of admission revealed influenced general status, pallor, dry lips, and diminished cutaneous turgor, abdominal tenderness, and diarrheic stools, weight 16.5 kg.
The laboratory tests at the time of admission were worse in comparison the his sister, revealing more elevated levels of liver enzymes (AST 597 U/L, ALT 784 U/L), hyperbilirubinemia (TBi 4.192 mg/dL, DBi 3.747 mg/dL), hyponatremia (Na 133 mmol/L), hypopotassemia (K 3.2 mmol/L), hypoalbuminemia (Alb 2.55 mg/dL), and altered coagulation tests (APTT 73.1 seconds, INR 3.68). The abdominal ultrasound showed hepatomegaly and ascites. After approximately 24 hours from admission, the hepatic cytolysis syndrome worsened (AST 1960 U/L, ALT 2544 U/L), and he was transferred to the PICU.
Similar to the case presented above, the little brother also received penicillin G by vein, glucose, electrolytes, and amino acids perfusion, and activated charcoal within the first hour after admission. Nevertheless, his condition continued to worsen and therapeutic plasma exchange along with the same supportive measures as in the case of his sister, were initiated in the PICU. Despite these therapeutic efforts, his liver enzymes continued to increase (AST 4386.7 U/L, ALT 5156.2 U/L) associating also renal dysfunction (creatinine 2.18 mg/dL). Liver transplantation was not a viable option under these circumstances. Unfortunately, the patients died after approximately 100 hours from the time of admission.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [5, 'years'], 'weight': [16.5, 'kg'], 'Sodium': [133.0, 'mmol/L']}",-0.495,-0.47025,-0.51975,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 5 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 16.5 kg. The concentration of sodium is 133.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 16.5 * (133.0/140 - 1) = -0.495 L. The patient's free body water deficit is -0.495 L."
6082,38,Free Water Deficit,lab test,decimal,pmc-2633086-1,Extracted,"A 26-year old woman was admitted to our hospital for further evaluation of a perirenal mass. Five days earlier, she had visited an outside emergency department with complaints of a high fever and left flank pain, which radiated to the iliac fossa and posterior back. An abdominal ultrasound (US) revealed a left perinephric mass (). The abdominal computed tomography (CT) scan revealed a perirenal hematoma confined to the left kidney. However, other perinephric structures, including the pancreas, adrenal grand, and additional vasculature, remained unaffected ().
The patient had a long history of insulin dependent diabetes mellitus (IDDM), and had been treated with insulin since the age of 16. She had no other medical illness (i.e. vasculitis, immunodeficiency, hypertension, or tuberculosis) and had no relevant medication history (i.e. aspirin or non-steroid anti-inflammatory drugs (NSAIDs)). However, in an attempt to lose weight, the patient had been exercising 30 minutes daily for about six months, using a hula-hoop. She recalled experiencing intermittent left flank pain whilst exercising with the hula-hoop.
A physical examination revealed an ill-appearing woman with a body temperature of 38℃, blood pressure of 130/80mmHg, and a heart rate of 98 beats/min. Her body weight was 54kg, and her height was 162cm (BMI, 20.1kg/m2). Her abdomen was soft, not distended, and remarkable for left costovertebral angle tenderness.
Laboratory examination revealed a WBC of 11,700/mm2 (64.5% segmental neutrophils and 10.9% lymphocytes), hemoglobin of 11.1g/dL, hematocrit of 34.8%, platelet 340 × 103, fasting blood glucose of 99mg/dL, postprandial glucose of 207mg/dL, hemoglobin A1C of 16.2%, serum sodium of 143mmol/L, potassium of 4.6mmol/L, blood urea nitrogen of 19mg/dL, creatinine 0.9 of mg/dL, lipase 78 of IU/L and a lactate dehydrogenase of (LDH) 396IU/L. Urine analysis was negative for blood and protein, and showed 0-1 WBC and 0-1 RBC. The 24-hour total protein was 473mg/day, and creatinine clearance was 77 mL/min/1.73m2. Coagulation parameters and the liver functions were normal.
An abdominal US was rechecked at our hospital. The US showed a 1.2cm diameter mass encircling the left kidney (). The size of the left perirenal hematoma was smaller than the previous image, which was conducted at a previous hospital about five days prior. Signs of persistent bleeding were absent, and the left kidney was well preserved and encapsulated. No vascular malformation was identified. She was treated with hydration and intravenous antibiotics (cephazedone, 2g/day), and her blood glucose level was well-controlled with insulin. Four days later, her fever subsided and her general condition improved. She was discharged, and a third abdominal US was repeated 20 days later in an outpatient setting. The US revealed an overall reduction in the size of the perirenal hematoma ().",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [26, 'years'], 'weight': [54.0, 'kg'], 'Sodium': [143.0, 'mmol/L']}",0.57857,0.54964,0.6075,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 26 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 54.0 kg. The concentration of sodium is 143.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 54.0 * (143.0/140 - 1) = 0.57857 L. The patient's free body water deficit is 0.57857 L."
6083,38,Free Water Deficit,lab test,decimal,pmc-5346915-1,Extracted,"A 28-year-old woman was admitted to our hospital with short-term memory problems, confusion, incoherent and delusional thinking, and self-neglect since 2 weeks. There was also loss of appetite and she had lost 7 kg of weight in the last 2 months. She was of mixed European/African ethnicity, and her previous medical history mentioned an attention deficit hyperactivity disorder for which she used methylphenidate 10 mg daily. Her psychiatric history showed a short period of paranoid features when she was 20 years old, possibly induced by overuse of methylphenidate.
On physical examination there was a body temperature of 34.8°C, an RR of 95/57 mm Hg, and a pulse rate of 80 beats/min. She had symptoms of bradyphrenia, bradykinesia, and slowed, halting speech and was disorientated in time and place. The Mini-Mental State Examination (MMSE) score was 26/30. The remaining physical and neurological examinations were unremarkable. Extensive ancillary testing was performed. Laboratory testing showed a leukocytosis of 27.7 × 109/L, a C-reactive protein level of 2.1 mg/L, and a mild hypernatremia of 148 mmol/L. Her thyroid function was normal and there were no vitamin deficiencies. A urine sample showed no abnormalities and drug testing was negative. HIV and lues screening was negative. A brain CT scan was normal.
She was admitted to our neurology ward, but after 2 days she was transferred to our medical psychiatric ward because of progressive confused behavior. The psychiatrist suspected a first psychotic episode with catatonic features; methylphenidate was discontinued and she was treated with lorazepam 0.5 mg twice a day. An antipsychotic drug was not yet started, because a somatic cause of her behavior had not been ruled out completely. She then developed hypothermia (32.6°C) and hypercapnia and was therefore transferred to the intensive care unit because of a suspected autonomic dysregulation. On the intensive care unit, her mental status deteriorated. A brain MRI showed an abnormal hyperintense signal on T2-weighted images and fluid-attenuated inversion recovery images of the hypothalamus (Fig. ) and, to a lesser extent, of the right optic nerve, with enhancement after gadolinium. A cerebrospinal fluid examination revealed a mild pleocytosis of 60 cells/µL, a normal protein level of 0.45 g/L, and a normal glucose level of 3.6 mmol/L.
The differential diagnosis at that moment included hypothalamic encephalitis either caused by an autoimmune disorder or of viral origin, a systemic autoimmune disease, or a paraneoplastic disorder. Cerebrospinal fluid cultures showed no abnormalities and the paraneoplastic antibodies were negative. A CT scan of the thorax and abdomen showed no signs of sarcoidosis or an underlying malignancy. Anti-dsDNA and anti-Sm antibodies were absent, ruling out systemic lupus erythematosus. Anti-Sjögren syndrome-related antigen B (anti-SSB) antibodies were positive, but in combination with a negative test for anti-SSA and normal findings at a lip biopsy, Sjögren syndrome was considered highly unlikely.
The patient was treated with intravenous methylprednisolone pulse therapy for 3 days, at 1,000 mg per day, which resulted in resolution of the hypothermia and hypercapnia. A second cerebrospinal fluid analysis showed an IgG index of 0.52 with oligoclonal bands. Considering all the normal results on testing and the prompt reaction to steroids, an NMOSD was considered and was confirmed by positive tests for serum anti-AQP4 antibody. After the 3-day course of intravenous methylprednisolone, we continued treatment with oral prednisolone at 30 mg twice a day and azathioprine at 50 mg twice a day. Because she developed apraxia and hypomanic features such as hypersexuality and overeating in combination with the preexisting cognitive and behavioral problems, she was retransferred to the medical psychiatric ward and treated with haloperidol at 2.5 mg and with lorazepam. Her MMSE score at that moment was 14/30. An ophthalmologist confirmed vision of 0.5/200 and 20/25, respectively, in the right and the left eye. On treatment with haloperidol and lorazepam, the hypomanic symptoms and delusional thinking subsided. After 6 weeks, she was discharged to a rehabilitation center with severe memory and visual problems. Oral prednisolone was continued in a 22-month tapering schedule; azathioprine was continued at 50 mg twice a day. After a couple of weeks in rehabilitation, she was again transferred to a psychiatric unit with a compulsive eating disorder and aggressive behavior probably due to a combination of treatment with prednisolone and a brain injury caused by the initial brain lesions. A repeat MRI scan 3 months later showed almost complete recovery of the hypothalamic lesions, and there were no signs of new disease activity.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [28, 'years'], 'weight': [7.0, 'kg'], 'Sodium': [148.0, 'mmol/L']}",0.2,0.19,0.21,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 28 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 7.0 kg. The concentration of sodium is 148.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 7.0 * (148.0/140 - 1) = 0.2 L. The patient's free body water deficit is 0.2 L."
6084,38,Free Water Deficit,lab test,decimal,pmc-4388017-1,Extracted,"A 47-year-old woman was admitted to our clinic with the complaints of nausea, intermittent vomiting, constipation, fatigue, and palpitation. She also had progressive weight loss of 10 kg since last 5 months. She had a history of bilateral surrenalectomy 3 years ago due to Cushing's syndrome associated with adrenocorticotropic hormone (ACTH) independent macronodular adrenal hyperplasia. The patient was taking prednisolone 7.5 mg and fludrocortisone 0.1 mg orally once a day. Her family history was significant for breast cancer in her mother, gastric cancer in her aunt, and coronary artery disease in her uncle. Physical examination revealed tachycardia, presence of lid lag, warm skin, and orthostatic hypotension. The thyroid gland was enlarged and had a bruit. Pertinent laboratory values included a serum thyroid stimulating hormone (TSH) of 0.005 mIU/L (normal, 0.4 to 4.2) with a free T4 value of 7.7 ng/dL (normal, 0.93 to 1.7) and free T3 value of 16 pg/mL (normal, 2 to 4.4). Thyroglobulin antibody (Anti TG) and thyroid receptor antibody (TRAB) were elevated (anti-TG 718 IU/mL (normal, 0 to 115) and TRAB 14.91 U/mL (normal, 0 to 1.1)). Thyroid scan showed bilateral mildly increased, diffuse, and homogenous uptake in the thyroid gland. Radioactive iodine uptake was calculated to be 19% at two hours and 39% at 24 hours. Thyroid ultrasonography revealed an enlarged and heterogeneous thyroid gland. The patient's serum calcium level was 16 mg/dL (normal, 8.4 to 10.2), serum phosphorus was 3.9 mg/dL (normal, 2.5 to 4.5), albumin level was in the normal range, and intact parathyroid hormone (iPTH) was found to be suppressed to the level of 7.99 pg/mL (normal, 15 to 65). The 25-OH vitamin D was slightly decreased (21 ng/dL (normal, 30 to 50)) and serum alkaline phosphatase was normal. Serum creatinine was in the normal range, serum sodium was 136 mmol/L (normal, 136 to 145), and potassium was 5.1 mmol/L (normal, 3.5 to 5.1). The electrocardiogram showed sinus tachycardia at a rate of 120 beat per minute (bpm) and shortened QT interval. In the lights of these initial physical and laboratory investigations, the diagnosis of thyrotoxicosis complicated by hypercalcemia and acute adrenal failure was confirmed. Emergent treatment with intravenous saline, methylprednisolone 20 mg intravenously 3 times a day, methimazole 10 mg orally 3 times a day, and propranolol 20 mg orally 2 times a day was started. Fludrocortisone at a dose of 0.1 mg orally was continued. After infusion of 2 liters of isotonic saline, furosemide was added to the therapy and saline infusion was continued at rate of 250 mL/hour. Zoledronic acid at a dose of 4 mg intravenously was also given to the patient. On the third day of the admission, the patient's calcium level was 9.5 mg/dL, and saline and furosemide infusion were stopped. The free T4 level was 4.67 ng/dL and free T3 level was 5.98 pg/mL. On the fourth day of admission, the patient complained of acute onset right upper quadrant pain. The laboratory examinations revealed that transaminase levels were elevated to approximately three times of the upper limit of normal. As her initial transaminase values were within the normal range, hepatotoxicity due to the methimazole administration was suspected and the drug was stopped. Hepatobiliary ultrasonography was consistent with acute hepatitis and viral serologic examinations were negative. After three days while off methimazole serum transaminase values were normalized and the patient had no more pain in the right upper quadrant, we started the patient on cholestyramine 8 g orally 3 times a day, lithium 600 mg orally 2 times a day, increased the propranolol dose to 40 mg 3 times a day, and continued methylprednisolone at the same dose. The investigations to rule out a possible malignancy including thorax and abdominal computed tomography (CT), bone marrow examination, gastroscopy, bone scan, gynecologic and mammographic examinations, and PET-CT were all negative. After being euthyroid the patient received 10 millicuries (mCi) radioactive iodine (RAI). The patient was discharged from the hospital with a steroid taper schedule aiming at 8 mg dose decrease every 5 days until the final dose of 7.5 mg per day of prednisolone was reached. Three months later, the patient was readmitted to the hospital with similar complaints and laboratory examinations revealed a mild thyrotoxicosis, mild hypercalcemia, hyponatremia, and hyperpotassemia. The clinical picture and laboratory findings of the patient were less remarkable at that time as she had increased the steroid dose one week before her admission. She was using prednisolone 5 mg orally three times a day and these supraphysiological doses of steroid may have potentially prevented the development of more severe adrenal failure and thus hypercalcemia. An additional dose of 15 mCi RAI was administered to the patient. She became hypothyroid and was started on levothyroxine replacement therapy 3 months later. At her last follow-up visit, she was euthyroid and normocalcemic and her iPTH was 41 pg/mL.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [47, 'years'], 'sex': 'Female', 'weight': [10.0, 'kg'], 'Sodium': [136.0, 'mmol/L']}",-0.14286,-0.13572,-0.15,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 47 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 10.0 kg. The concentration of sodium is 136.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 10.0 * (136.0/140 - 1) = -0.14286 L. The patient's free body water deficit is -0.14286 L."
6085,38,Free Water Deficit,lab test,decimal,pmc-4041959-1,Extracted,"A 31-year-old female patient with a height of 164 cm and weight of 60 kg was admitted to undergo ethanol sclerotherapy for a large painful vascular malformation in her left leg. Magnetic resonance imaging revealed an AVM measuring 28 × 7 × 4 cm in her left calf (). All preoperative examinations, including laboratory tests, electrocardiography, and chest X-ray, were normal. Vital signs before general anesthesia were stable: her blood pressure was 130/80 mmHg and her heart rate was 82 beats/min. Following the application of routine hemodynamic monitoring (3-lead electrocardiogram, noninvasive blood pressure, and pulse oximetry), anesthesia was induced using a bolus intravenous injection of 120 mg propofol and 40 mg rocuronium. A 20-gauge catheter was inserted into the radial artery to monitor her arterial blood pressure continuously. The target controlled infusion of 2% propofol and remifentanil (2-3 µg/ml and 2-5 ng/ml of the effect-site concentrations, respectively) was applied to maintain anesthesia. Immediately following the injection of ethanol, the patient's blood pressure and heart rate rose slightly to 160/100 mmHg and 100 beats/min, respectively. Thereafter, the patient's blood pressure and heart rate were stable throughout the procedure while she was in the prone position. A total dose of 50 ml of 99% ethanol was injected into the lesion over a period of 30 minutes without the use of a tourniquet. As soon as the patient was turned from prone to supine after finishing the procedure, an abrupt drop in her arterial blood pressure occurred, 40-50 mmHg systolic and 10-15 mmHg diastolic blood pressure with a simultaneous increase in her heart rate to 100-110 beats/min. To restore blood pressure, 20 mg of ephedrine was immediately injected, but the patient's heart rate rather decreased abruptly to < 30 beats/min. Chest compressions were performed along with the simultaneous injection of 50 µg of epinephrine. A few minutes later, the patient's blood pressure and heart rate recovered to 180/100 mmHg and 100-110 beats/min. At that moment, the arterial blood gas analysis showed metabolic acidosis with otherwise normal findings (pH 7.29, PaCO2 28 mmHg, PaO2 466 mmHg, SaO2 100%, base excess -11.6, Hematocrit 38%, Na+ 137 mEq/l, K+ 3.7 mEq/l, and Ca2+ 1.11 mmol/l). The patient was transferred to the intensive care unit with the endotracheal tube in place. Transthoracic echocardiograph (TTE) and embolism computed tomography (CT) were performed to confirm pulmonary hypertension or pulmonary embolism. There was no evidence of pulmonary embolism on CT. In addition, the peak tricuspid regurgitation jet velocity on TTE was 2.3 m/s, indicating no evidence of pulmonary hypertension at that moment (). However, TTE revealed dilated right ventricle () and severely decreased right ventricular function.
On postoperative day 1, the patient regained her consciousness and was discharged five days after the operation without any complications.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [31, 'years'], 'weight': [60.0, 'kg'], 'sex': 'Female', 'Sodium': [137.0, 'mEq/L']}",-0.64286,-0.61072,-0.675,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 31 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 60.0 kg. The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 60.0 * (137.0/140 - 1) = -0.64286 L. The patient's free body water deficit is -0.64286 L."
6086,38,Free Water Deficit,lab test,decimal,pmc-7526953-1,Extracted,"An 80-year-old male with a past medical history of Crohn's disease presented to the emergency department with complaints of nausea and multiple episodes of coffee-ground emesis for one day and was initially diagnosed with upper gastrointestinal bleed. His prior medical conditions included longstanding Crohn's disease, hypertension, diabetes, and coronary artery disease. He had undergone previous abdominal surgery for the complication of small intestinal obstruction due to Crohn's disease in 2017. On initial evaluation, he had a blood pressure of 159/74 mmHg, pulse of 84 per minute, respiratory rate of 18 per minute, oxygen saturation levels (SpO2) of 98% on room air, and body weight 125 pounds. On physical examination, the patient was noted to have a mildly tense and tender abdomen with hyperactive bowel sound. The fluid thrill and shifting dullness were negative.
His blood work revealed creatinine of 1.27 mg/dL, blood urea nitrogen of 27 mg/dL, sodium of 147 mmol/L, potassium of 3.6 mmol/L, chloride of 103 mmol/L, bicarbonate of 27 mmol/L, bilirubin of 2.3 mg/dL, lactate of 1.3 mg/dL, cardiac troponins of <0.10 (normal), WBC of 22,000 cells/mm3, and hemoglobin of 14.2 mg/dL. Imaging studies included CT abdomen and pelvis, which showed a markedly distended stomach filled with the enteric contrast, rotated in mesenteroaxial (MA) rotation, and localized fluid in the left upper quadrant with the caudal displacement of the spleen due to left upward stomach (Figures , ). The gastric outflow tract was pinched to the left of the midline superior to the esophagogastric junction related to the gastric volvulus, with a small amount of contrast material passing into the small intestine, suggesting a short segment of focal narrowing at the level of antrum or proximal duodenum (Figures , ). This was consistent with the diagnosis of gastric volvulus. After the initial resuscitation, the gastroenterologist decided to perform endoscopic detorsion, which was unsuccessful due to the twisting of the distal stomach in the antrum and stricture at the level of the antrum. The area was traversed multiple times without achieving clear untwisting due to adhesions.
The patient was taken to the operating room and laparoscopy was performed to find a redundant stomach without adhesions or masses. The stomach was detorsed. The gastroenterologist was consulted in the operating room and endoscopy was performed. The narrowing at the junction of the antrum and proximal duodenum was identified. Gastric and duodenal mucosa were healthy, without lesions or masses, and gastropexy was performed. Postoperatively, the patient was kept under observation for one week and was discharged home with outpatient follow-up. At his biweekly follow up, the patient was found to be doing well.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [80, 'years'], 'sex': 'Male', 'weight': [125.0, 'lbs'], 'Sodium': [147.0, 'mmol/L']}",1.41748,1.34661,1.48835,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 80 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 125.0 lbs so this converts to 125.0 lbs * 0.453592 kg/lbs = 56.699 kg. The concentration of sodium is 147.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 56.699 * (147.0/140 - 1) = 1.41748 L. The patient's free body water deficit is 1.41748 L."
6087,38,Free Water Deficit,lab test,decimal,pmc-6283186-1,Extracted,"In spring of 2013, a 32-year-old woman sought medical attention at the Jilin University First Bethune Hospital with complaints of intermittent pruritus and fatigue. Liver function tests revealed significantly increased levels of γ-glutamyltransferase (γ-GT, 468 U/L) and alkaline phosphatase (ALP, 968 U/L). The patient was diagnosed with hypothyroidism 3 years ago due to the use of I31I therapy and was treated with euthyrox (250 mg/d). She had no hypertension, diabetes, special drug, hepatitis, or consumption of alcohol history, as well as no any family history. No positive signs were observed on physical examination. Serology for hepatitis virus A, B, or C was negative. Immunologic tests showed that serum antinuclear antibodies were positive (1:640), accompanied by increased concentrations of serum immunoglobulin M (IgM, 5.01 g/L) and the presence of an anti-mitochondrial M2 antibody (AMA-M2, >200 RU/mL); however, the anti-Ro (SS-A) and anti-La (SS-B) antibodies were negative. A liver biopsy showed stage II PBC (Fig. A and B). The patient was eventually diagnosed with PBC and was treated with ursodeoxycholic acid (UDCA, 250 mg/d). The cholestatic enzyme levels and symptoms of pruritus were significantly improved.
In April 2016, the patient visited our hospital because of repeated fatigue for 2 years. Liver and kidney function, serum glucose levels, and blood routine tests were normal. Laboratory tests mainly revealed that the level of serum potassium (2.42 mmol/L) was low. The patient was treated intermittently with potassium citrate. However, the therapeutic effect was not satisfactory, and the cause of low potassium was unknown.
In July 2016, the patient visited the superior hospital for further treatment. She weighed 43 kg, and her height was 155 cm. Blood tests showed the following: pH, 7.347; PaCO2, 33.1 mm Hg; HCO3−, 17.7 mmol/L; PaO2, 103 mm Hg; Na+, 141 mmol/L; K+, 3.4 mmol/L; Cl−, 113 mmol/L; Mg2+, 0.94 mmol/L; serum creatinine, 70 μmol/L. In addition, the plasma anion gap (AG) was normal: AG = [Na+] – [Cl− + HCO3−] = 141 – (113 + 17.7) = 10.3 mmol/L (normal, 10–14 mmol/L). Urine routine showed a pH of 7.5, and 24-hour urine analysis demonstrated that the urine potassium concentration was 94 mmol/24 h. The aldosterone renin ratio was normal. Baseline data of the patient are summarized in Table . An abdominal ultrasound showed evidence of cirrhosis and gallstones. Adrenal CT showed bilateral nephrocalcinosis and no tumor. Whole-body bone mineral density was 0.99 g/cm2 with a T score of −1.3. According to the patient's history and related test results, she was finally diagnosed with RTA in PBC and was then treated with a combination of UDCA, potassium citrate, calcium supplements and activated vitamin D. One year after the treatment, the patient's liver function remained stable, and the clinical symptoms were significantly improved.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [32, 'years'], 'weight': [43.0, 'kg'], 'Sodium': [141.0, 'mmol/L']}",0.15357,0.14589,0.16125,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 32 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 43.0 kg. The concentration of sodium is 141.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 43.0 * (141.0/140 - 1) = 0.15357 L. The patient's free body water deficit is 0.15357 L."
6088,38,Free Water Deficit,lab test,decimal,pmc-5314848-1,Extracted,"A 1-year-old, previously healthy, 10 kg male child, presented to Accident and Emergency (A and E) department following a domestic accident. On admission, he was irritable and drowsy (Glasgow Coma Score = 7) with a mild right-sided weakness and unequal pupils (right 5+ and left 3+). There were no external injuries. As venous access was difficult, an intra-osseous (IO) needle was placed in the right tibia. He was intubated using 4.0 cuffed endotracheal tube after induction with fentanyl 2 mcg/kg, propofol 2 mg/kg, and rocuronium 0.8 mg/kg through the IO needle and hand ventilated to maintain a normal end-tidal carbon dioxide. His immediate head computed tomography scan conducted under general anesthesia showed an acute right-sided subdural hematoma with a significant midline shift. Therefore, he was immediately transferred to the operating theater for a right frontal craniotomy and evacuation of the acute subdural hematoma.
On arrival in theater, his systolic blood pressure was 98 mmHg with good pulses. However, his peripheries were mottled, with a pale blue skin. Therefore, venous access was gained through a left femoral triple lumen central line. Arterial pressure monitoring was established through a right femoral 22G cannula. His tympanic membrane temperature was 36.0°C. At this time, it became evident that he had had received 30 ml/kg of (3%) HS instead of the 3 ml/kg dose prescribed in A and E department. Surgery commenced regardless and anesthesia was maintained with O2/N2O and sevoflurane and positive pressure ventilation.
He passed a large volume of urine on his bed at the induction of anesthesia. Based on clinical judgment, a total of 400 ml (40 ml/kg) of Hartmann's solution was infused during surgery in 5 ml/kg boluses to maintain blood pressure during anesthesia. Blood loss was moderate, but a transfusion was not required. An arterial blood gas during surgery recorded a mixed respiratory acidosis (pH – 7.08, PCO2-9.2 KPa, PO2-31.6 KPa, Na+ – 154 mmol/L, K+ – 3.0 mmol/L, Cl – 129 mmol/L, Ca++ – 1.36 mmol/L, glucose – 14.1 mmol/L, lactate – 0.8 mmol/L, hemoglobin [Hb] – 10.0 g/L, base excess – 9.8). The highest serum sodium recorded during the surgery was 158 mmol/L. Hb was 8.0 g/dl at the end of the surgery. His right fronto-occipital hematoma was evacuated. He was transported to the pediatric Intensive Care Unit (PICU), ventilated, and sedated with midazolam 3 mcg/kg/min and morphine 20 mcg/kg/h infusions.
He was extubated 2 h after surgery in the PICU. His postoperative fluid intake was maintained at 2/3rd of daily requirement orally. He demonstrated a good urine output of 1–2 ml/kg/h. SaO2 was 98%–100% self-ventilating room air, respiratory rate was 24–28 bpm, there was no respiratory distress, heart rate was 140/min, and blood pressure was 112/66 mmHg. Pupils were equal and reacted to light. He was awake and alert. His electrolytes showed a normal Na+ (139–141 mmol/L) but a lower and normalizing K+ (3.4, 3.6, 3.8 mmol/L) during the next 24 h. He developed a single temperature spike to 38.8°C that resolved with paracetamol. The drug error with regard to HS overdose was explained to parents in keeping with the duty of candor. He made an uneventful recovery with no detectable residual defects either due to subdural hematoma or due to salt overdose. There was no evidence of renal injury or residual brain damage during the immediate postoperative period or at subsequent follow-up after 1 month.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [1, 'years'], 'weight': [10.0, 'kg'], 'sex': 'Male', 'Sodium': [158.0, 'mmol/L']}",0.77143,0.73286,0.81,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 1 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 10.0 kg. The concentration of sodium is 158.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 10.0 * (158.0/140 - 1) = 0.77143 L. The patient's free body water deficit is 0.77143 L."
6089,38,Free Water Deficit,lab test,decimal,pmc-3193049-1,Extracted,"An 84-year-old female was admitted for elective coronary angiography due to chest pain. Her height and body weight were 135 cm and 42.7 kg, respectively. She was healthy except for hypertension which was treated with amolodipine besilate (5 mg qd) and hydrochlorothiazide (12.5 mg qd). The blood creatinine was 0.9 mg/dL, the blood urea nitrogen (BUN) was 15.4 mg/dL, the glucose was 105 mg/dL, the sodium was 142 mmol/L, and the potassium was 3.8 mmol/L. Coronary angiography was performed from the left radial artery under local anesthesia. One hundred mL of Visipaque 320 (Iodixanol) contrast media was used. The coronary angiography showed minimal luminal narrowing of the mid-left anterior descending artery and was completed without complication. Twelve hours later, however, the patient had severe nausea and vomiting. Sixteen hours following coronary angiography, she was markedly confused, and was in a stuporous state with recurrent generalized tonic-clonic-type seizures. The neurologic examination was without focality. A brain MRI and electroencephalography were normal (). The diagnosis of hyponatremia was not entertained until blood was drawn and showed a sodium of 115 mmol/L, a potassium of 3.4 mmol/L, a glucose of 205 mg/dL, a creatinine of 0.6 mg/dL, a BUN of 7.3 mg/dL, a uric acid of 3.1 mg/dL, and an osmolarity of 241 mosm/L. A laboratory error was suspected until a second blood sample confirmed the initial results. With a differential diagnosis of hypo-osmolar hyponatremia, we measured the serum-free T4 and thyroid stimulating hormone, which were normal. A rapid Adenocorticotropic hormone stimulation test was performed and the results were within the normal range. The patient was treated with hypertonic saline (3% NaCl) at a rate of 2 mL/hr. She improved slowly over the following 26 hours. The serum and urine sodium levels returned to normal within 48 hours, together with a full clinical recovery ().",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [84, 'years'], 'weight': [42.7, 'kg'], 'sex': 'Female', 'Sodium': [142.0, 'mmol/L']}",0.2745,0.26078,0.28823,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 84 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 42.7 kg. The concentration of sodium is 142.0 mmol/L. Plugging in these values into the equation, we get 0.45 * 42.7 * (142.0/140 - 1) = 0.2745 L. The patient's free body water deficit is 0.2745 L."
6090,38,Free Water Deficit,lab test,decimal,pmc-2876866-1,Extracted,"A 23 year-old female patient, 160 cm tall and 48 kg, was diagnosed with acute appendicitis and admitted for a laparoscopic appendectomy. She had no abnormalities in her pediatric medical history, but from the age 18, she had slowly begun experiencing headaches in her left temporal lobe, nausea, and vomiting. In June of that year, she experienced generalized convulsions and aphasia. In a brain MRI and MRA, an infarction in the posterior divisions of the left mesencephalic arteries was found. Also, in a blood test, an increase in lactic acid was discovered (7.54 mM/L [normal level: 0.5-2.254 mM/L]). The patient was suspected to have MELAS syndrome. She was diagnosed with MELAS after testing (adenosine-to-guanine transition at t-RNA nucleotide 3243 in PCR sequencing). After she turned 21, she was diagnosed with Type I DM. The patient had to orally ingest 200 mg of carbamazepine and 100 mg of aspirin per day and subcutaneously inject 30 units of insulin in the morning and 20 units in the evening. She had no history of total anesthesia.
In a physical examination before the anesthesia, the patient was able to read but had auditory aphasia such that she could not understand spoken words. In the physical examination, there were no signs of hypotonia or amyotrophy of the limbs. The laboratory results showed hyponatremia (126 mEq/L), hyperglycemia (257 mg/dl), and light metabolic acidosis (pH 7.346, PaCO2 36.3 mmHg, HCO3 20.1 mM/L, BE -5.3 mM/L). There were no abnormal findings in the chest X-ray and electrocardiogram. One year prior to her admission to the hospital, she had an ECG that revealed a cardiac index of 67% and no abnormal findings. For sugar control, 4 units of shortacting insulin were injected, and 0.9% normal saline was administered to control hyponatremia. No other pre-operative measures were performed.
After the patient was taken to the operating room, we attached ECG standard leads II, noninvasive monitors for blood pressure, heart rate, arterial oxygen saturation, capnogram, and bispectral index (BIS), and a nerve stimulator to the patient using the Multi Channel Anesthesia Monitor S/5™ (Datex-Ohmeda, USA). Preliminary vital signs were as follows: blood pressure 115/65 mmHg, heart rate 100 beats/min, oxygen saturation rate 97%, and the ECG results appeared normal. The patient underwent 3 minutes of denitrogenation with 100% oxygen through a face mask. Afterwards, we administered lidocaine (40 mg) with the Master TCI (Fresenius Vial S.A., France); we then injected 2% propofol (Fresofol®, Fresenius Kabi, Austria) and remifentanil (Ultiva™, GlaxoSmithKline, UK) at target concentrations of 4 µg/ml (Marsh-model) and 5 ng/ml (Minto-model), respectively. After roughly 90 seconds had passed, we checked lid reflexes and found that the patient had lost consciousness. We administered atracurium (0.5 mg/kg), the BIS was 50, and we saw that there was no response to TOF stimulation with the nerve stimulator placed on the ulnar nerve. Endotracheal intubation was then performed without complications. We started mechanical respiration with air (1.5 L/min), oxygen (1.5 L/min), respiratory volume of 450 ml, and respiratory rate of 12 breaths per minute. To control ventilation, the capnogram was kept at 35-40 mmHg. We used spirometry to measure the respiratory volume and pulmonary compliance. We started invasive blood pressure monitoring through the radial artery and measured the esophageal temperature with a body temperature monitor. During the operation, we used a forced-air warming blanket (Bair Hugger™, Austine Medical, USA) to stabilize the patient's body temperature. For fluid maintenance, we administered 0.9% normal saline at 200 ml per hour. During the operation, the patient's vitals were kept stable with blood pressure at 120-140/60-80 mmHg, heart rate 80-100 beats/min, oxygen saturation 100%, body temperature 37.0-37.4℃, and BIS 40-60. Thirty minutes after inducing anesthesia, the arterial blood gas study showed pH 7.44, PaCO2 32 mmHg, PaO2 299 mmHg, HCO3 23.3 mM/L, BE -2.1 mM/L; her electrolytes were Na+ 125 mEq/L, K+ 3.8 mEq/L, Cl- 88 mEq/L; and her blood sugar was 176 mg/dl. Twenty minutes prior to the end of the operation, we administered ondansetron (4 mg) to prevent post-operative nausea and vomiting. After suturing the peritoneum, we stopped injecting remifentanil, kept the level of propofol in the target effect site at 2 µg/ml, and restored spontaneous breathing. After the operation was over, we stopped injecting propofol and stabilized spontaneous breathing at 300 ml per breath on the spirometer. On the nerve stimulator, the TOF rate was kept at 0.95. To reverse the muscle relaxant effects, we administered glycopyrrolate (0.4 mg) and pyridostigmine (15 mg). Afterwards, the patient responded to voice commands and opened her eyes. With stabilized spontaneous breathing, she was extubated. The operation lasted around 1 hour, and during the operation, 350 ml of 0.9% normal saline were used. We then moved the patient to the recovery room and kept her under observation with blood pressure, electrogram, and oxygen saturation monitors. In the recovery room, we gave her oxygen at 5 L/min through the facial mask. The arterial blood gas study showed pH 7.32, PaCO2 43 mmHg, PaO2 219 mmHg, HCO3 21.2 mM/L, and BE -3.6 mM/L; her electrolyte levels were Na+ 128 mEq/L, K+ 4.1 mEq/L, and Cl- 90 mEq/L; and her blood sugar level was 120 mg/dl. We then moved the patient to the ward where we performed a lactic acid test, which measured 3.6 mM/L. Three days after the operation, the patient showed no complications from the operation or anesthesia, so she was released from the hospital.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [23, 'years'], 'weight': [48.0, 'kg'], 'sex': 'Female', 'Sodium': [128.0, 'mEq/L']}",-2.05714,-1.95428,-2.16,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 23 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 48.0 kg. The concentration of sodium is 128.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 128.0 mEq. To convert from 128.0 mEq to mmol, convert from mEq to mmol. The compound 128.0 has a valence of 1, and so divide the valence by the value of mEq to get, 128.0 mEq/(1 mEq/mmol) = 128.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 128.0 mEq sodium/L converts to 128.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 48.0 * (128.0/140 - 1) = -2.05714 L. The patient's free body water deficit is -2.05714 L."
6091,38,Free Water Deficit,lab test,decimal,pmc-7837787-1,Extracted,"A 74-year-old male was admitted to hospital with a chief complaint of general weakness since the last 3 months and increasingly burdensome. There was nausea, vomiting, but no heartburn, decreased appetite for the last 5 months, and weight loss of around 7 kg in the last 6 months. There is no fever, headaches are often felt since the last 6 months and usually do not improve even after taking analgetics, and patients also sometimes find it difficult to sleep. There is no cough and dyspnoea; the patient often feels pain in the right chest which only decreases after taking analgetics. Urination is smooth, but the volume of urine was less, irregular defecation as long as this complaint.
Previous medical history: the patient was treated at hospital with a diagnosis of moderate differentiation of invasive squamous cell esophageal carcinoma, suspected lung and brain metastases with electrolyte balance disorders. The patient received chemotherapy 13 times and radiotherapy 30 times during treatment at a hospital in another country six months ago. Laboratory results of the last serum sodium after chemotherapy is 124 mmol/L. One month before admission in our hospital, the patient received a total of 10 bottles of 3% sodium infusion in another hospital. The serum sodium levels after correction were 111 mmol/L, 112 mmol/L, and 117 mmol/L, respectively. There was no history of swelling, hypertension, diabetes mellitus, and thyroid disease.
Physical examination found vital signs within normal limits, good consciousness, and body mass index (BMI) 18.4 kg/m2. No signs of anemia and jaundice, no palpable tumor mass, and no lymphadenopathy were found. Thoracic, cardiac, and abdominal physical examinations were within normal limits. There was no extremity edema and abdominal ascites.
The results of laboratory tests are as follows: leukocytes 4,600/mm3, erythrocytes 3.35 × 106/mm3, hemoglobin 10.6 gr/dL, hematocrit 28.5%, platelets 99,000/mm3, MCV 85.1 pg, MCHC 37.0 gr/dL, neutrophils 76.9%, lymphocytes 20.1%, RBG 156 mg/dL, ALT 17 U/L, AST 14 U/L, creatinine 0.9 mg/dL, blood urea 26 mg/dL, sodium 117 mmol/L, potassium 3.2 mmol/L, clorida 83 mmol/L, and plasma osmolality 216 mMol/kg. Other examinations found normal electrocardiography and abdominal ultrasound within normal limit, except for cysts in the right kidney (6.5 × 5.7 mm). Histopathological examination of esophageal tumor tissue biopsy was moderate differentiation of invasive squamous cell esophageal carcinoma. Thoracic CT-scan impression was sicculer esophageal tumors as high as the middle third with a mark of adhesions with the posterior portion of the aorta, no metastasis to lymph nodes and lung. The impression of PET-CT scan results postradiotherapy was increased FDG uptake is seen at a long segment of the thoracic esophagus. In view of previous radiation, considerations include esophagitis versus residual tumor. No increase was seen at the right hilum. The previously seen coeliac axis node is much smaller and non-FDG-avid. There is no evidence of hypermetabolic hepatic metastasis. A tiny nodule in the lingula is nonspecific. Increased uptake is seen at the right parietal brain parenchyma. This may be related to recent fall versus metastasis.
Based on the history, physical examination, laboratory, and radiography investigation, the initial working diagnosis was esophageal carcinoma with SIADH. Management at that time was correction of hyponatremia with NaCl 3% based on the calculation of the patient's requirement. During treatment, the patient always complains of feelings of weakness, nausea but no vomiting, no appetite, headache, insomnia, and right chest pain that is temporarily improving by giving analgesics. There was no coughing and dyspnoea. Urine production per day was between 350 and 600 cc and irregularly defecating. On physical examination, blood pressure fluctuates within normal limits but once blood pressure reaches 160/100 mmHg, the patient has experienced a decrease in consciousness with laboratory results of sodium at that time: 108 mmol/L.
Laboratory results for four times electrolyte control tests after correction showed sodium levels of 108, 108, 122, and 112 mmol/L, respectively, never reached the normal levels although correction of sodium with 3% sodium based on the calculation of patient requirement was given repeatedly; low plasma osmolality and urine osmolality higher than the plasma osmolality were also found in this patient. Furthermore, the management of SIADH was given fluid restriction; hyponatremia was corrected with 3% sodium based on the calculation of the patient's requirement, injection of furosemide 40 mg intravenous daily, tetracycline 500 mg twice daily. We follow-up urine production daily, urine sodium, urine osmolality, and plasma osmolality.
The general condition of the patient improves; complaints often felt during hospitalization have diminished. Physical examination results: vital signs are within normal limits, and urine production increases around 1100 cc daily. Laboratory examination results: levels of sodium are 140 mmol/L. Results of urine examination are within normal limits (urine density: 1.010). The patient is permitted to outpatient with recommended continue oral therapy, calculate urine production daily, and electrolyte control.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [74, 'years'], 'weight': [7.0, 'kg'], 'Sodium': [140.0, 'mmol/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 74 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 7.0 kg. The concentration of sodium is 140.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 7.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
6092,38,Free Water Deficit,lab test,decimal,pmc-3044576-1,Extracted,"A boy aged 4 years and 7 months was admitted to the emergency room with a chief complaint of unsteady walking that had started 10 h earlier. He felt drowsy and dizzy and was hypoactive. Following the neurological symptoms, he had a large volume of watery diarrhea. Before that, he was in good health, with no history of neurological or metabolic disease, fever or abdominal pain.
On admission, the child was dehydrated, but had normal temperature and blood pressure. His weight was 17 kg (25th percentile), and his height was 108 cm (50th percentile). The physical examination showed moderate muscle hypotrophy, scarce adiposity, abdominal distention and no visceromegaly. The neurological examination showed unsteady walking, dysarthria, hand dysmetria and isochoric light reagent pupils. He had irritability and self-aggressive behavior. Glasgow coma scale was 15. Drug screening tests were negative.
The child was born at term; birth weight was normal, and he was breastfed until 5 months of age. From the age of 2, he had sporadic diarrhea controlled with a low-fiber diet and lactose-free milk, and a diagnosis of irritable bowel syndrome was made. Enteropathogenic agents and blood in the stools were absent on all occasions. Serology tests for antigliadin (AGA) and antiendomysium antibodies (EMA) IgA and IgG were negative for CD at ages 2 and 4.
Laboratory test results showed hyponatremia (133 mEq/L), hypokalemia (3.1 mEq/L), hyperchloremic metabolic acidosis (pH 7.2; bicarbonate: 7 mmol/L; BE: –19.9). Serum chloride was 122 mEq/L, and lactate (<2 mmol/L) and glucose (85 mg/dL) levels were normal. Blood tests were normal. Liver and kidney functions were normal (TGO: 46 U/mL; TGP: 35 U/mL; urea: 10 mg/dL; creatinine: 0.3 mg/dL). Levels of serum iron, ferritin, cholesterol and albumin were extremely low. Stool analyses revealed no parasites, rare leukocytes and erythrocytes; cultures were negative and no Clostridium difficile toxins were detected. Radiographs showed global abdominal distension; cranial magnetic resonance imaging (MRI), computed tomography (CT) scans and cerebrospinal fluid tests were normal. Both sleep and waking electroencephalograms were normal.
Similar episodes were observed four consecutive times at 1-week intervals. Before each admission, the child ingested large amounts of bread, cakes and pizza. In the first three hospital admissions, his neurological symptoms faded within 2 days, but the hyperchloremic metabolic acidosis persisted without any evident cause. He had received intravenous hydration and was placed on a low-fiber and hypoallergenic diet without gluten restriction. The need for bicarbonate and potassium chlorate was high, so it was suggested that the loss of potassium and bicarbonate was probably associated with fecal loss because his kidney function was normal. During his fourth admission, a complete investigation for malabsorption was carried out.
Fecal analysis revealed an increased loss of fats. Serum IgA EMA and IgA anti-tissue transglutaminase antibody (anti-tTG) was reagent, over 100 U/mL. CD was suspected. The mucosa magnified by endoscope showed microhemorrhage, reduction in duodenal folds and multiple erosions (). Histological examination showed partial and total villous atrophy, intraepithelial lymphocytes and increased length crypts (Marsh 3C) ().
After the introduction of a gluten-free diet, the child improved progressively, and a supplement of folic acid, iron and calcium was introduced.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [4, 'years', 7, 'months'], 'weight': [17.0, 'kg'], 'sex': 'Male', 'Sodium': [133.0, 'mEq/L']}",-0.51,-0.4845,-0.5355,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 4 years, and 7 months old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 17.0 kg. The concentration of sodium is 133.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 133.0 mEq. To convert from 133.0 mEq to mmol, convert from mEq to mmol. The compound 133.0 has a valence of 1, and so divide the valence by the value of mEq to get, 133.0 mEq/(1 mEq/mmol) = 133.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mEq sodium/L converts to 133.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 17.0 * (133.0/140 - 1) = -0.51 L. The patient's free body water deficit is -0.51 L."
6093,38,Free Water Deficit,lab test,decimal,pmc-8681225-1,Extracted,"A 48-year-old man with a past medical history of hypertension, alcohol dependence, macrocytic anemia (secondary to a well-established clinical entity of monoclonal gammopathy associated with B-cell lymphoma, with an elevated IgG kappa level of 1380 mg/dL on immunoelectrophoresis), and a smoking history presents to the emergency department with multiple complaints including severe weight loss, poor appetite, fatigue, and nonproductive cough with sinus drainage for the past month. According to the patient, he has lost around 50 pounds in the span of four to five months and has been complaining of early satiety for the past two months. The patient denied any abdominal pain, dysphagia, or odynophagia and denies any history of esophagogastroduodenoscopy (EGD) or colonoscopy in the past. The patient admits to drinking more than one pint of hard liquor a day for the past four years and has been smoking half a pack a day for the past 30+ years. The patient had no family history of cancer. The patient is a homosexual and has multiple sexual partners and does not use protection. During his visit to the emergency department, the patient had two episodes of vomitus with large bright red blood; the patient denies any history of varices or variceal bleeding.
Initially, the patient had a WBC count of 10.37 k/mcl (Normal: 4-11) with a hemoglobin of 4.8 g/dL (Normal: 13.5-17.5) and MCV of 117.5 fl (Normal: 80-100) with a platelet count of 72 k/mcl (Normal: 150-450). The patient's creatinine was 2.64 mg/dl (Normal: 0.70-1.5) with an unknown baseline with a sodium of 124 mmol/L (Normal: 135-145), potassium 3.1 mmol/L (Normal: 3.5-5.4), and alkaline phosphatase of 226 IU/L (Normal: 20-130) with AST of 94 IU/L (Normal: 0-45), and a total protein of 9.8 g/dL (Normal: 6.2-8.1). The patient's urine drug analysis was negative and tested negative for coronavirus/SARS-CoV-2 (COVID-19). Vital signs show a heart rate of 120 beats/minute and were afebrile, and the rest of the vital signs were within normal limits. Physical exam showed that the patient was cachectic but not in acute distress. No enlarged lymph nodes were appreciated. Cardiovascular examination showed S1 plus S2 with no audible murmurs, and lungs were clear to auscultation bilaterally. Gastrointestinal examination showed a soft, non-tender abdomen with positive bowel sounds. The patient had 5/5 strength in the upper and lower extremities. Rectal examination showed multiple genital warts, which were coliform in nature, and the guaiac test was negative for any bleeding. Initially, the chest x-ray showed no acute disease; however, an abdominal ultrasound showed fatty changes in the liver but was negative for any gallbladder pathology. Computed tomography (CT) scan of the abdomen/pelvis without contrast was initially done and was negative for any acute pathology. The patient was resuscitated with intravenous (IV) fluids and two units of packed red blood cells and was started on octreotide drip for possible variceal bleed. The patient subsequently underwent EGD for his hematemesis, and a friable, ulcerated circumferential mass lesion was seen in the distal esophagus extending from 28 to 40 cm from the incisors with active oozing that was seen from the mass (Figure , Panels A and B).
Multiple biopsies were obtained and sent to pathology. Oncology was subsequently consulted. Moreover, the patient’s syphilis screen was nonreactive, he had a normal thyroid-stimulating hormone (TSH) level, hepatitis panel was negative, and tested negative for cytomegalovirus (CMV). Furthermore, the patient was tested for HIV which was positive with a viral load of 219,000 cpy/mL, with appropriate HIV 1 genotyping. The absolute lymphocyte number was 0.93 k/mcl with an absolute CD4 T-helper count of 24 /mm3. The patient subsequently underwent CT of the chest abdomen pelvis with IV contrast, which demonstrated a distended esophagus to about 2.5-3 cm with an air-fluid level (Figure ) and a subcarinal mass-like encirclement of the esophagus with splaying of the carina and mass-effect along the left atrium and inferior pulmonary veins, measuring 7.36 x 5.38 cm in the greatest transverse and anterior/posterior dimensions (Figure ). Pathologic analysis of esophageal biopsy showed a diffuse perforation of the large, atypical cells associated with brisk mitotic activity consistent with plasmablastic lymphoma (Figure ). Immunohistochemical (IHC) stains were positive for CD79a, CD138, MUM-1, and CD10 (Figures -, respectively) and were negative for CD20, PAX-5, CD3, CD5, BCL6, BCL2, cyclin D1, CD30, anaplastic lymphoma kinase (ALK), and epithelial membrane antigen (EMA). C-MYC by immunohistochemistry was positive and in-situ hybridization for Epstein-Barr virus (EBV) was positive (Figure ). The patient also underwent a bone marrow biopsy, which showed hypercellular marrow with 90% cellularity and decreased trilineage hematopoiesis, plasma cells, histiocytes, and lymphocytes. Immunohistochemistry showed the CD-79a highlights with scattered B cells and numerous plasma cells, which were also highlighted by CD-138. Flow cytometry showed CD45-positive lymphocytes and was negative for CD20, CD10, CD 200, CD5, and lambda light chain. The patient was started on chemotherapy with dose-adjusted etoposide, prednisolone, vincristine, cyclophosphamide, doxorubicin (V-EPOCH) and highly active antiretroviral therapy (HAART) with Truvada and Dolutegravir. The patient underwent a total of six cycles of V-EPOCH with dose-adjusted cyclophosphamide due to elevated bilirubin and low CD4 counts. Therapy was complicated by multiple episodes of febrile neutropenia requiring hospitalization and severe peripheral neuropathy requiring multiple dose adjustments; however, the patient tolerated therapy generally well and is now discussing the option of allogeneic bone marrow transplantation.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [48, 'years'], 'weight': [50.0, 'lbs'], 'sex': 'Male', 'Sodium': [124.0, 'mmol/L']}",-1.55517,-1.47741,-1.63293,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 48 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 50.0 lbs so this converts to 50.0 lbs * 0.453592 kg/lbs = 22.6796 kg. The concentration of sodium is 124.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 22.6796 * (124.0/140 - 1) = -1.55517 L. The patient's free body water deficit is -1.55517 L."
6094,38,Free Water Deficit,lab test,decimal,pmc-3965956-1,Extracted,"A six-year-old female patient was admitted to the emergency room with her mother after four hours of disease characterized by nausea and vomiting of food content, abdominal pain, difficulty in breathing, salivation, headache, blurred vision, and psychomotor agitation. A physical examination found the following: weight 22 kg, blood pressure 80/60 mmHg, respiratory rate 32 breaths per minute, and heart rate 148 beats per minute.
Her skin was pale, and her eyes were sunken, underactive, clouded, and irritable to stimulus.
The patient was initially treated for severe dehydration resulting from food poisoning. However, with the development of wheezing and unresponsiveness to stimuli, she was transferred to the shock trauma unit for worsening respiratory distress, deep breathing with panting (Kussmaul) breathing, unresponsiveness to stimuli, Glasgow 10, to receive ventilator support.
The laboratory findings were as follows: yellow urine, specific gravity 1.025, pH 7.0, trace glucose, leukocytes 8−10x field, erythrocytes 2-3x field, the leukocyte blood count 8,180x mm3, segmented 69%, eosinophils 5%, lymphocytes 26%, Hb 12 g/dL, sodium 133 mEq/L, potassium 6 mEq/L, chloride 107 mEq/L, aspartate aminotransferase 4490 IU/L, alanine aminotransferase 8030 IU/L, and lactate dehydrogenase 2609 UI/L.
Arterial blood gases showed severe mixed acidosis, metabolic and respiratory with high anion gap (pH 6.9, PaO2: 108 mmHg, PaCO2: 26 mmHg, and HCO3: 3 mEq/L). We therefore assumed the possibility of diabetic ketoacidosis, salicylate poisoning, or methanol poisoning. Evaluation of renal function showed urea 33 mg/dL and creatinine 0.6 mg/dL; glucose was normal. Therapy was initiated with vigorous hydration with sodium chloride 9/1000 and supplemental intravenous sodium bicarbonate. The toxicology results showed a serum methanol of 1.47 mg/dL. Emergency hemodialysis therapy was initiated; the patient was dialyzed for an hour for two sessions.
The family gave us new information that the girl regularly took a drink called Kola Ingles. They stated that the patient had found a 250 mL pink perfume bottle and that she had ingested 200 mL of its contents, thinking it was the cola drink.
The patient improved progressively after hemodialysis with correction of her metabolic acidosis, liver function tests, and lactic dehydrogenase (Tables and ).
The child was discharged from the hospital in five days recovering full health.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [6, 'years'], 'weight': [22.0, 'kg'], 'sex': 'Female', 'Sodium': [133.0, 'mEq/L']}",-0.66,-0.627,-0.693,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 6 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 22.0 kg. The concentration of sodium is 133.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 133.0 mEq. To convert from 133.0 mEq to mmol, convert from mEq to mmol. The compound 133.0 has a valence of 1, and so divide the valence by the value of mEq to get, 133.0 mEq/(1 mEq/mmol) = 133.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mEq sodium/L converts to 133.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 22.0 * (133.0/140 - 1) = -0.66 L. The patient's free body water deficit is -0.66 L."
6095,38,Free Water Deficit,lab test,decimal,pmc-5641499-1,Extracted,"A 17-year-old girl (height, 150 cm; weight, 54 kg; body mass index, 24 kg/m2) presented with polyuria (7 L/day) and polydipsia for one year. She did not have an underlying disease, including diabetes, and denied the use of any medication. Initial urine osmolality was 113mOsm/kg H2O, and specific gravity was <1.005. Her vital signs were normal. Laboratory findings were as follows: white blood cells 5,700/mm3, hemoglobin 13.0 g/dL, and platelets 229 K/mm3; blood urea nitrogen 8.6mg/dL and creatinine 0.5 mg/dL; sodium 141mEq/L, potassium 4.1mEq/L, and chloride 107mEq/L; serum osmolality 282mOsm/kg; and urine sodium 33mEq/L, potassium 11.1mEq/L, and chloride 41mEq/L. Urine analysis revealed no hematuria or proteinuria. Following 6 h of fluid restriction, serum plasma osmolality reached 300mOsm/kg H2O, whereas urine osmolality was 108mOsm/kg H2O. shows that urine osmolality was increased by 427% from 108 to 557 mOsm/kg after vasopressin challenge. These remarkable changes in urine osmolality can be used to diagnose central diabetes insipidus. Figure () shows a well-defined hyper signal intensity sellar lesion without an enhanced portion on gadolinium-enhanced fat-suppressed T1-weighted imaging, suggesting Rathke's cleft cyst. Extensive examinations were performed to determine the pathological states of the patient's hypopituitarism(). Other abnormalities in the release and stimulation of other hormones were not detected. These findings indicate a sole diagnosis of central diabetes insipidus, possibly derived from the atypical occupation of a Rathke's cleft cyst at the pituitary stalk. The patient was discharged with desmopressin nasal spray (10 µg); her urine output was maintained at 2-3 L/day, and urine osmolality was >300 mOsm/kg. She was scheduled for follow-up magnetic resonance imaging (MRI), and pituitary surgery was postponed due to a personal matter.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [17, 'years'], 'weight': [54.0, 'kg'], 'sex': 'Female', 'Sodium': [141.0, 'mEq/L']}",0.23143,0.21986,0.243,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 17 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 54.0 kg. The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 54.0 * (141.0/140 - 1) = 0.23143 L. The patient's free body water deficit is 0.23143 L."
6096,38,Free Water Deficit,lab test,decimal,pmc-5343247-1,Extracted,"A 27-year-old African American male with a history of morbid obesity status post-Roux-en-Y gastric bypass 9 years prior presented with painful nonbloody mucoid diarrhea, icterus, and dark urine of four-day duration. He described recent travel with family to a beach resort in the United States during which he noted that two family members had developed a self-limited diarrheal illness. Three days after exposure, he noted abdominal cramps followed by hourly watery yellow stools without blood. He also had intermittent nausea and an episode of bilious vomiting and reports not eating since onset of diarrheal illness. He noticed a 17-pound weight loss over 1 week. He had no fevers, chills, or rash. There was no preceding history of eating uncooked fish or meats and he had no tick exposure. Medication history included Lisinopril and Amlodipine, and he denied any new medications or alcohol use. He admitted to homosexual intercourse.
He was acutely ill-looking with icteric sclera and dry mucus membranes. Vitals signs showed low-grade fever of 100.2°F and pulse rate of 126 beats per minute. Cardiac, lung, and skin examinations were unremarkable. Abdomen was diffusely tender with hyperactive bowel sounds without peritoneal signs.
Laboratory data was remarkable for leukopenia of 2200/μL, hemoglobin of 12.7 g/dL, normal platelet of 158,000/μL, sodium of 128 meq/L and potassium of 3.2 meq/L, acute kidney injury with creatinine of 1.59 mg/dL (baseline of 0.63 mg/dL), BUN of 41 mg/dL, and anion gap of 19. After intravenous hydration, hemoglobin dropped to 10.1 g/dL and platelet to 96,000/μL. Sodium, BUN, and creatinine also improved with rehydration. He was also noted to have elevated transaminases AST 201 IU/L and ALT 73 IU/L, elevated total bilirubin of 8.2 mg/dL, direct bilirubin of 4.4 mg/dL, normal alkaline phosphatase of 66 IU/L, albumin of 3.2 g/dL, normal lipase of 40 U/L, and elevated lactate of 3.5 meq/L. INR was elevated to 1.8; however, he had normal haptoglobin 236 mg/dL (36–195 mg/dL) and LDH 177 IU/L (normal: 94–202 IU/L). Hepatitis panel was negative. Patient also tested negative for HIV, CMV, EBV, and Parvovirus B19 infection. Tylenol level was normal. Urinalysis showed moderate bilirubinuria. Stool study was positive for Shigella sonnei but was otherwise negative for bacteria, ova, or parasites. Rickettsia rickettsii IgM was positive and he was treated with Doxycycline. Other workup for tick-borne infection including Lyme, Babesia, Ehrlichia, and Anaplasma was negative. Autoimmune workups including ANA, antismooth muscle, liver/kidney microsome, and mitochondrial antibodies were negative. Alpha-1 antitrypsin and ceruloplasmin were also normal.
Abdominal ultrasound showed a diffusely increased heterogeneous liver echogenicity with underlying hepatomegaly consistent with hepatic steatosis. Hepatoportal duplex showed patent portal vein and hepatic artery. Computed tomography of the abdomen and pelvis was significant for hepatic steatosis, hepatomegaly, mild right colitis, and absence of gallstones. Magnetic resonance cholangiopancreatography (MRCP) was unremarkable with normal intra- and extrahepatic biliary tree.
During his hospital course, bilirubin trended up to 9 mg/dL and INR peaked at 2.9. Patient was not encephalopathic. Given impending hepatic failure, recommendation was made to transfer the patient to a transplant center but he declined. He was treated with N-acetylcysteine. Blood culture initially reported as Gram-negative rods presumptively Escherichia coli (E. coli) was later confirmed to be Shigella sonnei. Urine culture remained negative. He was treated with ciprofloxacin based on sensitivity results with an improvement in diarrhea frequency and downward trend in transaminases. He remained stable and was discharged home on Day 8. He was doing well 4 months later with normal cell counts, normal liver, and kidney function.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [27, 'years'], 'weight': [17.0, 'lbs'], 'sex': 'Male', 'Sodium': [128.0, 'mEq/L']}",-0.39657,-0.37674,-0.4164,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 27 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 17.0 lbs so this converts to 17.0 lbs * 0.453592 kg/lbs = 7.71106 kg. The concentration of sodium is 128.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 128.0 mEq. To convert from 128.0 mEq to mmol, convert from mEq to mmol. The compound 128.0 has a valence of 1, and so divide the valence by the value of mEq to get, 128.0 mEq/(1 mEq/mmol) = 128.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 128.0 mEq sodium/L converts to 128.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 7.71106 * (128.0/140 - 1) = -0.39657 L. The patient's free body water deficit is -0.39657 L."
6097,38,Free Water Deficit,lab test,decimal,pmc-3371495-1,Extracted,"A 70-year-old obese woman (weight=85 kg, body mass index=33.2 kg/m2) was admitted to our institute with a history of cough, cold and breathlessness since 10 days. She was on antibiotics prescribed by the primary physician. On examination in the emergency department, she was conscious, drowsy, tachypneic (respiratory rate=45/min) and cyanosed. Her pulse rate was 136/min, blood pressure was 170/110 mmHg, arterial oxygen saturation measured by pulse oximeter was 78% and heart sounds were muffled on auscultation. The respiratory system examination showed a grossly reduced bilateral air entry with silent chest. She was a known diabetic for the past 20 years and was currently on treatment with insulin. She was on Tab. Ramipril 2.5 mg once daily for essential hypertension for the past 10 years. She was a biopsy-proven case (hilar lympadenopathy) of sarcoidosis with interstitial lung disease and COPD, for which she was on salbutamol and budesonide metered-dose inhaler. There was no history of smoking. Quinidine had been used 10 years back for treating ventricular tachycardia but, presently, she did not need treatment for the same. Coronary angiography performed at that time failed to reveal any perfusion-related problem. On further enquiry, her husband revealed that she used to sleep in a sitting position for the past 6 months. Her recent travel history included visits to places with a high risk of Swine flu (H1N1).
She was administered O2 12 L/min by a non-rebreathing mask, salbutamol nebulization, intravenous deriphylline and hydrocortisone. Her initial blood gas analysis showed pH=7.13, PaO2=111 mmHg, PaCO2=47.6 mmHg, bicarbonate=14, base deficit=–13, oxygen saturation=95.7%, Na+=131 meq/L and K+=5.89 meq/L. A chest X-ray showed diffuse infiltrates in both the lung fields. After about 45 min, she developed severe bradycardia followed by cardiac arrest and one episode of convulsion. She was successfully resuscitated and put on mechanical ventilation with pressure control mode and dopamine infusion (5 μg/kg/min). She was shifted to the surgical intensive care unit (SICU) for further management.
Possibility of Swine flu, community-acquired pneumonia and infection by atypical organisms was considered at this stage. Samples for bacterial and viral (H1N1) culture were taken from the throat, nasopahrynx, trachea and blood. Right subclavian central venous and radial artery catheters were secured. Central venous pressure and invasive blood pressure monitoring were initiated. Broad-spectrum antibiotics, bronchodilators, oseltamavir (75 mg twice daily for 5 days through a nasogastric tube), methyl prednisolone (125 mg intravenously, thrice daily), low-molecular weight heparin and sedation were started. She developed two episodes of severe bronchospasm on separate occasions following tracheal suctioning that required treatment with inhaled salbutamol, ipratropium bromide, adrenaline and infusion of intravenous lignocaine and magnesium sulphate. Results of the laboratory tests ruled out H1N1 infection.
On the 4th day, her blood gas improved (pH=7.37, PaO2=70 mmHg, PaCO2=44 mmHg, bicarbonate=24, base deficit=–0.4 and oxygen saturation=93% on 50% O2 with PEEP=8 cmH2O). Her chest X-ray showed bilateral pericardiac/perihilar interstitial inhomogeneous opacities with waxing/waning airspace consolidation. The oral endotracheal tube was changed to nasal; she was weaned from sedation and ventilation and put on pressure support ventilation. On the 6th day, the trachea was extubated and she was put on non-invasive ventilation, which she tolerated only for 2 h. She was reintubated and put back on mechanical ventilation. A surgical tracheostomy was performed on the next day in view of anticipated difficulty in weaning and for better pulmonary care. Six days after the tracheostomy, the tube was changed to a silicon tracheostomy tube. Aggressive chest physiotherapy was started. On the 11th day, the chest X-ray showed segmental collapse of the right lower lobe. The tracheal aspirate grew Acinetobacter, and antibiotics were changed accordingly. An echocardiography showed concentric left ventricular hypertrophy, moderate pulmonary artery hypertension (56 mmHg) and 60% left ventricle ejection fraction.
She was successfully weaned from the ventilator and put on T-piece on the 18th day and transferred to the ward 4 days later after decannulating tracheostomy. Three days later, she started developing intermittent stridor on exertion. She was evaluated for the cause of stridor. An indirect laryngoscopy showed a normal upper airway and vocal cords. A lateral neck X-ray showed soft tissue swelling in the region of thyroid gland and tracheal narrowing just below the site of the tracheostomy. The computed tomography (CT) scan [Figures and ] demonstrated a short segment narrowing of the trachea (luminal caliber 0.8 cm × 0.7 cm) just distal to the partially closed tracheostomy stoma. There appeared a definitive bulge into the tracheal lumen at the above-mentioned region, both from the anterior as well as the posterior walls. An abnormal thyroid encircling the trachea (above the stoma) was also noted without any tracheal narrowing at that level.
She was shifted to another centre which dealt with tracheal problems. She developed severe stridor there and had to be intubated emergently. She was subjected to a bronchoscopic evaluation, which showed a long-segment tracheomalacia up to the carina with dynamic collapse of the anterior tracheal wall. The patient was offered the option of tracheal stenting or conservative management, but the relatives of the patient opted for the latter. At the time of writing this report (1 year later), the patient was on conventional T-tube and was doing well at home. The patient gave consent for publishing this report.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [70, 'years'], 'weight': [85.0, 'kg'], 'sex': 'Female', 'Sodium': [131.0, 'mEq/L']}",-2.45893,-2.33598,-2.58188,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 70 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 85.0 kg. The concentration of sodium is 131.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 131.0 mEq. To convert from 131.0 mEq to mmol, convert from mEq to mmol. The compound 131.0 has a valence of 1, and so divide the valence by the value of mEq to get, 131.0 mEq/(1 mEq/mmol) = 131.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 131.0 mEq sodium/L converts to 131.0 mmol sodium/L. Plugging in these values into the equation, we get 0.45 * 85.0 * (131.0/140 - 1) = -2.45893 L. The patient's free body water deficit is -2.45893 L."
6098,38,Free Water Deficit,lab test,decimal,pmc-8296630-1,Extracted,"A 53-year-old Asian man presented to us with a 7-day history of fever and tremor, and was admitted to our hospital. The symptoms had persisted/become worse despite treatment with cefditoren pivoxil and acetaminophen for 6 days, and levofloxacin and loxoprofen for 3 days prior to the hospitalization. Two days prior to admission, he had developed generalized malaise, which was sufficiently severe to cause difficulty in walking, and blood tests, chest X-ray examination, whole-body CT, and head CT had been performed at another hospital. The cause of the patient’s symptoms, however, remained unclear. Thereafter, he developed hiccups.
On admission, he complained of persistent generalized fatigue, tremor, and hiccups. He did not have any headache or altered sensorium. His height was 174.5 cm and body weight was 72.0 kg. His body temperature was 36.5 °C at admission, and he remained afebrile while in hospital. His blood pressure was 117/77 mmHg, and pulse rate and respiratory rate were 109 beats/minute and 20 breaths/minute, respectively, both regular rhythm. There were no significant gastrointestinal symptoms, respiratory symptoms, dry skin, or xerostomia. There was no edema or evidence of dehydration. Neurologically, the patient exhibited intention tremor, ataxic gait, and dysmetria on both the finger–nose test and knee–heel tests. Notably, there was no quadriplegia (manual muscle testing revealed full power), sensory disorder, headache, photophobia, or signs of meningeal irritation, including nuchal rigidity, positive Kernig’s sign, or positive Brudzinski’s sign. Laboratory examinations revealed a white blood cell count (WBC) of 8900/μL, red blood cell count of 506 × 104/μL, hemoglobin level of 15.7 g/dL, and platelet count of 20.3 × 104/μL. Serum C-reactive protein level was 0.04 mg/dL. Blood urea nitrogen level was 15 mg/dL, serum creatinine was 0.79 mg/dL, and estimated glomerular filtration rate (eGFR) was 80.3 mL/minute/1.73 m2. These results indicated absence of any inflammation or renal dysfunction. Serum electrolyte levels were Na 123 mEq/L, K 3.9 mEq/L, and Cl 86 mEq/L. Plasma osmolarity was 255 mOsm/kg H2O, while urinalysis revealed a urinary Na level of 87 mEq/L and urinary osmotic pressure of 691 mOsm/kg H2O. The serum ADH level was 1.6 pg/mL, suggesting that inappropriate secretion of ADH was responsible for the excessive excretion of sodium and hypotonic hyponatremia. Measurement of the serum hormone levels showed a plasma adrenocorticotropic hormone (ACTH) concentration of 30.7 pg/mL (normal range 7.4–55.7 pg/mL), cortisol concentration of 14.5 μg/mL (4.5–21.1 μg/mL), thyroid-stimulating hormone (TSH) concentration of 0.397 μIU/mL (0.2–5.0 μIU/mL), free thyroxine (FT4) concentration of 1.38 ng/dL (0.70–1.48 ng/dL), free triiodothyronine (FT3) concentration of 2.29 (1.71–3.71 pg/mL), aldosterone concentration of 98.4 pg/mL (29.9–159 pg/mL), and plasma renin activity of 0.9 ng/mL/hour (0.3–2.9 ng/mL/hour). Thus, there was no evidence of adrenal dysfunction. The physical and laboratory findings were consistent with the diagnosis of SIADH.
The results of the chest X-ray examination, fundus photographs, contrast-enhanced whole-body CT, contrast-enhanced head CT, and gadolinium-enhanced head magnetic resonance imaging revealed no potential cause for the SIADH. Serum levels of neuron-specific enolase and progastrin-releasing peptide, both small lung carcinoma makers, were within normal limits, and the T-SPOT.TB test, a test for tuberculosis infection, was also negative. 18F-FDG PET-CT revealed an area of tracer accumulation along the cervical cord (Fig. , arrow). Based on this PET-CT finding, meningitis was suspected. Examination of the cerebrospinal fluid (CSF) revealed the following findings: cell count 302 cells/3 μL (most were mononuclear cells); total protein 211 mg/dL; albumin 1323 µg/mL; glucose 49 mg/dL; β2-microgroblin 8447 ng/mL (440–1240 ng/mL); immunoglobulin G (IgG) 16.6 mg/dL (1–3 mg/dL); IgG index 0.61 (< 0.73); adenosine deaminase 10.2 U/L (< 9.0 U/L); myelin basic protein 175.1 pg/mL (< 102 pg/mL); no oligoclonal band detected. No organisms were detected on Gram staining or culture of the CSF. We considered these findings as being diagnostic of aseptic meningitis or partially treated meningitis, in particular, the findings that the cells were predominantly composed of mononuclear cells and that there was no apparent evidence of bacterial infection or underlying autoimmune diseases such as systemic lupus erythematosus and Behçet’s disease as the cause of the meningitis/encephalitis.
Although both intravenous infusion of physiological saline for a day and oral administration of sodium chloride were started, the serum sodium level remained below 125 mEq/L, and improved only after fluid restriction to 800 mL/day (Fig. , arrow) and initiation of treatment with tolvaptan 7.5 mg/day (Fig. ). Thereafter, the serum sodium level remained stable (at least until 4 months after admission). Aseptic meningitis was suspected as the cause of the tremor and hiccups. Baclofen 15 mg/day and clonazepam 1 mg/day were administered as symptomatic treatment for the hiccups and tremor, respectively. The hiccups rapidly resolved in response to this treatment, and the tremor tended to improve after the dosage of clonazepam was increased to 2 mg/day. A repeat CSF examination performed on day 22 before discharge of the patient confirmed a reduction of the CSF cell count to 125/3 μL from 302/3 μL, the latter count recorded in the earlier examination. Thus, our patient showed spontaneous partial remission of the aseptic meningitis. The administration of tolvaptan, baclofen, and clonazepam was gradually reduced after discharge and discontinued by a month after discharge. At 4 months after discharge, the symptomatic improvement was maintained. Throughout the observation period of 4 months, normonatremia was maintained without further treatment with tolvaptan.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [53, 'years'], 'weight': [72.0, 'kg'], 'Sodium': [123.0, 'mEq/L']}",-5.24571,-4.98342,-5.508,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 53 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 72.0 kg. The concentration of sodium is 123.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 123.0 mEq. To convert from 123.0 mEq to mmol, convert from mEq to mmol. The compound 123.0 has a valence of 1, and so divide the valence by the value of mEq to get, 123.0 mEq/(1 mEq/mmol) = 123.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 123.0 mEq sodium/L converts to 123.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 72.0 * (123.0/140 - 1) = -5.24571 L. The patient's free body water deficit is -5.24571 L."
6099,38,Free Water Deficit,lab test,decimal,pmc-4826363-1,Extracted,"A 41-year-old man with a history of liver cirrhosis caused by non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC) within the Milan criteria was referred to our hospital for possible living donor liver transplantation (LDLT) from his healthy 35-year-old brother. The patient was obese from childhood, with a peak body weight of 140 kg. He had been treated for HCC by radiofrequency ablation 2 years earlier and by transarterial chemoembolization 5 months earlier. Laboratory data included white blood cell count 3320/mL, hemoglobin 12.6 g/dL, platelet count 5.6 × 104/mL, total protein 6.4 mg/dL, albumin 2.7 g/dL, creatinine 0.87 mg/dL, total bilirubin 3.7 mg/dL, aspartate aminotransferase (AST) 91 U/L, alanine aminotransferase (ALT) 53 U/L, sodium 137 mEq/L, ammonia, 135 mg/dL, and prothrombin time 32 %. The patient was classified as Child-Pugh grade C with 11 points, and his model for end-stage liver disease score was 20. He was negative for hepatitis B surface antigen and antibody to hepatitis C virus. Tumor markers included α-fetoprotein 5.1 ng/mL and PIVKA-II 10,848 U/mL.
Laparotomy revealed a cirrhotic liver and an enlarged spleen. The recipient’s liver was removed, and the donated right lobe graft was implanted. The graft weight was 798 g, corresponding to 57.4 % of the recipient’s standard liver weight. Splenectomy was also performed. The total operating time was 819 min, and total blood loss was 3450 mL. There are three hepatocellular carcinomas in the resected specimen. The largest tumor size was 20 mm in diameter. Histological examination showed a well-differentiated hepatocellular carcinoma growing in trabecular and focally pseudo-glandular patterns. The surrounding liver tissues showed micronodular cirrhotic change with mild chronic inflammatory infiltrate the fibrous stroma (A1F4) with 5 % macrovesicular steatosis, which was compatible with burn-out NASH.
On the day of surgery, the patient received transfusions of 20 units of red blood cell concentrates, 12 units of fresh frozen plasma, and 20 units of platelet concentrate. On postoperative day (POD) 1, he was transfused with 16 units of fresh frozen plasma and 20 units of platelet concentrate. Subsequent transfusions included four units of fresh frozen plasma on POD 2, two units of red blood cell concentrate on POD 9, and four units of red blood cell concentrate on POD 13 (Table ).
Following LDLT, immunosuppression was started, including tacrolimus, mycophenolate mofetil, and steroids. The patient was discharged from the hospital on POD 22. Treatment with mycophenolate mofetil was discontinued on POD 32. His liver-enzyme became elevated (AST 46 U/L, ALT 56 U/L, total bilirubin 0.5 mg/dL) on POD 60. Immunosuppression was maintained including tacrolimus to the trough of 10 to 15 ng/mL and prednisolone 5 mg/day. At the same time, nationwide survey to clarify the presence of HEV infection after liver transplant in Japan was started and his blood samples taken on POD 81 showed positive for HEV RNA and IgG and IgM antibodies to HEV. To determine the time of HEV infection, stored blood samples taken just before transplantation and on PODs 1, 3, 7, and 14 were assayed for the presence of HEV RNA and anti-HEV antibodies. Blood samples from the donor were also assayed to determine whether infection was graft mediated. These assays showed that the patient first became positive for HEV RNA on POD 3, remaining positive thereafter. The donor sample was negative for anti-HEV antibodies and HEV RNA (Fig. ).
The transplantation protocol of our institution does not permit patients to ingest raw meat or raw fish until 1 year after LDLT. This patient had not ingested such foods after LDLT, precluding the likelihood of foodborne infection with HEV.
Eliminating the possibilities of donor and foodborne sources of HEV suggested that this patient may have become infected through a blood transfusion. Assays of the transfused samples, supplied by Fukuoka Prefecture Red Cross Blood Center, showed that HEV RNA was present in the platelet concentrate transfused into this patient on POD 1 (lot number 5020364476).
The genomic sequences of the HEV strain detected in the patient and the transfused platelet concentrate were compared. Sequences compared included a 326-nucleotide (nt) 5′-terminal region of the open reading frame (ORF)1, a 505-nt region of the proline-rich hinge (V) domain within the ORF1, and a 412-nt region of the ORF2. The two strains differed by one nt in the ORF1 and by two nts in the V domain, but their ORF2 sequences were identical.
Phylogenetic analysis of the HEV strains, conducted according to the previously described method [], revealed that the HEV strains in the transfused sample, and the patient were both classifiable into genotype 3 (subgenotype 3b) (Fig. ). These two isolates were closest to an HEV strain (95.6 % identity) isolated from a wild boar that had been captured in Saga Prefecture on Kyushu Island of Japan. These findings suggested that the source of infection was HEV strains circulating on Kyushu Island, Japan.
Treatment with steroids was decreased gradually and discontinued on POD 150. Thereafter, immunosuppressive therapy was done with tacrolimus monotherapy and the dosage was reduced to the target trough of 5–10 ng/mL. The patient remained positive for both HEV RNA and anti-HEV antibodies on POD 284, more than 6 months after diagnosis of HEV infection. Although a liver biopsy was not obtained, this patient was considered a chronic carrier of HEV. Treatment with ribavirin 800 mg/day was started on POD 327. AST and ALT became normal on POD 382, and he became negative for HEV RNA on POD 417. The therapy was done until POD 467. HEV RNA remained negative on POD 536.
Chronic hepatitis E is characterized by mild derangement in liver enzymes, persistently detectable HEV RNA in serum and stool for >3 months, delayed/absent HEV seroconversion, and histological features of chronic viral hepatitis, such as dense lymphocytic periportal infiltrates with piecemeal necrosis []. Screening for HEV RNA in the sera of liver transplant recipients showed that the prevalence of HEV infection in Europe was <1 % [, ].
The inability to clear HEV viremia is directly related to the degree of immunosuppression of these patients at the time of infection. Therefore, infections that occur shortly after transplantation and rejection episodes, and when patients have low total lymphocyte counts, are more likely to become chronic. Treatment with tacrolimus, as opposed to cyclosporine, was also shown to be a risk factor for chronic HEV in posttransplant patients []. Our immunosuppression strategy was initiated using a protocol based on either tacrolimus (Prograf; Astellas Pharma, Tokyo, Japan) or cyclosporine A (Neoral; Novartis Pharma K.K., Tokyo, Japan) with steroids with or without mycophenolate mofetil. The target tacrolimus trough concentration was set at 10 ng/mL for 3 months after LDLT and 5–10 ng/mL thereafter. The target trough concentration of cyclosporine A was set at 250 ng/mL for 3 months after LDLT and 150–200 ng/mL thereafter. Methylprednisolone was initiated on the day of LDLT, after which the dosage was tapered and prednisolone substituted for 7 days after LDLT. Prednisolone treatment was tapered and discontinued 6 months after LDLT. Mycophenolate mofetil was beginning with 1–2 g/day on the day after LDLT; the dosage was tapered and discontinued 6 months after LDLT. In this case, immunosuppression including tacrolimus might have influenced the chronicity of HEV infection.
Chronic HEV infection is frequently related to the consumption of undercooked pork or, in some cases, mussels or game meat []. Transmission of HEV via an infected liver graft has also been reported []. Transfused blood products are another potentially important mode of acquisition. In the UK, it was recently estimated that one in 2848 blood donors has hepatitis E viremia at the time of donation []. The first case of HEV infection via a blood transfusion in Japan was reported in 2004 []. A nationwide survey of the prevalence of HEV infection in Japan showed that 431 (3.4 %) of 12,600 donated blood samples were positive for anti-HEV IgG []. Although all donated blood samples are not checked for HEV, samples donated on Hokkaido Island are assayed by PCR amplification of HEV specific sequences, as the prevalence of acute hepatitis E is higher in Hokkaido than elsewhere in Japan []. In the present, screening of donated blood for HEV has only been conducted in the Hokkaido area. Patients receiving transfusion include many immunocompromised patients, so screening of blood donors for HEV in other areas in Japan is probably desirable.
Immunocompromised patients diagnosed with hepatitis E should be closely followed up, with regular monitoring of blood HEV RNA viral load, liver function tests, and liver stiffness. Delay in the management of persistent viremia should be minimized due to the potentially rapid onset of irreversible liver injury. Reduction in immunosuppression should be considered for patients with HEV viremia persisting for more than 3 months. In a previous study, reduction in immunosuppression, especially of calcineurin inhibitor, led to HEV clearance in one third of patients []. The remaining two third patients required antiviral therapy. If viremia still persists, treatment with ribavirin should be considered, as ribavirin monotherapy results in a sustained virological response rate of 78 % in patients with chronic hepatitis E [].",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [41, 'years'], 'weight': [140.0, 'kg'], 'sex': 'Male', 'Sodium': [137.0, 'mEq/L']}",-1.8,-1.71,-1.89,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 41 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 140.0 kg. The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 140.0 * (137.0/140 - 1) = -1.8 L. The patient's free body water deficit is -1.8 L."
6100,38,Free Water Deficit,lab test,decimal,pmc-6537048-1,Extracted,"A 78-year-old Hispanic female with a significant past medical history of type 2
diabetes mellitus, hypertension and hypothyroidism presented with altered mental
status. She was brought to the emergency department by her family members who
assisted with history gathering. According to her family, the patient had a cough
and worsening shortness of breath over 3 days prior to admission unrelieved by
over-the-counter antihistamine and antitussive medications. The family did not know
how long she had been diabetic or hypertensive. Nor could they list her medications.
Upon presentation she was lethargic, had labored breathing and was lying in bed
shaking. Her blood pressure was 142/67 mmHg in the supine position, heart rate
114 bpm, axillary temperature 36.7°C and she weighed 51.7 kg. On physical
examination, she was ill-appearing, obtunded, not following verbal commands and with
Glasgow coma scale of 9. She had decreased breath sounds over the left lung lower
field. The examination of the heart, abdomen and extremities was normal. On
neurological examination, she had hyperreflexia at the patellar and ankle joints, as
well as stimulated bilateral clonus and positive Babinski sign. The screening blood
tests performed upon her admission to the hospital were consistent with severe HHS.
Her initial laboratory findings revealed glucose 635 mg/dL (normal: 70–105), sodium
175 mEq/L (corrected Na: 188 mEq/L) (normal: 135–145 mEq/L), blood urea nitrogen
(BUN) 76 mg/dL (normal: 6–20 mg/dL), creatinine 1.61 mg/dL (normal: 0.5–1.2 mg/dL)
with a serum osmolality 410 mOsm/kg (normal: 280–300 mOsm/kg). Her urine ketones
were negative. On arterial blood gas her pH was 7.43, and HCO3 29 mEq/L
(normal: 22–29). Her initial hemoglobin (Hgb) was 16.8 g/dL, white blood cell count
(WBC) 18.3 × 103/µL and platelet count 194 × 103/µL. The
initial chest X-ray and noncontrast head computed tomogram (CT) were negative with
the head CT showing only mild diffuse cortical atrophy, proportional to the size of
the ventricular system. The calculated water deficit on admission was about 5.5 L.
In the emergency department, aggressive fluid resuscitation for volume replacement
was started using normal saline (NS), which initially caused worsening in sodium
values to 180 mEq/L (corrected Na: 193 mEq/L). After 2 L of NS, WBC was
23.2 × 103/µL, Hgb was 15.1 g/dL, platelet was
160 × 103/µL and her HCO3 was within normal limits in our
laboratory at 28 HCO3 mEq/L. She was admitted to the intensive care unit
(ICU), and nephrology was consulted. She was started on 0.45% NS and subsequently
switched to 5% dextrose in water. The sodium began to trend down, while maintaining
a mean steady decrease of 6 mEq/L of sodium daily, resulting in desired sodium range
within 5 days ().
An insulin drip was placed to control the severe hyperglycemia, which resolved
steadily over the first 48 h. The insulin drip was discontinued, and insulin
glargine with correctional insulin lispro was started. An abdominal pelvic CT was
negative. Due to her neurological findings, a continuous EEG (cEEG) was ordered,
which showed left frontocentral and temporal PLEDs on day 1. By day 2, the cEEG
showed only abnormal slowing without epileptiform discharges. During the
hospitalization, a nasogastric tube was placed and tube feeds were started due to
her poor mentation. Her kidney function improved and returned to baseline. She was
also found to have a left lower lobe infiltrate and was treated for community
acquired pneumonia. She was initially treated with ceftriaxone and azithromycin;
however, over the hospital course she clinically improved and was switched over to
oral cephalexin to finish the course. Her mental status improved and returned back
to baseline. In order to prevent potential aspiration, she underwent a successful
swallow study with modified barium and was started on regular diabetic diet. She
stayed in the hospital for 7 days and was diagnosed with severe hypernatremia
secondary to osmotic diuresis and dehydration from HHS. Her hemoglobin A1c was found
to be 9.9%, and upon discharge, she was placed on metformin, insulin glargine and
insulin lispro sliding scale. Due to her decline in functional status and
deconditioning, she was discharged to a skilled nursing facility. She received
diabetes teaching, which included lifestyle modifications, proper nutrition, insulin
administration and glucose checks. Unfortunately, there was no good follow-up with
the patient, because she returned to her home abroad.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [78, 'years'], 'weight': [51.7, 'kg'], 'sex': 'Female', 'Sodium': [175.0, 'mEq/L']}",5.81625,5.52544,6.10706,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 78 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 51.7 kg. The concentration of sodium is 175.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 175.0 mEq. To convert from 175.0 mEq to mmol, convert from mEq to mmol. The compound 175.0 has a valence of 1, and so divide the valence by the value of mEq to get, 175.0 mEq/(1 mEq/mmol) = 175.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 175.0 mEq sodium/L converts to 175.0 mmol sodium/L. Plugging in these values into the equation, we get 0.45 * 51.7 * (175.0/140 - 1) = 5.81625 L. The patient's free body water deficit is 5.81625 L."
6101,38,Free Water Deficit,lab test,decimal,pmc-3676995-1,Extracted,"An 18-year-old Caucasian female reported to the emergency service of our hospital in week 33 + 4 of her first pregnancy due to severe pain of sudden onset, located in the epigastric and left hypochondriac zone. The pain was described as continuous but with exacerbations. Previously the patient had been asymptomatic, with normal bowel habits, though upon questioning she explained that in the last two days the stools had been somewhat looser and scarcer than usual.
Before this episode the patient had been healthy, with normal menstruation and no medical or surgical antecedents of interest. Pregnancy up until that point had been normal. Upon admission, she weighed 52 kg, measured 155 cm in height, and had gained 10 kg in the course of pregnancy.
The vital functions were normal, with a temperature of 36°C and blood pressure 125/51 mmHg. Physical examination revealed a soft abdomen with pain in response to palpation in the epigastric and left hypochondriac zone but no signs of peritonism. The gynecological examination was normal, and the uterine cervix showed no modifications. The obstetric ultrasound findings were also normal, showing a fetus with longitudinal, cephalic presentation. The ultrasound measurements were consistent with dates, with normal placental insertion and amniotic fluid in normal quantities. The cardiotocographic recordings showed a reactive pattern with no contractions.
A peripheral venous catheter was inserted to administer analgesics, obtaining a very limited response. After the first hours of observation the pain proved more intense, irradiating to the subcostal region and left side of the chest. The blood tests showed a leukocyte count of 15,480 cells/mm3 (82.3% neutrophils), 10.9 g/dL hemoglobin and 269,000 platelets/mm3. The biochemical study was normal, with Na 143 mEq/L, K 4.2 mEq/L, and Cl 107 mEq/L. The transaminase, alkaline phosphatase, and amylase levels were within normal limits. Urine testing likewise showed no alterations.
Abdominal ultrasound initially revealed no renal or liver alterations. The chest X-ray study showed left hemi-diaphragmatic elevation secondary to abundant abdominal gas in the splenic angle of the colon, with normal lung parenchyma and no alterations of the cardiomediastinal silhouette ().
A rectal tube accompanied by postural changes and spasmolytic agents did not facilitate evacuation of the gas. Given the gradual worsening of the pain, a plain X-ray study of the abdomen was carried out, revealing notorious displacement of the gravid uterus to the right, important dilatation of the jejunal loops, and a redundant descending colon containing abundant gas. Colon obstruction was noted at pelvic level, consistent with obstructive ileus secondary to impaction of the fetal head in the dextroflexed uterus ().
Nasogastric intubation likewise failed to lessen the pain or facilitate intestinal evacuation. The general condition of the patient deteriorated as a result of intense pain. Accordingly, after 5 hours without improvement, and in view of the risk of bowel perforation as a result of the intense intestinal dilatation, we decided to perform an exploratory laparotomy, with possible fetal extraction. Betamethasone (one 12 mg dose) was administered to favor fetal pulmonary maturation. Surgery confirmed the presence of a dextroflexed uterus rotated about 90 degrees to the right, causing impaction of the head of the fetus over the sigmoid portion of the colon, compressing the lumen and producing the obstruction. There were no adherences or ischemic areas in the bowel loops suggesting other possible causes of obstruction. Cesarean section was performed, delivering a male weighing 1940 grams and with an Apgar score of 8/9.
The puerperal course was favorable, and 72 hours after cesarean section the patient presented complete intestinal transit, allowing us to remove the nasogastric tube and resume oral feeding (). The subsequent digestive study after puerperium did not reveal any intestinal pathology.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [18, 'years'], 'weight': [52.0, 'kg'], 'Sodium': [143.0, 'mEq/L']}",0.55714,0.52928,0.585,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 18 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 52.0 kg. The concentration of sodium is 143.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 143.0 mEq. To convert from 143.0 mEq to mmol, convert from mEq to mmol. The compound 143.0 has a valence of 1, and so divide the valence by the value of mEq to get, 143.0 mEq/(1 mEq/mmol) = 143.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mEq sodium/L converts to 143.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 52.0 * (143.0/140 - 1) = 0.55714 L. The patient's free body water deficit is 0.55714 L."
6102,38,Free Water Deficit,lab test,decimal,pmc-4396541-1,Extracted,"A 67-year-old man was admitted with epigastric pain. At the time of the admission, blood pressure was 100/60 mmHg, pulse was 92 beats/min, respiratory rate was 20 breaths/min, and temperature was 37.2°C. The patient was referred to our hospital with general weakness and a weight loss of 10 kg for the last 3 months. Mild epigastric tenderness was revealed during physical examination.
His laboratory tests revealed anemia with hemoglobin of 7.6 g/dL and leukocytosis with white blood cell count of 18,380/mm3. A comprehensive metabolic blood panel revealed a low albumin level of 2.5 g/dL, low sodium of 130 mEq/L, increased AST/ALT of 131/117 IU/L, and increased alkaline phosphatase of 539 IU/L. Renal functions were normal.
An electrocardiogram revealed right bundle branch block, with no changes compared to the previous exam. The levels of creatine kinase MB and troponin-I were normal.
Abdominal computed tomography (CT) revealed a heterogeneous left adrenal mass 6 cm in diameter, accompanied by hemorrhaging ().
Hormonal testing through 24 h urine collection showed the following results: epinephrine: 4.8 μg/day (range, 0~20); norepinephrine: 52.1 μg/day (range, 15~80); 17-ketosteroid: 5.76 mg/day (range, 10~25); and metanephrine: 0.47 mg/day (range, 0~1.3).
The levels of urine vanillylmandelic acid (VMA), 10.42 mg/day (range, 0~8), and urine-free cortisol, 491.4 μg/day (range, 55.5~286), were elevated. In addition, plasma ACTH, <1.0 pg/mL (range, 7.2~63.3), was suppressed, with normal plasma renin activity and aldosterone levels. With the suppression of ACTH and the elevation of urine-free cortisol, we performed a low-dose dexamethasone suppression test to check for Cushing's syndrome. The plasma cortisol level (6.13 μg/dL) showed no suppression at the end of test. We interpreted these results as subclinical Cushing syndrome because he had no symptoms or signs of Cushing's syndrome. 123I-Metaiodobenzylguanidine (123I-MIBG) scintigraphy was performed to check for the presence of pheochromocytoma. For this purpose, 3 mCi of 123I-MIBG was injected and whole body images were obtained after 6 h and after 24 h. From the 24 h images, eccentric uptake by a large left adrenal gland mass was confirmed (Figures and ). On the image of 123I-MIBG SPECT/CT, left adrenal gland tumor showed 123I-MIBG uptake in the peripheral portion ().
During preparation of surgery for suspected subclinical Cushing's syndrome and pheochromocytoma, chest X-ray and chest CT () confirmed metastatic lymphadenopathy of the mediastinum. PET-CT () and endobronchial ultrasound transbronchial needle aspiration (EBUS-TBNA) were also performed. From the lymph node biopsy obtained by EBUS-TBNA, metastatic carcinoma of unknown origin was suspected, and surgery was prepared in suspicion of malignant pheochromocytoma or adrenocortical carcinoma, accompanied by metastatic lymphadenopathy.
Starting from 2 weeks prior to the surgery, phenoxybenzamine and propranolol were administered. Laparoscopic left adrenalectomy was performed. The resected tumor measured 8.5 × 7.5 × 5.1 cm; central necrosis and hemorrhaging were present, with involvement of the resection margins (). Microscopically, the tumor revealed a solid sheet arrangement composed of pleomorphic cells. Tumor cells had enlarged pleomorphic nuclei with prominent nucleoli and abundant cytoplasm, while some cells show rhabdoid features with abundant eosinophilic cytoplasm and eccentric nuclei (). Pathologically, pheochromocytoma could be excluded since neuroendocrine markers (chromogranin, CD56, and NSE) were negative. The tumor was located within adrenal parenchyma with outside protruding feature in grossly. And inhibin and vimentin immunohistochemical stains were positive in tumor cells. Both antibodies are usually positive in adrenal cortical tumor. Grossly and immunohistochemically, this tumor was considered in primary adrenal tumor although it demonstrated histologically undifferentiated feature. A diagnosis of undifferentiated adrenal tumor with rhabdoid features was rendered.
Two days after tumor resection, the patient reported dyspnea and developed hypoxia; chest CT confirmed the presence of multifocal pulmonary thromboembolism, bilateral pneumonia, and pulmonary infarction. Mechanical ventilation, intensive care, and administration of antibiotics were continued, but the patient showed pneumonia aggravation, acute kidney injury, and fungemia, with no signs of improvement. The patient's legal guardian refused to continue intensive care and transferred the patient to another hospital for supportive treatment. The patient died 2 months after his initial diagnosis.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [67, 'years'], 'weight': [10.0, 'kg'], 'sex': 'Male', 'Sodium': [130.0, 'mEq/L']}",-0.35714,-0.33928,-0.375,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 67 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 10.0 kg. The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 10.0 * (130.0/140 - 1) = -0.35714 L. The patient's free body water deficit is -0.35714 L."
6103,38,Free Water Deficit,lab test,decimal,pmc-4219883-1,Extracted,"78-years-old man was admitted to our hospital due to 10-days history of intractable postprandial vomiting. He complained of progressive dysphagia presented initially to solid foods and then to liquids for a month. During this time, he had 15 kilogram weight loss.
He smoked for decades and noticed occasional productive cough with no relevant diagnostic work-up. He had history of hypothyroidism after being treated by radio –iodine for the primary hyperthyroidism when he was 60-years-old. However, at the time of presentation, he was in euthyroid state.
On clinical examination, he appeared ill and dehydrated. Except for bilateral temporal wasting, the whole clinical examination was normal. Tests of blood and electrolytes showed white blood cell (WBC): 9,700 /µl, Hb: 11.2 g/dl, MCV: 86/fl: Platelet count; 283,000 /µl: ESR; 125 mm/ hour, Na: 137 and K: 3.6 meq/ l. Renal and liver function assays were normal as serum protein electrophoresis study.
There was no evidence of hepatobiliary or splenic abnormality on abdominal sonography.
On upper endoscopy, esophagus appeared to be diffusely erythematous with multiple white plaques compatible with candidiasis; due to tight LES stenosis, attempts to pass the endoscope into stomach was futile. After dilatation with the Savary dilators, all parts of stomach were visualized that seemed to have normal mucosa. Multiple biopsies were obtained from distal esophagus and proximal stomach (both side of LES); but histologic examination revealed normal mucosa.
Abdominal and chest CT scan showed an abnormal soft tissue mass around distal esophagus with a solitary 2 cm pulmonary nodule (SPN) near right lung hilum. His medical records were unavailable to evaluate the growth rate of SPN.
On endosonography (EUS), a 42 mm hypoechoic mass was seen at LES extending beneath the mucosa ,involving all layers of esophageal wall albeit without any regional lymph node abnormality. Fine needle aspiration (FNA) guided by EUS was done (). Histological study of samples showed a well differentiated squamous cell carcinoma (). We did not evaluate the SPN as he refused to undergo further diagnostic work-up.
The tumor stage was T3N0M0. Therefore, he received chemo radiotherapy with platinium-based regimen. Thereafter, dysphagia improved significantly. Unfortunately, he died six months after treatment due to a heart attack.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [78, 'years'], 'weight': [15.0, 'kg'], 'Sodium': [137.0, 'mEq/L']}",-0.16071,-0.15267,-0.16875,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 78 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 15.0 kg. The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 15.0 * (137.0/140 - 1) = -0.16071 L. The patient's free body water deficit is -0.16071 L."
6104,38,Free Water Deficit,lab test,decimal,pmc-2799424-1,Extracted,"The patient, a 7 years and 6 months old boy, was the second child of unrelated healthy parents. He was born by cesarean section after a full term pregnancy. His birth weight was 3,250 kg (50 percentile), length 50 cm (50 percentile) and head circumference (HC) 35.5 cm (50 percentile). His perinatal period was without problems. The motor development was normal as he sat independently at the age of 7 months and walked unassisted at the age of 11 months. His language development was delayed; first words were spoken later than aged 2 years and 6 months, and at 5 years he was referred to logotherapy. His parents described him as a healthy, sociable and smart boy with low linguistic skills. When the patient attended 1st grade in the mainstream school he was referred by his schoolteacher for full developmental assessment because of learning difficulties and speech developmental delay.
On physical examination he was quite a sociable child, with mild dysmorphic facial features such as ocular hypertelorism, downward slanting palpebral fissures, epicanthal folds, flat nasal bridge, short nose with flat philtrum, and thin upper lip. Additionally, his neck was short and the feet were stubby and flat. His weight was 27 kg (50th percentile), height 122 cm (25th percentile) and his HC 52 cm (25th percentile). On developmental examination: his nonverbal skills were equivalent to a 5 years 9 months level with good language understanding, being able to spell, read and write small words, but his oral speech development was very poor. His expressive language was limited to small words and phrases with many phonological difficulties. According to Griffiths Mental Development Scales and Bayley Scales of Infant Development (2nd edition) his General Developmental Quotient (GDQ) was 78 with performance DQ of 86 and language DQ of 61. His behavior was normal for developmental age.
On neurological examination he was slightly hypotonic but without asymmetry. Heart auscultation revealed a mild systolic murmur. Audiological examination showed a mild bilateral selective high frequency hearing loss (4000-8000 Hz). Heart ultrasound (triplex) showed a single papillary muscle resulting in mild mitral valve regurgitation but without hemodynamic changes. The echocardiogram was normal. Full ophthalmologic examination was normal. Hematological tests revealed anemia with Hb of 9.3 g/100 ml, Ht of 30%, MCV of 57.9, MCH of 18, and MCHC of 31 g/100 ml, with normal blood cell and platelet counts 269,000/μl (140,000/μl-300,000/μl). Bleeding time was very elongated >17 min (2-4 min) and platelet aggregation test (PSA) was abnormal 196 sec (<142 sec).
Results of further biochemical tests were the following: urea: 34 mg/dl, blood sugar: 86 mg/dl, creatinine: 0.35 mg/dl, calcium: 9.4 mg/dl, Mg: 2.5 mg/dl, K: 4.8 mEq/l, Na: 140 mEq/l, Cl:106 mEq/l, SGOT: 40 U/l, SGPT: 30 U/l, GT: 8 U/l, cholesterol: 132 mg/dl, HD: 61 mg/dl, LDL: 59 mg/dl, CPK: 65 u/l, and ammonia: 0.69 μg/dl. Thyroid function and kidney-liver-spleen ultrasound were also normal.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [7, 'years', 6, 'months'], 'weight': [27.0, 'kg'], 'sex': 'Male', 'Sodium': [140.0, 'mEq/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 7 years, and 6 months old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 27.0 kg. The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 27.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
6105,38,Free Water Deficit,lab test,decimal,pmc-2760558-1,Extracted,"A 68 year-old Asian woman was admitted to our hospital presenting with a two-day history of high grade fever, diarrhea and nausea. The patient's symptoms began one day after eating grilled chicken and beef at a restaurant; however, she did not complain of abdominal pain, vomiting, or hematochezia. The patient was diagnosed with diabetes mellitus at the age of 50, had undergone haemodialysis due to diabetic nephropathy for the past 2 years, and was under three times weekly haemodialysis. She had also undergone an aortic mechanical valve replacement operation for aortic stenosis 7 months prior to the current admission.
Upon admission to our hospital, the patient's height was 149 cm and her body weight were 61.0 kg (dry weight). The patient's temperature was 106°F, blood pressure was 150/90 mmHg, heart rate was 152/min, and respiratory rate was 24/min. Cardiovascular examination revealed a Levine IV/VI systolic murmur at the right second intercostal space. Her bowel movements were slightly hypoactive and physical examination did not reveal any abdominal tenderness or rebound. No evidence of embolization including Osler node, Janeway lesion and petechiae was observed. No other abnormalities were noted on the systemic examination. Initial laboratory examinations revealed the following results: hemoglobin, 115 g/L [110-146 g/L]; total leukocyte counts, 10300/μL [3500-8200/μL] without left shift (Myelo 0.5%, Meta 0.5%, Stab 2.0%, Seg 90.0%, Lym 1.5%, Mono 5.5%); normal platelet counts, 1.42 × 103/μL [1.40-3.89 × 103/μL]; significantly elevated C-reactive protein, 18.54 mg/dL [<0.30 mg/dL]; Na 131 mEq/L, K 4.3 mEq/L, Cl 97 mEq/L, HCO3- 18.9 mmol/L; BUN 43.6 mg/dL, Cre 7.25 mg/dL (before haemodialysis); serum glucose, 173 mg/dL; and HbA1c, 7.3% [4.3-5.8%]. In addition, the patient was tested negative for HIV antibodies.
Salmonella enteritis or campylobacter enteritis was suspected due to the history of eating grilled chicken. Treatment was initiated with ciprofloxacin 300 mg q24hr, ceftriaxone 2 g q24hr, and clindamycin 600 mg q12hr intravenously, started on day of admission. Three days post-admission, a serial blood culture taken on admission revealed Salmonella enterica serotype Enteritidis (O9, H-g) that was sensitive to ceftriaxone (MIC <= 1) and ciprofloxacin (MIC <= 0.25) (Table ). After detection of the causable microorganism, ceftriaxone and clindamycin treatment was ceased, and the patient was treated with ciprofloxacin alone. Since the patient's aortic valve was a prosthetic, and Salmonella species have a high affinity for intravascular intima, there was a concern about prosthetic infective endocarditis. Therefore, the patient underwent transthoracic echocardiography (TTE) on day 7; however, no abnormalities were detected by TTE. On day 9, the patient showed a sudden disturbance in mental status, left conjugate deviation, and right hemiplegia. Diffusion-weighted imaging of the brain via MRI showed an acute cerebral infarction of the middle cerebral artery region (figure ). Following this discovery, the TTE was re-examined, followed by a transesophageal echocardiography (TEE) on day 13. The TEE revealed floppy vegetation on the mitral valve, which was 12 × 8 mm in size (figure ). We could not find any aberrance of the replaced aortic valve. Although surgery to remove the vegetation was considered, acute cerebral infarction contraindicated her from undergoing the operation. The ciprofloxacin dose was increased to 400 mg q24hr and was combined with ceftriaxone 2q q12hr, on day 12. Consequently, the patient was treated solely with ciprofloxacin for 8-day period (from day 4 to day 11). Although the patient's neurological deficit ameliorated gradually, she experienced another infarction at the left occipital lobe and the right cerebellar hemisphere on day 18. Conservative therapy with antibiotics was continued; however, her mental status progressively decreased and blood pressure deteriorated. Blood culture examinations were repeated, but they were all negative. haemodialysis ceased on day 35 due to the unstable haemodynamic status, although treatment with ciprofloxacin and ceftriaxone were continued. On day 39, the patient died of respiratory failure and cardiac arrest. Her clinical course is shown in figure . Autopsy revealed a rigid node on the mitral valve (figure ), associated with septic emboli (mass of gram-negative microorganisms) at the left occipital lobe (figure ).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [68, 'years'], 'weight': [61.0, 'kg'], 'sex': 'Female', 'Sodium': [131.0, 'mEq/L']}",-1.76464,-1.67641,-1.85287,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 68 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 61.0 kg. The concentration of sodium is 131.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 131.0 mEq. To convert from 131.0 mEq to mmol, convert from mEq to mmol. The compound 131.0 has a valence of 1, and so divide the valence by the value of mEq to get, 131.0 mEq/(1 mEq/mmol) = 131.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 131.0 mEq sodium/L converts to 131.0 mmol sodium/L. Plugging in these values into the equation, we get 0.45 * 61.0 * (131.0/140 - 1) = -1.76464 L. The patient's free body water deficit is -1.76464 L."
6106,38,Free Water Deficit,lab test,decimal,pmc-7942036-1,Extracted,"A 54-year-old man presented to the neurologic clinic of The Fourth Affiliated Hospital Zhejiang University School of Medicine, after episodes of seeing round, colored flickering lights, and reporting that he “can't see things in his right visual field” 7 d before admission.
One week prior to admission, the patient saw paroxysmal green and red flickering lights in his right visual field. He then experienced blurred vision in his right visual field. He visited a local ophthalmic clinic several days before coming to our hospital, and a visual field examination showed a right homonymous hemianopia (Figure ). His visual field defect improved partially without treatment. The paroxysmal flickering lights lasted for about 3 d before remission, but there was no further improvement in his hemianopia.
The patient was otherwise healthy. He denied a history of hypertension, diabetes mellitus (DM), prior cerebrovascular disease or other neurological complications.
The patient was a journalist with a height of 178 cm and weight of 76 kg. He had no history of drug use, drinking, smoking, or bad sexual life. One of his four siblings had DM, and there was no family history of stroke, epilepsy, or other neurologic diseases.
His general examination was unremarkable. Neurologic examination revealed right homonymous hemianopia with normal pupillary reactivity. No other positive neurologic signs were found.
His blood glucose was 645 mg/dL (35.83 mmol/L) without ketoacidosis, although his urine ketone test was weakly positive. Serum osmolarity was 297.09 mOsmol/L (range: 280-310 mOsmol/L), with serum sodium 126.42 mmol/L (range: 137-142 mmol/L), and serum potassium 4.21 mmol/L (range: 3.50–5.30 mmol/L). HbA1c was 14.4% (range: 3.6%-6.0%). Other laboratory tests were unremarkable.
Cranial magnetic resonance imaging (MRI) showed abnormalities in the left occipital lobe with decreased T2 and fluid-attenuated inversion recovery (FLAIR) signals in the white matter, restricted diffusion, and corresponding low signal intensity in the apparent diffusion coefficient map (Figure ). Magnetic resonance angiography imaging of the brain showed a mild stenosis of the right posterior cerebral artery, with arterial spin labeling showing decreased perfusion of the lesion (Figure ). The patient’s electroencephalogram (EEG) was mildly abnormal, showing slowing activities without spikes and sharp waves.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'weight': [76.0, 'kg'], 'sex': 'Male', 'Sodium': [126.42, 'mmol/L']}",-4.4232,-4.20204,-4.64436,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 54 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 76.0 kg. The concentration of sodium is 126.42 mmol/L. Plugging in these values into the equation, we get 0.6 * 76.0 * (126.42/140 - 1) = -4.4232 L. The patient's free body water deficit is -4.4232 L."
6107,38,Free Water Deficit,lab test,decimal,pmc-6164201-1,Extracted,"A 14-year-old girl came to Thammasat University Hospital for renal replacement therapy. She presented with end-stage renal disease (oliguria, anemia, and failure to thrive). She was the first child of healthy nonconsanguineous Thai parents. She was born at term to a 23-year-old mother and a 25-year-old father. Her prenatal and perinatal periods were uncomplicated. Her development was unremarkable until six months of age. She clawed by using her knees and elbows, instead of hands, at the age of 8 months. She was unable to walk on her feet but moved on her knees during her childhood period. She came to our hospital at the age of 12 years. Her weight was 25.4 kilograms (below the 3rd percentile) and her sitting height was 70 cm (below the 3rd percentile). Her vitals were normal, except high blood pressure at 120/80 mmHg (above 99th percentile for her age, sex, and height). She had pallor. Her distinctive facial features were the cloudy cornea, exophthalmos, underdeveloped ala nasi, maxillary hypoplasia, and micrognathia (). Upper extremity deformities included shortening of arms and forearms, flexion contracture of elbows, distorted wrists, and shortening of all fingers. Deformities of lower extremities were short thighs, short-bowed legs, and flexion contracture of knee. Distorted and restricted in motion of ankles, and deformities of feet were observed. Her heart, lungs, abdomen, and neurological examination were unremarkable. Her cognitive was appropriated with age.
Her initial investigations demonstrated blood urea nitrogen 120 mg/dL, serum creatinine 8.3 mg/dL, Na 134, K 4.5, Cl 95, HCO3 11 mmol/L, phosphate 2.6, calcium 3.8 mg/dL, albumin 0.6 g/dL, alkaline phosphatase (ALP) 13.5 U/L, with parathyroid hormone (PTH) level at 94 pg/ml. Her radiography of the upper extremities showed absence of carpal bones, osteolytic lesions of metacarpal, and distal ends of ulna and radial bones (). The radiography of the lower extremities demonstrated absence of tarsal bones, osteolytic lesions of metatarsal bones, and distal end of fibula (). In addition, severe cortical thinning of all bones indicating osteopenia was observed (Figures and ).
Ultrasonography showed small size of both kidneys and echocardiography demonstrated left ventricular hypertrophy. The diagnosis of end-stage renal disease was made with estimated glomerular filtration rate (GFR) of 7 mL/min/1.73 m2. All clinical presentation and investigations were compatible with the clinical diagnosis of MCTO. She received hemodialysis followed by continuous ambulatory peritoneal dialysis and medications including erythropoietin, ferrous fumarate, 0.50 µg of calcitriol, and 1400 mg of elemental calcium. Six months later, she developed generalized tonic-clonic seizure from hypercalcemia (12.4 mg/dL). Her serum chemistry demonstrated normal serum phosphorus level (3.9 mg/dL) and low serum alkaline phosphatase (4 U/L), with normal serum PTH level at 103 pg/mL. These findings indicated a marked reduction in the bone uptake of calcium after a period of calcium supplement. Calcium and calcitriol were discontinued until serum calcium returned to normal level, then only 720 mg of elemental calcium was reintroduced. Two years later, she had a slightly high serum calcium level (10.8 mg/dL), normal serum phosphorus level (3.5 mg/dL), and normal PTH level (113 pg/ml). Interestingly, during the past 2 years, we observed persistently low serum ALP levels (2.6–4.9 U/L) [], indicating poor osteoblastic activity and limited bone formation. Thus, impaired bone mineralization from dysregulation of osteoblast and osteoclast was suspected and MAFB mutation might be responsible for MCTO disease in this patient.
We performed a genetic testing, MAFB sequencing on her and her parental blood. The genomic were isolated from peripheral lymphocytes using Puregene DNA extraction kit (Qiagen, Valencia, CA). A short region of the amino-terminal transcriptional activation domain of the MAFB gene, containing mutation hotspots, was amplified by polymerase chain reaction (PCR). We designed primers by using software (Primer3Plus). The forward and reverse primer sequences for PCR amplification were 5′-GCTCAAGT TCGACGTGAAGA-3′ and 5′-GTAGTTGCTCGCCATCCAGT-3′, respectively. PCR products were visualized on a 2% agarose gel and purified using DyeEx 2.0 spin kit (Qiagen, Valencia, CA). The products were then sequenced by capillary electrophoresis. This study was approved by the ethic committee of the Faculty of Medicine, Thammasat University, Thailand (MTU-EC-PE-1-005/59).
We identified a de novo heterozygous missense mutation at nucleotide 197 from C to G (NM_005461.4; c.197C > G; ), predicting the change of amino acid at codon 66 from serine to cysteine (p.Ser66Cys). There was negative in both mother and father's result. This missense mutation occurred within the transactivation domain of MafB protein. This serine at the codon 66 is evolutionarily conserved among species, and in silico prediction of pathogenicity programs classify this variant as deleterious (SIFT) and probably damaging (PolyPhen).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [14, 'years'], 'weight': [25.4, 'kg'], 'sex': 'Female', 'Sodium': [134.0, 'mEq/L']}",-0.65314,-0.62048,-0.6858,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 14 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 25.4 kg. The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 25.4 * (134.0/140 - 1) = -0.65314 L. The patient's free body water deficit is -0.65314 L."
6108,38,Free Water Deficit,lab test,decimal,pmc-6392561-1,Extracted,"A 51-year-old woman visited our outpatient clinic because of latent tuberculosis infection detected by a screening examination performed by a healthcare worker. She had no relevant prior medical history. Laboratory findings were normal with a serum creatinine (Cr) level of 0.76 mg/dL (normal 0.6–1.5 mg/dL) and blood urea nitrogen (BUN) level of 12.8 mg/dL (normal 8–23 mg/dL). Antituberculosis treatment was started with isoniazid at 300 mg/d and rifampicin at 600 mg/d. During the 25-day antituberculosis therapy regimen, she complained of nausea, vomiting, general weakness, and edema. Serum Cr and BUN levels were 1.0 and 18 mg/dL, respectively. Rifampicin and isoniazid were discontinued. However, her symptoms progressed for 4 days and urinalysis revealed 4+ proteinuria (normal negative). She was admitted to the hospital for more detailed examinations.
On admission, her blood pressure was 110/80 mm Hg, body temperature was 36.5°C, height was 158 cm, and body weight was 68.6 kg. She had gained 8.6 kg in body weight over the preceding 1 month. The results of physical examination were unremarkable except for pitting edema on both lower extremities. Laboratory findings were as follows: white blood cell count 7490/mm3 (normal 4000–10,000/mm3) with 63.1% neutrophils and 1.4% eosinophils, hemoglobin 13.6 g/dL (normal 12–16 g/dL), platelet count in peripheral complete blood 295,000/mm3 (normal 140,000–440,000/mm3), BUN 45 mg/dL, serum Cr 1.72 mg/dL, total protein 3.67 g/dL (normal 6.5–8.2 g/dL), albumin 1.73 g/dL (normal 3.5–5.0 g/dL), total bilirubin 0.67 mg/dL (normal 0.1–1.2 mg/dL), aspartate transaminase 116 IU/L (normal 10–35 IU/L), alanine transaminase 94 IU/L (normal 0–40 IU/L), total cholesterol 453 mg/dL (normal 120–200 mg/dL), sodium (Na) 133 mEq/L (normal 135–145 mEq/L), potassium 5 mEq/L (normal 3.5–5.5 mEq/L), and chloride 103 mEq/L (normal 98–110 mEq/L). Urinalysis showed specific gravity >1.050 (normal 1.005–1.03), osmolality 687 mOsm/kg (normal 300–900 mOsm/kg), urine Na <10 mEq/L, and urinary Cr 267.34. The calculated fractional sodium excretion was 0.02%. The creatinine urine to plasma ratio was 155. Urinary sediment did not show either red blood cells or granular casts. A 24-h urine sample contained 12.2 g of protein. Serum and urine electrophoresis results showed no M-spike and nonselective proteinuria. The patient was negative for hepatitis B, hepatitis C, HIV, and syphilis serological markers. Rheumatoid factor, antinuclear antibody, antineutrophil cytoplasmic antibody, and antiglomerular basement membrane antibody tests were all negative. In addition, results for complement 3 (144.3 mg/dL, normal 90–180 mg/dL), complement 4 (32.4 mg/dL, normal 10–40 mg/dL), immunoglobulin G (551 mg/dL, normal 700–1600 mg/dL), immunoglobulin A (267 mg/dL, normal 70–400 mg/dL), and immunoglobulin M (111 mg/dL, normal 40–230 mg/dL) were negative. Chest X-ray revealed a small amount of bilateral pleural effusion (Fig. A). The patient was treated with torsemide at a dose of 50 mg/d for edema.
Renal biopsy was performed at 1 week after discontinuation of medication. However, she developed dyspnea and pulmonary edema on the day of the procedure (Fig. B). As we suspected nephrotic syndrome with acute nonoliguric renal failure, we performed dialysis and oral administration of prednisolone at 60 mg/d. Acute renal failure was confirmed with temporary loss of renal function that required dialysis, and with peaked serum Cr (2.68 mg/dL) that more than 3-fold increase in baseline Cr (0.76 mg/dL). Renal biopsy revealed nonsclerotic glomeruli with normocellularity and a mild focal tubular injury pattern on light microscopy (Fig. A and B). No deposition of immunoglobulins or complement components was observed in the glomeruli. Electron microscopy showed diffuse loss of the podocyte foot processes of glomerular epithelial cells, but the glomerular basement membrane showed normal thickness and architecture, consistent with MCD (Fig. A and B).
The diagnosis was confirmed to be MCD. Heavy proteinuria developed after using antituberculosis agents. We speculated that this was a case of antituberculosis medication-induced nephrotic syndrome and toxic hepatitis. Following discontinuation of rifampicin and isoniazid with the aid of prednisolone therapy, the patient's nausea, vomiting, and pulmonary edema improved after 1 week of steroid therapy, and dialysis was stopped. Her body weight recovered from 68.6 to 60.7 kg at 3 weeks after discontinuation of rifampicin and isoniazid, and she was then discharged. Proteinuria became negative and renal function tests showed normal results at 4 weeks (serum Cr, 0.86 mg/dL; BUN, 24.7 mg/dL). Furthermore, her albumin and cholesterol levels were 3.15 g/dL and 276 mg/dL, respectively, at 4 weeks after stopping the drugs. Prednisolone was then tapered and withdrawn 3 months after initiation. Recurrence of proteinuria was not observed during a 3-month follow-up. The patient's clinical course is summarized in Fig. .
Informed consents were obtained from the patient for the publication of clinical details and accompanying images. As this study is a clinical case report, no ethical committee approval was required for its conduction, which is in compliance with the institutional and national policies concerning research approvals.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [51, 'years'], 'weight': [68.6, 'kg'], 'sex': 'Female', 'Sodium': [133.0, 'mEq/L']}",-1.715,-1.62925,-1.80075,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 51 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 68.6 kg. The concentration of sodium is 133.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 133.0 mEq. To convert from 133.0 mEq to mmol, convert from mEq to mmol. The compound 133.0 has a valence of 1, and so divide the valence by the value of mEq to get, 133.0 mEq/(1 mEq/mmol) = 133.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mEq sodium/L converts to 133.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 68.6 * (133.0/140 - 1) = -1.715 L. The patient's free body water deficit is -1.715 L."
6109,38,Free Water Deficit,lab test,decimal,pmc-6942743-1,Extracted,"A 59-year-old Caucasian man with ESRD due to glomerulonephritis and failed kidney transplant who was undergoing CCPD for 7 months presented to the emergency department with periumbilical pain for several days. This was the first time the patient had experienced these symptoms since the initiation of CCPD. His medical history additionally included hypertension, valvular heart disease, degenerative arthritis, parathyroidectomy, and tobacco use. He had discontinued all of his immunosuppressive medications because his kidney transplant had been nonfunctional for several years.
Physical examination revealed a well-built, seemingly healthy man weighing 157 pounds with a blood pressure of 144/92 mmHg and a heart rate of 85 beats/min, without distress, and without jaundiced sclerae. He had clear lungs and systolic heart murmur. Abdominal examination revealed a soft abdomen with some fullness on the right lower quadrant proximal to his previous renal transplant, periumbilical tenderness, and intact exit site with no tunnel tenderness. He had active bowel sounds.
Laboratory testing revealed a white blood cell (WBC) count of 9.1 × 103/μL with 70% neutrophils, hemoglobin level of 12.9 g/dL, hematocrit count of 38.5%, and platelet count of 263 × 103/μL. Serum chemistry analysis showed the following levels: sodium 139 mmol/L, potassium 3.4 mmol/L, chloride 95 mmol/L, total carbon dioxide 28 mmol/L, glucose 127 mg/dL, blood urea nitrogen 31 mg/dL, and creatinine 12.46 mg/dL. The peritoneal fluid was colorless and appeared hazy. Initial analysis showed a WBC count of 4,470 cells/μL with 85% polymorphonuclear cells and 15% mononuclear cells. Gram staining of the peritoneal fluid was negative for any organisms, only showing WBCs.
Based on the available information, the patient was diagnosed with PD-peritonitis, and empiric treatment with 1 g of vancomycin and 1 g of ceftazidime was administered intravenously and daily infusions initiated. The final diagnosis was made through peritoneal fluid culture that showed light growth of P. multocida after 3 days. The isolate was sensitive to ampicillin, ceftriaxone, ceftazidime, gentamicin, and ciprofloxacin. Therefore, antibiotics were adjusted according to the bacterial cultures, where intravenous ampicillin-sulbactam was started and then switched to oral amoxicillin-clavulanate for a total of 3 weeks. Patient had subsequent improvement in symptoms and laboratory results. He was able to continue PD successfully without any interruption or the need for catheter removal.
Upon taking further history, the patient reported having several cats at home, none of which were kittens. At night, he would begin his PD treatment and go into a different room to watch television. Therefore, the cats were assumed to play with the dialysis equipment or chew on the tubing, possibly leading to infection, although the patient did not recall noticing any fluid leakage from the tubing. Prior to discharge, the patient's dialysis technique was confirmed by direct observation, and aseptic technique was ensured. The patient additionally decided to place his cats outside the home at night before starting PD treatment. He did not have any more episodes of PD-peritonitis caused by P. multocida after changing his routine.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [59, 'years'], 'weight': [157.0, 'lbs'], 'sex': 'Male', 'Sodium': [139.0, 'mmol/L']}",-0.3052,-0.28994,-0.32046,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 59 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 157.0 lbs so this converts to 157.0 lbs * 0.453592 kg/lbs = 71.21394 kg. The concentration of sodium is 139.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 71.21394 * (139.0/140 - 1) = -0.3052 L. The patient's free body water deficit is -0.3052 L."
6110,38,Free Water Deficit,lab test,decimal,pmc-7859974-1,Extracted,"A 56-year-old man (weight approximately 50 kg) with no medical history was admitted to the emergency department with shaking chills, loss of appetite, and difficulty in mobility, which had begun five days earlier. He was soon transferred to the ICU with a diagnosis of severe pneumonia. During our examination, he was alert, and his blood pressure, heart rate, cardiac rhythm, respiratory rate, oxygen saturation, and body temperature were 173/101 mmHg, 130 beats/min (atrial fibrillation), 42 breaths/min, 97% [high-flow nasal cannula (HFNC), 30 L/min, 30%], and 39.0 °C, respectively. Arterial blood gas findings were as follows: pH of 7.45, PaO2 of 110 (HFNC, 30 L/min, 30%), PaCO2 of 20, HCO3 of 16.9, and lactate of 13 mg/dL. The white blood cell (WBC) count was 13,400/μL, hemoglobin (Hb) level was 14.4 g/dL, and platelet (PLT) count was 92,000/μL. The blood urea nitrogen (BUN) level was 59.4 mg/dL, the Cre level was 4.09 mg/dL, alanine aminotransferase (ALT) level was 4,599, aspartate aminotransferase (AST) level was 12,743 U/L, total bilirubin (T-bil) level was 2.1 mg/dL, sodium (Na) level 128 mEq/L, potassium level was 3.6 mEq/L, and creatinine kinase (CK) level was 16,092 IU/L. The C-reactive protein (CRP) and procalcitonin (PCT) levels were both abnormal at 25.65 mg/dL and 106.3 ng/dL, respectively. Coagulation abnormalities were obvious, with an activated partial thromboplastin time (APTT) of 44.4 seconds, a prothrombin time (PT) of only 32.0% of the normal range, 307.9 μg/mL of fibrin/fibrinogen degradation products (FDP), D-dimer level of 155.0 μg/mL, a fibrinogen level of 667.0 mg/dL, and an antithrombin III (AT-III) level of only 45.6% of the normal range. The Sequential Organ Failure Assessment (SOFA) score [] was 7 points, and the Japanese Association for Acute Medicine Disseminated Intravascular Coagulation (JAAM DIC) diagnostic criteria score [] was 6 points. Chest X-ray findings showing widespread consolidation and air-alveologram in the left lung (Figure ), along with the detection of urinary Legionella antigen, led to a diagnosis of severe pneumonia due to Legionella. In the ICU, the patient received 500 mg intravenous levofloxacin every 24 hours, landiolol, recombinant human soluble thrombomodulin, and antithrombin gamma. We started continuous hemodiafiltration (CHDF) on the first day of ICU and switched to cPED the next day. After one session of cPED (48 hours), CHDF was reintroduced and terminated on day nine of the ICU stay. The patient was transferred to the general ward on the 11th day in a stable condition without oxygen administration.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [56, 'years'], 'weight': [50.0, 'kg'], 'Sodium': [128.0, 'mEq/L']}",-2.57143,-2.44286,-2.7,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 56 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 50.0 kg. The concentration of sodium is 128.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 128.0 mEq. To convert from 128.0 mEq to mmol, convert from mEq to mmol. The compound 128.0 has a valence of 1, and so divide the valence by the value of mEq to get, 128.0 mEq/(1 mEq/mmol) = 128.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 128.0 mEq sodium/L converts to 128.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 50.0 * (128.0/140 - 1) = -2.57143 L. The patient's free body water deficit is -2.57143 L."
6111,38,Free Water Deficit,lab test,decimal,pmc-4531633-1,Extracted,"A 27-year-old woman was admitted to evaluate the cause of secondary amenorrhea and recent weight gain. Her menstruation was very irregular and stopped a year ago. She had also gained 10 kg in the last two years. Her past medical history did not show anything significant. On admission, her blood pressure was 150/90 mmHg, pulse rate, 78/min, body temperature, 36.8°C, respiratory rate, 20/min, height 168.8 cm, and body weight was 67 kg. On physical examination, she had a moon face central obesity, and hypertrichosis. She also had many spotty skin and mucosal pigmentation on her lips, oral mucosa, fingers, and toes ().
Laboratory studies included WBC 9700/mm3 with 77% neutrophils and 14.7% lymphocytes and platelet 300×103/mm3. Her liver and renal function test results were normal. Concentrations of Na and K were 144 mEq/L, 4.1 mEq/L, respectively. Blood sugar after fasting was 100 mg/dL, and LH was 2.6 mlU/mL (1.1–7.0), FSH 4.0 mlU/mL (6.3–24), estradiol 24.3 pg/mL (30–400), and testosterone 1.30 ng/mL (0.14–0.76).
Looking at her history and physical examination, we suspected cushing’s syndrome. The levels of plasma ACTH and cortisol at 8 AM were 12.38 pg/mL and 27.8 ug/dL. The levels of plasma cortisol at 4 PM and midnight were 26.3 ug/dL and 27.5 ug/dL, respectively. The 24 hour urine-free cortisol was 902 ug/day, and the level of 17-ketosteroid slightly increased, while that of DHEA-S was within normal range. The results of low and high dose dexamethasone suppression test were shown in . The 24 hour urine-free cortisol excretion was not suppressed by the low and high dose dexamethasone suppression test. Abdominal CT scan was done under the impression of adrenal Cushing’s syndrome. A 2.3×1.7 cm-sized well defined homogenous mass was seen in the left adrenal gland (). However, at this time, we could not explain her skin pigmentation.
Although the abdominal CT scan findings were not typical of PPNAD, echocardiography was performed to search for cardiac myxoma, so that Carney complex could be excluded since right adrenal gland atrophy was not identified. However, the result turned out negative, prompting us to perform pituitary fossa MRI to exclude the diagnosis of adrenal nodular hyperplasia due to pituitary Cushing’s disease. We also measured the cathecholamine metabolites to exclude ectopic Cushing’s syndrome due to pheochromocytoma. The levels of vanylmandelic acid and metanephrine had not increased. However, there was a microadenoma in the inferior portion of the right pituitary gland (). At that time, baseline levels of all pituitary hormones were found to be within normal range (growth hormone: 0.63 ng/mL, prolactin: 15 ng/mL, TSH 0.94 ulU/mL, free T4 1.0 ng/dL). Jugular vein ACTH sampling was performed to rule out pituitary Cushing’s disease, but the ACTH level of the right jugular vein did not increase at twice the level of the peripheral vein (right jugular vein: 28.16 pg/mL, peripheral vein: 17.37 pg/mL). We planned to resect the left adrenal gland only because abdominal CT findings and echocardiographic findings were not typical of PPNAD, and because pituitary Cushing’s disease was not definitively ruled out by inferior petrosal sinus sampling. Left adrenalectomy was performed, and the cut surface of the surgical specimen showed a golden yellowish colored dominant nodule with multiple black pigmented small nodules (). On microscopic findings, variable multiple cortical nodules were noted and extracapsular nodules were also noted at periadrenal fat and abundant lipofuscin pigments were noted at the tumor cytoplasm (). We concluded that Cushing’s syndrome resulted from PPNAD and further studied whether she had other components of Carney complex. She mentioned that her father and grandmother also had the same skin pigmentation on the lips and oral mucosa, but we did not perform studies on her family. The 75 g oral glucose tolerance test and the measurement of IGF-1 were performed to exclude growth hormone secreting pituitary adenoma. The level of IGF-1 increased (721.6 ng/mL), but the level of growth hormone was suppressed during the oral glucose tolerance test (). Ultrasonography of the thyroid showed a 0.3 cm sized hypoechoic nodule at the right thyroid, while ultrasonography of the breasts showed multiple hypoechoic masses on both breasts (). However, the patient refused breast biopsy. We concluded with a final diagnosis of Carney complex including spotty skin pigmentation, Cushing’s syndrome due to PPNAD, nonfunctioning pituitary adenoma, and other suggestive findings such as breast and thyroid masses. After operation, the levels of plasma cortisol and 24 hour urine-free cortisol were normalized. However, 6 months after operation, 24- hour urine-free cortisol increased slightly (129.6 ug/day), causing us to consider resecting the contralateral adrenal gland.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [27, 'years'], 'weight': [67.0, 'kg'], 'sex': 'Female', 'Sodium': [144.0, 'mEq/L']}",0.95714,0.90928,1.005,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 27 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 67.0 kg. The concentration of sodium is 144.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 144.0 mEq. To convert from 144.0 mEq to mmol, convert from mEq to mmol. The compound 144.0 has a valence of 1, and so divide the valence by the value of mEq to get, 144.0 mEq/(1 mEq/mmol) = 144.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 144.0 mEq sodium/L converts to 144.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 67.0 * (144.0/140 - 1) = 0.95714 L. The patient's free body water deficit is 0.95714 L."
6112,38,Free Water Deficit,lab test,decimal,pmc-6051943-1,Extracted,"A 26-year-old man was admitted with known hypokalemia. He reported a 3-year history of nausea, vomiting, and diffuse muscle weakness. He complained of nausea and epigastric fullness in the absence of any identifiable organic gastrointestinal pathology, and his symptoms were known to subside after self-induced vomiting. Although he reported a normal appetite, he was known to vomit frequently, particularly after a large meal. He had been diagnosed with hypokalemia and had been treated with potassium supplements at a previous hospital. However, because of persistent nausea and vomiting, he was transferred to our hospital for evaluation of hypokalemia. His medical and family histories were unremarkable, and he did not report the use of medications such as diuretics and/or herbal medication. Physical examination upon admission showed he was 175 cm tall and weighed 44.5 kg, which indicated a weight loss from his previous weight of 58 kg over the previous 2 years. His body mass index was 14.53 kg/m2. Blood pressure was 100/60mmHg, pulse rate was 67/min, respiratory rate was 20/min, and his body temperature was 37.0℃.
Initial serum electrolyte testing showed the following: sodium 133 mEq/L, potassium 2.6 mEq/L, chloride 72 mEq/L, and total carbon dioxide 50mEq/L. Calcium/phosphorus were 11.2/4.1mg/dL, blood urea nitrogen/creatinine were 21.9/1.98mg/dL, the estimated glomerular filtration rate was 43.6mL/min/1.73m2, serum magnesium was 2.0mg/dL, blood glucose was 93mg/dL, and hemoglobin was 12.0 g/dL. Total cholesterol was 285mg/dL, serum protein/albumin were 8.1/5.3 g/dL. Thyroid and adrenal function tests, as well as serum renin and aldosterone levels were all within reference range. Arterial blood gas analysis showed pH 7.557, partial pressure of carbon dioxide was 65.8mmHg, and bicarbonate was 58.5 mEq/L. Urinary levels of sodium/potassium/chloride (Na/K/Cl) were 95/73.2/47mEq/L, respectively, his urinary creatinine measured 111.12mg/dL, and the trans-tubular potassium gradient was 17. Urinalysis showed the following findings: blood -, albumin ±, glucose -, and ketones -. Upper endoscopy and abdominal computed tomography showed no abnormalities. The SLC12A3 gene mutation test for Gitelman syndrome was observed to be negative. He was diagnosed with chloride-responsive metabolic alkalosis with kidney failure and treated with saline hydration, potassium supplementation, and spironolactone. Serum potassium increased to 3.0mEq/L; however, his nausea and vomiting persisted.
A renal biopsy was performed for the evaluation of renal dysfunction. Microscopically, interstitial mononuclear cell infiltration was identified. Renal tubular epithelial cells showed mild nuclear variation with conspicuous nucleoli and cytoplasmic vacuolization, indicating regenerative changes after acute tubular necrosis. Several foci of dystrophic calcification were identified among the tubular epithelial cells. A few shrunken glomeruli were observed suggesting ischemic damage; however, most glomeruli revealed no definitive abnormalities such as mesangial cell proliferation, segmental sclerosis, and/or deposition of immune complexes (). The patient showed an improvement in his gastrointestinal symptoms after treatment with mirtazapine. His serum potassium level increased to 3.5–4.4mEq/L and to date, he has been following-up at the outpatient clinic without any clinical signs and symptoms.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [26, 'years'], 'weight': [44.5, 'kg'], 'Sodium': [133.0, 'mEq/L']}",-1.335,-1.26825,-1.40175,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 26 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 44.5 kg. The concentration of sodium is 133.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 133.0 mEq. To convert from 133.0 mEq to mmol, convert from mEq to mmol. The compound 133.0 has a valence of 1, and so divide the valence by the value of mEq to get, 133.0 mEq/(1 mEq/mmol) = 133.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mEq sodium/L converts to 133.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 44.5 * (133.0/140 - 1) = -1.335 L. The patient's free body water deficit is -1.335 L."
6113,38,Free Water Deficit,lab test,decimal,pmc-8018181-1,Extracted,"A 65-year-old African American male with a history of chronic obstructive pulmonary disease (COPD), anemia, and heart failure with preserved ejection fraction (HFpEF) presented to the emergency department with complaints of unintentional weight loss, fevers, chills, and memory decline. He had lost 60 pounds within the past year, with associated functional decline and generalized fatigue. Within the past two months, he had developed fevers and night sweats, and within the past week, he had begun to experience cognitive decline described as being in a “fog,” which had led him to miss familiar exits on the highway and forget his way to his doctor’s office.
Upon presentation to the emergency department, his vitals included a blood pressure of 117/51 mmHg, heart rate of 95 beats per minute, respiratory rate of 18 breaths per minute, O2 saturation of 97%, and temperature of 98.3 °F. Physical exam showed a thin-appearing man in moderate distress secondary to shortness of breath and cognitive issues. Pertinent positives included bilateral shoddy cervical lymphadenopathy, increased respiratory effort with bilateral wheezing and inspiratory crackles, 1+ pretibial edema, and large bilateral axillary lymphadenopathy. A mini-mental status exam (MMSE) revealed a score of 24/30. Laboratory workup revealed WBC of 10.1 x 1000/mm3, Hemoglobin (Hb) of 9.5 g/dL, and platelet count of 400 x 1000/mm3. The basic metabolic panel (BMP) showed sodium of 130 mmol/L, potassium of 3.3 mEq/L, and creatinine of 0.84 mg/dL. Brain natriuretic peptide (BNP) was 225 pg/mL (normal range: 5-100). A chest X-ray showed cardiomegaly and mild interstitial edema with bilateral pleural effusions. CT brain revealed no acute findings. Given the patient’s functional decline, diffuse lymphadenopathy, and worsening mental status, he was admitted for further workup and management.
On day two of his admission, collateral information was obtained from the patient’s family, which revealed additional prior workup for his symptoms. Six months beforehand, the patient had been evaluated for worsening blurred vision and had been diagnosed with bilateral panuveitis. An extensive laboratory workup was performed, which is summarized below in Table .
Extensive radiology and pathology workup was performed and raised concerns for sarcoidosis. Although the patient had been prescribed methotrexate (MTX), he reported never starting it. One month prior to presentation, the patient had undergone a CT of the chest, abdomen, and pelvis with contrast, which had revealed multiple enlarged mediastinal and axillary lymph nodes and extensive bronchiectasis of bilateral lungs, with the lymphadenopathy (LAD) considered to be reactive versus neoplastic (Figure , Figure ).
Given this new information, rheumatology was consulted, inflammatory markers were drawn which showed an elevated C-reactive protein (CRP) of 50.4 mg/L (normal level: <5), and an erythrocyte sedimentation rate (ESR) of 97 mm/hr (normal range: 0-20); an excisional lymph node biopsy was pursued. Pathology from the axillary lymph node biopsy (Figure , Figure ) revealed increased epithelioid histiocytes and well-formed granulomas associated with multinucleated giant cells, most consistent with sarcoidosis. We also ruled out infectious etiologies with this biopsy with acid-fast bacilli (AFB) and Gomori methenamine silver (GMS) stains, both of which were negative, as shown in Figure and Figure . Given these results, initiating 40-mg prednisone and 15-mg MTX weekly was recommended. It is important to note that on every night during the patient’s hospitalization, he recorded a fever in the range of 101.4-102.4 °F. These fevers abated with acetaminophen and were never present during the day. Blood cultures were drawn at each instance, but they all returned free of organisms. The fevers were ultimately attributed to sarcoidosis.
Regarding the patient’s encephalopathy, neurology was consulted and an MRI brain was performed, which showed no evidence of infection, NS, CNS lymphoma, or neurodegenerative disease process. The patient’s mental status slowly improved over the course of the hospitalization, and a lumbar puncture was not pursued. In the outpatient setting, the patient was followed up with rheumatology and the steroid dose was slowly tapered. The patient also followed up with his primary care physician, stating improvements in his memory and his functional status. He has continued to live alone, retaining the ability to perform activities of daily living on his own.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [65, 'years'], 'weight': [60.0, 'lbs'], 'Sodium': [130.0, 'mmol/L']}",-0.97198,-0.92338,-1.02058,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 65 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 60.0 lbs so this converts to 60.0 lbs * 0.453592 kg/lbs = 27.21552 kg. The concentration of sodium is 130.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 27.21552 * (130.0/140 - 1) = -0.97198 L. The patient's free body water deficit is -0.97198 L."
6114,38,Free Water Deficit,lab test,decimal,pmc-4372569-1,Extracted,"In July 2010, a 64-year-old man was referred to our unit because of refractory congestive heart failure (HF). He had a history of chronic bronchitis, interstitial lung disease and arterial hypertension. In 1990, he had a large inferior myocardial infarction complicated by left ventricular aneurysm and HF, NYHA class III. In 1991, he underwent ventricular aneurysmectomy and mitral pericardial annuloplasty, complicated by mediastinitis. In 2004, he underwent restrictive mitral annuloplasty and in 2005 a cardioverter-defibrillator was implanted. The patient was neither eligible for heart transplantation nor for left ventricular assist device insertion. In August 2010, he presented worsening of dyspnea (NYHA class IV) and his Charlson's comorbidity index was 8 (1-year survival of 63%). His treatment was: frusemide 125 mg/day alternate to 250 mg/day, aldactone 100 mg/day, digoxin 0.125 mg 5 days/week, ramipril 2.5 mg/day and warfarin. In August 2010, he had severe peripheral oedema, his body weight was 85.7 kg and blood pressure 85/60 mmHg. Blood tests showed: creatinine 1.58 mg/dL, estimated GFR (eGFR) (four variables MDRD formula IDMS) 44 mL/min/1.73 m2, urea 25 mg/dL, sodium 130 mEq/L, potassium 3.08 mEq/L, calcium 8.9 mg/dL, haemoglobin 9.8 g/dL, albumin 3.8 g/dL, alanine transaminase (ALT) 5 IU/L, gamma glutamyl transpeptidase (GGT) 88 IU/L. Chest X-rays showed cardiomegaly, peribronchial thickening with initial perihilar consolidations and bilateral pleural effusion. At echocardiography, left atrium was enlarged (30 cm2) with severe mitral valve insufficiency and left ventricular enlargement (end diastolic volume 248 mL, end diastolic diameter 68 mm) with diffuse hypokinesis (ejection fraction 33%), while right atrium and ventriculum were normal. Estimated systolic pulmonary arterial pressure (sPAP) was 52 mmHg. Despite medical therapy, he had recurrent worsening of dyspnea and oliguria. High doses of IV frusemide were administered, followed by hypokalemia (3 mEq/L) and severe hyponatremia (113 mEq/L) without significant increase in diuresis. From March 2009 to August 2010 he was hospitalized 10 times and he spent 100 days in cardiac intensive care unit (CICU). At this stage of congestive refractory HF, according to both European Society of Cardiology and American College of Cardiology Foundation/American Heart Association guidelines (class IIa, level of evidence B), ultrafiltration is indicated. In August 2010, patient started home peritoneal UF. Daily therapeutic schedule included one icodextrin exchange (1 L 7.5%, 10 h dwell). Occasionally, 3.86% dextrose exchange (1 L, 2 h dwell) was administered according to clinical indications (dyspnea, body weight, ultrafiltration volume, diuresis). In November 2010, three months later, his therapy was unchanged except for withdrawal of ramipril and administration of bisoprolol 1.25 mg/die and darbepoetin alfa 60 mcg SC once weekly. His body weight was stably 81 kg and blood pressure 120/70 mmHg. He still had peripheral oedema. Blood tests were: serum creatinine 1.44 mg/dL, eGFR (MDRD) 49 mL/min/1.73 m2, serum urea 29 mg/dL, sodium 134 mEq/L, potassium 3.42 mEq/L, calcium 9.2 mg/dL, haemoglobin 11.3 g/dL, albumin 3.5 g/dL, ALT 17 IU/L and GGT 90UI/L. Chest X-rays showed reduction of interstitial oedema signs and only right pleural effusion. Echocardiographic data were unchanged except for decrease of sPAP (40 mmHg). The patient had no complications related to peritoneal UF. From August 2010 to January 2012 he was admitted twice to hospital for worsening dyspnea and spent in CICU only 10 days. In April 2011, he underwent biological mitral implantation with poor results and in January 2012, after further deterioration of cardiac function and acute worsening of HF, he died. In the 17 months following peritoneal UF, our patient improved his life quality, returning to a more normal life style.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [64, 'years'], 'weight': [85.7, 'kg'], 'Sodium': [130.0, 'mEq/L']}",-3.67286,-3.48922,-3.8565,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 64 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 85.7 kg. The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 85.7 * (130.0/140 - 1) = -3.67286 L. The patient's free body water deficit is -3.67286 L."
6115,38,Free Water Deficit,lab test,decimal,pmc-6464145-1,Extracted,"We report a case of a 47-year-old male patient from Mali, West Africa, who presented with intermittent fever, chills, increased fatigue, decreased appetite, and diffuse back and abdominal pain for three weeks. He reported a 35-pound weight loss over three months. He had a history of malarial infection six months before, which was treated. He endorsed traveling through Africa until a recent illness. At the time of admission, his temperature was 102.3 F, blood pressure was 103-110/59-64 mmHg, and heart rate was 92-113 bpm, saturating at 99% on room air. A blood examination showed a hemoglobin level of 4.4, a mean corpuscular volume (MCV) of 87.5, a platelet count of 13, a white blood cells (WBC) count of 6.4, and an international normalized ratio (INR) of 1.73. Other values included serum sodium 132, lactate 4.6, alkaline phosphatase 133, total bilirubin 1.9, direct bilirubin 1.6, and albumin 2.8. The malarial screen was negative. A chest X-ray showed bilateral lower lobes infiltrates consistent with pneumonia. A computed tomography (CT) scan of the chest, abdomen, and pelvis showed mild bilateral areas of focal infiltrates and consolidation consistent with pneumonia and small right scrotal hydrocele. A peripheral blood smear (Figure ) showed few monoblasts, few dysplastic features, and erythrocytes with intracellular inclusions. He received supportive care with blood and platelet transfusions. He was treated with intravenous ceftriaxone and intravenous azithromycin for community-acquired pneumonia and atovaquone for malaria.
A bone marrow aspirate was done (Figure ), and the smear showed hypercellular marrow with monoblasts, erythroblasts, maturation defect, and few megakaryocytes. Further examination showed hypercellular marrow for age with sheets of immature mononuclear cells (blasts and monocytes) diffusely occupying marrow cavities. Table shows the differential count of the bone marrow cells. Blasts comprised approximately 50% of marrow elements, confirmed by immunostaining with CD34 and CD117. Monocytes comprised approximately 20%-30% of marrow elements. The blasts were medium to large with increased nucleus-to-cytoplasm (N/C) ratio, fine chromatin, and prominent nucleoli.
Table presents the bone marrow differential count.
These results were consistent with a diagnosis of acute myeloid leukemia (non-APL), best classified as acute myelomonocyte leukemia (AMML). Flow cytometry analysis from the aspirate showed blasts (12%-15%) that were positive for CD34 (partial), CD117, HLA-DR, CD13, CD33, and CD38. Monocytes (~25%) were positive for CD2, CD4, CD11b, CD11c, CD13, CD14, CD33, CD38, CD45, CD64, and HLA-DR. CD56 was negative.
CCAAT/enhancer-binding protein alpha (CEBPA) mutational analysis was not detected. A fluorescence in situ hybridization (FISH) test (Figure ) showed no evidence of RARA rearrangement, no evidence of BCR/ABL rearrangement, no evidence of PML/RARA gene rearrangement, and no evidence for RUNX1/RUNX1T1 rearrangement; however, a subset of cells showed an abnormal hybridization pattern, consistent with gain of 8q or trisomy 8 (Figure ). There was no evidence of MLL gene locus 11q23 translocation and no evidence of CBFB [inversion (16) or translocation (16;16)] gene rearrangement.
OnkoSight TM (Bio-Reference Laboratories, Inc., NJ, USA) NGS AML panel sequencing identified a frameshift mutation in ASXL1 (p.Gly646Trpfs*12), a frameshift mutation in RUNX1 (p.Tyr281Leufs*319), and a hotspot missense mutation in DNMT3A (p.Arg882His). Cytogenetics revealed an abnormal male karyotype with tetrasomy of 8 (49, XY, 8+, 8+) (Figure ).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [47, 'years'], 'weight': [35.0, 'lbs'], 'Sodium': [132.0, 'mEq/L']}",-0.54431,-0.51709,-0.57153,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 47 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 35.0 lbs so this converts to 35.0 lbs * 0.453592 kg/lbs = 15.87572 kg. The concentration of sodium is 132.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 132.0 mEq. To convert from 132.0 mEq to mmol, convert from mEq to mmol. The compound 132.0 has a valence of 1, and so divide the valence by the value of mEq to get, 132.0 mEq/(1 mEq/mmol) = 132.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 132.0 mEq sodium/L converts to 132.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 15.87572 * (132.0/140 - 1) = -0.54431 L. The patient's free body water deficit is -0.54431 L."
6116,38,Free Water Deficit,lab test,decimal,pmc-2804057-1,Extracted,"We report on a 32-year-old female (62 kg bodyweight) with history of paranoid-hallucinatory schizophrenia and depression who was discovered by her companion in life 26 hours after ingestion of 36 g quetiapine (120 tablets of 100 mg and 80 tablets of 300 mg) and a suspected abuse of lorazepam. A previous suicide had been attempted 10 years before with haloperidol. Her past medical history was negative for cardiac dysrhythmia, hypertensive heart disease or a thyroid dysfunction. The emergency medical service found the patient comatose with response only to deep painful stimuli (Glasgow Coma Scale of 9), normotensive (127/83 mmHg), hyperglycemic capillary glucose level: 8.96 mmol/L = 160 mg/dl and tachycardiac with sinustachycardia of 140 bpm, capillary oxygen saturation was 98% and respiratory rate 12/min. There was no evidence of trauma or infection. During the transport to the hospital 40 mg of furosemide and 1000 mL saline were administered intravenously for detoxification and prophylaxis of hypotension. Vital signs were stable during transport.
On admission on the intensive care unit (ICU) the patient's condition worsened and she was intubated for airway protection. At this time venous blood gas on 30% FiO2 revealed pH of 7.38, pO2 of 45.3 mmHg, pCO2 42.2 mmHg, HCO3
− 24.4 mmol/L, base excess −0.1 mmol/L, Hb 13.8 g/dl, K+ 3,7 mmol/L, Na+ 140 mmol/L.
To prevent her from further absorption of quetiapine a gastric lavage was performed (no pill fragments of ingested tablets were recovered) and the patient enterally received 25 g of activated charcoal with 5 g Glauber's salt (sodium sulfate) every 3 to 4 hours until dejection of black stool.
Laboratory data on admission including serum electrolytes, liver, and renal function parameters and blood count remained normal except glucose of 8.12 mmol/L (145 mg/dl), CK of 333 U/L (control value remained unchanged) with no evidence of myocardial insufficiency or infarction, CRP of 32 mg/L (control value 8 hours later increased to 76 mg/L), TSH 6.0 mU/L (control value 8 hours later increased to 8.56 mU/L), and leucocytosis with 12.06 (×109/L).
The electrocardiogram at 36 hours postingestion revealed a moderately extended QTc interval measuring 436 millisseconds (at the upper limit of normal) compared to QTc interval of 388 ms after complete recovery. QTc-intervals were calculated using the Bazett formula [].
A comprehensive drug screen via immunoassay was positive for tricyclic antidepressants and benzodiazepines in particular, although these results could not be confirmed by UV-HPLC-methods.
One day after admission cardiac and pulmonary status was stable (without signs of QTc-prolongation, arrhythmia, or tachycardia), state of consciousness improved, so that she could be extubated and was transferred to psychiatric crisis ward within 67 hours after ingestion of quetiapine. The increased levels for glucose and TSH lasted for 2.5 days, CK turned to normal after 6 days and CRP after roughly two weeks, respectively (see ).
Serum-samples for pharmacokinetic analysis were collected directly on arrival in the emergency department, 5 hours after admission and the following two days (four samples in total). Quetiapine serum concentrations were determined by a validated UV-HPLC-method (linearity range 0.03–4.00 mg/L, lower limit of quantification (LLOQ) 0.03 mg/L, limit of detection (LOD) 0.01 mg/L). Drug concentrations and patient's data (gender, age, weight, height) as well as the ingested amount of quetiapine were processed by a commonly used pharmacokinetic program Mw/Pharm 3.50 []. Pharmacokinetic parameters were investigated based on an open two-compartment model and a Bayesian fitting procedure.
Elimination half-life was calculated as follows:
– t
1/2 = ln 2/λ
z (elimination, λ
z is the rate constant corresponding to the terminal elimination).
exemplifies the obtained quetiapine concentration levels and the software generated time-concentration profile based on a two-compartment model (solid-line). In addition, the expected time-concentration profile based on population-pharmacokinetic data is shown (dotted line). Absorption was supposed to be reduced because of anticholinergic effects of quetiapine on intestinal tract.
The elimination half-life was t
1/2 = 5.3 hours and was calculated based on the four obtained quetiapine concentration levels (c1 = 4.22 mg/L; c2 = 2.77 mg/L; c3 = 0.06 mg/L; c4 = 0.06 mg/L) with regard to patient's medical records and displayed a moderately increased elimination compared to population pharmacokinetic parameters. Additionally, the absorption rate constant ka (time)−1 had to be adjusted and displayed a reduced absorption of quetiapine after ingestion. In this case the patient was supposed to have ingested 36 g quetiapine corresponding to a dosage of 580 mg/kg quetiapine. Volume of distribution was within the expected range (Vd = 9 L/kg based on fitted solid line, ).
Expected peak quetiapine concentrations for population-pharmacokinetic data were higher than the fitted time-concentration profile based on measured quetiapine concentrations and a two-compartment model.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [32, 'years'], 'weight': [62.0, 'kg'], 'Sodium': [140.0, 'mEq/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 32 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 62.0 kg. The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 62.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
6117,38,Free Water Deficit,lab test,decimal,pmc-8604086-1,Extracted,"Clinical summary
A 43-year-old Danish man who had suffered from persistent occipito-nuchal pain for 10 years flew to Japan for sightseeing in June, 1979. He vomited in the airplane and complained of sever malaise. Next day, progressive muscle weakness and dyspnea on exertion appeared. On day 3, myalgia of both thighs started, and marked sweating happened on day 4. He was admitted to a local hospital in Tokyo on day 5. Urine excretion was kept, but the urine color was black. He smoked cigarettes and drank alcohol, but did not use any special medication. No family history of muscle disease was recorded. On admission, his mental status was clear. Hypothermia (35°C), tachycardia (120/minutes), and hypertension (150-170/100-120 mmHg) were pointed out. He complained of cold sensation on the lower extremities. Because of systemic myalgia with tenderness, he could not sit up on the bed. Decrease of urine volume (415 mL/day) with black-colored appearance persisted. The laboratory data on admission included neutrophilia (20,000/µL), blood urea nitrogen 42 mg/dL, creatinine 2.0 mg/dL, aspartate transaminase 700 IU/L, alanine aminotransferase 130 IU/L, lactate dehydrogenase 1,860 IU/L, sodium 137 mEq/L, potassium 5.4 mEq/L, chloride 95 mEq/L, and calcium 3.7 mEq/L. The urine revealed macroscopic hematuria but without red cells in the sediment. Myoglobin was immunologically detected in his urine. On day 7, he expired suddenly and unexpectedly. No dialysis therapy was given throughout his illness.
Autopsy findings
Autopsy was performed 6 hours after death in the Department of Pathology, Keio University School of Medicine, Tokyo, Japan. A well-muscled body weighed 72 kg, with height of 175 cm. No gross abnormality was discerned in skeletal and cardiac muscles (Figure ).
Microscopically, myolytic fibers were dispersed in both skeletal and cardiac muscles. Cellular reactions were sparse: infiltration of macrophages and neutrophils was minimal. The kidneys weighed 160 g (left) and 140 g (right). Eosinophilic granular casts were observed in the lower nephrons, and the casts were positive for Ralph’s benzidine reaction [] (Figure , ).
The casts in the FFPE sections showed myoglobin immunoreactivity with a peroxidase-antiperoxidase (PAP) method [] (Figure ). The direct cause of death was pulmonary edema due to acute heart failure. The cause for his persistent nuchal pain was not clarified.
Liquid chromatography tests for arsenics and heavy metals were negative in the liver. Viral isolation trials using the -20°C frozen striated muscles, kidney, and serum were unsuccessful: in vitro experiment with human erythroleukemia cells and in vivo experiment with suckling mice failed to identify any virus. Immunofluorescence studies for Coxsackie viruses (A12, B3, B4, and B5) and herpes simplex virus were negative.
The final anatomical diagnosis was idiopathic rhabdomyolysis with acute renal failure due to myoglobin cast formation.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [43, 'years'], 'weight': [72.0, 'kg'], 'sex': 'Male', 'Sodium': [137.0, 'mEq/L']}",-0.92571,-0.87942,-0.972,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 43 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 72.0 kg. The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 72.0 * (137.0/140 - 1) = -0.92571 L. The patient's free body water deficit is -0.92571 L."
6118,38,Free Water Deficit,lab test,decimal,pmc-7216462-1,Extracted,"A full-term 4-week old, African American male with an admission weight of 3,535 g presented to the emergency department with fever of 38.3 °C and nasal congestion. The patient’s mother reported no diarrhea, emesis, or cough and a recent diagnosis of thrush with initiation of nystatin therapy 2 days prior to presentation. Family history was significant for the mother, maternal uncle, and additional maternal relatives with renal tubular acidosis treated with bicarbonate supplements; however, the specific cause of RTA was never diagnosed. On admission, physical examination revealed a small appearing neonate with decreased subcutaneous fat in mild respiratory distress. An evaluation for sepsis was performed. Chemistry studies revealed serum bicarbonate of 5 mmol/L, serum sodium of 132 mmol/L, serum potassium of 3.4 mmol/L, serum chloride 114 mmol/L, serum creatinine of 0.49 mg/dL, blood urea nitrogen 19.3 mg/dL, serum phosphorus 5 mg/dL, and serum magnesium of 2.5 mg/dL. Venous blood gas revealed pH 7.16 and pCO2 of 19 mmHg. Urinalysis was notable for urine pH 6.0 and negative for glucose. These results were consistent with non-anion gap metabolic acidosis. Fractional excretion of bicarbonate was appropriate at 1%. The absence of diarrhea, lack of evidence of proximal tubular dysfunction (normal serum phosphorus, appropriate fractional excretion of bicarbonate, and absence of glucosuria), presence of low serum potassium, and the finding of inappropriately high urine pH led to clinical diagnosis of distal renal tubular acidosis. Intravenous sodium acetate was initiated with improvement in serum bicarbonate levels. Renal ultrasound showed normal kidneys with no evidence of nephrocalcinosis. The patient was discharged on oral sodium citrate 8.8 mEq/kg/day (10 mL 3 times daily) and potassium citrate supplementation 4.4 mEq/kg/day (2.5 mL 3 times daily) with plan for close outpatient follow-up. The bicarbonate supplementation formulation included sodium citrate solution 500 mg/334 mg per 5 mL (1 mL = 1 mEq of sodium ion and 1 mEq bicarbonate equivalent of citrate) and the potassium citrate and citric acid solution 1,100 mg/334 mg per 5 mL (1 mL = 2 mEq potassium ion and 2 mEq bicarbonate equivalent of citrate). Both solutions contained 2% v/v PG.
The evening after hospital discharge, the patient’s mother brought him back to our emergency room for concerns of lethargy. His mother stated that he appeared more tired and did not wake to feed. She noted that he was staring and blinking with his hand in his mouth, but denied noticing any shaking, tremor, emesis, skin color changes, or breathing issues. In the emergency room, the patient had a witnessed episode of staring without changes in vital signs, shaking, jerking, or emesis. CBC, CMP, and phosphorous levels were obtained and unremarkable. The patient was admitted for observation and evaluation of staring spells. During hospitalization, he returned to his baseline level of activity without initiation of anti-epileptic therapy and no additional staring spells were noted.
Upon medication review by a clinical pharmacist, concerns arose for possible excess exposure to PG. The PG content of sodium citrate and potassium citrate supplementation was verified with the manufacturer and estimated at 222 mg/kg/day, higher than the WHO limit for PG in food additives at 25 mg/kg/day. This high dose of citrate therapy was likely being administered for ~ 6 days prior to the onset of his symptoms. Review of medications for additional exposure to PG revealed that nystatin, swabbed to each side of mouth for treatment of thrush beginning 4 days prior to admission, also contained PG. Oral citrate supplementation and nystatin were stopped, and intravenous fluid with acetate was started. Toxicology service was consulted and PG levels were found to be elevated at > 15,000 µg/mL, a level consistent with PG toxicity and expected to cause altered mental status. Measured serum osmolality on admission was elevated at 306 mOsm/kg, and the calculated osmolal gap was 25 mOsm/kg. Serum osmolality 1 week later was normal at 283 mOsm/kg. The patient was then transitioned from intravenous sodium acetate to oral sodium bicarbonate supplementation (medication with no PG), and the dose was titrated to achieve a goal venous blood gas pH 7.35 – 7.45. The patient was transitioned back to oral sodium citrate supplementation at 1.3 mEq/kg/day. Two weeks following discharge, PG level was undetectable, and venous blood gas showed pH was in goal range at 7.36.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [4, 'weeks'], 'weight': [3535.0, 'g'], 'Sodium': [132.0, 'mmol/L']}",-0.1212,-0.11514,-0.12726,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 4 weeks old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 3535.0 g so this converts to 3535.0 lbs * kg/1000 g = 3.535 kg. The concentration of sodium is 132.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 3.535 * (132.0/140 - 1) = -0.1212 L. The patient's free body water deficit is -0.1212 L."
6119,38,Free Water Deficit,lab test,decimal,pmc-5590421-1,Extracted,"A 2-year-old male child from Villupuram, Tamil Nadu, was referred to us for a clinical suspicion of renal stones. The child was developmentally normal for age. Poor weight gain was reported by the parents, while there was no history of diarrhea, polyuria, polydipsia, pallor, dysuria, recurrent respiratory tract infections, or anorexia. He was born to third-degree consanguineous Tamil parents. At birth, he weighed 3.5 kg and his perinatal history was uneventful. He was immunized according to the age. At the age of 24 months, he weighed 9.7 kg (−1–−2 standard deviation [SD]), height 71 cm (−2–−3 SD), head circumference 46 cm, and vital signs and blood pressure (93/62 mmHg) being normal. No pallor, icterus, clubbing, edema, rickets, or lymphadenopathy was noted. Cardiovascular, abdominal, central nervous system and chest examinations were normal. No renal masses were appreciable. The abdominal X-ray showed nephrocalcinosis [].
He was fourth in birth order. His elder sister died at 9 years of age as a result of end-stage renal disease due to nephrocalcinosis. She had persistent vomiting at 3 months of age. She was admitted to another hospital where renal stones and high urinary oxalate levels (80 mg/24 h) were detected. A therapy based on potassium citrate and pyridoxine was suggested (at the age of 4 months), but was administered to the child only for 1 year, and then discontinued by the parents. At 8 years of age, she was found to have urinary tract infection and high serum creatinine levels (8.2 mg/dl). She was then kept on biweekly dialysis for 3 months and died at 9 years of age at home. No genetic testing was performed.
The two other siblings, aged 6 and 4 years, were healthy and did not have nephrocalcinosis, deranged renal function, or high urinary oxalate levels. Their parents were healthy; no further cases of nephrolithiasis were reported in the family.
In view of the family history and presence of nephrocalcinosis on abdominal X-ray, the child was investigated further: 24 h urinary oxalate level was high (75.7 mg/24 h), blood urea 32 mg/dl, serum creatinine 0.4 mg/dl (estimated glomerular filtration rate 80 mL/min/1.73 m2), serum calcium 9.2 mg/dl, phosphate 4.0 mg/dl, sodium 136 mEq/L, potassium 3.8 mEq/L, and hemoglobin 9.7 g/dl. The spot urine calcium: Creatinine ratio was 0.1 (normal for age). Venous blood gas analysis showed serum bicarbonate level 22 mEq/L. Renal ultrasonography showed medullary nephrocalcinosis.
The entire coding region of the AGXT gene (RefSeq NM_000030 2, Gene ID: 189) was amplified by polymerase chain reaction from genomic DNA extracted from blood. Analysis of the AGXT gene by means of Sanger sequencing[] revealed the presence of two single nucleotide substitutions in homozygous state: a transversion from C to G (c. 32C>G) in exon 1 resulting in the missense substitution p. Pro11Arg and a transversion from T to A (c. 167T>A) in exon 2 resulting in the missense substitution p. Ile56Asn []. Both variants have previously been reported and are classified as pathogenic. The other polymorphic sites of the gene were found in homozygosis and corresponded to the major haplotype.[] Following the current nomenclature,[] the AGXT gene mutations detected in this patient are described as: c.[32C>G; 167T>A];[32C>G; 167T>A] at the DNA level and p.[Pro11Arg; Ile56Asn];[Pro11Arg; Ile56Asn] at the protein level. Thus, the diagnosis of PH Type 1 was confirmed. Genetic testing of the parents was advised but not performed since they did not agree to undergo any further analysis.
The patient was treated with potassium citrate (0.5 mEq/kg/day) along with pyridoxine (5 mg/kg/day). He was advised to increase fluid intake to 3 L/m2/day, avoid oxalate-rich foods (such as tomato, spinach, and beetroot,), and take a low salt diet.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [2, 'years'], 'weight': [9.7, 'kg'], 'Sodium': [136.0, 'mEq/L']}",-0.16629,-0.15798,-0.1746,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 2 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 9.7 kg. The concentration of sodium is 136.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.0 mEq. To convert from 136.0 mEq to mmol, convert from mEq to mmol. The compound 136.0 has a valence of 1, and so divide the valence by the value of mEq to get, 136.0 mEq/(1 mEq/mmol) = 136.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mEq sodium/L converts to 136.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 9.7 * (136.0/140 - 1) = -0.16629 L. The patient's free body water deficit is -0.16629 L."
6120,38,Free Water Deficit,lab test,decimal,pmc-2859476-1,Extracted,"A 12-year-old male child presented with the complaints of polyuria and polydipsia of two months duration in April 2007. There was no history of weight loss, anorexia, nausea, vomiting, dysuria, hematuria, graveluria, recurrent urinary tract infection, or nocturnal enuresis. His past history included poor school performance and diminished distant vision since his age of eight years. He was born out of a nonconsanguinous marriage as a full-term normal vaginal delivery. He had a monozygotic twin and both had polydactyly in all limbs. There was no history of any illness in the neonatal period but his twin died at the age of two months due to a severe respiratory infection. His developmental milestones were however delayed.
Examination at presentation showed weight 44 kg (>75th percentile), height 128 cm (<5th percentile), BMI of 27.4 kg/m2, waist/hip ratio of 1.06, pulse 80/min, and BP 130/90 mmHg. He had pallor, no pedal edema and systemic examination was unremarkable. He had polydactyly in all four limbs [] and features of hypogonadism with testicular volume of 2 ml (normal 10–12 ml) and micropenis (<2.5 cm) []. Ophthalmological examination showed bilateral impaired distant vision, normal anterior segment and lens, and fundus features of retinitis pigmentosa. Psychological evaluation revealed borderline mental retardation with an IQ of 71–75.
Investigations showed Hb 7.9 gm/dl, TLC 7000/cmm, 1 + proteinuria with no active urinary sediment, 24-hour urine protein of 240 mg, BUN 43 mg/dl, creatinine 4.3 mg/dl, serum sodium 143 mEq/l, serum potassium 3.8 mEq/l, serum total protein 8.1 gm/dl, albumin 3.9 gm/dl, calcium 9.4 mg/dl, phosphorus 3.9 mg/dl, serum alkaline phosphatase 486 U/l, and blood sugar F/PP 80/96 mg/dl. Ultrasound showed small kidneys (right 6.3 cm, left 6.7 cm) with loss of cortico-medullary differentiation, mild cortical irregularity, and normal PCS. DTPA scan showed bilateral impaired renal function (GFR right kidney 16.1 ml/min, left kidney 15.8 ml/min, and total GFR 31.9 ml/min). Echocardiography showed normal systolic function and no structural abnormality.
He was diagnosed as BBS with stage III chronic kidney disease and started on conservative management and underwent amputation of extra digits of hands. He progressed to ESRD in April 2008 with creatinine remaining consistently around 11 mg/dl and calculated GFR of 5.68 ml/min. He underwent preemptive renal transplant on May 02, 2008, his mother aged 38 years being the donor. His immunosuppression consisted of Tacrolimus 0.15 mg/kg, Mycophenolate mofetil 500 mg BD, and Prednisolone 0.5 mg/kg. He remained anuric in immediate postoperative period and no bruit was audible at graft site and color doppler showed graft vein thrombosis. He was re-explored and the operative findings confirmed graft vein thrombosis with extension of the thrombus in the external iliac vein. The graft was reperfused and reanastomosis was done after thrombectomy. His graft showed gradual return of function and he was discharged on 14th postoperative day with a creatinine level of 1.2 mg/dl. At last follow-up on June 26, 2009 (14 months posttransplant), he was asymptomatic with urine output of >2 l/day, creatinine of 1.1 mg/dl, and DTPA scan GFR of graft kidney of 56.3 ml/min.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [12, 'years'], 'weight': [44.0, 'kg'], 'Sodium': [143.0, 'mEq/L']}",0.56571,0.53742,0.594,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 12 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 44.0 kg. The concentration of sodium is 143.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 143.0 mEq. To convert from 143.0 mEq to mmol, convert from mEq to mmol. The compound 143.0 has a valence of 1, and so divide the valence by the value of mEq to get, 143.0 mEq/(1 mEq/mmol) = 143.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mEq sodium/L converts to 143.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 44.0 * (143.0/140 - 1) = 0.56571 L. The patient's free body water deficit is 0.56571 L."
6121,38,Free Water Deficit,lab test,decimal,pmc-6959940-1,Extracted,"A 58-year-old man presented to the emergency department (ED) complaining of 3 days of low abdominal pain and dysuria. The abdominal pain was dull and especially aggravated just before defecating. The patient had previously heard from his parents that the he was born with ambiguous genitalia and some parts of the patient's external genitalia were excised when the patient was three years old. Since then, the patient was raised as male. The patient was married to a woman but had no children.
The height of the patient was 140 cm, and he weighed 50.1 kg and was bald. The patient had tenderness on the lower abdomen. The patient had micropenis and no palpable testis. The patient's urethral orifice was located on the perineum, not at the tip of the glans penis. The blood pressure was 114/72 mmHg and temperature was 37°C. White blood cell count was 15,100/μL, C-reactive protein (CRP) was 12.77 mg/dL, and sodium was 138 mMol/L. Urine analysis showed that the patient had pyuria. The ED physicians decided to perform an abdominal computed tomography (CT) for further evaluation. The CT showed
suspicious PID including left salpingitis;
a 10 cm myelolipoma in the left adrenal gland;
a 3.2 cm hypervascular mass in the small bowel mesentery (Fig. ).
The patient was admitted to the ED for evaluation of possible CAH and intravenous antibiotic administration of third generation cephalosporin and metronidazole was initiated. After 3 days of antibiotic treatment, CRP decreased to 1.65 mg/dL and the patient reported an improvement of the symptoms although the pain before defecation persisted. Along with antibiotics, a hormonal study regarding CAH was carried out (Table ). A high 17-OH-progesterone (17-OH-PG) level above 3500 ng/dL suggested that the patient had underlying CAH. Since the patient had ambiguous genitalia from birth and did not have electrolyte imbalance caused by salt wasting, we diagnosed the patient with classic simple virilizing CAH. Virilization of females can be caused by a deficiency in enzymes 21-OH and 11-beta hydroxylase. A deficiency in 11-beta hydroxylase deficiency presents with hypertension and low renin and aldosterone levels; however, the patient was suspected of having 21-OH deficiency due to the normal blood pressure, and normal levels of renin and aldosterone. Although the patient did not show symptoms of adrenal insufficiency, the rapid ACTH test results were abnormal, indicating a cortisol deficiency. During the ACTH stimulation test, response of 17-OH-PG to ACTH was exacerbated. This result further supported the diagnosis of CAH due to a 21-OH deficiency. The results are summarized in Table .
On the 12th day after admission, CRP decreased to 0.12 mg/dL, and intravenous antibiotics were suspended. Positron emission tomography-CT (PET-CT) was performed to evaluate whether the mesenteric mass was malignant. PET-CT demonstrated
a hypermetabolic mass with homogenous, intense fluorodeoxyglucose (FDG) uptake in the mesentery suggesting primary mesenteric tumor (peak standardized uptake value [SUV] = 11.8);
a hypermetabolic mass with heterogenous FDG uptake in the left adrenal gland suggesting benign adrenal gland tumor (peak SUV = 5.5) (Fig. ).
The patient opted for resection of the female genitalia along with the mesenteric and adrenal gland tumors in the near future. The physicians planned to administer stress-dosing corticosteroid during operation, and to decrease the dose to physiologic level afterward. The patient was safely discharged. Patient has provided informed consent for publication of the case.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [58, 'years'], 'weight': [50.1, 'kg'], 'sex': 'Male', 'Sodium': [138.0, 'mmol/L']}",-0.42943,-0.40796,-0.4509,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 58 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 50.1 kg. The concentration of sodium is 138.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 50.1 * (138.0/140 - 1) = -0.42943 L. The patient's free body water deficit is -0.42943 L."
6122,38,Free Water Deficit,lab test,decimal,pmc-7521777-1,Extracted,"An 89-year-old woman with a history of Alzheimer's disease was referred to our hospital for assessment by her physician because of acute deterioration in BPSD. In terms of activities of daily life, she was able to walk independently and was able to eat on her own when food was provided. Her most recent Revised Hasegawa Dementia Scale (HDS-R) score was nine points. She made use of a daycare service during the day. According to a report by a staff member at the daycare facility, her forgetfulness had worsened over the previous week, and she had experienced day-night reversal, night wandering, and the illusion that someone was resting on her head. She had almost no water intake, and she had consumed only a few mouthfuls of food, including both staple foodstuffs and side dishes, at meals. And multivitamin supplementation had not been commenced.
The findings at the first consultation were as follows. The patient was 127.5 cm in height and 34.3 kg in weight, with a BMI of 21.1. Her blood pressure was 127/69 mm Hg, heart rate 68 bpm, and body temperature 36.6°C.
Although conversation was possible, she could not tell the time or date, and she appeared disoriented. Furthermore, although she answered questions, she could not give correct answers as she did not understand the questions. Examination of her conjunctiva showed no sign of anemia, chest examination showed no murmur or abnormal breathing, and her abdomen was flat, soft, and without areas of tenderness. Her laboratory findings were as follows: white blood cell count, 6530/µL; red blood cell count, 417 × 104/µL; hemoglobin, 9.9 g/dL; hematocrit, 29.4%; platelet count, 33.4 × 104/µL; aspartate aminotransferase, 28 IU/L; alanine aminotransferase, 13 IU/L; alkaline phosphatase, 209 IU/L; lactate dehydrogenase (LDH), 327 IU/L; gamma-glutamyl transpeptidase, 8 IU/L; blood urea nitrogen, 26.3 mg/dL; creatinine, 1.2 mg/dL; sodium (Na), 140 mEq/L; potassium (K), 2.5 mEq/L; and chlorine (Cl), 86 mEq/L. Chest x-rays revealed no obvious congestion, cardiac enlargement, or infiltrative shadows. CT scans of the head showed atrophy of the frontal and temporal lobes and the hippocampus, and her electrocardiogram revealed mild ST depression in leads I, II, aVF, and V2-6 (possibly because of hypokalemia). Further interviews with a staff member at the daycare facility revealed that her oral food intake had been decreased for 2 months.
The worsening of her psychiatric symptoms within a period of only 2 weeks was considered to indicate delirium rather than the progression of Alzheimer's disease. In addition, TD was suspected from the fact that her dietary intake had been decreased for over 2 months and thiamine is only stored in the body for about 18 days. Therefore, as she satisfied 2 out of 4 of Caine's WE diagnostic criteria—eye signs, cerebellar signs, mild memory impairment or confusion, and signs of malnutrition—she was suspected of TD.
Thiamine disulfide (50 mg) was administered intravenously once a day for 3 days. In addition, we administered an infusion of maintenance fluid at 500 mL a day for 3 days because of her decreased water intake. Her symptoms such as day-night reversal, night wandering, and hallucinations disappeared a few days later. Several days after blood sampling, her serum thiamine level was found to be abnormally reduced to 19.4 (normal range: 21.3-81.9 ng/mL). Thereafter, she returned to her regular life.
The clinical findings, effective alleviation of delirious symptoms after thiamine and the administration of maintenance fluid infusion, low thiamine intake from food, and low level of thiamine in the serum fulfilled the Francis criteria for delirium induced by thiamine deficiency.
Over the following 9 months, the patient showed no recurrence of delirium. The VB1 blood concentration measured at that time was 37.0 ng/mL.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [89, 'years'], 'weight': [34.3, 'kg'], 'Sodium': [140.0, 'mEq/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 89 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 34.3 kg. The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. Plugging in these values into the equation, we get 0.45 * 34.3 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
6123,38,Free Water Deficit,lab test,decimal,pmc-3030016-1,Extracted,"A 52-year-old, 65 kg, 162 cm tall male patient was admitted for hepatoma. The patient was diagnosed as having hypertension and symptomatic ventricular premature complex and he was treated with a β-blocker and an angiotensin receptor blocker. The patient had been diagnosed with chronic renal failure two years previously and he had undergone transarterial chemoembolization (TACE) for hepatocellular carcinoma two months before the present admission. A preoperative blood test showed no hyperkalemia: the Na+ level was 44 mM/L, the K+ level was 4.6 mM/L, the BUN level was 29.8 mg/dl and the creatinine level was 10.4 mg/dl. His electrocardiogram (ECG) showed normal sinus rhythm.
Anesthesia was induced with 100 mg of propofol and 50 mg of rocuronium, and then 1.5-2 vol% sevoflurane was used for anesthetic maintenance. Remifentanil at 0.4-1 µg/kg/min was continuously infused intravenously. To measure the continuous arterial pressure, a 20 gauge catheter was inserted into the right radial artery, and a 7 Fr catheter was inserted into the right internal jugular vein for measuring the central venous pressure. After the surgery began, the arterial blood gas analysis and the level of electrolytes were checked every two hours. The results of the arterial blood gas analysis performed at the beginning of surgery showed no hyperkalemia ().
Neither a specific inotropic drug nor a vasoconstrictor was needed to maintain a systolic blood pressure of 150-90 mmHg and a diastolic blood pressure of 86-51 mmHg until the fourth hour of surgery. Thereafter, phenylephrine at 1-1.5 µg/kg/min was continuously infused to maintain a mean blood pressure above 60 mmHg. At the fifth hour of surgery, arterial blood gas analysis showed a K+ level of 4.89 mM, which was in the upper normal range, so additional treatment was not performed (). In surgical field, portal triad clampings were done before resecting each segment in order to confirm the resection margin. At 6.5 hours of surgery, a sudden decrease in arterial blood pressure was observed. The curvature of the radial artery diminished and the arterial blood pressure was 80/60 mmHg. At that time, trisegmentectomy had been completed, so the surgeon had begun suturing the muscle layer. No compression of the artery or vein was observed and the central venous pressure was 10 mmHg, which indicated there was no hypovolemic status. The phenylephrine infusion was increased to 2 µg/kg/min. QRS widening without a switching tall T wave was observed in the ECG, so an immediate arterial gas analysis was performed. No acidosis was observed, but the K+ level was 6.44 mM. Since hemolysis of the blood sample was possible, an arterial gas analysis was conducted again after ten minutes, and the result showed that K+ level had increased to 6.65 mM (). Calcium chloride (600 mg) was infused for several minutes and magnesium sulfate (2 mg) replacement was started for correcting the magnesium deficiency. As additional treatment was about to begin, a sudden onset of ventricular tachycardia was noted on the ECG.
The surgeon began chest compression and defibrillation at 200 J was performed twice. The cardiac arrest was thought to be due to hyperkalemia; therefore twenty units of insulin and 100 ml of 50% dextrose solution were mixed and infused continuously while 120 mg of sodium bicarbonate was being injected as well. One mg of epinephrine was administered repeatedly before performing defibrillation using 360 J. At 35 minutes after the initiation of cardiopulmonary resuscitation, a sinus rhythm on ECG and a systolic blood pressure of 70 mmHg were observed for five minutes and the total administered epinephrine was 41 mg. Nevertheless, the ventricular fibrillation continued. Due to the lack of a response to 100 mg injected lidocaine, an amiodarone infusion was started. After applying percutaneous extracorporeal support using the right femoral vein, the ECG and blood pressure appeared to stabilize, and the patient was transferred to the intensive care unit. Over 10 hours and 50 minutes of surgery, two units of packed red blood cells and 6,680 ml of crystalloid solution were administered. The total amount of urine was 710 ml, and 1,200 ml of blood was lost during the surgery.
Tests conducted one hour after resuscitation showed signs of liver damage with the laboratory results of AST/ALT: 255/156 IU/L, Na+: 152.5 mM and K+: 3.13 mM (). The bedside transthoracic echocardiography performed in the intensive care unit showed an inadequate volume in the ventricular chamber. The patient suffered multi-organ failure under anuria conditions, and the unstable vital signs continued despite the application of percutaneous extracorporeal cardiopulmonary support. Eight hours after his arrival in the intensive care unit, the patient suffered another cardiac arrest. After the administration of atropine and epinephrine, the sinus rhythm returned briefly, but the pulse rate dropped to lower than 40/min. When the ECG continued to be flat, the resuscitation attempts were discontinued.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [52, 'years'], 'weight': [65.0, 'kg'], 'sex': 'Male', 'Sodium': [44.0, 'mmol/L']}",-26.74286,-25.40572,-28.08,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 52 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 65.0 kg. The concentration of sodium is 44.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 65.0 * (44.0/140 - 1) = -26.74286 L. The patient's free body water deficit is -26.74286 L."
6124,38,Free Water Deficit,lab test,decimal,pmc-7713822-1,Extracted,"The present case report was published with the prior consent of the patient’s guardians.
A 23-year-old, 168 cm tall female patient, weighing 42 kg, visited the emergency room with a chief complaint of abdominal pain. The abdominal pain, accompanied by nausea and vomiting, kept increasing gradually for eight hours. The patient was diagnosed with major depression and bulimia nervosa nine years ago. The patient also had a history of frequent vomiting after episodes of binge eating, along with numerous suicide attempts. Ten hours before reporting to the hospital, the patient ate a very large quantity food, equivalent to approximately ten portions; however, the quantity of the vomit was much less, relative to the amount of food taken. The physical examination revealed abdominal pain and distension in the entire region, along with tenderness, but no rebound tenderness. Subsequent abdominal computed tomography (CT) revealed clear gastric distension. The results of various blood tests were normal. In the joint general surgery consultation that followed, it was decided that an immediate surgical treatment was not necessary; hence, the need for continuous observation of the condition was explained, and a gastroenterological or psychiatric hospitalization was advised, but both the patient and her guardians declined hospitalization. Afterward, they were warned of the possible complications, such as electrolyte imbalance, aspiration pneumonia, gastrointestinal perforation, ischemic changes, due to the pressure applied by gastrointestinal distension, and the possibility of death, in case the condition worsened. The self-discharge form was signed, and they returned home.
Seven hours after returning home, the patient re-visited the emergency room due to persistent abdominal pain, and mental confusion. At the time of the visit, the patient was unconscious. On physical examination, a more severe abdominal distension, and signs of abdominal rigidity were observed. Both legs of the patient had turned pale in color. No auscultation sounds were heard over the abdomen, and the dorsalis pedis pulse was not felt on either foot. Shock was suspected due to a 60/40 mmHg blood pressure, 160 beats/min heart rate, 22 times/minute aspiration rate, and 36.4℃ temperature. Other findings included pH 7.076, PaCO2 22.3 mmHg, PaO2 122 mmHg, HCO3- 6.3 mM/L, base excess (BE) 23.7 mM/L, and lactic acid 11.1 mM/L, which were measured in the arterial blood gas analysis and, thus, metabolic acidosis was confirmed. The electrolyte levels Na+ 157 mM/L, K+ 6.2 mM/L, and Cl- 130 mM/L, indicated that the electrolyte imbalance was severe (). In addition, the patient was in a severe hypoglycemic state with a blood sugar level of 15 mg/dl; because of an elevated creatinine level of 2.84 mg/dl, acute renal failure was suspected. First, to treat the metabolic acidosis, sodium bicarbonate was set at 80 mEq/h. In the abdominal X-ray, the gastrointestinal tract (GIT) was seen to be filled with a large amount of food but without any bowel gas (). Abdominal CT revealed a very large dilation of the stomach, esophagus, and the second part of the duodenum; it was suspected that the distended organs were pressing against the descending aorta, and the right kidney was pressed upwards (). One hour after the emergency room re-visit, the patient's mental state became lethargic—communication became impossible and spontaneous respiration decreased; as SpO2 was measured to be 88%, endotracheal intubation was performed. A Foley catheter was then inserted, but no urine was drained; an emergency hemodialysis was prepared, and for enough fluid supply, a central venous catheter was inserted into the right jugular vein. For continuous monitoring of changes in the vital signs, a conduit was placed in the right radial artery. An attempt was made to insert a nasogastric tube to relieve gastrointestinal pressure, but the food was not drained due to a blockage near the esophagus, which made further insertion impossible. An abdominal CT performed for follow-up observation revealed that the abdomen was still filled with food, and the nasogastric tube was twisted at the end of the esophagus (). It was also suspected that insertion was not possible due to gastroesophageal junction deviation or esophageal stenosis; however, no such sign was seen.
There was no decompression through the nasogastric tube, and as time passed, the mental state of the patient changed into a state of confusion. The patient’s vital signs became increasingly unstable. Since the symptoms and follow-up blood test results exacerbated, instead of performing a percutaneous drainage, it was decided to attempt a surgical decompression; subsequently, the patient was transferred to the operation room six hours after the re-visit. In the emergency room, a total of 3,170 ml of crystalloid fluid, in which a 5% glucose solution was included, was administered. Urine volume was not measured.
After reaching the operation room, the patient’s blood pressure was 70/46 mmHg and the heart rate was 128 beats/min. First, in order to improve the vital signs, crystalloid fluid was administered at the highest speed via the right arm’s peripheral venous catheter and via the central venous catheter of the right internal jugular vein. The instillation of norepinephrine was initiated with sustained dosing at an additional rate of 0.2 μg/kg/min, and continuous infusion of vasopressin at 4–8 unit/h was also initiated. Subsequently, general anesthesia was induced using sevoflurane 1–2 vol% and rocuronium 50 mg. In the arterial blood gas analysis conducted after entering the operating room, pH 7.45, PaCO2 20.8 mmHg, PaO2 335 mmHg, Na+ 161 mM/L, K+ 3.8 mM/L, glucose 205 mg/dl, lactate 13 mM/L, hemoglobin 6.8 g/dl, and HCO3- 14.4 mM/L were measured (). Four units of erythrocytes were prescribed to correct the reduced hemoglobin, and 20 mg of furosemide was injected due to a continuous lack of urination. Furthermore, for rapid transfusion, the rapid infusion system (RIS) was connected to the central venous catheter of the right internal jugular vein, and the transfusion of four erythrocyte units was initiated.
The operating surgeon planned and performed a gastrotomy, after making a skin incision of approximately 10 cm and within 20 min of beginning the surgery. The food and 5,000 ml of body fluid present in the stomach were drained via suction. Thirty minutes after the operation, blood pressure was maintained low at 60/40 mmHg and almost all food was drained; as a large amount of continuous gastric bleeding occurred after decompression, a total of 6,000 ml was drained into the suction bottle. In the follow-up arterial blood gas analysis, results showed: pH 6.75, PaCO2 46 mmHg, and lactate 20 mM/L. Acidosis had worsened, the blood sugar level had significantly increased to 469 mg/dl, electrolyte imbalance had exacerbated with K+ 7.5 mM/L, and hemoglobin had fallen to 4.3 g/dl, suggesting a large amount of bleeding. To correct this, 60 mEq of sodium bicarbonate, and two units of insulin were administered. Further, 1.2 g of calcium chloride was administered to treat hyperkalemia. Moreover, additional 20 μg of epinephrine was injected to correct persistent hypotension.
Bleeding in the stomach continued, and despite initiating erythrocyte transfusion via RIS, hemoglobin level decreased. As a result, a large amount of internal bleeding was suspected, and additional eight units of erythrocytes, and eight units of fresh frozen plasma were prescribed. The operating surgeon tried to determine the cause and area of bleeding, but as the surgical incision was only 10 cm, abdominal organs other than the stomach could not be identified with the naked eye. To reduce bleeding, the operating surgeon considered performing a total gastrectomy or extending the abdominal incision to confirm the bleeding areas from, other organs but concluded that the bleeding was due to ischemia-reperfusion injury after surgical decompression, and DIC. Since the patient’s vital signs steadily worsened, it was decided that the abdomen be closed urgently, and the patient moved to the intensive care unit (ICU).
One hour after the start of the operation, suturing after gastrectomy was completed. When the closing of the abdomen started, non-invasive blood pressure was not measured, and flat waveforms were observed in the catheter of the right radial artery. There was no pulse detected via palpation, and after confirming pulseless electrical activity through the observation of electrocardiogram, an additional 1 mg of epinephrine was injected, and cardiopulmonary resuscitation (CPR) was initiated.
A total of 3 mg of epinephrine was injected, with cardiac rhythm monitoring at 2 min intervals; afterward, 2 units of vasopressin were injected at 2 min intervals, totaling an injection of 4 units of vasopressin. After completing the abdominal closure while performing CPR, the patient was transferred to the intensive care unit, and no urine output was seen until the patient left the operation room.
The operation was conducted for 1 h 20 min, and the anesthesia time was 1 h 50 min. During the operation, a total of 800 ml, four erythrocyte units, were transfused, and 6,200 ml of crystalloid fluid were administered. A total of 6,000 ml was drained into the suction bottle—5,000 ml of food and body fluid through the suction unit via gastrectomy, and 1000 ml due to bleeding that had occurred after decompression from the start of the operation until finish; however, as mentioned earlier, the incision area was small, and bleeding occurring from other abdominal organs could not be confirmed, making it difficult to estimate the exact estimated blood loss. Additionally, prescribed erythrocytes and fresh frozen plasma were transfused through the RIS as the patient left the operation room.
After entering the ICU, CPR was stopped due to a return of spontaneous circulation, but the existing usage of epinephrine, norepinephrine, and vasopressin was preserved, and transfusion continued. However, blood pressure was still not measured, an additional 1,000 ml of bleeding was confirmed through the nasogastric tube, and bleeding from the closed abdominal area continued. Subsequently, as 3.5 g/dl hemoglobin was measured in the follow-up test, transfusion continued, and a 113.1-second prothrombin time, 180-s activated partial thromboplastin time, and platelet count of 22,000/μl were found, confirming that the patient was in a state of DIC. Despite continuous drug administration and transfusion, the hemoglobin level decreased to 1.8 g/dl, and after three hours in the ICU, the heartbeat disappeared, and the patient was declared dead.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [23, 'years'], 'weight': [42.0, 'kg'], 'sex': 'Female', 'Sodium': [157.0, 'mmol/L']}",2.55,2.4225,2.6775,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 23 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 42.0 kg. The concentration of sodium is 157.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 42.0 * (157.0/140 - 1) = 2.55 L. The patient's free body water deficit is 2.55 L."
6125,38,Free Water Deficit,lab test,decimal,pmc-5297160-1,Extracted,"A 61-year-old woman was admitted because of sudden onset of confusion and slurred speech. In preparation for an elective outpatient colonoscopy she had commenced bowel preparation four hours earlier with sodium picosulfate/magnesium citrate (PICOLAX ®). As instructed, she had ingested two liters of water and two liters of tea, albeit within two hours. Shortly thereafter, she felt nauseous, dizzy and vomited repeatedly. Her husband found her confused with unintelligible speech and unsteady gait and called the ambulance.
On physical examination, the patient appeared agitated and her speech was incomprehensible. She weighed 56 kg and her height was 168 cm (BMI 19.9 kg/m2). Vital signs were as follows: Afebrile, blood pressure 132/66 mmHg, pulse 82 beats/min. The patient was clinically euvolemic and could follow verbal commands. No lateralizing signs were found on neurological examination but generalized tremor was present. Acute CT scanning of the brain did not reveal any abnormalities.
Her medical records showed a history of hypothyroidism for which she took levothyroxine. She was a non-smoker and did not drink alcohol. Family history was unremarkable and there was no history of diuretic use or anorexia, as corroborated by her husband.
In the emergency department, biochemistry results were as follows: Serum sodium 122 mmol/l, potassium 3.1 mmol/l, chloride 87 mmol/l, BUN 14.8 mg/dl, creatinine 1.1 mg/dl, uric acid 4.1 mg/dl, glucose 108 mg/dl. Serum osmolality was 251 mOsm/kg. In view of the patient’s symptoms and the clear time of onset, acute hyponatremia was deemed likely and treatment with hypertonic saline (3%) at a rate of 50 ml/h was commenced. Urine osmolality was not done on admission but was 232 mOsm/kg with a urinary sodium of 39 mmol/l when tested two hours later. Thyroid-stimulating hormone was suppressed under replacement therapy. The sodium level increased to 128 mmol/l within the ensuing four hours. In parallel, the patient’s symptoms abated. Twelve hours after admission, she had voided 2600 ml of urine and her mentation and electrolytes had normalized.
On further questioning, it transpired that the patient had had very limited food intake prior to the scheduled procedure. On the day before admission (two days before the endoscopy appointment), her diet consisted of carrot-ginger soup with white bread for lunch and rusk with tea for dinner. The next day, a breakfast consisting of two slices of plain toast and a cup of coffee, followed by a broth at lunchtime, was all she had to eat. No additional salt had been added to her meals. Furthermore, the patient had been taking a nonsteroidal anti-inflammatory drug (NSAID) for the last five days because of shoulder pain (Diclofenac 50 mg bid). A diagnosis of hyponatremic encephalopathy due to acute water intoxication facilitated by poor dietary solute intake was made. On follow-up appointment 1 week later, the patient was well and electrolytes were normal. Adrenal function was tested and found to be intact.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [61, 'years'], 'weight': [56.0, 'kg'], 'Sodium': [122.0, 'mmol/L']}",-3.6,-3.42,-3.78,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 61 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 56.0 kg. The concentration of sodium is 122.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 56.0 * (122.0/140 - 1) = -3.6 L. The patient's free body water deficit is -3.6 L."
6126,38,Free Water Deficit,lab test,decimal,pmc-3668109-1,Extracted,"A 53-yr old woman (body weight: 63 kg, height: 162 cm) was scheduled for living donor liver transplantation due to acuteon-chronic liver failure. Thirteen years ago, she was diagnosed with hepatitis B related liver cirrhosis. Two days ago, she was intubated due to rapidly developing grade 3-4 hepatic encephalopathy. In the preoperative evaluation, the chest X-ray, electrocardiography, and echocardiography were within normal range. Her laboratory examination showed Hb 7.9 g/dl, platelet count 27 × 109/L, prothrombin time 3.5 international normalized ratio, fibrinogen 52 mg/dl, antithrombin III 6%, sodium 136 mmol/L, potassium 3.9 mmol/L, creatinine 3.8 mg/dl, glucose 163 mg/dl, albumin 3.1 g/dl, total bilirubin 52.8 mg/dl, and ammonia 205 µmol/L. Her Child-Pugh and Model for End-Stage Liver Disease scores were 12 and 49, respectively. However, brain computerized tomography and invasive ICP monitoring could not be performed because the acute exacerbation of her clinical condition requires urgent liver transplantation.
Upon arrival at the operating room, she was still intubated and was in a comatose state. Dopamine of 10 µg/kg/min, dobutamine of 15 µg/kg/min, and norepinephrine of 0.1 µg/kg/min had been administered continuously. Her systolic/diastolic/mean arterial blood pressure and heart rate were 100/50/67 mmHg and 80 beats/min, respectively. After establishing the standard monitoring used in our institute, ultrasound ONSD measurements were done by a physician well-trained in ocular ultrasonography before anesthetic induction. Based on the method described in a previous report [], both eyes were scanned using a 7.5-MHz probe (ProSound SSD-4000, ALOKA, Tokyo, Japan) through closed eyelids with the patient in the supine position. Right and left eyes were scanned in both sagittal and transverse planes, and the ONSD value was calculated by estimating the average results of these measurements. The ONSD was measured 3 mm posterior to the globe in each eye. Her ONSD just before anesthesia induction was 6.4 mm (). Simultaneously, TCD was performed to assess cerebral blood flow velocity and ICP noninvasively. Transtemporal insonation of the left middle cerebral artery was done using a 2-MHz probe (Companion III, Viasys Healthcare, Warwick, UK). TCD measurements showed her systolic/diastolic/mean cerebral flow velocities were 100/7/37 cm/s (normal reference values of systolic/diastolic/mean velocities [mean ± SD]: 77.1 ± 12.23/37.4 ± 7.13/50.6 ± 8.42 cm/s). The resistance index was 0.93 (normal reference value: 0.52 ± 0.05) and the pulsatility index was 2.5 (normal reference value: 0.80 ± 0.13), and the second systolic peak (Windkessel effect) was lost, suggesting elevated ICP () [,]. The bispectral index and suppression ratio were 30 and 20, respectively, and right and left regional cerebral oxygen saturations were 15/15%.
Anesthesia was induced with thiopental and vecuronium, and was maintained using 0.5-1% isoflurane, a 50% O2/air mixture, and continuous infusion with fentanyl and vecuronium. The patient's lungs were ventilated with a tidal volume of 10-12 ml/kg at a respiratory rate of 10-12 breaths/min to maintain hypocarbia (PaCO2: 28-32 mmHg) throughout the procedure. Also, mild hypothermia (34-35℃) was induced, and mannitol of 40 g was administered every six hours for the management of ICP. After anesthesia induction, her arterial blood gas analysis showed a pH of 7.33, a PaCO2 of 28 mmHg, a PaO2 of 209 mmHg, bicarbonate of 14.8 mEq/L, and base excess of -10.0 mmEq/L. Intraoperative hemodynamics and laboratory data were shown .
After finishing surgery, she was transferred to the surgical intensive care unit. On the second postoperative day, right and left pupil size were 3/3 mm. According to Glasgow coma scale evaluation, eye opening score was 4, best motor response score was 4, best verbal response score was not evaluated due to endotracheal intubation. Bispectral index score ranged from 70 to 90. However, on the third postoperative day, she was developed septic shock, and the patient died by septic shock on the fourth postoperative day.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [53, 'years'], 'weight': [63.0, 'kg'], 'sex': 'Female', 'Sodium': [136.0, 'mmol/L']}",-0.9,-0.855,-0.945,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 53 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 63.0 kg. The concentration of sodium is 136.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 63.0 * (136.0/140 - 1) = -0.9 L. The patient's free body water deficit is -0.9 L."
6127,38,Free Water Deficit,lab test,decimal,pmc-4722164-1,Extracted,"A one-day-old male was transferred to our neonatal intensive care unit from a local primary obstetric clinic several hours after birth due to respiratory difficulties. The patient was born at full term via caesarean section due to intermittent fetal heart deceleration during labor. There were no other remarkable perinatal complications or family history. Upon physical examination, the patient was seen to be large for his gestational age (physical profile: length, 55.0 cm [>95th percentile]; body weight, 4.4 g [>90th percentile]; head circumference, 37.5 cm [>95th percentile]). No other notable physical anomaly could be seen. His chest x-ray showed overall decreased lung volume, and decreased breathing sounds upon auscultation proved the need for respiratory support. He was put on noninvasive continuous positive end expiratory pressure ventilation for two days, after which he was weaned from it and kept in the room air.
Initial laboratory values at the time of admission showed the following: serum sodium, 137.0 mmol/L; serum potassium, 6.0 mmol/L; serum chloride, 100.0 mmol/L; blood-ureanitrogen, 14 mg/dL; serum creatinine, 0.9 mg/dL; serum calcium, 9.0 mg/dL; and serum inorganic phosphate, 5.3 mg/dL. His venous blood gas analysis showed pH 7.26, PCO2 55.9 mmHg, bicarbonate 25.9 mmol/L and base excess -2.0 mmol/L, reflecting mild respiratory acidosis. The patient's feeding proved to be poor, as he showed signs of nausea and vomiting with abdominal distention, and considering his age and health status, we assessed the cause to be nonspecific. As he needed respiratory support, the patient was put on intravenous fluid replacement (sodium 15 mEq mixed in 500 mL of 10% dextrose solution; infusion rate differed depending on the oral intake amount, with total intake limited to the patient's maintenance volume), and after he was weaned from respiratory support, feeding amounts were slowly increased until full enteral feeding was possible; this occurred by day 8 of admission. Routine laboratory examination was done on day 7, and no specific abnormality was noted.
Despite improved feeding, the patient continued to experience weight loss from his birth weight of 4.4 kg to 3.6 kg, nearly a 20% loss (). However, his overall physical condition was good. On day 9, intravenous fluid supplementation was cut, and capillary/venous electrolytes and a blood gas analysis were taken on the day after cessation of fluid therapy (day 10) to check for laboratory abnormalities. Laboratory results showed hyponatremia (128.0 mmol/L) combined with hyperkalemia (>9.0 mmol/L), but no electrical abnormality was detected on his electrocardiogram. Metabolic acidosis with respiratory compensation could be seen on his venous blood gas analysis. The results of the patient's newborn screening test and tandem mass spectra taken two days earlier had not been reported yet. Under the impression of congenital adrenal hyperplasia, a hormone study was done. Until laboratory results could confirm the patient's diagnosis, treatment with hydrocortisone and fludrocortisone was initiated, and electrolyte imbalances were medically managed. The above treatment was continued until day 21, when the patient's hormone study results were reported. Contrary to our expectation, the patient's renin activity and aldosterone levels were elevated to 307.5 ng/mL/hr (normal range, 1.4-7.8 ng/mL/hr) and 3,853.0 ng/dL (normal range, 17.0-154.0 ng/dL) respectively, and the Adrenocorticotropic hormone (ACTH) level had decreased to 2.7 pg/mL (normal rang, 10.0-60.0 pg/mL) . These results were suggestive of pseudohypoaldosteronism.
To confirm the diagnosis, genetic analysis of the patient's NR3C2 gene was done, and the results revealed heterozygous c.538G>A (p.V180I) and c.-2C>G substitution (). The patient was taken off steroid treatment, and sodium replacement (15 mEq/kg/day) was started. He showed gradual weight gain, along with stable serum electrolyte levels, and was discharged from our institution at postnatal age 25 days. The patient is currently 17 months old, his body profile shows height and weight in the 10th percentile, and he is achieving adequate developmental milestones. He is on tapering doses of oral sodium supplementation (down to 9.5 mEq/kg/day) and is receiving regular check-ups including serum electrolyte levels at the outpatient department (). His latest hormone study results taken in May this year were as follows and has relatively normalized since his initial study results; renin activity, 21.2 ng/mL/hr; aldosterone, 172.4 ng/dL; and ACTH, 31.0 pg/mL ().",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [1, 'days'], 'weight': [4.4, 'kg'], 'Sodium': [137.0, 'mmol/L']}",-0.05657,-0.05374,-0.0594,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 1 days old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 4.4 kg. The concentration of sodium is 137.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 4.4 * (137.0/140 - 1) = -0.05657 L. The patient's free body water deficit is -0.05657 L."
6128,38,Free Water Deficit,lab test,decimal,pmc-8238283-1,Extracted,"A 69-year-old man (body weight, 64. 4 kg; height, 156. 6 cm) was diagnosed with carcinoma of the ascending colon and scheduled to undergo laparoscopic right hemicolectomy and laparoscopic cholecystectomy. He had been diagnosed with hypertension a year ago and underwent pacemaker implantation due to SSS, complete AV block, and left bundle branch block (LBBB) in the same year. He had a dual-chamber pacemaker with atrial ventricular sensing, dual response, and rate-adaptive pacemaker (DDDR). In the preoperative evaluation, the electrocardiogram (EKG) revealed AV dual-paced rhythm with frequent premature ventricular contractions (PVCs). His heart rate (HR) was 68 beats/min, and QTc was 499 ms. PVC morphology has special characteristics of LBBB at V1, R/S transition in leads V3–4, and a tall R wave in leads II, III, and aVF, indicating PVC originating in the RVOT (Fig. ).[ Transthoracic echocardiography showed normal-sized cardiac chambers with preserved LV global systolic function (LVEF 64%) and normal valvular structure and function. The patient's pulmonary artery pressure was 37 mmHg, with no regional wall motion abnormalities. Moreover, there was no specific finding on performing coronary angiography. An adrenal mass was noted on performing abdominal CT and pheochromocytoma was ruled out.
Preoperative laboratory investigation showed no specific findings, with a hemoglobin (Hgb) level of 9.8 g/dL, sodium level of 142 mEq/L, potassium level of 3.54 mEq/L, chloride level of 103 mEq/L, and calcium level of 9.6 mg/dL.
Elective surgery was performed, which lasted for 4 hours and 35 minutes. Total time of anesthesia was 5 hours and 10 minutes. Preoperatively, the pacemaker mode was changed from DDDR to DOO (asynchronous mode). General anesthesia was induced totally with intravenous propofol which has anti-arrhythmic effects and remifentanil. Before intubation, 40 mg of lidocaine was injected intravenously, and 40 mg of rocuronium was used as a muscle relaxant. During the operation, the target concentration of anesthetics was maintained with propofol 2.5 to 3.0 mcg/mL, remifentanil 1 to 3 ng/mL, and rocuronium 5 mcg/kg/min. During the emergence, glycopyrrolate 0.2 mg, pyridostigmine 10 mg, and sugammadex 200 mg were administered. The vital signs of the patient were stable during surgery; frequent PVC was not observed, and his blood pressure was between 100 to 130 and 60 to 90 mmHg. His HR was maintained at 60 beats/min. The total estimated blood loss was approximately 400 mL, total urine output was 630 mL, and total administered fluid volume was 2100 mL of balanced crystalloids.
At the time of transfer from the operating room to PACU, the patient had a noninvasively measured blood pressure (NIBP) of 138/60 mmHg, HR of 60 beats/min, and temperature of 35.5°C. Immediately after entering the PACU, the patient complained of sharp throbbing pain at the surgical site (abdomen) with an numeral rating scale score (NRS) of 8 points and received 50 mcg of fentanyl. Subsequently blood pressure gradually decreased. Due to the delay in transfer to the general ward, the patient stayed in the PACU for a long time. Ninety minutes after PACU admission, NIBP dropped to 80/45 mmHg. To increase the blood pressure, 400 mL of fluid and 4 mg of ephedrine were administered, but the blood pressure did not increase, and the patient was sweating; however, he was mentally alert. The NRS score in the surgical area dropped from 8 to 3 points. Furthermore, 400 mL of fluid and 8 mg of ephedrine were administered again, but blood pressure remained low. After 20 minutes, NIBP decreased to 60/40 mmHg. There were no skin rashes or symptoms of allergy (Fig. ).
Continuous dopamine infusion was started at a rate of 5 mcg/kg/min with fluid therapy; however, after 10 minutes, blood pressure reduced to 60/35 mmHg, and dopamine infusion rate was increased to 10 mcg/kg/min. Ten minutes after infusion, NIBP was still at 61/19 mmHg, and HR suddenly increased to 200 to 230 beats/min. EKG was performed, and monomorphic VT was observed.
The patient was alert but sweating, and his femoral pulse was palpable. Monomorphic VT with pulse persisted and the patient was in sinus rhythm for 10 second intermittently. However, within a few seconds, HR again increased to 200 beats/min, and monomorphic VT with pulse continued. Arterial cannulation was performed. After administration of 2 mg of midazolam, DC cardioversion 120 J (biphasic) was performed. HR was maintained at 60 beats/min, arterial blood pressure (ABP) was 50/41 mmHg after DC cardioversion, and continuous infusion of norepinephrine was started at a rate of 0. 5 mcg/kg/min. (Fig. ) in approximately 7 minutes, the patient recovered with an ABP of 95/60 mmHg and HR of 80 to 90 beats/min; the patient showed improved symptoms, was nearly mentally alert, and was sweating less.
Immediate pacemaker interrogation was performed, but no abnormalities in the pacemaker were observed. The pacemaker had a pacing rate of 60 beats/min, which eliminated pacemaker-mediated tachycardia (Figs. and ). The pacemaker mode was changed from DOO (asynchronous mode) to DDDR, and the patient was transferred to the intensive care unit (ICU) for observation. The total fluid administered at the PACU was 1000 mL and ABGA showed pH of 7. 31, PCO2 of 42. 0 mmHg, PO2 of 97. 6 mmHg, sodium level of 143 mEq/L, potassium level of 4. 0 mEq/L, calcium level of 7. 2 mg/dL and an Hgb level of 10. 4 g/dL. The total urine output at the PACU was 100 mL.
A 12-lead EKG which was recorded in the ICU showed no PVCs, and portable transthoracic echocardiography revealed no specific findings.
One month later, the patient visited the emergency room (ER) with symptoms of dizziness, low blood pressure (systolic blood pressure of 80–90 mmHg), and presyncope. EKG at the ER showed AV dual-paced rhythm and frequent PVC with tall R waves in leads II, III, and aVF, which was the same as frequent PVC derived from the RVOT observed previously. QTc was 495 ms. The patient recovered after supportive care, including fluid loading, and was discharged.
This case report was approved and registered by the Institutional Review Board of Inha university hospital (IRB No. 2020–01–005). There was no potential conflict of interest relevant to this article. The patient has provided informed consent for publication of the case.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [69, 'years'], 'weight': [64.4, 'kg'], 'Sodium': [142.0, 'mEq/L']}",0.46,0.437,0.483,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 69 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 64.4 kg. The concentration of sodium is 142.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 142.0 mEq. To convert from 142.0 mEq to mmol, convert from mEq to mmol. The compound 142.0 has a valence of 1, and so divide the valence by the value of mEq to get, 142.0 mEq/(1 mEq/mmol) = 142.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mEq sodium/L converts to 142.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 64.4 * (142.0/140 - 1) = 0.46 L. The patient's free body water deficit is 0.46 L."
6129,38,Free Water Deficit,lab test,decimal,pmc-5477952-1,Extracted,"A 40-year-old woman came to the emergency room, accompanied by her mother, complaining of the progressive development of severe asthaenia, diffuse muscular pain and malaise. ‘I feel like I’m going to die’, she said repeatedly, ‘even if I do not know why’.
At admission, the clinical evaluation revealed a collaborative, suffering, lean and hypotensive woman (blood pressure 90/60 mmHg, last reported body weight 55 kg, height 175 cm), with normal heart rate (76 bpm, rhythmic), who was severely asthaenic. She looked dehydrated and her skin was diffusely hyperpigmented with hypertrichosis.
She denied any major problem in her past clinical history. The recent clinical history was also uneventful, except for an episode of gastroenteritis, about 10 days previously, after which she slowly improved for a few days, followed by the progressive development of the presenting complaints. Renal ultrasounds, performed in the emergency room, revealed kidneys of normal size, without signs of obstruction. Chest X-ray was normal. The patient was oligoanuric; she reported decreasing urinary output in the last few days and catheterization yielded <50 mL of urine. The EKG is shown in .
No previous blood test was available and the patient recalled having performed the last ones a few years before, when, on the occassion of the death of her father, she had undergone a general evaluation for having lost ‘considerable weight’.
The first blood tests performed in the emergency room revealed: serum creatinine, 5.55 mg/dL, active inflammatory signs [C-reactive protein, 41.2 mg/dL (normal < 0.8 mg/dL); fibrinogen, 938 mg/dL], massive leukocytosis (WBC, 67 000), suggestive of both severe haemoconcentration and infection, with severe sodium and potassium imbalance (Na, 107 mmol/L; K, 1.61 mmol/L), moderate, compensated metabolic acidosis (pH, 7.34; HCO3, 19.4 mmol/L; base excess, −4 mmol/L) and moderate hyperglycaemia (160 mg/dL). Haemoglobin level (15 g/dL) was normal. Elevated levels of creatinine–phosphokinase (26 186 UI/L) indicated concomitant rhabdomyolysis, probably as a result of infection and severe electrolyte imbalance, potentially contributing to the acute renal failure.
In the face of the complex metabolic disorder, a hierarchy of interventions was defined, starting from potassium supplementation with very slow sodium infusion, aimed at raising the sodium level by no more than 10–12 mEq/day. As it will be further discussed, the working diagnostic hypotheses are of an acute renal failure superimposed on a chronic kidney disease in the context of diuretic abuse. In spite of the need for rapid correction of the potassium and sodium levels, each of the interventions has, however, important limits and drawbacks and the anuric status limits the use of the most widely employed formulae guiding assessment and therapy in severe sodium imbalance ()
About 12 h after admission, in the absence of cognitive deficits, she suddenly developed flaccid tetraplegia and restrictive respiratory failure. A prompt transfer to the intensive care unit (ICU) was required because of respiratory failure. She was sedated and mechanical ventilation was started.
At transfer to the ICU and immediately after intubation (pO2, 193 mmHg; pCO2, 35.4 mmHg), the major electrolyte levels were the following: Na, 114 mmol/L; K, 0.8 mmol/L; HCO3, 15 mmol/L; lactate, 0.8 mmol/L; chloride, 83 mmol/L; ionized calcium, 1.16 mmol/L; pH, 7.255; base excess, −12 mmol/L; anion gap, 17 mmol/L. Calculated osmolarity was 278 mOsm/kg (according to the simplified formula: Osmolality = Sodium × 2 + Glucose/18 + BUN/2.8), the effect of the low sodium being partly counterbalanced by the high BUN (BUN, 116 mg/dL).
On account of the recent gastrointestinal viral disease, the flaccid paralysis with intact sensorium and the rapid course, the neurologist suspected Guillain–Barré syndrome (GBS) and performed a lumbar puncture, leading to a picture of albuminocytological dissociation (WBC, 7 mm3; proteins, 63 mg/dL; glucose, 90 mg/dL). In parallel with the slow correction of the electrolyte imbalance (), leading also to slow volume repletion, high-dose immunoglobulins were started (0.4 mg/kg/day for 5 days), with prompt clinical improvement and discharge from the ICU 7 days later, to be transferred to the internal medicine ward.
Diuresis gradually restarted in the following 12 h, reaching 800 mL by the second day. In keeping with the hypothesis of chronic kidney disease with impaired concentration ability, urinalysis showed low urine specific gravity (1010) and relatively high spot urinary sodium (39 mEq/L, with serum sodium, 121 mEq/L).
At discharge from the internal medicine ward 2 weeks later, serum creatinine was 1.38 mg/dL, BUN 16 mg/dL, creatinine clearance (24-h urine collection) ranged from 50 to 60 mL/min, proteinuria ranged from 0.2 to 0.3 g/day, Na 141 mmol/L, K 4.5 mmol/L, HCO3 24 mEq/L and PCR 0.04; urinalysis was normal. Renal ultrasounds revealed a decreased corticomedullary differentiation and slightly decreased thickness of the renal cortex, in keeping with the presence of chronic parenchymal disease; the presence of markedly hyperechogenic papillae is suggestive of nephrocalcinosis.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [40, 'years'], 'weight': [55.0, 'kg'], 'sex': 'Female', 'Sodium': [107.0, 'mmol/L']}",-6.48214,-6.15803,-6.80625,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 40 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 55.0 kg. The concentration of sodium is 107.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 55.0 * (107.0/140 - 1) = -6.48214 L. The patient's free body water deficit is -6.48214 L."
6130,38,Free Water Deficit,lab test,decimal,pmc-6751414-1,Extracted,"A 77-year-old man presented with a complaint of a lump on the upper abdominal wall for several weeks. His performance status (PS) was Grade 2 (Height, 168 cm; Weight, 58 kg; BMI, 20 kg/m2). He had a history of appendicitis that was operated upon. On physical examination, the tumor was located on the upper left side of the abdominal wall measuring around 5 cm with poor mobility and partial ulceration but without pain (Fig. ). At a nearby hospital, he had previously undergone physical examination and computed tomography (CT) for his symptoms. Advanced gastric cancer with invasion to the skin of the abdominal wall was suspected and, for more specific investigation and therapy, he was referred to our department. We obtained informed consent from all participants, and all procedures therapy were performed in accordance with the Declaration of Helsinki.
His blood investigation revealed the following: hemoglobin 8.7 g/dL, white blood cell count 6,060 /μL, platelets 321,000 /μL, prothrombin time-international nomarized ratio (PT-INR) 1.05, sodium 140 mmol/L, potassium 4.2 mmol/L, chlorine 105 mmol/L, creatinine 0.91 mg/dL, aspartate aminotransferase (AST) 13 U/L, alanine aminotransferase (ALT) 10 U/L, alkaline phosphatase 249 U/L, γ-guanosine triphosphate cyclohydrolase (γ-GTP) 14 U/L, LD 156 U/L, total bilirubin 0.8 mg/dL, C-reactive protein 0.41 mg/dL, carcinoembryonic antigen-S (CEA-S) 1.6 ng/mL, alpha-fetoprotein 1.83 ng/mL and carbohydorate antigen 19–9 (CA 19–9) <2 U/mL. There was moderate anemia but there was no organ failure and or elevation of tumor marker.
On Upper gastrointestinal endoscopy, a Type 3 tumor that measured around 40 mm was observed occupying from the angle of the stomach to the anterior wall of the antrum of the stomach (Fig. ).
On biopsy, the histological type was revealed as tubular adenocarcinoma (tub1) and immunostaining for HER2 was negative.
Thoracoabdominal enhanced CT revealed invasion of the tumor from the anterior wall of the stomach to the lateral region of the liver and infiltration from the abdominal wall to the skin. There was no evidence of metastasis or ascites (Fig. ).
On the basis of these findings, we diagnosed advanced gastric cancer (L-Less, Gre, type 3, 40 mm, tub1), cT4b (SI; liver, skin) N0M0 c Stage IIIA. Initially we anticipated chemotherapy considering that the patient's PS was Grade 2 and the defect of abdominal wall was too large for surgery. In addition, the patient did not want to undergo surgery. S-1+Cisplatin (SP) therapy was performed as first-line therapy every 3 weeks [].
Obvious shrinkage of the tumor invasion to the skin was observed, and we determined that PR was obtained at the end-point of 4th course of SP therapy. However, because of malaise (Grade 2), we had to set a 1-month interval. During the interval, the invasion to the skin gradually increased again; hence, another two courses of SP regimen were added with decreased dose. After six courses of SP therapy had been completed, PR was obtained again by the re-shrinkage of the skin tumor on physical examination and upper gastrointestinal endoscopy and CT (Fig. , ). At this point, the patient was not amenable to surgery or chemotherapy; hence, we adopted a “wait-and-see” approach. During this period, the skin tumor underwent re-growth gradually for which RAM/PTX therapy (3-week administration at 1-week intervals) was introduced as the second line chemotherapy, 2 months after the previous one []. Over the course of therapy, anemia (Grade 3) and neutropenia (Grade 2) were observed and we were compelled to skip one administration each of PTX in course 2 and 3but RAM dosage was completely administrated through all five courses (Fig. ). Throughout the second line of therapy, the skin tumor kept decreasing visually and enhanced abdominal CT revealed the shrinkage of the primary tumor and the invasion to the lateral area of the liver and skin. Similar findings were observed on gastrointestinal endoscopy; and hence, we determined that PR was obtained again (Fig. ). Since his general condition was observed have improved, we planned to perform surgery with the aim of reaching a chemotherapy-free status.
We performed open total gastrectomy with D2 lymph nodes dissection (Roux-en-Y reconstruction) with combined partial resection of the skin, abdominal wall, and liver. There were no findings of the peritoneal dissemination, metastasis to the liver, or ascites (Fig. ). The components separation method was performed for abdominal wall closure with the defect of the skin by exposure of the anterior sheath of abdominal rectal muscles and resection of partial aponeurosis of the right external abdominal oblique muscle.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [77, 'years'], 'weight': [58.0, 'kg'], 'Sodium': [140.0, 'mmol/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 77 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 58.0 kg. The concentration of sodium is 140.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 58.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
6131,38,Free Water Deficit,lab test,decimal,pmc-5984920-1,Extracted,"A 45-year-old Caucasian woman presented with abdominal pain, nausea, and vomiting for 17 h. At 22 h prior to admission, she went out to dinner and drank one glass of wine. A few hours after the meal, she developed epigastric and left upper quadrant abdominal pain that was moderate, persistent, cramping, and aching; the pain radiated to her left middle back and arm without exacerbating or alleviating factors. The pain was associated with nausea, vomiting, and she could not tolerate any oral intake. She felt thirsty and had polyuria and positional lightheadedness. She reported no fever, chills, chest pain, cough, sputum production, dysuria, hematuria, diarrhea, hematochezia, and melena.
On further questioning, the patient shared that she had a history of gestational glucose intolerance 6 years ago, and has had occasional impaired fasting glucose of 81–107 mg/dL for the past 6 years. She began following an American Diabetes Association (ADA) diet 2 years ago and lost 25 lb. Additionally, she had a past medical history of supraventricular tachycardia, irritable bowel syndrome, social alcohol use, cholecystectomy, and thyroid papillary adenocarcinoma status post partial thyroidectomy complicated by postsurgical hypothyroidism. Home medications included metoprolol tartrate, levothyroxine, and meloxicam. The patient reported no family history of diabetes.
Temperature 97.7 °F, pulse 130 bpm, respiratory rate 28 bpm, BP 134/71 mmHg, weight 87 kg, height 1.68 m, BMI 31 kg/m2, SpO2 99% on room air.
The patient was in moderate distress. There was no acanthosis nigricans. Cardiovascular system revealed tachycardia. A pulmonary exam revealed tachypnea, accessory muscle usage with moderate respiratory distress. Abdominal exam revealed central obesity, normoactive bowel sounds, left upper quadrant and epigastric tenderness to palpation, no rigidity or guarding. No costovertebral angle tenderness.
CBC: WBC 25.9 × 109/L, hemoglobin 14.7 g/dL, hematocrit 45.8%, platelet 386 × 109/L, MCV 100.2 µm3. BMP: sodium 135 mmol/L, potassium 7.4 mmol/L, chloride 89 mmol/L, bicarbonate 5 mmol/L, BUN 37 mg/dL, creatinine 1.27 mg/dL, glucose 931 mg/dL, eGFR 46 mL/min.
Liver chemistry: Total bilirubin 0.2 mg/dL, AST 23 U/L, ALT 54 U/L, ALP 138 U/L, total protein 7.5 g/dL, albumin 4.5 g/dL. Calcium 8.7 mg/dL, phosphate 1.4 mg/dL, magnesium 2.1 mg/dL. VBG: pH 6.92. Repeated ABG 2 h later: pH 7.21, pCO2 16 mmHg, pO2 129 mmHg, HCO3− 6.4 mmol/L, SaO2 98% on 2 L/min oxygen by nasal cannula. Beta-hydroxybutyrate 28 mmol/L, lactic acid 4.0 mmol/L. Urinalysis showed urine ketones 80 mg/dL, leukocyte esterase negative, urine culture no growth. HbA1c 6.4%. Lipid profile: triglycerides 89 mg/dL, total cholesterol 144 mg/dL, LDL 91 mg/dL, HDL 35 mg/dL. TSH 3.12 mIU/mL, free T4 1.26 ng/dL. Troponin I < 0.01 ng/mL.
Ultrasonography of the abdomen revealed mild hepatic steatosis, incidental mild to moderate right-sided hydronephrosis, status post cholecystectomy. ECG on admission: sinus rhythm, HR 126 bpm, peaked T waves at lead V2–V6 consistent with hyperkalemia, no ischemic changes.
All procedures performed in this study were in compliance with the ethical standards of the institutional and/or national research committee and with the 1964 Declaration of Helsinki and its later amendments or comparable ethical standards. Informed consent was obtained from the individual participant for being included in the study.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'years'], 'weight': [87.0, 'kg'], 'sex': 'Female', 'Sodium': [135.0, 'mmol/L']}",-1.55357,-1.47589,-1.63125,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 45 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 87.0 kg. The concentration of sodium is 135.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 87.0 * (135.0/140 - 1) = -1.55357 L. The patient's free body water deficit is -1.55357 L."
6132,38,Free Water Deficit,lab test,decimal,pmc-5023858-1,Extracted,"A 25-month-old male was admitted to the hospital with generalized tonic clonic seizure and loss of consciousness that continued for longer than 1 week. The patient had been diagnosed with communicating hydrocephalus at 19 months of age and delayed development. He could only turn inside. His past admission history was pneumonia at 3 month ago. Of his family, there is no one who had neurologic, metabolic, or cerebrovascular disease. On examination, his mental status was drowsy, and the muscle strength of his lower extremities was decreased to grade 2/5 with spasticity. He could not sit up by himself, and his deep tendon reflexes were accelerated. He also had microcephaly (44 cm < 3rd percentile). His nutritional state was very poor and cachectic (body weight 10 kg <3rd percentile). His first sodium–potassium–chloride level was 132–4.6–98 mmol/L checked. Complete blood count was 8800–14.1–382 K with C-reactive protein negative. Serum pH was 7.32, bicarbonate 16.9. Total protein, albumin, creatinine, and glucose levels were normal. All test results were normal. However, further brain evaluations were conducted because his mental status was gradually worsened. EEG revealed depressed background activities with moderately increased slow waves in the right hemisphere and frequent sharp waves in the left frontal area.
Brain MRI showed high-signal intensity in the peri-aqueductal and hypothalamic areas on T2/FLAIR-weighted images and lateral ventricle dilatation (Fig. ). These findings are consistent with Wernicke encephalopathy. To support this diagnosis, we measured urine organic acid, lactic acid, pyruvic acid, and lactic/pyruvic acid ratio, but we could not determine the serum thiamine level because thiamine therapy was initiated before sampling. The lactic acid level in the serum and urine was elevated, and the lactic acid/pyruvic acid ratio was 13890, which is also observed with WE. We prescribed anti-epileptics and 50 mg of thiamine per day for 3 weeks. Additionally, we administrated mannitol, methylprednisolone (2 mg/kg/day), phenytoin, and oxcarbamazepine for seizure control and hydrocephalus treatment not using diuretics.
Because his initial volume state euvolemic, we did not check blood pressure and follow-up electrolyte level during first 1 week. On the 6th hospital day, although his seizure attacks progressively improved, he started projectile vomiting 7 times per day. On the 7th hospital day, he had dark-colored loose stool. We decided that he needed a total parenteral nutrition (TPN) time of about 3 days. We supplied combination TPN material (350 kcal/day) and 1:4 SD fluid (100 cc/kg/day contained sodium 2.87 mEq/kg/day). Regardless of the sufficient fluid supplementation, the follow-up lab 3 days later (i.e., day 10) revealed a seriously decreased serum sodium level (96 mmol/L). Fortunately, the patient was in a light drowsy mental state. Simultaneously, we could suggest decreased “effective arterial blood volume,” because mean corpuscular hemoglobin concentration (MCHC), white blood cell (WBC) count, and BUN was elevated (MCHC – 40.5 g/dL, WBC-43000/μL, BUN 21 mg/dL).[ That day, his urine osmolality decreased to 129 mOsm/kg with a normal serum osmolality of 290 mOsm/kg. His 24-hour urine output was 516 mL (2.15 mL/kg/h) with a measured fluid intake of 343 mL. Because of the decreased urine osmolality, we considered the possibility that hyponatremia had induced GI bleeding or 3rd space sodium loss. To rule out other causes of hyponatremia, we examined sodium regulating hormone, for example, ACTH, ADH, cortisol, renin, aldosterone, and thyroid hormone. Except the low range of TSH, all hormone study revealed normal results. Massive sodium replacement was performed for 3 days, after which, the serum sodium level gradually recovered to 139 mmol/L. Other lab finding also recovered, MCHC, WBC and BUN were dramatically decreased after one day hydration therapy (MCHC 41.1 g/dL, WBC 19540/ mL, BUN 10 mg/dL).
However, on the 3rd day after recovery (i.e., day 13), the patient's serum sodium level suddenly decreased again to 117 mmol/L. At this stage, the urine osmolality was 512 mOsm/kg, and serum osmolality had decreased (273 mOsm/kg). The 24-hour urine output was 1198 mL (5 mL/kg/h) with a fluid supply of 1221 mL. On the basis of low serum osmolality, high urine osmolality, dehydration state, increased urine output, and negative water balance, a diagnosis of CSWS was made, and a 3% NaCl supply regimen was started. During the next 24 hour (i.e., day 14), serum osmolality decreased to 251 mOsm/kg, and urine osmolality increased to 1189 mOsm/kg (Fig. ).
The urinary output continued to be high, varying between 50 and 60 mL/kg/h during the next 3 days. On day 17, we changed the treatment plan to 0.2 mg fludrocortisone orally in an attempt to reduce the urinary sodium excretion.
This treatment resulted in a decrease in urine output (i.e., 24–39 mL/h) and a plasma sodium increase to 137 mmol/L. There was also a reduction in urinary sodium osmolality from 1189 to 281 mOsm/kg (i.e., day 20). Similar to findings from other CSWS cases, fludrocortisone was an effective treatment for urinary sodium loss (Table ).[.
From day 20 to day 30, the patient maintained a serum sodium level between 131 and 138 mmol/L. However, thiamine supplementation and electrolyte correction could not recovery his neurologic condition with lactate accumulation up to 17 mmol/L. He was discharged on the 30th day with well-controlled serum sodium level and seizures.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [25, 'months'], 'weight': [10.0, 'kg'], 'Sodium': [139.0, 'mmol/L']}",-0.04286,-0.04072,-0.045,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
This means that the patient is 2 years and 1 oldThe patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 10.0 kg. The concentration of sodium is 139.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 10.0 * (139.0/140 - 1) = -0.04286 L. The patient's free body water deficit is -0.04286 L."
6133,38,Free Water Deficit,lab test,decimal,pmc-6971472-1,Extracted,"A 56-year-old woman was admitted to our emergency department (ED) with disturbance of consciousness and respiratory failure. She had influenza-like symptoms including cough and fatigue without fever 2 days prior to presentation. She did not have a medical history but took an over-the-counter drug that contains ibuprofen for headache.
The patient's height was 139 cm and weight was 29.0 kg. Her vital signs were: blood pressure, 131/78 mm Hg; heart rate, 78 b.p.m. and regular; axillary temperature, 35.1°C; respiratory rate, 30 breaths/min; SpO2, 85% with oxygen delivered through a face mask (3 L/min); and a Glasgow Coma Scale score of E3V3M5 on admission.
Rapid viral testing was positive for influenza A virus. Significant laboratory results included hypoglycemia (serum glucose, 48 mg/dL), transaminitis (aspartate aminotransferase [AST] 12,548 IU/L and alanine aminotransferase [ALT] 5,725 IU/L), hyperbilirubinemia (total bilirubin 3.5 mg/dL and direct bilirubin 1.6 mg/dL), elevated international normalized ratio (INR; 3.16), hyperammonemia (ammonia 102 μg/dL), lactic acidosis (7.0 mmol/L), azotemia (blood urea nitrogen 55 mg/dL), hypercreatinemia (serum creatinine 2.32 mg/dL), hyponatremia (134 mmol/L), hyperkalemia (6.7 mmol/L), hypolipidemia (total cholesterol 114 mg/dL and triglyceride 29 mg/dL). Carnitine was normal (223 μmol/L). Her liver function was normal 5 days before presentation.
The head computed tomography (CT) revealed no specific findings, although the head magnetic resonance imaging showed hyperintense signals at the bilateral globus pallidus in diffusion-weighted images and fluid attenuation inversion recovery (FLAIR)-weighted images and a hyperintense signal at the left front parietal lobe in FLAIR-weighted images (Fig. ). Abdominal CT revealed fatty and enlarged liver. Chest CT showed diffuse alveolar type infiltrates in the patient's right middle lobe with air bronchograms and respiratory muscle loss. Based on these findings, we diagnosed the patient with RS induced by influenza A virus and pneumonia. The clinical course of the patient is shown in Figure . She was intubated and placed on mechanical ventilation in the ED then transferred to the intensive care unit for supportive care. She was treated with prednisolone (500 mg/day for 3 days) and peramivir (100 mg/day for 5 days) for influenza encephalopathy. The patient's liver function gradually improved with supportive care, fresh frozen plasma, and vitamin K. Her transaminase trended down from AST 7,546 IU/L and ALT 4,127 IU/L on day 2, to AST 85 IU/L and ALT 704 IU/L on day 7, and to AST 23 IU/L and ALT 169 IU/L on day 14 of hospitalization. Her INR trended down from 3.16 on day 1, to 1.28 on day 7, and to 1.07 on day 14. A tracheostomy was carried out on day 12 because of respiratory insufficiency type II due to muscle atrophy with chronic malnutrition.
On 14 day, the patient's condition had dramatically improved, with no abnormal neurological findings. Her appetite returned to normal and anorexia resolved. Her total duration of hospital stay was 71 days, and she was transferred to a rehabilitation hospital without neurological deficits.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [56, 'years'], 'weight': [29.0, 'kg'], 'sex': 'Female', 'Sodium': [134.0, 'mmol/L']}",-0.62143,-0.59036,-0.6525,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 56 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 29.0 kg. The concentration of sodium is 134.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 29.0 * (134.0/140 - 1) = -0.62143 L. The patient's free body water deficit is -0.62143 L."
6134,38,Free Water Deficit,lab test,decimal,pmc-7096564-1,Extracted,"A 32-year-old woman found to have polyhydramnios at 34 weeks of pregnancy was referred to the Division of Pediatric Gastroenterology at Karabuk Education and Training Hospital in September 2017. She had some concerns because her first child was diagnosed as having CCD. She wondered whether the fetus had CCD disease. In the family history, there was no consanguinity. Two weeks later, a female baby was born by cesarean section.
The female newborn weighed 3200 g, its length was 50 cm, with Apgar score 7 (1 min) and 9 (5 min). Watery diarrhea and vomiting started soon after birth. She required admission to the neonatal intensive care unit (NICU) because of dehydration and poor feeding with 15% weight loss. A physical examination revealed a distended abdomen. Blood gas and serum biochemical analysis were performed after birth. Blood analyses showed hypochloric hypokalemic metabolic alkalosis with pH 7.55, and base excess +3.2 sodium (Na+) 129 mmol/L, potassıum (K+) 3.4 mmol/L, and chloride (Cl-) 86 mmol/L. The stool test was initially within normal limits. Both abdominal X-ray and ultrasound revealed diffuse dilated intestinal loops. The family history along with polyhydramnios, watery diarrhea, bowel distension, and metabolic alkalosis led to a suspicion of CCD. Therefore, additional laboratory studies were performed: stool and urine electrolyte, sweat Cl, and plasma renin levels. Her stool electrolytes were as follows: Na+ of 52 (ref: 20–30) mmol/L, K+ of 61 (ref: 55–65) mmol/L, and Cl- of 125 (ref: 5–20) mmol/L. Cystic fibrosis was ruled out through a negative sweat test. The other laboratory results showed a low urine Cl concentration of 28 (ref: 110–250) mmol/L, high plasma renin activity and aldosterone levels, 42.6 (ref: 2.9–40) ng/mL/hour and 892.9 (ref: 29.5–162) pg/mL, respectively. The first results were similar to Bartter syndrome (BS); however, after intravenous fluid and electrolyte therapy, the plasma renin and aldosterone levels returned to normal values (). She was diagnosed as having CCD based on its typical clinical signs and a high concentration of stool Cl-. Consent was obtained from the patient’s parent.
The diagnosis was confirmed through genetic analysis. Our patient and her sister carry the same mutation c.2024_2026dup TCA (pIle675_Arg676insIle) in exon 18 of the SLC26A3 gene in a homozygous state. She was initially treated with intravenous fluids, administration of oral NaCl (3 mg/kg/day) and KCl (2 mg/kg/day) supplementation with lansoprazole (2 mg/kg/day) was changed to peroral therapy within 1 week. She tolerated oral salt supplementations with lansoprazole well. At six months of age, she still had diarrhea 5–6 times a day despite salt supplementations with lansoprazole.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [32, 'years'], 'weight': [3200.0, 'g'], 'Sodium': [129.0, 'mmol/L']}",-0.12571,-0.11942,-0.132,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 32 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 3200.0 g so this converts to 3200.0 lbs * kg/1000 g = 3.2 kg. The concentration of sodium is 129.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 3.2 * (129.0/140 - 1) = -0.12571 L. The patient's free body water deficit is -0.12571 L."
6135,38,Free Water Deficit,lab test,decimal,pmc-6031976-1,Extracted,"An 18-year-old male (height 155 cm and weight 51 kg) was accidentally hit by an unfastened crane hook and suffered serious injuries to the right side of his neck and jaw. He presented to the hospital emergency room with severe neck pain, bleeding from the mouth, and a deep lacerated injury on the right side of his jaw and upper part of the neck, with surgical emphysema (). His Glasgow Coma Scale (GCS) score was E4V5M5, and his pupils were bilaterally equal and 2 mm in size. His initial recorded vital signs were: blood pressure of 96/60 mmHg, heart rate of 100 beats/min, respiratory rate of 18/min, and SpO2 of 93% in room air. A computerized tomography (CT) scan of his facial bones and upper cervical spine revealed a comminuted displaced fracture, which involved the angle and body of the right hemimandible, with adjacent soft tissue laceration, hematoma, and air pockets (). There was a displaced comminuted fracture of the right transverse process of the atlas that extended into the right lateral mass, and a fracture of the right occipital condyle that extended to the foramen transversarium margin (). The atlas was rotated, with displacement of the atlanto-occipital and atlanto axial joints. A magnetic resonance image (MRI) scan of neck showed the absence of right vertebral artery flow void and a thrombus in the right vertebral artery (). Bilateral vertebral artery Doppler was performed, which showed right vertebral artery flow stasis, indicating a thrombus. The nasal bones, nasal cavity, nasopharynx, and laryngeal cartilages were normal. There was no intracranial injury and no involvement of the spinal cord; hence, no sensory motor deficits or bladder or bowel involvement were identified. A thin pre-vertebral hematoma was seen extending from level C1 to C4, and the rest of the cervical vertebrae were normal. Since the inner cortex of the mandible was comminuted and shattered, the right inferior alveolar artery was cut completely, with bleeding into the oral cavity. Mouth opening was restricted, and the inter incisor distance was 1 cm.
After the neck wound was covered with dressing, a cervical collar was applied. The patient was admitted to the high dependency unit (HDU); and after proper explanation of the anesthetic and surgical plan to the patient and his guardian, he underwent an open reduction and internal fixation of the mandible and exploration of the neck injury the next day. His basal oxygen saturation was at 95%, and an arterial blood gas analysis in room air revealed a pH of 7.36, PaCO2 of 40 mmHg, PaO2 of 110 mmHg, bicarbonate level of 22 mmol/L, and arterial oxygen saturation of 98%. His blood investigations revealed hemoglobin levels of 11.9 gm%, platelets of 2.04 lakhs/mm3, serum urea of 22.0 mg/dL, serum creatinine of 0.6 mg/dL, serum glucose of 93 mg/dL, sodium of 140 meq/dL, and potassium of 3.9 meq/dL. A large bore intravenous cannula was inserted into the dorsum of the left hand, and ringer lactate was started. He was connected to a multipara monitor that displayed his electrocardiogram (ECG), noninvasive arterial pressure, pulse oximetry, endtidal carbon dioxide (ETCO2) and core temperature. The ECG showed a sinus rhythm, with a heart rate of 92/min and a normal axis, blood pressure of 110/65 mmHg and respiratory rate of 14/min. Glycopyrrolate (0.2 mg) was given intravenously. An awake fiber-optic nasotracheal intubation was planned, with a backup emergency surgical airway kit in case the first method failed. The nasal cavity was anesthetized by packing with cotton tape gauze soaked in 2% lidocaine and 0.05% oxymetazoline hydrochloride, and the oropharynx was nebulized with 2% lidocaine spray. The larynx and trachea were anaesthetized by nebulization with lignocaine, and supplemental oxygen was administered via a nasal catheter. A 5.5 mm fiber-optic bronchoscope was taken, and a 7.0 mm size cuffed reinforced endotracheal tube was slid up the full length of the shaft and gently secured to the beveled end of the bronchoscope.
The oral cavity was full of clots as the right inferior alveolar artery was cut. The oral cavity was intermittently cleared, to enable clear visualization. The fiber-optic bronchoscope was introduced into the left nasal cavity and gently advanced through the glottis into the trachea to just above the carina. Then, the endotracheal tube was gently railroaded and advanced into the trachea. Successful placement of the tube in the trachea was verified by capnography and bilateral equal air entry. The cuff was inflated to seal the airway, and the tube was securely fixed. Fentanyl (50 µg, 1 µg/kg), propofol (80 mg), and atracurium (25 mg) were given intravenously. A throat pack was inserted gently through the available inter incisor space. Anesthesia was maintained using a mixture of 50% oxygen, 50% nitrous oxide, and 1–1.5% isoflurane, with intermittent doses of atracurium. Intermittent positive pressure ventilation was instituted, and ETCO2 was maintained at 35 mm Hg. The perioperative period was uneventful, without significant changes in blood pressure or heart rate (systolic pressure 110–130 mmHg, diastolic pressure 70–86 mmHg, heart rate 85–108 beats/min). The mean arterial pressure (MAP) was maintained between 90 to 100 mmHg to maintain perfusion and reduce the risk of posterior circulation ischemia. A total of 1000 mL of crystalloids was given perioperatively. At the end of the procedure, which lasted 90 minutes, neuromuscular blockade was reversed with neostigmine (2.5 mg) and glycopyrrolate (0.4 mg), which were given intravenously. The throat pack was removed and the trachea was extubated when the patient was awake with protective airway reflexes, and the neuromuscular transmission recovered to a train of four (TOF) ratio of 0.9. Paracetamol (1,000 mg) was given intravenously for postoperative analgesia, and ondansetron (4 mg) was given intravenously for antiemetic prophylaxis. The patient was transferred to the HDU for observation, and he made an uneventful recovery and was started on IV antibiotics and enoxaparin for anticoagulation, 48 hours following surgery for one week, to establish vertebral artery flow. This was later replaced with oral aspirin. The neurosurgical intervention included cervical immobilization using a cervical collar brace for 12 weeks, to achieve spinal stabilization and prevent further nerve damage, including injury to the brain stem.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [18, 'years'], 'weight': [51.0, 'kg'], 'sex': 'Male', 'Sodium': [140.0, 'mEq/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 18 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 51.0 kg. The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 51.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
6136,38,Free Water Deficit,lab test,decimal,trec-ct-2021-39,Extracted,"A 3-day-old Asian female infant presents with jaundice that started a day ago. She was born at 38w3d of gestation, after an uncomplicated pregnancy. The family history is unremarkable. The baby is breastfed.
Vital signs are reported as: axillary temperature: 36.3°C, heart rate: 154 beats/min, respiratory rate: 37 breaths/min, and blood pressure: 65/33 mm Hg. Her weight is 3.2 kg, length is 53 cm, and head circumference 36 cm. Her sclera are yellow and her body is icteric. No murmurs or any other abnormalities are  detected in the heart and lung auscultation. Her liver and spleen are normal on palpation.
Laboratory results are as follows: 
Serum total bilirubin: 21.02 mg/dL
Direct bilirubin of 2.04 mg/dL
AST: 37 U/L
ALT: 20 U/L
GGT: 745 U/L
Alkaline phosphatase: 531 U/L
Creatinine: 0.3 mg/dL
Urea: 29 mg/dL
Na: 147 mEq/L
K: 4.5 mEq/L
CRP: 3 mg/L
Complete blood cell count within the normal range.
She is diagnosed with uncomplicated neonatal jaundice that may require phototherapy.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [3, 'days'], 'weight': [3.2, 'kg'], 'sex': 'Female', 'Sodium': [147.0, 'mEq/L']}",0.096,0.0912,0.1008,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 3 days old. This means the patient is 0 years old.
The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 3.2 kg. The concentration of sodium is 147.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 147.0 mEq. To convert from 147.0 mEq to mmol, convert from mEq to mmol. The compound 147.0 has a valence of 1, and so divide the valence by the value of mEq to get, 147.0 mEq/(1 mEq/mmol) = 147.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 147.0 mEq sodium/L converts to 147.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 3.2 * (147.0/140 - 1) = 0.096 L. The patient's free body water deficit is 0.096 L."
6137,38,Free Water Deficit,lab test,decimal,pmc-3531538-1,Extracted,"A 31-year-old woman with height of 164 cm and weight of 42 kg (BMI; 15.62, normal; 18.5-23) was admitted for hysteroscopic myomectomy, under general anesthesia. Except penicillin allergy, she had no history of cardiovascular diseases, nor did she have any coronary risk factors, including smoking, diabetes mellitus, hyperlipidemia, hypertension, coagulative disorder, oral contraceptive use, and/or family history of myocardial disease. Physical examination and routine preoperative laboratory tests, including chest X-ray, and electrocardiogram (ECG) were unremarkable with total cholesterol and high density lipoprotein within normal range.
After arriving at the operating room, ECG, pulse oximetry, non-invasive blood pressure, and end-tidal carbon dioxide (EtCO2) monitoring were attached to the patient. For induction of general anesthesia, thiopental sodium 200 mg, followed by rocuronium 20 mg, were injected intravenously and classic laryngeal mask airway (No. 4) was inserted. Then, she was positioned to lithotomy for the operation. Anesthesia was maintained with desflurane 5.0-6.0 vol% in 50% nitrous oxide and oxygen. The operation was uneventful for 30 minutes, with stable vital signs, except slight tachycardia with heart rate 105 to 120 beats/min. Further, the estimated blood loss was negligible.
At the end of the surgery, ergonovine maleate 0.2 mg distilled with normal saline 10 ml was intravenously administered slowly for a minute at the request of the surgeon for the uterine contraction. About 2 minutes later, EtCO2 suddenly decreased to 20 mmHg from 33 mmHg, followed by a loss of plethysmographic wave. The patient was cyanotic, but anesthetic monitor showed no noticeable change in the airway pressure and expiratory tidal volume. The blood pressure, although measured at 119/89 mmHg a few minutes ago, was not checkable with un-palpable radial pulse, and ECG showed severe bradycardia, followed by asystole.
Immediately, 1 mg epinephrine was injected intravenously, FiO2 increased to 100%, and thereafter, chest compression was started. Laryngeal mask airway was changed to endotracheal tube (No. 7), under direct laryngoscopy, right internal jugular vein cannulated and arterial line in the right radial artery established, while chest compression continued, inotropics infused and intermittent atropine and other drugs were administered. Even with these measures, the patient responded poorly and cardiac rhythm couldn't be detected. The patient was just showing low blood pressure of about 40/20 mmHg, which was observed via arterial line, probably due to chest compression. About 20 minutes after cardiac arrest, ECG returned to sinus rhythm but with tachycardia and ST elevation. Blood pressure increased to 60/20 mmHg, heart rate was at 130 beats/min, SpO2 85%, and arterial blood gas analysis with pH 7.2, PCO2 42.7 mmHg, PO2 54.3 mmHg, bicarbonate 18.2 mmol/L, base -8.2 mmol/L, and sO2 82%. Other hematologic and electrolyte were within normal limits and the results were as follows: Hemoglobin 12.2 g/dl, Hematocrit 39.7%, Na+ 136 mmol/L, K+ 3.1 mmol/L, Ca2+ 4.5 mg/dl, and Cl- 117 mg/dl. With continued intotropic support, nitroglycerin 100 µg was intravenously administered with the suspicion of myocardial ischemia. Within 5 minutes, blood pressure further increased to 123/80 mmHg, heart rate to 128 beats/min, SpO2 100%. However, afterwards, the systolic blood pressure decreased to 75 mmHg and SpO2 88% again, despite inotropic support.
Chest X-ray, taken immediately after arrival to the intensive care unit, showed bilateral diffuse pulmonary edema (). Even though ECG didn't show definite ST abnormalities, except sinus tachycardia (), cardiac enzymes were elevated as follows; troponin I 3.2 ng/ml (normal < 0.78), CK-MB 12.08 ng/ml (normal < 5). Transthoracic echocardiography showed the ejection fraction of only 22% (normal 56-78%), with severe hypokinesia in the inferior and septal area. Patient was unresponsive, blood pressure still low with systolic pressure below 80 mmHg and oxygen saturation around 75-82%. So, the patient was managed with the extracorporeal membrane oxygenation (Capiox SP Pump controller 101, Terumo, Japan) through left femoral veno-right femoral arterial route with initial blood flow of 2-2.5 L/min. After that, the hemodynamics and oxygenation became stable with blood pressure 100/47 mmHg, and SpO2 100%.
She regained consciousness at the night of the operative day, and endotracheal tube was removed the following day. Extracorporeal membrane oxygenation was weaned and inotrope infusion was stopped at the third postoperative day. Afterwards, she recovered and was discharged without cardiopulmonary complication.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [31, 'years'], 'weight': [42.0, 'kg'], 'sex': 'Female', 'Sodium': [136.0, 'mmol/L']}",-0.6,-0.57,-0.63,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 31 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 42.0 kg. The concentration of sodium is 136.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 42.0 * (136.0/140 - 1) = -0.6 L. The patient's free body water deficit is -0.6 L."
6138,38,Free Water Deficit,lab test,decimal,pmc-4047694-1,Extracted,"A 21-year-old, 52 kg weight, male patient was admitted in the surgery department to undergo elective surgery. His preoperative biochemical and other baseline parameters were within normal limits. On the day of surgery, he was administered 2 ml of 0.5% of injection bupivacaine for spinal anesthesia. Following which he immediately went into shock. His blood pressure (BP) fell drastically to systolic 60 mg of Hg and diastolic not recordable and had thready pulse and tachypnea. His parameters PCO2-50.6 mm Hg; PO2-54.00 mm Hg; pH - 7.308; HCO3-24.5 mmol/L; hemoglobin (Hb) - 15 g/dl; serum Na + 142 mmol/L; serum K+2.7 mmol/L; blood urea 152 mg%, serum cretanine - 4.6 mg%; blood sugar - 126 mg%, serum alanine aminotransferase: 26.17 μkat/L, serum aspartate aminotransferase: 25.12 μkat/L and lipid profile were normal. Patient was given injection dopamine, mephentramine along with antibiotics and was put on ventilator support, but he succumbed within 1 day.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [21, 'years'], 'weight': [52.0, 'kg'], 'sex': 'Male', 'Sodium': [142.0, 'mmol/L']}",0.44571,0.42342,0.468,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 21 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 52.0 kg. The concentration of sodium is 142.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 52.0 * (142.0/140 - 1) = 0.44571 L. The patient's free body water deficit is 0.44571 L."
6139,38,Free Water Deficit,lab test,decimal,pmc-7683122-1,Extracted,"The patient is a 19-year-old female with a history of 6q24-related TNDM and Hashimoto's thyroiditis who was diagnosed with neonatal diabetes mellitus at birth.
She was born to a 25-year-old G3P2 mother, with a weight of 1927 grams, at 36 weeks of gestation via vaginal delivery after induction due to IUGR at an outside hospital. The pregnancy was significant for intrauterine growth restriction noted at 5 months of gestation. The pediatrician was at the delivery, and no resuscitation was needed. Apgar scores were 8 at 1 minute and 9 at 5 minutes. Macroglossia was noted. Umbilical hernia and hypotonia were not found. The infant was noted to have hypoglycemia on day of life one and was given intravenous glucose and went on to develop hyperglycemia. Glucose levels were the 400 mg/dl, and an insulin drip was started. The infant was transferred to the NICU from the outside hospital due to hyperglycemia and concerns for necrotizing enterocolitis (NEC). Due to concerns for NEC, oral feeds were discontinued and she was placed on TPN, providing a steady glucose load. No surgical intervention was necessary for the NEC. Glucose was difficult to control even while on TPN with blood sugar levels ranging from the 100s to >200 mg/dl. At about 1 month of age, glucose levels started dropping and insulin was weaned. During this time, due to an IV infiltrate, IV insulin was briefly discontinued and blood glucose was 268 mg/dl. Insulin infusion was restarted and was discontinued at about 1 month of age. Blood sugar levels ranged between 80 and 150 mg/dl. The infant was discharged shortly afterward, feeding ad lib and checking blood sugar before meals. She required intermittent subcutaneous insulin at home, which was finally discontinued at approximately 4 months of age. Since then, the patient did not require insulin or have diabetes symptoms. All developmental milestones were on time. At 15 years of age, she chipped her tooth and went to the dentist for evaluation. The dentist noted extensive tooth decay. Jaw X-rays showed bone loss of nearly 80% in the left mandible. Due to her history of TNDM, she was sent to her primary care provider for further workup and diabetes screening where blood glucose was 369 mg/dl and urinalysis showed positive ketones. She was sent to the emergency department, and laboratory examination showed blood glucose of 361 mg/dl, Na+ of 131 mEq/L, K+ of 3.4 mmol/L, bicarbonate of 19 mmol/L, 2+ urine ketones, anion gap of 16, and pH of 7.4. HbA1c was 15.4% during her admission. The diabetes autoimmune panel was negative (ICA-512, GAD-65, and Insulin Antibodies).
She endorsed long-standing polydipsia, polyphagia, and polyuria. She denied weight loss, nausea, vomiting, abdominal pain, confusion, blurry vision, fatigue, fever, and difficulty breathing. Family history was negative for autoimmune diseases except for hypothyroidism in the paternal grandmother and maternal great-grandmother. Physical exam showed a weight of 58.4 kg (70th percentile), height of 163 cm (55th percentile), and BMI of 21.98 kg/m2 (70th percentile). She was a well-appearing adolescent without thyromegaly and acanthosis nigricans and had Tanner Stage 5 breast. She was started on basal bolus insulin regimen consisting of 23 units of Glargine at bedtime and fast-acting insulin Lispro 1 unit per 10 grams of carbohydrates with meals.
She received the appropriate diabetes education. Laboratory examination also noted a TSH of 66 IU/ml (reference range: 0.35–5.5 uIU/ml); free T4 was 0.94 ng/dl (reference range: 0.8–1.8 ng/dl), and positive antibodies to thyroid peroxidase was 8580 IU/ml. She was treated with 75 mcg Levothyroxine that was titrated to a dose of 100 mcg. The 6q24 methylation-specific multiplex ligation-dependent probe amplification (MPLA) genetic test for transient neonatal diabetes identified hypomethylation within the 6q24 region. Deletion/duplication analysis ruled out paternal duplication of 6q24. Therefore, the hypomethylation could be the result of either paternal uniparental disomy of chromosome 6 (UPD6) or hypomethylation of the maternal allele. Via testing, UPD6 has been confirmed, meaning both copies of the 6q24 chromosome region in our patient were paternally inherited. This results in an epigenetic phenomena where both copies are still active. Typically, the paternal copy is active and the maternal copy is methylated and turned off. Epigenetic changes are typically de novo, as they depend on the parent of origin and are reset with each pregnancy, rather than DNA sequencing changes. Thus, risk of recurrence for parents, siblings, and offspring is unlikely. After diagnosis and her initial HbA1c of 15.4%, her HbA1c has ranged since then from 6.3% to 6.8%.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [19, 'years'], 'weight': [58.4, 'kg'], 'sex': 'Female', 'Sodium': [131.0, 'mEq/L']}",-1.87714,-1.78328,-1.971,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 19 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 58.4 kg. The concentration of sodium is 131.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 131.0 mEq. To convert from 131.0 mEq to mmol, convert from mEq to mmol. The compound 131.0 has a valence of 1, and so divide the valence by the value of mEq to get, 131.0 mEq/(1 mEq/mmol) = 131.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 131.0 mEq sodium/L converts to 131.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 58.4 * (131.0/140 - 1) = -1.87714 L. The patient's free body water deficit is -1.87714 L."
6140,38,Free Water Deficit,lab test,decimal,pmc-4241337-1,Extracted,"Mr. A, a 22-year-old Hispanic male with past psychiatric history of methamphetamine dependence and bipolar disorder type 1, came to the emergency department because of suicidal ideation with a plan to slash his throat with a machete. The patient was very agitated in triage and during initial assessment. In the emergency room (ER), the patient reported that he had been using methamphetamine for the last two years. His last use was a few hours before coming to the ER and that was his only use during the past six to eight weeks.
On physical examination, temperature was found to be 96.5 degree Fahrenheit, pulse 105/minute, blood pressure 124/78 mm Hg, weight 68.0 kg, and height 173 cm. His pupils were 5 mm in diameter and reactive. In the review of systems, the patient denied any pulmonary, cardiac, renal, and abdominal complaints. There was no increased lacrimation. Lungs were clear and the heart rate was regular without murmurs. Bowel sounds were normoactive. The patient was not oriented to time. His affect was flat and irritable. He was evasive and tangential while answering questions. A chest radiograph and electrocardiogram were normal. His urinary drug screen was positive for amphetamines, methamphetamines, and cannabinoids. Blood chemistry concentrations/counts/percent of the following analyses were mainly within reference limits: alcohol <5 mg/dL, salicylate <4 mg/dL, sodium 141 mmol/L, potassium 3.8 mmol/L, chloride 107 mmol/L, blood urea nitrogen 10 mg/dL, creatinine 0.9 mg/dL, aspartate transaminase 23 U/L, alanine transaminase 18 U/L, alkaline phosphatase 69 U/L, thyroid stimulating hormone 0.57 μIU/mL, white blood cells 10.7 K/uL, red blood cells 4.49 Mu/L, haemoglobin 13.9 g/dL, hematocrit 42.2%, and platelets 239 K/uL. Urinalysis revealed nothing abnormal.
The patient was transferred to the inpatient psychiatry unit. The next day, the patient was disoriented, refused to talk to the treatment team, and slept most of the day. On his third hospital day, the patient was much more oriented and reported that he was unable to get methamphetamine for the past six to eight weeks because he could not afford it. He claimed to use an insecticide, mostly cockroach killer, to “get high.” He would either “electrocute” the bottle or spray it on a heated metal sheet, and when the contents of the bottle turned into crystal, he would either inhale it or smoke it. The patient would use the crystals formed from one bottle for four to seven days. He claimed that his friends used those crystals intravenously after diluting them. The patient reported that it would give him the same high as methamphetamine and he would occasionally have feelings of deja vu. The patient also reported having olfactory hallucinations when he was on “crystal roach killer” but could not elaborate on that. He said that he liked the increase in heart rate and the “rush” he used to get after every use.
The patient's last use of the “crystal roach killer” was three days before coming to the ER. The patient reported that he would sleep most of the day when he was using it. He denied unwanted adverse effects during his use except for frequent headaches upon waking up which were relieved by over-the-counter analgesics. The patient had been using the insecticide for six to eight weeks and only used methamphetamine one (1) day before coming to the ER. The patient claimed that he had been compliant with his medications for bipolar disorder until he started using “crystal roach killer.” The patient was taking divalproex sodium 500 mg twice daily and quetiapine extended-release 300 mg at bedtime. He voiced that he, since a few weeks before coming to the ER, got scared that he might get cancer because of the frequent use of the insecticide, which led him to have suicidal ideation.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [22, 'years'], 'weight': [68.0, 'kg'], 'Sodium': [141.0, 'mmol/L']}",0.29143,0.27686,0.306,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 22 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 68.0 kg. The concentration of sodium is 141.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 68.0 * (141.0/140 - 1) = 0.29143 L. The patient's free body water deficit is 0.29143 L."
6141,38,Free Water Deficit,lab test,decimal,pmc-5704414-1,Extracted,"A 34-year-old, 47 kg male farmer presented to the emergency department with a history of consumption of around 150 ml of plant growth stimulant (nitrobenzene 20%) about 8 h before admission with suicidal intention. On examination, he was pale, irritable, tachypneic, and there was bitter almond-like pungent smell from patient's mouth. Blood pressure was 100/70 mmHg with pulse rate of 128/min and respiratory rate of 28/min. Arterial blood gas blood samples were dark-brown, which was suggestive of respiratory alkalosis. Electrocardiogram showed sinus tachycardia. X-ray chest was within normal limits. He was treated with gastric lavage (with normal saline), IV fluids, and IV methylene blue 50 mg. His kidney and liver function tests were normal on the day of admission. His serum cholinesterase enzyme level was 10,778 U/L. After 24 h of admission, the patient developed hypoxia (O2 saturation 86%), icterus, and decrease in urine output of about 100 ml in the last 6 h. Withdrawn blood for investigation was dark brown, which showed following serum values: total bilirubin 2.8 mg/dl (direct 1.0 mg/dl and indirect 1.8 mg/dl), serum glutamic oxaloacetic transaminase 121 U/L, serum glutamic pyruvic transaminase 45 U/L, alkaline phosphatase 45 U/L, creatinine 11.1 mg/dl, sodium 150 mEq/L, potassium 3.5 mEq/L, lactate dehydrogenase 780 U/L, and reticulocyte count of 4.0%; blood urea 279 mg/dl, hemoglobin 5.8 g/dl, total leukocyte count 11,800/mm3, and platelet count 7.54 lakh/mm3. Hemodialysis was initiated on an urgent basis through double-lumen internal jugular vein catheter with blood transfusions and was transferred to nephrology ward for the same. Peripheral blood smear showed normocytic, normochromic red blood cells that demonstrated anisocytosis and teardrop cells consistent with hemolysis. Coombs tests, both direct and indirect were negative. Urine was deep brown colored, and dipstick test was positive for hemeprotein. His methemoglobin level was sent and was found high (16.8%). Moreover, afterward, his G6PD enzyme level was found deficient. Hence, a diagnosis of methemoglobinemia in a G6PD-deficient patient due to compounds methylene blue and nitrobenzene with acute kidney injury was made. He was treated with ascorbic acid 500 mg three times a day along with supportive treatment. He was dialyzed on alternate days for the next 10 days with repeated blood transfusions. On the 11th day, his urine output gradually improved to 1000 ml and kidney functions started recovering. He was discharged after 20 days with following parameters: hemoglobin: 10.6 g/dl, total leukocyte count: 6600/mm3, and platelet count: 1.7 lakh/mm3. Serum creatinine was 1.1 mg/dl with normal serum electrolytes. Serum lactic dehydrogenase level was 186 U/L with normal liver function test.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [34, 'years'], 'weight': [47.0, 'kg'], 'Sodium': [150.0, 'mEq/L']}",2.01429,1.91358,2.115,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 34 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 47.0 kg. The concentration of sodium is 150.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 150.0 mEq. To convert from 150.0 mEq to mmol, convert from mEq to mmol. The compound 150.0 has a valence of 1, and so divide the valence by the value of mEq to get, 150.0 mEq/(1 mEq/mmol) = 150.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 150.0 mEq sodium/L converts to 150.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 47.0 * (150.0/140 - 1) = 2.01429 L. The patient's free body water deficit is 2.01429 L."
6142,38,Free Water Deficit,lab test,decimal,pmc-4085269-1,Extracted,"A 6-year-old girl 102 cm tall and weighing 17 kg, with chronic intestinal pseudo-obstruction was scheduled for multivisceral organ transplantation. Four-years earlier, she visited a hospital for abdominal distention and was diagnosed with gastric volvulus and congenital megacolon, for which she underwent gastropexy and segmental resection of the transverse colon. Since her symptoms did not improve over the next year, she was referred to our center and underwent a transverse colostomy. After that, she was repeatedly hospitalized and maintained on total parenteral nutrition due to continuously recurring mechanical ileus, malnutrition, and electrolyte imbalance. Two months before surgery, she was admitted due to abdominal distension and a malfunctioning colostomy. The colostomy function was normalized 2 days later, and she received conservative medical care, including total parenteral nutrition.
The patient was scheduled for multivisceral organ transplantation, including seven abdominal organs, the liver, spleen, stomach, duodenum, small bowel, colon and pancreas. Cadaveric donor was 5-year-old female 110 cm tall and weighed 21 kg, who had brain death due to increased intracranial pressure caused by medulloblastoma. Histidine-tryptophan-ketoglutarate solution was used as preservation solution and ischemic time was 170 min. Intraoperative gross finding of the grafts showed no significant abnormality. The recipient was not premedicated and arrived at the operating room with her father. Her blood pressure was 120/64 mmHg, her heart rate was 120 beats/min, and her oxygen saturation on pulse oxymetry was 100% before induction of anesthesia. Pre-operative blood laboratory data were within normal ranges, including hemoglobin (9.4 g/dl), Na+ (142 mmol/L), K+ (3.7 mmol/L), creatinine (0.34 mg/dl), aspartate transaminase (AST; 43 IU/L), alanine transaminase (ALT; 35 IU/L), total bilirubin (0.5 mg/dl), albumin (4.4 g/dl), and prothrombin time (1.00 INR). Anesthesia was induced with 75 mg of pentothal sodium, 15 mg of rocuronium, and 50 µg of fentanyl. After tracheal intubation, anesthesia was maintained with 1% sevoflurane in 50% oxygen in air and continuous infusion of fentanyl (100 µg/h) and vecuronium (2 mg/h). Her brachial artery was cannulated for continuous arterial blood pressure monitoring. A central venous catheter was inserted into her right internal jugular vein and a second into her subclavian vein to monitor central venous pressure and venous oxygen saturation. Femoral venous pressure was also monitored. Ten minutes before graft reperfusion, her vital signs and arterial gas analysis were as follows; mean arterial blood pressure (MAP) was 86 mmHg, heart rate was 90 bpm, central venous pressure was 4 mmHg, femoral venous pressure was 16 mmHg, and body temperature was 36.7℃, pH was 7.32 with a base excess of -9.5 mEq/L, arterial lactate concentration was 5.6 mmol/L, Na+ was 142 mmol/L, K+ was 2.5 mmol/L, Ca2+ was 0.83 mmol/L, hemoglobin was 10.8 g/dl, and blood glucose was 98 mg/dl.
After injection of 20 mEq of NaHCO3, graft reperfusion was performed. Just after reperfusion, MAP rapidly decreased to 39 mmHg. Femoral venous pressure decreased after IVC unclamping from 16 mmHg to 4 mmHg and central venous pressure was maintained around 4 mmHg. Because the decrease of arterial pressure was too severe to expect spontaneous recovery and met the definition of PRS (≥ 30% decrease in MAP occurring within 5 minutes after reperfusion and lasting for at least 1 minute). She was immediately administered 5 µg of epinephrine, resulting in an MAP of 44 mmHg. However, repeated injections of 10 µg epinephrine and volume replacement were required to increase her MAP due to prolonged hypotension. Hypotension was sustained over 10 minutes, during which her averaged arterial pressure was 38 mmHg despite intermittent surge of MAP > 60 mmHg (). Arterial blood gas analysis 5 minutes after reperfusion showed severe metabolic acidosis, with a arterial blood pH of 7.09 with a base excess of -17.9 mEq/L, and the arterial lactate concentration was 8.5 mmol/L, K+ was 4.8 mmol/L, Ca2+ was 0.84 mmol/L, glucose was 114 mg/dl, and hemoglobin was 8.5 g/dl. To correct metabolic acidosis and hypotension, she was immediately and repeatedly injected with 30 mEq of NaHCO3 and 10 µg of epinephrine. Her body temperature had decreased to 33.4℃ just after reperfusion, with hypothermia sustained for 30 min (nadir body temperature: 33.0℃) despite active warming with an air warmer. Subsequently, continuous infusion of norepinephrine (0.1 µg/kg/min) until the end of the operation was required to maintain her MAP within an acceptable range. At the end of surgery, her body temperature increased to 35.7℃, but metabolic acidosis was sustained despite frequent administration of NaHCO3 (arterial pH: 7.23; base excess: -10.0 mEq/L). During the surgery, the patient was infused with a total of 2,900 ml of fluid, including 1,500 ml of balanced crystalloid solution, 100 ml of half-normal saline, 300 ml of 5% dextrose water, and 1,000 ml of 5% albumin, as well as 2 units of packed red blood cells. After 9 hours of surgery, the patient was transferred to intensive care unit. Hemodynamic and laboratory changes during the operation are shown in .
After surgery, the AST and ALT concentrations of the patient increased rapidly (immediate postoperative AST 2,108 IU/L and ALT 2,351 IU/L), reaching 7,300 IU/L and 6,400 IU/L, respectively, on the second day after the operation. She required continuous infusion of fresh frozen plasma due to prolongation of prothrombin time (3.07-5.69 INR). Her total bilirubin concentration, which was 0.5 mg/dl preoperatively, increased to 3.4 mg/dl postoperatively. The patient was diagnosed with primary hepatic graft failure and scheduled for re-transplantation of the liver. An adult to child living donor liver transplantation was performed on the third day after multivisceral transplantation. During this operation, the patient's vital signs remained stable until reperfusion, including a MAP of 70-80 mmHg. Ten minutes before reperfusion, her arterial blood pH was 7.49 with a base excess of -0.1 mEq/L, arterial lactate concentration was 3.8 mmol/L, Na+ was 137 mmol/L, K+ was 3.3 mmol/L, Ca2+ was 0.97 mmol/L, hemoglobin was 8.2 g/dl, and blood glucose was 170 mg/dl. After reperfusion, PRS developed again and lasted over 1 min. She received three injections each of 4 µg epinephrine and 20 µg of phenylephrine to maintain MAP within an acceptable level. Her arterial lactate concentration was 3.1 mmol/L at pH 7.44 with a base excess of -2.2 mEq/L, Na+ concentration was 138 mmol/L, K+ was 2.9 mmol/L, Ca2+ was 1.00 mmol/L, and hemoglobin was 6.8 g/dl. After transfusion of one unit of packed red blood cells, her vital signs remained stable (MAP: 70-76 mmHg) until the end of the operation. At that time, plasma hemoglobin concentration was 11.9 g/dl, AST was 453 IU/L, ALT was 695 IU/L, total bilirubin was 3.6 mg/dl, creatinine was 0.6 mg/dl, albumin was 2.9 g/dl, and prothrombin time was 1.74 INR. Her serum AST and ALT concentrations decreased gradually. On the seventh day after liver transplantation, AST and ALT concentrations had declined to 69 IU/L and 150 IU/L, respectively, her total bilirubin was 1.4 mg/dl, prothrombin time was 1.07 INR, and feeding through gastrostomy tube was started. The patient was managed conservatively for 3 months including 50 day stay in the Intensive Care Unit and discharged in an improved condition 139 days after multivisceral transplantation.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [6, 'years'], 'weight': [17.0, 'kg'], 'sex': 'Female', 'Sodium': [142.0, 'mmol/L']}",0.14571,0.13842,0.153,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 6 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 17.0 kg. The concentration of sodium is 142.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 17.0 * (142.0/140 - 1) = 0.14571 L. The patient's free body water deficit is 0.14571 L."
6143,38,Free Water Deficit,lab test,decimal,pmc-3277472-1,Extracted,"MR was a 14-year-old Muslim Kurdish student living in Sulimania, northeast of Iraq. His parents were of an educated middle class family who enjoyed good health and stable relationships. He was brought by his mother to the hospital on 18th July 2010 for refusing to eat, which had led to severe weight loss and generalized weakness. His condition began seven months prior when his friends teased him about his plumpness and greedy appetite. Consequently, he started restricting his food intake, avoiding high-calorie foods and indulging routinely in extensive exercise. His parents tried to convince him to eat regular meals, but he refused. He was obsessed about his body shape and measured his waist and thigh circumferences regularly. His food intake decreased rapidly until his daily meal became no more than a cup of yogurt and pieces of cucumber. A few weeks before his visit to the hospital, he experienced severe fatigue, headaches, joints aches and attacks of epigastric pain followed by vomiting. He was treated by the local doctor with multivitamins, anti-emetics and anti-spasmodics, but without improvement.
The patient seemed to be overprotected by his mother. He was the youngest of seven siblings and a clever boy. She described him as being a graceful and obedient child, but somewhat of a perfectionist. There was neither a history of physical or mental illness nor sexual abuse during childhood.
On admission to the hospital, he appeared to be severely ill. He was pale, emaciated and dehydrated. He had lost about 20 kg during the past four months, according to his mother, who reported episodes of irritability and depressed mood with the decrease in weight. His body weight was 28 kg and height 147 cm, which is below the 2nd percentile for his age according to the growth chart. His BMI was 13.0, reflecting a 37% deficit in weight for his height [].
Upon examination, he showed generalized muscle wasting, and his skin was dry and covered by lanugo hair. His chest was clear, and he had a scaphoid soft abdomen. His blood pressure was 90/60 mmHg, heart rate 55 bpm and body temperature 37.8°C. Laboratory tests were as follows: blood glucose: 60 mg/dl, blood urea: 18 mg/d, serum sodium: 136 mg/dl, serum creatinine: 0.6 mg/dl, serum cholesterol: 147 mg/dl, WBC: 2200, platelet count: 150000, ESR: 1, and HB: 12 mg/dl. Blood proteins were low with slightly elevated liver enzymes. The blood culture was negative. Thyroid functions tests and steroid hormones were normal. General urine examination and culture revealed an acute bacterial infection, which accounted for his fever. Skull, spine and chest x-ray, brain scan and abdominal ultrasound were all normal. A previous gastroscopy at another hospital showed mild mucosal atrophy. An ECG revealed sinus bradycardia. The patient was smaller and shorter than his matching peers. He looked attentive but indifferent to his serious condition. His speech was rational and did not reveal delusions or hallucinations. However, he expressed strong denial of his body appearance and insisted he had a normal body shape. His mood was depressed, but he denied suicidal ideation.
The patient was admitted on 18th July 2010 to Sulimania General Hospital and was referred later for psychiatric consultation. A liaison treatment plan was designed by the attending physician, psychiatrist and dietitian focusing on scheduled feeding under the dietitian's advice, which was to be achieved through a nasogastric tube. Caloric intake was measured to reach 2000 calories per day, and he was instructed to rest in bed under a nurse's supervision. This ameliorated his previous hypoglycemic attacks. He was prescribed oral cephalosporin 250 mg qds to treat his urinary infection. On the second day of his admission, the psychiatrist prescribed a 20 mg daily dose of fluoxetine to treat his depressed mood and food-related obsessions. A 5 mg nightly dose of olanzapine was prescribed to resolve the distorted thoughts about his body image and promote sedation. Nasogastric refeeding was continued for the first week in the hospital until oral feeding was established. The tube was removed on the 6th day. In addition, a few sessions of cognitive psychotherapy were conducted with the patient.
At the end of the third week, he became more realistic and rational about his body weight and was more compliant with eating normal meals. His mood and irritability improved. He was discharged after 24 days in the hospital, advised to abide by the regulations of the dietitian and continue his medication for three months. He was to report to the psychiatry clinic on alternate weeks. His body weight had increased to 30 kg.
He did not keep his appointments and appeared six months later at the clinic weighing 38 kg. He was enjoying better health, although he was still having eating peculiarities. He had maintained his daily exercise but was reluctant to gain more weight. After consultation, he was advised to continue on fluoxetine for another three months. The family was advised to escort him regularly for psychotherapy sessions and watch his dietary intake.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [14, 'years'], 'weight': [38.0, 'kg'], 'sex': 'Male', 'Sodium': [136.0, 'mEq/L']}",-0.65143,-0.61886,-0.684,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 14 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 38.0 kg. The concentration of sodium is 136.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.0 mEq. To convert from 136.0 mEq to mmol, convert from mEq to mmol. The compound 136.0 has a valence of 1, and so divide the valence by the value of mEq to get, 136.0 mEq/(1 mEq/mmol) = 136.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mEq sodium/L converts to 136.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 38.0 * (136.0/140 - 1) = -0.65143 L. The patient's free body water deficit is -0.65143 L."
6144,38,Free Water Deficit,lab test,decimal,usmle-264,Extracted,"A 5-year-old African-American boy is brought to the physician because of fatigue and night sweats for the past month. During this time, he has also lost 3 kg (6.6 lbs). Before the onset of symptoms, he had been healthy except for a febrile seizure as an infant. His brother had chickenpox 2 months ago. He is at the 75th percentile for height and 50th percentile for weight. He appears markedly fatigued. His temperature is 38°C (100.4°F), pulse is 95/min, respirations are 19/min, and blood pressure is 100/60 mm Hg. Lung and cardiac examination is normal. There are enlarged, nontender lymph nodes bilaterally in the neck. The abdomen is soft and nontender. A complete blood count shows:
Leukocyte count 8,000/mm3
Hemoglobin 9.1 g/dL
Hematocrit 26.9%
Platelet count 34,000/mm3
Serum
Na+ 135 mEq/L
K+ 4.5 mEq/L
Cl- 101 mEq/L
HCO3- 27 mEq/L
Urea nitrogen 9 g/dL
Creatinine 0.7 g/dL
Ca2+ 8.8 mg/dL
PCR testing demonstrates a 9:22 chromosomal translocation.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [5, 'years'], 'weight': [3.0, 'kg'], 'sex': 'Male', 'Sodium': [135.0, 'mEq/L']}",-0.06429,-0.06108,-0.0675,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 5 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 3.0 kg. The concentration of sodium is 135.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 135.0 mEq. To convert from 135.0 mEq to mmol, convert from mEq to mmol. The compound 135.0 has a valence of 1, and so divide the valence by the value of mEq to get, 135.0 mEq/(1 mEq/mmol) = 135.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mEq sodium/L converts to 135.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 3.0 * (135.0/140 - 1) = -0.06429 L. The patient's free body water deficit is -0.06429 L."
6145,38,Free Water Deficit,lab test,decimal,pmc-3542923-1,Extracted,"We report the case of an athletic 49-year-old female with no medical records who has run the 2011 Marathon of Paris (42.195 Km). In view of the marathon, the patient started to train a few months ahead as per two to three runs weekly. She completed the marathon within 5 h 30, with an average speed of 7.5 Km/h, on a warm day (27 degrees celsius). Along the run, she drunk 4 L of mineral water (5 mg/L NaCl), and had some energy bars at the various feeding stations. Four hours after completion of the marathon, the patient felt dizzy and nauseous, with a strong asthenia and encompassed three vomiting periods associated with disorientation and confusion. She was then admitted to the emergency room 7 hours after the afore-mentioned symptoms occurred.
Upon admission, the patient was conscious but disoriented, clouded, with a Glasgow coma score of 13. She was apyretic and presented no circulatory failure. The neurological examination revealed acute spreadover of osteotendinous reflexes the four limbs, no systematic deficiencies and cutaneous plantar reflexes in flexion, isochoric and reactive pupils. Her body weight was 53.4 Kg (normal average body weight of 50 Kg).
The patient was then transferred to the intensive care unit (ICU) for diagnosis and treatment. Four hours later, the patient had a generalized tonic-clonic seizure that resolved following 1 mg clonazepam IV injection. The cerebral CT-scan showed a diffused supratentorial cerebral oedema (). The initial biological parameters were natremia 121 mmol/L, chloremia 88 mmol/L, protidemia 70 g/L, glycemia 8.5 mmol/L, kalemia 3.3 mmol/L, bicarbonates 18 mmol/L, blood urea nitrogen 3.7 mmol/L, creatinemia 68 μmol/L, blood urea nitrogen 2.9 mmol/L, uric acid 214 mmol/L, Glycemia 6.6 mmol/L, calcemia 1.8 mmol/L, phosphorus 0.87 mmol/L, magnesemia 1.04 mmol/L, CPK 14486 UI/L, Hb 10.1 g/dL, platelet count 172 G/L, and leukocytes 11.06 G/L. The calculated osmolality was 260 mosm/kg and the measured osmolality was 246 mosm/kg. Arterial blood gases showed a respiratory alkalosis to compensate an increased plasmatic anion gap metabolic acidosis, with initial blood lactate 10.5 mmol/L. The initial collection of a urine sample showed an urinary osmolality of 489 mosm/L. We report a natriuresis and kaliuresis of 86 and 75 mmol/L, respectively. The measure of the free cortisol was 1250 nmol/L at 8 am, and 1350 nmol/L following the ACTH test, by which therefore eliminate an adrenal origin of hyponatremia.
The patient was given a calculated bolus of isotonic saline as per the Adrogue formula. As no further clinical improvements followed, with a persistent hyponatremiaof 121 mmol/L, the patient was given a treatment based on 3% hypertonic saline solution. Natremia was recorded and indicated 128 mmol/L and 136 mmol/L at 4 hours and 7 hours after beginning of the treatment, respectively. Despite a rapid correction of natremia abnormalities, biological improvement was associated with the resolution of the neurological perturbations without apparition of new neurological symptoms.
The patient was discharged after 7 days following complete resolution of clinical and biological disorders.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [49, 'years'], 'weight': [53.4, 'kg'], 'Sodium': [121.0, 'mmol/L']}",-3.62357,-3.44239,-3.80475,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 49 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 53.4 kg. The concentration of sodium is 121.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 53.4 * (121.0/140 - 1) = -3.62357 L. The patient's free body water deficit is -3.62357 L."
6146,38,Free Water Deficit,lab test,decimal,pmc-5594813-1,Extracted,"A 4-year-old girl with 8 kg weight and 90 cm height admitted for femur fracture []. The onset of the disease was manifested at 6 months of age with a bulging anterior fontanel due to hydrocephalus with a subsequent ventriculoperitoneal shunting. Physical examination revealed short stature, growth delay, facial deformity, optimal mouth opening and neck extension, heart murmur grade III/VI, and splenomegaly. Heart and respiratory rates of the patient were 150/min and 20/min, respectively, with a 100/56 mmHg blood pressure. Laboratory results of the patients at the baseline were as follows – hemoglobin: 3.5 g/dL (anisocytosis, hypochromia, ovalocytosis, and elliptocytosis) and platelet: 39 × 109/L, which reached to 9.1 g/dL and 91 × 109/L after receiving two units of blood and platelet, respectively. White blood cell: 8.6 × 103/μL, red blood cell: 3.9 × 106/μL, alkaline phosphatase: 1279 U/L, lactate dehydrogenase: 832 U/L, phosphorus 3.5 mg/dL, Na: 135 mEq/L, K: 4.2 mEq/L, and calcium 9.3 mg/dL.
Echocardiography showed that the left ventricle volume was increased and the left ventricular ejection fraction was 30–40%, moderate tricuspid regurgitation. Sonography showed normal-sized liver with splenomegaly. The patient was on medication: Captopril 2.5 mg PO three times daily and Lanoxin (digoxin) 8 cc PO two times daily. Because of the femur fracture, the patient was candidate for applying a Spica cast under general anesthesia.
Due to the probability of difficult airway management (regarding facial abnormality), necessary precautions were made in the setting of anesthesia before induction [].
The equipment for difficult airway management was included into the preparation setting which were laryngoscopes with Mackintosh and Miller types blades (sizes 0-2), ventilation face masks sizes 1-2, stylets with endotracheal tubes sizes 3.5-4.5 mm ID (un-cuffed), a pediatric size Glidescope and fiberoptic, percutaneous jet-ventilation catheter.
Before anesthesia induction, the patient was monitored with electrocardiography, noninvasive blood pressure, oxygen saturation (SpO2), and end-tidal carbon dioxide (ETCO2). Balanced isotonic solution was administered with a rate of 10 cc/kg perioperatively due to heart failure during the anesthesia management.
Midazolam 0.15 mg/kg and fentanyl 1 μg/kg with 0.02 mg/kg atropine were administered as premedication. General anesthesia was induced and maintained by ketamine 1 mg/kg. The patient was ventilated by an anesthesia face mask. During the anesthesia, the heart rate was 110–120/min, blood pressure 100/70 mmHg, SPO2 = 99%, and ETCO2 28–30 mmHg. The course of anesthesia and recovery was uneventful.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [4, 'years'], 'weight': [8.0, 'kg'], 'sex': 'Female', 'Sodium': [135.0, 'mEq/L']}",-0.17143,-0.16286,-0.18,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 4 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 8.0 kg. The concentration of sodium is 135.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 135.0 mEq. To convert from 135.0 mEq to mmol, convert from mEq to mmol. The compound 135.0 has a valence of 1, and so divide the valence by the value of mEq to get, 135.0 mEq/(1 mEq/mmol) = 135.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mEq sodium/L converts to 135.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 8.0 * (135.0/140 - 1) = -0.17143 L. The patient's free body water deficit is -0.17143 L."
6147,38,Free Water Deficit,lab test,decimal,pmc-2816905-2,Extracted,"A 4.3-yr-old boy came to the Department of Plastic Surgery with chief complaints of Down syndrome, syndactyly of the third and fourth toes on both feet, and trigonocephaly. Plastic surgeons performed cranial vault remodeling for craniosynostosis and managed the patient cooperatively with pediatricians for the postoperative polyuria and exacerbation of the general condition. The findings on the first and second postoperative day were as follows; daily urine amounts of 798 mL and 1,790 mL during 24 hr, CVP 5-8 cmH2O and 2-6 cmH2O, blood loss of 99 mL and 64 mL, and blood pressure of 100/60 mmHg and 96/60 mmHg, respectively. On the third postoperative day, the values were changed to 2,375 mL of 24-hr urine amount, 3-6 cmH2O of CVP, 9.5 mL of blood loss, and 90/50 mmHg of blood pressure. The 24-hr urine amount, CVP, and blood pressure were 2,360 mL, 1-3 cmH2O, and 90/50 mmHg, respectively, on the fourth postoperative day and were 1,750 mL, 5-7 cmH2O, and 100/60 mmHg on the fifth postoperative day. The findings on the eighth postoperative day were as follows; 24-hr urine amount of 463 mL, CVP of 6-7 cmH2O, blood loss of 45 mL, and blood pressure of 110-60 mmHg. Since then, the 24-hr urine amount was maintained at less than 700 mL, and the blood pressure was also stabilized at 100-110/50-65 mmHg. On the thirteenth postoperative day, there was no more blood loss, and the suction drain was removed.
Growth percentiles at admission were 15 kg (0-25 percentile) in weight, 96 cm (3-10 percentile) in height, 45 cm (0-3 percentile) in head circumference. Vital signs were 37.7℃ of body temperature, 92 beats/min of pulse, 22 times/min of respirations, and 110/60 mmHg of blood pressure. While the patient had clear consciousness and good nutritional condition, the intelligence quotient and the physical quotient were comparatively retarded corresponding to about 15 months and 24 months, respectively. No abnormal rash or pigmented lesions were found on skin examination. The conjunctivae were a little pale but the sclera was anicteric. There were no pharyngeal injections or tonsillar hypertrophy. The thorax and the abdomen did not show any specific abnormalities. In extremities, syndactyly was shown on the third and the fourth toes of both feet. There was no neurological abnormality.
Preoperative laboratory findings included normocytic anemia with hemoglobin 9.5 mg/dL and MCV 83.5 fL. Biochemical test was normal, and electrolyte levels showed Na+ 140 mEq/L, K+ 4.5 mEq/L, Cl- 106 mEq/L, urine-specific gravity of 1.015, PmOsm of 293 mOsm/kg, and UmOsm of 408 mOsm/kg. The changes of electrolytes and osmolarity of serum and urine after surgery are shown in . Preoperative values of ADH, ANP, and HBNP were 3.25 pg/mL, 14 pg/mL, and HBNP 4.1 pg/mL, respectively. On the day of operation, the values were ADH 2.3 pg/mL, ANP 92 pg/mL, and HBNP 63 pg/mL. On the fifth postoperative day, they were ADH 1.38 pg/mL, ANP 36 pg/mL, and HBNP 6.4 pg/mL. The patient was diagnosed as having CSW syndrome when the postoperative 24-hr urine amount was over 1,500 mL, and did not show hyponatremia after the water and sodium supply through normal saline. Since the eighth postoperative day, the patient was in good general condition with the urine output gradually decreasing and normal blood pressure. Then, the patient was discharged from the hospital on the seventeenth postoperative day without circulatory or neurologic sequelae.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [3, 'years'], 'weight': [15.0, 'kg'], 'Sodium': [140.0, 'mEq/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 3 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 15.0 kg. The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 15.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
6148,38,Free Water Deficit,lab test,decimal,pmc-4459668-1,Extracted,"A 45-year-old, 58 kg, 156 cm woman presented with increased and prolonged vaginal bleedings. A physical examination and an ultrasound showed a submucosal leiomyoma of the uterus. There were no other symptoms or pathological findings. Preoperative blood tests, which included electrolytes analyses, a full blood exam, and coagulation parameters, showed no anomalies. Most notably, both creatinine and sodium were within normal levels, i.e. 0.7 mg/dL and 137 mEq/L, respectively. The patient had a history of encephalopathy during childhood of an unknown origin without sequelae, an elective caesarean section (1997) due to leiomyoma, laparoscopic myomectomy and removal of an endometrial cyst of the ovary (1999), and a second caesarean section (2000) due to an uterine instability subsequent to the first caesarean section and myomectomy. The patient had no known allergies. She was taking daily doses of ethinyl estradiol (0.02 mg) and levonorgestrel (0.1 mg) continuously over a period of six months. The patient refused a hysterectomy but an endoscopic removal of the leiomyoma and an endometrial ablation was decided on, subsequent to which the patient gave written informed consent. The patient was administered with 7.5 mg midazolam orally 60 min preoperatively. Subsequent to placing the patient in the lithotomy position, the application of a peripheral venous catheter and the attachment of standard monitoring equipment (electrocardiogram, non-invasive blood pressure cuff and a peripheral capillary oxygen saturation analyzer), anaesthesia was induced intravenously with propofol (2 mg/kg) and sufentanil (0.3 μg/kg).
A laryngeal mask was inserted, and after the correct positioning was verified, the lungs were ventilated with a fraction of inspired oxygen (FiO2) of 0.5 and a minute volume (MV) of 74 mL/min/kg at a ventilation frequency of 10/min in volume controlled mode (IPPV). The positive end-expiratory pressure (PEEP) level was 0 Pa and the peak pressure was 900 Pa. Anaesthesia was maintained with propofol (8 mg/kg/h). After anaesthesiological clearance the endoscopy commenced. Purisole® SM (Fresenius Kabi Inc., Germany) was utilized as the distension medium. This standard hypotonic solution contains 27 g sorbitol and 5.4 g mannitol per liter. A pressure of 16 kPa (120 mmHg) was applied to unfold the uterine cavity. Endometrial ablation and dissection of the submucosal myoma were performed within 70 min by monopolar resection. The duration of the procedure was prolonged due to the reduced visibility caused by excessive bleeding and cervical leakage of distension medium, which impeded proper expansion of the uterine cavity. The ventilation pressure increased slowly and continuously 60 min subsequent to the start of surgery. The compliance of the lungs, as well as the achievable minute volume within the acceptable airway pressure limit of 2 kPa, decreased. It was presumed that the level of anaesthesia was insufficient and was followed by the increased administration of propofol (10 mg/kg/h). The additional inhalation of fenoterol did, however, not improve the situation. As ventilation continued to be difficult, the laryngeal mask was replaced by a 7.0 cm (inside diameter) cuffed tube subsequent to the administration of 100 mg succinylcholine as a muscle relaxant. Approximately 50 mL of a foamy, transparent liquid was aspirated from the trachea. Testing with litmus paper indicated an alkaline pH and, therefore, not the aspiration of gastric content. The amount of the pulmonary oedema increased and, despite high levels of peak airway pressures at this point approximately 3 kPa (= set peak pressure limit), adequate ventilation was not possible. Blood gas and electrolyte analyses indicated acidosis, as well as a severe hyponatremia (pH 7.11; Na 74 mEq/L; partial pressure of CO2 49.9 mmHg; saturation of O2 97 % at FiO2 1.0). Cardiopulmonary changes remained minimal. 40 mg of furosemide and 500 mL of 3 % NaCl solution were immediately administered at an infusion rate of 500 mL/h, with constant monitoring for electrolyte changes. As the patient showed clinical signs of impaired haemostasis, the operation procedure was stopped. The patient was admitted to the intensive care unit with continuous administration of 3 % NaCl at a rate of 50 mL/h and electrolyte control. Plasma sodium levels increased from 74 mEq/L to 103 mEq/L after one hour, and to 130 mEq/L after 7 h (Fig. ). All together 800 mL of 3 % NaCl solution were administered within 7 h totalling at 24 g. Subsequently, sodium replenishment was stopped and the patient was extubated without problems. Immediate neurological assessment revealed no detectable deficits. 20 h after the onset of hyponatremia, the patient’s sodium levels returned to within the normal range. Until then, the cumulative renal excretion was 8.5 L. 9 L of distension medium was used intraoperatively with a calculated uptake of 5 L. The patient was relocated to the gynaecologic ward the following day and was released from the hospital on the third postoperative day without any detectable sequelae.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [45, 'years'], 'weight': [58.0, 'kg'], 'Sodium': [137.0, 'mEq/L']}",-0.62143,-0.59036,-0.6525,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 45 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 58.0 kg. The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 58.0 * (137.0/140 - 1) = -0.62143 L. The patient's free body water deficit is -0.62143 L."
6149,38,Free Water Deficit,lab test,decimal,pmc-4169830-1,Extracted,"A 16-year-old Caucasian boy had been affected by T1DM since the age of 16 months. The diagnosis of insulin- dependent diabetes was confirmed by the following autoimmune profile: glutamic acid decarboxylase antibodies (GADA), 134 IU/ml; islet cell antibodies (ICA), 126 IU/ml; and antibodies directed towards protein tyrosine phosphatase-like protein (IA2-ab), 12 IU/ml. At the age of 4 years, autoimmune thyroiditis was diagnosed and treatment with levo-tiroxine was started. In the last 4 years, the patient had been treated with continuous subcutaneous insulin infusion (CSII), which, combined with an adequate lifestyle (balanced diet and daily physical activity), allowed to obtain an optimal glycaemic control.
During a follow-up visit, he reported sporadic episodes of hypoglycaemia in the preceding three months; one of these episodes was severe with loss of consciousness, and required admission to the hospital. At physical examination we observed: height = 180 cm; weight = 67 kg; body mass index (BMI) = 20.7 Kg/m2; blood pressure = 120/75 mmHg. General examination showed no abnormalities. Glycated haemoglobin was 7.5%. The patient was on a total daily insulin dose of 1.1 IU/Kg/day, with a percentage of basal insulin of 41%. We prescribed a reduction of the total insulin dose, and the insulin/carbohydrate ratio was reset, reassessing patient’s food diary.
The patient was revaluated three months later: other episodes of hypoglycaemia had occurred with one episode of severe hypoglycaemia characterized by seizure and treated with glucagon. At physical examination, body weight was unchanged; blood pressure was 105/55 mmHg, and glycated haemoglobin was significantly reduced (6.6%). General examination revealed no clinical signs indicative of any associated disease. The patient, spontaneously, had gradually reduced basal insulin (total 0.92 IU/kg/day) and had continued to show an adequate compliance with dietetic and therapeutic regimens. Both the patient and his parents denied alcohol abuse or improper lifestyle. Routine blood chemistry resulted negative, excluding the presence of liver and kidney diseases. Screening for celiac disease was also negative. Hence, we decided to further reduce the total dose of insulin.
At the following visit, the patient reported frequent hypoglycaemic episodes and marked asthenia. The clinical picture appeared clearly deteriorated: a significant weight loss was observed (weight 61 kg; BMI 18.7 Kg/m2). Downloaded data of the insulin pump indicated a further reduction of total insulin by more than 30% (0.75 IU/kg/day). Glycated haemoglobin value was 6.3%. At clinical examination, the patient presented scrotal hyperpigmentation and blood pressure = 80/50 mmHg.
Adrenal insufficiency was immediately suspected, and the patient was admitted to the hospital for further investigation. Blood tests showed: sodium, 129 mEq/L (136–145); potassium, 5.3 mEq/L (3.5-5.1); basal serum cortisol, 1.5 ng/ml; ACTH, 1274 pg/ml (<60). Blood cortisol levels in response to the ACTH test (1 μg i.v.) were the following: basal levels, 1.5 ng/ml; levels at 20’, 1.1 ng/ml; and levels at 30’ , 1.1 ng/ml. Adrenal antibodies could be detected.
The diagnosis of AD was confirmed and cortisone acetate (14 mg/m2 in three doses) was prescribed.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [16, 'years'], 'weight': [61.0, 'kg'], 'Sodium': [129.0, 'mEq/L']}",-2.87571,-2.73192,-3.0195,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 16 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 61.0 kg. The concentration of sodium is 129.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 129.0 mEq. To convert from 129.0 mEq to mmol, convert from mEq to mmol. The compound 129.0 has a valence of 1, and so divide the valence by the value of mEq to get, 129.0 mEq/(1 mEq/mmol) = 129.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 129.0 mEq sodium/L converts to 129.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 61.0 * (129.0/140 - 1) = -2.87571 L. The patient's free body water deficit is -2.87571 L."
6150,38,Free Water Deficit,lab test,decimal,pmc-6077600-1,Extracted,"A 59-year-old male was scheduled for elective open retropubic prostatectomy for a benign enlarged prostate weighing approximately 65 grams. The patient's weight was 89 kg, ASA physical status II, diagnosed with essential hypertension two years ago, and controlled with ACE-I, Ramipril 10 mg once daily. No other morbidities were associated and no other medications were taken by the patient. The preoperative assessment did not reveal any other abnormality related to anaesthesia with normal vital signs, omitting Ramipril for 48 hours before the operation and normal baseline laboratory results including renal profile (creatinine 87 micromole/L, urea 7.9 mmol/L, Na 140 mmol/L, and K 4.1 mmol/L).
Following discussion with the patient and the surgical team, the anaesthetic plan was general anesthesia (GA) with postoperative patient-controlled analgesia (PCA) with morphine. Relatively uneventful induction of GA by propofol (2mg/kg), fentanyl (100 micrograms), and rocuronium (0.6 mg/kg) with endotracheal intubation, radial arterial cannulation for IBP monitoring, and two wide-bore peripheral cannulas (18G) were inserted. Induction was accompanied by hypotension (BP dropped from 112/68 to 73/46) and bradycardia (HR dropped from 78/min. to 38/min.) that required two successive doses of ephedrine each 6 mg were followed by restoration of BP and HR. Baseline arterial blood gas (ABG) after positioning was normal (). At 2 hours after the start of surgery, the estimated blood was about 350 ml and the urinary output (UOP) was 120 ml (over 2 hours) with mean arterial pressure (MAP) being maintained above 70 mmHg without further vasopressors required other than the initial 12 mg of ephedrine required immediately after induction. An arterial blood gas (2 hours after start of surgery) was initially performed for monitoring haemoglobin level showed hyperkalaemia (6.1 mmol/L) with acidosis (pH 7.33 and PCo2 6.2 kPa). The initial explanation was respiratory acidosis, and ventilation parameters were increased. Twenty-five minutes later ABG showed a decrease of PCo2 to normal with normal anion gap acidosis and increasing potassium to 6.5 mmol/L. Hyperkalaemia was treated with glucose-insulin (10 units of insulin added to 1 litre of glucose 10%) and mild hyperventilation and furosemide (20 mg bolus) with a change of the maintenance fluid from compound lactate solution to normal saline with the same rate (225ml/h). Forty minutes later, these measures had reduced potassium from 6.5 mmol/L to 4.1 mmol/L.
Despite normalization of potassium level (k 4.1 mmol/L) following the measures mentioned above, the acidosis persisted with maintained normal bicarbonate level and normal PCo2 (). From the time of normalized potassium, the acidosis required three hours to normalize which was two hours after recovery from GA. The presence of acidosis did not affect emergence from anaesthesia or recovery of the patient.
Postoperative follow-up of the renal function tests and electrolytes () revealed normalization over a period of two days postoperatively with the patient restored intake of ACE-I on day one postoperatively with no effect on potassium level.
At the end of surgery, the estimated blood loss was about 635 ml, UOP was 700 ml (over an operative time of 4 hours), and the infused fluids included 450 ml of Hartman's solution (over the first 2 hours), 950 ml of 0.9% normal saline, and 500 ml of Gelofusine 4% (over the second 2 hours) in addition to 1 litre of glucose 10% with insulin. No blood transfusion was required and no MAP <70 mmHg was recorded.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [59, 'years'], 'weight': [89.0, 'kg'], 'Sodium': [140.0, 'mmol/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 59 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 89.0 kg. The concentration of sodium is 140.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 89.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
6151,38,Free Water Deficit,lab test,decimal,pmc-5440537-1,Extracted,"An 18-year-old girl was referred to our department of pediatric nephrology due to elevated serum creatinine level. She was born premature and dysmature (gestational age 31 weeks + 5 days, birth weight 1210 g) to consanguineous parents. She had a good start but a very low blood glucose level directly after birth (0.2 mmol/L); this was corrected with an intravenous glucose infusion, and there was no further hypoglycemia in the neonatal period. She had mild bilateral eyelid ptosis from birth. Psychomotor development was normal. During childhood, she had a history of recurrent airway infections and bronchitis, mild failure to thrive, and mild anemia for which she visited a general pediatrician regularly. At age 4 years, routine serum creatinine measurements were 58 μmol/L, with an estimated glomerular filtration rate (eGFR) of 60 ml/min/1.73 m2. The lower than expected eGFR escaped the attention of the local pediatrician, and it was only at age 15 years, during routine testing, that a mildly elevated serum creatinine was noted for the first time (106 μmol/L, eGFR 53 ml/min/1.73 m2). At age 18 years, the serum creatinine level had increased to 139 μmol/L (eGFR 48 ml/min/1.73 m2), and she was referred to our university hospital for further examination. At that time, she reported exercise intolerance and lightheadedness on rising in the morning. Physical examination showed a height of 1.56 m (−2 standard deviations [SD]), a weight of 60 kg (+1SD), and a supine blood pressure of 106/55 mmHg; results were normal for heart, lungs, and abdomen examination, and, with the exception of the eyelid ptosis, for the neurological examination. Her symptoms and signs, especially the exercise intolerance and eyelid ptosis, raised the suspicion of a mitochondrial disorder. Laboratory investigations showed normal values for serum lactate and electrolytes (Na+ 140 mmol/L, K+ 4.4 mmol/L, Ca2+ 2.2 mmol/L, Mg2+ 0.75 mmol/L, P3− 1.33 mmol/L). There was no proteinuria nor hematuria. Kidney size and structure were normal on the renal ultrasound images. In order to obtain a diagnosis, we performed a renal biopsy. Light microscopic examination revealed a few vascular sclerosed glomeruli with only discrete interstitial fibrosis. Electron microscopic examination revealed notable abnormal, fused mitochondria in the proximal tubules but not in the distal tubules (Fig. ). This prompted the performance of a muscle biopsy for further evaluation of a mitochondrial defect. However, muscle histology was normal, and extensive biochemical testing of the respiratory chain also did not show any evidence of a mitochondrial disorder []. Mutation analysis of mitochondrial DNA was performed in leucocytes and muscle tissue, but did not show any abnormalities. At that time, current techniques, such as whole exome sequencing, were not yet available, and so the patient was managed further by our department without a classifying diagnosis. At age 19 years, she fainted while her height was being measured during a routine visit to the outpatient clinic. She reported that she was increasingly suffering from dizziness, especially in the morning. Orthostatic blood pressure measurements were performed, showing severe orthostatic hypotension with preserved heart rate increase. Her blood pressure decreased from supine values of 116/76 mmHg (heart rate 54 bpm) to 56/30 mmHg (heart rate 84 bpm) after standing for 3 min. Upon asking, she reported that sweating was normal.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [18, 'years'], 'weight': [60.0, 'kg'], 'Sodium': [140.0, 'mEq/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 18 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 60.0 kg. The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 60.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
6152,38,Free Water Deficit,lab test,decimal,pmc-8635746-1,Extracted,"A 2-day-old male neonate was referred to our neonatal intensive care unit (NICU) due to anuria for more than 48 h. He was born by cesarean section at 35 weeks of gestation at a regional hospital and weighed 1,675 g at birth. Antenatally, his mother had developed oligohydramnios; this was related to the premature rupture of membranes during the second trimester. At birth, the patient suffered from meconium aspiration, cyanosis, and bradycardia. Following resuscitation, his heart rate improved; Apgar scores were 5 and 7 at 1 and 5 min, respectively. A septic workup was performed, and the patient was administered antibiotics (vancomycin and ceftazidime) prior to referral based on their antibiotic policy. The patient was then referred to our hospital for further management.
On arrival, his vital signs were stable. However, fluid overload was noted (body weight: 1,892 g; 13% fluid overload). General edema was noted without skin rash. Laboratory analysis showed no evidence of leukocytosis (13,400/cumm), left shifting (Band: 1%, Seg: 77%), or eosinophilia (1%). Biochemical evaluations revealed elevated levels of creatinine (4.81 mg/dl) and blood urea nitrogen (28 mg/dl), hyponatremia (114 mmol/L), and non-anion gap metabolic acidosis (HCO3: 17.2 mmol/L). Renal ultrasound revealed increased renal echogenicity bilaterally without structural abnormality of the kidneys and bladder. We suspected acute tubular necrosis.
Intravenous furosemide was provided for diuresis, although the response was poor. Due to the overload of refractory fluid, we decided to commence continuous venovenous hemofiltration (CVVH) therapy. One 7-Fr dual lumen central venous catheter (CVC) (ARROW® Teleflex, Wayne, PA, USA) was placed in his umbilical vein under ultrasound guidance to provide vascular access; radiography was used to confirm the position of the catheter's tip. Heparin solution (10 U/ml) was locked in CVC before initiation of CKRT. Before the catheter was connected to the machine, the dialysis circuit was rinsed with heparin and primed with packed red blood cells (hematocrit: 70–80%) to combat low body weight. No more heparin was given because his activated clotting time (ACT) was 180–230 s initially. Blood flow was initially set to 12 ml/min (6.6 ml/kg/min). The filtration fraction was 0.1–0.2, and ultrafiltration was initially 50 ml/h (26 ml/kg/h). In total, 50% of the replacement fluid was given as predilution; the remainder was given as postdilution. The net ultrafiltration rate was set based on the infusion fluid to remove fluid gently. Due to the patient's coagulopathy, no anticoagulant was given initially.
Initially, the 7-Fr CVC provided an appropriate circuit life span of 49.5 h but varied from 0.5 to 12 h in subsequent courses. Therefore, when guiding the wire, we changed the vascular access to a larger 8-Fr Hemocath (MedCOMP® Medical Components, Inc., Harleysville, PA, USA) that was placed in the umbilical vein (). A permanent PD tube was also inserted preemptively by a pediatric surgeon since it was not possible to predict the recovery of renal function. CKRT was continued as a bridging therapy. We increased the blood flow to 20 ml/min (10 ml/kg/min) thereafter, and the circuit life span ranged from 12 to 71.9 h.
Urinary output and laboratory data improved after CVVH. Therefore, we stopped dialysis. The infant was subsequently discharged, and the PD tube was removed.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [2, 'days'], 'weight': [1892.0, 'g'], 'Sodium': [114.0, 'mmol/L']}",-0.21082,-0.20028,-0.22136,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 2 days old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 1892.0 g so this converts to 1892.0 lbs * kg/1000 g = 1.892 kg. The concentration of sodium is 114.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 1.892 * (114.0/140 - 1) = -0.21082 L. The patient's free body water deficit is -0.21082 L."
6153,38,Free Water Deficit,lab test,decimal,pmc-2733967-2,Extracted,"A 26-day-old girl was referred for evaluation of renal failure. She was born at 38+5 weeks' gestational age with a birth weight of 3,200 g. She was well until two days before admission when she developed generalized tonic clonic seizure. At a local clinic, hypocalcemia, hyperkalemia and azotemia were detected and she was referred to us. On admission, generalized edema was noted. Her external genitalia were normal female. Laboratory findings showed: hemoglobin, 9.8 g/dL; cholesterol, 120 mg/dL; total serum protein, 3.7 g/dL; serum albumin, 1.5 g/dL; BUN, 75 mg/dL; serum creatinine, 4.1 mg/dL; total calcium, 5.9 mg/dL; phosphorus, 12.7 mg/dL; sodium, 136 mEq/L; potassium, 5.5 mEq/L; chloride, 113 mEq/L; tCO2 7.8 mEq/L. Albuminuria and hematuria were detected. An ultrasonogram revealed enlarged kidneys with increased parenchymal echogenicity and poor corticomedullary differentiation. A renal biopsy was performed at the age of 29 days and light microscopy showed small glomeruli with various degrees of mesangial sclerosis (). The tubules were dilated with regenerative activity. Her karyotype was 46 XX. Analysis of the sequence of WT1 exon 9 revealed the presence of a heterozygous G to T base substitution, converting 396Asp to 396Tyr, and a heterozygous 395 Ser (TCC) > Ser (TCA) polymorphism (). Both parents showed normal sequence at these sites. Peritoneal dialysis was commenced with a temporary shift to hemodiafiltration because of dialysate leakage at the exit site. Sustained hypertension (120/80 mmHg) responded to an angiotensin-converting enzyme inhibitor. She was maintained on total parenteral nutrition due to uncontrolled chylothorax that resulted from internal jugular vein catheterization, and the patient died at the age of six months due to multiple serious infections and failure to thrive. Autopsy was not performed.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [136.0, 'mEq/L'], 'sex': 'Female', 'weight': [3.2, 'kg'], 'age': [26, 'days']}",-0.05486,-0.05212,-0.0576,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 26 days old. This means the patient is 0 years old.
The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 3.2 kg. The concentration of sodium is 136.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.0 mEq. To convert from 136.0 mEq to mmol, convert from mEq to mmol. The compound 136.0 has a valence of 1, and so divide the valence by the value of mEq to get, 136.0 mEq/(1 mEq/mmol) = 136.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mEq sodium/L converts to 136.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 3.2 * (136.0/140 - 1) = -0.05486 L. The patient's free body water deficit is -0.05486 L."
6154,38,Free Water Deficit,lab test,decimal,pmc-8705311-1,Extracted,"An 18-year-old adolescent female was evaluated at 15 weeks’ gestation for history of persistent emesis for four weeks, extreme fatigue and red colored urine for one day. There was no history of fever, diarrhea, abdominal pain, or urinary tract infection.
Past medical history was unremarkable for diabetes mellitus, rheumatoid arthritis, or other autoimmune diseases. She was not known to have hyperthyroidism in the past. Pregnancy had been uneventful except for persistent episodes of emesis for past one month. There was no prior history of mood symptoms or altered mental status. There was no history of heat intolerance, diarrhea, or weight loss. There was no recent history of usage of corticosteroid, loop or thiazide diuretic, strenuous exercise, vaginal bleeding, vaginal discharge of grape-like vesicles, seizures, alcohol intake, and carbohydrate load. Family history was notable only for type 2 diabetes in the father. There was no known family history of autoimmune diseases, thyroid disorders, hypokalemia, and periodic paralysis. There was no consanguinity.
Vital signs upon presentation showed blood pressure (BP) 142/87 mm Hg, pulse 120 beats per minute, oral temperature 38.9 °C (102.02 °F), respiratory rate 18 per minute, and oxygen saturation of 97%. Her height was 172.7 cm and weight was 109 kg (240 lb 4.8 oz). Physical examination was remarkable for an overweight female who was awake but slow to respond. There was no goiter and ophthalmopathy. There was mild scleral icterus. There was no tremor or pretibial edema.
Serum beta-human chorionic gonadotropin (hCG) level was 246,000 mIU/mL and sonogram confirmed the presence of a single viable intrauterine fetus of approximately 15 weeks gestation with expected uterine size. Renal function test showed sodium 127 mmol/L, potassium 2.5 mmol/L, bicarbonate 33 mmol/L, blood urea nitrogen (BUN) 123 mg/dL, serum creatinine 4.2 mg/dL (MDRD estimated glomerular filtration rate (eGFR) 17 mL/min/1.73 m2), calcium 9.5 mg/dL, phosphorus 2.7 mg/dL and magnesium of 1 mg/dL. Liver function test showed aspartate aminotransferase 140 IU/L, alanine aminotransferase 203 IU/L, total bilirubin 2.9 mg/dL, ammonia 55 µmol/L, and serum albumin 3.1 gm/dl. Renal function test two months prior to pregnancy showed normal serum creatinine of 0.8 mg/dL (MDRD eGFR 113 mL/min/1.73 m2) and normal electrolytes (serum sodium 138 mmol/L, potassium 3.9 mmol/L, bicarbonate 24 mmol/L, calcium 9.4 mg/dL, phosphorus 3.9 mg/dL, and magnesium was not available) Serum creatine kinase was normal at 121 U/L (normal 0–180 U/L). Urine sodium was <10 mmol/L, urine creatinine 84 mg/dL, urine potassium 28 mmol/L and urine osmolality was 344 mOsm/kg. Fractional excretion of sodium was 0.4%. Urinalysis showed 1+ proteinuria, no microscopic hematuria, 5 white cells per high power field, no ketonuria, pH 5, specific gravity of 1.015, and negative nitrites and leukocytes. Plasma renin activity was 14 ng/mL/h (normal 0.5–4 ng/mL/h, upright) and serum aldosterone was 13 ng/dL (normal 4–31 ng/dL, upright). Blood and urine cultures were negative. Other extensive investigations for infectious etiologies were also negative. Urine for Chlamydia and Neisseria was negative. SARS-CoV-2 DNA PCR from the nasopharyngeal swab was negative. Other labs were notable for undetectable thyroid stimulating hormone (TSH) level < 0.030 mIU/L (reference 0.4–5 mIU/L), total T3 238 ng/dL (reference 87–178 ng/dL), and free T4 > 6.99 ng/dL (reference 0.6–1.2 ng/dL). Computed tomography of the head showed no acute intracranial abnormalities.
Initial management included administration of intravenous fluids (IVF), propranolol, potassium iodide, propylthiouracil (PTU), and hydrocortisone. A presumptive diagnosis of hyperemesis gravidarum with thyroid storm and AKI secondary to persistent emesis was made. She met criteria for thyroid storm due to elevated serum free T4 and total T3 with undetected TSH, along with pyrexia, tachycardia, icterus, and altered mental status. Her clinical condition improved somewhat after receiving PTU, propranolol, and hydrocortisone as heart rate, blood pressure, and free T4 began to decrease. Her mental status improved and she became more alert and engaged in conversation. Given tachycardia and hypertension, she was started on propranolol 60 mg every 4 hours which was later converted to 160 mg daily.
Other thyroid studies showed thyroid peroxidase antibody 0.3 IU/mL (reference < 9 IU/mL), TSH receptor antibody (TRAb) < 0.90 (reference < 1.75 IU/L), and undetected thyroid stimulating immunoglobulin (TSI) of < 0.10 (reference ≤ 0.54 IU/L). Given negative TRAb, Graves’ disease was highly unlikely. Serum free T4 normalized in ten days, TSH in two weeks and total T3 in five days. Given pregnancy, further modalities including radioactive iodine uptake study were not pursued, given risk of fetal hypothyroidism, mental retardation, and increased risk of malignancy. Partial molar pregnancy was initially considered due to presentation of thyroid storm, however, the beta-hCG level was trending down and the patient did not show any signs of pre-eclampsia. Thyroid sonogram showed normal sized thyroid with homogenous thyroid texture and without increased vascularity, making Grave’s disease unlikely. Investigations for AKI included renal sonogram which showed right kidney measuring 12.8 cm in length and left kidney measuring 12.6 cm in length with bilateral normal cortical echogenicity without evidence of hydronephrosis or nephrocalcinosis. Hepatic sonogram showed gallbladder sludge. A chest X-ray was normal without pulmonary edema or cardiomegaly. Electrocardiogram showed normal Q-T interval. Echocardiogram was normal with ejection fraction of 65%. Cardiac enzymes were normal.
PTU was later changed to methimazole as she was no longer in the first trimester of pregnancy and as she demonstrated signs of liver insufficiency. Anti-emetics and IVF were discontinued after few days as the patient was able to tolerate well by mouth. Hydrocortisone was discontinued after two days. Subsequently, propranolol was discontinued along with methimazole, as the beta-hCG mediated hyperemesis was thought to be the likely etiology of thyroid symptoms. Her vital signs, including BPs, remained stable and her thyroid levels returned to normal without anti-thyroid drugs. Serum beta-hCG at discharge was 175,557 mIU/mL. Given decreasing level of hCG without other signs or symptoms of gestational trophoblastic disease, molar pregnancy was unlikely. She was discharged without any thyroid medications.
During the hospitalization, her serum potassium remained around 2.4–2.9 meq/L along with serum bicarbonate 30–38 meq/L despite resolution of emesis. Serum magnesium remained low, as well as with values ranging from 1–1.4 mg/dL. Twenty-four hour urine collection showed a urine calcium of 0.04 mg/kg/day. Random urine calcium to creatinine ratio was also low at 0.005. She required multiple intravenous potassium and magnesium supplements. Discharge serum potassium and magnesium was 3.5 meq/L and 1.2 mg/dL, respectively. She was discharged on magnesium oxide 400 mg daily and potassium chloride 10 meq twice daily. BUN and serum creatinine slowly improved with intravenous hydration. Kidney biopsy was not performed and renal replacement therapy was not required. Discharge BUN and serum creatinine was 15 mg/dL and 0.97 mg/dL (MDRD eGFR 90 mL/min/1.73 m2), respectively. Due to the persistent hypokalemia, alkalosis, hypomagnesemia and hypocalciuria despite resolution of emesis, a genetic testing by next generation sequence analysis was done which showed that the patient was homozygous in the SLCA123 (NM_001126108.2) gene for a known sequence variant designated c.2581C>T (p.Arg861Cys) (Prevention Genetics, Marshfield, WI, USA). No further in vitro functional studies were performed, hence the exact functional implication of this variant was unknown. However, to determine the pathogenicity of this variant, in silico tests were performed using SIFT, PolyPhen-2, FATHMM and MutationTaster. The resulting prediction utilizing these in silico tools was “Pathogenic”. At 37 weeks gestation, a healthy infant of 3.5 kilograms was born vaginally without any perinatal complications. The serum creatinine remained stable at 0.7 mg/dL after delivery (MDRD eGFR 132 mL/min/1.73 m2).",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [18, 'years'], 'weight': [109.0, 'kg'], 'Sodium': [127.0, 'mmol/L']}",-5.06071,-4.80767,-5.31375,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 18 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 109.0 kg. The concentration of sodium is 127.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 109.0 * (127.0/140 - 1) = -5.06071 L. The patient's free body water deficit is -5.06071 L."
6155,38,Free Water Deficit,lab test,decimal,pmc-4241302-1,Extracted,"A 73-year-old woman was admitted to our hospital because of severe headache, anorexia, malaise, weight loss, and vomiting. She had progressive headache and lost weight by 6 kg during about a half year. One month prior to admission, she began to have frequent vomiting. Her past history was noncontributory, and her family history showed hepatocellular carcinoma in mother and stomach cancer in siblings. She did not smoke and drank little alcohol.
She was 160 cm tall and weighed 59.5 kg, body temperature 36.8°C. Her blood pressure was 108/65 mmHg with a regular sinus rhythm of 115 bpm. Physical examinations of the chest, abdomen, and extremities were normal. Neither axillar or pubic hair loss nor abnormal skin pigmentation was noted. Ophthalmologic examination revealed left temporal hemianopia and optic nerve atrophy and right incomplete hemianopia.
Laboratory data showed slightly high serum sodium (149 mEq/L) and high plasma osmolality (296 mOsm/L). Liver and renal functions were normal. Endocrine data () showed very low levels of both ACTH and cortisol consistent with secondary adrenal insufficiency. The suppressed TSH level in the presence of elevated free T3 and free T4 levels is consistent with primary hyperthyroidism. Other pituitary hormones included low GH level and normal IGF-1 level for her age, elevated PRL level, low gonadotropin levels, and relatively low arginine vasopressin (AVP) level for high plasma osmolality. Anti-thyroid peroxidase antibody, TSH receptor antibody, and thyroid-stimulating antibody were all negative except positive anti-thyroglobulin antibody. 123I-Thyroid scintigraphy showed a markedly reduced uptake rate (0.24%). These thyroid function data are compatible with the diagnosis of thyrotoxicosis due to silent thyroiditis.
The dynamic endocrine stimulation tests with CRH, LH-RH, and GRH performed just after admission except TRH test which was performed after improvement of thyrotoxicosis are shown in : a normal response of ACTH and delayed response of cortisol after CRH, low responses of TSH and PRL after TRH, a low response of LH and a delayed response of FSH after LH-RH, and a low response of GH after GRH. Insulin tolerance test (0.1 U/kg) showed normal responses of both ACTH and cortisol and a low response of GH (). Rapid ACTH test () showed a low response of cortisol consistent with secondary adrenal insufficiency. These data are compatible with the diagnosis of hypopituitarism due to the impairment at pituitary and/or hypothalamic level.
MRI of the brain revealed a large cystic pituitary mass (18 × 12 × 12 mm) extending suprasellarly to the optic chiasm (); high intensity signal on T1 weighted-images and the rim effect enhanced by gadolinium contrast are suggestive of RCC.
Based on the diagnosis of central adrenal insufficiency, she was treated with glucocorticoid replacement (hydrocortisone: 10 mg), which markedly increased urine volume (5000–6000 mL/day) associated with high serum osmolality (301 mOsm/L), low urine osmolality (91 mOsm/L), and low AVP level (0.95 pg/mL). Thus, development of overt diabetes insipidus following glucocorticoid replacement is compatible with the diagnosis of “masked” diabetes insipidus. Nasal administration of DDAVP (15 μg) dramatically decreased urine volume (1500–2000 mL/day). Furthermore, because her thyrotoxicosis became hypothyroidism (TSH: 2.13 μIU/mL, free T3: 1.1 pg/mL, free T4: 0.47 ng/dL) during the natural course, she was treated with thyroid hormone (levothyroxine: 25 μg). After replacement with levothyroxine, most of her nonspecific symptoms, such as poor appetite, malaise, weight loss, and vomiting, gradually improved, but her headache persisted.
She underwent transsphenoidal surgery with complete cyst evacuation and partial wall excision; RCC was confirmed histopathologically. Postoperatively, her headache resolved, but bitemporal hemianopia persisted. Postoperative endocrine data () showed elevated levels of ACTH, cortisol, TSH, and AVP but low levels of thyroid hormones and gonadotropin and normal PRL level. Postoperative dynamic endocrine stimulation tests () showed normal responses of ACTH and cortisol after CRH, a delayed response of TSH and a low response of PRL after TRH, delayed responses of LH and FSH after LH-RH, and a normal response of GH after GRH. Postoperative rapid ACTH test () showed a normal response of cortisol after ACTH stimulation. Based on the postoperative endocrine data, replacements with glucocorticoid and desmopressin were stopped, while thyroid hormone was continued.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [149.0, 'mEq/L'], 'sex': 'Female', 'weight': [59.5, 'kg'], 'age': [73, 'years']}",1.72125,1.63519,1.80731,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 73 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 59.5 kg. The concentration of sodium is 149.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 149.0 mEq. To convert from 149.0 mEq to mmol, convert from mEq to mmol. The compound 149.0 has a valence of 1, and so divide the valence by the value of mEq to get, 149.0 mEq/(1 mEq/mmol) = 149.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 149.0 mEq sodium/L converts to 149.0 mmol sodium/L. Plugging in these values into the equation, we get 0.45 * 59.5 * (149.0/140 - 1) = 1.72125 L. The patient's free body water deficit is 1.72125 L."
6156,38,Free Water Deficit,lab test,decimal,pmc-4049549-1,Extracted,"A 21-year-old woman with TS was admitted because of auditory hallucinations and altered behavior for last 2 months. At the age of 13 years, she was first diagnosed with TS, mosaic karyotype 45,X/46,XX, combined by central obesity, hyperlipidemia, and type 2 diabetes mellitus. Also, she had been diagnosed concomitant with idiopathic central diabetes insipidus presenting polyuria (4 L/day) and polydipsia (4-5 L/day) for 1 year. A water deprivation test showed central diabetes insipidus, and the initial finding of sellar magnetic resonance imaging (MRI) showed a thickening of the pituitary stalk with normal high signal intensity in the posterior pituitary gland. She had been managed with metformin, estrogen, and oral 1-deamino-8-D-arginine vasopressin, to which she had maintained well with about 2 L of daily urine volume. Follow-up MRI imaging had taken 2 years later demonstrated a nearly normal pituitary stalk thickness.
At the age of 14 years, she had been treated with additional drug, levothyroxine due to Hashimoto's thyroiditis induced primary hypothyroidism. At the age of 18 years, her intelligence quotient (IQ) score was 52, suggestive of mild mental retardation, while her social quotient was at a level of 8 years. After graduated high school, she entered a vocational school for mentally disabled people. In school, she volunteered for a class senator, attended school punctually at any situation. She actively talked in school, so she earned the nickname 'radio'. She was active and honest daughter who lives with parents and younger brother. There was no history of alcohol or drug abuse. None of family members had psychiatric illness or mental retardation.
Before 2 months prior to admission, she suddenly avoided to talk and go to school and redundantly wanted to sleep without social interaction. She developed excessive daytime sleepiness and bizarre behavior with auditory hallucination 2 weeks ago. After taking oral medication prescribed by a psychiatric clinic, her symptoms including insomnia, visual and auditory hallucination were exacerbated. On mental status examination at admission, she showed poverty of speech, dysarthria, anxious mood, auditory hallucination, visual hallucination, persecutory delusion, social withdrawal, soliloquy, avolition, and aggressive behavior. Her orientation was intact for time, place, and person.
At admission to our hospital, the patient's height was 145 cm (percentile<3th) and her weight was 51.5 kg (25th<percentile <50th). Her body mass index was 24.5 kg/m2. She had a blood pressure of 123/82 mmHg, pulse of 103 beats per minute, respiration rate of 18 breaths per minute, and a temperature of 36.8℃. On physical examination, typical somatic features including dysmorphic face, webbed neck, low hairline, broad chest, and cubitus valgus were observed. Neurological examinations were normal. Laboratory findings revealed serum glucose, 107 mg/dL (normal, 70-100 mg/dL); glycosylated hemoglobin, 6.8% (normal, 4.0%-6.0%); normal free T4 level, 1.96 ng/dL (normal, 0.80-1.90 ng/dL); and thyroid-stimulating hormone, 0.80 mIU/L (normal : 0.17-5.65 mIU/L); sodium, 133 mEq/L (normal, 133-145 mEq/L); potassium, 3.8 mEq/L (normal, 3.5-5.5 mEq/L); chloride 96, mEq/L (normal, 95-110 mEq/L); serum osmolarity, 280 mOsm/kg (normal, 288-302 mOsm/kg); urine osmolarity, 464 mOsm/kg (normal, 300-900 mOsm/kg). The last follow-up MRI showed no significant interval change of pituitary stalk thickening compared to previous MRI finding and no abnormal pituitary mass or brain parenchymal abnormality. After diagnosed as having psychotic disorder, she was started on oral ziprasidone, which was gradually increased. She showed significant improvement after 1 month, but her symptoms were waxing and waning without full remission. She is under regular follow-up for the last 10 months.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [21, 'years'], 'weight': [51.5, 'kg'], 'Sodium': [133.0, 'mEq/L']}",-1.2875,-1.22313,-1.35188,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 21 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 51.5 kg. The concentration of sodium is 133.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 133.0 mEq. To convert from 133.0 mEq to mmol, convert from mEq to mmol. The compound 133.0 has a valence of 1, and so divide the valence by the value of mEq to get, 133.0 mEq/(1 mEq/mmol) = 133.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mEq sodium/L converts to 133.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 51.5 * (133.0/140 - 1) = -1.2875 L. The patient's free body water deficit is -1.2875 L."
6157,38,Free Water Deficit,lab test,decimal,pmc-5815706-1,Extracted,"A 69-year-old patient (G6 P6) (height, 155 cm; weight, 66 kg) reported vaginal prolapse for several years and incontinence, abdominal pain and hematuria. Comorbidities: type 2 diabetes for 20 years, circulatory failure, paroxysmal atrial fibrillation, anaemia, urinary tract infection, hypertension, chronic biliary gastritis, cervical osteoarthritis.
Physical examination on admission revealed anterior vaginal and uterine walls prolapse, with 8 cm in diameter large ulcerated lesion (Fig. ) located on the anterior vaginal wall. Diagnostic biopsy of the lesion revealed squamous cell carcinoma (Fig. ).
Additional tests: hemoglobin 11.0 g/dL (12.0–16.0); hematocrit 33.9% (37.0–47.0); erythrocytes 4.34 × 106/uL (4.00–5.00); MCV 78.1 fL (80–94); MCH 25.3 pg (27.0–31.0); MCHC 32.4 g/dL 931.0–37.0); RDW-SD 48.3 fL (36.4–46.3); RDW-CV 17.7% (11.7–14.4); Blood Plate 296 × 103/Ul (140–400); plate distribution width (PDW) 11.6 fL (9.80–16.20); MPV 9.8 fL (9.40–12.50); platelet large cell ratio (P-LCR) 24.1% (19.10–46.60); WBC 8.12 × 103/ul (4.0–10.0); Macro R 6.7%; Micro R 7.9%; total protein 7.1 g/dL (range 6.3–8.2); chlorides 112.0 mmol/L (98.0–107.0); activated partial thromboplastin time (APTT) 29.0 s (25.9–36.6); prothrombin time 9.2 s (7.6–11.4); Prothrombin index 103.7% (80.0–120.0); INR 1.0 (0.9–1.3); D-dimer 2 208.8 ng/mL (<500.0); fibrinogen 503.9 mg/dL (180.0–400.0); glomerular filtration rate (GFR) 27 mL/min/1.73 m2 (>60.0); glucose 115 mg/dL (70–99); creatinine 1.85 mg/dL (0.52–1.04); urea 66 mg/dL (15–43); potassium 4.9 mmol/L (3.5–5.1); sodium 144.0 mmol/L (137.0–145.0); TSH 0.50 uIU/mL (0.27–4.20).
Sagittal pelvic CT showed protruded vagina, infiltrated bladder wall, uterus, and rectum. In frontal CT scan of abdomen, enlarged pelvic iliac nodes, hydronephrosis of the left kidney with left hydroureter, in the right kidney nephrostomic catheter were observed (Fig. ).
Cystoscopy-mucosal lesions were found in the bladder (Fig. ). The diagnostic biopsies were collected from the urethra and the bladder (Fig. ).
Symptomatic treatment included: InsulinueGensulin R t.i.d. (2–6 units)sc, Amlodypinum 2 × 10 mg, 0.9%NaCl 2 × 500 ml iv., Clexan (Enoxaparinumnatricum) 2 × 0.6 sc, Ramiprilum 5 mg 1 × 1, Captoprilum 25 mg 1 × 1.
The patient was disqualified from surgery due to the severity of the disease, lymph node metastases, and coexisting comorbidities. Only palliative nephrostomy was performed.
The patient signed informed consents. In our case the patient accepted regular and proved diagnosis and therapy in Clinical Department of Urology, so the ethical approval was not necessary.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [69, 'years'], 'weight': [66.0, 'kg'], 'Sodium': [144.0, 'mmol/L']}",0.84857,0.80614,0.891,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 69 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 66.0 kg. The concentration of sodium is 144.0 mmol/L. Plugging in these values into the equation, we get 0.45 * 66.0 * (144.0/140 - 1) = 0.84857 L. The patient's free body water deficit is 0.84857 L."
6158,38,Free Water Deficit,lab test,decimal,pmc-8383643-1,Extracted,"Review of this case and presentation in this format was in accordance with the guidelines of the Institutional Review Board of Nationwide Children’s Hospital (Columbus, OH).
The patient was an 18-year-old, 63.8-kg previously healthy male who presented for posterior spinal fusion (T7 - 12) for correction of AIS. He was first evaluated for AIS 4 months prior to surgery at which point posterior spinal fusion was recommended due to the severity of the curve. He denied systemic signs or symptoms. Magnetic resonance imaging demonstrated severe scoliosis (62°) S-shaped rotary scoliosis with the dextro-scoliotic apex at T7 - 8 and the levo-scoliotic apex at L1 - 2. There was no evidence of intraspinal pathology and no canal or foraminal stenosis.
On the day of the procedure, the patient was held nil per os for 6 h. Preoperative vitals were normal with the patient being afebrile with a normal heart rate and blood pressure (BP) of 132/57 mm Hg. Preoperative laboratory analyses, obtained 2 weeks prior to surgery, were normal (sodium 141 mEq/L, potassium 4.5 mEq/L, blood urea nitrogen 15 mg/dL, and creatinine 0.96 mg/dL). The patient was transported to the operating room and standard American Society of Anesthesiologists’ monitors were placed. After the inhalation of 50% nitrous oxide in oxygen, a peripheral intravenous cannula was placed. Anesthesia was induced with propofol (150 mg), sufentanil (30 µg), lidocaine (60 mg), ketamine (30 mg), and methadone (7.1 mg). Neuromuscular blockade was achieved with rocuronium (40 mg) to facilitate direct laryngoscopy with a Macintosh 3 laryngoscope and endotracheal intubation with an 8.0-mm cuffed endotracheal tube. A radial arterial cannula and a second peripheral intravenous cannula were placed. Maintenance anesthesia included desflurane (titrated to maintain the bispectral index at 50 - 60), sufentanil infusion (0.1 - 0.5 µg/kg/h), lidocaine 30 (µg/kg/min), ketamine (0.25 mg/kg/h), and esmolol 5 - 35 (µg/kg/h). A tranexamic acid infusion (50 mg/kg bolus followed by 5 mg/kg/h) and intraoperative cell saver were used to limit the need for allogeneic blood products. Intravenous fluids were provided using Normosol®. Arterial blood gases, electrolytes, and hemoglobin were analyzed at regular intervals during the course of the procedure using point-of-care testing (POCT). The initial POCT at 8:56 am showed a normal pH 7.37, sodium 140 mEq/L, hemoglobin 12.6 g/dL and potassium of 3.9 mEq/L. The surgical procedure proceeded uneventfully without excessive blood loss (total estimated blood loss for the case was 200 mL) or hemodynamic instability. Report POCT testing performed at 10:24 am was remarkable for an increase of the potassium level to 5.3 mEq/L (). No change in the electrocardiogram (ECG) was noted. Given the unexplained increase in the serum potassium, the minute ventilation was increased by approximately 20% and a repeat serum potassium was obtained in 1 h. At 11:22 am, the serum potassium was 5.9 mEq/L. At this point, the esmolol infusion was discontinued, the Normosol® was discontinued and 0.9% normal saline was used for intraoperative fluid replacement. Sodium bicarbonate (50 mEq) was administered to treat a base deficit of -3 and furosemide (10 mg) administered intravenously. The furosemide resulted in an increase in urine output to 100 - 250 mL/h over the next 2 - 3 h. Due to the concern for an occult myopathy and rhabdomyolysis, the inhalational anesthetic agent was discontinued and total intravenous anesthesia with a propofol infusion (75 - 100 µg/kg/min) titrated to maintain the bispectral index at 50 - 60 []. Throughout this time, no change in the ECG was noted. Pharmacy was contacted to verify there had been no inadvertent use of concentrated potassium solutions to mix the intraoperative infusions. No high potassium concentration solutions are available in the operating room pharmacy. Dissection of the paraspinal muscles and exposure of the spine was completed at 10:45 am. POCT at 11:46 am showed that the potassium had decreased to 5.7 mEq/L, and then to 4.7 mEq/L at 1:09 pm. At the conclusion of the surgical procedure, the patient’s trachea was extubated, and he was transferred to the post-anesthesia care unit. On postoperative day 1, the serum potassium was 3.6 mEq/L. Creatinine phosphokinase was mildly elevated at 848 U/L (range of 36 - 289 U/L), which was attributed to the surgical dissection. The remainder of his postoperative course was uneventful.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [18, 'years'], 'weight': [63.8, 'kg'], 'Sodium': [140.0, 'mEq/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 18 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 63.8 kg. The concentration of sodium is 140.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 140.0 mEq. To convert from 140.0 mEq to mmol, convert from mEq to mmol. The compound 140.0 has a valence of 1, and so divide the valence by the value of mEq to get, 140.0 mEq/(1 mEq/mmol) = 140.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mEq sodium/L converts to 140.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 63.8 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
6159,38,Free Water Deficit,lab test,decimal,pmc-4851541-1,Extracted,"A 6-year-old boy was admitted to our department due to vomiting, weakness, polyuria, polydipsia, irritability and weight loss in the last few weeks. The patient is the third child of the fourth pregnancy, one of which ended up with abortion. He was born at term, through Cesarean section, weighting 3400 g. Down syndrome was suspected clinically at birth and confirmed by karyotyping (47XX, t21).
The body weight on admission was 14.5 kg and the body height was 93 cm (20th and 5th percentile for sex and age in Down syndrome, respectively) ().
Typical features of Down syndrome were present, including typical facies and generalized hypotonia. A 3/6 heart murmur was heard on auscultation, and transthoracic echocardiography revealed a low grade aortic regurgitation. The rest of his physical examination was unremarkable.
Laboratory studies revealed red blood cell count 2.14 × 1012/l, Hb 6.1 gr/dL, Htc 17.5%, platelet count 272000/mm3, white blood cell count 7800/mm3, ESR 60 mm/h, CRP 26 mg/l, urea 12.7 mmol/1, creatinine 160 umol/1, Na 136 mEq/L, K 2.7 mEq/L, Cl 108 mEq/L, Ca 9.8 mg/dL, ionised Ca 1.28 mmol/1, Mg 1.0 mmol/1, total serum proteins 59.6 g/l, albumins 32.3 g/l, fasting blood glucose 5.6 mmol/l, cholesterol 6,1 mmol/l, triglycerides 2.3 mmol/l and alkaline phosphatase 49 U/l. Results of the capillary blood gas analysis were as follows: pH 7.25, PCO2 26 mmHg, HCO3 14 mEq/L and serum anion gap 14 mEq/L.
Routine urine analysis showed mild proteinuria (+) and negative glucose. Urine microscopy showed 15 erythrocytes/hpf, 20 leucocytes/hpf and 20-30 bacteria/hpf; specific gravity was 1.005, and urinary pH was 7.0. Urine culture resulted positive for E. Coli.
Urinary uric acid was low at 774.0 umol/24h (normal values 1480-4430 umol/24h) as was citrate 21 mg/24h (normal value >115mg/24h). The urine calcium to creatinine ratio was 1.2 mmol/mmol (normal value < 1.1 mmol/mmol). In the view of normal anion gap hyperchloremic metabolic acidosis, alkaline urine and hypokalemia the diagnosis of dTRA was made.
Additional analysis searching for etiology of dTRA revealed serum 1,25-dihydroxyvitamin D 1.2 ng/ml (normal values 10.8-54 ng/ml), parathyroid hormone 27.2 pg/ml (normal values 6.5-36.8 pg/ml), free serum T4 2.20 pmol/l (normal values 10.3-25.8 pmol/l) and thyroid-stimulating hormone >1000.0 mU/l (normal values 0.54-4.21 mU/l). Prolactin was 163.9 ng/mL (normal values 3.2-20 ng/mL), while other hormonal profiles such as adrenocorticotropic hormone, luteinizing hormone, follicle-stimulating hormone and growth hormone were normal. Anti-thyroid peroxidase (TPO) antibody was >1000.0 IU/ml (normal value <50 IU/ml) and Thyroglobulin (hTg) was 3.41 ng/ml (normal values 0.2-70.0 ng/ml). Hence, Hashimoto thyroiditis as a possible cause was postulated. Moreover, antinuclear antibodies (ANA) test resulted negative.
The renal ultrasound showed hyper-echoic regions in the renal medulla consistent with bilateral nephrocalcinosis grade I (), also confirmed by abdominal CT (). Brain magnetic resonance imaging revealed pituitary enlargement ().
Treatment and follow up
Intravenous rehydration was started. The bicarbonate deficit was calculated, and KCl was added after the patient had his first urinary void. Blood gas analysis after 12 hours revealed increasing pH, HCO3 and K values. Packed red blood cells were then administered. The patient was put on potassium citrate and thyroid hormone substitution therapy. Also, intravenous antibiotherapy and oral ferrous supplements were started to treat urinary tract infection and anemia, respectively. On follow-up after six months, no evidence of metabolic acidosis and a nearly normal serum potassium level (3.4 mEq/L) were found. Urinary random analysis was normal. Patient’s weight was 16 kg and his height 98 cm (25th and 10th percetile, respectively). His thyroid hormone profile was within normal range. Also, prolactin, cholesterol, triglycerides and complete blood count analysis were normalizing. The patient is on regular follow-up.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [6, 'years'], 'weight': [14.5, 'kg'], 'Sodium': [136.0, 'mEq/L']}",-0.24857,-0.23614,-0.261,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 6 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 14.5 kg. The concentration of sodium is 136.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 136.0 mEq. To convert from 136.0 mEq to mmol, convert from mEq to mmol. The compound 136.0 has a valence of 1, and so divide the valence by the value of mEq to get, 136.0 mEq/(1 mEq/mmol) = 136.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mEq sodium/L converts to 136.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 14.5 * (136.0/140 - 1) = -0.24857 L. The patient's free body water deficit is -0.24857 L."
6160,38,Free Water Deficit,lab test,decimal,usmle-2148,Extracted,"A 3200-g (7.1-lb) female newborn is delivered at 38 weeks' gestation to a 24-year-old woman. The mother had regular prenatal visits throughout the pregnancy. The newborn's blood pressure is 53/35 mm Hg. Examination in the delivery room shows clitoromegaly and posterior labial fusion. One day later, serum studies show:
Na+ 131 mEq/L
K+ 5.4 mEq/L
Cl− 102 mEq/L
Urea nitrogen 15 mg/dL
Creatinine 0.8 mg/dL
Ultrasound of the abdomen and pelvis shows a normal uterus and ovaries.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [131.0, 'mEq/L'], 'sex': 'Female', 'weight': [3200.0, 'g'], 'age': [0, 'years']}",-0.12343,-0.11726,-0.1296,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 0 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 3200.0 g so this converts to 3200.0 lbs * kg/1000 g = 3.2 kg. The concentration of sodium is 131.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 131.0 mEq. To convert from 131.0 mEq to mmol, convert from mEq to mmol. The compound 131.0 has a valence of 1, and so divide the valence by the value of mEq to get, 131.0 mEq/(1 mEq/mmol) = 131.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 131.0 mEq sodium/L converts to 131.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 3.2 * (131.0/140 - 1) = -0.12343 L. The patient's free body water deficit is -0.12343 L."
6161,38,Free Water Deficit,lab test,decimal,pmc-4024691-1,Extracted,"A 58-year-old male patient (weight 70 kg, height 175 cm) with grade III benign hypertrophic hyperplasia was posted for TURP surgery. His general, systemic, and airway examinations were normal and he is a non-smoker. The laboratory investigations were within normal limits except for the ECG which showed left bundle branch block (LBBB). Echocardiography (ECHO) showed LBBB and left ventricular diastolic dysfunction (LVDD) grade I with ejection fraction (EF) = 51%. Stress thallium revealed mild reversible perfusion defect in apical and anteroseptal areas. Pre-operative electrolyte levels were: serum Na+ = 138 mEq/l, K+ = 4.78 mEq/l, and Cl− = 103 mEq/l. His average pre-operative blood pressure was 116/70 mmHg and heart rate was 78 beats/min. Since the patient was asymptomatic with good effort tolerance and no other co-morbidities, spinal anesthesia was administered with 2 ml of hyperbaric bupivaciane (0.5%) with 25 µg fentanyl at L3-4 level. Routine monitoring with ECG (leads II and V), non-invasive blood pressure (NIBP), pulse oximetry, and temperature was done. Inj. Midazolam 0.5 mg was given IV for sedation. T8 level was achieved before the surgery started.
At 120 min of surgery, the surgeon told that there was accidental opening of the prostatic venous sinus and patient started complaining of tightness in the chest with difficulty in breathing. He developed no other neurological or cardiovascular symptoms and his hemodynamic parameters were normal. SPO2 dropped to 86-88% within minutes. Bilateral basal crepts were present on auscultation of chest. We immediately informed the surgeon to terminate the surgery quickly and stopped the irrigation. We increased the fraction of inspired oxygen concentration and the patient was conscious and oriented. The chest examination revealed fine crepts in the basal areas. There was tachycardia, but no other ECG changes, and his BP was maintained. Right radial artery was cannulated for invasive blood pressure monitoring and arterial blood gas (ABG) sample was sent. Right central venous line was inserted. Central venous pressure (CVP) was 15 mmHg. A total of 20 l of 1.5% glycine was used during the procedure. The patient was given 1.5 l of crystalloid. There was no significant blood loss. We monitored blood gases which showed serum Na+ = 95 mEq/l, K+ = 3.56 mEq/l, Cl− = 72 mEq/l, pH = 7.266, PO2= 51.3, PCO2= 46.7, HCO3= 21.8, base excess (BE)= −5.6, and oxygen saturation (SPO2) = 80.1. A diagnosis of TURP syndrome was made.
Furosemide 20 mg IV was given. Rapid correction of hyponatremia was started with 3% hypertonic NaCl at 150 ml/h and the patient was shifted to postoperative ICU for further monitoring and optimization.
Serum electrolytes improved to Na+ = 104 mEq/l, K+ = 3.69 mEq/l, Cl− = 80 mEq/l, pH = 7.285, PO2= 54.9, PCO2= 44.7, HCO3= 20.8, BE = −5.8, and SPO2= 88.1. Symptoms of tightness in the chest wall and breathlessness improved.
About 150 ml more of 3% NaCl was infused over 1 h. ABG showed Na+ = 112 mEq/ q/ l, K+ = 3.87 mEq/l, Cl− = 86 mEq/l, pH = 7.311, PO2= 61.7, PC q/ O2= 44.4, HCO3= 21.9, BE = −4.3, and SPO2= 91.3%.
Patient was dehydrated as the urine output was 1.5 l over 2 h. Patient was rapidly infused with 500 ml of 0.9% NaCl. In the postoperative ICU, further infusion of 0.9% NaCl at 100 ml/h was maintained and blood gases were monitored when the serum Na+ reached 118 mEq/l after 6 h and 122 mEq/l after 12 h. The oxygen saturation and electrolytes continued to improve overnight and the serum sodium level increased to 132 mEq/l with potassium level of 3.35 mEq/l by the next evening.
Cardiac troponin levels measured 6 h after the event and on the next day were 0.2 and 0.15 ng/ml, respectively. Postoperative ECG and ECHO findings were similar to those seen in the pre-operative evaluation.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [58, 'years'], 'weight': [70.0, 'kg'], 'Sodium': [132.0, 'mEq/L']}",-2.4,-2.28,-2.52,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 58 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 70.0 kg. The concentration of sodium is 132.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 132.0 mEq. To convert from 132.0 mEq to mmol, convert from mEq to mmol. The compound 132.0 has a valence of 1, and so divide the valence by the value of mEq to get, 132.0 mEq/(1 mEq/mmol) = 132.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 132.0 mEq sodium/L converts to 132.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 70.0 * (132.0/140 - 1) = -2.4 L. The patient's free body water deficit is -2.4 L."
6162,38,Free Water Deficit,lab test,decimal,pmc-6177662-1,Extracted,"A 53-day-old girl was hospitalized owing to diabetic ketoacidosis (DKA) and a generalized tonic-clonic seizure in March 2017. The patient was born at 38 weeks of gestation and demonstrated intrauterine growth retardation. She was delivered via normal spontaneous vaginal delivery and weighed 2,520 g (standard deviation score [SDS], -1.89) at birth. She was the first child and had no siblings. Her family had no history of diabetes. Laboratory results at diagnosis were as follows: blood glucose, 702 mg/dL; pH, 6.979; HCO3-, 4.5 mmHg; base excess, -25.7 mmol/L; total CO2, 5 mmol/L; sodium, 141 mEq/L; corrected sodium, 149 mEq/L; potassium, 6.5 mEq/L; chloride, 105 mEq/L; urine glucose, 3+; urine ketone, 3+; glycated hemoglobin (HbA1c), 7.8%; C-peptide, <0.01 ng/mL; insulin 6.6 μIU/mL; insulin antibody 6.6% (0.0–7.0); glutamic acid decarboxylase II antibody, 0.59 U/mL (0.0–1.0); and islet cell antibody, negative. The patient recovered from DKA, and the continuous insulin treatment was subsequently discontinued. Instead, the patient had an injection of glargine (Lantus) once daily and regular insulin twice daily. Her insulin requirement gradually increased to 0.9 U/kg/day, and the seizure was no longer observed. No abnormal findings were observed on both the electroencephalogram and brain magnetic resonance image. She was hospitalized for a total of 14 days. Direct sequencing of the KCNJ11 and ABCC8 genes using genomic DNA extracted from peripheral lymphocytes was conducted during the hospitalization; her parents were not subjected to genetic testing. Six weeks later, direct sequencing of the KCNJ11 gene, encoding the Kir6.2 subunit of the KATP channel, confirmed the presence of a heterozygous mutation, KCNJ11:c.158G>A (p.G53D) (). ABCC8 mutation was not detected. By then, the patient was 3 months of age, and insulin was administered at 1 U/kg/day. She could lift her head and did not demonstrate signs of developmental delay. We immediately started sulfonylurea (glimepiride) at 0.3 mg/kg/day and gradually tapered the insulin dosage. Five weeks later, insulin was discontinued, and the dosage of glimepiride was adjusted to 0.75 mg/kg/day. The patient is now 11 months of age, and her weight is 9.7 kg (SDS, 0.07). She can sit without help, pull herself to the standing position, and respond well to simple verbal requests. She is also able to pronounce simple words like ""mama."" She maintains excellent blood glucose control without hypoglycemic events, with an HbA1c level of 6.3%. Six months after the initiation of glimepiride therapy, her serum C-peptide level was 2.53 ng/mL, which was higher than the initial level of <0.01 ng/mL. Her current glimepiride dose is 0.6 mg/kg/day. Thus far, no further episodes of seizure have been reported.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [53, 'days'], 'weight': [9.7, 'kg'], 'Sodium': [149.0, 'mEq/L']}",0.37414,0.35543,0.39285,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 53 days old. This means the patient is 0 years old.
The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 9.7 kg. The concentration of sodium is 149.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 149.0 mEq. To convert from 149.0 mEq to mmol, convert from mEq to mmol. The compound 149.0 has a valence of 1, and so divide the valence by the value of mEq to get, 149.0 mEq/(1 mEq/mmol) = 149.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 149.0 mEq sodium/L converts to 149.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 9.7 * (149.0/140 - 1) = 0.37414 L. The patient's free body water deficit is 0.37414 L."
6163,38,Free Water Deficit,lab test,decimal,pmc-8428511-2,Extracted,"An 80-year-old man was referred to the endocrinology clinic for headache, thirst, and polyuria of 4 months duration. He was known to have hypertension, diverticulosis, and vitamin B12 deficiency. He drank at least 5 L of fluids per day. He also lost 6 kg of weight. He had no other systemic or alarming symptoms.
On examination, he had normal visual fields and absence of cranial nerve palsy. He weighed 83.9 kg, and his body mass index was 28.4 kg/m. Clinical examination was unremarkable, with no features suggestive of acromegaly, Cushing's, or any other endocrinopathies.
Results of baseline investigations were as follows: sodium of 147 mEq/L, plasma osmolality of 301 mosm/kg, prolactin of 1062 mU/L, and normal levels of other pituitary hormones.
The water deprivation test showed results consistent with cranial diabetes insipidus. At baseline, his urine osmolality was 65 mosm/kg; after 2 h of water deprivation, it was 319 mosm/kg; and after subcutaneous administration of desmopressin, it increased to 416 mosm/kg. He was started with desmopressin and demonstrated good therapeutic response.
MRI of the pituitary gland showed a 10-mm mixed cystic/soft tissue mass lesion filling the posterior aspect of the pituitary sella, with infiltration of the pituitary stalk (). He continued to experience headache. Full-brain MRI confirmed the presence of a small nodule in each frontal lobe in addition to the pituitary mass lesion, likely metastatic deposits.
Computed tomography (CT) of the chest, abdomen, and pelvis showed a central tumor of the right lung (CT stage tbl4), prominent para-aortic and left hilar lymph nodes, and metastatic deposit in tbl11.
His general condition deteriorated very quickly, so he was not fit for palliative chemotherapy. He was referred to the palliative care team for symptom management. He died within 1 month of his diagnosis.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [80, 'years'], 'weight': [83.9, 'kg'], 'Sodium': [147.0, 'mEq/L']}",2.0975,1.99263,2.20238,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 80 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 83.9 kg. The concentration of sodium is 147.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 147.0 mEq. To convert from 147.0 mEq to mmol, convert from mEq to mmol. The compound 147.0 has a valence of 1, and so divide the valence by the value of mEq to get, 147.0 mEq/(1 mEq/mmol) = 147.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 147.0 mEq sodium/L converts to 147.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 83.9 * (147.0/140 - 1) = 2.0975 L. The patient's free body water deficit is 2.0975 L."
6164,38,Free Water Deficit,lab test,decimal,pmc-5175055-1,Extracted,"A 68-year-old female patient presented to our emergency service with inability to pass gas and feces for 2 days, abdominal distension, and vomiting. Her personal medical history was unremarkable, without any previous disease or operation. This multipara patient was 155 cm tall, and weighed 40 kg. Her vital signs were as follows: ABP: 120/70 mmHg, pulse rate: 78/min, respiratory rate: 23/min, body temperature: 36.7°C. Physical examination revealed abdominal distension without abdominal guarding, and rebound tenderness. The rectal ampulla was empty on digital rectal examination. Other system examinations were unremarkable. Results of laboratory tests were as follows: Htc: 43.1%; WBC: 11700/mm3, glucose: 125 mg/dL, BUN: 61mg/dL, creatinine: 1.21 mg/dL, sodium: 135 mEq/L, potassium: 4.3 mEq/L. Standing KUB revealed air-fluid level of intestines (). On whole abdominal ultrasound, dilated intestinal loops, and free fluid between intestinal loops were detected. Computed tomography (CT) demonstrated obstructive obturator hernia on the left side (Figures , ). The patient was operated urgently with the diagnosis of intestinal obstruction caused by strangulated obturator hernia. On exploration, a strangulated intestinal loop was detected within the left obturator channel, and reduced. Intestinal ischemia, necrosis or perforation were not detected, so additional intervention was not performed. The defect was repaired using a polypropylene mesh placed in the preperitoneal region. The patient was lost on postoperative 3rd day because of acute respiratory failure.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [68, 'years'], 'weight': [40.0, 'kg'], 'Sodium': [135.0, 'mEq/L']}",-0.64286,-0.61072,-0.675,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 68 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 40.0 kg. The concentration of sodium is 135.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 135.0 mEq. To convert from 135.0 mEq to mmol, convert from mEq to mmol. The compound 135.0 has a valence of 1, and so divide the valence by the value of mEq to get, 135.0 mEq/(1 mEq/mmol) = 135.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mEq sodium/L converts to 135.0 mmol sodium/L. Plugging in these values into the equation, we get 0.45 * 40.0 * (135.0/140 - 1) = -0.64286 L. The patient's free body water deficit is -0.64286 L."
6165,38,Free Water Deficit,lab test,decimal,usmle-1978,Extracted,"A 68-year-old woman comes to the physician because of increasing heartburn for the last few months. During this period, she has taken ranitidine several times a day without relief and has lost 10 kg (22 lbs). She has retrosternal pressure and burning with every meal. She has had heartburn for several years and took ranitidine as needed. She has hypertension. She has smoked one pack of cigarettes daily for the last 40 years and drinks one glass of wine occasionally. Other current medications include amlodipine and hydrochlorothiazide. She appears pale. Her height is 163 cm (5 ft 4 in), her weight is 75 kg (165 lbs), BMI is 27.5 kg/m2. Her temperature is 37.2°C (98.96°F), pulse is 78/min, and blood pressure is 135/80 mm Hg. Cardiovascular examination shows no abnormalities. Abdominal examination shows mild tenderness to palpation in the epigastric region. Bowel sounds are normal. The remainder of the examination shows no abnormalities. Laboratory studies show:
Hemoglobin 10.2 g/dL
Mean corpuscular volume 78 μm
Mean corpuscular hemoglobin 23 pg/cell
Leukocyte count 9,500/mm3
Platelet count 330,000/mm3
Serum
Na+ 137 mEq/L
K+ 3.8 mEq/L
Cl- 100 mEq/L
HCO3- 25 mEq/L
Creatinine 1.2 mg/dL
Lactate dehydrogenase 260 U/L
Alanine aminotransferase 18 U/L
Aspartate aminotransferase 15 U/L
Lipase (N < 280 U/L) 40 U/L
Troponin I (N < 0.1 ng/mL) 0.029 ng/mL
An ECG shows normal sinus rhythm without ST-T changes.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [137.0, 'mEq/L'], 'sex': 'Female', 'weight': [75.0, 'kg'], 'age': [68, 'years']}",-0.72321,-0.68705,-0.75937,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 68 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 75.0 kg. The concentration of sodium is 137.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 137.0 mEq. To convert from 137.0 mEq to mmol, convert from mEq to mmol. The compound 137.0 has a valence of 1, and so divide the valence by the value of mEq to get, 137.0 mEq/(1 mEq/mmol) = 137.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mEq sodium/L converts to 137.0 mmol sodium/L. Plugging in these values into the equation, we get 0.45 * 75.0 * (137.0/140 - 1) = -0.72321 L. The patient's free body water deficit is -0.72321 L."
6166,38,Free Water Deficit,lab test,decimal,pmc-8553378-1,Extracted,"The 36-year-old male presented to the emergency department (ED) of a London hospital with a three-week history of intermittent loose stools, cramping abdominal pain, and fevers. On the day of admission, the patient developed rigors and a headache with blurred vision which led him to attend hospital. Notably, he collapsed in the waiting room following which he was transferred to a resuscitation bay.
This young male who works in IT had no past medical history, took no regular medications, and had no relevant travel or family history. He was a non-smoker and reported no alcohol consumption in the month coming up to his admission. He also had no history of consumption of illicit drugs.
On assessment, he was noted to have a heart rate of 111 beats per minute (BPM), a blood pressure of 94/58 mmHg, and a fever of 40.1 degrees Celsius. His oxygen saturations were 100% on room air and his respiratory rate was 24 BPM.
On general examination the patient was noted to be pale. Respiratory examination found clear lung bases with good bilateral air entry. Examination of the cardiovascular system consisted of normal heart sounds, warm peripheries, and a capillary refill of less than two seconds. Right upper quadrant tenderness was noted during abdominal examination though his abdomen was soft with no signs of peritonism. No hepatomegaly was noted, bowel sounds were normal, and a digital rectal examination was unremarkable.
Investigations
A venous blood gas taken on admission to the ED revealed a lactate of 6.3 mmol/L, a base excess of -5.8 mmol/L, and a pH of 7.39 in keeping with the developing clinical picture of sepsis. The patient’s blood tests later revealed deranged liver function with raised inflammatory markers also. The tests found a C-reactive protein level (CRP) of 322 mg/L, white cell count of 5.01 x 109/L, neutrophils of 4.86 x 109/L, and eosinophils of 0.00 x 109/L. Liver function tests showed an alkaline phosphatase (ALP) of 193 IU/L, alanine transaminase (ALT) of 76 IU/L, bilirubin of 26 μmol/L, and albumin of 35 g/L. Renal bloods notably found a potassium of 2.9 mmol/L as well as an acute kidney injury (creatinine=149 mmol/L, urea=4.5 mmol/L, estimated glomerular filtration rate - eGFR=48 mL/min/1.73m², sodium=132 mmol/L). A rapid coronavirus polymerase chain reaction (PCR) test was also negative.
In the ED the patient also underwent imaging with a plain chest radiograph and CT scanning (CT abdomen and pelvis with contrast, non-contrast CT Head, CT pulmonary angiogram). The patient’s chest X-ray (Figure ) demonstrated clear lung fields with no effusion or pneumothorax, a normal mediastinum, and no cardiomegaly. CT scanning of the abdomen and pelvis found a central lesion of low attenuation measuring 7 cm x 6 cm x 6 cm which demonstrated no arterial enhancement and was reported as most likely representing a LA (Figure ). In addition, gross inflammatory change affecting a cluster of the small bowel beneath the cecum was noted and was thought to represent appendicitis or terminal ileitis. Gall bladder swelling was noted, though there was no sign of cholecystitis. There were normal appearances of the pancreas, spleen, and kidneys and no abdominal or pelvic free fluid.
The patient was also reviewed by the hospital’s cardiology team during his admission. This specialist review was requested due to the finding of ST depression and sinus tachycardia on his admission electrocardiograms (ECGs) (Figure ). Admission blood tests also revealed an elevated troponin T level of 40 ng/L which had risen to 59 13 hours later. This was followed by a transthoracic echocardiogram (TTE) which found a mildly dilated, globally hypokinetic left ventricle, mild left ventricular impairment and moderately dilated right ventricle but good longitudinal and radial function and trace mitral and tricuspid regurgitation (Figure ).
The evening following the patient’s admission he underwent ultrasound-guided percutaneous drainage of the abscess under the interventional radiology team. Some 100 mL of frank pus was aspirated which was then sent for microbiological assessment with a 12 Fr pigtail drain left in situ. A repeat ultrasound two days later revealed resolution of the collection, following which the drain was removed. Three days following sampling, the abscess fluid culture found growth of Streptococcus constellatus. Otherwise stool bacterial PCR, Clostridium difficile testing, ova/cysts/parasite microscopy, amoebic serology, and modified Ziehl-Nielsen testing for Cryptopsoridium were negative.
Given its role as a part of normal gut flora and suspected translocation from the bowel leading to the LA, a colonoscopy was arranged under the gastroenterology team for visual evaluation of the gastrointestinal (GI) tract. This found a severely distorted and inflamed terminal ileum with an impassable stricture (Figure ). Terminal ileum biopsies taken at the time found fragments of ulcerated mucosa and superficial submucosa which showed granulation tissue with a heavy lymphoplasmacytic inflammatory infiltrate. The infiltrate displayed no atypical morphological features and no granulomas or microorganisms were seen.
Treatment
Despite fluid resuscitation with three liters of crystalloid fluid and IV metronidazole, the patient was persistently shocked with a blood pressure of 89/40 mmHg and a urine output of approximately 40 mL/h (weight=83 kg). This led to escalation of his care to the intensive care team and subsequent vasopressor support with noradrenaline. At this time, advice was sought from the microbiology team who advised adding IV cefuroxime to his regular regime alongside metronidazole, as well as a single dose of IV gentamicin.
By day three of the patient’s admission he had no further requirement for vasopressor support, his acute kidney injury had resolved (urea=4.5 mmol/L, creatinine=81 mmol/L, eGFR=>90 mL/min/1.73m²) and his vital signs had normalized (afebrile, heart rate=89 BPM, blood pressure=108/53 mmHg). Given the patient’s stable condition, he was stepped down from the ICU to a normal ward environment under the care of the infectious diseases team.
Outcome and follow-up
Following the colonoscopy, after a total of 10 days admission, the patient was allowed to go home with a four-week course of oral co-amoxiclav. On outpatient clinic review three weeks later by the infectious diseases team, the patient reported no persisting abdominal symptoms. Examination was also normal. Bloods taken on the day also demonstrated resolution of his raised inflammatory markers with good kidney function (white cell count=6.00 x 109/L, CRP=17.0 mg/L, creatinine=84 mmol/L). Deranged liver function persisted to some extent but had dramatically improved when compared to tests taken at discharge.
Two months after discharge, the patient’s case was discussed in the gastroenterology inflammatory bowel disease (IBD) multi-disciplinary team meeting due to concerns raised about possible Crohn’s disease from the admission CT and following colonoscopy findings. Given the absence of relevant IBD symptoms, a reassuring outpatient MRI small bowel (found considerable resolution of the right iliac fossa inflammatory process) and a fecal calprotectin of 29 four months post discharge (normal=0-51 μg/g), it was concluded the terminal ileum changes were most likely accounted for by a complicated course of appendicitis. When reviewed in a telephone clinic 10 weeks post discharge he was found to have no persistent GI symptoms and was subsequently discharged.
Given the patient’s abnormal admission ECG and TTE findings, outpatient follow-up with the cardiology department was also arranged. While the inpatient TTE found a mildly impaired ejection fraction of 47%, a cardiac MRI (adenosine stress protocol) carried out 10 weeks after discharge found normal pump function. However, there was persistent mild left ventricular dilatation (end diastolic volume=202 mL; normal range=99-199 mL). A telephone clinic consultation at four months following discharge revealed the patient had no cardiac symptoms and was undertaking four exercise sessions weekly (including two 10 km runs). He was discharged from regular clinic review with a follow-up echocardiogram scheduled for three years’ time.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [36, 'years'], 'weight': [83.0, 'kg'], 'Sodium': [132.0, 'mmol/L']}",-2.84571,-2.70342,-2.988,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 36 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 83.0 kg. The concentration of sodium is 132.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 83.0 * (132.0/140 - 1) = -2.84571 L. The patient's free body water deficit is -2.84571 L."
6167,38,Free Water Deficit,lab test,decimal,pmc-4763642-1,Extracted,"A 32-year-old male patient was admitted to the outpatient clinic with complaints of weight gain, dry mouth, and fatigue. In 2002, some eruptions appeared on the skull. Two (2) years later, skin eruptions spread all over his body. At that time, he was diagnosed with psoriasis and prescribed topical clobetasol propionate. He had not been reexamined after that and has been using clobetasol propionate 0.005% routinely for 10 years. He has applied the drug to his arms, legs, and all over the trunk. Over the past year, he put on weight obviously (8 kg). He stopped the treatment 1 month ago, at the time of writing. He has been complaining of dry mouth and fatigue for the last month. On his physical examination, moon face, central adiposity, and purple-red striae on the abdomen under umbilicus were observed. There were scaly patches and erythematous plaques on the skull, interscapular area, sacrum, arms, legs, knees, and elbows []. Other systemic examinations were all normal. Blood pressure was 130/90 mmHg, pulse 75/min, height 1.76 m, weight 77 kg, and body mass index 24.8 kg/m2. On laboratory examination, fasting blood glucose: 152 mg/dL (N: 70-105), creatinine: 1 mg/dL (N: 0.72-1.25), triglyceride: 160 mg/dL (N: 0-200), total cholesterol: 240 mg/dL (N: 0-200), high-density-lipoprotein (HDL)-cholesterol: 44 mg/dL (N: 45-55), low-density-lipoprotein (LDL)-cholesterol: 164 mg/dL (N: 0-130), ALT: 42 u/L (N: 0-55); AST: 27 u/L (N: 0-34); sodium: 140 mmol/L (N: 136-145); potassium: 4.6 mmol/L (N: 3.5-5.1); calcium: 9.9 mg/dL (N: 8.4-10.2); phosphorus: 3.5 mg/dL (N: 2.3-4.7); albumin: 4.6 g/dL (N: 3.2-5.2); intact-parathyroid hormone (iPTH): 38 pg/mL (N: 14-72); 25-OH Vitamin D: 4.9 ng/mL (N: 24-50); white blood cell (WBC) count: 12.76-103 /uL (N: 4.23-9.07); hemoglobin (Hb) count: 14.7 gr/dL (N: 13.7-17.5); platelet: 217-103 /uL (N: 150-400); morning (8 AM) adrenocorticotropic hormone (ACTH): 5.6 pg/mL (N: 0-46); morning (8 AM) serum cortisol: <0.2 μg/dL (5.5 nmol/L) (N: 4.3-22.4). According to these findings, the patient was diagnosed with iatrogenic Cushing's syndrome secondary to topical steroid use. For adrenal insufficiency, 20 mg/day hydrocortisone treatment was commenced, and for vitamin D deficiency, vitamin D replacement. As the patient had high blood glucose levels, dyslipidemia, and large waist circumference (101 cm), he was diagnosed with metabolic syndrome, and a low-calorie diet and exercise were advised. Metformin treatment at a dose of 2000 mg/day was commenced for glucose regulation. The patient consulted at the dermatology department for his psoriasis, and calcipotriol pomade and emollients were prescribed. One (1) month after that, 1 μg tetracosactide i.v. was applied and cortisol levels were measured at 30 min and at 60 min. As both measured levels were below 3 μg/dL, glucocorticoid maintenance treatment was continued.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [32, 'years'], 'weight': [77.0, 'kg'], 'Sodium': [140.0, 'mmol/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 32 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 77.0 kg. The concentration of sodium is 140.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 77.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
6168,38,Free Water Deficit,lab test,decimal,pmc-8290566-1,Extracted,"A 44-year-old Moroccan Jew woman (gravida 4, para 4) was admitted to an internal medicine ward for general weakness and drowsiness, which began 2 days before admission. Her past medical history included morbid obesity and related complications of type 2 diabetes, which were controlled by metformin treatment; dyslipidemia, which was treated with atorvastatin; gastroesophageal reflux disease, which was not being managed with regular treatment; and fatty liver disease with no other known comorbidities. Her family history included untimely deaths of two of her four children, whose symptoms were similar to those in Leigh’s disease; her other two children are alive and healthy. Aiming to lose weight and control additional comorbidities, she underwent gastric band surgery at the age of 30 years. At the age of 38 years, owing to insufficient weight loss, she underwent gastric sleeve bariatric surgery, which resulted in a weight loss of 30 kg; however, she rapidly regained the lost weight. She subsequently remained morbidly obese, with a body mass index of 48.4. She was approved for a third bariatric surgery involving gastric bypass, and was admitted at the age of 44 years, weighing 126 kg. The surgery began with a laparoscopic approach, but, because of bleeding and gastrointestinal leakage, the procedure was converted to an open laparotomy. The procedure included an omega loop gastric bypass and an elective gallbladder resection, but was complicated by heavy postoperative bleeding. During the next several months, she underwent prolonged hospitalization with continuous mechanical ventilation, which required insertion of a tracheostomy tube, several recurring surgeries for peritoneal lavage, and repeated abscess drainage from the internal abdomen and abdominal wall. During this period, the patient also experienced recurrent episodes of sepsis, which required treatment with multiple courses of broad-spectrum antibiotics. Eventually, after 8 months of postoperative hospitalization, she recovered and was transferred to the rehabilitation department.
After 44 days in the rehabilitation department, she gradually developed new symptoms including slow psychomotor response, weakness, worsening peripheral edema, and drowsiness. Her vital signs on admission to the internal medicine department were unremarkable: temperature 36.4 °C, blood pressure 110/72 mmHg, pulse rate 84 beats per minute, respiratory rate 22 breaths per minute, and oxygen saturation on room air 97%. Her weight was 95 kg. Physical examination revealed grade 3 encephalopathy with asterixis, and neurological evaluation revealed hyporeflexia with symmetric weakness and decreased muscle tone. Other findings included peripheral edema grade 3. The surgical wounds in the abdominal wall had closed, and no signs of infection were seen. No tenderness was observed during abdominal palpation. Laboratory blood examinations showed an elevated international normalized ratio (1.6; normal range: below 1.1), severe hypoalbuminemia (1.5 g/dL; normal range: 3.4–5.4 g/dL), and highly elevated blood ammonia (285 µg/dL; normal range: 15–45 µg/dL). Other results included hemoglobin 9.2 g/L, white blood cell count 7200/µL, platelets 234,000/µL, glucose 91 mg/dL, urea 33 mg/dL, creatinine 0.7 mg/dL, sodium 137 mmol/L, potassium 4.3 mmol/L, magnesium 2.4 mmol/L, calcium 7.2 mmol/L, phosphorus 3.4 mmol/L, aspartate aminotransferase (AST) 28 IU/L, alanine aminotransferase (ALT) 31 IU/L, alkaline phosphatase 131 IU/L, gamma glutamyl transpeptidase 34 IU/L, lactate dehydrogenase 413 IU/L, total bilirubin 0.9 mg/dL, creatine phosphokinase 89 IU/L, pH 7.34, bicarbonate 23 mg/dL and PCO2 39.6 mmHg. Her C-reactive protein level was 1.2 mg/L (normal: 0–0.5 mg/L), and her blood ketones were negative. Further laboratory tests revealed normal levels of factor 5 and normal lactate levels (0.6 mg/dL). Imaging studies, including abdominal ultrasound and computerized tomography (CT), did not reveal any signs of cirrhosis; apart from previously known postsurgical changes, only diffuse fatty infiltrates of the liver were found (Fig. ). Brain CT, including venography and angiography, showed no signs of intracranial pathology, ischemia, or early or late enhancement. Her electroencephalographic findings supported the diagnosis of encephalopathy.
The most likely diagnosis was urea cycle disorder (UCD), as supported by the high ammonia levels, low blood protein levels, and advanced encephalopathy. Imaging studies showed no signs of cirrhosis, and laboratory investigations excluded hepatocellular injury. Hepatic cellular function was preserved, as reflected by standard factor 5 levels. Plasma amino acid analysis revealed a decrease in levels of several amino acid: taurine 17 µM, aspartate 13 µM, citrulline 4 µM, valine 105 µM, leucine 14 µM, tyrosine 25 µM, and histidine 58 µM. Other amino acids were in normal ranges. An acylcarnitine profile showed elevated carnitine with no further abnormalities. The urine organic acid profile revealed markedly elevated 4-hydroxyphenyllactate, but this test was inconclusive because the high levels of antibiotics in the blood might have influenced the results. Karyotyping revealed no irregularities.
Empirical treatments with the ammonia scavenger sodium benzoate, N-carbamylglutamate, l-arginine, carnitine, and low-protein total parenteral nutrition were administered in addition to nutritional supplements, which included thiamine, zinc, and vitamins C, B, and E. The patient’s encephalopathy condition continued to deteriorate, with new-onset fever and hemodynamic instability combined with respiratory failure. She was placed on mechanical ventilation, supported by vasopressors, started on a course of broad-spectrum antibiotics, and transferred to the internal intensive care unit, where a second ammonia level test was conducted and indicated a marked increase to 455 µg/dL. Her high ammonia levels were controlled by hemofiltration, in addition to the above treatment, and by administration of supplemental intravenous amino acids. Hemofiltration helped control her ammonia levels, which gradually decreased to baseline levels within 5 days.
A sepsis investigation began after fever and hemodynamic instability further complicated her condition, but no infectious source was found, and all cultures were negative. Total body CT and cardiac echocardiography were performed and yielded normal results.
With the resolution of systemic inflammatory response syndrome (SIRS), our patient was gradually weaned from mechanical ventilation and vasopressors, and her nutrition was steadily shifted from parenteral nutrition to enteral nutrition, and later to oral nutrition. The patient recovered neurologically and regained normal cognitive function. She subsequently developed critical care polyneuropathy, owing to the use of muscle relaxants, and was discharged to undergo rehabilitation in a designated hospital without a further need for nutritional supplements.
After 2 months in the rehabilitation department, she was discharged home. At a 2-year follow up after the hospitalization described above, her hyperammonemia had not recurred, and she had recovered from critical care polyneuropathy. During the follow-up period, no liver disease was found, and her ammonia levels remained stable and in the normal range, as did all other examined blood measurements.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [44, 'years'], 'weight': [95.0, 'kg'], 'Sodium': [137.0, 'mmol/L']}",-1.01786,-0.96697,-1.06875,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 44 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 95.0 kg. The concentration of sodium is 137.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 95.0 * (137.0/140 - 1) = -1.01786 L. The patient's free body water deficit is -1.01786 L."
6169,38,Free Water Deficit,lab test,decimal,pmc-4172392-1,Extracted,"A 44 year old Caucasian female (weight: 65 kg height: 170 cm) with a history of bipolar disorder and Wolf-Parkinson-Withe syndrome was transferred from a local hospital to our intensive care unit due to somnolence with a GCS (Glasgow Coma Scale) of 9 and polyuria after acute lithium intoxication. The patient was treated with a lithium medication for years. She took 4 tablets of perazindimalonat, 29 tablets of lithium (0.022 g Lithium per pill) and 10 tablets of zolpidemtartrat in suicidal attempt. On admission to our emergency room the patient’s history could not be obtained due to somnolence. Patient’s heart rate was 60 bpm, blood pressure was 120/80 mmHg, respiratory rate 14 per minute, cardiac and pulmonary auscultation were unremarkable as was the remainder of the physical exam. The patient was polyuric (4 l urine in 24 hours). Laboratory work-up showed a serum creatinine of 57 μmol/l, a serum sodium of 140 mmol/l and a serum potassium of 4.0 mmol/l. Liver function test, blood gas analysis and whole blood count were normal. Lithium serum level on admission was 3.9 mmol/l. Subsequently it rose to a concentration of 4.2 mmol/l two hours after admission. Due to the combination of the rising lithium serum level and the neurological symptoms the patient was transferred to the ICU for monitoring and the critical care nephrology department was consulted.
For fast reduction of lithium levels an intermittent hemodialysis using the GENIUS dialysis batch system (FMC, Germany) with a 90 liters dialysate tank volume and a 1.3 m2 F60S polysulfone high-flux dialyzer (FMC, Germany) was started. Blood and dialysate flow rate was started at 350 ml/min. As the patient woke up and became more vigilant but also agitated after one dialysis treatment, the flow rate had to be reduced to 200 ml/min to avoid frequent system alarms and the need to restrain the patient. Ultrafiltration rate was adjusted at minimum rate of 50 ml/h. Anticoagulation was provided by unfractionated heparin medication with an initial bolus of 1000 IE and a continuous dose of 500 IE per hour. Lithium serum levels were measured right before the start of the treatment, as well as within an interval of 15 minutes, 30 minutes, 1 hour, 2 hours and 3.5 hours after treatment initiation. One of the peculiarities of the GENIUS dialysis system is that fresh and spent dialysate are separated by virtue of temperature differences and difference in uremic solute concentration []. To prevent an early contamination of the fresh with the spent dialysate as seen in GENIUS therapy in patients without renal failure [], dialysis therapy was stopped after 4 hours of treatment. Plasma dialyzer clearance rates were measured 30 minutes and 3 hours after dialysis initiation using established dialyzer clearance equations reported previously []. Lithium dialyzer clearance was calculated according to the following equation: Kplasma = QB × (1 – Hct/100) × ((Cart – Cven)/Cart). Pre dialyzer concentrations (Cart) and post dialyzer concentration (Cven) were drawn at a time of minimal ultrafiltration (50 ml/h).
After the marked clinical improvement already occruing after the first hour of intermittent hemodialysis a subsequent extended dialysis with dialysate and blood flow of 140 ml/min was initiated right after the completion of the first dialysis session using a second GENIUS machine. As there was no gap between treatments a rebound could not be assessed.During the first dialysis lithium serum level was lowered by 71.5%. Plasma dialyzer clearance rate was 177.4 ml/min after 30 minutes of dialysis at a blood flow of 350 ml/min and 129.6 ml/min after 3 hours of dialysis at a blood flow of 260 ml/min. We mixed the total spent dialysate of the first dialysis tank by air insufflation and collected a sample for laboratory measurement. Lithium dialysate level was 0.4 mmol/l in the dialysate tank of 90 liters volume. Accordingly we found a total amount of 250 mg of lithium in the total spent dialysate. 5.5 hours after the initiation of the second dialysis therapy serum lithium level was 0.79 mmol/l (Figure ). No neurological symptoms were detectable after the patient woke up fully. Blood pressure rose to 175/85 mmHg prompting treatment with urapidil. Crystalloids were administered to compensate for polyuria. The morning after admission, the patient had fully recovered. Intensive monitoring was no longer required and the patient was retransferred to the psychiatric hospital. Blood pressure rose meanwhile up to 175/85 mmHg and urapidil therapy was initiated. Crystalloid solutes were administered to provide adequate fluid supply during polyuria. The morning after admission, the patient had fully recovered. Monitoring was no longer required and the patient was retransferred to the psychiatric hospital.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [44, 'years'], 'weight': [65.0, 'kg'], 'Sodium': [140.0, 'mmol/L']}",0,0,0,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 44 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 65.0 kg. The concentration of sodium is 140.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 65.0 * (140.0/140 - 1) = 0 L. The patient's free body water deficit is 0 L."
6170,38,Free Water Deficit,lab test,decimal,pmc-8183082-1,Extracted,"A 4-week-old, 2.8 kg Caucasian girl presented to the emergency department of a general hospital with a 1-day history of upper airway infection and poor feeding. She was born at 35 weeks of gestational age with a birth weight of 2.380 kg, Apgar 10, in a context of emergency C-section subsequent to preeclampsia and had no risk factor for mother-to-infant infection. She was admitted to the pediatric ward with a diagnosis of mild bronchiolitis with signs of rhinitis and reduced food intake, but showed no sign of dehydration. Upon admission, the patient was apyretic (37.5 °C), heart rate (HR) was at 172 beats per minute, blood pressure (BP) was 90/50 mmHg, and respiratory rate (RR) was 32 breaths/minute. She had no signs of hypoperfusion, and heart sounds were regular, with no audible murmur. Respiratory examination showed bilateral crackles, with moderate respiratory distress signs, and saturation was 100% under oxygen therapy 0.5 L/minute. She had moderate axial hypotonia, normal cries, and normotensive anterior fontanelle. There were no other findings on physical examination. Chest X-ray showed a chest distension without apparent infectious site (Fig. ). Respiratory panel test was negative, including for respiratory syncytial virus (RSV) and influenza, as well as aerobic and anaerobic blood cultures. Blood tests at admission reported hyponatremia and hyperkalemia (Na+ 126 mmol/L, K+ 5.6 mmol/L, bicarbonate 22.3 mmol/L, creatinine 20 μmol/L, urea 5.4 mmol/L, white blood cells (WBC) 9.2 × 109/L, hemoglobin (Hb) 10.9 g/dL, platelets (Plt) 553 × 109/L, C-reactive protein (CRP) < 5 mg/L) (Fig. ). She received continuous intravenous infusion of hypotonic fluid (sodium chloride 34 mmol/L, potassium 20 mmol/L, calcium 2.26 mmol/L, and glucose 5%) at a rate of 122 mL/kg/day, plus enteral feeding via nasogastric tube (130 mL/kg/day), supplemental oxygen 0.5 L/minute, respiratory physiotherapy, and oral betamethasone (0.375 mg once daily for 2 days).
After 48 hours, she was found drowsy and hypotonic, still reactive to stimulation with no other sign of intracranial hypertension. She presented respiratory distress, intermittent desaturation, hypothermia (35.5 °C), and normal hemodynamic parameters (HR 140 beats per minute and BP 95/50 mmHg). The blood tests showed: glycemia 6.10 mmol/L, Na+ 94 mmol/L, K+ 5.2 mmol/L, Cl− 67 mmol/L, osmolality 194.1 mmol/kg, creatinine 10 μmol/L, urea 3 mmol/L, WBC 18.4 × 109/L, Hb 10.8 g/dL, Plt 734 × 109/L, CRP < 5 mg/L and urine tests: Na+ 48 mmol/L, K+ 50 mmol/L, Cl− 102 mmol/L and osmolarity 456 mosm/L. NaCl was added to the MIVF (total Na+ content: 100 mmol/L), total intravenous intakes were restricted to 85 mL/kg/day, and feedings were stopped. Cerebral tomodensitometry showed widespread cerebral edema (Fig. ). Four hours later, the blood tests showed persistent severe hyponatremia (98 mmol/L). Patient transfer to the Pediatric Intensive Care Unit (PICU) was then decided. Upon arrival of the pediatric transport team, the child was unconscious (Glasgow Coma Scale: 8) and presented respiratory pauses and hemodynamic symptoms of intracranial hypertension (HR 115 bpm, BP 110/60 mmHg). Auscultation revealed a decrease of the left vesicular murmur, and hemodynamics remained stable. No other abnormal clinical signs were found. She immediately received osmotherapy (3 mL/kg of NaCl 3% w/v). She was then sedated with propofol (3 mg/kg) and paralyzed with succinylcholine (1 mg/kg) for rapid sequence intubation and intubated with a 3.5-cuffed tracheal tube. Afterwards, she received isotonic MIVF (dextrose 5% with NaCl 145 mmol/L) with a total intake restricted to 80 mL/kg/day. Upon PICU admission, she was sedated with continuous infusions of midazolam (30 μg/kg/hour) and morphine (30 μg/kg/hour), without any clinical sign of intracranial hypertension.
Three hours after admission, transcranial Doppler ultrasound (TDU) showed elements of intracranial hypertension (pulsatility index (PI): 1.40, diastolic velocity (Vd): 16 cm/second). TDU was normalized (PI: 1.02, Vd: 30 cm/second) after a second IV bolus of NaCl 3% w/v (3 mL/kg).
Thirteen hours postadmission, the patient presented with transient polyuria (5.4 mL/kg/hour) associated with a decrease in urinary density to 1.005 g/mL, urinary Na+ < 10 mmol/L, and a rapid increase in natremia (Fig. ). Intravenous desmopressin 0.1 μg/kg was given to control polyuria and stabilize natremia. Subsequently, diuresis and natremia normalized with isotonic MIVF and fluid restriction for 2 days until resumption of enteral feedings.
Amplitude-integrated electroencephalography (aEEG) did not report any comitial activity and sedation was weaned 24 hours after admission. The infant showed signs of awakening. She was extubated 2 days after admission, and then received supplemental oxygen for 5 days and systemic steroids (intravenous dexamethasone 0.15 mg/kg every 6 hours for 24 hours) for postextubation laryngeal stridor.
Three days after admission, the child’s EEG reported elements of cerebral suffering and some left central acute elements for which epileptic origin was not confirmed. EEG performed on day 6 was normal. Magnetic resonance imaging (MRI), performed on day 4, showed significant regression of cerebral vasogenic edema with multiple small areas of supratentorial cytotoxic edema, whose distribution did not match any typical aspect of osmotic demyelination syndrome (ODS) and were imputed to ischemic injuries. This lack of ODS-related lesion was later confirmed by another MRI 6 months later.
SIAD assessment was performed with elimination of dysthyroidism [TSH 3.16 mUI/L (N)] and adrenal insufficiency [8 a.m. cortisol: 52.3 µg/L (N)], but antidiuretic hormone dosage was not available. Blood samples remained normal afterwards.
Eight days after PICU admission, neurological examination was normal. The infant was transferred to the general pediatric ward on day 8 and discharged home on day 12. In the weeks following discharge, she presented with feeding difficulties and suffered episodes of acute discomfort with desaturation, bradycardia, and laryngeal spasm requiring rehospitalization in the pediatric ward and then in the PICU. Upon admission, HR was at 175 bpm, BP 120/68 mmHg, RR 40/minute, and saturation 100% under high-flow oxygen therapy with FiO2 30%. She had inspiratory dyspnea with severe respiratory distress, and other clinical signs were normal. Faced with a serious acute airway obstruction episode and an inability to intubate, urgent tracheostomy was performed. A subglottic stenosis was later found (Fig. ). A tracheostomy remained in place until the age of 14 months. She had multiple dilations of the subglottic stenosis with good results. At 2 years of age, she has a normal neurological clinical examination. She suffers from moderate asthma and is fed by a gastrostomy because of an orality disorder.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [126.0, 'mmol/L'], 'sex': 'Female', 'weight': [2.8, 'kg'], 'age': [4, 'weeks']}",-0.168,-0.1596,-0.1764,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 4 weeks old. This means the patient is 0 years old.
The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 2.8 kg. The concentration of sodium is 126.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 2.8 * (126.0/140 - 1) = -0.168 L. The patient's free body water deficit is -0.168 L."
6171,38,Free Water Deficit,lab test,decimal,pmc-1810538-1,Extracted,"A 52-year-old male with a history of hepatitis C, genotype 1b, was nearing completion of a one-year course of treatment with pegylated interferon 2a (180 ug subcutaneously each week) and ribavirin (1200 mg orally each day). His initial hepatitis C viral RNA had declined from 2.2 × 106 IU/ml at onset of treatment, to <65 IU/ml by six months, and remained undetectable thereafter. Toward the end of his course of treatment, he developed fatigue, malaise, drenching night sweats, intermittent fever and chills. On the last visit for hepatitis C treatment, axillary and cervical lymphadenopathy was noticed. His symptoms were initially attributed to adverse effects of interferon α, prompting premature discontinuation of treatment after 10.5 months. One month after onset of symptoms, he presented to a nearby hospital for further workup.
He was transferred to the Buffalo VA Western New York Healthcare System with complaints of malaise and left sided mid back pain. He had a documented weight loss of 40 lbs over the previous year. He appeared chronically ill and fatigued. He had a temperature of 101°F and a heart rate of 105 beats per minute. Generalized lymphadenopathy was noted, including cervical, axillary, inguinal and right epitrochlear lymph nodes. The nodes were 1–2 cm wide, firm, movable and nontender. He had left sided abdominal fullness and mild tenderness, but no guarding or rebound. The remainder of his examination was noncontributory.
CBC revealed hemoglobin of 11.7 g/dl (13.5–17), white blood cell count of 7.6 K/cmm (4.4–10.7), platelet count of 511 K/cmm (140–375) and ESR of 80 mm/hr. Serum chemistries included a sodium of 130 mEq/L (135–145), creatinine of 0.9 mg/dl (0.7–1.4). SGOT was 68 units/l (12–34), SGPT: 95 units/l (25–65). A serum ELISA for human immunodeficiency virus was negative. Rheumatoid and anti-nuclear antibody titers were also negative.
Computerized tomography (CT) scan of chest and abdomen revealed mild lymphadenopathy and multiple contrast enhancing hypodense lesions in the spleen (Figure ).
Initial clinical suspicion included lymphoma and he underwent a lymph node biopsy. Further history revealed exposure to numerous cats. He frequented a neighbor who had 6–9 cats, including kittens, with which the patient had played, and from whom he received numerous scratches. Serologic studies were sent for antibodies to Bartonella, Chlamydia, Toxoplasma and Brucella. He was given ibuprofen for symptomatic relief.
A biopsy of an epitrochlear lymph node displayed necrotizing granulomata with peripheral palisading epithelioid cells, with an admixture of plasma cells and lymphocytes. Areas of stellate necrosis with microabscesses were evident, consistent with cat scratch disease (Figure ). Stains for acid-fast bacilli and fungi showed no organisms. Lymph node biopsy material was cultured for routine pathogens, acid-fast bacilli and fungal organisms. Although the Gram stain displayed abundant white blood cells, all cultures were sterile.
Over the next 3–4 days, the patient defervesced and improved symptomatically on ibuprofen alone. By the eighth day, serum antibody titers (IgG and IgM) for Bartonella henselae were reported as >1:16,384. He continued to improve without further treatment. Six months later he was doing well and had regained 25 lbs of weight. An abdominal CT scan revealed complete resolution of splenic lesions.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [130.0, 'mEq/L'], 'sex': 'Male', 'weight': [40.0, 'lbs'], 'age': [52, 'years']}",-0.77759,-0.73871,-0.81647,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 52 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 40.0 lbs so this converts to 40.0 lbs * 0.453592 kg/lbs = 18.14368 kg. The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 18.14368 * (130.0/140 - 1) = -0.77759 L. The patient's free body water deficit is -0.77759 L."
6172,38,Free Water Deficit,lab test,decimal,usmle-1453,Extracted,"A previously healthy 10-year-old boy is brought to the emergency room by his mother 5 hours after the onset of abdominal pain and nausea. Over the past 2 weeks, he has also had progressive abdominal pain and a 4-kg (8.8-lb) weight loss. The mother reports that her son has been drinking more water than usual during this period. Last week he wet his bed three times despite being completely toilet-trained since 3 years of age. His temperature is 37.8°C (100°F), pulse is 128/min, respirations are 35/min, and blood pressure is 95/55 mm Hg. He appears lethargic. Physical examination shows deep and labored breathing and dry mucous membranes. The abdomen is soft, and there is diffuse tenderness to palpation with no guarding or rebound. Serum laboratory studies show:
Na+ 133 mEq/L
K+ 5.9 mEq/L
Cl- 95 mEq/L
HCO3- 13 mEq/L
Urea nitrogen 25 mg/dL
Creatinine 1.0 mg/dL
Urine dipstick is positive for ketones and glucose.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [10, 'years'], 'weight': [4.0, 'kg'], 'Sodium': [133.0, 'mEq/L']}",-0.12,-0.114,-0.126,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 10 years old. The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 4.0 kg. The concentration of sodium is 133.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 133.0 mEq. To convert from 133.0 mEq to mmol, convert from mEq to mmol. The compound 133.0 has a valence of 1, and so divide the valence by the value of mEq to get, 133.0 mEq/(1 mEq/mmol) = 133.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mEq sodium/L converts to 133.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 4.0 * (133.0/140 - 1) = -0.12 L. The patient's free body water deficit is -0.12 L."
6173,38,Free Water Deficit,lab test,decimal,pmc-5500080-1,Extracted,"A 3-day-old girl was admitted due to progressive tachypnoea and recurrent seizures for 1 day.
The patient was delivered by caesarean section at a gestational age of 39 weeks and weighed 3500 g at birth. No abnormalities were documented during her birth. Her antenatal history was uneventful. Her mother was 29 years old. The parents did not have a consanguineous marriage, and no congenital diseases were documented in the family. She had a healthy 7-year-old brother.
Poor feeding, low activity, and tachypnoea were observed, with rapid progression on day 2 after birth. Irregular respiration and 3 seizures (involving hypertonia and spasms of the upper limbs), each of approximately 1 minutes in duration, were documented before admission. Noninvasive ventilation, antibiotics, and anticonvulsants were administered. Because the symptoms were not relieved, the baby was intubated and transferred to our hospital.
Upon admission, the patient's vital signs were a temperature of 38°C, a heart rate of 192 bpm, a respiratory rate of 70 breaths per minute, and a blood pressure of 94/52 mm Hg. Her body weight was 3040 g. She was unconscious, with moderate jaundice. Lung auscultation revealed coarse rales. Obvious hypotonia was observed, and the patient's primitive reflexes were absent. Bloody fluids from the gastric tube were found after admission.
Peripheral blood counts and blood gas were normal upon admission. Elevated levels of alanine aminotransferase (203 U/L) and unconjugated hyperbilirubinemia (234 μmol/L) as well as a mildly elevated serum creatine level (104 μmol/L) were found. Hypoglycemia (blood glucose of 2.01 mmol/L), hypernatremia (Na+ of 153.8 mmol/L) and hyperchloremia (Cl− of 114.2 mmol/L) suggested a potential disturbance in homeostasis. A coagulation function test indicated a mildly prolonged prothrombin time of 16.8 seconds. A chest X-ray revealed pneumonia with atelectasis of the superior lobe of the right lung. However, sputum culture, blood culture, and cerebrospinal fluid examination were negative.
Dysfunction of multiple organs and systems, neonatal sepsis, and upper digestive tract bleeding were considered, and intracranial infection was suspected upon admission. The patient was on mechanical ventilation at the time of admission. In addition, meropenem and anticonvulsants were administered, as were other supporting therapies, such as fasting for 3 days. Symptoms were relieved, and the patient was weaned off ventilation.
Oral feeding recommenced after extubation. Feeding difficulties became the main problem because the patient did not respond well to routine swallow training. Therefore, parenteral nutritional support was added. Seizure and tachypnoea reappeared as intravenous amino acids were provided. Vomiting, dyspnoea, and lethargy were present concurrently, with rapid deterioration. Blood gases suggested respiratory alkalosis with or without metabolic acidosis. Further examination indicated severe hyperammonemia (serum ammonia level >500 μmol/L). Brain MRI (Fig. ) revealed extensive abnormalities in deep white matter of the bilateral cerebral hemisphere, subcortical white matter, caudate nuclei, the dorsal thalamus, and the cerebellar hemisphere, which suggested hereditary metabolic leukoencephalopathy. Blood tandem mass spectrometry revealed hypocitrullinemia (a serum citrulline level of 2.57 μmol/L), whereas urine gas mass spectrometry produced normal results. Urea cycle disorder was considered. Fasting, the withdrawal of amino acids and plans to treat hyperammonemia were immediately implemented.
An EDTA-anticoagulated blood sample was sent to Joy Orient Translational Medicine Research Center Co, Ltd, after informed consent was obtained from both parents. DNA was extracted and amplified via polymerase chain reaction (PCR). Sequencing and comparison with the NCBI RefSeq database revealed 2 heterozygous mutations in the CPS1 gene (Fig. ): c.2407C > G (p.803, R > G) in exon 20 and C.323G > A (p.108, G > E) in exon 4. The diagnosis of CPS1D was confirmed. However, the parents decided to discontinue medical care and refused to allow further genetic examination of the family. Written informed consent was obtained from the parents of the patient for publication of this case report and any accompanying images.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [3, 'days'], 'weight': [3040.0, 'g'], 'Sodium': [153.8, 'mmol/L']}",0.17979,0.1708,0.18878,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 3 days old. This means the patient is 0 years old.
The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 3040.0 g so this converts to 3040.0 lbs * kg/1000 g = 3.04 kg. The concentration of sodium is 153.8 mmol/L. Plugging in these values into the equation, we get 0.6 * 3.04 * (153.8/140 - 1) = 0.17979 L. The patient's free body water deficit is 0.17979 L."
6174,38,Free Water Deficit,lab test,decimal,pmc-4724850-1,Extracted,"A 51-year-old woman without underlying disease presented with generalized tonic clonic seizure for several minutes followed by dizziness and generalized weakness. There was no history of recent head trauma or infectious disease. She did not have smoking, alcohol drinking and specific family history. By obtaining her detailed history, we determined that she had overconsumed large amounts of ginkgo nuts 1 kg for 1 hour. About half a day later, the seizure occurred.
At the time of emergency room visit, her vital signs were blood pressure 121/81 mmHg, pulse rates 76bpm, respiratory rates 18 bpm, body temperature 36.2°C and O2 saturation 98%. Neurologic examination showed normal findings except for drowsiness. Blood tests revealed slightly elevated white blood cell (10,600/mL) and normal ranges of hemoglobin (12.6 g/dL), platelet (188,000/uL) and C-reactive protein (0.03 mg/dL). Arterial blood gas analysis indicated metabolic acidosis (pH 7.337, pCO2 38.7 mmHg, pO2 36.7 mmHg, HCO3 20.3 mmol/L, base excess −5.50 mmol/L and O2 saturation 68.9%) which became normalized after adequate hydration and oxygenation. Serum electrolyte and chemistry levels were normal (sodium 138 mmol/L, potassium 4.0 mmol/L, aspartate aminotransferase 44 IU/L, alanine aminotransferase 22 IU/L, blood urea nitrogen 14.5 mg/dL, and creatinine 1.06 mg/dL) and muscle enzyme levels were mildly increased (creatine kinase 256 IU/L, lactate dehydrogenase 540 IU/L). Blood vitamin B6 level was decreased (2.2 ug/L, normal range: 5.0–50.0 ug/L). The electrocardiography and brain magnetic resonance imaging findings were normal. Initial electroencephalography (EEG) revealed intermittent generalized slow waves, but no epileptiform discharges were observed (). Cerebrospinal fluid (CSF) study was performed due to prolonged decreased mentality and her CSF analysis showed normal findings (pressure 14 cmH2O, red blood cell 0/mL, white blood cell 2/mL, polymorphonuclear cell 0%, lymphocyte 0%, monocyte 0%, CSF glucose 83 mg/dL, blood glucose 128 mg/dL and protein 15.0 mg/dL).
After admission, she was taken to supportive management without anticonvulsants medication and received 50 mg oral pyridoxine daily. No more seizures recurred and her mental function was resolved completely. Three weeks later, her blood vitamin B6 level was within normal range (12.1 ug/L), and EEG findings returned to normal ().",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [138.0, 'mmol/L'], 'sex': 'Female', 'weight': [1.0, 'kg'], 'age': [51, 'years']}",-0.00714,-0.00678,-0.0075,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 51 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 1.0 kg. The concentration of sodium is 138.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 1.0 * (138.0/140 - 1) = -0.00714 L. The patient's free body water deficit is -0.00714 L."
6175,38,Free Water Deficit,lab test,decimal,pmc-7501118-1,Extracted,"A 15-year-old girl with a recent diagnosis of Crohn’s disease was admitted to Emma Children’s Hospital with complaints of right lower quadrant abdominal pain, nausea, anorexia, and reduced urine output with anuria for the last 8 h. She had no fever and no diarrhea. She had lost 5 kg in weight during the past month but put on again 1.5 kg in the last week.
On admission, her blood pressure was mildly elevated to 127/90 mmHg (95–99th percentile), with a heart rate of 90 BPM. Her height was 155 cm and weight 41.5 kg. On physical examination, she was well appearing, with right lower quadrant and bilateral flank tenderness. She had no rash, no edema, and normal capillary refill. Laboratory tests showed a hemoglobin of 10.5 mg/dL (5.2 mmol/l), thrombocytosis of 930,000 per microliter, leukocytosis of 12,300 per microliter, with an absolute neutrophil count of 9800 per microliter, and normal eosinophil count (40 per microliter). C-reactive protein was 38 mg/L. Serum creatinine was elevated to 2.5 mg/dL (220 micromol/L), blood urea nitrogen was normal (10.3 mg/L, i.e., 3.7 mmol/L). Albumin was 3.8 g/dL (38 g/L), phosphorus 5.1 mg/dL (1.65 mmol/L), sodium 135 mmol/L, and potassium 4.1 mmol/L. Blood gases were normal with a bicarbonate of 24 mmol/L.
Her urine sediment was positive for leukocytes (244 per microliter) and epithelial cells, with no RBC, casts, or crystals. There was moderate proteinuria with a protein/creatinine ratio of 0.9 mg/mg (104 mg/mmol). Urine sodium was < 20 mmol/L, and urine urea 43 mmol/L, with fractional excretions of 0.6% and 43%, respectively. Urine osmolality was 118 mOsmol/kg. Abdominal ultrasound showed stable ileocecal inflammation and normal renal size and structure. Urine culture was sterile.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [15, 'years'], 'weight': [41.5, 'kg'], 'Sodium': [135.0, 'mmol/L']}",-0.88929,-0.84483,-0.93375,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 15 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 41.5 kg. The concentration of sodium is 135.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 41.5 * (135.0/140 - 1) = -0.88929 L. The patient's free body water deficit is -0.88929 L."
6176,38,Free Water Deficit,lab test,decimal,pmc-5385225-1,Extracted,"A 24-year-old man with a protein-losing gastroenteropathy due to an intestinal lymphangiectasia was treated with glucocorticoids (prednisolone, 7.5 mg/day) and developed low-grade fevers 7 months before admission. He did not have any remarkable life histories. Five months before admission, the man complained of headaches, fatigue, and a hearing abnormality. Then, he experienced nausea, diarrhea, and drowsiness for 6 days and subsequently sought evaluation at our hospital. The physical examination at the time of admission revealed that he was slow to respond (Japan Coma Scale 1-1). The following measurements were obtained: height, 161.2 cm; weight, 51.0 kg; BMI, 19.6 kg/m2; blood pressure, 119/78 mmHg; heart rate, 62 bpm; and body temperature, 37.4°C. The remainder of the examination findings were normal, without any signs of meningitis.
The initial laboratory data showed a white blood cell count of 11700/μL, with 87.0% neutrophils (86% segmented and 1% band neutrophils), 2.0% lymphocytes, 10%monocytes, 0% eosinophils, 1% metamyelocytes, hemoglobin = 15.7 g/dL, and a platelet count of 157,000/μL. The serum C-reactive protein level was slightly elevated (0.80 mg/dL). Although the serum sodium level was slightly decreased (130 mEq/L), the potassium (4.6 mEq/L), chloride (97 mEq/L), creatinine (0.59 mg/dL), fasting glucose (85 mEq/L), and HbA1c (5.1%) concentrations were normal.
An abdominal computed tomography (CT) showed bilateral adrenal enlargement (right, 10.0 × 20.0 mm; left, 29.0 × 29.0 mm). A retrospective analysis of the CT images revealed that the enlargement in the left adrenal gland developed 5 months before admission (), which coincided with the onset of fevers and headaches. Subsequently, the bilateral adrenal enlargement progressed (). The differential diagnosis of adrenal enlargement includes metastatic carcinoma, bilateral adrenal hyperplasia, tuberculosis, and fungal infections. A whole-body examination failed to find a primary malignant lesion. The QuantiFERON-TB test and HIV antibody titer were negative.Although there were no signs of meningeal irritation, a diagnostic lumbar puncture was performed. The cerebrospinal fluid revealed an increased white blood cell count (240/μL), a normal protein level, a decreased glucose level (0.10 g/l), and a positive cryptococcal antigen titer. The pathologic specimen showed the presence of yeast-like organisms, such as Cryptococcus spp. on Alcian blue staining, which was subsequently determined to be Cryptococcus neoformans.
Although the level of serum adrenocorticotropic hormone (ACTH) was elevated (131.3 pg/mL; normal range, 7.2–63.3 pg/mL) at the time of the diagnosis of cryptococcosis (), cortisol release in response to ACTH (Cortrosyn), which was evaluated 1 day after prednisolone cessation, was increased (). Oral prednisolone (7.5 mg/day) was then resumed as treatment for the protein-losing gastroenteropathy. The other endocrinological data of adrenal gland ruled out the possibility of pheochromocytoma and aldosterone-secreting tumors in this patient ().
Amphotericin B (250 mg/day) was initiated, followed by the addition of fluconazole (400 mg/day). The symptoms improved gradually after beginning antifungal treatment. Fluconazole alone was continued after discharge. After the initiation of antifungal treatment, the elevated ACTH levels were decreased and varied during the treatment (), suggesting a stressed condition with infection at the diagnosis and unstable absorption of prednisolone due to the protein-losing gastroenteropathy. Mild hyponatremia probably due to relative adrenal insufficiency was improved to the normal range (138 mEq/L) one month after the initiation of the antifungal treatment.
An abdominal CT, which was routinely obtained during follow-up, showed that the size of the adrenal glands decreased following antifungal therapy and became normal without any abnormal findings, including calcifications, 6 months after starting treatment ().",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [24, 'years'], 'weight': [51.0, 'kg'], 'Sodium': [130.0, 'mEq/L']}",-2.18571,-2.07642,-2.295,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 24 years old. The patient's is a Male.
The patient's age is between 18 and 64 and so the patient is an adult. For adult male's the total body water percentage value is 0.60.
The patient's weight is 51.0 kg. The concentration of sodium is 130.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 130.0 mEq. To convert from 130.0 mEq to mmol, convert from mEq to mmol. The compound 130.0 has a valence of 1, and so divide the valence by the value of mEq to get, 130.0 mEq/(1 mEq/mmol) = 130.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mEq sodium/L converts to 130.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 51.0 * (130.0/140 - 1) = -2.18571 L. The patient's free body water deficit is -2.18571 L."
6177,38,Free Water Deficit,lab test,decimal,pmc-2647935-1,Extracted,"The patient was a 20-day-old Spanish male infant with a body weight of 2.5 kg, transferred from the neonatal unit on the ninth day after the surgical correction of Fallot's tetralogy and pulmonary atresia. On admission to the pediatric intensive care unit, the infant required mechanical ventilation, an infusion of vasoactive drugs (dopamine 6 mcg/kg/minute, dobutamine 10 mcg/kg/minute and milrinone 0.5 mcg/kg/minute) and furosemide in a continuous infusion of 0.4 mg/kg/hour. The patient had received treatment with vancomycin and amikacin up to 2 days earlier. On examination, there was marked generalized edema. The initial blood tests revealed a creatinine level of 0.5 mg/dL, urea 75 mg/dL, albumin 2.8 g/dL, sodium 132 mmol/L, potassium 4.6 mmol/L and chloride 96 mmol/L. In order to decrease the doses of intravenous vasoactive drugs, it was decided to administer digitalis to the patient, prescribing a dose of digoxin of 10 mcg/kg enterally. Four hours after the administration of the drug, the child presented with progressive oliguria, with a fall in diuresis from 4 to 1.5 mL/kg/hour, and with no change in the hemodynamic situation (blood pressure 65/40 mmHg, lactate 1.1 mmol/L, heart rate 140 bpm). Blood tests revealed a rise in creatinine to 0.7 mg/dL and in urea to 89 mg/dL and a fall in sodium to 121 mmol/L. There were no neurological clinical symptoms or alterations in the cerebral echography that suggested cerebral edema. The urinalysis was normal. Initially, to exclude hypovolemia, volume expansion was performed with 5% albumin (20 mL/kg). Intravenous sodium replacement was started according to the equation (135 - 121) × 0.6 × weight (kg) in 24 hours and the dose of dopamine was increased from 7.5 to 15 mcg/kg/minute in order to raise the mean blood pressure and improve renal perfusion. Subsequently, on persistence of the oliguria, the infusion of furosemide was increased from 0.4 to 1 mg/kg/hour, though no improvement in the diuresis was achieved. The medication chart was reviewed and the error was detected. Instead of digoxin, indomethacin had been prescribed at a dose of 25 mg (10 mg/kg), which is 50 to 100 times higher than the therapeutic dose.
Initially, it was decided to maintain a conservative approach. The child remained hemodynamically stable but presented with anuria and an increase in edema; continuous venovenous hemofiltration was therefore started after 12 hours. This therapy was continued for 33 hours, with a negative balance of 25 mL/hour, after which diuresis and renal function recovered (Table ). The subsequent course was favorable and the infant was discharged from the pediatric intensive care unit with a creatinine level of 0.2 mg/dL, urea 15 mg/dL and normal diuresis. No alteration of renal function has been detected on subsequent follow-up.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'age': [20, 'days'], 'weight': [2.5, 'kg'], 'Sodium': [121.0, 'mmol/L']}",-0.20357,-0.19339,-0.21375,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 20 days old. This means the patient is 0 years old.
The patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 2.5 kg. The concentration of sodium is 121.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 2.5 * (121.0/140 - 1) = -0.20357 L. The patient's free body water deficit is -0.20357 L."
6178,38,Free Water Deficit,lab test,decimal,pmc-5903093-1,Extracted,"A 59-year-old Japanese woman was admitted to our hospital for evaluation of muscle weakness. Hypertension had been detected at the age of 30 years. When she was 47, ADPKD was diagnosed because computed tomography showed polycystic kidneys and her father had this disease. At 53 years, primary aldosteronism was diagnosed after detection of hypokalemia and a left adrenal tumor. Spironolactone was administered. An angiotensin II receptor blocker (ARB; olmesartan at 40 mg/day) was added to treat hypertension, after which her blood pressure and serum potassium level were normalized despite discontinuation of spironolactone (Table ). At 58 years, tolvaptan therapy was started at 60 mg/day (morning and afternoon doses of 45 and 15 mg) to treat her renal disease (Table ; Fig. ). Hypertension became more severe after the initiation of tolvaptan. Although the dual action beta blocker/alpha-1 blocker carvedilol (15 mg/day), calcium channel blocker cilnidipine (20 mg/day), and ARB telmisartan (40 mg/day) were added, her hypertension was not controlled. Eight months after starting tolvaptan, muscle weakness and numbness of the lower limbs became problematic. At 12 months, she was admitted to our hospital.
On admission, the patient was 152 cm tall, weighed 61 kg, and had a blood pressure of 182/84 mm Hg. Laboratory tests revealed that serum creatinine was 1.1 mg/dL (eGFR: 39.7 mL/min/1.73 m2), urea nitrogen was 24 mg/dL, Na was 144 mmol/L, K was 2.5 mmol/L, and Cl was 99 mmol/L. Renin activity was < 0.2 ng/mL/h (normal: 0.3–2.3), and the aldosterone concentration was 130 ng/dL (normal: 3.0–15.0). Urinary K excretion was 65 mmol/day, Na excretion was 130 mmol/day, and Cl excretion was 120 mmol/day (Table ).
Before admission, hypokalemia was exacerbated after starting tolvaptan therapy, and her hypertension became refractory (Fig. ). The patient hoped to continue tolvaptan use. Therefore, a potassium supplement was administered, but her serum potassium only increased to 3.5 mmol/L. Tolvaptan was discontinued temporarily, and serum potassium increased to 4.0 mmol/L. Next, tolvaptan (60 mg/day) and spironolactone (50 mg/day) were administered concomitantly, but the serum potassium level dropped to 3.0 mmol/L. Subsequently, tolvaptan was tapered to a daily dose of 30 mg, and spironolactone was increased to a daily dose of 100 mg. Thereafter, serum potassium remained above 4.0 mmol/L, and control of the blood pressure improved.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [59, 'years'], 'weight': [61.0, 'kg'], 'Sodium': [144.0, 'mmol/L']}",0.87143,0.82786,0.915,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 59 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 61.0 kg. The concentration of sodium is 144.0 mmol/L. Plugging in these values into the equation, we get 0.5 * 61.0 * (144.0/140 - 1) = 0.87143 L. The patient's free body water deficit is 0.87143 L."
6179,38,Free Water Deficit,lab test,decimal,pmc-7714909-3,Extracted,"An 8-year-old girl attended the hospital reporting cyanosis on the lips and unconsciousness after exertion. The patient, who had rales on auscultation, was admitted with the diagnosis of pneumonia, and antibiotic therapy was commenced. She began on NIV for hypercarbia and this was followed by intubation and mechanical ventilation. Hyponatremia and liver dysfunction were present in her laboratory tests. Pulmonary hypertension was detected in her echocardiography. She was admitted to our PICU after 4 days of hospitalization where a further assessment was undertaken.
She was born at term with adequate birth weight and length. There was no consanguinity between parents and she had three healthy siblings. She had rapid weight gain with uncontrollable eating, starting at 5 years of age. For the past 1 month, her mother noticed that she was holding her breath asleep. She had excessive sweating. During hospitalization, we noticed that she did not complain or cry when she underwent needle phlebotomy. Her weight was 50 kg (+3.52 SDS), and her height was 135 cm (+1.43 SDS) with a body mass index (BMI) 27.4 kg/m2 (+3.44 SDS).
Laboratory evaluation revealed sodium (Na), 155 mmol/L [normal range (NR): 135–145 mmol/L]; aspartate transaminase, 315 U/L (NR: 8–45 U/L); alanine aminotransferase, 798 U/L (NR: 7–55 U/L); and urine density, 1,021. The remaining biochemical studies of blood were normal. As the patient had no polydipsia, hypernatremia was assumed to be due to insufficient intake. The hypernatremia was corrected (Na: 141 mmol/L) with intravenous fluid replacement therapy. No abnormal value was detected in her hormonal tests and pituitary MRI was normal. Diffusion restriction in white matter was detected in cranial MRI; therefore, cranial MRI spectroscopy was performed but no pathology was detected. Thoracic postural drainage was initiated in the patient due to widespread atelectasis on thorax CT. The patient was extubated after 24 h in the PICU and NIV treatment was initiated. She was discharged from the PICU 3 days later. The patient's CO2 retention continued during sleep when off NIV support, and she was therefore discharged using BPAP in ST mode (with IPAP: 15 CWP, EPAP: 7 CWP, back up respiratory rate of 15/min) during sleep. In the outpatient follow-up 1 month later, the patient was again diagnosed as having adipsic hypernatremia, which was treated with oral fluid support. She was referred to pediatric psychiatrist because the family expressed emotional lability in the patient.
Clinical, laboratory, and imaging findings at the time of diagnosis are presented also in , .",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'weight': [50.0, 'kg'], 'age': [8, 'years'], 'Sodium': [155.0, 'mmol/L']}",3.21429,3.05358,3.375,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 8 years old. The patient's is a Female.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 50.0 kg. The concentration of sodium is 155.0 mmol/L. Plugging in these values into the equation, we get 0.6 * 50.0 * (155.0/140 - 1) = 3.21429 L. The patient's free body water deficit is 3.21429 L."
6180,38,Free Water Deficit,lab test,decimal,pmc-3655504-1,Extracted,"A 77-year-old woman with a history of interstitial pneumonia and uveitis visited our institution complaining of general fatigue. Chest radiography revealed a mass in the upper lung fields (), and she was thus admitted for further examinations.
Her blood pressure was 130/71 mmHg, heart rate was 106 beats/min, body temperature was 36.8°C, and O2 saturation was 96% in room air. She had a history of smoking 15 cigarettes per day for 55 years but no history of alcohol consumption. On initial clinical examination, her weight was of 50.8 kg, height was 158 cm, body mass index was 20.3 kg/m2, and BSA was 150 m2. Mild anemia was revealed in the palpebral conjunctiva. No abnormal murmur could be heard on auscultation although dry rales were heard in both lungs.
Laboratory test results demonstrated a markedly elevated white blood cell count (266 × 102/μL; normal: 39–94 × 102/μL) with 81% neutrophils, mild anemia (red blood cell count: 322 × 104/μL; normal: 367–479 × 104/μL; hemoglobin: 9.8 mg/dL; normal: 11.5–14.9 mg/dL), elevated platelet count (56.9 × 104/μL; normal: 13–33 × 104/μL), mild renal dysfunction (serum creatinine: 0.96 mg/dL; normal: 0.47–0.79 mg/dL; serum urea nitrogen: 23.4 mg/dL; normal: 7–20 mg/dL), mild hyponatremia (133 mEq/mL; normal: 137–146 mEq/mL), mild hypercalcium (11.4 mg/mL; normal: 8.4–10 mg/dL), and markedly elevated C-reactive protein level (14.0 mg/dL; normal: 0–0.3 mg/dL). The tumor marker squamous cell carcinoma antigen was also elevated (5.5 ng/mL; normal: 0–1.5 ng/mL).
Chest computed tomography (CT) revealed interstitial shadows in both lungs. Chest CT also showed a 5.2 cm irregular mass with cavity and speculated margin in the right S3 as well as a 7.6 cm irregular mass with cavity and air bronchogram sign, which were adjacent to the pleural walls (Figures and ). A few nodules were found in the right lung. Left hilar and subcarinal lymph nodes were swollen. The pathological findings for an endoscopic biopsy specimen revealed squamous cell carcinoma (Figures and ). Abdominal CT and brain magnetic imaging showed no lesion suggestive of metastasis. Radiographic findings confirmed T4N3M0 lung cancer of stage IIIB.
After admission (), high-grade fever developed and laboratory tests revealed sustained elevated white blood cell counts and C-reactive protein level. Therefore, the cooccurrence of a respiratory tract infection was suspected. The administration of antibiotics was initiated (sulbactam/ampicillin at 3.0 g/day for 6 days, and, subsequently, pazufloxacin at 1000 mg/day for 4 days). However, the elevated inflammatory marker levels and high-grade fever were not resolved. After administering nonsteroidal anti-inflammatory drugs (loxoprofen sodium hydrate at 180 mg/day), her temperature returned to normal.
The cause of fever and elevated inflammatory reaction levels was suspected as cytokine production by tumor cells. Therefore, serum G-CSF and IL-6 levels were measured, which showed that both serum G-CSF (117 pg/mL; normal: <57.5 pg/mL) and IL-6 (83.5 pg/mL; normal: <2.41 pg/mL) levels were high. Immunohistochemical examination of biopsy specimens showed positive staining with anti-G-CSF monoclonal and anti-IL-6 monoclonal antibodies (Figures and ). Therefore, diagnosis of G-CSF- and IL-6-producing tumor was established.
Although surgical treatment was considered, it was not indicated because her respiratory function was poor because of interstitial pneumonia. Chemotherapy was recommended, but she declined. Therefore, she was administered best supportive therapy. She was discharged 19 days after her admission, after which she visited our institution regularly. However, she was transferred by ambulance because of dyspnea, and she died of hypoxemia due to interstitial pneumonia exacerbation two months after diagnosis of lung cancer.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'age': [77, 'years'], 'weight': [50.8, 'kg'], 'Sodium': [133.0, 'mEq/L']}",-1.143,-1.08585,-1.20015,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 77 years old. The patient's is a Female.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly female's, the total body water percentage value is 0.45.
The patient's weight is 50.8 kg. The concentration of sodium is 133.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 133.0 mEq. To convert from 133.0 mEq to mmol, convert from mEq to mmol. The compound 133.0 has a valence of 1, and so divide the valence by the value of mEq to get, 133.0 mEq/(1 mEq/mmol) = 133.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mEq sodium/L converts to 133.0 mmol sodium/L. Plugging in these values into the equation, we get 0.45 * 50.8 * (133.0/140 - 1) = -1.143 L. The patient's free body water deficit is -1.143 L."
6181,38,Free Water Deficit,lab test,decimal,pmc-6240427-1,Extracted,"A 67-year-old Japanese man with a past medical history of hypertension, diabetes mellitus, and angina presented with a history of generalized weakness, lethargy, cold intolerance, weight loss, and loss of appetite. The patient was a smoker who had been smoking a half-pack per day for 47 years. His family history was unremarkable.
One and one-half months prior to admission, the patient had symptoms of lethargy and anorexia, with a 7-kg weight loss in only 1 month. On the admission day, he could not move because of overall weakness and lethargy and was transferred to our hospital. He was conscious and oriented, and his blood pressure was low (104/70 mmHg) compared with his previous hypertension. His blood glucose on arrival was low (64 mg/dl). His body temperature was 35.8 °C, heart rate (HR) was 60 beats/min, and respiratory rate was 20 breaths/min. No conjunctival pallor or thyromegaly was appreciated. Cardiac and pulmonary examination results were normal, other than a positive tilt test. His neurological examination revealed that his higher cognitive functions were normal, as were the cranial pairs, with no visual defect.
Laboratory studies revealed that the patient’s complete blood count and coagulation were normal. Biochemistry tests revealed a sodium level of 134 mEq/L (reference range, 135–147) and hypoglycemia, but the other electrolytes were within normal limits. Notably, the level of thyroid-stimulating hormone (TSH) was 0.505 μIU/ml (reference range, 0.38–4.31), that of free thyroxine (FT4) was 0.61 ng/dl (reference range, 0.82–1.63), and that of free triiodothyronine was 1.67 ng/dl (reference range, 2.17–3.34) (see Table ). An electrocardiogram showed a sinus bradycardiac rhythm (HR, 53 beats/min) with no conduction or repolarization abnormalities. The echocardiogram revealed no abnormalities. We suspected hypopituitarism based on the patient’s hypoglycemia, hypotension, nonelevated TSH, and low FT4, and also based on the results of head computed tomography (CT) and magnetic resonance imaging (MRI).
CT of the head demonstrated a high-density area in the pituitary-hypothalamic axis, which suggested a hemorrhagic lesion (Fig. ). Subsequently, MRI of the brain was performed, revealing multiple masses (Fig. a, b) and a 10-mm mass on the recessus infundibulum in T2 star-weighted sequences, which were also consistent with hemorrhagic masses (Fig. c, d). In addition, a chest x-ray revealed a left hilar mass (Fig. ). We also noted a suspicious shadow in the left lung hilum shown in the chest radiograph. Subsequently, CT of the thorax revealed a mass in the left hilum (Fig. ), which was confirmed on biopsy by bronchoscopy later. There were no emphysematous changes on the chest CT scan, but some mediastinal lymphadenopathies were detected.
After the patient’s admission, we first performed a hormone loading test on day 4. The results of the hormone profile at baseline were as follows: TSH 0.586 μIU/ml, follicle-stimulating hormone (FSH) 0.7 mIU/ml (reference range, 2–8.3), luteinizing hormone (LH) < 0.1 mIU/ml (reference range, 1.2–7.1), prolactin 37.9 ng/ml (reference range, 3.6–12.8), testosterone < 4.3 ng/dl (reference range, 142.4–923.1), adrenocorticotropic hormone (ACTH) 5.6 pg/ml (reference range, 7.2–63.3), and cortisol 0.2 μg/dl (reference range, 4.5–21.1). The results showed a TSH response to thyrotropin-releasing hormone: serum TSH 4.526 μIU/ml at 30 min and 4.591 μIU/ml at 60 min. We demonstrated an adequate cortisol and ACTH response to corticotropin-releasing hormone: serum cortisol was 5.6 μg/ dl at 60 min and had a peak of 5.7 μg/ dl at 90 min, whereas serum ACTH showed a peak of 106.3 pg/ml at 30 min, 84.0 pg/ml at 60 min, and 62.4 pg/ml at 90 min. It also showed a delayed LH and FSH response to LH-releasing hormone: serum LH showed a value of 0.8 mIU/ml at 30 min, 1.1 mIU/ml at 60 min, and peak of 1.3 mIU/ml at 90 min, whereas serum FSH was 1.5 mIU/ml at 30 min, 1.8 mIU/ml at 60 min, and peak of 2.1 mIU/ml at 90 min (Fig. a). Those results suggested hypothalamic pan-hypopituitarism.
Tumor markers demonstrated elevated pro-gastrin-releasing peptide with a value of 678 pg/ml (reference range, 0–80.0) and neuron-specific enolase 18.6 ng/ml (reference range, 0–12), which are typical markers for small cell lung cancer. We performed lung biopsy by bronchoscopy. Endobronchial ultrasound of bronchoscopy was used, and transbronchial lung biopsies were performed. The pathological results eventually revealed a small cell lung cancer (Fig. ).
We made a diagnosis of pan-hypopituitarism secondary to suprasellar metastases from a small cell lung cancer and first initiated hormone replacement therapy with hydrocortisone and levothyroxine. Right after the replacement therapy, the symptoms of lethargy, loss of appetite, and hypotension were improved. There was no evidence of diabetes insipidus during those therapies. The patient’s clinical stage was stage IV (cT3N2M1b), and his performance status was 0 to 1; thus, he was treated with adjuvant cranial radiotherapy on day 24 and chemotherapy with cisplatin and etoposide on day 45. We reevaluated the hormone loading test on day 59 after admission, which revealed an improvement in ACTH and cortisol secretions (Fig. ). We also performed a brain MRI in T2 star-weighted sequences again on day 62, which demonstrated disappearance of the suprasellar tumor (Fig. e, f). The patient was subsequently treated with four cycles of chemotherapy, but he died 10 months later due to the progression of the lung cancer. An autopsy was not performed, because the patient’s family denied permission.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'weight': [7.0, 'kg'], 'age': [67, 'years'], 'Sodium': [134.0, 'mEq/L']}",-0.15,-0.1425,-0.1575,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 67 years old. The patient's is a Male.
The patient's age is greater than 64 years and so the patient is considered elderly. For elderly male's, the total body water percentage value is 0.50.
The patient's weight is 7.0 kg. The concentration of sodium is 134.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 134.0 mEq. To convert from 134.0 mEq to mmol, convert from mEq to mmol. The compound 134.0 has a valence of 1, and so divide the valence by the value of mEq to get, 134.0 mEq/(1 mEq/mmol) = 134.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mEq sodium/L converts to 134.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 7.0 * (134.0/140 - 1) = -0.15 L. The patient's free body water deficit is -0.15 L."
6182,38,Free Water Deficit,lab test,decimal,pmc-2816905-1,Extracted,"A 21-month-old boy had an operation for syndactyly of both hands at 6 months after the birth, and then underwent cranial vault remodeling due to craniosynostosis with a chief complaint of trigonocephaly in the Department of Plastic Surgery. The patient developed postoperative polyuria and hypotension, and his general condition was exacerbated after two postoperative days. The patient urinated 50-60 mL/hr (1,510 mL/24 hr) on the first postoperative day, and revealed 3-4 cmH2O of central venous pressure, 136 mL of blood loss through a suction drain, and 90/60 mmHg of blood pressure. After the third postoperative day, polyuria was developed with a change of urination to over 80 mL/hr (1,965 mL/24 hr), and the blood pressure and central venous pressure (CVP) decreased to 70/30 mmHg and to 1-3 cm H2O of CVP, respectively, which was associated with blood loss (52 mL) through the surgical drain. From the sixth postoperative day, the amount of the urine reduced to 70 mL/hr (1,730 mL/24 hr) and the blood pressure was maintained within the normal range at 100/50 mmHg because there was no more blood loss. Since then, the amount of urine was gradually decreased and finally stabilized at 30-40 mL/hr from the twelfth postoperative day.
At admission to the hospital, the patient was 12.6 kg (50-75 percentile) in weight and 85 cm (50-75 percentile) in height. The temperature was measured at 36.5℃, the pulse was at 100/min, and the respiration was at 25/min. The blood pressure was 100/60 mmHg. The patient had a clear consciousness, a little pale conjunctivae, and anicteric sclera. No cervical lymph node was palpated, and the thorax was symmetrically expanded without showing sunken thorax. We could not find any abdominal abnormalities but detected operational scars in both hands. There was not neurological abnormality.
Preoperatively microcytic anemia was observed with hemoglobin 9.7 g/dL, hematocrit 29.5%, and MCV 61.9 fL. Serum electrolyte levels were sodium (Na+) 138 mEq/L, potassium (K+) 4.5 mEq/L, and chloride (Cl-) 107 mEq/L, and urine specific gravity was 1.015. Postoperative data of electrolytes and osmolarity of serum and urine are shown in . Preoperative levels of ADH and atrial natriuretic peptide (ANP) were 4 pg/mL and 19 pg/mL (<40 pg/mL), respectively. The ANP and human brain natriuretic peptide (HBNP) were 89 pg/mL and 68.7 pg/mL (<100 pg/mL) on the first postoperative day, respectively. On the fifth and ninth postoperative day ADH was 1.29 pg/mL and 3.68 pg/mL, ANP 65 pg/mL and 51 pg/mL, and HBNP 13.8 pg/mL and 31.9 pg/mL, respectively.
The infant was diagnosed as having CSW syndrome that developed after cranial vault remodeling, and was supplied with water and sodium through intravenous normal saline administration from the early stage. The amount of urine was decreased from the sixth postoperative day, and the sodium level was stabilized. The infant currently shows normal in growth and development, weight gain, serum electrolytes, and urine osmolarity.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Male', 'weight': [12.6, 'kg'], 'age': [21, 'months'], 'Sodium': [138.0, 'mEq/L']}",-0.108,-0.1026,-0.1134,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
This means that the patient is 1 year and 9 oldThe patient's is a Male.
The patient is less than 18 years old and so the patient is a child. This means total body water percentage value is 0.6.
The patient's weight is 12.6 kg. The concentration of sodium is 138.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 138.0 mEq. To convert from 138.0 mEq to mmol, convert from mEq to mmol. The compound 138.0 has a valence of 1, and so divide the valence by the value of mEq to get, 138.0 mEq/(1 mEq/mmol) = 138.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mEq sodium/L converts to 138.0 mmol sodium/L. Plugging in these values into the equation, we get 0.6 * 12.6 * (138.0/140 - 1) = -0.108 L. The patient's free body water deficit is -0.108 L."
6183,38,Free Water Deficit,lab test,decimal,pmc-3391843-1,Extracted,"A 40-year-old (45-kg weight) previously healthy woman was admitted to the intensive burn care unit approximately 90 min after an assault chemical burn following conjugal violence. The total burned surface area was estimated at 35% (neck, face, head, arms, thorax, abdomen, and left leg), third degree []. There were severe bilateral eyes and ears lesions. Injury was due to sulfuric acid (battery acid, pH measured at 0.9). As the patient and relatives were in panic, irrigation with water was not performed at the scene of the accident but was started immediately after the arrival in the burn center. The emergency medical team began fluid resuscitation (Parkland's formula), and orotracheal intubation was performed on-site after evidence of the severity of facial burns. The patient was sedated for hospital transfer and presented the following vital signs: arterial blood pressure 70/30 mmHg, pulse 110 bpm, SpO2 >90% with normal lung auscultation.
The admission electrocardiogram and chest X-ray examination did not reveal significant abnormalities. Laboratory investigations mainly revealed a profound metabolic acidosis with a pH at 6.92, PaCO2 42 mmHg, total bicarbonate 8.6 mEq/l, base deficit 23.4 mEq/l, sodium 148 mEq/l, potassium 4.1 mEq/l, chloride 117 mEq/l, calcium 6.1 mg/dl, and phosphorus 15.1 mg/dl. The lactate level was within the normal range: 1.7 mmol/L. Renal function was initially preserved (serum creatinine 0.83 mg/dl), with no evidence for rhabdomyolysis. Blood coagulation tests on admission were disturbed, with fibrinogen 117 mg/dl, activated partial thromboplastin time (APTT) 69 s, and International Normalized Ratio (INR) 2.23. Platelets count was 169 000/mm3. Metabolic acidosis was progressively corrected by the administration of a total of 300 mmol of sodium bicarbonate over 14 h and of 140 mmol of lactate from Hartmann's solution over the first 24 h . The adjustment of the ventilator settings was complicated by the progressive development of a thoracic rigidity secondary to the chemical burns.
During the ICU stay, the patient developed several complications. Mechanical ventilation was required for 40 days, and a percutaneous tracheostomy had been performed after 1 month. The hemodynamic condition required mild inotropic support (maximal dose of dobutamine, 5 μg/kg/min) for a period of 15 days. Echocardiography demonstrated a moderate alteration of the left ventricular function. While urine output was maintained during the first week, continuous venovenous hemofiltration had to be started after this interval and was continued for 7 weeks. The patients also developed multiple episodes of wound-related sepsis treated by adapted antimicrobial therapy. In addition, iterative surgery was required with a total of 15 procedures for excision and grafting. After 5 months, the patient left the intensive care unit for rehabilitation.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'weight': [45.0, 'kg'], 'age': [40, 'years'], 'Sodium': [148.0, 'mEq/L']}",1.28571,1.22142,1.35,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 40 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 45.0 kg. The concentration of sodium is 148.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 148.0 mEq. To convert from 148.0 mEq to mmol, convert from mEq to mmol. The compound 148.0 has a valence of 1, and so divide the valence by the value of mEq to get, 148.0 mEq/(1 mEq/mmol) = 148.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 148.0 mEq sodium/L converts to 148.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 45.0 * (148.0/140 - 1) = 1.28571 L. The patient's free body water deficit is 1.28571 L."
6184,38,Free Water Deficit,lab test,decimal,usmle-3434,Extracted,"A 48-year-old woman comes to the physician for the evaluation of 24-hour blood pressure monitoring results. Over the last 3 months, she has had intermittent nausea, decreased appetite, and increasing weakness and fatigue during the day. She has been treated twice for kidney stones within the past year. Her current medications include lisinopril, amlodipine, and furosemide. She is 178 cm (5 ft 10 in) tall and weighs 97 kg (214 lb); BMI is 31 kg/m2. Her blood pressure is 152/98 mm Hg. Physical examination shows no abnormalities. Serum studies show:
Na+ 141 mEq/L
Cl− 101 mEq/L
K+ 4.5 mEq/L
HCO3− 24 mEq/L
Calcium 12.9 mg/dL
Creatinine 1.0 mg/dL
Twenty-four-hour blood pressure monitoring indicates elevated nocturnal blood pressure.",What is the patient's free water deficit in terms of kg? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'sex': 'Female', 'weight': [97.0, 'kg'], 'age': [48, 'years'], 'Sodium': [141.0, 'mEq/L']}",0.34643,0.32911,0.36375,"The formula for computing the free water deficit is (total body water percentage) * (weight) * (sodium/140 - 1), where the total body water percentage is a percentage expressed as a decimal, weight is in kg, and the sodium concentration is in mmol/L.
The total body water percentage is based on the patient's age and gender.
Adult male: 60% (i.e., use 0.6 in the equation)
Adult female: 50% (0.5)
Elderly male: 50% (0.5)
Elderly female: 45% (0.45)
Child: 60% (0.6)
The patient is 48 years old. The patient's is a Female.
The patient's age is between 18 and 64 and so the patient is an adult. For adult female's the total body water percentage value is 0.50.
The patient's weight is 97.0 kg. The concentration of sodium is 141.0 mEq/L. We need to convert the concentration to mmol/L. Let's first convert the mass of sodium from mEq to mmol. The mass of sodium is 141.0 mEq. To convert from 141.0 mEq to mmol, convert from mEq to mmol. The compound 141.0 has a valence of 1, and so divide the valence by the value of mEq to get, 141.0 mEq/(1 mEq/mmol) = 141.0 mmol sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mEq sodium/L converts to 141.0 mmol sodium/L. Plugging in these values into the equation, we get 0.5 * 97.0 * (141.0/140 - 1) = 0.34643 L. The patient's free body water deficit is 0.34643 L."
6185,39,Anion Gap,lab test,decimal,pmc-3986739-1,Extracted,"A ten-year-old girl was admitted to our hospital with complaints of cough, fever, vomiting, weakness and lack of appetite. She also suffered from alopecia and persistent/recurring respiratory infections. Both parents were reported to be healthy and they were consanguineous (first cousins). Their four children except for our patient were healthy.
Physical examination of the patient revealed normal vital signs. The percentiles of her weight and height were between the 3rd and 10th percentiles. She had pale skin, total alopecia and pitting in the nails of her hands and feet (). A crackling sound was heard during inspiration. Her puberty was stage I according to Tanner stages.
Her hematology results revealed a hemoglobin level of 7.0 g/dL, hematocrit 19.9%, white blood cells 13200/mm3, platelets 35000/mm3, MCV 84fL and reticulocytes of 8.14%, as well as negative direct Coombs test result. Blood smear showed schistocytes (). Her biochemical investigation revealed: urea 142 mg/dL, creatinine 4.61 mg/dL, AST 97 U/L, ALT 79 U/L, LDH 2218 U/L, total bilirubin 1.5 mg/dL, direct bilirubin 0.55 mg/dL, sodium 134 mmol/L, potassium 5.9 mmol/L, chloride 109 mmol/L, calcium 8.7 mg/dL, phosphorus 4.0 mg/dL, uric acid 8.0 mg/dL, ph 7.44, HCO3- 21 mmol/L and glucose 76 mg/dL. The urinalysis showed the following: pH 7.5, density 1010, protein (++), erythrocytes (+++), leucocytes (-) and dysmorphic erythrocytes in the urinary sediment.
Based on these biochemical and urinary abnormalities, the patient was diagnosed as HUS. After seven plasma exchange sessions, the hemolysis finally stopped and the laboratory abnormalities and renal function reverted to normal. The respiratory infection was treated with appropriate antibiotic regimens.
In the hormonal evaluation, free thyroxine (fT4) was 1.11 ng/dL (0.8-2.2), thyroid-stimulating hormone (TSH) 3.028 mU/mL (0.6-5.5), anti-peroxidase (anti-TPO) antibody 62 IU/ mL (<20), anti-thyroglobulin (anti-TG) antibody 65 IU/mL (<4.0), cortisol 25.5 mg/dL (3-21), adrenocorticotropic hormone (ACTH) 28.1 pg/mL (10-60), estradiol 14 ng/dL (0.2.0), follicle-stimulating hormone (FSH) 0.32 mIU/mL, luteinizing hormone (LH) 0.07 mIU/mL (0.02-0.3), anti-pancreatic islets antibody 1/100 (<1/10), parathyroid hormone (PTH) 65.9 ng/mL (10-65), renin 72 ng/L (5-35), aldosterone 248 pg/mL (20-300), vitamin B12 456 pg/mL (150-883) and folic acid 4.2 ng/mL (3.1-20.5) before plasma exchange therapy. Although thyroid ultrasonography was normal and the patient was not on Na-L-T4 treatment, both anti-TPO antibody and anti-TG antibody tests were positive. These findings suggested early diagnosed autoimmune thyroiditis. Cortisol response to ACTH stimulation test (1 μg ACTH) was as follows: initial 1 mg/dL, 30th minute 8.1 mg/dL, 60th minute 11.2 mcg/dL, 90th minute 14.1 mg/dL, and 120th 14.7 mg/dL. The cut-off level of this test was 14 mg/dL (9). These results were interpreted as a normal response to ACTH stimulation test and indicated that there was no adrenal insufficiency. In immunological evaluation, IgA was 24 mg/dL (29-384), IgM 24 mg/dL (50-278), IgG 464 mg/dL (625-1579), IgE 464 IU/mL (0-170), C3 90 mg/dL (90-180), C4 26 mg/dL (10-40), anti-nuclear antibody (ANA) (-), anti-double strain DNA antibody (-), p-ANCA (-), c-ANCA (-) and anti-HBs (-) before plasma exchange therapy. Lymphocyte subsets were CD3 78% (55-78), CD19 2% (10-31), CD4 39% (27-53) and CD8 51% (19-34). The complement factor H gene region was proliferated by PCR method. Sequences which have single nucleotide polymorphism on complement factor H have been determined. CT homozygote polymorphism for His402Tyr was detected. This factor is considered to be a risk factor for development of HUS (). In radiological evaluation, pulmonary X-ray showed bilateral diffuse infiltration and abdominal ultrasonography was normal except for hepatomegaly and grade I increase in renal echogenicity.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [109.0, 'mmol/L'], 'Bicarbonate': [21.0, 'mmol/L'], 'Sodium': [134.0, 'mmol/L']}",4,3.8,4.2,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 134.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 134.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 134.0 mmol * 1 mEq/mmol = 134.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mmol sodium/L converts to 134.0 mEq sodium/L. 
The concentration of chloride is 109.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 109.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 109.0 mmol * 1 mEq/mmol = 109.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 109.0 mmol chloride/L converts to 109.0 mEq chloride/L. 
The concentration of bicarbonate is 21.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 21.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 21.0 mmol * 1 mEq/mmol = 21.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 21.0 mmol bicarbonate/L converts to 21.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 134.0 mEq/L - (109.0 mEq/L + 21.0 mEq/L) = 4.0 mEq/L. Hence, The patient's anion gap is 4.0 mEq/L."
6186,39,Anion Gap,lab test,decimal,pmc-7377651-2,Extracted,"An 11-year-old boy brought to the ED with a history of sudden onset of bright red urine at the end of micturition (terminal hematuria) with small blood clots that started three hours prior to his presentation. He had associated painful micturition and urgency. There was no history of fever, flank pain, vomiting, trauma, body edema, or ingestion of medications or any type of red-colored food. Two weeks prior to his presentation, he had diarrheal illness without blood in his stool, which resolved spontaneously. He sought medical advice at that time, but no stool culture was taken. When he presented with blood in his urine, he had no current diarrhea. The child is an otherwise healthy boy with no history of recurrent urine or other body site infections in the past. He had no previous history of gross hematuria. No petechia, ecchymosis, or bleeding from other orifices. He underwent a routine circumcision as a neonate. His growth and development are appropriate for his age. There is no family history of hematuria, kidney or urological disorders, malignancy, bleeding, nor immunodeficiency disorders.
On examination, he looked well and hydrated. His body temperature was 36.8 °C, respiratory rate was 20 breaths/minute, heart rate was 76 beats/minute, and his blood pressure was 103/60 mmHg. He was not in pain. He had no edema or skin rash, and his abdomen was soft with no distension, tenderness, or organomegaly. Local examination revealed normal male genitalia with no local signs of infection or inflammation.
Urine analysis showed cloudy urine with a light orange color and urine pH of 8.5, specific gravity of 1.017, negative for glucose, negative for ketones, +3 blood, leukocyte esterase 500, negative nitrite, and +3 protein. Urine microscopy showed >30 red blood cells per high power field, five to 10 white blood cells per high power field.
His initial blood work showed prothrombin time was 12.3 seconds, partial thrombin time was 30.3 seconds, international normalized ratio of 1.03, white blood cell count of 9.8 x 109/L with cell differential count of neutrophils 7.35 x 109/L. His lymphocyte level was 1.60 x 109/L, eosinophils were 0.04 x 109/L, basophils were 0.03 x 109/L, and monocytes were 0.70 x 109/L. Blood chemistry showed serum sodium levels at 137 mmol/L, potassium at 4.1 mmol/L, chloride at 105 mmol/L, HCO3 at 23 mmol/L, blood urea nitrogen at 3.5 mmol/L, and creatinine at 52 μmol/L. The rest of the blood work showed a hemoglobin level of 148 g/L, platelet count of 356 x 109/L, and blood glucose levels of 105 mmol/L.
A midstream urine sample was collected two different times, and both samples were sent for culture before starting antibiotics. Both cultures were incubated and grew more than 100,000 colony forming units per ml of Gram-negative bacteria. Afterward, the identification and susceptibility test showed Salmonella Nontyphi species. It was sensitive to ampicillin, ceftriaxone, ciprofloxacin, and trimethoprim-sulfamethoxazole. No further serotype identification was made due to a lack of test kit availability.
Renal ultrasound showed a urinary bladder wall thickness of 0.3 cm in a full bladder with luminal mobile echogenic foci at 2 cm x 1.3 cm. Otherwise, both kidneys were healthy in size, echogenicity, and corticomedullary differentiation with no hydronephrosis or ureteronephrosis (Figure ).
The patient was admitted to the hospital and was started empirically on intravenous amoxicillin/clavulanic acid, which was continued for four days until the final urine culture result was assessed. Then, the patient was discharged home to complete three more days on the same antibiotic.
The patient was seen one month after discharge for follow-up; he was doing well with no gross hematuria episodes and no microscopic hematuria in urine analysis. The urology team saw him, and the plan was to consider cystoscopy if he became symptomatic again with another UTI. He was last seen seven months after the treatment of Salmonella UTI, and he was doing well with no recurrence of infection in the urinary tract.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [137.0, 'mmol/L'], 'Chloride': [105.0, 'mmol/L'], 'Bicarbonate': [23.0, 'mmol/L']}",9,8.55,9.45,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 137.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 137.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 137.0 mmol * 1 mEq/mmol = 137.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mmol sodium/L converts to 137.0 mEq sodium/L. 
The concentration of chloride is 105.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 105.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 105.0 mmol * 1 mEq/mmol = 105.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 105.0 mmol chloride/L converts to 105.0 mEq chloride/L. 
The concentration of bicarbonate is 23.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 23.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 23.0 mmol * 1 mEq/mmol = 23.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 23.0 mmol bicarbonate/L converts to 23.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 137.0 mEq/L - (105.0 mEq/L + 23.0 mEq/L) = 9.0 mEq/L. Hence, The patient's anion gap is 9.0 mEq/L."
6187,39,Anion Gap,lab test,decimal,pmc-6506427-1,Extracted,"A previously healthy 23-month-old boy presented to our hospital with a 2-day history of fever, postprandial diffuse abdominal pain, and non-bilious vomiting (>5 episodes/day) that began 1 day before admission. After admission, the patient developed a watery diarrhea. In addition to food refusal, he was observed to produce lesser urine than usual upon void review. His medical and birth history were unremarkable (he was not administered any medications, he had no known allergies, and his immunizations were up to date). His family medical history was unremarkable, and he had no travel history at that time.
Upon examination, the patient looked acutely ill and dehydrated. He was 90.2 cm (in the 75–85th percentile) tall and weighed 11.6 kg (in the 15–25th percentile). His abdomen was soft and flat with normoactive bowel sounds. Upon palpation of the abdomen the examination revealed the existence of a mild tenderness over the entire abdomen, without rebound tenderness or muscle guarding or rigidity. The rest of his physical examination was noted to be normal. The patient's vital signs showed a heart rate of 141 bpm, respiratory rate of 22 with a normal respiratory pattern, temperature of 38.6°C, and oxygen saturation at 98% on room air. He was observed to be mentally alert at the time of the examination. The initial laboratory tests revealed the following: white blood cells (WBCs) 6,500 cells/μL, hemoglobin (Hb) 13.2 g/dL, platelets 423,000/μL, C-reactive protein (CRP) 6.35 mg/dL, sodium 130 mmol/L, potassium 4.1 mmol/L, chloride 90 mmol/L, and total carbon dioxide 14.4 mmol/L. All other blood tests were within the reference range. His stool occult blood test was positive (748 ng/mL). It is noted that the tests for rotavirus and norovirus antigen were negative. An erect chest X-ray did not show pneumoperitoneum; however, an erect abdominal X-ray demonstrated abnormal dilatation of the small bowel loops with air-fluid levels suggestive of possible SBO (). The abdominal ultrasonography revealed mild wall thickening of the small bowel loops suggestive of acute enteritis, several enlarged lymph nodes in the right lower quadrant, and a normal-appearing proximal appendix (the tip of the appendix was not visualized), without any evidence of mechanical bowel obstruction such as an intussusception.
The patient was resuscitated using normal saline and received conservative management. At that time, cefotaxime was empirically administered intravenously. The following day, his condition rapidly deteriorated, and he developed a state of septic shock. Upon examination, the patient's vital signs now were: blood pressure (BP) 87/39 mmHg, heart rate 170 bpm, respiratory rate 56, temperature 38.1°C, and oxygen saturation 93% on room air. Our surgical team urgently came to the patient and performed physical examination; his abdomen was soft with mild tenderness and slight muscle guarding on palpation. They recommended continuing medical supportive care, but frequent physical examinations needed to be performed to detect subtle changes in the patient's signs and symptoms. The patient's laboratory tests were repeated and revealed: WBCs 5,300 cells/μL, Hb 9.7 g/dL, platelets 186,000/μL, CRP 28.96 mg/dL, sodium 129 mmol/L, potassium 3.7 mmol/L, chloride 95 mmol/L, and albumin 2.6 g/dL. Upon review, the coagulation tests revealed an abnormally prolonged prothrombin time at 21.5 seconds and an activated partial thromboplastin time at 56 seconds. The patient's venous blood gas analysis demonstrated metabolic acidosis: pH 7.28 and bicarbonate 15 mmol/L. Upon review, other blood tests remained within reference range. A plain abdominal X-ray was repeated and showed worsening of small bowel ileus. At that time, an urgent contrast-enhanced abdominal CT was performed in order to confirm the presence of a surgical abdomen. The imaging revealed diffuse dilatation of the large and small bowel loops (suggestive of paralytic ileus) with uniform enhancement of bowel wall and no lead point of bowel obstruction, mesenteric lymphadenitis, and mild ascites (). However, the radiologists were of the view that obstructive ileus could not be completely ruled out in this case. They did not find an abnormal appendix, but the condition of an acute appendicitis could not be excluded either. The patient was maintained on a nil per os status, and fluid resuscitation was continued. We tried rectal tube decompression, however, his condition did not show much improvement except the passage of small amount of rectal gas. He received albumin, packed red blood cells, and fresh frozen plasma intravenously. At that time, Metronidazole was additionally administered empirically, and his vital signs were closely monitored for any significant changes.
On the third hospital day, the patient became more lethargic despite medical therapy. His BP was observed to have normalized; however, it was noted that tachycardia and tachypnea persisted. On repeated physical examination, his abdomen now showed distention with hypoactive bowel sounds, however, muscle guarding or tenderness could not be clearly ascertained on palpation. The patient developed generalized edema and oliguria. Based on the patient's clinical condition, we decided to perform an urgent exploratory laparotomy at 44 hours after admission.
Upon opening the peritoneum, approximately 400 mL of ascitic fluid was drained. Next, a segment of markedly dilated and infarcted small bowel was identified 30 cm proximal to the ileocecal valve (). It is noted that the total length of the necrotic small bowel was approximately 60 cm. The omentum and the colon appeared to be intact. Upon review, the small bowel intussusception or volvulus was not identified. Even at laparotomy, our surgical team could not find the lead point of bowel obstruction. The appendix appeared unremarkable macroscopically. In this case, after decompression of the bowel following an incision on an infarcted small bowel segment, 110 cm of the distal small bowel containing the necrotic segment was resected and end-to-end small bowel anastomosis was performed in addition to a prophylactic appendectomy.
Histopathological examination of the surgical specimen revealed multiple areas of mucosal necrosis with diffuse congestion. The patient blood cultures did not reveal any bacteria, and stool cultures did not reveal Salmonella or Shigella. His postoperative course was considered to be uneventful, and oral nutrition could be initiated on postoperative day 5. The patient was discharged in a good general condition on postoperative day 11. After discharge, the patient was noted as asymptomatic and did not report any serious residual complications.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [90.0, 'mmol/L'], 'Bicarbonate': [15.0, 'mmol/L'], 'Sodium': [130.0, 'mmol/L']}",25,23.75,26.25,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 130.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 130.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 130.0 mmol * 1 mEq/mmol = 130.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mmol sodium/L converts to 130.0 mEq sodium/L. 
The concentration of chloride is 90.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 90.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 90.0 mmol * 1 mEq/mmol = 90.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 90.0 mmol chloride/L converts to 90.0 mEq chloride/L. 
The concentration of bicarbonate is 15.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 15.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 15.0 mmol * 1 mEq/mmol = 15.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 15.0 mmol bicarbonate/L converts to 15.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 130.0 mEq/L - (90.0 mEq/L + 15.0 mEq/L) = 25.0 mEq/L. Hence, The patient's anion gap is 25.0 mEq/L."
6188,39,Anion Gap,lab test,decimal,pmc-8260195-1,Extracted,"A 73-year-old Caucasian male presented to the hospital for acute renal failure secondary to diarrhea and dehydration. The patient was found to have C. difficile infection which was treated with oral vancomycin and Flagyl. He had a past medical history of diabetes on metformin, hypertension, and hyperlipidemia, all diagnosed in the last six months before presentation. Family history was significant for coronary artery disease (CAD) in his brother at an unknown age. There was no family history of hematological malignancy or autoimmune disorders. There was no history of chronic non-steroidal anti-inflammatory drug (NSAID) use. The patient denied any history of smoking or recreational drug use. He used to drink alcohol occasionally and worked in a coffee factory all his life. There was no history of radiation exposure.
Upon presentation, the patient's basic metabolic panel showed creatinine of 15, sodium of 140, potassium of 5.6, chloride of 106, blood urea nitrogen of 95, calcium of 9.2, and bicarbonate of 20. Complete blood count showed a WBC count of 8.3X103/μL, neutrophils 74%, hemoglobin 12.7 g/dL, and platelet count of 253 X103/μL. Renal biopsy was done which showed acute tubular injury with an increased number of calcium oxalate crystals and arteriolosclerosis. It also showed low-grade large B-cell lymphoma immunophenotypically most consistent with extranodal marginal zone lymphoma of MALT, involving approximately 10% of the kidney tissue. Immunohistochemistry of the kidney tissue showed CD 19, CD20 positive B cells, that were negative for CD5, CD10, CD23, CD200, CD38, and MYD 88. The Ki-67 proliferative index was low.
CT of the abdomen and pelvis showed no bowel obstruction or appendicitis or acute inflammatory change. Non- obstructing right renal lithiasis was found. No hydronephrosis or obstructive uropathy was noted. No lymphadenopathy was noted on the CT. Autoimmune workup including antinuclear antibodies (ANA), anti-double-stranded DNA, and antineutrophil cytoplasmic antibodies (ANCA) was negative. HIV and hepatitis panel, including hepatitis B and hepatitis C, were nonreactive.
A positron emission tomography (PET) scan (Figure ) showed uniform activity in renal parenchyma with no other significant hyper-metabolic activity or lymphadenopathy.
Bone marrow biopsy showed normocellular marrow involved by low-grade B-cell non-Hodgkin lymphoma consistent with marginal zone lymphoma, approximately 10%-15% involvement. Flow cytometric analysis of the bone marrow aspirate showed approximately 33% of lymphocytes that were monotypic B-cells, expressing CD19, CD20, CD22, CD45, and showed lambda light chain restriction. The B-cells were negative for CD5, CD10, CD23, CD200, and CD38.
The patient was started on dialysis, and he remained on intermittent hemodialysis three times a week for two months. However, his renal function improved without any treatments and interventions for his MZL. The patient eventually came off dialysis. Since the patient now remains completely asymptomatic, he did not receive any treatment for his MZL. The patient will follow up in a lymphoma clinic in three months with a repeat CT abdomen pelvis for close monitoring of his disease.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [106.0, 'mEq/L'], 'Bicarbonate': [20.0, 'mEq/L'], 'Sodium': [140.0, 'mEq/L']}",14,13.3,14.7,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mEq/L. 
The concentration of chloride is 106.0 mEq/L. 
The concentration of bicarbonate is 20.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (106.0 mEq/L + 20.0 mEq/L) = 14.0 mEq/L. Hence, The patient's anion gap is 14.0 mEq/L."
6189,39,Anion Gap,lab test,decimal,pmc-4241748-1,Extracted,"A 47-year-old man arrived to the emergency room due to generalized tonic-clonic seizures and altered mental status. He had a history of long-standing uncontrolled type 2 diabetes treated irregularly with insulin and metformin (HbA1c 10.1%), with no known microvascular or macrovascular complications. He had no history of alcohol consumption and twenty-four hours earlier he referred nocturia, polyuria and polydipsia. On the day of admission, while asleep, he suddenly developed three consecutive episodes of generalized tonic-clonic seizures along with urinary sphincter loss and subsequent postictal state.
On physical examination he was hemodynamically stable with a blood pressure of 130/80 mmHg, heart rate of 85 beats per minute, respiratory rate of 20 per minute, temperature 36.5°C, and room-air oxygen saturation of 98%. His body mass index was 32.2. Mucous membranes were remarkably dry. The patient was lethargic and had a Glasgow coma scale of 11/15, muscle strength was 4/5 in both lower extremities, and deep tendon reflexes were diminished. Cranial nerves were normal, sensitivity was preserved, and meningeal signs and primitive reflexes were absent. Due to the patient status cerebellum function could not be evaluated. Finger-stick glucose could not be recorded due to high blood glucose levels and venous blood gas analysis reported pH 7.36, PCO2 42 mmHg, PO2 32 mmHg, lactate 1.2 mmol/L, and bicarbonate 23.7 mEq/L. Urinary and plasma ketones were negative. Hydration with intravenous normal saline solution at 500 mL/h and an insulin infusion at 0.14 U/kg were started. Plasma glucose was 838 mg/dL (46.5 mmol/L), blood nitrogen urea 21 mg/dL, creatinine 1.1 mg/dL with a MDRD calculated glomerular filtration rate of 71 mL/min, serum sodium 133 mmol/L, and chlorine 89 mmol/L. Calcium, potassium, phosphorous, magnesium, hemoglobin, white blood count, and platelets were all within normal limits. Serum albumin was 2.1 g/dL, alkaline phosphatase 192 UI/L, alanine aminotransferase 19 U/L, aspartate aminotransferase 21 U/L, total bilirubin 0.8 mg/dL, and serum osmolality 320 mOsm/kg ().
Head computed tomography, electrocardiogram, and chest X-ray were normal. The patient after 24 hours of treatment continued with altered mental status and paraparesis progressed (3/5). Plasma glucose was lowered down carefully at a rate of 30–40 mg/dL/hr and was within 200–300 mg/dL []. Serum osmolality dropped down to 305 mOsm/Kg (). Twenty-four hours after admission a brain magnetic resonance imaging (MRI) was ordered and revealed increased signal intensity on T2-weighted FLAIR images with restricted diffusion in the medulla and central pons (). Mammillary bodies, thalamus, third ventricle, and both hemispheres were respected. Lumbar puncture was normal, electroencephalogram showed a nonspecific wave activity, and urinary and serum toxicology panel were negative. During all his admission serum sodium was documented to be within normal range. ODS was diagnosed and aggressive supportive therapy was started. During the next 3 weeks the patient progressively regained consciousness and muscle strength and was able to feed himself. At 6-month follow-up, the patient was asymptomatic and MRI showed no residual damage.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [89.0, 'mmol/L'], 'Bicarbonate': [23.7, 'mEq/L'], 'Sodium': [133.0, 'mmol/L']}",20.3,19.285,21.315,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 133.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 133.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 133.0 mmol * 1 mEq/mmol = 133.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mmol sodium/L converts to 133.0 mEq sodium/L. 
The concentration of chloride is 89.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 89.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 89.0 mmol * 1 mEq/mmol = 89.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 89.0 mmol chloride/L converts to 89.0 mEq chloride/L. 
The concentration of bicarbonate is 23.7 mEq/L. 
Plugging in these values into the anion gap formula gives us 133.0 mEq/L - (89.0 mEq/L + 23.7 mEq/L) = 20.3 mEq/L. Hence, The patient's anion gap is 20.3 mEq/L."
6190,39,Anion Gap,lab test,decimal,pmc-3658294-1,Extracted,"An 83-year-old bed bound female, with a history of dementia who had an indwelling urinary catheter in place for last 3 months, presented to us in the outpatients department with the complaints of nausea, vomiting, decreased oral intake, chronic constipation, and purplish discoloration of the urine bag and tubing. She had been having these complaints on and off (three times over a period of 1 month) before coming to us and every time she was treated empirically with oral antibiotics (records not available) for suspected UTI. Her urinary catheter and bag were changed each time she would get purple discoloration and her symptoms would get better. When she presented to our facility, she was hemodynamically stable and was afebrile. Physical examination was unremarkable except for mild dehydration. She was noticed to have purple colored urine in the urine bag, along with purplish discoloration of the tubing and the bag []. Investigations revealed a hemoglobin of 12 g/dl and total leukocyte count of 11 × 109. Her blood urea was 40 mg/dl, serum creatinine 0.9 mg/dL, serum sodium 135 mEq/L, potassium 4.2 mEq/L, chloride 110 mEq/L, and bicarbonate was 20 mEq/L. Her urine dipstick showed a pH of 8.0, specific gravity 1.020, and it was positive for nitrite. Urine microscopy revealed 4-6 leucocytes, 3-5 red blood cells, and triple phosphate crystals. Urine culture was sent and she was started on oral cefixime (third generation cephalosporin). Lactulose was also prescribed for relieving constipation. The patient was seen after 3 days, and reported resolution of symptoms and disappearance of purple color. Urine culture grew greater than 105 colony forming units of Escherichia coli sensitive to cefixime. She completed a 10 days course of cefixime and has been symptom free till the last follow-up visit.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [110.0, 'mEq/L'], 'Bicarbonate': [20.0, 'mEq/L'], 'Sodium': [135.0, 'mEq/L']}",5,4.75,5.25,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 135.0 mEq/L. 
The concentration of chloride is 110.0 mEq/L. 
The concentration of bicarbonate is 20.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 135.0 mEq/L - (110.0 mEq/L + 20.0 mEq/L) = 5.0 mEq/L. Hence, The patient's anion gap is 5.0 mEq/L."
6191,39,Anion Gap,lab test,decimal,pmc-8215722-1,Extracted,"An 11-year-old female with a history of seizure disorder controlled on Trileptal, learning disability, attention deficit hyperactivity disorder, and pica presented with altered mental status and vomiting. She was ill with fever, cough, nausea, and anorexia for two weeks prior to presentation and had completed a five-day course of azithromycin to treat atypical pneumonia. On the morning of presentation, she had multiple episodes of emesis and an inability to tolerate oral intake, which prompted evaluation in the emergency department.
In the emergency department, she was found to be lethargic and hypoxic with oxygen saturation in the 70s on room air. Vital signs showed a temperature of 36.8°C, heart rate of 100 beats per minute, blood pressure of 120/71 mmHg, and respiratory rate of 19 breaths per minute. She was placed on high-flow nasal cannula 20 liters per minute and 0.5 FiO2. Physical examination showed a lethargic child in no acute distress. Neurologic examination revealed cranial nerves II-XII intact, and normal speech, motor, and sensation examinations. Respiratory effort was normal, and there were end-expiratory rales bilaterally. She was mildly tachycardic with regular rhythm and normal distal perfusion. Abdominal examination was benign without hepatosplenomegaly.
Initial laboratory evaluation showed venous blood gas of pH 7.39, pCO2 of 65 mmHg (8.64 kPa), and HCO3 of 40 mEq/L (40 mmol/L). Chemistry was significant for sodium of 130 mEq/L (130 mmol/L), chloride of 87 mEq/L (87 mmol/L), bicarbonate of 37 mEq/L (37 mmol/L), blood urea nitrogen (BUN) of 28 mg/dL (10 mmol/L), and creatinine of 0.57 mg/dL (43.46 µmol/L). Liver enzymes were increased with aspartate aminotransferase (AST) of 1,396 U/L (23.31 µkat/L) and alanine aminotransferase (ALT) of 1,003 U/L (16.75 µkat/L). Urine drug screen was negative. Chest X-ray, as read by the radiologist, revealed bilateral perihilar opacities with no focal infiltrate (Figure ). On admission to the pediatric intensive care unit, she was escalated to BiPAP (bilevel positive airway pressure) support, but due to progressive alteration in mentation, she was orally intubated for acute hypoxic and hypercapnic respiratory failure. Shortly after intubation, she was awake, alert, and requested a quick extubation.
After extubation, repeat physical and neurologic examinations were nonfocal with normal cranial nerve function. However, it was noted that her carbon dioxide levels continued to rise. During the day, she could be coached to take deep breaths to lower her carbon dioxide level. At night, her carbon dioxide levels rose to 96 mmHg (12.8 kPa), which could only be controlled with noninvasive ventilation. Multiple studies including drug screen, thyroid studies, lead levels, hepatitis screen, cerebrospinal fluid cell counts and cultures, and urine electrolytes were sent and normal. Encephalopathy panel revealed N-type calcium channel receptor, for which the patient was started on intravenous immunoglobulin. Head imaging with CT and MRI were normal. On further history taking, it was revealed she had significant intellectual impairment and tremendous daytime somnolence with failing school performance. In combination with the fact that most laboratory studies were negative or unrevealing and that she had no respiratory drive in response to hypercarbia, genetic studies for CCHS were sent on day 2 of hospitalization and resulted positive for heterozygous c.765_779dup PHOX2B gene variant on day 22 of hospitalization.
After the diagnosis of LO-CCHS was made, a multi-disciplinary team including pulmonology, neurology, otolaryngology, social work, and child life met with the family to discuss treatment options. After discussing options with the family and patient, she had a tracheostomy placed and was discharged on invasive mechanical ventilation only during the night time and at times of rest. She had improvement in lab values following tracheostomy placement, as venous blood gas revealed pH of 7.40, pCO2 of 43 mmHg (5.7 kPa), and HCO3 of 26.4 mEq/L (26.4 mmol/L). Chemistry results were as follows: sodium of 135 mEq/L (135 mmol/L), chloride of 98 mEq/L (98 mmol/L), bicarbonate of 33 mEq/L (33 mmol/L), BUN of 10 mg/dL (3.57 mmol/L), and creatinine of 0.2 mg/dL (15.25 µmol/L). She was discharged home after 43 days of hospitalization.
At home with tracheostomy ventilation at night time, she has done remarkably well with significant improvement in mental status and excessive daytime tiredness. Her end-tidal carbon dioxide has been maintained between 35 to 45 mmHg (4.7 to 5.9 kPa) with normalization of her acid-base balance. She has returned full-time to school and has accelerated to the top 25% of her class within eight months of treatment.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [98.0, 'mEq/L'], 'Bicarbonate': [33.0, 'mEq/L'], 'Sodium': [135.0, 'mEq/L']}",4,3.8,4.2,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 135.0 mEq/L. 
The concentration of chloride is 98.0 mEq/L. 
The concentration of bicarbonate is 33.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 135.0 mEq/L - (98.0 mEq/L + 33.0 mEq/L) = 4.0 mEq/L. Hence, The patient's anion gap is 4.0 mEq/L."
6192,39,Anion Gap,lab test,decimal,pmc-2481241-1,Extracted,"A 52-year-old white male with O2-dependent COPD, hypertension, GERD, idiopathic gastroparesis, and chronic low back pain was noted to have persistent hypokalemia in the 2.7–3.3 meq/L range over more than 2 years. He complained also of chronic generalized weakness and fatigue. He denied nausea or vomiting, but did have occasional loose stools. The hypokalemia persisted despite discontinuation of diuretic treatment for hypertension and fludrocortisone that had been prescribed briefly for orthostatic hypotension. There was no improvement with aggressive oral potassium supplementation in amounts up to 120 meq per day. The patient's serum potassium level normalized on three occasions when he was hospitalized and given supplemental potassium (COPD exacerbations in 7/06 and 1/07, pseudoseizures in 7/07), but the hypokalemia promptly recurred after discharge from the hospital (Figure ). His medications were paroxetine, trazodone, pregabalin, sustained-release morphine, loratadine, isosorbide mononitrate, lisinopril, metoprolol, simvastatin, omeprazole, metoclopramide, potassium chloride, calcium/vitamin D tablets, alendronate, and mometasone, tiotropium, and albuterol inhalers. He smoked one-half pack of cigarettes per day and did not drink alcohol.
On physical examination, he was a chronically ill-appearing man wearing a nasal cannula. Height was 69 inches, weight 205 pounds. There were no cushingoid facies, buffalo hump, or abdominal striae. Vital signs were temperature 98.6 degrees, pulse 95, respiratory rate 14, blood pressure 128/73. There was no thyromegaly or lymphadenopathy. Lungs showed decreased breath sounds and mild expiratory wheezes bilaterally. Heart sounds were regular with no murmurs, rubs, or gallops. The abdomen was soft and non-tender, with no masses or organomegaly. Extremities showed no edema, clubbing or cyanosis. The neurologic examination revealed mild generalized muscular weakness (4+/5) and normal deep tendon reflexes.
Laboratory results include serum sodium 137 mg/dL, potassium 3.0 mg/dL, chloride 95 mmol/L, CO2 30.0 mmol/L, blood urea nitrogen 5 mg/dL, creatinine 0.8 mg/dL, calcium 9.3 mg/dL, phosphorus 4.1 mg/dL, albumin 3.6 g/dL, ferritin 126 ng/mL, hemoglobin 12.7 g/dL, white blood cell count 10.6 K/cmm, and platelet count 160 K/cmm. Serum aldosterone was 4.8 ng/dL (normal 4–31 ng/dL) and the plasma renin activity was 0.33 ng/mL/hr (normal 1.31–3.96 ng/mL/hr upright, 0.15–2.33 ng/mL/hr supine). Spot urine potassium was 8.6 mEq/L, urine sodium was < 10 mEq/L, and urine chloride was 16 mmol/L.
In the absence of a clear explanation for this patient's chronic hypokalemia, he was asked to give the details of his diet. He admitted to drinking 4 liters of Pepsi-Cola per day for the past several years. It was his habit to sip cola slowly but almost continuously, throughout the day. When hospitalized, he had stopped drinking cola and his potassium levels had temporarily normalized. In early May 2008, he decreased his cola intake to 2 liters per day, with a resultant increase in the serum potassium from 3.0 to 3.5 mg/dL (Figure ).",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [95.0, 'mmol/L'], 'Bicarbonate': [30.0, 'mmol/L'], 'Sodium': [137.0, 'mg/dL']}",-65.4,-62.13,-68.67,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 137.0 mg/dL. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mg to mEq. The mass of sodium is 137.0 mg. To convert from 137.0 mg to mEq, first convert from mg to mmol.To convert 137.0 mg of sodium to g, multiply by the conversion factor 0.001, giving us 137.0 mg sodium * 0.001 g/mg = 0.137 g sodium. To convert from grams of sodium to moles, divide by the molar mass 22.99 g/mol, which will give 0.137 g/(22.99 g sodium/mol) = 0.00596 mol sodium. To convert 0.00596 mol of sodium to mmol, multiply by the conversion factor 1000.0, giving us 0.00596 mol sodium * 1000.0 mmol/mol = 5.96 mmol sodium. To convert from 5.96 mmol sodium to mEq, multiply the mmol amount by the valence, to get 5.96 mmol * 1 mEq/mmol = 5.96 mEq sodium. The current volume unit is dL and the target volume unit is L. The conversion factor is 0.1 L for every unit of dL. Our next step will be to divide the mass by the volume conversion factor of 0.1 to get the final concentration in terms of mEq/L. This will result to 5.96 mEq sodium/0.1 L = 59.6 mEq sodium/L. The concentration value of 137.0 mg sodium/dL converts to 59.6 mEq sodium/L. 
The concentration of chloride is 95.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 95.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 95.0 mmol * 1 mEq/mmol = 95.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 95.0 mmol chloride/L converts to 95.0 mEq chloride/L. 
The concentration of bicarbonate is 30.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 30.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 30.0 mmol * 1 mEq/mmol = 30.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 30.0 mmol bicarbonate/L converts to 30.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 59.6 mEq/L - (95.0 mEq/L + 30.0 mEq/L) = -65.4 mEq/L. Hence, The patient's anion gap is -65.4 mEq/L."
6193,39,Anion Gap,lab test,decimal,pmc-3608317-1,Extracted,"A 91-year-old Puerto Rican man presented for evaluation of progressively worsening shortness of breath over the past six months associated with two weeks of productive cough of yellowish sputum. The patient also had complaints of fatigue, palpitations and dyspnea with minimal exertion. His past medical history was significant for pulmonary tuberculosis in 1969 for which he received approximately 24 months of medical treatment. The patient also had a history of coronary artery disease, bronchiectasis, moderate pulmonary hypertension, moderate chronic obstructive pulmonary disease (COPD), and has had multiple exacerbations of his bronchiectasis and COPD which did not require hospitalization. He had a history of smoking 30 cigarette packs per year but discontinued cigarette smoking 45 years prior to his admission. He denied alcohol or drug use and had no history of prior surgeries. He had been followed by a pulmonologist for over seven years, and spirometry testing done four months before his presentation showed an forced expiratory volume1 (FEV1) to forced vital capacity (FVC) ratio of 64%, FEV1 of 71%, and FVC of 84%. One year prior to presentation, an echocardiographic assessment demonstrated left ventricular hypertrophy with moderate pulmonary hypertension, and a dobutamine stress echocardiogram demonstrated a defect in the inferior wall consistent with a previous infarction.
On physical examination, the patient was tachycardic at a heart rate of 140 beats per minute, tachypneic with a respiratory rate of 18 breaths per minute and saturating oxygen at 94% on atmospheric air. The patient was awake, alert, and oriented to person, time, and place and able to speak in full sentences. He did not demonstrate jugular venous distention, but his trachea was deviated towards his right side. There was no evidence of stridor. The patient’s breath sounds were diminished bilaterally with more prominently diminished sounds over his right lung fields. Coarse rhonchi were notable over his right lower lung. No wheezing or rales were appreciated. Heart sounds were more prominent on the right side of the chest and were characterized as an irregular tachycardia, with no murmurs, gallops or accentuated heart sounds appreciated. Laboratory studies demonstrated a white blood cell count of 7100/mm3, hemoglobin level 9.1g/dL, hematocrit 28.0%, sodium 137mEq/L, potassium 4.0mEq/L, chlorine 101mEq/L, bicarbonate 30mEq/L, blood urea nitrogen 16mg/dL, serum creatinine 0.6mg/dL, glucose 140mg/dL, troponin I: 0.03ng/mL, B-type natriuretic peptide 320ng/L, and normal liver and kidney function. Arterial blood gas showed a pH of 7.480, partial pressure of carbon dioxide of 46, partial pressure of oxygen of 116 and an oxygen saturation of 99% on two L of oxygen. An electrocardiogram showed a multifocal atrial tachycardia without T wave or ST segment changes (Figure ). A chest X-ray demonstrated opacification of the right hemithorax with a marked mediastinal shift to the right and hyperinflation of the left lung (Figure ). A computed tomography scan of the patient’s chest showed hyperinflation of his left lung, cystic bronchiectasis, mediastinal shifting to the right with clockwise rotation of his trachea and marked absence of normal lung parenchyma in his right lung (Figures , ). Venous Doppler ultrasound of his lower extremities was negative for venous thrombosis. The patient’s presentation was attributed to a cardiac arrhythmia secondary to his extensive lung disease and was treated with calcium channel blockers to control his heart rate. However, four days into his hospital course, he became lethargic with a three gram drop of his hemoglobin and subsequently went into cardiac arrest. The patient was immediately intubated and was resuscitated according to Advanced Cardiac Life Support protocol. During the arrest he was noticed to have profound coffee ground emesis. Despite resuscitation efforts, the patient remained pulseless and subsequently died.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [101.0, 'mEq/L'], 'Bicarbonate': [30.0, 'mEq/L'], 'Sodium': [137.0, 'mEq/L']}",6,5.7,6.3,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 137.0 mEq/L. 
The concentration of chloride is 101.0 mEq/L. 
The concentration of bicarbonate is 30.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 137.0 mEq/L - (101.0 mEq/L + 30.0 mEq/L) = 6.0 mEq/L. Hence, The patient's anion gap is 6.0 mEq/L."
6194,39,Anion Gap,lab test,decimal,pmc-8058752-1,Extracted,"An 85-year-old woman called an emergency medical service (EMS) for hematochezia. Her medical history included atrial fibrillation, hypertension, chronic constipation, and chronic low back pain. Her medications were apixaban 5 mg/day in 2 doses, furosemide 40 mg/day, bisoprolol 10 mg/day, and perindopril 10 mg/day. Her height was 150 cm and weight 42 kg (body mass index 18.7 kg/m2). She lived at home with her husband and was completely independent with acts of daily life.
A basic life support ambulance was dispatched. When they arrived, the ambulance crew noted cyanosis in bilateral hands and feet. The patient was awake, alert, and oriented to place, person, and date, and conversant, with a Glasgow Coma Scale of 15. She had been complaining of tiredness, anorexia, and constipation for 8 days and blood in her stools. Blood pressure was 130/40 mmHg, heart rate 143 beats/min, respiratory rate 14 cycles/min, and temperature 37 °C. Oxygen saturation (SpO2) was hard to measure with a high variability of the results displayed on the oxymeter. A medical team (advance life support ambulance with an emergency physician on board) was sent for additional support.
When the medical team arrived on the scene, the medical history found that hematochezia had started within the last 24 h, but was also associated, in the past several days, with melena and diffuse abdominal pain. The clinical examination showed signs of tissue hypoperfusion with skin mottling of the lower limbs, peripheral vasoconstriction, increased capillary refill time, and peripheral cyanosis. The skin was very pale. Blood pressure was 112/40 mmHg, heart rate 86 beats/min, respiratory rate 20 cycles/min, temperature 37 °C, and SpO2 remained difficult to measure due to severe peripheral vasoconstriction. Placed at the ear, the oxymeter was able to show an SpO2 of 90% while the patient was on oxygen at 9 L/min via mask. The electrocardiogram showed atrial fibrillation with inverted T waves in V4, V5, and V6. The hemoglobin, measured twice on a capillary and venous point of care sample, was 5 g/dL. Capillary blood glucose, controlled three times, was not measurable despite the normal level of consciousness of the patient.
Management consisted of oxygen at 9 L/min via high flow mask, intravenous catheterization and rapid intravenous fluid infusion with 500 mL of isotonic saline solution (0.9% NaCl), and intravenous administration of 12 g of glucose with a 30% glucose solution. Anemia correction was deferred. Thirty-nine minutes after the medical team arrival, the patient was transported to an intensive care unit (ICU).
At the hospital, the symptomatology was unchanged. Laboratory results were are follows (normal values in parentheses): pH 7.30 (7.3–7.42), pCO2 30 mmHg (35–45), pO2 297 mmHg (> 90), bicarbonate 15 mmol/L (22–26), sodium 140 mmol/L (136–145), potassium 5.0 mmol/L (3.7–5.2), chloride 108 mmol/L (95–105), glucose 5.9 mmol/L (3.8–6.1), lactate 0.56 mmol/L (0.60–2.00), creatinine 251 μmol/L (55–100), and urea 45.1 mmol/L (2.5–7.5). Hematology was as follows: leukocytes 19,000/mL (4000–10,000), red blood cells 1,980,000/mL (4,000,000–5,2000,000), hemoglobin 4.8 g/dL (12.5–15.5), and platelets 324,000/mL (150,000–400,000). The prothrombin level was 39% (70–125). The apixaban anti-Xa was 484 ng/mL.
Therapies consisted of 50 IU/kg of 4-factor prothrombin complex concentrate to reverse apixaban, transfusion of 6 units of packed red blood cells, and 3 units of plasma. An esogastroduodenal fibroscopy did not show any lesions. A colonoscopy visualized, in the left angle and in the sigmoid colon, an ischemic colitis with ulcerations responsible for the bleeding in the previous days. No active bleeding was seen. The final diagnosis was hemorrhagic shock secondary to intestinal bleeding on ischemic colitis in the context of apixaban overdose, itself complicated by acute kidney injury and metabolic acidosis.
During the remainder of the patient’s stay in the ICU, there was no hemorrhagic or hypoglycemia recurrence, the acid-base balance was restored, and the kidneys recovered normal function. The patient was discharged to the internal medicine department on day 10. Her mental status was closely monitored and remained normal throughout her hospital stay.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [108.0, 'mmol/L'], 'Bicarbonate': [15.0, 'mmol/L'], 'Sodium': [140.0, 'mmol/L']}",17,16.15,17.85,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 140.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 140.0 mmol * 1 mEq/mmol = 140.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mmol sodium/L converts to 140.0 mEq sodium/L. 
The concentration of chloride is 108.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 108.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 108.0 mmol * 1 mEq/mmol = 108.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 108.0 mmol chloride/L converts to 108.0 mEq chloride/L. 
The concentration of bicarbonate is 15.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 15.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 15.0 mmol * 1 mEq/mmol = 15.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 15.0 mmol bicarbonate/L converts to 15.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (108.0 mEq/L + 15.0 mEq/L) = 17.0 mEq/L. Hence, The patient's anion gap is 17.0 mEq/L."
6195,39,Anion Gap,lab test,decimal,pmc-514562-1,Extracted,"A 24-year-old man was admitted to our intensive care unit (ICU) with a possible diagnosis of seizure disorder and sepsis. He had a past medical history of cerebral palsy and spastic quadriparesis. Three years ago, he had an ITB pump implanted for spasticity refractory to the high doses of oral baclofen. He had a significant improvement in spasticity, social and functional capacity in the past three years.
Later, he developed some disorientation and increased spasticity. He was taken to a local physician who prescribed oral baclofen (120 mg daily in four divided doses) for his increased spasticity. He also advised him to have his ITB pump checked immediately. The following day, his spasticity increased even after taking oral baclofen. He developed multiple seizures and respiratory distress in the next 24-hour period. Subsequently, he was admitted in a local hospital where he was orally intubated and transferred to our ICU for aggressive management.
On presentation, his temperature was 104.6°F (40.3°C), heart rate 127 beats per minute, and the blood pressure was 85/45 mm/Hg. His ventilator settings were: assist-control ventilation mode; respiratory rate, 15 breaths per minute; tidal volume, 650 mL; positive end expiratory pressure (PEEP), 5 cm H2O; and FiO2, 60%. His spontaneous respiratory rate was 18 breaths per minute and an oxygen saturation of 100% was noted on pulse oximetry. In the local hospital, he was documented to have a high fever of 107°F (41.6°C) and he had received intravenous lorazepam, phenytoin, pantoprazole, piperacillin/tazobactem and dopamine. On physical examination, neurologically he was unconscious with decerebrate posturing and his Glasgow coma scale was 6. He had an absent corneal and gag reflexes. He was moving all four limbs in response to noxious stimuli. He was also noted to have an extreme spasticity in all four limbs. Lung examination revealed decreased breath sounds in the left lower base. Cardiac examination was unremarkable. He had a palpable baclofen pump on abdominal wall and bowel sounds were heard. The differential diagnoses were septic shock, meningitis, neuroleptic malignant syndrome and malignant hyperthermia.
The initial laboratory results showed serum creatinine phosphokinase (CPK) 5250 U/L (Normal, 25–235 U/L) and CPK-MB fraction 12.1 ng/ml (Normal, 0.5–6.3 U/L). Serum chemistry revealed sodium 142 mmol/L, potassium 5.1 mmol/L, chloride 120 mmol/L, bicarbonate 13 mmol/L, and creatinine 2.1 mg/dl. Hemogram showed white blood cell count 12.2 K/UL, hemoglobin 16.5 g/dl and platelet count 9 K/UL (Normal, 130–400 K/UL). Liver function test showed aspartate aminotransferase (ALT) 1128 U/L, alanine aminotransferase (AST) 1140 U/L, alkaline phophatase 90 U/L, total bilirubin 1.2 mg/dl, conjugated bilirubin 0.7 mg/dl, prothrombin time 20.2 seconds (Normal, 10–12.5 seconds), and INR 2.0 (Normal, 0.9–1.1). Blood and urine cultures were obtained. Chest radiograph was normal. A computed tomography (CT) scan of the chest revealed atelectasis of the left lung base. His CT scan of head did not show any acute infarct or bleeding. His initial management included intravenous fluids, norepinephrine, platelet transfusion, phenytoin, propofol and broad-spectrum antibiotics (vancomycin, ceftriaxone) for suspected meningitis and septic shock. He received intravenous lorazepam (4–8 mg every four hours) for his spasticity. Next day, his spasticity improved and an ITB specialist investigated his baclofen pump. His baclofen pump analysis revealed that it was stopped due to some programming error, which was restarted at a previously prescribed baclofen rate (260 μg/day).
On third hospital day, his serum CPK was 15,878 U/L, AST was 2566 U/L, ALT was 2993 U/L, while CPK-MB fraction came down to 3.4 ng/ml. His urine output decreased (<400 ml/ day) and serum creatinine increased in the range of 5–6 mg/dl. Later, he was hemodialyzed few times during the course of hospitalization due to acute renal failure. His echocardiogram showed left ventricular ejection fraction of 20–25% and severe global hypokinesis. His electroencephalogram did not reveal any epileptogenic activity. He developed full-blown multisystem organ failure with an evidence of shock liver, renal failure, respiratory failure, disseminated intravascular coagulation and myocardial depression. His nutrition was started on nasogastric tube feedings, and proper ventilator care was taken through a tracheostomy tube. His serum baclofen obtained at the time of admission was less than 0.02 μg/ml (Expected values, 0.08–0.4 μg/ml). After a three-week course of aggressive management in ICU, he was weaned off from the ventilator and his multiple organ shock resolved. At a six-month follow-up, he was observed in a nursing home with his baseline functional, social, and family activities.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [142.0, 'mmol/L'], 'Chloride': [120.0, 'mmol/L'], 'Bicarbonate': [13.0, 'mmol/L']}",9,8.55,9.45,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 142.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 142.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 142.0 mmol * 1 mEq/mmol = 142.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mmol sodium/L converts to 142.0 mEq sodium/L. 
The concentration of chloride is 120.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 120.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 120.0 mmol * 1 mEq/mmol = 120.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 120.0 mmol chloride/L converts to 120.0 mEq chloride/L. 
The concentration of bicarbonate is 13.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 13.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 13.0 mmol * 1 mEq/mmol = 13.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 13.0 mmol bicarbonate/L converts to 13.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 142.0 mEq/L - (120.0 mEq/L + 13.0 mEq/L) = 9.0 mEq/L. Hence, The patient's anion gap is 9.0 mEq/L."
6196,39,Anion Gap,lab test,decimal,pmc-3731624-1,Extracted,"A 10-month-old boy with a body weight of 9.6 kg presented with progressive lethargy. His past medical history was unremarkable. He had suffered from gastritis 2 weeks before and started vomiting again 2 days before admission. The patient had no fever, excessive sweating or diarrhea, and his urine output was normal. Physical examination revealed a sleepy but easily arousable infant with a heart rate of 160 per minute, a respiration rate of 32 per minute and a body temperature of 37.7°C. On all four extremities, a blood pressure of 135/95 mm Hg was measured, a value above the 99th percentile (P) by age and height (e.g. P 95th is 103/56 mm Hg). There were no signs of meningitis or intracranial hypertension, no abnormalities in sensibility and strength, and reflexes were normal. Cardiopulmonary examination revealed no heart murmurs, and breath sounds were normal. The abdomen was not painful to palpation and there were no masses. No edema was found, and the skin was unremarkable. Based on the combination of hypertensive crisis and the neurological findings, the diagnosis of malignant hypertension was made and the patient was admitted to our pediatric intensive care unit for evaluation and intravenous antihypertensive therapy [, , ]. Nicardipine at 1 mcg/kg/min lowered his blood pressure to an acceptable level of 105/55 mm Hg (P 95th) within a few hours.
Laboratory results showed a normal complete blood cell count, serum electrolytes (Na 137 mmol/l, K 4.1 mmol/l, Cl 104 mmol/l), creatinine 13 µmol/l, urea 3.6 mmol/l and glucose 5.6 mmol/l. Glomerular filtration rate was 118 ml/min, and blood lactate as well as ammonia levels were normal. An arterial blood gas analysis revealed a mild meta-bolic acidosis with respiratory compensation (pH 7.40, bicarbonate 17.7 mmol/l, pCO2 29 mm Hg).
A computed tomography of the brain revealed no intracranial bleeding, no tumor and no signs of elevated intracranial pressure. An abdominal ultrasound showed normal kidneys without hydronephrosis, and Doppler studies were unremarkable. On the ultrasound, an abdominal mass with the characteristic ‘target sign’ of an ileocecal intussusception was visualized in the right lower quadrant (fig. ). Radiographically guided hydrostatic reduction with water-soluble contrast failed. Laparotomy was performed, which confirmed the diagnosis of intussusception. After repositioning, intestinal perfusion was adequate and bowel resection was not necessary. The anesthetics used during the surgery had no major influence on the blood pressure. Following surgery, the mental status returned to normal and antihypertensive medication could be discontinued. His blood pressure decreased to a normal level (P 50th 90/40 mm Hg).",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [104.0, 'mmol/L'], 'Bicarbonate': [17.7, 'mmol/L'], 'Sodium': [137.0, 'mmol/L']}",15.3,14.535,16.065,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 137.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 137.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 137.0 mmol * 1 mEq/mmol = 137.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mmol sodium/L converts to 137.0 mEq sodium/L. 
The concentration of chloride is 104.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 104.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 104.0 mmol * 1 mEq/mmol = 104.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 104.0 mmol chloride/L converts to 104.0 mEq chloride/L. 
The concentration of bicarbonate is 17.7 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 17.7 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 17.7 mmol * 1 mEq/mmol = 17.7 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 17.7 mmol bicarbonate/L converts to 17.7 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 137.0 mEq/L - (104.0 mEq/L + 17.7 mEq/L) = 15.3 mEq/L. Hence, The patient's anion gap is 15.3 mEq/L."
6197,39,Anion Gap,lab test,decimal,pmc-3471405-1,Extracted,"The patient was a 33-year-old Caucasian male with advanced AIDS (CD4+ cell count: 59 cells/mm3, HIV-1 RNA level of 308,000 copies/mL) and an extensive history of opportunistic infections including prior disseminated histoplasmosis, disseminated Mycobacterium avium complex (MAC), Pneumocystis jirovecii (PCP) pneumonia, cutaneous varicella-zoster infection, and cytomegalovirus (CMV) gastric ulcer. He had been placed on combination antiretroviral therapy (cART) with emtricitabine/tenofovir and raltegravir as well as opportunistic infection prophylaxis with itraconazole, azithromycin, trimethoprim/sulfamethoxazole (TMP/SMX), and valganciclovir, although the patient reported being poorly adherent to all prescribed medications. He presented to the hospital with a two-week history of worsening cough, shortness of breath, intermittent fever and chills, and black tarry stools. On admission, he appeared cachectic, chronically ill, and in obvious distress. Vital signs were notable for tachycardia and mild tachypnea. Physical examination revealed facial Molluscum contagiosum, ulcerations on the right lateral tongue, oropharyngeal thrush, mild diffuse abdominal pain, and moderate hepatosplenomegaly. A complete blood count was significant for pancytopenia with a leukocyte count of 2,800 cells/μL (93% neutrophils, 4% lymphocytes, and 1% monocytes), hematocrit of 20% (down from the patient's baseline of 30%), and platelet count of 28,000/mL. The results of a comprehensive metabolic panel were as follows: sodium 133 mmol/L, potassium 4.1 mmol/L, chloride 102 mmol/L, bicarbonate 22 mmol/L, blood urea nitrogen 16 mg/dL, creatinine 0.76 mg/dL, glucose 103 mg/dL, calcium 7.7 mg/dL, AST 113 units/L, ALT 25 units/L, and alkaline phosphatase 450 units/L.
On the evening of admission, the patient became febrile to 39.5°C and increasingly tachycardic, tachypneic, and hypoxic requiring supplemental oxygen, several liters of intravenous fluids, and two units of packed red blood cells. A chest radiograph was obtained which showed a diffuse miliary pattern concerning for PCP pneumonia and/or disseminated opportunistic infectious process such as tuberculosis, MAC, or fungal infection. He was started on empiric treatment with vancomycin, piperacillin/tazobactam, high dose TMP/SMX, prednisone, ethambutol, azithromycin, and liposomal amphotericin B. He responded well to broad-spectrum treatment over the next few days and subsequently underwent diagnostic bronchoscopy with bronchoalveolar lavage (BAL). BAL cultures returned positive for H. capsulatum. The patient also underwent esophagogastroduodenoscopy (EGD) given his persistent melanotic stools and progressively declining hematocrit (nadir of 18%) requiring multiple blood transfusions. EGD was significant for a well-healed scar on the greater curvature of the stomach from prior CMV gastric ulcer and new diffuse erosions throughout the second, third, and fourth segments of the duodenum (). Multiple biopsies were taken which showed duodenal mucosa with granulomatous inflammation. Gomori's methenamine silver (GMS) stain identified macrophages with small intracellular yeasts consistent with disseminated histoplasmosis (). Bone marrow involvement was also suspected in light of the patient's significant pancytopenia, but he had previously refused bone marrow biopsy. Urine Histoplasma antigen came back markedly elevated at >39 ng/mL (above the upper limit of detection for this particular assay) confirming the diagnosis, and the patient was treated with a two-week course of intravenous liposomal amphotericin B followed by indefinite oral itraconazole.
Following a two-week inpatient hospitalization, the patient demonstrated excellent improvement. All major presenting symptoms were resolved, including the melanotic stools, and his hematocrit was stable at his baseline. By the time of discharge, the patient had regained his prior level of functioning including full ambulatory capacity. Several weeks after discharge, sputum acid-fast culture returned positive for MAC for which he was continued on ethambutol and azithromycin.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [102.0, 'mmol/L'], 'Bicarbonate': [22.0, 'mmol/L'], 'Sodium': [133.0, 'mmol/L']}",9,8.55,9.45,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 133.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 133.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 133.0 mmol * 1 mEq/mmol = 133.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mmol sodium/L converts to 133.0 mEq sodium/L. 
The concentration of chloride is 102.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 102.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 102.0 mmol * 1 mEq/mmol = 102.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 102.0 mmol chloride/L converts to 102.0 mEq chloride/L. 
The concentration of bicarbonate is 22.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 22.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 22.0 mmol * 1 mEq/mmol = 22.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 22.0 mmol bicarbonate/L converts to 22.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 133.0 mEq/L - (102.0 mEq/L + 22.0 mEq/L) = 9.0 mEq/L. Hence, The patient's anion gap is 9.0 mEq/L."
6198,39,Anion Gap,lab test,decimal,pmc-3479936-1,Extracted,"A. M. is a 59-year-old man who developed sudden onset of progressively enlarging swelling on both feet immediately following a 10-hour journey in a tightlypacked bus. He initially was unable to walk out of the bus due to sudden weakness of both lower limbs with marked numbness but no pain and was later supported out of the bus. Initially, swelling was painless but later became mildly painful as the swelling increased in size. He experienced numbness and pins and needles sensation in gloves and stocking distribution for the previous one year. He has no history of intermittent claudication and no frothiness of urine but was said to have experienced deteriorating vision for the previous one year. A known type 2 diabetic diagnosed 11 years ago on account of osmotic symptoms was regular on antidiabetic (metformin,) and subsequently controlled on subcutaneous mixtard insulin. He was also diagnosed hypertensive one year prior to presentation and was placed on Nifedipine XL 30 mg daily Lisinopril 10 mg daily but not regular on clinic visit or medication. He has never smoked a cigarette or ingested alcohol.
Anthropometric examination showed that waist circumference = 107 cm, hip circumference = 102 cm, and waist-hip ratio = 1.05 (central obesity).
Dorsal and plantar surface of left the foot contained 10 cm × 12 cm bullae each, and the right foot had a 14 cm × 14 cm bullae on the plantar aspect extending to the anteromedial aspect all containing clear fluid, nontender, no differential warmth, and no redness (). Dorsalis pedis pulses were full bilaterally, and the pattern of sensory loss was of “gloves and stocking” distribution.
Pulse rate is 88 bpm, blood pressure is 140/90 mmHg, apex beat is at the 5th left intercostals space 2 cm lateral to the midclavicular line, with left ventricular heave, heart sounds were normal S1 and loud A2.
Blood glucose (fasting = 6.1 mmol/L, 2 hours postprandial = 11.1 mmol/L), urinalysis negative for protein, ketones, glucose, nitrite with normal pH.
Parked cell volume = 27%, white blood cell = 11.0 × 109 with neutrophil 56%, lymphocyte 40% monocyte 4%.
Serum urea electrolytes, with urea = 22 mmol/L, sodium = 135 mmol/L, potassium = 5.2 mmol/L, chloride = 102 mmol/L, bicarbonate = 21 mmol/L.
Serum total cholesterol = 7.1 mmol/L, low density lipoprotein cholesterol = 4.1 mmol/L, high density lipoprotein cholesterol = 0.6 mmol/L, triglycerides = 5.3 mmol/L, TC : HDL ratio = 11.8.
The right foot bullae ruptured spontaneously with purulent fluid exuded on the 5th day post-bullae formation, while the left foot was surgically drained following suppuration. Patient was empirically placed on flucloxacillin. Culture of aspirate revealed Staphylococcus aureus.
Serial sections of tissue biopsy shows hyperkeratotic focally acanthotic pigmented epidermis with subcorneal separation of the granular layer of the epidermis by aggregates of viable and nonviable polymorphs and lymphocytes. There is mild acantholysis of the epidermis. The dermis is fibrocollagenized and moderately infiltrated by lymphocytes.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [102.0, 'mmol/L'], 'Bicarbonate': [21.0, 'mmol/L'], 'Sodium': [135.0, 'mmol/L']}",12,11.4,12.6,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 135.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 135.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 135.0 mmol * 1 mEq/mmol = 135.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mmol sodium/L converts to 135.0 mEq sodium/L. 
The concentration of chloride is 102.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 102.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 102.0 mmol * 1 mEq/mmol = 102.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 102.0 mmol chloride/L converts to 102.0 mEq chloride/L. 
The concentration of bicarbonate is 21.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 21.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 21.0 mmol * 1 mEq/mmol = 21.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 21.0 mmol bicarbonate/L converts to 21.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 135.0 mEq/L - (102.0 mEq/L + 21.0 mEq/L) = 12.0 mEq/L. Hence, The patient's anion gap is 12.0 mEq/L."
6199,39,Anion Gap,lab test,decimal,pmc-7389983-1,Extracted,"A 59-year-old male with a 30-year history of neurofibromatosis presented with shortness of breath and ataxia for the last 10 days. Other past medical history includes tobacco abuse with 30 pack-year history, quitting 11 years prior to presentation. On arrival to the emergency department (ED), he was tachycardic with a heart rate of 101 beats per minute and tachypneic with a respiratory rate of 24 breaths per minute. The rest of his vital signs were within normal limits. His physical exam revealed no acute distress; he was awake, alert, and oriented to person, place, and time. Skin exam revealed multiple soft cutaneous neurofibromas and cafe au lait spots. Lung auscultation revealed good air entry bilaterally. Cardiac examination revealed a regular rate and rhythm, with no murmurs or gallops appreciated. Laboratory test illustrated a white blood count of 15.9 k/ul, hemoglobin of 12.2 gm/dl, glomerular filtration rate (GFR) >90 mL/min/1.73 m2, glucose of 66 mg/dl, blood urea nitrogen (BUN) of 12 mg/dl, creatinine of 0.68 mg/dl, sodium of 136 mmol/dl, potassium of 3.5 mmol/L, chloride of 104 mmol/L, CO2 of 26 mmol/L, calcium of 8.6 mg/dl, aspartate aminotransferase (AST) of 19 u/l, alanine aminotransferase (ALT) of 26 u/l, alkaline phosphatase of 275 u/l. An electrocardiogram showed biatrial enlargement and rightward axis deviation, compatible with pulmonary disease pattern.
A chest radiograph revealed a left lower lobe infiltrate concerning for pneumonia (Figure ), and a computed tomography (CT) scan of the chest was recommended. CT of the chest was positive for left basilar consolidation with surrounding ground-glass opacities and innumerable bilateral thin-walled cysts (Figures , ). The latter finding raised suspicion for neurofibromatosis-associated diffuse lung disease (NF-DLD). On chart review of previous hospital admissions, a CT of the chest from two years ago showed emphysema with scattered fibrosis and scarring, but no cysts were reported. Intravenous fluid resuscitation and antibiotics were initiated. The patient was admitted with sepsis secondary to community-acquired pneumonia.
After consultation with pulmonology, recommendations were to continue treatment for pneumonia and follow up with high-resolution CT of the chest and complete pulmonary function testing in 12 weeks.
The patient’s ataxia was investigated by neurology; CT and magnetic resonance imaging (MRI) of the brain were unremarkable. The ataxia was thought to be secondary to sepsis. His balance improved after the infection was treated. Follow-up with the movement disorder clinic was recommended. After seven days of hospitalization, the patient was discharged in a stable condition with close follow-up with pulmonary specialists.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [136.0, 'mmol/dL'], 'Chloride': [104.0, 'mmol/L'], 'Bicarbonate': [26.0, 'mmol/L']}",1230,1168.5,1291.5,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 136.0 mmol/dL. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 136.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 136.0 mmol * 1 mEq/mmol = 136.0 mEq sodium. The current volume unit is dL and the target volume unit is L. The conversion factor is 0.1 L for every unit of dL. Our next step will be to divide the mass by the volume conversion factor of 0.1 to get the final concentration in terms of mEq/L. This will result to 136.0 mEq sodium/0.1 L = 1360.0 mEq sodium/L. The concentration value of 136.0 mmol sodium/dL converts to 1360.0 mEq sodium/L. 
The concentration of chloride is 104.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 104.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 104.0 mmol * 1 mEq/mmol = 104.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 104.0 mmol chloride/L converts to 104.0 mEq chloride/L. 
The concentration of bicarbonate is 26.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 26.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 26.0 mmol * 1 mEq/mmol = 26.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 26.0 mmol bicarbonate/L converts to 26.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 1360.0 mEq/L - (104.0 mEq/L + 26.0 mEq/L) = 1230.0 mEq/L. Hence, The patient's anion gap is 1230.0 mEq/L."
6200,39,Anion Gap,lab test,decimal,usmle-4284,Extracted,"A 22-year-old woman with a history of type I diabetes mellitus presents to the emergency department with nausea, vomiting, and drowsiness for the past day. Her temperature is 98.3°F (36.8°C), blood pressure is 114/74 mmHg, pulse is 120/min, respirations are 27/min, and oxygen saturation is 100% on room air. Physical exam is notable for a confused and lethargic young woman. Initial laboratory values are notable for the findings below.

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 2.9 mEq/L
HCO3-: 9 mEq/L
BUN: 20 mg/dL
Glucose: 599 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.2 mg/dL
AST: 12 U/L
ALT: 10 U/L

An initial ECG is notable for sinus tachycardia.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [100.0, 'mEq/L'], 'Bicarbonate': [9.0, 'mEq/L'], 'Sodium': [139.0, 'mEq/L']}",30,28.5,31.5,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 139.0 mEq/L. 
The concentration of chloride is 100.0 mEq/L. 
The concentration of bicarbonate is 9.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 139.0 mEq/L - (100.0 mEq/L + 9.0 mEq/L) = 30.0 mEq/L. Hence, The patient's anion gap is 30.0 mEq/L."
6201,39,Anion Gap,lab test,decimal,pmc-7011916-1,Extracted,"A 67-year-old man with past medical history of coronary artery disease (CAD) status post coronary artery bypass graft (CABG), history of alcoholism, and history of chronic kidney disease stage 3 presented with chest pain for 1 week. Chest pain was intermittent, left sided, 8/10 in severity, non-radiating, dull in nature, exacerbated by exertion and mildly relieved by rest. Remaining review of system was negative. He stopped taking all his cardiac medications for 1 year. Vitals were as follows: blood pressure 130/76 mm Hg, pulse 142/beat per minute respiratory rate 18/min. Pulse oximetry was 97% on 2 L nasal cannula. Cardiac examination was significant for tachycardia with irregularly irregular pulse but no murmur, rub or gallops. Lungs were clear to auscultation. Other system examinations were unremarkable. Laboratory data showed sodium 137 (136 - 145 mmol/dL), potassium 5.1 (3.5 - 5.2 mmol/dL), chloride 105 (96 - 110 mmol/dL), bicarbonate 22 (24 - 31 mmol/dL), blood urea nitrogen (BUN) 37 (5 - 25 mg/dL), creatinine 1.85 (0.44 - 1.0 mg/dL), glucose 130 (70 - 99 mg/dL), aspartate transaminase (AST) 176 (10 - 42 IU/L), alanine transaminase (ALT) 208 (10 - 60 IU/L), international normalized ratio (INR) 1.39, and thyroid stimulating hormone (TSH) 6.87 (0.3 - 4.5 IU/mL). Serum troponin was 0.01 (reference value < 0.04 ng/mL). Electrocardiogram (EKG) showed 2:1 atrial flutter. Initially patient was given cardizem and β-blocker boluses but heart rate did not improve. He was loaded with amiodarone 150 mg intravenous push (IVP) over 10 min and continued on amiodarone drip 1 mg/min over 6 h. Heparin drip was started for anticoagulation. On the following day morning labs showed significantly elevated liver enzymes and worsening renal function from his base line on the day of admission. AST was 4,250 (10 - 42 IU/L), ALT 2,422 (10 - 60 IU/L), and INR 2.28. Creatinine was 3.2 mg/dL (0.44 - 1.0 mg/dL), and BUN 44 mg/d reference value (5 - 25 mg/dL). At that moment patient was hemodynamically stable with blood pressure (BP) of 105/55 mm Hg, HR 70 beats per min and pulse ox of 95% on room air. Six hours later, patient became confused and unable to protect his airways. A rapid response was called, and the patient was intubated for airway protection and transferred to intensive care unit (ICU). Amiodarone was immediately stopped. Right upper quadrant ultrasound, a computed tomography (CT) of the chest, abdomen and pelvis without contrast were normal. Blood cultures, toxicology screen including acetaminophen level, hepatitis panel, antinuclear antibodies (ANAs), anti-smooth muscle antibody (ASMA), antimitochondrial antibody (AMA) were all negative. Alpha-1 antitrypsine (A1AT) was 126 (90 - 200 mg/dL), and ceruloplasmin 18 (17 - 54 mg/dL). Hereditary hemochromatosis mutation with C282Y heterozygote and H63D was negative. Patient was immediately started on N-acetylcysteine drip for 72 h. Patient’s liver enzymes continued to rise and peaked at 21,000 (10 - 42 IU/L) for AST and 9,020 (10 - 60 IU/L) for ALT (, ). Total bilirubin increased to 3.9 (, ). INR was 3.8 (day 3 of admission) (). Patient was deemed not a candidate for liver transplant due to history of alcoholism and acute-on-chronic kidney injury. As patient’s kidney function continued to worsen, he was started on hemodialysis (on the fifth day). His platelets count began to drop on day 3. Heparin-induced thrombocytopenia was suspected and heparin was stopped. Heparin-induced platelet antibodies with reflex to serotonin were positive. Patient was started on argatroban but serotonin release assay came back negative. Patient was successfully extubated to nasal cannula on day 8. LFTs improved and came down AST 79, ALT 192, and albumin of 2.5. INR was falsely high when patient was receiving argatroban () but improved after argatroban was stopped. Kidney function eventually improved, and he did not need more hemodialysis.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [137.0, 'mmol/dL'], 'Chloride': [105.0, 'mmol/dL'], 'Bicarbonate': [22.0, 'mmol/dL']}",100,95,105,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 137.0 mmol/dL. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 137.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 137.0 mmol * 1 mEq/mmol = 137.0 mEq sodium. The current volume unit is dL and the target volume unit is L. The conversion factor is 0.1 L for every unit of dL. Our next step will be to divide the mass by the volume conversion factor of 0.1 to get the final concentration in terms of mEq/L. This will result to 137.0 mEq sodium/0.1 L = 1370.0 mEq sodium/L. The concentration value of 137.0 mmol sodium/dL converts to 1370.0 mEq sodium/L. 
The concentration of chloride is 105.0 mmol/dL. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 105.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 105.0 mmol * 1 mEq/mmol = 105.0 mEq chloride. The current volume unit is dL and the target volume unit is L. The conversion factor is 0.1 L for every unit of dL. Our next step will be to divide the mass by the volume conversion factor of 0.1 to get the final concentration in terms of mEq/L. This will result to 105.0 mEq chloride/0.1 L = 1050.0 mEq chloride/L. The concentration value of 105.0 mmol chloride/dL converts to 1050.0 mEq chloride/L. 
The concentration of bicarbonate is 22.0 mmol/dL. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 22.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 22.0 mmol * 1 mEq/mmol = 22.0 mEq bicarbonate. The current volume unit is dL and the target volume unit is L. The conversion factor is 0.1 L for every unit of dL. Our next step will be to divide the mass by the volume conversion factor of 0.1 to get the final concentration in terms of mEq/L. This will result to 22.0 mEq bicarbonate/0.1 L = 220.0 mEq bicarbonate/L. The concentration value of 22.0 mmol bicarbonate/dL converts to 220.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 1370.0 mEq/L - (1050.0 mEq/L + 220.0 mEq/L) = 100.0 mEq/L. Hence, The patient's anion gap is 100.0 mEq/L."
6202,39,Anion Gap,lab test,decimal,pmc-3583747-1,Extracted,"Mr. R.E. is a 72-year-old man who presented to the emergency department with a four-day history of abdominal pain, nausea, vomiting and diarrhea, which at one point progressed to confusion and slurred speech. Past medical history was most significant for a fall four months previously that resulted in fracture of several ribs on his left side. On presentation he was alert, oriented, and hemodynamically stable with: temperature 36.7°C, BP 143/83 mmHg, HR 85 beats per minute, RR 20 breaths per minute, oxygen saturation at 96% on room air. He denied shortness of breath, fever, chills, night sweats, or weight loss. Cardiac, pulmonary, and neurological examinations were unremarkable. Abdominal examination revealed extreme diffuse pain to palpation and percussion, positive rebound tenderness, but no evidence of hepatosplenomegaly. Mucous membranes were dry, and petechiae were observed along the inner left thigh.
Initially laboratory investigations revealed: hemoglobin (Hb) 138 g/L, white blood cell count (WBC) 14.7×109/L, neutrophil count 13×109/L, platelets 28×109/L, sodium 132 mmol/L, chloride 95 mmol/L, potassium 4.2 mmol/L, bicarbonate 27 mmol/L, BUN 18.6 mmol/L, plasma creatinine 112 μmol/L, total bilirubin 22.2 μmol/L, international normalized ratio (INR) 1.1, prothrombin time (PTT) 30 seconds, aspartate aminotransferase (AST) 95 U/L, alkaline phosphatase 57 U/L, serum creatine kinase (CK) 807 U/L, troponin-T < 0.01 μg/L, lactate dehydrogenase (LDH) 282 U/L, serum lipase 13 U/L and total amylase 58 U/L. Urinalysis was positive for blood with 20 to 30 erythrocytes per high power field, protein 1.0 g/L and pH of 6.5. A CT of the abdomen with contrast showed the entire spleen to be non-enhancing suggesting complete infarction, which was suspected to be caused by spontaneous embolization of the splenic artery at the hilum (Figure ). No definite active vascular extravasation was seen, however there was soft tissue stranding, a small amount of high attenuating fluid in the perisplenic fat and along the right paracolic gutter, and a small to moderate volume of hemoperitoneum in the pelvis.
Although an atypical presentation, the initial concern was a microangiopathic disorder such as thrombocytopenic thrombotic purpura (TTP), hemolytic uremic syndrome (HUS), or idiopathic thrombocytopenic purpura (ITP). Additional investigations for other vasculitic or autoimmune causes showed: C3 complement level 0.55 g/L (normal 0.66 to 1.68 g/L), C4 complement level 0.07 g/L (normal 0.10 to 0.40 g/L), antinuclear antibody (ANA) very weakly positive. pANCA, cANCA and anti-glomerular basement membrane antibodies were all negative. Direct and indirect Coombs tests, as well as anti-phospholipid IgM and IgG were likewise all negative. Five units of platelets were transfused but it did not increase the platelet count. Thirty-six hours following presentation the hemoglobin remained stable (125 g/L), WBC decreased to 7.5×109/L, erythrocyte sedimentation rate (ESR) was elevated at 38 mm/h, and C reaction protein (CRP) was elevated at 346.3 mg/L. The peripheral blood smear showed reactive granulocytosis but no evidence of hemolysis, and the patient remained afebrile.
Forty-eight hours after presentation the patient’s condition began to deteriorate with: T 37.8°C, HR 110, RR 26, oxygen saturation at 92% on room air. The patient had high fever, chills, rigor and low back pain, but physical examination was unremarkable. Platelet count further decreased to less than 10×109/L, hemoglobin decreased to 109 g/L, serum LDH increased to 306 U/L, and total bilirubin increased to 45.7 μmol/L along with an increase in creatinine from 74 to 102 μmol/L. There was no evidence of disseminated intravascular coagulopathy (DIC) given a normal Klaus fibrinogen level at 4.30 g/L, INR 1.1, and PTT 26 seconds.
On day three of admission, peripheral blood smears showed some evidence of mild schistiocytes, suggesting the presence of microangiopathic hemolytic anemia (MAHA). Pulmonary condition began to deteriorate, with increased requirement to 6 liters of oxygen per minute producing an oxygen saturation of 88 to 90%. The patient became hemodynamically unstable with a BP 95/58 and experienced decreased level of consciousness. Chest X-ray showed bilateral pulmonary infiltrates with evidence of pulmonary edema. He was transferred to the intensive care unit and intubated due to hypoxic respiratory failure and decreased level consciousness. The nephrology service was consulted and plasma exchange therapy was empirically initiated on the suspicion for TTP as the etiology of his deterioration. Following initiation of plasma exchange, blood culture results obtained on admission to the hospital were found to contain gram-negative rods, and piperacillin-tazobactam 4.5 grams IV Q8H was initiated. Two subsequent blood cultures both showed evidence of an unknown gram-negative organism and the patient remained febrile with temperature 39.5°C. Cardiac echocardiogram did not reveal any valvular vegetation and a head CT scan was also unremarkable. Plasma exchange was stopped on day five of admission due to failure of platelet count to increase with plasma exchange therapy, the presence of gram negative blood cultures, and the degree of thrombocytopenia being largely out of proportion to the level of LDH rise.
On day six of admission, the microbiology laboratory reported that the gram-negative organism identified to be a capnocytophaga species based on its fastidious growth and morphology on gram stain (Figures and ). Antibiotic therapy was switched to imipenem 500 mg IV Q6H given reports of some capnocytophaga species being resistant to certain beta-lactams []. Subsequently, on day seven of admission the platelet count increased to 60×109/L, but the patient continued to be febrile with a temperature of 38.0°C and WBC count continued to increase to 22.5×109/L. Due to his persistent confusion and decreased level of consciousness, antibiotic therapy was changed to meropenem 2 grams IV Q6H to decrease the risk of imipenem induced seizure activity. In an attempt to identify the cause of the splenic infarction a trans-esophageal echo was performed, but it did not demonstrate valvular vegetations.
The patient’s condition began to improve clinically with meropenem. Fever gradually resolved, platelet count continued to increase, and WBC count began to normalize. Following extubation the patient’s neurological status continued to improve. On further questioning, the patient reported that several days prior to his presentation to the hospital he sustained a cut to his hand while performing automobile repairs. He reports that shortly after sustaining this cut that his dog licked his wound. The patient also reported that he plays with his dog in the evenings on a regular basis and often receives minor bites or scratches to his hands.
The patient was discharged home from the hospital on day twenty-one of his admission with no further antibiotic therapy. On discharge his WBC count was 14.2×109/L and platelets were 295×109/L. Blood culture samples were sent to the Central Public Health Laboratory, Toronto, Canada and through gene sequencing the organism C. canimorsus was isolated.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [95.0, 'mmol/L'], 'Bicarbonate': [27.0, 'mmol/L'], 'Sodium': [132.0, 'mmol/L']}",10,9.5,10.5,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 132.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 132.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 132.0 mmol * 1 mEq/mmol = 132.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 132.0 mmol sodium/L converts to 132.0 mEq sodium/L. 
The concentration of chloride is 95.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 95.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 95.0 mmol * 1 mEq/mmol = 95.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 95.0 mmol chloride/L converts to 95.0 mEq chloride/L. 
The concentration of bicarbonate is 27.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 27.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 27.0 mmol * 1 mEq/mmol = 27.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 27.0 mmol bicarbonate/L converts to 27.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 132.0 mEq/L - (95.0 mEq/L + 27.0 mEq/L) = 10.0 mEq/L. Hence, The patient's anion gap is 10.0 mEq/L."
6203,39,Anion Gap,lab test,decimal,pmc-7749864-1,Extracted,"An 80 year-old female presented to the emergency department with a chief complaint of repeated twitching in her upper chest and arm. The patient and her family reported that this had been going on for the past three days, however there was no accompanying chest pain. The patient reported a history of asthma, hypertension, congestive heart failure, and diabetes mellitus. The patient also had an automatic implantable defibrillator (AICD).
On presentation, these twitches were observed to occur rhythmically and regularly, in approximately 3-5 second intervals, in the bicep, shoulder, and upper chest on her left side. The patient’s skin and soft tissue around the AICD were normal, with no signs of erythema, tenderness, or swelling, and no palpable hematoma.
Her initial vital signs were: pulse 74 beats per minute; blood pressure 120/54 mmHg; respiratory rate 18 breaths per minute; temperature 36.30C; O2 Sat 97%. Her physical examination was unremarkable except for an AICD in the upper left chest wall. Initial blood work showed a white blood cell count of 7.42 x103/m3, hemoglobin of 12.1 g/dL, sodium 136 mmol/L; potassium 5.4 mmol/L; Cl 103 mmol/L; HCO3 31 mmol/L; BUN 37 g/dL; creatinine 1.86 g/dL; glucose 204 mg/dL; Troponin I <0.02 ng/ml. An electrocardiogram was obtained showing an intermittent atrial pacing at 100 beats per minute, left axis deviation, artifacts, premature ventricular contractions, right bundle branch block, non-specific diffused ST-T changes; and no ST elevations (Figure ).
Upon consultation with a representative of the AICD manufacturer to interrogate the device, the contractions were noted to be occurring in conjunction with its firing. Supine portable chest x-ray revealed a fractured and coiled lead on the upper portion of the device (Figure ).
The AICD device representative reprogrammed the device, ceasing its firing, and accordingly the patient’s muscle twitching ceased. The patient was admitted and care transferred to an electrophysiological cardiologist to remove the fractured wire and replace the AICD.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [103.0, 'mmol/L'], 'Bicarbonate': [31.0, 'mmol/L'], 'Sodium': [136.0, 'mmol/L']}",2,1.9,2.1,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 136.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 136.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 136.0 mmol * 1 mEq/mmol = 136.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mmol sodium/L converts to 136.0 mEq sodium/L. 
The concentration of chloride is 103.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 103.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 103.0 mmol * 1 mEq/mmol = 103.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 103.0 mmol chloride/L converts to 103.0 mEq chloride/L. 
The concentration of bicarbonate is 31.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 31.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 31.0 mmol * 1 mEq/mmol = 31.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 31.0 mmol bicarbonate/L converts to 31.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 136.0 mEq/L - (103.0 mEq/L + 31.0 mEq/L) = 2.0 mEq/L. Hence, The patient's anion gap is 2.0 mEq/L."
6204,39,Anion Gap,lab test,decimal,usmle-1292,Extracted,"Two days after admission to the hospital, a 74-year-old man develops confusion and headache. He has also been vomiting over the past hour. His temperature is 36.7°C (98°F), pulse is 98/min, respirations are 22/min, and blood pressure is 140/80 mm Hg. He is lethargic and oriented only to person. Examination shows flushed skin. Fundoscopic examination shows bright red retinal veins. Serum studies show:
Na+ 138 mEq/L
K+ 3.5 mEq/L
Cl- 100 mEq/L
HCO3- 17 mEq/L
Creatinine 1.2 mg/dL
Urea nitrogen 19 mg/dL
Lactate 8.0 mEq/L (N = 0.5 - 2.2 mEq/L)
Glucose 75 mg/dL
Arterial blood gas analysis on room air shows a pH of 7.13.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [100.0, 'mEq/L'], 'Bicarbonate': [17.0, 'mEq/L'], 'Sodium': [138.0, 'mEq/L']}",21,19.95,22.05,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 138.0 mEq/L. 
The concentration of chloride is 100.0 mEq/L. 
The concentration of bicarbonate is 17.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 138.0 mEq/L - (100.0 mEq/L + 17.0 mEq/L) = 21.0 mEq/L. Hence, The patient's anion gap is 21.0 mEq/L."
6205,39,Anion Gap,lab test,decimal,pmc-6954747-1,Extracted,"A 27-year-old man with no medical history presented with headache since the morning and increasing nausea and drowsiness during the day. He became progressively confused in the late afternoon after which his partner consulted a doctor. On arrival at the emergency department he had an epileptic seizure with spontaneous recovery. Neurological and physical examination were unremarkable. Clinically he was euvolemic. CT head showed diffuse sulcal effacement without signs of haemorrhage, basilar artery thrombosis, cerebral venous sinus thrombosis or an intracranial tumour. Venous blood gas analysis, taken minutes after the seizure, showed a pH of 6.89, Pco2 10.8 kPa, bicarbonate 15.4 mmol/L, base excess −19.4 mmol/L and a lactate of 18.0 mmol/L. Blood chemistry was remarkable for sodium 131 mmol/L, chloride 82 mmol/L, albumin 51 g/L and an osmolality of 278 mOsmol/kg. The urine toxicology test was positive for acetaminophen but negative for opiates, amphetamines and cocaine. He was then treated with ceftriaxone, amoxicillin, acyclovir and dexamethasone awaiting the results of the lumbar puncture but the examination of the cerebrospinal fluid was normal.
This prompted us to reconsider the laboratory results. Patients relatively high haematocrit (0.48 L/L), together with the increased albumin level, were suggestive for haemoconcentration. However, we realised that measurements were done in a venous blood sample, which may have been ‘haemoconcentrated’ by water influx into the muscles during rhabdomyolysis. Therefore, we suggested that his arterial sodium concentration could well be lower, possibly low enough to explain the seizure. And indeed, in an arterial blood gas analysis taken 45 min after the seizure, the plasma sodium level was 118 mmol/L. Analysis of this hyponatremia revealed a urine sodium level of <20 mmol/L and an osmolality of 92 mOsmol/kg. He was diagnosed with primary polydipsia (the polyuria explaining the relatively low urine sodium concentration) and was admitted to the intensive care unit. In the first hours after admission his urine production was over 1 L/hour and the plasma sodium level rapidly increased to 128 mmol/L.
After regaining consciousness he told he had been drinking an excessive amount of water extra throughout the day (4–5 L) because he thought that his headache was caused by dehydration. He further explained that he was living a healthy lifestyle in which drinking ample amounts of water played a central role.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [82.0, 'mmol/L'], 'Bicarbonate': [15.4, 'mmol/L'], 'Sodium': [131.0, 'mmol/L']}",33.6,31.92,35.28,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 131.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 131.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 131.0 mmol * 1 mEq/mmol = 131.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 131.0 mmol sodium/L converts to 131.0 mEq sodium/L. 
The concentration of chloride is 82.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 82.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 82.0 mmol * 1 mEq/mmol = 82.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 82.0 mmol chloride/L converts to 82.0 mEq chloride/L. 
The concentration of bicarbonate is 15.4 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 15.4 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 15.4 mmol * 1 mEq/mmol = 15.4 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 15.4 mmol bicarbonate/L converts to 15.4 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 131.0 mEq/L - (82.0 mEq/L + 15.4 mEq/L) = 33.6 mEq/L. Hence, The patient's anion gap is 33.6 mEq/L."
6206,39,Anion Gap,lab test,decimal,pmc-3461311-1,Extracted,"The patient, a 55-year-old woman, was admitted to our hospital on February 3rd, 2012. Her chief complaint was repeated consciousness obstacle over two years. She had been in good health with normal menstrual cycles until her third delivery in 1988. She started to get mild hypofunction of gonad, thyroid, and adrenal cortex after severe postpartum hemorrhage. Unfortunately, owing to the limited medical resources in her hometown, she was not diagnosed as Sheehan's syndrome and did not receive enough professional treatment. Her menstrual periods prolonged (about 40–50 days) with little volume and short duration. In 1990, she conceived naturally for the fourth time but the symptoms got worse after delivery, especially in recent years. From 2000, she had unconsciousness for three times. She gradually had serious hypoglycemia, progressive fatigue, loss of cutaneous pigment, dryness, and furfuration of the skin, loss of muscle strength, and a decrease in libido after the fourth delivery. Nevertheless, she had no symptoms of vomiting, nausea, abdominal pain, or orthostatic dizziness. The family history of similar symptoms and previous history of hypertension or diabetes were not found.
The general physical examination showed that the blood pressure, heart rate, and temperature were within normal limits. She was in a coma and appeared chronically ill and pale with dryness and furfuration of the skin. Her eyebrows (), glandebalaes and pubes fell off. There was no remarkable abnormality in lung, heart, and neurological examinations.
Routine laboratory findings demonstrated a red blood cell count of 3.32 × 1012/L, a hemoglobin of 101 g/L, a hematocrit of 30.3%, the random blood glucose 2.89 mmol/L, the serum sodium 121.0 mmol/L, the chloride 94.5 mmol/L, carbon dioxide combining power (CO2CP) 17.2 mmol/L, the uric acid 63 μmol/L, the aspartate transaminase (AST) 72 U/L, the total protein (TP) 51.3 g/L, the albumin (ALB) 28.6 g/L, the globulin (GLB) 22.7 g/L, the triglyceride (TG) 2.83 mmol/L, the total cholesterol 7.62 mmol/L, the low-density lipoprotein cholesterol (LDL-C) 6.43 mmol/L, and the high-density lipoprotein cholesterol (HDL-CH) 0.67 mmol/L. The urine routine and stool routine were normal.
As the clinical manifestations suggested Sheehan's syndrome, related endocrinological tests were finished as follows. The thyroid function test revealed a serum triiodothyronine (T3) of 0.31 ng/mL (normal 0.6 to 1.81), a thyroxine (T4) of 0 μg/dL (normal 4.5 to 12.5), a free triiodothyronine (FT3) of 0.88 pg/mL (normal 1.8 to 4.2), a free thyroxine (FT4) of 0.16 ng/mL (normal 0.8 to 1.76), a thyroid-stimulating hormone (TSH) level of 1.547 μIU/mL (normal 0.35 to 5.5), and a thyroglobulin autoantibody of 83.6 U/mL (normal 0 to 60). The plasma adrenocorticotropic hormone (ACTH) level was 4.8 pg/mL (normal 0 to 46). The plasma crotisol level was 0.75 μg/dL (normal 3.9 to 22.4). The growth hormone (GH) level was 0.049 ng/mL (normal 0 to 10). The follicle-stimulating hormone (FSH) was 4.30 mIU/mL, the luteinizing hormone (LH) was 1.78 mIU/mL and the estradiol (E2) was 10.52 pg/mL.
The brain magnetic resonance imaging (MRI) showed a diminutive pituitary and an empty sella turcica (). There was no evidence of hemorrhage, intracranial mass, or aneurysm ().
She was diagnosed as Sheehan's syndrome and pituitary crisis. Replacement therapy was instituted with hydrocortisone and levothyroxine sodium.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [94.5, 'mmol/L'], 'Bicarbonate': [17.2, 'mmol/L'], 'Sodium': [121.0, 'mmol/L']}",9.3,8.835,9.765,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 121.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 121.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 121.0 mmol * 1 mEq/mmol = 121.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 121.0 mmol sodium/L converts to 121.0 mEq sodium/L. 
The concentration of chloride is 94.5 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 94.5 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 94.5 mmol * 1 mEq/mmol = 94.5 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 94.5 mmol chloride/L converts to 94.5 mEq chloride/L. 
The concentration of bicarbonate is 17.2 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 17.2 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 17.2 mmol * 1 mEq/mmol = 17.2 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 17.2 mmol bicarbonate/L converts to 17.2 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 121.0 mEq/L - (94.5 mEq/L + 17.2 mEq/L) = 9.3 mEq/L. Hence, The patient's anion gap is 9.3 mEq/L."
6207,39,Anion Gap,lab test,decimal,pmc-4530232-1,Extracted,"A 21-year-old Tarahumara male was transferred from his community hospital with a 4-month history of cough, hemoptysis, progressive dyspnea, intermittent fever, and significant weight loss. On admission, he presented with a bad general condition, with the following vital signs: blood pressure of 90/60 mmHg, heart rate of 140 bpm, respiratory rate of 35 breaths per minute, and core body temperature of 99.5°F. The physical examination revealed a cachectic young man with evident signs of ARF including tachypnea, breathy speech, and accessory muscle use. Chest auscultation evidenced fine inspiratory crackles, mainly in the right apex. Arterial blood-gas (ABG) analysis while he breathed supplemental oxygen via a mask showed a pH of 7.37, PaO2 of 98 mmHg, PaCO2 of 36.5 mmHg, and HCO3
− of 20.8 mEq/L. Laboratory admission tests showed Hb of 11.1 g/dL, white blood count (WBC) of 11.6 cells/μL, neutrophils count of 10.9/μL, lymphocytes count of 0.2/μL, Na+ of 136 mmol/L, Cl− of 98 mmol/L, K+ of 4.02 mmol/L, Ca2+ of 7.6 mg/dL, glucose of 77 mg/dL, Cr of 0.36 mg/dL, blood urea nitrogen (BUN) of 6.1 mg/dL, uric acid of 3.7 mg/dL, cholesterol of 91 mg/dL, triglycerides of 98 mg/dL, and albumin of 2.1 g/dL. The HIV and hepatitis B and C tests were all negative. Sputum acid-fast stains were positive since his previous hospitalization and a real-time polymerase chain reaction (PCR) assay performed with another sputum sample confirmed the presence of Mycobacterium tuberculosis DNA. A chest X-ray showed diffuse alveolar and nodular opacities, as well an extensive right upper lobe cavitary disease (). Based on the above findings, we calculated an APACHE II score of 13. The patient was treated with hydrocortisone 100 to 250 mg intravenously for 8 hours, and a daily regimen of intravenous amikacin 750 mg, and moxifloxacin 400 mg, along with antituberculosis treatment of 3 tablets of a fixed-dose combination (DoTBal, SILANES Laboratories) of rifampicin 150 mg, isoniazid 75 mg, pyrazinamide 400 mg, and ethambutol 300 mg. The patient was admitted to the intensive care unit but on day 4 in the hospital, the increased work of breathing required the initiation of NIPSV with a single-limb-circuit bilevel ventilator (VPAP III, ResMed) through an oronasal interface at pressures of 8–12/4 cm H2O. The DoTBal dose was increased to 4 tablets per day; however, the characteristic red color of the urine produced by rifampicin was no longer observed and the serum levels in a random sample were undetectable. Over the next 4 days despite slight improvement in PaCO2, it was not possible to wean the patient from NIPSV due to the persistent tachypnea. After a discussion regarding alternative therapies and under the respective observations of the local board of pharmacovigilance, the medical team decided as an extraordinary measure to administer etanercept (Enbrel, Wyeth Laboratories) 25 mg subcutaneously. The following day the patient showed a general improvement and an improved respiratory condition (). After 2 days, he could finally be separated from NIPSV and undergo continued care in an isolated hospital ward breathing supplemental oxygen via nasal prongs. Three days after the first dose of etanercept, a second dose was administered without significant changes in the clinical condition of the patient. However, 4 days after the second dose of etanercept, the patient experienced exacerbation of respiratory symptoms, malaise, and fever of 100.5°F (). Due to the short half-life of etanercept, this scenario was attributed to a paradoxical reaction and resolved promptly with the administration of a final third dose of etanercept along with hydrocortisone 200 mg intravenously. Within a few days, the clinical condition of the patient allowed his transfer to a unit with long-term care facilities, and after a month with negative smears for acid-fast bacilli he was finally discharged to their community under a directly observed therapy (DOT) program.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [98.0, 'mmol/L'], 'Bicarbonate': [20.8, 'mEq/L'], 'Sodium': [136.0, 'mmol/L']}",17.2,16.34,18.06,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 136.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 136.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 136.0 mmol * 1 mEq/mmol = 136.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mmol sodium/L converts to 136.0 mEq sodium/L. 
The concentration of chloride is 98.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 98.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 98.0 mmol * 1 mEq/mmol = 98.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 98.0 mmol chloride/L converts to 98.0 mEq chloride/L. 
The concentration of bicarbonate is 20.8 mEq/L. 
Plugging in these values into the anion gap formula gives us 136.0 mEq/L - (98.0 mEq/L + 20.8 mEq/L) = 17.2 mEq/L. Hence, The patient's anion gap is 17.2 mEq/L."
6208,39,Anion Gap,lab test,decimal,pmc-5649858-1,Extracted,"A 77-year-old woman was diagnosed with T1N0 Mx papillary serous endometrial adenocarcinoma. She underwent total abdominal hysterectomy, bilateral salphingo-oophorectomy, and lymph node dissection in 2000. In 2006, following an abnormal Pap smear, a biopsy of the vaginal cuff revealed metastases to this region. Positron emission tomography (PET) scan showed recurrence of the pelvic tumor, with lymph node metastases, and obstructive uropathy. Bilateral ureteral stenting was performed and the patient was treated with Carboplatin and Paclitaxel infusions from November 2006 to April 2007. The treatment was tolerated well except for the development of chronic anemia for which she received three units of packed red cell transfusion. In September 2007, a follow-up PET scan showed a recurrence of the pelvic tumor for which the patient was restarted on cyclical chemotherapy with weekly infusions of Carboplatin and Paclitaxel. During the fifth cycle of Carboplatin infusion, she became unresponsive and hypotensive. Carboplatin infusion was stopped and the patient was transferred to the emergency department (ED) at the same institution. In the ED she was unresponsive, with a blood pressure of 60/30 mmHg, heart rate of 110 beats per minute, respiratory rate of 26 breaths per minute, and oxygen saturation of 85% on 50% oxygen by ventimask. On physical examination she looked pale, with cool and clammy extremities. Her lungs were clear and the rest of the physical examination was normal. Laboratory tests showed: a hemoglobin of 3.8 g/dl (Her hemoglobin just prior to the Carboplatin infusion was 10.4 g/dl), arterial blood gases (ABG) were pH of 6.97, PCO2 of 14.4 and PaO2 of 271.7 mm Hg. Sodium was 130 mmol/lit (normal value 135 - 145 mmol/lit), with potassium of 4.6 mmol/lit (normal value 3.5 - 5.00 mmol/lit), chloride of 95 mmol/lit (normal value 97 - 108 mmol/lit), bicarbonate of 11 mmol/lit (normal value 22 - 29 mmol/lit), blood urea nitrogen of 32 mg/dl (Normal value 5-20 mg/dl), creatinine of 1.57 mg/dl (normal value 0.5 - 1.0 mg/dl), negative troponins and a slightly elevated creatinine kinase levels. Head CAT scan was normal. Peripheral blood smear showed clumped red blood cells (RBC’s). Serologic studies were sent for direct and indirect coombs test. The patient was intubated, and received three units of packed red blood cells and was resuscitated with intravenous normal saline, intravenous bicarbonate solution, steroids, and vasopressors. Despite aggressive treatment, she expired in seven hours. Later on, her serum was found to be positive for direct Coomb’s test. Carboplatin-dependent antibody was also detected. Direct anti-globulin (Coomb’s) test (DAT) was positive and showed the presence of anti-IgG and anti-C3 on the patient’s RBC’s. Elute prepared from patient’s RBC’s reacted when tested against red blood cells in the presence of Carboplatin and did not react with other cells, supporting an “immune complex-mediated destruction of RBC’s. The patient’s serum reacted with untreated RBC’s in the presence of Carboplatin, with titers at room temperatures and 37o Celsius of 2048. Titers for the antiglobulin test was 1024, supporting the presence of Carboplatin-dependent antibody and the diagnosis of Carboplatin-induced fatal hemolytic anemia.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [130.0, 'mmol/L'], 'Chloride': [95.0, 'mmol/L'], 'Bicarbonate': [11.0, 'mmol/L']}",24,22.8,25.2,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 130.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 130.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 130.0 mmol * 1 mEq/mmol = 130.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mmol sodium/L converts to 130.0 mEq sodium/L. 
The concentration of chloride is 95.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 95.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 95.0 mmol * 1 mEq/mmol = 95.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 95.0 mmol chloride/L converts to 95.0 mEq chloride/L. 
The concentration of bicarbonate is 11.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 11.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 11.0 mmol * 1 mEq/mmol = 11.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 11.0 mmol bicarbonate/L converts to 11.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 130.0 mEq/L - (95.0 mEq/L + 11.0 mEq/L) = 24.0 mEq/L. Hence, The patient's anion gap is 24.0 mEq/L."
6209,39,Anion Gap,lab test,decimal,usmle-1029,Extracted,"A 68-year-old man is brought to the emergency department because of fever, progressive weakness, and cough for the past five days. He experienced a similar episode 2 months ago, for which he was hospitalized for 10 days while visiting his son in Russia. He states that he has never fully recovered from that episode. He felt much better after being treated with antibiotics, but he still coughs often during meals. He sometimes also coughs up undigested food after eating. For the last 5 days, his coughing has become more frequent and productive of yellowish-green sputum. He takes hydrochlorothiazide for hypertension and pantoprazole for the retrosternal discomfort that he often experiences while eating. He has smoked half a pack of cigarettes daily for the last 30 years and drinks one shot of vodka every day. The patient appears thin. His temperature is 40.1°C (104.2°F), pulse is 118/min, respirations are 22/min, and blood pressure is 125/90 mm Hg. Auscultation of the lungs shows right basal crackles. There is dullness on percussion at the right lung base. The remainder of the physical examination shows no abnormalities. Laboratory studies show:
Hemoglobin 15.4 g/dL
Leukocyte count 17,000/mm3
Platelet count 350,000/mm3
Na+ 139 mEq/L
K+
4.6 mEq/L
Cl- 102 mEq/L
HCO3- 25 mEq/L
Urea Nitrogen 16 mg/dL
Creatinine 1.3 mg/dL
An x-ray of the chest shows a right lower lobe infiltrate.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [102.0, 'mEq/L'], 'Bicarbonate': [25.0, 'mEq/L'], 'Sodium': [139.0, 'mEq/L']}",12,11.4,12.6,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 139.0 mEq/L. 
The concentration of chloride is 102.0 mEq/L. 
The concentration of bicarbonate is 25.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 139.0 mEq/L - (102.0 mEq/L + 25.0 mEq/L) = 12.0 mEq/L. Hence, The patient's anion gap is 12.0 mEq/L."
6210,39,Anion Gap,lab test,decimal,pmc-5519313-1,Extracted,"The patient is a 63-year-old man with a past medical history of MALToma of the lung who presented with generalized weakness for the past one month associated with cough, fever, night sweats, and shortness of breath. The patient also had anorexia and weight loss of 15 pounds over one month. He denied a history of smoking. The patient was under treatment with isoniazid and pyridoxine for latent tuberculosis based on a positive skin tuberculin test.
On physical examination, his blood pressure was 110/59 mmHg, heart rate 118 beats per minute (bpm), respiratory rate 18/min, saturating 99% on room air with a temperature of 98.9oF. The patient was in no cardiopulmonary distress. A cardiovascular examination revealed no jugular venous distension, normal S1-S2, and no murmurs. On lung auscultation, the patient had rales at the left lung base.
Laboratory data showed sodium 134 mEq/L, potassium 4.2 mEq/L, chloride 103 mEq/L, bicarbonate 25 mEq/L, blood urea nitrogen 17 mg/dl, creatinine 0.9 mg/dl, glucose 96 mg/dl, hemoglobin 6.6 g/dl, hematocrit 20.1%, white blood cell count 5.5 x 103/microliter, and platelets 128 x 103/microliter. The coagulation profile showed prothrombin time (PT) 17.2 sec, partial thromboplastin time (PTT) 44.3 sec, and international normalized ratio (INR) 1.38.
Chest X-ray (CXR) and computed tomography (CT) scan showed right middle lobe opacity (Figures -). Repeat imaging after six months showed multiple masses in the lung and an osteoblastic bone lesion involving the left ilium (Figures -). Esophagogastroduodenoscopy showed a normal gastro-esophageal junction with erythematous mucosa in the stomach. The gastric biopsy was normal.
A lung biopsy done at initial presentation from the right middle lobe mass showed dense lymphoid infiltrate with proliferation of monocytoid B lymphocytes consistent with extranodal marginal zone lymphoma (BALToma/MALToma).
A CT-guided core needle biopsy from the left posterior pelvic mass that was noted six months after the initial presentation showed high grade diffuse large B-cell lymphoma involving skeletal muscles. The pathology report showed diffuse proliferation of lymphocytes, which were positive for cluster of differentiation (CD) 20 and B-cell lymphoma (BCL)-2 by immunohistochemistry tests. He was started on chemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) with subsequent complete clinical and radiologic remission (Figure ).",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [103.0, 'mEq/L'], 'Bicarbonate': [25.0, 'mEq/L'], 'Sodium': [134.0, 'mEq/L']}",6,5.7,6.3,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 134.0 mEq/L. 
The concentration of chloride is 103.0 mEq/L. 
The concentration of bicarbonate is 25.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 134.0 mEq/L - (103.0 mEq/L + 25.0 mEq/L) = 6.0 mEq/L. Hence, The patient's anion gap is 6.0 mEq/L."
6211,39,Anion Gap,lab test,decimal,pmc-4527798-1,Extracted,"We present a 60-year-old white female with a history of borderline personality disorder, hypertension (outpatient records indicate office readings for systolic blood pressure ranging from 120 to 130 mmHg on treatment), and chronic lumbago who reported to the emergency department with nausea and vomiting for 2 days and intentional amlodipine overdose. She reported taking approximately 300 mg of amlodipine 10 h prior to admission. The patient’s other medications included oxycodone, docusate, ibuprofen, and pantoprazole, all of which she reported taking as prescribed. On presentation, the patient was alert and oriented with a Glascow Coma Score (GCS) of 15. Vital signs showed a noninvasive blood pressure of 90/56 mmHg with no other abnormality. Examination revealed equal and mildly diminished radial pulses, normal heart rate and rhythm, clear lung fields, sluggish bowel sounds, no peripheral edema and no pallor. Initial laboratory results included an unremarkable complete blood count, a basic metabolic panel showing a sodium of 136 mmol/L, potassium of 5.3 mmol/L, chloride of 102 mmol/L, bicarbonate of 17 mmol/L, urea nitrogen of 22 mg/dL and a creatinine of 1.58 mg/dL (baseline 0.44 mg/dL). Further, urinalysis on admission was remarkable for the presence of ketones. Urine and serum toxicology including salicylate and acetaminophen were negative. Procalcitonin was 0.1 ng/mL and lactic acid was 2 mmol/L. Cardiac troponins were trended and were not elevated. Activated charcoal was not administered on admission due to the amount of time that had passed from ingestion to presentation. The patient was admitted to the medical transitional care unit for observation.
The medical intensive care team was notified 7 h after admission when the patient’s noninvasive mean arterial pressure (MAP) fell to the low 50s and was not responsive to fluid resuscitation and her mental status deteriorated to a GCS of 7. She was transferred to the medical intensive care unit where she required intubation for airway protection, had two central lines placed for medication compatibility concerns, and had an arterial line placed. In the ICU, lactic acid was found to be 6.4 mmol/L, and arterial blood gas showed a pH of 6.95, partial pressure of carbon dioxide (pCO2) of 43 mmHg, a partial pressure of oxygen (pO2) of 79 mmHg, and calculated bicarbonate of 9 mmol/L on 60% fraction of inspired oxygen (FiO2). Electrocardiogram at that time showed normal sinus rhythm, rate of 72 beats per minute, QTc of 408 ms, and low voltage in precordial leads.
A dopamine drip (10 μg/min titrated to 20 μg/min at maximum) through peripheral line, glucagon drip (5 mg loading dose followed by 5 mg/h drip), and a bolus of 3 amps of 8.4% sodium bicarbonate (150 mEq NaCO3 in 1L) in 1L D5W were subsequently started. After central access was obtained, calcium carbonate (12 mg/hr), norepinephrine (starting at 75 μg/min titrated up to 100 μg/min at maximum), epinephrine (5 μg/min titrated up to 10 μg/min), dobutamine (10 μg/kg/min titrated up to 25 μg/kg/min), methylprednisolone (100 mg every 8 h), and phenylephrine (100 μg/min) were started in rapid succession. Despite these interventions, arterial line MAPs were ranging between 45 and 60. Poison control was consulted and recommended continuing calcium carbonate while monitoring ionized calcium every 2 h, along with the bicarbonte drip in D5W, and glucagon drip. They also recommended starting an insulin drip which was administered per hospital ICU protocol targeting blood glucose of 180 mmol/L. Hemodynamic state was monitored using an arterial line and target MAP was >65.
Cardiology was consulted and performed a stat two-dimensional transthoracic echocardiogram, which showed mildly reduced left ventricular contractility with the ejection fraction measured at 51%. Methylene blue (2 mg/kg administered over 1 h) and vasopressin (0.04 units/min at set rate) were started per cardiology’s recommendations.
Within 18 h of these therapies, the patient’s MAP stabilized above 65, and vasopressors were slowly weaned starting with dobutamine, as echocardiogram result made cardiogenic shock unlikely. Phenylephrine, dopamine, and vasopressin were also weaned off on the first day. Epinephrine, insulin, and steroids were discontinued in ICU day 2. On day 3, the patient required only norepinephrine and glucagon drips to maintain a MAP >65. By day 4, the patient was requiring no vasopressors, was following commands, and was extubated. She was transferred to the floor the next day for treatment of acute kidney injury and aspiration pneumonia. She was discharged without sequelae on hospital day 7.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [136.0, 'mmol/L'], 'Chloride': [102.0, 'mmol/L'], 'Bicarbonate': [17.0, 'mmol/L']}",17,16.15,17.85,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 136.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 136.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 136.0 mmol * 1 mEq/mmol = 136.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mmol sodium/L converts to 136.0 mEq sodium/L. 
The concentration of chloride is 102.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 102.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 102.0 mmol * 1 mEq/mmol = 102.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 102.0 mmol chloride/L converts to 102.0 mEq chloride/L. 
The concentration of bicarbonate is 17.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 17.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 17.0 mmol * 1 mEq/mmol = 17.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 17.0 mmol bicarbonate/L converts to 17.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 136.0 mEq/L - (102.0 mEq/L + 17.0 mEq/L) = 17.0 mEq/L. Hence, The patient's anion gap is 17.0 mEq/L."
6212,39,Anion Gap,lab test,decimal,pmc-8451257-1,Extracted,"Case #1
A 51-year-old male patient with past medical history of alcohol and IVDU, untreated hepatitis C, heart failure with reduced ejection fraction (left ventricular ejection fraction, LVEF 40%-45%), thoracic vertebral bacterial osteomyelitis, infective bacterial endocarditis with S. marcescens, s/p bioprosthetic aortic and tricuspid valves replacement was brought to the emergency department by emergency medical services (EMS) for evaluation of altered mental status, after being found unresponsive on the street. The patient had been previously admitted to the hospital a month prior to this presentation with similar complaints and was diagnosed with sepsis secondary to bacterial endocarditis and vertebral osteomyelitis with an epidural abscess. Blood cultures obtained on the prior admission grew Gram positive cocci in clusters, later identified as S. marcescens. The patient was treated with prolonged courses of antibiotics, after which his sepsis resolved, and he was discharged shortly after. Presumably, in the time between the two admissions, the patient had had valve replacement surgery performed, as he presented with a sternotomy scar and a trans-thoracic echocardiogram performed on this admission revealed bioprosthetic aortic and tricuspid valves as seen in Video . On the current presentation, the patient’s mentation was altered so no history could be gathered at the time of admission. On presentation, the patient was febrile, body temperature 101.8°F, blood pressure (BP) 11/64 mmHg, heart rate (HR) 110 bpm, respiratory rate (RR) 25/min, and his O2 saturation was 95% on room air. The complete blood count (CBC) revealed hemoglobin (Hgb) 11.2 g/dL (12-16 g/dL) with a mean corpuscular volume (MCV) of 77.9, white blood cell (WBC) count 3.6 (4.8-10.8) with absolute neutrophils of 2.8 (1.4-6.5) and platelet count 18k (130-400k).
The basic metabolic panel (BMP) revealed blood glucose 99 mg/dL (74-118 mg/dL), creatinine 1.04 mg/dL (0.4-1.0 mg/dL), sodium 125 mmol/L (136-146 mmol/L), potassium 3.9 mmol/L (3.6-5.1 mmol/L), chloride 95 mmol/L (101-111 mmol/L), bicarbonate 21 mmol/L (22-32 mmol/L), magnesium 1.0 mg/dL (1.8-2.5 mg/dL), and phosphorus 1.6 mg/dL (2.4-4.7 mg/dL). Lactic acid was 1.2 mmol/L (0.5-2.2 mmol/L). Radiology was insignificant, as a chest X-ray revealed sternal sutures consistent with open heart and valve replacement surgery but showed no acute cardiopulmonary events. CT studies of the head and cervical spine were negative for acute, strokes, bleeds, or fractures as well.
The patient was bloused with 3 L of lactated Ringer in the ED, as code sepsis was called, and he was given STAT doses of vancomycin and zosyn for broad spectrum coverage. Blood and urine cultures were drawn for culture and sensitivity studies. The patient was started on standing doses of antibiotics and was admitted for further management. Unfortunately, the patient’s serum sodium dropped rapidly to 121 mmol/L, likely secondary to massive IV fluid transfusion, his serum osmolarity at the time was 260 mOsm/kg (280-295 mOsm/kg) and his urine osmolarity was 611 mOsm/kg; he was started on normal saline intravenous fluids (IVF), and was upgraded to the intensive care unit (ICU) for closer monitoring and correction of his electrolytes. The patient gradually regained consciousness, and his serum sodium improved to 127 in the span of eight hours, so the IV fluids were discontinued, and he was fluid restricted to prevent over-correction. Shortly after the patient became fully oriented, he opted to sign out of the hospital against medical advice. The risks were explained to the patient regarding the critical nature of his condition, but he decided to leave and not continue his hospital course.
A few hours later, the patient was again brought by the EMS after being found once again unconscious on the highway. His previous management was continued as mentioned before, and he regained consciousness shortly after admission. His condition improved in terms of body temperature, BP, and HR. Blood cultures obtained revealed Gram positive bacteremia, so his antibiotic regimen was narrowed to vancomycin alone. The patient then reported that he was on methadone treatment for heroine dependence and withdrawal and expressed the wish to be continued on it. A few hours later, the patient again wanted to leave the hospital against medical advice, and he was again counseled on the severity of his condition and the importance of completing his antibiotic regimen and hospital course, but he was adamant about leaving and left the hospital before the complete resolution of his symptoms.
Case #2
The patient was a 51-year-old Hispanic female with past medical history of hypertension, depression, chronic hepatitis C, and IV substance abuse who was brought to emergency room by ambulance with chief complaint of severe acute low back pain. Low back pain was started three days before her presentation. It was constant, radiating to legs, worsened with movement, with no alleviating factor, associated with malaise. The patient was actively using IV heroin and had previous history of heroin overdose. Her last heroin injection was two to three days before admission, around the same time that the pain started. Upon admission, the patient denied fevers, chills, chest pain, dyspnea, nausea, vomiting, diarrhea, skin lesions, numbness, tingling, and weakness of the lower extremities.
In the ED, initial vital signs were within normal limits. Physical examination was remarkable for disorientation, 3/6 systolic murmur, in addition to opiate withdrawal sings. Labs were significant for sodium 129 (136-144 mmol/L), blood urea nitrogen (BUN) 30 (8-20 mg/dL), creatinine 1.5 (0.4-1.0 mg/dL), WBC 19.3 (4.8-10.8 k/uL) with neutrophil predominance, platelet 71 (130-400 K). Urinalysis was also positive for large blood and leuko esterase. MRI of spine showed degenerative changes but no concrete evidence of abscess or osteomyelitis. Trans thoracic echocardiogram was unremarkable. Trans esophageal echocardiogram showed moderate sized (1.6 cm x 2 cm) vegetation on the anterior leaflet of the mitral valve of high embolic potential and ischemic cardiomyopathy of the left ventricle as seen in Video . CT of the abdomen showed multiple splenic and renal infarcts as seen in Figures -. The patient was started on empirical treatment with vancomycin and cefepime after first sets of blood culture was done. Blood cultures turned to be positive for S. marcescens and later antibiotics were changed to ceftriaxone based on the sensitivity results.
During hospital course, the patient’s mental status was further deteriorated. Severe tachypnea and respiratory distress resulted in intubation and mechanical ventilation of the patient in the ICU. Brain MRI showed multiple foci of acute non-hemorrhagic infarcts secondary to cardioembolic disease.
Antibiotic therapy was continued for the patient and second sets of blood culture were negative. The patient was evaluated by cardiothoracic surgeon. She was not a candidate for surgery intervention, due to unstable medical condition and multiple brain and myocardium infarcts. Hospitalization was further complicated by pneumonia with positive respiratory culture for S. marcescens and later Clostridium difficile infection. Due to multiple failed weaning trials, tracheostomy was placed for the patient. After two months of hospitalization, the patient was transferred to long-term acute care hospital. The patient was alert, able to follow simple commands, and remained ventilator dependent by the time of the discharge.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [95.0, 'mmol/L'], 'Bicarbonate': [21.0, 'mmol/L'], 'Sodium': [125.0, 'mmol/L']}",9,8.55,9.45,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 125.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 125.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 125.0 mmol * 1 mEq/mmol = 125.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 125.0 mmol sodium/L converts to 125.0 mEq sodium/L. 
The concentration of chloride is 95.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 95.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 95.0 mmol * 1 mEq/mmol = 95.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 95.0 mmol chloride/L converts to 95.0 mEq chloride/L. 
The concentration of bicarbonate is 21.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 21.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 21.0 mmol * 1 mEq/mmol = 21.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 21.0 mmol bicarbonate/L converts to 21.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 125.0 mEq/L - (95.0 mEq/L + 21.0 mEq/L) = 9.0 mEq/L. Hence, The patient's anion gap is 9.0 mEq/L."
6213,39,Anion Gap,lab test,decimal,pmc-8677960-1,Extracted,"An 8-year-old Chinese boy with no specific family or psychosocial history was admitted to our hospital with an emergency occurrence of purpura, severe hematemesis, large bloody stools, and sharp abdominal pain. His symptoms had begun 2 weeks prior to admission, with abdominal pain and an erythematous pinpoint rash on his arms. The rash developed from his upper limbs (opisthenar and arms) to his lower limbs. Laboratory examination in the outpatient clinic revealed no abnormalities in indicators such as white blood cell count, platelet count, and hemoglobin. After oral medication (specific unknown), his abdominal symptoms began to reduce, as did the purpura. Ten days prior, the rash progressed mostly on the legs, and he experienced deeper abdominal pain in the form of persistent pain with abdominal gassiness and emesis. He was admitted to another hospital with a diagnosis of HSP. Seven days prior, he had melena. After fasting and fluid replacement, there was no obvious improvement in the symptoms. Half a day prior, his face and lips appeared pale, and he had increased abdominal pain, accompanied by numerous bloody stools and hematemesis. He was immediately treated with methylprednisolone, posterior pituitary injection, somatostatin, and hemocoagulase, together with the infusion of large blood products (Table ). At this stage, the patient still produced large amounts of blood in the vomit and stool. His vital signs were extremely unstable, and he was transferred to the pediatric intensive care unit of our hospital. The patient had purpura with lower limb predominance and abdominal pain (consistent with one of the following 4 criteria: abdominal pain, histopathology, arthritis or arthralgia, and renal involvement), and was diagnosed with HSP.[
On admission, he had severe anemia, with a blood pressure of 76/44 mm Hg, pulse of 135 beats/min, and respiratory rate of 25 breaths/min. There was also a palpable purpura rash on both legs, tenderness in the abdomen, and absence of bowel sounds. Routine blood examination revealed a hemoglobin level of 70 g/L, white blood cell count of 11.48 × 109/L, and platelet count of 13 × 109/L. The liver function test showed albumin 10 g/L. The serum electrolytes showed sodium 140 mmol/L, potassium 2.92 mmol/L, chloride 112.1 mmol/L, and bicarbonate 15.9 mmol/L (Table ) with coagulopathy. Therefore, HSP complicated with an alimentary tract hemorrhage was diagnosed. He was immediately treated with intravenous methylprednisolone (2 mg/kg per day), infusion of blood products, and somatostatin but after 2 days after treatment (day 3), he still had massive gastrointestinal hemorrhage, poor circulation, a reduced level of consciousness, and unstable vital signs. Abdominal ultrasonography and plain abdominal radiography revealed no enterobrosis. The patient was also evaluated by pediatric surgeons, and the continuation of medical treatment was suggested. However, his condition deteriorated, and he needed to rely on a life-supporting blood transfusion. He developed signs of peritonitis with abdominal distension. Gastrointestinal tract perforation was suspected. A contrast-enhanced computed tomography (CT) scan of the whole abdomen revealed curved liquid samples and gas shadows on the left and front of the stomach, supporting the possibility of gastrointestinal tract perforation (Fig. ). On day 4, an emergency laparotomy was performed. The surgery revealed that the anterior wall of the descending duodenum was thinner with a 1 cm × 1 cm diameter perforation, and the posterior wall had a 3 cm × 1 cm ulcer, which had penetrated into the peritoneum of the pancreas and experienced active bleeding from the broken end of the vessel. The intraoperative hemorrhage volume was approximately 3000 mL, including intragastric bleeding and intestinal blood clots. Pathological examination indicated chronic inflammation of the intestinal wall mucosa in the descending part of the stomach and duodenum, with hemorrhage, ulceration, interstitial congestion, and edema. Immunofluorescence microscopy of paraffin sections showed granular and lumpy IgA focal deposition in the blood vessel walls (Fig. ). Postoperatively, he was administered nasal continuous positive airway pressure-assisted ventilation, anti-infection treatment, albumin transfusion, platelet transfusion, abdominal drainage, methylprednisolone, fluconazole antifungal treatment, and wound dressing. The general symptoms gradually improved, vital signs were stable, and abdominal pain was relieved. The drainage tube was assessed after discharge, the abdominal CT was repeated after 1 month and the duodenostomy tube was removed 50 days after surgery. There was no evidence of rebleeding during the 2-month follow-up assessment.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [112.1, 'mmol/L'], 'Bicarbonate': [15.9, 'mmol/L'], 'Sodium': [140.0, 'mmol/L']}",12,11.4,12.6,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 140.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 140.0 mmol * 1 mEq/mmol = 140.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mmol sodium/L converts to 140.0 mEq sodium/L. 
The concentration of chloride is 112.1 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 112.1 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 112.1 mmol * 1 mEq/mmol = 112.1 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 112.1 mmol chloride/L converts to 112.1 mEq chloride/L. 
The concentration of bicarbonate is 15.9 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 15.9 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 15.9 mmol * 1 mEq/mmol = 15.9 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 15.9 mmol bicarbonate/L converts to 15.9 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (112.1 mEq/L + 15.9 mEq/L) = 12.0 mEq/L. Hence, The patient's anion gap is 12.0 mEq/L."
6214,39,Anion Gap,lab test,decimal,pmc-3245397-2,Extracted,"A 77-year-old woman was admitted to our hospital with nausea, vomiting, and abdominal pain. Her family members reported that, 15 hours earlier, she had ingested 100 mL of cold wave neutralizer (10% sodium bromate) in a suicide attempt. Upon admission, she appeared ill and physiological examination revealed the following: blood pressure was 115/75 mmHg, heart rate was 85/min, respiration rate was 18/min, and body temperature was 36.5℃. Serological testing was performed, and the results were are follows: white blood cell count, 10,020/µL; hemoglobin, 13.6 g/dL; platelet count, 225,000/µL; serum sodium, 146 mEq/L; potassium, 4.3 mEq/L; chloride, 106 mEq/L; blood urea nitrogen 27.39 mg/dL; creatinine, 3 mg/dL; bicarbonate, 21 mmol/L; amylase, 1,706 U/L; and lactate dehydrogenase, 1,310 U/L. Liver transaminase levels were normal.
Urinalysis revealed her urine chloride to be 119 mEq/L; she also showed scores of 3+ for urine protein and 1+ for blood. On the second day of hospitalization, her daily urinary volume decreased to 300 mL and she complained of hearing loss; pure tone audiometry confirmed sensorineural hearing loss. Hemodialysis was initiated and repeated daily for three days following, and then every other day. On the seventh day, the patient's serum amylase level had decreased to normal, but her hearing loss and daily urine output had not improved. On the eleventh hospital day, her daily urinary volume increased to 1,000 mL, but her serum creatinine level remained at 6.1 mg/dL. Hemodialysis was continued, but the patient died of septic shock on hospital day 104.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [106.0, 'mEq/L'], 'Bicarbonate': [21.0, 'mmol/L'], 'Sodium': [146.0, 'mEq/L']}",19,18.05,19.95,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 146.0 mEq/L. 
The concentration of chloride is 106.0 mEq/L. 
The concentration of bicarbonate is 21.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 21.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 21.0 mmol * 1 mEq/mmol = 21.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 21.0 mmol bicarbonate/L converts to 21.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 146.0 mEq/L - (106.0 mEq/L + 21.0 mEq/L) = 19.0 mEq/L. Hence, The patient's anion gap is 19.0 mEq/L."
6215,39,Anion Gap,lab test,decimal,pmc-8015958-1,Extracted,"A 39-year-old woman presented with an established diagnosis of systemic lupus erythematosus (SLE) with lupus nephritis. She was being managed at a tertiary health care center in South Nigeria for approximately 4 years. She had been on conservative management but had been having a progressive worsening of her biochemical parameters with a progressive increase in her serum urea and creatinine and serum potassium.
In addition, the patient was also getting progressively anemic. The patient eventually became uremic with uremic encephalopathy, uremic gastritis, and pulmonary edema. On account of the patient's clinical condition, doctors at the tertiary hospital where the patient was being managed had prescribed hemodialysis, but the patient refused hemodialysis because she was advised to have a blood transfusion prior to hemodialysis on account of severe anemia. She refused transfusion on account of being a Jehovah's Witness and discharged herself from the tertiary hospital to a private dialysis center.
On examination at presentation, the patient was in respiratory distress, markedly pale (packed cell volume [PCV] 15%) with marked edema. The patient also had bilateral mid-zone and low-zone crepitations. The abdomen was distended, full with epigastric tenderness. The liver was palpably enlarged 3 cm below the right costal margin. The spleen and kidneys were not palpably enlarged.
CNS examination showed that the patient was well oriented in time, place, and person. There was no focal neurologic deficit, but there was moderate asterixis.
Initial electrolyte, urea, and creatinine results were as follows: urea – 215.8 mg/dL, creatinine – 7.45 mg/dL, Na – 132 mmol/L, K – 5.24 mmol/L, Cl – 108 mmol/L, and HCO3– 13.2 mmol/L.
The patient was on prednisolone, azathioprine, hydroxychloroquine, hydrochlorothiazide, and valsartan.
Computed tomography (CT) done previously did not reveal any deficit.
The scanogram was unremarkable. Five millimeter pre- and post-intravenous contrast-enhanced axial CT slices were taken from the base of the skull to the vertex. There was no shift of the midline brain structures. The lateral ventricles, third and fourth ventricles, as well as the basal cistern appeared grossly normal. The paranasal sinuses as well as the mastoid air cells appeared grossly normal. The orbit was grossly normal with no demonstrable defect in the bony orbit or intraocular mass lesion. The overlying soft tissue appeared grossly normal.
Conclusion: Normal cranial CT scan.
PCV done was 15%.
The patient and her relations were counseled for dialysis and blood transfusion. They revealed that they left the tertiary health center when they were told that the patient needed a blood transfusion before she could be dialyzed which they declined on religious grounds. They claimed even in life-threatening conditions; they would not accept a blood transfusion.
The patient was dialyzed, and over the next few weeks, she gradually improved clinically even though hemodialysis was markedly irregular.
The patient continued to improve and returned to the tertiary hospital for the continuation of dialysis since the PCV was now 23% and could be dialyzed without a mandatory transfusion.
The patient presented again in a few weeks with a different complaint. She was speaking English with a distinctly American accent. It had started 3 days prior to presentation. She claimed that the accent was distressing and embarrassing and a source of worry to herself and her family.
The examination revealed a calm patient. There was no neurologic deficit. Mini-mental state examination was within reference values. The patient scored 26. The speech had normal content, but the accent was American and markedly different from her previous speech pattern. The patient had a slightly elevated mood.
Her past medical history showed that she had a previous episode 6 years earlier when she recovered from a coma at the University of Benin Teaching Hospital Intensive Care Unit. She claimed that the symptoms resolved spontaneously after a few days. There has been no other episode since that time.
As stated earlier, a previous CT did not reveal any abnormality. PCV was 27%. All other systems were grossly normal.
Urea and creatinine results showed urea of 126 mg/dl and creatinine was 4.5 mg/dl. There was no asterixis. There were also no gross abnormalities on cranial CT scan, and uraemic encepalopathy had resolved. On account of these, a diagnosis of FAS post uraemic encepalopathy with possible hypomania was made.
The patient was referred to the mental health physician and was eventually placed on haloperidol 2.5 mg/dL and symptoms resolved gradually over the next 2–3 weeks.
Haloperidol was gradually stopped over a 1 month period, and there has been no relapse over the past 10 months. The patient has been stable clinically without any relapse to a foreign accent.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [108.0, 'mmol/L'], 'Bicarbonate': [13.2, 'mmol/L'], 'Sodium': [132.0, 'mmol/L']}",10.8,10.26,11.34,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 132.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 132.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 132.0 mmol * 1 mEq/mmol = 132.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 132.0 mmol sodium/L converts to 132.0 mEq sodium/L. 
The concentration of chloride is 108.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 108.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 108.0 mmol * 1 mEq/mmol = 108.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 108.0 mmol chloride/L converts to 108.0 mEq chloride/L. 
The concentration of bicarbonate is 13.2 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 13.2 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 13.2 mmol * 1 mEq/mmol = 13.2 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 13.2 mmol bicarbonate/L converts to 13.2 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 132.0 mEq/L - (108.0 mEq/L + 13.2 mEq/L) = 10.8 mEq/L. Hence, The patient's anion gap is 10.8 mEq/L."
6216,39,Anion Gap,lab test,decimal,pmc-7787899-1,Extracted,"The study was approved by the Institutional Review Board of the Catholic University of Korea (IRB No: PC20ZASI0046) with waiver of informed consent.
An 87-year-old man visited the outpatient clinic owing to poor oral intake. According to his medical history, he had undergone surgery for benign prostatic hyperplasia 6 years ago and had discontinued the medication for benign prostatic hyperplasia 4 months before hospitalization. Recently, he was diagnosed with cognitive dysfunction based on a mini-mental status examination score of 22, and a global deterioration scale of 3. And was started on appropriate medication. At the time of admission, he was prescribed choline alfoscerate 400 mg twice daily and donepezil 5 mg for the control of Alzheimer disease.
A review of systems did not reveal abnormal findings. His vital signs were as follows: blood pressure (BP), 180/70 mmHg; pulse rate, 72 beats/min; respiratory rate, 20 breaths/min; body temperate, 36.7℃. To determine the cause of poor oral intake, routine investigations were performed, including complete blood count, blood chemistry, urine analysis, electrocardiogram, and chest X-ray. The presence of subtle pneumonia on the chest X-ray and hypokalemia (serum potassium 2.6 mmol/L) was detected. Initial serum inflammatory markers showed the following results: plasma leukocyte count, 7,500/mm3; serum c-reactive protein, 0.74 mg/dL (range, 0.01–0.5 mg/dL). Except for potassium, blood chemistry revealed the following: serum albumin, 4.0 g/dL (range, 3.5–5.2 g/dL); blood urea nitrogen, 10.9 mg/dL; serum creatinine, 0.72 mg/dL (range, 0.61–1.20 mg/dL); serum sodium, 140 mmol/L; serum chloride, 91 mmol/L; serum magnesium, 2.4 mg/dL; serum osmolality, 290 mOsm/kg. Urinalysis and urine sediment examination presented the following: urine pH, 7.5; urine specific gravity, 1.011; urine white blood cells, 0–2/high power field; urine red blood cells, 0–2/high power field. Blood gas analysis revealed compensated metabolic alkalosis as follows: arterial blood pH, 7.52; arterial blood pCO2, 46.6 mmHg; arterial blood pO2, 73.7 mmHg; arterial blood HCO3¯, 36.8 mmol/L. Chest X-ray and inflammatory markers suggested that the pneumonia was not severe. Therefore, hypokalemia could be the cause of underlying poor oral intake.
The patient was admitted to treat pneumonia and hypokalemia. For pneumonia treatment, he received ceftriaxone and clarithromycin as antibiotic agents. To determine the cause of hypokalemia, further investigations were performed. No clues indicating hypokalemia were detected in the medical history and review of systems. Next, his renal potassium excretion was measured to determine the potassium/creatinine ratio, fractional excretion of potassium, and transtubular potassium gradient (TTKG), using blood chemistry and spot urine chemistry. The results of spot urine chemistry were as follows: urea nitrogen, 392.8 mg/dL; creatinine, 90.8 mg/dL; total protein, 29.9 mg/dL; sodium, 35 mEq/L; potassium, 29.2 mEq/L; chloride, 45 mEq/L; osmolality, 309 mOsm/kg. Additionally, the following values were determined and suggested renal potassium wasting: urine potassium/creatinine ratio, 32.2 mEq/g; fractional excretion of potassium, 8.9%; TTKG, 10.5. Those findings suggested renal potassium wasting. Next, computed tomography demonstrated no abnormalities in the bilateral adrenal glands and both kidneys (). A hormone study was conducted to evaluate the cause of high BP. The thyroid function test was in the normal range. The adrenocorticotropic hormone (ACTH) level was 36.02 pg/mL (range, 10.0–60.0 pg/mL) and the cortisol level was 10.51 µg/dL (range, 9.41–26.06 µg/dL), which were within the normal range, revealing no mineral corticoid excess. Plasma renin activity was determined as 0.19 ng/mL/hr (range, 0.3–2.9 ng/mL/hr), aldosterone concentration was 14.93 pg/mL (range, 29.9–158.8 pg/mL), and the aldosterone/renin ratio was 7.86, indicating hyporeninemic hypoaldosteronism. However, unlike Liddle syndrome, the serum sodium level was normal at 140 mmol/L. The serum magnesium level was normal at 2.4 mg/dL, which was far from that observed in Gitelman syndrome. Hence, no obvious cause of hypokalemia was determined.
During investigations analyzing the possible cause of hypokalemia, he underwent potassium supplementation using intravenous and oral formulations. Until the fourth day of hospitalization, his serum potassium level demonstrated difficulty increasing beyond 3.0 mmol/L despite sufficient potassium administration (). As the hypokalemia was poorly corrected, clinicians suspected other causes of hypokalemia. A thorough review of the therapeutic agents prescribed for cognitive dysfunction was conducted. On examining possible adverse effects, we identified evidence suggesting that donepezil causes hypokalemia as a rare adverse event [,]. Therefore, donepezil was immediately discontinued. Thereafter, his potassium demand, supplemented intravenously, gradually decreased and was modified to oral potassium agents. On the third day after donepezil cessation, his serum potassium level recovered to 3.5 mmol/L under oral potassium supplementation of 32 mEq/day (). During hypokalemia evaluation and correction, pneumonia was properly controlled. Finally, he was able to maintain serum potassium of 3.3 mmol/L under oral potassium supplementation of 32 mEq/day and was discharged on the ninth day of hospitalization. At the time of discharge, the results of blood chemistry and spot urine chemistry were as follows: serum creatinine, 0.73 mg/dL; serum potassium, 3.5 mmol/L; serum magnesium, 2.3 mg/dL; serum osmolality, 295 mOsm/kg; urine creatinine, 120.6 mg/dL; potassium, 46.7 mEq/L; osmolality, 330 mOsm/kg. Additionally, the following values were determined: urine potassium/creatinine ratio, 38.7 mEq/g; fractional excretion of potassium, 8.1%; TTKG, 11.9.
Conversely, in the past, he had presented a systolic BP of less than 130 mmHg and diastolic BP of 80 mmHg during several visits to the outpatient clinic, with no history of medication-related hypertension. However, for 24 hours after hospitalization, BP was continuously confirmed as 160/90 mmHg or more, including a maximum of 185/105 mmHg, and amlodipine 5 mg was initiated. As BP measurements were above 140/90 mmHg on average after the addition of amlodipine 5 mg, the patient was additionally prescribed olmesartan 20 mg on the fifth day of hospitalization. Finally, in the outpatient clinic follow-ups, serum potassium was measured as 4.5 mmol/L, and oral potassium agents were withheld.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [91.0, 'mmol/L'], 'Bicarbonate': [36.8, 'mmol/L'], 'Sodium': [140.0, 'mmol/L']}",12.2,11.59,12.81,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 140.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 140.0 mmol * 1 mEq/mmol = 140.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mmol sodium/L converts to 140.0 mEq sodium/L. 
The concentration of chloride is 91.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 91.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 91.0 mmol * 1 mEq/mmol = 91.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 91.0 mmol chloride/L converts to 91.0 mEq chloride/L. 
The concentration of bicarbonate is 36.8 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 36.8 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 36.8 mmol * 1 mEq/mmol = 36.8 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 36.8 mmol bicarbonate/L converts to 36.8 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (91.0 mEq/L + 36.8 mEq/L) = 12.2 mEq/L. Hence, The patient's anion gap is 12.2 mEq/L."
6217,39,Anion Gap,lab test,decimal,pmc-7526960-1,Extracted,"Our patient was a 63-year-old male, a previously diagnosed case of degenerative cervical disorder, hypertension, and alcoholism. He underwent an aortic valve replacement surgery in 2011 and was on warfarin since then, maintaining a target international normalized ratio (INR) of 2.5-3.5 (normal range: 0.8-1.1). The patient presented with sudden onset right scapular swelling, which was tender on palpation. An ultrasound of the swelling revealed a well-defined heterogeneous mass in the right posterior chest wall having a depth of around 2.3 cm. No definite vascularity was observed, and swelling was labeled as a hematoma/collection. The patient started to sweat profusely and was rushed to the emergency room immediately because he lost consciousness but eventually regained it on the way. His vitals displayed a picture of hypotensive episode secondary to suspected hemorrhagic shock and was administered intravenous fluids and atropine. Hematological investigations revealed moderate normocytic anemia with hemoglobin of 9.0 g/dL (normal in males: 13.5-17.5 g/dL), hematocrit of 26% (normal in males: 38.3%-48.6%), and platelet count of 155,000/mcL (normal: 150,000-450,000/mcL). Prothrombin time and INR were elevated at 32.8 seconds (normal: 10-13 seconds) and 2.9 (normal: 0.8-1.1), respectively, while partial thromboplastin time was at the normal upper limit, 35.5 seconds (normal: 25-35 seconds). Laboratory tests revealed serum urea 30 mg/dL (normal: 17-49 mg/dL) and creatinine level 0.79 mg/dL (normal in males: 0.9-1.3 mg/dL). Serum electrolytes were as follows: sodium 140 mEq/L (normal: 136-149 mEq/L), potassium 4.1 mEq/L (normal: 3.8-5.2 mEq/L), chloride 107 mEq/L (normal: 98-107 mEq/L), and bicarbonate 25.5 mEq/L (normal: 23-29 mEq/L). C-reactive protein was 3.5 mg/L (normal < 10 mg/L) and liver function tests were alanine transaminase 40 IU/L (normal: 0-45 IU/L) and aspartate transaminase 60 IU/L (normal: 0-35 IU/L). Serum N-terminal pro b-type natriuretic peptide (NT-pro-BNP) was 69 pg/mL (normal < 125 pg/mL) indicating absence of possible heart failure.
Once his vitals became stable, he was scheduled for a contrast-enhanced CT (CECT) chest to localize the bleeding points. During the arterial phase, the scan displayed that no active arterial bleed was present within the hematoma in the right lateral chest wall. However, delayed phase images revealed focal extravasation of contrast within the hematoma in close proximity of the right seventh rib (as displayed by the arrow in Figure ). The bleeding point was deduced to originate from a tiny branch of the intercostal artery in the right seventh intercostal space. A large acute hematoma was identified in the right upper and mid-lateral chest wall measuring 13.1 x 3.2 cm (anteroposterior x transverse) (Figure ). There was no evidence of aortic dissection or mediastinal hematoma and no large mass, cavitation, consolidation, or pleural effusion was seen.
The patient was taken to an angiography suite where emergency transcatheter right intercostal artery angiography and embolization were carried out using a 5 French (Fr) vascular sheath placed in the right common femoral artery and a 5 Fr C2 catheter. On angiography, the active bleeder was identified as a small branch of the intercostal artery in the right seventh intercostal space (contrast extravasation from active bleeder as shown by the arrow in Figure ). The aortic prosthetic valve was also noted.
Subsequently, the vessel was selectively cannulated using a microcatheter, and embolization was performed using 150-250 microns polyvinyl acetate (PVA) particles and two 10-mm pushable microcoils. Hence, complete occlusion of the abnormal actively bleeding vasculature was achieved (demonstrated by the absence of contrast extravasation in Figure ). The patient was shifted to the intensive care unit, where blood products were transfused. He was kept under strict monitoring of vitals and INR because anti-hypertensives and warfarin were put on hold due to hemodynamic instability.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [107.0, 'mEq/L'], 'Bicarbonate': [25.5, 'mEq/L'], 'Sodium': [140.0, 'mEq/L']}",7.5,7.125,7.875,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mEq/L. 
The concentration of chloride is 107.0 mEq/L. 
The concentration of bicarbonate is 25.5 mEq/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (107.0 mEq/L + 25.5 mEq/L) = 7.5 mEq/L. Hence, The patient's anion gap is 7.5 mEq/L."
6218,39,Anion Gap,lab test,decimal,pmc-3390736-1,Extracted,"A 25-yr-old Korean man was admitted to Pusan National University Hospital, Busan, Korea, on May 26, 2011, complaining flaccid paralysis of the lower extremities and numbness of hands. On arrival at the emergency room, his blood pressure was 110/70 mmHg, and the heart rate was 72 beats/min. He was alert with a respiratory rate of 18 breaths/min and a body temperature of 36.5℃. No heat intolerance, weight loss, changes in bowel habits, and other symptoms of hyperthyroidism were reported. On physical examination, he had a thyroid of normal size and consistency. Auscultation of the thyroid revealed no bruit. No exophthalmos or skin change was present. The lower limbs had flaccid paralysis with intact sensory function. No respiratory or visual difficulties were detected. He had no significant medical history and had received no medication; his family history was negative for familial hypokalemic periodic paralysis or thyroid disease. Laboratory tests revealed the following serum metabolite levels ; on the day of admission, sodium 143.6 mEq/L, potassium 2.42 mEq/L, chloride 104.7 mEq/L, creatinine 0.6 mg/dL, calcium 9.4 mg/dL and phosphorus 3.4 mg/dL. Arterial blood gas analysis showed arterial pH 7.408 mmHg, PO2 74.8 mmHg, PCO2 35.7 mmHg and bicarbonate 23.7 mM/L. A thyroid function test showed a thyroid-stimulating hormone level of 0.00 µIU/mL (normal: 0.3-5.0 µIU/mL), a T3 level of 205.1 ng/dL (normal: 80-170 ng/dL) and a free T4 level of 2.38 ng/dL (normal: 0.75-2.00 ng/dL). Thyroid autoantibodies showed a prominent elevated thyroglobulin antibody 93.40 U/mL (normal: 0-60 U/mL) and thyroid peroxidase antibody 642.82 U/mL (normal: 0-60 U/mL), but the level of TSH receptor antibody (by human TRAK RIA kit, BRAHMS, Hennigsdorf, Germany) was 0.37 IU/L (normal: 0-1.5 IU/L). An ultrasound revealed a normal sized thyroid gland, and neither nodules nor lymphadenopathy was detected (). A thyroid scan with Tc-99m revealed little or no uptake in the thyroid area compatible with thyroiditis (). Finally, we diagnosed this patient as thyrotoxic periodic paralysis associated with transient thyrotoxicosis due to painless thyroiditis.
He was given 40 mEq/L of intravenous potassium chloride in the emergency department and was then started on a normal saline infusion with 20 mEq/L of potassium chloride. He was also prescribed on an oral potassium and propranolol, which resulted in resolution of his lower extremity paralysis. On the second day of admission, his serum potassium level increased to 4.33 mEq/L. There was clinical improvement, concomitant with a progressive normalization of serum electrolytes. Complete remission of symptoms was obtained in 24 hr. Upon discharge, the patient had completely recovered his neuromuscular functions and serial measurement of his serum potassium level in the hospital remained within normal limits without oral potassium supplements.
He did not experience a hypokalemic paralytic attack during the subsequent 2 months. After 2 months of follow-up, thyroid function test was re-checked on outpatient department. The thyroid-stimulating hormone level was 11.11 µIU/mL (normal: 0.3-5.0 µIU/mL), a T3 level was 89.8 ng/dL (normal: 80-170 ng/dL), and a free T4 was 1.19 µg/dL (normal: 0.75-2.00 µg/dL); follow-up thyroid function survey was compatible with subclinical hypothyroidism. However, he remained symptom free.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [104.7, 'mEq/L'], 'Bicarbonate': [23.7, 'mmol/L'], 'Sodium': [143.6, 'mEq/L']}",15.2,14.44,15.96,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 143.6 mEq/L. 
The concentration of chloride is 104.7 mEq/L. 
The concentration of bicarbonate is 23.7 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 23.7 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 23.7 mmol * 1 mEq/mmol = 23.7 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 23.7 mmol bicarbonate/L converts to 23.7 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 143.6 mEq/L - (104.7 mEq/L + 23.7 mEq/L) = 15.2 mEq/L. Hence, The patient's anion gap is 15.2 mEq/L."
6219,39,Anion Gap,lab test,decimal,pmc-2908655-1,Extracted,"An 84-year-old female with history of major depression and anxiety was evaluated by her psychiatrist for worsening anxiety and given a single dose of 3 mg of paliperidone. Eight hours later she became increasingly agitated and, according to her daughter, “looked like she was going to crawl out of her skin.” She then told her daughter “make it go away, make it go away,” and subsequently stopped speaking and responding to any physical or verbal stimuli, although she appeared awake and alert. She had no prior documented episodes of catatonia. Her daughter brought her into the local emergency department (ED).
In the ED, she had a temperature of 37.3°C, pulse 80 beats per minute, blood pressure 161/72 mm Hg, respiratory rate 20 breaths per minute and oxygen saturation of 98% on room air. Her medications were citalopram, trazodone, levothyroxine, and paliperidone. She lived with her daughter, who related no recent trauma. The patient previously took risperidone, but it had been discontinued after several months because of mild akathisia, with both restlessness and tremor.
Physical exam showed an alert, well appearing elderly female in no acute distress. Her pupils were equal round and reactive to light; she would not comply with extraocular muscle testing. She did open her mouth on request and stuck out her tongue midline; there was no erythema, and mucous membranes were moist. Cardiopulmonary exam was unremarkable; abdominal palpation did not cause any change in her facial expression and was soft without masses. While she complied with several requests for the cranial nerve exam she would not move her fingers or toes when asked, but was noted to turn her head in all directions and roll from side to side, moving all extremities equally. Her brachioradialis and achilles reflexes were equal and Babinski reflexes were downgoing. She exhibited stupor and mutism with fixed postures.
Finger-stick glucose was 114 mg/dL. Intravenous diphenhydramine, 25 mg and benztropine, 0.5 mg were given for dystonia without any change. Noncontrast head computed tomography (CT) was performed due to concern for stroke and was unremarkable. Laboratory tests showed white blood cell count of 7.4 K/mm3 with 60% neutrophils, her hematocrit was 37.6%, and platelets were 203 K/mm3. Electrolytes and renal function showed sodium 135 mmol/L, potassium 3.5 mmol/L, chloride 101 mmol/L, bicarbonate 20 mmol/L, calcium 9.8 mg/dL, blood urea nitrogen 12 mg/dL, and creatinine 1.0 mg/dL.
Due to the lack of inpatient psychiatric beds, she was observed in the ED for 12 hours. Psychiatric consultation had no specific recommendations. Sixteen hours after the dose of paliperidone, without other therapy, she began to talk and interact. More detailed neurological exam showed no focal deficits. Her mood and affect were appropriate. She did not recall the events of the previous evening but remembered her daughter talking, although she was unable to respond.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [101.0, 'mmol/L'], 'Bicarbonate': [20.0, 'mmol/L'], 'Sodium': [135.0, 'mmol/L']}",14,13.3,14.7,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 135.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 135.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 135.0 mmol * 1 mEq/mmol = 135.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mmol sodium/L converts to 135.0 mEq sodium/L. 
The concentration of chloride is 101.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 101.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 101.0 mmol * 1 mEq/mmol = 101.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 101.0 mmol chloride/L converts to 101.0 mEq chloride/L. 
The concentration of bicarbonate is 20.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 20.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 20.0 mmol * 1 mEq/mmol = 20.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 20.0 mmol bicarbonate/L converts to 20.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 135.0 mEq/L - (101.0 mEq/L + 20.0 mEq/L) = 14.0 mEq/L. Hence, The patient's anion gap is 14.0 mEq/L."
6220,39,Anion Gap,lab test,decimal,usmle-8747,Extracted,"A 45-year-old woman comes to the emergency department complaining of abdominal pain for the past day. The pain is situated in the right upper quadrant, colicky, 8/10, and radiates to the tip of the right shoulder with no aggravating or relieving factors. The pain is associated with nausea but no vomiting. She tried to take over-the-counter antacids which relieved her pain to a certain extent, but not entirely. She does not smoke cigarettes or drink alcohol. She has no past medical illness. Her father died of pancreatic cancer at the age of 75, and her mother has diabetes controlled with medications. Temperature is 38°C (100.4°F), blood pressure is 125/89 mm Hg, pulse is 104/min, respiratory rate is 20/min, and BMI is 29 kg/m2. On abdominal examination, her abdomen is tender to shallow and deep palpation of the right upper quadrant.
Laboratory test
Complete blood count
Hemoglobin 13 g/dL
WBC 15,500/mm3
Platelets 145,000/mm3
Basic metabolic panel
Serum Na+   137 mEq/L
Serum K+ 3.6 mEq/L
Serum Cl-   95 mEq/L
Serum HCO3- 25 mEq/L
BUN   10 mg/dL
Serum creatinine        0.8 mg/dL
Liver function test
Total bilirubin   1.3 mg/dL
AST   52 U/L
ALT 60 U/L
Ultrasonography of the abdomen shows normal findings.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [95.0, 'mEq/L'], 'Bicarbonate': [25.0, 'mEq/L'], 'Sodium': [137.0, 'mEq/L']}",17,16.15,17.85,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 137.0 mEq/L. 
The concentration of chloride is 95.0 mEq/L. 
The concentration of bicarbonate is 25.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 137.0 mEq/L - (95.0 mEq/L + 25.0 mEq/L) = 17.0 mEq/L. Hence, The patient's anion gap is 17.0 mEq/L."
6221,39,Anion Gap,lab test,decimal,pmc-3208579-1,Extracted,"A 63-year-old G2P2 female presented ambulatory to the ED with the chief complaint of abdominal pain, described further to the triage nurse as abdominal cramping and a mass in her vagina. The patient described that she had had a ""bulge"" in her vagina for the past 2 years and was currently being treated by her gynecologist for an enterocele with estrogen cream. Elective surgical repair of an enterocele was planned. She complained to the triage nurse of abdominal pain intermittently for the preceding 1 week. She stated that when she coughed something protruded from her vagina and she believed that her rectum had prolapsed. She was initially triaged to the lower acuity area of the emergency department, but due to worsening pain, she was brought back to a room on the acute care side approximately 30 min after her arrival. She described working in her garden when she coughed, experiencing a ""bulge"" extending through and out of her vagina. According to the patient, this ""bulge"" had been worsening for 2 months but had never extended past her labia. The patient complained of severe cramping in the left lower quadrant of her abdomen, but denied any diffuse abdominal pain. Her past medical history was significant for hypertension and breast cancer treated with surgery and chemotherapy without radiation. The patient did not have a history of vaginal or vulvar cancer. Her surgical history was significant for mastectomy and breast reconstruction, laparoscopic-assisted vaginal hysterectomy and bilateral oopherectomy (5 years previously), and pubovaginal sling (4 years previously).
On examination she was pleasant, appearing well and in no acute distress, with a temperature of 36.8 C°, pulse of 70, and blood pressure of 142/97 mmHg. Initial abdominal examination demonstrated no tenderness to palpation and no peritoneal signs. On genitourinary exam approximately 15 cm of small bowel protruded through the vaginal introitus (see Figure ). The bowel exhibited peristaltic waves and was dark red in color. Manual reduction was attempted to reduce strangulation, but was unsuccessful because of the large amount of bowel present and to the patient's discomfort during the attempt. Intravenous morphine was administered for pain control. Sterile moist gauze was placed over the eviscerated bowel, and the gynecology department was immediately consulted for surgical management of the patient. The patient was given a bolus of 1 l normal saline and intravenous ertapenam and metronidazole to cover enteric organisms.
Laboratory data results included white blood cell count, 5.9 k/ul; hemoglobin, 13.1 g/dl; hematocrit, 38.6%; platelets, 287 k/ul; prothrombin time and partial thromboplastin time were normal. Sodium was 142 mEq/l; chloride, 109 mEq/l; potassium, 3.8 mEq/l; bicarbonate 23 mEq/l; glucose, 123 mg/dl; blood urea nitrogen, 17 mg/dl; creatinine, 0.7 mg/dl; calcium 9.3 mg/dl. The electrocardiogram showed normal sinus rhythm, with left atrial enlargement.
While awaiting surgical consultation and 45 min after being placed in a room, the patient developed relative hypotension; her blood pressure decreased from 183/108 to 107/63 mmHg. She became less responsive and experienced rigors. Repeat abdominal exam showed diffuse abdominal tenderness with peritoneal signs that rapidly progressed to frank peritonitis. The herniated bowel had become dark and dusky. A second large bore IV was placed, and aggressive fluid resuscitation with 2 l normal saline was initiated. Her bed was placed in the Trendelenburg position to reduce tension on the eviscerated bowel, and preparations were made to intubate the patient because of her rapid decline. The fluid resuscitation was successful in improving her mental status and blood pressure, and she did not require intubation. She was transported quickly to the operating room for repair by both gynecology and general surgery physicians. General surgery resected approximately 20 cm of the distal ileum, which they noted to be inflamed and thickened with two areas of ischemia. This was followed by resection and repair of the vaginal cuff by gynecologic surgery. The patient was discharged from the hospital 6 days later in improved condition.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [142.0, 'mEq/L'], 'Chloride': [109.0, 'mEq/L'], 'Bicarbonate': [23.0, 'mEq/L']}",10,9.5,10.5,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 142.0 mEq/L. 
The concentration of chloride is 109.0 mEq/L. 
The concentration of bicarbonate is 23.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 142.0 mEq/L - (109.0 mEq/L + 23.0 mEq/L) = 10.0 mEq/L. Hence, The patient's anion gap is 10.0 mEq/L."
6222,39,Anion Gap,lab test,decimal,usmle-5250,Extracted,"A 55-year-old male comes to the emergency department complaining of blood in his urine and severe back pain. He reports that the pain is left-sided, colicky, and began acutely this morning. The pain occasional radiates to his left groin. He also reports increased urinary frequency and an episode of blood-tinged urine. According to the patient, this has happened multiple times before. His medical history is also notable for hypertension, type II diabetes mellitus, and obstructive sleep apnea. His current medications include aspirin, metformin, and lisinopril. The patient’s temperature is 100.4°F (38°C), blood pressure is 148/85 mmHg, pulse is 71/min, and respirations are 14/min with an oxygen saturation of 98% on room air. Physical examination is significant for left-sided costovertebral angle tenderness. A urine dipstick is heme-positive. A urinalysis is pending. Labs are drawn, as shown below:

Serum:
Na+: 144 mEq/L
Cl-: 95 mEq/L
K+: 4.3 mEq/L
HCO3-: 23 mEq/L
Urea nitrogen: 18 mg/dL
Glucose: 142 mg/dL
Creatinine: 1.0 mg/dL
Calcium: 7.8 mg/dL

A radiograph is obtained, as shown in Figure A.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [95.0, 'mEq/L'], 'Bicarbonate': [23.0, 'mEq/L'], 'Sodium': [144.0, 'mEq/L']}",26,24.7,27.3,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 144.0 mEq/L. 
The concentration of chloride is 95.0 mEq/L. 
The concentration of bicarbonate is 23.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 144.0 mEq/L - (95.0 mEq/L + 23.0 mEq/L) = 26.0 mEq/L. Hence, The patient's anion gap is 26.0 mEq/L."
6223,39,Anion Gap,lab test,decimal,pmc-5719915-1,Extracted,"An 82-year-old woman with no significant medical history presented with a 2-month history of abdominal pain and nausea. Vital signs were as follows: blood pressure, 130/80 mm Hg; heart rate, 72 beats/minute (bpm); respiratory rate, 20/minute; and body temperature, 36.4°C. She appeared chronically ill and the findings of a physical examination of the thorax, heart, and abdomen were unremarkable. Laboratory studies revealed a white blood cell (WBC) count of 8,110/μL (neutrophils, 78.5%; and lymphocytes, 17.5%) and a hemoglobin (Hb) of 11.5 g/dL. Serum biochemical values were as follows: blood urea nitrogen (BUN), 12 mg/dL; serum creatinine (Cr), 0.8 mg/dL; aspartate aminotransferase/alanine aminotransferase, 21/14 U/L; albumin, 4.0 g/dL; total bilirubin, 0.6 mg/dL; and amylase 2,460 U/L. Electrolyte levels were as follows: Na, 139 mmol/L; K, 4.0 mmol/L; and Cl, 102 mmol/L. Carbohydrate antigen 19-9 (CA19-9) levels were 37.0 U/mL.
An abdominal computed tomography (CT) scan revealed a 2-cm mass near the ampulla of Vater with mild dilation of the intrahepatic and common bile ducts as well as the pancreatic ducts (). There was no evidence of invasion of other organs. Both kidneys were normal sized without apparent abnormalities.
Endoscopic retrograde cholangiopancreatography with endoscopic ultrasound (EUS) revealed a 2-cm adenoma-like protruding lesion in the ampulla of Vater. EUS showed a well-defined isoechoic homogeneous mass without bile or pancreatic duct invasion (-). The mass was resected using a snare and a plastic stent was inserted into the bile duct; insertion of a plastic stent into the pancreatic duct failed. No specific complications, including severe bleeding or perforation, were observed (). Six hours post-procedure, the patient vomited 50 mL of blood and complained of abdominal pain. A second episode of hematemesis (<30 cc) occurred approximately 5 hours later. Immediately after the second episode, treatment with 1 g of tranexamic acid and 2 KU of hemocoagulase administered three times per day along with ceftriaxone (2 g intravenous) and a proton pump inhibitor for suspected bleeding at the resection site was initiated. Her vital signs were unremarkable. The WBC count was 7,090/μL, Hb was 10.1 g/dL, BUN was 14 mg/dL, Cr was 0.8 mg/dL, and amylase/lipase was 69/54 U/L. After the initial two episodes of hematemesis, no further hematemesis, melena, or hematochezia was observed and the patient’s vital signs remained stable. Her Hb level remained >10 g/dL. Four days after the papillectomy, the patient’s daily urine volume abruptly decreased to <100 cc and she complained of dyspnea. Her blood pressure was 103/86 mm Hg, heart rate was 134 bpm, respiratory rate was 30/minute, and body temperature was 37.0°C. Laboratory studies were as follows: Hb, 9.1 g/dL; amylase/lipase, 415/418 U/L; BUN/Cr, 73/3.9 mg/dL; and brain natriuretic peptide, 5,000 pg/mL. Venous blood gas analysis revealed the following: pH, 6.92: pCO2, 37 mm Hg; and HCO3, 7.6 mmol/L. Pulmonary edema was observed on a chest radiograph and continuous renal replacement therapy (CRRT) was performed to treat metabolic acidosis and pulmonary edema caused by acute renal failure. Although there were no signs of bleeding at that time, 2 units of packed red blood cells were transfused.
Approximately 10 hours after the CRRT was initiated, the patient was noted to have melena mixed with a small amount of hematochezia. Melena continued to occur 2–3 times/day with a total daily volume of 200–400 cc. Her vital signs were relatively stable: blood pressure, 120–175/65–100 mm Hg; heart rate, 90–120 bpm; respiratory rate, 20–25/minute; and body temperature, 36.0°C–37.8°C. The daily serum Hb level was 7.1–9.5 g/dL and the tranexamic acid with hemocoagulase were continued. The patient received a total of 13.5 g of tranexamic acid and 36 KU of hemocoagulase and received three additional units of packed red blood cells until the sixth day post-procedure, when no further signs of bleeding were observed. However, her daily urine output was nearly zero despite the CRRT. A contrast-enhanced abdominal CT scan was performed on day 12 to assess the cause of her anuric acute renal failure and showed normal-sized kidneys with enhancement of the renal medulla but not of the renal cortex, a finding consistent with acute RCN (). Histopathology revealed a villotubular high-grade adenoma with clear resection margins. Conventional hemodialysis was continued, but renal function did not improve and the oliguria persisted post-discharge. Presently, 6 months after the endoscopic procedure, she continues to undergo hemodialysis. Her most recent BUN/Cr was 22/6.1 mg/dL.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [102.0, 'mmol/L'], 'Bicarbonate': [7.6, 'mmol/L'], 'Sodium': [139.0, 'mmol/L']}",29.4,27.93,30.87,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 139.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 139.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 139.0 mmol * 1 mEq/mmol = 139.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mmol sodium/L converts to 139.0 mEq sodium/L. 
The concentration of chloride is 102.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 102.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 102.0 mmol * 1 mEq/mmol = 102.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 102.0 mmol chloride/L converts to 102.0 mEq chloride/L. 
The concentration of bicarbonate is 7.6 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 7.6 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 7.6 mmol * 1 mEq/mmol = 7.6 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 7.6 mmol bicarbonate/L converts to 7.6 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 139.0 mEq/L - (102.0 mEq/L + 7.6 mEq/L) = 29.4 mEq/L. Hence, The patient's anion gap is 29.4 mEq/L."
6224,39,Anion Gap,lab test,decimal,pmc-2876866-1,Extracted,"A 23 year-old female patient, 160 cm tall and 48 kg, was diagnosed with acute appendicitis and admitted for a laparoscopic appendectomy. She had no abnormalities in her pediatric medical history, but from the age 18, she had slowly begun experiencing headaches in her left temporal lobe, nausea, and vomiting. In June of that year, she experienced generalized convulsions and aphasia. In a brain MRI and MRA, an infarction in the posterior divisions of the left mesencephalic arteries was found. Also, in a blood test, an increase in lactic acid was discovered (7.54 mM/L [normal level: 0.5-2.254 mM/L]). The patient was suspected to have MELAS syndrome. She was diagnosed with MELAS after testing (adenosine-to-guanine transition at t-RNA nucleotide 3243 in PCR sequencing). After she turned 21, she was diagnosed with Type I DM. The patient had to orally ingest 200 mg of carbamazepine and 100 mg of aspirin per day and subcutaneously inject 30 units of insulin in the morning and 20 units in the evening. She had no history of total anesthesia.
In a physical examination before the anesthesia, the patient was able to read but had auditory aphasia such that she could not understand spoken words. In the physical examination, there were no signs of hypotonia or amyotrophy of the limbs. The laboratory results showed hyponatremia (126 mEq/L), hyperglycemia (257 mg/dl), and light metabolic acidosis (pH 7.346, PaCO2 36.3 mmHg, HCO3 20.1 mM/L, BE -5.3 mM/L). There were no abnormal findings in the chest X-ray and electrocardiogram. One year prior to her admission to the hospital, she had an ECG that revealed a cardiac index of 67% and no abnormal findings. For sugar control, 4 units of shortacting insulin were injected, and 0.9% normal saline was administered to control hyponatremia. No other pre-operative measures were performed.
After the patient was taken to the operating room, we attached ECG standard leads II, noninvasive monitors for blood pressure, heart rate, arterial oxygen saturation, capnogram, and bispectral index (BIS), and a nerve stimulator to the patient using the Multi Channel Anesthesia Monitor S/5™ (Datex-Ohmeda, USA). Preliminary vital signs were as follows: blood pressure 115/65 mmHg, heart rate 100 beats/min, oxygen saturation rate 97%, and the ECG results appeared normal. The patient underwent 3 minutes of denitrogenation with 100% oxygen through a face mask. Afterwards, we administered lidocaine (40 mg) with the Master TCI (Fresenius Vial S.A., France); we then injected 2% propofol (Fresofol®, Fresenius Kabi, Austria) and remifentanil (Ultiva™, GlaxoSmithKline, UK) at target concentrations of 4 µg/ml (Marsh-model) and 5 ng/ml (Minto-model), respectively. After roughly 90 seconds had passed, we checked lid reflexes and found that the patient had lost consciousness. We administered atracurium (0.5 mg/kg), the BIS was 50, and we saw that there was no response to TOF stimulation with the nerve stimulator placed on the ulnar nerve. Endotracheal intubation was then performed without complications. We started mechanical respiration with air (1.5 L/min), oxygen (1.5 L/min), respiratory volume of 450 ml, and respiratory rate of 12 breaths per minute. To control ventilation, the capnogram was kept at 35-40 mmHg. We used spirometry to measure the respiratory volume and pulmonary compliance. We started invasive blood pressure monitoring through the radial artery and measured the esophageal temperature with a body temperature monitor. During the operation, we used a forced-air warming blanket (Bair Hugger™, Austine Medical, USA) to stabilize the patient's body temperature. For fluid maintenance, we administered 0.9% normal saline at 200 ml per hour. During the operation, the patient's vitals were kept stable with blood pressure at 120-140/60-80 mmHg, heart rate 80-100 beats/min, oxygen saturation 100%, body temperature 37.0-37.4℃, and BIS 40-60. Thirty minutes after inducing anesthesia, the arterial blood gas study showed pH 7.44, PaCO2 32 mmHg, PaO2 299 mmHg, HCO3 23.3 mM/L, BE -2.1 mM/L; her electrolytes were Na+ 125 mEq/L, K+ 3.8 mEq/L, Cl- 88 mEq/L; and her blood sugar was 176 mg/dl. Twenty minutes prior to the end of the operation, we administered ondansetron (4 mg) to prevent post-operative nausea and vomiting. After suturing the peritoneum, we stopped injecting remifentanil, kept the level of propofol in the target effect site at 2 µg/ml, and restored spontaneous breathing. After the operation was over, we stopped injecting propofol and stabilized spontaneous breathing at 300 ml per breath on the spirometer. On the nerve stimulator, the TOF rate was kept at 0.95. To reverse the muscle relaxant effects, we administered glycopyrrolate (0.4 mg) and pyridostigmine (15 mg). Afterwards, the patient responded to voice commands and opened her eyes. With stabilized spontaneous breathing, she was extubated. The operation lasted around 1 hour, and during the operation, 350 ml of 0.9% normal saline were used. We then moved the patient to the recovery room and kept her under observation with blood pressure, electrogram, and oxygen saturation monitors. In the recovery room, we gave her oxygen at 5 L/min through the facial mask. The arterial blood gas study showed pH 7.32, PaCO2 43 mmHg, PaO2 219 mmHg, HCO3 21.2 mM/L, and BE -3.6 mM/L; her electrolyte levels were Na+ 128 mEq/L, K+ 4.1 mEq/L, and Cl- 90 mEq/L; and her blood sugar level was 120 mg/dl. We then moved the patient to the ward where we performed a lactic acid test, which measured 3.6 mM/L. Three days after the operation, the patient showed no complications from the operation or anesthesia, so she was released from the hospital.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [90.0, 'mEq/L'], 'Bicarbonate': [21.2, 'mmol/L'], 'Sodium': [128.0, 'mEq/L']}",16.8,15.96,17.64,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 128.0 mEq/L. 
The concentration of chloride is 90.0 mEq/L. 
The concentration of bicarbonate is 21.2 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 21.2 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 21.2 mmol * 1 mEq/mmol = 21.2 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 21.2 mmol bicarbonate/L converts to 21.2 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 128.0 mEq/L - (90.0 mEq/L + 21.2 mEq/L) = 16.8 mEq/L. Hence, The patient's anion gap is 16.8 mEq/L."
6225,39,Anion Gap,lab test,decimal,pmc-6318142-1,Extracted,"A 32-year-old homeless man with a past medical history of ethanol use disorder (sober for 40 days prior to presentation) was brought in by emergency medical personnel after being found unresponsive in a Walmart parking-lot. After regaining consciousness, the patient stated that the last thing he remembered was “huffing” six to ten cans of the computer cleaning product, Dust-Off. He endorsed sharp, substernal chest and anterior neck discomfort made worse by deep inspiration. Initially, he was given two amps of bicarbonate, as well as empiric antibiotics. Physical exam was unremarkable with the exception of what appeared to be frost-bite on his fingertips of the right hand. Laboratory work was notable for leukocytosis of 17.7 thousand per microliter (K/uL), sodium of 127 millimoles per liter (mmol/L), potassium of 3.5 mmol/L, chloride of 90 mmol/L, bicarbonate of 20 mmol/L, creatinine of 1.63 milligram per deciliter (mg/dl), normal liver enzymes and a negative toxicology screen. Troponin was elevated to 4.34 nanograms per milliliter (ng/mL), creatinine kinase was 1163 units per liters (U/L) and creatinine kinase-muscle/brain (CK-MB) was 21.3 ng/mL. His initial electrocardiogram revealed sinus rhythm with a partial right bundle branch block and a prolonged corrected QT segment (QTc) of 518 milliseconds. On chest X-ray, the patient was found to have pneumomediastinum and pneumopericardium (Figure ).
Computed tomography of the chest demonstrated extensive air around the tracheal and laryngeal structures, extending down the cervical tissue planes and into the mediastinum and pericardium (Figure ).
Cardiothoracic surgery was consulted and the decision was made to observe the patient as he remained hemodynamically stable and he was protecting his airway. The patient did well, and prior to discharge, his kidney function improved, he had a normal echocardiogram, normalization of his electrocardiogram, and minimal residual mediastinal and pericardial air on repeat chest X-ray. He was provided extensive education and support for cessation of inhalant and alcohol use.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [90.0, 'mmol/L'], 'Bicarbonate': [20.0, 'mmol/L'], 'Sodium': [127.0, 'mmol/L']}",17,16.15,17.85,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 127.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 127.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 127.0 mmol * 1 mEq/mmol = 127.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 127.0 mmol sodium/L converts to 127.0 mEq sodium/L. 
The concentration of chloride is 90.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 90.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 90.0 mmol * 1 mEq/mmol = 90.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 90.0 mmol chloride/L converts to 90.0 mEq chloride/L. 
The concentration of bicarbonate is 20.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 20.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 20.0 mmol * 1 mEq/mmol = 20.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 20.0 mmol bicarbonate/L converts to 20.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 127.0 mEq/L - (90.0 mEq/L + 20.0 mEq/L) = 17.0 mEq/L. Hence, The patient's anion gap is 17.0 mEq/L."
6226,39,Anion Gap,lab test,decimal,pmc-7263001-1,Extracted,"A 61-year-old man presented to the ED after having black stools for 24 hours. This episode was preceded by the spontaneous onset of abdominal cramps, followed by dyspnea, fatigue, and light-headedness. His prior medical history included multiple hospital admissions for upper GI bleeding. There was no history of smoking, alcohol intake, or illicit drug use. On initial examination, he appeared lethargic, with a blood pressure of 101/55 mmHg, a pulse of 83 beats/minute, a respiratory rate of 16 breaths/minute, and oxygen saturation of 100% while breathing room air. He had conjunctival pallor. Cardiovascular examination revealed a systolic ejection murmur with late systolic peaking and soft second heart sounds. Laboratory tests showed a blood glucose concentration of 101 mg/dL, a white blood cell count of 4.6 x 109/L, a hemoglobin concentration of 8 g/dL, and a platelet count of 207 x 109/L. Other laboratory tests showed sodium 138 mEq/L, potassium 3.9 mmol/L, chloride 105 mmol/L, carbon dioxide 22 mEq/L, blood urea nitrogen 21 mg/dL, and creatinine 0.9 mg/dL. He was deficient in high molecular weight multimers of von Willebrand factor (vWF). Abdominal CT and upper GI endoscopy yielded negative results. A previous capsule examination of the small bowel had been negative. Two-dimensional transthoracic echocardiogram revealed a severely sclerotic aortic valve with area of 0.65 cm2 and left ventricular ejection fraction 65% (Figure ).
The patient was treated with intravenous administration of the proton pump inhibitor octreotide as well as two units of packed red blood cells. Because of his history of chronic GI bleeding, anemia, and AS, he was diagnosed with Heyde syndrome, a diagnosis supported by the deficiency in high molecular weight multimers of vWF.
The patient underwent a minimally invasive aortic valve replacement, with the insertion of a 27-mm tissue valve. At the present writing, three years after the procedure, the patient has been asymptomatic with no further episodes of bleeding.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [105.0, 'mmol/L'], 'Bicarbonate': [22.0, 'mEq/L'], 'Sodium': [138.0, 'mEq/L']}",11,10.45,11.55,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 138.0 mEq/L. 
The concentration of chloride is 105.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 105.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 105.0 mmol * 1 mEq/mmol = 105.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 105.0 mmol chloride/L converts to 105.0 mEq chloride/L. 
The concentration of bicarbonate is 22.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 138.0 mEq/L - (105.0 mEq/L + 22.0 mEq/L) = 11.0 mEq/L. Hence, The patient's anion gap is 11.0 mEq/L."
6227,39,Anion Gap,lab test,decimal,usmle-5468,Extracted,"A 33-year-old woman presents to the emergency department after she found out she had a blood pressure of 165/100 mmHg at a local pharmacy. The patient is not followed by a primary care physician and is not currently taking any medications. She has no other complaints at this time. A bedside ultrasound with Doppler of the abdomen is within normal limits. Laboratory values are ordered as seen below.

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
HCO3-: 33 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.2 mg/dL

The patient is given hydrochlorothiazide and sent home. An ECG performed at a subsequent follow up appointment is seen in Figure A.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [100.0, 'mEq/L'], 'Bicarbonate': [33.0, 'mEq/L'], 'Sodium': [139.0, 'mEq/L']}",6,5.7,6.3,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 139.0 mEq/L. 
The concentration of chloride is 100.0 mEq/L. 
The concentration of bicarbonate is 33.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 139.0 mEq/L - (100.0 mEq/L + 33.0 mEq/L) = 6.0 mEq/L. Hence, The patient's anion gap is 6.0 mEq/L."
6228,39,Anion Gap,lab test,decimal,pmc-6398077-1,Extracted,"Clinical History. A 27-year-old African American male with a history of unprovoked recurrent right lower extremity deep vein thrombosis and bilateral testicular hydrocele presented with a 4-week history of bilateral flank and generalized nonradiating lower abdominal pain. The pain was described as constant ache, associated with early satiety, but without nausea/vomiting, diarrhea, melena, or hematochezia. He denied weight loss or any urinary symptoms. Social history was negative for tobacco smoking and alcohol or recreational drug use. Medications included diphenhydramine as needed for sleep and apixaban.
Physical Exam. Vital vital signs revealed temperature 37.1°C, blood pressure 121/69 mmHg, pulse 96 beats/minute, and respiratory rate 16/minute. Lungs and heart exams were unremarkable. Lower half abdomen was mildly tender with palpation, but without mass, rebound, or guarding. There was mild right costovertebral angle tenderness and trace bilateral pedal edema. Genitalia were within normal limits without edema.
Initial Laboratory Data. Routine chemistry revealed serum sodium 133 mEq/L, potassium 5.0 mEq/L, chloride 98 mEq/L, bicarbonate 25 mEq/L, blood urea nitrogen 57 mg/dL, creatinine 12.6 mg/dL (baseline of 1.0 mg/dL one month prior), estimated glomerular filtration rate 6 mL/min/1.73 m2, and calcium 8.6 mg/dL. Urinalysis revealed specific gravity 1.014, pH 8.0, no red or white blood cells, 100 mg/dL protein, and no glucose or blood. Urine protein to creatinine and albumin to creatinine ratios were 0.5 and 0.293 g/g creatinine respectively. Renal ultrasound and abdomen/pelvis CT without contrast revealed mild bilateral hydroureteronephrosis with nonspecific inflammatory changes ().
The bland urinalysis and lack of significant proteinuria/albuminuria suggest tubulointerstitial injury (late phase of acute tubular necrosis, chronic tubulointerstitial nephritis) or obstructive uropathy. Differential diagnoses of obstructive uropathy relevant to current African American patient with unknown sickle cell history include recently passed papillary necrotic tissues or bladder stone, complicated medullary carcinoma (associated with sickle cell trait), diphenhydramine-induced neurogenic bladder, or retroperitoneal fibrosis (RPF). Rapidly progressive glomerulonephritis is thought to be less likely given the bland urinalysis.
Additional Investigations. Given the mismatched relatively benign findings of both urinalyses and imaging studies and degree of kidney failure and associated symptomology suspicious for RPF, an abdomen and pelvis CT with intravenous contrast was obtained.
Abdomen and pelvis computed tomogram with intravenous contrast revealed mild bilateral hydroureteronephrosis with point of obstruction at the level of distal abdominal aorta and inferior vena cava. There was an ill-defined, infiltrative soft tissue mass encasing both aorta, and inferior vena cava (approximately 7.2 cm). The mass appeared to infiltrate along the bilateral proximal common iliac vessels ().
Serologies to evaluate for autoimmune diseases and infectious etiologies including C-reactive-protein, human-immunodeficiency-virus, QuantiFERON gold, and antinuclear-antibody were negative. Serum lactate dehydrogenase obtained for possible lymphoproliferative disorder was mildly elevated at 248 IU (reference <192 IU). IgG4 level was 44.2 mg/dL (reference 4-86 mg/dL). Laparoscopic retroperitoneal mass biopsy revealed dense fibroadipose tissue with lymphocytic aggregates, focal scattered IgG4 positive plasma cells, and fibrin deposition without malignant cells.
Diagnoses. The diagnosis of idiopathic RPF was made. Kidney failure was thought to be due to severe bilateral ureteral encasement by RPF.
Clinical Follow-Up. Patient underwent bilateral nephrostomy placement with rapid improvement of serum creatinine. In addition, patient received a trial of prednisone 40 mg daily. At 4-month follow-up, kidney function normalized and CT revealed marked reduction in RPF size ().",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [98.0, 'mEq/L'], 'Bicarbonate': [25.0, 'mEq/L'], 'Sodium': [133.0, 'mEq/L']}",10,9.5,10.5,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 133.0 mEq/L. 
The concentration of chloride is 98.0 mEq/L. 
The concentration of bicarbonate is 25.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 133.0 mEq/L - (98.0 mEq/L + 25.0 mEq/L) = 10.0 mEq/L. Hence, The patient's anion gap is 10.0 mEq/L."
6229,39,Anion Gap,lab test,decimal,pmc-3531538-1,Extracted,"A 31-year-old woman with height of 164 cm and weight of 42 kg (BMI; 15.62, normal; 18.5-23) was admitted for hysteroscopic myomectomy, under general anesthesia. Except penicillin allergy, she had no history of cardiovascular diseases, nor did she have any coronary risk factors, including smoking, diabetes mellitus, hyperlipidemia, hypertension, coagulative disorder, oral contraceptive use, and/or family history of myocardial disease. Physical examination and routine preoperative laboratory tests, including chest X-ray, and electrocardiogram (ECG) were unremarkable with total cholesterol and high density lipoprotein within normal range.
After arriving at the operating room, ECG, pulse oximetry, non-invasive blood pressure, and end-tidal carbon dioxide (EtCO2) monitoring were attached to the patient. For induction of general anesthesia, thiopental sodium 200 mg, followed by rocuronium 20 mg, were injected intravenously and classic laryngeal mask airway (No. 4) was inserted. Then, she was positioned to lithotomy for the operation. Anesthesia was maintained with desflurane 5.0-6.0 vol% in 50% nitrous oxide and oxygen. The operation was uneventful for 30 minutes, with stable vital signs, except slight tachycardia with heart rate 105 to 120 beats/min. Further, the estimated blood loss was negligible.
At the end of the surgery, ergonovine maleate 0.2 mg distilled with normal saline 10 ml was intravenously administered slowly for a minute at the request of the surgeon for the uterine contraction. About 2 minutes later, EtCO2 suddenly decreased to 20 mmHg from 33 mmHg, followed by a loss of plethysmographic wave. The patient was cyanotic, but anesthetic monitor showed no noticeable change in the airway pressure and expiratory tidal volume. The blood pressure, although measured at 119/89 mmHg a few minutes ago, was not checkable with un-palpable radial pulse, and ECG showed severe bradycardia, followed by asystole.
Immediately, 1 mg epinephrine was injected intravenously, FiO2 increased to 100%, and thereafter, chest compression was started. Laryngeal mask airway was changed to endotracheal tube (No. 7), under direct laryngoscopy, right internal jugular vein cannulated and arterial line in the right radial artery established, while chest compression continued, inotropics infused and intermittent atropine and other drugs were administered. Even with these measures, the patient responded poorly and cardiac rhythm couldn't be detected. The patient was just showing low blood pressure of about 40/20 mmHg, which was observed via arterial line, probably due to chest compression. About 20 minutes after cardiac arrest, ECG returned to sinus rhythm but with tachycardia and ST elevation. Blood pressure increased to 60/20 mmHg, heart rate was at 130 beats/min, SpO2 85%, and arterial blood gas analysis with pH 7.2, PCO2 42.7 mmHg, PO2 54.3 mmHg, bicarbonate 18.2 mmol/L, base -8.2 mmol/L, and sO2 82%. Other hematologic and electrolyte were within normal limits and the results were as follows: Hemoglobin 12.2 g/dl, Hematocrit 39.7%, Na+ 136 mmol/L, K+ 3.1 mmol/L, Ca2+ 4.5 mg/dl, and Cl- 117 mg/dl. With continued intotropic support, nitroglycerin 100 µg was intravenously administered with the suspicion of myocardial ischemia. Within 5 minutes, blood pressure further increased to 123/80 mmHg, heart rate to 128 beats/min, SpO2 100%. However, afterwards, the systolic blood pressure decreased to 75 mmHg and SpO2 88% again, despite inotropic support.
Chest X-ray, taken immediately after arrival to the intensive care unit, showed bilateral diffuse pulmonary edema (). Even though ECG didn't show definite ST abnormalities, except sinus tachycardia (), cardiac enzymes were elevated as follows; troponin I 3.2 ng/ml (normal < 0.78), CK-MB 12.08 ng/ml (normal < 5). Transthoracic echocardiography showed the ejection fraction of only 22% (normal 56-78%), with severe hypokinesia in the inferior and septal area. Patient was unresponsive, blood pressure still low with systolic pressure below 80 mmHg and oxygen saturation around 75-82%. So, the patient was managed with the extracorporeal membrane oxygenation (Capiox SP Pump controller 101, Terumo, Japan) through left femoral veno-right femoral arterial route with initial blood flow of 2-2.5 L/min. After that, the hemodynamics and oxygenation became stable with blood pressure 100/47 mmHg, and SpO2 100%.
She regained consciousness at the night of the operative day, and endotracheal tube was removed the following day. Extracorporeal membrane oxygenation was weaned and inotrope infusion was stopped at the third postoperative day. Afterwards, she recovered and was discharged without cardiopulmonary complication.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [136.0, 'mmol/L'], 'Chloride': [117.0, 'mg/dL'], 'Bicarbonate': [18.2, 'mmol/L']}",84.8,80.56,89.04,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 136.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 136.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 136.0 mmol * 1 mEq/mmol = 136.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mmol sodium/L converts to 136.0 mEq sodium/L. 
The concentration of chloride is 117.0 mg/dL. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mg to mEq. The mass of chloride is 117.0 mg. To convert from 117.0 mg to mEq, first convert from mg to mmol.To convert 117.0 mg of chloride to g, multiply by the conversion factor 0.001, giving us 117.0 mg chloride * 0.001 g/mg = 0.117 g chloride. To convert from grams of chloride to moles, divide by the molar mass 35.45 g/mol, which will give 0.117 g/(35.45 g chloride/mol) = 0.0033 mol chloride. To convert 0.0033 mol of chloride to mmol, multiply by the conversion factor 1000.0, giving us 0.0033 mol chloride * 1000.0 mmol/mol = 3.3 mmol chloride. To convert from 3.3 mmol chloride to mEq, multiply the mmol amount by the valence, to get 3.3 mmol * 1 mEq/mmol = 3.3 mEq chloride. The current volume unit is dL and the target volume unit is L. The conversion factor is 0.1 L for every unit of dL. Our next step will be to divide the mass by the volume conversion factor of 0.1 to get the final concentration in terms of mEq/L. This will result to 3.3 mEq chloride/0.1 L = 33.0 mEq chloride/L. The concentration value of 117.0 mg chloride/dL converts to 33.0 mEq chloride/L. 
The concentration of bicarbonate is 18.2 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 18.2 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 18.2 mmol * 1 mEq/mmol = 18.2 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 18.2 mmol bicarbonate/L converts to 18.2 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 136.0 mEq/L - (33.0 mEq/L + 18.2 mEq/L) = 84.8 mEq/L. Hence, The patient's anion gap is 84.8 mEq/L."
6230,39,Anion Gap,lab test,decimal,pmc-6803752-1,Extracted,"This is a 73-year-old Caucasian female with history of hypertension and irritable bowel syndrome who presented to the hospital due to sudden onset retrosternal, squeezing, nonradiating chest heaviness during an episode of diarrhea. The pain was associated with minimal shortness of breath. She received aspirin 325 mg by EMS along with sublingual nitroglycerin. On examination in the emergency room, she had a blood pressure of 115/64 mm Hg, a regular heart rate of 67 beats per minute, a respiratory rate of 18 breaths per minute, and saturating 97% on room air. She had normal breath sounds and heart sounds on examination. She was started on nitroglycerin infusion, after which her chest heaviness partially improved but persisted. Initial EKG showed no acute changes but prolonged PR interval of 324 milliseconds ().
The patient was known to have a history of prolonged PR interval noted on prior EKGs. Initial labs showed serum sodium 136 mmol/L, potassium 4.1 mmol/L, bicarbonate 22 mmol/L, chloride 102 mmol/L, BUN 42 mg/dL, creatinine 1 mg/dL, glucose 118 mg/dL, calcium 8.7 mg/dL, white cell count 7.3/nL, hemoglobin 12.1 g/dL, and platelet count 219/nL. Coagulation profile and hepatic function panel were also within normal limits. Initial troponin was 0.46 ng/dL which increased to 3.06 ng/dL after five hours. An initial diagnosis of NSTEMI was made, and the patient was started on a heparin infusion. Urgent coronary catheterization was organized.
Coronary angiogram demonstrated a nonobstructive coronary artery disease (Figures and ) with a ventriculogram showing apical ballooning and ejection fraction of 40% suggestive of takotsubo cardiomyopathy (Figures and ). The patient was admitted to the CCU, and a transthoracic echo was done and consistent with the findings of coronary catheterization: it showed an ejection fraction of 45% with hyperdynamic inferobasal and anterior basal walls with apical ballooning indicative of takotsubo cardiomyopathy (). She was diagnosed as having takotsubo syndrome, and her heparin infusion was discontinued. Her hospitalization was complicated by Mobitz 1 AV block (), wide complex escape rhythms, and subsequent complete heart block (). Because of her baseline prolonged PR interval and very high projected pacing burden, biventricular pacer was inserted. The patient remained hemodynamically stable and was discharged home after a couple of days.
A repeat echocardiogram was done outpatient, two months after hospitalization, and showed improvement: she had an ejection fraction of 55-60% with resolution of the apical ballooning and hyperdynamic wall motion changes, which were initially noted during hospitalization (). Pacemaker interrogation revealed 100% ventricular pacing and continues to show 100% ventricular pacing even twenty months after hospital discharge. This signifies the persistence and chronicity of the AV block even after her hospitalization and after the resolution of her cardiomyopathy.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [136.0, 'mmol/L'], 'Chloride': [102.0, 'mmol/L'], 'Bicarbonate': [22.0, 'mmol/L']}",12,11.4,12.6,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 136.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 136.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 136.0 mmol * 1 mEq/mmol = 136.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mmol sodium/L converts to 136.0 mEq sodium/L. 
The concentration of chloride is 102.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 102.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 102.0 mmol * 1 mEq/mmol = 102.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 102.0 mmol chloride/L converts to 102.0 mEq chloride/L. 
The concentration of bicarbonate is 22.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 22.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 22.0 mmol * 1 mEq/mmol = 22.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 22.0 mmol bicarbonate/L converts to 22.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 136.0 mEq/L - (102.0 mEq/L + 22.0 mEq/L) = 12.0 mEq/L. Hence, The patient's anion gap is 12.0 mEq/L."
6231,39,Anion Gap,lab test,decimal,usmle-9340,Extracted,"A 69-year-old African American man is brought to the emergency department with sudden onset lower limb paralysis and back pain. He has had generalized bone pain for 2 months. He has no history of severe illnesses. He takes ibuprofen for pain. On examination, he is pale. The vital signs include: temperature 37.1°C (98.8°F), pulse 68/min, respiratory rate 16/min, and blood pressure 155/90 mm Hg. The neurologic examination shows paraparesis. The 8th thoracic vertebra is tender to palpation. An X-ray of the thoracic vertebrae confirms a compression fracture at the same level. The laboratory studies show the following:
Laboratory test
Hemoglobin 9 g/dL
Mean corpuscular volume 95 μm3
Leukocyte count 5,000/mm3
Platelet count 240,000/mm3
ESR 85 mm/hour
Serum
Na+ 135 mEq/L
K+ 4.2 mEq/L
Cl− 113 mEq/L
HCO3− 20 mEq/L
Ca+ 11.5 mg/dL
Albumin 4 g/dL
Urea nitrogen 18 mg/dL
Creatinine 1.2 mg/dL
Serum electrophoresis shows a monoclonal protein level of 38 g/L.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [113.0, 'mEq/L'], 'Bicarbonate': [20.0, 'mEq/L'], 'Sodium': [135.0, 'mEq/L']}",2,1.9,2.1,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 135.0 mEq/L. 
The concentration of chloride is 113.0 mEq/L. 
The concentration of bicarbonate is 20.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 135.0 mEq/L - (113.0 mEq/L + 20.0 mEq/L) = 2.0 mEq/L. Hence, The patient's anion gap is 2.0 mEq/L."
6232,39,Anion Gap,lab test,decimal,pmc-3712158-1,Extracted,"A 53-year-old male patient visited the emergency room for worsening symptoms of productive cough, fever, and chills that developed the day before. The patient, with no specific occupation, had a 30-pack/year history of cigarette smoking and consumed alcohol in moderation. He was successfully treated for CAP in another hospital 2 years prior and had experienced no other problems. Upon admission, the patient appeared acutely ill. His blood pressure was 82/46 mmHg, respiratory rate was 22 breaths per minute, pulse rate was 120 beats per minute, and body temperature was 40℃. A regular heart rhythm was observed and there were coarse breathing sounds with crackles on the right lower lung field.
The laboratory chemistry values were as follows: white blood cell count of 11,500/mm3 with 86.1% neutrophils, 11.5% lymphocytes, 1.9% monocytes, 0.2% eosinophils; hemoglobin 14.4 g/dL; platelet count 188,000/mm3; C-reactive protein 1.28 mg/dL. The arterial blood gas analysis at room air was pH of 7.47, pCO2 of 22.4 mmHg, pO2 of 52.5 mmHg, HCO3- of 16 mmol/L, and O2 saturation of 89%. Blood chemistries showed a blood urea nitrogen (BUN)/creatinine (Cr) level of 9/2.05 mg/dL and the serum sodium, potassium, and chloride were 139, 4.1, and 105 mmol/L, respectively. The urine sodium was 19 mmol/L, urine Cr was 222.31 mg/dL, and the calculated fractional excretion of sodium was 0.1%. A simple chest radiograph showed moderate patchy consolidation in the right lower lobe (). We made a presumptive diagnosis of sepsis caused by CAP.
Septic shock was suspected due to low blood pressure. A central line catheter was promptly inserted, along with fluid resuscitation, and oxygen was administered via nasal cannula. Cultures of blood, sputum, and urine samples were also completed. Empiric piperacillin/tazobactam with ciprofloxacin injections were administered simultaneously. The patient was admitted into the intensive care unit for directed therapy of septic shock. The initial APACHE II score was 25. Low blood pressure persisted after vigorous fluid therapy; thus, the vasoactive agent norepinephrine was administered. Vasopressin was later added when the mean arterial pressure did not normalize. Sixteen hours after admission, respiratory distress worsened, resulting in acute respiratory failure with arterial blood gas analysis showing a pH of 7.085, pCO2 of 61.4 mmHg, and HCO3- of 19 mmol/L. The patient was immediately intubated with mechanical ventilation at FiO2 of 1.0 and positive end expiratory pressure at 14 cmH2O; however, hypoxia persisted and respiratory and metabolic acidosis continued to deteriorate. Twenty-four hours after admission, follow-up arterial blood gas analysis showed a pH of 7.096, pCO2 of 63.7 mmHg, pO2 of 77.6 mmHg, HCO3- of 20 mmol/L, and O2 saturation of 89%. The follow-up chest radiograph showed more exacerbated consolidation in the right lung field with the beginning of patchy opacities in the left lower lobe (). The antibiotics were then switched to meropenem with teicoplanin. Twenty-eight hours after admission, oliguria ensued along with deteriorating acute kidney injury with BUN/Cr at 26/3.66 mg/dL. Continuous renal replacement therapy was promptly initiated. After 36 hours of intensive treatment, septic shock and acute respiratory failure did not improve and the patient went into cardiac arrest. Cardiopulmonary resuscitation was performed for 30 minutes but the patient did not recover.
After the patient expired, AB was identified in both the culture of sputum and two pairs of blood samples taken during the emergency room visit. Bacterial sensitivity to antibiotics was measured using isolates from both sputum and blood cultures. The bacterial isolate was susceptible to piperacillin/tazobactam, ceftazidime, cefepime, imipenem, meropenem, gentamicin, and tobramycin; tolerant to ampicillin, amoxacillin/clavulanic acid, cafalotin, cefoxitin, and trimethoprim/sulfamethoxazole; and moderately tolerant to cefotaxime and levofloxacin (). A VITEK device (VITEK 2, Biomerieux, Marcy I'Etolile, France) was used for culturing, and the sensitivity test was conducted in accordance to the Clinical and Laboratory Standards Institute.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [105.0, 'mmol/L'], 'Bicarbonate': [20.0, 'mmol/L'], 'Sodium': [139.0, 'mmol/L']}",14,13.3,14.7,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 139.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 139.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 139.0 mmol * 1 mEq/mmol = 139.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mmol sodium/L converts to 139.0 mEq sodium/L. 
The concentration of chloride is 105.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 105.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 105.0 mmol * 1 mEq/mmol = 105.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 105.0 mmol chloride/L converts to 105.0 mEq chloride/L. 
The concentration of bicarbonate is 20.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 20.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 20.0 mmol * 1 mEq/mmol = 20.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 20.0 mmol bicarbonate/L converts to 20.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 139.0 mEq/L - (105.0 mEq/L + 20.0 mEq/L) = 14.0 mEq/L. Hence, The patient's anion gap is 14.0 mEq/L."
6233,39,Anion Gap,lab test,decimal,usmle-286,Extracted,"A 73-year-old woman presents to the emergency department with diffuse abdominal pain, nausea, and vomiting. Her daughter who accompanies her says she was in her usual state of health until two days ago when she started to complain of abdominal pain and was unable to tolerate oral intake. She has hypertension, congestive heart failure, atrial fibrillation, and osteoarthritis. She underwent an exploratory laparotomy for an ovarian mass a year ago where a mucinous cystadenoma was excised. Her medications include aspirin, nifedipine, lisinopril, metoprolol, warfarin, and Tylenol as needed for pain. She does not drink alcohol or smoke cigarettes. She appears ill and disoriented. Her temperature is 37.9°C (100.3°F), blood pressure is 102/60 mm Hg, pulse is 110/min and irregular, and respirations are 16/min. Examination shows diffuse tenderness to palpation of the abdomen. The abdomen is tympanitic on percussion. Bowel sounds are hyperactive. The lungs are clear to auscultation bilaterally. There is a soft crescendo-decrescendo murmur best auscultated in the right second intercostal space. Laboratory studies show:
Hemoglobin 10.2 g/dL
Leukocyte count 14,000/mm3
Platelet count 130,000/mm3
Prothrombin time 38 seconds
INR 3.2
Serum
Na+ 132 mEq/dL
K+ 3.6 mEq/dL
Cl- 102 mEq/dL
HCO3- 19 mEq/dL
Urea nitrogen 36 mg/dl
Creatinine 2.3 mg/dL
Lactate 2.8 mEq/dL (N= 0.5-2.2 mEq/dL)
An x-ray of the abdomen shows multiple centrally located dilated loops of gas filled bowel. There is no free air under the diaphragm. A nasogastric tube is inserted and IV fluids and empiric antibiotic therapy are started. Emergent exploratory laparotomy is planned.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [102.0, 'mEq/dL'], 'Bicarbonate': [19.0, 'mEq/dL'], 'Sodium': [132.0, 'mEq/dL']}",110,104.5,115.5,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 132.0 mEq/dL. We need to convert the concentration to mEq/L. The mass units of the source and target are the same so no conversion is needed. The current volume unit is dL and the target volume unit is L. The conversion factor is 0.1 L for every unit of dL. Our next step will be to divide the mass by the volume conversion factor of 0.1 to get the final concentration in terms of mEq/L. This will result to 132.0 mEq sodium/0.1 L = 1320.0 mEq sodium/L. The concentration value of 132.0 mEq sodium/dL converts to 1320.0 mEq sodium/L. 
The concentration of chloride is 102.0 mEq/dL. We need to convert the concentration to mEq/L. The mass units of the source and target are the same so no conversion is needed. The current volume unit is dL and the target volume unit is L. The conversion factor is 0.1 L for every unit of dL. Our next step will be to divide the mass by the volume conversion factor of 0.1 to get the final concentration in terms of mEq/L. This will result to 102.0 mEq chloride/0.1 L = 1020.0 mEq chloride/L. The concentration value of 102.0 mEq chloride/dL converts to 1020.0 mEq chloride/L. 
The concentration of bicarbonate is 19.0 mEq/dL. We need to convert the concentration to mEq/L. The mass units of the source and target are the same so no conversion is needed. The current volume unit is dL and the target volume unit is L. The conversion factor is 0.1 L for every unit of dL. Our next step will be to divide the mass by the volume conversion factor of 0.1 to get the final concentration in terms of mEq/L. This will result to 19.0 mEq bicarbonate/0.1 L = 190.0 mEq bicarbonate/L. The concentration value of 19.0 mEq bicarbonate/dL converts to 190.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 1320.0 mEq/L - (1020.0 mEq/L + 190.0 mEq/L) = 110.0 mEq/L. Hence, The patient's anion gap is 110.0 mEq/L."
6234,39,Anion Gap,lab test,decimal,pmc-4572425-1,Extracted,"A 59-year-old Caucasian female with history of recurrent bilateral pleural effusions was admitted with worsening dyspnea and a nonproductive cough present over the course of one week. She had undergone outpatient right-sided thoracentesis on the day prior to admission, with drainage of 1500 mL of pleural fluid.
The recurrent pleural effusions had been occurring for three months prior to this presentation, and she had undergone thoracentesis twice for the right-sided pleural effusion and six times for the left-sided pleural effusion without any conclusive diagnosis. Results from all of thoracentesis procedures were suggestive of transudative effusions and cultures were negative.
On physical exam, this patient was mildly dyspneic but without retractions or accessory muscle use. There were decreased breath sounds at both lung bases. Temperature was 98.5°F, heart rate was 94/min, respiratory rate was 18/min, blood pressure was 97/55 mm Hg, and oxygen saturations were 99% on room air. Complete blood count and basic metabolic panel showed WBC 8.6 thou/μL, Hb 14.1 g/dL, Hct 44.2 g/dL, Plt 356 thou/μL, sodium of 140 mmol/L, potassium of 4 mmol/L, chloride of 101 mmol/L, bicarbonate 32 mmol/L, BUN 13 mg/dL, Creatinine 0.8 mg/dL, and glucose 112 mg/dL. Serum immunofixation electrophoresis showed small lambda monoclonal protein and no Bence-Jones proteinuria. Chest X-ray taken at the time of admission demonstrated a moderate to large left-sided pleural effusion as well as a right lower lobe consolidation. CT scan of chest showed bilateral pleural effusions, greater on the left side (). During her hospitalization, the patient underwent thoracentesis which showed WBC 484 mm3, RBC 38 mm3, lymphocyte count of 99%, monocyte count of 1%, glucose of 106 mg/dL, total bilirubin of 2.4 gm/dL, lactate dehydrogenase (LDH) of 80 U/L, amylase 19 U/L, cholesterol of 45 mg/dL, triglyceride 17 mg/dL, and adenosine deaminase of 2.3 U/L, and the cultures for routine, acid fast bacilli, and fungus were negative. Cytology demonstrated benign findings with numerous lymphocytes present. The patient underwent biopsy of the left upper lobe of the lung as well as chemical pleurodesis for her recurrent left-sided pleural effusion. Lung biopsy showed diffuse pulmonary amyloidosis, and Congo Red staining was positive confirming the diagnosis (Figures 
–). Biopsy of the pleura was negative for any pathologic findings.
The patient underwent hematology/oncology evaluation. Echocardiogram showed left concentric ventricular hypertrophy. Rheumatoid factor and thyroid stimulating hormone levels were normal. Follow-up immunoglobulin and electron microscopy as well as bone marrow biopsy were performed and favored plasma cell myeloma over primary amyloidosis. There were 6% plasma cells on aspirate smears and 15–20% on CD138 immunohistochemical staining of biopsy and clot sections. Flow cytometry showed 1.4% of monoclonal plasma cells typical of a plasma cell dyscrasia.
The patient was started on Cyclophosphamide, Dexamethasone, and Bortezomib (Velcade) therapy and was discharged in stable condition with outpatient follow-up. She had no recurrent pleural effusions at four-month follow-up.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [101.0, 'mmol/L'], 'Bicarbonate': [32.0, 'mmol/L'], 'Sodium': [140.0, 'mmol/L']}",7,6.65,7.35,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 140.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 140.0 mmol * 1 mEq/mmol = 140.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mmol sodium/L converts to 140.0 mEq sodium/L. 
The concentration of chloride is 101.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 101.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 101.0 mmol * 1 mEq/mmol = 101.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 101.0 mmol chloride/L converts to 101.0 mEq chloride/L. 
The concentration of bicarbonate is 32.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 32.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 32.0 mmol * 1 mEq/mmol = 32.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 32.0 mmol bicarbonate/L converts to 32.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (101.0 mEq/L + 32.0 mEq/L) = 7.0 mEq/L. Hence, The patient's anion gap is 7.0 mEq/L."
6235,39,Anion Gap,lab test,decimal,usmle-6290,Extracted,"A 45-year-old man is brought to the emergency department by police. He was found passed out in a store. The patient is dressed in soiled clothing that smells of urine and his pants are soaked in vomit. The patient has a past medical history of IV drug use, alcohol use, and multiple fractures secondary to scurvy. He is not currently taking any medications. His temperature is 99.5°F (37.5°C), blood pressure is 90/63 mmHg, pulse is 130/min, respirations are 15/min, and oxygen saturation is 95% on room air. The patient is started on IV fluids, thiamine, and dextrose. The patient becomes arousable at this point and begins vomiting into a basin. On physical exam, the patient appears poorly kempt and uncomfortable. His epigastric region is tender upon palpation. Cardiac exam reveals a normal rate and rhythm. Pulmonary exam is clear to auscultation bilaterally. A CT scan of the abdomen is ordered as seen in Figure A. Laboratory values are ordered as seen below:

Serum:
Na+: 139 mEq/L
Cl-: 102 mEq/L
K+: 4.0 mEq/L
HCO3-: 26 mEq/L
BUN: 20 mg/dL
Glucose: 73 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.2 mg/dL
Lipase: 295 U/L
AST: 57 U/L
ALT: 39 U/L

Hemoglobin: 9 g/dL
Hematocrit: 30%
Mean corpuscular volume: 120 µm^3
Leukocyte count: 8,500/mm^3 with normal differential
Platelet count: 199,000/mm^3

The patient continues to vomit and is observed in the emergency department. Several hours later his temperature is 99.5°F (37.5°C), blood pressure is 110/72 mmHg, pulse is 97/min, respirations are 15/min, and oxygen saturation is 95% on room air. Physical exam reveals a cardiac and pulmonary exam that are within normal limits. HEENT exam reveals suprasternal crepitus, an oropharynx that is blood-stained, and no signs of lymphadenopathy. Inspection of the patient’s lower extremities is within normal limits.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [102.0, 'mEq/L'], 'Bicarbonate': [26.0, 'mEq/L'], 'Sodium': [139.0, 'mEq/L']}",11,10.45,11.55,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 139.0 mEq/L. 
The concentration of chloride is 102.0 mEq/L. 
The concentration of bicarbonate is 26.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 139.0 mEq/L - (102.0 mEq/L + 26.0 mEq/L) = 11.0 mEq/L. Hence, The patient's anion gap is 11.0 mEq/L."
6236,39,Anion Gap,lab test,decimal,usmle-1270,Extracted,"A 54-year-old woman comes to the physician with abdominal distention and mild diffuse abdominal discomfort. She has not had nausea, vomiting, fever, or chills. She was diagnosed with alcoholic liver cirrhosis 2 years ago. Examination shows a protruding, distended abdomen that is dull to percussion with a positive fluid wave. Ultrasonography shows mild to moderate ascites. Appropriate treatment of the patient's condition is started. Four days later, the patient experiences palpitations and chest pain at home. She is brought to the emergency department, where her temperature is 37.3°C (99.1°F), pulse is 182/min, respirations are 18/min, and blood pressure is 82/50 mm Hg. An ECG shows ventricular tachycardia. Initial laboratory studies show:
Serum
Na+ 131 mEq/L
K+ 2.9 mEq/L
Cl- 92 mEq/L
Bicarbonate 34 mEq/L
Urea nitrogen 42 mg/dL
Creatinine 4.8 mg/dL
Glucose 90 mg/dL
Ca2+ 8.1 mg/dL
Mg2+ 1.5 mg/dL
Phosphate 4.7 mg/dL
Arterial Blood Gas
pH 7.52
pCO2 45 mm Hg
pO2 90.2 mm Hg
She is successfully cardioverted to normal sinus rhythm.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [92.0, 'mEq/L'], 'Bicarbonate': [34.0, 'mEq/L'], 'Sodium': [131.0, 'mEq/L']}",5,4.75,5.25,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 131.0 mEq/L. 
The concentration of chloride is 92.0 mEq/L. 
The concentration of bicarbonate is 34.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 131.0 mEq/L - (92.0 mEq/L + 34.0 mEq/L) = 5.0 mEq/L. Hence, The patient's anion gap is 5.0 mEq/L."
6237,39,Anion Gap,lab test,decimal,usmle-1910,Extracted,"A 25-year-old man is brought to the physician because of fatigue, lethargy, and lower leg swelling for 2 weeks. He also noticed that his urine appeared darker than usual and for the last 2 days he has passed only small amounts of urine. His temperature is 37.5°C (98.6°F), pulse is 88/min, respirations are 15/min, and blood pressure is 154/98 mm Hg. Examination shows 2+ pretibial edema bilaterally. Laboratory studies show:
Hemoglobin 10.9 g/dL
Leukocyte count 8200/mm3
Platelet count 220,000/mm3
Serum
Na+ 137 mEq/L
Cl- 102 mEq/L
K+ 4.8 mEq/L
HCO3- 22 mEq/L
Glucose 85 mg/dL
Urea nitrogen 34 mg/dL
Creatinine 1.4 mg/dL
Urine
Blood 2+
Protein 3+
Glucose negative
RBC 10–12/HPF with dysmorphic features
RBC casts numerous
Renal biopsy specimen shows a crescent formation in the glomeruli with extracapillary cell proliferation.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [102.0, 'mEq/L'], 'Bicarbonate': [22.0, 'mEq/L'], 'Sodium': [137.0, 'mEq/L']}",13,12.35,13.65,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 137.0 mEq/L. 
The concentration of chloride is 102.0 mEq/L. 
The concentration of bicarbonate is 22.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 137.0 mEq/L - (102.0 mEq/L + 22.0 mEq/L) = 13.0 mEq/L. Hence, The patient's anion gap is 13.0 mEq/L."
6238,39,Anion Gap,lab test,decimal,usmle-1673,Extracted,"A 38-year-old man is brought to the emergency room because of diarrhea for 2 days. He has abdominal cramps and has also noticed a dark red tint to his stool. He returned from a trip to Mexico 3 weeks ago, where he completed a marathon. He has a history of mild anemia. He does not smoke and drinks 3–4 beers on weekends. He takes fish oil, a multivitamin, and iron supplements to improve his athletic performance. His temperature is 101.8°F (38.8°C), pulse is 65/min, and blood pressure is 120/75 mm Hg. Lungs are clear to auscultation. Cardiac examination shows no abnormalities. There is mild tenderness to palpation of the left lower quadrant without rebound or guarding. Laboratory studies show:
Hematocrit 37.1%
Leukocyte count 4,500/mm3
Platelet count 240,000/mm3
Serum
Na+ 136 mEq/L
K+ 4.5 mEq/L
Cl- 102 mEq/L
HCO3- 26 mEq/L
Urea nitrogen 14 mg/dL
Creatinine 1.2 mg/dL
Stool culture demonstrates organisms with ingested erythrocytes.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [102.0, 'mEq/L'], 'Bicarbonate': [26.0, 'mEq/L'], 'Sodium': [136.0, 'mEq/L']}",8,7.6,8.4,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 136.0 mEq/L. 
The concentration of chloride is 102.0 mEq/L. 
The concentration of bicarbonate is 26.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 136.0 mEq/L - (102.0 mEq/L + 26.0 mEq/L) = 8.0 mEq/L. Hence, The patient's anion gap is 8.0 mEq/L."
6239,39,Anion Gap,lab test,decimal,pmc-6552952-1,Extracted,"A 4.5-month-old boy, presenting dry cough since two weeks that did not respond to antibiotics (amoxicillin-clavulanic acid), was admitted to the pediatric intensive care unit due to tachycardia and respiratory distress. He also presented anorexia and weight loss, without any episode of diarrhea and vomiting. The vital signs were as follows: RR = 30, HR = 90, BP = 80/60, and T = 37°C.
He was the first child of the family (no serious medical history of the mothers) and his birth weight was 3.5 kg, whereas at the time of admission he weighed 4.5 kg. The patient was calm during the examination and appeared normal with no sign of dehydration. Sodium electrolytes, blood gas analysis, and CBC were performed, and the patient was treated with fluid therapy and intravenous antibiotics.
The test results of patient tests were as follows: PH = 7.60/ PCO2 = 48/HCO3 = 46.1/ BE = 24; Na = 122 mEq/L/ K = 2.1 mEq/L/CL = 60 mEq/L/ Mg = 1.2 mEq/L.
The patient had hypocalcemia metabolic alkalosis, hypokalemia, and hyponatremia. Urine electrolytes measured were as follows: Na = 67 mEq/L, CL = 63 mEq/L, and K = 14 mEq/L. Transtubular K gradient (TTKG) was found to be 2.5.
Sodium and potassium concentrations were measured after every six hours. Liquid therapy with half saline and 60 mEq/L potassium was prescribed to the patient. Since K urine excretion was <15 mEq/L, the cause of hypokalemia was nonrenal excretion. Barter syndrome was thus not the diagnosis.
Twelve hours after the initiation of the treatment with liquid therapy, Na and K were 136 mEq/L and 3.9 mEq/L, respectively.
The patient responded appropriately to Na and K administration. Serum potassium and chloride levels decreased to 40 mEq/L, and therefore, oral potassium was also administered. Sonography did not show any positive signs of nephrocalcinosis and hypertrophic pyloric stenosis.
In response to respiratory symptoms and underweightness and metabolic alkalosis presented by the patient, sweat test was performed twice. Initially, the sweat chlorine and sodium were 58 mEq/L and 60 mEq/L, respectively, whereas, later, the levels of chlorine and sodium were increased to 65 mEq/L and 68 mEq/L, respectively.
Two weeks later, tests were repeated: Urine Na = 28 mmol/L/ Urine K = 11 mmol/L/ Urine CL = 16 mmol/L.
Liver enzymes were seen to be increased; however, urea, creatinine, glucose, albumin, potassium, sodium, and magnesium were normal in serum. During first examination, fat drop stool was not seen, but in the next test, fesses were seen with many fat drops, and the Sudan III test showed more than 100 fat drop.
The activity of trypsin was decreased by 1/24, where its normal rate is 1/96. Fecal elastase activity was 20 μg/g (normal > 200), seen as severe decrease in stool elastase.
Due to clinical and laboratory findings, such as positive sweat tests and other signs of metabolic alkalosis in infants, cystic fibrosis (CF) was diagnosed.
The patient was treated with fat-soluble vitamins, chest physiotherapy, antibiotics, MCT oil and pancreatic enzymes (due to gastrointestinal involvement and absorption of the patient), and amniotic nerve fibrosis and was discharged with good general condition.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [60.0, 'mEq/L'], 'Bicarbonate': [46.1, 'mEq/L'], 'Sodium': [122.0, 'mEq/L']}",15.9,15.105,16.695,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 122.0 mEq/L. 
The concentration of chloride is 60.0 mEq/L. 
The concentration of bicarbonate is 46.1 mEq/L. 
Plugging in these values into the anion gap formula gives us 122.0 mEq/L - (60.0 mEq/L + 46.1 mEq/L) = 15.9 mEq/L. Hence, The patient's anion gap is 15.9 mEq/L."
6240,39,Anion Gap,lab test,decimal,pmc-3651988-1,Extracted,"A previously healthy, 39-year-old woman was admitted to our hospital with generalized edema lasting 1 month and with sudden-onset pain in her right lower leg, particularly when walking. On admission, her general appearance was acutely ill and generally edematous. A physical examination revealed that her blood pressure was 120/80 mmHg, her heart rate was 90/min, her respiratory rate was 22/min, and her body temperature was 36.5℃. Her breathing sounds were clear, and her heartbeat was regular without murmur. A subsequent examination of her lower limbs showed asymmetric bilateral pretibial pitting edema predominantly in the left lower limb. In contrast, the right lower limb was less edematous and had very weak popliteal and pedal pulses. Delayed capillary refilling was also found in the right toes. The Homan's sign was negative.
Serum laboratory findings at admission were as follows: white blood cell count of 5,300/mm3, hematocrit of 39.5% with hemoglobin of 13.1 g/dl, and platelet count of 286,000/mm3. The serum sodium concentration was 141 mEq/L, the potassium concentration was 4.1 mEq/L, the chloride concentration was 104 mEq/L, and total CO2 was 28 mEq/L. The blood urea nitrogen concentration was 12.1 mg/dl, the creatinine concentration was 0.86 mg/dl, the serum total protein concentration was 4.3 g/dl, the albumin concentration was 2.2 g/dl, the total cholesterol concentration was 349.4 mg/dl, the low-density lipoprotein cholesterol concentration was 214.4 mg/dl, the high-density lipoprotein cholesterol concentration was 111 mg/dl, and the triglyceride concentration was 120.1 mg/dl. The results of liver function tests were normal. The coagulation profile showed an activated partial thromboplastin time of 32.0 s, prothrombin time of 9.7 s, anti-thrombin III value of 82% (70-120%), protein C activity of 143% (70-130%), and protein S activity of 65% (58.7-119.2%). The anti-nuclear antibody titer was less than 1:40, the anti-double-stranded DNA titer was 30.9 IU/ml, the C3 level was 158 mg/dl, and the C4 level was 19 mg/dl. Anti-cardiolipin immunoglobulin G, anti-cardiolipin immunoglobulin M, and lupus anticoagulant were all negative. Urinalysis revealed 3+ proteinuria (spot urine protein-to-creatinine ratio was 10.9 g/g creatinine; spot urine albumin-to-creatinine ratio was 7,406.2 mg/g creatinine) and trace hematuria (1-3 red blood cells/high-power field). To investigate the etiology of nephrotic syndrome, an urgent renal biopsy was performed.
Thereafter, although she had no risk factors for thrombosis such as immobilization, heart failure, atrial fibrillation, morbid obesity, or a recent orthopedic or gynecologic surgery, to rule out arterial thrombosis of the right lower extremity, lower extremity computed tomography (CT) angiography was performed. The CT imaging revealed that the right superficial femoral artery was occluded and there was no identifiable proximal source of thromboembolism in other large arteries (). On the basis of these CT angiographic findings, right lower extremity angiography was performed, which revealed a total occlusion of the right superficial femoral artery (). For the treatment of this condition, balloon dilatation was initially tried at the distal superficial femoral artery but failed. Hence, thrombectomy was performed with the Fogarty balloon catheter and the thrombi were successfully aspirated. After the interventional treatment, a good distal arterial flow was reestablished (). Thereafter, warfarin (5 mg/day) as an anticoagulant and corticosteroid treatments were initiated.
Subsequent transthoracic and transesophageal echocardiographic studies showed no evidence of intracardiac thrombus, vegetation, or other structural abnormalities including patent foramen ovale. Quantitation of proteinuria was confirmed by using a 24-hour urine collection that showed 10.2 g/day of protein excretion and 7.8 g/day of albumin excretion, respectively. Afterwards, with administration of warfarin and corticosteroid, the patient had nearly completely recovered from the edema and claudication and was discharged. The renal pathologic results were consistent with minimal change disease ( and ). Two months after discharge, her urine protein-to-creatinine ratio decreased to less than 0.1 g/g creatinine, her serum albumin level was maintained at 4.1 g/dl, and she had no further symptoms or signs of arterial thrombosis.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [104.0, 'mEq/L'], 'Bicarbonate': [28.0, 'mEq/L'], 'Sodium': [141.0, 'mEq/L']}",9,8.55,9.45,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 141.0 mEq/L. 
The concentration of chloride is 104.0 mEq/L. 
The concentration of bicarbonate is 28.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 141.0 mEq/L - (104.0 mEq/L + 28.0 mEq/L) = 9.0 mEq/L. Hence, The patient's anion gap is 9.0 mEq/L."
6241,39,Anion Gap,lab test,decimal,usmle-4195,Extracted,"A 65-year-old obese man presents to his primary care clinic feeling weak. He was in the military and stationed in Vietnam in his youth. His current weakness gradually worsened to the point that he had to call his son to help him stand to get on the ambulance. He smokes a pack of cigarettes every day and drinks a bottle of vodka a week. He has been admitted for alcohol withdrawal multiple times and has been occasionally taking thiamine, folic acid, and naltrexone. He denies taking steroids. His temperature is 98°F (36.7°C), blood pressure is 170/90 mmHg, pulse is 75/min, and respirations are 20/min. He is obese with a significant pannus. Hepatomegaly is not appreciable. Abdominal striae are present. His workup is notable for the following:

Serum:
Na+: 142 mEq/L
Cl-: 102 mEq/L
K+: 3.9 mEq/L
HCO3-: 25 mEq/L
BUN: 24 mg/dL
Glucose: 292 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 10.1 mg/dL
AST: 7 U/L
ALT: 14 U/L
24-hour urinary cortisol: 400 µg (reference range < 300 µg)
Serum cortisol: 45 pg/mL (reference range < 15 pg/mL)

A 48-hour high dose dexamethasone suppression trial shows that his serum cortisol levels partially decrease to 25 pg/mL and his adrenocorticotropin-releasing hormone (ACTH) level decreases from 10 to 6 pg/mL (reference range > 5 pg/mL).",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [102.0, 'mEq/L'], 'Bicarbonate': [25.0, 'mEq/L'], 'Sodium': [142.0, 'mEq/L']}",15,14.25,15.75,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 142.0 mEq/L. 
The concentration of chloride is 102.0 mEq/L. 
The concentration of bicarbonate is 25.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 142.0 mEq/L - (102.0 mEq/L + 25.0 mEq/L) = 15.0 mEq/L. Hence, The patient's anion gap is 15.0 mEq/L."
6242,39,Anion Gap,lab test,decimal,pmc-3886212-1,Extracted,"A 54-year-old woman presented to the emergency room of a community hospital with hematochezia and lightheadedness. Her past medical history was significant for end-stage renal disease (ESRD) due to type 1 diabetes mellitus (DM), for which she had undergone deceased donor kidney and pancreas transplant in 1989. The exocrine pancreas drained into the bladder. The pancreas failed and she underwent pancreatectomy in 2006. The kidney failed soon thereafter. She preemptively received a second kidney allograft from a friend and a deceased pancreas allograft (exocrine enteric drainage, and systemic venous system drainage) in 2008. The second pancreas failed in February 2011 when she once more became insulin dependent. Diffuse large B-cell lymphoma was diagnosed in 2009 for which she underwent R-CHOP chemotherapy and rituximab along with a decrease in immunosuppression. She has remained in remission with negative positron emission tomography (PET) scans.
At the time of admission, her home medications included tacrolimus, prednisone, furosemide, omeprazole, and insulin. Physical examination revealed a blood pressure of 115/57 mmHg, heart rate of 75 beats per minute and regular, and temperature of 98.4°F. The abdomen was soft, nontender with multiple incision scars, and a nontender left lower quadrant kidney allograft. Laboratory data revealed a white blood cell count of 4.0 k/mcL, hemoglobin 9.1 gm/dL, hematocrit 26.1%, and platelet count 208 k/mcL. Serum sodium was 145 mEq/L, potassium 4.1 mEq/L, chloride 111 mEq/L, and bicarbonate 27 mEq/L. Blood urea nitrogen was 16 mg/dL, creatinine 0.81 mg/dL, and glucose 145 mg/dL. Serum calcium was 8.6 mg/dL, phosphorus 3.7 mg/dL, and magnesium 1.6 mg/dL. Fecal occult blood tested positive. Esophagoduodenoscopy (EGD) and colonoscopy were performed which failed to reveal a source of gastrointestinal (GI) bleeding. She was transfused two units of packed red blood cells and subsequently discharged home.
Two days after discharge, she experienced episodes of coffee ground emesis and was admitted to another hospital. On this occasion hemoglobin was 7.7 g/dL. EGD was performed which again was inconclusive. After transfusion of 2 units of packed red blood cells (PRBCs), she was transferred to our hospital for further evaluation. When seen, BP was 115/56 mmHg, heart rate was 79 beats per minute and regular, and temperature of 98°F. Heart and lung examinations were unremarkable. The abdomen was soft, nondistended, with no tenderness over the graft. No peripheral edema was noted. A capsule endoscopy was undertaken, which showed a small nonbleeding arterial-venous malformation (AVM) in the duodenum, gastritis, but no blood in the stomach. At this time, hemoglobin was 9.3 g/dL, BUN 19 mg/dL, and creatinine 0.9 mg/dL.
On day 2 after transfer, she had two bloody bowel movements with a concomitant drop in hemoglobin to 7.6 g/dL and received 2 additional units of PRBCs. Repeat colonoscopy was technically limited due to poor bowel preparation but no active bleeding was detected. Later that day, she underwent a technetium-labeled RBC imaging scan which failed to reveal active gastrointestinal bleeding. On day 3 after transfer, she underwent repeat colonoscopy which again was nondiagnostic. Following colonoscopy, she became hypotensive with a systolic blood pressure of 70 mmHg without signs of active bleeding. Repeat hemoglobin was 9.9 g/dL and she received 2 liters of normal saline. On day 4, the hemoglobin dropped to 5.9 g/dL and 2 more units of PRBCs were administered. On day 5, she developed slurred speech and became unresponsive. She was intubated for airway protection and arterial-line systolic blood pressure measured 30–50 mmHg. Physical examination now revealed abdominal distension with hypoactive bowel sounds. An oral-gastric (OG) tube aspiration revealed 2,400 mL of bright red blood. Repeat hemoglobin was 4.4 g/dL. She received 5 liters of normal saline, 4 units of PRBCs, and pressure support with intravenous infusion of vasopressin and norepinephrine. An emergent endoscopy at bedside showed no active bleed from the duodenum; however, active bleeding was noticed from the proximal jejunum.
Emergent angiography with hand injection of contrast into the superior mesenteric artery was executed. Run off images revealed intense vasospasm and extravasation of contrast medium from the right external iliac artery (). Using the injector device, a right external iliac artery aneurysm was identified which communicated with the jejunum (). Coil embolization was attempted, but abandoned because of hemodynamic instability. Two iCast 7 mm × 59 mm covered stents (Atrium Medical Corp., Hudson, NH, USA) were deployed into the right external iliac artery over the site of the aneurysm (). Normal directional blood flow was instantaneously restored and hemodynamic stability was rapidly attained. Repeat hemoglobin was 12.7 g/dL and serum creatinine was 1.8 mg/dL. The hemoglobin remained stable for the next two days, and no further blood transfusion was required. Of note, during the hospitalization, the patient received a total of 20 units of PRBCs, 14 units of fresh frozen plasma (FFP), 10 units of platelets, 2 units of cryoprecipitate, and 3 units of factor IX.
On day 6 of admission, anuric acute kidney injury became manifested, presumably consequent to ischemic acute tubular necrosis. Continuous renal replacement therapy was instituted for the following 6 days for control of metabolic and volume status. A follow upcomputed tomography (CT) angiogram of the abdomen and pelvis showed a patent right iliac stent with no extravasation on contrast medium. On day 13, the patient was successfully extubated, but remained hemodialysis dependent until day 19 at which point creatinine stabilized at 3.2 mg/dL. On day 20, she was transferred to the hospital where she originally underwent deceased donor pancreas transplantation in 2008. No further intervention was undertaken and the patient was discharged home one week later. Her hemoglobin remained stable at 11.1 g/dL and 11.8 g/dL and serum Cr 3.0 mg/dL and 3.1 mg/dL at the 6, and 12-month followup points, respectively.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [111.0, 'mEq/L'], 'Bicarbonate': [27.0, 'mEq/L'], 'Sodium': [145.0, 'mEq/L']}",7,6.65,7.35,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 145.0 mEq/L. 
The concentration of chloride is 111.0 mEq/L. 
The concentration of bicarbonate is 27.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 145.0 mEq/L - (111.0 mEq/L + 27.0 mEq/L) = 7.0 mEq/L. Hence, The patient's anion gap is 7.0 mEq/L."
6243,39,Anion Gap,lab test,decimal,pmc-4847367-1,Extracted,"A 64-year-old Hispanic man with traumatic paraplegia presented with a urinary tract infection (UTI). He had a neurogenic bladder and a history of recurrent UTIs but no prior history of psychiatric diseases. On examination, he was noted to have a temperature of 100.7 °F (38.17 °C), blood pressure of 93/56 mm Hg, a pulse of 147 beats per minute, and a respiratory rate of 28 breaths per minute. He had labored breathing, suprapubic tenderness, and frank pus in his urine when a urinary catheter was placed. He was emergently intubated and mechanically ventilated because his cardiorespiratory status deteriorated. At the time of admission, our patient’s white blood cell (WBC) count was 16,500/μL (neutrophils 75 %, lymphocyte 12.5 %, and bands 8.4 %). His biochemical parameters were within physiological limits except for his serum creatinine at 2.4 mg/dL (estimated glomerular filtration rate [eGFR], 25 mL/min/1.73 m2) and blood urea nitrogen (BUN) at 52 mg/dL. Two sets of blood culture and a urine culture grew Klebsiella pneumoniae (a final report including the culture antibiotic sensitivity was reported on day 4 of his hospitalization). A renally adjusted dose of imipenem-cilastatin was initiated because of his prior history of extended-spectrum beta-lactamase (ESBL) Klebsiella UTIs. Sedatives were discontinued, and our patient was successfully extubated after he demonstrated clinical improvement. Our patient was oriented to place, person, time, and situation after extubation; an assessment using the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU) did not demonstrate any delirium. His family noted that he looked better and was conversing normally. The dose of imipenem-cilastatin was readjusted (increased) on his third day of hospitalization owing to the recovery of his renal function. On the fourth day of hospitalization, he was restless and agitated by paranoid thoughts (Fig. ). He reported seeing and hearing people from his church planning to burn him at the stake.
The differential diagnoses entertained at this time were ICU delirium, encephalitis, endocrine dysfunction, structural neurological lesions (possibly stroke), or toxic ingestion. Our patient was oriented to place, person, and time with no new neurological deficits except for the visual and auditory hallucinations. Despite having an acute change in his baseline mental status (Richmond Agitation Sedation Score [RASS] 0 to 1+), he did not demonstrate any inattention (as demonstrated by picking ‘2’s) and, therefore, CAM-ICU was not diagnostic for ICU delirium. When our patient’s laboratory tests were repeated at the time of the psychotic symptoms, his WBC count was 9400/μL (neutrophils 74.2 %, lymphocyte 14.2 %). His biochemistry panel revealed serum creatinine of 0.9 mg/dL (eGFR, 65 mL/min/1.73 m2), BUN of 15 mg/dL, serum sodium of 138 mEq/L, serum potassium of 4.1 mEq/L, serum chloride of 102 mEq/L, and serum bicarbonate of 22 mEq/L. His 8 a.m. cortisol level was 18 μg/dL and his thyroid function was within physiological limits (TSH 1.04 mIU/L, free T4 7.4 μg/dL, and free T3 83 ng/dL). Repeat urine and blood cultures performed while he was experiencing psychotic symptoms were later reported to have tested negative for any infection. Further neurological imaging or invasive neurological procedures were not performed because he did not have any new focal neurological deficits.
Brief psychotic episode was diagnosed as per the fifth edition Diagnostic and Statistical Manual of Mental Disorders (DSM-5) criteria, and delirium was excluded because inattention could not be demonstrated. All reversible causes of psychosis were sought. The only change in the management of our patient was a change in the dose of imipenem-cilastatin; this was considered to be a possible etiology for psychosis. Objective evidence of a causal relationship between the drug and psychosis was assessed using the Naranjo Probability Scale. Our patient’s Naranjo adverse drug reaction (ADR) probability scale score was calculated to be +7; imipenem-cilastatin was the probable culprit []. Imipenem-cilastatin was discontinued, and he was switched to ceftriaxone according to susceptibilities from the blood and urine culture. His mood and behavior improved; all visual and auditory hallucinations resolved by his sixth day of hospitalization. He experienced similar psychiatric symptoms 2 months later when imipenem-cilastatin was initiated empirically for complicated UTI. On this readmission, the Naranjo ADR probability scale score was +9, definite, when he was rechallenged with imipenem-cilastatin. His hallucinations resolved within 48 hours of discontinuing imipenem-cilastatin, as in the first instance. Unfortunately, on both occasions, the levels of imipenem or cilastatin were not estimated owing to laboratory and logistic issues.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [102.0, 'mEq/L'], 'Bicarbonate': [22.0, 'mEq/L'], 'Sodium': [138.0, 'mEq/L']}",14,13.3,14.7,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 138.0 mEq/L. 
The concentration of chloride is 102.0 mEq/L. 
The concentration of bicarbonate is 22.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 138.0 mEq/L - (102.0 mEq/L + 22.0 mEq/L) = 14.0 mEq/L. Hence, The patient's anion gap is 14.0 mEq/L."
6244,39,Anion Gap,lab test,decimal,pmc-3066742-1,Extracted,"A 48 year old male from Jammu presented to the Emergency Room with complaints of generalized weakness and altered sensorium for three days. The patient was a diagnosed case of Alcoholic liver disease in decompensated cirrhosis and pulmonary tuberculosis on a hepatic sparing regime. There was no history of seizures, chest pain or trauma. He was also a reformed alcoholic and a non smoker with no prior history of hypertension or Diabetes mellitus. In fact during his prior admission 6 months back all his documented sugar levels were normal. There was no history of use of sedatives or statins.
On admission the patient was drowsy and clinically dehydrated with Glasgow coma scale of E3M6V1. He was hemodynamically stable with pulse rate of 94/min, regular. Blood pressure was 110/90 mmHg and temperature of 36.8 centigrade degree. In view of altered sensorium and high plasma glucose of 1026 mg/dl the patient was shifted to the intensive care unit where he was managed with rehydration and insulin infusion. Laboratory parameters on admission revealed sodium 148 mmol/L; potassium 4.4 mmol/L; chloride 108 mmol/L: Bicarbonate 23.5 mmol/L; blood urea nitrogen 39 mmol/L and calculated serum osmolality came to 392 mosm/L (). Serum acetone was negative.
Creatinine phosphokinase (cpk) was sent on admission because of tall t waves in electrocardiogram () and it was 61530 U/L (). However with a normal echo the high cardiac enzymes were attributed to rhabdomyolysis. Urine routine and myoglobin were within normal limits. Cpk progressively returned towards normal () with treatment and control of sugars. The patient was finally moved to the ward where he was put on premeal insulins.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [108.0, 'mmol/L'], 'Bicarbonate': [23.5, 'mmol/L'], 'Sodium': [148.0, 'mmol/L']}",16.5,15.675,17.325,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 148.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 148.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 148.0 mmol * 1 mEq/mmol = 148.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 148.0 mmol sodium/L converts to 148.0 mEq sodium/L. 
The concentration of chloride is 108.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 108.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 108.0 mmol * 1 mEq/mmol = 108.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 108.0 mmol chloride/L converts to 108.0 mEq chloride/L. 
The concentration of bicarbonate is 23.5 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 23.5 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 23.5 mmol * 1 mEq/mmol = 23.5 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 23.5 mmol bicarbonate/L converts to 23.5 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 148.0 mEq/L - (108.0 mEq/L + 23.5 mEq/L) = 16.5 mEq/L. Hence, The patient's anion gap is 16.5 mEq/L."
6245,39,Anion Gap,lab test,decimal,pmc-4170087-1,Extracted,"A 52-years-old female was visited to our hospital emergency department due to abrupt onset of headache, fever, and vomiting. On her past history she suffered from chronic sinusitis 10 years ago. Two years ago, she received right total maxillectomy for treatment of right maxillary sinus infection with necrosis. Since one year ago, she experienced orthopedic surgery of open reduction and internal fixation of both femur due to slip down injury (). She had no history of hypertension, diabetes, hepatitis, and tuberculosis. Family history of other family members could not obtained except her elder sister because she did not wanted disclose her disease further to her family members. Her elder sister diagnosed osteopetrosis 12 years ago during dental procedure and had past history of femur fracture since 22 years ago. On her social history, she took intermittent alcohol consumption without smoking.
On arrival at the emergency department, she had a systolic blood pressure of 110 mmHg, diastolic pressure of 70 mmHg, pulse rate of 133 per minute, breathing rate of 22 per minute, body temperature of 38.3℃. She had 153 cm of height, 40.1 kg of body weight, and 17.1 kg/m2 of body mass index (BMI). On physical and neurological examination, she showed right eye proptosis and lateral gaze palsy, left hearing disturbance, and left facial nerve area sensory deficit.
Laboratory examinations were performed at the time of visiting; leukocyte was 14,000/mm3 (reference range 4,000-10,000), hemoglobin was 10.6 g/dL (reference range 12.0-16.0), platelet count was 354,000/mm3 (reference range 140,000-400,000), erythrocyte sedimentation rate was 81 mm/hr (reference range 0-20), and C-reactive protein was 18.12 mg/dL (reference range 0-0.50). Blood chemistry showed serum albumin 3.7 g/dL (reference range 3.5-5.0), total calcium 7.8 mg/dL (reference range 7.8-10.0), phosphorus 1.6 mg/dL (reference range 2.9-4.3), ionized calcium 0.89 mM/L (reference range 0.96-1.40), sodium 125 mM/L (reference range 137-150), potassium 4.1 mM/L (reference range 3.5-5.3), chloride 87 mmol/L (reference range 99-110), bicarbonate 28 mmol/L (reference range 22-34).
Radiographs of chest and PNS showed diffuse sclerotic change in bony structures (). Brain magnetic resonance imaging (MRI) showed leptomeningitis with abscess formation along right Meckel's cave and right cavernous sinus wall ().
Empirical parenteral antibiotics were started with ceftriaxone, metronidazole, and vancomycin for cavernous sinus thrombophlebitis and meningitis. Antibiotics were changed to ceftriaxone alone after obtained blood culture results with streptococcus constellatus, milleri infection.
Ten days after admission, she showed symptoms of febrile sensation, vomiting, whirling type vertigo, and generalized tonic chronic seizure attack. Mental status changed from alert to deep drowsy. On brain MRI scan, epidural empyema along right frontotemporal convexity and aggravation of meningeal enhancement were seen (). She was moved to intensive care unit and antibiotics were changed to vancomycin and metronidazole because antibiotics therapy with ceftriaxone alone caused aggravation of patient's symptom. Intravenous (IV) steroid and mannitol were administered to control increased intracranial pressure. Prompt neurosurgical decompression was indicated, but neurosurgery was not done due to refusal of operation by family members, patient's poor nutritional status like extremely low BMI and sclerotic bone disease with possibility of nonunion after operation. On cerebrospinal fluid (CSF) examination, red blood cell 0/mm3, leukocyte 800/mm3 on fluid analysis, but micro-organism was not grown.
Thirteen days after admission, she was transferred to general ward because her mental status changed to alert again with no further seizure attack. Seventeen days after admission, fever was developed again, so metronidazole was changed to meropenem to cover broader spectrum of infection. Vancomycin was stopped for 2 weeks later because fever was developed during previous vancomycin usage, and maintained meropenem alone for further 10 weeks. On endoscopic examination, sphenoid sinus was suspected to focus of infection. Five weeks after admission, she got a right sphenoidotomy under local anesthesia. Complete resolution of infection was obtained after broad spectrum antibiotic therapy for 12 weeks.
For etiologic evaluation, we tested further examination for diffuse sclerosing bony structure. Laboratory data revealed elevated serum levels of tartrate resistant acid phosphatase (TRAP) without carbonic anhydrase II DNA mutation, the intact parathyroid hormone (PTH) was elevated by 144.04 pg/mL (reference range 15-65), the 1,25-dihydroxy-vitamin D (1,25-[OH]2D) was elevated by 91.0 pg/mL (reference range 20.0-60.0), and the 25-hydroxy-vitamin D3 (25-[OH]D3) was decreased by 11.43 ng/mL (reference range 20-30). Results of bone formation and resorption marker were various with the value of bone alkaline phosphatase isoenzyme 34.2 g/L (age and gender specific reference range below 22), osteocalcin 10.4 ng/mL (age and gender specific reference range 4.0-12.0), and deoxypyridinoline 9.5 nM deoxypyridinoline (DPD)/mM (reference range 3.0-7.4), respectively. A plain radiograph of the spine showed end-plate thickening and sclerosis producing the classic ""sandwich vertebra"" appearance (). Bone mineral densitometry showed increased lumbar spine vertebral bone density and bone mineral content values (bone mineral density 2.713 g/cm2 with T-score +14.84, bone mineral content of lumbar spine 173.28 g). For evaluation of chloride channel 7 (CLCN7) deficiency osteopetrosis, we performed a CLCN7 gene mutation analysis using genomic DNA which was extracted from peripheral blood using genomic DNA prep kit (Solgent Co. Ltd., Daejeon, Korea). But we could not found any mutations on 24 and 25 exon of CLCN7 gene. And her older sister's spine X-ray also showed sandwich vertebra appearance () and the CLCN7 gene mutation was not found, too.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [125.0, 'mmol/L'], 'Chloride': [87.0, 'mmol/L'], 'Bicarbonate': [28.0, 'mmol/L']}",10,9.5,10.5,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 125.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 125.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 125.0 mmol * 1 mEq/mmol = 125.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 125.0 mmol sodium/L converts to 125.0 mEq sodium/L. 
The concentration of chloride is 87.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 87.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 87.0 mmol * 1 mEq/mmol = 87.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 87.0 mmol chloride/L converts to 87.0 mEq chloride/L. 
The concentration of bicarbonate is 28.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 28.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 28.0 mmol * 1 mEq/mmol = 28.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 28.0 mmol bicarbonate/L converts to 28.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 125.0 mEq/L - (87.0 mEq/L + 28.0 mEq/L) = 10.0 mEq/L. Hence, The patient's anion gap is 10.0 mEq/L."
6246,39,Anion Gap,lab test,decimal,pmc-8182158-1,Extracted,"A 12-year-old boy who experienced a cardiac arrest was referred to our emergency department from a local hospital in January 2020. His medical history revealed a cardiac fibroma that was detected prenatally. After birth, the fibroma was partially resected twice at another hospital, as the size and extent of the tumor prohibited single-stage resection. Heart transplantation was considered at the time. At the age of 2 years, he experienced cardiac arrest and was admitted to the same hospital. At that time, ventricular tachycardia was repeatedly detected. He developed central nervous system complications, including hypoxic-ischemic encephalopathy and quadriplegia, after which he had received oral amiodarone. Later, hydrocephalus was detected on brain magnetic resonance imaging, and he was treated with a ventriculo-peritoneal shunt.
The patient’s medication was discretionally discontinued at 10 years of age. At 12 years of age, he experienced a cyanotic spell at home and was unable to breathe. He received cardiopulmonary resuscitation from his father. When the rescue squad arrived, they determined that he was in ventricular fibrillation. Defibrillation was performed, and sinus rhythm was restored. The boy was transported to a local hospital where he received endotracheal intubation. Thereafter, he was referred to our hospital, where he was admitted to the pediatric intensive care unit.
On admission, the patient’s blood pressure and heart rate were 115/70 mm Hg and 151 beats per minute, respectively. He was intubated and was in a stuporous state. Cardiac murmurs were not heard on chest auscultation. Venous blood gas analysis revealed pH, 7.22; pCO2, 58 mm Hg; pO2, 28 mm Hg; HCO3, 18.9 mmol/L; and SvO2, 39%. Serum biochemical analysis showed a lactate level of 9.25 mmol/L. The levels of serum electrolytes were as follows: sodium, 142 mEq/L; potassium, 3.6 mEq/L; chloride, 109 mEq/L; total calcium, 8.4 mEq/L; ionized calcium, 2.3 mEq/L; inorganic phosphorous, 4.0 mg/dL; and magnesium, 1.7 mg/dL. Serum cardiac enzyme levels were as follows: creatine kinase, 155 IU/L; creatine kinase-MB, 3.37 ng/mL; troponin-T, 0.137 ng/mL; and pro-brain natriuretic peptide, 85.9 pg/ml. Cardiomegaly was observed on chest radiography (). Electrocardiogram showed sinus tachycardia with intermittent monomorphic ventricular premature contractions (VPCs). On the 1st day of hospitalization, the patient was supported by mechanical ventilation, without an intravenous inotropic agent. On the 2nd day, VPCs preceded abrupt ventricular fibrillation. He was resuscitated with sinus rhythm restoration following cardiopulmonary resuscitation and defibrillation (2 J/kg). Transthoracic echocardiography () and cardiac computed tomography () demonstrated a known fibroma (about 9.5 cm × 5.5 cm) in the anteroseptal wall of the left ventricle without blood flow obstruction. Soon after, he developed ventricular tachycardia (), and direct current cardioversion was performed along with intravenous amiodarone administration. Additionally, intravenous dopamine was administered for hypotension management. From the third to 9th days of hospitalization, he experience recurrent ventricular tachycardia refractory to multiple (45 times) direct current cardioversions (2 to 4 J/kg) and aggressive administration of antiarrhythmic agents (intravenous amiodarone and lidocaine). Although we suspected that the fibroma induced the arrhythmia, we believed additional partial resection of the tumor would not prevent it. Further, the patient’s poor neurocognitive and psychomotor states posed additional considerations for management. On the 10th day of hospitalization, he underwent an electrophysiology study, and a single-chamber implantable cardioverter defibrillator (ICD) generator (Visia AF MRI XT VR SureScan; Medtronic, Minneapolis, MN, USA) with a lead (model 6935M-62cm, Medtronic) attached to the right ventricle was inserted (). On the 11th day, weaning from mechanical ventilation was initiated. Additionally, the intravenous antiarrhythmic agents were discontinued, and oral amiodarone (10 mg/kg/day) and propranolol (0.75 mg/kg/day) were prescribed. On the 18th day, in the absence of an episode of ventricular arrhythmia from ICD memory for five days, he was discharged in stable condition with the ICD generator and followed up in the outpatient clinic.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [109.0, 'mEq/L'], 'Bicarbonate': [18.9, 'mmol/L'], 'Sodium': [142.0, 'mEq/L']}",14.1,13.395,14.805,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 142.0 mEq/L. 
The concentration of chloride is 109.0 mEq/L. 
The concentration of bicarbonate is 18.9 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 18.9 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 18.9 mmol * 1 mEq/mmol = 18.9 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 18.9 mmol bicarbonate/L converts to 18.9 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 142.0 mEq/L - (109.0 mEq/L + 18.9 mEq/L) = 14.1 mEq/L. Hence, The patient's anion gap is 14.1 mEq/L."
6247,39,Anion Gap,lab test,decimal,pmc-8298207-1,Extracted,"We present the case of an 82-year-old Caucasian male who presented to the hospital with a near-syncopal episode. The patient also complained of dyspnea on exertion for the past few weeks. He has a past medical history significant for hypertension, hypothyroidism, type 2 diabetes mellitus, and coronary artery disease status post coronary artery bypass grafting. The patient was diagnosed with COVID-19 four weeks prior to presentation to the hospital. He was treated with remdesivir and low dose dexamethasone. He was discharged after a three-day hospital stay. He noticed epistaxis the night prior to the presentation. He had also noted diffuse bruising on his arms several days prior to his current presentation. He denied a history of hematologic disorders.
On admission, his vital signs showed a temperature of 98.7 F, pulse rate of 82 beats per minute, respiratory rate of 17 breaths per min, blood pressure of 141/63 mmHg, and oxygen saturation of 89% on room air.
Physical examination revealed large areas of ecchymosis on the upper extremities, scattered ecchymosis on his lower extremities, some dried blood in his nares, and left lower lobe rales and rhonchi. Laboratory values yielded a white blood cell count 7,430/mm3, hemoglobin 10.3 g/dL, platelet count 1,000/mm3, prothrombin time 10.0 seconds, international normalized ratio 1.01, activated partial thromboplastin time 29 seconds, sodium 132 mmol/L, potassium 4.2 mmol/L, chloride 99 mmol/L, carbon dioxide of 25 mmol/L, blood urea nitrogen 45 mg/dL, and creatinine 1.4 mg/dL.
The patient was admitted to the medical floor. Hematology was consulted for severe thrombocytopenia.
On day 3 of his hospitalization, he started complaining of melena. His hemoglobin count dropped to a low of 6.8 g/dL on hospital day 4. One unit of packed red blood cells (pRBC) was transfused, which resulted in an increase of his hemoglobin to 8.0 g/dL. Gastroenterology was consulted to further evaluate. An esophagogastroduodenoscopy was performed, which revealed mild-to-moderate diffuse gastritis. Diffuse petechiae were also noted in the entire stomach (Figures , ).
The patient received four units of platelets without a satisfactory increase in his platelet count. The patient was then started on therapy with IVIG. He received a total of four doses of 0.4 g/kg of IVIG and was started on high-dose intravenous dexamethasone. This regimen raised his platelet count from 1,000/mm3 prior to administration to 161,000/mm3 after four doses (Table ). His hemoglobin count also remained stable with the normalization of his platelets.
The patient was discharged with a 14-day course of 60 mg prednisone daily. The patient was seen four weeks later in the hematology-oncology clinic and was faring well with no recurrent bleeding or thrombocytopenia.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [132.0, 'mmol/L'], 'Chloride': [99.0, 'mmol/L'], 'Bicarbonate': [25.0, 'mmol/L']}",8,7.6,8.4,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 132.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 132.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 132.0 mmol * 1 mEq/mmol = 132.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 132.0 mmol sodium/L converts to 132.0 mEq sodium/L. 
The concentration of chloride is 99.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 99.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 99.0 mmol * 1 mEq/mmol = 99.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 99.0 mmol chloride/L converts to 99.0 mEq chloride/L. 
The concentration of bicarbonate is 25.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 25.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 25.0 mmol * 1 mEq/mmol = 25.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 25.0 mmol bicarbonate/L converts to 25.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 132.0 mEq/L - (99.0 mEq/L + 25.0 mEq/L) = 8.0 mEq/L. Hence, The patient's anion gap is 8.0 mEq/L."
6248,39,Anion Gap,lab test,decimal,pmc-7410512-1,Extracted,"A 66-year-old African American male with a past medical history of hypertension, alcohol use, and asthma presented with facial swelling. He was discharged two months prior for a similar event related to lisinopril. On initial presentation, the patient's vitals were significant for heart rate of 104 beats per minute, respiratory rate of 30 breaths per minute, blood pressure of 190/100 mmHg, and oxygen saturation of 99% with a non-rebreather mask at 15 liters. Physical exam was significant for moderate to severe respiratory distress, inspiratory stridor, and subcostal and intercostal retractions. Lungs were clear to auscultation. The patient was otherwise alert and oriented. Arterial blood gas showed pH 7.447, pCO2 39, pO2 197, and HCO3 27 on 60% FiO2. His initial metabolic panel was significant for sodium 104 mmol/L, potassium 2.6 mmol/L, chloride 66 mmol/L, blood urea nitrogen (BUN) 5 mg/dL (baseline 20 mg/dL), and creatinine 0.6 mg/dL (baseline 1.0 mg/dL). Glucose was 165 mg/dL. Magnesium and phosphorus were 1.1 and 2.1 mg/dL, respectively. Serum uric acid was low at 2.7 mg/dL. Complete blood count showed no leukocytosis or anemia. Urinalysis had a specific gravity of 1.010, moderate blood, and 15-29 red blood cells. Urine electrolytes were notable for a sodium of 48 mmol/L and osmolality of 217 mOsm/kg. Serum osmolality was 215 mOsm/kg. Urine and serum toxicology were negative for any substances. Alcohol level was negative.
Due to concern for airway protection, the patient was intubated and admitted to the intensive care unit. Initial chest x-ray held concern for infectious process, but antibiotics were stopped after infectious workup was negative. The patient was given two units of fresh-frozen plasma, famotidine, and Benadryl, and started on methylprednisolone 60 mg every six hours for angioedema. Lisinopril was held at this time. For his hyponatremia, the patient's labs were suspicious for syndrome of inappropriate antidiuretic hormone (SIADH) and a one-liter fluid restriction was initiated with nephrology consult. Thyroid and adrenal workup to rule out other causes of SIADH was unremarkable. A CT chest scan was done to evaluate for malignancy as a cause of SIADH, but did not demonstrate overt suspicious lung pathology (Figure ). The patient's hyponatremia appropriately corrected over the course of one week and was 130 mmol/L upon discharge. Lisinopril was discontinued and marked as an allergy for the patient. On follow-up approximately nine months later, the patient's sodium had corrected and remained within normal limits.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [66.0, 'mmol/L'], 'Bicarbonate': [27.0, 'mmol/L'], 'Sodium': [104.0, 'mmol/L']}",11,10.45,11.55,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 104.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 104.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 104.0 mmol * 1 mEq/mmol = 104.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 104.0 mmol sodium/L converts to 104.0 mEq sodium/L. 
The concentration of chloride is 66.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 66.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 66.0 mmol * 1 mEq/mmol = 66.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 66.0 mmol chloride/L converts to 66.0 mEq chloride/L. 
The concentration of bicarbonate is 27.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 27.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 27.0 mmol * 1 mEq/mmol = 27.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 27.0 mmol bicarbonate/L converts to 27.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 104.0 mEq/L - (66.0 mEq/L + 27.0 mEq/L) = 11.0 mEq/L. Hence, The patient's anion gap is 11.0 mEq/L."
6249,39,Anion Gap,lab test,decimal,pmc-5295522-1,Extracted,"A 27-year-old African American female presented to the hospital after a sudden onset of severe retrosternal chest pain. Past medical history was insignificant for hypertension or diabetes mellitus. Patient has a history of smoking cigarettes, beginning at age 9, and frequent marijuana use. The patient was treated with morphine and Percocet for pain. Lab data and urine toxicology screen were negative for troponins and significant for marijuana, respectively. Urine drug screen was negative for cocaine and amphetamines. Drug screen was positive for opiates, but this result is most likely an artifact of morphine and Percocet treatment for chest pain. Initial laboratory findings included hemoglobin 12 g/dL, hematocrit 12.6%, platelets 223 × 103/μL, glucose 156 mg/dL, BUN 9 mg/dL, creatinine 0.8 mg/dL, sodium 135 mEq/L, potassium 4 mEq/L, chloride 101 mEq/L, and bicarbonate 18 mEq/L. In the emergency room, vital signs demonstrated a pulse rate of 98 beats/min, respiratory rate 22 breaths/min, blood pressure 132/89 mm Hg, temperature 98.1 °F, and oxygen saturation 100% on room air. The remainder of the physical examination was unremarkable. Initial electrocardiogram (ECG) demonstrated normal sinus rhythm, and the patient was admitted to telemetry for observation. The subsequent morning, the patient actively experienced chest pain and ECG changes. ECG demonstrated ST segment elevations in leads II and III, and T-wave inversions in V1-V3. Stat troponin level was found to be elevated at 11.07 ng/mL (< 0.30 ng/mL). The patient immediately underwent cardiac catheterization which demonstrated a 99% blockage of the left anterior descending artery and revascularization was performed (, ). Two-dimensional echocardiogram demonstrated a left ventricular ejection fraction of 40% with anterior wall akinesis. Transesophageal echocardiogram ruled out an apical mural thrombus, but confirmed the ejection fraction and wall akinesis from the previous echocardiogram. The patient was also found to have hyperlipidemia after the conduction of a lipid panel. Hypercoaguable state and vasculitis workup was negative.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [101.0, 'mEq/L'], 'Bicarbonate': [18.0, 'mEq/L'], 'Sodium': [135.0, 'mEq/L']}",16,15.2,16.8,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 135.0 mEq/L. 
The concentration of chloride is 101.0 mEq/L. 
The concentration of bicarbonate is 18.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 135.0 mEq/L - (101.0 mEq/L + 18.0 mEq/L) = 16.0 mEq/L. Hence, The patient's anion gap is 16.0 mEq/L."
6250,39,Anion Gap,lab test,decimal,pmc-4241635-1,Extracted,"A 61-year-old white woman presented in February 2013 with fatigue, decreased appetite and right upper quadrant abdominal pain for 2 weeks. She denied nausea, vomiting, weight loss and jaundice. Two weeks prior to presentation, the patient was found to have elevated liver enzymes by routine blood workup (AST 151 IU/l, ALT 199 IU/l), for which atorvastatin and ezetimibe were both discontinued (although she had been taking both for a long time). She was known to have MS (as she had clumsiness and optic neuritis with white matter hyperintensities by brain MRI, at that time not on any treatment, but treated with interferon in 2000 with resulting drug-induced hepatitis which resolved after discontinuation of interferon), hypothyroidism on levothyroxine (secondary to radioactive iodine ablation for Graves disease), hyperlipidemia and asthma.
On physical examination, blood pressure was 113/77 mm Hg, heart rate 64 beats/min and temperature 36.3°C. She was not jaundiced and her heart and respiratory sounds were normal. Her abdomen was soft, not tender, not distended, without hepatomegaly or splenomegaly and with normal bowel sounds. She was alert and oriented, the cranial nerves were grossly intact, muscle bulk, tone and power were normal, there was no sensory deficit, and coordination and gait were both unremarkable. Laboratory tests on admission revealed white blood cells 6.1 × 103/μl, hemoglobin 14 g/dl, platelets 433 × 103/μl, sodium 138 mEq/l, potassium 4.6 mEq/l, chloride 103 mEq/l, bicarbonate 29 mmol/l, BUN 11 mg/dl, creatinine 0.7 mg/dl and glucose 94 mg/dl. Liver function test showed AST 1,740 IU/l, ALT 1,497 IU/l, alkaline phosphatase (ALP) 140 IU/l, total bilirubin 2.4 mg/dl (direct bilirubin 1.3) – later on it went up to 5.1 mg/dl, gamma-glutamyl transferase (GGTP) 501 IU/l (normal 7–64 IU/l), total protein 8.3 g/dl and albumin 3.8 g/dl. Coagulation panel showed prothrombin time 13.6 s, international normalized ratio 1.44 and partial thromboplastin time 30.9 s. Urine drug screen was negative. The results of thyroid function testing were thyroid-stimulating hormone 10.3 mIU/ml and free thyroxine 0.8 ng/dl. She had normal alpha-fetoprotein and a negative ethanol level. Serum protein electrophoresis showed high gamma fraction of protein 2.1 g/dl. Viral hepatitis was ruled out by negative hepatitis panel including negative hepatitis C virus RNA PCR. Complete serological tests revealed positive anti-smooth muscle antibodies at 1:320 (normal titer <1:40), negative anti-mitochondrial antibodies, negative anti-nuclear antibodies, negative anti-neutrophil cytoplasmic antibodies, negative anti-myeloperoxidase antibodies, negative proteinase-3 antibodies and negative liver kidney microsomal antibodies. Ultrasound of the liver was performed and showed no significant abnormality in the liver, gallbladder or pancreas. There was no sign of gallstone or pericholecystic fluid formation. Abdominal computed tomography with contrast showed only mild fatty changes of the liver.
While the patient was in the hospital, ultrasound-guided liver biopsy was done; she was started on oral prednisone 60 mg daily and discharged home on that dose awaiting the liver biopsy result. Later on this confirmed our diagnosis of AIH as it showed lobular lymphoplasmacytic infiltrate (fig. ), Councilman bodies and spotty necrosis. Bile duct damage and bridging periportal fibrosis were present (fig. ). In March 2013, the patient had improved clinically. Her liver enzymes were checked while she was still taking 60 mg prednisone daily with the following values: AST 360 IU/l, ALT 602 IU/l, ALP 92 IU/l, GGTP 398 IU/l and total bilirubin 2.9 mg/dl. After receiving the liver biopsy result, she was prescribed oral azathioprine 50 mg daily while tapering the prednisone dose. Her liver function was periodically checked with continuous improvement. In April 2013, she was taking both 20 mg prednisone and 50 mg azathioprine daily. In June 2013, the azathioprine was stopped and she was kept on oral prednisone 10 mg daily, which later on (in September 2013) was decreased to 5 mg daily. Her liver function has been always within the normal range since July 2013 with AST 40 IU/l, ALT 35 IU/l, ALP 37 IU/l, total bilirubin 0.9 mg/dl, GGTP 60 IU/l, total protein 6.8 g/dl and albumin 3.9 g/dl.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [103.0, 'mEq/L'], 'Bicarbonate': [29.0, 'mmol/L'], 'Sodium': [138.0, 'mEq/L']}",6,5.7,6.3,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 138.0 mEq/L. 
The concentration of chloride is 103.0 mEq/L. 
The concentration of bicarbonate is 29.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 29.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 29.0 mmol * 1 mEq/mmol = 29.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 29.0 mmol bicarbonate/L converts to 29.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 138.0 mEq/L - (103.0 mEq/L + 29.0 mEq/L) = 6.0 mEq/L. Hence, The patient's anion gap is 6.0 mEq/L."
6251,39,Anion Gap,lab test,decimal,pmc-5971350-1,Extracted,"A 63-year-old female who was visitor from Veracruz, Mexico, presented to the emergency room with complaints of progressively worsening abdominal pain and distention for three days. She also had fever and altered mentation. Her past medical history was significant for hypertension, diabetes mellitus, hyperlipidemia, and end-stage renal disease. She had been on PD for four years and denied any recent changes in technique. She had two episodes of peritonitis in the past while in Mexico but was unaware of the details of those episodes. Her surgical history was significant for appendectomy, cholecystectomy, and tubal ligation and she denied any recent abdominal procedure. She denied smoking, alcohol intake, or use of recreational drugs.
On examination, her blood pressure was 172/85 mm of Hg, pulse 88/min, oral temperature 39.5°C (103.1°F), respiratory rate 14/min, and oxygen saturation on room air 94%. She was lethargic and confused. She had abdominal distention and diffuse tenderness without any rebound or guarding. Her PD catheter exit site was clean and dry. Laboratory studies showed white blood cell count of 14.5 × 103/μL with 87.1% granulocytes, hemoglobin of 6.3 g/dL, and hematocrit of 18.4%. Serum chemistries showed sodium of 130 mmol/L, potassium of 2.7 mmol/L, chloride of 90 mmol/L, bicarbonate of 27 mmol/L, blood urine nitrogen of 30 mg/dL, and creatinine of 7.7 mg/dL. Her liver function tests were within normal limits. Computed tomography of abdomen and pelvis without intravenous or oral contrast showed peritoneal thickening consistent with peritonitis, and there was no evidence of perforation or obstruction (). PD fluid analysis showed white cell count of 2173 per mm3 with 96% neutrophils and red blood cells of <3000 per mm3.
Blood and PD fluid cultures were sent, and she was empirically treated for bacterial peritonitis with intraperitoneal cefazolin and ceftazidime. PD fluid gram stain revealed budding yeast; blood and PD fluid cultures did not reveal bacterial growth. Given the high suspicion of fungal peritonitis, immediate removal of the PD catheter was discussed with the patient. She chose not to have the catheter removed, leave to Mexico, and get treated by her own nephrologist. Hence oral fluconazole was started for presumed Candida peritonitis. However, six days later, the fungal culture [Mycosel Agar and Brain Heart Infusion Agar] of the PD fluid grew H. Capsulatum.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [90.0, 'mmol/L'], 'Bicarbonate': [27.0, 'mmol/L'], 'Sodium': [130.0, 'mmol/L']}",13,12.35,13.65,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 130.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 130.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 130.0 mmol * 1 mEq/mmol = 130.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mmol sodium/L converts to 130.0 mEq sodium/L. 
The concentration of chloride is 90.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 90.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 90.0 mmol * 1 mEq/mmol = 90.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 90.0 mmol chloride/L converts to 90.0 mEq chloride/L. 
The concentration of bicarbonate is 27.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 27.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 27.0 mmol * 1 mEq/mmol = 27.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 27.0 mmol bicarbonate/L converts to 27.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 130.0 mEq/L - (90.0 mEq/L + 27.0 mEq/L) = 13.0 mEq/L. Hence, The patient's anion gap is 13.0 mEq/L."
6252,39,Anion Gap,lab test,decimal,usmle-302,Extracted,"A 52-year-old man comes to to the emergency department with fatigue and shortness of breath that has become progressively worse over the past week. He had an upper respiratory tract infection 2 weeks ago, for which he was given an antibiotic. He has hypertension, type 2 diabetes mellitus, and colonic polyps diagnosed on screening colonoscopy 2 years ago. His mother has systemic lupus erythematosus and his brother has a bicuspid aortic valve. He does not smoke cigarettes or drink alcohol. Current medications include lisinopril and metformin. His temperature is 37.3°C (99.1°F), pulse is 91/min, respirations are 18/min, and blood pressure is 145/84 mm Hg. His conjunctivae are pale. Cardiac examination shows a late systolic crescendo-decrescendo murmur at the right upper sternal border. Laboratory studies show:
Leukocyte Count 9,500/mm3
Hematocrit 24%
Platelet Count 178,000/mm3
LDH 215 U/L
Haptoglobin 22 mg/dL (N=41–165 mg/dL)
Serum
Na+ 140 mEq/L
K+ 4.6 mEq/L
CL- 100 mEq/L
HCO3- 25 mEq/L
Urea nitrogen 21 mg/dL
Creatinine 1.2 mg/dL
Total bilirubin 1.9 mg/dL
A peripheral blood smear is shown.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [100.0, 'mEq/L'], 'Bicarbonate': [25.0, 'mEq/L'], 'Sodium': [140.0, 'mEq/L']}",15,14.25,15.75,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mEq/L. 
The concentration of chloride is 100.0 mEq/L. 
The concentration of bicarbonate is 25.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (100.0 mEq/L + 25.0 mEq/L) = 15.0 mEq/L. Hence, The patient's anion gap is 15.0 mEq/L."
6253,39,Anion Gap,lab test,decimal,usmle-5278,Extracted,"A 44-year-old woman presents to her primary care physician for worsening dysuria, hematuria, and lower abdominal pain. Her symptoms began approximately 2 days ago and have progressively worsened. She denies headache, nausea, vomiting, or diarrhea. She endorses feeling ""feverish"" and notes to having foul smelling urine. She has a past medical history of Romano-Ward syndrome and is not on any treatment. She experiences profuse diarrhea and nausea when taking carbapenems and develops a severe rash with cephalosporins. Her temperature is 100.4°F (38C), blood pressure is 138/93 mmHg, pulse is 100/min, and respirations are 18/min. On physical exam, the patient appears uncomfortable and there is tenderness to palpation around the bilateral flanks and costovertebral angle. A urinalysis and urine culture is obtained and appropriate antibiotics are administered. On her next clinical visit urine studies and a basic metabolic panel is obtained, which is shown below:

Serum:
Na+: 140 mEq/L
Cl-: 101 mEq/L
K+: 4.2 mEq/L
HCO3-: 22 mEq/L
BUN: 20 mg/dL
Glucose: 94 mg/dL
Creatinine: 2.4 mg/dL

Urinalysis
Color: Yellow
Appearance: Clear
Blood: Negative
pH: 7 (Normal 5-8)
Protein: Negative
Nitrite: Negative
Leukocyte esterase: Negative
Cast: Epithelial casts
FeNa: 3%

Urine culture
Preliminary report: 10,000 CFU/mL E.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [101.0, 'mEq/L'], 'Bicarbonate': [22.0, 'mEq/L'], 'Sodium': [140.0, 'mEq/L']}",17,16.15,17.85,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mEq/L. 
The concentration of chloride is 101.0 mEq/L. 
The concentration of bicarbonate is 22.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (101.0 mEq/L + 22.0 mEq/L) = 17.0 mEq/L. Hence, The patient's anion gap is 17.0 mEq/L."
6254,39,Anion Gap,lab test,decimal,usmle-5168,Extracted,"A 5-year-old boy presents to the emergency department with sudden onset nausea and vomiting that started 2 hours ago. The patient's parents can not recall any inciting event and state that he very suddenly started acting irritable, started vomiting, and experienced 1 episode of diarrhea. His temperature is 98.7°F (37.1°C), blood pressure is 90/50 mmHg, pulse is 160/min, respirations are 29/min, and oxygen saturation is 99% on room air. The patient experiences 1 episode of bloody emesis while in the emergency department. Laboratory values are ordered as seen below.

Serum:
Na+: 140 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 19 mEq/L
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.2 mg/dL

Radiography is performed and is notable for radiopaque objects in the gastrointestinal tract.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [100.0, 'mEq/L'], 'Bicarbonate': [19.0, 'mEq/L'], 'Sodium': [140.0, 'mEq/L']}",21,19.95,22.05,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mEq/L. 
The concentration of chloride is 100.0 mEq/L. 
The concentration of bicarbonate is 19.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (100.0 mEq/L + 19.0 mEq/L) = 21.0 mEq/L. Hence, The patient's anion gap is 21.0 mEq/L."
6255,39,Anion Gap,lab test,decimal,pmc-3401823-1,Extracted,"A 58-year-old male presented to the Emergency Department with a three-day history of fever, worsening perineal erythema, and pain. His medical history revealed only mild seasonal allergies; his functional status was very good. His surgical history was significant for an inguinal herniorrhaphy three years prior to his current presentation. His medications consisted of fexofenadine and pseudoephedrine for seasonal allergies. He was not in acute distress. On physical examination, he was noted to have significant perineal cellulitis and pain. His preoperative chest X-ray revealed no infiltrates, pulmonary edema or cardiomegaly. Computed tomography (CT) demonstrated extensive inflammation of the perineum and scrotum as well as subcutaneous air, consistent with the diagnosis of Fournier's gangrene. Preoperatively the patient was normotensive, but tachycardic (heart rate 110 – 120 beats / minute). No cardiac murmurs were identified. His electrocardiogram on admission to the Intensive Care Unit (ICU) did not show any ST, T-wave changes. He did not demonstrate a third heart sound, peripheral edema, or jugular venous distention. His lungs were clear on auscultation bilaterally. His baseline SpO2 was 98% on room air. His hemoglobin and hematocrit were 14.9 g / dL and 44%, white blood cell count was 12.7 × 103 / mL, and platelet count was 146,000 / mL. His electrolyte panel featured sodium of 135 mmol / L, potassium 4.3 mmol / L, chloride 99 mmol / L, HCO3 26 mmol / L, blood urea nitrogen 16 mg / dL, and creatinine 1.14 mg / dL. He was without nourishment for > 8 hours preoperatively.
The patient was taken to the Operating Room for emergency surgical debridement of the Fournier's gangrene. He was premedicated with 2 milligrams (mg) of midazolam intravenously (IV) and anesthesia was induced with IV propofol (200 mg) and fentanyl (100 micrograms [mcg]). There was no central venous pressure monitor placed. A laryngeal mask airway (LMA, size number 4) was placed without difficulty. Anesthesia was maintained with sevoflurane 2 – 3%, with 50% oxygen and air. The patient received fentanyl 500 mcg and 1 mg of dilaudid for intraoperative analgesia. He remained hemodynamically stable throughout, but was tachypneic, with a respiratory rate of 35 breaths / minute. Surgical blood loss was ~200 mL and the procedure was otherwise uneventful. At the conclusion of surgery sevoflurane was discontinued and the patient was able to follow commands. However, before LMA removal the patient forcefully bit down on the LMA. Immediately after LMA removal, a laryngospasm was noted, with concurrent tachycardia and hypertension. Application of positive pressure via face mask (FiO2 100%) was unsuccessful in providing effective ventilation. Intravenous propofol and succinylcholine were administered to facilitate orotracheal intubation with a 7.5 endotracheal tube (ETT). Auscultation revealed bilateral rales, and pink frothy secretions were suctioned from the ETT. He did develop a brief episode of tachycardia (120 – 130 beats per minute) and hypertension (170 – 180 / 90 – 100 mmHg) on extubation. His SpO2 remained at 85 – 88% despite an FiO2 of 100%. His arterial blood gas (ABG) in the operating room showed pH 7.27, PaCO2 59 mmHg, PaO2 46 mmHg, HCO3 of 16 mmol / L, base excess of –1.9, and oxygen saturation of 75%, with a lactate of 1.27 mmol / L. He was on synchronized intermittent mechanical ventilation (SIMV) at 12 cycles / minute, tidal volume 750 mL, pressure support 10 cm H2O, with positive end-expiratory pressure (PEEP) of 10 cm H2O. After PEEP was increased to 12 cm H2O, his SpO2 recovered to > 90%. Of note, his peak and plateau pressures were only minimally elevated and his ability to generate a negative pressure was adequate (> –25 cm H2O). He was transferred to the intensive care unit (ICU) where he was continued on SIMV, with a tidal volume of 580 mL, FiO2 100%, pressure support 15 cm H2O, and PEEP of 12 cm H2O. His initial ABG in the ICU showed pH 7.6, PaCO2 25 mmHg, PaO2 165 mmHg, HCO3 27 mmol / L, and SpO2 99% (FiO2 of 80%). Appropriate ventilatorory adjustments were made. An ICU admission chest radiograph demonstrated bilateral patchy infiltrates, no pneumothoraces or effusions, and a normal heart size; these changes were central and peripheral and not in the dependent areas of the lung []. Over the subsequent 12 hours his FiO2 was weaned to 40%, and his ABG showed pH 7.45, PCO2 41 mmHg, PaO2 78 mmHg, HCO3 28 mmol / L, base excess 3.8, and oxygen saturation 96%. Postoperatively, during the first few days he was in positive fluid balance, however, he was in a negative fluid balance thereafter. His arterial line did demonstrate pulse wave variability.
The patient was taken for a planned re-debridement on postoperative day #2 and was not extubated until postoperative day #3. Shortly after extubation, he complained of acute shortness of breath, with an ABG showing pH 7.49, PCO2 39 mmHg, PaO2 62 mmHg, HCO3 29 mmol / L, and SpO2 93% (FiO2 of 80%). He was placed on intermittent continuous positive airway pressure (CPAP, 10 cm H2O) via full face mask. Although the chest radiogram showed an improvement from the index postoperative film, the patchy infiltrates persisted []. After ensuring adequate volume status, furosemide (40 mg intravenous) was administered, with resultant improvement in oxygenation, shortness of breath, and subsequent roentgenographic examination. The patient received two additional doses of furosemide (20 mg intravenous) over the next 24 hours, as determined on the basis of clinical re-evaluation. He was weaned off oxygen on postoperative day six as his chest radiogram showed near complete resolution of the pulmonary edema and his oxygenation was appropriate []. He was discharged from the hospital on postoperative day seven. The patient was doing well on follow-up at three months, and underwent uneventful skin grafting of the residual perineal wound without any general anesthesia-related complications.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [99.0, 'mmol/L'], 'Bicarbonate': [26.0, 'mmol/L'], 'Sodium': [135.0, 'mmol/L']}",10,9.5,10.5,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 135.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 135.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 135.0 mmol * 1 mEq/mmol = 135.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 135.0 mmol sodium/L converts to 135.0 mEq sodium/L. 
The concentration of chloride is 99.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 99.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 99.0 mmol * 1 mEq/mmol = 99.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 99.0 mmol chloride/L converts to 99.0 mEq chloride/L. 
The concentration of bicarbonate is 26.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 26.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 26.0 mmol * 1 mEq/mmol = 26.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 26.0 mmol bicarbonate/L converts to 26.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 135.0 mEq/L - (99.0 mEq/L + 26.0 mEq/L) = 10.0 mEq/L. Hence, The patient's anion gap is 10.0 mEq/L."
6256,39,Anion Gap,lab test,decimal,pmc-4003264-1,Extracted,"The patient is a 14-year-old girl diagnosed with pharyngitis 1 week before admission. She was referred to the Dr Humberto Notti Pediatric Hospital for macroscopic hematuria accompanied by oliguria, with suspicion of nephritic syndrome. On examination, the patient appeared healthy with a body mass index of 22.5 kg/m2, with no fever or edema. Her blood pressure was 110/90 mmHg (normal blood pressure levels for age, height and sex), with dispersed abdominal pain, aching shoulders, and myalgias. Family history was not significant and there was no history of illicit drugs.
Initial laboratory data were as follows: serum creatinine 3.10 mg/dL, urea 50 mg/dL, hemoglobin concentration 10.3 g/dL, and urinalysis with more than 100 red blood cells, some of them dysmorphic without crystals or hyaline cylinders. Negative 24-hour proteinuria was reported. Laboratory data 12 hours after admission into hospital were as follows: serum creatinine 5.7 mg/dL, urea 85 mg/dL, leukocytes 12,500/μL, platelet count 115 × 103/μL, C-reactive protein (CRP) 2.27 mg/dL (227.3 mg/L), ferritin 313 ng/mL (6–70 ng/mL), fibrinogen 476 mg% (200–400 mg%), potassium 3.4 mEq/L, sodium 133 mEq/L, chloride 93 mEq/L, calcium 8.59 mg/dL, acid base balance pH 7.4/PCO2 29.7 mmHg/HCO3 20 mmol/L, lactate dehydrogenase 800 U/L, and decreased glomerular filtration rate 14.4 mL/m/1.73 m2 by Schwartz formula. Chest radiograph with diffuse interstitial infiltrate in both lungs was demonstrated. Renal ultrasound showed increased kidney size with increased renal parenchymal echogenicity consistent with parenchymal disease.
Twenty-four hours after admission, peritoneal dialysis was started. The next day, creatinine and uremia continued to increase. A percutaneous renal biopsy was performed and intravenous steroid pulses at 10 mg/kg/day were begun.
Serology tests demonstrated the presence of positive C-ANCA by indirect immunofluorescence with documented proteinase 3-specific ANCA (PR3-ANCA). P-ANCA and peroxidase-specific antineutrophil cytoplasmic autoantibodies (MPO-ANCA) were negative. Rheumatoid factor and C3, C4 complement levels were normal. Anti-DNA antibody titers measured by enzyme-linked immunosorbent assay (ELISA) and anti-nuclear antibody (ANA) by immunofluorescence were at normal levels. Viral serology (hepatitis B and C, HIV), and blood and throat cultures were negative. Anti-streptolysin O (ASO) titers were within the normal limits.
Diagnosis of renal involvement was confirmed through biopsy. Microscopic optic study in 20 glomeruli revealed renal parenchyma with less than 50% glomeruli presenting segmental capillary fibrinoid necrosis with neutrophil exudate surrounding glomeruli. Tubule interstitial infiltrate was also shown (). Cellular crescent was seen in 20% of the glomeruli (). Immunofluorescence with antibodies against IgG, IgA, IgM, and C3 was negative for immunoglobulins, and the intensity of immunofluorescence staining was very weak (trace or trace to 1+) for C3. The final diagnosis was focal segmental necrotizing glomerulonephritis.
To investigate other organs affected with small vessel vasculitis, nasal cavity and sinuses computer tomography (CT) showed rhinosinusitis signals and inflammatory tissue. Chest CT showed bilateral pleural effusion.
Immunosuppressive therapy was started with three methylprednisolone pulses, following by cyclophosphamide intravenous pulses (each with a dosage of 750 mg/m2 body surface) continued at monthly intervals for 12 months. After 23 days, the patient’s renal function recovered. The early normalization of the glomerular filtration rate made plasma exchange in the protocol treatment unnecessary.
Further, the remission treatment consisted of a daily dose of mycophenolate mofetil 750 mg/m2 in two divided doses and oral prednisolone (1 mg/kg for 6 weeks) followed by slow tapering. She was discharged after 5 weeks. Neither symptoms nor signs of vasculitis were seen at the last clinical control. Six months after diagnosis, the patient was negative for PR3-ANCA.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [93.0, 'mEq/L'], 'Bicarbonate': [20.0, 'mmol/L'], 'Sodium': [133.0, 'mEq/L']}",20,19,21,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 133.0 mEq/L. 
The concentration of chloride is 93.0 mEq/L. 
The concentration of bicarbonate is 20.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 20.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 20.0 mmol * 1 mEq/mmol = 20.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 20.0 mmol bicarbonate/L converts to 20.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 133.0 mEq/L - (93.0 mEq/L + 20.0 mEq/L) = 20.0 mEq/L. Hence, The patient's anion gap is 20.0 mEq/L."
6257,39,Anion Gap,lab test,decimal,pmc-7327387-1,Extracted,"A 57-year-old female was presented to our emergency center with severe anxiety and general weakness. She was undergoing regular follow-up after concomitant chemoradiation therapy (CCRT) for cervical cancer 3 months ago. Also she was taking an amlodipine as an antihypertension drug. The patient usually consumed bay salt with her wrong belief that eating salt would be helpful to cure cancer. Two days before the hospital visit, her family member got to know that the patient had been taking 4 teaspoons of bay salt a day. In addition, the patient's oral intake had been markedly decreased, and had intermittent vomiting several days before the visit.
On arrival on our hospital, the patient showed dehydrated features such as dry tongue and reduced skin turgor. Blood pressure was 210/100mmHg and heart rate was 74 beats/min in the supine position. Initial laboratory tests showed the following values: serum sodium 203mEq/L [135–145], potassium 2.9mEq/L [3.5–5.0], chloride 167 mEq/L [96–108], bicarbonate 26.7mEq/L [21–28], inorganic phosphorus 1.1mg/dL [2.5–5.5], blood urea nitrogen (BUN) 42.5 mg/dL [8–23], creatinine 2.21mg/dL [0.5–1.3], serum osmolality 415mOsm/kg [280–295], urine osmolality 369 mOsm/kg [300–900], urine sodium 158mEq/L [40–220]. Owing to the patient's inappropriately high BP and peripheral cyanosis, we checked transthoracic 2D-echocardiography. Echocardiography revealed markedly decreased the left ventricular (LV) chamber size and resultant concentric remodeling, which are caused by depletion of circulating volume. Kidney ultrasonography showed enlarged kidney (both kidney size about 12 cm) with increased corticomedullary differentiation, which was compatible findings with acute kidney injury. Brain CT showed no significant abnormal findings such as cerebral infarction, hemorrhage, hydrocephalus and infection.
She was transferred to the medical intensive care unit. For the proper hydration, we calculated free water deficit: estimated free water deficit [free water deficit = total body water × ((serum sodium/140) − 1)] was calculated as 12 liters. Hydration was initiated with hypotonic fluid (5% dextrose and 0.45% sodium chloride). During initial aggressive hydration serum sodium level was even more elevated to 238 mEq/L 2 hours later, therefore we increased the replacement rate of water deficit. After that, however, serum sodium was unintendedly corrected at rates above 1mEq/L per hour (203mEq/L to 177mEq/L for 24 hours) and after 72 hours, the serum sodium concentration was nearly corrected to the normal level (less than 155mEq/L) (). Serum creatinine level also decreased to normal (0.8mg/dL) at the fourth day of hospitalization. Despite the high correction rate of hypernatremia, but the patient was completely recovered without any significant neurologic complications, and was discharged to home. In an outpatient clinic conducted after discharge, the patient's serum sodium level was well maintained around 140mEq/L. And she did not show any neurological signs including headache in at least six months of outpatient care.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [167.0, 'mEq/L'], 'Bicarbonate': [26.7, 'mEq/L'], 'Sodium': [203.0, 'mEq/L']}",9.3,8.835,9.765,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 203.0 mEq/L. 
The concentration of chloride is 167.0 mEq/L. 
The concentration of bicarbonate is 26.7 mEq/L. 
Plugging in these values into the anion gap formula gives us 203.0 mEq/L - (167.0 mEq/L + 26.7 mEq/L) = 9.3 mEq/L. Hence, The patient's anion gap is 9.3 mEq/L."
6258,39,Anion Gap,lab test,decimal,pmc-8206651-1,Extracted,"The patient was a 20-year-old female, 29 weeks pregnant, who was admitted to the obstetrics and gynecology service of our hospital with preterm premature rupture of membranes. She was previously healthy and had no history of chronic medical conditions. Three days after admission, a trial of induction of labor was attempted by administration of 10 units of oxytocin in 500 ml lactated ringer’s solution at a rate of 2 mU/min for five hours. This resulted in successful vaginal delivery of the fetus. Four hours after delivery, the patient suddenly started to complain of shortness of breath and chest discomfort. She had no fever, cough, or sputum production. She has a respiratory rate of 30 breaths per minute. Oxygen saturation was 95% on room air. Blood pressure was normal. There was no evidence of jugular venous distention. Chest auscultation revealed the presence of bilateral inspiratory crepitations. There was no swelling or erythema of the lower limbs. Laboratory tests showed a serum sodium level of 139 mEq/L (136-145), potassium level of 3.6 mEq/L (3.5 to 5.1), chloride level of 106 mEq/L (96 to 106), bicarbonate level of 23 mEq/L (23 to 30), creatinine of 0.38 mg/dL (0.50-0.90), WBC of 14,580 cells/dL (4,000-11,000), hemoglobin of 10 g/dL (11 to 13), C-reactive protein (CRP) of 33.8 mg/L (<5), N-terminal pro-brain natriuretic peptide (NT-pro-BNP) of 1234 pg/mL (0-130), troponin T of 5.52 ng/L (<14), D-dimer of 5.77 microgram/mL (<0.5). A chest X-ray done on the patient revealed evidence of pulmonary edema as shown in Figure .
Total fluid intake over the last 24 hours was 2.3 liters. Urine output, over the same period of time, was 1.8 liters. Polymerase chain reaction (PCR) test for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) on a nasopharyngeal swab was negative. An electrocardiogram showed normal sinus rhythm with no ischemic changes or evidence of right heart strain as demonstrated in Figure .
CT pulmonary angiogram was done as shown in Figure . It was reported as showing a small right-sided pleural effusion, no consolidation, and no evidence of pulmonary embolism.
Transthoracic echocardiography showed normal left ventricular systolic function with an ejection fraction of 60%. Furthermore, it showed no evidence of valvular heart disease or pericardial effusion. The patient was given 20 mg of furosemide intravenously every 12 hours for one day. She reported an improvement in her symptoms after the first dose of IV furosemide. High vaginal swab culture obtained on the day of admission grew normal vaginal flora. A repeat chest X-ray done three days later showed complete resolution of the pulmonary edema as seen in Figure , and hence the patient was discharged home in good health. The patient was scheduled to have a follow-up appointment at the clinic after discharge, but unfortunately, she did not attend the scheduled appointment.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [106.0, 'mEq/L'], 'Bicarbonate': [23.0, 'mEq/L'], 'Sodium': [139.0, 'mEq/L']}",10,9.5,10.5,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 139.0 mEq/L. 
The concentration of chloride is 106.0 mEq/L. 
The concentration of bicarbonate is 23.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 139.0 mEq/L - (106.0 mEq/L + 23.0 mEq/L) = 10.0 mEq/L. Hence, The patient's anion gap is 10.0 mEq/L."
6259,39,Anion Gap,lab test,decimal,usmle-5833,Extracted,"A 72-year-old man is seen in the hospital for a sacral rash. The patient has been hospitalized for the past 3 weeks for a heart failure exacerbation. When the nurse went to bathe him this morning, she noticed a red rash over his sacrum. The patient reports mild discomfort and denies pruritus. The patient has chronic kidney disease, urinary incontinence, ischemic cardiomyopathy, gout, and poor mobility. His current medications include aspirin, furosemide, metoprolol, lisinopril, spironolactone, and prednisone that was started for a recent gout flare. The patient’s temperature is 97°F (37.2°C), blood pressure is 110/62 mmHg, pulse is 68/min, and respirations are 13/min with an oxygen saturation of 98% on room air. On physical examination, there is a 4 cm x 6 cm patch of non-blanchable erythema over the patient’s sacrum that is mildly tender to palpation. Labs are obtained, as shown below:

Leukocyte count: 10,000/mm^3 with normal differential
Hemoglobin: 15.2 g/dL
Platelet count: 400,000/mm^3

Serum:
Na: 138 mEq/L
K+: 4.3 mEq/L
Cl-: 104 mEq/L
HCO3-: 25 mEq/L
BUN: 26 mg/dL
Creatinine: 1.5 mg/dL
Glucose: 185 mg/dL

A hemoglobin A1c is pending.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [104.0, 'mEq/L'], 'Bicarbonate': [25.0, 'mEq/L'], 'Sodium': [138.0, 'mEq/L']}",9,8.55,9.45,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 138.0 mEq/L. 
The concentration of chloride is 104.0 mEq/L. 
The concentration of bicarbonate is 25.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 138.0 mEq/L - (104.0 mEq/L + 25.0 mEq/L) = 9.0 mEq/L. Hence, The patient's anion gap is 9.0 mEq/L."
6260,39,Anion Gap,lab test,decimal,pmc-4162725-1,Extracted,"An otherwise healthy 34-year-old white female presented to the emergency department (ED) with one-hour history of back pain. The pain began gradually in the center of her thoracic spine at the level of T7–T8 and progressively became worse. She described the pain as a severe dull pain, constant, radiating through to the chest, up the back into the neck and down the back into both buttocks. She attempted to relieve the pain by soaking in warm water; when that was unsuccessful her family member brought her to the ED. She denied history of back pain, trauma, fever, abdominal pain, paresis, paralysis, urinary retention, or paresthesias.
On initial examination, the patient was uncomfortable and moaning. Vital signs were blood pressure 155/90 mm Hg, pulse rate 82 beats/min, respiratory rate 20 breaths/min, and temperature 36.2 degrees C (97.1 F). She was mildly tender over the mid thoracic spine. Heart sounds were regular, pulses were equal in both extremities and bilaterally in the groin, and no other abnormalities of the physical exam were found.
Electrocardiogram performed upon arrival was interpreted as normal sinus bradycardia, rate of 58 bpm, with nonspecific ST segment and T-wave changes. Laboratory evaluation revealed hemoglobin 13.6 g/dL (12.0 to 15.3 g/dL), WBC 11.0 × 103/μL (4.0 to 11.0), platelet count 286 × 103 /μL (150 to 450 × 103 μ/L), sodium 141 mmol/L (135–145 mmol/L), potassium 3.3 mmol/L (3.5–5.1 mmol/L), chloride 106 mmol/L (98 – 109 mmol/L), bicarbonate 29 mmol/L (23 to 31 mmol/L), blood urea nitrogen 13 mg/dL (6 to 26 mg/dL), creatinine 0.83 mg/dL (0.5 to 1.20 mg/dL), and glucose 120 mg/dL (70 – 99 mg/dL). Troponin level was <0.01 ng/mL (<0.01 ng/mL = Expected range for 99% population), myoglobin was 7534 ng/mL (28 – 72 mg/mL) and creatine kinase 2336 IU/L (24 – 170 IU/L). Urinalysis revealed large blood by dipstick with 31 to 50 RBCs (patient was menstruating), negative results for nitrite and leukocyte esterase. Urine toxicology was negative for illicit drugs, and the urine pregnancy test was negative. Chest radiograph was negative for any lung pathology, mediastinum was normal width and no pathology was seen on the thoracic vertebrae. Computed tomography angiogram of the chest was normal; no aortic dissection was found.
An intravenous catheter was inserted when blood was drawn for laboratory evaluation. Hydromorphone 0.5 mg and diazepam 2.5 mg was intravenously given for pain relief and normal saline was begun at 150 ml/hour. Approximately one hour after arrival the patient complained of aching all over and then began to vomit, undigested food with no blood. She mentioned to the staff that a friend with whom she had had dinner had called her and told her that she was also ill. The patient explained that they had eaten fish that her friend had purchased at a local market and cooked for dinner. It was buffalo fish (Ictiobus).
After reviewing the laboratory values, the rate of intravenous normal saline was increased to 300 ml/hour. The patient was further questioned for an etiology of the rhabdomyolysis and an ingestion of a toxin was considered. An Internet search was performed looking at buffalo fish and rhabdomyolysis, and information on Haff disease was identified. The Illinois Poison Control Center was notified. The Illinois Poison Control Center subsequently contacted the Cook County Board of Health and all buffalo fish were removed from the local market.
The patient was admitted to the hospital for continued hydration. On day two the creatine kinase peaked at 30,549 IU/L, approximately 19 hours after arrival. Blood urea nitrogen and creatinine remained normal. Creatine kinase levels began to decline, and the patient was discharged on day three.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [106.0, 'mmol/L'], 'Bicarbonate': [29.0, 'mmol/L'], 'Sodium': [141.0, 'mmol/L']}",6,5.7,6.3,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 141.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 141.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 141.0 mmol * 1 mEq/mmol = 141.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mmol sodium/L converts to 141.0 mEq sodium/L. 
The concentration of chloride is 106.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 106.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 106.0 mmol * 1 mEq/mmol = 106.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 106.0 mmol chloride/L converts to 106.0 mEq chloride/L. 
The concentration of bicarbonate is 29.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 29.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 29.0 mmol * 1 mEq/mmol = 29.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 29.0 mmol bicarbonate/L converts to 29.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 141.0 mEq/L - (106.0 mEq/L + 29.0 mEq/L) = 6.0 mEq/L. Hence, The patient's anion gap is 6.0 mEq/L."
6261,39,Anion Gap,lab test,decimal,pmc-3542891-1,Extracted,"The patient is a 38-year-old male that was transferred to our emergency department (ED) from an outside hospital status post cardiac arrest. The patient was an inmate at a local prison who was found unresponsive in his prison cell. Emergency Medical Services (EMS) was called for medical support. Minimal health information was provided by the prison. The patient was found by EMS to be in ventricular tachycardia with a palpable pulse and was intubated on the scene. The patient was given 150 mg of amiodarone, and transportation to an outside facility was initiated. On laboratory evaluation at the outside hospital, the patient was noted to have a potassium level of 9. Treatment of the patient's hyperkalemia with insulin, beta-agonists, and calcium was initiated. After initial resuscitation, the patient was transported to our ED. While en route, the patient experienced an episode of pulseless ventricular tachycardia, requiring two episodes of cardioversion. Return of spontaneous circulation was achieved prior to ED arrival.
Upon arrival to our ED, vitals were as follows: blood pressure 91/48, heart rate 145 beats per minute, respiratory rate 14 breaths per minute, oxygen (O2) saturation 99%, temperature 35.3 Celsius (C). An electrocardiogram (ECG) was performed, which documented ventricular tachycardia at a rate of 140 without ST segment or T wave changes. On exam, the patient was noted to be intubated. Head, ears, eyes, nose, and throat (HEENT) exam revealed 3 millimeter (mm) pupils that were sluggishly reactive to light and equal bilaterally and an endotracheal tube at 25 centimeters (cm) at the teeth. The remainder of the HEENT exam was unremarkable. Neck exam revealed a cervical collar in place with no cervical spine step-off noted. Cardiovascular exam revealed a heart rate of 140 beats per minute with palpable distal pulses. Lungs were clear to auscultation bilaterally. Abdomen was soft with good bowel sounds and no evidence of distension. On neurological exam, the patient was noted to be sedated with a Glasgow coma scale (GCS) of 3T.
The patient had blood sent to the lab for multiple studies. The patient's complete blood count (CBC) revealed a white blood cell count of 23.6 thou/cu mm, a hemoglobin of 14.7 g/dL, a hematocrit of 45.5%, and a platelet count of 181 thou/cu mm. His basic metabolic panel revealed a sodium of 143 mmol/L, a potassium of 8.7 mmol/L, a chloride of 120 mmol/L, a bicarbonate of 16 mmol/L, a BUN of 22 mg/dL, a creatinine of 1.06 mg/dL, and a glucose of 191 mg/dL. Venous blood gas revealed a pH of 7.06, pCO2 of 58 mmHg, and pO2 of 77 mmHg. International normalized ratio (INR) was 1.4. Cardiac markers and urinalysis were both unremarkable. A urine drug screen was positive for benzodiazepines.
The patient's emergency department management began with initial stabilization. Due to his persistent ventricular tachycardia, the patient was given another bolus of amiodarone upon arrival and a subsequent amiodarone infusion was started. Due to low mean arterial pressures, two liter of normal saline was given intravenously, a right subclavian central venous line was placed, and a left radial arterial line was placed. A levophed drip was started at 0.1 mcg/kg/min and titrated to maintain a mean arterial pressure (MAP) of 65 for pressure support. Treatment for hyperkalemia was readministered concurrently, consisting of insulin, beta-agonists and kayexalate. Chest X-ray revealed clear lungs with radio paque capsules in the fundus of the stomach. Over the next thirty minutes, the patient's rhythm converted to normal sinus rhythm and slowed to around 70 beats per minute. Repeat potassium lab draw revealed persistently elevated potassium level of 8.3 mmol/L, and hyperkalemia treatment was repeated. At this point, nephrology was consulted for emergent dialysis, and the medical intensive care unit (MICU) was notified for admission. We later found out, from the MICU team, that the patient had an esophagogastroduodenoscopy (EGD) performed to remove the unknown pills from the patient's stomach, which were found to be potassium chloride pills. After removal of the pills and multiple episodes of dialysis, the patient stabilized and was weaned from pressure and ventilator support. The patient's leukocytosis was believed to be a stress response as the MICU team was never able to determine a source of infection; however, the patient remained on-broad spectrum intravenous antibiotics over the course of his stay.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [120.0, 'mmol/L'], 'Bicarbonate': [16.0, 'mmol/L'], 'Sodium': [143.0, 'mmol/L']}",7,6.65,7.35,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 143.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 143.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 143.0 mmol * 1 mEq/mmol = 143.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mmol sodium/L converts to 143.0 mEq sodium/L. 
The concentration of chloride is 120.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 120.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 120.0 mmol * 1 mEq/mmol = 120.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 120.0 mmol chloride/L converts to 120.0 mEq chloride/L. 
The concentration of bicarbonate is 16.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 16.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 16.0 mmol * 1 mEq/mmol = 16.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 16.0 mmol bicarbonate/L converts to 16.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 143.0 mEq/L - (120.0 mEq/L + 16.0 mEq/L) = 7.0 mEq/L. Hence, The patient's anion gap is 7.0 mEq/L."
6262,39,Anion Gap,lab test,decimal,pmc-8270600-1,Extracted,"A 60-year-old Korean woman was admitted to our hospital for a renal biopsy. She had presented to the nephrology outpatient department due to edema 9 months earlier. She was diagnosed with T2DM and hypertension 5 years ago and took 4 mg glimepiride, 1000 mg metformin, 50 mg gemigliptin, 15 mg pioglitazone, 5 mg amlodipine, 100 mg losartan, and 25 mg carvedilol. The pioglitazone was withdrawn, while the other medicines were maintained, after the initial visit to our hospital. Her serum creatinine level had been gradually increasing (Fig. ) without significant changes in other laboratory findings. She denied symptoms and signs indicating deterioration of renal function, such as edema, oliguria, fever, chills, general weakness, malaise, arthralgia, myalgia, skin rash, and urine color changes during the 9-month follow-up. She also denied ingestion of known toxins, Chinese herbal medicines, drugs (including non-steroidal anti-inflammatory drugs), and nutraceuticals that can affect the serum creatinine level. Her hypertension and serum glucose were well controlled. She was admitted for renal biopsy and management of AKI.
Her initial vital signs were as follows: blood pressure, 120/80 mmHg; heart rate, 68 beats/min; respiratory rate, 18 breaths/min; and body temperature, 36.5°C. No lymph nodes were palpated on a neck examination. Heart sounds were normal and no wheezing or rales was heard in either lung field. No organomegaly was present in the abdomen, and bowel sounds were audible. No skin color changes on the torso or pitting edema were observed on the legs. Her blood urea nitrogen and serum creatinine levels were 29.7 mg/dL (range: 8.0–20.0 mg/dL) and 1.45 mg/dL (range: 0.51–0.95 mg/dL) on admission, whereas they were 14.1 and 0.53 mg/dL, respectively, 9 months before admission (Fig. ). The hematocrit and hemoglobin levels were 34% (range: 36%–48%) and 11.4 g/dL (range: 12–16 g/dL), respectively. Platelet and red blood cell counts were 232 × 109/L (normal range: 130–400 × 109/L) and 3.82 × 1012/L (normal range: 4.0–5.40 × 1012/L), respectively. The white blood cell count was 6.76 × 109/L (normal range: 4.0–10.0 × 109/L), with 63.5% segmented neutrophils (normal range: 50%–75%), 27.5% lymphocytes (normal range: 20%–44%), 6.7% monocytes (normal range: 50%–75%), and 1.9% eosinophils (normal range: 1.0%–5.0%). Other laboratory test results included sodium, 138 mmol/L (range: 135–145 mmol/L); potassium, 4.6 mmol/L (range: 3.3–5.1 mmol/L); chloride, 104 mmol/L (range: 98–110 mmol/L); glucose, 177 mg/dL (range: 70–110 mg/dL); HbA1c, 6.8% (range: 4.2%–5.9%); calcium, 9.0 mg/dL (range: 8.6–10.2 mg/dL; phosphorus, 3.9 mg/dL (range: 2.7–4.5 mg/dL); and total CO2, 28 mmol/L (range: 21–31 mmol/L). The C3 and C4 levels were 129.7 mg/dL (range: 90–180 mg/dL) and 34.8 mg/dL (range: 10–40 mg/dL), respectively. Urinalysis (dipstick test) revealed no protein or blood, and no red blood cells or white blood cells. The urine albumin creatinine ratio was 14.9 mg/g (range: 0–20 mg/g). The thyroid function test was within normal limits, and anti-neutrophil cytoplasmic antibodies and the anti-glomerular basement membrane antibody were negative.
Kidney ultrasound revealed normal-sized kidneys (right, 10.4 cm; left, 10.4 cm) and echogenicity without evidence of hydronephrosis or nephrolithiasis. A renal biopsy was performed on day 2 of admission. There was edematous interstitium, detachment of tubular epithelial cells, and lymphoplasmacytic infiltration into the interstitium (Fig. A). Tubulitis was indicated by tubular cell detachment and epithelial casts including numerous neutrophils were observed in the lumen of renal tubules and a few eosinophils were also observed among the increased interstitial inflammatory cell infiltrates (Fig. B). However, the glomeruli were normal (Fig. ). After the renal biopsy, we again enquired regarding the consumption of drugs, Chinese herbal medicines, and nutraceuticals that could evoke AIN on day 3 of admission. She disclosed that she had been ingesting an M charantia extract for 7 months to control her T2DM. She took about 600 mg almost every day in liquid form during the first 3 months, and had taken 1200 mg per day during the last 4 months. The M charantia extract was immediately withdrawn and 0.5 mg/kg/day of prednisolone was prescribed, and tapered, and then stopped after 3 months. Her serum creatinine decreased to 0.65 mg/dL after 3 months (Fig. ), while still using the other medicines.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [138.0, 'mmol/L'], 'Chloride': [104.0, 'mmol/L'], 'Bicarbonate': [28.0, 'mmol/L']}",6,5.7,6.3,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 138.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 138.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 138.0 mmol * 1 mEq/mmol = 138.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mmol sodium/L converts to 138.0 mEq sodium/L. 
The concentration of chloride is 104.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 104.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 104.0 mmol * 1 mEq/mmol = 104.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 104.0 mmol chloride/L converts to 104.0 mEq chloride/L. 
The concentration of bicarbonate is 28.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 28.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 28.0 mmol * 1 mEq/mmol = 28.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 28.0 mmol bicarbonate/L converts to 28.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 138.0 mEq/L - (104.0 mEq/L + 28.0 mEq/L) = 6.0 mEq/L. Hence, The patient's anion gap is 6.0 mEq/L."
6263,39,Anion Gap,lab test,decimal,pmc-3741440-1,Extracted,"A 40 year-old-female
Altered mentality
This previously healthy 40-year-old female was transported to the emergency room by her neighbors, who heard her moaning in her house. She lived alone, and 1 month prior to her admission, she developed the paranoid idea that her water was poisoned, and did not drink any water or beverages since then.
Non-contributory
Non-contributory
Her blood pressure was 100/60 mmHg, pulse rate 106/min, respiration rate 16/min, and body temperature 36.5℃. She looked chronically ill, and her skin and mucosa were extremely dehydrated. There was no evidence of trauma. A chest examination revealed a regular heart beat and clear breathing sounds. The abdomen was soft and flat with no palpable mass.
She was light, drowsy and disorientated. Her pupils were intact and reactive. The Glasgow Coma Scale was 11. No cranial nerve problem or peripheral nerve dysfunction was found.
White blood cell count 21,900/mm3 (4000-10,000/mm3), hemoglobin 11.2 g/dL(men 13-17 g/dL: women 12-16 g/dL), hematocrit 51%(men: 42-50%: women 36-44%), and platelets 207,000/mm3 (150,000-400,000/mm3). Her coagulation profile showed an international normalized ratio of 1.71 (1.2 below) and activated partial thromboplastin time of 177.4 sec (24-33 sec). Laboratory chemistry showed blood urea nitrogen 208mg/dL (8.0-20 mg/dL), creatinine 4.90mg/dL(0.6-1.2mg/dL), serum osmolality 452mOsm/L(289-302mOsm/L), protein 7.5 g/dL (6.5-8.2mg/dL), albumin 4.5 g/dL(3.5-5.1 g/dL), ionized calcium 4.6mg/dL (4.2-5.4mg/dL), magnesium 4.5mg/dL (1.9-2.5 mg/dL), serum sodium 172mEq/L(135-145mEq/L), potassium 4.4mEq/L(3.5-5.5mEq/L), chloride 127mEq/L(98-110 mEq/L), total CO2 21mEq/L (24-31mEq/L), aspiratetransaminase 22 IU/L (0-40 IU/L), alanine aminotransferase 16 IU/L (0-40 IU/L), total bilirubin 1.1mg/dL(0.2-1.1 mg/dL), myoglobin 1,949 ng/mL (28-72 ng/mL), creatine phsphokanase 389 IU/L (190 below IU/L), anti-diuretic hormone 8.95 pg/mL(0.0-6.7 pg/mL), adrenocorticotropic hormone (ACTH) 111 pg/mL(10-60 pg/mL), and cortisol 71 g/mL (morning 9.4-26.1/evening 1.8-12.7 g/mL). Breathing room air, the arterial blood gas analysis revealed pH 7.422, PaCO2 35.4mmHg, PaO2 106mmHg, and bicarbonate 22.6mEq/L. Urinalysis showed specific gravity was >1.030, urine pH 5.0, urine osmolality 698mOsm/L (300-900mOsm/L), and urine sodium/potassium/chloride34/85.6/8mEq/L.
Brain computerized tomography (CT) was normal.
She was diagnosed with uremic encephalopathy due to severe prerenal acute renal failure. Her estimated water deficit was 5.94 L. We started intravenous dextrose for 4h, but the changein serum sodium was minimal (171mEq/L). We therefore started hemodialysis to treat the uremic encephalopathy. The dialysate sodium level was 150mEq/L. After dialysis, the serum sodium decreased to 160mEq/L, potassium was 4.2mEq/L, chloride 124 mEq/L, and total CO2 23mEq/L. After a second dialysis treatment, the sodium was 150mEq/L and she became alert without neurological sequelae. We continued an intravenous dextrose fluid infusion with oral hydration, and the sodium level normalized on day 3 of hospitalization (). After discharge, her sodium and chemistry profile remained normal.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [127.0, 'mEq/L'], 'Bicarbonate': [22.6, 'mEq/L'], 'Sodium': [172.0, 'mEq/L']}",22.4,21.28,23.52,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 172.0 mEq/L. 
The concentration of chloride is 127.0 mEq/L. 
The concentration of bicarbonate is 22.6 mEq/L. 
Plugging in these values into the anion gap formula gives us 172.0 mEq/L - (127.0 mEq/L + 22.6 mEq/L) = 22.4 mEq/L. Hence, The patient's anion gap is 22.4 mEq/L."
6264,39,Anion Gap,lab test,decimal,pmc-3544065-1,Extracted,"A 51-year-old male from Tanzania, a hypertensive, on maintenance hemodialysis since June 2005, underwent a live related renal transplantation on 13/09/2005. His serology for HIV 1 and 2, hepatitis B, hepatitis C was negative. He had a history of blood transfusion (6 units) in June 2005 in his native country. His post-operative period was uneventful. He was inducted with a single dose of basiliximab on the day of transplantation and his immunosuppressants were prednisolone 15 mg, Mycophenolate Mofetil (MMF)–500 mg B.D, cyclosporin 175/150 microemulsion on discharge while returning to his country. The patient developed new onset diabetes after transplantation (NODAT). On discharge (6/10/2005) his blood urea was 31 mg/dL and serum creatinine was 1.1 mg/dL.
He returned to Tanzania and was followed-up there. He came back for a review 1 year later when his investigations showed urea 36 mg/dL, creatinine 1.2 mg/dL. Three months later, he presented with a rapidly progressive ulcerative lesion on his right thigh associated with swelling of the right lower limb. The ulceroproliferative lesion was 20 × 15 cm with skin discoloration and bilateral palpable inguinal lymph nodes. Investigations showed urea 53 mg/dL, creatinine 1.4 mg/dL, sodium 133.4 mEq/L, potassium 4.09 mEq/L, chloride 107 mEq/L, and bicarbonate 23.2 mEq/L. Wedge biopsy of the skin lesion showed pseudoepitheliomatous hyperplasia and inguinal lymph node biopsy suggesting features consistent with Kaposi sarcoma []. Repeated testing of HIV was negative and staining for acid-fast bacilli was negative Epstein-Barr virus IgG 22.6 and IgM 8.5. He was started on chemotherapy (liposomal doxorubicin). MMF was stopped, and cyclosporin and prednisolone were tapered with the plan of stopping in 2-3 weeks. He was started on sirolimus 5 mg once a day. On discharge, his investigations were urea 44 mg/dL, creatinine 2.3 mg/dL, sodium 124.6 mEq/L, potassium 5.03 mEq/L, chloride 96 mEq/L, bicarbonate 18.6 mEq/L, Hb 8.4 gm/dL, and TWBC 7500 cells/mm3. He received three doses of chemotherapy.
On follow-up, his Kaposi sarcoma lesion had regressed. His blood urea was 37 mg/dL and creatinine 1.3 mg/dL. He was given one dose of liposomal doxorubicin 40 mg on 15/3/2007. His right leg venous Doppler was normal. He was discharged with sirolimus monotherapy. His follow-up on 8/12/2007 was uneventful with blood urea 42 mg/dL, creatinine 1.5 mg/ dL, and he was continued on the same line of treatment.
On 20/05/2011, he presented with hematuria and high-grade fever. He had diarrhea for 3 days without blood or mucus. Stool analysis was unremarkable and the diarrhea settled. His investigations were blood urea 91 mg/dL, creatinine –3.1 mg/dL, sodium 133 mEq/L, potassium 3.7 mEq/L, chloride 98 mEq/L, bicarbonate 25.8 mEq/L, c alcium 9.2 mg/dL, phosphorus 3.4 mg/dL. Imaging of the chest did not show any lung parenchymal or pleural lesion. He tested positive for HIV with a viral load of 564407 IU/mL, CD4 count was 241 cells/mL and CD8 was 846 cells/mL. He denied any risky sexual behavior or IV drug abuse. Renal biopsy suggested features of chronic allograft nephropathy (CAN) [] with ill- defined granulomas suggestive of TB []. Nuclear amplification test of the urine for TB was positive. He was also diagnosed with BK viremia. He was started on antituberculous therapy (ATT) (isoniazid 150 mg once a day, pyrazinamide 750 mg twice a day, levofloxacin 500 mg twice a day, pyrodoxine 40 mg once a day). Antiretroviral drugs (zidovudine 300 mg twice a day, lamivudine 150 mg twice a day, efavirenz 600 mg twice a day) were initiated after discussion with ID consultant. His sirolimus dose was reduced to 3 mg once daily with a through level of 4.56 ng/dL. He became afebrile after a week of ATT and macroscopic hematuria disappeared. He was discharged with advice of regular follow-up.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [133.0, 'mEq/L'], 'Chloride': [107.0, 'mEq/L'], 'Bicarbonate': [23.2, 'mEq/L']}",2.8,2.66,2.94,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 133.0 mEq/L. 
The concentration of chloride is 107.0 mEq/L. 
The concentration of bicarbonate is 23.2 mEq/L. 
Plugging in these values into the anion gap formula gives us 133.0 mEq/L - (107.0 mEq/L + 23.2 mEq/L) = 2.8 mEq/L. Hence, The patient's anion gap is 2.8 mEq/L."
6265,39,Anion Gap,lab test,decimal,pmc-3533887-1,Extracted,"A 25-year-old Thai woman (gravida 3, para 3) had her third uneventful vaginal delivery followed by TS by modified Pomeroy technique on the following day. She experienced a persistent low-grade fever and abdominal pain that began in the third post-partum week and deteriorated over time. Her medical history was unremarkable. She denied any history of intravenous drug abuse, smoking, alcohol intake, or abdominal trauma. She reported being monogamous. Her partner was healthy and denied any history of sexually transmitted infections. Her previous obstetric history was unremarkable at 8 years and 5 years prior to this delivery. The vaginal delivery of her third baby took place 2 hours after a spontaneous rupture of membranes and progressed uneventfully. Post-partum TS was performed by request without any remarkable findings. She recovered well and was discharged with her baby from the hospital 3 days later.
With a persistent and progressive fever for 1 week, she was admitted to the hospital. On admission, she looked very sick. A physical examination showed a high-grade fever (39°C), tachycardia (pulse rate of 112 beats per minute), tachypnea (respiratory rate of 26 per minute), and a blood pressure of 110/60mmHg. An abdominal examination showed a small transverse subumbilical incision scar (from the TS) without any signs of wound infection. A 16-week, pregnancy-sized, non-mobile pelvic mass was found on the left side of her pelvis. The mass and other areas of her pelvis and abdomen were tender, suggesting peritonitis. A pelvic examination revealed a large amount of purulent vaginal discharge, a marked degree of pain elicited upon cervical excitation, a bulging cul-de-sac, and the tender pelvic mass as described in the abdominal examination findings. The results of the rest of the physical examination were unremarkable.
Ultrasonograms showed a uterus of 10.1×6.2×5.1cm in size and a smooth thin endometrial lining. A multiloculated mass of 6.2×8.2×10.9cm in size was seen over the left adnexal region. The right adnexal region was unremarkable. Approximately 50mL of free fluid was noted in the cul-de-sac. Laboratory testing revealed a hematocrit level of 32.2%, a white blood cell count of 33,170/mm3 (90.2% were polymorphonuclear neutrophils), and a platelet count of 422,000/mm3. Levels of blood urea nitrogen and creatinine were 6.2 and 0.5mg/dL, respectively. Blood electrolytes were as follows: sodium 138mmol/L, potassium 3.4mmol/L, chloride 106mmol/L, and bicarbonate 22mmol/L. A slightly prolonged coagulogram was found: a prothrombin time of 15.3 (10 to 13) seconds and a partial thromboplastin time of 34.7 (21 to 30) seconds. The results of a liver function test were normal. The results of a cervical swab and blood culture were negative.
The clinical diagnosis was a ruptured TOA. After counseling for a diagnosis and a plan for an urgent exploratory laparotomy, intravenous clindamycin 2700mg per day and gentamicin 240mg per day were initiated. Fluid resuscitation and preparation of blood components were executed.
The operative findings showed 50mL of bloody purulent intraperitoneal fluid. A left tubo-ovarian complex (Figures and ) of 7×7cm in size was seen. The mass contained 30mL of malodorous pus and had a 2cm rupture site on its posterior surface (Figures and ). The rupture site was walled off by a 30cm loop of severely inflamed ileum (Figure ). The two free ends of proximal and distal parts of the left fallopian tubes were evidenced (Figure ) without residual pieces of chromic catgut used for the sterilization. The uterus was markedly inflamed. The right adnexal region appeared grossly normal.
A total hysterectomy with left salpingo-oophorectomy, ileal resection with end-to-end anastomosis, abdominal toileting, and Penrose drain placement were performed. The operation took 4 hours, and the estimated blood loss was 2000mL. A Gram stain of pus from the abdominal cavity demonstrated numerous polymorphonuclear cells and numerous coccoid pleomorphic Gram-negative rods. An abdominal fluid culture revealed no growth, whereas the pus culture showed Fusobacterium necrophorum. The organism was identified as F. necrophorum subsp. funduliforme by microscopic examination, biochemical characteristics, and 16S ribosomal deoxyribonucleic acid (rDNA) sequencing. The isolate was designated as SIRD333. The 658 base-pair fragment of SIRD333 16S rDNA was submitted to GenBank (accession number JX103157). The surgical pathology showed chronic endometritis, TOA, and ileitis.
Our patient recovered well after the operation and had further treatment with intravenous antibiotics (clindamycin and gentamicin) until being clinically stable for 48 hours (4 days of intravenous antibiotics in total). She was discharged on the 10th post-operative day. She continued oral antibiotics (clindamycin) for six more weeks. She was clinically well during all of her follow-up visits.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [106.0, 'mEq/L'], 'Bicarbonate': [22.0, 'mEq/L'], 'Sodium': [138.0, 'mEq/L']}",10,9.5,10.5,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 138.0 mEq/L. 
The concentration of chloride is 106.0 mEq/L. 
The concentration of bicarbonate is 22.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 138.0 mEq/L - (106.0 mEq/L + 22.0 mEq/L) = 10.0 mEq/L. Hence, The patient's anion gap is 10.0 mEq/L."
6266,39,Anion Gap,lab test,decimal,pmc-5906769-1,Extracted,"A 73-year-old female presented initially to our emergency department complaining of cough for three weeks duration. She reported productive cough of white-colour sputum, right-sided pleuritic chest pain, exertional shortness of breath and acute limitation of functional capacity to less than two blocks. There was no history of haemoptysis, fever, night sweats, chills, recent infections or hospitalization. She had loss of appetite and unintentional weight loss of ten pounds over a period of 5 months. Past medical history was non-contributory. She was a lifetime nonsmoker with no history of alcohol or illicit drug abuse. She was afebrile, normotensive and maintaining optimal oxygen saturation on room air. The rest of the physical examination was unremarkable. Laboratory testing showed white blood cell count of 5.1 × 103/µL, haemoglobin 10.8 g/dl, haematocrit 32.4% and platelet count 276 × 103/µL. Comprehensive metabolic panel revealed serum sodium 141 mmol/L, potassium 4.4 mmol/L, chloride 103 mmol/L, bicarbonate 31 mmol/L, BUN 12 mg/dl, creatinine 0.6 mg/dl, calcium 9.3 mg/dl, bilirubin total 0.5 mg/dl, AST 15 mg/dl, ALT 6 mg/dl, ALP 78 mg/dl, total protein 7 g/dl of which albumin was 3.5 g/dl. Serum Β2-microglobulin was 3.3 mg/L. Thyroid function tests and iron studies were within normal limits. Chest x-ray () revealed right lower lobe consolidation and pleural effusion. In comparison, an old chest x-ray performed 3 years ago showed no active lung disease (). Computerized tomography of the chest without IV contrast () on second day of hospital stay revealed moderate right-sided pleural effusion and right lower lobe consolidation. Treatment with levofloxacin was started. She was clinically stable and was discharged with a plan to continue antibiotic for total duration of 7 days. She was scheduled for follow up with chest clinic in 2 weeks. The patient came back after 2 months for follow up at chest clinic. She reported unchanged cough and worsening shortness of breath. Since her symptoms were worsening, she was admitted to the hospital for further evaluation. On the second hospital admission vital signs were stable, chest CT scan () revealed no significant change in complete consolidation of right lower lobe as compared to previous chest CT scan there was a moderate right-sided pleural effusion and new right upper lobe infiltrate. Abdomen and pelvis CT scan revealed homogeneous attenuation of the liver. Size and contour were maintained with no focal lesions, the pancreas was intact without ductal dilatation, the spleen was normal in size, the adrenal glands were intact, no enlarged lymph nodes were found, no ascites was present and no worrisome osseous lesions were demonstrated. PET/CT scan revealed 2.5 cm infiltrate in right upper lobe and another larger lesion in right lower lobe, both with significant uptake. Moderate right pleural effusion. Bronchoscopy showed polypoid nodularities surrounded by black discoloured mucosa in the sub-segmental bronchi of the right lower lobe, transbronchial biopsy specimen revealed minute fragments of respiratory epithelium with atypical B cell-rich lymphocytes with no evidence of amyloid deposition. Polymerase chain reaction confirmed a clonal B cell gene rearrangement, findings suggestive of low-grade B cell lymphoma. Pleural fluid was sampled and analysis revealed straw-coloured fluid, pH 7.3, white blood cell count of 6400 cells, red cell count of 3750, fluid albumin of 2.2 g/dl (serum albumin 3.0 g/dl), fluid lactate dehydrogenase 52 IU/L (serum lactate dehydrogenase 199 IU/l). Pleural fluid cytology () with immunophenotypic flow cytometry revealed plasmacytoid lymphocytes. Serum immunofixation and free light-chain analysis unveiled large quantity of monoclonal paraproteins which was classified as IgM Kappa immunoglobulin. Concentration of IgM was 1491 mg/dl (range 26–217 mg/dl) while IgG and IgA levels were normal. Urine contained free kappa light chains. The clinical picture, serum IgM paraprotein, bronchoscopy specimen findings and pleural fluid analysis led to the diagnosis of Extramedullary Waldenström’s Macroglobulinemia. Patient was started on cyclophosphamide, prednisone and rituximab. Plan was to follow up with IgM level monthly and Chest CT scan after four months.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [103.0, 'mmol/L'], 'Bicarbonate': [31.0, 'mmol/L'], 'Sodium': [141.0, 'mmol/L']}",7,6.65,7.35,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 141.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 141.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 141.0 mmol * 1 mEq/mmol = 141.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mmol sodium/L converts to 141.0 mEq sodium/L. 
The concentration of chloride is 103.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 103.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 103.0 mmol * 1 mEq/mmol = 103.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 103.0 mmol chloride/L converts to 103.0 mEq chloride/L. 
The concentration of bicarbonate is 31.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 31.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 31.0 mmol * 1 mEq/mmol = 31.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 31.0 mmol bicarbonate/L converts to 31.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 141.0 mEq/L - (103.0 mEq/L + 31.0 mEq/L) = 7.0 mEq/L. Hence, The patient's anion gap is 7.0 mEq/L."
6267,39,Anion Gap,lab test,decimal,pmc-4421656-1,Extracted,"A 50-year-old female was diagnosed with Gitelman syndrome at the age of 20 years. She was treated with spironolactone (100 mg/day), magnesium lactate (1.2 g/day), potassium chloride (5.4 g/day) and indometacin (25 mg/day).
The patient was recently admitted to our Nephrology Department with oliguria and progressive facial and lower limb oedema 15 days in duration. Her blood analyses showed urea 60 mg/dL, creatinine 0.93 mg/dL, Na 138 mmol/L, K 3.3 mmol/L, Cl 98 mmol/L, Mg 2.1 mg/dL, Ca 8.2 mg/dL (ionic 1.08), P 3.1 mg/dL, total proteins 4.5 g/dL, albumin 1.7 g/dL, bicarbonate 30.1 mmol/L, cholesterol 441 mg/dL, triglycerides 151 mg/dL, high-density lipoprotein 101 mg/dL, low-density lipoprotein 339 mg/dL. Anti-nuclear antibodies, antineutrophil cytoplasmic antibodies and serologic tests for hepatotropic virus, human immunodeficiency virus and treponema were negative, and her complement system, haemogram and thyroid function were normal. Urinalysis findings were proteinuria 11.7 g/day, Na 74 mmol/L, K 152.6 mmol/L, Ca 5.7 mg/dL (136.8 mg/day) and Mg 3.8 mg/dL. A renal biopsy showed: subendothelial and mesangial segmental C1q deposits, mainly located in the distal areas of the capillary loops (), with discrete mesangial proliferation, slight interstitial fibrosis and hyperplasia of the juxtaglomerular apparatus ().
Her definitive diagnosis was nephrotic syndrome secondary to C1q nephropathy, probably minimal change type. Treatment with steroids at a dose of 1 mg/kg/day was started. The nephrotic syndrome resolved after 6 weeks of treatment.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [138.0, 'mmol/L'], 'Chloride': [98.0, 'mmol/L'], 'Bicarbonate': [30.1, 'mmol/L']}",9.9,9.405,10.395,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 138.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 138.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 138.0 mmol * 1 mEq/mmol = 138.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mmol sodium/L converts to 138.0 mEq sodium/L. 
The concentration of chloride is 98.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 98.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 98.0 mmol * 1 mEq/mmol = 98.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 98.0 mmol chloride/L converts to 98.0 mEq chloride/L. 
The concentration of bicarbonate is 30.1 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 30.1 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 30.1 mmol * 1 mEq/mmol = 30.1 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 30.1 mmol bicarbonate/L converts to 30.1 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 138.0 mEq/L - (98.0 mEq/L + 30.1 mEq/L) = 9.9 mEq/L. Hence, The patient's anion gap is 9.9 mEq/L."
6268,39,Anion Gap,lab test,decimal,usmle-1453,Extracted,"A previously healthy 10-year-old boy is brought to the emergency room by his mother 5 hours after the onset of abdominal pain and nausea. Over the past 2 weeks, he has also had progressive abdominal pain and a 4-kg (8.8-lb) weight loss. The mother reports that her son has been drinking more water than usual during this period. Last week he wet his bed three times despite being completely toilet-trained since 3 years of age. His temperature is 37.8°C (100°F), pulse is 128/min, respirations are 35/min, and blood pressure is 95/55 mm Hg. He appears lethargic. Physical examination shows deep and labored breathing and dry mucous membranes. The abdomen is soft, and there is diffuse tenderness to palpation with no guarding or rebound. Serum laboratory studies show:
Na+ 133 mEq/L
K+ 5.9 mEq/L
Cl- 95 mEq/L
HCO3- 13 mEq/L
Urea nitrogen 25 mg/dL
Creatinine 1.0 mg/dL
Urine dipstick is positive for ketones and glucose.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [133.0, 'mEq/L'], 'Chloride': [95.0, 'mEq/L'], 'Bicarbonate': [13.0, 'mEq/L']}",25,23.75,26.25,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 133.0 mEq/L. 
The concentration of chloride is 95.0 mEq/L. 
The concentration of bicarbonate is 13.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 133.0 mEq/L - (95.0 mEq/L + 13.0 mEq/L) = 25.0 mEq/L. Hence, The patient's anion gap is 25.0 mEq/L."
6269,39,Anion Gap,lab test,decimal,pmc-4591497-1,Extracted,"A 71 year-old Caucasian male ex-smoker without any significant past medical history presented to the emergency department complaining of worsening redness and swelling in his left lower leg. He presented five days earlier and was given antibiotic treatment which did not resolve the problem. On physical exam BP 119/68 mHg, Pulse 61/min, Resp 17/min, Temp: 96.6°F, O2 saturation 96% on Room air. Laboratory testing showed hemoglobin 12.2 g/dL, WBC 7.3 K/uL, Platelet count 26 K/uL, Neutrophils 29, Lymphocytes 20%, MCV 73.2 fL, glucose 120 mg/dL, BUN 14 mg/dL, Creatinine 0.8 mg/dL, Calcium 8.7 mg/dL, albumin 4.3 g/dL, Sodium 137 mmol/L, Potassium 4 mmol/L, Chloride 100 mmol/L, and CO2 25 mmol/L. Liver enzymes were within normal limits. X-ray ruled out osseous contribution to his problem and venous Doppler was negative for DVT. Subsequently a diagnosis of cellulitis was made. CBC demonstrated multiple cytopenias, including thrombocytopenia ( and ). A review of hospital records noted previous findings of thrombocytopenia as far as four years earlier. Considering pancytopenia an oncology consult was called who reviewed the peripheral smear which showed slight anisocytosis, monocytosis with marked thrombocytopenia with some giant platelets, No pseudo-Pelger-Huet cells or circulating blasts were noted (). Given the laboratory findings, leukemia was considered as a differential and therefore a bone marrow biopsy was performed which showed the differential () granulopoiesis, hypercellular marrow with increased myelomonocytic cells and megakaryocytogenesis (Figure 1B,C). Immunohistochemistry showed CD117: about 5-10% positive cells, consistent with immature cells/blasts, CD34: No increase in CD34 positive cells, CD163: Highlights predominantly monocytic component, CD123: Negative. Reticulin staining showed mild diffuse reticulin fibrosis. Immunophenotyping by flow cytometry analysis FLG13-859 shows mild myelomonocytic abnormalities. PCR study for JAK2 is negative. FISH was performed for BCR/ABL1 to detect the (9:22) translocation associated with CML and less commonly ALL or AML were normal. Cytogenic testing demonstrated an abnormal karyotype 46, XY, del(20)(q11.2q13.3)(20) (). Other 15 metaphase spreads examined showed a normal male karyotype, 46, XY. Patient was diagnosed with myelodysplastic syndrome, Unclassified (MDS-U) with refractory thrombocytopenia.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [100.0, 'mmol/L'], 'Bicarbonate': [25.0, 'mmol/L'], 'Sodium': [137.0, 'mmol/L']}",12,11.4,12.6,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 137.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 137.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 137.0 mmol * 1 mEq/mmol = 137.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mmol sodium/L converts to 137.0 mEq sodium/L. 
The concentration of chloride is 100.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 100.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 100.0 mmol * 1 mEq/mmol = 100.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 100.0 mmol chloride/L converts to 100.0 mEq chloride/L. 
The concentration of bicarbonate is 25.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 25.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 25.0 mmol * 1 mEq/mmol = 25.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 25.0 mmol bicarbonate/L converts to 25.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 137.0 mEq/L - (100.0 mEq/L + 25.0 mEq/L) = 12.0 mEq/L. Hence, The patient's anion gap is 12.0 mEq/L."
6270,39,Anion Gap,lab test,decimal,pmc-6385391-1,Extracted,"A 4-year-old boy, who had no systemic or inherited disease, presented with a 3-week history of intermittent vomiting without diarrhea or abdominal pain. In the past year, he experienced polydipsia and polyuria. Physical examination revealed body weight 17.5 kg (50th percentile), body height 100 cm (15~50th percentile), blood pressure 230/120 mmHg, heart rate 138 /min, and decreased skin turgor. There was no focal neurological deficit, blood pressure discrepancy between upper and lower extremities, palpable mass, nor any appreciation of an abdominal thrill. Laboratory studies revealed serum Na+ 124 mmol/L, K+ 2.4 mmol/L, Cl− 87 mmol/L, Ca2+ 8.5 mg/dL, HCO3− 34.5 mEq/L, creatinine 0.41 mg/dL, albumin 3.4 g/dL, IgG 247 mg/dL, and osmolality 290 mOsm/KgH2O. Urine analysis was significant for creatinine 11.2 mg/dL, Na+ 24 mEq/L, K+ 18 mEq/L, Cl− 24 mEq/L, osmolality 232 mOsm/KgH2O, RBC 168/μL, FENa 6%, and nephrotic-range proteinuria (55 mg/m2/hour). Survey for possible glomerulonephritis demonstrated the absence of anti-streptolysin O, p-ANCA, c-ANCA, ANA, and normal immunoglobulin A, C3, and C4 levels. In addition, work-up for secondary hypertension included: free T4 1.51 (normal range 0.8–2.0 ng/dL), TSH 5.7 (normal range 0.25–5.00 μIU/mL), cortisol 40.18 (normal range 4.3–25 μg/dL), ACTH 9.32 (normal range < 46 pg/mL), renin 1745 (normal range 2–15 ng/L), aldosterone 92.6 (normal range 4–25 ng/dL), and urine vanillylmandelic acid 3.8 (normal range 1.9–9.9 g/day). Renal ultrasonography revealed hyperechoic right kidney (7.6 cm in length) and small left kidney (5.3 cm in length). Due to the presence of hyperreninemic hypertension, natriuretic-hyponatremia, hypokalemia, and nephrotic range proteinuria, HHS was highly suspected. Computed tomography angiography confirmed high-grade renal artery stenosis with hypoplasia of the left kidney (Fig. ).
In terms of management for this case, we began with volume repletion by normal saline administration. Subsequently, his blood pressure declined from 210/120 mmHg to 180/90 mmHg. Intravenous calcium channel blocker was used to treat his hypertensive emergency, while oral captopril was prescribed for RAA axis blockage after diagnosis of unilateral renal artery stenosis. The systolic blood pressure gradually declined to 150~160 mmHg on the 3rd day. Potassium supplement was infused for his profound hypokalemia and generalized muscle weakness. Due to the severity of left renal artery stenosis, he was not a candidate for angiographic intervention, and decision was made to proceed with left nephrectomy. Overall, electrolyte abnormalities such as hyponatremia and hypokalemia were corrected within 1 week after admission, and resolution of polyuria, polydipsia, proteinuria, and hypertension were achieved 2 weeks after nephrectomy (Additional file : Table S1).",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [87.0, 'mmol/L'], 'Bicarbonate': [34.5, 'mEq/L'], 'Sodium': [124.0, 'mmol/L']}",2.5,2.375,2.625,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 124.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 124.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 124.0 mmol * 1 mEq/mmol = 124.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 124.0 mmol sodium/L converts to 124.0 mEq sodium/L. 
The concentration of chloride is 87.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 87.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 87.0 mmol * 1 mEq/mmol = 87.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 87.0 mmol chloride/L converts to 87.0 mEq chloride/L. 
The concentration of bicarbonate is 34.5 mEq/L. 
Plugging in these values into the anion gap formula gives us 124.0 mEq/L - (87.0 mEq/L + 34.5 mEq/L) = 2.5 mEq/L. Hence, The patient's anion gap is 2.5 mEq/L."
6271,39,Anion Gap,lab test,decimal,pmc-3891198-1,Extracted,"A 93-year-old male, 70 kg, 165 cm, was admitted to (the first of three hospitals) with a diagnosis of congestive heart failure attributed to right ventricular dysfunction. He required a walker for ambulation. He had a past medical history of a coronary artery disease, atrial fibrillation, mitral regurgitation, aortic stenosis, diverticular bleeding, hypertension, advanced chronic kidney disease, gout (remote), and nonAlzheimer's dementia. His surgical history included coronary artery bypass grafting with mitral valve and aortic valve replacement (tissue valves). His medications were donepezil for dementia, calcium carbonate, potassum chloride, isosorbide mononitrate, metamucil, pantoprazole, diltiazem, hydralazine, and bumetanide.
The laboratory evaluation demonstrated: Sodium 140 mmol/L, potassium 4.0 mmol/L, chloride 95 mmol/L, serum bicarbonate 36 mmol/L, phosphorus 3.4 mg/dl, magnesium 2.2 mg/dL, glucose 108 mg/dL, blood urea nitrogen (BUN) 73 mg/dL, creatinine 2.13 mg/dL, glomerular filtration rate (GFR) 29 mL/min, occult blood negative, total protein 6.3 g/dL, albumin 3.8 g/dL, thyroid function tests were normal, hemoglobin 9.7 g/dL, hematocrit 29.3%, white blood cell count 4.6 K/μL, and platelets 90 K/μL.
Physical examination revealed bilateral pulmonary rales, tachypnea, pedal edema, and rate-controlled atrial fibrillation (confirmed by electrocardiogram). Chest roentgenogram showed bilateral pleural effusions and pulmonary edema.
A furosemide infusion promoted a 6 kg loss in 5 days; tachypnea, pedal edema, pulmonary edema, and pleural effusions improved. Concurrently he complained of leg pain and received tramadol 50 mg every 8 hours. His cognitive function worsened over 72 hours (days 3-5 of diuresis). He also became incontinent, needed skilled nursing care, and was transferred to a covalesent facility where he was difficult to arouse upon arrival. He had lost intravenous access and none was started. No laboratory studies were drawn. The staff suggested that the patient be made “comfort care” only. The next morning his condition remained unchanged. The family expressed concern and transferred the patient to a third institution.
Subsequent examination revealed a Glasgow coma scale of 10, mild bilateral rales, rate controlled atrial fibrillation, no pretibial edema, and an edematous left foot with an erythematous, warm great toe. Urine output was diminished. Laboratory examination revealed a BUN of 81 mg/dL (GFR < 30 mL/min), potassium, sodium, and chloride were normal, and serum bicarbonate 43 mmol/L, and arterial blood gas was pH of 7.37, PaCO2 65, and PaO2 of 90 (2 liters nasal cannula). His uric acid level was 450 μmol/L.
He received crystalloid fluids at 100 mL/hour for 24 hours, and bilevel noninvasive mechanical ventilation 12/4 cm H2O. He subsequently improved over 36 hours. His ME from a compensated metabolic alkalosis with hypercapnea was corrected, and urine output improved. He could now converse, feed himself, and walk 50 feet with his walker.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mmol/L'], 'Chloride': [95.0, 'mmol/L'], 'Bicarbonate': [36.0, 'mmol/L']}",9,8.55,9.45,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 140.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 140.0 mmol * 1 mEq/mmol = 140.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 140.0 mmol sodium/L converts to 140.0 mEq sodium/L. 
The concentration of chloride is 95.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 95.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 95.0 mmol * 1 mEq/mmol = 95.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 95.0 mmol chloride/L converts to 95.0 mEq chloride/L. 
The concentration of bicarbonate is 36.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 36.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 36.0 mmol * 1 mEq/mmol = 36.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 36.0 mmol bicarbonate/L converts to 36.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (95.0 mEq/L + 36.0 mEq/L) = 9.0 mEq/L. Hence, The patient's anion gap is 9.0 mEq/L."
6272,39,Anion Gap,lab test,decimal,pmc-8346271-1,Extracted,"A 43-year-old male with a past medical history of paranoid schizophrenia presented to the emergency department (ED) with esophageal symptoms (throat pain, dysphagia/odynophagia, nausea, and vomiting) two days after ingesting a bottle of caffeine pills (about 30 g of caffeine) in an apparent suicide attempt. His vital signs on presentation to the ED included a blood pressure of 106/70 mmHg, heart rate of 136 beats per minute, body temperature of 98.5°F, and saturation of 91% on room air. His abdomen was soft and non-distended but was mildly tender to palpation in the epigastric region with no rebound or guarding; his bowel sounds were normal. There were no respiratory or cardiovascular findings. His Glasgow Coma Scale was 15. All other physical examination findings were normal.
Pertinent laboratory findings were white blood cell count of 11.9 × 109/L (neutrophils 89.9%, lymphocytes 3.7%, monocytes 5.7%), hemoglobin 20.0 g/L, platelet 241 × 109/L, sodium 134 mEq/L, potassium 3.7 mEq/L, chloride 86 mEq/L, bicarbonate 40 mEq/L, blood urea nitrogen 44 mg/dL, creatinine 3.9 mg/dL, aspartate aminotransferase 83 U/L, alanine aminotransferase 44 U/L, and creatinine kinase of 2,588 U/L. The urine drug screen was negative. Urine chemistry was suggestive of acute tubular necrosis. Urinalysis showed 2+ proteinuria and trace ketonuria, but was otherwise unremarkable. Electrocardiography showed a normal sinus rhythm. The patient’s blood caffeine level was not assessed.
He was found to have rhabdomyolysis and acute renal failure. Despite receiving aggressive intravenous fluid hydration in the ED with 2 L of normal saline intravenous (IV) bolus followed by lactated ringers at 125 cc/hour on the medical floor, his renal function continued to worsen peaking at 7.61 mg/dL on day three of the admission, warranting initiation of hemodialysis. His renal failure gradually recovered after three months of intermittent hemodialysis. A renal biopsy was not performed.
Esophagogastroduodenoscopy (EGD) done on day seven of hospital stay due to persistent esophageal symptoms despite being on famotidine showed severe erosive esophagitis (Figure ) and gastric subepithelial lesion​. Pathology reports of the gastric biopsy were consistent with mild chronic inactive gastritis, while that of the gastric subepithelial lesion was consistent with leiomyoma. His esophageal symptoms markedly improved following the initiation of proton pump inhibitor (pantoprazole 40 mg IV twice daily). He did not show up for a repeat EGD. This case highlights the risk of concurrent renal and gastrointestinal injuries after ingesting excessive caffeine tablets. Our experience suggests that for patients who have ingested excessive caffeine tablets, endoscopic evaluation is advisable in the setting of persistent esophageal symptoms to evaluate for chemical esophagitis.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [86.0, 'mEq/L'], 'Bicarbonate': [40.0, 'mEq/L'], 'Sodium': [134.0, 'mEq/L']}",8,7.6,8.4,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 134.0 mEq/L. 
The concentration of chloride is 86.0 mEq/L. 
The concentration of bicarbonate is 40.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 134.0 mEq/L - (86.0 mEq/L + 40.0 mEq/L) = 8.0 mEq/L. Hence, The patient's anion gap is 8.0 mEq/L."
6273,39,Anion Gap,lab test,decimal,pmc-4901012-1,Extracted,"A 51-year old man had a breakfast cooked with wild mushrooms that he had gathered one day earlier during summer vacation in August, 2010 at the Jujak mountain located on the province of Jeollanam-do, the southern area of Korea. He was a bus driver. He had no particular past medical or social history other than the occasional ingestion of wild mushrooms during recreational hiking. He was healthy before this admission. He did not have a history of trauma, infection, other known underlying cause, or medication use that could explain the occurrence of rhabdomyolysis. He shared the meal with his wife and son who did not eat any more mushrooms due to nausea after ingesting a single piece of mushroom. However, he ate the mushrooms without immediate symptom. Six hours later, he began to complain of vomiting, diarrhea, and myalgia. He visited a local hospital where his general condition worsened and systolic BP fell to 60 mmHg requiring dopamine treatment and endotracheal intubation. Twenty-eight hours after ingestion of the mushrooms, he was transferred to the intensive care unit of our hospital. At the time of admission, he was alert, but acute ill-looking. He complained of generalized myalgia, chest discomfort, palpitations, and dyspnea. Blood pressure was 80/56 mmHg, heart rate 121/min, respiratory rate 25/min, and body temperature 36.3oC. Oliguria was noted with no response to intravenous fluid and furosemide. Systolic murmurs were present on auscultation. Laboratory tests showed the following: hemoglobin 15.9 g/dL, hematocrit 45.9%, leukocyte count 20,740/μL with neutrophil 89.6%, platelet 253,000/μL, C-reactive protein (CRP) 8.36 mg/dL, blood urea nitrogen (BUN) 38.5 mg/dL, serum creatinine 2.84 mg/dL, serum osmolarity 314 mOsm/kg, sodium 140 mEq/L, potassium 4.7 mEq/L, chloride 100 mEq/L, ionized calcium 0.75 mmol/L, glucose 187 mg/dL, cholesterol 221 mg/dL, albumin 4.0 g/dL, aspartate aminotransferase (AST) 1,214 U/L, alanine aminotransferase (ALT) 343 U/L, total bilirubin 0.51 mg/dL, alkaline phosphatase 92 IU/L, creatine kinase (CK) 69,121 U/L, CK-MB > 500 ng/mL, lactate dehydrogenase (LDH) 2,196 U/L, troponin I 1.86 ng/mL, N-terminal pro brain natriuretic peptide (NT-pro BNP) 7,414 pg/mL, amylase 1,930 U/L, lipase 18 U/L, prothrombin time (PT) 10.2 seconds. (INR 0.86), activated partial thromboplastin time (aPTT) 28.2 seconds, urine osmolarity 341 mOsm/kg, sodium 22 mEq/L, potassium 59.2 mEq/L, chloride 14 mEq/L, creatinine 123.8 mg/dL, myoglobin 51.7 ng/mL, and fractional excretion of sodium 0.36%. Urine analysis showed pH 5.0, specific gravity 1.020, protein 2+, ketone 2+, blood 4+, RBC 5-9/high-power field, and WBC 0-1/high-power field. Blood and urine cultures were all negative for microorganism. Arterial blood gas analysis was pH 7.04, PaCO2 69 mmHg, PaO2 172 mmHg, and HCO3
- 18.7 mmol/L. Chest radiographs revealed mild cardiomegaly without lung lesion. Electrocardiogram (ECG) showed sinus tachycardia with QT prolongation. The enlarged left ventricle (LV), severe LV systolic dysfunction (ejection fraction 30%), and akinesia of LV mid to apex wall suggesting stress induced cardiomyopathy were noted on echocardiography. He received ventilator support, hemodynamic monitoring, continuous venovenous hemodiafiltration, and conservative care including intravenous fluid and electrolyte repletion. Seventy hours after ingestion of the mushrooms, BUN 41.9 mg/dL, serum creatinine 3.46 mg/dL, AST 3,271 U/L, ALT 1,254 U/L, total bilirubin 1.55 mg/dL, CK 121,397 U/L, CK-MB >500 ng/mL, LDH 6,102 U/L, troponin I 11.77 ng/mL, amylase 2,779 U/L, lipase 601 U/L, PT 42.1 seconds. (INR 3.34), and aPTT > 150 seconds. Blood pressure continued to decrease despite intravenous fluid and inotropics. Ventricular tachycardia developed, and he died due to cardiogenic shock 72 hours after ingestion of the mushrooms.
The leftover samples of the mushrooms that he had ingested were sent to Agricultural Microbiology Division, National Academy of Agricultural Science, Rural Development Administration, Suwon, Korea. Those were identified as R. subnigricans by their gross morphology (). Further examination by microscopy also confirmed the presence of spores from R.
subnigricans.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mEq/L'], 'Chloride': [100.0, 'mEq/L'], 'Bicarbonate': [18.7, 'mmol/L']}",21.3,20.235,22.365,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mEq/L. 
The concentration of chloride is 100.0 mEq/L. 
The concentration of bicarbonate is 18.7 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 18.7 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 18.7 mmol * 1 mEq/mmol = 18.7 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 18.7 mmol bicarbonate/L converts to 18.7 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (100.0 mEq/L + 18.7 mEq/L) = 21.3 mEq/L. Hence, The patient's anion gap is 21.3 mEq/L."
6274,39,Anion Gap,lab test,decimal,pmc-6709832-1,Extracted,"A sixty years old male was admitted to our multidisciplinary ICU with complaints of aggression, altered sensorium, tremors, sweating, clonus in legs (myoclonus) and irrelevant talks. Initially he was managed in medicine emergency where a working diagnosis of gastroenteritis induced hyponatremia with sepsis was made. The patient received infusion of 3% NaCl, antibiotics and oxygen supplementation @ 6 L/min through venturi mask. In view of aggression and altered sensorium, CT brain was done, which was normal. An assessment by neurologist was done, who advised for MRI Brain for further evaluation. Patient was kept nil per oral in view of possibility of further deterioration and need for mechanical ventilation. Since there was no improvement, patient was shifted to ICU. In ICU, the intensivist took a detailed history from the attendants of the patient. His medical history included long standing hypertension, diabetes mellitus type 2, coronary artery disease with PTCA for triple vessel disease and a major depressive disorder. Relatives denied any allergies or illicit drug abuse. Patient was taking metoprolol 25 mg once daily, olmesartan 10 mg twice daily, ecospirin 75 mg once daily, atorvastatin 10 mg at night, metformin 1 g twice daily twice daily, pioglitazone 50 mg once daily, regular insulin 16 U and 20 U subcutaneous, pantoprazole 40 mg once daily along with some herbal powder for his comorbidities for the past 10 years. For last two years, patient's depression was controlled with escitalopram (SSRI) 10 mg and clonazepam (benzodiazepine) 0.5 mg. The patient had an acute episode of anxiety five days before admission to ICU, for which psychiatrist had prescribed another SSRI paroxetine 20 mg and alprazolam 0.5 mg. Symptoms did not subside, rather patient developed restlessness in his legs with current like sensation along with loose motions. His symptoms worsened over next 2 days, and he presented to the medical emergency with severe agitation and presenting complaints as described above.
In the ICU, patient was hemodynamically stable but severely agitated and restless and not responding to commands. Laboratory parameters measured included Hb 12.8 g%, TLC 10800/mm3, platelet count 2.7 lakh/mm3, INR 1.0, Na+ 117meq/L, K+ 4.5meq/L, serum creatinine 0.9 mg/dL and ABG pH 7.424/PaO2 109/PaCO2 28.9/HCO3 18.6/BD −4.3/SpO2 99%/lactate 0.7/Na+ 117/K+ 3.9/iCa+2 3.55/glucose 90 mg/dL/Cl− 83 mEq/L. In view of the recent escalation in the doses and addition of other antidepressants (SSRI) and benzodiazepines with concomitant intake of drugs like metoprolol, pantoprazole and some herbal medications associated with typical features, presumptive diagnosis of SS was made as per Hunters criteria. All antidepressants were stopped. Sedation using titrated doses of propofol (10 mg/hr) to maintain Ramsay score of 2–3 was started to alleviate the symptoms and allow the complete excretion of drugs. Patient received oxygen by face mask and was monitored continuously. Over the next 24 hours his agitation subsided and patient was awake and started responding to commands. Later propofol sedation was gradually tapered off. Thereafter, patient was discharged from ICU and referred back to psychiatrist for further management.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [83.0, 'mEq/L'], 'Bicarbonate': [18.6, 'mEq/L'], 'Sodium': [117.0, 'mEq/L']}",15.4,14.63,16.17,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 117.0 mEq/L. 
The concentration of chloride is 83.0 mEq/L. 
The concentration of bicarbonate is 18.6 mEq/L. 
Plugging in these values into the anion gap formula gives us 117.0 mEq/L - (83.0 mEq/L + 18.6 mEq/L) = 15.4 mEq/L. Hence, The patient's anion gap is 15.4 mEq/L."
6275,39,Anion Gap,lab test,decimal,pmc-5225336-1,Extracted,"A 66-year-old male who was a long standing inmate in a forensic psychiatric hospital presented to the Emergency Department with a complaint of abdominal distention. The patient denied any nausea or vomiting but reported a decreased appetite which he attributed to abdominal discomfort. His last bowel movement was five days ago. The patient also endorsed dysuria. A computerized tomography (CT) scan of the abdomen and pelvis was performed prior to ED arrival and the images were brought with patient.
The patient had a past medical history notable for paranoid schizophrenia, bipolar disorder, latent tuberculosis, and ascending aortic aneurysm. There was no known history of liver disease. The patient's medications included clozapine, fluphenazine, lithium, paroxetine, lorazepam, and haloperidol. He had no known drug allergies and had no recent medication changes. Complete review of systems was otherwise negative. The patient had no history of previous surgeries, did not smoke, drink, or consume illicit drugs, and had a noncontributory family history.
On initial presentation to the ED his vital signs were heart rate (HR), 104; blood pressure (BP), 147/101; respiratory rate (RR), 22; pulse oximetry, 93% on room air; and temperature, 36.4 degrees Celsius.
On examination of the patient, his oral mucosa was noticeably dry. His cardiac exam was unremarkable with normal S1 and S2, no murmurs, rubs, or gallops, and 2+ pulses in all four extremities and his lungs were clear to auscultation bilaterally. The patient's abdomen was firm and grossly distended and was noted to resemble a full-term pregnant patient. Dilated superficial veins were noted on the abdomen and palpation revealed mild, diffuse tenderness without rebound or guarding. The patient was awake, alert, and orientated to time, date, and environment.
Labwork was notable for sodium of 115 mmol/L and a serum osmolality of 251 mOsm/kg. The potassium level was 5.2 mmol/L, chloride 80 mmol/L, bicarbonate 21 mmol/L, creatinine 1.58 mg/dL, lactic acid 1.5 mmol/L, troponin T < 0.01 ng/mL, and lithium level 1.0 mmol/L. The patient was mildly anemic with a hemoglobin of 11.5 g/dL, while his remaining complete blood count (CBC) was unremarkable with a white blood cell (WBC) count of 9.44/L and platelets of 318/L. An electrocardiogram was obtained during the ED evaluation () which showed a sinus tachycardia of 105 beats per minute, QRS 98s, QTc 415 ms, and peaked T waves in the precordial leads.
Upon review of the CT, large dilated loops of colon were noted up to 12 cm (Figures and ).
During the ED course, the acute care surgical service was consulted for further management. A rectal exam was performed by the resident physician with a plan for disimpaction immediately following. The patient was positioned on his left side. Soft stool was found on rectal exam. During the rectal examination, the nurse in the room noted that the patient was apneic and a code was called. The patient was unresponsive for less than one minute prior to the nurse noticing his status change. The patient had no new complaints prior to his arrest.
Unfortunately, the patient was not on a cardiac monitor at this time. Upon immediately placing the patient on a monitor, a bradycardic rate was noted. Following a pulse check, the patient was then found to be in pulseless electrical activity. Cardiopulmonary resuscitation (CPR) was started and advanced cardiac life support (ACLS) protocol was followed including intubation. Initial bedside ultrasound showed no cardiac activity. Following multiple rounds of CPR and ACLS medications, return of spontaneous circulation (ROSC) was obtained. The patient then again went into PEA with a bradycardic rhythm but ROSC was again obtained and remained. A postarrest arterial blood gas was notable for pH 6.84, pCO2 100 mmHg, and pO2 94.5 mmHg. The patient was then admitted to Intensive Care Unit (ICU) on epinephrine, norepinephrine, and vasopressin infusions. At time of ICU admission the patient was in a normal sinus rhythm of 98. Eight days later the patient expired following confirmation of anoxic brain injury and a decision made to provide comfort care.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [80.0, 'mmol/L'], 'Bicarbonate': [21.0, 'mmol/L'], 'Sodium': [115.0, 'mmol/L']}",14,13.3,14.7,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 115.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 115.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 115.0 mmol * 1 mEq/mmol = 115.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 115.0 mmol sodium/L converts to 115.0 mEq sodium/L. 
The concentration of chloride is 80.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 80.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 80.0 mmol * 1 mEq/mmol = 80.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 80.0 mmol chloride/L converts to 80.0 mEq chloride/L. 
The concentration of bicarbonate is 21.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 21.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 21.0 mmol * 1 mEq/mmol = 21.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 21.0 mmol bicarbonate/L converts to 21.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 115.0 mEq/L - (80.0 mEq/L + 21.0 mEq/L) = 14.0 mEq/L. Hence, The patient's anion gap is 14.0 mEq/L."
6276,39,Anion Gap,lab test,decimal,pmc-3186895-1,Extracted,"Case : A 30-year-old male was admitted to our hospital with general weakness and drowsy mental status. He had eaten only 3-4 spoons of brown rice and fresh vegetable without salt for 3 months to treat his tic disorder, and he had been in bed-ridden state. He had taken propolis and enema by himself, and his past medical history was unremarkable except tic disorder since high school. His blood pressure was 100/70 mm Hg, pulse rate 72/min, and respiratory rate 18/min, body temperature 36℃. He had lost 14 kg in the past 3 months. Physical examination presented cracking over his skin around his neck and both shoulders.
Serum laboratory results were as follows; hemoglobin 16.2 g/dL, white blood cell (WBC) 4.9 × 103/µL, platelet 201 × 103/µL, total protein 5.6 g/dL, albumin 3.4 g/dL, aspartate aminotransferase (AST) 114 IU/L, alanine aminotransferase (ALT) 101 IU/L, alkaline phosphatase (ALP) 57 IU/L, γ-glutamyl transferase (GGT) 13 IU/L, bilirubin (total/direct) 3.22/0.8 mg/dL, glucose 166 mg/dL, amylase 98 IU/L, blood urea nitrogen (BUN) 33.6 mg/dL, creatinine 0.41 mg/dL, total CO2 20.2 mEq/L, sodium 101 mEq/L, potassium 4.0 mEq/L, chloride 68 mEq/L, calcium 6.8 mg/dL, inorganic phosphorus 2.7 mg/dL, magnesium 1.5 mEq/L, uric acid 1.0 mg/dL, C-reactive protein (CRP) 1.87 mg/dL, osmolality 213 mOsm/kg H2O, creatine phosphokinase (CPK) 1,472 IU/L (29-145), myoglobin 1,278 ng/mL, lactate dehydrogenase (LDH) 1,472 IU/L (0-500), total cholesterol 231 mg/dL, triglyceride 97 mg/dL, high density lipoprotein (HDL)-cholesterol 127 mg/dL, low density lipoprotein (LDL)-cholesterol 83 mg/dL, prealbumin 10.7 mg/dL, hemoglobin A1c 5.4%, thyroid stimulating hormone (TSH) 1.26 uIU/mL, free T4 0.75 ng/dL, and international normalized ratio (INR) 1.61. Urinalysis revealed a specific gravity of 1.012, pH 7.0, trace protein, glucose 2+, occult blood 3+, myoglobin 2,687 ng/m, urine sodium 62 mEq/L, potassium 34.4 mEq/L, chloride 43.1 mEq/L, and osmolality 484 mOsm/kg H2O.
Chest AP X-ray showed mediastinal emphysema and extensive soft tissue emphysema in his neck and chest wall. Abdominal ultrasonography revealed a small amount of ascites and small amount of fluid collection in his bilateral perinephric space. Chest CT showed extensive soft tissue emphysema in his neck and chest wall, extensive mediastinal emphysema, small right pneumothorax, and pericardial fluid (). To rule out esophageal perforation esophagography with gastrographin was performed and it showed no evidence of contrast leakage from his esophagus. The diagnosis of orthorexia nervosa with hyponatremia, rhabdomyolysis, pneumomediastinum, pneumothorax, and soft tissue emphysema was made. We started on intravenous fluid supplementation based on treatment of hyponatremia and refeeding syndrome, and oral feeding. He gradually improved, but his total protein and albumin decreased on the 5th hospital day to 4.4 g/dL and 2.5 g/dL, respectively. On the 7th hospital day, his platelet and WBC levels decreased to 27 × 103/µL and 1.2 × 103/µL, respectively. On the 12th hospital day his hemoglobin level decreased to 7.2 g/dL from his hospital 2nd day. Peripheral blood smear showed normochromic normocytic anemia with anisopoikilocytosis 2+, neutropenia, lymphocytopenia, relative monocytosis 14%, and thrombocytopenia. His iron level was 88 µg/dL, total iron binding capacity (TIBC) 168 µg/dL, ferritin 908.6 ng/mL, vitamin B12 988 pg/mL, folate 2.8 ng/mL, and his Coomb's test, plasma hemoglobin, haptoglobin, and serology were within normal limits. We transfused 6 units of platelet concentrate by his hospital 7th day and granulocyte colony-stimulating factor (G-CSF) 150 µg due to absolute neutrophil count (ANC) 560 and methicillin-susceptible Staphylococcus aureus (MSSA) bacteremia by his hospital 16th day. By his hospital 8th day, serum laboratory results were as follows; sodium 138 mEq/L, potassium 3.7 mEq/L, chloride 99 mEq/L, calcium 8.1 mg/dL, inorganic phosphorus 1.9 mg/dL, magnesium 1.4 mEq/L, total CO2 32.5 mEq/L, osmolality 271 mOsm/kg H2O, CPK 270 IU/L, myoglobin 57.8 ng/mL, LDH 1,011 IU/L, and total cholesterol 140 mg/dL. By hospital 18th day, his AST level was 25 IU/L, ALT 59 IU/L, ALP 89 IU/L, bilirubin (total/direct) 0.35/0.12 mg/dL, and by hospital 28th day, his LDH was 514 IU/L. Until his hospital 20th day, his platelet level steadily increased to 1,475 × 103/µL, and gradually decreased to 382 × 103/µL by the hospital 37th day. By his hospital 37th day, his hemoglobin increased to 12.1 g/dL and WBC also stabilized to 3.4 × 103/µL (neutrophil 48%).
He was discharged by his hospital 38th day in an improving state, and followed up at our rehabilitation department for physical therapy and psychological department for supportive therapy.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [68.0, 'mEq/L'], 'Bicarbonate': [20.2, 'mEq/L'], 'Sodium': [101.0, 'mEq/L']}",12.8,12.16,13.44,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 101.0 mEq/L. 
The concentration of chloride is 68.0 mEq/L. 
The concentration of bicarbonate is 20.2 mEq/L. 
Plugging in these values into the anion gap formula gives us 101.0 mEq/L - (68.0 mEq/L + 20.2 mEq/L) = 12.8 mEq/L. Hence, The patient's anion gap is 12.8 mEq/L."
6277,39,Anion Gap,lab test,decimal,pmc-6425342-1,Extracted,"A 64-year-old woman with no past medical history and no prescribed medications was found unresponsive at home after ingestion of 208 tablets of Tylenol PM™ (APAP 500 mg with diphenhydramine 25 mg) approximately three hours prior to transportation to the ED. She was endotracheally intubated by prehospital staff due to decreased level of consciousness, vomitus, and agonal respiration. On arrival to the ED, vital signs included temperature of 33.9°C, heart rate of 57 bpm, blood pressure of 139/102 mmHg, respiratory rate of 19 rpm, and oxygen saturation of 99% on 100% FiO2. Physical examination demonstrated a Glasgow Coma Scale score 3 without spontaneous respiration. The patient subsequently became hypotensive requiring five IV push-dose epinephrine doses (total 100 µg), followed by dopamine (10 µg/kg/min increased to 15 µg/kg/min), and then a norepinephrine infusion (10 µg/min). An electrocardiogram (ECG) showed sinus rhythm of 58 bpm, PR of 144 ms, QRS of 112 ms, and QTc of 659 ms. Serum chemistries measured as follows: lactate 7.6 mmol/L (0.5-1.0 mmol/L), glucose 193 mg/dL (70-100 mg/dL), Na+ 142 mEq/L (136-144 mEq/L), K+ 3.2 mEq/L (3.7-5.2 mEq/L), Cl− 110 mmol/L (96-106 mmol/L), CO2 18 mmol/L (20-29 mmol/L), BUN 16 mg/dL (7-20 mg/dL), Cr 1.17 mg/dL (0.6-1.1 mg/dL), AST 21 IU/L (10-34 IU/L), ALT 99 IU/L (8-37 IU/L), and INR 1.2 (0.8-1.1). Initial ABG measured as follows: pH 7.32 (7.35-7.45), pCO2 30 mmHg (35-45 mmHg), pO2 249 mmHg (80-100 mmHg), and HCO3 16 (CMV FiO2 65%, PEEP 6, RR 16, and TV 500 mL). Initial serum APAP concentration measured 1,017 µg/mL. Serum salicylate and ethanol concentrations measured 7 mg/dL and negative, respectively. A preliminary urine drug screen of abuse detected only methadone. Expanded serum liquid chromatography/mass spectroscopy detected caffeine, dihydrocodeine/hydrocodol, lidocaine, monoethylglycinexylidide, and diphenhydramine. A chest X-ray revealed mild interstitial edema. Head computed tomography was unremarkable. The patient was admitted to the intensive care unit. There was no repeat ECG performed prior to transfer to transplant center; however, no dysrhythmias were observed on telemetry monitoring.
The medical toxicology service was consulted and recommended IV sodium bicarbonate (for prolonged QRS interval), IV NAC, IV 4-MP (15 mg/kg), and immediate HD. APAP concentration decreased to 825 µg/mL after initiation of IV NAC, and serial concentrations exponentially decreased during “triple therapy” (Figures and ). During HD, the IV NAC rate of administration was doubled to 200 mg/kg and then tripled to 300 mg/kg, and a subsequent dose of IV 4-MP 10 mg/kg was administered; these were performed due to concern of HD removal of both antidotes.
The patient's mental status improved during HD; however, she did not follow commands. Due to concern for potential severe liver injury given the massive initial APAP concentration and lack of institutional transplant services, she was transferred to a liver transplant center on hospital day one. On arrival to the liver transplant center, she was maintained on IV NAC and received an additional HD treatment. 4-MP was not readministered. IV NAC was discontinued when APAP concentrations were undetectable. The patient was awake and following commands but failed extubation due to respiratory distress and pneumonia. She was ultimately extubated to BiPAP and discharged to an inpatient psychiatry unit approximately eight days after ED presentation in a normal state of health.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [110.0, 'mmol/L'], 'Bicarbonate': [18.0, 'mmol/L'], 'Sodium': [142.0, 'mEq/L']}",14,13.3,14.7,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 142.0 mEq/L. 
The concentration of chloride is 110.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 110.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 110.0 mmol * 1 mEq/mmol = 110.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 110.0 mmol chloride/L converts to 110.0 mEq chloride/L. 
The concentration of bicarbonate is 18.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 18.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 18.0 mmol * 1 mEq/mmol = 18.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 18.0 mmol bicarbonate/L converts to 18.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 142.0 mEq/L - (110.0 mEq/L + 18.0 mEq/L) = 14.0 mEq/L. Hence, The patient's anion gap is 14.0 mEq/L."
6278,39,Anion Gap,lab test,decimal,pmc-7850349-1,Extracted,"A 66-year-old female presented to the emergency department with sudden onset of diffuse abdominal pain for 1 day. The pain was severe, constant, dull/achy, non-radiating, and aggravated by palpation. She also had nausea, multiple episodes of bilious vomiting, diarrhea, and melena. The patient denied fever, chills, hematemesis, or hematochezia. She had been on ferrous sulfate 325 mg daily for chronic microcytic anemia and pantoprazole 40 mg twice daily for gastroesophageal reflux disease at home. On admission, her blood pressure was 76/38 mm Hg, heart rate 98 bpm, respiratory rate 16/minute, and temperature 98.8 Fahrenheit. On physical examination, she had lower abdominal tenderness to palpation with rebound tenderness. The examination of the heart and lungs was normal. Laboratory results are as follows: hemoglobin 11.2 g/dL, white blood cell count 18,470/μL, platelet count of 450,000/μL, PT 11.9 seconds, INR 1.05, sodium 127 mmol/L, potassium 5.4 mmol/L, chloride 95 mmol/L, bicarbonate 23 mmol/L, BUN 40 mg/dL, creatinine 2.07 mg/dL, glucose 155 mg/dL, AST 31 units/L, ALT 8 units/L, alkaline phosphatase 220 units/L, and total bilirubin 0.3 mg/dL. Lactate was elevated at 3.4 mmol/L. She tested negative for hepatitis B and C. A fecal occult blood test was positive. Her initial CT abdomen/pelvis without contrast on admission showed mild wall thickening of the stomach, likely from gastritis. The patient was started on intravenous fluid, pantoprazole, and piperacillin/tazobactam to treat her possible colitis. Colorectal surgery was consulted, and on third day of hospitalization, she underwent an esophagogastroduodenoscopy and flexible sigmoidoscopy, which showed partial gastric outlet obstruction/severe gastritis and diverticulosis with partial stricture in the sigmoid colon, respectively.
From hospitalization day 2 to 4, her blood pressure was elevated, ranging from SBP 140s to 180s and DBP 70s to 100s. On the fourth hospitalization day, she developed hypotension (BP 61/38) and was transferred to the intensive care unit (ICU) for closer observation. Her ICU stay was uncomplicated, and she was transferred out to the floor in 1 day. On the 6th hospitalization day, however, she started developing worsening abdominal pain, along with worsening leukocytosis and anemia, which required 2 units of packed RBC transfusions. She also developed transaminitis with AST 669 units/L, ALT 374 units/L, ALP 130 units/L, and total bilirubin 0.3 mg/dL. A repeat CT abdomen/pelvis with contrast was performed on sixth day, and it showed a new large 5.28 cm subcapsular hematoma, surrounding the right lateral liver margin with displacement of the liver caudally into the left with small free intraperitoneal fluid collections, and a 1.5 × 1 cm pseudoaneurysm (). The patient was treated with embolization of the pseudoaneurysm, located at the right hepatic artery (). The patient’s abdominal pain improved, and her hemoglobin remained stable at around 8 g/dL for the next 10 days in the hospital. Prior to discharge, her hemoglobin was 8.2 g/dL, WBC 9,190/µL, platelets 700,00/µL.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [127.0, 'mmol/L'], 'Chloride': [95.0, 'mmol/L'], 'Bicarbonate': [23.0, 'mmol/L']}",9,8.55,9.45,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 127.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 127.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 127.0 mmol * 1 mEq/mmol = 127.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 127.0 mmol sodium/L converts to 127.0 mEq sodium/L. 
The concentration of chloride is 95.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 95.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 95.0 mmol * 1 mEq/mmol = 95.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 95.0 mmol chloride/L converts to 95.0 mEq chloride/L. 
The concentration of bicarbonate is 23.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 23.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 23.0 mmol * 1 mEq/mmol = 23.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 23.0 mmol bicarbonate/L converts to 23.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 127.0 mEq/L - (95.0 mEq/L + 23.0 mEq/L) = 9.0 mEq/L. Hence, The patient's anion gap is 9.0 mEq/L."
6279,39,Anion Gap,lab test,decimal,usmle-5161,Extracted,"A 69-year-old woman presents to the emergency department in severe abdominal pain. She states she was discharged from the hospital three days ago after being treated for a kidney infection with intravenous antibiotics. Over the last five days days, she has developed watery diarrhea and has been in almost constant pain which has now increased to an intensity of 10/10. On exam, her vitals are T 102.3F, HR 125, BP 89/45, RR 20. She has pain with palpation along her lower quadrants with questionable guarding. Her CBC is significant for a white blood cell (WBC) count of 25,000 cells/mcL along with Na 140, K 3.3, Cl 90 and HCO3- 15. Her lactic acid is 3.6 mmol/L. Figure A illustrates a radiograph of her abdomen.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mEq/L'], 'Chloride': [90.0, 'mEq/L'], 'Bicarbonate': [15.0, 'mEq/L']}",35,33.25,36.75,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mEq/L. 
The concentration of chloride is 90.0 mEq/L. 
The concentration of bicarbonate is 15.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (90.0 mEq/L + 15.0 mEq/L) = 35.0 mEq/L. Hence, The patient's anion gap is 35.0 mEq/L."
6280,39,Anion Gap,lab test,decimal,pmc-7294477-1,Extracted,"A 60-year-old man presented with fever and productive cough for 2 days. He had a history of type 2 diabetes for 12 years and received peritoneal dialysis for diabetic nephropathy for 5 years. He also received antihypertensive drugs for hypertension for 10 years. There was no personal or family history of coagulopathy or stroke, trauma, chest pain, or illicit intravenous drug use.
Admission physical examination revealed the patient to be febrile (39.1°C), tachycardic with a pulse of 112/min, a respiratory rate of 22/min, and hypertensive with a blood pressure of 170/80 mm Hg. Bibasilar crackles were heard on auscultation. The peritoneal dialysis catheter was correctly positioned in the right lower abdomen, with no local erythema. There was no exudate buildup in catheter dressings. His systemic examination was otherwise unremarkable, with no tenderness, ecchymosis, or other external signs of trauma.
Initial blood workup showed neutrophilic leukocytosis with a white blood cell count of 12.8 × 109/L (normal reference: 4.0–10 × 109/L) and 82.6% neutrophils (normal reference: 50%–70%). The patient was anemic (hemoglobin 95 g/L; normal reference: 120–160 g/L), with a normal platelet count (181 × 109/L; normal reference: 100–300 × 109/L). Both his prothrombin time (PT; 12.1 s, normal reference: 10–14 s) and activated partial thromboplastin time (aPTT; 34.1 s, normal reference: 20–40 s) were normal. Blood chemistry showed elevated blood urea nitrogen (20.5 mmol/L; normal reference: 3.2–7.1 mmol) and creatinine (1125 µmol/L; normal reference: 53–106 µmol/L). Blood glucose was 6.4 mmol/L (normal reference: 3.9–6.1 mmol/L), K+ 4.14 mmol/L (normal reference: 3.5–5.5 mmol/L), Na+ 145 mmol/L (normal reference: 135–145 mmol/L), Cl+ 108 mmol/L (normal reference: 95–105 mmol/L), and Ca++ 2.1 mmol/L (normal reference: 2.25–2.58 mmol/L). Liver function test was normal. Arterial blood gas analysis showed pH 7.40 (normal reference: 7.35–7.45), PaO2 60.1 mm Hg (normal reference: 95–100 mm Hg), PaCO2 44.8 mm Hg (normal reference: 35–45 mm Hg), and HCO3– 29.6 mmol/L (normal reference: 22–27 mmol/L). Chest X ray revealed patchy opacities in the right lower lung. The right diaphragmatic surface and costophrenic angle were also blurred. Furthermore, the cardiac silhouette was enlarged.
Treatment for pulmonary infection with cefoperazone-sulbactam (1.5 g every 12 h) was initiated. The patient also received subcutaneous insulin (30 units/day) and oral nifedipine sustained release tablet (30 mg daily). Peritoneal dialysis continued with 2.5% low calcium peritoneal dialysate.
At day 3 post admission, the patient became disoriented. He was still febrile (40.3°C). SPO2 declined to 88% despite of 5 L/min oxygen via a nasal cannula. Blood gas analysis showed pH 7.30, PaO2 53.10 mm Hg, PaCO2 58.50 mm Hg, and HCO3– 29.3 mol/L. Blood chemistry revealed that blood urea nitrogen (22.7 mmol/L) and serum creatinine (1345 µmol/L) continued to rise, and his plasma glucose also increased (8.4 mmol/L). K+, Na+, Cl+, and Ca++ were within normal range. His C-Reactive Protein (CRP) was 183 mg/L (normal reference: <8 mg/L), and procalcitonin 66.06 ng/mL (normal reference: <0.5 ng/mL). The liver function, platelet count, aPTT, and PT were normal. Thromboelastogram showed normal coagulation factor reaction time (9.9 min; normal reference: 5–10), fibrinogen reaction time (1.9 min; normal reference: 1–3), α (alpha) angle (64.9°; normal reference: 53°–72°), shear stress coefficient strength (19,233 d/s; normal reference: 4500–11,000 d/s), and hyperfibrinolysis (0.0%; normal reference: <8%) with increased platelet function (79.4 mm; normal reference: 50–70).
The patient was diagnosed with respiratory failure (type II) and pulmonoencephalopathy, and transferred to the intensive care unit (ICU) and placed on mechanical ventilation. Imipenem (0.5 g every 6 h) was added, and low-molecular-weight heparin (enoxaparin, 3500–5500 Da, 5–10 IU/kg/h) and insulin were delivered continuously by pumps. Peritoneal dialysis was discontinued and CVVH was undertaken at 32 mL/kg/h for renal insufficiency. The patient became oriented. Arterial blood gases showed normal pH (7.43), improved PaO2 (88.6 mm Hg), normal PaCO2 (36.5 mm Hg), and HCO3– (23.5 mmol/L). However, fever persisted (39.5°C), and the patient had difficulty weaning off mechanical ventilation.
Abdominal computed tomography (CT) at day 5 showed a hypointense shadow in the left hepatic lobe (61 mm × 56 mm) with an indistinct border (). Liver abscess was confirmed upon ultrasound-guided drainage. The culture revealed Klebsiella pneumonia that was sensitive to third-generation cephalosporin and imipenem. Imipenem (1.0 g every 8 h) and metronidazole (0.5 g every 8 h) were given, and mechanical ventilation and CVVH continued.
At day 12, the patient complained left back pain, which improved the next day without treatment. Platelet count (243 × 109/L) was normal, but both aPTT (67.5 s) and PT (17.3 s) were prolonged; his thromboelastogram (heparin cup) was normal. No cutaneous and mucosal bleeding was observed. The patient had no hemoptysis and his fecal occult blood test was negative. Abdominal CT scan at day 16 revealed left iliopsoas swelling, about 61.7 mm × 64.1 mm, with inhomogeneous densities, and occasional hyperintense opacities and an indistinct border (). A diagnosis of iliopsoas hematoma was made. Anticoagulation therapy with low-molecular-weight heparin was discontinued and switched to ex vivo anticoagulation with citrate. Mechanical ventilation and anti-infection therapy (imipenem 1.0 g every 8 h, metronidazole 0.5 g every 8 h) continued. No improvement was seen, and 3 days later, the patient died after his family decided to terminate therapy.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [145.0, 'mmol/L'], 'Chloride': [108.0, 'mmol/L'], 'Bicarbonate': [29.6, 'mmol/L']}",7.4,7.03,7.77,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 145.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 145.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 145.0 mmol * 1 mEq/mmol = 145.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 145.0 mmol sodium/L converts to 145.0 mEq sodium/L. 
The concentration of chloride is 108.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 108.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 108.0 mmol * 1 mEq/mmol = 108.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 108.0 mmol chloride/L converts to 108.0 mEq chloride/L. 
The concentration of bicarbonate is 29.6 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 29.6 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 29.6 mmol * 1 mEq/mmol = 29.6 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 29.6 mmol bicarbonate/L converts to 29.6 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 145.0 mEq/L - (108.0 mEq/L + 29.6 mEq/L) = 7.4 mEq/L. Hence, The patient's anion gap is 7.4 mEq/L."
6281,39,Anion Gap,lab test,decimal,pmc-7330196-1,Extracted,"A 64-year-old male visited a family medicine clinic due to lower extremity weakness lasting 1 month. The patient could not walk without assistance or walking aids. He was fully conscious and presented at the clinic in a wheelchair. He had numbness and a tingling sensation in his feet. There had been a 7 kg weight loss (from 60 to 53 kg) in a month. The patient had a past medical history of T2DM, diagnosed approximately 10 years previously. His medications were metformin 1000 mg daily and glipizide 10 mg daily; though he had irregularly attended his diabetes clinics, his adherence to medications was variable and he had had no recent follow-up or blood tests.
His vital signs were blood pressure, 141/93 mmHg; pulse, 108 beats per minute; respiratory rate, 20 breaths per minute; and temperature, 36.5°C. Physical examination of the nervous system revealed a decrease in motor power related to both hip flexion and elbow extension (grade 4). Pain sensation (tested by a pin prick test) was normal. Deep tendon reflexes of the knees and ankles indicated a slightly slow response (1+). The rest of his physical examination was normal.
Blood tests indicated a fasting plasma glucose (FPG) level of 650 mg/dL (36.1 mmol/L). Serum electrolytes were as follows: sodium, 135.3 mEq/L, potassium, 4.7 mEq/L, chloride, 97.3 mEq/L; and bicarbonate, 22.4 mEq/L. Serum creatinine was 1.4 mg/dL, and estimated glomerular filtration rate was 48.8 ml/min/1.73 m2. Thyroid function tests were normal. A glycated haemoglobin (HbA1c) was not taken at initial presentation.
The patient was referred to a district hospital because of symptomatic hyperglycaemia and poor mobility. During the patient’s 4-day hospital stay, the injectable insulin was prescribed to control his glucose level. The plasma glucose level was under control during the hospital stay and the weakness of the lower extremities improved. The patient could walk without assistance after hospital discharge. Subcutaneous insulin (30%/isophane 70% [mixtard 100 IU/ml] at 26 IU before breakfast and 14 IU before dinner) was prescribed after discharge from hospital. Six weeks later, the patient could walk to attend a follow-up visit at the family medicine clinic. Physical examination of the nervous system revealed normal muscle strength and normal muscle tone. The patient gained 5.9 kg of body weight (58.9 kg). The FPG was 281 mg/dL (15.6 mmol/L), and HbA1c was 10.9%. By the next follow-up visit (4 weeks later), the patient had made a full recovery from lower extremity weakness and could perform all activities of daily living. His body weight was 63 kg. His glycaemic test results were improved (FPG, 121 mg/dL [6.7 mmol/L]; HbA1c, 6.6%).",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [97.3, 'mEq/L'], 'Bicarbonate': [22.4, 'mEq/L'], 'Sodium': [135.3, 'mEq/L']}",15.6,14.82,16.38,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 135.3 mEq/L. 
The concentration of chloride is 97.3 mEq/L. 
The concentration of bicarbonate is 22.4 mEq/L. 
Plugging in these values into the anion gap formula gives us 135.3 mEq/L - (97.3 mEq/L + 22.4 mEq/L) = 15.6 mEq/L. Hence, The patient's anion gap is 15.6 mEq/L."
6282,39,Anion Gap,lab test,decimal,pmc-2703772-1,Extracted,"An 11-year-old female patient with a prior history of cardiac arrest arrived at the emergency room (ER) 35 minutes after losing consciousness. Her mother had immediately administered basic life support. The patient was born in the 40th gestational week by normal spontaneous vaginal delivery and weighed 4.0 kg. There was no specific family history of syncope or sudden cardiac death. Six years ago, she experienced a brief syncopal episode. Electroencephalography (EEG) at that time showed no specific abnormality. Six months after this first event, she was admitted to the ER for sudden loss of consciousness. Ventricular fibrillation (VF) was noted, and the normal sinus rhythm was restored by defibrillation. Neither delta wave nor QT interval prolongation was observed on a resting electrocardiogram (ECG) (). Echocardiography did not reveal any structural abnormalities, and Holter monitoring did not reveal specific arrhythmias. Brain magnetic resonance imaging (MRI) revealed no abnorzmalities. EEG was remarkable for dysrrhythmic waves and low amplitude voltage compatible with hypoxic encephalopathy. Although the definite cause of VF was not determined, it was recommended that the patient takes a beta-blocker (atenolol, 12.5 mg bid). She then underwent rehabilitation for cognitive function defects which resulted from hypoxic brain damage. She did not suffer any more attacks and stopped taking atenolol after several years.
Upon this ER arrival, the patient was unconscious, pulseless, and without spontaneous respirations. Blood pressure was undetectable, and her body temperature was 36.5℃. The initial ECG showed VF. Normal sinus rhythm was restored after 2 monophasic direct current defibrillations at 200 J (). On chest X-ray, no cardiomegaly or pulmonary congestion was observed. The laboratory test results were as follows: white blood cell count, 12,400/mm3; hemoglobin, 14.5 g/dL; platelet count, 188,000/mm3; sodium, 138 mmol/L; potassium, 5.7 mmol/L; chloride, 111 mmol/L; ionized calcium, 1.42 mmol/L; ionized magnesium, 1.06 mmol/L; creatine kinase, 124 U/L; and creatine kinase-MB, 0.9 ng/mL. An arterial blood gas test revealed the following: pH 7.13; PaCO2, 55.5 mmHg; PaO2, 59.8 mmHg; HCO3, 17.7 mmol/L; and SaO2, 80.1%.
After defibrillation and intubation, the patient was moved to the coronary care unit (CCU). During nasogastric tube insertion, VF redeveloped. Sinus rhythm was successfully restored by 2 defibrillations at 200 J. A review of telemetry monitoring in the CCU revealed that sinus tachycardia precipitated bidirectional ventricular tachycardia that in turn degenerated into VF ().
The patient was diagnosed with CPVT accompanied by typical bidirectional ventricular tachycardia which was triggered by sinus tachycardia. After intravenously administered beta-blocker (labetalol, 10 mg), tachyarrhythmia was no longer observed. After stabilization, echocardiography revealed an ejection fraction of 68% without any structural abnormalities. She was prescribed an oral beta-blocker (metoprolol, 100 mg bid) and discharged from hospital. She is currently being followed up.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [111.0, 'mmol/L'], 'Bicarbonate': [17.7, 'mmol/L'], 'Sodium': [138.0, 'mmol/L']}",9.3,8.835,9.765,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 138.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 138.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 138.0 mmol * 1 mEq/mmol = 138.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mmol sodium/L converts to 138.0 mEq sodium/L. 
The concentration of chloride is 111.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 111.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 111.0 mmol * 1 mEq/mmol = 111.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 111.0 mmol chloride/L converts to 111.0 mEq chloride/L. 
The concentration of bicarbonate is 17.7 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 17.7 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 17.7 mmol * 1 mEq/mmol = 17.7 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 17.7 mmol bicarbonate/L converts to 17.7 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 138.0 mEq/L - (111.0 mEq/L + 17.7 mEq/L) = 9.3 mEq/L. Hence, The patient's anion gap is 9.3 mEq/L."
6283,39,Anion Gap,lab test,decimal,usmle-187,Extracted,"A 62-year-old man is brought to the emergency department with fatigue, dry cough, and shortness of breath for 3 days. He reports a slight fever and has also had 3 episodes of watery diarrhea earlier that morning. Last week, he attended a business meeting at a hotel and notes some of his coworkers have also become sick. He has a history of hypertension and hyperlipidemia. He takes atorvastatin, hydrochlorothiazide, and lisinopril. He appears in mild distress. His temperature is 102.1°F (38.9°C), pulse is 56/min, respirations are 16/min, and blood pressure is 150/85 mm Hg. Diffuse crackles are heard in the thorax. Examination shows a soft and nontender abdomen. Laboratory studies show:
Hemoglobin 13.5 g/dL
Leukocyte count 15,000/mm3
Platelet count 130,000/mm3
Serum
Na+ 129 mEq/L
Cl- 100 mEq/L
K+ 4.6 mEq/L
HCO3- 22 mEq/L
Urea nitrogen 14 mg/dL
Creatinine 1.3 mg/dL
An x-ray of the chest shows infiltrates in both lungs.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [100.0, 'mEq/L'], 'Bicarbonate': [22.0, 'mEq/L'], 'Sodium': [129.0, 'mEq/L']}",7,6.65,7.35,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 129.0 mEq/L. 
The concentration of chloride is 100.0 mEq/L. 
The concentration of bicarbonate is 22.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 129.0 mEq/L - (100.0 mEq/L + 22.0 mEq/L) = 7.0 mEq/L. Hence, The patient's anion gap is 7.0 mEq/L."
6284,39,Anion Gap,lab test,decimal,pmc-2923795-1,Extracted,"A 74-yr-old woman was transferred to our emergency department from the local general hospital with an initial diagnosis of brain stem infarct on January 17, 2009. The patient was found unconscious and in a bed-ridden state during the early morning on the presenting day. The patient's breathing was shallow and irregular. The patient was unable to walk well due to a coccyx fracture two years ago, but she was able to perform daily life activities with minor help. One week ago, her facial edema started and she complained dry cough and general weakness three days ago. No other medical, familial, or social history was reported, and the patient had not taken any medication. There was also no evidence of intoxication.
According to the records of the local general hospital, the patient had an impending respiratory arrest and comatose mental status. Her blood pressure was 71/48 mmHg, her body temperature was 36.0℃, and her pulse rate was 99 beats/min with a sinus rhythm by electrocardiography (ECG). Neurologic examination revealed pinpoint pupils and a lack of brain stem reflexes, including the light reflex, corneal reflex, gag reflex, and doll's-eye phenomenon. She also showed decerebrated rigidity in response to painful external stimuli. The patient was assigned a score of 5 on the Glasgow Coma Scale, and the Babinski sign was detected at both feet. Brain computed tomography (CT) produced unremarkable results. Endotracheal intubation was performed for protection of the patient's airway, assisted ventilation was initiated, and an inotropic agent was injected to support the patient's state of shock, which did not respond to fluid therapy (1 L of normal saline). Prior to transfer, the patient's blood pressure was increased, but her neurologic findings were not improved. She was transferred to our hospital for further evaluation and treatment of a brain stem infarct.
On arrival, the patient's blood pressure was 70/40 mmHg, her pulse rate was 59 beats/min, and an intravenous infusion of premixed dopamine was administered (500 mL/800 mg, 20 µg/kg/min). The patient's body temperature was 34.8℃ according to a tympanic membrane thermometer, and her self-respiration was slow and shallow. The patient's lungs on auscultation were bilaterally clear, and cardiac examination showed a regular rate and rhythm without murmurs, gallops, or rubs. The patient's abdomen was soft without signs of guarding, tenderness, or rebound tenderness. A rectal examination revealed no masses, and the patient's stool was guaiac negative. No soiling due to urine or feces was noted on her undergarments.
The patient's face and extremities were edematous, and she presented with non-pitting edema. Her skin was dry, cool, pale, and slightly mottled and desquamated; however, there was no evidence of petechiae or purpura ().
The patient's level of consciousness was stupor to semi-coma. A neurologic examination revealed intact cranial nerves and she didn't show lateralizing signs. The patient's pupils were 3 mm across and briskly reactive. It was impossible to check for visual abnormalities and focal cerebellar findings. The results of the Babinski reflex test were negative.
The patient's laboratory values were as follows: WBC count 6,000/µL (86% neutrophils), hemoglobin 11.8 g/dL, sodium 121 mEq/L, potassium 4.2 mEq/L, chloride 87 mEq/L, BUN 1.3 mg/dL, creatinine 0.6 mg/dL, glucose 104 mg/dL, ALT 113 U/L, AST 74 U/L, albumin 3.3 g/dL, CK 499 IU/L, CK-MB 21.4 ng/mL, troponin-I <0.02 ng/mL, lactate 1.2 mM/L, urine RBCs 1-4/HPF, and urine WBCs 0-1.5/HPF. Arterial blood gas analysis (FiO2 1.0) revealed a pH of 7.486, a pCO2 of 30.6 mmHg, a pO2 of 36.4 mmHg, a HCO3- concentration of 22.9 mM/L, and an oxygen saturation of 77%.
A portable chest radiography revealed infiltration of the right lower lung zone and cardiomegaly. ECG revealed sinus bradycardia with no evidence of ischemia; the intervals and axis were normal except for a prolonged QTc interval. Echocardiography revealed a small amount of pericardial effusion, but it did not affect the patient's hemodynamic status.
During our resuscitative efforts, the patient's blood pressure didn't respond and additional laboratory test results confirmed hypothyroidism. The patient's free thyroxine was 0.05 ng/dL (0.93-1.7) and her TSH was 30.12 µIU/mL (0.27-5.0). A diagnosis of myxedema coma exacerbated by community-acquired pneumonia was thus assigned.
The patient was referred to the Department of Endocrinology and admitted to the intensive care unit for treatment and ventilatory support. The patient received 1,000 µg of levothyroxine orally for two days, followed by 300 µg/day for an additional three days and finally maintained on levothyroxine 0.1 mg orally each day. Following the administration of synthetic thyroid hormones for hypothyroidism and antibiotics for pneumonia, the patient regained consciousness and respiration. She was transferred to a general ward after two weeks in the intensive care unit and discharged from the hospital one week later.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [87.0, 'mEq/L'], 'Bicarbonate': [22.9, 'mmol/L'], 'Sodium': [121.0, 'mEq/L']}",11.1,10.545,11.655,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 121.0 mEq/L. 
The concentration of chloride is 87.0 mEq/L. 
The concentration of bicarbonate is 22.9 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 22.9 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 22.9 mmol * 1 mEq/mmol = 22.9 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 22.9 mmol bicarbonate/L converts to 22.9 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 121.0 mEq/L - (87.0 mEq/L + 22.9 mEq/L) = 11.1 mEq/L. Hence, The patient's anion gap is 11.1 mEq/L."
6285,39,Anion Gap,lab test,decimal,pmc-4590547-1,Extracted,"A 55-year-old nonsmoking unmedicated black woman without past surgical or medical history apart from mild untreated hypertension presented with deteriorated general condition, lethargy, and confusion. There was no personal or family history of thrombosis. A few weeks prior to admission, she had polyuria, polydipsia, and polyphagia. Laboratory findings mainly showed diabetic ketoacidosis (DKA) in the context of a new-onset diabetes with a pH of 7.22, partial pressure of carbon dioxide (pCO2) 12 mmHg, bicarbonates 5 mmol/L, random glucose 56.8 mmol/L, urinary ketones 7.8 mmol/L, sodium 158 mmol/L, chloride 111 mmol/L, potassium 7.9 mmol/L, urea 24.0 mmol/L, creatinine 302 µmol/L, international normalized ratio (INR) 1.16, partial thromboplastin time 25.5 s, and fibrinogen 5.92 g/L. The calculated osmolarity of 396.8 mOsm and intensity of the hyperglycemia evoked mixed features of hyperglycemic hyperosmolar state (HHS). A DKA protocol composed of intravenous insulin and normal saline fluid was started, and the latter rapidly changed to a quarter-normal saline and then dextrose 5% in water due to initial hypernatremia. Cerebral computed tomography scan showed no intracranial hemorrhage or other acute problems. No thromboprophylaxis was given. One of the two blood cultures returned positive for Gram-positive cocci in clusters 29.8 hours after admission for which vancomycin was started. Institutional Review Board approval as well as informed, written consent was not deemed necessary for the following retrospective review. All principles outlined in the Declaration of Helsinki were followed.
A peripherally inserted central catheter (PICC) line was installed on the left side on day 3 to facilitate fluid administration. The patient’s level of consciousness improved, as she was no longer confused. With regard to thromboprophylaxis, compression stockings were preferred to heparin because of thrombocytopenia (platelets at 199×109/L at arrival to 49 on day 4) with a normal coagulogram. Thrombotic thrombocytopenic purpura was contemplated, but no schistocyte was seen that day or on the two subsequent blood films. On day 4, the INR was slightly elevated at 1.33 (prothrombin time of 16.2 s) with a normal activated partial thromboplastin time of 27.5 s, a marginally low fibrinogen of 1.98 g/L, elevated D-dimers at >2 mg/L, and lactate dehydrogenase (LDH) of 334 U/L, revealing some extent of disseminated intravascular coagulation. On day 5, those values were stable, and the patient reported mild catheter-related discomfort that was relieved by acetaminophen. On day 6, platelet count was at 29×109/L and LDH was 848 U/L, and the patient was found to have dyspnea and tachypnea without chest pain, and left arm pain from shoulder to wrist as well as erythema without induration or edema. The patient had a blood pressure of 115/81 mmHg, heart rate 104/min, oxygen saturation 97%, respiratory rate 40/min, and temperature 36.7°C. On the left arm, no exudate was seen at the PICC line site. Radial pulse was nearly absent, and capillary refill was prolonged. There was hand numbness and motor function impairment from the elbow to the distal hand extremity. Arterial thrombosis and pulmonary emboli were suspected.
The vascular surgery team was contacted, and the patient immediately underwent a Doppler ultrasonography and angioscan which showed bilateral deep vein thrombosis (DVT) in legs, bilateral multiple pulmonary embolisms, and left subclavian artery thrombosis with significant extension in descending aorta. The concomitant events raised suspicions of paradoxical embolus through a patent foramen ovale (PFO). There was no evidence of cerebral involvement. A left subclavian thrombectomy was performed. The venous aspect of the clot clinically heightened the probability of a PFO. This was confirmed by transesophageal echocardiography (TOE) which showed left-to-right and spontaneous right-to-left shunts through a PFO but no thrombus. Unfractionated heparin was given as treatment for pulmonary embolisms as the patient was hemodynamically stable. Platelet transfusions were given as platelets count reached 25×109/L. Bacteria in the previously positive blood culture was identified as Micrococcus sp., a commensal organism considered nonpathogenic, so vancomycin was discontinued. Over 2 days, creatine kinase went from a high of 25,367 U/L to 6,331 U/L. Factor V (506) Leiden mutation and prothrombin 20210A mutation were ruled out. At discharge, the patient had regained most of her left arm’s motricity and had scheduled physiotherapy appointments. Warfarin bridging was done using tinzaparin until therapeutic INRs of 2–3 were reached. Long-term – possibly lifelong – anticoagulation was discussed, while PFO closure was not promoted.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [111.0, 'mmol/L'], 'Bicarbonate': [5.0, 'mmol/L'], 'Sodium': [158.0, 'mmol/L']}",42,39.9,44.1,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 158.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 158.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 158.0 mmol * 1 mEq/mmol = 158.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 158.0 mmol sodium/L converts to 158.0 mEq sodium/L. 
The concentration of chloride is 111.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 111.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 111.0 mmol * 1 mEq/mmol = 111.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 111.0 mmol chloride/L converts to 111.0 mEq chloride/L. 
The concentration of bicarbonate is 5.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 5.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 5.0 mmol * 1 mEq/mmol = 5.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 5.0 mmol bicarbonate/L converts to 5.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 158.0 mEq/L - (111.0 mEq/L + 5.0 mEq/L) = 42.0 mEq/L. Hence, The patient's anion gap is 42.0 mEq/L."
6286,39,Anion Gap,lab test,decimal,pmc-6629602-1,Extracted,"A 68-year-old man with sudden blindness presented at our emergency room. The day before, he had eaten sashimi and eel, and drank alcohol for dinner. Afterward, he experienced nausea, vomiting, and dizziness. His medical history included diabetes and hypertension. His diabetes, diagnosed more than 20 years ago, was at the time treated with metformin 1,000mg twice a day, glimepiride 2mg once a day, and linagliptin 5mg once a day. Concurrently, his hypertension was treated with telmisartan 80mg/amlodipine 5mg once a day.
At the time of admission to the emergency room, the patient's blood pressure was 104/57mmHg, heart rate 86 beats/min, body temperature 34.3℃, and the pulse oximeter reading was 98% on room air. The patient was alert and although the light reflex was intact, the patient reported seeing no light in either eye even when a penlight was shone into the eyes. No other focal neurological deficits were observed.
Brain computed tomography (CT) and brain magnetic resonance imaging & angiography (MRI & MRA) were performed. Brain CT and MRI showed no acute lesions. No significant stenosis of the cerebral artery was seen on MRA.
The first venous blood gas analysis (VBGA) test at admission showed pH, 6.78; pCO2, 26.7mmHg; pO2, 38 mmHg; bicarbonate, 4.0mmol/L; and total CO2<5 mmol/L. The first arterial blood gas analysis (ABGA) test showed pH, 6.93; pCO2, 16mmHg; pO2, 120mmHg; bicarbonate, 3.4mmol/L; total CO2, 4mmol/L; and SaO2, 95%. The initial laboratory data revealed the following: white blood cell (WBC), 35,300/µL; hemoglobin (Hb), 15.0 g/dL; platelets, 284,000 K/µL; BUN, 36.8mg/dL; creatinine, 2.31mg/dL; sodium 141.1mEq/L; potassium, 5.80mEq/L; chloride, 99.2mEq/L; total calcium, 9.9 mg/dL; phosphorus, 11.6mg/dL. Lactic acid was measured as >11mmol/L on admission. Urinalysis showed protein 2+, glucose −, and ketone 1+, and urine microscopy showed red blood cell (RBC) 3–5/HPF and WBC 6–10/HPF.
Massive hydration and intravenous sodium bicarbonate replacement were initiated for severe metabolic acidosis (lactic acidosis), but the metabolic acidosis did not change. Nevertheless, after three hours of hydration and sodium bicarbonate supplementation, while the metabolic acidosis remained unchanged, the patient's vision gradually recovered.
After 30 minutes of visual recovery, an ophthalmologic examination was performed. Diabetic retinopathy and cataract were found. No lesions that would cause blindness were identified ().
Although field of vision and visual acuity were restored, metabolic acidosis did not resolve completely (pH, 7.11; pCO2, 18mmHg; pO2, 77mmHg; bicarbonate, 5.7 mmol/L; total CO2, 6mmol/L; SaO2, 93% on ABGA). Hemodialysis (HD) was performed once, which resulted in decreased metabolic acidosis (pH, 7.49; pCO2, 30mmHg; pO2, 111mmHg; bicarbonate, 22.9mmol/L; total CO2, 23.8mmol/L; SaO2, 99% on ABGA). shows change in vital signs after admission. shows changes in metabolic acidosis and after admission.
shows the results of the tests performed during hospitalization. The patient did not undergo any further hemodialysis after admission. Metformin was discontinued, glimepiride was increased, and the patient was discharged after 6 days of hospitalization.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [141.1, 'mEq/L'], 'Chloride': [99.2, 'mEq/L'], 'Bicarbonate': [3.4, 'mmol/L']}",38.5,36.575,40.425,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 141.1 mEq/L. 
The concentration of chloride is 99.2 mEq/L. 
The concentration of bicarbonate is 3.4 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 3.4 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 3.4 mmol * 1 mEq/mmol = 3.4 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 3.4 mmol bicarbonate/L converts to 3.4 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 141.1 mEq/L - (99.2 mEq/L + 3.4 mEq/L) = 38.5 mEq/L. Hence, The patient's anion gap is 38.5 mEq/L."
6287,39,Anion Gap,lab test,decimal,pmc-3079651-1,Extracted,"A 23-year-old previously healthy Taiwanese male soldier presented with right ear pain and an eleven-day history of intermittent high fever, up to 39°C, after training in the jungle. He was admitted to a local clinic and amoxicillin/clavulanate 1 g was prescribed every 6 hours for otitis media, but the fever persisted. Furthermore, he developed a maculopapular skin rash over whole body and cramping abdominal pain with watery diarrhea appeared on the sixth day of fever. He was referred to our institution as his clinical condition has deteriorating with progressive dysponea and cough in the 4 preceding days. Physical examination showed an appearance of cardiopulmonary distress, icteric sclera, an eschar (Figure ) in the right external auditory canal and bilateral basal rales. Laboratory evaluation revealed a white blood cell count of 9100/mm3 (reference range [RR]: 4000-11000/mm3) with 87.9% segmented neutrophils, hemoglobin 14.6 g/dL (RR: 14-16 g/dL), platelet counts 24 × 103/mm3 (RR: 140-400 × 103/mm3), blood urea nitrogen 25 mg/dL, creatinine 1.5 mg/dl (RR: 0.7-1.4 mg/dL), sodium 140 mEq/L, potassium 3.9 mEq/L, chloride 108 mEq/L, calcium 8.2 mg/dL, total protein 5.8 g/dL (RR: 6.0-8.0 g/dL), albumin 3 g/dL (RR: 3.5-5.0 g/dL), total bilirubin 4.8 mg/dL (RR: 0.1-1.2 mg/dL), direct bilirubin 2.7 mg/dL (RR: 0.0-0.2 mg/dL), C-reactive protein 16.23 mg/dL (RR <0.3 mg/dL), aspartate aminotransferase (AST) 368 IU/L (RR: 8-38 IU/L), alanine aminotransferase (ALT) 271 IU/L (RR: 4-44 IU/L), alkaline phosphatase (ALK) 324 IU/L (RR: 50-190 IU/L), lactate dehydrogenase 783 IU/L (RR: 120-240 IU/L), glucose 94 mg/dL, creatine phosphokinase 229 IU/L (RR: 10-160 IU/L), and a positive for Weil-Felix reaction with a Proteus OX-K titer of 1:1280 on day 11 of fever. Arterial blood gas analysis was pH 7.501, PaCO2 38.1 mmHg, PaO2 76 mmHg, HCO3- 30.1 mmol/l, and BEB 7.2 with a FiO2 of 60%. A central venous line was setup for monitoring his central venous pressure and fluid replacement because of hypotension. Chest x-ray (Figure ) revealed bilateral diffuse infiltration. An endotracheal intubation was performed due to progressive dyspnea and desaturation, and then he was admitted to the intensive care unit. Doxycycline of 100 mg was prescribed every 6 hours for a clinical therapeutic trial of scrub typhus with ARDS and MOF. Fever subsided dramatically the next day and the endotracheal tube was removed on day 3. Chest x-ray abnormalities resolved gradually and full blood count and biochemistry results returned to normal ranges without sequelae. He was discharged on day 7 with tetracycline 500 mg every 6 hours for 7 days.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [108.0, 'mEq/L'], 'Bicarbonate': [30.1, 'mmol/L'], 'Sodium': [140.0, 'mEq/L']}",1.9,1.805,1.995,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mEq/L. 
The concentration of chloride is 108.0 mEq/L. 
The concentration of bicarbonate is 30.1 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 30.1 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 30.1 mmol * 1 mEq/mmol = 30.1 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 30.1 mmol bicarbonate/L converts to 30.1 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (108.0 mEq/L + 30.1 mEq/L) = 1.9 mEq/L. Hence, The patient's anion gap is 1.9 mEq/L."
6288,39,Anion Gap,lab test,decimal,pmc-8101516-1,Extracted,"An 81-year-old man presented to the gastroenterology clinic complaining of progressive dysphagia to solid food for 6 months. He had poor appetite and weight loss of 22 kg. He denied chest pain, regurgitation, cough, abdominal pain, nausea, vomiting, diarrhea, hematochezia, or melena. His past medical history was significant for essential hypertension, coronary artery disease, chronic hepatitis B infection, hypothyroidism, and sarcoidosis. The patient’s past surgical history was significant for coronary artery bypass grafting (CABG) surgery, bilateral cataract surgery, and multiple tooth extractions. Family history was noncontributory. Home medications included aspirin, quinapril, atenolol, levothyroxine, and entecavir. He denied using tobacco, alcohol, or illicit drugs.
On physical examination, the patient appeared chronically ill and cachectic. Vital signs demonstrated a temperature of 36.8 °C, blood pressure of 128/60 mmHg, heart rate of 65 beats per minute, and respiratory rate of 12 breaths per minute. Cardiovascular and lung exams were unremarkable. Abdominal exam showed a soft and non-tender abdomen with normal bowel sounds. Complete blood count (CBC) revealed a low hemoglobin of 11.6 g/dL and a mean corpuscular volume (MCV) of 63 fL consistent with microcytic anemia. Otherwise, the patient had a normal white blood cell (WBC) of 6.6 × 109/L and platelets of 167 × 109/L. Comprehensive metabolic panel (CMP) was within normal limits: Sodium 143 mmol/L, potassium 3.8 mmol/L, chloride 106 mmol/L, CO2 25 mmol/L, glucose 121 mg/dL, creatinine 0.81 mg/dL, BUN 12 mg/dL, calcium 9.4 mg/dL, total protein 6.5 g/dL, albumin 4.2 g/dL, total bilirubin 1.0 mg/dL, AST 12 U/L, ALT 12 U/L, and alkaline phosphatase 100 U/L.
An esophagogastroduodenoscopy (EGD) was performed to investigate the cause of dysphagia. EGD revealed a normal appearing esophagus, patchy erythema in the gastric antrum, normal appearing gastric body, and normal appearing duodenum (). A gastric biopsy was obtained, and histologic examination revealed glandular atrophy with acellular, eosinophilic deposits in the lamina propria and submucosa. Congo red stain revealed apple-green birefringence on polarized light consistent with gastric amyloidosis.
Further workup followed to evaluate the etiology of amyloidosis. Serum protein electrophoresis (SPEP) did not show a monoclonal (M) band. Urine protein electrophoresis (UPEP) did reveal the presence of proteinuria, but also failed to show an M band. Immunofixation showed elevated free kappa light chains of 104.90 mg/dL and an elevated free Kappa/Lambda ratio of 156.57. At this point, the patient was referred to a hematology/oncology specialist for a bone marrow biopsy. Bone marrow biopsy showed that plasma cells constituted 28.5% of the bone marrow consistent with multiple myeloma. The patient was started on lenalidomide, bortezomib, and dexamethasone. One month later, he was seen for a follow-up visit at the oncologist’s office. He reported improvement in dysphagia and weight gain of 1 kg. Unfortunately, the patient’s malignancy progressed, and his condition continued to deteriorate over the next 5 months. He eventually developed pneumonia complicated by septic shock, respiratory failure, and acute kidney injury. He was admitted to the intensive care unit where he suffered a sudden cardiac arrest and expired.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [106.0, 'mmol/L'], 'Bicarbonate': [25.0, 'mmol/L'], 'Sodium': [143.0, 'mmol/L']}",12,11.4,12.6,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 143.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 143.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 143.0 mmol * 1 mEq/mmol = 143.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mmol sodium/L converts to 143.0 mEq sodium/L. 
The concentration of chloride is 106.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 106.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 106.0 mmol * 1 mEq/mmol = 106.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 106.0 mmol chloride/L converts to 106.0 mEq chloride/L. 
The concentration of bicarbonate is 25.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 25.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 25.0 mmol * 1 mEq/mmol = 25.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 25.0 mmol bicarbonate/L converts to 25.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 143.0 mEq/L - (106.0 mEq/L + 25.0 mEq/L) = 12.0 mEq/L. Hence, The patient's anion gap is 12.0 mEq/L."
6289,39,Anion Gap,lab test,decimal,pmc-4446924-1,Extracted,"A 38-year-old man presented with nausea, vomiting and loose stools of 2 days duration. Patient gave history of consumption of a tuber taken from the nearby forest with the intent of deliberate self-harm. Patient has consumed the tuber 6 days prior to the presentation. It was followed by nausea, vomiting, loose stools and haematochezia on 4th day. He also complained haematuria and bleeding from gums and rectum on 5th day. On 6th day he observed scalp hair fall, and easy pluckability of beard, moustache and body hair. He also complained oliguria on day 6. Patient's wife has brought the tuber. It was identified as G. superba. Patient revealed that he had consumed 250 g of the tuber along with water.
Patient had no history of any illness. He was apprehensive, with pulse rate of 120 bpm, blood pressure 70/40 mmHg, febrile, with congestion of conjunctivae. The pillow and bed were full of his hair. Patient himself demonstrated easy pluckability of hair. His investigations were, haemoglobin 6.0 g/dl, total leucocyte count 14,000/mm3, differential count: polymorphs: 60, lymphocytes 30, monocytes 5, eosinophils 5%, erythrocyte sedimentation rate 40 mm after first hour, platelet counts 0.24 lakhs/mm3, peripheral smear showed no abnormal cells and no features of haemolysis, there was thrombocytopenia, random blood glucose 120 mg/dl, serum creatinine 5.4 mg/dl, blood urea 188 mg/dl, serum sodium 127 mEq/L, serum potassium 3.9 mEq/L, serum chloride 88 mEq/L, serum bicarbonate 12.0 mmol/L, serum bilirubin 1.0 mg/dl, serum glutamic oxaloacetic transaminase 45 U/L, serum glutamic pyruvic transaminase: 65 U/L, serum alkaline phosphatase 125 U/L, serum proteins 6.9 g/dl, serum albumin 4.3 g/dl, serum creatinine kinase 65 IU/L (reference range: 40–200 IU/L), fractional excretion of sodium <1%, urine microscopy showed plenty of red blood cells and urine myoglobin was negative. Ultrasound abdomen revealed normal sized kidneys. Electrocardiogram showed T inversion in V4, V5, and V6. Chest radiograph was normal.
He was initiated on intravenous fluids, sodium bicarbonate supplementation and ionopressors. He was transfused with two units of whole blood. Blood pressure improved after 24 h. The bleeding manifestations subsided over next 72 h. Serum creatinine fell over next 6 days. Hair loss continued for next 10 days. He lost entire scalp hair. Patient regained scalp hair after 4 months.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [88.0, 'mEq/L'], 'Bicarbonate': [12.0, 'mmol/L'], 'Sodium': [127.0, 'mEq/L']}",27,25.65,28.35,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 127.0 mEq/L. 
The concentration of chloride is 88.0 mEq/L. 
The concentration of bicarbonate is 12.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 12.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 12.0 mmol * 1 mEq/mmol = 12.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 12.0 mmol bicarbonate/L converts to 12.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 127.0 mEq/L - (88.0 mEq/L + 12.0 mEq/L) = 27.0 mEq/L. Hence, The patient's anion gap is 27.0 mEq/L."
6290,39,Anion Gap,lab test,decimal,pmc-4421254-1,Extracted,"A 47-year-old female was diagnosed with end-stage renal disease of unknown aetiology and on chronic haemodialysis twice weekly since 1994. She received a living-related kidney transplant in December 2003. Unfortunately, her transplant was complicated by graft rejection in December 2004 and haemodialysis became necessary in July 2005. In November 2007, she developed anaemia despite receiving 80 U/kg/week of erythropoietin. She was diagnosed with pure red cell aplasia from hypocellular bone marrow and positive anti-EPO in January 2008 and she needed chronic blood transfusions, of about 1–2 units of packed red blood cells per month. She developed iron overload in May 2008 with a serum ferritin level of 2650 ng/mL. She was treated with deferoxamine 1500 mg twice weekly.
In August 2008, the patient was struck by a fish bone in the right hand while she was boning fresh water fish. Subsequently, she developed a high-grade fever and generalized muscle pain the next day. Due to the progressive pain and redness of the wound, she presented to our hospital on the third day of fever.
On admission, the patient's body temperature was 39.2 °C, with a pulse rate of 100/min, a respiratory rate of 24/min and a blood pressure of 140/90 mmHg. The wound at the ridge of her right hand was swollen but there was no fluctuation (Figure ). Her right hand and right arm were also swollen and tender. Marked generalized muscle tenderness was noted which caused the patient to avoid moving her arms or legs. Initial laboratory investigation revealed that her white blood cell count (WBC) was 9700 cells/ mm3 with a neutrophil predominance. The haematocrit was 22.5% and platelet count was 101 000/mm3. Blood biochemistries showed sodium 129 mEq/L, potassium 6.23 mEq/L, chloride 93 mEq/L, bicarbonate 22.8 mEq/L, blood urea nitrogen 84 mg/dL, creatinine 15.9 mg/dL, aspartate transaminase 31 U/L, alanine transaminase 35 U/ L and creatinine phosphokinase (CPK) 1218 U/L. Urinalysis was marked positive for blood with marked proteinuria without red blood cell or white blood cell sediment.
Because of the severe sepsis, the patient received meropenem and vancomycin as empirical antibiotics. Blood cultures revealed Aeromonas hydrophila that was susceptible to the second and third generation of cepha- losporins, gentamicin, trimethoprim–sulfamethoxazole and fluoroquinolones. The antibiotics were switched to ceftriaxone after the results of the blood culture. Although fever rapidly subsided within 3 days, the WBC and CPK continued to rise. Meanwhile, she developed pustular skin lesions compatible with septic embolism over all extremities (Figure ). On the sixth day of admission, ciprofloxacin was added. Cultures from the skin lesion also recovered A. hydrophila. WBC peaked at 43 300 cells/mm3 on the 7th day of admission and returned to a normal value on the 15th day. CPK peaked at 13 317 U/L on the fourth day of admission and returned to a normal value on the ninth day (Figure ). She needed more frequent haemodialysis than her previous schedule during the first few days because of severe hyperkalaemia caused by rhabdomyolysis. No further skin lesion developed after the 11th day of admission. She was discharged on the 19th day of admission. The clinical course is shown in Figure .",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [93.0, 'mEq/L'], 'Bicarbonate': [22.8, 'mEq/L'], 'Sodium': [129.0, 'mEq/L']}",13.2,12.54,13.86,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 129.0 mEq/L. 
The concentration of chloride is 93.0 mEq/L. 
The concentration of bicarbonate is 22.8 mEq/L. 
Plugging in these values into the anion gap formula gives us 129.0 mEq/L - (93.0 mEq/L + 22.8 mEq/L) = 13.2 mEq/L. Hence, The patient's anion gap is 13.2 mEq/L."
6291,39,Anion Gap,lab test,decimal,usmle-5561,Extracted,"A 40-year-old woman with body mass index of 38 kg/m^2 presents to the emergency department with persistent bouts of epigastric pain for the past 2 hours with worsening nausea and vomiting. She has a history of polycystic ovarian syndrome and gastroesophageal reflux disease diagnosed by endoscopy, for which she takes omeprazole. She had a laparoscopic appendectomy 2 years ago. Her temperature is 98.3°F (36.8°C), blood pressure is 130/70 mmHg, pulse is 95/min, and respirations are 18/min. Her pulse oximeter reads 99% on room air. Abdominal tenderness is reproducible on physical exam without radiation in the upper abdomen. Her laboratory results are notable for the following:

Leukocyte count and differential:
Leukocyte count: 20,000/mm^3
Segmented neutrophils: 95%
Bands: 15%
Eosinophils: 2%
Basophils: 1%
Lymphocytes: 1%
Monocytes: 1%

Serum:
Na+: 135 mEq/L
Cl-: 100 mEq/L
K+: 4.2 mEq/L
HCO3-: 22 mEq/L
Urea nitrogen: 30 mg/dL
Glucose: 110 mg/dL
Creatinine: 1.1 mg/dL
Alkaline phosphatase: 50 U/L
Aspartate aminotransferase (AST, GOT): 25 U/L
Alanine aminotransferase (ALT, GPT): 15 U/L
Gamma-Glutamyltransferase (GGT): 1 U/L
Lipase: 250 IU/dL
Amylase: 300 IU/dL

She is admitted to the medical floor after being started on lactated ringer's solution and oxycodone as needed. Overnight, the patient complains that her pain is inadequately controlled. Her temperature is 98.3°F (36.8°C), blood pressure is 110/70 mmHg, pulse is 110/min, and respirations are 25/min. Her pulse oximeter reads 90% on room air. Her breathing is audible and labored with crackles heard on auscultation of her lungs bilaterally. After the patient is started on 10 liters of oxygen via nasal cannula, her SpO2 improves to 95%. An arterial blood gas is obtained:

pH 7.41
pCO2 30 mm Hg
pO2 125 mm Hg
HCO3 21 mEq/L
Base Excess +2

A chest radiograph is shown in Figure A.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [100.0, 'mEq/L'], 'Bicarbonate': [22.0, 'mEq/L'], 'Sodium': [135.0, 'mEq/L']}",13,12.35,13.65,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 135.0 mEq/L. 
The concentration of chloride is 100.0 mEq/L. 
The concentration of bicarbonate is 22.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 135.0 mEq/L - (100.0 mEq/L + 22.0 mEq/L) = 13.0 mEq/L. Hence, The patient's anion gap is 13.0 mEq/L."
6292,39,Anion Gap,lab test,decimal,pmc-6545788-1,Extracted,"A 27-year-old man with history of polysubstance abuse was witnessed to inhale “K2,” a synthetic cannabinoid. Over the next hour, he became unresponsive and was brought to an emergency room where he was found to be hypoxemic. There was no evidence of traumatic injury. He was intubated and admitted to the intensive care unit (ICU).
He had no other significant past medical history. Physical examination revealed an intubated and sedated patient; temperature was 97.1 °F, blood pressure was 144/84 mmHg, pulse was 98 beats/min, and oxygen saturation was 100% on FiO2 0.5; and bilateral coarse crackles were audible on chest auscultation.
Laboratory evaluation revealed WBC 10,900/dL, hemoglobin 12.6 g/dL, hematocrit 39.8 %, platelets 191,000/dL, sodium 140 meq/L, potassium 3.7 meq/L, chloride 102 meq/L, bicarbonate 19 mmol/L, BUN 13 mg/dL, creatinine 1.2 mg/dL, and creatine kinase 1,952 IU/L. Computed tomography (CT) of the brain showed no acute intracranial pathology. His initial arterial blood gas (ABG) values were pH 7.28, pCO2 58 mmHg, and pO2 125 mmHg on 50% oxygen. Chest radiography revealed alveolar opacities in the right upper lobe ().
The patient was started on broad-spectrum antibiotics. A urine and blood toxicology screen was positive for benzodiazepines (which he received after intubation) and negative for amphetamines, barbiturates, cocaine, opiates, phencyclidine, methadone, and cannabinoids. On the second day, frank blood was noted on suction from the endotracheal tube. His gas exchange worsened requiring a FiO2 1.0 to maintain adequate oxygenation. A blood gas showed profound hypoxemia with a pO2 110 mmHg. A chest radiograph revealed worsening bilateral alveolar infiltrates (). A CT of the chest revealed patchy ground glass opacities and diffuse lung consolidation (). Bronchoscopy was performed and showed oozing of blood from all right lung airways and the left lower lobe bronchus. Sequential bronchoalveolar lavage (BAL) confirmed diffuse alveolar hemorrhage by demonstrating increasingly bloody return. Hemosiderin laden macrophages were seen in BAL fluid on microscopy. Measurements of serum anti-nuclear antibody, anti-neutrophil cytoplasmic antibody, and anti-glomerular basement membrane antibody were negative. Urine analysis was negative for hematuria. BAL was negative for an infectious etiology. An echocardiogram was normal. There was no evidence of coagulopathy. UR- 144 N (4/5-hydroxypentyl), a metabolite of UR-144, was identified in the patient's blood by qualitative enzyme-linked immunosorbent assay (ELISA).
The patient was empirically treated with high-dose steroid for 3 days, followed by prednisone 40 mg/day that was tapered to 10 mg/day over 4 days and then discontinued. Over the 48 hours after corticosteroid administration, his oxygenation improved significantly. A chest radiograph performed 96 hours after admission showed complete resolution of the alveolar opacities. The patient was successfully extubated and transferred out of ICU. He was discharged 10 days after admission, neurologically and functionally intact.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [102.0, 'mEq/L'], 'Bicarbonate': [19.0, 'mmol/L'], 'Sodium': [140.0, 'mEq/L']}",19,18.05,19.95,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mEq/L. 
The concentration of chloride is 102.0 mEq/L. 
The concentration of bicarbonate is 19.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 19.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 19.0 mmol * 1 mEq/mmol = 19.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 19.0 mmol bicarbonate/L converts to 19.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (102.0 mEq/L + 19.0 mEq/L) = 19.0 mEq/L. Hence, The patient's anion gap is 19.0 mEq/L."
6293,39,Anion Gap,lab test,decimal,usmle-9759,Extracted,"A 71-year-old African American man is brought to the emergency department with a worsening productive cough and dyspnea for 2 days. He has had generalized bone pain for 2 months. He was admitted for pyelonephritis last month. He also received outpatient treatment for pneumonia almost 2 months ago. Over the past 2 months, he has been taking over-the-counter ibuprofen for pain as needed. He appears anxious. The vital signs include: temperature 38.8°C (101.8°F), pulse 95/min, respiratory rate 20/min, and blood pressure 155/90 mm Hg. The conjunctivae are pale. Crackles are heard in the right lower lobe. The cardiac examination shows no abnormalities. The laboratory studies show the following:
Hemoglobin 9 g/dL
Mean corpuscular volume 95 μm3
Leukocyte count 13,500/mm3
Segmented neutrophils 75%
Lymphocytes 25%
Platelet count 240,000/mm3
ESR 85 mm/hr
Serum
Na+ 135 mEq/L
K+ 4.2 mEq/L
Cl− 113 mEq/L
HCO3− 20 mEq/L
Ca+ 12.4 mg/dL
Albumin 4 g/dL
Urea nitrogen 38 mg/dL
Creatinine 2.2 mg/dL
A chest X-ray shows a right lower lobe opacity and blurring of the ipsilateral diaphragmatic dome. Skull and pelvic X-rays are performed (see image).",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [113.0, 'mEq/L'], 'Bicarbonate': [20.0, 'mEq/L'], 'Sodium': [135.0, 'mEq/L']}",2,1.9,2.1,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 135.0 mEq/L. 
The concentration of chloride is 113.0 mEq/L. 
The concentration of bicarbonate is 20.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 135.0 mEq/L - (113.0 mEq/L + 20.0 mEq/L) = 2.0 mEq/L. Hence, The patient's anion gap is 2.0 mEq/L."
6294,39,Anion Gap,lab test,decimal,pmc-7923710-1,Extracted,"A 32-year-old Caucasian female with a history of recently diagnosed systemic lupus erythematosus (SLE) presented to the emergency department with sudden-onset left-sided flank pain. The pain was dull and constant in origin with a score of 10 out of 10. She reported nausea but denied dysuria, hematuria, fever, chills, chest pain, shortness of breath, or changes in bowel function.
Seven weeks prior to this admission, she was hospitalized for autoimmune hemolytic anemia with a nadir hemoglobin level of 4.6 g/dL. Her hematologic workups were remarkable for positive antiglobulin test (Coombs test), nuclear dense fine speckled pattern on antinuclear antibodies screening with 1:640 titer, and positive anti-double-stranded DNA antibody of 259 IU/mL. Her recent C3 and C4 levels were diminished at 27 and 4 mg/dL, respectively. She was treated with intravenous methylprednisolone followed by packed red cell transfusion. Her hospital course was complicated by acute kidney injury with a presenting serum creatinine level of 2.20 mg/dL. Urine analysis showed 3+ occult blood and 2+ protein with a urine protein-creatinine ratio of 1.95 g/g. CT of the abdomen and pelvis was notable for small pericardial effusion and normal renal morphology. She was started on intravenous fluid and her serum creatinine level gradually improved. Her anemia and acute kidney injury improved, thus she was discharged home. At that time her hemoglobin level was 8.9 g/dL and her serum creatinine level was 1.22 mg/dL. Kidney biopsy was arranged as an outpatient procedure.
One week after discharge (or 9 days prior to the recent admission), she underwent a CT-guided core needle biopsy of the left kidney. The cortex was obtained from the lower pole of the left kidney. There were no immediate complications and the patient was discharged on the same day. The kidney biopsy showed immune complex-mediated proliferative glomerulonephritis, 2/5 global glomerulosclerosis, and mild arteriolar hyalinosis. These findings were consistent with International Society of Nephrology/Renal Pathology Society class III or IV lupus nephritis. No structures similar to small arterial aneurysmal wall were identified from the obtained core tissue. Induction therapy was not initiated at that time.
In this recent admission, the patient presented with sudden-onset left-sided flank pain. Initial vital signs were a temperature of 36.4°C, a heart rate of 100/min, a respiratory rate of 20/min, a blood pressure of 151/108 mm Hg, and an oxygen saturation of 100% on room air. She appeared pale and her left flank was tender to palpation, without discoloration or abdominal distention. Other parts of physical examination were unremarkable.
Initial investigations demonstrated hemoglobin 7.1 g/dL, hematocrit 20.5%, platelets 183,000/μL, and international normalization ratio 1.1. Metabolic panel showed serum sodium 140 mEq/L, serum potassium 3.8 mEq/L, serum chloride 104 mEq/L, serum bicarbonate 28.1 mEq/L, serum creatinine 1.11 mg/dL, and blood urea nitrogen 24 mg/dL.
A CT scan of the abdomen and pelvis with intravenous contrast medium (Fig. ) revealed a large hyperdense left perinephric collection consistent with perinephric hematoma with a moderate amount of retroperitoneal stranding most prominent on the left side extending across the midline to the right side. The retroperitoneal stranding stems from the level of the left hemidiaphragm to the left lower pelvis. Contrast extravasation was suspected in the lower pole of the left kidney consistent with active bleeding site. Chronic stranding in the right perinephric space was also noted.
The patient underwent emergent selective left renal artery coil embolization. The procedure was successful without any complications. Left renal angiography showed an approximately 2 × 1 cm intraparenchymal pseudoaneurysm in the lower pole of the left kidney with active extravasation. The coils were placed in the medial and lateral branches supplying the pseudoaneurysm (Fig. ). Small microaneurysms were also noted on angiography.
The patient followed with her nephrologist and hematologist after hospital discharge. Her flank pain completely resolved, and she received an induction therapy followed by maintenance therapy for her lupus nephritis.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [104.0, 'mEq/L'], 'Bicarbonate': [28.1, 'mEq/L'], 'Sodium': [140.0, 'mEq/L']}",7.9,7.505,8.295,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mEq/L. 
The concentration of chloride is 104.0 mEq/L. 
The concentration of bicarbonate is 28.1 mEq/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (104.0 mEq/L + 28.1 mEq/L) = 7.9 mEq/L. Hence, The patient's anion gap is 7.9 mEq/L."
6295,39,Anion Gap,lab test,decimal,usmle-11198,Extracted,"A 27-year-old female is brought in by ambulance with altered mental status. She is in a comatose state, but is breathing spontaneously with deep and rapid respirations. Her vital signs are as follows: T 100.2F, BP 92/54 mmHg, HR 103 bpm, RR 28, and SpO2 97% on room air. Complete blood count reveals: WBC 12.7, hemoglobin 11.3, platelets 254. Basic metabolic panel reveals: sodium 137, potassium 4.2, chloride 100, bicarbonate 16, creatinine 1.78 An ABG is performed which showed pH 7.38, PaO2 94, PaCO2 26.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [100.0, 'mEq/L'], 'Bicarbonate': [16.0, 'mEq/L'], 'Sodium': [137.0, 'mEq/L']}",21,19.95,22.05,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 137.0 mEq/L. 
The concentration of chloride is 100.0 mEq/L. 
The concentration of bicarbonate is 16.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 137.0 mEq/L - (100.0 mEq/L + 16.0 mEq/L) = 21.0 mEq/L. Hence, The patient's anion gap is 21.0 mEq/L."
6296,39,Anion Gap,lab test,decimal,pmc-6590859-2,Extracted,"Case 2 presentation
The patient is a 62-year-old African American male with an unknown past medical history who was brought by EMS after being found down at his home without heat by his neighbor.
On physical examination, his vital signs were: rectal temperature was 28.5 °C, heart rate 94 bpm, respiratory rate 22 breaths/min, and blood pressure 170/100 mmHg. On presentation, his Glasgow Coma Scale was 8 (E4 V1 M3). He was found to be non-responding verbally, pupils were reactive to light, lungs clear to auscultation, the heart had regular rate and rhythm. He was intubated in the emergency department.
Initial laboratory with blood gas analysis showed a metabolic and respiratory acidosis with the following pH 7.103; pCO2 65.6 mmHg; pO2 514.9 mmHg; HCO3 20.0 mmHg on the following ventilator settings: tidal volume 450 mL, respiratory rate 18 breaths/min, fraction of inspired oxygen (FiO2) 100% and positive end-expiratory pressure (PEEP) of 5 cmH2O. Other laboratory findings were the following: sodium 165 mmol/L, potassium 3.0 mmol/L, chloride 122 mmol/L, carbon dioxide (CO2) 18 mmol/L, glucose 182 mg/dL, blood urea nitrogen (BUN) 86 mg/dL, creatinine 1.83 mg/dL, AST 92 U/L, ALT 56 U/L, lipase 300 U/L, creatinine kinase 1,661 U/L, troponin 0.02 ng/mL, white blood cell count (WBC) 29.50 x 103 cmm, hemoglobin 5.4 g/dL, platelets 225 x 103 cmm, PT 17 sec, INR 1.5, APTT 36.4 sec, lactic acid 6.3 mmol/L. Urine drug screening was negative for any substances and alcohol level was <10 mg/dL. Initial EKG showed atrial fibrillation with premature ventricular complexes, left axis deviation, lateral injury pattern. Initial chest x-ray showed diffuse opacities on bilateral lung fields consistent with aspiration pneumonitis or infection.
The patient was admitted to the Intensive Care Unit (ICU) for rewarming with IV fluids and Bair Hugger (3M temperature management system). He developed multifactorial shock and was started on vasopressors, blood transfusion, and antibiotics. An echocardiogram was done 2 days after admission for shock investigation which demonstrated moderate left ventricular hypertrophy, anteroseptal and anterior akinesis with global hypokinesis, ejection fraction 25% with suspicion of apical thrombus and left atrial enlargement (Figure ).
Outcome and Follow-up
The patient was later started on anticoagulation after anemia resolved but anticoagulation was later held as he developed a psoas hematoma. He had 2 subsequent echocardiograms including a transesophageal echocardiogram during hospitalization that were concerning for apical thrombus. The patient was later discharged to a nursing home facility after 80 days of hospitalization with multiple complications.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [122.0, 'mmol/L'], 'Bicarbonate': [20.0, 'mmol/L'], 'Sodium': [165.0, 'mmol/L']}",23,21.85,24.15,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 165.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 165.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 165.0 mmol * 1 mEq/mmol = 165.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 165.0 mmol sodium/L converts to 165.0 mEq sodium/L. 
The concentration of chloride is 122.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 122.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 122.0 mmol * 1 mEq/mmol = 122.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 122.0 mmol chloride/L converts to 122.0 mEq chloride/L. 
The concentration of bicarbonate is 20.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 20.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 20.0 mmol * 1 mEq/mmol = 20.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 20.0 mmol bicarbonate/L converts to 20.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 165.0 mEq/L - (122.0 mEq/L + 20.0 mEq/L) = 23.0 mEq/L. Hence, The patient's anion gap is 23.0 mEq/L."
6297,39,Anion Gap,lab test,decimal,pmc-5458028-1,Extracted,"A 58-year-old male with dyslipidemia, an eight-year history of T2DM, a family history, his mother, of T2DM, with no known micro- or macrovascular complications, was admitted to the emergency department for malaise, epigastric pain, polyuria, and progressive dyspnea which had begun 10 h ago. He had experienced a 2-kg weight loss over the last few days. His usual medications included aspirin 100 mg q24 h, atorvastatin 40 mg q24 h, and metformin 850 mg q8 h, which had been switched to dapagliflozin 20 days before, due to poor glycemic control, with HbA1c 12% (108 mmol/mol). His vital signs included a heart rate of 122 bpm, respiratory rate 33 rpm, blood pressure 142/70 mmHg, temperature 36.1°C, and body mass index 22.5 kg/m2. On physical examination, somnolence, dry skin and mucous membranes, a Kussmaul breathing pattern, and a capillary refill of 3 sec were observed. Blood tests revealed hemoglobin 17.1 g/dL (13.5–18), leukocytes 19.5 × 103 (4–10 × 103), platelets 296 × 103 (150–450 × 103), glucose 248 mg/dL (60–100), creatinine 0.97 mg/dL (0.67–1.17), sodium 136 mmol/L (135–145), potassium 4.7 mmol/L (3.5–5.5), chloride 101 mmol/L (95–112), phosphate 4.9 mg/dL (2.5–4.5), amylase 70 U/L (10–115), lipase 28 U/L (1–67), pH 6.95 (7.35–7.45), pCO2 23 mmHg (35–45), HCO3 5 mmol/L (22–26), lactate 1.8 mmol/L (0–1.5), urine ketone bodies >150 mg/dL (0–0), CK 112 U/L (1–190), CK-MB 7.3 ng/mL (0.1–5), and troponin I 0.07 ng/mL (0.001–0.05). The electrocardiogram (EKG) showed sinus rhythm with right bundle branch block, and nonspecific repolarization abnormalities. Because of the right bundle branch block was not previously known, a new troponin test was performed six hours later with a peak value of 4.28 ng/mL. Treatment with crystalloids, continuous infusion of intravenous insulin, and administration of potassium and sodium bicarbonate were begun in the emergency room (ER). Due to a poor response over the first two hours, with the persistence of lactic acidosis, the patient was transferred to the intensive care unit (ICU), where more aggressive rehydration with crystalloids was started, without further modifications of the original therapeutic plan.
Two days later, the patient was discharged from the ICU to the endocrinology ward. Because of his coronary risk factors and the elevated troponin on admission, a coronary angiography was performed, showing triple-vessel disease. Successful bypass surgery without extracorporeal circulation was performed a few days later, with internal mammary artery grafts to the anterior descendent and marginal obtuse arteries and a saphenous vein graft to the right coronary artery. He was discharged 3 days later on Lantus™ Sanofi-aventis S.p.a Valcanello,03012 Anagni (FR), Italia (insulin glargine) 20 IU and Insulina Novorapid™: Novo Nordisk A/S. Hallas Allé, DK-4400. Kalundborg, Dinamarca (insulin aspart) 6-4-4-0 IU subcutaneous insulin, aspirin, clopidogrel, enalapril, bisoprolol, atorvastatin, and furosemide. The oral antidiabetic treatment with dapagliflozin was not restarted. During follow-up by endocrinology, C-peptide, anti-GAD, and IA-2 antibodies were required due to normal BMI and lack of family history suggested T1DM or a latent autoimmune diabetes of adults (LADA) rather than T2DM as etiology of his diabetes. C-peptide was 1 mg/dL (0.9–7.1) with glycemia 214 mg/dL (60–100), anti-GAD <5 U/mL (0–12.5), and anti-IA-2 <7.5 U/mL (0–7.5).",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [101.0, 'mmol/L'], 'Bicarbonate': [5.0, 'mmol/L'], 'Sodium': [136.0, 'mmol/L']}",30,28.5,31.5,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 136.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 136.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 136.0 mmol * 1 mEq/mmol = 136.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mmol sodium/L converts to 136.0 mEq sodium/L. 
The concentration of chloride is 101.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 101.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 101.0 mmol * 1 mEq/mmol = 101.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 101.0 mmol chloride/L converts to 101.0 mEq chloride/L. 
The concentration of bicarbonate is 5.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 5.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 5.0 mmol * 1 mEq/mmol = 5.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 5.0 mmol bicarbonate/L converts to 5.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 136.0 mEq/L - (101.0 mEq/L + 5.0 mEq/L) = 30.0 mEq/L. Hence, The patient's anion gap is 30.0 mEq/L."
6298,39,Anion Gap,lab test,decimal,pmc-7236346-1,Extracted,"A 63-year-old male with hypertension and seizure disorder presented to the renal clinic with a blood pressure of 220/110 mmHg, headache and neck pain and was sent to the emergency department. His review of systems showed that he had a 2-month history of bilateral ankle pain, anasarca, progressive renal impairment, weakness and fatigue, associated with a history of loss of appetite for this period of time. A renal workup revealed nephrotic-range proteinuria and microscopic hematuria, with urinalysis showing red cells and protein. CBC showed a hemoglobin of 8.6 g/dL, white cell count of 7.7 K/uL and a platelet count of 146 K/uL. Blood chemistry showed sodium of 146 mmol/L. potassium of 4.5 mmol/L, bicarbonate of 25 mmol/L, chloride of 113 mmol/L, BUN of 61 mg/dL and a creatinine of 4.08 mg/dL. Serology was negative for antinuclear antibody, antineutrophil cytoplasmic antibodies, rheumatoid factor, anti-double stranded DNA antibody, lupus anticoagulant, cryoglobulins and viral markers (HBV, HCV and HIV). Complement levels were normal. Serum and urine protein electrophoresis were negative for a monoclonal protein. Although he had slightly low haptoglobin, his ADAMTS13 level was within normal limits. A renal core biopsy showed predominantly medulla and a small cortical sample, containing up to 12 glomeruli of which one glomerulus was globally sclerosed. All patent glomeruli showed segmental or global occlusion of capillary loops by PAS-positive eosinophilic pseudothrombi which were non-argyrophilic and stained magenta red on trichrome (Fig. a-c); some of the glomeruli had a membranoproliferative pattern associated with mild mesangial hypercellularity and segmental double contours (Fig. b, PAS stain). A single artery sampled showed moderate arteriosclerosis but no thrombi. The interstitium was unremarkable except for patchy fibrosis. On immunofluorescence microscopy (IF), the pseudothrombi stained for IgA, kappa and lambda (Fig. d-f) and were negative for the other immunoreactants; some pseudothrombi also showed intensely staining bright foci that were more numerous in kappa than in lambda (arrow). Electron microscopy (EM) of 2 glomeruli showed several capillary loops lined by swollen endothelial cells, with occluding intra-luminal electron-dense crystals; all the crystals showed a lattice-like substructure with parallel linear arrays. No conventional immune complex-type electron-dense deposits or fibrin tactoids were seen within the glomeruli (Fig. a-c). Crystals were also not seen within proximal tubular epithelial cells. Occasional loops showed mild subendothelial widening along with rare cell interposition. A diagnosis of crystalglobulin-associated nephropathy (CAN) with possible kappa restriction was favored. Paraffin-IF with pronase digestion could not be performed as no glomeruli remained in the paraffin block. Subsequent testing with immunogold EM showed preferential association of kappa particles for the crystals, confirming kappa restriction of the crystals (Fig. d-f). A repeat serum electrophoresis 3 months later showed IgA kappa and trace amount of IgG lambda while urinary protein electrophoresis remained negative; a free light chain assay showed a kappa/lambda ratio of 3.9. Bone marrow and peripheral blood flow cytometry at this time showed a small clonal B-cell population (0.19 K/uL) with kappa restriction and a chronic lymphocytic leukemia (CLL) phenotype, co-expressing CD5 and CD23 and being negative for CD10 and CD103. No organomegaly or lymphadenopathy was present in the patient. A diagnosis of CAN presenting as MGRS in the background of monoclonal B-cell lymphocytosis (MBL) was confirmed in the patient. Since the diagnosis, the patient has been dialysis-dependent. A hemato-oncology referral was sought in view of the patient’s MGRS finding but because of the low clonal B-cell count coupled with extreme frailty and recurrent episodes of C.difficile diarrhea in the patient, no specific hematologic treatment was decided to be initiated by the clinical team till the patient became clinically more stable.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [113.0, 'mmol/L'], 'Bicarbonate': [25.0, 'mmol/L'], 'Sodium': [146.0, 'mmol/L']}",8,7.6,8.4,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 146.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 146.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 146.0 mmol * 1 mEq/mmol = 146.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 146.0 mmol sodium/L converts to 146.0 mEq sodium/L. 
The concentration of chloride is 113.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 113.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 113.0 mmol * 1 mEq/mmol = 113.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 113.0 mmol chloride/L converts to 113.0 mEq chloride/L. 
The concentration of bicarbonate is 25.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 25.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 25.0 mmol * 1 mEq/mmol = 25.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 25.0 mmol bicarbonate/L converts to 25.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 146.0 mEq/L - (113.0 mEq/L + 25.0 mEq/L) = 8.0 mEq/L. Hence, The patient's anion gap is 8.0 mEq/L."
6299,39,Anion Gap,lab test,decimal,pmc-4893599-1,Extracted,"An 81-year-old lady was admitted to our hospital with recurrent falls associated with brief loss of consciousness. She denied any other cardiac symptoms. Her past medical history included an embolic cerebrovascular event a year earlier with no residual focal neurology, hypertension, treated hypothyroidism, diverticulosis, anaemia of chronic disease, and chronic noninfective diarrhoea of 3 years' duration. This had been extensively investigated by several gastroenterologists and colorectal surgeons.
On admission she was passing 8–10 loose motions a day. She was on treatment with levothyroxine 125 micrograms OD, clopidogrel 75 mg OD, aspirin 75 mg OD, atorvastatin 40 mg OD, ranitidine 150 mg BD, zopiclone 7.5 mg OD, citalopram 10 mg OD, folic acid 5 mg OD, loperamide 2 mg TDS, co-codamol 8/500 2 tablets QDS, and desloratadine 5 mg OD.
On examination she was apyrexial, the pulse was 60 beats per minute and regular, and the supine blood pressure was 157/55 mmHg. Saturation on air was 95%. The rest of the cardiovascular, respiratory, and abdominal examination was within normal limits. There were no history of liquorice use, no clinical evidence of somatic neuropathy, and no evidence of adrenal adenomas on abdominal CT examination done prior to admission.
The investigations were as follows: haemoglobin 12.7 g/L, sodium 143 mmol/L, potassium 3.0 mmol/L, chloride 101 mmol/L, bicarbonate 27.6 mmol/L, pH 7.46, magnesium 0.72 mmol/L, adjusted calcium 2.21 mmol/L, phosphate 1.08 mmol/L, TSH 0.22 μ/mL, free T4 25 pmol/L, and C Reactive Protein (CRP) 89 mg/L. The admission resting ECG revealed ventricular bigeminy and prolongation of the QTc at 519 msec (normal for females < 470 msec), measured using Bazett's formula as heart rate was less than 65 bpm. Telemetry and Holter analysis confirmed the presence of multiple episodes of polymorphic VT (Torsades de Pointes) (). An echocardiogram confirmed a structurally normal heart with a normal ejection fraction of greater than 55%. Coronary angiography confirmed normal appearances with no evidence of overt coronary artery disease.
The patient's episodes of polymorphic VT stopped following administration of intravenous and oral potassium as well as magnesium supplementation () and the discontinuation of citalopram, which has been associated with development of long QT syndrome and Torsade de Pointes as an adverse drug reaction []. The QTc normalised within 48 hours following this. The patient was treated with loperamide 4 mg prn and amiloride 5 mg daily to correct the hypokalaemia. Following these interventions potassium levels remained above 4.0 mmol/L. Despite the administration of amiloride and normalisation of the potassium the patient was still experiencing ongoing diarrhoea. Additionally there were past blood tests (ordered by the patient's GP) documenting low potassium levels in the preceding 2 years. With that in mind the cardiology MDT felt that the precipitating cause of the Torsades de Pointes was not fully addressed and thus an ICD would offer the best change of preventing an arrhythmic death. An ICD (dual chamber, Medtronic Evera) was thus prophylactically implanted. Due to the patient's age and in the absence of any previous or family history of syncope and ventricular arrhythmias no genetic tests were performed.
On follow-up after six months, she remained asymptomatic with no further syncopal events or symptoms of light headedness, blurred vision, or feeling faint. Repeat blood tests by her GP at 3 and 6 months showed potassium of 4.1 and 4.2 mmol/L, respectively, and she was continuing to take amiloride. No arrhythmias were detected on interrogation of the ICD at the follow-up.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [101.0, 'mmol/L'], 'Bicarbonate': [27.6, 'mmol/L'], 'Sodium': [143.0, 'mmol/L']}",14.4,13.68,15.12,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 143.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 143.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 143.0 mmol * 1 mEq/mmol = 143.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mmol sodium/L converts to 143.0 mEq sodium/L. 
The concentration of chloride is 101.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 101.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 101.0 mmol * 1 mEq/mmol = 101.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 101.0 mmol chloride/L converts to 101.0 mEq chloride/L. 
The concentration of bicarbonate is 27.6 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 27.6 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 27.6 mmol * 1 mEq/mmol = 27.6 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 27.6 mmol bicarbonate/L converts to 27.6 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 143.0 mEq/L - (101.0 mEq/L + 27.6 mEq/L) = 14.4 mEq/L. Hence, The patient's anion gap is 14.4 mEq/L."
6300,39,Anion Gap,lab test,decimal,usmle-8822,Extracted,"A 55-year-old man is brought to the emergency department with altered mental status. The patient is in acute distress and cannot provide history due to disorientation. Temperature is 38.7°C (101.6°F), blood pressure is 80/50 mm Hg, pulse is 103/min, respiratory rate is 22/min, and BMI is 20 kg/m2. On examination, his sclera and skin are icteric. On abdominal examination, the patient moans with deep palpation to his right upper quadrant.
Laboratory test
Complete blood count
Hemoglobin 14.5 g/dL
MCV 88 fl
Leukocytes 16,500/mm3
Platelets 170,000/mm3
Basic metabolic panel
Serum Na+ 147 mEq/L
Serum K+ 3.8 mEq/L
Serum Cl- 106 mEq/L
Serum HCO3- 25 mEq/L
BUN 30 mg/dL
Serum creatinine 1.2 mg/dL
Liver function test
Total bilirubin 2.8 mg/dL
AST 50 U/L
ALT 65 U/L
ALP 180 U/L
The patient is treated urgently with intravenous fluid, dopamine, and broad spectrum antibiotics. The patient’s blood pressure improves to 101/70 mm Hg. On ultrasound of the abdomen, the common bile duct is dilated.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [106.0, 'mEq/L'], 'Bicarbonate': [25.0, 'mEq/L'], 'Sodium': [147.0, 'mEq/L']}",16,15.2,16.8,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 147.0 mEq/L. 
The concentration of chloride is 106.0 mEq/L. 
The concentration of bicarbonate is 25.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 147.0 mEq/L - (106.0 mEq/L + 25.0 mEq/L) = 16.0 mEq/L. Hence, The patient's anion gap is 16.0 mEq/L."
6301,39,Anion Gap,lab test,decimal,pmc-5661137-1,Extracted,"A 63-year-old woman with biopsy-confirmed SCLC metastatic to the liver developed rash and lesions to the face, chest, back, and oral mucosa that coincided with initiating topotecan therapy ( and B). A physical examination revealed erythematous edematous plaques with central tense bullae and crusting on the forehead, posterior auricular region, and chest. Multiple bullae drained serosanguinous fluid, Nikolsky’s sign was absent, and multiple ulcers were found within the oral mucosa.
A skin biopsy revealed dermatitis that was initially suspected to be due to a drug reaction. However, her symptoms worsened despite oral prednisone therapy and discontinuation of topetecan. One week after rash onset, she developed angioedema, generalized weakness, and myalgia most prominent in her proximal extremities. The patient also reported difficulty transferring from her bed or lifting her upper extremities. Laboratory findings revealed abnormal levels of: creatine phosphokinase (CPK) 25,865 IU/L (normal range 26-174), aldolase 40.3 U/L, sodium 125 mmol/L (normal range 135-146), chloride 71 mmol/L (normal range 96-107), bicarbonate 17 mmol/L (normal range 21-31), lactic acid 7.1 mmol/L (normal range 0.5-22), aspartate transaminase (AST) 878 IU/L (normal range 0-32), alanine transaminase (ALT) 312 IU/L (normal range 10-35), white blood cells 15.45 K/uL (normal 4.8-10.8). Urine analysis found large blood on dipstick and <1 red blood cell per high-powered field.
Bedside sonogram showed trace pericardial effusion and grossly preserved cardiac contractility. Magnetic resonance imaging of her neck revealed soft tissue thickening and diffuse heterogeneous enhancement of muscles. Histopathologic examination of her left bicep muscle showed strongly-positive HLA Class I immunohistochemistry without myofiber necrosis and mild-to-moderate type 2 myofiber atrophy ( and B). Antinuclear antibody titer was positive at a 1:640 dilution with a speckled pattern. Antip155/ 140 antibody was positive. The remainder of the myositis antibody comprehensive panel, extractable nuclear antigen screening (anti-ENA), and paraneoplastic autoantibody panel were negative (anti-Jo- 1, anti-SSA 52, anti-SSA 60, anti-Mi-2, anti-PL-7, anti-PL-12, anti-EJ, anti-Ku, anti-U2 sn RNP, anti-SRP, anti-OJ, anti PM/Scl complex, anti-neuronal nuclear antibody types 1, 2, and 3; anti-glial nuclear antibody, anti-PCA-1, anti-PCA2, anti- PCA-Tr, anti-Amphiphysin, anti-CRMP-5, anti-striational, anti-P/Q-type calcium channel, anti-N-type calcium channel, anti- Ach receptor binding antibody, anti-ACHr Ganglionic neuronal antibody).
The patient was initially treated with intravenous fluids and oral prednisone. She was then advanced to intravenous methylprednisolone and intravenous immunoglobulin therapy, resulting in a gradual decline of the CPK level to less than 1300 IU/L and improvement of her rash and erythematous plaques. During this time, she had progressive dysphagia, odynophagia, and oral thrush concerning for esophageal candidiasis. Despite treatment with oral nystatin rinses, which resolved her oral thrush, the patient continued to have worsening symptoms of dysphagia. Videoscopy revealed acutely-worsening dysphagia and CT-imaging demonstrated laryngeal edema. She was intubated to protect her airway, started on plasmapheresis, and fed through a nasogastric tube. Although the CPK level declined to less than 1000 IU/L, her edema and weakness persisted. Thereafter, the patient was transferred to hospice care and comfort measures were implemented.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [71.0, 'mmol/L'], 'Bicarbonate': [17.0, 'mmol/L'], 'Sodium': [125.0, 'mmol/L']}",37,35.15,38.85,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 125.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 125.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 125.0 mmol * 1 mEq/mmol = 125.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 125.0 mmol sodium/L converts to 125.0 mEq sodium/L. 
The concentration of chloride is 71.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 71.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 71.0 mmol * 1 mEq/mmol = 71.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 71.0 mmol chloride/L converts to 71.0 mEq chloride/L. 
The concentration of bicarbonate is 17.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 17.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 17.0 mmol * 1 mEq/mmol = 17.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 17.0 mmol bicarbonate/L converts to 17.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 125.0 mEq/L - (71.0 mEq/L + 17.0 mEq/L) = 37.0 mEq/L. Hence, The patient's anion gap is 37.0 mEq/L."
6302,39,Anion Gap,lab test,decimal,pmc-4949203-1,Extracted,"A 42-year-old man presenting an anterior chest pain, visited the emergency room. According to his medical history, although he visited the hospital with a chest pain repeatedly, heart work up, like electrocardiography and cardiac muscle enzymes, showed non-specific findings and a trans-thoracic echocardiogram revealed normal heart function. He did not take any drugs or herbal medications. On physical examination, blood pressure was 110/60mmHg and pulse rate was 82/min and regular. There was no pretibial edema or other neurologic abnormalities. The results of the blood test showed: sodium 140mEq/L, potassium 2.7mEq/L, chloride 91mEq/L, total calcium 9.3mg/dL (9.5-10.9), ionized calcium 2.09mmol/L(2.3-2.58), magnesium 1.1mg/dL (1.9-2.5), ionized magnesium 0.26mmol/L (0.45-0.6) and trans-tubular potasium gradient (TTKG) 12.68. Arterial blood gas analysis showed: pH 7.459, pCO2 42.4mmHg, pO2 88.5mmHg, HCO3 29.7mEq/L, and SaO2 97.3%. The results of urinalysis showed: sodium 80mEq/L, potassium 28.2mEq/L, chloride 148mEq/L, calcium 2.3mg/dL, creatinine 21.7mg/dL, spot urine Ca/Cr 0.1, and 24 hours urine magnesium 21.0mEq/L/day (5-17). Laboratory test showed hypochloremic metabolic alkalosis with hypokalemia, hypomagnesemia and hypocalciuria. Chest X-ray and kidney ultrasonography showed nonpathognomonic findings.
To evaluate for hypokalemia, which persists over 10 years combined with other electrolyte imbalances, we took an ultrasonography guided kidney biopsy. There were 3 global sclerosises among 51 glomeruli, and the light microscopy finding was normal without minimal increase of mesangial cell proliferation. Immunofluorescence findings showed all negativity for IgG, IgA, IgM, C3, C4, C1q, and lambda in the glomerulus. The result of the immunohistochemistry of NCC on tubules, and the expression degree was decreased compared with the control ().
We performed genetic analysis for diagnosis of GS. Although his family (parents and 3 sisters) did not show any clinical abnormality or electrolyte imbalances, we analyzed genomic DNA of the patient and his family in Keimyung University Medical Genetics Institute. Genomic DNA was isolated from peripheral blood by using the Wizard Genomic DNA Purification Kit according to the manufacture's instruction (Promega, Madison, WI, USA). Amplification of the coding sequence of the SLC12A3 gene by polymerase chain reaction was carried out as previously described. Polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP) was performed. PCR products in the patient, his family, and normal control were electrophoresed through 10% polyacrylamide gels. The result in patient, a double mutant band was found, his family had only one band ().
To get apparent result of sequencing, PCR products were cloned by TOPOTA cloning (Invitrogen Ltd., Paisley, United Kingdom) and direct sequencing was performed on those PCR products that showed altered band mobility in the above analysis. Variations in the sequences between GS and matched normal sample were performed using the ABI 3730 DNA sequencer (Bionics Inc, Korea). The result revealed that the patient had homozygous missense mutation of nucleotide 179, cytosine to threonine (ACG to ATG) on exon 1 of the SLC12A3 gene. His family has heterozygous mutation at the same region, and supports the diagnosis of GS and carrier (, ).",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mEq/L'], 'Chloride': [91.0, 'mEq/L'], 'Bicarbonate': [29.7, 'mEq/L']}",19.3,18.335,20.265,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mEq/L. 
The concentration of chloride is 91.0 mEq/L. 
The concentration of bicarbonate is 29.7 mEq/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (91.0 mEq/L + 29.7 mEq/L) = 19.3 mEq/L. Hence, The patient's anion gap is 19.3 mEq/L."
6303,39,Anion Gap,lab test,decimal,usmle-4395,Extracted,"A 72-year-old man presents to the emergency department for a change in his behavior. The patient's wife called 911 and he was brought in by emergency medical services. She noticed that he seemed somnolent and not very responsive. The patient has a past medical history of type II diabetes, obesity, osteoarthritis, and migraine headaches. His current medications include naproxen, insulin, atorvastatin, metformin, ibuprofen, omeprazole, and fish oil. His temperature is 99.5°F (37.5°C), blood pressure is 170/115 mmHg, pulse is 80/min, respirations are 19/min, and oxygen saturation is 98% on room air. On physical exam, the patient is somnolent and has a Glasgow Coma Scale of 11. Cardiac and pulmonary exams are notable for bibasilar crackles and a systolic murmur that radiates to the carotids. Neurological exam is deferred due to the patient's condition. Laboratory values are shown below.

Hemoglobin: 12 g/dL
Hematocrit: 36%
Leukocyte count: 9,500 cells/mm^3 with normal differential
Platelet count: 199,000/mm^3

Serum:
Na+: 144 mEq/L
Cl-: 98 mEq/L
K+: 4.0 mEq/L
HCO3-: 16 mEq/L
BUN: 44 mg/dL
Glucose: 202 mg/dL
Creatinine: 2.7 mg/dL
Ca2+: 9.2 mg/dL
AST: 12 U/L
ALT: 22 U/L

The patient is started on IV fluids.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [98.0, 'mEq/L'], 'Bicarbonate': [16.0, 'mEq/L'], 'Sodium': [144.0, 'mEq/L']}",30,28.5,31.5,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 144.0 mEq/L. 
The concentration of chloride is 98.0 mEq/L. 
The concentration of bicarbonate is 16.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 144.0 mEq/L - (98.0 mEq/L + 16.0 mEq/L) = 30.0 mEq/L. Hence, The patient's anion gap is 30.0 mEq/L."
6304,39,Anion Gap,lab test,decimal,pmc-3593508-1,Extracted,"A 70-year-old male was brought to the emergency department with complaints of increasing difficulty in breathing, cough with expectoration and fever of about one-week duration. The patient was suffering from cough with expectoration, breathlessness on and off for the past two years and vague abdominal discomfort for the past six months. The patient was not a diabetic or hypertensive but smoker for the past 40 years. On examination, the patient was thin built, ill-looking and pale. His pulse rate was 86/min and blood pressure was 140/80 mm of Hg. On palpation, the abdomen was tender in the epigastric and right hypochondriac region. There was no evidence of lymphadenopathy. Papules and excoriations were seen over the perianal region. The patient was conscious and coherent. No abnormality of central nervous system (CNS) was noted. Normal vesicular breathing with rales and course crackles were found in both the lung fields. Examination of cardiovascular system (CVS) was unremarkable.
At the time of admission, random blood sugar was 85 mg/dl, blood urea - 44 mg/dl, creatinine - 4 mg/ dl, hemoglobin - 9.3 g/dl, total count - 7200 cells/cmm, differential count- P67%, L29%, E04%, absolute esinophil count - 480 cells/cmm, erythrocyte sedimentation rate -10 mm and 24 mm at half an hour and one hour respectively. Serum sodium was 123 mmol/l, serum potassium - 3.3 meq/l, chloride - 89 meq/l and bicarbonates- 26 meq/l. Mantoux test and test for anti-human immunodeficiency virus (HIV) antibodies were negative. Electrocardiogram showed sinus tachycardia. Chest X-ray was suggestive of multiple fluid-filled cavities in the left lung and pending the results of sputum examination, the patient was empirically put on injection deriphylline, amoxycillin-clavulanic acid, gentamicin, ranitidine and metronidazole with a provisional diagnosis of acute exacerbation of chronic obstructive pulmonary disease (COPD)/lung abscess.
On day three of admission, the patient continued to have difficulty in breathing. Physical examination showed bilateral wheeze and no other abnormality. Electrocardiogram (ECG) showed sinus tachycardia. The patient was put on increasing dose of bronchodilators following which he appeared to be relieved temporarily. SPO2 was 96% without O2 Sputum for acid fast bacilli (AFB) was negative on three consecutive days. Wet mount of the sputum showed plenty of actively motile larvae of S. stercoralis [, ]. Routine culture of sputum yielded a moderate growth of Escherichia coli which was susceptible to gentamicin and amikacin. Examination of stool and repeat sputum was requested by our laboratory following the detection of larvae in the sputum. Stool sample and sputum sample collected on two consecutive days showed plenty of motile larvae of S. stercoralis []. The patient was put on albendazole 400 mg bid for three days. Repeat chest X-ray showed persistence of lung abscess on the left side. Ivermectin 12 mg OD was subsequently added to the treatment regimen and albendazole continued for further three days. Repeat stool examination done on the two consecutive days did not show any larvae of S. stercoralis. Sputum could not be examined as the patient could not submit the sample as there was no expectoration. Repeat chest X-ray showed clearance of fluid in the lung abscess with only thick fibroid wall of the cavity. He became afebrile and appetite improved. The patient was feeling better and was discharged at request with advice to report after two weeks. Follow-up of the patient four weeks later showed the patient was asymptomatic and stool examination did not show any parasites.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [89.0, 'mEq/L'], 'Bicarbonate': [26.0, 'mEq/L'], 'Sodium': [123.0, 'mmol/L']}",8,7.6,8.4,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 123.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 123.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 123.0 mmol * 1 mEq/mmol = 123.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 123.0 mmol sodium/L converts to 123.0 mEq sodium/L. 
The concentration of chloride is 89.0 mEq/L. 
The concentration of bicarbonate is 26.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 123.0 mEq/L - (89.0 mEq/L + 26.0 mEq/L) = 8.0 mEq/L. Hence, The patient's anion gap is 8.0 mEq/L."
6305,39,Anion Gap,lab test,decimal,pmc-5308422-1,Extracted,"We present a case of a 39-year-old woman with a history significant for infertility, a type II diabetes mellitus, and a body mass index (BMI) of 27.5, who presented to our emergency department (ED) 10 days after an IVF procedure with severe epigastric pain and several episodes of nausea and vomiting that started one day prior to presentation. On initial evaluation in the ED, she was afebrile and hemodynamically stable. Her physical examination was significant only for epigastric and left upper quadrant pain. Her BMI was 27.5. Initial laboratory work-up could not be accurately interpreted due to severe lipemia (); however, it revealed a serum level of lipase of 2470 U/L, amylase of 1000 U/L, blood glucose of 301 mg/dL, sodium of 117 meq/L, chloride of 92 meq/L, bicarbonate of 12 meq/L, aspartate transaminase of 60 U/L, alanine transaminase of 24 U/L, gamma-glutamyl transferase of 14 U/L, and alkaline phosphatase of 66 U/L. Arterial serum lactate was 0.78 meq/L, and urine ketone levels was valued as 4+ on urine dipstick. An ultrasound of the abdomen was performed and revealed fatty liver infiltration. A computed tomography scan of the abdomen and pelvis, done 48 h later, revealed acute hemorrhagic pancreatitis with peri-pancreatic fluid. The patient was admitted with a diagnosis of severe hypertriglyceridemia-induced acute pancreatitis, hypertriglyceridemia associated pseudo-hyponatremia, and possible diabetic ketoacidosis. The patient was admitted to the intensive care unit and started on aggressive intravenous (IV) hydration and intravenous insulin. The second day, her triglycerides dropped to 9234 mg/dL, her low-density lipoprotein (LDL) was 366 mg/dL, and her high-density lipoprotein (HDL) was 40 mg/dL. Her symptoms improved progressively every day and her pain became better. The third day, triglycerides dropped to 1455 mg/dL, and after confirmation of absence of pregnancy, she was started on fibrates and statins on day 3 of admission, after which her triglyceride level continued to drop ().
The patient had a negative family history for dyslipidemia. No previous history of acute pancreatitis. She was maintained at home on oral metformin 850 mg daily for mild type II diabetes mellitus, estradiol 2 mg daily, progesterone 200 mg twice daily, aspirin 100 mg daily, and subcutaneous hydroxyprogesterone 500 mg daily and enoxaparin 40 mg daily as part of a regimen for IVF.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [92.0, 'mEq/L'], 'Bicarbonate': [12.0, 'mEq/L'], 'Sodium': [117.0, 'mEq/L']}",13,12.35,13.65,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 117.0 mEq/L. 
The concentration of chloride is 92.0 mEq/L. 
The concentration of bicarbonate is 12.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 117.0 mEq/L - (92.0 mEq/L + 12.0 mEq/L) = 13.0 mEq/L. Hence, The patient's anion gap is 13.0 mEq/L."
6306,39,Anion Gap,lab test,decimal,pmc-5588234-1,Extracted,"An 81-year-old man with a medical history of chronic kidney disease secondary to hypertension (stage III/IV) and peptic ulcer disease presented with epigastric pain, a weight loss of 25 pounds over several months, melena for 2 weeks and hematemesis for 2 days. He had a remote history of alcohol abuse, but had remained abstinent for 4 decades. His medications included 20 mg of omeprazole twice daily and 20 mg of furosemide daily. He had no known allergies.
His vital signs on admission were temperature: 36.3°C, heart rate: 90 bpm, respiratory rate: 20 breaths/min and blood pressure: 173/63 mm Hg. Physical examination findings included generalized jaundice and a distended abdomen tender to palpation in the right upper quadrant with no peritoneal signs. There was profound hepatomegaly without splenomegaly. A rectal examination revealed guaiac-positive melenic stools. No palmar erythema, spider angiomas, asterixis or fluid wave were appreciated. The patient was started on intravenous fluids and a pantoprazole drip, and he remained clinically stable for the 4-day hospital course.
Initial laboratory tests showed hemoglobin of 11.6 g/dl (decreased from 13.6 g/dl 1 month previously), a white blood cell count of 10.8 × 109 cells/l, a platelet count of 342 × 109/l, total bilirubin of 10.1 mg/dl, direct bilirubin of 6.1 mg/dl, aspartate aminotransferase 727 U/l, alanine aminotransferase 333 U/l and alkaline phosphatase 333 U/l. Electrolytes revealed levels of sodium: 141 mEq/l, potassium: 4.9 mEq/l, chloride: 107 mEq/l, bicarbonate: 16 mEq/l, blood urea nitrogen: 68 mg/dl, creatinine: 2.2 mg/dl, glucose: 81 mg/dl, phosphorous: 6.0 mg/dl and calcium: 9.2 mg/dl. Electrolytes showed no trend toward significant acute kidney injury or tumor lysis syndrome during the hospital course. Lactate was elevated at 6.6 mmol/l. Urinalysis was unremarkable. P-lipase was normal. Urine drug screen, hepatitis panel and blood and urine cultures were negative. Arterial blood gas revealed two primary acid-base disorders: metabolic acidosis and respiratory alkalosis (pH: 7.43, pCO2: 24.6 mm Hg, pO2: 85.5 mm Hg and HCO3-: 16.1 mmol/l).
Diagnostic procedures included right upper quadrant abdominal ultrasound, which did not show common bile duct dilatation or gallstones. Esophagogastroduodenoscopy revealed a 2-cm, ulcerated mass on the retroflexion of the cardia. Biopsies of the mass revealed a poorly differentiated α-fetoprotein (AFP)-positive adenocarcinoma (fig. , ). A diagnosis of gastric adenocarcinoma was made. Positron emission tomography/computed tomography showed uptake of fluorodeoxyglucose in the cardia of the stomach, diffuse and intense uptake in the liver and focal uptake in several pulmonary nodules and the pelvis (fig. ). Lactate remained persistently elevated throughout the hospital course (range 4.0-6.6 mmol/l). Tumor marker tests were significant for the levels of AFP (896 ng/ml, normal range: 0-8) and cancer antigen 19-9 (100 U/ml, normal range: 0-35). Due to the extent of his disease and his poor performance status, the patient was thought to be a poor candidate for antineoplastic intervention. The findings were discussed with the patient and his family, and he opted for discharge to hospice care. He died several days later.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [107.0, 'mEq/L'], 'Bicarbonate': [16.0, 'mEq/L'], 'Sodium': [141.0, 'mEq/L']}",18,17.1,18.9,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 141.0 mEq/L. 
The concentration of chloride is 107.0 mEq/L. 
The concentration of bicarbonate is 16.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 141.0 mEq/L - (107.0 mEq/L + 16.0 mEq/L) = 18.0 mEq/L. Hence, The patient's anion gap is 18.0 mEq/L."
6307,39,Anion Gap,lab test,decimal,usmle-10047,Extracted,"A 59-year-old male with a history of aortic stenosis secondary to a bicuspid aortic valve treated with aortic valve replacement (AVR) presents with fever and shortness of breath. Patient states a gradual onset of symptoms approximately five days ago that have been getting steadily worse. He reports that he has trouble getting up and walking across a room before becoming short of breath. Past medical history is significant for a mechanical AVR three years ago for severe aortic stenosis, removal of a benign polyp last year following a colonoscopy, and a tooth extraction 2 weeks ago. Current medications are warfarin 5 mg orally daily, rosuvastatin 20 mg orally daily, and enalapril 10 mg orally twice daily. Vital signs are: temperature 39°C (102.2°F), blood pressure 100/65 mm Hg, pulse 96/min, respiration rate 18/min, and oxygen saturation 96% on room air. On physical exam, patient is alert but dyspneic. Cardiac exam is significant for a systolic ejection murmur that is loudest at the upper right sternal border and radiates to the carotids. Lungs are clear to auscultation. Abdomen is soft and nontender. Splenomegaly is present. Extremities are pale and cool to the touch. Laboratory tests are significant for:
Sodium  136 mEq/L
Potassium 4.1 mEqL
Chloride  107 mEq/L
Bicarbonate 21 mEq/L
BUN  13 mg/dL
Creatinine  1.0 mg/dL
Glucose (fasting)   75 mg/dL
  Bilirubin, conjugated 0.3 mg/dL
Bilirubin, total   1.1 mg/dL
AST (SGOT) 34 U/L
ALT (SGPT)      40 U/L
Alkaline phosphatase 39 U/L
  WBC            12,500/mm3
RBC 5.15 x 106/mm3
Hematocrit  32.1%
Hemoglobin  13.0 g/dL
Platelet count    215,000/mm3
  Troponin I (cTnI)  < 0.02 ng/mL
INR   2.4
Chest X-ray shows no evidence of dehiscence or damage to the mechanical valve. ECG shows the following in the picture. Transesophageal echocardiography shows a possible large vegetation on one of the mechanical aortic valve leaflets.  Left ventricular ejection fraction is 45% due to outflow tract obstruction. High flow supplemental oxygen and fluid resuscitation are started. Blood cultures x 2 are drawn.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [107.0, 'mEq/L'], 'Bicarbonate': [21.0, 'mEq/L'], 'Sodium': [136.0, 'mEq/L']}",8,7.6,8.4,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 136.0 mEq/L. 
The concentration of chloride is 107.0 mEq/L. 
The concentration of bicarbonate is 21.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 136.0 mEq/L - (107.0 mEq/L + 21.0 mEq/L) = 8.0 mEq/L. Hence, The patient's anion gap is 8.0 mEq/L."
6308,39,Anion Gap,lab test,decimal,pmc-7417115-1,Extracted,"The patient is a 49-year-old Vietnamese male with a past medical history of latent TB and non-insulin-dependent diabetes mellitus type 2. He presented with nausea, vomiting, and progressively decreasing urine output for one week. The patient described his urine color dark brown like “Coca-Cola”. He had associated symptoms of generalized weakness and lower back pain. About two months before the current presentation, he was admitted to the hospital for pneumonia and diagnosed with latent TB. Chest CT at that time revealed multifocal pulmonary nodules or nodular consolidations widely distributed throughout each lung area. The consolidations were largest in the perihilar portion of the right lung and throughout the dependent portion of the left lung base that contained numerous internal air bronchograms (Figure ).
CT-guided biopsy of a right pulmonary nodule was negative for malignancy or granuloma without any evidence of focal necrosis. Due to his country of origin in Southeast Asia, TB was suspected. Both sputum and bronchoalveolar lavage samples taken from broncoscopy were negative for acid-fast bacilli (AFB) stain or cultures. His purified protein derivative test revealed an induration of 31 mm, and the QuantiFERON®-TB Gold test was positive. He did not have any active TB symptoms of fevers, cough, weight loss, or night sweats, etc. He was then diagnosed with latent TB and discharged with supervised TB treatment with rifampin 300 mg weekly and isoniazid 900 mg weekly with a local health department.
About two weeks before the current presentation, he missed taking rifampin and isoniazid due to the unavailability of a home health nurse. On the day of his current presentation, he had mild leukocytosis with white blood cell (WBC) count of 11.6 x 109/L, hemoglobin 13.4 g/dL, hematocrit 26.4%, platelet count 132 x 109 /L, blood urea nitrogen (BUN) 133 mmol/L, creatinine 16.1 mg/dL, glomerular filtration rate (GFR) 3 mL/min/1.73 m2 (compared to baseline creatinine 0.7 mg/dL, GFR 95 mL/min/1.73 m2 two months ago), normal transaminases (total bilirubin 0.5 µmol/L, aspartate aminotransferase [AST] 13 units/L, alanine aminotransferase [ALT] 12 units/L), sodium 132 mEq/L, potassium 4.9 mmol/L, chloride 97 mEq/L, bicarbonate 18 mEq/L, glucose 208 mg/dL, and a fractional excretion of sodium (FENa) less than 1%. His renal ultrasound was unremarkable with normal-sized bilateral kidneys and the absence of hydronephrosis. CT chest findings in present admission were mostly unchanged from CT chest done in the previous admission two months ago. He did not report any symptoms of active TB comprising of fevers, cough, weight loss, or night sweats. On the day of admission, his home rifampin 300 mg weekly dose was re-administered after a drug-free interval of two weeks. During the first two days of admission, he received aggressive fluid hydration to address hypovolemia from vomiting. He started to exhibit clinical symptoms of volume overload without significant improvement in his renal function. He continued to remain oliguric, and hemodialysis was commenced. Over first four days after rifampin resumption, his hemoglobin-hematocrit continued to decline from 13.4 g/dL-26.4% to 8.5 g/dL-24%, respectively. His total bilirubin increased to 2.4 µmol/L with a direct component of the bilirubin value of 0.5 µmol/L. On day 4, since admission, his urine analysis revealed a pH of 7.5, urine protein 1+, urine occult blood 3+, and trace red blood cells (RBCs). The urinalysis was suspicious for hemoglobin or myoglobin pigment-related kidney injury due to the marked presence of urine occult blood while lacking a significant number of RBCs. His serum creatinine kinase (CK) was mildly elevated at 300 units/L that ruled out myoglobin-induced acute renal failure (ARF), i.e., rhabdomyolysis. Coombs test was positive, and lactic acid dehydrogenase (LDH) was 450 units/L. Based on published reports of RARF and convincing laboratory data, it was concluded that his acute renal injury was worsened by intravascular hemolysis triggered by the re-introduction of rifampin. Due to limited resources, we were not able to check the anti-rifampin antibodies in his serum. On the sixth day post rifampin administration, despite receiving three hemodialysis sessions, his renal function did not improve, and a renal biopsy was performed. His renal biopsy revealed acute tubular injury with intratubular hemoglobin casts, concerning of intravascular hemolysis and hemoglobinuria (Figures -).
Rifampin was discontinued. Subsequently, after five more hemodialysis sessions, his renal function exhibited steady improvement with a decrease in serum creatinine and an increase in GFR. When his urine output increased over 50 cc/hour with concomitant near normalization of creatinine and GFR, his hemodialysis was discontinued. He was discharged home, and rifampin was permanently removed from the discharge medication list. His latent TB treatment from the previous admission comprising of dual therapy with rifampin and isoniazid was substituted for monotherapy with isoniazid for a total of six months. In subsequent outpatient follow-ups of over 10 months to date, his renal function has remained within normal limits.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [97.0, 'mEq/L'], 'Bicarbonate': [18.0, 'mEq/L'], 'Sodium': [132.0, 'mEq/L']}",17,16.15,17.85,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 132.0 mEq/L. 
The concentration of chloride is 97.0 mEq/L. 
The concentration of bicarbonate is 18.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 132.0 mEq/L - (97.0 mEq/L + 18.0 mEq/L) = 17.0 mEq/L. Hence, The patient's anion gap is 17.0 mEq/L."
6309,39,Anion Gap,lab test,decimal,usmle-9635,Extracted,"A 55-year-old woman visits the clinic after experiencing what she describes as an odd episode of tingling in her fingers and the sensation of smelling sour milk. She denies loss of consciousness, confusion, or incontinence. She also denies a history of head trauma or the ingestion of toxic substances. Past medical history is significant for type 2 diabetes mellitus, which is well controlled with metformin. Her temperature is 36.8°C (98.2°F), the heart rate is 98/min, the respiratory rate is 15/min, the blood pressure is 100/75 mm Hg, and the O2 saturation is 100% on room air. The physical exam, including a full neurologic and cardiac assessment, demonstrates no abnormal findings. Laboratory findings are shown. Brain MRI does not indicate any areas of infarction or hemorrhage. ECG is normal, and EEG is pending.
BUN 15 mg/dL
pCO2 40 mmHg
Creatinine 0.8 mg/dL
Glucose 95 mg/dL
Serum chloride  103 mmol/L
Serum potassium 3.9 mEq/L
Serum sodium 140 mEq/L
Total calcium 2.3 mmol/L
Magnesium 1.7 mEq/L
Phosphate 0.9 mmol/L
Hemoglobin 14 g/dL
Glycosylated hemoglobin 5.5%
Total cholesterol 4 mmol/L
Bicarbonate (HCO3) 19 mmol/L
Urine toxicology screen is negative.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [103.0, 'mmol/L'], 'Bicarbonate': [19.0, 'mmol/L'], 'Sodium': [140.0, 'mEq/L']}",18,17.1,18.9,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mEq/L. 
The concentration of chloride is 103.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 103.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 103.0 mmol * 1 mEq/mmol = 103.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 103.0 mmol chloride/L converts to 103.0 mEq chloride/L. 
The concentration of bicarbonate is 19.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 19.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 19.0 mmol * 1 mEq/mmol = 19.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 19.0 mmol bicarbonate/L converts to 19.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (103.0 mEq/L + 19.0 mEq/L) = 18.0 mEq/L. Hence, The patient's anion gap is 18.0 mEq/L."
6310,39,Anion Gap,lab test,decimal,pmc-6620230-1,Extracted,"We report a case of a 37-year-old male with PWS who suffered from ESKD. At 3 years of age, he started overeating and developed obesity. At 5 years of age, PWS was suspected based on the patient’s body type, facial expression, and overeating. Dietary restriction was instructed; however, at 17 years of age, he was diagnosed with type 2 DM (T2DM). At 30 years of age, a diagnosis of PWS was confirmed by genetic testing. At age 32 years, he suffered from nephrotic syndrome, and diabetic retinopathy was diagnosed at the same time.
By June 2015, renal function had continuously deteriorated and his serum creatinine reached 8.9 mg/dL (eGFR at 5.0 mL/min/1.73 m2). Therefore, the patient was admitted to the hospital for initiating RRT. At admission, physical examination revealed: 150.8 cm height, 80.3 kg BW, BP 112/64 mmHg, HR 110/min, SO2 99% (room air). He showed systemic edema and urine volume decreased to 800 mL/24 h. The patient’s IQ was inferred 40–60. Blood chemistry showed: TP 6.4 g/dL, albumin 2.4 g/dL, CRP 10.9 mg/dL, BUN 83 mg/dL, UA 6.4 mg/dL, Na 136 mEq/L, K 5.4 mEq/L, Cl 110 mEq/L, Ca 7.1 mg/dL, P 12.7 mg/dL and HCO3− 14.7 mEq/L. Complete blood count was: WBC 16,770/μL, RBC 354 × 104/μl, Hgb 8.1 g/dL, Ht 27.6%, MCV 78 fl, MCH 22.9 pg, MCHC 29.3% and Plt 54.2 × 104/μl. Urinalysis showed massive proteinuria (4839 mg/24 h) without hematuria or pyuria. He had been receiving insulin injection 4 times a day. Random blood glucose level was 156 mg/dL and HbA1c was 6.8%.
After admission, restricted fluid intake, nutritional management, and temporary HD was performed 6 times for 2 weeks since massive edema prevented insertion of PD catheter. The reasons for choosing PD were as follows: vessels in his both forearms looked premature for creating A-V fistula at that time, suspecting intolerance in hemodialysis session for long hours and difficult cessation of fluid and food intake which are necessary for hemodialysis. Negative aspect of PD was specifically considered as a difficulty in maintaining sanitary in inlet of PD catheter. In either modality, family burden for supporting his dialysis was also considered.
Substantially his body weight decreased to 64 kg (− 16 kg from admission; BMI 28.4 kg/m2) and a catheter for PD was inserted using the non-stylet method under general anesthesia combined with epidural anesthesia at the 14th day of admission. We selected the JBS-2 semi-long PD Catheter with the exit site placed in the left upper abdomen (Fig. ). The catheter position was not ideally located initially but it functioned well for the following PD session after the surgery (Fig. ). From the third postoperative day, nocturnal intermittent PD (NIPD) was started. Since he could not sufficiently understand the procedure of PD, instructions for PD as well as insulin self-injection were provided to his father. He was discharged at the day 35 of hospitalization.
At the 2nd, 5th, 7th, and 13th month after NIPD introduction, a subcutaneous tunnel infection occurred (Fig. ). Since additional antibiotic therapy could not terminate infection, he underwent subcutaneous pathway diversion and PD catheter replacement for three times consequently. However, that was the last infection episode and infection-free PD was observed until the present time for next 27 months. With regard to the dialysis modality, NIPD was chosen first because he desired to continue his daytime job for handicapped person. At the 7th month after NIPD introduction, the treatment was switched to continuous cycling PD (CCPD) and 7.5% icodextrin solution (Extraneal™, Baxter, Tokyo, Japan) was added daytime because urine output gradually decreased, and ultrafiltration volume became insufficient. At the 10th month after NIPD introduction, glucose concentration in peritoneal dialysate increased from 1.5 to 2.5% (Reguneal™, Baxter, Tokyo, Japan). “Hybrid dialysis”, which combined daily PD with once-a-week HD, was started by creating A-V fistula at the 16th month after NIPD introduction. Owing to this “hybrid dialysis”, adequate ultrafiltration volume was maintained for following 17 months. Dialysis efficiency has been checked by blood tests and chest X-ray once a month and revealed adequate dialysis without major problems; accordingly, BUN level was below 50 mg/dL and serum potassium level below 5 mEq/L. Blood sugar was well maintained by daily intensive insulin therapy with oral dulaglutide initially and then this regimen was successfully replaced with once-weekly GLP-1 agonist associated with once a day ultralong-acting insulin finally. HbA1c had been maintained under 7% since NIPD introduction. His maximum body weight without overhydration reached to 71 kg (BMI 31.6 kg/m2) during this period. Finally, he lost his A-V fistula twice and returned to PD (CCPD) alone at the 38th month of NIPD introduction because of difficulty in creating another vascular access. For evaluating efficacy of PD, serum β2-microglobulin level was monitored every 2 months and revealed between 34 and 40 mg/L during the latest CCPD alone period.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [110.0, 'mEq/L'], 'Bicarbonate': [14.7, 'mEq/L'], 'Sodium': [136.0, 'mEq/L']}",11.3,10.735,11.865,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 136.0 mEq/L. 
The concentration of chloride is 110.0 mEq/L. 
The concentration of bicarbonate is 14.7 mEq/L. 
Plugging in these values into the anion gap formula gives us 136.0 mEq/L - (110.0 mEq/L + 14.7 mEq/L) = 11.3 mEq/L. Hence, The patient's anion gap is 11.3 mEq/L."
6311,39,Anion Gap,lab test,decimal,pmc-3519780-1,Extracted,"A 43 year-old male was referred to the Emergency Department (ED) of our hospital after his workplace colleagues noted increasingly strange behavior for three days. The patient arrived complaining of generalized fatigue, lethargy, fevers, severe band-like headache, slurred speech, and increasing confusion. Though it was felt that the patient’s history was not completely reliable secondary to confusion, he was able to deny throat pain, chest pain, diarrhea, abdominal pain, recent sick contacts, or recent travel. Review of systems was limited secondary to altered mental status, but he did admit to mild dry cough.
Though initially denying immune compromise in the ED, the patient later disclosed he was HIV+. He could not recall his CD4 count but stated that his last viral load was undetectable. Past medical history was significant for hypertension and hypercholesterolemia. Outpatient medications included Atripla, spironolactone, and gemfibrozil. He had a history of unprotected anal sex with men but denied new partners. He had no recent contact with animals. He smoked a pack of cigarettes per day but did not drink or use drugs.
In the ED, the patient’s temperature was 103.9°F (39.9°C). Heart rate was 121 beats per minute, and respiratory rate was 30 breaths per minute. Oxygen saturation was 94% on room air. Blood pressure was 142/90. The patient appeared unwell. He was somnolent but easily aroused. Pertinent findings on general physical exam included a supple neck and decreased breath sounds diffusely. On neurologic exam, he was noted to be dysarthric. He had general slowness of thought and processing. He was slightly confused, though he was oriented and able to name the days of the week forwards and backwards if given sufficient time.
Initial laboratory evaluation was notable for a white blood cell (WBC) count of 10.1 × 103 cells/mm3, [lab reference range 4.0–10.8], hemoglobin of 15.7 g/dL [lab range 14.0–18.0], platelet count of 135 × 103/mm3 [lab range 150–350]. Automated differential showed 87.5% segmented cells (lab range 30-85%), 9.3% lymphocytes (lab range 15-55%), 2.4% monocytes (lab range 0-10%), 0.8% eosinophils (lab range 0-5%), and 0% basophils. No manual differential was performed. A basic metabolic panel showed serum sodium of 134 mmol/L [lab range 137–145], serum potassium of 4.2 mmol/L (lab range 3.5-5.1), serum chloride of 100 mmol/L (lab range 98–107), and CO2 of 19 mmol/L [lab range 22.0–30.0]. Blood urea nitrogen, serum creatinine, and serum glucose were elevated at 33 mg/dL [lab range 9–20], 1.8 mg/dL [lab range 0.7–1.3] and 159 mg/dL [lab range 70–99], respectively. C-reactive protein (CRP) was high at 581 mg/dL [lab range 0–10]. Liver function studies showed an albumin level of 4.4 g/dL (lab range 3.5-5.0), total protein of 7.6 g/dL (lab range 6.3-8.2), total bilirubin of 0.7 mg/dL (lab range 0.2-1.3), direct bilirubin of 0.5 mg/dL (lab range 0–0.3), alkaline phosphatase of 62 U/L (lab range 38–126), alanine aminotransferase (ALT) of 49 U/L (lab range 13–69), and aspartate aminotransferase (AST) of 89 U/L (lab range 15–46). Urinalysis showed 2+ albumin, 3+ blood, trace WBC esterase, negative nitrite, 5–10 WBC, 0–5 red blood cells (RBC), 5–10 epithelial cells, 5–10 hyaline casts, 3+ amorphous cells, and 1+ mucous. A non-contrast computed tomography (CT) scan of the head did not reveal any abnormalities. Nasopharyngeal influenza assay was negative.
Due to the combination of altered mental status, headache, and fever, a lumbar puncture was performed. The results demonstrated an elevated cerebrospinal fluid (CSF) glucose of 97 mg/dL [normal 40–70], CSF protein of 37 mg/dL [normal 12–60], and normal cell count and gram stain. Blood cultures were sent.
A chest x-ray was done and was read as a left hilar mass extending down towards the left lower lobe (see Figure 
). A chest CT was obtained to better characterize the hilar mass (see Figure 
). This chest CT demonstrated a left lower lobe consolidation with air bronchograms suggesting a diagnosis of pneumonia. Based upon the aforementioned findings, the patient was started on azithromycin and ceftriaxone for community-acquired pneumonia, as well as empiric acyclovir for herpes encephalitis.
Given the findings of dysarthria and altered mental status in an HIV + individual with unknown CD4+ count, a brain MRI was obtained. No contrast was administered secondary to acute renal injury. The diffusion-weighted coronal cut can be seen in Figure 
, demonstrating abnormal restricted diffusion and swelling of the splenium of the corpus callosum without other significant abnormalities. Abnormal T2-weighted signal in the SCC can be seen in Figure 
. These MRI findings in an HIV + individual raised concern for CNS opportunistic infection. However, since the patient was hemodynamically stable, was on antiretroviral therapy, and had a negative lumbar puncture, it was decided to treat the pneumonia initially and closely monitor the patient’s mental status.
Over the first two to three days of hospitalization, the patient continued to have high fevers, confusion, and dysarthria. His laboratory markers improved on antibiotics. His serum CRP trended down from 581 mg/L at admission to 200 mg/L on day three. After day three the patient began to demonstrate significant clinical improvement. The patient’s admission CD4+ count returned on day three at 156 cells/mm3, and an HIV viral load came back on day four at <20 copies/mL. On day four, urine antigens for Streptococcus pneumoniae and Legionella pneumophila serogroup 1 were sent. By day five the patient’s neurologic symptoms had resolved, as had his acute renal insufficiency. This same day his Legionella pneumophila urinary antigen returned positive.
On hospital day six a repeat MRI was obtained to monitor radiologic progression of the SCC lesion. This repeat study showed partial interval clearing of the previously noted abnormalities: restricted diffusion, abnormal increased flair, and abnormal T2 signally in the SCC. On hospital day seven the patient was discharged home on oral azithromycin. He had no residual deficits. Initial CSF viral studies including herpes simplex virus 1 and 2, varicella, cytomegalovirus, enterovirus, and JC virus all returned negative, as did the syphilis, hepatitis B, and hepatitis C serologies. Sputum for acid fast bacilli and routine culture were negative. Legionella antibody IgG titers sent on day four later came back at 1:64.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [100.0, 'mmol/L'], 'Bicarbonate': [19.0, 'mmol/L'], 'Sodium': [134.0, 'mmol/L']}",15,14.25,15.75,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 134.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 134.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 134.0 mmol * 1 mEq/mmol = 134.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mmol sodium/L converts to 134.0 mEq sodium/L. 
The concentration of chloride is 100.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 100.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 100.0 mmol * 1 mEq/mmol = 100.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 100.0 mmol chloride/L converts to 100.0 mEq chloride/L. 
The concentration of bicarbonate is 19.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 19.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 19.0 mmol * 1 mEq/mmol = 19.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 19.0 mmol bicarbonate/L converts to 19.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 134.0 mEq/L - (100.0 mEq/L + 19.0 mEq/L) = 15.0 mEq/L. Hence, The patient's anion gap is 15.0 mEq/L."
6312,39,Anion Gap,lab test,decimal,pmc-6942743-1,Extracted,"A 59-year-old Caucasian man with ESRD due to glomerulonephritis and failed kidney transplant who was undergoing CCPD for 7 months presented to the emergency department with periumbilical pain for several days. This was the first time the patient had experienced these symptoms since the initiation of CCPD. His medical history additionally included hypertension, valvular heart disease, degenerative arthritis, parathyroidectomy, and tobacco use. He had discontinued all of his immunosuppressive medications because his kidney transplant had been nonfunctional for several years.
Physical examination revealed a well-built, seemingly healthy man weighing 157 pounds with a blood pressure of 144/92 mmHg and a heart rate of 85 beats/min, without distress, and without jaundiced sclerae. He had clear lungs and systolic heart murmur. Abdominal examination revealed a soft abdomen with some fullness on the right lower quadrant proximal to his previous renal transplant, periumbilical tenderness, and intact exit site with no tunnel tenderness. He had active bowel sounds.
Laboratory testing revealed a white blood cell (WBC) count of 9.1 × 103/μL with 70% neutrophils, hemoglobin level of 12.9 g/dL, hematocrit count of 38.5%, and platelet count of 263 × 103/μL. Serum chemistry analysis showed the following levels: sodium 139 mmol/L, potassium 3.4 mmol/L, chloride 95 mmol/L, total carbon dioxide 28 mmol/L, glucose 127 mg/dL, blood urea nitrogen 31 mg/dL, and creatinine 12.46 mg/dL. The peritoneal fluid was colorless and appeared hazy. Initial analysis showed a WBC count of 4,470 cells/μL with 85% polymorphonuclear cells and 15% mononuclear cells. Gram staining of the peritoneal fluid was negative for any organisms, only showing WBCs.
Based on the available information, the patient was diagnosed with PD-peritonitis, and empiric treatment with 1 g of vancomycin and 1 g of ceftazidime was administered intravenously and daily infusions initiated. The final diagnosis was made through peritoneal fluid culture that showed light growth of P. multocida after 3 days. The isolate was sensitive to ampicillin, ceftriaxone, ceftazidime, gentamicin, and ciprofloxacin. Therefore, antibiotics were adjusted according to the bacterial cultures, where intravenous ampicillin-sulbactam was started and then switched to oral amoxicillin-clavulanate for a total of 3 weeks. Patient had subsequent improvement in symptoms and laboratory results. He was able to continue PD successfully without any interruption or the need for catheter removal.
Upon taking further history, the patient reported having several cats at home, none of which were kittens. At night, he would begin his PD treatment and go into a different room to watch television. Therefore, the cats were assumed to play with the dialysis equipment or chew on the tubing, possibly leading to infection, although the patient did not recall noticing any fluid leakage from the tubing. Prior to discharge, the patient's dialysis technique was confirmed by direct observation, and aseptic technique was ensured. The patient additionally decided to place his cats outside the home at night before starting PD treatment. He did not have any more episodes of PD-peritonitis caused by P. multocida after changing his routine.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [139.0, 'mmol/L'], 'Chloride': [95.0, 'mmol/L'], 'Bicarbonate': [28.0, 'mmol/L']}",16,15.2,16.8,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 139.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 139.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 139.0 mmol * 1 mEq/mmol = 139.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 139.0 mmol sodium/L converts to 139.0 mEq sodium/L. 
The concentration of chloride is 95.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 95.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 95.0 mmol * 1 mEq/mmol = 95.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 95.0 mmol chloride/L converts to 95.0 mEq chloride/L. 
The concentration of bicarbonate is 28.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 28.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 28.0 mmol * 1 mEq/mmol = 28.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 28.0 mmol bicarbonate/L converts to 28.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 139.0 mEq/L - (95.0 mEq/L + 28.0 mEq/L) = 16.0 mEq/L. Hence, The patient's anion gap is 16.0 mEq/L."
6313,39,Anion Gap,lab test,decimal,pmc-5292295-1,Extracted,"A 77-year-old woman lost consciousness 6 hours before being admitting to a local clinic where she underwent brain CT. The patient was promptly referred to our department with suspected basal ganglion ICH based on the brain CT. The patient had no medical history other than diabetes. Her premorbid Eastern Cooperative Oncology Group score was 3 due to dementia but she had normal cognitive functioning. The patient had stopped taking her diabetic medication 2 months earlier, on her own volition, and had been suffering progressive debilitation. No other symptoms were present. The patient did not take any sedatives or tranquilizers. The initial vital signs were blood pressure 180/98 mmHg, pulse rate 110/min, respiratory rate 18/min, and body temperature 36.8°C. A neurological examination revealed stupor, intact brainstem signs, and greater than grade III motor strength in all four extremities without lateralizing signs. She did not exhibit any abnormal movements of the extremities. No specific abnormalities were found on a systemic physical examination. The initial serum laboratory test results were blood glucose 607 mg/dL, hemoglobin 12.8 g/dL, white blood cells 6,720/mm3, platelets 193,000/mm3, aspartate aminotransferase 32 IU/L, alanine aminotransferase 38 IU/L, blood urea nitrogen 17 mg/dL, serum creatinine 1.2 mg/dL, sodium 120 mEq/L, potassium 5.0 mEq/L, chloride 89 mEq/L, serum osmolarity 280 mOsm, and lactate 12.5 mg/dL. No serum ethanol was detected, and an arterial blood gas analysis revealed the following: pH 7.454, pCO2 37.0 mmHg, pO2 78.1 mmHg, HCO3 25.4 mmol/L, and base excess 1.6 mmol/L. No ketones were detected in the urinalysis. Barbiturates, benzodiazepines, and tricyclic antidepressants were not found during a toxin-screening test. The initial brain CT showed a hyperdense lesion in the right basal ganglion (). On magnetic resonance imaging, T1-weighted images revealed high signal intensity indicative of changes due to nonketotic hyperglycemia; diffusion weighted imaging (DWI) and an apparent diffusion coefficient map showed restricted diffusion (). Blood glucose level was controlled with regular insulin, and conservative treatment and fluid resuscitation were provided. Electroencephalography revealed findings compatible with diffuse encephalopathy, but no signs of seizure were detected. After admission to the intensive care unit, the patient gradually recovered consciousness and was alert after 24 hours, as blood glucose and sodium were controlled. No abnormal movement disorder was noted after a return to consciousness. The patient was discharged 10 days after admission without any complications.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [120.0, 'mEq/L'], 'Chloride': [89.0, 'mEq/L'], 'Bicarbonate': [25.4, 'mmol/L']}",5.6,5.32,5.88,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 120.0 mEq/L. 
The concentration of chloride is 89.0 mEq/L. 
The concentration of bicarbonate is 25.4 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 25.4 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 25.4 mmol * 1 mEq/mmol = 25.4 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 25.4 mmol bicarbonate/L converts to 25.4 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 120.0 mEq/L - (89.0 mEq/L + 25.4 mEq/L) = 5.6 mEq/L. Hence, The patient's anion gap is 5.6 mEq/L."
6314,39,Anion Gap,lab test,decimal,pmc-5965203-1,Extracted,"A 69-year-old man with a past medical history of untreated hypertension, chronic back pain, and heavy smoking was brought in by ambulance to a community emergency department (ED) for severe bilateral leg pain and paraplegia. He had been unable to ambulate and remained lying on the floor for the prior three days. The patient also admitted to chronic low back pain that had worsened over the preceding week and not improved with his usual pain medications of naproxen and aspirin. He had no other complaints and denied any fevers or chills.
The patient’s initial vital signs were as follows: temperature 36.6 degrees Celsius, blood pressure 157/84 mmHg, heart rate 95 beats/min, respiratory rate 38 breaths/min, oxygen saturation 94% on room air. On physical examination, the patient appeared cachectic and chronically ill. His cardiac exam revealed a regular heart rate and rhythm without murmur. He had no palpable femoral, popliteal, or dorsalis pedis pulses bilaterally. A Doppler ultrasound performed at bedside further demonstrated a lack of pulses bilaterally from the femoral to the dorsalis pedis arteries. Abdominal examination showed a scaphoid, soft, non-tender abdomen without a pulsatile mass. There was no midline spinal tenderness or step-offs on musculoskeletal examination. Neurological evaluation demonstrated complete sensory loss from T10 and ending on the S1dermatome bilaterally. He had 5/5 motor strength in both upper extremities and 0/5 strength in hip flexion and extension as well as ankle dorsiflexion and plantar flexion bilaterally. The dermatological examination of the lower extremities revealed pale, cold, and mottled-appearing skin from the hips to the ankles bilaterally.
Initial laboratory data for the patient revealed white blood cells (WBC) 26.9 x109/L with neutrophil count 88.8%, hemoglobin 14.3 g/L, hematocrit 44.4%, and platelets 288 x 109/L complete metabolic panel showed the following: sodium (Na) 127 mmol/L, potassium (K) 7.3 mmol/L, chloride (Cl) 99 mmol/L, carbon dioxide (CO2) 18 mmol/L, blood urea nitrogen (BUN) 82 mg/dL, creatinine (Cr) 4.4 mg/dL, glucose 123 mg/dL, alanine transaminase 288 units/L, aspartate transaminase 1,372 units/L, albumin 3.4g/dL, alkaline phosphatase 86 units/L, direct bilirubin 1.0 mg/dL, indirect bilirubin 0.2 mg/dL, and total bilirubin 1.2 mg/dL. Prothrombin time, international normalized ratio, and partial thromboplastin time were 11.0, 1.0, and 26.9 seconds, respectively. Lactic acid was 3.36 mmol/L and creatinine kinase was 111,693 units/L. Troponin was also elevated at 3.850 ng/mL, and the electrocardiogram showed diffuse and deep T-wave inversions in the inferior, anterior, and lateral leads.
Point-of-care ultrasound of the abdominal aorta revealed a linear hyperechoic shadow in the aorta. Chest radiograph displayed a mildly tortuous ectatic aorta and evidence of chronic obstructive pulmonary disease (COPD). CT of the chest demonstrates a Stanford Type B aortic dissection (). The dissection starts from the subclavian and extends well into the infrarenal region of the abdominal aorta with significant mural thrombosis. On three-dimensional reconstructed images of the CTA abdominal aorta and bilateral lower extremities with runoff, significant stenosis is visible in both renal arteries, especially in the left (). The right lower extremity demonstrates near-complete occlusion of the right common iliac artery and both internal and external iliac arteries. The popliteal artery and arteries below the right knee are occluded. No blood flow to the right lower extremity is noted. The left lower extremity also demonstrates severe narrowing with moderate thrombosis in the iliac arteries with complete occlusion of the left external iliac artery. The left popliteal artery is likewise occluded, and no blood flow to the left lower extremity is visible. In addition to the above findings, intramuscular gas is seen in the thighs bilaterally, raising suspicion for myonecrosis ().
In the ED, the patient was aggressively resuscitated with an initial two-liter bolus of normal saline. A central venous catheter was inserted in the left internal jugular vein and the patient was started on an intravenous (IV) esmolol drip. He also received IV heparin, calcium chloride, sodium bicarbonate, insulin, glucose, and morphine during his ED stay. Shortly thereafter, the patient was taken for emergent dialysis in the intensive care unit (ICU) to further correct his electrolyte abnormalities, renal failure, and rhabdomyolysis prior to operative treatment. The laboratory abnormalities were partially corrected to a WBC of 17.5 with neutrophil count of 79.7%, K of 6.6, BUN of 87 and Cr at 3.6. The patient subsequently underwent open bilateral iliofemoral aortic popliteal thrombectomy, stent placement in the abdominal aorta and bilateral iliac arteries and bilateral femoral endarterectomy and patch angioplasty. While in the operating room, the patient became hypotensive and bradycardic and eventually suffered cardiopulmonary arrest. Despite a brief return of spontaneous circulation after resuscitative efforts, the patient died shortly thereafter in the ICU.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [99.0, 'mmol/L'], 'Bicarbonate': [18.0, 'mmol/L'], 'Sodium': [127.0, 'mmol/L']}",10,9.5,10.5,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 127.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 127.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 127.0 mmol * 1 mEq/mmol = 127.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 127.0 mmol sodium/L converts to 127.0 mEq sodium/L. 
The concentration of chloride is 99.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 99.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 99.0 mmol * 1 mEq/mmol = 99.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 99.0 mmol chloride/L converts to 99.0 mEq chloride/L. 
The concentration of bicarbonate is 18.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 18.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 18.0 mmol * 1 mEq/mmol = 18.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 18.0 mmol bicarbonate/L converts to 18.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 127.0 mEq/L - (99.0 mEq/L + 18.0 mEq/L) = 10.0 mEq/L. Hence, The patient's anion gap is 10.0 mEq/L."
6315,39,Anion Gap,lab test,decimal,pmc-3044576-1,Extracted,"A boy aged 4 years and 7 months was admitted to the emergency room with a chief complaint of unsteady walking that had started 10 h earlier. He felt drowsy and dizzy and was hypoactive. Following the neurological symptoms, he had a large volume of watery diarrhea. Before that, he was in good health, with no history of neurological or metabolic disease, fever or abdominal pain.
On admission, the child was dehydrated, but had normal temperature and blood pressure. His weight was 17 kg (25th percentile), and his height was 108 cm (50th percentile). The physical examination showed moderate muscle hypotrophy, scarce adiposity, abdominal distention and no visceromegaly. The neurological examination showed unsteady walking, dysarthria, hand dysmetria and isochoric light reagent pupils. He had irritability and self-aggressive behavior. Glasgow coma scale was 15. Drug screening tests were negative.
The child was born at term; birth weight was normal, and he was breastfed until 5 months of age. From the age of 2, he had sporadic diarrhea controlled with a low-fiber diet and lactose-free milk, and a diagnosis of irritable bowel syndrome was made. Enteropathogenic agents and blood in the stools were absent on all occasions. Serology tests for antigliadin (AGA) and antiendomysium antibodies (EMA) IgA and IgG were negative for CD at ages 2 and 4.
Laboratory test results showed hyponatremia (133 mEq/L), hypokalemia (3.1 mEq/L), hyperchloremic metabolic acidosis (pH 7.2; bicarbonate: 7 mmol/L; BE: –19.9). Serum chloride was 122 mEq/L, and lactate (<2 mmol/L) and glucose (85 mg/dL) levels were normal. Blood tests were normal. Liver and kidney functions were normal (TGO: 46 U/mL; TGP: 35 U/mL; urea: 10 mg/dL; creatinine: 0.3 mg/dL). Levels of serum iron, ferritin, cholesterol and albumin were extremely low. Stool analyses revealed no parasites, rare leukocytes and erythrocytes; cultures were negative and no Clostridium difficile toxins were detected. Radiographs showed global abdominal distension; cranial magnetic resonance imaging (MRI), computed tomography (CT) scans and cerebrospinal fluid tests were normal. Both sleep and waking electroencephalograms were normal.
Similar episodes were observed four consecutive times at 1-week intervals. Before each admission, the child ingested large amounts of bread, cakes and pizza. In the first three hospital admissions, his neurological symptoms faded within 2 days, but the hyperchloremic metabolic acidosis persisted without any evident cause. He had received intravenous hydration and was placed on a low-fiber and hypoallergenic diet without gluten restriction. The need for bicarbonate and potassium chlorate was high, so it was suggested that the loss of potassium and bicarbonate was probably associated with fecal loss because his kidney function was normal. During his fourth admission, a complete investigation for malabsorption was carried out.
Fecal analysis revealed an increased loss of fats. Serum IgA EMA and IgA anti-tissue transglutaminase antibody (anti-tTG) was reagent, over 100 U/mL. CD was suspected. The mucosa magnified by endoscope showed microhemorrhage, reduction in duodenal folds and multiple erosions (). Histological examination showed partial and total villous atrophy, intraepithelial lymphocytes and increased length crypts (Marsh 3C) ().
After the introduction of a gluten-free diet, the child improved progressively, and a supplement of folic acid, iron and calcium was introduced.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [122.0, 'mEq/L'], 'Bicarbonate': [7.0, 'mmol/L'], 'Sodium': [133.0, 'mEq/L']}",4,3.8,4.2,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 133.0 mEq/L. 
The concentration of chloride is 122.0 mEq/L. 
The concentration of bicarbonate is 7.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 7.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 7.0 mmol * 1 mEq/mmol = 7.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 7.0 mmol bicarbonate/L converts to 7.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 133.0 mEq/L - (122.0 mEq/L + 7.0 mEq/L) = 4.0 mEq/L. Hence, The patient's anion gap is 4.0 mEq/L."
6316,39,Anion Gap,lab test,decimal,pmc-7703305-1,Extracted,"This 74-year-old woman was admitted to a community hospital in a rural area of the Mideast USA with the sudden onset of progressive symmetrical weakness of hands and feet, and numbness in a stocking glove distribution. Two weeks prior, she had an episode of abdominal pain and fecal incontinence that resolved. The patient had a 25-year history of hypertension. She also had a history of asthma, chronic obstructive pulmonary disease, mild depression, urinary tract infections, appendectomy, cholecystectomy, hysterectomy, thyroid lobectomy, cosmetic leg vein stripping, and repair of a ventral hernia. She had a remote history of smoking and did not drink alcohol. Her medications included enalapril, furosemide, potassium, montelukast, and amitriptyline plus perphenazine.
Computed tomography (CT) of the head and spine showed no acute processes. CT of the abdomen showed diverticulosis. The patient was started on empiric ciprofloxacin and metronidazole for presumptive urinary tract infection. Four days later, she was transferred to a nursing home for rehabilitation. Two days after that, she was brought back to the community hospital emergency room with profound weakness of her arms and inability to grasp with either hand. She also had increasing paresthesia of her feet. Her serum sodium was 127 mEq/L (reference range [RR]: 135-145 mEq/L). She was admitted with suspected Guillain Barré syndrome. A few days later, she was transferred to a referral hospital for further neurological evaluation.
On admission to the referral hospital, the patient was afebrile, with pulse 125/minute, blood pressure 140/90 mm Hg, respirations 18/minute and oxygen saturation 97% on supplemental oxygen at 3 L/min. She had distal extremity weakness, worse on the right (0/5) than the left (1-2/5). Sensory examination revealed numbness up to the ankles and wrists. Distal tendon reflexes were absent. Her sodium was 122 mEq/L, potassium 4.2 mEq/L (RR: 3.6-5 mEq/L), chloride 91 mEq/L (RR: 98-108 mEq/L), bicarbonate 26 mEq/L (RR: 22-26 mEq/L), glucose 98 mg/dL (RR: 65-100 mg/dL), blood urea nitrogen (BUN) 8 mg/dL (RR: 7-21 mg/dL), creatinine 0.4 mg/dL (RR: 0.5-1.4), hemoglobin 14.3 g/dL (RR: 12.0-15.2 g/dL), mean corpuscular volume 81.8 fL (RR: 78-101 fL), platelets 243,000/mm3 (RR: 140,000-450,000/mm3), white blood cell (WBC) count 13,500/mm3 (RR: 4,100-10,900/mm3) (83% neutrophils, 12% bands, 2% lymphocytes, 2% monocytes), erythrocyte sedimentation rate (ESR) 42 mm/hr (RR: <30 mm/hr), rheumatoid factor 226 IU/dL (RR: 40-60 IU/dL), C-reactive protein 16.8 mg/L (“high risk” >3 mg/L) and anti-nuclear antibody <40 IU/L (RR: <40 IU/L). Lumbar puncture showed cerebrospinal fluid with 1 WBC/mm3 and protein 73 mg/dL (RR: 15-60 mg/dL).
The next day, electromyography showed evidence of a severe axonal and demyelinating sensorimotor peripheral neuropathy. Magnetic resonance imaging of the brain showed age-related volume loss with chronic microangiopathic disease. Blood and urine testing for lead and mercury poisoning returned negative. Intravenous immunoglobulin therapy was started.
The next day, the patient was pleasant and conversant despite persistent sodium levels between 120 and 129 mEq/L. Her upper and lower extremities showed 2+ edema. CT showed marked elevation of the left hemidiaphragm, a small left pleural effusion and left basilar atelectasis. CT of the abdomen and pelvis was negative. Serology for human immunodeficiency virus, hepatitis B, hepatitis C, and Lyme disease IgM returned negative. The syndrome of inappropriate antidiuretic hormone was suspected and fluid restriction commenced.
The next day, a rheumatologist elicited a history of 2 episodes in the past 9 months of frontal headache, dry mouth, anorexia and early satiety; also, the patient had been told by an optometrist that she had dry eyes, but this was asymptomatic. The patient had remained afebrile in the hospital, with blood pressure 117-142 / 50-70 mm Hg. On examination by the rheumatologist, the patient had a non-blanching erythematous skin rash over her feet, palpable purpura over her left breast, loss of sensation from her feet up to her knees and from her fingertips to her elbows, inability to move her legs and right arm, areflexia, and glossitis, but no salivary or parotid gland enlargement. The WBC count was 13,700/mm3, hemoglobin 12.7 g/dL, BUN 8 mg/dL, and creatinine 0.3 mg/dL. The rheumatologist suspected vasculitis and prednisone (50 mg daily) was started. C3 complement was later reported 110 mg/dL (RR: 79-152 mg/dL), C4 complement <10 mg/dL (RR: 13-75 mg/dL), and serum protein electrophoresis and cryoglobulin test negative. Over the next few days, there was no neurological improvement, but the patient's serum sodium rose to 132 mEq/L.
The next day, the patient reported feeling much better, but that night began having episodes of confusion and delirium. Immunoglobulin therapy was discontinued and trazodone was started. The following day, she remained afebrile and hemodynamically stable. Her oxygen saturation was 98-100%. She appeared comfortable. Her lungs were clear. Her neurological status remained unchanged. The next day, serology for anti-Ro/SSA and anti-La/SSB was negative. The following day, open biopsies of the peroneus brevis muscle and peroneal and sural nerves were performed, which revealed necrotizing vasculitis of vessels in muscle and sural nerve, active and chronic neurogenic muscular changes, epineural fibrosis and chronic axonal loss.
The next day, the patient developed a large hematoma of unclear etiology in her upper right arm. Her platelet count dropped from 230,000/mm3 to 136,000/mm3. Chest radiograph showed unchanged left basilar atelectasis. The patient was receiving stress-ulcer prophylaxis as well as deep venous thrombosis prophylaxis. Bilateral venous duplex examination of her upper extremities showed no evidence of deep venous thrombosis. Immunofluorescence for anti-neutrophilic cytoplasmic antibodies was reported negative at a dilution of 1:20 (normal <1:40).
The following day, the patient exhibited acute mental status changes. Her hemoglobin dropped from 11.7 g/dL to 9.2 g/dL over 12 hours. CT showed a large left parietotemporal intraparenchymal hematoma with surrounding vasogenic edema; this compressed the posterior aspect of the left lateral ventricle and induced a small amount of midline shift. A decompressive craniotomy was performed. Follow-up CT showed a decrease in compression of the left ventricle and decreased midline shift. Electroencephalogram showed severely abnormal diffuse slowing, periodic lateralized epileptiform discharges, bi-hemispheric epileptiform discharges, and an electrographic seizure. Intravenous phenytoin (100 mg) was given.
The patient’s family was informed that she was not likely to make a meaningful recovery. A decision was reached with the family to provide comfort measures only and the patient died several days later.
Postmortem examination revealed necrotizing vasculitis in skeletal muscle, ( and ), peripheral nerves, esophagus, stomach, small intestine, pancreas, liver, adrenals, kidneys, lungs and pericardium, involving predominantly medium-sized arteries, but also some large parenchymal arteries in the liver, associated with multifocal thromboses in liver (up to 2 cm), myocardium, thoracic lymph nodes and left adrenal gland, and hemorrhages in left parietal-occipital cerebrum (7 × 6 × 5 cm), upper right arm (29 × 18 cm), stomach, intestines, bladder, pericardium, trachea, mesentery, omentum, right ovary and right breast. In addition to and , a virtual (digital) slide of skeletal muscle is available for viewing at the Larry Nichols collection. It is case 003.
Autopsy also revealed leukocytoclastic vasculitis involving arterioles, capillaries and venules in the skin ().
Autopsy also revealed a small, 0.6 cm, moderately differentiated, invasive adenocarcinoma in the cecum. The cerebral blood vessels had severe hypertensive vasculopathy and moderate atherosclerosis in those of the circle of Willis, but no vasculitis. There was severe acute transmural ischemic colitis of the rectum, a microscopic acute infarct of the left adrenal, and moderate coronary atherosclerosis, with up to 60% stenosis of the left anterior descending coronary artery. The myocardium had a microscopic area of necrosis adjacent to a thrombosed arteriole. The aorta had moderate atherosclerosis and mild cystic medial degeneration, but no aortitis. The pulmonary arteries contained a branched, recently formed (4 × 0.5 × 0.3 cm) thrombus in the left lower lobe, a branched, recently formed (6 × 1 × 0.5 cm) thrombus in the right middle lobe, microscopic non-occlusive thrombi, and multifocal fibrous intimal thickening suggestive of previous organized thromboemboli, but no vasculitis. The skin had petechiae and ecchymoses on the trunk and limbs. The kidneys had arteriolar nephrosclerosis, but no vasculitis or glomerulonephritis.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [122.0, 'mEq/L'], 'Chloride': [91.0, 'mEq/L'], 'Bicarbonate': [26.0, 'mEq/L']}",5,4.75,5.25,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 122.0 mEq/L. 
The concentration of chloride is 91.0 mEq/L. 
The concentration of bicarbonate is 26.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 122.0 mEq/L - (91.0 mEq/L + 26.0 mEq/L) = 5.0 mEq/L. Hence, The patient's anion gap is 5.0 mEq/L."
6317,39,Anion Gap,lab test,decimal,usmle-672,Extracted,"A 9-year-old girl is admitted to the hospital with a one-day history of acute abdominal pain and vomiting. She also has a two-day history of fever, headache, and neck pain. Her immunizations are up-to-date. She is confused and oriented only to place and person. Her temperature is 39.7°C (103.5°F), pulse is 148/min, blood pressure is 90/50 mm Hg, and respiratory rate is 28/min. Cervical range of motion is limited by pain. The remainder of the neurologic examination shows no abnormalities. Laboratory studies show:
Hemoglobin 10.9 g/dL
Leukocyte count 44,000/mm3
Serum
pH 7.33
Na+ 130 mEq/L
Cl- 108 mEq/L
K+ 6.1 mEq/L
HCO3- 20 mEq/L
Urea nitrogen 34 mg/dL
Glucose 180 mg/dL
Creatinine 2.4 mg/dL
Urine ketones negative
A CT scan of the head shows enhancement of the arachnoid and pia mater. Cerebrospinal fluid analysis shows a leukocyte count of 3,400/μL (90% neutrophils), a glucose concentration of 50 mg/dL, protein concentration of 81 mg/dL, and no erythrocytes. Gram stain of the CSF shows gram-negative diplococci.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [108.0, 'mEq/L'], 'Bicarbonate': [20.0, 'mEq/L'], 'Sodium': [130.0, 'mEq/L']}",2,1.9,2.1,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 130.0 mEq/L. 
The concentration of chloride is 108.0 mEq/L. 
The concentration of bicarbonate is 20.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 130.0 mEq/L - (108.0 mEq/L + 20.0 mEq/L) = 2.0 mEq/L. Hence, The patient's anion gap is 2.0 mEq/L."
6318,39,Anion Gap,lab test,decimal,usmle-6092,Extracted,"A 33-year-old man presents to the emergency department with joint pain. He states that it has been steadily worsening and also generally feels weak. The patient does not routinely see a physician and is not currently taking any medications. Review of systems is notable only for increased urination. Laboratory values are ordered as seen below.

Leukocyte count: 6,250/mm^3 with normal differential
Platelet count: 197,900/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 25 mEq/L
Glucose: 229 mg/dL
AST: 98 U/L
ALT: 90 U/L

Radiography is performed as seen in Figure A.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [100.0, 'mEq/L'], 'Bicarbonate': [25.0, 'mEq/L'], 'Sodium': [139.0, 'mEq/L']}",14,13.3,14.7,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 139.0 mEq/L. 
The concentration of chloride is 100.0 mEq/L. 
The concentration of bicarbonate is 25.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 139.0 mEq/L - (100.0 mEq/L + 25.0 mEq/L) = 14.0 mEq/L. Hence, The patient's anion gap is 14.0 mEq/L."
6319,39,Anion Gap,lab test,decimal,usmle-8171,Extracted,"A 25-year-old man presents to his primary care physician with complaints of coughing up blood in his sputum and dark-colored urine for 1 week. There are streaks of blood intermixed with phlegm. He also expresses concerns about his urine being grossly dark brown. He denies any history of major bleeding from minor injuries. He is currently not taking any medications. His family history is negative for bleeding disorders. The vital signs include blood pressure 160/100 mm Hg, pulse 88/min, temperature 36.8°C (98.2°F), and respiratory rate 11/min. On physical examination, there are no significant clinical findings. The urinalysis results are as follows:
pH 6.7
Color dark brown
Red blood cell (RBC) count 12–14/HPF
White blood cell (WBC) count 3–4/HPF
Protein absent
Cast RBC and granular casts
Glucose absent
Crystal none
Ketone absent
Nitrite absent 
24 hours of urine protein excretion 1 g
    His renal function test showed:
Sodium 136 mEq/L
Potassium 5.1 mEq/L
Chloride 101 mEq/L
Bicarbonate 22 mEq/L
Albumin 3.5 mg/ dL
Urea nitrogen 28 mg/dL
Creatinine 2.5 mg/dL
Uric Acid 6.8 mg/ dL
Calcium 8.7 mg/ dL
Glucose 111 mg/dL
HPF: high-power field
A kidney biopsy is obtained and the immunofluorescence shows linear immunoglobulin G (IgG) deposition in the glomeruli.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [101.0, 'mEq/L'], 'Bicarbonate': [22.0, 'mEq/L'], 'Sodium': [136.0, 'mEq/L']}",13,12.35,13.65,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 136.0 mEq/L. 
The concentration of chloride is 101.0 mEq/L. 
The concentration of bicarbonate is 22.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 136.0 mEq/L - (101.0 mEq/L + 22.0 mEq/L) = 13.0 mEq/L. Hence, The patient's anion gap is 13.0 mEq/L."
6320,39,Anion Gap,lab test,decimal,pmc-5518485-2,Extracted,"A 58-year-old Thai female patient with hypertension, hyperlipidemia, and type 2 diabetes mellitus was infected with HIV 1.5 years ago. She had been taking antiretroviral drugs including tenofovir, emtricitabine, and boosted darunavir thereafter and achieved virological control after 6 months of therapy. Her CD4-positive T-lymphocyte count was 532/mm3 (40%). Her other medications were amlodipine 5 mg/day, enalapril 10 mg/day, fenofibrate 300 mg/day, and metformin 500 mg/day. She gradually developed anorexia, nausea, and fatigue over two weeks' duration. She also noticed a decrease in her daily urine volume and new-onset nocturia together with swelling in both of her legs particularly in the evening. She reported no fever, rash, or joint pain. She denied taking over-the-counter medication or nonsteroidal anti-inflammatory drugs. On examination, she was alert and had normal vital signs except for mild hypertension (body temperature 37.0°C, pulse rate 70/min, respiratory rate 16/min, and blood pressure 140/70 mmHg). She also had mildly pale conjunctivae and pitting edema in both of her legs. Laboratory tests showed severe azotemia (BUN 21.4 mmol/L, Cr 1,370 µmol/L) compared to baselines labs 1 month earlier (Cr 124 µmol/L). She also had hyponatremia, hypokalemia, metabolic acidosis, and elevated muscle enzyme (sodium 127 mEq/L, potassium 5.5 mEq/L, chloride 94 mEq/L, bicarbonate 10 mEq/L, and creatine phosphokinase 1,904 U/L; normal value 22–165 U/L). Urinalysis revealed isosthenuria, albuminuria, leukocyturia, and microhematuria without dysmorphic RBC (specific gravity 1.010, proteinuria 2+, glucose negative, WBC 3–5/hpf, and RBC 20–30/hpf). Renal ultrasonography demonstrated normal size but mildly increased parenchymal echogenicity of both kidneys without hydroureter or hydronephrosis. AKI was diagnosed. Differential diagnoses of AKI included tenofovir-induced ATN, HIV-associated nephropathy/immune complex glomerulonephritis, and rhabdomyolysis.
RRT was initiated soon after admission due to uremia and volume overload. After successful insertion of flexible double-cuff PD catheter, automated PD (Homechoice cycler; Baxter) using total dialysate (Dianeal; Baxter) volume of 10 L was started (fill volume of 2 L, five cycles, therapy time 12 hours) on the first day of admission resulting in adequate control of fluid, electrolytes, and acid-base balance. The doses of PD by total weekly Kt/V and total weekly CCr were 3.63 and 91.94 L/week, respectively. Renal biopsy was later performed revealing evidence of acute granulomatous interstitial nephritis (AIN) and ATN without evidence of glomerular or vascular injury. Antiretroviral drugs-induced ATN/AIN was diagnosed. The attending physician then switched antiretroviral regimen to stavudine/lamivudine/boosted darunavir regimen. During fourth week of admission, her urine volume had increased to 0.8–1.0 L per day but the measured renal CCr was still low (6.62 mL/min/1.73 m2). She was discharged from the hospital anyway and was prescribed to continue automated PD during night time at home (night intermittent PD; NIPD) at a similar dose (fill volume of 2 L, five cycles, therapy time 12 hours). Eventually, PD was successfully discontinued 9 months after the onset of AKI in August 2014. At that time, her serum Cr was 159 µmol/L, and measured renal CCr was stable at 17.3 mL/min/1.73 m2 with daily urine volume of 2,480 mL. Afterwards, she remained in chronic kidney disease (CKD) stage 4 with stable renal function for another whole year.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [94.0, 'mEq/L'], 'Bicarbonate': [10.0, 'mEq/L'], 'Sodium': [127.0, 'mEq/L']}",23,21.85,24.15,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 127.0 mEq/L. 
The concentration of chloride is 94.0 mEq/L. 
The concentration of bicarbonate is 10.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 127.0 mEq/L - (94.0 mEq/L + 10.0 mEq/L) = 23.0 mEq/L. Hence, The patient's anion gap is 23.0 mEq/L."
6321,39,Anion Gap,lab test,decimal,usmle-4379,Extracted,"A 75-year-old man with coronary artery disease and mitral valve stenosis status-post coronary artery bypass graft and mitral bioprosthetic valve replacement is evaluated in the intensive care unit. His postsurgical course was complicated by ventilator-associated pneumonia and bilateral postoperative pleural effusions requiring chest tubes. He has been weaned from the ventilator and has had his chest tubes removed but has required frequent suctioning to minimize aspirations. He has been dependent on a percutaneous gastrostomy tube for enteral nutrition for the past four weeks. He is currently on aspirin, carvedilol, atorvastatin, ceftazidime, and pantoprazole. He has a history of prostate cancer status post radical prostatectomy. His temperature is 96°F (35.6°C), blood pressure is 95/55 mmHg, pulse is 50/min, and respirations are 20/min. On physical exam, he is not alert and oriented but responds with moans when stimulated. His laboratory data are listed below:

Serum:
Na+: 145 mEq/L
Cl-: 110 mEq/L
K+: 3.4 mEq/L
HCO3-: 26 mEq/L
BUN: 10 mg/dL
Glucose: 112 mg/dL
Creatinine: 1.4 mg/dL
Thyroid-stimulating hormone: 10 µU/mL
Ca2+: 11.1 mg/dL
PO4-: 1.0 mg/dL
AST: 6 U/L
ALT: 10 U/L
Albumin: 2.5 mg/dL
Lactate dehydrogenase: 200 U/L (140-280 U/L)
Haptoglobin: 150 mg/dL (30-200 mg/dL)
1,25-(OH)2 D3: 10 pg/mL (15-75 pg/mL)
Parathyroid hormone: 9 pg/mL (10-60 pg/mL)

Leukocyte count: 10,000 cells/mm^3 with normal differential
Hemoglobin: 9 g/dL
Hematocrit: 30 %
Platelet count: 165,000 /mm^3

His electrocardiogram and chest radiograph are shown in Figures A and B.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [110.0, 'mEq/L'], 'Bicarbonate': [26.0, 'mEq/L'], 'Sodium': [145.0, 'mEq/L']}",9,8.55,9.45,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 145.0 mEq/L. 
The concentration of chloride is 110.0 mEq/L. 
The concentration of bicarbonate is 26.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 145.0 mEq/L - (110.0 mEq/L + 26.0 mEq/L) = 9.0 mEq/L. Hence, The patient's anion gap is 9.0 mEq/L."
6322,39,Anion Gap,lab test,decimal,pmc-3825672-1,Extracted,"A 21-year-old woman was admitted to the emergency department 4 hours after taking 20 tablets of CBS in a suicide attempt. Each tablet included 300 mg of CBS, which is equivalent to 120 mg of Bi2O3. There was no alcohol or another intravenous drug usage. In the emergency service, the patient underwent gastric lavage and received intravenous fluid therapy, after which she was admitted to the internal medicine intensive care unit.
Physical examination upon admission was unremarkable: blood pressure, 100/60 mm Hg; pulse, 76 beats/minute; respiration rate, 12 breaths/minute; and body temperature, 36.5°C. Laboratory tests were as follows: white blood cell count, 7860/mm3; hemoglobin, 10.8 g/dL; platelet count, 445,000/mm3; serum sodium, 141 mEq/L; potassium, 4.3 mEq/L; chloride, 104 mEq/L; glucose, 108 mg/dL; amylase, 85 U/L; aspartate aminotransferase (AST), 35 U/L; alanine aminotransferase (ALT), 14 U/L; lactate dehydrogenase (LDH), 150 U/L; hepatitis B surface antigen, nonreactive; and anti-hepatitis C virus, nonreactive. Her INR was reported to be normal at 1.1. Thyroid function tests were normal. Chest radiography also showed no abnormalities. Abdominal ultrasonography demonstrated slightly increased echogenicity in the renal parenchyma. Electrocardiography and echocardiography findings were normal. The patient rapidly became oliguric (<500 mL/day) and thereafter was anuric (0 mL/day). Blood creatinine increased to 2.6 mg/dL (blood urine nitrogen [BUN], 8 mg/dL) during the first 24 hours and to 3.1 mg/dL (BUN, 11 mg/dL) the next day. The baseline creatinine value was normal. Nevertheless, levels of LDH, ALT, and AST were elevated at 1,129 U/L, 62 U/L, and 139 U/L, respectively. Her scleraes were anicteric. The abdomen was soft, flat, and without palpable organomegaly. There was no edema. Arterial blood gases showed metabolic acidosis with a pH of 7.28, PaCO2 of 30 mmHg, PaO2 of 80 mmHg, BE of −11 mmol/L, and HCO3 of 14 mmol/L. Blood chemistry and urine sediment showed signs of proximal tubular dysfunction (Fanconi’s syndrome) with hypophosphatemia, hypouricemia, metabolic acidosis, and renal glycosuria despite normal plasma glucose concentration.
After consultation with personnel at Turkey’s National Poison Information Center, we started oral treatment with the chelating agent sodium-2,3-dimercapto-1-propanesulfonate (DMPS), which is related structurally to 2,3-dimercapto-1-propanol (dimercaprol, also known as British anti-Lewisite), using the following regimen: DMPS, 600 mg orally every 8 hours for 14 days. Hemodialysis was performed because of anuria and severe metabolic acidosis. Hemodialysis was conducted daily for the first 4 days and then three times weekly. Arterial blood gases returned to normal. Afterwards, the patient’s urine output progressively increased. Levels of LDH, ALT, and AST also returned to normal. The patient recovered clinically and was discharged after 15 days in hospital. Her serum creatinine and BUN levels upon discharge were 5.2 mg/dL and 20.0 mg/dL, respectively. Eight weeks after discharge, the patient’s renal function (serum creatinine and BUN) test results remained high. The patient is still on hemodialysis approximately 1 year later.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [141.0, 'mEq/L'], 'Chloride': [104.0, 'mEq/L'], 'Bicarbonate': [14.0, 'mmol/L']}",23,21.85,24.15,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 141.0 mEq/L. 
The concentration of chloride is 104.0 mEq/L. 
The concentration of bicarbonate is 14.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 14.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 14.0 mmol * 1 mEq/mmol = 14.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 14.0 mmol bicarbonate/L converts to 14.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 141.0 mEq/L - (104.0 mEq/L + 14.0 mEq/L) = 23.0 mEq/L. Hence, The patient's anion gap is 23.0 mEq/L."
6323,39,Anion Gap,lab test,decimal,pmc-7029460-1,Extracted,"A 76-year-old white man presented to our emergency department (ED) with recent onset of unsteady gait, poor oral intake, dysarthria, and dizziness for 1 week prior to presentation. His wife called an ambulance and had him brought to our ED as she noticed he was short of breath for the prior 12 hours. He did not have any symptoms suggestive of a recent upper respiratory tract infection or gastroenteritis. He denied exposure to sick contacts, recent immunizations, or consumption of canned foods or beverages. He did have a past medical history significant for esophageal stricture (diagnosed 2 years before) for which he had been undergoing routine endoscopic balloon dilation (last attempt was 3 months before). He lived in a rural upstate New York county and had retired as a meat-cutter 15 years before. His only medications at the time were ferrous sulfate (324 mg daily), pantoprazole (40 mg twice daily), and a multivitamin. He did not have a history of tobacco smoking. He consumed approximately two standard drinks in a week. He had no known allergies. While in our ED, his vital signs were: temperature, 37 ºC (98.6 ºF); heart rate, 100–110 beats per minute; blood pressure, 141/82 mmHg; and oxygen saturation 82% on room air and requiring 100% fraction of inspired oxygen (FiO2) via facemask to maintain saturations above 96%. On physical examination, he was in marked respiratory distress but not toxic-appearing. He was awake but drowsy, oriented only to self. His pupils were equal and symmetrical with appropriate response to light. His extra-ocular movements were intact. There was no facial droop; there was no deviation of tongue or uvula. His gag reflex was impaired. He could move all four extremities spontaneously and on command. However, motor strength appeared to be symmetrically and mildly diminished in all extremities and accompanied by decreased tone. Diminished knee and ankle reflexes were noted bilaterally. He had a diminished flexor plantar response bilaterally. Sensation was grossly intact in his face, trunk, and extremities. Coordination was impaired in upper and lower extremities with dysmetria and dysdiadochokinesia. Gait was not assessed. He had no visible involuntary movements. His neck was supple without signs of meningismus. A cardiovascular examination was unremarkable, with normal heart sounds and equal symmetrical pulses in bilateral extremities. His abdominal, musculoskeletal, and skin examinations were unremarkable. Although he was hemodynamically stable, he became lethargic with stridor and progressive hypoxia. Given concern for airway protection, he was emergently intubated with a 7.5 mm endotracheal tube on first attempt and placed on mechanical ventilatory support. For intubation, he was administered 1.5 mg/kg of succinylcholine and 0.3 mg/kg of etomidate intravenously. Maintenance fluids (normal saline at 125 cc/hour) and empiric intravenous administration of ceftriaxone at a dose of 2 g every 24 hours (to cover for possible aspiration pneumonia) was initiated. He was transferred to our intensive care unit for further management. A nasopharyngolaryngoscopy revealed bilateral true vocal cord paralysis. After stabilization on a ventilator, he underwent a tracheostomy on day 3 of admission and was transitioned successfully to a tracheostomy collar. Following extubation, he had consistent and gradual recovery of mental status. This was not, however, accompanied by any progressive improvement in motor function. He continued to have vocal cord immobility and flaccid weakness of his extremities.
On presentation, laboratory testing revealed a white blood cell (WBC) count, 13,800 cells/μL; hemoglobin, 14.7 g/dl; platelet count, 235,000 cells/μL; sodium, of 143 mmol/L; potassium, 4.2 mmol/L; chloride, 105 mmol/L; glucose, 176 mg/dL; bicarbonate, 27 mmol/L; creatinine, 0.53 mg/dL; blood urea nitrogen (BUN), 15 mg/dL; and calcium, 8.0 mg/dL. A hepatic function panel revealed a total protein level, 5.2 g/dL; serum albumin, 3.5 g/dL; total bilirubin, 0.5 mg/dl; aspartate aminotransferase (AST), 18 U/L; alanine aminotransferase (ALT), 21 U/L; international normalized ratio (INR), 1.08; creatine kinase, 127 U/L; and troponin I less than 0.015 ng/mL. Urine analysis demonstrated cloudy urine with specific gravity 1.018, pH 4.8, with 116 red blood cells (RBCs) and 4 white blood cells (WBCs), negative leukocyte esterase and nitrite. An electrocardiogram and chest X-ray were unremarkable. A urine drug screen and serum alcohol levels were negative. Serum thyroid-stimulating hormone (TSH) and cortisol levels were within normal limits. Thiamine, vitamin B6, and B12 levels were normal. Serological tests were negative for Lyme disease, human immunodeficiency virus (HIV), syphilis, hepatitis B, and hepatitis C. Blood and urine cultures obtained at presentation showed no growth. Non-contrast computed tomography (CT) of his head and magnetic resonance imaging (MRI) of his brain were normal except for mild ventriculomegaly (Fig. ). CT angiography of his head and neck revealed patent intracranial vasculature. A repetitive nerve stimulation electromyographic (EMG) study demonstrated patchy, moderate to severe, peripheral motor nerve denervation consistent with AIDP. A lumbar puncture was performed and analysis of the obtained cerebrospinal fluid (CSF) showed albuminocytologic dissociation with less than 3 nucleated cells per mL of fluid, elevated CSF protein of 62 mg/dl, and normal glucose levels (88 mg/dl). CSF cultures did not demonstrate any growth. Anti-GQ1B antibody and anti-acetylcholine receptor (AChR) antibody levels were negative.
A subacute presentation with ataxia, stridor with respiratory distress, and areflexia with weakness of bilateral upper and lower extremity offers a challenging differential (Table ).
It is prudent to first rule out an acute vascular cause such as stroke, especially involving the cerebellum and brainstem; for example, for example, an absence of any lateralizing neurological signs and disturbed consciousness would rule out stroke, especially one with brainstem involvement. Next, metabolic abnormalities due to alcoholism, vitamin deficiencies, or electrolyte deficiencies would be evident on a metabolic panel and on serum vitamin and ethyl alcohol levels. An absence of a suggestive history of exposure to Clostridium botulinum, such as consumption of canned or tinned foods, cosmetic use of botulinum toxin injection, or intravenous drug use, significantly lowers the possibility of botulism. An absence of fever and meningeal signs, and analysis of CSF obtained on lumbar puncture, can rule out meningitis and encephalitis. Spinal cord trauma and spinal shock in the initial stages would result in flaccid paralysis of extremities aside from obvious signs of trauma. Also, concomitant bulbar paralysis is highly unlikely. Overlapping autoimmune demyelinating syndromes such as Guillain–Barré syndrome (GBS) and Bickerstaff’s brainstem encephalitis (BBE) must be considered. GBS is more likely to have a characteristic pattern of ascending paralysis. BBE is considered to lie on the same spectrum as MFS as it may present with ataxia and ophthalmoplegia and can have positive anti-GQ1b antibodies. However, BBE is characterized more by hyperreflexia and somnolence. New-onset MG can be suspected but, in our patient, motor involvement was patchy, the anti-AChR antibody test result was negative, and EMG was not suggestive of MG.
Based on the above, a diagnosis of MFS involving the bulbar muscles was made and our patient was started on a 5-day course of intravenous immunoglobulin at a daily dose of 0.4 mg/kg body weight per day. Following completion of this course, he showed clinical improvement in phonation, overall muscle strength, as well as tone. Although he initially did require overnight ventilatory support through his tracheostomy, the need for this gradually diminished and he was weaned off the ventilator altogether.
Subsequent follow-up laryngoscopies after 1, 2, and 4 weeks showed improvement in vocal cord abduction. His overall respiratory status also improved with decreasing oxygen requirement and decreased need for tracheostomy suctioning. He continued to have moderate pharyngeal dysphagia and required placement of a jejunostomy tube for feeding. His hospitalization was also complicated with development of aspiration pneumonia. He was eventually discharged to a skilled nursing facility on a tracheostomy collar and jejunostomy tube after a total of 6 weeks of hospitalization and subsequently discharged home after making suitable progress in physical rehabilitation. He continued to follow-up with the physical medicine and rehabilitation (PMR) out-patient clinic and remained tracheostomy-dependent at 6 months following hospitalization. He was able to ambulate with a walker at that time.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [105.0, 'mmol/L'], 'Bicarbonate': [27.0, 'mmol/L'], 'Sodium': [143.0, 'mmol/L']}",11,10.45,11.55,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 143.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 143.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 143.0 mmol * 1 mEq/mmol = 143.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mmol sodium/L converts to 143.0 mEq sodium/L. 
The concentration of chloride is 105.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 105.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 105.0 mmol * 1 mEq/mmol = 105.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 105.0 mmol chloride/L converts to 105.0 mEq chloride/L. 
The concentration of bicarbonate is 27.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 27.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 27.0 mmol * 1 mEq/mmol = 27.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 27.0 mmol bicarbonate/L converts to 27.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 143.0 mEq/L - (105.0 mEq/L + 27.0 mEq/L) = 11.0 mEq/L. Hence, The patient's anion gap is 11.0 mEq/L."
6324,39,Anion Gap,lab test,decimal,usmle-5071,Extracted,"A 68-year-old man presents to the emergency department with confusion. The patient lives in a nursing home and has Alzheimer dementia at baseline. His nurse noticed that he was more confused than usual and was somnolent for the past 12 hours. The patient’s nurse also noticed that he was soiling his diapers more frequently with copious amounts of urine. The patient has lost 15 pounds since his last physician appointment 3 weeks ago. Laboratory values are ordered as seen below.

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 12.2 mg/dL
PTH: 8 pg/mL

The patient is referred to another physician for a more thorough workup including laboratory work and CT imaging.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [100.0, 'mEq/L'], 'Bicarbonate': [25.0, 'mEq/L'], 'Sodium': [139.0, 'mEq/L']}",14,13.3,14.7,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 139.0 mEq/L. 
The concentration of chloride is 100.0 mEq/L. 
The concentration of bicarbonate is 25.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 139.0 mEq/L - (100.0 mEq/L + 25.0 mEq/L) = 14.0 mEq/L. Hence, The patient's anion gap is 14.0 mEq/L."
6325,39,Anion Gap,lab test,decimal,usmle-1081,Extracted,"A 55-year-old man comes to the emergency department because of headache, fever, chills, shortness of breath, and abdominal pain for 1 week. He also feels tired and nauseous. He returned from a trip to Botswana 2 weeks ago. He has type 2 diabetes mellitus. He has smoked one pack of cigarettes daily for the past 30 years and drinks a glass of beer daily. His only current medication is metformin. His temperature is 39.3°C (102.8°F), pulse is 122/min, respirations are 28/min, and blood pressure is 109/84 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 94%. Examination shows jaundice. A few scattered inspiratory crackles are heard in the thorax. The liver is palpated 2 cm below the right costal margin. Laboratory studies show:
Hemoglobin 9.2 g/dL
Leukocyte count 9,400/mm3
Platelet count 90,000/mm3
Serum
Na+ 137 mEq/L
Cl- 102 mEq/L
K+ 5.2 mEq/L
HCO3- 13 mEq/L
Glucose 69 mg/dL
Lactate dehydrogenase 360 U/L
Creatinine 0.9 mg/dL
Bilirubin
_ Total 4.2 mg/dL
_ Direct 0.8 mg/dL
AST 79 U/L
ALT 90 U/L
Urine
Blood 3+
Protein trace
RBC 0–1/hpf
WBC 1–2/hpf
Arterial blood gas analysis on room air shows a pH of 7.31.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [102.0, 'mEq/L'], 'Bicarbonate': [13.0, 'mEq/L'], 'Sodium': [137.0, 'mEq/L']}",22,20.9,23.1,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 137.0 mEq/L. 
The concentration of chloride is 102.0 mEq/L. 
The concentration of bicarbonate is 13.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 137.0 mEq/L - (102.0 mEq/L + 13.0 mEq/L) = 22.0 mEq/L. Hence, The patient's anion gap is 22.0 mEq/L."
6326,39,Anion Gap,lab test,decimal,usmle-1827,Extracted,"A 42-year-old man comes to the physician for a health maintenance examination. He has had generalized fatigue and muscle aches since his previous visit 6 months ago. He has hypertension and gastroesophageal reflux disease. Current medications include amlodipine and omeprazole. His temperature is 37.1°C (98.1°F), pulse is 88/min and blood pressure is 156/102 mm Hg. Physical examination shows no abnormalities. Serum studies show:
Na+ 143 mEq/L
K+ 2.3 mEq/L
Cl- 100 mEq/L
HCO3- 31 mEq/L
Urea nitrogen 14 mg/dL
Creatinine 1 mg/dL
His blood pressure medication is discontinued. One week later his plasma aldosterone concentration is 35 ng/dL (N=3.6 - 24.0 ng/dL) and plasma renin activity is 0.4 ng/mL/h (N=0.3 to 4.2 ng/mL/h). An oral sodium loading test over 3 days fails to reduce aldosterone. A contrast-enhanced CT scan of the abdomen and pelvis shows a 3-cm, homogenous, right-sided adrenal mass with rapid contrast washout. He is counseled about his treatment options and chooses to pursue surgery.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [100.0, 'mEq/L'], 'Bicarbonate': [31.0, 'mEq/L'], 'Sodium': [143.0, 'mEq/L']}",12,11.4,12.6,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 143.0 mEq/L. 
The concentration of chloride is 100.0 mEq/L. 
The concentration of bicarbonate is 31.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 143.0 mEq/L - (100.0 mEq/L + 31.0 mEq/L) = 12.0 mEq/L. Hence, The patient's anion gap is 12.0 mEq/L."
6327,39,Anion Gap,lab test,decimal,pmc-5845528-1,Extracted,"A 22-year-old Hispanic male who recently emigrated from Guatemala within the last six months, without any previous medical history presented with a chief complaint of rectal and abdominal pain. Onset of the pain was four days before; however, he had been experiencing other symptoms for approximately three months. He reported productive cough, pyrexia, chills, night sweats, fatigue, and weight loss. He denied nausea, vomiting, diarrhea, melena, hematochezia, and rectal manipulation. Vital signs revealed temperature of 99.8°F, blood pressure 105/67 mmHg, pulse 91 bpm, respiratory rate 20 bpm, and oxygen saturation 99%. Labs revealed sodium 136 mEq/L, potassium 4.5 mEq/L, chloride 99 mEq/L, bicarbonate 22 mEq/L, creatinine 0.54, WBC 9.3 k/μl, hemoglobin 11.0 g/dl, and platelet 416 k/μl.
On physical examination, there was palpable right lower quadrant tenderness accompanied by abdominal rigidity and involuntary guarding. The patient was not amenable to digital rectal examination due to reported pain. However, illuminated visual examination of the rectum did not reveal any abnormalities. Due to the constellation of travel history, cough, and constitutional symptoms, a chest X-ray (CXR) was performed. It revealed biapical pleural thickening associated with parenchymal scarring, bronchiectasis, nodularity, and superimposed infiltrates (). Pulmonary tuberculosis (TB) was highly suspected, and the patient was placed in an isolation room. Further imaging was accomplished with computed tomography (CT) of the abdomen and pelvis with intravenous and oral contrast. This revealed acute appendicitis in the right lower quadrant congruent with earlier physical examination findings (). It also revealed a 3.1 × 1.9 cm dumbbell-shaped loculated fluid collection anterior to the anus consistent with perirectal abscess () confirming the etiology of his rectal discomfort. Finally, CT gave more insight into suspected pulmonary TB as it revealed nodular and patchy consolidation in both lung bases along with dense consolidation, fluffy airspace infiltrates, distended, and distorted bronchi ().
The patient was taken to the operating room expeditiously where he underwent diagnostic bronchoscopy with bronchoalveolar lavage (BAL), laparoscopic appendectomy, and incision and drainage of the perirectal abscess. By postoperative day one, cultures from BAL, sputum, and perirectal abscess were positive for acid-fast bacilli (AFB). Cultures from the perirectal abscess were also positive for beta-hemolytic group C streptococcus. Gross pathology of the appendix revealed a dusky, congested, red-brown serosa. When sectioned, we appreciated a dilated lumen measuring approximately 0.5 cm in diameter and an appendiceal wall thickness averaging at 0.3 cm. The mucosa was noted to be tan-pink, glistening, and congested. The lumen of the appendix contained abundant gray-pink semisolid contents. A discrete perforation was not appreciated. Histologic analysis revealed a focally effaced mucosa albeit where present, the epithelium was without atypia. Foci of acute and granulomatous inflammation were appreciated () along with epithelioid histiocytes and multinucleated giant cells (). Initial acid-fast staining was negative, but a repeat stain revealed the presence of acid-fast bacilli in the cytoplasm of a multinucleated giant cell ().
The patient was started on antitubercular drugs that included a combination of rifampin, isoniazid, pyrazinamide, and ethambutol. Based on sensitivities, he was also started on antibiotics for management of the streptococcal infection. The patient did well postoperatively and tolerated both antibacterial and antitubercular treatments without complication.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [136.0, 'mEq/L'], 'Chloride': [99.0, 'mEq/L'], 'Bicarbonate': [22.0, 'mEq/L']}",15,14.25,15.75,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 136.0 mEq/L. 
The concentration of chloride is 99.0 mEq/L. 
The concentration of bicarbonate is 22.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 136.0 mEq/L - (99.0 mEq/L + 22.0 mEq/L) = 15.0 mEq/L. Hence, The patient's anion gap is 15.0 mEq/L."
6328,39,Anion Gap,lab test,decimal,pmc-2783075-1,Extracted,"A 42-year-old African-American man with HIV/AIDS, not taking any medications including HAART and pneumocystis jiroveci prophylaxis since January 2007, presented in August 2007 with complaints of progressing shortness of breath, right-sided pleuritic chest pain, non-productive cough, and low-grade fever for last several weeks. He was diagnosed with HIV initially in 1999, during hospitalization for community-acquired pneumonia. The patient also had a history of facial herpes simplex virus type 2 (HSV-2) which has been recurrent and a history of pneumocystis pneumonia in June 2005. Previous laboratory studies from November 2006 revealed a CD4+ lymphocyte count of 20 and viral load HIV RNA of 65,833 copies/ml. He was a social drinker and had never used illicit drugs or tobacco products. HIV was presumed to be acquired sexually.
On initial assessment in the emergency department, he was cachectic but was in no acute distress. He had a fever of 38°C, blood pressure of 92/60 mmHg and regular pulse of 85 beats per minute. He was breathing at 20 breaths per minute. Oxygen saturation was 95% on room air, which decreased to 90% during ambulation. There were no oral lesions. His neck was supple. Examination of the lungs revealed bilateral expiratory wheezes and rare rhonchi. Cardiac examination demonstrated normal first sound, second sound with a regular rhythm and no murmurs. His abdomen was soft, nontender, nondistended with normoactive bowel sounds. His extremities were warm and his skin was dry with multiple small herpetic ulcers on the left ear and the left side of the face.
Laboratory tests revealed the following concentrations: sodium 138 mmol/L, potassium 4.5 mmol/L, chloride 103 mmol/L, bicarbonate 26 mmol/L, BUN 2.9 mmol/L, creatinine 61 μmol/L, glucose 4.78 mmol/L, white blood cell 3.4 × 109/L, neutrophils 86%, hemoglobin 7.1 mmol/L, hematocrit 33%, platelets 322 × 109/L, LDH 497 U/L, CD4+ lymphocyte count of 2. Chest X-ray was negative for infiltrate (Figure ), but high resolution CT of the chest revealed subtle right middle lobe and right upper lobe ground-glass opacity (Figure ).
The patient was admitted to the medical ward with a working diagnosis of pneumocystis pneumonia. A sputum sample was collected spontaneously for a culture work-up (Bartlett score: +3). No sputum sample was collected for mycobacterial stains. Empiric treatment with trimethoprim-sulfamethoxazole (1 tablet double-strength × 3 per day) and prednisone (40 mg × 2 per day) was started. The patient was also placed on treatment for HSV with acyclovir (400 mg × 3 per day). The prednisone doses were reduced as part of initial therapy for pneumocystis pneumonia. On the third day, direct fluorescent antibody test for Pneumocystis jiroveci was negative, but the culture was positive for Bordetella bronchiseptica. The patient was placed on droplet precautions; treatment was switched to levofloxacin (400 mg per day). Trimethoprim-sulfamethoxazole dose was modified to (1 tablet single-strength per day) for pneumocystis prophylaxis and azithromycin (1200 mg once per week) for Mycobacterium avium complex prophylaxis began. The patient subsequently improved on levofloxacin and on the seventh day was discharged home on levofloxacin, trimethoprim-sulfamethoxazole, azithromycin, and acyclovir. After eleven days, the patient visited our office. The patient had no complaints, no fever and no cough and his shortness of breath was fully resolved. On retrospect, the patient reported that he had been visited by his brother and his brother's dog at his home about a week prior to the illness.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [103.0, 'mmol/L'], 'Bicarbonate': [26.0, 'mmol/L'], 'Sodium': [138.0, 'mmol/L']}",9,8.55,9.45,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 138.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 138.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 138.0 mmol * 1 mEq/mmol = 138.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 138.0 mmol sodium/L converts to 138.0 mEq sodium/L. 
The concentration of chloride is 103.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 103.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 103.0 mmol * 1 mEq/mmol = 103.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 103.0 mmol chloride/L converts to 103.0 mEq chloride/L. 
The concentration of bicarbonate is 26.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 26.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 26.0 mmol * 1 mEq/mmol = 26.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 26.0 mmol bicarbonate/L converts to 26.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 138.0 mEq/L - (103.0 mEq/L + 26.0 mEq/L) = 9.0 mEq/L. Hence, The patient's anion gap is 9.0 mEq/L."
6329,39,Anion Gap,lab test,decimal,pmc-4400448-1,Extracted,"A 17-year-old girl presented herself in our emergency department in the morning after suicidal ingestion of 250–300, 325 mg acetylsalicylic acid (Aspirin®). She announced that she had ingested the tablets on the previous evening. She developed vomiting and tinnitus prior to admission. She was 167 cm tall and weighed 52 kg. Her blood pressure was 132/74 mmHg, heart rate 110/min and the respiratory rate 26/min. She was alert, her pupillary response slightly delayed, she had mild epigastric tenderness and the bowel sounds were diminished. Her blood values were as following: pH 7.51, pO2 121 mmHg (16.1 kPa), pCO2 18 mmHg (2.38 kPa), HCO3
− 14 mmol/L, lactate 0.8 mmol/L, sodium 142 mmol/L, potassium 3.2 mmol/L, chloride 123 mmol/L, ionized calcium 0.98 mmol/L, creatinine 72 μmol/L (0.81 mg/dL). The serum salicylate concentration was 6.4 mmol/L (88 mg/dL).
We administered 100 mL sodium bicarbonate 8.4%, 40 mmol potassium, 2 mg tropisetron and 80 mg esomeprazole intravenously. Furthermore, a central venous catheter was introduced into the internal jugular vein and haemodialysis was begun. Haemodialysis was continued until the salicylate levels decreased sufficiently. The clinical course was uneventful and we transferred her to our psychiatric department.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [123.0, 'mmol/L'], 'Bicarbonate': [14.0, 'mmol/L'], 'Sodium': [142.0, 'mmol/L']}",5,4.75,5.25,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 142.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 142.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 142.0 mmol * 1 mEq/mmol = 142.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 142.0 mmol sodium/L converts to 142.0 mEq sodium/L. 
The concentration of chloride is 123.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 123.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 123.0 mmol * 1 mEq/mmol = 123.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 123.0 mmol chloride/L converts to 123.0 mEq chloride/L. 
The concentration of bicarbonate is 14.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 14.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 14.0 mmol * 1 mEq/mmol = 14.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 14.0 mmol bicarbonate/L converts to 14.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 142.0 mEq/L - (123.0 mEq/L + 14.0 mEq/L) = 5.0 mEq/L. Hence, The patient's anion gap is 5.0 mEq/L."
6330,39,Anion Gap,lab test,decimal,pmc-7216313-1,Extracted,"A 73-year-old woman with rheumatoid arthritis and Gilbert syndrome was admitted to the hospital with clinical evidence of encephalopathy. On presentation her temperature was 36.5° C, blood pressure 165/73 mmHg, pulse rate 76 bpm, and respiratory rate 16 breaths/minute. Her physical examination was otherwise notable for encephalopathy in which she was initially agitated and combative followed by lethargy and disorientation to time, place, and person. There were no focal neurological deficits nor stigmata suggestive of central nervous system infection, vasculitis or cirrhosis. Laboratory investigations included a leukocyte count of 4900 cell/mm3 (normal: 4.8-10.8 * 103cells/mm3), hemoglobin 12.2 g/dL (14.0-18.0 g/dl), platelet count 339,000/mm3 (140,000-440,000/mm3), prothrombin time (PT) 11.5 sec (9.4-11.7), international normalized ratio (INR) 1.03 (0.93-1.11), sodium 144 mmol/L (136-145 mmol/L), potassium 4.0 mmol/L (3.5-5.1 mmol/L), chloride 113 mmol/L (98-111 mmol/L), bicarbonate 25 mmol/L (21-31 mmol/L), blood urea nitrogen (BUN) 10 mg/dL (6-20 mg/dl), creatinine 0.5 mg/dL (0.6-1.2 mg/dl), calcium 9.6 mg/dL (8.6-10.0 mg/dl), albumin 3.8 g/dL (3.4- 4.8 g/dl), total protein 6.4 g/dL (6.4-8.3 g/dl), aspartate aminotransferase 20 U/L (8-20 U/L), alanine aminotransferase 15 U/L (10-40 U/L), alkaline phosphatase 68 U/L (25-100 U/L), total bilirubin 1.8 mg/dL (0.3-1.2 mg/dl), direct bilirubin 0.44 mg/dL (0.0-0.19 mg/dL) and ammonia level 165 mcmol/L (19-60 mcmol/L). Urinalysis and blood cultures were negative.
CT of the brain was unremarkable. Further laboratory testing revealed a negative human immunodeficiency virus (HIV) screen, hepatitis panel, and anti-smooth muscle antibodies. Abdominal ultrasonography revealed normal size and echotexture of the liver along with a dilated portal vein and dilated vascular channel within the right hepatic lobe. The liver appeared non-cirrhotic and a liver elastography showed a Metavir score of F1 indicating no evidence of cirrhosis.
Abdominal CT angiography revealed a dilated portal vein measuring up to 1.8 cm at the porta-hepatis along with dilated superior mesenteric and splenic veins. Multiple dilated vascular channels were seen within the right hepatic lobe. An intrahepatic portosystemic shunt between an enlarged middle hepatic vein and two separate branches of the right portal vein was visualized (Figures -).
A liver biopsy showed normal architecture with no sign of inflammation or fibrosis. She received conservative management with lactulose and rifaximin. Hyperammonemia and encephalopathy resolved after the second day of admission and she was discharged with close outpatient follow up by gastroenterology and interventional radiology.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [113.0, 'mmol/L'], 'Bicarbonate': [25.0, 'mmol/L'], 'Sodium': [144.0, 'mmol/L']}",6,5.7,6.3,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 144.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 144.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 144.0 mmol * 1 mEq/mmol = 144.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 144.0 mmol sodium/L converts to 144.0 mEq sodium/L. 
The concentration of chloride is 113.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 113.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 113.0 mmol * 1 mEq/mmol = 113.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 113.0 mmol chloride/L converts to 113.0 mEq chloride/L. 
The concentration of bicarbonate is 25.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 25.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 25.0 mmol * 1 mEq/mmol = 25.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 25.0 mmol bicarbonate/L converts to 25.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 144.0 mEq/L - (113.0 mEq/L + 25.0 mEq/L) = 6.0 mEq/L. Hence, The patient's anion gap is 6.0 mEq/L."
6331,39,Anion Gap,lab test,decimal,usmle-5686,Extracted,"A 14-year-old male presents to the emergency department with altered mental status. His friends who accompanied him said that he complained of abdominal pain while camping. They denied his consumption of anything unusual from the wilderness, or any vomiting or diarrhea. His temperature is 100.5°F (38.1°C), blood pressure is 95/55 mmHg, pulse is 130/min, and respirations are 30/min. His pupils are equal and reactive to light bilaterally. The remainder of the physical exam is unremarkable. His basic metabolic panel is displayed below:

Serum:
Na+: 116 mEq/L
Cl-: 70 mEq/L
K+: 4.0 mEq/L
HCO3-: 2 mEq/L
BUN: 50 mg/dL
Glucose: 1010 mg/dL
Creatinine: 1.2 mg/dL

While the remainder of his labs are pending, the patient becomes bradypneic and is intubated. His ventilator is adjusted to volume control assist-control with a respiratory rate (RR) of 14/min, tidal volume (Vt) of 350 mL, positive end-expiratory pressure (PEEP) of 5 cm H2O, and fractional inspired oxygen (FiO2) of 40%. His height is 5 feet 5 inches. Intravenous fluids and additional medical therapy are administered.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [70.0, 'mEq/L'], 'Bicarbonate': [2.0, 'mEq/L'], 'Sodium': [116.0, 'mEq/L']}",44,41.8,46.2,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 116.0 mEq/L. 
The concentration of chloride is 70.0 mEq/L. 
The concentration of bicarbonate is 2.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 116.0 mEq/L - (70.0 mEq/L + 2.0 mEq/L) = 44.0 mEq/L. Hence, The patient's anion gap is 44.0 mEq/L."
6332,39,Anion Gap,lab test,decimal,usmle-2638,Extracted,"A 17-year-old boy is brought to the physician by his father because of a 7-month history of fatigue, recurrent leg cramps, and increased urinary frequency. His pulse is 94/min and blood pressure is 118/85 mm Hg. Physical examination shows dry mucous membranes. Laboratory studies show:
Serum
Na+ 130 mEq/L
K+ 2.8 mEq/L
Cl- 92 mEq/L
Mg2+ 1.1 mEq/L
Ca2+ 10.6 mg/dL
Albumin 5.2 g/dL
Urine
Ca2+ 70 mg/24 h
Cl- 375 mEq/24h (N = 110–250)
Arterial blood gas analysis on room air shows a pH of 7.55 and an HCO3- concentration of 45 mEq/L.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [92.0, 'mEq/L'], 'Bicarbonate': [45.0, 'mEq/L'], 'Sodium': [130.0, 'mEq/L']}",-7,-6.65,-7.35,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 130.0 mEq/L. 
The concentration of chloride is 92.0 mEq/L. 
The concentration of bicarbonate is 45.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 130.0 mEq/L - (92.0 mEq/L + 45.0 mEq/L) = -7.0 mEq/L. Hence, The patient's anion gap is -7.0 mEq/L."
6333,39,Anion Gap,lab test,decimal,usmle-1550,Extracted,"A 46-year-old man comes to the emergency department because of a 4-week history of fatigue and headache that have gotten progressively worse. He has allergic asthma treated with inhaled salbutamol. He immigrated to the USA from Thailand 9 years ago. He lives by himself and works as a waiter in a restaurant. He has had 6 lifetime male sexual partners and uses condoms inconsistently. He drinks 1–2 beers daily. His temperature is 38.2°C (100.8°F), pulse is 88/min, and blood pressure is 128/76 mm Hg. Examination of the mouth shows several white patches on the tongue and oral mucosa that can be easily scraped off with a tongue blade. On mental status examination, the patient is somnolent and has short-term memory deficits. The remainder of the examination shows no abnormalities. Laboratory studies show:
Hemoglobin 13.6 g/dL
Leukocyte count 9,600/mm3
Segmented neutrophils 80%
Eosinophils 1%
Lymphocytes 17%
Monocytes 2%
CD4+ T-lymphocytes 80/mm3 (Normal ≥ 500)
Platelet count 328,000/mm3
Serum
pH 7.36
Na+ 135 mEq/L
Cl- 101 mEq/L
K+ 4.8 mEq/L
HCO3- 22 mEq/L
Glucose 95 mg/dL
Creatinine 0.9 mg/dL
BUN 16 mg/dL
Bilirubin, total 0.7 mg/dL
AST 13 U/L
ALT 15 U/L
Erythrocyte sedimentation rate 10 mm/hour
HIV test positive
A lumbar puncture is performed and an opening pressure of 150 mm H2O is noted. Cerebrospinal fluid analysis shows a leukocyte count of 25/mm3 (60% lymphocytes), protein concentration of 52 mg/dL, and a glucose concentration of 37 mg/dL. India ink stain shows organisms with prominent capsules. Blood cultures are drawn.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [101.0, 'mEq/L'], 'Bicarbonate': [22.0, 'mEq/L'], 'Sodium': [135.0, 'mEq/L']}",12,11.4,12.6,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 135.0 mEq/L. 
The concentration of chloride is 101.0 mEq/L. 
The concentration of bicarbonate is 22.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 135.0 mEq/L - (101.0 mEq/L + 22.0 mEq/L) = 12.0 mEq/L. Hence, The patient's anion gap is 12.0 mEq/L."
6334,39,Anion Gap,lab test,decimal,pmc-3966100-1,Extracted,"The present case is about a 11-year-old Saudi boy who was referred to our service for bilateral adrenalectomy. The patient had been diagnosed by the pediatric endocrinologist with cycling Cushing disease. He presented with a history of rapid weight gain, decreased school performance and emotional disturbances in the previous 18 months. These complaints came in cycles, each lasting 2-4 months before the patient returned to normal. Adrenal ultrasound and computed tomography scan showed normal adrenal glands, magnetic resonance imaging of the brain also showed normal pituitary and hypothalamic area. During one of these cycles, his weight increased by 4 kg, blood pressure was 140/100 and he exhibited the typical signs of Cushing's disease. Blood work confirmed Cushing's disease. His serum cortisol at 1 PM was elevated at 16.6 mcg/dL. Electrolytes showed sodium 143 mEq/L, potassium 4 mEq/L, chloride 103 mEq/L, total CO2 27, blood urea nitrogen 9 mg/dL and creatinine 0.3 mg/dL. 24 h urine for free cortisol was high at 542 mcg/24 h (normal 5-55 mcg/24 h). At 2 months later, the patient presented with a third episode and was admitted for a full work-up. Urine free cortisol was elevated at 350 mcg/24 h, at midnight serum cortisol was 19.9 mcg/dL and serum adrenocorticotropic hormone (ACTH) was <4 pg/ml. Am cortisol was 15.7 mcg/dL and ACTH was 5.4 pg/ml. The patient was subjected to small and high doses of dexamethasone suppression tests (1 mg and 5 mg respectively) but there was no change in cortisol or ACTH serum levels. These findings confirmed a diagnosis of Cushing's disease of adrenal origin and its cyclic nature presented Carney's complex syndrome as a possibility. Further investigations to exclude Endocrine and cardiac tumors as part of Carney's complex included ultrasound of the thyroid and echocardiography which were normal. Ultrasound of the testes showed bilateral diffuse macro-calcification as well as 0.8 × 0.8 cm hypo-echoic mass within the left testicle, which strengthened the diagnosis of Carney's complex. The patient had no abnormal skin rash and the family history was negative for any endocrine problems. Deoxyribonucleic acid analysis on our patient did not show the known mutation in Carney's complex (PRKAR1A) which is found in only 50% of those patients.
Bilateral adrenalectomy was the treatment of choice in this patient. The plan was to start with right laparoscopic adrenalectomy and proceed to left adrenalectomy with the possibility of converting to open. The patient underwent a successful simultaneous bilateral adrenalectomy; the operative time was 3 h and 30 min. The estimated blood loss was 50 ml. The patient resumed his diet and ambulated on the 1st post-operative day and was discharged from hospital on the 2nd post-operative day. The post-operative course was smooth and uneventful and he was started on replacement therapy post-operatively. At 3 months later, he was doing well with a remarkable improvement in his behavior and school performance. Histopathology report of his adrenal gland was consistent with micronodular adrenocortical hyperplasia.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [103.0, 'mEq/L'], 'Bicarbonate': [27.0, 'mEq/L'], 'Sodium': [143.0, 'mEq/L']}",13,12.35,13.65,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 143.0 mEq/L. 
The concentration of chloride is 103.0 mEq/L. 
The concentration of bicarbonate is 27.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 143.0 mEq/L - (103.0 mEq/L + 27.0 mEq/L) = 13.0 mEq/L. Hence, The patient's anion gap is 13.0 mEq/L."
6335,39,Anion Gap,lab test,decimal,pmc-5089155-1,Extracted,"A 50-year-old African-American male with a history of moderate alcohol use and non-insulin-dependent diabetes mellitus presented to the emergency department for worsening right foot pain for 2 months after a heavy object landed on his right foot. He reported intense swelling of the foot with associated weeping of the skin on the right calf but denied paresthesias. Vitals were blood pressure 141/67 mmHg, heart rate 83 bpm, temperature 97.8°F, and 22 respirations per minute. Physical examination showed darkening of the skin on the dorsum of the right foot, bullous formation on the right calf, and tenderness to palpation at right calf (). The left calf also had darkening of the skin, but no muscle tenderness or rigidity on examination (). Pulses were present bilaterally. A basic metabolic panel showed sodium 121 mEq/L (135–145 mEq/L), potassium 3.8 mEq/L (3.5–5.0 mEq/L), chloride 91 mEq/L (95–105 mEq/L), bicarbonate 14 mEq/L (22–29 mEq/L), blood urea nitrogen (BUN) 27 mg/dL (6–20 mg/dL), and creatinine 3.75 mg/dL (0.6–1.3 mg/dL). A complete blood count (CBC) showed a white blood cell count (WBC) of 7.6×109/L (3.5–10.5×109/L), hemoglobin 9.6×109/L (13.5–17.5 g/dL), and platelets 93×109/L (150–450×109/L). Labs were significant for a lactate of 4.5 mmol/L (0.5–2.2 mmol/L) and aspartate aminotransferase (AST) 142 U/L (8–48 U/L). Clinical presentation was suggestive of severe sepsis secondary to the right calf infection. Blood cultures were drawn. Afterward, he was given vancomycin and piperacillin/tazobactam and was taken for surgical debridement of the wound. A tissue sample from the right leg was taken. Exploration of the wound revealed suppurative fluid in the right lower extremity on the medial and lateral sides as well as dead subcutaneous soft tissue. Fascia below was viable and found healthy. After the procedure, he was transferred to ICU due to hemodynamic instability.
His medical condition worsened. The morning of his second hospital day (post-operative day 1 from right leg debridement), his WBC was 22.4×109/L, lactate 11.4 mmol/L, troponin 1.34 ng/mL (<0.05 ng/mL), creatine kinase- MB (CK-MB) 16,887 (30–200 IU/L). Dark brown urine was noted in the Foley bag. Urine analysis showed blood, but urine microscopy lacked RBCs. He temporarily began renal replacement therapy for worsening renal failure and was given a blood transfusion for coagulopathy in the setting of liver failure. Due to lack of improvement with medical intervention, the patient was taken to the operating room for right leg fasciotomy. The anterior, medial, and superficial posterior compartment muscle groups showed gross tissue swelling without necrosis. Post-operatively, the CK-MB decreased to 16,134 IU/L.
The patient's WBC raised to 29.9×109/L following the surgery and his creatine phosphokinase (CPK) decreased from 16,134 to 14,461 U/L after his right leg fasciotomy, the following day. CT scan, without contrast, of the lower extremities showed diffuse soft tissue edema bilaterally but no gas/abscess under the muscle groups (). Due to lack of clear clinical improvement from his first two surgeries, increased tissue tension in the left lower extremity, the decision was made to perform an exploratory fasciotomy on the contralateral leg. Surgery revealed bulging muscles of the anterior and medial compartments under pressure. All tissues were viable on clinical examination intraoperatively. After the left leg fasciotomy, the patient's CPK levels decreased sharply in the following hours from 14,461 to 7,009 U/L. On post-operative day 1, from the left leg fasciotomy, the CPK fell to 5,301 U/L. Blood cultures were negative. Tissue sample from the right leg debridement showed group A beta hemolytic streptococcus. Clindamycin with intravenous immunoglobulin was added to the treatment plan. His clinical picture gradually improved until the patient was awake and was able to follow commands. He was transferred to the burn unit for further management.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [121.0, 'mEq/L'], 'Chloride': [91.0, 'mEq/L'], 'Bicarbonate': [14.0, 'mEq/L']}",16,15.2,16.8,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 121.0 mEq/L. 
The concentration of chloride is 91.0 mEq/L. 
The concentration of bicarbonate is 14.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 121.0 mEq/L - (91.0 mEq/L + 14.0 mEq/L) = 16.0 mEq/L. Hence, The patient's anion gap is 16.0 mEq/L."
6336,39,Anion Gap,lab test,decimal,trec-ct-2021-52,Extracted,"A 34 year old man comes to the clinic complaining of dizziness and severe diarrhea since yesterday. He has returned from an international trip few days ago and was living in a camp in Sudan for a month. He developed abdominal pain followed by bloating and nausea as well as loose bowel movements. Soon he was having profuse watery diarrhea without odor. The stool is watery and white but the patient has no fever. Blood pressure is 95/62 lying down and drops to 75/40 standing. The skin turgor has reduced. HR is 110 and he looks ill with dry mucosa. V. cholerae was seen in dark-field microscopy of a fresh stool specimen. The lab study is as bellow:
Sodium                           137 meq/L
Potassium                      2 meq/L
Chloride                         94meq/L
CO2                                 15 meq/L
Fecal leukocytes           None seen
Fecal occult blood        Negative",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [94.0, 'mEq/L'], 'Bicarbonate': [15.0, 'mEq/L'], 'Sodium': [137.0, 'mEq/L']}",28,26.6,29.4,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 137.0 mEq/L. 
The concentration of chloride is 94.0 mEq/L. 
The concentration of bicarbonate is 15.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 137.0 mEq/L - (94.0 mEq/L + 15.0 mEq/L) = 28.0 mEq/L. Hence, The patient's anion gap is 28.0 mEq/L."
6337,39,Anion Gap,lab test,decimal,pmc-6923966-1,Extracted,"A 2-year-old male with no significant past medical history presented to the ED for cough, congestion, rhinorrhea, and intermittent fever for 3-day duration. The patient had no recent travel, was fully immunized, and was on no medications. His parents report multiple loose, brown, non-bloody episodes of diarrhea for the past 1 day with associated decreased oral intake. Other associated symptoms included non-specific bilateral flank pain, abdominal pain, and body aches. After multiple episodes of vomiting throughout the night and discovery of a temperature of 100.3 °F at home, the family brought the patient to the ED. Vitals on arrival were as follows: 98.2 °F (ibuprofen noted to be given prior to arrival), heart rate 90 beats/min, respiratory rate 25 breaths/min, and an oxygen saturation of 100% on room air. Physical exam revealed a well-appearing male in no acute distress. His nose exhibited clear rhinorrhea. Examination of the posterior pharynx revealed mild erythema with a clear post-nasal drip. His abdominal exam revealed diffuse non-specific tenderness, however, without distention or any surgical signs. Chest radiography revealed bilateral perihilar peribronchial cuffing. A point of care glucose was 194. Urinalysis revealed a specific gravity of 1.008, pH 6.5, ketones 40 mg/dL, 11–24 white blood cells/hpf, +nitrites, 2+ leukocyte esterase, and 2+ bacteria. Influenza and respiratory syncytial virus (RSV) detection by PCR was negative. He received intravenous fluids, was able to tolerate liquids/food in the ED, and was discharged home on trimethoprim/sulfamethoxazole (Septra) for a urinary tract infection.
Over the next few days, the family noted increasing abdominal pain and localized right flank pain with associated chills and nausea. Six days after his initial ED visit, the family reported he appeared to be shaking and had a decreased activity level, prompting a second visit to the ED. Vitals on arrival were as follows: 102.9 °F, heart rate 110 beats/min, respiratory rate 28 breaths/min, and an oxygen saturation of 100% on room air. On physical exam, his extremities felt cold without cyanosis, however, with a capillary refill of 3–5 s. He had voluntary guarding to the right upper and lower quadrants. His right flank exhibited costovertebral angle tenderness. His remaining physical exam including examination of his skin and genitourinary region was unremarkable. Code sepsis was activated based on vitals and physical exam. A total of 20 cc/kg fluid resuscitation was initiated, and a blood culture was drawn. Laboratory evaluation was notable for a white blood cell count (WBC) of 22.5 (5–15 bil/L), lactic acid of 2.3 (0.5–2.2 mmol/L), sodium of 131 (138–145 mmol/L), potassium 3.3 (3.5–5.2 mmol/L), chloride 92 (98–110 mmol/L), carbon dioxide 22 (20–29 mmol/L), glucose of 112 (60–99 mg/dL), C-reactive protein (CRP) of 23.9 (0.0–0.8 mg/dL), and an erythrocyte sedimentation rate (ESR) of 79 (0–15 mm/h). All remaining laboratory evaluation was unremarkable, including a hepatic function panel. Abdominal radiography was also negative for the acute process.
An ultrasound of the appendix was performed with unsuccessful visualization of the appendix. Given his positive urinalysis and clinical deterioration, suspicion arose for possible acute pyelonephritis, for which a complete ultrasound of the abdomen was done (Fig. ), revealing a hypoechoic avascular area within the right upper quadrant. This complex fluid collection appeared to have an intimate relationship with the liver parenchyma. Subsequent CT of the abdomen/pelvis with intravenous contrast (Fig. ) revealed a retrocecal dilated appendix coursing cranially with adjacent inflammatory changes. Additionally, a focus of air and fluid was seen within the posterior right hepatic lobe measuring 9.0 × 5.3 × 6.3 cm. These findings were suggestive of an intrahepatic abscess, possibly the result of acute appendicitis. The patient was started on intravenous piperacillin/tazobactam (100 mg/kg/dose q8h) for both a urinary tract infection and acute appendicitis with development of a hepatic abscess. He was transferred to a tertiary care facility with pediatric general surgery capabilities.
On day 2, the urine culture that was obtained by catheterization grew 10,000–50,000 CFU/mL of Escherichia coli. In addition, he underwent ultrasound-guided placement of a 10 French pigtail catheter into the intrahepatic abscess with resulting 100 mL of purulent drainage removed. By day 3, the patient was clinically improving with resolution of fever and nausea. Gram stain of the abscess fluid revealed Gram-positive cocci/Gram-positive bacilli consistent with a polymicrobial infection. Deep wound culture grew Pseudomonas aeruginosa. Anaerobic culture grew Bacteroides fragilis and Peptostreptococcus with susceptibilities to piperacillin/tazobactam. A PICC line was placed for outpatient antibiotic infusions. His percutaneous drain was removed on day 7 and repeat imaging demonstrated resolution of the intrahepatic abscess. He was discharged on day 8 with outpatient pediatric infectious disease and general surgery follow-up and continued antibiotic therapy for 4 weeks with weekly outpatient laboratory evaluation. After completion of his antibiotic course, the patient returned for an elective laparoscopic appendectomy. At his most recent post-operative visit, the patient is doing well.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [92.0, 'mmol/L'], 'Bicarbonate': [22.0, 'mmol/L'], 'Sodium': [131.0, 'mmol/L']}",17,16.15,17.85,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 131.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 131.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 131.0 mmol * 1 mEq/mmol = 131.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 131.0 mmol sodium/L converts to 131.0 mEq sodium/L. 
The concentration of chloride is 92.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 92.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 92.0 mmol * 1 mEq/mmol = 92.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 92.0 mmol chloride/L converts to 92.0 mEq chloride/L. 
The concentration of bicarbonate is 22.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 22.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 22.0 mmol * 1 mEq/mmol = 22.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 22.0 mmol bicarbonate/L converts to 22.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 131.0 mEq/L - (92.0 mEq/L + 22.0 mEq/L) = 17.0 mEq/L. Hence, The patient's anion gap is 17.0 mEq/L."
6338,39,Anion Gap,lab test,decimal,pmc-4842364-1,Extracted,"A 71-year-old male with past medical history significant for bladder cancer status after radical cystectomy on chemotherapy, diabetes, coronary artery disease, and hypertension presented to the emergency room with complaints of fever and shivering. Three days prior to admission, his oncologist diagnosed him with anemia. He had complaints of cough with white sputum consisting of up to half a cup per day. He denied any shortness of breath, diarrhea, hematuria and dysuria, or weight loss.
Upon physical examination patient was febrile with a temperature of 100.7 F, blood pressure of 110/62 mmHg, heart rate of 114/min, and respiratory rate of 20/min and had O2 saturation of 100% on two liters' nasal cannula. Pertinent findings revealed irregular rate and rhythm with distant heart sounds. The remainder of the physical exam was otherwise unremarkable. Laboratory data demonstrated hemoglobin of 7.0 g/dL, hematocrit of 21.7%, white blood cell count of 5.7 K/μL with absolute neutrophil count 5.0 K/μL, and platelet count 37 K/μL. Basic metabolic panel revealed glucose of 100 mg/dL, blood urea nitrogen of 27 mg/dL, creatinine of 0.7 mg/dL, calcium 8.0 mg/dL, albumin 2.9 g/dL, sodium 134 mmol/L, potassium 4.4 mmol/L, chloride 103 mmol/L, and bicarbonate 20 mmol/L. Electrocardiogram showed atrial fibrillation with low voltage. Chest X-ray showed marked enlargement of the cardiac silhouette with a possibility of large pericardial effusion ().
The patient was admitted to the intensive care unit for sepsis and large pericardial effusion. He was started on empiric antibiotics. Computed tomography scan of the chest was ordered to rule out any metastasis which revealed a large pericardial effusion that was 2.2-cm in thickness (). Echocardiography demonstrated large circumferential pericardial effusion.
A cardiothoracic surgeon was called on consult and the patient underwent a pericardial window where 800 mL of hemorrhagic pericardial effusion was drained. Pericardial biopsy illustrated metastatic urothelial carcinoma (). Immunostains were performed which were positive for pancytokeratin, CK7, CK20, and uroplakin and negative for PSA. Patient remained critical and, despite all the efforts, the patient deteriorated and expired over the course of a few days due to his relatively poor prognosis.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [103.0, 'mmol/L'], 'Bicarbonate': [20.0, 'mmol/L'], 'Sodium': [134.0, 'mmol/L']}",11,10.45,11.55,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 134.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 134.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 134.0 mmol * 1 mEq/mmol = 134.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mmol sodium/L converts to 134.0 mEq sodium/L. 
The concentration of chloride is 103.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 103.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 103.0 mmol * 1 mEq/mmol = 103.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 103.0 mmol chloride/L converts to 103.0 mEq chloride/L. 
The concentration of bicarbonate is 20.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 20.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 20.0 mmol * 1 mEq/mmol = 20.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 20.0 mmol bicarbonate/L converts to 20.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 134.0 mEq/L - (103.0 mEq/L + 20.0 mEq/L) = 11.0 mEq/L. Hence, The patient's anion gap is 11.0 mEq/L."
6339,39,Anion Gap,lab test,decimal,pmc-3932381-1,Extracted,"A 78-year-old Korean male was admitted to our hospital in November for severe hypothermia. He had been diagnosed with hypertension at the age of 65 years, and had been treated with medications. He was found comatose on a mountaineering path 4 hours prior to admission. The temperature on the mountain, where he was lying, was reported to be 14℃. Upon admission, the patient was in deep stupor. His blood pressure, as measured in the supine position, was 80/50 mmHg, heart rate was 85 beats per minute, and respiratory rate was 19 per minute. The body temperature was below 34.0℃ (exceeding the measurement range of 34.0℃ to 44.0℃ of the thermometer, which had an error of measurement of ± 0.2℃). Electrocardiography showed J waves, prolonged QT, and occasional premature ventricular complexes (). Therefore, we estimated that his body temperature was indicative of moderate to severe hypothermia.
Chest radiography appeared normal, and ultrasonography of the kidneys showed normal echogenicity and intact corticomedullary differentiation without hydronephrosis. The patient's kidneys were within the normal range in size (the right kidney measured 9.3 × 5.4 cm, and the left kidney measured 9.9 × 4.6 cm). Renal scan (technetium-99m MAG3) indicated normal excretion and secretion functions. Urinalysis showed no proteinuria, and urine microscopic exam showed 10 to 19 red blood cells per high-power field with no casts. Blood urea nitrogen and serum creatinine concentrations were 25 mg/dL (normal range, 8 to 20) and 2.7 mg/dL (normal range, 0.6 to 1.2), respectively. In addition, fractional excretion of sodium was 4.5% and renal failure index was 2.25. The results of hormonal assays were as follow: plasma cortisol 14.6 µg/dL (normal range, 4.0 to 18.3), thyroid simulating hormone 1.43 µIU/mL (normal range, 0.17 to 4.05), free triiodothyronine 0.49 ng/dL (normal range, 0.78 to 1.82), and free thyroxine 1.25 ng/dL (normal range, 0.93 to 1.20). Anterior pituitary hormone levels were normal.
The results of arterial blood gas analysis were as follows: pH 7.260, pCO2 28.0 mmHg, pO2 151.0 mmHg, and HCO3- 12.6 mmol/L. Other laboratory studies produced the following results: serum calcium 8.8 mg/dL, serum phosphate 8.0 mg/dL, serum sodium 141 mEq/L, serum potassium 3.7 mEq/L, serum magnesium 3.1 mg/dL, hemoglobin A1c 5.4%, lactic acid 11.4 mmol/L, serum myoglobin 1,685.0 ng/mL, serum lactate dehydrogenase 159 IU/L, serum creatine phosphokinase 68 U/L, and serum amylase 582 U/L. Urinary concentrations of sodium, potassium, chloride were 95, 44.1, and 114 mEq/L, respectively. Urine osmolality was 537 mOsm/kg.
Upon hospitalization, the patient was wrapped in a warm blanket. We provided him with a forced-air warming system (Warm Touch, Mallinckrodt Medical Inc., Dublin, Ireland) infused with warmed saline (42℃) by pressure infusion (Ranger, Alrizant Healthcare Inc., Eden Prairie, MN, USA). Five hours of warming resulted in an increase in body temperature to 37.3℃, and the patient regained consciousness. Subsequently, electrocardiography showed a normal sinus rhythm (). After supportive care, the serum creatinine levels decreased gradually from 2.7 to 1.1 mg/dL on the fourth day of the hospital stay. The patient was discharged after 12 days of hospitalization, and the serum creatinine and body temperature were 1.2 mg/dL and 36.5℃ at discharge ().",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [141.0, 'mEq/L'], 'Chloride': [114.0, 'mEq/L'], 'Bicarbonate': [12.6, 'mmol/L']}",14.4,13.68,15.12,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 141.0 mEq/L. 
The concentration of chloride is 114.0 mEq/L. 
The concentration of bicarbonate is 12.6 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 12.6 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 12.6 mmol * 1 mEq/mmol = 12.6 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 12.6 mmol bicarbonate/L converts to 12.6 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 141.0 mEq/L - (114.0 mEq/L + 12.6 mEq/L) = 14.4 mEq/L. Hence, The patient's anion gap is 14.4 mEq/L."
6340,39,Anion Gap,lab test,decimal,pmc-3845239-1,Extracted,"A male patient aged 4 years and 3 months presented to the ER (emergency room) of our hospital with vomiting, diarrhea, and seizures. On day 1 of the illness, he had developed gastrointestinal symptoms, including vomiting and watery diarrhea that occurred 4-5 times per day. Four days later, bilateral generalized tonic-clonic seizures began, for which he was transported to our hospital. The seizures lasted up to 1 minute and subsided spontaneously. The patient was in a restless state of consciousness (level E3V4M5 according to the Glasgow Coma Scale and level II-10 according to the Japan Coma Scale). He stared, averted his gaze, continued to cry, and threw objects. This disturbance of consciousness persisted for 7 hours. The patient was sedated with midazolam, and MRI was performed. On awakening after 2 hours, the patient had regained a normal state of consciousness, after which there was no recurrence of disturbance of consciousness or seizures.
On admission, the patient's vital signs were as follows: temperature, 37.7°C; heart rate, 130 beats/minute; blood pressure, 100/60 mmHg; and SpO2, 98% (room air). No central nervous system abnormality, meningeal irritation, paralysis, or abnormalities in the thoracoabdominal region were observed. MRI revealed a hyperintense signal in the splenium of the corpus callosum on DWI and a hypointense signal in the ADC-map (). The patient's peripheral circulation was good.
The patient's medical history was unremarkable. He was born by spontaneous cephalic delivery after 39 weeks and 3 days of gestation (birth weight, 2664 g). No remarkable observations were noted during the pregnancy or perinatal period. The patient's growth and development were normal. The family medical history revealed that the father had febrile seizures.
The results of the patient's biochemical blood tests were as follows: WBCs, 3900/μL; Hb, 13.4 g/dL; Plt, 26.1 × 104/μL; BUN, 16 mg/dL; Cre, 0.3 mg/dL; Na, 132 mEq/L; K, 4.5 mEq/L; Cl, 101 mEq/L; AST, 41 IU/L; ALT, 21 IU/L; CRP, 2.59 mg/dL; Glu, 84 mg/dL; lactic acid, 7.8 mg/dL; pyruvic acid, 0.32 mg/dL; NH3, 49 μg/dL; pH, 7.424; PCO2, 39.6 mmHg; HCO3, 25.5 mmol/L; and BE, 1.6 mmol/L. No abnormality was detected on blood amino acid analysis or tandem mass screening. Cerebrospinal fluid (CSF) examination revealed a cell count of 4 cells (all mononuclear), a glucose concentration of 95 mg/dL, and a total protein concentration of 16 mg/dL.
On day 2 of admission, an electroencephalogram was obtained during sedated sleep. The spindle wave was appropriate for the patient's age. No bursts were observed. The patient's stool was positive for RV antigen. RT-PCR did not reveal RV RNA in the blood or CSF. RT-PCR analysis of RNA extracted from the stool revealed that the RV genotype was G5P[6].
On day 5 of admission, no recurrences were observed, and the patient was discharged. Eight days after admission, all abnormal signals had disappeared (). The clinical course was typical of MERS.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [101.0, 'mEq/L'], 'Bicarbonate': [25.5, 'mmol/L'], 'Sodium': [132.0, 'mEq/L']}",5.5,5.225,5.775,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 132.0 mEq/L. 
The concentration of chloride is 101.0 mEq/L. 
The concentration of bicarbonate is 25.5 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 25.5 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 25.5 mmol * 1 mEq/mmol = 25.5 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 25.5 mmol bicarbonate/L converts to 25.5 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 132.0 mEq/L - (101.0 mEq/L + 25.5 mEq/L) = 5.5 mEq/L. Hence, The patient's anion gap is 5.5 mEq/L."
6341,39,Anion Gap,lab test,decimal,pmc-8700017-1,Extracted,"A 20-day-old girl was admitted to the neonatal intensive care unit with a chief complaint of poor oral intake through the emergency room. She was lethargic and did not suck well with swallowing only 10 to 20 mL of formula at a time in the last two days. However, the amount of urine did not decrease, and diapers were changed 10 to 14 times per day. Vomiting and diarrhea were not observed. She was born at 38+2 weeks of gestation with 3380 g (50th–75th percentile) via cesarean section. No abnormal findings were noted during the prenatal and immediate postnatal periods. She was the first child of healthy, nonconsanguineous Korean parents, and her family history was unremarkable. At admission, her weight was 3100 g (25th–50th percentile), length was 53 cm (50th–75th percentile), and head circumference was 36 cm (50th–75th percentile). Although vital signs were appropriate for her age (heart rate 150 beats/min, blood pressure 78/50 mmHg, respiratory rate 48 breaths/min, and body temperature 36.5 °C), her lips were dry, and the capillary refill time was prolonged to 5–6 s. Physical examination revealed both thumbs in palms, frontal bossing, prominent upper lip, high arched palate, sparse frontal scalp hair, and bilateral 5th finger clinodactyly. An initial capillary blood gas analysis showed severe metabolic acidosis (pH 7.16, pCO2 28.3 mmHg, pO2 42 mmHg, HCO3−—17.3 mmol/L, base excess—17.3 mmol/L). With an impression of dehydration, 20 mL/kg normal saline was infused intravenously for over 1 h before other laboratory results were obtained.
The laboratory tests at admission were as follows: serum sodium 113.3 mEq/L, serum potassium 8.79 mEq/L, serum chloride 90.8 mEq/L, total CO2 8.1 mEq/L, serum lactic acid 1.0 mmol/L, serum ketone body 24 µmol/L, blood glucose level 83 mg/dL, blood urea nitrogen 55.1 mg/dL, and serum creatinine 0.65 mg/dL. Her urinalysis revealed a specific gravity of 1.014 and pH 5.0 and was negative for white blood cells and red blood cells. Her spot urine sodium and potassium levels were 74 and 27.7 mEq/L, respectively. The serum and urine osmolality values were 232 and 229 mOsm/kg, respectively. All the results of the neonatal screening test were normal, which included TSH (1.2 mIU/L), 17-hydroxyprogesterone (1.6 ng/mL), total galactose (1.0 mg/dL), and mass spectrometry for amino acid, organic acid, fatty acid, purine, peroxisome, and carbohydrate metabolic disorders. The plasma ammonia level was within the normal limit as 97 µg/dL. The plasma renin activity and serum aldosterone level were markedly elevated to 142.0 ng/mL/h (normal range, 0.32–1.84 ng/mL/h) and 4560 ng/dL (normal range, 4.2–20.9 ng/dL), respectively. Renal ultrasonography revealed no abnormalities except mild hydronephrosis in the right kidney (). No abnormal findings were found in cardiac echocardiography or brain magnetic resonance imaging.
To correct severe hyponatremia, 60 mL of 3% sodium chloride was initially intravenously administered over 8 h. Her urine output on the first day of admission was 8.45 mL/kg/h. Hyponatremia and hyperkalemia were improved with intravenous fluid and oral sodium chloride supplementation (8 mEq/kg/day). The patient consumed an adequate amount of milk (170–200 mL/kg/day), and weight gain was appropriate (40–80 g/day) after oral sodium chloride supplementation.
For the genetic diagnosis of the patient, targeted exome sequencing (TES) was performed. Genomic DNA was extracted from proband blood. All exon regions of all human genes (~22,000) were captured by a Twist Human Core Exome Kit (Twist Bioscience, South San Francisco, CA, USA). The captured regions of the genome were sequenced using a NovaSeq 6000 sequencing machine (Illumina, San Diego, CA, USA). In TES, no other pathogenic/likely pathogenic single-nucleotide variants (SNVs) or small insertion and deletion variants associated with the clinical phenotypes were identified. However, her clinical phenotypes and biochemical results indicated PHA1. Therefore, we performed a chromosomal microarray (CMA) to identify deletion-encompassing genes responsible for PHA1. CMA (CytoScan Dx, Affymetrix Cytogenetics, Santa Clara, CA, USA) revealed a 203 kb heterozygous deletion at 4q31.23: arr[GRCh37] 4q31.23(148865586_149069090)x1 (). This deletion spans exons 7–9 of NR3C2 and exons 15–23 of the ARHGAP10 gene. Haploinsufficiency of the NR3C2 gene, which encodes the mineralocorticoid receptor, is responsible for ADPHA1. However, the details of the functional role of the ARHGAP10 gene in human disease remain unclear. Parental testing showed that the deletion was paternally inherited. Her father had no history of clinical PHA1 manifestation and had normal plasma electrolytes and serum aldosterone values with only slightly elevated plasma renin activity at testing.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [90.8, 'mEq/L'], 'Bicarbonate': [17.3, 'mmol/L'], 'Sodium': [113.3, 'mEq/L']}",5.2,4.94,5.46,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 113.3 mEq/L. 
The concentration of chloride is 90.8 mEq/L. 
The concentration of bicarbonate is 17.3 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 17.3 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 17.3 mmol * 1 mEq/mmol = 17.3 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 17.3 mmol bicarbonate/L converts to 17.3 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 113.3 mEq/L - (90.8 mEq/L + 17.3 mEq/L) = 5.2 mEq/L. Hence, The patient's anion gap is 5.2 mEq/L."
6342,39,Anion Gap,lab test,decimal,pmc-3722985-1,Extracted,"A 31-year-old male presented to the emergency room complaining of progressive dyspnea and productive cough over the course of 4 months. He also noted decreased appetite with a 50-pound weight loss over the past 5 months. He had no significant past medical or surgical history and was not taking any medications. His family history was unremarkable. He quit smoking tobacco two months ago due to worsening respiratory status; he rarely used alcohol and never used recreational drugs. He was unmarried and in a long-term heterosexual relationship and denied multiple sexual partners. He was currently working in an automobile parts factory as a janitor. After high school he had enlisted in the army and served for four years; at that time he was stationed in Hawaii. While in Hawaii he visited a single prostitute on several occasions.
Initial vital signs revealed temperature was 99.9 F, blood pressure 128/83 mmHg, pulse 134 beats per minute, and respiratory rate 22 breaths/minute; oxygen saturation was 92% on room air. He was in moderate respiratory distress, yet was awake, alert, and cooperative. Extraocular muscles were intact; there was no nystagmus or scleral icterus. Pupils were equal, round, and reactive to light. He had thrush under his tongue and on the palate. There was no palpable lymphadenopathy. Heart rate was regular with no murmurs, rubs, or gallops by auscultation. There were no palpable thrills. He had equal chest rise bilaterally. Breath sounds were diminished throughout, with rales and dullness to percussion in the lower lung fields bilaterally. Sensory and motor examination was grossly intact.
Laboratory data revealed white blood count 13,900/mcL, hemoglobin 7.2 g/dL, platelets 370,000/mcL, sodium 131 mmol/L potassium 5.8 mmol/L, chloride 99 mmol/L, carbon dioxide 17 mmol/L, blood urea nitrogen 155 mg/dL, and serum creatinine 8.9 mg/dL. Arterial blood gases showed a pH of 7.39, pCO2 32.2 mmHg, bicarbonate 19.1 mmol/L, and pO2 74.5 mmHg on 3 L nasal cannula. Chest X-ray showed diffuse bilateral reticulonodular opacities (). He was found to be HIV positive with CD4 count of <5 cells/cc and viral load of 1,180,000 copies. Bronchoalveolar lavage was preformed; Grocott's methenamine silver stain of the washings demonstrated Pneumocystis jiroveci (). He received antibiotics and steroids with gradual improvement.
On hospital day 14, he became confused and acutely developed nystagmus with both a horizontal and prominent vertical component. He was also found to have ataxia with finger to nose testing and difficulty sitting up without support. Considering his immunosuppressed state, infectious and neoplastic etiologies were the primary diagnostic considerations. Lumbar puncture revealed clear CSF, normal opening pressure, and normal cell counts. Polymerase chain reactions for Epstein-Barr virus, Herpes simplex virus, cytomegalovirus, and John Cunningham (JC) virus were negative. Nontreponemal serological screening for syphilis (VDRL), toxoplasmosis antibody, and Cryptococcus antigen titers were negative. CT of the head did not show any intracranial mass, hemorrhage, or other acute findings. MRI of the brain revealed a slight increase in T2 signal within the medial aspect of thalamus bilaterally (). After excluding infection and neoplasm, the clinical diagnosis of Wernicke's encephalopathy was made. Intravenous thiamine was administered resulting in resolution of symptoms, which confirmed the diagnosis.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [99.0, 'mmol/L'], 'Bicarbonate': [19.1, 'mmol/L'], 'Sodium': [131.0, 'mmol/L']}",12.9,12.255,13.545,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 131.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 131.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 131.0 mmol * 1 mEq/mmol = 131.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 131.0 mmol sodium/L converts to 131.0 mEq sodium/L. 
The concentration of chloride is 99.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 99.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 99.0 mmol * 1 mEq/mmol = 99.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 99.0 mmol chloride/L converts to 99.0 mEq chloride/L. 
The concentration of bicarbonate is 19.1 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 19.1 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 19.1 mmol * 1 mEq/mmol = 19.1 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 19.1 mmol bicarbonate/L converts to 19.1 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 131.0 mEq/L - (99.0 mEq/L + 19.1 mEq/L) = 12.9 mEq/L. Hence, The patient's anion gap is 12.9 mEq/L."
6343,39,Anion Gap,lab test,decimal,usmle-8725,Extracted,"A 68-year-old man presents with shortness of breath, particularly when walking up stairs and when lying down to go to sleep at night. He also complains of a chronic cough and states that he now uses 2 extra pillows at night. The patient has a history of type 2 diabetes that is well-managed with metformin. He also takes Prozac for a long-standing history of depression. The patient has a 60-pack-year smoking history. He also has a history significant for alcohol abuse, but he quit cold turkey 15 years ago when his brother was killed in a drunk driving accident. Both he and his brother were adopted, and he does not know other members of his biological family. Despite repeated efforts of patient counseling, the patient is not interested in quitting smoking. The physical exam is significant for an obese male using accessory muscles of aspiration. The vital signs include: temperature 36.8°C (98.2°F), heart rate 95/min, respiratory rate 16/min, and blood pressure 130/85 mm Hg. The oxygen saturation is 90% on room air. Additional physical exam findings include cyanotic lips, peripheral edema, hepatomegaly, and ascites. The cardiovascular exam is significant for an S3 heart sound and elevated JVP. The pulmonary exam is significant for expiratory wheezing, diffuse rhonchi, and hyperresonance on percussion. The laboratory test results are as follows:
BUN 15 mg/dL
pCO2 60 mm Hg
Bicarbonate (HCO3) 32 mmol/L
Creatinine 0.8 mg/dL
Glucose 95 mg/dL
Serum chloride 103 mmol/L
Serum potassium 3.9 mEq/L
Serum sodium 140 mEq/L
Total calcium 2.3 mmol/L
Hemoglobin 26 g/dL
Bilirubin total 0.9 mg/dL
Bilirubin indirect 0.4 mg/dL
Iron 100
Ferritin 70
TIBC 300
The l posterior-anterior chest X-ray is shown in the image.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Chloride': [103.0, 'mmol/L'], 'Bicarbonate': [32.0, 'mmol/L'], 'Sodium': [140.0, 'mEq/L']}",5,4.75,5.25,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mEq/L. 
The concentration of chloride is 103.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 103.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 103.0 mmol * 1 mEq/mmol = 103.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 103.0 mmol chloride/L converts to 103.0 mEq chloride/L. 
The concentration of bicarbonate is 32.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 32.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 32.0 mmol * 1 mEq/mmol = 32.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 32.0 mmol bicarbonate/L converts to 32.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (103.0 mEq/L + 32.0 mEq/L) = 5.0 mEq/L. Hence, The patient's anion gap is 5.0 mEq/L."
6344,39,Anion Gap,lab test,decimal,pmc-7796785-1,Extracted,"A 77-year-old woman walked into the emergency department with an episode of syncope and vomiting. She had a 6-week history of lower extremity weakness and had presented at an orthopedic clinic, where cervical and lumbar MRI findings were unremarkable. Five weeks later, she developed fingertip numbness followed by appetite loss 3 days before admission. The patient had been diagnosed with hypertension, hyperuricemia, and dyslipidemia. Aspirin 81 mg/d, telmisartan 40 mg/d, spironolactone 25 mg/d, allopurinol 100 mg/d, metoprolol tartrate 60 mg/d, and pravastatin sodium 10 mg/d were prescribed. She was conscious, with a temperature of 35.7°C; heart rate, 37 beats/min, and blood pressure, 185/54 mm Hg. Electrocardiography (ECG) in the emergency room revealed bradycardia, with a heart rate of 37 beats/min, decreased P-wave amplitude, normal QRS width and a tall, tented T wave in limb and chest leads (Figure ). Laboratory findings revealed serum sodium 134 mEq/L, potassium 9.2 mEq/L, chloride 113 mEq/L, blood urea nitrogen 45 mg/dL, creatinine 2.2 mg/dL, and eGFR 17.7 mL/min/1.73 m2. Blood gas analysis (oxygen via nasal cannula 2 L/min) showed pH 7.234, pO2 118.6 mm Hg, pCO2 32.1 mm Hg, HCO3- 13.1 mmol/L, BE −13.2, Hb 8.7 g/dL, TSH 0.76 μIU/mL, and Ca 9.5 mg/dL. Five months before admission, her serum creatinine was 1.5 mg/dL and eGFR was 26.2 mL/min/1.73 m2.
We considered that chronic kidney disease (CKD) and medication with telmisartan, spironolactone, and metoprolol tartrate had caused the hyperkalemia. We discontinued these medications. Furthermore, sodium bicarbonate, calcium gluconate and glucose-insulin therapy was added. Her general condition gradually improved. By hospital day 4, her serum potassium improved to 4.5 mEq/L, ECG findings showed a normal sinus rhythm and an improved tented T wave (Figure ). Her symptoms of lower extremity weakness, fingertip numbness and appetite loss disappeared. Abdominal CT and upper/lower gastrointestinal endoscopy revealed no significant findings. Antihypertensive drugs were replaced with a calcium antagonist. She was discharged on hospital day 19.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [134.0, 'mEq/L'], 'Chloride': [113.0, 'mEq/L'], 'Bicarbonate': [13.1, 'mmol/L']}",7.9,7.505,8.295,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 134.0 mEq/L. 
The concentration of chloride is 113.0 mEq/L. 
The concentration of bicarbonate is 13.1 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 13.1 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 13.1 mmol * 1 mEq/mmol = 13.1 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 13.1 mmol bicarbonate/L converts to 13.1 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 134.0 mEq/L - (113.0 mEq/L + 13.1 mEq/L) = 7.9 mEq/L. Hence, The patient's anion gap is 7.9 mEq/L."
6345,39,Anion Gap,lab test,decimal,pmc-7476800-1,Extracted,"A 65-year-old man was referred to the hospital in 5th July 2019 because of refractory edema in both legs.
The patient had a history of CKD stage 3a, a hypotrophic left kidney, and hypertension. He had been prescribed amlodipine 2.5 mg for hypertensive medication. He also underwent radical prostatectomy for prostate cancer two years earlier. He underwent pelvic MRI using gadoterate meglumine (15 mL), immediately after iodide contrast-enhanced chest and abdomen computed tomography (CT) for cancer surveillance. Thirty days before CT scan, his creatinine level was 1.28 mg/dL and his estimated glomerular filtration rate (eGFR) was 58 mL/min/1.73 m2. After 185 days, he visited a local clinic because of edematous changes in both lower extremities. CT angiography of the lower extremities was performed; no stenosis or occlusion of vessels was observed. Although diuretics were administered for 2 weeks, the edema worsened and was accompanied by pruritus and pain (). Eventually, he was referred to our hospital for further evaluation.
Upon admission, his body temperature was 36.8°C and his blood pressure was 110/60 mmHg. His height was 161.3 cm, weight was 53.2 kg and body mass index was 20.4 kg/m2. Physical examination revealed grade 2+ pretibial pitting edema with redness, mild heat, and tenderness in both lower extremities. Both inguinal lymph nodes were not enlarged.
Initial laboratory findings at admission (about 210 days after MRI scan) were as follows: white blood cell count, 6,200 /μL (neutrophil 66%, lymphocyte 22%, monocyte 10.3%, eosinophil 0.5%); hemoglobin, 10.7 g/dL; platelet, 253,000 /μL; blood urea nitrogen, 41 mg/dL; serum creatinine, 2.07 mg/dL; eGFR, 32 mL/min/1.73 m2; serum sodium, 134 mmol/L; potassium, 3.4 mmol/L; chloride, 102 mmol/L; total CO2, 20 mmol/L; calcium, 9.3 mg/dL; phosphate, 1.5 mg/dL; total protein, 6.9 g/dL; albumin, 4.0 g/dL; aspartate transaminase, 43 U/L; alanine aminotransferase, 15 U/L; and C-reactive protein, 0.96 mg/dL. Routine urine analysis revealed a pH of 6.0 and trace proteins. Red and white blood cells were absent in the urine. The spot urine protein/creatinine ratio was 209 mg/g and the spot urine albumin/creatinine ratio was 60 mg/g. Thyroid function tests were normal: thyroid stimulating hormone, 2.47 μIU/mL and free T4, 0.98 ng/dL. Fractional excretion of Na 0.1% and Fractional excretion of urea on admission was 17.6%, which suggested the patient was prerenal AKI.
Chest radiography and echocardiogram findings were normal. During doppler sonography of both lower extremities, the venous velocity was normal and there was no evidence of thrombosis. None of the aforementioned findings were suggestive of refractory edema.
Fluid therapy was administered to treat the AKI, which was probably caused by the diuretics he was given during his two-week stay in the local clinic. Subsequently, his renal function improved: serum creatinine, 1.18 mg/dL; and eGFR, 63.9 mL/min/1.73 m2. Since the redness and tenderness of both legs were suggestive of cellulitis-associated edema, intravenous cefazolin was administered for two weeks. However, the lesion gradually spread from his ankle to his thigh and changed into fibrotic induration. Contracture of the ankle and knee joints also occurred ().
To detect diffuse or localized systemic sclerosis, antinuclear antibody, anti-Scl 70 antibody, and anti-centromere antibody tests were performed, but the results were all negative. Also, eosinophilia and paraproteinemia was not seen, which is commonly accompanied in scleromyxedema or eosinophilic fasciitis. Although approximately 50 weeks had passed since he was exposed to the gadolinium, the characteristic clinical features led to the suspicion of NSF. A biopsy of the right anterior tibial skin lesion was performed to examine tissue for disease. This revealed unique features of the NSF such as dermal thickening with collagen fibers extending into the subcutaneous septa and a large number of spindle-shaped fibrocytes (). Neither eosinophilic tissue infiltration nor fat necrosis with calcification of adipocytes was found.
Systemic methylprednisolone (20 mg/day) was administered for two weeks to treat the NSF. Additionally, UV-A1 topical phototherapy of 1.5 joule (J)/cm2 was administered to the lower leg lesion twice a week. The patient underwent intensive physical therapy including stretching, pneumatic compression, and Transcutaneous Electric Nerve Stimulation . We administered MTX 15 mg weekly while reducing the methylprednisolone dose weekly by half until a dose of 2 mg/day was administered. Simultaneously, the UV-A1 intensity was gradually increased to 3.0 J/cm2. After 6 months of treatment, the reddish edema improved and the skin induration decreased. Although the contracture of the ankles was still present (), there was no further disease progression. Currently, the patient receives MTX (10 mg) weekly and methylprednisolone (2 mg) daily.
Informed consent for publication of clinical data was submitted by the patient and the images are published with the consent of the patient.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [134.0, 'mmol/L'], 'Bicarbonate': [20.0, 'mmol/L'], 'Chloride': [102.0, 'mmol/L']}",12,11.4,12.6,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 134.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 134.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 134.0 mmol * 1 mEq/mmol = 134.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 134.0 mmol sodium/L converts to 134.0 mEq sodium/L. 
The concentration of chloride is 102.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 102.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 102.0 mmol * 1 mEq/mmol = 102.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 102.0 mmol chloride/L converts to 102.0 mEq chloride/L. 
The concentration of bicarbonate is 20.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 20.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 20.0 mmol * 1 mEq/mmol = 20.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 20.0 mmol bicarbonate/L converts to 20.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 134.0 mEq/L - (102.0 mEq/L + 20.0 mEq/L) = 12.0 mEq/L. Hence, The patient's anion gap is 12.0 mEq/L."
6346,39,Anion Gap,lab test,decimal,pmc-4020898-1,Extracted,"The subject was a 23-year-old Japanese man with no abnormalities identified on examination and no particular medical history. Two weeks prior to onset of cardiac arrest, he noticed slight fever, coughing, loss of appetite, and weight loss of 3 kg. He did not have symptoms such as nausea, vomiting, or diarrhea. While jogging, the patient became aware of back pain and lost consciousness. A bystander immediately administered basic life support. Then, emergency medical technician-paramedics continuously administered cardiac pulmonary resuscitation using an automated external defibrillator to the subject, who was thereafter transported by ambulance to our hospital, Yamaguchi Grand Medical Center.
At the time of transfer to the hospital, the blood pressure of the subject could not be measured. An electrocardiogram (ECG) monitor indicated that his heart rate was 30 bpm (pulseless electrical activity) (). In addition, his body temperature was 37.3°C and he had a Glasgow coma scale score of E1M1V1 (no eye opening, no verbal response, no motor response). Physical examination revealed swelling of the thyroid gland on the anterior side of the neck; however, there were no signs of jaundice or peripheral edema. In addition, there were no signs of exophthalmos, finger tremor, loss of hair, or nail lesions. Because of pulseless electrical activity, cardiac arrest was diagnosed using an ECG, and administration of medication (epinephrine and atropine) led to ventricular fibrillation ( and ). As a result, defibrillation was administered using a direct current (DC) type 360-J monophasic defibrillator (Nihon Kohden Corporation, Tokyo, Japan) and the sinus rhythm was restored. Nonetheless, heart rate and breathing sounds were normal.
The laboratory findings were as follows: a white blood cell count of 13,800/μL; hemoglobin, 12.0 g/dL; platelets, 434,000/μL; C-reactive protein, 0.2 mg/dL; aspartate aminotransferase, 51 IU/L; alanine aminotransferase, 74 IU/L; lactic dehydrogenase, 217 IU/L; creatine kinase 61 IU/L; creatine kinase MB 46 IU/L; troponin T, <0.05 ng/mL; blood urea nitrogen, 16.4 mg/dL; creatinine, 0.81 mg/dL; blood glucose, 77 mg/dL; sodium, 143 mmol/L; potassium, 5.8 mmol/L; chloride, 97 mmol/L; calcium, 9.2 mg/dL; arterial blood gases (FiO2:100%, timing of return of spontaneous circulation and post-tracheal intubation); pH 7.53; PaCO2 30.8 mmHg; PaO2 184 mmHg; and HCO3 11.4 mEq/L.
Chest radiography revealed no congestion or pneumothorax in the lung field. After the sinus rhythm improved, an ECG revealed no significant changes in ST-T or QT interval prolongation (). In the echocardiography results, there was no cardiac wall motion dyssynchrony suggestive of ischemic heart disease, and the ejection fraction was 70%. There were no right side of the heart findings indicative of cardiac tamponade and thromboembolism. Thyroid ultrasound imaging showed that the parenchyma was marginally irregular and heterogeneous with rich blood flow.
On examination of thyroid function, the following findings were obtained: thyroid-stimulating hormone (TSH) level: <0.005 (reference range: 0.24–3.72), free thyroxine (T4) level: 5.03 (reference range: 0.94–1.52), free triiodothyronine (T3) level: >30.00 (reference range: 2.01–3.72), TSH receptor antibody: 30.2% (reference values: <15), and TSH-stimulating receptor antibody: 146% (reference values: <180).
After spontaneous circulation was returned, the reduced level of consciousness persisted and artificial respiration and cerebral hypothermia were administered. Hyperthyroidism-induced thyroid storm was strongly suspected and the patient was treated with thiamazole 60 mg/day, inorganic iodine (iodine solution 150 mg/day), hydrocortisone 300 mg/day, and metoprolol tartrate (beta-blocker) 120 mg/day for 2 weeks. After the initial 2 weeks, thiamazole 60 mg/day and metoprolol tartrate (beta-blocker) 120 mg/day were taken.
On day 22 of hospitalization, the subject was weaned from the artificial respirator; however, hypoxic encephalopathy- induced higher cerebral dysfunction persisted.
On day 30 of hospitalization, follow-up testing revealed that free T4 and free T3 levels had returned to normal (free T4 level: 1.46 and free T3 level: 3.43), but TSH suppression persisted (TSH <0.005). Because of higher cerebral dysfunction, coronary angiogram and magnetic resonance imaging (MRI) of the heart were not performed in accordance with the wishes of his family. On day 55, the subject was transferred to another hospital for long-term medical care. TSH level was 0.14 at the time.
At the present 1-year follow-up, no signs of recurrent ventricular fibrillation or other cardiac arrest rhythms have been observed in the other hospital in which the patient is receiving long-term medical care.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [143.0, 'mmol/L'], 'Bicarbonate': [11.4, 'mEq/L'], 'Chloride': [97.0, 'mmol/L']}",34.6,32.87,36.33,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 143.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 143.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 143.0 mmol * 1 mEq/mmol = 143.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 143.0 mmol sodium/L converts to 143.0 mEq sodium/L. 
The concentration of chloride is 97.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 97.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 97.0 mmol * 1 mEq/mmol = 97.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 97.0 mmol chloride/L converts to 97.0 mEq chloride/L. 
The concentration of bicarbonate is 11.4 mEq/L. 
Plugging in these values into the anion gap formula gives us 143.0 mEq/L - (97.0 mEq/L + 11.4 mEq/L) = 34.6 mEq/L. Hence, The patient's anion gap is 34.6 mEq/L."
6347,39,Anion Gap,lab test,decimal,pmc-3104540-1,Extracted,"An 8-year-old, thin, lean boy presented with a history of two episodes of syncope. On examination, pulse rate was 110 beats per minute and the blood pressure was 210/110 mmHg. There was no radio-femoral delay. A heaving apex in the fifth intercostal space inside the mid-clavicular line, a wide, but not-fixed split S2 with normal P2 and a grade II/VI systolic murmur at the apex were noted. On abdominal examination, a renal bruit was heard on the left side. Neurological examination and fundus were normal. His electrocardiogram revealed sinus tachycardia with corrected QT interval of 520 msec and occasional premature ventricular complexes [Figures and }. There was no family history of deafness or sudden death.
Laboratory studies were remarkable for serum sodium 136 mEq/L, potassium 2.1 mEq/L, chloride 99 mEq/L, bicarbonate 31 mEq/L, blood urea 22 mg/dL and serum creatinine 0.8 mg/dL. Serum calcium, 24-h urinary vanillyl mandelic acid (VMA) levels and complete blood counts were within normal limits. Results of the urinalysis were normal.
Echocardiography revealed concentric left ventricular hypertrophy and mild mitral regurgitation. There was no evidence of left ventricular outflow tract obstructive disease. The patient initially received intravenous magnesium and potassium, nitroglycerine, oral beta blockers and angiotensin receptor antagonists. His QTc normalized, premature ventricular ectopics disappeared, blood pressure got controlled and the patient became asymptomatic. Renal ultrasound Doppler was suggestive of replacement of left kidney by a necrotic mass (5 cm × 4.8 cm), with invasion of the left renal artery with normal vascular flow profile. A contrast enhanced computed tomography scan of the abdomen confirmed a cystic mass replacing the left kidney and compressing the left renal vein, with normal adrenal glands. A differential diagnosis of Bosnaik type IV cyst and Wilm's tumor were considered [].
The patient was referred for resection of the left renal mass. Nephrectomy was performed and a histopathological examination of the specimen revealed features suggestive of reninoma []. The post-operative period remained uneventful. Patient's blood pressure became normal. His symptoms resolved and he is asymptomatic on one and half years follow up.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [136.0, 'mEq/L'], 'Bicarbonate': [31.0, 'mEq/L'], 'Chloride': [99.0, 'mEq/L']}",6,5.7,6.3,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 136.0 mEq/L. 
The concentration of chloride is 99.0 mEq/L. 
The concentration of bicarbonate is 31.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 136.0 mEq/L - (99.0 mEq/L + 31.0 mEq/L) = 6.0 mEq/L. Hence, The patient's anion gap is 6.0 mEq/L."
6348,39,Anion Gap,lab test,decimal,pmc-4945810-1,Extracted,"A 74-year-old woman, with a past medical history of end-stage renal disease, mild chronic obstructive pulmonary disease, left ventricular hypertrophy, mild chronic iron deficiency anemia, chronic gastroesophageal reflux disease treated with proton pump inhibitors, and no known autoimmune disorders presented with dysphagia for solids without abdominal pain or other gastrointestinal (GI) symptoms, and without systemic ‘B’ symptoms of pyrexia, night sweats, or weight loss. She had a 10-pack-year history of smoking cigarettes, but had quit smoking 10 years earlier. She drank alcohol only socially and did not use any illicit drugs. Physical examination revealed a blood pressure of 145/78 mm Hg, a heart rate of 98 beats/min, and a temperature of 36.5°C. The abdominal examination was unremarkable, including findings of a nontender abdomen, normoactive bowel sounds, and no hepatosplenomegaly. Rectal examination revealed no fecal occult blood. Laboratory analysis showed a hemoglobin level of 10.3 g/dl, a mean corpuscular volume of 87 fl, a serum iron level of 25 μg/dl, and a total iron binding capacity of 223 μg/dl (iron saturation 11%, compatible with iron deficiency anemia). The serum levels of sodium were 136 mmol/l, potassium 3.7 mmol/l, chloride 98 mmol/l, and bicarbonate 26 mmol/l. The serum creatinine level was 2.71 mg/dl, and blood urea nitrogen was 27 mg/dl. Serum tests of liver function were all within normal limits, except that the alkaline phosphatase level was 263 U/l. The albumin level was low at 2.7 g/dl. The lactate dehydrogenase level was 206 U/l (normal range 100–238). A barium esophagogram revealed no abnormalities. EGD revealed no gross duodenal lesions and some digested food obscuring about 20% of the descending duodenal mucosa despite her having fasted for 8 h before EGD (fig. ). There were no gastric or esophageal lesions. Histologic analysis of esophageal biopsies, performed because of dysphagia, revealed no lesions. Histologic analysis of endoscopic biopsies of the descending duodenum, performed to exclude celiac disease in a patient with suspected iron deficiency anemia, revealed a prominent submucosal lymphocytic infiltrate with scattered plasma cells, consistent with low-grade B-cell non-Hodgkin's lymphoma and otherwise normal mucosa (fig. ). Immunohistochemistry predominantly revealed B cells, with a strong expression of CD43 and a coexpression of BCL2, findings highly compatible with extranodular marginal zone MALToma (fig. ). Microscopic examination of gastroduodenal biopsies using a modified Giemsa stain (Diff Quick stain; Electron Microscopy Sciences, Hatfield, Pa., USA) was negative for H. pylori, as was immunohistochemistry using antibodies to H. pylori. The serum IgG antibody level to H. pylori was 0.41 U/ml (levels of 0.00–0.89 U/ml compatible with no infection). Serum tissue transglutaminase IgA antibody levels were 7.1 U/ml (<20 U/ml negative for celiac disease), with a normal serum IgA level and no monoclonal gammopathy. An abdominal PET scan revealed small, minimally fludeoxyglucose-avid, mesenteric and periaortic lymph nodes. The patient agreed to undergo treatment for duodenal MALToma in the future.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [136.0, 'mmol/L'], 'Bicarbonate': [26.0, 'mmol/L'], 'Chloride': [98.0, 'mmol/L']}",12,11.4,12.6,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 136.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 136.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 136.0 mmol * 1 mEq/mmol = 136.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 136.0 mmol sodium/L converts to 136.0 mEq sodium/L. 
The concentration of chloride is 98.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 98.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 98.0 mmol * 1 mEq/mmol = 98.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 98.0 mmol chloride/L converts to 98.0 mEq chloride/L. 
The concentration of bicarbonate is 26.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 26.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 26.0 mmol * 1 mEq/mmol = 26.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 26.0 mmol bicarbonate/L converts to 26.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 136.0 mEq/L - (98.0 mEq/L + 26.0 mEq/L) = 12.0 mEq/L. Hence, The patient's anion gap is 12.0 mEq/L."
6349,39,Anion Gap,lab test,decimal,usmle-2005,Extracted,"A 32-year-old man comes to the physician because of a 2-week history of a cough and shortness of breath. He also noted several episodes of blood-tinged sputum over the last 4 days. He has a 3-month history of progressive fatigue. His temperature is 37.5°C (98.6°F), pulse is 86/min, respirations are 17/min, and blood pressure is 150/93 mm Hg. Examination shows pale conjunctivae. Crackles are heard on auscultation of the chest. Laboratory studies show:
Hemoglobin 10.2 g/dL
Leukocyte count 9200/mm3
Platelet count 305,000/mm3
Serum
Na+ 136 mEq/L
Cl- 101 mEq/L
K+ 4.5 mEq/L
HCO3- 25 mEq/L
Urea nitrogen 28 mg/dL
Creatinine 2.3 mg/dL
Anti-GBM antibodies positive
Antinuclear antibodies negative
Urine
Blood 2+
Protein 2+
RBC 11–13/hbf
RBC casts rare
He is started on prednisone and cyclophosphamide.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [136.0, 'mEq/L'], 'Bicarbonate': [25.0, 'mEq/L'], 'Chloride': [101.0, 'mEq/L']}",10,9.5,10.5,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 136.0 mEq/L. 
The concentration of chloride is 101.0 mEq/L. 
The concentration of bicarbonate is 25.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 136.0 mEq/L - (101.0 mEq/L + 25.0 mEq/L) = 10.0 mEq/L. Hence, The patient's anion gap is 10.0 mEq/L."
6350,39,Anion Gap,lab test,decimal,usmle-5198,Extracted,"A 27-year-old man presents to his primary care physician with worsening cough and asthma. The patient reports that he was in his usual state of health until 1 month ago, when he developed a cold. Since then his cold has improved, but he continues to have a cough and worsening asthma symptoms. He says that he has been using his rescue inhaler 3 times a day with little improvement. He is studying for an accounting exam and states that his asthma is keeping him up at night and making it hard for him to focus during the day. The patient admits to smoking tobacco. His smoking has increased from a half pack per day since he was 17 years old to 1 pack per day during the past month to cope with the stress of his exam. The patient’s temperature is 99°F (37.2°C), blood pressure is 110/74 mmHg, pulse is 75/min, and respirations are 15/min with an oxygen saturation of 97% on room air. Physically examination is notable for mild expiratory wheezes bilaterally. Labs are obtained, as shown below:

Serum:
Na+: 144 mEq/L
Cl-: 95 mEq/L
K+: 4.3 mEq/L
HCO3-: 23 mEq/L
Urea nitrogen: 24 mg/dL
Glucose: 100 mg/dL
Creatinine: 1.6 mg/dL

Leukocyte count and differential:
Leukocyte count: 13,000/mm^3
Segmented neutrophils: 63%
Eosinophils: 15%
Basophils: < 1%
Lymphocytes: 20%
Monocytes: 1.3%
Hemoglobin: 13.5 g/dL
Hematocrit: 50%
Platelets: 200,000/mm^3

Urinalysis reveals proteinuria and microscopic hematuria.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [144.0, 'mEq/L'], 'Bicarbonate': [23.0, 'mEq/L'], 'Chloride': [95.0, 'mEq/L']}",26,24.7,27.3,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 144.0 mEq/L. 
The concentration of chloride is 95.0 mEq/L. 
The concentration of bicarbonate is 23.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 144.0 mEq/L - (95.0 mEq/L + 23.0 mEq/L) = 26.0 mEq/L. Hence, The patient's anion gap is 26.0 mEq/L."
6351,39,Anion Gap,lab test,decimal,usmle-6085,Extracted,"A 33-year-old woman presents to the emergency department with numbness and severe fatigue. She states that her symptoms started yesterday and have been gradually worsening. The patient is generally healthy, drinks alcohol on the weekends, and does not smoke. She was ill recently but recovered spontaneously. Her temperature is 102°F (38.9°C), blood pressure is 127/68 mmHg, pulse is 120/min, respirations are 17/min, and oxygen saturation is 98% on room air. Physical exam is notable for an anxious young woman who appears mildly confused. Neurological exam reveals she has decreased sensation to light touch bilaterally on her upper and lower extremities. Dermatologic exam reveals petechiae. Laboratory values are ordered as seen below.

Hemoglobin: 7.2 g/dL
Hematocrit: 25%
Leukocyte count: 6,500/mm^3 with normal differential

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 5.4 mEq/L
HCO3-: 22 mEq/L
BUN: 30 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.9 mg/dL
Ca2+: 10.2 mg/dL

A peripheral smear is performed as seen in Figure A.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [139.0, 'mEq/L'], 'Chloride': [100.0, 'mEq/L'], 'Bicarbonate': [22.0, 'mEq/L']}",17,16.15,17.85,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 139.0 mEq/L. 
The concentration of chloride is 100.0 mEq/L. 
The concentration of bicarbonate is 22.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 139.0 mEq/L - (100.0 mEq/L + 22.0 mEq/L) = 17.0 mEq/L. Hence, The patient's anion gap is 17.0 mEq/L."
6352,39,Anion Gap,lab test,decimal,pmc-7722635-1,Extracted,"An 81-year-old man with a medical history of chronic kidney disease stage III, obesity with a body mass index of 52.0, cholecystectomy, and appendectomy presented in April 2020 from an assisted living facility with two weeks of lower abdominal pain, anorexia, and abdominal distention. He also reported at least 3 days of progressive dyspnea and the absence of bowel movements. Upon presentation to the hospital, he required 2 L/min oxygen by nasal cannula, but was afebrile and hemodynamically stable. Physical examination revealed abdominal distention with tenderness to palpation, voluntary guarding, and an umbilical hernia.
Admission laboratory testing revealed a white blood cell count of 25.7 K/cmm, sodium of 133 mmol/L, chloride of 95 mmol/L, bicarbonate of 28 mmol/L, creatinine of 1.0 mg/dL, total bilirubin of 2.0 mg/dL with normal transaminase levels, lactate dehydrogenase of 186 units/L, lactate of 4.1 mmol/L, procalcitonin of 0.15 ng/mL, ferritin of 143.87 ng/mL, and high-sensitivity C-reactive protein of 23.0 mg/L. Respiratory pathogen panel was negative, and SARS-CoV-2 was not detected by reverse transcriptase-polymerase chain reaction (RT-PCR) on nasopharyngeal swab. Two sets of blood cultures and one urine culture were obtained. Computed tomography of the abdomen and pelvis with intravenous contrast showed a distended stomach, dilated loops of small bowel, a fat-containing ventral wall hernia, and an umbilical hernia containing small bowel that was concerning for a transition point (). A nasogastric tube was placed by the general surgery team in the emergency department with immediate return of 2 liters of feculent material. The patient's umbilical hernia was manually reduced with palliation of the abdominal pain. The patient also received 3 liters of crystalloid fluid with improvement in both lactate and white blood cell count.
After the initial improvement in exam and inflammatory markers with nasogastric decompression and crystalloids, the patient was admitted to the general surgery service for conservative management of suspected small bowel obstruction. Over the next 4 hospital days, the patient had decreased abdominal pain, was stable on room air, and had resolution of all laboratory abnormalities. His initial blood cultures on admission remained negative. On hospital day 5, the patient's nasogastric tube was removed without complication after he began passing flatus. Several hours later, he became hypoxemic to 88% on room air with increased abdominal distension, hypotension, and tachycardia. Empiric vancomycin, piperacillin-tazobactam, doxycycline, and crystalloids were instituted after repeat blood and urine culture collection. Portable upright abdominal radiograph showed distended loops of bowel without free air, while chest radiograph showed new patchy bibasilar opacities. Evaluation by the surgical team revealed a stable abdominal exam without rebound tenderness following resuscitation and antibiotics. Surgical bowel exploration was considered, but deferred due to his stable abdominal exam and high intraoperative mortality risk. He remained afebrile, but had increasing tachypnea and required up to 4 L/min oxygen by nasal cannula. Further imaging studies were deferred at the time due to the patient's tenuous respiratory status. Laboratory studies revealed a white blood cell count increase to 14.6 k/cmm, creatinine of 2.5 mg/dL, ferritin of 691.79 ng/dL, procalcitonin level of 15.93 ng/mL, D-dimer of 1203 ng/mL, lactate dehydrogenase of 241 units/L, high-sensitivity C-reactive protein of greater than 160 mg/L, and lactate of 3.1 mmol/L (). COVID-19 pneumonia was suspected, and a repeat SARS-CoV-2 RT-PCR test was sent and was negative. Given concerns for a false-negative RT-PCR test result, the patient was transferred to the dedicated COVID-19 unit for airborne isolation in a negative pressure room. The following day, the patient's inflammatory markers worsened with persistent hypoxemia. A third nasopharyngeal swab was sent for RT-PCR, but was negative. On hospital day 7, both sets of repeat blood cultures grew a Gram-positive bacillus later identified as Clostridium sporogenes. Sensitivities were not performed as per the microbiology laboratory's protocol for anaerobic organisms, but the isolate was beta-lactamase negative.
After stabilization, repeat computed tomography of the chest, abdomen, and pelvis without intravenous contrast revealed focal ground glass opacities in the left upper lobe, bibasilar airspace disease, and new asymmetric thickening of the left rectus muscle with fluid consistent with abscess formation. The patient's creatinine peaked at 4.5 mg/dL before decreasing with judicious administration of intravenous crystalloid for suspected acute tubular necrosis. Urine culture showed no growth, and urine legionella antigen was not detected. The patient was treated with piperacillin-tazobactam and later meropenem with improvement of most inflammatory markers, but with persistent leukocytosis. On hospital day 10, after discussion with the surgery service regarding surgical intervention and the associated mortality risk, the patient decided to pursue comfort measures only. He was transferred to an inpatient hospice facility and died two days later.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [133.0, 'mmol/L'], 'Bicarbonate': [28.0, 'mmol/L'], 'Chloride': [95.0, 'mmol/L']}",10,9.5,10.5,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 133.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 133.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 133.0 mmol * 1 mEq/mmol = 133.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 133.0 mmol sodium/L converts to 133.0 mEq sodium/L. 
The concentration of chloride is 95.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 95.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 95.0 mmol * 1 mEq/mmol = 95.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 95.0 mmol chloride/L converts to 95.0 mEq chloride/L. 
The concentration of bicarbonate is 28.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 28.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 28.0 mmol * 1 mEq/mmol = 28.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 28.0 mmol bicarbonate/L converts to 28.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 133.0 mEq/L - (95.0 mEq/L + 28.0 mEq/L) = 10.0 mEq/L. Hence, The patient's anion gap is 10.0 mEq/L."
6353,39,Anion Gap,lab test,decimal,usmle-1509,Extracted,"A 44-year-old man is brought to the emergency department 45 minutes after being involved in a high-speed motor vehicle collision in which he was the restrained driver. On arrival, he has left hip and left leg pain. His pulse is 135/min, respirations are 28/min, and blood pressure is 90/40 mm Hg. Examination shows an open left tibial fracture with active bleeding. The left lower extremity appears shortened, flexed, and internally rotated. Femoral and pedal pulses are decreased bilaterally. Massive transfusion protocol is initiated. An x-ray of the pelvis shows an open pelvis fracture and an open left tibial mid-shaft fracture. A CT scan of the head shows no abnormalities. Laboratory studies show:
Hemoglobin 10.2 g/dL
Leukocyte count 10,000/mm3
Platelet count <250,000/mm3
Prothrombin time 12 sec
Partial thromboplastin time 30 sec
Serum
Na+ 125 mEq/L
K+ 4.5 mEq/L
Cl- 98 mEq/L
HCO3- 25 mEq/L
Urea nitrogen 18 mg/dL
Creatinine 1.2 mg/dL
The patient is taken emergently to interventional radiology for exploratory angiography and arterial embolization.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [125.0, 'mEq/L'], 'Bicarbonate': [25.0, 'mEq/L'], 'Chloride': [98.0, 'mEq/L']}",2,1.9,2.1,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 125.0 mEq/L. 
The concentration of chloride is 98.0 mEq/L. 
The concentration of bicarbonate is 25.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 125.0 mEq/L - (98.0 mEq/L + 25.0 mEq/L) = 2.0 mEq/L. Hence, The patient's anion gap is 2.0 mEq/L."
6354,39,Anion Gap,lab test,decimal,pmc-8022897-1,Extracted,"A 66-year-old morbidly obese woman presented to the ED with generalized weakness over the last seven days, oliguria, poor appetite, and thirst. Her past medical history included hypertension, hyperlipidemia, congestive heart failure, pulmonary hypertension, restrictive lung disease, morbid obesity, and type 2 diabetes mellitus. She had no history of cancer or multiple myeloma, or renal disease as evident from past admissions.
Upon presentation to the ED, she was found to have a serum creatinine of 5 mg/dL (her baseline was 0.5 mg/dL) and a serum calcium level of 23.1 mg/dL (normal reference range: 8-10.4 mg/dL) and ionized calcium of 3.23 mg/dL (normal reference range: 4.23-5.11 mg/dL). Her albumin was 3.9 g/dL, within normal range, indicating true hypercalcemia. CT of her abdomen and pelvis revealed an 18 mm cyst in upper pole of the right kidney with a parapelvic cyst measuring 18 mm x 18 mm (Figure ). Chest X-ray (CXR), CT of head also did not show any significant pathology. Her other labs included a white blood cell (WBC) 14.14, hemoglobin 11.8 g/dL, platelet 427,000 platelets per microliter, sodium 131 mEq/L, potassium 3.8 mEq/L, chloride 89 mEq/L, carbon dioxide 36 mEq/L (normal reference 20-32 mEq/L), blood urea nitrogen (BUN) 62 mg/dL, magnesium 3 mEq/L, aspartate aminotransferase (AST) 71 IU/L, alanine aminotransferase (ALT) 46 IU/L, troponin 39 ng/mL, B-type natriuretic peptide (BNP) 435 pg/mL, international normalized ratio (INR) less than 0, and partial thromboplastin time (PTT) more than 212 s. Her electrocardiogram (EKG) showed intraventricular right bundle branch block (Figure ). Her vitals included a temperature of 97.8 degrees Fahrenheit, pulse of 72 beats/min, and blood pressure of 160 over 83 millimeters of mercury. A hypercalcemia work-up was done which included parathyroid hormone (PTH), PTH-related protein, and serum protein electrophoresis. PTH was found to be low at 13.9 pg/mL (normal range 15-75 pg/mL) and PTH-related protein (PTHrP) was less than 2 pmol/L, normal. Serum immunofixation showed no monoclonal band, and serum and urine protein electrophoresis were unremarkable. Viral hepatitis serologies were negative. Thyroid stimulating hormone (TSH) was 3.14 uIU/mL, normal. Vitamin D 25-hydroxy was normal, 50.3 ng/mL.
Treatment was initiated with fluid resuscitation (1 L normal saline bolus), the bisphosphonate Zometa (Sagent Pharmaceuticals, Schaumburg, IL), and Miacalcin (Mylan, Rockford, IL). A temporary dialysis catheter was placed and dialysis treatment was initiated 12 h later (day two), and again on day three due to a persistently elevated serum calcium level of 11.5 mg/dL. Dialysis was necessary as Zometa and Miacalcin were not working fast enough to ensure a positive outcome alone. In addition, there was concern for acute tubular necrosis due to Zometa in our patient with a creatinine clearance of less than 30 mL/min (Figures -, Table ). The patient’s serum creatinine and calcium levels improved by day six and patient was discharged home with outpatient follow-up.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [131.0, 'mEq/L'], 'Chloride': [89.0, 'mEq/L'], 'Bicarbonate': [36.0, 'mEq/L']}",6,5.7,6.3,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 131.0 mEq/L. 
The concentration of chloride is 89.0 mEq/L. 
The concentration of bicarbonate is 36.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 131.0 mEq/L - (89.0 mEq/L + 36.0 mEq/L) = 6.0 mEq/L. Hence, The patient's anion gap is 6.0 mEq/L."
6355,39,Anion Gap,lab test,decimal,pmc-3190515-1,Extracted,"A 48-year-old morbidly obese African-American male with a medical history of congestive heart failure, hypertension, obstructive sleep apnea on 2 l of home oxygen and non-complaint with continuous positive airway pressure at night presented to the emergency department (ED) with worsening shortness of breath and lower extremity oedema over one week. Vital signs in the ED were temperature, 98.7 degrees Fahrenheit; blood pressure, 116/66 mmHg; heart rate, 130 beats per minute; respiratory rate, 30; oxygen saturation, 85% on 2 l nasal cannula; weight, 162 kg and body mass index, 47. Physical examination revealed a morbidly obese male in acute respiratory distress with an irregularly irregular pulse and one plus lower extremity pitting oedema. Laboratory values in the ED include white blood cell count, 9 800/μl; haemoglobin, 14.2 g/dl; platelet count, 230 000/μl; sodium, 140 mEq/l; potassium, 4.5 mEq/l; chloride, 104 mEq/l; bicarbonate, 29 mEq/l; blood urea nitrogen (BUN), 38 mg/dl; creatinine, 1.4 mg/dl; glucose, 105 mg/dl; aspartate aminotransferase (AST), 51 U/l; alanine aminotransferase (ALT), 40 U/l; alkaline phosphatase, 68 U/l; total bilirubin, 1.5 mg/dl; albumin, 3.4 g/dl; total protein, 7.1 g/dl; international normalised ratio (INR), 1.2; myoglobin, 97 μg/l; troponin, 0.07 ng/ml and B-type natriuretic peptide, 934 pg/ml. Urine toxicology screen was positive for cocaine. Arterial blood gas showed a pH 7.33, paCO2 68.5 and paO2 88.6 on FiO2 of 40%. Electrocardiogram confirmed atrial fibrillation with a rapid ventricular response. Echocardiogram revealed a myopathic severely enlarged left ventricular chamber with moderate concentric left ventricular hypertrophy and severe global hypokinesis with an ejection fraction of 8 to 10%. The patient's work of breathing and oxygenation improved with Bipap. He was started on diltiazem and diuresis was initiated. The patient was admitted to the step-down unit with a new diagnosis of atrial fibrillation.
On hospital day number eight, the overnight nurse found the patient unresponsive. A code blue was called. His initial rhythm was ventricular fibrillation and he was shocked with 200 J twice before regaining pulses. When stabilised, he was transferred to the intensive care unit (ICU) where he regained consciousness and full neurologic function within one hour of the event. The following day, an automatic implantable cardioverter defibrillator (AICD) was placed. Intraoperatively, the patient had runs of ventricular tachycardia with hypotension to 80 mmHg systolic. Postoperatively, the patient was found to have a right fixed mid-dilated pupil, flaccid paralysis of the left arm and leg with hyperreflexia throughout the left side. Computed tomography (CT) of the head revealed a right midbrain and thalamic stroke thought to be secondary to transient arrhythmia-induced hypoperfusion, intraoperatively.
On postoperative day number three, after AICD placement and stroke, the patient acutely developed a rigid distended board-like abdomen with dullness to percussion. Vitals at that time were temperature, 98.4 degrees Fahrenheit; blood pressure, 112/67 mmHg; heart rate range, 55 beats per minute, and respiratory rate 26 on ventilator settings of assist control volume control with a rate of 26; tidal volume, 500 ml; FiO2, 40% and positive end-expiratory pressure of 5. His peak inspiratory pressure on the ventilator had risen from 26 to 72 mmHg; his plateau had risen from 15 to 48 mmHg with oxygen desaturation from 93 to 85%. The patient had received 1.5 l in and urinated 4.5 l over the 24 hours, leading up to this event. His laboratory values from that morning were unchanged from previous (white blood count, 10 400/μl; haemoglobin, 12.6 g/dl; platelets, 200 000/μl; sodium, 139 mEq/l; potassium, 4.7 mEq/l; chloride, 100 mEq/l; bicarbonate, 34 mEq/l; BUN, 36 mg/dl; creatinine, 1.41 mg/dl; glucose, 78 mg/dl; calcium, 8.3 mg/dl; magnesium, 2.0 mEq/l; phosphorus, 3.0 mg/dl; AST, 77 U/l; ALT, 94 U/l; alkaline phosphatase, 186 U/l; total bilirubin, 1.3 mg/dl). This constellation of findings prompted the team to measure an abdominal compartment pressure which was elevated to 53 cm H2O (40 mmHg) with an abdominal perfusion pressure (APP) of 42 mmHg. A CT scan of the abdomen and pelvis was performed which showed no dilated loops of bowel, no ileus, no evidence of free air, abscess or obstruction and minimal free fluid []. Pertinent labs from the event revealed a lactate of 1.0 mg/dl; lipase, 159 U/l; amylase, 76 U/l; creatinine, 1.53 mg/dl. Surgery was consulted and the FiO2 was increased to 100%, which improved his oxygen saturation to 96% despite his elevated peak inspiratory pressures.
Surgical recommendations were for an emergent bedside surgical abdominal decompression. The patient was administered 10 mg of intravenous cisatracurium besylate by anaesthesia in preparation for surgical management. Shortly following paralytic administration, his peak inspiratory pressure corrected from 72 to 23 mmHg, his plateau pressure from 48 to 16 mmHg and his oxygenation status tolerated a decrease in FiO2 down to 40% with his oxygen saturation returning to baseline. Measurement of his abdominal compartment pressure revealed a drop from 53 (40 mmHg) to 23 cm H2O (17 mmHg) and then normalised to 15 cm H20 (11 mmHg) over a three-hour period. During this entire event, the patient averaged 100 to 200 cc/hr of urine output and laboratory values from the following day showed a drop in creatinine from 1.53 to 1.29 mg/dl. Given this correction, surgical management was postponed and the patient was monitored. The patient remained hospitalised for an additional 73 days. He was ultimately transferred to a skilled nursing facility without return of symptoms.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mEq/L'], 'Bicarbonate': [29.0, 'mEq/L'], 'Chloride': [104.0, 'mEq/L']}",7,6.65,7.35,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mEq/L. 
The concentration of chloride is 104.0 mEq/L. 
The concentration of bicarbonate is 29.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (104.0 mEq/L + 29.0 mEq/L) = 7.0 mEq/L. Hence, The patient's anion gap is 7.0 mEq/L."
6356,39,Anion Gap,lab test,decimal,pmc-4008352-2,Extracted,"A 79-year-old white man presented to the emergency room with a weight gain of 15 lbs. (6.8 kg) over two weeks associated with progressive bilateral pitting edema and paroxysmal nocturnal dyspnea. His medical history included a non-dilated ischemic cardiomyopathy with LVEF of 30% (New York Heart Association class III), status-post CABG, status-post biventricular automatic implantable cardioverter defibrillator (AICD), and CKD stage 4 due to cardiorenal syndrome. Physical examination revealed temperature of 37.1 C, blood pressure of 103/55 mmHg, heart rate of 68/min, respiratory rate of 17/min, and oxygen saturation of 96% in room air. His weight was 88.8 kilograms. He had jugular venous distention. Cardiac exam revealed regular S1/S2 with a II/VI SEM radiating to left lateral axilla. His lung exam revealed bibasilar rales. His abdomen was markedly distended with ascites. The lower extremities had gross pitting edema up to the waist. His serum sodium was 130 mmol/L (mEq/L), potassium was 5.1 mmol/L (mEq/L), bicarbonate was 29 mmol/L (mEq/L), and creatinine was 2.5 mg/dL (221 μmol/L), with chloride of 100 mmol/L (mEq/L) and B-type natriuretic peptide of 442 pg/mL (ng/L). Electrocardiogram showed no signs of acute ischemia. Chest roentgenogram showed pulmonary vascular congestion. He was managed with the triple diuretics and aquaretic regimen () for ADHF. Over four days, the patient achieved a 28.2 lb. (12.8 kg) weight loss. His serum creatinine improved to 2.18 mg/dL (192.7 μmol/L) with stable serum electrolytes as shown in . He remained out of the hospital for over thirty days.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [130.0, 'mEq/L'], 'Bicarbonate': [29.0, 'mEq/L'], 'Chloride': [100.0, 'mEq/L']}",1,0.95,1.05,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 130.0 mEq/L. 
The concentration of chloride is 100.0 mEq/L. 
The concentration of bicarbonate is 29.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 130.0 mEq/L - (100.0 mEq/L + 29.0 mEq/L) = 1.0 mEq/L. Hence, The patient's anion gap is 1.0 mEq/L."
6357,39,Anion Gap,lab test,decimal,pmc-5624136-1,Extracted,"23-year-old female presented to the Emergency Room with carpopedal spasms and tingling numbness in hands. Patient endorsed tingling sensation in hand since a month which was intermittent and unrelated to wrist movement. She denied history of preceding trauma and swelling in hands. There was no history of similar complaints in the past or any prior surgery. She denied complaints like nausea, vomiting, and diarrhea. Tingling in hands was not associated with paresthesia in other extremities and sensory or motor deficits. Patient was a known case of multidrug resistant tuberculosis and was being treated with the following drugs for two months: amoxicillin-clavulanate, ethionamide, intramuscular capreomycin, linezolid, and para-aminosalicylate (PAS) granules. Patient was afebrile and her initial vital signs were normal with a pulse of 78/min and blood pressure of 110/76 mm of Hg. On examination, flattening of chest wall on the left side was noted. Trail's sign was positive with a deviation of the trachea to the left side. On auscultation of lung fields, breath sounds were diminished on the left. These findings suggested presence of tuberculous fibrosis in the left lung. No other stigmata of TB were noted and rest of the physical examination was unremarkable.
Initial blood-work at the time of presentation revealed a low serum calcium level of 6.98 mg/dL. Patient was hospitalized and detailed investigations were done. Coexisting with hypocalcemia, other electrolyte abnormalities noted were as follows: serum sodium of 130 mEq/L, potassium of 1.8 mEq/L, chloride of 95 mEq/L, calcium of 6.98 mg/dL, and magnesium of 0.5 mg/dL. Serum albumin was 4 g/dL. Serum creatinine was normal and remained so throughout the course of hospitalization. The arterial blood gas evaluation showed metabolic alkalosis without respiratory compensation with pH of 7.5, HCO3 of 30 mEq/L, and PaCO2 of 30 mmHg. Routine urine examination revealed a 2–4 pus cells, 1-2 RBCs, and 1-2 epithelial cells, in the absence of proteinuria and glycosuria. Urine calcium/creatinine ratio was 0.49 (>0.2), which confirmed hypercalciuria. Urinary prostaglandin-E level was not performed as this assay is not readily available in our institute.
Vitamin D and serum parathyroid levels were found to be in the normal range, thus ruling out hypovitaminosis D and secondary hyperparathyroidism, respectively. Patient was treated symptomatically; injectable calcium, magnesium, and potassium were administered to correct electrolyte abnormalities. Due to the association of aminoglycoside antibiotics with alterations in electrolyte levels, capreomycin was discontinued. Subsequently, the electrolytes started to rise after two days of stopping capreomycin (). Patient was discharged once her symptoms resolved and the serum electrolytes were normalized. On follow-up, there were no complains of tingling sensations or carpopedal spasms and electrolytes remained to be in the normal range.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [130.0, 'mEq/L'], 'Bicarbonate': [30.0, 'mEq/L'], 'Chloride': [95.0, 'mEq/L']}",5,4.75,5.25,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 130.0 mEq/L. 
The concentration of chloride is 95.0 mEq/L. 
The concentration of bicarbonate is 30.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 130.0 mEq/L - (95.0 mEq/L + 30.0 mEq/L) = 5.0 mEq/L. Hence, The patient's anion gap is 5.0 mEq/L."
6358,39,Anion Gap,lab test,decimal,pmc-5139819-1,Extracted,"A 57-year-old Turkish woman presented to an emergency department with a 7-day history of fever, jaundice, abdominal distention, personality changes, slurred speech, and constipation. The patient was born in a village and lived in the eastern part of Turkey. The patient had a history of hepatic Echinococcus multilocularis, which had been diagnosed 8 years earlier, and she was receiving oral albendazole at a dose of 800 mg per day. At the time of evaluation, she appeared ill. He had a temperature of 38.2 °C, a blood pressure of 80/50 mm Hg, and a heart rate of 86 beats per minute. Her conjunctivas were icteric. There was moderate hepatomegaly with tense ascites. There was no splenomegaly. Her neurologic examination showed flapping tremor (asterixis) and somnolence. The remainder of the physical examination was normal. Blood tests showed a white-cell count of 11,800/mm3. An automatic differential cell count revealed 52% eosinophils, 40% neutrophils, and 8% lymphocytes. The hemoglobin level was 10 g/dl, the platelet count was 209,000/mm3, the prothrombine time was 17 seconds, and D-dimer level was 5.5 (normal range, 0 to 0.5). The serum sodium level was 125 mmol/L; chloride, 102 mmol/L; potassium, 3.8 mmol/L; bicarbonate, 21 mmol/L; blood urea nitrogen, 10 mg/dl; creatinine, 0.7 mg/dl; glucose, 80 mg/dl; albumin level, 2.8 g/dl; globulin level 4.8 g/dl; aspartate aminotransferase level, 56 U/L (normal range, 0 to 41); alanine aminotransferase level, 48 U/L (normal range, 0 to 40); alkaline phosphatase level, 378 U/L (normal range, 40 to 125); gammaglutamyl transferase level 121 U/L (normal range, 0 to 45) and total bilirubin level, 8 mg/dl (normal range, 0.0 to 0.8 ). Blood ammonia level was 212 mmol/L (normal range 11 - 51) and C-reactive protein level was 48 U/L (normal range 0 - 5). The ELISA test for E. multilocularis was also positive.
An abdominal paracentesis showed 800/mm3 white cell (50% eosinophil); the further examinations in ascitic fluid revealed the glucose level was 87 mg/dl, the protein level was 3.7 mg/dl and the albumin level was 1.5 mg/dl. Serum ascites-albumin gradient was calculated as 1.3 g/dl. At the time of emergency admission, an abdominal ultrasonography showed a hepatic mass, ascites and lack of the visualization of the hepatic veins. An abdominal CT scan also demonstrated multiple hepatic masses in the right lobe of the liver, the largest of which was 12 cm in diameter, nonuniform contrast enhancement of the liver parenchyma, an enlarged caudate lobe, and hepatic and portal vein thrombosis with ascites (). Her echocardiography revealed no major cardiac abnormality. The patient was considered as hepatic encephalopathy due to acute BCS and was given dextrose-containing intravenous fluids with low molecular weight heparin. Ammonia-lowering therapy with rifaximin was also initiated. On day 5 of the patient’s hospitalization, her ammonia level was in normal ranges and clinical parameters were gradually normalized. At this time, albendazole (15 mg/kg per day in divided doses) was also started as adjunctive therapy and she was discharged from hospital with close follow-up.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [125.0, 'mmol/L'], 'Bicarbonate': [21.0, 'mmol/L'], 'Chloride': [102.0, 'mmol/L']}",2,1.9,2.1,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 125.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 125.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 125.0 mmol * 1 mEq/mmol = 125.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 125.0 mmol sodium/L converts to 125.0 mEq sodium/L. 
The concentration of chloride is 102.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 102.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 102.0 mmol * 1 mEq/mmol = 102.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 102.0 mmol chloride/L converts to 102.0 mEq chloride/L. 
The concentration of bicarbonate is 21.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 21.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 21.0 mmol * 1 mEq/mmol = 21.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 21.0 mmol bicarbonate/L converts to 21.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 125.0 mEq/L - (102.0 mEq/L + 21.0 mEq/L) = 2.0 mEq/L. Hence, The patient's anion gap is 2.0 mEq/L."
6359,39,Anion Gap,lab test,decimal,pmc-3109782-1,Extracted,"A 72-year-old man presented with high-grade fever with chills and dysuria for last 10 days, decreased urine output, and worsening breathlessness since 1 day. He denied any history of hematuria, pain in abdomen, skin rashes, or joint pains. He was a diabetic and hypertensive on regular treatment since 5 years. Physical examination revealed a middle aged man in acute respiratory distress with a respiratory rate of 32 beats/min. His blood pressure was 150/90 mmHg and his temperature was 100° F. The jugular venous pressure was elevated, he had bilateral pitting edema of the legs, and sinus tachycardia was present (108/min with an S3 gallop). Auscultation of the lungs revealed pulmonary congestion.
His laboratory investigations were as follows: hemoglobin 9.1 g/dL, total leukocyte count 23,200/cmm, platelet count 592,000/cmm, BUN 65 mg/dL, creatinine 1.8 mg/dL, sodium 139 mEq/L, potassium 4.3 mEq/L, chloride 95.3 mEq/L, bicarbonate 13.8 mEq/L, total bilirubin 1.3 mg/dL, direct bilirubin 0.3 mg/dL, SGOT 32 IU/L, SGPT 25 IU/L, ALP 210 IU/L, total proteins 7.7 g/dL, albumin 3.1 g/dL, C-reactive protein 142, amylase 71, lipase 82, procalcitonin 1.4. His urine microscopy revealed trace proteins with entire field full of pus cells. A chest radiograph confirmed pulmonary edema. His abdominal sonography was unremarkable except for moderate ascites. CT-abdomen and pelvis revealed acute pyelonephritis with perinephric fat stranding.
The patient was transferred to the intensive care unit. Diuretic therapy was intensified (frusemide infusion), he was put on noninvasive ventilation, and broad-spectrum intravenous antibiotics were administered (meropenem, teicoplanin, aztreonem). His urine culture came positive for Escherichia coli, whereas blood culture was sterile. He continued to have high-grade fever and went into septic shock, with the acute physiology and chronic health evaluation (APACHE) II score of 21 and the sepsis-related organ failure assessment (SOFA) score of 9. He was intubated, put on ionotropic support, and antibiotics were changed according to sensitivity reports (tigecycline, colistin, vancomycin, clindamycin). His blood pressure stabilized at 100/50 mmHg on dopamine infusion at 20 μg/kg/min, noradrenaline at 15 μg/kg/min, adrenaline at 0.1 μg/kg/min, and vasopressin at 0.02 U/min. He was initiated on sustained low-efficiency hemodialysis (SLED), following anuria, worsening azotemia, and severe metabolic acidosis. In view of on-going sepsis and unstable hemodynamics, decision was taken to initiate him on direct hemoperfusion using PMX-DHP.
After priming the cartridge and blood lines, 2 hrs of direct hemoperfusion was performed using a blood flow rate of 100 mL/min and heparin anticoagulation. Twelve hours after the initiation of PMX-DHP therapy, vasopressin and adrenaline infusions were tapered, and there was a noticeable improvement in his urine output. 24 hr after initiation of PMX-DHP, vasopressin and adrenaline infusions were stopped. After another 24 hours, the dopamine and noradrenaline doses were decreased, and the urine output increased to approximately 0.7 mL/kg/hr. Under these conditions, the heart rate was maintained at 110 bpm; blood pressure 135/60 mmHg with a mean arterial pressure (MAP) of 85 mmHg []. The SOFA score improved from 9 to 6, and the APACHE II score improved from 21 to 11 (since the patient was under sedation, the score for the central nervous system was excluded). He required four more days of SLED, and his urine output increased to greater than 1 mL/kg/hr and he was taken off dialysis. He was discharged 60 days after the hemoperfusion therapy, with a stable creatinine of 2 mg/dL and on empirical antitubercular therapy.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [139.0, 'mEq/L'], 'Bicarbonate': [13.8, 'mEq/L'], 'Chloride': [95.3, 'mEq/L']}",29.9,28.405,31.395,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 139.0 mEq/L. 
The concentration of chloride is 95.3 mEq/L. 
The concentration of bicarbonate is 13.8 mEq/L. 
Plugging in these values into the anion gap formula gives us 139.0 mEq/L - (95.3 mEq/L + 13.8 mEq/L) = 29.9 mEq/L. Hence, The patient's anion gap is 29.9 mEq/L."
6360,39,Anion Gap,lab test,decimal,pmc-7362642-1,Extracted,"A 76-year-old man with a past medical history of prostate cancer, paroxysmal atrial fibrillation, and recurring pneumonia was found to have a 10-mm nodule in the left lower lung without hilar or mediastinal lymphadenopathy on CT of the chest with IV contrast (Figure ). CT/PET scan showed abnormal uptake in the lung nodule (Figure ) and grade II cervical lymphadenopathy. CT-guided biopsy of the left lower lung was performed. Histopathology showed a malignant neoplasm of plasmacytoid cells (Figure ). A panel of immunohistochemical stains was performed to further evaluate the lesion. The tumor cells were strongly and diffusely immunoreactive for the melanocytic marker MART-1 (Figure ). However, stains for AE1/AE3, CK7, TIF-1, Napsin, P63, PSA, and PASP were negative. The immunohistochemical results confirmed a diagnosis of metastatic melanoma of unknown primary origin (MUP) to the cervical lymph nodes (LNs) and lungs. The patient had just finished four cycles of ipilimumab when he presented to our clinic complaining of fatigue, generalized weakness, dizziness, nausea, abdominal pain, and a 10-pound weight loss. The patient denied any fever, chills, chest pain, shortness of breath, or diarrhea. He denied any smoking or drug-use history. Vital signs included a blood pressure of 98/60 mmHg, heart rate of 92 bpm, respiratory rate of 20 bpm, and oxygen saturation of 92% on room air. The physical exam was unremarkable except for a slightly enlarged left cervical LN, dark pigmentation of the lips and gingiva, and sinus tachycardia without abnormal heart sounds or murmurs. The complete blood count was within normal limits.
The labs before starting ipilimumab were as follows - sodium (Na): 140 mEq/L (normal range: 135-145 mEq/L), potassium: (K) 3.6 mEq/L (normal range: 3.5-5.2 mEq/L), chloride (Cl): 105 mEq/L (normal range: 96-106 mEq/L), carbon dioxide (CO2): 28 mEq/L (normal range: 23-29 mEq/L), blood urea nitrogen (BUN): 19 mg/dL (normal range: 6-20 mg/dL); creatinine (Cr): 1.3 mg/dL (normal range: 0.8-1.2 mg/dL); albumin: 3.9 g/dL, and glucose: 110 mg/dL (normal range: 64-100 mg/dL); morning cortisol: 17 μg/dL (normal range: 5-25 μg/dL), adrenocorticotropic hormone (ACTH): 14 pg/mL (normal range: <80 pg/mL), thyroid-stimulating hormone (TSH): 2.4 μU/mL (normal range: 0.4-5 μU/mL), and free thyroxin: 1.2 ng/dL (normal range: 0.8-2.8 ng/dL).
The labs after four cycles of ipilimumab were as follows - Na: 131 mEq/L, K: 4.1 mEq/L, Cl: 87 mEq/L, CO2: 27 mEq/L, BUN: 6 mg/dL, Cr: 1.1 mg/dL, albumin: 3.7 g/dL, and glucose: 89 mg/dL; morning cortisol: 5 μg/dL, ACTH: 120 pg/mL, TSH: 5 μU/mL, free thyroxin: 0.9 ng/dL, testosterone: 437 ng/dL (normal range: 270-1,070 ng/dL), follicle-stimulating hormone (FSH): 3.5 mIU/mL (normal range: 1.5-12.4 mIU/mL), luteinizing hormone (LH): 6.8 mIU/mL (normal range: 1.24-7.8 mIU/mL), prolactin: 11 ng/mL (normal range: 2-18 ng/mL). Aldosterone was undetectable, and renin was 31 ng/mL/h (normal range for normal sodium diet: 0.6-4.3 ng/mL/h). The patient's HbA1C was 5.7%, and blood culture showed no growth. Urinalysis showed no abnormality and procalcitonin was negative. After the administration of 250 μg intravenous (IV) cosyntropin, cortisol was found to be 6.8 μg/dL at 30 mins, and 10.2 μg/dL at 60 mins, confirming the diagnosis of PAI.
He was diagnosed with grade 3 toxicity of ipilimumab and, given his severe symptoms limiting his daily activities, was hospitalized. The patient was immediately started on IV fluid resuscitation and hydrocortisone 100 mg IV bolus, followed by 50 mg IV every six hours. A CT of the abdomen and pelvis with and without IV contrast revealed no evidence of intraabdominal or pelvic pathology. MRI of the brain with and without contrast revealed no evidence of hypophysitis and no evidence of intracranial metastatic disease. Symptomatic improvement was seen at 24 hours. He was discharged with a four-day taper of hydrocortisone as per the recommendations of the endocrinologist. On his follow-up at the endocrinology clinic, his symptoms continued to improve. A repeat cosyntropin stimulation test showed cortisol levels within normal limits. The patient was started on a second checkpoint inhibitor, nivolumab, for 16 cycles of treatment while being followed up by an endocrinologist to monitor any side effects. A repeat CT/PET FDG 12 months later showed complete disappearance of the left lung nodule, indicating tumor remission (Figure ).",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [131.0, 'mEq/L'], 'Chloride': [87.0, 'mEq/L'], 'Bicarbonate': [27.0, 'mEq/L']}",17,16.15,17.85,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 131.0 mEq/L. 
The concentration of chloride is 87.0 mEq/L. 
The concentration of bicarbonate is 27.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 131.0 mEq/L - (87.0 mEq/L + 27.0 mEq/L) = 17.0 mEq/L. Hence, The patient's anion gap is 17.0 mEq/L."
6361,39,Anion Gap,lab test,decimal,pmc-5414514-1,Extracted,"A 51-year-old man was diagnosed with phospholipase A2 receptor (PLA2R) positive, primary membranous nephropathy. He was initially treated with prednisone and cyclophosphamide without significant improvement. The patient was subsequently started on tacrolimus and became calcineurin inhibitor-dependent. Due to a relapse despite being on tacrolimus, rituximab treatment was recommended. His past medical history was remarkable for multiple episodes of deep venous thrombosis on chronic anticoagulation, hypertension, and dyslipidemia. He did not have any previous cardiac history and denied any concerning preceding cardiac symptoms of chest pain, dyspnea, syncope, orthopnea, or paroxysmal nocturnal dyspnea. The patient had a 33-pack-year history of smoking but quit two years previously. His 12-lead electrocardiogram (ECG) prior to rituximab treatment showed normal sinus rhythm. He worked as a carpenter and had been carrying heavy equipment at work without significant physical limitation. His family history is significant for coronary artery disease in his father at 50 years of age and dilated cardiomyopathy (DCM) in his brother. Due to significant cardiovascular diseases in his family members the patient underwent a cardiolite treadmill stress test which showed normal exercise tolerance and functional class I on Bruce protocol for 15 minutes. There was no evidence of fixed or reversible defect.
The patient was 179 cm tall with a body weight of 88 kg and body surface area (BSA) of 2.1 m2. Rituximab was administered at a dosage of 1000 mg intravenous (IV) at a starting infusion rate of 50 mL/h. Oral acetaminophen (1000 mg), oral diphenhydramine (50 mg), and IV methylprednisolone (100 mg) were also given as premedication. He underwent his first rituximab infusion without any immediate side effects. Forty-eight hours after the infusion, the patient presented to the hospital and reported having woken up from sleep with chest tightness and shortness of breath. He also had nausea and emesis. His physical examination was unremarkable with no evidence of heart failure.
A 12-lead ECG showed a new left bundle branch block (LBBB) as shown in . Troponin I level was 0.08 ng/mL (normal <0.03 ng/mL). Otherwise, Laboratory testing revealed the following values: hemoglobin 11.2 g/dL (reference range 13.5-17.5 g/dL), white blood cell count 9.6×109/L (reference range 3.5-10.5 ×109/L), platelet 157×109/L (reference range 150-450 ×109/L), serum creatinine 1.5 mg/dL (reference range 0.8-1.3 mg/dL), BUN 41 mg/dL (reference range 8-24 mg/dL), sodium 141 mmol/L (reference range 135-145 mmol/L), potassium 5.0 mmol/L (reference range 3.6-5.2 mmol/L), chloride 111 mmol/L (reference range 100-108 mmol/L), bicarbonate 22 mmol/L (reference range 22-29 mmol/L). Computed tomography angiogram of the chest was negative for pulmonary embolism without evidence of significant coronary calcification. An urgent transthoracic echocardiogram demonstrated moderately reduced left ventricular (LV) systolic function with an ejection fraction (EF) of 30% with moderate hypokinesis of the anteroseptal myocardium. There was no significant valvular disease. The patient subsequently underwent left and right heart catheterization with coronary angiography which revealed a cardiac output of 5.9 L/min (normal range: 4-8L/min) and a cardiac index of 2.88 L/min/m2(normal range: 2.6–4.2 L/min/m2). There was no significant atherosclerotic disease noted in the coronary vessels. However, there was moderate diffuse hypokinesis of the LV on ventriculogram. Right heart catheterization demonstrated mildly elevated right and left-sided filling pressures. Thus, the diagnosis of non-ischemic cardiomyopathy was made, and the underlying etiology of his non-ischemic cardiomyopathy was postulated to be due to rituximab treatment.
The patient received medical treatment for the cardiomyopathy with carvedilol 3.125 mg orally twice a day as well as lisinopril 10 mg and rosuvastatin 10 mg orally once a day. The patient was also subsequently placed on a life vest due to prevent sudden cardiac death. The patient was restarted on tacrolimus for his treatment of membranous nephropathy. He did not receive any further treatment with rituximab. A repeat echocardiogram one month later still demonstrated severe LV enlargement with a calculated EF of 26%. There was persistent generalized LV hypokinesis with abnormal ventricular septal wall motion due to LBBB. Otherwise, there was a mild valvular heart disease. His follow-up ECG showed normal sinus rhythm with LBBB. Carvedilol was increased to 6.25 mg twice a day and slowly titrated up to 25 mg twice a day. At 9-month follow-up, despite that he had better optimization of his medical therapy, his transthoracic echocardiogram still showed reduced LVEF of 31% with moderate−severe LV enlargement. Thus, the patient was evaluated and underwent cardiac resynchronization therapy with implantable cardioverter defibrillators (CRT-D) implantation. At 3 month after initiation of CRT therapy, the patient had significant improvement in his functional status with LVEF of 52%. Although the patient still had proteinuria at 607 mg/dL/24 hours, his kidney function remained stable with creatinine of 1.6 mg/dL and creatinine clearance of 69 mL/min/BSA.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [141.0, 'mmol/L'], 'Bicarbonate': [22.0, 'mmol/L'], 'Chloride': [111.0, 'mmol/L']}",8,7.6,8.4,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 141.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 141.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 141.0 mmol * 1 mEq/mmol = 141.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 141.0 mmol sodium/L converts to 141.0 mEq sodium/L. 
The concentration of chloride is 111.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 111.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 111.0 mmol * 1 mEq/mmol = 111.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 111.0 mmol chloride/L converts to 111.0 mEq chloride/L. 
The concentration of bicarbonate is 22.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 22.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 22.0 mmol * 1 mEq/mmol = 22.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 22.0 mmol bicarbonate/L converts to 22.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 141.0 mEq/L - (111.0 mEq/L + 22.0 mEq/L) = 8.0 mEq/L. Hence, The patient's anion gap is 8.0 mEq/L."
6362,39,Anion Gap,lab test,decimal,pmc-4440465-1,Extracted,"A 42-year-old male with history of untreated hepatitis C and polysubstance abuse was admitted for AKI and severe metabolic alkalosis. One day prior to admission, he admitted to having injected a massive amount of heroin and subsequently presented with nausea, vomiting and altered mental status. On presentation, his vital signs revealed a blood pressure of 120/80, heart rate of 98, respiratory rate of 10 and a temperature of 98°F. The rest of his physical exam was normal. His blood chemistry showed Na 138 meq/L, Cl 63 meq/L, HC03 more than 56 meq/L, BUN 67 mg/dL, creatinine 4 mg/dL, and normal creatinine kinase. Arterial blood gas showed pH 7.55, pCO2 82, and tC02 73 consistent with severe metabolic alkalosis and concomitant respiratory acidosis. His urine electrolytes revealed Na 40 meq/L, Cl 28 meq/L, creatinine 43 mg/dL, and osmolality 261 mOsm/kg, with a fractional excretion of sodium (FENa) of 2.72%. Urinalysis was negative for glucose, blood, protein, white blood cells or eosinophils, while the urine pH was >8. Urine microscopy showed packed crystals that resembled broomsticks without renal tubular epithelial cells or casts (Figure low power and Figure high power). Renal ultrasound showed two normal size echogenic kidneys without hydronephrosis or calculi.
Despite the initial fluid resuscitation with 4 L of intravenous normal saline, the patient remained oliguric with 350 mL urine output in the first 24 h of admission. Because of the lack of improvement in his serum creatinine and urine output in the first 72 h, a kidney biopsy was performed. Light microscopy revealed diffuse acute tubular injury with numerous intratubular crystals demonstrating an unusual, finely granular to ‘fluffy,’ deeply basophilic appearance ( and ). Focally, the crystals were associated with tubular rupture and interstitial inflammation. The glomeruli were unremarkable, and there was no significant interstitial fibrosis or tubular atrophy. Direct immunofluorescence microscopy was negative for immune complex deposition. Electron microscopy demonstrated occasional intratubular crystals with peripheral radiating spicules, located within tubular epithelial cells and in the tubular lumens ( and ).
After 5 days of continued IV saline infusion the patient's creatinine improved to 2.9 mg/dL with a urine output of 1500 mL/24 h. Repeat urinalysis showed a pH of 6.5 and significantly less crystals. The final diagnosis was severe metabolic and AKI from heroin crystal nephropathy.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [138.0, 'mEq/L'], 'Bicarbonate': [56.0, 'mEq/L'], 'Chloride': [63.0, 'mEq/L']}",19,18.05,19.95,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 138.0 mEq/L. 
The concentration of chloride is 63.0 mEq/L. 
The concentration of bicarbonate is 56.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 138.0 mEq/L - (63.0 mEq/L + 56.0 mEq/L) = 19.0 mEq/L. Hence, The patient's anion gap is 19.0 mEq/L."
6363,39,Anion Gap,lab test,decimal,usmle-1545,Extracted,"A 54-year-old woman comes to the emergency department because of two episodes of bright red blood per rectum within the past day. She has a history of migraine, which is treated prophylactically with verapamil. She appears well and is hemodynamically stable. Cardiac exam reveals a regular heart rate without any murmurs or gallops. Lungs are clear to auscultation. Her abdomen is mildly tender without rebound or guarding. Digital rectal examination shows fresh blood on the glove. Laboratory studies show:
Hemoglobin 10.4 g/dL
Leukocyte count 5,000/mm3
Platelet count 175,000/mm3
Partial thromboplastin time 35 seconds
Serum
Na+ 140 mEq/L
K+ 3.7 mEq/L
Cl- 101 mEq/L
HCO3- 25 mEq/L
Mg2+ 1.8 mEq/L
A routine ECG shows a heart rate of 75/min, a normal axis, PR interval of 280 ms, QRS interval of 80 ms with a QRS complex following each p wave, and no evidence of ischemic changes.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [140.0, 'mEq/L'], 'Bicarbonate': [25.0, 'mEq/L'], 'Chloride': [101.0, 'mEq/L']}",14,13.3,14.7,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 140.0 mEq/L. 
The concentration of chloride is 101.0 mEq/L. 
The concentration of bicarbonate is 25.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 140.0 mEq/L - (101.0 mEq/L + 25.0 mEq/L) = 14.0 mEq/L. Hence, The patient's anion gap is 14.0 mEq/L."
6364,39,Anion Gap,lab test,decimal,pmc-7226683-1,Extracted,"A 62-year-old female with hypertension and diabetes presented to the emergency department with one month of shortness of breath, orthopnea, worsening exercise tolerance, paroxysmal nocturnal dyspnea, palpitation, and bilateral leg swelling. She had been compliant with her medications which included Nifedipine, Irbesartan and Metformin.
On admission, her vital signs were a respiratory rate (RR) of 16 cycles/min, heart rate (HR) of 102 bpm, blood pressure (BP) of 104/75 mmHg and saturating 94% on room air. Physical examination revealed bibasilar crepitations, elevated jugular venous pulsation, and bilateral pitting leg edema. Laboratory work up revealed Na-132mmol/L, K- 4.9mmol/L, Cl- 109mmol/L, HCO3- 27mmol/L, BUN- 17mg/dL, Cr- 1.1mg/dL, GFR- 50ml/min/1.73m2, AST-17U/L, ALT- 27U/L, HbA1c- 6.5, WBC- 4.9, HGB- 12.7, BNP-246, Troponin - normal, D-dimer- normal, TSH/T4- normal.
Electrocardiogram revealed atrial fibrillation with the rapid ventricular rate (RVR) of 150bpm and a chest x-ray revealed bilateral pleural effusion with mild pulmonary vascular congestion. However, no pulmonary emboli were identified on computed tomography pulmonary angiogram (figures , ). An Echocardiogram showed an left ventricular ejection fraction of 55-65%, with grade II diastolic dysfunction, moderate to severely dilated left atrium, severe mitral regurgitation, moderate tricuspid regurgitation (thought to be functional regurgitation, no structural valve abnormality seen), dilated inferior vena cava and increased pulmonary artery systolic pressure (figure ).
The patient was diagnosed with acute decompensated diastolic heart failure with new-onset atrial fibrillation in rapid ventricular response with a CHADSVASc of 4. Patient was administered diltiazem initially for rate control and commenced on intravenous furosemide 40mg twice daily and later continued on metoprolol succinate PO 25 mg twice daily for rate control and Rivaroxaban 15 mg PO daily. On day 7 of admission, she had significant improvement in symptoms and was clinically euvolemic with atrial fibrillation in controlled ventricular response on metoprolol succinate. A transesophageal echocardiography (TEE) was done which showed similar findings to the initial echocardiography but with no evidence of thrombus in the atrial appendage with interval improvement in mitral and tricuspid valve regurgitation. During the index admission, we achieved a sinus rhythm with direct current cardioversion of 200 joules after the TEE and was afterward discharged on Rivaroxaban, Metoprolol succinate, Amiodarone, Losartan, and Furosemide.
However, she was admitted 24 hours after discharge with shortness of breath which got worse with exertion, orthopnea, paroxysmal nocturnal dyspnea and decreased urine output despite being compliant with her discharge medication. She was dyspneic and required BiPAP, and she was later switched to 2L intranasal oxygen by nasal cannula. Her vital signs were as follows: HR of 93bpm, RR of 45cycles/min, BP of 116/95mmHg. Examination revealed crackles at the mid lungs bilaterally and bilateral pitting edema. Laboratory investigations revealed BNP-130, BUN 56mg/dL, Cr 2.2mg/dL (initial Cr from previous admission was 1.1 mg/dL), Na- 130mmol/L, WBC- 6.2, HB 13g/dL. Urine microscopy showed many white blood cells, but no muddy casts. This admission was further complicated by bradycardia, hypotension, hyponatremia, and hyperkalemia and was managed conservatively by withholding ACEI/ARB and beta-blockers. The patient continued to receive intravenous furosemide.
A repeat transthoracic echocardiogram showed an ejection fraction of 55-65%, no wall motion abnormalities, Doppler parameters consistent with restrictive physiology indicative of decreased left ventricular diastolic compliance and/or increased left atrial pressure, right ventricular volume, and pressure overload as evidenced by the diastolic and systolic flattening of the ventricular septum, moderate mitral and tricuspid regurgitation with normal IVC size. Subsequently, the serum creatinine increased to 2.5mg/dL and then plateaued before gradually trending downwards to 1.9mg/dL after a few days (table ). On 4th day of admission, recurrence of atrial fibrillation was noted, despite the fact that the patient was on amiodarone for rhythm maintenance after DCCV. The patient was switched to metoprolol 12.5mg and amiodarone was discontinued. The patient was seen in clinic 3 months after with a creatinine level of 1.3 showing continuing renal improvement since discharge.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [132.0, 'mmol/L'], 'Bicarbonate': [27.0, 'mmol/L'], 'Chloride': [109.0, 'mmol/L']}",-4,-3.8,-4.2,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 132.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 132.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 132.0 mmol * 1 mEq/mmol = 132.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 132.0 mmol sodium/L converts to 132.0 mEq sodium/L. 
The concentration of chloride is 109.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 109.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 109.0 mmol * 1 mEq/mmol = 109.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 109.0 mmol chloride/L converts to 109.0 mEq chloride/L. 
The concentration of bicarbonate is 27.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 27.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 27.0 mmol * 1 mEq/mmol = 27.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 27.0 mmol bicarbonate/L converts to 27.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 132.0 mEq/L - (109.0 mEq/L + 27.0 mEq/L) = -4.0 mEq/L. Hence, The patient's anion gap is -4.0 mEq/L."
6365,39,Anion Gap,lab test,decimal,usmle-5234,Extracted,"A 33-year-old homeless man presents to the emergency department with an altered mental status. The patient was found minimally responsive at a local mall and was brought in by police. The patient has a past medical history of polysubstance abuse, anxiety, depression, and panic disorder. His current medications include sertraline, clonazepam, and amitriptyline. His temperature is 98.7°F (37.1°C), blood pressure is 117/68 mmHg, pulse is 80/min, respirations are 10/min, and oxygen saturation is 98% on room air. Physical exam is notable for a somnolent man. Neurological exam reveals 4 mm pupils, which are equal and reactive to light, and a patient who responds incoherently to questions when stimulated. The patient has normoactive bowel sounds and is non-tender in all 4 quadrants. Laboratory values are ordered as seen below.

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 25 mEq/L
BUN: 20 mg/dL
Glucose: 99 mg/dL
Creatinine: 1.1 mg/dL
Ca2+: 10.2 mg/dL
Ethanol: negative

An initial ECG is unremarkable.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [139.0, 'mEq/L'], 'Chloride': [100.0, 'mEq/L'], 'Bicarbonate': [25.0, 'mEq/L']}",14,13.3,14.7,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 139.0 mEq/L. 
The concentration of chloride is 100.0 mEq/L. 
The concentration of bicarbonate is 25.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 139.0 mEq/L - (100.0 mEq/L + 25.0 mEq/L) = 14.0 mEq/L. Hence, The patient's anion gap is 14.0 mEq/L."
6366,39,Anion Gap,lab test,decimal,usmle-6106,Extracted,"A 30-year-old man with history of intravenous drug use and methamphetamine-associated chronic thromboembolic pulmonary hypertension (CTEPH) is brought to the emergency department by his girlfriend for worsening abdominal pain and fevers. The patient said the pain was initially around his umbilicus, but he is now experiencing intense tenderness near his groin. He was initially prescribed rivaroxaban, but due to insurance issues, he was switched to warfarin for management of CTEPH two weeks ago. His temperature is 102°F (38.9°C), blood pressure is 95/60 mmHg, pulse is 95/min, respirations are 22/min. He states that his blood pressure usually runs low. His physical exam is notable for an unremarkable cardiac exam, bibasilar crackles, and RLQ tenderness with rebound tenderness when the LLQ is palpated. Laboratory results are shown below:

Hemoglobin: 11 g/dL
Hematocrit: 35 %
Leukocyte count: 16,000/mm^3 with normal differential
Platelet count: 190,000/mm^3

Serum:
Na+: 137 mEq/L
Cl-: 100 mEq/L
K+: 3.7 mEq/L
HCO3-: 23 mEq/L
BUN: 40 mg/dL
Glucose: 110 mg/dL
Creatinine: 0.8 mg/dL
Ca2+: 9.1 mg/dL
AST: 34 U/L
ALT: 45 U/L

International normalized ratio (INR): 6.2
Prothrombin time (PT): 40 seconds
Partial thromboplastin time: 70 seconds

Blood type: O
Rhesus: Positive
Antibody screen: Negative

A clinical diagnosis is made and supported by the surgical consult team in lieu of imaging. The next operating room for an add-on procedure will not be available for another 5 hours. Appropriate medical therapy is initiated.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Sodium': [137.0, 'mEq/L'], 'Bicarbonate': [23.0, 'mEq/L'], 'Chloride': [100.0, 'mEq/L']}",14,13.3,14.7,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 137.0 mEq/L. 
The concentration of chloride is 100.0 mEq/L. 
The concentration of bicarbonate is 23.0 mEq/L. 
Plugging in these values into the anion gap formula gives us 137.0 mEq/L - (100.0 mEq/L + 23.0 mEq/L) = 14.0 mEq/L. Hence, The patient's anion gap is 14.0 mEq/L."
6367,39,Anion Gap,lab test,decimal,pmc-2556317-1,Extracted,"A 55 year old post menopausal Caucasian female presented with vitiligo on her face, arms and legs. Her past medical history included only mild asthma requiring only intermittent bronchodilators without glucocorticoids. There was no other significant personal or family medical history. Clinical examination showed a well woman, weight of 69.1 kg, height 1.67 metre (body mass index ~25). Her blood pressure was 120/75 lying and 120/70 sitting with a regular pulse of 78 beats per minute. There were 3 vitiligo patches each measuring approximately 3 × 5 cm on her forehead, anterior abdomen and left cubital fossa. No goitre or liver enlargement was detected. Biochemical investigations are as follow: sodium 130 mmol/L (reference range (RR), 136–146), potassium 5.4 mmol/L (RR, 3.5–5.5), chloride 99 mmol/L (RR, 98–108), bicarbonate 21 mmol/L (RR, 24–30), urea 9.1 mmol/L (3.0–7.0), creatinine 90 umol/L (RR, 40–90), bilirubin 18 μmol/L (6–10), alanine aminotransferase 105 IU/L (RR, < 50), aspartate aminotransferase 56 IU/L (RR, < 45), alkaline phosphatase 136 IU/L (RR, < 110), γ-glutamyl transferase 40 IU/L (< 60), albumin 33 g/L (RR, 35–45), plasma aldosterone 172 pmol/L (RR, 80–1040), plasma renin activity > 35.7 ng/mL/hr (RR, 1.2–2.8). In essence, they showed mild hyperkalaemic metabolic acidosis and hepatocellular dysfunction. Because the latter persisted, chronic hepatitis C was confirmed with positive serology of genotype 1. The liver biopsy showed changes consistent with chronic persistent hepatitis, the inflammatory and fibrotic changes were both graded 1 according to the scoring method []. Together with additional biochemical and immunological studies, other causes of persistent abnormal liver function tests were excluded. In view of her vitiligo, hepatitis C and biochemical disturbance, the Adrenocorticotropin (ACTH) stimulation test (AST), also known as the Cosyntropin or Short Synacthen test, was performed which revealed the presence of subclinical adrenal insufficiency (AI), additional file . Further investigations for the causes of AI revealed positive adrenal cell antibody (ACA) serology. Computerised tomographic scan showed small adrenal glands bilaterally with normal anatomy and appearance.
The patient underwent routine combination treatment of Interferon-α2β (IFN) and Ribavirin (RBV) for 48 weeks for her genotype 1 HCV infection. The patient's subclinical adrenal disease was also followed closely using salivary as well as serum cortisol levels to assess the hypothalamo-pituitary-adrenal axis (HPA) every 12 weeks, starting at baseline, during treatment, 6 and 12 month follow-ups. The results suggested a progressive decline of her adrenal function during the treatment phase. Glucocorticoid replacement therapy was seriously considered but with apprehension due to possible exacerbation of the hepatitis. The risks were discussed in detail with the patient and her family and it was decided to continue with anti-viral therapy but without glucocorticoid supplement. The patient and her husband were counselled comprehensively regarding the emergency management of Addisonian crisis, provided with a carrying note and required to wear an alert bracelet. Other immediate family members were also involved in her management plan, with her consent. Her management plan was also forwarded to the local hospital Emergency Department and Hepatitis C Service. Fortunately, there was no crisis other than the common side effects of the treatment regimen. Her pattern of steroid profile and ACA returned to its pre-existing state and remained unchanged at 6 and 12 month follow-up after the cessation of therapy. The patient has remained well since but her subclinical AI persists.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Bicarbonate': [21.0, 'mmol/L'], 'Chloride': [99.0, 'mmol/L'], 'Sodium': [130.0, 'mmol/L']}",10,9.5,10.5,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 130.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 130.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 130.0 mmol * 1 mEq/mmol = 130.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 130.0 mmol sodium/L converts to 130.0 mEq sodium/L. 
The concentration of chloride is 99.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 99.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 99.0 mmol * 1 mEq/mmol = 99.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 99.0 mmol chloride/L converts to 99.0 mEq chloride/L. 
The concentration of bicarbonate is 21.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 21.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 21.0 mmol * 1 mEq/mmol = 21.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 21.0 mmol bicarbonate/L converts to 21.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 130.0 mEq/L - (99.0 mEq/L + 21.0 mEq/L) = 10.0 mEq/L. Hence, The patient's anion gap is 10.0 mEq/L."
6368,39,Anion Gap,lab test,decimal,pmc-7455384-1,Extracted,"A 57-year-old man was admitted to the ED with complaints of syncope and weakness. We noticed that in his medical history, leeches were applied to treat the diabetic wounds on his feet two hours before he attended our clinic. After this, the leeches spontaneously detached but he observed bleeding from his bites and bleeding did not stop in spite of compression with tight bandages. A review of the patient’s past medical history revealed hypertension, diabetes mellitus, diabetic foot, ischemic heart disease and coronary artery bypass surgery.
Vital signs were as follows; fever: 36.6°C, blood pressure: 85/50 mmHg, heart rate: 112/min and respiratory rate: 28/min. Physical examination revealed tenderness in the whole abdomen. Ampulla was empty with rectal examination. There was an ulcerative lesion with size 5x3 cm on the site of the amputated first toe. Additionally, there were multiple bites due to leech therapy on both feet (Figure ).
Laboratory tests indicated the following: hemoglobin: 7.6 g/dL, white blood cells: 9370/mm3, platelets: 147000/mL, blood urea nitrogen: 29.1 mg/dL, creatinine: 1.98 mg/dL, glucose: 527 mg/dL, Na: 127 mmol/L, K: 6 mmol/L, CL: 94.5 mmol/L, C-reactive protein: 1.27 mg/dL and other routine blood tests and coagulation functions were all normal. Blood gas analysis revealed pH: 7.26, pO2: 86 mmHg, and bicarbonate: 20.2 mmol/L. Abdominal ultrasonography (USG) showed gas in the intrahepatic biliary ducts. No obstructive pathology was found to mesenteric blood flow on Doppler USG. CT without intravenous contrast was performed because of abnormal renal function tests. CT revealed gas near the stomach, among colon segments (pneumatosis cystoides intestinalis, PSI) and intrahepatic biliary ducts in central and left hepatic lobe (hepatic portal venous gas, HPVG) (Figure , Figure , respectively).
The patient was referred to another hospital that had an intensive care unit and started conservative treatment with antibiotics and intravenous fluid. Twelve hours after treatment, his general condition did not improve and signs of diffused peritonitis were observed on abdominal examination. The patient underwent exploratory laparotomy. Necrosis was found in the terminal ileum and the entire colon during laparotomy. Doppler USG detected low flow in the vessels supplying these necrotic segments. However, resection was decided due to necrosis of these segments. These necrotic intestinal segments were resected and an end-ileostomy was performed. He had an uneventful recovery and was discharged on the 17th postoperative day.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Bicarbonate': [20.2, 'mmol/L'], 'Chloride': [94.5, 'mmol/L'], 'Sodium': [127.0, 'mmol/L']}",12.3,11.685,12.915,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 127.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 127.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 127.0 mmol * 1 mEq/mmol = 127.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 127.0 mmol sodium/L converts to 127.0 mEq sodium/L. 
The concentration of chloride is 94.5 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 94.5 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 94.5 mmol * 1 mEq/mmol = 94.5 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 94.5 mmol chloride/L converts to 94.5 mEq chloride/L. 
The concentration of bicarbonate is 20.2 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 20.2 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 20.2 mmol * 1 mEq/mmol = 20.2 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 20.2 mmol bicarbonate/L converts to 20.2 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 127.0 mEq/L - (94.5 mEq/L + 20.2 mEq/L) = 12.3 mEq/L. Hence, The patient's anion gap is 12.3 mEq/L."
6369,39,Anion Gap,lab test,decimal,pmc-7360221-1,Extracted,"A 39-year-old male patient (173 cm, 135 kgm, body mass index: 45.1) was a case of morbid obesity. He had undergone laparoscopic SG for morbid obesity on August 21, 2018, which led to his poor appetite, nausea and vomiting. In following 3 weeks, he lost 17 kilograms of body weight. On September 16, 2018, he was sent to our hospital due to persistent watery diarrhea, dehydration, and general weakness for 3 days. Upon the arrival at our hospital, his vital signs were blood pressure 117/57 mm Hg, pulse rate 108/min, respiratory rate 18/min, body temperature 37.1°C. Electrocardiography showed sinus tachycardia. The laboratory data revealed severe hypokalemia (K 2.6 mmol/L [3.6–5.1]), acute kidney injury (Bun 29 mg/dL [8–20], Cr 4.36 mg/dL [0.44–1.03] estimated Glomerular filtration rate 16 [mL/min]), and normal liver, pancreas, cardiac enzymes as well as other electrolytes (Na 137 mmol/L [136–144], Cl 111 mmol/L [100–111], bicarbonate 26 mmol/L [22–26]) (Table ). Other positive findings were mild anemia and leukocytosis (white blood cell 10.1^103/uL [3.8–10.0], Hemoglobin 10.6 g/dL [12–16]), elevated C-Reactive protein 2.3 mg/dL (<1.0) and lactic acid 3.1 mmol/L (0.5–2.2).
He was admitted for aggressive intravenous hydration. On the third day of admission, the patient's potassium level (3.2 mmol/L) and kidney function (Bun 23 mg/dL, Cr 2.57 mg/dL, eGFR 30 mL/min) were getting better, but he was getting deteriorated with drowsy consciousness. The brain computed tomography revealed no significant findings. Tracing his medical history, he was diagnosed as a bipolar affective disorder for 20 years. He was under regular follow-up in the psychiatric clinic with lithium carbonate 600 mg twice daily, risperidone 2 mg twice daily, and flurazepam 60 mg once daily. He was still taking the same dosage during these days after surgery. Lithium level was found to be 3.42 mEq/L and lithium toxicity was diagnosed. Lithium carbonate was discontinued immediately, and urgent hemodialysis was suggested by nephrologist.
After 3 courses of hemodialysis, his serum lithium level subsequently declined to 0.63 mEq/L and creatinine level to 1.58 mg/dL, while his consciousness returned normal. In the following days, neurologic sequelae were noted by muscle weakness (muscle power 2 points over bilateral dorsi-flexors and plantar-flexors) and pain sensation in both feet. The nerve conduction test revealed sensorimotor polyneuropathy with conduction block. The patient was discharged thirty-five days after admission, while his serum lithium and creatinine level declined to 0.06 mEq/L and 1.05 mg/dl, respectively. He was advised to keep a passive range of motion exercise until the nerve function recovers. Lithium carbonate was replaced by lamotrigine now.",What is the patient's anion gap in terms of mEq/L?  You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Bicarbonate': [26.0, 'mmol/L'], 'Chloride': [111.0, 'mmol/L'], 'Sodium': [137.0, 'mmol/L']}",0,0,0,"The formula for computing a patient's anion gap is: sodium (mEq/L) - (chloride (mEq/L)+ bicarbonate (mEq/L)).
The concentration of sodium is 137.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of sodium from mmol to mEq. The mass of sodium is 137.0 mmol. The compound, sodium, has a valence of 1, and so multiply the valence by the value of mmol to get, 137.0 mmol * 1 mEq/mmol = 137.0 mEq sodium. The volume units is L so no volume conversion is needed. Hence, the concentration value of 137.0 mmol sodium/L converts to 137.0 mEq sodium/L. 
The concentration of chloride is 111.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of chloride from mmol to mEq. The mass of chloride is 111.0 mmol. The compound, chloride, has a valence of 1, and so multiply the valence by the value of mmol to get, 111.0 mmol * 1 mEq/mmol = 111.0 mEq chloride. The volume units is L so no volume conversion is needed. Hence, the concentration value of 111.0 mmol chloride/L converts to 111.0 mEq chloride/L. 
The concentration of bicarbonate is 26.0 mmol/L. We need to convert the concentration to mEq/L. Let's first convert the mass of bicarbonate from mmol to mEq. The mass of bicarbonate is 26.0 mmol. The compound, bicarbonate, has a valence of 1, and so multiply the valence by the value of mmol to get, 26.0 mmol * 1 mEq/mmol = 26.0 mEq bicarbonate. The volume units is L so no volume conversion is needed. Hence, the concentration value of 26.0 mmol bicarbonate/L converts to 26.0 mEq bicarbonate/L. 
Plugging in these values into the anion gap formula gives us 137.0 mEq/L - (111.0 mEq/L + 26.0 mEq/L) = 0 mEq/L. Hence, The patient's anion gap is 0 mEq/L."
6370,44,LDL Calculated,lab test,decimal,pmc-7038555-1,Extracted,"An 18-year-old Black female who had been diagnosed with SCD in childhood, subsequently suffering frequent pain crises and undergoing repeated transfusions, presented to the emergency room with a 21-day history of progressive lower limb oedema accompanied by dyspnoea and orthopnoea. In addition, she reported a 3-day history of severe chest pain, together with a productive cough and fever as high as 38 °C. She reported no reduction in urine volume and no recent history of skin infection or tonsillitis. On physical examination, she was found to be very pallid and normotensive (blood pressure, 130/80 mmHg), with a heart rate of 104 bpm, a respiratory rate of 28 breaths/min, and oxygen saturation of 94% on room air, as well as being found to have developed anasarca. One month prior, she had undergone outpatient laboratory tests, which had shown that her renal function was normal—with a serum creatinine concentration of 0.75 mg/dl and an estimated glomerular filtration rate (eGFR), as determined by the Chronic Kidney Disease–Epidemiology Collaboration (CKD–EPI) equation, of 134.9 ml/min/1.73 m2—urine analysis showing no haematuria or proteinuria.
Blood tests performed at admission to the emergency room revealed the following: haemoglobin, 6.1 g/dl; haematocrit, 18.8%; haptoglobin, < 10 mg/dl; reticulocyte fraction, 6.11%; no schistocytes; lactate dehydrogenase, 433 U/L; indirect bilirubin, 0.36 mg/dl; leucocyte count, 18,820 cells/mm3; neutrophil count, 13,630 cells/mm3; lymphocyte count, 2790 cells/mm3; platelet count, 622;000 cells/mm3; and urea, 29 mg/dl. The patient showed signs of hyperfiltration, including a serum creatinine concentration of 0.49 mg/dl and a CKD–EPI-determined eGFR of 148.5 ml/min/1.73 m2, although no hydroelectrolytic or acid-base disorders were identified. A urine sample was found to contain 100 leucocytes/field and 70 erythrocytes/field. In addition, 24-h proteinuria was 8.99 g. Further analysis of the blood samples showed the following: total proteins, 3.9 g/dl; albumin, 1.2 g/dl; globulins, 2.7 g/dl; total cholesterol, 210 mg/dl, low-density lipoprotein, 114 mg/dl; high-density lipoprotein, 37 mg/dl; triglycerides, 205 mg/dl; C4, 26.1 mg/dl (normal range, 10–38 mg/dl); C3, 62 mg/dl (normal range, 73–149 mg/dl); C-reactive protein, 24.9 mg/dl (normal range, < 5 mg/dl). The serology was negative for HIV, hepatitis B, and hepatitis C. The patient also tested negative for antinuclear factor, anti-DNA, rheumatoid factor, and antineutrophil cytoplasmic antibodies. Serum protein electrophoresis showed hypoalbuminaemia and an anti-streptolysin O level of 816 IU/ml (normal range, < 200 IU/ml). Blood and urine cultures were negative. A chest X-ray showed mild congestion and infiltrate in the right lung base. Ultrasound of the kidneys and urinary tract showed that the kidneys were normal in size and appearance.
Given the clinical presentation, the diagnostic hypothesis was pneumonia and anasarca due to nephritic-nephrotic syndrome. The patient was started on ceftriaxone (1 g, twice daily). Computed tomography angiography of the chest ruled out pulmonary thromboembolism and acute chest syndrome, thus indirectly confirming the diagnosis of pneumonia.
After the infection had been controlled, the patient underwent renal biopsy. Light microscopy revealed 7 glomeruli with global endocapillary proliferation; neutrophil and macrophage infiltrate (Fig. a); synechiae in 10% of the glomeruli; occasional splitting of the glomerular basement membrane; and a preserved Bowman’s capsule. The tubules were dilated, with foci of epithelial regeneration and neutrophils within their lumina. There was focal oedema in the interstitium. The interlobular arteries had a normal aspect, with intimal proliferation in the arterioles. Immunofluorescence performed on frozen sections showed intensity of deposition of C3 (2+/3+), IgG (1+/3+), IgA (1+/3+) and lambda light chains (1+/3+), with a granular pattern, distributed diffusely throughout the capillary loop. Collectively, the histological findings were consistent with a diagnosis of APIGN accompanied by microangiopathic changes related to the underlying disease.
Treatment with a diuretic and an anti-proteinuric agent (angiotensin-converting enzyme inhibitor) was instituted, and the patient evolved to clinical improvement (normalisation of blood pressure, as well as resolution of the proteinuria and haematuria). However, the signs of hyperfiltration persisted even after resolution of the proteinuria. In the final evaluation, the serum creatinine concentration was 0.33 mg/dl and the CKD–EPI-determined eGFR was 187.8 ml/min/1.73 m2. Evolution of laboratorial tests are available in Fig. .",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [37.0, 'mg/dL'], 'Triglycerides': [205.0, 'mg/dL'], 'Total cholesterol': [210.0, 'mg/dL']}",132,125.4,138.6,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 210.0 mg/dL. 
The concentration of hdl cholesterol is 37.0 mg/dL. 
The concentration of triglycerides is 205.0 mg/dL. 
Plugging in these values will give us 210.0 mg/dL - 37.0 mg/dL - (205.0/5) mg/dL = 132.0 mg/dL.
The patients concentration of LDL cholestrol is 132.0 mg/dL."
6371,44,LDL Calculated,lab test,decimal,pmc-6484933-2,Extracted,"Ms. A, 12 years and 10 months, female
Hyperglycemia
Father with type 2 diabetes under treatment
No significant history
12-year-old female who presented to Konkuk University Medical Center with post-prandial hyperglycemia of 330 mg/dL measured by her father one day prior to admission. Menarche occurred 1 year prior and her menstrual cycles were regular.
On admission, the patient’s height was 158.9 cm (25–50th percentile), weight was 75.5 kg (>97th percentile), and BMI was 29.9 kg/m2 (>97th percentile) (). Her vital signs were within the normal range with a blood pressure of 112/68 mmHg, pulse of 72 beats/min, respiratory rate of 20 breaths/min, and temperature of 36.6°C. She had a clear mental status, warm skin, and moist mucous membranes. A chest examination revealed no specific findings, while an abdominal examination revealed no hepatomegaly or splenomegaly. The rest of the physical examination was unremarkable.
Laboratory tests at the time of admission revealed an HbA1c level of 9.9%, fasting blood glucose level of 202 mg/dL, insulin level of 15.85 μIU/mL, and C-peptide level of 2.97 ng/mL. Liver function tests showed an elevated AST level at 47 IU/L and ALT level at 69 IU/L. A lipid panel and comprehensive metabolic panel showed a total cholesterol level of 165 mg/dL, triglyceride level of 104 mg/dL, HDL-C of 50 mg/dL, total protein of 7.6 g/dL, and albumin of 4.8 g/dL (). The free fatty acid level was elevated at 671 μEq/L.
There were no significant findings on a chest radiograph. An abdominal ultrasound showed moderate fatty liver.
For glycemic control, combination therapy of oral medication (metformin 500 mg BID) and lifestyle modification through adjustments in dietary habits was prescribed. We evaluated her dietary and nutritional knowledge and then counseled her to consume regular meals with 70–90 g of protein per day, maintain daily nutritional requirements of approximately 1800 kcal, and eat a low-carb, low-fat diet. She was recommended to modify her habitual preference of salty and spicy foods, reduce her salt intake, track her meals, and attend outpatient monitoring appointments every 1–2 months.
For an exercise program, she was instructed to include aerobic and weight exercises that improve muscle strength. She was advised to walk >1 hour at least 5 days per week and visit a health training center for ≥1 hour of strength exercises at least 3 times per week. We measured her height and weight every 2 months, and used InBody720, a type of BIA for accurate assessment of obesity. On diagnosis, patient’s BMI was 29.9 kg/m2 (FMI, 12.7 kg/m2; FFMI, 17.2 kg/m2) and PBF was 42.5%. Two years later after the diagnosis, an abdominal ultrasound showed improvements in her fatty liver and her HbA1c was successfully reduced to 6.0%. The oral medication was discontinued due to the successful glycemic control. At the time, her fasting blood sugar was 97 mg/dL, insulin level was 5.62 μIU/mL, and C-peptide level was 2.79 ng/mL. Her BMI (FMI+FFMI) was 23.2 kg/m2 (7.0 kg/m2+16.2 kg/m2), which was within the overweight range (85–90th percentile), and her PBF was 30.2%. Her BMI at that point was 6.7 kg/m2 lower than that prior to therapy, with a 5.7 kg/m2 reduction observed in her FMI (). Liver function tests and a lipid panel revealed the following: AST, 20 IU/L; ALT, 34 IU/L; total cholesterol, 115 mg/dL; triglycerides, 70 mg/dL; and HDL-C, 30 mg/dL (). The changes in the patient’s weight and body composition during treatment are shown in . Since discontinuing the oral medication, the patient has maintained an HbA1c level <6.5%.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Total cholesterol': [165.0, 'mg/dL'], 'Triglycerides': [104.0, 'mg/dL'], 'high-density lipoprotein cholesterol': [50.0, 'mg/dL']}",94.2,89.49,98.91,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 165.0 mg/dL. 
The concentration of hdl cholesterol is 50.0 mg/dL. 
The concentration of triglycerides is 104.0 mg/dL. 
Plugging in these values will give us 165.0 mg/dL - 50.0 mg/dL - (104.0/5) mg/dL = 94.2 mg/dL.
The patients concentration of LDL cholestrol is 94.2 mg/dL."
6372,44,LDL Calculated,lab test,decimal,pmc-4543188-1,Extracted,"A male patient aged four years and 10 months was brought in with a complaint of short stature. It was indicated that although his development was normal until 12 months of age, it halted afterwards. It was found out that the patient was born at term in breech position through cesarean section with a normal Apgar score and birth weight of 3,750 g, hospitalized postnatally for five days due to birth in breech position and was not noted to be hypothermic and hypoglycemic, was diagnosed with LCP at four years of age following detailed examination due to complaints of pain in the hips, and consequently underwent surgery (). Family history indicated that the patient's parents were related to each other within the second degree of consanguinity. His first sibling was being followed up for Tangier disease, and his second sibling was being followed up for hyperlipidemia by the Department of Pediatric Metabolism. Physical examination findings showed that the patient was prepubertal, and that he had a height of 96 cm (standard deviation score [SDS], -3.2), body weight of 14.6 kg (SDS, -1.9), 2 cm shorter left leg compared to right leg, a surgical scar in the left inguinal region, and stretched penile length of 4.5 cm. Other systemic examination findings were normal. While the patient's chronological age was four years and 10 months, his bone age was consistent with a 2-year-old's (according to Greulich and Pyle).
Laboratory tests yielded the following results: white blood cell count, 11,300/mm3; hemoglobin, 12.1 g/dL; thrombocyte, 320,000/mm3; urea, 7 mg/dL; creatinine, 0.9 ml/dL; serum sodium, 148 mmol/L; potassium, 4.3 mmol/L; chloride, 102 mmol/L; calcium, 9.7 mg/dL; phosphorus, 4.4 mg/dL; normal liver function; fasting blood glucose, 92 mg/dL; total cholesterol, 130 mg/dL; high-density lipoprotein, 41 mg/dL; low density lipoprotein cholesterol, 69 mg/dL; triglyceride, 50 mg/dL; and urine density, 1,022 g/cm3.
Detailed laboratory analyses showed thyroid function consistent with central hypothyroidism (sT4, 0.49 ng/dL [0.8-1.9 ng/dL]; thyroid-stimulating hormone, 2.57 mU/L [0.5-5 mU/L]). The patient was also determined to have hypocortisolemia (basal serum cortisol level of 2.75 g/dL, stimulated serum cortisol level of 5.71 g/dL [with low-dose adrenocorticotropic hormone]) and GHD (peak GH values in glucagon and levodopa tests while the patient was euthyroid were 0.257 and 0.46 ng/mL, respectively). Serum IGF-1 level was 15 ng/mL (SDS, -3) and Insulin-like growth factor binding protein-3 (IGFBP3) level was 900 ng/mL (SDS, -2.6). An etiology-oriented hypophyseal magnetic resonance imaging was performed due to high prolactin levels (37.4 ng/mL [normal range, 0-25 ng/mL]), which revealed in the sellar cavity center that the adenohypophyseal gland height was 3 mm, neurohypophyseal localization was abnormal, and that there was no signal intensity. In addition, T1A hyperintense nodular appearance with dimensions of 3 mm×2.5 mm showing diffused homogeneous contrast retention following injection of contrast agent was observed at the median eminence level (ectopic neurohypophysis). The pituitary stalk was not identified as a separate structure (). Considering the patient's medical history, it was deduced and evaluated as a pituitary stalk interruption syndrome due to difficult birth. The patient was sequentially started on hydrocortisone, L-thyroxin, and GH therapy.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [41.0, 'mg/dL'], 'Triglycerides': [50.0, 'mg/dL'], 'Total cholesterol': [130.0, 'mg/dL']}",79,75.05,82.95,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 130.0 mg/dL. 
The concentration of hdl cholesterol is 41.0 mg/dL. 
The concentration of triglycerides is 50.0 mg/dL. 
Plugging in these values will give us 130.0 mg/dL - 41.0 mg/dL - (50.0/5) mg/dL = 79.0 mg/dL.
The patients concentration of LDL cholestrol is 79.0 mg/dL."
6373,44,LDL Calculated,lab test,decimal,pmc-6221513-1,Extracted,"A 49-year-old African American male presented to our hospital center after ventricular fibrillation cardiac arrest with return of spontaneous circulation achieved after 10 minutes of cardiopulmonary resuscitation and defibrillation by emergency services. Personal cardiovascular risk factors included untreated hyperlipidemia and hypertension. Cardiac past medical history included one episode of diaphoresis and palpitations, four years prior to this admission. Per the patient, workup at that time at another local hospital revealed an unspecified arrhythmia and cardiac hypertrophy, but the patient did not follow up. The patient denied a family history of recurrent syncope or unexplained cardiac death, but reported unspecified cardiac hypertrophy and unspecified arrhythmia in one brother, and coronary artery disease in mother and brother.
On arrival to the emergency department, the patient was asymptomatic. Clinical examination showed a blood pressure of 135/67, with irregular heartbeat of 72 beats per minute, decreased heart sounds and soft systolic murmur but no S4 on cardiac auscultation. Troponin-T was minimally elevated at 0.021 ng/mL. Lipid panel was deranged – cholesterol 239 mg/dL, triglycerides 149 mg/dL, low-density lipoprotein cholesterol 170 mg/dL, and high-density lipoprotein cholesterol 48 mg/dL. Transaminitis (aspartate aminotransferase 504 unit/L, alanine aminotransferase 332 unit/L), elevated creatinine 1.5 mg/dL and anion gap were noted on laboratory studies. Other labs were unremarkable including normal white blood cell count, hemoglobin and thyroid-stimulating hormone.
Serial 12-lead ECGs showed deep T inversions in V3-V6 and early repolarization in V1 and V2 leads (Figures , ). On arrival, the patient was also in atrial fibrillation with rapid ventricular response (Figure ), which resolved with intravenous Amiodarone. Septal infarct of undetermined age, possible inferior subendocardial injury, possible anterolateral subendocardial injury, and prolonged QT were also reported on automated interpretation of ECG. The patient underwent cardiac catheterization, which showed patent coronary arteries, however, the classic ace of spades sign was seen on ventriculogram (Figure ). Initial transthoracic echocardiogram without contrast was interpreted as normal left ventricular wall thickness, with an ejection fraction of 70% and no wall motion abnormalities.
The patient was treated with aspirin 81 mg daily, carvedilol 6.25 mg twice a day, hydrochlorothiazide 25 mg daily, atorvastatin 40 mg daily, and an automated implantable cardioverter-defibrillator (AICD) for secondary prevention of another cardiac arrest. The patient was asymptomatic up to discharge three days after admission. Liver function enzymes (aspartate aminotransferase and alanine aminotransferase) trended down to 65 unit/L and 199 unit/L, respectively. Creatinine also normalized to 1.1 mg/dL.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [48.0, 'mg/dL'], 'Triglycerides': [149.0, 'mg/dL'], 'Total cholesterol': [239.0, 'mg/dL']}",161.2,153.14,169.26,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 239.0 mg/dL. 
The concentration of hdl cholesterol is 48.0 mg/dL. 
The concentration of triglycerides is 149.0 mg/dL. 
Plugging in these values will give us 239.0 mg/dL - 48.0 mg/dL - (149.0/5) mg/dL = 161.2 mg/dL.
The patients concentration of LDL cholestrol is 161.2 mg/dL."
6374,44,LDL Calculated,lab test,decimal,pmc-7038555-2,Extracted,"A 12-year-old White male, who had also been diagnosed with SCD in childhood, sought treatment for a 20-day history of non-productive cough and lower limb oedema, which had evolved to anasarca, together with a new onset of hypertension. He had previously experienced one episode of pain and had undergone one transfusion. He reported no reduction in urine volume and no recent history of skin infection or tonsillitis. On physical examination, he was found to be pallid (+ 3/+ 4) and hypertensive (blood pressure, 160/90 mmHg), with a heart rate of 112 bpm, a respiratory rate of 36 breaths/min, and oxygen saturation of 92% on room air.
Blood tests performed at admission to the emergency room revealed the following: haemoglobin, 5.9 g/dl; haematocrit, 17.8%; haptoglobin, < 10 mg/dl; negative result on the Coombs direct antibody test; reticulocyte fraction, 4.26%; no schistocytes; lactate dehydrogenase, 970 U/L; indirect bilirubin, 0.65 mg/dl; leucocyte count, 17,330 cells/mm3; neutrophil count, 13,100 cells/mm3; lymphocyte count, 1700 cells/mm3; platelet count, 622;000 cells/mm3; and urea, 45 mg/dl. He also showed signs of hyperfiltration, with a serum creatinine concentration of 0.65 mg/dl, and an eGFR, as determined with the Schwartz formula, of 140.0 ml/min/1.73 m2, although no hydroelectrolytic or acid-base disorders were identified. An urine sample obtained at submission was found to contain 20 leucocytes/field and > 100 erythrocytes/field; 24-h proteinuria was 12.5 g. Metabolic analysis of the blood samples showed the following: total proteins, 6.1 g/dl; albumin, 2.6 g/dl; globulins, 3.1 g/dl; total cholesterol, 211 mg/dl, low-density lipoprotein, 118 mg/dl; high-density lipoprotein, 66 mg/dl; triglycerides, 133 mg/dl; C4, 25 mg/dl (normal range, 10–38 mg/dl); C3, 106 mg/dl (normal range, 73–149 mg/dl); C-reactive protein, 2.1 mg/dl (normal range, < 5 mg/dl). The serology was negative for HIV, hepatitis B, and hepatitis C. Tests for antinuclear factor, anti-DNA, rheumatoid factor, and antineutrophil cytoplasmic antibodies were also negative. Serum protein electrophoresis showed hypoalbuminaemia. Blood and urine cultures were negative. A chest X-ray showed cardiomegaly and signs of mild pulmonary congestion. Ultrasound of the kidneys and urinary tract showed that the kidneys were normal in size and appearance.
The patient underwent renal biopsy. Light microscopy showed 43 glomeruli with diffuse endocapillary hypercellularity (numerous lymphocytes and neutrophils). Synechiae were observed in 10% of the glomeruli in Bowman’s capsule. There was also occasional splitting of the glomerular basement membrane, as well as overall expansion of the mesangial matrix (Fig. b). There were no changes in the tubules, interstitium or arterioles. Immunofluorescence showed deposition of C3 (2+/3+) and lambda light chains (1+/3+), with a granular pattern, distributed throughout the capillary loop—the so-called “starry sky” pattern—consistent with a diagnosis of APIGN.
Treatment with a diuretic and an anti-proteinuric agent (angiotensin-converting enzyme inhibitor) was instituted, and the patient evolved to clinical improvement, including normalisation of blood pressure and a significant reduction in the level of proteinuria (24-h proteinuria, 1.34 g) after 10 days. Renal function was preserved. The patient left outpatient treatment after 18 months. In the final evaluation, he still presented no proteinuria or haematuria, although the signs of hyperfiltration persisted, his serum creatinine concentration being 0.5 mg/dl and his Schwartz-derived eGFR being 182 ml/min/1.73 m2. Evolution of laboratorial tests are available in Fig. .",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [66.0, 'mg/dL'], 'Triglycerides': [133.0, 'mg/dL'], 'Total cholesterol': [211.0, 'mg/dL']}",118.4,112.48,124.32,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 211.0 mg/dL. 
The concentration of hdl cholesterol is 66.0 mg/dL. 
The concentration of triglycerides is 133.0 mg/dL. 
Plugging in these values will give us 211.0 mg/dL - 66.0 mg/dL - (133.0/5) mg/dL = 118.4 mg/dL.
The patients concentration of LDL cholestrol is 118.4 mg/dL."
6375,44,LDL Calculated,lab test,decimal,usmle-5115,Extracted,"A 64-year-old man presents to his physician 6 months after experiencing a myocardial infarction. The patient currently denies any symptoms and is only in for a check up. The patient's past medical history is notable for diabetes (type II), obesity, hypertension and cyclothymia. His current medications are hydrocholorthiazide, metoprolol, metformin, insulin, fluoxetine, and fish oil. On physical exam you note a calm elderly man who is moderately obese and in no current distress. The patient's cardiovascular exam is notable for a S4 heart sound. The patients lab work is below.

Serum:
Na+: 140 mEq/L
Cl-: 100 mEq/L
K+: 4.4 mEq/L
HCO3-: 23 mEq/L
BUN: 20 mg/dL
Glucose: 120 mg/dL
Creatinine: 1.6 mg/dL
Ca2+: 10.1 mg/dL
AST: 11 U/L
ALT: 9 U/L
Cholesterol: 190 mg/dL
Triglycerides: 150 mg/dL
High density lipoprotein associated cholesterol: 11 mg/dL
Low density lipoprotein associated cholesterol: 149 mg/dL

The physician updates the patient's medication regimen after this visit.

The patient returns 2 weeks later and presents his blood glucose diary to you demonstrating a mean blood glucose of 167 mg/dL. He is also complaining of flushing that occurs occasionally but otherwise is doing well.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [11.0, 'mg/dL'], 'Triglycerides': [150.0, 'mg/dL'], 'Total cholesterol': [190.0, 'mg/dL']}",149,141.55,156.45,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 190.0 mg/dL. 
The concentration of hdl cholesterol is 11.0 mg/dL. 
The concentration of triglycerides is 150.0 mg/dL. 
Plugging in these values will give us 190.0 mg/dL - 11.0 mg/dL - (150.0/5) mg/dL = 149.0 mg/dL.
The patients concentration of LDL cholestrol is 149.0 mg/dL."
6376,44,LDL Calculated,lab test,decimal,pmc-8080730-1,Extracted,"A 46-year-old woman with a family history of ADPKD presented to our emergency department with acute chest pain.
Her chest pain lasted for 1 day and radiated to the back of her left shoulder.
Her ADPKD had affected kidney function (eGFR: 15.98 mL/min/1.73 m2), and she exhibited extrarenal features of polycystic liver as shown in Figure .
She had no cardiovascular risk factors except a long history of hypertension and emotional stress. Blood pressure at admission was 142/70 mmHg.
Auscultation revealed that the heart sounds were normal, without rales in the lungs.
At the emergency department, her troponin I was 0.268 ng/mL and the peak value during hospitalization was 1.928 ng/mL. Hematological examination found no signs of inflammation and anemia. The low-density lipoprotein cholesterol was 3.32 mmol/L, High density lipoprotein cholesterol cholesterol was 1.10 mmol/L, total cholesterol was 4.07 mmol/L, triglyceride was 0.82 mmol/L, and body mass index was 21.87 kg/m2.
Her initial electrocardiogram in the emergency room was normal without any changes in ST segment and T wave (Figure ). Transthoracic echocardiography revealed mild dilation of the left atrium (left atrium inner diameter 42 mm), normal left ventricular ejection fraction (62%), and mild mitral regurgitation.
After three days of antiplatelet therapy, we performed coronary angiography which found no obvious characteristics of coronary dissection (Figure and ). Given the particularity of the patient, IVUS examination was performed at the same time to further examine the condition of her coronary artery. Interestingly, obvious IMH formation from the distal to proximal was found in the left circumflex (Figure ). IVUS was also performed on the left anterior descending artery, and found only a few atherosclerotic plaques (Figure ).",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [1.1, 'mmol/L'], 'Triglycerides': [0.82, 'mmol/L'], 'Total cholesterol': [4.07, 'mmol/L']}",100.71,95.6745,105.7455,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 4.07 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of total cholesterol from mmol to mg. The mass of total cholesterol is 4.07 mmol. To convert 4.07 mmol of total cholesterol to mol, multiply by the conversion factor 0.001, giving us 4.07 mmol total cholesterol * 0.001 mol/mmol = 0.00407 mol total cholesterol. To convert from mol total cholesterol to grams, multiply by the molar mass 386.654 g/mol, which will give 0.00407 mol total cholesterol * 386.654 g/mol = 1.57368 g total cholesterol. To convert 1.57368 g of total cholesterol to mg, multiply by the conversion factor 1000.0, giving us 1.57368 g total cholesterol * 1000.0 mg/g = 1573.68 mg total cholesterol. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1573.68 mg total cholesterol/10.0 dL = 157.368 mg total cholesterol/dL. The concentration value of 4.07 mmol total cholesterol/L converts to 157.368 mg total cholesterol/dL. 
The concentration of hdl cholesterol is 1.1 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of hdl cholesterol from mmol to mg. The mass of hdl cholesterol is 1.1 mmol. To convert 1.1 mmol of hdl cholesterol to mol, multiply by the conversion factor 0.001, giving us 1.1 mmol hdl cholesterol * 0.001 mol/mmol = 0.0011 mol hdl cholesterol. To convert from mol hdl cholesterol to grams, multiply by the molar mass 386.654 g/mol, which will give 0.0011 mol hdl cholesterol * 386.654 g/mol = 0.42532 g hdl cholesterol. To convert 0.42532 g of hdl cholesterol to mg, multiply by the conversion factor 1000.0, giving us 0.42532 g hdl cholesterol * 1000.0 mg/g = 425.32 mg hdl cholesterol. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 425.32 mg hdl cholesterol/10.0 dL = 42.532 mg hdl cholesterol/dL. The concentration value of 1.1 mmol hdl cholesterol/L converts to 42.532 mg hdl cholesterol/dL. 
The concentration of triglycerides is 0.82 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of triglycerides from mmol to mg. The mass of triglycerides is 0.82 mmol. To convert 0.82 mmol of triglycerides to mol, multiply by the conversion factor 0.001, giving us 0.82 mmol triglycerides * 0.001 mol/mmol = 0.00082 mol triglycerides. To convert from mol triglycerides to grams, multiply by the molar mass 861.338 g/mol, which will give 0.00082 mol triglycerides * 861.338 g/mol = 0.7063 g triglycerides. To convert 0.7063 g of triglycerides to mg, multiply by the conversion factor 1000.0, giving us 0.7063 g triglycerides * 1000.0 mg/g = 706.3 mg triglycerides. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 706.3 mg triglycerides/10.0 dL = 70.63 mg triglycerides/dL. The concentration value of 0.82 mmol triglycerides/L converts to 70.63 mg triglycerides/dL. 
Plugging in these values will give us 157.368 mg/dL - 42.532 mg/dL - (70.63/5) mg/dL = 100.71 mg/dL.
The patients concentration of LDL cholestrol is 100.71 mg/dL."
6377,44,LDL Calculated,lab test,decimal,pmc-2687573-1,Extracted,"A 28-year-old obese man presented at the Emergency Room of our hospital complaining of epigastric pain radiated to the back for one day. He had been admitted to our hospital 3 times previously due to acute pancreatitis with hyperlipidemia. He had type 2 diabetes mellitus and active pulmonary tuberculosis. He was treated with dietary restriction, daily NPH insulin injection, and lipid lowing medication such as fibrate derivatives. His father was noted to have hypertension, old cerebral infarction and type 2 diabetes mellitus. His mother had hyperlipidemia (type IV) and his elder brother had recurrent acute pancreatitis and diabetes mellitus. He didn't have xanthoma or xanthelasma. He had no alcohol drinking history and no biliary calculus disease. His height was 176 cm and weight was 87 kg, showing marked obesity. On physical examination, his abdomen was slightly distended with hypoactive bowel sounds and he had direct tenderness on epigastrium without rebound tenderness. On admission, laboratory data showed white blood cell count of 15,210/mm3. Blood chemistry tests revealed fasting blood sugar level of 228 mg/dL, lactate dehydrogenase level of 379 IU/L, and aspartate aminotransferase level of 20 IU/L. The serum amylase level of 160 mg/dL was slightly higher than the normal range (25~125 mg/dL). Serum lipase level was increased to 1596 U/L (normal range of 13~60 U/L). Serum calcium level and blood urea nitrogen level were within normal limits. The lipid profiles such as total cholesterol, triglyceride, high density cholesterol and low density cholesterol were 272 mg/dL, 605 mg/dL, 28 mg/dL and 98 mg/dL, respectively. A diagnosis of type IIb hyperlipoproteinemia was made based on serum lipoprotein electrophoresis [0% of chylomicron (0-2.0), 62.9% of β-lipoprotein (36.5-59.1), 22.5% of pre-β-lipoprotein (3.8-33.8), and 14.6% of α-lipoprotein (20.4-46.4)]. Hemoglobin A1c level was 10.4% and fasting C-peptide and postprandial C-peptide were 2.7 and 3.7 ng/mL, respectively. Abdominal CT scan revealed diffusely enlarged pancreas, peripancreatic fat infiltration and pelvic ascites, which were compatible with acute pancreatitis grade C (). He was treated with dietary restriction, hydration, NPH insulin injection and lipid lowering agents. For the purpose of distinguishing infective pancreatitis from hyperlipidemic pancreatitis, we prescribed antibiotics (2 g of meropenem® per day) for two days until abdominal CT information was obtained. His abdominal pain was resolved within a few days, and white blood cell count was normalized. He was discharged after 8 days, with complete recovery from acute pancreatitis.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [28.0, 'mg/dL'], 'Triglycerides': [605.0, 'mg/dL'], 'Total cholesterol': [272.0, 'mg/dL']}",123,116.85,129.15,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 272.0 mg/dL. 
The concentration of hdl cholesterol is 28.0 mg/dL. 
The concentration of triglycerides is 605.0 mg/dL. 
Plugging in these values will give us 272.0 mg/dL - 28.0 mg/dL - (605.0/5) mg/dL = 123.0 mg/dL.
The patients concentration of LDL cholestrol is 123.0 mg/dL."
6378,44,LDL Calculated,lab test,decimal,pmc-4595366-1,Extracted,"A 47-year-old female visited our cardiology clinic due to dyspnea that had been progressive over the previous few months. The patient complained of resting dyspnea and peripheral pitting edema. She had no prior medical history or family history of cardiovascular disease. On physical examination, her height was 160 cm and body weight was 70 kg. Her blood pressure was 230/145 mm Hg, and her heart rate was 100 beats per minute. Auscultation of the chest revealed a coarse breathing sound with crackling and regular heart beats with no murmur. The liver and spleen were not palpable, and her bowel sounds were normal.
A blood examination revealed a 7,200/mm3 leukocyte count, 16.5 g/dL hemoglobin, a 274,000/mm3 platelet count, 296 mg/dL random glucose, 8.3% hemoglobin A1c (HbA1c), 28 mg/dL blood urea nitrogen, 1.5 mg/dL creatinine, 7.0 g/dL protein, 3.6 g/dL albumin, 33 IU/L aspartate aminotransferase, 24 IU/L alanine aminotransferase, 292 IU/L alkaline phosphatase, 2.58 mg/L high-sensitivity C-reactive protein, 248 mg/dL total cholesterol, 111 mg/dL triglycerides, 41 mg/dL high density lipoprotein, 181 mg/dL low density lipoprotein, 136 mmol/L sodium, and 4.2 mmol/L potassium. The results of a routine urinalysis were as follows: proteinuria, 2+; glycosuria, 2+; red blood cell, 0 to 1/high power field (HPF) and white blood cell, 5 to 9/HPF; and spot urine protein to creatinine ratio, 428 mg/g. A thyroid function test (TFT) revealed 88 ng/dL T3 (normal range, 78 to 182), 1.44 ng/dL free T4 (normal range, 0.8 to 1.78), and 9.86 mIU/L thyroid stimulating hormone (normal range, 0.17 to 4.05). The TFT results showed subclinical hypothyroidism, but thyroid autoantibodies were negative.
Cardiomegaly was detected on a chest radiograph, and the cardiothoracic ratio was 66% (). The electrocardiogram showed inverted T waves in the lateral and inferior leads, with no significant ST changes. A transthoracic echocardiogram revealed LV hypertrophy and severe systolic dysfunction (). The interventricular septal diameter was 1.3 cm, the LV posterior wall diameter was 1.8 cm, the LV internal diameter in diastole was 5.8 cm (normal range, 3.9 to 5.3), the LV internal diameter in systole was 5.1 cm (normal range, 2.1 to 4.0), and the left ventricular ejection fraction (LVEF) was 25% (). Coronary angiography was performed, and the results were normal.
The patient was treated with multiple antihypertensive drugs, including calcium channel blockers, diuretics, angiotensin converting enzyme inhibitors, and β-blockers to control a hypertensive crisis, but her blood pressure remained >160/100 mm Hg. Abdominal computed tomography was performed to evaluate secondary hypertension, which revealed no abnormalities in either the renal arteries or adrenal glands.
To manage diabetes mellitus, she was referred to Department of Endocrinology and Metabolism at Kyung Hee University Hospital at Gangdong. Because the patient had uncontrolled hypertension, newly diagnosed diabetes mellitus, and soft tissue and bone overgrowth, a diagnosis of acromegaly was suspected. Rough and thick skin was observed, and skin tags were noted around the neck. An enlarged jaw and protruded frontal bones were observed, and soft tissue overgrowth of the heel was noted on a lateral view of a foot X-ray (). The basal IGF-1 level was measured as 183.8 ng/mL, which was within the normal range (90 to 360). Acromegaly was diagnosed after performing a 75-g glucose-loading GH suppression test (). In a thyrotropin-releasing hormone stimulation test, GH levels were found to be increased (). MRI of the sella revealed a 5-mm microadenoma on the left side of the pituitary gland (). A combined pituitary stimulation test performed before surgery revealed that both basal and stimulated hormone levels were normal.
Hyperglycemia was treated with 500 mg metformin twice a day and 12 U insulin glargine once a day via subcutaneous injection. We performed a diabetic complication test, and fundoscopy showed severe nonproliferative diabetic retinopathy ().
Three weeks after admission, combination antihypertensive therapy caused a reduction in blood pressure to <140/80 mm Hg. A follow-up echocardiogram showed no significant difference in LV hypertrophy, but LVEF was improved to 66% ().
After transsphenoidal resection of the pituitary tumor, the tumor was identified as a GH-secreting adenoma () that showed strong staining with anti-GH antibodies in immunohistochemical analysis ().
We performed a follow-up 75-g glucose-loading GH suppression test 2 weeks after surgery, and GH levels were suppressed to 0.15 ng/mL, which means cure state (). The levels of GH and IGF-1 were 0.57, 243.7 ng/mL on postoperative day (POD) 3, 0.38, 295.4 ng/mL on POD 50, and 0.4, 249.5 ng/mL 6 months after surgery (). A follow-up transthoracic echocardiography 6 months after surgery revealed improved LV hypertrophy and LVEF compared with preoperative values.
The patient was prescribed calcium channel blockers and angiotensin-receptor blockers. Her blood pressure was maintained at 120/70 mm Hg 1 year after surgery. Her blood glucose levels were well controlled, with an HbA1c of 5.4%, using only 500 mg/day metformin without insulin. The degree of diabetic retinopathy was improved somewhat, and the patient was followed-up at the outpatient clinic.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [41.0, 'mg/dL'], 'Triglycerides': [111.0, 'mg/dL'], 'Total cholesterol': [248.0, 'mg/dL']}",184.8,175.56,194.04,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 248.0 mg/dL. 
The concentration of hdl cholesterol is 41.0 mg/dL. 
The concentration of triglycerides is 111.0 mg/dL. 
Plugging in these values will give us 248.0 mg/dL - 41.0 mg/dL - (111.0/5) mg/dL = 184.8 mg/dL.
The patients concentration of LDL cholestrol is 184.8 mg/dL."
6379,44,LDL Calculated,lab test,decimal,pmc-8414937-1,Extracted,"A 19-year-old man was admitted to the emergency room with persistent substernal chest pain
for 3 hours after staying up late for 1 week. He had been in good health without
hypertension, hyperlipemia, or other related diseases.
An electrocardiogram showed a normal sinus rhythm with ST-segment elevation and towering T
waves in the V1 to V6 leads () and the cardiac troponin level was 0.248 ng/L (upper limit of normal:
0.1 ng/L). His left ventricular ejection fraction was 55% and glycated hemoglobin level was
5.0%. The patient’s lipid levels were as follows: total cholesterol, 3.67 mmol/L; total
triglycerides, 1.53 mmol/L; high-density lipoprotein cholesterol, 0.91 mmol/L; and
low-density lipoprotein cholesterol, 2.42 mmol/L. He was diagnosed with acute anterior
myocardial infarction. His vital signs on presentation were stable with a pulse of
88 beats/minute, blood pressure of 145/85 mmHg, respiratory rate of 18 breaths/minute,
arterial blood oxygen saturation of 99% on room air, and temperature of 36.2°C. The current
evidence did not support the diagnosis of aortic dissection, acute pericarditis, acute
pulmonary embolism, pneumothorax, or digestive tract diseases. Therefore, we carried out
follow-up treatment after obtaining the patient’s consent. After he received aspirin 300 mg,
ticagrelor 180 mg, and a bolus of 3000 units of intravenous heparin, he underwent emergency
coronary angiography (CAG). CAG showed thrombosis in the proximal left anterior descending
artery (pLAD), and Thrombolysis in Myocardial Infarction (TIMI) thrombus grade 4 and TIMI
grade 1 distal flow (),
but a normal circumflex artery and right coronary artery. A bolus of heparin (3500 IU) and a
glycoprotein IIb/IIIa antagonist (tirofiban) was administered, and a 6F BL3.5 guide catheter
(Terumo, Tokyo, Japan) was inserted, followed by repeated manual thrombus aspiration.
Subsequent CAG showed TIMI grade 3 flow (). After taking into consideration the patient’s age, intracoronary OCT
was performed to assess whether more interventions were essential. OCT showed a residual red
and white thrombus and plaque erosion in the pLAD. The minimal lumen diameter of the pLAD
was 1.92 mm, the area was 2.95 mm2, and the area of stenosis was 48% (). Accordingly, stent
implantation was avoided for the patient. He was discharged with optimal medical therapy,
which comprised aspirin, ticagrelor, metoprolol, and a statin, for 12 months as recommended
by guidelines for prevention of secondary coronary events. CAG and OCT 1 month after primary
percutaneous coronary intervention showed that an organized thrombus remained in the pLAD
and that a lipid plaque was under the endomembrane with an unbroken fibrous cap and no
plaque rupture ().
Cholesterol crystals and microphage infiltration were detected. The patient has remained
asymptomatic and no adverse events were observed during 6 months of follow-up.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [0.91, 'mmol/L'], 'Triglycerides': [1.53, 'mmol/L'], 'Total cholesterol': [3.67, 'mmol/L']}",80.359,76.34105,84.37695,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 3.67 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of total cholesterol from mmol to mg. The mass of total cholesterol is 3.67 mmol. To convert 3.67 mmol of total cholesterol to mol, multiply by the conversion factor 0.001, giving us 3.67 mmol total cholesterol * 0.001 mol/mmol = 0.00367 mol total cholesterol. To convert from mol total cholesterol to grams, multiply by the molar mass 386.654 g/mol, which will give 0.00367 mol total cholesterol * 386.654 g/mol = 1.41902 g total cholesterol. To convert 1.41902 g of total cholesterol to mg, multiply by the conversion factor 1000.0, giving us 1.41902 g total cholesterol * 1000.0 mg/g = 1419.02 mg total cholesterol. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1419.02 mg total cholesterol/10.0 dL = 141.902 mg total cholesterol/dL. The concentration value of 3.67 mmol total cholesterol/L converts to 141.902 mg total cholesterol/dL. 
The concentration of hdl cholesterol is 0.91 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of hdl cholesterol from mmol to mg. The mass of hdl cholesterol is 0.91 mmol. To convert 0.91 mmol of hdl cholesterol to mol, multiply by the conversion factor 0.001, giving us 0.91 mmol hdl cholesterol * 0.001 mol/mmol = 0.00091 mol hdl cholesterol. To convert from mol hdl cholesterol to grams, multiply by the molar mass 386.654 g/mol, which will give 0.00091 mol hdl cholesterol * 386.654 g/mol = 0.35186 g hdl cholesterol. To convert 0.35186 g of hdl cholesterol to mg, multiply by the conversion factor 1000.0, giving us 0.35186 g hdl cholesterol * 1000.0 mg/g = 351.86 mg hdl cholesterol. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 351.86 mg hdl cholesterol/10.0 dL = 35.186 mg hdl cholesterol/dL. The concentration value of 0.91 mmol hdl cholesterol/L converts to 35.186 mg hdl cholesterol/dL. 
The concentration of triglycerides is 1.53 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of triglycerides from mmol to mg. The mass of triglycerides is 1.53 mmol. To convert 1.53 mmol of triglycerides to mol, multiply by the conversion factor 0.001, giving us 1.53 mmol triglycerides * 0.001 mol/mmol = 0.00153 mol triglycerides. To convert from mol triglycerides to grams, multiply by the molar mass 861.338 g/mol, which will give 0.00153 mol triglycerides * 861.338 g/mol = 1.31785 g triglycerides. To convert 1.31785 g of triglycerides to mg, multiply by the conversion factor 1000.0, giving us 1.31785 g triglycerides * 1000.0 mg/g = 1317.85 mg triglycerides. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1317.85 mg triglycerides/10.0 dL = 131.785 mg triglycerides/dL. The concentration value of 1.53 mmol triglycerides/L converts to 131.785 mg triglycerides/dL. 
Plugging in these values will give us 141.902 mg/dL - 35.186 mg/dL - (131.785/5) mg/dL = 80.359 mg/dL.
The patients concentration of LDL cholestrol is 80.359 mg/dL."
6380,44,LDL Calculated,lab test,decimal,pmc-4532003-1,Extracted,"A 32-year old Korean female was admitted with a complaint of edema and pain on the left leg for 2 months. In January 1993, she was diagnosed as SLE at another hospital and manifested gross hematuria, proteinuria, azotemia, anemia, thrombocytopenia, hypocomplementemia, positive FANA, positive anti-ds DNA antibody and positive anti-ENA antibody. In May 1993, she was transferred to Kangnam St. Mary’s Hospital with steroid (prednisolone 1mg/kg) medication. We checked the titer of anticardiolipin antibody (ACA), which was 100 GPL IU/ml and followed up the titer of ACA regularly at 2 months’ intervals and the titer of ACA IgG was persistently elevated. Her parity was 0-0-0-0 and she showed thrombocytopenia (35,000/mm3) and prolonged partial thromboplastin time (59.2 sec, control 27.0 sec). Her clinical features were Antiphospholipid syndrome in SLE and she was treated with baby aspirin 100 mg/day and steroid (prednisolone 1mg/kg) at the outpatient clinic. From April 1994, she suffered from edema and pain on the left leg and was admitted to our hospital in June 1994. On admission, she had polyarthralgia but did not complain of fever, malar rash, photosensitivity, oral ulcer, Raynaud’s phenomenon, xerostomia, xerophalmia and allopecia. On physical examination, her blood pressure was 120/80 mmHg. pulse rate 76 beats per minute, respiration rate 20 per minute and body temperature 36.5°C. There were no pathologic lesions in her eyes, ears, nasal or oral mucosa. Chest auscultation and abdomen palpation revealed no abnormalities and peripheral arterial pulsation was normal. There were no cutaneous vasculitis and abnormal neurologic signs.
On laboratory findings, hemoglobin was 10.6 g/dl, hematocrit 32%, white blood cell 8.1×103/mm3 (neutrophil 82%. lymphocyte 10%) and platelet 122×103/mm3. Renal function showed blood urea nitorgen 5.3 mg/dl, creatinine 0.9 mg/dl and 24hr urine protein 6.18 g/day. Urinanalysis showed 0 to 2 white cells and 10 to 20 red cells per high power fields. Lipid profile revealed total cholesterol 170 mg/dl. triglyceride 98 mg/dl and HDL-cholesterol 51 mg/dl. The AST was 16 IU/L. ALT 12 IU/L, alkaline phosphatase 229 IU/L, total bilirubin 0.7 mg/dl, total protein 4.1 g/dl and albumin 2.1 g/dl. The prothrombin time was 11.8 sec (control 12.1 sec) and activated partial thromboplastin time 59.2 sec (control 26.6 sec). On immunologic studies, FANA was positive (homogenous pattern, titer 1 : 1280), anti-ds DNA antibody 5 IU/ml, C3 21 mg/dl and C4 15 mg/dl. Rheumatoid factor was negative and ANCA was positive (GS-ANA, titer 1 : 80). Anti-cardiolipin antibody Ig G was 100 GPL IU/ml. Lupus anticoagulant was positive by the Kaolin clotting test. Anti-ENA and anti-Ro antibodies were all negative. The direct and indirect Coombs’ tests were all negative. The erythrocyte sedimentation rate was 18 mm/hr and C-reactive protein 2.4 mg/l. The immunoglobulin G, A, M levels revelaed 928, 274, 106 mg/dl, respectively. The serum viral hepatitis markers revealed that HBs antigen was negative, HBs antibody positive and HCV antibody negative. Gastrofiberscope showed esophageal varix, grade 2, and gastric fundal varix. Abdominal ultrasonography showed a moderate amount of ascites, moderate splenomegaly and marked coarse increased liver echogenecity. At computed tomography of the abdomen, we could not trace the inferior vena cava at the intrahepatic portion(). Doppler ultrasonography of the left leg showed no thrombosis in the superficial femoral vein and popliteal vein. Inferior and superior venocavograms showed obstructions at the intrahepatic portion of IVC and at both subclavian veins and abnormal collateral vessels were found around the obstructions (, ). We injected Heparin 5,000 units and Urokinase 500,000 units intravenously at the bolus during venocavogram and further thrombolytic therapy (Heparin 5,000 units/day and Urokinase 500,000 units/day continuously all day long) was done for additional two days. We followed the venocavogram to evaluate the extent of thrombosis, compared with pre-thrombolytic therapy, but we could not find any interval change. We decided to give the patient Warfarin 5 mg/day, Prednisolone 1 mg/kg and baby aspirin 100 mg/day and to follow her up at the outpatient clinic.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Total cholesterol': [170.0, 'mg/dL'], 'high-density lipoprotein cholesterol': [51.0, 'mg/dL'], 'Triglycerides': [98.0, 'mg/dL']}",99.4,94.43,104.37,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 170.0 mg/dL. 
The concentration of hdl cholesterol is 51.0 mg/dL. 
The concentration of triglycerides is 98.0 mg/dL. 
Plugging in these values will give us 170.0 mg/dL - 51.0 mg/dL - (98.0/5) mg/dL = 99.4 mg/dL.
The patients concentration of LDL cholestrol is 99.4 mg/dL."
6381,44,LDL Calculated,lab test,decimal,pmc-6199550-1,Extracted,"A 22-year-old male patient with a past medical history of nephrotic syndrome due to membranous nephropathy, which was diagnosed by renal biopsy 1 year ago, was admitted to the emergency room and transferred to our cardiac care unit with the complaint of chest pain along with dizziness, headache, and radiating pain to his left arm for 4 hours. The patient took no drugs in the past 6 months. On clinical examination, his pain was reported to be 5/10 according to the visual analogue pain scale, he was afebrile, with a maximum temperature of 36.6°C, and had ortho-arteriotony, with a blood pressure of 128/85 mmHg, and no tachycardia or bradycardia (pulse rate of 66 beats per minute). The patient’s face was bloated, but there was no jugular venous distention, muffled breath sounds, rhonchi or moist rale, the third or fourth heart sound gallop, pericardial rub, peritoneal irritation, hepatosplenomegaly, or leg oedema. Electrocardiogram on admission showed that ST elevated to 0.1–0.2 mv in II, III, aVF, and V4–V6 ().
Initial abnormal serum laboratory results were as follows: troponin I, 3.499 ug/L; myoglobin, 1200 ug/L; creatine kinase-MB, 69 U/L; creatine kinase, 678 U/L; lactate dehydrogenase, 343 U/L; cholesterol, 6.43 mmol/L; low-density lipoprotein cholesterol, 5.02 mmol/L; glucose, 2.44 mmol/L; high-density lipoprotein cholesterol, 0.76 mmol/L; prothrombin time, 10.3 s; activated partial thromboplastin time, 24.5 seconds; serum total protein, 39.1 g/L; albumin, 20.2 g/L; and 24-hour urine protein, 11.054 g/24 hours.
According to the results, our preliminary diagnosis was acute inferior myocardial infarction (Killip grade I) combined with nephrotic syndrome, and we performed a percutaneous intervention procedure, which was followed by 300 mg aspirin and 300 mg clopidogrel orally immediately. During the operation, we saw that the left coronary artery had thickened and the left main artery, left circumflex artery, and right coronary artery were normal. However, there was a great deal of thrombi blocking the anterior and middle anterior descending branch, resulting in 95% stricture () and leading to bloodstream classification at thrombolysis and thrombin inhibition in myocardial infarction grade II. Next, we applied the thrombus suction technique and injected 13 ml of tirofiban to dissolve blood clots. Unfortunately, there was still medium thrombi remaining and 60% stricture in the re-examination of coronary arteriography (). The bloodstream classification at thrombolysis and thrombin inhibition in myocardial infarction grade III. Because the anterior descending branch dilatation made it unsuitable for stent implantation, we had to stop further operation. Next, we gave him a therapeutic regimen of low-molecular-weight heparin for 7 days, 100 mg aspirin per day, and 90 mg ticagrelor twice a day to fight platelet aggregation, and 40 mg atorvastatin per night to remedy hyperlipidaemia persistently.
One day after the operation, his postoperative electrocardiogram showed that the elevated ST segments in II, III, aVF, and V4–V6 were down to baseline, and an inverted T wave began to appear in V2–V6 (). An echocardiography performed 3 days after admission showed a left ventricular ejection fraction of 48.2%, enlarged bilateral atrium, dilated left ventricle, segmental weak pulse of left ventricular wall, mild regurgitation of bicuspid valve or of tricuspid valve, and the estranged left ventricular cells (). Laboratory tests on the same day showed a higher troponin I of 31.833 ug/L, lower myoglobin of 27.9 ug/L, creatine kinase-MB of 21 U/L, creatine kinase of 74 U/L, and lactate dehydrogenase of 489 U/L. After 4 days, the serum laboratory results showed the following results: troponin I, 6.912 ug/L; myoglobin, 29.5 ug/L; creatine kinase-MB, 17 U/L; creatine kinase, 36 U/L; lactate dehydrogenase, 330 U/L; cholesterol, 2.86 mmol/L; low-density lipoprotein cholesterol, 1.63 mmol/L; triglyceride, 2.28 mmol/L; and high-density lipoprotein cholesterol, 0.57 mmol/L. All the related indexes were decreased. On the 14th day after the operation, the patient had a third examination of coronary arteriography, which revealed that there was barely any blockage caused by thrombi in the anterior descending branch and no stricture in the coronary artery (). The patient was discharged on the 17th day, as his vitals were stable and symptoms disappeared.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [0.57, 'mmol/L'], 'Triglycerides': [2.28, 'mmol/L'], 'Total cholesterol': [2.86, 'mmol/L']}",49.267,46.80365,51.73035,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 2.86 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of total cholesterol from mmol to mg. The mass of total cholesterol is 2.86 mmol. To convert 2.86 mmol of total cholesterol to mol, multiply by the conversion factor 0.001, giving us 2.86 mmol total cholesterol * 0.001 mol/mmol = 0.00286 mol total cholesterol. To convert from mol total cholesterol to grams, multiply by the molar mass 386.654 g/mol, which will give 0.00286 mol total cholesterol * 386.654 g/mol = 1.10583 g total cholesterol. To convert 1.10583 g of total cholesterol to mg, multiply by the conversion factor 1000.0, giving us 1.10583 g total cholesterol * 1000.0 mg/g = 1105.83 mg total cholesterol. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1105.83 mg total cholesterol/10.0 dL = 110.583 mg total cholesterol/dL. The concentration value of 2.86 mmol total cholesterol/L converts to 110.583 mg total cholesterol/dL. 
The concentration of hdl cholesterol is 0.57 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of hdl cholesterol from mmol to mg. The mass of hdl cholesterol is 0.57 mmol. To convert 0.57 mmol of hdl cholesterol to mol, multiply by the conversion factor 0.001, giving us 0.57 mmol hdl cholesterol * 0.001 mol/mmol = 0.00057 mol hdl cholesterol. To convert from mol hdl cholesterol to grams, multiply by the molar mass 386.654 g/mol, which will give 0.00057 mol hdl cholesterol * 386.654 g/mol = 0.22039 g hdl cholesterol. To convert 0.22039 g of hdl cholesterol to mg, multiply by the conversion factor 1000.0, giving us 0.22039 g hdl cholesterol * 1000.0 mg/g = 220.39 mg hdl cholesterol. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 220.39 mg hdl cholesterol/10.0 dL = 22.039 mg hdl cholesterol/dL. The concentration value of 0.57 mmol hdl cholesterol/L converts to 22.039 mg hdl cholesterol/dL. 
The concentration of triglycerides is 2.28 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of triglycerides from mmol to mg. The mass of triglycerides is 2.28 mmol. To convert 2.28 mmol of triglycerides to mol, multiply by the conversion factor 0.001, giving us 2.28 mmol triglycerides * 0.001 mol/mmol = 0.00228 mol triglycerides. To convert from mol triglycerides to grams, multiply by the molar mass 861.338 g/mol, which will give 0.00228 mol triglycerides * 861.338 g/mol = 1.96385 g triglycerides. To convert 1.96385 g of triglycerides to mg, multiply by the conversion factor 1000.0, giving us 1.96385 g triglycerides * 1000.0 mg/g = 1963.85 mg triglycerides. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1963.85 mg triglycerides/10.0 dL = 196.385 mg triglycerides/dL. The concentration value of 2.28 mmol triglycerides/L converts to 196.385 mg triglycerides/dL. 
Plugging in these values will give us 110.583 mg/dL - 22.039 mg/dL - (196.385/5) mg/dL = 49.267 mg/dL.
The patients concentration of LDL cholestrol is 49.267 mg/dL."
6382,44,LDL Calculated,lab test,decimal,pmc-4722418-1,Extracted,"A 31-year-old woman was diagnosed with hypertension by a private clinic in August 2013, based upon a systolic blood pressure of 160 mm Hg and she was prescribed antihypertensive drugs to treat the condition. Initial therapy consisted of hydrochlorothiazide 12.5 mg and losartan 50 mg daily. After 1 week, her blood pressure was still high, so the doctor changed her medication to amlodipine 5 mg, losartan 100 mg, and indapamide 2.5 mg per day. Five days after initiating this second regimen of drugs, she developed pretibial pitting edema, and thorough workup was done for the symptom. There were bilateral adrenal masses on abdominal-pelvic computed tomography (CT). Routine blood tests revealed the following: potassium 2.2 mmol/L, plasma renin activity (PRA) 0.12 ng/mL/hr, plasma aldosterone concentration (PAC) 16.76 ng/dL, and an aldosterone/renin ratio (PAC/PRA) >30, indicative of primary hyperaldosteronism.
Following her possible diagnosis of primary hyperaldosteronism, the patient was referred to our hospital for additional testing. At the time of admission, her blood pressure was 155/111 mm Hg, height was 164.5 cm, and weight was 63.5 kg (body mass index, 23.47 kg/m2). Pretibial pitting edemas were detected, but no physical signs of Cushing syndrome were observed.
A routine blood test at the time of admission showed the following: white blood cell 6,900/µL, hemoglobin 13.5 g/dL, platelet 351,000/µL, total protein 6.9 g/dL, albumin 4.1 g/dL, aspartate aminotransferase 76 U/L, alanine aminotransferase 126 U/L, blood urea nitrogen 7.3 mg/dL, creatinine 0.71 mg/dL, sodium 141 mmol/L, potassium 2.9 mmol/L, chloride 101 mmol/L, total cholesterol 210 mg/dL, triglyceride 104 mg/dL, high density lipoprotein 50 mg/dL, low density lipoprotein 141 mg/dL, and hemoglobin A1c 5.9%. Biochemical evaluation of pheochromocytoma showed no excessive catecholamine production. The transtubular potassium concentration gradient was 12.64%, suggesting the possibility of hyperaldosteronism or hypercortisolism. PAC and PRA were 24.4 ng/dL and 0.76 ng/mL/hr, respectively, and the PAC/PRA ratio was 32.11 (). After correcting for hypokalemia, a saline loading test was performed, which revealed no suppression of the aldosterone level after saline administration, consistent with a diagnosis of hyperaldosteronism (the basal PAC 24.4 ng/dL increased to 27.3 ng/dL after a 2 L saline infusion). Dexamethasone suppression tests (DSTs) resulted in no suppression of cortisol levels (). Adrenal CT demonstrated two bilateral adrenal masses in each of the adrenal glands, including a 1.6-cm mass on the right and a 2-cm mass on the left adrenal gland (). An adrenal cortical scan using iodine-131-6β-iodomethyl-19-norcholesterol (NP-59) showed focally increased radioactive uptakes in the bilateral adrenal gland areas, with a substantially higher uptake on the left side ().
Bilateral adrenal venous sampling (AVS) with adrenocorticotropic hormone (ACTH) stimulation () revealed inadequate right adrenal venous blood sampling (right adrenal vein cortisol level/peripheral blood cortisol level [CRt/CP] <10), whereas the cortisol concentration in the left adrenal venous blood showed successful sampling on the left side. One explanation for this difference may be that the low level of CRt was the result of suppressed cortisol secretion due to excessive cortisol secretion from the left adrenal mass. The left adrenal vein aldosterone/cortisol (ALt/CLt) ratio was lower than that of peripheral blood, implying the possibility of suppressed aldosterone secretion from this side caused by a contralateral adrenal mass which might secrete excessive aldosterone []. Four days after the first AVS, a second AVS was performed using low-dose DST but without ACTH infusion (). This time, we also measured the epinephrine levels in the both adrenal veins and peripheral blood; a large peripheral-to-adrenal gradient of epinephrine assured successful catheterization on both sides []. CLt/CP testing confirmed that the left adrenal mass was a cortisol-secreting adenoma [].
Even though those two AVS results appeared to provide clear evidence of the lateralization of functioning adrenal masses, such an independent functioning of bilateral masses was highly suspicious. We therefore concluded that sequential adrenalectomies, rather than concurrent operations, would be beneficial for making a definitive diagnosis. Moreover, the patient agreed to do sequential operations. The first procedure was a laparoscopic partial adrenalectomy of the right adrenal gland to remove the putative aldosterone-producing mass, with the goal of controlling hypertension and hypokalemia. A firm, 1.5-cm ovoid, well-circumscribed, bright yellow tumor mass lacking necrosis or hemorrhage was arising from the cortex of the adrenal gland in the pathologic specimen. Within 24 hours after surgery, the patient's blood pressure had fallen to 110/80 mm Hg without antihypertensive medication, serum potassium normalized at 4.5 mmol/L, and PAC decreased to 3 ng/dL. These large postoperative changes strongly suggested that the right adrenal adenoma was producing excessive aldosterone. By day 3, an overnight DST continued to show no cortisol suppression, indicating persistent secretion of corticosteroid from the left adrenal mass. To limit the likelihood of subclinical Cushing syndrome progressing to overt Cushing syndrome, we opted to completely remove the left adrenal gland as a means of controlling hypercortisolism. The excised portion of the adrenal mass contained an encapsulated brown solid mass.
The patient began taking prednisolone 10 mg once a day for steroid replacement 1 day after the second surgery. By 2 months she had lost 5 kg of body weight. At that time, a rapid ACTH test revealed adrenal insufficiency (). At 16 months after surgery, the patient has gradually reduced her prednisolone intake to 5 mg every other day. Her blood pressure and serum potassium levels have remained within normal ranges, without the need for additional antihypertensive medications or potassium supplements.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [50.0, 'mg/dL'], 'Triglycerides': [104.0, 'mg/dL'], 'Total cholesterol': [210.0, 'mg/dL']}",139.2,132.24,146.16,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 210.0 mg/dL. 
The concentration of hdl cholesterol is 50.0 mg/dL. 
The concentration of triglycerides is 104.0 mg/dL. 
Plugging in these values will give us 210.0 mg/dL - 50.0 mg/dL - (104.0/5) mg/dL = 139.2 mg/dL.
The patients concentration of LDL cholestrol is 139.2 mg/dL."
6383,44,LDL Calculated,lab test,decimal,pmc-4438415-1,Extracted,"A 19-year-old-male presented in May 2007 with swelling of the lower limbs and periorbital puffiness of 2 months’ duration. Evaluation at his primary health centre had revealed albuminuria on dipstick analysis, prompting referral to our institution. He gave no history of recent infections, arthralgia, oral ulcers, cough or haemoptysis. On examination, he had bilateral leg oedema extending up to his knees. The blood pressure was 110/70 mmHg, pulse rate was 90 b.p.m. and respiratory rate 14/min. The cardiovascular, abdomen, chest and nervous system examinations were within normal limits. Urinalysis showed 4+ proteinuria, but no erythrocytes or leucocytes. The 24-h urine protein excretion was 6.3 g. The serum creatinine was 71 μmol/L (0.8 mg/dL); serum total protein and albumin were 55 and 17 g/L (5.5 and 1.7 g/dL), respectively, and aspartate and alanine aminotransferases were 12 and 14 IU/L, respectively. Serum cholesterol was 10.4 mmol/L (400 mg/dL), triglyceride 2.8 mmol/L (250 mg/dL), low-density lipoprotein 7.2 mmol/L (280 mg/dL) and high-density lipoprotein 1.3 mmol/L (50 mg/dL). He tested negative for hepatitis B surface antigen, anti-HCV antibody and human immunodeficiency virus I/II. The antinuclear antibody test was negative.
Kidney biopsy (A) revealed 10 glomeruli, which were normal on light microscopy (LM), as were the tubulointerstitial and vascular compartments. Immunofluorescence did not reveal any immune deposits and electron microscopy (EM) showed diffuse foot process effacement.
A diagnosis of minimal-change disease (MCD) was made and the patient was started on oral prednisolone at 1 mg/kg/day. However, the proteinuria did not show any reduction. At the end of 4 months, the daily urinary protein excretion remained at 5 g. He was deemed to be steroid resistant and treated first with oral cyclophosphamide at 2 mg/kg for 3 months, followed by oral cyclosporine (4 mg/kg/day, average C0 120 ng/mL) and oral prednisolone (0.1 mg/kg/day) for 6 months, mycophenolate mofetil 2 g/day for 6 months and finally a combination of tacrolimus (0.1 mg/kg/day, average Tac C0 7 ng/mL) and oral prednisolone (0.1 mg/kg/day). The nephrotic state persisted throughout this period, with serum albumin <20 g/L (2.0 g/dL) and the serum creatinine 62–80 μmol/L (0.7–0.9 mg/dL) (). During the entire course of his illness, he was continued on supportive therapy with torsemide 10–20 mg twice daily, atorvastatin 20 mg/day and losartan 150 mg/day.
At this time, the kidney biopsy was repeated. LM revealed 13 glomeruli, 2 of which showed segmental collapse of the capillary tuft with an overlying crown of podocytes along with synechiae formation, 2 showed segmental endocapillary cellularity with foam cells, 2 were globally sclerosed and the remaining 7 did not show any significant abnormality (B). Tubules showed abundant protein absorption droplets along with patchy tubular atrophy occupying 20% of the biopsy area. Tubules close to the medulla showed marked nucleomegaly along with nuclear smudging associated with tubular necrosis, interstitial oedema and mild-to-moderate patchy plasma cell-rich interstitial inflammation occupying 10% of the biopsy area. Blood vessels were within normal limits. Immunofluorescence was negative for all immunoglobulins, C1q and light chains. EM showed segmental sclerosis with evidence of collapse (C). There was diffuse and extensive foot process effacement, and no reticular aggregates were seen. Ki 67 immunostain showed nuclear positivity in the podocytes of glomeruli showing collapse (D). CD 20 staining was negative. A final diagnosis of CG was made. The patient's serum tested negative by polymerase chain reaction for cytomegalovirus and parvovirus B-19.
In view of his resistance to the above therapies and a persistently severe nephrotic state with the biopsy showing many plasma cells, the patient was treated with 4 weekly injections of rituximab (375 mg/m2/dose). His oedema subsided and he stopped requiring the diuretic 3 months after the last dose. Six months after the last dose of rituximab, the 24-h urine protein was 1.8 g with a serum albumin of 37 g/L (3.7 g/dL). The patient has now been followed up for 18 months and remains asymptomatic. On his last follow-up, his 24-h urine protein is 1.2 g, serum creatinine 80 μmol/L (0.9 mg/dL) and serum albumin 47 g/L (4.7 g/dL). shows the evolution of his clinical and laboratory parameters during the course of the treatment.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [1.3, 'mmol/L'], 'Triglycerides': [2.8, 'mmol/L'], 'Total cholesterol': [10.4, 'mmol/L']}",303.62,288.439,318.801,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 10.4 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of total cholesterol from mmol to mg. The mass of total cholesterol is 10.4 mmol. To convert 10.4 mmol of total cholesterol to mol, multiply by the conversion factor 0.001, giving us 10.4 mmol total cholesterol * 0.001 mol/mmol = 0.0104 mol total cholesterol. To convert from mol total cholesterol to grams, multiply by the molar mass 386.654 g/mol, which will give 0.0104 mol total cholesterol * 386.654 g/mol = 4.0212 g total cholesterol. To convert 4.0212 g of total cholesterol to mg, multiply by the conversion factor 1000.0, giving us 4.0212 g total cholesterol * 1000.0 mg/g = 4021.2 mg total cholesterol. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 4021.2 mg total cholesterol/10.0 dL = 402.12 mg total cholesterol/dL. The concentration value of 10.4 mmol total cholesterol/L converts to 402.12 mg total cholesterol/dL. 
The concentration of hdl cholesterol is 1.3 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of hdl cholesterol from mmol to mg. The mass of hdl cholesterol is 1.3 mmol. To convert 1.3 mmol of hdl cholesterol to mol, multiply by the conversion factor 0.001, giving us 1.3 mmol hdl cholesterol * 0.001 mol/mmol = 0.0013 mol hdl cholesterol. To convert from mol hdl cholesterol to grams, multiply by the molar mass 386.654 g/mol, which will give 0.0013 mol hdl cholesterol * 386.654 g/mol = 0.50265 g hdl cholesterol. To convert 0.50265 g of hdl cholesterol to mg, multiply by the conversion factor 1000.0, giving us 0.50265 g hdl cholesterol * 1000.0 mg/g = 502.65 mg hdl cholesterol. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 502.65 mg hdl cholesterol/10.0 dL = 50.265 mg hdl cholesterol/dL. The concentration value of 1.3 mmol hdl cholesterol/L converts to 50.265 mg hdl cholesterol/dL. 
The concentration of triglycerides is 2.8 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of triglycerides from mmol to mg. The mass of triglycerides is 2.8 mmol. To convert 2.8 mmol of triglycerides to mol, multiply by the conversion factor 0.001, giving us 2.8 mmol triglycerides * 0.001 mol/mmol = 0.0028 mol triglycerides. To convert from mol triglycerides to grams, multiply by the molar mass 861.338 g/mol, which will give 0.0028 mol triglycerides * 861.338 g/mol = 2.41175 g triglycerides. To convert 2.41175 g of triglycerides to mg, multiply by the conversion factor 1000.0, giving us 2.41175 g triglycerides * 1000.0 mg/g = 2411.75 mg triglycerides. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 2411.75 mg triglycerides/10.0 dL = 241.175 mg triglycerides/dL. The concentration value of 2.8 mmol triglycerides/L converts to 241.175 mg triglycerides/dL. 
Plugging in these values will give us 402.12 mg/dL - 50.265 mg/dL - (241.175/5) mg/dL = 303.62 mg/dL.
The patients concentration of LDL cholestrol is 303.62 mg/dL."
6384,44,LDL Calculated,lab test,decimal,pmc-4557151-1,Extracted,"A 22-year-old nonalcoholic male with 6 days history of intermittent fever with chills presented with 2 days history of upper abdomen pain radiating to back, reduced by sitting. The pain was associated with vomiting. His pulse rate was 134/min regular and of feeble volume, and blood pressure (BP) was 80/60 mmHg. The respiratory rate was 24 breaths/min and temperature was 36.7°C by axilla. The abdomen was distended with the presence of shifting dullness. Upper abdomen was tender. Heart sounds were feeble. There was reduced air entry bilaterally. His consciousness was intact and had no neurological deficit. There was reduced urine output. The patient had no history of similar episodes of abdominal pain in the past. There was no significant medical or surgical history in the past.
The investigations revealed hemoglobin 12.7 g/dL, (12–16), total leukocyte count 14,190/mm3 (4000–11,000) with differential leukocyte count of neutrophils 73%, lymphocytes 20%, and eosinophils 1%, and platelet count 159,000/mm3. Blood urea was 190 mg/dL (14–40), serum creatinine 4.27 mg/dL (0.5–1.2), serum Na+ 142 mEq/L (135–145), K+ 4.5 mEq/L (3.5–5.0), serum Ca2+ 8.8 mg/dL (8.5–10.2), and blood glucose 110 mg/dL (70–110). Serum bilirubin was 2.94 mg/dL (0.3–1.3) with direct 1.02 mg/dL (0.1–0.4), serum glutamic pyruvic transaminase 54 U/L (8–40 U/L) and serum glutamic oxaloacetic transaminase 99 U/L (10–38), alkaline phosphatase 125 U/L (13–100), and serum albumin 3.7 g/dL (3.5–5.5). The serum amylase was 1882 U/L (10–200), S. lipase 210 U/L (10–140), and serum lactate dehydrogenase (LDH) 478 U/L. The coagulation profile showed bleeding time 1 min 30 s, clotting time 3 min, prothrombin time 13 s (control 13) INR 1, and activated partial thromboplastin time was 34.6 s (control 32.2). The lipid profile showed S. cholesterol 121 mg/dL, S. triglyceride 197 mg/dL, S. low-density lipoprotein 49 mg/dL, S. high-density lipoprotein 36 mg/dL. C-reactive protein level was 170 mg/dL (0–6).
The peripheral blood film showed ring form of trophozoite of P. vivax []. The antigen testing including parasite LDH tested positive for P. vivax and negative for P. falciparum. The chest X-ray PA view and two-dimensional echocardiogram were normal. Ultrasonography of abdomen showed bulky pancreas, moderate ascites, and edematous both kidneys. There was no gallstone. A non contrast computerised tomography scan of the abdomen revealed finding suggestive of acute pancreatitis [Figure and ]. Ascitic fluid examination was hemorrhagic and had protein 3.0 g/dL, sugar 110 g/dL, white blood cell 2200 mm3 with 83% neutrophils, 11% lymphocyte, 6% monocyte, and numerous red blood cell (RBC). The ascitic fluid amylase was 550 U/L. A diagnosis of P. vivax infection, acute pancreatitis, acute renal failure, and shock was made. The patient was put on intravenous chloroquine, inotropic support, and antibiotics. The BP normalized after 2 days of treatment. He tested negative for P. vivax after 3 days of treatment. After normalization of BP, he was put on hemodialysis. He improved over a period of next 4 weeks and was discharged. At the time of discharge, his blood urea was 56 mg/dL, S. creatinine 1.1 mg/dL, C-reactive protein was 4 mg/dL. Other investigations had normalized.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [36.0, 'mg/dL'], 'Triglycerides': [197.0, 'mg/dL'], 'Total cholesterol': [121.0, 'mg/dL']}",45.6,43.32,47.88,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 121.0 mg/dL. 
The concentration of hdl cholesterol is 36.0 mg/dL. 
The concentration of triglycerides is 197.0 mg/dL. 
Plugging in these values will give us 121.0 mg/dL - 36.0 mg/dL - (197.0/5) mg/dL = 45.6 mg/dL.
The patients concentration of LDL cholestrol is 45.6 mg/dL."
6385,44,LDL Calculated,lab test,decimal,pmc-4974739-1,Extracted,"In January 2014, a 45-year-old Japanese man was referred to our clinic owing to obesity, daytime sleepiness, and snoring during sleep. His Epworth Sleepiness Scale score was 10 points. He underwent overnight diagnostic polysomnography in February 2014. Upon admission, his height was 178.6 cm, weight was 130.7 kg, abdominal circumference was 122 cm, and BMI was 41.0 kg/m2. Physical examination showed that the thyroid gland was not palpable. His serum levels of creatine kinase and creatinine were elevated at 1581 U/L and 1.46 mg/dL, respectively, while his other laboratory results were as follows: aspartate aminotransferase, 57 U/L; alanine aminotransferase, 49 U/L; lactate dehydrogenase, 353 U/L; total cholesterol (TC), 335 mg/dL; high-density lipoprotein cholesterol, 45 mg/dL; triglycerides (TGs), 211 mg/dL; low-density lipoprotein cholesterol, 248 mg/dL; fasting blood sugar, 86 mg/dL; glycated hemoglobin (HbA1c), 6.1 %; thyroid-stimulating hormone (TSH), >500 μIU/mL; free triiodothyronine, 1.4 pg/mL; free thyroxine, <0.15 ng/dL; thyroid peroxidase antibody, 10 IU/mL; and thyroglobulin antibody, >4000 IU/mL (Table ). Blood samples were evaluated using routine methods at Sapporo Clinical Laboratory Inc. (Sapporo, Hokkaido, Japan). Based on these results, indicating hypothyroidism and thyroglobulin antibody positivity, the patient was diagnosed with severe primary hypothyroidism (Hashimoto’s thyroiditis). His dyslipidemia and impaired glucose tolerance were considered as secondary changes due to primary hypothyroidism and obesity. Because polysomnography showed an apnea–hypopnea index (AHI) of 71.2 events/h (normal, <5 events/h) and a minimal SpO2 of 60 %, he also was diagnosed with severe OSA associated with autoimmune hypothyroidism. Therefore, in the beginning of March 2014, nasal CPAP (ICON+Auto, auto-adjusting CPAP; Fisher & Paykel Healthcare Limited, Auckland, New Zealand; minimal pressure, 4.0 cmH2O; maximal pressure, 18.0 cmH2O) and low-dose levothyroxine (12.5 μg/day) were initiated. Upon initiation of the CPAP therapy, the patient was informed that he would have to continue with the CPAP therapy unless his body weight decreased sufficiently.
In April 2014, the patient’s body weight had decreased to 125.2 kg, and post-CPAP polysomnography indicated improved OSA (AHI, 2.8 events/h; minimal SpO2, 88 %). A monthly follow-up visit was scheduled to check his body weight and adherence to CPAP. The memory stick of the CPAP machine showed that he used CPAP for an average of 6 h per night, 6 days a week, and that he had an AHI of approximately 2.0 events/h. In the course of gradually increasing the dose of levothyroxine, the patient reportedly felt better and had recovered from his fatigue and lethargy.
To address his weight loss as a priority, an LCD was initiated in July 2014 []. Yamada et al. [] reported the benefits of a non-calorie-restricted LCD with the amount of carbohydrates limited to 70–130 g/day for Japanese patients with type 2 diabetes. The patient consumed 50 g of white rice per meal in addition to vegetables, fish, eggs, and meat in the morning and at noon; however, he did not eat rice, noodles, or other carbohydrates at night. In February 2015, the dose of 175 μg/day levothyroxine appeared to maintain a euthyroid state (TSH, 0.75 μIU/mL), and his other laboratory results were within normal limits, including an HbA1c level of 5.3 %, TC level of 194 mg/dL, and TG level of 89 mg/dL.
Finally, in July 2015, the patient’s body weight reached 98.3 kg, a reduction of 32.4 kg (25 % of his initial body weight), while his BMI decreased from 41.0 to 30.8 kg/m2. Figure shows changes in his body weight and TSH level over time. The patient felt motivated by the prospect of discontinuing the CPAP therapy, and was encouraged by the consistent weight loss at the monthly clinical visits. He also wanted to continue with the LCD because he did not find it difficult.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Total cholesterol': [335.0, 'mg/dL'], 'high-density lipoprotein cholesterol': [45.0, 'mg/dL'], 'Triglycerides': [211.0, 'mg/dL']}",247.8,235.41,260.19,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 335.0 mg/dL. 
The concentration of hdl cholesterol is 45.0 mg/dL. 
The concentration of triglycerides is 211.0 mg/dL. 
Plugging in these values will give us 335.0 mg/dL - 45.0 mg/dL - (211.0/5) mg/dL = 247.8 mg/dL.
The patients concentration of LDL cholestrol is 247.8 mg/dL."
6386,44,LDL Calculated,lab test,decimal,pmc-8051553-1,Extracted,"A 53-year-old Caucasian male with a past medical history significant only for heterozygous FVL deficiency presented with a complaint of typical angina of two weeks duration. The patient reported an athletic lifestyle, with recent exertional chest pain while kayaking and cycling. The patient reported that his most recent episode of pain awoke him from his sleep, prompting him to seek evaluation in the emergency department.
Laboratory testing revealed an elevated troponin I of 0.43 ng/mL (normal: <0.08 ng/mL), troponin T of 0.13 ng/mL (normal: <0.01 ng/mL), and pro B-type natriuretic peptide of 898 pg/mL (normal: <125 pg/mL). ECG showed normal sinus rhythm with deep symmetrical T wave inversions across anterior precordial leads suggestive of Wellens syndrome with Type B findings (Figure ).
Significant risk factors were evaluated and not found to be present. The patient was found to have a lipid profile of cholesterol 145 mg/dL, high-density lipoprotein (HDL) 32 mg/dL, low-density lipoprotein 95 mg/dL, non-HDL 113 mg/dL, triglycerides 88 mg/dL, very low-density lipoprotein 18 mg/dL, and hemoglobin A1c of 5.6%. The patient denied any history of hypertension and presented with a blood pressure of 122/79 mmHg on admission. He was recorded to have a body mass index of 26.3 kg/m2 and denied any smoking or alcohol history. No familial history of premature CAD was present. The patient was considered a moderate risk based on the HEART Score for six-week risk of major adverse cardiac events.
The patient underwent emergent cardiac catheterization, which revealed one-vessel CAD with a complete ostial occlusion of the LAD (Figure ). The right coronary artery (RCA) and left circumflex artery did not have any angiographically significant disease. Well-established collaterals were present from the dominant RCA, which supplied the mid-segment of the LAD (Figures , ). Due to the proximal location and nature of the occlusion, no intervention was attempted, and the patient was immediately referred to cardiac surgery for coronary artery bypass graft (CABG).
The patient underwent successful CABG with the left internal mammary artery to the LAD. He was ultimately discharged home on guideline-directed medical therapy, dual anti-platelet therapy with aspirin and clopidogrel, and without any complications from the procedure.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [32.0, 'mg/dL'], 'Triglycerides': [88.0, 'mg/dL'], 'Total cholesterol': [145.0, 'mg/dL']}",95.4,90.63,100.17,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 145.0 mg/dL. 
The concentration of hdl cholesterol is 32.0 mg/dL. 
The concentration of triglycerides is 88.0 mg/dL. 
Plugging in these values will give us 145.0 mg/dL - 32.0 mg/dL - (88.0/5) mg/dL = 95.4 mg/dL.
The patients concentration of LDL cholestrol is 95.4 mg/dL."
6387,44,LDL Calculated,lab test,decimal,pmc-5256339-1,Extracted,"A 72-year-old female was admitted to our hospital with acute onset dysarthria and right hemiparesis. The patient was a non-smoker and had no cardiovascular disease. Two years prior, she was diagnosed with MDS of the refractory anemia with excess blasts-2 subtype, according to World Health Organization classification. The International Prognostic Scoring System score was 3 and classified as high risk group. Following induction chemotherapy with azacitidine until the 16th cycle, the patient achieved complete remission. Chromosome analysis showed hyperdiploid clone with complex karyotypic abnormalities including trisomy 8 (55,XX, +1, +4, del(5)(q13), +6, +8, +9, +10, +14, +21, +22[17]/46, XX[3]).
The patient had been diagnosed with diabetes mellitus (DM) 2 years previously. Serum glucose level was controlled without complications such as diabetic retinopathy or nephropathy including microalbuminuria.
Laboratory test revealed pancytopenia (hemoglobin concentration, 6.0 g/dL; white blood cell count, 2.25×109/L; platelet count, 12×109/L); slightly abnormal serum lipid profile (total cholesterol, 213 mg/dL; high-density lipoprotein, 26 mg/dL; triglyceride, 284 mg/dL); normal prothrombin time and activated partial thromboplastin time; and elevated levels of fibrinogen, fibrin degradation product and D-dimer. Thrombolytic therapy and antiplatelet drugs were contraindicated due to thrombocytopenia. Electrocardiography and echocardiography showed no abnormal result.
On physical examination, the patient was alert and hemodynamically stable. Her initial National Institutes of Health Stroke Scale (NIHSS) score was 6 (facial palsy 1, right arm motor 4, dysarthria 1). Brain magnetic resonance imaging (MRI) revealed scattered acute infarction in the left cerebral deep white matter near primary motor cortex-white matter junction, corona radiata, and angular gyrus. Brain magnetic resonance angiography indicated severe stenosis and/or acute thrombosis of left proximal M1. And, perfusion MRI showed abnormal perfusion with delayed mean transit time (, , ).
On the third day of admission, she underwent rehabilitation consult. Manual muscle strength test (MMT) of right arm was grade 1 proximally and grade 0 at wrist; and the strength of right leg was grade 3 at whole lower limb. The patient scored 40 on the Korean version of Modified Barthel Index, suggesting total dependency of activities of daily living (ADL), and exhibited anomic aphasia. On the 27th day of admission, the patient was unable to open her right eye. The result of follow-up MMT was grade 0 at right whole upper limb, grade 1 at right hip and knee, and grade 2 at right ankle. Further radiologic study was not done despite possibility of progression. During the hospitalization period, conservative treatments alone were administered including intravenous hydration, transfusion, antibiotics for the recurrent infection, and bedside rehabilitative therapy. Additional chemotherapy was not possible because of poor general condition. On the 44th day of admission, the patient was transferred to a secondary referral hospital. On the day of discharge, her NIHSS score was 10 (facial palsy 2, right arm motor 3, right leg motor 2, limb ataxia 1, sensory 1, dysarthria 1), which was increased from that on admission.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Total cholesterol': [213.0, 'mg/dL'], 'high-density lipoprotein cholesterol': [26.0, 'mg/dL'], 'Triglycerides': [284.0, 'mg/dL']}",130.2,123.69,136.71,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 213.0 mg/dL. 
The concentration of hdl cholesterol is 26.0 mg/dL. 
The concentration of triglycerides is 284.0 mg/dL. 
Plugging in these values will give us 213.0 mg/dL - 26.0 mg/dL - (284.0/5) mg/dL = 130.2 mg/dL.
The patients concentration of LDL cholestrol is 130.2 mg/dL."
6388,44,LDL Calculated,lab test,decimal,pmc-8027099-1,Extracted,"In December 2020, a 51-year-old non-obese Japanese man presented to the Diabetes Care Center at Jinnouchi Hospital in Kumamoto, Japan, because of the suspicion of T2DM with hyperglycemia by an annual health screening (fasting glucose; 164 mg/dL, hemoglobin A1c (HbA1c); 8.8 %). He was initially pointed out his hyperglycemia at fasting condition by a health screening three years ago (fasting glucose; 140 mg/dL, HbA1c; 7.6 %) but he did not go to the hospital because he had no symptoms and did not recognize his own disease severity. He was an office worker and did not have a habit of excessive soft drink intake, and an unbalanced diet caused zinc deficiency. He was a current smoker (10 cigarettes/day) and had a daily drinking habit (30 g of alcohol/day). He did not have an active exercise habit. He did not have a family history of T2DM, cardiovascular disease, or any habitual medications.
At his first visit to our outpatient service, clinical examination showed a body height of 168.1 cm, bodyweight of 62.2 kg, body mass index (BMI) of 22.2 kg/m2 (non-obese), blood pressure of 150/79 mmHg (hypertension), and regular pulse rate of 77 beats/min. Physical examination revealed no abnormalities. Laboratory examination showed hyperglycemia (fasting blood glucose concentration, 172 mg/dL); elevated concentration of HbA1c (8.5 %) with normoinsulinemia (4.2 μU/mL; normal rage: 2.2~12.4 μU/mL), high total cholesterol (248 mg/dL), and high triglyceride (342 mg/dL); and a reduced high-density lipoprotein cholesterol level (39 mg/dL) (Table ).
He did not have diabetic retinopathy, neuropathy, nephropathy, thyroid dysfunction, or adrenal abnormality. He was non-obese but not salcopenic, and he had no evidence of excess fat accumulation assessed by bioelectrical impedance analyzer [] and abdominal computed tomography (Table ).
We performed 75-gram oral glucose tolerance test (75g-OGTT) and we found the well-maintained basal insulin secretion without hyperinsulinemia, prolonged hyperglycemia, and poor elevating insulin response to glucose load (Table ).
Based on the results of blood insulin levels in 75g-OGTT, we possibly speculated the presence of pancreatic β-cell dysfunction as his primary pathogenic cause of diabetes (Table ).
Three weeks after his first visit, he was admitted to our hospital for assessment and treatment of his hyperglycemia. We found that his antibody titer to glutamic acid decarboxylase was undetectable (<5.0 U/mL) and his daily urinary C-peptide immunoreactivity (CPR) excretion was unexpectedly accelerated at 182.07 µg/day, thus establishing a definitive diagnosis of T2DM (Table ).
After admission, we provided the hospitalized dietary (1800 Kcal/day) and exercise therapies according to our standard protocol []. On the second day of hospitalization (before treatment), his blood glucose levels were still elevated under the optimal dietary therapy (Table ).
On the third day of hospitalization, a hyperinsulinemic-euglycemic clamp examination [] revealed no insulin resistance (M-value>8.0), enhanced insulin sensitivity (M/I>12.0), and elevated insulin clearance assessed by the metabolic clearance rate of insulin (MCRI>500) (Table ).
We also found the strongly increased hepatic insulin clearance assessed by the molar ratio of CPR/insulin at fasting condition (Table ). Abdominal computed tomography showed normal subcutaneous and abdominal fat deposition and normal hepatic fat accumulation as assessed by the liver-to-spleen attenuation ratio (Table ). His pathogenic condition of abnormal glucose-metabolism suggested the possibility of attenuated insulin actions by the elevated insulin clearance but neither pancreatic β-cell dysfunction nor insulin resistance.
Because of the preserved capacity of endogenous insulin secretion from pancreatic β-cells and the absence of insulin resistance, the patient initially received lifestyle modification therapy with stopping smoking and drinking, taking adequate calorie intake, reducing salt intake, and introducing an exercise habit during the hospitalized treatments []. He also received an explanation for his diabetic conditions and his novel pathogenesis of hyperglycemia with elevated insulin clearance. Because we have no established and evidence-based interventional strategies to treat his elevated insulin clearance, we started to treat him with metformin (initial dose of 500 mg/day and maintenance dose of 1000 mg/day) and followed up his hyperglycemia. His hyperglycemia was not life-threatening at the time of hospital admission (no ketosis and no symptom), and dietary therapy and metformin were effective for his hyperglycemia. During the hospitalized therapy, we measured fasting blood glucose levels every morning and measured the daily blood glucose profile. At the same time, we started statin (rosuvastatin; 5 mg/day), fibrate (fenofibrate; 160 mg/day), and angiotensin-converting enzyme inhibitor (enalapril; 5 mg/day) to treat his hyperlipidemia and hypertension, and we subsequently added ezetimibe 10 mg/day and α-glycosidase inhibitor (voglibose; 0.9 mg/day). On the fourteenth day of hospitalization, his blood glucose concentration and blood pressure (blood pressure; 119/71 mmHg) were well-controlled (Table ). We finally found a decrease in daily urinary CPR excretion (103.75 µg/day) and blood insulin level (1.8 μU/mL) as compared to the pre-treatment condition. His elevated hepatic insulin clearance was not rapidly changed after the two weeks of hospital therapies (molar ratio of CPR/insulin at fasting condition; 41.8). After 17 days of in-hospital therapies and education, the patient was discharged with the recommendation to continue appropriate dietary therapy (1800 kcal/day as described above) and at least 30 minutes of daily exercise. The patient continued treatment with all the medications described above and underwent monthly outpatient follow-ups.
After discharge, we followed him at our outpatient service as usual [], which led to an improvement in his blood glucose and glycated hemoglobin (HbA1c) concentrations. In March 2021, his blood glucose, blood pressure, and lipid parameters have been well managed at our outpatient service (fasting glucose; 117 mg/dL, and HbA1c; 6.6 %, blood pressure; 112/71 mmHg, low-density lipoprotein cholesterol; 59 mg/dL, and triglyceride; 75 mg/dL). We want to re-perform the hyperinsulinemic-euglycemic clamp examination to evaluate insulin clearance and insulin sensitivity at our outpatient service after 12 months of treatment or after glycemic control had been improved. We are not sure whether we will be able to re-evaluate the elevated insulin clearance in the future.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [39.0, 'mg/dL'], 'Triglycerides': [342.0, 'mg/dL'], 'Total cholesterol': [248.0, 'mg/dL']}",140.6,133.57,147.63,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 248.0 mg/dL. 
The concentration of hdl cholesterol is 39.0 mg/dL. 
The concentration of triglycerides is 342.0 mg/dL. 
Plugging in these values will give us 248.0 mg/dL - 39.0 mg/dL - (342.0/5) mg/dL = 140.6 mg/dL.
The patients concentration of LDL cholestrol is 140.6 mg/dL."
6389,44,LDL Calculated,lab test,decimal,usmle-7444,Extracted,"A 66-year-old man presents to your office for a regular checkup. His only current complaint is periodic difficulty falling asleep at night. He takes captopril and hydrochlorothiazide for hypertension, atorvastatin for hyperlipidemia, and aspirin for cardiovascular disease prevention. His past medical history is significant for tympanoplasty performed 8 years ago for tympanic membrane rupture after an episode of purulent otitis media and intussusception that required surgical intervention 10 years ago. He also had a severe anaphylactic reaction after his 2nd Tdap administration 3 years ago. His blood pressure is 145/90 mm Hg, heart rate is 88/min, respiratory rate is 12/min, and temperature is 36.4°C (97.5°F). Physical examination only reveals a laterally displaced point of maximum impulse. Blood analysis shows the following findings:
Sodium
139 mEq/L (139 mmol/L)
Potassium
5.0 mEq/L (5.0 mmol/L)
Chloride
100 mEq/L (100 mmol/L)
Bicarbonate
22 mEq/L (22 mmol/L)
Albumin
3.8 mg/dL (38 g/L)
Urea nitrogen
8 mg/dL (2.86 mmol/L)
Creatinine
2.1 mg/dL (0.185 mmol/l)
Uric acid
5.8 mg/ dL (0.34 mmol/L)
Calcium
8.9 mg/ dL (2.22 mmol/L)
Glucose
106 mg/ dL (5.89 mmol/L)
Total cholesterol
254 mg/dL (5.57 mmol/L)
Low-density lipoprotein
58 mg/dL (1.5 mmol/L)
High-density lipoprotein
77 mg/dL (2.0 mmol/L)
Triglycerides
159 mg/dL (1.8 mmol/L)
The patient is concerned about pneumococcal infection. He has never been vaccinated against pneumococcus, and he would like to get the appropriate vaccination. You advise him that he should not be vaccinated with PCV13 (pneumococcal conjugate vaccine) and should instead be administered PPSV23 (pneumococcal polysaccharide vaccine).",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [77.0, 'mg/dL'], 'Triglycerides': [159.0, 'mg/dL'], 'Total cholesterol': [254.0, 'mg/dL']}",145.2,137.94,152.46,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 254.0 mg/dL. 
The concentration of hdl cholesterol is 77.0 mg/dL. 
The concentration of triglycerides is 159.0 mg/dL. 
Plugging in these values will give us 254.0 mg/dL - 77.0 mg/dL - (159.0/5) mg/dL = 145.2 mg/dL.
The patients concentration of LDL cholestrol is 145.2 mg/dL."
6390,44,LDL Calculated,lab test,decimal,pmc-7586627-1,Extracted,"A 40-year old male presented with painful swelling of the right foot. The swelling had been gradually increasing in size for the last 1 year. On local examination, the first tarso-metatarsal joint of the right foot was swollen. There was no history of trauma. There was no significant past or family history. She was a case of uncontrolled diabetes mellitus with a blood glucose level of 282 mg/dL and HbA1c of 8.1%. Erythrocyte sedimentation rate (ESR) and C-reactive protein were normal. Biochemical parameters showed serum calcium of 8.1 mg/dL (Normal 9–11 mg/dL), phosphate of 3.3 mg/dL (Normal 2.5–4.5 mg/dL), and uric acid of 4.5 g/dL (Normal 3.4–7.0 g/dL). Her rheumatoid factor (RF), anti-cyclic citrullinated peptide, and antinuclear antibody (ANA) were negative. Her lipid profile study showed total serum cholesterol of 315 mg/dL (normal <200 mg/dL), low density lipoproteins of 250 mg/dL (normal <100 mg/dL), triglyceride of 100 mg/dL (normal <150 mg/dL), and high density lipoproteins of 55 mg/dL (normal >40 mg/dL).
Plain radiographs of the right foot did not show any bony or joint erosion. There was no evidence of tendon xanthomas or tendinitis. Synovial fluid was aspirated from the first tarso-metatarsal joint of the right foot by a 24 gauge needle. Wet mount preparation from the fluid showed crystals plates with notched ends []. Under polarized light microscopy these crystals were positively birefringent []. May Grunwald Giemsa (MGG) stain showed mainly extracellular rhomboid and square-shaped crystals along with scattered foreign body giant cells []. The background showed chronic inflammatory cells consisting of lymphocytes and histiocytes.
A diagnosis of hypercholesterolemic arthritis was made. The blood glucose was controlled. The patient was started with atorvastatin and paracetamol. After 3 months, the lipid levels returned to normal with significant improvement in arthritis.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [55.0, 'mg/dL'], 'Triglycerides': [100.0, 'mg/dL'], 'Total cholesterol': [315.0, 'mg/dL']}",240,228,252,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 315.0 mg/dL. 
The concentration of hdl cholesterol is 55.0 mg/dL. 
The concentration of triglycerides is 100.0 mg/dL. 
Plugging in these values will give us 315.0 mg/dL - 55.0 mg/dL - (100.0/5) mg/dL = 240.0 mg/dL.
The patients concentration of LDL cholestrol is 240.0 mg/dL."
6391,44,LDL Calculated,lab test,decimal,pmc-7953395-1,Extracted,"A-61-year-old male of Han ancestry was admitted to our hospital on July 15, 2020 due to a 4-yr history of progressive swollen soft masses at multiple sites.
The patient presented with progressive soft masses over the abdomen for more than four years, swellings in the mandible, back of the neck and elbows also gradually enlarged during these four years.
The patient was a heavy drinker with an average of 500 mL liquor per day for 45 years. He had a smoking history of approximately 20 cigarettes/day for 45 years,. The patient was diagnosed with type 2 diabetes more than 20 years previously, with poorly controlled glucose for many years. He had a history of hypertension for 18 years and did not take any antihypertensive drugs.
He had no family history of similar diseases and denied previous special drug use.
Physical examination upon admission revealed the following: The patient was conscious; a body mass index of 21.0 kg/m2; subcutaneous masses in the mandible, back of the neck, abdomen and elbows (Figure ); no signs of moon face, paper skin, hirsutism, or purple stria.
Laboratory tests showed a total cholesterol level of 92.16 mg/dL, low-density lipoprotein cholesterol level of 35.28 mg/dL, high-density lipoprotein cholesterol level of 37.44 mg/dL, triglyceride level of 20.7 mg/dL, hemoglobin A1c of 5.4% and 24 h urinary albumin was 343.5 mg/d. Thyroid function was in the normal range. His basal cortisol level as well as his 1 mg dexamethasone suppression test were normal. Hepatitis B, hepatitis C, human immunodeficiency virus and syphilis were all negative.
Ultrasonography showed diffuse lipomatosis and lymph node echo in the neck in January 2018. The thickest part of the mass in the neck was about 28 mm. In July 2020, ultrasonography showed that the thickest part of the mass in the neck was about 44 mm. Ultrasonography of the elbow suggested that there was a hypoechoic mass between the palmaris muscles on both sides of the elbow, with a range of about 51 mm × 15 mm × 34 mm on the left and 46 mm × 14 mm × 35 mm on the right. The boundary was clear and the internal echo was not uniform, with strong echoes of several fiber spacers, similar to the echoes of adipose tissue. Simultaneously, excessive fat deposition was suggested on the mandible and the abdominal area of the patient by ultrasonic examination. Computed tomography showed diffuse and marked fatty deposits in the subcutaneous superficial fascia space of the neck without internal lesions (Figure ). A breast ultrasound examination showed that both sides of the breast had excessive fat deposition and a flaky strong echo was seen in the deep side of the areola. The left side was about 33 mm × 3 mm × 25 mm and the right side was about 44 mm × 8 mm × 31 mm. The internal lobular structure was disordered, and small hypoechoic areas were seen, but no obvious mass echo and mammary duct expansion was found.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [37.44, 'mg/dL'], 'Triglycerides': [20.7, 'mg/dL'], 'Total cholesterol': [92.16, 'mg/dL']}",50.58,48.051,53.109,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 92.16 mg/dL. 
The concentration of hdl cholesterol is 37.44 mg/dL. 
The concentration of triglycerides is 20.7 mg/dL. 
Plugging in these values will give us 92.16 mg/dL - 37.44 mg/dL - (20.7/5) mg/dL = 50.58 mg/dL.
The patients concentration of LDL cholestrol is 50.58 mg/dL."
6392,44,LDL Calculated,lab test,decimal,pmc-4802030-1,Extracted,"The 35-year-old male patient presented to our clinic with the complaints of headache, sore throat, a one-month history of a rapidly growing mass in the neck, and weight loss. At presentation, the patient had been followed up due to the diagnosis of ulcerative colitis for the last 10 years. Physical examination revealed a pain in the neck and a 1 cm nodule in the thyroid isthmus on palpation. Moreover, the breath sounds were decreased in the right lung. Laboratory tests were as follows: white blood cell: 3800/mm3, hemoglobin: 12.6 g/dL, platelet: 159,000/L, C-reactive protein (CRP): 25 mg/L (normal, 0 to 1 mg/dL), glucose: 90, urea: 47, creatinine: 1.07 mg/dL (0.84–1.25), aspartate transaminase (AST): 26 U/L (8–40), alanine transaminase (ALT): 43 U/L (5–35), sodium: 139 mmol/L (136–146), potassium: 4.7 mmol/L (2.5–4.5), triglyceride: 342 mg/dL (35–150), HDL: 35 mg/dL (40–60), total cholesterol: 302 mg/dL (120–200), and sedimentation: 76/h. The cardiothoracic ratio was increased on the PA-AC graph. Pericardial effusion was detected during the consultations with the relevant departments. During the investigation of the etiology of the pericardial effusion, nephrotic-range proteinuria (3.6 gr/day) was detected. Subcutaneous biopsy was performed on suspicion of amyloidosis in the etiology of proteinuria but no sign of amyloidosis was found in the immunohistochemical analysis. Duodenal and rectal mucosal biopsies were performed but amyloid was detected only in the rectal mucosa. The presence of amyloid was confirmed by the appearance of Congo Red and apple-green birefringence and immunohistochemical staining patterns. Thyroid function tests were as follows: Ft3: 2.14 pg/mL (normal, 2.5 to 3.9 pg/mL), Ft4: 1.01 ng/dL (0.61–1.12), TSH: 0.29 μIU/mL (0.34–4.2), anti-thyroid peroxidase (Anti-TPO): 28 IU/mL (0–35), and antithyroglobulin (AntiTG): 110 IU/mL (0–115). On ultrasonography, both thyroid parenchymata were heterogeneous, whereas a 12 × 8 mm heterogeneous, degenerated, mixed nodule was detected in the isthmus and a 13 × 8 mm cystic nodule was detected in the inferior segment of the right lobe. Thyroid scintigraphy revealed low thyroid activity and increased background activity in the thyroid area. Fine needle aspiration of the thyroid gland revealed a 12 × 8 mm mixed nodule with benign cytological results in the isthmus and an 18 mm cystic nodule at the junction of the left lobe with the isthmus. Thyroid scintigraphy was normal. In the follow-up period, total thyroidectomy was performed due to euthyroidism. Pathological analysis revealed amyloid deposition in the entire thyroid gland and deposition of amorphous eosinophilic material between the follicular structures. Amyloid was histochemically stained with PAS and Congo Red stains and was immunohistochemically classified as AA (Figures , , and ). The patient has been followed up for the last 15 months, and he is currently undergoing the treatment of levothyroxine intoxication and is in remission for amyloidosis that developed secondary to ulcerative colitis.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [35.0, 'mg/dL'], 'Triglycerides': [342.0, 'mg/dL'], 'Total cholesterol': [302.0, 'mg/dL']}",198.6,188.67,208.53,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 302.0 mg/dL. 
The concentration of hdl cholesterol is 35.0 mg/dL. 
The concentration of triglycerides is 342.0 mg/dL. 
Plugging in these values will give us 302.0 mg/dL - 35.0 mg/dL - (342.0/5) mg/dL = 198.6 mg/dL.
The patients concentration of LDL cholestrol is 198.6 mg/dL."
6393,44,LDL Calculated,lab test,decimal,pmc-3811690-1,Extracted,"A 53-year-old female presented to our hospital complaining of a 6-month history of backache. Judging from the blood testing results, she had hypercalcemia, and alkaline phosphatase (ALP) was increased to 1,253 U/L (normal range, 35 to 130); the patient was sent to the endocrinology department. Her past history was significant for a surgical procedure for fibrocystoma of her right humerus 20 years ago, and she had donated one of her kidneys to a relative 7 years previously. She had taken atorvastatin 10 mg, amlodipine 5 mg, and omega-3 fatty acid 1,000 mg daily for the past 3 years to treat high blood pressure and dyslipidemia. The patient had been misdiagnosed with a thyroid nodule and hypothyroidism at another hospital 4 years previously and had immediately been prescribed levothyroxine 50 µg/day. At that time, the thyroid ultrasonography revealed two nodules that were 0.3 and 0.5 cm in diameter on her right lobe and another nodule that was 2.3×1.3 cm in size that was projected backwards. She had fine needle aspiration cytology for the nodule on the left lobe, and this had revealed a benign nodule. She had been followed up every 6 months by neck ultrasonography. Two years later, when the nodule on the left lobe of the thyroid had increased in size to 2.9×1.7 cm, they carried out radiofrequency ablation. However, the thyroid nodule remained the same size even after the radiofrequency ablation, so they monitored its size every 6 months for 2 more years (). During that time, the patient began experiencing backache and visited the orthopedics department of our hospital where she was suspected of having metabolic bone disease due to the high serum ALP value.
The patient presented with generalized weakness and fatigue without other hypercalcemic symptoms. The peripheral blood examination was as follows: leukocyte count, 7,020/mm3; hemoglobin, 9.3 g/dL; platelet count, 249,000/mm3; prothrombin time (PT), 14.4 seconds (normal range, 11.9 to 14.3); activated partial thromboplastin time (aPTT), 31.3 seconds (normal range, 29.1 to 43.5); serum iron, 65 µg/dL (normal range, 40 to 160); total iron binding capacity (TIBC), 258 µg/dL (normal range, 230 to 430); transferrin saturation, 25%; and ferritin, 158.6 ng/mL (normal range, 13 to 150). Serum chemistry values were also obtained: blood urea nitrogen, 26.9 mg/dL; creatinine, 1.98 mg/dL; glucose, 110 mg/dL; ALP, 1,011 U/L; aspartate aminotransferase, 23 U/L; and alanine aminotransferase, 11 U/L. Serum calcium was 14.6 mg/dL, phosphate was 3.5 mg/dL, and ionized calcium was 7.2 mg/dL. Serum protein and serum albumin were 6.9 and 3.7 g/dL, respectively. The results of the serum electrolyte test revealed that sodium was 135.7 mmol/L, potassium was 4.3 mmol/L, chloride was 104.0 mmol/L, and serum osmotic pressure was 286 mOsm/kg. According to the serum lipid examination, the total cholesterol was 146 mg/dL, triglyceride was 95 mg/dL, high density lipoprotein was 33 mg/dL, and low density lipoprotein was 79 mg/dL. A thyroid function test found T3 was 108.9 ng/dL (normal range, 80 to 200), thyroid stimulating hormone was 0.40 mIU/L (normal range, 0.27 to 4.2), and free T4 was 0.74 ng/dL (normal range, 0.93 to 1.70). Under dual energy X-ray absorptiometry-based bone density examination, the T-score of the lumbar region was -1.4, while the T-scores of the neck were -1.2 on the left and -1.8 on the right. Except for the fifth lumbar vertebra, which had spondylolisthesis, nothing remarkable was found on magnetic resonance imaging.
According to further blood tests, 25-hydroxyvitamin D3 was 9.6 ng/mL (normal range, 4.8 to 52.8), and 1,25-dihydroxyvitamin D3 was 10.5 pg/mL (normal range, 19.6 to 54.3), while the intact parathyroid hormone (iPTH) was 1,911 pg/mL (normal range, 15 to 65). When we performed bone scanning with 99mTc, the amount of cortical bone radioactive isotope uptake increased very high (). Because we suspected hyperparathyroidism, we carried out a 99mTc sestamibi scan and suspected the lesion that had been previously diagnosed as a left thyroid nodule was likely a parathyroid adenoma (). Using thyroid Doppler ultrasonography, we discovered a hypervascular adenoma that was 5-cm-sized solid mass with similar echo of surrounding thyroid tissue in the center, and slightly low echo in outer part in the inferior site of left thyroid gland (), while on the right thyroid parenchyma we discovered two thyroid nodules, 0.3 and 0.5 cm each in diameter, that the patient had had 4 years before. We performed neck computed tomography and found there was no neck lymph node metastastasis and local invasion of other organs ().
The patient received both hydration and diuretic treatments until she underwent a surgical operation to control the hypercalcemia; she also had pamidronate 90 mg intravenous injections twice a week. On the 11th day after hydration and diuretic treatment, her condition had improved; serum calcium was reduced to 11.6 mg/dL, and creatinine improved to 1.11 mg/dL. On the 12th day, the patient had left parathyroid excision and was diagnosed with a parathyroid adenoma (). Following the surgical procedure, iPTH normalized to 42.5 pg/mL, but calcium and vitamin D were prescribed for 9 months to cure the hypocalcemia that had developed due to hungry bone syndrome. It has been a year since the surgical operation, and her calcium, phosphate, ALP, and iPTH all remain at normal levels.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [33.0, 'mg/dL'], 'Triglycerides': [95.0, 'mg/dL'], 'Total cholesterol': [146.0, 'mg/dL']}",94,89.3,98.7,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 146.0 mg/dL. 
The concentration of hdl cholesterol is 33.0 mg/dL. 
The concentration of triglycerides is 95.0 mg/dL. 
Plugging in these values will give us 146.0 mg/dL - 33.0 mg/dL - (95.0/5) mg/dL = 94.0 mg/dL.
The patients concentration of LDL cholestrol is 94.0 mg/dL."
6394,44,LDL Calculated,lab test,decimal,pmc-4421656-1,Extracted,"A 50-year-old female was diagnosed with Gitelman syndrome at the age of 20 years. She was treated with spironolactone (100 mg/day), magnesium lactate (1.2 g/day), potassium chloride (5.4 g/day) and indometacin (25 mg/day).
The patient was recently admitted to our Nephrology Department with oliguria and progressive facial and lower limb oedema 15 days in duration. Her blood analyses showed urea 60 mg/dL, creatinine 0.93 mg/dL, Na 138 mmol/L, K 3.3 mmol/L, Cl 98 mmol/L, Mg 2.1 mg/dL, Ca 8.2 mg/dL (ionic 1.08), P 3.1 mg/dL, total proteins 4.5 g/dL, albumin 1.7 g/dL, bicarbonate 30.1 mmol/L, cholesterol 441 mg/dL, triglycerides 151 mg/dL, high-density lipoprotein 101 mg/dL, low-density lipoprotein 339 mg/dL. Anti-nuclear antibodies, antineutrophil cytoplasmic antibodies and serologic tests for hepatotropic virus, human immunodeficiency virus and treponema were negative, and her complement system, haemogram and thyroid function were normal. Urinalysis findings were proteinuria 11.7 g/day, Na 74 mmol/L, K 152.6 mmol/L, Ca 5.7 mg/dL (136.8 mg/day) and Mg 3.8 mg/dL. A renal biopsy showed: subendothelial and mesangial segmental C1q deposits, mainly located in the distal areas of the capillary loops (), with discrete mesangial proliferation, slight interstitial fibrosis and hyperplasia of the juxtaglomerular apparatus ().
Her definitive diagnosis was nephrotic syndrome secondary to C1q nephropathy, probably minimal change type. Treatment with steroids at a dose of 1 mg/kg/day was started. The nephrotic syndrome resolved after 6 weeks of treatment.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [101.0, 'mg/dL'], 'Triglycerides': [151.0, 'mg/dL'], 'Total cholesterol': [441.0, 'mg/dL']}",309.8,294.31,325.29,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 441.0 mg/dL. 
The concentration of hdl cholesterol is 101.0 mg/dL. 
The concentration of triglycerides is 151.0 mg/dL. 
Plugging in these values will give us 441.0 mg/dL - 101.0 mg/dL - (151.0/5) mg/dL = 309.8 mg/dL.
The patients concentration of LDL cholestrol is 309.8 mg/dL."
6395,44,LDL Calculated,lab test,decimal,pmc-6180275-1,Extracted,"A 22-year-old female was admitted to our hospital with the chief complaint of heavy menstrual bleeding for 10 days. Blood loss was severe, requiring around 4–5 tampon changes per day, and she complained of feeling dizzy and weak. She was unmarried and had no history of similar menorrhagia.
About 10 months earlier she had prolonged menstrual bleeding at that time, but as the menstrual cycle was normal and the bleeding was not very severe, she had not sought gynecological advice. About 3 weeks earlier she had experienced generalized muscle aches and joint pains (especially involving the upper and lower extremities), along with low-grade fever and bleeding from the gums. She had visited a primary healthcare center, where laboratory examination showed thrombocytopenia (50,000 dL) and anemia (6.5 g/dL). Dengue fever was suspected, and she was given a blood transfusion.
At our hospital she was initially admitted to the obstetrics and gynecology emergency department because of the severe menstrual bleeding. However, after ultrasound examination ruled out gynecological abnormalities, she was referred to the internal medicine department. On examination, her vital signs were within normal limits, but the conjunctiva was pale, and her hair showed a tendency to fall out easily. Multiple erythematous macules were present on the skin; however, there was no “butterfly rash” on the face. Systemic examination was otherwise normal.
Hemogram showed the following: hemoglobin 11.3 g/dL; hematocrit 36%; MCV 76.4 fL; MCHC 31.4 g/dL; serum iron 45 µg/dL; TIBC 279 µg/dL; transferrin saturation 16%; thrombocyte count 55,200/dL; and leucocyte count 7,310/dL (with normal differential count). Kidney function tests showed normal serum urea and creatinine levels, with eGFR of 129.8 mL/min/1.73 m2 (calculated using the Chronic Kidney Disease Epidemiology Collaboration equation). The random blood glucose level was 105 mg/dL. The lipid profile showed total cholesterol, 218 mg/dL; low-density lipoprotein 161 mg/dL; high-density lipoprotein 27 mg/dL; and triglyceride 150 mg/dL. Liver function tests and serum electrolyte levels were within normal limits. Coagulation function tests showed partial thromboplastin time 9.7 s (11.3); activated partial thromboplastin time 31.8 s (34.7); fibrinogen level 429.9 mg/dL; and D-dimer 0.2 mg/dL. Antinuclear antibody was positive at a titer of 1/1,000, with C3 86.4 mg/dL, C4 15.4 mg/dL, CRP 2.4 mg/dL, and anti-dsDNA 614.5 IU/mL. Lactic acid dehydrogenase was 464 U/L, reticulocyte count 1.42%, immature platelet fraction 6.7%, and serum albumin 3.87 g/dL. Urinalysis showed a large number of erythrocytes, epithelial cells, and amorphous crystals. Proteinuria was present (2+). Total 24-h protein excretion was 1,148 mg. Kidney ultrasound examination was done as a part of routine examination, which revealed bilateral dilatation of the pelvicalyceal systems showing hydronephrosis grade 1 on the left kidney (Fig. ) and grade 2 on the right kidney (Fig. ) without evidence of kidney cyst or stones. Moreover, ultrasound examination on the urinary bladder shows an increased bladder wall thickness (Fig. ).
Based on these findings, we diagnosed SLE complicated by lupus nephritis and lupus cystitis. Treatment was started with intravenous methylprednisolone (62.5 mg/day; 1.5 mg/kg/day). The vaginal bleeding stopped within 2 days, and the patient's general condition improved. Laboratory parameters also showed good response to corticosteroid therapy. After 5 days of intravenous therapy, the patient was switched to oral methylprednisolone (1 mg/kg/day). She was discharged from hospital on the 8th day, with the advice to continue methylprednisolone at the same dose and she is scheduled for follow-up after 1 month.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [27.0, 'mg/dL'], 'Triglycerides': [150.0, 'mg/dL'], 'Total cholesterol': [218.0, 'mg/dL']}",161,152.95,169.05,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 218.0 mg/dL. 
The concentration of hdl cholesterol is 27.0 mg/dL. 
The concentration of triglycerides is 150.0 mg/dL. 
Plugging in these values will give us 218.0 mg/dL - 27.0 mg/dL - (150.0/5) mg/dL = 161.0 mg/dL.
The patients concentration of LDL cholestrol is 161.0 mg/dL."
6396,44,LDL Calculated,lab test,decimal,pmc-7021239-1,Extracted,"A 33-year-old male with a significant medical history of hypertension and smoking presented to outpatient department with complaints of left-sided chest pain, SOB and episodic cough. The pain was moderate to severe in intensity, radiating to left arm and neck, continuous in nature, aggravated with movements with no relieving factors. It was not associated with fever, headache, vomiting or abdominal symptoms. The SOB was mostly experienced on walking and occasionally when lying flat. His family history was positive for cardiovascular disease as his father had fatal MI at a young age.
Past medical records depicted that he was admitted to a local hospital in 2014 with a diagnosis of right-sided weakness secondary to cerebrovascular accielectrocardiogram dent. The magnetic resonance imaging scans of brain showed an acute infarction of area supplied by the left middle cerebral artery (MCA). Magnetic resonance angiography of the circle of Willis depicted occlusion of the left MCA at the horizontal M1 segment. The extracranial arteries did not show any abnormalities like plaque formation on evaluation by cervical echography. After initial management with intravenous (IV) aspirin, the patient was administered with IV clopidogrel. Long-term anticoagulation was not prescribed since no cause was identified. There were no complications and the patient’s hemiparesis gradually improved during the following months. Later in 2017, he developed SOB with acute retrosternal chest pain. His electrocardiogram (ECG) showed ST-segment elevation in leads V2-V4. Troponin T was raised up to 7,120 ng/L [normal (N)= 0-14]. Transthoracic echocardiogram (TTE) showed moderate left ventricular (LV) systolic dysfunction, concentric LV hypertrophy, regional wall motion abnormities and mild mitral regurgitation (Figure ). The patient was initially administered with xylocaine, heparin, nitroglycerine, atropine, metoprolol, clopidogrel and loop diuretics. Cardiac catheterization revealed total occlusion of the left anterior descending (LAD) artery for which the patient underwent primary angioplasty to LAD with a drug-eluting stent. After adequate management, the patient was discharged on aspirin, clopidogrel, bisoprolol, rosuvastatin, spironolactone, hydroxyzine and loop diuretics.
On examination, his blood pressure (BP) was 165/90 mmHg, respiratory rate was 24 breaths per minute and heart rate was 70 beats per minute with no arrhythmia. General physical examination revealed palmar erythema, splinter hemorrhages and mild pedal edema. The SOB of New York Heart Association class III along with orthopnea was accompanied by productive cough and hemoptysis. Apex beat could not be palpated while lung fields were found to be clear on auscultation. Neurological examination showed no focal neurological deficits with a Glasgow Coma Scale score of 15/15. Other systemic examinations were insignificant.
Laboratory evaluation on admission revealed hemoglobin of 14.5 g/dL (N=13.8-17.2), total leukocyte count of 7 x 109/L (N=4-11), platelet count of 249 x 109/L (N=150-400), prothrombin time of 10.7 seconds (N=11-13.5), activated partial thromboplastin time of 16.7 seconds (N=26-36) and international normalized ratio of 1.10 (N≤ 1.1). Serum electrolytes were normal, and creatinine was documented to be 0.8 mg/dL (N=0.6-1.2). Total bilirubin, albumin and globulin levels were within the normal range. Lipid profile was also normal with serum cholesterol of 114 mg/dL (N< 200), low-density lipoprotein of 55 mg/dL (N=60-130), high-density lipoprotein of 60 mg/dL (N=60), and triglyceride level of 75 mg/dL (N<150). However troponin I levels were raised up to 0.1 ng/mL (N≤ 0.04).
The initial ECG had 1-2 mm ST-segment elevation in leads I, V2-V5 and aVL with ST-segment depression in reciprocal leads (Figure ). Chest X-ray showed an enlargement of the cardiac silhouette with diffuse pulmonary edema (Figure ). The patient was initially managed with ascard, atorvastatin, clopidogrel, valsartan, bisoprolol, spironolactone,and omeprazole.
TTE showed dilated LV with moderate dysfunction, akinetic LV apex, apical mid interventricular septum and inferior wall, and an ejection fraction (EF) of 35%. Carotid Doppler and duplex study of neck vessels (common carotid, external carotid, internal carotid and vertebral arteries) were found to be normal. Cardiac catheterization revealed a patent stent and thrombotic occlusion of the LAD. Considering the past history of stroke and MI in this young patient, blood samples were sent for a detailed coagulation profile. The serum homocysteine level was found to be 10 µmol/L (N=4-15), while factor V Leiden was also negative. Deficiency of PC and PS was finally diagnosed; values seen were 41.9% (N=70-123) and 53% (N=70-140), respectively.
Although the patient recovered from SOB and pedal edema, the EF showed no improvement despite adequate antiplatelet therapy. The BP also dropped to 100/70 mmHg. The patient was discharged with anticoagulants, diuretics, beta-blockers and nitrates. The patient was advised for regular follow-ups, but unfortunately, he could not maintain follow-ups.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Total cholesterol': [114.0, 'mg/dL'], 'high-density lipoprotein cholesterol': [60.0, 'mg/dL'], 'Triglycerides': [75.0, 'mg/dL']}",39,37.05,40.95,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 114.0 mg/dL. 
The concentration of hdl cholesterol is 60.0 mg/dL. 
The concentration of triglycerides is 75.0 mg/dL. 
Plugging in these values will give us 114.0 mg/dL - 60.0 mg/dL - (75.0/5) mg/dL = 39.0 mg/dL.
The patients concentration of LDL cholestrol is 39.0 mg/dL."
6397,44,LDL Calculated,lab test,decimal,pmc-6188040-1,Extracted,"A 58-year-old male with a past medical history of hypertension, hyperlipidemia, and tobacco use presented to the emergency department with abdominal pain localized to the epigastric and periumbilical areas. The pain was intermittent, not related to eating, and lasted for 3 days prior to admission. He had no fever, nausea, vomiting, or other gastrointestinal symptoms. The patient also denied any history of abdominal trauma or surgeries. On arrival, blood pressure was 156/104 mm Hg, and heart rate was 80 beats per minute (). His abdomen was soft, non-tender and non-distended, and with normal bowel sounds. The rest of the physical examination was unremarkable. The patient had a normal complete blood count (CBC), coagulation panel, and comprehensive metabolic panel (CMP). Lipid panel showed a total cholesterol level of 221 mg/dL, low-density lipoprotein of 153 mg/dL, high-density lipoprotein of 46 mg/dL, and triglyceride of 110 mg/dL. Computed tomography (CT) of the abdomen and pelvis with contrast revealed a short (1.7 cm) segment dissection of the superior mesenteric artery with mild induration of the adjacent fat (). The distal branches of the SMA appeared patent. The patient was treated conservatively with bowel rest, fluid resuscitation, intravenous heparin, and serial abdominal examinations. Home antihypertensive medications including daily amlodipine 5 mg, lisinopril 20 mg, and triamterene-hydrochlorothiazide 37.5-25 mg were resumed and his blood pressure was well controlled throughout admission (). The patient’s condition improved and he was discharged on the third day of admission with a blood pressure of 103/70 mm Hg and on warfarin with a target INR of 2 - 3.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [46.0, 'mg/dL'], 'Triglycerides': [110.0, 'mg/dL'], 'Total cholesterol': [221.0, 'mg/dL']}",153,145.35,160.65,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 221.0 mg/dL. 
The concentration of hdl cholesterol is 46.0 mg/dL. 
The concentration of triglycerides is 110.0 mg/dL. 
Plugging in these values will give us 221.0 mg/dL - 46.0 mg/dL - (110.0/5) mg/dL = 153.0 mg/dL.
The patients concentration of LDL cholestrol is 153.0 mg/dL."
6398,44,LDL Calculated,lab test,decimal,pmc-8583680-1,Extracted,"Case 1 is a 47-year-old male who recalls gradually worsening illness starting around the age of 25 that he partially attributes to poor food choices and opioid use. By the age of 36, he recalls knowing that he had “undeniable, serious illness,” and by the age of 38, he weighed over 400 pounds and suffered from severe sleep apnea, asthma and trouble breathing, eczema, allergies, hypertension (SBP/DBP = 255/155 on 2 medications), high total cholesterol (300 mg/dL), high triglycerides (279 mg/dL), and chronic shoulder and joint pain. He had difficulty moving and completing basic activities of daily living, such as putting on his shoes. He was on a number of medications that cost him approximately USD 7680 out of pocket, annually, while his insurance company paid a total of USD 19,646 for medications in 2009 alone. In addition to seeing a physician at least once every 1–2 weeks for his various conditions, he attended monthly appointments to aspirate fluid from his knees, had multiple visits to the ER, underwent shoulder surgery, and had one ankle reconstruction surgery with a second one imminent. Around 2012, at the age of 38, he decided to pursue gastric bypass surgery; however, his physician did not clear him to undergo the procedure, due to his poor underlying health. This event, combined with the recent deaths of two close family members, is what ultimately prompted him to begin considering lifestyle changes to improve his health. Initially, his approach to change was “going one step further than the day before.” First, he forced himself to simply get up from his chair once, and then twice per day, and then he progressed to being able to go on walks and walk up the stairs. He began researching additional lifestyle changes and watched documentaries, such as Forks Over Knives, which he describes as providing an entirely new perspective on food. He adopted dietary changes that began with a green juice fast followed by calorie restrictions, reducing red meat, and changing from full to lower fat dairy. On 1 January 2013, he adopted a strict, whole-food, plant-based (WFPB) dietary pattern. Thus, what started initially as a set of small lifestyle changes ultimately fostered a completely new lifestyle approach—one where fitness and plant-based eating were the focus. Approximately 6 months into the lifestyle change, Case 1 had lost 150–200 pounds, and although he does not recall his exact numbers, his cholesterol was cut in half, and triglyceride levels were in the normal range. By 2015, his cholesterol was 112 mg/dL and triglycerides were 74 mg/dL. In just 3–4 years, he went from barely standing up from a chair to running his first marathon in May 2016; by 2017, he was completing Ironman competitions and later ran an ultra-marathon. His current laboratory values as of 20 May 2021 include a total cholesterol of 103 mg/dL, HDL cholesterol 36 mg/dL, triglycerides 61 mg/dL, non-HDL cholesterol 67 mg/dL, and blood pressure 122/78. Post lifestyle change, he also notes significant improvement in his level of happiness and quality of life, specifically with respect to being able to enjoy time with his family, traveling, and gaining a new outlook on life.
Aside from the possibility of gastric bypass surgery (USD 18,000–35,000) [], Case 1 was a candidate for a Continuous Positive Airway Pressure (CPAP) machine for obstructive sleep apnea (USD 1000–3000) [] and a Transcutaneous Electrical Nerve Stimulator (TENS) machine for pain management (approximately USD 100–500) [] prior to his lifestyle change, highlighting an approximate average savings of USD 28,800 in discreet medical costs potentially avoided. Post lifestyle change, he reports spending only USD 61 per year on medications (B12 injections), as opposed to his previous approximated average spending of USD 7600+ in annual medication costs. Pharmaceutical costs covered by his insurance company decreased from USD 19,000+ in 2009 to USD 122.24 in 2015 and 2016 combined. In addition, his grocery costs are approximately half of what they were prior to his lifestyle change.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Total cholesterol': [103.0, 'mg/dL'], 'high-density lipoprotein cholesterol': [36.0, 'mg/dL'], 'Triglycerides': [61.0, 'mg/dL']}",54.8,52.06,57.54,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 103.0 mg/dL. 
The concentration of hdl cholesterol is 36.0 mg/dL. 
The concentration of triglycerides is 61.0 mg/dL. 
Plugging in these values will give us 103.0 mg/dL - 36.0 mg/dL - (61.0/5) mg/dL = 54.8 mg/dL.
The patients concentration of LDL cholestrol is 54.8 mg/dL."
6399,44,LDL Calculated,lab test,decimal,pmc-4966213-1,Extracted,"A 65-year-old female with a history of hypertension, smoking, and gastroesophageal reflux disease came to the emergency department for evaluation of progressive fatigue, weakness, and lightheadedness over the course of weeks. She also reported intermittent, atypical episodes of sharp chest pain, unrelated to exertion, lasting <5 min at a time. On initial assessment, her blood pressure was 146/102 mmHg, with a heart rate of 80 beats/min and regular. Her physical examination was significant for obesity, dry skin, and trace edema of her lower extremities. Her complete blood count, comprehensive metabolic panel, and D-dimer were within normal limits. Her initial troponin was <0.01 ng/dL. Her chest X-ray did not reveal any acute abnormality. Initial electrocardiographic (ECG) showed normal sinus rhythm with no ischemic signs.
During her evaluation in the Emergency Department where she had an episode of severe chest pain associated with palpitations and lightheadedness. A 30 second run of accelerated junctional rhythm at a rate of 87 beats/min was documented at the time. Troponin levels at 3 h peaked at 0.42 ng/dL and declined to 0.35 ng/dL at 6 h. Repeat ECG showed normal sinus rhythm with new T-wave inversions in anterolateral leads. At that point, the patient was medically managed as a non-ST segment elevation myocardial infarction.
Additional laboratory data included a thyroid-stimulating hormone (TSH) of 77 mIU/L with suppressed peripheral thyroid hormones as well a total cholesterol level of 348 mg/dL, high-density lipoprotein of 75 mg/dL, low-density lipoprotein of 248 mg/dL with triglycerides of 122 mg/dL. Twelve hours later, the patient underwent a left heart catheterization, which showed no evidence of obstructive coronary artery disease []; ventriculogram revealed a mildy depressed ejection fraction, with basal hypercontractility and apical akinesis, consistent with TCM []. She was started on oral levothyroxine, metoprolol, aspirin, and atorvastatin. She was discharged on the day 4 with no recurrence of symptoms.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [75.0, 'mg/dL'], 'Triglycerides': [122.0, 'mg/dL'], 'Total cholesterol': [348.0, 'mg/dL']}",248.6,236.17,261.03,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 348.0 mg/dL. 
The concentration of hdl cholesterol is 75.0 mg/dL. 
The concentration of triglycerides is 122.0 mg/dL. 
Plugging in these values will give us 348.0 mg/dL - 75.0 mg/dL - (122.0/5) mg/dL = 248.6 mg/dL.
The patients concentration of LDL cholestrol is 248.6 mg/dL."
6400,44,LDL Calculated,lab test,decimal,pmc-4532117-1,Extracted,"A 49-year-old man with a 3-year history of exertional chest pain was hospitalized due to acute myocardial infarction in June 1990. After an uneventful discharge, he still had exertional chest pain. In October 1990, he was admitted to another hospital due to progressive chest pain. Septal defect was found on echocardiography, but no specific management for septal rupture was done. After discharge, he had chest pain which was relieved by isonid spray. He was readmitted due to chest pain in December 1990 and referred to our hospital for definitive management of septal defect and postinfarction angina.
On physical examination, he was in relatively good condition and not dyspneic. Vital singns were blood pressure 100/70 mmHg, pulse rate 70 times per minute, and body temperature 36.2°C. The conjunctiva was not anemic. On chest auscultation, a pansystolic murmur was heard along the left sternal border, and the point of maximal intensity was Erb’s area. On abdominal examination, the liver was palpated by 5 cm below the right costal margin.
At admission, a hemogram revealed hemoglobin 13.1 g/dl, WBC 5400/mm3, and platelet 142 k/mm3. Lipid profiles were cholesterol 149 mg/dl, triglyceride 114 mg/dl, and HDL 24 mg/dl. CK and LDH were within normal range.
A chest roentgenogram showed cardioimegaly and bilateral pleural effusions (). An electrocardiogram showed a Q wave in leads V3–V6, II, III, and aVF, along with ST segment elevation in V3–V5 ().
On echocardiogram, apical dilatation and apical septal defect through which a jet flow traversed were noticed (). Wall motions in the basal septum and left ventricular posterior wall were relatively well preserved and the ejection fraction was 80%.
Cardiac catheterization revealed increased main pulmonary arterial, right ventricular and right atrial pressures (MPA 64/18/32 mmHg, RV 60/2/18 mmHg, RA 18/18/14 mmHg). A left ventriculogram showed an apical aneurysm with apical and anterolateral wall hypokinesia and contrast filling to the right ventricle and pulmonary artery through interventricular septal defect. A coronary angiogram showed no definite abnormality. The pulmonary-systemic flow ratio was 3.76.
On the 9th hospital day, an operation was done. The patient was found to have pericardial effusion and septal defect which measured 1×3 cm and were located in the apex. Fibrosis around the septal defect was noticed The septal defect was closed with a Dacron patch. The left ventriculotomy was closed with 2 Gore-Tex strips and buttressed by prolene horizontal matress suture. Finally, a Gore-Tex patch was attached to the LV wall. His postoperative recovery was uneventful, and echocardiography before his dicharge showed akinetic apical wall without septal defect.
On the 34th hospital day, he was discharged witout any complication and treated with digoxin, diltiazem, and isosorbide dinitrate at OPD.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [24.0, 'mg/dL'], 'Triglycerides': [114.0, 'mg/dL'], 'Total cholesterol': [149.0, 'mg/dL']}",102.2,97.09,107.31,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 149.0 mg/dL. 
The concentration of hdl cholesterol is 24.0 mg/dL. 
The concentration of triglycerides is 114.0 mg/dL. 
Plugging in these values will give us 149.0 mg/dL - 24.0 mg/dL - (114.0/5) mg/dL = 102.2 mg/dL.
The patients concentration of LDL cholestrol is 102.2 mg/dL."
6401,44,LDL Calculated,lab test,decimal,pmc-4026617-1,Extracted,"A 52-year-old male with a history of hypertension for 3 years and a smoking history of 30 pack/year suffered an electrical shock on his right hand from a contact with a 220 V of alternating current. It was presumed that the current entered his right hand and exited through his left hand. He did not have any significant symptoms immediately after the shock, so he did not seek treatment. After 1 week, however, he perceived weakness in both upper extremities. The strength of his left arm gradually improved, but the weakness in his right arm progressed. The patient visited our hospital 2 weeks post-injury.
According to the manual muscle test (MMT; Medical Research Council), both lower extremities were normal, but an examination of the right upper extremity revealed shoulder flexion and abduction (2/5), elbow flexion and extension (3/5), wrist flexion and extension (3/5), and finger extension (2/5). Motor power in his left upper extremity was graded as 5/5, except for the shoulder flexion and abduction (4/5) and wrist extension (4/5). Nerve conduction study (NCS) and electromyography were performed 4 weeks post-injury, and motor power of the right side improved to 4/5, except for the right index finger extensor (3/5). Sensory function was intact, muscle stretch reflexes were normoactive, no pathological reflexes were identified, and all the other cranial nerve and cerebellar functions were normal. A sensory NCS was normal but a motor NCS revealed delayed-onset latency and reduced amplitude of compound muscle action potentials in the right radial nerve (). There were no abnormal spontaneous activities during the needle electromyography, but a reduced recruitment of motor unit action potentials was observed in the right elbow flexor, wrist extensor, and finger extensor muscles (). The patient was diagnosed with an incomplete right radial nerve injury and received physical therapy at another hospital.
At 5 weeks after the injury, the patient visited an emergency department for a sudden-onset of weakness on the right-side with an aphasia. He had central-type facial palsy and weakness of the right upper and lower extremities, with proximal MMT grade of 3/5 and distal MMT grade of 2/5. His muscle stretch reflexes were hyperactive in the right upper and lower extremities, and Hoffman sign was observed on his right side. Laboratory results were within the normal ranges, except for the increased liver enzymes (aspartate aminotransferase/alanine aminotransferase [AST/ALT], 32/71 IU/L) and dyslipidemia (total cholesterol, 263 mg/dL; high-density lipoprotein-cholesterol, 38 mg/dL; low-density lipoprotein-cholesterol, 158 mg/dL; triglyceride, 217 mg/dL). Holter monitoring for 24 hours revealed a normal sinus rhythm, an echocardiogram revealed mild-to-moderate left ventricular hypertrophy, and a brain magnetic resonance imaging scan revealed an acute cerebral infarction of the left middle cerebral artery (MCA) (). Additionally, magnetic resonance angiography showed marked focal stenosis in the left MCA and proximal anterior cerebral artery, as well as stenosis of the proximal basilar artery and right proximal cervical internal carotid artery (). Because the patient visited the hospital 18 hours after the attack, oral aspirin was administered. He received rehabilitation treatment including physical, occupational, and speech therapies. One week after the admission, his right-side motor power had improved in the upper extremity (3/5), proximal lower extremity (4/5), and distal lower extremity (3/5). He was discharged 2 weeks after the admission (Korean Modified Barthel Index score, 91).",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [38.0, 'mg/dL'], 'Triglycerides': [217.0, 'mg/dL'], 'Total cholesterol': [263.0, 'mg/dL']}",181.6,172.52,190.68,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 263.0 mg/dL. 
The concentration of hdl cholesterol is 38.0 mg/dL. 
The concentration of triglycerides is 217.0 mg/dL. 
Plugging in these values will give us 263.0 mg/dL - 38.0 mg/dL - (217.0/5) mg/dL = 181.6 mg/dL.
The patients concentration of LDL cholestrol is 181.6 mg/dL."
6402,44,LDL Calculated,lab test,decimal,pmc-4107385-1,Extracted,"A 27-year-old African American female was referred for nephrotic syndrome in 2012. In 2005, during her first pregnancy, she had developed proteinuria and preeclampsia. The proteinuria subsided after she had given birth; however, it recurred during a second pregnancy in 2006 and increased to the nephrotic range. The second pregnancy was otherwise uneventful, and after delivery, the degree of proteinuria trended down to a nadir of 120 mg/g creatinine by 2009. She subsequently presented to our hospital in 2012 when the proteinuria again increased, reaching 4,600 mg/24 h (or 2,900 mg/g creatinine).
The patient had no past medical history of diabetes, hypertension, or other systemic illnesses. She was not taking any medications, had no known allergies and denied ever smoking or having used illicit drugs. Of note, both her father and maternal grandmother had type 2 DM and her father had had a stroke at age 50.
On examination, her blood pressure was 100/60 mm Hg and her BMI was 33. There was no edema, acanthosis nigricans, or hirsuitism. Fundoscopy did not reveal any diabetic retinopathy. Laboratory values included 0.7 mg/dl serum creatinine, 167 mg/dl total cholesterol, 42 mg/dl HDL cholesterol, and 77 mg/dl triglycerides. Urinalysis showed 3+ proteinuria with no hematuria. Tests for HIV, RPR, HBV, HCV, ANA, C3, and C4 were all negative or normal. Fasting glucose was 80 mg/dl and HbA1C was 5.8%. Renal ultrasound revealed kidneys 12 cm in size.
A renal biopsy was obtained in October 2012. Of the 7 glomeruli present, none were globally or partially sclerotic. Glomerulomegaly was not present. Using an eyepiece micrometer, the mean glomerular diameter was 175 ± 12 μm, a value within the reported normal range. One glomerulus evidenced segmental hyalinosis. Otherwise, the glomeruli were unremarkable by light microscopy (fig. ). Evidence of chronicity such as interstitial fibrosis and tubular atrophy was absent. Immunofluorescence microscopy revealed mild (1–2+) pseudolinear staining of the glomerular basement membrane (GBM) for IgG. No other immunoglobulin classes or complement components were detectable. Electron microscopy showed that the lamina densa of the GBMs were diffusely thickened, averaging 700–900 nm (fig. ). The podocytes were not vacuolated and, importantly, their foot processes were not effaced (fig. ). The endothelial cells were swollen with loss of fenestrations. Hyaline deposits were also noted in the glomerular capillary wall (fig. ), a finding corresponding to the light microscopic changes mentioned above.
Our patient was serially evaluated for impaired glucose metabolism. Fasting blood glucoses ranged from 80 to 111 mg/dl (with only two values ≥100 mg/dl). HbA1C ranged from 5.6 to 5.9%. Fluorescein angiography was negative for diabetic retinopathy. An oral glucose tolerance test (OGTT) was normal with a 2-hour glucose level of 109 mg/dl. The homeostasis model assessment of IR (HOMA-IR) was elevated at 2.93 and 3.74, a result that indicates IR (normal value: 1) in the face of adequate insulin secretion to maintain normoglycemia and a normal OGTT.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Total cholesterol': [167.0, 'mg/dL'], 'high-density lipoprotein cholesterol': [42.0, 'mg/dL'], 'Triglycerides': [77.0, 'mg/dL']}",109.6,104.12,115.08,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 167.0 mg/dL. 
The concentration of hdl cholesterol is 42.0 mg/dL. 
The concentration of triglycerides is 77.0 mg/dL. 
Plugging in these values will give us 167.0 mg/dL - 42.0 mg/dL - (77.0/5) mg/dL = 109.6 mg/dL.
The patients concentration of LDL cholestrol is 109.6 mg/dL."
6403,44,LDL Calculated,lab test,decimal,pmc-6416668-1,Extracted,"A 44-year-old male patient was admitted to our institution with a past medical history remarkable for CKD as a result of congenital left renal hypoplasia and adaptive focal segmental glomerulosclerosis due to long-term obesity. The patient started peritoneal dialysis at the age of 26. After 3 years, he underwent a cadaveric kidney transplant. During the postoperatory period, slow graft function was seen, which recovered satisfactorily over time. Immunosuppressive therapy was initiated with cyclosporine, mycophenolate mophetil and prednisolone. Nevertheless, multiple celular rejection episodes lead to chronic graft glomerulopathy and hemodialysis requirement after 8 years. At the time, the patient’s BMI was 30 kg/m2. Progressively, weight gain increased BMI to 42 kg/m2 with difficult-to-control hypertension and severe sleep apnea. At that point, the patient’s waist circumference was 120 cm and fasting glucose was 100 mg/dL. As for the lipid panel, total cholesterol was 145.8 mg/dL, high-density cholesterol was 33 mg/dL and triglycerides were 117.1 mg/dL. Uric acid was 7.9 mg/dL and albumin was 3.9 g/L. Regarding dialysis adequacy parameters: single-pool Kt/V was 1.47, body fat measured through bioelectrical impedance (BIA) was 45%, phosphorus was difficult to control, and oscillated between 5 and 8 mg/dL.
Behavioral, nutritional and pharmacologic measures were not sufficient for an adequate weight control, thus in order to allow access to a second kidney transplant, the patient’s case was brought to consideration by a multidisciplinary board where a surgical approach was decided. A gastric sleeve was performed. There were no early or late post-operatory complications after a 12-month follow-up period.
On the initial dialysis sessions after surgery, due to rapid weight loss, the patient displayed cramps, dehydration and hypotension, which required several adjustments of dry weight (DW) by BIA, almost daily at first and weekly thereafter in order to better define the optimal ultrafiltration rate and symptom resolution.
The patient achieved a BMI of 28.6 kg/m2, adequate blood pressure control and reduced severity of sleep apnea. He then met all required criteria, and was registered in the kidney transplant waitlist.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [33.0, 'mg/dL'], 'Triglycerides': [117.1, 'mg/dL'], 'Total cholesterol': [145.8, 'mg/dL']}",89.38,84.911,93.849,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 145.8 mg/dL. 
The concentration of hdl cholesterol is 33.0 mg/dL. 
The concentration of triglycerides is 117.1 mg/dL. 
Plugging in these values will give us 145.8 mg/dL - 33.0 mg/dL - (117.1/5) mg/dL = 89.38 mg/dL.
The patients concentration of LDL cholestrol is 89.38 mg/dL."
6404,44,LDL Calculated,lab test,decimal,pmc-6427864-1,Extracted,"A 35-year-old Han Chinese male football player presented with abnormal ECGs for 8 years without any evident subjective discomfort. The patient recently complained about slight exertional dyspnea with reduced sport/physical tolerance and was admitted to our hospital. This patient had been employed as a professional football player from the age of 10 years and had been a physical education teacher from the age of 26 years. He was a longtime local resident and never went to any affected areas (areas with high prevalence of infectious diseases). He reported being formerly healthy without any medical histories or current comorbidities, and he reported taking no medications. He has smoked 20 cigarettes per day for 7 years and consumed alcohol for 10 years at 100 to 250 g per day. His parents were healthy, and his family history was unremarkable. His physical examination revealed no abnormal findings. His body temperature was 36.5 °C, blood pressure was 121/73 mmHg, respiratory rate was 18 breaths/min, pulse was 69/min, heart rate was 70 beats/min, and reflexes were normal. He had no pathology reflex, and his body mass index was 22.81 kg/m2. Laboratory evaluation revealed slightly elevated cardiac troponin T level of 0.017 ng/ml, N-terminal probrain natriuretic peptide level of 291.80 pg/ml, and C-reactive protein level of 0.40 mg/L. The patient’s blood lipid levels, liver function, and renal function were within the normal range with glutamic oxaloacetic transaminase level of 23 U/L, glutamic-pyruvic transaminase level of 31 U/L, alkaline phosphatase level of 84 U/L, total protein level of 67.9 g/L, albumin level of 41 g/L, globulin level of 26.9 g/L, total cholesterol level of 4.01 mmol/L, triglyceride level of 1.42 mmol/L, high-density lipoprotein level of 1.08 mmol/L, low-density lipoprotein level of 2.14 mmol/L, uric acid level of 353 μmol/L, epidermal growth factor receptor level of 105.48 ml/min/1.73 m2; serum K+ level of 4.05 mmol/L, serum Ca2+ level of 2.16 mmol/L, serum Mg2+ level of 0.88 mmol/L, and serum Na+ level of 141 mmol/L. The results of routine blood test and urinalysis were negative, thyroid function was normal, and microorganisms were not detected. Chest radiography showed an apparently normal morphology of the heart and lungs (Fig. ). ECGs revealed progressively deepened and widened Q waves on the II, III, and avF leads and contiguous TWIs on the I and avL leads (Fig. , Table ). Echocardiography revealed an increasingly thickened interventricular septum from 10 mm to 13 mm, an enlarged left atrium and ventricle, and a reduced left ventricular ejection fraction from 73% to 63% (Fig. ). Coronary angiography (CAG) was performed and showed no distinct stenosis. Emission computed tomography (ECT) revealed mild myocardial ischemia of the left ventricular inferior wall (Fig. ). All of these clinical tests supported the diagnosis of HCM, which became gradually evident with time. For further identification, we proposed other examination techniques for this patient, including cardiac magnetic resonance imaging (CMRI) to better evaluate the left ventricular wall thickness and to identify potential areas of myocardial fibrosis, Holter monitor recordings and an exercise test to evaluate possible “dynamic” changes of repolarization abnormalities, as well as genetic testing. However, the patient refused all of these suggestions and was discharged. In the subsequent follow-up visits at 1 month, 3 months, and 6 months after discharge, the patient showed poor compliance and was eventually lost to follow-up.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [1.08, 'mmol/L'], 'Triglycerides': [1.42, 'mmol/L'], 'Total cholesterol': [4.01, 'mmol/L']}",88.827,84.38565,93.26835,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 4.01 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of total cholesterol from mmol to mg. The mass of total cholesterol is 4.01 mmol. To convert 4.01 mmol of total cholesterol to mol, multiply by the conversion factor 0.001, giving us 4.01 mmol total cholesterol * 0.001 mol/mmol = 0.00401 mol total cholesterol. To convert from mol total cholesterol to grams, multiply by the molar mass 386.654 g/mol, which will give 0.00401 mol total cholesterol * 386.654 g/mol = 1.55048 g total cholesterol. To convert 1.55048 g of total cholesterol to mg, multiply by the conversion factor 1000.0, giving us 1.55048 g total cholesterol * 1000.0 mg/g = 1550.48 mg total cholesterol. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1550.48 mg total cholesterol/10.0 dL = 155.048 mg total cholesterol/dL. The concentration value of 4.01 mmol total cholesterol/L converts to 155.048 mg total cholesterol/dL. 
The concentration of hdl cholesterol is 1.08 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of hdl cholesterol from mmol to mg. The mass of hdl cholesterol is 1.08 mmol. To convert 1.08 mmol of hdl cholesterol to mol, multiply by the conversion factor 0.001, giving us 1.08 mmol hdl cholesterol * 0.001 mol/mmol = 0.00108 mol hdl cholesterol. To convert from mol hdl cholesterol to grams, multiply by the molar mass 386.654 g/mol, which will give 0.00108 mol hdl cholesterol * 386.654 g/mol = 0.41759 g hdl cholesterol. To convert 0.41759 g of hdl cholesterol to mg, multiply by the conversion factor 1000.0, giving us 0.41759 g hdl cholesterol * 1000.0 mg/g = 417.59 mg hdl cholesterol. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 417.59 mg hdl cholesterol/10.0 dL = 41.759 mg hdl cholesterol/dL. The concentration value of 1.08 mmol hdl cholesterol/L converts to 41.759 mg hdl cholesterol/dL. 
The concentration of triglycerides is 1.42 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of triglycerides from mmol to mg. The mass of triglycerides is 1.42 mmol. To convert 1.42 mmol of triglycerides to mol, multiply by the conversion factor 0.001, giving us 1.42 mmol triglycerides * 0.001 mol/mmol = 0.00142 mol triglycerides. To convert from mol triglycerides to grams, multiply by the molar mass 861.338 g/mol, which will give 0.00142 mol triglycerides * 861.338 g/mol = 1.2231 g triglycerides. To convert 1.2231 g of triglycerides to mg, multiply by the conversion factor 1000.0, giving us 1.2231 g triglycerides * 1000.0 mg/g = 1223.1 mg triglycerides. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1223.1 mg triglycerides/10.0 dL = 122.31 mg triglycerides/dL. The concentration value of 1.42 mmol triglycerides/L converts to 122.31 mg triglycerides/dL. 
Plugging in these values will give us 155.048 mg/dL - 41.759 mg/dL - (122.31/5) mg/dL = 88.827 mg/dL.
The patients concentration of LDL cholestrol is 88.827 mg/dL."
6405,44,LDL Calculated,lab test,decimal,pmc-6128601-1,Extracted,"A 31-year-old Asian American female with past medical history of chewing of betel leaf with betel nuts and non-smoker, who immigrated to the USA from Burma four years previously, was referred to the Digestive Health Center at the University of Virginia for evaluation of elevated transaminases discovered upon routine testing. She reported no previous history of liver test abnormality or liver disease. She was not using any hepatotoxic prescription or over the counter medications or supplements and reported rare consumption of alcohol. Besides, she had no family history of liver disease, hepatocellular carcinoma, autoimmune disorders or diabetes mellitus.
The physical examination was significant for obesity with weight 66 kg, height 146 cm, body mass index (BMI) 31, hepatomegaly, nonpalpable spleen, and lack of stigmata of chronic liver disease. Extensive laboratory workup revealed normal complete blood count, renal function, serum electrolytes, iron studies, serum immunoglobulin levels, and ceruloplasmin. Also, hepatitis B and C serologic tests and autoimmune markers were negative. Fasting lipid profile revealed dyslipidemia (total cholesterol 260 mg/dL, triglycerides 267 mg/dL, high density lipoprotein 45 mg/dL, and low density lipoprotein 170 mg/dL). Fasting blood glucose was 165 mg/dL with simultaneous fasting insulin level of 4.8 mill international units/liter and a homeostasis model assessment of insulin resistance score of 2.9, thus has insulin resistance. Hemoglobin (Hgb) A1c level at this time was 6.8% which was higher than previous values from eight months prior (6.1%), 16 months prior (6.1%) and 39 months prior (4.8%).
Ultrasonographic evaluation of the abdomen revealed hepatomegaly, hyperechogenic liver indicative of severe hepatic steatosis, an ill-defined liver mass, and standard spleen size. Magnetic resonance examination defined the liver mass as hemangioma in addition to hepatomegaly and severe hepatic steatosis. Ultrasound-guided liver biopsy (sample size of 3.5 cm) showed severe macrosteatosis with mild lobular and periportal inflammation associated with focal hepatocyte damage (Figure , Panel A). Trichrome staining revealed focal portal, periportal and perisinusoidal fibrosis consistent with stage II (Figure , Panel B) with a NASH activity score (NAS) of 7. The patient was instructed to exercise routinely and follow a healthy diet. She was seen in follow-up for three months at which time her weight was unchanged. Physical examination revealed dark brownish red pigment on the teeth, tongue, and oral mucosa. Upon questioning the patient about this finding, she admitted to chewing betel on an average of 10 times per day for the last eight years. The patient reported an associated weight gain of around 16 kg from her baseline weight maintained for many years at 50 kg (BMI 23.5). This significant weight gain could not be reversed despite daily physically demanding work and following a healthy diet recommended by her primary care physician.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [45.0, 'mg/dL'], 'Triglycerides': [267.0, 'mg/dL'], 'Total cholesterol': [260.0, 'mg/dL']}",161.6,153.52,169.68,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 260.0 mg/dL. 
The concentration of hdl cholesterol is 45.0 mg/dL. 
The concentration of triglycerides is 267.0 mg/dL. 
Plugging in these values will give us 260.0 mg/dL - 45.0 mg/dL - (267.0/5) mg/dL = 161.6 mg/dL.
The patients concentration of LDL cholestrol is 161.6 mg/dL."
6406,44,LDL Calculated,lab test,decimal,pmc-3568860-2,Extracted,"Patient B, a 52-year-old man (weight: 118.2 kg; BMI: 38) had experienced severe dizzy spells a few hours following a meal. Although he was not diabetic, he was classified as having the metabolic syndrome (central weight distribution, hypertension, total cholesterol: 4.6 mmol/L; HDL-cholesterol: 0.8 mmol/L; triglycerides: 3.9 mmol/L). Due to the postprandial symptoms an eGTT was carried out and the relevant biochemistry test results are presented in and . He became symptomatic (neuroglycopenic symptoms: dizziness and blurred vision) after 180 min and the test was stopped at 200 minutes due to lack of recovery, and fast acting glucose energy tablets were given.
We have presented 2 cases demonstrating differing patterns of postprandial reactive hypoglycaemia. Both patients experienced symptoms due to hypoglycaemia at different times following the glucose load. Patient A did not demonstrate any features of the metabolic syndrome in contrast to patient B. The blood glucose increased rapidly in both patients within 30 minutes; in patient A, it stopped increasing at that point, while in the insulin resistant patient B, it continued to rise. The plasma insulin levels also increased in both patients, albeit the patterns were different as seen in . In patient A, plasma insulin concentration increased earlier with peak levels observed after 60 minutes (, ). This was followed by a rapid decrease in blood glucose. The peak insulin concentration was of smaller magnitude following half the glucose load () with improvement in symptoms. In contrast, patient B demonstrated a greater increase in insulin concentration with peak levels occurring after 90 minutes. The decrease in blood glucose also took place later.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Total cholesterol': [4.6, 'mmol/L'], 'high-density lipoprotein cholesterol': [0.8, 'mmol/L'], 'Triglycerides': [3.9, 'mmol/L']}",79.7446,75.75737,83.73183,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 4.6 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of total cholesterol from mmol to mg. The mass of total cholesterol is 4.6 mmol. To convert 4.6 mmol of total cholesterol to mol, multiply by the conversion factor 0.001, giving us 4.6 mmol total cholesterol * 0.001 mol/mmol = 0.0046 mol total cholesterol. To convert from mol total cholesterol to grams, multiply by the molar mass 386.654 g/mol, which will give 0.0046 mol total cholesterol * 386.654 g/mol = 1.77861 g total cholesterol. To convert 1.77861 g of total cholesterol to mg, multiply by the conversion factor 1000.0, giving us 1.77861 g total cholesterol * 1000.0 mg/g = 1778.61 mg total cholesterol. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1778.61 mg total cholesterol/10.0 dL = 177.861 mg total cholesterol/dL. The concentration value of 4.6 mmol total cholesterol/L converts to 177.861 mg total cholesterol/dL. 
The concentration of hdl cholesterol is 0.8 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of hdl cholesterol from mmol to mg. The mass of hdl cholesterol is 0.8 mmol. To convert 0.8 mmol of hdl cholesterol to mol, multiply by the conversion factor 0.001, giving us 0.8 mmol hdl cholesterol * 0.001 mol/mmol = 0.0008 mol hdl cholesterol. To convert from mol hdl cholesterol to grams, multiply by the molar mass 386.654 g/mol, which will give 0.0008 mol hdl cholesterol * 386.654 g/mol = 0.30932 g hdl cholesterol. To convert 0.30932 g of hdl cholesterol to mg, multiply by the conversion factor 1000.0, giving us 0.30932 g hdl cholesterol * 1000.0 mg/g = 309.32 mg hdl cholesterol. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 309.32 mg hdl cholesterol/10.0 dL = 30.932 mg hdl cholesterol/dL. The concentration value of 0.8 mmol hdl cholesterol/L converts to 30.932 mg hdl cholesterol/dL. 
The concentration of triglycerides is 3.9 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of triglycerides from mmol to mg. The mass of triglycerides is 3.9 mmol. To convert 3.9 mmol of triglycerides to mol, multiply by the conversion factor 0.001, giving us 3.9 mmol triglycerides * 0.001 mol/mmol = 0.0039 mol triglycerides. To convert from mol triglycerides to grams, multiply by the molar mass 861.338 g/mol, which will give 0.0039 mol triglycerides * 861.338 g/mol = 3.35922 g triglycerides. To convert 3.35922 g of triglycerides to mg, multiply by the conversion factor 1000.0, giving us 3.35922 g triglycerides * 1000.0 mg/g = 3359.22 mg triglycerides. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 3359.22 mg triglycerides/10.0 dL = 335.922 mg triglycerides/dL. The concentration value of 3.9 mmol triglycerides/L converts to 335.922 mg triglycerides/dL. 
Plugging in these values will give us 177.861 mg/dL - 30.932 mg/dL - (335.922/5) mg/dL = 79.7446 mg/dL.
The patients concentration of LDL cholestrol is 79.7446 mg/dL."
6407,44,LDL Calculated,lab test,decimal,pmc-7282361-1,Extracted,"A 52-year-old female presented to our outpatient department with increasing exertional dyspnea and chest pain for the past two months. Her medical history was positive for ischemic heart disease, diabetes mellitus, and hypertension. Five years ago, she underwent cardiac catheterization followed by a percutaneous coronary intervention (PCI) with an implantation of five stents. Her ongoing medication included subcutaneous insulin, antianginals (diltiazem, nitroglycerine, ranolazine, TriCardin®), clopidogrel, and an antacid.
On presentation, the patient was afebrile with a blood pressure 162/82 mmHg, heart rate 92/min, respiratory rate 24/min, and oxygen saturation 98% on room air. Due to the worsening of her angina symptoms, she was admitted for elective coronary angiography to assess the status of previously placed stents. On admission, her labs revealed poor diabetic control (hemoglobin A1C 9.3%) and dyslipidemia (total cholesterol 214 mg/dl, triglycerides 203 mg/dl, low-density lipoprotein 165 mg/dl, very low density lipoprotein 41 mg/dl, and high-density lipoprotein 45 mg/dl). Cardiac enzymes were not raised (creatine kinase-myocardial band 19.4 U/l and troponin-I 0.44 ng/ml). Blood counts, serum electrolytes, renal and liver function tests, viral markers, and coagulation profile were within normal limits. Her previous transthoracic echocardiography was significant for hypokinesis of the inferoseptal segment of the left ventricle and an ejection fraction of 50%.
An elective coronary angiography revealed critical ISR in the distal right coronary artery (RCA) stent (Figure ). Furthermore, critical stenosis (80%) at the mid-distal junction of the left anterior descending (LAD) artery and 40%-50% stenosis of the proximal ostium were also seen (Figure ). Patent stents were present in the proximal RCA and mid-LAD artery segments. The patient refused to undergo coronary artery bypass grafting. Therefore, a two-staged elective PCI involving the RCA and LAD artery was planned to treat the ISR. Stage I PCI to RCA was performed after pre-dilating the vessel. RCA ostium was intubated with guiding catheter JL3.5-6Fr. The lesion was crossed using the Hi-Torque Balance Middleweight Universal II Guidewire (Abbott Cardiovascular, Santa Clara, CA). The area was then dilated with a Mini-Trek balloon (2 x 20 mm; Abbott Cardiovascular). Finally, a Xience Xpedition® everolimus-eluting cobalt-chromium coronary stent (2.5 x 48 mm; Abbott Cardiovascular) was deployed at 17 atmospheres (ATMs) while overlapping the previous stent. The entire length of the stent was post-dilated with an NC-Trek balloon (2.75 x 15 mm; Abbott Cardiovascular). An excellent final angiographic result with well-deployed stents and thrombolysis in myocardial infarction (TIMI) III distal blood flow was achieved.
Stage II PCI to the LAD artery was performed two days later. Left mainstem ostium was intubated with guiding catheter JL3.5-6Fr. The stenosed area was crossed using a Hi-Torque Balance Middleweight Universal II Guidewire. The mid-LAD artery lesion was directly stented with a Xience PrimeTM everolimus-eluting cobalt-chromium coronary stent (2.5 x 18 mm; Abbott Cardiovascular) and deployed at 13 ATMs overlapping the previously placed mid-LAD artery stent. Next, the overlapped segment and the previously placed stent were post-dilated with the same stent balloon at 15 ATMs. Ostial proximal LAD artery lesion was directly stented with another Xience PrimeTM coronary stent (2.5 x 18 mm) and deployed at 13 ATMs overlapping the first stents. Then the entire length of the stents was post-dilated with an NC-TREK balloon (2.5 x 15 mm) at 17 ATMs. An excellent final angiographic result with well-deployed stents and TIMI III distal blood flow was achieved in this case as well (Figure ). The patient was counseled regarding risk factors and diet modification. Finally, the patient was discharged on antianginal and anti-hypertensive medication.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'high-density lipoprotein cholesterol': [45.0, 'mg/dL'], 'Triglycerides': [203.0, 'mg/dL'], 'Total cholesterol': [214.0, 'mg/dL']}",128.4,121.98,134.82,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 214.0 mg/dL. 
The concentration of hdl cholesterol is 45.0 mg/dL. 
The concentration of triglycerides is 203.0 mg/dL. 
Plugging in these values will give us 214.0 mg/dL - 45.0 mg/dL - (203.0/5) mg/dL = 128.4 mg/dL.
The patients concentration of LDL cholestrol is 128.4 mg/dL."
6408,44,LDL Calculated,lab test,decimal,pmc-2771785-1,Extracted,"An 81-year-old female patient with exertional dyspnea visited the emergency room of our hospital and complained of aggravated dyspnea and chest pain. She was diagnosed with hypertension 6 years ago, and has taken medicine without any additional examination since she was hospitalized for congestive heart failure 2 years ago.
At the time of her visit, her blood pressure was 150/95 mmHg, pulse rate 150 beats/min, respiratory rate 35 breaths/min, and body temperature 36.5℃. She was conscious and but looked ill. Thoracic auscultation revealed a Grade IV/VI pansystolic murmur at the apex, a continuous murmur along the left third sternal border, and a rale in both the lung fields.
No significant findings were seen in the abdomen, and 1+pitting edema was found in both the legs. The hemoglobin level was 12.9 g/dL, leukocyte 7,600/mm3, and blood platelet 235,000 mm3, and in arterial blood gas analysis, pH was 7.355, PCO2 28.7 mmHg, PO2 91.7 mmHg, HCO- 316.2 mM/L, and oxygen saturation 96.9%. Biochemical analysis was Na 141 mEq/L, K 5.2 mEq/L, Cl 109 mEq/L, blood urea nitrogen (BUN) 32.9 mg/ dL, creatinine 1.9 mg/dL with high N-terminal pro-B-type natruretic peptide (NT-proBNP) >35,000 pg/mL. Serological analysis showed creatine phosphokinase 108 IU/L, creatinine kinase-MB isoenzyme 7.5 ng/mL, troponin-I 0.58 µg/L, total cholesterol 218 mg/dL, low density lipoprotein 186 mg/dL, high density lipoprotein 30 mg/dL, and triglyceride 55 mg/dL. Chest X-ray showed dilatation of the left mediastinum accompanied by right axis deviation of the bronchus, and right costophrenic (CP) angle blunting with medium cardiomegaly, suggesting pleural effusion (). The electrocardiogram showed transient atrial fibrillation with approximately 150 beats/min pulse rate and left ventricular hypertrophy, and T wave inversion accompanied by ST-segment depression (2 mm-3 mm) in V3-V6 ().
In transthoracic echocardiography, left ventricle function was normal as 64% of ejection fraction, and no sign of regional wall motion abnormality. Left ventricle end-diastolic dimension was dilated as big as 52 mm (3.7 cm/m2) and the size of the left atrium was dilated as big as 42 mm (3 cm/m2) by M-mode. Doppler echocardiography showed a thick mitral valve and moderate mitral regurgitation and moderate pulmonary hypertension (right ventricle systolic pressure=60 mmHg) accompanied by tricuspid regurgitation. The aortic root was also dilated as big as 41 mm, abnormal blood flow from the aorta to the dilated pulmonary artery (31 mm) was suspected at the aortic root level on the parasternal short axis view, and aliasing flow (Vmax=2.3 m/s) was detected around the pulmonary artery ().
In the chest multi-detector CT, pulmonary edema was present in both lungs, with a slight pleural effusion in both thoracic cavities resulting in subsegmental atelectasis in the right lower and middle lobes. A large aortic aneurysm (about 7 cm) from the aortic arch out and downward was detected. The core was filled with low density thrombus, and the downside of aortic aneurysm connected with the main pulmonary artery, resulting in aortopulmonary fistula. Both the ascending aorta and pulmonary artery were also dilated to about 4.7 cm and 4.2 cm respectively. No compression of the surrounding organs, aortic dissection, or aortic rupture were detected ().
This aortopulmonary fistula by an aortic aneurysm caused heart failure. Although medical treatment was given before surgical treatment, heart failure worsened and pulmonary edema and pleural effusion were aggravated in the chest X-ray. She refused surgery because of her age and lack of a direct guardian. Though we tried medical treatment and thoracentesis, she died from refractory heart failure without aortic dissection or rupture 13 days after she was hospitalized.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Total cholesterol': [218.0, 'mg/dL'], 'Triglycerides': [55.0, 'mg/dL'], 'high-density lipoprotein cholesterol': [30.0, 'mg/dL']}",177,168.15,185.85,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 218.0 mg/dL. 
The concentration of hdl cholesterol is 30.0 mg/dL. 
The concentration of triglycerides is 55.0 mg/dL. 
Plugging in these values will give us 218.0 mg/dL - 30.0 mg/dL - (55.0/5) mg/dL = 177.0 mg/dL.
The patients concentration of LDL cholestrol is 177.0 mg/dL."
6409,44,LDL Calculated,lab test,decimal,pmc-3830285-1,Extracted,"A 37-year-old female was referred by Ophthalmologist to our endocrine unit with a presumptive diagnosis of acromegaly. She had primary complaints of increased watering from both eyes for the past 4 years, which increased on lying down and on exposure to sunlight. There had also been gradual protrusion of both the eyes (left > right) for the past 2-3 years. She had shown to multiple ophthalmologists earlier without much respite with the therapy. She had also received ayurvedic medications with no relief. The Ophthalmologist took note of her change in physical features and referred to the endocrine unit with a presumptive diagnosis of acromegaly.
She had noticed changes in physical appearance with gradual changes in face, feet and hands for the past 4 years. There had also been mild generalized headache for the past 3 years. She had been amenorrheic for 7 months. She had developed hypertension 2 years back. Examination revealed an average built female with body mass index - 25.6 kg/m2. There was frontal bossing, bulbous lips, prognathism, macroglossia, thickened skin of palms and feet and skin tags on the neck. Systemic examination was normal.
Eye examination revealed axial proptosis in the left eye with normaloculor motility and visual equity in both eyes. Lacrimal gland was enlarged in both eyes (left > right) []. Schirmer's test was normal.
Lab evaluation revealed normal hemogram, liver function and kidney function tests. Fasting and postprandial blood glucose levels were in the diabetic range (201 mg/dl and 220 mg/dl respectively) and lipid profile was deranged (T. cholesterol - 208 mg/dl, high density lipoprotein - 46 mg/dl, low density lipoprotein - 122 mg/dl, very low density lipoprotein - 40 mg/dl and triglycerides - 207 mg/dl). Hormone profile showed normal thyroid function test (TFT) and cortisol. Prolactin levels were 52.4 ng/ml and S. testosterone was low with normal luteinizing hormone (LH) and follicle stimulating hormone (FSH) levels (S. testosterone - 1.75 nmol/l, LH - 2.8 mIU/ml and FSH - 3.7 mIU/ml). Basal and post-glucose GH levels were elevated (0 h - 69.5 ng/ml, 1 h post-glucose GH - 358 ng/ml).
Magnetic resonance imaging (MRI) brain showed a moderately enhancing sellar mass (1.6 cm × 2.2 cm × 2.3 cm) with extension into suprasellar cistern and left cavernous sinus causing left internal carotid artery encasement suggestive of pituitary macroadenoma.
MRI orbit revealed proptosis left eye with bilateral lacrimal gland enlargement [Figure and ].",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Total cholesterol': [208.0, 'mg/dL'], 'Triglycerides': [207.0, 'mg/dL'], 'high-density lipoprotein cholesterol': [46.0, 'mg/dL']}",120.6,114.57,126.63,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 208.0 mg/dL. 
The concentration of hdl cholesterol is 46.0 mg/dL. 
The concentration of triglycerides is 207.0 mg/dL. 
Plugging in these values will give us 208.0 mg/dL - 46.0 mg/dL - (207.0/5) mg/dL = 120.6 mg/dL.
The patients concentration of LDL cholestrol is 120.6 mg/dL."
6410,44,LDL Calculated,lab test,decimal,pmc-6439373-1,Extracted,"In October 2015, a 40-year-old female patient with a history of sinus venous thrombosis and hypertension sought medical consultation. Her blood pressure was resistant despite treatment. She had a good NYHA Class I/IV and exercised frequently. She was adherent to dietary approach to stop hypertension (DASH) and regularly attended medical visits.
A review of systems was negative. She did not have toxic habits. On her physical exam she had normal respiratory sounds, her cardiac exam was normal without murmurs or rubs, the heart sounds were regular and rhythmic, and her point of maximal impulse (PMI) was non-displaced. No murmurs nor bruits were found on her anterior abdomen or on her lumbar regions. Her body mass index was measured at 20 kg/m2.
Her prior treatment plan included verapamil 160 mg po qd, losartan 100 mg po qd, hydrochlorothiazide 25 mg po qd, aspirin 100 mg po qd, and clopidogrel 75 mg po qd. Despite treatment, the patient was found with diastolic blood pressures >100 mmHg. In that visit, verapamil was increased to 240 mg po qd.
Her laboratory results included: creatinine 0.55 mg/dL (NV 0.4–1.1 mg/dL), BUN 11.4 mg/dL (NV 3–20 mg/dL), K 4.27 mEq/L (NV 3.5–5.1 mEq/L), glucose 86 mg/dL (NV 70–99 mg/dL), total cholesterol 191 mg/dL (NV < 200 mg/dL), HDL 65 mg/dL (NV 50–60 mg/dL), triglycerides 72 mg/dL (NV < 100 mg/dL), and uric acid 2 mg/dL (NV 1.9–7.5 mg/dL). She had a normal electrocardiogram and transthoracic echocardiogram.
Based on the results of the October 2015 visit, the treatment plan was changed to: verapamil/trandolapril 240/4 mg po qd, hydrochlorothiazide 25 mg po qd, and spironolactone 25 mg po qd. In addition, ambulatory blood pressure monitoring (ABPM) was ordered as a precautionary measure (Figure ).
She was seen again in December of 2015; the ABPM showed good blood pressure control, but the patient complained of intolerance to spironolactone, which was subsequently stopped (Figure ).
A renal artery Doppler was completed in March of 2016 with all results being normal.
In July 2016, the patient complained of frontal headaches that were resolved with conventional analgesics. Her systolic blood pressure was 170 mmHg, so her treatment plan was supplemented with prazosin 3 mg po qd and eplerenone 25 mg po qd.
Despite the pharmacological changes, her blood pressure remained greater than 160/100 mmHg.
In May 2017, an angio-CT of the renal arteries was performed (Figures and ), and it showed bilateral renal fibromuscular dysplasia. The right renal artery was 100% abnormal, and the left renal artery was affected on its distal third.
A subsequent Doppler of renal arteries was completed in June 2017 (Figure ) and showed abnormal findings. The right renal/aortic index was 3.9; a high suspicion of FMD exists when the renal/aortic index is greater than 3.5. The peak-systolic velocity at the right renal artery was measured at 267 cm/s with a stenosis of 60%. The left renal artery was normal; a possible explanation for this normal finding could be the distal FMD at the left renal artery found in the angio-CT. The intra-renal blood flow had a spectrum type tardus et parvus, prolonged acceleration times, and normal resistance indexes.
The patient underwent renal arteriography (Figure ) and balloon angioplasty in June 2017. The most critical stenosis had a 5 mm diameter on the left side and 6 mm on the right side. 5 × 40 mm and 6 × 20 mm balloons were used on the left side, inflated to 8 atmospheres for two and a half minutes. The right side (more severely affected by FMD) was treated with a 6 × 20 mm balloon starting on the distal part of the vessel, inflated to 8 atmospheres for two and a half minutes. The medium and proximal thirds of the vessel were treated with a 6 × 20 mm balloon, inflated to 10 atmospheres.
There was a good angiographic result after the procedure, the stenosis improved significantly and there were no spasms or dissections observed. There were no complications. The patient remained in the clinic for a short period to monitor for possible complications and variations in her blood pressure.
After discharge, the patient has displayed good control of blood pressure; she is under treatment with only losartan/amlodipine 50/2.5 mg po qd. She has been asymptomatic and in good overall clinical condition.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Total cholesterol': [191.0, 'mg/dL'], 'Triglycerides': [72.0, 'mg/dL'], 'high-density lipoprotein cholesterol': [65.0, 'mg/dL']}",111.6,106.02,117.18,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 191.0 mg/dL. 
The concentration of hdl cholesterol is 65.0 mg/dL. 
The concentration of triglycerides is 72.0 mg/dL. 
Plugging in these values will give us 191.0 mg/dL - 65.0 mg/dL - (72.0/5) mg/dL = 111.6 mg/dL.
The patients concentration of LDL cholestrol is 111.6 mg/dL."
6411,44,LDL Calculated,lab test,decimal,pmc-4937936-1,Extracted,"The 26-year-old Chinese lady was an immigrant from the Inner Mongolia and incidentally found in the 8th week of pregnancy. She had being lived on cow milk products for 24 years in Inner Mongolia before she married a man in Guilin. As an aboriginal inhabitant, fresh milk and milk products were her favorite. She had 1-year history of renal biopsy-proven MGN with persistent proteinuria (2.5–5.5 g/24 hours). The lady was admitted to the Affiliated Hospital of Guilin Medical University in March 2014.
The patient was first admitted to the People's Hospital of Guilin with complaints of generalized edema in her face and legs in March 2013. No other abnormalities had previously been detected on her annual physical examinations.
The results of physical examination revealed normal, except for 2+ pitting pretibial edema and lower eyelids swelling. Laboratory measurements were as follows: total serum protein, 44.8 g/L (normal 60–80 g/L); albumin, 24.6 g/L (normal 35–50 g/L); total cholesterol, 7.91 mmol/L (normal 3.1–6.0 mmol/L), triglycerides, 1.22 mmol/L (normal 0.48–1.6 mmol/L), high-density lipoprotein, 1.49 mmol/L (normal 1.0–1.9 mmol/L); and low-density lipoprotein, 4.43 mmol/L (normal 2.1–3.36 mmol/L). The levels of liver enzymes, blood electrolytes, and the results of blood routine examination were basically within the normal ranges. Urinalysis showed the presence of urine dipstick protein of 3+, 24-hour urine protein level of 5.5 g/day (normal 0.04–0.23), blood urea nitrogen of 2.65 mmol/L (normal 3.2–7.5 mmol/L), and creatinine of 55.5 μmol/L (normal 44–115 μmol/L).
She was hospitalized to have percutaneous kidney biopsy performed on the 21st March, 2013. Renal tissues were obtained by core needle biopsy under ultrasound control on the basis of written informed consent from the patient. One third each of the renal biopsy specimen was processed for histochemical stains (HE, periodic acid-Schiff [PAS], periodic Schiff-methenamine, and Masson trichrome) with light microscopy; immunofluorescence stains for the monoclonal IgG, IgA, IgM, C1q, and C3c; and ultrastructural examination with transmission electron microscopy (Supplementary methods).
PAS stain with light microscopy showed diffused thickening of GBM (Figs. –). Mesangial expansion, proliferation, and sclerosis, and hyalinosis of glomerular arterioles and intralobular arteries were not significant.
Silver stain of periodic Schiff-methenamine highlighted the irregular GBM thickening due to subepithelial deposits to form spikes (Figs. –). The spikes were not evident by stains of HE, PAS, and Masson trichrome.
Immunofluorescence microscopy demonstrated strong global granular GBM reactivity for IgG (3+, Fig. ). Immunofluorescence for IgA, IgM, C1q, and C3c was not significant.
Electron microscopy pinpointed diffuse, irregular, and numerous electron-dense deposits along the GBM in subepithelial spaces (Fig. ).
Tubular changes mainly occurred in the proximal convoluted tubules and were characterized by loss of tubular brush border and formation of lipid peroxidation (Fig. ). Characteristic changes in interstitial compartments were lipid-laden foam cell infiltration (Fig. ).",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Total cholesterol': [7.91, 'mmol/L'], 'Triglycerides': [1.22, 'mmol/L'], 'high-density lipoprotein cholesterol': [1.49, 'mmol/L']}",227.2154,215.85463,238.57617,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 7.91 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of total cholesterol from mmol to mg. The mass of total cholesterol is 7.91 mmol. To convert 7.91 mmol of total cholesterol to mol, multiply by the conversion factor 0.001, giving us 7.91 mmol total cholesterol * 0.001 mol/mmol = 0.00791 mol total cholesterol. To convert from mol total cholesterol to grams, multiply by the molar mass 386.654 g/mol, which will give 0.00791 mol total cholesterol * 386.654 g/mol = 3.05843 g total cholesterol. To convert 3.05843 g of total cholesterol to mg, multiply by the conversion factor 1000.0, giving us 3.05843 g total cholesterol * 1000.0 mg/g = 3058.43 mg total cholesterol. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 3058.43 mg total cholesterol/10.0 dL = 305.843 mg total cholesterol/dL. The concentration value of 7.91 mmol total cholesterol/L converts to 305.843 mg total cholesterol/dL. 
The concentration of hdl cholesterol is 1.49 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of hdl cholesterol from mmol to mg. The mass of hdl cholesterol is 1.49 mmol. To convert 1.49 mmol of hdl cholesterol to mol, multiply by the conversion factor 0.001, giving us 1.49 mmol hdl cholesterol * 0.001 mol/mmol = 0.00149 mol hdl cholesterol. To convert from mol hdl cholesterol to grams, multiply by the molar mass 386.654 g/mol, which will give 0.00149 mol hdl cholesterol * 386.654 g/mol = 0.57611 g hdl cholesterol. To convert 0.57611 g of hdl cholesterol to mg, multiply by the conversion factor 1000.0, giving us 0.57611 g hdl cholesterol * 1000.0 mg/g = 576.11 mg hdl cholesterol. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 576.11 mg hdl cholesterol/10.0 dL = 57.611 mg hdl cholesterol/dL. The concentration value of 1.49 mmol hdl cholesterol/L converts to 57.611 mg hdl cholesterol/dL. 
The concentration of triglycerides is 1.22 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of triglycerides from mmol to mg. The mass of triglycerides is 1.22 mmol. To convert 1.22 mmol of triglycerides to mol, multiply by the conversion factor 0.001, giving us 1.22 mmol triglycerides * 0.001 mol/mmol = 0.00122 mol triglycerides. To convert from mol triglycerides to grams, multiply by the molar mass 861.338 g/mol, which will give 0.00122 mol triglycerides * 861.338 g/mol = 1.05083 g triglycerides. To convert 1.05083 g of triglycerides to mg, multiply by the conversion factor 1000.0, giving us 1.05083 g triglycerides * 1000.0 mg/g = 1050.83 mg triglycerides. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1050.83 mg triglycerides/10.0 dL = 105.083 mg triglycerides/dL. The concentration value of 1.22 mmol triglycerides/L converts to 105.083 mg triglycerides/dL. 
Plugging in these values will give us 305.843 mg/dL - 57.611 mg/dL - (105.083/5) mg/dL = 227.2154 mg/dL.
The patients concentration of LDL cholestrol is 227.2154 mg/dL."
6412,44,LDL Calculated,lab test,decimal,pmc-4209686-1,Extracted,"A 47-year-old woman diagnosed with type 1 diabetes at the age of 15 years and on subcutaneous insulin injections (insulin analog aspart) was admitted to the hospital with complaint of unsightly painless swelling in the lower abdomen at the injection site, which she noticed to be gradually increasing in size over the past 10 years. She also gave past history of recurrent abscesses at the same site.
On examination, the patient was of lean build with a body weight of 69 kg and a height of 167 cm with a body mass index of 24.7 kg/m2. Blood pressure and pulse were normal. No pedal or sacral edema or lymphadenopathy noted. Chest and the cardiovascular system were normal. Abdominal examination revealed the presence of a large mass measuring 8 × 8 cm in left lower paraumbilical region []. The mass was firm to hard with irregular surface and in the subcutaneous plane with restricted mobility. Overlying skin was scarred. No other clinical abnormality was evident. Hematological and some biochemical investigations were practically normal (complete blood count, blood urea, creatinine, liver function tests, electrolytes, and and thyroid function tests). Glycosylated hemoglobin was 12.0% and fasting blood glucose was 371 mg/dl. Serum calcium and phosphorous levels were 9.3 mg/dl and 3.7 mg/dl respectively. Lipid profile revealed cholesterol of 178, triglycerides 81, high density lipoproteins 39, and low density lipoproteins 123. Electrocardiogram and X-ray chest was normal. A diagnosis of lipodystrophy at insulin injection site was made in view of the past history, clinical, and laboratory investigations. Patient was posted for a mini abdominoplasty to remove redundant skin and for cosmetic purpose after control of blood sugar. Intraoperative findings showed necrotic subcutaneous fat with calcified areas corresponding to the swelling in the left lower abdomen. Partial excision was done as the swelling was found to be attached to the overlying skin. Histopathology revealed areas of fat necrosis with foreign body giant cell reaction along with thick fibrocollagenous tissue with extensive deposits of calcium (dystrophic calcification) [].
Postoperatively, the patient was advised to avoid the abdominal site for injecting insulin and was instructed to use the multiple rotation method for injections. Subsequently, the glycemic control improved marginally with fasting blood glucose falling to 179 mg/dl.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Total cholesterol': [178.0, 'mg/dL'], 'Triglycerides': [81.0, 'mg/dL'], 'high-density lipoprotein cholesterol': [39.0, 'mg/dL']}",122.8,116.66,128.94,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 178.0 mg/dL. 
The concentration of hdl cholesterol is 39.0 mg/dL. 
The concentration of triglycerides is 81.0 mg/dL. 
Plugging in these values will give us 178.0 mg/dL - 39.0 mg/dL - (81.0/5) mg/dL = 122.8 mg/dL.
The patients concentration of LDL cholestrol is 122.8 mg/dL."
6413,44,LDL Calculated,lab test,decimal,pmc-4363061-1,Extracted,"A 23-year-old Chinese man presented with edema in both legs and a mass in ulnar side of his right upper arm on August 8th 2013. The patient reported that the edema had been present for 11 days and that the mass had been palpable for 3 years, and was first detected in October 2010. According to the patient’s recollection, it had apparently increased in size since June 2013 with accompanying warmth of the overlying skin. The patient had not received any prior treatment for these conditions.
Before admission to our hospital, the patient developed worsened lower limb edema, abdominal distention, and oliguria. Two days later, an ultrasound examination revealed swollen lymph nodes in the medial aspect of his right upper arm, proximal to the elbow. Because the appearance of the swollen nodes was consistent with inflammation, the patient was prescribed cefprozil, which resulted in a reduction in the swelling.
The patient was admitted on August 19th 2013 as a result of edema, severe proteinuria, and low serum albumin levels. Tender epitrochlear nodes that were poorly mobile were palpable in his right upper arm, with the largest being approximately 30 × 20 mm in size in physical examination. Hematology revealed a white blood cell count of 7.7 × 109 cells/L, 48.5% eosinophils, and a platelet count of 172 × 109 platelets/L. Urinalysis revealed 4+ albuminuria and 2+ red blood cells per high power field. His 24-hour urinary protein excretion was 9,3g. A blood panel yielded the following results: total serum protein, 50.3 g/L; serum albumin, 16 g/L; serum cholesterol; 13.36 mmol/L; serum triglycerides, 1.85 mmol/L; high-density lipoprotein, 2.32 mmol/L; and low-density lipoprotein level, 9.37 mmol/L. In immunological tests, IgE level was as high as 1,510 IU/ml (reference value 0-100 IU/ml), with normal C3, C4, IgG, IgA, and IgM (1.54g/L, 0.37g/L, 5.82g/L, 3.69g/L and 1.44g/L respectively).
On magnetic resonance imaging (MRI) examination, a soft tissue-density mass was observed within the right medial upper arm, distributed along the brachial artery (Figure A). A biopsy of the epitrochlear nodes revealed eosinophilic hyperplastic lymphogranulomatous tissue. A renal biopsy indicated focal segmental glomerulosclerosis (FSGS) (cellular variant) with no infiltration of eosinophil in renal interstitium (Figure B). The results of immune-staining on the renal biopsy were negative for immunoglobulin G (IgG), IgA, IgM, C3 and C1q. The electron microscopic analysis showed podocyte effacement. Analysis of a bone marrow sample obtained by aspiration indicated an abnormally high proportion of eosinophils (total eosinophils 14%, metamyelocyte eosinophils, 2%; rod nuclear eosinophils, 2%; and leaf nuclear eosinophils, 10%). A bone marrow biopsy showed a predominance of eosinophils among the granulocytes. The patient had a normal karyotype, and mutation screening from a peripheral blood sample revealed no gene fusions of FIP1L1-PDGFRα and ETV6-PDGFRβ. No abnormalities were identified at 8p12/8p11.1-q11.1 using fluorescence in situ hybridization and the V617F single nucleotide polymorphism of JAK2.
The final diagnosis for this patient was KD associated with nephrotic syndrome (FSGS, cellular variant). He was given intravenous methylprednisolone (80 mg/day) for 3 days beginning on August 29th, 2013, followed by oral methylprednisolone (36 mg/d, once a day). Meanwhile, he received famotidine (20 mg, twice a day), rocaltrol (0.25 μg, once a day), and caltrate D (300 mg, twice a day) for symptomatic treatment. Six days after the initiation of glucocorticoid treatment, the edema had largely resolved, his serum albumin levels had improved, and his urine was negative for proteinuria. Additionally, the tumor-like mass reduced in size, and his eosinophil ratio and eosinophil counts normalized. Two weeks later, the serum albumin levels had increased to within the normal range and only one soft, smooth, mobile lymph node (5 × 5 mm cross-sectional area) was palpable in his right arm. Therefore, the patient was discharged on September 17th 2013. After a 2-month period of methylprednisolone at a dose of 36 mg/day, the prescribed methylprednisolone dose was tapered by 4 mg every 2 weeks until a maintenance dose of 8 mg/day was reached. During the year following discharge, serum albumin levels and urinalysis test results remained normal and no relapses occurred.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Total cholesterol': [13.36, 'mmol/L'], 'Triglycerides': [1.85, 'mmol/L'], 'high-density lipoprotein cholesterol': [2.32, 'mmol/L']}",394.9964,375.24658,414.74622,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 13.36 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of total cholesterol from mmol to mg. The mass of total cholesterol is 13.36 mmol. To convert 13.36 mmol of total cholesterol to mol, multiply by the conversion factor 0.001, giving us 13.36 mmol total cholesterol * 0.001 mol/mmol = 0.01336 mol total cholesterol. To convert from mol total cholesterol to grams, multiply by the molar mass 386.654 g/mol, which will give 0.01336 mol total cholesterol * 386.654 g/mol = 5.1657 g total cholesterol. To convert 5.1657 g of total cholesterol to mg, multiply by the conversion factor 1000.0, giving us 5.1657 g total cholesterol * 1000.0 mg/g = 5165.7 mg total cholesterol. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 5165.7 mg total cholesterol/10.0 dL = 516.57 mg total cholesterol/dL. The concentration value of 13.36 mmol total cholesterol/L converts to 516.57 mg total cholesterol/dL. 
The concentration of hdl cholesterol is 2.32 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of hdl cholesterol from mmol to mg. The mass of hdl cholesterol is 2.32 mmol. To convert 2.32 mmol of hdl cholesterol to mol, multiply by the conversion factor 0.001, giving us 2.32 mmol hdl cholesterol * 0.001 mol/mmol = 0.00232 mol hdl cholesterol. To convert from mol hdl cholesterol to grams, multiply by the molar mass 386.654 g/mol, which will give 0.00232 mol hdl cholesterol * 386.654 g/mol = 0.89704 g hdl cholesterol. To convert 0.89704 g of hdl cholesterol to mg, multiply by the conversion factor 1000.0, giving us 0.89704 g hdl cholesterol * 1000.0 mg/g = 897.04 mg hdl cholesterol. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 897.04 mg hdl cholesterol/10.0 dL = 89.704 mg hdl cholesterol/dL. The concentration value of 2.32 mmol hdl cholesterol/L converts to 89.704 mg hdl cholesterol/dL. 
The concentration of triglycerides is 1.85 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of triglycerides from mmol to mg. The mass of triglycerides is 1.85 mmol. To convert 1.85 mmol of triglycerides to mol, multiply by the conversion factor 0.001, giving us 1.85 mmol triglycerides * 0.001 mol/mmol = 0.00185 mol triglycerides. To convert from mol triglycerides to grams, multiply by the molar mass 861.338 g/mol, which will give 0.00185 mol triglycerides * 861.338 g/mol = 1.59348 g triglycerides. To convert 1.59348 g of triglycerides to mg, multiply by the conversion factor 1000.0, giving us 1.59348 g triglycerides * 1000.0 mg/g = 1593.48 mg triglycerides. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 1593.48 mg triglycerides/10.0 dL = 159.348 mg triglycerides/dL. The concentration value of 1.85 mmol triglycerides/L converts to 159.348 mg triglycerides/dL. 
Plugging in these values will give us 516.57 mg/dL - 89.704 mg/dL - (159.348/5) mg/dL = 394.9964 mg/dL.
The patients concentration of LDL cholestrol is 394.9964 mg/dL."
6414,44,LDL Calculated,lab test,decimal,pmc-3438269-1,Extracted,"A 52-year-old male was transferred to our hospital because of skin necrosis on his left arm. Forty-eight years ago, he had experienced a severe scalding burn on his left arm from boiling water. Two months ago, he had undergone acupuncture treatment at a private oriental clinic because of a tingling sensation in his left elbow and wrist. Uncontrolled skin ulcers developed at the acupuncture site and he had skin grafts at a local plastic surgery clinic, but the wound continued to worsen. At admission, the circulation of the left arm was poor and the grafted skin was nearly necrotized. He had been on anti-hypertensive medication 5 years ago. He had no history of angina or dyspnea on exertion. He also had no history of smoking, alcohol intake, or specific familial disease including coronary artery disease.
The patient's blood pressure was 92/54 mm Hg on the left arm and 140/80 mm Hg on the right arm. Blood chemistry analysis showed that total cholesterol was 128 mg/dL, triglyceride was 190 mg/dL, high density lipoprotein was 32 mg/dL, and low density lipoprotein was 61 mg/dL. The erythrocyte sedimentation rate was 76 mm/hour (normal range 1-20) and high-sensitivity C-reactive protein was 94.9 mg/L (normal range ≤8.0). Blood test results for autoimmunity showed positive anti-nuclear antibody and negative anti-neutrophilic cytoplasmic antibody. Upper extremity angiography was performed for a possible musculo-cutaneous flap operation. The left axillary artery showed aneurismal change with distal total occlusion and the right axillary and brachial arteries had multiple aneurismal changes (). A biopsy was performed from the skin and subcutaneous nodule and the pathological findings were compatible with PAN (). During his inpatient stay, the patient had resting chest discomfort and a consultation was made with our cardiovascular team for coronary angiography. The electrocardiography was normal except for the Q wave at lead III. The total creatinine kinase was 38 IU/L (normal range 38-160) and creatine kinase-MB was 0.7 ng/mL (normal range 0-3.6). The echocardiography showed normal left ventricular wall motions with an ejection fraction of 58%. The left coronary angiography showed large aneurysms on both the left anterior descending and left circumflex coronary arteries with CTO on distal segments (). The proximal right coronary artery (RCA) also showed huge aneurismal change with CTO lesion (). After these investigations, the patient was prescribed with immunosuppressive agents and anti-anginal medications with aspirin and statin.",What is the patient's LDL cholestrol concentration? Please outuput your answer in terms of mg/dL. You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Total cholesterol': [128.0, 'mg/dL'], 'Triglycerides': [190.0, 'mg/dL'], 'high-density lipoprotein cholesterol': [32.0, 'mg/dL']}",58,55.1,60.9,"To compute the patient's LDL cholestrol, apply the following formula: LDL cholesterol = total cholesterol - HDL - (triglycerides / 5), where the units for total cholestrol, HDL cholesterol, and triglycerides are all mg/dL.
The concentration of total cholesterol is 128.0 mg/dL. 
The concentration of hdl cholesterol is 32.0 mg/dL. 
The concentration of triglycerides is 190.0 mg/dL. 
Plugging in these values will give us 128.0 mg/dL - 32.0 mg/dL - (190.0/5) mg/dL = 58.0 mg/dL.
The patients concentration of LDL cholestrol is 58.0 mg/dL."
6415,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-5711,Extracted,"A 32-year-old man is brought into the emergency department by his friends. The patient was playing soccer when he suddenly became short of breath. The patient used his albuterol inhaler with minimal improvement in his symptoms. He is currently struggling to breathe. The patient has a past medical history of asthma and a 25 pack-year smoking history. His current medications include albuterol, fluticasone, and oral prednisone. His temperature is 99.5°F (37.5°C), blood pressure is 137/78 mmHg, pulse is 120/min, respirations are 27/min, and oxygen saturation is 88% on room air. On pulmonary exam, the patient exhibits no wheezing with bilateral minimal air movement. The patient’s laboratory values are ordered as seen below.

Hemoglobin: 15 g/dL
Hematocrit: 43%
Leukocyte count: 5,500/mm^3 with normal differential
Platelet count: 194,000/mm^3

Serum:
Na+: 138 mEq/L
Cl-: 102 mEq/L
K+: 4.4 mEq/L
HCO3-: 24 mEq/L
BUN: 20 mg/dL
Glucose: 120 mg/dL
Creatinine: 1.0 mg/dL
Ca2+: 10.2 mg/dL
pH: 7.44
PaCO2: 10 mmHg
PaO2: 60 mmHg
AST: 12 U/L
ALT: 10 U/L

The patient is started on an albuterol nebulizer, magnesium sulfate, and tiotropium bromide. Repeat vitals reveal an oxygen saturation of 90% with a pulse of 115/min.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [137.0, 'mm hg'], 'respiratory rate': [27.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Confusion': False, 'Diastolic Blood Pressure': [78.0, 'mm hg'], 'age': [32, 'years']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 32 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 20.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 27 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 137 mm Hg. The patient's diastolic blood pressure is 78 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6416,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-6306916-1,Extracted,"A 42-year-old Hispanic man with diabetes mellitus (DM) type 2 diagnosed five years ago and regularly treated with glybenclamide 5 mg once daily. Otherwise, the patient’s personal and familiar past medical history was unremarkable. He also denied consumption of alcohol, cigarettes, and illegal drugs. He presented to emergency department (ED) on 1 September 2017 with a history of malaise, headache, fever, and generalized body pain during the last 6 days. Three days before admission, he developed watery diarrhea (3 to 4 times a day), tachypnea, and confusion. During the following days, malaise and bowel movement frequency increased (up to 6 times a day). On the day of admission, the patient became drowsy, dyspneic, and looked very ill.
Physical examination: Body weight 50 kg, Body Mass Index 16.8 kg/m2, blood pressure: 60/30 mmHg, respiratory rate: 32 bpm, heart rate: 78 bpm, axillar temperature: 36 °C, SatO2: 99% (FiO2: 0.21); the patient was severely dehydrated, thyroid gland was not palpable; respiratory system: tachypnea, Kussmaul’s breathing; cardiovascular system: Sweaty mottled skin, and cold extremities with prolonged capillary refill time; neurologic system: Tremor in both hands, patellar and ankle hyperreflexia.
Lab: Hemoglobin 12.9 g/dL, hematocrit 40, platelets 198,000/mm3, white blood cells 10,100/mm3, segmented neutrophils 70%, bands 1%; serum glucose 460 mg/dL, urea 115 mg/dL, creatinine 1.3 mg/dL. Arterial blood gas analyses (ABG) are shown in . Liver function tests were normal, except for hypoalbuminemia and hypoproteinemia (3.0 g/dL and 5.18 g/dL, respectively). Urinalysis: pH 5, urine density 1030, leukocytes 2–4/field, granular casts 3+, glucose 3+, ketones 2+, and leucocyte esterase was negative.
Treatment with intravenous normal saline, potassium chloride, insulin infusion, sodium bicarbonate, norepinephrine, and empiric antibiotics (ceftriaxone + metronidazole) was administered. After 10 h of intensive treatment, ABG did not change significantly. So, differential diagnosis was extended and complementary exams were ordered: plasmatic amylase 96 U/L (reference range: 28–100 U/L), lipase 17 U/L (13–60 U/L), TSH 0.024 μIU/L (adult reference range: 0.27–4.2 μIU/L), free-T4 2.16 ng/dL (reference range: 0.82–1.63 ng/dL), total-T3 0.18 ng/mL (reference range: 0.5–2.0 ng/mL), free-T3 0.42 pg/mL (reference range: 2.1–3.8 pg/mL); CPK-MB 101.3 U/L (reference range: 0–25 U/L), total CPK 505.7 U/L (normal: 39–308 U/L); troponin T 25.0 ng/mL (reference range: 0.12–0.6 ng/mL). Based on these results, hydrocortisone 100 mg every 8 h, methimazole 20 mg every 8 h, and Lugol’s solution 10 drops every 8 h, were added on the second day of treatment. Because of shock, beta-blocker was not administered. On the third day of treatment a good evolution was observed, norepinephrine and insulin infusion were discontinued, and NPH insulin was initiated. Based on physical examination, chest x-ray (CXR) ( and ), and progressive decrease in partial oxygen pressure () compatible with acute lung edema, intravenous furosemide 20 mg every 12 h was administered for 2 days.
Although ECG was normal, troponin determinations were repeated over the next days and persisted elevated. Echocardiography (5 September 2017) showed borderline pulmonary artery systolic pressure (35 mm Hg), severe LV systolic dysfunction (LV ejection fraction 35%), diastolic dysfunction of restrictive type and global hypokinesia ().
On the 6th day of treatment, hydrocortisone and Lugol’s solution were stopped, and methimazole was reduced by half. The patient was discharged on 7 September 2017, with almost complete recovery.
We also performed other complementary exams: Twenty-four hour-urine sodium, chloride, and potassium levels were also normal. Direct stool examination showed 0–1 leucocytes/HPF, no parasites, no blood, no erythrocytes. Urine culture and HIV serology was negative. Anti-TPO and anti-thyroglobulin antibodies were negative. Cardiac catheterization and endomyocardial biopsy were not performed. Follow-up echocardiography at 6 months was completely normal. After the patient was discharged, no additional (blood or imaging) study was performed, other than echocardiography.
Written informed consent was obtained from the patients for publication of this article and accompanying images.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [42, 'years'], 'Systolic Blood Pressure': [60.0, 'mm hg'], 'Diastolic Blood Pressure': [30.0, 'mm hg'], 'respiratory rate': [32.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [115.0, 'mg/dL'], 'Confusion': True}",4,4,4,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 42 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient has confusion, 1 point is added to score making the current total 0 + 1 = 1.
The concentration of BUN is 115.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 32 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 2 + 1 = 3.
The patient's systiolic blood pressure is 60 mm Hg. The patient's diastolic blood pressure is 30 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 3 + 1 = 4.
The patient's CURB-65 score is 4."
6417,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-5704843-1,Extracted,"An 85-year-old male presented to our hospital with a 2-month history of a productive cough with white phlegm and a 2-day history of hemoptysis in October 2014. He reported no fever, chest pain, chills, night sweats, or dyspnea.
On physical examination, the patient was afebrile. His heart rate was 80 beats per minute and regular, blood pressure 136/72 mm Hg, respiratory rate 20 breaths per minute, and oxygen saturation 99% while breathing ambient air. He was alert and not in acute distress. There was no lymphadenopathy in the neck. The lungs were clear and there were no heart murmurs. His abdomen was not tender, and there was no organomegaly. The neurological examination was unremarkable.
The patient's white blood cell (WBC) count was 3430/mL, with 51.3% neutrophils, 32.9% lymphocytes, and 10.8% monocytes; his hemoglobin was 117 g/L; his hematocrit was 38.9%; and his platelet count was 207,000/mL. The patient's C-reactive protein (CRP) level was normal. Serum chemistry tests showed the following results: sodium, 142.3 mmol/L; potassium, 3.9 mmol/L; chloride, 106.2 mmol/L; blood urea nitrogen, 5.9 mmol/L; creatinine, 86.3 μmol/L; aspartate aminotransferase, 21 U/L (normal range 15–40 U/L); and alanine aminotransferase, 16 U/L (normal range 9–50 U/L). The international normalized ratio was 1.02, the partial-thromboplastin time was 27.1 seconds, and the d-dimer level was 180 μg/L. The brain natriuretic peptide was 17.0 pg/mL; tumor marker tests revealed: carcinoembryonic antigen, 2.32 ng/mL; squamous cell carcinoma antigen, 0.90 ng/mL; neuron-specific enolase, 6.24 ng/mL; and CY211, 2.25 μg/L.
Computed tomography (CT) revealed a mass in the right lower lobe (Fig. A). Electrocardiography revealed sinus rhythm, with a ventricular rate of 79 beats per minute. No metastatic lesions were found on brain magnetic resonance imaging or in bone using emission CT.
The hemoptysis was treated with 30 mg of ambroxol and 600 mg of p-aminomethyl benzoic acid daily. Sputum cultures were negative. Lung function tests after inhaling 400 μg of albuterol yielded an FEV1/FVC = 59.7% and FEV1 = 46.2%. Bronchoscopy showed stenosis in the posterior basal segment of the right lower lobe (Fig. ). A CT-guided transthoracic needle lung biopsy showed SCLC after histopathological and immunohistochemical examinations (Fig. ).
Seven days after the transthoracic needle lung biopsy, the patient's temperature increased to 40°C and he developed a worsening cough with purulent sputum. Repeat laboratory tests showed a WBC count of 13,890/mL, with 87.0% neutrophils, 6.5% lymphocytes, and 0.9% monocytes; hemoglobin, 128 g/L; hematocrit, 38.70%; platelet count, 138,000/mL; and CRP, 88.0 mg/L. The patient was treated with cefuroxime (1.5 g) twice per day for 7 days and his WBC and CRP level normalized.
He refused radiotherapy or chemotherapy. After obtaining consent, we treated the tumor with RFA. Before RFA, we evaluated the size and spatial relationships of the tumor using CT and determined the needle angle and depth via the shortest route from the surface to the mass. The puncture point was infiltrated with 5 mL of 2% lidocaine. The multipolar needle was directed to avoid bone, large blood vessels, and pulmonary bullae. A rapid biopsy of the lung tumor was performed. Heating was directed to an area within 0.5 to 1 cm of the tumor margin and to the needle track (Fig. B). After closing the puncture wound, repeat CT showed pneumothorax (Fig. C), which was treated with bed rest and inhaled oxygen. The patient had some chest pain the next day, but there was no fever or hemoptysis in the first week after RFA.
At the 2-year follow-up examination, the efficacy of the RFA was evaluated as a partial response (PR) (Fig. D–G). The patient was last seen in January 2017, when he developed community-acquired pneumonia (Fig. H).",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [85, 'years'], 'Systolic Blood Pressure': [136.0, 'mm hg'], 'Diastolic Blood Pressure': [72.0, 'mm hg'], 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [5.9, 'mmol/L'], 'Confusion': False}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 85 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 1.
The concentration of BUN is 5.9 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of BUN from mmol to mg. The mass of BUN is 5.9 mmol. To convert 5.9 mmol of BUN to mol, multiply by the conversion factor 0.001, giving us 5.9 mmol BUN * 0.001 mol/mmol = 0.0059 mol BUN. To convert from mol BUN to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0059 mol BUN * 28.02 g/mol = 0.16532 g BUN. To convert 0.16532 g of BUN to mg, multiply by the conversion factor 1000.0, giving us 0.16532 g BUN * 1000.0 mg/g = 165.32 mg BUN. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 165.32 mg BUN/10.0 dL = 16.532 mg BUN/dL. The concentration value of 5.9 mmol BUN/L converts to 16.532 mg BUN/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 1.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 136 mm Hg. The patient's diastolic blood pressure is 72 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6418,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-6381853-1,Extracted,"A 42-year-old Saudi male from Jizan, with a comorbidity of hypertension and type 2 diabetes mellitus diagnosed 6 years prior (well controlled by oral antidiabetic agents: metformin 1000 mg twice daily and gliclazide 30 mg once daily), presented with impaired renal function and hematuria. After basic laboratory investigations, kidney biopsy was performed. Histological examination with light microscope revealed a global sclerosed glomeruli, minimal interstitial fibrosis and tubular atrophy []. A diagnosis of glomerulonephritis of unknown etiology was made and treatment with mycophenolate (1 g PO twice daily) and prednisone (20 mg PO once daily) was initiated.
After 3 months, the patient presented with a 3-week history of fever, abdominal pain and fatigue. The fever was subjective, intermittent, associated with chills and rigors, especially at night, and not relieved by paracetamol. The abdominal pain was intermittent, diffuse and colicky in nature and was associated with nausea and vomiting without blood (2–3 times/day). During these 3 weeks, the patient's appetite decreased, owing to which he lost 7 kg in weight. In addition, the patient reported a history of animal contact (goat and sheep), ingestion of raw goat milk and swimming in the valley water. There was no history of rash, cough, hemoptysis, jaundice, diarrhea, constipation, dysuria, change in urine color, arthralgia, visual disturbances, oral ulcers, genital rash, discharge or contact with tuberculosis patients.
On physical examination, the patient was found to be obese, sweating, not jaundiced or cyanosed. He was conscious, alert and oriented to time, place and person. His vital signs were as follows: body temperature, 38.6°C; pulse rate, 98 beats/min; respiratory rate, 24 breaths/min; blood pressure, 125/85 mmHg; and oxygen saturation, 100% on room air. He was pale, with normal jugular venous pressure and no oral ulcers or thrush. Abdominal examination revealed mild epigastric tenderness and a palpable liver 4 cm below the costal margin with a 15-cm liver span. The rest of the examinations were within normal limits.
Laboratory investigations on admission revealed a white blood cell (WBC) count of 2.65/mcL (neutrophils, 72.1%; lymphocytes, 23.2%; monocytes, 4%; and eosinophils, 0.7%). Results of other hematological examinations were as follows: hemoglobin level, 8.8 g/L; erythrocyte sedimentation rate, 88 mm/h; platelet count, 87,000/mcL; and reticulocyte count, 1.28%. Level of ferritin was 1000 ng/mL, with a transferrin saturation of 11.22 mg/dL. Estimation of electrolytes showed sodium 138 mEq/L, potassium 3.2 mEq/L and bicarbonate 25 mmol/L. Liver function tests showed that total protein was 6.1 g/dL, albumin 3.2 g/dL, total bilirubin 1.2 mg/dL, alanine transaminase 71 IU/L, aspartate transaminase 42 IU/L, alkaline phosphatase 179 IU/L and gamma-glutamyl transferase 447 IU/L. International normalized ratio was 0.8. Renal function tests showed that blood urea nitrogen was 12 mg/dL and creatinine 2.15 mg/dL. Level of lactate dehydrogenase was 732 U/L and C-reactive protein 53 mg/L. Urine analysis showed 2–5 WBCs/high-power field and 10–25 red blood cells/high-power field with no nitrites. Sickling test and direct/indirect Coombs test were negative, and the stool test result was normal.
Chest X-ray and electrocardiogram were normal. Abdominal ultrasound showed an enlarged liver (16.2-cm liver span) and a mildly enlarged spleen (14 cm in length). Kidneys were normal in size, with a mild increase in the echogenicity of renal parenchyma, but no hydronephrosis or ascites.
The serological tests for viral hepatitis, human immunodeficiency virus, Epstein–Barr virus, cytomegalovirus, Toxoplasma and Brucella were negative. Rheumatoid factor, antinuclear antibody, antineutrophil cytoplasmic antibody, antiglomerular basement membrane antibody, anti-Sjögren's syndrome A and B antibodies and cryoglobulin were negative. Malaria smear and blood cultures were also negative.
The patient's condition continued to deteriorate and he developed continuous fever of up to 40.5°C. Repeated tests after 5 days revealed the following: WBC, 1.4/mcL; hemoglobin, 6.7 g/dL; platelet, 55,000/mcL; creatinine, 3.3 mg/dL; C-reactive protein, 151 mg/L; total bilirubin, 2.9 mg/dL; alkaline phosphatase, 460 IU/L; alanine aminotransferase, 80 IU/L; aspartate aminotransferase, 138 IU/L; gamma-glutamyl transferase, 651 IU/L; albumin, 2.5 g/dL; and lactate dehydrogenase, 1400 U/L.
Bone marrow aspirate showed mild hypocellular marrow with no evidence of dysplasia or malignancy. Bone marrow culture for Brucella was negative. Further, Leishman-Donovan bodies were not detected by light microscope. Polymerase-chain reaction test for the diagnosis of tuberculosis, serological tests for dengue fever and Q fever as well as β-D-Glucan and galactomannan antigen tests were all negative. Liver biopsy showed granulomatous hepatitis with extramedullary hematopoiesis. After 1 week of admission, the patient was treated empirically with broad-spectrum antibiotic (meropenem intravenously, 1 g every 8 h for 6 days); however, there was no improvement.
Additional serological testing using enzyme-linked immunosorbent assay (ELISA) releveled the presence of anti-Leishmania antibodies. Based on this, the patient was started on liposomal amphotericin B course as a treatment for VL (4 mg/kg intravenous on Days 1–5, 10, 17, 24, 31 and 38), despite the lack of a definitive diagnosis. After 1 week, the patient improved clinically, the fever subsided, the laboratory parameters began to improve and at the end of liposomal amphotericin B course, all tests returned to normal.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [125.0, 'mm hg'], 'respiratory rate': [24.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [12.0, 'mg/dL'], 'Confusion': False, 'Diastolic Blood Pressure': [85.0, 'mm hg'], 'age': [42, 'years']}",0,0,0,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 42 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 12.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 24 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 0.
The patient's systiolic blood pressure is 125 mm Hg. The patient's diastolic blood pressure is 85 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 0.
The patient's CURB-65 score is 0."
6419,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-5557,Extracted,"A 71-year-old man presents to the emergency department for shortness of breath. The patient was returning from a business trip to China, when he suddenly felt short of breath during the taxi ride home from the airport. The patient has a past medical history of poorly controlled diabetes mellitus and a 50 pack-year smoking history. The patient is non-compliant with his medications and is currently only taking ibuprofen. An initial ECG demonstrates sinus tachycardia. A chest radiograph is within normal limits. Laboratory values are notable for a creatinine of 2.4 mg/dL and a BUN of 32 mg/dL as compared to his baseline creatinine of 0.9 mg/dL. His temperature is 98.8°F (37.1°C), pulse is 122/min, blood pressure is 145/90 mmHg, respirations are 19/min, and oxygen saturation is 93% on room air. On physical exam, you note an older gentleman in distress. Cardiac exam is notable only for tachycardia. Pulmonary exam is notable for expiratory wheezes.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [145.0, 'mm hg'], 'respiratory rate': [19.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [32.0, 'mg/dL'], 'Confusion': False, 'Diastolic Blood Pressure': [90.0, 'mm hg'], 'age': [71, 'years']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 71 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 1.
The concentration of BUN is 32.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 19 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 145 mm Hg. The patient's diastolic blood pressure is 90 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6420,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-12510,Extracted,"A 77-year-old woman is brought to the emergency department from her nursing home because she was found down overnight. On presentation she was found to be delirious and was unable to answer questions. Chart review shows that she is allergic to cephalosporins. Her temperature is 102.2°F (39°C), blood pressure is 105/52 mmHg, pulse is 94/min, and respirations are 23/min. Physical exam reveals a productive cough. A metabolic panel is obtained with the following results:

Serum:
Na+: 135 mEq/L
Cl-: 95 mEq/L
K+: 4 mEq/L
HCO3-: 19 mEq/L
BUN: 40 mg/dL
Creatinine: 2.5 mg/dL
Glucose: 150 mg/dL

Based on these findings two different drugs are started empirically. Gram stain on a blood sample is performed showing the presence of gram-positive organisms on all samples. One of the drugs is subsequently stopped.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [77, 'years'], 'Systolic Blood Pressure': [105.0, 'mm hg'], 'Diastolic Blood Pressure': [52.0, 'mm hg'], 'respiratory rate': [23.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [40.0, 'mg/dL'], 'Confusion': True}",4,4,4,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 77 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient has confusion, 1 point is added to score making the current total 1 + 1 = 2.
The concentration of BUN is 40.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 2 + 1 = 3.
The patient's respiratory rate is 23 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 3.
The patient's systiolic blood pressure is 105 mm Hg. The patient's diastolic blood pressure is 52 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 3 + 1 = 4.
The patient's CURB-65 score is 4."
6421,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-5410879-1,Extracted,"In June 2014, a 50-year-old man was brought to the emergency room with pain abdomen, high-grade fever with chills, generalized malaise, night sweats and significant weight loss (>10 kg in 45 days). The patient is a milk vendor by occupation in rural Bangalore and routinely consumes unpasteurized or raw milk due to a belief that raw milk is healthier. The patient is an ex-smoker and alcoholic with consuming about 20 g (whiskey) per day from 10 years. Patient's medical records and history from relatives revealed fever with night sweats and pain abdomen from 2 months for which he was evaluated as fever of unknown origin. The patient denied any recent travel or contact with persons having a similar illness.
His physical examination during admission was remarkable for fever (40°C), hypotension (BP: 86/60 mmHg), and increased respiratory (30 min–1) and heart (120 min–1) rates. He was severely dehydrated and pale, but no scleral icterus, clubbing, cyanosis, edema or lymphadenopathy was noted. Systemic examination of the abdomen showed tenderness in the left hypochondriac region. The liver was nontender with normal span. The spleen was not palpable but castell's sign was elicited (dullness noted in lower eighth intercostal space on inspiration). Cardiovascular and respiratory system examination was normal. Nervous system examination was normal.
Investigations revealed total white blood cell count of 32 100 mm–3 (neutrophils 64%, lymphocytes 30%, eosinophils 3% and monocytes 3%), ESR of 100 mm/h, C-reactive protein of 92 mg/l, hemoglobin of 10 mg/dl and platelet count was 199 000 μm–1. The arterial blood gasses had pH of 7.36, a PO2 of 68 mmHg, PCO2 of 35.5 mmHg and 17.9 mmol/l of bicarbonate. Renal function test was abnormal with creatinine of 2.0 mg/dl and blood urea of 70 mg/dl. Liver function test was normal. Electrocardiogram showed tachycardia and nonspecific ST–T changes in leads 2 and aVF. Echocardiography was normal with the ejection fraction of 60% and no features of endocarditis were found.
Brucella slide and tube agglutination tests (Wright, at 1/640) were positive. Ultrasound abdomen and computerized tomography of the abdomen showed splenomegaly and well-demarcated hypodense lesion, which is nonenhancing and measuring 3.2 × 2.8 × 2.8 cm in the upper pole of spleen with perisplenic fat stranding. Blood cultures confirmed infection by Brucella melitensis on Day 1 and Day 3. Chest radiograph showed bilateral pleural effusion with basal atelectasis. Upper gastrointestinal (GI) endoscopy was normal. The patient was treated with percutaneous drainage along with oral doxycycline (200 mg/day) and rifampin (600 mg/day) for 6 weeks.
The patient improved symptomatically over a period of 10 days with the absence of fever and reduction of pain abdomen. The patient was discharged on Day 10 with advice for review ultrasound abdomen examinations. The patient remained asymptomatic without recurrence at 6 months after completion of treatment. Repeat ultrasound abdomen showed mild splenomegaly without any other abnormalities.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [50, 'years'], 'Systolic Blood Pressure': [86.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg'], 'Blood Urea Nitrogen (BUN)': [70.0, 'mg/dL'], 'respiratory rate': [30.0, 'breaths per minute'], 'Confusion': False}",3,3,3,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 50 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 70.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 30 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 1 + 1 = 2.
The patient's systiolic blood pressure is 86 mm Hg. The patient's diastolic blood pressure is 60 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 2 + 1 = 3.
The patient's CURB-65 score is 3."
6422,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-3960818-1,Extracted,"A 17-year-old male patient, student and nonsmoker, consulted a local physician at Murshidabad, West Bengal with high grade intermittent fever with chills but no rigors, cough with scanty mucoid expectoration, dull aching chest pain, and generalized weakness for 5 days. The patient's chest X-ray postero-anterior (PA) view at that time showed middle lobe consolidation []. The patient was treated as CAP with oral amoxicillin + clavulanic acid (625 mg) 8 hourly and levofloxacin (500 mg) daily was added afterwards. As the patient's condition deteriorated with documented weight loss of 5 Kg in 2 weeks, his father brought him to our hospital. On examination, the patient was very toxic with blood pressure 90/60 mmHg, pulse rate 130/min regular, respiratory rate 32/min with moderate pallor. Examination of the respiratory system revealed crepitations in the right mammary area. Examinations of other systems were normal. We treated the case as non-resolving pneumonia and did antibiotics adjustment with the intravenous cefoperazone-sulbactam (1.5 g) 8 hourly and oral clarithromycin (500 mg) twice daily along with the other supporting treatment. The investigations revealed hemoglobin 6.4 g%, total white cell count 15200/mm3 with 94% neutrophils; fasting blood sugar 86 mg/dl, urea 45 mg/dl, creatinine 0.8 mg/dl, total bilirubin 0.96 mg/dl, alanine transaminase 78 U/L, aspartate transaminase 82 U/L and alkaline phosphatase 238 U/L. Routine urine examination was normal and culture revealed no growth after 72 h of incubation. Blood culture (two samples) was negative for bacteria. His sputum smear was negative for acid-fast bacilli for 3 consecutive days. Enzyme-linked immunosorbent assay (ELISA) for HIV 1 and 2 was non-reactive. Mantoux test with 5 T.U. was negative. HBsAg and anti-HCV were negative. USG whole abdomen showed hepatosplenomegaly. The patient's condition deteriorated further with appearance of right-sided pleural effusion [] and hepatosplenomegaly. Examination of pleural fluid showed cell count of 560/mm3 with 70% lymphocytes, protein 3.4 gm/dl, sugar 46 mg/dl, lactate dehydrogenase 600 U/L and adenosine deaminase 36 U/L. The patient's contrast enhanced computed tomography (CECT) of thorax showed organization of right middle lobe consolidation with enlargement of right paratracheal and subcarinal lymph nodes with central necrosis []. Fibre-optic bronchoscopy revealed pus coming from the right main bronchus and a gelatinous mass in the posterior wall of trachea and a widened carina with constricted right main bronchus []. Bronchoscopic biopsy from the mass showed inflammatory granulation tissue with proliferation of capillaries and infiltration of a large number of inflammatory cells. Gomori's methenamine silver stain showed fungal spores morphologically resembling Histoplasma capsulatum []. Bronchoalveolar lavage (BAL) and transbronchial needle aspiration (TBNA) from subcarinal lymph node also showed the presence of capsulated round microorganism on a background of inflammatory exudates compatible with Histoplasma capsulatum. Post-bronchoscopic sputum for fungal culture showed a growth of Histoplasma capsulatum. The patient did not have any past history suggestive of exposure to Histoplasma capsulatum. The patient was treated with intravenous amphotericin B 50 mg/day for 1 week followed by oral itraconazole 200 mg twice daily. Significant clinical improvement was noticed by 7 days and follow-up chest X-ray after one month showed a significant radiological resolution [].",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'respiratory rate': [32.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [45.0, 'mg/dL'], 'Diastolic Blood Pressure': [60.0, 'mm hg'], 'age': [17, 'years']}",3,3,3,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 17 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 45.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 32 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 1 + 1 = 2.
The patient's systiolic blood pressure is 90 mm Hg. The patient's diastolic blood pressure is 60 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 2 + 1 = 3.
The patient's CURB-65 score is 3."
6423,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-7735994-1,Extracted,"A 60-year-old male came to the emergency department of a tertiary care hospital, in Pakistan, with complaints of fever for one week, cough, and shortness of breath for two days. He was tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) before admission. The polymerase chain reaction (PCR) test came positive and chest X-ray revealed bilateral infiltrates as shown in Figure . The patient was diagnosed with severe COVID-19 infection and was admitted to our dedicated COVID-19 ICU. His past medical history included essential hypertension for the past 10 years, which was in control by his medication.
Examination at the time of admissions showed a regular heart rate of 100 beats per minute, non-invasive blood pressure (NIBP) of 155/88 mmHg, temperature 37.5°C, respiratory rate of 30 breaths per minute, and pulse oximeter showed 80% saturation on room air. The patient was immediately given non-invasive 100% FiO2, which improved saturation to 95%. Continuous monitoring of vitals was done using the Life Scope VS BSM-3000 series monitor (Nihon Kohden, Tokyo, Japan) for NIBP measurement, pulse oximetry, and electrocardiogram.
Initial lab investigations showed an elevated white blood cell (WBC) count of 13.9×109/L, elevated neutrophil percentage of 91%, decreased lymphocyte percentage of 6%, and a decreased platelet count of 95×109/L. The biochemical examination displayed normal serum creatinine 0.7 mg/dL, slightly elevated blood urea nitrogen 25 mg/dL, serum lactate dehydrogenase 1397 U/L. C-reactive protein (CRP) was markedly increased with a level of 82.5 mg/L, and procalcitonin was normal at 0.3 ng/mL. Coagulation function displayed an elevated D-dimer level of 1.96 mg/L, normal prothrombin time of 14.2 seconds, elevated international normalized ratio of 1.35, and elevated activated partial thromboplastin time of 28.4 seconds on Day 1. Arterial blood gases showed a slightly alkalotic pH of 7.48, decreased pCO2 of 27 mmHg, decreased pO2 of 60.7 mmHg, and increased lactate level of 3.2 mmol/L. His laboratory findings are shown in Table . However, one of the limitations to this study is that his complete cytokine assay was not performed.
The patient's treatment plan included antibiotics, prophylactic enoxaparin, 40 mg subcutaneous once daily, symptomatic, and supportive treatment, including steroids and vitamins. The patient was also found to have CRS by aggravated inflammatory markers, for example, CRP levels []. Intravenous TCZ 6 mg per kg was given on the day of admission. Oral feed along with oral and intravenous hydration was continued.
On the third day of admission, the patient's oxygen requirements decreased. The WBC count increased to 45×109/L, pO2 increased to 82 mmHg, and inflammatory markers were reduced. Chest X-ray also showed improvement. On the same day, the patient began complaining of pain in the right lower limb. A physical examination revealed hypothermia, numbness, and mild blackening of the right foot as shown in Figures , . Peripheral pulses of the right foot were not palpable. The vascular ultrasound of lower limbs showed no vascular flow in the popliteal, anterior tibial, posterior tibial, and dorsalis pedis artery. A severe arterial insufficiency was diagnosed, and the Vascular Surgery department was consulted immediately. They declared the limb unsalvageable and counselled for right limb above-knee amputation after the patient's condition had stabilized. Administering a therapeutic anticoagulant dose to prevent any other athero-embolic event was also suggested. Enoxaparin was then increased to 80 mg subcutaneous twice daily. Broad-spectrum antibiotics were added for the raised white cell count. On the ninth day of admission, the patient was maintaining oxygen saturation of 94% on room air. Chest X-ray showed a significant reduction in bilateral patchy infiltrates as shown in Figure . The right foot was blackened and atrophied, which extended up to the knee. No progression in ischemia was noted. The patient was stepped down to high dependency unit (HDU) and was placed on the vascular surgery operating room list for above-knee amputation. The surgery took place under spinal anesthesia. After all aseptic measures, fish-mouth incision was given at the mid femur level through the skin, superficial fascia, and subcutaneous tissue. Deep tissue dissection and muscle transection was done. Neurovascular structures were identified, ligated, and transected. Lastly, the bone was lacerated, hemostasis was secured, and the wound was closed. Aseptic pressure dressing was applied, and the patient remained hemodynamically stable. Postoperatively, the patient was monitored in the HDU for 48 hours. The patient was then discharged and advised tablet rivaroxaban 10 mg once daily for one month.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [60, 'years'], 'Systolic Blood Pressure': [155.0, 'mm hg'], 'Diastolic Blood Pressure': [88.0, 'mm hg'], 'respiratory rate': [30.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [25.0, 'mg/dL']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 60 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 25.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 30 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 1 + 1 = 2.
The patient's systiolic blood pressure is 155 mm Hg. The patient's diastolic blood pressure is 88 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6424,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-3948856-1,Extracted,"A 53-year-old male presented with cough, sputum, and headache for 2 weeks.
Five years previously, he had been diagnosed with HIV. He noted the onset of cough, sputum, and headache. The cough worsened, his sputum turned more yellowish and headaches accompanied by neck stiffness were related to coughing.
Over the first five years following the diagnosis of HIV, he was treated with antiretroviral medications (lamivudine and zidovudine; Combivir, Ritonavir; Norvir, atazanavir sulfate; Reyataz).
Vital signs were as follows: temperature, 38.0℃; blood pressure, 110/70 mm Hg; pulse rate, 90/min; respiratory rate, 20/min. He was alert mentally. Auscultation revealed rales in the right lower lung field. A Brudzinski-Kernig test was positive.
Complete blood count results were white blood cell 18.43×103/µL (neutrophils 91.3%, lymphocytes 3.5%), hemoglobin 14.0 g/dL, hematocrit 40.3%, and platelets 290×103/µL. Serum chemistry showed blood urea nitrogen 14 mg/dL, creatinine 0.66 mg/dL, aspartate aminotransferase 25 IU/L, alanine aminotransferase 23 IU/L, total bilirubin 1.92 mg/dL, and C-reactive protein 38.51 mg/dL. Cerebral spinal fluid (CSF) showed a white blood cell count of 108/µL, red blood cell count 0/µL, glucose 53 mg/dL, and protein 123 mg/dL. CSF and sputum bacterial cultures were negative. A CD4 T-cell count of 139/µL and HIV RNA of 20.7 copies/mL were recorded.
Plain chest radiography showed ground glass opacity and consolidation in both lung fields (especially the right lower) (). Contrast-enhanced chest computed tomography showed multiple irregular nodular infiltration in both lungs and patchy consolidation with ground glass opacity of the right middle and lower lung (). Contrast-enhanced cervical spine magnetic resonance imaging (MRI) showed a posterior epidural abscess: a peripheral rim-enhancing lesion at the posterior C2-3 epidural space (); osteomyelitis; mild scanning enhancement of the clivus and cervical spine; early leptomeningitis; and prominent leptomeningeal enhancement ().
The patient was administered vancomycin (1 g q 12 hr IV), ceftriaxone (2 g q 24 hr), clindamycin (600 mg q 12 hr) and fluconazole (400 mg q 24 hr). The patient's fever reduced 3 days following admission. His epidural abscess was discussed with the neurosurgeon in our hospital. There were no neurological symptoms, no surgical treatment was performed and antibiotic therapy was maintained. At follow-up 5 days after admission, a plain chest radiograph showed improvement, and S. pneumoniae was detected in two blood cultures that showed sensitivity to most antibiotics. The patient was thus switched from vancomycin plus ceftriaxone to ampicillin (2 g) plus sulbactam (1 g q 6 hr IV). Fifteen days after admission, neck stiffness had improved and cough and sputum production reduced. A plain chest X-ray showed decrease in both ground glass opacity and consolidation in both lung fields (). Twenty-six days after admission, laboratory analysis was as follows: white blood cell count 5.42×103/µL, neutrophils 55.9%, lymphocytes 25.9%, and C-reactive protein 0.26 mg/dL. The patient wished to be discharged, so antibiotic therapy was switched from intravenous to oral (amoxicillin/clavulanate 625 mg PO tid). Since discharge, no recurrence of symptoms or evidence of pneumonia according to plain chest radiography have been observed. One year after discharge, there is no abnormal finding on cervical MRI ().",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [53, 'years'], 'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg'], 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [14.0, 'mg/dL'], 'Confusion': False}",0,0,0,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 53 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 14.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 0.
The patient's systiolic blood pressure is 110 mm Hg. The patient's diastolic blood pressure is 70 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 0.
The patient's CURB-65 score is 0."
6425,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-3816164-1,Extracted,"A 63-year-old Korean woman with a past medical history of hypertension and a 25-year history of SLE presented with a 3-week history of shortness of breath. She had been treated with hydroxychloroquine 400 mg/day and varying doses of prednisone between 5 and 15 mg/day for the SLE. Additionally, the hypertension was under control with carvedilol 25 mg/day. On examination, her blood pressure was 110/70 mmHg, pulse rate was 112 beats/min, respiratory rate was 24 breaths/min, and body temperature was 36.5℃. Jugular venous distention was noted on inspection. On cardiac auscultation, her rhythm was noted to be tachycardic but regular, weak summation gallops were heard at the cardiac apex, and no pericardial friction rubs were appreciated. Blood tests showed a white blood cell count of 4000/mm3 (normal, 4300-9400/mm3), hemoglobin of 11.5 g/dL (normal, 12-14.3 g/dL) and platelet count of 67000/mm3 (normal, 169-365/mm3). The C-reactive protein level was found to be 0.29 mg/L (normal, 0-0.75 mg/L). A blood chemistry panel revealed a blood urea nitrogen level of 25.0 mg/dL (normal, 7-20 mg/dL), creatinine of 1.3 mg/dL (normal, 0.5-1.5 mg/dL), total protein of 6.7 g/dL (normal, 6.0-8.3 gm/dL), and albumin of 3.2 g/dL (normal, 3.5-4.5 mg/dL). Analysis of the urinary sediment revealed 1-4 white blood cells/high power field (hpf), many red blood cells/hpf, and trace levels of proteinuria. Cardiac enzymelabs were drawn and found to be elevated: CK-MB of 8.7 U/L (normal, 0.6-6.3 U/L), troponin-I of 0.35 ng/mL (normal, 0.0-0.2 ng/mL), and pro-brain natriuretic peptide of 8110 pg/mL (normal, 0-125 pg/mL). Chest X-ray revealed an enlarged cardiac silhouette and an electrocardiogram revealed ST elevation in leads V1-6 (). Immunofluorescence tests were negative for double-stranded DNA antibodies and anti-extractable nuclear antigen antibodies (anti-Ro and anti-La). Complement levels were found to be low (C3 0.39 g/L, normal 0.8-1.7 g/L; C4 0.04 g/L, normal 0.12-0.36 g/L). Viral markers for cytomegalovirus, Coxsackie virus B type 2, herpes simplex virus, and Epstein-Barr virus were all negative. Echocardiography demonstrated moderate left ventricular systolic dysfunction [left ventricular ejection fraction (LVEF) was 42%] with apical akinesia but no evidence of pericardial effusion (). Echocardiography performed 2 years earlier showed mild concentric left ventricular hypertrophy with a LVEF of 70%. A coronary angiography showed normal coronary arteries.
We suspected takotsubo cardiomyopathy. However there was no trigger event as physical and emotional stress. The patient was treated with angiotensin converting enzyme inhibitor, furosemide, and intravenous nitrates. The dose of glucocorticoids was between 0.5 to 1 mg/kg for the control of SLE activity. Her dyspnea gradually improved, however, a three-week follow-up echocardiography test revealed persistent apical ballooning and a newly developed apical thrombus (size, 1.10 × 2.12 cm) () with no significant improvement in LVEF. Heparin was then administered followed by oral anticoagulation therapy with warfarin. There were no embolic events during the patient's hospital stay. On the 35th day of hospital admission, follow-up echocardiography showed slightly improved wall motion of the left ventricular apex with a partially resolved thrombus and a LVEF of 50%. Although cardiac enzymes remained elevated (CK-MB 12.80 U/L and troponin-I 0.64 ng/mL), the patient was discharged on oral anticoagulation therapy.
Three months later, she was readmitted to the hospital due to a severe herpes zoster outbreak on her left shoulder. Cardiac enzymes were again found to be elevated (CK-MB 8.8 U/L and troponin-I 0.98 ng/mL). Electrocardiography revealed persistent ST segment elevation () and echocardiography revealed mild apical hypokinesia with a LVEF 50%, but no apical thrombus (). During her hospital stay she developed a mild fever and candidemia which was treated with an intravenous antifungal agent. Unfortunately, she developed septic shock and expired on day 54 of hospital re-admission.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [63, 'years'], 'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg'], 'respiratory rate': [24.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [25.0, 'mg/dL']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 63 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 25.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 24 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 110 mm Hg. The patient's diastolic blood pressure is 70 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6426,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-5843145-1,Extracted,"A 39-year-old man presented to the emergency department complaining of a 3-day history of shortness of breath and dry cough. He had no known significant co-morbidities and did not report any further associated symptoms. He reported that he was treated with antibiotics for a lower respiratory tract infection (LRTI) by a private physician in the previous 3 days with no improvement in symptoms. He was unsure of his HIV status and was not on antiretroviral therapy (ART).
His admission vitals were a blood pressure of 123/70 (82) mmHg, heart rate of 116 beats per minute, respiratory rate of 30 breaths per minute and a temperature of 36.9 °C. On examination, he had no significant lymphadenopathy and was not found to have mucosal or skin lesions associated with advanced HIV. No other obvious stigmata of advanced HIV were noted. He was in severe respiratory distress with scattered bilateral predominantly basal crackles on auscultation. Wheezing was not present on auscultation. He had an oxygen saturation of 62% on a partial rebreather mask with an inspired oxygen fraction (FiO2) of 80%.
Laboratory investigations revealed a white cell count (WCC) of 14.5 × 109 cells/L, haemoglobin (Hb) of 11.6 g/L, platelets of 298 × 109 cells/L, urea of 6.3 mmol/L, creatinine of 108 μmol/L, C-reactive protein (CRP) of 102 mg/L and beta-d-glucan (BDG) of > 500 pg/mL. His admission blood gas showed a mixed respiratory and metabolic acidosis with type II respiratory failure and a markedly increased alveolar-arterial gradient (pH = 7.36, pCO2 = 34.7, pO2 = 64.8, HCO3 = 19.2, BE = -4.9, SpO2 = 96.9, Hb = 13.4, Lac = 4.4). His chest X-ray (CXR) showed diffuse bilateral alveolar infiltrates and granular opacities. A transthoracic echocardiogram performed at the time of admission showed normal left ventricular function, no evidence of pulmonary embolus and normal heart valves. Based on clinical suspicion, hypoxaemic respiratory failure with typical chest radiograph changes, the patient’s normal echocardiogram, elevated BDG, and the relative absence of clinical signs usually associated with a multilobar pneumonia, the diagnosis of Pneumocystis pneumonia (PCP) was considered.
On the basis of his clinical condition and investigations, the patient was intubated, ventilated and admitted to the intensive care unit (ICU) for respiratory support. He was empirically started on treatment for partially treated community acquired pneumonia (CAP) (piperacillin and tazobactam and a macrolide) as well as PCP, on the basis of clinical case definition as suggested by the World Health Organisation (WHO), with high-dose intravenous trimethoprim-sulfamethoxazole (TMP-SMX) and high-dose intravenous corticosteroids (hydrocortisone). He consented to HIV testing on admission and was found to be HIV-infected with a CD4 count of 7 cells/μL. Additional sputum and blood investigations for Mycobacterium tuberculosis (TB) including TB culture (sputum and blood) and Auramine O stain, real-time polymerase chain reaction (PCR) (TB GeneXpert), sputum gram stain and bacterial culture and direct fluorescence antigen test for PCP were negative. Standard aerobic and anaerobic blood cultures yielded no pathogenic organisms.
The patient was intubated and ventilated for 3 days and spent a week in our unit. During this period, we adopted a lung protective ventilation strategy, permissive hypoxaemia as well as meticulous fluid management. Through his week-long admission, he had a cumulative fluid balance of -332 mL. Initial pre-admission ventilator settings of FiO2 = 1, PEEP = 14 and ΔP = 8 were successfully weaned to FiO2 = 0.6, PEEP = 10 and ΔP = 10 on day one of admission. We accepted oxygen saturations in the region of 70%–80% and PaO2 measurements in the region of 50 mmHg – 60 mmHg whilst maintaining tidal volumes of 4 mL/kg – 6 mL/kg. On day four of admission, despite oxygen saturations in the region of 80%, the patient was successfully extubated and placed on non-invasive ventilation (NIV). He required NIV (positive end expiratory pressure of 6 cm H2O and pressure support of 6 cm H2O) for a total of 3 days before being weaned onto oxygen supplementation with an FiO2 of 0.4. He maintained oxygen saturations in the region of 85%–90%. He was discharged to the ward on nasal cannula after a 7-day ICU stay.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [123.0, 'mm hg'], 'respiratory rate': [30.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [6.3, 'mmol/L'], 'Confusion': False, 'Diastolic Blood Pressure': [70.0, 'mm hg'], 'age': [39, 'years']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 39 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 6.3 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of BUN from mmol to mg. The mass of BUN is 6.3 mmol. To convert 6.3 mmol of BUN to mol, multiply by the conversion factor 0.001, giving us 6.3 mmol BUN * 0.001 mol/mmol = 0.0063 mol BUN. To convert from mol BUN to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0063 mol BUN * 28.02 g/mol = 0.17653 g BUN. To convert 0.17653 g of BUN to mg, multiply by the conversion factor 1000.0, giving us 0.17653 g BUN * 1000.0 mg/g = 176.53 mg BUN. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 176.53 mg BUN/10.0 dL = 17.653 mg BUN/dL. The concentration value of 6.3 mmol BUN/L converts to 17.653 mg BUN/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 30 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 0 + 1 = 1.
The patient's systiolic blood pressure is 123 mm Hg. The patient's diastolic blood pressure is 70 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6427,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-7580483-2,Extracted,"A 41-year-old female, without any significant past history presented to department of critical care medicinewith altered sensorium, fever, cough, shortness of breath, palpitation for 2 days. At presentation, her Glasgow Coma Scale (GCS) -12/15, pulse rate-190 beats/per min irregularly irregular, blood pressure-80/40 mm of Hg, respiratory rate-31breaths/ min, oxygen saturation-91% at five liter oxygen, and temperature -100°F. On examination thyroid swelling, bilateral pitting edema and jaundice were present.On auscultation of chest, bilateral crepitation was present. Cardiovascular examination showed tachycardia without murmur. Abdominal examination was normal. BWPS was 50.
Her investigation profile were TLC-15000/ mm3,platelets-110000/mm3, Hb-9gm/dl, urea 90-mg/dl, creatinine-1.6 mg/dl, sodium and potassium were within normal range. Total bilirubin was 5mg/dl in which direct bilirubin corresponds to 2mg/dl, total protein-5.9mg/dl in which albumin-2.9 mg/dl, ALT-256U/L, AST-201U/L, FT3-8 ng/dl, FT4-5 ng/dl and TSH-0.01 μlU/ml.Chest X-ray showed bilateral pneumonia ().
Immediately the patient was resuscitated with fluid, hydrocortisone, broad spectrum antibiotics and cardio version. Heart rate got controlled with Digoxin followed by Propanolol (20 mg) three times a day orally. Carbimazole (20mg) was started thrice a day. The patient was transferred from Intensive Care Unit (ICU) on the fourth day. She was followed up at OPD after 2 weeks, thyroid function test was done and carbimazole was continued.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [80.0, 'mm hg'], 'respiratory rate': [31.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [90.0, 'mg/dL'], 'Confusion': True, 'Diastolic Blood Pressure': [40.0, 'mm hg'], 'age': [41, 'years']}",4,4,4,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 41 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient has confusion, 1 point is added to score making the current total 0 + 1 = 1.
The concentration of BUN is 90.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 31 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 2 + 1 = 3.
The patient's systiolic blood pressure is 80 mm Hg. The patient's diastolic blood pressure is 40 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 3 + 1 = 4.
The patient's CURB-65 score is 4."
6428,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-2846739-1,Extracted,"A 15-year-old girl was admitted to our hospital with a 1-week history of fever as well as dry cough, dyspnea, and myalgia that started on the day of admission. She had been healthy prior to admission and had no notable history of respiratory or allergic disease. In her family history, her father was being treated for liver cirrhosis. She had started smoking 3-5 cigarettes daily 3 weeks before admission, but stopped smoking 1 week before admission due to discomfort after smoking. On admission, the patient had clear consciousness but appeared acutely ill. Her blood pressure was 112/70 mmHg, pulse rate 121/minute, respiratory rate 24/minute, and body temperature 36.4℃. The conjunctivae were pink, and the sclerae showed no sign of jaundice. No cervical lymph nodes were palpable. On physical examination, rales and coarse breathing sounds were audible, but heart sounds were normal. There were no abnormal findings in the abdomen.
On admission, routine blood tests revealed white blood cells, 19,400/µL; hemoglobin, 14.4 g/dL; erythrocyte sedimentation rate, 17 mm/hour; platelets, 241,000/µL; neutrophils, 90.8%; lymphocytes, 3.7%; monocytes, 4.0%; and eosinophils, 1.4%. Arterial blood gas analysis performed in room air exhibited pH 7.45; PaCO2, 31 mmHg; PaO2, 64 mmHg; HCO3, 22.0 mEq/L; base excess, -1.4 mEq/L; and oxygen saturation, 93%. Blood biochemical tests showed total protein, 5.9 g/dL; albumin, 3.3 g/dL; aspartate aminotransferase, 17 IU/L; alanine aminotransferase, 8 IU/L; C-reactive protein, 4.22 mg/dL; total bilirubin, 1.1 mg/dL; blood urea nitrogen, 4.0 mg/dL; and creatinine, 0.4 mEq/L. Chest X-ray showed diffuse bilateral infiltrates, especially in the peripheral region () and chest CT exhibited multiple nodular lesions with ground-glass appearance (). The patient was negative for rheumatoid factor, antinuclear antibody, anti-neutrophil cytoplasmic antibody (ANCA), antibody against Mycoplasma, and cold agglutinin. The levels of IgG, IgA, IgM, complement C3 and C4 were within the normal limits, and the total IgE level was 113 KU/L. Cultures of blood and sputum were negative for bacteria and fungi. Urine tests were negative for antigens of Legionella and Pneumococcus, and IgG tests against parasites were negative for Paragonimus westermani and Clonorchis sinesis. Stool examination was negative for parasite ova. Immediately after admission, ampicillin/sulbactam and cefotaxime, as well as oseltamivir, were administered under the suspicion of pandemic H1N1 infection, but hypoxia, dyspnea, and pneumonic infiltration on chest X-ray were aggravated abruptly. Non-invasive ventilation was maintained. On the second day in hospital, bronchoscopy revealed no abnormal findings, but BALF tests exhibited white blood cells, 280/µL; macrophages, 19%; neutrophils, 10%; lymphocytes, 26% eosinophils, 35% (eosinophilia); and basophils, 4% (). BALF cultures were negative for bacteria and fungi. The patient was negative for PCR and culture of viruses, including respiratory syncytial virus, influenza virus, parainfluenza virus, adenovirus, and human metapneumovirus; real-time RT-PCR for the novel influenza virus H1N1; antigen tests for Aspergillus and Pneumocystis jiroveci; PCR and culture of cytomegalovirus and Chlamydia pneumonia; PCR of Epstein-Barr virus; and acid-fast bacillus smear. On the third day in hospital, thoracoscopy-assisted lung biopsy was performed in the middle and lower lobes of the left lung, which showed eosinophilic infiltrates suggestive of interstitial pneumonia (). Based on these results, the patient was diagnosed with acute eosinophilic pneumonia. On the fifth day in hospital, urine cotinine level, which was determined to confirm smoking, was 47 ng/mL. Furthermore, routine blood test revealed white blood cells, 5,500/µL; neutrophils, 45.8%; lymphocytes, 26.0%; monocytes, 9.0%; and eosinophils (19.0%, eosinophilia). Methylprednisolone (125 mg) was administered every 6 hours. The day after methylprednisolone administration, hypoxia and dyspnea improved, and infiltrates on chest X-ray improved 2 days after drug administration (). Methylprednisolone was tapered from the fourth day of drug administration. The patient was discharged from the hospital on day 9 and was followed up periodically. At the time of discharge from the hospital, routine blood tests revealed white blood cells, 10,300/µL; neutrophils, 59.6%; lymphocytes, 31.5%; monocytes, 6.3%; and eosinophils, 2.4% (within the normal limits). There were no specific findings in pulmonary function, methacholine provocation, and skin prick tests. Methylprednisolone is being tapered at the outpatient clinic. On day 15 of follow-up, chest X-ray showed no infiltrates.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [112.0, 'mm hg'], 'respiratory rate': [24.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [4.0, 'mg/dL'], 'Confusion': False, 'Diastolic Blood Pressure': [70.0, 'mm hg'], 'age': [15, 'years']}",0,0,0,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 15 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 4.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 24 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 0.
The patient's systiolic blood pressure is 112 mm Hg. The patient's diastolic blood pressure is 70 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 0.
The patient's CURB-65 score is 0."
6429,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-5667273-1,Extracted,"A 74-year-old man with a history of diabetes mellitus and chronic obstructive pulmonary disease suffered cervicalgia and a stiff shoulder after engaging in farm work. He was a chicken farmer and produced a fertilizer that utilized cow and poultry manure. He went to a nearby clinic 2 days after the onset of symptoms as he experienced difficulty swallowing. Tetanus was strongly suspected from his clinical condition, and he was transferred to the emergency room 3 days after the initial symptoms began. His vital signs were as follows: Glasgow Coma Scale score, 15 (E4V5M6); blood pressure, 144/63 mmHg; heart rate, 79 b.p.m.; respiratory rate, 24 breaths/min; and body temperature, 36.5°C. The level of oxygen saturation showed 96%. Painful contracture of the neck was observed. Trismus, risus sardonicus, and strong muscle spasms in the platysma and sternocleidomastoideus were observed (Fig. ). Laboratory tests revealed slight inflammation and rhabdomyolysis (white blood cell count, 12,600 cells/mm3; C-reactive protein, 0.04 mg/dL; lactase dehydrogenase, 276 U/L; creatine kinase, 340 IU/L; blood urea nitrogen, 25.5 mg/dL). A computed tomography scan showed emphysematous bulla in the lung and patchy pneumonia in the right upper lobe. Tetanus was clinically diagnosed and he was admitted into the intensive care unit (Fig. ). Polyethylene glycol-treated human anti-tetanus immunoglobulin (3,000 units) was injected and benzylpenicillin potassium (8,000,000 units/day) was administered. Both KT (7.5 g/day) and SKT (7.5 g/day) were given by nasogastric tube to release muscle tension. One to three packages of each Kampo extract was dissolved in tap water (20 mL). Trismus and generalized convulsions were temporarily improved 30 min after treatment with KT and SKT (Fig. B). Fluctuation of systolic blood pressure (100–170 mmHg) was observed for the first 3 days of hospitalization. It was most severe on day 1 (70–180 mmHg). On day 3 of hospitalization, mechanical ventilation was introduced to treat the complications of pneumonia. Blood gas analysis revealed pH 7.47, PaO2 87 mmHg, PaCO2 41 mmHg, base excess (BE) 5.6 mEq/L (FIO2 0.6, synchronized intermittent mandatory ventilaton (SIMV) 13/min, pressure control (PC) 10 cmH2O, pressure support (PS) 8 cmH2O, positive end-expiratory pressure (PEEP) 4 cmH2O). After 11 days of hospitalization, doses of KT and SKT were reduced to 5.0 g/day, as the tetanic convulsions were controlled without the use of muscle relaxants. After 17 days of hospitalization, the patient was weaned from the ventilator. The patient was discharged from the intensive care unit after 25 days; after 27 days, treatment with all Kampo medicines was terminated. After 30 days of hospitalization, he was discharged from the hospital without sequelae.
The blood culture at the time of the patient's admission showed negative results; however, on day 4 of hospitalization, Klebsiella oxytoca was detected from the sputum culture.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [144.0, 'mm hg'], 'respiratory rate': [24.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [25.5, 'mg/dL'], 'Confusion': False, 'Diastolic Blood Pressure': [63.0, 'mm hg'], 'age': [74, 'years']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 74 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 1.
The concentration of BUN is 25.5 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 24 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 144 mm Hg. The patient's diastolic blood pressure is 63 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6430,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-7171607-2,Extracted,"A 78-year-old male patient presented to the emergency department with chief complaints of fever with productive cough since last ten days and altered sensorium with chest pain for one day. The patient was apparently well ten days back when he developed high grade fever and cough with haemoptysis and yellowish sputum. It was also associated with shortness of breath. He was a known case of type 2 diabetes mellitus with uncontrolled sugar. There was no past history of taking antitubercular drugs and no exposure to pets. On examination, he was febrile; heart rate was 122 beats/min, respiratory rate was 28/min; blood pressure was 122/75 mm Hg; and oxygen saturation was 84% while breathing room air. The patient had bilateral pedal oedema. Respiratory system examination revealed bilateral crepitation with occasional rhonchi. The total leucocyte count was 14000/mm3 with 95% neutrophils and 3% lymphocytes. The haemoglobin was 11.67 g/dl, and the erythrocyte sedimentation rate was 110/h. Serum urea was 43 mg, and creatinine was 0.7 mg/dl. On chest radiography, there were bilateral fluffy opacities. Inj Ceftriaxone 1 gm IV BD was started empirically along with Inj Azithromycin 500 mg BD along with other supportive treatment. On the same day, as the patient was rapidly desaturating, he was shifted to the respiratory ICU where he was intubated and kept on ventilator. Neurologist opinion was taken for the altered sensorium and a normal contrast CT scan of the head was done. Sputum sample was collected which came out negative for AFB but surprisingly KOH mount revealed weak, acid-fast, and filamentous bacilli resembling Nocardia spp. On day 4, the empirical regimen was stopped, and the patient was started on Inj Imipenem and Inj Amikacin. However, the patient developed hypotension with tachycardia, as a result of which IV fluids and inotropic support was given. Despite this on day 8, he had severe bradycardia with profound hypotension. CPR was started with repeated cycles and DC shock, but the patient could not be revived and was declared dead.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [78, 'years'], 'Systolic Blood Pressure': [122.0, 'mm hg'], 'Diastolic Blood Pressure': [75.0, 'mm hg'], 'respiratory rate': [28.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [43.0, 'mg/dL'], 'Confusion': True}",3,3,3,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 78 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient has confusion, 1 point is added to score making the current total 1 + 1 = 2.
The concentration of BUN is 43.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 2 + 1 = 3.
The patient's respiratory rate is 28 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 3.
The patient's systiolic blood pressure is 122 mm Hg. The patient's diastolic blood pressure is 75 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 3.
The patient's CURB-65 score is 3."
6431,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-2478653-1,Extracted,"A 76-year-old female who had never smoked came to the hospital because of chronic cough. The chest radiograph showed bilateral consolidation with a cavity (Figure ). The chest computed tomography (CT) scan showed multiple consolidations in both lungs with cavities in the left upper lobe (Figure ). The acid-fast stain of the sputum smear was positive, and the sputum culture and the PCR were also positive for M. tuberculosis. Thus, the patient was diagnosed as having pulmonary tuberculosis, and she was admitted to hospital for treatment. Three days later from admission to prior hospital, the patient developed acute abdominal pain with guarding. An abdominal radiograph showed marked dilatation of the small intestine (Figure ). On enhanced abdominal CT (Figure ), intestinal obstruction caused by a mass lesion with a target sign in the ascending colon was seen. A concentric ring of intraluminal mesenteric fat interposed between the central portion and the outer edematous colonic wall gives this lesion its characteristic appearance. In addition, the small intestine was enlarged and filled with fluid. The patient was diagnosed as having intussusception and was admitted to our hospital to treat both the pulmonary tuberculosis and the intussusception. On physical examination, her body temperature was 37.8°C, the heart rate was 86 beats/min, and the respiratory rate was 18 breaths/min. Her blood pressure was 150/72 mmHg. Coarse crackles were audible in the left lung. The patient had no peripheral lymphadenopathy, no skin lesions, and no neurological deficits. On abdominal examination, the mass lesion was palpable in the right lower abdominal region, and guarding was present. On laboratory examination, the white blood cell count was elevated (15.4 × 103/mm3), the serum C-reactive protein (CRP) level was increased (5.43 mg/dl), and the erythrocyte sedimentation rate was increased (70 mm/h). Other laboratory results included: total protein, 5.9 g/dl; serum albumin, 3.4 g/dl; serum creatinine, 0.5 mg/dl; blood urea nitrogen, 14.0 mg/dl; and serum lactate dehydrogenase, 301 IU/l. The serum glucose concentration and liver function tests were normal, and the serum complement prothrombin time was 97%. The HIV antibody was negative and the numbet of CD4 positive T-lymphocyte was normal. Arterial blood gases were improved on 2L O2 given nasally (PaO2, 80.1 Torr; PaCO2, 52.1 Torr; pH, 7.46; HCO3, 36.5 mmol/L; BE 11.3 mmol/L). Abdominal ultrasonography showed the bull's eye sign at the site of the mass lesion (Figure ). Since there was a possibility of intestinal necrosis, ileocecal resection was done on the day of admission. Macroscopically, it could be seen that the terminal ileum gained entry to the ascending colon. Pathologically, there were large areas of ischemic enteritis due to intussusceptions, and caseous necrosis with epithelioid cell granulomas was seen (Figure ). There was no evidence of any neoplasm or diverticulum that could have caused the intussusception. Thus, this patient was diagnosed as having intussusception due to intestinal tuberculosis. The patient was treated with isoniazid (300 mg/day), rifampicin (600 mg/day), ethambutol (750 mg/day), and pyrazinamide (750 mg/day). The patient's postoperative course was uneventful, and there has been no recurrence.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [76, 'years'], 'Diastolic Blood Pressure': [72.0, 'mm hg'], 'Systolic Blood Pressure': [150.0, 'mm hg'], 'respiratory rate': [18.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [14.0, 'mg/dL'], 'Confusion': False}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 76 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 1.
The concentration of BUN is 14.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 1.
The patient's respiratory rate is 18 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 150 mm Hg. The patient's diastolic blood pressure is 72 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6432,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-5885493-1,Extracted,"A 56-year-old Hispanic male with no comorbid conditions presented to our emergency department with a 2-day history of fever, generalized weakness, abdominal pain, nausea, and vomiting. He had no hemoptysis, hematemesis, arthralgia, or headache. He denied recent contact with sick humans, exposure to pets or birds, or travel. He smoked 5 cigarettes per day for over 20 years but denied using alcohol or recreational drugs.
On physical examination, the patient was in respiratory distress, with a respiratory rate of 24 breaths per minute and pulse oxygen saturation of 90% on 2 liters per minute oxygen via a nasal cannula. His temperature was 101.5°F, heart rate was 68 beats per minute, and blood pressure was 80/50 mm·Hg. On lung examination, bilateral rales were noted. His heart sounds were normal. His abdomen was soft upon palpation, with slight tenderness in the right upper quadrant; no organomegaly was noted. Neurologic examination was unremarkable. The patient was intubated immediately because of his respiratory distress, and an intravenous infusion of norepinephrine was begun for the presumptive diagnosis of septic shock.
Relevant laboratory results on the day of admission were as follows: leukocytosis (white blood cell count: 20 × 103 cells/µL), lactic acidosis (serum lactate: 17.5 mmol/L), pH of 7.15, bicarbonate of 15 mEq/L, blood urea nitrogen of 37 mg/dL, serum creatinine of 4.5 mg/dL, and increased serum aspartate transaminase (1532 unit/L), alanine aminotransferase (683 unit/L), and alkaline phosphatase (149 unit/L). Chest X-ray showed bilateral diffuse alveolar infiltrates ().
The patient underwent fiberoptic bronchoscopy with bronchoalveolar lavage; diffuse alveolar hemorrhage was excluded, and cultures from the lavage samples were negative. Bedside ultrasound of the abdomen revealed acalculous acute cholecystitis, and a percutaneous cholecystostomy tube was placed. Blood cultures from admission grew P. multocida, and gram-negative Pasteurella rods were seen on gram stain during examination via light microscopy. Cultures from the gallbladder fluid were negative. Transthoracic echocardiography showed a left ventricular ejection fraction of 74% and no vegetations.
The patient was diagnosed with multiorgan failure, septic shock with severe lactic acidosis, acute respiratory distress syndrome (ARDS), and renal failure requiring hemodialysis. Broad-spectrum intravenous antibiotics were begun. His condition rapidly deteriorated, and his clinical course was further complicated by disseminated intravascular coagulation, gastrointestinal bleeding, and refractory shock requiring multiple vasopressor medications. He subsequently died of a cardiopulmonary arrest. Despite all measures, the serum lactic acid at the time of his death was 12 mmol/L.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [80.0, 'mm hg'], 'respiratory rate': [24.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [37.0, 'mg/dL'], 'Confusion': False, 'Diastolic Blood Pressure': [50.0, 'mm hg'], 'age': [56, 'years']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 56 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 37.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 24 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 80 mm Hg. The patient's diastolic blood pressure is 50 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 1 + 1 = 2.
The patient's CURB-65 score is 2."
6433,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-4842364-1,Extracted,"A 71-year-old male with past medical history significant for bladder cancer status after radical cystectomy on chemotherapy, diabetes, coronary artery disease, and hypertension presented to the emergency room with complaints of fever and shivering. Three days prior to admission, his oncologist diagnosed him with anemia. He had complaints of cough with white sputum consisting of up to half a cup per day. He denied any shortness of breath, diarrhea, hematuria and dysuria, or weight loss.
Upon physical examination patient was febrile with a temperature of 100.7 F, blood pressure of 110/62 mmHg, heart rate of 114/min, and respiratory rate of 20/min and had O2 saturation of 100% on two liters' nasal cannula. Pertinent findings revealed irregular rate and rhythm with distant heart sounds. The remainder of the physical exam was otherwise unremarkable. Laboratory data demonstrated hemoglobin of 7.0 g/dL, hematocrit of 21.7%, white blood cell count of 5.7 K/μL with absolute neutrophil count 5.0 K/μL, and platelet count 37 K/μL. Basic metabolic panel revealed glucose of 100 mg/dL, blood urea nitrogen of 27 mg/dL, creatinine of 0.7 mg/dL, calcium 8.0 mg/dL, albumin 2.9 g/dL, sodium 134 mmol/L, potassium 4.4 mmol/L, chloride 103 mmol/L, and bicarbonate 20 mmol/L. Electrocardiogram showed atrial fibrillation with low voltage. Chest X-ray showed marked enlargement of the cardiac silhouette with a possibility of large pericardial effusion ().
The patient was admitted to the intensive care unit for sepsis and large pericardial effusion. He was started on empiric antibiotics. Computed tomography scan of the chest was ordered to rule out any metastasis which revealed a large pericardial effusion that was 2.2-cm in thickness (). Echocardiography demonstrated large circumferential pericardial effusion.
A cardiothoracic surgeon was called on consult and the patient underwent a pericardial window where 800 mL of hemorrhagic pericardial effusion was drained. Pericardial biopsy illustrated metastatic urothelial carcinoma (). Immunostains were performed which were positive for pancytokeratin, CK7, CK20, and uroplakin and negative for PSA. Patient remained critical and, despite all the efforts, the patient deteriorated and expired over the course of a few days due to his relatively poor prognosis.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [27.0, 'mg/dL'], 'Confusion': False, 'Diastolic Blood Pressure': [62.0, 'mm hg'], 'age': [71, 'years']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 71 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 1.
The concentration of BUN is 27.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 110 mm Hg. The patient's diastolic blood pressure is 62 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6434,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-3125360-1,Extracted,"A 27-year-old Iranian woman, recipient of a living, unrelated renal transplant five years earlier, presented with a productive cough, weight loss and fever. The cause of her end-stage renal disease was chronic pyelonephritis. Six weeks prior to her admission, her immunosuppressant regimen was switched from oral cyclosporine (100 mg, twice daily) to oral sirolimus (1 mg, twice daily) with a diagnosis of chronic allograft nephropathy (serum creatinine level of 2 mg/dL). Her mycophenolate mofetil dose was decreased from 2000 to 1000 mg/day and prednisolone was continued with the previous dose (5 mg, daily). Four weeks later, she developed a mild cough, weakness and anorexia. Her condition progressed to a more constant cough and weight loss until she was hospitalized.
Physical examination revealed her blood pressure to be 110/60 mm/Hg, respiratory rate 20/min, pulse rate 92/min and body temperature 38°C. A chest examination revealed fine crackles mainly on her lower lung fields. On admission, the laboratory findings were as follows: white blood cell count 5.1 × 109/L, hemoglobin 7.2 g/dL, hematocrit 22.4%, mean corpuscular volume 75 fL (normal range, 77-97 fL), mean corpuscular hemoglobin 24 pgm (normal range, 26-32 pgm), mean corpuscular hemoglobin concentration 32% (normal, 32-36%), platelet count 213 × 109/L, fasting blood glucose 105 mg/dL, blood urea 62 mg/dL, serum creatinine 1.9 mg/dL, sodium 135 mEq/L, potassium 4.5 mEq/L, aspartate aminotransferase 37 IU/L, alanine aminotransferase 45 IU/L, alkaline phosphatase 1106 IU/L and total bilirubin 1 mg/dL. A urine analysis was unremarkable.
On the first day of admission, sirolimus and mycophenolate mofetil were discontinued and cyclosporine (200 mg/day) was started. The dose of prednisolone was not altered (5 mg, daily). A chest X-ray showed fine miliary nodules throughout the entire lung fields. Echocardiography revealed normal pericardium and cardiac chambers. Her left ventricular ejection fraction was 65%. An ultrasound examination of her renal allograft did not reveal any pathologic finding. A 6 mm induration was observed on a TB skin test. Sputum and bronchial aspirate examination was positive for acid-fast bacilli, suggestive of Mycobacterium tuberculosis infection. A chest computed tomography (CT) scan illustrated widespread miliary nodules throughout the lung fields, compatible with miliary TB (Figure ).
In the evening of her fourth day of admission, our patient developed an increasing right lower quadrant abdominal pain spreading to her entire abdomen. Physical examination revealed widespread abdominal tenderness and rebound. An ultrasonographic study of her abdomen disclosed a small fluid collection in the right lower quadrant. Two cysts were detected in her left ovary (54 × 32 mm and 33 × 31 mm). An abdominal CT scan with oral contrast revealed that her pancreas and spleen were normal. Her colonic wall thickness was measured as 4 mm and free fluid was visible in dependent parts of her abdominal cavity. Her peritoneal cavity was then opened with a midline incision and widespread peritonitis was found. Her inflamed appendix (9 × 6 cm) was perforated at its tip. Her ileocecal area and cecum were inflamed with fragile tissues. A cecostomy was performed and a drain was placed. Histopathological examination of the resected appendix revealed caseating epithelioid granulomas, epithelioid histiocytes and Langhans giant cells in the sub-mucosa and sub-serosa of her appendix (Figure ). The histological picture, along with positive mycobacterial cultures from the sputum and bronchial aspirate, was suggestive of tuberculous appendicitis. After surgery, chemotherapy for TB was started and continued for nine months. An immunosuppressive regimen was continued with cyclosporine, mycophenolate mofetil and prednisolone. During follow-up visits, the pulmonary and abdominal signs and symptoms were resolved.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg'], 'age': [27, 'years'], 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [62.0, 'mg/dL']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 27 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 62.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 110 mm Hg. The patient's diastolic blood pressure is 60 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 1 + 1 = 2.
The patient's CURB-65 score is 2."
6435,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-4005210-2,Extracted,"A 40-year-old female from Ralegaon village, Yavatmal district, farm laborer by occupation was admitted in drowsy state with history of fever for 10 days, cough and progressive shortness of breath for last 5 days, and pain in right side of abdomen and vomiting for last 3 days. On general physical examination, she was febrile (39.2°C), icteric, and drowsy. She had pulse of 114 beats per min, blood pressure of 110/80 mmHg, and respiratory rate of 26 breaths per min. Her GCS score was E2M5V4. A 1.5 cm sized black crusted ulcer (eschar) was found on the lateral aspect of right thigh []. Her chest examination revealed bilateral crackles. Chest radiograph showed bilateral diffuse infiltrates []. She was treated with oral doxycycline 100 mg twice a day. Arterial blood gas analysis revealed metabolic acidosis and PaO2/FiO2 ratio of 54. In view of her respiratory distress, she was intubated and put on mechanical ventilator.
Her laboratory investigations revealed TLC of 21,300 mm3, hemoglobin of 7.8 gm/dl, and platelet count of 116,000 mm3; AST, 373; ALT, 238; total bilirubin, 3.6 mg/dl; albumin, 1.7 gm/dl; total protein, 4 gm/dl; creatinine, 2.4 mg/dl; and urea, 84 mg/dl. CSF examination did not reveal any abnormality. Abdominal USG was normal. Her Weil-Felix test was positive for the OX-K antigen in titers of 1:320. Biopsy of eschar showed a lymphohistiocytic vasculitis, perivascular collections of lymphocytes with areas of ulceration, and necrosis of overlying epidermis. She was also started on chloramphenicol, but in spite of the intensive supportive care and antibiotic coverage, the patient succumbed to her illness on the 7th day of hospitalization due to multiorgan failure (MOF).",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'respiratory rate': [26.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [84.0, 'mg/dL'], 'Confusion': True, 'Diastolic Blood Pressure': [80.0, 'mm hg'], 'age': [40, 'years']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 40 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient has confusion, 1 point is added to score making the current total 0 + 1 = 1.
The concentration of BUN is 84.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 26 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 110 mm Hg. The patient's diastolic blood pressure is 80 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6436,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-4384458-1,Extracted,"A 55-year-old male patient without a prior medical history was admitted to the emergency room of our university hospital for treatment of a severe headache and vomiting on May 12th, 2010. His vital signs included blood pressure of 180/100 mmHg, pulse rate of 88/min, respiratory rate of 24/min, and body temperature of 36.0℃. An initial head computed tomography (CT) scan revealed an acute extensive subarchnoid hemorrhage filling the basilar cisterns. Subsequent CT angiography showed an anterolaterally-directed ruptured aneurysm on the left mid-cranial artery bifurcation. As a result of these findings, microsurgical clipping was proposed. During the left pterional craniotomy and dural reflection, an intraoperative rupture was encountered and a rapid corticectomy with a retraction of the temporal lobe made the aneurysm clipping amenable.
Post-operatively, the patient was stuporous and responded only to basal stimuli. On post-operative day 2, a controlled mandatory ventilation mode mechanical ventilator was applied along with intravenous sedatives. The patient's neurologic status was stationary. Around post-operative day 5, the patient's body temporal temperature elevated to 38.1℃, and the arterial oxygen saturation levels dropped to 90%. Additional laboratory examinations revealed elevated C-reactive protein (27.0 mg/dL), leukocytosis (20,990/mm3) with a high neutrophil percentage (93%) and a left-shift. A chest CT discovered diffused bilateral lower lobe interstitial infiltrates with pleural effusion, consistent with a diagnosis of ARDS. Following this, the patient was placed on a regimen of IV teicoplanin (200 mg every 12 h), moxifloxacin (400 mg every 24 h) and meropenem (0.5 g every 12 h). On post-operative day 7, a culture of a sputum specimen was found to be positive for multi-drug-resistant Acinetobacter baumannii and methicillin-resistant Staphylococcus aureus, but they were not isolated later. Consequently, the administration of meropenem was changed to colistimethate sodium (160 mg every 12h). However, oxygenation deteriorated further (PaO2/FiO2 90-150 mmHg) and the patient became hemodynamically unstable despite the use of volume resuscitation and mechanical ventilation.
Despite the previous 10 days of regimented intravenous antibiotics and inotropics, the patient's condition worsened and progressed into severe sepsis. On May 27, lab results revealed a white blood cell count of 18,400/mm3, hemoglobin 8.8 g/dL, creatinine 2.8 mg/dL, blood urea nitrogen 111 mg/dL, alanine transaminase 116 IU/L, aspartate transaminase 88 IU/L, alkaline phosphatase 183 IU/L, sodium 155 mEq/L, potassium 4.7 mEq/L, and chloride 116 mEq/L. The erythrocyte sedimentation rate was 75 mm/hr and C-reactive protein was 23.5 mg/L. At this point, the patient's arterial oxygen saturation levels had dropped to 86%. In response, in addition to the existing assist-controlled mechanical ventilation, the patient was treated with 2 liters of IV normal saline, dopamine (3 µg/kg/min) and dobutamine (7 µg/kg/min). On post-operative day 17, gram-positive bacilli were detected in the patient's blood cultures. Blood was drawn from peripheral veins on both arms and feet, and six isolates could be obtained from six blood cultures. Of these, isolate 100604-2 was subjected to species identification, but it could not be identified using conventional methods in the clinical microbiology laboratory, including VITEK2 (bioMerieux, Hazelwood, MO, USA) and Microscan (Dade-Microscan, West Sacramento, CA, USA) analyses. On post-operative day 23, it was ascertained that there was little hope of recovery and his family requested the patient be transferred to a hospital located closer to their house. As a result the patient was discharged and transferred to the requested hospital. The patient died 3 days later.
The isolates including the isolate 100604-2 formed translucent, flat colonies of gram-positive bacilli, and showed no hemolysis on blood agar. To identify isolate 100604-2, 16S rRNA gene analysis was performed. A portion of the 16S rRNA gene was amplified and sequenced using the primer set fD1/rp2 []. Determined sequences (1,425 bp) were compared with the GenBank public database using the BLASTN program () and the EzTaxon public database () []. Sequences showing high similarities were retrieved from the database and were aligned using the CLUSTALX program. A phylogenetic tree was also constructed by the neighbor-joining method and bootstrap values were evaluated from 1,000 replications.
The 16S rRNA gene sequence (1,425 bp) of the isolate 100604-2 showed the highest similarity (99.6%) with a sequence of P. pasadenensis SAFN-007T (AY167820), followed by P. humicus PC-147T (AM411528) (98.0%), P. kobensis DSM 10249T (AB073363) (95.0%), and P. pinihumi S23T (GQ423057) (94.7%). Thus, the isolate 100604-2 was identified as P. pasadenensis. The constructed phylogenetic tree also indicated that isolate 100604-2 clustered with P. pasadenensis SAFN-007T (AY167820), which was supported strongly by bootstrap analysis ().
In vitro antimicrobial susceptibility testing was performed by the broth microdilution method according to the guidelines of the Clinical and Laboratory Standards Institute (CLSI) []. Isolate 100604-2 showed a low minimum inhibitory concentration for several antimicrobial agents that included ceftazidime (1 mg/L), imipenem (≤0.06 mg/L), penicillin (≤0.06 mg/L), polymyxin B (1 mg/L), vancomycin (0.12 mg/L), and trimethoprim/sulfamethoxazole (0.06/1.18 mg/L).",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'Systolic Blood Pressure': [180.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg'], 'respiratory rate': [24.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [111.0, 'mg/dL'], 'Confusion': True}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 55 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient has confusion, 1 point is added to score making the current total 0 + 1 = 1.
The concentration of BUN is 111.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 24 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 180 mm Hg. The patient's diastolic blood pressure is 100 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6437,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-9759,Extracted,"A 71-year-old African American man is brought to the emergency department with a worsening productive cough and dyspnea for 2 days. He has had generalized bone pain for 2 months. He was admitted for pyelonephritis last month. He also received outpatient treatment for pneumonia almost 2 months ago. Over the past 2 months, he has been taking over-the-counter ibuprofen for pain as needed. He appears anxious. The vital signs include: temperature 38.8°C (101.8°F), pulse 95/min, respiratory rate 20/min, and blood pressure 155/90 mm Hg. The conjunctivae are pale. Crackles are heard in the right lower lobe. The cardiac examination shows no abnormalities. The laboratory studies show the following:
Hemoglobin 9 g/dL
Mean corpuscular volume 95 μm3
Leukocyte count 13,500/mm3
Segmented neutrophils 75%
Lymphocytes 25%
Platelet count 240,000/mm3
ESR 85 mm/hr
Serum
Na+ 135 mEq/L
K+ 4.2 mEq/L
Cl− 113 mEq/L
HCO3− 20 mEq/L
Ca+ 12.4 mg/dL
Albumin 4 g/dL
Urea nitrogen 38 mg/dL
Creatinine 2.2 mg/dL
A chest X-ray shows a right lower lobe opacity and blurring of the ipsilateral diaphragmatic dome. Skull and pelvic X-rays are performed (see image).",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [71, 'years'], 'Systolic Blood Pressure': [155.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg'], 'Blood Urea Nitrogen (BUN)': [38.0, 'mg/dL'], 'respiratory rate': [20.0, 'breaths per minute']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 71 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 1.
The concentration of BUN is 38.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 155 mm Hg. The patient's diastolic blood pressure is 90 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6438,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-8185934-1,Extracted,"A 78-year-old Japanese female was diagnosed with focal epilepsy two years prior to admission based on repeated right hemiconvulsion evolving into generalized tonic–clonic seizure with an electroencephalography finding of frequent sharp waves in the left parietal lobe. Her status was stable on treatment with levetiracetam (LEV) 2000 mg/day orally, however, episodic disturbance of consciousness appeared and gradually worsened one month prior to admission. Phenytoin (PHT) 200 mg/day was given in conjunction with LEV at another hospital 16 days prior to admission. Nevertheless, there was little improvement in the frequency of impaired consciousness, and she was transferred to our hospital to adjust AEDs.
At the time of admission, her level of consciousness was alert and there was no obvious evidence of epileptic seizures. Physical examination on admission revealed blood pressure (BP) 106/52 mm Hg, heart rate (HR) 76 beats per minute (bpm), body temperature (BT) 37.5 °C, and respiratory rate (RR) 22 breaths per minute, and the electrocardiogram (ECG) showed no arrhythmia and PR interval was normal (0.16 s). Her height, body weight, and body mass index (BMI) were 152 cm, 42 kg, and 18.2 kg/m2, respectively. Figure A shows the clinical course and the chronological laboratory findings of the patient. Her complete blood cell counts (CBCs) showed total white blood cell (WBC) counts of 7100 /μL with neutrophil counts of 5893 /μL, hemoglobin level of 7.0 mg/dL, red blood cell counts of 413 × 104 /μL, mean corpuscular volume of 63.7 fl, mean corpuscular hemoglobin concentration of 26.6%, and platelet counts of 19.6 × 104 /μL, indicating hypochromic microcytic anemia due to iron deficiency. Her blood chemistry tests showed normal liver and renal function: aspartate aminotransferase (AST) of 13 U/L, alanine aminotransferase (ALT) of 8 U/L, blood urea nitrogen (BUN) of 15.1 mg/dL, and creatinine (Cr) of 0.34 mg/dL. Her serum C-reactive protein (CRP) was mildly elevated to 6.6 mg/dL and chest computed tomography showed mild aspiration pneumonia in the left S10 segment of left lung. Since she was in good condition without decreased percutaneous oxygen saturation (SpO2), antibiotics were not administered. LEV 2000 mg/day was continued orally and PHT was discontinued, thereafter, the patient was initiated on LCM at 100 mg/day orally because the patient did not accept to increase the LEV dose due to drug-induced drowsiness. The stool occult blood on admission was positive, but the patient did not agree to undergo a gastrointestinal endoscopy, thereafter, the patient received a blood transfusion containing 4 units of red blood cell concentrates (RCC) on the 4th hospital day to treat anemia.
The dose of LCM was increased to 200 mg/day on the 9th hospital day, as per the Japanese guidelines for maintenance doses, and subsequently on the 10th hospital day, a sinus bradycardia with HR of 20 bpm suddenly began to appear, with a maximum sinus arrest of 5.6 s (Fig. B). The PR interval was 0.16 s and did not change during her hospitalization. There was no decrease in BP or no symptomatic syncope due to SND, while WBC counts were decreased to 2300/μL on the 10th hospital day. The additional blood chemistry tests showed AST of 16 U/L, ALT of 10 U/L, BUN of 15.8 mg/dL, Cr of 0.33 mg/dL, and potassium of 4.45 mmol/L. Drug-induced SND and leukopenia were suspected and LCM was immediately discontinued. The bradycardia gradually improved until the next day with HR of 59 bpm. There was no evidence of sepsis causing neutropenia at this point, and CRP was decreased to 1.2 mg/dL.
On the 11th hospital day, a decrease in SpO2 requiring high-flow oxygen appeared. An analysis of arterial blood (O2 10 L/min via non-rebreather mask) showed a pH of 7.49, a partial pressure of carbon dioxide of 31.9 mm Hg, and a partial pressure of oxygen of 72.3 mm Hg. Although serum N-terminal pro-brain natriuretic peptide level was elevated to 1320 pg/mL (reference range < 125 pg/mL), a transthoracic echocardiogram showed a normal ejection fraction of the left ventricle (63%) without signs of asynergy and pulmonary hypertension, and normal inferior vena cava diameter (13 mm) with normal inspiratory collapse. A chest X-ray showed an infiltrative shadow in the left lung field, which was suspected to be exacerbation of the pneumonia recognized at admission. The WBC counts decreased to 500/μL and the neutrophil counts to 49/μL, leading to a diagnosis of drug-induced agranulocytosis. Fever of over 39 °C appeared. After blood, sputum, and urine cultures were submitted, meropenem (3 g/day) and granulocyte-colony stimulating factor (G-CSF) (100 μg/day) were administered. No bacterial growth was confirmed in the blood and urine cultures, while the sputum cultures showed a growth of Acinetobacter baumannii/calcoaceticus complex and Klebsiella pneumoniae that were sensitive to carbapenem antibiotics. Since LCM was discontinued, LEV was replaced from oral to intravenous administration, and the dose was increased to 3000 mg/day in order to reinforce the treatment of epilepsy.
On the 12th hospital day, the vital signs were worsened to BP 69/49 mm Hg, HR 123 bpm, BT 39.4 °C, RR 34 breaths per minute, and she became unresponsive to calls. Consequently, fluid resuscitation was started, and vancomycin was administered with dose adjustment based on therapeutic drug monitoring (TDM). Since hypotension did not improve even with adequate fluid resuscitation, norepinephrine was started and increased to maintain mean arterial pressure at 65 mm Hg. The WBC counts were 600/μL and the neutrophil counts were 24/μL with still no improvement in agranulocytosis, and serum procalcitonin level was markedly elevated at 25.55 ng/mL (reference range < 0.50 ng/mL), suggesting severe sepsis. Generally, 28–49% of severe sepsis cases are known to show negative cultures [] Although the blood cultures of the patient were negative, septic shock was strongly suspected due to fever associated with agranulocytosis, hypotension unresponsive to adequate rehydration, tachypnea, disturbance of consciousness, and the absence of other diseases causing hypotension.
On the 14th hospital day, the patient’s WBC and neutrophil counts improved to 4000/μL and 3640/μL, respectively, therefore, G-CSF administration was discontinued. Although the SND and agranulocytosis improved, the patient could not recover from septic shock, and died on the 15th hospital day.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [78, 'years'], 'Systolic Blood Pressure': [69.0, 'mm hg'], 'Diastolic Blood Pressure': [49.0, 'mm hg'], 'Blood Urea Nitrogen (BUN)': [15.8, 'mg/dL'], 'respiratory rate': [22.0, 'breaths per minute'], 'Confusion': True}",3,3,3,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 78 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient has confusion, 1 point is added to score making the current total 1 + 1 = 2.
The concentration of BUN is 15.8 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 2.
The patient's respiratory rate is 22 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 69 mm Hg. The patient's diastolic blood pressure is 49 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 2 + 1 = 3.
The patient's CURB-65 score is 3."
6439,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-6186,Extracted,"A 70-year-old man with history of asthma and chronic obstructive pulmonary disease presents to the emergency department with resting dyspnea for the past 2 hours after watching his granddaughter play soccer. Despite albuterol, ipratropium, magnesium, methylprednisolone, and high flow nasal cannula, the patient agrees to elective intubation and is transferred to the intensive care unit. His hospital course is prolonged by pneumonia, which is managed with vancomycin, pipercillin-tazobactam, and gentamicin to cover for ventilator-associated etiologies. He is maintained on nasogastric tube feeds, lactated ringer fluid boluses, and subcutaneous heparin for deep vein thrombosis prophylaxis. On hospital day 7, the patient proves difficult to wean from his ventilator due to labored tachypnea. As the nurse rotates the patient to change his sacral pressure ulcer dressing, the patient's peak airway pressure increases sharply to 55 cm H2O. The nurse noted that the patient was wincing at the time. His temperature is 100.1°F (38.1°C), blood pressure is 100/50 mmHg, and pulse is 100/min. His respirations are 22/min on the ventilator despite a set respiratory rate of 14/min. His laboratory results are shown below:

Leukocyte count and differential:
Leukocyte count: 18,000/mm^3
Segmented neutrophils: 90%
Bands: 10%
Eosinophils: 5%
Basophils: 2%
Lymphocytes: 2%
Monocytes: 1%

Serum:
Na+: 135 mEq/L
Cl-: 107 mEq/L
K+: 3.2 mEq/L
HCO3-: 18 mEq/L
Urea nitrogen: 45 mg/dL
Glucose: 89 mg/dL
Creatinine: 1.3 mg/dL
Alkaline phosphatase: 100 U/L
Aspartate aminotransferase (AST, GOT): 250 U/L
Alanine aminotransferase (ALT, GPT): 300 U/L
Gamma-Glutamyltransferase (GGT): 2 U/L
Amylase: 10 IU/dL
Lipase: 5 IU/dL

Bedside ultrasound imaging is shown in Figure A.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [70, 'years'], 'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [50.0, 'mm hg'], 'Blood Urea Nitrogen (BUN)': [45.0, 'mg/dL'], 'respiratory rate': [22.0, 'breaths per minute']}",3,3,3,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 70 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 1.
The concentration of BUN is 45.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 22 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 100 mm Hg. The patient's diastolic blood pressure is 50 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 2 + 1 = 3.
The patient's CURB-65 score is 3."
6440,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-3546438-1,Extracted,"A 68-year-old white male with a history of hypertension, gastroesophageal reflux disease, and congestive heart failure was found by his son lying on the floor of his home. The son activated the EMS system, and the paramedics found the patient with altered mentation, responsive to pain and mumbling. The patient was incontinent of feces and urine. The son last spoke to the patient two days earlier and reports that he was in his normal health. The patient's history included depression, benzodiazepine dependence, and anxiety disorder. The patient's daily medications included furosemide 40 mg, isosorbide dinitrate 30 mg, lisinopril 20 mg, and atorvastatin 10 mg. The patient was known to ingest large amounts of over-the-counter antacids and baking soda mixed with water for indigestion. His social history was significant for tobacco and alcohol.
Upon arrival to the emergency department (ED) the patient's blood pressure was 218/111, the cardiac monitoring showed sinus tachycardia at 127/minute, a rectal temperature 98.6°F was measured, the room air SPO2 was 94%, and respirations were 16/minute. The patient was able to follow simple commands. He opened his eyes to voice and moved his extremities, including pulling his EKG wires. The patient had pale skin, lateral nystagmus, and signs of poor hygiene. The remainder of the physical exam was unremarkable except for abdominal pain, nausea, vomiting, or generalized pain. The patient was given labetalol 10 mg for hypertension and aggressive intravenous fluid hydration and IV folic acid, magnesium sulfate, multivitamin, and thiamine.
Significant laboratory results included calcium of 18.7 mg/dL, bicarbonate 45 mmol/L, BUN 55 mg/dL, creatinine 4.5 mg/dL, chloride 83 mmol/L, and WBC 22.46 K/cumm. Arterial blood gas revealed a pH of 7.54, pCO2 of 58 mmHg, and pO2 of 60 mmHg. Parathyroid hormone was undetectable (normal range is 14–72). Liver function tests, coagulation studies, and lipase were normal. EKG showed sinus tachycardia and head CT showed no acute changes.
The patient was admitted to the intensive care unit with a BP of 184/116, pulse 88/min, and respirations of 16/min. A chest X-ray showed infiltrates, concerning for pneumonia. The patient was placed on a nitroglycerin drip to control his blood pressure, antibiotics for presumed infection, IV fluids and a bisphosphonate for hypercalcemia, and risperidol for signs of delirium.
The patient was admitted for a total of 16 days. Upon discharge the patient's mental status had returned to nearly normal, the patient was found to have an underlying dementia not previously diagnosed. The discharge blood values showed calcium 8.5 mg/dL, bicarbonate 21 mmol/L, BUN 19.0 mg/dL, creatinine 1.4 mg/dL, and WBC 10 K/cumm. demonstrates the progressive resolution of the patient's metabolic alkalosis, hypercalcemia, and renal failure throughout this hospital course. The patient was placed on Protonix for reflux, given instruction to avoid antacid use and to follow up with the internal medicine clinic.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [68, 'years'], 'Systolic Blood Pressure': [218.0, 'mm hg'], 'Diastolic Blood Pressure': [111.0, 'mm hg'], 'respiratory rate': [16.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [55.0, 'mg/dL'], 'Confusion': True}",3,3,3,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 68 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient has confusion, 1 point is added to score making the current total 1 + 1 = 2.
The concentration of BUN is 55.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 2 + 1 = 3.
The patient's respiratory rate is 16 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 3.
The patient's systiolic blood pressure is 218 mm Hg. The patient's diastolic blood pressure is 111 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 3.
The patient's CURB-65 score is 3."
6441,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-6549348-1,Extracted,"A 69-year-old Chinese woman was admitted to our hospital with fever and myalgia persisting for 2 days on August 12, 2017. The patient was not treated at a local clinic. Except a history of hypertension for 3 years, she had no other specific diseases or familial medical history. She lived in a rural area from her birth and often worked in fields. The vital signs were body temperature 39.0 °C, heart rate 122/min, respiratory rate 23/min and blood pressure 130/80 mmHg. The positive physical examination included a poor general condition, petechiae in the chest, palpable lymph nodes in the neck and axilla, and rough breathing sounds in lungs. Upon admission, hematologic tests revealed that her leukocyte count was 1.1 × 109 /L, erythrocyte count 2.88 × 1012 /L, hemoglobin 102 g/L, platelet count 36.0 × 109 /L, and abnormal lymphocytes 3%. Blood biochemistry showed blood urea nitrogen 14.17 mmol/L, creatinine 135.1 μmol/L, lactic dehydrogenase 989.4 IU/L, ferritin > 2000 μg/L and procalcitonin 66.29 ng/ml. The prothrombin time was 18.7 s, partial thromboplastin time 86.3 s, fibrinogen 1.90 g/L and D-Dimer over 20 μg/ml. Enzyme-linked immunosorbent assays of IgM and IgG antibodies for HFRS were both positive and the serotype of hantaviruses was HTNV. Additional serologic tests showed that antibodies against EBV, cytomegalovirus, herpes, adenovirus, respiratory syncytial virus, influenza virus A and B, human immunodeficiency virus, Hepatitis A, B, and C viruses, Legionella pneumophila, mycoplasma pneumoniae, chlamydia pneumoniae and rickettsia were negative. The scan of chest and abdomen by computed tomography demonstrated that hypostatic pneumonia and hepatosplenomegaly. The ultrasound examination to superficial lymph nodes revealed that multiple lymphadenectasis in the neck, axilla and groin. After 4-day hyperthermia (a peak temperature of up to 42 °C) from admission, the patient’s condition deteriorated gradually. Blood test showed that leukocyte count was 2.6 × 109 /L, erythrocyte count 1.91 × 1012 /L, hemoglobin 70 g/L, platelet count 10.0 × 109 /L, abnormal lymphocytes 18%, blood urea nitrogen 13.64 mmol/L, creatinine 200.6 μmol/L, lactic dehydrogenase 1169.0 IU/L, alanine aminotransferase 63.4 U/L, aspartate aminotransferase 260.7 U/L, albumin 28.3 g/L, creatine kinase 1859.4 U/L, creatine kinase-MB 58.3 IU/L, hydroxybutyrate dehydrogenase 816.0 IU/L, HDL-cholesterol 0.51 mmol/L, LDL-cholesterol 0.38 mmol/L, total cholesterol 1.34 mmol/L, triglyceride 1.04 mmol/L, the prothrombin time 18.5 s, partial thromboplastin time 100.2 s and fibrinogen 1.34 g/L. For clear comparison and understanding, the results of these blood parameters with their normal range on admission day 1 and day 4 were listed in Table . The immature cells and nucleated erythrocytes were found by peripheral blood smears. The concurrently cultures of blood, urine and sputum did not reveal any pathogen. The formation of histiocytes with prominent hemophagocytosis was discovered through bone marrow aspiration (Fig. ).
In the treatment of the patient, we just focused on the original disease HFRS, mainly taking the measurements of antiviral agent ribavirin, diuretic and intermittent hemodialysis in the initial and oliguric stages, antibacterial drug cefoperazone sodium and sulbactam sodium in dealing with pulmonary infection, maintenance of water and electrolyte acid-base balance and other supportive therapies when needed. No corticosteroids and specific therapy were applied. The patient recovered completely after the above comprehensive treatments on day 26. Bone marrow aspiration was performed again on September 7 and the result only showed secondary anemia but no signs of hemophagocytosis. The 3 months follow-up blood tests after her discharge from our hospital demonstrated normal outcomes.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [69, 'years'], 'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg'], 'respiratory rate': [23.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [14.17, 'mmol/L']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 69 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 1.
The concentration of BUN is 14.17 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of BUN from mmol to mg. The mass of BUN is 14.17 mmol. To convert 14.17 mmol of BUN to mol, multiply by the conversion factor 0.001, giving us 14.17 mmol BUN * 0.001 mol/mmol = 0.01417 mol BUN. To convert from mol BUN to grams, multiply by the molar mass 28.02 g/mol, which will give 0.01417 mol BUN * 28.02 g/mol = 0.39704 g BUN. To convert 0.39704 g of BUN to mg, multiply by the conversion factor 1000.0, giving us 0.39704 g BUN * 1000.0 mg/g = 397.04 mg BUN. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 397.04 mg BUN/10.0 dL = 39.704 mg BUN/dL. The concentration value of 14.17 mmol BUN/L converts to 39.704 mg BUN/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 23 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 130 mm Hg. The patient's diastolic blood pressure is 80 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6442,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-2769317-1,Extracted,"A 46-year-old white male presented to the emergency department (ED) complaining of progressive dyspnea. He was healthy until three days prior to hospital admission when he developed a sore throat and fever. He went to his primary care physician’s (PCP) office where he had a positive group A rapid antigen test. His PCP gave him a prescription for cefdinir 300 mg twice daily for ten days and he began taking the antibiotic. His throat felt worse the next day and his fever increased to 105 degrees Fahrenheit. He called the PCP’s office but was not given an office appointment that day. On day 3, he returned to the PCP’s office with complaints of persistent fever, sore throat and new onset of redness and swelling over the left side of his neck. He received a shot of ceftriaxone and promethazine (to treat his nausea) and was told to put an ice pack on his neck swelling. That night, the patient’s wife noted he began acting confused and had some trouble sleeping. The following morning, the patient developed severe shortness of breath with intermittent air gasping. His wife called EMS, who transported him emergently to the hospital. The ED physicians observed him in acute respiratory distress leading to intubation. In addition to sedation/paralytic meds for intubation, he was given acetaminophen 650 mg per rectum, clindamycin 600 mg IV, ceftriaxone 2 gm IV, vancomycin 1 gm IV, and two liters of normal saline bolus. In the ED, he was later noted to have falling systolic blood pressures to the 60’s and was started on a dopamine drip and admitted to the ICU.
His past medical history included impaired fasting glucose and hypercholesterolemia, without history of surgeries. His home medications consisted of metformin 500 mg twice daily, resuvastatin 5 mg nightly, fish oil, flax seed, and niacin. Socially, he currently resides with his wife, denies tobacco or drug use and drinks alcohol occasionally.
On initial physical exam, his temperature was 104 degrees Fahrenheit. His first recorded blood pressure and heart rate were 141/81 and 117 respectively, but systolic blood pressure dropped to the 60s after some time in the ED. After intubation, his respiratory rate was 20 and his oxygen saturation was 100% on the ventilator.
In general, he was an average sized white male who seemed comfortable on the ventilator. He had normal sclera, conjunctiva and mucous membranes, but his oropharynx was poorly visualized due to ET and OG tubes in place. A large firm swelling over his left neck, which was erythematous and warm, was noted. His lungs were clear to auscultation bilaterally without wheezes or crackles and his cardiac exam revealed a fast rate and regular rhythm with S1 and S2 audible, without murmurs, rubs, or gallops. His peripheral pulses were strong and no significant edema was noted. His abdomen was soft and nondistended with positive bowel sounds. His skin had no evident rashes or lesions. The neurological exam and mental status was poorly tested due to paralytics given in the ED.
Initial laboratory data revealed a white blood cell count of 6.96, hemoglobin of 13.2, hematocrit of 38.4, and platelet count of 134. The basic metabolic panel showed sodium of 125, potassium of 4.0, chloride of 91, bicarbonate of 22, BUN of 7, creatinine of 0.9, glucose of 140, and calcium of 8.5. The hepatic panel was within normal limits. His cardiac enzymes, including CK, CKMB and troponin, were normal. Initial arterial blood gas after intubation showed a pH of 7.13, pCO2 of 61, pO2 of 136, and oxygen saturation of 98% on 100% O2. After ventilator adjustment the pH normalized to 7.41 with a pCO2 of 35.
On imaging, his head computerized tomography (CT) scan showed no acute disease. His neck CT scan showed extensive soft tissue edema along the nasopharynx and orophyarnx involving the prevertebral and parapharyngeal spaces, in addition to a left peritonsillar abscess that completely obliterated the airspace except for the endotracheal tube ().
The patient was started on dexamethasone intravenously soon after admission. The otolaryngologist performed a bedside incision and drainage (I&D) of the abscess. Over the next couple of days, the patient was weaned off the ventilator and dopamine was discontinued. Due to an adverse reaction to clindamycin on day 1 of hospitalization, we changed his antibiotic regimen to vancomycin and piperacillin-tazobactam. On hospital day 4, we extubated the patient. Unfortunately, that night he had a recurrence of dyspnea with stridor, which required transfer back to the ICU with repeat I&D of the abscess. After the repeat drainage, the patient had a smooth recovery and was discharged 3 days later on continued antibiotics and oral steroids. His final peritonsillar wound culture results revealed group C and group G streptococcus and his blood cultures indicated septicemia with group C streptococcus.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [60.0, 'mm hg'], 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [7.0, 'mg/dL'], 'Confusion': True, 'Diastolic Blood Pressure': [81.0, 'mm hg'], 'age': [46, 'years']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 46 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient has confusion, 1 point is added to score making the current total 0 + 1 = 1.
The concentration of BUN is 7.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 1.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 60 mm Hg. The patient's diastolic blood pressure is 81 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 1 + 1 = 2.
The patient's CURB-65 score is 2."
6443,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-1670,Extracted,"A 43-year-old woman comes to the physician because of a fever, nausea, and a nonproductive cough for 7 days. During this period, she has had headaches, generalized fatigue, and muscle and joint pain. She has also had increasing shortness of breath for 2 days. She has type 2 diabetes mellitus and osteoarthritis of her left knee. Current medications include insulin and ibuprofen. She had smoked two packs of cigarettes daily for 20 years but stopped 10 years ago. Her temperature is 38.1°C (100.6°F), pulse is 94/min, respirations are 18/min, and blood pressure is 132/86 mm Hg. The lungs are clear to auscultation. There are multiple skin lesions with a blue livid center, pale intermediate zone, and a dark red peripheral rim on the upper and lower extremities. Laboratory studies show:
Hemoglobin 14.6 g/dL
Leukocyte count 11,100/mm3
Serum
Na+ 137 mEq/L
K+ 4.1 mEq/L
Cl- 99 mEq/L
Urea nitrogen 17 mg/dL
Glucose 123 mg/dL
Creatinine 0.9 mg/dL
An x-ray of the chest is shown.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [43, 'years'], 'Systolic Blood Pressure': [132.0, 'mm hg'], 'Diastolic Blood Pressure': [86.0, 'mm hg'], 'Blood Urea Nitrogen (BUN)': [17.0, 'mg/dL'], 'respiratory rate': [18.0, 'breaths per minute']}",0,0,0,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 43 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 17.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 18 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 0.
The patient's systiolic blood pressure is 132 mm Hg. The patient's diastolic blood pressure is 86 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 0.
The patient's CURB-65 score is 0."
6444,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-7814410-1,Extracted,"An 84-year-old male with a medical history significant for multiple myeloma not in remission, insulin-dependent type II diabetes mellitus, hypertension, and hyperlipidemia presented to our emergency department to be tested for COVID-19 infection. He was diagnosed with multiple myeloma about 6 months ago at another institute and was undergoing cycles of outpatient chemotherapy with Revlimid, Velcade, and Dexamethasone (RVD; 1.3 mg/m2 SC). He was sent to the ED to rule out COVID-19 infection prior to him continuing his chemotherapy sessions. At that time, he was experiencing nonspecific symptoms such as malaise, fatigue, hyporexia, and aguesia for the past 7 days but denied fever, chest pain, cough, difficulty in breathing, rhinorrhea, nasal congestion, sore throat, sneezing, or any other URI symptoms at the time of presentation. He was in close contact with his daughter who was diagnosed with COVID-19 infection. Home medications included basal bolus of insulin, acarbose, liraglutide, and linagliptin for his diabetes and carvedilol, lisinopril, furosemide, and verapamil for his hypertension and was on high-intensity statin therapy. He was a former smoker who quit about 35 years ago. He reported no use of alcohol or illicit drugs. He was followed up by an oncologist part of our healthcare system.
On physical examination at the time of presentation, the patient was afebrile (36°C), with a blood pressure of 156/64 mmHg, heart rate of 94 beats/min, respiratory rate of 19 breaths/min, and oxygen saturation of 95% on room air. He was not in acute distress, and chest auscultation revealed normal breath sounds. Rest of the physical examination was unremarkable. Initial blood tests revealed the following: hemoglobin level 11.3 g/dL, leucocyte count 3,600 cells/mm3, with 74% neutrophils, 17.6% lymphocytes, and 6.4% monocytes, platelet count 106,000/mm3, serum sodium level 135 mmol/L, urea 40 mg/dL, creatinine level 2.42 mg/dL, lactate dehydrogenase 373 U/L, high sensitive C-reactive protein 17.40 mg/l, and ferritin level 415 ng/ml. Xpert-SARS-CoV-2 obtained through a nasopharyngeal swab was positive. Chest radiograph revealed patchy areas of interstitial infiltrates in mid to lower lung zones ().
The patient was admitted to telemetry floors with the diagnosis of mild COVID-19 pneumonia and acute kidney injury (AKI). He was started on hydroxychloroquine and azithromycin for COVID-19 pneumonia, supplemental oxygen as needed to maintain an oxygen saturation >92%, Lovenox for thromboembolism prophylaxis, supportive measures with intravenous fluids, and electrolyte abnormalities correction for his AKI. Except for spikes in temperature and mild hypoxia requiring 4 L of O2 through a nasal cannula, his hospital course was unremarkable for the first 5 days.
On the sixth day of admission, the patient was found to have hematochezia associated with a significant drop in his hemoglobin from 10 mg/dL to 7.1 mg/dL. He had a history of diverticulosis from previous colonoscopy. He was managed conservatively with holding antiplatelet and anticoagulation and started on intravenous proton-pump inhibitors. After the acute blood loss anemia, the patient became more hypoxic with an increment in supplemental oxygen requirements. He underwent emergent intubation and mechanical ventilation in the setting of acute hypoxemic respiratory failure and was transferred to an intensive care unit. He was also resuscitated with intravenous blood products. Repeat chest radiograph was remarkable for worsening bilateral infiltrates, and the patient was started on empiric treatment for superimposed bacterial infection with cefepime 2 g IV and vancomycin. At that time, his COVID-19 infection was reassessed as severe multifocal COVID-19 pneumonia. IL-6 level and hepatitis B and C were ordered for possible consideration of tocilizumab therapy. Convalescent plasma and remdesivir trials were also considered for treatment therapy. His IL-6 level was elevated at 38.73 pg/mL and also found to have hepatitis B surface antigen, core antibody. It was decided to abstain from tocilizumab therapy given the possibility of reactivation of his chronic hepatitis B. He was able to be weaned off the mechanical ventilation and was switched to nonrebreather after 5 days of intubation and mechanical ventilation.
On the 11th day of admission, the patient was found to be bradycardic and in shock and eventually found to be in asystole prompting ACLS with return of circulation after 7 minutes and 2 rounds of epinephrine. The patient developed cardiac arrest and had to be reintubated and mechanically ventilated. His labs showed worsening inflammatory markers, as well as kidney function, requiring renal replacement therapy. He received both convalescent plasma and remdesivir 200 mg IV BID loading dose followed by 100 mg IV BID daily for 4 days for treatment of COVID-19 pneumonia.
He was kept on mechanical ventilation with a low-stretch tidal volume strategy, 6 ml/kg TV, goal plateau pressure less than 30, permissive hypercapnia with pH >7.20, and high PEEP with the goal for lower FiO2 to prevent hyperoxia; however, he continued to have significant shunt hypoxemia due to volume overload and severe pneumonitis. In the following days, he remained on mechanical ventilation and hemodialysis without any significant improvement in the ventilator settings. In the context of shock, requiring vasopressors such as norepinephrine, increased FiO2, bandemia (18%), and positive procalcitonin level, repeat cultures were sent. CXR revealed worsening infiltrates (). New-onset septic shock with possible ventilator-associated pneumonia was considered. Repeat blood and sputum cultures came back positive for the growth of acid-fast beaded bacilli. With uncertainty, if the results were contamination versus an isolated line infection, repeat AFB blood cultures from 2 sites including the lines were sent along with AFB sputum culture for confirmation. While awaiting final culture and sensitivity reports, his antibiotics were upgraded to cover possible nocardia infection with imipenem/cilastatin 500 mg IV and trimethoprim/sulfamethoxazole IV 5 mg/kg. Unfortunately, he was unable to withstand multiorgan failure with septic shock and ARDS complicated by AFB bacteremia. He developed asystole with fixed and dilated pupils and was pronounced dead after approximately 2 months being hospitalized. Blood and sputum cultures 1 week after came back positive for AFB bacilli Mycobacterium abscessus.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [156.0, 'mm hg'], 'Diastolic Blood Pressure': [64.0, 'mm hg'], 'age': [84, 'years'], 'respiratory rate': [19.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [40.0, 'mg/dL'], 'Confusion': False}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 84 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 1.
The concentration of BUN is 40.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 19 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 156 mm Hg. The patient's diastolic blood pressure is 64 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6445,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-6467430-1,Extracted,"An 80-year-old Caucasian female who was an active smoker with a 40 pack year smoking history and a past medical history of primary hypertension and chronic obstructive pulmonary disease (COPD) presented to our hospital emergency department (ED) in February, 2017 with fatigue, generalized weakness, and shortness of breath for the last two days. She had been noticing progressively worsening shortness of breath on exertion without any fever, chills, cough, chest pain, orthopnea or paroxysmal nocturnal dyspnea. She did not have any sick contacts and had not travelled anywhere recently.
Upon arrival to the hospital, she was noted to have a heart rate of 122 beats per minute, a respiratory rate of 30 breaths per minute with an oxygen saturation of 85% on room air, and a blood pressure of 161/86 mmHg. Further physical examination revealed a thin and cachectic female who appeared to be in mild respiratory distress. She was noted to have normal heart sounds without any murmurs, rubs, or gallops. A pulmonary examination revealed expiratory wheezing bilaterally without any rales or rhonchi. She did not have rashes or peripheral edema. Due to her respiratory distress she was started on non-invasive ventilatory support in the emergency department (ED), which led to improvement in her respiratory status.
Laboratory investigation revealed a hemoglobin count of 15.1 g/dL (reference range [ref], 12.3-15.3), a peripheral white blood cell count of 21,130 cells/mm3 (ref, 4400-11,300) with a relative neutrophil percentage of 80% (ref, 37%-77%), a platelet count of 301,000/mm3 (ref, 145,000-445,000), a sodium level of 134 mmol/L, a serum creatinine level of 0.30 mg/dL (ref, 0.70-1.5), and a blood urea nitrogen of 8 mg/dL (ref, 9-20). Her liver enzymes were within normal limits. Venous blood gas analysis revealed a pH of 7.26 and a CO2 of 83 mmHg (ref, 41-51). Initial serum procalcitonin was 0.07 ng/mL and a chest radiograph was only significant for hyper-inflated lungs (Figure ).
She was admitted to the hospital for management of mild COPD exacerbation and treated with inhaled bronchodilators and systemic steroids. Repeat blood work obtained 12 hours after initial presentation was significant for a serum procalcitonin of 2.07 ng/mL and a peripheral white blood cell count of 35,170 cells/mm3 with a relative neutrophil percentage of 91% and 2% bands. Due to concerns for development of CAP, sputum cultures, two sets of blood cultures via peripheral blood draw and urinary antigens for S. pneumoniae and L. pneumophila were obtained. She was started on intravenous ampicillin-sulbactam 3 grams every six hours and azithromycin 500 milligrams every 24 hours. A computed tomography scan of the chest revealed tree-in-bud opacities along with regions of bronchial wall thickening in the bilateral lower lobes (Figure ).
A sputum Gram stain revealed many Gram-positive rods, rare Gram-positive cocci, less than 10 squamous epithelial cells and greater than 25 white blood cells per low power field. Her blood cultures remained negative and the final sputum culture grew normal respiratory flora. Surprisingly, urinary antigens for both S. pneumoniae and Lp1 returned positive. Antibiotics were then de-escalated to intravenous levofloxacin 500 mg every 24 hours for a total of five days. The patient’s clinical status improved, and she was discharged home in a stable condition after a one-week hospital stay.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [80, 'years'], 'Systolic Blood Pressure': [161.0, 'mm hg'], 'Diastolic Blood Pressure': [86.0, 'mm hg'], 'Blood Urea Nitrogen (BUN)': [8.0, 'mg/dL'], 'respiratory rate': [30.0, 'breaths per minute'], 'Confusion': False}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 80 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 1.
The concentration of BUN is 8.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 1.
The patient's respiratory rate is 30 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 1 + 1 = 2.
The patient's systiolic blood pressure is 161 mm Hg. The patient's diastolic blood pressure is 86 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6446,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-3008949-1,Extracted,"A 37-year-old man with stage V diabetic nephropathy was admitted in the nephrology unit of a tertiary care hospital with complaints of decreased urine output, low grade fever and puffiness of face and pedal edema for one week. He is a known diabetic and hypertensive on regular treatment. He is an A.C technician by occupation, working in the Middle East. He had undergone dialysis five times in the Middle East for the same complaints. At the time of admission, he had a temperature of 100.8°F, BP – 130/90 mm Hg, Pulse -80 beats/min, Respiratory rate – 20 breaths / min. On physical examination, he had pitting pedal edema. Hemogram showed hemoglobin 8.9gm%, total count 8300/cu mm with 71 % neutrophils, 22% lymphocytes, 6% eosinophils. Other investigations showed blood urea 125 mg/dl, s. creatinine 9.4 mg/dl, S. uric acid 5.3 mg/dl, total proteins 5.0 g/dl, Albumin 2.3 g/dl, A/G ratio 0.9, Random blood sugar 110 mg/dl. HIV, HBsAg and HCV ELISA were negative.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [125.0, 'mg/dL'], 'Diastolic Blood Pressure': [90.0, 'mm hg'], 'age': [37, 'years']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 37 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 125.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 130 mm Hg. The patient's diastolic blood pressure is 90 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6447,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-6080,Extracted,"A 67-year-old man presents to the emergency department with a fever and altered mental status. The patient has a history of Alzheimer dementia and is typically bed bound. His son found him confused with a warm and flushed complexion thus prompting his presentation. The patient has a past medical history of dementia, diabetes, and hypertension and typically has a visiting home nurse come to administer medications. Prior to examination, he is given haloperidol and diphenhydramine as he is combative and will not allow the nurses near him. His temperature is 102.9°F (39.4°C), blood pressure is 104/64 mmHg, pulse is 170/min, respirations are 22/min, and oxygen saturation is 100% on room air. Physical exam is notable for dry and flushed skin and a confused man. There is no skin breakdown, and flexion of the patient’s neck elicits no discomfort. Laboratory studies are drawn as seen below.

Hemoglobin: 15 g/dL
Hematocrit: 45%
Leukocyte count: 4,500/mm^3 with normal differential
Platelet count: 227,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.3 mEq/L
HCO3-: 24 mEq/L
BUN: 30 mg/dL
Glucose: 97 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 10.2 mg/dL
AST: 12 U/L
ALT: 10 U/L

Urine:
Color: Yellow
Bacteria: Absent
Nitrites: Negative
Red blood cells: Negative

An initial chest radiograph is unremarkable. The patient is given 3 liters of Ringer's lactate and an electric fan to cool off. Two hours later, his temperature is 99°F (37.2°C), blood pressure is 154/94 mmHg, pulse is 100/min, respirations are 17/min, and oxygen saturation is 100% on room air. The patient’s mental status is at the patient’s baseline according to the son.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [104.0, 'mm hg'], 'respiratory rate': [22.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [30.0, 'mg/dL'], 'Confusion': True, 'Diastolic Blood Pressure': [64.0, 'mm hg'], 'age': [67, 'years']}",3,3,3,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 67 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient has confusion, 1 point is added to score making the current total 1 + 1 = 2.
The concentration of BUN is 30.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 2 + 1 = 3.
The patient's respiratory rate is 22 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 3.
The patient's systiolic blood pressure is 104 mm Hg. The patient's diastolic blood pressure is 64 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 3.
The patient's CURB-65 score is 3."
6448,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-1580,Extracted,"A 36-year-old woman comes to the physician because of a 4-day history of fever, malaise, chills, and a cough productive of moderate amounts of yellow-colored sputum. Over the past 2 days, she has also had right-sided chest pain that is exacerbated by deep inspiration. Four months ago, she was diagnosed with a urinary tract infection and was treated with trimethoprim/sulfamethoxazole. She appears pale. Her temperature is 38.8°C (101.8°F), pulse is 92/min, respirations are 20/min, and blood pressure is 128/74 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 99%. Examination shows pale conjunctivae. Crackles are heard at the right lung base. Cardiac examination shows no abnormalities. Laboratory studies show:
Hemoglobin 12.6 g/dL
Leukocyte count 13,300/mm3
Platelet count 230,000/mm3
Serum
Na+ 137 mEq/L
Cl- 104 mEq/L
K+ 3.9 mEq/L
Urea nitrogen 16 mg/dL
Glucose 89 mg/dL
Creatinine 0.8 mg/dL
An x-ray of the chest shows an infiltrate at the right lung base.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [128.0, 'mm hg'], 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [16.0, 'mg/dL'], 'Diastolic Blood Pressure': [74.0, 'mm hg'], 'age': [36, 'years']}",0,0,0,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 36 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 16.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 0.
The patient's systiolic blood pressure is 128 mm Hg. The patient's diastolic blood pressure is 74 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 0.
The patient's CURB-65 score is 0."
6449,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-7357312-1,Extracted,"A 27-year-old Hispanic male with a past medical history of obesity (BMI: 28.59 kg/m²), long-standing uncontrolled HTN, stage 3 CKD, and obstructive sleep apnea presented to the hospital with complaints of fatigue, generalized weakness, and bleeding from the upper lip. Approximately a week ago, he got a cut on his lip while drinking from an open can and since then was suffering from slow oozing of blood from the wound site. He also reported 25-30 pounds unintentional weight loss over the past two months. He denied dysuria, hematuria, urgency, cloudy urine, abdominal pain, diaphoresis, fever, chills, syncopal attacks, palpitations, headache, blurry vision, dyspnea, or lower extremity swelling.
The patient was diagnosed with HTN at the age of 13. Three years ago, he was evaluated for exertional chest pain and uncontrolled HTN, which led to the diagnosis of CKD stage III/IV with a baseline creatinine of 2.9 mg/dL. Cortisol level was normal, aldosterone level was less than 1 ng/dL, and renin activity level was elevated at 24.40 ng/mL/hour, but the patient was on lisinopril and repeat testing after discontinuing lisinopril was normal at 1.4 ng/mL/hour. Vasculitis work-up including antinuclear antibody (ANA), anti-neutrophilic cytoplasmic antibody (ANCA) screen, anti-double stranded DNA antibody, and C3 and C4 complement levels were all within the normal range. Renal artery duplex had shown no signs of renal artery stenosis, and CT of the chest had shown a 3.7 cm (borderline) ascending thoracic aorta but no signs of coarctation. Transthoracic echocardiography findings were within the normal range. Exercise cardiac stress test showed no evidence of myocardial ischemia. No secondary cause of HTN could be elicited, and the patient was diagnosed with primary essential HTN. He was placed on three anti-hypertensive drugs: amlodipine 10 mg daily, carvedilol 25 mg two times a day, and hydralazine three times a day. He had stopped taking his blood pressure (BP) medication about one year ago due to insurance issues.
He reported consumption of two beers a week but denied smoking and recreational drug abuse. The patient was adopted at the age of 6 when he immigrated from Mexico to the United States; hence, substantial medical history of his biological family could not be obtained.
On arrival, the patient was afebrile with temperature of 98.7°F, respiratory rate of 14 breaths per minute, heart rate of 98 beats per minute, elevated BP of 175/99 mm Hg, 100% oxygen saturation at room air, and BMI of 27.12 kg/m². Systolic BP in his previous outpatient visits ranged from 140 to 180 mm Hg, indicative of poorly controlled BP. On physical examination, the patient appeared well built but he was pale and lethargic. He had a scab on his upper lip and on removal of the scab, slow oozing of blood was noted. Rest of his examination including cardiovascular, respiratory, abdominal, and neurological showed no abnormalities. Blood chemistry revealed serum sodium of 137 mmol/L, potassium of 5.0 mmol/L, chloride of 98 mmol/L, bicarbonate of 9 mmol/L, anion gap of 30 mmol/L, serum phosphorus of 11.7 mg/dL, corrected calcium of 7 mg/dL, blood urea nitrogen (BUN) of 228 mg/dL, and serum creatinine of >37 mg/dL (Architect Analyzer, Abbott Laboratories, Abbott Park, IL, USA, alkaline picrate kinetic [AP-K] method) []. The glomerular filtration rate (GFR) was unmeasurable and therefore not reported. The calculated GFR using the Modification of Diet in Renal Disease (MDRD) equation was less than 1.5 mL/minute/1.73 m². His baseline creatinine was around 2.9 mg/dL. Complete blood count showed hemoglobin of 4.7 g/dL, hematocrit of 15.8%, mean corpuscular volume of 87.3 fL, and platelet count of 127 x 103/mcL. Peripheral smear showed poikilocytosis, ovalocytes, and elliptocytes. Parathyroid hormone levels were elevated at 1,008 pg/mL. Uric acid levels and creatine phosphokinase levels were elevated at 16.5 mg/dL and 353 U/L, respectively. Protime was mildly elevated to 15.2 seconds, with an unremarkable international normalized ratio (INR) of 1.2. On gross inspection, the urine sample was pale yellow and cloudy in appearance. The urinalysis showed a specific gravity of 1.012, with pH of 5.0, two plus proteinuria, two plus blood, three plus white blood cell esterase, and positive for leukocytes and red blood cells. Urine culture grew Escherichia coli (100,000 CFU/mL). Serological work-up including human immunodeficiency virus (HIV) antigen/antibodies and hepatitis B core IgM antibody, and urine drug screen were all negative.
Chest X-ray did not show any signs of fluid overload such as pulmonary edema or pleural effusion (Figure ). Electrocardiogram showed prolonged QT (QTc 493 ms) (Figure ) and transthoracic echocardiogram revealed mild left ventricular hypertrophy (Figure ). Renal ultrasound reported bilaterally increased parenchymal echogenicity and cortical thinning consistent with chronic renal insufficiency (Figure ).
The patient emergently underwent transfusion with two units of packed red blood cells. HTN was controlled with amlodipine and intravenous hydralazine. His metabolic acidosis was slowly corrected with intravenous bicarbonate infusion. An internal jugular venous hemodialysis catheter was placed, and the patient underwent emergent hemodialysis. With initiation of hemodialysis, bleeding and electrolyte imbalances resolved. During his hospital course, he was also treated with a five-day course of ceftriaxone for urinary tract infection. At discharge, his creatinine level had come down to 15.1 mg/dL, BUN was down to 56 mg/dL, potassium was down to 3.9 mmol/L and hemoglobin was 7.5 g/dL. Eventually, the patient was transitioned to peritoneal dialysis. Unfortunately, due to the patient's non-compliance with dialysis, he has been admitted multiple times over the past year with similar presentations.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [27, 'years'], 'Systolic Blood Pressure': [175.0, 'mm hg'], 'Diastolic Blood Pressure': [99.0, 'mm hg'], 'respiratory rate': [14.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [228.0, 'mg/dL'], 'Confusion': False}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 27 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 228.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 14 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 175 mm Hg. The patient's diastolic blood pressure is 99 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6450,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-4127409-1,Extracted,"A 54-year-old Korean man presented with a month-long history of cough and yellowish sputum, an 8-kg weight loss over the course of three months and Modified Medical Research Council Dyspnea Scale grade 1 dyspnea. He had no history of surgery or other medical illness and he was a current smoker (30 pack-years). On examination, his blood pressure was 100/80 mm Hg, pulse rate was 76 beats/min, respiratory rate was 24 breaths/min, and body temperature was 36.5℃. On chest auscultation, breathing sounds were abnormal with coarse rales in both upper lung fields. Initial arterial blood gas results were pH 7.428, pCO2 32.8 mm Hg, pO2 85.1 mm Hg, HCO3- 21.2 mmol/L, and SaO2, 97.8% in ambient air. Blood tests showed a white blood cell count of 6,700/mm3 (normal, 4000-10000/mm3), hemoglobin of 12.8 g/dL (normal, 12.5-15 g/dL), and a platelet count of 178/mm3 (normal, 150-450/mm3). The C-reactive protein level was found to be 5.23 mg/L (normal, 0-0.75 mg/L). A blood chemistry panel revealed a blood urea nitrogen level of 45.3 mg/dL (normal, 7-20 mg/dL), creatinine of 1.0 mg/dL (normal, 0.5-1.5 mg/dL), total protein of 8.3 g/dL (normal, 6.0-8.3 g/dL), albumin of 3.2 g/dL (normal, 3.5-4.5 mg/dL), and aspartate aminotransferase/alanine aminotransferase of 78/54 IU/L (normal, 8-40/5-35, respectively). Cardiac enzyme labs were found to be elevated: CK-MB, 33.21 ng/mL (normal, 0-5 ng/mL); troponin-I, 0.904 ng/mL (normal, 0.0-0.2 ng/mL); and brain natriuretic peptide, 183.20 pg/mL (normal, 0-99 pg/mL). Electrocardiography (ECG) revealed nonspecific ST- or T-wave abnormalities. Initial chest radiographs showed numerous nodules in both apices suggestive of active pulmonary tuberculosis (). Chest computed tomography (CT) showed two large cavities in the right upper lobe and small nodules in both lungs (). There were no abnormal lesions present in either adrenal gland. There was a 1.9-cm ovoid filling defect in the apex of the left ventricle (LV) suggestive of a thrombus (). Echocardiography showed a balloon-like akinesia of the apex wall (), a 1.65×1.21-cm apical thrombus (), and the left ventricular ejection fraction was 56.7%.
We started anticoagulation with low molecular weight heparin for the LV thrombus. Coronary CT angiography showed normal epicardial coronary arteries. The next day, CK-MB and troponin I levels normalized to 1.09 ng/mL and 0.267 ng/mL, respectively. Follow-up ECG showed T-wave inversion at the V3-V6 leads in contrast to the normal initial ECG. Sputum studies showed positive results for acid fast stain and polymerase chain reaction for mycobacterium tuberculosis. We started first-line anti-tuberculosis medication (rifampin, isoniazid, ethambutol, and pyrazinamide) immediately. Ten days later, follow-up echocardiography showed normalized LV apical wall motion and no evidence of akinesia of the apex wall (). The left ventricular ejection fraction was 58%. The LV thrombus was still noted on imaging, but decreased in size (). Seventeen days later, we confirmed a diagnosis of pulmonary tuberculosis through positive tuberculosis culture. Drug susceptibility test revealed all sensitive results. He completed a six months of treatment with rifampin, isoniazid, ethambutol and pyrazinamide for two months, followed by rifampin and isoniazid for four months. During the follow-up period, there was no physical evidence of recurrence in TTC.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [54, 'years'], 'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg'], 'respiratory rate': [24.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [45.3, 'mg/dL']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 54 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 45.3 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 24 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 100 mm Hg. The patient's diastolic blood pressure is 80 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6451,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-4531584-1,Extracted,"An 84-year-old man with end stage renal disease secondary to diabetic nephropathy for 1 year was admitted to hospital because of dyspnea and poor oral intake of 1 weeks duration. He had been diagnosed with gout 13 years previously, and had been managed at another clinic for glaucoma, diabetes mellitus and hypertension 10 years previously. He had a history of admission to our hospital due to chronic renal failure 1 year previously, after which he had not been followed up at our OPD unit. He did not have any allergic or family medical history. Physical examination at admission revealed blood pressure of 140/80 mmHg, heart rate of 107/min, body temperature of 36.8°C, and respiratory rate of 20/min; other findings were unremarkable. At that time, complete blood count revealed a hemoglobin level of 11.1 g/dL, WBC count was 24,500/mm3 (neutrophil, 93%; lymphocyte, 5%; monocyte, 2%), platelet count was 216,000/mm3, serum BUN was 143 mg/dL, Cr was 5.7 mg/dL, uric acid was 13.3 mg/dL, calcium was 9.3 mg/dL, phosphorus was 7.4 g/dL, albumin was 3.5 g/dL, alkaline phosphatase was 94 IU/L, total bilirubin was 1.1 mgf/dL, AST/ALT was 29/28 IU/L, and parathyroid hormone was 92.26 pg/mL. Urine analysis was albumin (++), blood (+), RBC count 3-5/HPF, and WBC count 20–30/HPF. Twenty-four hour urine protein level was 467 mg/day. Twenty-four hour urine creatinine clearance level was 5.4 mL/min. He was started on hemodialysis with temporary internal jugular catheter. On the twenty-fifth day after admission, a peritoneal catheter was inserted. Three weeks after peritoneal catheter insertion, he was started on peritoneal dialysis with a 6-hour exchange of 2L 1.5% peritoneal dialysate. On the ninth day after the start of peritoneal dialysis, he developed turbid peritoneal effluents with fever (38.4°C), abdominal pain and tenderness. Dialysate WBC count was 180/mm3 (neutrophil, 20%; lymphocyte, 4%; eosinophil, 76% [eosinophil count: 136/mm3]).
Complete blood count was WBC of 7,650/mm3 (eosinophil, 5.5%), hemoglobin level of 8.9 g/dL, and platelet count level of 337,000/mm3. Peripheral blood eosinophilia was not observed. Cultures of peritoneal fluid showed no growth of aerobic or anaerobic bacteria, or of fungus. AFB stain was negative. CAPD was commenced, and he was started on intraperitoneal ceftazidime (1.0 g/day) and cefazolin (1.0 g/day) with heparin at 8000 unit. After two weeks, dialysate had cleared up and clinical symptoms were improved. Dialysate WBC count decreased to 8/mm3 and eosinophils were not detected in peritoneal fluid ().
There was no recurrence of eosinophilic peritonitis on follow-up evaluation and he continued with CAPD. However, he died of sepsis and pneumonia fifteen weeks after admission.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [84, 'years'], 'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg'], 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [143.0, 'mg/dL']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 84 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 1.
The concentration of BUN is 143.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 140 mm Hg. The patient's diastolic blood pressure is 80 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6452,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-5823,Extracted,"A 77-year-old man presents to the emergency department for shortness of breath. The patient states that over the past month he has felt short of breath when doing everyday tasks, and today he even felt short of breath while taking a nap. The patient has a past medical history of obesity, diabetes, hypertension, and asthma. His current medications include lisinopril, insulin, metformin, and an albuterol inhaler. His temperature is 99.5°F (37.5°C), blood pressure is 130/90 mmHg, pulse is 85/min, respirations are 11/min, and oxygen saturation is 96% on room air. An EKG is ordered as seen in Figure A. A chest radiograph is ordered as seen in Figure B. Laboratory studies are ordered as seen below:

Serum:
Na+: 137 mEq/L
K+: 3.9 mEq/L
Cl-: 100 mEq/L
HCO3-: 24 mEq/L
Urea nitrogen: 9 mg/dL
Glucose: 122 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 10.2 mg/dL
Mg2+: 1.5 mEq/L
AST: 15 U/L
ALT: 9 U/L
Alkaline phosphatase: 32 U/L
Glutamyltransferase (GGT): 12 U/L
Albumin: 3.9 g/dL
Total protein: 6.9 g/dL
Total bilirubin: 0.9 mg/dL
Direct bilirubin: 0.2 mg/dL

On physical exam the patient appears obese and in distress. He has bilateral lower extremity pitting edema and yellowing of his toenails. Pulmonary exam is notable for bilateral crackles. Cardiac exam demonstrates a normal rate and rhythm with a displaced cardiac apex. There is JVD to the angle of the mandible.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [77, 'years'], 'Systolic Blood Pressure': [130.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg'], 'Blood Urea Nitrogen (BUN)': [9.0, 'mg/dL'], 'respiratory rate': [11.0, 'breaths per minute']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 77 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 1.
The concentration of BUN is 9.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 1.
The patient's respiratory rate is 11 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 130 mm Hg. The patient's diastolic blood pressure is 90 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6453,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-7939513-1,Extracted,"A 44-year-old previously healthy male was transferred to our hospital in February 2020 with a 4-month history of productive cough and one month of intermittent fever. He had no relevant transplantation and no significant medical history (particularly no corticosteroid and no immunosuppressive drug history), and never had any episode of tuberculosis or chronic pulmonary disorders. He was a never-smoker and no alcoholism. He had no family history of chronic lung disease. He had no recent travel history of Wuhan. Four months prior, the patient developed cough with white phlegm, accompanied with chest tightness and shortness of breath when he coughed severely. Sometimes he had blood-streak sputum. He was suspected as upper respiratory tract infection and given symptomatic treatment, but the cough was not relieved. One month later, chest x-ray showed pulmonary infection. With the treatment of clarithromycin, ribavirin and ampicillin for 5 days, cough was relieved. However, one month prior, he developed low-grade fever. 22 days prior, he had a fever with maximum body temperature of 39.4°C. He was admitted to local hospital. Blood tests showed a white blood cell (WBC) count of 8.32×10E9/L and C-reactive protein (CRP) of 128.06mg/L. Chest computed tomography (CT) scan showed bilateral infiltrations. Piperacillin tazobactam, oseltamivir and doxycycline were initiated after admission to treat pulmonary infection. One day later, chest CT showed the aggravated infection of both lungs. He developed to be hypoxia, septic shock. Acute respiratory distress syndrome (ARDS) was diagnosed. Then he was treated with meropenem, voriconazole, doxycycline. Reexamination of chest CT showed the infection was relieved. Five tests of nucleic acid of Corona Virus Disease 2019 (COVID-19) were all negative, which were carried out by regional Centers for Disease Control and Prevention (CDC). Eight days prior, the metagenomic next-generation sequencing (mNGS) of blood detected the sequences of P. jirovecii and Cytomegalovirus (CMV). Caspofungin, trimethoprim–sulfamethoxazole (TMP-SMX) and methylprednisolone (MP) were used for antifungal therapy. One day prior, the oxygen saturation decreased again. Then he was transferred to our hospital and admitted to our department.
Chest CT on admission showed bilateral infiltrations, ground glass opacity, crazy paving pattern ( and ). Blood tests performed on admission showed WBC count of 9.38×10E9/L, absolute value of lymphocyte (LYMP) of 0.65×10E9/L, hemoglobin (Hb) level of 126g/L, platelet count of 291×10E9/L, aspartate aminotransferase (AST) of 37 IU/L, alanine aminotransferase (ALT) of 40 IU/L, blood urea nitrogen (BUN) of 5.6mmol/L, and serum creatinine of 68umol/L. Hypersensitive C-reactive protein (hsCRP) was 43.2mg/L, and procalcitonin (PCT) was 0.025ng/mL. The physical examination showed blood pressure of 125/69mmHg, heart rate of 94 beats/minute, respiratory rate of 25 rates/minute, and temperature of 37.7°C, oxygen saturation of 99% with therapy of high-flow nasal cannula (HFNC) with fraction of inspiration (FiO2) 0.55). Moist rales were audible over bilateral lungs, without lower-extremity edema. Physical examination of the heart and abdomen were normal. The arterial blood gas analysis revealed a pH of 7.45, the partial pressure of oxygen (PO2) was 124mmHg, the partial pressure of carbon dioxide (PCO2) was 45mmHg, PaO2/FiO2 was 113mmHg, alveolar-arterial oxygen gradient ((A-a) DO2) was 212mmHg. Intravenous moxifloxacin (400mg/day), ganciclovir (250mg, every 12 hours), caspofungin (50mg/day), clindamycin (600mg, every 8 hours) and methylprednisolone (40mg/day), and oral trimethoprim–sulfamethoxazole (TMP-SMX) (3 tablets (240/1200mg) every 6 hours, with each tablet containing 80mg trimethoprim and 400mg sulfamethoxazole) were prescribed. Human immunoglobulin for intravenous injection (IVIG) was given with the dosage of 10g for 5 days. Thymalfasin was used with the dosage of 1.6mg for 12 days. Hepatitis B and C viruses, HIV, and Syphilis were all tested negative by serology. The sputum analysis of acid-fast bacilli smear and mycobacterial culture was negative. Mycobacterium tuberculosis complex was negative based on blood test with the GeneXpert MTB/RIF assay. The immunofluorescence staining of sputum smear did not find Pneumocystis organisms. Serum 1,3-beta-D-glucan (BDG) level was normal (<3.836pg/mL). In addition, bronchoalveolar lavage fluid (BALF) culture revealed no growth of bacteria or fungi. The DNA copies of CMV was 9E2 copies/mL. The lactate dehydrogenases level was 429 U/L. Antinuclear antibody (ANA), anti-double stranded DNA antibody(dsDNA), anti-neutrophil cytoplasmic antibody (ANCA) series and extractable nuclear antigen (ENA) series were all negative. Flow cytometry of peripheral blood cells showed CD3+T cells/lymphocyte was 86% (normal range 50%-84%), CD3+CD4+T cells/lymphocyte was 17%, CD3+CD8+T cells/lymphocyte was 55%, CD3+CD4+T cells/CD3+CD8+T cells was 0.31, B cells/lymphocyte was 12%, NK cells (CD3-CD16+ or CD3-CD56+)/lymphocyte was 2%. The thyroid stimulating hormone (TSH) level was normal. Peripheral blood and bronchoalveolar lavage fluid (BALF) samples collected on day 3 were sent for mNGS test, which was performed by Vision Medicals CO. Ltd (Guangzhou, China) using Illumina NextSeq 550 (USA). On day 4, the mNGS detected M. abscessus with 1315 high-confidence sequence reads, CMV with 649 high-confidence sequence reads and P. jirovecii with 44 high-confidence sequence reads in BALF sample. mNGS detected CMV with 74 high-confidence sequence reads and P. jirovecii with 368 high-confidence sequence reads in blood (). The M. abscessus sequence reads mapped to a M. abscessus reference genome (NC_010397.1), the P. jirovecii sequence reads assembled to a P. jirovecii reference genome (NW_017264779.1), and the sequence reads for CMV allowed assembly of a CMV reference genome (NC_006273.2) ().
Meanwhile, the oxygen saturation decreased to about 90%, and the partial pressure of oxygen dropped to 54 mmHg. Moxifloxacin (400 mg/day) was switched to imipenem cilastatin (1.0g every 8 hours) for the treatment of M. abscessus infection. Linezolid (600mg every 12 hours) was synergistically used on day 6 to anti-M. abscessus. On day 9, The patient discontinued HFNC, and be treated with nasal catheter for oxygen inhalation, and chest CT was performed and revealed that worsening infiltration in lower lungs and absorbing of other lungs ( and ). With the treatment, the patient still had intermittent low-grade fever, with the highest temperature of 38.2 °C, and the heat peak was gradually decreased, the body temperature returned to normal on day 10. The symptom of cough and sputum was also significantly relieved, the hsCRP decreased to 4.8mg/L. The PCT was 0.022ng/mL. On day 12, the patient was transferred to General Medical Wards. Moxifloxacin (400 mg/day), imipenem cilastatin (1.0g every 8 hours) and linezolid (600mg every 12 hours) were used to treat M. abscessus infection. Caspofungin (50mg/day), TMP-SMX (240/1200mg, every 6 hours), clindamycin (600mg, every 8 hours) and MP (20mg/day) were used to treat PJP. The copies of CMV were below 500 copies/mL tested on Day 11, so the ganciclovir was discontinued. On day 17, MP was switched to oral taken with 16mg/day for 7 days, then it was reduced to 12mg/day for 3 days. Chest CT performed on day 17 revealed absorbing infiltrations ( and ). On day 18, the count of WBC dropped to 3×10E9/L, recombinant human granulocyte stimulating factor injection was given. On day 20, caspofungin was discontinued, and clindamycin was changed from intravenous to oral administration with the dosage of 450mg/day (150mg every 8hours), moxifloxacin was also switched to oral taken (400mg/day). On day 23, linezolid was discontinued for the plantlet dropping to 89×10E9/L. On day 26, chest CT showed pulmonary infection was significantly absorbed ( and ). The level of LYMP elevated to 1.1×10E9/L, with the WBC of 3.97×10E9/L. The levels of AST, ALT, BUN and creatinine was normal. On day 27, he was discharged with 7-day oral medicines (SMZ 240/1200mg every 6hours, clindamycin 150mg every 8hours, MP 8mg/day, clarithromycin 500mg every 12hours, levofloxacin 0.5g/day). The important laboratory results on admission and after treatment are summarized in . The details of antibiotic and main process of disease are summarized in . Five months after discharge, he returned to our hospital for reexamination of chest CT which showed the inflammation in both lungs was basically completely absorbed ( and ). During this period, the patient had no symptoms such as cough and fever. Unfortunately, the patient refused blood tests including flow cytometry test.
To further confirming P. jirovecii, the BALF and blood samples detected by mNGS were sent for PCR. The commercial PneumoGenius® real-time PCR (PathoNostics, Maastricht, The Netherlands) performed by Shanghai GeneDx Biotech Co., Ltd, according to the manufacturers’ instructions using an LC480 Ⅱ real-time system, detected Pneumocystis mitochondrial large subunit of ribosomal RNA (mtLSU) gene and wild-type sequence at the dihydropteroate synthase (DHPS) locus both in BALF and blood samples. The cycle threshold (Ct) value for mtLSU of BALF and blood were 32.5 and 36.31, respectively ().",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [44, 'years'], 'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [69.0, 'mm hg'], 'respiratory rate': [25.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [5.6, 'mmol/L']}",0,0,0,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 44 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 5.6 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of BUN from mmol to mg. The mass of BUN is 5.6 mmol. To convert 5.6 mmol of BUN to mol, multiply by the conversion factor 0.001, giving us 5.6 mmol BUN * 0.001 mol/mmol = 0.0056 mol BUN. To convert from mol BUN to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0056 mol BUN * 28.02 g/mol = 0.15691 g BUN. To convert 0.15691 g of BUN to mg, multiply by the conversion factor 1000.0, giving us 0.15691 g BUN * 1000.0 mg/g = 156.91 mg BUN. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 156.91 mg BUN/10.0 dL = 15.691 mg BUN/dL. The concentration value of 5.6 mmol BUN/L converts to 15.691 mg BUN/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 25 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 0.
The patient's systiolic blood pressure is 125 mm Hg. The patient's diastolic blood pressure is 69 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 0.
The patient's CURB-65 score is 0."
6454,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-7752485-1,Extracted,"A 69-year-old man was admitted to the hospital because of anorexia and fever. He had suffered an acute middle cerebral artery territory stroke 45 days previously and underwent treatment. The only medications he was taking were for stroke (aspirin 100 mg, cilostazol 100 mg, atorvastatin 80 mg, and rabamipide 100 mg). On the initial physical examination, his vital signs were as follows: blood pressure, 162/79 mm Hg; pulse rate, 104 beats/min; respiratory rate, 20 breaths/min; and temperature, 37.8°C. He had severe dysarthria and right extremity weakness due to the stroke. No malar rash, oral ulcers, jugular venous distension, or lymphadenopathy were observed. Bilateral fine crackles were detected on chest auscultation, and his abdomen was soft but there was no organomegaly. Multiple pinkish reticulated patches were observed on the lower leg. The results of initial laboratory tests were as follows: white blood cell (WBC) count, 17 630/μL (4000-10 000/μL); hemoglobin, 9.1 g/dL (13.0-17.0 g/dL); blood urea nitrogen, 24.3 mg/dL (6-20 mg/dL); creatinine, 1.52 mg/dL (0.6-1.2 mg/dL); C-reactive protein, 153.5 mg/dL (0.0-5.0 mg/dL); MPO–ANCA, 100.0 U/mL (0-4.9 U/mL); and PR3–ANCA, negative. The urinalysis revealed the following findings: protein, 2+; blood, 2+; red blood cells, 5-9/high power fields (HPF); and WBC, 5-9/HPF. Serum/urine protein electrophoresis and immunofixation showed nonspecific findings (Table ). Pulmonary interstitial fibrosis was noted on a chest X-ray (CXR). Brain magnetic resonance imaging revealed no evidence of a newly developed infarction, but the hemorrhagic transformation of the left MCA infarction lesion was detected (frontoparietal lobes, basal ganglia, and insular region). His baseline serum creatinine was 0.71 mg/dL, which increased to 1.52 and 2.24 mg/dL on days 1 and 3 of admission, respectively. A percutaneous renal biopsy was performed on day 7 of admission. Seven fibrocellular crescents out of 17 glomeruli were observed on light microscopy (Figure ). Some were associated with fibrinoid necrosis, and numerous neutrophils were detected in the capillary lumen. In addition, a few small vessels with neutrophil infiltration and fibrin deposition were evident, indicating acute necrotizing vasculitis (Figure ). Most of the interstitial area was infiltrated by numerous plasma cells and several neutrophils. The possibility of crescentic glomerulonephritis, associated with plasma-cell proliferative disease or IgG-related disease, was considered. Kappa and Lambda in situ hybridization revealed a positive staining pattern, indicating polyclonality (Figure ). In addition, IgG4-positive plasma cells were up to 200/HPF in the interstitial area. Unlike IgG4-tubulointerstitial nephritis, there was no sclerosing lymphoplasmacytic inflammation or apparent obliteration of the tubules. Therefore, the patient was diagnosed with microscopic polyangiitis having pauci-immune crescentic glomerulonephritis with fibrinoid necrotizing vasculitis. A bone marrow (BM) aspiration and biopsy showed a normocellular marrow with no increase in plasma cells (1.8% of all nucleated cells), and no evidence of BM involvement by monoclonal plasma cells. His Birmingham vasculitis activity score was 27. Serum creatinine peaked at 3.1 mg/dL. He received three pulses of methylprednisolone (500 mg/day) followed by prednisone (1 mg/kg/day) and cyclophosphamide (1.5 mg/kg/day). After treatment, his serum creatinine improved to 2.3 mg/dL, and the microscopic hematuria disappeared. Furthermore, his fever and skin lesions improved. He was discharged with prednisolone 40 mg/day (1 mg/kg/day), peroral cyclophosphamide 50 mg/day, and his renal function remained stable until 2 months after discharge. No side effects were observed due to the immunosuppressive agents. The dose of azathioprine was maintained, and the dose of prednisolone was tapered to 30 mg/day. He was subsequently lost to follow-up and died 16 months later due to pneumonia.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [162.0, 'mm hg'], 'Diastolic Blood Pressure': [79.0, 'mm hg'], 'age': [69, 'years'], 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [24.3, 'mg/dL'], 'Confusion': False}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 69 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 1.
The concentration of BUN is 24.3 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 162 mm Hg. The patient's diastolic blood pressure is 79 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6455,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-4969,Extracted,"A 38-year-old female presents to the emergency department for cough. She reports that two days ago she developed a nonproductive cough with moderate shortness of breath. On review of systems, the patient also endorses chills and sweats as well as several episodes of diarrhea over the past three days. Her husband also reports that the patient seemed confused this morning when he spoke to her before he left for work. The patient’s past medical history is significant for diabetes mellitus type II for which she takes metformin and glipizide. She drinks 8-10 beers per week and has a 15 pack-year smoking history. She works as a sales manager at a local retail company. Her temperature is 102.6°F (39.2°C), blood pressure is 126/72 mmHg, pulse is 82/min, and respirations are 18/min. On physical exam, she is alert and oriented to person and place only. She has crackles bilaterally extending up to the mid-lung fields. Her abdomen is soft and non-distended without rebound or guarding. Laboratory testing is performed and reveals the following:

Serum:
Na+: 129 mEq/L
K+: 3.6 mEq/L
Cl-: 99 mEq/L
HCO3-: 17 mEq/L
Urea nitrogen: 16 mg/dL
Creatinine: 1.1 mg/dL

Leukocyte count: 16,300/mm^3
Hemoglobin: 13.2 g/dL
Mean corpuscular volume: 87 µm^3
Platelet count: 348,000/mm^3

A chest radiograph is performed and can be seen in Figure A.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [126.0, 'mm hg'], 'respiratory rate': [18.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [16.0, 'mg/dL'], 'Confusion': True, 'Diastolic Blood Pressure': [72.0, 'mm hg'], 'age': [38, 'years']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 38 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient has confusion, 1 point is added to score making the current total 0 + 1 = 1.
The concentration of BUN is 16.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 1.
The patient's respiratory rate is 18 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 126 mm Hg. The patient's diastolic blood pressure is 72 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6456,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-4531665-1,Extracted,"A 64-year-old woman was referred to our hospital for bronchial asthma with atypical pneumonia unresolved by antibiotic treatment. She had no history of being diagnosed as asthma but had suffered from intermittent sensation of chest constriction by exposure to cold air.
She had taken steroid for her joint arthritis without consulting a doctor for several years. She has never smoked and had no history of tuberculosis, diabetes mellitus or other cardiovascular disease. About 20 days before admission, the patient suffered from fever, cough, sputum and dyspnea. She visited another hospital and was treated with antibiotics and steroids. Despite treatment, there was no clinical improvement of her symptoms. She was referred to our hospital for further evaluation.
On admission, her body temperature was 37.2°C, pulse rate was 110/min, respiration rate was 24/min and blood pressure was 160/100 mmHg. Physical examination revealed bilateral diffuse inspiratory crackle without wheezing. Laboratory tests were performed: white blood cell count was 48,220/μL (neutrophils were 98%, monocytes 1% and lymphocytes 1%), hemoglobin 11.2 g/dL, hematocrit 32.1% and platelet count 394,000/μL on complete blood cell counts. Arterial blood gas analysis findings were pH 7.497, PaCO2 42.5 mmHg, PaO2 63.4 mmHg, bicarbonate 32.6 mmol/L and oxygen saturation 93.3% on oxygen 3 L/min via nasal prong. Sodium was 126 mEq/L, potassium 2.7 mEq/L, chloride 98 mEq/L, urea nitrogen 13.9 mg/dL, creatinine 1.24 mg/dL, cholesterol 168 mg/dL, total protein 5.1 mg/dL, albumin 2.6 mg/dL, AST 22 IU/L, ALT 22 IU/L and total bilirubin was 0.82 mg/dL on blood chemistry. Chest radiography and high-resolution computed tomography (HRCT) showed multifocal variable-sized consolidation with reticulonodular opacities () and cavitary lesion in both upper lobes and right lower lobe. There were also multiple small nodular densities and ground glass attenuation around the consolidation ().
Microscopic examination of sputum showed no acid-fast bacilli. Other laboratory findings, including IgG, IgM, IgA, IgE PRIST, C3, C4, CH50, rheumatoid factor (RF), antinuclear antibody (ANA), anti-neutrophil cytoplasmic antibody (ANCA), antistreptolysin-O (ASO), VDRL and cold cryoglobulin, were all negative.
Despite empiric broad-spectrum antibiotics and steroid treatment, dyspnea progressively aggravated. Open lung biopsy was done on the tenth hospital day. Histopathologic findings of the biopsy specimen showed large areas of necrotizing pneumonia with an infarct-like appearance (). There were some scattered fungal hyphae within the lung parenchyma (). The bronchi and bronchioles often showed dilated lumen which were filled with mucus, numerous necrotic debris, inflammatory cells and branching septated hyphae characteristic of aspergillus. Some terminal bronchioles were found to be destroyed and were replaced by granulomatous inflammation (). The bronchocentric granulomatous reaction extended into the adjacent lung parenchyma to a degree. Gomori-Methenamine-Silver (GMS) staining revealed many fungal hyphae consistent with aspergillus species. There was no evidence of angioinvasion by aspergillus or aspergillous emboli. With an impression of invasive aspergillus infection with BCG-like elements, 15 mg of amphotericin-B once day was administered intravenously and the dose was increased up to 30 mg daily. Steroids was tapered progressively. There were some improvement in her clinical symptoms. However despite vigorous antifungal treatment, sudden respiratory arrest occurred due to acute tracheobronchial tree obstruction with bronchial casts on the thirty-fourth hospital day. Histopathologic examination of the casts revealed fibrinoid necrotic tissue containing neutrophils, a few metaplastic squamous cell nests and variably fragmented fungal hyphae ().",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [64, 'years'], 'Systolic Blood Pressure': [160.0, 'mm hg'], 'Diastolic Blood Pressure': [100.0, 'mm hg'], 'respiratory rate': [24.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [13.9, 'mg/dL'], 'Confusion': False}",0,0,0,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 64 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 13.9 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 24 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 0.
The patient's systiolic blood pressure is 160 mm Hg. The patient's diastolic blood pressure is 100 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 0.
The patient's CURB-65 score is 0."
6457,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-4260105-1,Extracted,"A 48-year-old Caucasian man was diagnosed with GERD and hiatal hernia 15 years before presentation. His symptoms included chronic heartburn and nighttime cough that did not improve with lifestyle modification, histamine 2 blockers, and PPIs. Esophageal 24-hour pH-impedance monitoring confirmed the diagnosis of GERD. He underwent TIF after failing conservative therapy. A few hours after surgery, the patient developed midsternal chest pain. Physical examination revealed a mildly distressed state with rapid shallow breathing. His respiratory rate was 18 breaths per minute, heart rate was 140 beats per minute, O2 saturation was 88% on a 40% venturi mask, temperature was 36℃, and blood pressure was 154/93 mm Hg. The pulmonary, cardiovascular, and abdominal examinations were normal. Electrocardiogram showed no acute ST/T wave changes. His chest radiograph showed new small bilateral pleural effusions and bilateral lung opacities. The next day, the patient had worsening chest pain, severe back pain, and shortness of breath. Physical examination revealed decreased breath sounds on the left side. The patient's respiratory status deteriorated, and he was intubated for mechanical ventilation. Another chest radiograph showed a large left-sided pleural effusion and bilateral pulmonary infiltrates consistent with consolidation and/or atelectasis.
Laboratory studies revealed a white blood count of 16.9×109/L, a hemoglobin level of 16 g/dL, a blood urea nitrogen level of 22 mg/dL, a serum creatinine level of 1.2 mg/dL, a serum lactate level of 2.7 mmol/L, a total protein level of 5.7 g/dL, and a lactate dehydrogenase (LDH) level of 170 U/L. Arterial blood gases revealed pH 7.27, PaCO2 46.7 mm Hg, PaO2 53.2 mm Hg, and HCO3 21 mmol/L. Computed tomography of the chest showed moderate-to-large left-sided and moderate right-sided pleural effusions, a left-sided pneumothorax, and pneumomediastinum, findings consistent with distal esophageal perforation (). Computed tomography of the abdomen showed pneumoperitoneum. The patient was started on vancomycin and ertapenem. A left-sided chest tube was inserted, and purulent, brown-greenish fluid was drained (1,300 mL) during the tube placement. Pleural fluid analysis showed an exudative effusion consistent with esophageal perforation and empyema with a white blood cell count of 1.75×109/L (mainly neutrophils), a protein level of 44 g/L, an LDH level of 7,589 U/L, a fluid protein/serum protein ratio of 0.77, a fluid LDH/serum LDH ratio of 4.46, an amylase level of 335 U/L, a lipase level of 1,188 U/L, and a glucose level of 20 mg/dL.
The patient had a fever for 5 days and leukocytosis despite the antibiotic coverage, chest tube placement, and nasogastric decompression. Blood cultures were negative on two occasions; pleural fluid cultures grew coagulase-negative Staphylococcus nitric oxide synthase and diphtheroids. On postoperative day 8, a left-sided thoracotomy and decortication for nonresolving empyema was performed. The patient required mechanical ventilation for 12 days. At his most recent follow-up visit, the patient had been hospitalized at another hospital for 2 weeks because of the nonresolving right-sided empyema and had undergone right thoracotomy with decortication.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [154.0, 'mm hg'], 'respiratory rate': [18.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [22.0, 'mg/dL'], 'Diastolic Blood Pressure': [93.0, 'mm hg'], 'age': [48, 'years']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 48 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 22.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 18 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 154 mm Hg. The patient's diastolic blood pressure is 93 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6458,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-4528890-1,Extracted,"A 39-year-old man with no significant past medical history who works as an oil well driller presented to the emergency department (ED) with a 3-day history of significant shortness of breath and a productive cough. Two weeks prior, he had presented to the ED with symptoms of shortness of breath and productive cough and was treated with a onetime dose of azithromycin 500 mg, a 4-day course of azithromycin 250 mg once daily, a 5-day course of prednisone 10 mg 4 times daily, and albuterol 17 two puffs 4 times daily. He remained short of breath at rest and with activity. He complained of a productive cough with yellowish sputum and occasional streaks of blood. Pleuritic chest pain was present with coughing. He also had mild epigastric abdominal pain, nausea, and vomiting for the previous 7 to 10 days with no aggravating or alleviating factors. He denied any diarrhea or constipation. He denied any recent fever but had recently noticed significant diaphoresis. He denied any recent sick contacts, recent travel, and any history of asthma or tuberculosis. He had smoked 1 pack of cigarettes per day for an undocumented amount of time until 1 month previously when he quit.
His vital signs were as follows: blood pressure 167/104 mm Hg, heart rate 114 beats per minute, respiratory rate 24 breaths/min, temperature 98.7°F, O2 saturation 92% on room air, and body mass index 47.5 kg/m2. On examination he was mildly dyspneic and diaphoretic. He had no oral lesions. He had diffuse rhonchi bilaterally on inspiration and expiration and crackles on the right. His abdomen was soft, nontender, and nondistended with active bowel sounds.
His labs were as follows: white blood cell (WBC) 19,300/µL, hemoglobin 12.1 g/dL, hematocrit 36.4%, normal electrolytes, creatinine 1 mg/dL, glucose 117 mg/dL, total bilirubin 2.2 mg/dL, albumin 3.1 g/dL, alanine aminotransferase (ALT) 63 IU/L, and aspartate aminotransferase (AST) 38 IU/L. Cardiac enzymes were negative. Hepatitis panel was negative. His chest x-ray revealed bilateral lung infiltrates. The chest computed tomography (CT) showed no evidence of pulmonary thromboembolism and extensive patchy ground glass opacities in both lungs consistent with possible pulmonary edema, ARDS, or severe pneumonitis. The patient was admitted to the hospital and started on levofloxacin 750 mg once daily, piperacillin/tazobactam 3.375 g 3 times daily, vancomycin 1.25 g twice daily, and methylprednisolone 80 mg 4 times daily. The methylprednisolone dose and frequency was tapered down to 40 mg once daily over a 7-day period before it was discontinued.
His blood cultures showed no growth after 5 days, and his sputum culture grew 2+ normal upper respiratory flora and <1+ Staphylococcus aureus, resistant only to penicillin. Studies for Legionella pneumophila, HIV, and Pneumocystis jiroveci were negative. Five days after admission, he underwent bronchoscopy with bronchial alveolar lavage (BAL) from the right upper and lower lobes. The bronchoscopist found inflamed mucosa throughout the tracheobronchial tree, which was worse on the right side, thin mucoid secretions, especially in the right upper lobe, and no focal mucosal lesions. Transbronchial biopsies showed focal pneumonitis with plentiful intra-alveolar macrophages. His respiratory virus immunofluorescent assays (IFA) from the BAL were negative for adenovirus, influenza types A and B, respiratory syncytial virus, metapneumovirus, and parainfluenza virus types 1, 2, and 3. Direct fluorescent antibody (DFA) for PCP and CMV were negative. Herpes simplex DFA screening was positive for herpes simplex virus 1 (HSV-1) both from bronchial washings and both BAL specimens using the D3 DFA Herpes Simplex virus identification and typing kit (Diagnostic Hybrids, Athens, OH). (The kit’s positive and negative percent agreements for HSV-1 were 92.7% to 100% and 98.9% to 100%, respectively. Positive and negative percent agreements are used instead of sensitivity and specificity when standard references are not available to form the results. The term percentage therefore measures the percent agreement with a reference that is not standard rather than the accuracy of the study.) After 7 days, no herpes simplex virus was isolated on culture. No yeast or fungal elements were seen; aerobic cultures were negative on BAL and bronchial washing. Anaerobic cultures grew <1+ Staphylococcus saccharolyticus and <1+ Campylobacter gracilis. BAL fluid analysis showed a red blood cell count of 4232/mm3 and a WBC count of 224/mm3. The WBC differential was 85% neutrophils, 2% lymphocytes, 2% monocytes, 2% eosinophils, 8% macrophages, and 1% mesothelial cells. A 14-day course of acyclovir 1.3 g 3 times daily was started for herpes infection. Piperacillin/tazobactam 3.375 g twice daily, levofloxacin 750 mg once daily, and methylprednisolone 40 mg twice daily were continued. Vancomycin was discontinued.
Six days after admission, the patient’s breathing became labored and tachypneic, and he was intubated due to respiratory failure (). His PPD was negative, and his CD4 and CD8 counts were 613/µL (normal range = 347-872/µL) and 380/µL (normal range = 224-872/µL), respectively. Piperacillin/tazobactam and levofloxacin were discontinued on day 9, and methylprednisolone was discontinued on day 10. The patient was intubated for a total of 9 days. Two days after extubation, he was discharged.
Twelve days after discharge, the patient returned with increasing shortness of breath and bloody sputum for the previous 3 days. His vital signs were as follows: blood pressure 142/91 mm Hg, heart rate 99 beats per minute, and respiratory rate 24 breaths/min. His physical examination was significant for decreased breath sounds especially on the right side and bilateral crackles with occasional wheezing. His labs were as follows: WBC 13,300/µL, hemoglobin 11.3 g/dL, hematocrit 35.4%, sodium 140 mmol/L, potassium 3.2 mmol/L, BUN 8 mg/dL, creatinine 0.8 mg/dL, glucose 117 mg/dL, total bilirubin 1.6 mg/dL, albumin 3.7 g/dL, ALT 23 IU/L, AST 17 IU/L. Cardiac enzymes were negative. A chest CT showed worsening consolidation of the lungs bilaterally, especially in the right lung. Sputum and blood cultures were negative. He was started on vancomycin 2 g 3 times daily, azithromycin 500 mg once daily, cefepime 1 g 3 times daily, and acyclovir 1.2 g 3 times daily but showed little improvement. He was intubated 4 days after admission for a total of 21 days (). Ten days after admission he had an open lung right wedge biopsy that showed organizing pneumonia changes with interstitial pneumonitis ( and ). Pathology also showed diffuse alveolar damage with hyaline membranes, intra-alveolar macrophages, and pleural fibrosis. He was started on methylprednisolone 40 mg 4 times daily over the next 14 days and his oxygenation improved. Three days after extubation the patient left against medical advice (AMA). He presented in the internal medicine clinic for a follow-up appointment where he stated that he was admitted to a different hospital the same day he left AMA. He stayed at the other hospital for 2 weeks and was continued on prednisone. At the clinic he reported a cough but no dyspnea or limitations of activity. He was off prednisone.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [167.0, 'mm hg'], 'Diastolic Blood Pressure': [104.0, 'mm hg'], 'age': [39, 'years'], 'respiratory rate': [24.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [8.0, 'mg/dL']}",0,0,0,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 39 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 8.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 24 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 0.
The patient's systiolic blood pressure is 167 mm Hg. The patient's diastolic blood pressure is 104 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 0.
The patient's CURB-65 score is 0."
6459,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-7263243-1,Extracted,"A 57-year-old man, with past medical history significant for hypertension on amlodipine and type II diabetes on insulin glargine, presented to the emergency department with one day history of acute dizziness, most prominent with head movements and exacerbated with standing. It was associated with retrosternal burning pain especially after meals. At that time, he was investigated for coronary artery disease, with normal ECG and negative serial troponins. Serum sodium was 128mEq/L (reference range 135–145 mEq/L), however, it was not investigated initially. He was discharged on betahistine.
Three days later, he presented again with increasing severity of dizziness, along with nausea, fatigue, and generalized headache. There was no fever, chills, cough or shortness of breath. The patient denied any change of his oral intake of fluid, introduction of new medications or change in his urinary habits. He was afebrile, with blood pressure of 152/90 mmHg, heart rate of 88 beats per minute and respiratory rate of 19 breaths per minute with oxygen saturation of 98 % on room air. Physical exam was unremarkable, with no signs of overload or dehydration.
Laboratory findings were significant for serum sodium of 112 mEq/L (normal range 136–145 mEq/L). Three days before his serum sodium was 128 mEq/L, and 137 mEq/L noted on a prior admission for a urinary tract infection three years ago. Laboratory investigations revealed normal BUN of 8.96 mg/dL (reference range: 7–20 mg/dL) and creatinine of 0.79 mg/dL (normal range: 0.5–1.2 mg/dL). Random blood glucose was 9.6 mmol/L. Further workup revealed urine osmolarity of 237 mOsm/kg, urinary sodium 63 mEq/L with low serum osmolality of 240 mOsm/kg. Thyroid stimulating hormone and ACTH stimulation test were normal. A chest X-ray did not show any infiltrates. Electrocardiogram showed no abnormality. Head computed tomography scan was unremarkable. As COVID-19 was widespread in the community of Qatar, and a case series in our center recently reported an association between COVID-19 and SIADH, we sent a nasopharyngeal swab for SARS-CoV-2 PCR which came back positive. Since all workup for pulmonary and central nervous system disorders remained negative, the patient was diagnosed as having SIADH due to underlying COVID-19 infection.
The treatment with slow hypertonic saline 3% infusion was initiated with remarkable improvement in his symptoms. Oral fluid restriction was initiated. Serum sodium levels were monitored for the next 72 h, and fluctuated between 124–130 mEq/L. The patient was transferred to a quarantine facility; however, he did not develop any respiratory symptoms or fever.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [152.0, 'mm hg'], 'respiratory rate': [19.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [8.96, 'mg/dL'], 'Confusion': False, 'Diastolic Blood Pressure': [90.0, 'mm hg'], 'age': [57, 'years']}",0,0,0,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 57 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 8.96 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 19 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 0.
The patient's systiolic blood pressure is 152 mm Hg. The patient's diastolic blood pressure is 90 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 0.
The patient's CURB-65 score is 0."
6460,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-5127219-1,Extracted,"A 65-year-old female patient previously diagnosed with rheumatic valve disease was submitted to surgical mitral valve repair in 1996 and percutaneous exchange of the mitral valve in 2007. This patient visited the cardiology outpatient clinic and complained of dyspnea on the slightest effort, paroxysmal nocturnal dyspnea, orthopnea, dry cough, and daily episodes of fever between 38 and 38.5 °C persisting for 1 month. The patient also reported being treated for dengue fever in another health service 40 days previously. During the hospital stay, the patient experienced an episode of paroxysmal atrial flutter. Ten days later, the patient’s level of consciousness decreased abruptly (Glasgow coma scale of 13), and she presented anisocoric pupils. The patient was referred to the intensive care unit (ICU). Upon admission to the ICU, she was drowsy, pale, hydrated, acyanotic, anicteric, and afebrile (37.3 °C). The arterial blood pressure was 122/73 mm Hg, the heart rate was 96 beats per minute, and the respiratory rate was 14 breaths per minute. Heart auscultation was normal; murmurs were absent. Respiratory auscultation and abdomen examination were normal. There was mild edema in the lower limbs.
Laboratorial records revealed the following data: hemoglobin 8.5 g/dL, hematocrit 25%, white blood cells 16,200/mm3, platelets 192,000/mm3 without left shift and with mild anisocytosis and microcytosis, urea 67 mg/dL, creatinine 2.39 mg/dL, sodium 132 mmol/L, potassium 3.6 mmol/L, and C reactive protein 11.2 mg/dL. At admission, the patient’s Acute Physiology and Chronic Health Disease Classification System (APACHE) II score was 22 (which corresponded to a death risk of 45%) [, ], and her Sequential Organ Failure Assessment (SAPS) III score was 64 (which corresponded to a death risk of 44%) [, ]. Dental evaluation indicated precarious dentition.
Blood culture samples were collected and empirical treatment with ceftriaxone associated with gentamicin was initiated. Transesophageal echocardiogram revealed an approximately 8-mm filamentous image with chaotic motion in the ventricular face of the anterior mitral valve leaflet compatible with vegetation. After 10 days in hospital, the patient’s level of consciousness decreased, and she presented sensitive conduction aphasia and mild right central paralysis. Ischemic stroke with high probability of septic etiology was suspected. Brain tomography demonstrated hypodense left insular lobe corresponding to incipient ischemia. Mechanical thrombectomy was indicated, but the arteriogram did not show occlusion of the proximal vessels. Failed partial filling of the parietal branch of the left middle cerebral artery was observed. The patient progressed with worsened level of consciousness, hemodynamic instability, and need for hemodialysis. Orotracheal intubation was performed, vasoactive drugs were initiated, and brain tomography was repeated. The tomography evidenced brain edema in the posterior circulation region and hypodensity in the left thalamus. The patient presented septic shock refractory to the therapeutic measures and died.
The transesophageal echocardiogram evidenced pronounced dilation of the left atrium, moderate double mitral lesion, mild to moderate tricuspid insufficiency, moderate pulmonary hypertension, and approximately 8-mm filamentous image with chaotic motion in the ventricular face of the anterior mitral valve leaflet compatible with vegetation.
Haemophilus parainfluenzae grew in the four blood culture samples. Blood culture was conducted in diffusion discs. The microorganism was sensitive to all the tested B-lactamic compounds.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [65, 'years'], 'Systolic Blood Pressure': [122.0, 'mm hg'], 'Diastolic Blood Pressure': [73.0, 'mm hg'], 'respiratory rate': [14.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [67.0, 'mg/dL'], 'Confusion': True}",3,3,3,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 65 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient has confusion, 1 point is added to score making the current total 1 + 1 = 2.
The concentration of BUN is 67.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 2 + 1 = 3.
The patient's respiratory rate is 14 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 3.
The patient's systiolic blood pressure is 122 mm Hg. The patient's diastolic blood pressure is 73 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 3.
The patient's CURB-65 score is 3."
6461,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-6374832-1,Extracted,"A 53-year-old Caucasian man was admitted to the emergency department (ED) with complaints of diarrhea of 3 days' duration, general weakness leading to multiple falls, abdominal pain with lack of appetite, dry cough, and dyspnea on exertion since the last 6 months. His medical past history included chronic alcoholism with 28 units of alcohol per week, active tobacco smoking (22,5 pack-years), sleep apnea syndrome treated with nocturnal continuous positive airway pressure (CPAP) ventilation, high arterial blood pressure controlled by a daily dose of perindopril 5mg and bisoprolol 10 mg, and a morbid obesity with a body mass index (BMI) of 47,3 kg/m2. There was no history of abdominal surgery. Vital signs in the ED were arterial blood pressure 106/64 mmHg, sinus tachycardia with heart rate ranging from 104 to 144 bpm, respiratory rate 37/min, temperature 36.2°C, and oxygen peripheral saturation (SpO2) 92% at room air. Initial examination revealed crackles at the basis of the right lung and abdominal distension with decreased bowel sounds. There were no clinical signs of muscular injury.
The relevant laboratory investigations were the following: CRP 192 mg/L (< 5), platelet count 115.000 /μL, serum creatinine 4.48 mg/dL, BUN 94 mg/dL, sodium 126 mmol/L, and potassium 3mmol/L. A major rhabdomyolysis was early noted: CK 96,012 IU/L (< 397), troponin-I 103.3 ng/L (< 34.2), AST 818 IU/L (< 37), and LDH 2,960 IU/L (< 214). The CK level further increased to 120,059 IU/L 4 hours after hospital admission. Arterial blood gas analysis was consistent with a compensated metabolic acidosis: pH 7.44, pCO2 21.8 mmHg, pO2 79.7 mmHg, bicarbonate 18.6 mmol/L, base excess -7.2 mmol/L, and lactate level 2 mmol/L (< 1.6). Urine analysis revealed moderate proteinuria (++).
The electrocardiogram showed new onset atrial fibrillation (144/min). The diagnosis of left basal pneumonia with a contralateral pleural effusion was made on chest X-ray. Small and large bowel distension was evident from abdomen X-ray with some air fluid levels ().
The patient was transferred to the intensive care unit (ICU) for further management. He remained hypotensive (79/43 mmHg), with atrial fibrillation (166/min) and hypoxemia requiring nasal oxygen administration (5L/min). Initial therapy included fluid replacement, vasopressors, and potassium supplementation for persisting hypokalemia (2.9 mmol/L). Cefuroxime and clarithromycin were initially chosen for empirical antimicrobial therapy. No sputum was available for culture and blood cultures remained sterile. Urine Legionella testing returned positive for L. pneumophila serogroup 1 antigen and clarithromycin was continued alone.
Further clinical course was characterized by a progressive weaning of vasopressors and decrease of arterial lactate. Ileus persisted. Contrast enhanced abdominal computed tomography (CT) showed a diffuse distension of the large intestine and terminal ileum and a diffuse enhancement of the intestinal wall without evidence of bowel ischemia or stenosis (). Renal failure worsened and the patient became anuric on day 2 with serum creatinine 7.18 mg/dl and BUN 146 mg/dl. Intermittent hemodialysis was then started. The peak level of CK (202,000 IU/L) was reached on day 2.
Mechanical ventilation was ultimately required from hospital day 4 to 10 due to the progression of hypoxemia with hypercapnia; there was also a suspicion of inhalation pneumonia secondary to persisting ileus. During the period of mechanical ventilation, the patient did not receive opioid medications that could have resulted in a decreased intestinal motility.
Despite noncontributive abdominal CT findings, an explorative laparotomy was decided on day 12 that failed to demonstrate any mechanical occlusion.
Two weeks after ICU admission, patient was transferred to the nephrology ward with persisting ileus leading to a full month of parenteral nutrition. Antimicrobial therapy was stopped after 21 days. The patient was discharged home after two months. Hemodialysis was definitely stopped after 5 weeks, and renal function returned to normal values after 6 weeks.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [53, 'years'], 'Systolic Blood Pressure': [106.0, 'mm hg'], 'Diastolic Blood Pressure': [64.0, 'mm hg'], 'respiratory rate': [37.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [94.0, 'mg/dL'], 'Confusion': True}",3,3,3,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 53 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient has confusion, 1 point is added to score making the current total 0 + 1 = 1.
The concentration of BUN is 94.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 37 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 2 + 1 = 3.
The patient's systiolic blood pressure is 106 mm Hg. The patient's diastolic blood pressure is 64 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 3.
The patient's CURB-65 score is 3."
6462,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-5458001-1,Extracted,"A 43-year-old woman, with postliver transplant (2008) secondary to primary sclerosing cholangitis-related cirrhosis, maintained on tacrolimus, presented to our hospital with 4-day history of sore throat and fever and 2-day history of skin rash. On examination, patient was found to be febrile with temperature of 38.2 celsius, B.P 100/80 mmHg, respiratory rate (R.R) 24/min, and heart rate (H.R.) 130/min. Oxygen saturation on room air was 85%. Systemic examination revealed congested eyes, pharyngeal erythema, maculopapular skin rash involving face, upper limbs, and trunk. Chest examination revealed decreased breath sounds on the right basal area and crackles on the left side posteriorly till the mid-zone. Basic laboratory work-up was as follows: WBC: 9.8 × 103/μL, neutrophil: 7.7 × 103/UL, lymphocyte: 0.9 × 103/UL, BUN:2.80 mmol/L, creatinine: 88 μmol/L, Na: 129 mmol/L, K: 4 mmol/L, Cl: 99 mmol/L, HCO3: 18 mmol/L mmol/L, bilirubin T: 7.6 μmol/L, albumin: 28 gm/L, ALT: 50 U/L, AST: 84 U/L, ALP: 268 U/L, INR: O.9, CRP: 53, ESR: 29 and tacrolimus level: 3.4. Hepatic transaminases showed progressive increase over 2 days. Ultrasound of abdomen and liver was normal. A CT pulmonary angiogram was ordered due to the presence of tachypnoea, tachycardia and drop in oxygen saturation. It did not show any evidence of PE but showed bilateral basal lung infiltrates more on the right side with associated two large size basal lung cysts (Fig. ) .
Patient was admitted as a case of viral exanthemata fever and bronchopneumonia with airborne precautions and was treated with intravenous antibiotics and fluids. The respiratory viral panel came negative. Viral serology results were positive for CMV Ab IgG, EBV nuclear antigen IgG, EBV capsid antigen IgG, rubella IgG Ab, measles IgG Ab, and measles IgM Ab. Autoimmune serologies and tuberculosis work-up were negative. On day 2 of admission, patient's skin rash started to fade from the face and patient showed clinical improvement with regard to fever and constitutional symptoms. Bronchoscopy with bronchoalveolar lavage to evaluate lung infiltrates and cystic lung disease showed negative work-up for acid-fast bacilli, Pneumocystis jiroveci pneumonia, and fungi. Measles virus PCR in serum was reported positive. She was managed with fluids and supportive measures. The patient improved clinically with the fading of skin rash gradually and normalization of liver enzymes over the next 5 days and was discharged home.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg'], 'age': [43, 'years'], 'respiratory rate': [24.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [2.8, 'mmol/L']}",0,0,0,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 43 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 2.8 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of BUN from mmol to mg. The mass of BUN is 2.8 mmol. To convert 2.8 mmol of BUN to mol, multiply by the conversion factor 0.001, giving us 2.8 mmol BUN * 0.001 mol/mmol = 0.0028 mol BUN. To convert from mol BUN to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0028 mol BUN * 28.02 g/mol = 0.07846 g BUN. To convert 0.07846 g of BUN to mg, multiply by the conversion factor 1000.0, giving us 0.07846 g BUN * 1000.0 mg/g = 78.46 mg BUN. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 78.46 mg BUN/10.0 dL = 7.846 mg BUN/dL. The concentration value of 2.8 mmol BUN/L converts to 7.846 mg BUN/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 24 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 0.
The patient's systiolic blood pressure is 100 mm Hg. The patient's diastolic blood pressure is 80 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 0.
The patient's CURB-65 score is 0."
6463,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-7839278-1,Extracted,"An 85-year-old female patient with a history of coronary artery disease, aortic valve replacement (AVR), type 2 diabetes mellitus, and end-stage renal disease (ESRD) on PD presented to the emergency department with difficulty breathing and altered mental status. Her son, the primary caregiver, shared that the patient was recently discharged from subacute rehab following a below-knee amputation (BKA) and had been having diarrhea. No further review of systems was obtainable due to her clinical status.
Upon arrival, her blood pressure was 113/48 mmHg, heart rate of 69 beats per minute, respiratory rate of 20 breaths per minute, oxygen saturation of 99% on 100% non-rebreather mask, the temperature of 36.6° C. Physical exam revealed an elderly, frail female who was not oriented. She had bilateral coarse rhonchi on auscultation of her lungs with decreased breath sounds at the right lung base. The heart exam was normal. The abdomen was tender to palpation as facial grimacing was noted. A PD catheter was in place, and the site was clean. The patient did not follow commands, but the neurologic exam was non-focal.
Further workup revealed blood urea nitrogen (BUN) 27 mg/dL, creatinine 3.8 mg/dL (at baseline), mild hypokalemia at 3.5 mMol/L, leukocytosis at 13.5/mm3. A stat computed tomography of her head showed no acute intracranial process, and a chest X-ray revealed a right pleural effusion with possible right lower lobe opacities, which were unchanged from the previous studies (Figure ).
She was then started on empiric antibiotics, including vancomycin, cefepime, and doxycycline, and admitted to the intensive care unit for severe sepsis. Infectious disease was consulted and recommended switching cefepime to ceftriaxone as the patient’s mental status continued to deteriorate, in addition to sending peritoneal fluid for analysis and culture. While awaiting PD fluid cultures, her blood cultures grew Methicillin-resistant Staphylococcus aureus (MRSA), leading to concerns for infective endocarditis given her AVR history. The peritoneal fluid analysis revealed neutrophilic predominance with results as follows: 3,938 nucleated cells, 82% neutrophils, 9% lymphocytes, 8% monocytes, and 1% eosinophils. Although receiving empiric antibiotic therapy, the patient’s clinical condition continued to deteriorate. On the fifth hospital day, the patient’s peritoneal fluid culture revealed Enterococcus gallinarum resistant to vancomycin. The patient was subsequently placed on IV daptomycin and cefazolin for synergy with improvement in her mental status within 48 hours. Repeat peritoneal fluid analysis showed decreased leukocytes and clearance of her E. gallinarum on repeated fluid cultures. The susceptibilities for E. gallinarum are listed in Table .
A transthoracic echocardiogram was performed as the patient also had persistent MRSA bacteremia, which did not show any vegetations or mass. A transesophageal echocardiogram (TEE) subsequently revealed a large globular deformation of the posterior mitral leaflet bulging into the left atrium, measuring 2.0 x 1.9 cm in size that was concerning for mitral valve abscess (Figures -). Unfortunately, due to the patient's worsening clinical status and considering the overall prognosis, the patient was placed in hospice care and died several days later. An autopsy was not performed.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [85, 'years'], 'Systolic Blood Pressure': [113.0, 'mm hg'], 'Diastolic Blood Pressure': [48.0, 'mm hg'], 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [27.0, 'mg/dL'], 'Confusion': True}",4,4,4,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 85 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient has confusion, 1 point is added to score making the current total 1 + 1 = 2.
The concentration of BUN is 27.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 2 + 1 = 3.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 3.
The patient's systiolic blood pressure is 113 mm Hg. The patient's diastolic blood pressure is 48 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 3 + 1 = 4.
The patient's CURB-65 score is 4."
6464,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-3870642-1,Extracted,"A 57-year-old Chinese male with a past medical history significant for hypertension, hyperlipidemia, and moderate mitral regurgitation secondary to mitral valve prolapse presented with a 3-week history of progressive hemoptysis and worsening dyspnea. The symptoms started insidiously and progressed to a point where his exercise tolerance was reduced to a few steps. He was a plumber by profession and a lifetime nonsmoker. He denied wheezing, fever, night sweats, chest pain, and weight loss. He had no history of hemoptysis or bleeding from any other body sites. He did not use any medications and denied recent travel or sick contacts. On physical examination, he appeared to be in moderate respiratory distress, tachycardia, and tachypnea. His vital signs were blood pressure of 146/80 mmHg, heart rate of 116/min, respiratory rate of 34/min, temperature of 99.1 F, and saturating at 96% on 3 liters of oxygen by nasal cannula. He was oriented to time place and person and was found to be using his accessory muscles of respiration. His chest examination was notable for coarse crackles on the right side without any wheezing. His cardiac examination revealed tachycardia with a 3/6 pansystolic murmur best heard over the mitral area. The rest of his physical examination was unremarkable. His extremities were perfusing well and no peripheral edema was noted. His labs were notable for leukocytosis with neutrophilia (WBC: 12.7 k/mm3; neutrophils: 84%; eosinophils < 1%), his electrolytes were within normal range, and renal function was deranged with elevated blood urea nitrogen (BUN) and creatinine (Na: 143 mEq/L; K: 4.6 mEq/L; Cl: 107 mEq/L; HCO3: 23 mEq/L; BUN: 40 mg/dL; creatinine: 1.5 mg/dL). His liver function tests (LFTs) were notable for elevated liver enzymes (AST: 48 U/L; ALT: 127 U/L). His arterial blood gas (ABG) was notable for a pH of 7.44, pCO2 of 31 mmHg, and a pO2 of 84 mmHg. His chest X-ray (CXR) showed right sided fluffy infiltrates (). He was admitted to the medical floor and started on ceftriaxone and azithromycin for presumed community acquired pneumonia. However, his respiratory status deteriorated and he was transferred to the Cardiac Intensive Care Unit where he was started on noninvasive mechanical ventilation (inspiratory pressure of 15 mmHg, expiratory pressure of 8 mmHg at 100% oxygen supplementation). An ABG showed a pH of 7.13, pCO2 of 64 mmHg, and a pO2 of 68 mmHg indicative of acute respiratory acidosis. His respiratory condition continued to deteriorate and he was intubated and mechanically ventilated with a positive end expiratory pressure (PEEP) of 5 mmHg and 50% oxygen supplementation. The patient's CXR revealed infiltrates which were more dense and confluent (). His labs were significant for up-trending leukocytosis (15 k/mm3). The patient's blood and urine cultures were negative. Tests for legionella, mycoplasma, HIV, and influenza were also negative. Autoimmune and vasculitis panels [antinuclear antibody (ANA), antineutrophil cytoplasmic antibodies (ANCA), and antiglomerular basement membrane antibody (GBM)] tests were negative. An ABG after commencing mechanical ventilation showed a pH of 7.44, pCO2 of 31 mmHg, and a pO2 of 81 mmHg. Computed tomography (CT) of his chest confirmed the presence of dense infiltrates predominantly located in the right upper and middle lobes (Figures and ). Transthoracic echocardiogram showed an ejection fraction (EF) of 70%, mildly dilated left atrium, significant prolapse of the posterior mitral leaflet, and moderate tricuspid regurgitation. Right heart catheterization showed a pulmonary artery pressure of 56/23/35 mmHg (systolic/diastolic/mean); pulmonary capillary wedge pressure (PCWP) of 22 mmHg, right atrial pressure of 4 mmHg, RV: 53/6 mmHg (systolic/diastolic); cardiac Index (by thermo dilution) of 2.1 liters/min/m2, and a pulmonary artery resistance of 9 wood units. Bronchoscopy revealed fresh blood in all the lobes with no obvious source and no endobronchial lesions. Sequential lavage from the right middle lobe was not progressively bloodier and hence less consistent with diffuse alveolar hemorrhage. Bronchoalveolar lavage was negative for cytology, acid fast bacillus (AFB), fungal stain, and pneumocystis carinii pneumonia (PCP). Thoracentesis yielded 150 cc of serous fluid with a pH of 7.6, LDH of 80 U/L, protein of 0.9 g/dL, glucose of 120 mg/dL, cell count with a differential of 55% of neutrophils, lymphocytes of 25%, and mesothelial cells of 10%. This was consistent with a transudative pleural effusion. The cytology and culture results of the fluid from thoracentesis were also negative. A transesophageal echocardiogram (TEE) showed thickening and elongation of the anterior leaflet of the mitral valve consistent with myxomatous degeneration, up to 1 cm in thickness at the margin of the anterior leaflet, prolapse of posterior leaflet into left atrium, aneurysm measuring 1 × 1.6 cm2 and perforation into left atrium and severe mitral regurgitation but no vegetations. The patient continued to have increased oxygen requirements and persistent hemoptysis and eventually underwent an emergent mitral valve repair. Perioperative TEE revealed hypertrophied right and left ventricles, normal right and left ventricular function with EF of 55%, mild anteroseptal wall hypokinesis, prolapse of the posterior mitral leaflet with a flail P3 segment, and severe mitral regurgitation with systolic flow reversal in right upper pulmonary vein (Figures and ). A final diagnosis of alveolar hemorrhage secondary to severe acute mitral regurgitation from myxomatous degeneration of mitral valve was made. Notably, his hemoglobin had decreased from 14.5 gm/dL to 11.7 gm/dL. Postoperative TEE did not show any evidence of mitral valve regurgitation (). A repeat bronchoscopy 3 days after the mitral valve repair showed clearing of the alveolar hemorrhage (Figures , , and ). The patient rapidly recovered thereafter as was reflected in his CXR ().",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [146.0, 'mm hg'], 'Diastolic Blood Pressure': [80.0, 'mm hg'], 'age': [57, 'years'], 'respiratory rate': [34.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [40.0, 'mg/dL'], 'Confusion': False}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 57 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 40.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 34 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 1 + 1 = 2.
The patient's systiolic blood pressure is 146 mm Hg. The patient's diastolic blood pressure is 80 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6465,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-4620336-1,Extracted,"A 54-year-old female was admitted to our hospital with subacute cough for the last month. The patient had a history of multilobar (right middle lobe and right upper lobe) pneumonia over the past 2 years, and had been admitted to a nearby hospital with the chief complaint of a cough that had worsened over the previous month. She usually had a dry cough after a cold, which did not last for more than 2 months. Following a diagnosis of acute eosinophilic bronchitis and focal pneumonia, the patient was administered antibiotics. However, her pneumonia did not improve and she was transferred to our hospital for further examination.
She had no disease and no operation history. She was nonsmoker and social drinker. She had no family history and her occupation was teacher.
Blood pressure was 110/60 mm Hg, pulse rate was 60 beats per minute, respiration rate was 20 per minute, and body temperature was 36.8℃. General findings indicated no pain, but chest auscultation revealed minor rales in the right middle lobe. Heart auscultation revealed a normal beat without cardiac murmur. No edema was observed in the abdomen or extremities, and no lymph node enlargement was apparent.
The results of an arterial blood gas examination performed at the time of admission were PH 7.43, PaCO2 33 mm Hg, PaO2 78 mm Hg, and HCO3- 22 mEq/L. A peripheral blood examination revealed a hemoglobin level of 13.1 g/dL, hematocrit 44%, a white blood cell count of 8,600/mm3, and a platelet count of 250,000/mm3.
The results of biochemical analysis were a total protein level of 6.8 g/dL, albumin 4.1 g/dL, aspirate aminotransferase 38 IU/L, alkaline phosphatase 200 mg/dL, erythrocyte sedimentation rate 30 m/hr, blood urea nitrogen 12.9 mg/dL, and creatinine 0.9 mg/dL. Electrolytes and blood glucose levels were normal, and urine examination revealed specific gravity of 1.025, pH 6.0, no proteinuria, and a red blood cell count of 30-49 per high-power field. Subsequent examination revealed no worsening of hematuria. Empirical antibiotic treatment, acid-fast bacillus (AFB) sputum smear, and sputum eosinophil tests were performed, in order to differentiate community-acquired pneumonia and pulmonary tuberculosis (TB). Sputum bacteria examination did not yield specific findings, and very few sputum eosinophils were observed. The concentration of the tumor marker carcinoembryonic antigen detected was 1.3 ng/mL(with-in normal range), and an interferon-gamma release assay was positive. However, the AFB smear and TB polymerase chain reaction were negative, and AFB culture yielded no-growth. Tests for rheumatic factors and antinuclear antibody yielded no specific findings, and the patient did not complain of rheumatic-disease-related symptoms. Electrocardiography and echocardiography yielded normal results, and pulmonary function examination revealed a forced vital capacity (FVC) of 2.83 L (90% of reference), forced expiratory volume in the first second (FEV1) 2.27 L (93% of reference), FEV1/FVC 92%, and diffusion capacity adjusted by the alveolar volume 97%, indicating mild obstructive ventilation disturbance.
Simple chest radiography revealed nodular lesions around the pulmonary hilum of the right upper lobe (). Chest computed tomography (CT) revealed a 1.8-cm speculated nodule around the inferior margin of the right upper lobe, and the differential diagnosis of focal pneumonia or lung cancer was required (). A bronchoscopy revealed no abnormalities in the bronchi. Kidney ultrasonography and a gastroscopy that were performed to confirm the amyloidosis lesions did not yield specific findings; so video assisted thoracic surgery (VATS)-assisted pulmonary wedge resection was conducted for early differentiation of lung cancer. No surgical complications were encountered.
Histology indicated a thickened interstitium due to eosinophilic amorphous material deposits, with some giant cells and histiocyte infiltration (). Congo red staining for amyloidosis was positive, and under a polarized microscope the nodule exhibited a unique apple-green birefringence ().
Additional examinations for amyloidosis, blood and urine immunoelectrophoresis, and immunofixation were performed. IgG, IgM, IgA, IgE, and IgD concentrations were normal, as were the immunofixation results (). A bone marrow biopsy was not performed, in accordance with the patient's request.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg'], 'age': [54, 'years'], 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [12.9, 'mg/dL']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 54 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 12.9 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 0.
The patient's systiolic blood pressure is 110 mm Hg. The patient's diastolic blood pressure is 60 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 0 + 1 = 1.
The patient's CURB-65 score is 1."
6466,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-7850343-1,Extracted,"We present a 62-year-old female with a past medical history of hypertension, bipolar disorder, chronic obstructive pulmonary disease, and opioid use disorder. She was hospitalized at an inpatient psychiatric facility in 2017. She was started on valproate 500 mg twice daily and duloxetine 60 mg. The patient has been following with outpatient psychiatric clinic, who changed valproate to risperidone 2 mg twice daily. Her current home medications are oxycodone 15 mg 4 times a day, trazadone 100 mg daily at night, duloxetine 60 mg daily, risperidone 2 mg twice daily, and metoprolol tartrate 25 mg daily.
She was brought to the emergency department by EMS after she was found unresponsive by her family. When the EMS arrived at her home, she was given 4 mg naloxone intranasally, which resulted in the improvement of her mental status.
In the Emergency Department, vital signs on initial arrival were as follows: Temperature: 99.0 F, Blood Pressure: 115/74, Heart Rate: 64, Respiratory Rate: 15, Pulse Oximetry: 97% on room air. On physical examination, the patient was sleepy but arousable by verbal stimulation. She had small pupils bilaterally. She was oriented to place and person but wasn’t answering questions or following commands properly. Lung and heart exam revealed a normal bilateral vesicular breathing sounds with no wheezes or crackles. She had a regular rate and normal rhythm S1, S2 sounds no murmurs or gallops. She had no lower limb edema bilaterally. She was not in respiratory distress. She received additional three doses of IV 0.4 mg of naloxone as she was drowsy. Laboratory was remarkable for elevated creatinine of 1.74. A urine drug screen was positive for opiates, methadone, and benzodiazepines. The patient later in the emergency department was noted to become short of breath, with oxygen saturation decreasing to 80%. She was also tachycardic to 120 s. A Non-rebreathing mask was applied and resulted in an improvement of oxygen saturation to 95%.
Upon auscultation of the chest, she was noted to have bilateral crackles. A portable chest x-ray was obtained that showed findings highly suggestive of interstitial edema, pulmonary vascular congestion, and early pulmonary edema ().
Arterial blood gases were obtained while the patient was on 2 L nasal cannula (28% oxygen) PH 7.37, PO2 64, PCO2 55, HCO3 28.5, O2 saturation of 94% consistent with hypoxemia and chronic respiratory acidosis.
COVID 19 PCR was negative. WBC 12.7 k/ul [Normal range 4.8–10.8], Hemoglobin 13.9 gm/dl, platelets 160 [130–400 k]. AST 16[15–41 u/l], bilirubin total 0.8 mg/dl [0.2–2 mg/dl],
Alk 62 u/l [Normal range 38–126], ALT 14 u/l [Normal range 14–54 u/l], BUN 28 [8–20 mg/dl], Cr 1.76 mg/dl [Normal range 0.4–1 mg/dl], glucose 238, calcium 8.9, sodium 131 mmol/l, potassium 5 mmol/l, CPK 38 u/l, blood alcohol level <10 mg/dl, troponin I 0.04 ng/ml, acetaminophen level 5 ul/ml, salicylate level <4, BNP 111. CT scan of the head without contrast showed no evidence of an acute intracranial abnormality. EKG showed normal sinus rhythm, left ventricular hypertrophy with repolarization abnormalities. She was given furosemide 40 mg intravenously and was admitted to the intensive care unit.
Initially, the patient remained sleepy but easily arousable. She was maintaining an oxygen saturation of 92 on 4 L nasal cannula. She never required intubation, a trial of noninvasive mechanical ventilation was not attempted because of fluctuating mental status. She was kept in the ICU for monitoring and started on IV furosemide 40 mg daily. Repeat ABG in the morning was still showing hypoxemia and chronic compensated respiratory acidosis with a PH of 7.41, PCO2 53, PO2 54, HCO3-30, oxygen saturation of 90% on 4 L nasal cannula. She was more awake the next day. The patient reports that she might have taken multiple oxycodone at one time. An echocardiogram was obtained, which showed normal global left ventricular systolic function with left ventricular ejection fraction is 55% to 60%, moderate concentric left ventricular hypertrophy, and a mildly dilated left atrium (4 cm). Diastolic grading could not be performed on the echo due to fusion of E/A waves (however other parameters were normal; E/e’ Ratio: 8.3, TR max velocity 2.8 cm). Suspicion for heart failure as a cause of pulmonary edema was low given the absence of significant findings on echo. Pulmonology consultation was obtained; the patient was started on incentive spirometry and acapella. On the third day, she was maintaining saturation of 100% on room air; however, she remained in sinus tachycardia up to 120 s, serum creatinine improved to 1.4 mg/dl. A repeat chest X-ray showed improvement of mild interstitial prominence ().
Psychiatry was consulted and restarted the patient on her psychiatric medications and determined that the patient had the capacity to make her decisions. The patient signed out against medical advice later that day.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [62, 'years'], 'Systolic Blood Pressure': [115.0, 'mm hg'], 'Diastolic Blood Pressure': [74.0, 'mm hg'], 'Blood Urea Nitrogen (BUN)': [28.0, 'mg/dL'], 'respiratory rate': [15.0, 'breaths per minute'], 'Confusion': True}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 62 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient has confusion, 1 point is added to score making the current total 0 + 1 = 1.
The concentration of BUN is 28.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 15 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 115 mm Hg. The patient's diastolic blood pressure is 74 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6467,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-2365966-1,Extracted,"A 42-year-old Caucasian female presented with a history of high-grade fever and yellow productive cough for one day. The cough was associated with pleuritic chest pain and shortness of breath at rest. The patient described chronic dyspnea for approximately 15 years limiting her ability to perform household activities. A review of systems was significant for chronic fatigue and weakness for 15 years, and chronic loose stools with occasional constipation for 10 years. The patient had been transferred from the hospital to a rehabilitation facility one week prior following a prolonged stay in the intensive care unit with multiorgan failure secondary to septic shock. She required ventilatory support for two weeks and temporary hemodialysis for approximately two weeks secondary to acute kidney injury. She was discharged in a stable condition.
Past medical history included asthma for 15 years, chronic obstructive pulmonary disease for 5 years, recurrent cough and sinus infections since adolescence requiring antibiotics, severe ear infection requiring emergent mastoidectomy 4 years prior, gastroesophageal reflux disease, irritable bowel syndrome for 10 years, migraine headaches and bipolar disorder for 2–3 years, and tonsillectomy as a child. She had a normal mammogram 4 years prior and a normal colonoscopy approximately 10 years prior, which was performed as part of a work-up for irritable bowel syndrome. She admitted to a 20 pack year smoking history, but denied any alcohol or illicit drug abuse. Medications included levalbuterol, montelukast, fluticasone/salmeterol for 10–15 years, lansoprazole and loratidine/pseudoephedrine as required for a few years, and hydrocodone, quetiapine fumarate and topiramate for approximately 3 years.
On examination, she appeared chronically ill and anxious. She had a temperature of 99.8°F, was tachycardic (137/min), tachypneic (26/min) with a blood pressure of 109/59 mmHg and was saturating 88% on 2 l/min nasal oxygen. Physical examination was significant for bibasilar rhonchi and a central venous catheter in the left internal jugular vein, which had been placed for hemodialysis. She had no clubbing or nasal polyps. The remainder of the physical examination was within normal limits.
Her white blood cell (WBC) count was elevated at 15,800/mm3; this was 8,000/mm3 at discharge. Her blood urea nitrogen (BUN) and creatinine levels were slightly elevated at 24/1.6 mg/dl; however, these were on a downward trend since discharge (29/2.4 mg/dl). Chest X-ray was significant for improving bibasilar infiltrates when compared with a previous chest X-ray at the time of discharge. Cardiac enzymes were normal and arterial blood gas (ABG) showed a pH of 7.5, PC02 of 32 mmHg, PO2 of 48 mmHg and HCO3 of 25 mEq/l on 2 l/min nasal oxygen. The A-a gradient was markedly increased at 104 mmHg. Computerized tomography (CT) of the chest following the pulmonary embolism protocol did not reveal any evidence of pulmonary embolism. Sputum Gram stain with cultures and blood cultures were sent for analysis and she was started on intravenous levofloxacin and vancomycin.
A high-resolution CT thorax scan without contrast was carried out for better delineation of lung parenchyma and was significant for bronchial wall thickening and dilatation predominantly in the lower lung fields consistent with bronchiectasis (Figure ).
A CT scan of the sinuses revealed chronic maxillary sinusitis. The patient showed clinical improvement by the next day and the blood culture did not have any growth at 72 hours. Sputum culture showed moderate growth of Streptococcus pneumoniae.
Given the patient's recurrent respiratory infections since adolescence and bronchiectasis, a wide differential diagnosis was considered to include genetic conditions such as cystic fibrosis, immotile cilia syndrome, alpha 1 antitrypsin deficiency and immunodeficiency. A work-up was initiated which revealed a negative sweat chloride test and normal alpha 1 antitrypsin levels. Human immunodeficiency virus (HIV) screening test was negative. Ig levels were significantly reduced: IgA 11 mg/dl (normal 70–400 mg/dl), IgM 2 mg/dl (normal 40–230 mg/dl) and IgG 53 mg/dl (normal 700–1,600 mg/dl). The presumptive diagnosis of CVID was confirmed by an inadequate antibody response to pneumococcal vaccine and tetanus toxoid. The patient was given 400 mg/kg of intravenous immunoglobulin (IVIG). She was initially started on a four-week regimen of IVIG infusion, which was later switched to a three-week regimen as the patient had respiratory infections on the four-week regimen. Since initiation of this regimen 18 months ago, the patient has required no hospital admissions or antibiotic treatments and reported a significant improvement in quality of life.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [42, 'years'], 'Systolic Blood Pressure': [109.0, 'mm hg'], 'Diastolic Blood Pressure': [59.0, 'mm hg'], 'Blood Urea Nitrogen (BUN)': [24.0, 'mg/dL'], 'respiratory rate': [26.0, 'breaths per minute']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 42 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 24.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 26 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 109 mm Hg. The patient's diastolic blood pressure is 59 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 1 + 1 = 2.
The patient's CURB-65 score is 2."
6468,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-3833937-1,Extracted,"A 67-year-old man was admitted with a 1-month history of increasing dyspnea of modified Medical Research Council grade 3. The patient had undergone mitral valve replacement 20 years earlier and had been treated for heart failure, diabetes, and hypertension. His medications included warfarin, digoxin, furosemide, losartan, isosorbide mononitrate, glimepiride, and thiotacid. He had no smoking history. At the time of hospitalization, the patient was alert and the following findings were noted in a physical examination: blood pressure, 140/60 mm Hg; pulse rate, 84 beats/min; respiratory rate, 20 breaths/min; and body temperature, 37.6℃. He had no history of chest trauma or any prominent abnormalities on chest, abdominal, and lower-extremity examinations. Other results of the physical examination were non-specific.
On a physical examination, decreased breath sounds were auscultated on the left lower thorax. A chest radiograph showed blunting of the left costophrenic angle (). Chest computed tomography images obtained after therapeutic thoracentesis revealed pleural thickening and calcification on the right posterior pleura but no nodule, mass, or lesion in the lung parenchyma showing in connective tissue disease (). Transthoracic echocardiography revealed enlargement of both atria, dilatation of the left-sided ventricle, and concentric left ventricular hypertrophy with left ventricle ejection fraction 57%. Mild mitral regurgitation and tricuspid regurgitation (grade II) were noted, but no definite change could be observed. There was no pericardial effusion or pericardial thickening, and no valvular vegetations were seen. Although a dose of diuretics had been added for several days, the amount of the left pleural effusion increased markedly, and the patient was referred to a pulmonologist. Laboratory examinations showed the following findings: white blood cell count, 9,300/mm3; hemoglobin, 11.7 g/dL; platelet count, 338,000/mm3; aspartate aminotransferase, 29 IU/L; alanine aminotransferase, 24 IU/L; total protein, 7.8 g/dL; blood urea nitrogen, 22 mg/dL; creatinine, 1.4 mg/dL; C-reactive protein, 8.3 mg/dL; and NT-pro B-type natriuretic peptide (BNP), 1,324 pg/mL. Arterial blood gas analysis in room air yielded results within normal ranges. Analysis of the pleural effusion revealed the following findings: color, yellow; pH, 7.4; specific gravity, 1.010; red blood cell count, 13,760/mm3; white blood cell count, 990/mm3 (neutrophils, 2%; lymphocytes, 29%; eosinophils, 34%); protein, 4.2 g/dL; lactate dehydrogenase, 384 U/L; glucose, 117 mg/dL; carcinoembryogenic antigen, 0.2 ng/mL; adenosine deaminase, 31 IU/L; negative acid-fast staining, culture, non-specific cytology, and negative results in real-time polymerase chain reaction for Mycobacterium tuberculosis. Diagnostic thoracentesis revealed a pleural effusion appearing as an exudate with an elevated eosinophil count (34%). Serological tests for parasites (Clonorchis sinesis, Paragonimus westermani, Cysticercus cellulosae, Sparganum) yielded negative results. Serological test for rheumatologic diseases and vasculitides yielded positive results for the antinuclear antibody (>1:1,280, speckled pattern) and the anti-SS-A/Ro (179.09 EU) and anti-SS-B/La antibodies (208.98 EU). Serological tests for rheumatoid factor (RF) (<20 IU/mL), anti-ds DNA, and complement (C3, C4) yielded negative results. Of the medications the patient was receiving, although warfarin was associated with EPE, he had been taking the drug without any side effects since the mitral valve replacement surgery. Therefore, we considered that the possibility of warfarin-associated EPE was low. The patient complained of xerostomia but not of xerophthalmia, Raynaud's phenomenon, skin lesion, or arthralgia. The patient's heart failure was well controlled; he showed no pitting edema, and his NT-pro BNP level had reduced from 2,419 pg/mL to 1,324 pg/mL in a 1-month period. EPE associated with UCTD was considered, and the patient was discharged after 1 L of excess fluid was removed by therapeutic thoracentesis. About 2 weeks later, his dyspnea worsened and the left pleural effusion increased again. Repeated therapeutic thoracentesis temporarily relieved the symptoms, but they aggravated again within 2 weeks. The administration of systemic corticosteroid was considered but was contraindicated by chronic anticoagulation therapy, uncontrolled blood sugar levels, and the patient's age.
Because we were reluctant to administer systemic corticosteroid therapy, a single dose of 125 mg methylprednisolone was injected directly into the pleural space. A chest X-ray image obtained 2 weeks later showed a marked decrease in the pleural effusion (). No recurrence was observed during a 1-year follow-up, and serological tests for autoantibodies yielded similar results to those obtained in the previous year ().",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [67, 'years'], 'Systolic Blood Pressure': [140.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg'], 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [22.0, 'mg/dL'], 'Confusion': False}",3,3,3,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 67 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 1.
The concentration of BUN is 22.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 140 mm Hg. The patient's diastolic blood pressure is 60 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 2 + 1 = 3.
The patient's CURB-65 score is 3."
6469,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-4554223-1,Extracted,"A 29-year-old female with no significant past medical history presented to the emergency department with complaints of shortness of breath and productive cough consisting of green phlegm. The symptoms started a month prior for which she visited her primary medical doctor and was treated for pneumonia. Her symptoms continued to persist and gradually worsen at which point she was also treated with tamiflu for influenza. Her other symptoms however continued to progress and consisted of fever, chills, cough, body aches, and shortness of breath. The patient is a non-smoker, drinks alcohol socially, and works in a pharmacy.
On physical examination, the patient was tachycardia with a heart rate of 118, blood pressure of 111/72, respiratory rate of 24, and was saturating 88% on room air. At the time, she was afebrile with a temperature of 99.1 °F. Significant findings on examination showed diffuse rhonchi bilaterally with crackles on lung examination. Laboratory data demonstrated hemoglobin of 13, hematocrit of 39, white blood cell of 10.9, and platelets of 344,000. Sodium was 136, potassium 3.8, chloride 98, bicarbonate 21, blood urea nitrogen 15, creatinine 1.0, and glucose of 113. Troponins were negative. D-dimer was elevated at 0.71 and CT angiogram (CTA) was conducted to rule out pulmonary embolism. CTA of the chest was negative for pulmonary embolism but showed tree-in bud changes in the right upper lobe suspicious for an infectious or inflammatory process (). Similar findings were also seen in the right lower lobe. There were linear changes in the lower lobes bilaterally which most likely represented atelectasis and there was a 7.6 mm nodule in the left lower lobe.
The patient was admitted to telemetry for the management of pneumonia with azithromycin and ceftriaxone initially. Patient was found to be positive for Mycoplasma pneumonia and medications were adjusted accordingly. Patient continued to have persistent hypoxia and continued to desaturate to 88% upon ambulation. She was later found to have hemophilus influenza growth in sputum culture, which was properly being managed by her antibiotic regimen. During her hospital stay, although the patient was receiving solumedrol and antibiotics she continued to have diffuse bilateral crackles and productive cough. Patient was found to have leukocytosis as high as 19.6, but this could be attributed to her steroid treatment. However, this train of thought remained unclear as the patient was also found to have a bandemia of 21. Her antibiotics for methicillin-resistant Staphylococcus aureus (MRSA) were adjusted to consist of doxycycline, zyvox, and fluconazole. The patient continued to deteriorate and systemic workup including allergy test, antineutrophil cytoplasmic autoantibody (cANCA), perinuclear anti-neutrophil cytoplasmic antibodies (pANCA), antinuclear antibody (ANA), purified protein derivative (PPD), QuantiFERON, and human immunodeficiency virus (HIV) test was all conducted. Full systemic workup returned negative for any findings. After completing her course of antibiotics, she was also removed from her steroids but would continue to desaturate and lung findings remained unchanged. Patient underwent bronchoscopy but no significant mass or lesion was found to biopsy and her postoperative diagnosis remained as non-resolving pneumonia. Repeat CT scan was performed which showed minimal improvement and continue to suggest pneumonia and possibly underlying interstitial lung disease ().
The patient was scheduled for video-assisted thoracoscopic surgery (VATS) procedure with biopsy of the right middle and lower lobes. Right lower lobe wedge biopsy on pathology showed lung parenchyma with consolidation, atelectasis, and areas of fibrosis (). Right mid lung biopsy also showed foci of consolidation but also consisted of varying stages of questionable emphysema (). As the findings were highly unusual and emphysematous changes were not found on patient’s CT scans, the pathology was sent to a specialist, who confirmed the results but again noted them to be very non-specific. The patient’s post-operative status was complicated and patient desaturated overnight and required intubation. Alpha-1 antitrypsin was sent but returned elevated. The patient was successfully extubated after 2 days. She was placed back on steroids and was clinically improving over the course of another 1 week. Her pulse oximetry however on room air remained around 86% even after a week of steroids and thus the patient would be discharged on home oxygen therapy. Pulmonary function tests were significant for a forced vital capacity (FVC) moderately reduced at 1.65 L (60%), forced expiratory volume in 1 second (FEV1) severely reduced at 0.98 L (40%), FEV1/FVC ratio reduced at 59%, and MVV severely reduced at 28%. Flow volume loop demonstrated a combined obstructive and restrictive contour (). Lung volumes showed a vital capacity reduced at 1.65 L (60%), total lung capacity (TLC) reduced at 2.08 L (56%), and residual volume (RV) reduced at 0.43 L (43%). Her diffusion capacity (DLCO) was also severely reduced at 38%. These findings were suggestive of combined severe, irreversible obstructive and restrictive lung disease with severely reduced diffusion capacity. She would follow up with infectious disease and a pulmonary specialist as an outpatient for further workup and repeat CT scan in 3 weeks with further discussion with regard to possible lung transplant options.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [29, 'years'], 'Systolic Blood Pressure': [111.0, 'mm hg'], 'Diastolic Blood Pressure': [72.0, 'mm hg'], 'respiratory rate': [24.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [15.0, 'mg/dL']}",0,0,0,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 29 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 15.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 24 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 0.
The patient's systiolic blood pressure is 111 mm Hg. The patient's diastolic blood pressure is 72 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 0.
The patient's CURB-65 score is 0."
6470,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-7729390-2,Extracted,"A 62-year-old male with a past medical history of hypertension, diabetes mellitus, and coronary artery disease presented to the ED with complaints of generalized weakness, myalgia, exertional dyspnea, pleuritic chest pain, and dry cough of 5-day duration. On admission, he had a temperature of 102.8 degrees Fahrenheit, blood pressure of 150/79, heart rate of 120 bpm, and respiratory rate of 20 with oxygen saturation of 90% on room air. He was comfortable at rest with a normal physical exam. He was treated with supplemental oxygen via a 4 L nasal cannula. Complete blood count on admission showed white blood cells of 11,200/mcL with an elevated neutrophil count. He was noted to be in acute renal failure with a BUN and creatinine of 28 mg/dL and 1.69 mg/dL, respectively. Procalcitonin was elevated at 2.18 ng/mL. Chest X-ray showed bilateral lower lobe infiltrates (), and he was empirically treated for community-acquired pneumonia with doxycycline. On the second day of admission, he tested positive for SARS-CoV-2 via PCR of nasal swab as well as Streptococcus pneumoniae urine antigen. He was started on Plaquenil and continued antibiotic therapy. On the second day of admission, he no longer required supplemental oxygen, and he was successfully discharged home with 5 days of oral doxycycline.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [150.0, 'mm hg'], 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [28.0, 'mg/dL'], 'Confusion': False, 'Diastolic Blood Pressure': [79.0, 'mm hg'], 'age': [62, 'years']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 62 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 28.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 150 mm Hg. The patient's diastolic blood pressure is 79 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6471,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-8398,Extracted,"A 17-year-old boy presents to the emergency department of a hospital located in the town of Recuay (which is situated at 3,400 meters above mean sea level [MAMSL]) in the Ancash Region (Peru), 48 hours after returning from a 21-day stay in Lima (the capital city of Peru at 0 MAMSL). The patient has no previous medical history. His current complaints include cough, dyspnea at rest, hemoptysis, chest pain, and vomiting. His vital signs include: blood pressure 90/60 mm Hg; heart rate 149/min; respiratory rate 37/min; temperature 36.5°C (97.7°F); and O2 saturation 71%. Physical examination reveals polypnea, perioral cyanosis, intercostal retractions, and diffuse pulmonary crackles. His laboratory results are as follows:
Hemoglobin 19.2 g/dL
Hematocrit 60%
Leukocytes 13,000 (Bands: 12%, Seg: 78%, Eos: 0%, Bas: 0%, Mon: 6%)
Urea 25 mg/dL
Creatinine 0.96 mg/dL
A chest X-ray is shown.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [17, 'years'], 'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg'], 'respiratory rate': [37.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [25.0, 'mg/dL']}",3,3,3,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 17 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 25.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 37 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 1 + 1 = 2.
The patient's systiolic blood pressure is 90 mm Hg. The patient's diastolic blood pressure is 60 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 2 + 1 = 3.
The patient's CURB-65 score is 3."
6472,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-4716279-1,Extracted,"A 17-year-old boy presented to the emergency room (ER) complaining of shortness of breath and pleuritic chest pain that had developed 2 hours earlier. The patient was a high school student who had been well until 1 month before this visit. In the subsequent month, he had a dry cough, fatigue, and weight loss of 2 kg. He had no febrile sensation or myalgia. The day before, he developed fever, chills, and pleuritic chest pain rated 3 points on a 0-10 numeric pain intensity scale. The pain was located on the anterior chest wall and was aggravated when the patient inspired deeply. Two hours before visiting the ER, shortness of breath developed, and the pleuritic chest pain was aggravated and radiated to the shoulder and jaw. He did not smoke nor drink alcohol, and did not have any trauma.
The patient was alert but appeared acutely ill. Vital signs included a body temperature of 39.0℃, blood pressure of 107/70 mmHg, heart rate of 110 beats/min, respiratory rate of 30/min, and 98% oxygen saturation with pulse oximetry on room air. Results of examinations of the head, eye, ear, nose, and throat were unremarkable. The jugular vein was not distended. On chest examination, lung auscultation was normal, but a rapid and distant heart sound was heard. On abdominal examination, there was no tender point or organomegaly. No pitting edema on the peripheral limbs was observed.
Initial laboratory findings were as follows: white blood cell count was 20,100/mm3 with 88.4% neutrophils, hemoglobin 12.6 g/dL, hematocrit 37.3% and the platelet count was 394,000/mm3. Additional findings included the following: blood urea nitrogen, 7.2 mg/dL (reference range, 7-20 mg/dL); serum creatinine, 0.78 mg/dL (reference range, 0.6-1.4 mg/dL); C-reactive protein, 21.7 mg/dL (reference range <0.3 mg/dL); aspartate aminotransferase, 84 U/L (reference range, 5-40 U/L); alanine aminotransferase, 177 U/L (reference range, 5-45 U/L), D-dimer, 2.97 mg/L (reference range, 0-0.24 mg/L); B-type natriuretic peptide, 97 pg/mL (reference range 0-100 pg/mL); and troponin I, 0.04 ng/mL (reference range 0.01-0.06 ng/mL). An HIV antibody test result was negative. On electrocardiography, sinus tachycardia (heart rate 116 beats/min), elevation of PR segment in aVR, and depression of PR in the other leads were observed. A chest radiograph showed cardiac silhouette enlargement with left lower lobar consolidation (). In a computed tomography (CT) scan of the chest, pericardial effusion with pericardial enhancement and multiple necrotic lymph nodes containing air in the mediastinal area were observed, which suggested a broncho-lymph nodal fistula (). Echocardiography showed a large amount of pericardial effusion with normal cardiac wall motion. TB pericarditis and lymphadenitis were presumed, and the patient was admitted to the intensive care unit. Intravenous ceftriaxone was administered from the first day of his arrival at the ER.
Six hours after admission, he began to breathe faster (40 breaths/min) and his blood pressure dropped to 90/50 mmHg. Jugular venous distention was observed. Cardiac tamponade was presumed, and emergency fluoroscopy-guided percutaneous pericardiocentesis was performed during which 200 mL of pus-like fluid was drained. The catheter was left in the pericardial space for drainage. Fluid specimens were sent for culture and chemical analysis. Chemical analysis findings of initial pericardial fluid were as follows: white blood cell count, 197,840/mm3 with 98% neutrophils; red blood cell count, 70,000/mm3, lactate dehydrogenase, 1,894 U/L; triglycerides, 31 mg/dL; glucose, 3 mg/dL; and adenosine deaminase, 91.8 U/L. Microbiologic results of the pericardial fluid culture are shown in .
On the following day, a Mycobacterium tuberculosis polymerase chain reaction (TB PCR) test performed on the pericardial fluid yielded positive results. Acid-fast bacillus (AFB) staining and Gram staining were all negative. Isoniazid, rifampin, ethambutol, and pyrazinamide with pyridoxine were administered. On hospital day 3, we learned that yeast was growing in the initial pericardial fluid culture so we added intravenous fluconazole. On hospital day 4, Candida parapsilosis was identified in the initial pericardial fluid culture. The amount of fluid drained from the pericardial catheter decreased to 70 mL/day, but his fever persisted. We learned that gram-positive bacterium was growing in the pericardial fluid drained on the first hospital day. We used vancomycin and ciprofloxacin in addition to fluconazole as treatment for pyogenic pericarditis. On hospital day 7, the fever developed daily, and vital signs included a body temperature of 38.1℃, blood pressure of 110/75 mmHg, heart rate of 98 beats/min and respiratory rate of 18/min. Chest radiography showed that the cardiac silhouette had decreased in size but that pneumopericardium had developed (). Subsequent chest CT image showed that pneumopericardium newly developed and the pericardial wall became more thickened and septated (). We switched vancomycin and ciprofloxacin with vancomycin and ertapenem for the uncontrolled, mixed infection because of the pneumopericardium. On hospital day 9, Peptostreptococcus asaccharolyticus and Streptococcus anginosus in addition to C. parapsilosis were identified from the initial pericardial fluid culture. Methicillin-sensitive S. aureus and Prevotella oralis were also determined to the causative organisms of pyogenic pericarditis in this case, isolated respectively from pericardial fluid drained on hospital day 4 and hospital day 7. At this point, we understood that the multiple organisms in the pericardial fluid would be from the oral cavity through a broncho-lymph nodal fistula and possibly a lymph nodal-pericardial fistula. Upon reviewing the chest CT image, we observed that the subcarinal lymph node with air density was shown to contact with the parietal pericardium at coronal section images (panel D in ). Because of persistent pericardial drainage, pericardial thickening, and probable broncho-lymph node-pericardial fistula, a pericardiectomy was performed on hospital day 10. Pus, inflammatory material, and multiple septations were observed within the pericardium during the procedure, and irrigation with suction and removal of septations were performed for smooth drainage of the pericardial fluid. There was neither gross pericardial fistula nor evidence of mediastinitis. In order to identify the suspected tracheobronchial fistula, an air leakage test was performed, but no leakage was observed. The thickened pericardium and epicardium were removed (mostly on the anterior right ventricle side). Therefore, subcarinal and paratracheal lymph nodes were not dissected. Pericardial tissue biopsy revealed acute and chronic inflammation with liquefactive necrosis. The patient began to improve postoperatively. TB cultures of the pericardial fluid were all negative. One month after admission, the patient was discharged with oral antifungal, antibiotic and anti-TB medication. We stopped amoxicillin/clavulanic acid after three months and fluconazole after six months, but patient remained on anti-TB medication. Six months after discharge, the patient returned to normal activity including playing soccer, and his heart rate was around 70 beats/min. Echocardiography showed no cardiac relaxation abnormality, although the ejection fraction was minimally decreased.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [50.0, 'mm hg'], 'age': [17, 'years'], 'respiratory rate': [40.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [7.2, 'mg/dL'], 'Confusion': False}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 17 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 7.2 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 40 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 0 + 1 = 1.
The patient's systiolic blood pressure is 90 mm Hg. The patient's diastolic blood pressure is 50 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 1 + 1 = 2.
The patient's CURB-65 score is 2."
6473,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-3856144-1,Extracted,"An 18-year-old man was brought to the emergency department (ED) because of altered mental status. Family reported that he had nausea and vomiting before presenting to the ED. Past medical history was significant for diabetes, diabetic ketoacidosis (DKA), and hypothyroidism. Past surgical and social histories were unremarkable. Home medication was insulin glargine.
Physical exam revealed a lethargic patient. Vitals were blood pressure 130/70 mmHg, pulse 96/minute, respiration 28/minute, temperature was normal. Lung auscultation showed left basal crackles.
Chest radiograph (CXR) showed lower lobe infiltrates and pneumomediastinum (PM). Laboratory results: Arterial blood gas: PH 6.930 (7.350–7.450), PCO2 16 mmHg (35–45), PO2 138 mmHg (81–110), and serum bicarbonate 3 mmol/L (22–26); serum electrolytes: sodium 129 mmol/L (136–144), potassium 6.4 mmol/L (3.3–5.1), and chloride 100 mmol/L (101–111); glucose 1087 mg/dL (60–250), blood urea nitrogen 40 mg/dL (8–26), and creatine 2.68 mg/dL (0.70–1.20). Blood counts were normal.
The patient was intubated for airway protection because of altered mental status. A postintubation CXR showed PM, lower lobe infiltrates, and an air-filled distended stomach. An oral-gastric (OG) tube was placed easily, to decompress the air-filled distended stomach after bagging prior to intubation and in view of nausea and vomiting. A chest computed tomography scan showed multilobar infiltrates suggestive of aspiration pneumonia, PM, and the tip of the OG tube to be in the right hemithorax. The patient underwent a right thoracotomy with the intention to repair the esophageal rupture. Intraoperatively, the tip of the OG tube was found to be retracted into the esophageal lumen. Inspection of the esophagus did not reveal a clear rupture. An OG tube was placed intraoperatively, and a chest tube was placed into the right pleural space.
The patient was given intravenous (IV) fluid for hydration, IV insulin drip, IV metronidazole, and IV levofloxacin. Serial CXRs showed clearing of pneumonic infiltrates and PM. The chest tube was discontinued, and the patient was successfully extubated. After extubation, an esophagogram was performed and showed no extravasation of contrast.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [130.0, 'mm hg'], 'respiratory rate': [28.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [40.0, 'mg/dL'], 'Confusion': True, 'Diastolic Blood Pressure': [70.0, 'mm hg'], 'age': [18, 'years']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 18 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient has confusion, 1 point is added to score making the current total 0 + 1 = 1.
The concentration of BUN is 40.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 28 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 130 mm Hg. The patient's diastolic blood pressure is 70 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6474,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-6133457-1,Extracted,"A 57-year-old man was admitted to the Pneumology Department of the Affiliated Hospital of Medical School, Ningbo University in December 2016 for cough and sputum production for half a month and hemoptysis for 1 day. He had a medical history of pulmonary aspergillosis and type 2 diabetes.
On admission, blood pressure was 125/76 mm Hg, the body temperature was 36.6°C, respiratory rate was 19 breaths/min, and heart rate was 79 beats/min. Results of laboratory tests included the following values: urea nitrogen 12.4 mmol/L, creatinine 139.7 μmol/L, uric acid 539 μmol/L, potassium 4.43 mmol/L, glucose 7.83 mmol/L, leukocytes 12 × 109/L, with 75.6% neutrophils, hemoglobin 11.4 g/dL, lactic acid 1.9 mmol/L, and pH 7.37.
Intravenous voriconazole (200 mg q/12 h, first dose doubling) was used to treat pulmonary fungal infection. The results of a sputum smear examination showed gram-positive cocci+, gram-positive bacilli+, and gram-negative bacilli++. According to the results of sputum smear examination and the clinical manifestations, community-acquired pneumonia cannot be excluded and moxifloxacin (400 mg q/d) was added on day 3. Five days later, the patient presented with shortness of breath and became febrile up to 38.8°C. Chest radiography showed aggravated infection. Intravenous imipenem and cilastatin sodium (500 mg q/8 h) was substituted for moxifloxacin.
The patient was transferred to the intensive care unit on day 10 for severe pneumonia-induced respiratory failure. The antibiotic therapy was escalated to vancomycin. Because of poor renal function (estimated renal clearance 36 mL/min), intravenous linezolid (600 mg q/12 h) was introduced as an alternative treatment to vancomycin. After 3 doses of linezolid, the patient's blood lactate had risen up to 10.0 mmol/L, blood pressure was 50/40 mm Hg, heart rate was 42 beats/min, and creatinine was 335.8 μmol/L. Noradrenaline and dopamine were administered with a minipump to maintain a relatively normal pressure. As linezolid was implicated as a possible cause of the lactic acidosis, the agent was discontinued.
The patient required mechanical ventilation because of respiratory failure and continuous renal replacement therapy for 6 days to normalize his blood pH and clear linezolid from his plasma. However, the lactic acidosis improved only marginally, and his blood pressure decreased to 30/22 mm Hg. The patient died on day 17.
We searched for cases of linezolid-induced lactic acidosis reported in English in PubMed from their inception until April 2017. Literature searches included keywords for “linezolid” or “Zyvox” and “lactic acidosis” or “hyper-lactatemia.”
Two reviewers (Yiyang Mao and Danping Dai) independently screened all titles and abstracts for eligible articles. Cases presented in the articles were included if the lactic acidosis was induced by linezolid and the data were extractable.
Two authors extracted data independently (Yiyang Mao and Danping Dai). Any dispute was settled by discussion or by a third investigator. Study characteristics were extracted from each case, including first author identification, gender, age, comorbidities, reason for use, duration of linezolid, dosage, lactate concentration before linezolid, peak lactate concentration after linezolid, treatment for lactic acidosis, and outcome.
Seven, fourteen, and twenty-eight days were selected to be the cut-off points in statistics according to the treatment duration recommended in the drug instruction. The treatment duration of linezolid was expressed in days in the calculations. The dosage of linezolid was assumed to be 600 mg/bid, when it was not reported according to the drug instruction. Only the lactic acidosis-related deaths were included when analyzing and evaluating the data. Patients ≥65 years were defined as elderly according to the WHO's definition.
All statistical analyses were conducted using the SPSS software package (version 18.0). Statistical evaluations were carried out using the chi-squared tests with P values of <.05 considered to be statistically significant. All statistical tests were 2-sided. Fisher exact test was used when the sample size was <40.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [57, 'years'], 'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [76.0, 'mm hg'], 'respiratory rate': [19.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [12.4, 'mmol/L'], 'Confusion': False}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 57 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 12.4 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of BUN from mmol to mg. The mass of BUN is 12.4 mmol. To convert 12.4 mmol of BUN to mol, multiply by the conversion factor 0.001, giving us 12.4 mmol BUN * 0.001 mol/mmol = 0.0124 mol BUN. To convert from mol BUN to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0124 mol BUN * 28.02 g/mol = 0.34745 g BUN. To convert 0.34745 g of BUN to mg, multiply by the conversion factor 1000.0, giving us 0.34745 g BUN * 1000.0 mg/g = 347.45 mg BUN. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 347.45 mg BUN/10.0 dL = 34.745 mg BUN/dL. The concentration value of 12.4 mmol BUN/L converts to 34.745 mg BUN/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 19 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 125 mm Hg. The patient's diastolic blood pressure is 76 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6475,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-1307,Extracted,"A 36-year-old man is brought to the emergency department by his neighbor because of altered mental status. He was found 6 hours ago stumbling through his neighbor's bushes and yelling obscenities. The neighbor helped him home but found him again 1 hour ago slumped over on his driveway in a puddle of vomit. He is oriented to self but not to place or time. His temperature is 36.9°C (98.5°F), pulse is 82/min, respirations are 28/min, and blood pressure is 122/80 mm Hg. Cardiopulmonary exam shows no abnormalities. He is unable to cooperate for a neurological examination. Muscle spasms are seen in his arms and jaw. Serum laboratory studies show:
Na+ 140 mEq/L
K+ 5.5 mEq/L
Cl- 101 mEq/L
HCO3- 9 mEq/L
Urea nitrogen 28 mg/dL
Creatinine 2.3 mg/dL
Glucose 75 mg/dL
Calcium 7.2 mg/dL
Osmolality 320 mOsm/kg
Calculated serum osmolality is 294 mOsm/kg. Arterial blood gas shows a pH of 7.25 and lactate level of 3.2 mmol/L (N=< 1 mmol/L). Examination of the urine shows oxalate crystals and no ketones.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [122.0, 'mm hg'], 'respiratory rate': [28.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [28.0, 'mg/dL'], 'Confusion': True, 'Diastolic Blood Pressure': [80.0, 'mm hg'], 'age': [36, 'years']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 36 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient has confusion, 1 point is added to score making the current total 0 + 1 = 1.
The concentration of BUN is 28.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 28 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 122 mm Hg. The patient's diastolic blood pressure is 80 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6476,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-5124,Extracted,"A 45-year-old homeless man is brought to the emergency department by the police. He was found intoxicated and passed out in a library. The patient has a past medical history of IV drug abuse, diabetes, alcohol abuse, and malnutrition. The patient has been hospitalized previously for multiple episodes of pancreatitis and sepsis. Currently, the patient is minimally responsive and only withdraws his extremities in response to painful stimuli. His temperature is 99.5°F (37.5°C), blood pressure is 90/48 mmHg, pulse is 150/min, respirations are 17/min, and oxygen saturation is 95% on room air. Physical exam is notable for tachycardia, a diastolic murmur at the left lower sternal border, and bilateral crackles on pulmonary exam. The patient is started on IV fluids, vancomycin, and piperacillin-tazobactam. Laboratory values are ordered as seen below.

Hemoglobin: 9 g/dL
Hematocrit: 30%
Leukocyte count: 11,500/mm^3 with normal differential
Platelet count: 297,000/mm^3

Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 4.0 mEq/L
HCO3-: 28 mEq/L
BUN: 33 mg/dL
Glucose: 60 mg/dL
Creatinine: 1.7 mg/dL
Ca2+: 9.7 mg/dL
PT: 20 seconds
aPTT: 60 seconds
AST: 1,010 U/L
ALT: 950 U/L

The patient is admitted to the medical floor. Five days later, the patient's neurological status has improved. His temperature is 99.5°F (37.5°C), blood pressure is 130/90 mmHg, pulse is 90/min, respirations are 11/min, and oxygen saturation is 99% on room air.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [48.0, 'mm hg'], 'age': [45, 'years'], 'respiratory rate': [17.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [33.0, 'mg/dL'], 'Confusion': True}",3,3,3,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 45 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient has confusion, 1 point is added to score making the current total 0 + 1 = 1.
The concentration of BUN is 33.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 17 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 90 mm Hg. The patient's diastolic blood pressure is 48 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 2 + 1 = 3.
The patient's CURB-65 score is 3."
6477,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-2783075-1,Extracted,"A 42-year-old African-American man with HIV/AIDS, not taking any medications including HAART and pneumocystis jiroveci prophylaxis since January 2007, presented in August 2007 with complaints of progressing shortness of breath, right-sided pleuritic chest pain, non-productive cough, and low-grade fever for last several weeks. He was diagnosed with HIV initially in 1999, during hospitalization for community-acquired pneumonia. The patient also had a history of facial herpes simplex virus type 2 (HSV-2) which has been recurrent and a history of pneumocystis pneumonia in June 2005. Previous laboratory studies from November 2006 revealed a CD4+ lymphocyte count of 20 and viral load HIV RNA of 65,833 copies/ml. He was a social drinker and had never used illicit drugs or tobacco products. HIV was presumed to be acquired sexually.
On initial assessment in the emergency department, he was cachectic but was in no acute distress. He had a fever of 38°C, blood pressure of 92/60 mmHg and regular pulse of 85 beats per minute. He was breathing at 20 breaths per minute. Oxygen saturation was 95% on room air, which decreased to 90% during ambulation. There were no oral lesions. His neck was supple. Examination of the lungs revealed bilateral expiratory wheezes and rare rhonchi. Cardiac examination demonstrated normal first sound, second sound with a regular rhythm and no murmurs. His abdomen was soft, nontender, nondistended with normoactive bowel sounds. His extremities were warm and his skin was dry with multiple small herpetic ulcers on the left ear and the left side of the face.
Laboratory tests revealed the following concentrations: sodium 138 mmol/L, potassium 4.5 mmol/L, chloride 103 mmol/L, bicarbonate 26 mmol/L, BUN 2.9 mmol/L, creatinine 61 μmol/L, glucose 4.78 mmol/L, white blood cell 3.4 × 109/L, neutrophils 86%, hemoglobin 7.1 mmol/L, hematocrit 33%, platelets 322 × 109/L, LDH 497 U/L, CD4+ lymphocyte count of 2. Chest X-ray was negative for infiltrate (Figure ), but high resolution CT of the chest revealed subtle right middle lobe and right upper lobe ground-glass opacity (Figure ).
The patient was admitted to the medical ward with a working diagnosis of pneumocystis pneumonia. A sputum sample was collected spontaneously for a culture work-up (Bartlett score: +3). No sputum sample was collected for mycobacterial stains. Empiric treatment with trimethoprim-sulfamethoxazole (1 tablet double-strength × 3 per day) and prednisone (40 mg × 2 per day) was started. The patient was also placed on treatment for HSV with acyclovir (400 mg × 3 per day). The prednisone doses were reduced as part of initial therapy for pneumocystis pneumonia. On the third day, direct fluorescent antibody test for Pneumocystis jiroveci was negative, but the culture was positive for Bordetella bronchiseptica. The patient was placed on droplet precautions; treatment was switched to levofloxacin (400 mg per day). Trimethoprim-sulfamethoxazole dose was modified to (1 tablet single-strength per day) for pneumocystis prophylaxis and azithromycin (1200 mg once per week) for Mycobacterium avium complex prophylaxis began. The patient subsequently improved on levofloxacin and on the seventh day was discharged home on levofloxacin, trimethoprim-sulfamethoxazole, azithromycin, and acyclovir. After eleven days, the patient visited our office. The patient had no complaints, no fever and no cough and his shortness of breath was fully resolved. On retrospect, the patient reported that he had been visited by his brother and his brother's dog at his home about a week prior to the illness.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [42, 'years'], 'Systolic Blood Pressure': [92.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg'], 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [2.9, 'mmol/L']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 42 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 2.9 mmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of BUN from mmol to mg. The mass of BUN is 2.9 mmol. To convert 2.9 mmol of BUN to mol, multiply by the conversion factor 0.001, giving us 2.9 mmol BUN * 0.001 mol/mmol = 0.0029 mol BUN. To convert from mol BUN to grams, multiply by the molar mass 28.02 g/mol, which will give 0.0029 mol BUN * 28.02 g/mol = 0.08126 g BUN. To convert 0.08126 g of BUN to mg, multiply by the conversion factor 1000.0, giving us 0.08126 g BUN * 1000.0 mg/g = 81.26 mg BUN. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 81.26 mg BUN/10.0 dL = 8.126 mg BUN/dL. The concentration value of 2.9 mmol BUN/L converts to 8.126 mg BUN/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 0.
The patient's systiolic blood pressure is 92 mm Hg. The patient's diastolic blood pressure is 60 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 0 + 1 = 1.
The patient's CURB-65 score is 1."
6478,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-3318852-1,Extracted,"A 65-years-old male patient presented to emergency department with complaints of progressive dyspnea, dysuria, and change in mental status in last six hours. The patient had a history of hypertension, type-2 diabetes mellitus, coronary artery disease, hypertriglyceridemia, peripheral vascular disease, chronic pancreatitis, gastroesophageal reflux disease, chronic back pain and depression. Surgical history included left popliteal-femoral bypass and coronary artery stenting. He had 25-pack-years history of smoking, but denied significant alcohol or illicit drug use. His customary medications were lantus insulin, glimeperide, verapamil, losartan, aspirin, rosuvastatin, fenofibrate, cilostazole, esomeprazole, dicyclomine, eszopiclone, venlafaxine, alprazolam, testosterone lotion, and hydrocodone-acetaminophen.
On physical examination, he was alert but not oriented, and in severe respiratory distress. Blood pressure (BP) was 160/94 mmHg in right arm, pulse rate was 140 per minute, respiratory rate was 30 breaths per minute, and temperature was 38.4oC. The Oxygen saturation via pulse oximeter was 86% while the patient was breathing 100% O2 by non-rebreather mask. There was decreased air movement at both lung bases, and consolidation at right lung base. Cardiac examination showed no abnormalities except tachycardia. The remainder of the examination was unremarkable.
The initial labs and arterial blood gas (ABG) analysis are shown in and . Serum lactate at the beginning was elevated at 4.1 mmol/L (normal: 0.5-1 mmol/L). Initial electrocardiogram showed sinus tachycardia with rate of 144 beats per minute. A chest radiograph showed increased interstitial markings and right lower lobe infiltrates (). Urine analysis study revealed presence of urinary tract infection and results are shown in . He was immediately started on fluid replacement, intravenous (IV) antibiotics which included levofloxacin, piperacillin/tazobactam and vancomycin, and high flow oxygen, and was transferred to medical intensive care unit (ICU) for further care.
Later on, patient went into severe respiratory distress, and endotrachial intubation was performed. Soon after intubation, patient went into pulseless electrical activity, and a code blue was called. Cardio-pulmonary resuscitation was performed as per standard protocol for 15 minutes, and patient came back to sinus rhythm. After the code, patient was hypotensive and required three vasopressors including epinephrine, norepinephrine and dopamine to maintain systolic BP more than 90. Oxygen saturation was 90% on 100% FiO2. After one hour, patient again went into cardiac asystole, then ventricular fibrillation, and then pulseless electrical activity. Successful resuscitation was done for 15 minutes. After this second code, the systolic BP was in 80s, and IV phenylephrine was added. Hear rate was 146 beats per minute, and oxygen saturation 88% on 100% FiO2. The laboratory results showed lactate level of 12.1 mmol/L; transaminase in 1000's and blood urea nitrogen and creatinine of 53 mg/dl and 4.9 mg/dl respectively. Serum troponin level was 2.92 ng/ml (normal ≤ 0.04 ng/ml). Arterial blood gas (ABG) revealed worsening metabolic acidosis.
An emergent two-dimensional echocardiogram was obtained and revealed normal left and right ventricular function. His left ventricular ejection fraction was found to be 50%, and there was no pericardial effusion, or right ventricular strain. Patient was started on IV hydrocortisone, and anidulafungin was added to cover for fungal pathogens. A decision was also made to start patient on activated protein C infusion considering high risk of death. In addition, bicarbonate drip was also started.
Twelve hours after his admission to this hospital, patient started showing signs of anoxic brain injury. At that time, he was on maximum doses of five vasopressors, but was still hypotensive and tachycardic. The oxygen saturation decreased to 88% on 100% of FiO2. ABG at that time is shown in . Family meeting was called, and they requested for withdrawal of care. Thirty minutes later, care was withdrawn and patient expired within 10 minutes of extubation and stopping IV medications. Family refused autopsy. The next day, two out of four blood cultures were positive for Escherichia coli.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [160.0, 'mm hg'], 'respiratory rate': [30.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [53.0, 'mg/dL'], 'Confusion': True, 'Diastolic Blood Pressure': [94.0, 'mm hg'], 'age': [65, 'years']}",4,4,4,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 65 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient has confusion, 1 point is added to score making the current total 1 + 1 = 2.
The concentration of BUN is 53.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 2 + 1 = 3.
The patient's respiratory rate is 30 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 3 + 1 = 4.
The patient's systiolic blood pressure is 160 mm Hg. The patient's diastolic blood pressure is 94 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 4.
The patient's CURB-65 score is 4."
6479,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-6823011-1,Extracted,"The patient was a 72-year-old Caucasian male with a past medical history of long-standing gastroesophageal reflux disease, tobacco dependence (over 50 packs/year), cerebrovascular disease, and chronic kidney disease. He was admitted to the medical intensive-care unit (MICU) for the evaluation of pneumomediastinum. Two weeks before admission, the patient had been seen in a community emergency department with a three-day history of fevers, dyspnea, and cough. He had been diagnosed with aspiration pneumonia and treated with amoxicillin-clavulanic acid. The patient had subsequently returned to the emergency department two days later with worsening symptoms and hematemesis. At the MICU, a CT of the chest showed a right lower lobe consolidation and pneumomediastinum (Figure ). The pneumomediastinum tracked from the right paratracheal region along the right lateral aspect of the esophagus to the gastroesophageal junction. There was also a marked thickening of the distal esophagus (Figure ). Vital signs on arrival included a temperature of 38.3° Celsius, a heart rate of 92 beats per minute, respiratory rate of 30 breaths per minute, blood pressure of 144/65, and an oxygen saturation of 97% on 15 liters of supplemental oxygen via non-rebreather. Physical examination revealed bilateral diffuse rhonchi. Laboratory studies on arrival were remarkable for a white blood cell (WBC) count of 19.75 x109/L, hemoglobin of 13.8 g/dL, and platelet count of 354 x109/L. Renal function was diminished with a serum creatinine of 1.69 mg/dL (baseline: 1.4 mg/dL) and blood urea nitrogen of 39 mg/dL. Abnormal serum chemistry lab results included albumin level of 2.9 g/dL, and liver enzymes were elevated with an alkaline phosphatase of 172 units/L, aspartate aminotransferase and alanine aminotransferase at 112 units/L and 66 units/L, respectively. Procalcitonin and C-reactive protein (CRP) were both elevated at 3.53 ng/mL and 43.95 mg/dL, respectively. Arterial blood gas on a 60% fraction of inspired oxygen (FiO2) demonstrated a pH of 7.472, pCO2 of 32.1 mmHg, pO2 of 72.7 mmHg, and HCO3 of 23.2 mmol/L. The alveolar-arterial gradient was elevated at 315 mmHg.
The differential diagnosis of pneumomediastinum in the setting of esophageal wall thickening includes Boerhaave’s syndrome (retching- associated esophageal rupture), malignancy-associated esophageal rupture, infectious infiltration of the esophagus, and esophagitis-related esophageal rupture. Initial management of our patient included intubation for increased respiratory rate and acute hypoxemic respiratory failure. Once intubated, the patient was placed on a strict nil-per-os (NPO) status. Intravenous (IV) pantoprazole was scheduled every 12 hours, and empiric broad-spectrum antibiotic therapy was started for suspected pneumonia after bedside bronchoscopy. Bronchoscopy showed no obvious airway deformities or perforations on inspection but did reveal thick copious secretions that were therapeutically aspirated and sent for culture.
A Gastrografin (Schering AG, Berlin, Germany) study was ordered but could not be performed as nasogastric or orogastric tubes could not be placed due to concern for esophageal perforation. Thoracic surgery was consulted and an esophagogastroduodenoscopy (EGD) was performed in the operating room. EGD demonstrated no obvious tear or perforation but did show swollen and black mucosa primarily involving the distal esophagus (Figure ). The gastric mucosa was unaffected. Tissue cultures from the EGD grew Klebsiella pneumoniae, which was also grown from the bronchial wash and bronchoalveolar lavage (Table ). EGD findings were consistent with acute esophageal necrosis (AEN), and the patient continued to remain NPO. Total parenteral nutrition was considered but deferred as a jejunostomy tube had been placed by thoracic surgery to provide the patient with enteral nutrition to promote healing. Though surgical esophagectomy was considered by the thoracic surgeons, the patient was ultimately deemed to be a poor surgical candidate given his multiple comorbidities.
The patient’s hospitalization was complicated by critical limb ischemia of the right lower extremity, which prompted the use of a heparin drip. Unfortunately, the patient developed a gastrointestinal bleed while on therapeutic anticoagulation. After a goals-of-care discussion with the patient’s family, the decision was made to extubate the patient to focus on comfort measures. The patient passed away peacefully soon thereafter.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [144.0, 'mm hg'], 'Diastolic Blood Pressure': [65.0, 'mm hg'], 'age': [72, 'years'], 'respiratory rate': [30.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [39.0, 'mg/dL']}",3,3,3,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 72 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 1.
The concentration of BUN is 39.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 30 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 2 + 1 = 3.
The patient's systiolic blood pressure is 144 mm Hg. The patient's diastolic blood pressure is 65 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 3.
The patient's CURB-65 score is 3."
6480,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-8548205-1,Extracted,"A 43-year-old male patient underwent aortic valve and mitral valve replacement with CarboMedics valves (Sultzer CarboMedics Inc., Austin, TX, USA) at a university hospital in 1994 and subsequently took warfarin. Wisdom teeth were extracted without prophylactic antibiotics in early 2018 at a follow-up visit. The patient experienced coughing and sputum for several days before visiting the emergency room. In addition, the patient experienced generalized weakness, deteriorated fever, and shortness of breath at noon on the day of the emergency room visit. When he arrived at the local hospital, endotracheal intubation was performed immediately because his oxygen saturation was 68%. Transthoracic echocardiography showed normal left ventricular ejection and left atrial dilatation was confirmed. However, the vegetation and valve function of the aortic and mitral mechanical valves could not be evaluated at that time. The patient was transferred to our hospital due to uncontrolled pulmonary edema.
All lung zones were auscultated with crackle sounds. At the emergency room examination, the patient’s blood pressure was 110/90 mm Hg, the pulse was 169 beats/min, the respiratory rate was 35 breaths/min, the body temperature was 38.6°C, and the oxygen saturation was 83%. The following blood lab values were obtained: C-reactive protein, 54.6 mg/L; white blood cell count, 32,820/μL; procalcitonin, 3.21 ng/mL; creatine kinase-MB, 2.6 ng/mL; troponin-I, 0.276 ng/mL; pro-brain natriuretic peptide, 12,454 pg/mL; D-dimer, 493 ng/mL; international normalized ratio, 1.71; blood urea nitrogen, 34 mg/dL; and creatinine, 3.2 mg/dL. Meropenem and vancomycin were administered for suspected infectious endocarditis and pneumonia as a cause of fever. Hypoxia caused by acute respiratory distress syndrome worsened and the patient’s blood pressure was not maintained with vasopressors. To evaluate the cause of cardiogenic shock, we performed coronary angiography.
On coronary angiography, only 1 leaflet was found in the mitral valve, but the diagnosis of mitral valve regurgitation due to leaflet fracture was missed (). On the second day of hospitalization, transthoracic echocardiography was performed. We found no vegetation on the aortic and mitral valves and the function of the aortic valve was good. However, 1 of the leaflets of the mitral valve was not seen and severe mitral regurgitation was confirmed. On the third day of hospitalization, the thoracic surgery department was contacted because mobility of the mitral valve leaflet could not be observed with transesophageal echocardiography (). Subsequently, an emergency redo-mitral valve replacement (29 mm; St. Jude Medical Inc., St. Paul, MN, USA) was performed.
In the operating room, no vegetation of the mitral valve was observed, but a single leaflet was completely separated from the existing CarboMedics mechanical valve () and the formation of a pannus was severe around the sewing ring. The left atrium, left ventricle, and pulmonary vein were examined using a video endoscope in the operating room, but the missing leaflet could not be found.
After valve replacement surgery, the patient was admitted into the intensive care unit with veno-venous extracorporeal membrane oxygenation due to persistent hypoxia. On the ninth day after surgery, computed tomography of the chest and abdomen was performed to find the missing leaflet. A 14.4-mm piece of the valve was found in the left common iliac artery and a 13.9-mm piece was found in the left external iliac artery. On the 23rd day after surgery, the leaflet inside the left external iliac artery was removed via a transverse incision from the mid-inguinal ligament to the lateral side, under general anesthesia. The leaflet fragment in the left common iliac artery was not easy to reach. Therefore, the fragment was removed using a fluoroscopy device (C-arm) in the operating room (). After 2 operations, the patient was discharged 33 days after hospitalization. The patient underwent outpatient follow-up without specific findings 1 year after surgery.
The study was approved by the Institutional Review Board of Samsung Medical Center (IRB approval no., 202010014). The patient provided written informed consent for the publication of his clinical details and images.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [43, 'years'], 'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg'], 'respiratory rate': [35.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [34.0, 'mg/dL']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 43 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 34.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 35 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 1 + 1 = 2.
The patient's systiolic blood pressure is 110 mm Hg. The patient's diastolic blood pressure is 90 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6481,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-5895835-1,Extracted,"A 67-year-old male presented with multiple tender erythematous nodules and pustules distributed over his face and upper and lower extremities (). The first skin lesion developed on his left hand about 8 months previously. Despite surgical drainage of his left hand with topical antibiotic treatment at a local hospital, the lesion spread to the face and upper and lower extremities. He complained of general weakness and loss of appetite. Respiratory symptoms such as cough and sputum were not evident. Generalized swelling of the upper and lower extremities was observed.
The patient had been employed by a deep-water fishery for more than 30 years. He had been taking oral hypoglycemic agents for treatment of diabetes mellitus for 3 years. He had a history of intermittent steroid injections for treatment of arthralgia at the local hospital for the past 6 months. He recalled experiencing multiple minor skin lacerations while working but not sufficiently severe to require medical care.
On admission, the patient had a blood pressure of 90/60 mmHg, pulse rate of 68 beats/min, respiratory rate of 20/min, and a body temperature of 36.3°C. Laboratory findings were as follows: white blood cell count 12,500/mm3, hemoglobin level 11.1 g/dL, platelet count 88,000/mm3, C-reactive protein 30.15 mg/dL, blood urea nitrogen 32.6 mg/dL, creatinine 0.9 mg/dL, total protein 4.5 g/dL, and albumin 1.7 g/dL. Levels of aspartate aminotransferase, alanine transaminase, alkaline phosphatase, and lactate dehydrogenase were 45 U/L, 18 U/L, 228 U/L and 886 U/L, respectively. The serum concentration of hemoglobin A1c was 11.2%. Needle aspiration from a skin nodule on left wrist was performed for microbiological examination. Intravenous cefazolin was started as an empirical antibiotic.
On day 3 since admission, fever was detected, together with aggravation of the skin lesion on the left hand and thrombocytopenia. Two sets of blood cultures were performed, both of which showed no growth. Neutrophilia with a left shift to myelocytes and thrombocytopenia were observed in a peripheral blood smear. On day 5 since admission, pus culture from day 1 revealed methicillin-resistant Staphylococcus epidermidis; for this reason, cefazolin was changed to vancomycin. His fever persisted and he began exhibiting altered consciousness (Glasgow coma scale 13) with no improvement of the tender multiple nodules. On day 7 since admission, a rapid adrenocorticotropic hormone stimulation test was performed due to the patient’s recent history of steroid injection. The test results showed evidence of adrenal insufficiency. The patient was prescribed an oral hydrocortisone at 40 mg per day. Chest and abdomen computed tomography (CT) with enhancement was performed to identify any other fever foci. Multiple, peribronchial nodules of variable size in both lungs were observed on chest CT (). Other than mild fatty liver, no sign of liver cirrhosis or splenomegaly was evident on abdomen CT. The patient complained of worsening multiple arthralgias in both wrists and ankles. A three-phase bone scan revealed arthritic changes in the right shoulder, both wrists, and the right ankle. The amount of synovial fluid was insufficient for aspiration. Examination of the skin discharge from the left forearm was repeated, and acid-fast bacilli (AFB) staining and TB culture, as well as bacterial and fungal culture of sputum were performed. AFB were seen in pus and sputum samples stained with Ziehl–Neelsen. Sputum Mycobacterium tuberculosis (MTB) PCR with hybridization was negative. Skin biopsies from the left cheek and left 2nd finger were performed, and pathologic examination revealed acute suppurative inflammation and a positive Ziehl–Neelsen stain. Empirical treatment for both MTB and nontuberculous Mycobacterium (NTM) was initiated with isoniazid (300 mg once per day), rifampin (600 mg once per day), ethambutol (1,200 mg once per day), pyrazinamide (1,500 mg once per day), clarithromycin (500 mg twice per day), and intravenous cefoxitin (3 g three times per day). After 9 days of medication, the fever gradually subsided and the platelet level returned to the normal range; however, painful erythematous nodules remained. CT of the face () and both femurs () showed multiple abscess pockets in the subcutaneous layer where nodules were present. Surgical debridement of the abscess was performed under local anesthesia. NTM grew in culture of two sputum and pus samples. The organism was later identified as M. marinum using NTM-specific DNA probes (hybridization with Geno type mycobacterium CM ver. 1.0®, Hain Lifescience GmbH, Nehren, Germany). The M. marinum isolate showed resistance to doxycycline, rifampin, and trimethoprim-sulfamethoxazole. According to the microbiological results, daily medication was changed to clarithromycin (500 mg twice per day), moxifloxacin (400 mg once per day), and ethambutol (1,200 mg once per day). The patient’s symptoms gradually improved and he was discharged on day 39 since admission.
During outpatient follow-up, he continued the medications for 3 months, during which time the skin nodules disappeared and the chest radiological findings improved. However, at 3 months of follow-up, he presented to the emergency center due to an altered mental state. On chest CT, the previous peribronchial nodules were no longer visible and newly developed peribronchial consolidation and perilesional ground glass opacities were seen in the left lung and the posterior basal segment of the right lower lung. Pseudomonas aeruginosa was grown in blood culture. Streptococcus pneumoniae antigen in urine, respiratory virus, and pneumobacter PCR results were negative. The patient died during the course of the pneumonia and subsequent Pseudomonas bacteremia treatment.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [67, 'years'], 'Systolic Blood Pressure': [90.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg'], 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [32.6, 'mg/dL'], 'Confusion': True}",4,4,4,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 67 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient has confusion, 1 point is added to score making the current total 1 + 1 = 2.
The concentration of BUN is 32.6 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 2 + 1 = 3.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 3.
The patient's systiolic blood pressure is 90 mm Hg. The patient's diastolic blood pressure is 60 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 3 + 1 = 4.
The patient's CURB-65 score is 4."
6482,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-1971,Extracted,"A 67-year-old woman is brought to the emergency department for the evaluation of fever, chest pain, and a cough productive of a moderate amount of greenish-yellow sputum for 2 days. During this period, she has had severe malaise, chills, and difficulty breathing. She has hypertension, hypercholesterolemia, and type 2 diabetes mellitus. She smoked one pack of cigarettes daily for 20 years, but quit 5 years ago. Current medications include simvastatin, captopril, and metformin. Temperature is 39°C (102.2°F), pulse is 110/min, respirations are 33/min, and blood pressure is 143/88 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 94%. Crackles are heard on auscultation of the right upper lobe. Laboratory studies show a leukocyte count of 12,300/mm3, an erythrocyte sedimentation rate of 60 mm/h, and a urea nitrogen of 15 mg/dL. A chest x-ray is shown.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [143.0, 'mm hg'], 'respiratory rate': [33.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [15.0, 'mg/dL'], 'Diastolic Blood Pressure': [88.0, 'mm hg'], 'age': [67, 'years']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 67 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 1.
The concentration of BUN is 15.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 1.
The patient's respiratory rate is 33 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 1 + 1 = 2.
The patient's systiolic blood pressure is 143 mm Hg. The patient's diastolic blood pressure is 88 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6483,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-8310679-1,Extracted,"A 61-year-old female with a past medical history of ulcerative colitis status post colectomy and colostomy presented to the emergency department (ED) with altered mental status and severe generalized weakness for an unknown duration. Upon arrival, the patient was alert but disoriented to person, place, and time, and unable to provide pertinent history. She was noted to be allergic to sulfa drugs and had not been following any primary care physician for the past 15 years with limited recent medical records available. Physical examination revealed erythematous and excoriated wounds draining purulent material over her left abdomen at the site of her colostomy bag and left superolateral thigh near the buttocks. Surgery was consulted for concern of possible necrotizing fasciitis at the site of her thigh wound, but it was determined that there was no surgical intervention needed with a recommendation for further resuscitative measures. Her vital signs on arrival revealed a blood pressure of 151/86 mmHg, pulse rate of 118 beats/minute, the temperature of 98.2 °F, respiratory rate of 29 breaths/minute, and oxygen saturation of 92% on 2 L nasal cannula. Initial laboratory results (Table ) revealed the following: WBC 14.7 × 103/µL with a left shift, neutrophils 75%, blood urea nitrogen (BUN) 49 mg/dL, creatinine 2.1 mg/dL, glomerular filtration rate (GFR) 25 ml/min, HCO3 13 mmol/l, AG 15, Cl 103 mmol/l, C-reactive protein (CRP) 18 g/dl, ABG: pH 7.278, pCO2 26.5 mm Hg, pO2 121 mm Hg, and bicarbonate 12.0 mmol/l on 3 L oxygen. Chest X-ray revealed bilateral airspace disease (Figure ). Computed tomography (CT) of the abdomen (Figures and 3) showed a fatty liver, sludge in the gallbladder, scattered punctate nonobstructive renal calculi, and a large right paramedian ventral hernia sac containing abdominal contents.
Blood cultures grew anaerobic Gram-positive cocci and Staphylococcus aureus. Culture from the abdomen wound revealed 2+ Gram-positive cocci and 1+ Gram-positive bacilli, while culture from the left thigh wound showed 3+ Gram-positive cocci, 3+ Gram-negative bacilli, and 1+ Gram-positive bacilli. She was diagnosed with severe sepsis secondary to diffuse extensive abdominal wall and bilateral lower extremity purulent cellulitis, community-acquired pneumonia, and acute renal failure due to prerenal azotemia from dehydration. Treatment was initiated in the ED with multiple intravenous antibiotics including piperacillin/tazobactam and vancomycin. She was subsequently admitted to a general medical floor and her antibiotics were changed to meropenem, doxycycline, and vancomycin. On day 6, owing to the improvement of her cellulitis and pneumonia, her antibiotics were de-escalated to ceftriaxone, metronidazole, and vancomycin per a recommendation from an infectious disease specialist. On day 8, she developed a maculopapular rash on the back of the thigh. Suspecting drug eruption, ceftriaxone was changed to ertapenem, and vancomycin and metronidazole remained unchanged. The rash continued to worsen, and blisters developed on the abdominal surface with denuded skin. At this time, there were multiple fluid-filled blisters on the abdominal wall and upper extremities. Some of the blisters ruptured and exposed the underlying tissue. Subsequently, all antibiotics were discontinued due to suspected SJS/TEN and intravenous methylprednisolone was started. As per the infectious disease specialist, daptomycin and metronidazole were restarted for prophylactic coverage, although repeat blood cultures did not reveal any growth. The rash continued to worsen, involving more than 20% of body surface area (BSA) with denuded skin. Blisters spread to the face, abdominal surface, and upper extremities, but spared the oral mucosa (Figure ). Meanwhile, the patient developed oliguric renal failure due to suspected acute interstitial nephritis and required hemodialysis. Skin biopsy revealed overlapping features of AGEP and SJS/TEN (Figures -). Due to the uncontrolled progression of her rash, she was transferred to the burn unit of a higher care center.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [61, 'years'], 'Systolic Blood Pressure': [151.0, 'mm hg'], 'Diastolic Blood Pressure': [86.0, 'mm hg'], 'Blood Urea Nitrogen (BUN)': [49.0, 'mg/dL'], 'respiratory rate': [29.0, 'breaths per minute'], 'Confusion': True}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 61 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient has confusion, 1 point is added to score making the current total 0 + 1 = 1.
The concentration of BUN is 49.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 29 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 151 mm Hg. The patient's diastolic blood pressure is 86 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6484,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-7507594-2,Extracted,"A 72-year-old male visited the hospital with a recent history of cough, phlegm and increased focal opacity in of left lower lung field (LLLF) on CXR (Fig. b-Pre). On admission, BP was 120/70 mmHg, PR was 90/min, RR was 20/min, and BT was 36.6 °C. Chest CT showed consolidation in the LLLF (Fig. b). The leukocyte count was 4700/uL (neutrophils, 58%), Hb was 12.6 g/dL, ESR was 26 mm/hr., CRP was 5.3 mg/L, procalcitonin was 0.03 ng/mL, Na was 139 mEq/L, BUN was 15.1 mg/dL, Cr was 0.8 mg/dL, and albumin was 2.8 g/dL. An anti-HIV antibody screening test was negative. To confirm the cause of pneumonia, TBLB and bronchoalveolar lavage (BAL) were performed under R-EBUS. The lung biopsy results suggested OP (Fig. b). AFB stain of bronchial wash fluid was negative, but the MTB PCR was positive. Since the biopsy and radiologic examination results did not show findings appropriate for TB, the MTB PCR result was determined to be a false-positive. Therefore, he received corticosteroid treatment while maintaining antibiotic treatment. CXR showed that LLLF infiltration improved after steroids, but 3 weeks later M. tuberculosis was confirmed on AFB culture of BAL fluid. Therefore, the steroid was discontinued and anti-tuberculosis treatment was started. The microbe was sensitive to all anti-tuberculosis drugs and CXR revealed that all lesions improved thereafter (Fig. b-Post).",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg'], 'age': [72, 'years'], 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [15.1, 'mg/dL']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 72 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 1.
The concentration of BUN is 15.1 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 1.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 120 mm Hg. The patient's diastolic blood pressure is 70 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6485,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-4701793-1,Extracted,"A 58-year-old man visited our hospital with cough, purulent sputum, and dyspnea since a month prior. The patient presented no medical history except a 30 pack-year smoking history.
On admission, the patient's vital signs were as follows: blood pressure 100/70 mm Hg, pulse rate 92 beats per minute, body temperature 37.4℃, and respiratory rate 35 breaths per minute. Auscultation of lungs revealed coarse breathing sounds with crackle and wheezing on both lower lung fields. The oxygen saturation was 94%, pH 7.48, PaO2 63.0 mm Hg, and PaCO2 32.0 mm Hg while the patient was breathing ambient air. A complete blood count showed a white blood cell (WBC) count of 6,920/mm3 (neutrophils 70.9%, lymphocytes 21.9%, monocytes 20.9%, and eosinophils 9.8%), a hemoglobin of 12.4 g/dL, and platelets 198,000/mm3. Serum chemistry showed blood urea nitrogen 18.6 mg/dL, creatinine 1.0 mg/dL, aspartate aminotransferase 158 IU/L, alanine aminotransferase 439 IU/L, alkaline phosphatase level of 386 IU/L, and a C-reactive protein 7.0 mg/dL. The following day, WBC increased to 19,220/mm3 with neutrophil 91.4%; and C-reactive protein increased to 8.5 mg/dL. An electrocardiogram revealed normal sinus rhythm and cardiac enzyme within was normal range.
Plain chest radiography on admission showed cardiomegaly and consolidation on both lung fields (). Contrast-enhanced chest computed tomography demonstrated diffuse ground glass opacity and consolidation in both lungs. Underlying emphysematous and bullous changes were also noted predominantly in the lower lobes (). An echocardiography showed an ejection fraction of 10% and severe left ventricular systolic dysfunction with no regional wall motion abnormality.
Initially, we suspected bacterial pneumonia and heart failure consequent to pulmonary edema. Empirically, levofloxacin, piperacillin-tazobactam, and diuretics were started intravenously. At 7 days follow-up after admission, 2 sputum cultures showed R. planticola with showed sensitivity to most antibiotics except for ampicillin and ciprofloxacin; no different bacteria were detected. Blood cultures were sterile. We diagnosed a pneumonia caused by R. planticola. We stopped levofloxacin based on the sputum result and continued piperacillin-tazobactam treatment.
Seven days after hospitalization, dyspnea had improved and cough and sputum production was reduced. Fifteen days after admission, laboratory analysis was as follows: a WBC count of 5,420/mm3 (neutrophils 55.9%) and C-reactive protein 0.26 mg/dL. At 3 weeks follow-up after admission, chest radiography showed decrease in both ground glass opacity and consolidation in both lung fields; in addition, contrast-enhanced chest computed tomography showed improvement of pneumonia (). The patient continued antibiotic therapy for 4 weeks and was discharged. Since discharge, he has been followed up at an outpatient clinic without evidence of recurrence.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg'], 'age': [58, 'years'], 'respiratory rate': [35.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [18.6, 'mg/dL']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 58 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 18.6 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 35 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 0 + 1 = 1.
The patient's systiolic blood pressure is 100 mm Hg. The patient's diastolic blood pressure is 70 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6486,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-8101516-1,Extracted,"An 81-year-old man presented to the gastroenterology clinic complaining of progressive dysphagia to solid food for 6 months. He had poor appetite and weight loss of 22 kg. He denied chest pain, regurgitation, cough, abdominal pain, nausea, vomiting, diarrhea, hematochezia, or melena. His past medical history was significant for essential hypertension, coronary artery disease, chronic hepatitis B infection, hypothyroidism, and sarcoidosis. The patient’s past surgical history was significant for coronary artery bypass grafting (CABG) surgery, bilateral cataract surgery, and multiple tooth extractions. Family history was noncontributory. Home medications included aspirin, quinapril, atenolol, levothyroxine, and entecavir. He denied using tobacco, alcohol, or illicit drugs.
On physical examination, the patient appeared chronically ill and cachectic. Vital signs demonstrated a temperature of 36.8 °C, blood pressure of 128/60 mmHg, heart rate of 65 beats per minute, and respiratory rate of 12 breaths per minute. Cardiovascular and lung exams were unremarkable. Abdominal exam showed a soft and non-tender abdomen with normal bowel sounds. Complete blood count (CBC) revealed a low hemoglobin of 11.6 g/dL and a mean corpuscular volume (MCV) of 63 fL consistent with microcytic anemia. Otherwise, the patient had a normal white blood cell (WBC) of 6.6 × 109/L and platelets of 167 × 109/L. Comprehensive metabolic panel (CMP) was within normal limits: Sodium 143 mmol/L, potassium 3.8 mmol/L, chloride 106 mmol/L, CO2 25 mmol/L, glucose 121 mg/dL, creatinine 0.81 mg/dL, BUN 12 mg/dL, calcium 9.4 mg/dL, total protein 6.5 g/dL, albumin 4.2 g/dL, total bilirubin 1.0 mg/dL, AST 12 U/L, ALT 12 U/L, and alkaline phosphatase 100 U/L.
An esophagogastroduodenoscopy (EGD) was performed to investigate the cause of dysphagia. EGD revealed a normal appearing esophagus, patchy erythema in the gastric antrum, normal appearing gastric body, and normal appearing duodenum (). A gastric biopsy was obtained, and histologic examination revealed glandular atrophy with acellular, eosinophilic deposits in the lamina propria and submucosa. Congo red stain revealed apple-green birefringence on polarized light consistent with gastric amyloidosis.
Further workup followed to evaluate the etiology of amyloidosis. Serum protein electrophoresis (SPEP) did not show a monoclonal (M) band. Urine protein electrophoresis (UPEP) did reveal the presence of proteinuria, but also failed to show an M band. Immunofixation showed elevated free kappa light chains of 104.90 mg/dL and an elevated free Kappa/Lambda ratio of 156.57. At this point, the patient was referred to a hematology/oncology specialist for a bone marrow biopsy. Bone marrow biopsy showed that plasma cells constituted 28.5% of the bone marrow consistent with multiple myeloma. The patient was started on lenalidomide, bortezomib, and dexamethasone. One month later, he was seen for a follow-up visit at the oncologist’s office. He reported improvement in dysphagia and weight gain of 1 kg. Unfortunately, the patient’s malignancy progressed, and his condition continued to deteriorate over the next 5 months. He eventually developed pneumonia complicated by septic shock, respiratory failure, and acute kidney injury. He was admitted to the intensive care unit where he suffered a sudden cardiac arrest and expired.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [81, 'years'], 'Systolic Blood Pressure': [128.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg'], 'respiratory rate': [12.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [12.0, 'mg/dL']}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 81 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 1.
The concentration of BUN is 12.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 1.
The patient's respiratory rate is 12 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 128 mm Hg. The patient's diastolic blood pressure is 60 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 1 + 1 = 2.
The patient's CURB-65 score is 2."
6487,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-6198694-1,Extracted,"A 24-year-old male presented to the emergency department with a 3-day history of fever, fatigue, and severe headache. He had been living in a rural area and had been working in a forest for 1 month where he got wet in the rain 3 days before his presentation. History of tick and rodent contact was unclear. His medical history was positive for six pack-years of cigarette smoking. His family history was unremarkable. On physical examination, his temperature was 39.1°C, heart rate 92/min, blood pressure 120/70 mmHg, and respiratory rate was 16/min. His throat and conjunctiva were hyperemic and tongue and mucosa were dry. Pulmonary sounds were normal on auscultation. Spleen was palpable below the left costal margin. Other physical examination findings were normal. Laboratory values were white blood cell: 7.3 K/uL (n = 4–10.5), hemoglobin: 14.6 g/dL (n = 12-17.5), platelet: 34,000/mm3 (n = 140,000–450,000), urea: 18.7 mg/dL (n = 16.6–48.5), creatinine: 0.81 mg/dL (n = 0.7–1.2), alanine transaminase: 21 U/L (n = 0–41), aspartate aminotransferase: 39 U/L (N: 0-40), creatine kinase: 375 U/L (n = 39–308), and C-reactive protein: 59.5 mg/L (n = 0–5). HIV was negative. Urinalysis showed mild proteinuria and microscopic hematuria. Chest X-ray was within normal limits. Abdominal ultrasound showed a mild increase in the long axis of both kidneys and splenomegaly (long axis of spleen: 143 mm). He was admitted to inpatient clinic with a presumptive diagnosis of acute respiratory system infection. After collection of blood and urine cultures, ceftriaxone intravenous was started empirically. Serum samples were sent to the National Arboviruses and Viral Zoonoses Reference Laboratory to rule out Crimean-Congo hemorrhagic fever and hantavirus infection. Platelet transfusions were given to treat the thrombocytopenia. On the 3rd day of hospitalization, he suddenly developed severe dyspnea, massive dry cough and a dramatic decrease in oxygen saturation which was 79% on a finger pulse oximeter. During the deterioration, his blood pressure was normal (110/70 mmHg), platelet count was 67,000/mm3, renal function tests were urea: 28 mg/dL, creatinine: 1.51 mg/dL. Liver function tests and coagulation profile were in normal limits. On oxygen supplementation, arterial blood gas analysis was: pH: 7.43 (n = 7.35–7.45), PaCO2:29.9 (n = 35–45), PaO2:53.2 (n = 60–100). There was no hemoptysis. To rule out pulmonary embolism, computed tomography angiography of the thorax was done. There was no evidence of pulmonary embolism, however, bilateral extensive infiltrations and bilateral pleural effusion were detected []. As the patient had no finding of hemodynamic instability such as hypotension or bleeding, clinical exacerbation was thought to be related to impaired pulmonary ventilation due to infective process rather than pulmonary hemorrhage. Mild clinical and laboratory findings despite severe radiological findings suggested atypical pneumonia as the diagnosis. Intravenous moxifloxacin was added to the treatment. Then, the patient was referred to a tertiary care hospital due to possible risk of acute respiratory distress syndrome and admitted to its intensive care unit. Treatment was continued with ampicillin/sulbactam, clarithromycin, and oseltamivir. The next day, he was transferred to the ward as there was improvement in his clinical status. His renal function tests and arterial blood gas analysis returned to normal. There was no growth in blood and urine cultures. Legionella urinary antigen was negative. Other relevant microbiological agents were all negative []. Hantavirus IgM and IgG were positive on indirect immunofluorescence assay (Anti-Hantavirus IIFT, Euroimmun, Germany) immunoblot analysis (Antibodies against antigens of Hantavirus, Hanta Profile 1 Euroline, Euroimmun, Germany) and evaluation of the test strips using EUROLineScan program. The sensitivity of the Anti-Hantavirus IIFT test is reported to be 96% for IgM and 99% for IgG and the specificity 100% for IgM and 98% for IgG. The sensitivity of the Hanta Profile 1 Euroline IgM test is reported to be 91.4% for IgM and 84.5% for IgG, and the specificity 86% for IgM and 95.1% for IgG by the manufacturer. The serotype of the virus was detected as Puumala. Immunoblot strips and evaluation form images are shown in . After a 10-day hospital stay, the patient was discharged on oral cefdinir and clarithromycin. At 1 month follow-up, he was asymptomatic and his blood tests and computed tomography of the thorax were normal. At 2 months follow-up, antibody levels against hantavirus were increased by four-fold on immunofluorescence assay. Thus, the final diagnosis in our patient was HPS due to PUUV.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg'], 'age': [24, 'years'], 'respiratory rate': [16.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [18.7, 'mg/dL'], 'Confusion': False}",0,0,0,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 24 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 18.7 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 16 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 0.
The patient's systiolic blood pressure is 120 mm Hg. The patient's diastolic blood pressure is 70 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 0.
The patient's CURB-65 score is 0."
6488,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-3712158-1,Extracted,"A 53-year-old male patient visited the emergency room for worsening symptoms of productive cough, fever, and chills that developed the day before. The patient, with no specific occupation, had a 30-pack/year history of cigarette smoking and consumed alcohol in moderation. He was successfully treated for CAP in another hospital 2 years prior and had experienced no other problems. Upon admission, the patient appeared acutely ill. His blood pressure was 82/46 mmHg, respiratory rate was 22 breaths per minute, pulse rate was 120 beats per minute, and body temperature was 40℃. A regular heart rhythm was observed and there were coarse breathing sounds with crackles on the right lower lung field.
The laboratory chemistry values were as follows: white blood cell count of 11,500/mm3 with 86.1% neutrophils, 11.5% lymphocytes, 1.9% monocytes, 0.2% eosinophils; hemoglobin 14.4 g/dL; platelet count 188,000/mm3; C-reactive protein 1.28 mg/dL. The arterial blood gas analysis at room air was pH of 7.47, pCO2 of 22.4 mmHg, pO2 of 52.5 mmHg, HCO3- of 16 mmol/L, and O2 saturation of 89%. Blood chemistries showed a blood urea nitrogen (BUN)/creatinine (Cr) level of 9/2.05 mg/dL and the serum sodium, potassium, and chloride were 139, 4.1, and 105 mmol/L, respectively. The urine sodium was 19 mmol/L, urine Cr was 222.31 mg/dL, and the calculated fractional excretion of sodium was 0.1%. A simple chest radiograph showed moderate patchy consolidation in the right lower lobe (). We made a presumptive diagnosis of sepsis caused by CAP.
Septic shock was suspected due to low blood pressure. A central line catheter was promptly inserted, along with fluid resuscitation, and oxygen was administered via nasal cannula. Cultures of blood, sputum, and urine samples were also completed. Empiric piperacillin/tazobactam with ciprofloxacin injections were administered simultaneously. The patient was admitted into the intensive care unit for directed therapy of septic shock. The initial APACHE II score was 25. Low blood pressure persisted after vigorous fluid therapy; thus, the vasoactive agent norepinephrine was administered. Vasopressin was later added when the mean arterial pressure did not normalize. Sixteen hours after admission, respiratory distress worsened, resulting in acute respiratory failure with arterial blood gas analysis showing a pH of 7.085, pCO2 of 61.4 mmHg, and HCO3- of 19 mmol/L. The patient was immediately intubated with mechanical ventilation at FiO2 of 1.0 and positive end expiratory pressure at 14 cmH2O; however, hypoxia persisted and respiratory and metabolic acidosis continued to deteriorate. Twenty-four hours after admission, follow-up arterial blood gas analysis showed a pH of 7.096, pCO2 of 63.7 mmHg, pO2 of 77.6 mmHg, HCO3- of 20 mmol/L, and O2 saturation of 89%. The follow-up chest radiograph showed more exacerbated consolidation in the right lung field with the beginning of patchy opacities in the left lower lobe (). The antibiotics were then switched to meropenem with teicoplanin. Twenty-eight hours after admission, oliguria ensued along with deteriorating acute kidney injury with BUN/Cr at 26/3.66 mg/dL. Continuous renal replacement therapy was promptly initiated. After 36 hours of intensive treatment, septic shock and acute respiratory failure did not improve and the patient went into cardiac arrest. Cardiopulmonary resuscitation was performed for 30 minutes but the patient did not recover.
After the patient expired, AB was identified in both the culture of sputum and two pairs of blood samples taken during the emergency room visit. Bacterial sensitivity to antibiotics was measured using isolates from both sputum and blood cultures. The bacterial isolate was susceptible to piperacillin/tazobactam, ceftazidime, cefepime, imipenem, meropenem, gentamicin, and tobramycin; tolerant to ampicillin, amoxacillin/clavulanic acid, cafalotin, cefoxitin, and trimethoprim/sulfamethoxazole; and moderately tolerant to cefotaxime and levofloxacin (). A VITEK device (VITEK 2, Biomerieux, Marcy I'Etolile, France) was used for culturing, and the sensitivity test was conducted in accordance to the Clinical and Laboratory Standards Institute.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [53, 'years'], 'Systolic Blood Pressure': [82.0, 'mm hg'], 'Diastolic Blood Pressure': [46.0, 'mm hg'], 'respiratory rate': [22.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [9.0, 'mg/dL'], 'Confusion': True}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 53 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient has confusion, 1 point is added to score making the current total 0 + 1 = 1.
The concentration of BUN is 9.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 1.
The patient's respiratory rate is 22 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 82 mm Hg. The patient's diastolic blood pressure is 46 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 1 + 1 = 2.
The patient's CURB-65 score is 2."
6489,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-5196,Extracted,"A 28-year-old woman presents to the emergency department with shortness of breath. She immigrated from Uganda two months ago. She reports cough with occasional blood-tinged sputum and night sweats for the past week. She denies any chest pain or discomfort currently. The patient denies any sexual activity or intravenous drug use. She denies any history of cancer in her family. She currently lives in an apartment with several other female migrant workers. She received a vaccination against tuberculosis when she lived in Uganda. Her temperature is 99°F (37.2°C), blood pressure is 110/70 mmHg, pulse is 100/min, respirations are 20/min, and oxygen saturation is 94% on room air. Breath sounds are decreased in the left posterior lower and middle lung fields; egophony is present on the left middle lung field. The remainder of the physical exam is unremarkable. A complete blood count and basic metabolic panel are obtained:

Serum:
Na+: 135 mEq/L
Cl-: 100 mEq/L
K+: 3.5 mEq/L
HCO3-: 26 mEq/L
BUN: 10 mg/dL
Glucose: 105 mg/dL
Creatinine: 0.6 mg/dL

Leukocyte count: 20,000/mm^3
Segmented neutrophils: 69 %
Bands: 10 %
Eosinophils: 2 %
Basophils: 1 %
Lymphocytes: 25 %
Monocytes: 3 %

Hemoglobin: 11 g/dL
Hematocrit: 33 %
Platelet count: 400,000/mm^3

An electrocardiogram reveals sinus tachycardia without acute ST-T wave changes. Chest radiography is obtained in Figure A.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [110.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg'], 'age': [28, 'years'], 'Confusion': False, 'respiratory rate': [20.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [10.0, 'mg/dL']}",0,0,0,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 28 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 10.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 0.
The patient's respiratory rate is 20 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 0.
The patient's systiolic blood pressure is 110 mm Hg. The patient's diastolic blood pressure is 70 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 0.
The patient's CURB-65 score is 0."
6490,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-8691,Extracted,"A 58-year-old man is brought to the Emergency Department after 2 days of shortness breath, orthopnea, and lower limb edema. His past medical history is significant for hypertension and a myocardial infarction 3 years ago that required a coronary arterial bypass graft. He has not been able to take prescribed medicine in several months due to recent unemployment and issues with insurance. On admission, his blood pressure is 155/92 mmHg, heart rate is 102/min, respiratory rate is 24/min, and temperature is 36.4°C (97.5°F). On physical examination there are fine rales in both lungs, regular and rhythmic cardiac sounds with an S3 gallop and a grade II/VI holosystolic murmur. Initial laboratory tests are shown below:
Na+ 140 mEq/L
K+ 4.2 mEq/L
Cl- 105 mEq/L
BUN 20 mg/dL
Creatinine 0.8 mg/dL
The patient is stabilized and admitted to the hospital. The next day his blood pressure is 110/60 mmHg, heart rate is 110/min, respiratory rate is 18/min, and temperature is 36.4°C (97.5°F).",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [155.0, 'mm hg'], 'Diastolic Blood Pressure': [92.0, 'mm hg'], 'age': [58, 'years'], 'respiratory rate': [24.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 58 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 20.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 24 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 155 mm Hg. The patient's diastolic blood pressure is 92 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6491,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-6350018-1,Extracted,"A 42-year-old male with a history significant for chronic obstructive pulmonary disease (COPD), asthma, polyneuropathy, ½-pack-per-day smoker for 30 years was admitted to hospital for non-resolving cough and left-sided chest pain in November 2016. One month prior to this admission, he was in the Emergency Department and was treated with a 5-day course of azithromycin for a presumed, left upper lobe pneumonia. Seeing no significant relief of his symptoms, he went to his primary care provider and was prescribed a 10-day course of levofloxacin. The patient reported good adherence to and completion of both courses of antibiotic. Despite these two courses of treatment, respiratory symptoms persisted, which led to hospitalization and further diagnostic work-up.
At the time of hospital admission, the patient was afebrile, had a blood pressure of 113/77 mm Hg, heart rate of 96 beats per minute, respiratory rate of 16 breaths per minute, and a body mass index of 17.5 kg/m2. Physical exam revealed anterior cervical lymphadenopathy and coarse rhonchi in left upper zone anteriorly. Initial laboratory examination revealed the following: white blood cell count, 11.4 × 103 cells/µL; neutrophils, 78.4%; red blood cell count, 4.08 × 103 cells/µL; hemoglobin, 12.2 g/dL; hematocrit, 37.0%; platelets, 570 × 103 cells/µL; sodium, 140 mEq/L; potassium, 4.5 mEq/L; chloride, 104 mEq/L; CO2, 28 mmol/L; anion gap, 8 mEq/L; blood urea nitrogen (BUN), 20 mg/dL; creatinine, 0.87 mg/dL; glomerular filtration rate (GFR) > 60 mL/min; magnesium, 2.2 mEq/L; aspartate aminotransferase (AST), 14 units/L; alanine aminotransferase (ALT), 25 units/L; albumin, 3.4 g/dL; and troponin < 0.01 ng/mL. Chest X-ray showed left upper lobe consolidation, and a computed tomography (CT) of chest showed dense consolidation and cavitation in the left upper lobe along with advanced COPD changes in his lungs ().
The patient was admitted to the medical service for non-resolving pneumonia. Given his symptoms, there was high suspicion of mycobacterial lung infection. He was placed in a negative pressure isolation room and work-up was started. Sputum for Gram stain and acid-fast bacilli (AFB) stain and culture were obtained, and purified protein derivative (PPD) test was placed. Three separate sputum samples were sent for AFB stain and culture based on our laboratory protocol, which includes a digestion-decontamination method using N-acetyl-l-cysteine-sodium hydroxide and cultivation with Lowenstein Jensen Medium and BACTEC MGIT 960 system (Becton Dickinson, MA, USA). Human immunodeficiency virus (HIV) screening was also ordered to assess for a possible source of immunosuppression which could pre-dispose the patient to NTM infection. The PPD, HIV test, and routine sputum cultures were negative; however, two out of three acid-fast smears came back positive with a semi-quantitative result of +1 AFB, reflective of 1–9 organisms per high powered field. Due to the long turnaround time for mycobacterial organism identification and susceptibility determination, the patient was started empirically on a four-drug treatment regimen of isoniazid, rifampin, ethambutol and pyrazinamide.
The patient’s condition slowly improved, though he remained symptomatic throughout his hospitalization. Initially, he experienced some nausea and vomiting associated with the antimycobacterial drugs; however, this improved with modification of the timing of his doses relative to meals. Once the patient was tolerating his medications, plans were made to discharge the patient. Coordination with the local health department helped facilitate the discharge to home, with instructions for staying at home and avoiding close contact with others for at least the first month of therapy. The discharge medication regimen included ethambutol 1200 mg oral daily, isoniazid 300 mg oral daily at bedtime, pyrazinamide 1500 mg oral daily at bedtime, pyridoxine 50 mg oral daily at bedtime and rifampin 600 mg oral daily at bedtime.
The AFB isolate was later identified as M. szulgai, using MALDI-TOF mass spectrometry analysis. Real-time polymerase chain reaction (PCR) was negative for M. tuberculosis complex DNA and MAC DNA . The species were discriminated using MALDI-TOF mass spectrometry analysis as M. szulgai. Specimens were later submitted to reference lab at National Jewish Health, Denver, CO, USA for drug susceptibility testing. Reference lab performed agar proportion antimicrobial susceptibility testing methodology using Middlebrook 7H11 agar. As there are no standard treatment regimens for this organism, he was continued on the four-drug regimen for 2 months of treatment, during which he showed progressive clinical improvement. Based on the susceptibility test results, the regimen was streamlined accordingly to rifampin, isoniazid and azithromycin after 2 months of standard anti-tubercular therapy. His sputum culture was negative for AFB within 2 months of therapy initiation and remained negative for throughout his treatment course. A repeat CT was done, which showed complete resolution of left lung consolidation with remnant scarring (). Treatment was stopped after 10 total months of therapy. He was closely followed up and had surveillance sputum cultures which remained negative. Given the persistent scar, he had a positron emission tomography (PET) scan which showed increased uptake in left upper lobe, which could be reflective of either malignancy or mycobacterial infection. Given the patient’s history of cigarette smoking and concern for associated neoplasm, he was advised to undergo wedge resection, which was done 6 months after the completion of therapy. Pathology revealed old granulomas, and AFB culture of the resected tissue was negative. No evidence of malignancy was identified. The patient’s clinical symptoms had resolved prior to the surgery and remained stable after the resection.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [113.0, 'mm hg'], 'respiratory rate': [16.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [20.0, 'mg/dL'], 'Diastolic Blood Pressure': [77.0, 'mm hg'], 'age': [42, 'years']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 42 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 20.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 16 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 113 mm Hg. The patient's diastolic blood pressure is 77 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6492,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-1029,Extracted,"A 68-year-old man is brought to the emergency department because of fever, progressive weakness, and cough for the past five days. He experienced a similar episode 2 months ago, for which he was hospitalized for 10 days while visiting his son in Russia. He states that he has never fully recovered from that episode. He felt much better after being treated with antibiotics, but he still coughs often during meals. He sometimes also coughs up undigested food after eating. For the last 5 days, his coughing has become more frequent and productive of yellowish-green sputum. He takes hydrochlorothiazide for hypertension and pantoprazole for the retrosternal discomfort that he often experiences while eating. He has smoked half a pack of cigarettes daily for the last 30 years and drinks one shot of vodka every day. The patient appears thin. His temperature is 40.1°C (104.2°F), pulse is 118/min, respirations are 22/min, and blood pressure is 125/90 mm Hg. Auscultation of the lungs shows right basal crackles. There is dullness on percussion at the right lung base. The remainder of the physical examination shows no abnormalities. Laboratory studies show:
Hemoglobin 15.4 g/dL
Leukocyte count 17,000/mm3
Platelet count 350,000/mm3
Na+ 139 mEq/L
K+
4.6 mEq/L
Cl- 102 mEq/L
HCO3- 25 mEq/L
Urea Nitrogen 16 mg/dL
Creatinine 1.3 mg/dL
An x-ray of the chest shows a right lower lobe infiltrate.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [68, 'years'], 'Systolic Blood Pressure': [125.0, 'mm hg'], 'Diastolic Blood Pressure': [90.0, 'mm hg'], 'respiratory rate': [22.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [16.0, 'mg/dL']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 68 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 1.
The concentration of BUN is 16.0 mg/dL. The patient's BUN concentration is less than or equal to 19 mg/dL and so 0 points are added to score, keeping the current total at 1.
The patient's respiratory rate is 22 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 125 mm Hg. The patient's diastolic blood pressure is 90 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6493,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-3229794-1,Extracted,"A 21-year-old male, on treatment for alcohol and tobacco dependence, presented to the emergency department within 12 hours after alleged consumption of 10 tablets of extended release baclofen (20 mg). On admission, his heart rate was 76 beats /min, blood pressure was 158/70 mm of Hg, respiratory rate was 40/min and SpO2 was less than 80% on 60% venturi mask. His Glasgow Coma Scale (GCS) was 3/15, bilateral (B/L) pupils were dilated, deep tendon reflexes were brisk and B/L plantars were extensor. Bilateral crepitations were heard on chest auscultation. He was intubated and put on mechanical ventilation. His baseline renal function tests were: S. Urea 33 mg/dl, S. Creatinine 1.3 mg/dl, S. Sodium 138 meq/l, S. Potassium 4.4 meq/l; his blood counts, liver function test and arterial blood gas analysis (on mechanical ventilation) were normal. His GCS did not show any improvement in the next 12 hours. He underwent two sessions of hemodialysis with a Fresenius hemodialysis machine on consecutive days. Following dialysis, his sensorium improved dramatically and he was successfully extubated. He underwent psychiatric evaluation and counselling prior to discharge.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [158.0, 'mm hg'], 'respiratory rate': [40.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [33.0, 'mg/dL'], 'Confusion': True, 'Diastolic Blood Pressure': [70.0, 'mm hg'], 'age': [21, 'years']}",3,3,3,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 21 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient has confusion, 1 point is added to score making the current total 0 + 1 = 1.
The concentration of BUN is 33.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 40 breaths per minute. Because the respiratory rate is greater than 30 breaths per minute, 1 point is added to the score, making the current total 2 + 1 = 3.
The patient's systiolic blood pressure is 158 mm Hg. The patient's diastolic blood pressure is 70 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 3.
The patient's CURB-65 score is 3."
6494,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-6182792-2,Extracted,"A 69-year-old (height 160.0 cm, weight 37.1 kg) Japanese man was admitted to our ICU from the emergency room due to severe dyspnea. His past medical history included extracorporeal shock wave lithotripsy due to urinary calculus (56 years of age), endoscopic colon polypectomy because of colon polyps (66 years of age), and esophagectomy with gastric reconstruction for esophageal cancer after a stint of preoperative chemoradiation therapy (66 years of age). He smoked 30 cigarettes/day for 40 years and drank whisky (1 bottle/4 days). He was not on any medication. Regarding family history, his grandmother died of liver cancer. On physical examination, he was confused and restless, and his breathing was shallow with reduced air entry to both lungs. A neurological examination was not significant. His vital signs were as follows: heart rate 122 beats/minute, blood pressure 80/58 mmHg, respiratory rate 26 breaths/minute, and temperature 38.7 °C. Arterial blood gases exhibited respiratory acidosis: pH 7.21, PaCO2 117 mmHg, PaO2 76 mmHg, and bicarbonate ion (HCO3−) 45.9 mmol/L with mask oxygen at 6 L/minute. Even bag-valve-mask ventilation could not provide proper ventilation. He was immediately intubated, and numerous food particles, such as beans and rice, were aspirated from his trachea. Therefore, we removed these food particles by bronchoscope as soon as possible. A chest X-ray revealed diffuse bilateral pulmonary infiltrates (Fig. ). He was diagnosed as having aspiration pneumonia and placed on mechanical ventilation. Laboratory findings revealed white blood cell count 0.9 × 109/L, red blood cell count 4.66 × 1012/L, hemoglobin 12.1 g/dL, hematocrit 41.0%, platelet 297 × 109/L, aspartate aminotransferase 17 U/L, alanine aminotransferase 7 U/L, total bilirubin 0.59 mg/dL, albumin 2.2 g/dL, urea nitrogen 26 mg/dL, creatinine 0.75 mg/dL, and C-reactive protein 1.7 mg/dL on ICU admission.
He underwent tracheostomy on ICU day 32 due to prolonged mechanical ventilation. Although his oxygenation was good (PaO2/FIO2 > 300 mmHg), he had restrictive pulmonary dysfunction: tidal volume 210–220 mL, static compliance 16–17 mL/cmH2O with 10 cmH2O pressure support ventilation, respiratory rate 30 beats/minute and PaCO2 46 mmHg. We tried to wean him from mechanical ventilation with support by HFT (flow at 40 L/minute with FIO2 of 0.25). Table presents the respiratory parameters over the 4-day period HFT was administered. On HFT day 4, his arterial blood gases were pH 7.41, PaCO2 58 mmHg, PaO2 68 mmHg, and HCO3− 35.7 mmol/L. Judging his condition as satisfactory, we switched from HFT to a 3 L/minute oxygen T-piece. One hour after the T-piece was commenced, he complained of dyspnea and his arterial blood gases moderately worsened (pH 7.34, PaCO2 72 mmHg, PaO2 106 mmHg, and HCO3− 37.3 mmol/L). At that time, his tidal volume was 200 mL. We decided to switch back to HFT (flow at 40 L/minute with FIO2 of 0.25), and his arterial blood gases improved 1 hour later: pH 7.40, PaCO2 60 mmHg, PaO2 71 mmHg, and HCO3− 35.9 mmol/L. On HFT day 5, his PaCO2 increased to 70 mmHg. This condition suggested respiratory muscle fatigue; however, no complaints of dyspnea were noted. We decided to apply the HFT at daytime and switch to a ventilator (10 cmH2O pressure support with 5 cmH2O PEEP) at night, and the treatment regimen was continued accordingly for the next 8 days.
We evaluated tracheal pressure during HFT using a flow analyzer (CITREX®, TOKIBO, Co. Ltd, Tokyo, Japan) to measure airway pressure and at the entrance of the tracheostomy tube. The measured values were as follows: 0.21– 0.3 cmH2O, 0.21–0.56 cmH2O, 0.54–0.91 cmH2O, 0.76–2.01 cmH2O, 1.17–2.01 cmH2O, and 1.76–2.01 cmH2O at 10 L/minute, 20 L/minute, 30 L/minute, 40 L/minute, 50 L/minute, and 60 L/minute, respectively. The airway pressure was continuously positive and did not become negative even during inspiration. These results suggest that HFT reduces inspiratory effort. Under respiratory support with HFT and physiotherapy rehabilitation, our patient was successfully weaned from the ventilator. He was discharged from the ICU to the general ward on ICU day 51. His physiotherapy rehabilitation continued for 1 month. He was discharged to home on day 86 of hospitalization and returned for a follow-up visit.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [69, 'years'], 'Systolic Blood Pressure': [80.0, 'mm hg'], 'Diastolic Blood Pressure': [58.0, 'mm hg'], 'respiratory rate': [26.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [26.0, 'mg/dL'], 'Confusion': True}",4,4,4,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 69 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient has confusion, 1 point is added to score making the current total 1 + 1 = 2.
The concentration of BUN is 26.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 2 + 1 = 3.
The patient's respiratory rate is 26 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 3.
The patient's systiolic blood pressure is 80 mm Hg. The patient's diastolic blood pressure is 58 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 3 + 1 = 4.
The patient's CURB-65 score is 4."
6495,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-2769299-1,Extracted,"A 47-year-old Caucasian man presented with a three-week history of progressive dyspnea, productive cough, and weight loss of 10 kg in the preceding 3 months. He suffered from several episodes of respiratory infection in preceding months that improved after antibiotic therapy. He smoked 16 packs per year.
Upon admission, physical examination showed an ill looking patient who was thin, pale, acyanotic and tachycardic. His blood pressure was 100/70 mmHg, his pulse 100 beats/min, and his respiratory rate was 26 breaths/min. There was no cervical, axillary, or inguinal lymphadenopathy. Lung auscultation revealed diffusely scattered crackles and rhonchi bilaterally. A physical examination of the heart and abdomen revealed no abnormal findings.
Laboratory tests showed the following blood analysis results: red blood cell count, 4.7 milion/mm3; hemoglobin, 11.1 g/dL; hematocrit, 34.8%; white blood cells, 4,300/mm3; and platelets, 200,000/mm3. Arterial blood gas analysis while breathing room air showed an arterial oxygen tension (PaO2) of 80 mmHg and an arterial carbon dioxide tension (PaCO2) of 32 mmHg. Blood analysis further revealed the following molecular concentrations: sodium, 136 mEq/L; potassium, 4.5 mEq/L; blood urea nitrogen, 26 mg/dL; and creatinine, 1.1 mg/dl. Liver function tests were normal. Serology for HIV and tests for acid-fast bacilli and fungi in three sputum samples were negative. Respiratory function tests demonstrated a moderate obstructive disease. Echocardiography revealed a normal ejection fraction with no myocardial or valvular abnormalities.
A chest radiograph () and computed tomography (CT) on the thorax () showed multiple pulmonary nodular opacities and masses of soft tissue density that had irregular contours, and were diffusely and bilaterally distributed. Most of the nodules and masses contained calcifications, but none were cavitated. Radiographs () and CT of the thorax () had been performed at another institution six years prior, showing nodular lesions with calcifications that were smaller than at present. Since he was asymptomatic at the time, he did not return for further examinations.
Bronchoscopy showed no abnormalities. A bronchoalveolar lavage was negative for tuberculosis, fungi or malignancy. An open lung biopsy was performed and histopathological analysis showed pulmonary amyloidosis. Three months later, the patient died from a respiratory infection.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [47, 'years'], 'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg'], 'respiratory rate': [26.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [26.0, 'mg/dL']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 47 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 26.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 26 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 100 mm Hg. The patient's diastolic blood pressure is 70 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6496,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-6363593-1,Extracted,"A 70-year-old Caucasian male presented to emergency with 10 days of dry cough, dyspnoea, and fatigue. His respiratory rate was 18 per minute with saturations of 93% on 2 L of nasal prong oxygen, heart rate 75 beats per minute and in sinus rhythm, blood pressure 104/60 and was afebrile. Examination demonstrated globally reduced air entry with bibasal crackles with no other pertinent findings.
His medical history included HIV diagnosed in 1997 and well controlled with combination anti-retroviral therapy (sequential viral loads undetectable and CD4 >500/mm3) and Barrett's oesophagus. His surgical history included a trans-urethral prostate resection for hypertrophy as well as a left total knee replacement and a decompression for spinal stenosis. Medications were allopurinol, rosuvastatin, atazanavir, ritonavir, lamivudine, zidovudine, and pantoprazole. He had a 40 pack-year smoking history (quit 15 years ago), minimal alcohol, and no illicit substance history. He worked in an office, was an active swimmer, and not in a relationship. Vaccines were up to date.
Initial investigations revealed a haemoglobin of 115 g/L, neutrophils 8.19 × 109/L, lymphocyte 0.49 × 109/L, eosinophils 0.17 × 109/L, and platelets 390 × 109/L. Creatinine was 441 micromol/L (86 six months prior), urea 25.4 mg/dL, and C-reactive protein 148 mg/L. Chest film demonstrated diffuse bilateral infiltrates predominantly in the lower zones. Urinalysis demonstrated >500 erythrocytes, 10 leucocytes, and no bacteria.
With a provisional diagnosis of pneumonia he was commenced on ceftriaxone, azithromycin, and oxygen. Intravenous fluids continued.
The following day his creatinine increased to 512 despite 3 L of intravenous fluid. An arterial blood gas showed type 1 respiratory failure with a haemoglobin 98 g/L. A broad screen for infectious and non-infectious aetiologies was performed, and a routine HIV viral load taken 4 days prior to presentation was 146 copies/mL. Anti-retrovirals were changed to dolutegravir, efavirenz, and lamivudine due to renal failure.
By day 3 his fatigue and dyspnoea had worsened without new symptoms. Repeat chest film demonstrated worsening infiltrates (Fig. ). His oxygen requirement had increased to 50 L/min, 50% FiO2 via hi-flow nasal cannulae. Dialysis was commenced with red cell transfusions as his haemoglobin was now 82 g/L. A repeat urine had >500 erythrocytes, protein 1100 mg/L, creatinine 188 g/mol, myoglobin 14 μg/L, and normal haemosiderin.
Day 4 returned a Perinuclear-ANCA (P-ANCA) titre >1:640 with all other diagnostic investigations unremarkable, and a provisional diagnosis of MPA was made. Treatment with intravenous cyclophosphamide (800 mg second weekly, three doses), plasma exchange (second daily, seven sessions) and methylprednisolone (500 mg daily for 3 days, then long-course prednisolone) was started. He also received prophylactic trimethoprim/sulphamethoxazole, intravenous iron, and darbepoetin alfa.
With a substantial clinical and radiological improvement (Fig. ) he was discharged after a 29-day stay with ongoing thrice weekly haemodialysis. Renal biopsy five days after discharge demonstrated crescentic-class pauci-immune necrotizing glomerulonephritis without granulomata, consistent with MPA.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [70, 'years'], 'Systolic Blood Pressure': [104.0, 'mm hg'], 'Diastolic Blood Pressure': [60.0, 'mm hg'], 'respiratory rate': [18.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [25.4, 'mg/dL']}",3,3,3,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 70 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 1.
The concentration of BUN is 25.4 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 18 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 104 mm Hg. The patient's diastolic blood pressure is 60 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because at least one of these statements is true, 1 point is added to score, making the current total 2 + 1 = 3.
The patient's CURB-65 score is 3."
6497,45,CURB-65 Score for Pneumonia Severity,risk,integer,usmle-302,Extracted,"A 52-year-old man comes to to the emergency department with fatigue and shortness of breath that has become progressively worse over the past week. He had an upper respiratory tract infection 2 weeks ago, for which he was given an antibiotic. He has hypertension, type 2 diabetes mellitus, and colonic polyps diagnosed on screening colonoscopy 2 years ago. His mother has systemic lupus erythematosus and his brother has a bicuspid aortic valve. He does not smoke cigarettes or drink alcohol. Current medications include lisinopril and metformin. His temperature is 37.3°C (99.1°F), pulse is 91/min, respirations are 18/min, and blood pressure is 145/84 mm Hg. His conjunctivae are pale. Cardiac examination shows a late systolic crescendo-decrescendo murmur at the right upper sternal border. Laboratory studies show:
Leukocyte Count 9,500/mm3
Hematocrit 24%
Platelet Count 178,000/mm3
LDH 215 U/L
Haptoglobin 22 mg/dL (N=41–165 mg/dL)
Serum
Na+ 140 mEq/L
K+ 4.6 mEq/L
CL- 100 mEq/L
HCO3- 25 mEq/L
Urea nitrogen 21 mg/dL
Creatinine 1.2 mg/dL
Total bilirubin 1.9 mg/dL
A peripheral blood smear is shown.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [145.0, 'mm hg'], 'respiratory rate': [18.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [21.0, 'mg/dL'], 'Diastolic Blood Pressure': [84.0, 'mm hg'], 'age': [52, 'years']}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 52 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Whether the patient has confusion is not reported in the note. Hence, we assume this to be false, and so 0 points are added to the score, making the current total 0.
The concentration of BUN is 21.0 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 18 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 145 mm Hg. The patient's diastolic blood pressure is 84 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6498,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-7780870-2,Extracted,"Case 2: A 74-year-old male with a 3-day history of fever, anorexia, vomiting, and shortness of breath was admitted to our hospital. The patient had no history of drug and alcohol abuse and was a non-smoker. His vital signs at admission were as follows: temperature of 38.2 °C, pulse rate of 110 beats per minute, blood pressure of 130/80 mm Hg, respiratory rate of 20 breaths per minute, and SpO2 of 90% in ambient air. After a thorough workup including routine tests and computerized tomography, he received a treatment for COVID-19 and was discharged with good condition and reduced inflammatory markers. Twelve days later, he was readmitted with worsening dyspnea, palpitation, lethargy, confusion, drowsiness, blurring of vision, and generalized weakness. The initial vital signs included body temperature of 38 °C, pulse rate of 120 beats per minute, blood pressure of 140/80 mm Hg, respiratory rate of 22 breaths per minute, and SpO2 of 85% while breathing ambient air. Cranial nerves examination was normal and his pupils were midsize and reactive to light and accommodation.
Laboratory data were as follows: blood glucose level, 102 mg/dL; BUN, 29.6 mg/dL; creatinine (Serum), 0.9 mg/dL; sodium, 138 mEq/L; potassium, 4.6mEq/L; magnesium: 1.7 mg/dL; phosphures, 4 mg/dL; calcium, 8.9mg/dL; ALP, 706 U/L; AST: 66 U/L, ALT: 53 U/L, and troponin level, 4 ng/mL. The blood sample revealed the following results: WBC count 10.4×109/L with 7% lymphocytes and 91% neutrophils; CRP and erythrocyte sedimentation rate (ESR) of 128 mg/L and 57 mm/h, respectively. Chest CT scan showed bilateral GGOs which was expected due to the underlying COVID-19 infection (). The axial unenhanced CT image of the brain showed a hypodense lesion in the superior and lateral aspects of the left cerebellar hemisphere without significant mass effect (). Due to his atrial fibrillation (AF) pattern in the electrocardiogram (ECG), along with his fluctuating SpO2, the patient was admitted to the intensive care unit (ICU). Patient received heparin-based prophylaxis. A single 500 mg oral dose of chloroquine phosphate, Kaletra (lopinavir/ ritonavir) two 200 mg tablets twice daily, meropenem 1 g IV q8hr and vancomycin 1 gram q12hr were administered. After 3 days, his drowsiness diminished and he was able to tolerate oral diets. Also, his CRP level decreased to 63 mg/L. Therefore, he was transferred to the infectious diseases ward. Four days later, he developed arrhythmia, confusion and new-onset hemiplegia. At the time, WBC count was 10.00×109/L with 9.5% lymphocytes; pro BNP, 8930 pg/mL; D-dimer, 7500 μg/L; CRP, 203 mg/L and PCT, 0.2 ng/mL. Anticoagulant was started for him and he was readmitted to ICU. Nine days later, his condition improved and he was discharged with an SpO2 of 95% and CRP of 30 mg/L.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Systolic Blood Pressure': [140.0, 'mm hg'], 'respiratory rate': [22.0, 'breaths per minute'], 'Blood Urea Nitrogen (BUN)': [29.6, 'mg/dL'], 'Confusion': True, 'Diastolic Blood Pressure': [80.0, 'mm hg'], 'age': [74, 'years']}",3,3,3,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 74 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient has confusion, 1 point is added to score making the current total 1 + 1 = 2.
The concentration of BUN is 29.6 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 2 + 1 = 3.
The patient's respiratory rate is 22 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 3.
The patient's systiolic blood pressure is 140 mm Hg. The patient's diastolic blood pressure is 80 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 3.
The patient's CURB-65 score is 3."
6499,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-3326990-1,Extracted,"An 80-year-old woman was admitted to Gachon Gil Medical Center due to severe right upper quadrant (RUQ) abdominal pain of 2 days, before which she had been diagnosed as hilar cholangiocarcinoma (). An endoscopic retrograde biliary stent was placed for biliary drain-age 2 months prior to the current admission. She had no medical history, such as diabetes mellitus or biliary surgery. Symptoms related to cholangitis were resolved with biliary stenting and her general condition showed improvement. Because of her refusal to undergo surgical treatment, radiotherapy was applied after palliative biliary stenting. Computed tomography (CT) performed for simulating a radiation therapy taken 17 days prior to admission revealed ideal placement of an endoscopic retrograde biliary drainage stent (). She received 9 times of radiotherapy with a total dose of 16.2 Gy (1.8 Gy×9 fractions).
On admission, she was conscious and acutely ill in appearance. Her vital signs included a temperature of 36.7℃, a heart rate of 100 beats/min, a blood pressure of 120/70 mmHg, a respiratory rate of 18 breaths/min, and an oxygen saturation of 94% on room air. Her sclera was icteric and her liver was palpable approximately 2 cm below the right costal margin. Right upper quadrant tenderness of the abdomen was present. The spleen was not palpable. Initial complete blood count showed a white blood cell count of 36,130 mm3, hematocrit of 28.2%, and hemoglobin of 9.3 mg/dL. Blood urea nitrogen was 34.9 mg/dL and creatinine was 1.4 mg/dL. C-reactive protein was 26.56 mg/dL. On liver function tests, aspartate transaminase of 882 IU/L, alanine transaminase of 257 IU/L, alkaline phosphatase of 464 IU/L, and total bilirubin of 17.9 mg/dL. Prothrombin time was normal. Abdominal CT scan demonstrated hepatic parenchymal emphysema measuring approximately 6.3×4.4 cm in the superior segment of the right liver (S7/S8) with pneumoperitoneum finding in the perihepatic space (). Urgent percutaneous drainage was attempted under the peritonitis impression; however, no fluid was drained. A diagnosis of emphysematous hepatitis with spontaneous rupture into the peritoneal cavity was made.
On the second day of admission, aggravated laboratory tests were noted as follows: WBC 26,000 mm3, aspartate transaminase 978 IU/L, alanine transaminase 257 IU/L, alkaline phosphatase 367 IU/L, total bilirubin 27.4 mg/dL, blood urea nitrogen 50.2 mg/dL, creatitine 1.2 mg/dL, prothrombin time INR 1.19. Clostridium perfringens and Escherichia coli were grown on blood culture. She was empirically treated with cefotaxime and metronidazol. Despite intensive therapy in the ICU, the patient's condition did not show improvement and she expired on the third day of admission.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [80, 'years'], 'Systolic Blood Pressure': [120.0, 'mm hg'], 'Diastolic Blood Pressure': [70.0, 'mm hg'], 'Blood Urea Nitrogen (BUN)': [34.9, 'mg/dL'], 'respiratory rate': [18.0, 'breaths per minute'], 'Confusion': False}",2,2,2,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 80 years old. The patient's age is greater than or equal to 65 years, and so we add 1 point to the score, making the current total 0 + 1 = 1.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 1.
The concentration of BUN is 34.9 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 1 + 1 = 2.
The patient's respiratory rate is 18 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 2.
The patient's systiolic blood pressure is 120 mm Hg. The patient's diastolic blood pressure is 70 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 2.
The patient's CURB-65 score is 2."
6500,45,CURB-65 Score for Pneumonia Severity,risk,integer,pmc-7445494-1,Extracted,"A 20-year-old Nepalese male was admitted to our hospital after a 3-day history of a high fever and cough. He had been previously seen at another local clinic where he was diagnosed with influenza and treated with oral oseltamivir for the first 3 days. On the fourth day, he developed dyspnea and was admitted to our hospital on the same day. He did not have any relevant past history and had not been prescribed any medications. He came to Japan for employment almost five years ago with his parents and took his residence in Saitama Prefecture.
His vital signs on the day of admission were as follows: level of consciousness, E3V4M6/Glasgow Coma Scale; blood pressure, 100/72 mmHg; heart rate, 133 beats per minute; body temperature, 38.4 °C; respiratory rate, 24 breaths per minute; and peripheral capillary oxygen saturation level at an O2 flow rate of 2 liters per minute, 94%. Physical examination revealed lower respiratory sounds, and a few moist rales were heard in both lungs on chest auscultation. Laboratory data revealed a white blood cell (WBC) count of 700/mm3, a blood platelet count of 82,000/mm3, a C-reactive protein (CRP) level of 23.2 mg/dl, a blood urea nitrogen (BUN) level of 26.3 mg/dl, and a serum creatinine level of 2.2 mg/dl. The results of liver function tests were normal except for a lactate dehydrogenase (LDH) level of 618 IU/l. A chest computed tomography (CT) scan showed infiltrative and nodular shadows with pneumatocele formation in the right upper lobe ().
At first, we diagnosed severe bacterial pneumonia after influenza and septic shock and initiated the administration of lactate Ringer’s solution, noradrenalin infusion, and intravenous tazobactam/piperacillin (TAZ/PIPC) (4.5 g, 4 times daily) and azithromycin (AZM) (500 mg, once a day). However, his vital signs did not improve, and he developed respiratory failure requiring mechanical ventilation support. After rapid deterioration of his arterial oxygenation level, we introduced veno-veno extracorporeal membrane oxygenation support. Because gram-positive staphylococci were detected from sputum and blood samples collected on admission, we added linezolid (600 mg, 2 times daily, intravenously) on day 2. On the same day, we performed a bronchoscopy, which showed diffuse inflammatory changes and easy bleeding (). Therefore, we suspected necrotizing pneumonia caused by CA-MRSA. He underwent multidisciplinary treatment; however, his respiratory condition gradually worsened. Despite resuscitation efforts, he died of multiple organ failure on day 7. The isolates from the culture of blood and sputum samples on the day of hospital admission were MRSA strains TUM18988 and TUM18989. Additionally, his father, who lived with him in Japan, had a negative nasal swab test for MRSA.",What is the patient's CURB-65 score? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [20, 'years'], 'Systolic Blood Pressure': [100.0, 'mm hg'], 'Diastolic Blood Pressure': [72.0, 'mm hg'], 'Blood Urea Nitrogen (BUN)': [26.3, 'mg/dL'], 'respiratory rate': [24.0, 'breaths per minute'], 'Confusion': False}",1,1,1,"The CURB-65 Score criteria are listed below:

1. Confusion: No = 0 points, Yes = +1 point
2. BUN >19 mg/dL (>7 mmol/L urea): No = 0 points, Yes = +1 point
3. Respiratory Rate ≥30: No = 0 points, Yes = +1 point
4. Systolic BP <90 mmHg or Diastolic BP ≤60 mmHg: No = 0 points, Yes = +1 point
5. Age ≥65: No = 0 points, Yes = +1 point

The total CURB-65 score is calculated by summing the points for each criterion.

The CURB-65 score is current at 0 points.
The patient is 20 years old. The patient's age is less than 65 years, and so we add 0 points to the score, keeping the current total at 0.
Because the patient does not have confusion, 0 points are added to the score, keeping the score at 0.
The concentration of BUN is 26.3 mg/dL. The patient's BUN concentration is greater than 19 mg/dL and so we add 1 point to score making the current total 0 + 1 = 1.
The patient's respiratory rate is 24 breaths per minute. Because the respiratory rate is less than 30 breaths per minute, 0 points are added to the score, keeping the current total at 1.
The patient's systiolic blood pressure is 100 mm Hg. The patient's diastolic blood pressure is 72 mm Hg. For a point a point to be added, the systiolic blood pressure must be less than 90 mm Hg or the diastolic blood pressure must be less than or equal to 60 mm Hg. Because neither of these statements are true, 0 points are added to score, keeping the current total to 1.
The patient's CURB-65 score is 1."
6501,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8610462-1,Extracted,"A 73-year-old female was brought by emergency medical services (EMS) to the emergency department (ED) after a motor vehicle collision (MVC). She was driving when her car crashed into a streetlamp at 40 miles per hour. The EMS team reported that the pole intruded into the passenger compartment and the patient required a prolonged extrication. She had a Glasgow Coma Scale score (GCS) of 11 when EMS arrived at the scene, which improved to a 15 after repeated evaluations. She was conscious, alert, and oriented at the scene and during transport.
The patient had difficulty recalling the events before the collision. She remembered feeling “like I was having a panic attack” just before the crash, and she did not recall the car impacting the streetlamp. In the ED, she complained of substernal chest pressure. The patient’s history was limited due to her continued difficulty recalling the events of the accident. The patient’s son was contacted and he stated that she lives alone and is active and independent. He stated that she had experienced syncopal episodes over the last several years, all associated with paroxysms of panic when driving, and she had undergone extensive workups without any clear etiology identified. She had magnetic resonance imaging (MRI) of her brain with and without contrast four years prior for stroke-like symptoms after a syncopal event. Per his report, no abnormalities were found.
The patient had a past medical history of anxiety, migraines, Hashimoto thyroiditis, and hyperlipidemia. She had been diagnosed with breast cancer in 2012, which was treated with a left mastectomy followed by five years of tamoxifen and letrozole treatment. She had a family history of dementia, diabetes, and heart disease. She denied using tobacco, alcohol, or illicit substances. She was prescribed, and was taking, the following medications: levothyroxine 25 micrograms daily; atorvastatin 20 milligrams (mg) nightly; rizatriptan 10 mg as needed for headaches; and multivitamins.
On physical exam, the patient’s temperature was 36.5° Celsius, her heart rate was 92 beats per minute, and her blood pressure was 142/72 millimeters of mercury. She was breathing at a rate of 21 breaths per minute with an oxygen saturation of 98% on room air. She weighed 125 pounds and was 5 feet, 3 inches tall, with a body mass index of 22.1 kilograms per meter squared. She did not appear to be in any acute distress, was healthy appearing, and was oriented to her name, date, and location. Her head was normocephalic and atraumatic; she had no Battle sign, raccoon eyes, or other signs of trauma. She had hearing aids in place bilaterally. She had normal extraocular movements with equal pupils that were reactive to light. She had a cervical collar in place. Later, when it was safe to remove her collar, her neck had a normal range of motion without rigidity or pain.
On auscultation, her heart had a regular S1 and S2 at a normal rate and was without murmurs. She had normal pulses bilaterally. Her lungs were clear without wheezing or rhonchi, and she was noted to have normal effort without respiratory distress. Her abdomen was soft and flat, without tenderness or guarding. Her musculoskeletal exam showed an overall normal range of motion without deformities. She had no step-offs of the spinous processes or tenderness along the midline spine. The remainder of her skeletal exam only revealed tenderness over the left wrist. She had a capillary refill of less than two seconds. On her skin exam, she had minor contusions to the left upper chest near the axilla with superficial abrasions along the left wrist. She was not diaphoretic. Neurologically she had no cranial nerve deficits, with no motor weakness or sensory deficits peripherally. She had a normal gait and normal coordination as well. She could not recall her birth date and had slow verbalization with some word-finding difficulty. Psychiatrically, she was normal in mood and behavior.
Point-of care-ultrasound did not find evidence of free fluid within the abdominal or thoracic cavities and was negative for a pericardial effusion. Point-of-care ultrasound examination of her chest revealed normal lung sliding bilaterally. Chest radiograph showed no acute abnormalities. A radiograph of her pelvis showed no fracture or malalignment of the bones. A computed tomography (CT) of her head and brain showed no intracranial injury. A CT of the cervical spine and chest with contrast in the arterial phase was performed, which showed normal vertebral body height and alignment without fracture. The CT did show some mild atherosclerosis of the carotid and vertebral arteries, but no vascular injury and no obvious narrowing. Her trachea and mainstem bronchi were patent, she had no mediastinal abnormalities, the thoracic aorta was normal in appearance, and she had no pericardial effusion or pneumothorax ().
A CT of her abdomen and pelvis with contrast in the venous phase was also performed, which showed patent vasculature including a normal caliber aorta and inferior vena cava, normal appearing spleen, pancreas, adrenal glands and kidneys/ureters, a small hiatal hernia but otherwise normal appearing bowel, and no ascites or pneumoperitoneum. The radiologist did not find any fractures on her imaging or any soft tissue injuries. Initial laboratory studies (), laboratory studies after administration of intravenous fluids (), and the patient’s electrocardiograms (ECG) () are shown. A test was then performed and a diagnosis was made.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [73, 'years'], 'Heart Rate or Pulse': [92.0, 'beats per minute'], 'Hemoptysis': False, 'O₂ saturation percentage': [98.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': True, 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 73 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 92.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
Hence, the number of PERC rule criteria met by the patient is 3."
6502,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-4928,Extracted,"A 34-year-old woman is assaulted and suffers a number of stab wounds to her abdomen. Bystanders call paramedics and she is subsequently taken to the nearest hospital. On arrival to the emergency department, her vitals are T: 36 deg C, HR: 110 bpm, BP: 100/60, RR: 12, SaO2: 99%. A FAST and abdominal CT are promptly obtained which are demonstrated in Figures A and B, respectively. Her chart demonstrates no other medical problems and vaccinations/boosters up to date. The patient is diagnosed with a Grade V splenic laceration and is immediately brought to the OR for emergent splenectomy. The splenectomy is successfully performed with removal of the damaged spleen (Figure C).",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [34, 'years'], 'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'O₂ saturation percentage': [99.0, '%'], 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 34 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 110.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6503,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-5965117-1,Extracted,"A 66-year-old man with a history of hypertension and hyperlipidemia was brought to the ED for altered mental status. The patient’s wife reported that two hours prior to arrival, he had ingested two glasses of wine and took a nap. Prior to napping the wife noted no unusual symptoms. Upon awaking, he was noted to have dysarthria and discoordination of his extremities and was brought to the ED. His wife reported that his home medications included bupropion, dutasteride, lisinopril, and tolterodine.
His vital signs were blood pressure 115/78 millimeters mercury, heart rate 83 beats per minute, respiratory rate 16 breaths per minute, temperature 36.8° Celsius, and oxygen saturation of 95% on room air. On exam, the patient was noted to have waxing and waning alertness, but he could intermittently answer questions and follow commands. His pupils were reactive, sluggish, and with horizontal and vertical nystagmus. His face was symmetric and his tongue was midline. His speech was dysarthric. He was unable to follow commands for strength testing, but he was moving all extremities without appreciable asymmetry. He had bilateral dysmetria on finger-to-nose and heel-to-shin testing. He had truncal ataxia in the seated position. His mental status and ataxia progressively worsened during his ED stay of approximately 1.5 hours.
Given the acute onset of symptoms, an institutional stroke alert was activated and a head computed tomography angiogram was obtained, which was negative for hemorrhage or other abnormality. Laboratory values, including complete blood count, chemistry panel, coagulation panel, and urinalysis were within normal limits. His blood alcohol level was 57 mg/dL. Electrocardiogram showed normal sinus rhythm with a QRS of 108 ms and a QTc of 497 ms. A dose of naloxone 0.4 milligrams was trialed without improvement in patient’s somnolence. He was evaluated by the neurology consultant team and determined to have a National Institute of Health Stroke Scale of 11. Given concern for a posterior circulation stroke, tissue plasminogen activator was administered for thrombolysis. The patient was subsequently intubated for airway protection due to increasing somnolence and admitted to the intensive care unit (ICU).
While intubated in the ICU, the patient developed status epilepticus, characterized by three periods of generalized tonic clonic activity, each lasting approximately five minutes. He received multiple doses of benzodiazepine and phenytoin, in addition to the propofol infusion for sedation, resulting in cessation of seizure activity. Subsequent electroencephalogram did not demonstrate ongoing seizure activity, and the patient did not have an additional seizure during the hospital course while maintained on phenytoin.
Magnetic resonance imaging of the brain did not show evidence of acute stroke. Comprehensive urine drug screen by gas chromatography and mass spectrometry was positive for clozapine and clozapine metabolites, in addition to caffeine and bupropion, a home medication. No drugs of abuse or other medications were detected. However, the patient had never been prescribed clozapine. In discussion with his wife, it was learned that the patient’s family member takes clozapine for a psychiatric condition. The patient manages the family member’s medication and they frequently take their respective medications at the same time. It was concluded that the patient must have mistaken the family member’s medication for his and accidently ingested the family member’s usual dose of 200 mg of clozapine, hours prior to his presentation. The patient was extubated on hospital day three and discharged with a normal neurologic exam and no further seizure activity on hospital day five.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [66, 'years'], 'Heart Rate or Pulse': [83.0, 'beats per minute'], 'O₂ saturation percentage': [95.0, '%'], 'Hormone use': False, 'Unilateral Leg Swelling': False, 'Recent surgery or trauma': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 66 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 83.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 95.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6504,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4908703-1,Extracted,"A 78-year-old female with a past medical history significant for breast cancer and moderate COPD presented to Emergency Department with syncope. Nine months prior to admission, she underwent left total mastectomy for invasive ductal carcinoma and was started on Tamoxifen 20 mg daily. Home medications included GB 50 mcg once daily, Salbutamol, calcium and a multi-vitamin. GB was started 3 months prior to her presentation for syncope.
The day prior to admission, she received an IV vitamin infusion consisting of a mixture of thiamine, folic acid, multivitamin and magnesium sulfate at a naturopath clinic. Shortly after completion of the IV infusion, she developed emesis and took 2 tablets of dimenhydrinate. The following day, she reported dizziness as she walked across the kitchen and passed out after sitting in a chair. The patient reported no palpitations, chest discomfort, nausea, warm sensation or diaphoresis prior to the syncope event. She was not witnessed to have any seizure like activity and when she regained consciousness, reported immediate awareness of surroundings with no neurological deficits, no tongue biting, bowel or urinary incontinence. There was no previous history of syncope and no family history of sudden cardiac death. Her initial blood pressure in the ambulance was 70/50 mm Hg. Hemodynamics normalized after administration of intravenous fluid and her symptoms resolved. Oxygen saturation was above 97 % and telemetry revealed normal sinus rhythm with a heart rate of 77. Precordial examination was unremarkable with regular normal heart sounds and no murmurs. In the Emergency Department, blood tests including complete blood count (CBC), serum electrolytes (potassium, calcium, magnesium), glucose, creatinine and thyroid stimulating hormone were normal. Electrocardiogram (ECG) showed a corrected QT interval using Fridericia (QTcF) and Bazett’s formula (QTcB) of 603 and 631 ms respectively (Fig. ) and she was admitted to the cardiology service for further investigation of the etiology for her QT prolongation.
Prior to starting Tamoxifen her QTcF and QTcB were 439 and 440 ms respectively (Fig. ), however no ECG was obtained after initiation of Tamoxifen and prior to starting GB. Her last dose of Tamoxifen and GB were the day of admission with both medications discontinued at presentation.
An echocardiogram revealed that her left ventricular ejection fraction was >60 % with no valvular or regional wall motion abnormalities. Serial electrocardiograms demonstrated corrected QTcF and QTcB respectively of 603 and 631 ms day 0, 496 and 514 ms day 1, and 446 and 455 ms on day 2 and 442 and 460 ms on day 3 (Fig. ). There were no arrhythmias seen on telemetry. Syncope was felt to be secondary to orthostatic changes and she was discharged on day 3 after admission.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [78, 'years'], 'Hormone use': True, 'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [77.0, 'beats per minute'], 'Hemoptysis': False, 'O₂ saturation percentage': [97.0, '%'], 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 78 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 77.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 97.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'recent surgery or trauma'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
Hence, the number of PERC rule criteria met by the patient is 2."
6505,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8186916-1,Extracted,"A 40-year-old previously healthy man with a past medical history only notable for a body mass index of 27 presented to the Emergency Department (ED) with several days of fever and cough. He tested positive for SARS-CoV-2 on polymerase chain reaction (PCR) nasopharyngeal swab. His vital signs on examination were notable for a heart rate of 110 beats per minute and a temperature of 38.2°C. His chest X-ray was unremarkable. Given his clinical stability, further labwork was deferred and the patient was discharged from the ED to self-quarantine at home. Over the subsequent 3 weeks, the patient’s symptoms completely resolved. He had repeat COVID-19 testing prior to returning to work, which was negative.
Two months after his negative COVID-19 testing, the patient developed progressive dyspnoea with minimal exertion. He had an episode of syncope which prompted him to return to the ED for further evaluation. On presentation, his blood pressure was 126/99 mmHg, heart rate 122 beats per minute, temperature 37.5°C, and oxygen saturation 97% on room air. Physical examination was notable for tachycardia with regular rhythm, 3/6 holosystolic murmur at the lower left sternal border, positive jugular venous distention to 10 cm, lungs clear to auscultation bilaterally, and no evidence of lower extremity oedema.
Labwork was significant for a troponin of 0.12 ng/mL (normal < 0.02 ng/mL), brain natriuretic peptide of 1321 pg/mL (normal < 100 pg/mL), lactate 2.5 mm/l (normal 0.9–1.7 mm/l), and a D-dimer of 19 014 ng/mL fibrinogen equivalent units (FEU) (normal < 100 ng/mL FEU). Electrocardiogram revealed sinus tachycardia with an S1Q3T3 pattern (see ). Given the significantly elevated D-dimer and history of SARS-CoV-2 infection, a computed tomography angiogram with PE protocol was obtained that demonstrated acute bilateral PE described as a central obstructive clot with acute thrombus and a high obstructive score as defined by a modified Miller score of 15 (see ). Bedside echocardiography revealed severe right ventricular (RV) enlargement (6.5 cm) (), positive McConnell’s sign, moderate to severe tricuspid regurgitation (), right ventricular outflow tract velocity time integral (RVOT VTI) of 6.69 cm (normal > 10 cm) (), tricuspid annular plane systolic excursion of 10 mm (normal > 18 mm) (), and an right ventricular:left ventricular ratio of 2.4 (normal < 1) (). Repeat SARS-CoV-2 PCR testing returned positive, and the patient was admitted to the coronary care unit on a heparin infusion.
After a multidisciplinary pulmonary embolism response team discussion, it was recommended that the patient be escalated to catheter-directed thrombolysis given the multiple high-risk features for acute decompensation. Unfortunately, prior to the procedure the patient had an episode of bradycardia and hypoxia followed immediately by cardiopulmonary arrest with pulseless electrical activity (PEA). Cardiopulmonary resuscitation was immediately initiated and full-dose systemic alteplase was administered. Cardiothoracic surgery was consulted for consideration of veno-arterial extracorporeal membrane oxygenation. Unfortunately, return of spontaneous circulation was unable to be achieved due to persistent PEA and asystole.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [40, 'years'], 'Heart Rate or Pulse': [122.0, 'beats per minute'], 'Hemoptysis': False, 'O₂ saturation percentage': [97.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Previously Documented Pulmonary Embolism': True, 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 40 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 122.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 97.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is reported to have been diagnosed with pulmonary embolism in the past. At least one of the criteria is met and so we increment the criteria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6506,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-5771133-1,Extracted,"An 84-year-old woman presented to our hospital with complaints of a 1-week history of abdominal pain and appetite loss. The patient had no history of cough, sputum, fever, chills, weight loss, or night sweats. She had no history of tobacco smoking, tuberculosis or exposure to individuals with tuberculosis. She did not have a history of malignancy, diabetes mellitus, cytotoxic therapy or corticosteroid use. Her family history was unremarkable. Physical examination revealed a heart rate of 90 beats/min, blood pressure of 157/76 mmHg, respiratory rate of 24 breaths/min, temperature of 37.8 °C and oxygen saturation of 98% on room air. Respiratory, cardiac and abdominal examination were unremarkable. Chest radiograph showed multiple small nodules in both lung fields and chest computed tomography (CT) showed diffuse micronodules in random patterns in both lung lobes, cardiomegaly and bilateral pleural effusion (Figs. and ). White blood cell count, C-reactive protein and procalcitonin levels were 2800 /μl, 7.50 mg/dl (normal range 0.00–0.10 mg/dl) and 0.373 ng/ml (normal range 0.000–0.046 ng/ml), respectively. Serum carcinoembryonic antigen, carbohydrate antigen 19–9 and soluble IL-2 receptor were elevated at 9.4 ng/ml (normal range 0.0–5.0 ng/ml), 188.4 U/ml (normal range 0.0–37.0 U/ml) and 6163 U/ml (normal range 0–500 U/ml), respectively. Angiotensin-converting enzyme, mycoplasma antibody and blood sugar were within normal ranges. Serum QuantiFERON testing was positive. CD4/8 ratio, CD4 count and CD8 count were 1.73 (normal range 0.6–2.9), 422 /μl (normal range 344–1289) and 244 /μl (normal range 110–1066), respectively. IgG, IgA and IgM were 998 mg/dl (normal range 870–1700), 128 mg/dl (normal range 110–410), 59 mg/dl (normal range 46–260), respectively. Testing for human immunodeficiency virus infection was negative. Expectorated sputum smears were negative for bacteria and acid-fast bacilli. Urinary antigen testing (Binax NOW; Binax, Inc., Portland, ME) for Streptococcus pneumoniae and Legionella pneumophila was negative. According to these results, we initially suspected intraabdominal malignancy including malignant lymphoma. However, abdominal CT and magnetic resonance imaging showed no abnormalities. Therefore, we suspected miliary tuberculosis or pulmonary sarcoidosis. Liver, skin and bone marrow biopsies were subsequently performed and showed epithelioid cell granuloma without caseous necrosis. Gastric aspirate smear was positive for acid-fast bacilli and polymerase chain reaction (Loopamp; Eiken Chemical Co., Ltd. Tokyo, Japan) was positive for Mycobacterium tuberculosis. Although these microbiological findings might indicate the presence of non-viable M. tuberculosis, miliary tuberculosis was suspected and antimycobacterial therapy [oral isoniazid (INH) 200 mg/day, rifampicin (RFP) 300 mg/day and ethambutol (EB) 500 mg/day] was initiated on hospital day 12. Gastric aspirate culture was positive for M. tuberculosis after 1 week of culture. After a 2-month treatment course, chest radiograph showed gradual improvement, oral EB was discontinued and the patient was discharged. Although INH and RFP therapy was continued, chest radiograph showed new multiple nodules in the right middle lung field after a 6-month treatment course. Chest CT showed that a right S6 small nodule, presumed to be miliary tuberculosis, had increased and new multiple nodules appeared in the right lower lobe (Fig. ). The patient’s white blood cell count and C-reactive protein at this time were 2400 /μl and 0.09 mg/dl, respectively. Flexible fiberoptic bronchoscopy was subsequently perfomed. Microbiological testing of bronchial lavage fluids did not reveal any bacteria, mycobacteria or fungi. However, cytology showed a small number of Periodic acid-Schiff-positive bodies, suggesting Cryptococcus species (Fig. ). Moreover, serum cryptococcal antigen testing (Serodirect “EIKEN” Cryptococcus; Eiken Chemical Co., Ltd. Tokyo, Japan) was positive (×128). According to these findings, pulmonary cryptococcosis was diagnosed, although the culture was negative. Oral fluconazole (FLCZ; 300 mg/day) was subsequently initiated. After a 6-month treatment course, chest radiograph showed gradual improvement and oral FLCZ was discontinued. The patient received a total of 12 months of antimycobacterial therapy. On follow-up, she has remained asymptomatic with suspect to pulmonary disease, with no recurrence.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [84, 'years'], 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 84 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 90.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6507,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-5063,Extracted,"An 18-year-old girl comes to the emergency room with abdominal pain. She states that the pain started 6 hours ago, is 8/10, and localizes to the right lower abdomen. She recalls a similar episode last month. Her older brother was hospitalized 2 years ago for perforated appendicitis. Her mother has diverticulitis. The patient got her first menstrual period at age 14. Her periods occur regularly every 28 days. Her last menstrual period was 2 weeks ago. She is sexually active with multiple partners and uses condoms inconsistently. The patient’s temperature is 99°F (37.2°C), blood pressure is 110/74 mmHg, pulse is 89/min, and respirations are 14/min with an oxygen saturation of 98% on room air. On physical exam, the patient is in moderate distress. There is lower abdominal tenderness with guarding. A pelvic examination reveals clear mucous in the vaginal introitus, a mobile uterus, and tenderness of the right adnexa. Labs are obtained, as shown below:

Leukocyte count: 10,000/mm^3 with normal differential
Hemoglobin: 13.5 g/dL
Platelet count: 200,000/mm^3
Beta-human chorionic gonadotropin: Pending

A pelvic ultrasound demonstrates a small fluid collection in the cul-de-sac posterior to the uterus.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [18, 'years'], 'Heart Rate or Pulse': [89.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Recent surgery or trauma': False, 'Hormone use': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",0,0,0,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 18 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 89.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 0.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 0.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 0.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
Hence, the number of PERC rule criteria met by the patient is 0."
6508,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4918863-1,Extracted,"History: A 37-year old female with history of migraine and recent diagnosis of hypertension presented to the ED complaining of chest pressure and dyspnea on exertion for two weeks prior to presentation. She described pressure in the sternal area of her chest, constant, 7/10, radiating to her back, her jaw and her right arm. Patient reported being admitted to a nearby hospital with similar symptoms a month earlier. She had a transient left bundle branch block (LBBB) on her electrocardiogram and was worked up for acute coronary syndrome. Her cardiac biomarkers were negative, and she underwent a stress echocardiogram during which she exercised for 6 minutes on a Bruce protocol, achieving 7.1 metabolic equivalents (METS), and had normal left ventricular chamber size diminution and a normal baseline ejection fraction (~65 percent). Exercise was stopped secondary to fatigue, and the only concerning finding was that she had septal hypokinesis that was read as possible ischemia versus a consequence of her LBBB.
On the basis of her abnormal stress echocardiogram she also underwent stress perfusion imaging that showed possible anterior ischemia – again in the setting of her LBBB. On this basis she underwent a coronary angiography at the local hospital that revealed no obstructive coronary disease. She was discharged home, with a diagnosis of non-cardiac chest pain.
Over the next week, patient’s symptoms worsened with chest pain radiating down right arm, associated with profound fatigue, dizziness, lightheadedness, tingling in the jaw. These symptoms disrupted her work as a postal worker and brought her to the second emergency department for evaluation.
Past Surgical History: Right lower leg surgery for fracture, left ear surgery, laparoscopy, tonsillectomy.
Medications: Aspirin 81 mg, multivitamins.
Allergies: Bactrim, cephalosporins.
Family History: Mother had angioplasty at age 39, maternal grandfather with MI at 38, deceased from myocardial infarction (MI) at 42. Second cousin passed from massive MI at age 45.
Social History: Denies any current/past use/abuse of tobacco, alcohol, or illicit drugs. She was married with one child and worked full time.
Height/Weight/BMI: 5'4"", 160 pounds, body mass index of 27.5.
Physical Exam: Patient appeared well in no distress. Vitals: Blood pressure 113/63 | Pulse 85 | Temperature 98.9 °Fahrenheit (Oral) | Respiration 18 | Oxygen saturation 98%. She had no jugular venous distention. Cardiovascular exam showed normal rate, regular rhythm, normal heart sounds and intact distal pulses. Chest exam showed normal effort and breath sounds normal. She exhibited no chest wall tenderness. Her neurological exam showed alert woman with normal speech and no focal findings.
Patient was admitted to the ED chest pain observation unit for further evaluation.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [37, 'years'], 'Heart Rate or Pulse': [85.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 37 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 85.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 0.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
Hence, the number of PERC rule criteria met by the patient is 0."
6509,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-2741488-1,Extracted,"A 66-year-old Caucasian man with no significant past medical history presented with flu-like symptoms, progressively worsening shortness of breath, difficulty in breathing (NYHA class III) and dry cough over the past 2 weeks prior to presentation. He denied any fever, chills, sputum production, orthopnea or paroxysmal nocturnal dyspnea, anorexia, weight loss, recent or past exposure to tuberculosis, sick contacts, pets, recent travel or past exposure to cigarette smoke (active or passive), asbestos, silica, coal dust or chemicals. He maintained an active lifestyle walking 5 miles three times a week without overt dyspnea. He had no prior history of connective tissue disease or HIV and denied any history of skin rash or joint pains. Past surgical, social and family histories were non-contributory. He also had no history of prior use of any long term medications. He had presented to the hospital 4 days prior to present admission and a provisional diagnosis of community acquired pneumonia was made based on chest radiograph findings and he was discharged home on 2L of oxygen and Levofloxacin, but came back to the hospital due to lack of obvious improvement.
On examination, he appeared tired with shortness of breath. The temperature was 99.9°F, the pulse 124/min, respiratory rate 26/min and oxygen saturation of 86% on 2L. Skin was diaphoretic. There was no evidence of rash, pallor, lymphadenopathy, clubbing, joint swelling or edema. Auscultation of chest revealed diminished breath sounds with bilateral velcro-like fine inspiratory crackles. Laboratory studies showed a normal complete blood count, metabolic panel, liver function tests, cardiac enzymes, BNP, lactate, PT/INR, aPTT, fibrinogen and TSH. D-dimer was elevated at 15.4 (normal <1.6). ESR was 52 mm/hour. Rheumatoid factor was <5 (negative). ANA, p-ANCA and c-ANCA were negative. Blood cultures (bacterial/fungal/mycobacterial), urine legionella and streptococcal antigen were negative. Viral respiratory panel, including cytomegalovirus & Herpes Simplex Virus PCR were also negative. ABG showed hypoxemia with respiratory alkalosis. Pulmonary function tests showed restrictive pattern of lung disease. Transthoracic echocardiogram showed normal cardiac chamber sizes and left ventricular ejection fraction of 81%.
Plain chest radiograph (Fig. ) showed bilateral basilar infiltrates and a peripheral reticulonodular pattern superimposed on generalized interstitial changes, involving the upper lobes as well as lung bases. High Resolution Computed Tomography (HRCT) of the chest (Fig. and ) revealed moderate to severe thickening of intralobular septa, septal line formation, parenchymal band formation and peribronchial thickening, ground glass opacities and mild mediastinal lymphadenopathy (likely reactive, largest lymph node being 1.1 cm) was noted. This was consistent with idiopathic interstitial pneumonia (IIP) without a specific pattern. At this time, treatment with levofloxacin was continued and solumedrol was added for empirical therapy. Computed Tomogram (CT) of the abdomen/pelvis was normal with no evidence of retroperitoneal lymphadenopathy. Despite steroid therapy, the patient's respiratory status deteriorated over the next day requiring intubation and mechanical ventilation. Consequently, consent for wedge biopsy of the lung was obtained for a pathological diagnosis to guide further therapy.
A right lung wedge biopsy was obtained by video-assisted thoracoscopic surgery (VATS). A polymorphic lymphoid infiltrate composed of large atypical cells, small lymphocytes and many plasma cells was noted, with lymphoid cells infiltrating blood vessels and bronchial walls (Fig. ). Multinucleated large Reed Sternberg-like cells were also present along with foci of necrosis. Bronchial washings showed atypical benign bronchial cells and pulmonary macrophages with a few rare atypical Reed-Sternberg-like cells. Bone marrow biopsy was normal.
Immuno-histochemical studies of lung tissue showed predominance of T cells expressing CD3, CD5 and CD43 with a smaller population of large atypical cells expressing CD20 and CD79a (B cell markers) (Fig. ). Many CD138+ plasma cells exhibiting polyclonal staining pattern for kappa and lambda immunoglobulin light chains were also seen. Bone marrow biopsy revealed normal cellularity with no evidence of lymphoma. In situ hybridization for EBV encoded RNA (EBER) was positive within scattered large lymphoid cells throughout the biopsy specimen (Fig. ).
Based on the pathological and immuno-histochemical findings, a diagnosis of Lymphomatoid Granulomatosis was made. Treatment with high dose steroids and rituximab showed significant clinical improvement and he was extubated 4 days after starting therapy. Treatment was continued with cyclophosphamide, vincristine, doxorubicin and prednisolone chemotherapy and he showed gradual but slow resolution of clinical and x-ray findings. However, he subsequently developed pancytopenia consequent to chemotherapy, septic shock requiring increasing doses of pressors and acute renal failure which did not respond to aggressive management and he was terminally weaned per family wishes 4 weeks later. A chest-only autopsy revealed diffuse alveolar damage, likely secondary to sepsis or chemotherapy or both, but no evidence of residual LG was noted within the lungs (Fig. ).",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [66, 'years'], 'Heart Rate or Pulse': [124.0, 'beats per minute'], 'O₂ saturation percentage': [86.0, '%'], 'Hemoptysis': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Recent surgery or trauma': False, 'Hormone use': False, 'Unilateral Leg Swelling': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 66 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 124.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 86.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 2 + 1 = 3.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6510,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-791,Extracted,"A 55-year-old man is brought to the emergency department 30 minutes after the sudden onset of severe, migrating anterior chest pain, shortness of breath, and sweating at rest. He has hypertension, hypercholesterolemia, and type 2 diabetes mellitus. Medications include atorvastatin, hydrochlorothiazide, lisinopril, and metformin. He has smoked one pack of cigarettes daily for 25 years. He is in severe distress. His pulse is 110/min, respirations are 20/min, and blood pressure is 150/85 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 98%. Cardiac examination shows a grade 3/6, high-pitched, blowing, diastolic murmur heard best over the right sternal border. The lungs are clear to auscultation. Femoral pulses are decreased bilaterally. An ECG shows sinus tachycardia and left ventricular hypertrophy.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Hormone use': False, 'Unilateral Leg Swelling': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 55 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 110.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6511,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-5214,Extracted,"A 59-year-old man presents to the emergency department with a sudden-onset sensation that the room is spinning causing him to experience several episodes of nausea and vomiting. Upon arriving, the patient’s symptoms have resolved. He states his symptoms occurred as he was going to bed. He has never experienced this before, but felt extremely dizzy for roughly 3 minutes. He currently feels at his baseline. The patient is otherwise healthy and only has a history of eczema. His temperature is 97.7°F (36.5°C), blood pressure is 134/85 mmHg, pulse is 85/min, respirations are 13/min, and oxygen saturation is 98% on room air. Physical exam is notable for a healthy man with a normal gait. The patient has a physiologic nystagmus and his cranial nerve exam is unremarkable. The patient’s head is turned to the left and he is laid back on the stretcher, which exacerbates severe symptoms with a nystagmus notable. The patient’s symptoms improve after 2 minutes of being in this position.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [59, 'years'], 'Heart Rate or Pulse': [85.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 59 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 85.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6512,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-1802,Extracted,"Four days after undergoing a Whipple procedure for newly-diagnosed pancreatic cancer, a 65-year-old man has shortness of breath. His surgery was complicated by bleeding for which he required intraoperative transfusion with 4 units of packed red blood cells and 1 unit of platelets. His temperature is 38.8°C (101.8°F), pulse is 110/min, respirations are 26/min, and blood pressure is 95/55 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 85%. Cardiac examination shows normal heart sounds and no jugular venous distention. Auscultation of the lungs shows diffuse crackles bilaterally. The extremities are warm and there is no edema. Laboratory studies show a leukocyte count of 17,000/mm3 and hemoglobin concentration of 9.8 g/dL. Arterial blood gas on room air shows:
pH 7.35
PaO2 41 mm Hg
PaCO2 38 mm Hg
HCO3- 25 mEq/L
The patient is intubated and mechanical ventilation is initiated. An x-ray of the chest is shown. Transthoracic echocardiography shows a normally contracting left ventricle.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [65, 'years'], 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'O₂ saturation percentage': [85.0, '%'], 'Recent surgery or trauma': True, 'Unilateral Leg Swelling': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",4,4,4,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 65 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 110.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 85.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 2 + 1 = 3.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 3 + 1  =  4.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 4.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 4.
Hence, the number of PERC rule criteria met by the patient is 4."
6513,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4008028-1,Extracted,"A 28-year-old woman gave birth to a healthy male infant following a normal, uneventful vaginal delivery (gravida 10, para 8). The patient was admitted to the emergency department six days postpartum with the acute onset, two hours prior, of substernal chest pain radiating to the left arm and interscapular region. The patient had no coronary risk factors such as hypertension, diabetes, or dyslipidemia, had no family history of heart disease, and did not have a history of oral contraceptive use. She did not smoke and did not use alcohol or drugs.
On physical examination, her blood pressure was 110/65 mmHg and her heart rate 89 beats/min, temperature of 37.2°C, and oxygen saturation of 94%. Auscultation of heart and lung fields was normal. Physical examination revealed no signs of heart failure. Chest X-ray was normal. Electrocardiography demonstrated the presence of ST-segment elevation in leads I, aVL (both 1 mm) and V1–V5 (all 3 mm), along with reciprocal ST segment depression in leads II, III, and aVF (all 2 mm). The initial laboratory analyses were within normal limits.
Subsequent cardiac catheterization revealed spontaneous dissection of the left anterior descending artery (LAD) (). There was a 80% stenosis of the true lumen of the mid-LAD caused by external compression by the hematoma in the false lumen. The right coronary artery (RCA) and left circumflex artery (LCX) were angiographically normal. The patient underwent percutaneous transluminal coronary angioplasty with bare-metal stent (3.0 × 18 mm) placed in the LAD (). We continued with low-molecular-weight heparin, clopidogrel, ramipril, metoprolol, and aspirin. The patient was discharged with good hemodynamic balance on the fourth day after admittance. One month after the control examination, the patient had no chest pain at all. Follow-up echocardiography revealed normal left ventricular function.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [28, 'years'], 'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [89.0, 'beats per minute'], 'Hemoptysis': False, 'O₂ saturation percentage': [94.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 28 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 89.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 94.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6514,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-5637961-1,Extracted,"A 17-year-old female presented with 1-month history of more noticeable weight loss and increased tiredness. Over the last 6 years since immigrating to the United States with her family from Burma and going through puberty, her body habitus has changed to a very thin appearance. This period of time began with menarche, which subsequently demonstrated intermittent oligomenorrhea occasionally alternating with amenorrhea. Apparently, workup by a gynecologist was negative and a yearlong period of oral contraceptive use did little to change the scant flow pattern. She discontinued these 6 months ago. The patient’s diet history revealed 3 meals a day of normal type foods but always smaller portions than other members of her family. Mother agreed that she does not eat much fried or fast foods, usually what is prepared for the family at home. The patient eventually suggested after repetitive questions that there was an increase in early satiety over the last month and she clearly was overall more tired. Five months ago, she had an outpatient visit for viral syndrome with vomiting and diarrhea, which resolved in 48 hours. At that time, her weight was 42 kg and no fever noted. Review of systems was notable for fatigue, intermittent chills, hair loss with nonvigorous brushing, intermittent “shakiness” when getting up, and shortness of breath on exertion. She denied any fever, upper respiratory tract infection symptoms, coughing, nausea, vomiting, dysuria, abdominal pain other than associated with her menstrual cycle, rashes, easy bruising or bleeding. Her past medical history was notable for the oligomenorrhea and scoliosis, but prior testing for anemia reported negative 6 months ago, and all chronic diseases, including in other members of the family, was denied, including anemia, thalassemia, and tuberculosis. The patient reports feeling “sad sometimes” but denied any suicidal or homicidal ideation. In the emergency department, her physical exam (PE) was notable for a tired appearing but otherwise well teenage girl with a temperature of 101.6°F, heart rate 125, respiratory rate 16, pulse oxygenation saturation of 97% on room air, weight 40 kg, height 144.78 cm, body mass index 20.1, some hair loss with brushing, II/VI systolic murmur over LUSB, and mild nonpitting bilateral edema. The remainder of the PE was unremarkable. Laboratory values were remarkable for white blood cell count 4700/µL with neutrophilic predominance, hemoglobin 7.3 g/dL, hematocrit 24.8%, mean corpuscular volume 74.9 fL, red cell distribution width 18.4%. Chemistry panel was within normal limits except for low albumin 2.9 g/dL, and a slightly elevated aspartate transaminase 54 U/L. Thyroid studies demonstrated slightly elevated thyroid-stimulating hormone of 6.68 mIU/L (05-6.0) with normal free T4 of 1.08 ng/dL (0.7-1.9). C-reactive protein and erythrocyte sedimentation rate were elevated to 65.4 mg/L (normal 0-5) and 132 mm/h (normal 0-20), respectively. Urinalysis was unremarkable and urine pregnancy test was negative. Additional iron studies demonstrated levels of iron 29 µg/dL, ferritin 3 ng/mL, and a total iron binding capacity of 144 µg/dL. Given the severe anemia and elevated inflammatory markers, the decision was made to admit the patient for further workup.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [17, 'years'], 'Heart Rate or Pulse': [125.0, 'beats per minute'], 'O₂ saturation percentage': [97.0, '%'], 'Hormone use': True, 'Recent surgery or trauma': False, 'Unilateral Leg Swelling': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 17 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 125.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 97.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
Hence, the number of PERC rule criteria met by the patient is 2."
6515,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-5788,Extracted,"A 62-year-old woman presents to the emergency department after an episode of light-headedness. She was using the bathroom when she felt light-headed and fell to the floor. Her daughter found her and brought her into the emergency department right away. The patient has a past medical history of obesity and diabetes mellitus. She came to the emergency department 1 week ago for a similar complaint. The patient states that she has otherwise felt well with the exception of fatigue, constipation, an odd sensation in her chest, and a decreased appetite and desire to drink recently causing her to lose 10 pounds. Her temperature is 98.0°F (36.7°C), blood pressure is 122/88 mmHg, pulse is 92/min, respirations are 14/min, and oxygen saturation is 99% on room air. Physical exam reveals a cardiopulmonary exam within normal limits and stable gait. The patient has an obese abdomen with abdominal distension. Strength is 5/5 in the upper and lower extremities.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [62, 'years'], 'Heart Rate or Pulse': [92.0, 'beats per minute'], 'O₂ saturation percentage': [99.0, '%'], 'Hemoptysis': False, 'Unilateral Leg Swelling': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 62 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 92.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6516,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-6076,Extracted,"A 66-year-old man presents to the emergency department for a cough and fatigue. The patient was brought in from a nursing home with documentation stating that he has seemed confused for the past day according to the staff. The patient has a past medical history of diabetes and hypertension. He is currently taking insulin, metformin, lisinopril, and atorvastatin. His temperature is 102°F (38.9°C), blood pressure is 107/58 mmHg, pulse is 120/min, respirations are 15/min, and oxygen saturation is 98% on room air. Physical exam reveals crackles on pulmonary exam and S4 on cardiac auscultation.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [66, 'years'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Hormone use': False, 'Recent surgery or trauma': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 66 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 120.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6517,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8445139-1,Extracted,"A 56-year-old man presented to a peripheral hospital with a history of severe acute central chest pain accompanied by sweating. He has been suffering from diabetes mellitus for 3 years for which he was taking oral hypoglycemic agent (glibenclamide 5 mg, BID). However, he was not on regular follow-up. He was hypertensive for 3 years and for which he was on regular medication.
He was diagnosed with acute ST-segment elevation extensive anterior wall myocardial infarction and was given Streptokinase due to unavailability of reteplase/alteplase. Although the chest pain improved, his post lysis ECG showed poor resolution. However, next morning the ECG showed transient inferior leads ST elevation with fast atrial fibrillation (AF). He was given a bolus intravenous amiodarone (300 mg). While he was on amiodarone infusion, he became hypotensive and dobutamine was started at low dose (5 mcg/kg/min). Eventually, his case was discussed and it was decided he needed a tertiary care hospital. He was shifted with 12 hours for further management.
On arrival, his radial arterial blood pressure was 106/70 mmHg, mean arterial BP was 59 mmHg. He was maintained on low dose dobutamine. The PR was 96 b.p.m, in sinus rhythm. His urine output was 75 ml / hour. On physical examination, he had bilateral fine crepitation and a pan systolic murmur at the left lower sternal area, radiating to the right precordium. Further examination showed the jugular venous pulse was mildly raised but no lower leg edema and warm touch. Oxygen saturation was 98% on 4 L/min oxygen facemask.
Electrocardiography [] revealed sinus rhythm with persistent ST-segment elevation in the anterior (V1-V6) with established Q-waves in anterior leads. Chest X-ray [] showed bilateral mild pulmonary congestion.
Transthoracic echocardiography revealed multiple (2–3 mm) apical muscular ventricular septal defects (VSD) with the largest VSD measuring 1 cm [], and a left to right shunt []. Left ventricular (LV) systolic function was mildly impaired with an ejection fraction of 45%. The left ventricular apex was akinetic. There was Grade-I diastolic dysfunction with normal right side dimension and functions. There was no significant valvular regurgitation or stenosis, but there was moderate pericardial effusion measuring 1.6 cm posteriorly and 1.1 cm anteriorly []. There was no sign of cardiac tamponade. The results of the biochemical Labs were unremarkable except for mild renal impairment (creatinine 105 mmol/L, eGFR-65) and raised Troponin T (364 pg/ml). Lactate level was 2.1mmol/L.
Coronary angiography (CAG) revealed the left anterior descending artery had tight lesions in the proximal (95%) and mid segment (85%) with diffusely diseased distal LAD []. Right coronary had proximal 30% stenosis; the right posterior descending artery had ostial (90%) lesion []. There was non-significant lesion at distal left circumflex artery. LV Angiography showed Apical VSR with LV to RV flow [Figure and ].
His Society for Cardiovascular Angiography and Intervention (SCAI) cardiogenic shock (CS) stage was determined to be Stage B. At this time cardiac surgeons were consulted, who advised to continue medical treatment with an intention to heal infarct area spontaneously and they would consider either for coronary artery bypass graft (CABG) plus VSD repair versus Percutaneous Coronary Intervention (PCI) plus device closure.
The patient was initially treated medically with intravenous diuretics, inotropes, and with oral aspirin and statin. Gradually, all inotropes were tapered off and he was clinically asymptomatic with stable hemodynamics without support of intra-aortic balloon pump (IABP). Later, low dose of lisinopril and carvedilol was added as vasodilators to reduce afterload.
Eventually, at the eighteenth day of admission, the patient underwent CABG (one venous graft to r-PDA) with simultaneous repair of VSD with Gortex patch with infarct exclusion technique. The LAD artery could not be grafted due to poor visualization hence dit was decided for PCI later if needed.
Postoperatively, the patient remained stable and was extubated the next day. Follow-up echocardiography revealed no residual intra-cardiac shunt. He was discharged on the 7th post-operative day in stable condition. Due to expatriate issue, a follow-up was arranged over telephone at 2 weeks. After two months, he was asymptomatic, hemodynamically stable and could perform routine daily activities. Later a clinic follow- up was arranged with echocardiography.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [56, 'years'], 'Heart Rate or Pulse': [96.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 56 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 96.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6518,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-6101341-1,Extracted,"A 70-year-old man presented with dyspnoea and palpitations on exertion to the emergency department (ED). His medical history was significant for stage IV clear cell RCC, chronic atrial fibrillation on anticoagulation with warfarin, coronary artery disease status post the placement of two stents with an ischaemic cardiomyopathy and a LVEF of 40%–45%. He was recently started on pazopanib for systemic treatment of metastatic RCC. Pazopanib was started at 75% of the recommended dose. At the initiation of therapy, the patient had a creatinine of 1.2 mg/dL and was able to walk 90 min a day without any complaints.
Within the first week of starting pazopanib, the patient developed dyspnoea on exertion that progressed rapidly to dyspnoea on minimal exertion. He was no longer able to conduct his daily walks. On the 10th day after starting pazopanib, he was unable to shave himself due to dyspnoea, which prompted his ED presentation. In the ED, his blood pressure (BP) was 122/70 mm Hg, heart rate (HR) was 93 beats per minute (bpm), respiratory rate (RR) was 22 breaths/min, and oxygen saturation was 94% on room air. On physical examination, auscultation of the heart was significant for an irregular rhythm with no additional heart sounds or signs of volume overload. His lungs were clear to auscultation, and the remainder of the examination was unremarkable.
Initial labs were significant for a creatinine of 1.4 mg/mL and a supratherapeutic international normalised ratio of 4.0. Blood counts, electrolytes and liver function tests were within normal limits. His B-natriuretic peptide (BNP) was 2685 pg/mL. His troponin results were negative. An ECG showed atrial fibrillation without significant changes compared with previous tracings. A CT angiogram (CTA) of the chest in the ED showed heterogeneous opacification of the left main pulmonary artery with concern for a non-occlusive thrombus.
The patient was admitted to the hospital and empirically started on anticoagulation with enoxaparin for presumed pulmonary embolism (PE). On the second day, he presented with worsening shortness of breath and compromised mental status. On physical examination, he was dyspnoeic and tachypnoeic with RR of 40 breaths/min and oxygen saturation of 95% on 2 L of oxygen by nasal cannula. His HR ranged between 140 and 150 bpm and his BP was 96/53 mm Hg. He was in respiratory distress, unable to speak in full sentences but alert and following commands.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [70, 'years'], 'Heart Rate or Pulse': [93.0, 'beats per minute'], 'O₂ saturation percentage': [94.0, '%'], 'Previously documented Deep Vein Thrombosis': False, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Hormone use': False, 'Previously Documented Pulmonary Embolism': True}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 70 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 93.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 94.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is reported to have been diagnosed with pulmonary embolism in the past. At least one of the criteria is met and so we increment the criteria met by 1, making the current total 2 + 1 = 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6519,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-10856,Extracted,"A 36-year-old male suffered a gun-shot wound to the abdomen that required an emergent exploratory laparotomy to repair and resect damaged portions of the bowel. Four days later, the patient reports increased generalized abdominal pain. His vital signs are as follows: T 38.5, HR 110, BP 110/60, RR 18, SpO2 96%. Physical exam reveals extreme tenderness to palpation of the abdomen as well as rebound tenderness, worse in the bilateral lower quadrants. The abdomen is mildly distended with guarding and decreased bowel sounds. The surgical and bullet-entrance wounds appear intact without any evidence of leakage/drainage, erythema, or warmth. Initial lab-work shows an elevated white blood cell count of 17.1 x 10^9 cells/L. A CT scan of the abdomen shows a 4 cm abscess in the left lower quadrant.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'O₂ saturation percentage': [96.0, '%'], 'Recent surgery or trauma': True, 'age': [36, 'years'], 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 36 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 110.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 96.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6520,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8272663-1,Extracted,"A 69-year-old Caucasian male was admitted to the emergency department of our hospital after returning from a one-month vacation to Myanmar that included horseback riding. The patient had not taken malaria prophylaxis and did not receive any vaccinations prior to his departure. The patient's medical history was remarkable for gout, ciguatera, and neurosurgical reconstruction of the skull after a basilar skull fracture. The latter occurred 5 years before this event (after a fall from a horse), and it was complicated by cerebrospinal fluid (CSF) leakage and right-sided glossopharyngeal and vagal nerve damage, which resulted in right-sided vocal cord paralysis with hoarseness and sporadic aspiration. The patient did not take any medications and did not smoke, but he drank wine regularly.
For the last few days, the patient had been increasingly tired and somnolent, with complaints of headache, left-sided ear pain, and night sweats. One day prior to admission, the patient had become increasingly confused. On the day of his admission, he was found by his wife lying on the floor of his home, confused, agitated, shivering, and incontinent of urine. At the emergency department, the patient's temperature was 39.2 °C, and his heart rate was 111 beats per minute, with a respiratory rate of 20 breaths per minute and a blood pressure of 161/88 mmHg. The patient's peripheral oxygen saturation was 87%, and his Glasgow Coma Scale was scored as 9 (E2 M5 V2). Clinical examination revealed fasciculations of the face and lower legs and crepitation over the right lower lung on pulmonary auscultation. There was no purpura or nuchal rigidity.
At that time, blood results revealed a leukocyte count of 34 900 × 109/l (normal: 4 300–10 000) (>95% being neutrophils) and a C-reactive protein (CRP) level of 204 mg/l (normal value <3). A chest X-ray revealed no abnormalities. A CT scan of the brain showed only nonspecific white matter lesions but no haemorrhage or oedema. Lumbar puncture examination revealed a leukocyte count of 1160/mm3 (almost all neutrophils), a normal glucose level, and a total protein level of 128 mg/dl (normal value 15–40) accompanied by an elevated lactate level of 6.1 meq/l. Gram stain showed irregularly shaped cocci. Bacterial meningitis was suspected, and after obtaining two sets of blood cultures, empirical therapy with 2 g of intravenous ceftriaxone every 12 h, 2 g of ampicillin every 4 h and 10 mg/kg of acyclovir every 8 h was initiated. Shortly after starting the antibiotic therapy, the patient became more somnolent and developed a left-sided hemiplegia, left-sided central facial palsy, and right-sided head and eye deviation, and the patient was admitted to the intensive care unit (ICU). Because of increasingly obstructive respirations and an increasing oxygen need by the next day, the patient was intubated and ventilated.
Cerebrospinal fluid (CSF) cultures showed β-hemolytic colonies; blood and CSF cultures were positive for Streptococcus equi. Intravenous treatment with 2 g of ceftriaxone every 12 h was continued for 21 days, while ampicillin and acyclovir were discontinued. In vitro testing confirmed a sensitivity to ceftriaxone. Fluid-attenuated inversion recovery images (FLAIR) showed a “dirty CSF” appearance in the right parietal region (, white arrow). Axial () and sagittal () T1-weighted images after the intravenous administration of gadolinium-chelate revealed a focal area of superficial contrast enhancement overlying the cerebral cortex, presumably representing a thickened pia mater and opacification of the left mastoid. In view of the MRI lesions and the left hemiplegia, one gram of intravenous methylprednisolone once daily was added to the treatment for 3 days with gradual tapering afterwards because meningoencephalitis with accompanying cerebral vasculitis was suspected []. After 4 days, the patient was weaned from the ventilator and extubated. Initially, the patient remained very agitated and disoriented and was temporarily treated with 25 mg of twice daily quetiapine and 100 mg of daily trazodone. Nine days after admission to the ICU, the patient was transferred to the neurology department. Later, this Streptococcus equi was identified as S. equi subspecies equi (at the National Reference Center for Invasive Non-Group B Beta-Hemolytic Streptococci, Belgium).
The patient initially recovered completely and had no complaints apart from mild gait disturbances and light-headedness at a follow-up appointment 3 months after discharge. Because of the patient's prior medical history of basilar skull fracture and opacification of the left mastoid on brain MRI, despite a lack of clinical evidence of acute otitis or mastoiditis, an additional CT scan of the base of the skull was performed to rule out possible portals of entry for central nervous system (CNS) infection. The CT scan revealed only an asymmetrical widening of the left squamosal suture; therefore, we opted for a conservative approach.
One month later (5 months after the initial referral), the patient was readmitted with intracranial bleeding, and consecutive CT scans showed multiple right-sided cerebral haemorrhages, with the largest located precentrally in the frontal lobe with small perilesional parietal and temporal haemorrhages accompanied by a left hemiparesis and aphasia (). CT angiography examination (, para-axial MPR) showed multiple tortuous, engorged pial veins of the right hemisphere. Cerebral angiography confirmed the presence of a suspected superficial dural arteriovenous fistula (, lateral projection of right internal carotid artery injection, large black arrow) in the right parietal region. The arterial feeders were mainly meningeal branches originating from the right ophthalmic artery and transosseous feeders from the right superficial temporal and occipital arteries (, lateral projection right external carotid artery injection); in addition, there was limited arterial supply to the fistula from the left middle meningeal artery across the midline (not shown). Venous drainage was through a large, right temporal draining vein (large white arrow) with reflux into multiple tortuous, superficial frontotemporal veins, as shown in , indicating a fistula with high risk of haemorrhage.
Comparison of the axial T2-weighted images of MRI examinations at initial admittance () and at the second admission () showed the new finding of dilated pial veins (encircled), demonstrating de novo development of the dural AV fistula.
The dural AV fistula was excised by the neurosurgeon. Microscopy of the resected dura showed a previously damaged vein with inflammatory remnants and granulation tissue in its wall (Figures and ). The patient was discharged to home with a hemiparesis that was still present. Seven months later, after this second event, the patient's GCS was 15/15, and the hemiparesis had almost completely disappeared.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [69, 'years'], 'Heart Rate or Pulse': [111.0, 'beats per minute'], 'O₂ saturation percentage': [87.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 69 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 111.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 87.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 2 + 1 = 3.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6521,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7872601-1,Extracted,"A 52-year-old male was brought to the emergency department (ED) via emergency medical services (EMS) with complaints of chest pain and pressure after a motor vehicle collision. The patient was the restrained driver in a collision while traveling at approximately 45 miles per hour when a car turned in front of him at an intersection. His airbags deployed; he did not lose consciousness and was able to self-extricate from the vehicle. After extrication, he started to experience substernal chest pressure, which was not present prior to the accident. When EMS arrived he was placed in a cervical collar and given aspirin, and an electrocardiogram (ECG) was obtained (). He was transported to the ED.
On arrival, a repeat ECG was performed, and the emergency physician alerted a cardiac activation given concern for an ST-elevation myocardial infarction (STEMI). He complained of substernal chest pain and pressure that was non-radiating and exacerbated by deep inspiration. Additional review of systems was negative.
On examination in the ED, the patient’s temperature was 36.6° Celsius, heart rate 76 beats per minute, respirations 15 breaths per minute, blood pressure 102/60 millimeters mercury, and an oxygen saturation of 97%. He was in no acute distress. He had tenderness to palpation over the sternum with no evidence of contusion or seatbelt sign on chest or abdomen. He had no abnormalities on cardiac, lung, or abdominal exams. He had no bony point tenderness of extremities and had full range of motion of all extremities.
He had no prior medical history but had not had regular medical care in the prior 30 years. He had smoked 1.5 packs per day of cigarettes for many years, consumed alcohol on social occasions, and denied recreational drug use. He had no known drug allergies. He had never had surgery. He denied any family history of coronary artery disease and denied any personal history of hypertension, hyperlipidemia, or coronary artery disease.
Chest radiography demonstrated only mild left lung base atelectasis. Point-of-care echocardiography by the cardiology service was limited by difficult windows and pain on transducer pressure, but demonstrated a relatively preserved ejection fraction, no pericardial effusion, and no obvious wall motion abnormalities. Initial troponin-I was elevated at 0.045 nanograms per milliliter (ng/mL) (reference range 0.02–0.04 ng/mL), and B-type natriuretic peptide was 10 picograms (pg)/mL (<=99 pg/mL).
While the diagnosis of cardiac contusion was entertained, the field ECG could not be ignored. With no contraindications to angiography identified, the patient was fully anticoagulated and taken emergently for coronary angiography. Coronary angiogram demonstration 100% occlusion of the mid left anterior descending artery (LAD) without dissection (). There was also a mid-right coronary artery (RCA) ragged 70–90% lesion. After intervention on the LAD lesion, the patient’s pain subsided. The next day, he complained of chest pain on deep inspiration and chest heaviness. He had a staged intervention of the RCA the following day. In the interim, he was discovered to have a sternal fracture by computed tomography ().",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [52, 'years'], 'Heart Rate or Pulse': [76.0, 'beats per minute'], 'O₂ saturation percentage': [97.0, '%'], 'Hormone use': False, 'Unilateral Leg Swelling': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 52 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 76.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 97.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6522,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-6717387-1,Extracted,"A 71-year-old male with a past medical history of hypertension presented to our community emergency department (ED) transported by emergency medical services (EMS) with the chief complaints of chest pain, difficulty breathing, back pain, and weakness of both lower extremities. He had an abrupt onset of chest pain, described as a sharp and stabbing pain, while using his rototiller in the garden, 6 h prior to arrival. His symptoms continued to progress to the point that he was having difficulty breathing and starting to have trouble walking for which EMS was called. Per EMS, they noted rapidly progressing symptoms while en route to the ED. Vitals on arrival to the ED are as follows: 94.5 °F, blood pressure of 91/64 mmHg, heart rate of 109 beats/min, respiratory rate of 22 breaths/min, and 100% pulse oximetry on room air. On physical exam, he was toxic appearing, in acute distress, and diaphoretic. Jugular venous distention was present. Cardiopulmonary exam was notable for tachycardia, distant heart sounds, and the presence of bibasilar rales. His skin/lower extremities were pale, mottled, and he was unable to move them. Carotid pulses were 2+ bilaterally, radial pules 1+ bilaterally, femoral pulses 1+ bilaterally, with absent popliteal pulses. On neurological exam, he had dysarthric speech, left-sided facial droop, and loss of strength and sensation in his lower extremities.
The patient was placed on non-invasive positive pressure. Electrocardiography revealed sinus tachycardia with premature atrial complexes, a right bundle branch block, with non-specific ST/T wave changes in the anterior leads. Portable chest radiography taken in an upright position (Fig. ) demonstrated a widened mediastinum at about 10.5 cm. A bedside point of care cardiac ultrasound revealed a significant pericardial effusion. Computed tomography (CT) of the head without contrast was unremarkable for any acute process. Pertinent laboratory evaluation:
Hemoglobin of 9.2 (13.5–17 g/dL) Arterial blood gas: pH 7.01, pCO2 45, p02 116, HCO3 12 Initial lactic acid of 8.3 (0.5–2.2 mmol/L) that increased to 14.8 Blood/urea/nitrogen of 42 (8–22 mg/dL) Creatinine of 3.06 (0.6–1.4 mg/dL).
CT angiography of the chest, abdomen, and pelvis with and without intravenous contrast revealed a Stanford type A dissection with an intimal tear beginning at the level of the aortic root and extending throughout the course of the thoracic aorta and into the abdominal aorta (Figs. , , and ). Additional findings on CT included involvement of the origins of the great vessels (brachiocephalic trunk, left common carotid artery, left subclavian artery). Hemopericardium is visualized with high suspicion for pericardial tamponade. There is dilation of the ascending thoracic aorta measuring up to 5.2 cm. The dissection continues distally (Figs. and ) to involve the left common iliac artery and bilateral external iliac arteries.
He was transferred emergently to a tertiary center and was taken immediately to the operating room for definitive repair. The patient underwent sternotomy, repair of Stanford type A dissection with right groin cannulation, and repair of the right femoral artery and vein. He arrived in the surgical intensive care unit in guarded condition, his sternotomy was left open secondary to severe coagulopathy intraoperatively, and he was on an epinephrine, norepinephrine, and vasopressin infusion. By day 2, continuous renal replacement therapy (CCRT) was initiated for acute tubular necrosis. Vascular surgery was consulted to evaluate a pulseless right lower extremity status post right femoral artery cannulation for cardiopulmonary bypass. Given the patient had an open sternotomy with five chest tubes with significant output requiring transfusion of multiple blood products throughout the night, vascular surgery could not perform a femoral-femoral bypass or axillofemoral bypass without heparinization.
By day 3, he underwent mediastinal irrigation and sternal closure with cardiothoracic surgery. He was then taken for a right common femoral endarterectomy, iliofemoral and lower extremity embolectomy, and right lower extremity four-compartment fasciotomy secondary to acute ischemia of the right lower extremity. In addition, neurosurgery evaluated the patient because he was not spontaneously moving his extremities after surgery and there was concern that the dissection had caused an infarction of his thoracic spinal cord, resulting in paraplegia. By day 4, he remained stuporous off sedation and on maximum pressor support (norepinephrine infusion at 30 mcg/min, epinephrine infusion at 10 mcg/min, and a vasopressin infusion at 0.04 units/min). He continued to have upper extremity non-epileptic myoclonic jerks secondary to continued renal failure. CT of the head revealed multiple 1 to 2 cm foci consistent with likely subacute infarcts related to embolic disease. By day 5, a family discussion was had regarding a poor neurological prognosis for independent neurological recovery with likely permanent cognitive and motor deficits. His code status was subsequently changed to do not resuscitate (DNR) with no further escalation of care. The patient continued to deteriorate throughout the night, became asystolic, and expired.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [71, 'years'], 'Heart Rate or Pulse': [109.0, 'beats per minute'], 'O₂ saturation percentage': [100.0, '%'], 'Unilateral Leg Swelling': True, 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",4,4,4,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 71 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 109.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 100.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 3 + 1  =  4.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 4.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 4.
Hence, the number of PERC rule criteria met by the patient is 4."
6523,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-4381,Extracted,"A 65-year-old man arrives to the emergency department (ED) complaining of pain and swelling in his right leg. The patient reports he recently underwent a total hip replacement. His past medical history is significant for hypertension and diabetes. His current medications include aspirin, lisinopril, metformin, and atorvastatin. On arrival, his temperature is 99°F (37.2°C), blood pressure is 135/82 mmHg, pulse is 88/minute, and oxygen saturation is 99% O2. He denies chest pain or shortness of breath. On physical exam, his right leg appears moderately erythematous, swollen, and is tender to palpation. Other physical exam findings are negative.

A complete blood count (CBC) was performed with the following findings:

Hemoglobin: 13.0 g/dL
Leukocyte count: 6500/mm^3
Platelet count: 150,000/mm^3

The appropriate anti-coagulation therapy is started. Seven days later the patient arrives back to the ED complaining of crushing substernal chest pain. An electrocardiogram is performed and is shown in Figure A.

A CBC was performed with the following findings:

Hemoglobin: 13.5 g/dL
Leukocyte count: 8500/mm^3
Platelet count: 58,000/mm^3
INR: 2.5
aPTT: 34 seconds
Fibrinogen level: 200 mg/dL
Troponin T: 0.2 ng/mL

On physical exam, the right leg is again swollen and tender to palpation. However, a new lesion has also formed, as shown in Figure B.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [65, 'years'], 'Heart Rate or Pulse': [88.0, 'beats per minute'], 'O₂ saturation percentage': [99.0, '%'], 'Recent surgery or trauma': True, 'Unilateral Leg Swelling': True, 'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 65 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 88.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6524,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-3881409-1,Extracted,"A 37-year-old male visited the emergency department at Samsung Medical Center, Seoul, Korea, presenting with a chief complaint of dyspnea. Initial symptoms had begun 1 week prior to his visit, characterized by fever and chills, followed by progressive respiratory difficulty. He appeared acutely ill. A crackling sound was heard upon chest examination. His heartbeat was regular without a murmur. A purplish discoloration of the right ankle was observed, but there were no local heat or tenderness. Initial blood pressure was 163/91 mmHg, pulse rate was 114 beats/min, respiratory rate was 24 breaths/min, and body temperature was 38℃. Oxygen saturation was initially detected as 87%, and increased to 95% upon oxygen supplement via nasal cannula at 5 L/min. Following oxygen supplementation, arterial blood gas analysis (ABGA) showed a pH of 7.39, partial pressure of carbon dioxide (PaCO2) of 40.9 mmHg, partial pressure of oxygen (PaO2) of 113.7 mmHg, and oxygen saturation of 98%.
Laboratory tests revealed peripheral eosinophilia and thrombocytopenia with a white blood cell count of 22,580/µL (50% neutrophils, 31% eosinophils, 10% lymphocytes), Hb levels at 13.7 g/dL, and a platelet count of 26,000/µL. Prothrombin and activated partial thromboplastin times were 15 sec, and 35.4 sec respectively. Fibrinogen levels were within the normal range, but the concentration of D-dimer was markedly elevated at 26.69 µg/mL. Serum total IgE and ECP levels (939.4 IU/mL and 201.0 ng/mL, respectively) were both elevated, too. Tests for both anti-nuclear antibodies and anti-neutrophil cytoplasmic antibodies were negative. A test for parasites in the stool and serum were negative. Bone marrow biopsy showed normal cellularity with increased eosinophils. Fip1-like1 and platelet-derived growth factor receptor alpha (FIP1L1-PDGFRA) gene fusion was not detected. Patchy consolidation with ground-glass opacity in both lower lung zones was noticed in the initial chest radiography ().
During the initial workup, the patient became progressively tachypneic with increased oxygen demand to 15 L/min via facial mask. The patient was transferred to the intensive care unit and oxygen supply was increased to 100% by high-flow nasal cannula. Despite supplementation, PaO2 levels remained low (49.9 mmHg) leading to a diagnosis of ARDS, and then the patient underwent intubation and mechanical ventilation.
Bronchoalveolar lavage (BAL) revealed marked eosinophilia (187/200 evaluated cells, 93.5% eosinophils). Skin biopsy of the right ankle showed diffuse eosinophilic perivascular infiltration of the dermis () and eosinophilic abscess of subcutaneous fat (). Duplex sonography revealed deep vein thrombosis in the left popliteal, soleal, and peroneal veins. Nerve conduction test and electromyography showed neuropathy in the right posterior tibial nerve.
A diagnosis of IHES was reached based on the presence of peripheral and tissue eosinophilia, along with the exclusion of other causes of eosinophilia. High-dose corticosteroid (methylprednisone 1 mg/kg/day) therapy was initiated on the first day of admission. By day 3, eosinophil counts decreased to the normal range (). Extubation was performed on day 4 as a result of clinical and radiological improvements.
A chest CT scan was obtained on day 9 to evaluate symptoms of mild dyspnea despite the dramatic improvement seen by simple radiography (). Pulmonary thromboembolism (PTE) was detected in the bilateral lobar and segmental branches of the pulmonary arteries (), and we started anticoagulant therapy. On day 23, the patient was discharged from the hospital with a gradual tapering of corticosteroids.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [37, 'years'], 'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [114.0, 'beats per minute'], 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': True, 'O₂ saturation percentage': [87.0, '%'], 'Unilateral Leg Swelling': True, 'Hormone use': False, 'Recent surgery or trauma': False}",4,4,4,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 37 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 114.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 87.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. At least one of the criteria is met and so we increment the criteria met by 1, making the current total 3 + 1 = 4.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 4.
Hence, the number of PERC rule criteria met by the patient is 4."
6525,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-6215582-1,Extracted,"A 26-year-old male patient with no remarkable medical and social history presented with a five-day history of a cough and fever. Before coming to our hospital, he went to a clinic and received amoxicillin, which resulted in no improvement of his symptoms. He visited another hospital three days before presenting to us and was hospitalized with a diagnosis of bacterial pneumonia. Although he received tazobactam/piperacillin, his clinical symptoms showed deterioration. Two days later, he was admitted to our hospital.
His vital signs were as follows: temperature, 38.1°C, heart rate of 112 beats/min, blood pressure of 98/60 mmHg, respiratory rate of 24 breaths/min, and saturation of peripheral oxygen of 94% with a reservoir mask of 6 L/min. On physical examination, weak respiratory sounds and coarse crackles were heard in the lower left chest.
His initial white blood cell count was 6,800/μL, hemoglobin was 14.0g/dL, platelet count was 133,000/μL, and C-reactive protein level was 34.30 mg/dL (). Arterial blood gas (reservoir mask of 6 L/min) showed that the pH was 7.44, PCO2 was 41.1 mmHg, PO2 was 69.2 mmHg, HCO3− was 27.2 mmol/l, and BE was 2.8 mmol/L. Among the viral and bacterial rapid tests performed, only the Mycoplasma antigen tested positive.
Chest radiography indicated an infiltrating shadow in left middle lung field and right lower lung field. A chest CT indicated lobar pneumonia in the lower left lobe and an infiltrating shadow in the left whole lung lobe and the lower right lobe (). Based on these findings, the patient was diagnosed with severe mycoplasma pneumonia.
Azithromycin 500 mg/day and prednisolone 30 mg/day were initiated. After admission, his respiratory condition worsened until a reservoir mask 15 L/min was required. We then changed the reservoir mask to a nasal high-flow oxygen (40 L/min, FiO2:0.8) and increased the prednisolone to 60 mg/day. In case of macrolide resistance, we additionally administrated minocycline 200 mg/day. On hospital day 4, the patient's respiratory status and inflammatory markers on laboratory findings improved. On hospital day 20, he was discharged.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [26, 'years'], 'Heart Rate or Pulse': [112.0, 'beats per minute'], 'O₂ saturation percentage': [94.0, '%'], 'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Recent surgery or trauma': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 26 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 112.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 94.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6526,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-5330230-1,Extracted,"A 71-year-old man was admitted to our emergency department after being found unconscious and hypoxemic in front of his house. He had a history of alcohol- and nicotine-abuse and lived a reclusive life. One week prior he had visited his general practitioner because of dyspnea. He was prescribed oral steroids and bronchodilators for presumed exacerbation of chronic obstructive pulmonary disease (COPD).
On physical examination he looked ill, was haemodynamically stable and hypercapnic. His body temperature was 37.2 °C. His blood pressure was 154/66 mmHg, with a regular pulse of 116 beats min−1. He was tachypneic, respiration rate of 27 min−1, with a peripheral oxygen saturation of 97 % with a non-rebreathing mask. Lung auscultation revealed weak breath sounds. Further physical examination revealed a wound between his first and second toe on his right foot in which a great number of maggots were present (). Signs of chronic venous insufficiency were present, but no signs of arterial insufficiency. The remaining physical examination was unremarkable. Haematological and biochemical investigations showed a white blood cell count of 17.9×109 l−1[reference range (ref.) 4–10×109 l−1], with 81 % neutrophils (ref. 40–75 %), C-reactive protein 51 mg l−1 (ref. <10), glucose level of 257.6 mg dl−1 (ref. 72.1–115.1) and otherwise normal results for haemoglobin level, platelet count, liver enzymes, electrolytes and creatinine. Arterial blood-gas analysis showed a marked respiratory acidosis with a pH of 7.19 and pCO2 of 12.1 kPa. A chest X-ray did not reveal signs of pneumonia. He was admitted to our Intensive Care Unit and non-invasive ventilation was started with a diagnosis of exacerbation of his COPD without an apparent trigger, possibly upper respiratory tract infection. Steroids, bronchodilators and a broad-spectrum antibiotic (amoxicillin/clavulanic acid) were given. Two days later he was transferred to the pulmonology ward. Two blood culture sets each containing one aerobic and one anaerobic bottle (BACTEC Plus Aerobic/F and Anaerobic/F Culture Vials using the BACTEC FX system; Becton Dickinson) drawn upon admission revealed growth of Gram-negative rods in one of the aerobic bottles after incubation for 48 h. Upon subculturing of the Gram-negative rod, an oxidase-positive, aerobic, catalase-positive strain was found. Determination by Vitek2Combo with ID-GN card (bioMérieux) revealed Acinetobacter iwoffii with 98 % probabil ity. API NE tests (bioMérieux) could not assign the strain to a specific species. The above results were conflicting with colony morphology and oxidase reaction. A RapID-ANA test (Remel) was done to test for enzymatic reactions that could possibly provide a clue to the identification. Positive reactions for urease, arginine and serine hydrolysis were found. Although we even considered this strain to be a non-fermentative contaminant, the combination of the positive oxidase reaction and the growth characteristics finally let us consider Wohlfahrtiimonas species as we knew the patient had a wound full with maggots. However , a positive urease reaction is not compatible with Wohlfahrtiimonas. We offered the strain to an external laboratory (BaseClear, Leiden, The Netherlands) for identification by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) (VITEK MS; bioMérieux) and MicroSEQ analysis, a 16S rRNA gene amplification and sequencing method (Life Technologies). MALDI-TOF MS did not reveal a reliable result (VITEK MS industry database v2.0) and even the MicroSEQ analysis with the validated database was unsuccessful. To our complete surprise a species of the genusIgnatzschineria was identified when the 489 basepair 16S rRNA gene sequence was blasted against the NCBI and SMARTgene databases. The colony morphology, growth characteristics, oxidase and urease reaction were all compatible with this identification as well as the clinical story. The complete 16S rRNA gene was amplified and analysed. The resulting sequence (1392 nucleotides) showed 98.7, 98.5 and 98.2 % similarity, respectively to the type strains of Ignatzschineria ureiclastica, Ignatzschineria larvae and Ignatzschineria indica (GenBank accession numbers , and ). shows a phylogenetic tree displaying the relations with close proximate species. The sequence was submitted to the GenBank database and assigned accession number . Antimicrobial susceptibility testing performed by Etest (bioMérieux) revealed minimal inhibitory concentrations (MIC) for amoxicillin/clavulanic acid of 0.25 mg l−1, amoxicillin 0.047 mg l−1 and ciprofloxacin 0.064 mg l−1. A beta-lactamase test (Oxoid) was positive. According to EUCAST non-species related breakpoints all these antibiotics could be considered sensitive based on Pk/Pd data. The positive beta-lactamase test argues against amoxicillin as appropriate treatment. The in vitro sensitivity to amoxicillin by Etest in conjunction with a positive beta-lactamase test is suggestive of an inducible beta-lactamase. A culture of the wound on the right foot of the patient taken two days after start of antimicrobial treatment and admission did only reveal Providencia stuartii. Even with the knowledge of the blood culture result we could not find species of the genus Ignatzschineria in this culture. A two-week course of amoxicillin/clavulanic acid was completed with good clinical response. The wound on the patient's foot was successfully treated with application of povidone-iodine (betadine) and low adherent highly absorbent (melonin) dressings. His pulmonary condition improved, elevated glucose level and venous insufficiency were taken care of and he gradually improved and was discharged three weeks after admission.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [71, 'years'], 'Heart Rate or Pulse': [116.0, 'beats per minute'], 'O₂ saturation percentage': [97.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 71 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 116.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 97.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6527,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7876339-1,Extracted,"A 56-year-old man was admitted to our institution with an 11-day history of persistent dry cough, fever, and progressive shortness of breath. On arrival at the hospital, he was hypoxemic, with a SpO2 of 91% and a respiratory rate of 35 breaths per minute requiring ambient oxygen therapy with a flow of 15 L/min via a non-rebreather mask. Hemodynamically, he showed a stable profile with a blood pressure of 120/80 mmHg and a heart rate of 84 bpm. His body temperature was 38.1°C. Laboratory tests revealed an elevated C-reactive protein concentration of 37 mg/L (reference: <5 mg/L), a leukocyte count of 7.7 × 109/L (reference: 4–10 × 109/L) and D-dimer of 0.41 mg/L (reference: <0.50 mg/L). The chest radiograph demonstrated bilateral basal consolidations. The suspicion of Covid-19 was confirmed by real-time reverse transcription polymerase chain reaction (RT-PCR) analysis of nasopharyngeal swab samples.
The patient was primarily admitted to a designated Covid-19 ward for further observation and oxygen therapy. Due to severe hypoxemic respiratory failure within 24 h after admission, he was immediately transferred to the intensive care unit (ICU) where he was intubated. On the 5th day of ICU admission (T0), the patient developed a high fever accompanied with an increase in inflammatory parameters (). Hemodynamic parameters did not indicate an unstable course (). Microcirculatory monitoring was carried out sublingually using Cytocam-IDF imaging (CytoCam, Braedius Medical, Huizen, The Netherlands). Image analysis which was performed offline using MicroTools, showed an increase in microcirculatory density (total vessel density and perfused vessel density) and perfusion parameters (proportion of perfused vessels and microvascular mean flow index) as well as in red blood cell (RBC) velocity (). Subsequent CT-scan demonstrated extensive subcutaneous emphysema and pneumomediastinum as well as a thrombus in the right jugular vein extending to the superior vena cava and into the right brachial vein (). A tracheal defect was ruled out by bronchoscopy. There was no pneumothorax or evidence of esophageal rupture.
The patient was ventilated for 19 days and a temporary tracheostomy was performed for a gradual wean from the ventilator. Unfractionated heparin was given in therapeutic doses for his venous thrombus. Chest CT obtained at 19th (T1) and 25th day of ICU admission (T2) showed complete resorption of mediastinal air and venous thrombus (). Concurrent microcirculatory images revealed a recovery of microcirculatory alterations ( and ). Thereupon on the 30th day of ICU admission, the tracheostomy was removed and the patient was discharged to the ward after 32 days of ICU stay in stable hemodynamic and respiratory condition.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [56, 'years'], 'Heart Rate or Pulse': [84.0, 'beats per minute'], 'O₂ saturation percentage': [91.0, '%'], 'Hemoptysis': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': True}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 56 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 84.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 91.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note does not report a status on 'recent surgery or trauma'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. At least one of the criteria is met and so we increment the criteria met by 1, making the current total 2 + 1 = 3.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6528,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7883749-1,Extracted,"A 45-year-old African female nursing assistant presented to the emergency department with four days of diarrhea, nausea, and vomiting. She endorsed recent contact with COVID-19-positive patients. She denied cough, shortness of breath, chest pain, and fever. She was a non-smoker and was not on any medications. Vital signs showed a blood pressure of 113/85 mm Hg, heart rate of 116 beats per minute (bpm), respiration of 18 breaths per minute, a temperature of 96.0 degrees Fahrenheit, and oxygen saturation of 98% on room air. Her examination was remarkable for an overweight, diaphoretic female in distress with abdominal tenderness and cold and clammy extremities.
An electrocardiogram (EKG) showed sinus tachycardia and diffuse ST-segment elevation in I, II, augmented Vector Left (aVL), and V3-V6 (Figure ).
Laboratory testing was remarkable for a white blood cell count of 3.8 103/uL (reference range: 4.0 - 11.0 103/uL), platelets 144 103/uL, (reference range 150 - 400 103/uL), international normalized ratio (INR) 1.26 (reference range 0.8 - 1.1), lactic acid 2.97 mmol/L (reference range: 0.5 - 2.00 mmol/L), ferritin 562 ng/mL (reference range: 13 - 150 ng/mL), C-reactive protein (CRP) 24.1 mg/L, (reference range: 0 - 5 mg/L); serum aspartate aminotransferase (AST) 141 U/L (reference range: 10 - 34 U/L), lactate dehydrogenase (LDH) 464 U/L (reference range: 135 - 235 U/L), creatine kinase (CK) 693 U/L (reference range: 26 - 192 U/L), N-terminal pro-B-type natriuretic peptide (NT-proBNP) 4,585 pg/mL (reference range: 0 - 450 pg/mL), and troponin T 0.43 ng/mL (reference: 0 - 0.02). The chest x-ray showed patchy infiltrates bilaterally (Figure ). SARS-CoV-2 reverse transcription-polymerase chain reaction (RT-PCR) was positive.
The patient initially received 2 liters of normal saline, hydroxychloroquine 400 mg, aspirin 325 mg, and atorvastatin 80 mg for presumptive COVID-19-associated myocarditis. She improved symptomatically and remained hemodynamically stable. Two hours later, she became lethargic with a heart rate of 130 bpm. Pulses were unmeasurable. She received another liter bolus of normal saline and was immediately transferred to the intensive care unit. A bedside echocardiogram showed a left ventricular ejection fraction of approximately 10% with global hypokinesis and no pericardial effusion.
Ultimately, the patient developed cardiogenic shock. She was intubated and started initially on norepinephrine and subsequently required additional pressor support with phenylephrine and dopamine. She received intravenous immunoglobulin and methylprednisolone. She subsequently became asystolic. She received four doses of intravenous (IV) epinephrine and 1 ampule of IV bicarbonate. The patient expired after 15 minutes of resuscitation.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'years'], 'Heart Rate or Pulse': [130.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Hormone use': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 45 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 130.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'recent surgery or trauma'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6529,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8138369-1,Extracted,"A case study was done after obtaining ethical clearance from the institutional ethics committee and after obtaining informed written and oral consent from the patient.
A 72-year-old male patient presented to Bapuji teaching hospital attached to JJM medical college, Davangere on July 24, 2020 with hiccups in the last 5 days. There was no history of fever, cough, breathlessness, loose stools, burning micturition, chest pain or headache.
The patient was apparently normal 5 days back after which he developed intractable hiccups, insidious in onset, which failed to subside with home remedies. The patient got prolonged episodes every 3 hours which caused discomfort. Hiccups did not affect sleep or appetite. The patient is a known case of hypertension well controlled on 5 mg Amlodipine OD. The patient is not a known case of diabetes mellitus, bronchial asthma, tuberculosis, epilepsy, ischemic heart disease, or chronic kidney disease.
On general physical examination (GPE):
The patient was febrile at the time of examination
BP: 140/90 mmHg
PR: 92 bpm
SPO2: 92% @ room air
Temperature: 100° F
No signs of pallor icterus clubbing cyanosis lymphadenopathy or edema.
Head to toe examination appears to be normal.
On systemic examination:
RS: B/L crepitations +
B/L air entry equal
CVS: S1S2 heard, no murmurs
P/A: soft, non-tender, no organomegaly
CNS: clinically normal",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [72, 'years'], 'Heart Rate or Pulse': [92.0, 'beats per minute'], 'O₂ saturation percentage': [92.0, '%'], 'Hormone use': False, 'Unilateral Leg Swelling': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 72 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 92.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 92.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6530,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7290260-1,Extracted,"A 38-year-old Caribbean-Black (Afro-Trinidadian) female with a medical history of endometriosis, intermittently adherent with the oral contraceptive pill, initially presented to the adult emergency department with acute dyspnea during the preceding 2 days. Her vital signs reflected systolic blood pressures of 142 mm Hg, heart rate of 112 beats per minute, and respiratory rate of 20 breaths per minute with an oxygen saturation of 92% on room air. Her physical examination revealed a mildly elevated jugular venous pulse (10 cm of water), right chest stony dullness, no peripheral edema, and active menses.
A 12-lead electrocardiogram revealed sinus tachycardia with an incomplete right bundle branch block, right ventricular hypertrophy, and subtle secondary ST-T segment changes (see ). A portable chest radiograph revealed a large-sized, right pleural effusion with mild perihilar congestion (see ). Pertinent diagnostic laboratory investigations included a D-dimer 208 ng/dL (normal ≤500 ng/mL), pro–brain natriuretic peptide (pro-BNP) 323 pg/mL (normal ≤300 pg/mL), cardiac troponin I (cTnI) 0.08 ng/mL (normal = 0.0-0.15 ng/mL). The patient’s arterial blood gas was consistent with mild hypoxia on 24% fractional inspiration of oxygen (FiO2) with an alveolar-arterial gradient (A-a gradient) of 14 mm Hg.
The patient was subsequently admitted for an inpatient hospitalization, and computed tomography (CT)-guided therapeutic thoracentesis was performed with a resultant hemorrhagic exudative effusion. Despite this intervention, the pleural effusion recurred within 48 hours, and cardiothoracic surgery was consulted for a video-assisted thoracoscopic surgery (VATS) pleural biopsy, which later affirmed the presence of endometrial tissue on clinicopathological examination. The tentative diagnosis at this juncture was recurrent catamenial pleural effusions. On further interview, the patient acknowledged that she often experienced dyspneic episodes during menstruation.
During the ensuing hospitalization, she continued to experience persistent shortness of breath with an episode of paroxysmal atrial fibrillation (PAF). A 2-dimensional transthoracic echocardiogram (TTE) revealed preserved left ventricular function with moderate right heart enlargement, septal flattening, and mild pHTN with estimated right ventricular systolic pressures of approximately 45 mm Hg. A 2-dimensional and 3-dimensional transesophageal echocardiogram (2D/3D-TEE) also revealed an intact interatrial septum with agitated saline “bubble” study. The PVs were incompletely visualized and hence the rationale for further advanced imaging (see ). A cardiac CT angiogram (CCTA) affirmed the presence of the suspected PAPVC of the left inferior PV to the left brachiocephalic (innominate) vein with angiographically normal coronary arteries (see ). The patient also underwent cardiac magnetic resonance imaging (CMRI), which demonstrated the same aberrant connection with the remaining pulmonary venous vasculature appearing dilated in addition to the RA, right ventricle, and main pulmonary artery (see and , respectively). Left heart catheterization established angiographically normal coronary arteries with right heart catheterization revealing a significant hemodynamic left-to-right shunt with Qp:Qs ratio of 3:1, mild pHTN, and elevated pulmonary vascular resistance (see for a summary of the pertinent cardiovascular investigations).
Cardiothoracic surgery was reconsulted regarding the surgical repair of the PAPVC. In the interim, the patient was instituted on an optimal cardiovascular regimen that included apixaban for her PAF, angiotensin receptor blocker with a neprilysin inhibitor (ARNI), β-blocker (BB), mineralocorticoid receptor antagonist (MRA) for her heart failure and nitrates, tadalafil, and calcium channel blockade (CCB) for her pHTN. The rest of her hospital course was uneventful, and she was discharged home with scheduled corrective surgery in 2 months (due to our limited resource setting pending consultation from an international specialist CHD cardiothoracic surgeon).",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [38, 'years'], 'Heart Rate or Pulse': [112.0, 'beats per minute'], 'O₂ saturation percentage': [92.0, '%'], 'Hormone use': True, 'Unilateral Leg Swelling': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 38 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 112.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 92.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note does not report a status on 'recent surgery or trauma'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
Hence, the number of PERC rule criteria met by the patient is 3."
6531,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7472409-1,Extracted,"A 26-year-old Somalian woman (Gravida 2, Para 1) who had been living in Sweden for a year presented at the Emergency Department of Skåne University Hospital in Malmö on April 17th, 2020 pregnant at 32 + 1 weeks of gestation. She was transferred to the Infectious Diseases Department with suspicion of COVID-19. A diagnostic test, based on quantitative real time polymerase chain reaction (qRT-PCR), from a nasopharyngeal swab, was positive for SARS-CoV-2.
She had recently moved from Stockholm to Malmö. In 2015 she had a normal vaginal delivery in Somalia. The patient had an appendectomy and a cholecystectomy in Somalia. Her medical history also included hypothyroidism, currently treated with 150 ug Levothyroxine daily. The body mass index (BMI) on admission to prenatal care was 47 kg/m2 with length 163 centimetres (cm), weight 126 kg (kg). Apart from the obesity, her pregnancy had been without complications. She had received an intramuscular injection of Anti-D immunoglobulin at 28 + 5 weeks of gestation since she was Rhesus D (RhD) negative and the fetus was RhD positive.
On admission, the patient described a nine-day history of shortness of breath, dry cough, myalgia, nausea, abdominal pain and fever (Fig. 1). She had significant abdominal pain on admission but the surgeon did not find any signs of an acute abdominal event. The patient had also noticed reduced fetal movements for the last two days. Obstetric examination including cardio-tocography (CTG) and an abdominal ultrasound showed no abnormalities.
The patient’s respiratory rate was 22 breaths/minute, oxygen saturation 95%, blood pressure 116/71, pulse 113 beats/minute and temperature 37.2 degrees Celsius (oC). The laboratory tests are shown in Table . The patient was given morphine, paracetamol and oxycodone for pain relief and also received thromboprophylaxis, Dalteparin 7500 units /day subcutaneously. No additional oxygen was needed.
On day 2 (18/4/2020), the patient was relatively stable apart from two short episodes of fever up to 38.9 oC. Due to risk for preterm labour, the patient received 12 milligrams (mg) of Betamethasone intramuscularly to aid fetal lung maturity. Daily fetal monitoring using CTG showed no signs of fetal distress.
The patient was discharged on day 3 (19/4/2020) with a planned obstetric follow-up including fetal growth assessment after recovery. She was prescribed dalteparin for four weeks.
The patient returned to the Emergency Department the next day (20/4/2020) with a sore throat and severe difficulties in swallowing. Apart from tachypnoea (25–35 breaths/minute) and tachycardia (118 beats/minute), other vital signs were normal. After examination, she was discharged with a prescription of Betamethasone tablets for three days (6, 4 and 3 mg) for swallowing difficulties and potassium supplements for the hypokalaemia noted in the blood tests (Table ).
The patient was readmitted to the Infectious Diseases Department the next day (21/4/2020) (Fig. ). Her COVID-19 symptoms (cough, myalgia, abdominal pain and fever) had worsened and she now presented with dyspnoea. At readmission, the patient’s respiratory rate 42 breaths/minute, blood pressure 114/61, pulse was 120 beats/minute and temperature 38.9 oC. During episodes of coughing, her oxygen saturation fell to 86%, but with 5 L of oxygen on mask the saturation rose to 99%. Laboratory tests are shown in Table .
Her condition deteriorated on day 2 (22/4/2020) of the readmission. In addition to the generalized pain and tenderness, the pain in her right upper abdomen had worsened. Blood tests showed elevation of aspartate aminotransferase (ASAT), interleukin-6 (IL-6) and ferritin concentrations. There was impaired coagulation as shown by a prolonged activated partial thromboplastin time (APTT), high D-dimer, falling platelet count and decreased level of Anti-thrombin III (Table ). Hemolysis was indicated by a fall in the hemoglobin concentration and rising lactate dehydrogenase levels although haptoglobin concentrations only were slightly elevated (Table ). Despite her worsening condition, the patient felt active fetal movements and normal intermittent CTG controls were registered. Intravenous antibiotic treatment with Cefotaxime (2 g, 3 times daily) was initiated due to suspicion of concomitant bacterial infection (Table ). Blood and urine cultures were taken but since the general condition of the patient had worsened, a decision was made to deliver by Caesarean section (32 + 6 gestational weeks), on maternal indication. The operation was performed in spinal analgesia in an operating theatre with negative air ventilation. The local hospital guidelines were followed to prevent the spread of COVID-19 []. An uncomplicated operation was completed within 40 min and the total blood loss was 200 millilitres (mL).
After two hours in the post-operative unit, the patient returned to the ward and received thromboprophylaxis, dalteparin at a total dose of 10.000 units divided in two doses. A computed tomography (CT) lung scan, performed later the same day, showed bilateral diffuse, ground-glass opacities with both peripheral and perihilar distribution, but no signs of pulmonary embolism (Fig. ).
Due to deranged liver values, the patient was unable to receive paracetamol and due to the COVID-19 infection not able to receive ibuprofen []. The pain relief was managed by administering 2.5 mL of intravenous morphine as needed. However, the patient’s condition worsened during the night and on examination, the patient was somnolent and lethargic but answered adequately when woken up (Reaction Level Scale 2). The patient’s pain was mostly localized to the upper right quadrant of the abdomen and epigastrium. Her uterus was well contracted and there were no signs of postoperative complications such as bleedings and local infection. On examination, the patient had miotic pupils that reacted poorly to light stimulation. Even though the patient only was given 7.5 mg of morphine over the course of 8 h, a morphine over-dose was suspected, and intravenous morphine was replaced by a combination of orally administered Naloxone and Oxycodone. Post-operative mobilization was initiated one day after surgery where after the patient made a steady recovery.
Table illustrates the drastic improvement in the patient’s blood tests on day 3 (23/4/2020) of the readmission. The patient was discharged in good health on the 30th of April, 2020 with thromboprophylaxis planned for 6 weeks postpartum and a follow-up visit to the Obstetrics Clinic.
A male baby was delivered with birth weight 2085 g (37th percentile), birth length 48 cm (99th percentile) and head circumference 33.5 cm (99th percentile). The cord was clamped immediately after birth and the baby was shown briefly to the mother before being taken to a neonatal resuscitation station. At 1-minute after delivery, the baby had a normal heart rate but was gasping and had absent tone and no spontaneous movements. Positive pressure ventilation by a T-piece (neopuff) was given with peak inspiratory pressure (PIP) 20 cmH2O and positive end expiratory pressure (PEEP) between 5 and 7 cmH2O intermittently during the first seven minutes of life. At ten minutes, the baby was spontaneously breathing, albeit grunting, through T-piece continuous positive airway pressure (CPAP) with preductal oxygen saturation between 90–95% at FiO2 (fraction of inspired oxygen) 0.4. Fine crackles could be heard on lung auscultation. Intermittent intercostal retractions were also seen. Skin colour, tone and reflex irritability improved gradually during the stabilisation process. Apgar score; 1 min: 4 (appearance 1, pulse 2, reflex irritability 0, activity 1, respiration 0), 5 min: 6 (appearance 1, pulse 2, reflex irritability 1, activity 1, respiration 1), 10 min: 8 (appearance 2, pulse 2, reflex irritability 1, activity 1, respiration 2). Vitamin K was given intramuscularly and a nasogastric tube was inserted. Nasal CPAP with PEEP 6 cmH2O was started.
Arterial umbilical cord blood gas showed mild combined respiratory and metabolic acidosis with pH 7.28, partial pressure of oxygen (pO2) 3.45 (kilopascal) kPa, partial pressure of carbon dioxide (pCO2) 6.97 kPa and base excess − 6.8.
The baby was put in an incubator and transferred to the neonatal intensive care unit (NICU) and placed in an airborne infection isolation room (AIIR) with negative pressure ventilation. It was given preterm formula supplemented with intravenous glucose infusion. Venous blood gas was analysed at 4 h of age: pH 7.27, pO2 5 kPa, pCO2 7.3 kPa, BE -1.8, Hb 184 g/l and lactate 2.7 mmol/l.
After parental consent, formula was changed to donated breast milk. The mother was supplied with a breast pump and instructed in its use. After the initial need of breathing support and supplemental oxygen during day one of life the baby has enjoyed an uneventful clinical course. Nasopharyngeal swabs for SARS-CoV-2 detection were collected at 48 and 96 h of life and were found to be negative in both instances.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [26, 'years'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'O₂ saturation percentage': [86.0, '%'], 'Recent surgery or trauma': True, 'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 26 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 120.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 86.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6532,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-11907,Extracted,"A 31-year-old, G1P0 woman at 35 weeks of gestation comes to the emergency room for a severe headache. She reports that she was washing the dishes 2 hours ago when a dull headache came on and progressively worsened. She also reports 2 episodes of intermittent blurred vision over the past hour that has since cleared. Nothing similar has ever happened before. She denies any precipitating events, trauma, mental status changes, abdominal pain, lightheadedness, fever, ulcers, or urinary changes. Her temperature is 98.9°F (37.1°C), blood pressure is 160/110 mmHg, pulse is 98/min, respirations are 12/min, and oxygen saturation is 98%. A physical examination demonstrates a rash on her face that she attributes to a recent change in cosmetics. A urine test demonstrates the presence of protein.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Hormone use': True, 'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [98.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'age': [31, 'years'], 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 31 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 98.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 0.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 0.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 0.
The patient note does not report a status on 'recent surgery or trauma'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 0.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 0.
The patient note reports 'hormonal use' to be present for the patient and so we increment the criteria count by 1, making the current total 0 + 1  =  1.
Hence, the number of PERC rule criteria met by the patient is 1."
6533,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7935285-1,Extracted,"This study presents a case of a 21-year-old male patient with T-cell acute lymphoblastic lymphoma status post induction chemotherapy with lineage switch to acute myelogenous leukemia. He received high-dose chemotherapy with cyclophosphamide, total body irradiation (TBI), and later received a matched unrelated donor blood stem cell transplantation. His post-transplant course was complicated by biopsy proven chronic graft-versus-host disease in the gastrointestinal tract requiring daily steroid use. He also developed Cytomegalovirus (CMV) pneumonitis, BK virus-induced hemorrhagic cystitis, Candida glabrata fungemia, and Streptococcus viridans bacteremia-all of which were appropriately treated and resolved.
Eleven months after his stem cell transplant, he presented with acute onset of copious blood-tinged phlegm, shortness of breath and left pleuritic chest pain. Upon initial evaluation, the patient was afebrile, respiratory rate was 30 breaths per minute, pulse 180 beats per minute, blood pressure 90/67 mmHg, and oxygen saturation 91% on room air. Broad-spectrum antibiotics including intravenous vancomycin and antifungals were started. The patient later was hypotensive with blood pressure of 70/46 despite aggressive intravenous hydration. Due to septic shock, intravenous norepinephrine drip was started in the intensive care unit. Laboratory studies were significant for pancytopenia with white blood cell count of 2.79 x 103 cells/µL. Intravenous steroids were started given septic shock and patient’s known history of chronic steroid use due to chronic GVHD. Electrolytes and renal function were unremarkable. Arterial blood gas was significant for PaO2 of 64 mmHg. Blood cultures grew methicillin-resistant Staphyloccocus aureus (MRSA). A chest CT scan as seen in Figure showed left lower lobe consolidation in the setting of multiple bilateral cavitary nodules.
The infectious disease service was consulted. Blood cultures grew methicillin resistant Staphyloccocus aureus. Given the patient had not been hospitalized recently, it was determined that he had community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) bacteremia. Bronchoscopy was done and was remarkable for the presence of purulent secretions in the tracheobronchial tree. Respiratory culture from bronchoscopy also grew methicillin resistant Staphylococcus aureus. The rest of the infectious workup from the bronchoscopy was unremarkable. A transthoracic echocardiogram was ordered to evaluate for the possibility of endocarditis. The echocardiogram showed a left ventricular ejection fraction of 50%, mild global hypokinesis, and no evidence of vegetation suggestive of endocarditis. After a few days of treatment, the patient had significant clinical improvement and blood cultures were negative. He was discharged with a two week course of intravenous vancomycin which he completed.
Two months later, the patient was admitted to the hospital for fevers, productive cough with green sputum, and shortness of breath. He was found to have recurrent MRSA bacteremia and recurrent MRSA pneumonia. The CT chest findings as seen in Figure showed multiple bilateral cavitary nodules consistent with a necrotizing process.
Initially, intravenous vancomycin was started, however this was later switched to intravenous linezolid. This was done because the patient had recurrent MRSA bacteremia despite prior intravenous vancomycin therapy. Blood cultures were negative after two days of treatment. Transthoracic echocardiogram showed an improved left ventricular ejection fraction of 60-70% and no vegetations were identified. After clinical improvement, the patient was discharged on oral linezolid for six weeks per infectious disease team recommendations. After completing this course he was placed on prophylaxis with oral doxycycline to prevent further CA-MRSA infections.
Six months later, he had a repeat CT of the chest as seen in Figure . This CT showed the presence of permanent pneumatoceles from the focal loss of lung parenchyma.
Our patient was readmitted on several occasions mainly due to bouts of community-acquired viral pneumonia (adenovirus, parainfluenza, and influenza) along with a secondary Pseudomonas aeruginosa pneumonia. He did not have recurrent CA-MRSA pneumonia. His chest CT scan as seen in Figure from 2.5 years after the original MRSA infection demonstrated bronchiectasis and persistent pneumatoceles from his original infection with CA-MRSA.
His initial recurrent community-acquired pneumonias with secondary MRSA and his recent recurrent episodes of pseudomonas infection suggest the patient was likely chronically colonized.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [21, 'years'], 'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [180.0, 'beats per minute'], 'Hemoptysis': True, 'O₂ saturation percentage': [91.0, '%'], 'Hormone use': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 21 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 180.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 91.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6534,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-3002912-1,Extracted,"57-year old man presented to emergency department of regional hospital with chest pain, which started after walking in the morning. Dull pain was localized in the middle of his chest and was accompanied with nausea, fatigue and difficult breathing.
He had no history of heart problems, but was a former smoker and had elevated cholesterol levels. During last summer, he noticed varicose veins on right groin and was wearing elastic bandage. He had no history of cardiovascular disease, took no medications, had no known allergies and was in good physical condition. His father died at the age of 80 due to cerebrovascular insult and his mother had pulmonary embolism at the age of 74.
Since chest pain, dyspnea and fatigue didn't subside he called an ambulance. Upon arrival to emergency department he was pale and hypotensive (102/60 mmHg), heart rate was 100 b.p.m. and respiratory rate 22 breaths/min. Oxygen saturation was 95% while breathing 100% oxygen. His body temperature was 36.6 C°. Beside varicose veins on right groin, his physical examination was unremarkable.
On 12-lead ECG there was sinus rhythm with incomplete right bundle branch block, ST segment elevations up to 3 mm in precordial leads V1-V4 and negative T wave in lead III (Figure ).
On the basis of ECG changes and clinical presentation, acute ST segment elevation myocardial infarction (STEMI) was suspected. After receiving aspirin 500 mg, morphine 5 mg i.v., thiethylperazine, unfractionated heparin 5000 IU i.v. and nitroglycerin sublingually, he was immediately transferred to our University medical center for primary coronary intervention (PCI). In case of STEMI, quick referral from local hospital or directly from the field, to catheterisation laboratory is a standard of care in Slovenia. That is why no further diagnostic procedures, which would delay transport to PCI were performed in regional hospital.
The coronaroangiography reveled normal ascending aorta, coronary arteries without atherosclerotic lesions and acute occlusion, however there was a small separate conus artery arising from aortic root with embolic occlusion (Figure , additional file ). The affected artery was too small to attempt PCI.
On admission to medical intensive care unit (ICU) his first blood tests were available. His white blood cell count was slightly elevated (13.4 109/L), so were troponin I (0.128 μg/l - cut off 0.1 μg/l) and D-dimmer (1172 μg/l - cut off 350 μg/l). 4 hours after the onset of symptoms brain pro-BNP concentration was still normal (332.8 ng/l - cut off 500 ng/L). Lactate concentration was not elevated. Arterial blood gas analysis while breathing 6 liters of oxygen via bi-nasal catheter showed pH 7.41, carbon dioxide pressure of 4.3 kPa, oxygen pressure of 17.3 kPa, bicarbonate concentration of 19.9 mM and BE -3.7 mM.
Transthoracic echocardiography reviled good left ventricular systolic function without segmental contraction defects. Right cardiac chambers were enlarged, paradoxical movement of interventricular septum was noted but contractility of right ventricle was not impaired and right heart pressure was estimated to be 40 mmHg + central venous pressure.
With bedside transesophageal echocardiography pulmonary embolism was confirmed; thrombi were seen in both pulmonary arteries (Figure , additional file ); right to left intra-atrial communication was diagnosed after contrast application (Figure , additional file ).
At the time of diagnosis of pulmonary embolism he was hemodynamically stable. He received continuous infusion of unfractionated heparin and was soon transferred to step down telemetry unit. Maximal troponin I value of 3.08 μg/l was reached 24 h after admission. ST segment elevations of precordial leads returned to baseline and inverse T waves appeared on leads V1-V3. Ultrasound of lower extremity veins reveled right popliteal vein thrombosis. In a few days heparin infusion was substituted for warfarin and he was discharged.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [57, 'years'], 'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'Previously documented Deep Vein Thrombosis': True, 'O₂ saturation percentage': [95.0, '%'], 'Unilateral Leg Swelling': True, 'Hormone use': False}",4,4,4,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 57 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 100.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 95.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
The patient note does not report a status on 'recent surgery or trauma'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. At least one of the criteria is met and so we increment the criteria met by 1, making the current total 3 + 1 = 4.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 4.
Hence, the number of PERC rule criteria met by the patient is 4."
6535,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4793133-1,Extracted,"A 74-year-old normotensive, nondiabetic, male smoker (30-pack years) presented with progressively increasing shortness of breath, cough, white, mucoid expectoration, and retrosternal and right sided parasternal, oppressive chest pain for last 2 months. Chest pain and shortness of breath were increased in severity on exertion and were associated with palpitation, but there is no history of sweating, orthopnoea, paroxysmal nocturnal dyspnoea, unconsciousness, and convulsion. There was no radiation of chest pain. Chest pain was suddenly increased for last five days and the patient was admitted in the emergency department with a suspicion of acute myocardial infarction (AMI). There was no history of fever, hemoptysis, leg swelling, and facial puffiness. History of significant weight loss and anorexia were present. There was no history of household contact with the patient of sputum smear positive tuberculosis. The patient received formoterol + tiotropium metered dose inhaler (2 puffs once daily with spacer) and oral doxofylline (400 mg twice daily) for last five years, as he suffered from chronic bronchitis predominant chronic obstructive pulmonary disease (COPD) which resulted in persistent breathlessness, cough, and expectoration.
General survey revealed anemia and clubbing, but there was no cyanosis, edema, and engorged neck vein. There were multiple cervical and supraclavicular enlarged lymph nodes on left side, which were hard in consistency, discrete, nontender, and fixed to underlying structure, but not fixed to overlying skin, and there was no discharging sinus. His temperature was 37°C, respiratory rate 24 breaths/minute, pulse rate 120 beats/minute, regular blood pressure 94/64 mmHg, oxygen saturation in capillary blood (SpO2) 96% @ room air, and FiO2 0.21.
Examination of respiratory system revealed no abnormality, except vesicular breath sound with prolonged expiration on both sides, bilateral crackles, mainly over the bases of the lungs, and occasional wheezes. Examination of other system was normal. Complete hemogram showed anemia with hemoglobin concentration of 7.1 g/dL. Blood biochemistry was normal. Electrocardiogram (ECG) showed atypical ST segment elevation and T wave inversion in lateral chest leads (Lead V4, Lead V5, and Lead V6). Initial rapid troponin-t-test was inconclusive, but repeat one after 12 hours of first test was negative. Sputum for acid fast bacilli and Gram stain was negative, and pyogenic culture of sputum showed no growth. Chest X-ray posteroanterior (PA view) showed cardiothoracic ratio was more than 0.5; that is, size of the cardiac silhouette was increased, but lung parenchyma was normal. Contrast enhanced computed tomography (CECT) of thorax showed a large, nonhomogenous mass lesion in right lower lobe which invaded the left atrium and was compressing the adjacent ventricular walls (). There was also mediastinal and hilar lymphadenopathy. CT-guided fine needle aspiration cytology (FNAC) showed discrete clusters of malignant epithelial cells which showed nuclear pleomorphism, hyperchromasia, high nucleocytoplasmic ratio, pale cytoplasm, and ill-defined cell boundary—suggestive of non-small-cell carcinoma, possibly squamous cell variety (). FNAC of left sided supraclavicular lymph nodes showed metastatic squamous cell carcinoma. Sputum for malignant cell was negative and fibre optic bronchoscopy did not show any abnormality. Echocardiogram showed a large echogenic mass of 15 × 12 mm, attached to the roof of the left atrium adjacent to right pulmonary venous openings, encroaching to interatrial septum, an extension of the tumour from adjacent lung parenchyma. Ejection fraction was 66%. Ultrasound of abdomen and CECT scan of brain were normal. Hence the diagnosis was a non-small-cell carcinoma of lower lobe of right lung with invasion of the left atrium and compression of adjacent ventricular wall (T4 disease) with contralateral supraclavicular metastatic lymphadenopathy (N3 disease). First cycle chemotherapy regimen comprising intravenous cisplatin (100 mg on day 1) and etoposide (100 mg on days 1, 2, and 3) was given, but unfortunately he died just after completion of first cycle.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [74, 'years'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Hemoptysis': False, 'O₂ saturation percentage': [96.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 74 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 120.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 96.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6536,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4673375-1,Extracted,"A 57-year-old Caucasian male was brought to our emergency department (ED) following an allergic reaction (flushing, chest rash, and drop in blood pressure [BP] to 90/60 mm Hg) to intravenous (i.v.) amiodarone administered by the emergency medical service (EMS) to treat atrial fibrillation. Upon admission, he was anxious and complained of palpitations. He had a history of palpitations and experienced several episodes of irregular heart rhythm following lack of sleep, or periods of work-related stress. He had arterial hypertension for 2 years, and was regularly taking his prescribed medication (5 mg ramipril and 5 mg amlodipine). In his family history, there were no serious diseases and cardiovascular emergencies. His palpitations started 6 hours before presenting to the EMS. An electrocardiogram (ECG) at the EMS showed AF with fast ventricular response (125 bpm). Blood pressure was 180/110 mm Hg and physical examination showed no abnormalities other than irregular heart rhythm on auscultation. He was administered 300 mg amiodarone in 250 mL 5% dextrose solution, and in a matter of minutes had a drop in BP, a rash appeared on his chest, and he complained of flushing. Amiodarone was stopped, and 150 mg propafenone in 250 mL 5% dextrose solution i.v. was admistered as an alternative. This attempt at cardioversion was unsuccessful, and he was transferred to our ED.
Upon arrival to our ED he was agitated and complained of palpitations. His physical examination findings were unremarkable other than irregular heart rhythm on heart auscultation.
His BP was 130/80 mm Hg, pulse above 125 bpm, pulse oximeter showed 98% oxygenation. His body mass index was 29.2 kg/m2, body temperature 36.7°C. The ECG showed atrial fibrillation with an average ventricular response of 107 bpm. He had left electrical axis and left anterior fascicular block. There were no signs of accessory electrical conduction pathway in ECG. There were no radiological or clinical signs of cardiac decompensation, and we ruled out acute coronary or pulmoembolic syndrome. We performed both transtoracic and transesophageal echocardiography, which showed structurally normal heart with normal heart cavities and good systolic function of the left ventricle, with no visible thrombus. He was on telemetry monitoring during the index hospitalization. After having ruled out immediate and life-threatening causes, such as cardiac ischemia, congestive heart failure, and pulmonary embolism, other possible causes of paroxysmal AF were considered. The common causes of atrial fibrillation are well known, and diagnostic tests revealed no underlying structural heart disease. Thyrotoxicosis was excluded and there were no electrolyte disorders.
According to AF treatment guidelines and patient workup results, we decided for rhythm-control strategy rather than rate-control strategy since paroxysmal FA lasted less than 48 hours. Propafenone was prescribed in an oral dose of 150 mg twice a day, bisoprolol 2.5 mg in the morning, and standard thromboprophylaxis with nadroparine 0.8 ml subcutaneously once a day. A betablocator was excluded from therapy due to AF with bradycardic ventricular response (<60 bpm), and a drop of arterial BP to 105/75 mm Hg. He was very anxious and experienced palpitations, therefore we decided to treat him with acupuncture before performing a transesophageal ultrasound. He was scheduled for electrocardioversion for the upcoming day. Acupuncture was administered by a physician accredited at the Croatian Society for Acupuncture, a member of the International Council of Medical Acupuncture and Related Techniques. He was stimulated bilaterally with acupuncture needles (Tewa coated needle PB 2540, 0.25 × 40 mm) at 3 acupuncture points (HT-7, ST-36 and PC-6). Manual stimulation of the acupuncture point was performed until “De-Qui” effect (sensation of numbness, distension, or electrical tingling at the needling site) was produced, and then needles were left for 25 minutes. There was an instant drop of ventricular response rate during treatment and 2 hours after acupuncture therapy cardioversion to sinus rhythm occurred. There was no significant drop of arterial BP during or after acupuncture therapy. He received additional ambulatory acupuncture therapy during 10 treatments every third day in addition to propafenone at peroral dose of 300 mg twice a day. No anticoagulation was recommended due to CHA2DS2-VASC score of zero (0). He was urged to minimize work-related stress and keep a diary of his symptoms.
Twenty-four-hour Holter ECG performed after one month showed sinus rhythm with median frequency of 72/min. At 3 month follow-up examination, ECG showed sinus rhythm. No palpitations or other symptoms were reported by the patient. Events and interventions are summarized in the timeline (). A written consent was provided by the patient regarding presenting his case.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [57, 'years'], 'Heart Rate or Pulse': [125.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 57 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 125.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6537,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8672649-1,Extracted,"A 55-year-old male, with a history of chronic kidney disease for many years, received a living kidney transplant in 2013 and thereafter followed a regular immunosuppressive regimen, including mycophenolate mofetil (MMF) (0.5 g twice daily), tacrolimus (2 mg twice daily, the concentration was maintained at 4–5 ng/mL.), and methylprednisolone (5 mg once daily) (Fig. ). His creatinine levels were maintained at around 100 μmol/L most of the time, but increased to 180 μmol/L on Jan 15, 2020. He used to experience shortness of breath on exertion. He also had a history of heart failure, regularly taking oral medications, including clopidogrel (75 mg once daily) and aspirin (100 mg once daily), and occasionally taking furosemide (60 mg once daily).
The patient presented to a local clinic in Wuhan on Jan 31, 2020, complaining of oliguria for two weeks. Chest computed tomography (CT) revealed bilateral lung lesions, with a lot of speckle consolidation shadows seen in both lungs. An oropharyngeal swab from this patient was positive for SARS-CoV-2 as shown by the reverse transcription-polymerase chain reaction (RT-PCR) assay, suggesting that he suffered from pneumonia caused by SARS-CoV-2. He displayed no fever, cough, dyspnea, diarrhea or vomiting at that time. He was then isolated in a makeshift hospital for further treatment.
On Feb 8 (Day 0 of the illness, Day 0), the patient showed a mild cough without sputum, but developed dyspnea by Feb 12 (Day 4). He was then transferred to an intensive care unit in Tongji Hospital of Huazhong University of Science and Technology (Wuhan, China), a site designated for treating severe and critically ill COVID-19 patients on Feb 13 (Day 5). On admission, he had a blood pressure of 90/60 mm Hg, a pulse of 104 beats per minute, and an oxygen saturation of 94% while breathing ambient air. His laboratory testing showed lymphocytopenia, hypercreatinemia, and increased levels of D-dimers, C-reactive protein (CRP), and cardiac troponin I (Table ). Moreover, his CT images showed bilateral lung interstitial disease, especially near the hilum, with ground-glass opacities (GGO) (Fig. a). A combined strategy was adopted to treat him, including cessation of tacrolimus and methylprednisolone, and initial supportive treatments (oxygen delivery via nasal cannula, furosemide therapy and injection of thymosin α1 and immunoglobulin) (Fig. ). Thymosin α1 is a peptide originally isolated from thymic tissue, and shown to regulate immune function in many diseases, such as sepsis and chemotherapy-induced immunosuppression []. The patient responded well to the therapy.
On Feb 20 (Day 12), the patient showed improved clinical symptoms (BP 118/81 mm Hg, HR 84 bpm, RR 16 bpm; the patient displayed good consciousness and spirit and showed no obvious cough, expectoration, fever, chill, abdominal pain, or diarrhea; the patient had a measured SpO2 of 100% when receiving 4 L/min oxygen through a nasal cannula) and was transferred to a general ward. Due to incomplete improvement in imaging results, high levels of CRP (34.6 mg/L) and procalcitonin (0.14 ng/mL) (Table ), as well as a positive SARS-CoV-2 RNA test on an oropharyngeal swab, the patient received anti-bacterial and anti-viral treatment with beta-methylcarbapenem (0.3 g twice daily) and oral lopinavir/ritonavir (1000 mg/d), respectively. During this anti-bacterial and anti-viral therapy period, methylprednisolone (20 mg once daily), gradually reduced MMF dosage, and an adjusted dosage of tacrolimus, were also re-introduced (Fig. ). While the patient subsequently showed improved clinical symptoms, his chest CT images on Feb 24 (Day 11) still showed extensive GGO (images not shown).
To identify potential respiratory pathogens associated with the abnormal image findings, several laboratory tests were ordered. On Feb 25 (Day 17), his oropharyngeal swab remained positive for SARS-CoV-2. Microscopic analysis of his expectorated sputum (also Feb 25) did not detect P. jirovecii or Mycobacterium tuberculosis. The result of his HIV test was negative. On Feb 28 (Day 20), his serum (1, 3)-beta-D glucan (BDG) level was 89.3 pg/mL, slightly above the normal range (< 70 pg/mL). He was suspected of carrying a fungal infection, especially PJP, based on the positive BDG test, his chest CT features and long immunosuppressive state. However, his impaired kidney function (with high creatinine level) at that time precluded empiric treatment with trimethoprim/sulfamethoxazole (TMP-SMX). Instead, he was treated with micafungin (50 mg IV gtt once daily), an echinocandin that inhibits the synthesis of BDG []. Additionally, the anti-bacterial regimen with beta-methylcarbapenem was maintained empirically. Considering the possibility of lopinavir/ritonavir in increasing the concentration of tacrolimus in his blood, anti-viral treatment was replaced with umifenovir (0.2 g three times daily). After one week of micafungin treatment, serum BDG levels fell within the normal range (61.61 pg/mL). His clinical symptoms and laboratory findings continued to improve (Table ), with chest CT images on Mar 1 (Day 22) and Mar 8 (Day 29) showing gradual absorption of the ground-glass lesions (Fig. b and c). With his oropharyngeal swabs being SARS-CoV-2 negative on Mar 4 (Day 24) and 7 (Day 27), he was discharged on Mar 11 (Day 32). Since then, MMF was discontinued, but methylprednisolone (20 mg once daily) and tacrolimus (1 mg twice daily, the drug concentration was maintained at 2-3 ng/ml) were maintained. He remained well as of April 2 (Day 54), with lower serum creatinine level (112 μmol/L) (Table ) and moderately improved chest CT images (Fig. d).
Given the incomplete absorption of the lesions in the lung but nearly normal serum creatinine level (112 μmol/L), we retrospectively analyzed the patient’s sputum collected on Feb 25 for the presence of P. jirovecii by a more sensitive method. Using a laboratory-developed quantitative real-time polymerase chain reaction (qPCR) assay that targets the mitochondrial large subunit ribosomal RNA gene of P. jirovecii [], we found that the levels of P. jirovecii in his sputum were almost tenfold higher than those in a PJP positive sputum (collected from a non-COVID-19 patient). This finding suggested that the patient probably suffered from PJP. Accordingly, the patient received one month of anti-PJP treatment with TMP-SMX starting on April 4 (0.96 g twice daily), resulting in a favorable outcome, including significantly improved symptoms and imaging.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'Heart Rate or Pulse': [104.0, 'beats per minute'], 'O₂ saturation percentage': [94.0, '%'], 'Hemoptysis': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 55 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 104.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 94.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 2 + 1 = 3.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6538,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7944982-1,Extracted,"A 16-year-old girl with a history of psoriasis presented to the emergency department for fever, cough and unintentional weight loss. Her symptoms began 4 months prior to presentation with intermittent, non-productive daytime cough associated with pleuritic chest pain. She describes daily tactile fevers and chills. She has also had intermittent diffuse, ‘crampy’ abdominal pain with associated non-bloody, non-bilious emesis occurring approximately three times per week. Additionally, she described nausea and anorexia, resulting in a 15 kg weight loss over the past 4 months. She denied upper respiratory symptoms, sore throat, dysphagia, haematemesis, haemoptysis, cyanosis, diarrhoea, melena, haematochezia, dysuria, haematuria or rashes. She denied syncope, presyncope or seizures. She reported her last menstrual period as 3 months prior and denied any current vaginal symptoms. She denied recent travel, known sick contacts, sexual activity or illicit and recreational drug use. She was born in Ethiopia, moved to the USA relatively soon after birth and last travelled there 9 years ago. She had no contact with recent international travellers or prisoners.
She reported that during the past 4 months, she had been seen at an urgent care facility multiple times and treated with three different oral antibiotics for pneumonia; she cannot recall the names of these prescriptions. She has also been seen in an outpatient gastroenterology clinic and had an oesophagogastroduodenoscopy that demonstrated oesophageal candidiasis, for which she was treated with fluconazole. She was previously healthy with the exception of psoriasis. Regarding her psoriasis, she reported that she previously had diffuse skin involvement, but has never had arthritis. She was initially treated with adalimumab, a monoclonal antibody against tumour necrosis factor (TNF)-α, but was changed to methotrexate after being diagnosed with pneumonia. Her psoriatic symptoms are currently well controlled. She presented to the emergency department due to lack of improvement in systemic symptoms after the above management and a new sensation of a racing heartbeat.
In the emergency department, her initial vital signs were: temperature 39.2°C, heart rate of 140 beats/min, respiratory rate of 18 breaths/min, blood pressure of 115/61 mm Hg, oxygen saturation of 94% on room air and weight 54.6 kg. On examination, she was tired and chronically ill-appearing, but non-toxic. Her physical examination was remarkable for tachycardia without murmur, bounding radial pulses and mild respiratory distress with asymmetrically (right>left) diminished basilar aeration. She does not have lymphadenopathy, hepatosplenomegaly, ascites or peripheral oedema. The remainder of her examination was normal. Laboratory studies were remarkable for normocytic anaemia, lymphopenia, hypoalbuminemia, elevated prothrombin time and elevated inflammatory markers. Electrolytes, transaminases, thyroid profile and urine pregnancy test were normal. HIV antibody and viral load were negative. Review of records shows that her outside chest X-ray was remarkable for rounded opacities scattered throughout both lungs and a right upper lobe cavitary lesion. A chest CT was obtained, which reveals a cavitary right upper lobe mass ().",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [16, 'years'], 'Heart Rate or Pulse': [140.0, 'beats per minute'], 'O₂ saturation percentage': [94.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Hemoptysis': False, 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 16 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 140.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 94.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6539,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-6327855-1,Extracted,"A 45-year-old woman with a 3-year history of chronic anemia was followed up at the Gastroenterology outpatient department of another hospital, with a 6-month history of abdominal pain. The pain was intermittent, worse in the mornings, and localized to the epigastric region. The patient noticed that her abdomen became distended after meals and distension was relieved after a bowel movement. The patient noticed a 12-kg weight loss over the last 6 months. There was a history of nausea but no vomiting. The patient denied any history of loss of appetite, diarrhea or constipation, and upper or lower gastrointestinal bleeding. There was no significant past medical history other than anemia and multiple blood transfusions. The patient denied any history of tobacco smoking, alcohol consumption, drug abuse, Helicobacter pylori (H. pylori) infection, chronic renal failure, peptic ulcer disease, and chronic pancreatitis. Her family history was unremarkable. The patient did not have any prior surgeries or history of malignancy. Workup for her chronic anemia included CT scan of the abdomen and pelvis with intravenous and oral contrast, which revealed duodenal intussusception. The patient was booked for upper gastrointestinal endoscopy in the referral hospital but missed her appointment and asked for a referral to another hospital.
Upon arrival at our hospital, she appeared underweight (height, 162 cm; weight, 43 kg). Her vitals were stable, and she was afebrile (blood pressure, 118/67 mm/Hg; heart rate, 96 bpm; respiratory rate, 23 bpm; oxygen saturation, 98% in room air; temperature: 36.9 °C). On examination, her abdomen was soft and laxative, with no tenderness, or organomegaly. A complete blood count on the day of admission revealed the following: low hemoglobin level, 7.2 g/dL (12.0–17.0 g/dL); mean corpuscular volume (MCV), 78.0 fL (80.0–100.0 fL); low hematocrit, 24.8% (40.0%–51.0%); leukocyte count, 8.2 × 109/L (4.5-11.0 × 109/L); and platelet count, 323 × 109/L (150-450 × 109/L). Other laboratory profiles were unremarkable. Contrast CT of the abdomen and pelvis revealed significant dilation of the stomach with no detectable gastric lesion. The third part of the duodenum was distended by a sausage-shaped intraluminal structure with alternating fat planes and dilated vessels reaching up to the first part of the duodenum, suggesting retrograde jejuno-duodenal intussusception. There was no detectable soft tissue lesion, and the rest of the bowel was unremarkable (A–C). Endoscopic examination of the upper digestive tract revealed a large, long, mobile submucosal longitudinal and tortuous bulge extending from the first to the second part of the duodenum that moved freely with bowel contraction. The papilla of Vater was normal with no neoplastic process.
The patient underwent laparoscopic exploration, which revealed antiperistaltic intussusception in the proximal jejunum (). A jejunostomy was performed, and the mass was pulled through in the proximal jejunum (A).
A cholecystectomy was performed, and a pediatric feeding tube was passed through the cystic duct to locate the ampulla of Vater. The mass was not resectable without affecting the ampulla, so the decision was made to perform a pancreas-sparing duodenal resection. The excised duodenum with mass was sent for histopathological examination (B).
Pathological findings showed a large polypoid mass with the mucosa pedunculated from the bowel lumen, measuring 12 × 7.5 × 2.0 cm3. Microscopic examination revealed a bowel mucosa with underlying submucosa showing lobules of benign normal-appearing Brunner's glands separated by fibrous stroma. The nodular proliferation of Brunner glands was accompanied by cystically dilated ducts and adipose tissue with no microscopic features of malignancy (A–C). The patient was discharged postoperatively in good condition, given an appointment after 1 month.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [45, 'years'], 'Heart Rate or Pulse': [96.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Hormone use': False, 'Unilateral Leg Swelling': False, 'Hemoptysis': False, 'Recent surgery or trauma': False}",0,0,0,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 45 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 96.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 0.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
Hence, the number of PERC rule criteria met by the patient is 0."
6540,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-6198549-1,Extracted,"A 34-year-old male presented to our Emergency Department via emergency medical services complaining of palpitations, shortness of breath, and cough with one episode of hemoptysis that started earlier that day. The patient reported that his symptoms rapidly progressed a few hours prior to arrival shortly after smoking crystal methamphetamine. The patient reported chronic methamphetamine use for 10 years, becoming an everyday user 3 years ago. He admitted to occasional polysubstance use that included ketamine, ecstasy, and alcohol, although those were limited to a few times a month. Past medical history was significant for two remote spontaneous pneumothoraces, but the patient stated that his current symptoms felt unrelated. Past surgical history was noncontributory and he denied allergies or taking any prescribed medications. Reviews of systems were positive for myalgias and fatigue. The patient denied any chest pain, chest tightness or abdominal pain.
Initial vital signs include the following: HR: 153 bpm, RR: 20, BP: 115/56 mmHg, Temp (O): 102.1 °F, and SpO2 96% (RA).
The physical exam demonstrated a well-nourished, well-kept male appearing in his stated age in good physical shape. The patient appeared anxious and diaphoretic with dry mucus membranes and labored breathing. The patient was alert and oriented but found to have mild confusion upon detailed questioning. The rest of the neurologic exam was normal and the patient did not display any meningeal signs. Auscultation of the chest revealed rales at the lung bases. Cardiac exam demonstrated a regular, tachycardic rhythm without the presence of obvious murmurs, rubs, or gallops. There was no lower extremity edema present and patient displayed normal muscle tone. The rest of the physical exam was unremarkable.
Upon the patient's initial presentation, orders for initial management were with a normal saline bolus of 2 liters, supplemental oxygen with 2 liters on nasal cannula, broad spectrum antibiotics (piperacillin/tazobactam and vancomycin), antipyretics, and multiple doses of IV lorazepam with the aim of treating his tachycardia with a mixed picture of sepsis, dehydration, and methamphetamine intoxication.
Point-of-care ultrasound (POCUS) of the inferior vena cava (IVC), heart, and lungs was obtained. The IVC diameter measured 1.85 cm (max) in inspiration and 1.71 cm (min) in expiration (Images -, ). Cardiac views demonstrated gross biatrial and biventricular dilation on visual inspection with a severely reduced left ventricular ejection fraction (LVEF) and a small pericardial effusion (Images -, Videos -). Lung ultrasound demonstrated bilateral lung sliding anteriorly and B-lines in bilateral inferolateral lung fields (Images -, Videos -). With the information obtained via US, the decision was made to consult cardiology and to restrict IVF administration by giving the patient 1 liter of normal saline over the course of two hours instead of a 2-liter bolus.
Electrocardiogram (ECG) revealed sinus tachycardia with a normal axis and without ST elevations, PR depressions, or significant T-wave inversions (). Chest X-ray demonstrated a right lower lobe consolidation with evidence of central pulmonary venous congestion and cephalization (). Significant laboratory findings included a WBC count of 21,000 with a neutrophilic predominance of 81%, lactic acid of 1.8 mmol/L, Pro-BNP of 1,741 pg/ml, and Troponin I < 0.04 ng/ml. The rest of the basic blood works including renal function and electrolytes were within normal limits for our institution. Computed tomography (CT) pulmonary angiogram was performed and demonstrated a right lower lobe consolidation and no evidence of pulmonary embolism. Also evident on CT were atrial and ventricular enlargement, central pulmonary venous congestion, and signs of early pulmonary edema (Images -).
The patient was admitted to the ICU and was continued on broad-spectrum antibiotics and a normal saline infusion of 75 ml/hr. On day two, all IV fluids were discontinued and diuresis was employed for decompensated heart failure with developing hypoxia. The patient grew 2/2 positive blood cultures for Streptococcus pneumoniae and was found to be Influenza B positive. Comprehensive 2D Echocardiogram revealed dilated cardiomyopathy with LVEF of 16%, restrictive left ventricular filling pattern, elevated filling pressures with E/e'=30, moderate/severe mitral regurgitation, and severe tricuspid regurgitation.
The patient improved during hospitalization and was discharged on day 9 with a diagnosis of severe sepsis, right lower lobe pneumonia, Streptococcus pneumoniae bacteremia, Influenza B, and Methamphetamine-Associated Cardiomyopathy.
He was discharged on antibiotic therapy and a heart failure regimen consisting of lisinopril and metoprolol.
His cardiac dysfunction improved with drug abstinence and medical therapy. A four-month echocardiogram demonstrated resolution of dilated atrial and ventricular chambers, with improvement of LVEF to 45% and improvement in valvular dysfunction to only trace mitral and tricuspid regurgitation.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Hormone use': False, 'Unilateral Leg Swelling': False, 'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [153.0, 'beats per minute'], 'Hemoptysis': True, 'O₂ saturation percentage': [96.0, '%'], 'Recent surgery or trauma': False, 'age': [34, 'years'], 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 34 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 153.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 96.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6541,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7934556-1,Extracted,"A 73-year-old female patient, who was hospitalized since 3 months, presented with complaints of paroxysmal dry cough since 2 weeks. The patient was admitted initially due to progressive dyspnea. Respiratory distress occurred 2 days later and she was transferred to the intensive care unit (ICU) after intubation for mechanical ventilation. Her past medical history included hypertension and diabetes mellitus for approximately 20 years; both of which were in a stable condition with regular medication. Six months before admission, she underwent a median sternotomy and thymectomy for thymoma. She denied having a recent travel history aboard but reported contact with a large pigeon population as there was a large dovecot near her residence. A series of examinations were performed for the unexplained respiratory failure, and myasthenic crisis was diagnosed based on high levels of acetylcholine receptor antibodies (> 4 nmol/L) and neurophysiological study findings. Consequently, she received several courses of plasma exchange followed by a high dose of prednisolone (30 mg daily) and azathioprine (25 mg daily) to treat the myasthenic crisis. Her respiratory condition improved after the therapy. She was transferred to the general ward after successfully weaning off mechanical ventilation. Oral prednisolone and azathioprine therapy was continued. After receiving prednisolone and azathioprine therapy for nearly 3 months, she developed dry cough. Physical examination revealed that respiratory rate was 15 breaths/min, blood pressure was 140/88 mmHg, heart rate was 80 beats/min, and body temperature was in the normal range. The remainder of the examination including cardiovascular, respiratory, and other organ systems was unremarkable. Laboratory evaluation included a peripheral white blood cell count of 8870/µL; hemoglobin, 10.8 g/dL; and platelet count of 299,000/µL. Her serum alanine aminotransferase level was 9 U/L; aspartate aminotransferase level was 19 U/L; blood urea nitrogen level was 13 mg/dL; creatinine level was 0.3 mg/dL; level of procalcitonin was 0.1 ng/Ml, and level of C-reactive protein was 1.78 mg/dL. Arterial blood gas analysis (with the patient breathing ambient air) revealed pH 7.47, PaCO2 56.9 mmHg, PaO2 66.7 mmHg, and oxygen saturation 99%.
A thoracic CT scan was performed. On comparing it with the previous thoracic CT scan performed on admission (Fig. a), a newly developed 2-cm consolidative nodule was observed on the upper lobe of the left lung (Fig. b). Serum aspergillus galactomannan antigen testing, fungus stain and fungus culture of sputum, polymerase chain reaction (PCR) of sputum for mycobacterium tuberculosis were all negative. The CT-guided biopsy was performed, and its pathology revealed chronic granulomatous inflammation with multinucleated giant cells engulfing thick-wall micro-organisms (Fig. a). These organisms were 4–6 microns in diameter, stains bright red with Periodic Acid Schiff (Fig. b) and black in Gomori Methenamine-Silver (Fig. c), consistent with those of cryptococcus. A subsequent serum titer of cryptococcal antigen was 1:8 using Remel Cryptococcus Antigen Test Kit (Remel, Lenexa, KS, USA). Because there were no neurologic symptoms and signs indicated cryptococcus meningoencephalitis, lumbar puncture was not performed. Immune status of the patient was then assessed. Except for recent immunosuppressive therapy for the myasthenic crisis, the patient revealed no evidence of malignancy or vasculitis, and human immunodeficiency virus testing was negative. To determine the possibility of cross transmission from infected patients, we reviewed the incidence of cryptococcal infection cases in the ICU and the general ward for up to 1 month before the patient was diagnosed, but no new cryptococcal infection cases were reported. Intravenous fluconazole, 400 mg daily, was administered for pulmonary cryptococcal infection for 14 days. Respiratory symptoms nearly resolved after treatment and the patient was discharged for outpatient follow-up with continuation of oral fluconazole 400 mg daily. The chest CT scan, 3 months after discharge, revealed complete clearance of the lesion (Fig. c) and the relevant inflammatory biomarkers were in the normal range. No recurrence of the Cryptococcal infection has occurred to date.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [73, 'years'], 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'O₂ saturation percentage': [99.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Hemoptysis': True, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 73 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 80.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6542,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-5107867-1,Extracted,"A 58-year-old female after allogeneic stem cell transplant (SCT) for acute myelogenous leukemia (AML) presented with cough productive of brown sputum and right shoulder pain. Her symptoms progressed over the course of 2 weeks. She did not have fever, chills, or shortness of breath. She denied chest pain, vomiting, or diarrhea and she did not report headache, loss of consciousness, or seizures.
She was diagnosed with AML 2 years ago for which she underwent allogeneic SCT. Thereafter she developed chronic graft versus host disease (cGVHD), which was treated with steroids and mycophenolate mofetil. Her home medications included prednisone, mycophenolate mofetil, and dapsone.
On examination, she was afebrile with a heart rate of 57, blood pressure of 150/74, and oxygen saturation of 93% on room air. Lung examination revealed reduced air entry and rhonchi over the right upper lung zone. Heart exam revealed regular heart sounds without murmurs and her abdomen was soft without tenderness or organomegaly.
Laboratory tests showed white blood cell count of 7.6 × 109 cells/L (88% neutrophils), hemoglobin of 94 g/L, platelets of 34 × 109 cells/L, and creatinine of 70 μmol/L. Chest computed tomography (CT) scan was done and is shown in . Bronchoalveolar (BAL) stains and cultures were negative for bacteria, mycobacteria, and fungi. Serum as well as BAL galactomannan and serum cryptococcal antigen were negative. Her prednisone dose was reduced and she was discharged home on ertapenem and voriconazole that were given on empirical basis.
The patient's symptoms persisted, so a follow-up chest CT scan was done 2 weeks into treatment (). She was readmitted to the hospital and started on broad-spectrum antibiotics: linezolid, imipenem, amikacin, and liposomal amphotericin B. Her vital signs on admission were stable with an oxygen saturation of 93% on room air. Labs were within her baseline. A repeated BAL was performed.
What is your diagnosis?",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [58, 'years'], 'Hormone use': True, 'Heart Rate or Pulse': [57.0, 'beats per minute'], 'Hemoptysis': False, 'O₂ saturation percentage': [93.0, '%'], 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 58 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 57.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 93.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
Hence, the number of PERC rule criteria met by the patient is 3."
6543,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-5818954-1,Extracted,"A 42-year-old female was seen in the emergency department with three days of severe abdominal pain and sepsis. Medical history included menometrorrhagia due to uterine fibroids and previous endometrial ablation in 2015. She used a contraceptive vaginal ring for three months prior and Provera for 2 days prior to presentation for persistent vaginal bleeding. Physical examination revealed the following vital signs: temperature 39.2°C; blood pressure 136/78 mmHg, pulse 132 beats/min, and respiratory rate 16 breaths/min. Oxygen saturation was 100% on room air. Physical exam revealed tenderness throughout the lower abdomen with voluntary guarding. Labarotory data revealed WBC of 12,000/µL, Hgb of 7.8 gm/dL and Hct of 25.7, sodium of 127 mmol/L, and chloride of 96 mmol/L. Lactate was normal at 1.5 mmol/L. Initial CT scan showed uterine masses, consistent with known fibroids, and minimal pelvic fluid ().
She was initially admitted to the medical service for sepsis. Given her lower abdominal pain, Gynecology was consulted for presumed pelvic inflammatory disease (PID). She was started on empiric antibiotics for PID (ceftriaxone IV 1 g every 24 hours, azithromycin IV 500 mg every 24 hours, and metronidazole IV 500 mg every 8 hours). Blood, urine, and stool cultures were sent upon admission, all of which were negative.
Her pain continued to progress with rising leukocytosis to 20,000/µL. A repeat CT scan on hospital day four showed interval development of ascites (). Surgical consultation was obtained, and she was found to have an acute abdomen. She was taken for a diagnostic laparoscopy, which revealed a dense fibrinous exudate and significant ascites in all four quadrants of the abdomen (). Multiple peritoneal biopsies were taken, and peritoneal fluid was sent for gram stain, cultures, and cytology.
Postoperatively, carcinoembryonic antigen (CEA) and CA-125 levels were obtained. CEA was within the normal range, and CA-125 was mildly elevated at 56.8 U/mL (normal 0–35.0 U/mL). Her WBC fluctuated between 15,000 and 25,000/µL. The peritoneal fluid gram stain did not reveal any bacteria. Cytology revealed rare mesothelial cells and abundant neutrophils but no malignant cells. Final pathology report stated the presence of benign fibromembranous tissue with severe acute inflammation and extensive necrosis, consistent with “severe necrotizing acute peritonitis.”
Given the extensive inflammatory reaction, infectious disease was consulted. Group A Strep (GAS) peritonitis was suspected, and recommendations were made to continue ceftriaxone at 1 g IV every 24 hours in addition to one dose of clindamycin 600 mg IV. Azithromycin was added to ceftriaxone three days later (IV 500 mg every 24 hours). A streptolysin O antibody (ASO) titer was sent but came back normal at 61 I U/mL (normal range 0–330 IU/mL), arguing against GAS peritonitis. Ceftriaxone was stopped, and azithromycin was transitioned to oral 500 mg daily.
She continued to have persistent abdominal pain and anorexia. A repeat CT scan obtained nine days after surgery () showed peritoneal enhancement and several fluid collections. A diagnostic paracentesis was performed, and the peritoneal fluid was sent to an outside institution for 16S ribosome analysis, to isolate bacterial RNA.
Her abdominal pain and leukocytosis slowly improved. She continued to have severe anorexia and food aversion, despite reassuring physical exam findings. On hospital day 23, she was discharged home on oral azithromycin. Several days after discharge, 16S ribosome testing revealed Mycoplasma hominis RNA within the peritoneal fluid. Her outpatient antibiotic was changed to oral doxycycline 100 mg twice daily for three months. She was closely followed as an outpatient and gradually demonstrated clinical improvement. She remains well ten months after hospitalization.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [42, 'years'], 'Heart Rate or Pulse': [132.0, 'beats per minute'], 'O₂ saturation percentage': [100.0, '%'], 'Hormone use': True, 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 42 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 132.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 100.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
Hence, the number of PERC rule criteria met by the patient is 3."
6544,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7798777-1,Extracted,"A 75-year-old female presented to the emergency department with dyspnoea. She had been treated for recurrent lower respiratory tract infections by the general practitioner (GP) with oral antibiotics (12 cases in the past 14 months). Her relevant medical history included chronic kidney disease stage 3 (baseline creatinine 80–110 µmol/L), polymyalgia rheumatica requiring long-term steroids, asthma and chronic back pain. The pneumonia diagnosis was confirmed by a chest radiograph and CT showing multifocal nodular consolidation in the right lower lobe with cavitations and blood cultures were taken that grew Staphylococcus aureus.
Her medical history otherwise included depression, hypercholesterolaemia, gastro-oesophageal reflux disease, spondylosis, glaucoma, hypertension, lacunar stroke, transient ischaemic attack, vitamin B12 deficiency and vascular dementia.
Her long-term treatment included hydromorphone, paracetamol, topiramate, paracetamol–codeine–doxylamine, doxylamine, colecalciferol, aspirin, duloxetine, pantoprazole, prednisolone, docusate, macrogol, hydroxocobalamin, salbutamol and denosumab.
On presentation, she was initially afebrile, heart rate of 95 bpm, respiratory rate of 25 breaths per minute and oxygen saturation of 96%. On examination, there were crackles on the right base, dual heart sounds with no murmurs and no peripheral stigmata of infective endocarditis. She was subsequently treated for pneumonia and urinary tract infection with intravenous piperacillin–tazobactam. The working diagnosis was S. aureus bacteraemia secondary to a pulmonary source.
The patient was transferred to the closest tertiary hospital as the eventual need for further investigations, including a trans-oesophageal echo, was anticipated in the context of S. aureus bacteraemia. The treatment of her bacteraemia was eventually changed to intravenous flucloxacillin (2 g four times daily) once sensitivities were confirmed. Flucloxacillin was planned to continue for a further 5 weeks via peripherally inserted central catheter (PICC) on an 8 g/24 hours infuser that was monitored via hospital in the home (HITH).
Four weeks into the HITH treatment, the patient developed nausea and was investigated with blood results that showed worsening renal function associated with HAGMA. She was subsequently referred back to the regional hospital. Her heart rate was 105 bpm, respiratory rate of 20 breaths per minute and O2 sat 98% on room air. At that point, HAGMA was attributed to an acute kidney injury (AKI). Following adequate fluid resuscitation, HAGMA and AKI persisted. She was investigated for the AKI with a renal ultrasound which was negative and there were no eosinophils found in the urine. Interstitial nephritis secondary to flucloxacillin use was considered as another reason for her AKI but was deemed unlikely. The treatment plan was to commence sodium bicarbonate 840 mg once daily following consultation with the renal team. Ultimately, further investigations for the AKI were completed at the tertiary hospital. The HAGMA was suspected to be caused by the concurrent use of flucloxacillin and paracetamol. As a result of this, flucloxacillin was changed to cefazolin and the patient transferred again to a tertiary facility pending further investigations as well as suspected pulmonary embolism following reports of chest pain.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [75, 'years'], 'Heart Rate or Pulse': [105.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 75 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 105.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6545,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4623380-1,Extracted,"A dyspneic 69-year-old male was referred for further management to our tertiary referral hospital with suspicion of pericardial effusion and cardiac tamponade. He suffered typical chest pain, diaphoresis, and an anterior myocardial infarction 3 days before admission to our hospital and was treated with streptokinase in a general medical center. He also underwent dopamine and dobutamine therapy in that center because of a significant reduction in his blood pressure.
On admission, he had a pulse rate of 105 bpm, a blood pressure of 80/65 mmHg, and a respiratory rate of 25 (O2 saturation = 92%). On physical examination, he had muffled heart sounds and a fine crackle in the lower two-thirds of both lungs. His jugular venous pressure was higher than normal, and his electrocardiography showed sinus rhythm with significant Q waves in V1 through V6 precordial leads.
Initial transthoracic echocardiography showed a severe abnormal left ventricular ejection fraction (LVEF = 20%) with a massive pericardial effusion with hemodynamic effect (right ventricular outflow tract collapse). The results were highly suggestive for rupture of the apical septal myocardium with clot formation.
The operation was performed through a standard median sternotomy. The proximal part of pericardium was partially opened, and a controlled amount of blood was removed gradually, which immediately improved his hemodynamic indices. Standard cardiopulmonary bypass (CPB) was performed with mild hypothermia (32°C) and standard cardioplegic myocardial preservation. The heart was arrested, and the pericardium was opened completely. Thereafter, the remaining blood was drained. A large myocardial infarction in the apex was seen, and the sub-epicardial hematoma extended to the lateral side of left and right ventricular free wall. This resulted in intramural perforation of the apex (). The distal part of the LAD was inside the hematoma and was not suitable for graft anastomosis. Under dry conditions, a 95 × 48 mm piece of TachoSil® patch was positioned on the area and was pressed to the surface of the ventricle for 5 minutes. This was repeated two times after which no bleeding was observed. Thereafter, a large autologous pericardial patch was fixed over the surface covered by TachoSil® fleece far from fragile necrotic tissue with a few separate 6 - 0 Prolene sutures to obtain maximal adhesion to the epicardial surface. Finally, a generous Teflon felt patch was sewn over all previous patches to reinforce adhesion and avoid blood oozing (). The aortic cross-clamp was released, and the patient was weaned from CPB after normothermia with normal sinus rhythm, epinephrine, and insertion of an intra-aortic balloon pump. The CPB and aortic cross-clamp times were 112 and 47 minutes, respectively. No bleeding occurred during the follow-up period.
The patient was alive and had a good clinical status 12 months later. Postoperative and follow-up transesophageal echocardiography showed normal left and right ventricular size (LVEF of 30% - 35%) without pseudo-aneurysm. All apical, inferoseptal, and anteroseptal segments showed akinesia. Echocardiography also revealed anterior hypokinesia. There was no ventricular septal defect. The pericardium was normal without any effusion.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [69, 'years'], 'Heart Rate or Pulse': [105.0, 'beats per minute'], 'O₂ saturation percentage': [92.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 69 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 105.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 92.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 2 + 1 = 3.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6546,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4309308-1,Extracted,"A previously healthy 50-year-old intoxicated man was driving on a road on a May afternoon when he attempted to move a snake off the road with a stick to prevent it from being run over. He was bitten on the dorsum of his right hand by a positively identified 6-foot long diamondback rattlesnake (). He immediately called his wife who called emergency medical services (EMS) while he drove home. When EMS arrived, he was found to be confused, nauseated, and vomiting, with altered mental status and intermittent combativeness. Once in the transport vehicle, an intravenous line was established and he was given 25 mg of intravenous (IV) diphenhydramine.
Upon arrival in the emergency department (ED) less than one hour after the initial injury, the patient was noted to be tachycardic (HR 131), hypotensive (92/79), and stridorous. On physical examination, he had decreased mental status, voice change, and significant perioral, pharyngeal, and marked glossal edema. Rapid sequence intubation (RSI) was initiated due to impending complete upper airway obstruction. The patient was pretreated with 100 mcg of phenylephrine IV to prevent hemodynamic decompensation during RSI. During video-assisted laryngoscopy, pronounced epiglottal and cord edema was noticed, and multiple attempts of passing a styletted endotracheal tube and gum elastic bougie failed. Bag valve mask ventilation was difficult despite use of an oral airway with a decline in his oxygen saturation to 78%. Thus the decision was made to proceed with emergency cricothyrotomy using a bougie-assisted landmark-guided technique, which was successful on its first attempt. A cuffed 6-0 endotracheal tube was passed over the bougie, with good chest rise and end-tidal capnography. At the time of securing the airway, the patient's oxygen saturation had returned to 100% secondary to continued uninterrupted two-person oral airway assisted bag valve mask ventilation.
Initial arterial blood gas analysis showed a pH of 7.03, pCO2 of 56.1 mmHg, and pO2 of 174.0 mmHg on 60% FiO2. He received 125 mg IV methylprednisolone and 1 L Plasma-Lyte A with improvement of his blood pressure to 119/76.
His right upper extremity was noted to have fang marks 2.5 cm apart in the first dorsal webspace (). There was severe amount of edema over the palmar and dorsal surface of the right hand extending proximally to the wrist with mottling and ecchymoses of the right hand. The compartments remained compressible, capillary refill remained brisk, and oxygen saturation remained 95–99% SpO2 in all five fingers. Orthopedic surgery was consulted by the emergency physicians for the evaluation of progressive swelling and potential compartment syndrome; no surgical intervention was performed as the patient maintained a radial pulse by Doppler signal and brisk capillary refill.
The state's poison center was simultaneously consulted in the ED; an initial bolus of 6 vials of FabAV (CroFab) was administered. Initial pre-FabAV laboratory findings from the emergency department demonstrated consumptive coagulopathy: thrombocytopenia (platelets 20 × 103 mm−3), d-dimer > 20 μg mL−1, fibrinogen < 35 mg dL−1, INR > 8, PTT > 240 sec, and PT > 150 sec. The patient was subsequently admitted to the medical intensive care unit for further management.
The state's poison control recommended boluses of CroFab per their protocol, which initially corrected his coagulopathy. His coagulation panel at the time of administration of FabAV throughout his hospitalization is shown in . The first week of his hospitalization was uneventful. The edema of his right upper extremity stabilized within 24 hours and did not require surgical intervention. He was successfully extubated on day 5.
On day 8 of his hospitalization, his fibrinogen and platelet count trended downwards, and his PT and INR trended upwards. He remained hemodynamically stable with no drop in his blood pressure, hemoglobin, or hematocrit and did not exhibit signs or symptoms of bleeding from his coagulopathy. There was no recurrence of swelling. Hematology was consulted, and decision was made to start him on FabAV infusions each over 6 hours instead of 1 hour. After six vials of FabAV were infused over 6 hours each, his coagulopathy resolved. The resolution of his coagulopathy is demonstrated in . His coagulopathy resolved by day 12 and he was subsequently discharged from the hospital.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [50, 'years'], 'Heart Rate or Pulse': [131.0, 'beats per minute'], 'O₂ saturation percentage': [78.0, '%'], 'Hormone use': False, 'Unilateral Leg Swelling': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 50 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 131.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 78.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 2 + 1 = 3.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6547,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-5139857-1,Extracted,"A 33 years old Caucasian male presented to the emergency room of St.Vincent Mercy Medical Center at Toledo, Ohio with a history of intermittent hemetemesis for last couple of weeks which has increased in severity during the last 24 hours, progressing to 4 episodes of a cup full of blood. He also had complaints of light headedness and dizziness. He had no history of hemetochezia, melena, fever, chills, constipation, diarrhea, abdominal pain or nausea. He had no recent NSAIDs use, headache, chest pain, shortness of breath or palpitation.
Patient had past history of Diabetes Mellitus type 1 and is on Insulin. Patient had history significant for Gallstone pancreatitis which resulted in Pseudocyst formation. Patient had undergone Cholecystectomy and Cystojejunostomy in 2007. He had history of Spinal Stenosis, right knee surgery and Tonsillectomy. Patient was allergic to Avandia, Fentanyl, and Metfromin. Patient was on Tramadol, Neurontin, Insulin, Zolpidem and Omeprazole. Patient had no history of Gastrointestinal (GI) disease in family. His father had diabetes and mother had COPD and pernicious anemia. Patient was a non smoker, non alcoholic and denied using any illicit drugs. His bowel and bladder functions were unaltered.
On presentation his vitals were Temp: 36.3 °C, Pulse: 114/min, Blood pressure: 102/54 mm of Hg, Oxygen saturation: 99% on room air and Respiratory rate: 16/min. On physical examination he was conscious, coherent, pale looking and weak with warm and moist skin without dermatosis. No signs of Jaundice or generalized Lymphadenopathy were found. He had no obvious spinal or limb deformities. He had normal pulses in all extremities without any signs of cyanosis. His oral cavity was normal without ulcerations. His chest was symmetrically expanding with good breath sounds and without labored breathing. He had adynamic precordium with apex beat located in 5th intercostal space at midclavicular line. He had normal heart sounds without any murmur. His abdomen was soft and flat. He had tenderness in epigastric region. No organomegaly or masses were found and bowel sounds were normal. Patient had normal neurological examination with grossly intact cranial nerves and normal reflexes. Pupils were equal and reacting to light normally.
His initial investigations were Hemoglobin 6.3 gm/dl, Hematocrit of 18.7%, MCV: 88.8 fL, White cell count 8.4 k/ul (Neutrophils 84, Lymphocytes 10, Monocytes 6, Eosinophils 0, Basophils 0), Platelet count: 327 k/ul, Sodium: 137 meq/l, Potassium: 4.7 mEq/l, Bicarbonate: 24.5 mEq/l, Chloride: 103 mEq/l, Blood Urea Nitrogen: 35 mg/dl, Creatinine: 0.59 mg/dl, Glucose: 231 mg/dl, Bilirubin: Direct: 0.12 and total 0.28 mg/dl, Proteins total: 4.4 g/dl, Albumin: 2.7 g/dl, AST: 31 units/L, ALT: 44 units/l, Calcium: 7.9 mEq/l, Alkaline phosphatase: 53 units/l, Lipase: 23 units/l, pCO2 46, pO2 84, pH 7.34, PTT: 23.4 (20.3-30.9 sec), Prothrombin time: 12.5 (9.7-12 sec), INR: 1.2, Fibrinogen: 420(140-420 mg/dl). Hepatitis serology and ANA screen were negative. He had undergone Liver biopsy was performed during surgery which was found normal without any changes of cirrhosis of liver ().
On upper GI endoscopy (EGD) esophageal and stomach mucosa were found normal without any active sites of bleeding. Fundus was clearly seen without varices. Pylorus was patent and the duodenal bulb was normal. The major papilla was identified in the descending duodenum and had normal appearance. Just distal to the major papilla in the 2nd portion of duodenum, there was a large submucosal bulge suspicious for an ectopic duodenal varix (). On withdrawal of the scope findings were confirmed.
Abdominal and pelvic CT scan with contrast showed massive gastric distention. Gastric outlet obstruction was suspected. Pancreatic Pseudocyst in the tail of the pancreas had significantly increased in size from the previous study. Changes of chronic pancreatitis were present.
Mesenteric Arteriogram showed slow contrast filling of the superior mesenteric vein with significant limiting of flow. Superior Mesenteric Vein obstruction was suspected. Multiple venous varicosities around the distal stomach and the pancreatic head region were found (). Possibility of at least partial thrombosis of the Superior Mesenteric Vein (SMV) near the pancreatic head region was suspected secondary to pancreatitis. Splenic vein was found of normal caliber without any varicosities.
Patient had undergone end to side Mesocaval Anastomosis with a Dacron 10 mm graft between the Superior Mesenteric Vein and the Inferior Vena Cava along with adhesionolysis and liver biopsy. During surgery no varicosities found in the gastric and esophageal region or no dilation found in the splenic or inferior mesenteric venous system. There were multiple adhesions found in the tail region of pancreas possibly because of previous Cystojejunostomy in that area. Similarly many adhesions found in the peripancreatic region most likely due to changes of chronic pancreatitis. Patient was discharged without any complications and found asymptomatic in the follow up visits with normal hemoglobin level and without any evidence of bleeding. Considering the young age of the patient and relatively absent varices at other sites Mesocaval shunt surgery was chosen as a treatment over Transjugular Intrahepatic Portosystemic Shunt (TIPS) and duodenal resection.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [33, 'years'], 'Heart Rate or Pulse': [114.0, 'beats per minute'], 'O₂ saturation percentage': [99.0, '%'], 'Hemoptysis': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Hormone use': False, 'Unilateral Leg Swelling': False, 'Recent surgery or trauma': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 33 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 114.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6548,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-3492683-1,Extracted,"A previously healthy 75-yr-old Korean woman was hospitalized with a 7-day history of exertional dyspnea and fever on August 16, 2011. She had not raised any pet dogs or cats. On admission, her vital signs showed body temperature 38.3℃, blood pressure 147/63 mmHg, heart rate 86/min, and respiratory rate 18/min. On physical examination, a grade 3 diastolic heart murmur was detected at left upper sternal border. Her complete blood count showed WBC 7,910/µL (neutrophils 90.8%, lymphocytes 7.5%), hemoglobin 12.7 g/dL and platelet 71,000/µL. Chemistry profiles showed total bilirubin 0.8 mg/dL, AST 16 IU/L, ALT 4 IU/L, alkaline phosphatase 79 IU/L, total protein 6.1 g/dL and albumin 2.8 g/dL. BUN 17.1 mg/dL, creatinine 0.87 mg/dL and CRP 1.4 mg/dL. Arterial blood gas analysis showed pH 7.537, pO2 65.9 mmHg, pCO2 31.3 mmHg, O2 saturation 92.2%, and HCO3 26 mM. Urinalysis revealed microscopic hematuria and microalbuminuria. A chest radiograph and electrocardiogram showed no abnormality. Echocardiography demonstrated the presence of oscillating vegetation (0.46 × 1.77 cm) attached to the aortic valve, as well as moderate aortic regurgitation. Ceftriaxone was empirically given in a dose of 2 g/day after repeated blood cultures. On hospital day 2, she underwent urgent valve replacement surgery due to the risk of embolization. Intraoperative findings revealed 0.5 × 1.5 cm sized oscillating mass on left coronary cusp. Blood cultures obtained prior to antibiotic administration were all negative. Microbiological examination of the excised aortic valve and vegetation revealed no organism on the Gram stain and the culture grew no organism. Histology revealed fibromyxoid valvulopathy and chronic active inflammation with vegetation, which were consistent with infective endocarditis. Empirical ceftriaxone treatment was continued under the diagnosis of culture-negative endocarditis.
Bacterial DNA was extracted from surgically excised valve tissue and vegetation, directly. A 16S rRNA fragment was amplified with the universal primers 4F (5'-TTGGAGAGTTTGATCCTGGCT-3'), 534R (5'-TACCGCGGCTGCTGGCAC-3'), 27F (5'-AGAGTTTGATCMTGGCTCAG-3'), and 801R (5'-GGCGTGGACTTCCAGGGTATCT-3').
The 16S rRNA gene sequence showed 100% (707/707) similarity to that of the Bartonella quintana strain (accession no. BX897700 and AJ250247) in the GenBank database (). The next closest sequences were those of Bartonella henselae, and it showed 98.7% (699/708) similarity (accession no. DQ645426 and BX897699). Identification to the Bartonella species can be accepted if there is a ≥ 99% match with the 16S rRNA gene sequence and a difference of greater than 0.8% between those of other different species, according to the Clinical and Laboratory Standards Institute (CLSI) guideline MM18-A (). B. quintana was also only the best-matched strain in the BIBI database (). Based on the molecular identification using GenBank and BIBI databases, we concluded that B. quintana was the best matched species.
In addition, serologic testing with the indirect fluorescent antibody (IFA) method, which was performed at the Korea Center for Disease Control and Prevention showed an IgG titer of 1:512 to Bartonella spp. After she was finally diagnosed with B. quintana endocarditis, gentamicin was added to ceftriaxone in a dose of 1.7 mg/kg q8h. She was discharged after ceftriaxone treatment for 4 weeks in combination with gentamicin for the last 2 weeks.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [75, 'years'], 'Heart Rate or Pulse': [86.0, 'beats per minute'], 'O₂ saturation percentage': [92.2, '%'], 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': True, 'Hemoptysis': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 75 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 86.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 92.2 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6549,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7406867-1,Extracted,"The patient was a 32-year-old female, mother of a 13-month-old boy who was directly breastfed since birth with complementary food added at 6 months of age. On January 20, 2020, the patient and her son had a family meal with relatives who returned to Yiwu from Wuhan for the Spring Festival. Two weeks later the patient had nasal congestion, and her son had a fever with a peak temperature of 38.4 °C, dry cough, and nasal congestion. Two days after the onset (February 2, 2020), tests for SARS-CoV-2 nucleic acid performed at the Fourth Affiliated Hospital, Zhejiang University School of Medicine, were positive in both the mother and the son, whereas the patient’s husband had a negative result. The results were confirmed by the Yiwu Center for Disease Control and Prevention. The patient suffered from postpartum depression, felt deeply anxious, and insisted on staying with her child. At the same time, the husband asked to accompany his wife and son due to concerns about the patient’s mental health. To respect the wish of the patient and her family, and after consultation with psychiatrists, the family was treated in the same negative-pressure isolation ward room.
On admission, the mother had nasal congestion, but no rhinorrhea, cough, sputum, fever, or fatigue. The physical examination revealed a body temperature of 36.4 °C, respiratory rate of 18 breaths per minute, a pulse of 90 beats per minute, blood pressure of 102/74 mmHg, and oxygen saturation of 98% while breathing ambient air. Lung auscultation indicated no abnormalities. The results of a routine blood tests (complete blood count, liver and renal function), C-reactive protein and chest Xray were normal. Respiratory virus antigen quadruplet test (Influenza A and B virus, respiratory syncytial virus, adenovirus) and the nucleic acid test for Influenza A and B virus were negative. The patient received atomized inhalation of recombinant human interferon α-2b 5 million International Unit (IU) in 2 mL sterilized water twice a day as the antiviral treatment from hospital day one to day 28 and traditional Chinese medicine as a supplemental therapy from hospital day four to day 28. She continued directly breastfeeding four to five times every day. The symptom of nasal congestion improved on hospital day 2, and white blood cell count declined to 2.7 × 109/L, while the lymphocyte count was 0.9 × 109/L. The nasopharyngeal swab specimens were positive for SARS-CoV-2 nucleic acid, but the serum was negative. On hospital day 3, the symptoms of nasal congestion disappeared, not to return. The mother’s body temperature and oxygen saturation without oxygen inhalation were monitored and remained within the normal range, and the patient was in stable condition. On hospital day 4, the plain chest CT scan indicated the presence of density-increased patchy consolidation and ground-glass shadow in the lower lobe of the right lung, and viral pneumonia was the likely diagnosis (Fig. a). Subsequently, on hospital day 10, white blood cell and lymphocyte counts returned to a normal level, and liver and renal function and myocardial enzyme tests continued to be normal. During the period of hospitalization, the mother’s serum, milk and feces specimens tested negative for SARS-CoV-2 nucleic acid, but the nasopharyngeal swabs were repeatedly positive. Chest CT scans on hospital days 10 and 23 showed the gradual clearing of the lungs. (Fig. b, c). On hospital days 9 and 25 after admission, the breastmilk tests yielded a positive result for SARS-CoV-2 IgG and negative for IgM. Similarly, the maternal serum was positive for SARS-CoV-2 IgG and negative for IgM on hospital days 16 and 20. On hospital day 28, the patient was discharged as three consecutive nasopharyngeal swabs were negative for SARS- CoV-2 nucleic acid. The major laboratory results of the patient are listed in Table .
The patient’s 13-month-old son had a fever, occasional dry cough, and nasal congestion at admission to the hospital. The physical examination revealed a body temperature of 37.6 °C, respiratory rate of 23 breaths per minute, a pulse of 105 beats per minute, blood pressure of 95/56 mmHg, oxygen saturation of 99% while breathing ambient air, and bodyweight of 10 kg. There was no abnormality in lung auscultation. During the hospitalization, antiviral treatment with atomized inhalation of recombinant human interferon α-2b 1.5 million International Unit (IU) in 2 mL sterilized water was performed twice a day for 8 days, from day 1 to day 8 of hospitalization. On the day of admission, the white blood cell count was low at 3.7 × 109/L, and lymphocyte count was 2 × 109/L. The infant’s serum tested negative for SARS-CoV-2 IgG and IgM. On hospital day 2, the temperature returned to the normal value, and remained normal thereafter, but occasional dry cough and runny nose continued. On hospital day 4, feces and nasopharyngeal swab specimens were positive for SARS-CoV-2 nucleic acid, and plain chest CT scan revealed ground-glass shadows in the lower lobe of the right lung (Fig. a). On hospital day 6, the child’s cough was essentially resolved, while occasional rhinorrhea persisted. At that time, the counts of white blood cells and lymphocytes were 6.9 × 109/L and 5.1 × 109/L, respectively. The child became free of symptoms on hospital day 7. On hospital day 14, the serum was negative for SARS-CoV-2 nucleic acid, but positive for SARS-CoV-2 IgG and IgM. Nasopharyngeal swabs and feces specimens repeatedly tested positive for SARS-CoV-2 nucleic acid. On hospital day 28, when the child tested negatively two consecutive times for SARS-CoV-2 nucleic acid in nasopharyngeal swabs and chest CT indicated that the ground-glass shadows in the lungs were essentially absorbed (Fig. b), the child was discharged. The major laboratory results of the child are listed in Table .",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [32, 'years'], 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Hormone use': False, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",0,0,0,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 32 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 90.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 0.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 0.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
Hence, the number of PERC rule criteria met by the patient is 0."
6550,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8114276-1,Extracted,"A 71-year-old African American male presented for routine follow-up with his primary care physician 3 months after initiating atorvastatin 80 mg and pioglitazone 15 mg daily. His lipid panel revealed a total cholesterol of 152 mg/dL, triglycerides of 83 mg/dL, high-density lipoprotein cholesterol of 59 mg/dL, and a calculated low-density lipoprotein cholesterol (LDL-c) of 76 mg/dL. LFTs were notable for an aspartate aminotransferase (AST) of 1093 U/L (upper limit of normal [ULN] 41 U/L), an alanine transaminase (ALT) of 1385 U/L (ULN 58 U/L), and an alkaline phosphatase (ALP) of 265 U/L (ULN 129 U/L; R Factor 11.6; ). Total bilirubin was elevated to 1.5 mg/dL (ULN 1.2 mg/dL). The patient denied myalgias, pruritus, or abdominal pain. He was admitted for further management.
The patient denied known hypotensive episodes or recent use of alcohol, herbal supplements, antibiotics, or acetaminophen. Gamma glutamyl-transferase was elevated to 551 U/L (ULN 50 U/L). Serum acetaminophen and ethanol were undetectable. Hepatitis A virus IgM/IgG, hepatitis B virus core IgM/IgG, hepatitis C virus (HCV), and human immunodeficiency virus-1 (HIV-1) antibodies were negative, as were hepatitis B surface antigen (HBsAg) and HIV-1 and HCV RNA. Anti-neutrophil cytoplasmic, anti-mitochondrial, and liver-kidney microsome antibodies were not detected. Serum IgG, copper, and ceruloplasmin levels were normal. Remaining workup was unrevealing except for a borderline-positive smooth muscle antibody titer of 1:20 (normal <1:20) and a ferritin of 1469 ng/mL (ULN 336 ng/mL). Serum albumin (3.4 g/dL) and prothrombin time international normalized ratio (1.01) were within normal limits. Liver ultrasound revealed “mildly increased echogenicity, coarsened echotexture, and attenuation of sound beam” suggestive of “hepatic steatosis and/or diffuse hepatocellular disease.” The right lobe measured 14.1 cm. A prior abdominal computerized tomography scan with contrast at age 60 years revealed only a punctate calcification, likely a granuloma, within the right lobe.
On admission, his temperature was 36.8 °C, heart rate was 67 beats per minute, blood pressure was 123/63 mm Hg, respiratory rate was 16 breaths per minute, and oxygen saturation was 97% on room air. Physical examination revealed no scleral icterus, a soft and nontender abdomen without palpable masses or organomegaly, and normal mental status. Atorvastatin and pioglitazone were discontinued on admission with rapid improvement in LFTs (see ). Liver biopsy was therefore not performed. The patient remained asymptomatic and was discharged on hospital day 4 with normalization of LFTs within 1 month. Simvastatin 20 mg daily and pioglitazone 15 mg daily were started 3 and 10 months after discharge, respectively. Contrast-enhanced computed tomography (CT) scan of the abdomen at 3 months again showed a likely granuloma but no steatosis. Serum LFTs have since remained within normal limits.
Before starting atorvastatin, the patient had been taking simvastatin 40 mg daily for 11 years for an elevated LDL-c of 137 mg/dL and a 10-year ASCVD risk of 18.9%. Other pertinent medical history included type 2 diabetes mellitus, hypertension, and stage 2 chronic kidney disease. He had no history of ASCVD. His baseline serum LFTs were within normal limits. No change in LFTs or other side effects were noted while on simvastatin. His LDL-c reached a nadir of 74 mg/dL at age 70 years.
Three months prior to this presentation, the patient’s LDL-c was elevated to 93 mg/dL, at which point simvastatin was stopped and atorvastatin 80 mg daily was started. A goal LDL-c below 70 mg/dL was targeted for secondary prevention out of concern for prior ischemic stroke resulting in bilateral superior altitudinal hemianopsia noted on visual field testing 6 months prior. Pioglitazone 15 mg daily was started simultaneously with atorvastatin for an elevated hemoglobin A1c of 8.1%. He was continued on his other medications, including gabapentin 300 mg 3 times daily for diabetic neuropathy, glipizide 20 mg twice daily, lisinopril 5 mg daily, metformin 1000 mg twice daily, omeprazole 20 mg twice daily, paroxetine 20 mg daily, and trazodone 100 mg as needed. Subsequent review of medication history revealed that he had not refilled his simvastatin for almost 6 weeks before starting on atorvastatin.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [71, 'years'], 'Heart Rate or Pulse': [67.0, 'beats per minute'], 'O₂ saturation percentage': [97.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Unilateral Leg Swelling': False, 'Hemoptysis': False, 'Hormone use': False, 'Recent surgery or trauma': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 71 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 67.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 97.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6551,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-5348628-1,Extracted,"A 65-year-old man presented to our hospital emergency room (ER) with complaints of bilateral flank pain. He denied nausea, vomiting and change in bowel habit. He reported decrease in appetite and loss of 15-pound (lbs.) weight in one month.
His medical history was significant for mild intermittent bronchial asthma, benign essential hypertension, major depressive disorder and prostate cancer treated with radiation therapy 5 years prior to current hospital admission which is currently in remission. He did not undergo any surgical procedures in the past. There were no gastrointestinal malignancies diagnosed in his immediate or distant family members. He never used tobacco products, alcohol or recreational drugs. He was not allergic to any medications.
On initial evaluation he was afebrile with heart rate of 75 beats per minute, respiratory rate of 18 per minute and blood pressure of 150/70 millimeters of mercury (mm of Hg). His oxygen saturation was 95% on room air. Abdomen was non-distended, soft and non-tender to palpation. On auscultation bowel sounds were noted to be normoactive. Digital rectal examination (DRE) revealed a hard palpable, non-mobile mass on the posterior rectal wall. Cardiorespiratory and neurological examination was within normal limits.
Laboratory results were significant for microcytic anemia with hemoglobin of 8.5-g percent with normal white cell counts and platelets. Coagulation parameters were within normal limits. Liver function tests showed elevated alkaline phosphatase of 482 units per liter, with remaining liver parameters being unremarkable. Tumor markers showed mildly elevated carcinoembryonic antigen level of 38.2 nanogram/milliliter and Cancer antigen-125 (CA-125) of 682.8 units/milliliter. Serum prostate specific antigen (PSA) level was 0.12 nanogram/milliliter. Computerized tomography of chest, abdomen and pelvis showed an area of opacity measuring 8.8 cm × 4.6 cm × 6.3 cm in the left upper lobe of the lung, diffuse mediastinal adenopathy and moderate to large left sided pleural effusion (Figure ). There was diffuse osteo-sclerosis of multiple bones suspicious for osteoblastic metastatic disease. Also, noted were several intrahepatic masses suspicious for metastatic disease and shotty mesenteric and portocaval adenopathy. Magnetic resonance imaging (MRI) confirmed computed tomography (CT) findings of liver metastases (Figure ).
Gastroenterology consultation was obtained in view of anemia and possible liver lesions. Patient underwent upper gastrointestinal endoscopy, colonoscopy and subsequent endoscopic ultrasound under monitored anesthesia care. Upper gastrointestinal endoscopy showed a 15-millimeter crated gastric ulcer without any stigmata of recent bleeding which was biopsied (Figure ). Colonoscopy showed a large mass in the rectum (Figure ) and four polyps in the cecum, all of which were biopsied. Subsequent endoscopic ultrasound (EUS) of the rectal lesion revealed irregular hypoechoic lesion causing thickening of the submucosal layer and irregular out-borders suggestive of malignant nature of the lesion. Patient also underwent CT guided left thoracentesis and liver biopsy.
Pathology from both rectal mass and gastric ulcer showed metastatic adenocarcinoma, consistent with lung primary (Figure ). Immuno-histochemical staining was positive for cytokeratin 7 (CK 7), thyroid transcription factor-1 (TTF-1) and napsin-A antibodies (Figure ). It was negative for PSA, prostate specific acid phosphatase, CK 20, CDX-2, cancer antigen 19-9 (CA 19-9) and P504 antibodies consistent with lung primary. Results from thoracentesis and liver biopsy yielded similar results showing metastatic adenocarcinoma of the lung origin. Patient was started on chemotherapy with combination of Carboplatin and Paclitaxel. After receiving two cycles of chemotherapy, patient and family opted for palliative care and he expired five months after the diagnosis was made.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [65, 'years'], 'Heart Rate or Pulse': [75.0, 'beats per minute'], 'O₂ saturation percentage': [95.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 65 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 75.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 95.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6552,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7182625-1,Extracted,"A 28-year-old man was admitted in our hospital on Jul 13, 2018 because of recurrent cough and yellow-phlegm accompanied by fever for more than 10 months. The symptoms were repeated after routine symptomatic treatment. A chest computed tomography (CT) scan taken in January 2018 had showed that his right lung was spotted by small piece of shadow, accompanied by a cavity. The patient refused to initiate antitubercular therapy. The symptoms were improved after self-administration of cephalosporin as anti-infection treatment for 1 week. In May, the cough and sputum were aggravated, accompanied by fever in the afternoon, with body temperature around 38 °C. In the beginning of July, chest CT showed that the patchy shadow was scattered in two lungs with multiple cavities. The large consolidation in the right upper lung was significantly progressed compared with half a year ago. Considering combination of pulmonary tuberculosis and pulmonary infection, he was hospitalized.
At admission, physical examination revealed the following: weight 53 kg; BMI 16.7, body temperature 38.7 °C, pulse 85/min, blood pressure 118/72 mmHg, finger oxygen saturation degree (FOSD) 98%. The lungs had lower breath sounds, with no obvious dry or wet rale. The auxiliary examination showed that the following test items were normal, including blood routine, biochemistry, coagulation, erythrocyte sedimentation rate, arterial blood gas analysis and echocardiography. D-dimer was 13.17 mg/L. Electrocardiogram showed sinus tachycardia. The details of chest CT was shown in Fig. . Acid-fast bacilli staining test for sputum sample was positive (4+/3+), which confirmed the diagnosis of pulmonary tuberculosis.
Routine anti-tuberculosis regimen was initiated, including isoniazid (300 mg/day), rifampin (450 mg/day), pyrazinamide (1500 mg/day) and ethambutol (750 mg/day). After 3 days of treatment, the body temperature dropped down to the normal, and the cough was relieved. Respiratory symptoms were also improved after 15 days of treatment. At that time, the patient suddenly felt chest tightness, chest pain, and shortness of breath after increased activity (three times more than the usual). Physical examination revealed: heart beats 138/m, blood pressure 88/58 mmHg, FOSD 86%. Even after 6 L high-flow oxygen intake, FOSD was maintained at 90%. Arterial blood gas analysis without oxygen inhalation indicated: pH 7.44, PO2 48 mmHg, PCO2 33 mmHg, SPO2 86%, Oxygenation Index 228.57 mmHg, D-dimer 14.03 mg/L. Electrocardiogram showed atrial tachycardia, non-specific ST elevation. Taking together, all the data highly suggested PTE. Emergency computer tomography pulmonary angiography (CTPA) inspection showed signs of filling defects in the trunk and branches of the left pulmonary artery and the right lower pulmonary artery (Fig. ).
According to the CTPA result, the patient was diagnosed as a large-scale PTE, and the risk stratification was medium-high. The patient was prescribed with low-molecular-weight heparin (LMWH) (0.1 mL/10 kg) for anticoagulation. Then, under pulmonary angiography, a combined thrombolytic therapy including mechanical thrombolysis, aspiration, and topical urokinase (300,000 U) was applied to the left pulmonary artery. Fortunately, as shown in Fig. , the filling defect of left pulmonary artery disappeared. After the interventional therapy, the patient received intravenous pumping of 20,000 U urokinase every 1 h for 24 h. The symptoms of chest tightness, chest pain and shortness of breath were significantly improved, while the blood oxygen saturation and blood pressure returned to normal, and the vital signs were stable. Neither hemoptysis nor gastrointestinal bleeding occurred during the period of thrombolysis. The deep vein B-ultrasound of double lower limbs was performed and found a flocculent echo in the superior cavity of the upper right femoral vein, and extended into the external iliac vein. Then protein C, protein S activity, coagulation factor V leiden mutation, prothrombin 20210A, lupus anticoagulant, homocysteine, were determined and no abnormality was found. Anti-tuberculosis and warfarin anticoagulant therapy were continued, and international normalized ratio (INR) value was monitored and adjusted between 2 and 3. The patient was discharged with self-administration of oral anti-TB drugs and anticoagulant drug. At follow-up after 20 days of discharge, B-ultrasound showed that the deep vein thrombosis (DVT) of right lower extremity of the patient disappeared. At follow-up of 4 months, the patient was re-examined with chest enhanced CT in the outpatient department of our hospital and no obvious emboli was found.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [28, 'years'], 'Heart Rate or Pulse': [138.0, 'beats per minute'], 'O₂ saturation percentage': [86.0, '%'], 'Hemoptysis': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': True, 'Hormone use': False, 'Recent surgery or trauma': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 28 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 138.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 86.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. At least one of the criteria is met and so we increment the criteria met by 1, making the current total 2 + 1 = 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6553,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-5965173-1,Extracted,"A 35-year-old female presented to the emergency department via ambulance with a chief complaint of chest pain and dyspnea for two hours, described as constant in nature and sudden in onset. She could identify no precipitating events and was resting in bed when it started. The patient complained of severe pain in the back of her neck and left arm, which worsened with inhalation. She found nothing to relieve the symptoms and denied fever, chills, productive cough, leg pain, and lower extremity swelling.
Her medical history included coronary artery disease, uncontrolled diabetes mellitus type 2, obesity, deep vein thrombosis, dyslipidemia, gastroesophageal reflux, headaches, and hypertension. Her surgical history was significant for three-vessel coronary artery bypass grafting. Her medications and allergies were reviewed but not pertinent. The patient used caffeine daily and denied having ever used alcohol or recreational drugs. She reported on her last primary care visit to be a former smoker. Initial examination revealed tachycardia at 126 beats per minute, 18 labored respirations per minute, temperature of 98°F and blood pressure of 140/90 mmHg, and was 97% on 2 liters (L) of oxygen. Emergency medical services initiated their chest pain protocol as well as oxygen but did not obtain room air saturation. The patient was noted to be awake, alert, and oriented to person, place, and time, with an anxious affect. Head, ears, eyes, nose, and throat exam was unremarkable. Respiratory exam showed increased work of breathing with moderate distress, but no adventitious lung sounds. Cardiac auscultation revealed a regular rhythm, without murmur, rub, or gallop. Abdominal exam was notable for obesity but non-tender. Lower extremity exam revealed no edema or calf pain.
The patient was treated with aspirin, hydromorphone, ondansetron, diphenhydramine for itching, 2L per minute oxygen via nasal cannula, and 1L of normal saline bolus followed by 100 ml/hr continuous infusion. She was placed in the clinical decision unit and an extensive investigation was undertaken. Acute coronary syndrome, pulmonary emboli, and pneumonia led the differential diagnoses. The patient received a repeat dose of hydromorphone due to sustained pain. Her electrocardiogram (ECG) showed sinus tachycardia normal axis and nonspecific t-wave changes similar to prior. She was found to have an unchanged chest radiograph compared to two years prior with hyperlucent lungs, sternotomy wires, and vascular clips. Specifically, no pneumothorax, consolidations, vascular redistribution patterns, or pleural fluid were identified. She had a normal complete blood count, procalcitonin, creatine kinase, and troponin. A measured glucose of 667 mg/dL with pseudohyponatremia 128mmol/L, chloride of 96 mmol/L, and her D-Dimer was noted to be slightly elevated. She received eight units of subcutaneous insulin and a second liter of normal saline.
A computed tomography (CT) angiogram of the chest was ordered to rule out pulmonary emboli. Before receiving the CT, the patient experienced a brief oxygen desaturation to 83% and was subsequently placed on a 5L per minute high-flow oxygen mask. During the CT, she was slightly confused and refused to lie flat. She then experienced several episodes of desaturation and at that point was requiring 12L per minute on a high-flow oxygen mask to maintain 90% saturation by pulse oximetry. After completing the CT, the patient had an arterial blood gas performed to clarify the extent of her hypoxia. Her pH was 7.42, PaCO2 36 mmHg, PaO2 50 mmHg, and HCO3 23 mEq/L. methemoglobin was 0.4% and carboxyhemoglobin was 1.1%. Arterial lactate was 2.4 mmol/L. Biphasic positive airway pressure (BIPAP) support was initiated in an attempt to supplement the patient’s respiratory efforts and prevent intubation.
The CT was reported with nodular infiltrates centered in the lower lung zones () with some confluence at the lung bases not previously seen on chest radiograph. Mediastinal adenopathy not previously seen on CT from two years prior and a nodular thickening of the hila were also noted. In addition, there was a 1.5 × 1.5 cm collection of hypodense fluid and loss of distinction in the cortex of the right kidney suggestive of trauma.
A broader history was elicited from the patient and husband to discern a possible infectious or inflammatory etiology of the observed lower respiratory pneumonitis/inhalational injury pattern. The patient and her spouse denied trauma, fever, “huffing” paint, methamphetamine use or production, bonfires, and open fires at home. The husband interjected with commentary on the patient’s heavy use of ENDS. The patient admitted to daily use of two refill containers she knew to be 2.5%/ml or 25mg/ml in nicotine concentration, which she believed was equal to a pack of cigarettes. The husband was unable to identify the single refill product that was the most recently used at home, and the patient had three different ENDS.
The patient was transferred to the intensive care unit (ICU) and upon arrival she was noted to have extensive rales, with notable work of breathing that caused truncated speech. The patient tolerated the BIPAP well, but became increasingly dyspneic despite pressure support from the BIPAP. Her increased work of breathing and impending respiratory failure urged endotracheal intubation and mechanical ventilation. A bronchoscopy was performed that demonstrated erythema of the tracheal tissues extending to the carina that appeared cobblestoned and/or leathery. The main bronchi had a yellow, vesicular appearance with interspersed erythema and increased friability of the tissue. The right mainstem bronchus and remaining airways had a rust-colored appearance along with erythema extending into the visible lower airways (). The pattern was postulated to be inhalational injury by pulmonary medicine.
Upon ICU admission the patient was treated empirically for bacterial pneumonia with meropenem levofloxacin and vancomycin. The right lower lobe bronchial alveolar lavage culture resulted in heavy growth of methicillin-resistant Staphylococcus aureas (MRSA) 48 hours after admission. Her urine culture was positive for Escherichia coli.
The patient continued to decline over the next 48 hours. She was transferred to a tertiary care center for possible ECMO, burn expertise, and continued intensive care.
Upon arrival to the tertiary care center, she was persistently hypoxemic and failed a trial of mechanical ventilation with inhaled epoprostenol. Repeat bronchoscopy was performed showing persistent vesicular injury pattern (). She underwent emergent placement of veno-venous ECMO. She was stabilized and subsequent examinations showed a left hemiparesis. The neurologic insult was diffuse on magnetic resonance imaging and read as hypoxic, toxic and or metabolic insult. She improved on ECMO, eventually receiving a tracheostomy, which was decannulated 14 days later. She was returned to the long-term rehabilitation unit at the initial treatment center. There she progressed well, where she was ambulating with an assist device and made significant progress toward an independent return to home.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [35, 'years'], 'Heart Rate or Pulse': [126.0, 'beats per minute'], 'O₂ saturation percentage': [97.0, '%'], 'Hormone use': False, 'Unilateral Leg Swelling': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': True}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 35 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 126.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 97.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. At least one of the criteria is met and so we increment the criteria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6554,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-3891071-1,Extracted,"A 25-year-old woman was admitted to our hospital with nonresolving pneumonia. The patient had felt well until two weeks before her admission, when she began to experience a dry cough, dyspnea and pleuritic pain. Her respiratory symptoms did not respond to a 5-day course of oral cephalosporin, and macrolide antibiotics had been prescribed before her admission. She was a non-smoker with unremarkable past medical history.
On admission the body temperature was 36.6℃, the heart rate was 84/min, the respiration rate was 20/minute and the blood pressure was 100/80 mmHg. On physical examination, the patient was alert and not in great discomfort. There was a crackle sound over the left lower lung zone. There was no organomegaly or lymphadenopathy. Detailed examination of the cardiovascular system and abdomen was unremarkable. Chest radiography disclosed a pneumonic infiltration on the left lower lung field and there was no cardiomegaly (). Computed tomography (CT) scanning of the chest revealed a consolidation with air-bronchogram in the left lower lobe and a small amount of pleural effusion (). The complete blood count showed a normal white cell count (8.4×109/L). There was no hypoxemia on the blood gas analysis (pH 7.4, PaCO2 37.2 mmHg, SaO2 98%) when she was breathing room air. The other laboratory investigations showed normal electrolytes and renal and liver function tests. The fasting glucose was normal. The serum anti-HIV antibody was negative. The serum immunoglobulin levels (including IgG, IgA and IgM) were normal. Pulmonary function testing showed a mild restrictive pattern (the forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) was 2.50/2.32L; the ratio was 93%), and there was a normal diffusion coefficient for carbon monoxide (DLco: 109%). The initial examination of the sputum for acid-fast bacilli with gram staining and culture did not reveal any organisms. The blood culture was sterile after 7 days incubation. We then conducted a bronchoscopic examination. There were no endobronchial abnormalities. Bronchoalveolar lavage (BAL) revealed the lymphodominant nature (a lymphocyte count of 70%, the macrophages were 28%). The BAL fluid culture was negative and there were neither acid-fast bacilli nor any pathogens.
During the first six days of this patient's admission to our hospital, her annoying respiratory symptoms and lung consolidation did not improved for all the combination antibiotic treatment (intravenous cefuroxime and oral clarithromycin). We performed a subsequent computed tomography guided percutaneous needle biopsy on the sixth hospital day. The tissue pathology revealed granulomatous lesion including multinucleated giant cells and fungal spores. The specimens were stained with Hematoxilin-Eosin, mucicarmine, Gomori-Methenamine silver (GMS), and periodic-acid-Schiff (PAS). The Hematoxilin-Eosin and GMS stain showed granulomatous inflammation with numerous yeast-like organisms that were surrounded by clear halos, and these organisms were present within multinucleated giant cells and in the intercellular spaces (). Mucicarmine staining for capsular material was negative. With performing additional Fontana-Masson silver staining (FMS), the black color in the walls of the organism was disclosed (). This special stain pattern is a characteristic of C. neoformans, and especially for the capsule deficient form. Subsequently, the antibiotic regimen was replaced by 1-week of once-a-day intravenous fluconazole treatment and the patient was discharged on oral fluconazole. Further cultures of the lung specimen yielded moderate growth of Cryptococcus neoformans afterward. During the 6-months follow up period her respiratory symptoms and abnormal radiologic feature were markedly improved ().",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [25, 'years'], 'Heart Rate or Pulse': [84.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False, 'Recent surgery or trauma': False}",0,0,0,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 25 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 84.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 0.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
Hence, the number of PERC rule criteria met by the patient is 0."
6555,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-5062238-1,Extracted,"A 15-year-old female presented in preanesthetic checkup clinic for rush nail removal of femur. She was a known case of OI type I and history of recurrent fractures for which she had been operated three times uneventfully under general anesthesia. There was no history of OI in the family.
On general examination, she was short statured with a height of 103 cm, weighing 49 kg, blue sclera, fragile bones, progressive hearing loss, kyphoscoliosis. Her blood pressure was 130/80 mmHg, and heart rate was 80 beats/min. There was no pallor, icterus, cyanosis, clubbing, lymphadenopathy, or pedal edema. Respiratory system revealed barrel-shaped chest with bilateral equal air entry, and cardiovascular system revealed normal heart sounds. Electrocardiogram (ECG), liver function test, renal function test, and coagulation profile were normal. Chest X-ray was normal except mediastinal widening; X-ray of the spine revealed dorsolumbar kyphoscoliosis to the left. Pulmonary function test was suggestive of mildly restrictive disease. Airway assessment showed acceptable flexion and extension at neck with adequate mouth opening and normal dentition, Mallampatti Class III. The patient was accepted for surgery as American Society of Anesthesiologists Grade III; in view odontoaxial dislocation and normal coagulation profile, we decided to proceed with a spinal anesthetic technique. Thorough operating room preparation was completed including difficult airway equipment, and measures made ready to deal with hyperthermias if any.
The patient was positioned very carefully on the operation table, and pressure points were padded adequately. An 18-gauge intravenous (i.v.) cannula was inserted on the dorsum of the right hand. Monitors including ECG, sphygmomanometer, and SpO2 were placed on the patient.
Her baseline blood pressure was 128/80 mmHg, heart rate was 90 beats/min, and O2 saturation on room air was 98%. An i.v. preload of 500 ml Ringer's lactate was administered. Despite the kyphoscoliosis, no difficulty was experienced in finding the subarachnoid space, and spinal anesthesia was given in the sitting position in the space L3–L4 space with 25-gauge Quincke needle with 2.5 ml of bupivacaine heavy 0.5%. The motor block was up to T 10 level. The operation lasted for 1 h and 45 min. There was no significant variation in the vitals, and the recovery was uneventful.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [15, 'years'], 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': True, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Hemoptysis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 15 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 90.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 0 + 1  =  1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6556,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-1730,Extracted,"A 43-year-old woman is brought to the emergency department because of severe central chest pain, mild shortness of breath, and one episode of coughing up blood since waking up that morning. The pain worsens on inspiration, and she describes it as 8 out of 10 in intensity. Three months ago, she underwent a left modified radical mastectomy for invasive ductal carcinoma. Her temperature is 37.8°C (100°F), pulse is 103/min, respirations are 20/min, and blood pressure is 102/74 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 93%. The lungs are clear to auscultation. Cardiac examination shows no abnormalities. The left lower extremity is swollen and erythematous. Laboratory studies show a normal complete blood count, creatinine of 1.0 mg/dL, and a creatinine clearance of 81 mL/min (N = 75–115). Arterial blood gas analysis on room air shows:
pH 7.49
PCO2 29 mm Hg
PO2 69 mm Hg
HCO3- 22 mEq/L
An x-ray of the chest shows no abnormalities.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [43, 'years'], 'Heart Rate or Pulse': [103.0, 'beats per minute'], 'O₂ saturation percentage': [93.0, '%'], 'Hemoptysis': True, 'Unilateral Leg Swelling': True, 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",5,5,5,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 43 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 103.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 93.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient note reports 'hemoptysis' to be present for the patient and so we increment the criteria count by 1, making the current total 3 + 1  =  4.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 4 + 1  =  5.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 5.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 5.
Hence, the number of PERC rule criteria met by the patient is 5."
6557,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-5053,Extracted,"A 24-year-old woman presents to the emergency department for chest pain and shortness of breath. She was at home making breakfast when her symptoms began. She describes the pain as sharp and located in her chest. She thought she was having a heart attack and began to feel short of breath shortly after. The patient is a college student and recently joined the soccer team. She has no significant past medical history except for a progesterone intrauterine device which she uses for contraception, and a cyst in her breast detected on ultrasound. Last week she returned on a trans-Atlantic flight from Russia. Her temperature is 98.4°F (36.9°C), blood pressure is 137/69 mmHg, pulse is 98/min, respirations are 18/min, and oxygen saturation is 99% on room air. Physical exam reveals an anxious young woman. Cardiac and pulmonary exam are within normal limits. Deep inspiration and palpation of the chest wall elicits pain. Neurologic exam reveals a stable gait and cranial nerves II-XII are grossly intact.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [24, 'years'], 'Heart Rate or Pulse': [98.0, 'beats per minute'], 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False, 'O₂ saturation percentage': [99.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': True, 'Recent surgery or trauma': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 24 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 98.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 0.
The patient note reports 'hormonal use' to be present for the patient and so we increment the criteria count by 1, making the current total 0 + 1  =  1.
Hence, the number of PERC rule criteria met by the patient is 1."
6558,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-5182,Extracted,"A 60-year-old man presents to the emergency department with shortness of breath, cough, and fever. He states that his symptoms started a few days ago and have been progressively worsening. The patient recently returned from international travel. He works from home and manages a chicken coop as a hobby. He has a past medical history of an ST-elevation myocardial infarction and recently has had multiple sick contacts. His temperature is 102°F (38.9°C), blood pressure is 187/108 mmHg, pulse is 120/min, respirations are 17/min, and oxygen saturation is 93% on room air. A radiograph of the chest reveals bilateral pleural effusions. Pleurocentesis demonstrates the findings below:

Protein ratio (pleural/serum): 0.8
Lactate dehydrogenase ratio (pleural/serum): 0.75
Glucose: 25 mg/dL

Further analysis reveals a lymphocytic leukocytosis of the pleural fluid.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [60, 'years'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'O₂ saturation percentage': [93.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Hemoptysis': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 60 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 120.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 93.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 2 + 1 = 3.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6559,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-5091,Extracted,"A 57-year-old man presents to the emergency department with epigastric pain. The patient states that he was at home watching television when his symptoms began. Otherwise, the patient has no complaints. The patient has a past medical history of obesity, hypertension, alcohol abuse, diabetes, and constipation. His current medications include insulin, metformin, lisinopril, and sodium docusate. His temperature is 99.5°F (37.5°C), blood pressure is 160/95 mmHg, pulse is 90/min, respirations are 14/min, and oxygen saturation is 98% on room air. Laboratory values and an abdominal ultrasound are ordered and are currently pending. An abdominal radiograph is ordered as seen in Figure A. On physical exam, the patient is clinically intoxicated. Cardiopulmonary exam is within normal limits. The patient is started on IV fluids and given morphine.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [57, 'years'], 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 57 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 90.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6560,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7962500-1,Extracted,"A 46 years old female with a history of unspecified arthritis presented to the emergency department with complaints of substernal chest pain and right leg numbness of one-hour duration. The chest pain was radiating to the left shoulder and was associated with diaphoresis and dyspnea. On examination, vitals revealed a blood pressure of 92/69 mmHg, heart rate of 54/min, oxygen saturation of 100% on room air, and afebrile at 98.3°F. There was a soft systolic murmur in the right upper sternal border. Pulsation on dorsalis pedis and posterior tibial artery and sensation on right lower extremity was decreased. Electrocardiogram (EKG) revealed complete heart block with junctional escape rhythm and ST elevation in anterior precordial leads with ST depression in leads I and aVL (Figure ). Pertinent labs revealed initial troponin-I of 0.05 ng/ml. The remaining blood work, including complete blood count and the basic metabolic panel, was unremarkable.
In the emergency department, the patient received immediate dual antiplatelet therapy, and cutaneous pacer pads were applied. Due to the focal exam findings, a computerized tomography angiogram (CTA) was performed rapidly with quick review ruling out dissection. CTA however revealed a small transverse, linear defect in the proximal aorta (Figure ). This defect was noted to propagate towards the root of the aortic valve on its anterior leaflet suggesting possible vegetation on the aortic valve. Given the ST changes and ongoing chest pain, the patient was taken immediately for cardiac catheterization which revealed a distal thrombus in the posterior left ventricular branch of the right coronary artery which was not amenable for intervention (Figures , ). During cardiac catheterization, right lower extremity pain and coolness suddenly worsened. Angiogram of the right lower extremity showed 100% occlusion of the right anterior and posterior tibial arteries (Figure ). The patient then went for emergent thrombo-embolectomy of the right tibio-peroneal trunk, with a marked resolution of symptoms. Transesophageal echocardiography was performed later confirming the vegetation in the aortic valve measuring about 6.5x4.0 mm (Figure ). Three sets of blood cultures were negative. Significant remarkable lab findings included C-reactive protein (CRP) of 10.5 ng/dl, erythrocyte sedimentation rate (ESR) of 60 mm/hr, and positive rheumatoid arthritis screen. Extensive rheumatological and hypercoagulable workup including anti-nuclear antibodies, complement levels, anti-thrombin III activity, protein C & S levels, homocysteine levels, and other procoagulant markers were within the normal range. Specific testing for systemic scleroderma, Sjogren’s, and polymyositis were also unremarkable. Confirmatory testing with anti-cyclic citrullinated protein showed levels of >250 units establishing the diagnosis of RA. The patient was treated with systemic oral anticoagulation and was initiated on steroids.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [46, 'years'], 'Heart Rate or Pulse': [54.0, 'beats per minute'], 'O₂ saturation percentage': [100.0, '%'], 'Unilateral Leg Swelling': True, 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 46 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 54.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 100.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 0 + 1  =  1.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6561,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4345244-1,Extracted,"An eighty-five-year-old female presented to the emergency room with complaints of sudden onset substernal chest pain and dizziness. Her past medical history was significant for atrial fibrillation. She had a pacemaker inserted at another facility 2 weeks before. No perioperative complications were reported and patient had been doing well without any complaints till the day of presentation. Medications included dabigatran for her atrial fibrillation. On examination, the patient was diaphoretic but in no respiratory distress. Temperature was 97°F, pulse 96/minute, irregular; systolic blood pressure was 70 mm Hg; respiratory rate was 22/minute; and oxygen saturation was 95% on room air. No jugular venous distension was noted. Cardiac examination revealed irregular rhythm, no murmur or rub. Lung auscultation revealed slightly diminished breath sounds at left base. Chest X-ray showed a mild-to-moderate left-sided pleural effusion; pacemaker leads appeared to be in the right ventricle (). Electrocardiogram (EKG) showed trioventricular (AV) sequential pacing (). Echocardiogram (ECHO) revealed no wall motion abnormality with normal ejection fraction. Pacemaker leads were visualized in the right ventricle (RV) on ECHO. Her hemoglobin was 8 gm%; prothrombin time (PT) was 19 seconds; and INR was 2.9.
No pacing or sensing failure was noted on device interrogation. The patient's hypotension persisted despite vigorous intravenous fluid resuscitation including transfusion of 2 units of blood cell and 6 units of fresh frozen plasma and improvement in her hemoglobin to 11 gm%. A computed tomogram (CT) of the chest was performed which showed a moderate left pleural effusion, with the pacemaker wire extending to the left pleural cavity and a small localized pericardial effusion adjoining the pleural effusion (). The patient's hemodynamic instability was not due to tamponade effect as the pericardial effusion was small but due to continued hemorrhage into the pleural cavity due to her coagulopathic state from being on dabigatran for her atrial fibrillation, which was not fully corrected by fresh frozen plasma infusion.
The patient was taken to the operating room where she underwent a median sternotomy. The pacemaker lead was found to be protruding out of the right ventricle (). The external portion was cut with the remaining intracardiac portion of the pacemaker lead left in place. The perforation of the RV wall was repaired. The hemothorax and hemopericardium were evacuated. Subsequently, the patient's hemodynamic status improved. Two days later, the remaining portion of the pacemaker lead was removed transvenously. A new pacemaker was inserted transvenously and placed on the right ventricular septum. The patient did not have further complications and was discharged home subsequently. On follow-up 6 weeks later, she was doing well.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [85, 'years'], 'Heart Rate or Pulse': [96.0, 'beats per minute'], 'O₂ saturation percentage': [95.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Hemoptysis': False, 'Recent surgery or trauma': True}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 85 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 96.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 95.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6562,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-6346,Extracted,"A 62-year-old woman presents to her primary care physician for problems with her legs. The patient states that she is easily tired whenever she walks. She claims that sometimes she experiences pain and swelling in her legs that can be difficult for her to cope with. The patient has a past medical history of obesity, hypertension, hyperlipidemia, myocardial infarction, and a 52 pack-year smoking history. She lives at home with her husband who assists her with daily acts of living. She endorses falling recently. Her temperature is 99.5°F (37.5°C), blood pressure is 177/108 mmHg, pulse is 90/min, respirations are 17/min, and oxygen saturation is 95% on room air. Cardiopulmonary exam is notable for mild expiratory wheezes and a murmur along the right sternal border. Inspection of the patient's lower extremities reveals the finding in Figure A.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [62, 'years'], 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'O₂ saturation percentage': [95.0, '%'], 'Unilateral Leg Swelling': True, 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 62 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 90.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 95.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6563,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8169091-1,Extracted,"A 56-year-old man presented to the emergency department with pleuritic chest pain and four episodes of hemoptysis hours after attempting to siphon fuel from a gasoline tank with his mouth []. His past medical history was remarkable for hypertension and type II diabetes mellitus. On initial presentation, respiratory rate was 30 breaths per minute, heart rate was 130 beats per minute, blood pressure was 196/102 mmHg, and oxygen saturation was 91% on room air. Physical examination was notable for normal oral mucosa with increased lacrimation, patent airway, diminished breath sounds with bilateral rales, and no accessory muscle use []. He was alert and oriented without any focal neurologic deficits. He was immediately placed on a non-rebreather mask.
The white blood cell count was 11.2 109/L. Arterial blood gas revealed the following: pH 7.410, pCO2 37.2 mmHg, pO2 104 mmHg on 100% FiO2. Chest radiograph demonstrated right middle and lower lobe infiltrates (Figure ) []. Chest computed tomography (CT) with contrast showed patchy airspace disease and air bronchograms in the aforementioned areas with a right infrahilar mass measuring 3.3 × 2.6 cm near the right middle lobe bronchi (Figure ) [].
He was admitted to the intensive care unit, ultimately requiring intubation and mechanical ventilation. Sputum and blood cultures drawn on admission revealed no growth. A repeat chest radiograph demonstrated the development of a pleural effusion, felt to be parapneumonic. A thoracentesis was performed with removal of 300 cc of yellow-colored fluid []. Pleural fluid analysis was exudative with a negative gram stain and culture. Bronchoscopy demonstrated friable mucosa in the bronchi of the right middle and lower lobes []. Purulent fluid was noted, which was suggestive of abscess formation. Gram stain of the aspirated fluid was remarkable for white blood cells without organisms.
The patient underwent thoracotomy with right middle lobe resection []. Surgical pathology revealed extensive acute and chronic inflammation with lipoid droplets, extensive necrosis, and obliteration of alveolar spaces. These findings were consistent with the diagnosis of necrotizing lipoid pneumonia with abscess formation following hydrocarbon aspiration. The patient’s hospitalization was further complicated by an acute cerebellar stroke. He required tracheostomy and percutaneous endoscopic gastrostomy tube placement. He was ultimately discharged to a long-term acute care hospital.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [56, 'years'], 'Heart Rate or Pulse': [130.0, 'beats per minute'], 'Hemoptysis': True, 'O₂ saturation percentage': [91.0, '%'], 'Unilateral Leg Swelling': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",4,4,4,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 56 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 130.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 91.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 2 + 1 = 3.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'hemoptysis' to be present for the patient and so we increment the criteria count by 1, making the current total 3 + 1  =  4.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 4.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 4.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 4.
Hence, the number of PERC rule criteria met by the patient is 4."
6564,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-3071487-1,Extracted,"A 35-year-old woman with Marfan syndrome was admitted at 37 weeks gestational age (GA). She was diagnosed with Marfan syndrome at 16 years of age. A previous pregnancy at 33 years of age culminated in a missed abortion at 6 weeks GA, for which a dilatation and curettage was performed at our hospital under monitored anesthesia with propofol and remifentanil. She underwent a Bentall operation due to aortic regurgitation at 20 years of age. She underwent a vitrectomy at 27 years of age for subluxation of the right lens. She had orthostatic headaches 3 years ago, and dural ectasia at the 5th lumbar and sacrum, which was identified on lumborsacral spine magnetic resonance myelography, was thought to be the cause of the symptoms. At the time of admission, she had a 35-mm abdominal aortic aneurysm for 8 years. The cardiac functions were stable because the previous aortic surgical procedures were well-maintained during the current pregnancy. She was medicated with verapamil, atenolol, and warfarin, which were switched to labetalol and enoxaparin during the pregnancy.
She had the pathognomic body habitus of Marfan syndrome (height, 179 cm; weight, 76.2 kg; and arachnodactyly). A metallic click and systolic murmur were auscultated with a stethoscope. Her initial vital signs showed a blood pressure of 130/70 mmHg, a heart rate of 80/min, and an oxygen saturation of 100% on room air. A pre-operative echocardiography revealed a normal left ventricle ejection fraction (55-60%) and a well-functioning prosthetic aortic valve. Mild ectatic changes in the proximal descending thoracic aorta and distal abdominal aorta (32 × 36 and 34 × 31 mm, respectively) were confirmed with no interval changes compared to the last study checked 1 year ago.
An elective cesarean section was recommended by the obstetricians, cardiologists, and anesthesiologists involved in the patient's care. Combined spinal-epidural anesthesia is the standard anesthetic choice for cesarean section at our hospital. However, the presence of dural ectasia at the 5th lumbar and sacrum, and a neurosurgeon's warning against spinal anesthesia for the possible recurrence of headache associated with CSF leakage, led us to decide on epidural anesthesia. Enoxaparin was discontinued one day before the scheduled cesarean section and unfractionated conventional heparin was administered until 6 hours before the operation.
With the patient in the right lateral position, a 17-gauge Tuohy needle was inserted at the L3-4 interspace under sterile conditions using a midline approach with the loss-ofair resistance technique. Then, a 19-gauge epidural catheter (FlexTip Plus®; Arrow, USA) was inserted via the Tuohy needle and fixed at 9 cm. Eight ml of 2% lidocaine with epinephrine (1 : 200,000) and fentanyl (50 µg) were injected via an epidural catheter as a divided first dose, and the total 27 ml of 2% lidocaine with epinephrine (1 : 200,000) and fentanyl (100 µg) was injected incrementally over 10 minutes. Twenty minutes after the last epidural injection of lidocaine, the sensory block was sufficiently high (T4) for the cesarean section. The systolic blood pressure was decreased by 25% and 3 doses of phenylephrine (100 µg) and 1 dose of ephedrine (10 mg) were administered to maintain the blood pressure at 100/50 mmHg. She was sedated with propofol after the infant was delivered and transferred to the post-anesthesia care unit. The baby had been diagnosed prenatally with possible Marfan syndrome and was transferred to the neonatal intensive care unit. The patient's post-operative vital signs were stable with a blood pressure of 106/68 mmHg, a heart rate of 83/min, and an oxygen saturation of 100%. Heparin was re-infused 6 hours after the cesarean section. The post-operative pain was managed with patient-controlled epidural analgesia for 3 days post-operatively. The epidural catheter was removed 6 hours after stopping the continuous heparin injection on the 3rd post-operative day. She was transferred to the Cardiology Department for postpartum management and discharged without cardiovascular complications.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [35, 'years'], 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'O₂ saturation percentage': [100.0, '%'], 'Hormone use': True, 'Previously Documented Pulmonary Embolism': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 35 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 80.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 100.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 0.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 0.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 0.
The patient note reports 'hormonal use' to be present for the patient and so we increment the criteria count by 1, making the current total 0 + 1  =  1.
Hence, the number of PERC rule criteria met by the patient is 1."
6565,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8592315-1,Extracted,"A 73-year-old woman presented with three days of progressively worsening sharp non-radiating reproducible left-sided thoracic pain exacerbated by movement of the ipsilateral upper extremity. Her past medical history was significant for a myocardial infarction two decades prior with resultant ischemic cardiomyopathy and congestive heart failure with moderately reduced left ventricular ejection fraction and a biventricular pacemaker and defibrillator in place. Initial examination revealed normal vital signs, non-distended neck veins, and left-sided chest wall tenderness to palpation. Electrocardiography displayed a ventricular-paced rhythm and left bundle branch block not meeting the Sgarbossa criteria for ischemia. Three serial troponin I assays were negative. Chest radiograph showed dual chamber pacer wires in place without cardiomegaly, pulmonary edema, or pleural effusions. Biventricular pacemaker interrogation revealed no arrhythmic events but indicated the need for battery replacement. Her symptoms were attributed to noncardiac musculoskeletal chest pain, and she was discharged home with plans for elective pacemaker battery replacement.
Two weeks later, the patient presented with dyspnea, orthopnea, and retrosternal chest pain. On physical examination, the patient was afebrile, and she had a blood pressure of 172/64 mmHg, pulse rate of 67 beats/minute, and respiration rate of 18 breaths/minute. Her oxygen saturation was 99% on 3 L of oxygen per minute. Cardiac examination revealed non-distended neck veins, normal heart sounds, diminished bilateral lung sounds, and mild bilateral pedal edema. Electrocardiogram was similar to the prior, and serial cardiac enzymes were normal. The brain natriuretic peptide level was elevated at 2,042 pg/mL. Chest radiograph showed increased vascular markings and cardiomegaly. Immediate intravenous loop diuretics and noninvasive positive pressure ventilation were initiated with symptomatic improvement. In the setting of unstable angina with decompensated heart failure, urgent cardiac catheterization was performed, revealing a totally occluded right coronary artery, normal left coronaries, and a calcified, well-demarcated, large left ventricular infero-basal aneurysm with a 28 mm neck opening (Figure ). Cardiac computed tomography with angiography (Figures and 3) and transesophageal echocardiography (Figure ) showed a 46 x 45 x 47 mm aneurysm originating just at the takeoff of the posterior mitral valve leaflet (increased in size when compared with prior images) and severe mitral regurgitation. The patient underwent surgical mitral valve repair, aneurysmectomy, and pericardial patching. Left ventricular ejection fraction improved from 30%-35% to 40%-45% postoperatively. Following the initial recovery period, the patient reported better exercise tolerance and improved quality of life, and she did not require further heart failure or angina-related hospitalizations to date.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [73, 'years'], 'Heart Rate or Pulse': [67.0, 'beats/minute'], 'O₂ saturation percentage': [99.0, '%'], 'Recent surgery or trauma': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 73 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 67.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6566,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7314363-1,Extracted,"A 55-year-old African American male with past medical history of hypertension, diabetes, and hyperlipidemia was admitted for fever and difficulty breathing for several days. His associated symptoms were chest tightness without any pain. A diagnosis of possible community-acquired coronavirus was made. His vital signs were a temperature of 101.8 °F, heart rate of 100 beats/min, blood pressure of 163/101 mmHg, respiratory rate of 16 breaths/min, and pulse oximetry of 96% on room air. Physical examination was remarkable for decreased breath sounds without any rales or rhonchi. The patient was placed on nasal cannula. Tests for influenza and respiratory syncytial virus by PCR were negative. Initial chest X-ray (CXR) revealed right upper lobe and bilateral lower lobe infiltrates (Figure ), without hilar fullness, congestion, or Kerley lines. Complete blood count and complete metabolic panel were remarkable for sodium of 133 mmol/L, blood glucose of 230 mg/dL, and a creatinine of 1.51 mg/dL. Troponin was elevated at 0.307 ng/ml and it slowly trended down afterwards. He was transferred to our facility on hospital day 2. The initial workup at our facility was unremarkable with a creatinine of 1.2 mg/dL and negative troponin level. Hemoglobin A1c was 8.7%. His inflammatory markers were markedly elevated, with a C-reactive protein (CRP) of 34.86 mg/dL and a D-dimer of 462. A CXR showed bilateral infiltrate (Figure ). He was placed on airborne and contact precautions. He was started on oral hydroxychloroquine and intravenous ceftriaxone with the eventual addition of doxycycline for a suspected superimposed bacterial pneumonia. His home medication of Losartan was held during hospitalization. Repeated nasal COVID PCR swabs on hospital day 2 and 3 were negative. Blood and urine cultures were negative as well. Electrocardiogram revealed left bundle branch block. Echocardiogram suggested by cardiologist revealed a reduced ejection fraction of 35%. The patient was placed on 4-5 liters of oxygen via nasal cannula throughout the hospital course and his symptoms were well controlled. Subsequently, he was able to wean off the supplemental oxygen. His CRP and D-dimer trended down. He was discharged with instructions on self-isolation.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'O₂ saturation percentage': [96.0, '%'], 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 55 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 100.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 96.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6567,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-5587959-1,Extracted,"A 64-year-old African American man presented to a university hospital with one-week history of worsening dyspnea, cough, and lower extremity edema. He endorses frequently forgetting to take his medications as well as nonadherence with dietary and fluid restrictions. Past medical history is pertinent for morbid obesity, paroxysmal atrial fibrillation (prior radiofrequency ablation, currently anticoagulated), coronary artery disease (prior stent to mid-left anterior descending (LAD) artery), hypertension, ventricular septal defect (VSD), and previous motor vehicle collision approximately ten years prior.
Upon arrival to the emergency department, he was noted to have blood pressure of 106/77 with heart rate of 94 and respirations of 23. He was saturating at 86% on 4-5 L nasal cannula and was subsequently started on Bilevel Positive Airway Pressure (BiPAP) to improve respiratory status. Physical exam was notable for bibasilar crackles, grades II/VI holosystolic murmur, mildly elevated jugular venous pressure, and 1+ bilateral lower extremity edema. Admission labs were unremarkable (including normal B-natriuretic peptide, troponin-I, and albumin). Chest X-ray demonstrated interstitial pulmonary vascular congestion (), and EKG was sinus tachycardia with first-degree AV block. He was admitted to the cardiology inpatient service for continued management of presumed acute decompensated heart failure.
Given the persistent hypoxemia, transthoracic echocardiogram (TTE) and computed tomography pulmonary angiogram (CTPA) were ordered. TTE demonstrated normal biventricular systolic function, grade 2 diastolic dysfunction, and a small, 5 mm distal inferoseptal/apical VSD (). CTPA was without evidence of pulmonary embolism but did demonstrate a 6.4 × 4.3 cm calcified lesion concerning for giant LAD coronary artery aneurysm (), though image quality was limited by lack of gating. Diuresis was continued with symptomatic improvement, but given these findings, the decision was made to proceed with invasive angiography.
Heart catheterization revealed elevated right-sided (right atrium (RA) 9 mmHg, right ventricle (RV) 52/12 mmHg, pulmonary artery 71/29 mmHg (mean 45 mmHg), pulmonary capillary wedge pressure 14 mmHg), and left-sided pressures (left ventricle 183/31 mmHg, systemic arterial pressure 171/97 mmHg (mean 128 mmHg)) without evidence of step-up intracardiac RV shunt (RA 59%, RV 61% saturation). There was elevated cardiac output (Fick—11.1 L/min (index 4.39 L/min); Thermodilution—14.4 L/min (index 5.73 L/min). Coronary angiography revealed mild luminal irregularities only, with normal ejection fraction and no evidence of LAD aneurysm (). There was no apparent mass lesion evident with fluoroscopy and ventriculogram showed normal left ventricular wall motion.
Follow-up imaging was performed to elucidate these findings, and cardiac magnetic resonance imaging (MRI) clarified the anomaly as a 5.4 × 4.1 × 4.9 cm pseudoaneurysm arising from the mid-apical free wall of the RV with a 9 mm neck (). Cardiac CT angiogram was well performed and confirmed pseudoaneurysm arising superiorly from the mid-apical free wall of the RV measuring up to 6.1 cm in maximal diameter with a 15 mm neck as well as 4 × 11 mm mid-apical VSD (). A review of the previously performed CTPA was conducted at this point and revealed a previously healed rib fracture anterior to the pseudoaneurysm ().
Given the high output heart failure noted on angiography, an abdominal ultrasound was performed and revealed evidence of a cirrhotic liver. Upon further questioning, our patient admitted to prior longstanding alcohol abuse, now in remission. Remote motor vehicle accident was the presumed etiology to the rib fracture, and in the subsequent years, our patient developed RV pseudoaneurysm as well as VSD from the penetrating fracture. The patient was seen by cardiothoracic surgery for further evaluation, with plan to continue close surveillance per patient preference.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [64, 'years'], 'Heart Rate or Pulse': [94.0, 'beats per minute'], 'O₂ saturation percentage': [86.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Unilateral Leg Swelling': True, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 64 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 94.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 86.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6568,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-2938507-1,Extracted,"A 65-year-old male presented with an abrupt onset of sharp, burning, constant right lower abdominal pain after previously been feeling well. There was no history of trauma, fever, vomiting, diarrhea, chest pain, shortness of breath, syncope, dysuria, hematuria or melena. His past medical history included hypertension, atrial flutter and cardiomyopathy, and he had an implantable cardioverter/defibrillator (ICD). There was no prior history of abdominal aortic aneurysm in the patient or in his family. His past surgical history included an inguinal hernia repair. His medications included aspirin, valsartan, metoprolol and atorvastatin. He did not smoke, use alcohol or illicit drugs.
Physical exam showed vitals signs as follows: body temperature of 36.3°C, blood pressure of 140/82 mmHg, heart rate of 52 beats per minute, respiratory rate of 18 breaths per minute and pulsoximetry of 98% on room air. He was alert, but appeared in mild distress due to pain. His abdominal exam revealed tenderness to palpation in the right lower quadrant, with no rebound, guarding, distention or organomegaly. The remainder of the exam was normal.
The initial emergency department evaluation included an electrocardiogram that showed atrial flutter with a 4:1 block. Laboratory assessment revealed trace hematuria, no leukocytosis, creatinine of 1.3 mg/dL (normal range, 0.7–1.4 mg/dL), mildly elevated lipase to 85 U/L (normal range, 12–70 U/L), mild hyperglycemia and mildly elevated aspartate aminotransferase to 46 U/L (normal range, 7–40 U/L). The lactate and coagulation profiles were within normal limits. Lactate dehydrogenase was not ordered at presentation, but obtained 2 days after admission, and was elevated at 1,479 U/L (normal range, 100–220 U/L). Lactate dehydrogenase is present in the renal tissue and elevates in serum after kidney insult, and it is unknown whether this level correlates to the severity of the infarct.
Given the nature of the pain and the hematuria seen on urinalysis and the history of cardiomyopathy with atrial flutter, both nephrolithiasis and mesenteric ischemia were strongly considered as causes for this acute pain. Therefore, both non-contrast- and contrast-enhanced helical computed tomography (CT) images [Figures and ] were obtained, which showed extensive infarction involving the upper pole of the right kidney with multiple patchy infarcts into the lower pole, a patent right renal artery, but no visualization of the interparenchymal arterial branches within the mid and upper poles of the right kidney, suggesting arterial thromboembolic disease. There was poor opacification of the right renal vein, and, therefore, renal vein thrombus could not be ruled out. A 2-mm left renal calculus was also identified.
The urology and vascular surgery services were consulted, and both recommended conservative treatment with anticoagulation. In addition to normal saline and dilaudid for pain control, a heparin bolus of 80 mg/kg was given and an infusion at 18 mg/kg/h was initiated, with the patient being admitted to the general medicine service.
It was concluded his renal artery thrombosis was most likely embolic and a 2-D echocardiogram was ordered, which showed no intramural thrombus. He was discharged 5 days later, on coumadin. His creatinine, which was 1.3 mg/dL on admission, rose to 1.8 mg/dL and fell to 1.7 mg/dL by discharge. One month later, the creatinine levels had declined to 1.6 mg/dL.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [65, 'years'], 'Heart Rate or Pulse': [52.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Hemoptysis': False, 'Previously Documented Pulmonary Embolism': False, 'Recent surgery or trauma': False, 'Hormone use': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 65 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 52.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6569,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-3109763-1,Extracted,"Our patient was a 25-year-old previously healthy female at 36th week gestation presented to the hospital with 4 days of progressive dyspnea and right-sided pleuritic chest pain. Her past medical history was pertinent for gestational thrombocytopenia which resolved spontaneously but no history of epistaxis or family history of Osler-Weber-Rendu syndrome was noted. She was found to be hypotensive and hypoxic on ventilator support. Chest X-ray revealed right-sided pleural effusion which caused complete hemithorax opacification.
Patient underwent emergent cesarean delivery due to unstable vital signs and frequent fetal decelerations. Due to persistent hypoxia and hypotension, patient was admitted to ICU with ventilator support. Physical exam was significant for decreased breath sounds on the right side, dull percussion note, and decreased vocal tactile fremitus but no evidence of cyanosis.
Vital signs were systolic blood pressure of 80 mm Hg, diastolic blood pressure of 40 mm Hg, pulse rate 142/min, pulse oximetry saturation 86% to 88% on 100% inspired oxygen, afebrile, and respiratory rate of 30/min. Patient was visibly diaphoretic using accessory muscles with sinus tachycardia noted on monitor.
Initial labs revealed normal platelets, normal coagulation panel, and hemoglobin of 6.5 gm/dL. Critical care panel showed pH of 7.4, pCO2 of 50 mm hg, pAO2 60 mm hg, and saturation of 88%.
A chest tube was placed which revealed a hemothorax. four liters of frank blood was removed with the chest tube placement which also resulted in normalization of the blood pressure and improved oxygenation on the monitor. Repeat chest X-ray showed continued opacification of the right lung, and the patient's hemoglobin continued to fall (). CT-chest with IV contrast showed a likely 1 cm area of active contrast extravasation along with compressive atelectasis of the right lower lobe.
Pulmonary angiography confirmed an AVM with feeding branch of a basilar right pulmonary artery supplying aneurysmal AVM and dilated draining vein. Embolisation of the culprit vessel was performed ().
Repeat chest X-ray showed continued opacification of the right lung and suspecting an organized blood clot thoracoscopic evacuation was performed.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [25, 'years'], 'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [142.0, 'beats per minute'], 'Hemoptysis': False, 'O₂ saturation percentage': [88.0, '%'], 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 25 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 142.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 88.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6570,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4100447-4,Extracted,"A 77-year-old African American female came to our hospital complaining of shortness of breath. The patient was experiencing severe left-sided abdominal pain for the past two weeks. It was not associated with any alleviating or aggravating factors. On the day of presentation, she became lightheaded and experience shortness of breath. The discomfort was associated with two episodes of nonbloody emesis and left-sided pleuritic chest pain. She did not have any retrosternal chest pain, diaphoresis, or syncopal episode. She was, additionally, complaining of right lower leg cramping. Her medical history included hypertension, diabetes, and deep vein thrombosis, which was treated with an oral anticoagulant for six months. The initial vitals were blood pressure of 125/62 mmHg, heart rate of 92 beats per minute, respiratory rate of 18 breaths per minute, and oxygen saturation of 99% on room air; she was afebrile. The cardiopulmonary exam was unremarkable. The initial troponin level was 0.02 ng/mL (normal: 0–0.10 ng/mL), eight hours apart. The pro-BNP level was at 7511 pg/mL (normal: 50–92 pg/mL). An electrocardiogram showed normal sinus rhythm without significant findings. A CT-chest with contrast showed diffuse bilateral pulmonary emboli in the right and left main pulmonary arteries and straightening of the interventricular septum suggestive of right ventricular strain (). The echocardiogram showed preserved ejection fraction, hypokinetic RV, mild pulmonary hypertension (RVSP of 49 mmHg), and RV/LV > 1 (). The ultrasound with Doppler of the lower extremities did not show deep vein thrombosis.
The patient was diagnosed with submassive PE, and she was decided to be treated with UAT. The UAT catheters were placed in both arteries and local alteplase was administered for 12 mg with heparin over 12 hours after receiving 2 mg of bolus. There were no peri- or postprocedural complications. The next day, the patient experienced marked improvement in dyspnea. Next day, a repeated echocardiography showed preserved ejection fraction with mildly depressed right ventricular function with RV/LV <1 () and RVSP of 40 mmHg. The patient was discharged on oral rivaroxaban. Refer to for data summary.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [77, 'years'], 'Heart Rate or Pulse': [92.0, 'beats per minute'], 'O₂ saturation percentage': [99.0, '%'], 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': True, 'Previously Documented Pulmonary Embolism': True, 'Unilateral Leg Swelling': True, 'Hormone use': False, 'Recent surgery or trauma': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 77 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 92.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is reported to have been diagnosed with deep vein thrombosis in the past. The patient is reported to have been diagnosed with pulmonary embolism in the past. At least one of the criteria is met and so we increment the criteria met by 1, making the current total 2 + 1 = 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6571,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-5748310-1,Extracted,"A 29-year-old man presented to the emergency department after one week of repeated bouts of crampy abdominal pain and diarrhea, which became bloody on the day of arrival. There was no fever, nausea, or vomiting.
He was evaluated several times in the Emergency Medicine Department during the previous three months, with various abdominal complaints that resolved after symptomatic relief without further investigation. The patient reported no additional symptoms or relevant personal or familial medical history. He worked as a bus driver, smoked cigarettes for many years, and did not drink alcohol regularly.
The patient reported daily usage of “Mr. Nice Guy” for the last few months but denied use of any other drugs or supplements. Consumption of SCs was via smoking, and he denied other means of administration such as oral or intravenous. This information was validated by collateral anamnesis of visiting friends.
In the emergency department, the patient was hemodynamically stable with initial BP recordings of 159/100 mmHg, regular heart rate of 99 bpm, and oxygen saturation of 99% on ambient air. Physical examination was unremarkable except for intense borborygmi and mild abnormal tenderness. Initial blood work showed leukocytosis of 20,000 cells/mcL with neutrophilia (80%) and normal hemoglobin (15.1 grams/dL). Biochemistry, including electrolytes, kidney function tests, liver, and pancreatic enzymes, were all within normal limits. Urinalysis was unremarkable, and urine toxicology screen was slightly positive for amphetamines and benzodiazepines but negative for other screened drugs including THC, opiates, and cocaine. Upon repeated questioning, patient once again denied use of any other stimulant including amphetamines, besides “Mr. Nice Guy.” White cell count increased to 28,000 cells/mcL six hours later, and an abdominal computed tomography (CT) performed without IV or PO contrast enhancement was unremarkable. Over the next four days the patient continued to complain of intermittent episodes of crampy abdominal pain with episodic diarrhea, followed by pain-free periods during which he strolled freely around the hospital, admitting that he was still smoking “Mr. Nice Guy,” provided to him by his friends. Additional toxic screens were not performed during hospitalization due to lack of the patient's cooperation. Leukocytosis gradually resolved. Blood, stool, and urinary cultures were negative and other laboratory data were unremarkable, with the exception of hypophosphatemia (0.5 mmol/L, normal = 0.8–1.4) and increasing C-reactive protein (22 mg/dL, normal < 0.5 mg/dL). During his hospitalization we abstained giving the patient medications from the family of benzodiazepines, potent opiates, and any medications which involve potential future addiction.
On the fifth hospitalization day, an abdominal X-ray, taken during a bout of abdominal pain, demonstrated dilated small bowel loops without features of intestinal obstruction or perforation, consistent with paralytic ileus. Later that day, the pain subsided and the patient requested to take a walk around the hospital, as our internal medicine ward regulations permit stable patients to leave their rooms. Obviously, hospitalized patients are not permitted to use any form of drug or medication not provided to them by hospital staff.
However upon returning from his walk, the patient admitted that he had once again consumed “Mr. Nice Guy” with one a friend who came to visit him. Routine checkup of vital signs revealed elevated blood pressure 180/110 mmHg with a heart rate of 120/min, without fever. Six hours later, he developed sudden extreme abdominal pain and was found to be in profound shock vomiting “coffee ground” material. Physical examination revealed abdominal guarding and rebound tenderness compatible with peritonitis, and laboratory evaluation disclosed hypoglycemia, lactic acidosis, thrombocytopenia, and worsening kidney function. An emergent surgical intervention was considered for an evolving abdominal catastrophe, but the patient quickly went into pulseless electrical activity with subsequent cardiac arrest.
A request for autopsy was declined by the patient's family, but a postmortem CT scan one hour after death revealed extensive pneumatosis intestinalis of the entire small bowel, right colon and sigmoid, gas in the portal system, and blood vessels, with free air and unclear fluid in the peritoneal cavity (Figures and ). These findings were consistent with acute intestinal perforation most probably due to a nonobstructive mesenteric infarction (NOMI) as the cause of death. There was no evidence of single vessel infarction, rather of diffuse ischemia, possibly due to splanchnic vasospasm. Air in the aorta, right ventricle, and biliary tract were conceivably postmortem changes. Urinary toxic screen sampled during hemodynamic resuscitation was positive for methadone, THC, and benzodiazepines, but negative for cocaine, opiates, and amphetamines. Unfortunately, due to technical failure, the final urine sample was not sent for confirmatory mass spectrometry testing.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'Hemoptysis': False, 'O₂ saturation percentage': [99.0, '%'], 'Recent surgery or trauma': False, 'age': [29, 'years'], 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 29 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 120.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6572,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-5889269-1,Extracted,"We report the case of a 9-year-old Saudi male who presented at King Abdulaziz University Hospital with a 3-day history of pallor, lethargy, shortness of breath, and headache. Along with these manifestations, the family noticed a yellowish discoloration of the sclera. The patient was in optimal health, with no significant medical complaints, until 2 weeks prior to hospital admission, a time when he developed symptoms of upper respiratory tract infection (i.e., a sore throat, cough, and mild subjective fever). One week later, he developed diarrhea with a frequency greater than 5 times daily. The diarrhea was yellowish in color and without blood. Furthermore, the diarrhea was associated with epigastric pain and vomiting, and it resolved a few days later; however, the epigastric pain became more severe, and his vomiting continued. Due to this situation, the patient had been unable to maintain his usual appetite and had lost some weight. The patient also reported a decrease in the amount of his urine and a change of the urine's color, which was described by the mother as tea-colored. No rash or edema was reported.
The patient was referred to our tertiary hospital by a dispensary after their results revealed red and granular casts in the urine and abnormal kidney function.
An initial assessment revealed that the patient had a rapid but regular heart rate of 118 beats/min. His respiratory rate was 20/min, his blood pressure was 119/61 mmHg, and his oxygen saturation was 100%.
Examination showed that the patient was conscious and oriented; he was pale and had yellowish sclera but exhibited no other significant signs (i.e., no periorbital or lower limb edema, skin rash, or petechia). His chest was clear, and the heart sounds were normal, with no additional sounds or murmurs. A neurological examination was unremarkable.
Based on the initial assessment and the laboratory work-up, (Table ) hemolytic uremic syndrome was strongly suspected due to the presence of the classical triad of the disease. The diagnosis of PSGN was unlikely for several reasons, although the patient had a high ASO titer; this only confirmed a previous exposure and not an infection. Additionally, another more probable disease, i.e., HUS, better explained the abnormal kidney function and urine analysis. Unfortunately, we were unable to obtain a throat swab results and get an evidence of a streptococcal infection. Thus, PSGN could not be completely ruled out.
There are few similar cases reported in the literature involving patients with SLE who initially present with HUS , , , , , . (Table )
Surprisingly, the patient also exhibited a positive immune profile for SLE (i.e., ANA and dsDNA).So far, a clear diagnosis of the acute kidney injury was difficult to be made. For this reason, a kidney biopsy was indicated.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [9, 'years'], 'Heart Rate or Pulse': [118.0, 'beats per minute'], 'O₂ saturation percentage': [100.0, '%'], 'Unilateral Leg Swelling': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 9 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 118.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 100.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6573,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-3106,Extracted,"A 28-year-old woman, gravida 3, para 2, at 34 weeks' gestation comes to the physician because of a 1-day history of dyspnea, dry cough, and chest pain. Her pulse is 112/min, respirations are 24/min, and blood pressure is 108/78 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 90%. Examination shows jugular venous distention and bilateral pitting edema below the knees that is worse on the right side. There is dullness to percussion over the right lung base.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [28, 'years'], 'Heart Rate or Pulse': [112.0, 'beats per minute'], 'O₂ saturation percentage': [90.0, '%'], 'Unilateral Leg Swelling': True, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 28 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 112.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 90.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note does not report a status on 'recent surgery or trauma'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6574,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4454912-1,Extracted,"A 62-year-old woman underwent a right mastectomy with axillary node dissection for a poorly differentiated ductal carcinoma. One month later she underwent left nephrectomy for renal cell carcinoma. After 14 days, she received her first cycle of CMF as a part of her breast cancer treatment. Two weeks later, she developed progressive shortness-of-breath, dry cough, and mild fever, for which she was started on antibiotics for possible pneumonia. Two days later, her respiratory status deteriorated and she required intubation and mechanical ventilation. Because of hemodynamic instability and hypotension, she was started on inotropes and transferred to the intensive care unit. On examination, her blood pressure was 110/70 mm Hg, pulse of 104 beats per minute, normal temperature, and her jugular venous pressure was 8 cm above the sternal angle. Chest examinations revealed bilateral bronchial breathing and diffuse crackles. Cardiovascular and abdominal examinations were unremarkable. Her initial chest x-ray showed bilateral mixed alveolar and interstitial infiltrates with volume loss (). Her arterial blood gases on room air prior to intubation, were partial pressure of oxygen 47torr, partial pressure of carbon dioxide 32torr, pH 7.49, bicarbonate 21, O2 saturation was 85%. The PAP was 36/21 mm Hg, pulmonary capillary wedge pressure 12 mm Hg, central venous pressure 20 cm H2O, cardiac index of 2.0 L/min/m2, and calculated PVR was 560 dynes sec/cm-5 (). A spiral CT of the chest showed a non-occlusive saddle pulmonary embolism with multiple bilateral pulmonary emboli (Figures ). She was treated with thrombolytics (100 mg rt-PA) followed by heparin without complications. She improved hemodynamically, and the inotropes were discontinued. Doppler ultrasound of the legs confirmed bilateral deep vein thrombosis. Because of persistent pulmonary infiltrates (Figures ), she underwent a fiberoptic bronchoscopy with bronchoalveolar lavage, which was negative. This was followed by open lung biopsy that showed loose organizing granulation tissue in the small airways consistent with BOOP (). She was treated with a pulse of steroids (1 g of methylprednisolone intravenously daily for 3 days followed by 1 mg/kg of prednisone daily). She was extubated 8 days later. She was transferred to the medical ward and was discharged home on long-term anticoagulation and steroids 2 weeks later. She had a chest x-ray before discharge, which showed near resolution of the infiltrate and restoration of lung volumes ().",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [104.0, 'beats per minute'], 'Hemoptysis': False, 'O₂ saturation percentage': [85.0, '%'], 'Recent surgery or trauma': True, 'age': [62, 'years'], 'Previously documented Deep Vein Thrombosis': True}",5,5,5,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 62 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 104.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 85.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 2 + 1 = 3.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 3 + 1  =  4.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is reported to have been diagnosed with deep vein thrombosis in the past. The patient is reported to have been diagnosed with pulmonary embolism in the past. At least one of the criteria is met and so we increment the criteria met by 1, making the current total 4 + 1 = 5.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 5.
Hence, the number of PERC rule criteria met by the patient is 5."
6575,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-5116,Extracted,"A 29-year-old woman is recovering on the obstetrics floor after vaginal delivery of 8 pound twin boys born at 42 weeks gestation. The patient is very fatigued but states that she is doing well. Currently she is complaining that her vagina hurts. The next morning, the patient experiences chills and a light red voluminous discharge from her vagina. She states that she feels pain and cramps in her abdomen. The patient's past medical history is notable for diabetes which was managed during her pregnancy with insulin. Her temperature is 99.5°F (37.5°C), blood pressure is 107/68 mmHg, pulse is 97/min, respirations are 16/min, and oxygen saturation is 98% on room air.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [29, 'years'], 'Heart Rate or Pulse': [97.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Hormone use': True, 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 29 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 97.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 0.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 0.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 0 + 1  =  1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
Hence, the number of PERC rule criteria met by the patient is 2."
6576,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-6970351-1,Extracted,"A 22-year-old female G2P0010 at 36 weeks gestation presented to an outside hospital with a 24-hour history of left flank pain and nausea. The pain was sharp, stabbing, constant, and radiated to the left mid-abdomen. She denied fever, chills, dysuria, hematuria, urinary frequency, or urgency. She underwent a CT scan that was concerning for adrenal hemorrhage [Figures and ]. She was noted to have blood pressure in the non-severe range. Later she developed severe range blood pressure and was found to have normal preeclampsia labs and negative urine spot. She was treated with antihypertensive medications including IV hydralazine 10 mg × 1, 20 mg × 2. She underwent an MRI that confirmed left adrenal hemorrhage []. Subsequently, she was transferred to our hospital.
Upon transfer, the patient's vital signs were as follows: blood pressure 168/110 mmHg, heart rate 92 beats per minute, oxygen saturation 99% on room air, and respiratory rate 18 per minute. The abdomen was gravid, soft and non-tender to palpation. Her laboratory values were notable for a white blood cell count of 19,000/uL, hematocrit (Hct) of 30.8% and spot protein/creatinine ratio of 0.3 g/day. All other laboratory values including liver function and coagulation tests were within normal limits.
A review of her history revealed an uneventful pregnancy without prior history of chronic hypertension, gestational hypertension, episodic hypertension, flushing, diarrhea, malignancy, endocrine dysfunction, coagulation disorder, family or personal history of a bleeding disorder, or blunt trauma to the abdomen. Her past medical history was notable only for migraine headaches and anxiety/depression not requiring pharmacological therapy. Her past surgical history included right laparoscopic oophorectomy for a large simple cyst.
A plan was made for conservative management of her adrenal hemorrhage and blood pressure control. Based on severe-range blood pressure on intravenous antihypertensive therapy, a diagnosis of preeclampsia with severe features was made. The patient was offered an external cephalic version for fetal breech presentation, but she declined. A decision was made to proceed with cesarean delivery. A combined spinal-epidural anesthetic was provided without complication. The patient tolerated the surgery well and was discharged home 5 days later.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [22, 'years'], 'Heart Rate or Pulse': [92.0, 'beats per minute'], 'O₂ saturation percentage': [99.0, '%'], 'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 22 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 92.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 0.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 0 + 1  =  1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6577,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-2773426-1,Extracted,"Our IV team was requested to insert a central line for parenteral nutrition in a 70-year-old female patient (weight: 57 kg; height: 160 cm; ASA: 2). Two days earlier, the patient had undergone intestinal and colic resections under general and epidural anaesthesia with a suspected diagnosis of pelvic abscess. No hysterectomy was performed during the intervention. Postoperative diagnosis was an endometrial adenocarcinoma with colic parietal infiltration through to the mucosa.
Prior to the procedure, our patient's transcutaneous oxygen saturation was 97% in room air, blood pressure was 135/80 mmHg, and pulse rate was regular at 110/minute. The patient has no history of pulmonary or pleural disease (), no history of cardiothoracic surgery or thoracic radiotherapy. No earlier central line placement insertions had been performed.
After placement of noninvasive monitoring a nasal prongs oxygen delivery device was installed administrating 2 L/minute of oxygen. Under maximal aseptic barrier protection a local anaesthesia with 1% lignocaine was placed under the right clavicula and a 18 Gauge introducer needle was introduced mid-clavicularly. The pleural space was punctured twice with the introducer needle after 2.5 cm, confirmed by the presence of air in the syringe. About one minute later, the patient started to complain of pain situated in the right side of the chest that increased at inspiration but without respiratory distress. Her oxygen saturation was at this stage 96%.
Subsequently the site of puncture was moved 2 cm medial compared to the first insertion site and the right subclavian vein was directly punctured at a depth of approximately 3 cm, just under the right-sided sterno-clavicular junction. The entire procedure was completed without any further complications and the patient's oxygen saturation was 94% at the end of the procedure.
A chest radiograph performed approximately ten minutes after the wound dressing revealed a complete left-side pneumothorax and a mild right-side pneumothorax (). At this time, the patient was starting to complain of respiratory distress. Her respiratory rate was 18/minute and her oxygen saturation was 91% with supplemental oxygen of 8 L/minute. Her pulse rate was 140/minute and her blood pressure 144/81 mmHg.
Thoracic surgeons were called and they inserted a chest tube on the left side of the chest. No clinical improvement was noticed and the patient had in between an oxygen saturation of 84% despite a face mask oxygen delivery device with reservoir.
A second chest radiograph was performed and showed a complete right-side tension pneumothorax that was not present on the prior radiograph (). The size of the left pneumothorax had decreased after the chest tube insertion. A second chest tube was inserted on the right side and the patient's symptoms resolved and oxygen saturation normalized.
Two days later a computed tomography (CT) of the chest showed persistent bilateral pneumothoraces and leftwards mediastinal shift, the chest tubes were wellplaced, and there were bilateral pleural effusions; furthermore, important bilateral subcutaneous emphysema was present. There was no evidence of emphysema or bulla in the partially expanded nonatelectatic lung parenchyma.
Seven days later, thoracic tubes were removed and one month later, after the first cycle of chemotherapy, the central venous catheter was taken off. Seven days later the patient was discharged without any further complications.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [70, 'years'], 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'O₂ saturation percentage': [97.0, '%'], 'Hemoptysis': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Unilateral Leg Swelling': False, 'Recent surgery or trauma': True}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 70 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 110.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 97.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6578,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-6906557-1,Extracted,"Sudden-onset chest pain for 1 d.
A 29-year-old man complained of sudden precordial pain with no remission for 1 d prior to hospital admission but denied hemoptysis, dyspnea, or syncope. He sought evaluation and was admitted for the purpose of intensive examination and treatment.
The patient had been addicted to N2O for 1 year; as a result, peripheral neuropathy had occurred and was treated with vitamin B12 (Vit B12). His medical history included poor blood glucose control and anxiety. However, he had no history of thrombosis, malignant tumor, recent trauma, or prolonged air travel.
The patient has smoked over 13 pack-years and did not have alcoholism or a positive family history.
The initial assessment revealed that the patient was overweight and fragile, with a body mass index of 31.12 kg/m2, temperature of 36.3 °C, blood pressure of 110-120/70-80 mmHg, heart rate over 110 beats/min, respiratory rate over 30 breaths/min, and pulse oximetry of 93% when the fraction of inspired oxygen was 49%. Moreover, the physical examination indicated diminished breath sounds on both sides and the accentuation of pulmonic second sounds.
Laboratory data showed a high leukocyte count and an increased hemoglobin level, suggested abnormal liver biochemistry and hyperlipidemia, and revealed HHcy (24.12 µmol/L), high Vit B12 (734 µmol/L), and normal folate (14.39 nmol/L). The results of the protein S, protein C, anti-thrombin III antibody, anti-cardiolipin antibody, lupus anticoagulant, anti-β2gp1 autoantibody, and other autoantibodies were within normal limits. The clotting profile was normal, other than the D-dimer value (1.13 mg/L), and thrombophilia screening was negative. As markers in the risk stratification of PE, the levels of brain natriuretic peptide (BNP) and cardiac troponin I (CTnI) were 533 pg/mL and 0.334 ng/mL, respectively. Arterial blood gas levels measured with an oxygen concentration of 49% showed the following: pH, 7.44; PaCO2, 30 mmHg; and PaO2, 74 mmHg.
An electrocardiogram (ECG, Figure ) showed sinus tachycardia with typical changes on SIQIIITIII (S wave in the aVL lead, Q wave and T wave in the III lead). Ultrasonic cardiogram demonstrated right ventricular enlargement with left ventricular compression. Color Doppler scans were used to explore femoral, popliteal, and calf muscular venous thrombosis in the right extremity. Computed tomographic pulmonary angiography (CTPA) revealed occlusion of the pulmonary artery trunk, lobar artery, and arterial branches on both sides and signs of increased right heart load (Figure and ).",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [29, 'years'], 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'O₂ saturation percentage': [93.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Hemoptysis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 29 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 110.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 93.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6579,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-3608307-1,Extracted,"A 20 years-old primigravida with seven months amenorrhea presented to the emergency department with giddiness and difficulty in breathing. The history of presenting complaints revealed that she had developed these complaints within few minutes of receiving first infusion of iron sucrose USP 5 ml injection (FERISE 5 brand of Intas Pharma Company) diluted in 100 ml normal saline for severe iron deficiency anemia in a primary health care centre.Parenteral iron therapy was initiated to her because she was noncompliant to oral iron and folic acid supplements.She had no history of allergies or significant past medical illness. On presentation, she was conscious,alert(Glasgow coma scale 15/15) and afebrile. Her pulse rate was 140/min, respiratory rate 28/min, oxygen saturation of 90% at room air and systolic blood pressure 70 mm of Hg. On physical examination, she had marked pallor in mucous membranes. Chest examination revealed bilateral diminished breath sounds; rest of the systemic examination was unremarkable. Her hemoglobin was 6.0 gm/dL, total leucocyte count 27900/μL, red blood cell count 2.86 million/cmm, platelet count 570000/μL, International normalized ratio (INR) 1.13 and APTT 34.4 seconds. Arterial blood gas analysis was suggestive of hypoxia (pH 7.37, po2 66, pco2 44,HCO3 20 and po2/Fio2 0.66 on 100% Fio2). Chest radiograph showed bilateral infiltrates. She had normal urine analysis, serum electrolytes, renal, liver and thyroid function tests. She was treated with intravenous adrenaline, hydrocortisone, antihistaminics and H2 blockers and transferred to the intensive care unit for ventilatory and inotropic support.
Despite intensive resuscitation attempts in the intensive care unit, the patient expired due to cardiac arrest within 24 hrs.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [140.0, 'beats per minute'], 'Hemoptysis': False, 'O₂ saturation percentage': [90.0, '%'], 'Recent surgery or trauma': False, 'age': [20, 'years'], 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 20 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 140.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 90.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6580,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4386195-1,Extracted,"A 56-year-old man was electively admitted for investigation of his abdominal pains. He had surgery for traumatic fracture of his right leg three weeks ago and was discharged without any complications. He did not have any other major co-morbidity and was not taking any regular medications. Few days into the hospital stay, he suddenly became short of breath and unwell with severe hypoxemia, hypotension and tachycardia. His peripheral oxygen saturations dropped to 85% on room air. His systolic blood pressure was 60 mmHg with heart rate of 120 per minute. After initial stabilization, urgent computerised tomography scan of the chest was performed that revealed filling defects in the distal main pulmonary artery extending bilaterally up to the interlobar and its segmental branches, consistent with thrombi (, top left). It also revealed dilated pulmonary trunk (24 mm) with a filling defect in the right atrium (, top right). A trans-thoracic echocardiography was immediately performed to assess the right atrial mass. It showed a free-floating thrombus in the right atrium (RA) with a ‘snake-like’ configuration (, bottom panel).
The right ventricle was moderately enlarged with systolic impairment. The inferior vena cava was free of masses. There was moderate pulmonary hypertension with peak pulmonary pressure of 45 mmHg. Serum biochemistry revealed markedly raised troponin and brain-natriuretic peptide levels. The patient was transferred to the intensive care unit where he was intubated and ventilated, and needed extensive support with vasopressors. He also received thrombolysis with reteplase. A repeat echocardiography after thrombolysis showed absence of the previously seen thrombus in the right atrium, which had likely lysed and migrated to the pulmonary vasculature. The patient, however, never recovered from this massive pulmonary vascular insult and remained in the intensive care unit for the next few days. He deteriorated gradually until he passed away.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [56, 'years'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'O₂ saturation percentage': [85.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': True, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False}",4,4,4,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 56 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 120.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 85.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 2 + 1 = 3.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 3 + 1  =  4.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 4.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 4.
Hence, the number of PERC rule criteria met by the patient is 4."
6581,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-5704843-1,Extracted,"An 85-year-old male presented to our hospital with a 2-month history of a productive cough with white phlegm and a 2-day history of hemoptysis in October 2014. He reported no fever, chest pain, chills, night sweats, or dyspnea.
On physical examination, the patient was afebrile. His heart rate was 80 beats per minute and regular, blood pressure 136/72 mm Hg, respiratory rate 20 breaths per minute, and oxygen saturation 99% while breathing ambient air. He was alert and not in acute distress. There was no lymphadenopathy in the neck. The lungs were clear and there were no heart murmurs. His abdomen was not tender, and there was no organomegaly. The neurological examination was unremarkable.
The patient's white blood cell (WBC) count was 3430/mL, with 51.3% neutrophils, 32.9% lymphocytes, and 10.8% monocytes; his hemoglobin was 117 g/L; his hematocrit was 38.9%; and his platelet count was 207,000/mL. The patient's C-reactive protein (CRP) level was normal. Serum chemistry tests showed the following results: sodium, 142.3 mmol/L; potassium, 3.9 mmol/L; chloride, 106.2 mmol/L; blood urea nitrogen, 5.9 mmol/L; creatinine, 86.3 μmol/L; aspartate aminotransferase, 21 U/L (normal range 15–40 U/L); and alanine aminotransferase, 16 U/L (normal range 9–50 U/L). The international normalized ratio was 1.02, the partial-thromboplastin time was 27.1 seconds, and the d-dimer level was 180 μg/L. The brain natriuretic peptide was 17.0 pg/mL; tumor marker tests revealed: carcinoembryonic antigen, 2.32 ng/mL; squamous cell carcinoma antigen, 0.90 ng/mL; neuron-specific enolase, 6.24 ng/mL; and CY211, 2.25 μg/L.
Computed tomography (CT) revealed a mass in the right lower lobe (Fig. A). Electrocardiography revealed sinus rhythm, with a ventricular rate of 79 beats per minute. No metastatic lesions were found on brain magnetic resonance imaging or in bone using emission CT.
The hemoptysis was treated with 30 mg of ambroxol and 600 mg of p-aminomethyl benzoic acid daily. Sputum cultures were negative. Lung function tests after inhaling 400 μg of albuterol yielded an FEV1/FVC = 59.7% and FEV1 = 46.2%. Bronchoscopy showed stenosis in the posterior basal segment of the right lower lobe (Fig. ). A CT-guided transthoracic needle lung biopsy showed SCLC after histopathological and immunohistochemical examinations (Fig. ).
Seven days after the transthoracic needle lung biopsy, the patient's temperature increased to 40°C and he developed a worsening cough with purulent sputum. Repeat laboratory tests showed a WBC count of 13,890/mL, with 87.0% neutrophils, 6.5% lymphocytes, and 0.9% monocytes; hemoglobin, 128 g/L; hematocrit, 38.70%; platelet count, 138,000/mL; and CRP, 88.0 mg/L. The patient was treated with cefuroxime (1.5 g) twice per day for 7 days and his WBC and CRP level normalized.
He refused radiotherapy or chemotherapy. After obtaining consent, we treated the tumor with RFA. Before RFA, we evaluated the size and spatial relationships of the tumor using CT and determined the needle angle and depth via the shortest route from the surface to the mass. The puncture point was infiltrated with 5 mL of 2% lidocaine. The multipolar needle was directed to avoid bone, large blood vessels, and pulmonary bullae. A rapid biopsy of the lung tumor was performed. Heating was directed to an area within 0.5 to 1 cm of the tumor margin and to the needle track (Fig. B). After closing the puncture wound, repeat CT showed pneumothorax (Fig. C), which was treated with bed rest and inhaled oxygen. The patient had some chest pain the next day, but there was no fever or hemoptysis in the first week after RFA.
At the 2-year follow-up examination, the efficacy of the RFA was evaluated as a partial response (PR) (Fig. D–G). The patient was last seen in January 2017, when he developed community-acquired pneumonia (Fig. H).",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [85, 'years'], 'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'Hemoptysis': True, 'O₂ saturation percentage': [99.0, '%'], 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 85 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 80.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient note does not report a status on 'recent surgery or trauma'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6582,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4666442-1,Extracted,"A 68-year-old man attended the Accident and Emergency department with increasing breathlessness but no chest pain, sputum production or haemoptysis. He had recently returned from holiday in Spain and his general practitioner prescribed amoxicillin for a presumed chest infection. He was a diet-controlled type 2 diabetic on treatment for hypertension. He had a 40-pack-year smoking history and had lost 4 kg in weight. Examination revealed an obese man with normal blood pressure, sinus tachycardia at 100 beats⋅min−1, with a respiratory rate of 26 breaths⋅min−1. His oxygen saturation was 96% on air. His white cell count was 11×109 cells⋅L−1 and C-reactive protein was 92 mg⋅L−1. Renal function and coagulation studies were normal.
The admitting medical team felt that there was a “complete whiteout” of the left hemithorax and initially treated him for suspected severe community-­acquired pneumonia with intravenous antibiotics and fluids, while arranging a respiratory opinion. Prophylactic low molecular weight ­heparin (LMWH) was also started. The respiratory team felt that an underlying malignancy may have been responsible for the radiographic appearances of left upper lobe collapse and suggested a ­computed tomography (CT) scan of the thorax. shows a “veil-like” opacity projected over the left lung field, a raised left hemidiaphragm with blunting of the left costophrenic angle consistent with left upper lobe collapse, volume loss and an associated pleural effusion.
The CT scan showed a large left hilar mass coalescing with the left upper lobe collapse. There were associated large para-aortic, subcarinal, mediastinal and supraclavicular nodes, a single liver metastasis and a second separate mass in the right lung. Lung cancer staging was T4N3M1b.
It was interesting to note that a separate mass was present in the right lung (c). He did have metastatic disease but this might represent a synchronous primary, although by strict definition, to diagnose this, we needed to prove that the second mass was of different histology to the primary mass or that it was of the same histology but with no mediastinal or metastatic spread [].
While awaiting a bronchoscopy, the patient coughed up ∼600 mL of fresh blood in 12 h, with worsening hypoxia. Repeat full blood count and coagulation studies were normal.
The patient was having massive haemoptysis, defined as coughing up anything between 100 mL and 600 mL of fresh blood in 24 h [].
He was seen by the on-call medical team and sat upright. Two large-bore cannulae were inserted in case of exsanguination. Sitting upright runs the risk of the blood spilling over into the normal lung. “Drowning” by filling up the bronchial tree with blood tends to occur before any true haemodynamic instability due to volume loss. As such, the mainstay of treatment in massive haem­optysis is to protect the normal lung and try to stop the bleeding [, ].
The respiratory team felt that a palliative approach was too premature, but it was explained to him that his prognosis was poor with limited treatment options available. He agreed to a “do not resuscitate” plan. A treatment escalation plan was agreed to ensure his treatment was limited to level 2 care. Hypoxia precluded a bronchoscopy or transfer to the local cardiothoracic centre. Bronchoscopic strategies to control pulmonary haemorrhage include balloon tamponade, iced saline lavage, administration of a topical vasoconstrictor or coagulant, laser therapy and electrocautery [].
The patient pointed to his left hemithorax when asked which side he felt the bleeding was coming from. Anecdotal experience suggests that patients with haemoptysis can often accurately indicate the side of the bleeding lesion. He was therefore positioned on his left side and tranexamic acid was administered intravenously. A pilot study evaluating the effect of tranexamic acid and the related antifibrinolytic agent aminocaproic acid included three patients with haemoptysis due to lung cancer []. All three patients experienced cessation of bleeding within 1–4 days without any recurrence. Patients received 1.5 g of intravenous tranexamic acid initially, followed by 1 g three times per day for a week after cessation of bleeding. The use of tranexamic acid in bleeding has been recognised for a long time [] and tranexamic acid may reduce both the duration and volume of bleeding, with low risk of short-term thromboembolic complications [].
His haemoptysis and hypoxia improved over the ensuing days, and at bronchoscopy an organised clot was visualised in the left upper lobe bronchus with no endobronchial masses and a normal right bronchial tree. Left upper lobe lavage revealed no malignant cells on cytology. At endobronchial ultrasound examination, a large paratracheal node was sampled and histology demonstrated a poorly differentiated necrotic squamous cell carcinoma.
The patient’s clinical condition slowly improved until 15 days into his admission, when overnight he developed acute dyspnoea with tachycardia at 120 beats⋅min−1. Arterial blood gas sampling measured his arterial oxygen tension (PaO) at 7.0 kPa on high flow oxygen via a reservoir bag, and an arterial carbon dioxide tension (PaCO) of 5.1 kPa. A repeat chest radiograph showed no change.
The PA–aO is a measure of the difference between the alveolar concentration (A) of oxygen and the arterial (a) concentration of oxygen. In room air (inspiratory oxygen fraction of 0.21) at sea level (atmospheric pressure of 760 mmHg) assuming 100% humidity in the alveoli, a simplified version of the equation is 21−((PaCO/0.8)−PaO), 0.8 being the respiratory quotient.
High flow oxygen delivers ∼85% oxygen, so 85−(5.1/0.8)−7=71.625, which is significantly raised. While his PA–aO was likely to be raised due to his cancer/effusion, such a disparity and the clinical picture points towards the possibility of a pulmonary embolus. The use of the PA–aO is a useful adjunct in diagnosis []. There are numerous case reports about tranexamic acid increasing the risk of pulmonary emboli [, ]. In this case, the patient had other significant risk factors such as disseminated malignancy and a prolonged period of immobility.
The patient understood that if left untreated, a large pulmonary embolus may prove fatal, but by treating it with anticoagulation, a major fatal haemoptysis was also more likely. He agreed to receive LMWH together with morphine for symptoms of dyspnoea and agitation. 6 h later, he had improved clinically and was able to safely lie flat briefly for a CT pulmonary angiogram. This confirmed large right-sided pulmonary emboli with associated right heart strain with reflux of contrast into the venous circulation (). The option of inferior vena cava filter insertion to prevent further embolic events was not available in our hospital, and he was too unstable to be transferred to an appropriate tertiary hospital. Over the following 2 days, urgent palliative radiotherapy to the left-sided tumour was arranged. After he had received a single fraction, further large volume haemoptysis recurred. LMWH was stopped and tranexamic acid restarted. The bleeding settled once more and he completed five fractions of radiotherapy. Slowly his oxygen saturations improved to 93% on air and he was discharged home on long-term full-dose LMWH with no recurrence of the haem­optysis.
He presented 3 weeks later with progressive respiratory failure and his symptoms were palliated according to his wishes.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [68, 'years'], 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'O₂ saturation percentage': [96.0, '%'], 'Hormone use': False, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 68 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 100.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 96.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6583,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7302682-1,Extracted,"A 46-year-old woman was urgently presented to a nearby hospital because of a femur fracture caused by an accident. Although she was alert on arrival, she began to experience sleepiness approximately 5 hours later. A follow-up helical computed tomography (CT) of the brain revealed the absence of any additional severe lesions or skull fractures. Chest CT confirmed an exudative lesion, and a pulmonary vascular computed tomography angiography (CTA) revealed no obvious abnormalities. Based on the clinical and imaging findings, the patient was suspected to have CFE. After 2 days, the patient was moved to our neurology department to receive the appropriate care. Immediate physical examination on arrival revealed a Glasgow Coma Scale score of 4, a positive bilateral Babinski sign, a positive Kernig sign, and neck stiffness. The patients left thigh presented bruising and swelling and had been fixed with external fixation with restrained movement in the previous hospital (Fig. A). She presented an arterial pressure of 148/80 mm Hg, heart rate of 124 bpm, and partial pressure of oxygen (PO2) of 64 mm Hg. Her blood gas analysis revealed a pH value of 7.4. Total body CT revealed a left femoral comminuted fracture with dislocation (Fig. B). Her bilateral lung presented an exudative lesion as well as pleural effusion (Fig. A). Brain magnetic resonance imaging (MRI) revealed diffuse abnormal signals in the bilateral cerebral hemisphere, brainstem, and cerebellum, which were suggestive of embolization (Fig. ). Combined with the patients trauma history and imaging findings of the lung and brain, the patient was initially diagnosed with FES, whose corresponding treatment is mainly supportive. Regarding the closed fracture of the left femur, the external fixation that had been performed at the previous hospital was appropriate, and no further treatment was applied. Subsequent cardiovascular screening, including echocardiography, cervical artery ultrasound and bilateral lower extremity vascular ultrasound, was performed, and all the findings were negative. Four days after the femur fracture, the patient presented with moderate dyspnea, and her arterial blood gas analysis retrieved a pH value of 7.4. PO2 was 35 mm Hg, partial pressure of carbon dioxide was 126 mm Hg, and arterial oxygen saturation was 97.5% under nasal oxygen. Fourteen days after the fracture, both the lung symptoms and lung CT findings were considerably improved (Fig. B). Transthoracic echocardiography ultrasound was performed again, and shunts through a PFO were observed (Fig. ). On the following day, there was a gradual improvement in consciousness. However, the patients speech indicated dysphasia. Under active supportive care and hormone therapy, the patient was finally discharged with dysphasia and an untreated closed fracture.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [46, 'years'], 'Heart Rate or Pulse': [124.0, 'beats per minute'], 'O₂ saturation percentage': [97.5, '%'], 'Unilateral Leg Swelling': True, 'Hormone use': True, 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",4,4,4,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 46 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 124.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 97.5 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be present for the patient and so we increment the criteria count by 1, making the current total 3 + 1  =  4.
Hence, the number of PERC rule criteria met by the patient is 4."
6584,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8059042-1,Extracted,"A 53-year-old man (height, 170 cm; weight, 89 kg) was admitted to the hospital because of a 1-year history of shortness of breath after exercise. The patient was a smoker, had a history of hypertension, and was taking captopril and nimodipine. Breathing was reduced in the left lung. However, neither rhonchus nor moist rales were heard during auscultation. Chest computed tomography revealed a GEB, and the left lung was compressed by about 95% with a right mediastinal shift (). An electrocardiogram showed normal findings, and echocardiography revealed that the heart was located in the right thoracic cavity. The left ventricular diastolic function was decreased, and the left ventricular ejection fraction was 64%. Laboratory tests showed no obvious abnormalities. Arterial blood gas analysis showed the following: pH: 7.43, PaCO2: 41 mmHg, PaO2: 94 mmHg, lactate: 1.4 mmol/L, potassium: 3.6 mmol/L, sodium: 138 mmol/L, calcium: 1.10 mmol/L, FiO2: 21%, and SpO2: 98%.
On the day of surgery, the patient’s electrocardiogram, blood pressure, SpO2, and bispectral index were monitored upon entry into the operating room. A radial artery catheter and right internal jugular venous catheter were placed. The patient’s arterial blood pressure was 175/109 mmHg, heart rate was 90 beats/minute, and SpO2 was 94%. Before anesthesia, 40 µg of dexmedetomidine was infused within 10 minutes. The thoracic surgeon then created a small incision at the intersection of the sixth intercostal space and the left mid-axillary line to puncture the lung bulla and insert an indwelling catheter (14 Ga, 16 cm in length; Arrow International/Teleflex, Wayne, PA, USA) into the GEB to drain it for 15 minutes. The patient was preoxygenated with 100% oxygen at 6 L/minute for 5 minutes. Anesthesia was administered using 100 mg of propofol, 30 µg of sufentanil, and 50 mg of rocuronium. A 37-Fr right double-lumen endotracheal tube was inserted with the help of a visual laryngoscope, and single-lung ventilation was performed after proper alignment had been confirmed by fiberoptic bronchoscopy. The tidal volume was set at 5 to 6 mL/kg, the respiratory rate was 15 to 17 breaths/minute, the positive end-expiratory pressure was set at 5 cmH2O, and the inhalation:expiration ratio was 1:2. Propofol, remifentanil, and sevoflurane were used to maintain anesthesia. The intraoperative bispectral index was maintained at 40 to 50. After resecting the GEB (), one-lung ventilation was switched to two-lung ventilation and the lungs slowly expanded with a low tidal volume until complete lung re-expansion was observed. During the 3-hour surgery, the patient experienced 50 mL of blood loss, was administered 1300 mL of lactated Ringer’s solution, and excreted 500 mL of urine. After the operation, the double-lumen endotracheal tube was replaced with a single-lumen endotracheal tube and the patient was sent to the intensive care unit for monitoring and further treatment. Two hours after entering the intensive care unit, the patient was fully awake and the tracheal tube was smoothly removed. The following day, the patient was transferred to the thoracic surgery ward, where he recovered; he was discharged 12 days later. Postoperative chest computed tomography showed that the lungs were well inflated with no abnormalities ().",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [53, 'years'], 'Heart Rate or Pulse': [90.0, 'beats/minute'], 'O₂ saturation percentage': [98.0, '%'], 'Hemoptysis': False, 'Recent surgery or trauma': True, 'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 53 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 90.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6585,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7813127-1,Extracted,"A 24-year-old man, a newly appointed automobile mechanic, presented to the emergency room of Tribhuvan University Teaching Hospital with a chief complaint of progressive shortness of breath, low-grade fever, bilateral chest pain, and nonproductive cough for three days. The shortness of breath was exertional, and the patient did not complain of any orthopnea, paroxysmal nocturnal dyspnea, or pedal edema. The low-grade fever occurred three days before dyspnea, had a Tmax of 99.8°F, was on and off, and was not associated with chills or rigors. There was no history of wheezing, sputum production, hemoptysis, night sweats, weight loss, or anorexia. He denies any rash, joint pain, numbness, or weakness in the extremities. On detailed inquiry, he revealed that he recently started working as an automobile mechanic and had to aspirate diesel from fuel tanks often. As he was new to this job, he had accidentally aspirated a small volume of diesel several times in the last two weeks. He was a nonsmoker and had never consumed alcohol in his lifetime. The patient had no past medical history of note, no history of allergies, and had not taken any drugs or medications recently.
On examination, he was ill-looking with a temperature of 98°F, a sphygmomanometric blood pressure of 140/90mmHg, a heart rate of 110 beats/minute, and a respiratory rate of 28/minute saturating poorly in ambient air (peripheral SpO2 87%, as measured by pulse oximetry). He had no pallor, icterus, lymphadenopathy, cyanosis, clubbing, edema, and dehydration. There was a decreased excursion of the chest wall on chest examination, diminished breath sounds bilaterally along with diffuse bilateral basal crepitations, and a dull stony percussion note bilaterally. The examination of other systems did not reveal any abnormalities. The patient had leukocytosis with a total WBC count of 13900/mm3, and differential leukocyte count consisted of 90% neutrophils and 10% lymphocytes. Hemoglobin, hematocrit, and platelet count were normal. Renal function test, liver function test, coagulation assay, and serology tests were regular. Arterial blood gas analysis was within the reference range.
Chest X-ray (CXR) done at admission (Figure ) showed pneumonic consolidation over the bilateral lung field with bilateral pleural effusion and pneumothorax. Chest tubes were inserted bilaterally under ultrasound guidance to alleviate pleural effusion and pneumothorax. On the second day of chest tube insertion, CXR (Figure ) was done again, revealing the left lung's expansion, persistent right-sided pneumothorax, and bilateral surgical emphysema. Contrast-enhanced computed tomography of thorax revealed right-sided pneumothorax, bilateral pleural effusion, bilateral patchy consolidated lung parenchyma, and bilateral chest tube in situ.
Owing to radiological findings, clinical features, and siphonage history, the diagnosis of hydrocarbon pneumonitis was made. Since Nepal is a tuberculosis endemic region, pulmonary tuberculous was also considered as alternative diagnosis. However, sputum examination did not reveal the acid-fast organism; neither did the GeneXpert PCR test. The patient was kept under intravenous piperacillin/tazobactam, nebulization was done six hourly, and high flow oxygen was administered. The patient developed no complications during his hospital stay. The patient was discharged after two weeks when there was significant radiological regression of consolidations (Figure ), improvements in pulmonary symptoms, and maintenance of oxygen saturation above 90% in room air. The patient was advised to follow-up regularly and is doing well at the time of writing.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [24, 'years'], 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'O₂ saturation percentage': [87.0, '%'], 'Hemoptysis': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Hormone use': False, 'Unilateral Leg Swelling': False, 'Recent surgery or trauma': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 24 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 110.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 87.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6586,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8142754-1,Extracted,"A 52-year-old male patient presented to the ED with abdominal pain and weakness for 2 days. His vital signs were as follows: blood pressure, 130/70 mm/Hg; pulse rate, 107 beats per minute; respiratory rate, 18 breaths per minute; temperature, 36.6°C; and oxygen saturation, 93%. Physical examination findings were normal bilateral breath sounds, abdominal guarding, absence of rebound tenderness, and dry tongue. The patient had CLL for 15 years. He underwent autologous stem cell transplantation, but he developed Richter transformation 6 months ago, recurrence was observed 3 months following transplantation, and treatment was stopped thereafter. He has taken 10 vials of vitamin D (cholecalciferol form) orally for the past 2 months.
Laboratory results are shown in . 25-Hydroxy vitamin D >100 ng/mL (normal range, 30–100 ng/mL) and chemiluminescence immunoassay total vitamin was examined with D-Roche Diagnostic. In diluted blood, the 25-hydroxy vitamin D level was >150 ng/mL. Laboratory tests performed 6 months ago revealed 9.75 mg/dL of calcium and 0.99 mg/dL of creatinine. Since the patient’s 25(OH)D level was >150 ng/mL, which indicated vitamin D poisoning, he developed hypercalcemia and acute renal failure.
Medical treatment was started, and emergency dialysis was planned. His case was consulted with the hematology, nephrology, and intensive care units, and he underwent hemodialysis. After dialysis, blood test values were as follows: urea, 44 mg/dL; creatinine, 1.65 mg/dL; albumin, 2.6 g/dL; sodium, 135 mmol/L; potassium, 2.9 mmol/L; calcium, 11.8 mg/dL (corrected calcium value 12.9 mg/dL). The patient was then admitted in the hematology clinic.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [52, 'years'], 'Heart Rate or Pulse': [107.0, 'beats per minute'], 'O₂ saturation percentage': [93.0, '%'], 'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 52 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 107.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 93.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 2 + 1 = 3.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6587,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7256686-1,Extracted,"A fit, physically active 32-year-old female with no underlying risk factors underwent a left knee anterior cruciate ligament (ACL) reconstruction and partial lateral meniscectomy. She was not taking oral contraceptives. She presented 19 days postoperatively with acute dyspnea, chest pain, tachycardia, and complaints of feeling light-headed of 5 days duration. In the emergency department, she had sinus tachycardia on electrocardiography, a heart rate of 126 bpm, blood pressure of 107/68 mmHg, respiratory rate of 18/min, and an oxygen saturation of 95% on room air. Her examination was noted to be otherwise unremarkable. There was no evidence of surgical site infection and no limb swelling noted. A complete blood count and electrolyte and metabolic panel were normal. Her troponin was 80 ng/L (normal 0–14 ng/L). A chest radiograph and D-dimer were not performed. Her pretest probability of pulmonary embolism was moderate based on Wells' criteria [].
Computed tomography pulmonary angiogram (CTPA) reported the patient as having PTE. Findings included saddle PE, extensive clot extending into lobar and segmental branches of all lobes () as well as evidence of right heart strain with marked right atrial (RA) and RV dilation as well as flattening and deviation of the interventricular septum. The RV/LV ratio was 1.3. Unfractionated low-molecular-weight heparin was immediately initiated. Her simplified PE Severity Index (sPESI) was 1 (high risk, 8.9% mortality) [].
The patient was admitted to the Internal Medicine service. On day 1, her clinical status was unchanged; laboratory indices were similar with a troponin level of 35 ng/L and NTpro-BNP of 3859 ng/L (normal 0–300). ICU was consulted on day 1 of admission, and a transthoracic echocardiogram (TTE) was immediately requested. This demonstrated a 3.3 cm maximum diameter multilobulated, mobile right atrial thrombus, which extended from the RV inlet through the pulmonic valve to the pulmonary artery (i.e., an RHTT). Intraventricular septal flattening and severe RV dilation with moderate systolic dysfunction and tricuspid regurgitation were also observed. McConnell's sign was present with apical hypercontractility and basal and mid-ventricular segmental hypokinesis. The right ventricular systolic pressure (RVSP) was 48.1 mmHg ().
She was transferred to the intensive care unit (ICU) with a diagnosis of clinical submassive pulmonary embolism with clot in transit. Arterial blood gas was pH 7.52, pCO2 29 mmHg, PaO2 74 mmHg, O2 saturation 96%, and lactate 0.8 mmol/L. The case, as well as treatment options, was reviewed with a member of the pulmonary embolism response team (PERT). A decision was made to proceed with low-dose thrombolysis, despite the recent surgery, employing the regimen described in the MOPETT trial []. The potential benefits and risks were discussed with the patient who consented. She received a 10 mg recombinant tPA bolus followed by an additional 40 mg over two hours intravenously (IV). IV heparin was continuously infused at 10 U/kg/hr during the thrombolysis as well and for three hours afterwards at which time the heparin nomogram infusion of 18 U/kg/hr with serial adjustments based on PTT was re-introduced. Serial echocardiograms at 2 hours after thrombolysis and the next day () demonstrated improvement in her RV function. The RVSP was 27 mmHg at 2 hours and 26 mmHg the following day. The in-transit clot was no longer visible on the posttreatment echocardiograms. She was eventually discharged home on day 5 on tinzaparin for two weeks and then transitioned to rivaroxaban. She was continued on anticoagulation for 6 months.
Seven months after discharge, she was doing very well. Her breathing had returned back to baseline, and she was rehabilitating well from her reconstruction. She had no bleeding complications from the rivaroxaban therapy. Her DASH score [] was 1 (3.9% annual risk of DVT recurrence), and her HERDOO2 score [] was 0 (3% risk of major recurrent venous thromboembolism per 100 patient years). The anticoagulation was discontinued. She had returned to the gym, though had not yet returned to more vigorous-intensity physical activities, such as basketball. A repeat echocardiogram at this time demonstrated normal left and right ventricular systolic function with no hemodynamically significant valvular disease. Serial D-dimers, every three months, for the following year were scheduled. Testing for inherited thrombophilia was negative.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [32, 'years'], 'Hormone use': False, 'Unilateral Leg Swelling': False, 'Heart Rate or Pulse': [126.0, 'beats per minute'], 'O₂ saturation percentage': [95.0, '%'], 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 32 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 126.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 95.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6588,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7325384-1,Extracted,"A 39-year-old male with a medical history of diabetes mellitus presented to the emergency room for the evaluation of jaundice. He complained of fever for the last seven days that was associated with nausea, intermittent headache, and dry cough. He also had diffuse arthralgia. The patient took over-the-counter antipyretic and analgesic but did not get any relief. The initial evaluation revealed a temperature of 100°F, blood pressure of 110/70 mmHg, heart rate of 101 beats per minute, respiratory rate of 20 per minute, and oxygen saturation of 99% on room air. The physical examination showed severe jaundice with the icteric sclera. He had diffuse arthralgia with tenderness. Cardiac and chest examination was normal. The abdomen was soft with normal bowel sounds and no organomegaly.
Initial laboratory analysis is shown in Tables and 2. The patient’s platelet count, hemoglobin, and hematocrit were within the normal ranges, except white blood cells. His serum metabolic panel was unremarkable, except for elevated total bilirubin and creatinine.
Extensive workup for severe jaundice involved serum iron studies, cytomegalovirus (CMV) antibody, and antinuclear antibody (ANA), all of which were negative. Common causes of hyperbilirubinemia such as hepatitis A, B, and, C were negative. His low-density lipoprotein (LDL) was 50 mg/dL, high-density lipoprotein (HDL) was 55 mg/dL, serum cholesterol was 180 mg/dL, and serum triglyceride was 152 mg/dL.
On abdominal ultrasound, the liver, gall bladder, and spleen were normal in size and texture. CT of thorax and abdomen was performed, which revealed diffuse pulmonary and hilar infiltrates in both lung bases. It was suspected that the patient had a possible chest infection, and he was started on intravenous ampicillin-sulbactam. The patient’s kidney function was concerning due to high creatinine, but creatinine improved to 2.0 mg/dL on the third hospital day.
On further investigation, the patient reported that he visited Connecticut, USA, one week ago. He had no history of tick bite. Peripheral smear examination of blood was performed, which revealed no abnormality in the morphology of blood cells. Serologic tests for Lyme disease were performed. He was treated with doxycycline at a dose of 100 mg twice a day on the third hospital day. The radiograph of the joints revealed no abnormality.
His total bilirubin remained high during the hospital stay in the beginning, and his bilirubin was 12.0 mg/dL (direct: 10.3 mg/dL) on the third hospital day (Figure ). His white blood cell count remained elevated at 18 × 103/µL. However, his liver enzymes remained normal (Figure ).
The patient’s fever resolved on hospital day 4, and joint pain also got better. Repeat ultrasound of the abdomen was conducted due to the worsening of laboratory results, which revealed no mass or calcification, except few changes in liver echotexture suggesting the possible fatty/fibrotic change. The gallbladder was thin-walled and anechoic, with no stones. Portal vein appeared red-orange, and the hepatic artery was yellow (indicating higher flow velocity). The decision was made for invasive workups such as biopsy and magnetic resonance cholangiopancreatography (MRCP), but the patient denied it.
Serum ELISA (enzyme-linked immunosorbent assay) for Lyme disease was performed. The results of ELISA screen were positive for Lyme disease, which was further confirmed by Western blot. He continued on doxycycline. His bilirubin gradually improved. He was discharged with outpatient follow-up. The patient remained afebrile and symptom-free throughout his hospital stay, without any significant pulmonary or gastrointestinal symptoms. His bilirubin was 9.0 mg/dL on the day of discharge from the hospital.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [101.0, 'beats per minute'], 'Hemoptysis': False, 'O₂ saturation percentage': [99.0, '%'], 'Recent surgery or trauma': False, 'age': [39, 'years'], 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 39 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 101.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6589,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7891256-1,Extracted,"A 29-year-old male presented to the Emergency Department with a penetrating stab wound to the anterior left second intercostal space, 2 cm medial to the mid-clavicular line. Previous medical history consisted of a right tibia-fibula fracture with intra-medullary nailing 7 years prior.
The patient presented haemodynamically unstable, in grade 3 haemorrhagic shock and after resuscitation, improved as a transient fluid responder. A left-sided intercostal drain was inserted for a large haemothorax. Vital signs after resuscitation: heart rate 100; respiratory rate 14; saturating at 95% on room air; blood pressure 101/64. Post-resuscitation, no angina was reported. On examination: no features of cardiac failure, central cyanosis, bruits, or murmurs were elicited. No ST or other rhythm abnormalities were noted on electrocardiogram (). Pertinent findings were that of chronic septic hardware of the right lower limb which on further enquiry, had not been formally assessed by an orthopaedic service. Microbiological workup of the local septic limb was deferred until after haemodynamic stabilization.
A preliminary diagnosis of local septic hardware led to screening for methicillin-resistant Staphylococcus aureus, and antibiotic prophylaxis with broad-spectrum coverage.
Focused Assessment with Sonography for Trauma scan demonstrated a 1 cm pericardial effusion. A contrasted computed tomographical scan of the chest and cardiac TTE was ordered.
Computed tomographical findings () demonstrated a right ventricular outflow tract (RVOT) injury at the level of the pulmonary valve and an associated suspected thrombus. A small aortic root injury with a small pseudo-aneurysm and intimal flap was also observed. The injury tract extended to the medial superior vena cava (SVC) and a high index of suspicion for an SVC injury was entertained.
Transthoracic cardiac ECHO () findings did not demonstrate valvulopathies, clear flow reversal or shunting, regional wall motion abnormalities, tamponade, or features of infective endocarditis. The patient had a preserved left ventricular ejection fraction. A large dense lesion was noted immediately beneath the pulmonary valve which demonstrated beat to beat movement and was noted to be highly suggestive of a clot.
Pertinent laboratory findings showed that the patient had normal renal and liver function with a normocytic normochromic anaemia (haemoglobin = 10.9) and no coagulation abnormalities (normal prothrombin and partial thromboplastin time).
The patient was intubated under general anaesthesia with a single lumen endotracheal tube (). Femoral cardiopulmonary bypass was initiated via the left groin. A median sternotomy was performed and no active bleeding was seen.
The aorta was then clamped and the heart arrested with cold blood cardioplegia administered into the aortic root. Cardioplegia was given every 20 min throughout the procedure.
A large clot was found within a defect in the medial wall of the RVOT, abutting the ascending aorta, and was subsequently removed. The RVOT was repaired with continuous 3/0 prolene sutures.
The aorta was opened via a transverse ‘J’ incision (). There was a 0.5 cm laceration in the aortic wall, ∼1 mm left of the right coronary ostium which was repaired primarily. The plane between the main pulmonary artery (PA) and ascending aorta was dissected and opened. The right coronary artery was not injured. The contralateral side of the ascending aorta (right side) also had a defect through it and there was a small point injury to the base of the SVC which were both primarily repaired.
Pre-operative radiological findings had a good correlation with the intra-operative findings and no other intra-operative injuries were noted.
The patient was weaned off of cardiopulmonary bypass and closure of the femoral cannulation site, and sternum was performed successfully. The patient remained intubated and was transported to intensive care unit.
A complete recovery was made with no residual thrombus or intracardiac shunt at early follow-up. There was no cardiac, respiratory, or neurological sequelae at 30-day follow-up.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [29, 'years'], 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'O₂ saturation percentage': [95.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Unilateral Leg Swelling': False, 'Hemoptysis': False, 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 29 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 100.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 95.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6590,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8296770-1,Extracted,"An 81-year-old woman with a history of Graves’ disease, treated with both levothyroxine 50 µg and thiamazole 5 mg, was diagnosed with stage IIIB malignant mesothelioma in 2017. She underwent chemotherapy with carboplatin and pemetrexed for 10 courses. As disease progression was observed during chemotherapy, nivolumab (240 mg every 2 weeks) was initiated in October 2018. In January 2019, after the eighth course of nivolumab treatment, the patient underwent laparoscopic sigmoid colectomy for sigmoid colon cancer. During the perioperative period, nivolumab administration was continued. Just after the surgery, she noted mild intermittent abdominal pain, which continued for 2 months. An abdominal CT scan was performed but showed no causative abnormalities, even at the surgical sites. Two weeks later, just after the 12th course of nivolumab, the patient visited an emergency department and complained of worse abdominal pain and general fatigue.
On physical examination, her level of consciousness was normal, and her vital signs were as follows: blood pressure 88/77 mm Hg, pulse rate 115 beats per minute, SpO2 95% on ambient air, respiratory rate 16 per minute, and body temperature 37.2°C. Even after infusion of 1.5 litres of intravenous physiologic saline, her blood pressure remained around 100/80 mm Hg. Vasopressor drugs were not used. Abdominal examination showed tenderness in the right lower quadrant without signs of peritoneal irritation. The physical examination was otherwise normal.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [81, 'years'], 'Heart Rate or Pulse': [115.0, 'beats per minute'], 'O₂ saturation percentage': [95.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Hemoptysis': False, 'Recent surgery or trauma': True, 'Unilateral Leg Swelling': False, 'Hormone use': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 81 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 115.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 95.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6591,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-6099001-1,Extracted,"A 65-year-old female, known case of metastatic breast cancer with brain involvement, presented to our emergency department because of dyspnea, tachypnea, tachycardia and hypotension since 2 hours ago.
She had history of triple positive (ER+, PR+, HER2+) breast cancer and left radical mastectomy 15 years ago after which systemic chemotherapy and hormone therapy (Letrozole/Tamoxifen) was implemented. Three years before current presentation, bilateral hystero-salpingo-ovoforectomy, was performed. About 2 months ago, routine clinical examination by her oncologists revealed left axillary lymphadenopathy (2 × 3 cm) with fixed, firm and nontender node and an additional fixed mass (1 × 3 cm) in the anterior left forearm. Both lesions were excisionally biopsied. Further Imaging showed bilateral hilar lymphadenopathy and multiple metastatic lesions in the liver & abdomen and chest. PET scan showed 2 metastatic lesions in brain.
Pathologic examination of excised node revealed metastatic breast cancer (ER+/HER2+) and salvage chemotherapy with Paclitaxel 100 mg and Gemcitabin 1000 mg weekly plus Herceptin (Trastuzumab) 440 mg and Perjecta (Pertuzumab) 14 mg/kg tri weekly was initiated. One day after the first dose of Herceptin and Perjecta and the fourth dose of Gemcitabin and Paclitaxel, the right lower extremity swelling developed and subsequent Compression ultrasound and Doppler studies revealed acute extensive thrombus formation in the superficial femoral vein of the right leg. The patient was admitted and anticoagulation therapy with LMVH (60 mg BID) was initiated under the supervision of an oncologist at a private hospital. Preliminary laboratory tests revealed mild pancytopenia with a platelet count of 60 000 that was attributed to recent chemotherapy.
Two days after anticoagulation initiation she was discharged home.
Shortly after discharge, she presented to our emergency department with complaint of severe shortness of breath beginning abruptly 2 hours ago.
Her vital signs upon arrival to the emergency department showed a systolic blood pressure of 70 mm Hg, a heart rate of 155 beats per minute, a respiratory rate of 40 per minute & oxygen saturation of 70% in ambient air. She was apparently pale, agitated, diaphoretic and unable to speak in full sentence. Jugular veins were distended and cardiac exam showed moderate tachycardia and a right ventricular heave.
Pulmonary examination was unremarkable except for decreased breath sounds at the mid-zone of the left lung and the base of right lung.
Radial pulses were very weak bilaterally with no palpable pulse in lower extremities. The initial electrocardiogram showed sinus tachycardia at a rate of 135 per minute, right bundle branch block with a QRS duration of 130 ms and right axis deviation of 110 degrees (Figure ).
Bedside echocardiography performed despite severe agitation of the patient demonstrated preserved EF (EF = 50%-55%), severe right ventricular (RV) dilation and estimated pulmonary artery pressure (PAP) of 45-50 mm Hg.
Repeat laboratory findings showed Hemoglobin: 8 (g/dL), Platelets count: 50/mm3.
Immediately a 500 cc bolus of normal saline was administered and norepinephrine was initiated as vasopressor of choice.
Pulmonary CT angiography (CTA) confirmed large bilateral pulmonary thromboemboli with radiological evidence of RV strain (Figure ).
According to hemodynamic compromise resulting from the massive pulmonary embolism and absolute contraindication for thrombolytic therapy due to brain metastases and concurrent thrombocytopenia, she became candidate for emergent catheter or surgical embolectomy. Surgical consult with cardiothoracic surgeon was requested but due to critical condition of the patient complicated by refractory hypoxia and unstable hemodynamic parameters surgery and anesthesiology team declared the patient as inoperable and there was no equipment and specialist for catheter embolectomy in our center.
Ultimately the critical decision was made, despite absolute contraindications, to treat the patient with systemic thrombolysis. Alteplase was selected as thrombolytic of choice and was prescribed according to approved dosage for massive PTE (100 mg infusion over a 2 hours’ period).
Approximately 1 hour after termination of thrombolytic therapy, the norepinephrine was discontinued. Blood pressure returned to 110/70 mm Hg, with a heart rate of 100 beats per minute and a respiratory rate of 20 per minute with an oxygen saturation of 90% in ambient air. Electrocardiogram now shows sinus tachycardia at a rate of 100 per minute, normal QRS duration and normal axis, Figure .
Heparin infusion was initiated with half-dose because of concurrent thrombocytopenia.
After 30 hours, heparin infusion stopped due to a drop in platelet count (platelet count: 23 000/mm3), consulted with hematologist colleagues, they believed it was due to recent chemotherapy, so 10 units of platelets were transfused. One day later platelet count reached 123 000/mm3, heparin infusion was resumed, and after 24 hours it changed to a therapeutic dose of subcutaneous enoxaparin (LMWH with a dose of 60 mg twice a day). The patient continued to improve clinically and was discharged from hospital after 5 days with LMWH. Last echocardiography performed immediately before discharge demonstrated mild RV enlargement & dysfunction and pulmonary artery pressure of 20-25 mm Hg. One week after discharge, laboratory findings showed Hemoglobin: 11.5 (g/dL), Platelet count: 227/mm.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [65, 'years'], 'Hormone use': True, 'Unilateral Leg Swelling': True, 'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [155.0, 'beats per minute'], 'O₂ saturation percentage': [70.0, '%'], 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': True}",6,6,6,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 65 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 155.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 70.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 2 + 1 = 3.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 3 + 1  =  4.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 4.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 4.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is reported to have been diagnosed with deep vein thrombosis in the past. The patient is reported to have been diagnosed with pulmonary embolism in the past. At least one of the criteria is met and so we increment the criteria met by 1, making the current total 4 + 1 = 5.
The patient note reports 'hormonal use' to be present for the patient and so we increment the criteria count by 1, making the current total 5 + 1  =  6.
Hence, the number of PERC rule criteria met by the patient is 6."
6592,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8665683-1,Extracted,"A 43-year-old man presented to the emergency department reporting sudden-onset feeling of palpitations and near syncope after strenuous heavy lifting. He was pale and diaphoretic; blood pressure was measured 90/70 mmHg, oxygen level 99%, heart-rate 210–230 b.p.m., and body temperature 36.6°C. Past medical history was clear for cardiac disease, syncope, or pre-syncope. No history of sudden cardiac death (SCD) or cardiomyopathy into his family was stated. He denied recent flu-like symptoms, smoking, illicit drug use, or excessive alcohol consumption. Physical examination was unremarkable. Initial electrocardiogram (ECG) depicted an irregularly irregular, broad QRS complex tachycardia (). No previous ECG recordings were handed. Direct current (DC) cardioversion restored sinus rhythm with manifest ventricular pre-excitation and clear ‘delta’ waves () confirming our initial clinical suspicion for underlying WPW syndrome. Shortest pre-excited RR interval (SPERRI) during AF was estimated at 160 ms (), indicating an AP with extremely short antegrade effective refractory period (ERP) at risk for mediating SCD. Echocardiography ruled out abnormalities associated with WPW, including Ebstein’s anomaly, valve lesions, cardiac hypertrophy, atrial aneurysms, and septal defects. Cardiac ischaemia was also excluded on the basis of clinical, electrocardiographic, echocardiographic, and laboratory data. The patient was put on enoxaparin 80 mg b.i.d. and propafenone 150 mg t.i.d. and his clinical course remained uneventful. Electrophysiological study (EPS) was performed at a tertiary centre on Day 10 post-diagnosis; programmed atrial stimulation induced pre-excited AF with markedly increased SPERRI = 264 ms and a left anterolateral AP with antegrade only conduction properties was ablated (). The patient was scheduled for routine cardiologic follow-up and advised to abstain from intense physical activity for at least 1-month post-discharge. In case of palpitations, ECG and 24-h Holter monitoring were suggested. CHA2DS2-VASc Score was calculated zero, so 1 month of rivaroxaban 20 mg daily was deemed sufficient post-ablation. Family members were also screened for pre-excitation. The patient remained symptom free without pre-excitation on surface ECG on his latest follow-up visit 3 months after the procedure.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [43, 'years'], 'Heart Rate or Pulse': [210.0, 'beats per minute'], 'O₂ saturation percentage': [99.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Hormone use': False, 'Hemoptysis': False, 'Recent surgery or trauma': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 43 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 210.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6593,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7789174-1,Extracted,"A 75-year-old woman, who was being treated with prednisolone 5 mg/day for polymyalgia rheumatica, presented with anorexia and general malaise for 3 days and then developed vomiting and diarrhea. She experienced difficulty moving her body, and her consciousness deteriorated. The patient was brought to our hospital on an ambulance. The consciousness level on admission, body temperature, blood pressure, pulse rate, respiratory rate, and peripheral oxygen saturation were E3V4M6, 39.5 °C, 153/88 mmHg, 124 beats/minute, 25 breaths/minute, and 90% (with oxygen mask 6 L/min), respectively. Her bulbar conjunctiva was congested on both sides, and coarse crackles were heard in the right lung field. Reticular dermatosis was found on both of her lower legs, and erythematous dermatosis was observed on the lower side of the back. Laboratory blood tests on admission showed elevated inflammatory markers (white blood cell count and C-reactive protein), creatine phosphokinase, and liver aminotransferase. Further, a rapid influenza diagnostic test was positive for influenza A (Table ). Chest computed tomography (CT) showed diffuse airspace opacification in the right middle lobe (Fig. ). Head CT demonstrated a slight fluid collection in the right upper sinus suggesting sinusitis.
Her clinical signs and symptoms fulfilled three out of five clinical criteria of TSS with a fever of 38.9 °C or higher, diffuse erythroderma, and multisystem involvement (conjunctival congestion, gastrointestinal symptoms of vomiting and diarrhea, hepatic dysfunction, and disorientation). At this time point, she had not developed desquamation yet and had no hypotension. Therefore, the patient was clinically diagnosed with influenza with bacterial pneumonia and potential TSS, and her treatment was started with meropenem (1 g every 8 h), vancomycin (1 g every 12 h, therapeutic drug monitoring: ≥15 μg/mL), and clindamycin (600 mg every 8 h).
The next day, S. simulans, a CoNS strain, was detected in both sets of blood cultures. Furthermore, pneumococci and methicillin-sensitive Staphylococcus aureus (MSSA) were identified in sputum cultures (Geckler 4 group) and pharyngeal cultures (small number of colonies), respectively. Exotoxins, such as TSST-1, and staphylococcal enterotoxins (type A, B, C, and D), which are known to cause TSS, were not detected in culture samples of MSSA and S. simulans. We used the reversed passive latex agglutination method to evaluate the exotoxins and enterotoxins; the minimum detection sensitivity of sensitized latex using this method was found to be 1–2 ng/mL. We changed the antimicrobial therapy to cefazolin (1 g q8h) and clindamycin (600 mg q8h), based on microbiologic test results, and this therapy was administered for 14 days. Finger desquamation appeared on the 8th day of hospitalization, fulfilling four out of five clinical criteria for TSS. Therefore, we diagnosed the case as probable TSS.
Serum levels of inflammatory cytokines were high: neopterin 62 mmol/L (reference range, ≤5 mmol/L) and IL-6 38 pg/mL (reference range, ≤5 pg/mL). Lymphocyte subpopulation distribution was then analyzed in peripheral blood (Fig. ), showing prominent CD57 expression in CD8+ T cells, suggesting strong activation of this T lymphocyte subset.
Furthermore, T cell receptor (TCR) Vβ repertoire distribution analysis was carried out (Fig. ). A specific subset of CD8+ T cells, including Vβ7.2 and Vβ14 cells, was increased, indicating the oligoclonal activation of CD8+ T cells likely due to antigen exposure. However, the distribution of CD4+ T cell TCR Vβ repertoire was normal. The activation of Vβ2+ population, which is characteristic for TSST-1, was not observed.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [75, 'years'], 'Heart Rate or Pulse': [124.0, 'beats/minute'], 'O₂ saturation percentage': [90.0, '%'], 'Hormone use': False, 'Recent surgery or trauma': False, 'Hemoptysis': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 75 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 124.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 90.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 2 + 1 = 3.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6594,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7724120-2,Extracted,"An 88-years-old woman (height 146 cm, weight 50 kg) presented with complaints of low back and bilateral buttock pain as well as numbness in both lower extremities. The patient was suffering from a gait disorder which severely restricted her mobility without a wheelchair. A history of congestive heart failure and cerebral infarction was reported. The patient also had a 5-year history of lumbar nerve root and epidural blocks to manage her symptoms. MRI revealed multiple old compression fractures (T10–12, L2–4), vertebroplasty at T7, 10, 11, and L4 and spinal canal stenosis (severe central stenosis L1/2, bilateral mild foraminal stenosis T10–L1) (). On presentation, a fluoroscopy-guided epidural steroid injection was scheduled. In the prone position, the injection site was disinfected and 1% lidocaine was injected. The L5/S1 interspace was identified by fluoroscopy, and an 18-gauge Tuohy needle was advanced into the interlaminar space under an AP fluoroscopic view. The needle was advanced into the epidural space using the LOR technique with a 1-ml air-filled syringe though the LF and a location where the syringe would not rebound. However, CSF aspirated, and on injecting 0.5 ml of the contrast, a dural puncture was confirmed through the fluoroscopic AP and lateral images (). The procedure was aborted immediately. After explaining the occurrence of the dural puncture to the patient, she was sent to the recovery room. Her blood pressure was 103/61 mmHg, HR was 87 beats/min and oxygen saturation was 96%. Normal saline was infused intravenously and oxygen (5 L/min) was administered using a facial mask with a reservoir. One hour later, she complained of severe (NRS score 5–6) bilateral temporal headache and pain on the top of her head that persisted regardless of posture changes. Tramadol administration did not reduce her headache. A case of pneumocephalus was suspected. Brain CT examination showed the presence of air at the ventricular frontal horn, anterior interhemispheric fissure, right ambient cistern, and around bilateral cavernous sinuses (). The patient was admitted to the hospital after an explanation was provided to her and her guardian. After the admission, oxygen (5 L/min) was administered. Twenty-two hours later, the headache was reduced by 70%. Follow-up brain CT confirmed the reduction of the pneumocephalus. Therefore, she was discharged the next day. Follow-up 2 weeks after discharge, indicated complete resolution with no complaint of headache. Her physical examination was negative for pneumocephalus.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [88, 'years'], 'Heart Rate or Pulse': [87.0, 'beats per minute'], 'O₂ saturation percentage': [96.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False, 'Unilateral Leg Swelling': False, 'Recent surgery or trauma': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 88 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 87.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 96.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6595,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8665831-1,Extracted,"Prior to COVID-19 vaccination becoming widely available, a previously healthy, 20-year-old Caucasian male with no significant past medical history presented with two weeks history of progressive dyspnea. About four days prior to presentation, he was evaluated at the emergency department with dyspnea, nonproductive cough, malaise, emesis, diarrhea, intermittent fever with a temperature max of 103°F, and found to have leukocytosis of 20,000 and negative COVID-19 test. Chest X-ray (CXR) showed bilateral interstitial patchy opacities and he was prescribed a five-day course of azithromycin for possible atypical pneumonia. He failed to improve after four days of treatment with azithromycin. He presented with worsening hypoxemia associated with fever, cough, emesis, and diarrhea.
On presentation, vitals showed temperature of 100.8°F, heart rate 99, blood pressure 129/81, respiratory rate 40, SpO2 85% on room air which improved to >90% on 4L nasal cannula. The patient was not in respiratory distress and a physical exam showed crackles over right lung fields and left lingula with expiratory wheezes in the same distribution. Labs were significant for leukocytosis (18x10^3/uL) with eosinophilia (7%). CXR demonstrated diffuse bilateral airspace and interstitial opacity concerning for infection or inflammatory process including COVID-19 (Figure ). Azithromycin was continued and ceftriaxone was initiated for possible community-acquired pneumonia (CAP).
The patient was placed in isolation for CXR findings, as mentioned above, which was concerning for COVID infection. Repeat testing for COVID came back negative. Further workup was significant for elevated ferritin 1,258 ng/mL, lactate dehydrogenase (LDH) 734 units/L, c-reactive protein (CRP) 27.20 mg/dL, procalcitonin 0.58 ng/mL suggestive of possible false-negative COVID-19 infection vs. CAP. Eosinophilic pneumonia vs. allergic bronchopulmonary aspergillosis (ABPA) was considered for eosinophilia and it was noted on initial complete blood count (CBC); further workup with IgE was unremarkable with 9.7 U/ml. Extensive infectious work up with influenza, mycoplasma, chlamydia nucleic acid amplification test (NAAT), sputum culture, urine antigen testing for legionella, Histoplasma, blastomycosis, aspergillus all came back negative. Human immunodeficiency virus (HIV) and QuantiFERON (QFT-G, Cellestis Limited, Carnegie, Vi Australia) were both negative.
On further evaluation, the patient reported living in his parent’s basement around the time of dyspnea onset but denied being exposed to mold. He moved out to go to college within a few days of symptoms onset and he has been living with three housemates since then. The patient initially denied tobacco use, recreational drug use, or being sexually active, and later admitted to binge drinking and vaping (dapping, use of nicotine, and delta-9-tetrahydrocannabinol (THC) products) once a week during social gatherings, and the last time he vaped was two days prior to the onset of dyspnea. The urine drug screen came back positive for cannabinoids.
Acute hypoxemic respiratory failure (AHRF) acutely worsened while on empiric therapy for CAP requiring a high flow nasal cannula (HFNC) with 35 to 45 L/min O2 and 0.4 to 0.6 FiO2, and he was started on treatment with methylprednisolone 40 mg every six hours and albuterol-ipratropium nebulizers. Infectious disease and pulmonology were consulted. Work up with CT chest demonstrated diffuse bilateral lower lobe predominant ground-glass opacities with relative sparing of the subpleural regions and associated interstitial thickening (Figure ). Suspicion of COVID infection remained high but he had a few more negative tests. An echocardiogram showed normal size lateral ventricles and normal systolic function with an ejection fraction of 63%; left pleural effusion was noted. AHRF improved significantly to 2L of nasal cannula after two days of receiving methylprednisolone. The patient was diagnosed with EVALI as a diagnosis of exclusion and AHRF resolved with steroid therapy.
Infectious disease recommended discontinuing all antibiotics for low concern of infectious etiology. Pulmonology service recommended checking antinuclear antibodies (ANA), vasculitis panel with ANA, anti-glomerular basement membrane (anti-GBM) for initial eosinophilia. All these labs were negative, and eosinophilia was later resolved. He underwent bronchoscopy with bronchoalveolar lavage (BAL) and transbronchial biopsy. Infectious work-up on the BAL sample was unremarkable for viral, fungal, and bacterial pathogens and cytology demonstrated small clusters of atypical cells with a high nuclear to cytoplasmic ratio. The patient briefly required being on HFNC after bronchoscopy, but he was back on room air the third day after initiating methylprednisolone. Repeat CXR showed marked improvement in bilateral interstitial and soft tissue opacities (Figure ).
The patient was hospitalized for a total of seven days, and he was discharged on prednisone 60 mg tapered dose over two weeks and supplementary oxygen (3 L of O2 with exertion). Five weeks after the hospital admission, the patient was evaluated at the pulmonary clinic for follow-up. He has been asymptomatic and AHRF has completely resolved.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [20, 'years'], 'Heart Rate or Pulse': [99.0, 'beats per minute'], 'O₂ saturation percentage': [85.0, '%'], 'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False, 'Recent surgery or trauma': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 20 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 99.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 85.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6596,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-2672256-1,Extracted,"A 59-year-old female presented to the ED with a chief complaint of abdominal pain. Her abdominal pain began three hours before presentation and had awoken her from sleep. This abdominal pain was described as “achy,” 5/10, intermittent, and located in the left lower quadrant without radiation. She denied nausea or vomiting and had no diarrhea or blood in her stools. Review of systems revealed that the patient had symptoms of dysuria for one day and left-sided flank pain along with her abdominal pain. She denied fevers or chills. She stated that, despite taking her prescribed insulin injections, her blood sugars have been persistently elevated above 400 with her personal glucometer. Her past medical history was significant for insulin-dependent diabetes mellitus (DM), hypertension, and prior cerebrovascular accident. She denied ever having any surgeries. She used regular insulin, Lantus (insulin glargine), and Ibuprofen. Her family history was noncontributory, and she denied alcohol, tobacco, or illicit drug use.
Physical exam revealed a temperature of 36.5° C, respiratory rate of 18 breaths per minute, heart rate of 93 beats per minute, blood pressure of 166/81 mm Hg, oxygen saturation of 99% on room air, and capillary blood glucose of 447 mg/dL. She was awake, alert, and interacting appropriately. Her pupils were equally round and reactive to light. The cardiac exam was normal and lungs were clear with breath sounds bilaterally. The abdomen was soft with minimal tenderness to palpation in the left periumbilical and left lower quadrant. There was no guarding or rebound. Extremities were warm and well-perfused. The neurological exam revealed no deficit.
The metabolic panel revealed sodium of 132 mEq/L (normal 135–145), BUN of 45 mg/dL (normal 8–22), Creatinine of 2.0 mg/dL (normal 0.5–1.3), glucose of 473 mg/dL, and an anion gap of 8.0. A CBC revealed a white blood cell count of 12.0 K/MM3 (normal 4.5–11.0) and a manual differential with 10.10 K/MM3 Neutrophils (normal 0.80–7.70). The hepatic panel was remarkable for an alkaline phosphatase of 189 U/L (normal 35–115). The urine was visibly clear and non-turbid. Urinalysis was leukocyte esterase and nitrate negative, but revealed large occult blood, glucosuria, protein of 300 mg/DL, and 3–6 WBC/HPF (normal 0–3).
While laboratory studies were pending, the patient received one liter IV normal saline, four mg of morphine sulfate IV for pain, and 10 units of regular insulin. Despite fluid administration and analgesia, the patient continued to have worsening 6/10 abdominal pain. Given the patient’s presentation of undifferentiated abdominal pain without clear etiology and her immunocompromised state, a non-contrast computed tomography (CT) scan of the abdomen was ordered. The CT scan revealed significant air in the bladder wall and lumen consistent with EC, severe left hydroureter and hydronephrosis without evidence of stones, and significant left perinephric stranding without gas in the renal parenchyma ().
A gram of Ceftriaxone and 500 mg of Gentamycin were started empirically along with a repeat fluid bolus and placement of a Foley catheter. While awaiting consultation and admission to the Urology service, the patient complained of increased abdominal pain and was increasingly tender in the left lower quadrant and suprapubic region. Her heart rate was persistently tachycardic (in the 130s), and she developed a fever to 39.4°C. In light of developing urosepsis and the potential for rapid progression to Emphysematous pyelonephritis, Interventional Radiology (IR) was consulted and placed a left nephrostomy tube to relieve the functional obstruction of the urinary tract just eight hours after the patient presented to the ED. After nephrostomy tube placement by IR, the patient was admitted to the ICU for close monitoring. The urine culture grew out Klebsiella pneumoniae and the patient was continued on IV antibiotics. Three days after admission, the nephrostomy tube was removed as the patient was able to void without use of a foley catheter and was able to control her pain. She was subsequently discharged and given a prescription for Levofloxacin 500 mg every day for fourteen days.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [59, 'years'], 'Heart Rate or Pulse': [93.0, 'beats per minute'], 'O₂ saturation percentage': [99.0, '%'], 'Recent surgery or trauma': False, 'Hormone use': False, 'Hemoptysis': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 59 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 93.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6597,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7279916-2,Extracted,"A 73-year-old woman with a history of lower limb venous insufficiency, obesity, dyslipidaemia and impaired fasting glucose, who was not taking any medications, was admitted to another hospital due to compressive chest pain. Chest CT angiography demonstrated a proximal ascending aorta dissection. The patient was transferred to our tertiary medical centre and admitted to the cardiac surgery department. Since she came from an endemic area, she was tested for COVID-19 infection by RT-PCR testing of a nasopharyngeal swab, which came back positive. The cardiac surgeons postponed surgery, asked the patient to avoid mobilization, and kept her blood pressure low by administering intravenous labetalol. Physical examination upon arrival at the intensive care unit was notable for an oral temperature of 36.8°C, heart rate of 72 beats/min, respiratory rate of 24 breaths/min, blood pressure of 106/55 mmHg, and oxygen saturation of 94% in room air. Laboratory tests showed no leucocytosis, D-dimer blood levels of 7,353 ng/ml, and CRP blood levels of 129 mg/l. Another chest CT angiogram showed no change in the aortic dissection. The patient was not treated with thromboprophylaxis because of the high risk of aortic rupture and bleeding, but a pneumatic compression device on both legs was used in order to prevent deep vein thrombosis.
Over the next days the patient was asymptomatic, oxygen saturation was normal most of the time, CRP blood levels decreased to 67 mg/l, and four RT-PCR tests for COVID-19 infection on nasopharyngeal swabs came back negative. However, there was a discrepancy between these signs and laboratory findings and the steady increase in D-dimer blood levels that reached 3,1041 ng/ml (). A third CT angiogram showed no change in the aortic dissection, but a new bilateral PE was demonstrated (). Thereafter, the patient underwent aortic dissection repair and thrombectomy.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [73, 'years'], 'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [72.0, 'beats per minute'], 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False, 'O₂ saturation percentage': [94.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': True}",4,4,4,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 73 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 72.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 94.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is reported to have been diagnosed with pulmonary embolism in the past. At least one of the criteria is met and so we increment the criteria met by 1, making the current total 3 + 1 = 4.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 4.
Hence, the number of PERC rule criteria met by the patient is 4."
6598,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7543835-2,Extracted,"A 43-year-old Brazilian man arrived at the ED in May 2020 with a history of cough with hemoptoic sputum for more than 1 month, evolving to mild respiratory distress in the last 7 days. He did not show signs of a fever and other symptoms. He had a previous history of HIV/AIDS with no adherence to antiretroviral therapy, illicit drug abuse, and had generalized anxiety disorder. He had lost clinical and laboratory follow-up in the last 5 years. In 2015, the HIV viral load was 9,054 copies/mm3, and the T-CD4 cell count was 407/mm3. On physical examination, his weight was 55 kg, heart rate was 79 bpm, respiratory rate was 18 rpm, and SPO2 was 96%. No lymphadenopathy was observed. Blood cell count presented low hemoglobin (9.9 g/dL) and hematocrit levels (29.7%), and normal platelet and white cell count ranges. Lactate dehydrogenase and C-reactive protein levels were 312 U/L, above reference limits (140–271 U/L), and 52.3 mg/dL, respectively. The D-dimer level (0.6 mcg/mL) exceeded the normal range. Troponin, AST, ALT, and ferritin levels were in normal range.
Chest CT revealed bilateral glass-ground opacities occupying approximately 25% of both lungs (). Respiratory secretion was collected with a nasopharyngeal swab and tested positive for SARS-CoV-2. Mycobacterium tuberculosis DNA was detected using PCR (GeneXpert MTB/RIF assay) without RIF resistance. Treatment was initiated with azithromycin (500 mg/day), HCQ (400 mg/day) for 5 days, and ceftriaxone (2 g/day). He was treated with isoniazid, ethambutol, pyrazinamide, and RIF. Antiretroviral therapy was not started to avoid complications with anti-TB treatment. The patient was clinically stable and discharged to home after 1 week. Currently, the patient is under follow-up and remains asymptomatic without developing relapses.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [43, 'years'], 'Heart Rate or Pulse': [79.0, 'beats per minute'], 'O₂ saturation percentage': [96.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': True, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 43 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 79.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 96.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'hemoptysis' to be present for the patient and so we increment the criteria count by 1, making the current total 0 + 1  =  1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6599,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4879800-1,Extracted,"A 26-year-old female presented to the emergency department with sudden onset of dyspnea and left precordial pain of 6 hr duration. She had no history of exertional dyspnea, fever, weight loss, prolonged immobilization, syncope, focal neurological deficits, substance abuse, endocrine disorders and dermatological ailments in the past. She had no family history of cardiac disorders, including cardiac tumors. The patient's physical examination revealed blood pressure of 94/60 mmHg, heart rate of 120 beats/min, respiratory rate of 40/min, elevated jugular venous pressure with prominent ‘v’ wave. On cardiovascular system examination, S1 was normal, S2 was narrowly split with loud P2; a pan-systolic murmur of grade III/VI intensity was present along left sternal border. Tumor plop was audible. Chest was clear on auscultation. Abdominal examination was normal. Electrocardiogram revealed sinus tachycardia, right axis deviation and QR in V1 lead. Pulse oximetry revealed a saturation of 85% at room air increasing to 90% with 100% oxygen at 6 L/min. Laboratory examination revealed hemoglobin - 12.6 g/dl, total leukocytes count - 12.600/µL and platelet count of 1,00,000/µL. Liver function tests and renal function tests were normal. Chest roentgenogram was unremarkable.
Transthoracic echocardiogram showed a large pedunculated mobile mass in RA with heterogenous echotexture attached to RA free wall and another mass attached to interatrial septum near fossa ovalis []. Another mass was seen in RV measuring 11 mm × 11 mm just beneath the septal leaflet of tricuspid valve []. Larger RA mass was prolapsing into RV producing severe eccentric TR jet with a gradient of 60 mmHg [, supplementary movie 1]. RV outflow tract and PA was dilated []. Inferior vena cava was free of any mass or thrombus (supplementary movie 2). HRCT thorax revealed embolization to the lateral aspect of right PA and along the medial aspect of left PA causing subtotal obstruction with pulmonary infarct in left lung [Figure and ]. Ultrasonography of abdomen and bilateral lower limb Doppler was unremarkable. Contrast-enhanced computed tomography scan of the abdomen was normal.
Once the diagnosis of multicentric RA and RV myxoma with tumor fragment embolization to PA was made, emergency surgery was performed by standard median sternotomy and cardio-pulmonary bypass using bicaval and ascending aortic cannulation to prevent further embolic events. Systemic hypothermia was used, and cardioplegia was administered for myocardial protection. The RA was then opened and a round lobulated mass measuring 3 cm × 2.5 cm × 2.5 cm was found attached to the RA free wall by a pedicle. Another mass attached to interatrial septum near fossa ovalis was excised. Multiple degenerating tumor strands were detected in RA, which were not visualized by transthoracic echocardiography. Another solitary mass was excised from the RV originating beneath the septal leaflet of tricuspid valve [Figure and ]. After the direct closure of RA, patient was weaned off the extra-corporeal circulation.
Gross pathological examination revealed multiple flesh-colored soft to firm lobulated mass. Gross foci of degeneration were detected. Microscopy revealed hypocellular tumor tissue with myxoid background, isolated spindle and stellate cells with no abnormal mitosis or pleomorphism [Figure and ]. Gross pathology and histopathological examination were consistent with the diagnosis of cardiac myxoma.
After the surgical excision of the tumor, severity of TR decreased from severe to mild. Her breathlessness decreased. Patient was administered anticoagulation therapy postsurgery. Echocardiographic follow-up at 6 months revealed no recurrence.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [26, 'years'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'O₂ saturation percentage': [85.0, '%'], 'Unilateral Leg Swelling': False, 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 26 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 120.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 85.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6600,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-3530248-1,Extracted,"Mrs. A.O., a 40-year-old known SCD patient with hemoglobin SS genotype was referred to the pulmonary division on account of dry cough of 3 weeks, difficulty in breathing of 2 weeks, and bilateral leg swelling of 4 days. There was low-grade fever, no weight loss, and no contact with chronic cough index. Difficulty in breathing initially occurred on exertion but later occurred even at rest. There was orthopnea but no paroxysmal nocturnal dyspnea. There was bilateral leg swelling, which worsened progressively. No swelling in other parts of the body. No reduction in her urine volume. She was not a diagnosed asthmatic, hypertensive, or diabetic and she was not previously treated for tuberculosis or any other chronic lung diseases. She was only admitted for childbirth in her adulthood years. She had a single episode of blood transfusion when she was 6 years old. Afterwards, she has been crisis free for more than 20 years. She neither smokes cigarettes nor consumes alcoholic drinks. No history of exposure to cigarette smoke from others. She is married in a monogamous family with two girls and one boy. Her last childbirth was 15 years prior to presentation. She works as a secretary in the registration office of a state polytechnic. No history of exposure to occupational dust or fumes. No history of chronic drug use and no history of allergy.
On general examination, she was a middle aged looking woman, conscious, dyspneic with central cyanosis, afebrile (Temperature=36.5), not pale, anicteric, not dehydrated, grade 3 digital clubbing, bilateral pitting pedal edema up to the lower third of the leg, weight=84 kg, height=1.65 m, and BMI=30.9 kg/m2. Oxygen saturation in room air was 78% and this increased to 92% on 5 L/min of oxygen via nasal prong.
Respiratory examination revealed that she was in respiratory distress as evidenced by respiratory rate of 42/ min, flaring of alae nasi, and use of accessory muscles of respiration, and the trachea was central with symmetrical chest movement. Percussion note was resonant with coarse crepitations over the entire right lung and posterior lower zone of the left lung.
Cardiovascular examination: pulse=100 beats/min, regular with premature beats, full volume; arterial wall was not thickened. No locomotor brachialis. BP was 105/60 mmHg. JVP was raised to the angle of the jaw. She had a right parasternal heave and apex beat was in the 5th left intercostal just lateral to the mid-clavicular line. Heart sounds were S1, S2, S3 gallop rhythm with loud pulmonary component of second heart sound.
Abdomen – full, moves with respiration, liver was 4 cm below the costal margin, mildly tender, smooth surface, and span of 16 cm. Spleen and kidneys were not enlarged. No demonstrable ascites.
Other systems were within normal limits.
Her packed cell volume was 32% with a white blood cell count of 13.5 ×109/L (neutrophil=52%, lymphocyte=38%, other=9%) and erythrocyte sedimentation rate of 3 mm/h. Sputum examination for acid and alcohol fast bacilli was negative in three samples; sputum culture did not yield any growth. Chest X-ray showed widespread reticulonodular opacities involving the whole of the right lung field and left upper zone with an area of hyperluscency in the left mid and lower zones. Electrocardiography revealed sinus tachycardia of 120 beats/min, P pulmonale, and right ventricular hypertrophy with ventricular extrasystole. Echocardiography demonstrated tricuspid regurgitation with pulmonary hypertension. Spirometry showed severe restrictive pattern {FVC=1.13 L (36% of predicted); FEV1=0.84 L (35% of predicted) FEV1/FVC ratio=74.5% (92% of predicted)}. Chest CT demonstrated diffuse ground glass opacity with thickening of interlobar septa in the entire right lung field as well as left apex and part of the left lower region. There were multiple bullae with reduced attenuation (suggestive of compensatory emphysema of the remaining lung tissue) in the left lung field, sparing the apex. The pulmonary trunk was prominent and there was cardiomegaly [Figures –].
She was admitted and managed initially in the intensive care unit with intranasal oxygen, cardiopulmonary monitoring, tablet levofloxacin 500 mg daily, intravenous frusemide 60 mg 8 hourly, tablet spironolactone 25 mg twice daily, and tablet aspirin 75 mg daily.
The heart failure gradually improved but she continued to desaturate in room air. She was advised on domiciliary oxygen, which she initially rejected but later purchased a cylinder of oxygen (did not purchase oxygen concentrator because of poor power supply) and pulse oximeter. She was discharged home, on 1–3 L/min of domiciliary oxygen (to be titrated with the pulse oximeter readings), aspirin, and oral diuretics, after 1 month of hospitalization. She was re-admitted 1 week later with productive cough and features of right heart failure. She was managed with oxygen, diuretics, antibiotics, and aspirin. She improved and was discharged after 3 weeks. She has remained relatively stable at subsequent clinic visits. Her clinic oxygen saturation was 91-94% (off oxygen) during clinic visits.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [40, 'years'], 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'O₂ saturation percentage': [78.0, '%'], 'Unilateral Leg Swelling': True, 'Recent surgery or trauma': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 40 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 100.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 78.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6601,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7873810-1,Extracted,"A 64-year-old male presented to the emergency department with a 10-day history of fatigue, shortness of breath, and peripheral oedema.
His medical history included: bioprosthetic aortic valve replacement (AVR) and coronary artery bypass graft (CABG) surgery, 5 months prior, for critical aortic stenosis and significant coronary artery disease, hypertension, type-2 diabetes mellitus, hypercholesterolaemia, nephrotic syndrome, and pulmonary embolism. He was an active gentleman, often completing several rounds of golf per week.
Medications included: warfarin, clopidogrel 75 mg OD, losartan 25 mg OD, atorvastatin 20 mg OD, prednisolone 60 mg OD, gliclazide 240 mg/40 mg BD, and linagliptin 5 mg OD.
At presentation, his blood pressure was 110/60 mmHg, heart rate 72 b.p.m., respiratory rate 25 b.p.m., oxygen saturations 100% on air, and he had a temperature of 37.7°C. On physical examination, he appeared breathless on minimal exertion, had fine right basal crepitations, a pan-systolic and early diastolic murmur, and bilateral mild pitting oedema. Initial laboratory investigations revealed a haemoglobin of 117 g/L, white cell count of 11.57 × 109/L (neutrophil count 9.26 × 109/L), C-reactive protein 11 mg/L, and creatinine 96 μmol/L [estimated glomerular filtration rate (eGFR) 72 mL/min].
The primary components of the admission differential diagnosis included: infective endocarditis, aortic valve dehiscence or thrombosis, congestive cardiac failure of alternative cause, and pneumonia.
Urgent echocardiography was performed which demonstrated dehiscence of the aortic valve with mild aortic regurgitation. On 2D echo imaging, a hypoechoic tract could be visualized from the left ventricular outflow tract (LVOT) to the RA (Figure ). The suspicion of a Gerbode defect was confirmed on colour flow mapping, with a large jet demonstrated between the two chambers (Figure and C).
Computerized tomography (CT) revealed a complex aortic root pseudoaneurysm with LVOT to RA fistulation and a large left-to-right shunt (Figure and B).
Three peripheral blood cultures taken on admission returned positive for Staphylococcus warneri, a coagulase-negative Staphylococcus. Treatment with intravenous gentamicin, vancomycin, and rifampicin was initiated and after 10 days of therapy, he underwent a surgical aortic valve replacement and LV–RA fistula repair. After 1 month in hospital, he was discharged home, and 2 months later was back on the golf-course, albeit with a very limited swing on account of his recent sternotomy.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [64, 'years'], 'Heart Rate or Pulse': [72.0, 'beats per minute'], 'O₂ saturation percentage': [100.0, '%'], 'Hemoptysis': False, 'Previously Documented Pulmonary Embolism': True, 'Unilateral Leg Swelling': True, 'Hormone use': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 64 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 72.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 100.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is reported to have been diagnosed with pulmonary embolism in the past. At least one of the criteria is met and so we increment the criteria met by 1, making the current total 2 + 1 = 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6602,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7771626-1,Extracted,"Our patient is an otherwise previously healthy, active, nonsmoking, 40-year-old male who presented to an outside hospital on April 2, 2020, with a 7-day history of fevers (Tmax: 102.7°F, 39.3C) and worsening shortness of breath. On presentation, he was saturating 80% on room air, which improved to 96% with 6 l of the nasal cannula. His other vitals at presentation included: heart rate of 87 beats/min, respiratory rate of 18 breaths/min, the temperature of 39.1C, and blood pressure of 135/60 mmHg. His height was 188 cm, weight 87.7 kg, and body mass index was 25. His C-reactive protein (CRP) was 19.8 mg/dL (normal: 0.3–1.0 mg/dL). Other admission laboratories included a point of care troponin (normal, 0.0 ng/ml), creatinine of 1.17 mg/dL, carbon dioxide of 27 mmol/L, procalcitonin of 0.31 ng/ml, lactic acid of 1.5 mmol/L, normal liver transaminases, normal prothrombin time, white blood cell count (8.9 10^9/L) and differential, hemoglobin of 13.5 g/dL. No D-Dimer or brain natriuretic peptide testing was performed and per the initial assessment, since there were no complaints of leg swelling, a computed tomography (CT) scan of the chest was not performed, however, a chest X-ray demonstrated “multi-focal consolidation most consistent with typical viral bronchopneumonia” []. No other source of bacterial infection or cause of acute respiratory failure was identified, and a COVID polymerase chain reaction test was positive. He required mechanical ventilation (initial setting: rate: 24/min; positive end-expiratory pressure: 14 mmHg; peak inspiratory pressure: 31 mmHg; tidal volume: 460 ml; FIO2: 0.70) the following day with a CRP of 23.6 mg/dL and a ferritin of 1039 ng/mL (normal: 38–380 ng/mL). His COVID-19 therapies are listed in . D-Dimer testing on April 9th was elevated to 5.25 mg/L.
However, due to the worsening of his respiratory failure, including poor response to prone positioning and inhaled nitric oxide (40 parts/million), he was transferred to our institution for ECMO on April 7, 2020 []. On arrival, he was immediately assessed by our ECMO Team (respiratory ECMO survival prediction score: 3, Class II risk, 76% predicted survival)[] and placed on percutaneous veno-veno ECMO at the bedside (21 Fr single-stage inflow, 25 Fr multi-stage drainage cannulas with Maquet CardioHelp circuit (Maquet Cardiovascular, Wayne NJ USA). ECMO was initiated 96 h postinitiation of mechanical ventilation. At the time of cannulation, his arterial PaO2 to FiO2 (P/F) ratio was 45. He was treated with tocilizumab on April 11, and the following day, an additional unit of convalescent plasma was given. Neither he did receive remdesivir, nor did he receive steroids. Systemic heparin for the ECMO circuit was used with a target partial thromboplastin time of 40–60 s. A lung-protective strategy was employed using an airway pressure release ventilation mode that was frequently adjusted to minimize airway pressures and atelectasis.
He was successfully decannulated on April 15, 2020 (189 h on ECMO) and was extubated to the nasal cannula by April 17 with a P/F ratio of 213.
He was discharged home with his family on April 21, 2020, on room air []. His COVID-19 test (Cepheid Xpress SARS-CoV-2 assay) on the day before discharge was still positive, and he was advised to self-isolate. His only medication at discharge was apixaban 5 mg po BID for a peroneal deep-vein thrombosis discovered post-ECMO.
Formal pulmonary function testing was obtained on May 6, 2020 [] and reported no abnormalities. The final interpretation was: “no evidence of obstruction, restriction, or diffusion impairment.” Outpatient COVID-19 testing was negative. The patient reported no respiratory symptoms, was walking and eventually running at least 6 miles a day and was encouraged to pursue more intensive exercise as tolerated (of note, the patient was an avid marathon runner before his illness). As he has been doing well, not further chest imaging has been performed. Although no family member tested positive for the disease, his wife tested positive for antibodies, suggesting she had been infected previously. However, she never required hospitalization or treatment and never manifested significant clinical signs or symptoms.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [40, 'years'], 'Heart Rate or Pulse': [87.0, 'beats per minute'], 'O₂ saturation percentage': [80.0, '%'], 'Hemoptysis': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 40 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 87.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 80.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6603,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-6306,Extracted,"A 67-year-old man presents to his primary care physician for a follow up appointment. He was released from the hospital 1 week ago for an appropriately managed ST-elevation myocardial infarction (STEMI); however, he has not filled any of his prescriptions and did not attend his follow up appointment as scheduled. The patient has a past medical history of hypertension and peripheral vascular disease. His temperature is 97.5°F (36.4°C), blood pressure is 167/118 mmHg, pulse is 90/min, respirations are 14/min, and oxygen saturation is 99% on room air. Physical exam is notable for jugular venous distention and bilateral lower extremity pitting edema. Echocardiography demonstrates an ejection fraction of 55%.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [67, 'years'], 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'O₂ saturation percentage': [99.0, '%'], 'Unilateral Leg Swelling': True, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 67 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 90.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6604,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-5536,Extracted,"A 22-year-old woman presents to the emergency department for abdominal pain. The patient has been trying to get pregnant and was successful recently, but now she is experiencing abdominal pain, contractions, and a bloody vaginal discharge. According to her last appointment with her primary care provider, she is 10 weeks pregnant. The patient has a past medical history of constipation, anxiety, and substance abuse. She is not currently taking any medications. Her temperature is 99.5°F (37.5°C), blood pressure is 107/58 mmHg, pulse is 90/min, respirations are 17/min, and oxygen saturation is 98% on room air. Physical exam is notable for a bloody vaginal discharge and an open cervix. The patient is initially extremely grateful for the care she is receiving and thanks the doctor and the nursing staff for saving her baby. Upon hearing the news that she is having a spontaneous abortion, the patient becomes angry and aggressive and states that her physician and the medical staff are incompetent, evil, and she is going to sue all of them. The patient is left to grieve but upon entering the room again you notice that the patient has new lacerations over her wrists and that some of the medical equipment in the room is broken.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [22, 'years'], 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False, 'O₂ saturation percentage': [98.0, '%'], 'Hormone use': False, 'Recent surgery or trauma': False, 'Previously Documented Pulmonary Embolism': False}",0,0,0,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 22 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 90.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 0.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 0.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
Hence, the number of PERC rule criteria met by the patient is 0."
6605,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7530872-1,Extracted,"The patient was a 52-year-old man who referred to the Poursina Hospital in Rasht while complaining of abdominal pain from the day before hospitalization. The patient reported a history of tiredness, fever, and nausea. In the examinations performed, there was a brief tenderness in the patient’s epigastrium. The patient’s initial pressure was 80.120 with a pulse rate of 95. The patient’s fever was not detected upon arrival. For the patient, an upright abdominal radiograph, abdominal and pelvic ultrasounds, and blood tests including CBC,BUN,Cr,PT,PTT,INR,LFT,Amylase,Lipase,LDH were requested.
The patient’s upright abdominal radiograph was normal. Perihepatic and perisplenic fluid and gallstones were seen on the patient’s ultrasound. On laboratory findings, White Blood Cells (WBC) = 4000 /μL with 30% lymphocytes were reported. Hemoglobin (Hb) = 11 g/dL and Platelets (PLT) = 245,000 /μL were found. Other findings were normal. No pathological lesion was observed on the patient’s lung CT scan (Fig. ). A small amount of perihepatic and perisplenic fluid was observed on the patient’s CT scan (Fig. ).
The patient was monitored and about 12 h after hospitalization, ill appearance, respiratory (respiratory distress) symptoms, and high fever were reported for the patient. The patient’s O2Sat was 96%. Due to the exacerbation of the patient’s respiratory symptoms, the CT scan of the lungs was requested again for the patient and the tests were repeated for suspicion of coronavirus.
The second CT scan was performed about 18 h after the initial examination. Patchy ground-glass lesions along with bilateral pleural effusion were seen on the CT scan of the patient’s lungs (Fig. ). A bilateral chest tube was inserted for the patient according to the volume of the fluid, and according to the patient’s CT scan and respiratory symptoms, he was transferred to the specialized COVID-19 unit. In the new blood tests, Hb = 9.5 g/dL, WBC = 4800/μL, and PLT = 195,000 /μL were observed. An extensive fluid collection around the spleen was observed on the CT scan performed for the patient (Fig. ). The examination of the patient’s abdomen changed significantly about 20 h after the initial examination and became generalized rebound tenderness. However, the patient’s blood pressure was still 70.110 and the pulse rate was 90. According to the examination, the patient was immediately transferred to the operating room and underwent laparotomy. During the operation, contrary to our expectations, a lot of blood (about 1000 cc) was observed in the patient’s abdomen. After blood suctioning, the left upper quadrant was bleeding and the rupture of the spleen could also be observed. Therefore, a splenectomy was performed (Fig. ).
In the examinations performed for the patient, the patient’s PCR confirmed COVID-19. The patient was admitted to the ICU after surgery, and within 3 days after surgery, the patient was extubated. The patient’s chest tubes were removed within 1 week after the surgery according to the radiographs performed. After a concomitant treatment for COVID-19 and during a two-week hospital stay, the patient was discharged in good general condition.
During the examinations performed and the history taken several times from the patient and the patient’s companion, no history of the trauma was given and the changes in the patient’s CT scan and the patient’s examinations occurred very quickly.
The LE cell, ANA, and HIV as well as the Monospot, RF and Wright agglutination test were negative. The peripheral blood smear and the Widal agglutination test were negative for malaria and VCA Antibody IgM and IgG were negative for Epstein - Barr virus (EBV).
In the macroscopic study of splenic pathology, a spleen tissue with dimensions of 11× 8 × 5 cm and a weight of 350 g and a laceration with a size of 2 × 2 cm were observed and in the microscopic study, a focally hemorrhagic area was reported.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [52, 'years'], 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'O₂ saturation percentage': [96.0, '%'], 'Previously Documented Pulmonary Embolism': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 52 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 90.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 96.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6606,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-3074556-1,Extracted,"A 44-year-old Hispanic woman presented to the hospital with a six-month history of generalized weakness, weight loss of 40 pounds over a four-month period and a two-week history of progressively worsening dyspnea. She had had hypertension for five years for which she was being treated with lisinopril but had been noncompliant for over three years because of financial constraints. The patient denied any alcohol or illicit drug use and was a lifelong non-smoker.
On admission, her blood pressure was 102/66 mm/Hg, her temperature was 37°C, her respiratory rate was 24 breaths/minute, her oxygen saturation level was 92% on room air and her pulse rate was 88 beats/minute. A physical examination revealed an ill-looking woman with mucosal pallor, generalized wasting and non-tender, rubbery axillary and inguinal lymphadenopathy. There was no evidence of cyanosis, digital clubbing, pitting edema, skin rash or joint deformities. Her abdomen was mildly distended but non-tender, with no organomegaly detected. Dullness to percussion and decreased breath sounds over the left base were noted on the respiratory system examination. The cardiovascular and neurological examinations were unremarkable.
Initial laboratory investigations (Table ) revealed anemia, leukopenia, elevated blood urea nitrogen and elevated serum creatinine. Urinalysis showed trace proteinuria. Chest radiography revealed bilateral pleural effusions that were determined to be exudative in nature on the basis of thoracocentesis. There was a high index of suspicion for malignancy; however, the results of chest, abdomen and pelvis computed tomography scans and an axillary lymph node biopsy did not confirm this. Human immunodeficiency virus and tuberculin skin tests were negative.
On day four of admission, she developed acute inflammatory arthritis of the elbows and knees. A serological workup revealed high anti-nuclear antibody, anti-double-stranded DNA antibody and anti-Smith antibody titers, with low complement 3 levels. An active sediment was noted on the basis of urinalysis (Table ). The patient's renal impairment persisted, and her glomerular filtration rate was estimated to be 53 ml/min/1.73 m2. A review of blood results since admission showed evidence of documented leukopenia on more than two occasions.
On day 5 of admission, the patient experienced dyspnea and pleuritic chest pain. Reaccumulated pleural effusions were noted on a chest radiograph, and an echocardiogram showed evidence of pericardial effusion. Arterial blood gas interpreted in conjunction with a corresponding basal metabolic panel (Table ) revealed the presence of a non-anion gap hyperkalemic metabolic acidosis consistent with type 4 RTA. Analysis of morning serum sample showed a serum aldosterone level less than 1 ng/dl.
The renal ultrasound obtained showed normal kidney morphology and no evidence of nephrolithiasis. A renal biopsy was done, which revealed diffuse global proliferative and membranous glomerulonephritis. This was consistent with lupus nephritis Renal Pathology Society/International Society of Nephrology 2003 class IV-G(A) and V, moderate activity index 9/24, minimal chronicity index 1/12; minimal tubulointerstitial fibrosis and acute tubular necrosis (Figure ).
She was diagnosed with SLE complicated by a generalized lupus flare, with a SLEDAI score of 29. Overall during this single admission, she demonstrated six of the 11 American College of Rheumatology criteria used in the diagnosis of SLE.
The patient was treated with a course of hydroxychloroquine and intravenous methylprednisone 1 g daily for three days. Thereafter she was placed on a prednisone, mycophenolate mofetil and hydroxychloroquine regimen. Complete resolution of the renal impairment (Figures and ) and type 4 RTA (Figure ) was achieved. She was discharged after 19 days to follow-up in the Rheumatology and Nephrology clinics. Her renal function remained normal at the one-month follow-up clinic visit.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [44, 'years'], 'Heart Rate or Pulse': [88.0, 'beats per minute'], 'O₂ saturation percentage': [92.0, '%'], 'Hormone use': False, 'Unilateral Leg Swelling': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 44 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 88.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 92.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6607,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4612483-1,Extracted,"A 63-year-old Caucasian male with a past history of supraventricular tachycardia and recurrent deep vein thrombosis, who had been non-compliant with his daily Rivaroxaban® 20 mg, presented with pleuritic chest pain and was found to have a right lower lobe pulmonary embolus. The patient was subsequently restarted on Rivaroxaban® and discharged. He presented again 5 days later with left arm weakness and was found to have multiple areas of punctuate infarctions of both cerebral and cerebellar hemispheres, more confluent within the right frontal lobe on magnetic resonance imaging (MRI) of the brain ( and ). He has been compliant with his Rivaroxaban® since the previous hospital discharge 5 days prior. The patient was admitted and subsequently started on unfractionated heparin. On admission, his vital signs were blood pressure 138/93, heart rate 65 beats per minute, respiratory rate 16, and oxygen saturation 97% on room air. Cardiopulmonary examination revealed regular rate and rhythm, without murmurs, rubs, or gallops and clear lungs on auscultation. Neurologic examination revealed intact cranial nerves, preserved strength in all extremities with an exception of mild dysmetria in the left upper extremity and an NIH score of 1. Electrocardiogram revealed normal sinus rhythm, non-specific ST changes, and a premature ventricular contraction. Transthoracic echocardiogram was notable for normal left ventricular function with mild tricuspid regurgitation and stage 1 diastolic dysfunction. Transesophageal echocardiogram was negative for intracardiac thrombus. The echocardiography with agitated saline contrast revealed microbubbles of moderate opacity entering the left atrium from the left lower pulmonary vein indicative of a grade 2 intra-pulmonary arteriovenous shunt (). There was no atrial septal defect or patent foramen ovale. Unfractionated heparin was continued, and the patient was transferred to a tertiary care center for embolization of the shunt. There, he developed recurrent cerebral infarctions while anticoagulation was temporarily held. Computed tomography of the abdomen and pelvis was done for persistent abdominal pain, and noted an omental mass, and subsequent exploratory laparotomy revealed an adenocarcinoma within the omentum with nodular peritoneal implants. The patient was placed on weight-based Enoxaparin® and discharged home with scheduled outpatient chemotherapy. Embolotherapy of the intrapulmonary shunt was deferred given this new diagnosis of malignancy.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [63, 'years'], 'Hormone use': False, 'Previously Documented Pulmonary Embolism': True, 'Heart Rate or Pulse': [65.0, 'beats per minute'], 'O₂ saturation percentage': [97.0, '%'], 'Previously documented Deep Vein Thrombosis': True}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 63 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 65.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 97.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'recent surgery or trauma'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is reported to have been diagnosed with deep vein thrombosis in the past. The patient is reported to have been diagnosed with pulmonary embolism in the past. At least one of the criteria is met and so we increment the criteria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6608,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-6366373-1,Extracted,"A 21-year-old woman presented to the ED with complaint of chest pain and shortness of breath. Prior to arrival to the ED she had an episode of near syncope. Her previous medical history included development of diffuse erythematous rash following a course of minocycline prescribed for acne three months prior to ED presentation. The minocycline was discontinued, and she was treated with 30 milligrams (mg) daily oral prednisone with improvement of the rash. Initial vitals included blood pressure of 81/68 millimeters of mercury (mmHg), heart rate of 121 beats per minute (bpm), and respiratory rate of 18 breaths per minute. She was afebrile (36.7ºC oral temperature) and had pulse oximetry (SpO2) of 100% on room air. Physical exam was within normal limits. Electrocardiogram (ECG) showed right bundle branch block and normal ST-T segments, but no previous ECG was available.
While in the ED the patient had an episode of syncope during peripheral venous catheter placement, and intravenous (IV) fluids were administered due to concern of vasovagal event. She was also administered 5 mg IV dexamethasone due to possibility of adrenal suppression from steroid use. Her systolic pressure improved. However, the patient complained of worsening chest pain and then became unresponsive with pulseless electrical activity arrest (PEA). Cardiopulmonary resuscitation (CPR) and Advanced Cardiac Life Support were initiated. She received two doses of 1 mg IV epinephrine with return of spontaneous circulation (ROSC) in normal sinus rhythm of 70 bpm and blood pressure of 72/48 mmHg. Due to persistent hypotension, norepinephrine infusion was administered with improvement of blood pressure to 88/56 mmHg. She was intubated for airway protection.
Due to concern for massive pulmonary embolus, computed tomography chest angiography was performed but was unremarkable. Point-of-care echocardiogram demonstrated no right heart strain and grossly reduced heart function. Telemetry demonstrated QRS widening and increasing bradycardia to 41 bpm. The patient then developed a second PEA arrest with ROSC after CPR and one dose of 1 mg IV epinephrine. She remained hypotensive with blood pressure of 60/40 mmHg despite norepinephrine infusion. Initial troponin-T measured was 8.56 nanograms/milliliter (ng/mL) (reference range 0.0–0.02 ng/mL) and complete blood count with differential showed leukocytosis of 17.5 × 103 cells/mL (reference range 4.0–10.0 × 103 cells/mL) and eosinophilia of 1.6 × 103 cells/mL r (reference range 0.0–0.4 × 103 cells/mL). The cardiology service was consulted and a formal echocardiogram demonstrated a severely reduced ejection fraction of 15% (normal range 55–70%).
The dermatology service was also consulted at bedside in the ED; concern for ANEM in setting of DRESS given the rapidity of onset of her cardiac dysfunction was discussed. Also, the differential diagnoses included coronary vasculitis, viral myocarditis, infiltrative cardiomyopathy, and sepsis. (She was administered 4.5 g piperacillin/tazobactam and 20 milligrams/kilogram (mg/kg) vancomycin, and 500 mg azithromycin IV.)
While in the ED the patient developed further hypotension with blood pressure of 61/40 mmHg despite multiple vasopressors (IV vasopressin and norepinephrine infusions) and had severe acidemia and hypoxemia despite high ventilator support. Ventilator settings were tidal volume of 360mL, positive end-expiratory pressure of 20 centimeters of water (cmH2O), and fraction of inspired oxygen of 100%, and respiratory rate of 28 breaths per minute. Arterial blood gas (ABG) revealed respiratory acidosis with pH of 7.06, carbon dioxide partial pressure (pCO2) of 78 mmHg (reference range 33–43 mmHg), low arterial oxygen (PaO2) of 61 mmHg (reference range 80–100 mmHg), and normal bicarbonate. Basal metabolic panel was within normal limits. Due to continued decline, she received cannulation for veno-arterial extracorporeal membrane oxygenation (VA-ECMO) within the ED. ECMO cannulation occurred within three hours of initial cardiac arrest. Once placed on ECMO she had significant improvement in her acidosis and hypoxemia on repeat ABG (pH 7.39, pCO2 41 mmHg, PaO2 135 mmHg) and was rapidly weaned from her vasopressors.
The patient was admitted to the cardiac intensive care unit (ICU) for further management. Due to concern of DRESS-induced myocarditis, dexamethasone with a dose of 1 mg/kg/day was administered intravenously. On hospital day (HD) eight, cardiac biopsy demonstrated diffuse active myocarditis with coagulative myocyte necrosis and mixed infiltrate including eosinophils consistent with DRESS myocarditis. She was decannulated from ECMO on HD 16. She was eventually discharged after 20 days in the ICU and 62 total days in the hospital with a life vest and continued cardiac follow-up. An echocardiogram performed three months later demonstrated improved ejection fraction of 34%.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [21, 'years'], 'Heart Rate or Pulse': [121.0, 'beats per minute'], 'O₂ saturation percentage': [100.0, '%'], 'Hemoptysis': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 21 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 121.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 100.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6609,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8047735-1,Extracted,"A 79-year-old African American female presented to the emergency room for shortness of breath with exertion and grade 2+ bilateral lower limb edema. The patient denied dizziness, palpitation, fever, chills, productive cough, abdominal pain, nausea, vomiting, hematemesis, melena, and hematochezia.
On examination, the patient's blood pressure was 94/66 mmHg, the temperature was 97.6 °F, the heart rate was irregular with a rate of 78 beats per minute, respiratory rate was 20 breaths per minute, and she was saturating 100% on room air. Sinus pauses were noted, up to 10 seconds in length, on the telemetry monitor. ECG and telemetry monitoring demonstrated SSS with sinus bradycardia, pauses up to three seconds, and atrial fibrillation (AF) with a rate of 130 beats per minute (bpm; Figure ). Her other medical history included paroxysmal atrial tachycardia, lower extremity venous insufficiency, diastolic heart failure (ejection fraction of 70-75%), chronic obstructive pulmonary disease, and gastroesophageal reflux disease, and no other medical history reported. The patient's home medications included fluticasone propionate/salmeterol inhaler, albuterol sulfate inhaler, torsemide, metolazone, potassium chloride, vitamin D3, pantoprazole, sotalol, and no other heart rate modulating medication reported. Laboratory workup revealed a potassium of 4.5 (3.5-5.1 mM/L), magnesium of 2.3 (1.7-2.7 mg/dL), thyroid-stimulating hormone of 1.54 (0.34-5.60 µIU/mL), and troponin of 0.1 (0.0-0.5 ng/mL). The patient underwent urgent pacemaker placement to prevent further sinus pauses.
The patient was also complaining of dysphagia and difficulty swallowing, for which an esophagogastroduodenoscopy (EGD) was performed. The procedure identified both esophageal and duodenal ulcers. The biopsy was performed during the EGD and sent for histopathological review. The esophagus contained small columnar pieces of mucosa and collections of eosinophilic, amorphous material demonstrated on congo red staining. The congo red stain contained one fragment with blood vessels that exhibited mural deposition of amyloid. In the duodenal biopsy, the lamina propria also had amyloid on congo red staining. Videofluoroscopic swallowing examination revealed no tracheal aspiration and no motility disorder. Eventually, the patient required percutaneous endoscopic gastrostomy tube placement for feeding secondary to dysphagia. TTE findings were consistent with restrictive cardiomyopathy, raising the possibility of cardiomyopathy secondary to amyloidosis and SSS as the initial presenting feature in our patient.
The patient had also developed a bifascicular block, which was potentially consistent with an infiltrative amyloid disease. The patient had a Kappa free light chain drawn, and this was markedly elevated at 146 mg/dL (reference range 0.3-1.9 mg/dL), Lambda 1.97 (0.5-2.6 mg/dL), with a Kappa/Lambda ratio of 74.1. We performed electrophoresis to investigate further and found an elevated gamma globulin of 1.75 g/dL (reference range 0.70-1.50 mg/dL).
Two months later the patient presented with persistent, progressive shortness of breath on minimal exertion and persistent lower limb edema. Laboratory work-up was significant for brain natriuretic peptide (BNP) of 838 (2-100 pg/mL), BUN of 37, creatinine of 1.85, white blood cell count of 10.3 (4.5-11.0 × 103/µL), hemoglobin of 10.7 (12.0-15.7 g/dl), and platelet count of 178 (140-440 × 103/µL). ECG was obtained and demonstrated an atrial paced rhythm, bifascicular block, left anterior fascicular block, right bundle branch block, and a pronounced low voltage pattern throughout all leads (Figure ). She had three negative troponins, and her pacemaker was found to be functioning appropriately. The patient did not have any compelling cardiac symptoms aside from the dyspnea on exertion.
TTE demonstrated an ejection fraction of 60%, a small pericardial effusion, an increased left ventricular wall thickness (left ventricular posterior wall diastolic thickness 1.4 cm (0.6-1.0/0.6-0.9 cm), right ventricular systolic pressure (RVSP) 56 mmHg, and mild to moderate biatrial enlargement (Figure ).
A renal biopsy and bone marrow biopsy were performed to confirm the diagnosis of amyloidosis. The results of these biopsies were consistent with our hypothesis that the patient had AL amyloid. She was intermittently treated with Dexamethasone and Bortezomib but ultimately evaluated by palliative care for comfort measures due to the prognosis of her condition.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [79, 'years'], 'Heart Rate or Pulse': [78.0, 'beats per minute'], 'O₂ saturation percentage': [100.0, '%'], 'Hemoptysis': False, 'Previously Documented Pulmonary Embolism': False, 'Previously documented Deep Vein Thrombosis': False, 'Unilateral Leg Swelling': True, 'Recent surgery or trauma': False, 'Hormone use': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 79 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 78.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 100.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6610,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4664794-1,Extracted,"A 57-year-old woman presented to the rheumatology clinic with recurrent fever and painful ulcers on her legs since two months. Eight months prior to current presentation, she developed vertigo and decreased hearing in her left ear which she felt was “full of air” all the time. She was found to have sensorineural deafness in her left ear. Two weeks later, she developed fever with chills. A chest radiograph revealed infiltrates in her right lung and an elevated ESR. She was treated with oral antibiotics which relieved her symptoms. Then she developed gingival hypertrophy and a CT scan of the paranasal sinuses revealed subcutaneous soft tissue thickening of the right buccal area suggestive of an inflammatory process. She was treated with ibuprofen and felt better. Her past medical history was notable for hypothyroidism for 20 years and she as well was maintained on 50 mcg of thyroxin daily. She had undergone hysterectomy for uterine fibroids 15 years ago. She reported no recent travel history. Of note, she revealed contact with sick animals. She nursed her paralyzed pet dog and also had cats. She was treated with antibiotics yet continued to spike fever and came to our center for comprehensive evaluation. On examination, she appeared weak and ill. The temperature was 37.5°C, the blood pressure 139/69 mm Hg, the pulse 78 beats per minute, and the respiratory rate 16 breaths per minute, with 99% oxygen saturation at room air. Erythematous tender nodules were noticed on bilateral lower extremities ().
The remainder of the examination was unremarkable. Her complete blood count revealed normocytic, normochromic anemia with normal white cell and platelet count. Her biochemistry showed normal kidney and liver function. No active sediment was present on urinalysis. Her three sets of blood cultures and one urine culture reported no growth. The test for latent tuberculosis by interferon gamma release assay (IGRA) was also negative. Serology for Brucella abortus and melitensis also came negative. Tests for chronic viral hepatitis B and C were also normal. Serological tests for connective tissue disease were negative as was the serum angiotensin converting enzyme level. Other relevant investigations are outlined in . An upper abdominal ultrasound showed hypoechoic, cystic lesions scattered across both lobes of the liver (). A subsequent CT scan of the abdomen with contrast showed multiple oval hypoattenuating lesions in both lobes of the liver ().
On liver biopsy there was evidence of cholestasis and multiple large irregular areas of necrosis, palisaded by epitheloid cells with associated granulomatous inflammation with a number of plasma cells ().
Acid-fast bacilli culture of liver biopsy specimen after six weeks came out negative. Meanwhile, the patient continued to spike fever with maximum temperature of 101°F. Leg lesions were becoming worse with central necrosis and purulent discharge (Figures and ).
Pus cultures were negative for bacterial, fungal, and mycobacterial growth. A biopsy of the skin was performed. Pathological examination of frozen sections revealed surface ulceration with fibrinoid necrosis and vasculitis involving superficial and deep dermal vessels along with granuloma formation, neutrophilic infiltration, and debris ().
Immunohistochemical testing was performed on biopsy specimen using immune-alkaline phosphatase technique which came negative for mycobacterial species. Real-time PCR for mycobacterial species also turned out to be negative. It was concluded from the skin biopsy that the patient had cutaneous granulomatous vasculitis. Treatment was commenced with prednisone 1 mg/kg/day and the patient was offered induction with cyclophosphamide which she refused due to associated toxicities. Meanwhile, azathioprine 2 mg/kg/day was added to prednisone. After seven weeks on prednisone and six weeks of azathioprine her lesions had healed almost completely (). She was maintained on prednisone 5 mg bid and azathioprine 50 mg bid with healing lesions. A repeat CT scan of the abdomen revealed normal architecture of hepatic parenchyma.
Therefore, considering a chronic inflammatory process characterized by hearing loss, gingival hypertrophy, granulomatous hepatic lesions, and cutaneous ulcers with necrotizing granulomatous inflammation on skin biopsy, a unifying diagnosis of granulomatosis with polyangiitis (GPA) was made.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [57, 'years'], 'Heart Rate or Pulse': [78.0, 'beats per minute'], 'O₂ saturation percentage': [99.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 57 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 78.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6611,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8177025-1,Extracted,"A 53-year-old male without known significant past medical history presented to the emergency department for a gunshot wound to the left foot. He reported leaving a bar when a shot was fired, hitting him in the foot. He noted pain and bleeding but was able to walk. His pain was worsened with palpation to the affected site. The patient denied any significant family history. His social history was significant for tobacco use of two packs per day and alcohol use of six to 12 beers a day.
Upon arrival, blood pressure was 152/85 mmHg, pulse was 76 bpm, respiratory rate was 18 bpm, the temperature was 97.6°F, and O2 saturation was 100% on room air. On examination, there was a wound with associated tenderness and edema to the medial aspect of the left foot with no other findings noted. A left foot x-ray was ordered and tetanus, diphtheria, and pertussis (Tdap) vaccine were administered intramuscularly. X-ray imaging revealed a large bullet fragment in the plantar soft tissue beneath the medial cuneiform as well as punctate fragments in the medial soft tissue near the large fragment. There were no fractures noted on imaging (Figure ).
Lidocaine 1% with epinephrine was administered locally and removal of the bullet was attempted. The bullet path was tracked by following pieces of thread detached from the patient’s shoe, which was found to be wrapped around the bullet (Figure ).
Bullet extraction was performed by pulling the shoe fibers along the bullet path. The severed tendon was visible upon extraction following bullet removal. Plantar and dorsiflexion of all toes of the left foot were intact. Orthopedic surgery was consulted and recommended a repeat x-ray which showed removal of the large bullet fragment in the plantar soft tissues (Figure ).
The patient was discharged with topical bacitracin and ciprofloxacin 500 mg tablet two times daily for seven days. He was provided with crutches and instruction for outpatient management with orthopedic surgery. The patient did not follow up for further management.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Hormone use': False, 'Unilateral Leg Swelling': True, 'Heart Rate or Pulse': [76.0, 'beats per minute'], 'Hemoptysis': False, 'O₂ saturation percentage': [100.0, '%'], 'Recent surgery or trauma': True, 'age': [53, 'years'], 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 53 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 76.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 100.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6612,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-6624151-1,Extracted,"A 55-year-old man with a history of type II diabetes mellitus, hypertension, obstructive sleep apnea, and depression developed pleuritic chest pain and shortness of breath, and had a syncopal episode during a car trip from Texas to Cleveland. In the emergency room (ER), his blood pressure was 120/83 mmHg, pulse 119/min, respiratory rate 22/min, temperature 36.6oC, and oxygen (O2) saturation was 93% on room air. Physical exam was notable for an obese male in no acute distress with tachycardia, regular rhythm, clear lungs, shallow breaths without accessory muscle usage, and mild epigastric tenderness. His electrocardiogram (ECG) demonstrated sinus tachycardia at 117 bpm with a deep S wave in lead I, a small Q wave and inverted T wave in lead III (Figure ).
Initial laboratory testing was significant for serum sodium 132 mmol/L, creatinine 1.6 mg/dL, ProBNP 3188pg/mL, and initial troponin 0.12, peaking at 0.2 on hospital day two. Computed tomography (CT) chest showed bilateral submassive pulmonary emboli in multiple branches of the right and left upper and lower lobe pulmonary arteries, with no indication of a saddle embolus or main pulmonary artery thrombus (Figures -).
The patient was started on an intravenous (IV) heparin drip and thrombolytics were deferred due to perceived hemodynamic stability and timing of presentation. While in the ER, he became more tachycardic with heart rate 130-140 bpm, and developed jugular venous distention and acute hypoxemia requiring 3 liters (L) nasal cannula to maintain normal O2 saturation. He was admitted to the medical intensive care unit (MICU) due to possible signs of acute decompensation.
In the MICU, ultrasound revealed a right popliteal deep vein thrombosis (DVT); an inferior vena cava filter was considered, but the patient was considered hemodynamically stable and placement of a filter was deferred. Over the second and third hospital days, he remained tachycardic at 105-130/min with blood pressures in the 110/80 mmHg range and stable O2 saturations on 3L per nasal cannula. Transthoracic echocardiogram revealed right ventricular strain and a mobile structure in the right atrium, possibly consistent with thrombus. On hospital day four, he remained hemodynamically stable but experienced mild pleuritic chest pain and shortness of breath. On hospital day five, the patient was switched from IV heparin to enoxaparin 120 mg twice daily with a two-hour overlap; he was noted to have a transient O2 desaturation but remained normotensive. In the early hours of day six, he became diaphoretic and developed sustained tachycardia at 140/min with a blood pressure of 100/70 mmHg. He then developed chest pain and worsening dyspnea and lethargy, and was found to be in atrial flutter with 2:1 block. In the early afternoon, while speaking with the medical team and later while working with physical therapy, the patient complained of worsening shortness of breath, and was noted to be diaphoretic and persistently tachycardic at 120/min. Shortly thereafter, he lost consciousness and was found to be in cardiac arrest. He was treated per advanced cardiac life support (ACLS) protocol with temporary restoration of circulation, but became asystolic and was pronounced dead after 30 minutes.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [55, 'years'], 'Heart Rate or Pulse': [119.0, 'beats per minute'], 'O₂ saturation percentage': [93.0, '%'], 'Hemoptysis': False, 'Previously Documented Pulmonary Embolism': True, 'Previously documented Deep Vein Thrombosis': True}",4,4,4,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 55 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 119.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 93.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 2 + 1 = 3.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note does not report a status on 'recent surgery or trauma'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is reported to have been diagnosed with deep vein thrombosis in the past. The patient is reported to have been diagnosed with pulmonary embolism in the past. At least one of the criteria is met and so we increment the criteria met by 1, making the current total 3 + 1 = 4.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 4.
Hence, the number of PERC rule criteria met by the patient is 4."
6613,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-9936,Extracted,"A 49-year-old woman is brought to the emergency department with progressive dyspnea and cough which she developed approx. 8 hours ago. 2 weeks ago she had a prophylactic ovariectomy because of a family history of ovarian cancer. She is known to have type 2 diabetes mellitus and stage 1 hypertension, but she does not take her antihypertensives because she is not concerned about her blood pressure. Also, she has a history of opioid abuse. She takes metformin 1000 mg and aspirin 81 mg. She has been smoking 1 pack of cigarettes per day for 22 years. Her vital signs are as follows: blood pressure 155/80 mm Hg, heart rate 101/min, respiratory rate 31/min, and temperature 37.9℃ (100.2℉). Blood saturation on room air is 89%. On examination, the patient is dyspneic and acrocyanotic. Lung auscultation reveals bilateral rales over the lower lobes. A cardiac examination is significant for S2 accentuation best heard in the second intercostal space at the left sternal border and S3 presence. There is no leg edema. Neurological examination is within normal limits.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [49, 'years'], 'Heart Rate or Pulse': [101.0, 'beats per minute'], 'O₂ saturation percentage': [89.0, '%'], 'Unilateral Leg Swelling': False, 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 49 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 101.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 89.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6614,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7032602-1,Extracted,"A 42-year-old African American female who recently emigrated from the Caribbean Islands initially presented with non-resolving productive cough and dyspnea for two weeks. She had no significant past medical history, no history of medication use, no history of surgery, or recent prolonged immobilization. Admission vitals were: blood pressure (BP) 110/75, temperature 98.2 F, respiratory rate 18/min, sPO2 95% room air, tachycardia with 110-120 beats/min. She was anxious on presentation. Rest of the physical exam including cardiovascular, gastrointestinal, and respiratory system findings, were unremarkable.
Initial investigations revealed the following: White blood cell count 9.9 x 109/L (ref 4-11 x 109/L), hemoglobin 11.7 gm/dl (reference 13-15 gm/dl), hematocrit 36.8% (reference range 39-48%), platelets 304,000/ml (reference 15,000 to 450,000/ml); arterial blood gas analysis suggested hypoxia, pO2 being 72% and had high A-a gradient of 37 mm Hg (normal 5-10 mm Hg); lactate dehydrogenase (LDH) was elevated to 508 unit/L (reference range 140-280 units/L). Electrocardiogram (EKG) showed sinus tachycardia. CT angiogram chest did not show any pulmonary embolus but showed diffuse ground glass lung opacities with hilar lymphadenopathy (Figure ). She underwent voluntary human immunodeficiency virus (HIV) testing as per New York State law, and the test came back reactive with CD4 count 46 cells/micro litre (reference range 500-1500 cells/micro litre) and HIV viral load 810231 copies/ml (reference range 40-50 copies/ml). The urine legionella antigen was negative. Treatment was initiated with oral Bactrim DS and Prednisone (for suspected Pneumocystis carinii pneumonia [PCP]), and further investigation by bronchoscopy specimen was positive for Pneumocystis carinii PCR confirming PCP. The patient improved clinically and was discharged home with continuation therapy of Bactrim DS and outpatient follow-up instructions. However, she was re-admitted to the hospital within a week of discharge with worsening dyspnea and cough with expectorations. Vitals showed sinus tachycardia with heart rate 110/min. Other vitals like BP, temperature, respiratory rate were normal. Chest X-ray on admission showed perihilar opacities unchanged from previous admission (Figure ). Physical examination revealed rales bilaterally. The rest of examinations, including gastrointestinal, neurological, cardiovascular system, were normal. Treatment was initiated with broad spectrum antibiotics Vancomycin and Meropenem intravenous (IV) in view of possible superadded bacterial infection. On day 2 of admission, she complained of severe epigastric pain radiating to back and also was noted to have pruritic macular rashes over face and neck. As initial suspicion was Varicella Zoster (VZ) infection vs. drug-induced rash, Bactrim was stopped, and she was started on Valacyclovir orally. Serum lipase and amylase were elevated at 160 IU/dl (reference range less than 50 IU/dl) and 133 IU/dl (reference range less than 110 IU/dl) respectively. The rest of the labs, including blood urea nitrogen, creatinine, calcium, sodium, potassium, phosphorus, were normal. She was also started on IV hydration with isotonic normal saline and pain management with opioids for pancreatitis. Her clinical condition continued to worsen gradually, and the rash became more generalized with pruritic vesicular-papular eruptions. She developed a low-grade fever and became hypotension - BP 70/40 (she required inotropic support with norepinephrine for three days). Other systemic organs were also involved, as evident by laboratory abnormalities. Over the course of hospital stay, her labs got worsened significantly - platelet counts dropped remarkably (125-66-30---26---24); Lipase/amylase continued to increase (160/133-379/663---254/491); liver functions worsened with aspartate aminotransferase (AST)/alanine aminotransferase (ALT) gradually increased (180/128---389/227---837/501) (reference range < 40 for both); LDH was high (2438---2565-1308); lactic acid increased (3.7-2.4) [reference range < 2 mmol/L]. Given the worsening clinical status, she was switched to Acyclovir 500 mg IV. Her blood culture and urine culture sent on admission day returned negative for any bacterial infection; four days later, her VZ virus DNA PCR from skin blister and serum both reported positive confirming active VZV infection.
Ultrasound abdomen did not reveal any gallstones. Echocardiogram did not suggest any source of septic emboli.
Her clinical condition improved gradually with near normalization of labs. She completed 14 days course of antimicrobials for disseminated varicella. Eventually, she was started on an anti-retroviral drug Stribild (Dolutegravir/Lamivudine) daily along with a prophylactic dose of Dapsone (for PCP). Post treatment completion, oral Valacyclovir was initiated for viral suppression. After the acute stay in hospital for three weeks, she recovered well and was followed up regularly in the clinic with no further recurrence in six months of follow-up.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [42, 'years'], 'Heart Rate or Pulse': [110120.0, 'beats per minute'], 'O₂ saturation percentage': [95.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 42 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 110120.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 95.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6615,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4914727-1,Extracted,"A 38-year-old G2P2 African American woman presented with 3-hour duration of severe abdominal pain, nausea, and vomiting. Her pain was acute in onset and constant in nature, radiated to both groins, and was progressively worsening. She denied any musculoskeletal pain. Her past medical history was significant for hypertension, fibroid uterus, and a cholecystectomy. She had worsening menorrhagia over the past two months. Her last gynecologic evaluation was three years prior to presentation. She reported tobacco use and denied alcohol or drug consumption. Physical examination revealed diffuse rebound tenderness and a palpable abdominal mass. Initial vital signs were as follows: temperature of 38.6°C, heart rate of 122 beats per minute, blood pressure of 48/37, and respiratory rate of 31 breaths per minute. Oxygen saturation was 88% and increased to 94% on 2 liters of nasal oxygen.
Biochemical testing showed an elevated white blood cell count (13.5 K/μL), significant neutrophilia (94.8%), an elevatedcreatinine (3.8 mg/dL), low hemoglobin (8.9 g/dL), low potassium (3.2 mEq/L), and an elevated myoglobin (2140 ng/mL, normal range: 0–101 ng/mL). A cardiac and skeletal muscle enzyme panel was normal. Baseline creatinine from a prior admission was normal (0.6 mg/dL). Urinalysis showed trace blood and amorphous sediment. A computed tomography scan of the abdomen and pelvis without contrast showed a 24 cm × 13 cm × 13 cm complex mass occupying the pelvis and extending to the upper abdomen (). Both kidneys appeared normal in size without perinephric inflammation, hydronephrosis, or hydroureter. Renal sonography revealed normal echotexture and ureteral caliber.
The working diagnosis was acute septic shock with associated acute renal failure. The patient had nonanion gap metabolic acidosis with a lactic acid level of 4.5 mmol/L (normal 0.4–2 mmol/L) and a pH of 7.40 with a compensatory decrease in PCO secondary to hyperventilation. Blood and urine cultures were obtained and the patient was started on intravenous fluid resuscitation, a bicarbonate drip, and broad-spectrum antibiotics. A norepinephrine infusion was used to maintain a normotensive state. The pelvic mass was thought to be the source of the patient's abdominal pain and represented a degenerating fibroid that was contributing to her critical presentation with worsening inflammation and myoglobinemia. Relevant tumor markers including CEA, AFP, CA-125, and inhibins A and B were normal.
The patient's overall status continued to worsen the following day. She became obtunded with loss of consciousness, in sinus tachycardia, and hypotensive despite all aforementioned measures. Endotracheal intubation then followed. Furthermore, her renal function continued to deteriorate (creatinine of 7 mg/dL). Urine and blood cultures had still not yielded any bacterial growth. Continuous renal replacement therapy (CRRT) was initiated and the decision to perform an exploratory laparotomy and remove the pelvic mass followed, as it was attributed to the patient's worsening critical state.
A large solitary fibroid was found within the left broad ligament that was densely adherent and contiguous with the uterus. The uterus and adnexal structures appeared significantly devitalized and edematous and were displacing the ureters without evidence of hydroureter. The bowels appeared normal. A total abdominal hysterectomy with bilateral salpingo-oophorectomy was performed with an estimated blood loss of 150 mL. The patient remained intubated and returned to the surgical intensive care unit. The postoperative period was complicated by atrial fibrillation that responded to intravenous amiodarone in addition to anemia (Hg 6.7 g/dL) requiring blood transfusion.
Dramatic biochemical improvement occurred over the next 48 hours with CRRT following surgery. Final blood and urine cultures were negative at 48 hours. Serum creatinine decreased to 1.4 mg/dL but however rebounded slowly over the following three days and peaked at 3.1 mg/dL. Serum myoglobin reached a nadir of 380.4 ng/mL by the fourth postoperative day (POD) and steadily increased and reached a plateau of 1074 ng/mL by POD-8 (). Clinical improvement followed with defervescence and normalization of vital signs by POD-3 and POD-5, respectively. Broad-spectrum antibiotics were discontinued at this time. The patient had normal sinus rhythm, was normotensive without any vasopressors, and was extubated uneventfully. The pathology reported a 29.4 × 20.8 × 19.7 cm large solitary leiomyoma weighing 3028 grams and showing extensive loss of nuclei from cells, stromal hyalinization, polymorphonuclear white blood cell infiltrate, and foci of calcifications reflecting various stages of early and late fibroid degenerative changes (). Both adnexal structures showed an extensive infiltrate of polymorphonuclear cells suggestive of severe and acute inflammation.
The patient was discharged on POD-8 in a stable condition. Serum creatinine remained stable at 2.9 mg/dL, and myoglobin was 1074 ng/mL. She showed complete biochemical and clinical remission by her 4-week follow-up with a return to baseline serum creatinine (0.6 mg/dL) and a normal serum myoglobin of 25 ng/mL (). The patient was placed on oral estradiol for hormone replacement therapy and her care was released to her primary care physician.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Hormone use': True, 'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [122.0, 'beats per minute'], 'O₂ saturation percentage': [88.0, '%'], 'Recent surgery or trauma': True, 'age': [38, 'years'], 'Previously documented Deep Vein Thrombosis': False}",4,4,4,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 38 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 122.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 88.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be present for the patient and so we increment the criteria count by 1, making the current total 3 + 1  =  4.
Hence, the number of PERC rule criteria met by the patient is 4."
6616,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7034194-1,Extracted,"A 48-year-old diabetic male was referred to us with a diagnosis of basal VSR, approximately 2 weeks before MI. He had a history of breathlessness of New York Heart Association class III with bilateral pedal edema and oliguria for the past 15 days. On admission, he was hemodynamically stable with a blood pressure of 120/80 mmHg and heart rate of 110/min. He had elevated cardiac markers (troponin I of 0.1 ng/mL) with electrocardiogram showing Q waves in leads II, III avf showing evolved inferior wall (IW) and right ventricle (RV) MI. A two-dimensional echocardiography showed hypokinetic basal septum and a huge VSR [] of 18 × 20 mm in size shunting left to right [] with severe pulmonary arterial hypertension (RV systolic pressure of 75 mmHg) and biventricular dysfunction and mild mitral regurgitation (MR) with an RV wall motion index (WMI) of 0.8. An elective coronary angiogram showed proximal tight occlusions of both the right coronary artery (RCA) and the obtuse marginal (OM) branch of the left circumflex. The left anterior descending artery was normal. He was planned for surgical closure of the VSR with grafts to OM and RCA territories after a week's time.
A Swan-Ganz catheter was inserted after induction showing a pulmonary capillary wedge pressure of 24 mmHg, a pulmonary artery systolic pressure (PASP) and diastolic pressure (DP) of 60 and 33 mmHg, respectively, and a diastolic pulmonary gradient of 9 mmHg. The central venous pressure (CVP) was 15 mmHg. Simultaneous right atrial and pulmonary artery saturations showed a step up of 30%. Cardiopulmonary bypass (CPB) was instituted with aorto bicaval cannulation and the heart was arrested by Del Nido cardioplegia (aortic root). After adequate retraction, a vertical left ventriculotomy was done parallel to the posterior descending artery (PDA) in the diaphragmatic surface of the heart. The VSR was visualized with difficulty by retracting the papillary muscle [] and its chordae tendinae. It was closed with bovine pericardium with interrupted 2-0 polypropylene sutures using David technique. The left ventriculotomy was closed [] followed by OM and PDA grafting as planned. After adequate period of CPB support with an aortic cross clamp time of 88 min and CPB time of 145 min, the patient was weaned off CPB. Transesophageal echo showed intact VSR patch with biventricular dysfunction. During closure, arterial pressures were 100/60 mmHg with a PASP of 45 and DP of 23 mmHg. The patient was shifted to the intensive care unit (ICU) with supports of inj. dobutamine 5 μg/kg/min, inj. adrenaline 0.08 μg/kg/min, and inj. vasopressin 2 IU/h. As the cardiac contractility was reasonably alright, IABP was not inserted in the operation theater with a low threshold of insertion in case of eventuality.
The patient was shifted to the ICU with continuous monitoring with cardiac output (CO) of 3.5 L/min and cardiac index (CI) of 1.9 L/min/m2 and systemic vascular resistance (SVR) of 1900 dynes-s/cm5. After 6 h, there was a drop in CO and SVR elevation, and hence a 40-cc IABP was inserted percutaneously through the right common femoral artery (CFA). The patient's hemodynamics improved and he was extubated on the second postoperative day (POD). As he was hemodynamically stable, on the fourth POD, IABP was removed with inj. dobutamine 5 μg/kg/min and inj. adrenaline 0.05 μg/kg/min. Six hours later, there was once again a drop in the CI and CO and echo showed severe RV dysfunction with a tricuspid annular plane systolic excursion (TAPSE) value of 8 mm. Inotropes were hiked with no further improvement. Twelve hours later, the patient became dyspneic, tachypneic with a mixed venous oxygen saturation (MVO2) of 35%, and a pulmonary vascular resistance of 250 dynes-s/cm5 and was electively re-intubated in view of hypoxia due to low cardiac output. A sheathless 34-cc IABP was re-inserted percutaneously through the left CFA. The hemodynamics improved and MVO2 improved to 70%. He was extubated the next day and a decision was made to retain the IABP. The IABP was removed after 10 days (1:1 augmentation for 8 days and 1:2 for the next 48 h and 1:3 for the next 24 h) and inotropes were reduced. Repeat echo showed improvement in the RV function with a TAPSE improving to 12 mm. He was discharged in a stable condition on 18th POD. Discharge echo revealed intact VSR patch [] with moderate biventricular dysfunctionand TAPSE value of 12 mm and moderate MR []. He is planned for MR follow-up and surgical intervention at a later date.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [48, 'years'], 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'O₂ saturation percentage': [70.0, '%'], 'Unilateral Leg Swelling': True, 'Hormone use': False, 'Recent surgery or trauma': True, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",4,4,4,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 48 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 110.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 70.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'unilateral leg swelling' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 3 + 1  =  4.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 4.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 4.
Hence, the number of PERC rule criteria met by the patient is 4."
6617,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7262979-1,Extracted,"A 69-year-old man with hepatitis C cirrhosis and hepatocellular carcinoma underwent
uncomplicated orthotopic liver transplantation. Additional history includes a
moderately dilated ascending aorta measuring 4.8 cm. Three days posttransplant,
shortly following extubation, he developed profound positional hypoxia. Vital signs
remained normal with recumbency with a blood pressure of 120/60 mm Hg, heart rate of
60 beats/min, and oxygen saturation of 94%. In an upright position, however, he
became tachycardic to 120 beats/min, tachypneic with respiratory rate of 24
breaths/min, hypertensive with blood pressure of 175/100 mm Hg, and hypoxic with
desaturations to 80% while receiving 100% supplemental oxygen via a non-rebeathing
facemask. Physical examination revealed no new murmurs, pulmonary rales, jugular
venous distension, nor peripheral edema.
Initial testing demonstrated a normal chest X-ray and ventilation perfusion scan.
Transthoracic echocardiography demonstrated normal biventricular size and function,
normal cardiac valve anatomy and function, and normal pulmonary artery, right
ventricular, and right atrial (RA) pressures. An agitated saline study revealed
evidence of a mild right to left shunting in the supine position with profound right
to left shunting in the upright position ( and ; Videos 1 and 2 [available online]).
While echocardiography suggested shunting at the atrial level, the patient’s history
of cirrhosis raised the possibility of intrapulmonary shunting. The patient was
brought forward for a right heart catheterization performed through the right
femoral vein demonstrating normal intracardiac pressures. The catheter course
confirmed the presence of an interatrial communication although oximetry did not
demonstrate a shunt while the patient was breathing spontaneously in the supine
position ().
Intracardiac echocardiography confirmed the presence of a patent foramen ovale (PFO)
without evidence of a septal aneurysm, unusually long tunnel, or a prominent
Eustacian valve. However, both the pressure catheter and intracardiac
echocardiography catheter course were biased posteriorly and medially due to an
acute angulation at the inferior vena cava (IVC)-RA junction.
An agitated saline study performed within the high IVC demonstrated brisk shunting
across the PFO. Additional agitated saline studies performed within the bilateral
branch pulmonary arteries showed no evidence of intrapulmonary shunting. As such, a
decision was made to proceed with transcatheter PFO closure, which was successfully
performed using a 25-mm Gore Cardioform septal occluder device (; Video 3 [available online]).
Postintervention, the patient experienced immediate improvement in oxygen saturations
and maintained oxygen saturations of 95%, in absence of supplement oxygen, in both
the supine and upright positions. The patient was discharged on postoperative day 12
in excellent condition. One month follow-up transthoracic echocardiography confirmed
complete occlusion of the interatrial shunt.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [69, 'years'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'O₂ saturation percentage': [80.0, '%'], 'Unilateral Leg Swelling': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 69 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 120.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 80.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 2 + 1 = 3.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note does not report a status on 'hormonal use'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6618,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7061779-1,Extracted,"History
A 52-year-old African American male presented to the emergency department complaining of pleuritic, sharp pain in his right chest wall that had begun three days prior to arrival. The pain had since worsened in intensity, and did not radiate. He had taken acetaminophen without relief of his symptoms. The patient denied any fever, cough, shortness of breath, headache, or rash. His review of symptoms was otherwise negative. The patient had no significant past medical history and was taking no medications. He denied any recent history of surgery or trauma, but did note weight lifting two days prior to the onset of symptoms. Family history was negative for coagulopathies and autoimmune conditions.
Exam findings
Vital signs on arrival were blood pressure 146/97, heart rate 97, temperature 36.2°C, respiratory rate 20, and SpO2 99% on room air. He was alert and oriented, and in no acute distress. Lung sounds were clear bilaterally and heart sounds were normal. A raised cord was visible crossing from the epigastrium across the right breast toward the axilla, that was tender to palpation and mobile. There was no warmth, erythema, or rash overlying the cord. Head/eyes/ears/nose/throat, abdominal, and neurological examinations were unremarkable.
Diagnostic evaluation
Basic metabolic panel and troponin levels were normal, and a complete blood count and differential was unremarkable with platelets of 212 bil/L. Chest radiograph showed clear lung fields but did reveal remote right-sided posterior fractures of ribs five through eight. Given the pleuritic nature of the pain, a computed tomography pulmonary angiogram was ordered to rule out pulmonary embolism. As shown in Figure , it revealed a subtle density in the right chest wall over the area of the palpable cord, with no evidence of a pulmonary embolism. The diagnosis of superficial chest wall thrombophlebitis, or Mondor’s disease, was made.
Patient course
The patient was treated with ibuprofen in the emergency department and discharged with a naproxen prescription. He was referred to his primary care physician for further work-up. The pain improved in the days following his emergency department visit, resolving within a week of discharge. The patient was contacted two months after his emergency department visit. He noted that he was still able to appreciate a firm mass in his chest wall with some reduction in size since it was first diagnosed.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [52, 'years'], 'Heart Rate or Pulse': [97.0, 'beats per minute'], 'O₂ saturation percentage': [99.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 52 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 97.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6619,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7211338-1,Extracted,"A 57-year-old white man presented with a 3-month history of new-onset, severe, bi-frontal headaches and a 13.6 kg (30-lb) weight loss. Local emergency room evaluation revealed a negative computed tomography (CT) scan of his head. Laboratory findings included an elevated erythrocyte sedimentation rate (ESR) of 80 mm/hour and C-reactive protein (CRP) of 55.3 mg/L. He was discharged with pain control.
During follow-up with his local primary provider, his headache persisted and bilateral jaw pain and left facial numbness had developed. He was started on prednisone 60 mg/day for presumed GCA with partial improvement in his headache. Bilateral temporal artery biopsies were performed 3 days later and were negative. Prednisone was subsequently discontinued. Two weeks later his headache progressed and right eye horizontal diplopia and perioral numbness developed. Magnetic resonance imaging (MRI) of his brain was performed and interpreted as normal. He was admitted for pulse-dose steroids (1000 mg daily for 3 days) which led to resolution of visual symptoms and was discharged on prednisone 60 mg/day. Tapering below 50 mg/day was unsuccessful due to rising inflammatory markers, symptom progression, and return of diplopia. Severe left hip pain developed for which plain radiographs were obtained but negative for fracture or avascular necrosis.
On referral to our institution he continued to have ongoing headache and left jaw numbness despite 6 weeks of high-dose glucocorticoids (80 mg/day). Left hip pain had worsened to the point of wheelchair dependency. His past medical history was remarkable for atrial fibrillation for which he was receiving warfarin 2 mg/day and diltiazem 240 mg/day. Social history was notable for lack of tobacco or alcohol use and absence of known environmental exposures during his employment as an office manager. Aside from prostate cancer in his father, our patient’s family history was negative for other pertinent diagnoses of additional malignancies or autoimmune conditions. Laboratory evaluation noted an ESR 72 mm/hour, CRP 53 mg/L, hemoglobin 11.1 g/dL, leukocytes 5.2 × 109/L and platelets 110 × 109/L, international normalized ratio (INR) 2.3, creatinine 1.04 mg/dL, calcium 11.6 mg/dL, alanine aminotransferase 106 U/L, aspartate aminotransferase 64 U/L, alkaline phosphatase 360 U/L, total bilirubin 1.2 mg/dL, total protein 5.1 g/dL, and albumin 3.4 g/dL. Previously obtained autoimmune serologies were negative for antinuclear and extractable nuclear antigens as well as rheumatoid factor, anti-cyclic citrullinated peptide, myeloperoxidase, and proteinase-3 antibodies.
His vital signs demonstrated a heart rate of 95 beats per minute, blood pressure of 94/44 mm Hg, respiratory rate of 12 per minute, oxygenation saturation of 96%, and weight of 144 kg with body mass index (BMI) of 48.6 kg/m2. An examination was notable for a Cushingoid appearance and morbid obesity. Evaluation of adenopathy and splenomegaly was limited due to body habitus. Pertinent cardiovascular findings included irregularly irregular pulse without murmurs. Upper and lower arterial pulses were normal and symmetric. Common superficial temporal artery palpation was without tenderness or nodularity. Trace pitting edema was noted to the ankle bilaterally. Breath sounds were equal and symmetric without wheezing or rhonchi. Aside from scattered bruising at site of venipuncture, no cutaneous abnormalities were noted. A neurologic examination showed normal speech without language deficits. Visual acuity was 20/20 bilaterally. Cranial nerves 2–12 were assessed and normal except for mild esotropia of his right eye and hypoesthesia to light touch and pinprick over the left mandibular region of the left trigeminal nerve. The remaining dermatomes evaluated showed normal sensation. Reflexes were normal and symmetric throughout and toes were down-going bilaterally. No ataxia was observed. A musculoskeletal examination demonstrated normal range of motion of upper extremities without deficit. Marked pain was noted on passive and active range of motion of his left hip.
Given the persistent headache despite high-dose glucocorticoids and atypical features, alternative etiologies were suspected. The local MRI of his brain was reviewed and evidence of abnormal enhancing soft tissue involving Meckel’s cave bilaterally with extension through the foramen ovale was noted (Fig. a). The differential diagnosis for infiltrative process in Meckel’s cave included sarcoidosis as well as primary or secondary neoplastic lesions such as meningioma, nasopharyngeal carcinoma, schwannoma, neurofibroma, and lymphoma [, ]. The presence of constitutional symptoms and elevated inflammatory markers suggested a secondary process with associated intracranial involvement. As such, positron emission tomography (PET)-CT was obtained. This demonstrated extensive hypermetabolic lesions throughout the axial and appendicular skeleton, including the skull base, as well as fluorodeoxyglucose (FDG)-avid lymph nodes above and below the diaphragm (Fig. c). MRI of his left hip revealed diffusely abnormal marrow signal suggestive of infiltrative disease. A cervical lymph node biopsy demonstrated evidence of diffuse large B cell lymphoma and staging bone marrow biopsy revealed a hypercellular marrow (90%) with diffuse large B cell lymphoma involving 70% of the total cellularity (Fig. ). Initiation of high-dose methotrexate (3.5 g/m2), rituximab (375 mg/m2), cyclophosphamide (750 mg/m2), hydroxydaunorubicin (50 mg/m2), Oncovin (vincristine; 2 mg), and prednisone (255 mg) (MR-CHOP; 21-day cycle) resulted in interval improvement in his headache and visual symptoms (Fig. b, d).
Ten months after initial diagnosis and 4 months after completion of his sixth cycle of MR-CHOP, our patient re-presented with bilateral lower extremity weakness and PET-CT showed recurrence of disease with evidence of neurolymphomatosis of multiple cervical, thoracic, and sacral nerve roots. Intrathecal cytarabine (50 mg) was given and ibrutinib (140 mg/day) was initiated, resulting in initial findings of improved strength and subsequent decreased nerve root FDG-avidity.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [57, 'years'], 'Heart Rate or Pulse': [95.0, 'beats per minute'], 'O₂ saturation percentage': [96.0, '%'], 'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 57 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 95.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 96.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6620,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-4450,Extracted,"A 44-year-old male presents to his primary care physician with complaints of fatigue, muscle weakness, cramps, and increased urination over the past several weeks. His past medical history is significant only for hypertension, for which he was started on hydrochlorothiazide (HCTZ) 4 weeks ago. Vital signs at today's visit are as follows: T 37.2, HR 88, BP 129/80, RR 14, and SpO2 99%. Physical examination does not reveal any abnormal findings. Serologic studies are significant for a serum potassium level of 2.1 mEq/L (normal range 3.5-5.0 mEq/L). Lab-work from his last visit showed a basic metabolic panel and complete blood count results to all be within normal limits.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [44, 'years'], 'Heart Rate or Pulse': [88.0, 'beats per minute'], 'O₂ saturation percentage': [99.0, '%'], 'Hormone use': False, 'Unilateral Leg Swelling': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",0,0,0,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 44 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 88.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 99.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 0.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 0.
Hence, the number of PERC rule criteria met by the patient is 0."
6621,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7872489-1,Extracted,"A 63-year-old male, a current heavy smoker with a smoking history of over 100-pack years, was referred due to complaints of dyspnea at rest and productive cough over the last three days. He had a history of COPD; he was diagnosed the previous year and treated with a combination of inhaled beclomethasone, formoterol, and glycopyrronium, with more of three hospitalizations due to infectious exacerbations the last six months. He had also a history of coronary artery disease with coronary artery bypass done nine years ago and circumflex artery angioplasty four years ago, as well as aortic valve replacement with metallic prosthesis, arterial hypertension, and dyslipidemia. The patient mentioned no severe lung infection during his childhood.
Clinical examination revealed decreased breath sounds in both lungs and wheezing. Blood pressure was 110/60 mmHg, heart rate was 90 beats per minute, oxygen saturation was 94% on room air, and body temperature 36.5°C. Arterial blood gas analysis revealed partial pressure of oxygen (pO2) 66 mmHg, partial pressure of carbon dioxide (pCO2) 41 mmHg, pH 7.47, and bicarbonate (HCO3−) 29.8 mmol/L on room air. Electrocardiography showed no abnormal findings. Laboratory findings were normal. Chest X-ray showed emphysematous lesions with lungs of large volume, flattened hemidiaphragms, horizontal ribs, small size of the heart, and increased retrosternal space (Figure ).
The patient underwent computed tomography (CT) of the chest in our hospital, which showed bronchiectasis on the left lower lobe. In addition, a reduced density in the same region was observed (Figure ). Pulmonary function tests (PFTs) revealed a non-reversible mild obstructive pattern. The measured values of forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) were of 65%/67% and 99%/102% of predicted values, pre and post-bronchodilator administration, respectively (Figure ). Based on clinical manifestations and imaging findings, a diagnosis of Swyer-James-MacLeod syndrome was confirmed.
The patient was treated with nebulized salbutamol/ipratropium, intravenous prednisolone for five days, and empirical antimicrobial therapy with piperacillin-tazobactam while sputum culture did not reveal any microorganism. The patient recovered and was discharged from our hospital with strong advice for smoking cessation and vaccination to prevent pulmonary infections.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [63, 'years'], 'Previously Documented Pulmonary Embolism': False, 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'Hemoptysis': False, 'O₂ saturation percentage': [94.0, '%'], 'Hormone use': False, 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 63 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 90.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 94.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note does not report a status on 'recent surgery or trauma'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6622,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4386897-1,Extracted,"The patient is a 75-year-old male with no relevant personal antecedents. He underwent
elective right hip arthroplasty, and, on the fourth postoperative day, after beginning
to walk, dyspnea, polypnea and low arterial oxygen saturation appeared.
His physical examination findings were as follows: arterial blood pressure 120/70 mm Hg;
heart rate 68 bpm; respiratory rate 30 bpm; peripheral saturation 80%. His cardiac and
pulmonary auscultations were uneventful, and neither jugular venous distention nor
peripheral edema was observed.
Regarding laboratory findings, his blood gas analysis (under supplementary oxygen at 5
L/minute) stood out, with an arterial oxygen partial pressure (PaO2) of 47 mm
Hg and respiratory alkalosis. Relevant changes were observed in neither hematological
nor biochemical parameters. The electrocardiogram and chest X-ray showed no significant
changes.
Chest computed tomography angiography (CT-angio) revealed small and hypodense filling
defects in the middle and right inferior lobar arteries, in addition to slight dilation
of the ascending aorta (45 mm).
The transthoracic echocardiogram findings were as follows: cardiac chambers of normal
dimensions; good left and right ventricular function; minimum tricuspid regurgitation;
no pulmonary hypertension; exuberant Eustachian valve; slightly dilation of the aortic
root and ascending aorta (45 mm). No ASD was identified.
Pulmonary embolism was diagnosed and enoxaparin therapy initiated. Periods of hypoxemia
related to the sitting position persisted, and total normalization of peripheral
saturation was obtained with the dorsal decubitus position.
Considering the hypothesis of intracardiac right-to-left shunt, transesophageal
echocardiogram (TEE) with agitaded saline contrast was performed, revealing exuberant
atrial septal (AS) aneurysm of the ostium secundum type, allowing the
contrast medium to pass to the left chambers, even with no Valsalva maneuver ().
In an attempt to clarify the positional variation of arterial oxygen saturation, TEE was
also performed on a tilt table, under serial blood gas monitoring. At 60º, the prolapse
of the AS aneurysm to the left atrium was maintained, and the contrast flow to the left
chambers was immediate and greater than that observed in the decubitus position (). Concomitantly, PaO2 decreased
from an initial value of 67 mm Hg, in the decubitus position, to 43 mm Hg (under normal
conditions).
After one week, the patient underwent a new high-resolution CT-angio, which showed no
filling defects in the pulmonary circulation, and the review of the previous exam raised
the possibility of a false-positive exam. Pulmonary ventilation/ perfusion scan showed
neither perfusion nor diffusion defects, and the functional respiratory tests showed no
obstructive, restrictive or diffusion changes.
The patient underwent percutaneous ASD closure by placement of a cribriform device under
fluoroscopic and intracardiac echography control.
The TEE with agitated saline was repeated and showed a well-positioned device adjacent
to the AS aneurysm, with persistence of the right-to-left contrast medium flow at a
lower degree than in the previous exam, and almost exclusively associated with the
Valsalva maneuver. That flow did not increase at the 60º position on the tilt table;
however, a PaO2 reduction from 102 mm Hg to 75 mm Hg was observed ().",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [75, 'years'], 'Heart Rate or Pulse': [68.0, 'beats per minute'], 'O₂ saturation percentage': [80.0, '%'], 'Recent surgery or trauma': True, 'Hormone use': False, 'Unilateral Leg Swelling': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False}",3,3,3,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 75 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 68.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 80.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 3.
Hence, the number of PERC rule criteria met by the patient is 3."
6623,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,usmle-3789,Extracted,"A 63-year-old woman comes to the physician because of worsening shortness of breath, cough, and a 4-kg (8.8-lb) weight loss over the last year. She has no history of serious illness and takes no medications. She has smoked one pack of cigarettes daily for 35 years. Her temperature is 37°C (98.6°F), pulse is 92/min, respirations are 20/min, blood pressure is 124/78 mm Hg, and pulse oximetry on room air shows an oxygen saturation of 93%. Physical examination shows decreased breath sounds. A flow-volume loop obtained via pulmonary function testing is shown.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [63, 'years'], 'Heart Rate or Pulse': [92.0, 'beats per minute'], 'O₂ saturation percentage': [93.0, '%'], 'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 63 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 92.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 93.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 2.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
Hence, the number of PERC rule criteria met by the patient is 2."
6624,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8536310-1,Extracted,"A 63-year-old Caucasian male with a history only significant for daily marijuana use received the J&J COVID-19 vaccine on May 7, 2021. One day later, he developed intractable nausea, vomiting, dyspnea, watery diarrhea, chills, sweats, and heavy chest pain. In the emergency department (ED), the patient was tachycardic at 120 beats per minute, hypoxic with oxygen 88% on room air, brain natriuretic peptide (BNP) 3421 pg/ml, elevated troponins at 1.29 ng/ml, procalcitonin 25 ng/ml, lactic acid 5.0 mmol/L, white blood cells 19 K/UL, thrombocytopenia at 101 K/UL, and creatinine 1.91 mg/dL. Initial chest X-ray showed bilateral airspace opacities consistent with atypical pneumonia. The patient was intubated because he was in severe respiratory distress with use of accessory muscles and decreased oxygen saturation. Ventilator settings are presented in Table .
Echo showed an ejection fraction (EF) of 25% with global hypokinesis and grade 3 diastolic dysfunction. A right heart catheterization was performed, showing severe pulmonary hypertension. An intra-aortic balloon pump was inserted, but his condition continued to decline, so a left-sided Impella device (Impella Cardiosystems AG, Aachen, Germany) was placed and milrinone and norepinephrine were started.
The patient was worked up for infectious causes and all were negative including two negative COVID-19 results, viral panel, blood cultures, urine cultures, sputum cultures, and urine legionella. A chest X-ray five days after presenting to the ED is shown below (Figure ).
Throughout his nine-day hospital stay, he continued to have rapid cyclical fluctuations of hypertension (260s/130s) and hypotension (40s/20s), persistent fevers up to 40.2 °C, and acute respiratory distress syndrome (ARDS)-like picture. His other problems included acute tubular necrosis (ATN) from an acute kidney injury (AKI), hypernatremia, arterial catheter-associated thrombosis in mid left radial artery leading to gangrene of left 1st and 2nd digits, non-ST-elevation myocardial infarction (NSTEMI) with cardiogenic shock (on May 10, 2021, EF was 55% with no diastolic dysfunction), subclinical hyperthyroidism, and electroencephalogram (EEG) showed diffuse slowing, with no epileptiform activity. Echo on May 15, 2021 showed EF of 43% with mild global hypokinesis.
Neuroendocrine crisis was suspected, and the patient was worked up for pheochromocytoma and carcinoid syndrome (Table ).
The results of retroperitoneal ultrasound are shown below (Figures -).
The first step in the diagnosis of pheochromocytoma is to discontinue medications that may interfere with metanephrine levels such as norepinephrine. Due to our patient's labile blood pressure measurements, he was on and off of vasopressors (such as norepinephrine) and anti-hypertensive medications (nitroglycerin). The results of significantly elevated 24-hour urine fractionated metanephrines and catecholamines or elevated fractionated plasma metanephrines confirms the diagnosis of pheochromocytoma. Imaging with CT or MRI is done to localize the tumor. Our patient was not stable enough for these imaging tests and thus we had to do an ultrasound. There were no previous imaging studies on record for this patient or a family history that could explain the etiology of his tumor.
The patient was transferred to the University of Michigan (U of M) hospital for mass resection on May 21, 2021. A CT was performed that day to confirm the ultrasound finding of a 7 cm heterogeneous right adrenal mass. The patient continued to suffer from acute hypoxemic respiratory failure and a tracheostomy was performed on June 07, 2021 due to prolonged intubation. His stay at U of M hospital was also complicated by episodes of non-sustained ventricular tachycardia (NSVT) that responded well to synchronized cardioversion. He was also placed on amiodarone. On June 18, 2021, an open right adrenalectomy was performed and on June 22, 2021, repeat plasma metanephrine was <0.2 nmol/L, and normetanephrine was 0.9 nmol/L. An echo performed on June 22, 2021 revealed a left ventricular EF of 63%, normal overall left ventricular systolic function, normal overall right ventricular systolic function, and no significant valvular dysfunction. Multiple upper and lower extremity deep vein thromboses (DVTs) were found on June 24, 2021. The patient was treated with blood thinners and stabilized for transfer to inpatient rehabilitation on July 02, 2021. The patient was then discharged on July 12, 2021 to stay with his sister. He has continued outpatient therapy and is now able to walk on his own and perform all of his activities of daily living independently. He will follow up with endocrine genetics for the etiology of his pheochromocytoma, cardiology, and physical medicine and rehabilitation. He will continue amiodarone for NSVT and rivaroxaban for the DVTs until the end of September 2021. The patient is doing very well overall.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [63, 'years'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'O₂ saturation percentage': [88.0, '%'], 'Previously documented Deep Vein Thrombosis': True, 'Hormone use': False, 'Recent surgery or trauma': True, 'Previously Documented Pulmonary Embolism': False}",5,5,5,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 63 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 120.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 88.0 percent. The saturated oxygen is less than 95%, and so we increment the perc critieria met by 1, making the current total 2 + 1 = 3.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
The patient note does not report a status on 'hemoptysis'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 3.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 3 + 1  =  4.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. At least one of the criteria is met and so we increment the criteria met by 1, making the current total 4 + 1 = 5.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 5.
Hence, the number of PERC rule criteria met by the patient is 5."
6625,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-7717955-1,Extracted,"The subject of this report is a 29 year old male, US citizen of Palestinian descent, who works full-time as a biomedical research technician. His health history is unremarkable, except for the fact that at age 16 he was diagnosed with ulcerative colitis and primary sclerosing cholangitis. Since then, he has been treated successfully with mesalamine (1.2 g, 2 times per day), azathioprine (50 mg, 3 times per day), and ursidiol (300 mg, 2 times per day). The subject has been able to live an active lifestyle and participate in a variety of sports including running, weightlifting, basketball, and baseball. The subject denies any history of smoking or use of alcohol, opioids, or illicit drugs. On April 22, 2020, the subject's father, who lives in the same house as the subject, and works for a major shipping company, was diagnosed with COVID-19. This was about 2 months after the first case of COVID had been confirmed in his state of residence, which was one of the early active zones of COVID-19 transmission in the US. On April 25, the patient began to experience general malaise and fatigue. Over the next 24 h, the symptoms worsened to include severe fatigue and weakness, loss of appetite, tiredness, slight dry cough, body aches, muscle pain, loss of taste and smell, sore throat and fever. The patient was then seen by his general practice physician. Vital signs at the time of examination were BP 110/72, pulse 97 BPM, respiration 14 per minute, oxygen saturation 98%, and body temperature 101.7°F. The patient was given a naso-pharyngeal swab, real-time RT-PCR test [COBAS (R) SARS-COV-@ test, Labcorp Laboratories, South Bend, IN] that confirmed a diagnosis of COVID-19. In compliance with standard medical practice standards, the patient was ordered to self-isolate and to start a 5-day course of azithromycin (250 mg, daily), and to also take 1 g of paracetamol (acetaminophen) every 6 h for treatment of pain and fever. Despite good adherence to the recommended treatment, the symptoms other than fever, did not improve, and he also started to feel depressed, demotivated, and spend long periods in bed. During this period, the patient experienced ongoing generalized myalgia and musculoskeletal pain. He described the pain as persistent and relatively severe (rated 7 on a scale of 1–10). Because of this discomfort, after 4 days the patient decided to consume kratom to relieve his symptoms. According to the patient, he had first used kratom 14 months earlier before his COVID-19 infection. He used kratom sporadically (no more than 4–5 times in total) as a cognitive enhancer and not to self-treat pain.
The patient decided to take 2.5 gms (or grams) of green kratom (as ground leaf powder suspended in water). The product was purchased at a local shop in April 2020 sold under the name “Green Bali.” After 30 min, he noticed a significant improvement in the intensity of the physical symptoms (mainly pain and fatigue), and within 60 min he felt a sensation of mild euphoria and well-being that lasted for about 5 h. After 6 h following consumption the effects of kratom wore off, and the patient administered another dose. He used kratom three times a day continuously for 3 days (for a total of 9 doses of 2.75 g each) with significant benefit.
When asked to score from 0 to 100% the improvement that kratom had on COVID-19 symptoms: fatigue and weakness (80% improvement), tiredness (70% improvement), body aches (80% improvement), muscle pain (90% improvement, “much better than paracetamol/acetaminophen”). The kratom did not seem to have an impact on: fever, cough, or sore throat. The patient also stated: “I didn't have anxiety or any psychological symptoms. For me, kratom mainly gave improvement in physical reaction.” “It also elevated my mood and made me feel less miserable, to the point where I was able to get out of bed, shower, look at work emails without feeling completely exhausted and drained”; “Kratom helped me more than antibiotic”; “I slept better, I essentially fell asleep immediately. Without kratom, sleep was not nice, with kratom less wake ups, about 6 h.” Over the next 2 weeks the patient's symptoms gradually subsided and on May 13 he had a televisit with his physician and a follow-up swab test that was negative for COVID-19. The subject was able to end his quarantine and return to work in early June. In a follow-up interview with us, the patient reported that he did not experience any side effects from using kratom, except for a very bad taste when swallowing it. The patient was also able to discontinue kratom use immediately without any evidence of physical or psychological withdrawal symptoms. The patient also informed us that he still had some of the kratom product that he had taken and he agreed to provide us with a sample for chemical analysis.
An established quantitative liquid chromatography mass spectrometry method was conducted () and found that the sample obtained from the patient is kratom due to the presence of mitragynine (102 mg/g kratom powder) and 7-hydroxymitragynine (0.8 mg/g kratom powder). The extracted kratom sample was analyzed for the presence of 13 opioids and 8 benzodiazepines by comparing the chromatograms to those of the reference mixtures Pain Management Multi-component Opiate Mixture-13 solution and Benzodiazepine Multi-component Mixture-8 solution. These data suggest the sample was not fortified with 7-hydroxymitragynine and there was also no evidence of adulteration with opioids or common benzodiazepines in the sample.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [29, 'years'], 'Heart Rate or Pulse': [97.0, 'beats per minute'], 'O₂ saturation percentage': [98.0, '%'], 'Hormone use': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': True, 'Recent surgery or trauma': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 29 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 97.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 0.
The saturated oxygen percentage in the room is 98.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 0.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 0.
The patient note reports 'hemoptysis' to be present for the patient and so we increment the criteria count by 1, making the current total 0 + 1  =  1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6626,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-3541795-1,Extracted,"A 59-year-old Hispanic male from Galveston, Texas presented to the Emergency Department on April 29, 2012 with complaints of headache and fever. His headache started two weeks prior, and he noted temperatures up to 40 degrees Celsius in the preceding five days. He denied neck pain, visual complaints, respiratory symptoms, or arthralgias. He denied recent travel, eating unpasteurized milk products, and sexual activity for the last several years. Two days prior to presentation, he was evaluated by the Emergency Department and was discharged with a presumed viral illness. Because of persistent fever and headache, he returned to the Emergency Department where he was admitted for further evaluation.
His medical history was significant for open-angle glaucoma and seasonal allergies. Outpatient medications included travoprost and dorzolamide ophthalmic drops. Multiple family members had diabetes mellitus and hypertension, and his father had a diagnosis of leukemia. He denied use of tobacco or illicit drugs. He drank alcohol rarely.
On examination, his temperature was 39.2 degrees Celsius, blood pressure 117/78 mmHg, heart rate 75 beats/minute, respiratory rate 16 breaths/minute, and oxygen saturation 95% on ambient air. He appeared ill, and skin examination was remarkable for a lightly erythematous macular rash on his chest and arms (). The examination was otherwise unremarkable.
Laboratory data revealed a leukocyte count of 3700/μL (3500 to 10,000/μL), erythrocyte sedimentation rate of 15 mm/hour (0 to 10 mm/hour), C-reactive protein of 12.3 mg/dL (0.0 to 0.8 mg/dL), ferritin of 1320 ng/mL (18 to 464 ng/mL), aspartate aminotransferase of 66 units/L (13 to 40 units/L), and alanine transaminase of 94 units/L (9 to 51 units/L). Serologic tests for viral hepatitis, HIV, cytomegalovirus, Epstein-Barr virus, syphilis, and Bartonella were nonreactive. Anti-nuclear antibody, antibodies to double-stranded DNA, and rheumatoid factor were negative. Blood and urine cultures were negative. Cerebrospinal fluid analysis was unremarkable. Chest radiograph and computed tomography of the head, abdomen, and pelvis were negative for lesions suggestive of malignancy or focal infectious process.
Throughout hospitalization, the patient continued to have daily fevers with temperatures up to 40 degrees Celsius. A careful revisitation of his history revealed exposure to opossums around his yard and home. This historical information in combination of his symptoms, rash, and mild transaminitis rendered murine typhus a likely diagnosis. Doxycycline was initiated and was followed by complete resolution of his symptoms within 48 hours. Although an immunofluorescence IgG assay for typhus group antibodies was nonreactive, the patient was discharged to complete a seven-day course of doxycycline.
One month after discharge, the patient returned to clinic and was free of symptoms. Serum obtained for an immunofluorescence IgG assay for typhus group antibodies was reactive at a dilution of 1 : 1024, confirming the diagnosis of murine typhus.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [59, 'years'], 'Heart Rate or Pulse': [75.0, 'beats/minute'], 'O₂ saturation percentage': [95.0, '%'], 'Unilateral Leg Swelling': False, 'Hormone use': False, 'Recent surgery or trauma': False, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False}",1,1,1,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 59 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 75.0 beats per minute. The patient's heart rate is less than 100 beats per minute, and so we do not increment the criteria count. The current total remains at 1.
The saturated oxygen percentage in the room is 95.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
Hence, the number of PERC rule criteria met by the patient is 1."
6627,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-4763561-1,Extracted,"A 69-year-old Caucasian woman presented to outside hospital with complaints of chest pain and shortness of breath. Chest pain started approximately a week ago and lasted for about 5 days but then subsided for a day. Next day, the patient was experiencing continuous chest tightness both on right and left side. She was also having dyspnea on exertion. The patient had a past medical history of hypertension, hyperlipidemia, obesity, and severe degenerative joint disease. Past surgical history was significant for hysterectomy. She denied any history of smoking cigarettes or using illicit drugs. The patient had a history of occasional alcohol intake. Medications at home included amlodipine/benazepril 10/20 mg daily, raloxifene 60 mg daily, celecoxib 200 mg BID, clonazepam 1 mg daily, fenofibrate 145 mg daily, a multivitamin tablet daily, a calcium tablet 600 mg daily, glucosamine 1500 mg daily, tramadol/acetaminophen 37.5/325 mg BID, and hydrocodone/acetaminophen 10/300 mg as needed for pain.
On arrival to the emergency department, the patient was tachycardic with a heart rate of 114/min, tachypneic with a respiratory rate of 24/min. She was normotensive at that time. Within the next few minutes, the patient became significantly hypotensive. Vitals at that time were blood pressure 78/52, heart rate 109/min, respiratory rate 22/min, and saturation of 96% on 3 L of oxygen via nasal cannula. On physical examination, the patient appeared to be in acute distress. On cardiovascular assessment, S1 and S2 were audible with no added murmur or gallop. She had bilateral pitting lower extremity edema. On lung examination, the patient had bilateral rhonchi and increased respiratory effort.
EKG showed sinus tachycardia with q waves and ST segment elevations of almost 2 mm in leads III and aVF. There was also left atrial enlargement (). Radiograph of chest showed interstitial edema. Laboratory results from admission included a basal metabolic panel that showed blood urea nitrogen of 40 mg/dL (6–20 mg/dL), creatinine of 1.2 mg/dL (0.7–1.2 mg/dL), and potassium of 4.2 mEq/L (3.5–5.0 mEq/L). First set of troponin levels were found to be 1.60 ng/mL (0.0–0.3 ng/mL) and first set of CK was 118 U/L (29–200 U/L). A Doppler echocardiogram was done in the emergency room, which showed normal ejection fraction of 60–65% with RV hypokinesis, which was consistent with RVI.
The patient was started on vasopressors and emergently transferred to our facility to undergo cardiac catheterization. Left heart catheterization revealed 99% stenosis to mid-right coronary artery and subsequently the patient underwent percutaneous coronary intervention (PCI) to the right coronary artery. An intra-aortic balloon pump was placed during cardiac catheterization as the patient was in cardiogenic shock. After successful PCI, the intra-aortic balloon pump was removed as her vitals seemed to have stabilized. Two days later, again the patient developed hypotension and worsening shortness of breath. Urgent bedside Doppler echocardiogram showed a new left-to-right shunt in the ventricle, which was noted to be a muscular VSD. The patient was transferred to a tertiary care medical center for surgical repair. At the tertiary care hospital, transesophageal echocardiogram (TEE) was done, which revealed large VSD with a dimension of 1.38×0.9 cm2 and an area of 0.9 cm2 located in the posterior wall of ventricle (). TEE also showed mildly reduced RV systolic function and moderate to severe tricuspid regurgitation ( and ).
The patient subsequently developed S. aureus bacteremia and Clostridium difficile colitis, which were successfully treated with intravenous antibiotics. She underwent cardiothoracic surgery for possible surgical versus percutaneous repair of the VSD. Based on the location of the VSD, the patient was considered to be an excellent candidate for percutaneous repair with amplatzer postinfarct VSD occluder device. After placement of the amplatzer VSD device, significant reduction in left-to-right shunt was noted on TEE. Also, hemodynamically the patient improved and her hypotension resolved, so the intra-aortic balloon pump was discontinued. Eventually, the patient developed sepsis secondary to C. difficile colitis, which resulted in development of disseminated intravascular coagulation, hemodynamic collapse, and death.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'age': [69, 'years'], 'Heart Rate or Pulse': [114.0, 'beats per minute'], 'O₂ saturation percentage': [96.0, '%'], 'Hormone use': True, 'Previously Documented Pulmonary Embolism': False, 'Hemoptysis': False, 'Recent surgery or trauma': True, 'Previously documented Deep Vein Thrombosis': False}",4,4,4,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 69 years old. The patient's age is greater than or equal to 50 years, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The patient's heart rate is 114.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 1 + 1 = 2.
The saturated oxygen percentage in the room is 96.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 2.
The patient note does not report a status on 'unilateral leg swelling'. Hence, we assume it to be absent, and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 2.
The patient note reports 'recent surgery or trauma' to be present for the patient and so we increment the criteria count by 1, making the current total 2 + 1  =  3.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 3.
The patient note reports 'hormonal use' to be present for the patient and so we increment the criteria count by 1, making the current total 3 + 1  =  4.
Hence, the number of PERC rule criteria met by the patient is 4."
6628,48,PERC Rule for Pulmonary Embolism,diagnosis,integer,pmc-8436833-1,Extracted,"A 27-year-old African American female patient with a history of stage IV endometriosis presented to the emergency department with exertional dyspnea of three-month duration. She also had an unintentional weight loss of approximately 25 pounds. The patient also endorsed night sweats, paroxysmal nocturnal dyspnea, and orthopnea, but she denied chest pain or lower extremity swelling. Of notice, the patient had an endometrial cyst removal performed five years ago and an endometriosis-related paracentesis performed three years ago. The last follow-up with obstetrics/gynecology was 13 months ago.
On presentation, the patient had a blood pressure of 120/78 mmHg, a temperature of 36.6°C, a heart rate range of 75-90 beats per minute, and a respiratory rate of 16 breaths per minute with an oxygen saturation of 97% on room air. Chest auscultation revealed absent breath sounds on the right side of the chest.
Laboratory studies were significant for a hemoglobin of 11.2 g/dl (12-16 g/dl). Other complete blood count parameters and electrolytes were within normal limits. Chest X-ray (CXR) showed complete opacification of the right chest with a left tracheal deviation (Figure ). Computed tomography of pulmonary arteries (CT-PA) was negative for pulmonary emboli, but it showed a massive right pleural effusion with complete atelectasis of the right lung in addition to a left-sided cardiomediastinal shift (Figure ). Thoracocentesis with the removal of 2 to 3 l of serosanguinous fluid was performed, fluids turned to be exudative with few glandular and endometrial cells on cytohistological examination. Because the patient’s condition was not improving, a chest tube was placed. Continuous chest tube drainage with serosanguinous fluid was noted for eight days. Because the patient’s condition did not significantly improve, a right video-assisted thoracoscopic surgery (VATS), a right diaphragm and pleural biopsy, and pleurodesis were performed, which revealed dense fibroconnective tissue with prominent chronic inflammation, including lymphoid aggregates and focal mesothelial hyperplasia (Figure ). No malignancy was reported in the histopathologic examination.
Ultrasonography of the abdomen and pelvis in addition to magnetic resonance imaging (MRI) of the thorax, abdomen, and pelvis was done; these investigations showed endometrioma of about 7.2 × 7.1 × 4.2 cm in the mid-upper pelvis with a moderate amount of hemorrhagic fluid in the pelvis and bilateral paracolic gutters (Figure ), and the latter finding was similar to a prior finding on a CT scan of the abdomen that was done three years ago. Because these fluids did not cause any symptoms to the patient, the obstetrics/gynecology team’s decision was not to drain, believing that the endometriosis treatment itself should improve this condition.
Transvaginal ultrasonography and complete pelvic duplex ultrasonography of the lower abdomen showed a large septate cystic lesion in the left adnexa, which has been present for three years. The lesion was consistent with endometrioma (Figure ). The patient was discharged on Leuprolide Depot 11.25 mg injections every three months and norethindrone hormonal therapy of 5 mg tablets daily to prevent menopausal symptoms, with a close outpatient follow-up.",What are the number of criteria met for the PERC Rule for Pulmonary Embolism (PE)? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'O₂ saturation percentage': [97.0, '%'], 'Hemoptysis': False, 'Previously documented Deep Vein Thrombosis': False, 'Previously Documented Pulmonary Embolism': False, 'Unilateral Leg Swelling': False, 'Recent surgery or trauma': False, 'Hormone use': True, 'age': [27, 'years'], 'Heart Rate or Pulse': [7590.0, 'beats per minute']}",2,2,2,"The PERC Rule critiera are listed below:

1. Age ≥50: No = 0 points, Yes = +1 point
2. Heart Rate (HR) ≥100: No = 0 points, Yes = +1 point
3. O₂ saturation on room air <95%: No = 0 points, Yes = +1 point
4. Unilateral leg swelling: No = 0 points, Yes = +1 point
5. Hemoptysis: No = 0 points, Yes = +1 point
6. Recent surgery or trauma (within 4 weeks, requiring treatment with general anesthesia): No = 0 points, Yes = +1 point
7. Prior pulmonary embolism (PE) or deep vein thrombosis (DVT): No = 0 points, Yes = +1 point
8. Hormone use (oral contraceptives, hormone replacement, or estrogenic hormone use in males or females): No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the points for each criterion.
    
The current count of PERC criteria met is 0.
The patient is 27 years old. The patient's age is less than 50 years, and so we do not increment the criteria count. The current total remains at 0.
The patient's heart rate is 7590.0 beats per minute. The patient's heart rate is greater than or equal to 100 beats per minute, and so we increment the perc critieria met by 1, making the current total 0 + 1 = 1.
The saturated oxygen percentage in the room is 97.0 percent. The saturated oxygen is greater than or equal to 95% and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'unilateral leg swelling' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'hemoptysis' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient note reports 'recent surgery or trauma' to be absent in the patient and so we do not increment the criteria count. The current total remains at 1.
The patient must be diagnosed with at least one of deep vein thrombosis or pulmonary embolism in the past for a PERC rule criteria to be met. The patient is not reported to have been diagnosed with deep vein thrombosis in the past. The patient is not reported to have been diagnosed with pulmonary embolism in the past. Neither criteria is met and so we do increment the criteria count, keep the current total at 1.
The patient note reports 'hormonal use' to be present for the patient and so we increment the criteria count by 1, making the current total 1 + 1  =  2.
Hence, the number of PERC rule criteria met by the patient is 2."
6629,51,SIRS Criteria,diagnosis,integer,pmc-7440216-1,Extracted,"A previously healthy 55-year-old woman with confirmed COVID-19 infection was hospitalised due to fatigue and near-syncope. Nine days prior to admission, her daughter returned from another European country and 3 days thereafter the daughter developed upper airways symptoms. The next day (day 0), the patient developed fatigue and unspecific body discomfort, with no airway symptoms. COVID-19 was confirmed in both the next days. Her medical condition improved temporarily until hospitalisation on day 7 due to several episodes of near-syncope and increased body and chest discomfort.
By admittance to hospital, the patient was isolated due to the COVID-19 infection. Blood pressure was 102/72 mm Hg, heart rate was 100 beats/min, respiratory rate was 17/min and rectal temperature was 37.2°C. Clinical examination revealed normal organ findings including pulmonary and cardiac examination. The ECG showed sinus tachycardia, insignificant ST-elevation in inferior leads and T-wave inversion in precordial leads (). Furthermore, there was low-voltage ECG with peak-to-peak QRS amplitude less than 5 mm in the standard leads and 10 mm in the precordial leads (V5 and V6). All ECG findings were stationary during the course. Laboratory findings showed glucose 7.2 mmol/L, normal electrolytes, mild elevation of C-reactive protein (CRP) 11 and significantly elevated leucocyte count 13.2×109/L, troponin T 108 ng/L, NT-proBNP 1025 ng/L. Comprehensive description of laboratory tests and therapy is shown in . Bedside cardiac ultrasound examination performed by the on-call cardiac resident using a hand-held ultrasound device revealed moderate concentric left ventricular hypertrophy, reduced left ventricular EF, dilated inferior caval vein with reduced respiratory variation and pericardial effusion at a maximum of 18 mm, a small right ventricle and a slight impression of the right atrium (). She was subsequently transferred to the ICU and treated with fluid support and norepinephrine. Day to day fluid and pressor treatment are highlighted in . The results of the point-of-care ultrasound examination were confirmed by echocardiography at the ICU. The left ventricle presented with a moderate concentric hypertrophy with a small cavity with end-diastolic volume less than 70 mL. Furthermore, there was a striking hyperechogenic pattern of the endocardium and epicardium ( and ). She deteriorated the following day with decreasing blood pressure and diuresis, with only a modest response on supportive treatment with fluid and pressor (norepinephrine (NA) and dobutamine). Fluid support was provided due to extensive peripheral capillary leakage. The extremities were cold and wet, but cognition was normal and beside international normalization ratio (INR) 1.2–1.3 there was no other sign of organ failure. Pericardiocentesis was performed at day 9 due to subacute deterioration and echocardiographic signs of a tamponade including compression of the right atrium, dilated inferior vena cava without inspiratory diameter reduction and respiratory variation in volumes and flow velocities ( and ). After initial drainage of 300 mL of serosal pericardial fluid, there was an immediate reduction of the respiratory variation of inflow patterns. The systolic blood pressure increased from 60 mm Hg to 95 mm Hg followed by increased diuresis. Size and function of the cardiac chambers together with mitral inflow pattern and filling of the left ventricle normalised gradually over the following days (, ). The left ventricular myocardial thickness and striking echogenicity were reduced in the same period. Cardiac output and blood pressure improved correspondingly. The patient needed supportive fluid therapy due to capillary leakage until day 15 when she was transferred to the ward.
The pericardial fluid tested negative in PCR for COVID-19. Cardiac (CMRI) study performed at day 15 was consistent with the diagnosis of acute perimyocarditis. T1-mapping showed relaxation times of 1260–1270 ms in the anterolateral wall compared with 1090 ms in the septum. The corresponding T2-mapping relaxation times were 60–61 ms and 52–53 ms, respectively. Inversion recovery sequences showed a moderate epicardial late gadolinium enhancement in the anterolateral wall (). Myocardial biopsy was postponed due to the COVID-19 situation and rapid improvement.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Heart Rate or Pulse': [100.0, 'beats per minute'], 'Temperature': [37.2, 'degrees celsius'], 'respiratory rate': [17.0, 'breaths per minute'], 'White blood cell count': [13200.0, 'L']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.2 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 100.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 13200.0 count/L. To convert 13200.0 count/L of white blood cell to mm^3, multiply by the conversion factor 1e-06 L/mm^3 which will give 13200.0 white blood cell count/L * 1e-06 L/mm^3 = 0.0132 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 17.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6630,51,SIRS Criteria,diagnosis,integer,pmc-7171472-1,Extracted,"A 42-year-old male on peritoneal dialysis presented with abdominal pain and cloudy effluent of one-day duration. The patient denied any fever and denied any in advent breach in the technique while making peritoneal dialysis connections. Moreover, the patient denied history of diarrhea or constipation. The patient has been on peritoneal dialysis for five years and had no prior history of peritonitis. Past medical history was signification for diabetes, hypertension, hyperlipidemia, hyperparathyroidism, end-stage renal disease on peritoneal dialysis. Home medications included metoprolol 100 milligrams (mg) twice a day, nifedipine 60 mg extendedrelease daily, atorvastatin 80 mg daily, sevelamer 2400 mg three times a day with meals, calcitriol 0.5 micrograms (mcg) daily, gabapentin 100 mg daily at bedtime, cinacalcet 30 mg daily, insulin glargine 15 units daily, insulin sliding scale.
The vital signs on presentation were the temperature of 36.4 Celsius, pulse rate of 84 beats per minute, respiratory rate of 16 breath per minute, blood pressure of 158/95 mm Hg. Physical examination revealed abdominal tenderness with a peritoneal dialysis catheter in the right lower quadrant. There was no exit site drainage or redness along the tunnel and the rest of the physical examination was nonsignificant.
Laboratory analysis showed white blood count 10300 mm3, hemoglobin 11.2 gm/dl, platelet count 22300 mm3, sodium 138 mmol/l, potassium 4.5 mmol/l, bicarbonate 22 mmol/l, blood urea nitrogen 58 mg/dl, creatinine 11.6 mg/dl, albumin 3.3 g/dl. The peritoneal fluid effluent revealed peritoneal fluid white blood cells (WBC) 1837 cells/ul with 85% predominant neutrophils. Peritoneal fluid gram stain revealed >100 WBC, and no organisms were seen. The patient was started on empiric treatment for peritonitis with intraperitoneal vancomycin and ceftazidime. Later on, peritoneal fluid culture grew Citrobacter freundii in both aerobic and anaerobic bottles. The sensitivities of Citrobacter freundii were listed in done by VITEK 2 method.
The patient was treated with double antibiotic coverage of intraperitoneal ceftazidime and oral ciprofloxacin for three weeks. The repeat peritoneal fluid cultures after finishing the antibiotic course yielded heavy growth of C. freundii again. The sensitivities of Citrobacter freundii are listed in done. Another three weeks course of double antibiotic treatment (intraperitoneal ceftazidime and intravenous imipenem) was given, which failed to clear the organism. The symptoms resolved when peritoneal dialysis catheter was removed after failing two double antibiotic courses. Subsequently, he did not require a further course of antibiotics. The dialysis modality of the patient was then switched to hemodialysis and the patient continues to be hemodialysis dependent after two years of follow up.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.4, 'degrees celsius'], 'Heart Rate or Pulse': [84.0, 'beats per minute'], 'respiratory rate': [16.0, 'breaths per minute'], 'White blood cell count': [10300.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.4 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 84.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 10300.0 count/m^3. To convert 10300.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 10300.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 16.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6631,51,SIRS Criteria,diagnosis,integer,usmle-9959,Extracted,"A 16-year-old man presents to the clinic accompanied by his father, with the complaints of high fever, sore throat, and bloody diarrhea for 4 days. He adds that he is also nauseous and vomited several times in the past 2 days. He denies any recent travel or eating outside. He recently started a dog-walking business. The father relates that two of the dogs had been unwell. His temperature is 37°C (98.6°F), respiratory rate is 16/min, pulse is 77/min, and blood pressure is 100/88 mm Hg. A physical examination is performed and is within normal limits including the abdominal exam.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.0, 'degrees celsius'], 'Heart Rate or Pulse': [77.0, 'beats per minute'], 'respiratory rate': [16.0, 'breaths per minute'], 'White blood cell count': [13100.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 77.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 13100.0 count/m^3. To convert 13100.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 13100.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 16.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6632,51,SIRS Criteria,diagnosis,integer,pmc-7780472-1,Extracted,"A 72-year-old man with diabetes mellitus, hypertension, and prostate cancer accompanied by multiple bone metastasis had sudden chest and back pain and difficulty in breathing at rest. His chest pain was accompanied by heaviness, squeezing, and discomfort. His prostate cancer had been treated with bicalutamide (80 mg/day) for ∼2 years, and his cancer stage was stable. He was brought to our hospital by ambulance and his vital signs were as follows: heart rate 72/min, respiratory rate 24/min, an axillary temperature 36.2°C, saturation of percutaneous oxygen under room air 90%, and peak blood pressure of 190/108 mmHg. There was no pleural effusion or congestion in the chest radiograph (). Electrocardiography showed sinus rhythm with a complete right bundle branch block (CRBBB) and no significant ST-segment changes (). His initial serum troponin I level was 0.05 ng/mL (normal value: <0.04 ng/mL) and the d-dimer level was 14.7 μg/mL (normal value: <1.0 μg/mL). White blood cell count was 12 900/μL (normal value: 4000–7500/μL) and brain natriuretic peptide was 110 pg/mL (normal value: <18.4 pg/mL); other laboratory values were within normal range. The echocardiogram did not show any wall motion abnormality, significant valve disease, right ventricle dilation, or obvious congenital heart disease such as a patent foramen ovale. His chest CT with contrast showed bilateral scattered PE and left deep vein thrombus (from popliteal vein to soleus vein) (). After admission, his chest pain persisted, and the serum troponin I level and ECG were checked repeatedly. Although his serial ECG did not show no significant changes (), his serum troponin I level 3 h after the admission was elevated to 0.90 ng/mL. Furthermore, reconstruction of the SDCT (IQon Spectral CT; Philips healthcare) images clearly showed a perfusion defect of the posterolateral left ventricle myocardium (), suggesting a combination of PE and non-ST-segment elevation myocardial infarction (NSTEMI).
Following these findings, coronary angiogram was then performed which showed total occlusion of the OM branch. Although atherosclerotic plaques were seen in multiple coronary arteries, significant stenosis was not observed except for the OM branch (). Consequently, percutaneous coronary intervention (PCI) was performed to the occlusion site. After thrombectomy, intracoronary imaging using intravascular ultrasound was performed, and atherosclerotic plaque lesions were observed (). Two drug-eluting stents were deployed (Synergy 2.75/28 mm and Synergy 2.25/20 mm), and Thrombolysis in Myocardial Infarction 3 flow was achieved (). The creatine kinase (CK) and CK-MB peaked at 2034 and 278 IU/L (normal values: CK 60–287 IU/L and CK-MB <25 IU/L) 8 h after the admission.
Following treatment of ACS, we began treatment for PE with an oral anticoagulant (OAC, rivaroxaban 30 mg/day). He was relieved of his chest symptoms and was rescued from a hypoxic state. He was discharged on the 14th day after admission. Enhanced SDCT and associated reconstructed images of effective atomic number (Z-effective) 6 months after the treatment started, until when dual antiplatelet therapy (aspirin 100 mg and clopidogrel 75 mg/day) and OAC therapy (rivaroxaban 30 mg/day for 3 weeks and 15 mg/day after 3 weeks) were continued, showed improvement in perfusion defects in both pulmonary fields () and the myocardium (). His treatment was deescalated to single antiplatelet therapy (clopidogrel 75 mg/day) and OAC, and he has had a good course without recurrence.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.2, 'degrees celsius'], 'Heart Rate or Pulse': [72.0, 'beats per minute'], 'respiratory rate': [24.0, 'breaths per minute'], 'White blood cell count': [12900.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.2 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 72.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 12900.0 count/µL. To convert 12900.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 12900.0 white blood cell count/µL * 1.0 µL/mm^3 = 12900.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 24.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 1 + 1 = 2 criteria met.
Hence, the the number of SIRS criteria met by the patient is 2."
6633,51,SIRS Criteria,diagnosis,integer,pmc-4620336-1,Extracted,"A 54-year-old female was admitted to our hospital with subacute cough for the last month. The patient had a history of multilobar (right middle lobe and right upper lobe) pneumonia over the past 2 years, and had been admitted to a nearby hospital with the chief complaint of a cough that had worsened over the previous month. She usually had a dry cough after a cold, which did not last for more than 2 months. Following a diagnosis of acute eosinophilic bronchitis and focal pneumonia, the patient was administered antibiotics. However, her pneumonia did not improve and she was transferred to our hospital for further examination.
She had no disease and no operation history. She was nonsmoker and social drinker. She had no family history and her occupation was teacher.
Blood pressure was 110/60 mm Hg, pulse rate was 60 beats per minute, respiration rate was 20 per minute, and body temperature was 36.8℃. General findings indicated no pain, but chest auscultation revealed minor rales in the right middle lobe. Heart auscultation revealed a normal beat without cardiac murmur. No edema was observed in the abdomen or extremities, and no lymph node enlargement was apparent.
The results of an arterial blood gas examination performed at the time of admission were PH 7.43, PaCO2 33 mm Hg, PaO2 78 mm Hg, and HCO3- 22 mEq/L. A peripheral blood examination revealed a hemoglobin level of 13.1 g/dL, hematocrit 44%, a white blood cell count of 8,600/mm3, and a platelet count of 250,000/mm3.
The results of biochemical analysis were a total protein level of 6.8 g/dL, albumin 4.1 g/dL, aspirate aminotransferase 38 IU/L, alkaline phosphatase 200 mg/dL, erythrocyte sedimentation rate 30 m/hr, blood urea nitrogen 12.9 mg/dL, and creatinine 0.9 mg/dL. Electrolytes and blood glucose levels were normal, and urine examination revealed specific gravity of 1.025, pH 6.0, no proteinuria, and a red blood cell count of 30-49 per high-power field. Subsequent examination revealed no worsening of hematuria. Empirical antibiotic treatment, acid-fast bacillus (AFB) sputum smear, and sputum eosinophil tests were performed, in order to differentiate community-acquired pneumonia and pulmonary tuberculosis (TB). Sputum bacteria examination did not yield specific findings, and very few sputum eosinophils were observed. The concentration of the tumor marker carcinoembryonic antigen detected was 1.3 ng/mL(with-in normal range), and an interferon-gamma release assay was positive. However, the AFB smear and TB polymerase chain reaction were negative, and AFB culture yielded no-growth. Tests for rheumatic factors and antinuclear antibody yielded no specific findings, and the patient did not complain of rheumatic-disease-related symptoms. Electrocardiography and echocardiography yielded normal results, and pulmonary function examination revealed a forced vital capacity (FVC) of 2.83 L (90% of reference), forced expiratory volume in the first second (FEV1) 2.27 L (93% of reference), FEV1/FVC 92%, and diffusion capacity adjusted by the alveolar volume 97%, indicating mild obstructive ventilation disturbance.
Simple chest radiography revealed nodular lesions around the pulmonary hilum of the right upper lobe (). Chest computed tomography (CT) revealed a 1.8-cm speculated nodule around the inferior margin of the right upper lobe, and the differential diagnosis of focal pneumonia or lung cancer was required (). A bronchoscopy revealed no abnormalities in the bronchi. Kidney ultrasonography and a gastroscopy that were performed to confirm the amyloidosis lesions did not yield specific findings; so video assisted thoracic surgery (VATS)-assisted pulmonary wedge resection was conducted for early differentiation of lung cancer. No surgical complications were encountered.
Histology indicated a thickened interstitium due to eosinophilic amorphous material deposits, with some giant cells and histiocyte infiltration (). Congo red staining for amyloidosis was positive, and under a polarized microscope the nodule exhibited a unique apple-green birefringence ().
Additional examinations for amyloidosis, blood and urine immunoelectrophoresis, and immunofixation were performed. IgG, IgM, IgA, IgE, and IgD concentrations were normal, as were the immunofixation results (). A bone marrow biopsy was not performed, in accordance with the patient's request.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.8, 'degrees celsius'], 'Heart Rate or Pulse': [60.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [8600.0, 'm^3'], 'PaCO2': [33.0, 'mm hg']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.8 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 60.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 8600.0 count/m^3. To convert 8600.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 8600.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 8.6e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 33.0 mm Hg, which is greater or equal to than 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6634,51,SIRS Criteria,diagnosis,integer,pmc-8453413-1,Extracted,"A 27-year-old man presented to the emergency room with complaints of lightheadedness, dyspnoea, orthopnoea, and bilateral lower extremity oedema over the course of a few weeks. His symptoms were associated with chest discomfort and he denied similar past episodes. He had no significant past medical history. Family history was remarkable for a brother diagnosed with BTHS by genetic testing. The patient denied alcohol use and recreational drug use. He endorsed active cigarette smoking (0.33 packs per day). On presentation, the patient was afebrile with a temperature of 36.7°C, hypotensive to 86/54 mmHg, tachycardic to 104 beats per minute (b.p.m.), breathing at a rate of 18 breaths per minute, with an oxygen saturation of 96% on room air. Physical examination was remarkable for diminished breath sounds at the lung bases bilaterally, tachycardia with regular rhythm, jugular venous distension to the earlobe, and 2+ pitting oedema in the lower extremities bilaterally. Complete blood count revealed leukopenia (2.9 k/μL; reference range: 4.0–10.8 k/μL), neutropenia (27.7%; reference range: 43.0–75.0%), and monocytosis (37.1%; reference range: 3.0–12.0%). Lipid panel showed total cholesterol of 91 mg/dL (reference range: 120–200 mg/dL), with a calculated LDL of 44 mg/dL (reference range: 0–99 mg/dL), and an HDL of 22 mg/dL (reference range: 40–59 mg/dL). Initial electrocardiogram showed sinus tachycardia with a ventricular rate of 128 b.p.m., criteria for left atrial enlargement, and a prolonged QTc interval of 589 ms (). The patient was admitted to the hospital for further evaluation, diagnostic interventions, and treatment. Echocardiographic exam revealed enlargement of all four chambers ( and Video 1), with significant dilatation of the left ventricle (end-diastolic diameter 6.0 cm, end-systolic diameter 5.8 cm) and severely reduced left ventricular ejection fraction (LVEF) of 15–20%. Additionally, mild pulmonary hypertension was present. Ischaemic workup with coronary angiography revealed patent vessels ( and Video 2), and ventriculogram showed an LVEF of 20%. Right heart catheterization was remarkable for pulmonary arterial pressure of 26/11 mmHg (mean of 16 mmHg), a calculated Fick cardiac output of 3.18 L/min (normal range: 4–8 L/min) and a cardiac index of 2.02 L/min/m2 (normal range 2.5–4 L/min/m2). HIV testing was negative, ethanol level was within normal limits, thyroid stimulating hormone (TSH) was mildly elevated at 5.12 μIU/mL (reference range: 0.4–4.0 μIU/mL), with free T4 within normal limits at 1.16 ng/dL. Based on the history of present illness, family history, physical examination findings, laboratory investigations, and diagnostic imaging results, the patient could likely have a diagnosis of BTHS. He was carefully diuresed to euvolemia, discharged in stable condition with a LifeVest wearable defibrillator for 3 months, and furosemide 20 mg per orum (PO) daily. He was also started on guideline-directed medical therapy including carvedilol 3.125 mg PO twice a day and sacubitril-valsartan 24–26 mg PO twice a day. At a 6-month follow-up visit, the patient had no further complaints, remained compliant with his discharge medications, and spironolactone 12.5 mg PO daily was added. An outpatient cardiac magnetic resonance imaging study with and without contrast for evaluation of infiltrative disease and other causes of non-ischaemic cardiomyopathy was non-suggestive of myocardial infarction, infiltrates, or other abnormal enhancement by late gadolinium enhancement imaging. The patient’s diagnosis was confirmed with outpatient genetic testing for TAZ gene mutation, and he continued to regularly follow-up with an advanced heart failure cardiologist. A repeat echocardiogram (Video 3) 2 years after the initial hospitalization showed evidence of cardiac remodelling with improvement in left ventricular size (end-diastolic diameter 5.02 cm, end-systolic diameter 4.06 cm) and LVEF (45–50%).",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.7, 'degrees celsius'], 'Heart Rate or Pulse': [104.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [2900.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.7 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 104.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 2900.0 count/µL. To convert 2900.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 2900.0 white blood cell count/µL * 1.0 µL/mm^3 = 2900.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6635,51,SIRS Criteria,diagnosis,integer,pmc-2582518-1,Extracted,"A 53-year-old Korean man who had undergone curative surgical resection for stage iii (T3N2M0) colon cancer was evaluated in clinic by his medical oncologist before the start of adjuvant chemotherapy. He appeared clinically well on assessment and proceeded to receive his first cycle of modified folfox-6 chemotherapy. This regimen consisted of oxaliplatin 85 mg/m2, folinic acid 400 mg/m2, and 5-fluorouracil (5-fu) 400 mg/m2 bolus on day 1, followed by 5-fu 2400 mg/m2 by continuous infusion over the next 46 hours. Dexamethasone 12 mg and ondansetron 8 mg were given as pre-medication before chemotherapy.
The patient experienced no acute side effects or complications in the chemotherapy unit. He was discharged home with an ambulatory 5-fu pump and was scheduled to return to the clinic at completion of his 5-fu infusion.
Twenty-four hours later, the patient presented to the emergency department with new symptoms of erratic behaviour and confusion. Collateral history from the accompanying family members revealed that he had suffered a brief generalized tonic–clonic seizure earlier in the day, but no apparent history of head injuries, infectious symptoms, or recent alcohol intake was present. The patient’s other medical problems included well-controlled hypertension, hyperlipidemia, polycystic kidney disease, chronic renal insufficiency (baseline creatinine: 172 mmol/L), and stable chronic hepatitis B carrier status without laboratory or radiologic evidence of cirrhosis. No history of epilepsy was present. The patient’s only oral medications were amlodipine, quinapril, hydrochlorothiazide, and atorvastatin. He was an ex-smoker, and he denied alcohol abuse and illicit drugs.
On examination in the emergency department, the patient was neither alert nor oriented. He was unable to follow commands, and his verbal responses were incomprehensible. He was agitated, and his limbs were tremulous at rest. Temperature was 35.9°C; heart rate, 82/min; respirations, 18/min; blood pressure, 130/84 mmHg; and O2 saturation on room air, 99%. The patient’s eyes appeared deviated to his left side, but pupils were equal and reactive. Spontaneous twitching of the extremities, on the left side more than on the right, was noted and attributed to possible complex partial seizures. No other focal neurologic deficits or evidence of trauma were present. The Brudzinski and Kernig signs were negative. Examinations of chest, heart, and abdomen were otherwise unremarkable. The patient was noted to be incontinent of urine during the assessment. He was treated with intravenous diazepam and phenytoin (given in a loading dose of 1000 mg) for his agitation and presumed seizure activity respectively. At this point, his 5-fu infusion pump was still attached and functioning.
Laboratory investigations showed leucocytosis (white blood cell count: 19.5 × 109/L) with left shift, but an otherwise normal complete blood cell count. Liver enzyme tests were within normal limits. Serum creatinine and blood urea nitrogen were elevated (239 mmol/L and 8.6 mmol/L respectively). Metabolic acidosis with an anion gap of 29 mmol/L was present. Imaging of the head and brain by computed tomography and magnetic resonance imaging scan respectively did not demonstrate evidence of infarction, hemorrhage, mass, or other abnormalities. Cerebrospinal fluid analysis was benign, and subsequent cultures of cerebrospinal fluid, blood, and urine were all negative. Of note, serum ammonia, at 316 mmol/L, and serum lactate, at 8.3 mmol/L, were elevated. The remainder of the toxicology screen was completely unremarkable. Vitamin B12 level and thyroid function tests were normal. An electroencephalogram showed a generalized slowing pattern consistent with metabolic encephalopathy.
Over the next 8 hours, the patient’s mental status progressively deteriorated to a comatose state. The 5-fu infusion pump was discontinued. Because the patient was no longer adequately protecting his airway, the critical care team was consulted for patient intubation and admission to the intensive care unit. With an apparent cause for the rapidly progressive cognitive dysfunction still lacking, lactulose at a dose of 30 mL every 4 hours was administered by nasogastric tube shortly thereafter in an effort to correct the patient’s encephalopathy. Phenytoin was continued.
Following the cessation of 5-fu and administration of lactulose, the patient gradually recovered over the next 48 hours from his acute confusional state. He experienced significant fatigue and muscle weakness, but no further seizures. Successive ammonia levels showed a decreasing trend. The patient was extubated, and phenytoin was discontinued. This man was discharged home on day 8 with instructions to follow up with his medical oncologist the following week.
After discharge, the patient required several weeks to recuperate before he could embark on additional chemotherapy. Considering his presumed neuropsychiatric complication from folfox chemotherapy, raltitrexed (3 mg/m2) and oxaliplatin (130 mg/m2) were given every 3 weeks as adjuvant treatment instead. This therapy was provided on an inpatient basis because of the insistence of the patient. No significant adverse reactions were noted. Unfortunately, re-staging investigations shortly thereafter revealed three metastatic lesions in the liver. We plan to continue with further chemotherapy for this patient with the goal of potential resection of his liver lesions in the future.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [35.9, 'degrees celsius'], 'Heart Rate or Pulse': [82.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [19500.0, 'L']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 35.9 degrees celsius. Because the temperature is less than 36 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 82.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 19500.0 count/L. To convert 19500.0 count/L of white blood cell to mm^3, multiply by the conversion factor 1e-06 L/mm^3 which will give 19500.0 white blood cell count/L * 1e-06 L/mm^3 = 0.0195 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6636,51,SIRS Criteria,diagnosis,integer,pmc-8302451-1,Extracted,"A 74-year-old male with a history of mild cognitive impairment presented to the emergency department with failure to thrive and generalized weakness of three weeks duration. He was having difficulty swallowing which he related to a poorly fitted denture. He had thirty pounds of unintentional weight loss in the last three months due to loss of appetite. His past medical history was significant for diabetes mellitus type II, hypertension, major depressive disorder, chronic pain syndrome, and hepatitis C. His social history was significant for 12.5 pack-year smoking and drinking (two to three glasses of wine/day). He denied any utilization of recreational drugs. In the emergency department, his vital signs were, BP-104/59 mmHg, HR-97 bpm, respiratory rate-14/minute, temperature-97.4 °F, and oxygen saturation was 99% on room air. He weighed 40 kg, and his BMI was 13.84 kg/m2. On physical examination, he was alert, oriented, and appeared weak and malnourished. The ill-fitted complete maxillary denture was removed. The oral cavity examination revealed a large (3 × 2 cm2) defect with an erythematous border that encompassed the mid-palatal structures and emanated from the hard palate into his nasal cavity (Figure ).
There was no discrete mass or ulcer and mucosa surrounding this defect appeared normal. On palpation, the lesion was non-tender without any palpable lymph node on the head and neck examination. His lungs, heart, neurological, and abdominal examinations were unremarkable. Laboratory data at admission showed Hb-11.7 g/dl, WBC’s-9.6 K/CMM, and platelets-190 K/CMM. The chemistry panel (BMP) was within the normal range. AST-23 U/L, ALT-25 U/L, and serum alkaline phosphatase were 114 U/L. Auto-immune work-up including anti-dsDNA, anti-proteinase-3 antibodies, myeloperoxidase (MPO) antibodies were negative. The patient was managed conservatively, with nutritional supplementation and supportive care. Contrast-enhanced CT of the neck demonstrates enlarged level 2A lymph nodes bilaterally (Figure and 2B), corresponding to increased fluorodeoxyglucose (FDG) avidity on PET CT (Figure ).
A biopsy of the palatal lesion was performed, which showed SCC (well-differentiated), with parakeratosis, acute, and chronic inflammation (Figure ).
Immunohistochemistry by p16 shows diffuse nuclear and cytoplasmic staining of well-differentiated SCC (Figure ). PD-L1 test showed a combined positive score of 10-15. CT chest, abdomen, and pelvis were negative for metastasis. NM bone scan showed radiotracer uptake in paranasal sinuses/facial bones. PET scan showed diffuse FDG activity in the hard palate, mildly hypermetabolic cervical, pretracheal, subcarinal, and left hilar nodes with minimal FDG activity. A diagnosis of locally advanced (stage IVa) oral cavity SCC was made. The patient was evaluated by a multidisciplinary team including an oncologist, head and neck surgeon, maxillofacial surgeon, radiation oncologist, and nutritionist for further management. The patient underwent prosthetic rehabilitation. A palatal obturator (prosthesis) was placed to improve his speech, eating, and prevent regurgitation. The patient opted for palliative care and did not want to pursue further treatment. He was discharged home.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [97.4, 'degrees fahrenheit'], 'Heart Rate or Pulse': [97.0, 'beats per minute'], 'respiratory rate': [14.0, 'breaths per minute'], 'White blood cell count': [9600.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 97.4 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 65.4 = 36.33333 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 97.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 9600.0 count/m^3. To convert 9600.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 9600.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 9.6e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 14.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6637,51,SIRS Criteria,diagnosis,integer,usmle-8344,Extracted,"A 63-year-old man presents to the physician with fever for 5 days. He has had increasing fatigue and dyspnea for the past 2 months. During this time, he has lost 3 kg (6.6 lb). He received outpatient treatment for pneumonia last month. He had urinary tract infection 2 weeks ago. He takes no other medications other than daily low dose aspirin and recent oral antibiotics. He does not smoke or drink alcohol. The vital signs include: temperature 38.5°C (101.3°F), pulse 93/min, respiration rate 18/min, and blood pressure 110/65 mm Hg. On physical examination, he has petechiae distally on the lower extremities and several purpura on the trunk and extremities. Several enlarged lymph nodes are detected in the axillary and cervical regions on both sides. The examination of the lungs, heart, and abdomen shows no abnormalities. The laboratory test results are as follows:
Hemoglobin 10 g/dL
Mean corpuscular volume 90 μm3
Leukocyte count 18,000/mm3
Platelet count 40,000/mm3
A Giemsa-stained peripheral blood smear is shown by the image.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.5, 'degrees celsius'], 'Heart Rate or Pulse': [93.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [18000.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.5 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 93.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 18000.0 count/m^3. To convert 18000.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 18000.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 2e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6638,51,SIRS Criteria,diagnosis,integer,pmc-6406221-1,Extracted,"The patient was a Japanese 72-year-old man, who had been diagnosed with atypical chronic myeloid leukemia (aCML) in 2014. He was an ex-smoker who did not regularly consume alcohol. In September 2015, treatment with oral cytarabine ocfosfate hydrate was initiated. After four cycles, he developed pneumonia, and treatment was terminated in February 2016. In April 2016, although he had no complaints, his serum C-reactive protein level was found to have re-increased to 4.6 mg/dL, and a chest X-ray and high-resolution computed tomography (HRCT) revealed scattered small nodular shadows and patchy consolidation (Figure A,B). The radiological findings did not improve despite the administration of antibiotics and antifungal drugs.
We performed bronchoscopy in May 2016. Bronchoalveolar lavage performed in the right upper lobe recovered 90 mL of 150 mL (60%) with 1.3 × 105/mL cells (neutrophils: 26%, lymphocytes: 36%, eosinophils: 1%, and macrophages: 37%). The histological examination of a specimen obtained from the right upper lobe via transbronchial lung biopsy revealed findings consistent with OP (Figure A). On immunofluorescence testing, the patient's antinuclear antibody titer was <40, and no other autoantibodies, including anti-SS-A, anti-aminoacyl tRNA synthetase antibody, rheumatoid factor, and anti-cyclic citrullinated peptide antibody, were detected. We diagnosed the patient with secondary OP associated with aCML. Treatment with prednisolone (30 mg, daily) was initiated, which resulted in the improvement of the laboratory and radiological findings, and the dose of prednisolone was then gradually tapered (Figure ). In September 2016, the patient developed general fatigue while under treatment with prednisolone (17.5 mg, daily). Chest CT revealed diffuse ground-glass opacities (GGOs). We considered the possibility of a recurrence of OP, and therefore increased the dose of prednisolone to 30 mg, daily; however, the patient's condition did not improve.
The patient was admitted to our hospital due to dyspnea on effort in November 2016. On admission, a physical examination revealed the following findings: respiratory rate, 15 breaths per minute; heart rate, 80 beats per minute; blood pressure, 106/60 mm Hg; and body temperature, 37.3°C. Chest auscultation revealed no abnormalities.
The laboratory tests performed on admission included an arterial blood gas analysis under ambient air, which showed the following findings: partial pressure of oxygen, 60.3 Torr; partial pressure of carbon dioxide, 30.4 Torr; and pH, 7.446. A blood analysis revealed the following findings: white blood cell count, 41 900/μL (neutrophil, 88.0%; lymphocytes, 5.0%; monocytes, 2.0%; promyelocytes, 1.0%; and myelocytes, 3.0%; metacytes, 1.0%); hemoglobin, 7.8 g/dL; platelet count, 34.2 × 104/μL; lactate dehydrogenase, 564 IU/L, Krebs von den Lugen-6, 2826 U/mL; and carcinoembryonic antigen, 15.6 ng/mL. The patient was negative for β-D glucan and cytomegalovirus antigen. HRCT showed diffuse GGOs in both lung fields (Figure C,D).
On the following day, we performed bronchoscopy with bronchoalveolar lavage in the right middle lobe. The bronchoalveolar lavage fluid showed a light milky appearance (Figure B) and was periodic acid-Schiff (PAS)-positive. Transbronchial lung biopsy revealed the precipitation of dense, homogenous, eosinophilic material, which had a fine granular appearance, and which filled the alveoli (Figure C); however, no evidence of OP was found. Based on these findings, he was diagnosed with PAP. Although the granulocyte/macrophage colony-stimulating factor autoantibody level was not measured, the diagnosis of sPAP was confirmed by compatible radiological findings and a pre-existing diagnosis of aCML.,
He gradually developed respiratory failure with the progression of PAP; whole-lung lavage was subsequently performed. Unfortunately, the patient died of acute enteritis within 1 month of whole-lung lavage.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.3, 'degrees celsius'], 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'respiratory rate': [15.0, 'breaths per minute'], 'White blood cell count': [41900.0, 'µL'], 'PaCO2': [30.4, 'mm hg']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.3 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 80.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 41900.0 count/µL. To convert 41900.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 41900.0 white blood cell count/µL * 1.0 µL/mm^3 = 41900.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 15.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 30.4 mm Hg, which is less than than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 1 + 1 = 2 criteria met.
Hence, the the number of SIRS criteria met by the patient is 2."
6639,51,SIRS Criteria,diagnosis,integer,pmc-5297566-1,Extracted,"A 60-year-old man was referred to our hospital for raised serum creatinine. The patient had abdominal pain for 15 days, which was mild, vague and non-radiating. It was followed by bilateral pedal edema in a day and in next three days followed by sudden onset bilateral foot drop with numbness. Patient gave history of nausea, vomiting, skin rash, anorexia and malaise since 20 days. He had weight loss of 10 kg in last 20 days. The past medical history was unremarkable. Alcohol consumption and drug abuse were absent. On physical examination, temperature was 38.4°C, blood pressure was 160/100 mm Hg, pulse rate 84/min and respiratory rate 20/min. Pedal edema was pitting, bilateral. Macular skin rashes around both ankles were present. Testicular tenderness was present. There was sensory and motor involvement in bilateral tibia and peroneal nerve distribution. Funduscopic examination showed grade 3 hypertensive retinopathy. Laboratory examination revealed a hemoglobin of 12.1 g/dl, white blood cell count of 24000/µl, platelet count of 485000/µl. Serum creatinine was 2.4 mg/dl, blood urea nitrogen 102 mg/dl, potassium 5.0 mEq/l, albumin 3.1 g/dl, aspartate aminotransferase 27 U/l, alanine aminotransferase 20 U/l, alkaline phosphatase 131 U/l and total cholesterol 198 mg/dl. Prothrombin and partial thromboplastin times were normal. Urinalysis revealed proteinuria, with two to three oval fat bodies per high-power field. Protein excretion was 3.4 g/day. Bence jones proteinuria, urine immunoelectrophoresis showed non selective proteinuria. On admission, HBsAg, HBeAg and anti-HBc IgM were positive. Anti-HBs, anti-HBe, anti-HCV and anti-HIV were negative. Serum HBV-DNA level (PCR) was 582917 copies/ml. ANA, anti-dsDNA, RF, p-ANCA, c-ANCA, and cryoglobulins were negative. Serum C3 and C4 complement levels were normal. Chest x-ray and electrocardiography were normal. The nerve conduction study was compatible with axonal and demyelinating polyneuropathy in bilateral lower limbs. A kidney biopsy was performed due to nephrotic range proteinuria and revealed membranous nephropathy (MN). All glomeruli were mildly enlarged. Capillary lumina were open and lined by thickened membranes and there was spikes on the external side of the glomerular basement membrane (GBM) (Jones stain). Mild uniform matrix accentuation with normal cell distribution was noted. Tubules were moderately degenerated. Interstitial area was moderately prominent for edema with leucocyte infiltration. Immunofluorescence study, showed significant granular IgG deposition along the membranes of capillary in a diffuse pattern (). There was no immunofluorescent staining for fibrinogen, IgA, or IgM. Congo-red staining for amyloid was negative. A liver biopsy was not performed. Doppler study for renal vessels was normal and there were no microaneurysms characteristic of PAN. Prednisolone (60 mg/day), plasmapheresis (5courses) and entecavir (0.5 mg/ every second day) were started. At 2 months follow up, patient improved in the form of grade 3/5 power in both lower limbs with sensory improvement. Twenty-four hours proteinuria decreased to 800 mg/day and serum creatinine was 1.5 mg/dl with no pedal edema.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.4, 'degrees celsius'], 'Heart Rate or Pulse': [84.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [24000.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.4 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 84.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 24000.0 count/µL. To convert 24000.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 24000.0 white blood cell count/µL * 1.0 µL/mm^3 = 24000.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6640,51,SIRS Criteria,diagnosis,integer,pmc-8293092-2,Extracted,"A 21-year-old female patient with no significant past medical history presented to the emergency department with presyncope. Three weeks prior to her presentation, she tested positive for COVID-19 infection after developing symptoms of shortness of breath and chest pain. She was quarantined at her home and treated symptomatically with improvement. She never required hospitalization for her symptoms nor medications. She denied smoking and alcohol or illicit drug use along with any other medication that could cause QT interval prolongation. Upon her presentation, her physical examination was noted to be significant for bradycardia. Her vitals were blood pressure of 118/63 mmHg, a heart rate of 45 bpm, a temperature of 98.3 °F, and a respiratory rate of 18 sating 100% on room air. Her electrocardiogram showed 45 bpm with narrow QRS complex and premature atrial complexes.
Significant laboratory results included a WBC of 18.24 k/μL (3.60–9.50), troponin negative at <0.03 ng/mL (≤0.04), normal TSH at 3.79 uIU/mL (0.34–5.60), CRP at 27.00 mg/L (≤10.00), ESR at 51 mm/h (0–20), procalcitonin at <0.02 ng/mL (0.00–0.10), a COVID-19 PCR positive, BNP at 160 pg/mL (≤100), lactate at 1.2 mmol/L (0.5–2.2), and a negative urine drug screen. The chest X-ray showed no acute events. The transthoracic echocardiogram was normal with an EF of 60%. The patient was walked on treadmill and her junctional heart rhythm increased to 91 bpm; she was given 1 mg of atropine IV over a period of 5 min, in which her sinus rate increased to >100 bpm. Given the improvement in the patient’s symptoms, there was no indication for a dual chamber pacemaker. Hence, she was started on theophylline 200 mg oral dose daily with follow up within 1 week at the clinic (A,B). Upon her follow up, she had a heart rate of 90 bpm while on theophylline and no side effects were reported. Later, at her 5-week follow up visit, a complete resolution of her symptoms was reported and theophylline use was discontinued.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [98.3, 'degrees fahrenheit'], 'Heart Rate or Pulse': [45.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [18240.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 98.3 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 66.3 = 36.83333 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 45.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 18240.0 count/µL. To convert 18240.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 18240.0 white blood cell count/µL * 1.0 µL/mm^3 = 18240.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6641,51,SIRS Criteria,diagnosis,integer,pmc-8403091-1,Extracted,"A 6-year-old girl (height 110 cm, weight 20.3 kg) with no medical history had a fever 1 month before surgery. She visited a clinic and general hospital due to jaundice and malaise. At admission to the general hospital 2 weeks before surgery, she was diagnosed with acute hepatitis and was given liver protection drugs (Stronger Neo-Minophagen C, Lactulose, Vitamin K) and fresh frozen plasma, although her liver and coagulation function deteriorated during the course of treatment, along with decrease in platelet count. She was transferred to the pediatric intensive care unit (PICU) of our children's medical center for blood purification therapy 4 days before surgery.
On examination, she looked ill. Physical examination revealed the following: blood pressure 95/56 mm Hg, pulse rate 72 beats/min, respiratory rate 20 breaths/min with SpO2 of 99% on room air, body temperature 37.3 °C, and Glasgow Coma Scale (GCS) score of E3V4M6. Abdominal examination was unremarkable, with no hepatosplenomegaly. Examination of the eyes and skin revealed icterus.
Initial laboratory investigations revealed thrombocytopenia (hemoglobin 13.0 g/dL, white cell count 3.4 × 103/μL, platelet count 9.1 × 104/μL). Electrolytes were normal (Na 139 mmol/L, K 4.2 mmol/L, Cl 103 mmol/L, Ca 9.5 mg/dL, Mg 2.3 mg/dL, P 3.9 mg/dL). Her coagulation profile was prolonged (prothrombin time 23%, prothrombin time-international normalized ratio 2.36, activated partial thromboplastin time 63.7 s) and liver function tests were abnormal (albumin 4.0 g/dL, total bilirubin 18.76 mg/dL, direct bilirubin 13.17 mg/dL, venous ammonia 70 μg/dL, lactate 2.2 mmol/L). Infectious disease screening tests were negative. Computed tomography (CT) scan of her abdomen showed lower absorption in the liver compared to the spleen, suggesting ALF. Cranial CT scan and fundus examination were normal. Electroencephalogram (EEG) showed slow spindle waves with a frequency of 1–2 Hz, without laterality or triphasic waves (Fig. a). Daily plasma exchange and continuous hemodiafiltration were started for ALF with HE. Mannitol was administered to prevent cerebral edema. A day before surgery, GCS scores worsened to E1VTM1. Clinically, she was unresponsive to pain and auditory stimuli, and her EEG showed high voltage continuous slow waves with a frequency of 0.5–1 Hz, without lateralization (Fig. b). Assuming deterioration of HE, emergency LT was considered vital. After obtaining informed consent from her family, urgent living donor LT with an extended left liver graft from her mother was planned on the 5th ICU day.
General anesthesia was induced with fentanyl (50 mcg) and rocuronium (20 mg) and maintained with remifentanil and rocuronium infusions (0.1–0.4 mcg/kg/min and 7 mcg/kg/min, respectively), along with sevoflurane inhalation at 0.5%. A BIS Quatro Brain Monitoring Sensor (Medtronic plc, Dublin, Ireland) was placed on the frontotemporal region, and her electroencephalogram, including BIS values, 95% spectral edge frequency (SEF95), and suppression ratio (SR), was continuously recorded at each phase of liver transplantation by the BIS monitor until the end of anesthesia (Fig. , Fig. a–d). The durations of anesthesia and surgery were 708 min and 637 min, respectively. The graft volume was 254 g, graft volume/recipient standard liver volume (GV/SLV) was 46.1%, and graft-to-recipient weight ratio (GRWR) was 1.27%. Warm and cold ischemia times were 40 min and 51 min, respectively. BIS values ranged from 10 to 20 from the start of the operation to reperfusion (Fig. ). From reperfusion to the end of the operation, BIS values ranged from 10 to 80, and the variation in BIS values also increased. The frequency of EEG waveforms and BIS values seen with BIS monitoring gradually increased (Fig. ). She was re-admitted to the PICU after surgery, extubated on postoperative day (POD) 2 and discharged from the PICU on POD 7. Follow-up EEG on POD 5 showed low amplitude and fast waves with a frequency of 9–10 Hz, without laterality or paroxysmal waves (Fig. c). However, she spoke only a few words until POD 7. Two weeks postoperatively, she was newly diagnosed with hepatitis-associated aplastic anemia. Her immunosuppressant regimen was changed and continued for post liver transplantation prophylaxis and aplastic anemia. She was discharged after 4 months of hospitalization. The cause of liver failure in the present case remains unknown.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.3, 'degrees celsius'], 'Heart Rate or Pulse': [72.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [3400.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.3 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 72.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 3400.0 count/µL. To convert 3400.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 3400.0 white blood cell count/µL * 1.0 µL/mm^3 = 3400.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6642,51,SIRS Criteria,diagnosis,integer,pmc-7149248-1,Extracted,"A 46-year-old Japanese man without a remarkable medical history visited our hospital with chief complaints of fever, fatigue, generalized edema, and abdominal distention. His fever started two weeks prior to admission. Abdominal distention and edema gradually worsened, and he gained 7 kg of weight within two weeks, despite low food intake owing to loss of appetite. He denied previous episodes of infectious diseases. At initial presentation, he appeared exhausted. His vital signs were as follows: body temperature, 37.8 °C; blood pressure, 160/93 mmHg; heart rate, 109 beats/min; respiratory rate, 22 breathes/min; and oxygen saturation, 90% with room air. On physical examination, generalized pitting edema was observed. His heart sounds were normal, but his lung sounds were weak at the lung base on both sides. Jaundice was not observed, but a distended abdomen and hepatomegaly were observed. Blood test results on the day of admission revealed an elevated white blood cell (WBC) count (14,600/μL), mild anemia (hemoglobin level, 11.1 g/dL), thrombocytopenia (platelet count, 11.1 × 104/μL), renal impairment (blood urea nitrogen level, 60.7 mg/dL and serum creatinine level, 2.94 mg/dL), an elevated C-reactive protein (CRP) level (14.25 mg/dL), an elevated ALP level (768 U/L), polyclonal hypergammaglobulinemia (immunoglobulin G [IgG], 2461 mg/dL), and an elevated IgG4 level (235 mg/dL). Immunological screening test results for autoantibodies were negative, except for positive antinuclear antibody (× 40) and anti-SS-A antibody. Polymerase chain reaction for HHV-8 DNA in a serum sample was negative (Table ). Computed tomography (CT) performed on the day of admission revealed massive pleural effusions and ascites, generalized mild lymphadenopathy (< 1.5 cm in diameter), and hepatosplenomegaly (Fig. ). Echocardiography performed on day 2 revealed normal wall motions without any sign of valvular disease, but a collapsed inferior vena cava was observed (maximum diameter < 5 mm). 18F–fluorodeoxyglucose positron emission tomography (FDG-PET) revealed no apparent FDG uptake, except for slight uptake in the para-aortic lymph nodes (Fig. ). Considering the positive anti-SS-A antibody finding, lip biopsy was performed on day 6, but the pathological findings did not meet the criteria for Sjögren syndrome (SjS). On ophthalmological examination, keratoconjunctivitis was not observed; however, bilateral optic edema was remarkable (Fig. ). Serum IL-6 and plasma VEGF levels were assessed in a blood sample obtained on day 9, and both were elevated (25.2 pg/mL and 224 pg/mL, respectively). Abdominal paracentesis was performed on the same day, and the levels of IL-6 and vascular endothelial growth factor (VEGF) in ascites were remarkably high (3310 pg/mL and 335 pg/mL, respectively). Bone marrow examination was performed on day 9. Bone marrow aspiration was dry tap, and bone marrow biopsy revealed a mild increase in megakaryocytes and mild reticulin myelofibrosis on silver impregnation staining (Fig. ). Biopsy of a cervical lymph node was performed on day 10, and the pathological findings were compatible with a mixed-type MCD histology (Fig. ). We suspected TAFRO syndrome and methylprednisolone (mPSL) pulse therapy (500 mg/day for three consecutive days) was initiated on day 10 after lymph node biopsy, followed by intravenous PSL (40 mg/day) and oral CsA administration. The disease severity of TAFRO syndrome one day prior to treatment initiation was very severe (grade 5) []. After the initiation of immunosuppressive treatment, the patient became afebrile and the CRP level returned to the normal range within two weeks. However, the patient’s platelet count and serum creatinine level as well as his overall condition did not improve, even after the initiation of immunosuppressive treatment (Fig. ). A central venous catheter was inserted and total parenteral nutrition was started as he could not eat owing to loss of appetite and refusal of tubal feeding. Diuretics, including furosemide, potassium canrenoate, trichlormethiazide, and tolvaptan were administered during hospitalization; however, the amount of ascites did not decrease (Fig. ). Urinalysis performed on day 25 revealed mild proteinuria (0.34 g/day) with a fractional excretion of sodium of 5.1% and a fractional excretion of urea nitrogen (FEUN) of 20.7%. Because urinalysis was performed under diuretics use, considering FEUN level and intravascular hypovolemia on echography, intravenous fluid replacement was performed to correct the pre-renal factor responsible for renal impairment. However, the patient’s volume depletion and blood pressure did not respond well to intravenous fluid replacement. Abdominal paracentesis was again performed on day 40, and it revealed persistently high levels of IL-6 and VEGF (4320 pg/mL and 421 pg/mL, respectively). Although urine volume was initially preserved with diuretic administration, the patient became oliguric from day 47 and anuric from day 49. He was hemodynamically unstable on day 50 (body temperature, 37.5 °C; blood pressure, 84/52 mmHg; heart rate, 109 beats/min; respiratory rate, 24 breaths/min; oxygen saturation, 95% with room air). As the patient was undergoing immunosuppressive therapy and his CRP levels increased by 10.08 mg/dL on the same day, systemic examination was performed to rule out the possibility of infectious disease. Analysis of ascites was performed on the same day, revealing purulent ascites, and Escherichia coli was isolated. E. coli was also isolated from blood cultures. CT of the chest showed a mass in the right lung (Fig. ) in addition to scattered appearance of high intensity regions in the myocardium, which were newly observed (Fig. ). Blood tests performed on day 50 revealed elevated β-d-glucan levels (23.0 pg/mL) and positive cytomegalovirus (CMV) antigenemia (41 cells/5 × 104 WBCs on the C7-HRP test). Aspergillus, Candida mannan, and Cryptococcus neoformans antigens were negative. We suspected bacterial peritonitis and fungal pneumonia. Intravenous meropenem, vancomycin, and caspofungin were initiated on the same day. Continuous renal replacement therapy (CRRT) using a polymethyl-methacrylate membrane was also initiated on the same day because anuria did not improve and the patient was hemodynamically unstable. Conditions of CRRT were as follows: mode, continuous hemodiafiltration; dialysis membrane, CH-1.8 W (Toray Medical Co., Ltd., Tokyo Japan); and anticoagulant, nafamostat mesilate. The blood, dialysate, substitute, and filtration flow rates were 100 mL/min, 400 mL/h, 400 mL/h, and 800 mL/h, respectively.
However, approximately 10 h after CRRT initiation, cardiac arrest (ventricular fibrillation followed by pulseless electrical activity) suddenly occurred. Return of spontaneous circulation (ROSC) was achieved by cardiopulmonary resuscitation with epinephrine injections. STEMI was suspected from electrocardiography findings obtained immediately after ROSC (Fig. ). Echocardiography performed immediately after ROSC revealed a generalized hypokinesis and akinesia of the anterior wall, septum, and apex without any apparent calcification of the cardiac wall. Blood tests performed after ROSC revealed a slightly elevated serum creatine kinase-MB level (80 U/L, normal range: < 25 U/L) and a remarkably elevated troponin I level (1.2904 ng/mL, normal range: < 0.0262 ng/mL), indicating the acute phase of MI. Emergent coronary angiography (CAG) was performed on the same day. On CAG, complete occlusion of the left anterior descending coronary artery was observed, and reperfusion was achieved through percutaneous old balloon angioplasty (Fig. ). An intra-aortic balloon pump was inserted to increase coronary blood flow and improve cardiogenic shock. However, even after successful coronary intervention, the patient was still hemodynamically unstable. Despite intensive care, the patient died on day 52.
Autopsy was performed after obtaining consent from the patient’s relatives. The histological findings of autopsy are shown in Fig. . In this case, multiple infections, including bacterial peritonitis (small abscesses were observed in the abdominal space, and gram-positive cocci and gram-negative rods were identified), systemic CMV infection (including the lungs, pancreas, and adrenal glands), and Trichosporon asahii infection in the lungs (T. asahii was isolated from sputum culture) were observed. Intravascular invasion of fungal hyphae was noted in the lungs. On histological evaluation of the heart, coagulation necrosis and neutrophil infiltration were observed, findings that were compatible with MI that occurred a few days before the autopsy. Considering that intravascular invasion of fungal hyphae was observed, embolization caused by fungal hyphae was a possible cause of MI in this case. Necrotic changes were observed in most internal organs. We considered multiple organ failure due to multiple severe infections and circulatory failure due to MI as the main causes of death in this patient. Although there was no stenotic lesion and vascular calcification was not apparent in the left anterior descending coronary artery, myocardial calcification was noted. Calcification in the skeletal muscle cells of the diaphragm and iliopsoas muscle without vascular calcification was also noted. The pathological findings of the kidney were compatible with thrombotic microangiopathy (TMA) and endothelial injury was noted, although fibrin thrombi were not observed in arterioles. IgA, IgG, and IgM were negative on immunofluorescence. Tubulointerstitial changes could not be evaluated because most of the tissue was necrotic due to changes after death and circulatory failure prior to death. In the bone marrow reevaluation, the number of megakaryocytes did not increase, and reticulin myelofibrosis was not remarkably changed. In the lymph node reevaluation, infiltration of plasma cells was decreased, and immunosuppressive therapy appeared partially effective, although the amount of ascites and IL-6 levels in ascites did not decrease in the present case. Fibrotic changes in the fat tissue of the anterior mediastinum were noted.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.8, 'degrees celsius'], 'Heart Rate or Pulse': [109.0, 'beats per minute'], 'respiratory rate': [22.0, 'breaths per minute'], 'White blood cell count': [14600.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.8 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 109.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 14600.0 count/µL. To convert 14600.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 14600.0 white blood cell count/µL * 1.0 µL/mm^3 = 14600.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6643,51,SIRS Criteria,diagnosis,integer,pmc-3548148-1,Extracted,"An 81-year-old woman was referred to the emergency department with abdominal pain and vaginal discharge that had lasted for 4 days. Medical history included right nephrectomy for a renal stone 21 years earlier and medication for arterial hypertension 4 years earlier. The pain was localized to the lower abdomen without aggravating factors. Upon admission to the department of gynecology, the patient looked ill and had a temperature of 37.4℃, a blood pressure of 134/59 mmHg, a pulse of 77 beats/min, and a respiratory rate of 18 breaths/min. The abdomen was slightly distended and tender over the lower abdomen, without signs of generalized peritoneal irritation. Pelvic examination showed an atrophied vagina and cervix, and a yellowish foul odorous vaginal discharge from the cervical os. Laboratory test results were within normal limits, except for a white blood cell count of 27,580/µL and a neutrophil fraction of 88.3%. Culture of the vaginal discharge revealed Escherichia coli and Enterococcus avium. Endovaginal sonography showed fluid collection measuring 2.7 × 2.4 cm in the endometrium, suggesting a pyometrium. Abdominopelvic computed tomography (CT) showed a myometrial abscess cavity in the uterus and diverticulosis of the sigmoid colon. Tomography also showed that the uterine had joined to the thick sigmoid wall (). However, no definite fistula tract was visible. A colouterine fistula caused by diverticulitis was suspected. Therefore, fistulography was performed. When contrast fluid was injected through the cervical os, spillage of the contrast fluid into the sigmoid colon via the left side of the abscess cavity of the uterine fundus was observed (). On colonoscopy, multiple diverticula were noted at the sigmoid colon, and a suspected lesion of the fistula opening with surrounding edema and emission of air bubbles was detected approximately 25 cm from the anal verge (). The patient was diagnosed with a colouterine fistula caused by diverticulitis and was transferred to the department of surgery for a collaborative operation.
During the operation, inflammatory adhesion of the distal sigmoid colon to the posterior wall of the uterus was found (). The colon was dissected off the uterus, and a fistula between the sigmoid colon and the endometrial cavity was identified. Primary resection of the sigmoid colon, including the affected segment, with anastomosis and repair of the fistula tract of the uterus were performed. The intrauterine purulent content was drained through the cervical os. In terms of gross appearance, the excised portion showed a fistula tract in the colonic wall (). The postoperative course was uneventful, and the patient was discharged on the ninth postoperative day.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.4, 'degrees celsius'], 'Heart Rate or Pulse': [77.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [27580.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.4 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 77.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 27580.0 count/µL. To convert 27580.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 27580.0 white blood cell count/µL * 1.0 µL/mm^3 = 27580.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6644,51,SIRS Criteria,diagnosis,integer,pmc-6803741-1,Extracted,"A 65-year-old African American female with past medical history significant for noninsulin-dependent type 2 diabetes mellitus, essential hypertension, dyslipidemia, chronic back pain, morbid obesity (body mass index (BMI) was 41), gastroesophageal reflux disease (GERD), uterine fibroids, generalized anxiety disorder, and former tobacco abuse presented to the emergency department (ED) complaining of generalized abdominal pain of 3 weeks' duration with intermittent diarrhea and constipation. Upon review of systems, she complained of atypical chest pain which was pleuritic and reproducible on palpation. The chest pain was nonexertional but she had exertional dyspnea. Of note, she had no prior history of cardiovascular disease.
Past surgical history was remarkable for cesarean section and hysterectomy. Prior to admission medications included metformin, hydrochlorothiazide, propranolol, ranitidine, and acetaminophen. Family history was remarkable for diabetes. In terms of social history, she was a former tobacco smoker, drank alcohol socially, and denied illicit drug use. She had a history of allergy to hydroxyzine, propoxyphene, and zomepirac.
In the ED, measurement of vital signs showed a temperature of 37.0°C, heart rate of 88 beats per minute, respiratory rate of 18 breaths per minute, blood pressure of 148/82, and pulse oxygen saturation of 99% on room air. Initial physical examination was normal except for obesity, depressed mood, chest wall tenderness, mild abdominal distention with tympanic note to percussion and mild generalized nonspecific tenderness to palpation. Rectal exam showed small nonbleeding external hemorrhoids. Complete blood count and basic metabolic panel were normal except for blood glucose of 240 milligrams/deciliter (mg/dL). Hemoglobin A1c was 9.3%. Troponin I was slightly elevated at 0.07 and it trended down on second measurement. Electrocardiogram showed normal sinus rhythm with new T-wave inversion in the inferolateral leads. Computed tomography angiography (CTA) of the chest, abdomen, and pelvis was only remarkable for fecal stasis in the rectum. Her abdominal pain and constipation was partially relieved after administration of IV morphine and senna-docusate.
She was also given aspirin for the chest pain. After her abdominal symptoms moderately improved, she was placed in the observation unit for cardiology consultation. After evaluation by the cardiologist, she was admitted to a telemetry unit for an inpatient cardiac stress test. She was receiving 81 mg aspirin daily. On day 2 of hospital admission, she underwent myocardial perfusion scan using the standard 0.4 mg regadenoson (LEXISCAN) injection. The stress test showed reversible perfusion defect involving the apex and lateral wall of the left ventricle, suggesting myocardial ischemia. At that time, clopidogrel (Plavix) was added to aspirin and the patient was started on IV heparin per ACS protocol pending cardiac catheterization. On day 4, coronary angiography was performed and it showed no significant occlusive coronary artery disease (CAD). During the catheterization procedure, the patient received IV heparin and IV nitroglycerin in addition to midazolam for sedation and fentanyl for analgesia. The radio contrast used was iohexol (OMNIPAQUE 350). Post-procedure, IV heparin was discontinued while DAPT with aspirin and Plavix were resumed.
After recovery from sedation, the patient complained of a headache which got progressively worse within a few hours. It did not improve with repeated doses of oral hydrocodone and oral/IV acetaminophen. After around 12 hours of cardiac catheterization, the patient developed acute left-sided ptosis, deviated gaze (down and outward palsy), and anisocoria with left pupillary dilation (mydriasis) consistent with acute left 3rd nerve palsy (). The patient did not complain of decreased vision and visual field testing by confrontation was normal. She had no other sensory or motor deficits. Her mental status examination did not show evidence of confusion. Her vital signs were normal. STAT CT head without contrast (per stroke protocol) was read as negative for acute intracranial process. CTA of the head and neck was negative for arterial stenosis or aneurysms. The next day, MRI head and orbit with and without contrast were done using Gadodiamide as the MRI contrast agent. The MRI report, as read in our hospital, indicated a nonenhancing heterogeneous pituitary mass measuring 1.9 × 2.0 cm in the greatest dimension and slightly compressing on the optic chiasm suggestive of pituitary macroadenoma (). There was no report of any bleed/infarction by either CT or MRI report.
A multidisciplinary team approach was undertaken with involvement of neurology, endocrinology, ophthalmology, otolaryngology (ENT), and neurosurgery. A full ophthalmological examination was normal except for complete left 3rd nerve palsy and mild cataracts. Visual field testing was normal. Hormonal studies were ordered and the results were as shown in . Of note, prolactin was lower than normal, while adrenocorticotropic hormone (ACTH) level was above the reference range. Both follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were considered low given the patient's postmenopausal status. The patient had normal random cortisol and free T4 level. She did not receive any IV glucocorticoids. The next day after the third nerve palsy, the patient developed a mild fever at 37.9°C with mild neutrophilic leukocytosis (white blood cell count 14.2 K/UL). The patient was transferred to a neuro step-down unit for close observation. Her vital signs remained mostly normal. Subjectively, she neither had a progression of symptoms nor developed new symptoms. Her headache was controlled with oral hydrocodone/acetaminophen. Her full neurologic examination remained normal except for isolated complete left oculomotor palsy. Leukocytosis gradually normalized over several days.
Pituitary apoplexy was highly suspected as a cause of the third nerve palsy, but the diagnosis was challenged by the fact that our radiologist's interpretation of imaging did not mention bleed or cavernous sinus extension. The diagnosis of diabetic neuropathy of the third nerve from microvascular ischemia was contemplated but it was felt less likely because it is usually pupil-sparing []. Neurosurgery requested ENT help for trans-sphenoidal pituitary resection. ENT did not feel comfortable with the plan and recommended transfer to a higher level center. The patient and her family were involved in decision making. They were truthfully told that our medical center is not a high volume center for such pituitary cases and the patient might benefit from a transfer to a more experienced center. They chose to transfer and the patient was transferred by ambulance to an academic center of excellence on day 7 of presentation.
There, neuroradiologists read the images obtained at our hospital differently. The new CT scan report indicated increased attenuation of the sella turcica and in the suprasellar cistern at the site of the patient's pituitary mass, suggestive of possible hemorrhage within the tumor (). The new MRI report indicated that there was a sellar/suprasellar mass lesion which appeared to show central intrinsic T1 shortening and hypoenhancement with peripheral right-sided enhancement. There was mass effect on the optic chiasm superiorly. The lesion appeared to extend laterally into the left cavernous sinus with mild mass effect on the cavernous internal carotid artery. The overall hypoenhancing portion measured 2.1 × 1.9 × 1.3 cm (Figures and ).
The physicians in the other hospital decided to proceed with surgical intervention hoping to relieve the pressure on the third nerve. On day 9 of symptoms, the patient underwent successful trans-sphenoidal pituitary resection. Intraoperatively, the neurosurgeon reported a typical contused apoplectic adenoma. A frozen section biopsy report, as well as final pathology report, confirmed necrotic pituitary tumor with evidence of recent hemorrhage. The apoplectic adenoma was removed and the pituitary gland was left intact. Postoperatively, the laboratory assessment indicated central hypothyroidism and secondary adrenal insufficiency. Vital signs were stable. No major sodium abnormalities were noted. The patient was started on oral hydrocortisone and levothyroxine. Otherwise, the immediate postoperative course was uneventful and the patient was discharged home on day 11 of symptoms development. One-month follow-up at the neurosurgeon's office was remarkable for persistence of oculomotor palsy. A six-month follow-up is scheduled.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.0, 'degrees celsius'], 'Heart Rate or Pulse': [88.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [14.2, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 88.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 14.2 count/µL. To convert 14.2 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 14.2 white blood cell count/µL * 1.0 µL/mm^3 = 14.2 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6645,51,SIRS Criteria,diagnosis,integer,pmc-2770472-1,Extracted,"A 33-year-old man presented with fever, dyspnea, and odynophagia. Five months prior to admission, the patient had been treated for dental caries at a local hospital, and at that time examination revealed seropositivity for human immunodeficiency virus. On admission, temperature was 39.0'C, pulse 92 beats per minute, respiratory rate 20 breaths per minute and blood pressure 130/80 mmHg. Physical examination revealed oral thrush, consistent with findings of extensive esophageal candidiasis in endoscopic gastroduodenscopy performed five days before admission. Laboratory data on admission revealed a WBC count of 1,760/uL, Hb 10.9 g/dL, and platelet count of 297,000/uL. Arterial blood gas analysis while breathing room air revealed PaO2 of 48.0 mmHg, PaCO2 of 32.7 mmHg, and saturation of 88.5%, and the calculated (A-a)DO2 was 53.7. CD4 count and HIV viral load were 4/uL and 130,000 IU/mL, respectively. Diffuse bilateral infiltrates of both lung fields were noted, and no cystic lesions were observed on the chest X-ray and high resolution computed tomography (HRCT) taken on admission. Bronchoscopic alveolar lavage for diagnosis of P. jirovecii was carried out, and microscopic examination of the bronchoalveolar lavage fluid obtained showed P. jirovecii; no other microorganisms were detected by culture. Treatment with trimethoprim/sulfamethoxazole, fluconazole and corticosteroids at standard dosages was started. The patient had never been on HAART therapy prior to admission. HAART therapy was added to the treatment on the 8th hospital day. During the treatment with trimethoprim/sulfamethoxazole, pancytopenia worsened. Bone marrow biopsy revealed inflamed marrow and partial necrosis. Granulocyte colony stimulating factor was used without avail. On the 22nd hospital day, the chest X-ray obtained as the patient's hypoxemia worsened revealed pneumomediastinum. HRCT showed newly formed cystic lesions in both lung fields. Pneumomediastinum was treated conservatively with high oxygen supply. CD4 cell count and HIV levels were not followed during treatment. However, as the general condition of the patient deteriorated, the patient was started on intravenous pentamidine on the 23rd hospital day. On the 25th hospital day, his oxygen requirement increased. Without intubation, as the patient and guardian refused the patient being put on a ventilator due to multiple economical and sociological reasons, the patient died on the 26th hospital day.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.0, 'degrees celsius'], 'Heart Rate or Pulse': [92.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [1760.0, 'µL'], 'PaCO2': [32.7, 'mm hg']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.0 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 92.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 1760.0 count/µL. To convert 1760.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 1760.0 white blood cell count/µL * 1.0 µL/mm^3 = 1760.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 32.7 mm Hg, which is greater or equal to than 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6646,51,SIRS Criteria,diagnosis,integer,pmc-3346838-1,Extracted,"A 22-month-old girl was admitted to our hospital with a three-day history of cough and rhinorrhea, a one-day history of fever, and an episode of generalized tonic clonic seizure with fever that lasted around 10 to 15 minute at 15 hours before admission.
Upon arrival at the emergency center, her pulse rate was 140/min, blood pressure was 115/74 mmHg, respiratory rate was 28 breaths/min, and body temperature was 40.2℃. She had no spontaneous movement, no response to painful stimuli, no pupillary reflex, and no corneal reflex. Doll's eye movement was absent. Her pupils were 1 mm in diameter and nonreactive to light. Deep tendon reflexes were absent.
Approximately 1 hour after arrival she had a second generalized tonic clonic seizure with fever that lasted 10 seconds, and was treated with 0.3 mg/kg of intravenous diazepam. She had dark brown-colored hematemesis, so we performed L-tube irrigation with normal saline. A computed tomography (CT) scan indicated diffuse symmetric low density in the basal ganglia, thalami, and pons with brain swelling (). Because of brain swelling, unstable vital sign, and thrombocytopenia, we decided to defer lumbar puncture and after all we did not make it. She was admitted to the intensive care unit.
Her platelet count was 32,000/µL, white blood cell was 6,240/µL, aspartate aminotransferase was 4,579 U/L, alanine aminotransferase was 2,787 U/L, ammonia was 38 mmol/L and C-reactive protein was 1.0 mg/dL. Coagulation testing for prothrombin, partial thromboplastin and thrombin times, fibrin degradation products, and D-dimer were elevated. Blood urea nitrogen was 30 mg/dL and serum creatinine was 1.3 mg/dL. Creatine kinase-MB, myoglobin, and troponin-T were elevated. Respiratory virus polymerase chain reactions for influenza A and B, respiratory syncytial virus, adenovirus, metapneumovirus, and rhinovirus were negative, but the test for parainfluenza virus was positive on a nasal wash specimen. Serological tests for hepatitis viruses, mycoplasma, herpes virus, Japanese encephalitis virus, and salmonella were all negative.
Electroencephalography indicated extremely low voltage and featureless background rhythms (). Brain MRI performed on the day of hospitalization indicated diffuse bilateral symmetric signal changes of both basal ganglia, thalami, periventricular white matter, pons, and cerebral white matter, as well as generalized swelling of the brain. The involved areas were diffusely hypointense on T1W images () and hyperintense on T2W images (). We diagnosed the patient with ANE based on the clinical symptoms and MRI findings.
The patient was intubated and mechanically ventilated because of shallow breathing and profound alteration of sensorium on the day of hospitalization and she was treated with ceftriaxone, vancomycin, acyclovir, intravenous immunoglobulin, and methylprednisolone. A chest X-ray was normal at admission, but indicated right perihilar infiltration on the 5th day of admission. Her consciousness had no interval change, and blood pressure, heart rate, and urine output decreased on day 13. The 14th day of admission, she died due to multiple organ failure.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [40.2, 'degrees celsius'], 'Heart Rate or Pulse': [140.0, 'beats per minute'], 'respiratory rate': [28.0, 'breaths per minute'], 'White blood cell count': [6240.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 40.2 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 140.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 6240.0 count/µL. To convert 6240.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 6240.0 white blood cell count/µL * 1.0 µL/mm^3 = 6240.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 28.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6647,51,SIRS Criteria,diagnosis,integer,pmc-7667610-1,Extracted,"A 77-year-old male patient presented to the emergency department with intractable nausea and bilious and non-bloody vomiting of one-day duration. This was associated with diffuse abdominal pain which he described as dull, non-radiating, and moderate in severity. His symptoms were exacerbated by oral intake. Prior to his presentation, he had normal bowel movements. He denied chest pain, shortness of breath, cough, dysphagia, diarrhea, or constipation. Past medical and surgical histories were noncontributory. The patient previously smoked 1.5 packs per day for 20 years but quit 31 years ago. He reported moderate alcohol use and denied illicit drug use.
Three weeks prior to his presentation to the emergency department, he was diagnosed with stage IV pancreatic adenocarcinoma. He did not receive chemotherapy and elected for conservative management as well as palliative care. One day prior to his presentation, he underwent EUS-guided CPN for palliation of his debilitating pain. The procedure involved injecting bupivacaine and 98% absolute alcohol under general anesthesia to induce unilateral celiac plexus neurolysis. There were no immediate post-procedure complications, and the patient was discharged home in a stable condition soon after completion of the neurolysis. Of note, the patient was using oxycodone 5 mg oral tablets three times per day as needed for pain since his cancer diagnosis. In the last three weeks prior to the procedure, he did not complain of nausea or constipation. He also denied taking the medication more frequently than usual.
In the emergency department, vital signs demonstrated blood pressure of 115/73 mmHg, heart rate of 82 beats per minute, respiratory rate of 15 breaths per minute, and temperature of 37.2℃. Abdominal exam was significant for minimal epigastric tenderness without guarding or rebound tenderness. The remainder of the physical exam was noncontributory. Complete blood count (CBC) showed white blood cell (WBC) of 10.0 × 103/µL, hemoglobin of 12.3 g/dL, and platelet count of 295 × 103/µL. Basic metabolic panel (BMP) showed sodium of 135 mmol/L, potassium of 5.1 mmol/L, chloride of 96 mmol/L, creatinine of 1.34 mg/dL, glucose of 384 mg/dL, and anion gap of 9 mmol/L. Liver function tests showed aspartate transaminase (AST) of 12 U/L, alanine transaminase (ALT) of 17 U/L, alkaline phosphatase of 74 U/L, and total bilirubin of 0.4 mg/dL. Lipase was within reference range at 5.0 U/L. Urinalysis did not reveal ketones. Hemoglobin A1c was unremarkable at 5.4% and glucose levels normalized without treatment, suggesting that the initial hyperglycemia was probably related to stress.
The patient initially received intravenous fluids and was placed on a bowel rest regimen. Computed tomography (CT) scan of the abdomen showed significant gastric distension, which was concerning for obstruction at the level of the duodenum (Figure ).
Next, esophagogastroduodenoscopy (EGD) showed large amounts of fluids within the gastric fundus and body, which was also concerning for duodenal obstruction. The examined first and second parts of the duodenum were normal (Figure ).
As a result, upper gastrointestinal series with barium swallow was performed to look for an obstruction distal to the second part of the duodenum. Although it showed delayed gastric emptying of the contrast, contrast was seen in the third part of the duodenum and jejunum ruling out a complete obstruction in the duodenum (Figure ).
Finally, a push enteroscopy was performed to visualize the entire duodenum. It showed angulation in the third part of the duodenum but no obstruction or mucosal abnormalities in the third or fourth parts of the duodenum (Figure ).
At that point, extensive gastrointestinal workup ruled out small bowel obstruction, and the diagnosis of ileus was made. The patient received ondansetron and polyethylene glycol as needed, and his diet was advanced slowly. His symptoms improved over the course of a few days, and he experienced a return of normal bowel activity. He eventually tolerated a regular diet and was discharged home in a stable condition.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.2, 'degrees celsius'], 'Heart Rate or Pulse': [82.0, 'beats per minute'], 'respiratory rate': [15.0, 'breaths per minute'], 'White blood cell count': [10000.0, 'µL']}",0,0,0,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.2 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 82.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 10000.0 count/µL. To convert 10000.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 10000.0 white blood cell count/µL * 1.0 µL/mm^3 = 10000.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 0.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 15.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 0.
Hence, the the number of SIRS criteria met by the patient is 0."
6648,51,SIRS Criteria,diagnosis,integer,pmc-5494575-1,Extracted,"A 74-year-old woman visited the emergency department in our institute after multiple wasp stings. She complained of dizziness and whole body pain. More than 40 stings marks were found across her head, neck, both upper and lower extremities, buttocks, and back. On admission, blood pressure was 60/49 mmHg and pulse rate was 120 per minute. She was given intravenous fluids, hydrocortisone, and antihistamines. Her vital signs and symptoms recovered, and she was discharged. The next day, she returned to the hospital complaining of dyspnea, nausea, general ache, edema, and decreased amount of urine. She has a history of diabetes mellitus and hypertension for 20 years. She had chronic kidney disease stage III, and her estimated glomerular filtration rate (eGFR) has been measured at 55.4 ml/min/1.73 m2 four months before the wasp stings. She had undergone surgery and chemotherapy for colon cancer nine years ago. She was taking medications including telmisartan 40 mg, pravastatin 10 mg, glimepiride 2 mg, metformin 500 mg, and acetylsalicylic acid 100 mg.
Her mentality was drowsy, and blood pressure was 158/83 mmHg, pulse rate 118/min, body temperature 36.2°C, and respiratory rate 20/min. There was mild tenderness in the epigastric area without rebound tenderness. Urine color was dark brown, and the hourly urine output was 10–20 cc. The initial laboratory results were serum hemoglobin 11.7 g/dL, white blood cell count 18,200 cells per microliter, platelets 213,000/uL, blood urea nitrogen 66 mg/dL, creatinine 3.97 mg/dL, eGFR 10.6 ml/min/1.73 m2, sodium 130 meq/L, potassium 8.0 meq/L, ionized calcium 1.01 mmol/L, phosphorous 12.5 mg/dL, serum bilirubin 4.7 mg/dL, aspartate aminotransferase 10380 IU/L, alanine aminotransferase 3302 IU/L, lactate dehydrogenase 8356 IU/L (reference: 140–271 IU/L), creatinine kinase (CK) 98,862 IU/L (reference: <171 IU/L), PT 18 sec (reference: 11.8–14.3 sec), PTT 121.3 sec (reference: 29–44 sec), D-dimer 4499.69 ng/mL (reference: <500 ng/mL), FDP 5~20 ug/mL (reference: <5 ug/mL), fibrinogen 441 mg/dL (reference: 180–400 mg/dL), amylase 205 IU/L (reference: 22–85 IU/L), and lipase 622 IU/L (reference: 21–67 U/L). Arterial blood gas analysis results were pH 7.11, pCO2 26 mmHg, HCO3 9.5 mmol/L, and oxygen saturation 93%. Urine analysis revealed a 1.025 specific gravity, protein 3+, occult blood 4+, RBC 5–9/HPF, and WBC 1–4/HPF. Viral markers for hepatitis B, hepatitis C, and HIV were negative. Chest X-ray did not show pulmonary edema or abnormal infiltration. Electrocardiography revealed sinus tachycardia, absent P wave, and tall T wave.
Abdominal computed tomography showed peripancreatic fat infiltration in the tail portion, suggesting acute pancreatitis grade C (). Whole body bone scintigraphy showed multiple radioiodine uptake in the head, shoulder, hip, and both upper and lower extremities (). Approximately 1–3-cm sized blisters were formed at the sites of the wasp stings and lasted for one week (). The skin biopsy showed subdermal bullae with eosinophilic infiltration.
Continuous renal replacement therapy (CRRT) was initiated 30 hours after the wasp stings. Serum CK level and liver function test were significantly improved during maintenance of CRRT for three days. Serum amylase and lipase level were decreased to less than three times the upper reference limit six days after the wasp stings. However, AKI was persistent and peak serum creatinine level was 8.58 mg/dL on the 13th day after admission. We underwent 11 sessions of conventional hemodialysis until renal function was restored. Ten months after the wasp stings, her serum creatinine level had improved to 1.6 mg/dL (eGFR 30 ml/min/1.73 m2).",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.2, 'degrees celsius'], 'Heart Rate or Pulse': [118.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [18200.0, 'µL'], 'PaCO2': [26.0, 'mm hg']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.2 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 118.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 18200.0 count/µL. To convert 18200.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 18200.0 white blood cell count/µL * 1.0 µL/mm^3 = 18200.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 26.0 mm Hg, which is less than than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6649,51,SIRS Criteria,diagnosis,integer,pmc-7389190-1,Extracted,"We present a 20-year-old female with no previous medical history who was brought to the hospital by her parents. Two days prior she became nauseated and had one episode of emesis, then she became sleepy and subsequently became less responsive. On initial assessment, she was obtunded, had a temperature of 36.9°C, a heart rate of 110 beats per minute, a blood pressure of 100/55 mmHg, oxygen saturation of 98% on room air. On neurological assessment both pupils were three millimeters, equal and reactive to light, her eyes were open spontaneously, she was moving all her limbs spontaneously, but was not following command, she was also making incomprehensible sounds, not responding to questions. The examination of her lungs, heart, and abdomen was unremarkable.
Complete blood count revealed white blood cells 18.5 cells/µL (normal 3.5-10.6 cells/µL), hemoglobin 13.0 g/dL (normal 13.3-17.1 g/dL), and platelet 280 x 10^3 /microliter. Biochemical labs showed abnormalities consistent with DKA, beta-hydroxybutyrate 128 mg/dL (normal 0.2-2.8) (Table ). Her labs also revealed acute kidney injury (AKI) with creatinine (Cr) of 4.54 mg/dL (normal 0.70-1.30) (Table ). A urine drug screen was negative. Infectious workup with chest X-ray, COVID-19 nasal swab, urine analysis, urine culture, and blood culture were done but were unremarkable. She was started on an insulin drip and IV fluids for DKA, in less than 24 hours a repeat lab is done (Table ).
Later on the second day of admission, her mental status deteriorated further, she became none responsive, her Glasgow Coma Scale (GCS) dropped to three and she was subsequently intubated for airway protection and her ventilator settings were set at a respiratory rate of 18 breaths/minute, a tidal volume of 500 mL, a fraction of inspired oxygen of 100%, and a positive end-expiratory pressure of five cm H2O. CT scan of her brain was obtained quickly and showed changes consistent with CE (Figure ). Neurology team was consulted, she had electroencephalography (EEG) done which showed moderate to severe degree of cerebral dysfunction consistent with metabolic/hypoxic encephalopathy, the waveforms were not epileptiform in nature. Despite multiple interventions including lowering PaCO2 to 25-30 mmHg, hypertonic saline 3%, pentobarbital coma, and cooling the patient to 35°C (95°F), she did not show any signs of improvement.
On the third day and fourth day of admission, her condition continued to worsen, and so on the fifth day and because she was not exhibiting response to painful stimuli, no brainstem reflexes, neurology proceeded with a brain death exam, which she had no arousal to voice or sternal rub, no withdrawal to painful stimuli, no cough response, gag or corneal reflexes, her pupils were dilated and fixed, nonreactive to light.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.9, 'degrees celsius'], 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [18500.0, 'µL'], 'PaCO2': [25.0, 'mm hg']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.9 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 110.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 18500.0 count/µL. To convert 18500.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 18500.0 white blood cell count/µL * 1.0 µL/mm^3 = 18500.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 25.0 mm Hg, which is less than than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6650,51,SIRS Criteria,diagnosis,integer,pmc-4825171-1,Extracted,"A 71-year-old male presented in September 2014 with right flank pain, 10 kg weight loss over past 1 month. He had a past medical history of gout, but no past surgical history. The patient was a current smoker with a 20-pack-year smoking history and chronic alcoholics, with a 0.5 bottle per day, over 40 yrs. He had no prior liver insult.
Physical examination revealed no specific finding. He did not have palpable lymph nodes on the head, neck, and inguinal area. There was no suspicious skin lesion. Digital rectal examination was negative, and no perirectal mass or lesion was found. Breathing sound was clear without wheezing or crackle.
Initial vital sign was non-specific (blood pressure 110/70 mmHg, pulse rate 70/min, respiratory rate 20/min, body temperature 36.3°C). Laboratory work-up showed an elevated alkaline phosphatase (ALP)/Gamma-guanosine triphosphate (r-GTP) level of 345/245 IU/L. But total bilirubin 0.44 mg/dL, serum glutamic oxalacetic transaminase (AST) 22 IU/L and serum glutamic pyruvic transaminase (ALT) 27 IU/L level were within normal limits. Complete blood count showed leukocytosis with neutrophilia (WBC 14,800/mm3, segmented neutrophil 79.5%), anemia (Hemoglobin 10.2 g/dL) and thrombocytosis (Platelet 485 ×103/mm3). Hepatitis viral markers were all negative, and Ca 19-9 level was slightly elevated (28.58 U/mL). Alpha fetoprotein (AFP) 1.38ng/mL, protein induced by vitamin K absence or antagonist II (PIVKA-II) 55 mAU/mL, carcino-embryonic Antigen (CEA) level were 4.45 ng/mL, all of them were within normal limits.
A computed tomography (CT) scan of the abdomen and pelvis with contrast revealed a 10 × 6 cm sized low attenuated mass involving segment VIII and left lobe of the liver, invading left portal vein and bile duct. Unlike primary hepatocellular carcinoma, liver mass showed delayed fill-in enhancement pattern, which mimics cholangiocarcinoma, rather than primary hepatocellular carcinoma (). But Tumor thrombi was invading the middle hepatic vein, extending to the right atrium via inferior vena cava, which was unusual finding for mass-forming cholangiocarcinoma ().
Also, there were multiple metastatic lymphadenopathy involving porta hepatis, portocaval, retrocaval and paraaortic space, with benign-looking multiple cysts in the both kidneys, 2.2 cm cyst in the uncinate process of pancreas.
Non-enhanced Chest CT from other hospital showed metastasis to the right ninth rib and surrounding paravertebral soft tissue with osteolytic change (). As mass size was huge and showed the aggressive form, we decided to perform positron emission tomography-CT (PET-CT) for evaluating disease extent.
Additionally, PET-CT scan revealed a small hypermetabolic lymph node in the left supraclavicular area, which was suspected as metastatic lesion (). Excisional biopsy on supraclavicular lymph node returned negative. In turn, we had to perform an ultrasonography guided needle biopsy of the liver for pathologic confirmation. Pathology of the liver mass showed infiltrating feature with squamoid shaped cells with varying degrees of differentiation and atypia, which suggests tumor mass as poorly differentiated adenocarcinoma or squamous cell carcinoma (). Immunohistochimistry and special staining for needle biopsy specimens were positive for cytokeratin (CK) 7, 8, 19, and p63. And anti-hepatocyte was negative, suggesting tumor as primary or metastatic squamous cell carcinoma of the liver ().
The patient underwent an extensive workup to search for a primary squamous carcinoma lesion, including neck CT, chest CT, duodenoscopy, sigmoidoscopy, laryngoscopy and ENT survey, all of which turned out to be negative. Taken together, we concluded the tumor as a primary SCC of the liver.
During the hospital day, patient presented uncontrolled high and recurrent fever, which was suspected to be the cancer fever. Patient’s general condition continued to get worsen. First, we considered palliative chemotherapy, however we failed to conduct due to his poor general condition (Eastern Cooperative Oncology Group 3). The patient started palliative radiotherapy for right paravertebral mass. After 10 times of radiation therapy, patient refused further treatment and transferred to the local hospital for hospice care, and passed away about a month after discharge.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.3, 'degrees celsius'], 'Heart Rate or Pulse': [70.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [14800.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.3 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 70.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 14800.0 count/m^3. To convert 14800.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 14800.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6651,51,SIRS Criteria,diagnosis,integer,pmc-6687419-1,Extracted,"An 88-year-old woman with a history of dementia, end-stage renal disease on hemodialysis, hypertension, and chronic cholelithiasis presented with nausea and non-bloody emesis for two days. No abdominal pain, fever, chills, dysuria, hematuria, melena, or hematochezia were exhibited.
She was hospitalized three years prior for a similar presentation. At that time, a CT scan was obtained which showed a large stone within the gallbladder (Figure ). During that presentation, the patient refused any surgical intervention and was treated conservatively. One year later, the patient returned with a similar presentation in which a second CT was obtained (Figure ) which showed a gall stone, as well as inflammatory changes and possible duodenal stricture. Thereafter, an esophagogastroduodenoscopy was performed and showed duodenopathy with a post-bulbar duodenal stricture. It was thought that the cholelithiasis may have caused inflammatory changes of the duodenum and led to the stricture formation. Pathological examination failed to demonstrate malignancy or Helicobacter pylori infection. She was treated conservatively per her request to avoid surgical intervention.
Examination on this admission revealed a core temperature of 98.6, a heart rate of 78, a respiratory rate of 16, and an elevated blood pressure of 171/89. The patient had a normal mental status, respiratory, and cardiovascular examination. Abdominal examination was significant for moderate abdominal distention but otherwise unremarkable. Murphy’s sign was negative. There was no guarding or rigidity, no hernia was observed, and no masses or enlarged liver or spleen were palpated. Laboratory investigations were remarkable for an alkaline phosphatase of 283 unit/L (normal: 25 - 100), serum glucose of 171 mg/dl, and leukocytosis of 16.7 with a left shift. In addition, the renal panel was abnormal with a blood urea nitrogen of 33 and creatinine of 6.3. Other hepatic, hematologic, and metabolic studies were unremarkable.
An abdominal roentgenogram showed an abnormal gas pattern with distended gastric outline and gastrectasis which was increased compared to her prior studies obtained two years ago. A moderate stool burden was noted throughout the inferior colon and rectum representing fecal impaction. No free air or significant calcification were noted. An abdominal CT scan (Figure ) showed a large 4 cm gallstone in the duodenal bulb with interval development of air within the biliary tree and common duct. A nasogastric tube was placed and drained > 1 liter of dark, red-tinged fluid. Endoscopic studies revealed a normal esophagus, gastric antrum, and pylorus. Debris and fluid were found in the stomach and were suctioned using a gastroscope. A normal duodenal bulb with a large gallstone (4 - 5 cm) at the apex into the duodenal sweep was found. This was surrounded by mucosal edema. Because of the stone angulation, it was difficult to obtain purchase on the stone. Different devices were used in attempts to free the stone from the duodenum and manipulating it into the stomach. Efforts failed due to the calcified nature of the stone, the angulation of the duodenum, extensive inflammatory changes surrounding the stone, and the size of the stone. Subsequently, surgical management was discussed with the patient and her family who agreed to proceed with the operation.
Diagnostic laparoscopy was attempted but failed due to the difficulty accessing the area of interest laparoscopically. Thus, an exploratory laparotomy was carried out. A midline incision was made and dissection was carried down until the duodenum was once again palpated. Attempts were made trying to move the stone proximally into the stomach; however, there was significant inflammation, as well as adhesions, in the duodenum from the longstanding cholecystitis and cholecystoduodenal fistula. Multiple attempts were made to try to lyse the adhesions, trying to free the angle into the stomach or make it less acute. Despite lysing all the adhesions and performing a limited Kocher maneuver, the attempts to move the stone into the stomach were unsuccessful. The surgical team then attempted to pass the stone more distally in an attempt to take it out through a jejunal enterotomy. The stoned moved freely down to D3/D4, but unfortunately, we were unable to move the stone beyond the ligament of Treitz. The ligament of Treitz was taken down, along with adhesions in the area; however, we were still unable to remove the stone. As there was some hematoma forming in this area, we elected to then proceed with a duodenotomy to retrieve the stone. The stone was moved back to D2, and electrocautery was used to make a 5 cm duodenotomy on the lateral antimesenteric border of the duodenum. The stone was encountered, freed, and extracted from the duodenum (Figure ). Repair of the duodenum and omental flap creation were performed. This was followed by placement of a gastrojejunostomy feeding tube.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [98.6, 'degrees fahrenheit'], 'Heart Rate or Pulse': [78.0, 'beats per minute'], 'respiratory rate': [16.0, 'breaths per minute'], 'White blood cell count': [16.7, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 98.6 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 66.6 = 37.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 78.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 16.7 count/m^3. To convert 16.7 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 16.7 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1.67e-08 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 16.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6652,51,SIRS Criteria,diagnosis,integer,pmc-3891035-2,Extracted,"A 40-year-old man was hospitalized due to jaundice and lethargic fatigue that started 10 days prior to admission. The patient had complaints of weight loss and night sweats. Four months prior to this admission, he had visited to the Department of ENT at another hospital with the complaint of nasal stuffiness. At that time, the serologic testing for hepatitis B antigen and anti-HIV antibody were positive. He has been treated with zidovudine, lamivudine and efavirenz for two months until admission. He assumed that his AIDS was transmitted from heterosexual contact at abroad ten years ago. On admission, the blood pressure was 120/70 mmHg, the pulse rate 90/min, the respiratory rate 20/min and the body temperature was 36.6℃. He was icteric on the physical examination. The liver was tender and firm in consistency. It was palpated at a three-finger breadth below the right costal margin. His spleen and lymph nodes were not enlarged. The laboratory results were normal apart from an ESR of 120 mm/h; leukopenia 3,930/mm3 (neutrophils: 58.8%, lymphocytes: 31% and monocytes: 8.4%) and hemoglobin 9.4 g/dL. The liver function tests were abnormal: total bilirubin 8.9 mg/dL (direct bilirubin: 6.05 mg/dL), AST 171 IU/L, ALT 100 IU/L and LDH 1063 IU/L. The total number of CD4 and CD8 T lymphocytes was 290/mm3 and 568/mm3, respectively, and the ratio of CD4/CD8 was 0.51. Abdominal enhanced CT scanning revealed multifocal and variable sized homogenous hypodense masses in both hepatic lobes (). A liver biopsy showed a heavy infiltration composed mainly of large lymphoid cells (). Immunohistochemical staining revealed the atypical cells to be CD20 positive (), which established a diagnosis of diffuse large B-cell lymphoma according to the WHO classification. Bone marrow biopsy demonstrated normal cellularity with normal maturation of all three cell lines. There was no malignant cell infiltration. After the patient was diagnosed as having diffuse large B-cell lymphoma, he received VAD (vincristine 0.4 mg, adriamycin 9 mg/m2, dexamethasone 40 mg on days 1-4, and additional dexamethasone on days 9-12 and days 17-20). The patient seemed to show a little clinical improvement, but before starting the second chemotherapy, he developed signs of spinal cord compression (). Emergency radiation therapy was delivered to the spine lesion. CHOP chemotherapy (cyclophosphamide 750 mg/m2, adriamycin 50 mg/m2 and vincristine 1.4 mg/m2 on day 1 and prednisone 100 mg/m2 on days 1-5) and laminectomy induced temporary improvement (). Alas, the paraplegia continued and his clinical condition progressively worsened. He passed away 103 days after starting the second round of chemotherapy from complications of pressure sores, deep vein thrombosis and pulmonary thromboembolism.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.6, 'degrees celsius'], 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [3930.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.6 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 90.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 3930.0 count/m^3. To convert 3930.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 3930.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 3.93e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6653,51,SIRS Criteria,diagnosis,integer,pmc-4531665-1,Extracted,"A 64-year-old woman was referred to our hospital for bronchial asthma with atypical pneumonia unresolved by antibiotic treatment. She had no history of being diagnosed as asthma but had suffered from intermittent sensation of chest constriction by exposure to cold air.
She had taken steroid for her joint arthritis without consulting a doctor for several years. She has never smoked and had no history of tuberculosis, diabetes mellitus or other cardiovascular disease. About 20 days before admission, the patient suffered from fever, cough, sputum and dyspnea. She visited another hospital and was treated with antibiotics and steroids. Despite treatment, there was no clinical improvement of her symptoms. She was referred to our hospital for further evaluation.
On admission, her body temperature was 37.2°C, pulse rate was 110/min, respiration rate was 24/min and blood pressure was 160/100 mmHg. Physical examination revealed bilateral diffuse inspiratory crackle without wheezing. Laboratory tests were performed: white blood cell count was 48,220/μL (neutrophils were 98%, monocytes 1% and lymphocytes 1%), hemoglobin 11.2 g/dL, hematocrit 32.1% and platelet count 394,000/μL on complete blood cell counts. Arterial blood gas analysis findings were pH 7.497, PaCO2 42.5 mmHg, PaO2 63.4 mmHg, bicarbonate 32.6 mmol/L and oxygen saturation 93.3% on oxygen 3 L/min via nasal prong. Sodium was 126 mEq/L, potassium 2.7 mEq/L, chloride 98 mEq/L, urea nitrogen 13.9 mg/dL, creatinine 1.24 mg/dL, cholesterol 168 mg/dL, total protein 5.1 mg/dL, albumin 2.6 mg/dL, AST 22 IU/L, ALT 22 IU/L and total bilirubin was 0.82 mg/dL on blood chemistry. Chest radiography and high-resolution computed tomography (HRCT) showed multifocal variable-sized consolidation with reticulonodular opacities () and cavitary lesion in both upper lobes and right lower lobe. There were also multiple small nodular densities and ground glass attenuation around the consolidation ().
Microscopic examination of sputum showed no acid-fast bacilli. Other laboratory findings, including IgG, IgM, IgA, IgE PRIST, C3, C4, CH50, rheumatoid factor (RF), antinuclear antibody (ANA), anti-neutrophil cytoplasmic antibody (ANCA), antistreptolysin-O (ASO), VDRL and cold cryoglobulin, were all negative.
Despite empiric broad-spectrum antibiotics and steroid treatment, dyspnea progressively aggravated. Open lung biopsy was done on the tenth hospital day. Histopathologic findings of the biopsy specimen showed large areas of necrotizing pneumonia with an infarct-like appearance (). There were some scattered fungal hyphae within the lung parenchyma (). The bronchi and bronchioles often showed dilated lumen which were filled with mucus, numerous necrotic debris, inflammatory cells and branching septated hyphae characteristic of aspergillus. Some terminal bronchioles were found to be destroyed and were replaced by granulomatous inflammation (). The bronchocentric granulomatous reaction extended into the adjacent lung parenchyma to a degree. Gomori-Methenamine-Silver (GMS) staining revealed many fungal hyphae consistent with aspergillus species. There was no evidence of angioinvasion by aspergillus or aspergillous emboli. With an impression of invasive aspergillus infection with BCG-like elements, 15 mg of amphotericin-B once day was administered intravenously and the dose was increased up to 30 mg daily. Steroids was tapered progressively. There were some improvement in her clinical symptoms. However despite vigorous antifungal treatment, sudden respiratory arrest occurred due to acute tracheobronchial tree obstruction with bronchial casts on the thirty-fourth hospital day. Histopathologic examination of the casts revealed fibrinoid necrotic tissue containing neutrophils, a few metaplastic squamous cell nests and variably fragmented fungal hyphae ().",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.2, 'degrees celsius'], 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'respiratory rate': [24.0, 'breaths per minute'], 'White blood cell count': [48220.0, 'µL'], 'PaCO2': [42.5, 'mm hg']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.2 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 110.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 48220.0 count/µL. To convert 48220.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 48220.0 white blood cell count/µL * 1.0 µL/mm^3 = 48220.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 24.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is 42.5 mm Hg, which is greater or equal to than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6654,51,SIRS Criteria,diagnosis,integer,pmc-7290114-1,Extracted,"Six weeks following an uncomplicated delivery via low-transverse C-section for arrest of labor (placenta not sent to pathology), a 23-year-old G3P2011 woman presented to the ED with pleuritic chest pain and severe shortness of breath for two days. The patient’s prenatal course was unremarkable. Following delivery, she was discharged home on post-operative day three with a hemoglobin (Hgb) of 10.8 g/dL and a hematocrit (Hct) of 32.4%. Her post-partum history was notable for endometritis, excessive vaginal bleeding throughout the post-partum period with evidence of increased endometrial blood flow, as well as an endometrium measuring 1.5 cm via transvaginal ultrasound. She required hospitalization for antibiotics and transfusion of two units of packed red blood cells (PRBCs) two weeks prior, but did not have any curettage performed at that time. Upon initial evaluation, she was afebrile (37.0° C), tachycardic (145 beats per minute), hypertensive [blood pressure (BP) 156/82 mmHg], and in severe respiratory distress with a respiratory rate (RR) of 30 breaths per minute, oxygen saturation of 99% while breathing 100% oxygen via nonrebreather mask. A chest X-ray showed diffuse pulmonary edema and bilateral airspace disease with bilateral pleural effusions (Figure ).
Initial arterial blood gas analysis showed severe hypoxemia, metabolic acidosis, and concomitant respiratory alkalosis (pH 7.31, pO2 197, pCO2 18, base excess −8, HCO3 18 on 100% O2 via bag-valve-mask). Labs demonstrated a Hgb of 4.9 g/dL and Hct of 15.6% with gross intraperitoneal blood found on sonographic exam, leukocytosis (white blood cell count 16,700 with 82% neutrophils), elevated d-dimer (>5,000 ng/mL), normal fibrinogen, and transaminitis with aspartate aminotransferase/alanine aminotransferase/alkaline phosphatase of 363/356/274 units/L, respectively. Additionally, the patient was found to have a serum beta-human chorionic gonadotropin (hCG) of 2,800 mIU/mL, a creatinine of 1.10 mg/dL, and a lipase of 453 units/L. The patient was transfused with three units of PRBCs, and subsequently intubated with a tidal volume (TV) of 6 mL/kg ideal body weight, a respiratory rate of 16, and a positive end-expiratory pressure (PEEP) of 5 cm H2O and an inspired oxygen fraction of 60%.
Initial transabdominal ultrasound revealed a hypervascular uterus with internal echogenic material, as well as an endometrial lining measuring 3.7 cm, suspicious for GTD (Figure ).
A CT angiogram with contrast of the chest, abdomen, and pelvis showed free fluid in the abdomen, multiple lesions within the liver, spleen, bilateral pleural effusions, and bilateral thromboses in the gonadal veins, raising concern for septic emboli vs. disseminated GTD. The patient was transferred to a quaternary center, where she was started on broad-spectrum antibiotics and cisplatin/etoposide for two cycles prior to full-dose chemotherapy with etoposide, methotrexate, actinomycin D, cyclophosphamide, and vincristine due to concern of acute hemorrhage given her high tumor burden. Bacterial cultures of blood, urine, and tracheal aspirate were negative.
On hospital day seven, the patient developed massive hemoptysis with marked respiratory distress. Bronchoscopy showed active hemorrhage with predominant bleeding from the right upper lobe. The patient underwent interventional radiology-guided embolization of her right bronchial artery. She continued to have DAH (Figure ).
Recruitment maneuvers (pressure-controlled inflations of 40 cm H2O sustained for 20 s) and neuromuscular blockade failed to improve gas exchange on assist-control ventilation with a TV of 4.5 mL/kg ideal body weight, RR of 23, a PEEP of 16 cm H2O, and an inspired oxygen fraction of 100% while minimizing driving pressure. She was placed on veno-venous ECMO on hospital day eight.
Under ultrasound guidance, a 23 French drainage cannula was placed percutaneously in the left femoral vein, and a 21 F return cannula was placed into the right internal jugular vein. Blood was drained from the left femoral vein into the ECMO circuit. ECMO flows were initiated at 4 L/min with a sweep gas flow of 2 L/min, titrated to keep oxygen saturation >88% and pCO2 within normal parameters. The ECMO for Protective Ventilation (EMPROVE) protocol, a lung-protective strategy utilized at our institution, was initiated on the ventilator. The protocol has been described in detail elsewhere, but in brief, it utilizes either pressure control or airway pressure release ventilation to maintain a peak pressure ≤ 30 or a plateau pressure ≤ 25. The respiratory rate is lowered to 5-8 breaths per minute, and moderate PEEP is used to keep the lungs expanded during low TV ventilation. The FiO2 is set at ≤ 50%. ECMO provided a gradual improvement in hypercapnia over the initial 45 min (PCO2 48-42, pH 7.48-7.45). Using the EMPROVE protocol her TVs declined from ~300 to ~200 mL, reducing peak airway pressures from 46 to 30 cmH2O. Her respiratory rate was maintained at 7 and her PEEP at 14 cm H2O.
Due to the hemorrhagic nature of GTD, the patient was not anticoagulated. Partial thromboplastin time measured between 25 and 36 s while on ECMO. Platelets were transfused to maintain count > 50,000/µL, as per local hospital practice. There were no thrombotic complications. The patient’s clinical condition gradually improved and extracorporeal support was discontinued after 23 days (Figure ).
Sedation was weaned and she was alert and oriented, however, with significant debility. She underwent tracheostomy placement and was weaned to T-piece. Sadly, while nearing transfer status to a decreased level of care, the patient suffered a catastrophic hemorrhage from a brain metastasis and subsequently expired on hospital day 42.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.0, 'degrees celsius'], 'Heart Rate or Pulse': [145.0, 'beats per minute'], 'respiratory rate': [30.0, 'breaths per minute'], 'White blood cell count': [16700.0, 'µL'], 'PaCO2': [18.0, 'mm hg']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 145.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 16700.0 count/µL. To convert 16700.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 16700.0 white blood cell count/µL * 1.0 µL/mm^3 = 16700.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 30.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is 18.0 mm Hg, which is less than than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6655,51,SIRS Criteria,diagnosis,integer,pmc-5361634-2,Extracted,"A previously healthy 10-month-old Mestizo boy was admitted with a 1 day history of 12 watery stools and fever. He had not received any previous medications. On examination, the child was irritable, had sunken eyes with no tears, dry oral mucosa and thirst. Abdominal distention and increased peristalsis was also observed. He had normal skin turgor and a capillary refill of 3 s. Vitals signs on admission were as follows: temperature, 38.5 °C; pulse, 140 beats min−1; and respiration, 46 breaths min−1. His weight was 8.6 kg and length was 72 cm. His weight-for-age and length-for-age were between the 0 and −2 z scores, and his weight-for-length between the 0 and −1 z scores. He was classified as adequately nourished. The CBC reported haemoglobin, 11.3 g dl−1; leukocytes, 13.8×103 µl−1; neutrophils, 9.6×103 µl−1; platelets, 356×103 µl−1. His dehydration was classified as moderate, with an estimated fluid deficit of 5–10 %, and he was prescribed plan B with oral rehydration therapy (ORS) [(mEq l−1): Glucose 75; Sodium 75; Chloride 65; Potassium 20; Citrate 20. Osmolarity 245] at 100 mlkg−1 for 4 h. He presented three episodes of vomiting during the first 2 h and was switched to intravenous rehydration therapy with isotonic solution at 180 mlkg−1day−1 for 8 h; he also received one dose of 120 mg acetaminophen when his temperature reached 39.5 °C. He was discharged in good condition the next day and sent home with ORS and trimethoprim/sulphamethoxazole (64 mg/320 mg) for 5 days. The E. coli strain isolated from his stools was resistant to nalidixic acid and the β-lactam antibiotics ampicillin, ceftriaxone and ceftazidime, and susceptible to all other tested antibiotics, including trimethoprim/sulphamethoxazole. His stool pattern returned to normal after 4 days from onset.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.5, 'degrees celsius'], 'Heart Rate or Pulse': [140.0, 'beats per minute'], 'respiratory rate': [46.0, 'breaths per minute'], 'White blood cell count': [13800.0, 'µL']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.5 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 140.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 13800.0 count/µL. To convert 13800.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 13800.0 white blood cell count/µL * 1.0 µL/mm^3 = 13800.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 46.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6656,51,SIRS Criteria,diagnosis,integer,pmc-8304195-1,Extracted,"An 18-year-old male with a past medical history of MID and a notable surgical history of small bowel, liver, and pancreas transplant, who was maintained on tacrolimus 2 mg and prophylactic trimethoprim-sulfamethoxazole 400-80 mg, presented to the emergency room (ER) with four days of hematochezia and lightheadedness. He had experienced recurrent GI bleeding, most recently a year ago, and had undergone multiple endoscopies by pediatric gastroenterology in the past, which had been negative for active bleeding or any possible source. The patient denied nausea, vomiting, abdominal pain, fevers, shortness of breath, cough, or chest pain. His vitals on presentation were as follows: BP of 136/67 mmHg, heart rate (HR) of 114 beats per minute, respiratory rate (RR) of 22 breaths per minute, O2 saturation of 96% on room air, and temperature of 36.9 °C.
The serologic evaluation was pertinent for hemoglobin of 9.6 g/dL, white blood cell count of 4.66 K/uL, platelets of 130 K/uL, and prothrombin time (PT)-international normalized ratio (INR) of 1.152. Liver function tests including aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and bilirubin were all within normal limits. The patient was admitted and scheduled to undergo evaluation with esophagogastroduodenoscopy (EGD). The following day, he continued to deteriorate with ongoing bleeding resulting in a hemoglobin drop to 6.7 g/dL, requiring transfusion of one unit of packed red blood cells. EGD with push enteroscopy showed an enteroenterostomy with a hemorrhagic appearance in the jejunum. The area adjacent to the anastomosis was biopsied to rule out rejection. The region near the anastomosis had grape-like clustering raising concern for varices, and noted hemorrhage post-biopsy (Figure ). Hemostasis was achieved with argon plasma coagulation and epinephrine (Figure ). A metallic clip was placed for radiographic identification for the purpose of an interventional radiology (IR) procedure (Figure ). Subsequently, the patient remained intubated and was transferred to ICU on an octreotide drip.
The case was discussed with IR and Transplant Hepatology, as endoscopic management with sclerosing agents or glue was not available. The complex nature of the post-surgical vascular anatomy and concern for an interrupted inferior vena cava prompted IR to perform a CT angiography (CTA) of the abdomen, with the possibility of embolization. The results of the CTA demonstrated a massive tangle of jejunal submucosal varices, as well as reported cecal submucosal varices and massive splenomegaly (Figures , ). Furthermore, due to atrophic hepatic vein and systemic collaterals to the azygos vein, transjugular intrahepatic portosystemic shunting (TIPS) was deemed not feasible at the time. Subsequent discussion involving Transplant Surgery at the hospital where the patient had received his small bowel and liver transplant prompted a decision to transfer the patient for open surgical evaluation and combined IR embolization of varices. The patient was then stabilized and transferred.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.9, 'degrees celsius'], 'Heart Rate or Pulse': [114.0, 'beats per minute'], 'respiratory rate': [22.0, 'breaths per minute'], 'White blood cell count': [4660.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.9 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 114.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 4660.0 count/µL. To convert 4660.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 4660.0 white blood cell count/µL * 1.0 µL/mm^3 = 4660.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 1 + 1 = 2 criteria met.
Hence, the the number of SIRS criteria met by the patient is 2."
6657,51,SIRS Criteria,diagnosis,integer,pmc-2726475-1,Extracted,"A 9-year-old mildly obese boy with a medical history significant for recurrent otitis media presented with sudden, one day, onset of sharp right-sided neck pain and neck stiffness that awakened him from sleep. He rated the pain 10 out of 10 in intensity, and noted it to be non-radiating, without alleviating or aggravating factors.
He admitted to subjective fever 1 week before presentation, associated neck stiffness, a frontal headache, right otalgia, pharyngitis and dysphagia. He also admitted to a single episode of vomiting clear fluid 1 day before experiencing the neck pain. He denied rash, tinnitus, odynophagia, cough, dyspnea, recent travel or exposure to sick contacts. However, 2 weeks before this presentation, he was treated with antibiotic eardrops for an episode of otitis media. The patient had no known drug allergies. His immunizations were up to date, and he was not taking any medications at the time of presentation.
In the emergency room, his temperature was 100.8°F, blood pressure 103/66, heart rate was 103, and respiratory rate at 22. On examination, he was a young, mildly obese boy in moderate distress, with no rash or skin lesions. His face was plethoric with tenderness to palpation appreciated along the right side of the sternocleidomastoid. Cervical lymphadenopathy was noted on palpation in this region of the neck. There was diminished range of motion on turning his neck to the right, secondary to pain. Kernig's and Brudzinski's signs were negative. No oropharyngeal erythema or oral lesions were noted. The right ear and mastoid were tender to palpation, and bilateral middle ear effusions were appreciated. He was tachycardic with regular rhythm, clear breath sounds, and normal abdominal exam. He was alert and oriented to person, place, and time, and cranial nerves II-XII were grossly intact. He had no focal neurologic deficits.
White blood cell count was 12,000/mm3, neutrophils 81.6%, lymphocytes 10%, monocytes 7.6%, eosinophils 0.3%, platelets 236 TH/CM, hemoglobin 11.3gm/dL, hematocrit 34.1% and erythrocyte sedimentation rate was 58mm/hour.
The patient was initially started on a combination regimen of clindamycin and ceftriaxone.
Computed tomography (CT) scan of the head demonstrated hyperdensity in the region of the right transverse sinus, and bilateral mastoiditis with decreased pneumatization, greater on the right than left (Figure ). Further sections of head CT scan and magnetic resonance imaging (MRI) showed thrombosis of the right internal jugular vein (Figures and ). The classic cord sign, illustrative of transverse venous thrombosis, was also demonstrated via MRI (Figure ). Magnetic resonance venography (MRV) demonstrated diminished perfusion of the superior sagittal, straight, transverse and sigmoid sinuses (Figure ). The patient was subsequently started on therapeutic lovenox. Ceftriaxone was discontinued secondary to an allergic reaction.
Given the patient's predisposition for recurrent otitis media, prophylactic bilateral myringotomy and tympanostomy tubes were placed.
The patient improved significantly, with complete resolution of symptoms, and he was treated as an outpatient on therapeutic enoxaparin at 65mg subcutaneously every 12 hours for a duration of 4-6 weeks and oral clindamycin 300mg three times a day for a duration of 4 weeks. At follow-up, the patient was completely asymptomatic, and appeared to have recovered without any residual effects.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [100.8, 'degrees fahrenheit'], 'Heart Rate or Pulse': [103.0, 'beats per minute'], 'respiratory rate': [22.0, 'breaths per minute'], 'White blood cell count': [12000.0, 'mm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 100.8 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 68.8 = 38.22222 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 103.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 12000.0 count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6658,51,SIRS Criteria,diagnosis,integer,pmc-5646314-1,Extracted,"A 51-year-old male with a past medical history of HIV, COPD, and hypertension presented with a four-day history of fever, shortness of breath, and nonproductive cough associated with headache and reduced appetite. He had a 30-pack-year history of smoking cigarettes and had not been compliant with his HIV medications as well as trimethoprim-sulfamethoxazole. He had no history of nonsteroidal anti-inflammatory drug (NSAID), herbal drug, or cocaine use. He denied recent ill contacts, recent travel, or camping. On examination, he was in respiratory distress with blood pressure 143/95 mmHg, pulse 135 beats per minute, respiratory rate 24 breaths per minute, temperature 39.5 degrees Celsius, and sPO2 92% on room air and 98% on 2 litres nasal cannula. He had bronchial breath sounds in the left mid and lower lung fields with crackles, but no wheezing. His heart sounds were normal. Abdomen was soft and nontender, with normal bowel sounds. Other aspects of his examination were unremarkable.
His white cell count was 4.6 (4.5–11 × 103/uL); haemoglobin was 10.7 (12–16 g/dL); platelet was 246 (140–440 thou/cu mm); mean corpuscular volume was 94 (82–101 fl); Prothrombin Time (PT) was 12.9 (11–13.5 seconds); international normalised ratio (INR) was 1.0 (0.8–1.2); partial thromboplastin time (PTT) was 34 (25–35 seconds); HbA1c was 5.7% (4–5.6%); procalcitonin was 31.2 ng/mL (<0.15 ng/mL); thyroid stimulating hormone (TSH) was 0.705 (0.27–4.2 uIU·ml); sodium was 137 (135–145 mmol/L); potassium was 4.5 (3.3–4.6 mmol/L); chloride was 95 (101–110 mmol/L); BUN was 56 (6–22 mg/dL); creatine was 6.98 (0.6–1.17 mg/dL); calcium was 7.8 (8.6–10 mg/dL); albumin was 2.6 (3.8–4.9 g/dL); phosphorus was 5.5 (2.5–4.5 mg/dL); aspartate aminotransferase was 789 (14–33 IU/L); ALT was 235 (10–42 IU/L); anion gap was 22 (4–16); direct bilirubin was 3.3 (0–0.2 mg/dL); indirect bilirubin was 0.4 mg/dL (0.2–1.2 mg/dL); total bilirubin was 3.7 (0.2–1.0 mg/dL); alkaline phosphatase was 66 (40–129 IU/L); total creatine kinase was 51092 U/L (22–195 U/L), and urine was positive for myoglobin. His CD 4 count was 41 cells/ul, and HIV viral load was 34900 copies/mL.
Urine analysis with Alere BinaxNOW lateral flow immunochromatographic assay for Legionella antigen serogroup 1 was positive; urine pneumococcal antigen was negative; blood culture, respiratory culture, and urine culture were without bacterial growth; respiratory viral panel was reported negative for influenza, parainfluenza, rhinovirus, respiratory syncytial virus (RSV) virus, human metapneumovirus, H1, and H3.
His electrocardiogram showed sinus tachycardia. Chest X-ray (CXR) showed a homogenous consolidation in the left lower lung field (). CT chest showed consolidation in the left lingual with air bronchograms consistent with lobar pneumonia, without pleural effusion (Figures and ). Echocardiograph showed a left ventricular ejection fraction of 65%. Renal ultrasound showed normal sized kidneys with normal echogenicity without hydronephrosis.
He was diagnosed with Legionella pneumonia, rhabdomyolysis, and acute renal failure and started on levofloxacin and atovaquone. He became further oliguric, with rising creatine and BUN, with worsening respiratory status requiring intubation and ventilation in addition to dialysis which were commenced on the second day of admission. Azithromycin was added to his antibiotic regimen in the ICU. His maximum creatine was 13.04 mg/dL, and BUN was 153 mg/dL during his hospital course. His respiratory and renal function improved during his ICU stay. He was extubated after six days. With improvement in his urine output and renal indices; he no longer required dialysis. On discharge, after 28 days of hospital stay and seven days of ICU stay, his creatine was 2.6 md/dL, BUN 36 md/dL, total creatine kinase (CK) 69 U/L, aspartate aminotransferase (AST) 16 IU/L, alanine aminotransferase (ALT) 30 IU/L, direct bilirubin 0.1 mg/dL, indirect bilirubin 0.1 mg/dL, and total bilirubin 0.2 mg/dL. After three-weeks follow-up in the outpatient setting, his creatine was back to normal at 1.06 (0.6–1.17 mg/dL), with resolution of the chest X-ray consolidation (). Renal biopsy was not pursued in light of recovery of normal renal function.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.5, 'degrees celsius'], 'Heart Rate or Pulse': [135.0, 'beats per minute'], 'respiratory rate': [24.0, 'breaths per minute'], 'White blood cell count': [4600.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.5 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 135.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 4600.0 count/µL. To convert 4600.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 4600.0 white blood cell count/µL * 1.0 µL/mm^3 = 4600.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 24.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6659,51,SIRS Criteria,diagnosis,integer,pmc-3285709-1,Extracted,"A 75-year-old woman was admitted to the emergency department with acute right abdominal pain of 2-hour duration. Her medical history included a hysterectomy 30 years ago. From several decades ago, she had almost always voided with abdominal strain. Also, she suffered from tenesmus and weak stream. On examination, she was oriented and cooperative. Her vital signs were as follows: blood pressure, 150/75 mmHg; pulse, 84 beats per minute and regular; respirations, 20 per minute; and body temperature, 36.0℃. Clinical examination revealed diffuse pain in the right abdomen with tenderness. However, costovertebral angle (CVA) tenderness was not prominent. Bowel sounds were increased.
Urinalysis showed 2 to 4 red cells and 0 to 1 white cells per field under high-power magnification. Complete blood cell count results were as follows: 8,500/mm3, with 44.5% neutrophils. Serum chemical analysis showed a urea level of 26 mg/dl, a creatinine level of 1.5 mg/dl, and a C-reactive protein (CRP) level of 0.99 mg/dl. Other values were within the normal limits.
After analgesic injection, her pain subsided. With a presumptive diagnosis of acute gastroenteritis, she was discharged with medication.
The following day, the patient was admitted to the gastrointestinal department with persistent right abdominal pain. An abdominal computed tomographic (CT) scan was performed, which showed a dilated urinary bladder, hydronephroureterosis, and perinephric fluid collection. The patient was referred to our urologists, who recommended insertion of an indwelling Foley catheter. About 2 L of urine was drained shortly after catheter indwelling. Because there was no delayed phase on CT, we performed a non-enhanced CT scan immediately. It showed extravasation of radiocontrast from the right upper ureter at the L3 to 4 transverse process level and improved hydronephroureterosis ().
A 8.5 F pigtail percutaneous nephrostomy catheter was inserted into the renal pelvis. After 7 days, antegrade pyelography (AGP) performed through the nephrostomy catheter showed no extravasation of radiocontrast from the ureter (). A double-J catheter (6 F, 24 cm) was placed in the right ureter. The percutaneous nephrostomy catheter and Foley catheter were removed. The next day, she was discharged without complications.
After 2 weeks, the Double-J catheter was removed and we subsequently performed a video-urodynamic study. A total of 500 ml of normal saline was filled in the bladder. The patient then tried to void with abdominal straining, but could not. Maximal detrusor pressure did not exceed 10 cmH2O. In other words, the patient showed detrusor underactivity and no vesicoureteric reflux (VUR). A follow-up CT scan was performed 2 months later. It showed resorption of urinoma in the right peri-renal space and there was neither malignancy nor obstructing lesions. She was managed with alpha-blockers and clean intermittent catheterization.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.0, 'degrees celsius'], 'Heart Rate or Pulse': [84.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [8500.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 84.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 8500.0 count/m^3. To convert 8500.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 8500.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 8.5e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6660,51,SIRS Criteria,diagnosis,integer,pmc-7450893-1,Extracted,"In late June, a 51-year-old male presented to the ED with a chief complaint of shortness of breath. The patient reported sporadic fevers and chills at home over the past two weeks, but denied current fever, nausea, vomiting, diarrhea, abdominal pain, headache, or any urinary symptoms. The patient reported no past medical history and was not on any medications. His son, however, was diagnosed with COVID-19 two weeks prior, with a cough, fever, and typical viral syndrome type symptoms. The patient reported that he did not quarantine from his son even after the positive COVID-19 diagnosis, as they lived in the same house.
The patient’s vital signs were temperature 99.1°F, blood pressure 111/76 mmHg, pulse rate 87 beats per minute, respiration rate 18 breaths per minute, and oxygen saturation of 94% on room air. Physical examination revealed significantly decreased breath sounds bilaterally. The remainder of physical examination was unremarkable, including cardiovascular and neurological examination. Laboratory analysis showed signs of leukopenia (white blood cell count of 3,000 per cubic mm) but was negative for neutrophilia or lymphocytopenia. All electrolytes were within normal limits. The D-dimer count was elevated at 2.05 mg/L. Radiological examination included a chest x-ray that demonstrated scattered opacities throughout both lungs suggestive of multifocal atypical pneumonia (Figure ).
Chest CT showed multifocal ground glass opacities (GGO) throughout both lungs typical of underlying SARS-CoV-2 infection. There was no evidence for pulmonary embolism (Figure ).
He appeared well throughout the remainder of his stay in the ED with stable vitals. The patient was ambulated in the ED with no decrease in oxygen saturation noted. Although the patient had imaging findings typical of COVID-19 pneumonia and a corroborating history of present illness, the patient was nonetheless treated with 500 mg intravenous azithromycin and 1 g of ceftriaxone as empiric treatment for community-acquired pneumonia. Given that the patient had no other comorbidities, and wanted to go home, he was discharged home with a course of oral antibiotics. During a telephone follow-up three days after being discharged, the patient reported that he continued to feel better while at home.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [99.1, 'degrees fahrenheit'], 'Heart Rate or Pulse': [87.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [3000.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 99.1 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 67.1 = 37.27778 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 87.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 3000.0 count/m^3. To convert 3000.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 3000.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 3e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6661,51,SIRS Criteria,diagnosis,integer,usmle-11198,Extracted,"A 27-year-old female is brought in by ambulance with altered mental status. She is in a comatose state, but is breathing spontaneously with deep and rapid respirations. Her vital signs are as follows: T 100.2F, BP 92/54 mmHg, HR 103 bpm, RR 28, and SpO2 97% on room air. Complete blood count reveals: WBC 12.7, hemoglobin 11.3, platelets 254. Basic metabolic panel reveals: sodium 137, potassium 4.2, chloride 100, bicarbonate 16, creatinine 1.78 An ABG is performed which showed pH 7.38, PaO2 94, PaCO2 26.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [100.2, 'degrees fahrenheit'], 'Heart Rate or Pulse': [103.0, 'beats per minute'], 'respiratory rate': [28.0, 'breaths per minute'], 'White blood cell count': [12.7, 'µL'], 'PaCO2': [26.0, 'mm hg']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 100.2 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 68.2 = 37.88889 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 103.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 12.7 count/µL. To convert 12.7 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 12.7 white blood cell count/µL * 1.0 µL/mm^3 = 12.7 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 28.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is 26.0 mm Hg, which is less than than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6662,51,SIRS Criteria,diagnosis,integer,usmle-10017,Extracted,"A 55-year-old man presents with a 2-month history of an increasing sensation of fullness in the upper left side of his abdomen. He complains of increasing fatigue and dyspnea. He has no history of serious illness and takes no medications. His temperature is 36.7°C (98.1°F), pulse is 90/min, respiratory rate is 18/min, and blood pressure is 125/70 mm Hg. His conjunctivae are pale. The examination of the heart and lungs shows no abnormalities. The splenic margin is palpable 8 cm (3.1 in) below the costal margin. No abnormal lymph nodes are found. Laboratory studies show:
Hemoglobin 8 g/dL
Mean corpuscular volume 90 μm3
Leukocyte count 3,000/mm3
Platelet count 85,000/mm3
Peripheral blood smear shows small lymphocytes with cell membrane projections. Bone marrow aspiration is unsuccessful. Cell immunophenotyping is positive for CD25.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.7, 'degrees celsius'], 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [3000.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.7 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 90.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 3000.0 count/m^3. To convert 3000.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 3000.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 3e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6663,51,SIRS Criteria,diagnosis,integer,pmc-5083267-1,Extracted,"A 57-year-old man visited Inje University Ilsan Paik Hospital after experiencing abdominal pain, nausea, and vomiting for 3 weeks. He had visited our emergency room for the same symptoms 2 weeks prior, where he was suspected of having paralytic ileus. However, he was discharged against our medical advice, insisting that his symptoms were not severe. His symptoms had not improved since this visit. He had chronic renal disease for 10 years. Instead of taking prescription drugs, he had been using self-manufactured herbal medication for over 6 months. The herbal medication included more than 10 herbal ingredients such as sansisi (Gardenia jasminoides), hua shi (magnesium silicate), long gu (Mastodi ossis fossilia or talc), and mu li (Ostrea gigas). He had been taking no other medication except for the herbal medicine. He was a 15-pack-year current smoker, and did not drink alcohol.
The patient looked acutely ill; his blood pressure was 132/71 mmHg, pulse rate 97/min, respiratory rate 20/min, and body temperature 36.2℃. The patient's abdomen was distended and tympanic, and showed tenderness without rebound tenderness. In addition, his bowel sounds were decreased. Laboratory tests were as follows: white blood cell 6,970/mm3, hemoglobin 8.1 g/dL, platelet count 372,000/mm3, BUN 43 mg/dL, creatinine 4.52 mg/dL, and CRP 0.3 mg/dL. The electrolyte levels were within normal limits.
A plain radiograph showed diffuse small bowel distension and colon wall calcification along the colonic area (). Because of his reduced renal function, a non-contrast-enhanced CT scan was taken, which showed diffuse fluid-filled distension of the small bowel with colonic wall thickening and calcifications in the colon wall and at the mesocolon, suggesting atherosclerotic changes (). Paralytic ileus was suspected, and the patient was initially managed with supportive care including hydration, bowel rest, and nasogastric drainage. However, a follow-up CT taken on hospital day 7 did not show any improvement in bowel distention. Colonoscopy without bowel preparation performed on hospital day 8 showed diffuse bluish edematous mucosal change, multiple scarring, and loss of vascularity from the distal sigmoid to the transverse colon. There was a pinpoint stricture in the transverse colon, 65 cm from the anus, and scope passage was not possible (). A biopsy taken from the stricture site showed chronic inflammation and fibrosis with mild regenerative change (). Under the supposition of a PC diagnosis, a contrast-enhanced CT scan with delayed phase angiography was performed, which showed extensive calcifications along the colonic wall, mesenteric, and portal veins (). Total colectomy was recommended, but the patient refused. Fortunately, on the day after the colonoscopy, the patient's symptoms dramatically improved, and the ileus disappeared (). Presumably, this was due to the dilatational effect from the scope passage attempt, or dislodgement of a fecalith. Based on radiologic, endoscopic, and histologic findings, we diagnosed the patient with PC. After several days of a soft diet, the patient remained asymptomatic, and was discharged. The patient is currently symptom-free, after 2 months of follow-up.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.2, 'degrees celsius'], 'Heart Rate or Pulse': [97.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [6970.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.2 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 97.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 6970.0 count/m^3. To convert 6970.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 6970.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 6.97e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6664,51,SIRS Criteria,diagnosis,integer,pmc-7154252-1,Extracted,"A 25-year-old healthy Thai man presented with progressive dyspnea for 1 month. Four months earlier, the patient had developed generalized myalgia without clinical weakness that was predominant on both thighs (pain score 7/10) and a low-grade fever. Two months later, the fever persisted and he complained of difficulty climbing stairs. He had occasional knee pain on both sides and weight loss from 65 to 60 kg in 3 months. One month later, he developed rapidly progressive dyspnea and noticed a new-onset periorbital rash, which brought him to the hospital.
Vital signs on admission were temperature of 36.7°C, blood pressure of 115/75 mm Hg, pulse rate of 119 beats/min, respiratory rate of 30 breaths/min, and severe hypoxemia (SpO2 74% in room air). Physical examination revealed erythematous to violaceous patches on the periorbital areas (heliotrope rash), red to violaceous papules (Gottron's papules) with overlying ulcerations and crusts on the right 3rd metacarpophalangeal joint and 4th proximal interphalangeal joint, ill-defined violaceous erythema (Gottron's sign) on the left 3rd metacarpophalangeal joint, tender erythematous papules, and ulcerations on the palmar surfaces of the distal interphalangeal joints of both hands and medial aspect of the index fingers. Livedo reticularis was also detected on the palmar surfaces of the index fingers of both hands, and erythematous linear plaques (flagellate erythema) were noticed on both inner thighs (Fig. ). Mechanic's hands were not found. Chest auscultation was notable for bilateral basal lung crepitation. He had bilateral proximal muscle weakness grade IV/V at both the upper and lower extremities. No signs of arthritis were detected. Other findings were unremarkable.
Laboratory investigations showed mild anemia (Hb 9.1 g/dL), a white blood cell count of 10,370/µL (neutrophils 85%, lymphocytes 8%, monocytes 4%, eosinophils 3%), a C-reactive protein level of 3.53 mg/dL, and an erythrocyte sedimentation rate of 68 mm/h. Creatine kinase and aspartate aminotransferase were high at 505 mg/dL and 105 IU/L, respectively. Alanine aminotransferase was normal (20 IU/L). The anti-nuclear antibody titer was 1:80 (fine speckle type and cytoplasmic pattern), and anti-Ro-52 was positive. Anti-MDA5 antibody was positive, whereas anti-Jo-1, anti-Mi-2, and anti-SRP antibodies as well as other myositis panels were negative which were detected by Western blot.
An anteroposterior chest X-ray showed bilateral interstitial infiltration at both lungs. A high-resolution CT scan of the chest revealed multifocal areas of ground glass attenuation and alveolar opacity throughout the lung parenchyma and predominately at the peripheral and peribronchiolar regions (Fig. ). Electromyographic findings suggested inflammatory myositis. Histopathological findings from the right 3rd knuckle revealed interface changes with sparse inflammatory cell infiltrate (Fig. ).
The patient was diagnosed with RP-ILD with anti-MDA5 antibody-positive classical DM. He was initially treated with intravenous hydrocortisone (300 mg/day) and 125 g of intravenous immunoglobulin (0.4 g/kg/day) divided over 5 days due to impending respiratory failure. However, his condition deteriorated. He developed new-onset fever on the 7th day after admission and a chest X-ray showed progressive alveolar infiltration. Meropenem was administered intravenously at a dose of 1 g every 8 h. Bronchoalveolar lavage was performed and bronchoalveolar lavage fluid cultures were negative for microorganisms. Pathological transbronchial biopsy results revealed benign bronchial epithelium with fibrinous material and no malignancy. Dexamethasone was administered intravenously at a dosage of 20 mg per day in addition to the patient's existing treatment regimen. However, his status progressed towards respiratory failure, and he required ventilator support. He died due to respiratory failure on day 22.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.7, 'degrees celsius'], 'Heart Rate or Pulse': [119.0, 'beats per minute'], 'respiratory rate': [30.0, 'breaths per minute'], 'White blood cell count': [10370.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.7 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 119.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 10370.0 count/µL. To convert 10370.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 10370.0 white blood cell count/µL * 1.0 µL/mm^3 = 10370.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 30.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 1 + 1 = 2 criteria met.
Hence, the the number of SIRS criteria met by the patient is 2."
6665,51,SIRS Criteria,diagnosis,integer,pmc-6396484-1,Extracted,"A 39-year-old apparently healthy woman complained of fever and productive cough, in March, 2017. Her medical history did not reveal any specific illness, including acquired immune deficiency syndrome, collagen disease, and congenital immunodeficiency. She neither smoked nor consumed alcohol. Three days after onset (clinical day 3), she was admitted to a local general hospital, owing to progressive fever, malaise, and anorexia. On admission, her vital signs were as follows: body temperature, 39.2 °C; blood pressure, 106/64 mmHg; pulse, 80 beats/min with a regular rhythm; SpO2, 97% in an air-conditioned room; and respiratory rate, 16 breaths/min. Cyanosis, cardiac murmur, and abnormal breath sounds were absent. The patient’s liver, spleen and lymph nodes were not palpable. Her white blood cell count was 5600/μL, with a shift to the left (81.2% neutrophils). Her aspartate aminotransferase level was 23 IU/L; alanine aminotransferase, 12 IU/L; lactate dehydrogenase, 206 IU/L; and C-reactive protein, 2.4 mg/dL (normal range, 0–0.3 mg/dL). Moreover, the patient’s chest X-ray and chest computed tomography (CT) images revealed subsegmental consolidation in her right lower lobe (Figs. a, f). After admission, administration of ampicillin/sulbactam (ABPC/SBT), at 6 g/day, was initiated under a clinical diagnosis of severe community-acquired pneumonia. Azithromycin (AZM) was also given at 2 g/day p.o. stat on clinical day 3 (Fig. ). Her indirect hemagglutination titer for MP was negative (1:40) on clinical day 4. After admission (clinical day 7), her fever had not subsided, and the pulmonary lesions had extended to the entire right lower lobe as well as to the left lower lobe (Figs. b, g). Thus, bronchoalveolar lavage (BAL) and a transbronchial biopsy of the right lower lobe were performed. These examinations revealed nonspecific inflammation with neutrophil infiltration, but no pathogen was identified on pathological or microbiological examination. Contrary to the extremely rapid progression of the pulmonary lesions, her general condition had not significantly deteriorated, which was not compatible with severe bacterial infection. Owing to the unique clinical presentation, organizing pneumonia was considered. Therefore, treatment with prednisolone (PSL) was initiated at 40 mg/day from clinical day 7, and steroid pulse therapy (methylprednisolone 1 g/day) was given on clinical days 10–12. However, neither her symptoms nor her pulmonary lesion improved (Figs. c, h). Rather, her respiratory failure had worsened significantly, after steroid pulse therapy (clinical day 14), as she required oxygen inhalation at 15 L/min on her motion; therefore, she was transferred to our hospital (Hokkaido University hospital) for further examination and treatment. Considering the existence of lower respiratory tract infection due to any rare pathogens, ABPC/SBT was changed to meropenem (MEPM) on clinical day 14, and levofloxacin (LVFX) and minocycline (MINO) were also initiated concurrently. On admission (clinical day 14), her indirect hemagglutination titer for MP had elevated to 1:2560, which was more than that identified on clinical day 4 at the referring hospital. Moreover, BAL fluid (BALF) examination, which was performed on the day of admission to our hospital, using Ribotest™ Mycoplasma (Asahi Kasei Pharma Corporation, Japan), yielded positive results for the mycoplasma antigen. No other pathogen was identified on microbiological examination of the BALF. Based on these clinical findings, we confirmed our case as severe life-threatening MP pneumonia. Thereafter, we continued empirical antibiotic therapy with LVFX, MINO and MEPM, and corticosteroid therapy with PSL at 40 mg/day. Two days later (clinical day 16), her fever, malaise, and hypoxia had resolved, and her pulmonary lesions had significantly improved (Fig. d). Therefore, we replaced the antibiotics with garenoxacin (GRNX) as monotherapy, at 400 mg/day, and reduced the dosage of PSL from clinical day 18. The patient was discharged on day 24, and administration of GRNX and corticosteroid therapy were continued until clinical day 30 (Fig. ). Subsequently, she had an uneventful recovery with no recurrence of fever or pneumonia.
Due to the rarity of our patient’s clinical course, we performed further molecular identification using DNA extracted from her BALF. DNA of MP was identified by real-time polymerase chain reaction (PCR) with Mp181-F and Mp181-R primer pairs and an Mp181-P probe []. A previously described RFLP analysis of point mutation in domain V of MP 23SrRNA gene [] was used to identify mutations known to confer macrolide resistance (2063, 2064, and 2617 in the MP 23S rRNA gene domain V region). The result of the molecular analysis was positive for A2063G mutation, which was, at that time, a common macrolide-resistant mutant of MP in Japan. Based on these results and the clinical course, we confirmed our case as severe MP pneumonia due to a macrolide-resistant strain.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.2, 'degrees celsius'], 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'respiratory rate': [16.0, 'breaths per minute'], 'White blood cell count': [5600.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.2 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 80.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 5600.0 count/µL. To convert 5600.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 5600.0 white blood cell count/µL * 1.0 µL/mm^3 = 5600.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 16.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6666,51,SIRS Criteria,diagnosis,integer,pmc-7588679-1,Extracted,"A 16-year-old female with a complicated past medical history inclusive of recurrent and self-resolving episodes of ALI since birth presented to the emergency department with a 2-day history of right upper quadrant abdominal pain, vomiting, and altered mental status.
A detailed history, obtained from both parents, described chronic medical complexity with multiorgan system involvement. The patient, born at 26 weeks of gestation, was diagnosed with developmental delay, short stature, and learning disability. Due to failure to thrive, she was gastrostomy tube dependent until 11 years of age. She was being treated for polycystic ovarian syndrome (managed with norgestrel, ethinyl estradiol, metformin, and spironolactone), hypothyroidism (managed with levothyroxine), chronic constipation (managed with polyethylene glycol), and anxiety disorder (managed with sertraline). Since birth, she had experienced several self-resolving ALI episodes of unknown etiology, characterized by elevated hepatic enzymes. According to her parents, the last ALI episode was 10 years before, probably triggered by a febrile illness. Although these episodes required hospital admission, each resolved spontaneously without any apparent long-term complications. Several genetic and metabolic workups failed to establish a definitive etiology for the ALI. The parents denied exposure to potential hepatotoxic agents or a special diet. The patient's immunizations were up-to-date, and workup for immune deficiency was negative.
On admission, her vital signs were remarkable for hypertension (134/100 mm Hg), tachycardia (pulse of 114 beats/min), and tachypnea (respiratory rate of 28 breaths/min). Her oxygen saturation was 99% on room air. She was normothermic (body temperature of 36.9°C), her height was 147.3 cm (1st percentile), and her weight was 52.1 kg (36th percentile). On physical examination, she was found to be drowsy, weak, difficult to arouse, and slow to respond to questions. Also, unsteady gate and asterixis were noted. Her abdomen was soft, with slight tenderness to palpation over the right upper quadrant. There was no organomegaly or ascites, and the rest of the physical examination was unremarkable.
Initial laboratory evaluation included a white blood cell count of 25,600/μL, hemoglobin of 10.5 g/dL, and a platelet count of 270,000/mm3. Serum chemistries showed normal electrolytes and serum albumin, transaminitis with aspartate transaminase >15,000 U/L (reference 5–26 U/L) and alanine transaminase 13,799 U/L (reference 12–49 U/L), hyperbilirubinemia (total serum bilirubin of 2.9 mg/dL), hyperammonemia of 107 μmol/L (reference ≤32 μmol/L), elevated lipase levels of 1,381 U/L (reference 64–231 U/L), coagulopathy with an INR of 2.8 (reference 1.0–2.0), lactic acidosis with a lactate level of 8.2 mmol/L (reference 1.0–2.4 mmol/L), pH of 7.29, and serum bicarbonate of 15 mEq/L (reference 17–31 mEq/L). The patient's elevated serum creatinine of 2.7 mg/dL, with an estimated glomerular filtration rate of 22 mL/min/1.73 m2(Schwartz formula), was consistent with stage III AKI based on the Kidney Disease: Improving Global Outcomes (KDIGO) classification []. Urinalysis was positive for proteinuria and microscopic hematuria (>50 red blood cells per high-power field) without signs of infection. Chest radiography and computed tomography of the abdomen and pelvis were unremarkable, excluding any inflammatory or obstructive process. The toxicology screen was found to be negative as well.
While treated empirically with broad-spectrum parenteral antibiotics (piperacillin-tazobactam) and intravenous fluids, the patient's mental status improved, but her serum chemistries continued to worsen, prompting transfer to the pediatric intensive care unit with a diagnosis of ALI complicated by stage III AKI. On her second day of admission, preliminary infectious workup (including aerobic blood cultures, polymerase chain reaction, and serology for common viral etiologies) returned positive for influenza A infection, although she did not have fever, rhinorrhea, or any upper respiratory tract symptoms. Further diagnostic evaluation included acylcarnitine, urine organic acid, and amino acid profiles, all of which were within the normal range. To determine the etiology of the patient's ALI, she underwent a transjugular liver biopsy that revealed submassive hepatocellular necrosis with microvascular steatosis, suggesting metabolic rather than autoimmune etiology (Fig. ).
Although encephalopathy, hyperammonemia, and overall liver function improved with conservative medical management, the patient's renal function continued to deteriorate. Despite an adequate urine output, her serum blood urea nitrogen and creatinine continued to worsen (44 and 4.8 mg/dL, respectively), with an estimated glomerular filtration rate of 13 mL/min/1.73 m2. Due to the development of 5% fluid overload with pulmonary congestion and a new oxygen requirement, acute intermittent hemodialysis was initiated. An intrinsic kidney insult was suggested by urinary fractional excretion of sodium of 6.1% and elevated neutrophil gelatinase-associated lipocalin levels of 4,182 ng/mL (reference <50 ng/mL). Histology obtained by kidney biopsy demonstrated tubular injury with extensive tubular dilation, tubular epithelial necrosis, and glomerular sparing, most consistent with acute tubular necrosis (Fig. ).
During the patient's hospital course, while liver function resolved almost wholly, renal recovery was delayed until 1 week after hospital discharge. In the setting of recurrent episodes of ALI and new-onset AKI, exome sequencing analysis confirmed a biallelic abnormality in the NBAS gene that could retrospectively explain her convoluted liver history and perhaps this recent episode of kidney involvement as well.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.9, 'degrees celsius'], 'Heart Rate or Pulse': [114.0, 'beats per minute'], 'respiratory rate': [28.0, 'breaths per minute'], 'White blood cell count': [25600.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.9 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 114.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 25600.0 count/µL. To convert 25600.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 25600.0 white blood cell count/µL * 1.0 µL/mm^3 = 25600.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 28.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6667,51,SIRS Criteria,diagnosis,integer,pmc-5815698-1,Extracted,"A 30-year-old Taiwanese woman presented with intermittent spiking fever and sore throat for 5 days. She also described the migratory pain at sole, ankle, knee in previous 3 weeks. She visited our outpatient department, where salmon-like pink rash was found at her ankle and knee. According to the Yamaguchi criteria, she was newly diagnosed with AOSD. Because of relapsing spiking fever, she was medicated with high-dose systemic corticosteroid therapy for 3 days (methylprednisolone 500 mg/d) then shifted to oral prednisolone (0.5 mg/kg/d). Ten days later, she was readmitted because of intermittent fever and diarrhea. Chest radiography revealed mild left-sided pleural effusion. Blood cultures indicated the presence of S enteritidis bacteremia. She received intravenous ceftriaxone (2000 mg/d) for 1 week. S enteritidis was absent in follow-up blood cultures. Chest radiography and transthoracic echocardiography (TTE) were normal with no evidence of fluid accumulation.
However, she gradually suffered from dyspnea on exertion, nausea with vomiting, and frequent epigastric fullness in recent 2 months. In the emergency department, her initial vital signs were as follows: temperature, 36.2 oC; heart rate, 105 beats/minute; respiratory rate, 24 breaths/minute; blood pressure, 102/76 mmHg; and oxygen saturation, 95%. Chest auscultation revealed bilateral basal rales, and cardiac auscultation revealed mildly diminished heart sound without pericardial knock or friction rub. An electrocardiogram revealed sinus tachycardia without ST segment elevation. Chest radiography revealed massive left-sided pleural effusion. Blood investigations revealed severe infectious disorder, with a white blood cell count of 11800/L, C-reactive protein level of 118.2 mg/L, and procalcitonin level of 0.30 ng/mL. Blood cultures disclosed recurrence of S enteritidis bacteremia. She was admitted and treated with intravenous ceftriaxone (2000 mg/d). A pigtail catheter (8.5 French) was inserted and 500 mL of serosanguinous pleural effusion was drained out on the first day.
During hospitalization, the patient remained critically ill in spite of pigtail catheter drainage and antibiotic therapy. TTE was obtained which displayed a thickened pericardium with hyperechoic nonfloating bodies in the pericardial space, resulting in left ventricular posterior wall diastolic collapse (Fig. A). In addition, pulsed-wave Doppler analysis displayed exaggerated respiratory variation in mitral inflow velocity (Fig. B) and expiratory diastolic flow reversals of prominent hepatic vein, consistent with purulent constrictive pericarditis. Computed tomographic angiography confirmed the findings of TTE with loculated pericardial effusion and consolidation foci in the left lower lobe, and with no evidence of mycotic aneurysm (Fig. ).
After obtaining informed consent, she underwent subtotal pericardiectomy through a limited (9 cm) median sternotomy. The markedly thickened pericardium was observed and incised vertically by a scalpel. The purulent debris and loculations in the pericardial cavity were manually evacuated and sent for microbial study. Fibrous adhesions between the parietal and visceral pericardium were made free. Then, the pericardium was gently stripped from the right atrium to the right ventricle. Hemodynamic status remarkably improved during the operation, with central vein pressure from 20 to 11 mmHg and mixed venous oxygen saturation from 38% to 79%. Histopathologic examination of the resected pericardium revealed a fibrous thickening. Subsequent cultures of pericardial fluid yielded S enteritidis. The patient received the same antibiotic regimen of ceftriaxone (2000 mg/d) in the hospital for 1 month. The New York Heart Association functional classification downgraded from class III to class I. There are no reaccumulation of pericardial effusion and no recurrent constrictive pericarditis on serial postoperative TTE.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.2, 'degrees celsius'], 'Heart Rate or Pulse': [105.0, 'beats/minute'], 'respiratory rate': [24.0, 'breaths/minute'], 'White blood cell count': [11800.0, 'L']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.2 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 105.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 11800.0 count/L. To convert 11800.0 count/L of white blood cell to mm^3, multiply by the conversion factor 1e-06 L/mm^3 which will give 11800.0 white blood cell count/L * 1e-06 L/mm^3 = 0.0118 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 24.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6668,51,SIRS Criteria,diagnosis,integer,pmc-5040579-1,Extracted,"12-year-old boy presented with history of trauma to his right ankle three days back. He complained of pain and swelling of right ankle. He also gave a history of associated cough and fever since 5 days. The personal and past history was insignificant.
Patient was febrile with 38.5 degree Celsius temperature; tachycardia at 125/min and respiratory rate 25/min. Right ankle was mildly swollen with redness, local rise of temperature, tenderness over lateral malleolus, lower 3rd leg laterally (). There was restriction of ankle movements. No neurovascular deficits. Rest of the limb was normal. Plain X-ray of right ankle with leg was normal. His blood parameters were; haemoglobin-12.5gm%;total count- 21.28K/uL; neutrophils-19.77K/uL; lymphocytes-0.75K/uL%, CRP- 360.1mg/L(positive); ESR--60mm/hr; RAfactor-negative; ASO-titre- 400IU/ML; sickling-negative. Urine routine was performed and found to benormal. Patient was admitted for treatment of suspected cellulitis, pediatric opinion was sought for cough. Chest X-ray: revealed pneumonia, therefore he was started on IV Cloxacillin 1gm four times daily. Later blood culture revealed growth of Staphylococcus aureus which was sensitive to Cloxaciilin. On the 3rd day, patient’s general condition deteriorated with persistently elevated temperature, tachycardia (140/min), respiratory rate at 40/min and SPO2- 87% at room air with moderate swelling on whole of right leg with tender calf and a positive Homan sign. D-Dimer test was negative. CT angiogram of chest was carried out to rule out pulmonary embolism. There was no evidence of embolism, but showed right sided pleural effusion and bilateral patchy pneumonia. The duplex scan of right lower limb was suggestive of popliteal vein thrombosis (, ), thrombophilia work up for protein C &S; anti- thrombin III was negative. Patient was treated with low molecular heparin and IV cloxacillin (for pneumonia) in intensive care unit. Patient improved clinically, calf swelling was reduced and blood parameters were also reverting to normalcy at the time of discharge. Patient was discharged on 14th day and was treated with warfarin for next 3 months. Repeat duplex scan at 6 weeks was normal. Patient was followed up for period of 6 months, and there were no signs of recurrence.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.5, 'degrees celsius'], 'Heart Rate or Pulse': [140.0, 'beats per minute'], 'respiratory rate': [40.0, 'breaths per minute'], 'White blood cell count': [21280.0, 'µL']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.5 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 140.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 21280.0 count/µL. To convert 21280.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 21280.0 white blood cell count/µL * 1.0 µL/mm^3 = 21280.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 40.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6669,51,SIRS Criteria,diagnosis,integer,pmc-3685548-1,Extracted,"A 66 year-old man with a past medical history of hypertension, hypothyroidism, hyperhomocysteinemia, and major depressive disorder was transferred to our hospital for further evaluation of altered mental status. The patient had been cattle ranching four days prior to his initial hospital presentation. While cattle ranching, he began having malaise and cramping in his hands. He subsequently vomited and started having diarrhea. Given that the temperatures outside were above 100 degrees Farhanheit during the first two days while cattle ranching, the patient’s wife felt he was dehydrated and encouraged him to drink more fluids. On the third day of cattle ranching, the patients’ mental status deteriorated as he became increasingly lethargic. He was taken to an outside hospital and was intubated for airway protection. Outside hospital laboratories demonstrated the following significant laboratories: WBC 11.4 K/cmm, Hemoglobin 15.6 K/cmm , Na 143 mEq/L, K 5.9 mEq/L, Phosphorus 6.4 mEq/L, anion gap 22 mEq/L, creatinine 5.5 mg/dL, C-reactive protein (CRP) 22.7 mg/L, erythrocyte sedimentation rates (ESR) 50 mm/hr, lactate 2 mMol/L, and troponin 0.229 ng/mL, CK-MB 8.1 ng/mL, and lipase 1091 unit/L. The patient displayed evidence of multiorgan failure and was transferred to our hospital for further care.
Upon arrival (five days after his initial presentation to the outside hospital), the patient was euthermic at 97.8 F. His heart rate was 86, blood pressure 162/82, and respiratory rate 18. His neurological examination was significant for lethargy, dysarthria, impaired vertical eye movements, diffuse weakness in all limbs (4 out of 5 power in the extensors of the arms and flexors of the legs), bilateral ataxia on finger to nose, and bilateral extensor plantar responses. General physical examination was normal other than bilateral scattered crackles on lung auscultation. There were no stigmata of infectious endocarditis.
Laboratory findings upon transfer were remarkable for an elevated C-reactive protein of >190 mg/L, ESR of 111 mm/hr, ALT 91 U/L, AST 51 U/L, and a macrocytic anemia with a hemoglobin and hematocrit of 13.2/38.2 K/cmm. WBC, platelets, PTT/PT/INR, vitamin B12, folate, homocysteine, cardiac enzymes including CK, thyroid studies, creatinine, and blood cultures were normal. Abdominal ultrasound showed evidence of hepatic steatosis and transthoracic echocardiogram showed normal ejection fraction with left ventricular hypertrophy and diastolic dysfunction but no evidence of vegetations or wall motion abnormalities.
Diffusion weighted magnetic resonance imaging showed multiple punctate foci of restricted diffusion involving the frontoparietal cerebral cortex and cerebellum bilaterally as well as two larger foci in the dorsomedial and ventrolateral thalami bilaterally (Figure ). These abnormal lesions showed decreased ADC and heterogeneous postcontrast enhancement (Figure ). Magnetic resonance angiography of the head and neck vasculature showed normal flow-related signal within the intra and extracranial vessels. There was trace layering of intraventricular hemorrhage within the bilateral occipital horns on the GRE sequence.
After nine days of hospitalization, the patient started to awaken and became more alert. During hospitalization he was started on Amantadine and was eventually discharged to an acute rehabilitation facility. After two weeks of inpatient therapy, the patient had persistent cognitive deficits including poor short term memory.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [97.8, 'degrees fahrenheit'], 'Heart Rate or Pulse': [86.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [11400.0, 'µL']}",0,0,0,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 97.8 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 65.8 = 36.55556 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 86.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 11400.0 count/µL. To convert 11400.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 11400.0 white blood cell count/µL * 1.0 µL/mm^3 = 11400.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 0.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 0.
Hence, the the number of SIRS criteria met by the patient is 0."
6670,51,SIRS Criteria,diagnosis,integer,pmc-3318165-1,Extracted,"A 38-year-old female patient was diagnosed with clinical Stage IIIC (cT2cN3M0) infiltrating ductal carcinoma of the left breast with left supraclavicular lymph nodes metastases. She was treated with neoadjuvant chemotherapy consisting of docetaxel and doxorubicin. After six cycles of chemotherapy, the supraclavicular lymph node was not palpable with a partial response of the breast cancer and the axillary nodes. She underwent a curative resection for the breast cancer, and the final pathologic stage was ypStageIIIC (ypT2N3M0). Immunohistochemistry showed negative staining for the estrogen receptor (ER), progesterone receptor (PR), and human epithelial growth factor receptor 2 (HER2). Histological and nuclear grades were III/III and 3/3, respectively, and extensive endolymphatic tumor emboli were present. Adjuvant chemotherapy with cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) was commenced, but on her visit for the third cycle she complained of sudden-onset right chest pain and cough. Her chest X-ray was within normal limits (). Ten days later, she felt right inspiratory chest pain and was referred to the emergency department. She complained of dyspnea on exertion (DOE), cough, and a mild febrile sense, however, she denied the high fever, sputum, pitting edema, or orthopnea. Her initial vital signs were a heart rate of 97 beats per minute, respiratory rate of 20 per minute, blood pressure of 133/68 mmHg, body temperature of 36.5℃, and oxygen saturation 97% on room air. Signs of respiratory distress were not definite. Fine crackles in the right upper lung field were present on chest auscultation but a pleural friction rub was not present. A chest X-ray demonstrated patchy consolidation on the right upper lung field () and computed tomography (CT) showed right upper lobe (RUL) patchy consolidation with ill-defined small ground glass opacities (GGO) in the RUL and right lower lobe (RLL) (, respectively). The differential diagnosis from the radiological study was pneumonia with a fungal etiology but we could not rule out a bacterial etiology. The white blood cell count was 5,800/mm3, and the segmented neutrophil portion was 76.4%. The C-reactive protein level was 0.86 mg/dL (reference range, 0-0.5 mg/dL) and there was no evidence of pulmonary thromboembolism on chest CT.
We started empirical antibiotics with third generation cephalosporin and macrolide under the impression of community acquired pneumonia, but the follow-up chest CT at 1 week showed an increased extent of RUL patchy consolidation (, ). Furthermore, subjective symptoms of dyspnea and pleuritic chest pain rapidly aggravated. No microorganisms were identified on the initial respiratory specimen culture. Findings from chest X-rays and chest CT suggested fungal pneumonia, however, the patient had not experienced severe neutropenia for several months, and there were no predisposing clinical factors favoring a diagnosis of fungal pneumonia. We considered the probability of lymphangitic metastatic carcinoma or a fungal infection such as aspergillosis or mucormycosis. Therefore, we performed a video-assisted thoracoscopic lung biopsy for an accurate pathological diagnosis before administering antifungal agents. We thought it might be difficult to obtain a differential diagnosis using a percutaneous needle biopsy, because the nature of the lesion was infiltrative consolidation, not a mass.
We performed a wedge resection of the RUL. The specimen was 6×3×3 cm, and a gross examination of the sections showed focal brownish discoloration of lung parenchyma without definite evidence of necrosis, tumor, hemorrhage, or a calcified area. A microscopic examination showed metastatic carcinoma with extensive endolymphatic tumor emboli and hemorrhagic infarctions (, ). In contrast, Gram staining revealed no microorganisms and Gomori's methenamine silver and periodic-acid Schiff stains revealed no fungal hyphae. The Mycobacterium tuberculosis-polymerase chain reaction result was also negative.
We confirmed that the patient was not under infection, so we discontinued antimicrobial agents, enrolled the patient to the clinical trial and started first-line palliative chemotherapy consisting of ixabepilone (Ixempra™; Bristol-Myers Squibb, New York, USA) and capecitabine (Xeloda®; Roche, Basel, Switzerland), as the disease had relapsed just 4 months after neoadjuvant docetaxel and doxorubicin and during adjuvant CMF chemotherapy (). This study was supported by a grant of the Korean Health Technology R&D Project, Ministry of Health & Welfare, Republic of Korea (A110448). After chemotherapy, the size of the consolidative lesion in the RUL and the extent of focal GGO in RUL and RLL decreased markedly. The pleuritic chest pain and DOE also improved. Currently, after 17 months, she is under palliative chemotherapy and regular follow-up with partial response to the disease ().",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.5, 'degrees celsius'], 'Heart Rate or Pulse': [97.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [5800.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.5 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 97.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 5800.0 count/m^3. To convert 5800.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 5800.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 5.8e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6671,51,SIRS Criteria,diagnosis,integer,pmc-7179991-1,Extracted,"A 61-year-old morbidly obese African American female presented to emergency department with chief complaint of left-sided chest pain of one-hour duration with progressively worsening shortness of breath and cough and some body aches for past few days. Her medical history was pertinent for coronary artery disease requiring multiple stent placements, chronic obstructive pulmonary disease, pulmonary hypertension, smoking dependence, uncontrolled diabetes mellitus, obstructive sleep apnea with continuous positive airway pressure use, cerebrovascular accident, and gastro-esophageal reflux disease. She denied any fever, sore throat and gastrointestinal symptoms. She did not have any exposure to sick contacts.
Initial evaluation in the emergency room revealed temperature of 98.4 F, blood pressure of 146/84, respiratory rate in mid-30’s, heart rate of 99, and saturating 95% on 15 liters oxygen. Stat electrocardiogram (EKG) revealed ST elevations in leads II, III, aVF with reciprocal changes in V1, V2 consistent with acute inferior wall STEMI (Figure ).
Labs were significant for WBC of 9.8, elevated cardiac enzymes including CK of 606, CK-MB of 42, Troponin I of 3.53, elevated brain natriuretic peptide (BNP) of 4960, and elevated liver function tests including aspartate aminotransferase (AST) of 168 and alanine aminotransferase (ALT) of 93. Chest X-ray at that time showed diffuse bilateral pulmonary infiltrates consistent with cardiogenic edema (Figure ).
Cardiologist was notified immediately, and the patient was taken to the cardiac catheterization lab. Emergent left heart catheterization (LHC) showed subtotal occlusion of her previous stent located in right coronary artery (RCA). She was treated with aspiration thrombectomy and a drug eluting stent placement. Repeat EKG after the stent placement showed resolution of ST-elevation changes (Figure ).
Echocardiogram post LHC showed moderately reduced ejection fraction (EF) of 30-35%. Her previous echo from 2018 showed an EF of 65%. The patient was transferred to intensive care unit after the stent placement and was initially placed on bilevel positive airway pressure (BIPAP) followed by intubation due to worsening hypoxia. X-ray repeated at that time showed bilateral ground glass opacities more consistent acute respiratory distress syndrome (ARDS) (Figure ).
Covid-19 test was sent out and it came back positive.
She was started on hydroxy-chloroquine along with azithromycin immediately and continued on mechanical ventilation with ARDS protocol. Her troponins peaked to 18 and then started to trend down. Labs done the next day showed elevated lactic acid dehydrogenase (LDH) of 2850, D-Dimer of 2000. Currently, the patient is on a ventilator with positive end expiratory pressure (PEEP) of 10, and 100% Fio2.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [98.4, 'degrees fahrenheit'], 'Heart Rate or Pulse': [99.0, 'beats per minute'], 'respiratory rate': [30.0, 'mid’s breaths per minute'], 'White blood cell count': [9.8, 'L']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 98.4 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 66.4 = 36.88889 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 99.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 9.8 count/L. To convert 9.8 count/L of white blood cell to mm^3, multiply by the conversion factor 1e-06 L/mm^3 which will give 9.8 white blood cell count/L * 1e-06 L/mm^3 = 9.8e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 30.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6672,51,SIRS Criteria,diagnosis,integer,pmc-6453368-1,Extracted,"A 70-year-old woman with end-stage renal disease due to polycystic kidney disease (PKD) opted to undergo PD. Ten days after the initiation of automated PD consisting of 30 mL/kg peritoneal dialysate infusion three times a night, she suddenly complained of dyspnoea. Her blood pressure was 147/78 mm Hg, heart rate was 92 beats/min, temperature was 36.8°C, respiratory rate was 24/min and percutaneous oxygen saturation in room air was 88%. Her heart exam revealed normal S1 and S2 with no murmur, and her chest examination revealed attenuated breath sounds in addition to slight coarse crackle in the right lung field. The results of blood examination were as follows: white blood cell count=6.3×109/L, haemoglobin=112 g/L, platelet count=29.4×109/L, serum sodium=141 mmol/L, serum potassium=3.9 mmol/L, serum urea nitrogen=55.7 mg/dL, serum creatinine=6.64 mg/dL, serum albumin=3.4 g/dL, serum protein=6.6 g/dL, creatine kinase=64 IU/L, brain natriuretic peptide=113.8 pg/mL and C reactive protein<0.1 mg/dL. Electrocardiography revealed a normal sinus rhythm without ST-T segment abnormality. Chest X-ray radiography revealed massive right-sided pleural effusion (). At this point, she was suspected to have PPC. However, CT peritoneography using 40 mL/kg peritoneal dialysate mixed with 1.5 mL/kg contrast material on usual breath holding showed no leakage. Therefore, the phase of imaging was changed from the usual inspiratory level to the maximal inspiratory level. Accordingly, the patient was instructed to strain as if defecating, which resulted in the identification of a jet of contrast material from the peritoneal cavity flowing into the right pleural cavity and the exact site of the diaphragm defect (), which led to an accurate diagnosis of PPC. Due to the fact that PD during the daytime restart with 20 mL/kg peritoneal dialysate per session after the cessation of PD to improve her respiratory condition had induced hydrothorax again, she was expected to undergo a thoracoscopic surgery to continue PD. We could not identify the defect, although, we investigated the diaphragm thoroughly. Accordingly, using CO2 pneumoperitoneum through a PD catheter, we attempted to identify the exact defect (). There was no air leakage from the defect measuring <5 mm in diameter until the abdominal pressure was sufficiently increased with the CO2 pneumoperitoneum, and then closure of the defect and pleurodesis were performed.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.8, 'degrees celsius'], 'Heart Rate or Pulse': [92.0, 'beats per minute'], 'respiratory rate': [24.0, 'breaths per minute'], 'White blood cell count': [6.3, 'L']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.8 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 92.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 6.3 count/L. To convert 6.3 count/L of white blood cell to mm^3, multiply by the conversion factor 1e-06 L/mm^3 which will give 6.3 white blood cell count/L * 1e-06 L/mm^3 = 6.3e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 24.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6673,51,SIRS Criteria,diagnosis,integer,pmc-7354865-1,Extracted,"A previously healthy 5-year-old boy was transferred to our hospital because of melena and hematemesis. The child complained of periumbilical pain and vomiting four days before initial visit to our hospital, and a histamine 2 receptor (H2) antagonist and an antispasmodic agent were administered under the impression of acute enteritis. Powdered oral rehydration salts was also prescribed at a private clinic because of mild dehydration one day before the visit. Abdominal cramps and hematemesis occurred in two hours after taking ORS at home and the child was admitted at a private hospital. The medical history was unremarkable except that Helicobacter pylori infection was diagnosed in the mother of the child a few months ago. The vital signs at the first hospital were relatively stable and the hemoglobin level was 11.5 g/dL. However, the child was transferred to our hospital because of recurrent hematemesis, development of melena, and dizziness. Initial vital signs in our hospital were as follows: blood pressure, 104/66 mmHg; heart rate, 133/minutes; respiratory rate, 22/minutes; and body temperature, 36.8°C. The child looked acutely ill and dehydrated. Anemic conjunctivae and pale, dried lips were also noted. Chest auscultation revealed clear breath sounds and tachycardia. Abdominal examination revealed epigastric tenderness and rigidity. There was no hepatomegaly or splenomegaly. Pale skin without purpura or rash was noted. Mental status was alert. Abdominal X-ray was unremarkable, but abdominal computed tomography (CT), performed because of abdominal rigidity, showed duodenal and gastric wall thickening. Complete blood cell counts were, hemoglobin, 6.9 g/dL; white blood cell count, 12,970/mm3; and platelet count, 384,000/mm3. Among the blood coagulation tests, prothrombin time, activated partial thrombin time, and international normalized ratio were 15.4 (reference range: 11.9–14.3) s, 31.1 (29.1–43.5) s, and 1.20, respectively. Biochemical laboratory analyses were performed and the results were as follows: sodium, 130.0 mmoL/L (135–145); potassium, 4.4 mmoL/L (3.3–5.1); chloride, 93 mmoL/L; serum osmolarity, 272 mOsm/L (276–300); aspartate aminotransferase, 17 U/L (15–50), and alanine aminotransferase, 6 U/L(5–45). Urinary blood and red blood cells were negative. Stool wet smear and culture were unremarkable but occult blood in stool was positive (432.5 ng/mL, 0–12.0).
Transfusion of packed red blood cells, octreotide and a proton pump inhibitor were promptly initiated after exclusion of surgical abdomen. Gastroduodenofibroscopy was performed to identify the cause of melena and hematemesis, which revealed linear ulcers and scattered submucosal hemorrhages in the prepyloric area of stomach, and large circular ulcers in the first and second portions of the duodenum. The duodenal ulcers were along the folds. The mucosal margin of the ulcers was distinct and easily friable (). Pathologic examination showed ulcer debris, gastritis, and active duodenitis (). Serologic test for H. pylori immunoglobulin G and M, and rapid urease test were negative. H. pylori was also not detected on pathologic examination using Giemsa stain (). Additionally, there was no evidence of vasculitis on pathologic examination (). Serum gastrin level was 28.5 pg/mL (13–115). After the results were reported, the mother recalled that a packet of ORS was reconstituted with a lesser amount of water (≈50 mL) than the instructed amount on the manual (200 mL) when the aggravation of abdominal pain and hematemesis occurred. The ORS reconstituted in 50 ml of water had higher osmolarity (992 msom/kg) and higher concentrations of sodium (176.5 mEq/L), potassium (81.8 mEq/L), glucose (9,451 mg/dL), and citrate (122.6 mEq/L) compared with the ORS reconstituted in 200 mL of water (). The abdominal pain was resolved promptly and melena disappeared in two days after treatment was initiated. The child was discharged with good general condition after eight days of hospital stay. He has been in good general condition during the last six months.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.8, 'degrees celsius'], 'Heart Rate or Pulse': [133.0, 'beats per minute'], 'respiratory rate': [22.0, 'breaths per minute'], 'White blood cell count': [12970.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.8 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 133.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 12970.0 count/m^3. To convert 12970.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 12970.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6674,51,SIRS Criteria,diagnosis,integer,pmc-4307710-1,Extracted,"A 59-year-old Caucasian man with past medical history significant for hypertension and hyperlipidemia presented to the emergency department with a four-day history of increasing throat pain and bilateral neck swelling. Associated symptoms included voice hoarseness, shortness of breath, dysphagia, and odynophagia. He denied recent dental procedures, upper respiratory tract infection or history of similar symptoms. Patient’s social history was negative for smoking, alcohol and illicit drug use. Initial vital signs were Blood Pressure 109/68, Pulse 101, Repiratory Rate 16, Temperature 98.1, and O2 saturation of 100% on room air. On exam, the patient was noted to have edema and tenderness to palpation of his entire right neck, with erythema tracking from the superior border of his right clavicle to the angle of the jaw on the right. No induration, crepitus or bullae were noted on the skin. Oral examination was remarkable for edema and erythema of the right anterior tonsil, without exudates or fluctuance, with mild deviation of the uvula to left. The laboratory values were significant for elevated leukocyte count of 29,000 with 89.9 % neutrophils and blood urea nitrogen and creatinine of 37 and 2.32, respectively. Computed tomography (CT) of the neck without contrast showed extensive edema in the oropharynx/hypopharynx, with edema and air within the retropharyngeal and danger space, as well as debris within the piriform sinus ( and ). Given the clinical exam, CT findings highly suspicious for “a gas-forming organism or necrotizing fasciitis,” and his laboratory results, blood cultures were drawn and intravenous clindamycin, vancomycin and ceftriaxone were empirically started. Otolaryngology was emergently consulted and the decision was made to immediately take the patient to the operating room for incision, drainage and washout.
Following nasotracheal intubation in the operating room (OR), the right neck was explored laterally into the retropharyngeal space. Purulent drainage was found to track via an overlying necrotic fascial plane into the parapharyngeal spaces as well as inferiorly into the superior mediastinum. Intraoperative gram stain showed gram positive cocci in both chains and clusters, gram negative rods and gram positive rods. The antibiotic regimen was changed to piperacillin/tazobactam and metronidazole (with discontinuation of clindamycin and ceftriaxone). Final wound culture grew Streptococcus anginosus and coagulase negative staphylococcus. The patient remained intubated postoperatively, and a repeat CT was performed on postoperative day 4 due to persistent leukocytosis. A residual phlegmon in the bilateral piriform sinuses was discovered, and the patient was then taken back to the OR for repeat right neck exploration, direct laryngoscopy, and bilateral incision and drainage of the peritonsillar space. Intra-operatively, cardiothoracic surgery was consulted to perform an open lateral thoracotomy to drain a posterior mediastinal phlegmon.
Despite repeat drainage, the patient began to decompensate, requiring multiple vasopressors to maintain adequate perfusion, and he suffered from persistent fevers, acute renal failure and transaminitis (aspartate aminotransferase 4202, alanine aminotransferase 1922). His leukocytosis continued to rise, peaking at 51,600. On postoperative day 7, the patient suffered a cardiac arrest requiring one round of chest compressions and epinephrine before return of spontaneous circulation. On postoperative day 9, his multisystem organ failure began to improve and the patient was slowly weaned off vasopressors, with successful extubation on postoperative day 12. He was discharged to a rehabilitation institution on postoperative day 21 with a peripherally inserted central catheter line to continue vancomycin, clindamycin and metronidazole for a total of four weeks. On recent follow-up with otolaryngology six weeks after his discharge, he was noted to be doing well and has elected to undergo cosmetic revision of right neck scar, the date of which is to be determined.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [98.1, 'degrees fahrenheit'], 'Heart Rate or Pulse': [101.0, 'beats per minute'], 'respiratory rate': [16.0, 'breaths per minute'], 'White blood cell count': [29000.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 98.1 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 66.1 = 36.72222 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 101.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 29000.0 count/µL. To convert 29000.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 29000.0 white blood cell count/µL * 1.0 µL/mm^3 = 29000.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 16.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6675,51,SIRS Criteria,diagnosis,integer,pmc-6487166-1,Extracted,"A 16-year-old previously healthy male presented to the emergency department with chills, abdominal pain, worsening nausea, and shortness of breath. He was noted to have increased work of breathing. Abdominal examination revealed mild tenderness in the periumbilical area, but no rebound guarding. His oral temperature was 38.6°C, heart rate 123 beats/min, blood pressure 121/69, and respiratory rate 20 breaths per minute. He was noted to have poor perfusion with capillary refill of 4 seconds, which improved after fluid resuscitation. Complete blood count showed a white blood cell count at 18,300 mm3, platelet count at 78,000/mm3, and hemoglobin of 14.3 g/dL (14-17 g/dL). Blood chemistry demonstrated high blood urea nitrogen at 27 mg/dL, high creatinine at 2.3 mg/dL, high alanine aminotransferase at 442 IU/L, high aspartate aminotransferase at 343 IU/L, and high total bilirubin at 2.8 mg/dL. The patient received one dose of ceftriaxone in the emergency department. He was placed on vancomycin and piperacillin/tazobactam.
The patient was admitted to pediatric intensive care where he underwent abdominal ultrasound to investigate the acute renal and liver injury. Ultrasound revealed a complex 9.3 x 9.2 cm heterogeneous-appearing mixed soft tissue and cystic lesion within the dome of the right hepatic lobe (). After discussion with surgical and infectious disease teams, a CT-guided 10 French pigtail percutaneous drainage catheter (PD) was placed in the abscess and drained purulent brown fluid.
The drained fluid grew Streptococcus anginosus, which was penicillin susceptible, and antibiotic regimen was changed from piperacillin/tazobactam and vancomycin to ampicillin monotherapy. Metronidazole was added later in his hospital course. Following drainage of the abscess, he became hypotensive, necessitating norepinephrine infusion. He developed respiratory failure requiring noninvasive positive pressure ventilation. Minimal fluid was drained from PD in the first 3 days. Follow-up ultrasound two days after the PD placement demonstrated abscess enlargement (18.4 × 117 cm) (). After multispecialty discussion, open surgical drainage was deferred. Instead, tissue plasminogen activator (tPA) was instilled into the PD. Four milligrams tPA was diluted in 50 mL saline, capped for one hour, and then drained to gravity. This was performed every 6 hours for total of five doses. Following instillation of tPA, catheter drainage significantly increased, and the patient's respiratory status and fever curve improved significantly (). Follow-up ultrasound after 5 doses of tPA therapy demonstrated a decrease in abscess size to 11.3 × 6.2cm (). The patient was discharged home on amoxicillin/clavulanate and metronidazole, with the drain in place, after 14 days of hospitalization. Ultrasound performed eleven days after hospital discharge demonstrated further decrease in size of abscess to 7 × 4.9 cm. The PD was removed 34 days after initial placement.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.6, 'degrees celsius'], 'Heart Rate or Pulse': [123.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [18300.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.6 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 123.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 18300.0 count/m^3. To convert 18300.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 18300.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 2e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6676,51,SIRS Criteria,diagnosis,integer,pmc-4531962-1,Extracted,"A 72-year-old woman was referred to our hospital for the evaluation of the pancreatic mass.
She presented with a one month history of palpable abdominal mass and body weight loss of 5kg. Also, she complained of loose stool and dyspepsia occasionally for three months. Her family and past medical history were not contributory. On admission, pulse rate was 68/min, blood pressure 140/80mmHg, respiration rate 18/min and body temperature 36.7°C. On physical examination, she appeared relatively well and the sclerae were anicteric. There was a palpable nodular non-tender mass with hard consistency in the epigastric area. The remainder of the physical examination was normal.
Laboratory studies included hemoglobin 12.1g/dl, white blood cell 3,800/mm3, platelet 201,000/mm3, total protein 6.7g/dl, albumin 3.7g/dl, AST 18U/L, ALT 15U/L, total bilirubin 0.4mg/dl, direct bilirubin 0.1mg/dl, alkaline phosphatase 119U/L, fasting blood glucose 109mg/dl, serum amylase 66IU/L, lipase 159IU/L and CA 19-9 3.0U/ml.
The abdominal computed tomography (CT) scan showed 5cm-sized protruding cystic mass in the pancreatic tail with calcification (). The entire main pancreatic duct and its branches were markedly dilated and pancreatic parenchyme was severely atrophied (). During the endoscopic retrograde pancreatography (ERP), we found patulous orifice of the papilla, and mucin was extruded through it. ERP showed diffuse dilatation of the entire pancreatic duct, but opacification of the pancreatic duct was difficult due to the presence of thick mucin (). Sono-guided aspiration cytology of the cystic mass in the pancreatic tail revealed numerous large sheets of tall columnar cells within the mucinous background. The cells had cytoplasmic mucin vacuoles and showed nuclear enlargement with increased nuclear cytoplasmic ratio.
With the diagnosis of ductectatic type mucin producing tumor of the pancreas, exploratory laparotomy was done and resection of the body and tail of the pancreas and splenectomy were carried out. At operation, the pancreas appeared to have brownish, protruding tumorous lesion in its body and tail portion. There was no lymph node enlargement.
The resected portion of the pancreas revealed a cystic mass in the tail. The multilocular cyst was 6×5.5×4.5cm in size and connected with the branch duct. The main pancreatic duct was diffusely dilated and its maximal diameter was 2.4cm. The lumen of the pancreatic duct and cyst was filled with mucin and their walls showed diffuse intraluminal papillary protrusion ().
Microscopically, the ductal epithelium and cyst wall were replaced by papillary proliferation, tall columnar cells of mucinous type. The large proportion of duct and cyst showed papillary hyperplasia or adenomatous change of the epithelium and carcinomatous change in some areas (). There was multifocal mucin spillage with dystrophic calcification in the stroma, but definitive invasion of the stroma by tumor cells was not seen. The remaining pancreatic parenchyme revealed severe atrophy. There was no evidence of tumor metastasis in the peripancreatic lymph node. These findings were consistent with the intraductal papillary tumor with mucinous ductal ectasia.
At 3 months after the operation, the patient was clinically well.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.7, 'degrees celsius'], 'Heart Rate or Pulse': [68.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [3800.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.7 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 68.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 3800.0 count/m^3. To convert 3800.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 3800.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 3.8e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6677,51,SIRS Criteria,diagnosis,integer,usmle-2105,Extracted,"A 6-year-old boy is brought to the emergency department because of worsening confusion for the last hour. He has had high-grade fever, productive cough, fatigue, and malaise for the past 2 days. He has not seen a physician in several years. His temperature is 38.9°C (102°F), pulse is 133/min, respirations are 33/min, and blood pressure is 86/48 mm Hg. He is lethargic and minimally responsive. Mucous membranes are dry. Pulmonary examination shows subcostal retractions and coarse crackles bilaterally. Laboratory studies show a hemoglobin concentration of 8.4 g/dL and a leukocyte count of 16,000/mm3. A peripheral blood smear shows sickled red blood cells.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.9, 'degrees celsius'], 'Heart Rate or Pulse': [133.0, 'beats per minute'], 'respiratory rate': [33.0, 'breaths per minute'], 'White blood cell count': [16000.0, 'm^3']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.9 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 133.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 16000.0 count/m^3. To convert 16000.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 16000.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 2e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 33.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6678,51,SIRS Criteria,diagnosis,integer,pmc-8367390-1,Extracted,"A 57-year-old male with a past medical history pertinent for hyperlipidemia, pancreatic adenocarcinoma diagnosed six months prior and on chemotherapy, as well as recurrent bouts of pancreatitis presented to our institution due to shortness of breath, fever, chills, and epigastric abdominal pain radiating to his back and associated with nonbloody emesis that had been present for five days prior to arrival. Physical examination revealed a cachectic and frail man, with epigastric abdominal tenderness and voluntary guarding. Vital signs revealed a blood pressure of 102/63 mmHg, heart rate of 62 beats per minute, temperature of 36.9°C, oxygen saturation of 99% at room air, and a respiratory rate of 16 breaths per minute. Initial laboratory studies revealed an elevated lipase of 1671 U/L (10-140 U/L) and leukocytosis of 17.1 × 103/uL (4.0-10.5 × 103/uL) with a 75% neutrophilic predominance. A chest radiograph revealed a large right-sided apical cavitary lesion measuring up to 6 cm (Figure ).
A computed tomography (CT) scan of the chest with intravenous (IV) contrast was obtained to further characterize the findings evident on the chest radiograph which revealed a cavitary lesion with internal dependent debris and air-fluid level in the right upper lobe apical and anterior segment measuring 5.7 × 5.7 × 5.8 cm (Figure ).
The patient was started on aggressive IV fluid hydration with Ringer’s Lactate for the treatment of pancreatitis as well as IV piperacillin-tazobactam to cover for the possibility of bacterial cavitary pneumonia.
Bronchoscopy with bronchoalveolar lavage (BAL) was performed and fungal culture grew A. flavus with fungal smear revealing septate hyphae branching at 45-degree angles. A. flavus titers were elevated at 1:4, for which a diagnosis of CCPA was made. HIV testing was negative. Antifungal therapy with voriconazole 200 mg PO BID was initiated. Piperacillin-tazobactam was discontinued as the BAL cultures were negative for bacteria. BAL acid-fast bacilli culture grew M. avium intracellulare and the patient was started on ethambutol 800 mg PO QD, azithromycin 500 mg PO BID, and amikacin 250 mg IV BID.
The patient clinically improved with decreased oxygen requirement and down-trending white blood cell counts and was discharged from the hospital on voriconazole, ethambutol, azithromycin, and IV amikacin.
The patient returned to the emergency department at our institution with shortness of breath less than a week after being discharged. At this time, he had an oxygen saturation of 92% at room air, which improved to 97% with a 3 L nasal cannula. A chest radiograph showed evidence of a new right-sided spontaneous pneumothorax (Figure ), which was also demonstrated on CT chest with IV contrast (Figure ).
A right-sided chest tube was placed for the treatment of the right-sided pneumothorax (Figure ).
Daily chest radiographs were obtained to monitor the status of the pneumothorax. It continued to enlarge secondary to subsequent malpositioning of the chest tube. At this time, interventional radiology was consulted. A pigtail catheter was placed and the malpositioned chest tube was removed (Figure ).
Following pigtail catheter placement, the pneumothorax resolved within a week, and the catheter was removed without complications. A repeat chest radiograph demonstrated the resolution of the pneumothorax. The patient’s oxygen saturation improved to 98% on room air.
Amikacin was changed from IV administration to the inhaled formulation to avoid nephrotoxicity on discharge. The patient was additionally sent home with voriconazole, azithromycin, and ethambutol. He was instructed to continue with close follow-up at our Infectious Disease Clinic.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.9, 'degrees celsius'], 'Heart Rate or Pulse': [62.0, 'beats per minute'], 'respiratory rate': [16.0, 'breaths per minute'], 'White blood cell count': [17100.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.9 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 62.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 17100.0 count/µL. To convert 17100.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 17100.0 white blood cell count/µL * 1.0 µL/mm^3 = 17100.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 16.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6679,51,SIRS Criteria,diagnosis,integer,pmc-7568791-1,Extracted,"A 59-year-old woman with a history of recent placement of a dual-chamber permanent pacemaker (PPM) due to sick sinus syndrome was admitted to the hospital due to erythema, warmth, and fluctuance over the PPM site (). She was at 4 weeks after PPM placement. Her symptoms developed gradually over a course of 5 days. She denied any fever or chills. She did not have any specific exposures over the PPM area other than dressing changes and cleaning with water and soap. There was no recent travel or pet exposure. Her vital signs on admission showed a temperature of 36.5°C, heart rate of 93 beats per minute, respiratory rate of 18 breaths per minute, and blood pressure of 100/60 mmHg. Physical examination on admission revealed a nondistressed woman, and her chest showed erythema overlying the PPM site with pain to palpation, fluctuance, and evidence of pus from surgical scar (). Her laboratory workup showed a white blood cell (WBC) count of 7300/μL, with 80.3% neutrophils, hemoglobin (Hgb) of 12.8 g/dL, platelet count of 189000/μL, lactate of 1.4 mmol/L, glucose of 142 mg/dL, BUN of 9 mg/dL, and creatinine of 0.66 mg/dL.
On the day of admission, blood cultures were obtained, and she was started on broad-spectrum antibiotics with vancomycin 1250 mg IV every 12 hours and piperacillin/tazobactam 4.5 g IV every 8 hours. She then underwent PPM removal on the 2nd day of hospitalization. Dual-chamber leads were taken out, and intraoperative specimens from the pocket site were sent to microbiology for stains and cultures. Pathology samples were not sent except for the leads for gross pathological evaluation. No frank pus was obtained intraoperatively, and the leads were removed without any complications. Blood cultures remained negative, and initial gram stain from the intraoperative specimens showed no organisms and rare WBCs. On day 4 of hospitalization, microbiology reported scant growth of acid-fast bacilli from the deep wound cultures, and empiric therapy was changed to amikacin 10 mg/kg IV daily, imipenem 1 g IV twice daily, and linezolid 600 mg PO twice daily. The specimen was then sent to the National Jewish Health reference laboratory (Denver, Colorado, USA) for identification by rpoB gene sequencing, which showed Mycobacterium peregrinum.
The patient showed clinical improvement and was discharged from the hospital on day 5 with the proposed empiric intravenous regimen. At 3 weeks of follow-up, the patient reported no side effects from the antibiotics prescribed and had proper healing of the PPM pocket site. Full susceptibilities by broth microtiter dilution methodology were made available (), and she was switched to moxifloxacin 400 mg PO daily and trimethoprim/sulfamethoxazole 160/800 mg twice daily to complete a 4-month regimen. Of note, the erm(39) gene was not tested for this case, and it was not preincubated in subinhibitory concentrations of macrolide to check for inducible resistance.
The patient was seen at 2 months and completed therapy at 4 months with proper healing of the PPM pocket site (). She had no side effects from the antibiotics and did not require reimplantation of the PPM.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.5, 'degrees celsius'], 'Heart Rate or Pulse': [93.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [7300.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.5 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 93.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 7300.0 count/µL. To convert 7300.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 7300.0 white blood cell count/µL * 1.0 µL/mm^3 = 7300.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6680,51,SIRS Criteria,diagnosis,integer,pmc-7362622-1,Extracted,"An 87-year-old man presented with multiple episodes of non-bloody, watery diarrhea associated with nausea and epigastric pain for two days. He had a past medical history of hypertension, hyperlipidemia, and coronary artery disease with bypass surgery. He denied any fever, vomiting, sick contact, recent travel, or recent antibiotic use. On physical exam, his blood pressure was 146/90 mmHg, pulse rate was 90 beats per minute, respiratory rate was 20 breaths per minute, and temperature was 100.8°F. He was non-toxic-appearing without acute distress, mild epigastric tenderness with hypoactive bowel sounds was noted, without rebound tenderness or guarding. Normal vesicular breathing without any crackles or wheezing on chest exam. Laboratory findings showed normal blood counts except leukocytosis of 14,000/ml, elevated urea blood levels of 30 mmol/L, and creatinine level of 1.3 mg/dl. A contrast-enhanced computed tomography (CECT) scan of the abdomen and pelvis showed air in the portal vein and gastric wall, with minimal thickening of the proximal small bowel, which was concerning for emphysematous gastroenteritis (Figure ).
Further workup results were negative, including blood cultures, stool studies, Clostridium difficile toxins, and lactic acid levels. He was admitted to the intensive care unit (ICU) for closer monitoring and evaluated by surgery, gastroenterology, and infectious disease specialists. His care team decided to treat the patient nonoperatively based on his hemodynamic stability and a benign abdominal exam. The patient was placed on a “nil per os” (i.e., nothing by mouth) order and received intravenous (IV) fluids and IV antibiotics, including ciprofloxacin and metronidazole. With no other identifiable cause of PI, the patient’s presentation was ultimately thought to represent a mild bacterial infection yielding minimal clues to the definitive diagnosis aside from radiographic data. The patient recovered well with nonoperative management and was discharged on oral antibiotics after a few days, with plans to follow up with outpatient CT scan imaging.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [100.8, 'degrees fahrenheit'], 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [14000.0, 'mL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 100.8 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 68.8 = 38.22222 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 90.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 14000.0 count/mL. To convert 14000.0 count/mL of white blood cell to mm^3, multiply by the conversion factor 0.001 mL/mm^3 which will give 14000.0 white blood cell count/mL * 0.001 mL/mm^3 = 14.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6681,51,SIRS Criteria,diagnosis,integer,pmc-7291778-2,Extracted,"A 13-year-old boy came to a pediatric fever clinic in our hospital with intermittent fever having lasted 1 day on February 7, 2020 (). His mother was a suspected case of COVID-19. She developed a fever on February 1, 2020. Her CT showed a few signs of infection. She was hospitalized in Wuhan Central Hospital for 4 days, and the SARS-CoV-2 nucleic acid tests were negative twice. The boy had been in close contact with his mother.
Physical examination showed: temperature 37.4°C, pulse 88 beats per minute, respiration 23 breaths per minute, SpO2 100%. No abnormal respiratory signs were found. Nasopharyngeal swab samples were collected and tested negative for SARS-CoV-2. The serum IgM antibody of Influenza A was positive. A high-resolution chest computed tomography (HRCT) scan on February 7 demonstrated little ground glass nodules seen in the upper lobe of the right lung (). Other laboratory findings included a leukocyte count of 7.83 × 109/L, lymphocytes of 1.62 × 109/L, and C-reactive protein of < 0.1 mg/L ().
Based on the results of lab examination, the boy was also considered an influenza case, although COVID-19 could not be ruled out. Isolation treatment was recommended. Then, he started treatment with Tamiflu and lotus qingwen capsules. Five days later, his temperature was normal. Considering the boy's and his mother's medical history, serum antibody of SARS-CoV-2 and fecal nucleic acid were assessed on February 27. The subsequent results for both were positive, so this boy was also confirmed to be a COVID-19 case complicated with influenza A virus infection.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.4, 'degrees celsius'], 'Heart Rate or Pulse': [88.0, 'beats per minute'], 'respiratory rate': [23.0, 'breaths per minute'], 'White blood cell count': [7830.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.4 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 88.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 7830.0 count/µL. To convert 7830.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 7830.0 white blood cell count/µL * 1.0 µL/mm^3 = 7830.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 0.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 23.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 0 + 1 = 1 criteria met.
Hence, the the number of SIRS criteria met by the patient is 1."
6682,51,SIRS Criteria,diagnosis,integer,pmc-8114242-1,Extracted,"A 36-year-old African American male with a past medical history of HIV (diagnosed in 2005) presented to the emergency department for generalized weakness, fever, and dizziness on ambulation. The patient has not been taking his anti-HIV medications for past 3 years. Review of system positive for non-bloody diarrhea, 40 pounds weight loss over several months, chills, night sweats, and productive cough. Vital signs on presentation revealed blood pressure of 118/62 mm Hg, heart rate of 136 beats/minute, respiratory rate of 14 breaths/minute, temperature of 38.5 °C, and oxygen saturation of 99% on room air. On examination, there were palpable bilateral axillary lymphadenopathy. On initial laboratory evaluation, the following values were noted: total leucocyte count 9.4 × 103/µL (4.5-11 × 103/µL), hemoglobin 9.2 g/dL (12-15.5 g/dL), platelets 112 × 103/µL (140-440 × 103/µL), absolute neutrophil count 6.47 × 103/µL (1.7-7 × 103/µL), absolute lymphocyte count 0.50 × 103/µL (0.9-2.9× 103/µL), blood urea nitrogen 16 mg/dL (8.6-10.3 mg/dL), serum creatinine 1.07 mg/dL (0.60-1.30 mg/dL), troponin 0.045 ng/mL (<0.03 ng/mL), creatinine kinase 86 U/L (30-223 U/L), prothrombin time 13.7 seconds (9.9-13 seconds), international normalized ratio 1.0 (0.9-1.1), partial thromboplastin time 44.7 seconds (25.2-37.4 seconds), HIV viral load 1 423 440 copies/mL, CD4 helper cells 5/µL (359-1519/µL), CD4/CD8 ratio 0.03 (0.92-3.72), lactate dehydrogenase 359 U/L (140-271 U/L), ferritin level 4412.0 ng/mL (16.4-294 ng/mL), and lactic acid was 1.3 mmol/L (0.5-2.2 mmol/L). Electrocardiogram showed sinus tachycardia of 111 beats/minute. Computed tomography (CT) of the head without contrast was negative. Chest X-ray showed no active disease. Noncontrast CT of the chest, abdomen, and pelvis showed left supraclavicular adenopathy (), multiple enlarged mesenteric lymph nodes (), mildly enlarged retroperitoneal lymph node, and hepatosplenomegaly. An excisional biopsy of the left axillary lymph node revealed epithelioid histiocytic aggregates without caseating necrosis and acid-fast bacilli within the epithelioid histiocytes ( and ). Immunohistochemistry analysis was positive for CD68 () and negative for S100, CD21, CD1a, and CD35. These results were consistent with mycobacterial spindle cell pseudotumor. Blood, stool, and sputum cultures were positive for Mycobacterium avium. Polymerase chain reaction of the biopsy tissue was negative for Mycobacterium tuberculosis complex. The patient was started on ethambutol, azithromycin, and rifabutin. His symptoms including dizziness improved over the course of his hospital stay. Fever resolved after day 9 of initiation of antimycobacterial drugs. Antiretroviral therapy was started on day 10 post commencement of antimycobacterial drugs. He was seen in infectious disease outpatient clinic a month after the diagnosis and was improving clinically.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.5, 'degrees celsius'], 'Heart Rate or Pulse': [136.0, 'beats per minute'], 'respiratory rate': [14.0, 'breaths per minute'], 'White blood cell count': [9400.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.5 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 136.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 9400.0 count/µL. To convert 9400.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 9400.0 white blood cell count/µL * 1.0 µL/mm^3 = 9400.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 14.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6683,51,SIRS Criteria,diagnosis,integer,pmc-7643252-1,Extracted,"A 16-year-old African American male with a history of fibroma of the right knee presented to our emergency department with a three-week history of right knee pain, preceded by five days of subjective fever. Pain was severe and limited his ability to walk. Otherwise, the patient denied any history of trauma. He has no significant past medical or surgical history except for fibroma of the right knee and leg length discrepancy (unclear etiology if it was congenital or caused by fibroma). He had a basketball injury four years ago and a knee X-ray at that time showed non ossifying fibroma. No family history of bone diseases or sickle cell disease. The patient lives at home with his parents and usually plays basketball. He denied smoking, alcohol, or drug use, and no history of sexual activity was identified.
On physical examination, oral temperature was 98°F, heart rate 99 beats per minute, blood pressure 129/60 mmHg, respiratory rate 16 times per minute, and oxygen saturation was 100% on room air. Weight was 56.4 kg with body mass index (BMI) 21. The right knee exam showed mild edema, but no tenderness, warmth nor erythema. He was able to flex his legs about 30 degrees when supine. No signs of marked stiffness or joint deformities were evident in other joint examinations. Heart and lung exams were clear, and no skin rash or lesions were seen. The patient looked otherwise well developed with appropriate mood and affect.
Initial clinical laboratory assessment revealed elevated erythrocyte sedimentation rate (ESR) >100 mm/hr and c-reactive protein (CRP) 91.2 mg/L. Normal white blood cell (WBCs): 8.1 x103/µL. Mild decreased hemoglobin and hematocrit values, 10.4 g/dl, and 30.9%, respectively (Table ).
X-ray of the right knee showed lytic lesions; there were multiple cortically based ill-defined lytic lesions of the distal femoral metadiaphysis with surrounding reactive sclerosis (Figure ). The most proximal lesion was eccentrically located and demonstrated cortical thinning with questionable cortical breakthrough.
MRI of the right knee showed scattered enhancing areas of marrow edema and cystic changes involving the right distal femoral diaphysis, metaphysis, and epiphysis (Figure ). Also, there was extensive cellulitis and myositis surrounding the right knee and extended proximally to the level of the greater trochanter with small developing organized fluid collections within the proximal vastus lateralis and intermedius muscles, representing evolving abscesses.
Because of the lytic lesions noted on imaging, bone biopsy, and knee aspiration were subsequently performed. Synovial fluid analysis revealed hematogenous cloudy fluid, elevated WBCs 4,000/µL, and >90% of polymorphonuclear leukocytes (PMN) (Table ).
On day three, he underwent debridement and irrigation of the right knee in the operating room. Operative findings revealed large amounts of thick sanguineous fluid, as well as necrotic fat, and thick gelatinous fluid was obtained with purulent material. The patient was then started on intravenous (IV) ceftriaxone awaiting culture results. Joint fluid culture grew GBS sensitive to ceftriaxone. Bone biopsy showed acute on chronic osteomyelitis with infiltration of histiocytes and plasma cells. Synovial biopsy revealed fibro-purulent debris and focal granulation tissue.
On day seven, he was discharged to complete a four-week course of IV ceftriaxone followed by four weeks of amoxicillin. CRP and ESR values showed down-trending which normalized by day 70 (Table ).
Given the presence of histiocytes on bone biopsy, he was referred to oncology for further workup of Langerhans cell histiocytosis.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [98.0, 'degrees fahrenheit'], 'Heart Rate or Pulse': [99.0, 'beats per minute'], 'respiratory rate': [16.0, 'breaths per minute'], 'White blood cell count': [8100.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 98.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 66.0 = 36.66667 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 99.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 8100.0 count/µL. To convert 8100.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 8100.0 white blood cell count/µL * 1.0 µL/mm^3 = 8100.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 16.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6684,51,SIRS Criteria,diagnosis,integer,pmc-3322204-1,Extracted,"A 51-year-old, male patient was admitted to our hospital in May 2005, suffering with epistaxis. He had no history of previous medical disorders, and had never had a blood transfusion. He had not taken any kind of medication prior to manifestation of symptoms and was neither an alcoholic nor a heavy drinker. The patient's blood pressure was 126/77 mm Hg, his pulse rate was 87 beats/min, his respiratory rate was 22 breaths/min, and his body temperature was 36℃.His initial hemoglobin level was 14 g/dL, his hematocrit was 43.8% and his white blood cell count (WBC) was 4,400×103/µL. His platelet count was observed to be low, at 16×103/µL. Hepatomegaly and splenomegaly were both not observed during physical examination. Mild hepatosplenomegaly was seen in his liver scan accompanied by reticuloendothelial system dysfunction. Increased numbers of megakaryocytes were seen in the result of the patient's bone marrow aspiration (). He was diagnosed with ITP, and the patient started treatment with high-dose oral prednisolone at 1 mg/kg/day for 4 weeks, and his platelet count level subsequently rose to 204×103/µL. He was discharged and visited our outpatient clinic routinely for the next 6 months, continuing with low-dose oral prednisolone tapered to 5 mg.
Seven months later, during a routine visit to the clinic he complained that his face had developed a yellowish color. Upon physical examination, icteric sclera and anemic conjunctiva were revealed. Upon laboratory examination, his hemoglobin and hematocrit levels were observed to be 7.0 g/dL and 23.2%, respectively. His WBC and platelet counts were found to be 4,400/µL and 241×103/µL, respectively. His corrected reticulocyte count was 8.3% and reticulocyte production index (RPI) was 4.1. His total and direct bilirubin concentrations were observed to be 4.5 mg/dL and 0.6 mg/dL respectively. His lactate dehydrogenase concentration was high, at 937 IU/L, and his serum haptoglobin had decreased to 10 mg/dL. Acidified sucrose lysis (Ham's test), antinuclear antibody, and anti-dsDNA antibody tests all produced negative results. Both direct and indirect Coombs' tests both produced negative results. Flow cytometry for red blood cell CD55 and CD59 were 99.8% (neutrophil 99.1%) and 99.9% (neutrophil 99.9%), respectively. Peripheral blood smear revealed macrocytic normochromic anemia (). A bone marrow biopsy was repeated, which revealed normocellular marrow with increased erythroid and megakaryopoiesis (). Based on these findings, we concluded that the patient suffered from ITP and Coombs' negative AIHA. Since there is a well known association between LPDs and AIHA, an F-18 fluorodeoxyglucose positron emission tomography/computed tomography (F-18 FDG PET/CT) scan was conducted to investigate possible occurrence of LPDs, however, there was no sign of malignancy (). He was treated with a higher dosage of oral prednisolone of one [] mg/kg/day for 5 weeks. We attempted to taper the prednisolone dosage, but his hemoglobin level fluctuated in proportion to the dose. We determined that the patient was developing a steroid dependency and a resulting laparoscopic splenectomy was performed in November 2006. After the operation, his hemoglobin level and platelet count slowly increased and reached normal range. His hemoglobin level was 13.8 g/dL and his platelet count was 301×103/µL. We stopped the steroid treatment.
During a routine clinic visit four months later, the patient complained of a yellowish face color again. He also had a newly developed, palpable lymph node on the right side of his neck. His hemoglobin count had decreased to 7.4 g/dL and his platelet count had increased to 529×103/µL. His corrected reticulocyte count was 6.6% and his RPI was 3.3. His lactate dehydrogenase concentration had increased to 1,088 IU/L and his serum haptoglobin had fallen to 21.1 mg/dL. Direct and indirect Coombs' test results were again, both negative. A peripheral blood smear revealed macrocytic and normochromic erythrocytes with mild anisocytosis and poikilocytosis. His chest radiograph, taken on admission, revealed a right hilar prominence which was not apparent in the chest radiograph taken 4 months before. A chest CT scan and F-18 FDG PET/CT scan confirmed enlarged lymph nodes in the right hilum, mediastinum, and right neck (). A biopsy was performed using the enlarged lymph node on the right side of his neck, revealing diffuse proliferation of medium to large atypical lymphoid cells (). The patient was diagnosed with diffuse large B-cell lymphoma. Bone marrow aspiration and biopsy revealed hypercellular marrow, but no evidence of malignant lymphoma. He was treated with 8 cycles of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP). After the 8 cycles of chemotherapy, complete remission was achieved. The patient is still visiting our outpatient clinic regularly. Full blood count, including reticulocytes, and blood films have all remained within normal limits.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.0, 'degrees celsius'], 'Heart Rate or Pulse': [87.0, 'beats per minute'], 'respiratory rate': [22.0, 'breaths per minute'], 'White blood cell count': [4400.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 87.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 4400.0 count/µL. To convert 4400.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 4400.0 white blood cell count/µL * 1.0 µL/mm^3 = 4400.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 0.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 0 + 1 = 1 criteria met.
Hence, the the number of SIRS criteria met by the patient is 1."
6685,51,SIRS Criteria,diagnosis,integer,pmc-2769317-1,Extracted,"A 46-year-old white male presented to the emergency department (ED) complaining of progressive dyspnea. He was healthy until three days prior to hospital admission when he developed a sore throat and fever. He went to his primary care physician’s (PCP) office where he had a positive group A rapid antigen test. His PCP gave him a prescription for cefdinir 300 mg twice daily for ten days and he began taking the antibiotic. His throat felt worse the next day and his fever increased to 105 degrees Fahrenheit. He called the PCP’s office but was not given an office appointment that day. On day 3, he returned to the PCP’s office with complaints of persistent fever, sore throat and new onset of redness and swelling over the left side of his neck. He received a shot of ceftriaxone and promethazine (to treat his nausea) and was told to put an ice pack on his neck swelling. That night, the patient’s wife noted he began acting confused and had some trouble sleeping. The following morning, the patient developed severe shortness of breath with intermittent air gasping. His wife called EMS, who transported him emergently to the hospital. The ED physicians observed him in acute respiratory distress leading to intubation. In addition to sedation/paralytic meds for intubation, he was given acetaminophen 650 mg per rectum, clindamycin 600 mg IV, ceftriaxone 2 gm IV, vancomycin 1 gm IV, and two liters of normal saline bolus. In the ED, he was later noted to have falling systolic blood pressures to the 60’s and was started on a dopamine drip and admitted to the ICU.
His past medical history included impaired fasting glucose and hypercholesterolemia, without history of surgeries. His home medications consisted of metformin 500 mg twice daily, resuvastatin 5 mg nightly, fish oil, flax seed, and niacin. Socially, he currently resides with his wife, denies tobacco or drug use and drinks alcohol occasionally.
On initial physical exam, his temperature was 104 degrees Fahrenheit. His first recorded blood pressure and heart rate were 141/81 and 117 respectively, but systolic blood pressure dropped to the 60s after some time in the ED. After intubation, his respiratory rate was 20 and his oxygen saturation was 100% on the ventilator.
In general, he was an average sized white male who seemed comfortable on the ventilator. He had normal sclera, conjunctiva and mucous membranes, but his oropharynx was poorly visualized due to ET and OG tubes in place. A large firm swelling over his left neck, which was erythematous and warm, was noted. His lungs were clear to auscultation bilaterally without wheezes or crackles and his cardiac exam revealed a fast rate and regular rhythm with S1 and S2 audible, without murmurs, rubs, or gallops. His peripheral pulses were strong and no significant edema was noted. His abdomen was soft and nondistended with positive bowel sounds. His skin had no evident rashes or lesions. The neurological exam and mental status was poorly tested due to paralytics given in the ED.
Initial laboratory data revealed a white blood cell count of 6.96, hemoglobin of 13.2, hematocrit of 38.4, and platelet count of 134. The basic metabolic panel showed sodium of 125, potassium of 4.0, chloride of 91, bicarbonate of 22, BUN of 7, creatinine of 0.9, glucose of 140, and calcium of 8.5. The hepatic panel was within normal limits. His cardiac enzymes, including CK, CKMB and troponin, were normal. Initial arterial blood gas after intubation showed a pH of 7.13, pCO2 of 61, pO2 of 136, and oxygen saturation of 98% on 100% O2. After ventilator adjustment the pH normalized to 7.41 with a pCO2 of 35.
On imaging, his head computerized tomography (CT) scan showed no acute disease. His neck CT scan showed extensive soft tissue edema along the nasopharynx and orophyarnx involving the prevertebral and parapharyngeal spaces, in addition to a left peritonsillar abscess that completely obliterated the airspace except for the endotracheal tube ().
The patient was started on dexamethasone intravenously soon after admission. The otolaryngologist performed a bedside incision and drainage (I&D) of the abscess. Over the next couple of days, the patient was weaned off the ventilator and dopamine was discontinued. Due to an adverse reaction to clindamycin on day 1 of hospitalization, we changed his antibiotic regimen to vancomycin and piperacillin-tazobactam. On hospital day 4, we extubated the patient. Unfortunately, that night he had a recurrence of dyspnea with stridor, which required transfer back to the ICU with repeat I&D of the abscess. After the repeat drainage, the patient had a smooth recovery and was discharged 3 days later on continued antibiotics and oral steroids. His final peritonsillar wound culture results revealed group C and group G streptococcus and his blood cultures indicated septicemia with group C streptococcus.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [104.0, 'degrees fahrenheit'], 'Heart Rate or Pulse': [117.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [6.96, 'µL'], 'PaCO2': [61.0, 'mm hg']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 104.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 72.0 = 40.0 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 117.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 6.96 count/µL. To convert 6.96 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 6.96 white blood cell count/µL * 1.0 µL/mm^3 = 6.96 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 61.0 mm Hg, which is greater or equal to than 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6686,51,SIRS Criteria,diagnosis,integer,pmc-3052194-1,Extracted,"A 69-year-old Greek female patient presented at our emergency department (ED) with a two-hour history of abdominal pain and vomiting. Her medical history was unremarkable except for previous cholecystectomy and appendectomy. The patient did not take any medications, and she was not a smoker or an alcohol consumer.
She looked ill with a blood pressure of 130/85 mm/Hg, a pulse rate of 90 beats/min, respirations of 25 breaths/min and a temperature of 38.5°C. A thorough physical examination revealed diffuse abdominal tenderness on deep palpation without any other signs of peritonitis. The laboratory examination was unremarkable except for polymorphonuclear leucocytosis (white blood cell [WBC] count, 15 × 103/μL; neutrophils, 86%) and an elevated C-reactive protein (14 mg/dL; reference range, 0-5). An upright chest radiograph demonstrated free subdiaphragmatic air bilaterally (Figure ), which seemed to be increasing during air insufflation in the stomach via a nasogastric tube (Figure ). Abdominal ultrasound examination was unremarkable.
An emergency laparotomy was performed for a suspected perforation in the upper GI tract. A few adhesions caused by previous cholecystectomy and appendicectomy were observed without any signs of peritoneal irritation or peritoneal fluid. The stomach and duodenum were fully mobilized, and the lesser sac was explored, but no evidence of perforation was found in the distal esophagus, stomach or duodenum. The small bowel and colon were also examined, but no leakage was observed. Subsequently, dilution of methylene blue in normal saline was instilled into the stomach through the nasogastric tube, but no obvious leakage was noted. Afterward, the abdominal cavity was filled with 2000 cc of normal saline, and air was again infused through the nasogastric tube into the stomach, but no air leakage from the upper GI tract was noted. Finally, because no cause of the pneumoperitoneum had been found, the operation was completed by placing a double-lumen drain.
The postoperative course was uneventful, and the patient showed a significant and prompt recovery. The subdiaphragmatic air disappeared six days postoperatively (Figure ). The patient was discharged home on the seventh postoperative day. One month later, esophagogastroduodenoscopy, colonoscopy and abdominal computed tomography (CT) were performed, but no pathology was detected.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.5, 'degrees celsius'], 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'respiratory rate': [25.0, 'breaths per minute'], 'White blood cell count': [15000.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.5 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 90.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 15000.0 count/µL. To convert 15000.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 15000.0 white blood cell count/µL * 1.0 µL/mm^3 = 15000.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 25.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6687,51,SIRS Criteria,diagnosis,integer,pmc-7222299-1,Extracted,"A 24-year-old young man was admitted to our hospital with chief complaints of high-grade fever more than 1 week. Antibiotic treatment in local hospital was ineffective. He denied a history of hypertension or a family history of cardiac disease. Six months prior to admission, the patient developed acute aortic dissection DeBakey type-1 for which he underwent complex surgery including removing autologous aortic walls of the ascending aorta and arch, David procedure, elephant trunk stenting and dacron graft repair of the total arch.
On admission, his blood pressure was 104/84 mmHg, pulse rate 96 beats per minute, and respiratory rate 19 per minute. He was febrile with temperature of 37.8 °C. There was a swelling in the superior sternum fossa, the skin temperature was higher than that of the surrounding normal skin, and the yellow turbid pus flowed out from the surface breach. Hematological findings included C-reactive protein of 59.8 mg/L (reference range<7 mg/L), hemoglobin of 102 g/L (reference range from 120 to160g/L), white blood cell count of 23.35 G/L (reference range from 4 to 10 G/L). Blood bacterial culture was negative. Transthoracic echocardiography showed (Fig. a) an echolucent area consistent with fluid or blood around the ascending aorta conduit graft concerning for perigraft leak or abscess, but the valves were not involved. Liquid dark area was found in the subcutaneous tissue above the sternum with a few flocculent echo (Fig. b). Due to the concerning findings, a total aortic arch CTA scan with contrast was ordered and showed that the lesion surrounded the ascending aortic artery, aortic arch and its branches, extending into the level of the C7 vertebral body and going down to the origin of the aortic body (Fig. c;1d).
This case was diagnosed with perigraft abscess and treated surgically. We chose a median sternotomy and saw the abscess cavity when opening the skin of the suprasternal (Fig. a). After thoracotomy, the old thrombus was cleared, and then washed repeatedly with active iodine and warm saline. No obvious bleeding was found. On surgical exploration, purulent material was drained from the wall of the aorta around the graft and microbiological cultures were obtained. The graft were normal in shape with a little old thrombus tissue (Fig. b). Intraoperatively, it was found that there was a clear demarcation between the graft and the abscess collection, and therefore, a decision was made not to explant the graft. After thoracotomy, the thrombus was cleared, then washed repeatedly with active iodine. Bacterial culture of pus and tissues collected during the surgery was negative. All surveillance culture samples collected perioperatively were also negative. Patient was still continued on intravenous antibiotics (Vancomycin mainly) for 2 weeks from the day after surgery. It based on the empirical use of antimicrobial agents in the treatment of infections. He started to defervesce postoperatively and remained afebrile upon discharge. As of 3 months postoperatively, there has been no recurrence of the infection.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.8, 'degrees celsius'], 'Heart Rate or Pulse': [96.0, 'beats per minute'], 'respiratory rate': [19.0, 'breaths per minute'], 'White blood cell count': [23.35, 'L']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.8 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 96.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 23.35 count/L. To convert 23.35 count/L of white blood cell to mm^3, multiply by the conversion factor 1e-06 L/mm^3 which will give 23.35 white blood cell count/L * 1e-06 L/mm^3 = 2e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 19.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6688,51,SIRS Criteria,diagnosis,integer,pmc-3313756-1,Extracted,"A 70-year-old woman presented with 4-day history of fever, right flank pain, polyurea, and altered sensorium. She had been detected to have diabetes mellitus about a month back and was taking oral antidiabetic medication. The patient was ill looking, agitated, and talking irrelevant; she was febrile (temperature 100°F) and tachypnic (respiratory rate 34 per minute); her heart rate was 110 bpm and blood pressure was 90/60 mmHg. On systemic examination, air entry was reduced and crepitations were audible more on the right side; suprapubic and right renal angle tenderness was present and no abdominal mass was palpable. There was no neurodeficit or localizing sign. Initial laboratory evaluation included complete blood count (hemoglobin 9.9 g%, total leukocyte count 9500/μl with 86% neutrophils, and platelet count of 36,000/μl), kidney function tests (blood urea 95 mg/dl and serum creatinine 4.6 mg/dl), random blood glucose (408 mg/dl) and arterial blood gas analysis (pH 7.37, SaO2 89.5%, PCO2 18.3 mmHg, PO2 56.4 mmHg, and HCO3 10.4 meq/l). Numerous pus cells were seen on urine microscopic examination while ketones were absent. Bilateral pleural effusion was evident on posterioanterior chest radiograph and electrocardiogram showed sinus tachycardia. USG abdomen revealed left kidney size of 11.1 × 4.4 cm with mild increased echo pattern. Right kidney was 11 × 4.7 cm, showing dense acoustic shadow. NCCT of brain was normal; cerebrospinal fluid examination, performed in view of altered sensorium, was normal. Repeated urine and blood culture samples taken during the hospital stay failed to grow any organism. Computed tomography (CT) of the abdomen revealed the presence of gas in the right pelvicalyceal system and renal parenchyma, with air and debris in dilated right ureter. Left kidney was normal []. The diagnosis of EPN was made and the patient was managed with oxygen inhalation, intravenous fluids in the form of normal saline, and insulin infusion to achieve euglycemia. Empiric intravenous antibiotics in the form of pipericillin, tazobactum, and metronidazole were administered. Because of persistent fever, hypotension and worsening renal functions, the antibiotic spectrum was broadened in the form of addition of ciprofloxacin and vancomycin. Ionotropic support with dopamine was also initiated after the 2nd day. The patient's clinical condition started improving around the 4th day of treatment and NCCT on the 5th day revealed marked improvement in the form of decrease in the size and extent of EPN []. The patient made a remarkable recovery over the next 2 weeks. After 3 weeks, another NCCT abdomen revealed complete disappearance of features of EPN []. After this, parenteral antibiotics were stopped and the patient was put on oral third-generation cephalosporin (cefpodoxime proxitel + clavulanate) and ciprofloxacin. She recovered completely []. She was on oral diet and was discharged on two doses of premixed (30/70) insulin at the end of 4 weeks. When reviewed after two more weeks, the patient was asymptomatic and routine urine examination was normal. She was prescribed metformin 1 g/day with good glycemic control.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [100.0, 'degrees fahrenheit'], 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'respiratory rate': [34.0, 'breaths per minute'], 'White blood cell count': [9500.0, 'µL'], 'PaCO2': [18.3, 'mm hg']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 100.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 68.0 = 37.77778 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 110.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 9500.0 count/µL. To convert 9500.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 9500.0 white blood cell count/µL * 1.0 µL/mm^3 = 9500.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 34.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is 18.3 mm Hg, which is less than than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 1 + 1 = 2 criteria met.
Hence, the the number of SIRS criteria met by the patient is 2."
6689,51,SIRS Criteria,diagnosis,integer,pmc-4942937-1,Extracted,"A 23-years old female presented to Pitas District Hospital in northeast Sabah, Malaysia, with a 5-day history of fever, rigours, headache, and dizziness. She lived with her family in a malaria-endemic village surrounded by palm oil plantations, where long-tailed macaques were regularly seen. She had a history of beta thalassaemia major, diagnosed at 9 months of age and requiring splenectomy at age 13 years. She received iron chelation and second monthly blood transfusions at her local hospital. Her last blood transfusion had been 16 days prior to presentation, and her post-transfusion haemoglobin was 9.8 g/dL. She had recently commenced oral hypoglycaemic agents for type 2 diabetes mellitus.
On presentation at the district hospital her vital signs were within normal range, including an oxygen saturation of 98 %. Her haemoglobin was 8.7 g/dL, white cell count 48 × 103/µL and platelet count 129 × 103/µL. She was admitted with a provisional diagnosis of symptomatic anaemia. Later that day she developed respiratory distress with an oxygen saturation of 50 % on room air, improving to 72 % on high-flow oxygen, and she was transferred to a tertiary referral hospital in the state capital, Kota Kinabalu. On arrival her temperature was 38.6 °C, heart rate 139 beats/min, blood pressure 116/69 mm Hg, and oxygen saturation 93 % on high-flow mask with a respiratory rate of 36 breaths per minute. A blood film taken on arrival was positive for malaria parasites resembling P. knowlesi, with a parasite count of 84,000 parasites/µL. Further investigation revealed worsening anaemia (haemoglobin 6.0 g/dL) and further elevation of the white blood cell count (61 × 103/µL), in addition to metabolic acidosis (lactate 16 mmol/L, bicarbonate 8.4 mmol/L, pH 7.14), hyperbilirubinemia (80 µmol/L), acute kidney injury (creatinine 184 µmol/L), increased liver transaminases (alanine transaminase 181 U/L and aspartate transaminase 308 U/L), and hypoglycaemia (blood glucose 2.5 mmol/L) (Table ). Chest radiograph was initially unremarkable, however, on day 1 showed mild bilateral interstitial infiltrates. She was diagnosed with severe knowlesi malaria, admitted to the intensive care unit, and commenced on intravenous artesunate, intravenous antibiotics (initially piperacillin/tazobactam, then ceftriaxone) and inotropic support; she was transfused two units of whole blood. She made a good recovery, and on day 2 after completing three doses of intravenous artesunate, she was changed to oral artemether-lumefantrine (Riamet) for 3 days and discharged from the intensive care unit. Her blood film was negative for malaria parasites on day 3, and she was discharged from hospital on day 9. Dengue NS1 antigen and blood cultures taken prior to antibiotics were negative. PCR of her initial blood sample using previously described methods [] confirmed P. knowlesi.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.6, 'degrees celsius'], 'Heart Rate or Pulse': [139.0, 'beats per minute'], 'respiratory rate': [36.0, 'breaths per minute'], 'White blood cell count': [61000.0, 'µL']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.6 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 139.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 61000.0 count/µL. To convert 61000.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 61000.0 white blood cell count/µL * 1.0 µL/mm^3 = 61000.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 36.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6690,51,SIRS Criteria,diagnosis,integer,usmle-302,Extracted,"A 52-year-old man comes to to the emergency department with fatigue and shortness of breath that has become progressively worse over the past week. He had an upper respiratory tract infection 2 weeks ago, for which he was given an antibiotic. He has hypertension, type 2 diabetes mellitus, and colonic polyps diagnosed on screening colonoscopy 2 years ago. His mother has systemic lupus erythematosus and his brother has a bicuspid aortic valve. He does not smoke cigarettes or drink alcohol. Current medications include lisinopril and metformin. His temperature is 37.3°C (99.1°F), pulse is 91/min, respirations are 18/min, and blood pressure is 145/84 mm Hg. His conjunctivae are pale. Cardiac examination shows a late systolic crescendo-decrescendo murmur at the right upper sternal border. Laboratory studies show:
Leukocyte Count 9,500/mm3
Hematocrit 24%
Platelet Count 178,000/mm3
LDH 215 U/L
Haptoglobin 22 mg/dL (N=41–165 mg/dL)
Serum
Na+ 140 mEq/L
K+ 4.6 mEq/L
CL- 100 mEq/L
HCO3- 25 mEq/L
Urea nitrogen 21 mg/dL
Creatinine 1.2 mg/dL
Total bilirubin 1.9 mg/dL
A peripheral blood smear is shown.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.3, 'degrees celsius'], 'Heart Rate or Pulse': [91.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [9500.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.3 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 91.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 9500.0 count/m^3. To convert 9500.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 9500.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 9.5e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6691,51,SIRS Criteria,diagnosis,integer,usmle-4794,Extracted,"A 45-year-old man with a history of biliary colic presents with one-day of intractable nausea, vomiting, and abdominal pain radiating to the back. Temperature is 99.7 deg F (37.6 deg C), blood pressure is 102/78 mmHg, pulse is 112/min, and respirations are 22/min. On abdominal exam, he has involuntary guarding and tenderness to palpation in the right upper quadrant and epigastric regions. Laboratory studies show white blood cell count 18,200/uL, alkaline phosphatase 650 U/L, total bilirubin 2.5 mg/dL, amylase 500 U/L, and lipase 1160 U/L.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [99.7, 'degrees fahrenheit'], 'Heart Rate or Pulse': [112.0, 'beats per minute'], 'respiratory rate': [22.0, 'breaths per minute'], 'White blood cell count': [18200.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 99.7 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 67.7 = 37.61111 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 112.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 18200.0 count/µL. To convert 18200.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 18200.0 white blood cell count/µL * 1.0 µL/mm^3 = 18200.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6692,51,SIRS Criteria,diagnosis,integer,pmc-5017849-1,Extracted,"A 33-year-old male with a history of schizophrenia and polysubstance abuse presented to the emergency department (ED) with altered mental status. Emergency medical technicians reported that the patient was discovered in the middle of the street, agitated and confused with an empty box of baking soda in his pants pocket.
On initial evaluation, the patient appeared alert, tremulous and distressed. His vitals were temperature 35.7°C (96.2°F), heart rate 124 beats/min, respirations 18 breaths/min, blood pressure 126/93, oxygen saturation 94% on room air. The physical examination was significant for a thin male, rocking back and forth, mumbling incoherently and forcefully blinking his eyes. The head and neck examination was notable for horizontal nystagmus, intermittent involuntary facial twitching, moist mucus membranes and no facial droop. Pupils were equal, round, and reactive to light bilaterally. The cardiac examination revealed regular tachycardia. Neurologic examination was significant for a coarse tremor to his arms and upper torso. He would intermittently lift his legs and arms off the bed then slam them down on the stretcher. He was stuttering, disoriented, and unable to answer questions. Cerebellar function could not be tested due to the patient’s mental status. The rest of his exam was normal.
Initial laboratory values were Na 172mEq/L, K 2.5mEq/L, chloride 98mEq/L, CO2>45mEq/L, glucose 433mg/dL, BUN 16mg/dL, creatinine 1.85mg/dL, magnesium 3.2mg/dL, phosphate<1mg/dL, and calcium of 11mg/dL. Liver function tests were remarkable for a bilirubin of 1.4mg/dL, total protein of 8.5g/dL, albumin of 5.6g/dL. White blood cell count was 11.6 cells/microL and his hemoglobin was 17g/dL. A room air venous blood gas measurement 7.53, pCO2 60mmHg, pO2 39mmHg, HCO3 50mEq/L, with a base excess of 21.6mEq/L. The electrocardiogram (EKG) showed sinus tachycardia with a prolonged QTc of 528msec. Urinalysis: pH of 8.52 and granular casts. Serum osmolality was 364 mOsm/kg and venous lactate 12.3 mmol/L. A urine toxicology screen was negative for amphetamines, barbiturates, benzodiazepines, cocaine, methadone, opiates, phencyclidine, cannabionoids, and tricyclic antidepressants. Blood alcohol, acetaminophen, and salicylate levels were negative. A head computed tomography (CT) was obtained and revealed multiple areas of intracranial hemorrhage in the left temporal and bilateral cerebellar regions. Additionally there was subarachnoid hemorrhage in the left frontal lobe and right posterior frontal lobe (). CT angiography was normal without aneurysm. CT of the chest, abdomen, and pelvis was significant only for diffuse mild dilation of the small bowel and marked fluid content of the entire GI tract.
While in the ED, the patient received 2L normal saline and intravenous potassium replacement. Neurosurgery was consulted but did not recommend any surgical intervention. He was admitted to the intensive care unit where he continued to receive IV normal saline and electrolyte repletion. The patient’s mental status improved to his baseline over the next 24 hours and he was able to endorse that he had consumed an entire box of baking soda (net wt 16oz/454g). His estimated sodium burden was 5,403mEq. A repeat head CT showed stable intracranial hemorrhages. He denied suicidal ideation and after evaluation, psychiatry deemed the patient safe for discharge. He was discharged on hospital day 4 at which time he had a non-focal neurologic exam.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [35.7, 'degrees celsius'], 'Heart Rate or Pulse': [124.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [11.6, 'µL'], 'PaCO2': [60.0, 'mm hg']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 35.7 degrees celsius. Because the temperature is less than 36 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 124.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 11.6 count/µL. To convert 11.6 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 11.6 white blood cell count/µL * 1.0 µL/mm^3 = 11.6 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 60.0 mm Hg, which is greater or equal to than 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6693,51,SIRS Criteria,diagnosis,integer,pmc-4031816-1,Extracted,"The male patient, who was 37 years old from Brasilia (DF), was admitted to the intensive
care unit (ICU) with a condition of dry cough for 4 days with a fever (38.5C) and
progressive dyspnea. The patient was undergoing antineoplastic therapy for non-Hodgkin's
lymphoma with cyclophosphamide, doxorubicin, vincristine, prednisone and rituximab, and
the last session was 6 days prior to admission. The patient had no history of tobacco
smoking, prior lung disease or occupational or environmental exposure. Upon a physical
examination, the patient was tachycardic (115 beats per minute), normotensive (115/68
mmHg) and tachypneic (28 breathing cycles per minute) and had diffuse crackles on
pulmonary auscultation. Laboratory tests showed leukopenia (3,100 leucocytes/mm³ with
18% rods and 48% segmented), 273 U/L lactate dehydrogenase and 2.33 mg/dL
ultra-sensitive C-reactive protein. The arterial blood gasometry showed 44 mmHg oxygen
pressure (PaO2) and 82% oxygen saturation (SaO2). The patient
showed 62 mmHg PaO2 and 90% SaO2 following administration of
supplementary oxygen via a Venturi mask with 50% fraction of inspired oxygen
(FiO2). Thoracic computed tomography (CT) indicated extensive pulmonary
opacities with a predominantly ""ground glass"" appearance and bilateral diffuse
involvement ().
The introduction of noninvasive mechanical ventilation and empiric broad-spectrum
antibiotic therapy (piperacillin/tazobactam, clarithromycin, trimethoprim/
sulfamethoxazole and linezolid) was initially chosen.
On the 2nd day of ICU admission, the patient's respiratory mechanics and gas
exchange worsened with a drop in SaO2, and an orotracheal intubation (OTI)
and introduction of invasive mechanical ventilation (IMV) with a protective ventilation
strategy were chosen. On the 6th day of ICU admission, the patient showed an
improvement of gas exchange and respiratory mechanics, and he was extubated after
performing the spontaneous breathing test.
However, the patient's breathing worsened on the 15th day of ICU admission;
therefore, the patient was subjected to an IVM, and a new OTI was performed. The patient
also showed hemodynamic instability when norepinephrine was initiated. The white blood
cell count was in the normal range, and the PaO2/FiO2 ratio was
69. The blood, urine and bronchoalveolar lavage cultures were negative, as was the
analysis of acid-alcohol-resistant bacilli (AARB).
On the 19th day following ICU admission, the patient had an IMV
PaO2/FiO2 ratio of 74 and 88 mmHg PaCO2 with 15
cmH2O positive end-expiratory pressure (PEEP) and 6 L/min tracheal gas
insufflation. At that time, the OP diagnostic hypothesis was suggested. Pulse therapy
with methylprednisolone was initiated (1 g per day for 5 days), and the use of
clarithromycin was maintained (500 mg twice daily).
Upon ending the pulse therapy (23rd day), the patient showed a 116
PaO2/FiO2 ratio. A thoracic CT showed a large reduction of
""ground glass"" pulmonary opacities on the 25th hospital day ().
A tracheostomy was performed on the 27th day of ICU admission, and on the
31st day, the patient was removed from mechanical ventilation, showing a
402 PaO2/FiO2 ratio. The patient was discharged from the ICU on
the 42nd day of ICU admission and was discharged from the hospital 8 days
later. The patient still showed consolidated ""ground glass"" pulmonary opacities
bilaterally based on the therapeutic monitoring thoracic CT at hospital discharge, which
were more pronounced in the posterior and lateral basal segments of the inferior lobes,
albeit with significant decrease in the extent of pulmonary opacities (). The patient maintained outpatient
follow-up and used corticosteroid therapy with 60 mg of prednisone per day for another 6
months.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.5, 'degrees celsius'], 'Heart Rate or Pulse': [115.0, 'beats per minute'], 'respiratory rate': [28.0, 'breaths per minute'], 'White blood cell count': [3100.0, 'm^3'], 'PaCO2': [88.0, 'mm hg']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.5 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 115.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 3100.0 count/m^3. To convert 3100.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 3100.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 3.1e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 28.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is 88.0 mm Hg, which is greater or equal to than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6694,51,SIRS Criteria,diagnosis,integer,pmc-3891035-1,Extracted,"A 37-year-old male was admitted to our hospital because of his left sided hemiplegia that he had experienced for 3 months. He was known to be positive for HIV, as was determined during evaluation for idiopathic thrombocytopenic purpura in a foreign country about 6.5 years before this admission. At that time, he had been treated with zidovudine, lamivudine and saquinavir for the management of AIDS for 9 months and then he discontinued therapy of his own will. He was advised to restart treatment with zidovudine, lamivudine and indinavir at our hospital 4 years ago. He noticed weakness on the left side of his body during movement, which had slowly progressed and he finally developed left-sided hemiplegia 3 months previously. At the time of admission, he had complaints of headache and night sweats. He was diagnosed as having idiopathic thrombocytopenic purpura about 6.5 years ago and so splenectomy was done. Even after splenectomy, the thrombocytopenia continued. He was treated with steroid, vincristine, intravenous gammaglobulin, rituximab and danazole. He had also experienced liver abscess 4 years ago. He had received radiation for Kaposi sarcoma about 8 months before admission. On admission, the blood pressure was 90/60 mmHg, the pulse rate 100/min, the respiration rate 22/min and the body temperature was 38℃. Upon physical examination, the patient was in poor general condition with anemic conjunctiva. There were no signs of hemorrhagic diathesis or icterus. The laboratory finding were as follows; hemoglobin 7.4 g/dL, WBC 8,300/mm3 (neutrophila: 79.5%, lymphocytes: 14.6%, monocytes: 4.6%), platelets 10,000/mm3, erythrocyte sedimentation rate (ESR) 2 mm/h, AST 24 IU/L, ALT 9 IU/L, total bilirubin 0.7 mg/dL, LDH 473 IU/L, protein 3.9 g/dL, albumin 2.3 g/dL, BUN 9.5 mg/dL, creatinine 0.42 mg/dL, calcium 7.3 mg/dL, phosphorus 3.1 mg/dL, Na 130 mmol/L, K 3.0 mmol/L, the total number of CD4 and CD8 T lymphocytes was 46/mm3 and 621/mm3, respectively, and the ratio of CD4/CD8 was 0.07. The chest X-ray was not remarkable. Brain MRI () shows 4 cm-sized round mass involving the right frontal lobe. The T1 weighted image and the T2 weighted image () showed extensive areas of perilesional edema involving the right frontoparietal region and there was a mass effect upon the right lateral ventricle. Stereotactic biopsy of the brain lesion was performed, and histological examination disclosed atypical lymphoid cells with a predominant perivascular arrangement (). Immunohistochemical examination showed positivity for CD20. The diagnosis of diffuse large B-cell lymphoma involving the CNS was made. The patient was treated with brain radiation. Sadly, he died of pneumonia 13 days after brain radiation therapy.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.0, 'degrees celsius'], 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'respiratory rate': [22.0, 'breaths per minute'], 'White blood cell count': [8300.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 100.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 8300.0 count/m^3. To convert 8300.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 8300.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 8.3e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6695,51,SIRS Criteria,diagnosis,integer,pmc-7931525-1,Extracted,"Fourteen months prior to the referral to our institution, a 69-year-old Japanese woman presented at an orthopedic hospital with a painless mass, approximately 10 mm in diameter, in the right breast adjacent to the sternal border. Based on contrast-enhanced computed tomography (CT) findings, the breast mass was tentatively diagnosed as a benign tumor. However, the lesion gradually increased in size. Four months later, she was referred to the breast surgery department of a community hospital. Ultrasound imaging showed a 17 mm mass surrounded by fluid in the right breast. Cytology of the needle biopsy specimens revealed nonspecific inflammatory cells without atypical cells. Bacterial cultures of the specimens yielded no pathogens. She was administered cefcapene pivoxil 100 mg three times a day for 12 days; however, there was no improvement. She was diagnosed with nonspecific (non-purulent) mastitis, and incisional drainage of the lesion was performed.
Eight months later, the breast lesion, which still continued to increase in size, spontaneously discharged pus from the skin around the right nipple. The patient was referred to the breast surgery department at our hospital, and further referred to our department for the treatment of intractable mastitis.
Her medical history revealed miliary tuberculosis at the age of 25 years, for which she had been hospitalized and treated with three drugs, including streptomycin, for 1 year. She had been a homemaker since her twenties, living with her husband. Her socioeconomic status was not low. She had five pregnancies, three abortions, and two live births. She was an ex-smoker with a smoking history of 42 pack-years. Currently, she was taking clopidogrel and aspirin for ischemic heart disease, bisoprolol and enalapril for hypertension, and lovastatin for dyslipidemia. Her family history was unremarkable.
On examination, she appeared well with stable vital signs: body temperature, 36.7°C; blood pressure, 144/76 mm Hg; pulse rate, 96 beats per minute; and respiratory rate, 14 breaths per minute. The cervical and axillary lymph nodes were not palpable. Heart sounds were normal without murmurs, and the lung sounds were clear without crackles. Her abdomen was soft and flat with no hepatosplenomegaly. Clinical breast examination revealed palpable cord-like induration with mild tenderness from the right margin of the sternum to the skin around the right nipple. The formation of a fistula was observed near the right nipple, and it showed slightly cloudy and yellowish exudates (Fig. a).
The laboratory test results were as follows: white blood cell count, 5200/µL; hemoglobin, 11.9 g/dL; platelet count, 159,000/µL; albumin, 4.5 g/dL; aspartate aminotransferase, 21 U/L; creatinine, 0.65 mg/dL; and C-reactive protein, 0.08 mg/dL (reference: < 0.06 mg/dL). Interferon-gamma release assay (T-SPOT.TB®) showed positive results. She tested negative for human immunodeficiency virus.
Mammography showed distortion accompanied by retraction of the right nipple with regional microcalcifications. CT revealed high-density lesions suggesting inflammatory changes in the right breast and calcifications of the right apical pleura and mediastinal lymph nodes. Breast magnetic resonance imaging (MRI) showed no mass in the right mammary gland and a fistula formation between the parasternal area and skin of the right breast (Fig. a). T2 imaging showed enhanced high signal intensity lesions in the sternum, suggesting sternal osteomyelitis.
Pus drained from the fistula was collected with a clean syringe and immediately sent to the hospital laboratory to test for aerobic and anaerobic bacteria, mycobacteria, and fungus. Although Gram staining, Ziehl-Neelsen staining, and bacterial and fungal cultures showed negative results, polymerase chain reaction for M. tuberculosis was positive. Blood culture was not performed. Four weeks later, the M. tuberculosis isolate was cultured from the pus specimen and showed good sensitivity to isoniazid, rifampicin, ethambutol, streptomycin, and levofloxacin. She was diagnosed with tuberculous mastitis and sternal osteomyelitis. A 2-month intensive phase of therapy with isoniazid (300 mg daily), rifampicin (450 mg daily), ethambutol (750 mg daily), and pyrazinamide (1200 mg daily) was initiated, followed by 7-month continuation therapy with isoniazid and rifampicin. After completion of the treatment regimen, the fistula and deformity in the breast were healed (Fig. b), and MRI findings of the lesion showed considerable improvement (Fig. b). At the 2-year follow-up after treatment, she was cured of the disease and experienced no recurrence or relapse.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.7, 'degrees celsius'], 'Heart Rate or Pulse': [96.0, 'beats per minute'], 'respiratory rate': [14.0, 'breaths per minute'], 'White blood cell count': [5200.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.7 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 96.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 5200.0 count/µL. To convert 5200.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 5200.0 white blood cell count/µL * 1.0 µL/mm^3 = 5200.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 14.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6696,51,SIRS Criteria,diagnosis,integer,pmc-2908657-2,Extracted,"A 66-year-old male presented to the ED with a four-day history of intermittent lower abdominal pain associated with several episodes of nausea, vomiting, and diarrhea. He described the pain as dull and heavy, worse with lying on his back and better when he laid on his side, without prior episodes of similar pain. Review of symptoms was negative for fever, chills, weight loss, black or bloody stools, change in bowel caliber, urinary symptoms, recent travel, camping or unusual foods. He had no recent sick contacts. His past medical history included degenerative joint disease and a past surgical history of an appendectomy. He had no family history and a social history of cigarette smoking only.
Initial vital signs were within normal limits: temperature 98 degrees Celsius, blood pressure of 122/82 mm Hg, heart rate of 98 beats per minute, respiratory rate of 18 breaths per minute, and oxygen saturation of 97% on room air. Initial exam revealed a patient in mild distress and an exam significant only for moderate suprapubic tenderness without rebound or guarding. There were no masses or hepato-splenomegaly appreciated. In addition, bowel sounds were normal. Initial lab tests including a complete blood count, chemistry panel, urinalysis and coagulation profile were significant only for a WBC count of 19,000 cells/L (70% neutrophils, 18% lymphocytes, 9% monocytes, 3% basophils) and a hematocrit of 39%. CT scan of the abdomen and pelvis revealed evidence of ileocolic intussusception with edematous and possibly ischemic bowel (). A right hemicolectomy was subsequently performed with primary ileo-mid-transverse colostomy. Examination of the patient’s resected tissue revealed Duke’s C adenocarcinoma of the right colon. The Duke’s classification of colon cancer places patients into one of four categories based on spread of cancer. This patient’s classification indicates that he had cancer spread out of the confines of his bowel wall and into adjacent lymph nodes without spread of beyond the confines of the lymph nodes. His post-operative recovery was otherwise uneventful.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [98.0, 'degrees celsius'], 'Heart Rate or Pulse': [98.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [19000.0, 'L']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 98.0 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 98.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 19000.0 count/L. To convert 19000.0 count/L of white blood cell to mm^3, multiply by the conversion factor 1e-06 L/mm^3 which will give 19000.0 white blood cell count/L * 1e-06 L/mm^3 = 0.019 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6697,51,SIRS Criteria,diagnosis,integer,pmc-6458939-1,Extracted,"A 25-year-old man from Ghana was admitted to our hospital for an altered mental state, weight loss, neck pain, cough, fever, nausea, vomiting, and photophobia for 7 days. He reported a cough with greenish phlegm and blood-tinged sputum and a weight loss of ∼20 lb in the last month. He reported that he could not eat because he was always nauseous and experienced nonbilious, nonprojectile vomiting. He denied chest pain, difficulty breathing and swallowing, diarrhea, dysuria, and skin rashes. His past medical history included intermittent asthma and migraines, but he was not on any medications. He did not have any significant family history or prior surgeries. He reported that he smoked 10 cigarettes a day for the past 5 years, drank alcohol occasionally, and denied illicit drug use except for marijuana. He reported that he last traveled to Ghana 6 months priorly, and he denied having contact with sick persons. He reported that he was sexually active with many partners but denied any prior sexually transmitted diseases.
Examination revealed a cachectic young male with a heart rate of 102 beats/min, a blood pressure of 108/69 mmHg, a respiratory rate of 20 breaths/min, a temperature of 98°F, and a 96% oxygen saturation in ambient air. He had a body mass index of 19.2 kg/m2 and was lethargic but oriented. He had no icterus or cervical or axillary lymphadenopathy. He had clear bilateral breath sounds, and his cardiovascular and abdominal examinations were unremarkable. He had a good pulse and no peripheral edema.
On admission, the patient tested positive for HIV with a CD4 count less than 20 and a high viral load. Pneumonia and meningitis resulting from opportunistic infections were considered, and he was treated for bacterial meningitis and tuberculosis (TB) even though the lumbar puncture was delayed because the patient was restless and uncooperative. The lumbar puncture results showed a pressure of 23 cm·H2O, a white blood cell count of 2, a red blood cell count of 57, a protein level of 102 mg/dl, and a glucose level of 25 mg/dl. The Gram stain and bacterial antigen tests were negative.
There was a high suspicion of pulmonary TB and tuberculous meningitis due to recent travel to Ghana, and the initial chest X-ray showed multiple nodular opacities suggestive of miliary TB (). The micronodular appearance was confirmed by a chest CT scan without contrast (). Despite a quantiFERON negative test result, quadruple therapy for TB with isoniazid, pyrazinamide, ethambutol, and rifampin (RIPE) was continued.
On succeeding days, yeast was growing in the patient's blood cultures and a Gram stain of the patient's cerebrospinal fluid (CSF) showed presence of yeast cells. The titer of Cryptococcus in the CSF was greater than 1 : 1024 and was eventually identified as Cryptococcus neoformans. Thus, antibacterial meningitis treatment was discontinued, and the patient was started on amphotericin B and flucytosine. Anti-TB medications were continued. He underwent placement of a lumbar drain due to a persistent headache and photophobia. Antiretroviral treatment was not started, but the patient was treated with prophylaxis medications for opportunistic infections. At this time, the patient had four persistently negative acid-fast bacilli sputum smears and was negative for the sputum Mycobacterium tuberculosis PCR test.
The patient underwent FFB with BAL and TBBx. In the BAL, >100,000 CFU/mL of Staphylococcus haemolyticus grew; thus, the treatment for bacterial pneumonia was modified. Tissue culture and TBBx showed the presence of Cryptococcus neoformans. Higher magnification microscopy showed the presence of both hyphae and yeast cells (Figures and ). The patient showed clinical improvement and was discharged on oral fluconazole.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [98.0, 'degrees fahrenheit'], 'Heart Rate or Pulse': [102.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [2.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 98.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 66.0 = 36.66667 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 102.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 2.0 count/µL. To convert 2.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 2.0 white blood cell count/µL * 1.0 µL/mm^3 = 2.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6698,51,SIRS Criteria,diagnosis,integer,usmle-314,Extracted,"Twelve hours after undergoing an exploratory laparotomy for a perforated duodenal ulcer, a 36-year-old man has shortness of breath. He has asthma well controlled with an albuterol inhaler. His father died of lung cancer at 62 years of age. He has smoked one pack of cigarettes daily for 14 years. He does not drink alcohol. He appears uncomfortable. His temperature is 37.4°C (99.3°F), pulse is 98/min, respirations are 19/min, and blood pressure is 122/76 mm Hg. Examination shows reduced breath sounds over the left lung base. Cardiac examination shows no abnormalities. There is a clean, dry surgical incision over the midline of the abdomen. Bowel sounds are hypoactive. The calves are soft and nontender. His hemoglobin concentration is 12.9 g/dL, leukocyte count is 10,600/mm3, and platelet count is 230,000/mm3. An x-ray of the chest in supine position is shown.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.4, 'degrees celsius'], 'Heart Rate or Pulse': [98.0, 'beats per minute'], 'respiratory rate': [19.0, 'breaths per minute'], 'White blood cell count': [10600.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.4 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 98.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 10600.0 count/m^3. To convert 10600.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 10600.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 19.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6699,51,SIRS Criteria,diagnosis,integer,pmc-4485204-1,Extracted,"A 40-year-old Puerto Rican-born female presented to the emergency department with a 2-day history of subjective low-grade fever and pleuriticleft-sided chest pain localized to the pacemaker site. She reported chills and rigors as well as swelling with redness at the pacemaker site associated with left arm pain. She had a history of multiple pacemaker battery and wire exchanges utilizing pacemaker compounds made up of different metal materials in the past, with the last replacement done 2 weeks prior. In light of her history of multiple drug allergies (including penicillin, ciprofloxacin, daptomycin, sulfa drugs, linezolid, and metochlopropamide), she took azithromycin empirically to treat a possible cellulitis prior to presentation to the emergency department. Her medical history was significant for complete heart block, hypertension, migraine, and inherited thrombophilia (Prothrombin Gene Mutation G20210A), with a history of recurrent deep venous thrombosis and pulmonary embolism, the last one being 1 year ago. Her twin brother also had complete heart block with multiple pacemaker rejections, which had improved only after having a gold-plated pacemaker implanted.
Physical examination revealed a non-toxic looking female, who did not appear to be in any acute distress, with a maximal temperature of 96.9 F, pulse of 64/min, blood pressure of 104/64 mmHg, and respiratory rate of 18/min. A pacemaker was palpable on the left chest area, with overlying tenderness and fluctuant erythema around the skin.
Leukocyte count was 5,900/μL, with 43% polymorphonuclear cells and 49% lymphocytes, hemoglobin was 11.9, and platelet was 253, 000/μL. Results of her complete metabolic panel were within normal limits without any white cells, bacteria, nitrites, or esterase in her urinalysis. Chest x-ray and chest computed tomography scans with contrast were essentially unremarkable except for a left-sided pacemaker with atrioventricular leads. Electrocardiogram was normal sinus at a rate of 76 bpm with normal axis and no ST or T wave abnormality. She was initially managed as possible recurrent pacemaker infection and was started on intravenous ceftriaxone and vancomycin, which was discontinued after 2 sets of blood cultures and microbiology testing of removed pacemaker leads failed to demonstrate the growth of any microorganism.
She subsequently had an extensive metal and substance allergy testing, which revealed an allergic sensitivity to titanium, epoxy, and silicone. A course of steroid therapy without any response was prescribed. Keeping in mind the brother's similar pacemaker history, a special order for a gold-plated permanent pacemaker was made. It was subsequently implanted and resulted in the resolution of the symptom related to recurrent pacemaker allergic reactions.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [96.9, 'degrees fahrenheit'], 'Heart Rate or Pulse': [64.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [5900.0, 'µL']}",0,0,0,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 96.9 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 64.9 = 36.05556 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 64.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 5900.0 count/µL. To convert 5900.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 5900.0 white blood cell count/µL * 1.0 µL/mm^3 = 5900.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 0.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 0.
Hence, the the number of SIRS criteria met by the patient is 0."
6700,51,SIRS Criteria,diagnosis,integer,pmc-7336594-1,Extracted,"A 74-year-old Caucasian male presented to the ED with worsening shortness of breath and elevated blood pressure. On presentation, he was markedly tachypneic and in severe respiratory distress. Vital signs include an elevated blood pressure of 165/114 mmHg, a pulse of 122 beats per minute, a temperature of 99.1°F and a respiratory rate of 28/minute. On physical examination, the patient was in acute distress, diaphoretic, and using accessory muscles of respiration. Lung auscultation revealed diffuse rales. Regular rate and rhythm with no accessory heart sounds were appreciated on precordial auscultation. The patient was put on a non-rebreather mask with mild improvement in the respiratory status and subsequently intubated and transferred to the intensive care unit on mechanical ventilation.
The patient’s medical history was significant for obstructive sleep apnea with noncompliance to positive airway pressure therapy due to discomfort. He had grade 1 left ventricular diastolic dysfunction on an echocardiogram 8 months ago with normal biventricular size and function. He took a trip to Florida with his wife and noticed body aches, constant non-productive cough, headaches, fatigue, and fevers with a temperature of 101°F since his return 10 days prior. He reported sick contact at his vacation, which prompted him to get checked for viral pathogens and get a chest x-ray. The patient was diagnosed with COVID-19 8 days prior to presentation and was followed by the Cleveland Clinic’s distance health service with daily phone encounters while he was in isolation at home. His chest x-ray had shown left perihilar opacity and he was provided with doxycycline.
The differential diagnosis included viral pneumonia, bacterial pneumonia, PE, and COVID-19 acute respiratory distress syndrome (ARDS).
Laboratory work revealed hemoglobin of 17.3 g/dL, white blood cell count of 16,400/uL, elevated liver enzymes with ALT 336 U/L and AST 309U/L. C-reactive protein was elevated to 11.9 mg/dL, D-dimer elevated to 4,300 ng/mL, IL-6 was elevated to 52 pg/mL and ferritin was elevated to 5440 ng/mL. Electrocardiogram (EKG) was insignificant for any acute abnormality, troponin T was elevated to 0.0770 ng/mL and proBNP was elevated to 1312 pg/mL. Arterial blood gas analysis revealed acute hypoxemic respiratory failure with a P: F of 220 on 80% fractional inspired oxygen (FiO2). Chest x-ray revealed bilateral hazy opacities. The patient was kept in airborne precautions. Blood and urine cultures were drawn. The tracheal aspirate was sent for bacterial pneumonia workup. A point of care lower extremity ultrasound revealed left femoral deep venous thrombosis (Figure ).
Low tidal volume lung-protective ventilation was maintained with a high positive end-expiratory pressure (PEEP) and a low fraction of inspired oxygen (FiO2) strategy. The patient was initiated on hydroxychloroquine and azithromycin based on anecdotal data. The patient was a candidate for tocilizumab therapy but was avoided in the setting of abnormal liver function. His P: F ratio suddenly started to decrease along with the elevation of troponin T and pro-BNP. Suspicion of myocarditis, as well as a PE, were high on the differential. As multimodality imaging was limited due to strict precautions to prevent spread, transthoracic echocardiography was performed revealing a normal left ventricular size and systolic function but with a moderately dilated right ventricle with impaired right ventricular (RV) systolic function, severe hypokinesis of basal and mid RV walls and septum with normal contractility of distal RV wall and apex (Video ).
The pattern of RV wall motion was consistent with acute RV strain and a positive McConnell’s sign (Video ).
The patient was started on a heparin infusion. The patient’s acute inflammatory markers trended down with medical therapy and his ARDS improved. Troponin T also returned to baseline after 48 hours.
Hospital course was complicated by the development of ventilator-associated pneumonia and after being on the ventilator for 14 days. the patient was successfully extubated. The patient is currently recovering on the medical floor.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [99.1, 'degrees fahrenheit'], 'Heart Rate or Pulse': [122.0, 'beats per minute'], 'respiratory rate': [28.0, 'breaths per minute'], 'White blood cell count': [16400.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 99.1 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 67.1 = 37.27778 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 122.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 16400.0 count/µL. To convert 16400.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 16400.0 white blood cell count/µL * 1.0 µL/mm^3 = 16400.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 28.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6701,51,SIRS Criteria,diagnosis,integer,pmc-2688166-1,Extracted,"A 20-year-old female patient, who had taken synthetic thyroxine (100 µg/day) for Hashimoto's thyroiditis and overt hypothyroidism, was admitted to our hospital with symptoms of dizziness and generalized weakness in October 1997. Eight months prior, she had been diagnosed with primary hypothyroidism and had begun treatment with synthetic thyroxine (50 µg/day). Upon admission to our hospital, the patient had aggravated dizziness with accompanying nausea and vomiting. She has five siblings, none of whom has any autoimmune disorder.
On physical examination, the patient's blood pressure was 100/70 mmHg, body temperature, 36.8℃, respiration rate, 20 breaths/minute, and pulse rate, 110/minute. She weighed 51 kg and measured 151 cm height (body mass index 22.4 kg/m2).
She looked pale and acutely ill, and had anemic conjunctiva and icteric sclera. Exophthalmoses were not present. The thyroid gland was slightly enlarged and had a hard consistency on palpation, without tenderness. The abdomen was soft and flat, and the liver and spleen were not palpable.
The patient's initial hemoglobin (5.2 g/dL) and hematocrit (15.1%) levels were severely low. Her white blood cell count (WBC) was 9,150/µL (68% polymorphonuclear leukocytes, 18% lymphocytes, 12% monocytes and 2% metamyelocytes), and her platelet count was 576,000/µL. The reticulocyte count was 21.2%, the corrected reticulocyte count was 7.0% and the reticulocyte index was 2.8. Peripheral blood smear analysis revealed spherocytosis, macrocytosis, poikilocytosis, and polychromasia with hemolytic features, and adequate white blood cell and platelet counts (). Levels of both serum calcium and phosphorus were within normal ranges. Total bilirubin, alkaline phosphatase, aspartate transferase and alanine transferase in the serum were 61.2 µmol/dL (reference range [RR], 5.1-17), 87 IU/L (RR, 30-120), 45 and 62 U/L (RR, 5-45), respectively. Lactate dehydrogenase concentration was highly increased to 748 IU/L (RR, 30-170 IU/L), and serum haptoglobin was decreased to 11.8 ng/dL (RR, 50-320 ng/dL). Direct/indirect Coombs' tests and a hemosiderin test yielded strongly positive results. Antinuclear antibody (ANA), antiplatelet antibody, acidified sucrose lysis (Ham's) test and osmotic fragility test were all negative. Abdominal ultrasonography revealed that the patient had a normal sized spleen and liver. According to bone marrow aspiration and biopsy, the patient showed erythroid hyperplasia, which is consistent with hemolytic anemia.
The thyroid function tests performed during synthetic thyroxine (100 µg/day) treatment showed that the patient was at a euthyroid state. However, she had elevated levels of antithyroid antibodies [antithyroglobulin antibody 3,100 U/mL (RR, 0-60) and antimicrosomal antibody 541 U/mL (RR, 0-60)]. The technetium-99m scan () indicated that she had a slightly enlarged thyroid with an inhomogeneous uptake pattern (2.8%). Based on the above results, the patient was diagnosed as having autoimmune hemolytic anemia and Hashimoto's thyroiditis. Her HLA genotypes, HLA-A*020101/A*2602, HLA-B*270502/B*5401, HLA-Cw*0102/Cw*020202, HLA DRB1*0404/DRB1*0405, and DQB1*0302/DQB1*0401 were determined as previously described.
We started the patient on an oral administration of prednisolone (1 mg/kg) and continued synthetic thyroxine medication (100 µg/day). Her hemoglobin level increased and stabilized within two weeks after prednisolone treatment. She had regular follow-up with prednisolone (10 to 30 mg/day) and synthetic thyroxine (100 µg/day) for two years and five months. In April 2000, she complained of frequent epistaxis episodes and an increased amount of menstrual bleeding with her regular cycle. She denied ingestion of any drugs including alcohol or herbs during that time period. She had also adhered to the prescribed administration of prednisolone and synthetic thyroxine. Physical examination did not show any clues indicating systemic lupus erythematosus (SLE) such as arthritis, photosensitivity, oral ulcer, skin rash or psychosis. At that time, she had moderate and persisting thrombocytopenia (75,000-90,000/µL), and repeated ANA test results were negative for serum platelet autoantibody. Hepatosplenomegaly was not found by abdominal ultrasonography. Bone marrow biopsy showed normal findings, except a mildly increased number of megakaryocytes. Serum calcium, phosphorus and albumin were 2.3 mmol/L (RR 2.2-2.6), 1.3 mmol/L (RR, 1.0-1.4) and 4.1 g/dL (3.2-5.3), respectively. Her fasting serum glucose level was 4.8 mmol/L. On urinalysis, neither proteinuria nor microscopic hematuria were found.
Considering the occurrence of thrombocytopenia, and regardless of the prednisolone treatment for AIHA and a normal bone marrow biopsy, we concluded that she had refractory idiopathic thrombocytopenic purpura and autoimmune hemolytic anemia, called Evans' syndrome, associated with Hashimoto's thyroiditis. The severity of hemolytic anemia fluctuated with prednisolone dosage, so we were not able to lower her prednisolone dosage below 20 mg/day. In July 2000, the patient had shown aggravated hemolytic anemia, despite a prednisolone dosage of over 30 mg/day. We concluded that the patient was in a steroid dependent and steroid refractory state, and so carried out a laparoscopic splenectomy.
After the operation, the patient's hemoglobin level and platelet count were restored to 11.1 g/dL and 461,000/µL, respectively. We could then lower her prednisolone dosage to 10 mg/day. Currently, she is still taking 10 mg of prednisolone per day due to her steroid-dependent AIHA and ITP condition, and has regular follow-ups at our hospital's outpatient clinic.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.8, 'degrees celsius'], 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [9150.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.8 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 110.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 9150.0 count/µL. To convert 9150.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 9150.0 white blood cell count/µL * 1.0 µL/mm^3 = 9150.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6702,51,SIRS Criteria,diagnosis,integer,pmc-8107894-1,Extracted,"A 52-year-old female visited the emergency room of our hospital (Soonchunhyang University Bucheon Hospital) due to abdominal pain nausea and vomiting.
Five weeks before visiting the emergency room, she visited our outpatient clinic of gastroenterology department due to an increased level of liver enzyme alanine aminotransferase (ALT) (at 320 U/mL) that was accidentally found at a health screening test. Blood test showed positive autoimmune antibody (anti-nuclear antibody 1:1280 and anti-mitochondrial antibody positive). Her immunoglobulin G was elevated to 1577 mg/dL. Abdominal ultrasound and computed tomography (CT) showed coarse liver surface, indicating that she had chronic liver disease (Figure ). Therefore, a liver biopsy was performed and the patient was finally diagnosed with an overlap syndrome predominantly with features of an autoimmune hepatitis. After the biopsy, the patient started to take high dose of ursodeoxycholic acid (15 mg/kg) plus prednisolone 40 mg daily for two weeks. After two weeks from the initial treatment, the dose of ursodeoxycholic acid was maintained and prednisolone was reduced by 10 mg every week. Six days before the emergency room visit, prednisolone was reduced to 5 mg and azathioprine 50 mg was maintained.
From two days before visiting the emergency room, the patient had symptoms of mild heartburn and abdominal pain. One day before the emergency room visit, her abdominal pain worsened to the point that it interfered with her sleep. In addition, she had more symptoms of nausea, vomiting, and diarrhea. Thus, she finally visited the emergency room.
The patient had an unremarkable past medical history except for an overlap syndrome described above.
At the time of the emergency room visit, her blood pressure was normal with a systolic blood pressure of 130 mmHg and a diastolic blood pressure of 80 mmHg. She had a mild fever (37.6 °C) and tachycardia (heart rate of 110 beats/min). She also had tachypnea at 30 breaths per minute. She had abdominal tenderness in the epigastric to the left upper quadrant area. Her abdomen was a little hard. However, no rebound tenderness was observed.
During the outpatient treatment period, her counts of white blood cells, red blood cells, and platelets were all normal. However, at the time of the emergency room visit, her counts of white blood cells and platelets were reduced to 700/µL and 61000/µL, respectively. Since her neutrophil level was decreased to 5% and C-reactive protein level was elevated to 14.35 mg/dL, systemic infection was strongly suspected. Test results for liver enzymes were: aspartate aminotransferase, 347 U/L; ALT, 52 U/L; and gamma glutamyl transferase, 458 U/L. Her prothrombin time international normalized ratio was 1.2.
Contrast-enhanced abdominal CT revealed a huge stomach with layered wall thickening in the fundus and upper body (Figure ), which was not found before she received treatment (Figure ). Air in the stomach wall was observed in some areas. Decrease of mucosal enhancement was also detected.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.6, 'degrees celsius'], 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'respiratory rate': [30.0, 'breaths per minute'], 'White blood cell count': [700.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.6 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 110.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 700.0 count/µL. To convert 700.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 700.0 white blood cell count/µL * 1.0 µL/mm^3 = 700.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 30.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6703,51,SIRS Criteria,diagnosis,integer,pmc-7708882-1,Extracted,"A 50-year old female kidney transplant recipient presented to the transplant clinic with a progressive dry cough and fever that started three days ago.
She described accidentally being in contact with a symptomatic COVID-19 positive individual 7 d prior to her cough and fever.
She had received a standard criteria deceased donor kidney seven years ago with anti-thymocyte globulin induction. Since then her kidney function was stable with maintenance immunosuppressants consisting of tacrolimus (1.5 mg/d), mycophenolate mofetil (720 mg/d), and prednisone (5 mg/d).
She did not smoke, consume alcohol, or have coronary artery disease. Her only comorbidity was mild hypertension treated with amlodipine (10 mg/d). Her family history was unremarkable.
On examination, her temperature was 38 °C, heart rate 100 bpm, respiratory rate 14 breaths/min, blood pressure 120/60 mmHg, and oxygen saturation 96%. Auscultation of the chest revealed bilateral fine crackles at the base of the lungs.
Her graft function was stable with a minimum elevation from her baseline creatinine of 0.9 to 1.1 mg/dL. The glomerular filtration rate was 58.5 mL/min. Complete blood count showed increased white blood cells (20800/μL) with a total lymphocyte count of 1210/μL. The hemoglobin and platelet counts were 10.6 g/dL and 177.000/μL, respectively. The remaining biochemical parameters were within normal ranges. A high level of C-reactive protein (CRP) was noted (276 mg/L). Complete urine analysis was unremarkable. Lastly, her trough tacrolimus level was 5.5 ng/mL.
Chest X-ray was normal. Although the patient did not give a history of traveling abroad or contacting COVID-19 positive individuals, a chest computed tomography (CT) scan was obtained. The scan revealed consolidation areas with air bronchograms in the left lower lobe with pneumonic infiltrations (Figure ). A nasopharyngeal swab to test for COVID-19, influenza A/B was obtained. Additionally, blood samples for cytomegalovirus (CMV) and BK virus serology were sent to the microbiology department to diagnose opportunistic viral infections.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.0, 'degrees celsius'], 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'respiratory rate': [14.0, 'breaths per minute'], 'White blood cell count': [20800.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 100.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 20800.0 count/µL. To convert 20800.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 20800.0 white blood cell count/µL * 1.0 µL/mm^3 = 20800.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 14.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6704,51,SIRS Criteria,diagnosis,integer,pmc-6232278-1,Extracted,"A 35-year-old male with a past medical history of diabetes mellitus type 2, hypercholesterolemia and recurrent boils from methicillin-resistant Staphylococcus aureus (MRSA) initially presented with a right axillary boil. The patient reported that 5 days prior he noticed a red, hot area under his right arm which then progressed to a boil that spontaneously ruptured. Over the course of the next several days the boil drained foul smelling fluid and became progressively more painful causing him to seek medical attention. He reported subjective fevers during the first 2 days of his symptoms, but the fevers resolved after the boil ruptured. He denied any other symptoms.
Upon examination the patient was alert and oriented and was noted to have an area of black necrotic skin in his right axilla, with surrounding erythema and associated induration on the right chest wall (Fig. ). On admission his heart rate was 132 beats per minute, blood pressure 116/80 mmHg, temperature 38.3°C, respirations 30 per minute and oxygen saturation 96% on room air. Laboratory studies revealed a white blood count of 26.2 K cells/dL, hemoglobin of 13.2 g/dL, sodium of 129 mEq/L, glucose of 289 mg/dL, serum creatinine of 0.9 mg/dL, C-reactive protein of 36.8 mg/dL, hemoglobin A1C of 13.5% and lactate of 3.3 mmol/L. The remaining laboratory values were within normal limits. The patient’s calculated Laboratory Risk Indicator for Necrotizing Fasciitis score was 10 points, supporting the clinical diagnosis of NSTI []. A computed tomography scan revealed a moderate amount of subcutaneous gas within the soft tissue of the right axilla and lateral chest wall along with surrounding edema.
The patient was started on linezolid and piperacillin–tazobactam for broad-spectrum coverage. He was taken emergently to the operating room for sharp debridement of skin, subcutaneous tissue, fascia and muscle of the right axilla and lateral chest wall. Intraoperatively a large amount of purulent and necrotic tissue was found. Fluid and tissue cultures were taken. The excised area measured 17 × 9 × 6 cm3 (Fig. ). The patient underwent a subsequent operation for further debridement and returned to the operating room 3 days after that for delayed primary closure over a drain (Fig. ). On hospital Day 6, the initial operative cultures returned with abundant growth of Kocuria rosea and rare growth of coagulase negative Staphylococcus. Although susceptibility studies were not performed, literature has shown Kocuria to be susceptible to commonly used antibiotics []. The patient’s antibiotics were narrowed to intravenous ampicillin–sulbactam and linezolid while he remained in the hospital. The patient was discharged on hospital Day 9 on oral amoxicillin–clavulanate and linezolid to complete a 14-day antibiotic course. Although the culture data did not support the use of linezolid, it was continued given his past history of recurrent MRSA boils. He returned to the outpatient clinic 27 days after wound closure for drain and suture removal. The patient had no follow-up complications and was released from the surgical service.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.3, 'degrees celsius'], 'Heart Rate or Pulse': [132.0, 'beats per minute'], 'respiratory rate': [30.0, 'breaths per minute'], 'White blood cell count': [26200, 'dL']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.3 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 132.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 26200 count/dL. To convert 26200 count/dL of white blood cell to mm^3, multiply by the conversion factor 1e-05 dL/mm^3 which will give 26200 white blood cell count/dL * 1e-05 dL/mm^3 = 0.262 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 30.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6705,51,SIRS Criteria,diagnosis,integer,pmc-8173408-1,Extracted,"A 33-year-old primigravid woman with a twin pregnancy in the 31st week of gestation, who had conceived after in vitro fertilization (IVF), presented to the hospital with intermittent chest tightness for 12 wk, aggravation for 1 wk, and chest pain for 4 h.
Twelve weeks ago, the patient had begun to experience chest tightness after a full meal, which had lasted for approximately 30 min each time. One week prior, her chest tightness was aggravated but was not accompanied by any other discomfort; hence, the patient did not visit a clinician. However, 4 h before admission, the patient had suddenly experienced poststernal colic after having her meal, which was not relieved, accompanied by sweating and awareness of defecation. The patient reported having a fall without injuries. She also complained of nausea and non-jet vomiting. The vomiting included stomach contents, and she had no syncope or loss of consciousness.
Subsequently, the patient was admitted to Beijing United Family Hospital and underwent certain examinations. Electrocardiogram (ECG) showed ST-segment elevation in leads II, III, aVF, V3R-V5R, and V7-V9 (Figure ). The hypersensitive troponin level (TNI, 0.0074 μg/L) was increased, and the white blood cell (WBC, 16.5 × 109/L) count and D-dimer levels were elevated. Echocardiogram suggested akinesis of the inferior wall of the left ventricle and hypokinesis of the basic segment of the posterior wall. Despite the administration of ondansetron and saline, the patient’s chest pain failed to be relieved, after which she was intravenously administered with morphine. The patient was subsequently transferred to Beijing Anzhen Hospital.
The patient had no history of cardiovascular disease, conventional cardiovascular risk factors (such as hypertension, diabetes, and smoking), or relevant family history. Nonetheless, the patient was advised to rest in bed in the 24th week of gestation. She was also administered with nifedipine, dexamethasone, and progestin during the pregnancy and was subcutaneously administered with enoxaparin for her hypercoagulable state 1 wk prior to admission. In addition, the patient had been diagnosed with benign paroxysmal positional vertigo 2 wk prior to admission and was treated with Merislon. She was allergic to penicillin and egg yolk.
The patient had no relevant family history.
The patient was conscious on admission; her body temperature was 36.0 °C, pulse was 95 bpm, blood pressure was 119/73 mmHg, and respiratory rate was 20 breaths per minute. On physical examination, the patient appeared acutely ill, was in the left lying position, exhibited no special cardiopulmonary signs, and had a pregnant abdomen and irregular abdominal contractions.
Laboratory examination showed obviously elevated levels of the following: Creatine kinase 2924 U/L, lactate dehydrogenase 558 U/L, creatine kinase isoenzyme MB 21.5 ng/mL, TNI 47.72 ng/mL, and myoglobin 1442.7 ng/mL.
ECG showed that the ST segment in leads II, III, and aVF had dropped back to baseline levels, and the V3R-V5R leads were of the QS type.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.0, 'degrees celsius'], 'Heart Rate or Pulse': [95.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [16500.0, 'L']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 95.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 16500.0 count/L. To convert 16500.0 count/L of white blood cell to mm^3, multiply by the conversion factor 1e-06 L/mm^3 which will give 16500.0 white blood cell count/L * 1e-06 L/mm^3 = 0.0165 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6706,51,SIRS Criteria,diagnosis,integer,pmc-5507793-1,Extracted,"A 40-year-old male factory worker was admitted to the emergency room with severe abdominal pain and distension. Four hours prior, his friend blew out dust from the clothes of the patient with a compressed air gun () as was usually done in his work place. At this time, his friend placed air nozzle too close to the buttocks of the patient, but the intention of practical joke was denied according to a witness. Immediately, the patient experienced severe abdominal pain and gradual distension of the abdomen. At admission, his blood pressure was 170/104 mmHg, pulse rate was 133 beats/min, respiratory rate was 22 breaths/min, and body temperature was 36.8℃. The patient was pale and clammy. The abdomen was markedly distended with signs of tenderness and rebound tenderness. Large amounts of fresh and clotted blood gushed out on digital rectal examination. On laboratory blood test, white blood cell count was 6.78 × 103/µL, hemoglobin 16.1 g/dL, while the other parameters were not clinically significant. Abdominal X-ray showed large amounts of free peritoneal gas. Computed tomography of the abdomen and pelvis demonstrated large amounts of free gas in the peritoneal cavity, retroperitoneal area, and mediastinum (). Subcutaneous emphysema was seen in the perineal area and around the scrotum (). Percutaneous decompression of the tension pneumoperitoneum was performed by inserting a cannula into the abdomen for relief of pressure. Sigmoidoscopy was attempted after enema for the detection of the perforation site but it did not revealed any significant findings due to the presence of large amounts of fecal material and blood clot in the rectum. Emergency exploratory laparotomy was done under the lithotomy position, which provides a route for intraoperative colonoscopy when necessary. The peritoneum was assessed via a low midline incision. On opening the abdomen, large amounts of air whistled out of the abdominal cavity. Large amounts of gross fecal material and bloody ascites were found. A 4- × 4-cm-sized perforation (), which extended from the retroperitoneal part of rectum to the rectosigmoid junction, was found. Intraoperative endoscopic rectal examination after rectal irrigation was done to evaluate the entire length of the rectum since the presence of perineal air suggested additional rectal injuries; however, there was no other damage. Primary repair of the perforation or anastomosis after bowel resection seemed dangerous under the circumstance of severe fecal contamination. The damaged segment of the bowel was resected with closure of the distal rectal stump and construction of an end sigmoid colostomy (Hartmann procedure). His follow-up period was completed without any complication and he was discharged 8 days after operation. Reversal of the colostomy was done after 8 weeks and the postoperative period was uneventful.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.8, 'degrees celsius'], 'Heart Rate or Pulse': [133.0, 'beats per minute'], 'respiratory rate': [22.0, 'breaths per minute'], 'White blood cell count': [6780.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.8 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 133.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 6780.0 count/µL. To convert 6780.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 6780.0 white blood cell count/µL * 1.0 µL/mm^3 = 6780.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 1 + 1 = 2 criteria met.
Hence, the the number of SIRS criteria met by the patient is 2."
6707,51,SIRS Criteria,diagnosis,integer,pmc-4193390-1,Extracted,"In October, 2013, an 18-year-old African American young woman diagnosed in August of that year with SLE presented to a community hospital complaining of headache, neck and back pain for five days, and vomiting with non-bloody diarrhea for one day. Additionally, she reported right-sided weakness. Six weeks prior to this presentation, she met the criteria for a diagnosis of SLE with arthritis, a photosensitive malar rash, and serum serology positivity for anti-nuclear antibodies (1:5120) as well as anti-double stranded DNA and anti-ribonuclear protein antibodies. A regimen of oral prednisone (10 mg twice daily) and hydroxychloroquine (200 mg twice daily) was begun. In the weeks subsequent to the diagnosis and treatment of SLE, and prior to her hospitalization, the patient had a positive home pregnancy test, which was followed by an unusually heavy menstrual cycle and presumed spontaneous abortion. The patient did not seek medical attention, and therefore no uterine manipulation or evacuation was performed. The patient’s family history is significant for a maternal aunt and paternal cousin with SLE, and a maternal great-uncle who died from Libman-Sacks endocarditis.
At the time of the acute presentation, she was febrile to 38.9°C, oriented to self only, and had positive Kernig and Brudzinski signs. A computed tomography scan of the head revealed an extra-axial fluid collection in the right frontotemporal region, with a mild local mass effect, but no midline shift and normal ventricles. Intravenous vancomycin and ceftriaxone were initiated and the patient was transferred to our institution.
On arrival to our pediatric intensive care unit, the patient’s temperature was 38.8°C, blood pressure was 145/76 mmHg, heart rate was 70 beats per minute, respiratory rate was 22 breaths per minute, and oxygen saturation was 100% on room air. She was drowsy and irritable when aroused, complaining of continued severe headache and neck pain. Neurological exam was significant for photophobia and meningismus. The remainder of the neurological exam and the ocular exam were normal. Analysis of the cerebrospinal fluid (CSF) revealed 1525 white blood cells/µL (91% neutrophils), 65 red blood cells/µL, 252 mg/dL protein, and 56 mg/dL glucose. An MRI of the brain with and without contrast revealed a moderately sized extra-axial effusion with secondary inflammatory response (
 and
) and punctate diffusion abnormalities within the dependent portion of the lateral ventricles, consistent with pus or debris. The CSF culture was negative for bacteria, likely secondary to receipt of antibiotics prior to sampling, but the blood culture prior to antibiotic receipt grew GBS. Antibiotic susceptibility testing was not performed. CSF studies for other pathogens, including cryptococcal antigen, detection of herpes simplex and varicella viruses by PCR, and specific cultures for acid-fast bacilli and fungi, were negative. Upon identification of GBS, vancomycin and ceftriaxone were discontinued, and treatment was continued with intravenous penicillin G (4,000,000 units every 4 hours) for two weeks. The patient showed rapid improvement on antibiotic therapy and had resolution of all neurologic symptoms within one week of admission. She was discharged to receive intravenous ceftriaxone for one additional week at home.
Notably, the patient’s SLE was severely active during the course of this acute illness. Initial laboratory results at our institution demonstrated anti-Smith, anti-Ro and anti-La antibodies. She also had severe hypocomplementemia, doubling of serum creatinine, and nephrotic range proteinuria as assessed by 24-hour urine collection. Subsequent kidney biopsy demonstrated class V lupus nephritis. Induction therapy with intravenous methylprednisolone was started, which was then changed to oral prednisone (30 mg twice daily), mycophenolate mofetil (1000 mg twice daily), and hydroxychloroquine (400 mg once daily). Her serologically active SLE began to improve after her course of methylprednisolone, but was still active at the time of discharge.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.8, 'degrees celsius'], 'Heart Rate or Pulse': [70.0, 'beats per minute'], 'respiratory rate': [22.0, 'breaths per minute'], 'White blood cell count': [1525.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.8 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 70.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 1525.0 count/µL. To convert 1525.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 1525.0 white blood cell count/µL * 1.0 µL/mm^3 = 1525.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6708,51,SIRS Criteria,diagnosis,integer,pmc-6314392-1,Extracted,"A 69-year-old female presented to our emergency department with chief complaint of neck swelling, sore throat and difficulty swallowing for the past two days. She also complained of fever and voice hoarseness. Flexion and extension of the neck made the pain worse. She denied difficulty breathing, nausea, vomiting, or chest pain. She reported a non-productive cough. She stated that her daughter and grandchildren were sick with a cough and cold. She took diphenhydramine, acetaminophen and some old amoxicillin at home. Her past medical history was significant for salivary gland cancer nine years prior that was treated with chemotherapy and radiation.
Her vital signs were: pulse 103, blood pressure 120/62 mmHg, temperature 37.6°C, respirations 18/min, and room air pulse oximetry 100%. Laboratory analyses revealed an elevated white blood cell count of 33 K/mm3, and an elevated procalcitonin level of 23.67 ng/mL. Radiograph of the soft tissues of the neck revealed an enlarged epiglottis and aryepiglottic folds, consistent with epiglottitis. In addition, subglottic narrowing of the airway is demonstrated (Figure ). The patient received intravenous ampicillin-sulbactam, methylprednisolone and diphenhydramine in the emergency department with some improvement. The patient was initially admitted to the intensive care unit and evaluated by the otolaryngology service using a flexible nasopharyngoscope. The patient was gradually weaned off of intravenous medications and discharged on hospital day three. Blood and throat cultures were negative.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.6, 'degrees celsius'], 'Heart Rate or Pulse': [103.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [33000.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.6 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 103.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 33000.0 count/m^3. To convert 33000.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 33000.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 3e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6709,51,SIRS Criteria,diagnosis,integer,pmc-8178924-1,Extracted,"A Japanese four-year-old girl with a rhinorrhea and four days of fever was referred to our hospital. Her past history was as follows: she was delivered at 35 weeks of gestation by caesarian section because of nonimmune hydrops fetalis secondary to congenital chylothorax. She was diagnosed with Sturge-Weber syndrome at 2 years old due to hemangiomas in the trigeminal nerve distribution area, glaucoma, occipital lobe hemangioma and parenchymal atrophy in the same area, and developmental disabilities. Pleural effusion was present at three years of age because of Budd-Chiari syndrome due to occlusion of the hepatic portion of the inferior vena cava. After the placement of a pleuroperitoneal shunt, pleural effusions were improved. An abdominal computed tomography (CT) incidentally revealed a simple renal cyst in her right kidney, and the asymptomatic simple renal cyst was managed conservatively (Fig. a). Her immunizations were up-to-date, and she received a 13-valent pneumococcal conjugate vaccine four times.
On exam, she was initially febrile: her axillary temperature was 38.1 °C; respiratory rate was 28/min, with an O2 saturation of 97 % on room air; heart rate was 144/min; and blood pressure was 144/108 mmHg. She had tenderness on her back, and her breath sounds were decreased. Her white blood cell (WBC) count was 15,000/µl, with differential counts of neutrophils (72.6 %) and lymphocytes (20.2 %); her C-reactive protein level was markedly elevated (28.48 mg/dl, normal range 0-0.3 mg/dl); her serum total protein level was 6.8 g/dl and her serum albumin level was slightly decreased (3.0 g/dl, normal range 3.9–5.2 mg/dl). She did not show symptoms of nephrotic syndrome, such as edema and heavy proteinuria, or symptoms of protein losing enteropathy, such as diarrhea. Pyuria and bacteriuria were not present in her urinalysis. A chest X-ray showed massive pleural effusions on the right side (Fig. b). Analysis of the pleural fluid obtained by thoracentesis revealed the following: pH, 7.011; protein, 900 mg/dl; and WBC, 2,940 cells/µl (66 % neutrophils). We suspected pneumococcal infection or catheter-related blood stream infection due to the presence of a pleuroperitoneal shunt catheter and initiated 200 mg/kg cefotaxime (CTX) per day and 60 mg/kg vancomycin (VCM) per day. VCM was discontinued after two days. S. pneumoniae was detected from two sets of blood cultures on admission, chest CT showed infiltration in the left lower lobe and right upper lobe, and otitis media was noted by otological evaluation on the subsequent day. We diagnosed her with invasive pneumococcal disease, including pneumonitis and otitis media. Based on susceptibility test results, CTX was changed to 200 mg/kg ampicillin per day on day 5. Although transient improvement of her symptoms and a decrease in the WBC count (9,800/µl) and CRP level (11.9 mg/dl) were observed on hospital day 9, she complained of respiratory discomfort again on hospital day 12. Her WBC count (13,200/µl) and serum CRP level (16.41 mg/dl) were elevated. Ampicillin (ABPC) treatment was escalated to 300 mg/kg tazobactam-piperacillin (TAZ/PIPC) treatment per day empirically. However, her symptoms did not improve sufficiently. Ultrasonography on hospital day 20 revealed a fluid-fluid level, suggesting an abscess in the right renal cyst. Enhanced CT on hospital day 21 revealed enlargement of the right renal cyst and enhancement and thickening of the wall around the cyst, which was considered to be an infected simple renal cyst (Fig. c). A drainage procedure under general anesthesia was performed on hospital day 23. Twelve milliliters was removed of greenish white pus was removed, and Gram staining of the pus showed neutrophils with no organisms. The melting temperature (Tm) mapping method was performed using 50 µl of the pus. After bacterial DNA was isolated from the pellets using a DNA extraction kit (DNA Extraction Kit, Mitsui Chemicals, Japan) in accordance with the supplier’s instructions, we conducted nested polymerase chain reaction (PCR) on the DNA using seven universal bacterial primer sets and EvaGreen dye, which was performed on an analytical instrument with a high degree of thermal accuracy among PCR tubes. The data profile was analyzed using a Rotor-Gene Q® (QIAGEN, Germany), which can achieve temperature uniformity among samples (± 0.02 °C), and the Tm values were identified. The seven Tm values were determined and mapped on two dimensions, and by comparing the pattern to those in the database, S. pneumoniae was identified 4.5 hours after cyst drainage (Fig. ). We diagnosed her with a simple renal cyst infected with S. pneumoniae. The culture of the pus was negative, but we de-escalated TAZ/PIPC treatment to 200 mg/kg ABPC treatment per day on the basis of positive detection by the Tm mapping method on hospital day 27. Her convalescence was uneventful after the drainage, the drainage tube was removed on hospital day 29, and the antibiotic treatment was changed to oral amoxicillin (40 mg/kg per day) on hospital day 30. An asymptomatic scar approximately 1 cm in size was observed in her right kidney on ultrasonography, but she was discharged from our hospital with 5 days of oral amoxicillin on hospital day 32. Samples of fluid aspirated from the renal cyst did not grow any organisms in culture, but 16 S rRNA sequencing of the pus revealed a 100 % nucleotide identity to the respective sequence of a S. pneumoniae strain (ABI 3500 Genetic Analyzer, Applied Biosystems, Foster City, CA) in subsequent days. She was followed up for two years after discharge, and no recurrence of renal cyst infection was observed.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.1, 'degrees celsius'], 'Heart Rate or Pulse': [144.0, 'beats per minute'], 'respiratory rate': [28.0, 'breaths per minute'], 'White blood cell count': [15000.0, 'µL']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.1 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 144.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 15000.0 count/µL. To convert 15000.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 15000.0 white blood cell count/µL * 1.0 µL/mm^3 = 15000.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 28.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6710,51,SIRS Criteria,diagnosis,integer,pmc-7811565-1,Extracted,"In April 2020, a 46-year-old man with a past medical history of diabetes presented to the emergency room with symptoms of cough, shortness of breath, and fevers for four weeks. He was treated for suspected pneumonia with azithromycin two weeks prior to presentation and denied any improvement in respiratory symptoms thereafter. In addition, he developed a painful and pruritic rash that was progressively worsening over the last two weeks (see for timeline of patient course).
On physical examination, he was afebrile (36.9 C) with tachycardia (110 bpm), blood pressure 127/77 mm Hg, respiratory rate 20, and O2 saturation 94% on room air. He had erosions on bilateral nasal mucosa and vermillion lips with overlying crusts. Oropharynx was clear. There were purpuric macules and papules on bilateral palms, arms, and legs, few with overlying vesicular changes and collarettes of scale (Figures and ). He also had retiform purpuric macules and patches on buttocks and thighs (), as well as ulcerations on buttocks at the gluteal cleft.
Laboratory evaluation showed an elevated white blood cell count (15.3K/μL), decreased hemoglobin (10.3 g/dL), elevated blood urea nitrogen (48 mg/dL), creatine (2.9 mg/dL), and D-dimer (8,922 ng/mL). He was cANCA positive, coronavirus PCR negative via nasopharyngeal swab, and coronavirus antibody IgM positive and IgG negative. CT scan of the chest showed patchy ground-glass opacities in the lungs.
Biopsy of skin showed superficial and deep perivascular inflammation with thrombus formation (H&E stain, 10x) (). High-power view showed an infiltrate composed of lymphocytes, histiocytes, neutrophils, and eosinophils, with prominent erythrocyte extravasation, leukocytoclasia, and fibrinoid necrosis of vessels (H&E stain, 40x) (). Renal biopsy showed interstitial mixed cell infiltrates and intraglomerular thrombi and necrosis, concerning for GPA.
Based upon his clinical presentation, histologic findings, and laboratory studies, the patient was diagnosed with GPA in the setting of suspected coronavirus infection. He was first treated for coronavirus with five-day course of hydroxychloroquine, followed by treatment of GPA with systemic steroids and rituximab infusion. Kidney function improved, and his rash completely resolved. He was discharged on a steroid taper.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.9, 'degrees celsius'], 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [15300.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.9 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 110.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 15300.0 count/µL. To convert 15300.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 15300.0 white blood cell count/µL * 1.0 µL/mm^3 = 15300.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6711,51,SIRS Criteria,diagnosis,integer,pmc-3271399-1,Extracted,"A 25 year old female patient presented to us with the complaints of shortness of breath since 3 days, which was sudden in onset, associated with left sided chest pain. She was also giving history of fever and cough since 3 months. She had pallor, but no clubbing, jaundice or lymphadenopathy. On vitals examination pulse rate was 100/min; respiratory rate 30/min, blood pressure 100/70 mm Hg and temperature 99°F. Chest movements were diminished on the left side with a slight shift of trachea to the right side. Percussion revealed a hyperresonant note on the left side with markedly diminished breath sounds. Other systemic examinations findings were unremarkable. Laboratory investigations revealed a moderate anemia (8.6 gm%) with a normocytic, normochromic peripheral blood picture and a high total leucocytic count (12,400 mm3) with lymphocytosis (70%). ESR was 54 mm at the end of 1 hour. Chest roentgenogram done 10 days prior to admission showed bilateral miliary shadows. Chest roentgenogram (PA view) on admission showed a left sided pneumothorax with miliary mottling (). An intercostal chest tube drainage connected to an underwater seal bottle was put on the left side resulting in relief in symptoms, and patient was put on antitubercular treatment. Two days post intercostal chest tube drainage chest X-ray (PA view) showed complete resolution of pneumothorax () and intercostal chest tube drain was removed. Patient was discharged on antitubercular drugs. After 1 month patient again presented to us with severe breathlessness, on repeat chest X ray (PA view) pneumothorax again developed on left side (), urgent intercostal chest tube drainage was done, and patient relieved immediately. Patient was kept in the hospital for 12 days and intercostal chest tube drain was removed. Patient was discharged.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [99.0, 'degrees fahrenheit'], 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'respiratory rate': [30.0, 'breaths per minute'], 'White blood cell count': [12400.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 99.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 67.0 = 37.22222 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 100.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 12400.0 count/m^3. To convert 12400.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 12400.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 30.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6712,51,SIRS Criteria,diagnosis,integer,pmc-5331238-1,Extracted,"A four-week-old, Japanese, female infant was taken to the emergency department of an outside hospital because of episodic cyanotic spells. She had been previously healthy with normal growth and was born at 39 weeks of gestation with a birth weight of 3280 g. On examination, she was noted to become motionless with facial cyanosis after coughing. Oxygen saturation (SpO2) was 72% with ambient air, and her pulse was 198 beats per minute (bpm). After vigorous stimulation, she started breathing and rapidly returned to a healthy color with a 98% SpO2 with oxygen administration. She was transferred to our hospital for apnea monitoring.
Her mother and siblings also had a symptomatic nagging cough for more than 1 month. Two weeks prior to the birth of the patient, her nine-year-old brother began to cough, followed by her six-year-old sister and her 38-year-old mother. Her siblings had completed a series of vaccinations recommended by the National Childhood Immunization Program in Japan . These vaccinations included four doses of diphtheria, tetanus, and acellular pertussis (DTaP) vaccine at 7, 9, 11, and 27 months old. Her mother has not received pertussis vaccine for at least 30 years. The patient has not been immunized.
On arrival to our hospital, the patient appeared well. Vital signs were all within the normal range; the temperature was 37.1°C; the blood pressure 84/42 mmHg, the pulse 150 beats per minute, the respiratory rate 38 breaths per minute, and the oxygen saturation 98% while she was breathing ambient air. She had coarse crackles on the right side of the thorax and several episodes of transient apnea which lasted approximately 10–20 sec. The white cell count on admission was 26,690 WBC/μL; 72.0% were neutrophils and 22.5% were lymphocytes. The C-reactive protein level was 3.29 mg/dL. A chest X-ray showed infiltration in the right lower lung. Antipertussis toxin (PT) and antifilamentous hemagglutinin (FHA) IgG levels were negative, with values of 6 and 3 EU/mL, respectively. The assay cutoff level for negative results was 10 EU/mL for both tests.
The patient was admitted to our intermediate-level unit, specially staffed to provide close cardiopulmonary monitoring. Intravenous sulbactam/ampicillin (225 mg/kg/day for 10 days) and oral azithromycin (10 mg/kg/day for 5 days) were administered. We suspected pertussis complicated by aspiration pneumonia. Anti-PT- and anti-FHA-IgG tests were positive in the patient's mother (mother: PT-IgG, 146 EU/mL; FHA-IgG, ≥160 EU/mL) and siblings (brother: PT-IgG, 156 EU/mL; FHA-IgG, ≥160 EU/mL and sister: PT-IgG, ≥160 EU/mL; FHA-IgG, ≥160 EU/mL). The anti-PT-IgG test was considered positive at a value of >100 EU/mL, indicating recent infection with B. pertussis, regardless of the immunization history. In addition, lymphocytosis was observed on day 4 after admission (maximum lymphocyte fraction of 88.0%, Fig. ) and morphological examination of a peripheral blood smear showed numerous mature lymphocytes (Fig. ). These findings strongly supported the diagnosis of pertussis. Furthermore, polymerase chain reaction (PCR) for B. pertussis was positive in a nasopharyngeal swab from the patient, with a value of 440 copies/well. The cutoff value for a positive result was 100 copies/well.
Figure shows the trend of the occurrence of desaturation events and the patient's absolute lymphocyte count in our intermediate-level unit. Between desaturation events, the patient's SpO2 and pulse rate were stable and were maintained at an SpO2 of 98–100% with ambient air and approximately 130 bpm throughout her hospital stay. However, despite our treatment, she had repeated apnea episodes followed by desaturation and a decreased pulse rate. She also had repeated bradycardia (<85 bpm) episodes, despite oxygen administration by nasal cannula at 1–2 L/min, especially during the first week of hospitalization. Some apnea episodes typically occurred after consecutive bouts of coughing, and others occurred without warning (Fig. ). Apnea episodes gradually decreased and become less severe with time. The absolute lymphocyte count reached a peak level of 14,100/μL on the third hospital day and then gradually decreased. The patient was discharged home on the forty-fifth hospital day. Before discharge, we instructed her parents regarding pediatric basic life support in case of repeated life-threatening apnea. At follow-up in our outpatient clinic, her mother reported that she had no further apnea episodes after discharge. The total medical cost for care during hospitalization was ¥2,768,100 (approximately US $23,000).",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.1, 'degrees celsius'], 'Heart Rate or Pulse': [150.0, 'beats per minute'], 'respiratory rate': [38.0, 'breaths per minute'], 'White blood cell count': [26690.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.1 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 150.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 26690.0 count/µL. To convert 26690.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 26690.0 white blood cell count/µL * 1.0 µL/mm^3 = 26690.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 38.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6713,51,SIRS Criteria,diagnosis,integer,pmc-5687971-1,Extracted,"A 33-year-old Hispanic male of average build was admitted to our facility, complaining of dyspnea, fever, night sweats, and rapid weight loss (18 kg over a four-month period). A pertinent positive finding on the initial history taking was his having traveled to a country where tuberculosis is endemic. Physical examination revealed no acute distress and no stigmata of intravenous drug abuse. He was febrile (≤ 38.5°C), with a blood pressure of 124/72 mmHg, a heart rate of 76 bpm, a respiratory rate of 18 breaths/min, and a constant SpO2 at rest of 98%. The initial total leukocyte count was 8,200 cells/µL, with a predominant neutrophilic reaction. Blood culture was negative for aerobic and anaerobic microorganisms. Urine toxicology and HIV tests were negative. Chest X-ray and HRCT showed micronodules (1-3 mm in size) bilaterally in centrilobular distribution (). An IFN-γ assay and sputum smear microscopy for acid-fast bacilli were carried out in order to rule out mycobacterial infection. Although the results were negative for tuberculosis, the high clinical suspicion of the disease prompted empirical initiation of the four-drug antituberculous therapy. Four weeks later, the patient returned to the emergency room with worsening of the shortness of breath. A repeat HRCT revealed similar centrilobular nodules with no radiological improvement (). At that time, bronchoscopy with transbronchial lung biopsy was performed for further evaluation of the pulmonary micronodules. Examination of the BAL fluid, with Ziehl-Neelsen staining, revealed no acid-fast bacilli. Histopathological analysis of the transbronchial lung biopsy specimen showed multiple granulomas with birefringent material in the center (), confirming the diagnosis of PFBG. The patient strongly denied intravenous drug use. Unfortunately, he experienced a progressive course with a further decline in his lung function. After progressive fibrosis over the following one-year period, the patient died of chronic respiratory failure.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.5, 'degrees celsius'], 'Heart Rate or Pulse': [76.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [8200.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.5 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 76.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 8200.0 count/µL. To convert 8200.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 8200.0 white blood cell count/µL * 1.0 µL/mm^3 = 8200.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6714,51,SIRS Criteria,diagnosis,integer,pmc-8319662-1,Extracted,"A 66-year-old woman presented to the emergency department with complaints of shortness of breath and chest pain for the preceding 2 days.
She had a history of rheumatoid arthritis (RA) and systemic lupus erythematous (SLE), taking oral prednisolone (6 mg/day) and hydroxychloroquine (200 mg/day). She was a housewife and frequently worked with potting soils in her garden. She also had orange-coloured sputum (Figure ). Her vital signs upon admission were as follows: temperature, 36.1°C; blood pressure, 109/69 mmHg; pulse rate, 111 beats/min; respiratory rate, 30/min; and oxygen saturation, 96% on 9 L/min of oxygen mask with reservoir bags. She had clear consciousness. She had coarse crackles bilaterally.
Laboratory findings were as follows: white blood cell count 30,510/μl (neutrophils 99.5%), haemoglobin 10.1 g/dl, platelet count 5.0 × 104/μl, lactate dehydrogenase 341 U/L, urea nitrogen 30 mg/dl, creatinine 1.21 mg/dl and C-reactive protein 41.06 mg/dl. Blood gas analysis showed the following: pH 7.397, pCO2 34.4 torr, pO2 46.5 torr and HCO3
− 21.8 mEq/L (with room air).
Her chest x-ray showed consolidation in the upper and middle lung fields bilaterally (Figure ). Computed tomography (CT) of the chest showed consolidation of the right upper, middle and lower lobes and the left upper, and atelectasis of the left lower lobe (Figure ). Sputum Gram stain showed very few epithelial cells and some neutrophils, but not satisfactory to estimate causative bacteria. Both the BinaxNOW™ pneumococcal and Legionella urinary antigen test (Abott) were negative.
We suspected severe pneumonia and started with intravenous levofloxacin (500 mg q24h) and meropenem (500 mg q6h) empirically. Given her history of RA and SLE, and immunosuppressive state, we thought that viral/fungal infections, alveolar haemorrhage and interstitial pneumonia were important differential diagnoses. Thus, she underwent BAL by bronchoscopy under intubation. The colour of BALF was also orange (Figure ) and the cellular pattern was neutrophil predominant (90.0%) suggestive of bacterial infection. But, Gram stain of the BALF results was negative. Cytology of BALF revealed numerous neutrophils and a few macrophages which were not hemosiderin-laden. Because it has been clinically suggested that the colour of sputum obtained from patients with pneumonia caused by L. pneumophila is orange, we suspected non-pneumophila Legionella species pneumonia. We switched meropenem to azithromycin (500 mg q24h) and increased levofloxacin to maximum dose (750 mg q24h) targeting Legionella species pneumonia. Acid-fast bacillus cultures of sputum resulted negative. Two sets of blood cultures were negative. Polymerase chain reactions (PCR) for Pneumocystis, cytomegalovirus and SARS-CoV-2 were all negative. On the fifth day, mass spectrometry analysis of colonies obtained by culturing in BCYEα medium from BALF identified the presence of Legionella longbeachae.
On the sixth day, her respiratory condition deteriorated and contrast-enhanced CT showed exacerbation of ground-glass opacity (GGO) without pulmonary thromboembolism. We suspected organizing pneumonia secondary to L. longbeachae and started high-dose pulse intravenous steroid treatment with 1 g methylprednisolone for 3 days followed by prednisolone 1 mg/kg (60 mg/day) alongside levofloxacin that was administered 21 days in total. The following days she recovered gradually and she was extubated on Day 12. Eventually, consolidation and GGO improved on her chest CT of Day 23 and she was discharged home without oxygen on Day 34.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.1, 'degrees celsius'], 'Heart Rate or Pulse': [111.0, 'beats per minute'], 'respiratory rate': [30.0, 'breaths per minute'], 'White blood cell count': [30510.0, 'µL'], 'PaCO2': [34.4, 'mm hg']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.1 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 111.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 30510.0 count/µL. To convert 30510.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 30510.0 white blood cell count/µL * 1.0 µL/mm^3 = 30510.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 30.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is 34.4 mm Hg, which is greater or equal to than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6715,51,SIRS Criteria,diagnosis,integer,pmc-1112595-3,Extracted,"In July of 2002, a 36-year old obese woman [weight 200 pounds, height 5 feet 1 inch] with history of type 2 diabetes for 5 years, presented to the emergency department with 5 days history of fever, chills and cough with yellowish phlegm and sharp pain in her right lower chest that aggravated with deep breathing. Physical examination was unremarkable. She was afebrile and lungs were clear. Homen's sign was negative. Initial laboratory data showed slightly elevated d-dimer of 0.374 ug/mL [normal <0.25 ug/mL]. A chest X-ray (figure ) showed right lower lobe infiltrate. She was diagnosed with community acquired pneumonia and sent home on oral clarithromycin 500 mg BID, cefurox 500 mg BID for 7 days and acetaminophen as required.
She continued to have symptoms of fever, chills, night sweats with productive cough and dyspnea and presented to the hospital five days later. She denied hemoptysis. Physical examination revealed a temperature of 39 degree Celsius, mild tachycardia with heart rate of 104 beats per minute, normal blood pressure of 125/74 mmHg and respiratory rate of 18. Pulse oxymetry revealed oxygen saturation of 96% on room air. There was decreased air entry with bronchial breath sounds in right lower chest. A white cell count was slightly elevated at 13.5, with normal hemoglobin of 128 g/L and d-dimer between 0.25–0.50 ug/mL. A second chest X-ray (figure ) showed dense infiltrate in right lower lobe. She was admitted with the diagnosis of community-acquired pneumonia and started on intravenous levofloxacin 500 mg a day.
She had a positive Mantoux test in 1976. There was no history of travel save for visiting her sister's cottage at the local lake a weak before where she slept at the gazebo for two nights. There were no pets at home. She smoked one pack per day and entertained social drinks.
She continued to have temperature up to 39 degrees Celsius, productive cough and shortness of breath. Sputum Gram stain showed 4+ neutrophils and 1+ normal flora and blood cultures remained negative. She received intravenous levofloxacin and clindamycin for one week. Bronchoscopy performed on day 6 was unremarkable save for inflammatory changes in lower lungs and samples were collected for bacterial and tuberculosis cultures [in retrospect, the specimen was not sent for fungal cultures]. On 7th day because of ongoing symptoms, the antibiotics were changed to intravenous imipenem-cilastatin sodium 1 gm every 12 hour and she has had a CT scan of chest (figure ) that showed bibasilar consolidation with sparing of the apices. The white cell count fluctuated between 13.6 to 20.2 [normal 4.0–11.0 × 109 /L]. Hemoglobin decreased to 97 g/L. BUN, serum creatinine, electrolytes, AST, ALT, GGT and ALP were normal. Urinalysis was negative. Blood, urine and sputum cultures remained negative. Sputum gram stain showed 3-4+ neutrophils without organisms. ESR on day 8 was elevated at 112 mm/hr [normal 0–15]. Antinuclear antibody was negative. Arterial blood gas on day 8 showed pH of 7.46, pCO2 of 35, pO2 of 59 and oxygen saturation of 91% on room air. She was started on supplemental oxygen by nasal prongs. Bronchoscopic specimen cultures were negative save for pending TB cultures.
After five days of intravenous imipenem-cilastatin sodium therapy, there was no improvement in her clinical condition. Another medical consult was requested, when the author got involved in her care. She had a temperature of 39 C, pulse rate of 104 and blood pressure of 114/70 mmHg. There was no lymphadenopathy and heart sounds were normal. Her chest examination showed decreased breath sounds at both bases with egophony in right lower chest. There were no pleural rubs. There was no clubbing or cyanosis. The rest of the examination was unremarkable save for an obese benign abdomen.
Chest X-ray (figure ) now showed further deterioration of the bilateral infiltrates with nodular appearance and the radiologist remarked, ""The lesions are suspicious of metastases."" Sputum cytology showed a large number of acute inflammatory cells without malignant cells. The possibility of vasculitis was entertained because of markedly elevated ESR and antineutrophilic cytoplasmic antibody (ANCA) was negative.
The history of sleeping at the cottage for two nights, a week before her illness started; progressive bilateral pneumonia with ongoing high-grade fever, chills, and night sweats despite sufficient antibiotic coverage and sputum Gram stain showing a large number of neutrophils without organisms (culture negative) raised the author's suspicion for the possibility of fungal process such as acute blastomycosis pneumonia and the Public Health Laboratory (PHL) was specifically asked to perform wet preparation for blastomycosis on the sputum. The PHL laboratory confirmed the presence of 'round thick walled budding yeast like cells (figure ) suggestive of Blastomyces dermatitidis and this was confirmed on fungal cultures. She was promptly started on intravenous amphotericin B and responded well and later switched to oral itraconazole 400 mg twice a day for 6 months and then 200 mg a day for another 6 months. She recovered fully.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.0, 'degrees celsius'], 'Heart Rate or Pulse': [104.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [13500.0, 'µL'], 'PaCO2': [35.0, 'mm hg']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.0 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 104.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 13500.0 count/µL. To convert 13500.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 13500.0 white blood cell count/µL * 1.0 µL/mm^3 = 13500.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 35.0 mm Hg, which is greater or equal to than 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6716,51,SIRS Criteria,diagnosis,integer,pmc-3480933-1,Extracted,"A 25-year-old HIV-negative female presented to the emergency department with constant sharp left lower quadrant pain for 1 day accompanied by nausea and three episodes of vomiting. Her last menstrual period was 3 weeks prior to presentation. Although the patient had received treatment for PID 2 weeks prior to this visit, her male sexual partner had not been treated for any sexually transmitted infections. She denied diarrhea, fever, urinary symptoms, vaginal bleeding, or discharge. At triage, her temperature was 101.0°F, blood pressure was 100/60 mmHg, heart rate was 110 beats/min, respiratory rate was 20/min, and oxygen saturation was 96% on room air. The patient had no surgical history, and sexual history was significant for multiple male partners without consistent use of barrier protection.
On physical examination, the lungs were clear, the heart sounds were fast and regular, and the abdomen was soft with left lower quadrant tenderness without rebound or guarding. Pelvic examination was difficult to interpret as the patient was in a significant degree of discomfort. On speculum examination, there was no blood in the vaginal vault, and there was a small amount of clear discharge from the cervical os. On bimanual examination, the patient had tenderness of the cervical area, the uterus, and the bilateral adnexae, left greater than right. It was unclear if distinct CMT was present as the patient was uncomfortable with the entire bimanual examination. A point-of-care test of the urine was negative for pregnancy and infection.
A BUS was performed. The patient tolerated the probe insertion but had a significant amount of pain when the probe abutted the cervix (Figure ). With pressure applied to the probe to directly visualize the cervix, the patient felt a focal exacerbation of her pain, which the EP recognized, clarified, and confirmed as CMT. A coronal view of the left adnexal region demonstrated a complex heterogeneous collection thought to represent an abscess (Figure ).
The gynecology service was consulted, and an ultrasound in the department of radiology was obtained to further evaluate the adnexae and document blood flow to the ovaries. The left adnexa was found to be an enlarged tubo-ovarian complex. It was estimated to measure 8 cm in diameter with multiple irregular tubo-ovarian abscesses. The ovaries demonstrated bilateral blood flow. There was a small amount of free fluid in the posterior cul-de-sac.
Laboratory studies showed a WBC count of 15.0. The patient was started on intravenous antibiotics and admitted to the gynecology service. Microbiology result of the cervical culture was positive for N. gonorrhea.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [101.0, 'degrees fahrenheit'], 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [15.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 101.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 69.0 = 38.33333 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 110.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 15.0 count/µL. To convert 15.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 15.0 white blood cell count/µL * 1.0 µL/mm^3 = 15.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6717,51,SIRS Criteria,diagnosis,integer,pmc-3420607-1,Extracted,"A 61-year-old male with history of Alzheimer's dementia, diagnosed at the age of 50, was admitted for worsening mental status and paranoid behavior. He was started on olanzapine a few weeks prior to this admission. He was found to be lethargic, drowsy, lying down in the bed motionless. His home medications included donepezil, alprazolam, and trazodone in addition to recently started olanzapine. On physical examination he had a fever of 102.1°F, heart rate—122 beats/minute, blood pressure—106/77 mm of Hg, and respiratory rate—22 breaths/minute with 100% oxygen saturation on room air. He was drowsy lying down in bed, only opening eye to repeated verbal commands. He had opisthotonus, with diffuse rigidity; reflexes were not well elicitable in view of diffuse rigidity. The rest of system examination was noncontributory.
Laboratory data showed hemoglobin level of 12.5 mg/dL (reference range—13.5–17.5 g/dL), WBC—12.5 × 103/μL (reference range—4.5–10.8 × 103/μL), platelet—253 × 109/L (reference range—150–450 K/μL), and creatinine kinase (CK)—6400 units/L (reference range—38–174 units/L). Blood cultures were negative; CT scan of head, abdomen, and thorax was normal; Cerebrospinal fluid analysis was normal and the urine drug screen was negative. In view of rigidity, fever and increased CK along with the history of recently added olanzapine, a diagnosis of neuroleptic malignant syndrome (NMS) was made. He was managed in the intensive care unit and in addition to hydration was treated with intravenous dantrolene (which was later changed to oral bromocriptine). Throughout his stay in the hospital he was not physically restrained and was kept on deep venous thrombosis (DVT) prophylaxis with enoxaparin. On the fourth day of admission, the patient developed swelling of arms, neck, and right lower limb. Doppler studies revealed venous thrombosis involving the right axillary, right subclavian, right internal jugular vein, left axillary vein, and right common femoral vein. The patient was thus treated with intravenous heparin (with warfarin bridging). The standard workup for new onset DVT was negative. He had normal levels of Antithrombin III, Protein C, and Protein S. In addition he was negative for Factor V Leiden, ANA, and Lupus Anticoagulant.
Considering the temporal sequence of events and no previous history of DVT, either NMS or olanzapine or a combination of both could be implicated as the possible etiology for the extensive venous thrombosis. At time of discharge he was back to his baseline functional state. He was discharged on warfarin for a period of six months.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [102.1, 'degrees fahrenheit'], 'Heart Rate or Pulse': [122.0, 'beats per minute'], 'respiratory rate': [22.0, 'breaths per minute'], 'White blood cell count': [12500.0, 'µL']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 102.1 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 70.1 = 38.94444 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 122.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 12500.0 count/µL. To convert 12500.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 12500.0 white blood cell count/µL * 1.0 µL/mm^3 = 12500.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6718,51,SIRS Criteria,diagnosis,integer,pmc-8168998-1,Extracted,"A 39-year-old male with a five-year history of moderate ulcerative colitis (UC), as per Montreal classification, was admitted to the emergency department with worsening abdominal and rectal pain secondary to a C. diff infection of one week. Patient had a multi-week history of diarrhea that was waking him up at night leading up to the C. diff diagnosis. One week prior to ED admission, his GI had ordered precautionary leukocytes and C. diff due to history of UC, and both returned positive. Per GI note, ""Vancomycin prescribed as this patient has IBD and patients with IBD can develop spontaneous C. diff infections and need to be treated regardless of toxin presence."" He had no prior history of antibiotic use over the past three months or triggering factor for C. diff infection.
Over the course of the week, his symptoms progressed, and he claimed to have nausea, vomiting, and hematochezia.
The patient presented with a past medical history of depression, post-traumatic stress disorder, and obstructive sleep apnea. His allergies included trazodone and amoxicillin/clavulanate. His family history was unrevealing. His surgical history included cholecystectomy and thyroglossal duct cyst removal in 2019.
This patient was a nonsmoker. He denied alcohol or drug use. He tried to maintain a healthy diet of lean proteins, fruits, and vegetables.
Initial vitals on presentation included: temperature: 98.6 F, pulse: 90 beats per minute, respiratory rate: 15 breaths per minute, pulse oximetry: 95%, blood pressure: 119/87 mmHg, weight: 217.16 lbs, and body mass index: 32.14.
General surgery was consulted upon CT scan with IV contrast revealing new extraluminal gas in the perineum surrounding the anus and distal rectum (Figures , , , ). He was examined and subsequently diagnosed with rectal perforation.
Preoperatively, the patient’s physical exam revealed an uncomfortable looking young man in mild distress due to abdominal pain. An abdominal exam revealed no distention, masses, rebound, or guarding. The absence of McBurney’s sign, Murphy’s sign, and peritoneal inflammation was noted. There was no active rectal bleeding at the time of physical examination. Laboratory data revealed an elevated c-reactive protein of 66.4. Complete blood count and complete metabolic panel were otherwise within normal limits. Despite infection and imaging reflecting perforation, white blood count was found to be 5.9 k/cmm.
After review of the available data, assessment of clinical condition, and deliberation with the emergency department physicians and the patient’s primary gastroenterology physician, the surgery team decided the patient would require an urgent exploratory laparotomy with total abdominal colectomy and end ileostomy due to the diagnosis of rectal perforation secondary to C. diff colitis on chronic UC.
The patient was immediately brought to the operating room. The primary incision was made from the subxiphoid to the pubic symphysis within two hours of initial presentation to the hospital. The colon was visualized and resected; thus, a total colectomy was undergone. The pre-rectal space was opened to identify signs of purulence or injury, which found crepitus and severe UC causing circumferential ulcerations and a deep ulcer in the midline anteriorly. These ulcers traversed all layers of the rectal wall. A drain was placed to drain potential abscess or infection from the pre-rectal space.
The patient left the OR in stable condition after enduring no complications intraoperatively. He remained in the inpatient surgical unit for five days, during which he continued to advance his diet and ambulate successfully. He was discharged after an education session on ostomy bag maintenance and told to follow up with the general surgery team and gastroenterology team in one week. At his one-week follow-up post-op visit, the patient was doing well, ostomy output was draining appropriately, and he denied fever, nausea, or vomiting. No secondary follow-up surgery was required.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [98.6, 'degrees fahrenheit'], 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'respiratory rate': [15.0, 'breaths per minute'], 'White blood cell count': [5900.0, 'µL']}",0,0,0,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 98.6 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 66.6 = 37.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 90.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 5900.0 count/µL. To convert 5900.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 5900.0 white blood cell count/µL * 1.0 µL/mm^3 = 5900.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 0.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 15.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 0.
Hence, the the number of SIRS criteria met by the patient is 0."
6719,51,SIRS Criteria,diagnosis,integer,pmc-5309395-1,Extracted,"A 66-year-old African American female without significant personal or family medical history and who has not been followed by any physician for years came in to the emergency department due to acute onset altered mental status changes. As per patient's daughter, she was in good health until the night prior to admission after a two-mile walk. In the morning she was noticed to be drowsy and confused “trying to drink her hair as if it were a glass of water”. She could not identify her daughter and she was complaining of generalized weakness as well as right groin pain. As the morning went by she was progressively getting worse becoming somnolent and stopped responding to verbal commands. She was brought to the emergency room where she was found to be febrile (as high as 106 degrees Fahrenheit), tachycardic (145 beats per minute), and tachypneic (25 breaths per minute) with a normal blood pressure. She was only responsive to painful stimuli with no meningeal signs. No palpable organomegaly or cervical, supraclavicular, axillary, or inguinal lymphadenopathy was found.
Complete blood cell count showed normocytic anemia (Hb 6.6 g/dL; MCV 91), thrombocytopenia (platelet count 77,000), and slight leukocytosis with neutrophilia (WBC 13,400. ANC 11,800). Further testing revealed an elevated LDH 1248 U/L (125–220 U/L), reticulocyte count 3.5% (1-2%), mild indirect hyperbilirubinemia (total bilirubin 1.4 mg/dL and direct bilirubin 0.3 mg/dL), and mildly elevated creatinine (1.2 mg/dL). Vitamin B12 level, folate level, prothrombin time, partial thromboplastin time, and INR were all normal as well as fibrinogen level (402 mg/dL). Serum iron was 6 mcg/dL (50–170 mcg/dL), total iron binding capacity was 257 mcg/dL (179–378 mcg/dL), and ferritin was 378 ng/mL (10–204 ng/mL). Urinalysis showed microscopic hematuria and proteinuria (30 mg/dL). Antibodies to human immunodeficiency virus were negative. Peripheral smear showed marked schistocytosis () and dysplastic neutrophils (Figures and ).
Chest X-ray and computed tomography (CT) of the head were unremarkable. Because of the compelling evidence of microangiopathic hemolytic anemia (MAHA) associated with thrombocytopenia, alter mental status, fever, and renal involvement thrombotic thrombocytopenic purpura (TTP) was strongly considered. ADAMTS-13 was sent and she was started on daily plasmapheresis and steroids. Platelet count dropped even further in the next couple of days (nadir 9,000) and there was no improvement in the MAHA (including the persistent marked schistocytosis) . ESR was 5 (normal range: 0–20 MM/HR). Three days after the beginning of plasmapheresis the test results for haptoglobin as well as for ADAMTS-13 activity came back and they were 120 (14–250 mg/dL) and 52% (normal: 68–163%), respectively. Plasmapheresis was stopped. Urine culture and blood cultures were negative for infection. CT chest, abdomen, and pelvis with contrast as well as CT angiogram of the lower extremities were unremarkable. Flow cytometry showed no evidence of B-cell lymphoma, T-cell lymphoma, acute leukemia, or increase in blasts.
She underwent to bone marrow aspiration and biopsy which showed markedly hypercellular marrow, hyperplastic and dysplastic megakaryocytic, and dyspoietic erythroid elements with occasional binucleate forms and irregular contour, and myeloid elements showed slight left shift. There was mild increase in reticulin fiber content making a myelophthisic process as the underlying cause of schistocytosis unlikely (Figures –). There was no evidence of plasma cell disorder. Iron stain on biopsy showed mild increase in stainable iron (3+) and no ring sideroblasts. There was no increase in blasts.
Karyotype analysis in twenty metaphases was performed and revealed a complex karyotype in eight metaphases (Figures and ). Twelve metaphases were chromosomally normal. Due to all these findings the final diagnosis was MDS with multilineage dysplasia [] and she was referred for a clinical trial.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [106.0, 'degrees fahrenheit'], 'Heart Rate or Pulse': [145.0, 'beats per minute'], 'respiratory rate': [25.0, 'breaths per minute'], 'White blood cell count': [13400.0, 'µL']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 106.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 74.0 = 41.11111 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 145.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 13400.0 count/µL. To convert 13400.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 13400.0 white blood cell count/µL * 1.0 µL/mm^3 = 13400.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 25.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6720,51,SIRS Criteria,diagnosis,integer,pmc-8005271-1,Extracted,"A 19-year-old female (primigravida and nulliparous) with no known past medical history was admitted to the hospital at 40 weeks 5 days of gestational age for induction of labor and delivery. The patient had regular prenatal visits and all laboratory workup and fetal ultra-sonogram were done according to the gestational age and were unremarkable. Labor was induced with oxytocin and cervical misoprostol. The patient had a temperature of 102.2oF one hour before the delivery and was given one dose of acetaminophen 650 mg which helped in controlling the fever. She had stable vital signs otherwise. The patient had a normal vaginal delivery. Amniotic fluid was meconium stained. The infant had an APGAR score of 1 at one minute and a score of 6 after five minutes. After about half an hour of delivery, the patient became dyspneic with a respiratory rate of 30 breaths/minute, blood pressure of 82/52 mmHg, heart rate of 150 beats/minute, and oxygen saturation of 37% on room air. A rapid response was initiated (also known as urgent response team) and the patient was transferred to the ICU. A chest X-ray showed bilateral infiltrates (Figure ).
She was tried and failed the bilevel noninvasive ventilation for around 10 minutes and was immediately intubated and placed on the mechanical ventilation. She was sedated with fentanyl, propofol, and dexmedetomidine. Arterial blood gas (ABG) findings after intubation, pH was normalized to 7.39, pCO2 43.4, pO2 83.3, HCO3 25.9, vent rate 30/min, fiO2 100%, tidal volume 350 mL/breath, and PEEP 5 cm H2O. In view of persistent hypotension even after isotonic fluid bolus challenge, the patient had to be maintained on multiple vasopressor drips that included norepinephrine, phenylephrine, vasopressin, and epinephrine. Broad-spectrum empiric antibiotics coverage such as linezolid, cefepime, and metronidazole were also started. Complete blood count showed white blood cell (WBC) 24.5/uL (4.8-10.8), red blood cell (RBC) 2.21/uL (4.2-5.4), hemoglobin (Hgb) 7 g/dL (12-16), hematocrit 20.9% (37-47), and platelet 76/uL (150-450). Basic metabolic panel (BMP) showed sodium 139 mmol/L (133-145), potassium 3.1 mmol/L (3.6-5.2), chloride 104 mmol/L (100-108), CO2 mmol/L14 (22-32), blood urea nitrogen (BUN) 12 mg/dL (16-20), creatinine 1.86 mg/dL (0.6-1), lactic acid 15.6 mmol/L (0.5-2.2), calcium 7.5 (8.7-10.5); liver function tests revealed total bilirubin 2.9 mg/dL (0-1.0), aspartate aminotransferase (AST) 69 units/L (15-37), alanine aminotransferase (ALT) 9 units/L (30-65), and alkaline phosphate 834 units/L (50-130). Coagulation studies showed elevated prothrombin time (PT) 19.5 seconds (reference range 9.6-12.3), activated partial thromboplastin time (aPTT) 36.2 seconds (22.5-35.3), fibrinogen 144 mg/dL (200-400), INR 1.71, D-dimer > 7650 ng/mL FEU (<500). Initial disseminated intravascular coagulation (DIC) score was 7. The patient received three units of packed red blood cells (PRBC), two units fresh frozen plasma (FFP), two units cryoprecipitate, and two units platelets.
Initial troponin was 2.11 ng/mL which later increased to 5.96 ng/mL. CT angiogram chest showed small embolus in the right upper lobe and findings were concerning for AFE (Figures -).
The patient had an urgent bedside transthoracic echocardiogram (TTE) that showed ejection fraction (EF) > 70%, no regional wall motion abnormalities, normal diastolic function parameters, right ventricle dilation, reduced systolic function, systolic pressure severely increased in pulmonary arteries, estimated to be 65 mmHg. The TAPSE was not calculated. Given the patient’s critical condition, it was planned to send the patient to a higher center for ECMO support. The patient was placed on vena-arterial (VA) ECMO via a bi-femoral approach. The patient sustained a brief episode of pulseless electrical activity (PEA) cardiac arrest requiring one dose of epinephrine and 2 minutes of high-quality chest compression with the return of spontaneous circulation (ROSC). Postcannulation of VA ECMO, the patient required additional six units PRBC, one unit of platelet along with supplementation of calcium gluconate and sodium bicarbonate. The patient was on low-dose epinephrine that was eventually weaned off within day 2 of delivery. The patient was extubated on the second day. Hematology was consulted for coagulopathy with disseminated intravascular coagulation (DIC) that was deemed secondary to shock liver. As low antithrombin III levels may have decreased the effectiveness of heparin, she was given low dose bivalirudin bolus for ECMO continuation. Later the patient was transitioned to warfarin with enoxaparin bridging on discharge.
The patient was also noted to have anuric acute renal failure and elevated lactate with a high anion gap metabolic acidosis and hypernatremia. Nephrology initiated continuous renal replacement therapy (CRRT) which was discontinued before discharge with normalization of renal functions. The patient was weaned off ECMO on day 4. The patient's condition progressively stabilized and was discharged from the hospital on day 8.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [102.2, 'degrees fahrenheit'], 'Heart Rate or Pulse': [150.0, 'beats per minute'], 'respiratory rate': [30.0, 'breaths per minute'], 'White blood cell count': [24.5, 'µL'], 'PaCO2': [43.4, 'mm hg']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 102.2 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 70.2 = 39.0 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 150.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 24.5 count/µL. To convert 24.5 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 24.5 white blood cell count/µL * 1.0 µL/mm^3 = 24.5 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 30.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is 43.4 mm Hg, which is greater or equal to than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6721,51,SIRS Criteria,diagnosis,integer,pmc-6215582-1,Extracted,"A 26-year-old male patient with no remarkable medical and social history presented with a five-day history of a cough and fever. Before coming to our hospital, he went to a clinic and received amoxicillin, which resulted in no improvement of his symptoms. He visited another hospital three days before presenting to us and was hospitalized with a diagnosis of bacterial pneumonia. Although he received tazobactam/piperacillin, his clinical symptoms showed deterioration. Two days later, he was admitted to our hospital.
His vital signs were as follows: temperature, 38.1°C, heart rate of 112 beats/min, blood pressure of 98/60 mmHg, respiratory rate of 24 breaths/min, and saturation of peripheral oxygen of 94% with a reservoir mask of 6 L/min. On physical examination, weak respiratory sounds and coarse crackles were heard in the lower left chest.
His initial white blood cell count was 6,800/μL, hemoglobin was 14.0g/dL, platelet count was 133,000/μL, and C-reactive protein level was 34.30 mg/dL (). Arterial blood gas (reservoir mask of 6 L/min) showed that the pH was 7.44, PCO2 was 41.1 mmHg, PO2 was 69.2 mmHg, HCO3− was 27.2 mmol/l, and BE was 2.8 mmol/L. Among the viral and bacterial rapid tests performed, only the Mycoplasma antigen tested positive.
Chest radiography indicated an infiltrating shadow in left middle lung field and right lower lung field. A chest CT indicated lobar pneumonia in the lower left lobe and an infiltrating shadow in the left whole lung lobe and the lower right lobe (). Based on these findings, the patient was diagnosed with severe mycoplasma pneumonia.
Azithromycin 500 mg/day and prednisolone 30 mg/day were initiated. After admission, his respiratory condition worsened until a reservoir mask 15 L/min was required. We then changed the reservoir mask to a nasal high-flow oxygen (40 L/min, FiO2:0.8) and increased the prednisolone to 60 mg/day. In case of macrolide resistance, we additionally administrated minocycline 200 mg/day. On hospital day 4, the patient's respiratory status and inflammatory markers on laboratory findings improved. On hospital day 20, he was discharged.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.1, 'degrees celsius'], 'Heart Rate or Pulse': [112.0, 'beats per minute'], 'respiratory rate': [24.0, 'breaths per minute'], 'White blood cell count': [6800.0, 'µL'], 'PaCO2': [41.1, 'mm hg']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.1 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 112.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 6800.0 count/µL. To convert 6800.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 6800.0 white blood cell count/µL * 1.0 µL/mm^3 = 6800.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 24.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is 41.1 mm Hg, which is greater or equal to than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6722,51,SIRS Criteria,diagnosis,integer,usmle-7643,Extracted,"A 60-year-old man presents to his physician as part of his routine annual medical check-up. He has no specific complaints but mentions that he has often experienced fatigue over the past few months. His past medical history is noncontributory. On physical examination, his temperature is 37.2°C (98.8°F), pulse rate is 84/min, blood pressure is 130/86 mm Hg, and respiratory rate is 18/min. On general examination, mild pallor is present. Palpation of the abdomen reveals splenomegaly, which extends 6.35 cm (2.5 in) below the left costal margin. There is no hepatomegaly. Laboratory studies show the following values:
Hemoglobin 9.7 g/dL
Total leukocyte count 30,000/mm3
Granulocytes 83%
Lymphocytes 10%
Eosinophils 5%
Basophils 1%
Monocytes 1%
Platelet count 700,000/mm3
The physician orders a bone marrow biopsy analysis of hematopoietic cells. The report shows the presence of a t(9;22)(q34; q11) translocation.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.2, 'degrees celsius'], 'Heart Rate or Pulse': [84.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [30000.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.2 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 84.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 30000.0 count/m^3. To convert 30000.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 30000.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 3e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6723,51,SIRS Criteria,diagnosis,integer,usmle-6498,Extracted,"A 20-year-old male military recruit comes to the office with complaints of a fever and a non-productive cough that started 5 days ago. He also states having pain during swallowing. He has a mild headache and pain in his left ear. He does not have any relevant past medical history. His vitals include the following: blood pressure of 120/78 mm Hg, pulse of 100/min, temperature 37.8°C (100°F), respiratory rate 14/min. Physical exam reveals a congested left tympanic membrane and rhonchi on auscultation of the right lung base. The blood test results are given below:
Hemoglobin: 15 mg/dL
Hematocrit: 50%
Leukocyte count: 7,500/mm3
Neutrophils: 67%
Bands: 5%
Eosinophils: 1%
Basophils: 0%
Lymphocytes: 28%
Monocytes: 5%
Platelet count: 265,000/mm3
Low titers of cold agglutinins are detected. His chest radiograph shows poorly defined nodular opacities in the right lower lung zone.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.8, 'degrees celsius'], 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'respiratory rate': [14.0, 'breaths per minute'], 'White blood cell count': [7500.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.8 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 100.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 7500.0 count/m^3. To convert 7500.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 7500.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 7.5e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 14.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6724,51,SIRS Criteria,diagnosis,integer,pmc-8629823-1,Extracted,"A 73-year-old man admitted to Erfan hospital, Tehran, Iran, with fever, generalized weakness and dyspnea. He had history of cholecystectomy duoe to cholecystitis 56 days ago. Following surgery, he gradually developed shortness of breath but he did not seek care. Continued dyspnea and addition of fever, took him to the emergency room. He had history of hypertension and no history of addiction or diabetes mellitus. At presentation, temperature was 38°C, respiratory rate 18 breaths per minute, heart rate 84 beat per minute, blood pressure 130/70 mmHg and oxygen saturation 94%. Heart auscultation indicated early systolic and diastolic murmur. Laboratory test showed a total leukocyte count of 8700 with 90% polymorphs and anemia (Hb 7/5 gr/dl). His erythrocyte sedimentation rate was 19 mm/h and his serum level of C-reactive protein was 29 mg/dl. Blood urea, serum creatinin, sodium and potassium were in normal ranges. His chest CT scan demonstrated mild plural effusion in both lungs. In transthoracic echocardiography he had moderate MR and moderate TR with a mobile calcified mass on aorta valve. Transesophageal echocardiography indicated Mitral valve thickening with severe regurgitation and perforation of anterior leaflet; Aortic valve thickening with severe insufficiency and perforation of non-coronary cusp (NCC); mobile mass measuring about 6×7 mm on NCC and mild pericardial effusion posterior to right atrium (). Three sample of blood culture by hourly intervals was negative. After 2 weeks of treatment with vancomycin, ampicillin/sulbactam and gentamicin, there was no improvement in the patient. So, he underwent surgical excision and valves replacement that revealed vegetation on aorta and mitral valves. Pathologic specimen showed severe neutrophilic infiltration with areas of necrosis, granulation tissue, fibrous deposition and bacterial colonization (). Tissue sample was also placed in sterile screw-cap container and drops of sterile saline were added to keep it moist. It was transported to the microbiological laboratory in 15 minutes. The sample was cultured on MacConkey agar and chocolate blood agar and after 48 hours Gram-stained smear showed Gram-negative pleomorphic coccobacilli which grew as non lactose fermenting colonies. The organism was oxidase negative, catalase positive and non mobile. The isolate was identified as Acinetobacter baumannii complex based on glucose oxidation and Triple Suger Iron (TSI) test. Antimicrobial susceptibility testing was performed using the Kirby-Bauer disc diffusion method as per clinical and laboratory standard institute recommendation and based on that, the organism was XDR and was only sensitive to colistin. According to the antibiotic susceptibility pattern, medical treatment of the patient changed to intra-venous colistin and tigecycline. Finally, he discharged 42 days after operation and antibiotic therapy with no important complication and no vegetation on fallow up echocardiography.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.0, 'degrees celsius'], 'Heart Rate or Pulse': [84.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [8700.0, 'µL']}",0,0,0,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 84.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 8700.0 count/µL. To convert 8700.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 8700.0 white blood cell count/µL * 1.0 µL/mm^3 = 8700.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 0.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 0.
Hence, the the number of SIRS criteria met by the patient is 0."
6725,51,SIRS Criteria,diagnosis,integer,pmc-6341628-1,Extracted,"An 85-year-old Japanese man was admitted to our hospital with a two-day history of fever and worsening malaise. He denied respiratory tract symptoms. The patient had a medical history of diabetes mellitus (hemoglobin A1c level, 7.0%), but no past medical history of pulmonary disease. On admission, his vital signs were recorded as follows: heart rate, 90 beats/min; blood pressure, 123/77 mmHg; room-air oxygen saturation, 94%; respiratory rate, 19 breaths/min; and body temperature, 38.2 °C. Based on the laboratory test results, the patient was diagnosed with leukocytosis (12,000 cells/μL) and showed elevated levels of C-reactive protein (18.8 mg/dL); however, his liver and renal functions were normal. A chest radiograph showed multiple small pulmonary infiltrates in both lungs. Additional chest computed tomography (CT) scan revealed multiple bilateral pulmonary nodules mainly in subpleural areas (Fig. , left panel), suggesting the diagnosis of SPE.
While searching for the primary source of infection, transthoracic echocardiography was performed multiple times (on the day of admission and 5 days after admission), and showed the absence of vegetation on the heart valves. Additionally, contrast-enhanced CT scan of the neck, chest, abdomen, and pelvis revealed neither an abscess nor suppurative thrombosis on the day of admission. After collection of the blood sample, empiric treatment with meropenem (1 g every 8 h) and vancomycin (1 g every 12 h) was initiated. On the 3rd day of hospital stay, the blood culture with a BacT/ALERT 3D system (BioMérieux, France) was found to be positive for P. micra, identified by RapID-ANA II system (Innovative Diagnostic Systems, Inc., Atlanta, Ga), a qualitative micromethod employing conventional and chromogenic substrates for the identification of anaerobic bacteria. The isolate was highly susceptible to all β-lactams, clindamycin, and carbapenems. Repeated physical assessment to detect the source of infection revealed mild tenderness on the left temple. Oral examination by a dentist showed periapical periodontitis at the root of the second left maxillary premolar. Further, contrast-enhanced facial CT scan identified an abscess in the infratemporal fossa (Fig. a), and thus puncture drainage of pus was performed on the 9th day of hospital stay (Fig. b). Following a review of susceptibility test results, we changed the antibiotics to ampicillin-sulbactam (3 g every 8 h), targeting P. micra and all possible anaerobic bacteria. Although Gram stain of the sample taken from the infratemporal fossa abscess showed positive staining for polymicrobial patterns of Gram-positive cocci and Gram-negative rod strains, only Prevotella oris (not P. micra) was isolated from culture of the abscess. The isolation same method was used for Prevotella oris and P. micra. Isolated Prevotella oris was susceptible to ampicillin-sulbactam, clindamycin, and carbapenems, but intermediately susceptible to penicillin and ampicillin. P. micra was not recovered from the infratemporal fossa abscess, probably due to the effect of ampicillin-sulbactam and difficulty in culturing anaerobic organisms.
Thus, we diagnosed this case as periodontal disease-associated SPE and infratemporal fossa abscess. Following combined treatment with ampicillin-sulbactam, tooth extraction, and puncture drainage of the infratemporal fossa abscess, the patient’s symptoms including fever and malaise gradually improved (Fig. ). Intravenous antibiotic therapy with ampicillin-sulbactam was administered for 4 weeks, followed by continued oral treatment with clindamycin for 4 weeks. We confirmed complete remission of the lung lesions by CT scan (Fig. , right panel), and there has been no recurrence of symptoms after discontinuation of antibiotics.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.2, 'degrees celsius'], 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'respiratory rate': [19.0, 'breaths per minute'], 'White blood cell count': [12000.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.2 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 90.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 12000.0 count/µL. To convert 12000.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 12000.0 white blood cell count/µL * 1.0 µL/mm^3 = 12000.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 19.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6726,51,SIRS Criteria,diagnosis,integer,pmc-5471576-1,Extracted,"A 33-year-old female presented to the emergency room complaining of painful lesions on her right upper extremity that began approximately two days prior to presentation. She also noted generalized malaise, chills, subjective fever, nausea, vomiting, abdominal pain, and dyspnea on exertion. She became short of breath with minimal activity. Past medical history was significant for hepatitis C, polysubstance abuse, and nicotine dependence. Approximately six months prior to current illness, she was hospitalized and treated for staphylococcal left knee septic arthritis.
Initial vital signs were BP 144/71 mmHg, pulse 107 beats/min, temperature 98.1°F (36.7°C), respiratory rate 20 breaths/min, and oxygen saturation 99% breathing ambient air. Physical examination demonstrated petechiae and ecchymosis on all four extremities along with several tender erythematous nodules. She also had jugular venous distention to the angle of the mandible. There were bibasilar rales on pulmonary examination and a 2/6 intensity holodiastolic murmur was present at the 2nd right interspace on cardiac examination. There was mild bilateral lower extremity pitting edema. The remainder of the physical exam was unremarkable. Laboratory data demonstrated serum sodium 131 mEq/L, potassium 3.0 mEq/L, chloride 97 mEq/L, bicarbonate 24 mEq/L, BUN 21 mg/dl, creatinine 1.01 mg/dl, and glucose of 110 mg/dL. Cardiac troponin was undetectable. White blood cell count was 9.3 k/μl, hemoglobin 14.3 g/dl, hematocrit 41.5%, and platelet count 99 k/μl. Blood cultures grew Methicillin Sensitive Staphylococcus aureus (MSSA). Electrocardiogram demonstrated accelerated junctional rhythm at 99 beats/minute with retrograde P waves ().
Transthoracic echocardiogram revealed normal LV chamber dimension, wall motion, and left ventricular ejection fraction estimated at 60–65%. The aortic valve was not clearly visualized but aortic regurgitation was noted with continuous wave and color flow Doppler. Transesophageal echocardiogram revealed severe aortic regurgitation; pressure half-time of the regurgitant jet was 320 ms. A large mobile mass measuring 1.3 cm by 1.0 cm was attached to the septal wall of the left ventricular outflow tract (LVOT) (Figures and ). The mass was attached at the site of a jet lesion where the aortic valve regurgitant jet contacted the LVOT wall ().
She was treated with intravenous antibiotics. Due to the size and location of the vegetation, she was referred for aortic valve replacement and resection of the LVOT vegetation. Pathologic analysis of the native aortic valve revealed a 0.6 × 0.4 cm ovoid perforation of the noncoronary leaflet likely due to prior endocarditis with acute vegetation on the septal surface of the LVOT under the right coronary leaflet. The patient did well postoperatively and was treated adequately with a six-week course of intravenous antibiotics.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [98.1, 'degrees fahrenheit'], 'Heart Rate or Pulse': [107.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [9300.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 98.1 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 66.1 = 36.72222 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 107.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 9300.0 count/µL. To convert 9300.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 9300.0 white blood cell count/µL * 1.0 µL/mm^3 = 9300.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6727,51,SIRS Criteria,diagnosis,integer,usmle-8454,Extracted,"A 65-year-old woman presents to a physician with painful ankles for 2 days. Her symptoms began 1 week ago with a severe fever (40℃ (104℉)) for 3 days. When the fever subsided, she developed a maculopapular rash over the trunk and extremities with painful wrists and fingers. She also reports abdominal pain, nausea, vomiting, and headaches. Last week she returned from a trip to Africa where she spent several weeks, mostly in rural areas. Her temperature is 37.5℃ (99.5℉); pulse is 75/min; respiratory rate is 13/min, and blood pressure is 115/70 mm Hg. A maculopapular rash is observed over the trunk and limbs. Both ankles are swollen and painful to active and passive motion. The abdomen is soft without organomegaly. Laboratory studies show the following:
Laboratory test
Hemoglobin 11.4 g/d
Mean corpuscular volume 90 µm3
Leukocyte count 4,500/mm3
Segmented neutrophils 70%
Lymphocytes 15%
Platelet count 250,000/mm3
Ring-form trophozoites are absent on the peripheral blood smear.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.5, 'degrees celsius'], 'Heart Rate or Pulse': [75.0, 'beats per minute'], 'respiratory rate': [13.0, 'breaths per minute'], 'White blood cell count': [4500.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.5 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 75.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 4500.0 count/m^3. To convert 4500.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 4500.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 4.5e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 13.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6728,51,SIRS Criteria,diagnosis,integer,pmc-7385607-1,Extracted,"A 58-year-old woman presented with lower abdominal pain from the deep pelvis and frequent failure of flatulence for 4 mo.
She was referred from a department of gynecology and diagnosed with a suspicious leiomyosarcoma of the rectum or a pedunculated myoma of the uterus after colonoscopy and abdominopelvic computed tomography (CT) in a previous hospital. She visited the outpatient clinic after 10 d and was transferred to the emergency center because of severe lower left abdominal pain on 2 d before her scheduled admission. She had nausea, vomiting, and non-whirling dizziness. She was diagnosed with colonic cancer perforation with an abscess and was admitted for antibiotic treatment. We ensured that the acute septic condition was stabilized, and the patient underwent operation.
She had no co-morbid disease.
On digital rectal examination, a circumferential fungating mass with a central ulceration was palpated 8 cm from the anal verge, and it was fixed in the pelvic cavity. In the emergency center, the patient’s body temperature was 38.9 °C. The systolic and diastolic blood pressures were 110 mmHg and 70 mmHg respectively, pulse rate was 78 beats per minute, and respiratory rate was 20 breaths per minute.
Laboratory results were as follows: White blood cell count (23900/µL; 93.9% of neutrophil), hemoglobin (11.6 g/dL), platelet count (416000/µL), C-reactive protein (16.14 mg/dL), lipase (9 IU/L), albumin (3.2 g/dL), alkaline phosphatase (265 IU/L), sodium (132 mEq/L), chloride (93 mEq/L), and prothrombin time percentage (73.2%).
Chest X-ray showed a nodule in the right upper lung field. Besides this, there was no active lesion in the lungs. Colonoscopy revealed a huge submucosal mass-like lesion with focal ulceration located 8 to 15 cm from the anal verge. Abdominopelvic CT showed a poorly marginated mass measuring 7.4 cm × 6.3 cm × 5.5 cm in size located between the rectum and uterus and separated from the uterus by fat tissues. The mass had focal non-enhancing lesions without lymph node enlargement. To rule out the origin of the mass, the patient underwent pelvic magnetic resonance imaging (MRI) before the operation. MRI revealed an exophytic growing mass with a maximum diameter of 7.2 cm at the right lateral wall of the rectum with an internal cystic portion and hemorrhage, multiple lymph node enlargement at the iliac bifurcations, obturator, and presacral areas, and a 2.2-cm-sized multiseptated cystic mass in the fundus of uterus (Figure ). Positron emission tomography-CT revealed a high possibility of a malignant tissue with a hypermetabolic mass (SUVmax = 15.1) and cystic changes in the rectum, and this lesion was considered to directly invade the adjacent uterus. Multifocal FDG uptake (SUVmax = 4.0) was observed in the left common iliac, perirectal area, and presacral area (Figure ).
The tumor was a polypoid mass measuring 10 cm × 4 cm × 4 cm in size, and it invaded left ovary and salpinx via the serosal membrane (Figure ). No lymph node metastasis, lymphovascular invasion, or perineural invasion was observed. Microscopically, the tumor was a cellular mass that had a solid growth pattern with few glandular structures and many foci of intratumoral necrosis. Tumor cells had elongated nuclei and scant cytoplasm. Mitotic figures, including atypical ones, were also frequently observed. At the boundary between the tumor and normal tissue, tumor cells were arranged in a palisading pattern, resembling basal cell carcinomas of the skin (Figure ). Immunohistochemical examinations revealed that the tumor cells were focally positive for cytokeratin (CK) 7, p63, and Pan-CK and were negative for CK20; neuroendocrine markers, such as synaptophysin and CD56; and mesenchymal cell markers, including CD34, CD117, desmin, S100 protein, and α-smooth muscle actin. Additionally, the tumor cells were negative for vimentin, WT-1, calretinin, CD99, TTF-1, and CDX2.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.9, 'degrees celsius'], 'Heart Rate or Pulse': [78.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [23900.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.9 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 78.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 23900.0 count/µL. To convert 23900.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 23900.0 white blood cell count/µL * 1.0 µL/mm^3 = 23900.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6729,51,SIRS Criteria,diagnosis,integer,pmc-3326989-1,Extracted,"In January 2010, a 22-year-old male presented with acute renal failure at another hospital, and was diagnosed with acute hepatitis A. He was treated conservatively at that hospital for one month, during which time the symptoms and laboratory findings improved. At that time he didn't receive any antibiotics. Three days prior to the end of treatment, he developed a sudden fever and liver enzyme levels began rising again. Oseltamivir was prescribed empirically due to the possibility of pandemic swine influenza. One day after the administration of oseltamivir, he developed a whole body skin rash with intense itching. Records from the previous hospital admission indicated a persistent fever accompanied by a skin rash, and an abdomino-pelvic CT showed gall bladder wall thickening. Consequently, cefotaxime and metronidazole antibiotics were prescribed due to the suspicion of acute cholecystitis just one day before his arrival at our hospital.
The patient was referred to our hospital on February 9th due to the cholestatic hepatitis A, fever and skin rash symptoms. The initial vital signs were as follows: blood pressure 112/72 mmHg, heart rate 113/min, respiratory rate 20/min, and body temperature 38.0℃. Laboratory findings showed a white blood cell count of 15,900/mm3, a hemoglobin level of 11.9 g/dL, a platelet count of 321,000/mm3, an eosinophil count of 2,150/mm3 (8% [upper limit of normal (ULN) 7%]), a serum protein level of 5.0 g/dL, a serum albumin level of 1.9 g/dL, a serum aspartate aminotransferase (AST) level of 152 IU/L (ULN 40 IU/L), a serum alanine aminotransferase (ALT) level of 187 IU/L (ULN 40 IU/L), a serum creatinine level of 1.3 mg/dL (ULN 1.4 mg/dL), a serum total bilirubin level of 25.8 mg/dL (ULN 1.2 mg/dL), a serum direct bilirubin level of 15 mg/dL (ULN 0.5 mg/dL), and a prothrombin time (PT) (%) level of 22.4% (normal, 70-140%). The patient tested negative for herpes virus, cytomegalovirus (CMV), hepatitis B and C, and positive for IgG antibodies against the Epstein Barr virus (EBV) and HAV. The patient also tested positive for anti-HAV IgM.
The patient was treated using conservative management for the hepatitis A with prolonged cholestasis, including the administration of cefotaxime for 4-5 days for the persistent fever and jaundice.
By the 4th day after admission to our hospital, the fever and skin rash symptoms worsened, prompting a skin biopsy (). The biopsy revealed perivascular lymphocytic and eosinophilic infiltration, consistent with drug eruption (). After the 8th day of admission, a liver biopsy was performed to identify a possible cause of the fever. That biopsy revealed an eosinophilic microabscess (). The peripheral blood eosinophil count was 32.4% (6,059/mm3), and laboratory findings showed a total bilirubin level of 23 mg/dL, an AST level of 110 IU/L, an ALT level of 142 IU/L and a serum creatinine level of 4.4 mg/dL.
Upon consideration of the overall findings, we made a diagnosis of DRESS syndrome and prolonged cholestatic hepatitis A with renal azotemia. Therefore, cefotaxime administration was immediately ceased, and high-dose steroid (hydrocortisone 80 mg tid daily) and immunoglobulin (1 g/kg/day for 2 days) were administered. After a week of high-dose steroid administration, the fever and skin rash improved, and prednisolone was then continued at a maintenance dose.
After 20 days of treatment, the fever recurred. A CMV antigenemia test returned positive findings (41/200,000 WBC), and a CMV PCR showed 1,097,500 copies/mL. The steroid dose was rapidly reduced and ganciclovir was administered (). The steroid was discontinued on March 28th, and ganciclovir was ceased on April 7th.
Approximately 10 days after steroid discontinuation, the serum ALT level rapidly rose to 1,200 IU/L. The patient developed another fever and the PT level decreased to 53.9%. We performed further blood cultures and PCR assays for the detection of HAV, CMV and EBV, yet these tests all returned negative findings. This led us to suspect recurrent DRESS syndrome. Therefore, we commenced steroid pulse therapy (methylprednisolone 1 mg/kg/day) on April 14th. The patient improved and the steroid dose was tapered gradually such that it was 20 mg daily in the form of oral prednisone by the time of discharge on April 28th. The prednisone was further tapered to 10 mg/day at the outpatient clinic. A review in July 2010 showed that liver functions had normalized.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.0, 'degrees celsius'], 'Heart Rate or Pulse': [113.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [15900.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 113.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 15900.0 count/m^3. To convert 15900.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 15900.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 2e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6730,51,SIRS Criteria,diagnosis,integer,pmc-6288861-1,Extracted,"A 47-year-old female patient presented to the dialysis unit with decreased level of consciousness and sleepiness of two days duration. Her past medical history is end stage renal disease and regular hemodialysis 3 times/week for 2.5 years, controlled hypertension. She is non-diabetic. Her past surgical history included arteriovenous fistula before 2.5 years, appendectomy and tonsillectomy long time ago.
The patient was in her usual state of health of moderate exercise tolerance until two days before admission when she started to experience lower back and bilateral knee pain that was vague in nature and associated with insomnia. That time, she received one tablet of baclofen 25 mg from her sister. Her sister used to ingest baclofen for chronic neck pain. The patient fell into a deep sleep throughout that night and entire next day without any wakefulness periods. Two days later, she went to her usual hemodialysis session and there the medical personnel noticed her high blood pressure and a state of unconsciousness for which she was sent back to the emergency department after the hemodialysis session. The family denied any previous similar episodes or limb weakness, numbness, dysarthria, dysphagia or mouth deviation before the event. There is no history of fever, photophobia, neck stiffness, falling down or any psychosocial problems. She had not travelled or had any contact with sick people. She was compliant to her hemodialysis sessions. She is a 20 pack-year smoker but does not use any illegal drugs or consume alcoholic drinks. Her home medications were: Atenolol 50 mg/day, Amlodipine 5 mg/ day, CaCO3 600 mg /day and alfacalcidol 0.25 ugm/day.
On examination, the vital signs were as follows: Temperature: 36.4 °C, Blood pressure: 220/110, pulse: 95 beat/minute, respiratory rate: 14/min, oxygen saturation: 95% on room air. On admission, the Glasgow Coma Scale was 9/15. She was unconscious. Deep tendon reflexes were absent. There was no obvious facial asymmetry, left pupil was round and reactive to light (right eye is artificial due to previous trauma). Gag reflex was intact but the cranial nerves could not be assessed. The fundus was examined and no papilledema or hemorrhage were seen. The breathing sounds were heard bilaterally on the chest with no added sounds. Abdominal examination was unremarkable.
Lab results at admission were: Hemoglobin: 16.1 g/dL, White blood cells: 6.8 K/ul, platelets: 155 K/ul, Sodium: 138 mEq/L, potassium: 4.4 mEq/L, chloride: 95 mEq/L, CRP: 1.6 mg/L, Glucose: 99 mg/dL, ABG’s: pH:7.44, pCO2: 36.6 mmHg, pO2: 88 mmHg, HCO3: 24.4 mEq/L, albumin: 4.4 g/dL, alkaline phosphatase:88, total bilirubin: 0.5 mg/dL, direct bilirubin: 0.2 mg/dL, BUN: 27 mg/dL, Creatinine: 5.5 mg/dL. Liver function tests were within normal ranges. To rule out any brain ischemia or hemorrhage, brain computed topography (CT scan) was done on the day of admission and Magnetic resonance imaging (MRI) of the brain was done on the second day of admission. CT scan showed no significant lesions, no hemorrhage or any other defects. MRI showed no signs of recent ischemic stroke, intracranial hemorrhage, space-occupying lesion or midline shift. The hypertension was controlled by labetalol IV infusion pump.
After ruling out all possible causes of her decreased level of consciousness, including Posterior reversible encephalopathy syndrome (PRES), baclofen toxicity was considered as the cause. She was started on flumazenil 0.25 mg and on intensive daily ultrafiltration hemodialysis sessions since the first day of admission with total of three extra hemodialysis sessions. The improvement started to be noticed at the second day when she was semi-conscious, hallucinating, obeying commands as ordered but still not oriented to time, place or person. GCS was 10/15. The dramatic improvement was on the next day after a total of two extra hemodialysis sessions, she was fully awake, GCS 15/15, able to obey commands but still not well oriented so a third extra session was considered. After three days of admission and a total of five hemodialysis sessions, she was discharged after she had returned to her previous baseline state of health and she was instructed not to receive baclofen again.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.4, 'degrees celsius'], 'Heart Rate or Pulse': [95.0, 'beats per minute'], 'respiratory rate': [14.0, 'breaths per minute'], 'White blood cell count': [6800.0, 'µL'], 'PaCO2': [36.6, 'mm hg']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.4 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 95.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 6800.0 count/µL. To convert 6800.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 6800.0 white blood cell count/µL * 1.0 µL/mm^3 = 6800.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 14.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 36.6 mm Hg, which is greater or equal to than 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6731,51,SIRS Criteria,diagnosis,integer,pmc-6649211-1,Extracted,"A 50-year-old Caucasian female driver was brought to the Emergency Department
following a high-speed car accident. Vehicle extrication had to be performed on the
scene (duration 35 minutes). No information about seat belt use was available. Her
medical history included arterial hypertension and depression. Her drug regimen
included nebivolol 5mg d.i.d., lamotrigine 25mg b.i.d. and fluoxetine 25mg o.d. No
allergies were mentioned.
On admission, she presented with a Glasgow Coma Scale of E2/V3/M5 (Eye/Verbal/Motor
response), heart rate (HR) 70 beats/min, blood pressure 65/37mmHg, core temperature
(t°) 34°C, respiratory rate 9 breaths/min, oxygen pulse saturation (SpO2)
85% on oxygen mask (flow - 15L/min), mixed lung sounds on both sides upon
auscultation, and bruises all over the right upper limb and both lower limbs.
Moreover, right leg length discrepancy with concomitant right knee outer rotation
was noted. Alcohol odor on breath was recorded. Full spine immobilization and 1.2L
of crystalloids had already been given by the Emergency Medical Technicians. Her
Revised Trauma Score was 4 and Emergency Trauma Score was 7.
Rapid sequence intubation was performed, and further investigation (computed
tomography (CT), CT angiography and X-ray imaging) revealed multiple rib fractures
on both sides (4th - 6th ribs on the left and 9th -
12th ribs on the right), sternal body fracture, small left
pneumothorax, left lung contusions, right hepatic lobe contusion, and right distal
femoral fracture with knee involvement.
On admission to the intensive care unit (ICU), the patients Acute Physiology and
Chronic Health Evaluation (APACHE) II score was 31, and her Sequential Organ
Failure Assessment (SOFA) score was 11. An arterial blood gas exam
revealed severe mixed acidosis: pH 7.22, partial pressure of oxygen 54.2mmHg,
partial pressure of carbon dioxide 37.9mmHg, potassium 3.5mEq/L, sodium 140mEq/L,
bicarbonate15mEqL, basis excess 11.8, anion gap (corrected for albumin) 13.25mmol/L,
and lactate 10.4mmol/L. Further laboratory results were hemoglobin 7.8g/dL,
leukocytes 13.4k/dL, platelets 260k/dL, partial prothromboplastin time 32 sec,
prothrombin time 19.2 sec, serum creatinine 1.22mg/dL, urea 34mg/dL, serum glutamic
oxaloacetic transaminase 342IU/L, serum glutamic-pyruvic transaminase (SGPT)
221IU/L, creatine phosphokinase 2716IU/L, and troponin T 327mcg/L. Central venous
pressure measurement was 7cmH2O, and bulging of the right jugular vein
was noted (Lancisi's sign). A grade 2/6 holosystolic murmur that was augmented
during inspiration was noted at the left lower sternal border. Transthoracic
echocardiography (TTE) revealed signs of possible tricuspid valve injury. Subsequent
transesophageal echocardiography (TEE) revealed traumatic tricuspid valve papillary
muscle injury ( and ). During the following hours, positive
end-expiratory pressure (PEEP)-dependent (from 7 to 4cmH2O) hypoxia was
noted, and so a second TEE was performed. Injection of a micro-bubble through the
central line revealed a PFO, which was also displayed with color Doppler (). Right ventricular systolic pressure
was 42 - 44mmHg, yet with preserved systolic function. At the time, and for the rest
of her ICU hospitalization, plateau pressure was < 25mmHg and tidal volume was
< 8mL/kg.
Stabilization of the patient continued with fluid resuscitation and high doses of
vasopressors (noradrenaline 1.1µg/kg/min), active rewarming and reversal of
acid-base derangement.
Due to lack of a cardiosurgical unit in the hospital, communication with other
hospitals in the region was conducted. Transportation of the patient to a private
cardiosurgical unit was performed 5 days later.
At operation, a median sternotomy was performed and cardiopulmonary bypass was
instituted. The tricuspid valve was exposed through right atriotomy.
Intraoperatively, apart from the tricuspid valve papillary muscle rupture and PFO
(1cm), a 3cm length covert rupture of the right atrium was also noticed. Correction
included tricuspid valve annuloplasty with a Carpentier-Edward ring 28mm and
complementing valve leaflets, closure of the PFO and additional atrial wall defect
with continuous surgical suture. The postoperative course of the patient was
uneventful, and she was discharged from the hospital with a Glasgow Outcome Scale of
7. A year later, the woman had fully recovered, apart from a residual functional
defect of the right knee.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [34.0, 'degrees celsius'], 'Heart Rate or Pulse': [70.0, 'beats per minute'], 'respiratory rate': [9.0, 'breaths per minute'], 'White blood cell count': [13400.0, 'µL'], 'PaCO2': [37.9, 'mm hg']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 34.0 degrees celsius. Because the temperature is less than 36 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 70.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 13400.0 count/µL. To convert 13400.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 13400.0 white blood cell count/µL * 1.0 µL/mm^3 = 13400.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 9.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 37.9 mm Hg, which is greater or equal to than 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6732,51,SIRS Criteria,diagnosis,integer,pmc-8405453-1,Extracted,"A 59-year-old caucasian woman with a past medical history of chronic obstructive pulmonary disease, morbid obesity presented to the emergency department complaining of fevers, dry cough, and loss of taste and smell for about ten days prior to presentation. The woman tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) approximately nine days before admission.
Upon admission, vital signs included temperature 35.8° C (96.4° F), heart rate 116 beats per minute, respiratory rate of 22 breaths per minute, non-invasive blood pressure 138/67 mm Hg, and SpO2 67% on room air. An arterial blood gas analysis showed pH 7.4, PaCO2 36.9 mm Hg, PaO2 53 mm Hg; pertinent laboratory data upon admission included white blood cells 15,200 cells per microL, blood urea nitrogen 18 gm/dL, creatinine 1.32 gm/dL, aspartate transaminase 48 U/L. Inflammatory markers were: D-dimer 1.58 mg/L, ferritin 465 nanogram/mL, C-reactive protein 34.4 mg/dL, lactate dehydrogenase 619 U/L. Portable chest radiography at the time of admission showed bibasilar airspace disease. Pulmonary embolus protocol- computerized tomographic angiography showed severe, widespread bilateral ground glass (alveolar) airspace disease consistent with COVID19 pneumonia; no pulmonary embolism was noted.
The patient was initially placed on Bimodal Positive Airway Pressure (BiPAP) for hypoxia and was admitted to our step-down unit. She was treated with the then prevailing regimen of anti-viral remdesivir, high-titer anti-SARS-CoV-2 convalescent plasma, dexamethasone, and empiric therapeutic anticoagulation (shared decision making with the patient). Despite therapy and supportive care, she deteriorated and needed to be transferred to the ICU 12 days after admission.
On day #13 of this admission, the patient was endotracheally intubated and the ETT secured with a commercially available fastener {Hollister AnchorFast oral endotracheal tube fastener (Part # 9799), Libertyville, IL}. During the ICU course, she required vasopressors intermittently and daily prone sessions for severe ARDS. As she could not be weaned off from the ventilator, percutaneous tracheostomy (Cook Medical, Blue Rhino percutaneous tracheostomy, Bloomington, IN) was performed on day 21 of intubation.
After the tracheostomy had been inserted and was affixed in place, the Hollister AnchorFast oral endotracheal tube holder was gently removed, revealing - under the skin barrier pads - bilateral stage 2 pressure ulcers on her face; these had not been present prior to placement of the affixation device when the patient was endotracheally intubated (Figures , ).
While the pressure ulcers were managed with frequent (two times a day) cleaning with saline and the application of mupirocin our patient’s medical condition continued to deteriorate and, on day #31 post-intubation, her family (surrogate decision-maker) chose to withdraw life-sustaining treatment.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [35.8, 'degrees celsius'], 'Heart Rate or Pulse': [116.0, 'beats per minute'], 'respiratory rate': [22.0, 'breaths per minute'], 'White blood cell count': [15200.0, 'µL'], 'PaCO2': [36.9, 'mm hg']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 35.8 degrees celsius. Because the temperature is less than 36 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 116.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 15200.0 count/µL. To convert 15200.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 15200.0 white blood cell count/µL * 1.0 µL/mm^3 = 15200.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is 36.9 mm Hg, which is greater or equal to than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6733,51,SIRS Criteria,diagnosis,integer,usmle-9906,Extracted,"A 13-year-old African American boy with sickle cell disease is brought to the emergency department with complaints of abdominal pain over the last 24 hours. The pain is situated in the right upper quadrant and is sharp in nature with a score of 8/10 and radiates to tip of the right scapula. He also complains of anorexia and nausea over the past 2 days. He has been admitted into the hospital several times for pain episodes involving his legs, hands, thighs, lower back, and abdomen. His last hospital admission was 4 months ago for acute chest pain, and he was treated with antibiotics, analgesics, and intravenous fluid. He takes hydroxyurea with occasional red blood cell exchange. Both of his parents are in good health. Temperature is 38°C (100.4°F), blood pressure is 133/88 mm Hg, pulse is 102/min, respiratory rate is 20/min, and BMI is 18 kg/m2. On examination, he is in pain with a tender abdomen with painful inspiration. Soft palpation of the right upper quadrant causes the patient to cry out in pain.
Laboratory test
Complete blood count
Hemoglobin 8.5 g/dL
MCV 82 fl
Leukocytes 13,500/mm3
Platelets 145,000/mm3
Basic metabolic panel
Serum Na+ 135 mEq/L
Serum K+ 3.9 mEq/L
Serum Cl- 101 mEq/L
Serum HCO3- 23 mEq/L
Liver function test
Serum bilirubin 2.8 mg/dL
Direct bilirubin 0.8 mg/dL
AST
30 U/L
ALT 35 U/L
Serum haptoglobin 23 mg/dL (41–165 mg/dL)
Ultrasonography of abdomen shows the following image.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.0, 'degrees celsius'], 'Heart Rate or Pulse': [102.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [13500.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 102.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 13500.0 count/m^3. To convert 13500.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 13500.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6734,51,SIRS Criteria,diagnosis,integer,pmc-7249276-3,Extracted,"A 43-year-old male with no significant past medical history presented to the emergency room with shortness of breath, cough, fever, chest pain, and headache for about one week (). He was taking doxycycline for pneumonia before presentation; however, his symptoms did not resolve. He denied sick contacts, recent travel, or being in contact with someone who traveled. He also denied vomiting, diarrhea, or abdominal pain. Initial vitals showed a temperature of 98.7 Fahrenheit but rising to 101.2 Fahrenheit, pulse rate of 76 beats per minute, respiratory rate of 18 cycles per minute, blood pressure of 121/75 mmHg, and pulse oximetry of 95% on room air. Physical examination revealed breath sounds that were equal bilaterally. The initial laboratory showed a white blood cell count of 2.1 k/μL, hemoglobin of 12.8 g/dl, and platelets of 110 k/μL, but a complete metabolic panel was normal. Laboratory investigation was also negative for HIV 1 and 2, influenza A and B, and respiratory syncytial virus. A chest X-ray demonstrated mild fullness in the right perihilar region (.). He was diagnosed with COVID-19 and was started on levofloxacin but he received hydroxychloroquine for two days.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [101.2, 'degrees fahrenheit'], 'Heart Rate or Pulse': [76.0, 'beats per minute'], 'respiratory rate': [18.0, 'cycles per minute'], 'White blood cell count': [2100.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 101.2 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 69.2 = 38.44444 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 76.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 2100.0 count/µL. To convert 2100.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 2100.0 white blood cell count/µL * 1.0 µL/mm^3 = 2100.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6735,51,SIRS Criteria,diagnosis,integer,pmc-4010036-1,Extracted,"A 41-year-old man with an extensive medical history, including Child-Pugh B liver cirrhosis and chronic pancreatitis, consulted his family doctor with progressive dyspnea, retrosternal pain radiating to the back, repeated vomiting, and fever for 3 days. On admission at the emergency ward, the patient appeared confused and agitated. Core temperature was 38.5°C, heart rate was regular at 150 beats/min, and respiratory rate was 40 breaths/min. Physical examination revealed a supple but tender abdomen, normal peristalsis, and muffled breath sounds over the right lung. Blood analysis showed macrocytic anemia, 18500 leukocytes/mm³, normal enzymes, a C-reactive protein (CRP) of 303 mg/L, and a lactate level of 7.4 mmol/L. Chest X-ray showed a silhouette sign over the right heart border and small mediastinal radiolucent streaks of air (). A contrast-enhanced computed tomography (CT) scan of the thorax confirmed the pneumomediastinum () and showed a dilated oesophagus with a distal tear, bilateral pleural effusions, and heterogeneous retro- and paracardiac collections (). The diagnosis of Boerhaave's syndrome was made. Blood cultures were taken; intravenous antibiotic therapy (β-lactam + aminoglycoside) and ample fluid resuscitation were initiated. The patient was transferred to the ICU. Two hours after ICU admission, the patient became increasingly oxygen- and vasopressor-dependent. A new chest X-ray revealed a rapidly evolving right pleural effusion (). Subsequently, the patient was intubated and mechanically ventilated. A chest tube was inserted in the right pleural space. A brown, foul-smelling fluid was evacuated. The pleural fluid did not contain food particles, pH was 7, and amylase was 685 U/L. Gastroscopy confirmed an oesophageal tear in the lower one-third of the oesophagus. At that time, a severe concomitant mucosal inflammation precluded further endoscopic treatment because of a too high risk of oesophageal rupture. A control CT scan demonstrated a left-sided paravertebral encapsulated air-fluid collection and a left pleural effusion that had substantially increased in size. A pigtail catheter was inserted into the left pleural space. CT guided drainage of encapsulated pleural collections was performed. Four days after ICU admission, a self-expandable oesophageal stent was endoscopically placed. Despite stenting, continuous bilateral pleural drainage, and broad antimicrobial covering, the patient remained septic with hectic fever and persistently high leukocyte counts and CRP levels. Video-assisted thoracoscopic surgery was performed with drainage and rinsing of the mediastinum and pleural cavities. Thereafter, fever subsided and clinical and biological parameters progressively normalised. After an ICU stay of 33 days, the patient was discharged.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.5, 'degrees celsius'], 'Heart Rate or Pulse': [150.0, 'beats per minute'], 'respiratory rate': [40.0, 'breaths per minute'], 'White blood cell count': [18500.0, 'm^3']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.5 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 150.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 18500.0 count/m^3. To convert 18500.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 18500.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 2e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 40.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6736,51,SIRS Criteria,diagnosis,integer,pmc-3852629-1,Extracted,"A 21-year-old woman who was otherwise healthy before presented with severe abdominal pain. The pain was generalized, severe, acute onset and continuous. She was also found to have multiple episodes of vomiting for a period of 24 h. Otherwise, she had no fever, no history of previous abdominal surgery, no other co-morbids and no trauma.
On examination she was drowsy, tachycardic with a pulse rate of 120 beats/min, BP 130/78 mmHg, temperature 37.0°C, dehydrated and respiratory rate of 24 breaths/min. An abdominal examination revealed distended abdomen, generalized abdominal tenderness and guarding. Bowel sounds were absent.
Laboratory investigations results were normal, except for an elevated white blood cell count of 16 000/mm3.
In view of generalized peritonitis, the abdomen was explored through an emergency midline laparotomy after initial resuscitation.
Upon entering the peritoneal cavity, 2 l of hemorrhagic fluid was drained. A loop of ileum had herniated through a small mesenteric defect. A total of 180 cm ileum noted to be gangrenous with loss of peristalsis and absent pulsations (Fig. ). Terminal ileum and the ileocecal junction were also nonviable. Pulsations of mesenteric vessels were intact. The mesenteric defect measuring 3 × 3 cm located about 4 cm from the mesenteric edge of mid-jejunum. There was no evidence of malrotation. A limited right hemicolectomy with extensive gangrenous small bowel resection was performed and a stapled side-to-side functional anastomosis created. The mesenteric defect mentioned earlier was closed with interrupted sutures. The patient recovered well from the surgery. She was allowed orally on day 3 post surgery (Figs –).",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.0, 'degrees celsius'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'respiratory rate': [24.0, 'breaths per minute'], 'White blood cell count': [16000.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 120.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 16000.0 count/m^3. To convert 16000.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 16000.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 2e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 24.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6737,51,SIRS Criteria,diagnosis,integer,pmc-6169237-1,Extracted,"An 85-year-old black woman was admitted to the hospital with complaints of crampy abdominal pain, vomiting, and several episodes of watery diarrhea for two days. Her past medical history included end-stage renal disease (on continuous cycling peritoneal dialysis), congestive heart failure, atrial fibrillation, chronic obstructive pulmonary disease, and cervical cancer (status after total abdominal hysterectomy). She was started on peritoneal dialysis three months ago for her end-stage renal disease during a hospital admission for congestive heart failure. She was discharged to rehab, where she stayed for a month. Her last home dialysis session was a day prior to the onset of symptoms. She denied any fever, bloody stool, outside food ingestion, any sick contact, and recent travel history. On physical examination, her vital signs revealed a pulse rate of 76 beats per minute, blood pressure of 121/70 mmHg, respiratory rate of 16 breaths per minute, and a temperature of 99°F. Abdominal examination revealed nondistended abdomen with diffuse tenderness on palpation and hyperactive bowel sounds with voluntary guarding; however, dialysis catheter was intact with no surrounding erythema or purulent discharge. Initial laboratory analysis showed WBC of 13,400/μL, neutrophils of 88.5%, hemoglobin of 11 g/dl, and serum albumin of 2.9 mg/dl. Peritoneal fluid analysis revealed white blood cell count in peritoneal effluent of 8359/μL, with 93% neutrophil predominance. Gram strain did not show any microorganisms. Given the overall clinical status, peritonitis was suspected, and she received empiric vancomycin and ceftazidime. However, stool C. difficile toxin B assay returned positive. She was concurrently started on oral metronidazole. Within 24 hours, there was improvement in the clinical symptoms, and her broad-spectrum antibiotics were discontinued after a couple of days. The patient was diagnosed with PD-related peritonitis accompanying C. difficile-associated diarrhea, with continuation of oral metronidazole. Repeated effluent white blood cell count the day after starting metronidazole decreased to 133/μL, with complete resolution of peripheral leukocytosis. Surgical consultation done on admission concluded that the peritoneal catheter was not the source of infection and, therefore, the catheter was not removed. The patient's symptoms resolved, and she was then discharged on a total of three weeks of metronidazole with continuation of peritoneal dialysis.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [99.0, 'degrees fahrenheit'], 'Heart Rate or Pulse': [76.0, 'beats per minute'], 'respiratory rate': [16.0, 'breaths per minute'], 'White blood cell count': [13400.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 99.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 67.0 = 37.22222 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 76.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 13400.0 count/µL. To convert 13400.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 13400.0 white blood cell count/µL * 1.0 µL/mm^3 = 13400.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 16.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6738,51,SIRS Criteria,diagnosis,integer,pmc-6327550-1,Extracted,"A 48-years-old woman with trisomy 21 and history of ostium primum atrial septal defect and hypothyroidism, on effective replacement therapy, was transferred from the Cardiology of another hospital to our Internal Medicine Department because of dyspnea with acute and worsening respiratory failure. She had been in her usual health until 2 months before admission, when a flu-like syndrome occurred in November. After 15 days, during an admission in other hospital for syncope with sphincter incontinence, a mild pericardial effusion (7 mm) was diagnosed and treated with ibuprofen 600 mg every 8 h and colchicine 0.5 mg twice day. Two weeks later, due to worsening of dyspnea and appearance of diarrhea, therapy had to be suspended. Trans-thoracic echocardiogram showed a diffuse increase in pericardial effusion (30 mm) without inspiratory collapse of the inferior vena cava (Fig. ). Chest CT confirmed massive pericardial effusion and highlighted bilateral basal and left upper lobe pleural effusion with atelectasis. Therefore, a metilprednisolone 60 mg/day (1 mg/Kg) and furosemide 40 mg/day therapy was started.
On admission, blood pressure was 110/70 mmHg, heart rate 75 beats per minute, respiratory rate 16 breaths per minute, body temperature 99 °F, and oxygen saturation 86% while the patient was breathing ambient air. Cardiac examination revealed muffled heart sounds and a 3/6 ejection murmur on aortic area. Pulmonary evaluation revealed a stony dull percussion with diminished vesicular breath sounds on basal region bilaterally and widespread rhonchi. The total leukocyte count was 8400/μL (neutrophils 93% and lymphocytes 15%), erythrocyte sedimentation rate (ESR) 120 mm/h, CRP 16 mg/L, procalcitonin 0.05 ng/mL, MR-pro-adrenomedullin 0.96 nmol/L, ferritin 3799 ng/mL, NT-proBNP 254 pg/mL, and TSH 0.33 mcU/L; ANA, anti-dsDNA, ENA, c-ANCA and p-ANCA were in the normal range. Arterial blood gas analysis revealed severe hypoxemia with respiratory and metabolic alkalosis (pH 7.48, pO2 47.3 mmHg, pCO2 36.1 mmHg, HCO3− 26.6 mmol/l). ECG highlighted incomplete right bundle branch block, while trans-thoracic echocardiogram showed large circumferential pericardial effusion (25, 23, and 30 mm respectively on apical, posterior, and lateral ventricular walls, 20 mm on right ventricular wall) without right ventricular compression; grade 2 diastolic dysfunction; mild left-right shunt due to ostium primum atrial septal defect; mild tricuspidal and minimal mitral regurgitations with cleft of the anterior mitral valve leaflet; mild enlargement of the right cardiac chamber with pulmonary artery pressure of 40 mmHg. Chest X-ray showed widespread bronchial wall thickening and enlargement of the cardiac silhouette (Fig. ).
The absence of other causes for pericardial effusion and the history of recent flu-like syndrome rose the suspicion of a viral etiology; therefore, laboratory evaluation identified the presence of influenza B virus on molecular assay of tracheal aspirate. Antiviral therapy with oseltamivir 75 mg twice a day for 5 days was added to ongoing treatment with metilprednisolone 30 mg (0.5 mg/kg/day) and colchicine 0.5 mg/day therapy [].
The patient showed a progressive clinical and CRP improvement with disappearance of the pericardial effusion on 15-days echocardiographic follow-up.
The patient was discharged in good medical conditions with 1-month prednisone 30 mg/day followed by dose reduction of 2.5 mg every 5 days and 3-months colchicine 0.5 mg/day therapy [].
At 1-month follow-up, patient was asymptomatic with normal physical examination, CRP 1.1 mg/L, and echocardiogram showed mild pericardial detachment on right atrium without sign of compression (Fig. ). At 6-month follow-up, clinical and echocardiographic features was preserved, with complete normalization of inflammatory markers (CRP 0,26 mg/L) even when treatment was suspended.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [99.0, 'degrees fahrenheit'], 'Heart Rate or Pulse': [75.0, 'beats per minute'], 'respiratory rate': [16.0, 'breaths per minute'], 'White blood cell count': [8400.0, 'µL'], 'PaCO2': [36.1, 'mmhg']}",0,0,0,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 99.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 67.0 = 37.22222 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 75.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 8400.0 count/µL. To convert 8400.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 8400.0 white blood cell count/µL * 1.0 µL/mm^3 = 8400.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 0.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 16.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 36.1 mm Hg, which is greater or equal to than 32 mm Hg. Neither criteria met and so keep the current total at 0.
Hence, the the number of SIRS criteria met by the patient is 0."
6739,51,SIRS Criteria,diagnosis,integer,pmc-3421971-1,Extracted,"A previously healthy 7-year-old boy presented to the emergency department (ED) with a complaint of right lower extremity pain and fever. The preceding day his parents had noticed that he was limping upon returning home from school. The pain progressed that evening until he could no longer bear weight on his right leg. Overnight he developed a fever. The child reported no history of trauma. His parents stated that 2 days before presentation he had complained of contralateral leg pain, which had since resolved. On further questioning, his parents also reported that he had experienced left shoulder pain 3 days previously, which resolved within 36 hours. Neither the child nor his parents were aware of any recent tick exposures, but they did note that he had had tick bites several months prior during the summer. He was described as a very active child who enjoys playing outdoors. Other than a recent trip to Europe, there was no history of foreign travel. There were no known sick contacts. Review of systems was positive for fatigue, but negative for chills, weight loss, nausea, vomiting, diarrhea, abdominal pain, cough, congestion, rhinorrhea, sore throat, and urinary symptoms.
Physical examination revealed a pleasant, well-developed boy who appeared uncomfortable and localized his pain to the right anterior mid-thigh. His temperature was 38.0°C; heart rate, 132 beats/minute; respiratory rate, 24 breaths/minute; blood pressure, 106/54 mmHg; and O2 saturation, 99% on room air. He was unable to bear weight on the right leg owing to pain. He had no tenderness to palpation at the right hip or knee, but had pain with passive internal and external rotation of the affected hip. He could flex and extend the right knee without difficulty. He had no appreciable edema at the right knee or hip but did have an effusion at the asymptomatic left knee. There was no erythema or calor present in either lower extremity. A thorough inspection of the skin and scalp revealed no rash or signs of insect bites. The remainder of the physical examination was unremarkable.
Serologic studies revealed a white blood cell (WBC) count of 8,900/μL, erythrocyte sedimentation rate (ESR) of 53 mm/h, and C-reactive protein (CRP) of 5.7 mg/dL. Blood cultures and Lyme titers were obtained. Radiographs showed no abnormality at either hip, a small to moderate effusion of the right knee, and a moderate effusion of the left knee. Bedside ultrasonography was performed, revealing a hypoechoic fluid collection at the right hip () measuring 20 mm in the anterior synovial recess, which is the space between the anterior cortex of the femoral neck and the posterior surface of the joint capsule underlying the iliopsoas muscle. Normally, a fluid collection in this location, if present at all, should be no greater than 7.7 mm for a child of this age. Sonography of the left hip was normal ().
After applying topical anesthetic cream and injecting subcutaneous local anesthetic, an ultrasound-guided arthrocentesis of the right hip was performed in the ED under sterile conditions (video of procedure available online). Seven milliliters of turbid, yellow fluid was aspirated and sent for analysis. Repeated sonographic imaging of the right hip revealed a marked reduction in size of the effusion. After arthrocentesis, ceftriaxone was promptly administered intravenously, and the orthopedic service was consulted.
The synovial fluid had 109,495 white cells/mm3 (95% neutrophils). The gram stain results showed no organisms. When examined by the orthopedist approximately an hour after arthrocentesis, the patient had significant improvement in his pain and was able to bear weight on the affected leg. A second arthrocentesis, this time of the left knee, was performed by the orthopedic consultant that yielded 82,887 white cells/mm3 (92% neutrophils) and a negative gram stain result. In view of these findings, Lyme disease was believed to be the likely cause of the patient's illness. The patient was admitted to the family practice service, and ceftriaxone therapy was continued. The patient's symptoms improved in hospital, and after 3 days he was discharged and given a 4-week course of amoxicillin for presumptive Lyme arthritis. Ultimately, blood and synovial fluid cultures revealed no growth. Lyme studies, which were pending at the time of discharge, yielded positive results 3 days later by Western Blot analysis for IgG and IgM.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.0, 'degrees celsius'], 'Heart Rate or Pulse': [132.0, 'beats/minute'], 'respiratory rate': [24.0, 'breaths/minute'], 'White blood cell count': [8900.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 132.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 8900.0 count/µL. To convert 8900.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 8900.0 white blood cell count/µL * 1.0 µL/mm^3 = 8900.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 24.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 1 + 1 = 2 criteria met.
Hence, the the number of SIRS criteria met by the patient is 2."
6740,51,SIRS Criteria,diagnosis,integer,pmc-6701334-1,Extracted,"A 44-year-old female patient admitted to the university hospital for new-onset left-sided weakness and right-sided headache; dizziness, confusion, chest pain, and palpitations for four days; and generalized malaise for two months. Medical history was significant for hypertension, chronic hepatitis C treatment naive, hypothyroidism, recent IV drug abuse, and alcoholism, and she was a former heavy smoker. A CT scan (computerized tomography) of the head done at the outside hospital revealed acute infarctions in the right thalamus and right temporal lobe. EKG showed normal sinus rhythm, and a chest X-ray was normal.
On the day of admission, vital signs were blood pressure of 118/74 mmHg, pulse rate of 117/minute, respiratory rate of 20/minute, temperature of 38°C, and SpO2 of 98% on room air. Physical examination revealed the presence of poor oral hygiene and grade 3/6 systolic murmur at the cardiac apex. Neurological examination affirmed slurred speech, left-sided weakness with motor strength of 1/5 in upper and lower extremities, increased reflexes on the left side compared to the right, and right pupil dilation with sluggish response to light and right lateral ophthalmoparesis. EKG showed sinus tachycardia. TTE (transthoracic echocardiogram) () displayed an ejection fraction of 65%, dilated left atria, and severe mitral valve regurgitation with a 2 cm strand-like hypoechoic structure on its atrial surface suggestive of vegetation. CT angiogram of the head and neck displayed the patent carotid and vertebral basilar arterial system. Multifocal acute infarcts were detected at the right medial temporal lobe, right thalamus, right lateral pons, and midbrain with no hemorrhagic transformation on MRI (magnetic resonance imaging). TEE (transesophageal echocardiogram) () on day 4 revealed no evidence of thrombus or mass, ruptured chordae tendineae of the posterior mitral leaflet, and a small mobile density on the anterior mitral leaflet with no patent foramen ovale. Blood cultures obtained on day 3 of hospitalization for fever of 38.7°C resulted positive on day 5 for Gram-positive cocci in chains in 4 out of 4 bottles.
The infectious disease team was consulted on day 4 of admission. The intravenous (IV) antibiotic vancomycin 1.5 g every 12 hrs was initiated on day 5 to achieve a target vancomycin trough of 15 to 20 mcg/ml. Overall, blood cultures obtained on days 3 and 5 resulted positive in 4 out of 4 bottles. MALDI-TOF MS (matrix-assisted laser desorption ionization-time of flight mass spectrometry) was used to identify the organism due to difficulty in retrieving it from culture media. G. adiacens was confirmed on day 6 in all of the positive blood culture samples obtained. Isolated colonies determined insufficient to be transferred to a tertiary lab for antimicrobial susceptibility. IV vancomycin was continued as per treatment plan. From day 6 onwards, blood cultures remained negative for any growth. A cardiothoracic surgeon evaluated the patient for mitral valve replacement/repair surgery.
On day 9, the patient complained of acute low back pain. A CT scan of the lumbar spine with contrast revealed L3-L4 early discitis and osteomyelitis. On the same day, the patient's confusion worsened and was transferred to the neuroscience intensive care unit. The MRI brain was repeated for deteriorating confusion. It () revealed right thalamic and right medial temporal-occipital abscess (measuring 1.1 × 2.3 × 2.9 cm) associated with extensive vasogenic edema extending to the brainstem. Lumbar spine MRI () displayed L3-L4 discitis with osteomyelitis with no epidural or paravertebral abscess. The CSF (cerebrospinal fluid) analysis revealed an elevated total protein of 196 mg/dl, decreased glucose of 33 mg/dl, elevated white cell count of 385/mcl, lymphocyte predominant (85%), and RBC of 1040/mcl. The CSF BioFire panel for meningitis pathogens was negative. At this time, IV meropenem 2 g every 8 hrs was started alongside with vancomycin. The patient's confusion gradually cleared with improvement in speech and left-side strength. Cardiac catheterization revealed normal coronary arteries without any significant disease. Normal coronary arteries implied that ruptured chordae tendineae was due to infection. Cardiothoracic surgery reevaluated the patient and recommended transfer to a larger tertiary care facility due to the complex clinical condition and high surgical risk. Vancomycin trough (mcg/ml) was 14.6 on day 7, 21.4 on day 14, and 24.8 on day 20.
The tertiary care center transfer was on day 21 in a clinically stable condition. IV vancomycin and meropenem continued at transfer. Mitral valve replacement with Hancock type 2 MV tissue was done on day 31, and the patient was discharged on six-week course of IV vancomycin and ertapenem. On clinical follow-up at three months, mild residual weakness on the left side was noted, and brain imaging revealed resolving abscesses.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.0, 'degrees celsius'], 'Heart Rate or Pulse': [117.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [385.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 117.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 385.0 count/µL. To convert 385.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 385.0 white blood cell count/µL * 1.0 µL/mm^3 = 385.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6741,51,SIRS Criteria,diagnosis,integer,usmle-3824,Extracted,"A 60-year-old man is brought to the emergency room because of fever and increasing confusion for the past 2 days. He has paranoid schizophrenia treated with chlorpromazine. He appears diaphoretic. His temperature is 40°C (104°F), pulse is 130/min, respirations are 29/min, and blood pressure is 155/100 mm Hg. Neurologic examination shows psychomotor agitation and incoherent speech. There is generalized muscle rigidity. His deep tendon reflexes are decreased bilaterally. Serum laboratory analysis shows a leukocyte count of 11,300/mm3 and serum creatine kinase concentration of 833 U/L.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [40.0, 'degrees celsius'], 'Heart Rate or Pulse': [130.0, 'beats per minute'], 'respiratory rate': [29.0, 'breaths per minute'], 'White blood cell count': [11300.0, 'm^3']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 40.0 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 130.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 11300.0 count/m^3. To convert 11300.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 11300.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 29.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6742,51,SIRS Criteria,diagnosis,integer,usmle-10059,Extracted,"A 78-year-old woman living in New Jersey is brought to the emergency department in July with a fever for 5 days. Lethargy is present. She has had bloody urine over the last 48 hours but denies any nausea, vomiting, or abdominal pain. She has no history of serious illness and takes no medications. She has not traveled anywhere outside her city for the past several years. She appears ill. The temperature is 40.8℃ (105.4℉), the pulse is 108/min, the respiration rate is 20/min, and the blood pressure is 105/50 mm Hg. The abdominal exam reveals hepatosplenomegaly. Lymphadenopathy is absent. Petechiae are seen on the lower extremities. Laboratory studies show the following:
Laboratory test
Hemoglobin 8 g/dL
Mean corpuscular volume (MCV) 98 µm3
Leukocyte count 4,200/mm3
Segmented neutrophils 32%
Lymphocytes 58%
Platelet count 108,000/mm3
Bilirubin, total 5.0 mg/dL
Direct 0.7 mg/dL
Aspartate aminotransferase (AST) 51 U/L
Alanine aminotransferase (ALT) 56 U/L
Alkaline phosphatase 180 U/L
Lactate dehydrogenase (LDH) 640 U/L (N = 140–280 U/L)
Haptoglobin 20 mg/dL (N = 30–200 mg/dL)
Urine
Hemoglobin +
Urobilinogen +
Protein +
A peripheral blood smear is shown (see image).",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [40.8, 'degrees celsius'], 'Heart Rate or Pulse': [108.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [4200.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 40.8 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 108.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 4200.0 count/m^3. To convert 4200.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 4200.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 4.2e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6743,51,SIRS Criteria,diagnosis,integer,pmc-2803839-1,Extracted,"A 56-year-old Caucasian Greek male was referred to the emergency department of our hospital with a two-month history of recurring fever, loss of appetite and swelling in his neck.
Upon admission, he was obtunded and hyperthermic (axillary temperature, 38°C). The patient had a respiratory rate of 20 breaths/min and a heart rate of 100 beats/min. He had no skin lesions. Upon physical examination, he was found to have bilateral cervical, axillary and inguinal lymphadenopathy. His lymph nodes were tenacious, unmovable and tender, and measured from 1.0 × 1.5 cm to 3.0 × 3.5 cm. A respiratory examination revealed mild bilateral inspiratory fine crackles. Chest X-rays showed right hilar lymphadenopathy. Laboratory data showed hemoglobin levels at 10.81 g/dl, a white blood cell count of 6,800 cells/mm3 (70% neutrophils, 14% lymphocytes, 12% monocytes, 1% eosinophils) and a platelet count of 346.000 cells/mm3. His international normalized ratio was 1.11 and his activated partial thromboblastin time was 32.8 seconds.
The patient's erythrocyte sedimentation rate was 64 mm/h, and his C-reactive protein concentration was 9.97 mg/dl (normal range < 0.6 mg/dl). His total bilirubin was 0.13 mg/dl, his serum glutamic oxaloacetic transaminase (SGOT) was 113 IU/l, his serum glutamic pyruvic transaminase (SGPT) was 36 IU/l, his total protein was 7.69 mg/dl, and his creatinine phosphokinase (CPK) was 1777 IU/l. His renal function tests were within normal ranges, and an examination of his cerebrospinal fluid revealed no cells and its biochemical composition was normal. A Mantoux test was positive (20 mm), an arterial blood gas analysis while breathing room air showed pH 7.39, PaO277 mmHg, PaCO2 40.6 mmHg, and HCO3 25.1 mmol/l. A protein electrophoresis did not show any monoclonal spike. Serolologic tests for hepatitis A, B, and C viruses and HIV were negative.
An ultrasonography of the abdomen revealed hepatosplenomegaly and a computed tomography (CT) of the brain demonstrated no evidence of parenchymal lesions. A CT scan of the neck showed multiple enlarged lymph nodes in the right cervical chain, measuring up to 3.5 cm (Figure ). A chest CT scan revealed numerous paratracheal lymph nodes over the superior-anterior mediastinum, measuring up to 2.8 cm (Figure ). An abdominal CT showed lymph nodes in the lesser omentum, the mesentery, the anterior pararenal space, and the upper and lower para-aortic regions, measuring up to 2.5 cm (Figure ).
Cervical lymph node and bone marrow biopsies were performed. The bone marrow biopsy was normocellular with mature hematopoietic elements. The lymph node was completely effaced with a lot of epithelioid cells and occasional Langhans giant cells, constituting well-defined granulomas with caseous necrosis, typical of TB. Immunohistochemically, the cells were negative for CD3, CD20, CD30, kappa and light chains. A Ziehl-Neelsen stain for acid-fast bacilli (AFB) was negative, but the culture grew Mycobacterium tuberculosis complex. The patient was started on antituberculous treatment with the standard four-drug regimen consisting of rifampin, pyrazinamide, ethambutol and isoniazid. After two months of treatment, he was symptom-free, with a prominent reduction in most lymph node swelling. The patient was started on a two-drug regimen of isoniazid and rifampin for seven months. At the end of the therapy, the patient had residual lymph nodes in the neck and in the mediastinum.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.0, 'degrees celsius'], 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [6800.0, 'm^3'], 'PaCO2': [40.6, 'mm hg']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 100.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 6800.0 count/m^3. To convert 6800.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 6800.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 6.8e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 40.6 mm Hg, which is greater or equal to than 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6744,51,SIRS Criteria,diagnosis,integer,pmc-6825490-1,Extracted,"A 53-year-old man lacking medical care for seven years presented to the emergency department following a fall at home. His past medical history was significant for alcohol use disorder, consuming eight to ten or more drinks per day; his last drink was the evening prior to admission. Previous attempts at alcohol cessation were unsuccessful due to strong withdrawal symptoms, but there was no history of seizures or delirium tremens. When he fell, he had hit his head on the wall, and endorsed being down for one hour with no loss of consciousness. He also complained of three days of copious, watery, nonbloody diarrhea, abdominal pain, nausea, and poor per os (PO) intake. He denied any subjective fevers, chills, night sweats, vomiting, headache, confusion, sick contacts, or recent change in diet. He was a nonsmoker. Initial vital signs were body temperature 99.3 °F, pulse rate 115 bpm, blood pressure 165/87 mmHg, and respiration rate 18. Physical exam was unremarkable aside from rales heard on auscultation and positive egophany of the right lower lung lobe. There was no accessory muscle use, no general muscle tenderness or ecchymoses noted. Initial lab tests were significant for ethyl alcohol (EtOH) level 87 mg/dL (normal 0-10) with urine drug screen positive only for ethanol, serum sodium 123 mmol/L (136-148), bicarbonate 18 mmol/L (21-32), blood urea nitrogen (BUN) 21 mg/dL (8-20), creatinine 1.3 mg/dL (0.5-1.2), and troponin 0.1 ng/dL (0-0.05). The patient's baseline levels were largely unknown due to his infrequent health care use. Urinalysis was positive for blood, but no red blood cells were present - myoglobin is often detected as blood on urine dipstick testing. Initial Clinical Institute Withdrawal Assessment (CIWA) scores ranged from 9 to 12, and he was treated per hospital protocol with lorazepam. Chest X-ray revealed patchy right lower lobe infiltrates (Figure ).
The patient was treated with IV hydration, thiamine, folic acid, vitamin K, and IV ceftriaxone for community-acquired pneumonia. On hospital day two, he developed worsening leukocytosis to 14.82x10^3 cells/µL (3.6-11) and fever to 103.1 °F, and antibiotics were broadened to vancomycin, piperacillin-tazobactam, and azithromycin. The CPK rose to 10,221 U/L (0-250) on the morning of day two, peaked at 85,780 U/L late on day two, and remained elevated in the 65,000 to 76,000 U/L range through hospital day five; there was a concurrent rise in transaminases with a high AST/ALT ratio (AST:ALT 115:53 units/L on admission, trending upwards to peak of 451:213 units/L on hospital day six) (Figure ).
He was treated for rhabdomyolysis with aggressive IV hydration. Creatinine peaked at 1.3 mg/dL on hospital day two, and normalized at 0.9 mg/dL by hospital day five. Early on hospital day three, the Legionella urinary antigen returned positive (sputum cultures were also ordered and eventually tested positive, polymerase chain reaction (PCR) was not ordered), and the patient was switched to azithromycin monotherapy. On day five he defervesced, and on day six the CPK dropped dramatically to 13,125 U/L, and continued to decline steadily. A similar pattern was seen with the transaminases. White blood cell (WBC) count trended consistently down from admission, maintaining the lowest range counts of 5.42-6.05 x10^3 cells/µL between hospital days four through six (leukocytosis resolved between hospital days two and three). Blood, urine, and stool cultures and a Clostridium difficile PCR were all negative; the diarrhea resolved, and his hemodynamic and respiratory status remained stable throughout the hospitalization. He was discharged on hospital day nine after completing a six-day course of azithromycin.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [99.3, 'degrees fahrenheit'], 'Heart Rate or Pulse': [115.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [14820.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 99.3 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 67.3 = 37.38889 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 115.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 14820.0 count/µL. To convert 14820.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 14820.0 white blood cell count/µL * 1.0 µL/mm^3 = 14820.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6745,51,SIRS Criteria,diagnosis,integer,pmc-2845798-1,Extracted,"A 48-year-old woman was admitted to the Rheumatology clinic on 30 October 2008 with a 7-month history of pain and swelling in the right knee. The patient underwent arthroscopic arthroplasty 9 months before for relief of osteoarthritis pain. Because the pain and swelling in the right knee developed 7 months earlier, she underwent repeat arthroplasty 4 months before admission for removal of semilunar cartilage remnants. Despite the two arthroplasties, she continued to complain of pain and swelling.
Her medical history was negative for any rheumatoid diseases, cancer, renal diseases, and AIDS. She was a non-smoker, and did not take any steroids, antibiotics, or illegal drugs. On physical examination, the patient had no rashes, lymph node enlargement, or hepatosplenomegaly. The patient’s vital signs were as follows: blood pressure, 130/80 mmHg; heart rate, 88/min; respiratory rate, 20/min; and body temperature, 36.8°C (98.2°F). The patient was alert and oriented, and there were no oral ulcers or erythema. The conjunctivae were not anemic and the sclerae were not icteric. A chest X-Ray showed a normal cardiac silhouette with no signs of pulmonary edema, and an EKG showed a normal sinus rhythm.
The laboratory results were as follows: WBC, 3100/mm3 (4-10 x 103/mm3); hemoglobin, 15g/dL (12-16g/dL); PLT, 16.3 x 104/mm3 (15-45 x 104/mm3); ESR, 41 mm/hr (0-15 mm/hr); CRP, 28.9mg/dL (0-5mg/dL); total bilirubin, 0.6 mg/dL (0.2-1.4mg/dL); AST/ALT, 23/11 IU/L (5-35/5-40 IU/L); ALP, 130 IU/L (32-122 IU/L); r-GTP, 16 IU/L (7-50 IU/L); LDH, 553 IU/L (100-450 IU/L); BUN/Cr, 11.2/0.8 mg/dL (8-20/0.5-1.3 mg/dL); and uric acid, 2.2 mg/dL (2.5-8 mg/dL). Tests for anti-nuclear antibody (ANA), rheumatoid factor (RF), anti-dsDNA antibody, anti-Smith antibody, anti-Ro/La antibody, anti-RNP antibody, and HLA B27 were all negative. The C3 was 158 mg/dL (70-176 mg/dL) and the C4 was 21 mg/dL (16-45 mg/dL). The synovial fluid cytology findings were as follows: appearance, cloudy and reddish; WBC, 12,800/mm3 (0-200/mm3) with 85% neutrophils and 10% lymphocytes; RBC, 8,320/mm3 (0-400/mm3); protein, 3g/dL (1-3 g/dL); and glucose, 2 mg/dL (0-10 mg/dL). No crystals were detected in the joint aspirate. The Gram stain and acid-fast bacteria (AFB) stain showed no bacteria or tuberculosis. Candida parapsilosis was cultured in the synovial fluid on hospital day 7, which was confirmed on hospital day 8.
On hospital day 2, the radiographs of both knees showed a mottled appearance of the distal femur and proximal tibia and asymmetric joint space narrowing (Fig. ). A magnetic resonance imaging (MRI) of the right knee demonstrated a large joint effusion and enhanced synovium, indicating severe inflammation of the knee joint (Fig. ). Amphotericin B (0.7 mg/kg/day) was given intravenously for 3 weeks. As the pain and swelling of the knee subsided, the amphotericin B was discontinued and oral fluconazole (400 mg/day) was prescribed for 6 months. The last culture of synovial fluid was negative for C. parapsilosis and the patient had no complaints of pain or swelling.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.8, 'degrees celsius'], 'Heart Rate or Pulse': [88.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [3100.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.8 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 88.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 3100.0 count/m^3. To convert 3100.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 3100.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 3.1e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6746,51,SIRS Criteria,diagnosis,integer,pmc-7842242-1,Extracted,"A 33-year-old male with no significant past medical history presented to the emergency room with a chief complaint of a sore throat. He noted the symptoms began one week prior and were associated with dysphagia, decreased oral intake, and intermittent fevers. He denied symptoms of shortness of breath, chest pain, myalgias, joint pains, nausea, vomiting, or diarrhea. Vital signs upon admission revealed a temperature of 98.4 degrees F, blood pressure of 135/65 mmHg, heart rate of 81 beats per minute, a respiratory rate of 20 breaths per minute, and an oxygen saturation of 99% on ambient air. Physical exam upon admission revealed a comfortable, awake, alert, and oriented patient. Cardiac examination revealed a regular rate and rhythm with normal S1 and S2 and no murmurs. The pulmonary exam revealed clear lungs to anterior and posterior auscultation with no wheezes, rales, or diminished breath sounds. Abdominal exam revealed normal bowel sounds, and a soft, non-tender, non-distended abdomen. Oral and neck exam was significant for an erythematous and swollen right tonsil and tenderness to palpation of the right anterior neck with associated submandibular and supraclavicular lymphadenopathy, respectively. Laboratory findings were significant for a leukocytosis to 16.5 K/UL. A CT scan of the head and neck was obtained and was significant for right peritonsillar edema with tracking along the lateral pharyngeal wall consistent with phlegmon (Figure ).
Associated lymphadenopathy included the involvement of the internal jugular chain, posterior triangle, bilateral supraclavicular, and submandibular lymph nodes. The epiglottis was without enlargement. The paranasal sinuses and mastoid air cells were clear. A throat swab was obtained for bacterial culture, and meanwhile, clindamycin was started. Blood cultures were obtained too. When the cultures came back negative, the empiric antibiotic was stopped. A monospot was obtained which was negative. A nasopharyngeal swab for COVID-19 was positive for SARS-CoV-2 ribonucleic acid (RNA). The patient was discharged after one day in the hospital and was instructed to remain in quarantine. Upon telemedicine follow-up one week later, the patient reported marked improvement in dysphagia and denied fevers after symptomatic treatment and rest.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [98.4, 'degrees fahrenheit'], 'Heart Rate or Pulse': [81.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [16500.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 98.4 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 66.4 = 36.88889 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 81.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 16500.0 count/µL. To convert 16500.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 16500.0 white blood cell count/µL * 1.0 µL/mm^3 = 16500.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6747,51,SIRS Criteria,diagnosis,integer,pmc-3297043-1,Extracted,"A 59-year-old man with diabetes, hypertension, and hypercholesterolemia who had undergone coronary angioplasty three and a half years earlier underwent CABG in September 2008. The postoperative course was uneventful, and the patient was discharged nine days after the bypass surgery. The patient had been well until February 2009, when progressive and intense chest pain around the sternal wound and shoulders developed, followed by malaise and weight loss (approximately 7 kg). One week before admission, the patient experienced purulent discharge at the sternal wound. On evaluation, he appeared tired and restless; his blood pressure was 120 × 70 mmHg, his pulse was 100 beats per minute, his temperature was 36.9°C, and his respiratory rate was 18 breaths per minute. There was hyperemia limited to the sternal wound; the remainder of the examination was normal. Laboratory results at the time of admission revealed a robust increase in plasma C-reactive protein (181 mg/dL); hemoglobin 9.7 mg/dl; leukocytes 10800/mm3 (neutrophils 73%, lymphocytes 19%); platelets 633.000/mm3; urea 40 mg/dL; and creatinine 0.82 mg/dL. A chest tomography scan showed no bone abnormalities. All aerobic and anaerobic blood cultures (three samples) were sterile, and empiric intravenous therapy with vancomycin (1000 mg 12/12 hours) plus ciprofloxacin (400 mg 12/12 hours) was started. After four days, purulent wound discharge was observed. Technetium-99 m/Gallium-67 scintillography confirmed osteomyelitis in the region of the sternal wound.
The patient underwent aggressive surgical debridement by thoracic and plastic surgeons with the removal of steel stitches, which revealed bilateral infection in the 3rd to 8th costal cartilages (), which were partially removed (), and vacuum-assisted closure (VAC) was used. The subject remained on VAC until new surgical debridement was performed bilaterally on the 6th ribs four days later (). The VAC device was removed, a Portovac® tube was inserted, and the wound was closed primarily (). The patient had a favorable clinical evolution, without signs of systemic disseminated infection. Cartilaginous-bone tissue biopsies from the first and second surgical procedures showed Aspergillus osteomyelitis. The culture from the surgically removed sternal bone demonstrated the presence of Aspergillus spp. Treatment with a combination of vancomycin and ciprofloxacin was discontinued, and intravenous voriconazole (4 mg/kg per dose twice daily) was started six days after the first surgery. The Portovac® tube was removed three days later, and the patient was discharged on the 18th day after the first surgical procedure. Intravenous voriconazole therapy was continued for a total of 42 days, when it was changed to oral capsules for 4 more months. After 3 months of voriconazole therapy, plasma C-reactive protein normalized, and Technetium-99 m/Gallium-67 scintillography showed no evidence of osteomyelitis. The patient currently remains very well, and the sternal wounds have healed completely.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.9, 'degrees celsius'], 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [10800.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.9 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 100.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 10800.0 count/m^3. To convert 10800.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 10800.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6748,51,SIRS Criteria,diagnosis,integer,pmc-8039197-1,Extracted,"A 24-year-old lady on APD for almost two years secondary to type 1 diabetes mellitus. She was first diagnosed with type 1 diabetes mellitus at the age of 7. She has diabetic proliferative retinopathy and diabetic neuropathy with no previous history of peritonitis. She had two previous admissions 10 years ago due of diabetic ketoacidosis. She presented to our PD Unit on April 2020 with a history of lower abdominal pain for 3-days duration. The pain was moderate in severity, non-radiating, with no relieving or aggravating factors. It was not associated with fever, nausea, vomiting or turbid discoloration of PD fluid. There was no history of urinary symptoms or diarrhea or previous episodes of peritonitis.
The patient was vitally and clinical stable Her physical examination showed blood pressure of 125/70 mmHg, pulse rate of 90/min, respiratory rate of 18/min and temperature of 37.8°C. She has left eye diabetic proliferative retinopathy in addition to bilateral legs neuropathy and dermopathy. Her abdominal examination showed no evidence of hepatosplenomegaly. Her superficial palpation revealed mild tenderness in hypogastric area. The rest of her clinical examinations were unremarkable. Her investigations were normal apart from white blood cell count of 4500/microliter, hemoglobin of 10.6 gm/dL and glycated hemoglobin of 6.7%. She was well controlled on glargine 20 at bedtime and aspart insulin 3 units with meals.
The PD fluid was clear with no exit site discharge. PD fluid analysis, gram stain and culture were requested, and the patient was treated as a case of peritonitis and 1gm of ceftriaxone IP and 1gm of vancomycin IP were given as per our protocol. Her PD fluid analysis confirmed the presence of peritonitis with WBC >200, however, the initial results of PD fluid gram stain and cultures as well as exit site cultures all came negative.
The patient was receiving her daily dose of IP ceftriaxone when the second aerobic culture of the peritoneal fluid confirmed the presence of Bacillus licheniformis. Upon further questioning, she admitted having a cat and a dog at home. The antibiotic regimen was changed to 1000 mg of Vancomycin at 4 days interval and adjusted according to Vancomycin blood level with target of 10–15 mg/liter. The patient recovered completely from her peritonitis and did not develop any recurrence of her peritonitis over 6 months follow up following her course of treatment with Vancomycin.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.8, 'degrees celsius'], 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [4500.0, 'µL']}",0,0,0,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.8 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 90.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 4500.0 count/µL. To convert 4500.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 4500.0 white blood cell count/µL * 1.0 µL/mm^3 = 4500.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 0.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 0.
Hence, the the number of SIRS criteria met by the patient is 0."
6749,51,SIRS Criteria,diagnosis,integer,pmc-4070362-1,Extracted,"A 76-year-old woman with a past medical history of diabetes mellitus, leukemia, and pancytopenia presented to the emergency department with a twelve-hour history of leg pain. On arrival, the patient was alert and afebrile with normal vital signs (temp 36°C, BP 114/68 mmHg, HR 80 bpm, and RR 14 breaths/min). Clinical examination was normal except for an intense pain in the left thigh, aggravated by movement, with no signs of edema or cellulitis. There was no evidence of crepitations or fluctuation on physical. Chest radiography and ECG were unremarkable. Initial blood tests revealed that leukocytes 860/mm3 (370 neutrophils), C-reactive protein 5, creatinine phosphokinase (CK) 360 U/L, d-dimer 1145 ng/mL, and biochemical analyses were normal. No abnormalities of the femur were detected on plain film radiography. Ultrasound exploration showed edema and fluid bands around the anterior thigh muscles with air-on-fascia between rectus femoris and vastus medialis (see ). A computed tomography (CT) scan confirmed the ultrasound findings (see ) and clindamycin with piperacilin/tazobactan was started. Urgent surgical debridement and excision of necrotic tissue were performed. Surgical findings revealed grey necrotic tissue, with lack of blood supply, and noncontracting muscle. 48 hours later further debridement of subcutaneous tissue and muscle was carried out. Within hours, the patient collapsed with hemolytic anemia and multiorganic failure and died shortly after. CP was isolated from both tissue and blood cultures.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.0, 'degrees celsius'], 'Heart Rate or Pulse': [80.0, 'bpm'], 'respiratory rate': [14.0, 'breaths/min'], 'White blood cell count': [860.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 80.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 860.0 count/m^3. To convert 860.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 860.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 8.6e-07 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 14.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6750,51,SIRS Criteria,diagnosis,integer,pmc-5863263-1,Extracted,"A 12-year-old girl was admitted to our unit with syncope. She had fainted after climbing the stairs. She was born to non-consanguineous parents. Her history was negative for systemic disease, and she denied taking any medicine or exposure to toxins. She had experienced two syncope attacks during exercise, four months previously.
By physical examination, her the heart rate was 95 beats min-1, respiratory rate was 25 min-1, and blood pressure was 90/55 mmHg. Body temperature was 37 °C. While she was awake, the respiratory sounds were diminished. Laboratory examinations showed leukocytosis (13.5000 mm3) and elevated acute phase reactants (erythrocyte sedimentation rate: 83 mm/h; C-reactive protein: 8.2 mg/dL). Chest X-ray showed bilateral diffuse pneumonic consolidation and mild cardiomegaly. Except for a stable ST depression, electrocardiography (ECG) was normal (). Echocardiography showed thickening of the mitral and aortic valves and mild mitral valve insufficiency. The left ventricle was mildly dilated, but systolic function was within normal limits (the ejection fraction was 68%). The troponin-1 level was high (66 mcg/dL, upper limit: 0.04 mcg/dL). Influenza A virus DNA was detected by respiratory viral panel screening. The toxicologic screening was negative. Throat, blood, and urine cultures were negative. Antistreptolysin O titer was within normal limits. Cranial computed tomography and electroencephalography were normal. We did not detect any arrhythmia by 24 h ambulatory electrocardiographic monitoring. Intravenous immunoglobulin was given for treatment of myocarditis. We started combined wide-spectrum antibiotics and antiviral oseltamire treatments. At the third day, she had no complaint; acute phase reactants and cardiac markers were negative. Normal cardiac size and clear lung fields were detected by chest X-ray. We stopped giving antibiotics after ruling out bacterial infection. However, there was a stable ST depression in the inferior leads by ECG. Coronary angiography by computed tomography displayed a suspected atheroma plague in the left anterior descending (LAD) aorta. Meanwhile, she had experienced another syncope attack. ECG showed an ST depression in the inferior leads, but the cardiac marker was negative. A cardiovascular stress test showed significant ST depression in the inferior leads (). Conventional coronary angiography revealed a significant occlusion of the LAD artery and circumflex artery (). High serum levels of total cholesterol (756 mg/dL) and LD-cholesterol (LDL-C) (556 mg/dL) were noticed. Carotid artery Doppler imaging showed moderate occlusion in both carotid arteries. When the patient’s medical history was re-taken, we found that her grandmother had been diagnosed with heterozygous familial hypercholesterolemia (HeFH) and underwent a coronary bypass surgery at 50-years-of-age. Her parents and 4-year-old sister’s blood analyses showed hypercholesterolemia, which was suggesting of HeFH. Diagnosis of HoFH was made in our case based on elevated plasma cholesterol levels, premature CAD, and positive family history. Her coagulation and thrombus panel and thyroid function tests were normal, and metabolic screening tests were negative. She had no tendon xanthomas. A coronary bypass surgery was performed between the left internal mammary arteries (LIMA) and LAD. Rosuvastatin, ezetimibe (a calcium-canal blocker drug), and aspirin treatments were started. After 1 year, she was in good condition and had no complaint. Her electrocardiography was normal. On echocardiogram, mitral and aortic regurgitations persisted. The LDL cholesterol level was slightly decreased (350-450 mg/dL), and we have planned lipid apheresis. She was consulted by the Pediatric Gastroenterology and Transplantation committee at our hospital. Meanwhile, the combined and high doses of ezetimibe and rosuvastatin therapy have resulted in a 37% reduction in her serum LDL level. She has remained free from treatment-related adverse responses, and CVD during follow-up and her parents did not accept liver transplantation. Written informed consent was obtained from the parents.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.0, 'degrees celsius'], 'Heart Rate or Pulse': [95.0, 'beats per minute'], 'respiratory rate': [25.0, 'breaths per minute'], 'White blood cell count': [13500.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 95.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 13500.0 count/m^3. To convert 13500.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 13500.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 25.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6751,51,SIRS Criteria,diagnosis,integer,pmc-2946668-1,Extracted,"A 48-yr-old man was transferred to our hospital with the diagnosis of AKI due to HAV infection requiring dialysis on June 4, 2009. He had been admitted to another hospital with general weakness and jaundice. The initial laboratory examination revealed the presence of IgM anti-HAV antibody, aspartate transaminase 1212 (5-45) IU/L, alanine transaminase 2,462 (10-40) IU/L, total bilirubin 7.8 (0.3-1.4) mg/dL, direct bilirubin 6.2 (0-0.4) mg/dL, gamma-glutamyl transpeptidase 102 (0-39) IU/L, hemoglobin 14.4 (13.1-17.2) g/dL, white blood cell count 14,700 (4,500-11,000)/µL, and platelet count 163,000 (150,000-400,000)/µL. The blood urea nitrogen (BUN) and creatinine were 43.6 (7-20) and 9.3 (0.7-1.3) mg/dL, respectively, and hemodialysis was started. He developed fever on day 4 before transfer and vancomycin was administered for possible catheter-related bacteremia. Upon presentation to our hospital, he was markedly jaundiced, and complained of weakness, fever, and rash. The vital signs were as follows: blood pressure, 200/100 mmHg; pulse rate, 108 beats/min; respiratory rate, 24/min; and body temperature, 38.1℃. There were no palpable lymph nodes. The BUN and creatinine levels rose to 85 and 15.2 mg/dL, respectively, and the total bilirubin level progressively increased to 21.8 mg/dL, with a normal prothrombin time. Viral markers, including Ebstein-Barr virus (EBV) and cytomegalovirus, were negative; HAV was positive. Urinalysis showed dark-colored urine with 2+ bilirubin, a trace of blood, and 1+ proteinuria. A 24-hr urine test revealed albuminuria (197.2 mg). The daily urine output was maintained at 1,500-2,000 mL with furosemide. A chest roentgenogram initially showed pulmonary congestion with a bilateral pleural effusion that was improved by furosemide. Abdominal ultrasonography showed normal sized kidneys with increased echogenecity and splenomegaly. On the 3rd hospital day, a kidney biopsy was performed and showed a diffusely edematous interstitium with infiltration of inflammatory cells and severely damaged tubules, findings which were compatible with ATIN. An immunohistochemical study identified the infiltrating cells as predominantly CD3+ T cells and CD68+ activated macrophages (). The glomeruli were relatively well-preserved. On the 8th hospital day, consolidation in both upper lobes developed. All microbiological culture studies were negative and no endobronchial lesions were detected. Despite catheter exchange and empirical antibiotics, a high fever, consolidation, and rash persisted. With hemodialysis and supportive care, liver and kidney dysfunction gradually improved, while anemia worsened and leucopenia and thrombocytopenia developed; the hemoglobin was 7.4 g/dL (hematocrit, 22.2%), the absolute neutrophil count was 130/µL, and the platelet count was 141,000/µL. Granulocyte-colony stimulating factor (G-CSF) was given. A bone marrow biopsy revealed a normocellular marrow with occasional hemophagocytosis (); there was no evidence of malignancy. The ferritin level was 2678 (17-390) ng/mL, the triglycerides were 493 (55-327) mg/dL, and the fibrinogen was 557 (225-457) mg/dL. VAHS was highly suspected and steroids were added to the treatment regimen. Upon steroid treatment, the fever, rash, and bilateral consolidation rapidly subsided. Hemodialysis was stopped after 13 dialysis sessions and renal function remained stable with a serum creatinine level of 1.7 mg/dL. He was discharged on a steroid taper in the outpatient clinic. The creatinine level declined to 1.3 mg/dL about 1 month later.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.1, 'degrees celsius'], 'Heart Rate or Pulse': [108.0, 'beats per minute'], 'respiratory rate': [24.0, 'breaths per minute'], 'White blood cell count': [14700.0, 'µL']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.1 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 108.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 14700.0 count/µL. To convert 14700.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 14700.0 white blood cell count/µL * 1.0 µL/mm^3 = 14700.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 24.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6752,51,SIRS Criteria,diagnosis,integer,pmc-4277835-1,Extracted,"A 62 year old female presented to the emergency room with history of fall from one storey building. The impact was over the trunk region. On clinical examination the blood pressure was 90/60 mmHg, pulse rate was 110/min, temperature was 98.6 degree Farenheit and respiratory rate was 20/min. Pallor was present and the thyroid gland was enlarged. Pansystolic murmur was present over the mitral and tricuspid regions. Fine basal crepitations were heard over both lung fields. Left upper quadrant tenderness was present.
A complete blood count showed pancytopenia with hemoglobin 7.4gm/dl (normal: 12–16 gm/dl), WBC count 3400/μl (normal: 4000–11,000/μl) and platelet count 91,000/μl (normal 1,50,000-4,00,000/μl). Multiple ventricular premature complexes were present in the electrocardiogram (ECG). Ultrasound of the abdomen showed splenic laceration with splenic hematoma extending up to the hilum. Contrast enhanced computed tomography of the abdomen showed findings consistent with grade II splenic injury.
The patient was admitted to the intensive care unit (ICU) for conservative management and further workup with the impression of grade II splenic injury and pancytopenia.
Ultrasound of the neck showed multiple heteroechoic nodules with calcification in both lobes of thyroid, findings suggestive of multinodular goiter. Echocardiography showed severe tricuspid regurgitation and mitral regurgitation. Bone marrow aspiration showed mixed normocellular and a few hypercellular marrow fragments. Absolute retics and peripheral blood smear were normal. Hormonal studies showed features suggestive of hyperthyroidism (Table ).
The patients hemoglobin improved with two units of packed cells transfusion but the WBC and platelet count didn’t improve. On the third day of admission, she developed a temperature of 102 degree Farenheit, pulse rate of 150-160/min, respiratory rate of 30/min and oxygen saturation of 75-80% at 5 L/min of oxygen via face mask. On examination the patient was agitated and had diffuse crepitations over both lung fields. On ECG monitoring multiple VPCs per minute was present. A Burch Wartofsky Score of 95 was calculated (Table ). With the impression of thyroid storm, the patient was started on hydrocortisone, oral propranolol 40 mg q6hrly (intravenous preparation not available), and oral carbimazole 10 mg q8hrly. After 24 hours the patients pulse rate stabilized between 80–100 bpm, temperature was 99 degree farenheit and there were only few VPCs per minute. Propranolol was gradually tapered over a period of one week and her pulse rate stabilized at 60 to 80 bpm. After starting carbimazole, her WBC and platelet counts started improving and became normal at discharge (Table ).
The patient was advised for radionuclide thyroid scan and further treatment.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [102.0, 'degrees fahrenheit'], 'Heart Rate or Pulse': [150.0, 'beats per minute'], 'respiratory rate': [30.0, 'breaths per minute'], 'White blood cell count': [3400.0, 'µL']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 102.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 70.0 = 38.88889 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 150.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 3400.0 count/µL. To convert 3400.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 3400.0 white blood cell count/µL * 1.0 µL/mm^3 = 3400.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 30.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6753,51,SIRS Criteria,diagnosis,integer,pmc-4531545-1,Extracted,"A 23-year-old Asian man with chronic renal allograft dysfunction was admitted to our hospital in May 2001 with a 10-day history of fever, intermittent chills, dry cough and progressive dyspnea. He underwent renal transplantation in 1994 for end-stage renal disease of unknown cause diagnosed in 1993. He had been on a medication of cyclosporine 200 mg/day and prednisolne 5–20 mg/day. His temperature was 40°C, blood pressure 120/70 mmHg supine, pulse rate 120/min and respiratory rate 20/min. Respiratory examination revealed mildly decreased breathing sounds on the right lower chest. We also noted several erythematous tender macules measuring 0.5 cm in diameter on both shins. He had no neurological signs of meningitis. Chest radiograph obtained on admission demonstrated increased opacity on the right lower lobe. Arterial blood gas analysis on room air revealed a pH of 7.38, PaCO2 22.1 mmHg, PaO2 49.4 mmHg, and SaO2 85.3%. A complete blood count yielded a leukocyte count of 5,600/mm (91.6% neutrophils), hemoglobin 5.6 g/dL, and platelet count 267,000/mm3. The renal allograft function was in acute exacerbation on chronic dysfunction; BUN 113 mg/dL, Cr 8.5 mg/dL, Na 125 mmol/L, K 6.4 mmol/L, protein 5.2 g/dL, albumin 2.9 g/dL, glucose 102 mg/dL. The patient had been treated with empirical antibiotics for the presumed diagnosis of severe community-acquired pneumonia. On the next day, his respiratory status deteriorated dramatically with a rapid development of hypotension. A repeat chest radiograph showed nearly complete opacification of both lung fields (). The patient was intubated and placed on mechanical ventilation. Dobutamine and dopamine were administered. Urgent anti-CMV IgM, CMV PCR and anti-HIV were negative. Anti-mycoplasma antibody titer was <1:20. Acid-fast bacillus smear and methenamine silver stain of sputum yielded negative results. The initial three sputum and blood cultures were sterile. On the eighth hospital day, tender macules on both shins coalesced to form erythematous patches. Skin biopsy showed granulomatous inflammation in the dermis and numerous yeast organisms with clear thick capsules (). The cerebrospinal fluid (CSF) exam was clear with normal glucose and slightly increased protein (95 mg/dL). The cryptococcal antigen titer was elevated in CSF at >1:256 and at >1:516 in serum. However, the microscopic examination of CSF preparations with India ink was negative for encapsulated yeasts and CSF cultures were negative. The culture of skin biopsy isolated a yeast organism, which was identified as Cryptococcus albidus by characteristic morphology, fermentation, and carbon assimilation tests using the API 20c AUX system (bioMérieu, Marcy-l’Etoile, France). The patient was treated intravenously with fluconazole immediately after the skin biopsy. After 10 days of fluconazole therapy, his chest radiograph and CT scan showed marked clearing with only one cavitary nodular lesion on the left upper lobe (). Percutaneous needle aspiration was performed for the left upper pulmonary nodule. Cytologic examination of the aspirates also revealed a typical morphology of the numerous cryptococci (). The patient was discharged on an oral regimen of fluconazole (200 mg/day). Fluconazole maintenance therapy was continued for 12 months on a long-term basis for prevention of cryptococcosis. At the time of the most recent follow-up, July 2002, his chest radiograph was stable and we detected no evidence of recurrent cryptococcal infection.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [40.0, 'degrees celsius'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [5600.0, 'mm^3'], 'PaCO2': [22.1, 'mm hg']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 40.0 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 120.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 5600.0 count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 22.1 mm Hg, which is less than than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6754,51,SIRS Criteria,diagnosis,integer,pmc-7575311-1,Extracted,"A 61-year-old woman was admitted to the hospital with fever, leukocytosis, and severe pain in the anal area. The patient had been in her usual state of health until seven days before this admission, when perianal pain developed. She was evaluated by her primary care physician, who found an erythematous area in her perianal skin and prescribed her a course of oral clindamycin and an antibiotic cream. Seven days later, she returned to her primary care physician because her pain worsened. Ketorolac and empiric ceftriaxone were administered, and she was sent to the emergency department.
In the emergency department, the patient presented with severe perianal pain. She had a history of diabetes mellitus, hypertension, obesity, hypercholesterolemia, and hypothyroidism. Her medications included telmisartan, dapagliflozin, exenatide, atorvastatin, and levothyroxine. Shortness of breath, cough, smell or taste disturbances, and myalgia were not reported. No suspected or known exposure to SARS-CoV-2 was reported. On examination, the temperature was 100.1°F, blood pressure 110/52 mmHg, heart rate was 85 beats per minute, respiratory rate was 19 breaths per minute, and the oxygen saturation was 100% while the patient was breathing ambient air. The lungs were clear on auscultation. In the perianal area, there was an abscess that had begun to drain spontaneously. The white cell count was 11,400/µL (reference range: 4,800-10,900/µL), lactic acid was 2.32 mmol/L (reference range: 0.5-1.99 mmol/L), and anion gap was 14 mEq/L (reference range: 2-12 mEq/L). A decision for admission of the patient was made; therefore, a SARS antigen fluorescent immunoassay (FIA) screening test was performed, and the result was negative. Morphine and acetaminophen were administered for pain and fever. The surgery department was consulted, and a combination of vancomycin with piperacillin-tazobactam was recommended. In addition, a CT of the abdomen and pelvis was performed after the administration of intravenous contrast material.
The abdominopelvic CT scan revealed a loculated fluid collection posterior to the anus consistent with an abscess. In addition, there were peripheral ground-glass opacities in both imaged lung bases (Figure ). Five hours after the initial presentation, the patient was admitted. A nasopharyngeal swab was obtained for NAAT. Six hours after admission, the test was positive for SARS-CoV-2 RNA and the patient was transferred to the COVID-19 unit. A posteroanterior radiograph of the chest was performed, and the radiologist reported slightly increased interstitial markings, especially in the lung bases. Ten hours later, incision and drainage of the patient’s abscess were successfully performed in the operating room. The postoperative diagnoses included horseshoe perirectal abscess, perianal abscess, and asymptomatic SARS-CoV-2 infection. No specific therapy for COVID-19 was administered to the patient because she had no respiratory symptoms.
Three days after admission, a chest radiograph was performed, which did not reveal any abnormalities. The next day, the patient continued without any respiratory symptoms, and the perianal pain had significantly decreased. The vital signs were normal. The white cell count, the value of the serum anion gap, and the serum lactate levels were normal. The patient was subsequently discharged home with a prescription of levofloxacin. During her follow-up visit with the surgery department 36 days later, she did not report any symptoms whatsoever.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [100.1, 'degrees fahrenheit'], 'Heart Rate or Pulse': [85.0, 'beats per minute'], 'respiratory rate': [19.0, 'breaths per minute'], 'White blood cell count': [11400.0, 'µL']}",0,0,0,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 100.1 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 68.1 = 37.83333 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 85.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 11400.0 count/µL. To convert 11400.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 11400.0 white blood cell count/µL * 1.0 µL/mm^3 = 11400.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 0.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 19.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 0.
Hence, the the number of SIRS criteria met by the patient is 0."
6755,51,SIRS Criteria,diagnosis,integer,usmle-225,Extracted,"A 79-year-old woman comes to the physician for the evaluation of a 2-month history of a non-productive cough and fatigue. During this period, she also has had a 4.5-kg (10-lb) weight loss and has become increasingly short of breath with mild exertion. She has congestive heart failure and hypertension. Three months ago, she was in India for 3 weeks to attend a family wedding. She worked as a seamstress in a textile factory for 50 years. She has smoked one pack of cigarettes daily for 47 years. Her current medications include enalapril, digoxin, isosorbide, spironolactone, and metoprolol. She appears thin. Her temperature is 37.0°C (98.6°F), pulse is 90/min, respirations are 25/min, and blood pressure is 110/70 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 94%. There is dullness to percussion and decreased breath sounds over the right lung base. The remainder of the examination shows no abnormalities. Laboratory studies show a glucose level of 90 mg/dL, serum lactate dehydrogenase of 227 U/L, and serum protein of 6.3 g/dL. An x-ray of the chest shows nodular pleural lesions on the right side and a moderate-sized pleural effusion. Thoracentesis shows 250 ml of turbid fluid.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.0, 'degrees celsius'], 'Heart Rate or Pulse': [90.0, 'beats per minute'], 'respiratory rate': [25.0, 'breaths per minute'], 'White blood cell count': [4000.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 90.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 4000.0 count/m^3. To convert 4000.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 4000.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 4e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 25.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 1 + 1 = 2 criteria met.
Hence, the the number of SIRS criteria met by the patient is 2."
6756,51,SIRS Criteria,diagnosis,integer,pmc-6349969-1,Extracted,"A 57-year-old Caucasian woman with a past medical history of a provoked pulmonary embolism (04/2017), T2DM, hypertension, hyperlipidemia, and chronic headaches presented to the emergency department complaining of left-sided pelvic pain for the past 2 months. At this time, the patient also complained of diarrhea and fever for the past 2 months. The patient states the pelvic pain had increased gradually and had progressively gotten more painful. The pain was sharp, 10 out of 10 and radiated to the back and to the left hip. The patient stated the pain was constant and aggravated by movement. She also complained of non-bloody, loose diarrhea for the past 2 months with no resolution. The patient admitted to an episode of fever at home registering at 102.4°F. Upon further questioning, the patient had experienced proximal muscle weakness, with difficulty combing her hair and reaching for items above her head. The proximal muscle weakness was present in the shoulders and the hips bilaterally. The patient had experienced gait abnormalities secondary to the muscle weakness, causing her to lose balance on multiple occasions, but denies any falls. She stated the proximal muscle weakness was present prior to the onset of her localized pelvic pain. The patient had completed therapy with an anticoagulant for her pulmonary embolism and denies recent antibiotic use. She further denied any trauma, vision changes, chest pain, dyspnea, or blood in the stool. Review of systems was otherwise unremarkable. Patient denies current or prior diagnosis of retinopathy, nephropathy, or peripheral neuropathy.
Family history was significant for a father with T2DM, a sister with Friedreich’s ataxia, a first cousin with an unknown autoimmune disorder, a maternal uncle with colon cancer, and a paternal aunt with breast cancer.
Vital signs on admission were as follows: blood pressure, 150/73 mmHg; heart rate, 101 beats/min; respiratory rate, 20 breathes/min, temperature, 101.9°F; and oxygen saturation, 97% on room air. General physical examination revealed a patient who is alert and oriented, cooperative but in mild distress. Head, eyes, ears, nose, and throat examination (HEENT) was negative for facial edema, rashes, or visual defects. Abdominal exam was significant for left lower quadrant pain on superficial and deep palpation. Musculoskelatal exam revealed tenderness to palpation in the left anterior and lateral hip, with reduced range of motion (ROM) in both hips; the left more affected than the right. Upper extremities were non-tender and had full ROM. No rashes, lesions, or signs of trauma noted on skin examination. Neurological exam revealed normal muscle strength and deep tendon reflexes (DTRs) in both upper extremities. Motor strength was 2/5 in the left lower thigh and 3/5 in the right lower thigh, and DTR was 2+ in both lower extremities, including achilles and patellar tendons. Bedside monofilament test revealed no sensory deficits in the lower extremities. Cardiovascular and pulmonary examinations were normal.
Initial lab work up upon admission revealed mild anemia (hemoglobin: 10.1 g/dL and hematocrit: 31.5%) but no leukocytosis (white blood cells 10.6 K/uL). A comprehensive metabolic panel (CMP) revealed a low albumin (2.8 g/dL), a total protein of 7.9 g/dL, calcium of 9.1 mg/dL (10 mg/dL when corrected), blood urea nitrogen (BUN) and creatinine of 21 and 0.9 mg/dL, respectively, and a high serum glucose (296 mg/dL). Hemoglobin A1c was 9.7%. Blood and urine cultures were obtained to rule out an infectious systemic process. Serum protein electrophoresis (SPEP) and urine protein electrophoresis (UPEP) were obtained for a mildly increased protein gap and anemia. Blood cultures, urine cultures, SPEP, and UPEP were all negative. At this point, a myositis workup had been initiated secondary to proximal muscle weakness and reduced ROM on physical exam. Serum levels of creatine kinase (CK) were obtained on two separate occasions. In addition, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), lactate dehydrogenase (LDH), and aldolase were also obtained. CK levels, LDH, and aldolase were within normal limits; however, ESR (112 mm/h) and CRP (125.5 mg/L) were markedly elevated. Furthermore, specific markers for inflammatory myositis and general autoimmune pathologies were negative, including anti-Mi-2, anti–signal recognition particle (SRP), anti-Jo-1, antinuclear antibody (ANA), and anti-Smith/ribonucleoprotien (Sm/RNP).
An abdominal and pelvic computed tomography (CT) scan was obtained on day of admission with benign, non-specific findings. A follow-up abdominal and pelvic magnetic resonance imaging (MRI) with and without contrast was subsequently obtained 48 h later and had revealed edema ventral to the psoas and iliacus muscles bilaterally, enhancement of the left iliacus muscles () and asymmetrically enlarged left iliacus in comparison to the right ().
Basic lab work and vitals were monitored daily since admission with no significant changes noted. An extensive workup resulting in lack of conclusions had warranted a rheumatology consult, leading to a diagnosis of diabetic myonecrosis of the left iliacus muscle. Further inspection of laboratory results revealed an average serum glucose of 250 mg/dL and an extensive history of a hemoglobin A1c averaging around 10%. The patient was made aware of the diagnosis and informed of the conservative management of her diabetic myonecrosis. The patient’s medication list was reassessed and her oral metformin was discontinued. In addition, the patient’s previous basal insulin dose was increased with the introduction of bolus/prandial injections for better glycemic control.
The patient was seen during her follow-up visit with her primary-care physician approximately 6 weeks after discharge. Patient continues to have mild discomfort in the left pelvic area but reports significant improvement in both pain and ROM.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [101.9, 'degrees fahrenheit'], 'Heart Rate or Pulse': [101.0, 'beats/min'], 'respiratory rate': [20.0, 'breaths/min'], 'White blood cell count': [10600.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 101.9 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 69.9 = 38.83333 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 101.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 10600.0 count/µL. To convert 10600.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 10600.0 white blood cell count/µL * 1.0 µL/mm^3 = 10600.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6757,51,SIRS Criteria,diagnosis,integer,pmc-7814990-1,Extracted,"In January 2016, a 68-year-old woman with a medical history of hypertension, dyslipidemia, old cerebral infarction, and mild dementia was admitted to the emergency department with unconsciousness, disquiet, and severe anasarca. She had been bedridden and living alone. On the particular day with an outside temperature of approximately 0°C, she was lying on the bed at home without heating. Her relatives noticed that she was unconscious and called for an emergency. Her initial heart rate was 15 b.p.m., respiration rate was 8/min, blood pressure and O2 saturation could not be measured, and urinary bladder temperature was 25.4°C. Respiratory acidosis (pH 7.092, PO2 65 mm Hg, and PCO2 80 mm Hg) was observed in arterial blood gas. The following laboratory results were obtained: white blood cell count 15.4 × 103/μL, hemoglobin 10.8 g/L, platelet count 446 × 103/μL, C-reactive protein 4.57 mg/mL, total bilirubin 0.5 mg/mL, aspartate transaminase 69 U/L, alanine transaminase 52 U/L, lactate dehydrogenase 266 U/L, blood urea nitrogen 30.0 mg/mL, creatinine 1.06 mg/dL, sodium 140 mEq/L, potassium 4.7 mEq/L, and chloride 104 mEq/L.
According to her initial vital signs, she immediately underwent tracheal intubation without anesthesia and given i.v. atropine 0.5 mg to improve breathing and cardiac output, respectively. After an i.v. injection of atropine, an ECG revealed 85 b.p.m. with indeterminate rhythm, wide QRS complexes, and prominent J waves at the end of the QRS, with the highest amplitude recorded in limb leads I and II and precordial leads V3–6 (Fig. ). External and internal heating (2°C per hour) was immediately applied using an electric heat blanket, a forced-air warming device, and a respiratory warming/humidifying device, because there were no extracorporeal circulation circuit devices in the hospital at this time. Consecutive ECG monitoring during external heating showed that the J-wave amplitude decreased with the increase in the urinary bladder temperature, and the J wave disappeared at 32°C (Fig. ). Rewarming by external heating was continued until the core body temperature reached 36°C. After the patient regained consciousness, she was extubated the next morning. During rewarming therapy, ventricular premature contractions were observed, but no lethal arrhythmia was observed. The patient had severe systemic edema. A diuretic was used to reduce the body fluid for a while, and she was discharged after complete recovery after 1 month.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [25.4, 'degrees celsius'], 'Heart Rate or Pulse': [15.0, 'beats per minute'], 'respiratory rate': [8.0, 'breaths per minute'], 'White blood cell count': [15400.0, 'µL'], 'PaCO2': [80.0, 'mm hg']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 25.4 degrees celsius. Because the temperature is less than 36 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 15.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 15400.0 count/µL. To convert 15400.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 15400.0 white blood cell count/µL * 1.0 µL/mm^3 = 15400.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 8.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 80.0 mm Hg, which is greater or equal to than 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6758,51,SIRS Criteria,diagnosis,integer,pmc-7592528-1,Extracted,"An eight-year-old boy without significant past medical history was brought to the outpatient department by his parents with a four-day history of non-documented, low-grade intermittent fever, which became persistent from the very next day. There were no associated symptoms at the time of the presentation. Additionally, parents reported no history of sore throat, cough, nausea, vomiting, and bowel and bladder abnormalities. There was no history of any drug intake, contact with a sick patient, or known exposure to someone COVID-19 positive. Initial evaluation revealed a temperature of 99°F, blood pressure (BP) of 115/75 mmHg, heart rate (HR) of 90 beats/minute, respiratory rate (RR) of 18 breaths/minute, and oxygen saturation (SpO2) of 98% while breathing ambient air.
The patient was discharged on acetaminophen (Tylenol). The next day, the patient presented with a fever again, but this fever was accompanied by lethargy and tachypnea. He also developed mild-to-moderate maculopapular eruptions all over the body with sandpaper-like texture and a mild degree of bilateral conjunctivitis.
He was admitted to the pediatric floor, and per hospital protocol, reverse transcriptase-polymerase chain reaction for COVID-19 was also advised along with other laboratory investigations. Physical examination at the time of the second presentation demonstrated a temperature of 100°F, BP of 105/75 mmHg, HR of 95 beats/minute, RR of 27 breaths/minute, and SpO2 of 91%. His workup revealed the following: white blood cell count of 10 x 109/L, a prothrombin time of 19.3 seconds, an activated partial thromboplastin time of 33.2 seconds, C-reactive protein (CRP) of 41 mg/L, an erythrocyte sedimentation rate (ESR) of 30, and a D-dimer concentration of 1.8 µg/ml. A chest x-ray (CXR) showed a parenchymal opacification in the left upper lobe with pleural effusion on the same side (Figure ). His COVID-19 test result was negative.
The patient was empirically started on 1.2 g of intravenous (IV) ceftriaxone and 320 mg of IV vancomycin three times per day in normal saline at a slow rate. In addition, echocardiography was performed. On the following day, his fever was 101°F, and his SpO2 started dropping dramatically to 85% along with worsening tachypnea. He was started on supplemental oxygen at 2 L/min via face mask. A portable CXR was done, which showed worsened inflammatory changes with local patchy infiltrates in the right middle lobe (Figure ).
The echocardiography findings were unremarkable. Blood serology for measles was negative. Additionally, a strep throat test result was negative. After carefully ruling out all possible differentials like a drug-induced allergic reaction and infections (e.g., SSSS, scarlet fever, measles, varicella), the patient was highly suspected of having atypical KD based on the clinical presentation and history of fever. He was also started on high-dose IV immunoglobulins (IVIG) at 2 g/kg on day one (given the patient weighed 24 kg) along with a high dose of aspirin (80 mg/kg/day every six hours) as per guidelines. Moreover, an anti-severe acute respiratory syndrome-coronavirus-2 serologic test result was positive, with an immunoglobulin G titer level of 2.1. Hence, he was diagnosed with COVID-19-associated atypical KD.
Twenty-four hours after completion of IVIG, his breathing issues started resolving. His repeated CXR showed mild inflammatory changes without any new lung infiltrates or lesions. Additionally, his fever also subsided, and the rash started disappearing. His daily temperature chart is shown in Figure . On day six, he was discharged from the hospital on a low dose aspirin of (5 mg/kg/day) as maintenance therapy. On his follow-up visit, the patient was doing well.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [101.0, 'degrees fahrenheit'], 'Heart Rate or Pulse': [95.0, 'beats/minute'], 'respiratory rate': [27.0, 'breaths/minute'], 'White blood cell count': [10000.0, 'L']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 101.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 69.0 = 38.33333 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 95.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 10000.0 count/L. To convert 10000.0 count/L of white blood cell to mm^3, multiply by the conversion factor 1e-06 L/mm^3 which will give 10000.0 white blood cell count/L * 1e-06 L/mm^3 = 0.01 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 27.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6759,51,SIRS Criteria,diagnosis,integer,pmc-6343228-1,Extracted,"An HIV-infected 32-year-old male presented to Mulago National Referral Hospital, Uganda with a 2-week history of headache with fevers and a 1-day history of confusion (
). He had been on ART (zidovudine, lamivudine, efavirenz) and co-trimoxazole prophylaxis for 5 years. 5 months prior, he was diagnosed with pulmonary TB by positive sputum Xpert MTB/RIF (Cepheid, Sunnyvale, CA, USA). He had completed 2 months of induction TB therapy (rifampicin, isoniazid, ethambutol, pyrazinamide) and was 3 months into continuation phase (rifampicin, isoniazid). He endorsed poor adherence to both ART and anti-tuberculous medications.
On examination, the patient was febrile (38.6°C). His blood pressure was 112/71 mmHg, pulse 94 beats/minute, respiratory rate 48, and oxygen saturation 98%. He was wasted, dehydrated, and had overt rigors. His Glasgow Coma Scale was 14/15 with nuchal rigidity and positive Kernig’s sign. Cranial nerves were intact. He had normal tone and power in all limbs. A clinical diagnosis of HIV-associated meningitis was suspected and he was recruited into the ‘Improving Diagnostics and Neurocognitive Outcomes in HIV/AIDS-related Meningitis’ study (registration:
). Whilst awaiting further investigations, he received empiric therapy of ceftriaxone 2 g twice daily for possible bacterial meningitis.
A finger stick cryptococcal antigen lateral flow assay (CrAg LFA) (IMMY, Norman, Oklahoma, USA) was negative. Liver and renal function tests were normal. Cerebrospinal fluid (CSF) opening pressure was elevated to 33 cm CSF (normal <20 cm CSF), CSF white cells 590 /µl, protein 419 mg/dl (normal range 15–45 mg/dl), CSF lactate 9.5 mmol/L (normal range <2.5 mmol/l). CSF glucose was unavailable.
Mycobacterium tuberculosis in CSF was confirmed on Xpert MTB/RIF Ultra; there was no evidence of rifampicin resistance. On day 2, he was initiated on dexamethasone at 0.4 mg/kg/day and induction TB-medications were re-commenced (rifampicin, isoniazid, ethambutol, pyrazinamide) for TBM. The IV ceftriaxone was stopped, his ART was continued. He continued to spike high-grade fevers (39.6°C.) with tachycardia (pulse 118 beats/min). A peripheral blood smear showed
P. falciparum parasites (1+ trophozoites), despite a negative malaria histidine rich protein-2 (PfHPR2)-based rapid diagnostic test (Malaria
Plasmodium falciparum Rapid Test Cassette, Vaxpert, Florida, USA). Given his ongoing neurological symptoms, which could be compatible with cerebral malaria, the decision was made to treat for severe malaria. Drug-drug interactions (DDIs) between rifampicin and artemisinin compounds, and rifampicin and quinine are recognized (
); a decision was made to treat with IV artesunate as the most efficacious anti-malarial for severe malaria
. He received three doses of IV artesunate (3 mg/kg), after which a repeat peripheral blood smear showed no malaria parasites. He then completed 3 days of oral artemether/lumefantrine. His fevers subsided on day 6. He was discharged on day 8; medication adherence counselling was provided for the patient and his guardian and outpatient follow-up was arranged for the following week.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.6, 'degrees celsius'], 'Heart Rate or Pulse': [94.0, 'beats per minute'], 'respiratory rate': [48.0, 'breaths per minute'], 'White blood cell count': [590.0, 'µL']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.6 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 94.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 590.0 count/µL. To convert 590.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 590.0 white blood cell count/µL * 1.0 µL/mm^3 = 590.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 48.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6760,51,SIRS Criteria,diagnosis,integer,pmc-4528891-1,Extracted,"Our patient is a 33-year-old African American woman with a past history of hypertension and hypothyroidism who had repeated emergency room visits for pleuritic chest pain and dyspnea. On her initial presentation to the emergency room, she reported intermittent pleuritic pain in the right anterior region of her chest. The pain was described as 10/10 in severity, increased with both inspiration and palpation of the chest wall, and radiated into her back. Her pain was aggravated with walking and while lying flat to the point that she was sleeping on 3 or more pillows. The patient also reported a mild productive cough with clear-yellow sputum and some blood. She had no dysphagia. On chest x-ray, she had bilateral lower lobe and lingular airspace consolidation prompting the diagnosis of community-acquired pneumonia. The patient was treated with a 7-day course of antibiotics and antitussive medications. Over the next 4 months, the patient returned to the emergency room 5 times with similar complaints of pleuritic chest pain and dyspnea. She also noted pain in the neck, both arms, and upper back during this 4-month course. At her last emergency department visit, the patient still complained about left arm pain associated with paresthesias. Repeat imaging of her chest continued to show lower lobe consolidation/atelectasis. Since her symptoms had failed to improve with multiple courses of antibiotics, she was admitted to the internal medicine service for further evaluation.
The patient had a past history of hypertension and hypothyroidism. She had no history of recent surgery, trauma, infection, or radiation. Her family history was positive for hypertension in her father and lung cancer in her grandmother but negative for connective tissue disease. She was married, worked as a nurse’s aide, had an occasional alcoholic drink, and smoked 1 cigarette per day.
Initial vital signs included blood pressure 131/87 mm Hg, pulse rate 109 beats per minute, respiratory rate 18 breaths per minute, temperature 99.4°F, and oxygen saturation 98% on room air. Initial complete blood count included white blood cells 5300/µL, hemoglobin 9.5 gm/dL, and platelet count 278 000/µL. The initial complete metabolic panel was normal except for a low K+ (3.4 mmol/L). Creatine kinase was 29 IU/L (normal = 26-308 IU/L). The thyroid-stimulating hormone level was normal off thyroid replacement therapy. The erythrocyte sedimentation rate (ESR) was121 mm/h (normal = 0-20), and the C-reactive protein (CRP) level was 8.2 mg/dL (normal = 0-0.5). Other laboratory tests included a positive ANA using the BioPlex 2200 ANA screen (BioRad Laboratories, Inc, Hercules, CA). Additional testing included a positive chromatin with an Antibody Index (AI) of 2.9 (normal = 0.2-1.0). Anti-double stranded DNA and anti-Smith antibodies were negative. SS-A antibody was 8 AI (normal = 0.2 to1.0); the SS-B antibody was negative. The rheumatoid factor (RF) was 20 IU/mL (normal < 14), and the cyclic citrulline peptide was negative. The anti-RNP antibody was >8.0 AI (normal = 0.2-1.0). Blood cultures were negative. Her echocardiogram revealed a small atrial septal defect, mild pulmonary hypertension with right ventricular systolic pressure of 35 to 40 mm Hg, and an ejection fraction of 65% to 69%. The pulmonology medicine consultant noted that the patient had poor inspiratory expansion of the lower thorax, paradoxical movement of her abdomen, and bilateral basilar crackles. Her voice was normal. Neurosurgery was consulted and documented normal strength in the arms and legs, normal sensation to light touch, normal proprioception, normal reflexes, and normal coordination. Magnetic resonance imaging (MRI) of the cervical spine showed only some mild degenerative changes and no evidence of focal lesions that could cause radiculopathy. A fluoroscopic “sniff” test showed no movement of the left diaphragm and reduced movement on the right, consistent with bilateral phrenic nerve involvement and respiratory muscle weakness. She was subsequently prescribed muscle relaxants, pulmonary hygiene with a vibratory therapy system, incentive spirometry, and pain medication, including indomethacin for symptomatic relief. Her pain and dyspnea improved somewhat, and she was discharged home.
While in the hospital, she was started on incentive spirometry and an albuterol inhaler 1 to 2 puffs every 6 to 8 hours. Her inhalation volume on incentive spirometry was 500 mL initially in the hospital, 1000 mL after 1 month, and 1500 mL after 2 months. Pulmonary function tests done 2 months after the initial hospitalization revealed a forced expiratory volume in 1 second (FEV1) 1.4 L (43.9% predicted), forced vital capacity (FVC) 1.9 L (47.3% predicted), FEV1/FVC ratio 0.77, total lung capacity 3.7 (60.8% predicted), a normal residual volume 1.7 L (105.2% predicted), and a severely reduced diffusing capacity for carbon monoxide (36.4% predicted) that partially corrected with adjustment for alveolar volume (67.7% predicted). Pulmonary function tests were consistent with a severe restrictive ventilatory defect with a reduced diffusion capacity.
Two months later the patient described her chest pain as markedly improved compared to her first admission. She reported her pain at rest as 3/10, mild in intensity, in the lower part of her rib cage but nonradiating, and aggravated with daily routine activities. She denied fever, chills, nausea, vomiting, and joint pain in her hands but still reported mild shortness of breath at rest. She had had several visits to a rheumatologist who started her on a regimen of hydroxychloroquine, methotrexate, and low-dose prednisone (5 mg daily) for suspected lupus and seropositive rheumatoid arthritis and eventually added leflunomide and etanercept. The patient noted some symptomatic relief on this new regimen but now noticed her fingers turning white in cold temperatures. Over a 1-year follow-up period she had persistent pain and some joint tenderness on palpation but no synovitis. Repeat ANA was positive 3 months later, and a repeat ESR was 95 mm/h 6 months later. Skeletal x-rays done 6 months after her initial presentation with chest pain showed no evidence of rheumatoid arthritis.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [99.4, 'degrees fahrenheit'], 'Heart Rate or Pulse': [109.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [5300.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 99.4 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 67.4 = 37.44444 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 109.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 5300.0 count/µL. To convert 5300.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 5300.0 white blood cell count/µL * 1.0 µL/mm^3 = 5300.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6761,51,SIRS Criteria,diagnosis,integer,pmc-7559645-1,Extracted,"A 55-year-old male patient presented to the Gastroenterology Department of West China Hospital for dysphagia and weight loss for 1 mo.
The patient suffered dysphagia while eating solid or semi-solid food and lost 6 kg in 1 mo. He also felt slight retrosternal pain while changing position, without reflux, vomit, fever, or cough.
The patient had no specific previous illness or family history. On average, the patient had a smoking history of 60 cigarettes a day for 30 years and a drinking history of 80 g/d for 20 years.
At admission, the patient’s temperature was 36.5 °C, heart rate was 76 bpm, respiratory rate was 20 breaths per minute, blood pressure was 119/89 mmHg, oxygen saturation in room air was 99%, height was 172 cm, and weight was 63 kg. No other special finding was reported.
A routine blood test indicated leukocytosis with the white blood cell count at 12.08 × 109/L (normal range, 3.5 × 109/L to 9.5 × 109/L) and mainly neutrophils (81.9%; normal range, 40%-75%). The hemoglobin concentration and platelet count were normal. The serum albumin concentration had declined to 29.9 g/L (normal range, 40–55 g/L). The serum C-reactive protein concentration had increased to 74.8 mg/L (normal range, < 5.0 mg/L), and the erythrocyte sedimentation rate was 60 mm/h (normal range, < 21.0 mm/h). The serum tumor markers, including CEA, AFP, and CA 19-9, had normal concentrations.
An X-ray barium meal examination showed a huge intraluminal stalk-like mass along the middle and lower esophagus (Figure ). Computed tomography (CT) showed a prominently enhanced anterior area of the mass beside the esophageal wall, and the maximum sectional area was about 5.6 cm × 3.5 cm (Figure ). Endoscopy indicated that the mass was polypoid, gray-white, with a bulky pedicle, located in the esophagus 22-45 cm from the incisors and almost filled the whole esophageal lumen, but the endoscope could still pass through (Figure ).",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.5, 'degrees celsius'], 'Heart Rate or Pulse': [76.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [12.08, 'L']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.5 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 76.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 12.08 count/L. To convert 12.08 count/L of white blood cell to mm^3, multiply by the conversion factor 1e-06 L/mm^3 which will give 12.08 white blood cell count/L * 1e-06 L/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6762,51,SIRS Criteria,diagnosis,integer,pmc-6743666-1,Extracted,"A 49-year-old woman was admitted to the hospital for the evaluation of mild nausea and abdominal pain, which had evolved from burning, epigastric pain to aching, and right lower quadrant pain over a period of six hours. She described the pain as moderate to intense, continuous, and without alleviating or exacerbating factors. She denies anorexia, back and flank pain, and issues with bowel movements. She admitted to drinking on social occasions and revealed that she had quit smoking 20 years ago. Her past medical history was otherwise unrevealing. Her family history was significant for hypertension in her mother, and colon polyps and colon cancer in her brother and grandmother, respectively.
At initial evaluation, her vital signs were within normal limits with a temperature of 98.7ᵒF, a pulse rate 86 beats per minute, a respiratory frequency of 18 breaths per minute, and a blood pressure of 128/85. The abdominal exam revealed moderate to severe tenderness in the right lower quadrant with rebound. Normal bowel sounds on auscultation. There were no visible abdominal wall defects, and no pulsatile or pathological masses. The remainder of her physical exam was unremarkable. The laboratory evaluation was significant for an increased white blood cell count of 10.7K/mm3, and neutrophil count of 7.4K/mm3.
Abdominal ultrasonography was inconclusive, but computed tomography (CT) of the abdomen and pelvis revealed a dilated appendix measuring up to 1.1 cm with mild inflammatory periappendiceal fat stranding and no calcification (Figures -). Acute appendicitis was the main differential diagnosis, with the possibility of appendiceal neoplasm low on the list. A detailed discussion of the risks and benefits of a laparoscopic, possibly open, appendectomy was carried out, and informed consent was obtained. The surgery was performed without complications, and the post-operative diagnosis remained acute phlegmonous appendicitis. Surgical pathology, however, revealed a LAMN with serrated architecture, and secondary acute inflammation of the appendix (5 cm in length x 0.7 cm in diameter) with a congested and hemorrhagic serosal surface (Figures -). Margins were free and no fecaliths were identified on sectioning.
The patient tolerated and recovered well from surgery and was discharged home on day one after surgery.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [98.7, 'degrees fahrenheit'], 'Heart Rate or Pulse': [86.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [10700.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 98.7 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 66.7 = 37.05556 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 86.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 10700.0 count/m^3. To convert 10700.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 10700.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6763,51,SIRS Criteria,diagnosis,integer,pmc-7596015-1,Extracted,"A 32-year-old nulliparous woman presented into Emergency Room with colicky abdominal pain that lasted 48 h. Additionally, she had diarrhea, abdominal distension, nausea, vomiting, dry cough, nasal congestion, headache, and fever. She was taking antibiotics for H. pylori gastritis. Her medical history included endometriosis. She was taking oral contraceptives intermittently. She had right oophorectomy at age 22 due to endometrioma, and right salpingectomy at age 25 due to ectopic pregnancy. In-vitro fertilization and embryo transfer failed at age 29.
On physical examination: BP 80/60 mmHg. HR 120 bpm. RR 22 bpm. Temp. 39 °C. Her abdomen was diffusely distended, absent bowel sounds, generalised tenderness, without rebound. Vaginal examination was unremarkable. Rectal exam showed liquid stool. Leucocytes 18,000/μL. PaO2/FiO2 ratio 370. Abdominal CT scan with IV contrast showed small bowel diameter of 5 cm with air-fluid levels and transition point at 5 cm from the ileocecal valve (). PCR was positive for C. difficile as well as Influenza AH1N1.
Patient was admitted in the Intensive Care Unit. She was kept NPO. A nasogastric tube was placed, and 2 L of enteric fluid were drained. She was started on Vancomycin 500 mg QID and Oseltamivir 75 mg BID by nasogastric tube, as well as Tigecycline 50 mg BID IV. The organ failure resolved within 48 h.
On her second hospital day, laparoscopic exploration was performed. Small bowel was diffusely dilated, and extensive intra-abdominal and pelvic adhesions were seen. The point of obstruction was at the terminal ileum next to the ileocecal valve. That segment of bowel was severely stenosed. Ileal obstruction was induced by many blue-black nodules (). On the surface of the parietal and visceral peritoneum, many lesions were visualized and biopsied ().
Due to the complexity of the case, it was converted to midline laparotomy since the exposure was not adequate to perform the surgery safely. Extensive lysis of adhesions was done. At this point, right ileocolectomy was performed. Using a 60 mm stapler, ileo-transverse anastomosis was done. No complications were reported.
Patient's recovery was uneventful. She was started on total parenteral nutrition (TPN) on postoperative day (POD) 0. On POD 1, she had bowel sounds and slowly recovered her bowel function. On POD 4, she was stared on liquid diet. Her diet was slowly progressed and the TPN weaned. By POD 8, she was tolerating soft diet, having bowel function, and no signs of active infection. She was discharged home.
The macroscopic pathological examination consisted of a 20 cm long ileum segment and a 6 cm cecum and colon segment. The external surface was light brown, with congestive areas. The luminal surface had hematic material and showed a variable diameter secondary to stenotic areas, with purplish areas of hemorrhagic appearance. Cross sections showed small dilated cystic areas in relation to fibrosis and mural bleeding.
Microscopically, we found multiple foci along the enterocolonic wall of glandular and tubular structures, lined by epithelial cuboidal-columnar cells without atypia, surrounded by endometrial stroma with lymphoplasmacytic inflammatory infiltrate, focal hemorrhage, and hemosiderin-laden macrophages. There was important vascular proliferation as well as extensive subserosal fibrous bands. Immunostains for Estrogen Receptor and PAX8 were positive, which confirmed the endometrial nature of the lesions. The diagnosis of enterocolonic transmural endometriosis with serosal adhesions was established ().
Definite diagnosis was ileal obstruction secondary to transmural endometriosis. At one-year follow-up, patient remains asymptomatic. She has been referred to Gynecology for further treatment of endometriosis.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.0, 'degrees celsius'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'respiratory rate': [22.0, 'breaths per minute'], 'White blood cell count': [18000.0, 'µL']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.0 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 120.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 18000.0 count/µL. To convert 18000.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 18000.0 white blood cell count/µL * 1.0 µL/mm^3 = 18000.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6764,51,SIRS Criteria,diagnosis,integer,pmc-6613421-1,Extracted,"An 8-year-old male child from a village of central India was bitten by a street dog, sustaining Category III wound on the dorsum of the right thumb and index finger. He was treated by a medical officer at a primary health center where the wounds were washed under running tap water. Simultaneously, the child received the first dose of purified chick embryo cell rabies vaccine but not immunoglobulin. He also received three subsequent doses of the same vaccine on days 3, 7, and 14 after the bite. After 20 days of bite, he had developed moderate-to-high-grade fever, frontal headache, and episodes of vomiting. For these complaints, he received medication at the same primary health center. However, on the 5th day of illness, he had altered consciousness, not able to recognize parents, and unable to respond to oral command and stimulation. Hence, he was referred and admitted to our institute. On further inquiry, he had no history of convulsion, rash, diarrhea, recent episode of viral infection, and recent past vaccination other than rabies.
On examination, he was febrile (temperature 102.5°F), with pulse rate of 110/min regular, respiratory rate of 22/min, and blood pressure of 110/76 mmHg. There were no abnormal physical findings except congested eyes and throat. His Glasgow Coma Scale score was 9/15 (E3V3M3), and he did not respond to oral command but there was slight response on deep painful stimuli. His pupils were equal and reactive bilaterally, and fundus examination was within normal limit. The cranial nerves were intact. Motor system examination revealed hypertonia of all the four limbs with Grade 3/5 power. All the deep tendon reflexes were brisk bilaterally. Both planter responses were extensor. Signs of meningeal irritation were present. A provisional diagnosis of viral meningoencephalitis, viral encephalitis, and rabies encephalitis was made. Other possibilities of acute disseminated encephalomyelitis were considered as symptoms developed after rabies vaccination. Considering the possibility of febrile encephalopathy, initially he was treated with broad spectrum antibiotics and antimalarial agent and was investigated for possible etiologies. His hematological and biochemical parameters were normal. Screening for malaria, tuberculosis, and HIV was negative. Cerebrospinal fluid (CSF) analysis showed lymphocytic pleocytosis (white blood cell count – 20), elevated protein (72 mg/dl), normal glucose (58 mg/dl), blood glucose (110 mg/dl), and negative staining (Gram-stain, acid-fast bacilli, and India ink preparation) and culture. Magnetic resonance imaging (MRI) showed bilateral thalamus, basal ganglion, brainstem, and cerebellar hyperintensities in the T2-weighted image, and flair imaging with no diffusion restriction and blooming []. After 3 days of hospitalization, he had developed persistent high-grade fever, generalized convulsion, worsened sensorium, spasticity in all the four limbs, and weak gag reflex. Considering the possibility of post vaccine acute disseminated encephalomyelitis a standard course of intravenous methylprednisolone (30 mg/kg/day once daily for 3 days) followed by oral prednisolone was adminstered in tappering doses but there was no clinical improvement. The possible diagnosis of Japanese, herpes, or rabies encephalitis were made. The CSF and serum were negative for herpes and Japanese encephalitis. In view of the possibility of rabies encephalitis, he was evaluated using paired sera and CSF sample antibody titers. The paired sera showed antibody titers in excess of 1:50,000 dilutions after 50 days of vaccination. A viral antigen detection kit from reference Neurovirology Laboratory of the World Health Organization Collaborating Centre for Reference and Research on Rabies, NIMHANS, Bengaluru, showed positive result on serum. Diagnosis of rabies was made on the basis of neuroimaging finding, high antibody titers in sera and CSF and detection of viral antigen.
He was managed in the Pediatric Intensive Care Unit with ventilatory support, good nursing care, and strict universal precautions. Parents and caretakers were vaccinated against rabies. The intensive care course was complicated by catheter-associated urinary infection and management included antibiotics for Klebsiella, antiepileptic drugs, and aggressive physiotherapy. Nutritive support was fulfilled by the nasogastric tube. He was weaned off of the ventilatory support after 3 weeks of illness.
Over the next 1½ months, his consciousness had improved and was able to follow commands. Motor function was improved with spontaneous movements of limb and truncal muscle. He was continued with physiotherapy and, after 3 months of hospitalization, he was discharged in stable condition with neurological sequelae. MRI scan was repeated after 2 months of discharge which revealed reduction of hyperintensities along with cortical atrophy. During the last review, the patient was able to walk few steps and follow meaningful commands.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [102.5, 'degrees fahrenheit'], 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'respiratory rate': [22.0, 'breaths per minute'], 'White blood cell count': [20.0, 'µL']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 102.5 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 70.5 = 39.16667 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 110.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 20.0 count/µL. To convert 20.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 20.0 white blood cell count/µL * 1.0 µL/mm^3 = 20.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6765,51,SIRS Criteria,diagnosis,integer,pmc-3652051-1,Extracted,"A 31-year-old female presented to the emergency department of our hospital, complaining of high-grade fever with chills and shortness of breath while she had been well until two days earlier. She is refered with intravenous heroin use for more than fifteen years. The temperature was 39°C, the pulse rate was 95/min and the respirations were 25/min. Her physical examination revealed tenderness at the right site of the neck, redness and edema with mild regional lymphadenopathy (). Examination of the oropharyngeal cavity, tonsils, and lungs was unremarkable. Nuchal rigidity was not noticed. One hour after admission, she became hypotensive requiring vigorous intravenous fluid administration.
The patient mentioned, that during the last 10 months trying to gain a venous access, she frequently used the jugular veins. She denied any needle sharing or using of contaminated syringes. Her usual practice is to lubricate the needle with her saliva and injecting without cleaning the skin.
On routine laboratory testing, the hemoglobulin was 10 g per deciliter, the white cell count was 12200 per cubic millimeter with 90 percent neutrophilia, and elevated C-reactive protein (CRP: 13 mg/dL, normal limits < 0,5 mg/dL). The blood chemical findings were normal. Serological tests were positive for hepatitis C infection.
A contrast-enhanced helical computer tomography (CT) of the neck showed extensive thrombus in the right internal jugular vein and enlargement of the regional lymph nodules (). CT scan of the thorax and brain was negative. A cardiac ultrasonographic examination was also negative. Based on findings, a diagnosis of Lemierres syndrome was made. Empirical antibiotic treatment with intravenous meropenem, vancomycin (for the possibility of MRSA), and clindamycin was initiated, but clindamycin was discontinued three days later due to gastrointestinal symptoms. The patient became afebrile with clinical improvement. Blood cultures, five days after admission grew Fusobacterium necrophorum, and the antibiotic regimen changed to ampicillin-sulbactam plus metronidazole for fourteen days intravenously. At the time of discharge, the patient was in good health and she continued treatment per os for a duration of six weeks. Anticoagulation therapy was initiated with the diagnosis but was discontinued after hospital discharge because of poor compliance.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.0, 'degrees celsius'], 'Heart Rate or Pulse': [95.0, 'beats per minute'], 'respiratory rate': [25.0, 'breaths per minute'], 'White blood cell count': [12200.0, 'm^3']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.0 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 95.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 12200.0 count/m^3. To convert 12200.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 12200.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 25.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6766,51,SIRS Criteria,diagnosis,integer,pmc-4876221-1,Extracted,"The patient, a forty-seven-year-old male from Guinea, West Africa, presented to the emergency room with one-day history of fever and profuse diarrhea. His past medical history was significant for end stage renal disease requiring hemodialysis, hypertension, and type 2 diabetes mellitus. He reported an exposure to antibiotics two months prior to his current admission.
His vital signs included blood pressure of 166/106 mmHg, heart rate of 136 bpm, temperature of 100.7 F, and respiratory rate of 16 breaths/min. Physical examination was remarkable for generalized maculopapular rash and abdominal tenderness. The rest of the physical evaluation was unremarkable.
Pertinent laboratory analysis showed a white blood cell count of 27,000/mm3 with left shift, hemoglobin of 11.2 g/dL, blood urea nitrogen of 68 mg/dL, and creatinine of 6.6 mg/dL. Blood and urine cultures, hepatitis A and hepatitis B antigens, hepatitis C antibody, and cytomegalovirus antigen in the blood were all unremarkable. Stool work-up including clostridium difficile toxin B PCR, leukocytes in stool, stool culture, and cryptosporidium were negative. Ova and parasite stool examination revealed the presence of multiple microorganisms identified as Blastocystis sp.
Our patient was started on intravenous fluid hydration and antibiotic therapy with intravenous metronidazole. His diarrhea frequency lessened and white blood cell count improved three days after the initiation of therapy. The patient was discharged on oral metronidazole in light of the presence of Blastocystis sp. with total resolution of symptoms by day ten.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [100.7, 'degrees fahrenheit'], 'Heart Rate or Pulse': [136.0, 'beats per minute'], 'respiratory rate': [16.0, 'breaths per minute'], 'White blood cell count': [27000.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 100.7 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 68.7 = 38.16667 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 136.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 27000.0 count/m^3. To convert 27000.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 27000.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 3e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 16.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6767,51,SIRS Criteria,diagnosis,integer,pmc-5798034-1,Extracted,"A 19-year-old male was admitted to the emergency service complaining of pain in abdomen and testis. The pain began 4 days prior. Also, the patient complains of nausea and vomiting, fever and chills and loss of appetite without symptoms of urinary problems. He had habit of smoking but nothing about previous diseases and taking medications in his history. No history of trauma was mentioned. Physical examination revealed an ill man with following vital signs: blood pressure 120/80 mmHg, respiratory rate 18 breaths per minute, and temperature 39.5°C, pulse rate 100 beats per minute. Tenderness was appreciated in right lower quadrant (RLQ), right inguinal region and scrotum with radiating to the right groin area. Abdomen was soft, symmetric and no signs of distention, guarding, with positive rebound tenderness and Rovsing’s sign. Significant laboratory results included white blood cell count = 16.5 × 103/mic L (normal range 4.4–11.0), hematocrit = 40% (normal range 41.5–50.4), Sodium = 131 mEq/L (normal range 138–145), platelet distribution width = 10.1% (normal range 12.0–20.0) and the other laboratory tests such as: R.B.C Count, Hemoglobin, MCV, MCH, MCHC, Platelet, Lymphocytes count, Fasting Blood sugar, BUN, creatinine and urine analysis (U/A) were normal. Abdominal and pelvic ultrasonography revealed features in enlarged lymph node and free abdominal fluid in RLQ. Any significant inflammation, abscess and mass in appendix were not reported. Also, the radiologist recommended consideration of other clinical and paraclinical signs and symptoms to rule out appendicitis. In according to the order of urologist sonographic color-Doppler requested and no significant abnormal findings were reported. Hence, general surgeon decided to perform appendectomy at Mcburney’s point. As the report of surgeon appendix was suppurative. Also, surgeon observed 100 cm of ileum for any additional problems (Figs and ).",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.5, 'degrees celsius'], 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [16500.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.5 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 100.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 16500.0 count/µL. To convert 16500.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 16500.0 white blood cell count/µL * 1.0 µL/mm^3 = 16500.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6768,51,SIRS Criteria,diagnosis,integer,pmc-7249762-1,Extracted,"A 29-year-old man with a previous history of alcohol use disorder and injection drug use presented to our hospital with fever, cough, and shortness of breath, along with chronic diarrhea lasting for a few months. The patient reported feeling ill for two days prior to presentation but subsequently felt feverish and sweaty, prompting him to visit the emergency department. On examination, the patient was febrile with a temperature of 39.1 °C (102.3 °F) and tachycardic with a heart rate of 101 beats per minute. His blood pressure was borderline, 95/60 mmHg; he was hypoxic with 89% breathing in room air, and he was in a moderate degree of distress. Examination of his lungs revealed decreased air entry on the right side with some crackles, whereas examination of his mouth showed oral thrush. The findings of his abdominal examination were unremarkable, with no evidence of organomegaly or tenderness to abdominal palpation. Biochemical and hematological investigations revealed a healthy leukocyte count of 7,500 cells/µL (neutrophils 94%), low hemoglobin of 10.4 gm/dL (healthy mean corpuscular volume of 99), a healthy creatinine level of 0.4 mg/dL, an elevated aspartate transaminase level of 216 U/L (reference range is <39 U/L), a healthy alanine transaminase level of 49 U/L (reference range is <52 U/L), and an elevated total bilirubin level of 1.5 mg/dL (reference range is <1.00 mg/dL). A chest x-ray showed focal consolidation in the right middle lobe (Figure ) . Blood cultures , S. pneumoniae urine antigen and Legionella pneumophila urine antigen were performed, and the patient was started on empirical treatment with ceftriaxone and azithromycin. Further assessment of the patient revealed that he was in a monogamous relationship with a male partner and regularly participated in unprotected anal intercourse. A fourth-generation rapid HIV antigen-antibody test was, therefore, performed.
On the second day of admission, the patient continued to experience febrile episodes, was still coughing and experiencing shortness of breath, and was still hypoxic. Results of urinalysis showed that he was positive for S. pneumoniae antigen, and rapid HIV testing was also positive with a CD4 count of 18 cells/mm3. He was preliminary diagnosed with pneumonia due to S. pneumoniae. Treatment with ceftriaxone was therefore continued, but all other antibiotics were discontinued. On the third day, however, his condition deteriorated, and he developed respiratory failure. The patient was intubated with ventilator settings that included a respiratory rate of 18 breaths/minute, a tidal volume of 460 mL, a fraction of inspired oxygen of 60%, and a positive end-expiratory pressure of 5 cm H2O. His blood culture was positive for pan-susceptible S. pneumoniae, and repeated chest x-rays showed bilateral infiltrates (Figure ). Military tuberculosis was ruled out as three sputum samples were negative. Vancomycin was added, and bronchoscopy was performed to determine the presence of opportunistic infections. His bronchoalveolar lavage fluid was positive for Pneumocystis jirovecii and methicillin-resistant Staphylococcus aureus . He was therefore started on trimethoprim-sulfamethoxazole and corticosteroids. Two days later, his condition improved, and he was extubated to a high-flow nasal cannula (Figure ). He continued to improve and was discharged after being hospitalized for two weeks (Figure ).",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.1, 'degrees celsius'], 'Heart Rate or Pulse': [101.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [7500.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.1 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 101.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 7500.0 count/µL. To convert 7500.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 7500.0 white blood cell count/µL * 1.0 µL/mm^3 = 7500.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6769,51,SIRS Criteria,diagnosis,integer,pmc-6157216-1,Extracted,"A 40-year-old gentleman presented to the emergency with chief complaints of SOB, cough, and fever for about a week. He did not have any other any other known comorbidities. He had a history of dyspnea in the past also. On examination, his heart rate was 120 b.p.m., respiratory rate was 30–35 b.p.m., oxygen saturation (SpO2) was 90% on room air, and he was febrile with temperature of 100.2° F. There were decreased breath sounds on the right side and crepitations on the left side of the chest. He was administered noninvasive ventilation (NIV), and his SpO2 improved to 99%. Chest X-ray images showed extensive left-sided infiltrates, right-sided mediastinal shift, and loss of lung volume on the right side []. Subsequently, he was shifted to Intensive Care Unit, and as his chest X-ray images worsened despite NIV and broad-spectrum antibiotics, he was intubated and ventilated. His white blood cell count was 18,700 per uL and procalcitonin was 36.5 ng/mL. Arterial blood gas showed poor oxygenation and respiratory acidosis, eventually falling into category to ARDS, according to ratio of partial pressure of oxygen in arterial blood and fraction of inspired oxygen (PaO2-FiO2). Echocardiography revealed pulmonary arterial hypertension (PAH) and no other significant findings. Endotracheal tube aspirate showed Klebsiella pneumoniae, and he was administered the sensitive antibiotics. Ventilatory management of ARDS was done using 6 mL/kg of predicted body weight, keeping the plateau pressure goal of <30 cm H2O with applicable positive end-expiratory pressure. Due to nonresolution of the pulmonary infiltrates and PaO2-FiO2 despite lung protective ventilation, prone ventilation was done with adequate precautions. Prone position ventilation was administered for 16 h a day. Eventually, his oxygenation and CXR worsened. Due to this deterioration in spite of all possible lung protective ventilator measures and treatment, computerized tomography (CT) of the thorax and pulmonary angiography were done. It showed agenesis of the right pulmonary artery and hypoplasia of the right lung with hyperplastic left lung having nonhomogeneous infiltrates [Figures and ]. Three-dimensional thoracic angiogram also showed right pulmonary artery agenesis [Figures and ]. He was referred to a higher center for requirement of extracorporeal membrane oxygenation (ECMO) for the nonresolving ARDS, but due to financial restraints, the family was unable to take him to an ECMO center. He succumbed to his condition and expired despite multimodal treatment and management.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [100.2, 'degrees fahrenheit'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'respiratory rate': [30.0, 'breaths per minute'], 'White blood cell count': [18700.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 100.2 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 68.2 = 37.88889 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 120.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 18700.0 count/µL. To convert 18700.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 18700.0 white blood cell count/µL * 1.0 µL/mm^3 = 18700.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 30.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6770,51,SIRS Criteria,diagnosis,integer,pmc-8702258-2,Extracted,"An 80-year-old man presented to our emergency room with a 5-day history of cough, sputum, and fever. He was an ex-smoker with a 30 pack-years history. He also had a history of hypertension treated with medication. Five months prior, he was diagnosed with M. intracellulare lung disease with a subpleural cavitary lesion in the right lower lobe (Fig. A, B). However, he refused treatment for the NTM lung disease.
His blood pressure was 100/60 mm Hg and body temperature was 37.5°C. His pulse rate was 83 beats/min and respiratory rate was 20 breaths/min. A chest examination showed coarse crackles on the right lung.
The WBC count was 18500/μL, with a neutrophil differential of 80.6%. The C-reactive protein level was increased to 11.0 mg/dL. Chest radiography and computed tomography revealed aggravating pneumonic consolidation and a cavity in the right lower lobe with a newly developed pleural effusion (Fig. C, D). On the arterial blood gas analysis, the partial pressure of oxygen was 69 mm Hg and partial pressure of carbon dioxide was 25 mm Hg on room air.
The patient received tazobactam/piperacillin and underwent immediate thoracentesis. A pleural fluid analysis revealed an exudate with a WBC count of 2807/mm3, neutrophil differential of 39%, lymphocyte differential of 40%, adenosine deaminase 69.6 of IU/L, and pH of 7.4. The patient was admitted to the respiratory ward and treatment with antibiotics and drainage was continued. The multidrug regimen consisting of daily azithromycin 250 mg, rifampin 600 mg, and ethambutol 800 mg and intravenous amikacin 1.0 g 3 times a week was administered to treat the M. intracellulare lung disease. A pleural fluid culture also revealed M. intracellulare. On day 11, a chest X-ray revealed spontaneous secondary pneumothorax at the right hemithorax (Fig. A). A pigtail catheter was inserted with chest wall suction. However, the pneumothorax did not improve; therefore, a chest tube was inserted on day 29 instead of the pigtail catheter. Negative sputum culture conversion was achieved after 6 weeks of NTM treatment. However, due to persistent air leaks, the right lung was not fully expanded, suggesting the presence of a complicated bronchopleural fistula (Fig. B). We recommended surgical management to the patient, but he refused. On day 90, he was transferred to a local clinic with chest tube. However, 28 days later, he died of acute respiratory failure.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.5, 'degrees celsius'], 'Heart Rate or Pulse': [83.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [18500.0, 'µL'], 'PaCO2': [25.0, 'mm hg']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.5 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 83.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 18500.0 count/µL. To convert 18500.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 18500.0 white blood cell count/µL * 1.0 µL/mm^3 = 18500.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 25.0 mm Hg, which is less than than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 1 + 1 = 2 criteria met.
Hence, the the number of SIRS criteria met by the patient is 2."
6771,51,SIRS Criteria,diagnosis,integer,pmc-3510275-1,Extracted,"A 17-year-old girl was admitted to a university hospital with lymphadenopathy on the right side of the neck lasting for a week, and she was treated with antibiotics. However, she complained fever, sore throat, and otalgia beginning on the fourth day of hospitalization, and she was transferred to Seoul St. Mary's Hospital at her request on the seventh day of hospitalization.
Three years prior she had experienced fever with lymphadenopathy on the left side of the neck. She was admitted to the same hospital, treated with antibiotics, and recovered. At that time, she was investigated for nonfunctioning goiter. Thyroid function tests were normal and the levels of antithyroid antibodies were close to the upper limits of normal. The thyroid scan showed diffuse distribution of the radioisotope. Her mother and maternal grandmother have hypothyroidism.
She was conscious at the time of transfer to our hospital. Her blood pressure was 100/70 mmHg, heart rate was 78 beats/min, respiratory rate was 20 breaths/min, and body temperature was 38.4℃. She had multiple tender lymph nodes on the right lateral side of the neck and in the right supraclavicular area, and the largest lymph node was 3×2 cm in size. She also had a tender goiter.
Her laboratory tests showed anemia (hemoglobin 7.6 g/dL), leucopenia (white blood cell count 2,700/µL), and elevated levels of erythrocyte sedimentation rate (ESR) of 70 mm/hr, C-reactive protein of 0.93 mg/dL and lactate dehydrogenase (LDH) of 688 U/L. Laboratory tests for anemia revealed iron deficiency. The test for EBV infection, tuberculin skin test and blood culture were negative. She was negative for rheumatoid factor and antinuclear antibodies were detected (titer=1:100). Thyroid function tests were normal, but antithyroid peroxidase antibodies and antithyroglobulin antibodies were elevated (). Computed tomography of the neck revealed multiple enlarged lymph nodes at levels II, III, IV and V on both sides of the neck and in the right supraclavicular area of the neck ().
On the second day of hospitalization, she complained of pruritic skin rashes on her lower extremities. Despite antibiotic and analgesic treatment, the fever persisted, the skin rashes spread to her trunk and upper extremities, her cervical lymph nodes continued to enlarge, and the lymphadenopathy spread to the occipital area. On the sixth day of hospitalization, an excisional biopsy of the enlarged cervical lymph node was performed, and the histopathologic findings were consistent with KFD (). Her fever persisted after the excisional biopsy, so we started the administration of oral prednisolone (0.5 mg/kg/day) on the seventh day of hospitalization. On the ninth day of hospitalization, the fever disappeared and the skin rashes began to subside. Ultrasonography of her thyroid showed heterogeneous echogenicity of the thyroid gland and a solitary nodule.
We diagnosed her with autoimmune thyroiditis on the basis of her family history and the laboratory results. Thus, she was ultimately diagnosed with KFD and autoimmune thyroiditis. Her hemoglobin was 9.2 g/dL after one month of iron supplementation.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.4, 'degrees celsius'], 'Heart Rate or Pulse': [78.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [2700.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.4 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 78.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 2700.0 count/µL. To convert 2700.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 2700.0 white blood cell count/µL * 1.0 µL/mm^3 = 2700.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6772,51,SIRS Criteria,diagnosis,integer,pmc-3580925-1,Extracted,"A 43-year-old African American female presented to our Emergency Department (ED) with multiple painful purpuric skin rashes on her face, ears, and extremities that started 3 days before. The skin lesions started on the legs and later progressed to the thighs, arms, face, and ears and became confluent with some areas beginning to slough. The patient had associated odynophagia with mild dysphagia. She stated that she had a similar episode of a lesser degree a few months earlier but did not seek treatment. She was recently seen at a different hospital for an infected skin ulcer of her right knee and was treated with trimethoprim and sulfamethoxazole. The patient denied fever, chills, chest pain, and shortness of breath, cough, headache, blurred vision, or neck stiffness. Her only complaint was the painful lesions, and she asked for pain medication. She was homeless, and she reported a history of smoking crack cocaine for the past 20 years and had used it as recently as a day before admission to our ED. Her past medical history was significant for hypertension. She denied any medication use and had no known allergies.
On physical examination, she was an afebrile, cachexic female, in no acute distress. Her vital signs were blood pressure of 195/102 mmHg, pulse of 94 beats per minute, respiratory rate of 20 breaths per minute, temperature of 97.8° F, and oxygen saturation of 100% on room air. Cardiovascular, pulmonary, and abdominal examinations were unremarkable. Ear, nose, and throat examination revealed hyperemic purpuric lesions on her face, ears, and malar area with swollen lips. Dermatological examination revealed multiple confluent purpuric reticular plaques on her thighs, face, and ears with characteristic patterns containing central necrosis and erythematous borders (Figures , , and ).
Initial laboratory studies revealed neutropenia (WBC of 1,900 cells/mL, with 42% neutrophils and an absolute neutrophil count of 800.00) and increased sedimentation rate, with normal chemistry and coagulation panels. Toxicology screening of the urine was positive for cocaine. Urine revealed gross hematuria, and full analysis showed hematuria with numerous red blood cells and negative urine culture. Theserum levamisole level, detected by liquid chromatography tandem mass spectrometry, was positive. Treatment in the ED consisted of a normal saline bolus and 2 mg intravenous (IV) morphine sulphate for pain control, followed by 125 mg IV methylprednisolone, 25 mg IV antihistamine, and 50 mg IV ranitidine.
The dermatology service was consulted, and a presumptive diagnosis of levamisole-induced vasculitis was made based on the initial presentation of the lesions involving the ears and positive cocaine metabolites on urine toxicology screening. The patient was admitted to our hospital and started on 25 mg IV antihistamine every 6 hrs as needed for pruritus, 40 mg daily oral pantoprazole, and 125 mg IV methylprednisolone every 4 hrs for 2 days, followed by 80 mg every 8 hrs for 2 more days and finally a tapering daily oral dose of 30 mg prednisone. A biopsy specimen of purpuric skin lesions on her left thigh revealed fibrin thrombi in small-sized vessels consistent with vasculitis (). Laboratory results showed the following: HIV antibody negative, normal lymphocyte subset panel, RPR nonreactive, hepatitis B surface antibody negative, anticardiolipin antibody negative, ANA negative, RF negative, and HLA-B27 negative. The perinuclear pattern of ANCA (p-ANCA) was detected, consistent with ANCA-positive vasculopathy. These clinical findings also suggest toxic effects of levamisole.
After one week of hospitalization, the patient's WBC count normalized, and her skin lesions improved significantly. She was discharged with a tapering dose of prednisone and counseled to cease cocaine abuse. Arrangements were made for treatment at a rehabilitation unit. The patient was instructed to have a followup in the medicine and dermatology clinics of our hospital in 1-2 weeks.
The patient returned to our ED a few months later complaining of a recurrent painful skin rash on her nose and stated that the symptoms began 3 days prior after smoking crack cocaine, which she said was “cut with lamusol”. Laboratory results again showed neutropenia, reinforcing our original diagnosis of levamisole toxicity. Her WBC count improved with IV methylprednisolone, and she was discharged 3 days later with tapering prednisone. After counseling about cocaine use, she was treated at a rehabilitation unit.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [97.8, 'degrees fahrenheit'], 'Heart Rate or Pulse': [94.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [1900.0, 'mL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 97.8 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 65.8 = 36.55556 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 94.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 1900.0 count/mL. To convert 1900.0 count/mL of white blood cell to mm^3, multiply by the conversion factor 0.001 mL/mm^3 which will give 1900.0 white blood cell count/mL * 0.001 mL/mm^3 = 1.9 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6773,51,SIRS Criteria,diagnosis,integer,pmc-7891795-1,Extracted,"A 51-year-old Caucasian male with a medical history of coronary artery disease and multiple myeloma diagnosed six years ago presented to the emergency department (ED) complaining of nonradiating generalized chest pain that has been progressively worsening for one week. His multiple myeloma was in remission after he received treatment with four cycles of chemotherapy with ninlaro, darzalex, and venetoclax and stem cell transplant two years ago. He has since been started on daratumumab weekly with chronic dexamethasone. In the ED, his physical examination was unremarkable. Electrocardiogram (EKG) was unremarkable without ST-T segment changes and cardiac troponins were within normal limits (normal value: <0.04 ng/dL). Laboratory results revealed a hemoglobin level of 8.0 g/dL, white blood cell count of 3.2 10*3/uL, and platelet count of 20 10*3/uL. His aspartate aminotransferase (AST) level was 30 U/L and alanine aminotransferase (ALT) was 26 U/L. Vitals in the ED were a blood pressure of 117/70 mm Hg, heart rate of 120 beats per minute, temperature of 97.8 degrees Fahrenheit, respiratory rate of 18 breaths per minute and oxygen saturation of 100% on room air. He urgently received two units of platelets while in the ED. Hematology and oncology was consulted for possible disease reoccurrence.
While on the medical floors his platelet and hemoglobin levels continued to decrease, and he received several additional transfusions to maintain hemoglobin above 8.0 g/dL and platelet count >20 10*/uL. Six days after admission the patient was noted to become more confused and his mental status began to decline, a computed tomography (CT) scan of the head and CT of the sinuses showed complete opacification of the left frontal sinus and left frontal, maxillary and sphenoid sinus disease with small mucous retention cysts in the right sphenoid sinus, leftward nasal septal deviation seen, and innumerable mixed lytic and sclerotic lesions within the calvarium suspicious for multiple myeloma (Figure ). Protein panel for suspicious multiple myeloma was also obtained (Table ). An ammonia level at that time was 118 umol/L (normal levels: 9-35 umol/L). The infectious disease team started the patient on 1 gram of meropenem every eight hours and acyclovir 10 mg/kg every eight hours for possible meningitis however a lumbar puncture was unable to be safely performed due to a low platelet count. Two days after admission, he became more obtunded, tachypneic (30-40 breaths per minute), tachycardic (heart rate 140-150 beats per minute) and was eventually intubated and transferred to the intensive care unit (ICU) for further management.
A lumbar puncture was ultimately obtained with a dry tap. Ammonia level at this time was 256 umol/L and AST was 41 U/L and ALT was 45 U/L. CT scan of the abdomen and pelvis was unremarkable and hepatitis panel was negative. The patient was started on lactulose and rifaximin for hyperammonemia. A bone marrow biopsy was performed and resulted in showing markedly hypercellular marrow about 100% diffusely infiltrated by plasma cells (>70% of cellularity). Sheets of neoplastic plasma cells, frequent bi- or tri-nucleated forms, some plasma cells with prominent nucleoli, and increased mitotic activity were also noted on the biopsy. The overall morphologic features of plasma cells were noted to be intermediate to high histologic grade and maturing trilineage hematopoiesis were markedly reduced. Immunostains were performed on the biopsy with the following results: CD138: Highlights numerous plasma cells; involving more than 70% of bone marrow cellularity. P53: Strong nuclear expression of p53 in >60% of plasma cells (overexpressed). Ki67: High proliferation rate in plasma cells (70% nuclear expression). He was ultimately diagnosed with a relapse of his multiple myeloma. Despite being aggressively managed in the ICU, he remained on the ventilator and was unable to be weaned off by day 14. Due to a poor prognosis, the family ultimately decided to pursue palliative and comfort care.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [97.8, 'degrees fahrenheit'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [3200.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 97.8 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 65.8 = 36.55556 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 120.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 3200.0 count/µL. To convert 3200.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 3200.0 white blood cell count/µL * 1.0 µL/mm^3 = 3200.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6774,51,SIRS Criteria,diagnosis,integer,pmc-3880742-1,Extracted,"A 26-year-old nulliparous woman with a dichorionic-diamniotic twin pregnancy achieved by assisted reproductive techniques was admitted at 32 weeks of gestation. At admission, her complaints were epigastric pain and flank pain. Until that time, the patient had an uneventful pregnancy without history of vaginal bleeding, abdominal trauma, uterine contraction, or recent sexual intercourse. Her past medical history included neither abdominal surgery nor myoma uteri. On physical examination, the temperature was 36°C, the blood pressure was 110/70 mm Hg, the pulse was 92 beats per minute, and respiratory rate was 24 beats per minute and vital parameters were normal. At initial abdominal examination, she had no rebound tenderness. Pelvic examination was one cm dilated with a soft cervix. Cardiotocography showed irregular contractions with reactive fetal heart rate tracing. Hemoglobin (Hb) was 10.3 g/dL, hemotocrit level (Hct) was 31.4%, white blood cell count (WBC), C-reactive protein (CRP) level and other laboratory results were normal. Urinalysis revealed 100 mg/mL protein and leucocyte (++). Obstetrical ultrasonography examination revealed two otherwise healthy fetuses with apppropriate biometrical calculations and with normal amniotic fluid, Doppler flow velocimetry indices. Maternal abdominal ultrasound examination revealed minimal anechoic free fluid in the right lower quadrant but appendix was not observed. Transvaginal ultrasound examination revealed a 26 mm cervical length.
After hospitalisation, steroid therapy betamethasone (Celestone Chronodose, 1 ml, Schering Plough, Germany) was performed for lung maturation. Nifedipine 10 mg 6 times a day (Nidilat, Sanofi Aventis, France) and then beta-agonists was administered for 24 hours for accelerated uterine contractions. Within 24 hours of admission the patient gradually complained of progressive nausea and vomiting. The patient was consulted to general surgery department, and oral intake was stopped, a nasogastric catheter was placed, a proton pump inhibitor was started intravenously, and an antibiotic regimen was administered (ceftriaxone 2 gr/day (Rocephine, Saba, Turkey)) and metronidazole 1 gr/day (Flagyl, Ecz.Baxter, Turkey) for suspicion of appendicitis. Whole abdominal and pelvic magnetic resonance (MR) imagings were performed and revealed a minimal intra-abdominal free fluid without any pathological signs. On the second day, abdominal pain with nausea and vomiting gradually increased but no rebound tenderness was experienced. Hg level decreased to 9.53 g/dL, htc level decreased to 29.4%, and WBC increased in value of 19.4 × 103/UL. Since leucocyte counts increased gradually and symptoms became more obscure, surgery had been decided with the diagnosis of acute abdomen. Under spinal anesthesia, laparotomy was extended through pfannenstiel incision and 300–400 mL hemoperitoneum was observed in the peritoneal cavity. Pelvic exploration revealed blurish color on the posterior right side of the uterus, active bleeding from right uterine vessel, and a torn uterine serosa (). A 8-9 apgar, 1760 gr, female fetus and a 8-9 apgar, 1730 gr, male fetus were born by a Cesarean section. The placenta was normal in appearance without retroplacental hematoma, ablation, or previa. Uterine vein branch was sutured with polyglactin 910 number 1.0. (Ethicon,Johnson & Johnson) (). Postoperative period was uneventful without any necessity of blood transfusion, and the patient was discharged home on the second postoperative day.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.0, 'degrees celsius'], 'Heart Rate or Pulse': [92.0, 'beats per minute'], 'respiratory rate': [24.0, 'breaths per minute'], 'White blood cell count': [19400.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 92.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 19400.0 count/µL. To convert 19400.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 19400.0 white blood cell count/µL * 1.0 µL/mm^3 = 19400.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 24.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6775,51,SIRS Criteria,diagnosis,integer,pmc-7491108-1,Extracted,"A 74-year-old man was admitted to our hospital with a 4-day history of abdominal pain, appetite loss and vomiting. He took 40 mg telmisartan, 5 mg amlodipine besilate combined drug and 2.5 mg amlodipine besilate for hypertension with 100 mg celecoxib, 37.5 mg tramadol hydrochloride/325 mg acetaminophen and 0.5 mg etizolam. He drank 540 mL sake (rice wine; about 75 g ethanol/540 mL sake) [] every day. He had smoked half a pack of tobacco for 50 years and quit 5 years ago. His vital signs upon arrival at the emergency room were as follows: body temperature, 37.2 °C; pulse rate, 157 beats/min; respiratory rate, 32 breaths/min; blood pressure, 111/81 mmHg; and oxygen saturation, 100% on oxygen mask 6 L/min. His conscious level was alert. He had icterus on his conjunctiva. The neck was supple. His heart sounds were unremarkable. The lungs were clear to auscultation. His abdomen was not distended. There was no tenderness or hepatosplenomegaly. Neurological examination was unremarkable. Hematological and biochemical testing showed leukocytosis (white blood cell count of 13,900/mm3 with 92.3% neutrophils) and elevated C-reactive protein (26.93 mg/dL). He had no anemia (hemoglobin, 15.8 g/dL) or thrombocytopenia (323,000/μL). Other relevant data were as follows: blood urea nitrogen, 45.0 mg/dL; creatinine, 1.66 mg/dL; Na, 124 mEq/L; Cl, 92 mEq/L; and K, 5.8 mEq/L. Serum bilirubin was markedly elevated at 6.8 mg/dL (normal range: 0.3–1.3 mg/dL) with direct bilirubin elevation of 5.0 mg/dL (normal range: 0–0.3 mg/dL). Other liver enzymes were also elevated as follows: serum aspartate aminotransferase, 67 IU/L (normal range: 13–37 IU/L); serum alanine aminotransferase, 39 IU/L (normal range: 8–45 IU/L); lactate dehydrogenase, 612 IU/L (normal range: 122–228 IU/L); alkaline phosphatase, 1228 IU/L (normal range: 118–335 IU/L); and gamma-glutamyltransferase, 602 IU/L (normal range: 12–49 IU/L).
Contrast-enhanced computed tomography (CECT) on the day of admission revealed choledocholithiasis in the common bile duct with intrahepatic biliary dilatation (Fig. a and b) and also showed a gastric wall abscess and intra-abdominal abscess around the spleen (Fig. c and d).
Cefoperazone sodium/sulbactam sodium was administered soon after blood culture. Endoscopic retrograde cholangiopancreatography (ERCP) was performed and 6 gallstones in the common bile duct were removed on hospital day 4. Percutaneous drainage with an 8 French (Fr) catheter through the left side of the back was performed for the intra-abdominal abscess on hospital day 7 (Fig. b). The abscess had a bile-like color and bilirubin was markedly elevated at 8.1 mg/dL with direct bilirubin of 4.9 mg/dL. Both blood and abscess cultures were positive for E. tarda. On endoscopic examination, a large mass was noted at the greater curvature of the stomach (Fig. a, Supporting figure A, B, and C, which showed the greater curvature of the stomach (arrow)). Fistulography revealed connection between the intra-abdominal abscess and gastric submucosal abscess (Fig. b and c). The size of the intra-abdominal abscess was decreased; however, the size of the gastric submucosal abscess was not changed.
EUS-guided drainage with a 5 Fr pigtail catheter was performed for the gastric submucosal abscess on hospital day 22 (Fig. d, Supporting figure D and E, and Supporting figure , which showed layer of the stomach). The catheter successfully decreased the abscess size (Fig. a and b). Abscess culture at this time revealed Enterococcus faecalis and Candida, which were thought to be microbial substitution caused by long-term antibiotic therapy. The bilirubin level in the gastric submucosal abscess was elevated at 5.2 mg/dL with direct bilirubin of 2.4 mg/dL. The catheter was placed for 14 days then removed on hospital day 35. The patient was discharged on hospital day 36 without any complications. A CT scan taken 4 months after discharge showed complete disappearance of both the gastric submucosal abscess and intra-abdominal abscess (Fig. c and d).",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.2, 'degrees celsius'], 'Heart Rate or Pulse': [157.0, 'beats per minute'], 'respiratory rate': [32.0, 'breaths per minute'], 'White blood cell count': [13900.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.2 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 157.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 13900.0 count/m^3. To convert 13900.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 13900.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 32.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6776,51,SIRS Criteria,diagnosis,integer,pmc-3914224-1,Extracted,"A 26-year-old man with end-stage renal disease of undetermined etiology received a living donor renal transplantation on February 2012. The adult donor was his sister sharing 1-haplotype; the AHG-CDC cross match was negative, the PRA result was 1% and 0% for class I and class II, respectively. Time zero graft biopsy was not performed due to a limited subcapsular hematoma in the superior pole. He received basiliximab induction, followed by methylprednisolone, tacrolimus (TAC), and mycophenolate mofetil (MMF). Trimethoprim-sulfamethoxazole was given for bacterial prophylaxis. He was determined to have a low-risk CMV (D−/R−) status so no viral prophylaxis was administered in this regard. On day 5-posttransplantation (post-KT), a Doppler US was performed in which adequate renal perfusion and normal graft characteristics were observed. He was discharged on day 6 post-KT with a serum creatinine (SCr) of 1.2 mg/dL and an immunosuppressive regimen based on TAC, MMF, and prednisone administered at a dose of 6 mg/BID (trough levels 8 ng/dL), 500 mg/BID, and 10 mg/day, respectively.
After an uneventful posttransplant evolution, the patient was hospitalized 9 days later due to gross haematuria, dysuria, and an elevation of SCr to 1.5 mg/dL. A complete workup was performed. CBC showed Hb 11 g/dL, leukocytes 5.8 K/uL, and platelets 238 K/uL. Urine analysis showed 49 leukocytes and 135 erythrocytes per each high-power field. Ceftriaxone 2 g IV BID was administered for a possible urinary tract infection (UTI) along with IV fluids. His vital signs were as the following: temperature 36.7°C, blood pressure 130/65 mm/Hg, pulse rate 100 bpm, and respiratory frequency 20/min.
On day 1 of hospitalization, the patient developed fever of 39°C which was treated with paracetamol. Leukopenia, anemia, and thrombocytopenia became evident with Hb 7.5 mg/dL, leukocyte 2.0 K/uL, and platelets 124 K/uL. There was also an increase in SCr to 2.04 mg/dL. A Doppler US was performed in which an image compatible with a renal graft residual hematoma, evidence of moderate hydronephrosis and blood clots in the bladder, were observed. Computed tomography (CT) scan studies of the chest, abdomen, and pelvis exclusively showed a residual fluid collection surrounding the graft. Urine and blood cultures were negative for bacteria. A graft biopsy was performed which showed normal histology on light microscopy; routine panel of immunofluorescence was negative. Immunohistochemistry for adenovirus (cell marque 1 : 100), CMV (cell marque 1 : 50), SV-40 (cell marque 1 : 100), and LMP1 (cell marque 1 : 100) did not demonstrate the presence of viral particles (Figures and ). Cytomegalovirus (CMV) pp65 antigenemia and parvovirus B19 antigenemia were negative. BK virus was also negative in blood and urine analysis. On day 3, blood and urine real-time qualitative polymerase chain reaction for adenovirus yielded positive results.
On day 4 of hospitalization, a cystoscopy was performed due to persistent haematuria. There was evidence of clots but no active bleeding, although abnormal mucosal inflammation and petechia were evident. MMF was withdrawn, and the dose of TAC was reduced to reach a blood level of 5 ng/dL (previous blood level 15.3 ng/mL). The patient continued to be febrile with a temperature of 39°C, for which ceftriaxone was substituted by 1 g IV ertapenem QD. Twenty-four hours later, ertapenem was replaced by meropenem. A continuous cystoclysis was placed through the Foley catheter to relieve the haematuria. There was a SCr decrease to 1.53 mg/dL.
On day 7 of hospitalization, ribavirin was started at a dose of 800 mg/6 hr. It is worth mentioning that the antiviral drug was not available before this day. Renal function showed further deterioration with an elevation of SCr to 1.95 mg/dL, leukocytes count was 4.2 K/uL, platelets 233 K/uL, and Hb was 7.9 mg/dL. The fever persisted with a temperature of 40°C. On day 9, the SCr decreased to 1.48 mg/dL.
The treatment for adenovirus continued with ribavirin 800 mg/6 hr for 10 days until the dosage was reduced to 400 mg/6 hr due to evidence of leukopenia. The treatment continued for a total of 20 days until the urine and blood real-time PCR was negative and the patient was asymptomatic; the urine analysis was normal as well. Fifteen days later, the patient returned with gross haematuria, fever, and a positive blood real-time PCR for adenovirus. He received treatment with IVIG with a total dose of 2 g/kg. He was later discharged with a stable renal function.
Eight months later, his renal function is stable with aSCr of 1.33 mg/dL and is currently on treatment with TAC 10 mg/day (8.5 ng/dL), MMF 500 mg/day, and prednisone 5 mg/day. Viral serology for CMV with pp65 antigenemia and parvovirus B19 antigenemia has remained negative. Blood and urine real-time PCR for adenovirus has remained negative in 3 serial subsequent determinations (). A subsequent control graft biopsy was not performed.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.0, 'degrees celsius'], 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [4200.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.0 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 100.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 4200.0 count/µL. To convert 4200.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 4200.0 white blood cell count/µL * 1.0 µL/mm^3 = 4200.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6777,51,SIRS Criteria,diagnosis,integer,usmle-1261,Extracted,"A 49-year-old woman is brought to the emergency department by her daughter because of increasing arthralgia, headache, and somnolence for the past week. She has a history of systemic lupus erythematosus without vital organ involvement. She last received low-dose glucocorticoids 2 months ago. Her temperature is 38.6 °C (101.5 °F), pulse is 80/min, respirations are 21/min, and blood pressure is 129/80 mm Hg. She is confused and disoriented. Examination shows scleral icterus and ecchymoses over the trunk and legs. Neurological examination is otherwise within normal limits. Laboratory studies show:
Hemoglobin 8.7 g/dL
Leukocyte count 6,200/mm3
Platelet count 25,000/mm3
Prothrombin time 15 seconds
Partial thromboplastin time 39 seconds
Fibrin split products negative
Serum
Bilirubin
Total 4.9 mg/dL
Direct 0.5 mg/dL
A blood smear shows numerous fragmented red blood cells. Urinalysis shows hematuria and proteinuria.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.6, 'degrees celsius'], 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'respiratory rate': [21.0, 'breaths per minute'], 'White blood cell count': [6200.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.6 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 80.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 6200.0 count/m^3. To convert 6200.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 6200.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 6.2e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 21.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6778,51,SIRS Criteria,diagnosis,integer,pmc-5799638-1,Extracted,"An 84-year-old Japanese woman was brought to our emergency department. She had sustained a 40°C fever over 2 days. Intravenous ceftriaxone followed by oral levofloxacin was administered at the long-term care facility. There were no remarkable findings on physical examination except for cognitive impairment and paralysis of the left upper and bilateral lower extremities caused by a previous cerebral infarction and by disuse syndrome.
Her medical history was significant for paroxysmal atrial fibrillation, cerebral infarction, Parkinson's disease, and dementia. She had been confined to bed in a nursing home and was practically without any mobility for several years. She had a surgical history of superior mesenteric artery thrombosis and a chronic subdural hematoma.
After urine and sputum samples and two sets of blood cultures had been submitted for laboratory testing, intravenous amoxicillin and clavulanic acid were started on suspicion of some bacterial infection with an unknown focus at that point. Nevertheless, she remained febrile, and all cultures turned out to be sterile. On the fifth day of admission, the patient was referred to our infectious disease department.
On physical examination, her temperature was 38.2°C, pulse 125 bpm, blood pressure 110/54 mmHg, and respiratory rate 20 breaths/min. The Glasgow Coma Scale was E4V4M3, which was typical for her. Her right shoulder was red, swollen, and inflamed. Her shoulder pain was aggravated by pressing the right acromioclavicular joint or by abduction of the right arm. The remainder of the examination was normal.
Laboratory tests 1 day before consultation revealed the following values: white blood cell count 4700/mL (reference range, 3500–9700) with a normal differential cell count, hemoglobin level 10.1 g/dL (reference range, 11.2–18.3) and platelet count 71,000/μL (reference range, 140,000–397,000), aspartate aminotransferase level 38 U/L (reference range, 13–33), alanine aminotransferase level 23 U/L (reference range, 6–30), lactate dehydrogenase level 190 U/L (reference range, 119–229), and C-reactive protein level 22.94 mg/dL (reference range, <0.2). Other parameters, including the levels of creatinine, blood urea nitrogen, and electrolytes, were within normal limits.
We aspirated 40 mL of yellow turbid synovial fluid from the right shoulder joint. The analysis showed 7765 cells/μL (mostly polymorphonuclear neutrophils), a protein level of 3.0 g/dL, and glucose of 75 mg/dL. Radiography of the right shoulder showed osteoarthritic changes, and some metallic suture anchors in the greater and lesser tuberosities of the humerus, which indicated that she had undergone rotator cuff repair in the past. Magnetic resonance imaging showed massive fluid collection within the right glenohumeral joint with synovitis, showing an amorphous mass of intermediate signal intensity on T2-weighted images. The surgically repaired rotator cuff was diffusely reruptured.
No bacteria were found in the fluid sediment by Gram and acid-fast staining; however, we started intravenous piperacillin on suspicion of bacterial arthritis. While the temperature of the patient had decreased since the first fluid aspiration, frequent taps were required to control the arthralgia and fluid collection in the right shoulder joint. The cell count of the synovial fluid increased to 38,400 cells/μL (88% polymorphonuclear leukocytes, 4% lymphocytes, and 8% monocytes), and a significantly elevated adenosine deaminase level (61.0 U/L) was observed on the third tap.
Pseudomonas species was isolated, but only from the initial synovial fluid culture. However, our hospital's microbiological facility was not able to distinguish between Pseudomonas fluorescens and Pseudomonas putida. Antibiotic sensitivity could not be identified because there were too few bacterial colonies and poor growth. We discontinued piperacillin use because her arthritis had not improved after 1 week of medication and three taps, and also because the initial synovial fluid cultures in blood culture bottles had been sterile.
Two weeks later, debridement and synovectomy of the right shoulder were performed to control the patient's culture-negative nonresolving arthritis. Hyperplasia of the synovial membrane and the presence of rice bodies were observed during the operation (Fig. ). Histopathology demonstrated inflammatory granulomas filled with numerous multinucleated giant cells, which surrounded semitransparent and glossy surgical sutures (Fig. ). There were no pathological findings suggesting septic arthritis. Routine and acid-fast bacilli smear and culture and polymerase chain reaction amplification for Mycobacterium tuberculosis were negative. Postoperatively, her persistent arthritis subsided completely, and the function of the right shoulder improved gradually.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.2, 'degrees celsius'], 'Heart Rate or Pulse': [125.0, 'bpm'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [4700.0, 'mL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.2 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 125.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 4700.0 count/mL. To convert 4700.0 count/mL of white blood cell to mm^3, multiply by the conversion factor 0.001 mL/mm^3 which will give 4700.0 white blood cell count/mL * 0.001 mL/mm^3 = 4.7 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6779,51,SIRS Criteria,diagnosis,integer,pmc-8667193-2,Extracted,"A 41-year-old female was hospitalized with subjective fever, nausea, vomiting, and abdominal pain which were present for 3 weeks. Initial examination showed blood pressure 66/39 mmHg, pulse 135 bpm, temperature 36.6 °C, respiratory rate 35 bpm and SpO2 99%. Normal heart sounds and breath sounds were heard on auscultation. Initial workup () showed hemoglobin 7.9 g/dL (11.6–15), hematocrit 24.7% (35.5–44.9), platelet 33×109 (157–371), white cell count 1.1×109 (3.4–9.6), absolute neutrophil count 0.5×109 (1.56–6.45), troponin T 17 (<10 ng/L), triglyceride 970 mg/dL, fibrinogen 601 mg/dL (200–393), ferritin 5446 (11–307 mcg/L), LDH 534 (122–222 U/L), interleukin 2 receptor (CD25) soluble 1599 pg/mL (≤1033), IL-6 10.2 pg/mL, prothrombin time 14.4 (9.4–12.5 sec), INR 1.3 (0.9–1.1), activated partial prothrombin time 35 (25–37 sec) and elevation of liver enzymes (total bilirubin 3.1 mg/dL (<1.2), direct bilirubin 2.7 mg/dL (0–0.3), alanine aminotransferase 81 U/L (7–45), aspartate aminotransferase 241 U/L (8–43), alkaline phosphatase 117 U/L (35–104). Serial troponin T levels were 13 ng/L (day 2) and 18 ng/L D3 (day 3). Other laboratory workup included renal function panel and autoimmune screen were unremarkable. Her HScore was 152 based on the above results. Blood smear showed absolute leukopenia and lymphopenia. EKG showed sinus tachycardia with T inversions in V1.
Echocardiogram showed left ventricular ejection fraction 21% with a normal size and thickness left ventricle with multiple regional wall motion abnormalities in non−coronary distribution and associated global decrease in systolic function; grade 3/4 left ventricular diastolic dysfunction, consistent with severely elevated left ventricular filling pressure; normal right ventricular chamber size with mild global decrease in systolic function, right ventricular systolic pressure 42 mmHg, tricuspid annular plane systolic excursion (TAPSE) was 11 mm (20–22); mitral valve was normal with moderate mitral valve regurgitation and severe tricuspid valve regurgitation. Aortic and pulmonary valves were normal. No pericardial effusion. Normal size of both right and left atrium (). Abdominal ultrasound did not show splenomegaly/hepatomegaly. She was started on broad spectrum antibiotics (vancomycin, piperacillin and tazobactam) and admitted to ICU as she required inotropic support with milrinone starting at 0.375 mcg/kg/min and then titrated as needed to maintain blood pressure. Extensive workup for underlying infection including bacterial, viral, fungal and mycobacterial organisms were all negative. Bone marrow biopsy showed hypocellularity with left-shifted myelopoiesis, increased clusters of immature myeloid precursors, and increased CD68+ macrophages, which were predominantly type 2 macrophages negative for pSTAT1 and positive CD163 (). Chromosome analysis, AML FISH, NGS for myeloid neoplasms (11 gene panel), MPN panel (JAK2, CALR, and MPL), immunoglobulin gene rearrangement, and T-cell receptor gene rearrangements were all unremarkable. Macrophage activation associated cytokine-mediated systemic disease process was suspected and treated with anakinra (anti-IL1) 100 mg subcutaneous for 7 days, and dexamethasone 10 mg once daily for 7 days followed by a 6-week steroid taper. She clinically improved rapidly and was completely off inotropic support after 6 days of immunosuppression treatment. Repeat echocardiogram after 7 days of immunosuppressive treatment showed significantly improved left ventricular function with ejection fraction 70%; normal left ventricular chamber size and wall thickness with hyperdynamic systolic function; normal right ventricular chamber size and function; no regional wall motion abnormalities; no pericardial effusion (). Complete resolution of cytopenias and normalization of liver function was also seen. At 8 months follow up she has no clinical features of heart failure.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.6, 'degrees celsius'], 'Heart Rate or Pulse': [135.0, 'beats per minute'], 'respiratory rate': [35.0, 'breaths per minute'], 'White blood cell count': [1.1, 'L']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.6 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 135.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 1.1 count/L. To convert 1.1 count/L of white blood cell to mm^3, multiply by the conversion factor 1e-06 L/mm^3 which will give 1.1 white blood cell count/L * 1e-06 L/mm^3 = 1.1e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 35.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6780,51,SIRS Criteria,diagnosis,integer,pmc-5192989-1,Extracted,"A 56-year-old multigravida postmenopausal woman presented to the emergency department with complaints of persistent nausea, vomiting, and abdomen pain for the past 1 day and constipation for the past 4 days. The abdominal pain was left-sided, sharp, constant, nonradiating, and 10/10 in severity. The vomiting was nonbloody and nonbilious in nature. She took laxatives for constipation, without much relief. She denied fever, diaphoresis, shortness of breath, chest pain, or urinary symptoms. The past medical history was significant for diabetes, asthma, anxiety, and chronic back pain. She had multiple abdominal surgeries in the past, including cholecystectomy, appendectomy, hysterectomy, and bilateral salpingo-oophorectomy. Her family history was unremarkable. She was a chronic smoker, however, denied any alcohol or drug use. She was allergic to morphine, phenergan, and sulfa drugs.
On admission, the patient was in significant distress, secondary to the abdominal pain. She was afebrile with temperature of 97°F, tachycardic with heart rate of 108 beats/min and hypertensive with the blood pressure measuring 206/106 mmHg. Her respiration rate was 22 breaths/min, and the oxygen saturation was 93% on room air. Her neurologic, cardiovascular, and respiratory system examinations were within the normal limits. Her abdomen was distended with hypoactive bowel sounds. She was tender in the left upper quadrant without the presence of guarding, rigidity, and rebound tenderness. On laboratory analysis of her blood, the white blood cell count was 16,000, with hemoglobin and hematocrit of 14.2 g/dl and 42, respectively. Her platelet count was 196. The biochemistry and liver function test were within normal range except for mild hyponatremia (Na = 134 mmol/L).
An urgent contrast-enhanced computed tomography (CT) scan of the abdomen was performed. The CT scan demonstrated dilatation of the jejunum and proximal ileum with multiple air-fluid levels consistent with intestinal obstruction. Distal small bowel loops were collapsed, and there was a stricture noted in the small bowel. There was no evidence of pneumatosis. There was a small, irregular soft tissue mass in proximity to site of narrowing and acute angulation of the ileal loop [Figures and ].
The patient was observed for 24 h after the placement of the nasogastric tube. Repeat X-rays of the abdomen after 24 h demonstrated no interval improvement. The decision was made to proceed with exploratory laparotomy. Intraoperatively, significant ascites were noted, and approximately 500 cc of clear fluid was evacuated. The small bowel was extremely dilated throughout its proximal two-third. There was a stricture identified in the proximal ileum with an adhesive band, causing near complete obstruction. Extensive scarring of bowel wall was present and approximately 15 cm proximal to the terminal ileum, a small bowel mesenteric nodule was noted. The adhesions, the mesenteric nodule, and the obstructed segment of the small bowel were resected followed by functional end-to-end reanastomosis of the small bowel. The abdomen cavity was copiously irrigated at the end of the procedure.
The postoperative course was significant for hypertension, hypokalemia, and hypomagnesemia, which were successfully managed medically and her diet was gradually advanced. She was discharged home on postoperative day 5 in afebrile condition, tolerating regular diet, and having bowel movements. Histopathology of the mesenteric nodule associated with small bowel confirmed the presence of ovarian tissue consistent with diagnosis of ORS [].",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [97.0, 'degrees fahrenheit'], 'Heart Rate or Pulse': [108.0, 'beats/min'], 'respiratory rate': [22.0, 'breaths/min'], 'White blood cell count': [16000.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 97.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 65.0 = 36.11111 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 108.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 16000.0 count/µL. To convert 16000.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 16000.0 white blood cell count/µL * 1.0 µL/mm^3 = 16000.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6781,51,SIRS Criteria,diagnosis,integer,pmc-3665061-1,Extracted,"A 42-year-old woman presented with acute onset of dyspnea, chest pain, and fever of 10 days duration. She had insignificant past medical record. She was apparently healthy prior to 2 weeks. Her illness started after exposure to large amount of hay dust, which led to episode of sneezing. She developed acute onset of breathing difficulty and dry cough after that episode. She received treatment at local hospital with no symptomatic benefit. Her condition continued to deteriorate; she had new onset of dyspnea and started having fever. So, she was referred to our hospital for further management. She denied any history of hemotpysis, bleeding tendency, epistaxis, telengectasis, immobilization, hypertension, and catamenial hemoptysis. She was not on any medications like antiplatelets or anticoagulants. She denied any history of recent trauma or surgery. Family history was not contributory.
The patient was restless and anxious. Vital signs were as follows: Temperature: 37.8°C; heart rate: 114 beats/min; blood pressure: 102/60 mm Hg; respiratory rate: 30 breaths/min, and oxygen saturation: 95% while breathing on 10 L of oxygen. There was no clubbing, cyanosis, lymphadenopathy, edema of extremities, mucosal or vascular abnormalities, (telangiectasia) or visible thyroid swelling. Respiratory system examination was consistent with left-sided pleural effusion. The abdomen was soft with no appreciable organomegaly. The patient was alert and oriented with no neurologic deficits.
Laboratory findings included the following: Hemoglobin: 7.73 g/dL; hematocrit: 23%; white blood cell count: 30.5 × 103/mm3; 88% neutrophils; platelet count: 811 × 103/mm3; creatinine level: 0.7 mg/dL; total bilirubin 2.98 mg/dL; alanine aminotransferase: 52.4 IU/L; aspartate amino transferase: 82.3 IU/L; alkaline phosphatase: 95.5 IU/L; prothrombin time with international normalized ratio: 14.9/14.60/1.04 s, activated partial thromboplastin time: 40.5/32.2 s. Chest radiography demonstrated left opaque hemithorax with contralateral mediastinal shift [].
Diagnostic pleural aspiration revealed hemorrhagic fluid with hematocrit of 18%. Diagnosis of spontaneous hemothorax was made. (Serum hematocrit: 23%). Emergency multidetector computed tomography (MDCT) chest was done which confirmed left-sided hemothorax (high attenuation) with underlying collapsed left lung. It also showed a 2 × 1 cm, tortuous, tubular structure visualized in left lingular lobe suggestive of pulmonary arteriovenous malformation/venous varix []. She was subjected to left posterolateral thoracotomy. Left lingular lobe showed two nodules of approximately 3 × 2 cm in size; left lingular lobe was friable warranting lobectomy. Intercostal chest drain was inserted following the procedure. Entire specimen was sent for histopathology, which showed multiple large and small vascular spaces with variable smooth muscle layer, with absence of elastic lamina, suggesting arteriolization of veins. The histopathology findings were consistent with PAVM [].
Postoperative period was uneventful and she was successfully discharged on 8th postoperative day. Genetic testing for hereditary hemorrhagic telangiectasia was suggested for her as well as her family members.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.8, 'degrees celsius'], 'Heart Rate or Pulse': [114.0, 'beats/min'], 'respiratory rate': [30.0, 'breaths/min'], 'White blood cell count': [30500.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.8 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 114.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 30500.0 count/m^3. To convert 30500.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 30500.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 3e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 30.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6782,51,SIRS Criteria,diagnosis,integer,usmle-1523,Extracted,"A 5-year-old girl is brought to the emergency department because of abdominal pain, vomiting, and diarrhea for 6 days. Her mother says that over the last 24 hours she has developed a rash and has been urinating less frequently than usual. One month ago, she had a 3-day episode of high fever and sore throat that subsided without medical treatment. She appears weak. Her temperature is 37.7°C (99.8°F), pulse is 120/min, respirations are 28/min, and blood pressure is 114/72 mm Hg. Examination shows petechiae on the trunk and jaundice of the skin. The abdomen is diffusely tender with no peritoneal signs. Neurological examination shows no abnormalities. Laboratory studies show:
Hemoglobin 8 g/dL
Mean corpuscular volume 85 μm3
Leukocyte count 16,200/mm3
Platelet count 38,000/mm3
Serum
Blood urea nitrogen 43 mg/dL
Creatinine 2.9 mg/dL
pH 7.0
Urine dipstick is positive for blood and protein. A blood smear shows schistocytes and normochromic, normocytic cells.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.7, 'degrees celsius'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'respiratory rate': [28.0, 'breaths per minute'], 'White blood cell count': [16200.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.7 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 120.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 16200.0 count/m^3. To convert 16200.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 16200.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 2e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 28.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6783,51,SIRS Criteria,diagnosis,integer,pmc-3466021-1,Extracted,"We report the case of a 3-month-old male who presented with cough, catarrh, difficulty in breathing, and high-grade, continuous fever of one week duration. There was no history of contact with someone with chronic cough. The child was being exclusively breastfed. On examination at presentation, he was ill looking, mildly pale, dyspneic, not cyanosed, and not dehydrated. The weight for age and other anthropometric parameters were normal. Vital signs measurement revealed a heart rate of 180 beats/min, respiratory rate of 52 breaths/min, and a temperature of 37.8°C. Examination revealed widespread rhonchi in both lung fields and no crepitation was heard. An initial diagnosis of bronchopneumonia to rule out bronchiolitis was made. Initial full blood count done revealed packed cell volume of 25%, white cell count of 13,700/mm3 with relative neutrophilia (65%), and absolute platelet count of 617,000/mm3. Blood film for malaria was negative and Mantoux test done was negative (5 mm area of induration). A sample for blood culture was taken at the peak of pyrexia, and the patient was placed on intravenous antibiotics, (iv ampicillin/sulbactam 50 mg/kg/dose 8 hourly subsequently changed to iv cefuroxime 120 mg/kg/day 8 hourly and iv gentamicin 5 mg/kg/day), intravenous infusion, oxygen by nasal prongs, and intermittent salbutamol nebulization.
Patient did not however improve as the vital signs worsened after 3 days. Respiratory rate increased to 74 breaths/min. Chest Radiograph showed loss of costophrenic and cardiophrenic angles and homogenous opacification of the left lung.
Patient could not be managed in the intensive care unit (ICU) because there is no functional paediatric ICU. Arterial blood gases estimation machine is also not available. Left tube thoracostomy was inserted into the left pleural space. It drained purulent effluent which was subsequently taken for microscopy, culture and sensitivity, and acid fast bacilli. Seven days after thoracostomy, repeat chest radiograph revealed 2 huge pneumatoceles and several smaller ones (). A chest computerized tomography scan machine is not available at this center, and the patient was unable to afford one at the nearest center.
The result of the pleural fluid microscopy and blood culture yielded heavy growth of Enterobacter gergoviae sensitive to ciprofloxacin and gentamicin. The organism was isolated on sheep blood agar and MacConkey agar plates. The antibiotic sensitivity test is by modified Kirby-bauer disk diffusion method.
The patient's condition continued to deteriorate. His respiratory rate became 80 breaths/min and pulse rate 187 beats/min, The antibiotic regimen was changed from iv cefuroxime to iv ceftazidime 100 mg/kg/day and iv gentamicin 5 mg/kg/day was continued. There was marked improvement 36 hours after commencing ceftazidime.
A repeat chest radiograph revealed enlargement of the pneumatoceles causing massive mediastinal shift to the right (). Double thoracostomy tube drains were inserted into each pneumatocele separately (). There was a massive air escape into the underwater seal drain. The patient's condition continued to improve, and he was discharged after a month on admission on syrup ciprofloxacin 7.5 mg/kg/dose 12 hrly for one week. Chest radiograph done just before discharge revealed no obvious lung pathology. Subsequent clinical and radiologic evaluation in the outpatient clinic revealed no abnormality ().",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.8, 'degrees celsius'], 'Heart Rate or Pulse': [187.0, 'beats per minute'], 'respiratory rate': [80.0, 'breaths per minute'], 'White blood cell count': [13700.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.8 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 187.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 13700.0 count/m^3. To convert 13700.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 13700.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 80.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6784,51,SIRS Criteria,diagnosis,integer,pmc-7968225-1,Extracted,"A 9-year-old boy had normal perinatal history, growth, and development. He presented with a fever, abdominal pain, and vomiting, all starting 5 days before admission. Diarrhea and hematochezia were not noted. We examined a stool sample to test for bacterial pathogens, which were not detected. His condition was provisionally diagnosed as acute viral gastroenteritis based on the clinical manifestations. On admission, his vital signs were body temperature 38.0 °C, blood pressure 98/44 mmHg, heart rate 82/min, and respiratory rate 16/min with an O2 saturation of 99% on room air. Upper abdominal tenderness was found without abdominal swelling or hepatosplenomegaly. Complete blood count showed white blood cells 9540/μL, haemoglobin 13.9 g/dL, and platelets 140 × 103/μL. Biochemical parameters showed total bilirubin 0.56 mg/dL, aspartate transaminase 58 IU/L, alanine transaminase 47 IU/L, blood urea nitrogen 6.3 mg/dL, creatinine 0.23 mg/dL, sodium 134 mEq/L, potassium 4.1 mEq/L, and C-reactive protein (CRP) 3.7 mg/dL. Coagulation studies revealed prolonged activated partial thromboplastin time (aPTT) of 92.4 s, elevated D-dimer 3.7 μg/mL, LA positivity, and slightly low prothrombin activity 58% (reference range [RR] 75–135%) in combination with immunoglobin M (IgM) class anti-prothrombin antibody of 32.1 AU/mL (RR < 24.0 AU/mL). Immunoglobin G (IgG) class anti-phosphatidylserine/prothrombin antibody was also positive (> 50.0 units, RR < 2.0 units), which is associated with strong LA activity. The patient’s LA-positive plasma was examined using the thrombin generation test and clot waveform analyses (Fig. a, b, and c) as previously described []. The clotting times in LA-positive plasma were significantly prolonged, compared to a healthy control.
A diagnosis of LAHPS was made. The patient tested positive for anti-nuclear antibody (ANA) titer 1:160, anti-double-stranded DNA (dsDNA) antibody of IgG 22 IU/mL, anticardiolipin antibody of IgG 16 U/mL, and anti-β2-glycoprotein I antibody of IgG > 50 units, but the patient did not fit the Systemic Lupus International Collaborating Clinics (SLICC) 2012 Classification Criteria []. A contrast-enhanced computed tomogram revealed nodular lesions in the adrenal glands bilaterally (Fig. d and e). The diagnosis of acute adrenal failure due to adrenal haemorrhage was made on the basis of the clinical manifestations, mild hyponatremia (134 mEq/L), high plasma ACTH 1586 pg/mL (RR 7.2–63.3), low plasma cortisol 3.24 μg/dL (RR 6.2–18.0), blood glucose 37 mg/dL, low serum aldosterone 43.1 pg/mL, and relatively elevated plasma renin activity 9.1 ng/mL/hr. Hence, the patient received glucose (0.6 g/kg/dose), hydration (1700 mL/m2), and hydrocortisone (50 mg/m2/day). Hydrocortisone and fludrocortisone were continued for the adrenal replacement therapy at physiological doses. Repeated coagulation studies still showed positive LA and prolonged aPTT for 12 months (Fig. a).
At 10 years of age, he visited our hospital because of gait disturbances and weakness in all extremities after acute upper respiratory viral infection. He had butterfly rash, discoid rash, optic disc swelling, deranged renal function, and showed higher levels of ANA and anti-dsDNA antibody. Renal biopsy resulted in a diagnosis of lupus nephritis (Fig. b and c). His condition was diagnosed as SLE on the basis of the SLICC 2012 Classification Criteria []. Intravenous pulsed treatments with methylprednisolone (30 mg/kg/day) and cyclophosphamide (500 mg/m2) were immediately initiated, followed by mycophenolate mofetil 400 mg/m2/day. The patient’s clinical condition improved.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.0, 'degrees celsius'], 'Heart Rate or Pulse': [82.0, 'beats per minute'], 'respiratory rate': [16.0, 'breaths per minute'], 'White blood cell count': [9540.0, 'µL']}",0,0,0,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 82.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 9540.0 count/µL. To convert 9540.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 9540.0 white blood cell count/µL * 1.0 µL/mm^3 = 9540.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 0.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 16.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 0.
Hence, the the number of SIRS criteria met by the patient is 0."
6785,51,SIRS Criteria,diagnosis,integer,pmc-3546274-1,Extracted,"In May 2009, a 30-year-old woman came to the emergency room (ER) with a five-day history of acute progressive dyspnea on exertion (NYHA class III). In 2007, ductal carcinoma in situ was diagnosed by biopsy during pregnancy. In 2008, after a full-term delivery, findings on fluorodeoxyglucose positron emission tomography computed tomography (CT) and ultrasound of the right breast revealed diffuse microcalcification and skin thickening of the right breast, and metastatic axillary lymph nodes. The patient refused further management and was lost to follow up until the ER visit.
On admission, the patient's blood pressure was 126/76 mm Hg, heart rate was 120 beats per min, respiratory rate was 18 breaths per minute, and body temperature was 36.7℃. A chest radiograph showed that the lung field was clear. Results of arterial blood gas analysis in room air indicated hypoxemia: pH 7.446, pCO2 28.2 mm Hg, pO2 44.3 mm Hg, HCO3 19.1 mmol/L, SaO2 76.8%. D-dimers were elevated to 2.59 µg/mL (normal, <0.39 µg/mL) with an elevated troponin I level to 0.24 ng/mL (normal, <0.04 ng/mL) and a brain natriuretic peptide of 774 pg/mL (normal, <100 pg/mL). Diffuse enlargement of the right breast with skin thickening and many enlarged axillary lymph nodes consistent with locally advanced breast cancer was observed on CT.
On the second day of admission, the patient was consulted with the cardiology department for possible preoperative cardiac evaluation. An electrocardiogram showed an S1Q3T3 pattern with inverted or flattened T waves in leads V1 through V4. A transthoracic echocardiogram showed normal left ventricular systolic function with right ventricular enlargement and free wall hypokinesia sparing the apex. In addition, the echocardiogram showed typical findings of acute pulmonary thromboembolism with a D-shaped left ventricle, moderate tricuspid regurgitation, and moderate pulmonary hypertension with an estimated right ventricular systolic pressure of 61 mm Hg.
Other laboratory tests showed the following results: white blood cell 7,900/mm3 with normal differential counts, hemoglobin15.4 g/dL, platelets 144,000/mm3, alanine aminotransferase 50 IU/L (normal, 0 to 40 IU/L), aspartate aminotransferase 218 IU/L (normal, 0 to 40 IU/L), total bilirubin 1.4 mg/dL (normal, 0.2 to 1.2 mg/dL), C-reactive protein 0.81 mg/dL (normal, 0 to 0.30 mg/dL), prothrombin time (PT) international normalized ratio (INR) of 1.36 (normal, 0.8 to 1.2), activated partial thromboplastin time (aPTT) of 45.7 seconds (normal, 27.0 to 45.0 seconds), fibrinogen of 196 mg/dL (normal, 200 to 400 mg/dL), and fibrin degradation products (FDP) of 1 : 2 positive (normal, negative). A peripheral blood smear showed increased numbers of schistocytes and reticulocytes consistent with MAHA ().
We measured serum vascular endothelial growth factor (VEGF) and interleukin 6 (IL-6) in view of preexisting information on VEGF, a critical angiogenic molecule and IL-6, a multifunctional cytokine promoting tumor growth. Serum VEGF levels were 26.9 pg/mL on the second day in the hospital and 9.5 pg/mL on the third day in the hospital (normal, 88.7 to 1,048.7 pg/mL); IL-6 levels were 50.3 pg/mL and 25.6 pg/mL on the second and third days, respectively (normal range, 0.4 to 8.6 pg/mL).
Anticoagulation therapy with enoxaparin was startedunder the clinical diagnosis of submassive acute pulmonary thromboembolism. While no evidence of pulmonary thromboembolism was observed on pulmonary CT angiography (), an echocardiogram showed acute right ventricular pressure overload (), and a perfusion lung scan showed multiple small wedge-shaped perfusion defects throughout both lungs (). Therefore, with a diagnosis of PTTM based on clinical and laboratory findings, the patient was transferred to the intensive care unit and received 1 mg/kg enoxaparin subcutaneously, 0.05 mg/kg dexamethasone intravenously, and 2 mg warfarin sodium orally.
On the third day of admission, repeated transthoracic echocardiogram showed additional significant right ventricular pressure overload with an estimated right ventricular systolic pressure of 60 mm Hg. Abnormal liver function was the result of either passive congestion or hepatic metastasis, although the initial CT did not show definite systemic metastasis. The patient was scheduled to undergo surgical breast biopsy and appropriate chemotherapy, however, her general condition showed rapid deterioration, and she died within 48 hours of admission.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.7, 'degrees celsius'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [7900.0, 'm^3'], 'PaCO2': [28.2, 'mm hg']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.7 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 120.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 7900.0 count/m^3. To convert 7900.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 7900.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 7.9e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 28.2 mm Hg, which is less than than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6786,51,SIRS Criteria,diagnosis,integer,pmc-8686233-1,Extracted,"A 14-month-old Congolese male child with oculocutaneous albinism visited the Mbujimayi pediatric clinic with fever and fatigue. He was originally from Kasai Oriental, a region of the Democratic Republic of the Congo. He was the youngest in a family of five children, three of whom had oculocutaneous albinism. He himself has sickle cell disease and the rest of the siblings have a sickle cell trait (Fig. ). He was born at term with a birth weight of 3000 g, and presented with spontaneously resolutive neonatal jaundice. The other significant history was episodes of fever with a monthly frequency of two episodes. No vaso-occlusive crisis was clearly diagnosed, in particular no dactylitis episode was reported. The vaccination schedule according to the expanded program of immunization in the DRC was respected with Bacille Calmette et Guérin (BCG) vaccine against tuberculosis; diphtheria, tetanus and pertussis (DTP) vaccine; oral polio vaccine (OPV) against polio; hepatitis B and haemophilus influenzae vaccine (HepB-HiB1); rotavirus vaccine (Rotasiil1); pneumococcal vaccine (Prevenar); measles vaccine (VAR); and yellow fever vaccine (AAV). The patient has never been hospitalized and has always been treated on an outpatient basis in health centers during febrile episodes such as malaria or typhoid fever. The siblings reported no particular clinical history.
His parents are not albinos and have no specific medical history; they never benefited from a prenuptial test. They reported their fear of the judgment of others because they have albino children when they are not affected.
The patient was wide awake with good contact and interaction. Generalized pallor was noted with subicteric conjunctivae, and the irises were bluish gray and translucent, thus appearing red with nystagmus (Fig. ). The patient’s skin was pinkish white, depigmented, without any particular lesions or bruises.
On physical examination, weight and height were at the third and tenth percentile for age, respectively. There was no fever (temperature 36.5 °C), the respiratory rate was high (53 cycles/minute), as well as the heart rate (176 beats/minute), but the latter was regular with the presence of a 1/6 systolic murmur at the mitral focus. The oxygen saturation was 94%. The oral examination was normal. The lymph nodes were free, without lymphadenopathy. The lung examination was normal. The abdomen was supple and painless. There was stage III splenomegaly according to the Hackett classification. Laboratory tests showed a hemoglobin level of 48 g/L and white blood cells at 13,200/μl (complete blood count performed with the Sysmex poch-100i; Sysmex, Norderstedt, Germany).
The diagnosis of SCD has been suggested on the basis of pallor, jaundice, and severe anemia. It was confirmed first by a positive rapid test (BioMedomics, Inc, Morrisville, USA) and then by hemoglobin electrophoresis.
The diagnosis of albinism was proven by molecular genetics on a blood sample and identification of the mutation involved, that is homozygosity for the 2.7 kb deletion of OCA2 (laboratory “Centro Nacional de Biotecnologia CNB-CSIC Campus de Cantoblanco, Darwin 3, 28049 Madrid, Spain). A family investigation was then performed (see Fig. ).
Given the very low hemoglobin level, the patient’s age, and SCD, a blood transfusion was indicated. Antibiotic treatment (ceftriaxone and amikacin) was started in the hospital. The evolution was favorable. On discharge from hospital, routine prophylaxis with folic acid and oral penicillin was initiated, and advice on crisis prevention and medical monitoring was given to the parents.
A dedicated patient monitoring program has been set up for sickle cell anemia and albinism with hygiene advice and sun protection measures. The patient received a hat, sunglasses, and sun protection cream. Ophthalmologic follow-up has also been set up. The evolution remains dermatologically stable, no skin lesion was observed. For SCD, the patient received treatment with hydroxyurea since early 2020. It is still too early to objectify the benefit of this therapy but he had only one infectious episode, one vaso-occlusive crisis, and did not require blood transfusion for over a year.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.5, 'degrees celsius'], 'Heart Rate or Pulse': [176.0, 'beats per minute'], 'respiratory rate': [53.0, 'breaths per minute'], 'White blood cell count': [13200.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.5 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 176.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 13200.0 count/µL. To convert 13200.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 13200.0 white blood cell count/µL * 1.0 µL/mm^3 = 13200.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 53.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6787,51,SIRS Criteria,diagnosis,integer,pmc-3443729-1,Extracted,"A 31-year-old woman was admitted to our hospital with severe headache, nausea, and vomiting. About 6 months previously, she had given birth to her second child. No excessive postpartum bleeding occurred and no blood transfusion was required. Four months before admission to our hospital, she had visited the Department of Neurology due to a bilateral temporal headache. Neurologic examination and brain MRI showed no abnormal finding (), so she was treated pharmacologically with a nonsteroidal anti-inflammatory drug. However, her condition did not improve. Due to nausea and vomiting for 2 weeks, she was brought to the emergency room. No menstruation or galactorrhea was observed at that time. On physical examination, her blood pressure was 110/70 mmHg, pulse rate was 58 beat/min, respiratory rate was 16 breath/min, and body temperature was 36.6℃. A neurologic examination revealed bitemporal hemianopsia. Initial complete blood analysis revealed a white blood cell count of 4,860/mm3, a hemoglobin level of 12.4 g/dL, and a platelet count of 241,000/mm3. The biochemical test results were as follows: protein, 7.2 g/dL; albumin, 4.2 g/dL; aspartate aminotransferase, 16 IU/L; alanine aminotransferase, 6 IU/L; blood urea nitrogen, 5.9 mg/dL; and creatinine, 0.5 mg/dL. The electrolyte test results were as follows: sodium, 113 mEq/L; potassium, 4.3 mEq/L; and chloride, 82 mEq/L. The blood and urine osmolarities were 249 and 691 mOsm/kg, respectively. The thyroid function test results were as follows: serum thyroid-stimulating hormone (TSH) level, 0.56 µIU/mL (reference range, 0.27 to 4.2); free T4, 0.91 ng/dL (0.93 to 1.7); and T3, 0.89 ng/mL (0.8 to 2.0). We performed a combined pituitary stimulation function test and rapid adrenocorticotropic hormone (ACTH) stimulation test for further assessment. We injected regular insulin (0.1 µ/kg), thyrotropin-releasing hormone (200 µg), and luteinizing hormone (LH)-releasing hormone (100 µg); 2 hours later, the patient's blood glucose level fell to 60 mg/dL and she complained of hypoglycemic symptoms. The rapid ACTH stimulation test showed no increase in cortisol (). The combined pituitary function stimulation test showed no increase in serum growth hormone, ACTH, or TSH level. Serum levels of LH and follicle-stimulating hormone were normal over time, and mild hyperprolactinemia was present with normal increments over time (). T1- and T2-weighted MRI showed an 18 × 10-mm round mass with isosignal intensity in the sella. The lesion extended to the suprasella and slightly compressed the optic chiasm ().
Prednisolone and levothyroxine were prescribed and the mass was removed using a transsphenoidal approach. The pathologic findings revealed granulomatous changes with multinucleated giant cells (). Visual disturbances improved after surgery. The acid-fast bacilli stain, tuberculosis polymerase chain reaction, angiotensinogen-converting enzyme, and venereal disease tests yielded no abnormal finding. The patient was finally diagnosed with idiopathic granulomatous hypophysitis, and estradiol and progesterone were added to the prednisolone and levothyroxine for maintenance therapy. She is now under outpatient follow-up care.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.6, 'degrees celsius'], 'Heart Rate or Pulse': [58.0, 'beats per minute'], 'respiratory rate': [16.0, 'breaths per minute'], 'White blood cell count': [4860.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.6 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 58.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 4860.0 count/m^3. To convert 4860.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 4860.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 4.86e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 16.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6788,51,SIRS Criteria,diagnosis,integer,pmc-4641864-1,Extracted,"A 42-year-old man was admitted to the emergency department because of inability to remove an adult product from his rectum. The patient described the incidence as his first event, and he had no specific history. The patient denied homosexual identity. No abdominal pain, nausea, or vomiting was observed. The patient's blood pressure was 128/82 mm Hg; pulse rate, 92/min; respiration rate, 18/min; and body temperature, 36.6℃. Abdominal examination revealed a soft and flat abdomen with normal bowel sounds. Digital rectal examination revealed the hard plastic bottom of the object abutting the upper anal canal and normal anal sphincter tone. His laboratory data were as follows: hemoglobin level, 12.7 g/dL; white blood cell count, 8,940/mm3; and CRP level, 6.33 mg/L. The results of evaluations for hepatitis B surface antigen, hepatitis C antibody, and human immunodeficiency virus (HIV) antibody were all negative. Radiography revealed a vibrator in the rectum, without evidence of peritoneal or perirectal free air ().
Several attempts to remove the vibrator by endoscopic snare, alligator forceps, grasping forceps, and u-turn technique with a transparent hood were made to no avail. As the endoscopic maneuvers failed to remove the foreign body, surgical removal under spinal anesthesia was planned. However, the patient refused to receive spinal anesthesia. We attempted to remove the foreign body by blindly using tenaculum forceps but could not grasp it tightly and failed (). Finally, we decided to use the forceps under endoscopic assistance. After the endoscope was inserted in the anal canal, the tenaculum forceps was inserted and proceeded along the vision obtained by the endoscope until the distal ends reached the foreign body. Under direct endoscopic guidance, the tenaculum forceps was opened and used to grasp the end of the foreign body (). Finally, the object was removed successfully. The removed object was relatively large and heavy (length, 25 cm; diameter, 5 cm; weight, 650 g). Mucosal injury was observed during endoscopic examination immediately after the removal. However, the patient did not complain of abdominal pain and therefore was discharged.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.6, 'degrees celsius'], 'Heart Rate or Pulse': [92.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [8940.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.6 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 92.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 8940.0 count/m^3. To convert 8940.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 8940.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 8.94e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6789,51,SIRS Criteria,diagnosis,integer,pmc-3994264-1,Extracted,"A 54-year-old man visited Daegu Catholic University Hospital after a screening colonoscopy that revealed a sigmoid colon polyp that was diagnosed pathologically as a tubular adenoma. He denied other symptoms such as abdominal pain, weight loss, fever, general weakness, loss of appetite, or hematochezia. His blood pressure was 106/64 mm Hg, pulse rate 73 beats per minute, respiratory rate 20 breaths per minute, and body temperature 36.7℃. His consciousness was clear, and no lymphadenopathy was evident in the head and neck, axillary, or inguinal region. Abdominal examination revealed no tenderness or rebound tenderness. Bowel sounds were normal, and the liver and spleen were not palpable. The laboratory findings were as follows: white blood cells, 11,400/mm3 (neutrophils 81.8%, eosinophils 0.4%, lymphocytes 12.4%); hemoglobin, 13.4 g/dL; and platelet count, 202,000/mm3. The blood chemistry test showed the following results: aspartate aminotransferase, 16 IU/L; alanine aminotransferase, 21 IU/L; total bilirubin, 0.6 mg/dL; alkaline phosphatase, 129 IU/L; total protein, 6.5 g/dL; albumin, 4.4 g/dL; blood urea nitrogen, 12.2 mg/dL; creatinine, 0.9, mg/dL; Na, 139 mEq/L; K, 3.4 mEq/L; and Cl, 98 mEq/L. The serum carcinoembryonic antigen level was 2.69 ng/mL, which was within the reference range.
Colonoscopy revealed a semipedunculated polyp, approximately 2 cm in size, in the sigmoid colon. The surface of the polyp showed redness and nodularity (). In private clinics, the tumor was diagnosed as a tubular adenoma; however, a diagnosis of submucosal tumor was not completely ruled out. We performed EMR by en bloc resection of the polyp with a flex knife and a snare after injecting a glycerin solution into the submucosa ().
Resected specimens histologically showed lymphoepithelial lesions with diffuse proliferation of atypical lymphocytes, which immunohistochemically stained positively for CD20, CD5, and Bcl-6, but negatively for CD3, Bcl-2, and cyclin D1. In addition, the Ki-67 labeling index was 10% to 20%. These findings were compatible with low-grade B-cell MALT lymphoma ().
There was no evidence of lymph node metastasis or involvement of any other organ, except for a gallstone, in the thoracic and abdominal computed tomography performed for staging. According to the Ann Arbor staging system, the tumor was stage IE.
The resected lesion was replaced with normal mucosa on sigmoidoscopy 2 months after the EMR (). He has been free of disease during 10 months of follow-up.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.7, 'degrees celsius'], 'Heart Rate or Pulse': [73.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [11400.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.7 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 73.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 11400.0 count/m^3. To convert 11400.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 11400.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6790,51,SIRS Criteria,diagnosis,integer,pmc-3652097-2,Extracted,"A 9-year-old girl was admitted to the clinic with the complaint of fever and widespread skin rash. The history revealed that the girl had been taking VPA for five years for the treatment of epilepsy, and CBZ had been added one month before the admission. With the complaints of high fever and skin rash 25 days after initiation of CBZ treatment, the girl had been treated for the diagnosis of scarlet fever by her family doctor. Due to the continuation of complaints, she was referred to our hospital.
On examination, physical findings were as follows: temperature, 39°C, pulse rate, 88 bpm, respiration, 24 breaths/min, and blood pressure, 105/70 mmHg. Skin rash tended to be confluent and was widespread on body. Bilateral cervical and suboccipital enlarged lymph nodes and hepatomegaly were determined.
Laboratory findings revealed hemoglobin (11.2 g/dL) and leucocyte counts (9.3 × 103/mm3) with a differential of 59% lymphocytes (9% were composed of atypical lymphocytes), 24% neutrophils, and 15% monocyte. Eosinophils number was 0.77 × 103/mm3. Lymphocyte level (5.5 × 103/mm3) was above the laboratory limits (0.9–3.2 × 103/mm3). Aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and gamma-glutamyl transferase were elevated at 323, 216, 280, and 454 IU/L, respectively. C-reactive protein was 3.19 mg/dL (normal range < 5 mg/L). Erythrocyte sedimentation rate was 9 mm/h. Blood and throat cultures were negative. Virological examinations for hepatitis A, B, and C, the Epstein-Barr virus, parvovirus B-19, human herpes virus type 6, and cytomegalovirus were negative. Antistreptolysin O, antidouble-stranded DNA, and ANA profiles were negative. Lactate dehydrogenase level was elevated to 784 U/L (normal range 120–330 U/L). VPA and CBZ levels were 77.5 µg/mL and 8 µg/mL, respectively. Ultrasonography revealed hepatosplenomegaly.
The patient was diagnosed with definite case of DRESS syndrome based on clinical and laboratory findings. CBZ was abruptly discontinued, while VPA treatment was continued. Pulse methylprednisolone was given at a dose of 30 mg/kg (max 1 g/day) for 3 days. Fever and rash disappeared with resolving of facial edema in 8 days. While improving, marked peroral desquamation was remarkable (). The case was discharged from the hospital with oral prednisolone treatment at a dose of 1 mg/kg/day. After two weeks, all symptoms completely resolved, laboratory tests were normal, and oral prednisolone was discontinued.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.0, 'degrees celsius'], 'Heart Rate or Pulse': [88.0, 'beats per minute'], 'respiratory rate': [24.0, 'breaths per minute'], 'White blood cell count': [9300.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.0 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 88.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 9300.0 count/m^3. To convert 9300.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 9300.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 9.3e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 24.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6791,51,SIRS Criteria,diagnosis,integer,pmc-3510291-1,Extracted,"An 82-year-old man was admitted to our medical center because of nausea and vomiting that occurred after the first oral anti-tuberculosis medication. One week before the admission, the patient underwent a routine-biannual health check-up at a local healthcare facility, and his chest radiograph showed consolidation in the left upper lobe (LUL). The patient received immediate medical attention owing suspected pulmonary tuberculosis. The patient had been receiving routine-biannual health check-ups, and did not have any major disease, except hypertension and diabetes mellitus. He had no history of smoking and drinking. He had been under clinidipin and sitagliptin treatments for 5 years for hypertension and diabetes, respectively.
On physical examination, his blood pressure was 120/80 mm Hg, heart rate was 70 beats/min, respiratory rate was 18 breaths/min, and body temperature was 36.5℃. The findings of auscultation were insignificant. Signs of collagen vascular disease were not observed, and the remaining physical examination was unremarkable. His chest radiograph showed an increase in consolidation in the LUL as compared with the observation a week ago. Chest computed tomography (CT) showed a diffuse, patchy consolidation with ground-glass opacity in the LUL. Reticular opacities, on which our suspicion of idiopathic pulmonary fibrosis (IPF) was based, were found along the periphery of both the lower lobes (). No bronchiectasis or honeycombing was observed.
Laboratory findings were as follows: leukocyte count was 8,700/µL, C-reactive protein level was 103 mg/dL, and anti-nuclear antibody was not detected. Arterial blood gas analysis was not performed because the patient did not have dyspnea. The other data were within normal limits. Upon admission, 750-mg of levofloxacin was administered to the patient for the treatment of community-acquired pneumonia.
Blood and sputum cultures were negative. The results of the serologic tests for Mycoplasma pneumoniae, Legionella pneumophila, and Streptococcus pneumoniae were also negative. On day 4 after admission, bronchoalveolar lavage (BAL) was performed because the lesion in the LUL had not improved. Cellular components and lymphocyte subsets were not assessed for the BAL specimen. Culture, tuberculosis polymerase chain reaction, and cytology of the BAL specimen were negative. Video-assisted thoracoscopy was performed owing to increased infiltration observed on the chest radiograph obtained on day 10. Pathological examination of the tissue samples obtained from the anterior and posterior segment of the LUL showed that DAD was at its organizing stage ().
We immediately started treatment with high doses of parenteral methylprednisolone, and found that the consolidation of LUL decreased within 3 days after the initiation of the treatment. Further, antibiotic treatment was discontinued, and the steroid therapy was maintained for 3 weeks. A follow-up examination showed almost complete disappearance of the LUL infiltration, although reticular opacities on both the lower lobes remained ().",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.5, 'degrees celsius'], 'Heart Rate or Pulse': [70.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [8700.0, 'µL']}",0,0,0,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.5 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 70.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 8700.0 count/µL. To convert 8700.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 8700.0 white blood cell count/µL * 1.0 µL/mm^3 = 8700.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 0.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 0.
Hence, the the number of SIRS criteria met by the patient is 0."
6792,51,SIRS Criteria,diagnosis,integer,pmc-7470353-1,Extracted,"A 24-year-old native Japanese man presented to our hospital after developing high-grade fever. He had travelled to Vietnam and Cambodia for 14 days. After leaving Japan, he visited the beach in Halong Bay, the forest region near the border of China, and Siem Reap in Cambodia. During his stay, he had participated in forest trekking tourism and had stayed in a youth hostel. For dietary intake, he ate home-cooked food and drank beverages with ice, in a similar manner to local people. Fourteen days after he returned to Japan, he developed a mild headache, chills and malaise, and 2 days later, he developed a high fever with chills and rigors. He did not have any abdominal pain or diarrhoea. His past medical history, family history and social history were unremarkable. On examination, his temperature was 39 ℃, his blood pressure was 128/68 mmHg, his pulse was 101 beats per minute, his respiratory rate was 18 breaths per minute and his oxygen saturation was 98 % with room air. He did not present a rash, lymph node swelling, abdominal tenderness, or hepatosplenomegaly. His laboratory examination demonstrated elevated serum C-reactive protein (5.1 mg dl−1; normal range, 0–0.3 mg dl−1). The blood cell counts and the other biochemical tests were normal (WBC 6900 µl−1, AST 20 U l−1, ALT 19 U l−1). The HIV test result was negative, while contrast-enhanced computed tomography (CT) revealed ileocecal lymphadenopathy. We did not detect enterocolitis, arthritis, or abscesses. We also did not detect an aneurysm or abscess via brain magnetic resonance imaging (MRI).
Based on his travel history and clinical findings, we suspected primary bacteraemia from typhoid fever. He was admitted to our hospital for observation and treated with antibiotics. On the day of admission, ceftriaxone (2 g/day) and minocycline (200 mg/day) were administered. On hospital day two, the initial blood cultures yielded Gram-negative bacilli, which were identified as by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. The bacterial subspecies could not be identified by biochemical testing at our hospital. Antibiotic susceptibility testing revealed that the organism was not resistant to the following antibiotics: ampicillin, piperacillin, cefotiam, cefotaxime, ceftizoxime, ceftazidime, cefepime, imipenem, meropenem, azythromycin, levofloxacin, ciprofloxacin and fosfomycin. Only minomycin had an MIC90 value of >8 µg ml−1.
After 1 day of ceftriaxone and minocycline, his fever, malaise and headache remitted. We discontinued minocycline, and ceftriaxone was continued for 14 days. The patient was discharged on day 10 and had an uneventful recovery with no recurrence of fever.
Further testing using commercial O and H antisera (Denka Seiken Co. Ltd, Tokyo, Japan) according to the Antigenic Formulae of the (9th ed.) [] identified the organism as serovar Corvallis (at Hokkaido Institute of Public Health, Sapporo, Japan). Thus, serovar Corvallis was likely to have caused the primary bacteraemia in this patient, as described.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.0, 'degrees celsius'], 'Heart Rate or Pulse': [101.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [6900.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.0 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 101.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 6900.0 count/µL. To convert 6900.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 6900.0 white blood cell count/µL * 1.0 µL/mm^3 = 6900.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6793,51,SIRS Criteria,diagnosis,integer,pmc-5118515-1,Extracted,"A 59-year-old Haitian female with history of biopsy confirmed dermatomyositis (initially she presented with lower extremity weakness and creatinine kinase of 6547 u/L), on chronic steroid therapy (prednisone 30 mg daily) for six months, presented to the emergency room with a painful tongue lesion for two months and right shoulder pain. The patient described a four-month history of progressive right shoulder pain exacerbated by movement. An X-ray of the shoulder was unremarkable fourth months prior; however, a recent outpatient magnetic resonance image (MRI) of the right shoulder was suspicious for septic arthritis of the right acromioclavicular joint, and this prompted the current admission. In addition, she reported a tongue ulcer which started after biting her tongue and had progressed in size over the course of two months. She had been treated with a full course of oral acyclovir followed by famciclovir, without improvement. Her travel history included a visit to Haiti one year prior. The patient denied constitutional symptoms of fever, chills, night sweats, or weight loss. She had no cough, shortness of breath, hemoptysis, chest pain, or joint or back pain. She denied any gastrointestinal, genitourinary, or neurologic complaints.
On examination, the patient was found to have a temperature of 100.3° Fahrenheit, heart rate of 120 beats per minute, a blood pressure of 135/65 mmHg, a respiratory rate of 18 per minute, and an oxygen saturation of 98% in ambient air. She had a heliotrope rash, shawl sign, and Gottron's papules consistent with dermatomyositis. Head and neck examination revealed soft and mobile left anterior cervical adenopathy with the largest node measuring approximately 1 cm. On the tongue there was a tender, three by three centimeter fungated and ulcerated lesion on the left lateral aspect, with irregular indurated borders and a foul smelling white exudative material (). The lungs were clear on auscultation. A musculoskeletal examination demonstrated limited range of motion in the right shoulder due to pain associated with tenderness, warmth, and mild effusion. Serum chemistry was normal. WBC count was 7 × 103/µL with 86% neutrophils and 10% lymphocytes but otherwise the CBC was normal. She was hyperglycemic, with HbA1c of 11.1% (newly diagnosed steroid induced diabetes). She was HIV negative.
In the presence of known dermatomyositis, the nonhealing oral ulcer raised concerns for malignancy. Therefore, a biopsy of the tongue lesion was performed under local anesthesia. Pathology of the tongue biopsy was negative for carcinoma and demonstrated extensive ulceration with granulation tissue and noncaseating granulomas; AFB stain performed on the tissue returned positive for mycobacteria. Periodic acid-Schiff stain was negative for other microorganisms.
Given the positive AFB stain, we reviewed a routine chest radiograph which had been obtained in the emergency room and it revealed diffuse micronodular densities (). In contrast, the patient's chest radiograph obtained four months before demonstrated no consolidations or lesions. The patient was placed on airborne precautions and three induced sputum specimens were obtained. Induced sputum specimens returned positive for acid-fast bacilli (AFB), and culture demonstrated M. tuberculosis.
In further evaluation of her pulmonary disease, a computerized tomography (CT) scan of the chest was obtained which showed diffuse miliary nodules and an incidental finding of focal central sclerotic lesions throughout the thoracic vertebral bodies (). Therefore CT scans of the cervical, thoracic, and lumbar spine were also obtained and they were consistent with intraosseous tuberculosis. The MRI findings in the right shoulder were presumed to be due to tuberculosis arthritis; repeated joint aspiration was insufficient for microbiological confirmation.
The patient's prednisone was decreased. She was started empirically on quadruple antituberculous therapy (rifampin, isoniazid, pyrazinamide, and ethambutol with the addition of pyridoxine). Culture sensitivity revealed a pan-susceptible strain of Mycobacterium tuberculosis; therefore ethambutol was discontinued. Once the patient completed the initial phase of treatment, she was maintained on isoniazid and rifampin for a total of 12 months. At a five-month followup visit, the tongue lesion was noted to have completely resolved and repeat imaging of her right shoulder demonstrated improvement. A followup chest X-ray at the end of the 12-month treatment showed complete resolution of the previously described miliary nodules in the lung parenchyma ().",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [100.3, 'degrees fahrenheit'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [7000.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 100.3 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 68.3 = 37.94444 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 120.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 7000.0 count/µL. To convert 7000.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 7000.0 white blood cell count/µL * 1.0 µL/mm^3 = 7000.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6794,51,SIRS Criteria,diagnosis,integer,pmc-2700571-1,Extracted,"A 38-year-old woman, gravida 4, para 3, was admitted to the emergency room at the university hospital of Hassan II. She presented with a 2 day history of extreme right iliac fossa pain. She experienced heavy bleeding for one day. The last reported menstrual period was 10 weeks before presentation. She denied fevers, chills, vomiting, constipation, and diarrhea. Past medical, obstetric, gynaecological, and surgical histories were remarkable only for 3 uncomplicated live births and no history of sexually transmitted diseases or pelvic inflammatory disease. On examination, she was found to have a blood pressure of 120/80 mmHg, a pulse rate of 80 beats/min and a respiratory rate of 20 breaths/min; she was mildly pyrexial at 37.5°C. Abdominal examination revealed tenderness in the right iliac fossa. Gynaecological examination revealed a closed cervix and a right adnexal mass.
Serum level of β-human chorionic gonadotropin (β-hCG) was 3175 IU/ml and complete blood cell count was significant for a leukocyte count of 14,000/mm3 with 80% polymorphonuclear leukocytes, hematocrit of 0.30, and a platelet count of 300,000. A pelvic sonogram revealed echogenic mass in the right adnexa measuring 4×5 cm with empty uterine cavity. An abdominal sonogram showed a thickening of the appendix wall associated with a free intraperitoneal fluid.
Diagnoses of appendicitis and ectopic pregnancy were entertained preoperatively, but neither could be excluded by history, physical, laboratory, and radiology examinations.
Because of the uncertainty in diagnosis, emergency exploratory laparotomy was performed through a subumbilical incision, leading to the surprising finding of concurrent ruptured ectopic pregnancy and appendicitis. She was found to have 400 ml of blood free in the pelvis with a perforated right-sided tubal pregnancy and a grossly inflamed appendix. Right salpingectomy, appendectomy and evacuation of blood clot were performed without complications. Post-operatively the patient received intravenous antibiotics; she made an excellent recovery. She was discharged from the hospital in stable condition 3 days later with a prescription for oral antibiotics. Pathologic examination of the resected segment of appendix revealed edema and inflammation of the appendix without abscess formation, consistent with early appendicitis. Pathology of the resected right fallopian tube revealed immature placental tissue and villi consistent with ectopic pregnancy.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.5, 'degrees celsius'], 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [14000.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.5 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 80.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 14000.0 count/m^3. To convert 14000.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 14000.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6795,51,SIRS Criteria,diagnosis,integer,pmc-8255223-1,Extracted,"A 76-year-old Japanese man with diabetes and hypertension presented with left lower quadrant abdominal and medial femoral pain for the previous 10 days. He was diagnosed with a left common iliac aneurysm by the consultant who referred him to our hospital. He denied any gastrointestinal symptoms before admission. He had no known allergies and was prescribed angiotensin II receptor blocker for hypertension and insulin for diabetes; however, he had discontinued these medications two months before hospitalization based on his own judgment.
He was alert (Glasgow Coma Scale 15), and his vital signs were as follows: body temperature, 38.2 °C; blood pressure, 117/54 mmHg; heart rate, 67 beats/min; respiratory rate, 14 breaths/min; and oxygen saturation, 98 % on ambient air. Physical examination indicated mild tenderness on the left lower abdomen. The findings from other examinations, including the palpation of bilateral dorsalis pedis arteries, were normal.
The laboratory findings were as follows: albumin, 3.0 g/dL; alanine transferase, 11 U/L; aspartate aminotransferase, 15 U/L; lactate dehydrogenase, 139 U/L; creatine kinase, 30 U/L; lactate, 7.7 mg/dL; blood urea nitrogen, 17 mg/dL; creatinine, 0.94 mg/dL; C-reactive protein, 5.15 mg/dL; blood glucose, 155 mg/dL; hemoglobin A1c (HbA1c), 6.9 %; white blood cell count, 6400/μL with 68.7 % neutrophils; hemoglobin, 8.8 g/dL; and platelet count, 22.2 × 104/μL.
Abdominal computed tomography (CT) showed a 27 × 32 mm sized saccular pseudoaneurysm surrounded by inflammation in the left common iliac artery (; A, C). The inflammation affected the inferior mesenteric artery and the left ureter (A), which caused left hydronephrosis (B).
Two sets of aerobic and anaerobic blood cultures (BacT/Alert FAN plus, bioMérieux, Marcy I’Etoile, France) obtained at admission turned positive within 21 h. Gram staining showed Gram-positive rods (A), which were quickly and accurately identified as L. monocytogenes, using the matrix-assisted laser desorption ionization (MALDI) biotyper Sepsityper kit® (Bruker Daltonik GmbH, Bremen, Germany) with a high score value (2.03) and the Verigene® system (Luminex, Austin, Texas, USA), within 24 h of obtaining the blood cultures. Isolates grew on 5% sheep blood agar (Nihon Becton-Dickinson, Tokyo, Japan), following 24 h incubation at 5% CO2 and 37 °C and exhibited a narrow zone of beta-hemolysis (B). The E-test® (bioMérieux, Marcy I’Etoile, France) suggested minimum inhibitory concentrations (MICs) of 0.19, 0.125, and 0.064 μg/mL for penicillin, ampicillin, and sulfamethoxazole/trimethoprim, respectively, which indicated susceptibility, according to the Clinical and Laboratory Standards Institute (CLSI) document (M100-Ed30) (; C, D) []. There was no evidence of infective endocarditis, as evaluated by transthoracic and transesophageal echocardiography or bacterial meningitis, as observed from the cerebrospinal fluid examination on day 2. In addition, the stool culture obtained during admission was negative for L. monocytogenes.
The patient was diagnosed with an infected aneurysm caused by L. monocytogenes and treated with 2 g of intravenous ampicillin every 6 h. He became apyrexial without any massive rupture of the infected aneurysm, because of the administration of the appropriate antibiotic; his blood pressure was well controlled with an intravenous antihypertensive calcium channel blocker. Blood cultures from samples obtained on day 6 were negative for L. monocytogenes. Therefore, surgical debridement, followed by in-situ Y-graft (Japan Lifeline Co., Ltd., Tokyo, Japan) placement with revascularization including the inferior mesenteric artery and omental implantation, was performed on day 8. The resected specimen culture was negative for L. monocytogenes, which could be attributed to the intensive antibiotic therapy before the surgery. Postoperative CT on day 16 indicated that all the anastomoses were patent without any complications (). After three weeks, the antibiotic therapy was changed from intravenous ampicillin to oral amoxicillin and the patient was discharged on day 23. Oral amoxicillin was discontinued on day 85, when all anastomoses remained patent without left hydronephrosis in the follow-up CT, and the patient has remained disease-free without recurrence ().",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.2, 'degrees celsius'], 'Heart Rate or Pulse': [67.0, 'beats per minute'], 'respiratory rate': [14.0, 'breaths per minute'], 'White blood cell count': [6400.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.2 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 67.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 6400.0 count/µL. To convert 6400.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 6400.0 white blood cell count/µL * 1.0 µL/mm^3 = 6400.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 14.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6796,51,SIRS Criteria,diagnosis,integer,pmc-2642792-1,Extracted,"We report a case of 12 years old boy, black, student who was admitted to our department for a 1 year progressive slowly growing of not painful abdominal mass occupying the right flank and right-lower quadrant. The patient had history of chronic constipation of 2 years referring 1 bowel movements every third-fourth day with hard stools. He denies symptoms of vomiting, nausea, diarrhea, fever, hematocquezia, hematuria, anorexia, lost weight. Not learning or mental disabilities were reported from his parents.
The patient was hospitalized previously four times during his life by history of constipation treated with laxatives and enemas and discharged with food recommendations. Only family history of diabetes in his grandmother.
On initial evaluation, the patient had a temperature of 37°C, blood pressure of 100/70 mm Hg, a heart rate of 85 beats per minute, a respiratory rate of 18 breaths per minute, with weight 30 kg and height 133 cms (BMI = 16.5, 18th centile).
Physical examination revealed a good general condition, cardiac and lungs examination were unremarkable. Abdomen without scars, soft, not distended, tympanic in 4 quadrants, normoactive bowel sound, palpation revealing an abdominal mass smooth, mobile, nontender in the lower right flank and quadrant of ± 13 cm of diameter. Rectal examination revealed no palpable stool in the rectal vault and was hemoccult negative. No malformations were finding during the examination.
The laboratory test parameter during admission were: hemoglobin 13.2 g/dl, hematocrit of 39.5%, WBC 5.500, platelets 374.000 mm3; creatinine 0.8/BUN 70, Na:142, K:4.3, urinalysis and liver function tests were normal. Stool samples for parasites were negative.
Intravenous pyelogram revealed a large rounded mass of approximately 12 cm. in diameter at the colon which seemed to have an irregular mottled texture. The right ureter seemed to be somewhat displaced by the mass that produce a slightly enlargement of the renal pelvis (Fig. ). Roentgenologic examination of the colon after barium enema showed an intraluminal mass having a smooth contour and without any mucosal attachment (Fig. ).
Ultrasound of the abdomen showed a mass arising probably from the intestine with no evidence of hydronephrosis.
The flexible rectosigmoidoscopy was done and only passed through 25 cm of rectum which presented a normal rectum with a roomy sigmoid colon and a large, firm fecal ball. Sigmoidoscopic rectal biopsies were not performed and fragmentation was attempted but abandoned because of pain during the procedure. Repeated enemas and laxatives were unsuccessful in evacuating the fecal mass.
The patient underwent elective laparotomy. Preoperative bowel cleaning was performed with phosphosoda solution and lavage with warm saline until evacuations were liquid without fecal residue. A 20-cm midline incision (infraumbilical with supraumbilical extension) was made. During the procedure we founded an enlarged sigmoid colon lateralized to the right showing a large, rock-hard mass, smooth and ovoid in shape, measuring about 14 cm, which appeared to be a hardened mass of feces. The rest of the colon appeared normal and empty.
The sigmoid colon with the mass was resected (Fig. ) and an end-to-end anastomosis was done. The patient recovered for the surgical procedure and had an uneventful convalescence. After six months our patient refers 1 bowel movement per day performing soft stools with no recurrence of his symptoms leading a completely normal healthy life.
Examination of the gross specimen after incision of the intestinal wall showed a firm fecal mass covered with a white material (barium) which filled the lumen but was unattached to the wall of the colon (Fig. ). No lesions were observed at the sigmoid wall. Microscopic examination of the colon demonstrates normal intestinal mucosa without ulcers. Myenteric plexus shows nerve fibers with lack of ganglion cells (Fig. ).",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.0, 'degrees celsius'], 'Heart Rate or Pulse': [85.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [5500.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 85.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 5500.0 count/m^3. To convert 5500.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 5500.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 5.5e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6797,51,SIRS Criteria,diagnosis,integer,pmc-4411896-1,Extracted,"We report the case of a 53-year-old female who presented to the emergency room complaining of severe nausea and vomiting associated with abdominal cramps and intense diarrhea starting nine hours after ingesting wild mushrooms which she had picked herself. The patient was admitted to the hospital and started on an intense cocktail of therapeutic modalities. The patient reported that at 4 am she awoke with intense right upper quadrant (RUQ) abdominal pain, accompanied by severe nausea and innumerable amounts of emesis. In addition she reported having multiple episodes of watery diarrhea. The symptoms continued throughout the day until she arrived in the emergency room. In the emergency room she was noticed to be in no acute distress with a temperature of 97.3 degrees Fahrenheit, blood pressure of 153/84, pulse of 96, and a respiratory rate of 20. Her physical examination was notable for an abdominal examination significant for mild tenderness to palpation in the RUQ with no guarding or rebound, active bowel sounds, or stigmata of liver disease. Pertinent laboratory values on admission revealed a creatinine of 1.2 mg/dL, WBC of 14.2 K/uL, hemoglobin of 16.7 g/dL, hematocrit of 49.3%, INR of 1.1, total bilirubin 0.8 mg/dL, ALT of 54 u/L, and AST of 68 u/L.
Intravenous hydration with normal saline was started and the New York State Poison Control Center was contacted. They recommended administering a regimen consisting of oral-activated charcoal 50 g every 2 hours, penicillin G one million units/kg IVPB every 6 hours divided into four doses per day, famotidine 20 mg IVPB every 6 hours (used for the first 16 hours of care until cimetidine 300 mg IV could be acquired), and vitamin C 500 mg PO BID. The following morning the patient's blood tests showed an increased ALT of 223 u/L and an AST of 304 u/L. She reported that she no longer had anymore nausea, vomiting, diarrhea, or abdominal cramps and that she was feeling better. However early that afternoon the patient suddenly became hypotensive and obtunded. An arterial blood gas was obtained and revealed a severe anion gap metabolic acidosis with a pH of 7.13, PO2 113, PCO2 19.7, HCO3 6.5, and an SO2 of 92%. The patient was immediately intubated and transferred to the intensive care unit where vasopressors were started as well as sodium bicarbonate and N-acetylcysteine infusions. Repeat labs showed an ALT of 824 u/L, AST of 1258 u/L, and an INR of 2.1. At this point arrangements were immediately made to transfer the patient to our regional liver transplant center to be evaluated for a liver transplant as her condition was rapidly worsening. Upon reaching the transplant center her condition continued to degrade and within 24 hours developed fulminant liver failure accompanied by hepato-renal syndrome and died despite maximal supportive care. The culprit mushrooms that were cooked and ingested by the patient were obtained for analysis as well as any mushrooms remaining from her reported area of foraging. These samples were then examined by an expert mycologist and determined them to be of the species Amanita bisporigera.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [97.3, 'degrees fahrenheit'], 'Heart Rate or Pulse': [96.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [14200.0, 'µL'], 'PaCO2': [19.7, 'mm hg']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 97.3 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 65.3 = 36.27778 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 96.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 14200.0 count/µL. To convert 14200.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 14200.0 white blood cell count/µL * 1.0 µL/mm^3 = 14200.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 19.7 mm Hg, which is less than than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6798,51,SIRS Criteria,diagnosis,integer,pmc-2827808-1,Extracted,"A 63-year-old man was admitted for chest discomfort, orthopnea, and dyspnea on exertion lasting 5 days. His initial vital signs included a blood pressure of 100/60 mmHg, a pulse rate of 80 beats/min, a respiratory rate of 20/min, and a body temperature of 36.6℃.
The jugular vein was engorged, but no hepatomegaly or audible cardiac murmurs were detected. The laboratory tests revealed the following: a hemoglobin, 11.3 g/dL; hematocrit, 35.3%; white blood cell (WBC) count, 9,550/mm3; platelet count, 254,000/mm3; blood urea nitrogen, 14 mg/dL; serum creatinine, 1.0 mg/dL; alanine aminotransferase, 58 IU/L; aspartate aminotransferase, 40 IU/L; total bilirubin, 0.9 mg/dL; glucose, 166 mg/dL; lactate dehydrogenase, 444 IU/L; protein, 6.4 g/dL; and albumin, 3.7 g/dL. Chest radiography showed an increased cardiac silhouette with a round, flask-like appearance (). Computed tomography and transthoracic echocardiography showed a large inhomogeneous and focally-enhancing mass in the right atrium, and a massive amount of pericardial and right pleural effusion ().
While in the emergency room, the blood pressure dropped to 80/54 mmHg and the pulse rate increased to 101 beats/min; the patient complained of severe dyspnea and chest pain, suggesting cardiac tamponade. An emergency pericardiocentesis and drainage was performed. The pericardial effusion was blood-like in color; an effusion analysis showed the following: hemoglobin, 11.9 g/dL; red blood cell (RBC) count, 2.95×106/mm3; WBC, 15,210/mm3 (lymphocytes, 68%; neutrophils, 23%), glucose, 109 mg/dL; lactate dehydrogenase, 591 IU/L; and protein, 5.6 g/dL. The initial drainage of the pericardial effusion was 800 mL. There were no malignant cells in the pericardial effusion cytology. The chest pain and dyspnea were improved immediately after the pericardiocentesis. Transesophageal echocardiography showed a 5.5×5 cm mass without invasion of the inferior and superior vena cava ().
On hospital day (HD) 5, surgery was performed. After the mass was resected, the right atrium was repaired with a bovine pericardial patch. The mass was close to the tricuspid valve (only 2 mm from the resection margin). On HD 7, the patient was transferred to the general ward and on HD 13 he was discharged. The patient was scheduled to receive adjuvant radiotherapy and chemotherapy.
At the time of biopsy, a 6.8×6.5×2.5 cm gray-brown protruding endocardial mass was noted in the right atrial chamber. The pericardium was spared of malignant cells. The cut surface was diffusely hemorrhagic with a gray-white solid portion. The tumor was comprised of oval-to-spindle cells with intracytoplasmic RBCs. There were frequent mitoses (> 10/10 HPF). The tumor cells were positive for CD34 immunohistochemical staining with confirmed primary cardiac angiosarcoma ().",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.6, 'degrees celsius'], 'Heart Rate or Pulse': [101.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [9550.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.6 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 101.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 9550.0 count/m^3. To convert 9550.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 9550.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 9.55e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6799,51,SIRS Criteria,diagnosis,integer,pmc-5124474-2,Extracted,"A 6-year-old female was admitted to our facility with persistent cough over the previous month and fever over the previous three days. Additionally, she complained of neck pain for the previous three months without torticollis. In another hospital, neck pain was thought to be due to the neck lymphadenopathy. The initial physical examination revealed temperature 39.5°C, pulse 120 beats/min, respiratory rate 25 breaths/min, and blood pressure 100/60 mm Hg. Crepitation was heard in the right lung, and enlarged cervical lymph nodes were observed bilaterally (>1 cm), with no redness or tenderness detected. All of the other systems were normal, with exception of torticollis on left side. Her initial WBC was 17 × 103 cells/mm3 with 86% segments, ESR was 55 mm/hr, and CRP was 27 mg/dL. The chest X-ray and thoracic CT scan revealed consolidation in the middle and lower lobes of the right lung (). Retropharyngeal abscess was excluded and intravenous cefotaxime was given for the pneumonia. The torticollis was thought to be due to pleural irritation. This patient's conditions improved dramatically, and she was discharged after 10 days. One week later, she was readmitted with torticollis, but the detailed neurological examination was otherwise normal. MR scan of the neck was performed to rule out the retropharyngeal abscess, and an arachnoid cyst (2.5 × 1.5 cm2) was observed on the upper cervical spinal cord, markedly compressing the front of the spinal cord (Figures and ). Surgery was planned immediately, before any neurological deficits developed.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.5, 'degrees celsius'], 'Heart Rate or Pulse': [120.0, 'beats per minute'], 'respiratory rate': [25.0, 'breaths per minute'], 'White blood cell count': [17000.0, 'm^3']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.5 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 120.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 17000.0 count/m^3. To convert 17000.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 17000.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 2e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 25.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6800,51,SIRS Criteria,diagnosis,integer,pmc-6591983-1,Extracted,"A 50-year-old Hispanic man with known history of obesity and hypertension presented with a 3-month history of abrupt episodes of weakness and altered mental status. He referred severe psychomotor symptoms as well as anxiety, aggressiveness, agitation, weakness, diaphoresis, and decreased visual acuity occurring at any time of the day and improved by eating. Upon further questioning, our patient, who worked as a truck driver and whose symptoms had reflected poorly in his workplace, also expressed overall discomfort with life and wishes of death due to the intensity of his symptoms. He had no history of tobacco smoking or excessive alcohol consumption. Medications taken prior to admission included candesartan 16 mg and hydrochlorothiazide (HCTZ) 12.5 mg once a day for hypertension.
During the following weeks, the symptoms increased in severity and frequency, with continued unremitting anxiety and weakness accompanied by loss of consciousness and extreme burning sensation in his entire body. After this acute episode, he was evaluated by a primary care physician in a local hospital and hospitalized for 4 days, where he continued to present recurrent episodes of irritability and aggression to self and others. He was discharged and referred for psychologic evaluation by mental health services at another institution. No specific diagnoses were given.
Upon release from mental evaluation, he was evaluated by a third physician, who performed a 3-hour postprandial blood glucose test which revealed a blood glucose level of 58 mg/dL. Suspecting an insulinoma, our patient was admitted to a third-level hospital, and upon arrival his vital signs were: afebrile (37 °C), heart rate of 93 beats per minute, blood pressure of 161/84 mmHg, respiratory rate of 19 breaths per minute, and oxygen saturation of 98% on room air. A physical examination revealed an oriented, well-nourished, and hydrated patient, without any stigmata on skin, a normocephalic and atraumatic head, and no masses or lesions. His eyes and ear, nose, and throat examinations were all within normal limits. His lungs were clear to auscultation without any added sounds, and heart sounds had a regular rate and rhythm without any murmurs, rubs, or gallops. An abdominal examination revealed a soft and nontender abdomen without any masses or organomegaly. Extremities showed no deformities, edema, skin discoloration, swelling, or tenderness. A neurological examination was within normal limits and showed an alert patient oriented to person, time, and place with fluent speech and comprehension. Cranial nerves II–XII were intact, with steady gait, with grossly intact sensation in all extremities. The reflexes were symmetric and 2+ at the biceps, triceps, knees, and ankles and had full strength in all extremities. Initial laboratory studies revealed a hemoglobin level of 15.7 g/dL (normal range, 13.7–17.5 g/dL), white blood cell count of 9.51 K/uL (normal range, 4.23–9.07), and calcium levels of 9.60 mg/dL (normal range, 8.42–10.22).
He was placed on the standard 72-hour fast to induce a hypoglycemic episode and became symptomatic after 20 hours. Further laboratory testing revealed blood glucose of 29 mg/dL (normal range, 100–125 mg/dL), increased insulin at 426 mIU/L (normal range, 2.6–24.9 mIU/L), and C-peptide levels of 12.83 ng/mL (normal range, 0.5–2.0 ng/mL). Sulfonylurea levels, abdominal ultrasound, and contrast magnetic resonance imaging (MRI) were also performed without findings. Prolactin, parathyroid hormone (PTH), albumin, and calcium levels, as well as MRI of his brain were normal, ruling out multiple endocrine neoplasia type 1 (MEN-1).
Prior to imaging, liver and renal function tests were performed, revealing alanine aminotransferase (ALT) levels of 27 U/L (normal range, 21–72), aspartate aminotransferase (AST) of 24 U/L (normal rang, 17–59), and creatinine levels of 0.89 mg/dL (normal range, 0.66–1.25). Urine analysis revealed no abnormal findings. After negative initial imaging, a triple phased computed tomography (CT) scan was performed, with an early arterial phase revealing a 1.8 × 1.6 cm hypervascular mass located at the tail of the pancreas (Figs. , ). Both kidneys had normal size and morphology, and slight hepatomegaly was shown as well as round nodules less than 10 mm in size in segments 3, 7, and 8.
At the completion of imaging studies, our patient was presented to the surgical department and scheduled for distal pancreatectomy in addition to a splenectomy due to the tumor’s close proximity to his spleen.
During the course of surgery an incidental appendectomy was also performed. A 4.5 × 3.5 × 1.5 cm specimen (Fig. ) was collected during surgery and sent for pathologic analysis; the pathologic analysis reported the diagnosis of insulinoma, an encapsulated mass within the specimen that measured 1.5 × 1.5 × 1.0 cm and is consistent with the findings on CT scan.
Upon microscopic evaluation, histologic analysis revealed pancreatic tissue organized into islets within a vascularized stroma interspersed by hyaline tissue (Fig. ). Surgical margins were clear of invasion and no metastasis was found in liver or abdominal lymph nodes.
Our patient had no complications during the immediate postoperative period, in which he was tested for glucose (190 mg/dL, normal range < 126 mg/dL), lipase (207 U/L, normal range < 160 U/L), and calcium (8.5 mg/dL, normal range, 8.5–10.2 mg/dL), and administered omeprazole (40 mg intravenously once per day), insulin glargine (100 UI subcutaneous injection once per day), atenolol (100 mg orally once per day), HCTZ (25 mg orally once per day), metoclopramide (10 mg intravenously every 8 hours), nalbuphine (10 mg intravenously every 8 hours), and ceftriaxone (1 g intravenously every 12 hours). During the third postoperative day (POD), elevated respiratory rate, decreased oxygen saturation, and chest auscultation of diminished breaths sounds with rhonchi, pointed toward a diagnosis of left lobar pneumonia with pleural effusion. However, he was discharged on the fifth POD and prescribed ambulatory management and follow-up by endocrinology, pulmonology, and internal medicine units. On the ninth POD, he returned to our hospital with acute pain and serohematic secretions at the surgical site and was managed with drainage of the seroma and intravenously administered ketorolac (30 mg intravenously twice a day). A vaccination scheme was established on the 19th POD follow-up visit and started on the 18th POD with Prevnar-13® (pneumococcal 13-valent conjugate vaccine, diphtheria CRM197 protein), followed by Influenza (34th POD), and diphtheria and tetanus (DT) booster (53rd POD). On POD 21, he returned to our emergency room with acute pain, 10/10 intensity of both left quadrants. Laboratory results returned “within normal limits” and he was discharged on ambulatory management. He remains asymptomatic at 6-month follow-up and is currently being treated with ciprofibrate (100 mg orally once per day), amlodipine (10 mg orally once per day), enalapril (20 mg orally once per day), and aspirin (81 mg orally once per day)",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.0, 'degrees celsius'], 'Heart Rate or Pulse': [93.0, 'beats per minute'], 'respiratory rate': [19.0, 'breaths per minute'], 'White blood cell count': [9510.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 93.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 9510.0 count/µL. To convert 9510.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 9510.0 white blood cell count/µL * 1.0 µL/mm^3 = 9510.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 19.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6801,51,SIRS Criteria,diagnosis,integer,pmc-3432333-1,Extracted,"A 49-year-old female with active intravenous heroin use was admitted with fever, chills, night sweats, malaise, nausea, and 15 lb weight loss for 2 months. About a month prior to admission, the patient had a foul smelling, draining skin abscess in the left arm at the site of heroin injection, which was treated with a course of trimethoprim/sulfamethoxazole prescribed in the emergency room. Although the abscess resolved, her constitutional symptoms worsened. She reported no cough, vomiting, diarrhea, abdominal pain, or dysuria and was taking no regular medications. She used heroin daily and had a twenty pack-year smoking history. She had been incarcerated for 9 months about five years prior to admission.
On physical examination, the patient was cachectic and malnourished. She was awake, alert, fully oriented and in no acute distress. Temperature was 39.4°C, blood pressure 115/69, heart rate 127, respiratory rate 20, and oxygen saturation 99% on ambient air. The area of the previous injection site infection was healed. Multiple needle track marks in the cubital fossae were noted. There was no cervical and axillary lymphadenopathy, and the lungs were clear to auscultation. Cardiovascular exam showed a regular tachycardia with normal S1 and S2. There were no murmurs or extra heart sounds. Abdominal exam was significant for mild right-upper-quadrant tenderness to deep palpation and a liver span of 14 cm in the right midclavicular line.
Laboratory showed a leukocytosis of 11.2, a markedly elevated serum alkaline phosphatase of 1210 unit/L (normal 38–126) and gamma-glutamyl transpeptidase (GGT) 957 unit/L (normal 12–43), as well as slightly elevated AST 125 unit/L, ALT 55 unit/L, and total bilirubin 1.5 mg/dL with direct bilirubin 0.9 mg/dl. Chest X-ray showed a nodule in the left lower lung. Intravenous contrast-enhanced chest CT demonstrated a peripheral 1.7 cm cavitary nodule in the left lower lobe and a peripheral 3 cm mass-like infiltrate in the right lower lobe (). Abdominal ultrasound demonstrated hepatomegaly without focal abnormality. The patient was empirically started on vancomycin for suspected staphylococcal endocarditis and was placed on respiratory isolation for possible tuberculosis. Since the patient did not produce sputum, bronchoscopy was performed, and an AFB smear as well as bronchoalveolar lavage culture were negative. Transthoracic echocardiogram showed normal systolic function without vegetation. Hepatitis C serology was positive, and HIV was negative. The patient continued to be febrile and tachycardic on day 3, her blood pressure fell to 85/44, and piperacillin/tazobactam was added to vancomycin, along with intravenous fluid resuscitation. Although blood culture was negative initially, gram positive rods, which appeared to be branching, were grown in multiple cultures after 5 days. Nocardia was suspected, therefore, trimethoprim/sulfamethoxazole (TMP/SMX) was started, and vancomycin and piperacillin/tazobactam were continued. Subsequently, the infectious disease consult recommended switching from vancomycin to linezolid to cover adequately for possible disseminated Nocardia infection. Therefore, the patient was placed on linezolid, piperacillin/tazobactam, and TMP/SMX. After the antibiotics regimen was initiated, the patient became afebrile and normotensive and felt much better. On day 14, the patient was discharged home with oral linezolid and TMP/SMX; however, she failed to keep her follow-up appointment and did not take her medications. She was readmitted 14 days later with the recurrence of all prior symptoms.
Approximately 15 days after the first admission, the reference lab reported that the gram positive rods were also acid fast and identified them as Mycobacterium fortuitum. The organism was grown in 6 aerobic bottles of a total of 15 blood cultures obtained during the two hospital admissions. It was sensitive to linezolid, imipenem, ciprofloxacin, amikacin, doxycycline, and sulfamethoxazole; and was resistant to clarithromycin, cefoxitin, and tobramycin. During the second admission, the patient was placed on intravenous linezolid and ciprofloxacin, and oral TMP/SMX with clinical improvement. She underwent transesophageal echocardiogram, which showed aortic and tricuspid valve vegetations (). A liver biopsy showed granulomatous hepatitis (). No organisms could be identified on the liver biopsy culture. However, serum alkaline phosphatase level fell with antibiotic treatment ().
The patient completed a six-week course of intravenous antibiotics and was discharged on oral bactrim and ciprofloxacin with goal of continuing the antibiotics for 6–12 months. She was counseled regarding options for treating her narcotic addiction.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.4, 'degrees celsius'], 'Heart Rate or Pulse': [127.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [11.2, 'L']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.4 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 127.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 11.2 count/L. To convert 11.2 count/L of white blood cell to mm^3, multiply by the conversion factor 1e-06 L/mm^3 which will give 11.2 white blood cell count/L * 1e-06 L/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6802,51,SIRS Criteria,diagnosis,integer,pmc-3955505-1,Extracted,"A previously healthy 70-day-old male was brought to our clinic (Mugla Sitki Kocman University, Medicine Faculty, Department of Pediatrics, Mugla/Turkey; February 2012) with cyanosis on the perioral region, trunk and hands, three hours after he was administered locally prilocaine (Cytanest 2%; Astra Zeneca, Istanbul, Turkey) for circumcision. His previous health history and family history were unremarkable. On physical examination, temperature of 36 °C, blood pressure of 90/70 mm Hg, heart rate of 128 beats per minute regular with normal pulses and respiratory rate of 44 beats per minute with normal breathing. Oxygen saturation level was 76% (with pulse oximeter) on room air while he had prominent cyanosis on perioral region and the extremities. The rest of the physical examination was normal.
Intravenous line was obtained, and the blood collected for laboratory analysis had chocolate-color appearance. The laboratory results analysed by routinely calibrated equipments revealed; Hb 11 g/dl, WBC 9310/μL, PLT 622000/μL and all other biochemistry values were in normal range (Symex XT 2000i,Roche Diagnostics, Mannheim, Germany). Arterial blood gases (GEM premier 3000,instrument laboratory, Italy, calibrated in january 2012) revealed pH 7.43, pCO2 41 mmHg, pO2 97 mmHg and bicarbonates 28 mEq/L, and methemoglobin 24.5% (). After obtaining blood samples to check the methemoglobin levels, 300 mg IV ascorbic acid was slowly administered in 24 h. After 10 min, oxygen saturation began to increase and an hour later reached its normal levels. Methemoglobin levels were found to be 24.5% before ascorbic acid administration. After 24 hour of administration, methemoglobin level was seen to be 2%.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.0, 'degrees celsius'], 'Heart Rate or Pulse': [128.0, 'beats per minute'], 'respiratory rate': [44.0, 'breaths per minute'], 'White blood cell count': [9310.0, 'µL'], 'PaCO2': [41.0, 'mm hg']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 128.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 9310.0 count/µL. To convert 9310.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 9310.0 white blood cell count/µL * 1.0 µL/mm^3 = 9310.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 44.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is 41.0 mm Hg, which is greater or equal to than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 1 + 1 = 2 criteria met.
Hence, the the number of SIRS criteria met by the patient is 2."
6803,51,SIRS Criteria,diagnosis,integer,pmc-3492681-1,Extracted,"A 32-yr-old male patient visited infection clinic of our hospital for fever, abdominal pain and vomiting in April 2011. He had no past medical history, family history and history of tobacco, alcohol, illegal drug use, and travel. He had been suffering from recurrent periodic fever, abdominal pain, and vomiting every three months since 3 yr ago. He complained of abdominal discomfort for two days and fever for three days followed along with whole abdominal pain and vomiting, and then the symptoms resolved spontaneously and completely. He could maintain a normal daily life during the symptom free period. He had already taken several blood tests, abdominal CT, gastroscopy, and colonoscopy a year ago in two another hospitals, but the cause of his symptoms had not been found.
His vital signs were blood pressure 120/68 mmHg, pulse 97/min, respiratory rate 22/min, and body temperature 40.0℃ on admission. Mild tenderness and hypoactive bowel sound were checked on the whole abdomen. Initial laboratory results showed that leukocyte was 9,980/µL (neutrophil 8,830/µL), hemoglobin 16.8 g/dL, platelet 171,000/µL, C-reactive protein 85.71 mg/L, and the erythrocyte sedimentation rate 6 mm/hr. Various antibody tests screening for infection, antibody tests for autoimmune disease, blood complement levels, blood cultures, peripheral blood smear, tumor markers, and hormone tests were all negative.
In abdominal CT with contrast enhancement (), were observed edematous wall thickening of proximal jejunum, dilatation of proximal jejunum, accompanied by lymphadenopathy, and a small amount of ascites. Therefore capsule endoscopy was done for the evaluation of small intestine. Mild lymphangiectasia was observed throughout the small intestine in capsule endoscopy. Despite biopsies taken at suspicious lymphangiectasia through double balloon enterosocpy, there was non-specific, only mild inflammation of mucosa. His symptoms lasted for around 3 days and then were spontaneously subsided, and abdominal ultrasonography on the 4th day of admission showed that jejunal dilatation and lymphadenopathy almost completely disappeared.
Through several tests, we could exclude several suspected diseases such as infectious diseases, autoimmune diseases and neoplastic diseases, and based on his repetitive symptoms and age, we thought that it was highly likely to be FMF or tumor necrosis factor receptor-associated periodic syndrome (TRAPS) among periodic fever syndromes. We performed MEFV and TNFR1 gene test for definite diagnosis, and as two missense mutations were detected in the exon 2 of the MEFV gene, c.329T > C (p.Leu110Pro) in heterozygous and c.442G > C (p.Glu148Gln) in homozygous, this patient was diagnosed as FMF (, ).
The patient is current under treatment with colchicine 1.2 mg/day and the progress is being followed up with gradually improved severity and duration of the symptoms.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [40.0, 'degrees celsius'], 'Heart Rate or Pulse': [97.0, 'beats per minute'], 'respiratory rate': [22.0, 'breaths per minute'], 'White blood cell count': [9980.0, 'µL']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 40.0 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 97.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 9980.0 count/µL. To convert 9980.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 9980.0 white blood cell count/µL * 1.0 µL/mm^3 = 9980.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6804,51,SIRS Criteria,diagnosis,integer,pmc-6154823-1,Extracted,"A 56-year-old male patient with no known comorbidities presented to the emergency department with history of fever and headache for past 2 days with sporadic episodes of projectile vomiting, irrelevant talk, and poor sensorium for a day. On admission, the patient manifested fever (39 °C), a heart rate of 104 beats per minute, blood pressure of 130/60 mmHg, respiratory rate of 30/min, and capillary blood glucose of 140 mg/dl. His Glasgow Coma Scale (GCS) score was 9, with respective scores of 5, 2, and 2 for motor, eye, and verbal responses. There were no signs of meningeal irritation or focal neurological deficit. Clinical examination was otherwise normal except for a scar over the anterior bi-frontal region which was a surgical incision. On further inquiry, he had an accidental fall from a two-story building 23 years ago, causing a persistent CSF leak from the nose (rhinorrhea). He underwent complete repair for the CSF leak without any residual defect. There were no further hospitalizations for the past 23 years with symptoms suggestive of meningitis.
His computerized tomography (CT) scan showed cystic gliosis changes in the left frontal lobe which was communicating with the frontal horn of ipsilateral lateral ventricle. CSF analysis of the patient revealed hypoglycorrachia (< 20 mg/dl with corresponding blood sugar of 140 mg/dl), elevated protein > 300 mg/dl, and neutrophil-predominant pleocytosis (total cells 360/mm3 with 96% polymorphs) suggestive of acute pyogenic meningitis. He was started empirically on ceftriaxone 100 mg/kg/day in two divided doses, amoxycillin 100 mg/kg/day in four divided doses, and acyclovir 45 mg/kg/day in three divided doses. Initial peripheral blood WBC count was 14,760 with 85% neutrophils and serum lactate levels of 5.35 mmol/l. His renal and liver function tests were normal. Antibiotics (ceftriaxone, amoxycillin) were continued, and acyclovir was stopped as there were filamentous gram-negative rods in gram staining of the CSF, which was a rare morphology to be identified (Fig. ). Further, the sample was plated onto blood agar, MacConkey agar, and chocolate agar and incubated aerobically at 37 °C. Non-hemolytic colonies were formed on blood agar (Fig. ) which were lactose-fermenting colonies on MacConkey agar (Fig. ). The organism was identified to be Escherichia coli by Vitek 2 Compact (Biomerieux), and spectrum of antibiotic sensitivity was described in Table .
In accordance with the culture and sensitivity pattern, ceftriaxone was continued and amoxycillin was stopped. He was afebrile for the next 48 h, and his sensorium improved. Further work up was done to identify the source of seeding of E. coli to the meninges. Urine culture and blood cultures that were sent prior to initiation of antibiotics did not show any bacterial growth, and stool microscopy was negative for ova and cysts. CT scan of the abdomen revealed a non-obstructive renal calculus of 6 mm × 6mm at interpole of the left kidney without any signs of pyelonephritis. After the initial improvement, patient again had a drop in sensorium without any localizing signs. Magnetic resonance imaging (MRI) of the brain with contrast study was done to rule out secondary complications associated with meningitis like vascular infarcts or hydrocephalus. There was post-contrast enhancement of leptomeninges and subtle enhancement of ventricular wall and posterior fossa cisternal spaces in post-contrast T1 sequence, and the same findings along with exudates in the ventricles in T2 fluid attenuated inversion recovery (FLAIR) images, which were suggestive of ventriculitis (Figs. and ). CT cisternogram was performed to check for residual CSF leak at the past surgical site, in which there was an opacified density in the left frontal region representing a porencephalic cyst communicating with the left frontal horn. There was no CSF leak into the paranasal sinuses or nasal cavity (Fig. ).
In the CSF analysis repeated on day 7 of antibiotic therapy, there was improvement in cell count (total cell count of 26 with 100% of lymphocytes) and cultures were sterile. He was discharged from the hospital on day 10 and advised to continue intravenous antibiotics for 6 weeks in view of ventriculitis. On further follow-up, the patient has improved, with no neurological deficit and antibiotics have been stopped at the end of the sixth week.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.0, 'degrees celsius'], 'Heart Rate or Pulse': [104.0, 'beats per minute'], 'respiratory rate': [30.0, 'breaths per minute'], 'White blood cell count': [14760.0, 'µL']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.0 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 104.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 14760.0 count/µL. To convert 14760.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 14760.0 white blood cell count/µL * 1.0 µL/mm^3 = 14760.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 30.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6805,51,SIRS Criteria,diagnosis,integer,pmc-3499430-1,Extracted,"An 80-year-old male patient visited Bongseng Memorial Hospital for a regular medical examination. The patient had a blood pressure of 110/70 mmHg, a heart rate of 80 beats/min, a respiratory rate of 24 times/min, and a body temperature of 36.8℃. No particular symptoms were identified, and he had normal consciousness. Auscultation revealed that the heart sound was normal, but a crackle was observed in both lower lungs. Peripheral blood tests showed white blood cell, 5,700 mm2; neutrophils, 58.4%; hemoglobin, 13.4 g/dL; mean corpuscular volume, 38.8%; and platelets, 218,000 mm2. Blood biochemistry showed total protein, 7.3 g/dL; globulin, 3.2 g/dL; total billirubin, 0.9 mg/dL; serum glutamic oxalacetic transaminase, 20 IU/L; serum glutamic pyruvic transaminase, 9 IU/L; alkaline phosphatase, 288 IU/L; and lactic dehydrogenase, 293 IU/L.
Colonoscopy showed an irregular inflammatory lesion in the ascending colon, and an ulcerative mass that covered more than 1/3 of the intestinal tract was observed in the SC 15 cm superiorly to the anal verge. The ulcerative mass in the SC was suspected as a malignant lesion in the initial tests, so a biopsy was performed (). An abdominal computed tomography (CT) showed that no particular clinical finding, except for a slight enlargement of the intestinal wall of the ileocecal area, lymphadenopathy, multiple cysts in the liver, 1-cm gallstones, and gallbladder wall distension.
A chest X-ray () showed an increase in opacity in the bilateral lower lung, and a chest CT () showed bilateral pulmonary emphysema, an endobrachial nodule, and a pulmonary nodule. Thus, radiological findings were reasonable for the assumption of active tuberculosis. In addition, an AFB trace was found in a sputum smear. The result of the biopsy showed that the inflammatory lesion in the ascending colon was chronic colitis, and that the lesion in the SC was chronic granulomatous inflammation ().
As colon cancer was endoscopically suspected, a follow-up colonoscopy was conducted one month after anti-tuberculous medication. As a result, the ulcerative mass observed in the SC was improved, and inflammatory polyps were observed in the uncreative area (). A biopsy was additionally conducted, and chronic inflammation was the only finding. A chest X-ray showed that the opacity of both lower lungs had decreased. The patient's respiratory symptom was also improved. An improvement was confirmed in a follow-up colonoscopy conducted 6 months later. At present, the patient has completely recovered via anti-tuberculous medication for 9 months and has been following an outpatient follow-up schedule.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.8, 'degrees celsius'], 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'respiratory rate': [24.0, 'breaths per minute'], 'White blood cell count': [5700.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.8 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 80.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 5700.0 count/m^3. To convert 5700.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 5700.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 5.7e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 24.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 1 + 1 = 2 criteria met.
Hence, the the number of SIRS criteria met by the patient is 2."
6806,51,SIRS Criteria,diagnosis,integer,pmc-8040694-1,Extracted,"A 70-year-old man with a history of hypertension and paroxysmal atrial fibrillation presented with high fever and general fatigue 4 days before hospital admission (). He visited our hospital due to experiencing continued fever and general malaise with mild cough. His vital signs were as follows: heart rate (HR), 92 beats/min; respiratory rate (RR), 20 breaths/min; axillary temperature, 38.3°C; SaO2 97% (room air); and blood pressure, 161/91 mmHg. Chest computed tomography (CT) scan revealed progressive interstitial pneumonia with bilateral patchy ground-glass opacities on admission (). The patient was diagnosed with COVID-19 pneumonia after a positive severe acute respiratory syndrome–coronavirus (SARS-CoV)-2 real-time polymerase chain reaction (PCR) test and admitted to the general ward at our hospital.
Ciclesonide inhalation was started on day 1 of hospitalization. Due to continued fever, the patient received favipiravir on day 3 (at a dose of 3600 mg/day on day 3 and 1600 mg/day on days 4–16). On day 5, the patient experienced dyspnea, his SpO2 was 89% at room air, and his PaO2/FIO2 (P/F) ratio was 338. Oxygen was administered as was azithromycin. On day 6, the patient’s SpO2 was under 90% (reservoir mask oxygen, 8 L/min) with dyspnea, leading to the administration of a single dose (8 mg/kg) of tocilizumab. Blood C-reactive protein (CRP) levels decreased after tocilizumab administration. Nevertheless, the patient’s symptoms did not improve, and his P/F ratio was 92 and accompanied by dyspnea and tachypnea. The patient was admitted to the ICU on day 7. On day 8, the patient’s P/F ratio decreased to 73 and his RR was 27/min. The other blood tests before PMX-DHP on day 8 are follows: white blood cell count (WBC): 6800/µL, lymphocyte: 5.6% (absolute lymphocyte count: 526/µL), troponin I: 0.03 ng/mL, NT-pro BNP: 58 pg/mL, ferritin: 913 ng/mL, LDH 604 U/L, AST 44 U/L, procalcitonin 0.20 ng/mL. The patient then received the initial round PMX-DHP therapy for 6 h, with continued monitoring of blood cytokine levels. However, his condition did not improve, with the P/F ratio of 89 and RR of 25/min on day 10. He received the second round of PMX-DHP therapy over 6 h. The following day (on day 11, 10 h after the second round of PMX-DHP), the patient’s dyspnea improved, and his RR decreased to 22/min. On day 14, his P/F ratio was 149 and RR was 19/min. On day 18, both his P/F ratio and RR values reached 310 and 17/min, respectively, and oxygen therapy was discontinued. On day 20, the patient was discharged from the ICU. There was no decrease in blood pressure during the course of the ICU and hemodynamics were stable On day 95, his lungs recovered without the evidence of lung fibrosis on a chest CT scan (). The patient recovered without requiring mechanical ventilation during his hospitalization.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.3, 'degrees celsius'], 'Heart Rate or Pulse': [92.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [6800.0, 'µL']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.3 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 92.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 6800.0 count/µL. To convert 6800.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 6800.0 white blood cell count/µL * 1.0 µL/mm^3 = 6800.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6807,51,SIRS Criteria,diagnosis,integer,pmc-2846740-1,Extracted,"A 55-year-old woman developed generalized urticaria, itching, and a subsequent coma within 5 minutes of ingesting yacon roots. At the time, she was in a steam bath. She was treated at a regional hospital, and her systolic blood pressure was 60 mmHg. She was then referred to our clinic to determine the cause of her problem.
She had a 20-year history of hypothyroidism and had been taking amlodipine (5 mg) for hypertension for 3 years. There was no history of bronchial asthma, allergic rhinitis, or atopic dermatitis, although she frequently developed pruritus when preparing Codonopsis lanceolata. She did not smoke or consume alcohol. She reported that her one son developed urticaria and angioedema when he ingested shrimp, apple, or pear.
On physical examination, she appeared acutely ill, but her consciousness was clear. Her blood pressure was 100/60 mmHg; respiratory rate, 20/minute; pulse, 81/minute; and body temperature, 36℃. Her conjunctivae were not anemic, and no jaundice was observed in her sclera. On auscultation, no rales or stridor were heard. There were no abnormal findings in the abdomen or extremities.
Routine blood tests revealed a white blood cell count of 5,350/µL, 182/µL eosinophils (3.4% of all white blood cells), and an erythrocyte sedimentation rate (ESR) of 2 mm/hour. Thyroid function tests showed TSH at 5.99 mIU/L (normal range, 29-4.2 mIU/L), free T4 at 0.86 ng/dL (normal, 0.93-1.70 ng/dL), total T3 at 96.14 ng/dL (normal, 80-200 ng/dL), and anti-TPO antibody at 278.3 IU/mL (normal, 0-314 IU/mL). No abnormalities were observed by biochemical or serologic testing, urinalysis, stool examination, electrocardiography, and simple chest X-rays.
She refused skin prick tests with common inhalant allergens, although skin prick and intradermal tests were performed using juice extracted from cut raw yacon root. The skin prick test showed a 3.5×4.0/+ reaction to histamine (H), -/- reaction to normal saline, 4.5×7.0/+ reaction to yacon extract (allergen A), and a 3+ A/H ratio (positive reaction) (). An oral food provocation test was performed using 1-g pieces of yacon root. The patient complained of tingling, pain, and numbness in the oral cavity and around the lips at about 5 minutes after ingesting 2 g of the root. Headache, chest tightness, dizziness, and pruritus/urticaria extending to the neck and face developed about 10 minutes after ingesting the root. At that time, her blood pressure was 85/50 mmHg and her pulse was 115/minute. The oral provocation test was stopped because the patient complained of chest tightness and dizziness. The patient was given epinephrine (1:1,000, 3 mL, intramuscularly), dexamethasone (5 mg, intravenously), and fluids. Her symptoms improved immediately and her blood pressure normalized. She was definitively diagnosed with anaphylaxis to yacon root based on the oral provocation test results. She was instructed not to ingest yacon roots and to carry a portable epinephrine kit for use in an emergency. Levothyroxine (50 µg) was prescribed for her hypothyroidism.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.0, 'degrees celsius'], 'Heart Rate or Pulse': [81.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [5350.0, 'µL']}",0,0,0,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 81.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 5350.0 count/µL. To convert 5350.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 5350.0 white blood cell count/µL * 1.0 µL/mm^3 = 5350.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 0.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 0.
Hence, the the number of SIRS criteria met by the patient is 0."
6808,51,SIRS Criteria,diagnosis,integer,pmc-6652069-1,Extracted,"An 81-year-old man presented to our institution with a chief complaint of abdominal pain and distension. The patient reported one week of worsening, generalized abdominal pain with constipation that had progressed to obstipation. The patient also admitted to several episodes of nausea and vomiting over the last two days. Recently, the patient has undergone emergent sigmoidoscopy in another facility to decompress a twisted sigmoid colon, and it showed sigmoid colon with numerous polypoid-appearing lesions with grossly normal-appearing overlying mucosa (). Past medical history was significant for duodenal ulcer and chronic constipation. The patient is taking a proton-pump inhibitor but not regularly. His social history is significant for smoking 40 packs per year; the family history was noncontributory.
On presentation, the patient looked tired and dehydrated, and initial assessment revealed following vital parameters the following: blood pressure 110/50 mmHg, pulse 98/min, respiratory rate 20/min, saturation 94% on room air, and temperature 36.5°C. The patient complained of generalized abdominal tenderness but without peritoneal reaction. The abdomen was distended with generalized tenderness but without peritonitis signs or exaggerated bowel sounds. Rectal examination was normal and nasogastric tube revealed 1500 cc of stomach content fluid.
The patient's blood work was remarkable for the following results: WBC count was 12 k/μl, hemoglobin 9.6 g/dl, hematocrit 28.2%, and platelet count 167 k/μl.
The patient's abdominal CT scan showed massive distention of the stomach () with a cluster of air-filled sacs compatible with PI affecting the sigmoid colon and the intestine () and no free air or signs of acute sigmoid volvulus (SV).
Upper endoscopy was performed for diagnosis and gastric decompression purposes. It showed a copious amount of fluids in the stomach with considerable gastric distention; however, it was very difficult to proceed with endoscopy, and surgical decompression was recommended. After initial resuscitation, the patient was then taken to the operating room. The stomach was severely distended with signs of fibrotic pyloric mass. The sigmoid colon was remarkably redundant. There were findings of chronic sigmoid volvulus with a twisted sigmoid mesentery. PI was apparent externally and covering the entire sigmoid colon; however, there were no signs of perforation. Another extensive PCI disease was found covering the ileum () but without other intraoperative abnormalities. Partial distal gastrectomy, vagotomy, and Billroth II reconstruction were performed, and the intraoperative frozen section was negative for malignancy. The patient then also underwent a sigmoid resection (Figures and ) with primary anastomosis of the descending colon and the rectum. Postoperatively, the patient's diet was slowly advanced; he was discharged on the sixth postoperative day with unremarkable recovery period up to a 3-month follow-up.
The final histopathology on the surgically resected specimens revealed benign fibrotic stenotic pylorus with extensive PI involving the sigmoid colon.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.5, 'degrees celsius'], 'Heart Rate or Pulse': [98.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [12000.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.5 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 98.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 12000.0 count/µL. To convert 12000.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 12000.0 white blood cell count/µL * 1.0 µL/mm^3 = 12000.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6809,51,SIRS Criteria,diagnosis,integer,pmc-4688336-1,Extracted,"A 41-year-old woman was admitted to our hospital with a complaint of severe headache. She had headache for 3 years and expressed it as throbbing pain in both temporal regions accompanied by nausea. This pain was exacerbated by physical activity and under sunlight. Symptoms tended to occur once in 1~2 months, lasted for 1~3 days and then disappeared. A week before admission to our hospital, her headache symptoms were different from those in the past. She felt a twinge it the right posterior neck for the first time, and subsequently experienced severe pain in the entire head, but no nausea, vomiting, or fever. She was admitted to the neurology department of an outside hospital and underwent computerized tomography (CT) angiography 2 days after the headache developed; no bleeding was noticed yet multifocal vasospasms of intracranial arteries were revealed (). She was diagnosed with status migrainosus; hence, steroid pulse therapy with oral beta-blockers and non-steroidal anti-inflammatory drugs were given to relieve headache. However, her symptoms did not improve but rather worsened. Several hours before admission to our hospital, she started complaining of nausea and vomiting as well as very sharp tearing pain in the neck and back. According to the analysis of a cerebrospinal fluid (CSF) specimen that was obtained via lumbar puncture in an outside hospital 3 days after symptom onset, the levels of white blood cells (WBC), protein, and glucose were 4/µl, 62 mg/dl, and 46 mg/dl, respectively. Other CSF profiles were not provided. She had a history of hypertension and her blood pressure was well controlled with regular antihypertensive medication. She denied any history of auto-immune or cerebrovascular diseases. There was also no special family history of migraine or autoimmune disease. On admission to our hospital, her blood pressure was 195/114 mmHg; pulse, 60 beats/min; respiration, 20 breaths/min; and body temperature, 36.6℃. Mental status was alert and oriented. Cranial nerve examination and motor and sensory functions were normal. No pathologic reflexes were found, yet neck stiffness was suspected. According to the routine blood tests, the only abnormality was that the WBC count was increased to 18000/µl. In the blood coagulation test, prothrombin time-international normalized ratio and activated partial thromboplastin time were 0.99 s (normal range, 0.00~1.20 s) and 28 s (normal range, 20.0~36.0 s), respectively; both values were within the normal range. Aortic CT angiography revealed no evidence of aortic dissection. We started steroid pulse and mannitolization therapy. On day 2 after admission, her headache was alleviated, yet pain in the neck and back rapidly worsened and subsequently spread to the whole spine. Additionally, marked neck stiffness was observed. On day 3 after admission, brain magnetic resonance imaging (MRI) showed no intracranial hemorrhage, such as SAH (). On the same day, transfemoral cerebral angiography (TFCA) revealed multiple ICVSs (). Two hours after TFCA, weakness of both legs [Medical Research Council (MRC) grade 0 or I], bladder distension, and sensory deficit below both nipples developed. On spinal cord MRI, we found spinal cord compression by SDH, which was located from the ventral lower cervical to mid-thoracic level (C7 to T6) (). In subsequent CSF examinations, the red blood cell count was 340000/µl and WBC count was 30/µl (polymorphonuclear leukocytes, 59%; lymphocytes, 29%; and mononuclear cells, 12%), CSF was red, and no color change was observed in the three-tube test. Emergent total laminectomy was performed through the posterior approach, which was started 7 h after paraplegia. While incising the dura, we found that the spinal cord was swollen and large hematoma was present in the subdural and subarachnoid spaces. The hematoma was evacuated and no vascular malformation was found. After surgery, pain was relieved. On postoperative day 5, sensory symptoms and muscle power of the left leg (MRC grade II) partially improved.
Upon the request by the patient's guardian, the patient was transferred to another hospital on postoperative day 6. Three days after the transfer, the patient had weakness and alien hand syndrome of the left arm. Brain MRI showed bilateral multifocal acute infarction of the corpus callosum; the right side of the lesion was larger than the left side (). On CT angiography performed at the other hospital at 8 days after the transfer from our hospital, more exacerbated vasospasms were found in the anterior, posterior, and middle cerebral arteries than initial CT angiography after the headache onset. Upon medical treatment, symptoms in the left arm gradually improved. Four months after discharge from our hospital, she visited our out-patient clinic and no longer had any pain including headache. She did not complain of urinary symptoms yet complained of a tingling feeling in both legs. The muscle power of both legs and the left arm was approximately MRC grade IV, while the power of the right arm was MRC grade V, which represented considerable improvements in comparison with those parameters at the time of discharge from our hospital. Alien hand syndrome was also no longer observed.
About 1 year after symptom onset, muscle power recovered to an almost normal level in both legs and arms. Follow-up magnetic resonance angiography revealed no vasospasms in any of the intracranial arteries ().",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.6, 'degrees celsius'], 'Heart Rate or Pulse': [60.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [18000.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.6 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 60.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 18000.0 count/µL. To convert 18000.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 18000.0 white blood cell count/µL * 1.0 µL/mm^3 = 18000.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6810,51,SIRS Criteria,diagnosis,integer,pmc-5733958-1,Extracted,"This is a 47-year-old Caucasian male with a history significant for a living unrelated renal transplant two years prior to presentation and recent acute cytomegalovirus (CMV) infection. He presented with a two-day history of worsening, ascending lower extremity weakness, numbness, and tingling. The weakness had worsened rapidly to the point where he had difficulty ambulating and imbalance. Seven days prior to presentation, he had first presented with fever, chills, myalgias, and headache of one-week duration. Work-up at that time revealed acute CMV infection and he was started on oral valganciclovir at treatment doses. On review of systems, the patient complained of mild shortness of breath that worsened on exertion. He denied fever, chills, nausea, vomiting, diarrhea, lightheadedness, cough, lower extremity edema, or any changes in his urine output. He denied any recent travel, sick contacts, recent history of insect bites, or vaccinations.
His past medical history was significant for hypertension, dyslipidemia, asthma, and a distant history of melanoma. The etiology of his end stage kidney disease was biopsy proven focal segmental glomerulosclerosis presumed to be secondary to anabolic steroid use. He had a living unrelated kidney transplant two years prior to presentation. Induction was with steroids and basiliximab. His posttransplant course was complicated by biopsy proven BK Virus Nephropathy one year after transplant for which he was successfully treated with reduction in immunosuppression and intravenous immunoglobulin. At the time of transplantation, the donor was CMV positive, and the recipient was CMV negative. He received prophylaxis with valganciclovir for CMV more than one year. His current immunosuppression regimen consisted of prednisone 5 mg daily, tacrolimus 1.5 mg every twelve hours, and mycophenolate mofetil 500 mg every twelve hours.
On physical examination, the patient appeared anxious but was awake, alert, and oriented to person, place, and time. Vital signs included a blood pressure of 137/98 mmHg, pulse rate of 81/min, temperature of 97 degrees Fahrenheit, respiratory rate of 16 breaths/min, and a pulse oximetry of one hundred percent on room air. Physical examination was significant for a neurological examination, which demonstrated decreased motor strength in proximal and distal muscles in both upper and lower limbs (grades 3/5 and 2/5, resp.). He had absent deep tendon reflexes in his lower extremities. His gait could not be assessed due to lower extremity weakness and inability to ambulate. Two days before, his neurological exam was noncontributory except for decreased temperature sensation in his hands and feet.
Laboratory data from one week prior to presentation included mild thrombocytopenia, mild increase in liver transaminases, and a stable creatinine. Diagnosis of acute CMV infection was made based on a positive serum CMV IgM titer of 149 au/ml (normal < 30 au/ml), negative CMV IgG, and CMV PCR with 4800 copies/ml. Lumbar puncture and other serologic work-ups were negative. MRI of the brain done revealed no acute changes. Due to a diagnosis of acute CMV infection, he was started on oral valganciclovir. Laboratory data at this presentation included white blood cell count 5.9 k/microliter; hemoglobin 16.8 grams/deciliter; platelets 312 k/microliter; sodium 139 mmol/liter; potassium 3.6 mmol/liter; chloride 105 mmol/liter; bicarbonate 23 mmol/liter; blood urea nitrogen 17 mg/dl; and creatinine 1.28 mg/dl (at baseline). Urine heavy metal screen was negative for arsenic, cadmium, mercury, or lead. HIV, HTLV I/II, HBV, HCV, HSV, EBV, and HHV-6 PCR analyses were all negative. Lumbar puncture showed cerebrospinal fluid protein at 63 mg/dL, glucose of 68 mg/dL, cell count of 1, and albumin of 52.7 mg/dL. CMV PCR was positive in the CSF. Serum CMV PCR was 4000 copies/mL.
Based on positive serum and cerebrospinal fluid CMV PCR, the typical albuminocytologic dissociation of CSF analysis, and progressive neurological manifestations, a diagnosis of CMV associated Guillain-Barré Syndrome was made.
The patient was on an immunosuppression regimen that consisted of prednisone 5 mg daily, tacrolimus 1.5 mg every twelve hours, and mycophenolate mofetil 500 mg every twelve hours. The mycophenolate mofetil was discontinued, and the Prograf dosage was reduced to target FK506 troughs of 5–7. In addition to reduction in immunosuppression, the patient received eleven treatments of plasma exchange over a course of two weeks (each exchange consisted of two plasma volumes each with albumin as the replacement) and a total of 1 g/kg body weight of intravenous immunoglobulin (IVIG) in two divided doses. He was continued on valganciclovir 900 mg orally two times a day. After 72 hours, the patient began to improve with increased motor strength and improved negative inspiratory flow and vital capacity measurements. Every successive plasma exchange treatment seemed to subjectively show a favorable response to his motor recovery and muscle strength. After a two-week hospitalization, the patient regained his ability to ambulate and he was subsequently discharged on oral valganciclovir. He was continued on treatment doses of valganciclovir at 900 mg orally two times a day as an outpatient. His serum CMV PCR was negative after two weeks of treatment. One month later, the patient returned with lower extremity weakness and was readmitted for a presumed relapse. At this time, his CMV PCR was still negative. The patient was then treated with a total of 7 plasma exchanges. He regained his motor strength once again after initiation of plasma exchange and subjectively reported progressive improvement with each treatment. The patient had no adverse reactions to the IVIG or to the plasmapheresis. He has been in remission after treatment. His renal function has remained stable through all of this.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [97.0, 'degrees fahrenheit'], 'Heart Rate or Pulse': [81.0, 'beats per minute'], 'respiratory rate': [16.0, 'breaths per minute'], 'White blood cell count': [5900.0, 'µL']}",0,0,0,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 97.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 65.0 = 36.11111 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 81.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 5900.0 count/µL. To convert 5900.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 5900.0 white blood cell count/µL * 1.0 µL/mm^3 = 5900.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 0.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 16.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 0.
Hence, the the number of SIRS criteria met by the patient is 0."
6811,51,SIRS Criteria,diagnosis,integer,pmc-7255552-1,Extracted,"A 66-year-old male presented to the emergency department (ED) with complaints of abdominal pain. The patient provided a past medical history of rectal cancer, alcohol-induced cirrhosis, esophageal varices, stroke, paroxysmal atrial fibrillation, and hypertension. Vital signs at admission were temperature 99 degree Fahrenheit, heart rate 111 beats per minute, respiratory rate 19 blood breaths per minute, pressure 132/82 mmHg, and oxygen saturation 95%. Physical examination was positive for right upper quadrant tenderness. Laboratory results showed white blood count 14,000/mm3, hemoglobin 9.5 g/dL, platelet count 77 x 109/L, aspartate aminotransferase 19 U/L, alanine transaminase 12 U/L, alkaline phosphatase 85 U/L, prothrombin time/international normalized ratio 36/1.3. A CT of the abdomen and pelvis without contrast revealed cirrhotic liver, cholelithiasis, and a mass extending to the gallbladder from the medial segment of the left hepatic lobe (Figure ).
Ultrasound of the right upper quadrant revealed cholelithiasis with a distended gallbladder. The patient reported he had been recently treated with neoadjuvant chemotherapy and radiation for rectal cancer. His positron emission tomography/CT scan and MRI were negative one month prior to his ED visit. He developed multifocal atrial tachycardia and later wide QRS tachycardia soon after admission. The irregular rhythm was managed with beta-blocker therapy, oral metoprolol 50 mg twice a day. The patient had one episode of hematemesis and developed shock requiring aggressive intravenous fluid resuscitation and vasopressors. Rapid sequence intubation was required for acute hypoxemic respiratory failure due to possible aspiration. Bronchoscopy was performed afterwards and dark brownish secretions were suctioned. A repeat CT of the abdomen and pelvis without contrast showed bleeding from the gallbladder with hemoperitoneum and thickening of the ascending colon (Figure ). The patient was emergently taken to surgery and underwent laparoscopic cholecystectomy with evacuation and drainage of intra-abdominal hematoma/hemoperitoneum and abscess. During surgery, a large hemoperitoneum was found throughout the abdomen, and after evacuating 1.5 L of cold blood and bile, the gallbladder was visualized. Bright red blood was oozing from the cystic artery, and the gallbladder was perforated with leakage of bile and blood throughout the abdomen. Active bleeding from the cystic artery was stopped with a staple because artery dissection and placement of a clip were not possible. The patient had two drains placed intra-abdominally, and his gallbladder was sent for pathology. He remained hemodynamically stable and was extubated four days later. Gallbladder pathology did not show any evidence of malignancy. Intra-abdominal cultures were positive for Klebsiella pneumoniae and Enterobacter cloacae due to gallbladder perforation. The patient was treated with appropriate antimicrobial therapy (pipercillin/tazobactam and meropenem) per culture sensitivity for seven days. He had an outpatient follow-up with the general surgeon in two weeks, and no complications were noted.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [99.0, 'degrees fahrenheit'], 'Heart Rate or Pulse': [111.0, 'beats per minute'], 'respiratory rate': [19.0, 'breaths per minute'], 'White blood cell count': [14000.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 99.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 67.0 = 37.22222 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 111.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 14000.0 count/m^3. To convert 14000.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 14000.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 19.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6812,51,SIRS Criteria,diagnosis,integer,pmc-5696664-1,Extracted,"A 17-year-old female was admitted to bilateral blurring of vision, neck pain, and headache; she had experienced these symptoms for 5 days. She had neither a remarkable medical history nor infectious symptoms. She had been vaccinated for Bacillus Calmette–Guérin in infancy. Initial vital signs were within normal limits: body temperature 36.4°C, heart rate, 80 beats/min; blood pressure, 100/60 mmHg; and respiratory rate, 20/min. Her weight and height were 56 kg (percentile 50%) and 155 cm (percentile 10%), respectively. On physical examination, optic neuritis was diagnosed with pallor optical disc, although the cranial nerves, muscles power, and deep tendon reflexes were all normal. The result of other system examinations was unremarkable, except right cervical lymphadenopathy (2 cm × 2 cm). Her primary laboratory data were as follows: white blood cell counts, 9.700/mm3, neutrophils, 65%; lymphocytes, 25%; monocyte, 10%; hemoglobin 9.7 g/dL; platelets, 242.000/mm3; erythrocyte sedimentation rate, 50 mm/h; C-reactive protein, 12 mg/dL; urea, 43 mg/dL; and creatinine, 1.54 mg/dL. All other measures were within normal limits. MRI of the spine showed an intramedullary lesion that was isointense on the T1-weighted and hyperintense on the T2-weighted images, extending from the brainstem to the full lumbar spine []. Vertebrae, intervertebral discs, and brain MRI were normal. The MRI images were consistent with a diagnosis of holocord LETM. Lumbar puncture showed normal intracranial pressure (160 mmH2O). Cerebrospinal fluid (CSF) analysis revealed 11 cells/mm3 with lymphocyte, and elevated protein (148 mg/dL) and normal glucose (59 mg/dL) levels. CSF polymerase chain reaction (PCR) for MTB, herpes simplex virus, Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, and Enterovirus, acid-fast bacillus (AFB) stain, and an agglutination test for brucella were all negative. Serology results for Lyme and brucella in the blood were negative. CSF NMO antibodies and oligoclonal bands were negative. Serum viral serology was unremarkable, and an ELISA for human immunodeficiency virus was negative.
On follow-up, blood pressure was found to have remained high (220/110 mmHg), and urea and creatinine levels had progressively increased (132 mg/dL and 3 mg/dL, respectively). The markers for autoimmune and connective tissue disorders (i.e., antinuclear antibodies, anti-dsDNA, C3, C4, Coombs, anticardiolipin antibody, thyroid-stimulating hormone, and free T4) were all negative, and echocardiography and urine calcium testing were within normal limits. Sarcoidosis was ruled out by the laboratory tests. Chronic renal failure was diagnosed, but hypertension could not be controlled, despite aggressive medical therapy. The result of tuberculin skin testing (TST) was positive (23 mm), but the chest X-ray was normal. AFB and MTB-PCR on three consequtive sputum samples were negative. The results of the patient's immunological screening tests were normal. On follow-up, the patient had transient left upper limb muscle weakness (muscle power grade 4/5). Pulse steroid therapy was initiated. Computed tomography of the chest revealed a calcified lymph node (3 cm × 1.5 cm) in the right paratracheal region. On abdominal MRI, a few nodular lesions were detected on the left liver lobe. On the histopathological evaluation of the cervical lymph node and liver, necrotizing granulomatous inflammation with positive AFB was detected. The clinical and imaging findings supported a diagnosis of disseminated tuberculous with holocord LETM. Four antituberculous drugs (isoniazid, rifampin, pyrazinamide, and ethambutol) were administered with corticosteroid therapy (2 mg/kg/day). The patient received prednisone for the first 8 weeks. All sputum, tissue, and CSF cultures remained negative for MTB. After 16 weeks of treatment, her complaints disappeared, and the results of control spinal MR were completely normal []. At the end of the one year, antituberculosis therapy was stopped without any sequelae.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.4, 'degrees celsius'], 'Heart Rate or Pulse': [80.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [9700.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.4 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 80.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 9700.0 count/m^3. To convert 9700.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 9700.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 9.7e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6813,51,SIRS Criteria,diagnosis,integer,usmle-671,Extracted,"A 47-year-old woman comes to the emergency department 4 hours after the onset of abdominal and right shoulder pain. She has nausea and has had 2 episodes of vomiting. The pain began after her last meal, is constant, and she describes it as 7 out of 10 in intensity. She has had multiple similar episodes over the past 4 months that resolved spontaneously. She drinks 2 pints of vodka daily. She appears ill. Her temperature is 38.4°C (101.1°F), pulse is 110/min, respirations are 20/min, and blood pressure is 165/90 mm Hg. She is alert and fully oriented. Examination shows diaphoresis and multiple telangiectasias over the trunk and back. The abdomen is distended; there is tenderness to palpation in the right upper quadrant. When the patient is asked to inhale with the examiner's hand below the costal margin in the right midclavicular line, the patient winces and her breath catches. Voluntary guarding and shifting dullness are present. The liver is palpated 3 cm below the right costal margin. Laboratory studies show:
Hemoglobin 11.5 g/dL
Leukocyte count 16,300/mm3
Platelet count 150,000/mm3
Prothrombin time 20 sec (INR=1.3)
Serum
Urea nitrogen 16 mg/dL
Glucose 185 mg/dL
Creatinine 1.2 mg/dL
Bilirubin (total) 2.1 mg/dL
Albumin 3.1 g/dL
An abdominal ultrasound shows multiple small stones in the gallbladder and fluid in the gallbladder wall with wall thickening and pericholecystic fluid and stranding.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.4, 'degrees celsius'], 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [16300.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.4 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 110.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 16300.0 count/m^3. To convert 16300.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 16300.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 2e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6814,51,SIRS Criteria,diagnosis,integer,pmc-6823037-1,Extracted,"A 61-year-old man arrived at the emergency department reporting abdominal pain, persistent nausea, and vomiting for three weeks. It was localized to the upper-mid abdomen and was constant, dull, and 5-7 out of 10 in intensity and non-radiating. The pain was predominantly diurnal and aggravated with food intake but did not relieve with eructation, vomiting, bowel movements, or change in position. The pain was associated with nausea, followed by nonbilious, nonbloody vomiting unrelated to eating. He had not attempted to treat the symptoms with medications. He reported a 25-pound unintentional weight loss in the last month but denied fever, jaundice, change in the color of his urine or stool, chest pain, cough, shortness of breath, diarrhea, constipation, urinary symptoms, or fatigue.
Abdominal pain associated with nausea and vomiting is a common presenting symptom for patients seeking evaluation in the emergency department. A multitude of disorders affecting various organ systems such as the gastrointestinal tract, cardiovascular, endocrine, metabolic, CNS, renal, hematological, malignant and nonmalignant processes may be associated with such symptoms. A comprehensive history and physical examination need to be conducted to identify potential etiologies to the underlying processes.
The patient’s medical history was positive for atraumatic and intermittent back pain for the past six months. Lower back pain that persisted mostly during day-time worsened with a change in position. Family history was pertinent for high blood pressure and diabetes in both mother and brother. The patient denied taking any medications, herbal, or nutritional supplements. He denied smoking, alcohol intake, or drug use. He had not been sexually active for many years and did not have a history of sexually transmitted infection. The patient was originally from Latin America, but had not traveled outside the US in the past several years and had not seen a physician for the last 20 years. He lived alone and worked as a laborer. On physical examination, the patient appeared to be in no pain. The temperature was 97.1 °F, heart rate 81 beats per minute, blood pressure 140/88 mmHg, respiratory rate 20 breaths per minute, and oxygen saturation 100% at room air. Oral mucosa was dry. Sclera was anicteric. No conjunctival pallor was noted. The abdominal examination demonstrated normal bowel sounds, mild diffuse tenderness to deep palpation, which was most prominent over the epigastric region. There was no rigidity, guarding, or organomegaly. Murphy sign was negative. No abdominal bruits were noted. CVA tenderness was not elicited. Cardiac, respiratory, skin, musculoskeletal, and neurologic examinations were unremarkable.
Initial laboratory investigations revealed white cell count 8.5 k/uL (4.0-10.5), hemoglobin 12.1 g/dL (13.5-18.0), platelet count 203 k/uL (150-450), glucose 161 mg/dl (70-105), creatinine 10.8 mg/dl (0.7-1.3), blood urea nitrogen 65 mg/dl (7-25), bicarbonate 30 mg/dl (21-32), calcium 9.2 mg/dl (8.6-10.3), lipase 31 U/L (11-82), albumin 3.8 g/dl (3.5-5.0), globulin 3.0 g/dl, and total protein 6.8 g/dl (6.0-8.3). Hemoglobin A1c was 8.35. Urinalysis demonstrated trace leukocyte esterase, protein 30 mg/dl, and trace blood on dipstick. Microscopic analysis revealed no white blood cells, red blood cells, casts, crystals or bacteria.
The most remarkable finding on laboratory studies was the significantly reduced glomerular filtration rate. Given the history of nausea and vomiting over the past 2-3 weeks and the presence of elevated serum bicarbonate, it is likely that volume depletion and prerenal azotemia contributed to his kidney failure. On the other hand, the absence of hypotension or significant tachycardia made it unlikely that hypovolemia was the sole cause of his renal failure. The presence of mild proteinuria could be consistent with intrinsic renal disease. Elevated blood glucose and HbA1c suggested the possibility of diabetic nephropathy, which is the most common cause of end-stage renal disease, but it is highly unlikely that unrecognized diabetic nephropathy was the primary cause of renal failure in this case.
Abdominal ultrasonography showed normal-sized kidneys with normal cortical thickness, no hydronephrosis or evidence of urolithiasis, and no masses. The right kidney measured 11.7 cm longitudinally and the left kidney measured 12.3 cm longitudinally. Liver, spleen, gallbladder, and bile ducts were normal in size and appearance. A non-contrast computed tomography (CT) scan (Figure ) of the abdomen obtained in the emergency room confirmed normal size kidneys (arrows) and nonspecific bilateral perinephric stranding (arrowhead) and descending and sigmoid colon diverticulosis.
The patient initially received 2 L of intravenous crystalloid that was stopped when he developed dyspnea and jugular vein distension. His urine output over 12 hours was 1 liter. His vital signs remained stable, but the physical examination was consistent with a hypervolemic state. Creatinine levels decreased from 10.8 to 10.1 mg/dL.
The minimal improvement in kidney function with volume expansion excluded prerenal azotemia as the main cause of kidney failure. The imaging studies effectively ruled out the possibility of obstructive uropathy. The most striking feature of his imaging studies was the absence of gross evidence of chronic kidney damage such as decreased kidneys, increased echogenicity, decrease in cortical thickness, or cyst formation. A number of chronic kidney diseases, such as diabetic nephropathy, amyloidosis, HIV nephropathy, and autosomal dominant polycystic kidney disease, can be associated with preserved, or even enlarged kidney size despite advanced kidney failure. Alternatively, the imaging findings were consistent with an acute process or subacute process, resulting in a significant reduction in renal function over the span of 2 to 3 weeks before admission but unchanged kidney size. Such acute and subacute processes might include acute tubular necrosis, acute allergic interstitial nephritis, acute crystal-induced nephropathy, acute glomerulonephritis, monoclonal gammopathy of renal significance, and myeloma cast nephropathy as possible differentials. Further serological workup for HIV, hepatitis viruses, serum protein electrophoresis, quantification of urine protein excretion, urine protein electrophoresis, measurement of serum complements, and tests for ANA and antineutrophil cytoplasmic antibodies including anti-PR3 and anti-MPO antibodies were obtained.
Spot urine protein/creatinine was 1.96 g/day. Serum protein electrophoresis showed a small abnormality in gamma fraction. Serological studies for anti-PR3 and anti-MPO antibodies and ANA were negative. Serum complements were within the normal range. Hepatitis screen and HIV serology were also negative.
Despite only trace urine protein detected on the dipstick, spot urine protein to creatinine ratio indicates the presence of substantial proteinuria. This finding associated with the abnormality detected on serum protein electrophoresis was indicative of potential paraproteinemia-related kidney disease. On subsequent serum immunofixation and serum-free light chain assay, he was found to have a very elevated serum kappa free light chains 1240 mg/dl (normal range: 0.3300 to 1.94 mg/dl) and kappa/lambda ratio 816 (normal range: 0.2600 to 1.65).
Severe renal failure in the presence of very high levels of free light chains is diagnostic of monoclonal gammopathy. To accurately assess the characteristics of the monoclonal gammopathy, the patient underwent bone marrow and renal biopsies. Bone marrow biopsy (Figure ) depicted sheets of plasma cells (arrows) comprising up to 80% of marrow cells in some areas.
Renal biopsy (Figure ) demonstrated tubules containing casts of glassy to slightly granular proteinaceous material (arrow). The tubular epithelium appeared attenuated and flattened in some area (arrowhead) consistent with cast nephropathy.
The diagnosis of IgD MM with myeloma cast nephropathy was confirmed. Skeletal survey was obtained, which was normal. The patient’s urine output remained stable and he did not require hemodialysis.
The patient received one cycle of cyclophosphamide 1,692 mg intravenously with subcutaneous bortezomib of 2.4 mg and dexamethasone 40 mg intravenously. Acyclovir of 200 mg daily was initiated for Varicella zoster prophylaxis. The patient was discharged after the first cycle of chemotherapy. His creatinine level has decreased to 7.3 mg/dl by the day of discharge from 10.5 mg/dl on admission. He has since completed three cycles of chemotherapy and his creatinine level has improved significantly to 1.5 mg/dl.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [97.1, 'degrees fahrenheit'], 'Heart Rate or Pulse': [81.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [8500.0, 'µL']}",0,0,0,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 97.1 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 65.1 = 36.16667 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 81.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 8500.0 count/µL. To convert 8500.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 8500.0 white blood cell count/µL * 1.0 µL/mm^3 = 8500.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 0.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 0.
Hence, the the number of SIRS criteria met by the patient is 0."
6815,51,SIRS Criteria,diagnosis,integer,pmc-5798186-1,Extracted,"A 33-year-old white man presented to our hospital with sudden onset pleuritic chest pain and dyspnea of 1 day’s duration. The chest pain started when he was lifting a heavy trash bag and described the pain as sharp, constant, and radiating to his back. He also complained of diffuse body aches and chills but denied any fever, cough, hemoptysis, or weight loss. He denied any history of dental caries, recent travel, or exposure to sick contacts. He had no significant past medical history and was not taking any routine medications. He smoked half a pack of cigarettes a day for the past 10 years and denied any alcohol or illicit drug use. He worked as a waste collector in a garbage disposal firm.
At the time of presentation, he was: alert; oriented in time, place, and person; afebrile with a temperature of 37.06 °C (98.7 °F); tachycardic (heart rate of 110 beats/minute); and tachypneic (respiratory rate of 18/minute) with a blood pressure of 126/78 mmHg. An oral examination revealed normal dentition. A cardiopulmonary examination showed normal S1 and S2 with no murmurs and clear lung fields to auscultation bilaterally. An abdominal examination revealed a soft, non-tender abdomen with no organomegaly. A neurological examination showed intact cranial nerves and sensory system, and his muscle strength was 5/5 in all limbs with normal tone. Deep tendon reflexes were normal. An initial laboratory workup showed mild leukocytosis with white blood cell (WBC) count of 13,700 cells/mm3, elevated inflammatory markers of erythrocyte sedimentation rate (ESR) 48 mm/hour and C-reactive protein (CRP) 84 mg/dl, and moderately elevated serum transaminases of aspartate aminotransferase (AST) 634 U/L and alanine aminotransferase (ALT) 326 U/L. A basic metabolic panel was within normal limits. Three sets of cardiac enzymes done 8 hours apart were normal. An electrocardiogram was obtained which showed sinus tachycardia and diffuse ST segment elevations. A chest radiograph showed normal bilateral lung fields and normal cardiac silhouette. Computed tomography (CT) of his chest (Fig. ) ruled out aortic dissection but showed pericardial effusion. A transthoracic echocardiogram showed normal left ventricular systolic function with ejection fraction of 55% and a small pericardial effusion with no signs of tamponade physiology.
He was diagnosed as a case of acute pericarditis with minimal pericardial effusion. He was discharged home on indomethacin and was asked to follow up in the out-patient clinic. Two weeks later, when he was seen in our out-patient clinic, he complained of worsening dyspnea and chest pain. He was readmitted to hospital and an urgent transthoracic echocardiogram was obtained, which showed moderate to large pericardial effusion and tamponade physiology with right ventricular diastolic collapse and dilated inferior vena cava (Fig. ). An emergency pericardiocentesis was done and approximately 550 ml of purulent pericardial fluid was drained. The pericardial fluid was sent for culture, cell analysis, and cytology. Pericardial fluid WBC count was 15,376 cells/mm3 with 98% segmented neutrophils. A Gram stain of the pericardial fluid showed Gram-positive cocci in chains. He was started on broad-spectrum antibiotics with intravenously administered vancomycin (dosed on trough concentration) and piperacillin-tazobactam (3.375 g every 8 hours). Pericardial fluid cultures grew alpha hemolytic streptococci which were characterized as S. intermedius by matrix-assisted laser desorption/ionization time-of-flight mass spectroscopy (MALDI-TOF MS). S. intermedius was susceptible to penicillin and ceftriaxone. Anaerobic, fungal, and acid-fast bacilli cultures were negative. Pericardial fluid cytology was also negative for any malignant cells. Extensive workup with CT abdomen, CT chest, urine analysis, urine culture, and blood culture to look for source of infection failed to identify any other focus of infection. Human immunodeficiency virus (HIV) and tuberculosis QuantiFERON testing were negative. Antibiotics were deescalated to intravenously administered ceftriaxone (2 g every 24 hours) as per culture sensitivity.
His hospital course was complicated with the development of a pulmonary embolism for which he was started on an intravenously administered heparin infusion. However, within a few days of starting heparin, there was a steady decline in his platelets count. Heparin-induced thrombocytopenia (HIT) was suspected and heparin infusion was stopped. Our patient was started on argatroban infusion at a rate of 140 mcg/minute. HIT antibodies and serotonin release assay were sent which came back positive. He was subsequently transitioned to orally administered warfarin with target international normalized ratio (INR) range of 2 to 3. However, with the course of time, he did not have complete resolution of symptoms with persistence of chest pain and dyspnea. Hemodynamic and echocardiographic features were consistent with development of constrictive pericarditis. Surgical pericardiectomy with median sternotomy approach was performed which revealed thickened pericardium (Fig. ). He reported improvement in his symptoms after pericardiectomy. He was discharged home in a stable condition and received a total of 7 weeks of intravenously administered ceftriaxone. Six months post-discharge he reported complete resolution of his symptoms. A repeat echocardiography was normal and showed resolution of pericardial effusion.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.06, 'degrees celsius'], 'Heart Rate or Pulse': [110.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [13700.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.06 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 110.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 13700.0 count/m^3. To convert 13700.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 13700.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6816,51,SIRS Criteria,diagnosis,integer,pmc-3542890-1,Extracted,"A 58-year-old male presents to the Emergency Department via EMS as a possible stroke. Per spouse, he woke up from sleep with left-sided facial droop, slurred speech, and left arm weakness. He had gone to sleep at approximately 10 pm and awoke with the left-sided complaints at approximately 4 am the morning of arrival. He had a past medical history of adrenal adenoma, chronic gastritis, and a vasectomy in 1993. The patient's medications prior to admission were alprazolam, esomeprazole, probiotics, and a daily multivitamin. The patient is aware of his left-sided weakness and complains of heaviness on his left side. He reports no history of alcohol, tobacco, or illicit drug use. The patient's spouse reported that he had been unwell for three months with unexplained weight loss, fever, chills, and loss of appetite. At the time of presentation, various specialists including gastroenterology failed to determine an underlying cause for the patient's complaints besides “anemia of chronic disease.” Furthermore, he was scheduled for an upper and lower endoscopy the day of presentation and was in the process of preparation (cathartics) for that. He has been on a gluten-free diet for elevated tissue transglutaminase and gliadin antibody titers by his endocrinologist. Upon arrival at patient's residence, EMS reported a positive stroke screen with a Cincinnati score of 2, positive for left arm weakness, and left-sided facial droop. Vital signs upon arrival to the Emergency Department were temperature 36.4 degrees Celsius by tympanic reading, pulse 105 beats per minute, blood pressure 116/56 mmHg, respirations 18 breaths per minute, and pulse oximetry 98% on room air. His weight was recorded as 68 kilograms. He was not in any distress but appeared pale and cachectic. His neurologic exam was positive for a left facial droop with weakness of cranial nerves 3, 5, and 7. There was no uvular deviation, and pupils were equal and reactive bilaterally with intact extraocular movements. The upper extremities had symmetric sensation to fine touch with a left pronator drift and 3/5 strength in the proximal and distal muscle groups in comparison to the right. There was no dysmetria. The lower extremities had 5/5 strength bilaterally and absent Babinski reflexes. His NIH stroke scale score was 6. The rest of his physical exam was unremarkable.
Initial labs included a metabolic panel with measured sodium of 131 mmol/L and blood glucose of 125 mg/dL but were otherwise normal. The complete blood count showed a hemoglobin of 9.6 g/dL and a hematocrit of 29.9%. The white blood cell count was 12.5 thou/cu mm with 78.8% neutrophils and no bands. Cardiac enzymes and urinalysis were both normal. The point-of-care INR was 1.5. Stroke alert protocol imaging included a CT angiogram of the head and neck with and without contrast and postprocedure multiplanar reconstructions. These revealed acute/subacute CVA in the right insula cortex and right basal ganglia () as well as significant narrowing of the proximal M1 branch of the right middle cerebral artery (MCA) secondary to either embolus or atherosclerotic disease (). Perfusion images demonstrate elevated time to peak in the posterior right MCA distribution with normal capillary transit time and normal cerebral blood volume consistent with compensated collateral blood flow ().
The patient received 300 mg aspirin per rectum and IV fluids prior to admission to the neuro-ICU. The patient was deemed an unsuitable candidate for thrombolysis as onset was estimated approximately 6 hours prior to ED arrival. Neurosurgery was consulted and decided that the risks of endovascular therapy did not outweigh the benefits for the patient.
Followup the next day revealed that the patient had an echocardiogram that showed a mass on the posterior leaflet of the mitral valve with mitral regurgitation. Following echocardiogram, the patient had an acute sudden deterioration in his mental status and displayed respiratory compromise. On examination, his pupils were “blown” (enlarged) bilaterally and he was emergently intubated for airway protection. His emergent noncontrast CT of the head () showed a subcortical hemorrhage with intraventricular extension and subfalcine herniation. Neurosurgery emergently brought the patient to the operating room with a postoperative diagnosis of right intracranial hemorrhage secondary to ruptured mycotic MCA aneurysm. On postoperative day one, the family decided to withdraw care and the patient expired.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.4, 'degrees celsius'], 'Heart Rate or Pulse': [105.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [12500.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.4 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 105.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 12500.0 count/m^3. To convert 12500.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 12500.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6817,51,SIRS Criteria,diagnosis,integer,usmle-9296,Extracted,"A 51-year-old woman is brought to the emergency department after not being able to urinate for the past 12 hours. She also complains of a headache that is sharp in nature, 9/10, without radiation, and associated with nausea and vomiting. She neither smokes cigarettes nor drinks alcohol. She complains that her fingers have become numb and very painful on exposure to cold weather during the last few months. She has also noticed her fingers change color from blue to pale to red on cold exposure. Her face looks shiny with thickened, wrinkle-free skin. She has had joint pain and stiffness for the last 20 years. She takes over-the-counter omeprazole for heartburn, which she says improves her symptoms. She has unintentionally lost 9 kg (20 lb) in the last 6 months. She has no previous history of diabetes, hypertension, chest pain, orthopnea, or paroxysmal nocturnal dyspnea. Her mother has rheumatoid arthritis for which she takes methotrexate, and her father takes medications for hypertension and hypercholesterolemia. Her temperature is 37°C (98.6°F), blood pressure is 210/120 mm Hg, pulse is 102/min, respiratory rate is 18/min, and BMI is 22 kg/m2.
Laboratory test
Complete blood count:
Hemoglobin    9.5 g/dL
Leukocytes 15,500/mm3
Platelets 90,000/mm3
Serum haptoglobin 20 mg/dL (30–200 mg/dL)
Serum creatinine 2.3 mg/dL
Blood urea nitrogen 83.5 mg/dL
The peripheral blood film of the patient shows the following.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.0, 'degrees celsius'], 'Heart Rate or Pulse': [102.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [15500.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 102.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 15500.0 count/m^3. To convert 15500.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 15500.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 2e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6818,51,SIRS Criteria,diagnosis,integer,pmc-7727232-1,Extracted,"A 38-year-old healthy Japanese man from China was admitted to our hospital (day 1); thoracic computed tomography (CT) revealed abnormal lung lesions. The patient was a former smoker (two pack-years) with no history of illicit drugs use or dust exposure. Three months before admission, he had two episodes of loss of consciousness in China; however, echocardiography and head CT showed no abnormal findings. Two months previously, he noticed hemoptysis and experienced dyspnea. Immediately after he returned to Japan, thoracic CT (Fig. a, coronal view) evaluation was performed at a local hospital that demonstrated multiple scattered nodules, most of which were surrounded by ground-glass opacities (GGO), the so-called “halo signs,” which were located on the outer side of the lungs (Fig. b, c), suggesting hematological spread.
The patient’s vital signs were as follows: blood pressure, 108/60 mmHg; body temperature, 36 °C; respiratory rate, 18 breaths/min; tachycardia (heart rate, 108 beats/min); and hypoxemia (blood oxygen saturation using pulse oximetry of 89% on ambient air). Physical examination revealed conjunctival rim pallor and coarse crackles in the early to mid-inspiratory phase in both the lung fields.
Serum laboratory data showed severe anemia with a hemoglobin level of 5.6 g/dL, mild or moderate elevation in white blood cell counts of 11,700/µL, and C-reactive protein level of 10.2 mg/dL. On admission, chest radiograph (Fig. a) showed non-segmental bilateral lung infiltration predominantly seen in the right-sided middle to lower lung fields. Non-enhanced thoracic CT simultaneously showed non-segmental consolidation in both the lung lobes with scattered multiple nodules (Fig. b), but no apparent lymphadenopathies were noted. Serum data for Aspergillus galactomannan, Cryptococcus antigen, and T-SPOT tests were negative. No pathogens were isolated from sputum. Further, myeloperoxidase anti-neutrophil cytoplasmic antibodies and serine proteinase 3-anti-neutrophil cytoplasmic antibodies were also negative. Furthermore, none of the serum tumor marker, such as carcinoembryonic antigen, sialyl Lewis X-i antigen, α-fetoprotein, or human chorionic gonadotropin, was elevated.
Careful examination of contrast-enhanced thoracic CT suggested a filling defect in the right atrium (Fig. c, black asterisks), which corresponded to the inhomogeneously enhancing tumor in the right atrium (Fig. d, white asterisks) on enhanced electrocardiogram-gated cardiac CT. On day 2, acute respiratory failure occurred and the patient was placed on mechanical ventilation.
On day 8, urgent transcatheter endomyocardial biopsy was performed, which revealed abundant atypical cells invading the myocardial tissue (Fig. a, 40×) on hematoxylin–eosin staining. These atypical cells partly formed capillary-like spaces (Fig. b, 600×) and were stained with FLI-1 (figure not shown), CD-31 (Fig. c, 400×), and ERG (Fig. d, 400×) on immunohistochemical analysis, suggesting an endothelial origin of the tumor.
On day 10, based on the transcatheter biopsied specimen of the right atrium mass, the patient was tentatively diagnosed with primary cardiac angiosarcoma and treated with intravenous administration of doxorubicin (75 mg/m2). However, his respiratory status rapidly deteriorated, and he died on day 20. Postmortem autopsy demonstrated that the right atrium contained a massive tumor (Fig. a, asterisk), which also showed infiltrative growth in the myocardium (Fig. b, 20×). The tumor was composed of the similar atypical cells as seen in the transcatheter biopsied specimen (Fig. c, 200×). Cut surfaces of the right lung revealed multiple nodules, measuring 1 cm in diameter (Fig. d) together with a hemorrhagic infarct in peripheral areas (Fig. e). Histological features of the pulmonary nodules were identical to those of the cardiac tumor with accompanying intratumoral hemorrhagic necrosis and severe bleeding in the surrounding lung parenchyma (Fig. f). Hence, the patient was diagnosed with primary cardiac angiosarcoma derived from the right atrium with lung metastasis via hematological spread. The tumor also metastasized to the mediastinal and bilateral hilar lymph nodes and bilateral adrenal glands.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.0, 'degrees celsius'], 'Heart Rate or Pulse': [108.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [11700.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 108.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 11700.0 count/µL. To convert 11700.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 11700.0 white blood cell count/µL * 1.0 µL/mm^3 = 11700.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6819,51,SIRS Criteria,diagnosis,integer,usmle-557,Extracted,"Three days after undergoing an open cholecystectomy, a 73-year-old man has fever and abdominal pain. He has hypertension, type 2 diabetes mellitus, chronic obstructive pulmonary disease, and benign prostatic hyperplasia. He had smoked one pack of cigarettes daily for 40 years but quit 1 year ago. He does not drink alcohol. Prior to admission to the hospital, his medications included lisinopril, metformin, ipratropium, and tamsulosin. He appears acutely ill and lethargic. His temperature is 39.5°C (103.1°F), pulse is 108/min, respirations are 18/min, and blood pressure is 110/84 mm Hg. He is oriented only to person. Examination shows a 10-cm subcostal incision that appears dry and non-erythematous. Scattered expiratory wheezing is heard throughout both lung fields. His abdomen is distended with tenderness to palpation over the lower quadrants.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.5, 'degrees celsius'], 'Heart Rate or Pulse': [108.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [19000.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.5 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 108.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 19000.0 count/m^3. To convert 19000.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 19000.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 2e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6820,51,SIRS Criteria,diagnosis,integer,pmc-2934912-1,Extracted,"A 27-year-old woman was referred to the emergency department with complaints of icterus, nocturnal fever, arthralgia, and abdominal pain. The patient had been well until two weeks earlier, when symptoms developed. She was a farmer in a village and owned a lot of sheep. There were no allergies and no history of recent use of drugs but she was consuming a large amount of nonpasteurized traditional cheese.
On physical examination, the patient was nonedematous. Her temperature was 38.5°C, with a blood pressure of 70/45 mm Hg, a pulse rate of 70 beats per minute, and respirations of 18 per minute. The oxygen saturation was 96 percent while she was breathing room air.
The liver edge was palpable 5 cm below the costovertebral margin. Her right upper quadrant of abdomen was diffusely tender to palpation. Additionally, there was marginal splenomegaly. The heart sounds and the results of the remainder of the examination were normal.
Laboratory studies performed at admission revealed a WBC count of 5400 cells/mm³, a hemoglobin level of 10.6 g/dL, a platelet count of 216.000 platelets/mm³, an aspartate aminotransferase level of 224 U/L, an alanine aminostransferase of 159 U/L, an alkaline phosphatase level of 2340 U/L, a gamma glutamyl transferase level of 597 U/L, a direct bilirubin level of 3.1 mg/dL, an albumin level of 3.3 g/dL, a globulin level of 4.3 g/dL and a uric acid level of 1.4 g/dL. Serum pituitary, thyroid, and adrenal function tests were in normal ranges.
Her other laboratory parameters included erythrocyte sedimentation rate 47 mm/hr, C-Reactive Protein level 26 U/L, serum sodium level 124 mmol/L, potassium 4.4 mmol/L, chloride 95 mmol/L, and plasma osmolality 262 mmol/kg/H2O. Urine biochemistry showed osmolality 274 mmol/kg/H2O and urinary sodium 64 mmol/L. Serologic tests for Epstein-Barr virus, cytomegalovirus, and hepatitis viruses were negative. Electrocardiographic examination showed minimal ST-T elevations.
Ultrasonography and Computed Tomography scan (CT scan) of the abdomen showed a small pericardial effusion with mild splenomegaly and hepatomegaly (Figures and ). However, there was no evidence of biliary dilatation or cholecystitis. CT scan of thorax and brain revealed no abnormality. Echocardiography detected mild pericardial effusion without cardiac dysfunction.
At the next day, serum agglutination test for Brucella was positive and its titer was 1/1240. The diagnosis of SIADH in association with cholestatic hepatitis and pericardial effusion due to Brucellosis was made. After intramuscular streptomycin (1000 mg/day for 20 days) with oral Doxycycline (100 mg twice daily for 6 weeks), the patient's symptoms, cholestasis, pericardial effusion, and hyponatremia resolved dramatically.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.5, 'degrees celsius'], 'Heart Rate or Pulse': [70.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [5400.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.5 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 70.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 5400.0 count/m^3. To convert 5400.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 5400.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 5.4e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6821,51,SIRS Criteria,diagnosis,integer,usmle-10106,Extracted,"A 72-year-old man with chronic lymphocytic leukemia (CLL) comes to the physician with a 2-day history of severe fatigue and dyspnea. He regularly visits his primary care physician and has not required any treatment for his underlying disease. His temperature is 36.7°C (98.1°F), pulse is 105/min, respiratory rate is 22/min, and blood pressure is 125/70 mm Hg. The conjunctivae are pale. Examination of the heart and lungs shows no abnormalities. The spleen is palpable 3 cm below the costal margin. No lymphadenopathy is palpated.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.7, 'degrees celsius'], 'Heart Rate or Pulse': [105.0, 'beats per minute'], 'respiratory rate': [22.0, 'breaths per minute'], 'White blood cell count': [80000.0, 'm^3']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.7 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 105.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 80000.0 count/m^3. To convert 80000.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 80000.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 8e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6822,51,SIRS Criteria,diagnosis,integer,pmc-3212705-1,Extracted,"A 3-year-old girl was referred to the Samsung Medical Center, Seoul, Korea emergency department due to fever, respiratory distress, and decreased mental status during the peak influenza pandemic period in October 2009. She had been healthy until she developed fever and cough 7 days prior to hospitalization. Two days after her initial symptoms, she was seen by a general practitioner and was started on oseltamivir based on a positive rapid antigen test result. However, her condition deteriorated and she experienced difficult breathing and sleepiness despite antiviral treatment. She was taken to a general hospital near her home and was eventually referred to our center due to impending respiratory failure and decreased mental status. She did not have any significant past medical or family history, and she had not been vaccinated against 2009 H1N1 influenza or seasonal influenza.
On arrival, the patient's blood pressure was 117/67 mmHg, heart rate 181 beats/min, respiratory rate 40/min, and body temperature 37.5℃. Percutaneous oxygen saturation was 91% on 7 liters/min of oxygen via face mask. On physical examination, chest wall retraction was observed and left lung sounds were decreased. The patient did not have any abnormal focal neurological signs although she appeared drowsy. She was admitted to the pediatric intensive care unit and intubated immediately.
Her initial blood gas analysis showed pH 7.193, PaCO2 53.9 mmHg, PaO2 30.3 mmHg, bicarbonate 20.3 mmoL/L, and base excess -7.9 on 7 liters/min of oxygen via face mask. A complete blood count showed pancytopenia (white blood cell [WBC] count 710/µL, absolute neutrophil count 210/µL, hemoglobin 10.6 g/dL, platelets 81,000/µL) and her C-reactive protein was markedly elevated up to 37.18 mg/dL. Her immunoglobulin G level was decreased to 399 mg/dL. The patient was placed on high dose oseltamivir (60 mg/dose, body weight 13 kg) and intravenous immunoglobulin G was also given as 500 mg/kg/day for 2 days. The 2009 H1N1 influenza virus was detected by reverse transcriptase-polymerase chain reaction assay in both a respiratory specimen and spinal fluid. Her initial chest radiograph showed diffuse haziness in the entire left lung field and the right upper lung field (). Thoracentesis was performed and 100 mL of turbid chocolate-colored fluid was drained from the left lung (pleural fluid analysis results: red blood cell >1,000/µL, WBC >1,000/µL, polymorphonuclear neutrophil 93%, pH 7.4, glucose 11 mg/dL, protein 3,564.6 mg/dL). A culture of the pleural fluid did not grow any organisms.
On hospital day 3, a chest tube was inserted into the left pleural space due to increased pleural effusion causing tracheal deviation. On hospital day 6, chest computed tomography showed necrotizing pneumonia with a significant left pleural effusion (). She also had persistent high fever (39.1℃) and a striking leukocytosis (WBC count 24,250/µL, absolute neutrophil count 19,640/µL) despite broad spectrum antibiotics (cefotaxime and vancomycin). On hospital day 7, pneumothorax developed in the left lung () and the chest tube was replaced by one with a bigger sized lumen. As pneumothorax was waxed-and-waned on hospital day 8, more ventilator support (volume control mode, FiO2 1.0, positive end-expiratory pressure [PEEP] 5 cmH2O, TV 90 mL) was needed to maintain percutaneous oxygen saturation level near 90%. Peak inspiratory pressure was recorded at 23 to 34 cmH2O depending on the relief of pneumothorax. Due to her poor response to antibiotic treatment, cefotaxime was changed to meropenem. On hospital day 9, percutaneous oxygen saturation level was dropped to 77% due to progressive respiratory failure with a persistent purulent pleural effusion and a recurrent, massive pneumothorax (). To rescue the patient from progressing respiratory failure without raising positive airway pressure, which might aggravate pneumothorax, venovenous ECMO support was initiated.
Of note, multidrug resistant Acinetobacter baumannii started to grow from both blood and tracheal aspirate cultures on hospital day 10. Follow-up cultures persistently grew A. baumannii and Stenotrophomonas maltophilia from both tracheal aspirates and pleural fluid. Blood cultures became negative 5 days after ECMO discontinuation (bacteremia persisted from day 10 to day 18). The tracheal aspirate cultures were positive from hospital days 10 to 34, and pleural fluid cultures were positive from hospital days 11 to 41. The total duration of ECMO support was 6 days, and successful weaning was achieved without cardiovascular complications. At the time of ventilator weaning, blood gas analysis showed pH 7.371, PaCO2 64.0 mmHg, PaO2 111.9 mmHg, bicarbonate 36.3 mmoL/L, and base excess 9.2 with conventional mechanical ventilation. Various combinations of antibiotics were used including isepamicin, minocyclin, rifampicin, ceftazidime, TMP-SMX, and colistin in an attempt to control persistent infections due to multidrug resistant A. baumannii and S. maltophilia. Total duration of oseltamivir medication was 23 days (high dose for 18 days and usual dose for 5 days).
The patient was weaned from mechanical ventilation on hospital day 37, and all antimicrobials were discontinued on day 57. On day 63, the left chest tube was removed and she was discharged from the hospital alert and spontaneously breathing without difficulty in room air (). At the time this manuscript was submitted, the patient had no respiratory symptoms and a chest radiograph was markedly improved.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.5, 'degrees celsius'], 'Heart Rate or Pulse': [181.0, 'beats per minute'], 'respiratory rate': [40.0, 'breaths per minute'], 'White blood cell count': [710.0, 'µL'], 'PaCO2': [53.9, 'mm hg']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.5 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 181.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 710.0 count/µL. To convert 710.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 710.0 white blood cell count/µL * 1.0 µL/mm^3 = 710.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 40.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is 53.9 mm Hg, which is greater or equal to than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6823,51,SIRS Criteria,diagnosis,integer,pmc-3853597-1,Extracted,"A 25-year-old 6 months pregnant lady from a rural background was admitted to a private tertiary care hospital in north India with complaints of fever with chills since 4 days. The patient had a BP = 100/60 mm of Hg, pulse = 112 bpm, RR = 22/min, temperature = 101°F, and was maintaining a saturation of 96% with oxygen support at 2 l/min. The patient was dyspneic, had a blanching erythematous rash, pallor (+++) and the fetal heart sounds could be heard. The cardiovascular and neurological examination was, however, normal. A complete blood count with peripheral smear, ELISA for immunoglobulin G (IgG) and immunoglobulin M (IgM) for dengue, were sent along with the routine blood examinations. The patient was managed symptomatically and was given supportive treatment.
The patient had Hb = 4.1 gm/dl, TLC = 5000/mm3, DLC = P68%, L32%, E0, B0, Platelets = 50,000/mm3, blood urea = 58.8 mg/dl, Sr.creatinine = 1.8 mg/dl, Sr.Na+ = 145 meq/L, Sr.K+ = 4.3 meq/L, total bilirubin = 0.8 mg/dl with a direct bilirubin = 0.7 mg/dl and an indirect bilirubin = 0.1 mg/dl, total serum protein = 3.9 g/dl, Sr.albumin = 2.2 g/dl, Sr.globulin = 1.7 g/dl, Aspartate Amino transferase (AST) = 60 U/L, Alanine Aminotransferase (ALT) =13 U/L, Sr.Alkaline Phosphatase = 113 U/L. Dengue duo Nonprotein Surface (NS1) antigen combo kit manufactured by standardia using one step rapid immunochromatograpic test for detection of NS1 Antigen and IgG and IgM were employed for the detection of dengue infection. Peripheral smear examination revealed presence of gametocytes of P. vivax and P. falciparum. The histidine rich protein-2 card test was also positive for P. vivax and P. falciparum. A general blood picture was that of markedly reduced red cell mass, red blood cells were microcytic and hypochromic along with anisopoikilocytosis in the form of tear drop cells, target cells and helmet cells. The treatment was accordingly modified and anti-malarials were started in the form of artisunate based combination therapy. Paracetamol in divided doses was given to control the fever and proper care was taken for fetal well-being by fetal sonography. During fetal sonography the amount of amniotic fluid, blood flow through the Doppler study, fetal activity, placenta and cervix were examined to ensure that there was no fetal compromise. The patient was given four units of packed red blood cell transfusion and was discharged after 7 days of in-patient treatment with a live fetus and is on a regular follow-up.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [101.0, 'degrees fahrenheit'], 'Heart Rate or Pulse': [112.0, 'beats per minute'], 'respiratory rate': [22.0, 'breaths per minute'], 'White blood cell count': [5000.0, 'm^3']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 101.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 69.0 = 38.33333 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 112.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 5000.0 count/m^3. To convert 5000.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 5000.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 5e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 22.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6824,51,SIRS Criteria,diagnosis,integer,pmc-3714084-1,Extracted,"A 45-year-old African American male with a medical history significant for active IDU, hypertension, type II diabetes mellitus, hepatitis C, history of osteomyelitis and cerebrovascular accident was brought to emergency room for mental status changes. He was found to be in respiratory failure and was subsequently intubated in the ER.
Physical examination on presentation was significant for temperature of 39.3°C, controlled blood pressure, sinus tachycardia at a rate of 105 beats/min, and a respiratory rate of 28/min. Oxygen saturation was 98% on AC mode with 35% oxygen concentration. His pupils were pinpoint. The patient had multiple abscesses on the upper extremities at the sites of IV drug injection. Multiple pink, macular, irregular lesions were seen on the patient's right thumb and hand ().
Laboratory results included leukocytosis of 14.8 with 85.1% neutrophils, lactic acid 15.9, hyperglycemia 460 with negative ketones, and increased BUN/creatinine 24/2. HIV screening test was negative. Chest X-ray and head CT were initially unremarkable. CSF analysis revealed elevated protein 118 mg/dL, glucose 240 mg/dL with WBC 73 (segment 98%). However, CSF gram stain and culture were negative. Blood cultures were positive for MSSA.
The patient was admitted to the intensive care unit and antimicrobial treatment was initiated (ceftazidime 1 g IV q8h – later switched to ceftriaxone and vancomycin 1.5 g IV q12h). Transthoracic echocardiography (TTE) obtained on the day of admission did not reveal any detectable intracardiac vegetations. Despite the aggressive antibiotic treatment, the patient remained febrile. On the fifth day of his hospital stay, transesophageal echocardiography (TEE) was performed, and a 1.5 cm vegetation was found on the aortic valve. The antibiotic regimen was then changed to nafcillin (2 g IV q4h) and gentamicin (3 mg/kg qday for 5 days) for MSSA positive endocarditis. The patient, however, did not improve and 2 weeks after admission, had a cardiac arrest and died.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.3, 'degrees celsius'], 'Heart Rate or Pulse': [105.0, 'beats per minute'], 'respiratory rate': [28.0, 'breaths per minute'], 'White blood cell count': [14800.0, 'µL']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.3 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 105.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 14800.0 count/µL. To convert 14800.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 14800.0 white blood cell count/µL * 1.0 µL/mm^3 = 14800.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 28.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6825,51,SIRS Criteria,diagnosis,integer,pmc-6700676-1,Extracted,"The patient was a 78-year-old Caucasian woman, with a medical history including type 2 diabetes mellitus, hypertension and gout, who presented to the emergency department with disoriented speech, a temperature of 40°C (104°F), hypertension and tachycardic. There was an initial concern for heat stroke when she was admitted to the hospital considering the high temperature and humidity outside. She was admitted to the general medical floor where she rapidly deteriorated and developed respiratory distress with oxygen saturation declining to 86%. She was placed on non-invasive positive pressure ventilation (NIPPV) and transferred to the critical care unit (CCU). On CCU arrival, the patient’s vital signs showed a temperature of 39°C (102.3°F) with her blood pressure spiking to 204/74 mm Hg. She remained in sinus tachycardia at a rate of 124 beats/min and respiratory rate of 23 while on NIPPV. Physical exam findings revealed worsening mental status, severe nuchal rigidity and positive Brudzinski’s sign (forced flexion of neck causes reflex hip flexion) and Kernig’s sign (flexing at the hip and knee at 90° and subsequent knee extension is painful and patient resists).
On initial CCU history and chart review, it was found that she had no recent history of trauma or illness. She was taking amlodipine, atorvastatin, benazepril, calcium carbonate, glipizide, sitagliptin/metformin, insulin glargine and lisinopril at home. Her initial lab values showed multiple abnormalities, including hypokalaemia with a potassium of 3.3 mmol/L, glucose of 11.4 mmol/L mg/dL, Blood Urea Nitrogen (BUN) of 13.57 mmol/L, serum creatinine of 214.86 μmol/L, magnesium 0.64 mmol/L, phosphorus of 0.484 mmol/L, platelets at 86×109/L and a white blood cell (WBC) at 12.44×109/L.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.0, 'degrees celsius'], 'Heart Rate or Pulse': [124.0, 'beats per minute'], 'respiratory rate': [23.0, 'breaths per minute'], 'White blood cell count': [12440000.0, 'µL']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.0 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 124.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 12440000.0 count/µL. To convert 12440000.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 12440000.0 white blood cell count/µL * 1.0 µL/mm^3 = 12440000.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 23.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6826,51,SIRS Criteria,diagnosis,integer,pmc-8212922-1,Extracted,"A 29-year-old, previously healthy male walked into the outpatient department (OPD) of the National Hospital of Sri Lanka with dengue non-structural protein 1 (NS1) antigen-positive fever of three days duration. Other than the three-day history of fever, he had no other signiﬁcant past medical history except a failed military fitness test because of body temperature 40°C and muscle cramp after running 1 km four years previously. He denied a recent history of strenuous exercise or the use of illicit drugs. Urine or serum drug screen was not performed due to lack of facility.
On admission to the medical ward, he was conscious and rational. His temperature was 37.3°C, his heart rate was 80 bpm, and his blood pressure was 110/60 mmHg. Hematologic analysis revealed full blood count with WBC 4,850 per microliter (4.850 x 109/L), hematocrit 39%, and platelets 180,000 per microliter (180 x 109/L). One hour after being admitted to the medical ward, he developed a high fever with a temperature of 40.2°C which was treated with active cooling with IV cooled normal saline and ice water sponging. Other clinical features detected were diaphoresis, tachycardia with a heart rate of 140 beats/min, tachypnea with a respiratory rate of 40 breaths/min, skeletal muscle spasms, and limb rigidity. Arterial blood gas (ABG) revealed the following: pH - 6.9, PCO2 - 101 mmHg, HCO3 - 8 (mmol/L), BE - (-14), PO2 - 105 mmHg, SpO2 - 95%, and K+ - 6.8. Hyperkalemia was managed by giving intravenous 10 units of soluble insulin and 50% Dextrose infusion, Intravenous 8.4% bicarbonate 50 ml infusion. Intravenous 10% calcium gluconate 10 ml was given to protect cardiomyocytes.
The patient’s clinical condition deteriorated after 10 minutes, and he developed increasing muscle tone with trismus, opisthotonic posture, hyperthermia, severe metabolic and respiratory acidosis despite hyperventilation, refractory hyperkalemia (8.8 meq/l), and hypocalcemia. ABG results were as follows: PH - 7.03, PCO2 - 100 mmHg, HCO3 - low, and lactate - 10. Urine was brown in color and urine for myoglobinuria report received as positive after 4 hours.
Then the patient was emergently intubated after giving IV atracurium 60 mg (A non-depolarizing muscle relaxant). He progressed to asystolic cardiac arrest, which was treated according to the advanced life support (ALS) protocol. The patient’s hyperkalemia was refractory to insulin and dextrose infusion and bicarbonate infusion. Salbutamol was not started due to tachycardia. He expired after two hours of attempted resuscitation.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [40.2, 'degrees celsius'], 'Heart Rate or Pulse': [140.0, 'beats per minute'], 'respiratory rate': [40.0, 'breaths per minute'], 'White blood cell count': [4850.0, 'µL'], 'PaCO2': [101.0, 'mm hg']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 40.2 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 140.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 4850.0 count/µL. To convert 4850.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 4850.0 white blood cell count/µL * 1.0 µL/mm^3 = 4850.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 40.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is 101.0 mm Hg, which is greater or equal to than 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 2 + 1 = 3 criteria met.
Hence, the the number of SIRS criteria met by the patient is 3."
6827,51,SIRS Criteria,diagnosis,integer,usmle-10048,Extracted,"A 43-year-old Caucasian woman is admitted to the hospital with acute onset right upper quadrant (RUQ) pain. The pain started 6 hours ago after the patient had a large meal at a birthday party and has progressively worsened. She recalls having similar pain before but not so intense. No significant past medical history. Current medications are only oral contraceptive. Vitals are blood pressure 140/80 mm Hg, heart rate 79/min, respiratory rate 14/min, and temperature 37.6℃ (99.7℉). The patient’s BMI is 36.3 kg/m2. On exam, the patient appears slightly jaundiced. Her cardiac and respiratory examinations are within normal limits. Abdominal palpation reveals tenderness to palpation in the RUQ with no rebound or guarding, and there is an inspiratory arrest on deep palpation in this region. The remainder of the examination is within normal limits.
Laboratory tests are significant for the following:
RBC count 4.1 million/mm3
Hb 13.4 mg/dL
Leukocyte count 11,200/mm3
ESR 22 mm/hr
Platelet count 230,000/mm3
Total bilirubin 2 mg/dL
Direct bilirubin 1.1 mg/dL
ALT 20 IU/L
AST 18 IU/L
Amylase 33 IU/L
Ultrasound of the abdomen shows the following result (see image):
The common bile duct (CBD) (not shown in the image) is not dilated.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.6, 'degrees celsius'], 'Heart Rate or Pulse': [79.0, 'beats per minute'], 'respiratory rate': [14.0, 'breaths per minute'], 'White blood cell count': [11200.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.6 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 79.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 11200.0 count/m^3. To convert 11200.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 11200.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 14.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6828,51,SIRS Criteria,diagnosis,integer,pmc-8559634-1,Extracted,"A 27-year-old woman with a history of thalassemia minor was admitted to surgical ward due to clinical presentation of peritonitis suggestive of acute abdominal crisis with three days history of fever, bloody diarrhea, nausea and vomiting. At presentation, she looked pale without icterus and initial vital signs include: blood pressure of 135/85 mmHg, pulse rate 100 beats/minute, Respiratory rate 32 breaths/minute and axillary temperature 39C. Abdominopelvic computed tomography showed no signs of perforation or obstruction but there was prominent thickening of colonic wall from splenic flexure to rectum- compatible with colitis and evidence of ascites and bilateral pleural effusion ( and ). Peritoneal fluid paracentesis showed light red aspirate with 550/µl white blood cells (70% polymorphonuclears) and 9000/µl red blood cells.
Laboratory data showed the evidence of microangiopathic hemolytic anemia (MAHA) with considerable schistocytes () and thrombocytopenia. During evaluation, she experienced an episode of tonic-clonic seizure. She referred to internal medicine ward to evaluate thrombotic thrombocytopenic purpura/ hemolytic uremic syndrome (TTP/HUS).
During our physical examination the patient was ill, had periorbital and generalized 2+ pitting edema and was anuric. Further evaluation revealed 4+ proteinuria, rise in plasma creatinine and pericardial effusion (beside ascites and pleural effusion). Her immunologic markers of ANA, anti-dsDNA, Anti-Ro, anti-La and Coombs study were negative and her complement levels showed C3 of 77 ng/dl (normal range: 90-190) and normal C4 and CH50. (the lab data are given in ).
As she had uremic signs, we commenced her hemodialysis with left femoral catheter (only for two successive sections) and with the diagnosis of seronegative SLE, we commenced her intravenous cyclophosphamide and 3 successive days of methylprednisolone pulse. She dramatically responded to treatment but on the 4th day, she developed left common femoral vein thrombosis, therefore anticoagulant started and hemodialysis catheter removed. Antiphospholipid antibody panel was negative.
We performed a renal biopsy and sent her home. Tissue sample was compatible with stage III lupus nephritis (according to WHO classification) and the ANA became positive with 1:320 titer.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [39.0, 'degrees celsius'], 'Heart Rate or Pulse': [100.0, 'beats per minute'], 'respiratory rate': [32.0, 'breaths per minute'], 'White blood cell count': [550.0, 'µL']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 39.0 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 100.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 550.0 count/µL. To convert 550.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 550.0 white blood cell count/µL * 1.0 µL/mm^3 = 550.0 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 32.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6829,51,SIRS Criteria,diagnosis,integer,pmc-4890486-1,Extracted,"Fifty-four year old male
The chief complaint of the patient included breathing difficulty and coughing during exercise that developed 2 months previously.
Breathing difficulty and coughing aggravated further during mountain hiking. A pulmonary disease was suspected from the findings of chest radiographs. The patient was hospitalized to obtain an accurate diagnosis and for treatment.
On a special health examination performed 5 months before admission, no unusual findings were observed on the plain chest radiography. The patient had no ophthalmologic diseases, but complained of eye dryness for several months. He frequently used artificial tears because of the eye dryness.
The patient had a history of smoking 20 cigarettes a day for 20 years and then 10 cigarettes a day for 10 years; however, he quit smoking 3 months previously. He has a history of consuming five bottles (350 mL) of soju (approximately 18 % alcohol by volume) per week. No significant family history of autoimmune diseases was noted.
On admission, the patient’s vital signs were stable with blood pressure of 140/80 mmHg, pulse rate of 86 beats/min, respiratory rate of 20 breaths/min and body temperature of 37.0 °C. Although the patient showed an acute ill-looking appearance, his consciousness was clear, cardiac sound regular, and no heart murmur was heard. Fine inspiratory crackles were heard at both lower lung fields. Finger clubbing was not observed, but fingers were swollen and skin was thickened. The findings in the abdomen, extremities, and neurological examination were normal.
In a plain chest radiograph obtained on admission, ground glass opacities (GGOs) were observed at the lower part of both lungs (Fig. ). In a chest computed tomography image, reticulation and GGOs were observed in both lungs, leading to the diagnosis of interstitial lung disease (Fig. ).
In arterial blood gas analysis performed before hospitalization, pH was 7.4; PaCO2, 38 mmHg; PaO2, 94.2 mmHg; and oxygen saturation, 97.3 %. In a peripheral blood test, the leukocyte count was 8,300/μL; hemoglobin, 5.2 g/dL; and platelet count, 436,000/μL. In a lung function test, findings of restrictive lung function disorder were obtained with forced vital capacity (FVC) 2.62 L (67 % of the predicted value), forced expiratory volume in 1 s (FEV1) 2.31 L (80 % of the predicted value), the ratio of FEV1/FVC 88 %, forced expiratory flow 25–75 % 4.76 L/sec (154 % of the predicted value), and peak expiratory flow rate 8.16 L/sec (110 % of the predicted value).
The results of bronchoscopy and a lung lavage test revealed chronic inflammation with fibrosis. The results of lung biopsy were consistent with usual interstitial pneumonitis. Breathing difficulty was alleviated with systemic steroid therapy. During admission, the patient complained of dry mouth and difficulty of swallowing dry food without liquid. Immune serologic tests were performed under suspicion of autoimmune disease. The results of serologic tests were as follows; positive for antinuclear antibody (1:2560), negative for rheumatoid factor, positive for anti-SSA (Ro) antibody, negative for anti-SSB (La) antibody and positive for anti-Scl 70 antibody. The anti-ds DNA level was 7.64 IU/mL (reference level, <7.0 IU/mL). The secretory function of the salivary gland was considered to be decreased. In a salivary gland scan, the uptake increases in the parotid gland and submandibular gland were relatively normal; however, the ejection fraction of the salivary gland after stimulation decreased by more than the moderate level. Although the results of Schirmer’s test did not satisfy the diagnostic criteria for Sjögren’s syndrome, with the right eye showing a result of 12 mm in 5 min and the left eye showing a result of 7 mm in 5 min, they were found to be lower than the normal range. Other diseases such as hepatitis C, acquired immunodeficiency syndrome, lymphoma and sarcoidosis were excluded by medical history and the results of relevant laboratory tests. Clinical findings including ocular symptom of dry eyes, oral symptom of difficulty in swallowing dry food without liquid, oral sign of abnormal salivary scintigraphy and positive autoantibody of anti-SSA (Ro) antibody were compatible with diagnostic criteria for Sjögren’s syndrome (Table ) []. In addition, there were some features of systemic sclerosis (puffy fingers, interstitial lung disease and positive for systemic sclerosis related autoantibody [anti-Scl 70]) according to the revised classification criteria of systemic sclerosis (Table ) []. The patient has been followed for the overlap syndrome with Sjögren’s syndrome and systemic sclerosis.
The patient had worked for 25 years as a worker in the large-scale rolling department of a steel-manufacturing company. He was in charge of maintenance and repairs for the roughing mill and intermediate mill. His major tasks were the management of oils, roll exchange of the rolling mill for different sizes and stand-seating manufacture. Rolling is a plastic process in which the cross-sectional thickness of a material is reduced by successively pressing while passing it between two rollers. A roughing mill is the first process where slabs coming out of the furnace are rolled, and this produces dust containing silica. Hot rolling is a rolling process performed at a temperature of between 1100 °C and 1200 °C. A large amount of fumes develops at that high temperature. Generally, the hot rolling process is a wet process. As it progresses, oxidized film on the surface of the rolled material is removed and water is jet-sprayed to prevent the high generation of fumes. The final product is a scroll-shaped intermediate processed product called a coil, after which additional processing is performed in the cold rolling process. The large-scale milling process in which he was involved is a series of operations comprising the furnace, roughing mill, intermediate mill, finishing mill and cutting. The roll was being exchanged for different sizes more than once a day, depending on the work volume. To meet the production standards when changing the roll, the process of resting the new roll on a stand, dissembling the existing roll and performing the exchange was mainly performed near the rolling mill owing to the nature of the work. According to the report of working environment measurement, noise, dust, toxic metals and heat were identified as occupational hazards. In general, workers in the milling process take 30-min rest after 30-min working because of the high-heated working condition. The patient has worked on the three-shift system. The total ventilation system was applied in the plant, and the patient has regularly used personal protective equipment including mask and ear plugs.
It was verified that standard steel products produced by a series of hot rolling processes contain a maximum of 0.4 % silicon []. However, the concentration of free silica in the air was not measured directly. Instead, type 2 dust, which contains silicon dioxide up to 30 %, was measured as mineral dust. According to the report of working environment measurement in 2008, the concentration of type 2 dust was 1.444 mg/m3 and 0.417 mg/m3 in the roughing and intermediate mills, respectively (Table ). Potential toxic substances other than silica were found in the milling process such as nickel, chromium and manganese, but the ambient concentration was very low or not detectable. For example, the highest concentration of nickel and manganese were measured at the roughing mill site, which were 0.0026 mg/m3 and 0.0051 mg/m3, respectively (Table ).",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.0, 'degrees celsius'], 'Heart Rate or Pulse': [86.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [8300.0, 'µL'], 'PaCO2': [38.0, 'mm hg']}",0,0,0,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.0 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 86.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 8300.0 count/µL. To convert 8300.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 8300.0 white blood cell count/µL * 1.0 µL/mm^3 = 8300.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 0.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is 38.0 mm Hg, which is greater or equal to than 32 mm Hg. Neither criteria met and so keep the current total at 0.
Hence, the the number of SIRS criteria met by the patient is 0."
6830,51,SIRS Criteria,diagnosis,integer,pmc-4531946-1,Extracted,"An 18-year-old man was admitted to the Chonnam University Hospital because of general weakness for 4 weeks. His family had no medical problems. Nine years previously, he was admitted to the Department of Cardiac Surgery, and an echocardiographic examination showed mitral valve prolapse and moderate mitral regurgitation. Operation was recommended, but the patient refused and only received medical therapy.
The blood pressure was 130/80 mmHg, the pulse was 112/min, the temperature was 37.4°C, and the respirations were 20/min. On examination, he appeared chronically ill. He was noted to have tall and thin stature with long tapered extremities and spider-like appearance of both hands. A grade III/VI holosystolic murmur was heard at the apex, with prominent radiation to the axilla. There were no palpable hepatosplenomegaly and lymph nodes. An ophthalmic examination by slit lamp showed lower lens zonular fibers due to mild upward displacement of lens in both eyes, that is, ecopia lentis, but he had adequate vision ().
The blood count showed a white cell count 107,700/mm3, hemoglobin 11.6g/dL, and platelet count 93,000/mm3. Blood chemistry revealed total serum protein 7.3g/dL, albumin 4.3g/dL, alkaline phosphatase 77U/L, AST 58U/L, ALT 15U/L, BUN 10.6mg/dL, Cr 0.9mg/dL, LDH 3317U/L and uric acid 7.6mg/dL. Coagulation profiles were PT 14.2sec (control 12.5sec), aPTT 35.3sec (control from 28 to 40sec) and fibrinogen assay 170mg/dL.
An electrocardiogram revealed no abnormalities except for a sinus tachycardia at a rate of 112. A radiograph of the chest was normal. Both hand AP roentgenogram showed arachnodactyly (). A radiograph of spine showed no scoliosis and kyphosis. An echocardiogram revealed the prolapse of posterior mitral leaflet and mitral regurgitation, but not aortic regurgitation and dissection (). Peripheral blood smear showed markedly increased blasts and decreased platelet count. Findings on bone marrow examination showed that most of the nucleated cells were monoblasts () that were negative on myeloperoxidase and chloracetate esterase staining but demonstrated positivity on staining with non-specific esterase (). Immunophenotype of those cells showed CD13+, CD33+, CD56+ and HLA-DR+. Cytogenetic studies on the marrow showed 46 XY. He was diagnosed as acute monoblastic leukemia (M5a).
We recommended him to receive remission induction chemotherapy, but the patient gave up the therapy.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [37.4, 'degrees celsius'], 'Heart Rate or Pulse': [112.0, 'beats per minute'], 'respiratory rate': [20.0, 'breaths per minute'], 'White blood cell count': [107700.0, 'm^3']}",2,2,2,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 37.4 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 112.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 107700.0 count/m^3. To convert 107700.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 107700.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 0.00011 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 1 + 1 = 2.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 2.
Hence, the the number of SIRS criteria met by the patient is 2."
6831,51,SIRS Criteria,diagnosis,integer,pmc-7544388-1,Extracted,"In August 2018, a 66-year-old man visited the outpatient clinic for febrile sensations and chills that had been present for 6 months; he also complained of myalgia and dyspnea. The patient had undergone aortic valve replacement and central annuloplasty 10 years prior, due to severe aortic valve stenosis and moderate mitral valve regurgitation. On admission, he had a blood pressure of 100/60 mm Hg, pulse rate of 54 beats/min, respiratory rate of 18 breaths/min, and body temperature of 36.7°C. Physical examination revealed conjunctival hemorrhage in the left eye and petechial eruption on both lower extremities. Laboratory examinations revealed a white blood cell count of 4700/mm3 (44.6% neutrophils and 1.1% eosinophils), a hemoglobin level of 13.0 g/dL, and a platelet count of 96,000/mm3. Measurement of inflammatory markers showed a C-reactive protein level of 1.55 mg/dL, erythrocyte sedimentation rate of 40 mm/h, and a procalcitonin level of 0.273 ng/mL. Liver function tests showed an alkaline phosphatase level of 102 U/L, aspartate aminotransferase level of 41 U/L, alanine aminotransferase level of 18 U/L, lactate dehydrogenase level of 687 U/L, total bilirubin level of 0.78 mg/dL, and serum albumin level of 3.5 mg/dL. Renal function tests showed a blood urea nitrogen level of 16.5 mg/dL and a serum creatinine level of 1.68 mg/dL. The serum coagulation profiles showed activated partial thromboplastin and prothrombin times of 81.6 and 37.6 seconds, respectively. Transthoracic echocardiography was performed to evaluate infective endocarditis; this examination revealed a mobile mass-like lesion (0.92 × 1.57 cm) at the prosthetic aortic valve and a hypermobile mass-like lesion (0.96 × 0.67 cm) at the mitral valve. Thus, the patient was treated with injections of ceftriaxone and gentamycin. On day 3 of hospitalization, yeast-forming fungi were detected in blood culture; therefore, fluconazole was administered. The yeast-forming fungi were analyzed by sequencing of the internal transcribed spacer (ITS) (including the 5.8S rRNA gene) and D1/D2 regions of the 26S ribosomal DNA. rRNA genes were amplified using the primers pITS-F (5′-GTCGTAACAAGGTTAACCTGCGG-3′) and pITS-R (5′-TCCTCCGCTTATTGATATGC-3′) and NL1 (5′-GCATATCAATAAGCGGAGGAAAAG-3′) and NL4 (5′-GGTCCGTGTTTCAAGACGG-3′),[ respectively. BLAST search results indicated a 100% match (450/450 bp for ITS, 533/533 bp for D1/D2) with T mucoides (GenBank accession nos. KY107341 and KY103030). Commercial matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF MS) systems, the VITEK MS (bioMérieux, Marcy l’Etoile, France) with Knowledge Base version 3.0, and the MALDI-TOF Biotyper (Bruker Daltonics, Billerica, MA) identified the isolate as T mucoides. In vitro studies of susceptibility to amphotericin B, fluconazole, voriconazole, caspofungin, and micafungin were performed by the Clinical and Laboratory Standards Institute document M27-A3 broth microdilution method.[ The minimal inhibitory concentrations were as follows: amphotericin B, 1 mg/mL; fluconazole, 16 mg/mL; voriconazole, 0.25 μg/mL; caspofungin, >8 μg/mL; and micafungin, >8 μg/mL. On day 7 after admission, the patient's regimen was changed to intravenous voriconazole plus liposomal amphotericin B, due to continuous fever and new conjunctival hemorrhage.
On day 11 of hospitalization, repeat aortic valve replacement, mitral commissurotomy, and removal of the prosthetic ring and pannus were performed. The same fungus (T mucoides) was grown from pus from abscesses around the ring. Histopathology of the anterior petechial skin lesions on both lower extremities on day 4 showed mild dermal perivascular chronic inflammation with red cell extravasation, indicative of vasculitis. From suspected onychomycosis on the left big toe on day 5 after admission, a potassium hydroxide preparation was positive, but no causative fungus was isolated.
Liposomal amphotericin B treatment (3 mg/kg) was maintained for 22 days and voriconazole monotherapy was maintained for 3 months. More than 1.5 year after the end of treatment, the patient has shown no evidence of relapse.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.7, 'degrees celsius'], 'Heart Rate or Pulse': [54.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [4700.0, 'm^3']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.7 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 54.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 4700.0 count/m^3. To convert 4700.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 4700.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 4.7e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6832,51,SIRS Criteria,diagnosis,integer,pmc-6033244-1,Extracted,"A 30-year-old male, with no significant past medical history, came to the emergency department with complaints of fever and chills for a duration of 3 days. He also complained of myalgia and abdominal pain for the same duration. He reported diffuse abdominal pain, which was 6/10 in severity, nonradiating, and not related to food. He also reported 2 episodes of diarrhea without any blood or mucous, brown in color. He denied cough, shortness of breath, chest pain, night sweats, weight loss, history of trauma, extreme exercise, or any history of travel.
His abdominal examination was significant for abdominal tenderness in all four quadrants, but was soft and nondistended and bowel sounds were present. The rest of his examination was unremarkable. Triage vitals were significant for a temperature of 103.3°F, heart rate of 88 beats per minute, respiratory rate of 18 breaths per minute, blood pressure of 109/49, and pulse oximetry of 99% on room air.
Admission laboratory workup revealed leukocyte count of 6.1 × 103 µL (reference range 4.5–11.0 × 103) with 72% neutrophils, hemoglobin of 16.2 g/dL (reference range 13.0–17.0), hematocrit of 48.2% (reference range 39–53), platelet count of 149 × 103 µL (reference range 130–400 × 103), ESR of 4 mm/hr (reference range 0–20), BUN of 34 mg/dL (reference range 8–20), creatinine of 1.8 mg/dL (reference range 0.4–1.3), potassium of 4.7 mmol/L (reference range 3.6–5.1), phosphorous of 3.0 mg/dL (reference range 2.4–4.7), aspartate aminotransferase of 1,146 IU/L (reference range 15–41), alanine aminotransferase of 243 IU/L (reference range 17–63), and creatinine kinase of 39,125 IU/L (reference range 38–398). Urinalysis was significant for large blood, and urine red blood cells were 0–2.
In view of the high-grade fever, we attempted to find an infectious source to explain his history and presentation. Chest X-ray () and CT scan were obtained and showed no signs of pneumonia. Urinalysis and influenza rapid antigen test were performed and did not reveal any abnormalities. CT of the abdomen and pelvis was obtained and did not reveal any focal sources. Stool culture with ova and parasites, blood cultures, urinary toxicology including synthetic THC (K2), HIV, herpes simplex virus, hepatitis panel, Mycoplasma pneumoniae IgM antibody, urine Legionella antigen, QuantiFERON® test for tuberculosis, and TSH were all performed as well. All the test results were negative except immunoglobulin M antibodies for Mycoplasma pneumoniae that were detected by enzyme-linked immunosorbent assay. The antibodies were initially 781 U/mL, which is considered a low positive (reference range 770–950).
Our patient was empirically started on levofloxacin and metronidazole for possible gastroenteritis initially while culture and laboratory results were pending. He was managed for his acute renal failure and rhabdomyolysis with aggressive parenteral hydration. However, he continued to spike fevers during days 1–4 of the admission, but his diarrhea, abdominal pain, and myalgia resolved by day 3. One week later, mycoplasma antibody was recorded again and it was 976 U/ml, which is considered a true positive (reference range 950+). The fact that the antibody titer was trending up was clinically significant for a recent Mycoplasma pneumoniae infection. After mycoplasma was found to be positive, metronidazole was discontinued and he was continued with levofloxacin. His creatinine, liver function tests, and CK trended down to normal reference ranges (), and he was discharged on day 9 with planned outpatient follow-up.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [103.3, 'degrees fahrenheit'], 'Heart Rate or Pulse': [88.0, 'beats per minute'], 'respiratory rate': [18.0, 'breaths per minute'], 'White blood cell count': [6100.0, 'µL']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 103.3 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 71.3 = 39.61111 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 88.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 1.
The patient's concentration of white blood cell is 6100.0 count/µL. To convert 6100.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 6100.0 white blood cell count/µL * 1.0 µL/mm^3 = 6100.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6833,51,SIRS Criteria,diagnosis,integer,pmc-4531640-1,Extracted,"A 71-year-old female farmer, with a past history of diabetes mellitus, showed symptoms of diffuse myalgia, severe muscle weakness and fever for 4 days. She was dehydrated, and general myalgias and weakness were so severe that she was unable to walk. Physical examination revealed the following values: 38.5°C body temperature, 80/50 mmHg blood pressure, 100/min pulse rate, 20/min respiratory rate. In particular, an eschar, which is characteristic of tsutsugamushi disease, was found on her right flank area. Her Tsutsugamushi antibody titer, which was measured by serologic indirect fluoroimmunoassay, was 1:40960. Significant laboratory findings included serum creatine phophokinase (CPK) 3250 U/L (normal less than 200 U/L), serum aldolase 22.4 IU/mL (normal less than 8 IU/mL), blood urea nitrogen 95 mg/dL (normal less than 22 mg/dL), creatinine 4.6 mg/dL (normal less than 1.4 mg/dL), potassium 5.1 mg/dL, sodium 129 mg/dL, uric acid 12.4 mg/dL (normal less than 7 mg/dL), albumin 2.1 g/dL, aspartate transaminase 173 U/L, and alanine transaminase 89.5 U/L. The patient’s urine was red, and analysis revealed a large amount of blood (4+, 0–1 red blood cells/high power field, 5–9 white blood cells/high power field). Urine myoglobin was 23.5 ng/mL (normal less than 7 ng/mL). White blood cell count was 6.4×109/L, hemoglobin 14.9 g/dL, and platelet count 92×109/L. Chest X-ray, electrocardiogram, and abdominal film were normal. She was diagnosed with rhabdomyolysis and acute renal failure associated with tsutsugamushi infection and was treated with doxycycline and fluid resuscitation with normal saline. Five days into treatment, creatinine and other laboratory findings normalized () and other clinical symptoms and signs improved greatly, including fever, myalgia, weakness and hypotension. She was subsequently discharged after 12 days.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.5, 'degrees celsius'], 'White blood cell count': [6.4, 'L'], 'respiratory rate': [20.0, 'breaths per minute'], 'Heart Rate or Pulse': [100.0, 'beats per minute']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.5 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 100.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 6.4 count/L. To convert 6.4 count/L of white blood cell to mm^3, multiply by the conversion factor 1e-06 L/mm^3 which will give 6.4 white blood cell count/L * 1e-06 L/mm^3 = 6.4e-06 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 20.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6834,51,SIRS Criteria,diagnosis,integer,pmc-3617319-1,Extracted,"A 53-year-old male patient with a 20-year history of alcohol use (50 g/day) and confirmed liver cirrhosis, was admitted to this medical center for hematemesis on November 23, 2002. His vital signs on admission were heart rate of 120 beats per minute, blood pressure of 90/60 mmHg, respiratory rate of 18 per minute, body temperature of 36.4℃, and room air oxygen saturation of 100%. On physical examination, the patient appeared to be acutely ill; anemic conjunctiva, spider angioma on the anterior chest, abdominal distension, and shifting dullness were also observed. Laboratory data showed hemoglobin level of 7.4 g/dL, white blood cell count of 11,400/µL, platelet count of 67,000/µL, serum creatinine of 1.2 mg/dL, blood urea nitrogen of 35 mg/dL, serum total bilirubin of 1.9 mg/dL, alkaline phosphatase of 231 IU/L, aspartate aminotransferase of 285 IU/L, alanine aminotransferase of 95 IU/L, albumin of 2.1 g/dL, and prothrombin time of 14.8 sec (International Normalized Ratio 1.26). Serum hepatitis B surface antigen and serum hepatitis C antibodies were negative. His Child-Pugh score was 8 (class B).
We started somatostatin (6 g/day) and cefotaxime (3 g/day) infusion but not gastric acid-suppressive agents. Two units of packed red blood cells were transfused and urgent esophagogastroduodenoscopy (EGD; GIF-XQ240, Olympus Optical Co., Tokyo, Japan) was performed. EGD findings showed a small non-bleeding esophageal varix and a nodular shaped gastric varix with stigmata at the fundus of the stomach. EVL was performed for emergency hemostasis using endoscopic pneumoactivated ligating devices (Sumitomo Bakelite Co., Ltd, Tokyo, Japan) in the left lateral decubitus position (). A sufficient amount of the lesion was sucked into the ligator cap, and a rubber band was applied to fully ligate the lesion. The procedure was completed without any events at that time.
However, two days after the EVL, the patient complained of abdominal pain, and a perforation was observed at the post-EVL ulcer base on the gastric fundus at follow-up EGD (). Also, a few air bubbles were observed outside the posterior gastric wall of the fundus on abdominal computed tomography (). We diagnosed perforation after the band ligation of the gastric varices and recommended emergency surgery. However, the patient refused to undergo an emergency operation and was therefore treated with a supportive therapy consisting of nothing-by-mouth status, intensive care unit management, and continued intravenous administration of antibiotics for 10 days. After 10 days, findings on EGD revealed healing of the perforation site (). Oral intake was then resumed and the patient was discharged 25 days later. Three months after the discharge, a follow-up EGD indicated that the perforation site had healed completely ().",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.4, 'degrees celsius'], 'White blood cell count': [11400.0, 'µL'], 'respiratory rate': [18.0, 'breaths per minute'], 'Heart Rate or Pulse': [120.0, 'beats per minute']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.4 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 120.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's concentration of white blood cell is 11400.0 count/µL. To convert 11400.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 11400.0 white blood cell count/µL * 1.0 µL/mm^3 = 11400.0 white blood cell count/mm^3. Because the white blood cell count is between 4000 and 12000 count per mm^3, this does not meet SIRS criteria for white blood cell count, and so the current total remains at 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6835,51,SIRS Criteria,diagnosis,integer,pmc-6020389-1,Extracted,"A 24-year-old Sri Lankan man developed fever, profuse vomiting and diarrhoea followed by reduced level of consciousness over a 12-h duration. He had myalgia, arthralgia and frontal headache. He did not have photophobia, phonophobia, skin rash, fits, cough or urinary symptoms. He did not have any bleeding manifestations. He did not smoke tobacco or consume alcohol. There was no history of illicit drug abuse or high risk sexual behavior. He had been previously diagnosed with mild intermittent bronchial asthma.
On examination, he was febrile (101.3 °F), drowsy with a Glasgow coma scale of 11/15. There were no skin rashes or lymphadenopathy. No focal signs were noted in the neurological examination and fundoscopic examination was normal. His Pulse rate was 112 bpm; blood pressure was 100/60 mmHg with no postural hypotension; respiratory rate was 14/min. Rest of the general and systems examinations were normal.
His full blood count on admission showed white blood cells of 6 × 109/L (Normal range [NR] 4.0–11.0 × 109/L) with neutrophils of 59%; haemoglobin 14.3 g/dL (NR 13.5–16.5 g/dL) and platelet count of 74 × 109/L (NR 150–450 × 109/L). Erythrocyte sedimentation rate was 13 mm in first hour and C-reactive protein was 63 mg/l (NR < 5 mg/L). Serum electrolytes were normal with mild impaired renal function. Liver enzymes were elevated, alanine aminotransferase was 303 U/l (NR < 50 U/L) and aspartate aminotransferase was 482 U/l (NR < 50 U/L) with a total bilirubin of 10.6 µmol/L (NR 5–21 µmol/L). His urine analysis and coagulation profile were normal. Non-contrast CT brain demonstrated cerebral oedema. Lumbar puncture was precluded by a low platelet count.
Based on a working diagnosis of encephalitis, he was commenced on intravenous meropenem, vancomycin, aciclovir and dexamethasone, but were subsequently omitted once the diagnosis became evident.
On further investigation, dengue IgM antibody in serum was positive on day 6 of fever. Blood and urine cultures did not yield any microbial growth. Electroencephalography showed generalized slow wave activity. The cranial MRI showed an isolated ovoid hyperintensity in the splenium of the corpus callosum with homogeneous hyperintense signal on diffusion-weighted imaging (DWI) (Fig. ). A diagnosis of reversible splenial lesion syndrome (RESLES) was suspected based on the MRI appearance.
Standard dengue monitoring of vitals, urine output, haematocrit and platelet count were done. His platelet count dropped to a nadir of 31 × 109/L, but subsequently increased. The white cell count steadily increased to 14 × 109/L and then stabilized around 7 × 109/L. Fluid leakage was not detected on repeated ultrasound scanning during the acute phase of illness.
He was discharged from hospital on the tenth day of illness with complete clinical, heamatological and biochemical recovery. Follow–up cranial MRI done 1 month later showed complete resolution of the splenial lesion (Fig. ).",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [101.3, 'degrees fahrenheit'], 'White blood cell count': [6000.0, 'L'], 'respiratory rate': [14.0, 'breaths per minute'], 'Heart Rate or Pulse': [112.0, 'beats per minute']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 101.3 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 69.3 = 38.5 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 112.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 6000.0 count/L. To convert 6000.0 count/L of white blood cell to mm^3, multiply by the conversion factor 1e-06 L/mm^3 which will give 6000.0 white blood cell count/L * 1e-06 L/mm^3 = 0.006 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 14.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6836,51,SIRS Criteria,diagnosis,integer,pmc-3552714-1,Extracted,"A 42-year-old man presented with a painful, enlarging, lateral abdominal wall mass, which appeared after playing baseball. He gave no history of direct abdominal trauma such as collision with another player. He had a history of hyperuricemia; however, he had not undergone any therapy for the same. There was no family history of bleeding diathesis or hematological diseases. On physical examination, his vital signs were as follows: temperature 36.8°C, blood pressure 108/69 mm Hg, pulse rate 58 beats/min, and respiratory rate 12 breaths/min. A firm mass was palpable over the left lateral abdominal wall and it was tender. The skin color of the area was normal. Blood biochemistry on laboratory examination was within normal ranges and the platelet count was 174 ×103 cells/μl, prothrombin time was 11.8 s, international normalized ratio was 0.99, and activated partial thromboplastin time was 32.6 s.
Ultrasonography (US) showed a heteroechoic, well-defined mass in the patient’s left lateral abdominal wall (Figure
). An emergency noncontrast computed tomography (CT) of the abdomen showed a hyperdense mass in the left internal oblique muscle measuring 10.5 × 6.5 × 5.5 cm. Contrast-enhanced CT did not show extravasation of the contrast material within the mass (Figure
). The diagnosis of an oblique muscle hematoma was made. The patient was conservatively treated with analgesics. Four days after the first visit, the patient revisited our department for follow-up. His abdominal pain improved, but an ecchymosis was observed on the patient’s left lateral abdominal skin (Figure
).",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.8, 'degrees celsius'], 'White blood cell count': [174000.0, 'µL'], 'respiratory rate': [12.0, 'breaths per minute'], 'Heart Rate or Pulse': [58.0, 'beats per minute']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.8 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 58.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 174000.0 count/µL. To convert 174000.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 174000.0 white blood cell count/µL * 1.0 µL/mm^3 = 174000.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 12.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6837,51,SIRS Criteria,diagnosis,integer,pmc-5234096-1,Extracted,"A previously healthy, fully immunized, 4-year-old boy came to the Emergency Room of the Saint Anna Hospital in Como on July 21, 2016, presenting with sudden onset weakness and poor mobility in his left arm. Two days earlier, he had an upper respiratory illness with mild fever, rhinorrhoea, and cough. Past and recent clinical histories were negative for relevant diseases. At admission, physical examination of the patient showed that the child had a temperature of 38.5 °C, a heart rate of 131/min, a respiratory rate of 18/min, 98% oxygen saturation and a blood pressure of 110/70 mmHg. Respiratory, cardiovascular, and skin examinations were normal. Neurological evaluation demonstrated that the child was alert but had a stiff neck and weakness in his left arm, which was hypotonic and areflexic. The results of cranial nerve examination, including fundoscopy, and diagnoses of the right arm and bilateral leg strength were normal.
Results from a complete blood count were in the normal range, with the exception of slightly elevated white blood cell and neutrophil counts. Serum electrolytes, coagulation factors, liver enzymes, and C-reactive protein were within the normal limits. Fine bilateral perihilar infiltration was observed on a chest X-ray to give the diagnosis of probable community-acquired pneumonia of viral aetiology.
CSF examination showed a mild increase in white blood cell count (80/mm3, 41% neutrophils) with normal glucose (60 mg/dL) and slightly elevated protein (76 gm/dL) concentrations. Cultures for bacteria were negative, and molecular biology tests for detecting viral infection were negative for herpes simplex virus 1, herpes simplex virus 2, human herpesvirus 6, EV, varicella zoster virus, adenovirus, parvovirus, cytomegalovirus, and Epstein-Barr virus. Computed tomography of the head without contrast did not show abnormalities. Intravenous ceftriaxone and acyclovir were then administered.
Despite this therapy, the child’s neurological function deteriorated rapidly. Within 24 h, the muscle weakness extended to all four limbs, which exhibited greatly reduced mobility. Due to his worsening clinical prognosis, the child was transferred to the Pediatric Intensive Care Unit (PICU) of the Fondazione IRCCS Ca’ Granda, Ospedale Maggiore Policlinico, Milan, Italy.
When the child was admitted to the PICU on July 22, 2016, he was alert but was diagnosed with acute flaccid paralysis based on neurological examination. Together with the muscles of the four limbs, the respiratory muscles were also clearly involved. Moreover, a deficit of the right facial nerve with dysphagia was observed. The child required intubation and mechanical ventilation for adequate gas exchange. After 11 days, tracheotomy was performed. Nutrition was assured through percutaneous endoscopic gastrotomy.
Figure – summarizes the results of magnetic resonance imaging (MRI) of the brain at admission to the PICU, 3 days and about 24 h after the onset of respiratory and neurological manifestations, respectively. A focal signal alteration was found localized in the dorsal portion of the medulla oblongata, also involving the pontine tegmentum, without enhancement or diffusion restriction. Moreover, MRI of the spinal cord showed an extensive signal alteration of the cervical and dorsal spinal cord, reported as myelitis. The signal alteration was mainly localized in the central grey matter, most likely in the anterior horns. After contrast administration, a slight enhancement in some of the caudal roots was observed, without enhancement in the spinal cord.
The presence of somatosensory-evoked potentials confirmed that only the motor pathway was affected. Acute polyradiculoneuritis was excluded because there was no albumino-cytological dissociation and no antiganglioside antibodies in the CSF. There was no evidence of paraneoplasic syndrome or inflammatory disease.
Bacterial cultures of the nasopharyngeal aspirate and the bronchoalveolar lavage fluid were negative. Molecular biology tests for detecting viral infection were negative for herpes simplex virus 1, herpes simplex virus 2, human herpesvirus 6, varicella zoster virus, adenovirus, parvovirus, cytomegalovirus and EBV, but was positive for EV. Both the respiratory samples were reanalysed for the presence of EV-D68 using single-tube real-time PCR to amplify a 116 bp fragment of the 5′ non-translated region according to the method proposed by Poelman et al. []. Phylogenetic analysis based on the method used by Nix et al. [] verified the presence of a virus belonging to clade B3 of the EV-D68 phylogenetic tree (Fig. ). Sequence analysis showed that the 2016 strains were closely related to sequences of the recently described subclade B3, represented in Fig. , by four sequences obtained in China. The level of nucleotide divergence was 2.1% within B3, 5.5% between B1 and B3, and 7.3% between B2 and B3. The sequence from our Italian AFM case was closely related to Dutch AFM EV-D68 cases from 2016.
Serological analysis showed no infection with herpes simplex virus, varicella zoster virus, Epstein-Barr virus, cytomegalovirus, Mycoplasma pneumoniae, Borrelia burgdorferi, Cryptococcus neoformans, or Mycobacterium tuberculosis.
Treatment with intravenous methylprednisolone (30 mg/kg) was initiated. Plasmapheresis was conducted and intravenous immunoglobulins (1 g/kg/day) were administered during the first 3 days in the PICU. Intravenous steroid therapy was suspended after 5 days and substituted with oral prednisone (2 mg/kg/day) for 4 weeks, which was then tapered over an additional 2 weeks.
Significant weakness with reduced mobility of the four limbs and difficulty swallowing persisted with very slow regression. After 4 weeks of treatment, all the signs and symptoms of AFM were significantly reduced or disappeared, although a certain degree of weakness and tingling in the four extremities were still present. Moreover, deep tendon reflexes were generally reduced. However, as expected due to the recent onset of the disease, no muscle atrophy was observed. Moreover, the results of MRI performed about 1 month after the onset of the first neurological manifestations showed that the previously reported alterations were no longer present (Fig. ).",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.5, 'degrees celsius'], 'White blood cell count': [80.0, 'm^3'], 'respiratory rate': [18.0, 'breaths per minute'], 'Heart Rate or Pulse': [131.0, 'beats per minute']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.5 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 131.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 80.0 count/m^3. To convert 80.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 80.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 8e-08 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6838,51,SIRS Criteria,diagnosis,integer,pmc-5704834-1,Extracted,"A 34-year-old male presented at emergency department with pyrexia, chill, fatigue, anorexia, productive cough, body aches, and a right dorsal foot pain. The symptoms started 7 days ago and had been deteriorated after initial treatment with dexamethasone, levofloxacin, and vitamin B6 with suspicion of erysipelas in another hospital. There was no significant past medical history and he was not on any prescribed medications. On presentation, his vital signs were: temperature 38.7oC, respiratory rate 33 breaths per minute, pulse 99 beats per minute, blood pressure 108/64 mm Hg. Physical examination was remarkable for enlarged lymph nodes in the right groin, tumidness, and necrosis in dorsal part of the right foot with purulent fluid, ecchymosis on the anterior tibia of right lower limb, and macular erythematous rash over the body. Laboratory test results revealed a leukocyte count of 13.31 × 109, neutrophil was 79.94%, the neutrophil count was 10.64 × 109, and hemoglobin (Hb) was 129.0 g/L. C-reactive protein was 78.46 mg/L. Aspartate aminotransferase (AST) was 67 U/L, alanine aminotransferase (ALT) was 181 U/L, creatinine was 115 μmol/L, lactate dehydrogenase (LDH) was 365 U/L, α- hydroxybutyrate dehydrogenase (α-HBDH) was 246 U/L, total protein (TP) was 55.9 g/L, albumin was 30.9 g/L, and the ratio of albumin to globulin was 1.2. Urine latent blood was +++, red blood cell was 241.34/μL, and white blood cell (WBC) count was 53.3/μL. Total body computed tomography (CT) scan revealed multiple metal dense shadows of various organs in chest and abdomen, and bones (Fig. ). There was no gross intracranial abnormality. X-ray showed radio opaque deposits in the 2 lungs and subcutaneous deposits in dorsal part of the right foot (Fig. ). On further questioning, the patient's girlfriend, who works as a nurse, acknowledged that she had ever added hypnotics in his coffee, and then injected him 40 g mercury extracted from 40 thermometers through the veins at left elbow and back of right foot after he fell into deep sleep 11 days ago.
Based on an exposure history, symptoms, and imaging, a diagnosis of metallic mercury poisoning was established. The diagnosis was then confirmed with a urinary mercury concentration of 4828 μg/L. Chelation therapy was started on 12th day after mercury exposure with sessions of sodium dimercaptosulphonate (DMPS) and dimercaptosuccinic acid (DMSA) treatment: DMPS 250 mg was administrated intravenously every 12 hours with 7 days on and 3 days off, and DMSA 500 mg p.o. every 8 hours with 3 days on and 4 days off. Blood irrigation was performed once a day for 3 hours each time during first 5 days. Foreign body resections and debridement including ligating and excising the affected vessels at the injection sites were performed at the 16th, 35th, and 59th day. Alveolar lavage was performed at the 56th day, and the toxicity test of the alveolar lavage fluid was positive. In addition, sessions of plasma exchange were performed at the 47th, 65th, 84th, 107th, and 125th day; each session contains 3 times of plasma exchange in successive 3 days. At the end of the fourth month, toxicity test results showed that the mercury concentration in the blood and urine was decreased to 264 ng/mL and 940 ng/mL, respectively. Laboratory test results showed that the WBC count was 7.5 × 109, neutrophil was 58.5%, Hb was 136 g/L, ALT was 26 U/L, AST was 21 U/L, TP was 79.8 g/L, LDH was 165 U/L, α-HBDH was 144 U/L, creatinine was 70 μmol/L, urea was 3.83 mmol/L, 24-hour urine creatinine was 16290 μmol, 24-hour urine protein was 0.51 g, 24-hour urine beta 2-microglobulin was 0.39 mg, urinary N-Acetyl B-D-glucosamine was 22.56 U, 24-hour urine α 1-microglobulin was 12.38 mg, 24-hour urine nitrogen was 259.65 mmol, and the ratio of mercury to creatinine in the urine was 4294.5 μg/g. Pulmonary ventilation function was normal. Electrocardiogram and sonographic examination of heart was unremarkable. The patient has been continuously followed up after hospital discharge.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [38.7, 'degrees celsius'], 'White blood cell count': [13310.0, 'µL'], 'respiratory rate': [33.0, 'breaths per minute'], 'Heart Rate or Pulse': [99.0, 'beats per minute']}",4,4,4,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 38.7 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 99.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 13310.0 count/µL. To convert 13310.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 13310.0 white blood cell count/µL * 1.0 µL/mm^3 = 13310.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 33.0 breaths per minute, which is greater than 20 breaths per minute. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. At least one of the criteria is met, and so we increment the criteria count by 1 giving us a total of 3 + 1 = 4 criteria met.
Hence, the the number of SIRS criteria met by the patient is 4."
6839,51,SIRS Criteria,diagnosis,integer,pmc-7732970-1,Extracted,"A 73-year-old female with a past medical history of hypertension and prior cholecystectomy presented to the emergency room with acute onset of abdominal pain of 1-day duration. She described right lower quadrant abdominal pain that was constant and worsening since it started. She reported no prior occurrence. There were no alleviating or exacerbating factors. Her symptoms were preceded by five days of constipation refractory to stool softeners. She was briefly febrile four days prior to admission. Surgical history disclosed laparoscopic cholecystectomy in 2010 complicated with a perforated gallbladder. After being discharged following the surgery, she noted having had recurring fevers for ten days and experienced no other symptoms.
On initial assessment, her exam revealed an elderly woman, who was alert, well-oriented, and in mild distress. She had an oral temperature of 99°F, a heart rate of 89 bpm, blood pressure of 142/63 mmHG, and a respiratory rate of 18 breaths per minute. Her abdominal exam revealed a soft, non-distended stomach with moderate tenderness at the medial right lower quadrant abdomen. There was no guarding or rebound, and she had normal bowel sounds.
Initial labs showed an elevated WBC at 15.2 K/mcl, hemoglobin at 13.3 g/dL and a high platelet count of 552 K/mcl. The patient had normal values for the following: sodium at 135 mEq/L, potassium at 3.8 mEq/L, BUN at 16 mg/dL and creatinine at 0.92 mg/dL. A CT of the abdomen and pelvis with contrast showed hepatomegaly along with a 12.4 × 4.8 × 3.6 cm fluid collection within the right lateral abdominal wall with two radiopaque structures resembling gallstones (). The abscess extended superiorly to the level of Morison's pouch and inferiorly to the right iliac wing ().
The patient was admitted and started on intravenous piperacillin-tazobactam. Dr. Joseph Hartigan, who has over 20 years of experience in laparscopic surgery, performed a laparoscopic drainage of the abscess and removal of the gallstones. The origin of the abscess was found near the umbilicus and tracked cephalad up towards the liver. A 15 Blake drain was placed into the abscess cavity and left in place for four days. A phlegmon of approximately 100 cc's of purulent fluid was drained and cultures grew out E. Coli. The patient recovered well and was discharged on the 3rd postoperative day. The abscess formed by the gallstones was determined to be the cause of the abdominal pain in this case. The drain was removed during the follow-up appointment two weeks after the surgery. There were no complications. The patient was intrigued in the discovery and thankful for the outcome.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [99.0, 'degrees fahrenheit'], 'White blood cell count': [15200.0, 'µL'], 'respiratory rate': [18.0, 'breaths per minute'], 'Heart Rate or Pulse': [89.0, 'beats per minute']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 99.0 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 67.0 = 37.22222 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 89.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 15200.0 count/µL. To convert 15200.0 count/µL of white blood cell to mm^3, multiply by the conversion factor 1.0 µL/mm^3 which will give 15200.0 white blood cell count/µL * 1.0 µL/mm^3 = 15200.0 white blood cell count/mm^3. Because the white blood cell count is greater than 12000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6840,51,SIRS Criteria,diagnosis,integer,pmc-6629601-1,Extracted,"A 63-year-old man was admitted to the nephrology department for further evaluation of renal impairment and hypocalcemia. The patient was clinically diagnosed with TSC at another tertiary hospital approximately 40 years ago and had a history of hypertension and diabetes. He had not undergone thyroid or parathyroid gland surgery. Several episodes of seizures occurred when he was young. These were managed with anticonvulsants, which were maintained until several years ago. He had also been taking unidentified herbal medicine due to fatigue for a month. He had no cognitive or behavioral problems. He had large bilateral renal AMLs and underwent transcatheter arterial embolizations due to left and right side hemorrhages 24 years and 2 weeks ago, respectively. His two sons were also diagnosed with TSC based on genetic test results.
On admission, the patient complained of general weakness and muscle tremor without other neurologic symptoms, such as tetany or seizure. Physical examination revealed trace peripheral edema and facial angiofibroma only. His blood pressure was 113/67mmHg, with a pulse rate of 87/min, a respiratory rate of 18/min, and body temperature of 36.9℃. His initial laboratory findings were as follows: white blood cells, 12,760/mm3; hemoglobin, 7.9 g/dL; platelets, 365 K/mm3; blood urea nitrogen, 54 mg/dL; serum creatinine, 5.26mg/dL; alkaline phosphatase, 98 IU/L; magnesium, 2.1mg/dL; total calcium, 3.7 mg/dL (corrected calcium, 4.5mg/dL); ionized calcium, 0.591mmol/L; phosphrous, 5.0mg/dL; and albumin, 3.0 mg/dL. An electrocardiogram showed QT prolongation (QT 440 ms, QTc 508ms). Computed tomography (CT) demonstrated enlarged and distorted kidneys due to numerous AMLs and a large number of tiny nodules in both lungs, consistent with renal and pulmonary manifestations of TSC(). His baseline kidney function was not determined due to the lack of previous medical records; however, severely destructed renal parenchyma detected in CT suggested progression to advanced chronic kidney disease (CKD). Bone mineral density was within normal range (the lowest value was −0.6 for the total femur). To determine the cause of the hypocalcemia, hormonal status related to calcium homeostasis was examined, including parathyroid hormone (PTH) 44 pg/mL, 25-(OH) vitamin D3 9 ng/mL, and 1,25-(OH) 2 vitamin D3 2.8 pg/mL (reference range, 19.6-54.3 pg/mL). Urinary calcium concentration was very low(<0.8mg/dL), and the urinary calcium/creatinine ratio was <0.013mg/mg Cr. The fractional excretion of calcium(FECa) was 0.015.
The patient was initially treated with oral calcitriol 0.25 mg/day, calcium acetate 4.26 g/day, and cholecalciferol 400 IU/day, and intravenous calcium gluconate 2 g/day was administered on the first 2 days (). After 5 days of intensive calcium replacement, the total calcium concentration increased from 3.7 to 6.1mg/dL and ionized calcium from 0.591 to 0.749mmol/L, and his tremor improved. At the outpatient clinic 1 month after discharge, the total and ionized calcium levels were measured as 7.9mg/dL and 0.945mmol/L, respectively, with continuous administration of calcitriol 0.25mg/day and calcium citrate 750mg/cholecalciferol 400 IU/day.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'Temperature': [36.9, 'degrees celsius'], 'White blood cell count': [12760.0, 'm^3'], 'respiratory rate': [18.0, 'breaths per minute'], 'Heart Rate or Pulse': [87.0, 'beats per minute']}",1,1,1,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 36.9 degrees celsius. Because the temperature is between 36 and 38 degrees celsius, this does not meet SIRS criteria for temperature, and so the current total remains at 0.
The patient's heart rate is 87.0 beats per minute. Because the heart rate is less than 90 beats per minute, this does not meet SIRS criteria for heart rate, and so the current total remains at 0.
The patient's concentration of white blood cell is 12760.0 count/m^3. To convert 12760.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 12760.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 1e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 18.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 1.
Hence, the the number of SIRS criteria met by the patient is 1."
6841,51,SIRS Criteria,diagnosis,integer,pmc-8057120-1,Extracted,"A 45-year-old non-alcoholic female presented with a seven-day history of fever, generalized rashes, deep jaundice, and itching three weeks after initiation of dapsone 100 mg/day for leprosy neuritis. At the time of admission, she was conscious, cooperative, and oriented. The blood pressure was 110/70 mmHg, pulse rate 110 beats/min, respiratory rate 16 breaths/min, and the temperature was 101.5 degrees Fahrenheit. She had an oral ulcer, deep icterus, pallor, and erythematosus, desquamating rashes predominantly over the neck, trunk, and upper extremities. The liver and spleen were not palpable. Cardiac and respiratory system examinations were unremarkable.
Laboratory investigations revealed a hemoglobin level of 7.0 g/dL, leukocyte count 79,500/mm3 with differential blood counts of neutrophils 75%, lymphocytes 3%, eosinophils 1%, myelocytes 13%, meta-myelocytes 06%, and a severe thrombocytosis of 14,32000/mm3. Peripheral blood film examination showed microcytic hypochromic anemia, leukocytosis with a shift to the left, and thrombocytosis. Liver function tests revealed total bilirubin of 12.14 mg/dL with direct fraction 7.5 mg/dL, aspartate transaminase (AST) 148 IU/L, alanine transaminase (ALT) 189 IU/L, alkaline phosphatase 622 IU/L, and total protein with serum albumin 2.8 g/dL. Lactate dehydrogenase (LDH) was markedly elevated at 1830 IU/L. Blood urea was 45 mg/dL, serum creatinine 0.75 mg/dL, serum sodium 138 mEq/L, and serum potassium 3.4 mEq/L. Urinalysis was normal. Coagulation profiles including bleeding time, clotting time, prothrombin time, and activated prothrombin time were within normal limits. Serological tests for hepatitis A virus (anti-HAV IgM), hepatitis B virus (HBsAg), hepatitis C virus (anti-HCV), and hepatitis E virus (anti-HEV IgM) were negative. She tested negative for malaria, leptospirosis, typhus fever, cytomegalovirus, Epstein-Barr virus, and human immunodeficiency virus 1 and 2. Other laboratory tests including thyroid hormone profile, glucose-6-phosphate dehydrogenase level, and iron profile were within normal limits. The direct, as well as indirect agglutination tests, were negative. The serum ferritin level was 285 ng/mL, leukocyte alkaline phosphatase (LAP) score was 205, erythrocyte sedimentation rate (ESR) 55/hr at the first hour, and C- reactive protein >6 mg/dl. In autoimmune study antinuclear antibody, anti-mitochondrial antibodies, anti-smooth muscle antibody, anti-double-stranded DNA, and anti-liver-kidney-microsomal antibodies were negative. Serial laboratory investigations are mentioned in Table . Chest X-ray and electrocardiogram were unremarkable. Ultrasonography of the abdomen showed mild uniform enlargement of the liver with normal echo-texture, there was no evidence of biliary obstruction and portal hypertension. Microscopic examination of the liver biopsy showed diffuse fatty changes and steatosis. Bile pigment in hepatocytes and bile in bile canaliculi was present. The mild proliferation of the bile duct and mild inflammation of the portal triad were also present.
Clinical history of the patient and laboratory parameters with a prior history of dapsone therapy was consistent with a diagnosis of DHS with leukemoid reaction and thrombocytosis. She was treated with oral prednisolone 50 mg/day (1 mg/kg) for one month and then tapered off over the next month. She started improving after the first week with gradual subsidence of fever and rashes. Leukocytes, platelet count, and leukocyte alkaline phosphate (LAP) score showed a downward trend on repeated examination (Table ). After one month of follow-up, she was asymptomatic with complete resolution of rashes, icterus, with normal hematological parameters.",What are the number of SIRS critiera met by the patient? You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'White blood cell count': [79500.0, 'm^3'], 'Temperature': [101.5, 'degrees fahrenheit'], 'respiratory rate': [16.0, 'breaths per minute'], 'Heart Rate or Pulse': [110.0, 'beats per minute']}",3,3,3,"The rules for SIRS Criteria are listed below:
    
1. Temperature >38°C (100.4°F) or <36°C (96.8°F): No = 0 points, Yes = +1 point
2. Heart rate >90: No = 0 points, Yes = +1 point
3. Respiratory rate >20 or PaCO₂ <32 mm Hg: No = 0 points, Yes = +1 point
4. White blood cell count (WBC) >12,000/mm³, <4,000/mm³, or >10% bands: No = 0 points, Yes = +1 point

The total number of criteria met is taken by summing the score for each criteria.
    
The current count of SIRS criteria met is 0.
The patient's temperature is 101.5 degrees fahrenheit. To convert to degrees celsius, apply the formula 5/9 * [temperature (degrees fahrenheit) - 32]. This means that the patient's temperature is 5/9 * 69.5 = 38.61111 degrees celsius. Because the temperature is greater than 38 degrees celsius, we increment the criteria count by 1 making the current total 0 + 1 = 1.
The patient's heart rate is 110.0 beats per minute. Because the heart rate is greater than 90 beats per minute, this meets SIRS criteria and so we increment the criteria count by 1 making the current total 1 + 1 = 2.
The patient's concentration of white blood cell is 79500.0 count/m^3. To convert 79500.0 count/m^3 of white blood cell to mm^3, multiply by the conversion factor 1e-09 m^3/mm^3 which will give 79500.0 white blood cell count/m^3 * 1e-09 m^3/mm^3 = 8e-05 white blood cell count/mm^3. Because the white blood cell count is less than 4000 count per mm^3, we increment the criteria count by 1 making the current total 2 + 1 = 3.
The final SIRS criteria is whether the patient has a respiratory rate of more than 20 breaths per minute or if the patient's PaCO₂ partial pressure is less than 32 mm Hg. The patient's respiratory rate is 16.0 breaths per minute, which is less or equal to than 20 breaths per min. The patient's PaCO₂ partial pressure is not provided and so we assume that the patient's partial pressure is greater than or equal to 32 mm Hg. Neither criteria met and so keep the current total at 3.
Hence, the the number of SIRS criteria met by the patient is 3."
6842,56,QTc Fridericia Calculator,physical,decimal,22,Template,A patient has a heart rate of 70 bpm and a QT interval of 210 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [70, 'beats per minute'], 'QT Interval': [210, 'msec']}",221.07283,210.01919,232.12647,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 70 beats per minute.
The QT interval is 210 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/70 = 0.85714.
Hence, plugging in these values, we will get 210/√(0.85714) = 221.07283.The patient's corrected QT interval (QTc) is 221.07283 msec."
6843,56,QTc Fridericia Calculator,physical,decimal,23,Template,A patient has a heart rate of 58 bpm and a QT interval of 262 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [58, 'beats per minute'], 'QT Interval': [262, 'msec']}",259.05616,246.10335,272.00897,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 58 beats per minute.
The QT interval is 262 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/58 = 1.03448.
Hence, plugging in these values, we will get 262/√(1.03448) = 259.05616.The patient's corrected QT interval (QTc) is 259.05616 msec."
6844,56,QTc Fridericia Calculator,physical,decimal,24,Template,A patient has a heart rate of 103 bpm and a QT interval of 418 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [103, 'beats per minute'], 'QT Interval': [418, 'msec']}",500.50221,475.4771,525.52732,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 103 beats per minute.
The QT interval is 418 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/103 = 0.58252.
Hence, plugging in these values, we will get 418/√(0.58252) = 500.50221.The patient's corrected QT interval (QTc) is 500.50221 msec."
6845,56,QTc Fridericia Calculator,physical,decimal,25,Template,A patient has a heart rate of 133 bpm and a QT interval of 338 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [133, 'beats per minute'], 'QT Interval': [338, 'msec']}",440.70651,418.67118,462.74184,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 133 beats per minute.
The QT interval is 338 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/133 = 0.45113.
Hence, plugging in these values, we will get 338/√(0.45113) = 440.70651.The patient's corrected QT interval (QTc) is 440.70651 msec."
6846,56,QTc Fridericia Calculator,physical,decimal,26,Template,A patient has a heart rate of 113 bpm and a QT interval of 222 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [113, 'beats per minute'], 'QT Interval': [222, 'msec']}",274.15509,260.44734,287.86284,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 113 beats per minute.
The QT interval is 222 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/113 = 0.53097.
Hence, plugging in these values, we will get 222/√(0.53097) = 274.15509.The patient's corrected QT interval (QTc) is 274.15509 msec."
6847,56,QTc Fridericia Calculator,physical,decimal,27,Template,A patient has a heart rate of 117 bpm and a QT interval of 251 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [117, 'beats per minute'], 'QT Interval': [251, 'msec']}",313.58268,297.90355,329.26181,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 117 beats per minute.
The QT interval is 251 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/117 = 0.51282.
Hence, plugging in these values, we will get 251/√(0.51282) = 313.58268.The patient's corrected QT interval (QTc) is 313.58268 msec."
6848,56,QTc Fridericia Calculator,physical,decimal,28,Template,A patient has a heart rate of 72 bpm and a QT interval of 234 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [72, 'beats per minute'], 'QT Interval': [234, 'msec']}",248.66244,236.22932,261.09556,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 72 beats per minute.
The QT interval is 234 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/72 = 0.83333.
Hence, plugging in these values, we will get 234/√(0.83333) = 248.66244.The patient's corrected QT interval (QTc) is 248.66244 msec."
6849,56,QTc Fridericia Calculator,physical,decimal,29,Template,A patient has a heart rate of 166 bpm and a QT interval of 425 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [166, 'beats per minute'], 'QT Interval': [425, 'msec']}",596.63151,566.79993,626.46309,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 166 beats per minute.
The QT interval is 425 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/166 = 0.36145.
Hence, plugging in these values, we will get 425/√(0.36145) = 596.63151.The patient's corrected QT interval (QTc) is 596.63151 msec."
6850,56,QTc Fridericia Calculator,physical,decimal,30,Template,A patient has a heart rate of 103 bpm and a QT interval of 431 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [103, 'beats per minute'], 'QT Interval': [431, 'msec']}",516.06807,490.26467,541.87147,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 103 beats per minute.
The QT interval is 431 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/103 = 0.58252.
Hence, plugging in these values, we will get 431/√(0.58252) = 516.06807.The patient's corrected QT interval (QTc) is 516.06807 msec."
6851,56,QTc Fridericia Calculator,physical,decimal,31,Template,A patient has a heart rate of 130 bpm and a QT interval of 499 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [130, 'beats per minute'], 'QT Interval': [499, 'msec']}",645.69997,613.41497,677.98497,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 130 beats per minute.
The QT interval is 499 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/130 = 0.46154.
Hence, plugging in these values, we will get 499/√(0.46154) = 645.69997.The patient's corrected QT interval (QTc) is 645.69997 msec."
6852,56,QTc Fridericia Calculator,physical,decimal,32,Template,A patient has a heart rate of 157 bpm and a QT interval of 252 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [157, 'beats per minute'], 'QT Interval': [252, 'msec']}",347.25487,329.89213,364.61761,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 157 beats per minute.
The QT interval is 252 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/157 = 0.38217.
Hence, plugging in these values, we will get 252/√(0.38217) = 347.25487.The patient's corrected QT interval (QTc) is 347.25487 msec."
6853,56,QTc Fridericia Calculator,physical,decimal,33,Template,A patient has a heart rate of 98 bpm and a QT interval of 263 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [98, 'beats per minute'], 'QT Interval': [263, 'msec']}",309.72898,294.24253,325.21543,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 98 beats per minute.
The QT interval is 263 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/98 = 0.61224.
Hence, plugging in these values, we will get 263/√(0.61224) = 309.72898.The patient's corrected QT interval (QTc) is 309.72898 msec."
6854,56,QTc Fridericia Calculator,physical,decimal,34,Template,A patient has a heart rate of 159 bpm and a QT interval of 406 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [159, 'beats per minute'], 'QT Interval': [406, 'msec']}",561.83322,533.74156,589.92488,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 159 beats per minute.
The QT interval is 406 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/159 = 0.37736.
Hence, plugging in these values, we will get 406/√(0.37736) = 561.83322.The patient's corrected QT interval (QTc) is 561.83322 msec."
6855,56,QTc Fridericia Calculator,physical,decimal,35,Template,A patient has a heart rate of 58 bpm and a QT interval of 402 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [58, 'beats per minute'], 'QT Interval': [402, 'msec']}",397.48312,377.60896,417.35728,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 58 beats per minute.
The QT interval is 402 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/58 = 1.03448.
Hence, plugging in these values, we will get 402/√(1.03448) = 397.48312.The patient's corrected QT interval (QTc) is 397.48312 msec."
6856,56,QTc Fridericia Calculator,physical,decimal,36,Template,A patient has a heart rate of 166 bpm and a QT interval of 347 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [166, 'beats per minute'], 'QT Interval': [347, 'msec']}",487.13208,462.77548,511.48868,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 166 beats per minute.
The QT interval is 347 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/166 = 0.36145.
Hence, plugging in these values, we will get 347/√(0.36145) = 487.13208.The patient's corrected QT interval (QTc) is 487.13208 msec."
6857,56,QTc Fridericia Calculator,physical,decimal,37,Template,A patient has a heart rate of 176 bpm and a QT interval of 401 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [176, 'beats per minute'], 'QT Interval': [401, 'msec']}",574.02542,545.32415,602.72669,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 176 beats per minute.
The QT interval is 401 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/176 = 0.34091.
Hence, plugging in these values, we will get 401/√(0.34091) = 574.02542.The patient's corrected QT interval (QTc) is 574.02542 msec."
6858,56,QTc Fridericia Calculator,physical,decimal,38,Template,A patient has a heart rate of 51 bpm and a QT interval of 260 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [51, 'beats per minute'], 'QT Interval': [260, 'msec']}",246.28978,233.97529,258.60427,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 51 beats per minute.
The QT interval is 260 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/51 = 1.17647.
Hence, plugging in these values, we will get 260/√(1.17647) = 246.28978.The patient's corrected QT interval (QTc) is 246.28978 msec."
6859,56,QTc Fridericia Calculator,physical,decimal,39,Template,A patient has a heart rate of 170 bpm and a QT interval of 393 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [170, 'beats per minute'], 'QT Interval': [393, 'msec']}",556.10772,528.30233,583.91311,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 170 beats per minute.
The QT interval is 393 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/170 = 0.35294.
Hence, plugging in these values, we will get 393/√(0.35294) = 556.10772.The patient's corrected QT interval (QTc) is 556.10772 msec."
6860,56,QTc Fridericia Calculator,physical,decimal,40,Template,A patient has a heart rate of 175 bpm and a QT interval of 452 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [175, 'beats per minute'], 'QT Interval': [452, 'msec']}",645.80216,613.51205,678.09227,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 175 beats per minute.
The QT interval is 452 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/175 = 0.34286.
Hence, plugging in these values, we will get 452/√(0.34286) = 645.80216.The patient's corrected QT interval (QTc) is 645.80216 msec."
6861,56,QTc Fridericia Calculator,physical,decimal,41,Template,A patient has a heart rate of 160 bpm and a QT interval of 462 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [160, 'beats per minute'], 'QT Interval': [462, 'msec']}",640.66582,608.63253,672.69911,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 160 beats per minute.
The QT interval is 462 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/160 = 0.375.
Hence, plugging in these values, we will get 462/√(0.375) = 640.66582.The patient's corrected QT interval (QTc) is 640.66582 msec."
6862,56,QTc Fridericia Calculator,physical,decimal,42,Template,A patient has a heart rate of 146 bpm and a QT interval of 246 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [146, 'beats per minute'], 'QT Interval': [246, 'msec']}",330.87853,314.3346,347.42246,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 146 beats per minute.
The QT interval is 246 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/146 = 0.41096.
Hence, plugging in these values, we will get 246/√(0.41096) = 330.87853.The patient's corrected QT interval (QTc) is 330.87853 msec."
6863,56,QTc Fridericia Calculator,physical,decimal,43,Template,A patient has a heart rate of 61 bpm and a QT interval of 278 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [61, 'beats per minute'], 'QT Interval': [278, 'msec']}",279.53562,265.55884,293.5124,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 61 beats per minute.
The QT interval is 278 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/61 = 0.98361.
Hence, plugging in these values, we will get 278/√(0.98361) = 279.53562.The patient's corrected QT interval (QTc) is 279.53562 msec."
6864,56,QTc Fridericia Calculator,physical,decimal,44,Template,A patient has a heart rate of 86 bpm and a QT interval of 383 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [86, 'beats per minute'], 'QT Interval': [383, 'msec']}",431.8326,410.24097,453.42423,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 86 beats per minute.
The QT interval is 383 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/86 = 0.69767.
Hence, plugging in these values, we will get 383/√(0.69767) = 431.8326.The patient's corrected QT interval (QTc) is 431.8326 msec."
6865,56,QTc Fridericia Calculator,physical,decimal,45,Template,A patient has a heart rate of 135 bpm and a QT interval of 330 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [135, 'beats per minute'], 'QT Interval': [330, 'msec']}",432.42377,410.80258,454.04496,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 135 beats per minute.
The QT interval is 330 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/135 = 0.44444.
Hence, plugging in these values, we will get 330/√(0.44444) = 432.42377.The patient's corrected QT interval (QTc) is 432.42377 msec."
6866,56,QTc Fridericia Calculator,physical,decimal,46,Template,A patient has a heart rate of 92 bpm and a QT interval of 380 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [92, 'beats per minute'], 'QT Interval': [380, 'msec']}",438.19087,416.28133,460.10041,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 92 beats per minute.
The QT interval is 380 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/92 = 0.65217.
Hence, plugging in these values, we will get 380/√(0.65217) = 438.19087.The patient's corrected QT interval (QTc) is 438.19087 msec."
6867,56,QTc Fridericia Calculator,physical,decimal,47,Template,A patient has a heart rate of 175 bpm and a QT interval of 355 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [175, 'beats per minute'], 'QT Interval': [355, 'msec']}",507.21187,481.85128,532.57246,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 175 beats per minute.
The QT interval is 355 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/175 = 0.34286.
Hence, plugging in these values, we will get 355/√(0.34286) = 507.21187.The patient's corrected QT interval (QTc) is 507.21187 msec."
6868,56,QTc Fridericia Calculator,physical,decimal,48,Template,A patient has a heart rate of 145 bpm and a QT interval of 210 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [145, 'beats per minute'], 'QT Interval': [210, 'msec']}",281.81188,267.72129,295.90247,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 145 beats per minute.
The QT interval is 210 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/145 = 0.41379.
Hence, plugging in these values, we will get 210/√(0.41379) = 281.81188.The patient's corrected QT interval (QTc) is 281.81188 msec."
6869,56,QTc Fridericia Calculator,physical,decimal,49,Template,A patient has a heart rate of 56 bpm and a QT interval of 239 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [56, 'beats per minute'], 'QT Interval': [239, 'msec']}",233.56618,221.88787,245.24449,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 56 beats per minute.
The QT interval is 239 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/56 = 1.07143.
Hence, plugging in these values, we will get 239/√(1.07143) = 233.56618.The patient's corrected QT interval (QTc) is 233.56618 msec."
6870,56,QTc Fridericia Calculator,physical,decimal,50,Template,A patient has a heart rate of 59 bpm and a QT interval of 351 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [59, 'beats per minute'], 'QT Interval': [351, 'msec']}",349.03897,331.58702,366.49092,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 59 beats per minute.
The QT interval is 351 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/59 = 1.01695.
Hence, plugging in these values, we will get 351/√(1.01695) = 349.03897.The patient's corrected QT interval (QTc) is 349.03897 msec."
6871,56,QTc Fridericia Calculator,physical,decimal,51,Template,A patient has a heart rate of 141 bpm and a QT interval of 457 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [141, 'beats per minute'], 'QT Interval': [457, 'msec']}",607.58373,577.20454,637.96292,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 141 beats per minute.
The QT interval is 457 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/141 = 0.42553.
Hence, plugging in these values, we will get 457/√(0.42553) = 607.58373.The patient's corrected QT interval (QTc) is 607.58373 msec."
6872,56,QTc Fridericia Calculator,physical,decimal,52,Template,A patient has a heart rate of 90 bpm and a QT interval of 290 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [90, 'beats per minute'], 'QT Interval': [290, 'msec']}",331.96658,315.36825,348.56491,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 90 beats per minute.
The QT interval is 290 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/90 = 0.66667.
Hence, plugging in these values, we will get 290/√(0.66667) = 331.96658.The patient's corrected QT interval (QTc) is 331.96658 msec."
6873,56,QTc Fridericia Calculator,physical,decimal,53,Template,A patient has a heart rate of 107 bpm and a QT interval of 234 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [107, 'beats per minute'], 'QT Interval': [234, 'msec']}",283.76539,269.57712,297.95366,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 107 beats per minute.
The QT interval is 234 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/107 = 0.56075.
Hence, plugging in these values, we will get 234/√(0.56075) = 283.76539.The patient's corrected QT interval (QTc) is 283.76539 msec."
6874,56,QTc Fridericia Calculator,physical,decimal,54,Template,A patient has a heart rate of 86 bpm and a QT interval of 359 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [86, 'beats per minute'], 'QT Interval': [359, 'msec']}",404.77259,384.53396,425.01122,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 86 beats per minute.
The QT interval is 359 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/86 = 0.69767.
Hence, plugging in these values, we will get 359/√(0.69767) = 404.77259.The patient's corrected QT interval (QTc) is 404.77259 msec."
6875,56,QTc Fridericia Calculator,physical,decimal,55,Template,A patient has a heart rate of 158 bpm and a QT interval of 268 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [158, 'beats per minute'], 'QT Interval': [268, 'msec']}",370.08561,351.58133,388.58989,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 158 beats per minute.
The QT interval is 268 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/158 = 0.37975.
Hence, plugging in these values, we will get 268/√(0.37975) = 370.08561.The patient's corrected QT interval (QTc) is 370.08561 msec."
6876,56,QTc Fridericia Calculator,physical,decimal,56,Template,A patient has a heart rate of 176 bpm and a QT interval of 282 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [176, 'beats per minute'], 'QT Interval': [282, 'msec']}",403.67872,383.49478,423.86266,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 176 beats per minute.
The QT interval is 282 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/176 = 0.34091.
Hence, plugging in these values, we will get 282/√(0.34091) = 403.67872.The patient's corrected QT interval (QTc) is 403.67872 msec."
6877,56,QTc Fridericia Calculator,physical,decimal,57,Template,A patient has a heart rate of 116 bpm and a QT interval of 363 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [116, 'beats per minute'], 'QT Interval': [363, 'msec']}",452.21253,429.6019,474.82316,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 116 beats per minute.
The QT interval is 363 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/116 = 0.51724.
Hence, plugging in these values, we will get 363/√(0.51724) = 452.21253.The patient's corrected QT interval (QTc) is 452.21253 msec."
6878,56,QTc Fridericia Calculator,physical,decimal,58,Template,A patient has a heart rate of 69 bpm and a QT interval of 301 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [69, 'beats per minute'], 'QT Interval': [301, 'msec']}",315.35398,299.58628,331.12168,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 69 beats per minute.
The QT interval is 301 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/69 = 0.86957.
Hence, plugging in these values, we will get 301/√(0.86957) = 315.35398.The patient's corrected QT interval (QTc) is 315.35398 msec."
6879,56,QTc Fridericia Calculator,physical,decimal,59,Template,A patient has a heart rate of 67 bpm and a QT interval of 476 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [67, 'beats per minute'], 'QT Interval': [476, 'msec']}",493.83499,469.14324,518.52674,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 67 beats per minute.
The QT interval is 476 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/67 = 0.89552.
Hence, plugging in these values, we will get 476/√(0.89552) = 493.83499.The patient's corrected QT interval (QTc) is 493.83499 msec."
6880,56,QTc Fridericia Calculator,physical,decimal,60,Template,A patient has a heart rate of 108 bpm and a QT interval of 277 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [108, 'beats per minute'], 'QT Interval': [277, 'msec']}",336.95309,320.10544,353.80074,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 108 beats per minute.
The QT interval is 277 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/108 = 0.55556.
Hence, plugging in these values, we will get 277/√(0.55556) = 336.95309.The patient's corrected QT interval (QTc) is 336.95309 msec."
6881,56,QTc Fridericia Calculator,physical,decimal,61,Template,A patient has a heart rate of 158 bpm and a QT interval of 375 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [158, 'beats per minute'], 'QT Interval': [375, 'msec']}",517.84367,491.95149,543.73585,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 158 beats per minute.
The QT interval is 375 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/158 = 0.37975.
Hence, plugging in these values, we will get 375/√(0.37975) = 517.84367.The patient's corrected QT interval (QTc) is 517.84367 msec."
6882,56,QTc Fridericia Calculator,physical,decimal,62,Template,A patient has a heart rate of 169 bpm and a QT interval of 394 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [169, 'beats per minute'], 'QT Interval': [394, 'msec']}",556.42658,528.60525,584.24791,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 169 beats per minute.
The QT interval is 394 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/169 = 0.35503.
Hence, plugging in these values, we will get 394/√(0.35503) = 556.42658.The patient's corrected QT interval (QTc) is 556.42658 msec."
6883,56,QTc Fridericia Calculator,physical,decimal,63,Template,A patient has a heart rate of 130 bpm and a QT interval of 471 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [130, 'beats per minute'], 'QT Interval': [471, 'msec']}",609.4683,578.99488,639.94172,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 130 beats per minute.
The QT interval is 471 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/130 = 0.46154.
Hence, plugging in these values, we will get 471/√(0.46154) = 609.4683.The patient's corrected QT interval (QTc) is 609.4683 msec."
6884,56,QTc Fridericia Calculator,physical,decimal,64,Template,A patient has a heart rate of 123 bpm and a QT interval of 344 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [123, 'beats per minute'], 'QT Interval': [344, 'msec']}",436.99638,415.14656,458.8462,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 123 beats per minute.
The QT interval is 344 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/123 = 0.4878.
Hence, plugging in these values, we will get 344/√(0.4878) = 436.99638.The patient's corrected QT interval (QTc) is 436.99638 msec."
6885,56,QTc Fridericia Calculator,physical,decimal,65,Template,A patient has a heart rate of 116 bpm and a QT interval of 212 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [116, 'beats per minute'], 'QT Interval': [212, 'msec']}",264.10208,250.89698,277.30718,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 116 beats per minute.
The QT interval is 212 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/116 = 0.51724.
Hence, plugging in these values, we will get 212/√(0.51724) = 264.10208.The patient's corrected QT interval (QTc) is 264.10208 msec."
6886,56,QTc Fridericia Calculator,physical,decimal,66,Template,A patient has a heart rate of 90 bpm and a QT interval of 446 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [90, 'beats per minute'], 'QT Interval': [446, 'msec']}",510.5417,485.01461,536.06879,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 90 beats per minute.
The QT interval is 446 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/90 = 0.66667.
Hence, plugging in these values, we will get 446/√(0.66667) = 510.5417.The patient's corrected QT interval (QTc) is 510.5417 msec."
6887,56,QTc Fridericia Calculator,physical,decimal,67,Template,A patient has a heart rate of 179 bpm and a QT interval of 410 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [179, 'beats per minute'], 'QT Interval': [410, 'msec']}",590.22263,560.7115,619.73376,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 179 beats per minute.
The QT interval is 410 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/179 = 0.3352.
Hence, plugging in these values, we will get 410/√(0.3352) = 590.22263.The patient's corrected QT interval (QTc) is 590.22263 msec."
6888,56,QTc Fridericia Calculator,physical,decimal,68,Template,A patient has a heart rate of 125 bpm and a QT interval of 390 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [125, 'beats per minute'], 'QT Interval': [390, 'msec']}",498.10113,473.19607,523.00619,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 125 beats per minute.
The QT interval is 390 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/125 = 0.48.
Hence, plugging in these values, we will get 390/√(0.48) = 498.10113.The patient's corrected QT interval (QTc) is 498.10113 msec."
6889,56,QTc Fridericia Calculator,physical,decimal,69,Template,A patient has a heart rate of 170 bpm and a QT interval of 407 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [170, 'beats per minute'], 'QT Interval': [407, 'msec']}",575.91817,547.12226,604.71408,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 170 beats per minute.
The QT interval is 407 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/170 = 0.35294.
Hence, plugging in these values, we will get 407/√(0.35294) = 575.91817.The patient's corrected QT interval (QTc) is 575.91817 msec."
6890,56,QTc Fridericia Calculator,physical,decimal,70,Template,A patient has a heart rate of 47 bpm and a QT interval of 326 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [47, 'beats per minute'], 'QT Interval': [326, 'msec']}",300.51488,285.48914,315.54062,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 47 beats per minute.
The QT interval is 326 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/47 = 1.2766.
Hence, plugging in these values, we will get 326/√(1.2766) = 300.51488.The patient's corrected QT interval (QTc) is 300.51488 msec."
6891,56,QTc Fridericia Calculator,physical,decimal,71,Template,A patient has a heart rate of 138 bpm and a QT interval of 202 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [138, 'beats per minute'], 'QT Interval': [202, 'msec']}",266.64177,253.30968,279.97386,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 138 beats per minute.
The QT interval is 202 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/138 = 0.43478.
Hence, plugging in these values, we will get 202/√(0.43478) = 266.64177.The patient's corrected QT interval (QTc) is 266.64177 msec."
6892,56,QTc Fridericia Calculator,physical,decimal,72,Template,A patient has a heart rate of 92 bpm and a QT interval of 498 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [92, 'beats per minute'], 'QT Interval': [498, 'msec']}",574.26067,545.54764,602.9737,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 92 beats per minute.
The QT interval is 498 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/92 = 0.65217.
Hence, plugging in these values, we will get 498/√(0.65217) = 574.26067.The patient's corrected QT interval (QTc) is 574.26067 msec."
6893,56,QTc Fridericia Calculator,physical,decimal,73,Template,A patient has a heart rate of 138 bpm and a QT interval of 251 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [138, 'beats per minute'], 'QT Interval': [251, 'msec']}",331.3222,314.75609,347.88831,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 138 beats per minute.
The QT interval is 251 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/138 = 0.43478.
Hence, plugging in these values, we will get 251/√(0.43478) = 331.3222.The patient's corrected QT interval (QTc) is 331.3222 msec."
6894,56,QTc Fridericia Calculator,physical,decimal,74,Template,A patient has a heart rate of 160 bpm and a QT interval of 285 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [160, 'beats per minute'], 'QT Interval': [285, 'msec']}",395.21593,375.45513,414.97673,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 160 beats per minute.
The QT interval is 285 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/160 = 0.375.
Hence, plugging in these values, we will get 285/√(0.375) = 395.21593.The patient's corrected QT interval (QTc) is 395.21593 msec."
6895,56,QTc Fridericia Calculator,physical,decimal,75,Template,A patient has a heart rate of 120 bpm and a QT interval of 447 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [120, 'beats per minute'], 'QT Interval': [447, 'msec']}",563.18471,535.02547,591.34395,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 120 beats per minute.
The QT interval is 447 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/120 = 0.5.
Hence, plugging in these values, we will get 447/√(0.5) = 563.18471.The patient's corrected QT interval (QTc) is 563.18471 msec."
6896,56,QTc Fridericia Calculator,physical,decimal,76,Template,A patient has a heart rate of 163 bpm and a QT interval of 271 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [163, 'beats per minute'], 'QT Interval': [271, 'msec']}",378.13541,359.22864,397.04218,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 163 beats per minute.
The QT interval is 271 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/163 = 0.3681.
Hence, plugging in these values, we will get 271/√(0.3681) = 378.13541.The patient's corrected QT interval (QTc) is 378.13541 msec."
6897,56,QTc Fridericia Calculator,physical,decimal,77,Template,A patient has a heart rate of 157 bpm and a QT interval of 230 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [157, 'beats per minute'], 'QT Interval': [230, 'msec']}",316.93897,301.09202,332.78592,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 157 beats per minute.
The QT interval is 230 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/157 = 0.38217.
Hence, plugging in these values, we will get 230/√(0.38217) = 316.93897.The patient's corrected QT interval (QTc) is 316.93897 msec."
6898,56,QTc Fridericia Calculator,physical,decimal,78,Template,A patient has a heart rate of 60 bpm and a QT interval of 217 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [60, 'beats per minute'], 'QT Interval': [217, 'msec']}",217,206.15,227.85,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 60 beats per minute.
The QT interval is 217 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/60 = 1.0.
Hence, plugging in these values, we will get 217/√(1.0) = 217.0.The patient's corrected QT interval (QTc) is 217.0 msec."
6899,56,QTc Fridericia Calculator,physical,decimal,79,Template,A patient has a heart rate of 150 bpm and a QT interval of 489 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [150, 'beats per minute'], 'QT Interval': [489, 'msec']}",663.67511,630.49135,696.85887,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 150 beats per minute.
The QT interval is 489 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/150 = 0.4.
Hence, plugging in these values, we will get 489/√(0.4) = 663.67511.The patient's corrected QT interval (QTc) is 663.67511 msec."
6900,56,QTc Fridericia Calculator,physical,decimal,80,Template,A patient has a heart rate of 120 bpm and a QT interval of 349 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [120, 'beats per minute'], 'QT Interval': [349, 'msec']}",439.71245,417.72683,461.69807,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 120 beats per minute.
The QT interval is 349 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/120 = 0.5.
Hence, plugging in these values, we will get 349/√(0.5) = 439.71245.The patient's corrected QT interval (QTc) is 439.71245 msec."
6901,56,QTc Fridericia Calculator,physical,decimal,81,Template,A patient has a heart rate of 113 bpm and a QT interval of 432 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [113, 'beats per minute'], 'QT Interval': [432, 'msec']}",533.49099,506.81644,560.16554,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 113 beats per minute.
The QT interval is 432 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/113 = 0.53097.
Hence, plugging in these values, we will get 432/√(0.53097) = 533.49099.The patient's corrected QT interval (QTc) is 533.49099 msec."
6902,56,QTc Fridericia Calculator,physical,decimal,82,Template,A patient has a heart rate of 119 bpm and a QT interval of 225 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [119, 'beats per minute'], 'QT Interval': [225, 'msec']}",282.6929,268.55825,296.82755,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 119 beats per minute.
The QT interval is 225 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/119 = 0.5042.
Hence, plugging in these values, we will get 225/√(0.5042) = 282.6929.The patient's corrected QT interval (QTc) is 282.6929 msec."
6903,56,QTc Fridericia Calculator,physical,decimal,83,Template,A patient has a heart rate of 79 bpm and a QT interval of 291 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [79, 'beats per minute'], 'QT Interval': [291, 'msec']}",318.94733,302.99996,334.8947,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 79 beats per minute.
The QT interval is 291 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/79 = 0.75949.
Hence, plugging in these values, we will get 291/√(0.75949) = 318.94733.The patient's corrected QT interval (QTc) is 318.94733 msec."
6904,56,QTc Fridericia Calculator,physical,decimal,84,Template,A patient has a heart rate of 176 bpm and a QT interval of 320 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [176, 'beats per minute'], 'QT Interval': [320, 'msec']}",458.07515,435.17139,480.97891,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 176 beats per minute.
The QT interval is 320 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/176 = 0.34091.
Hence, plugging in these values, we will get 320/√(0.34091) = 458.07515.The patient's corrected QT interval (QTc) is 458.07515 msec."
6905,56,QTc Fridericia Calculator,physical,decimal,85,Template,A patient has a heart rate of 90 bpm and a QT interval of 291 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [90, 'beats per minute'], 'QT Interval': [291, 'msec']}",333.11129,316.45573,349.76685,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 90 beats per minute.
The QT interval is 291 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/90 = 0.66667.
Hence, plugging in these values, we will get 291/√(0.66667) = 333.11129.The patient's corrected QT interval (QTc) is 333.11129 msec."
6906,56,QTc Fridericia Calculator,physical,decimal,86,Template,A patient has a heart rate of 172 bpm and a QT interval of 368 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [172, 'beats per minute'], 'QT Interval': [368, 'msec']}",522.76406,496.62586,548.90226,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 172 beats per minute.
The QT interval is 368 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/172 = 0.34884.
Hence, plugging in these values, we will get 368/√(0.34884) = 522.76406.The patient's corrected QT interval (QTc) is 522.76406 msec."
6907,56,QTc Fridericia Calculator,physical,decimal,87,Template,A patient has a heart rate of 147 bpm and a QT interval of 465 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [147, 'beats per minute'], 'QT Interval': [465, 'msec']}",626.86806,595.52466,658.21146,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 147 beats per minute.
The QT interval is 465 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/147 = 0.40816.
Hence, plugging in these values, we will get 465/√(0.40816) = 626.86806.The patient's corrected QT interval (QTc) is 626.86806 msec."
6908,56,QTc Fridericia Calculator,physical,decimal,88,Template,A patient has a heart rate of 66 bpm and a QT interval of 392 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [66, 'beats per minute'], 'QT Interval': [392, 'msec']}",404.65394,384.42124,424.88664,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 66 beats per minute.
The QT interval is 392 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/66 = 0.90909.
Hence, plugging in these values, we will get 392/√(0.90909) = 404.65394.The patient's corrected QT interval (QTc) is 404.65394 msec."
6909,56,QTc Fridericia Calculator,physical,decimal,89,Template,A patient has a heart rate of 96 bpm and a QT interval of 226 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [96, 'beats per minute'], 'QT Interval': [226, 'msec']}",264.3312,251.11464,277.54776,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 96 beats per minute.
The QT interval is 226 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/96 = 0.625.
Hence, plugging in these values, we will get 226/√(0.625) = 264.3312.The patient's corrected QT interval (QTc) is 264.3312 msec."
6910,56,QTc Fridericia Calculator,physical,decimal,90,Template,A patient has a heart rate of 84 bpm and a QT interval of 261 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [84, 'beats per minute'], 'QT Interval': [261, 'msec']}",291.97723,277.37837,306.57609,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 84 beats per minute.
The QT interval is 261 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/84 = 0.71429.
Hence, plugging in these values, we will get 261/√(0.71429) = 291.97723.The patient's corrected QT interval (QTc) is 291.97723 msec."
6911,56,QTc Fridericia Calculator,physical,decimal,91,Template,A patient has a heart rate of 91 bpm and a QT interval of 409 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [91, 'beats per minute'], 'QT Interval': [409, 'msec']}",469.91593,446.42013,493.41173,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 91 beats per minute.
The QT interval is 409 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/91 = 0.65934.
Hence, plugging in these values, we will get 409/√(0.65934) = 469.91593.The patient's corrected QT interval (QTc) is 469.91593 msec."
6912,56,QTc Fridericia Calculator,physical,decimal,92,Template,A patient has a heart rate of 106 bpm and a QT interval of 263 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [106, 'beats per minute'], 'QT Interval': [263, 'msec']}",317.93625,302.03944,333.83306,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 106 beats per minute.
The QT interval is 263 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/106 = 0.56604.
Hence, plugging in these values, we will get 263/√(0.56604) = 317.93625.The patient's corrected QT interval (QTc) is 317.93625 msec."
6913,56,QTc Fridericia Calculator,physical,decimal,93,Template,A patient has a heart rate of 170 bpm and a QT interval of 345 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [170, 'beats per minute'], 'QT Interval': [345, 'msec']}",488.18617,463.77686,512.59548,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 170 beats per minute.
The QT interval is 345 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/170 = 0.35294.
Hence, plugging in these values, we will get 345/√(0.35294) = 488.18617.The patient's corrected QT interval (QTc) is 488.18617 msec."
6914,56,QTc Fridericia Calculator,physical,decimal,94,Template,A patient has a heart rate of 145 bpm and a QT interval of 407 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [145, 'beats per minute'], 'QT Interval': [407, 'msec']}",546.17826,518.86935,573.48717,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 145 beats per minute.
The QT interval is 407 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/145 = 0.41379.
Hence, plugging in these values, we will get 407/√(0.41379) = 546.17826.The patient's corrected QT interval (QTc) is 546.17826 msec."
6915,56,QTc Fridericia Calculator,physical,decimal,95,Template,A patient has a heart rate of 150 bpm and a QT interval of 272 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [150, 'beats per minute'], 'QT Interval': [272, 'msec']}",369.1608,350.70276,387.61884,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 150 beats per minute.
The QT interval is 272 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/150 = 0.4.
Hence, plugging in these values, we will get 272/√(0.4) = 369.1608.The patient's corrected QT interval (QTc) is 369.1608 msec."
6916,56,QTc Fridericia Calculator,physical,decimal,96,Template,A patient has a heart rate of 64 bpm and a QT interval of 449 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [64, 'beats per minute'], 'QT Interval': [449, 'msec']}",458.76391,435.82571,481.70211,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 64 beats per minute.
The QT interval is 449 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/64 = 0.9375.
Hence, plugging in these values, we will get 449/√(0.9375) = 458.76391.The patient's corrected QT interval (QTc) is 458.76391 msec."
6917,56,QTc Fridericia Calculator,physical,decimal,97,Template,A patient has a heart rate of 80 bpm and a QT interval of 460 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [80, 'beats per minute'], 'QT Interval': [460, 'msec']}",506.29551,480.98073,531.61029,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 80 beats per minute.
The QT interval is 460 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/80 = 0.75.
Hence, plugging in these values, we will get 460/√(0.75) = 506.29551.The patient's corrected QT interval (QTc) is 506.29551 msec."
6918,56,QTc Fridericia Calculator,physical,decimal,98,Template,A patient has a heart rate of 108 bpm and a QT interval of 388 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [108, 'beats per minute'], 'QT Interval': [388, 'msec']}",471.97762,448.37874,495.5765,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 108 beats per minute.
The QT interval is 388 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/108 = 0.55556.
Hence, plugging in these values, we will get 388/√(0.55556) = 471.97762.The patient's corrected QT interval (QTc) is 471.97762 msec."
6919,56,QTc Fridericia Calculator,physical,decimal,99,Template,A patient has a heart rate of 177 bpm and a QT interval of 211 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [177, 'beats per minute'], 'QT Interval': [211, 'msec']}",302.61545,287.48468,317.74622,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 177 beats per minute.
The QT interval is 211 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/177 = 0.33898.
Hence, plugging in these values, we will get 211/√(0.33898) = 302.61545.The patient's corrected QT interval (QTc) is 302.61545 msec."
6920,56,QTc Fridericia Calculator,physical,decimal,100,Template,A patient has a heart rate of 101 bpm and a QT interval of 492 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [101, 'beats per minute'], 'QT Interval': [492, 'msec']}",585.2683,556.00488,614.53171,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 101 beats per minute.
The QT interval is 492 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/101 = 0.59406.
Hence, plugging in these values, we will get 492/√(0.59406) = 585.2683.The patient's corrected QT interval (QTc) is 585.2683 msec."
6921,56,QTc Fridericia Calculator,physical,decimal,101,Template,Patient has a heart rate of 155 bpm and a QT interval of 330 msec.,"Using the Fridericia Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [155, 'beats per minute'], 'QT Interval': [330, 'msec']}",452.79979,430.1598,475.43978,"The corrected QT interval using the Fredericia formula is computed as  QTc = QT interval / (RR interval)**(1/3), where ** denotes an exponent, QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 155 beats per minute.
The QT interval is 330 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/155 = 0.3871.
Hence, plugging in these values, we will get 330/√(0.3871) = 452.79979.The patient's corrected QT interval (QTc) is 452.79979 msec."
6922,57,QTc Framingham Calculator,physical,decimal,22,Template,A patient has a heart rate of 66 bpm and a QT interval of 365 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [66, 'beats per minute'], 'QT Interval': [365, 'msec']}",379.00014,360.05013,397.95015,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 66 beats per minute.
The QT interval is 365 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/66 = 0.90909.
Hence, plugging in these values, we will get 365/(154 * ( 1- 0.90909 )) = 379.00014.
The patient's corrected QT interval (QTc) is 379.00014 msec."
6923,57,QTc Framingham Calculator,physical,decimal,23,Template,A patient has a heart rate of 82 bpm and a QT interval of 350 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [82, 'beats per minute'], 'QT Interval': [350, 'msec']}",391.31666,371.75083,410.88249,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 82 beats per minute.
The QT interval is 350 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/82 = 0.73171.
Hence, plugging in these values, we will get 350/(154 * ( 1- 0.73171 )) = 391.31666.
The patient's corrected QT interval (QTc) is 391.31666 msec."
6924,57,QTc Framingham Calculator,physical,decimal,24,Template,A patient has a heart rate of 82 bpm and a QT interval of 249 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [82, 'beats per minute'], 'QT Interval': [249, 'msec']}",290.31666,275.80083,304.83249,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 82 beats per minute.
The QT interval is 249 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/82 = 0.73171.
Hence, plugging in these values, we will get 249/(154 * ( 1- 0.73171 )) = 290.31666.
The patient's corrected QT interval (QTc) is 290.31666 msec."
6925,57,QTc Framingham Calculator,physical,decimal,25,Template,A patient has a heart rate of 147 bpm and a QT interval of 397 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [147, 'beats per minute'], 'QT Interval': [397, 'msec']}",488.14336,463.73619,512.55053,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 147 beats per minute.
The QT interval is 397 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/147 = 0.40816.
Hence, plugging in these values, we will get 397/(154 * ( 1- 0.40816 )) = 488.14336.
The patient's corrected QT interval (QTc) is 488.14336 msec."
6926,57,QTc Framingham Calculator,physical,decimal,26,Template,A patient has a heart rate of 106 bpm and a QT interval of 352 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [106, 'beats per minute'], 'QT Interval': [352, 'msec']}",418.82984,397.88835,439.77133,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 106 beats per minute.
The QT interval is 352 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/106 = 0.56604.
Hence, plugging in these values, we will get 352/(154 * ( 1- 0.56604 )) = 418.82984.
The patient's corrected QT interval (QTc) is 418.82984 msec."
6927,57,QTc Framingham Calculator,physical,decimal,27,Template,A patient has a heart rate of 116 bpm and a QT interval of 367 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [116, 'beats per minute'], 'QT Interval': [367, 'msec']}",441.34504,419.27779,463.41229,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 116 beats per minute.
The QT interval is 367 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/116 = 0.51724.
Hence, plugging in these values, we will get 367/(154 * ( 1- 0.51724 )) = 441.34504.
The patient's corrected QT interval (QTc) is 441.34504 msec."
6928,57,QTc Framingham Calculator,physical,decimal,28,Template,A patient has a heart rate of 85 bpm and a QT interval of 464 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [85, 'beats per minute'], 'QT Interval': [464, 'msec']}",509.29448,483.82976,534.7592,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 85 beats per minute.
The QT interval is 464 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/85 = 0.70588.
Hence, plugging in these values, we will get 464/(154 * ( 1- 0.70588 )) = 509.29448.
The patient's corrected QT interval (QTc) is 509.29448 msec."
6929,57,QTc Framingham Calculator,physical,decimal,29,Template,A patient has a heart rate of 70 bpm and a QT interval of 337 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [70, 'beats per minute'], 'QT Interval': [337, 'msec']}",359.00044,341.05042,376.95046,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 70 beats per minute.
The QT interval is 337 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/70 = 0.85714.
Hence, plugging in these values, we will get 337/(154 * ( 1- 0.85714 )) = 359.00044.
The patient's corrected QT interval (QTc) is 359.00044 msec."
6930,57,QTc Framingham Calculator,physical,decimal,30,Template,A patient has a heart rate of 150 bpm and a QT interval of 365 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [150, 'beats per minute'], 'QT Interval': [365, 'msec']}",457.4,434.53,480.27,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 150 beats per minute.
The QT interval is 365 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/150 = 0.4.
Hence, plugging in these values, we will get 365/(154 * ( 1- 0.4 )) = 457.4.
The patient's corrected QT interval (QTc) is 457.4 msec."
6931,57,QTc Framingham Calculator,physical,decimal,31,Template,A patient has a heart rate of 108 bpm and a QT interval of 423 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [108, 'beats per minute'], 'QT Interval': [423, 'msec']}",491.44376,466.87157,516.01595,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 108 beats per minute.
The QT interval is 423 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/108 = 0.55556.
Hence, plugging in these values, we will get 423/(154 * ( 1- 0.55556 )) = 491.44376.
The patient's corrected QT interval (QTc) is 491.44376 msec."
6932,57,QTc Framingham Calculator,physical,decimal,32,Template,A patient has a heart rate of 80 bpm and a QT interval of 475 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [80, 'beats per minute'], 'QT Interval': [475, 'msec']}",513.5,487.825,539.175,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 80 beats per minute.
The QT interval is 475 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/80 = 0.75.
Hence, plugging in these values, we will get 475/(154 * ( 1- 0.75 )) = 513.5.
The patient's corrected QT interval (QTc) is 513.5 msec."
6933,57,QTc Framingham Calculator,physical,decimal,33,Template,A patient has a heart rate of 49 bpm and a QT interval of 202 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [49, 'beats per minute'], 'QT Interval': [202, 'msec']}",167.42854,159.05711,175.79997,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 49 beats per minute.
The QT interval is 202 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/49 = 1.22449.
Hence, plugging in these values, we will get 202/(154 * ( 1- 1.22449 )) = 167.42854.
The patient's corrected QT interval (QTc) is 167.42854 msec."
6934,57,QTc Framingham Calculator,physical,decimal,34,Template,A patient has a heart rate of 137 bpm and a QT interval of 357 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [137, 'beats per minute'], 'QT Interval': [357, 'msec']}",443.55416,421.37645,465.73187,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 137 beats per minute.
The QT interval is 357 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/137 = 0.43796.
Hence, plugging in these values, we will get 357/(154 * ( 1- 0.43796 )) = 443.55416.
The patient's corrected QT interval (QTc) is 443.55416 msec."
6935,57,QTc Framingham Calculator,physical,decimal,35,Template,A patient has a heart rate of 126 bpm and a QT interval of 288 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [126, 'beats per minute'], 'QT Interval': [288, 'msec']}",368.66674,350.2334,387.10008,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 126 beats per minute.
The QT interval is 288 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/126 = 0.47619.
Hence, plugging in these values, we will get 288/(154 * ( 1- 0.47619 )) = 368.66674.
The patient's corrected QT interval (QTc) is 368.66674 msec."
6936,57,QTc Framingham Calculator,physical,decimal,36,Template,A patient has a heart rate of 164 bpm and a QT interval of 235 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [164, 'beats per minute'], 'QT Interval': [235, 'msec']}",332.6591,316.02614,349.29206,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 164 beats per minute.
The QT interval is 235 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/164 = 0.36585.
Hence, plugging in these values, we will get 235/(154 * ( 1- 0.36585 )) = 332.6591.
The patient's corrected QT interval (QTc) is 332.6591 msec."
6937,57,QTc Framingham Calculator,physical,decimal,37,Template,A patient has a heart rate of 110 bpm and a QT interval of 279 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [110, 'beats per minute'], 'QT Interval': [279, 'msec']}",349.0007,331.55066,366.45074,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 110 beats per minute.
The QT interval is 279 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/110 = 0.54545.
Hence, plugging in these values, we will get 279/(154 * ( 1- 0.54545 )) = 349.0007.
The patient's corrected QT interval (QTc) is 349.0007 msec."
6938,57,QTc Framingham Calculator,physical,decimal,38,Template,A patient has a heart rate of 165 bpm and a QT interval of 486 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [165, 'beats per minute'], 'QT Interval': [486, 'msec']}",583.99944,554.79947,613.19941,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 165 beats per minute.
The QT interval is 486 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/165 = 0.36364.
Hence, plugging in these values, we will get 486/(154 * ( 1- 0.36364 )) = 583.99944.
The patient's corrected QT interval (QTc) is 583.99944 msec."
6939,57,QTc Framingham Calculator,physical,decimal,39,Template,A patient has a heart rate of 108 bpm and a QT interval of 318 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [108, 'beats per minute'], 'QT Interval': [318, 'msec']}",386.44376,367.12157,405.76595,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 108 beats per minute.
The QT interval is 318 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/108 = 0.55556.
Hence, plugging in these values, we will get 318/(154 * ( 1- 0.55556 )) = 386.44376.
The patient's corrected QT interval (QTc) is 386.44376 msec."
6940,57,QTc Framingham Calculator,physical,decimal,40,Template,A patient has a heart rate of 164 bpm and a QT interval of 315 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [164, 'beats per minute'], 'QT Interval': [315, 'msec']}",412.6591,392.02614,433.29206,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 164 beats per minute.
The QT interval is 315 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/164 = 0.36585.
Hence, plugging in these values, we will get 315/(154 * ( 1- 0.36585 )) = 412.6591.
The patient's corrected QT interval (QTc) is 412.6591 msec."
6941,57,QTc Framingham Calculator,physical,decimal,41,Template,A patient has a heart rate of 178 bpm and a QT interval of 444 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [178, 'beats per minute'], 'QT Interval': [444, 'msec']}",546.08968,518.7852,573.39416,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 178 beats per minute.
The QT interval is 444 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/178 = 0.33708.
Hence, plugging in these values, we will get 444/(154 * ( 1- 0.33708 )) = 546.08968.
The patient's corrected QT interval (QTc) is 546.08968 msec."
6942,57,QTc Framingham Calculator,physical,decimal,42,Template,A patient has a heart rate of 124 bpm and a QT interval of 458 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [124, 'beats per minute'], 'QT Interval': [458, 'msec']}",537.48402,510.60982,564.35822,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 124 beats per minute.
The QT interval is 458 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/124 = 0.48387.
Hence, plugging in these values, we will get 458/(154 * ( 1- 0.48387 )) = 537.48402.
The patient's corrected QT interval (QTc) is 537.48402 msec."
6943,57,QTc Framingham Calculator,physical,decimal,43,Template,A patient has a heart rate of 164 bpm and a QT interval of 326 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [164, 'beats per minute'], 'QT Interval': [326, 'msec']}",423.6591,402.47615,444.84206,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 164 beats per minute.
The QT interval is 326 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/164 = 0.36585.
Hence, plugging in these values, we will get 326/(154 * ( 1- 0.36585 )) = 423.6591.
The patient's corrected QT interval (QTc) is 423.6591 msec."
6944,57,QTc Framingham Calculator,physical,decimal,44,Template,A patient has a heart rate of 125 bpm and a QT interval of 255 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [125, 'beats per minute'], 'QT Interval': [255, 'msec']}",335.08,318.326,351.834,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 125 beats per minute.
The QT interval is 255 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/125 = 0.48.
Hence, plugging in these values, we will get 255/(154 * ( 1- 0.48 )) = 335.08.
The patient's corrected QT interval (QTc) is 335.08 msec."
6945,57,QTc Framingham Calculator,physical,decimal,45,Template,A patient has a heart rate of 124 bpm and a QT interval of 300 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [124, 'beats per minute'], 'QT Interval': [300, 'msec']}",379.48402,360.50982,398.45822,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 124 beats per minute.
The QT interval is 300 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/124 = 0.48387.
Hence, plugging in these values, we will get 300/(154 * ( 1- 0.48387 )) = 379.48402.
The patient's corrected QT interval (QTc) is 379.48402 msec."
6946,57,QTc Framingham Calculator,physical,decimal,46,Template,A patient has a heart rate of 156 bpm and a QT interval of 421 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [156, 'beats per minute'], 'QT Interval': [421, 'msec']}",515.76852,489.98009,541.55695,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 156 beats per minute.
The QT interval is 421 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/156 = 0.38462.
Hence, plugging in these values, we will get 421/(154 * ( 1- 0.38462 )) = 515.76852.
The patient's corrected QT interval (QTc) is 515.76852 msec."
6947,57,QTc Framingham Calculator,physical,decimal,47,Template,A patient has a heart rate of 90 bpm and a QT interval of 372 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [90, 'beats per minute'], 'QT Interval': [372, 'msec']}",423.33282,402.16618,444.49946,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 90 beats per minute.
The QT interval is 372 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/90 = 0.66667.
Hence, plugging in these values, we will get 372/(154 * ( 1- 0.66667 )) = 423.33282.
The patient's corrected QT interval (QTc) is 423.33282 msec."
6948,57,QTc Framingham Calculator,physical,decimal,48,Template,A patient has a heart rate of 104 bpm and a QT interval of 412 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [104, 'beats per minute'], 'QT Interval': [412, 'msec']}",477.15432,453.2966,501.01204,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 104 beats per minute.
The QT interval is 412 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/104 = 0.57692.
Hence, plugging in these values, we will get 412/(154 * ( 1- 0.57692 )) = 477.15432.
The patient's corrected QT interval (QTc) is 477.15432 msec."
6949,57,QTc Framingham Calculator,physical,decimal,49,Template,A patient has a heart rate of 87 bpm and a QT interval of 469 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [87, 'beats per minute'], 'QT Interval': [469, 'msec']}",516.79236,490.95274,542.63198,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 87 beats per minute.
The QT interval is 469 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/87 = 0.68966.
Hence, plugging in these values, we will get 469/(154 * ( 1- 0.68966 )) = 516.79236.
The patient's corrected QT interval (QTc) is 516.79236 msec."
6950,57,QTc Framingham Calculator,physical,decimal,50,Template,A patient has a heart rate of 127 bpm and a QT interval of 215 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [127, 'beats per minute'], 'QT Interval': [215, 'msec']}",296.24424,281.43203,311.05645,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 127 beats per minute.
The QT interval is 215 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/127 = 0.47244.
Hence, plugging in these values, we will get 215/(154 * ( 1- 0.47244 )) = 296.24424.
The patient's corrected QT interval (QTc) is 296.24424 msec."
6951,57,QTc Framingham Calculator,physical,decimal,51,Template,A patient has a heart rate of 67 bpm and a QT interval of 433 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [67, 'beats per minute'], 'QT Interval': [433, 'msec']}",449.08992,426.63542,471.54442,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 67 beats per minute.
The QT interval is 433 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/67 = 0.89552.
Hence, plugging in these values, we will get 433/(154 * ( 1- 0.89552 )) = 449.08992.
The patient's corrected QT interval (QTc) is 449.08992 msec."
6952,57,QTc Framingham Calculator,physical,decimal,52,Template,A patient has a heart rate of 87 bpm and a QT interval of 261 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [87, 'beats per minute'], 'QT Interval': [261, 'msec']}",308.79236,293.35274,324.23198,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 87 beats per minute.
The QT interval is 261 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/87 = 0.68966.
Hence, plugging in these values, we will get 261/(154 * ( 1- 0.68966 )) = 308.79236.
The patient's corrected QT interval (QTc) is 308.79236 msec."
6953,57,QTc Framingham Calculator,physical,decimal,53,Template,A patient has a heart rate of 107 bpm and a QT interval of 275 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [107, 'beats per minute'], 'QT Interval': [275, 'msec']}",342.6445,325.51227,359.77672,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 107 beats per minute.
The QT interval is 275 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/107 = 0.56075.
Hence, plugging in these values, we will get 275/(154 * ( 1- 0.56075 )) = 342.6445.
The patient's corrected QT interval (QTc) is 342.6445 msec."
6954,57,QTc Framingham Calculator,physical,decimal,54,Template,A patient has a heart rate of 113 bpm and a QT interval of 485 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [113, 'beats per minute'], 'QT Interval': [485, 'msec']}",557.23062,529.36909,585.09215,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 113 beats per minute.
The QT interval is 485 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/113 = 0.53097.
Hence, plugging in these values, we will get 485/(154 * ( 1- 0.53097 )) = 557.23062.
The patient's corrected QT interval (QTc) is 557.23062 msec."
6955,57,QTc Framingham Calculator,physical,decimal,55,Template,A patient has a heart rate of 126 bpm and a QT interval of 468 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [126, 'beats per minute'], 'QT Interval': [468, 'msec']}",548.66674,521.2334,576.10008,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 126 beats per minute.
The QT interval is 468 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/126 = 0.47619.
Hence, plugging in these values, we will get 468/(154 * ( 1- 0.47619 )) = 548.66674.
The patient's corrected QT interval (QTc) is 548.66674 msec."
6956,57,QTc Framingham Calculator,physical,decimal,56,Template,A patient has a heart rate of 120 bpm and a QT interval of 351 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [120, 'beats per minute'], 'QT Interval': [351, 'msec']}",428,406.6,449.4,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 120 beats per minute.
The QT interval is 351 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/120 = 0.5.
Hence, plugging in these values, we will get 351/(154 * ( 1- 0.5 )) = 428.0.
The patient's corrected QT interval (QTc) is 428.0 msec."
6957,57,QTc Framingham Calculator,physical,decimal,57,Template,A patient has a heart rate of 104 bpm and a QT interval of 309 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [104, 'beats per minute'], 'QT Interval': [309, 'msec']}",374.15432,355.4466,392.86204,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 104 beats per minute.
The QT interval is 309 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/104 = 0.57692.
Hence, plugging in these values, we will get 309/(154 * ( 1- 0.57692 )) = 374.15432.
The patient's corrected QT interval (QTc) is 374.15432 msec."
6958,57,QTc Framingham Calculator,physical,decimal,58,Template,A patient has a heart rate of 122 bpm and a QT interval of 243 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [122, 'beats per minute'], 'QT Interval': [243, 'msec']}",321.2628,305.19966,337.32594,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 122 beats per minute.
The QT interval is 243 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/122 = 0.4918.
Hence, plugging in these values, we will get 243/(154 * ( 1- 0.4918 )) = 321.2628.
The patient's corrected QT interval (QTc) is 321.2628 msec."
6959,57,QTc Framingham Calculator,physical,decimal,59,Template,A patient has a heart rate of 58 bpm and a QT interval of 417 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [58, 'beats per minute'], 'QT Interval': [417, 'msec']}",411.69008,391.10558,432.27458,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 58 beats per minute.
The QT interval is 417 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/58 = 1.03448.
Hence, plugging in these values, we will get 417/(154 * ( 1- 1.03448 )) = 411.69008.
The patient's corrected QT interval (QTc) is 411.69008 msec."
6960,57,QTc Framingham Calculator,physical,decimal,60,Template,A patient has a heart rate of 72 bpm and a QT interval of 222 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [72, 'beats per minute'], 'QT Interval': [222, 'msec']}",247.66718,235.28382,260.05054,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 72 beats per minute.
The QT interval is 222 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/72 = 0.83333.
Hence, plugging in these values, we will get 222/(154 * ( 1- 0.83333 )) = 247.66718.
The patient's corrected QT interval (QTc) is 247.66718 msec."
6961,57,QTc Framingham Calculator,physical,decimal,61,Template,A patient has a heart rate of 157 bpm and a QT interval of 486 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [157, 'beats per minute'], 'QT Interval': [486, 'msec']}",581.14582,552.08853,610.20311,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 157 beats per minute.
The QT interval is 486 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/157 = 0.38217.
Hence, plugging in these values, we will get 486/(154 * ( 1- 0.38217 )) = 581.14582.
The patient's corrected QT interval (QTc) is 581.14582 msec."
6962,57,QTc Framingham Calculator,physical,decimal,62,Template,A patient has a heart rate of 67 bpm and a QT interval of 385 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [67, 'beats per minute'], 'QT Interval': [385, 'msec']}",401.08992,381.03542,421.14442,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 67 beats per minute.
The QT interval is 385 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/67 = 0.89552.
Hence, plugging in these values, we will get 385/(154 * ( 1- 0.89552 )) = 401.08992.
The patient's corrected QT interval (QTc) is 401.08992 msec."
6963,57,QTc Framingham Calculator,physical,decimal,63,Template,A patient has a heart rate of 165 bpm and a QT interval of 207 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [165, 'beats per minute'], 'QT Interval': [207, 'msec']}",304.99944,289.74947,320.24941,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 165 beats per minute.
The QT interval is 207 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/165 = 0.36364.
Hence, plugging in these values, we will get 207/(154 * ( 1- 0.36364 )) = 304.99944.
The patient's corrected QT interval (QTc) is 304.99944 msec."
6964,57,QTc Framingham Calculator,physical,decimal,64,Template,A patient has a heart rate of 59 bpm and a QT interval of 215 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [59, 'beats per minute'], 'QT Interval': [215, 'msec']}",212.3897,201.77022,223.00919,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 59 beats per minute.
The QT interval is 215 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/59 = 1.01695.
Hence, plugging in these values, we will get 215/(154 * ( 1- 1.01695 )) = 212.3897.
The patient's corrected QT interval (QTc) is 212.3897 msec."
6965,57,QTc Framingham Calculator,physical,decimal,65,Template,A patient has a heart rate of 144 bpm and a QT interval of 491 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [144, 'beats per minute'], 'QT Interval': [491, 'msec']}",580.83282,551.79118,609.87446,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 144 beats per minute.
The QT interval is 491 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/144 = 0.41667.
Hence, plugging in these values, we will get 491/(154 * ( 1- 0.41667 )) = 580.83282.
The patient's corrected QT interval (QTc) is 580.83282 msec."
6966,57,QTc Framingham Calculator,physical,decimal,66,Template,A patient has a heart rate of 104 bpm and a QT interval of 362 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [104, 'beats per minute'], 'QT Interval': [362, 'msec']}",427.15432,405.7966,448.51204,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 104 beats per minute.
The QT interval is 362 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/104 = 0.57692.
Hence, plugging in these values, we will get 362/(154 * ( 1- 0.57692 )) = 427.15432.
The patient's corrected QT interval (QTc) is 427.15432 msec."
6967,57,QTc Framingham Calculator,physical,decimal,67,Template,A patient has a heart rate of 123 bpm and a QT interval of 210 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [123, 'beats per minute'], 'QT Interval': [210, 'msec']}",288.8788,274.43486,303.32274,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 123 beats per minute.
The QT interval is 210 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/123 = 0.4878.
Hence, plugging in these values, we will get 210/(154 * ( 1- 0.4878 )) = 288.8788.
The patient's corrected QT interval (QTc) is 288.8788 msec."
6968,57,QTc Framingham Calculator,physical,decimal,68,Template,A patient has a heart rate of 134 bpm and a QT interval of 324 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [134, 'beats per minute'], 'QT Interval': [324, 'msec']}",409.04496,388.59271,429.49721,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 134 beats per minute.
The QT interval is 324 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/134 = 0.44776.
Hence, plugging in these values, we will get 324/(154 * ( 1- 0.44776 )) = 409.04496.
The patient's corrected QT interval (QTc) is 409.04496 msec."
6969,57,QTc Framingham Calculator,physical,decimal,69,Template,A patient has a heart rate of 112 bpm and a QT interval of 281 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [112, 'beats per minute'], 'QT Interval': [281, 'msec']}",352.50066,334.87563,370.12569,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 112 beats per minute.
The QT interval is 281 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/112 = 0.53571.
Hence, plugging in these values, we will get 281/(154 * ( 1- 0.53571 )) = 352.50066.
The patient's corrected QT interval (QTc) is 352.50066 msec."
6970,57,QTc Framingham Calculator,physical,decimal,70,Template,A patient has a heart rate of 102 bpm and a QT interval of 236 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [102, 'beats per minute'], 'QT Interval': [236, 'msec']}",299.41104,284.44049,314.38159,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 102 beats per minute.
The QT interval is 236 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/102 = 0.58824.
Hence, plugging in these values, we will get 236/(154 * ( 1- 0.58824 )) = 299.41104.
The patient's corrected QT interval (QTc) is 299.41104 msec."
6971,57,QTc Framingham Calculator,physical,decimal,71,Template,A patient has a heart rate of 98 bpm and a QT interval of 322 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [98, 'beats per minute'], 'QT Interval': [322, 'msec']}",381.71504,362.62929,400.80079,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 98 beats per minute.
The QT interval is 322 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/98 = 0.61224.
Hence, plugging in these values, we will get 322/(154 * ( 1- 0.61224 )) = 381.71504.
The patient's corrected QT interval (QTc) is 381.71504 msec."
6972,57,QTc Framingham Calculator,physical,decimal,72,Template,A patient has a heart rate of 59 bpm and a QT interval of 315 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [59, 'beats per minute'], 'QT Interval': [315, 'msec']}",312.3897,296.77022,328.00919,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 59 beats per minute.
The QT interval is 315 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/59 = 1.01695.
Hence, plugging in these values, we will get 315/(154 * ( 1- 1.01695 )) = 312.3897.
The patient's corrected QT interval (QTc) is 312.3897 msec."
6973,57,QTc Framingham Calculator,physical,decimal,73,Template,A patient has a heart rate of 164 bpm and a QT interval of 465 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [164, 'beats per minute'], 'QT Interval': [465, 'msec']}",562.6591,534.52614,590.79206,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 164 beats per minute.
The QT interval is 465 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/164 = 0.36585.
Hence, plugging in these values, we will get 465/(154 * ( 1- 0.36585 )) = 562.6591.
The patient's corrected QT interval (QTc) is 562.6591 msec."
6974,57,QTc Framingham Calculator,physical,decimal,74,Template,A patient has a heart rate of 141 bpm and a QT interval of 433 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [141, 'beats per minute'], 'QT Interval': [433, 'msec']}",521.46838,495.39496,547.5418,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 141 beats per minute.
The QT interval is 433 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/141 = 0.42553.
Hence, plugging in these values, we will get 433/(154 * ( 1- 0.42553 )) = 521.46838.
The patient's corrected QT interval (QTc) is 521.46838 msec."
6975,57,QTc Framingham Calculator,physical,decimal,75,Template,A patient has a heart rate of 121 bpm and a QT interval of 319 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [121, 'beats per minute'], 'QT Interval': [319, 'msec']}",396.63602,376.80422,416.46782,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 121 beats per minute.
The QT interval is 319 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/121 = 0.49587.
Hence, plugging in these values, we will get 319/(154 * ( 1- 0.49587 )) = 396.63602.
The patient's corrected QT interval (QTc) is 396.63602 msec."
6976,57,QTc Framingham Calculator,physical,decimal,76,Template,A patient has a heart rate of 156 bpm and a QT interval of 220 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [156, 'beats per minute'], 'QT Interval': [220, 'msec']}",314.76852,299.03009,330.50695,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 156 beats per minute.
The QT interval is 220 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/156 = 0.38462.
Hence, plugging in these values, we will get 220/(154 * ( 1- 0.38462 )) = 314.76852.
The patient's corrected QT interval (QTc) is 314.76852 msec."
6977,57,QTc Framingham Calculator,physical,decimal,77,Template,A patient has a heart rate of 63 bpm and a QT interval of 422 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [63, 'beats per minute'], 'QT Interval': [422, 'msec']}",429.33348,407.86681,450.80015,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 63 beats per minute.
The QT interval is 422 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/63 = 0.95238.
Hence, plugging in these values, we will get 422/(154 * ( 1- 0.95238 )) = 429.33348.
The patient's corrected QT interval (QTc) is 429.33348 msec."
6978,57,QTc Framingham Calculator,physical,decimal,78,Template,A patient has a heart rate of 173 bpm and a QT interval of 422 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [173, 'beats per minute'], 'QT Interval': [422, 'msec']}",522.58972,496.46023,548.71921,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 173 beats per minute.
The QT interval is 422 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/173 = 0.34682.
Hence, plugging in these values, we will get 422/(154 * ( 1- 0.34682 )) = 522.58972.
The patient's corrected QT interval (QTc) is 522.58972 msec."
6979,57,QTc Framingham Calculator,physical,decimal,79,Template,A patient has a heart rate of 173 bpm and a QT interval of 491 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [173, 'beats per minute'], 'QT Interval': [491, 'msec']}",591.58972,562.01023,621.16921,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 173 beats per minute.
The QT interval is 491 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/173 = 0.34682.
Hence, plugging in these values, we will get 491/(154 * ( 1- 0.34682 )) = 591.58972.
The patient's corrected QT interval (QTc) is 591.58972 msec."
6980,57,QTc Framingham Calculator,physical,decimal,80,Template,A patient has a heart rate of 133 bpm and a QT interval of 238 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [133, 'beats per minute'], 'QT Interval': [238, 'msec']}",322.52598,306.39968,338.65228,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 133 beats per minute.
The QT interval is 238 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/133 = 0.45113.
Hence, plugging in these values, we will get 238/(154 * ( 1- 0.45113 )) = 322.52598.
The patient's corrected QT interval (QTc) is 322.52598 msec."
6981,57,QTc Framingham Calculator,physical,decimal,81,Template,A patient has a heart rate of 112 bpm and a QT interval of 307 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [112, 'beats per minute'], 'QT Interval': [307, 'msec']}",378.50066,359.57563,397.42569,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 112 beats per minute.
The QT interval is 307 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/112 = 0.53571.
Hence, plugging in these values, we will get 307/(154 * ( 1- 0.53571 )) = 378.50066.
The patient's corrected QT interval (QTc) is 378.50066 msec."
6982,57,QTc Framingham Calculator,physical,decimal,82,Template,A patient has a heart rate of 143 bpm and a QT interval of 434 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [143, 'beats per minute'], 'QT Interval': [434, 'msec']}",523.38468,497.21545,549.55391,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 143 beats per minute.
The QT interval is 434 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/143 = 0.41958.
Hence, plugging in these values, we will get 434/(154 * ( 1- 0.41958 )) = 523.38468.
The patient's corrected QT interval (QTc) is 523.38468 msec."
6983,57,QTc Framingham Calculator,physical,decimal,83,Template,A patient has a heart rate of 87 bpm and a QT interval of 255 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [87, 'beats per minute'], 'QT Interval': [255, 'msec']}",302.79236,287.65274,317.93198,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 87 beats per minute.
The QT interval is 255 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/87 = 0.68966.
Hence, plugging in these values, we will get 255/(154 * ( 1- 0.68966 )) = 302.79236.
The patient's corrected QT interval (QTc) is 302.79236 msec."
6984,57,QTc Framingham Calculator,physical,decimal,84,Template,A patient has a heart rate of 147 bpm and a QT interval of 399 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [147, 'beats per minute'], 'QT Interval': [399, 'msec']}",490.14336,465.63619,514.65053,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 147 beats per minute.
The QT interval is 399 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/147 = 0.40816.
Hence, plugging in these values, we will get 399/(154 * ( 1- 0.40816 )) = 490.14336.
The patient's corrected QT interval (QTc) is 490.14336 msec."
6985,57,QTc Framingham Calculator,physical,decimal,85,Template,A patient has a heart rate of 107 bpm and a QT interval of 495 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [107, 'beats per minute'], 'QT Interval': [495, 'msec']}",562.6445,534.51227,590.77673,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 107 beats per minute.
The QT interval is 495 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/107 = 0.56075.
Hence, plugging in these values, we will get 495/(154 * ( 1- 0.56075 )) = 562.6445.
The patient's corrected QT interval (QTc) is 562.6445 msec."
6986,57,QTc Framingham Calculator,physical,decimal,86,Template,A patient has a heart rate of 139 bpm and a QT interval of 371 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [139, 'beats per minute'], 'QT Interval': [371, 'msec']}",458.5259,435.5996,481.4522,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 139 beats per minute.
The QT interval is 371 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/139 = 0.43165.
Hence, plugging in these values, we will get 371/(154 * ( 1- 0.43165 )) = 458.5259.
The patient's corrected QT interval (QTc) is 458.5259 msec."
6987,57,QTc Framingham Calculator,physical,decimal,87,Template,A patient has a heart rate of 104 bpm and a QT interval of 490 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [104, 'beats per minute'], 'QT Interval': [490, 'msec']}",555.15432,527.3966,582.91204,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 104 beats per minute.
The QT interval is 490 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/104 = 0.57692.
Hence, plugging in these values, we will get 490/(154 * ( 1- 0.57692 )) = 555.15432.
The patient's corrected QT interval (QTc) is 555.15432 msec."
6988,57,QTc Framingham Calculator,physical,decimal,88,Template,A patient has a heart rate of 146 bpm and a QT interval of 288 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [146, 'beats per minute'], 'QT Interval': [288, 'msec']}",378.71216,359.77655,397.64777,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 146 beats per minute.
The QT interval is 288 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/146 = 0.41096.
Hence, plugging in these values, we will get 288/(154 * ( 1- 0.41096 )) = 378.71216.
The patient's corrected QT interval (QTc) is 378.71216 msec."
6989,57,QTc Framingham Calculator,physical,decimal,89,Template,A patient has a heart rate of 75 bpm and a QT interval of 335 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [75, 'beats per minute'], 'QT Interval': [335, 'msec']}",365.8,347.51,384.09,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 75 beats per minute.
The QT interval is 335 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/75 = 0.8.
Hence, plugging in these values, we will get 335/(154 * ( 1- 0.8 )) = 365.8.
The patient's corrected QT interval (QTc) is 365.8 msec."
6990,57,QTc Framingham Calculator,physical,decimal,90,Template,A patient has a heart rate of 94 bpm and a QT interval of 208 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [94, 'beats per minute'], 'QT Interval': [208, 'msec']}",263.7018,250.51671,276.88689,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 94 beats per minute.
The QT interval is 208 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/94 = 0.6383.
Hence, plugging in these values, we will get 208/(154 * ( 1- 0.6383 )) = 263.7018.
The patient's corrected QT interval (QTc) is 263.7018 msec."
6991,57,QTc Framingham Calculator,physical,decimal,91,Template,A patient has a heart rate of 121 bpm and a QT interval of 446 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [121, 'beats per minute'], 'QT Interval': [446, 'msec']}",523.63602,497.45422,549.81782,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 121 beats per minute.
The QT interval is 446 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/121 = 0.49587.
Hence, plugging in these values, we will get 446/(154 * ( 1- 0.49587 )) = 523.63602.
The patient's corrected QT interval (QTc) is 523.63602 msec."
6992,57,QTc Framingham Calculator,physical,decimal,92,Template,A patient has a heart rate of 143 bpm and a QT interval of 359 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [143, 'beats per minute'], 'QT Interval': [359, 'msec']}",448.38468,425.96545,470.80391,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 143 beats per minute.
The QT interval is 359 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/143 = 0.41958.
Hence, plugging in these values, we will get 359/(154 * ( 1- 0.41958 )) = 448.38468.
The patient's corrected QT interval (QTc) is 448.38468 msec."
6993,57,QTc Framingham Calculator,physical,decimal,93,Template,A patient has a heart rate of 147 bpm and a QT interval of 351 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [147, 'beats per minute'], 'QT Interval': [351, 'msec']}",442.14336,420.03619,464.25053,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 147 beats per minute.
The QT interval is 351 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/147 = 0.40816.
Hence, plugging in these values, we will get 351/(154 * ( 1- 0.40816 )) = 442.14336.
The patient's corrected QT interval (QTc) is 442.14336 msec."
6994,57,QTc Framingham Calculator,physical,decimal,94,Template,A patient has a heart rate of 136 bpm and a QT interval of 339 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [136, 'beats per minute'], 'QT Interval': [339, 'msec']}",425.05828,403.80537,446.31119,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 136 beats per minute.
The QT interval is 339 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/136 = 0.44118.
Hence, plugging in these values, we will get 339/(154 * ( 1- 0.44118 )) = 425.05828.
The patient's corrected QT interval (QTc) is 425.05828 msec."
6995,57,QTc Framingham Calculator,physical,decimal,95,Template,A patient has a heart rate of 59 bpm and a QT interval of 333 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [59, 'beats per minute'], 'QT Interval': [333, 'msec']}",330.3897,313.87021,346.90919,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 59 beats per minute.
The QT interval is 333 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/59 = 1.01695.
Hence, plugging in these values, we will get 333/(154 * ( 1- 1.01695 )) = 330.3897.
The patient's corrected QT interval (QTc) is 330.3897 msec."
6996,57,QTc Framingham Calculator,physical,decimal,96,Template,A patient has a heart rate of 153 bpm and a QT interval of 222 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [153, 'beats per minute'], 'QT Interval': [222, 'msec']}",315.60736,299.82699,331.38773,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 153 beats per minute.
The QT interval is 222 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/153 = 0.39216.
Hence, plugging in these values, we will get 222/(154 * ( 1- 0.39216 )) = 315.60736.
The patient's corrected QT interval (QTc) is 315.60736 msec."
6997,57,QTc Framingham Calculator,physical,decimal,97,Template,A patient has a heart rate of 71 bpm and a QT interval of 469 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [71, 'beats per minute'], 'QT Interval': [469, 'msec']}",492.85922,468.21626,517.50218,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 71 beats per minute.
The QT interval is 469 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/71 = 0.84507.
Hence, plugging in these values, we will get 469/(154 * ( 1- 0.84507 )) = 492.85922.
The patient's corrected QT interval (QTc) is 492.85922 msec."
6998,57,QTc Framingham Calculator,physical,decimal,98,Template,A patient has a heart rate of 126 bpm and a QT interval of 232 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [126, 'beats per minute'], 'QT Interval': [232, 'msec']}",312.66674,297.0334,328.30008,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 126 beats per minute.
The QT interval is 232 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/126 = 0.47619.
Hence, plugging in these values, we will get 232/(154 * ( 1- 0.47619 )) = 312.66674.
The patient's corrected QT interval (QTc) is 312.66674 msec."
6999,57,QTc Framingham Calculator,physical,decimal,99,Template,A patient has a heart rate of 82 bpm and a QT interval of 376 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [82, 'beats per minute'], 'QT Interval': [376, 'msec']}",417.31666,396.45083,438.18249,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 82 beats per minute.
The QT interval is 376 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/82 = 0.73171.
Hence, plugging in these values, we will get 376/(154 * ( 1- 0.73171 )) = 417.31666.
The patient's corrected QT interval (QTc) is 417.31666 msec."
7000,57,QTc Framingham Calculator,physical,decimal,100,Template,A patient has a heart rate of 111 bpm and a QT interval of 322 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [111, 'beats per minute'], 'QT Interval': [322, 'msec']}",392.75684,373.119,412.39468,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 111 beats per minute.
The QT interval is 322 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/111 = 0.54054.
Hence, plugging in these values, we will get 322/(154 * ( 1- 0.54054 )) = 392.75684.
The patient's corrected QT interval (QTc) is 392.75684 msec."
7001,57,QTc Framingham Calculator,physical,decimal,101,Template,Patient has a heart rate of 74 bpm and a QT interval of 330 msec.,"Using the Framingham Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [74, 'beats per minute'], 'QT Interval': [330, 'msec']}",359.13526,341.1785,377.09202,"The corrected QT interval using the Framingham formula is computed as  QTc = QT Interval + (154 * (1 - rr_interval_sec)), where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 74 beats per minute.
The QT interval is 330 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/74 = 0.81081.
Hence, plugging in these values, we will get 330/(154 * ( 1- 0.81081 )) = 359.13526.
The patient's corrected QT interval (QTc) is 359.13526 msec."
7002,58,QTc Hodges Calculator,physical,decimal,22,Template,A patient has a heart rate of 125 bpm and a QT interval of 206 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [125, 'beats per minute'], 'QT Interval': [206, 'msec']}",319.75,303.7625,335.7375,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 125 beats per minute.
The QT interval is 206 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/125 = 0.48.
Hence, plugging in these values, we will get 206 + 1.75 * [(60/0.48) - 60] = 319.75.
The patient's corrected QT interval (QTc) is 319.75 msec."
7003,58,QTc Hodges Calculator,physical,decimal,23,Template,A patient has a heart rate of 56 bpm and a QT interval of 463 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [56, 'beats per minute'], 'QT Interval': [463, 'msec']}",455.99987,433.19988,478.79986,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 56 beats per minute.
The QT interval is 463 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/56 = 1.07143.
Hence, plugging in these values, we will get 463 + 1.75 * [(60/1.07143) - 60] = 455.99987.
The patient's corrected QT interval (QTc) is 455.99987 msec."
7004,58,QTc Hodges Calculator,physical,decimal,24,Template,A patient has a heart rate of 138 bpm and a QT interval of 469 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [138, 'beats per minute'], 'QT Interval': [469, 'msec']}",605.50145,575.22638,635.77652,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 138 beats per minute.
The QT interval is 469 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/138 = 0.43478.
Hence, plugging in these values, we will get 469 + 1.75 * [(60/0.43478) - 60] = 605.50145.
The patient's corrected QT interval (QTc) is 605.50145 msec."
7005,58,QTc Hodges Calculator,physical,decimal,25,Template,A patient has a heart rate of 111 bpm and a QT interval of 439 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [111, 'beats per minute'], 'QT Interval': [439, 'msec']}",528.25019,501.83768,554.6627,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 111 beats per minute.
The QT interval is 439 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/111 = 0.54054.
Hence, plugging in these values, we will get 439 + 1.75 * [(60/0.54054) - 60] = 528.25019.
The patient's corrected QT interval (QTc) is 528.25019 msec."
7006,58,QTc Hodges Calculator,physical,decimal,26,Template,A patient has a heart rate of 112 bpm and a QT interval of 350 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [112, 'beats per minute'], 'QT Interval': [350, 'msec']}",441.00157,418.95149,463.05165,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 112 beats per minute.
The QT interval is 350 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/112 = 0.53571.
Hence, plugging in these values, we will get 350 + 1.75 * [(60/0.53571) - 60] = 441.00157.
The patient's corrected QT interval (QTc) is 441.00157 msec."
7007,58,QTc Hodges Calculator,physical,decimal,27,Template,A patient has a heart rate of 69 bpm and a QT interval of 364 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [69, 'beats per minute'], 'QT Interval': [364, 'msec']}",379.74934,360.76187,398.73681,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 69 beats per minute.
The QT interval is 364 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/69 = 0.86957.
Hence, plugging in these values, we will get 364 + 1.75 * [(60/0.86957) - 60] = 379.74934.
The patient's corrected QT interval (QTc) is 379.74934 msec."
7008,58,QTc Hodges Calculator,physical,decimal,28,Template,A patient has a heart rate of 122 bpm and a QT interval of 428 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [122, 'beats per minute'], 'QT Interval': [428, 'msec']}",536.50142,509.67635,563.32649,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 122 beats per minute.
The QT interval is 428 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/122 = 0.4918.
Hence, plugging in these values, we will get 428 + 1.75 * [(60/0.4918) - 60] = 536.50142.
The patient's corrected QT interval (QTc) is 536.50142 msec."
7009,58,QTc Hodges Calculator,physical,decimal,29,Template,A patient has a heart rate of 86 bpm and a QT interval of 220 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [86, 'beats per minute'], 'QT Interval': [220, 'msec']}",265.50095,252.2259,278.776,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 86 beats per minute.
The QT interval is 220 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/86 = 0.69767.
Hence, plugging in these values, we will get 220 + 1.75 * [(60/0.69767) - 60] = 265.50095.
The patient's corrected QT interval (QTc) is 265.50095 msec."
7010,58,QTc Hodges Calculator,physical,decimal,30,Template,A patient has a heart rate of 88 bpm and a QT interval of 250 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [88, 'beats per minute'], 'QT Interval': [250, 'msec']}",298.99959,284.04961,313.94957,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 88 beats per minute.
The QT interval is 250 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/88 = 0.68182.
Hence, plugging in these values, we will get 250 + 1.75 * [(60/0.68182) - 60] = 298.99959.
The patient's corrected QT interval (QTc) is 298.99959 msec."
7011,58,QTc Hodges Calculator,physical,decimal,31,Template,A patient has a heart rate of 99 bpm and a QT interval of 398 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [99, 'beats per minute'], 'QT Interval': [398, 'msec']}",466.25017,442.93766,489.56268,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 99 beats per minute.
The QT interval is 398 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/99 = 0.60606.
Hence, plugging in these values, we will get 398 + 1.75 * [(60/0.60606) - 60] = 466.25017.
The patient's corrected QT interval (QTc) is 466.25017 msec."
7012,58,QTc Hodges Calculator,physical,decimal,32,Template,A patient has a heart rate of 72 bpm and a QT interval of 367 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [72, 'beats per minute'], 'QT Interval': [367, 'msec']}",388.0005,368.60047,407.40053,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 72 beats per minute.
The QT interval is 367 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/72 = 0.83333.
Hence, plugging in these values, we will get 367 + 1.75 * [(60/0.83333) - 60] = 388.0005.
The patient's corrected QT interval (QTc) is 388.0005 msec."
7013,58,QTc Hodges Calculator,physical,decimal,33,Template,A patient has a heart rate of 178 bpm and a QT interval of 255 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [178, 'beats per minute'], 'QT Interval': [255, 'msec']}",461.49875,438.42381,484.57369,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 178 beats per minute.
The QT interval is 255 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/178 = 0.33708.
Hence, plugging in these values, we will get 255 + 1.75 * [(60/0.33708) - 60] = 461.49875.
The patient's corrected QT interval (QTc) is 461.49875 msec."
7014,58,QTc Hodges Calculator,physical,decimal,34,Template,A patient has a heart rate of 71 bpm and a QT interval of 220 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [71, 'beats per minute'], 'QT Interval': [220, 'msec']}",239.25006,227.28756,251.21256,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 71 beats per minute.
The QT interval is 220 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/71 = 0.84507.
Hence, plugging in these values, we will get 220 + 1.75 * [(60/0.84507) - 60] = 239.25006.
The patient's corrected QT interval (QTc) is 239.25006 msec."
7015,58,QTc Hodges Calculator,physical,decimal,35,Template,A patient has a heart rate of 95 bpm and a QT interval of 420 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [95, 'beats per minute'], 'QT Interval': [420, 'msec']}",481.24972,457.18723,505.31221,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 95 beats per minute.
The QT interval is 420 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/95 = 0.63158.
Hence, plugging in these values, we will get 420 + 1.75 * [(60/0.63158) - 60] = 481.24972.
The patient's corrected QT interval (QTc) is 481.24972 msec."
7016,58,QTc Hodges Calculator,physical,decimal,36,Template,A patient has a heart rate of 63 bpm and a QT interval of 305 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [63, 'beats per minute'], 'QT Interval': [305, 'msec']}",310.25011,294.7376,325.76262,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 63 beats per minute.
The QT interval is 305 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/63 = 0.95238.
Hence, plugging in these values, we will get 305 + 1.75 * [(60/0.95238) - 60] = 310.25011.
The patient's corrected QT interval (QTc) is 310.25011 msec."
7017,58,QTc Hodges Calculator,physical,decimal,37,Template,A patient has a heart rate of 140 bpm and a QT interval of 406 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [140, 'beats per minute'], 'QT Interval': [406, 'msec']}",546.00082,518.70078,573.30086,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 140 beats per minute.
The QT interval is 406 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/140 = 0.42857.
Hence, plugging in these values, we will get 406 + 1.75 * [(60/0.42857) - 60] = 546.00082.
The patient's corrected QT interval (QTc) is 546.00082 msec."
7018,58,QTc Hodges Calculator,physical,decimal,38,Template,A patient has a heart rate of 65 bpm and a QT interval of 231 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [65, 'beats per minute'], 'QT Interval': [231, 'msec']}",239.74962,227.76214,251.7371,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 65 beats per minute.
The QT interval is 231 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/65 = 0.92308.
Hence, plugging in these values, we will get 231 + 1.75 * [(60/0.92308) - 60] = 239.74962.
The patient's corrected QT interval (QTc) is 239.74962 msec."
7019,58,QTc Hodges Calculator,physical,decimal,39,Template,A patient has a heart rate of 79 bpm and a QT interval of 361 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [79, 'beats per minute'], 'QT Interval': [361, 'msec']}",394.25067,374.53814,413.9632,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 79 beats per minute.
The QT interval is 361 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/79 = 0.75949.
Hence, plugging in these values, we will get 361 + 1.75 * [(60/0.75949) - 60] = 394.25067.
The patient's corrected QT interval (QTc) is 394.25067 msec."
7020,58,QTc Hodges Calculator,physical,decimal,40,Template,A patient has a heart rate of 83 bpm and a QT interval of 291 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [83, 'beats per minute'], 'QT Interval': [291, 'msec']}",331.25031,314.68779,347.81283,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 83 beats per minute.
The QT interval is 291 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/83 = 0.72289.
Hence, plugging in these values, we will get 291 + 1.75 * [(60/0.72289) - 60] = 331.25031.
The patient's corrected QT interval (QTc) is 331.25031 msec."
7021,58,QTc Hodges Calculator,physical,decimal,41,Template,A patient has a heart rate of 156 bpm and a QT interval of 381 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [156, 'beats per minute'], 'QT Interval': [381, 'msec']}",548.99672,521.54688,576.44656,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 156 beats per minute.
The QT interval is 381 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/156 = 0.38462.
Hence, plugging in these values, we will get 381 + 1.75 * [(60/0.38462) - 60] = 548.99672.
The patient's corrected QT interval (QTc) is 548.99672 msec."
7022,58,QTc Hodges Calculator,physical,decimal,42,Template,A patient has a heart rate of 61 bpm and a QT interval of 444 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [61, 'beats per minute'], 'QT Interval': [444, 'msec']}",445.74963,423.46215,468.03711,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 61 beats per minute.
The QT interval is 444 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/61 = 0.98361.
Hence, plugging in these values, we will get 444 + 1.75 * [(60/0.98361) - 60] = 445.74963.
The patient's corrected QT interval (QTc) is 445.74963 msec."
7023,58,QTc Hodges Calculator,physical,decimal,43,Template,A patient has a heart rate of 179 bpm and a QT interval of 213 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [179, 'beats per minute'], 'QT Interval': [213, 'msec']}",421.24582,400.18353,442.30811,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 179 beats per minute.
The QT interval is 213 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/179 = 0.3352.
Hence, plugging in these values, we will get 213 + 1.75 * [(60/0.3352) - 60] = 421.24582.
The patient's corrected QT interval (QTc) is 421.24582 msec."
7024,58,QTc Hodges Calculator,physical,decimal,44,Template,A patient has a heart rate of 170 bpm and a QT interval of 290 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [170, 'beats per minute'], 'QT Interval': [290, 'msec']}",482.50099,458.37594,506.62604,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 170 beats per minute.
The QT interval is 290 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/170 = 0.35294.
Hence, plugging in these values, we will get 290 + 1.75 * [(60/0.35294) - 60] = 482.50099.
The patient's corrected QT interval (QTc) is 482.50099 msec."
7025,58,QTc Hodges Calculator,physical,decimal,45,Template,A patient has a heart rate of 176 bpm and a QT interval of 296 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [176, 'beats per minute'], 'QT Interval': [296, 'msec']}",498.99918,474.04922,523.94914,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 176 beats per minute.
The QT interval is 296 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/176 = 0.34091.
Hence, plugging in these values, we will get 296 + 1.75 * [(60/0.34091) - 60] = 498.99918.
The patient's corrected QT interval (QTc) is 498.99918 msec."
7026,58,QTc Hodges Calculator,physical,decimal,46,Template,A patient has a heart rate of 157 bpm and a QT interval of 485 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [157, 'beats per minute'], 'QT Interval': [485, 'msec']}",654.74684,622.0095,687.48418,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 157 beats per minute.
The QT interval is 485 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/157 = 0.38217.
Hence, plugging in these values, we will get 485 + 1.75 * [(60/0.38217) - 60] = 654.74684.
The patient's corrected QT interval (QTc) is 654.74684 msec."
7027,58,QTc Hodges Calculator,physical,decimal,47,Template,A patient has a heart rate of 78 bpm and a QT interval of 432 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [78, 'beats per minute'], 'QT Interval': [432, 'msec']}",463.50014,440.32513,486.67515,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 78 beats per minute.
The QT interval is 432 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/78 = 0.76923.
Hence, plugging in these values, we will get 432 + 1.75 * [(60/0.76923) - 60] = 463.50014.
The patient's corrected QT interval (QTc) is 463.50014 msec."
7028,58,QTc Hodges Calculator,physical,decimal,48,Template,A patient has a heart rate of 174 bpm and a QT interval of 250 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [174, 'beats per minute'], 'QT Interval': [250, 'msec']}",449.49787,427.02298,471.97276,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 174 beats per minute.
The QT interval is 250 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/174 = 0.34483.
Hence, plugging in these values, we will get 250 + 1.75 * [(60/0.34483) - 60] = 449.49787.
The patient's corrected QT interval (QTc) is 449.49787 msec."
7029,58,QTc Hodges Calculator,physical,decimal,49,Template,A patient has a heart rate of 139 bpm and a QT interval of 341 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [139, 'beats per minute'], 'QT Interval': [341, 'msec']}",479.25264,455.29001,503.21527,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 139 beats per minute.
The QT interval is 341 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/139 = 0.43165.
Hence, plugging in these values, we will get 341 + 1.75 * [(60/0.43165) - 60] = 479.25264.
The patient's corrected QT interval (QTc) is 479.25264 msec."
7030,58,QTc Hodges Calculator,physical,decimal,50,Template,A patient has a heart rate of 74 bpm and a QT interval of 449 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [74, 'beats per minute'], 'QT Interval': [449, 'msec']}",473.50013,449.82512,497.17514,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 74 beats per minute.
The QT interval is 449 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/74 = 0.81081.
Hence, plugging in these values, we will get 449 + 1.75 * [(60/0.81081) - 60] = 473.50013.
The patient's corrected QT interval (QTc) is 473.50013 msec."
7031,58,QTc Hodges Calculator,physical,decimal,51,Template,A patient has a heart rate of 85 bpm and a QT interval of 254 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [85, 'beats per minute'], 'QT Interval': [254, 'msec']}",297.7505,282.86297,312.63803,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 85 beats per minute.
The QT interval is 254 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/85 = 0.70588.
Hence, plugging in these values, we will get 254 + 1.75 * [(60/0.70588) - 60] = 297.7505.
The patient's corrected QT interval (QTc) is 297.7505 msec."
7032,58,QTc Hodges Calculator,physical,decimal,52,Template,A patient has a heart rate of 64 bpm and a QT interval of 396 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [64, 'beats per minute'], 'QT Interval': [396, 'msec']}",403,382.85,423.15,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 64 beats per minute.
The QT interval is 396 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/64 = 0.9375.
Hence, plugging in these values, we will get 396 + 1.75 * [(60/0.9375) - 60] = 403.0.
The patient's corrected QT interval (QTc) is 403.0 msec."
7033,58,QTc Hodges Calculator,physical,decimal,53,Template,A patient has a heart rate of 121 bpm and a QT interval of 225 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [121, 'beats per minute'], 'QT Interval': [225, 'msec']}",331.74905,315.1616,348.3365,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 121 beats per minute.
The QT interval is 225 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/121 = 0.49587.
Hence, plugging in these values, we will get 225 + 1.75 * [(60/0.49587) - 60] = 331.74905.
The patient's corrected QT interval (QTc) is 331.74905 msec."
7034,58,QTc Hodges Calculator,physical,decimal,54,Template,A patient has a heart rate of 174 bpm and a QT interval of 424 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [174, 'beats per minute'], 'QT Interval': [424, 'msec']}",623.49787,592.32298,654.67276,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 174 beats per minute.
The QT interval is 424 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/174 = 0.34483.
Hence, plugging in these values, we will get 424 + 1.75 * [(60/0.34483) - 60] = 623.49787.
The patient's corrected QT interval (QTc) is 623.49787 msec."
7035,58,QTc Hodges Calculator,physical,decimal,55,Template,A patient has a heart rate of 46 bpm and a QT interval of 262 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [46, 'beats per minute'], 'QT Interval': [262, 'msec']}",237.49987,225.62488,249.37486,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 46 beats per minute.
The QT interval is 262 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/46 = 1.30435.
Hence, plugging in these values, we will get 262 + 1.75 * [(60/1.30435) - 60] = 237.49987.
The patient's corrected QT interval (QTc) is 237.49987 msec."
7036,58,QTc Hodges Calculator,physical,decimal,56,Template,A patient has a heart rate of 136 bpm and a QT interval of 275 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [136, 'beats per minute'], 'QT Interval': [275, 'msec']}",407.9981,387.59819,428.39801,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 136 beats per minute.
The QT interval is 275 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/136 = 0.44118.
Hence, plugging in these values, we will get 275 + 1.75 * [(60/0.44118) - 60] = 407.9981.
The patient's corrected QT interval (QTc) is 407.9981 msec."
7037,58,QTc Hodges Calculator,physical,decimal,57,Template,A patient has a heart rate of 158 bpm and a QT interval of 263 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [158, 'beats per minute'], 'QT Interval': [263, 'msec']}",434.4977,412.77281,456.22259,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 158 beats per minute.
The QT interval is 263 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/158 = 0.37975.
Hence, plugging in these values, we will get 263 + 1.75 * [(60/0.37975) - 60] = 434.4977.
The patient's corrected QT interval (QTc) is 434.4977 msec."
7038,58,QTc Hodges Calculator,physical,decimal,58,Template,A patient has a heart rate of 136 bpm and a QT interval of 209 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [136, 'beats per minute'], 'QT Interval': [209, 'msec']}",341.9981,324.89819,359.09801,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 136 beats per minute.
The QT interval is 209 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/136 = 0.44118.
Hence, plugging in these values, we will get 209 + 1.75 * [(60/0.44118) - 60] = 341.9981.
The patient's corrected QT interval (QTc) is 341.9981 msec."
7039,58,QTc Hodges Calculator,physical,decimal,59,Template,A patient has a heart rate of 174 bpm and a QT interval of 350 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [174, 'beats per minute'], 'QT Interval': [350, 'msec']}",549.49787,522.02298,576.97276,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 174 beats per minute.
The QT interval is 350 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/174 = 0.34483.
Hence, plugging in these values, we will get 350 + 1.75 * [(60/0.34483) - 60] = 549.49787.
The patient's corrected QT interval (QTc) is 549.49787 msec."
7040,58,QTc Hodges Calculator,physical,decimal,60,Template,A patient has a heart rate of 153 bpm and a QT interval of 358 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [153, 'beats per minute'], 'QT Interval': [358, 'msec']}",520.74786,494.71047,546.78525,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 153 beats per minute.
The QT interval is 358 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/153 = 0.39216.
Hence, plugging in these values, we will get 358 + 1.75 * [(60/0.39216) - 60] = 520.74786.
The patient's corrected QT interval (QTc) is 520.74786 msec."
7041,58,QTc Hodges Calculator,physical,decimal,61,Template,A patient has a heart rate of 54 bpm and a QT interval of 231 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [54, 'beats per minute'], 'QT Interval': [231, 'msec']}",220.50009,209.47509,231.52509,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 54 beats per minute.
The QT interval is 231 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/54 = 1.11111.
Hence, plugging in these values, we will get 231 + 1.75 * [(60/1.11111) - 60] = 220.50009.
The patient's corrected QT interval (QTc) is 220.50009 msec."
7042,58,QTc Hodges Calculator,physical,decimal,62,Template,A patient has a heart rate of 166 bpm and a QT interval of 358 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [166, 'beats per minute'], 'QT Interval': [358, 'msec']}",543.49661,516.32178,570.67144,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 166 beats per minute.
The QT interval is 358 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/166 = 0.36145.
Hence, plugging in these values, we will get 358 + 1.75 * [(60/0.36145) - 60] = 543.49661.
The patient's corrected QT interval (QTc) is 543.49661 msec."
7043,58,QTc Hodges Calculator,physical,decimal,63,Template,A patient has a heart rate of 138 bpm and a QT interval of 225 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [138, 'beats per minute'], 'QT Interval': [225, 'msec']}",361.50145,343.42638,379.57652,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 138 beats per minute.
The QT interval is 225 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/138 = 0.43478.
Hence, plugging in these values, we will get 225 + 1.75 * [(60/0.43478) - 60] = 361.50145.
The patient's corrected QT interval (QTc) is 361.50145 msec."
7044,58,QTc Hodges Calculator,physical,decimal,64,Template,A patient has a heart rate of 139 bpm and a QT interval of 465 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [139, 'beats per minute'], 'QT Interval': [465, 'msec']}",603.25264,573.09001,633.41527,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 139 beats per minute.
The QT interval is 465 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/139 = 0.43165.
Hence, plugging in these values, we will get 465 + 1.75 * [(60/0.43165) - 60] = 603.25264.
The patient's corrected QT interval (QTc) is 603.25264 msec."
7045,58,QTc Hodges Calculator,physical,decimal,65,Template,A patient has a heart rate of 69 bpm and a QT interval of 370 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [69, 'beats per minute'], 'QT Interval': [370, 'msec']}",385.74934,366.46187,405.03681,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 69 beats per minute.
The QT interval is 370 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/69 = 0.86957.
Hence, plugging in these values, we will get 370 + 1.75 * [(60/0.86957) - 60] = 385.74934.
The patient's corrected QT interval (QTc) is 385.74934 msec."
7046,58,QTc Hodges Calculator,physical,decimal,66,Template,A patient has a heart rate of 87 bpm and a QT interval of 291 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [87, 'beats per minute'], 'QT Interval': [291, 'msec']}",338.24893,321.33648,355.16138,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 87 beats per minute.
The QT interval is 291 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/87 = 0.68966.
Hence, plugging in these values, we will get 291 + 1.75 * [(60/0.68966) - 60] = 338.24893.
The patient's corrected QT interval (QTc) is 338.24893 msec."
7047,58,QTc Hodges Calculator,physical,decimal,67,Template,A patient has a heart rate of 49 bpm and a QT interval of 329 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [49, 'beats per minute'], 'QT Interval': [329, 'msec']}",309.74999,294.26249,325.23749,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 49 beats per minute.
The QT interval is 329 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/49 = 1.22449.
Hence, plugging in these values, we will get 329 + 1.75 * [(60/1.22449) - 60] = 309.74999.
The patient's corrected QT interval (QTc) is 309.74999 msec."
7048,58,QTc Hodges Calculator,physical,decimal,68,Template,A patient has a heart rate of 138 bpm and a QT interval of 305 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [138, 'beats per minute'], 'QT Interval': [305, 'msec']}",441.50145,419.42638,463.57652,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 138 beats per minute.
The QT interval is 305 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/138 = 0.43478.
Hence, plugging in these values, we will get 305 + 1.75 * [(60/0.43478) - 60] = 441.50145.
The patient's corrected QT interval (QTc) is 441.50145 msec."
7049,58,QTc Hodges Calculator,physical,decimal,69,Template,A patient has a heart rate of 64 bpm and a QT interval of 299 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [64, 'beats per minute'], 'QT Interval': [299, 'msec']}",306,290.7,321.3,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 64 beats per minute.
The QT interval is 299 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/64 = 0.9375.
Hence, plugging in these values, we will get 299 + 1.75 * [(60/0.9375) - 60] = 306.0.
The patient's corrected QT interval (QTc) is 306.0 msec."
7050,58,QTc Hodges Calculator,physical,decimal,70,Template,A patient has a heart rate of 150 bpm and a QT interval of 394 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [150, 'beats per minute'], 'QT Interval': [394, 'msec']}",551.5,523.925,579.075,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 150 beats per minute.
The QT interval is 394 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/150 = 0.4.
Hence, plugging in these values, we will get 394 + 1.75 * [(60/0.4) - 60] = 551.5.
The patient's corrected QT interval (QTc) is 551.5 msec."
7051,58,QTc Hodges Calculator,physical,decimal,71,Template,A patient has a heart rate of 133 bpm and a QT interval of 362 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [133, 'beats per minute'], 'QT Interval': [362, 'msec']}",489.74888,465.26144,514.23632,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 133 beats per minute.
The QT interval is 362 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/133 = 0.45113.
Hence, plugging in these values, we will get 362 + 1.75 * [(60/0.45113) - 60] = 489.74888.
The patient's corrected QT interval (QTc) is 489.74888 msec."
7052,58,QTc Hodges Calculator,physical,decimal,72,Template,A patient has a heart rate of 135 bpm and a QT interval of 207 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [135, 'beats per minute'], 'QT Interval': [207, 'msec']}",338.25236,321.33974,355.16498,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 135 beats per minute.
The QT interval is 207 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/135 = 0.44444.
Hence, plugging in these values, we will get 207 + 1.75 * [(60/0.44444) - 60] = 338.25236.
The patient's corrected QT interval (QTc) is 338.25236 msec."
7053,58,QTc Hodges Calculator,physical,decimal,73,Template,A patient has a heart rate of 122 bpm and a QT interval of 433 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [122, 'beats per minute'], 'QT Interval': [433, 'msec']}",541.50142,514.42635,568.57649,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 122 beats per minute.
The QT interval is 433 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/122 = 0.4918.
Hence, plugging in these values, we will get 433 + 1.75 * [(60/0.4918) - 60] = 541.50142.
The patient's corrected QT interval (QTc) is 541.50142 msec."
7054,58,QTc Hodges Calculator,physical,decimal,74,Template,A patient has a heart rate of 125 bpm and a QT interval of 469 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [125, 'beats per minute'], 'QT Interval': [469, 'msec']}",582.75,553.6125,611.8875,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 125 beats per minute.
The QT interval is 469 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/125 = 0.48.
Hence, plugging in these values, we will get 469 + 1.75 * [(60/0.48) - 60] = 582.75.
The patient's corrected QT interval (QTc) is 582.75 msec."
7055,58,QTc Hodges Calculator,physical,decimal,75,Template,A patient has a heart rate of 141 bpm and a QT interval of 306 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [141, 'beats per minute'], 'QT Interval': [306, 'msec']}",447.75111,425.36355,470.13867,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 141 beats per minute.
The QT interval is 306 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/141 = 0.42553.
Hence, plugging in these values, we will get 306 + 1.75 * [(60/0.42553) - 60] = 447.75111.
The patient's corrected QT interval (QTc) is 447.75111 msec."
7056,58,QTc Hodges Calculator,physical,decimal,76,Template,A patient has a heart rate of 123 bpm and a QT interval of 265 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [123, 'beats per minute'], 'QT Interval': [265, 'msec']}",375.25215,356.48954,394.01476,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 123 beats per minute.
The QT interval is 265 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/123 = 0.4878.
Hence, plugging in these values, we will get 265 + 1.75 * [(60/0.4878) - 60] = 375.25215.
The patient's corrected QT interval (QTc) is 375.25215 msec."
7057,58,QTc Hodges Calculator,physical,decimal,77,Template,A patient has a heart rate of 65 bpm and a QT interval of 456 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [65, 'beats per minute'], 'QT Interval': [456, 'msec']}",464.74962,441.51214,487.9871,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 65 beats per minute.
The QT interval is 456 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/65 = 0.92308.
Hence, plugging in these values, we will get 456 + 1.75 * [(60/0.92308) - 60] = 464.74962.
The patient's corrected QT interval (QTc) is 464.74962 msec."
7058,58,QTc Hodges Calculator,physical,decimal,78,Template,A patient has a heart rate of 62 bpm and a QT interval of 328 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [62, 'beats per minute'], 'QT Interval': [328, 'msec']}",331.50022,314.92521,348.07523,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 62 beats per minute.
The QT interval is 328 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/62 = 0.96774.
Hence, plugging in these values, we will get 328 + 1.75 * [(60/0.96774) - 60] = 331.50022.
The patient's corrected QT interval (QTc) is 331.50022 msec."
7059,58,QTc Hodges Calculator,physical,decimal,79,Template,A patient has a heart rate of 100 bpm and a QT interval of 419 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [100, 'beats per minute'], 'QT Interval': [419, 'msec']}",489,464.55,513.45,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 100 beats per minute.
The QT interval is 419 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/100 = 0.6.
Hence, plugging in these values, we will get 419 + 1.75 * [(60/0.6) - 60] = 489.0.
The patient's corrected QT interval (QTc) is 489.0 msec."
7060,58,QTc Hodges Calculator,physical,decimal,80,Template,A patient has a heart rate of 131 bpm and a QT interval of 376 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [131, 'beats per minute'], 'QT Interval': [376, 'msec']}",500.24763,475.23525,525.26001,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 131 beats per minute.
The QT interval is 376 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/131 = 0.45802.
Hence, plugging in these values, we will get 376 + 1.75 * [(60/0.45802) - 60] = 500.24763.
The patient's corrected QT interval (QTc) is 500.24763 msec."
7061,58,QTc Hodges Calculator,physical,decimal,81,Template,A patient has a heart rate of 115 bpm and a QT interval of 338 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [115, 'beats per minute'], 'QT Interval': [338, 'msec']}",434.24966,412.53718,455.96214,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 115 beats per minute.
The QT interval is 338 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/115 = 0.52174.
Hence, plugging in these values, we will get 338 + 1.75 * [(60/0.52174) - 60] = 434.24966.
The patient's corrected QT interval (QTc) is 434.24966 msec."
7062,58,QTc Hodges Calculator,physical,decimal,82,Template,A patient has a heart rate of 67 bpm and a QT interval of 358 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [67, 'beats per minute'], 'QT Interval': [358, 'msec']}",370.25031,351.73779,388.76283,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 67 beats per minute.
The QT interval is 358 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/67 = 0.89552.
Hence, plugging in these values, we will get 358 + 1.75 * [(60/0.89552) - 60] = 370.25031.
The patient's corrected QT interval (QTc) is 370.25031 msec."
7063,58,QTc Hodges Calculator,physical,decimal,83,Template,A patient has a heart rate of 160 bpm and a QT interval of 429 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [160, 'beats per minute'], 'QT Interval': [429, 'msec']}",604,573.8,634.2,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 160 beats per minute.
The QT interval is 429 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/160 = 0.375.
Hence, plugging in these values, we will get 429 + 1.75 * [(60/0.375) - 60] = 604.0.
The patient's corrected QT interval (QTc) is 604.0 msec."
7064,58,QTc Hodges Calculator,physical,decimal,84,Template,A patient has a heart rate of 148 bpm and a QT interval of 430 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [148, 'beats per minute'], 'QT Interval': [430, 'msec']}",583.99706,554.79721,613.19691,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 148 beats per minute.
The QT interval is 430 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/148 = 0.40541.
Hence, plugging in these values, we will get 430 + 1.75 * [(60/0.40541) - 60] = 583.99706.
The patient's corrected QT interval (QTc) is 583.99706 msec."
7065,58,QTc Hodges Calculator,physical,decimal,85,Template,A patient has a heart rate of 65 bpm and a QT interval of 389 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [65, 'beats per minute'], 'QT Interval': [389, 'msec']}",397.74962,377.86214,417.6371,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 65 beats per minute.
The QT interval is 389 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/65 = 0.92308.
Hence, plugging in these values, we will get 389 + 1.75 * [(60/0.92308) - 60] = 397.74962.
The patient's corrected QT interval (QTc) is 397.74962 msec."
7066,58,QTc Hodges Calculator,physical,decimal,86,Template,A patient has a heart rate of 79 bpm and a QT interval of 418 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [79, 'beats per minute'], 'QT Interval': [418, 'msec']}",451.25067,428.68814,473.8132,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 79 beats per minute.
The QT interval is 418 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/79 = 0.75949.
Hence, plugging in these values, we will get 418 + 1.75 * [(60/0.75949) - 60] = 451.25067.
The patient's corrected QT interval (QTc) is 451.25067 msec."
7067,58,QTc Hodges Calculator,physical,decimal,87,Template,A patient has a heart rate of 173 bpm and a QT interval of 294 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [173, 'beats per minute'], 'QT Interval': [294, 'msec']}",491.75071,467.16317,516.33825,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 173 beats per minute.
The QT interval is 294 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/173 = 0.34682.
Hence, plugging in these values, we will get 294 + 1.75 * [(60/0.34682) - 60] = 491.75071.
The patient's corrected QT interval (QTc) is 491.75071 msec."
7068,58,QTc Hodges Calculator,physical,decimal,88,Template,A patient has a heart rate of 170 bpm and a QT interval of 487 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [170, 'beats per minute'], 'QT Interval': [487, 'msec']}",679.50099,645.52594,713.47604,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 170 beats per minute.
The QT interval is 487 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/170 = 0.35294.
Hence, plugging in these values, we will get 487 + 1.75 * [(60/0.35294) - 60] = 679.50099.
The patient's corrected QT interval (QTc) is 679.50099 msec."
7069,58,QTc Hodges Calculator,physical,decimal,89,Template,A patient has a heart rate of 143 bpm and a QT interval of 458 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [143, 'beats per minute'], 'QT Interval': [458, 'msec']}",603.25025,573.08774,633.41276,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 143 beats per minute.
The QT interval is 458 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/143 = 0.41958.
Hence, plugging in these values, we will get 458 + 1.75 * [(60/0.41958) - 60] = 603.25025.
The patient's corrected QT interval (QTc) is 603.25025 msec."
7070,58,QTc Hodges Calculator,physical,decimal,90,Template,A patient has a heart rate of 68 bpm and a QT interval of 431 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [68, 'beats per minute'], 'QT Interval': [431, 'msec']}",445.0004,422.75038,467.25042,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 68 beats per minute.
The QT interval is 431 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/68 = 0.88235.
Hence, plugging in these values, we will get 431 + 1.75 * [(60/0.88235) - 60] = 445.0004.
The patient's corrected QT interval (QTc) is 445.0004 msec."
7071,58,QTc Hodges Calculator,physical,decimal,91,Template,A patient has a heart rate of 123 bpm and a QT interval of 302 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [123, 'beats per minute'], 'QT Interval': [302, 'msec']}",412.25215,391.63954,432.86476,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 123 beats per minute.
The QT interval is 302 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/123 = 0.4878.
Hence, plugging in these values, we will get 302 + 1.75 * [(60/0.4878) - 60] = 412.25215.
The patient's corrected QT interval (QTc) is 412.25215 msec."
7072,58,QTc Hodges Calculator,physical,decimal,92,Template,A patient has a heart rate of 57 bpm and a QT interval of 273 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [57, 'beats per minute'], 'QT Interval': [273, 'msec']}",267.75015,254.36264,281.13766,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 57 beats per minute.
The QT interval is 273 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/57 = 1.05263.
Hence, plugging in these values, we will get 273 + 1.75 * [(60/1.05263) - 60] = 267.75015.
The patient's corrected QT interval (QTc) is 267.75015 msec."
7073,58,QTc Hodges Calculator,physical,decimal,93,Template,A patient has a heart rate of 94 bpm and a QT interval of 408 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [94, 'beats per minute'], 'QT Interval': [408, 'msec']}",467.49945,444.12448,490.87442,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 94 beats per minute.
The QT interval is 408 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/94 = 0.6383.
Hence, plugging in these values, we will get 408 + 1.75 * [(60/0.6383) - 60] = 467.49945.
The patient's corrected QT interval (QTc) is 467.49945 msec."
7074,58,QTc Hodges Calculator,physical,decimal,94,Template,A patient has a heart rate of 94 bpm and a QT interval of 462 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [94, 'beats per minute'], 'QT Interval': [462, 'msec']}",521.49945,495.42448,547.57442,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 94 beats per minute.
The QT interval is 462 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/94 = 0.6383.
Hence, plugging in these values, we will get 462 + 1.75 * [(60/0.6383) - 60] = 521.49945.
The patient's corrected QT interval (QTc) is 521.49945 msec."
7075,58,QTc Hodges Calculator,physical,decimal,95,Template,A patient has a heart rate of 149 bpm and a QT interval of 307 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [149, 'beats per minute'], 'QT Interval': [307, 'msec']}",462.75296,439.61531,485.89061,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 149 beats per minute.
The QT interval is 307 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/149 = 0.40268.
Hence, plugging in these values, we will get 307 + 1.75 * [(60/0.40268) - 60] = 462.75296.
The patient's corrected QT interval (QTc) is 462.75296 msec."
7076,58,QTc Hodges Calculator,physical,decimal,96,Template,A patient has a heart rate of 154 bpm and a QT interval of 487 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [154, 'beats per minute'], 'QT Interval': [487, 'msec']}",651.50027,618.92526,684.07528,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 154 beats per minute.
The QT interval is 487 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/154 = 0.38961.
Hence, plugging in these values, we will get 487 + 1.75 * [(60/0.38961) - 60] = 651.50027.
The patient's corrected QT interval (QTc) is 651.50027 msec."
7077,58,QTc Hodges Calculator,physical,decimal,97,Template,A patient has a heart rate of 76 bpm and a QT interval of 234 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [76, 'beats per minute'], 'QT Interval': [234, 'msec']}",262.00062,248.90059,275.10065,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 76 beats per minute.
The QT interval is 234 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/76 = 0.78947.
Hence, plugging in these values, we will get 234 + 1.75 * [(60/0.78947) - 60] = 262.00062.
The patient's corrected QT interval (QTc) is 262.00062 msec."
7078,58,QTc Hodges Calculator,physical,decimal,98,Template,A patient has a heart rate of 120 bpm and a QT interval of 447 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [120, 'beats per minute'], 'QT Interval': [447, 'msec']}",552,524.4,579.6,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 120 beats per minute.
The QT interval is 447 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/120 = 0.5.
Hence, plugging in these values, we will get 447 + 1.75 * [(60/0.5) - 60] = 552.0.
The patient's corrected QT interval (QTc) is 552.0 msec."
7079,58,QTc Hodges Calculator,physical,decimal,99,Template,A patient has a heart rate of 146 bpm and a QT interval of 202 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [146, 'beats per minute'], 'QT Interval': [202, 'msec']}",352.49932,334.87435,370.12429,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 146 beats per minute.
The QT interval is 202 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/146 = 0.41096.
Hence, plugging in these values, we will get 202 + 1.75 * [(60/0.41096) - 60] = 352.49932.
The patient's corrected QT interval (QTc) is 352.49932 msec."
7080,58,QTc Hodges Calculator,physical,decimal,100,Template,A patient has a heart rate of 106 bpm and a QT interval of 441 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [106, 'beats per minute'], 'QT Interval': [441, 'msec']}",521.49926,495.4243,547.57422,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 106 beats per minute.
The QT interval is 441 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/106 = 0.56604.
Hence, plugging in these values, we will get 441 + 1.75 * [(60/0.56604) - 60] = 521.49926.
The patient's corrected QT interval (QTc) is 521.49926 msec."
7081,58,QTc Hodges Calculator,physical,decimal,101,Template,Patient has a heart rate of 108 bpm and a QT interval of 330 msec.,"Using the Hodges Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [108, 'beats per minute'], 'QT Interval': [330, 'msec']}",413.99849,393.29857,434.69841,"The corrected QT interval using the Hodges formula is computed as  QTc = QT interval + 1.75 * [(60 /rr_interval_sec) - 60], where QT interval is in msec, and RR interval is given as 60/(heart rate).
The patient's heart rate is 108 beats per minute.
The QT interval is 330 msec.
The RR interval is computed as 60/(heart rate), and so the RR interval is 60/108 = 0.55556.
Hence, plugging in these values, we will get 330 + 1.75 * [(60/0.55556) - 60] = 413.99849.
The patient's corrected QT interval (QTc) is 413.99849 msec."
7082,59,QTc Rautaharju Calculator,physical,decimal,22,Template,A patient has a heart rate of 81 bpm and a QT interval of 229 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [81, 'beats per minute'], 'QT Interval': [229, 'msec']}",255.71667,242.93084,268.5025,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 229 msec.
The patient's heart rate is 81 beats per minute.
Hence, plugging in these values, we will get 229 x (120 + 81) / 180 = 255.71667.
The patient's corrected QT interval (QTc) is 255.71667 msec."
7083,59,QTc Rautaharju Calculator,physical,decimal,23,Template,A patient has a heart rate of 67 bpm and a QT interval of 358 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [67, 'beats per minute'], 'QT Interval': [358, 'msec']}",371.92222,353.32611,390.51833,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 358 msec.
The patient's heart rate is 67 beats per minute.
Hence, plugging in these values, we will get 358 x (120 + 67) / 180 = 371.92222.
The patient's corrected QT interval (QTc) is 371.92222 msec."
7084,59,QTc Rautaharju Calculator,physical,decimal,24,Template,A patient has a heart rate of 109 bpm and a QT interval of 335 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [109, 'beats per minute'], 'QT Interval': [335, 'msec']}",426.19444,404.88472,447.50416,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 335 msec.
The patient's heart rate is 109 beats per minute.
Hence, plugging in these values, we will get 335 x (120 + 109) / 180 = 426.19444.
The patient's corrected QT interval (QTc) is 426.19444 msec."
7085,59,QTc Rautaharju Calculator,physical,decimal,25,Template,A patient has a heart rate of 52 bpm and a QT interval of 277 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [52, 'beats per minute'], 'QT Interval': [277, 'msec']}",264.68889,251.45445,277.92333,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 277 msec.
The patient's heart rate is 52 beats per minute.
Hence, plugging in these values, we will get 277 x (120 + 52) / 180 = 264.68889.
The patient's corrected QT interval (QTc) is 264.68889 msec."
7086,59,QTc Rautaharju Calculator,physical,decimal,26,Template,A patient has a heart rate of 112 bpm and a QT interval of 402 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [112, 'beats per minute'], 'QT Interval': [402, 'msec']}",518.13333,492.22666,544.04,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 402 msec.
The patient's heart rate is 112 beats per minute.
Hence, plugging in these values, we will get 402 x (120 + 112) / 180 = 518.13333.
The patient's corrected QT interval (QTc) is 518.13333 msec."
7087,59,QTc Rautaharju Calculator,physical,decimal,27,Template,A patient has a heart rate of 175 bpm and a QT interval of 268 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [175, 'beats per minute'], 'QT Interval': [268, 'msec']}",439.22222,417.26111,461.18333,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 268 msec.
The patient's heart rate is 175 beats per minute.
Hence, plugging in these values, we will get 268 x (120 + 175) / 180 = 439.22222.
The patient's corrected QT interval (QTc) is 439.22222 msec."
7088,59,QTc Rautaharju Calculator,physical,decimal,28,Template,A patient has a heart rate of 116 bpm and a QT interval of 460 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [116, 'beats per minute'], 'QT Interval': [460, 'msec']}",603.11111,572.95555,633.26667,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 460 msec.
The patient's heart rate is 116 beats per minute.
Hence, plugging in these values, we will get 460 x (120 + 116) / 180 = 603.11111.
The patient's corrected QT interval (QTc) is 603.11111 msec."
7089,59,QTc Rautaharju Calculator,physical,decimal,29,Template,A patient has a heart rate of 149 bpm and a QT interval of 446 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [149, 'beats per minute'], 'QT Interval': [446, 'msec']}",666.52222,633.19611,699.84833,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 446 msec.
The patient's heart rate is 149 beats per minute.
Hence, plugging in these values, we will get 446 x (120 + 149) / 180 = 666.52222.
The patient's corrected QT interval (QTc) is 666.52222 msec."
7090,59,QTc Rautaharju Calculator,physical,decimal,30,Template,A patient has a heart rate of 113 bpm and a QT interval of 392 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [113, 'beats per minute'], 'QT Interval': [392, 'msec']}",507.42222,482.05111,532.79333,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 392 msec.
The patient's heart rate is 113 beats per minute.
Hence, plugging in these values, we will get 392 x (120 + 113) / 180 = 507.42222.
The patient's corrected QT interval (QTc) is 507.42222 msec."
7091,59,QTc Rautaharju Calculator,physical,decimal,31,Template,A patient has a heart rate of 114 bpm and a QT interval of 391 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [114, 'beats per minute'], 'QT Interval': [391, 'msec']}",508.3,482.885,533.715,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 391 msec.
The patient's heart rate is 114 beats per minute.
Hence, plugging in these values, we will get 391 x (120 + 114) / 180 = 508.3.
The patient's corrected QT interval (QTc) is 508.3 msec."
7092,59,QTc Rautaharju Calculator,physical,decimal,32,Template,A patient has a heart rate of 122 bpm and a QT interval of 342 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [122, 'beats per minute'], 'QT Interval': [342, 'msec']}",459.8,436.81,482.79,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 342 msec.
The patient's heart rate is 122 beats per minute.
Hence, plugging in these values, we will get 342 x (120 + 122) / 180 = 459.8.
The patient's corrected QT interval (QTc) is 459.8 msec."
7093,59,QTc Rautaharju Calculator,physical,decimal,33,Template,A patient has a heart rate of 70 bpm and a QT interval of 323 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [70, 'beats per minute'], 'QT Interval': [323, 'msec']}",340.94444,323.89722,357.99166,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 323 msec.
The patient's heart rate is 70 beats per minute.
Hence, plugging in these values, we will get 323 x (120 + 70) / 180 = 340.94444.
The patient's corrected QT interval (QTc) is 340.94444 msec."
7094,59,QTc Rautaharju Calculator,physical,decimal,34,Template,A patient has a heart rate of 77 bpm and a QT interval of 403 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [77, 'beats per minute'], 'QT Interval': [403, 'msec']}",441.06111,419.00805,463.11417,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 403 msec.
The patient's heart rate is 77 beats per minute.
Hence, plugging in these values, we will get 403 x (120 + 77) / 180 = 441.06111.
The patient's corrected QT interval (QTc) is 441.06111 msec."
7095,59,QTc Rautaharju Calculator,physical,decimal,35,Template,A patient has a heart rate of 160 bpm and a QT interval of 238 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [160, 'beats per minute'], 'QT Interval': [238, 'msec']}",370.22222,351.71111,388.73333,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 238 msec.
The patient's heart rate is 160 beats per minute.
Hence, plugging in these values, we will get 238 x (120 + 160) / 180 = 370.22222.
The patient's corrected QT interval (QTc) is 370.22222 msec."
7096,59,QTc Rautaharju Calculator,physical,decimal,36,Template,A patient has a heart rate of 106 bpm and a QT interval of 407 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [106, 'beats per minute'], 'QT Interval': [407, 'msec']}",511.01111,485.46055,536.56167,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 407 msec.
The patient's heart rate is 106 beats per minute.
Hence, plugging in these values, we will get 407 x (120 + 106) / 180 = 511.01111.
The patient's corrected QT interval (QTc) is 511.01111 msec."
7097,59,QTc Rautaharju Calculator,physical,decimal,37,Template,A patient has a heart rate of 120 bpm and a QT interval of 445 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [120, 'beats per minute'], 'QT Interval': [445, 'msec']}",593.33333,563.66666,623,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 445 msec.
The patient's heart rate is 120 beats per minute.
Hence, plugging in these values, we will get 445 x (120 + 120) / 180 = 593.33333.
The patient's corrected QT interval (QTc) is 593.33333 msec."
7098,59,QTc Rautaharju Calculator,physical,decimal,38,Template,A patient has a heart rate of 159 bpm and a QT interval of 237 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [159, 'beats per minute'], 'QT Interval': [237, 'msec']}",367.35,348.9825,385.7175,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 237 msec.
The patient's heart rate is 159 beats per minute.
Hence, plugging in these values, we will get 237 x (120 + 159) / 180 = 367.35.
The patient's corrected QT interval (QTc) is 367.35 msec."
7099,59,QTc Rautaharju Calculator,physical,decimal,39,Template,A patient has a heart rate of 153 bpm and a QT interval of 292 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [153, 'beats per minute'], 'QT Interval': [292, 'msec']}",442.86667,420.72334,465.01,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 292 msec.
The patient's heart rate is 153 beats per minute.
Hence, plugging in these values, we will get 292 x (120 + 153) / 180 = 442.86667.
The patient's corrected QT interval (QTc) is 442.86667 msec."
7100,59,QTc Rautaharju Calculator,physical,decimal,40,Template,A patient has a heart rate of 143 bpm and a QT interval of 281 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [143, 'beats per minute'], 'QT Interval': [281, 'msec']}",410.57222,390.04361,431.10083,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 281 msec.
The patient's heart rate is 143 beats per minute.
Hence, plugging in these values, we will get 281 x (120 + 143) / 180 = 410.57222.
The patient's corrected QT interval (QTc) is 410.57222 msec."
7101,59,QTc Rautaharju Calculator,physical,decimal,41,Template,A patient has a heart rate of 48 bpm and a QT interval of 444 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [48, 'beats per minute'], 'QT Interval': [444, 'msec']}",414.4,393.68,435.12,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 444 msec.
The patient's heart rate is 48 beats per minute.
Hence, plugging in these values, we will get 444 x (120 + 48) / 180 = 414.4.
The patient's corrected QT interval (QTc) is 414.4 msec."
7102,59,QTc Rautaharju Calculator,physical,decimal,42,Template,A patient has a heart rate of 110 bpm and a QT interval of 362 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [110, 'beats per minute'], 'QT Interval': [362, 'msec']}",462.55556,439.42778,485.68334,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 362 msec.
The patient's heart rate is 110 beats per minute.
Hence, plugging in these values, we will get 362 x (120 + 110) / 180 = 462.55556.
The patient's corrected QT interval (QTc) is 462.55556 msec."
7103,59,QTc Rautaharju Calculator,physical,decimal,43,Template,A patient has a heart rate of 126 bpm and a QT interval of 362 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [126, 'beats per minute'], 'QT Interval': [362, 'msec']}",494.73333,469.99666,519.47,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 362 msec.
The patient's heart rate is 126 beats per minute.
Hence, plugging in these values, we will get 362 x (120 + 126) / 180 = 494.73333.
The patient's corrected QT interval (QTc) is 494.73333 msec."
7104,59,QTc Rautaharju Calculator,physical,decimal,44,Template,A patient has a heart rate of 99 bpm and a QT interval of 223 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [99, 'beats per minute'], 'QT Interval': [223, 'msec']}",271.31667,257.75084,284.8825,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 223 msec.
The patient's heart rate is 99 beats per minute.
Hence, plugging in these values, we will get 223 x (120 + 99) / 180 = 271.31667.
The patient's corrected QT interval (QTc) is 271.31667 msec."
7105,59,QTc Rautaharju Calculator,physical,decimal,45,Template,A patient has a heart rate of 62 bpm and a QT interval of 470 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [62, 'beats per minute'], 'QT Interval': [470, 'msec']}",475.22222,451.46111,498.98333,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 470 msec.
The patient's heart rate is 62 beats per minute.
Hence, plugging in these values, we will get 470 x (120 + 62) / 180 = 475.22222.
The patient's corrected QT interval (QTc) is 475.22222 msec."
7106,59,QTc Rautaharju Calculator,physical,decimal,46,Template,A patient has a heart rate of 159 bpm and a QT interval of 343 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [159, 'beats per minute'], 'QT Interval': [343, 'msec']}",531.65,505.0675,558.2325,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 343 msec.
The patient's heart rate is 159 beats per minute.
Hence, plugging in these values, we will get 343 x (120 + 159) / 180 = 531.65.
The patient's corrected QT interval (QTc) is 531.65 msec."
7107,59,QTc Rautaharju Calculator,physical,decimal,47,Template,A patient has a heart rate of 97 bpm and a QT interval of 204 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [97, 'beats per minute'], 'QT Interval': [204, 'msec']}",245.93333,233.63666,258.23,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 204 msec.
The patient's heart rate is 97 beats per minute.
Hence, plugging in these values, we will get 204 x (120 + 97) / 180 = 245.93333.
The patient's corrected QT interval (QTc) is 245.93333 msec."
7108,59,QTc Rautaharju Calculator,physical,decimal,48,Template,A patient has a heart rate of 145 bpm and a QT interval of 454 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [145, 'beats per minute'], 'QT Interval': [454, 'msec']}",668.38889,634.96945,701.80833,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 454 msec.
The patient's heart rate is 145 beats per minute.
Hence, plugging in these values, we will get 454 x (120 + 145) / 180 = 668.38889.
The patient's corrected QT interval (QTc) is 668.38889 msec."
7109,59,QTc Rautaharju Calculator,physical,decimal,49,Template,A patient has a heart rate of 47 bpm and a QT interval of 324 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [47, 'beats per minute'], 'QT Interval': [324, 'msec']}",300.6,285.57,315.63,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 324 msec.
The patient's heart rate is 47 beats per minute.
Hence, plugging in these values, we will get 324 x (120 + 47) / 180 = 300.6.
The patient's corrected QT interval (QTc) is 300.6 msec."
7110,59,QTc Rautaharju Calculator,physical,decimal,50,Template,A patient has a heart rate of 118 bpm and a QT interval of 349 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [118, 'beats per minute'], 'QT Interval': [349, 'msec']}",461.45556,438.38278,484.52834,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 349 msec.
The patient's heart rate is 118 beats per minute.
Hence, plugging in these values, we will get 349 x (120 + 118) / 180 = 461.45556.
The patient's corrected QT interval (QTc) is 461.45556 msec."
7111,59,QTc Rautaharju Calculator,physical,decimal,51,Template,A patient has a heart rate of 177 bpm and a QT interval of 368 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [177, 'beats per minute'], 'QT Interval': [368, 'msec']}",607.2,576.84,637.56,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 368 msec.
The patient's heart rate is 177 beats per minute.
Hence, plugging in these values, we will get 368 x (120 + 177) / 180 = 607.2.
The patient's corrected QT interval (QTc) is 607.2 msec."
7112,59,QTc Rautaharju Calculator,physical,decimal,52,Template,A patient has a heart rate of 106 bpm and a QT interval of 388 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [106, 'beats per minute'], 'QT Interval': [388, 'msec']}",487.15556,462.79778,511.51334,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 388 msec.
The patient's heart rate is 106 beats per minute.
Hence, plugging in these values, we will get 388 x (120 + 106) / 180 = 487.15556.
The patient's corrected QT interval (QTc) is 487.15556 msec."
7113,59,QTc Rautaharju Calculator,physical,decimal,53,Template,A patient has a heart rate of 111 bpm and a QT interval of 439 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [111, 'beats per minute'], 'QT Interval': [439, 'msec']}",563.38333,535.21416,591.5525,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 439 msec.
The patient's heart rate is 111 beats per minute.
Hence, plugging in these values, we will get 439 x (120 + 111) / 180 = 563.38333.
The patient's corrected QT interval (QTc) is 563.38333 msec."
7114,59,QTc Rautaharju Calculator,physical,decimal,54,Template,A patient has a heart rate of 114 bpm and a QT interval of 473 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [114, 'beats per minute'], 'QT Interval': [473, 'msec']}",614.9,584.155,645.645,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 473 msec.
The patient's heart rate is 114 beats per minute.
Hence, plugging in these values, we will get 473 x (120 + 114) / 180 = 614.9.
The patient's corrected QT interval (QTc) is 614.9 msec."
7115,59,QTc Rautaharju Calculator,physical,decimal,55,Template,A patient has a heart rate of 89 bpm and a QT interval of 401 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [89, 'beats per minute'], 'QT Interval': [401, 'msec']}",465.60556,442.32528,488.88584,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 401 msec.
The patient's heart rate is 89 beats per minute.
Hence, plugging in these values, we will get 401 x (120 + 89) / 180 = 465.60556.
The patient's corrected QT interval (QTc) is 465.60556 msec."
7116,59,QTc Rautaharju Calculator,physical,decimal,56,Template,A patient has a heart rate of 98 bpm and a QT interval of 342 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [98, 'beats per minute'], 'QT Interval': [342, 'msec']}",414.2,393.49,434.91,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 342 msec.
The patient's heart rate is 98 beats per minute.
Hence, plugging in these values, we will get 342 x (120 + 98) / 180 = 414.2.
The patient's corrected QT interval (QTc) is 414.2 msec."
7117,59,QTc Rautaharju Calculator,physical,decimal,57,Template,A patient has a heart rate of 99 bpm and a QT interval of 248 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [99, 'beats per minute'], 'QT Interval': [248, 'msec']}",301.73333,286.64666,316.82,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 248 msec.
The patient's heart rate is 99 beats per minute.
Hence, plugging in these values, we will get 248 x (120 + 99) / 180 = 301.73333.
The patient's corrected QT interval (QTc) is 301.73333 msec."
7118,59,QTc Rautaharju Calculator,physical,decimal,58,Template,A patient has a heart rate of 120 bpm and a QT interval of 485 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [120, 'beats per minute'], 'QT Interval': [485, 'msec']}",646.66667,614.33334,679,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 485 msec.
The patient's heart rate is 120 beats per minute.
Hence, plugging in these values, we will get 485 x (120 + 120) / 180 = 646.66667.
The patient's corrected QT interval (QTc) is 646.66667 msec."
7119,59,QTc Rautaharju Calculator,physical,decimal,59,Template,A patient has a heart rate of 178 bpm and a QT interval of 257 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [178, 'beats per minute'], 'QT Interval': [257, 'msec']}",425.47778,404.20389,446.75167,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 257 msec.
The patient's heart rate is 178 beats per minute.
Hence, plugging in these values, we will get 257 x (120 + 178) / 180 = 425.47778.
The patient's corrected QT interval (QTc) is 425.47778 msec."
7120,59,QTc Rautaharju Calculator,physical,decimal,60,Template,A patient has a heart rate of 48 bpm and a QT interval of 311 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [48, 'beats per minute'], 'QT Interval': [311, 'msec']}",290.26667,275.75334,304.78,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 311 msec.
The patient's heart rate is 48 beats per minute.
Hence, plugging in these values, we will get 311 x (120 + 48) / 180 = 290.26667.
The patient's corrected QT interval (QTc) is 290.26667 msec."
7121,59,QTc Rautaharju Calculator,physical,decimal,61,Template,A patient has a heart rate of 114 bpm and a QT interval of 340 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [114, 'beats per minute'], 'QT Interval': [340, 'msec']}",442,419.9,464.1,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 340 msec.
The patient's heart rate is 114 beats per minute.
Hence, plugging in these values, we will get 340 x (120 + 114) / 180 = 442.0.
The patient's corrected QT interval (QTc) is 442.0 msec."
7122,59,QTc Rautaharju Calculator,physical,decimal,62,Template,A patient has a heart rate of 156 bpm and a QT interval of 453 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [156, 'beats per minute'], 'QT Interval': [453, 'msec']}",694.6,659.87,729.33,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 453 msec.
The patient's heart rate is 156 beats per minute.
Hence, plugging in these values, we will get 453 x (120 + 156) / 180 = 694.6.
The patient's corrected QT interval (QTc) is 694.6 msec."
7123,59,QTc Rautaharju Calculator,physical,decimal,63,Template,A patient has a heart rate of 91 bpm and a QT interval of 393 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [91, 'beats per minute'], 'QT Interval': [393, 'msec']}",460.68333,437.64916,483.7175,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 393 msec.
The patient's heart rate is 91 beats per minute.
Hence, plugging in these values, we will get 393 x (120 + 91) / 180 = 460.68333.
The patient's corrected QT interval (QTc) is 460.68333 msec."
7124,59,QTc Rautaharju Calculator,physical,decimal,64,Template,A patient has a heart rate of 126 bpm and a QT interval of 463 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [126, 'beats per minute'], 'QT Interval': [463, 'msec']}",632.76667,601.12834,664.405,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 463 msec.
The patient's heart rate is 126 beats per minute.
Hence, plugging in these values, we will get 463 x (120 + 126) / 180 = 632.76667.
The patient's corrected QT interval (QTc) is 632.76667 msec."
7125,59,QTc Rautaharju Calculator,physical,decimal,65,Template,A patient has a heart rate of 63 bpm and a QT interval of 396 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [63, 'beats per minute'], 'QT Interval': [396, 'msec']}",402.6,382.47,422.73,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 396 msec.
The patient's heart rate is 63 beats per minute.
Hence, plugging in these values, we will get 396 x (120 + 63) / 180 = 402.6.
The patient's corrected QT interval (QTc) is 402.6 msec."
7126,59,QTc Rautaharju Calculator,physical,decimal,66,Template,A patient has a heart rate of 54 bpm and a QT interval of 302 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [54, 'beats per minute'], 'QT Interval': [302, 'msec']}",291.93333,277.33666,306.53,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 302 msec.
The patient's heart rate is 54 beats per minute.
Hence, plugging in these values, we will get 302 x (120 + 54) / 180 = 291.93333.
The patient's corrected QT interval (QTc) is 291.93333 msec."
7127,59,QTc Rautaharju Calculator,physical,decimal,67,Template,A patient has a heart rate of 171 bpm and a QT interval of 278 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [171, 'beats per minute'], 'QT Interval': [278, 'msec']}",449.43333,426.96166,471.905,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 278 msec.
The patient's heart rate is 171 beats per minute.
Hence, plugging in these values, we will get 278 x (120 + 171) / 180 = 449.43333.
The patient's corrected QT interval (QTc) is 449.43333 msec."
7128,59,QTc Rautaharju Calculator,physical,decimal,68,Template,A patient has a heart rate of 101 bpm and a QT interval of 227 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [101, 'beats per minute'], 'QT Interval': [227, 'msec']}",278.70556,264.77028,292.64084,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 227 msec.
The patient's heart rate is 101 beats per minute.
Hence, plugging in these values, we will get 227 x (120 + 101) / 180 = 278.70556.
The patient's corrected QT interval (QTc) is 278.70556 msec."
7129,59,QTc Rautaharju Calculator,physical,decimal,69,Template,A patient has a heart rate of 49 bpm and a QT interval of 404 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [49, 'beats per minute'], 'QT Interval': [404, 'msec']}",379.31111,360.34555,398.27667,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 404 msec.
The patient's heart rate is 49 beats per minute.
Hence, plugging in these values, we will get 404 x (120 + 49) / 180 = 379.31111.
The patient's corrected QT interval (QTc) is 379.31111 msec."
7130,59,QTc Rautaharju Calculator,physical,decimal,70,Template,A patient has a heart rate of 135 bpm and a QT interval of 448 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [135, 'beats per minute'], 'QT Interval': [448, 'msec']}",634.66667,602.93334,666.4,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 448 msec.
The patient's heart rate is 135 beats per minute.
Hence, plugging in these values, we will get 448 x (120 + 135) / 180 = 634.66667.
The patient's corrected QT interval (QTc) is 634.66667 msec."
7131,59,QTc Rautaharju Calculator,physical,decimal,71,Template,A patient has a heart rate of 113 bpm and a QT interval of 417 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [113, 'beats per minute'], 'QT Interval': [417, 'msec']}",539.78333,512.79416,566.7725,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 417 msec.
The patient's heart rate is 113 beats per minute.
Hence, plugging in these values, we will get 417 x (120 + 113) / 180 = 539.78333.
The patient's corrected QT interval (QTc) is 539.78333 msec."
7132,59,QTc Rautaharju Calculator,physical,decimal,72,Template,A patient has a heart rate of 114 bpm and a QT interval of 285 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [114, 'beats per minute'], 'QT Interval': [285, 'msec']}",370.5,351.975,389.025,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 285 msec.
The patient's heart rate is 114 beats per minute.
Hence, plugging in these values, we will get 285 x (120 + 114) / 180 = 370.5.
The patient's corrected QT interval (QTc) is 370.5 msec."
7133,59,QTc Rautaharju Calculator,physical,decimal,73,Template,A patient has a heart rate of 156 bpm and a QT interval of 311 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [156, 'beats per minute'], 'QT Interval': [311, 'msec']}",476.86667,453.02334,500.71,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 311 msec.
The patient's heart rate is 156 beats per minute.
Hence, plugging in these values, we will get 311 x (120 + 156) / 180 = 476.86667.
The patient's corrected QT interval (QTc) is 476.86667 msec."
7134,59,QTc Rautaharju Calculator,physical,decimal,74,Template,A patient has a heart rate of 64 bpm and a QT interval of 404 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [64, 'beats per minute'], 'QT Interval': [404, 'msec']}",412.97778,392.32889,433.62667,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 404 msec.
The patient's heart rate is 64 beats per minute.
Hence, plugging in these values, we will get 404 x (120 + 64) / 180 = 412.97778.
The patient's corrected QT interval (QTc) is 412.97778 msec."
7135,59,QTc Rautaharju Calculator,physical,decimal,75,Template,A patient has a heart rate of 83 bpm and a QT interval of 366 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [83, 'beats per minute'], 'QT Interval': [366, 'msec']}",412.76667,392.12834,433.405,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 366 msec.
The patient's heart rate is 83 beats per minute.
Hence, plugging in these values, we will get 366 x (120 + 83) / 180 = 412.76667.
The patient's corrected QT interval (QTc) is 412.76667 msec."
7136,59,QTc Rautaharju Calculator,physical,decimal,76,Template,A patient has a heart rate of 51 bpm and a QT interval of 365 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [51, 'beats per minute'], 'QT Interval': [365, 'msec']}",346.75,329.4125,364.0875,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 365 msec.
The patient's heart rate is 51 beats per minute.
Hence, plugging in these values, we will get 365 x (120 + 51) / 180 = 346.75.
The patient's corrected QT interval (QTc) is 346.75 msec."
7137,59,QTc Rautaharju Calculator,physical,decimal,77,Template,A patient has a heart rate of 153 bpm and a QT interval of 385 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [153, 'beats per minute'], 'QT Interval': [385, 'msec']}",583.91667,554.72084,613.1125,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 385 msec.
The patient's heart rate is 153 beats per minute.
Hence, plugging in these values, we will get 385 x (120 + 153) / 180 = 583.91667.
The patient's corrected QT interval (QTc) is 583.91667 msec."
7138,59,QTc Rautaharju Calculator,physical,decimal,78,Template,A patient has a heart rate of 178 bpm and a QT interval of 304 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [178, 'beats per minute'], 'QT Interval': [304, 'msec']}",503.28889,478.12445,528.45333,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 304 msec.
The patient's heart rate is 178 beats per minute.
Hence, plugging in these values, we will get 304 x (120 + 178) / 180 = 503.28889.
The patient's corrected QT interval (QTc) is 503.28889 msec."
7139,59,QTc Rautaharju Calculator,physical,decimal,79,Template,A patient has a heart rate of 57 bpm and a QT interval of 350 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [57, 'beats per minute'], 'QT Interval': [350, 'msec']}",344.16667,326.95834,361.375,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 350 msec.
The patient's heart rate is 57 beats per minute.
Hence, plugging in these values, we will get 350 x (120 + 57) / 180 = 344.16667.
The patient's corrected QT interval (QTc) is 344.16667 msec."
7140,59,QTc Rautaharju Calculator,physical,decimal,80,Template,A patient has a heart rate of 117 bpm and a QT interval of 335 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [117, 'beats per minute'], 'QT Interval': [335, 'msec']}",441.08333,419.02916,463.1375,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 335 msec.
The patient's heart rate is 117 beats per minute.
Hence, plugging in these values, we will get 335 x (120 + 117) / 180 = 441.08333.
The patient's corrected QT interval (QTc) is 441.08333 msec."
7141,59,QTc Rautaharju Calculator,physical,decimal,81,Template,A patient has a heart rate of 94 bpm and a QT interval of 453 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [94, 'beats per minute'], 'QT Interval': [453, 'msec']}",538.56667,511.63834,565.495,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 453 msec.
The patient's heart rate is 94 beats per minute.
Hence, plugging in these values, we will get 453 x (120 + 94) / 180 = 538.56667.
The patient's corrected QT interval (QTc) is 538.56667 msec."
7142,59,QTc Rautaharju Calculator,physical,decimal,82,Template,A patient has a heart rate of 85 bpm and a QT interval of 315 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [85, 'beats per minute'], 'QT Interval': [315, 'msec']}",358.75,340.8125,376.6875,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 315 msec.
The patient's heart rate is 85 beats per minute.
Hence, plugging in these values, we will get 315 x (120 + 85) / 180 = 358.75.
The patient's corrected QT interval (QTc) is 358.75 msec."
7143,59,QTc Rautaharju Calculator,physical,decimal,83,Template,A patient has a heart rate of 135 bpm and a QT interval of 488 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [135, 'beats per minute'], 'QT Interval': [488, 'msec']}",691.33333,656.76666,725.9,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 488 msec.
The patient's heart rate is 135 beats per minute.
Hence, plugging in these values, we will get 488 x (120 + 135) / 180 = 691.33333.
The patient's corrected QT interval (QTc) is 691.33333 msec."
7144,59,QTc Rautaharju Calculator,physical,decimal,84,Template,A patient has a heart rate of 66 bpm and a QT interval of 479 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [66, 'beats per minute'], 'QT Interval': [479, 'msec']}",494.96667,470.21834,519.715,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 479 msec.
The patient's heart rate is 66 beats per minute.
Hence, plugging in these values, we will get 479 x (120 + 66) / 180 = 494.96667.
The patient's corrected QT interval (QTc) is 494.96667 msec."
7145,59,QTc Rautaharju Calculator,physical,decimal,85,Template,A patient has a heart rate of 142 bpm and a QT interval of 356 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [142, 'beats per minute'], 'QT Interval': [356, 'msec']}",518.17778,492.26889,544.08667,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 356 msec.
The patient's heart rate is 142 beats per minute.
Hence, plugging in these values, we will get 356 x (120 + 142) / 180 = 518.17778.
The patient's corrected QT interval (QTc) is 518.17778 msec."
7146,59,QTc Rautaharju Calculator,physical,decimal,86,Template,A patient has a heart rate of 165 bpm and a QT interval of 359 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [165, 'beats per minute'], 'QT Interval': [359, 'msec']}",568.41667,539.99584,596.8375,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 359 msec.
The patient's heart rate is 165 beats per minute.
Hence, plugging in these values, we will get 359 x (120 + 165) / 180 = 568.41667.
The patient's corrected QT interval (QTc) is 568.41667 msec."
7147,59,QTc Rautaharju Calculator,physical,decimal,87,Template,A patient has a heart rate of 75 bpm and a QT interval of 252 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [75, 'beats per minute'], 'QT Interval': [252, 'msec']}",273,259.35,286.65,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 252 msec.
The patient's heart rate is 75 beats per minute.
Hence, plugging in these values, we will get 252 x (120 + 75) / 180 = 273.0.
The patient's corrected QT interval (QTc) is 273.0 msec."
7148,59,QTc Rautaharju Calculator,physical,decimal,88,Template,A patient has a heart rate of 154 bpm and a QT interval of 211 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [154, 'beats per minute'], 'QT Interval': [211, 'msec']}",321.18889,305.12945,337.24833,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 211 msec.
The patient's heart rate is 154 beats per minute.
Hence, plugging in these values, we will get 211 x (120 + 154) / 180 = 321.18889.
The patient's corrected QT interval (QTc) is 321.18889 msec."
7149,59,QTc Rautaharju Calculator,physical,decimal,89,Template,A patient has a heart rate of 103 bpm and a QT interval of 206 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [103, 'beats per minute'], 'QT Interval': [206, 'msec']}",255.21111,242.45055,267.97167,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 206 msec.
The patient's heart rate is 103 beats per minute.
Hence, plugging in these values, we will get 206 x (120 + 103) / 180 = 255.21111.
The patient's corrected QT interval (QTc) is 255.21111 msec."
7150,59,QTc Rautaharju Calculator,physical,decimal,90,Template,A patient has a heart rate of 141 bpm and a QT interval of 370 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [141, 'beats per minute'], 'QT Interval': [370, 'msec']}",536.5,509.675,563.325,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 370 msec.
The patient's heart rate is 141 beats per minute.
Hence, plugging in these values, we will get 370 x (120 + 141) / 180 = 536.5.
The patient's corrected QT interval (QTc) is 536.5 msec."
7151,59,QTc Rautaharju Calculator,physical,decimal,91,Template,A patient has a heart rate of 97 bpm and a QT interval of 296 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [97, 'beats per minute'], 'QT Interval': [296, 'msec']}",356.84444,339.00222,374.68666,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 296 msec.
The patient's heart rate is 97 beats per minute.
Hence, plugging in these values, we will get 296 x (120 + 97) / 180 = 356.84444.
The patient's corrected QT interval (QTc) is 356.84444 msec."
7152,59,QTc Rautaharju Calculator,physical,decimal,92,Template,A patient has a heart rate of 168 bpm and a QT interval of 276 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [168, 'beats per minute'], 'QT Interval': [276, 'msec']}",441.6,419.52,463.68,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 276 msec.
The patient's heart rate is 168 beats per minute.
Hence, plugging in these values, we will get 276 x (120 + 168) / 180 = 441.6.
The patient's corrected QT interval (QTc) is 441.6 msec."
7153,59,QTc Rautaharju Calculator,physical,decimal,93,Template,A patient has a heart rate of 89 bpm and a QT interval of 210 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [89, 'beats per minute'], 'QT Interval': [210, 'msec']}",243.83333,231.64166,256.025,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 210 msec.
The patient's heart rate is 89 beats per minute.
Hence, plugging in these values, we will get 210 x (120 + 89) / 180 = 243.83333.
The patient's corrected QT interval (QTc) is 243.83333 msec."
7154,59,QTc Rautaharju Calculator,physical,decimal,94,Template,A patient has a heart rate of 140 bpm and a QT interval of 376 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [140, 'beats per minute'], 'QT Interval': [376, 'msec']}",543.11111,515.95555,570.26667,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 376 msec.
The patient's heart rate is 140 beats per minute.
Hence, plugging in these values, we will get 376 x (120 + 140) / 180 = 543.11111.
The patient's corrected QT interval (QTc) is 543.11111 msec."
7155,59,QTc Rautaharju Calculator,physical,decimal,95,Template,A patient has a heart rate of 57 bpm and a QT interval of 484 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [57, 'beats per minute'], 'QT Interval': [484, 'msec']}",475.93333,452.13666,499.73,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 484 msec.
The patient's heart rate is 57 beats per minute.
Hence, plugging in these values, we will get 484 x (120 + 57) / 180 = 475.93333.
The patient's corrected QT interval (QTc) is 475.93333 msec."
7156,59,QTc Rautaharju Calculator,physical,decimal,96,Template,A patient has a heart rate of 107 bpm and a QT interval of 408 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [107, 'beats per minute'], 'QT Interval': [408, 'msec']}",514.53333,488.80666,540.26,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 408 msec.
The patient's heart rate is 107 beats per minute.
Hence, plugging in these values, we will get 408 x (120 + 107) / 180 = 514.53333.
The patient's corrected QT interval (QTc) is 514.53333 msec."
7157,59,QTc Rautaharju Calculator,physical,decimal,97,Template,A patient has a heart rate of 59 bpm and a QT interval of 496 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [59, 'beats per minute'], 'QT Interval': [496, 'msec']}",493.24444,468.58222,517.90666,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 496 msec.
The patient's heart rate is 59 beats per minute.
Hence, plugging in these values, we will get 496 x (120 + 59) / 180 = 493.24444.
The patient's corrected QT interval (QTc) is 493.24444 msec."
7158,59,QTc Rautaharju Calculator,physical,decimal,98,Template,A patient has a heart rate of 152 bpm and a QT interval of 365 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [152, 'beats per minute'], 'QT Interval': [365, 'msec']}",551.55556,523.97778,579.13334,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 365 msec.
The patient's heart rate is 152 beats per minute.
Hence, plugging in these values, we will get 365 x (120 + 152) / 180 = 551.55556.
The patient's corrected QT interval (QTc) is 551.55556 msec."
7159,59,QTc Rautaharju Calculator,physical,decimal,99,Template,A patient has a heart rate of 96 bpm and a QT interval of 284 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [96, 'beats per minute'], 'QT Interval': [284, 'msec']}",340.8,323.76,357.84,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 284 msec.
The patient's heart rate is 96 beats per minute.
Hence, plugging in these values, we will get 284 x (120 + 96) / 180 = 340.8.
The patient's corrected QT interval (QTc) is 340.8 msec."
7160,59,QTc Rautaharju Calculator,physical,decimal,100,Template,A patient has a heart rate of 56 bpm and a QT interval of 302 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [56, 'beats per minute'], 'QT Interval': [302, 'msec']}",295.28889,280.52445,310.05333,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 302 msec.
The patient's heart rate is 56 beats per minute.
Hence, plugging in these values, we will get 302 x (120 + 56) / 180 = 295.28889.
The patient's corrected QT interval (QTc) is 295.28889 msec."
7161,59,QTc Rautaharju Calculator,physical,decimal,101,Template,Patient has a heart rate of 56 bpm and a QT interval of 330 msec.,"Using the Rautaharju Formula for corrected QT interval, what is the patient's corrected QT interval in terms of msec?","{'Heart Rate or Pulse': [56, 'beats per minute'], 'QT Interval': [330, 'msec']}",322.66667,306.53334,338.8,"The corrected QT interval using the Rautaharju formula is computed as QTc = QT interval x (120 + HR) / 180, where QT interval is in msec, and HR is the heart rate in beats per minute.
The QT interval is 330 msec.
The patient's heart rate is 56 beats per minute.
Hence, plugging in these values, we will get 330 x (120 + 56) / 180 = 322.66667.
The patient's corrected QT interval (QTc) is 322.66667 msec."
7162,60,Body Surface Area Calculator,physical,decimal,pmc-6389502-1,Extracted,"The patient was a 34-year-old Japanese man, whose family history included a father with hypertension, and a mother that suffered a subarachnoid hemorrhage, but which did not include either a consanguineous marriage or any incidence of renal cysts. At the age of 31, the patient presented with mild albuminuria, and a serum creatinine (Cr) level of 2.98 mg/dL. At the age of 34, the patient was admitted to hospital with a creatinine level of 8.2 mg/dL.
Upon admission, the patient's height, weight, and blood pressure were 179 cm, 58 kg, and 126/80 mm Hg, respectively. The patient exhibited anemia (Hb 8.2 g/dL), azotemia (Cr 8.38 mg/dL), hyperphosphatemia, metabolic acidosis, and secondary hyperparathyroidism; thus, he was diagnosed with ESRD. An abdominal ultrasonography revealed that, although the size of both kidneys appeared to be normal, the patient's renal parenchyma showed increased brightness. We performed a percutaneous renal biopsy; histologically, six of 16 glomeruli displayed global sclerosis, along with mild cellular infiltration, conspicuous interstitial fibrosis, renal tubular atrophy, and cystoid irregular dilation (Figure ), suggesting an NPHP diagnosis. We performed targeted sequencing using a next-generation sequencer, with the approval by the research ethics committee of Tokyo Medical and Dental University in accordance with the Declaration of Helsinki and the patient's written informed consent. A homozygous full gene deletion of NPHP1 (NM_000272.3:g110879716-110962709) was resultantly identified, as well as heterozygous substitutions in PKD1 (NM_0001009944.2:c.6395T>G(p.Phe2132Cys)) (Figure ), BBS1 (NM_024649.4:c.908T>C(p.Val303Ala)), and INPP5E (NM_019892.4:c.1652C>T(p.Thr551Met)).",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [58.0, 'kg'], 'height': [179.0, 'cm']}",1.6982,1.61329,1.78311,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 179.0 cm. 
The patient's weight is 58.0 kg. 
Therefore, the patient's bsa is sqrt((58.0 (in kgs) * 179.0 (in cm))/3600) = 1.6982 m^2."
7163,60,Body Surface Area Calculator,physical,decimal,pmc-3337389-1,Extracted,"A 65-year-old woman (weight, 44 kg; height, 153 cm) was admitted to our hospital for an elective total thyroidectomy. She had been diagnosed with a papillary carcinoma of the thyroid. Her medical history included hypertension, minor depression, a cerebral infarction, and brain surgery. Her medications included aspirin, a calcium channel blocker, and antidepressant. The preoperative chest radiograph and electrocardiography revealed no abnormalities. Echocardiography revealed mild pulmonary hypertension. The blood tests were within the normal limits.
Her blood pressure, heart rate and SpO2 was 140/70 mmHg, 80 beats/min and 99%, respectively. General anesthesia was induced with thiopental 5 mg/kg and rocuronium 0.6 mg/kg. She was intubated without problems using a 7.0 mm oral endotracheal tube that was fixed 22 cm from the mouth. Anesthesia was maintained with air 1 L/min, O2 1 L/min, sevoflurane 1-2 vol% and a continuous infusion of remifentanil 0.01-0.05 µg/kg/min. Her vital signs, airway pressures, and end-tidal CO2 remained stable during surgery. The planned surgical procedure was performed uneventfully in 2 hours and 55 minutes. A total volume of 900 ml lactated Ringer's solution was administered. During surgery, the estimated blood loss was 200 ml and urine output was 300 ml. After reversing the muscle relaxant, the patient was extubated in the operating room after confirming her ability to obey commands and her full recovery of motor function as tested by the hand grip and head control.
On the way to the post-anesthesia care unit, the patient was unable to breath and became cyanotic. The initial blood pressure at the recovery room was 110/60 mmHg, heart rate was 90 beats/min, and SpO2 was 78%. The oral airway was maintained and manual bagging was started with 100% oxygen at 10 L/min but there was considerable resistance and adequate oxygenation could not be maintained. A decision was made to reintubate the patient with midazolam 2 mg and succinylcholine 2 mg/kg while inserting an arterial line catheter into the left radial artery. Direct laryngoscopy revealed no specific abnormalities, such as laryngeal edema or aspirate. The patient was intubated successfully with a 7.0-mm endotracheal tube and ventilated several times with a bag valve mask with less resistance. However, a large volume of pink, frothy fluid emerged from the endotracheal tube, prompting an interim diagnosis of pulmonary edema. Pulmonary auscultation revealed moist rales in the entire bilateral lung fields. Despite the continued manual ventilation and tracheal suction with 100% O2, the SpO2 remained at approximately 80%. The first arterial blood gas analysis was as follows: pH 7.40, PaCO2 30.4 mmHg, PaO2 35.0 mmHg, SaO2 66.8% at FiO2 1.0. A portable chest radiograph confirmed the typical pattern of pulmonary edema with symmetric bilateral infiltrates and a slightly enlarged heart (). As a treatment of pulmonary edema, morphine 3 mg and furosemide 20 mg were administered. After 10 minutes, spontaneous respiration was observed and the patient could reply to verbal commands.
The patient was transferred to the ICU for ventilatory support with a positive end-expiratory pressure (PEEP) of 7 cm H2O. The patient's SpO2 remained > 97% on 100% oxygen. The follow-up arterial blood gas analysis was as follows: pH 7.39, PaCO2 33.6 mmHg, PaO2 125 mmHg, SaO2 98.9% at FiO2 1.0. The cardiac enzyme studies and echocardiography were unremarkable. Extubation was attempted on the second postoperative day because her SpO2 remained at 100%, her breathing was spontaneous, and her chest radiograph had improved (). Immediately after extubation, however, the patient became cyanotic and hypoxia developed and she was reintubated. According to the advice of our cardiologist colleagues, repeated echocardiography and coronary angiography was performed, which suggested transient stress-induced cardiomyopathy. Dobutamine 5 µg/kg/min was infused. The patient was extubated successfully and weaned from the dobutamine infusion on the sixth postoperative day but still showed some degree of dyspnea on 3 L/min via nasal cannula. Otolaryngology consultation attributed the residual dyspnea and the initial upper airway obstruction to bilateral vocal cord dysfunction. Given the possibility of sudden respiratory arrest, the patient underwent a tracheostomy.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [44.0, 'kg'], 'height': [153.0, 'cm']}",1.36748,1.29911,1.43585,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 153.0 cm. 
The patient's weight is 44.0 kg. 
Therefore, the patient's bsa is sqrt((44.0 (in kgs) * 153.0 (in cm))/3600) = 1.36748 m^2."
7164,60,Body Surface Area Calculator,physical,decimal,usmle-15,Extracted,"A 34-year-old man with AIDS comes to the physician because of a 2-day history of decreasing vision and seeing black spots in his right eye. He has no pain and the left eye is asymptomatic. He was treated for fungal esophagitis 6 months ago with fluconazole. He was diagnosed with Kaposi's sarcoma 2 years ago. Current medications include efavirenz, tenofovir, emtricitabine, azithromycin, trimethoprim-sulfamethoxazole, multivitamins, and a nutritional supplement. He is 170 cm (5 ft 7 in) tall and weighs 45 kg (99 lbs);BMI is 15.6 kg/m2. His temperature is 37°C (98.6°F), pulse is 89/min, and blood pressure is 110/70 mm Hg. Examination shows cervical lymphadenopathy. There are multiple violaceous plaques seen over his trunk and extremities. Fundoscopic examination shows granular yellow-white opacities around the retinal vessels and multiple areas of dot-blot hemorrhages. His CD4+ T-lymphocyte count is 36/mm3.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.0, 'kg'], 'height': [170.0, 'cm']}",1.45774,1.38485,1.53063,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 170.0 cm. 
The patient's weight is 45.0 kg. 
Therefore, the patient's bsa is sqrt((45.0 (in kgs) * 170.0 (in cm))/3600) = 1.45774 m^2."
7165,60,Body Surface Area Calculator,physical,decimal,trec-ct-2021-71,Extracted,"The patient is a 34-year-old obese woman who comes to the clinic with weight concerns. She is 165 cm tall, and her weight is 113 kg (BMI: 41.5).  In the past, she unsuccessfully used  antiobesity agents and appetite suppressants. She is complaining of sleep apnea, PCO and dissatisfaction with her body shape. She is a high-school teacher. She is married for 5 years. She doesn't use any contraceptive methods for the past 4 months and she had no prior pregnancies. She rarely exercises and movement seems to be hard for her. She is not able to complete  the four-square step test in less than 15 seconds. She does not smoke or use any drugs. Her BP: 130/80, HR: 195/min and her BMI is: 41.54. Her lab results:
FBS: 98 mg/dl
TG: 150 mg/dl
Cholesterol: 180 mg/dl
LDL: 90 mg/dl
HDL: 35 mg/dl
She is considering a laparoscopic gastric bypass.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [113.0, 'kg'], 'height': [165.0, 'cm']}",2.27578,2.16199,2.38957,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 165.0 cm. 
The patient's weight is 113.0 kg. 
Therefore, the patient's bsa is sqrt((113.0 (in kgs) * 165.0 (in cm))/3600) = 2.27578 m^2."
7166,60,Body Surface Area Calculator,physical,decimal,pmc-4273471-1,Extracted,"GK is a 43-year-old right-hand dominant nonsmoking female who presented to our office with right shoulder pain. The patient had symptoms for nine months following a motor-vehicle accident where she was a restrained passenger. The patient stated she had severe pain at the anterolateral aspect of her right shoulder, difficulty lifting greater than five pounds, limited overhead motion, and subjective catching. Physical examination showed her height, weight, and body mass index were 61 inches, 135 pounds, and 25.51, respectively. After history, physical, and radiographic examination, the patient was diagnosed with a rotator cuff strain, long head biceps tenosynovitis, and acromioclavicular joint osteolysis. Over the course of one year, the patient attended 36 sessions of physical therapy, participated in a home exercise program and underwent a subacromial cortisone injection with only temporary relief. Due to her lack of progress with conservative measures, an MRI arthrogram was obtained which showed a moderate bursal-sided tear of the supraspinatus, moderate acromioclavicular joint osteolysis, and a type II superior labrum anterior posterior (SLAP) lesion. A discussion of nonoperative versus operative treatment options, outcomes, and complications occurred and the patient elected to go forward with surgery.
After being brought into the operating room, the patient underwent an interscalene nerve block for intraoperative and postoperative pain control using a nerve stimulator. Bilateral lower extremity sequential compression devices were applied for deep vein thrombosis prophylaxis. General endotracheal tube anesthesia (GETA) was administered. The patient was then positioned into the modified lateral decubitus position (patient rolled back 30 degrees) using a foam wedge with all bony prominences well padded. An axillary roll was placed one hand breadth distal to the axilla, and the patient was secured with Velcro straps. After sterile draping and time-out, the patient's operative extremity was placed in ten pounds of balanced suspension in the scapular plane.
Upon shoulder arthroscopy, the patient was found to have a type II SLAP lesion with a long head biceps that had inflammation and fraying. The articular side of the rotator cuff had mild fraying. When viewing the subacromial space, the patient's rotator cuff was found to have significant fraying, fragmentation, and thinning of the bursal side (type A1, B3). When probed, the supraspinatus was found to be of inadequate quality due to intrasubstance tearing. In addition, the acromioclavicular joint was arthritic. As a result, the patient underwent an arthroscopic take-down and repair of the rotator cuff, a distal clavicle excision, and a miniopen subpectoralis long head biceps tenodesis. The duration of the surgery was one hour and 45 minutes with the duration of balanced suspension one hour and 20 minutes. There were no complications intraoperatively. The patient was placed into a sling with an abduction pillow and awoken from the anesthesia with no incident. She was taken to the postanesthesia care unit in good condition.
At her initial postoperative visit six days after surgery, the patient presented with occasional pain in her shoulder with moderate swelling. She denied nausea, vomiting, fever, chills, and sweats and had no calf tenderness. She was not menopausal. She was taking Percocet as needed as with appropriate relief but otherwise denied any additional medication history. Her incisions were clean and dry, and the stitches were removed and steri-strips applied. The patient was instructed to continue wearing her sling and abduction pillow except when performing twice daily Codman's exercises. Exercises for elbow, wrist, and finger range of motion were demonstrated, and the patient was advised to perform these twice per day.
At four weeks postoperatively, the patient's pain was well-controlled with no requirement for pain medication, and her wounds were well-healed. She denied fevers, chills, and calf pain. Her sling was discontinued and formal physical therapy was initiated as per our standard rotator cuff repair and biceps tenodesis protocol.
41 days postoperatively, the patient called our office with new-onset right-hand swelling and trouble breathing. She also reported that she had been feeling “flu-like symptoms” and stomach pains. She had no calf pain or lower extremity swelling. The patient was able to send our office a picture of her swollen hand over a secure email service with patient identification removed (). After seeing the photograph, she was advised to immediately follow up with us where upper extremity swelling and slightly labored breathing were confirmed.
Vital signs were stable and we ordered a stat computed tomography (CT) pulmonary angiogram, which revealed that the patient had an acute pulmonary embolism (PE) in the subsegmental posterior basal segment artery of the right lower lobe (). A stat hematology consult was arranged, and the patient was admitted through the emergency room to the hematology service for further evaluation and management. The patient was started on a therapeutic dose of Lovenox and subsequently transitioned to per-oral Xarelto. Three days after admission, she underwent a bilateral upper extremity venous duplex ultrasound that was negative for deep vein thrombosis (DVT). An immediate ultrasound upon admission was not performed due to the hematologist service's need to stabilize the patient prior to additional testing. She had no pain, swelling, or tenderness in the left upper extremity or bilateral lower extremities. A full hematology analysis was performed and was negative for any predisposing genetic factors for VTE. In assessing the patient's objective risk factors for VTE, a Revised Geneva Score was calculated and resulted in a score of two, corresponding to low risk for DVT [].
Three days after initiation of anticoagulation therapy, the patient's constitutional symptoms and discomfort with breathing resolved. Two weeks later, her upper extremity swelling resolved. Although her preoperative pain was completely resolved, the patient developed postoperative stiffness, and at six months postoperatively she had a protracted humeral head with active forward elevation 130 degrees, external rotation 45 degrees, and internal rotation to L5. Her strength with regard to her supraspinatus, infraspinatus, subscapularis, and biceps was 5/5 with no pain, and a postoperative MRI at 6 months postoperatively showed complete healing of the supraspinatus repair and long head biceps tenodesis.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [135.0, 'lbs'], 'height': [61.0, 'in']}",1.62342,1.54225,1.70459,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 61.0 in, which is 61.0 in * 2.54 cm/in = 154.94 cm. 
The patient's weight is 135.0 lbs so this converts to 135.0 lbs * 0.453592 kg/lbs = 61.23492 kg. 
Therefore, the patient's bsa is sqrt((61.23492 (in kgs) * 154.94 (in cm))/3600) = 1.62342 m^2."
7167,60,Body Surface Area Calculator,physical,decimal,pmc-4564715-1,Extracted,"A 53-year-old female patient diagnosed with DM1 was transferred to the rehabilitation medicine department due to gait disturbance. She presented with myotonia, disabling distal weakness, dysarthria, dysphagia, dementia, and cataract. Dominant limb weakness started about a year prior. Since then she was housebound, and experienced difficulty in sit to stand with visible gait deviation which developed for the past 6 months. Anthropometric data at initial admission revealed a height of 160 cm, and weight of 46 kg with equivalent body mass index 18 kg/m2. Initial blood test showed total cholesterol 353 mg/dL, triglyceride 418 mg/dL, LDL cholesterol 147 mg/dL, HDL cholesterol 39 mg/dL, blood glucose 105 mg/dL, but parameters reflecting liver and thyroid function were within normal range. Clinical signs concerned with diabetes were not detected. She had been taking oral statin for 2 years before the admission. On electromyography, denervation potentials and myotonic discharges were evident in all tested muscles. Southern blot analysis revealed about 650 trinucleotide (CTG) repeats expansion in the DMPK gene. She was diagnosed as DM1. She had a smoking history of 7 pack/year and alcohol abuse for the past 10 years.
In the course of rehabilitation, she intermittently complained of vague claudication of both lower limbs. Physical exam revealed weak pulsation of dorsalis pedis arteries with pale coloration of both ankles. Under the impression of deep vein thrombosis or PAOD, the following studies were performed. Ankle-brachial index (ABI) values were 0.09 on right side and 0.42 on left side (). Duplex ultrasonography study of lower extremity revealed a pulsus tardus parvus on femoral, popliteal, tibial and dorsalis pedis arteries (). Three-dimensional reconstructed abdomen computed tomography (CT) angiography showed concentric wall thickening and tapering occlusion in the distal abdominal aorta at 3.5 cm below the renal artery (). Under the impression of PAOD, she was advised to undergo bypass surgery from a thoracic surgery specialist. Preoperative pulmonary function test showed severe restrictive pattern (FVC, 42%; FEV1, 47%). The expected high cardiopulmonary risks of general anesthesia and surgery made us reluctant to conduct bypass surgery. However, due to diffuse extensive occlusive lesions and the patient's strong desire for the surgery, aortobifemoral artery bypass was performed. Biopsy showed fibrous wall thickening with intimal yellow patch lesion, confirmative of PAOD. Postoperative CT angiography showed patent lumen of the bypassed artery (). However, she did not recover from the post-operative respiratory complications, and died of respiratory failure 54 days after the operation.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [46.0, 'kg'], 'height': [160.0, 'cm']}",1.42984,1.35835,1.50133,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 160.0 cm. 
The patient's weight is 46.0 kg. 
Therefore, the patient's bsa is sqrt((46.0 (in kgs) * 160.0 (in cm))/3600) = 1.42984 m^2."
7168,60,Body Surface Area Calculator,physical,decimal,pmc-6360029-1,Extracted,"A 64-year-old woman was referred to our hospital for the treatment of chest wall necrosis. She had undergone Halsted surgery and postoperative radiation therapy with cobalt-60 (30 Gray) and megavoltage X-rays (30 Gray) 25 years earlier. Following the treatment, her left upper limb became completely paralyzed.
Six years earlier, she had sustained a left clavicle fracture due to osteonecrosis, and she had subsequently developed a chronic cutaneous fistula measuring 1 cm in diameter. The fracture and cutaneous fistula failed to heal, and she experienced bleeding from the fistula since 1 year. Two months before visiting our hospital, she was hospitalized in the Department of Breast Surgery at another hospital for massive bleeding and local infection. She was treated with antibiotics and cleansing of the fistula and the infection subsided 2 months thereafter. She visited our hospital after discharge.
At initial examination, her height was 153 cm and weight was 34 kg. Necrosed clavicle was exposed through the 6-cm-wide skin defect in the left clavicular region, and air entered and exited the opening from deep within the chest while breathing (Fig. ). Computed tomography (CT) revealed the part of the first to third left ribs, part of the left clavicle, the subclavian artery, and the brachial plexus to be missing. Her upper left limb was nourished by retrograde blood flow from the thoracodorsal artery; however, blood flow was weak to the skin of the arm, the surface of which was cold, resulting in complete paralysis of the upper extremity. Several rounds of debridement eliminated the necrotic tissue, and the local infection was completely resolved. Debridement revealed a tissue defect measuring 4 cm × 8 cm and 4 cm deep at the base and approximately 10 bronchial stumps on the surface of the collapsed lung covered in granulation tissue, from which exhaled air and sputum were effusing (Fig. ). She presented with severe emaciation and malnutrition, but no other systemic anomalies were noted.
After treatment, she had almost no problem with daily life but frequently coughed while taking baths or when exposed to cold air. Therefore, she consented to undergo the surgical closure of the pulmonary fistula. A left latissimus myocutaneous flap could not be used as the reconstructive material due to the absence of vascular pedicle (Fig. ). A free rectus abdominis flap was considered, but an omental flap was ultimately selected for its perceived ability to create the best air seal. Owing to her severe emaciation, the volume of the omentum available for harvest was considered inadequate; therefore, she was administered a diet by a nutritionist for 9 months to improve her systemic nutritional state and thereby increase her resistance. Subsequently, her weight increased from 34 kg to 38 kg, and her serum albumin level improved from 3.0 g/dL to 3.7 g/dL. Reconstructive surgery was performed. Preoperative blood gas analysis revealed pH of 7.400, carbon dioxide partial pressure of 45.3 mmHg, and oxygen partial pressure of 84.3 mmHg. Lung function test performed while holding down the pulmonary fistula revealed forced vital capacity of 1.16 L and forced expiratory volume as 1% of 100%.
Surgery was performed under general anesthesia with selective one lung ventilation.
The damaged skin, clavicle, and ribs surrounding the defect were debrided. The base of the defect was covered with hemorrhagic granulation tissue and was only rubbed with gauze for debridement to avoid over expansion of the bronchial stumps. A free omental flap (approximately 155 cc) with the right gastroepiploic blood vessel as its pedicle was harvested under laparoscopy. The right transverse cervical artery and right anterior jugular vein were anastomosed with the right gastroepiploic blood vessel; the tissue defect was filled with the omentum. A 20/1000-in.-thick split-thickness skin graft was placed over the omentum, and the graft was immobilized with tie-over dressing (Fig. ).
The tie-over dressing was removed on the 5th postoperative day, and the engraftment of the omentum and skin graft was observed to ensure that there was no air leakage (Fig. ). However, a bulge that moved with breathing was noted on the skin graft over the omentum 2 weeks after surgery. CT confirmed this bulge to be the buildup of air between the transplanted omental tissues (omental emphysema). Pressure was applied to the bulge with scrunched up gauze and adhesive tape for 2 months; however, omental emphysema persisted even after 2 months; therefore, the dressing was removed, and she instructed to apply pressure with the hand when coughing. She is currently undergoing the follow-up and has not developed any subsequent emphysematous or respiratory infection (e.g., pneumonia). Omental emphysema persisted almost entirely without change for at least 2 years after surgery, but it spontaneously resolved by the 3rd postoperative year (Fig. ). Changes over time, as observed in CT, at 7 years after the surgery are presented in Fig. .",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [38.0, 'kg'], 'height': [153.0, 'cm']}",1.27083,1.20729,1.33437,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 153.0 cm. 
The patient's weight is 38.0 kg. 
Therefore, the patient's bsa is sqrt((38.0 (in kgs) * 153.0 (in cm))/3600) = 1.27083 m^2."
7169,60,Body Surface Area Calculator,physical,decimal,pmc-8196126-1,Extracted,"A 32-year-old, 70 kg, 155 cm female presented with a one-month history of fever, which she treated like a common cold. Her fever did not improve. Further examination showed elevated blood and urinary noradrenaline levels. We additionally noted increased uptake of iodine-123-metaiodobenzylguanidine in the left adrenal glands, leading to the diagnosis of pheochromocytoma.
On admission, she presented with a headache and general malaise. Her blood pressure (BP) was 126/76 mmHg, heart rate (HR) was 113 beats/min, and body temperature (BT) was 38.5 °C. Chest radiography results were unremarkable. Transthoracic echocardiography revealed no left ventricular hypertrophy. Magnetic resonance imaging revealed a 70-mm left adrenal gland mass. Laboratory tests revealed a high inflammatory state with the following results: a white blood cell count of 12,400/μl; C-reactive protein (CRP) levels at 27.9 mg/dL; anemia, coagulopathy, and malnutrition, with hemoglobin at 8.9 g/dl; a prothrombin time-international normalized ratio (PT-INR) of 1.49; and albumin levels at 2.1 g/dL. For catecholamines, there was a significant increase in serum noradrenaline (2.5 ng/ml [normal range 0.15–0.57]). Serum adrenaline (< 0.01 ng/mL) and dopamine levels (0.04 ng/mL) were almost normal. In addition, serum IL-6 (78.8 pg/mL [normal range < 4]) was elevated, while IL-1β (10 pg/mL) and tumor necrosis factor-alpha (TNF-α; 1.17 pg/mL) levels were normal, which led us to diagnose an IL-6-producing pheochromocytoma. Laparoscopic left adrenal tumor resection was subsequently scheduled (Table ).
After admission, oral loxoprofen administration was started to control systemic inflammation. We also initiated oral doxazosin, a common preoperative treatment for pheochromocytoma. The surgery was scheduled to take place after approximately 2 months to allow for incremental increases of the doxazosin dose. However, her persistently high inflammatory markers, anemia, malnutrition, and coagulopathy, led us to prepone her surgery. The dosage of doxazosin peaked at 12 mg. We did not reach 16 mg, as initially planned, because there were only 17 days before surgery. Anemia due to continued systemic inflammation was also prominent, and two units of packed red blood cells were administered daily starting 5 days before surgery (Fig. ).
Her BP was 111/68 mmHg on the day of surgery, HR was 95 beats/min, without arrhythmias, and BT was 37.0 °C. General anesthesia was performed, and an erector spinae plane block was used for perioperative analgesia. Epidural anesthesia was not performed because of coagulopathy. In addition to the standard monitors, an arterial catheter was placed in the radial artery. General anesthesia was induced with target-controlled infusion (TCI) of an effect-site propofol concentration set at 4.0 μg/ml, remifentanil 0.4 μg/kg/min, and rocuronium 50 mg. There were no hemodynamic fluctuations after tracheal intubation. Her BP surged to 146/79 mmHg when she was placed in a head-down position to insert the central venous catheter into the right internal jugular vein. Consequently, phentolamine (2 mg) was immediately administered. Flurbiprofen (50 mg) was administered before the start of surgery. After the start of pneumoperitoneum, the infusion rate of remifentanil was increased to 1.0–1.7 μg/kg/min, with 1 mg of phentolamine administered as appropriate. Meanwhile, her systolic BP was kept around 140 mmHg. During direct tumor manipulation, an increase in BP of 150/70 mmHg and tachycardia of 115 beats/min were observed, which required a bolus infusion of phentolamine (2 mg) for a total of 12 mg. Beta-blocker administration and continuous infusion of phentolamine were not necessary to control hemodynamic fluctuations. After tumor removal, the surgery was completed with a continuous infusion of noradrenaline 0.05–0.1 μg/kg/min. During the operation, the patient’s BT rose to 38.2 °C without a warmer and quickly dropped to 37 °C postoperatively. The duration of surgery and anesthesia time were 232 min and 361 min, respectively, with a volume of infusion of 2,200 mL, a blood loss of 50 mL, and a urine output of 1,450 mL (Fig. ).
Postoperatively, she was transferred to the intensive care unit, and a continuous infusion of 0.05 μg/kg/min noradrenaline was administered. This was eventually discontinued, and the patient moved to the general ward the next day. On postoperative day (POD) 1, chest radiography was normal without any findings of vascular hyperpermeability. Laboratory tests showed improved inflammatory markers. Further, her noradrenaline and IL-6 levels decreased, which normalized by POD7 (Table ). The patient was discharged with an uneventful postoperative course on POD8.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [155.0, 'cm']}",1.73606,1.64926,1.82286,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 155.0 cm. 
The patient's weight is 70.0 kg. 
Therefore, the patient's bsa is sqrt((70.0 (in kgs) * 155.0 (in cm))/3600) = 1.73606 m^2."
7170,60,Body Surface Area Calculator,physical,decimal,pmc-3982260-1,Extracted,"The baby boy was born full-term by spontaneous vaginal delivery to a 28-year-old healthy female mother as a fifth pregnancy. Immediately after birth, the infant cried but displayed no change in skin color, and his Apgar scores were 7 and 9 at one and 5 minutes, respectively. There was no history of a consanguineous marriage between the parents or the presence of a similar disease in the other children of the family or other family members. At birth, his weight was 2850 grams (10–50 percentile), height was 50 cm (50 percentile), and his head circumference was 34 cm (50 percentile). In his physical examination, there was no dysmorphic appearance and the other systems were found to be normal. On the postnatal second day, tonic and abnormal jerk-like seizures involving all the extremities were observed. The blood glucose was measured at 32 mg/dL during these seizures. The patient was diagnosed with hypoglycemic convulsion and given phenobarbital, after which he was sent to our clinic and hospitalized. His blood glucose was 32 mg/dL. The patient initially had subtle seizures like pedaling, licking lips, and swallowing which were then followed by generalized tonic convulsions. The patient first received 4 cc/kg intravenous 10% dextrose solution. Upon prolonged apnea and deterioration of his general condition both enteral and parenteral nutrition were started. Hormone tests, carried out to explain his resistant hypoglycemia, yielded normal results. Respiratory ventilation with continuous positive airway pressure (CPAP) was required for the pathologic apnea following convulsions. In the meantime, his cranial magnetic resonance imaging (MRI) and electroencephalogram (EEG) results were normal. Due to the persistence of the convulsions, midazolam infusion was given. In spite of the maximum dose of midazolam infusion and vitamin B6 supplements, the convulsions continued and levetiracetam was added to the treatment regimen. The urine and blood amino acids, the urine sulphite test, and the serum uric acid were all within normal ranges. Convulsions continued despite the normalization of the blood sugar level and the multiple antiepileptic drugs. Then, an important observation was made. It was observed that the patient was extremely alert to acoustic and tactile stimuli and that these stimuli triggered the convulsions. In the repeated EEG, there was no electroencephalographic abnormality accompanying the seizures triggered by stimuli and no other findings except for movement artefacts. Upon observing that the nasal pillow mask triggered seizures, the diagnosis of hyperekplexia was considered and treatment with clonazepam was started. The midazolam, phenobarbital, and levetiracetam that he had been taking were gradually reduced in dose and stopped. Considering the effects that minimal stimuli had, CPAP was replaced by an oxygen hood for ventilation and stimulating interventions were minimalized. The patient then displayed a significant decrease in the intensity and number of his seizures, started normal breast feeding, had normal blood glucose levels, and had no apnea. Where upon, he was discharged from the hospital with clonazepam treatment. During the 4-month follow-up period, he did not display apnea on the apnea monitor and he did not have any convulsions, only minimum-level contractions.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [2850.0, 'g'], 'height': [50.0, 'cm']}",0.19896,0.18901,0.20891,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 50.0 cm. 
The patient's weight is 2850.0 g so this converts to 2850.0 lbs * kg/1000 g = 2.85 kg. 
Therefore, the patient's bsa is sqrt((2.85 (in kgs) * 50.0 (in cm))/3600) = 0.19896 m^2."
7171,60,Body Surface Area Calculator,physical,decimal,pmc-3892058-1,Extracted,"An 89-year-old female was transferred to our institution with massive gross hematuria in March 2011. The patient’s medical history included uterine cervical cancer for which surgical treatment was performed at the age of 45 and gastric cancer treated by total gastrectomy at the age of 55. Medical history did not include renal biopsy, renal injury, percutaneous nephrolithotomy, or no trauma at the flank region. On admission, blood pressure was 143/67 mmHg, heart rate was 83 beats/min, body temperature was 37.2°C, and oxygen saturation was 99% on room air. On clinical examination, weight was 45 kg, height was 143 cm, and body mass index was 22.0 kg/m2. Inspection of the palpebral conjunctiva revealed evidence of anemia. Blood chemical analyses were shown in Table . A urinalysis revealed urine protein level of 3+, urine occult blood level of 3+, white blood cell count of 10–19/HPF, and red blood cell count of >100/HPF. Plain abdominal computed tomography (CT) revealed dilated left renal pelvis with high-density contents and hematoma was suspected (Figure A, B). Contrast enhanced CT was not performed because this condition was not considered to have association with renal vascular diseases. Subsequent plain abdominal magnetic resonance imaging revealed left hydronephrosis and blood retention in the dilated left renal pelvis. No cancer in the renal pelvis or ureter was detected (Figure C).
Despite conservative treatment with hemostatic agents (carbazochrome sodium sulphate and tranexamic acid), hematuria persisted. Repeated urinary cytology revealed no malignant cells. On day 9 after admission, consciousness deteriorated, systolic blood pressure decreased to 60 mmHg, and a high-grade fever of 39.0°C developed. Laboratory blood tests revealed a markedly elevated white blood cell count (35,000/μL), markedly elevated C-reactive protein levels (32.5 mg/dL), and moderate anemia (red blood cell count, 206 × 104/μL; hemoglobin, 6.0 g/dL). The patient went into septic and/or hemorrhagic shock. Therefore, fluid and catecholamine infusion, blood transfusion, and antibacterial drugs were rapidly initiated. Consciousness level and circulatory condition gradually improved. Repeated blood culture prior to administration of antibacterial drugs revealed no evidence of bacterial infection. On day 10 after admission, abdominal ultrasonography revealed expansion of hematoma in the left renal pelvis. Contrast-enhanced abdominal CT confirmed marked expansion of hematoma in the left renal pelvis and identified microaneurysms in the segmental arteries of the left kidney (Figure A, B).
Inflammation improved and a left double-J stent was inserted to improve hydronephrosis. Selective renal angiography that was simultaneously performed revealed renal arteriovenous malformation with microaneurysms in the left segmental arteries (Figure A). Catheter embolization using metallic coils was then successfully performed (Figure ); thus, hematuria ceased. Subsequent plain abdominal CT confirmed the absence of hematoma in the left renal pelvis (Figure A). Abdominal radiography revealed a well-positioned double-J stent (Figure B). The subsequent clinical course was uneventful. No postembolization syndrome (fever, lumbago, elevation of lactase dehydrogenase, or hematuria) was observed. The patient was ambulatory on discharge.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.0, 'kg'], 'height': [143.0, 'cm']}",1.33697,1.27012,1.40382,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 143.0 cm. 
The patient's weight is 45.0 kg. 
Therefore, the patient's bsa is sqrt((45.0 (in kgs) * 143.0 (in cm))/3600) = 1.33697 m^2."
7172,60,Body Surface Area Calculator,physical,decimal,pmc-6966921-1,Extracted,"A 33-year-old healthy woman (height, 159 cm; weight, 66 kg) underwent her second CS under spinal anesthesia. During the postoperative course, she experienced SM in the lower extremities. There were no preoperative neurological findings in her medical history, and preoperative laboratory examination results, including blood cell count, blood glucose level, and serum electrolyte concentrations, were within the normal range. Intrathecal administration of local anesthetic was performed at the L3/4 level using 0.5% hyperbaric bupivacaine (13 mg) without anesthetic premedication. Intermittent administration of ephedrine (at a total dose of 25 mg) was used to maintain the systolic blood pressure above 80 mmHg during the operation. Following the delivery of a healthy baby, droperidol (1.25 mg) was intravenously administered for nausea. Midazolam (2 mg) was also intravenously administered as a sedative at the patient’s request. Upon the completion of CS 67 min after induction of spinal anesthesia, the maximum level of sensory blockade was at the bilateral T2 level. Approximately 130 min after the intrathecal administration of local anesthetic, the patient complained of occasional myoclonic leg jerks in the maternity ward, which gradually increased in frequency and magnitude. The frequency and magnitude of the myoclonus were not constant, ranging from 2 to 30 times per minute. The patient’s pulse rate was 96 bpm, blood pressure was 120/78 mmHg, body temperature was 37.1 °C, and respiratory rate was 19 bpm, and her consciousness was clear. She presented severe postoperative lower abdominal pain associated with the myoclonic leg jerks; therefore, pentazocine (30 mg) and hydroxyzine (50 mg) were intravenously administered. No movement disorders were observed in the upper extremities. However, sensory perception in her lower extremities was not restored and she was unable to move her legs at will. The severity of the involuntary movements peaked at approximately 3 h after the induction of spinal anesthesia. The patient displayed bicycle-riding-like involuntary movements of the lower extremities; subsequently, these gradually decreased without treatments, and the sensation and voluntary movements in the lower extremities recovered. Approximately 5 h after the intrathecal administration of local anesthetic, the involuntary movements had almost disappeared. On postoperative day (POD) 1, neurological findings such as signs of meningitis, high fever, nuchal rigidity, impaired consciousness, or convulsions were absent. The patient was discharged on POD 8.
The patient underwent CS on three occasions. The first CS was at the age of 29 years and was performed under a combination of spinal and epidural anesthesia. Following placement of an epidural catheter at the T11/12 level, spinal anesthesia was performed at the L3/4 level using 0.5% hyperbaric bupivacaine (8.5 mg) and fentanyl (20 μg). Patient-controlled epidural analgesia was induced at a rate of 4 mL/h with 300 mL of 0.14% ropivacaine containing fentanyl (1.5 mg) and droperidol (7.5 mg). The third CS occurred at the age of 35 years and spinal anesthesia was performed at the L3/4 level using 0.5% hyperbaric bupivacaine (11.5 mg) and fentanyl (15 μg). Following delivery of a healthy baby, droperidol (1.25 mg) was intravenously administered for nausea. At the end of the CS, the maximum level of sensory blockade was at the bilateral T2 level. No postoperative neurological events occurred during the first or third CS.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [66.0, 'kg'], 'height': [159.0, 'cm']}",1.70734,1.62197,1.79271,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 159.0 cm. 
The patient's weight is 66.0 kg. 
Therefore, the patient's bsa is sqrt((66.0 (in kgs) * 159.0 (in cm))/3600) = 1.70734 m^2."
7173,60,Body Surface Area Calculator,physical,decimal,pmc-7863479-1,Extracted,"A 49-year-old Japanese man visited our department in November 2017 with chief complaints of indolent right scrotum enlargement and a right inguinal mass. History showed that the patient visited our department of gastroenterology with chief complaints of blackish feces and ill complexion in February 1997. Gastrointestinal fiberscopy was used to treat duodenal ulcer bleeding. Computed tomography (CT) showed a right retroperitoneal tumor, which was removed in the same month.
Histopathological examination showed a teratoma and yolk sac tumor (Fig. ). He was diagnosed with primary retroperitoneal EGCT and underwent three courses of chemotherapy (bleomycin/etoposide/cisplatin; BEP) starting in May 1997. He was closely followed using procedures including periodic imaging, tumor markers determination, and self-palpation.
He was followed up on an outpatient basis 5 years after treatment and was subsequently lost to follow-up. In August 1999, he underwent surgery of the right hydrocele. At that time, perioperative findings were unremarkable, indicating no clear tumor in either testicle.
At the first visit, his height was found to be 163 cm, and weight was 58.5 kg.
Blood pressure was 128/78 mmHg, heart rate was regular at 62 beats per minute, and body temperature was 36.4 °C.
He had no history of smoking or drinking, and there was nothing remarkable in the family history.
On physical examination, the right testicle was found to be elastic, hard, and enlarged to the size of 40 × 40 mm. A 45 × 40 mm sized induration was palpable in the right inguinal area and was adequately mobile. Neurological examination showed no abnormal findings. Blood biochemistry examination, urinalysis, and tumor markers (alpha-fetoprotein [AFP], human chorionic gonadotropin [HCG], and lactate dehydrogenase [LDH]) showed no abnormal findings.
Ultrasound findings showed a mosaic shadow inside the right testicle, with no abnormal findings in the left testicle.
During other diagnostic imaging procedures, enlargements of the right external iliac lymph node (24 × 14 mm) and right inguinal lymph node (43 × 29 mm) and a 31 × 22 mm mass with uneven contents were found in the right testicle (Fig. ). There was no evidence of any distant metastasis.
For the right testicular tumor, the patient underwent high orchiectomy and resection of the right inguinal lymph nodes in November 2017. The testicular tumor was 40 × 40 × 30 mm in size and weighed 34 g. The lymph node was 40 × 40 × 30 mm in size and weighed 21 g. The cut surfaces of both specimens were yellowish and solid, and the testicular tumor was localized in the testicle (Fig. ).
Histopathological findings showed irregular cobblestone proliferations of germ cell-like atypical cells with clear nucleoli and massive necrotic changes that partially resulted from self-destruction. The tumor did not extend into the tunica albuginea, and no vascular infiltration was found. Spermatic cord stumps were negative. Tumor diagnosis was a classical seminoma with no other elements. Lymph node metastases were also diagnosed as a result of the seminoma (Fig. ).
Based on the above findings, this seminoma was diagnosed as pT1, pN2, M0, S0, and TNM stage IIB [].
The patient received postoperative chemotherapy with one course of BEP therapy and three courses of etoposide and cisplatin (EP) therapy at the Japan Community Health care Organization Kani Tono Hospital starting in January 2018.
Post-chemotherapy CT confirmed a complete clinical response (cCR) at the right external iliac lymph node, and this response continued 12 months later (Fig. ).",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [58.5, 'kg'], 'height': [163.0, 'cm']}",1.6275,1.54612,1.70887,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 163.0 cm. 
The patient's weight is 58.5 kg. 
Therefore, the patient's bsa is sqrt((58.5 (in kgs) * 163.0 (in cm))/3600) = 1.6275 m^2."
7174,60,Body Surface Area Calculator,physical,decimal,pmc-3830271-1,Extracted,"A 22-year-old unmarried female presented with a 4-year history of general fatigue, weight loss and hypotension. She was born of non-consanguineous parents after a normal full term vaginal delivery. She reported no family or personal history of autoimmune diseases. She had no history of trauma and she did not have a history of receiving glucocorticoids.
There were no abnormal findings on clinical examination, she was normally pigmented, blood pressure was 95/60 mmHg with no postural fall, and she had normal body hair. Her height was 170 cm and her weight was 53 kg. Thyroid palpation was normal. She had normal pubertal development. Her menarche started at the age of 12 years and she had regular periods. She had no galactorrhea. She had no headaches, visual disturbances, polyuria, or polydipsia.
Blood examinations showed natremia of 138 mEq/L, kaliemia of 4.1 mmol/L, calcemiaof 2.38 mmol/L, plasma glucose of 4.3 mmol/L and normal blood cell count.
Clinical findings led us to consider the possibility of adrenocortical insufficiency, and the patient underwent detailed endocrine investigations, the results of which are shown in .
Cortisol deficiency was shown clearly by both insulin-induced hypoglycemia and depot Synacthen test [intravenous injection (IV), 1μg]. Secondary hypoadrenalism was confirmed by the finding of low basal ACTH level (13.8 pg/mL, reference range: 10.3-48.3), at which the plasma cortisol was 34 ng/mL. Prolactin level was elevated at 39 ng/mL (Normal range: 5-29 ng/mL in females). She had normal growth hormone levels concomitant to hypoglycemia. In contrast, basal concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol, thyroid stimulating hormone (TSH), and free thyroxine (FT4) were normal. These results excluded panhypopituitarism and led us to diagnose the patient with IAD. Magnetic resonance imaging (MRI) of the hypothalamus and pituitary showed a normal-sized pituitary (pituitary height 6 mm), with no mass lesion. Thepituitary stalk has a normal thickness of 2 mm and was not deviated. Thehyperintense signal of the posterior pituitary was in the normal location.
The diagnosis of IAD probably secondary to LYH was made. Investigation for autoimmune diseases, including assessment of anti-thyroid peroxidase antibody (anti-TPO), anti-thyroglobulin antibody (anti-TG), anti-ovarian antibodies, anti-adrenal antibodies, anti-glutamic acid decarboxylase (anti-GAD) antibodies, and antinuclear antibodies (ANA) was negative.
A daily dose of hydrocortisone (25 mg) was administered. After 8 months of follow-up, the patient was well-controlled, and she experienced no signs or symptoms of endocrine dysfunction.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.0, 'kg'], 'height': [170.0, 'cm']}",1.58202,1.50292,1.66112,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 170.0 cm. 
The patient's weight is 53.0 kg. 
Therefore, the patient's bsa is sqrt((53.0 (in kgs) * 170.0 (in cm))/3600) = 1.58202 m^2."
7175,60,Body Surface Area Calculator,physical,decimal,pmc-4674586-1,Extracted,"In November 2014, a 67-year-old male (height, 163 cm; weight, 44 kg) presented with epigastralgia, anorexia, and excessive weight loss (10 kg per month). Endoscopic studies revealed multiple small ulcers extending from the cardiac to the pyloric region and an irregular shaped ulcer in the angular region of the stomach; however, a biopsy was not performed and the patient was treated with a histamine H2-receptor antagonist. Two months later, the patient presented at our clinic with a high fever, epigastralgia, diarrhea, and continuous anorexia. On admission, the patient was neither anemic nor icteric. No lymphadenopathy was noted. The blood test results are summarized in . A second endoscopy of the upper gastrointestinal tract revealed several ulcers at the esophagogastric junction of the lower esophagus. The gastric mucosa was edematous and reddish, and multiple ulcers were found in the corpus, angular region and in the greater curvature of the stomach. These results indicated an increase in both the number and size of the ulcers. Biopsies from these lesions showed inflammatory cell infiltrates associated with typical CMV intranuclear inclusion bodies, suggesting the presence of esophagogastric CMV infection (Figures and ). We found it interesting that the patient was negative for CMV-IgM but was positive for CMV antigenemia. Colonoscopy identified two small ulcers in the terminal ileum and a large ulcer (3 cm) in the ileocecal valve. Histopathology of the biopsied tissues revealed CMV infection in the ileum and cecum (data not shown). Although the patient was initially suspected of having Behçet's disease, he was screened for immunodeficiency due to the opportunistic CMV gastroenteritis. The results revealed that the patient was HTLV-1-positive, with a high titer of anti-HTLV-1 antibodies (1 : 1024). He was HIV-negative. A blood smear was carefully reexamined and abnormal lymphocytes with bizarre, convoluted nuclei were identified, although these were not the flower cells typically observed in cases of HTLV-1 infection () []. An extremely high CD4+CD25+ T cell count in peripheral blood was identified by flow cytometry (). The patient was finally diagnosed with smoldering ATL. Initial treatment for Behçet's disease (mesalazine, 1.0 g, 3 times per day) and infliximab (one 300 mg infusion) was changed to ganciclovir (250 mg, twice per day for 14 days) to treat CMV gastroenteritis, which significantly improved CMV antigenemia. However, high fever continued to be unresponsive to prednisolone (maximum 30 mg/day) and intravenous immunoglobulin (5 g/day for 5 days). The patient was transferred to a university hospital for further care.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [44.0, 'kg'], 'height': [163.0, 'cm']}",1.41146,1.34089,1.48203,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 163.0 cm. 
The patient's weight is 44.0 kg. 
Therefore, the patient's bsa is sqrt((44.0 (in kgs) * 163.0 (in cm))/3600) = 1.41146 m^2."
7176,60,Body Surface Area Calculator,physical,decimal,pmc-4414761-1,Extracted,"A 51-year-old male patient was referred to Asan Medical Center on August 10, 2005 for a rectal NET that was found incidentally on screening colonoscopy. The patient had undergone hemorrhoidectomy in his twenties, but otherwise had no significant past medical history. He was a non-smoker and non-drinker. His height and weight were 164 cm and 59.3 kg, respectively. His initial vital signs included a blood pressure of 116/74 mmHg, pulse of 84 beats/minute, respiratory rate of 20 breaths/minute, and body temperature of 36.6℃.
Physical examination revealed no abnormalities. Laboratory data and the results of urinalysis and stool examination were all within normal limits. Chest and abdominal radiography were also unremarkable. Colonoscopy revealed a 5-mm-sized subepithelial tumor in the rectum, 5 cm above the anal verge; histological analysis of a forceps biopsy specimen revealed a rectal NET that was positive for both synaptophysin and chromogranin. Abdominopelvic CT showed no definite rectal lesions, but did reveal a 7-mm-sized perirectal lymph node. Considering the small size of the lymph node and the rare incidence of small metastatic rectal NETs, the malignant potential of the perirectal lymph node was regarded as very low. We discussed the CT findings with the patient, and finally decided to first remove the primary rectal NET endoscopically, with more invasive surgery to be considered if histological analysis revealed any other unfavorable findings, such as lymphovascular invasion, ≥2 mitoses per 50 high-power fields, and/or Ki-67 index >2%.
Endoscopic mucosal resection was performed (). The tumor measured 8×5×5 mm, and the vertical resection margin was positive. The tumor involved the mucosa and submucosa without angioinvasion. The Ki-67 index was 0.8%. Hence, the lesion was diagnosed as a well-differentiated grade 1 NET (). Given the favorable histological results of the resected specimen, we considered metastasis to the perirectal lymph nodes to be extremely unlikely; thus, we elected to follow-up the patient using endoscopy (annual sigmoidoscopy for the first 3 years, then colonoscopy every 3 years) and annual abdominopelvic CT.
For up to 7 years after endoscopic resection, the size of the perirectal lymph node remained unchanged on CT, and no intraluminal recurrence was identified on serial endoscopic follow-up examinations. However, 7 years after the resection, the lymph node was found to have enlarged slightly, from 7 to 10 mm (), although colonoscopy revealed no evidence of recurrence in the rectum. Transrectal ultrasound-guided biopsy was performed on the perirectal lymph node, and histological analysis revealed a well-differentiated NET. Preoperative MRI showed two perirectal lymph nodes suspicious for metastasis. Laparoscopic low anterior resection and lymph node dissection were also performed. The surgical specimen contained two metastatic lymph nodes, measuring 10×8×8 mm and 6×5×5 mm, respectively. Although lymphovascular and perineural invasion were present, the resection margins were clear. The specimen was positive for synaptophysin, but negative for chromogranin. The Ki-67 labeling index was ≤2%, but no mitosis was noted. Finally, the surgical specimen was diagnosed as a metastatic, well-differentiated, grade 1 NET (). The patient was discharged without complications and was scheduled to continue to receive follow-up examinations on a regular basis.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [59.3, 'kg'], 'height': [164.0, 'cm']}",1.64361,1.56143,1.72579,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 164.0 cm. 
The patient's weight is 59.3 kg. 
Therefore, the patient's bsa is sqrt((59.3 (in kgs) * 164.0 (in cm))/3600) = 1.64361 m^2."
7177,60,Body Surface Area Calculator,physical,decimal,pmc-8578920-2,Extracted,"The second patient (Fig.) is a 68-year-old male (75 kg, 164 cm) with SARS-Cov-2-induced ARDS and positive SARS-Cov-2 PCR test admitted to the university hospital. Co-morbidity is asthma. The CT scan showed bilateral ground glass opacities. Haemodynamically the patient was stable. The patient received tocilizumab on day 8 and favipiravir for 14 days; he did not receive dexamethasone. On day 2, the respiratory conditions deteriorated, and the PaO2/FiO2 ratio is 118 mm Hg (moderate ARDS according to the Berlin ARDS definition []). The patient was intubated and required mechanical ventilation. The initial ventilator settings include pressure control, peak inspiratory pressure 28 cm H2O, PEEP 13 cm H2O and respiratory rate 30/min. CRP was 10.6 mg/L, and KL-6 was 486 U/ml. White blood cell count, platelet count and urine production were normal. The ferritin levels remained >1000 ng/ml (100 μg/dl) during the entire ICU stay. Albumin was 2.9 g/dl. In the following 3 days, the PaO2/FiO2 ratio improved to around 150 mm Hg. The PaO2/FiO2 ratio dropped from 152 on day 5 to 84 mm Hg on day 6. CRP was increased to 22.9, and the KL-6 was increased to 762 U/ml. The patient was put in prone position and given muscle relaxants. Continuous intravenous lidocaine of 0.6 ml/kg/h was started. Albumin was 1.8 g/dl. On day 7, the PaO2/FiO2 ratio increased to 128 mm Hg, CRP dropped to 10.3 mg/mL and the lidocaine plasma concentration was 2.2 μg/ml. From day 3 until discharge from the ICU, D-dimer values were elevated reaching 75 nM/L on day 14. On day 8, although the PaO2/FiO2 ratio improved from 84 to 125 mm Hg, the mechanical ventilatory strategies were exhausted, and the patient was put on ECMO. The KL-6 was increased to 845 U/L, and lidocaine plasma level was 2.9 μg/ml. The PaO2/FiO2 ratio improved to 238 mm Hg on day 9, but on day 10, a sharp drop of the PaO2/FiO2 ratio to 60 mm Hg was observed, and CRP was 2.0 mg/ml. The patient’s ARDS status had changed from moderate to severe according to the Berlin ARDS criteria []. Lidocaine treatment was switched from continuous intravenous to continuous subdermal (dosage: 1 mg/kg/h). On day 14, the lidocaine plasma level was 2.7 μg/ml. KL-6 dropped to 549 U/l. On day 17, the clinical condition of the patient was improving, and the PaO2/FiO2 ratio reached 158 mm Hg. The patient was weaned from ECMO. The PaO2/FiO2 ratio improved further reaching 291 mm Hg on day 21, and the patient’s ARDS status has changed from moderate to mild ARDS []. On day 22, mechanical ventilation was discontinued, and the patient was extubated. The patient was orientated, and no signs of confusion were detected. CT scan on day 25 showed persistent ground glass opacities in both lungs, some pulmonary effusion (right >left), and no signs of vascular thrombosis. In addition, no signs of deep venous thrombosis were found in the lower extremities. Lidocaine treatment was continued until discharge from the ICU on day 30. No new ECG changes were observed during treatment with lidocaine. Blood metHb were within the normal range (0.1–0.6%). The patient was discharged home on day 37. At 3 months after admission, the patient is doing well.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [75.0, 'kg'], 'height': [164.0, 'cm']}",1.84842,1.756,1.94084,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 164.0 cm. 
The patient's weight is 75.0 kg. 
Therefore, the patient's bsa is sqrt((75.0 (in kgs) * 164.0 (in cm))/3600) = 1.84842 m^2."
7178,60,Body Surface Area Calculator,physical,decimal,pmc-4865707-1,Extracted,"A 43-year-old man (weight, 60.0 kg; height, 171.0 cm; body mass index, 20.5 kg/m2) was admitted to our hepatopancreatobiliary surgery department, an asymptomatic 14.0-cm mass in the right liver was diagnosed by ultrasound. The patient was infected by chronic HBV 20 years proir. The α-FP level was 1,000.00 ng/mL and the liver function was normal (Child-pugh A). CT scan showed that the liver was cirrhotic with a huge lesion in the right liver, which was considered as hepatocellular carcinoma, and a small lesion in the left liver was a typical hemangioma (). The FLR volume was calculated to be 356.0 cm3 (29.1% of 1,223.3 cm3 of the stander liver volume) based on the preoperative CT scan. It is reported that an FLR >30% of the stander liver volume is considered as a safe scope for hepatoectomy []. However, our criteria is FLR >45% of the stander liver volume for patients with cirrhosis. Given the high risk of postoperative liver failure for the patient, a 2-stage surgery should be adopted to increase the FLR. Although compared with portal vein embolization, ALPPS provides a better chance of complete resection for patients with primarily unresectable liver tumor, the morbidity from ALPPS was very high []. Thus, we decided to perform an AMAPS (a modified ALPPS) for this patient.
In the first stage of operation, abdominal laparotomy was performed under general anesthesia. After abdominal exploration and cholecystectomy, the right hepatic pedicle was dissected carefully, and the right hepatic artery was isolated and tagged with the homemade rubber strip, which also reduced adhesion around the right hepatic artery by the large flat area. Then, the right portal vein was freed and ligated (). After the falciform ligament was divided, the future transection plane was marked with ultrasound guiding. The microwave antenna, which was guided by ultrasound, was inserted into the liver parenchyma on the right future transection plane, setting a 4-minute and 70 watts output cycle (). This manner was repeated step by step every 2.5 cm to create an avascular groove along the future transection plane.
The duration of the first-stage operation was 210 minutes with a blood loss of 100 mL with no need for blood transfusion or intensive care unit (ICU) admission. The postoperative FLR was re-evaluated by CT scan weekly. The FLR was estimated at 430.6 cm3 (35.2% of the stander liver volume) after 1 week, and was increased to 500.3 cm3 (40.9% of the stander liver volume) after 2 weeks. On postoperative day 20, the volume of left hepatic was increased to 626.3 cm3 (51.2% of the stander liver volume; FLR increase 75.9%; daily FLR increase 13.5 cm3/day), without any metastatic tumors ().
The second-stage operation was performed 21 days after the first-stage operation. Little adhesion was found during the laparotomy. The right hepatic artery was easily identified and divided through the homemade rubber tag. The right portal vein was found below the right hepatic artery and was divided. Then, a bloodless blunt liver resection was performed along the future transaction plane with an anterior approach (). The right biliary duct was indentified and sutured during the parenchymal transection. The median and right hepatic veins were divided and sutured last.
The duration of the second-stage operation was 100 minutes with a blood loss of 200 mL, and there was no need for blood transfusion or ICU admission. The result of pathology demonstrated a hepatocellular carcinoma with poor differentiation, and the resection margin was tumor-free (R0). The patient recovered without any complications and was discharged on postoperative day 7. No tumor relapse or metastasis was detected (), and the α-fetoprotein level was normal at three months after the surgery.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.0, 'kg'], 'height': [171.0, 'cm']}",1.68819,1.60378,1.7726,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 171.0 cm. 
The patient's weight is 60.0 kg. 
Therefore, the patient's bsa is sqrt((60.0 (in kgs) * 171.0 (in cm))/3600) = 1.68819 m^2."
7179,60,Body Surface Area Calculator,physical,decimal,pmc-6906354-1,Extracted,"A 25-year-old woman complained of continuous pain in the right fifth finger, which
had started a few months previously without preceding trauma. She was a caregiver
and had belonged to a rowing club in her college days. The patient’s history was not
obtained at the first consultation in our hospital. Physical examination revealed a
Japanese woman of normal intelligence who looked androgynous and muscular. Her
height was 166 cm and weight 53 kg. Movement of her fifth finger was associated with
mild pain. Swelling or numbness was not observed. Her hands and feet were large as
observed in acromegaly. Her facial features were exaggerated due to prominence of
the mandibular bone. Hyperpigmentation was also observed. On radiographs, a lytic
bone lesion without calcification was observed in the fifth middle phalanx
accompanied by mild adjacent joint space narrowing and subchondral bone sclerosis
(). Enchondroma
was suspected first and magnetic resonance imaging (MRI) was performed. On MRI of
the right hand, bone marrow showed diffuse intermediate signal intensity (iso-signal
intensity to muscles) on T1-weighted (T1W) images and very high signal intensity on
T2-weighted (T2W) and STIR images (). On fat image with the DIXON method, an almost total lack of
subcutaneous and bone marrow fat was evident. The lytic lesion detected on
radiograph showed a similar signal to that of the surrounding bone marrow in all
sequences. Conditions showing serous bone marrow were suspected from the imaging
findings, and the patient’s history and medication history were taken.
The patient had been diagnosed with CGL since birth and genetically diagnosed as
having seipin-linked CGL2 when she was 15 years, when she started leptin replacement
therapy. One of her two younger brothers was also diagnosed with CGL. Laboratory
tests showed mild elevation of AST/ALT and HbA1c of 7.8%, with other parameters
within the respective normal ranges.
Bone survey was performed. Background bone mineral density was increased. Multiple
osteolytic lesions were noted in the bilateral phalanxes and metacarpal bones in
hands (), and
bilateral first to fifth metatarsal bones, phalanges, and navicular bones in the
feet (). Most of the
lytic lesions were located adjacent to subchondral bone. The lesions in the right
second, fifth, and left fifth intermediate phalanxes were accompanied by adjacent
joint space narrowing and subchondral bone sclerosis with or without geode
formation. Multiple epiphyseal osteolytic changes with coarsening of trabeculae were
also observed. There was a tendency in the feet to show honeycomb-like osteolytic
lesions. Multiple osteopoikilosis-like patchy sclerotic lesions were also observed
in the bilateral first metacarpal bones, third middle phalanxes, and left distal
radius. Enlargement of maxillary sinuses and prognathism with gaps between the teeth
was observed on the skull. Sella tunica was not enlarged. Coxa profunda was observed
in the bilateral hip joint. Other long tubular bones, spine, and pelvic bones showed
no obvious lytic or sclerotic lesion. Computed tomography (CT) of the right hand
also showed multiple lytic and sclerotic lesions without evident fracture or
periosteal reaction. The whole-body MRI performed 10 years ago when she was
diagnosed with seipin-linked CGL type 2 was reviewed. The study showed almost a
total lack of fat tissue, with only a small amount of fat preserved in the
retro-orbital, axillar, sole, and palmar regions (). Observation was selected due to the
patient’s poorly controlled diabetes, although curettage would normally be
undertaken for management of painful lytic lesions in a young active woman because
of concern about impending fracture.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.0, 'kg'], 'height': [166.0, 'cm']}",1.56329,1.48513,1.64145,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 166.0 cm. 
The patient's weight is 53.0 kg. 
Therefore, the patient's bsa is sqrt((53.0 (in kgs) * 166.0 (in cm))/3600) = 1.56329 m^2."
7180,60,Body Surface Area Calculator,physical,decimal,pmc-4911527-1,Extracted,"In July 2014, a 95-year-old Japanese woman was admitted to our hospital with a 3-month history of bilateral edema of the lower extremities. When she developed chronic diarrhea at 90 years of age (in 2009), laboratory tests revealed that serum creatinine (Cre) was 1.6 mg/dl, albumin was 3.2 g/dl, and urinary protein excretion was 0.32 g/day.
She had no history of smoking, alcohol intake, or malignancy. On admission, she was 153 cm tall and weighed 56.4 kg. Her blood pressure was 138/70 mm Hg. There were bilateral edema of the lower extremities.
Laboratory tests revealed a white blood cell count of 4,600/μl, a red blood cell count of 3.71×106/μl, hemoglobin of 11.7 g/dl, and platelet count of 21.3×104/μl. In addition, total protein was 6.3 g/dl, albumin was 2.4 g/dl, serum urea nitrogen was 26 mg/dl, serum Cre was 1.55 mg/dl, C-reactive protein was 1.6 mg/dl, and lactate dehydrogenase was 257 IU/l (normal: 119-229 IU/l). Immunological tests showed that antinuclear antibody, anti-double-stranded DNA antibody, and U1-nuclear ribonucleoprotein antibody were all negative. IgG was 1,340 mg/dl, IgA was 427 g/dl, and IgM was 266 mg/dl. The serum level of C3 was 123 mg/dl (normal: >86 mg/dl), C4 was 19 mg/dl (normal: >18 mg/dl), and CH50 was 38 U/ml (normal: >30 U/ml). The patient was negative for hepatitis B virus antibody, hepatitis C virus antibody, and Treponema antigen. Urinary protein excretion was 9.1 g/day, and the sediment contained 5-10 erythrocytes per high-power field. Urinary Bence Jones protein was negative by immunofixation electrophoresis.
No findings suggestive of malignancy were revealed by imaging studies such as computed tomography and ultrasonography. The long axis of the kidney was calculated to be 9.0 cm bilaterally. Serum anti-PLA2R autoantibody was positive according to the method of Akiyama et al. []. Renal biopsy was done to evaluate the renal changes in this patient.
Light microscopy of a renal biopsy specimen containing 36 glomeruli revealed global sclerosis in 22 of them (fig. ). The other 13 glomeruli showed mild mesangial matrix expansion (fig. ), but there was no definite spike formation, bubbling, or thickening of the glomerular basement membrane (GBM) (fig. ). In the tubulointerstitial region, atrophy or fibrosis affected 50-60% of the cortical tissue (fig. ). The arterioles displayed mild to moderate hyalinosis (fig. ), while the interlobular arteries showed mild to moderate fibroelastic intimal thickening (fig. ). Immunofluorescence microscopy demonstrated granular deposits of IgG and C3 along the GBM. Analysis of IgG subclasses revealed dominant staining for IgG4 (IgG4 > IgG1 > IgG3 > IgG2; fig. ), while staining for IgA and IgM was very weak. The anti-PLA2R binding in the biopsy was positive. Congo red staining was negative. Electron microscopy showed subepithelial electron-dense deposits (EDD) in the GBM, but these subepithelial EDD were not associated with spike-like protrusions arising from the basement membrane (fig. ). Stage 1 MGN was diagnosed due to these findings.
Anasarca was treated with diuretics (furosemide at 80 mg daily) and dietary restriction (6 g of salt and 700 ml of water daily), achieving weight loss from 56.4 to 51.0 kg. Because the patient did not want steroid therapy due to adverse effects such as bone disease, cyclosporin microemulsion (Neoral at 50 mg daily) was added, and the level at 2 h after administration was titrated in the range of 600-1,000 ng/ml. However, proteinuria persisted, and renal function deteriorated rapidly. Hemodialysis was started when Cre was 6.0 mg/dl and urea nitrogen was 102 mg/dl because of exacerbation of pleural effusion and generalized edema along with an increase in weight to 58 kg at 2 months after diagnosis.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [56.4, 'kg'], 'height': [153.0, 'cm']}",1.54822,1.47081,1.62563,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 153.0 cm. 
The patient's weight is 56.4 kg. 
Therefore, the patient's bsa is sqrt((56.4 (in kgs) * 153.0 (in cm))/3600) = 1.54822 m^2."
7181,60,Body Surface Area Calculator,physical,decimal,pmc-8314493-1,Extracted,"A 70-year-old Japanese man without any major family and psychosocial history was referred to our hospital to continue treatment for DME. At the patient’s former hospital, his major symptom was repeated visual disturbance of both eyes due to DME, and he received sub-Tenon’s triamcinolone acetonide injection and intravitreal anti-VEGF injection. Sub-Tenon’s triamcinolone acetonide injections were once in both eyes, and intravitreal anti-VEGF injections were 12 times in both eyes every 2–3 months (4 times with 0.5 mg ranibizumab and 7 times with 2 mg aflibercept in the right eye and once with aflibercept in the left eye) during the 2.5-year follow-up period. At the patient’s former hospital, the last anti-VEGF therapies were injected in the left eye in July 2016 and the right eye in December 2016.
At the patient’s first visit to our hospital in January 2017, his body height and weight was 160 cm and 52 kg [body mass index (BMI) 20.3], respectively. His HbA1c level was 6.3 %, and he has been suffering from diabetes mellitus for 10 years with only diet therapy. His blood pressure was 120/61 mmHg, and he had no hypertension. Although he had hyperlipidemia (total cholesterol 244 mg/dl, LDL cholesterol 148 mg/dl), he did not receive any pharmacological treatments for it. He has been treated with donepezil hydrochloride for mild cognitive impairment in the neurology department of Tokyo Takanawa Hospital. However, because he works regularly and can attend a hospital by himself, he has no hindrance to daily life. In addition, there was no issue on financial and language/cultural challenges. A dilated fundus examination showed mild nonproliferative diabetic retinopathy [], with several small hemorrhages without macular edema, and his best corrected visual acuity was 1.0 in both eyes. The central subfield macular thickness (CMT) on spectral-domain optical coherence tomography (SD-OCT) was 279/320 μm (right eye/left eye).
Five months later, he noticed blurred vision in both eyes (visual acuity was 0.8 in both eyes), and a fundus examination showed significant macular edema in both eyes (CMT, 404/478 μm). In June 2017, for the first time at our hospital, the patient received 2-mg intravitreal aflibercept injections in both eyes 1 week apart (6 June in the right eye and 13 June in the left eye). No laser therapy was applied. After short-term anti-VEGF therapies to both eyes, his systemic condition remained the same. The treatment was effective in both eyes, and 1 month later, his CMT recovered to 277/321 μm, and his blurred vision disappeared (visual acuity was 1.0 in right eye and 1.2 in left eye). Three months after the first treatment at our hospital (1 September 2017), significant macular edema relapsed in both eyes (CMT, 403/463 μm; Fig. ), visual acuity was 0.8 in right eye and 1.0 in left eye, and he desired continuous treatment for both eyes. In October 2017, he received intravitreal aflibercept injections in both eyes 1 week apart (3 October in the right eye and 10 October in the left eye). One month after treatment (10 November), his subjective complaint of blurred vision disappeared (0.8 in right eye and 1.2 in left eye), and the CMT decreased to 280/315 μm (Fig. ). During this period, his HbA1c levels were measured and kept at 6.5% (3 October, 10 October, and 10 November).
Upon initiating the intravitreal injection in the operating room, we measured his blood pressure as 141/69 mmHg (3 October) and 135/70 mmHg (10 October) without blood-pressure-lowering drugs (Fig. a). However, on 12 November, just 2 days after a follow-up visit to our hospital, he complained of a severe headache and walked to the emergency department at Tokyo Takanawa Hospital. He complained of a severe headache on the right back side of his head and visual disturbance of the left visual field with no other systemic neuropathological symptoms. He had no external injury presumed as trauma antecedent and no other apparent causes leading to cerebral hemorrhage. His blood pressure was elevated at 195/108 mmHg, and computed tomography (CT) of the brain revealed the presence of a high-density area (2.5 × 3.0 cm) in the right occipital lobe indicating a subcortical hemorrhage (Fig. a). The patient was treated with an intravenous injection of nicardipine hydrochloride to lower his systemic blood pressure to < 140 mmHg for 2 days. On 13 November, CT showed no enlargement of the high-density area (data not shown). On 15 November, 3 days after the stroke, magnetic resonance imaging (MRI) revealed a peripheral low-intensity zone in the same region (T2*-weighted MRI, Fig. b) and a low-intensity area (diffusion-weighted MRI, Fig. a) in the occipital lobe that was consistent with the CT results. Additionally, magnetic resonance (MR) angiography revealed no vascular anomalies or malformation (Fig. b), and T2*-weighted MRI revealed no cerebral microbleeds, thus ruling out cerebral amyloid angiopathy (Fig. b). He was therefore diagnosed with a hypertensive cerebral hemorrhage of the occipital lobe. On 14 November, 2 days after the stroke, the patient began oral treatment with 80 mg/day telmisartan, which was continued for 3 days. Starting 17 November, the telmisartan dose was reduced to 40 mg/day. During this period, his blood pressure was maintained at < 130/80 mmHg, and his symptoms of severe headache disappeared, and visual disturbance of the left visual field was alleviated. Ten days later, he was discharged from Tokyo Takanawa Hospital, and 20 days after discharge he visited our hospital to receive a follow-up ophthalmological examination. Two months after the stroke (5 January 2018), visual field tests with Goldmann perimetry at our hospital showed no apparent left homonymous hemianopsia (Fig. ). Follow-up CT (14 February 2018; Fig. c) and T2*-weighted MRI (24 July 2018; Fig. d) examinations revealed that the cerebral hemorrhage had been absorbed, and the lesion had decreased in size. One year after the cerebrovascular stroke, the telmisartan was discontinued because his blood pressure had stabilized to a normal level and remained around 110/60 mmHg.
The patient received no anti-VEGF therapy for 4 months prior to 3 October 2017 because his macular edema did not relapse. We happened to determine his plasma VEGF levels before and after the intravitreal anti-VEGF injections (October 2017) via specific enzyme-linked immunosorbent assay (SRL, Tokyo, Japan; Fig. b). The patient’s plasma VEGF level was 28 pg/ml on 3 October, just before the intravitreal injection of aflibercept in the right eye. However, the level rapidly decreased to below the detection limit (< 20 pg/ml) on 10 October, just before the injection in his left eye. Notably, the levels on 10 November (2 days before the cerebral hemorrhage) and 10 December were also below the detection limit. On 25 January 2018, we confirmed that his plasma VEGF level had recovered to 41 pg/ml. Thereafter, we continued to follow the patient for DME and diabetic retinopathy, and no cerebral hemorrhage recurred.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [52.0, 'kg'], 'height': [160.0, 'cm']}",1.52023,1.44422,1.59624,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 160.0 cm. 
The patient's weight is 52.0 kg. 
Therefore, the patient's bsa is sqrt((52.0 (in kgs) * 160.0 (in cm))/3600) = 1.52023 m^2."
7182,60,Body Surface Area Calculator,physical,decimal,pmc-6755925-1,Extracted,"A 51-year-old gentleman, recently diagnosed to have type 2 diabetes mellitus and systemic hypertension, presented to the cardiology outpatient clinic on 28th July 2016 with history of pricking chest pain and shortness of breath for the past 7 years and recurrent attacks of syncope since the previous year. He weighed 49 kg and with a height of 157 cm; body mass index was 19.88 kg/m2. His blood pressure (BP) was 120/80 mmHg and pulse rate was 78/min and regular in rhythm. He was afebrile. Systemic examination was unremarkable.
Laboratory findings revealed hemoglobin of 15.1 g/dL, hematocrit of 47%, white blood cell count of 11,300/mm3 (differential count of neutrophils of 56%, lymphocytes 26%, eosinophils 11%, and monocytes of 7%), and platelet count of 293,000/mm3. Urine on routine examination showed a pH of 6.0, specific gravity of 1015, and was negative for albumin, glucose, red blood cells, and pus cells. Blood glucose fasting was 115 mg/dL and post-prandial was 219 mg/dL with an HbA1C of 7.1%. Blood urea was 27 mg/dL and creatinine was 1.0 mg/dL. Serum electrolytes were as follows: sodium 141 mEq/L, potassium 4.3 mEq/L, chloride 103 mEq/L, and bicarbonate 28 mEq/L. Serum cholesterol was 183 mg/dL, serum triglyceride 121 mg/dL, and serum uric acid 3.9 mg/dl. Two-dimensional (2D) echocardiogram showed normal left ventricular dimensions, no regional wall motion abnormality, and a left ventricular ejection fraction of 69%. Holter monitoring showed occasional supraventricular and ventricular premature complexes. On 2nd August, coronary angiography showed insignificant coronary artery disease with dominant right coronary system and he was discharged with medical advice.
On 3rd August, he attended emergency department with complaints of severe back pain, palpitation, and sweating. His back pain was sudden in onset, gradually progressive, throbbing type, rating 8/10 in pain scale, radiating to the left flank, aggravated by exertion, and partially relieved by rest. He had no other complaints. He was on metformin and calcium channel blocker. He looked anxious, agitated, and restless but was oriented and afebrile. His pulse rate was 112/min, respiratory rate was 28/min, and BP was 210/120 mmHg in the right upper limb and 210/100 mmHg over the left upper limb in supine position. There was no radio-femoral delay. Systemic examination was unremarkable except for a mild tenderness in the lumbar region.
On investigation, electrocardiography, chest X-ray, complete blood counts, liver function tests, 2D echocardiography, urine analysis, and toxicology screen were all within normal limits. Serum amylase and lipase were normal. Blood urea was 58 mg/dL and serum creatinine was 2 mg/dL. Venous blood gas (VBG) analysis showed a pH of 7.21, bicarbonate of 18 mmol/L, base excess of −9.4 mmol/L, and a lactate of 10.81 mmol/L. Serum electrolytes were sodium 138 mmol/L, potassium 3.8 mmol/L, and chloride 108 mmol/L, and anion gap was 12 mmol/L.
The following were considered in the differential diagnosis of this situation: (a) acute mesentric ischemia, (b) aortic dissection (c) hypertensive emergency, and (d) pancreatitis. Contrast-enhanced computed tomography abdomen showed a lesion in the left adrenal gland measuring about 3.5 × 3.2 cm with mild enhancement in the arterial phase, features consistent with pheochromocytoma [: Contrast enhanced CT scan of abdomen showing the mildly enhancing left adrenal mass]. No additional extra-adrenal tumors were seen. There was no evidence of mesenteric ischemia, aortic dissection, or pancreatitis. Upon further questioning his family members, it was known that he was unwell in the previous 6 months with on and off headache, palpitation, and anxiousness, which they attributed to the recently diagnosed diabetes mellitus.
His BP was managed with alpha adreno-receptor blocker and calcium channel blocker. Phenoxybenzamine was added at a dose of 10 mg twice a day and later increased to 20 mg three times daily. Persistent tachycardia and BP were stabilized with addition of beta blocker.
On 5th August 2016, the level of 24-h urine metanephrines was 14,536 mcg (reference range: less than 350 mcg/24 h) and nor-metanephrines was 7,607 mcg (reference range: less than 600 mcg/24 h).
Laparoscopic removal of pheochromocytoma was done under general anesthesia on 12th August 2016. After the surgery, there was a brief episode of hypoglycemia and hypotension, which was managed with 25% dextrose and normal saline, respectively. Azotemia resolved and blood gases were normalized. Pathological examination of the resected mass revealed a well-encapsulated tumor of size 5 cm × 4 cm × 3 cm, without hemorrhage. It showed polygonal and round cells with abundant cytoplasm and increased vasculature. There was no capsular or vascular invasion. Tumor cells were seen in the background of spindle cells with ganglion cells and Schwanian stroma. These features were reported as consistent with a CP–ganglioneuroma of the left adrenal gland []. Immunohistochemistry examination showed positivity for chromogranin, synaptophysin, and S-100 stains and negativity for calretinin in pheochromocytoma cells. Calretinin, chromogranin, synaptophysin, and S-100 stains were positive in the ganglioneuromatous component. Vimentin was positive and cytokeratin was negative. These staining characteristics confirmed the composite nature of the tumor.
At the time of discharge, his blood pressure and blood glucose were normal. Upon review on 28th February 2017, his BP was 130/80 mmHg without antihypertensive medicine. Blood glucose fasting was 90 mg/dL and post-prandial 66 mg/dL, with an HbA1C of 6.1% without any antidiabetic medicine. The levels of 24-h urinary metanephrines and normetanephrines were 62 and 604, mcg, respectively.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [49.0, 'kg'], 'height': [157.0, 'cm']}",1.46183,1.38874,1.53492,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 157.0 cm. 
The patient's weight is 49.0 kg. 
Therefore, the patient's bsa is sqrt((49.0 (in kgs) * 157.0 (in cm))/3600) = 1.46183 m^2."
7183,60,Body Surface Area Calculator,physical,decimal,pmc-4973717-1,Extracted,"A 66-year-old female presented to the emergency department with 1 week duration of general weakness and poor oral intake. She had an underlying disease of diabetes and hypertension for 10 years and had been treated with medications at the local clinic, which included metformin, glimepiride, hydrochlorothiazide, losartan, and atorvastatin. She also had severe osteoarthritis at both knee joints and had multiple steroid injections at the local orthopedic clinic. Approximately 2 weeks before admission, she had been admitted for treatment of urinary tract infection (UTI). At that time, blood culture and urine culture showed growth of Escherichia coli and was treated with ceftriaxone and tazobactam. She was not on any antihypertensive medication for 2 weeks.
Physical examination showed the following findings: height 152 cm, body weight 57 kg, blood pressure 70/50 mmHg, heart rate 70 beats per minute, and respiratory rate 20 per minute, with body temperature 36.5°C. Decreased skin and tongue turgor were observed. Pulmonary, cardiac, abdominal, and neurologic examinations were unremarkable.
shows the laboratory data at admission and those 2 weeks before admission. Her outpatient laboratory data checked at 2 weeks prior to admission showed normal levels of serum creatinine and calcium. Serum magnesium level decreased to a lower limit of normal range at admission. Fractional excretion of sodium was 1.0%.
Having pyuria and hypotension, with a previous history of UTI, she was first diagnosed as UTI sepsis. She was admitted to the intensive care unit and antibiotics and massive hydration (30 mL/kg of crystalloids) were administered. The patient’s vital signs were stabilized after administration of crystalloids. Within 2 days, inflammatory signs and blood pressure were normalized. However, serum calcium and creatinine levels remained elevated, and the patient constantly complained about poor oral intake and general weakness.
On the third hospital day, administration of saline and calcitonin (40 IU per day) was begun. Serum calcium level decreased for the next 2 days (from 11.9 to 9.9 mg/dL) but began to increase again from the third day of calcitonin administration.
To evaluate the cause of hypercalcemia, contrast-enhanced computed tomography of chest and abdomen and whole body bone scintigraphy were performed, but the results showed no evidence of malignancy. Serum and urine protein electrophoresis, anti-neutrophil cytoplasmic antibody titers, and tumor marker studies were negative. Thyroid function profile revealed normal levels of thyroid stimulating hormone (0.68 μIU/L, normal range: 0.34–0.56 μIU/L) and free thyroxine (1.12 ng/dL, normal range: 0.58–1.64 ng/dL). The bone mineral density T-score was –1.4, which indicated osteopenia. Intact parathyroid hormone (PTH) was 7.5 pg/mL (normal range: 12–88 pg/mL), PTH-related peptide was undetectable (normal range: <1.1 pmol/L), and serum 25-hydroxy vitamin D was 16.32 ng/mL (normal range: 30–100 ng/mL). These results indicated a suppressed PTH–vitamin D axis.
We found that the patient had multiple steroid injections in both her knee joints in the past, although the amount of steroid could not be quantified. Adrenocortical function was assessed, and showed that her serum cortisol level was 2.36 μg/dL and adrenocorticotropic hormone (ACTH) was 32.51 pg/mL (normal range: 10–60 pg/mL). The ACTH stimulation test showed inadequate cortisol response to the pharmacological dose of ACTH (). As most people with secondary adrenal insufficiency fall within the range limit and usually below 35, the plasma ACTH level and ACTH stimulation test results suggested the diagnosis of secondary adrenal insufficiency. Hydrocortisone (1.5 mg/kg) was administered from the tenth hospital day. Her serum calcium level returned to normal within 3 days and her general weakness and anorexia were completely improved (). With the normalization of calcium level, magnesium level trended toward normal range. After 2 weeks of follow-up, serum calcium level was maintained at 8.7 mg/dL. As the patient was at a high risk of developing osteoporosis and needed corticosteroid replacement, regular monitoring for bone mineral density was considered, but the patient was lost for follow-up.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [57.0, 'kg'], 'height': [152.0, 'cm']}",1.55134,1.47377,1.62891,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 152.0 cm. 
The patient's weight is 57.0 kg. 
Therefore, the patient's bsa is sqrt((57.0 (in kgs) * 152.0 (in cm))/3600) = 1.55134 m^2."
7184,60,Body Surface Area Calculator,physical,decimal,pmc-5559909-1,Extracted,"A 27-year-old single Saudi woman presented with her parents on September 2016 at the gynecology outpatient clinic of the King Fahad Medical city, Saudi Arabia, with a gradually abdominal distension and discomfort over two years. The swelling was accompanied by vague abdominal pain and breathlessness which worsened on recumbency leading to decreased sleep. She also complained of constipation and poor appetite. There was no history of vomiting or other gastrointestinal symptoms, urinary symptoms, colicky pain, and fainting attacks. She had no previous history of any illnesses, allergies, or operations. She denied the use of any medications. There was no family history of malignancies. Her menarche commenced at the age of 11 years with subsequent regular cycles.
Her body weight was 71 kg, her height was 157 cm, and her BMI was 28.8. On physical examination, she was afebrile with a pulse rate of 79 b/min, blood pressure of 120/73 mm Hg, and respiratory rate of 20 cycles/min. There was no jaundice, edema, or lymphadenopathy. Secondary sexual characteristics were evident. Abdominal examination revealed abdomen was distended with large ill-defined pelvic-abdominal cystic mass extending from pubis to epigastrium with an abdominal girth of 106 cm with a dull note on percussion, without tenderness and the presence of dermal striae. Intestinal sounds were normal. The external genital examination was normal.
Plain radiograph of the chest (P-A view) was within normal limits. Transabdominal ultrasonography verified a large pelvic cystic mass about 29 × 18 cm with no evidence of solid components or septations. The uterus was normal and endometrial thickness was 10 mm. CA-125 was 25.3 IU/ml and another tumor marker was within the normal ranges. Abdominopelvic computerized tomography (CT) findings were consistent with a large well-defined homogeneously cystic lesion originating from the right ovary measuring 15.6 × 26.3 × 31.7 cm in the AP, transverse, and craniocaudal dimensions, respectively (). Most likely this represents ovarian cystadenoma, with no abdominopelvic metastases or lymphadenopathy. Our patient was counseled and signed informed consent for laparoscopic ovarian cystectomy, possible oophorectomy, and laparotomy if needed.
Intraoperatively, the patient was in a supine position, prepped and draped in the usual sterile fashion. The bladder had been drained with a Foley catheter that was placed in the bladder. Attention was then turned to the abdomen where an approximately 10 mm skin incision was made in the umbilical fold. Entry into the peritoneum was done using the Hasson technique. The 10 mm trocar was placed through the umbilical incision. The abdominal cavity was visualized with huge cyst arising from the right ovary which was seen, extending up to the level of the xiphoid process, and the liver was not visualized due to the huge cyst. Peritoneal wash was sent for cytology. The 10 mm second trocar was applied in the suprapubic catheter with direct opening in the cyst and being drained around 10,050 ml. However, with suction, a large globular piece of the cyst was obtained that appeared to be coagulated blood which was sent for cytology. Two trocars 5 mm were inserted in the lower quadrant bilaterally. The cyst wall was identified and was removed using blunt dissection with countertraction. The ovarian bed was then irrigated and dried. There was slight oozing noted near the edge of the ovary, with hemostasis obtained using electrocautery. The Endo Catch bag was placed through the 10 mm port (suprapubic) and the cyst wall components, and the right ovarian cyst was placed in the Endo Catch bag and removed through the 10 mm incision which was sent for histopathology (). After decompression of the ovarian cyst, the liver and the gallbladder were seen with no abnormality. The uterus and the left ovary were looking normal. Lymph nodes were not enlarged. The pelvis was copiously irrigated and dried. Hemostasis was assured. Operative time was 155 minutes. Estimated blood loss was minimal. The patient tolerated the procedure well. Total excised cyst measured 31 cm in size and 550 grams by weight (). Total volume of the cyst was calculated to approximately 11 kg. The postoperative period was uneventful.
She was discharged on the 2nd postoperative day. The patient was advised to follow up after 4 weeks. Patient weighed 60 kg with an abdominal girth of 80 cm on day 28 after operation. Cytological examinations were negative for malignancy. Histopathological examination revealed serous cystadenoma of the ovary. She recovered completely from her surgery and has gone back to her normal daily activity.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [71.0, 'kg'], 'height': [157.0, 'cm']}",1.75966,1.67168,1.84764,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 157.0 cm. 
The patient's weight is 71.0 kg. 
Therefore, the patient's bsa is sqrt((71.0 (in kgs) * 157.0 (in cm))/3600) = 1.75966 m^2."
7185,60,Body Surface Area Calculator,physical,decimal,pmc-7680296-1,Extracted,"A 77-year-old woman visited a local clinic because of persistent cough for the past 6 months. A tracheal tumor was suspected on imaging and she was referred to us for further evaluation and treatment. Her medical history included hypertension and atrial fibrillation, for which she was treated with medications. Her height was 156 cm and weight was 56 kg. Respiratory noise was audible on respiration. There was no enlargement of surface lymph nodes. Additionally, there were no abnormalities in blood biochemistry and tumor marker levels were normal. Radiography showed a mass in the trachea. Computed tomography (CT) and magnetic resonance imaging (MRI) findings revealed a 1.5 cm large border and a smooth surface nodule shadow on the posterior wall of the thoracic trachea approximately 5 cm below the glottis. Mass formation with a major axis of 1.0 cm in diameter extending from the trachea to the esophagus was observed. Based on MRI findings, the border with the surrounding organs was clear and it was diagnosed as primary tracheal tumor invasion (Fig. a, b) Furthermore, bronchoscopy showed a smooth-surfaced submucosal tumor with abundant neovessels, which accounted for 80% of the cross-sectional area of the trachea (Fig. ). Biopsy was not performed, because there was a strong possibility of airway obstruction due to bleeding. Fluorodeoxyglucose-positron emission tomography (FDG-PET) showed accumulation with a maximum standardized uptake value of 2.9 for the lesion and the possibility of malignancy could not be excluded (Fig. ). The patient was not in a state of respiratory distress and tumor resection using a bronchoscope was at risk of bleeding, we decided to remove the tumor by tracheal sleeve resection, because the patient had symptoms and was at risk of airway obstruction. Regarding anesthesia, the percutaneous cardiopulmonary support (PCPS) was put on standby in consideration of the possibility of suffocation due to intubation difficulties and bleeding during intubation. There were no problems during anesthesia except for the operation of the intubation tube. Surgery was performed via median sternotomy. The thymus and surrounding structures were separated to expose the trachea, and then five tracheal rings, including the tumor, were removed by sleeve resection. Separation from the esophagus was relatively easy. After resection of the trachea, the airway was secured by intubation. End-to-end anastomosis of the trachea was performed using 3-0 monofilament synthetic absorbable suture material. A continuous suture was initiated in the membranous portion. The orally inserted tracheal tube was then advanced to the distal portion to secure the airway and interrupted suture of the portion of the tracheal cartilage was performed. The anastomosis site was covered with the thymus (Fig. ). Five tracheal rings were excised for excision of one or more tracheal rings above and below the tumor. Based on the results of intraoperative pathology, it was judged that there was no tendency for tumor infiltration and additional resection was not performed. The postoperative course was favorable. There has been no recurrence for 2 years after surgery. The resected specimen showed a white–pink tumor (maximum diameter of 23 mm) protruding into the tracheal lumen and the membranous portion (Fig. ). Pathological examination showed a mass of hyperplastic atypical cells with spindle-shaped nuclei arranged in bundles running in various directions in the submucosa. On immunostaining, the tumor was positive for vimentin, CD34, and Bcl-2, and negative for α-smooth muscle actin (α-SMA). Based on these findings, the tumor was diagnosed as an SFT (Fig. , ). There were no malignant findings and the resected stump was negative. The postoperative course was favorable and there has been no evidence of recurrence for 2 years after the surgery.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [56.0, 'kg'], 'height': [156.0, 'cm']}",1.55778,1.47989,1.63567,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 156.0 cm. 
The patient's weight is 56.0 kg. 
Therefore, the patient's bsa is sqrt((56.0 (in kgs) * 156.0 (in cm))/3600) = 1.55778 m^2."
7186,60,Body Surface Area Calculator,physical,decimal,pmc-7479557-1,Extracted,"A 16-year-old male patient complained of a painful left ankle on the anteromedial side for more than 2 years. He presented to the out-patient department on November 2016.
Pain levels fluctuated, and the maximum pain was 7 on visual analogue scale and persisted over a week.
The patient’s height is 168 cm and weight is 75 kg (body mass index: 26.57 kg/m2). He did not have any underlying medical history. He visited local hospitals several times and was diagnosed with osteochondral lesion of the talus through radiologic study. The symptom was alleviated with medication or rest. He had no trauma history, genetic predisposition or degenerative joint disease.
The patient did not have limitation of ankle range of motion. He had problem of weight bearing walking due to pain.
There were no specific findings in preoperative laboratory examination.
We found bony abnormalities, including OLTs in the equator of the medial talar dome with subchondral cyst, in the X-ray of ankle (Figure ). Magnetic resonance image (MRI) was evaluated and found OLTs in the medial talar dome with subchondral cysts and subcortical depression. Also, we could see bony spurs at the anterior and posterior lips of the tibial plafond and tiny subchondral cyst at the anterior lip of the tibial plafond in MRI study (Figure ).
The primary impression of the presented case is osteochondral lesion of the talus.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [75.0, 'kg'], 'height': [168.0, 'cm']}",1.87083,1.77729,1.96437,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 168.0 cm. 
The patient's weight is 75.0 kg. 
Therefore, the patient's bsa is sqrt((75.0 (in kgs) * 168.0 (in cm))/3600) = 1.87083 m^2."
7187,60,Body Surface Area Calculator,physical,decimal,pmc-4557221-1,Extracted,"A 7.5-year-old boy presented to the Department of Endocrinology with symptoms of virilisation (presence of pubic hair, enlargement of penis), acne and adult body odour.
Our patient was born after a full-term, unremarkable pregnancy and exhibited normal development until the age of 5 years. At the age of 5.5 years, the first symptoms of virilisation started to appear (pubic hair and enlargement of penis) as well as acceleration of growth velocity. On admission to the Endocrinology Department, on physical examination the patient was found to have pubic hair (Tanner stage III/IV), a large penis measuring around 6 cm. His height was 144 cm (+3.25SD) with a weight 28.1 kg (5–10 centile according to the height) , a growth spurt was diagnosed (growth velocity 9 cm/year), his bone age was two years advanced. There was acne limited to the region of his face and adult body odour but no axillary hair and no striae. Testicular size (2 ml each) and structure were normal for age. Moreover, neurologic examination revealed that the patient had difficulty in walking (he walked on his toes), increased leg reflexes and right site foot-clonus. His bowel and bladder function were normal as well his sensation.
Laboratory investigations revealed significantly raised serum androgen levels (Table ), abnormally high concentrations of androgen metabolites in the urine steroid profile that were suggestive of a virilising tumour; and normal cortisol and ACTH levels.
There was no androgen suppression observed during the 4-day Dexamethasone test (2 days of 2 mg/d, 2 days of 8 mg/d) but normal cortisol suppression after the small dose of Dexamethasone. Urine catecholamine and their metabolites levels were normal.
The abdominal and thoracic computed tomography (CT) scan and the adrenal magnetic resonance imaging (MRI) revealed no abnormalities. The ultrasound of the testes was normal. Adrenal scintigraphy (131 J-norcholesterol) showed no adrenal autonomic function.
The brain MRI was normal, however spinal MRI T2- and contrast enhanced T1-weighted images demonstrated an ovoid, well-circumscribed, intradural extramedullary enhancing mass measuring approximately 2.8x2.1x6.0 cm (Fig. ). The mass occupied the entire cross-section of the spinal canal at levels L3 to L4/5 (Fig. ). The presence of myxopapillary ependymoma was suspected.
The patient underwent an L3-L4 laminectomy. Upon opening the dura, an extramedullary mass was seen. There were calcifications within the arachnoid. The white-grayish mass measured 3.0x2.0x5.0 cm, appeared well-circumscribed, and showed no invasion of surrounding tissues. The lesion was resected totally.
Microscopically features were of benign ectopic adrenocortical tumour (Fig. ). On the IHCM (immunohistochemistry and microscopy) panel the cells were positive for melan-A, locally positive for synaptophisin and for CD56. The cells were negative for glial fibrillary acidic protein (GFAP), cytokeratins AE1/AE3 and chromogranin. The proliferative activity ki67 index was low (locally up to 3 %).
Postoperative course was uneventful apart from transient urinary bladder function disturbances (difficulty urinating and patient required catheterisation regimen for several weeks). The patient was followed up and the normalization of androgen levels was observed in tests performed 9 days, 2 and 7 months after surgery (Table ). Neurologic examination at 9 month post surgery was normal apart from lack of right Achilles tendon reflex. There were no abnormalities on control MRI of the brain and spine performed 9 months post surgery. Unfortunately secondary to the endocrine activity of the tumour, central precocious puberty occurred and patient started the treatment with long acting LH-RH analogue. The boy is now 10 years of age, his height is 162 cm and bone age is three years advanced. Fig. shows his growth chart with final height prediction (the prediction was based on his height, bone age and parental heights) [].",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [28.1, 'kg'], 'height': [144.0, 'cm']}",1.06019,1.00718,1.1132,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 144.0 cm. 
The patient's weight is 28.1 kg. 
Therefore, the patient's bsa is sqrt((28.1 (in kgs) * 144.0 (in cm))/3600) = 1.06019 m^2."
7188,60,Body Surface Area Calculator,physical,decimal,pmc-6531112-1,Extracted,"A 77-year-old, Asian male patient (weight: 60 kg, height: 165 cm) with end-stage renal disease (ESRD) undergoing periodic hemodialysis, was hospitalized due to acute exacerbation of chronic obstructive pulmonary disease. He had no known history of psychosis prior to admission to the hospital. His social history was positive for alcohol consumption (25 mL a day for 10 years) and smoking (40 cigarettes a day for 30 years).
On admission, the patient was conscious and oriented to person, time, and place. Complete neurological examination including mental state was normal. The patient was in shortness of breath with the following vital signs: temperature 36.2 °C, blood pressure 156/91 mmHg, pulse 98 beats/min, and respiratory rate 20 per minute. He reported progressively worsening cough productive of yellow purulent sputum. Bilateral moist crackles were heard in both lungs on auscultation but with no wheezing. Markers of systemic inflammation were elevated (white blood cell count [WBC] 10.25 × 103/μL, C-reactive protein [CRP] 57.50 mg/L, procalcitonin [PCT] 0.49 ng/mL). Laboratory analysis revealed increased baseline serum creatinine (10.63 mg/dL, estimated creatinine clearance 4.94 mL/min). His liver function was moderately impaired and classified into Child-Pugh class B. Chest computed tomography (CT) scan showed diffuse inflammation and interstitial change and a small amount of pleural effusion in bilateral lungs.
Intravenous moxifloxacin was initiated 400 mg daily as empiric treatment for pulmonary infection on hospital day 1. A sputum sample was collected for microbiological culture before initiation of antibiotics and the result came back negative. On day 12, the patient was feeling tired and weak with hyperthemia (38.1 °C), hypertension (184/91 mm Hg), and worsened shortness of breath (26 beats/min). Plasma indicators for infection were elevated (WBC 11.50 × 109/L, neutrophils 97.1%, PCT 22.10 ng/mL). On the 13th day, moxifloxacin was switched to meropenem 500 mg intravenous every 8 hours. On 16th day, sputum culture revealed multidrug-resistant (MDR) A baumannii (resistant to carbapenem but sensitive to tetracycline). Then intraveous tigecycline was added to the regimen at a loading dose of 100 mg followed by 50 mg every 12 hours.
Fourteen hours after tigecycline initiation, the patient became confused, disoriented to location, and the time. He had difficulty understanding instructions and was clearly disturbed in attention during the conversation. He was agitated, fearing that people around him were trying to harm him. Then he became verbally aggressive toward his family members and medical staff. His mental disorder worsened in the next 2 to 3 hours then he began having hallucinations, seeing a huge ball in the ceiling and asking the nurse to take it down so he could eat it. He asked other people to gather together and said he had important things to announce. His Confusion Assessment Method, which is a valid tool for the detection of delirium, was negative prior to the initiation of tigecycline, but became positive after it was started. His clinical manifestations also met the key features listed by the Diagnostic and Statistical Manual of Mental Disorders fifth edition (DSM-V) criteria from the American Psychiatric Association that characterizes delirium.[
No focal neurological disease was noted after neurological examination. A computerized tomographic scan of the head was then performed, and no abnormalities were identified. Oxygen supplementation (4 L/min via nasal cannulae) was initiated after the arterial blood gas analysis showed hypoxemia (pH 7.41; PaCO2 25 mmHg; PaO2 68 mmHg; Na+ 132 mEq/L; K+ 5.5 mEq/L). The patient did not have any prior history of mental illness. Drug-induced delirium was suspected and tigecycline was speculated to be the most likely offending agent after medication review (Table ). Since his delirium was treated with little success with olanzapine, tigecycline therapy was discontinued the next morning after the patient stayed awake the whole night. During the following day after discontinuation of tigecyline, the patient's mental state improved and delirium cleared slowly. He restored the ability of focus and orientation. Perceptual disturbances disappeared, and no visual illusions or vague delusions of harm were noted again.
Meanwhile, markers of systemic inflammation were elevated (WBC 43.91 × 109/L, neutrophils 98.2%, PCT 34.04 ng/mL, CRP 89.09 mg/L). On Day 19, antibiotic therapy was switched to meropenem (i.v., 500 mg q8 h) combined with minocycline (p.o., 400 mg q12 h), and amikacin (i.v., 200 mg qd). The regimen continued for 5 days but the patient did not respond well, showing even higher systemic inflammation markers and exacerbated dyspnea. Antibiotic therapy was switched to meropenem 500 mg every 8 hours, and he started again on tigecycline 50 mg every 12 hours on 24th day with no loading dose.
In the morning of Day 25, the patient showed reduced psychomotor activity, decreased speech, but no obvious hallucinations. He had no idea of the time of day, nor where he was, although the day before he was fully orientated. The patient experienced a hypoactive state of delirium. CT examination of the chest showed increased inflammatory pulmonary lesions in bilateral lungs. Blood gas analysis revealed hypoxemia without carbon dioxide retention, and the electrolytes were found to be within range. Also, no significant changes in blood profile like levels of liver enzymes or serum creatinine was observed compared with the last test taken before the delirium appeared again. Tigecycline was discontinued and delirium resolved in the afternoon. Antibiotic treatment was then switched to levofloxacin (i.v., 600 mg qd) and minocycline (p.o., 100 mg q12 h). But the patient did not respond well to the present antibiotic therapy and his dyspnea exacerbated. He was transferred to the intensive care unit 6 days later as mechanical ventilation was required. Unfortunately, the patient died of recurrent attacks of left heart failure probably caused by uncontrolled serious infections on 33th day.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.0, 'kg'], 'height': [165.0, 'cm']}",1.65831,1.57539,1.74123,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 165.0 cm. 
The patient's weight is 60.0 kg. 
Therefore, the patient's bsa is sqrt((60.0 (in kgs) * 165.0 (in cm))/3600) = 1.65831 m^2."
7189,60,Body Surface Area Calculator,physical,decimal,pmc-3079672-2,Extracted,"Case 2 is a 30-year-old Japanese man who was transferred to the emergency department with diabetic ketoacidosis and was initially diagnosed with type 1 diabetes three years prior to this study. He has been using different doses and types of insulin since that diagnosis. However, his glutamic acid decarboxylase (GAD) and insulin antibodies were negative (below detectable range). Therefore, this patient has features of both type 1 and type 2 diabetes. However, because of his clinical picture, this patient may have non-autoimmune fulminant type 1 diabetes, which is rare in Caucasian populations but comprises approximately 10% of type 1 diabetes cases in Japan []. His endogenous insulin secretory capacity was almost completely lost, since his post-meal C-peptide levels were repeatedly undetectable (below 0.1 ng/ml). His post-meal glucagon level was 107 pg/ml (normal range, 23 to 197 pg/ml). His BMI was 17.5 (body weight/body height = 52 kg/172 cm). His HbA1c level was above 8% in the three months prior to this study. Sitagliptin (50 mg/day) was added to the therapeutic regimen to try to achieve better control of his diabetes. At that time, he was using premixed biphasic insulin aspart (30% insulin aspart and 70% protamine-complexed insulin aspart; Novorapid 30 MIX) three times daily before each meal (15U, 7U and 16U, respectively). He was also taking 625 mg metformin three times daily and 75 mg miglitol three times daily. His post-meal blood glucose level was 242 mg/dl, and his HbA1c level was 8.1% at baseline. In the first month after starting sitagliptin, he had occasional mild hypoglycemia, which he could manage by taking glucose drinks by himself. He had no hypoglycemic events after the second month of sitagliptin therapy. His HbA1c level was followed for 24 weeks and was reduced from 8.1% to 7.1% (1.0% reduction, Figure ). His post-meal C-peptide levels repeatedly remained undetectable (below 0.1 ng/ml) after the start of sitagliptin treatment. No adverse events were observed in kidney or liver function. No weight gain or gastrointestinal complaints were noted. At eight weeks, he could reduce the insulin dose by 2U before each meal. The doses of other drugs remained unchanged. Before and during sitagliptin treatment, no special difference in diet management or physical exercise was noted.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [52.0, 'kg'], 'height': [172.0, 'cm']}",1.57621,1.4974,1.65502,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 172.0 cm. 
The patient's weight is 52.0 kg. 
Therefore, the patient's bsa is sqrt((52.0 (in kgs) * 172.0 (in cm))/3600) = 1.57621 m^2."
7190,60,Body Surface Area Calculator,physical,decimal,pmc-7220147-1,Extracted,"A 56-year-old man (164 cm, 57 kg) who was previously diagnosed with left Aspergilloma, a tuberculosis destroyed lung, and diabetes mellitus was scheduled for a left pneumonectomy due to recurrence of Aspergilloma in his left lung. As shown in his chest x-ray and chest CT (Figs. and ), his left lung was nearly collapsed, and the result of a pulmonary function test was severely restricted. The patient's diffusing capacity for carbon monoxide was 63% and predicted postoperative forced expiratory volume in 1 second was 23.5%, suggesting he might require a postoperative mechanical ventilator. However, the patient's preoperative room air saturation was 98% and arterial blood gas analysis (ABGA) showed pH 7.428, pCO2 36.6 mmHg, pO2 98.6 mmHg, and HCO3- 24.9 mmol/L. As the patient's partial oxygen concentration was adequate despite his left lung being nearly totally collapsed, we thought that we would be capable of performing the pneumonectomy using a SLT. The thoracic surgeon also agreed to use a SLT. For a better surgical view, we planned lung isolation via insertion of a SLT deep into the bronchus.
On the day of the surgery, routine monitoring was done, including an electrocardiography, a noninvasive blood pressure measuring device, and pulse oximetry. Central venous line and arterial line were placed for better anesthetic care. Midazolam 2 mg, 2% propofol, and remifentanil were injected intravenously. After confirmation of unconsciousness, rocuronium 50 mg was injected for paralysis and a SLT was inserted into the patient's right bronchus. It was intubated deeper than the normal depth because we had to insert the tube into the right bronchus. After we checked via a fiberoptic bronchoscope and auscultated to confirm that the tube had been appropriately inserted, a silastic 7.0 sized single lumen tube (Covidien) was fixed 26 cm at the teeth. Total intravenous anesthesia was adjusted according to the bispectral index (BIS). The patient's position was changed from supine to right lateral decubitus and we reconfirmed through a fiberoptic bronchoscope that the tube was placed correctly. After opening the patient's thorax, the surgeon warned us that the patient's left lung had more adhesion than expected and therefore, a lot of bleeding could be expected. During the operation, there was excessive bleeding from the left lung, because of which we had to transfuse 2750 mL of packed red blood cells, 1200 mL of fresh frozen plasma, and 360 mL of platelets. We also carried out frequent tracheal suctions because there were large amounts of bloody secretions inside the tube. The patient's ABGA showed pH 7.425, pCO2 37.7 mmHg, pO2 169 mmHg, HCO3 24.7 mmol/L with fraction of inspired oxygen 50% and his blood pressure was 109/57 mmHg, the heart rate was 72 beats per minute, and his oxygen saturation was 100%. After tracheal suction was performed, we tried a lung recruitment maneuver and suddenly end-tidal carbon dioxide did not show on the monitor. We tried manual-bagging without success. The patient's oxygen saturation was gradually dropping from 100% to 37%. Tracheal suction was performed and there was a bloody discharge but saturation did not improve. When we decided to use a bronchoscope to see what happened inside the tube, the patient's blood pressure dropped and heart rate was decreasing. We thought that cardiopulmonary resuscitation (CPR) was needed; therefore, 1 mg of epinephrine was injected via the central line. Surgeons stopped the procedure and started cardiac massage. The patient was in a right lateral decubitus position; hence, we moved him into a supine position and maintained suction through the trachea. During CPR, an approximately 2-cm-sized hematoma (Fig. ) was removed from the endotracheal tube after vigorous suctioning. After removal of the hematoma, the ventilation and patient's vital signs recovered. To reduce risk, we reintubated the patient with a right-sided DLT and used a fiberoptic bronchoscope after intubation. After this event, the surgery was uneventful without any other complications. After surgery completion, the patient was transferred to an intensive care unit. Ten days after surgery, he was transferred to a ward and discharged on postoperative day 65 without any complications. The patient gave his permission to be included in the manuscript.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [57.0, 'kg'], 'height': [164.0, 'cm']}",1.61142,1.53085,1.69199,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 164.0 cm. 
The patient's weight is 57.0 kg. 
Therefore, the patient's bsa is sqrt((57.0 (in kgs) * 164.0 (in cm))/3600) = 1.61142 m^2."
7191,60,Body Surface Area Calculator,physical,decimal,pmc-3766784-1,Extracted,"An 84-year-old male patient, 165 cm in height and 84 kg in weight, visited the hospital to have TURP for hyperplasia of prostate with obstruction. The patient had no specific medical history. The preoperative chest X-ray and electrocardiogram (ECG) were within normal range. The hemoglobin level (Hb) was 14.2 g/dl, and the hematocrit level was 41.1%, which were within normal limits.
After arriving in the operating room, noninvasive blood pressure (NIBP), ECG, and pulse oximetry were attached. After a few minutes of rest, blood pressure was 150/95 mmHg, heart rate was 85 beats/min, respiratory rate was 15 breaths/min, and oxygen saturation (SaO2) was 94.0%. The patient's position was maintained at the right lateral decubitus position. After identifying the L4-5 intervertebral space, a 25 G Quincke spinal needle was inserted into the space. After the stylet was removed and cerebrospinal fluid was confirmed to be draining well, 11 mg of 0.5% bupivacaine (Marcaine®, AstraZeneca AB, Södertälje, Sweden) with 100 ug of epinephrine was injected. Ten minutes after he was placed in the supine position, the height of sensory block was increased to the T12 and checked by pin-prick test. The patient was placed in a lithotomy position. When bipolar TURP began, the irrigation fluid with 0.9% saline solution was injected from a height of about 150 cm without pressure. The patient had a severely enlarged right lobe of the prostate. At 120 minutes after anesthesia, 4 mg of ondansetron was injected because the patient vomited. At that time vital signs were stable (HR: 71 beats/min, NIBP: 150/85 mmHg). At 135 minutes after anesthesia, the patient complained of pain on operative site, considered to be caused by a low level of anesthesia. Therefore, with the consent of the patient, spinal anesthesia was switched to general anesthesia. Pre-oxygenation with 100% oxygen was conducted. After intravenous injection of 250 mg of thiopental and 40 mg of rocuronium, endotracheal intubation with a tube of internal diameter 7.5 mm was performed. Anesthesia was maintained with 2 L/min of oxygen, 2 L/min of air, and 2 vol% of sevoflurane. Tidal volume was 500 ml and respiratory rate was 10 breaths/min, so mechanical ventilation was initiated, when PIP was 24 cmH2O.
Forty minutes after switching to general anesthesia, the surgeon inserted a Foley catheter and finished the surgery. Glycopyrrolate 0.4 mg and neostigmine 1.5 mg were injected for reversal of muscle relaxation, the patient's spontaneous respiration and muscular strength recovered, and the endotracheal tube was removed. His blood pressure was well maintained at 140-100/100-70 mmHg throughout surgery, and the body temperature was around 36.2℃. However during emergence 10 mg of labetalol was injected twice due to high blood pressure (180/110 mmHg). The total anesthetic time was 3 hours and 15 minutes, and the total surgical time was 2 hours and 30 minutes. Seven hundred fifty ml of Ringer's lactate were injected, and 5 L of 0.9% saline solution was used as an irrigation fluid. When the patient was transferred to the PACU, SaO2 was measured as 80%. Although 10 L of O2 was provided with nonrebreathing reservoir facial mask, the SaO2 was not maintained at more than 90.0% (HR 77 beats/min, NIBP 190/110 mmHg). Arterial blood gas analysis showed a pH 7.159, PaCO2 53.5 mmHg, PaO2 58.9 mmHg, HCO3- 15.9 mmol/L, base excess -9.0 mmol/L, Na+ 139 mmol/L, K+ 3.5 mmol/L, Hb 14.2 g/dl and SaO2 81.8%. The patient complained of severe respiratory difficulties and abdominal pain. On physical examination, abdominal distension was founded. The surgeon suggested conducting an abdominal CT scan, but oxygen saturation was not maintained at more than 90% despite an Ambu-bagging with 10 L of 100% O2. The anesthesiologist decided to perform the endotracheal intubation again. Two hundred fifty mg of thiopental and 50 mg of rocuronium were injected, and endotracheal intubation with a tube of ID 7.5 mm was performed. A chest X-ray was taken and an intravenous injection of 10 mg of furosemide was conducted. In PACU NIBP was 180-140/110-85 mmHg and HR was 80-70 beats/min.
A chest X-ray was normal. After the abdominal CT scan, the patient was transferred to the intensive care unit (ICU). Findings of the abdominal CT scan are seen . In the ICU, pressure support 11 cmH2O, FIO2 0.45, and PEEP 6 cmH2O were maintained as a PSV mode. Arterial blood gas analysis showed a pH 7.380, PaCO2 26.1 mmHg, PaO2 73.9 mmHg, HCO3- 15.6 mmol/L, base excess -7.3 mmol/L, and SaO2 94.7%. After the test, intravenous injections of 10 mg of furosemide were injected twice. The total volume of urine on the day of the surgery was 1100 cc.
On the first day after surgery the endotracheal tube was removed and checked ABGA. Three hours later ultrasonography was conducted and showed that a great volume of fluid had accumulated around the liver. A percutaneous catheter drainage (PCD) was done into the right upper abdomen, and about 650 cc of clear yellowish fluid was drawn. The patient was transferred to a general ward on that day. The PCD catheter was removed on the fourth day after the surgery. The patient was discharged from the hospital on the tenth day after the surgery.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [84.0, 'kg'], 'height': [165.0, 'cm']}",1.96214,1.86403,2.06025,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 165.0 cm. 
The patient's weight is 84.0 kg. 
Therefore, the patient's bsa is sqrt((84.0 (in kgs) * 165.0 (in cm))/3600) = 1.96214 m^2."
7192,60,Body Surface Area Calculator,physical,decimal,pmc-3659367-1,Extracted,"A 22-year old female (height 158 cm, weight 43 kg, BMI 17.22) presented with a 1.5 year history of dysphagia in the retrosternal area. Initially, her dysphagia could be alleviated within 1–3 min by drinking warm water. Six months before hospital admission (Renmin Hospital of Wuhan University), her dysphagia became more frequent (once every 2–3 weeks), lasting for up to 10 min and could not be relieved by drinking warm water. The retrosternal chest pressure was relieved by regurgitation. These episodes were associated with hypersalivation and profuse sweating. Heartburn and retrosternal chest pain were frequent. Three weeks prior to hospitalization, she was unable to tolerate any solid food orally.
Physical examination showed no focal abnormality. Complete blood count, liver biochemistry, electrolytes and creatinine were normal. An upper gastrointestinal barium swallow study showed typical features of achalasia, demonstrating the bird's beak sign, no barium passed into the stomach during the investigation. Endoscopy, performed after two days of fasting, showed no mucosal abnormality although there was an increased resistance passing the endoscope through the LES.
Esophageal manometry using a 8-channel water perfused system with a Dent sleeve for LES pressure, showed high LES pressure and regular spontaneous rhythmic non-propagating contractions in the esophageal body at a frequency of 7/min, with an amplitude between 48 and 51 mm Hg (Figures , ). An initial dry swallow did not affect the contractile activity but two subsequent dry swallows decreased amplitude and frequency (Figure ). Subsequent wet swallows, using 20 ml of warm water, increased the frequency to 8/min and also increased the amplitude (Figure ). Drotaverine hydrochloride (40 mg intramuscular) was given to reduce the LES pressure; this markedly reduced the contraction frequency from 7 to 3/min without a significant effect on the amplitude; a subsequent wet swallow increased the frequency to 9/min and also increased the contraction amplitude (Figure ). Significant swallow-induced LES relaxation was still present.
Pneumatic balloon dilatation of the LES was performed uneventfully. The balloon was 35 mm in diameter, 80 mm in length, obtained from EndoFlex Germany. A small amount of blood was seen on the balloon after the dilation procedure. Omeprazole 40 mg iv daily was administered for 3 days. Thereafter the diet was advanced gradually as tolerated. By day 5, liquid meals passed down the stomach without pain. The patient was discharged 7 days after the dilatation. At the 23-month follow up visit, she reported a normal eating habit without any gastrointestinal symptoms.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [43.0, 'kg'], 'height': [158.0, 'cm']}",1.37376,1.30507,1.44245,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 158.0 cm. 
The patient's weight is 43.0 kg. 
Therefore, the patient's bsa is sqrt((43.0 (in kgs) * 158.0 (in cm))/3600) = 1.37376 m^2."
7193,60,Body Surface Area Calculator,physical,decimal,pmc-3546099-1,Extracted,"A 20-yr-old man, 173 cm in height and 58 kg in weight, underwent a microdiscectomy for a symptomatic right-sided disc herniation at the intervertebral space, confirmed by magnetic resonance imaging in 2002. Routine laboratory studies were unremarkable with a hemoglobin (Hb) level of 14.1 g/dL and hematocrit (Hct) of 41.6%. Anesthesia was induced with 250 mg thiopental, 100 mg succinylcholine, 25 mg atracurium and maintained with 1.5% isoflurane in 50% oxygen and 50% nitrous oxide with a fresh gas flow 2 L/min. A routine microdiscectomy was carried out in the prone position on Wilson's frame under general anesthesia. During operation the discectomy the surgeon felt some momentary downward slippage of the pituitary rongeur into the deep intervertebral space. At that moment unexplained profuse bleeding occurred in the disc space. Shortly after this event blood pressure (BP) suddenly decreased from 110/80 mmHg to 80/60 mmHg. It became normalized soon after the injection of ephedrine 10 mg and atropine 0.5 mg and the bleeding stopped spontaneously. In the recovery room, the patient experienced transient hypotension (90/60 mmHg) and tachycardia (95 bpm/min) which again responded well to volume replacement. On the first day after the surgery operation the patient complained of abdominal discomfort and wound pain. BP was 100/70 mmHg, HR 92 bpm/min and body temperature 38.4℃. Hb and Hct was 11 g/dL and 32% respectively. Neurologic examination revealed normal motor tone in his lower extremities. Physically, the abdomen was mildly distended with tenderness in the left lower quadrant of the abdomen on a physical examination. Bowel sounds were decreased. Apparently he was stabilized with volume expansion.
On the second day after the operation he started to complain of increasing abdominal pain in the left quadrant with dizziness and became restless and very pale. At that time BP was 100/60 mmHg, HR 100 b/min and body temperature 38.5℃. Hb was 9.2 g/dL and Hct was 26.9%. Abdominal examination revealed decreased bowel sounds and the left femoral and deep peroneal artery pulsation was absent on palpation. Three hours later, Hb became 6.8 g/dL and Hct was 19.7%. Four units of blood were transfused for stabilization. An urgent Doppler sonogram showed no flow in the common iliac artery suggesting segmental obstruction. Contrast-enhanced CT also revealed a low attenuation perfusion defect in the common iliac artery at the level of L4-5 with a moderate amount of retroperitoneal hematoma (). There was no leakage of contrast but a few small air densities were present around the obstructed artery probably coming out from the perforated anterior spinal ligaments. Angiography of the abdomen demonstrated a complete obstruction of the left common iliac artery, located about 2 cm distal to the aortic bifurcation (). The distal portion of the obstructed artery was filled with contrast material by collateral circulation through the internal and external iliac arteries. Fifty five hours after the L4-5 discectomy, an emergent laparotomy was performed. Anesthesia was induced with 250 mg thiopental, 100 mg succinylcholine, 25 mg atracurium and maintained with 1.5% isoflurane in 50% oxygen and 50% nitrous oxide with a fresh gas flow 2 L/min. During the operation, BP and HR were stable and the surgical field revealed a moderate retroperitoneal hematoma. There was no active bleeding. A small defect was observed in the anterior longitudinal ligament overlying the right side of the L4-5 disc space. The laceration was located at the posterior aspect of the left common iliac artery, made by a partial puncture with a pituitary rongeur. It was packed with thrombus and adhered densely to the punctured anterior longitudinal ligament at the surgical level so that it was spontaneously sealed. The arterial injury was repaired by the excision and interposition of an 8 mm polytetrafluoroethylene graft with the removal of the retroperitoneal hematoma. The postoperative course was uneventful and the patient remains in good condition over 10 yr later.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [58.0, 'kg'], 'height': [173.0, 'cm']}",1.6695,1.58603,1.75297,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 173.0 cm. 
The patient's weight is 58.0 kg. 
Therefore, the patient's bsa is sqrt((58.0 (in kgs) * 173.0 (in cm))/3600) = 1.6695 m^2."
7194,60,Body Surface Area Calculator,physical,decimal,pmc-3030060-1,Extracted,"A 50-year-old male patient visited the hospital to undergo synovectomy for left knee ostarthritis and tenosynovitis. The patient had suffered difficulties in walking from weakening of both lower limb muscles since 25 years ago, and recently the symptom of weakness of lower limb muscles became more serious and dyspnea at the level of ATS (American Thoracic Society) Dyspnea Grade I had occurred due to the weakening of the respiratory root. A molecular genetics examination conducted at another hospital discovered a deficit of the SMN1 gene, and considering the time of onset and clinical conditions, the patient was diagnosed with type IV spinal muscular atrophy. The patient stood 168 cm and weighed 63 kg, and there were no special opinions from ECG and simple radioactive examination before operation. Arterial blood gas analysis (ABGA) showed pH 7.435, PaO2 74.6 mmHg, PaCO2 36.9 mmHg, and HCO3- 24.2 mmHg. The patient was under drug treatment for hypertension. Administration before anesthesia was not conducted and vital signs examined after going into the operating room were blood pressure: 160/100 mmHg; respiration rate per minute: 20 times; ECG: normal sinus rhythm; and pulse oxymetry: 98%. From a manual muscle test before operation, both legs were at the 4th stage. At the genupectoral position, the epidural space was identified by loss of resistance technique using an 18 G Tuohy insertion needle in between the L2-L3 lumbar, and after a test dose injection of 1.5% lidocaine 3 ml containing 1 : 200,000 epinephrine, no increase of heart rate or spinal anesthesia symptom was detected. After injecting 0.75% ropivacaine 12 ml, a catheter was placed and maintained. To measure the level of motor block by time after anesthesia, a modified Bromage scale (0: One can stretch and raise his/her leg; 1: One cannot raise his/her leg and cannot bend his/her knee; 2: One cannot his/her knee but can bend his/her ankle; 3: One cannot bend his/her ankle) was applied.
The level of modified Bromage scale before anesthesia was 1, and 20 minutes after injecting ropivacaine, the level of modified Bromage scale was 3. The sensory nerves were blocked by T8 segment on pinprick examination. Vital signs during operation were blood pressure: 120-140/60-80 mmHg and pulse rate per minute: stable at 70-80 times. A Venti® mask with 35% of oxygen fraction in inspired air was used, and an ETCO2 capnometer was placed under the nose of the patient to monitor the end-tidal CO2. ETCO2 was stable at 35 mmHg and the pulse oxymetry was 100%. Due to the risk of aspiration of saliva or bronchial secretion during operation, sedation was not operated. The surgery was operated for an hour, and the epidural catheter was removed after operation. After finishing the operation, the level of modified Bromage scale was 3 and the sensory nerve block was decreased up to the T9 segment. Three hours after the operation, the level of modified Bromage scale was dropped to 2 and the sensory nerve block to the T11 segment; 5 hours after the operation, the stage of modified Bromage scale was 1, and the sensory nerve was declined to the L1 segment. Since the patient did not show adverse effects including vomiting, nausea, and dizziness in the recovery room, he was moved to a patient room. Twelve hours after finishing the operation, both the level of the modified Bromage scale and sensory nerve were recovered to the condition before operation, and also for the manual muscle test, both legs were maintained at the 4th stage. A physical exam conducted 24 hours after finishing surgery did not show special opinions. The patient recovered smoothly without complications and left the hospital 2 days after the operation.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [63.0, 'kg'], 'height': [168.0, 'cm']}",1.71464,1.62891,1.80037,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 168.0 cm. 
The patient's weight is 63.0 kg. 
Therefore, the patient's bsa is sqrt((63.0 (in kgs) * 168.0 (in cm))/3600) = 1.71464 m^2."
7195,60,Body Surface Area Calculator,physical,decimal,pmc-6769354-1,Extracted,"A 12-year-old girl had severe abdominal distention with increasing abdominal girth that had started 6 months earlier. She visited our hospital because her abdominal distention worsened despite her diet restriction.
Although she had menarche 9 months prior to presentation, her second menstruation had not come. Additionally, she had never experienced sexual relations.
The girl was 170 cm tall and weighed 63 kg. Her body mass index was 21.8. She had no fever or abdominal pain. Her abdomen was markedly distended without fluctuation.
Abdominal X-ray showed elevated diaphragms and a lesion occupying a large space in the abdominal cavity. Her routine blood analysis and renal functions were normal: white blood cell count, 4.40 × 103/mm3 (4.3-10.8 × 103); hemoglobin, 11.1 g/dL (12-18 g/dL); hematocrit, 34.3% (35-53%); platelet count, 220 × 103/μL (150-400 × 103/μL); alanine transaminase, 13 units/L (5-40 units/L); aspartate aminotransferase, 22 units/L (5-42 units/L); urea nitrogen, 16 mg/dl (8-20 mg/dL); and creatinine, 0.87 mg/dL (0.4-1.0 mg/dL).
The values of tumor markers were as follows: hCG (Human Chorionic Gonadotropin), < 0.003 units/mL (0-5 units/mL); α-fetoprotein, 0.7 ng/mL (< 5 ng/mL); carcinoembryonic antigen, 117.5 ng/mL (0-4.60 ng/mL); CA 19-9, 5029.0 units/mL (< 39 units/mL); and CA-125, 96.3 units/mL (0-35 units/mL). The patient’s CA 19-9 and CA-125 levels were high.
Abdominal US (Ultrasonography) showed a giant multilocular cystic lesion that had some solid lesions, which protruded into the inside of the giant lesion. There was an oviduct-like structure on the dorsal side (). T2-weighted MRI (Magnetic Resonance Imaging) also showed multilocular, high-intensity cysts with a stained-glass-like structure with a distinct septum and various concentrations of internal solution. Solid lesions had a lower intensity than that of the internal solution on T2-weighted images. On the bottom of the dorsal cyst wall, there was a structure that appeared to be an oviduct. Bilateral hydronephroses were caused by cyst oppression (). There was no finding suggesting peritoneal distant metastasis with MRI or CT (Computed Tomography).
We diagnosed a multilocular cyst connecting to the oviduct-like feature as an ovarian cystadenoma. Therefore, we performed a laparotomy.
We approached her abdomen by a lower abdominal horizontal incision and submitted her transparent ascites for cytology. The left oviduct was stretched and connected to the left lower side of the cyst. Although the border of the oviduct and tumor was clear, that of the ovarian parenchyma and tumor was ambiguous (Figure 3A,B). Therefore, we performed left oophorectomy. There were no findings that caused us to suspect membrane damage or lymph node metastasis or distant metastasis or dissemination in the peritoneal cavity. We thought the tumor was benign or borderline malignant. Therefore, we decided to preserve the oviduct. We ligated a thickened vessel entering the tumor from the mesometrium and removed the tumor. Adhesion to other organs was mild. Ascites cytology indicated that the tumor not malignant, and the intraoperative section diagnosis was diagnosed as an MCA. We sutured each layer of the abdominal wall and finished the operation.
The multilocular cystic tumor was 420 × 220 × 200 mm and 11.8 kg (Figure 3C,D). It contained mucinous fluid, and the luminal surface was covered with a single layer of endocervical-like epithelial cells. In some areas, nuclear stratification into 2 or 3 layers and the formation of reactive granulation tissue were observed pathologically. Nuclear fission, high nuclear atypia, and stromal invasion were not observed. Therefore, we diagnosed her tumor as an FIGO (International Federation of Gynecology and Obstetrics) stage IA (which is defined as tumor limited to 1 ovary, capsule intact, no tumor on surface, and negative washings) borderline MCA. Her postoperative course had no complications. Each tumor marker fell to within the normal range. The patient is doing well without recurrence or metastasis 5 years after the surgery.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [63.0, 'kg'], 'height': [170.0, 'cm']}",1.72482,1.63858,1.81106,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 170.0 cm. 
The patient's weight is 63.0 kg. 
Therefore, the patient's bsa is sqrt((63.0 (in kgs) * 170.0 (in cm))/3600) = 1.72482 m^2."
7196,60,Body Surface Area Calculator,physical,decimal,pmc-7310047-1,Extracted,"The proband, a 12 and a half years old female, is the only daughter of healthy and non-consanguineous Caucasian parents (the mother is 36 years old, the father 40 at conception). She was delivered by cesarean section for maternal reasons at 39 weeks of a spontaneous and unremarkable pregnancy. Amniocentesis was performed due to advanced maternal age resulting in a normal female karyotype (46,XX). The birth weight was 3000 g (25th percentile), length 50 cm (50th percentile), head circumference 35 cm (50th percentile), Apgar score was 8 and 10 at 1 and 5 min respectively. After birth she was referred as normal: she was breastfed for a few weeks, then artificially, weaned at 6 months. She walked independently at one year, spoke the first words at 18 months. At the admission to the kindergarten, at the age of 3, she was referred to the Child Neuropsychiatry Unit on account of language impairment. Intensive speech therapy was supplied for 2 years, then continued with less frequent sessions during the primary school with slowly but steadily positive results. During the second year of the primary school, at the age of 7, learning disability and behavioral disorders became evident. Cognitive assessment performed by Leiter R scale (specific for nonverbal intelligence) and by WPPSI-III, gave an IQ of 91 and 77, respectively (with VIQ = 68, PIQ =89 at the latter scale). A diagnosis of a neurodevelopmental disorder compatible with Gilles de la Tourette syndrome was made at age of 11 for the presence of motor and vocal tics, hyperactivity, motor and behavioral mannerisms, together with mild intellectual disability. During instrumental work up audiological examination, EEG and brain MRI were performed with normal results. At the last follow-up, when she was 12 years old, physical examination showed a height of 153 cm (35th percentile), weight of 61 kg (91th percentile). She had her first menstruation at the age of 11 years without dysmenorrhea or other related problems. Motor embarrassment and bilateral flat foot, corrected with orthotics, were persistent. The last cognitive assessment performed in 2015 by Leiter R gave an IQ score of 69, with WISC IV scale the results indicated total IQ of 57 (VCI = 60, PRI = 67, WMI = 61, PSI = 85) while the GAI was 59. The proband now attends the second class of the secondary school with a learning support teacher. Pharmacological treatment with Aripiprazole 8 mg/day is ongoing.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.0, 'kg'], 'height': [153.0, 'cm']}",1.61012,1.52961,1.69063,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 153.0 cm. 
The patient's weight is 61.0 kg. 
Therefore, the patient's bsa is sqrt((61.0 (in kgs) * 153.0 (in cm))/3600) = 1.61012 m^2."
7197,60,Body Surface Area Calculator,physical,decimal,pmc-3147132-1,Extracted,"A 28-year-old man was admitted to our hospital because of reduced livido and increased fatigability. He had been in good health until 1 year earlier, when he noticed reduced livido. Four months before admission, he noticed frequent headaches, thirst, polydipsia, and polyuria. Because he was voiding urine every hour, he visited his family doctor. Magnetic resonance imaging (MRI) revealed a suprasellar mass, and he was thus referred to our hospital for further evaluation and treatment. Although polydipsia and polyuria had been gradually relieved by the time of admission, he became aware of increased fatigability.
At the time of admission, he was 176 cm tall and weighed 72 kg. His temperature was 37.6°C, pulse rate was 60/min, and blood pressure was 110/60 mmHg. No goiter or enlargement of lymph nodes was noted. Axillar and pubic hair were lost and there was palpable erythematous rush on his forehead (). The remainder of the physical examination was unremarkable.
Laboratory results revealed the following results: blood urea nitrogen 9.6 mg/dL, creatinine 0.79 mg/dL, serum sodium 141 mEq/l, potassium 4.0 mEq/l, chloride 100 mEq/l, calcium 9.4 mg/dL, phosphate 3.7 mg/dL, fasting plasma glucose 80 mg/dL, and C-reactive protein 0.07 mg/dL. Endocrinologic data revealed a mild decrease in free T4 level (0.6 ng/dL) with normal thyroid-stimulating hormone (TSH) level (0.9106 μU/mL) and decreased cortisol (4.7 μg/mL), adrenocorticotropic hormone (ACTH; 6 pg/mL), luteinizing hormone (LH; 0.2 mIU/mL), follicle stimulating hormone (FSH; 1.3 mIU/mL), and testosterone (0.05 ng/mL) levels. Urinary cortisol was undetectable. Plasma osmolality was 288 mOsm/kgH2O, with a urinary osmolality of 239 mOsm/kgH2O, and arginine vasopressin (AVP) was undetectable (<0.15 pg/mL). Urinary output was from 1.5 to 2.2 L/day.
His clinical course and laboratory findings led us to suspect CDI with anterior pituitary dysfunction. We thus performed hormonal provocative tests. The patient was given an infusion of 5% saline at a rate of 0.05 mL/kg for 120 min. Although plasma AVP was undetectable before and after administration of hypertonic saline, urine osmolality (391 mOsm/kgH2O) increased above the plasma levels (296 mOsm/kgH2O) (). Hormonal provocative tests revealed that growth hormone (GH) response to GH-releasing hormone was normal, TSH response to TSH-releasing hormone was low and blunted, and FSH and LH response to LH-releasing hormone were low and blunted (). Although ACTH response to corticotrophin-releasing hormone (CRH) was normal, cortisol response to CRH was low (maximum 13.0 μg/mL). Cortisol response to rapid ACTH stimulation test was low (maximum 15.9 μg/mL). Results of these hormonal tests were compatible with the diagnosis of CDI with partial GC deficiency.
MRI revealed enhancing lesion centrally in the pituitary stalk, which spread continuously to the bottom of the third ventricle, and the high intensity of the posterior lobe was lost, compatible with the diagnosis of CDI (). Considering the patient's age, we first suspected of neurohypophysial germinoma. However, this was unlikely because cerebrospinal fluid was negative for malignant cells, and β-human chorionic gonadotropin (HCG) levels were normal. Next, we suspected sarcoidosis because chest X-ray revealed hilar enlargement. A biopsy from the skin of the forehead was performed, which revealed noncaseating granuloma composed of epithelioid cells (). Multinucleated giant cells were also present. Thus, the diagnosis of sarcoidosis was made.
While waiting for histologic confirmation of biopsy results, hydrocortisone replacement was begun with a dose of 20 mg daily. Soon after the replacement therapy was begun, moderate polyuria (3.5–4.0 liters daily) occurred (). After the diagnosis of sarcoidosis was confirmed, he was treated with 40 mg of prednisolone and his general condition improved. The hypertonic saline test was repeated while he was taking 40 mg of prednisolone. Plasma AVP was undetectable during the hypertonic saline test and urine osmolality was consistently below plasma levels, which was compatible with a diagnosis of CDI (). He was treated with 1-desamino-8-D-arginine vasopressin (dDAVP).
MRI following prednisolone therapy revealed a reduction in the size of the affected lesion. However, his pituitary function remained unchanged, and he is currently being treated with prednisolone, levothyroxine natrium, HCG, and dDAVP.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [72.0, 'kg'], 'height': [176.0, 'cm']}",1.87617,1.78236,1.96998,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 176.0 cm. 
The patient's weight is 72.0 kg. 
Therefore, the patient's bsa is sqrt((72.0 (in kgs) * 176.0 (in cm))/3600) = 1.87617 m^2."
7198,60,Body Surface Area Calculator,physical,decimal,pmc-8133044-9,Extracted,"A 79-year-old man (weight, 77 kg; height, 162 cm; BMI, 29 kg/m2) was scheduled to undergo radical prostatectomy. The MO was 3.5 fingers wide. No remarkable risk was noted. He had a K-score of 3. The intubation was smooth despite the relatively old age. The IDS score was 0, and the duration was 78 s. The lesson I learned from this case was to insert the laryngoscope slowly. If the laryngoscope is inserted too deep too quickly, it could disorient the inexperienced intubator, since the usual landmarks are absent on the screen.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [77.0, 'kg'], 'height': [162.0, 'cm']}",1.86145,1.76838,1.95452,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 162.0 cm. 
The patient's weight is 77.0 kg. 
Therefore, the patient's bsa is sqrt((77.0 (in kgs) * 162.0 (in cm))/3600) = 1.86145 m^2."
7199,60,Body Surface Area Calculator,physical,decimal,pmc-6966974-1,Extracted,"A 13-year-old girl (height, 151 cm; weight, 40.3 kg) with Kniest dysplasia was scheduled for surgery to recorrect talipes equinovarus. A flat nasal root and mandibular prognathism were present, but no symptoms of airway obstruction such as stridor, wheezing, or respiratory distress were detected preoperatively. The patients had no associated cartilage abnormalities, such as cleft palate, laryngomalacia, tracheomalacia, micrognathia, or platyspondyly.
She had previously undergone the same surgery at the age of 6 years, at which time laryngeal edema had rapidly developed after tracheal intubation, resulting in intensive care unit admission with tracheal intubation for 21 days. On the day of the scheduled reoperation at 13 years of age, her oxygen saturation upon entering the operating room was 99% on room air. Anesthesia was induced by intravenous administration of remifentanil at 0.5 μg/kg/min, thiopental at 200 mg, and rocuronium at 30 mg. Mask ventilation and laryngoscopy were easily performed. However, despite two attempts to perform tracheal intubation using uncuffed 6.0 and 6.5 mm standard tracheal tubes, tracheal intubation could not be achieved because of narrowing of the glottis. The tip of the tracheal tube did not pass the glottic level. False vocal cord swelling began after only two attempts and considering the history of prolonged laryngeal edema that had developed at the age of 6 years in this patient, the trial of tracheal intubation was discontinued. After placement of a size 2.5 laryngeal mask, anesthesia was maintained with 2.5% sevoflurane, and the airway was evaluated by a fiberscope 2 h later under spontaneous breathing through the laryngeal mask before the end of anesthesia. Although the end-tidal CO2 level was maintained at 40 to 46 mmHg and the capnogram waveform was plateaued without exhibiting an obstructive pattern or increase in the peak airway pressure, the development of laryngeal edema and glottic narrowing was observed using a fiberscope (Fig. ). Hydrocortisone 150 mg was intravenously administered, and the laryngeal mask was removed 139 min after the trials of tracheal intubation. We confirmed that the patient’s respiratory condition was not disturbed and returned her to the general ward. Her oxygen saturation upon exiting the operating room was 99% with the oxygen mask at 3 L/min. No postoperative exacerbation of her respiratory condition or decline in her oxygen saturation level was observed. Surgery was delayed until 1 month later.
1 month later, nasal endoscopy was performed by an otolaryngologist the day before the scheduled surgery. The otolaryngologist pointed out the small larynx and narrow glottis, but no vocal cord edema, thickness, or immobilization was observed throughout the laryngopharynx (Fig. ). In addition, no airway narrowing or deformity was detected from the glottis to the carina by cervical computed tomography (Fig. ). The airway was not compressed by the curve of the cervical vertebrae, and cervical retroflexion was not impaired preoperatively. The minimum diameter of the airway on the axial view was 7.08 mm (anteroposterior diameter) and 11.79 mm (transverse diameter) as identified at the glottic level (Fig. ). The second anesthesia was performed without tracheal intubation. Anesthesia was induced with midazolam 2 mg, fentanyl 25 mg, and dexmedetomidine 2 μg/kg/h, and spinal anesthesia was then performed at the L3/4 level with 2.5 ml of 0.5% bupivacaine. The catheter used for the sciatic nerve block was inserted by a subgluteal approach for postoperative analgesia. The patient was sedated with dexmedetomidine at 0.5 to 1.2 μg/kg/h during surgery. Adequate spontaneous breathing was maintained without symptoms of laryngospasm or airway obstruction such as stridor or wheezing and the oxygen saturation was maintained at > 99% during anesthesia. The surgery time was 175 min, and the anesthesia time was 209 min. The patient was transferred to the general ward for postoperative care without airway complications.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [40.3, 'kg'], 'height': [151.0, 'cm']}",1.30014,1.23513,1.36515,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 151.0 cm. 
The patient's weight is 40.3 kg. 
Therefore, the patient's bsa is sqrt((40.3 (in kgs) * 151.0 (in cm))/3600) = 1.30014 m^2."
7200,60,Body Surface Area Calculator,physical,decimal,pmc-7507522-1,Extracted,"Patient 1 was a 14.5-year-old girl born to a primigravida from Shandong Province. At conception, her father was 31 years old, and her mother was 30 years old. She was delivered in good general condition, without asphyxia or hypoxia. She was born at term but displayed features of intrauterine growth restriction (IUGR) during pregnancy. Her birth weight was 2100 g (<3 percentile), and her height was 44 cm (<3rd percentile). From day 3 on, the baby was exclusively artificially fed until 2 years old, which resulted in gradual low weight gain. Her psychomotor development was normal. She started to practice speaking at 12 months but walked at 19 months. At school age, she found it difficult to learn, especially in math, and the score was usually less than 20 (out of 100 points). Short stature was noted at birth but became more noticeable from the age of 12 years; however, her parents did not record the growth rate per year in detail. She was first seen in the endocrine clinic at age 14.5 years and was referred for the assessment of short stature.
At admission, we performed a systematic physical examination. She was noted to have partial lipodystrophy as well as a peculiar face, looking considerably older than her age. On examination, she was found to have short stature (137.3 cm, −4.0 SD), low weight (27 kg, −2.7 SD), and low BMI (14.3 kg/m2, −2.5 SD). Her face showed typical features, such as microcephaly, triangular shape, small chin, and so on. Physical examination showed abnormal abduction of the elbow joint (elbow valgus) and brachydactyly, short fingers/toes, metacarpal sign and bilateral toe deformities (Figure ). Her puberty stage was Tanner III but no menarche.
Her father was 170 cm in height and grew significantly at the age of 14 years. Her mother was 153 cm in height with menarche at the age of 13 years. Her younger brother was 6 years old and maintained a height above the 50th percentile of the population with the same age and gender. There was no family history of diabetes mellitus or short stature.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [27.0, 'kg'], 'height': [137.3, 'cm']}",1.01477,0.96403,1.06551,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 137.3 cm. 
The patient's weight is 27.0 kg. 
Therefore, the patient's bsa is sqrt((27.0 (in kgs) * 137.3 (in cm))/3600) = 1.01477 m^2."
7201,60,Body Surface Area Calculator,physical,decimal,pmc-8610885-1,Extracted,"A 26-year-old male patient was admitted with symptoms of fatigue, tiredness, generally being unwell, melena and anemia.
His illness had begun 2 wk before with intermittent dark stools. Three days to presentation, he had a fever of 39C and right quadrant pain. He experienced an unexplained weight loss of 13 kg within 2 wk. He denied current or prior alcohol consumption, smoking, or drug use.
The patient had a medical history of surgery for intestinal obstruction due to adhesion 2 mo before the current admission, which was associated with a previous operation for intussusception at the age of 13 years. Two years ago, he also had melena managed with blood transfusion and proton pump inhibitors.
No significant family history or risk factors for GI pathologies were found.
Physical examination showed clinical signs of anemia, otherwise within normal limits. No sign of jaundice was observed. His abdomen was flat and soft without tenderness or palpable mass. His height was 162 cm and his weight was 49 kg (body mass index 18.7 kg/m2).
Hematological investigations showed iron deficiency anemia with 72 g/L hemoglobin (normal range, 135–175 g/L). Other laboratory data revealed an elevated serum total bilirubin of 35 mol/L (normal range ≤ 17 mol/L), alkaline phosphatase of 380 U/L (normal range 40–129 U/L) and increased serum C-reactive protein of 30 mg/dL (normal range ≤ 0.05 mg/dL) and procalcitonin of 17.6 ng/mL (normal range ≤ 0.05 ng/mL) (Table ).
Dynamic abdominal computed tomography (CT) showed marked thickening of the duodenal walls and fatty replacement over the entire pancreatic parenchyma with no delineation between the pancreas and duodenum. The main pancreatic duct was not narrowed or dilated, and no tumor was detected (Figure ). Magnetic resonance imaging (MRI) with T1-weighted, T2-weighted, and fat-suppression images showed a large mass-like lesion containing adipose tissue from the pancreatic head to tail (Figure ). Fatty tissue infiltrated not only the pancreatic parenchyma but also the duodenal wall (Figure , ). Both CT and MRI findings suggested the diagnosis of LiPH. Furthermore, focal cystic dilatations of intrahepatic bile ducts in the left hepatic lobe (localized biliary ectasia) were also detected on CT and MRI (Figure , ). Esophagogastroduodenoscopy revealed a large submucosal mass along the C-shaped loop of the duodenum, the size of the tumor was about 100 mm in the longest diameter with central ulceration, which was considered the origin of bleeding (Figure ).",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [49.0, 'kg'], 'height': [162.0, 'cm']}",1.48492,1.41067,1.55917,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 162.0 cm. 
The patient's weight is 49.0 kg. 
Therefore, the patient's bsa is sqrt((49.0 (in kgs) * 162.0 (in cm))/3600) = 1.48492 m^2."
7202,60,Body Surface Area Calculator,physical,decimal,pmc-8504087-1,Extracted,"A 19-month-old Syrian boy was referred to our clinic for steatorrhea, vomiting, and abdominal distension. He was born a full-term, normal pregnancy without any complications after birth. The birth weight was 4 kg. The newborn screening test was normal. Since early infancy, he suffered from feeding intolerance and diarrhea described 5 times per day; oily, bulky, and foul-smelling without vomiting or bilious emesis. He was on breast and bottle feeding. By the age of 6 months, there was an obvious failure to weight gain and the family started seeking medical advice. Investigations were performed which excluded primary cystic fibrosis, alpha 1 antitrypsin, Metabolic disease (lipid metabolism disease), thyroid diseases, adrenal insufficiency, diabetes mellitus, and celiac disease. There were fatty drops in the stool examination. A diagnosis of non-specific malabsorption was made and the patient was treated with multivitamins without any improvement in general condition. The family started feeding him PediaSure® formula milk - only by chance- from around 10 months of age with partial improvement in his symptoms and observed weight gain. His development was normal for his age. The child underwent all the compulsory immunizations for his age. There was no relationship between the parents and the family history was noncontributory.
On physical examination, his body weight was 9 kg (− 3 SD), the length was 75 cm (− 3 SD), he was vitally stable and generally well. The abdomen was distended but soft, with no masses or organomegaly. The neurological assessment was normal. The patient underwent multiple investigations. Complete blood count (CBC), C- reactive protein (CRP), blood film, blood gases, renal and liver function, electrolytes, glucose, bilirubin, ammonia, amylase, lipase, and urine were normal (Table ). Stool microscopy revealed fat globules. Abdominal ultrasound showed revealed intestinal wall thickening with normal findings (Liver steatosis was not observed). An ophthalmologic (funduscopic examination), cardiac assessment (echocardiogram) was normal. We performed an Esophagogastroduodenoscopy (EGD) that showed a milky white “snow-storm” appearance of the duodenal mucosa (Fig. ) and the histological biopsies from the duodenum showed fat-laden vacuolization of enterocytes without villous atrophy (Fig. a, b). That suggested lipid trafficking disorder. The Differential Diagnosis included abetalipoproteinemia (ABL), hypobetalipoproteinemia (HBL), or CRD. Therefore, more specialized additional investigations were performed including total cholesterol (TC), Low-Density lipoprotein cholesterol (LDL-C), and total lipid which were markedly reduced; high-Density lipoprotein cholesterol (HDL-C) was borderline low with normal very-low-density lipoprotein (VLDL) and Triglycerides (TG). Total Creatine kinase (CK) was elevated. Vitamin A, D levels were borderline low with low vitamin E levels (Table ). Lipoprotein electrophoresis of postprandial plasma did not show the presence of chylomicrons. Immunoblot testing showed a decrease in apolipoprotein A1 and apolipoprotein B.
The clinical and laboratory findings were more consistent with CRD. A blood sample for genetic analysis in directional direct DNA sequencing (AB 3730 DNA analyses equipped with seascape software) of SARB coding exons and exonic-intronic junctions from genomic DNA was obtained. Genotyping identified a homozygous SAR1B gene variant as the deletion of one of the two repeated Glutamine in position 113 or 114. It was the first description of this variant in the fourth helix of SAR1B protein (NM_0161032.: c.[del340-342]; [del340-342], p. [Glu114del]; [Glu114del]). His parents were heterozygous for the same variant (NM_0161032.: c.[del340-342]; [=], p. [Glu114del]; [=]).
The patient was started on the restriction of dietary fats, hydrolyzed formula with a higher medium-chain triglyceride content, some vegetable oils (sun-seed, olive oil, almond oil) in his daily diet in addition to fat-soluble vitamin supplementation (hydrosoluble vitamin E 50 UI/kg/d; vitamin A 15,000 IU/d; vitamin K 15 mg/wk.; vitamin D 1000 UI/kg/d).
During follow-up, the child showed catch-up growth in weight–height and a clinical examination were unremarkable with normal laboratory findings (Table ) (Fig. ).",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [9.0, 'kg'], 'height': [75.0, 'cm']}",0.43301,0.41136,0.45466,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 75.0 cm. 
The patient's weight is 9.0 kg. 
Therefore, the patient's bsa is sqrt((9.0 (in kgs) * 75.0 (in cm))/3600) = 0.43301 m^2."
7203,60,Body Surface Area Calculator,physical,decimal,pmc-6661044-1,Extracted,"A 76-year-old woman (height 156 cm, weight 47 kg) had previously undergone intestinal resection procedures because of superior mesenteric artery occlusion and carotid artery stenting for bilateral internal carotid artery stenosis. As a result, she had a past medical history of old cerebral infarction.
We planned endovascular aneurysm repair (EVAR) for para-renal abdominal aortic aneurysm using the snorkel technique for the renal artery, but we failed to pass through the left subclavian artery when approaching from the left brachial artery because of AAO.
Before the operation, her pulse was palpable and there was no difference between the left and right upper extremity. Her upper arm blood pressure at that time exhibited no laterality (HR 87/min, BP right 149/90 mmHg, BP left 148/84 mmHg).
Preoperative enhanced computed tomography (CT) imaging revealed a para-renal abdominal aortic aneurysm with a maximum diameter of 58 × 63 mm. The axillary artery was densely calcified, but the AAO was not obvious since the contrast medium was injected from the left upper extremity during preoperative enhanced CT, and this caused severe halation at the axillar/subclavian vein, which made visualization of the adjacent left subclavian artery difficult or impossible.
We planned EVAR for her para-renal abdominal aortic aneurysm using the snorkel technique in the renal arteries. We attempted cannulation of the renal artery approaching from the left brachial artery, but failed to pass through the left subclavian artery because of AAO. Therefore, we decided to compromise the EVAR by landing the proximal stent in the short neck without the snorkel technique. Since the completion angiogram showed the absence of endoleak and complete exclusion of the aneurysm, we did not access the right upper extremity to perform the originally planned snorkel technique.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [47.0, 'kg'], 'height': [156.0, 'cm']}",1.42712,1.35576,1.49848,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 156.0 cm. 
The patient's weight is 47.0 kg. 
Therefore, the patient's bsa is sqrt((47.0 (in kgs) * 156.0 (in cm))/3600) = 1.42712 m^2."
7204,60,Body Surface Area Calculator,physical,decimal,pmc-8601284-1,Extracted,"A 48-year-old woman visited the referral university hospital to jaundice and nausea. She was referred to the outpatient clinic of gastroenterology department in a tertiary hospital due to jaundice and increased levels of liver enzyme detected during blood test tracking after 5 weeks of pazopanib therapy.
The patient's medical history included end-stage renal disease on hemodialysis, liver cirrhosis with hepatitis B virus carrier. The patient underwent right nephrectomy for RCC 2 years ago. Newly onset liver and lung metastasis were detected 3 months ago by liver biopsy. The patient started taking immunotherapy agent (pazopanib) and prophylactic antiviral agent (tenofovir disoproxil fumarate) from 2 months ago. Pazopanib prescribe was started at half dose considering the patient's clinical history of liver cirrhosis. After administration at 400 mg per day, which is half the dose for 2 weeks, liver enzyme level was kept in the normal range and showed no change, so the dosage was increased to a fixed amount of 800 mg per day and dosing was maintained for an additional 2 weeks.
Before first visiting the outpatient clinic, the patient had symptoms of nausea with vomiting and jaundice for 2 weeks. The patient was suspected to progress acute hepatitis considering jaundice and increased liver enzyme. Elevated serum total bilirubin persisted 2 weeks after pazopanib discontinuation and she was hospitalized for further evaluation and treatment.
At the time of admission, she was 160.5 cm tall, weighed 61.1 kg, and had a body mass index (BMI) of 23.72. Blood pressure of the patient was normal with a systolic blood pressure of 123 mm Hg and a diastolic blood pressure of 74 mm Hg. Mild elevated body temperature (37.8 °C) and normal heart rate (95 bpm) with normal breathing rate (18 breaths per minute) was seen. The patient presented with nausea and jaundice. The patient had a soft abdomen on physical examination.
Liver-function test at baseline shows no abnormal findings measured before pazopanib treatment and 2 weeks after the start of treatment. However, blood tests measured 5 weeks after the start of treatment revealed abnormal findings in liver function. At the time 5 weeks after starting treatment of pazopanib, levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) were 306, 427, and 227 U/L, respectively. Prothrombin time-international normalized ratio value was in normal range (0.99). The total bilirubin level was 1.98 mg/dL (Fig. ). Alpha-fetoprotein (AFP) level was 6.1 ng/mL with in normal range. The blood test results related to hepatitis virus infection are as follows, hepatitis B surface antigen (positive); anti-HBs (negative); hepatitis B e antigen (negative); anti-HBe (positive); hepatitis B virus DNA (120 copies/mL); anti-hepatitis C virus (negative). Child-Pugh score and class were 5 points and class A. The model for end-stage liver disease (MELD) score was 20 points and estimated 3-month mortality was 19.6%.
Contrast-enhanced abdominal computed tomography (CT) revealed liver cirrhosis and there was no significant change of about 1.3 cm sized enhancing hepatic nodule on right lobe which is pathologically proven metastatic RCC. There was no obstructive lesion on biliary tract (Fig. ). Abdominal ultrasound also revealed no significant abnormality other than hepatic nodule and liver cirrhosis.
There was a clinical possibility of DILI caused by pazopanib, and the Roussel Uclaf Causality Assessment Method (RUCAM) score was used to evaluate the possibility of the disease. The patient was of the mixed type. Symptoms started appearing 5 weeks after administration (+2). Total bilirubin, AST, and ALT were normalized within 180 days of the cessation of drug administration (+2). There were no risk factors such as alcohol, pregnancy, and the elderly over 55 years of age (0). Although tenofovir was taken as a concomitant drug, the possibility of hepatotoxicity by the drug was low, and the time interval was not consistent with the onset of symptoms (0). There were no acute viral hepatitis, bile duct obstruction, alcoholism, or recent hypotension that could cause liver damage other than drugs (+2). Pazopanib, which was taken, is a drug with a warning of hepatotoxicity on the product according to previous studies (+2). The possibility of DILI can be known more clearly through re-administration of the drug, but re-administration was not performed in this patient (0). Taking these factors into consideration, the patient's RUCAM score was 8 points, and it was in the probable group corresponding to 6 to 8 points, so the possibility of DILI was high. At the beginning of the clinical course, it was unknown whether there will be any improvement after the cessation of drug administration, so even if this score factor (course-change after stopping drug) was excluded, the RUCAM score was already 6 points, indicating a high possibility of DILI, so treatment for pazopanib-induced DILI was initiated.
Finally, for confirmatory diagnosis, liver biopsy was performed to establish the cause of jaundice. Liver biopsy revealed hepatocyte swelling and degeneration with cholestasis in centrilobular area and the protal tract showed only sparse chronic inflammation. The final diagnosis was confirmed as acute cholestatic hepatitis consistent with toxic hepatitis (Fig. ). Therefore, the patient was diagnosed with severe DILI due to pazopanib.
The patient started to take prednisolone 40 mg daily for 1 week for empirical treatment of DILI. The dose of prednisolone was gradually reduced every 1 week and it was discontinued finally after 7 weeks of dosing. After discontinuation of pazopanib and taking empirical steroid treatment, the patient's AST and ALT levels were maintained within the normal range and total bilirubin level was decreased significantly from the peak level of 24.61 to 1.06 mg/dL on 12-weeks after pazopanib discontinuation (Fig. ). After discontinuation of pazopanib treatment, jaundice improved rapidly and the patient is currently being observed in the outpatient clinic.
The study protocol was approved by the Institutional Review Board of Soonchunhyang University Bucheon Hospital, and conformed to the ethical guidelines of the World Medical Association Declaration of Helsinki. Written informed consent was obtained because of the retrospective design.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.1, 'kg'], 'height': [160.5, 'cm']}",1.65047,1.56795,1.73299,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 160.5 cm. 
The patient's weight is 61.1 kg. 
Therefore, the patient's bsa is sqrt((61.1 (in kgs) * 160.5 (in cm))/3600) = 1.65047 m^2."
7205,60,Body Surface Area Calculator,physical,decimal,pmc-6786676-1,Extracted,"A 55-year-old man was brought to emergency room after accidental ingestion of insecticide, methidathion (also known as methion in Korea) while he was drunken. According to his family member, he ingested a paper cup full of 40% original solution. He had history of non-insulin dependent diabetes mellitus. His body weight was 75 kg and height was 173 cm.
In the emergency room, he was semi-comatose, but had intermittent myoclonus-like movements. Blood pressure was 67/50 mmHg and heart rate was 48 beats per minute. His trachea was intubated and he was placed on mechanical ventilation. Initial resuscitation efforts included intravenous infusion of atropine (50 mcg/minute) after a bolus of 1 mg, norepinephrine (0.25 mcg/Kg of body weight/minute), vasopressin (0.3 units/minute), dobut-amine (30 mcg/Kg/min), epinephrine (0.25 mcg/Kg/min), and PAM-A (Pralidoxime chloride, cholinesterase reactivator, 2.5 mg/min), in addition to intravascular volume expansion with crystalloids, in efforts to keep the mean arterial pressure higher than 65 mmHg. Also given were midazolam, remifentanyl, and vecuronium. Gastric lavage was done. The initial arterial blood gas analysis while he was being mechanically ventilated with 100% of oxygen showed that pH was 6.96, PCO2 98 mmHg, PO2 85 mmHg, HCO-3 19 mEq/L, and BE -14.8. His ethanol level in blood was 144 mg/dl. Albumin was 4.4 g/dl, glucose 359 mg/dl, Hemoglobin A1c 11.4%, and total CO2 content 16.9 mEq/L. The levels of total bilirubin, aminotransferases, sodium, chloride, potassium and troponin I were normal, so were prothrombin time, international normalized ratio, and activated thromboplastin time. Leukocyte count was 17,400 cells/mm3, hemoglobin 15.4 g, hematocrit 46% and platelets 266,000/mm3 . The repeated analysis of arterial blood gases showed that pH was 7.09, PCO2 29 mmHg, PO2 66 mmHg, HCO-3 20 mEq/L, BE –11.3 and lactate 7.8 mEq/L. Urine output had been in the range of 200 to 600 mL/hour. Serum cholinesterase level was 12 (normal, 620-1,370) units/L.
The patient was transferred to intensive care unit. Tests for hepatitis A, B, and C were negative, so was human immunodeficiency virus test. Free T4 level was 3.84 mcg/L. Arterial blood gases showed that pH was 7.23, PCO2 59 mmHg, PO2 78 mmHg, HCO-3 24 mEq/L and lactate 1.7 mEq/L. Blood cultures, of which blood samples were taken from the central venous line, arterial line and percutaneous punctures, were all negative. Intravenous infusion of vecuronium was discontinued. On the 2nd hospital day, intravenous infusion of epinephrine was tapered off. The infusion of norepinephrine was reduced to 0.15 mcg/kg/min, vasopressin to 0.15 units/min and dobutamine to 20 mcg/kg/min. There was no longer metabolic acidosis. Urine output decreased to 300 ml/h. On the 4th hospital day, intravenous infusion of atropine was discontinued. Glycopyrrolate was given intermittently whenever heart rate became less than 60 beats per min. Urine output was running about 100 ml/h. Daily chest radiography had been unremarkable. Sputum culture revealed the growth of Klebsiella pneumoniae, which was sensitive to all antibiotics except ampicillin. Piperacillin/tazobactam was started. On the 5th hospital day, doses of vasopressors and inotropic were not able to be reduced. Interleukin-6 was 335 pg/ml and procalcitonin 92 ng/ml. Intravenous infusion of remifentanil and midazolam had been maintained for sedation. Despite the use of high doses of vasopressors and inotropic, the patient’s hands and feet were warm and pink, and there was no metabolic acidosis, thus indicating that there was no peripheral vasoconstriction or poor peripheral perfusion. On the 6th hospital day, lactate level was 1.3 mEq/L. Fibrinogen was 966 mg/dl and d-dimer 6.53 mg/L. The absence of deep vein thrombosis was confirmed with ultrasonography and transthoracic echocardiography ruled out an acute pulmonary embolism (no right ventricular dysfunction). Total parenteral nutrition was started. Enteral feeding was not considered appropriate at this time. On the 9th hospital day, intravenous midazolam infusion was discontinued. Over the following several days, vasopressors and inotropic were able to be reduced gradually. On the 11th day, all vasoactive medications were completely tapered off. The patient opened eyes on command. Intravenous infusion of ketamine was added. On the 14th hospital day, ulnar nerve stimulation test using train-of-four technique to assess neuromuscular junction activity revealed the presence of depolarizing block, indicating the persistent muscle paralysis by cholinergic crisis. Sputum culture showed the growth of methicillin-resistant Staphylococcus aureus. Vancomycin was started. On the 17th hospital day, pH of arterial blood decreased 7.29 from 7.41 and PCO2 increased to 56 mmHg from 42 mmHg in the afternoon, compared with those of morning values. Leukocyte count increased to 17,750 cells/mm3 from 12,000. Platelet count also increased to 765,000/mm3 from 576,000/mm3. Ultrasonography of abdomen showed a large amount of ascites. CT scan of abdomen revealed multiple perforations of small bowel. While the exploratory laparotomy was being arranged, pulmonary artery catheter was inserted via right subclavian vein under ultrasonographic guidance. Pulmonary artery pressure was 36/18 mmHg with pulmonary capillary wedge pressure of 12 mmHg. On laparotomy, almost the whole small bowel was found gangrenous and there were multiple perforations of small bowel. The portion of bowel from the distal duodenum to the ascending colon was resected. Since there was no gross evidence of peritonitis, the peritoneum was closed. Postoperatively, vasopressors and inotropic were required overnight, but quickly tapered off by the following morning. Urine output was running in the range of 100 to 300 ml/h. Analysis of arterial blood gases showed that pH was 7.44, PCO2 44 mmHg, PO2 83 mmHg and HCO-3 29.2 mEq/L, while the patient was on mechanical ventilator with 10 cmH2O and 0.6 of FiO2. Lactate was 1.8 mEq/L. Creatinine was 1.15 mg/dl. Leukocyte count was 17,690 cells/mm3 and platelet 352. Fibrinogen level was 305 mg/dl. On the 20th hospital day, glycopyrrolate was given for the last time. Cultures from the peritoneal drain and blood were all negative. Procalcitonin was 5.03 ng/dl, interleukin-6 92.2 pg/dl, C-reactive protein 16.32, fibrinogen 432 mg/dl and platelet count 230,000/mm3. Repeated ulnar nerve stimulation test using train-of-four technique revealed the presence of depolarizing block, indicating the persistent muscle paralysis by cholinergic crisis. Pathologic report of surgical specimen revealed the aspergillosis infection causing gangrene and abscess formation with multiple bowel perforations. Serum Aaspergillus antigen (galactomannan) was negative. Voriconazole was started. On the 27th hospital day (10th postoperative day), culture of peritoneal drain fluid showed the growth of methicillin-resistant S. aureus. Blood culture was negative. On the 31th hospital day, the second laparotomy revealed a diffuse peritonitis, gangrenous colon and abscess formation with perforations. Total colectomy was done. Postoperatively, the patient developed a severe septic shock, requiring vasopressors and inotropic in escalating doses. Intravascular volume expansion was done with guidance of pulmonary artery catheter. Thermodilution cardiac output was running in the range of 10 to 12 L/min. The patient developed a severe metabolic acidosis with rising level of lactate. On the 38th hospital day, lactate level rose to 10.7 mEq/L. Repeated test for Aspergillus antigen (galactomannan) became positive (5.42 index). The patient developed a sudden cardiac arrest. A prolonged effort of cardiopulmonary resuscitation became futile.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [75.0, 'kg'], 'height': [173.0, 'cm']}",1.89846,1.80354,1.99338,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 173.0 cm. 
The patient's weight is 75.0 kg. 
Therefore, the patient's bsa is sqrt((75.0 (in kgs) * 173.0 (in cm))/3600) = 1.89846 m^2."
7206,60,Body Surface Area Calculator,physical,decimal,pmc-6783222-1,Extracted,"A 6-year, 2-month-old boy was admitted to our hospital complaining of a 4-day history of weakness. His birth weight was 3.00 kg. No family history of endocrine, renal, celiac, and cardiovascular diseases or history of diuretic use was noted. Blood pressure was normal (91/63 mmHg). Initial biochemical analysis revealed metabolic alkalosis with hypokalemia (Table ) based on the following values: serum total calcium level was 2.40 mmol/L (normal range: 2.20–2.65 mmol/L), phosphorus was 1.25 mmol/L (normal range: 1.29–2.26 mmol/L), and serum magnesium level was very low compared to the normal range. Further investigations revealed high serum renin and aldosterone levels. The 24-hour urinalysis showed that calcium was 2.5 mg/24 hour, significantly lower than the normal range of 100–300 mg/24 hour. The patient had normal adrenal, hepatic, renal, parathyroid, and thyroid function. Abdominal ultrasound showed that the kidneys and liver were normal. Whole blood DNA sequencing revealed 2 heterozygous mutations in the SLC12A3 gene (c.473G>A p.R158Q and c.602-16G>A p. splicing) (Table ). Administration of oral replacement of magnesium oxide (MgO, 1 g/day), potassium chloride (KCl, 2.0 g/day), and spironolactone (2 mg/kg·day−1) was done. Serum potassium and magnesium levels increased to 3.0 mmol/L and 0.85 mmol/L, respectively. The frequency of weakness significantly decreased. However, his growth rate was just 4.2 cm/year, slightly higher than that before MgO and KCl therapy, which was only 3.2 cm/year.
His height was 108 cm (−2.78 standard deviation score [SDS]) and his weight was 18.7 kg (−1.58 SDS) at 9.50 years. The pubertal stage was genitalia stage I and pubic hair stage I, and his bone age (BA), according to the Greulich-Pyle method, was 6 years old. Growth hormone stimulation tests (GHSTs) (L-dopa and arginine) for short stature identified GHD, the peak GH level was 6.00 ng/mL (see Table ). Pituitary MRI revealed no remarkable findings. The patient was treated with 0.277 mg/kg/week of recombinant human growth hormone (rhGH), and he achieved a 10.6-cm height gain over 11 months.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [18.7, 'kg'], 'height': [108.0, 'cm']}",0.749,0.71155,0.78645,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 108.0 cm. 
The patient's weight is 18.7 kg. 
Therefore, the patient's bsa is sqrt((18.7 (in kgs) * 108.0 (in cm))/3600) = 0.749 m^2."
7207,60,Body Surface Area Calculator,physical,decimal,pmc-3809873-1,Extracted,"A 72-year-old woman underwent THA for idiopathic osteonecrosis of left femoral head in February, 2000. In 2012, she visited our emergency room for left hip pain with clunk sounds after squatting position 3 days ago. She had no problems in gait before the accident of squatting position. She has obese appearance; her height was 164 cm, weight was 90 kg, and bone mass index was 33.5 kg/m2. There was no evidence of infection including redness or heating sensation around left hip.
Plain radiographs showed ceramic head fractures with multiple fragments around the joint. The former arthroplasties included the cementless cup (Trilogy® acetabular system, Zimmer, Warsaw, IN, USA), cementless stem (Versys® hip system, Zimmer, Warsaw, IN, USA), polyethylene liner (Trilogy® acetabular system, UHMWPE, Zimmer, Warsaw, IN, USA), and ceramic head (Versys® hip system, 28 mm diameter, short neck length, zirconium oxide ceramic). The inclination of acetabular cup was 43 degree, and anteversion was 10 degree, which were within acceptable range ().
Revision operation was done. Posterolateral approach was used, similar to previous operation. After capsulectomy thorough posterolateral approach, various sizes of ceramic particles were observed. Intraoperatively, ceramic fragments were meticulously removed, and extensive capsulectomy was performed. Inner surface of polyethylene liner and metal neck taper junction of the femoral components were severely scratched to retain (). There were concerns about refracture of ceramic head and galvanic corrosion of metal head because of the scratched femoral neck. Thus, femoral stem was removed. In addition, the acetabular cup that was loosened because of osteolysis was also removed. After the removal of all components, massive irrigation and extensive synovectomy were done to remove microscopic ceramic fragments.
For revision, new cementless acetabular cup (Delta-PF Cup, Lima, Udine, Italy), full-coated modular cementless stem (Revision hip uncemented stem-Lima, Udine, Italy) were used. And, the 4th generation ceramic liner (Neutral liner, 36 mm I.D., Biolox Delta, CeramTec, Plochingen, Germany) was implanted for revision surgery. Full-coated modular cementless stem (Revision hip uncemented stem-diameter 16 mm, length 140 mm, Neck with screw-height 60 mm, Lima, Udine, Italy) was inserted with allogenic bone graft around proximal femur. Finally, the 4th generation ceramic head (Femoral head, 36 mm short taper 12/14, Biolox Delta, CeramTec, Plochingen, Germany) was applied. Intraoperative testing of the stability of the revised implants was advisable. The cup position was checked with 42 degree of abduction, and 31 degree of anteversion in postoperative plain radiographs ().
At her 6 months follow-up, she could return to her previous level of activity, and had Harris hip score of 82. In radiographs, the implant showed stable fixation without sign of osteolysis or loosening.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [90.0, 'kg'], 'height': [164.0, 'cm']}",2.02485,1.92361,2.12609,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 164.0 cm. 
The patient's weight is 90.0 kg. 
Therefore, the patient's bsa is sqrt((90.0 (in kgs) * 164.0 (in cm))/3600) = 2.02485 m^2."
7208,60,Body Surface Area Calculator,physical,decimal,pmc-7383637-1,Extracted,"A 71-year-old right-handed man [height: 185 cm; body weight: 87 kg; body mass index (BMI) 25.4 kg/m2] presented at the emergency department following involuntary movement of the left arm for 1 week. He had no history of diabetes but experienced polydipsia, polyuria, and a weight loss of about 10 kg in the previous month. He also reported a 24-year history of well-controlled hypertension and a 4-year history of percutaneous coronary intervention. He was on regular medication for the above two diseases. He had been diagnosed with lung adenocarcinoma 4 years before presentation and had been receiving icotinib (125 mg tid) since then. On neurological examination, muscle tone and strength of extremities were generally normal. No cranial nerve impairment or sensory disturbance was identified. Routine laboratory evaluation revealed random serum glucose up to 42.05 mmol/l with normal serum osmolarity (304.5 mmol/l). The artery gas analysis was normal. His urine glucose was positive (+++) and ketone was negative. His A1C (HbA1c) was 14% (130 mmol/mol). Cerebral CT was arranged instead of MRI because of the metal coronary stent and revealed a hyperdense lesion in the right basal ganglia (). After neurology and endocrinology consultation, other etiologies for HH including cerebrovascular condition, infection, and neurodegenerative disorders were excluded. The patient was diagnosed with diabetic HH and referred to the endocrinology department for further therapy.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [87.0, 'kg'], 'height': [185.0, 'cm']}",2.11443,2.00871,2.22015,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 185.0 cm. 
The patient's weight is 87.0 kg. 
Therefore, the patient's bsa is sqrt((87.0 (in kgs) * 185.0 (in cm))/3600) = 2.11443 m^2."
7209,60,Body Surface Area Calculator,physical,decimal,pmc-7336260-1,Extracted,"A 7-year-old girl with distinct facial features and short stature visited our hospital for diagnostic evaluation. She had been born via cesarean section at 36-week gestation without perinatal problems; her birth weight was 2.7 kg (25th–50th percentile). She was the second child of nonconsanguineous, healthy parents. Her midparental height was 160 cm (father's height, 180 cm; mother's height, 153 cm). Her elder brother exhibited normal growth and psychomotor development. There was no family history of genetic diseases.
At initial presentation, the patient’s height was 105.8 cm (-3.54 standard deviation score [SDS]); her weight was 16.3 kg (-2.45 SDS), and her head circumference was 51 cm (-0.3 SDS). Her bone age was 4.5 years. She had dysmorphic facial features, which included a small, triangular face with deep-set eyes, a broad and bulbous nose, a short philtrum, and thin lips as well as hand anomalies, such as clinodactyly and a short thumb with clubbing. X-rays revealed middle phalange dysplasia and genu varum ().
The patient's fine motor and gross motor development were appropriate for her chronological age. She demonstrated severe intellectual disabilities as well as obsessive-compulsive and aggressive behaviors. The patient attended a special-education school and had been receiving rehabilitation treatment for the previous 2 years. Electroencephalogram, brain magnetic resonance imaging, echocardiography, and ultrasound of the kidneys were normal. Chromosome analysis indicated a 46, XX karyotype. Ophthalmological examination revealed strabismus and mild diplopia. Results of blood biochemical and urine studies were within the normal ranges. Thyroid function test results were also normal. Serum insulin-like growth factor 1 (IGF-1) and IGF-binding protein 3 levels were 223.1 ng/mL (normal range, 26–320 ng/mL) and 2481.1 ng/mL (normal range, 2,188–4,996 ng/mL), respectively. The GH peak levels provoked by insulin and L-dopa were 44.30 ng/mL and 6.07 ng/mL, respectively.
Whole-exome sequencing was performed to search for causative genes. Previous Sanger sequencing of single target genes and panel gene tests regarding the phenotypes of short stature and skeletal dysplasia presenting with intellectual disabilities revealed no pathogenic variants.
Genomic DNA was extracted from the buccal mucosa. The library was prepared to capture all exon regions of all human genes (~22,000) using the SureSelect kit (Agilent Technologies, Santa Clara, CA, USA). The captured regions were sequenced using the Illumina platform (NovaSeq, Illumina, Inc., San Diego, CA, USA). Raw genome sequencing data analysis, including alignment to the reference sequence (original GRCh37 from NCBI, February 2009), was performed with a mean depth of coverage of 100× (10×=99.2%). Variant calling, annotation, and prioritization were performed as previously described []. Variants with minor allele frequencies <0.05% for dominant disease association or 2% for recessive disease association were analyzed using population genome databases, such as the 1,000 genomes site (), the Exome Variant Server (), and ExAC ().
A heterozygous c.7330C > T (p.Arg2444*) mutation in SRCAP was identified and confirmed by Sanger sequencing (). There were no pathogenic variations in other genes related to Rubinstein-Taybi syndrome, Shprintzen-Goldberg syndrome, or other short-stature syndromes, such as those linked to mutations in the CREBBP, EP300, SKI, and ACAN genes; coverage rates greater than 20X of exons and intronic flanking regions (20 bp) were 87%, 95.6%, 93.7%, and 94.8%, respectively.
At 8 years old, the patient’s height was 112.8 cm (-3.33 SDS). Recombinant human GH replacement therapy was initiated (1.0 U/kg/wk). After 55 months of GH therapy, her height was 141.3 cm (-2.7 SDS), and she showed a modest improvement in growth velocity of 6.2 cm/yr (). Her bone age was consistent with her chronological age by 12 years (), at which point her Tanner stage was breast III. No adverse events were observed during GH treatment.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [16.3, 'kg'], 'height': [105.8, 'cm']}",0.69213,0.65752,0.72674,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 105.8 cm. 
The patient's weight is 16.3 kg. 
Therefore, the patient's bsa is sqrt((16.3 (in kgs) * 105.8 (in cm))/3600) = 0.69213 m^2."
7210,60,Body Surface Area Calculator,physical,decimal,pmc-7495872-1,Extracted,"A 38-year-old female living donor (height 162.3 cm; weight 53.5 kg; body mass index 20.3 kg/m2) was scheduled for elective laparoscopic right hepatectomy for LT. She was clinically acceptable for donation surgery according to multidisciplinary assessments based on living liver donation guidelines [, ]. She had no history of diabetes mellitus, hypertension, cerebro- and cardiovascular diseases, hepatitis or pneumothorax, and there were nonspecific physical findings. The CXR and chest CT image findings were nonspecific, and there was no evidence of fatty liver or focal hepatic lesions in abdominal CT images. Sinus rhythm was recorded on an electrocardiogram. A central venous catheter (Arrow 7 Fr catheter; Teleflex, Wayne, PA, USA) was implemented to administer intravenous fluids and medications without complications in the right internal jugular vein under sonographic guidance, and the patency of catheterization was confirmed by CXR. Her laboratory findings were as follows: hemoglobin, 12.0 g/dL; white blood cell count, 6.94 × 109/L (neutrophils, 57.2%); platelet count, 271,000/μL; creatinine, 0.64 mg/dL; albumin, 4.2 g/dL; aspartate and alanine aminotransferase, 19 U/L and 11 U/L, respectively; total bilirubin, 0.39 mg/dL; and prothrombin time, 111.6% (INR: 0.94).
Balanced anesthesia was induced with 100 mg propofol (Fresenius Kabi, Bad Homburg, Germany) and 50 mg rocuronium (Merck Sharp & Dohme Corp., Kenilworth, NJ, USA), and was maintained with desflurane (Baxter, Deerfield, IL, USA) in oxygen/medical air (FiO2 50%) with volume-controlled mechanical ventilation (tidal volume: 400 mL; respiration rate: 12/min; inspiration and expiration ratio: 1:2). A neuromuscular block was maintained with rocuronium. Her vital signs (i.e., systolic [SBP] and diastolic [DBP] blood pressure; heart rate [HR]; and body temperature) and hypnotic depth (bispectral index monitor; Medtronic, Minneapolis, MN, USA) were continuously monitored and managed, as appropriate (Table ).
A laparoscopic hepatectomy was performed using the five-trocar technique and the trocars were placed uneventfully. Abdominal CO2 insufflation was performed with a pressure of 10–12 mmHg. The patient was placed in a 30° head-up position to assist with surgical exposure. The harmonic scalpel (Ethicon Inc., Cincinnati, OH, USA), with transaction and hemostasis of the liver around tissues, was meticulously applied for liver mobilization.
Saturation of peripheral oxygen (SpO2) decreased to 90%, and airway peak pressure reached 35 cmH2O 30 min after beginning the laparoscopic surgery. Chest auscultation revealed normal breath sounds over the left chest but reduced breath sounds on the right. Because we assumed that this could be due to kinking or migration of the endotracheal tube or due to obstructive secretions in the endotracheal tube, we carefully checked the tube and smoothly toileted inside the tube using a fiberoptic bronchoscope. Chest auscultation and movement seemed to recover during inspiration and expiration. However, airway peak pressure abruptly reached 38 cmH2O again and tidal volume simultaneously decreased to 180 mL. Her hemodynamic parameters began to change as SpO2 was 88%, end-tidal CO2 increased to 48 mmHg, SBP/DBP decreased to 82/41, and HR reached 110 beats/min. As a result, a sonographic examination of the lungs (Affiniti 70C ultrasound system; Philips, Amsterdam, the Netherlands) was performed to rule out pneumothorax, but we verified the lung points as a sonographic marker for occult pneumothorax in both anterior apical zones (Fig. ). A pneumothorax was suspected, and the surgeon was asked to temporarily pause the surgery and cease gas insufflation. Lung ultrasound using a sterile drape was meticulously performed in the anterior apical zone (i.e., the mid-clavicular line at the second to third intercostal space) and lateral zone (i.e., the lateral-clavicular line at lateral and slightly superior to the nipple) with the patient in the supine position, and the stratosphere sign was identified as a critical marker for pneumothorax (Fig. ). Portable CXR verified a right-dominant large pneumothorax with a small degree of left lung collapse; thus, a chest tube was inserted on the right side without complications (Fig. ). After passive decompression using a chest tube, her hemodynamic parameters fully recovered, and the surgery continued laparoscopically with the chest tube inserted and close monitoring of the left-side lung field using lung ultrasound and respiratory monitoring. The surgeon explored both the diaphragm and surrounding structures to detect any defects or injuries, but there were no specific abnormal findings (Fig. ). The surgery was completed uneventfully, and after manual deflation of the abdomen, an alveolar recruitment maneuver (i.e., manual inflation of 30 cmH2O for 30 s) was performed several times. We confirmed the return of both equal breath sounds, and the donor was extubated and transported to the postanesthesia care unit.
The postoperative recovery course was uneventful, and follow-up CXR and CT images revealed complete resolution of the two-sided pneumothorax (Fig. ). She was discharged on postoperative day 5 without any complications.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.5, 'kg'], 'height': [162.3, 'cm']}",1.55305,1.4754,1.6307,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 162.3 cm. 
The patient's weight is 53.5 kg. 
Therefore, the patient's bsa is sqrt((53.5 (in kgs) * 162.3 (in cm))/3600) = 1.55305 m^2."
7211,60,Body Surface Area Calculator,physical,decimal,pmc-4170086-1,Extracted,"In May, 2010, a 49-year-old woman presented with 4 year history of both buttock pain. The onset of the pain had been insidious with no significant history of trauma. The pain was localized to both buttock and lower back. She was referred to our hospital for further evaluation from other clinics. Laboratory findings revealed that serum alkaline phosphatase (ALP) level was 57 IU/L (reference range, 30 to 115 IU/L). A bone scan, which undergone at outside hospital 4 year ago, confirmed pagetic changes in the left ilium (). And, pelvis anterior-posterior radiograph obtained at our hospital revealed a typical mosaic pattern of PD in her pubic and left ilium ().
She had no family history of PD. Physical examination revealed the tenderness at the left iliac crest and posterior iliosacral joint. Her weight was 61.4 kg, height was 162 cm, and body mass index was 23.4 kg/m2. Range of motion at left hip was decreased due to pain, and she walked with a mild limp.
Although the level of ALP was within reference range, pamidronate treatment was started orally for 3 months, because she had a severe pain. However, her pain intensity level increased. The ALP was 44 IU/L, and bone scan show still hot uptake in her both ilium and lumbar vertebrae ().
Subsequently, she received intravenous zoledronate (5 mg) in a single dose at August, 2010. After this treatment, we evaluated clinical and biochemical remission and improvement in bone scan. Three months after administration zoledronate, ALP decreased 26 IU/L, and a severe pain and limping gait disappeared. Six months after intravenous zoledronate, ALP decreased 21 U/L, and bone scan showed the improvement, which means a response of zoledronate (). After then, she was lost to follow-up.
In March, 2012, she visited our hospital again, because of left hip pain. Although ALP was 34 IU/L, and bone scan showed hot uptake in both ilium and lumbar vertebrae ().
One year after second zoledronate, ALP was 37 IU/L, and the bone scan also improved (). She had no pain, and refused the third injection of zoledronate. There was no adverse drug reaction during the treatments.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.4, 'kg'], 'height': [162.0, 'cm']}",1.66223,1.57912,1.74534,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 162.0 cm. 
The patient's weight is 61.4 kg. 
Therefore, the patient's bsa is sqrt((61.4 (in kgs) * 162.0 (in cm))/3600) = 1.66223 m^2."
7212,60,Body Surface Area Calculator,physical,decimal,pmc-4049544-1,Extracted,"A 13-year-old female with type 1 DM was referred to our hospital complaining of abdominal pain and distention a month in duration. She had visited her local hospital and abdominal ultrasonography revealed marked hepatomegaly. She was diagnosed with type 1 DM at 11 years of age. None of her family had diabetes. Her height was 150.4 cm (10th-25th percentile) and her weight 51 kg (50th-75th percentile). Tanner stage was V (breasts and pubic hair) and bone age 15 years when she was 12 years of age (by the Greulich-Pyle method). She had been on intensive insulin therapy commencing 2 years prior (insulin aspart 8 U before meals in the morning, at noon, and in the evening; and 21 U of insulin detemir at 10 PM; total insulin dose 0.88 U/kg). However, her glycemic control was poor because she ate excessively and skipped her insulin detemir because of injection pain. She had not experienced hypoglycemia. Physical examination revealed a hard and rigid abdomen and back, and tender hepatomegaly (four fingers in breadth). Laboratory data included elevated serum liver transaminase concentrations aspartate aminotransferase, 105 U/L; alanine aminotransferase, 84 U/L and a raised lipid profile (total cholesterol, 273 mg/dL; triglycerides, 432 mg/dL; low-density lipoprotein cholesterol, 164 mg/dL). The glycated hemoglobin(HbA1C) concentration was 10.7%. Her urine contained ketones. Complete blood count data and the coagulation profile were normal. Abdominal computed tomography (CT) revealed hepatomegaly and marked liver attenuation (). Infectious causes were excluded, based on negative serological data for infection with cytomegalovirus, hepatitis B virus, hepatitis C virus, hepatitis A virus, and Epstein-Barr virus. The ceruloplasmin level was normal. We excluded autoimmune hepatitis. No antinuclear, antismooth muscle, anti-liver-kidney microsomal, or antimitochondrial antibodies, were detected. Liver biopsy revealed an intact lobular architecture and swollen hepatocytes with pale cytoplasm (). There was no evidence of inflammation, fibrosis, steatosis, or necrosis. Periodic acid-Schiff (PAS) staining revealed many PAS-positive granules within the cytoplasm of hepatocytes. Such staining after diastase digestion showed that the enzyme had destroyed the granules. The histological findings were consistent with GH. The insulin doses were adjusted to insulin aspart 8U in the morning, at noon, and in the evening, before meals; and 19 U of insulin detemir at 10 p.m. (0.84 IU/kg/day). She was re-educated on the importance of controlling nutrition and her diabetes.
With improved glycemic control, her abdominal pain and hepatomegaly decreased over 4 weeks. The HbA1C level fell to 9.5% and liver function returned to normal (aspartate aminotransferase, 44 U/L; alanine aminotransferase, 27 U/L) over 3 months.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [51.0, 'kg'], 'height': [150.4, 'cm']}",1.45968,1.3867,1.53266,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 150.4 cm. 
The patient's weight is 51.0 kg. 
Therefore, the patient's bsa is sqrt((51.0 (in kgs) * 150.4 (in cm))/3600) = 1.45968 m^2."
7213,60,Body Surface Area Calculator,physical,decimal,pmc-7490311-1,Extracted,"Written informed consent was acquired from the patient, and publication of this case report was approved by the institutional ethics committee (JHS19-011).
A 48-year-old male patient, 163 cm tall and weighing 53 kg, was diagnosed with atypical carcinoid tumor in the anterior mediastinum at a previous hospital and had already undergone three courses of chemo and radiation therapies. Computed tomography (CT) scans at admission (Fig. a–c and Fig. ) demonstrated that the maximal longitudinal and transverse diameters of the tumor were 11 cm and 16.5 cm, respectively. The tumor extended from the bifurcation of the innominate vein to the SVC, compressed the heart, and involved the left phrenic nerve, causing left phrenic nerve palsy and elevation of the left diaphragm. Although the left innominate vein was completely occluded, requiring preoperative heparinization, blood flow from the left jugular vein drained via well-developed collateral vessels, while flow in the right innominate vein connecting to the SVC was intact, but was surrounded by the tumor. He had ocular protrusion and remarkable dilatation of the internal jugular veins bilaterally, which was thought to be due to SVC syndrome. He had dyspnea in the left lateral position, although it decreased by changing to a forward tilt position. He could lay on his back with only slight dyspnea. The left pulmonary vein and the left upper pulmonary artery were slightly stenotic due to compression by the tumor, although blood flow in the pulmonary vessels was intact on enhanced CT images. His preoperative laboratory examinations and electrocardiogram were within normal limits. The results of respiratory function testing and arterial blood gas examination were as follows: vital capacity, 2.19 L (55.1% of normal values); FEV1.0, 1.42 L (42.5% of normal values); PaO2, 97 mmHg; PaCO2, 41.3 mmHg; BE, 0.7 mEq/L; and HCO3, 25.7 mEq/L.
Hence, he was scheduled to undergo surgical resection of the tumor with SVC replacement via right open thoracotomy.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.0, 'kg'], 'height': [163.0, 'cm']}",1.5491,1.47164,1.62655,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 163.0 cm. 
The patient's weight is 53.0 kg. 
Therefore, the patient's bsa is sqrt((53.0 (in kgs) * 163.0 (in cm))/3600) = 1.5491 m^2."
7214,60,Body Surface Area Calculator,physical,decimal,pmc-8423640-1,Extracted,"This 4-year-old boy had a known history of AS. He was born full term at 40 weeks’ gestation by Cesarean section secondary to cephalopelvic disproportion following an uncomplicated pregnancy. At 28 days of age, he underwent a Kasai procedure for biliary atresia. Due to progression of his liver disease, a liver transplantation was performed at 11 months of age after AS had been diagnosed. At 4 years of age, bilateral PE was detected in a routine ophthalmological examination.
He was then referred to the neuropediatric department for further evaluation. On clinical examination, he had a normal blood pressure, his weight was 16.5 kg, and his height 96 cm. Neuropediatric examination was normal. Laboratory studies including renal and liver function parameters were normal. An echocardiogram revealed no cardiovascular abnormalities.
Medication consisted of immunosuppressive therapy with ciclosporine (70 mg/day), mycophenolate mofetil (400 mg/day), and prednisolone (1 mg/day). The cyclosporine level was within normal range.
An MRI scan was performed in which hydrocephalus, mass effect, or structural lesion was ruled out. Subsequently, a lumbar puncture in propofol sedation was achieved revealing a recumbent opening pressure of 48 cm H2O. Examination of the CSF including bacteriological and viral panels showed no abnormalities. Consequently acetazolamide treatment was initiated at a 2 × 125 mg dosage. After 6 weeks, the PE persisted and also deterioration of the visual acuity was documented. In a repeat LP, the opening pressure was still elevated at 34 cm H2O. Repeat neuroimaging assessment remained unremarkable.
Given the progressive visual loss and the PE being refractory to medical treatment, the patient was referred to the Department of Neurosurgery for further evaluation and measurement of ICP dynamics.
An epidural sensor (Neurodur®, Raumedic, Münchberg, Germany) was implanted over the right frontal area via a precoronal burrhole, and the ICP was monitored for 2 days. ICP monitoring demonstrated massive dynamic ICP changes over time with markedly increased ICP values most of the time (Fig. ). The decomposition of pressure traces revealed pressure waves with amplitudes reaching values up to 60 mmHg for several minutes. B-waves dominated ICP dynamics superposing the slower ICP fluctuations in time. Additionally, a relatively high number of A-wave pressure transients were scattered in the traces. The majority of ICP values were measured to be within the range of 15 to 70 mmHg (83%).
Subsequent to ICP monitoring, a ventriculoperitoneal shunt was implanted using an optic-guided neuronavigation system (Medtronic, Minneapolis, MN, USA). A proGAV® valve with an integrated shuntassistant® (Aesculap-Miethke, Tuttlingen, Germany) was implanted at an opening pressure of 10 cm H20 []. The CT scan on the first postoperative day demonstrated an accurately placed ventricular catheter, and the patient was discharged on the seventh postoperative day.
One month after discharge, PE had completely resolved. Further follow-ups were unremarkable until a growth-related dislocation of the ventricular catheter was noted 3.5 years after the shunting procedure. An ophthalmological examination showed relapse of bilateral PE. The ventricular catheter was revised and the immediate postoperative course was uneventful. One month following discharge, the shunt system was explanted due to an infection with Staphylococcus aureus and an external ventricular drain was placed. Antibiotics were administrated intravenously for 3 weeks. When serial CSF bacterial cultures were negative, a new ventriculoperitoneal shunt was inserted guided by electromagnetic neuronavigation (AxiEM) []. The valve was set at an opening pressure of 6 cm H2O. Postoperative CT confirmed an accurately placed ventricular catheter. At long-term follow-up (12 years), there was no recurrence and both ophthalmological and neurological findings were unremarkable. The opening pressure has not been adjusted during the follow-up period.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [16.5, 'kg'], 'height': [96.0, 'cm']}",0.66332,0.63015,0.69649,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 96.0 cm. 
The patient's weight is 16.5 kg. 
Therefore, the patient's bsa is sqrt((16.5 (in kgs) * 96.0 (in cm))/3600) = 0.66332 m^2."
7215,60,Body Surface Area Calculator,physical,decimal,usmle-1385,Extracted,"A 34-year-old woman with HIV comes to the emergency department because of a 2-week history of diarrhea and abdominal cramping. She has had up to 10 watery stools per day. She also has anorexia and nausea. She returned from a trip to Mexico 4 weeks ago where she went on two hiking trips and often drank from spring water. She was diagnosed with HIV 12 years ago. She says that she has been noncompliant with her therapy. Her last CD4+ T-lymphocyte count was 85/mm3. She appears thin. She is 175 cm (5 ft 9 in) tall and weighs 50 kg (110 lb); BMI is 16.3 kg/m2. Her temperature is 38.3°C (100.9°F), pulse is 115/min, and blood pressure is 85/65 mm Hg. Examination shows dry mucous membranes. The abdomen is soft, and there is diffuse tenderness to palpation with no guarding or rebound. Bowel sounds are hyperactive. Microscopy of a modified acid-fast stain on a stool sample reveals oocysts.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [50.0, 'kg'], 'height': [175.0, 'cm']}",1.55902,1.48107,1.63697,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 175.0 cm. 
The patient's weight is 50.0 kg. 
Therefore, the patient's bsa is sqrt((50.0 (in kgs) * 175.0 (in cm))/3600) = 1.55902 m^2."
7216,60,Body Surface Area Calculator,physical,decimal,pmc-4066970-1,Extracted,"A 53-year-old, right-handed female (height 1.54 m; weight 48.2 kg) sustained a hemorrhagic right middle cerebral artery stroke 3 years earlier. The patient presented with left spastic hemiparesis involving, among others, the finger flexors. In addition, she exhibited weak voluntary finger and wrist extension. The patient underwent extensive physical and occupational therapy after the stroke and up to the time of presentation. A total of 50 units onabotulinum toxin A (BOTOX™, Allergan, Irvine, CA, USA) was administered to the left flexor digitorum superficialis (FDS) and flexor digitorum profundus, respectively. The injection was guided by percutaneous electrical stimulation of the motor points of these muscles.
After providing written consent, the subject attended three laboratory sessions before (Pre = Day 0), after (Post 1 = 10 days), and at the follow-up (Post 2 = 2.5 months) injection. Delays in grip initiation and release were assessed using electromyographic (EMG) signals in paretic and non-paretic sides, respectively. The Modified Ashworth Scale (MAS) was used to assess hypertonia. Bilateral grip strength was measured using a hand-held dynamometer (Lafayette Instruments, Lafayette, IN, USA), and the Functional Independence Measure (FIM) was used to evaluate clinical improvement.
During grip initiation and release tasks, the subject sat comfortably in a chair with a backrest to provide proper trunk support. The limb was supported and secured firmly on a customized apparatus on a desk and was placed with 45° shoulder abduction and flexion and a 90° elbow flexion. The wrist was placed and secured in a neutral position (with thumb pointing upward), and the hand was placed around a customized hand-held apparatus. The apparatus was fixed to the table and was adjusted to accommodate hand size, adjusting for comfort and a firm grip. First, the non-paretic hand was tested, followed by the impaired hand. In each 20-second trial, the subject was asked to relax the fingers for the first 10 seconds, maximally grip the apparatus and hold for 5 seconds, and then relax the hand for 10 seconds. Computer-generated audible tones cued the subject when to start and stop grip efforts. The subject was instructed to grip the apparatus as quickly as possible in response to the first tone (start), and then relax the hand as quickly as possible when the second tone (stop) was played. The patient practiced five trials prior to the grip initiation and release task, which allowed for familiarizing with the setting and task. After the practice sets, five trials for each side were performed.
Bipolar active surface electrodes (Delsys, Boston, MA, USA) were placed over the muscle bellies of FDS and extensor digitorum communis (EDC). The FDS muscle is the primary mover in power grip, and EDC muscle activity was recorded to monitor antagonist muscle activity. For consistency, electrode locations were recorded, and electrodes were placed at identical locations for all sessions. EMGs were recorded at 1 000 Hz using a Delsys amplifier and data acquisition system (National Instruments, Austin, TX, USA) controlled by custom LabView program (National Instruments). EMG signals were processed and analyzed offline using a custom Matlab program (The MathWorks, Natick, MA, USA). EMG signals were initially band-pass filtered (10-400 Hz), rectified, and then root-mean-square smoothed with a 40-ms time constant to create envelopes that clearly displayed aggregated muscle activity.
Delays in grip initiation and release were determined from the FDS EMG. The Teager-Kaiser energy operator was used to analyze surface EMG to improve the signal-to-noise ratio, as well as to optimize EMG onset/offset detection[]. The baseline FDS EMG was calculated as values for the EMG averaged across a 0.5-second window during the initial resting period of each trial. The FDS EMG onset time was identified when the EMG value increased more than the mean value plus 3 standard deviations of the baseline values. Grip initiation delay was calculated as the time difference between EMG onset and the “start” audible tone ().
The FDS EMG offset time was identified as the time when EMG values fell below the mean plus 3 standard deviations of the baseline values. The release delay was then calculated as the time difference between EMG offset and the “stop” audible tone ().
After BT injection to the finger flexor muscles (FDS and flexor digitorum profundus) of the paretic left hand, grip strength decreased at 10 days post-injection and returned to pre-injection levels at 2.5 months post-injection (Pre vs. Post 1 vs. Post 2: 2.3 vs. 1.0 vs. 2.2 kg), while grip strength of the non-paretic hand remained stable (Pre vs. Post 1 vs. Post 2: 22.7 vs. 20.4 vs. 22.2 kg). In parallel, the MAS scores of the affected finger flexors were as follows: Pre vs. Post 1 vs. Post 2: 2 vs. 0 vs. 1 for FDS; 2 vs. 0 vs. 1 for flexor digitorum profundus. FIM scores remained unchanged (FIM = 6 for Pre, Post 1, and Post 2), but the subject reported an improved overall ability for handling objects, as well as bimanual activities at home while performing activities of daily living in Post 1 and Post 2 measures.
Release delay time in the paretic hand resulted in dynamic changes (Pre: 2 223 ms; Post 1:1 024 ms; Post 2: 1 333 ms), without dramatic changes in grip initiation delay times in the paretic hand (Pre: 417 ms; Post 1: 439 ms; Post 2: 378 ms). It is noteworthy to mention that a decreased FDS release delay time was paralleled by shortened EDC and EDC EMGs (). In contrast, both grip initiation and release delay times in the non-impaired hand remained relatively stable in all measurements (Pre vs. Post 1 vs. Post 2: 468 ms vs. 404 ms vs. 371 ms for grip initiation delay; 725 ms vs. 740 ms vs. 691 ms for release delay).",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [48.2, 'kg'], 'height': [1.54, 'm']}",1.43593,1.36413,1.50773,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 1.54 m, which is 1.54 m * 100 cm/m = 154.0 cm. 
The patient's weight is 48.2 kg. 
Therefore, the patient's bsa is sqrt((48.2 (in kgs) * 154.0 (in cm))/3600) = 1.43593 m^2."
7217,60,Body Surface Area Calculator,physical,decimal,pmc-5290181-1,Extracted,"A 9-year-10-month-old Tajikistani girl visited our hospital through a missionary program. Her height was 110 cm, which was under the 3rd percentile for her age, and her weight was 23.1 kg, which was in the 5th–10th percentile. Her birth weight was 3.0 kg, which was in the 50th–75th percentile. She had incomplete upper eyelids (coloboma with ectopic cilia on the left side and cryptophthalmos with dermolipoma on the right) and sparse hair with separated alopecia. She had hyperpigmentation of the left hemibody with multiple café-au-lait macules on the left side of her face, trunk, and left extremity, and she had ipsilateral edema of the lower extremity. Her Tanner stage was Sexual Maturity Rating (SMR) 1. Her teacher mentioned that she displayed 2 years of retarded development compared with other children of the same age. She had no history of seizures. A grade I–II systolic heart murmur was heard on auscultation of the chest. Her family history was nonspecific. Her morphologic characteristics are shown in .
On the magnetic resonance imaging (MRI) of her brain, unilateral ventricular dilatation and an extra-axial cerebrospinal fluid space in the left hemisphere and posterior fossa were observed (), consistent with a minor MRI criterion for diagnosis of ECCL. Coarctation of the aorta (isthmic portion) with a velocity of 2.3–2.4 m/sec, which did not require any intervention, was observed on the 2-dimensional echocardiogram. Three major systems were involved and two major and two minor criteria, as defined by Moog, were met. Thus, she was diagnosed with definitive ECCL.
The baseline Insulin-like growth factor-binding protein 3 (IGFBP-3) (1,245 ng/mL) and Insulin-like growth factor 1 (IGF-1) (19.14 ng/mL) were under the normal range (IGFBP3 normal range, 1,389–4,260 ng/mL; IGF-1 normal range, 76–499 ng/mL). The levels of the other measured hormones (T3, T4, free T4, thyroid-stimulating hormone, follicle-stimulating hormone, luteinizing hormone, adrenocorticotropic hormone, cortisol, estradiol, progesterone, testosterone, aldosterone, and renin) were within the normal range.
Her bone age was estimated to be 8 years 4 months; this was significantly less than her chronological age of 9 years 10 months. To evaluate her short stature, we performed a GH provocation test using insulin and levo-dihydroxyphenylalanine and found GH deficiency (). MRI of the sella was not performed; however, the abnormal findings on the brain MRI were not associated with GH deficiency ().
To evaluate the lesions to her extremities, we performed X-ray and MRI (). Images of her extremities showed nonossifying fibromas involving the left proximal humerus, left distal femur, both proximal tibias, and left proximal fibula, suggesting JCS. Biopsy of the left tibia proximal bone and pretibial soft tissue were performed (). Pathologically, the results suggested nonossifying fibromatosis. Our present patient could be diagnosed with JCS because she had multiple café-au-lait macules and nonossifying fibromas, and no neurofibromatosis type-1 (NF1) mutation was found after genetic examination using a blood sample. Ultimately, she was diagnosed with GH deficiency combined with ECCL and JCS.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [23.1, 'kg'], 'height': [110.0, 'cm']}",0.84014,0.79813,0.88215,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 110.0 cm. 
The patient's weight is 23.1 kg. 
Therefore, the patient's bsa is sqrt((23.1 (in kgs) * 110.0 (in cm))/3600) = 0.84014 m^2."
7218,60,Body Surface Area Calculator,physical,decimal,pmc-5796503-1,Extracted,"A 25-year-old man was referred to vascular medicine clinic because of pain in the left calf while running, which had been occurring for the past 4 years.
This patient practiced almost daily physical activity that involved both combative and running (over 8 h per week), and he competed at a regional level (with a personal best of running of 36min12s/10000 m). In 2012, the patient had reported left calf pain when running, forcing him to stop. He described a calf swelling sensation that gradually increased with the intensity of running. While in the past he could easily run 15–20 km, the patient reported at that date that he could not run more than 2 km before having to stop. After stopping, the pain was deep and persisted for several minutes; it was also associated with swelling of the calf. This pain had led him to change his occupation to a less physically demanding job (military officer in the past, and now security officer). The consequences were a weight gain of 8 kg, and a cessation of all physical activity (running, fight sports). The patient also reported a loss of self-esteem.
Over a period of 4 years, the patient was seen by two general physicians, a rheumatologist, a neurologist, a sports physician and a vascular physician. Many explorations were carried out (spinal and pelvic x-ray, pelvic and lumbar spine scan, venous duplex scan, arterial duplex scan, and electromyography), all of which revealed no sign of dysfunction. The sports physician raised the possibility of diagnosis of a compartment syndrome, but the patient refused to submit to investigation of intramuscular pressure taken at rest and in immediately post exercise. Different therapies were proposed, including anti-inflammatory drugs, paracetamol and compression stockings (Class 2).
The patient interview revealed that a proximal deep vein thrombosis DVT (thrombosis in the iliac, femoral and popliteal veins) of the left lower limb had been diagnosed in 2012 and treated for 6 months by direct oral anticoagulant therapy (Rivaroxaban, Xarelto 20 mg per day) combined with compression stockings french class 3 worn (20–36 mmHg) for 6 months and then class 2 compression socks (15–20 mmHg) thereafter. This episode of DVT occurred spontaneously without major or minor contributing factors. There was no family history of venous thromboembolism disease. Clinical and laboratory tests had found no neoplasia. The biological thrombophilia test at distance of anticoagulation was negative.
The patient was 1.78 m and 79 kg (body mass index = 24.9 kg/m2). He was afebrile, and his brachial blood pressure was 120/70 mmHg. Upon examination the legs were hot and there was no trophic disorder. There was a difference in the circumference of the calves (left calf 2 cm > right calf). There were no visible or palpable varicose veins. Peripheral pulses were present and there was no sign of Lassegue. Palpation of the major lower limb joints (ankles, knees, hips) was not painful. Calves were flexible, painless, with good trophicity. No lymphadenopathy was found and no local inflammatory signs. When examined by auscultation, there were no vascular sounds along the vascular axes.
All Doppler ultrasound measurements were performed with a high-resolution ultrasound machine (Affiniti 70, Philips, Amsterdam, The Netherlands). The deep venous system was free and compressible when compressed by the ultrasound probe at calf level (posterior tibial veins, peroneal, gastrocnemius and soleus), at femoral popliteal level (popliteal veins, femoral and common femoral) and at ilio-cava level with no sign of recent deep vein thrombosis. There was wall thickening at the left common femoral vein CFV (anterior posterior diameter APD under compression = 3.9 mm) and at the left external iliac vein (APD under compression = 3.6 mm); this finding had already been highlighted when vascular physician examined the patient in 2013.
The Doppler examination showed a clear asymmetry of the respiratory modulations of blood velocity between right and left CFV. In the left CVT, respiratory modulations were almost absent and blood volume flow was not as high as on the right side. We found a reflux into the left internal iliac vein and dilation of the left gonadal vein. While standing, there was no significant deep venous reflux (> 1 s) at the popliteal vein (functional venous valves). The superficial venous system (great and small saphenous veins) was compressible and continent.
The diagnostic hypothesis of MTS was issued at the end of this first consultation, taking into account the following clinical and hemodynamic arguments:▪ History of the left proximal DVT without predisposing factor. ▪ Symptoms of left calf venous claudication due to effort (+/− associated with unilateral edema reported by the patient). ▪ Asymmetry respiratory modulation and venous blood volume flow at the left proximal deep vein (as a result of a downstream obstacle).
Additional morphological exploration was requested computed tomography angiography (CTA) and a surgical opinion was recommended and requested.
The CTA revealed compression of the left common iliac vein (CIV) between the right common iliac artery (CIA) and lumbar spine (Fig. ) and intraluminal spurs. There was also dissimilar venous systems collatorally with that was more highly developed on the left iliac axis relative to the right iliac axis, reflecting the need to create a system of substitution.
In this context of symptomatic MTS with compatible imaging, venography was performed in order to confirm the diagnosis and to treat the MTS at the same time. Venography showed patency of the left venous axis iliac featuring endoluminal spurs and a footprint at the terminal portion of the iliac vein (Fig. ).
Endovascular support was carried out with introduction of two Wallstent endo prostheses (Boston Scientific) into the common iliac and external iliac veins, associated with angioplasty intra stent to modulate the different areas of overlap, the diameters and lengths to achieve a harmonious assembly. The phlebographic control carried out at the end of the procedure was satisfactory.
At 3 and 6 months, the patient reported an improvement in symptoms. The patient restarted running, and initially venous claudication was not felt and the patient was once more able to run more than 10 km. He currently wears a compression class III especially during physical activity, as advised.
Angiographic assessment found normal stent patency at the iliac vein, with symmetrical respiratory modulations. It was also decided to carry out a duplex ultrasound scan at 3 months. At this scanning session the stents were in place and permeable. Pharmacological treatment in the form of an anti platelet (Clopidogrel 75 mg) was prescribed.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [79.0, 'kg'], 'height': [1.78, 'm']}",1.97639,1.87757,2.07521,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 1.78 m, which is 1.78 m * 100 cm/m = 178.0 cm. 
The patient's weight is 79.0 kg. 
Therefore, the patient's bsa is sqrt((79.0 (in kgs) * 178.0 (in cm))/3600) = 1.97639 m^2."
7219,60,Body Surface Area Calculator,physical,decimal,pmc-7238324-1,Extracted,"The case report involved a 75-year-old woman with no special medical history. The patient's height and weight were 147 cm and 49 kg, respectively. She visited a nearby clinic and presented with a tumor on the right clavicle and a sense of discomfort. Computed tomography (CT) revealed a large right-upper mediastinal tumor and micropulmonary metastases (Figures and ). The large tumor extended to the neck, subclavicle, and right-upper mediastinum. Partial resection of the lung metastasis was performed under thoracoscopy to diagnose the primary tumor. We did not biopsy the superior mediastinal tumor because it was an extrapulmonary lesion with no continuity with the lung lesion, which was covered by pleura. The pathological diagnosis was lung metastasis of papillary thyroid carcinoma. Although a small mass was also found in the thyroid gland, there was no malignant finding, and treatment was prioritized without further examination. Because the tumor obstructed the right brachiocephalic vein and approached the superior vena cava (SVC) junction, there was a risk of SVC occlusion and pulmonary embolism (). We decided to start treatment as soon as possible to avoid sudden death from pulmonary embolism. Lenvatinib treatment was started with approval from the Cancer Board of Kanagawa Cancer Center (IRB approval number 28–41). The tumor shrank upon treatment, and the major axis was reduced from 68 to 48 mm in diameter. The tumor embolus regressed from the junction of the SVC, permitting the right brachiocephalic vein to be clamped and ligated safely ().
The adverse events induced by lenvatinib included grade 2 HT, grade 2 hand-foot syndrome, and grade 2 anorexia, and thus, the dose was reduced to 10 mg after 3 weeks. After 16 weeks of treatment, her weight loss reached 10 kg, and it was clinically assessed that further continuation of lenvatinib was impossible. Then, surgery was performed 1 week after withdrawal of lenvatinib. Total thyroidectomy and resection of the first rib, right internal jugular vein, right subclavian vein, and tumor were performed, and the right brachiocephalic vein was clamped and separated from the SVC junction at the periphery. Infiltration of the subclavian artery and vagal nerve was found on the dorsal side of the tumor, and a tumor approximately 1 cm2 in size remained at the site. The risk of SVC syndrome and pulmonary embolism was resolved, and the tumor was largely resected. shows the schema of the surgical procedure and CT after the operation. The sternum was incised as shown in the figure, the sternoclavicular joint and collarbone were flipped outward, and surgery was performed. We planned to conduct follow-up of the efficacy of RAI therapy and thyroid stimulating hormone (TSH) suppression for small residual tumors and lung metastases.
No primary lesion remained in the thyroid gland, and the lenvatinib had a beneficial effect on papillary carcinoma originating from the upper mediastinum. presents a histopathological image of the central region of the papillary carcinoma lesion. presents a histopathological image of the periphery of the tumor. Extensive necrosis and fibrosis caused by lenvatinib were observed. Treatment efficacy was clearly recognized. The patient's preoperative thyroglobulin and TgAb levels were 4690 ng/mL and 18 IU/mL, respectively, decreasing to 451 ng/mL and <10 IU/mL, respectively, after the operation.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [49.0, 'kg'], 'height': [147.0, 'cm']}",1.41451,1.34378,1.48524,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 147.0 cm. 
The patient's weight is 49.0 kg. 
Therefore, the patient's bsa is sqrt((49.0 (in kgs) * 147.0 (in cm))/3600) = 1.41451 m^2."
7220,60,Body Surface Area Calculator,physical,decimal,pmc-7796768-5,Extracted,"A 31-year-old male patient (weight 90 kg, height 187 cm) was scheduled for emergency surgery of acute diverticulitis with abscess. Bilateral ESP block was performed at the Th10 level with 30 mL 0.25% bupivacaine on each side before surgery. The total amount of fentanyl given during surgery was 250 μg. In the postoperative period, at 2, 6, 12, 24, 36, 48, and 72 h, the patient didn't report having pain, pain scores were 0/10 at rest and on coughing, and thus, no analgesic was given.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [90.0, 'kg'], 'height': [187.0, 'cm']}",2.16217,2.05406,2.27028,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 187.0 cm. 
The patient's weight is 90.0 kg. 
Therefore, the patient's bsa is sqrt((90.0 (in kgs) * 187.0 (in cm))/3600) = 2.16217 m^2."
7221,60,Body Surface Area Calculator,physical,decimal,pmc-4975295-1,Extracted,"A 30 year old female presented to the neurology out patients department for cramps, rigidity, tremor and twitching and abnormal movements of hands and feet. The patient complained that this problem was continuing despite treatment for 6 years. On checking her old prescriptions and reports, it was found that she was being treated with antiepileptics [eptoin 100mg bid] along with vitamin E [Evion400mgod].A CTscan of brain (done outside) revealed basal ganglia calcification []. She was referred to Endocrinology department. While in the OPD; two bouts of tetany were witnessed by the doctor, followed by recovery in a few minutes. She was married for twelve years, had her first child six years back, who died at 6 months of age due to high grade fever. Two years later, she had a son. Six months after delivery, she began to experience convulsions, tetany, stiffness of hands and feet and would fall down, and then recover completely on her own, in a few minutes. This happened about twice or thrice a month. She had long standing generalized weakness. She was employed in a bangle making factory, and had to give up her job due to this recurring health problem.
On examination, she weighed 32 kg, height 144 cm, and blood pressure 90/60 mm Hg. All other systems were normal on examination. Findings from an electroencephalogram were normal. Her laboratory investigations were as follows [reference range in parantheses].Serum calcium was 5.39 mg/dl [8.4-10.2], ionized calcium at 0.7 mmol/L[1.12-1.32 ], 24 hour urine calcium 259 mg [100-300], thyroid stimulating hormone [TSH] 6.73 µ IU/ ml [0.25-5], intact parathyroid hormone [IPTH] 13.54 pg/ml [15-65],phosphorus 7.57 mg/dl [2.5-4.5], magnesium 1.9 mg/dl [1.6-2.5], hemoglobin 10.5g/dl [12-15], fasting plasma glucose 100.4 mg/dl [70-110]. Albumin and 25 hydroxyvitamin D levels were within reference range. No nutritional, familial, congenital, infiltrative or autoimmune cause of hypoparathyroidism was obvious. Our tests for ANA and APLA by IFA and ELISA respectively tested negative Patient never had surgery or irradiation of neck. Eye examination revealed no abnormality. Cortisol level was within reference range, excluding hypoadrenalism. On clinical examination, there was no evidence of mucormycosis or any other fungal infection
The patient was diagnosed as primary hypoparathyroidism and treated with activated vitamin D [1, 25 dihydroxycholecalciferol].Three months later, her calcium level is 8.9 mg/dl and phosphate 5.2 mg/dl, intact parathyroid hormone is 15.9 pg/ml [15-65] and she has not experienced the seizures since two weeks. She has also regained her happiness and confidence to get back to her livelihood again.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [32.0, 'kg'], 'height': [144.0, 'cm']}",1.13137,1.0748,1.18794,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 144.0 cm. 
The patient's weight is 32.0 kg. 
Therefore, the patient's bsa is sqrt((32.0 (in kgs) * 144.0 (in cm))/3600) = 1.13137 m^2."
7222,60,Body Surface Area Calculator,physical,decimal,pmc-3849883-1,Extracted,"This 12-year-old girl of Slavic origin is the first child of healthy, unrelated parents. During neonatal period intrauterine growth retardation (birth weight, 2700 grams) and microcephaly (head circumference, HC = 31 cm; < p3) were observed. Her past medical history revealed that she suffered from recurrent lung infections (otitis media, pneumonia) since infancy. At 18 months of age she was treated for bacterial meningitis. At 8 years of age she was hospitalized because of severe varicella complicated with pneumonia. At the same age she had an episode of hip pain diagnosed as transitory synovitis.
At 9 years of age she was referred to our Institute for investigation of repeated lung infections. Physical examination on admission included: height, 129 cm (p50) and the body weight, 29 kg (p50); microcephaly (head circumference = 46 cm, < p3); typical facial features with prominent midface, large ears and hyperthelorism with upward slant of the palpebral fissures (Figure ); hypopigmented spots on trunk and extremities; bilateral clinodactyly and syndactyly of the second and third toe were observed. Chest examination revealed bilateral basilar crackles due to bronchiectasis. Neurological examination and ophtalmologic slit-lamp examination were normal.
Immunologic investigations are presented in Table . Karyotype of peripheral blood lymphocytes revealed typical chromosomal rearrangements involving chromosomes 7 and 14. Final diagnosis of NBS was established by mutation analysis of the NBS1 gene that revealed homozygousity for typical 5 base-pair deletion (657del5). She was placed on regular substitution with intravenous immunoglobulin (IVIG) in a dose of 400 milligrams/kg/body weight every 4 weeks. With this treatment acute exacerbations of her chronic lung disease decreased in frequency.
At 10 years of age she was admitted because of pain, morning stiffness and bilateral swelling of her proxymal interphalangeal (PIP), wrist and knee joints (Figure ). Affected joints were hot, swollen and tender on passive or active motion. L Laboratory investigations at that time included: erythrocyte sedimentation rate 42 mm/hr, C-reactive protein 92 mg/l (normal < 5 mg/l), hemoglobin 121 g/l, WBC count 6.2 × 109/l with 58% of neutrophils, 30% of lymphocytes and 6% of monocytes, platelets were 346 × 109/l; urinalysis was normal; liver function tests was normal; serum lactate-dehydrogenase was not increased; serum concentrations of complement components C3, 1.99 g/l and C4, 0.46 g/l both were increased. Immunologic investigations including serum immunoglobulin concentrations, peripheral blood lymphocyte phenotype and proliferative response of lymphocytes to mitogen are presented in Table . Antinuclear antibodies, anti-double stranded DNA, anti-cyclic citrullinated protein antibodies and rheumatoid factor (RF) were all negative.
Diagnostic puncture of knee joint was done and 4 milliliters of cloudy, yellow sinovial exudate was obtained. Microscopic examination and bacterial culture of joint fluid specimen yielded no microogranism. Also, special cultures for Mycoplasma spp., Ureaplasma urealyticum and mycobacteria were negative.
An initial treatment included non-steroidal anti-inflammatory drug (NSAID) meloxicam together with azithromycin because of suspected mycoplasmal infection. After two months of treatment, no improvement was seen so that azithromycin was replaced for doxycycline in a daily dose of 4 mg/kg/body weight and with this treatment her joint symptoms transiently improved. However, over the next 6 months several relapses of arthritis were observed so hydroxychloroquine as disease-modifying antirheumatic drug (DMARD) was given.
After one year of treatment no objective improvement of polyarthritis using defined core set of six variables for JIA (physician global assessment of disease activity; parent global assessment of disease activity; number of joints with active arthritis; number of joints with limited range of motion; child health assessment questionaiire, erythrocyte sedimentation rate) was observed [,].
We decided to introduce rituximab in a standard dose regimen (375 mg/m2/month) used in children and adults affected with PID who developed autoimmune diseases []. She received six infusions of rituximab without major side-effects and continued to receive regular IVIG therapy. Treatment with rituximab led to complete clinical and laboratory remission of her polyarthritis lasting for 9 months (Table ).",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [29.0, 'kg'], 'height': [129.0, 'cm']}",1.0194,0.96843,1.07037,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 129.0 cm. 
The patient's weight is 29.0 kg. 
Therefore, the patient's bsa is sqrt((29.0 (in kgs) * 129.0 (in cm))/3600) = 1.0194 m^2."
7223,60,Body Surface Area Calculator,physical,decimal,pmc-3581789-1,Extracted,"A 64-year-old man (height 169 cm, weight 70 kg) was presented for laminoplasty C3-7 due to incomplete cervical spinal cord injury. He started taking antihypertensive medication daily a year ago. Except that, the patient was in good health until he fell from a three-meter-high cliff. Four weeks ago, he had an emergency operation, anterior cervical discectomy and fusion (ACDF) C3-7, under general anesthesia, and no specific events happened during the perioperative period. Anesthesia was induced using a propofol and remifentanil, and the paralysis was facilitated with rocuronium. Endotracheal intubation was achieved using a light-wand and a reinforced endotracheal tube of the inner-diameter 7.5 mm was successfully placed. Anesthesia was maintained with sevoflurane and 50% oxygen in the air. A three-pin head holder was affixed to the patient's head. After the patient was turned prone, the surgeons slightly moved his neck to find an appropriate position and fixed the holder with the head in a neutral position. The total anesthetic and operation time was 405 min and 310 min, respectively, and the blood loss was estimated to be 700 ml. The patient was extubated after a full recovery of respiration and consciousness, and was transferred to the general ward.
On the first postoperative day, the patient began to complain of dysphagia and recurrent aspiration, and the symptoms have persisted for two days. A rigid fiberoptic laryngoscope showed the deviation of the tongue to the left on protrusion, the absent movement of the left vocal cord and the pooling of saliva in the left pyriform sinus. Neurologic examination revealed the palsy of the left hypoglossal and recurrent laryngeal nerves. Video fluoroscopic swallowing study (VFSS) showed the impairment of pharyngeal contraction on swallowing and left side deviation and atrophy of the tongue. There was no uvula deviation or abnormality of the soft palate elevation. On neurologic examination, there were palsy of the left hypoglossal and recurrent laryngeal nerve, and the remainder was normal. On a magnetic resonance imaging of the brain and neck, there was no evidence to suspect central neurologic or vascular involvement. These findings suggested a peripheral type of Tapia's syndrome. Conservative management included intravenous corticosteroid, electrical stimulation therapy aimed at a restoration of swallowing ability and the nasogastric tube feeding to reduce the risk of aspiration. VFSS-guided balloon dilation of the esophagus was also performed. Seven weeks after the operation, the patient's symptoms began to improve and he started a soft diet. He gradually recovered thereafter, and was discharged three months later.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [169.0, 'cm']}",1.81276,1.72212,1.9034,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 169.0 cm. 
The patient's weight is 70.0 kg. 
Therefore, the patient's bsa is sqrt((70.0 (in kgs) * 169.0 (in cm))/3600) = 1.81276 m^2."
7224,60,Body Surface Area Calculator,physical,decimal,pmc-8560865-3,Extracted,"A 37-year-old woman (G1P1; height, 158 cm; weight, 78 kg) without a significant medical history was referred to our hospital with a diagnosis of PPCM. Postpartum day 4, she developed dyspnea with lower leg edema, shock, and LVEF was 33% (INTERMAX profile 1). Medical treatment was started with inotropes and diuretics for heart failure. Subsequently, LVEF reduced to 20%, LVEDd was 69 mm, and mitral regurgitation worsened. IABP, VA-ECMO, and anti-prolactin therapy were started on postpartum day 7. However, congestion progressed with dilation of the left ventricle and left ventricular vent was inserted on postpartum day 11, which resulted in improvement of congestion. Postpartum day 19, VA-ECMO was stopped due to thrombus in its circulation, and at this time the LVEF was 35% and CO 4.76 L/min. Postpartum day 23, we had no choice but to removed IABP and continued medical treatment. However, the cardiac dysfunction could not be controlled and the patient needed IABP again, postpartum day 118. Postpartum day 129, the implantable LVAD was implanted and mitral valve replacement was performed. Postpartum day 386, LVEF recovered to 55% and CO 4.36 L/min, and the LVAD was withdrawn and the patient was discharged from the hospital.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [78.0, 'kg'], 'height': [158.0, 'cm']}",1.85023,1.75772,1.94274,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 158.0 cm. 
The patient's weight is 78.0 kg. 
Therefore, the patient's bsa is sqrt((78.0 (in kgs) * 158.0 (in cm))/3600) = 1.85023 m^2."
7225,60,Body Surface Area Calculator,physical,decimal,pmc-4089302-1,Extracted,"A 55-year-old man (weight 80 kg, height 178 cm) with hepatitis B and hepatocellular carcinoma was treated with liver transplantation without veno-venous bypass. He was ASA status III and MELD score 25. His preoperative serum creatinine was 1.08 mg/dL. Routine monitoring was established, then anesthesia was induced. Anesthesia was maintained with isoflurane, morphine and atracurium (intravenous bolus doses).
Approximately, 30 min after initiation of the operation, his arterial blood pressure rapidly dropped to 50/30 mm Hg. Infusion of norepinephrine (0.1–0.8 µg/kg/min) and dopamine (2.0 µg/kg/min) was started. After 45 min, the patient had still poor response to increasing doses of norepinephrine; the cardiac output was high (8.0 L/min), and the systemic vascular resistance was low (460 dyn s/cm5). Therefore, epinephrine was administered at a rate of 0.9 µg/kg/min; dopamine was also given at a rate of 2.0 µg/kg/min. Fluids were administered via rapid infusion system to maintain a central venous pressure in the range of 8–12 mm Hg.
The anhepatic phase took 68 min. After the suprahepatic and infrahepatic vena cava and portal vein were unclaimed, the patient's need for epinephrine decreased.
Urine output was less than 1 mL/kg/min although the central venous pressure was maintained above 8 mm Hg and dopamine, furosemide and N-acetylcysteine were administered during the operation. Oxygen saturation and temperature remained within the normal range. Arterial blood gases and plasma potassium, sodium and hemoglobin also remained within acceptable ranges. The total operative time was 390 min ().
After surgery, the patient was transferred to the ICU, and epinephrine was infused in combination with dopamine 2.0 µg/kg/min to maintain the arterial blood pressure during the first 6 h of surgery. Continuous renal replacement therapy was initiated immediately post-operative in the ICU; the patient's endotracheal tube was removed 24 h later. On the first post-operative day, the serum creatinine level was 2.1 mg/dL; on the second day, it was 2.2 mg/dL. The patient was discharged from the ICU on day six with a serum creatinine level of 1.5 mg/dL. He was discharged from the hospital on post-operative day 20 without any further complications. After nine months of follow-up, the BUN and creatinine were 16 mg/dL and 1.1 mg/dL, respectively.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [80.0, 'kg'], 'height': [178.0, 'cm']}",1.98886,1.88942,2.0883,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 178.0 cm. 
The patient's weight is 80.0 kg. 
Therefore, the patient's bsa is sqrt((80.0 (in kgs) * 178.0 (in cm))/3600) = 1.98886 m^2."
7226,60,Body Surface Area Calculator,physical,decimal,pmc-4999489-1,Extracted,"We admitted a 52-year-old Caucasian man with a body mass index (BMI) of 38.3 kg/m2 (weight, 120 kg; height, 177 cm) who had experienced a massive weight loss of 120 kg using diet alone (initial BMI, 76.6 kg/m2). His chief complaint was a gigantic genital mass extending beneath his knees in standing position that had progressed over the previous years (). At the time of admission, he was immobilized due to this giant mass, and it was impossible for him to wear normal clothing. Additionally, his penis was completely covered by the mass, so that micturition was only possible in the standing position with assistance. Therefore, a urinary catheter was placed. Most likely due to his mild bipolar disorder and schizophrenia, the giant genital mass had been neglected for a long period of time. As expected, the patient additionally reported impotence. The patient lived in a convalescent home and was single. He and his family were not able to take care of him at home due to his physical status and the gigantic case of lymphedema. Moreover, his bipolar disorder and schizophrenia occasionally caused difficulties for his caregivers, although these conditions were stable due to treatment with quetiapine and olanzapine at the time of admission.
The physical examination revealed a very large, painless, soft, and non-adherent tissue in the suprapubic region, completely covering the penis and scrotum. The skin was thickened and hyperkeratotic, but not erythematous. After moving the mass upwards, the penile orifice as well as normal-sized testes could be observed (). His extremities were not edematous and no lymphadenopathy was detected. His medical history was otherwise unremarkable, apart from his stable bipolar disorder and schizophrenia. No history of trauma, radiotherapy, or tropical vacations was reported. In an abdominopelvic computed tomography scan, the huge genital mass demonstrated no signs of malignancy or inguinal hernia (). All laboratory findings, including tumor markers of testicular cancer, were within normal limits (α-fetoprotein=2.6 ng/mL, beta-human chorionic gonadotropin <1.2 mIU/mL, and lactate dehydrogenase=2.59 IU/L).
In order to facilitate normal urination and physical activities, as well as restoring acceptable sexual appearance and function, we performed a reductoplasty of the gigantic suprapubic mass as well as a puboscrotal reconstruction with a horizontal ellipsoid excision of the mass, leaving the penis and scrotum intact. The dilated veins and lymphatic vessels were meticulously ligated. Both spermatic cords were identified and marked using vessel loops (). Finally, a mass of 11 kg (measuring 40×27×14 cm) was resected ().
The histopathological examination revealed abundant lymphatic tissue and vessels with no sign of filariasis or a malignancy. Postoperatively, the wound healed by first intention, and the patient was discharged with satisfying functional and cosmetic results. The bladder catheter was removed one month after surgery, once the wound had completely healed. The family of the patient reported that he exhibited no dysfunctions involving micturition. However, the patient was not able to function sexually due to impotence. The treatment of impotence was postponed due to the patient's psychological status. In fact, the patient never attended postoperative follow-up examinations and refused any further medical interventions. His family was contacted and informed about the procedures necessary for planning further medical interventions if requested by the patient, which would most likely involve penile reconstructive surgery.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [120.0, 'kg'], 'height': [177.0, 'cm']}",2.42899,2.30754,2.55044,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 177.0 cm. 
The patient's weight is 120.0 kg. 
Therefore, the patient's bsa is sqrt((120.0 (in kgs) * 177.0 (in cm))/3600) = 2.42899 m^2."
7227,60,Body Surface Area Calculator,physical,decimal,pmc-5557159-1,Extracted,"A 17 year-old male (height: 1.803 m; weight: 83.235 kg; body mass index (BMI): 25.59 kg/m2) high school varsity athlete (football, basketball) was referred to an outside endocrinologist by his primary care provider after an approximate 2-year history of worsening episodes of exercise-induced excessive sweating accompanied by abdominal cramps, headaches, dizziness, occasional blurred vision, and paresthesia throughout his entire body during exercise. His sweating episodes were characterized by a heavy increase in sweating approximately 5 min after the onset of athletic activity. A complete general medical and endocrine evaluation was inconclusive. His comprehensive metabolic panel was within normal limits. His physical examination was unrevealing. The patient subsequently presented to our sports medicine clinic for evaluation of heavy sweating during athletic activities.
Subjective hyperhidrosis (HH) is a reasonably common clinical complaint, but frequently patients are found to have a normal sweat rate when tested. The first step in our clinical protocol for most patients who complain of excess sweating is to have them exercise in a hot and humid environment and measure their weight pre- and post-workout to get an estimate of their actual sweat rate. This patient ran for 33 min on a warm and humid afternoon (88°F, humidity 65%, heat index 97.5), did not urinate, and demonstrated a 3.2-kg weight loss which calculated to an estimated sweat rate of 5.8 L/h (69.9 mL/kg/h). Following this period of exertion, he had a normal resting heart rate at 70 beats per minute. His sweat pattern appeared normal with sweat noticeable on his head, chest, back, and all four extremities. Post-exertional labs were obtained within 5 min of exercise completion and demonstrated mild acidosis (CO2: 21; anion gap: 19), hyperphosphatemia (5.9 mg/dL), and hyperglycemia (123 mg/dL), but no other electrolyte or acid-base abnormalities. We discussed with the patient and his family the results including the excessively high rate of sweat loss (69.9 mL/kg/h vs normal rate of 10–20 mL/kg/h). We encouraged aggressive fluid resuscitation with sugar and electrolyte sports during prolonged exercise athletic events and continued abstinence from caffeine. We also discussed with the patient the possibility of using an aluminum hydroxide–based antiperspirant diffusely over his body in an attempt to limit the rate of sweating during athletic competitions.
Given the patient’s athletic participation, we also made a plan with the patient to test how glycopyrrolate therapy might alter his body temperature and sweat rates during strenuous physical activity. We obtained institutional review board (IRB) approval (the project was deemed exempt) and informed verbal consent from the patient’s father and verbal assent from the patient for a research protocol to test the patient’s physiologic response to glycopyrrolate therapy when physically stressed in a hot and humid environment.
The patient and one healthy control subject (healthy: 35-year-old male, senior author, A.R.P.) received three different trials of glycopyrrolate therapy 0 mg (Trial 1), 2 mg (Trial 2), and 4 mg (Trial 3). Each subject waited 2 h after each glycopyrrolate administration and then underwent an exercise protocol consisting of running on a treadmill (5.4–6.7 mile/h at 1° of incline) in a warm climate-controlled chamber (87 F, humidity 57%, heat index 92.5) for 30 min. Core temperature (CorTemp® Ingestible Core Body Temperature Sensor), heart rate (Polar® FT-1 Heart Rate Monitor), rate of perceived exertion (RPE), and sweat rate were monitored. Spearman correlations and partial effect sizes were calculated. Glycopyrrolate dose was non-significantly correlated with decreased sweat rate (r = −0.79, p = 0.06; ) and maximal core temperature (r = 0.60, p = 0.21; ). However, the clinical effect of reducing the sweat rate was very strong. The improvement of his sweat rate allowed him to successfully return to sport. The effect size of glycopyrrolate dose on sweat rate was high (partial eta-squared = 0.28), but the effect size of glycopyrrolate on core temperature was low (partial eta-squared = 0.07). The patient with HH decreased his sweat rate from 4.4 L/h (53 mL/kg/h) with 0 mg glycopyrrolate to 2.0 L/h (24 mL/kg/h) and 1.8 L/h (22 mL/kg/h) with 2 and 4 mg of glycopyrrolate, respectively (). This is in comparison to the control subject with a sweat rate of 2.0 L/h (26.7 mL/kg/h) with 0 mg of glycopyrrolate to 1.4 L/h (18.7 mL/kg/h) and 0.6 L/h (8.0 mL/kg/h) with 2 and 4 mg of glycopyrrolate, respectively (). The patient with HH’s core temperature was unchanged between the trials with 0 and 2 mg of glycopyrrolate (38.19°C and 37.96°C, respectively), but increased to 38.65°C with 4 mg glycopyrrolate (). The control subject had a similar maximal core temperature response as he was unchanged with 0 and 2 mg of glycopyrrolate (38.43°C and 38.28°C, respectively), but increased to 39.27°C with 4 mg of glycopyrrolate (). Neither subject had a significant change in heart rate with 2 or 4 mg of glycopyrrolate compared to 0 mg of glycopyrrolate ().",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [83.235, 'kg'], 'height': [1.803, 'm']}",2.04174,1.93965,2.14383,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 1.803 m, which is 1.803 m * 100 cm/m = 180.3 cm. 
The patient's weight is 83.235 kg. 
Therefore, the patient's bsa is sqrt((83.235 (in kgs) * 180.3 (in cm))/3600) = 2.04174 m^2."
7228,60,Body Surface Area Calculator,physical,decimal,pmc-5624279-1,Extracted,"A 44-year-old Japanese woman was admitted to our hospital for evaluation of abdominal distension. She was 164 cm tall and weighed 74 kg, with a blood pressure of 143/93 mm Hg. Laboratory tests revealed that her serum creatinine (Cre) value was 0.91 mg/dL, the estimated glomerular filtration rate (eGFR) was 53.7 mL/min/1.73 m2, and her albumin level was 3.6 g/dL. In addition, the total bilirubin level was 0.7 mg/dL, aspartate aminotransferase was 23 IU/L (normal range: 13–33), alanine aminotransferase was 15 IU/L (normal range: 8–42), lactate dehydrogenase was 173 IU/L (normal range: 103–190), alkaline phosphatase was 268 IU/L (normal range: 117–350), γ-glutamyl transpeptidase was 74 IU/L (normal range: 9–109), and C-reactive protein was 0.8 mg/dL. Urinary protein excretion was 0.1 g/day, and the urine sediment contained 1–4 erythrocytes per high-power field. Magnetic resonance imaging and computed tomography showed bilateral enlarged polycystic kidneys and a massive polycystic liver (Fig. ). ADPKD was diagnosed, since her mother had this disease. Liver volume was calculated to be 10,173 mL, indicating advanced PLD, while the total kidney volume was calculated as 2,614 mL by a previously reported method [].
First, 3 large cysts were treated by aspiration and sclerotherapy using minocycline hydrochloride according to a reported method []. Her abdominal fullness improved immediately after 1,750 mL of cyst fluid was removed, but the improvement was only temporary. Liver volume increased to 9,750 mL again after 6 months, along with the exacerbation of abdominal symptoms. Tolvaptan therapy was started at a dose of 60 mg daily to treat renal involvement (Cre of 0.89 mg/dL and eGFR of 54.6 mL/min/1.73 m2). After 1 month of tolvaptan therapy, abdominal fullness showed improvement and liver volume decreased to 9,219 mL, while it decreased further to 8,963 mL after 12 months of treatment and to 8,345 mL after 17 months. Total kidney volume was 2,714 mL at the start of tolvaptan therapy, while it was 2,640 mL after 1 month and 2,832 mL after 17 months. There was no significant change in kidney volume during the 17-month treatment period, and renal function was also unchanged (Cre of 0.92 mg/dL and eGFR of 52.3 mL/min/1.73 m2).",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [74.0, 'kg'], 'height': [164.0, 'cm']}",1.83606,1.74426,1.92786,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 164.0 cm. 
The patient's weight is 74.0 kg. 
Therefore, the patient's bsa is sqrt((74.0 (in kgs) * 164.0 (in cm))/3600) = 1.83606 m^2."
7229,60,Body Surface Area Calculator,physical,decimal,usmle-1547,Extracted,"A 20-year-old man comes to the emergency room because of palpitations and mild dyspnea for the last 2 hours. He has had similar episodes in the past that resolved within 20 minutes, but they have been worsening since he started training for his first marathon 1 month ago. Ten years ago, he was treated for streptococcal pharyngitis with a 10-day course of penicillin. His maternal uncle passed away unexpectedly from a heart condition at age 40. He is 180 cm (5 ft 11 in) tall and weighs 85 kg (187 lb); BMI is 26.2 kg/m2. His temperature is 36.5°C (97.7°F), pulse is 70/min, respirations are 18/min, and blood pressure is 132/60 mm Hg. On examination, there is a decrescendo early diastolic murmur heard best along the left sternal border. His head slightly bobs about every second. The remainder of the examination shows no abnormalities.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [85.0, 'kg'], 'height': [180.0, 'cm']}",2.06155,1.95847,2.16463,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 180.0 cm. 
The patient's weight is 85.0 kg. 
Therefore, the patient's bsa is sqrt((85.0 (in kgs) * 180.0 (in cm))/3600) = 2.06155 m^2."
7230,60,Body Surface Area Calculator,physical,decimal,pmc-3977502-4,Extracted,"A 57-year-old diabetic male (68 in, 184 lbs, BMI 28, smoking ~1/2 pack daily) presented with 5 months of left shoulder pain from a full thickness rotator cuff tear. Eleven days after undergoing subacromial decompression and rotator cuff repair, he reported significant elbow pain. His examination demonstrated well healing portals without evidence of infection. However, there were slight swelling and localized tenderness over the medial elbow and proximal forearm. Duplex ultrasound revealed occlusive thrombus in the basilic vein with multiple nonocclusive thrombi in the brachial vein. Treatment included rivaroxaban 15–20 mg daily for a total of 3 months with resolution of symptoms within 3 days. At follow-up of 11 weeks, he was doing very well with no pain in his shoulder.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [184.0, 'lbs'], 'height': [68.0, 'in']}",2.00107,1.90102,2.10112,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 68.0 in, which is 68.0 in * 2.54 cm/in = 172.72 cm. 
The patient's weight is 184.0 lbs so this converts to 184.0 lbs * 0.453592 kg/lbs = 83.46093 kg. 
Therefore, the patient's bsa is sqrt((83.46093 (in kgs) * 172.72 (in cm))/3600) = 2.00107 m^2."
7231,60,Body Surface Area Calculator,physical,decimal,pmc-6498274-1,Extracted,"A 68-year-old female was referred to the emergency department of our hospital in April 2016. She was suffering from anorexia, abdominal distension, abdominal pain in lower-right abdomen. Furthermore, a right-side inguinal hernia and uterine prolapse were revealed by a physical examination. Her height and weight were 154 cm and 65 kg, respectively, and she had no history of other diseases.
Laboratory data showed inflammatory changes, as indicated by a white blood cell count of 13,600/μl, CRP of 33.8 mg/dl, hypoalbuminemia at the serum albumin level 3.4 g/dl, and slight renal dysfunction (BUN 108 mg/dl, Creatinine 4.25 mg/dl); in addition, she had elevated levels of tumor markers CEA, CA19-9 and CA125 at 37 ng/ml, 113 U/ml, and 124 U/ml, respectively.
Abdominal computed tomography (CT) at admission revealed massive ascites and a cystic mass in the lower-right abdomen that ruptured to abdominal cavity (Fig. a). The CT density of the ascites was 10–20 Hounsfield units (H.U.) which was higher than serous ascites (0–5 H.U.) CT also revealed a right inguinal hernia containing the small intestine (Fig. b) and uterine prolapse (Fig. c). Magnetic resonance imaging revealed that the cystic tumor was arising from appendix (Fig. ). We had aspirated the ascites being yellow and cloudy. And cytology of the ascites showed mucus suggesting the diagnosis of PMP but no malignant cells (Fig. ).
Based on these findings, we diagnosed the patient with ruptured appendiceal mucinous adenoma and PMP and scheduled a laparotomy. Massive yellow and cloudy ascites and ruptured cystic tumor arising from the appendix were seen (Fig. a). Bilateral ovaries and peritoneum were covered with the yellow substance. We performed an appendectomy containing the cystic mass, bilateral oophorectomy and a biopsy for the peritoneum. We irrigated the abdominal cavity using 3000 ml of dextran solution.
Additionally, we fixed the pelvic diaphragm by sutures and repaired the inguinal hernia via the another incision.
The macroscopic findings showed a ruptured cystic mass measuring 5 × 4 cm arising from the middle of the appendix. We also noted small nodules inside the capsule. Mucous was retained in the vermis. The bilateral ovaries and peritoneum were also covered with yellow mucin. The pathologic findings revealed the presence of low-grade atypical cell inside the capsule, and fibrosis with hemosiderin and cholesterin was observed in the wall of the vermis (Fig. ) . However, no tumor cells were found on the surface of the ovary or peritoneum.
The postoperative course was uneventful, and the serum tumor marker levels subsequently decreased to CEA 3.1 ng/ml, CA19-9 47.6 U/ml, and CA125 17.7 U/ml, 2 months later.
We administered S1 (75 mg/body for 14 days every 21 days) to prevent the relapse. The patient is doing well in 1 year later.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [65.0, 'kg'], 'height': [154.0, 'cm']}",1.6675,1.58413,1.75087,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 154.0 cm. 
The patient's weight is 65.0 kg. 
Therefore, the patient's bsa is sqrt((65.0 (in kgs) * 154.0 (in cm))/3600) = 1.6675 m^2."
7232,60,Body Surface Area Calculator,physical,decimal,pmc-4766327-1,Extracted,"A 35-year-old pregnant Japanese woman (gravida 2, para 0-1-0-1) presented to our emergency outpatient department at 18 weeks' gestation with sudden dyslexia and worsening symptoms of aphasia and dyslexia. Brain magnetic resonance imaging (MRI) revealed a solid mass on the left temporal lobe ().
The patient's mother was diagnosed with breast cancer at 40 years of age and died as a result of the disease at 47 years of age; moreover, her grandmother also died of cancer (the affected organ was unclear) and her grandfather had pancreatic cancer. Her sisters and brother did not have cancer ().
At 29 years of age, she developed ovarian cysts and a salpingo-oophorectomy was performed. Subsequently, at 30 years of age, she was incidentally diagnosed with pregnancy-associated breast cancer during her first pregnancy; at that time, a cesarean section was performed at 36 weeks' gestation due to the termination of the pregnancy. Thereafter, right mastectomy and right axillary dissection were also performed. Computed tomography (CT), MRI, and bone marrow scintigraphy did not indicate any metastatic lesions, and the preoperative levels of tumor markers were as follows: NCC-ST-439, 22.5 U/mL (normal, ≤7.0 U/mL); CA15-3, 25.0 U/mL (normal, ≤27.0 U/mL); and CEA, 1.1 U/mL (normal, ≤5.0 U/mL). Furthermore, histopathological examination indicated that the tumor was an invasive ductal carcinoma. The tumor was located in the right breast and was 30 × 45 × 50 mm in size. Negative margins were obtained with surgery. No lymph node metastases were observed (0/14). The final pathological staging was T3, N0, M0, stage IIb. A hormone receptor assay indicated that the tumor was negative for both estrogen and progesterone receptors, and the human epidermal growth factor receptor 2 (HER-2)/neu test also yielded negative results. The Ki-67 expression index was 80% (). Because she had triple-negative cancer, adjuvant therapy was recommended; however, she refused this therapy due to the risk of infertility. Four years after the surgery, no increases in tumor marker levels were noted. She became pregnant naturally after 4 years and came to our hospital for a prenatal checkup.
On admission, the patient's height was 160 cm and weight was 60.8 kg (body mass index, 38.0). The levels of tumor makers were within the normal ranges, as follows: NCC-ST-439, ≤2.5 U/mL (normal, ≤7.0 U/mL); CA15-3, 7.7 U/mL (normal, ≤27.0 U/mL); and CEA, 0.5 U/mL (normal, ≤5.0 U/mL).
She underwent an urgent craniotomy. Histopathological examination of the tumor tissue indicated that the tumor was a metastasis of adenocarcinoma. The hormone receptor assay indicated that the tumor was negative for both the estrogen and progesterone receptors, and negative results were obtained on HER-2/neu testing. The Ki-67 expression index was 90%. To treat the recurrence of familial breast cancer during pregnancy, a multidisciplinary team including a breast surgeon, neurosurgeon, and radiotherapist discussed the case. To confirm whether there was metastasis at other locations, positron emission tomography-CT was also performed, and lung metastasis was detected (). The breast surgeon believed that long-term survival is difficult in the case of brain metastasis, and, hence, treatment could proceed rapidly and she could continue her pregnancy while receiving anticancer medication until the date of delivery. However, the neurosurgeon and radiotherapist believed that she should undergo cranial irradiation after terminating the pregnancy. The patient and her husband did not wish to terminate the pregnancy, and, therefore, we determined a course of treatment after several consultations with the patient and her husband. However, they consented to terminating the pregnancy after the symptoms associated with the brain metastasis worsened. Therefore, an artificial abortion was performed at 21 weeks' gestation using gemeprost, after which whole brain irradiation was performed. Thereafter, she was treated with adjuvant chemotherapy containing adriamycin and cyclophosphamide and underwent a partial pneumonectomy. At present, she has not shown any signs of recurrence (). Her family history, young-onset disease, and histopathological finding of triple-negative cancer were consistent with HBOC. Genetic counseling was performed. Though she understood the importance of a genetic test for her daughter, she did not wish to receive the genetic test. Her remaining ovary is regularly examined because she is at a high risk of developing HBOC.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.8, 'kg'], 'height': [160.0, 'cm']}",1.64384,1.56165,1.72603,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 160.0 cm. 
The patient's weight is 60.8 kg. 
Therefore, the patient's bsa is sqrt((60.8 (in kgs) * 160.0 (in cm))/3600) = 1.64384 m^2."
7233,60,Body Surface Area Calculator,physical,decimal,pmc-7788116-1,Extracted,"A 36-year-old Japanese female was referred to our hospital with morbid obesity and T1DM. She was diagnosed with T1DM at the age of 6 years, thereafter, treatment with multiple daily insulin was started. By the age of 20 years, she had a body weight of 70 kg, increasing to > 100 kg at the age of 34 years. Her required daily dose of insulin increased as a function of her body weight. At her initial assessment, she required 45 units of insulin aspart and 30 units of insulin glargine per day. Although a temporary weight loss and reduction in daily insulin dose was achieved with an in-hospital treatment, her weight rebounded shortly after discharge and the patient experienced difficulty in controlling her body weight. The patient expressed her intention for surgical treatment for weight loss, and she was referred to our department.
At the time of admission, her height was 159 cm and her weight 106.7 kg, BMI of 42.2 kg/m2. Blood analyses indicated HbA1c of 9.0%, and blood C-peptide levels were undetectable (< 0.01 ng/mL), suggesting her insulin secretion capacity was completely depleted. With medication, her blood lipid levels were within normal range. On computed tomography (CT) examination, the calculated visceral fat area was 162.6 cm2, with a subcutaneous fat area of 527.9 cm2, measured at level of the umbilicus (Fig. a, b). Upper gastrointestinal endoscopy revealed no abnormalities in the esophagus, stomach, or duodenum.
To prevent complications associated with rapid postoperative blood glucose improvement, she was admitted to our hospital 2 weeks before operation for strict glycemic control, dietary restrictions, and exercise therapy. As a result, preoperative HbA1c was reduced to 7.8% and body weight was reduced to 101.1 kg.
We performed a laparoscopic sleeve gastrectomy (LSG) [], using five ports,, as shown in Fig. a. The blood vessel along the wall of the greater curvature of the stomach was first dissected. We then inserted a 36 Fr (12 mm) bougie into the stomach and resected the greater curvature of the stomach, from a point, on the oral side, 4 cm from the pylorus to the His angle, using a linear stapler. The staple line was reinforced with continuous seromuscular sutures using non-absorbable stitches (Fig. b, c).
After the operation, a unit of insulin aspart was mixed with 5 g of glucose contained in the infusion solution and sliding scale insulin was added as needed. From postoperative day 2, insulin glargine was administered. Sliding scale insulin was added depending on fasting blood sugar level and oral intake and her daily insulin dose was determined accordingly.
There were no postoperative complications, including severe hypoglycemic episodes. One year after the procedure, her body weight had decreased to 81.0 kg, with a BMI of 32.2 kg/m2, with this decrease being mainly due to a decrease in the body fat mass. Her HbA1c level improved to 7.7%, and her daily required insulin dose had been reduced to 24 units (10 units of insulin aspart and 14 units of insulin glargine per day: Fig. a–d). On abdominal CT images, the visceral fat area, measured at level of the umbilicus, was 44.8 cm2, with a subcutaneous fat area of 408.8 cm2 (Fig. c, d). Therefore, there was a marked decrease in both visceral and subcutaneous fat.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [106.7, 'kg'], 'height': [159.0, 'cm']}",2.17085,2.06231,2.27939,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 159.0 cm. 
The patient's weight is 106.7 kg. 
Therefore, the patient's bsa is sqrt((106.7 (in kgs) * 159.0 (in cm))/3600) = 2.17085 m^2."
7234,60,Body Surface Area Calculator,physical,decimal,pmc-3253671-2,Extracted,26 year old female (upon admission). Diagnosed of Graves' disease at age 26 but presented with liver dysfunction with methimazole and mild neutropenia with propylthiouracil. Thyroid function was controlled with potassium iodide until surgery. She had a history of anorexia and bulimia since age 19. Her thyroid function and eating behavior were both stable at the time of surgery. There is no record of the use of SSRIs in the treatment of anorexia nervosa. Her height was 158.5 cm and her weight was 55.0 kg (BMI 21.9) at the time of surgery. Post operatively she was placed on 75 mcg of levothyroxine daily which maintained her thyroid function within normal levels. There was no relapse of her anorexia bulimia and her body weight increased slightly and gradually over the next seven years (to BMI 23.8).,What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.0, 'kg'], 'height': [158.5, 'cm']}",1.55613,1.47832,1.63394,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 158.5 cm. 
The patient's weight is 55.0 kg. 
Therefore, the patient's bsa is sqrt((55.0 (in kgs) * 158.5 (in cm))/3600) = 1.55613 m^2."
7235,60,Body Surface Area Calculator,physical,decimal,pmc-5690740-1,Extracted,"A boy was delivered at 38 weeks of gestation to a 25-year-old gravida1 paral1 by emergency cesarean section soon after the coagulation function of his mother had become normal. His mother had bled from oral mucosa for 3 days because of an unknown reason. Blood tests showed a prolonged prothrombin time (PT) exceeding 70 s (normal: 10.4–12.6 s) and activated partial thromboplastin time (aPTT) of 110.5 s (normal: 74.0–110.0 s). The addition of normal plasma in a 1:1 ratio resulted in complete correction of the coagulation abnormalities, and a coagulation factor deficiency was suspected. The results of factor assay were associated with vitamin K deficiency: the levels of factor II, factor VII, factor IV, and factor X were sharply low, but factor V and factor VIII were within normal ranges. The mother was given vitamin K intravenously, and the oral bleeding stopped after 8 hours. Serum screening for toxicant by using gas chromatography/mass spectrometry (GC/MS) was taken 6 hours after admission and the result showed a bromadiolone level of 126 ng/mL.[ She denied intentional ingestion of any kind of rodenticides. The most likely route of exposure might be ingestion of the food contaminated by bromadiolone.
The boy's APGAR scores[ were 2 (Pulse: 2), 5 (Activity: 1;Pulse: 2;Grimace: 1;and Respiratory effort: 1), and 5 (Activity: 1;Pulse: 2;Grimace: 1;Respiratory effort: 1) at 1, 5, and 10 minutes respectively. Blood gas analysis showed pH of 7.249, PCO2of 55.9mmHg, PO2of 32mmHg, and BE of −4.2mmol/L. Immediate intubation and resuscitation was necessary. The boy showed poor respiratory effort, decreased muscle tone, and pallor. He was transferred to the neonatal intensive care unit for further treatment. The patient presented no history of trauma and bleeding diathesis.
Upon admission, the boy's measurements were as follows: weight 3120 g; length 48 cm; and fronto-occipital head circumference 37 cm. All of these measurements were appropriate for the boy's gestational age. The boy presented with bulging anterior fontanelle, a heart rate of 169 bpm, and blood pressure of 68/40 mmHg. No external signs of spontaneous hemorrhage were noted. The pupils were dilated and fixed to light. Corneal, Moro, and rooting reflexes were absent. Hepatomegaly and splenomegaly were not found.
Laboratory tests revealed hemoglobin level of 74 g/L, white blood cell count of 17.57 × 109/L, and platelet count of 264 × 109/L. PT exceeded 70 s (upper limit of reference), and aPTT was greater than 150 s (upper limit of reference). Fibrinogen (3.02 g/L) and thrombin time (16.4 s) were normal. Serology assay showed the following values: ALT: 5U/L; Alb: 28 g/L; TBil: 27.4 μmol/L; Cr: 57 μmol/L; CK: 353U/L; and CKMB: 6.3 μg/L.
The neonate was treated with vitamin K, fresh-frozen plasma, and red blood cells. His oral mucosa started to bleed at 2 hours after birth. Muscle tone increased at 4 hours after birth. Generalized seizures started on day 1 of life. A head computed tomography showed a severe subdural hematoma causing midline shift, bilateral intraventricular hemorrhage, and subarachnoid hemorrhage (Fig. ). Serum from cord blood was screened for toxicants. The result showed bromadiolone level of 94 ng/mL. His parents requested to stop all treatment, and the neonate died shortly after. Autopsy was not obtained from the parents.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [3120.0, 'g'], 'height': [48.0, 'cm']}",0.20396,0.19376,0.21416,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 48.0 cm. 
The patient's weight is 3120.0 g so this converts to 3120.0 lbs * kg/1000 g = 3.12 kg. 
Therefore, the patient's bsa is sqrt((3.12 (in kgs) * 48.0 (in cm))/3600) = 0.20396 m^2."
7236,60,Body Surface Area Calculator,physical,decimal,pmc-6547317-1,Extracted,"A 62-year-old Chinese man complained of intermittent weakness in the extremities (particularly the calves), muscle pain, and walking difficulty.
The patient’s weakness in the extremities started 30 years ago, but spontaneously recovered in one week after each instance. Twenty years ago, he was admitted to the hospital because of difficulty walking upstairs and a diagnosis of hypokalemia was made. The patient’s symptoms quickly improved with potassium replacement therapy. Despite any medicine treatment, his serum potassium levels ranged from 2.8 to 3.1 mmol/L in the past 10 years. The patient presented with muscle pain and walking difficulty 15 d ago. He took potassium chloride sustained-release tablets 1.5 g per day for 5 d. Furthermore, he described dark-colored urine for 3 days. Thus, the patient was sent to the hospital for further evaluation. There was no history of diarrhea or vomiting, signs of infection or alcohol intoxication. He denied ever taking any statins. Upon further questioning, a detailed history revealed that he had con-sumed liquorice water daily for 7 days preceding admission.
The past medical history revealed only type 2 diabetes mellitus since the age of 52. For that reason, he was treated with 10 mg of dapagliflozin and 25 mg of alogliptin daily.
The patient denied tobacco, alcohol, and illicit drug use. His family history was unre-markable, and there were no similar cases in his family.
On admission, the patient’s body weight was 60.0 kg, and his height was 168.2 cm. His blood pressure was 128/92 mmHg and his pulse rate was 86 beats/min. There was generalized paralysis in all four limbs (power grade 3/5). There was no sensory deficit. The examination of the thyroid and other systems was unremarkable.
Table shows laboratory data of the patient. Serum potassium level was 1.84 mmol/L. Serum magnesium was 0.68 mmol/L. Creatinine phosphokinase (CK) was 10117 IU/L, and he had marked hemoglobinuria. Fractional chloride excretion and fractional magnesium excretion were calculated as 1.9% and 4.4%, respectively. Urinary calcium/creatinine ratio was calculated as 0.24. Plasma renin activity and aldosterone concentration were within the normal ranges. Serum alkaline pho-sphatase and parathormone levels were normal. According to the laboratory tests, the level of CK at presentation was 30 times more than the upper limit of the normal range. Furthermore, the level of serum myoglobin (MYO) was significantly increased. Consequently, rhabdomyolysis was diagnosed.
Rhabdomyolysis can have various causes, such as metabolic disease, direct trauma to muscle, muscle necrosis due to ischemia, muscle inflammation, or exposure to drugs and toxins[]. Recent studies suggest that liquorice can induce hypokalemia and muscle weakness and can even lead to life-threatening rhabdomyolysis[]. However, considering the medical history, the patient had a history of hypokalemia for 30 years. Moreover, considering the results of the laboratory tests including hypomagnesemia, normal plasma renin activity, and aldosterone concentration, the etiology of pre-existing hypokalemia should be considered. With informed consent, we investigated the SLC12A3 gene of the patient. Sequence analysis of the SLC12A3 gene of the patient revealed that he had compound heterozygous mutations. One missense mutation was a heterozygous G to A base pair substitution at position 1567 in exon 12, which caused an Ala to Thr substitution at position 523. A second missense mutation, a hetero-zygous G to A base pair substitution at position 2542 in exon 21, causing an Asp to Asn substitution at position 848, was also present (Figure ).
The 12-lead electrocardiogram (ECG) demonstrated a sinus rhythm with inverted T-waves on leads V1-V6 and ST-depression on leads V4-V6, but no prolongation of the QTc interval and U waves. Abdominal sonography did not reveal renal stones or nephrocalcinosis. Peripheral neuropathy in both lower limbs was found by examining the electromyogram. Muscle biopsy was rejected by the patient.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [60.0, 'kg'], 'height': [168.2, 'cm']}",1.67432,1.5906,1.75804,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 168.2 cm. 
The patient's weight is 60.0 kg. 
Therefore, the patient's bsa is sqrt((60.0 (in kgs) * 168.2 (in cm))/3600) = 1.67432 m^2."
7237,60,Body Surface Area Calculator,physical,decimal,pmc-4377186-1,Extracted,"A 72-year-old woman with a 10-year history of hypertension visited a local hospital presenting with anasarca and 15-kg weight gain in the past 3 months. She did not have fever, appetite loss, night sweats, or dyspnea. Because of elevated liver enzymes and abdominal computed tomography (CT) abnormalities, including splenomegaly and multiple splenic tumors, she was referred to our hospital.
On admission, physical examination of the patient revealed the following: temperature, 36.3 °C; pulse rate, 84 beats per minute, regular; blood pressure, 132/74 mmHg; and respiration rate, 18 breaths per minute. Although she had remarkable anasarca, she seemed in no distress. Her height was 143.5 cm, body weight 71 kg, and body mass index 34.2. She had no jugular venous distention. Lymphadenopathy was not noted. No crackles were audible, but there were diminished breath sounds in the base of the right lung. She had remarkable nonpitting and slow pitting mixed edema of the legs. A delayed relaxation time of the Achilles tendon reflex was observed.
Laboratory test results revealed the following: white blood cell count, 7,400 cells/mm3; hemoglobin, 11.6 g/dL; platelet count, 103,000/μL; total protein, 6.0 g/dL; albumin, 2.9 g/dL; aspartate aminotransferase, 27 IU/L; alanine aminotransferase, 20 IU/L; lactate dehydrogenase, 707 IU/L; alkaline phosphatase, 629 IU/L; total-bilirubin, 0.69 mg/dL; blood urea nitrogen, 11 mg/dL; creatinine, 0.65 mg/dL; creatinine kinase, 15 IU/L; thyroid-stimulating hormone (TSH), 0.45 μU/mL (standard value: 0.45-3.33 μU/mL); free thyroxine (FT4), 0.37 ng/dL (standard value: 0.84-1.44 ng/dL); free triiodothyronine (FT3), 0.89 pg/mL (standard value: 2.11-3.51 pg/mL); and soluble interleukin-2 receptor, 6,660 U/mL (standard value: 124–466 U/mL). Urinary protein level was 0.2 g/g creatinine. A contrast-enhanced CT of the head, neck, chest, abdomen, and pelvis revealed splenomegaly and multiple spleen tumors (Figure ), whereas there was no lymphadenopathy. CT-guided biopsy of the spleen was performed, which showed aggregated large atypical cells. The individual cells had the chromatin-rich nuclei and relatively abundant intracytoplasmic eosinophilic inclusion bodies (Figure ). Immunohistochemistry showed that the atypical cells were positive for CD20 and CD79a, and negative for CD3 and CD10. Histopathology and immunohistochemistry of the spleen led to the diagnosis of DLBCL.
We assessed the central hypothyroidism because of anasarca, delayed Achilles tendon reflex, and low FT4.
Head magnetic resonance imaging (MRI) revealed swelling of pituitary gland, but a normal-size of pituitary gland was confirmed in a head MRI performed 1 year before (Figure a, b). Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were also at low levels (LH 0.3 mIU/mL [standard value: 6.7-38.0 mIU/mL] and FSH 3.4 mIU/mL [standard value: 26.2-113.3 mIU/mL]). Cortisol level was 21.6 μg/dL [standard value: 4.0-18.3μg/dL] and ACTH was 33.4 pg/mL [standard value: 7.2-63.3 pg/mL]. Prolactin was 9.2 ng/mL[standard value: 3.12-15.39 ng/mL(menopause women) ]. AVP level was not measured but there were no polyuria and hyponatremia. We diagnosed pituitary anterior lobe hormone insufficiency.
Positron emission tomography (PET) scan revealed a localized accumulation in the pituitary gland, spleen, and para-abdominal aorta lymph nodes (Figure ). Pituitary gland biopsy was not performed; however, we clinically diagnosed central hypothyroidism caused by pituitary gland infiltration of DLBCL (clinical stage IV in the Ann Arbor staging classification).
She received 25 μg per day of levothyroxine for one week before the chemotherapy. However, the dose and duration of levothyroxine were not enough. The first course of chemotherapy for DLBCL including methotrexate, vincristine, ifosfamide, and dexamethasone, which improved anasarca remarkably and the patient’s body weight returned to what it was 3 months before. Moreover, thyroid hormone, LH, and FSH levels normalized and the pituitary gland swelling improved (Figure c), although thyroid hormone replacement therapy was not effective before chemotherapy (Figure ). We chose a second course of chemotherapy that comprised cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone (CHOP) because there were no atypical cells in the patient’s cerebrospinal fluid. This second course of chemotherapy led to remission and the same chemotherapy regimen was repeated.
Here, we describe a case of pituitary gland infiltration of DLBCL associated with central hypothyroidism, which caused remarkable anasarca. In this case, only a few clinical manifestation were anasarca and a delayed relaxation time of the Achilles tendon reflex, other than the typical symptoms of lymphoma (fever, night sweats, and weight loss).
Pituitary gland involvement as extranodal lymphoma is comparatively rare [,], and DLBCL is one of the most frequent histological types for pituitary gland involvement []. Infiltration of lymphoma cells to the pituitary gland lead to headache, opthalmoplegia, or hemianopia [], and often causes diabetes insipidus []. Anasarca is a rare symptom in patients with lymphoma [].
Moreover, lymphoma with pituitary gland infiltration seldom shows significant anasarca or weight gain caused by secondary central hypothyroidism. Some patients with lymphoma who have pituitary gland involvement have no symptom, and they are incidentally detected using PET or MRI []. We clinically diagnosed infiltration of a malignant lymphoma in the pituitary gland based on time-dependent changes in MRI findings, thyroid hormone, LH, and FSH levels before and after chemotherapy; and PET findings.
Infiltration of DLBCL cells to the pituitary gland caused secondary central hypothyroidism, and secondary central hypothyroidism led to anasarca and weight gain in our patient. Nonpitting edema was noted, provably caused by hypothyroidism, and slow pitting edema resulting from hypoalbuminemia was observed simultaneously.
Elderly people often have several disorders at the same time; however, we believe that, in explaining manifestations, one disorder should account for every symptom. In this case, the patient had remarkable anasarca because of DLBCL involvement of the pituitary gland. This case was very valuable because we could assess the patient’s abnormalities; that is to say, anasarca, weight gain, hypothyroidism, elevated lactate dehydrogenase and alkaline phosphatase, splenomegaly, and swelling of the pituitary gland caused by malignant lymphoma and its infiltration into the pituitary gland.
In this era of longevity, the prevalence of diseases increases, and we must anticipate the greater likelihood of multiple, simultaneous diagnoses []. Hickam’s dictum and Occam’s razor are well suited to this case. “A patient can have as many diagnoses as he darn well pleases” []. This is Hickam’s dictum. However, William of Ockham stated “Among competing hypotheses, favor the simplest one” []. This is known as Occam’s razor.
It was easy to assess laboratory abnormalities, splenomegaly, and multiple spleen tumors that resulted from the malignant lymphoma. It was also easy to assess anasarca that was due to hypothyroidism and hypoalbuminemia. In this case, however, we reached the correct diagnosis of pituitary gland involvement from DLBCL, which manifested significant anasarca, according to Occam’s razor. A pituitary gland lesion with central hypothyroidism should be considered as one of the differential diagnoses of edema, especially nonpitting edema in some cases.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [71.0, 'kg'], 'height': [143.5, 'cm']}",1.6823,1.59818,1.76642,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 143.5 cm. 
The patient's weight is 71.0 kg. 
Therefore, the patient's bsa is sqrt((71.0 (in kgs) * 143.5 (in cm))/3600) = 1.6823 m^2."
7238,60,Body Surface Area Calculator,physical,decimal,pmc-6967009-1,Extracted,"A 39-year-old, gravida 2, para 1, Japanese woman (158 cm/56.8 kg) with fetal congenital heart anomaly and polyhydramnios was scheduled for induction of delivery at 37 weeks of gestation. She requested labor analgesia.
The combined spinal-epidural block was placed at L3-L4 level, and 1.5 mg 0.5% isobaric bupivacaine with fentanyl 15 mcg was administered into the subarachnoid space. A catheter was introduced into the epidural space at cervix dilatation of 4 cm. Then, the labor analgesia was managed by programmed intermittent epidural bolus with 0.1% ropivacaine and fentanyl 2 mcg/mL was set at 8 mL with a 60-min interval. Due to polyhydramnios, pinhole amniotomy was performed at cervix dilation of 3 cm. There were no major complications until fetal bradycardia (80–90 beats per minute) occurred, which prompted the obstetric physician to go for vacuum extraction delivery. Patient delivered a female infant weighing 2468 g with an Apgar score of 7/8. Total delivery time was 2 h and 39 min (second stage of labor duration was 22 min).
After an episiotomy, a large amount of bleeding from the uterus was observed, and the obstetric physician suspected it as postpartum atony. Blood pressure was 112/89 mmHg, heart rate was 80 beats per minute, shock index was 1, and total amount of bleeding was 2800 mL at that time. We started to transfuse red blood cells and placed an intrauterine (Bakri®) balloon. At 30 min after the delivery, the total bleeding amount reached 3100 mL, and the blood pressure was decreased to 72/43 mmHg, shock index increased to 2, and SpO2 decreased to 86%. We started treatment based on a suspicious diagnosis of AFE due to sudden decrease of plasma fibrinogen level and uncontrollable bleeding from a needle hole. She was orotracheally intubated, and a central venous and a radial artery catheter was inserted. We ruled out pulmonary embolism because the central venous pressure was 5 mmHg. Besides administering low-dose noradrenaline, an occlusion balloon was inserted into the descending aorta. Uterine artery embolization was performed at radiology department. Red blood concentrates (RBCs) and fresh frozen plasma (FFP) were transfused using a rapid infusion system. In spite of those treatments, her bleeding was uncontrollable and obstetrics team decided to perform total hysterectomy, and the patient was transferred to the operating room. The time from the start of surgery to hysterectomy was 11 min. The fibrinogen level increased above 100 mg/dL after hysterectomy. However, the second interventional radiology (IVR) was required to control bleeding from the vagina. Embolization of the right internal pudendal artery and cervicovaginal branches of the right uterine artery was performed. At last, her bleeding was controlled, and the blood pressure became stable without norepinephrine administration. After hysterectomy, she was transferred to the ICU with intubation. The total bleeding amount was 12,000 mL, and the total amount of RBCs, FFP, platelet concentrate, and fibrinogen required were 38 U, 36 U, 60 U, and 8 V, respectively. The perioperative chart is shown in Fig. . The time series results of blood sampling are shown in Table .
She was extubated on the second day after surgery at ICU. On the third day, she was moved from the ICU to the general ward. On the 16th postoperative day, she was discharged from the hospital without any complications. Laboratory tests at when postpartum hemorrhage began showed that serum zinc coproporphyrin-1 and sialyl-Tn antigens were negative, but C3 (64.0 mg/dL), C4 component (10.0 mg/dL), and C1 esterase inhibitor levels (27%) were low. A month later, immunostaining examination revealed fetal components in the uterus, confirming a diagnosis of DIC type AFE.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [56.8, 'kg'], 'height': [158.0, 'cm']}",1.57889,1.49995,1.65783,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 158.0 cm. 
The patient's weight is 56.8 kg. 
Therefore, the patient's bsa is sqrt((56.8 (in kgs) * 158.0 (in cm))/3600) = 1.57889 m^2."
7239,60,Body Surface Area Calculator,physical,decimal,pmc-3819856-1,Extracted,"A 10-year-old male patient (30 kg, 122 cm) presented with short stature and a stooping posture due to pronounced kyphoscoliosis [] along with back pain for the past three years. History of snoring, breath holding, cyanosis, paradoxical chest movement, restless sleep, daytime somnolence and family history of dwarfism were absent. He was cooperative, had normal mental function and intellectual development without any neurological deficit. Airway examination revealed adequate mouth opening, Mallampati class-II and unrestricted neck extension.
Pulmonary functional tests and laboratory values were within regular limits. Chest and cervical region X-ray appeared normal, without subluxation on flexion and extension. Thoracic kyphosis was present with a Cobb's angle of 35° []. Magnetic resonance imaging of brain revealed hydrocephalus, ventriculomegaly, a short posterior fossa, tonsillar herniation and a 3-mm syrinx. Posterior fossa decompression by C1, C2 laminectomy with removal of a foramen magnum rim was planned.
On the night before surgery the patient was instructed to follow standard ASA fasting guidelines. Anticipating difficult venous cannulation due to the coarse and loose skin [], the AV300 Vein Viewing System was used to identify a vein in the dorsum of the left hand, which was marked.
On the day of surgery, the patient was brought to the operation theatre in a calm state and 5-lead ECG, non-invasive blood pressure and pulse oximetry were connected. A 20-G intravenous cannula was inserted into the previously marked site after application of EMLA cream.
The severe kyphoscoliosis and gibbus deformity prevented the patient from assuming a supine position for intubation []. We modified the position by placing a thick pillow that supported the occiput and compensated the gibbus deformity []. Keeping the difficult airway cart ready the child was sedated with intravenous midazolam (1 mg), fentanyl (60 g) and a bolus dose of propofol (60 mg). After confirming the ability to mask ventilate and glottic visualisation following a gentle check laryngoscopy, vecuronium (3 mg) was administered to facilitate intubation. Endotracheal tube size prediction in such patients is difficult.[] Age formula predicted an endotracheal tube size of 6.5 mm, but we could intubate the patient with a 5.5-mm cuffed, flexomettalic endotracheal tube. The operative site being near the brainstem, the left radial artery was cannulated for invasive blood pressure monitoring and an oesophageal temperature probe was inserted. Anesthesia was maintained with an air-oxygen mixture (1:1) and isoflurane, and intermittent boluses of vecuronium and fentanyl as needed.
After preloading with 200 ml of normal saline, the patient was positioned prone on pillows keeping the abdomen free for excursions and the pressure points were padded. Surgery was completed in about 2 h. Postoperatively the patient was turned supine and placed on a thick pillow in a position similar to intubation. The neuromuscular block was antagonised and the trachea was extubated after complete awakening. The patient was shifted to the ICU for monitoring. Injection of paracetamol (500 mg intravenously six-hourly) provided postoperative pain relief. After an uneventful postoperative period, the patient was discharged after 3 days with advice for spinal extension brace, physiotherapy and follow-up.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [30.0, 'kg'], 'height': [122.0, 'cm']}",1.0083,0.95788,1.05872,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 122.0 cm. 
The patient's weight is 30.0 kg. 
Therefore, the patient's bsa is sqrt((30.0 (in kgs) * 122.0 (in cm))/3600) = 1.0083 m^2."
7240,60,Body Surface Area Calculator,physical,decimal,pmc-7982238-1,Extracted,"A 65-year-old Asian man (173 cm/90 kg) was admitted with lower back pain that occurred 2 years prior. Degenerative spondylolisthesis at L4-5 was found on magnetic resonance imaging (MRI) and posterior lumbar interbody fusion L4-5 was scheduled.
He had a history of hypertension, diabetes mellitus, and chronic obstructive pulmonary disease. His medications were calcium channel blockers and beta-blockers for hypertension
On preoperative examination, there were no abnormalities in blood tests including cardiac markers performed before surgery, and ECG (Fig. ) and chest imaging were normal. On echocardiography, the ejection fraction was 59%, and other findings were normal except for diastolic dysfunction grade 2.
Glycopylorate (0.2 mg) was administered intravenously for premedication before surgery. The patient's vital signs were monitored through invasive arterial blood pressure (BP) monitoring using radial artery, ECG, capnometry, and pulse oximetry equipment. In the operating room, his initial BP, heart rate (HR), Sp02 were 164/91 mmHg, 78 beats/min and 98%, respectively. ECG was NSR. Oxygen (100%) was delivered for preoxygenation prior to anesthetic induction. General anesthesia was induced with 150 mg of propofol and isoflurane (INH) in oxygen. Five minute after the administration of 70 mg of rocuromium, tracheal intubation was performed. General anesthesia was maintained with INH (1 MAC), O2 at 2 L/min, nitrous oxide at 2 L/min. The right radial artery was cannulated for invasive arterial BP monitoring and frequent sampling.
The patient's vital signs before posture change for surgery were BP 110/70 mmHg and HR 75 beats/min. Five minutes after changing position from supine to prone, his vital signs were BP 95/62 mmHg, HR 80 beats/min, and QRS widening appeared in lead II.
To prepare for emergencies such as acute myocardial infarction and cardiac arrest, the patient was placed in the supine position, and a 12 lead ECG was taken immediately (Fig. ). QRS widening (0.174 ms), absence of Q wave in lead I and V6, and monomorphic R wave V1-4 appeared in 12 lead ECG. Five minutes after changing the position to supine, his vital signs were BP 118/73 mmHg, HR 73 beats/min, and ECG changed to NSR.
NSR and stable vital signs were observed for 20 minutes, and continuous 1.0 μg/kg/min nitroglycerin (NTG) was injected intravenously under the advice of a cardiologist. After the posture changed to the prone position, LBBB appeared again in lead II, the operation was performed with the LBBB maintained and vital signs were stable. The operation was completed without complications. After the operation, the ECG was normal in the post-anesthesia care unit. The patient complained of back pain only, and there was no chest pain or dyspnea.
The patient was transferred to the intensive care unit, and a cardiac marker test was performed 3 times every 8 hours, and Holter tests were also performed for 24 hours. Cardiac markers were normal, and 24-hour Holter test results were transient right bundle branch block, LBBB, second degree atrioventricular (AV) block Mobitz type II. After two weeks of treatment, the patient was discharged and visited a tertiary hospital for a detailed cardiac examination. His coronary angio-computed tomography results showed right coronary artery with 30%-40% stenosis and left circumflex artery with 40%–50% stenosis. He was diagnosed with stable angina and a second-degree AV block Mobitz type II. He was prescribed clopidogrel, statins, angiotensin II receptor blockers, and a permanent pacemaker was inserted. The patient provided informed consent for the publication of the case, and this case followed the CARE guidelines.[",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [90.0, 'kg'], 'height': [173.0, 'cm']}",2.07966,1.97568,2.18364,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 173.0 cm. 
The patient's weight is 90.0 kg. 
Therefore, the patient's bsa is sqrt((90.0 (in kgs) * 173.0 (in cm))/3600) = 2.07966 m^2."
7241,60,Body Surface Area Calculator,physical,decimal,pmc-6177046-1,Extracted,"A 12-year-old girl was referred to our clinic with diagnosis of anorexia. She refused to eat during the last months and was obviously underweight (weight 31 kg, height 145 cm, body mass index (BMI) =14.7 kg/cm2). She had no palpitation, syncope or any other cardiac complains. On admission, laboratory investigations revealed a normal complete blood count, electrolytes, sedimentation rate, liver and kidney function tests, amylase, cholesterol and thyroid-stimulating hormone. The follicle-stimulating hormone, luteinizing hormone and oestradiol were in normal levels for this age. To find the cause of underweighting, gastro-duodeno-oesophagoscopy and brain computer tomography (CT)-scan were performed. No abnormalities were found. Malabsorption syndrome characterized by anorexia, weight loss, and steatorrhoea was excluded. Anorexia nervosa was diagnosed by psychologist in an initial report, but it was called atypical, because does not clearly met common types of this pathology: restrictive or self-induced vomiting were not recorded. Commonly, restricting food intake may include excessive exercise, which was not reported in this case.
Twelve-lead resting electrocardiography revealed sinus rhythm with slight prolongation of PR interval (220 ms) (). The echocardiography revealed normal structure of the heart. The 40-h ambulatory electrocardiography (ECG) monitoring showed more than 70 episodes of 2:1 AV block and high degree (up to 7:1) of AV block with no escape rhythm [ventricular pauses up to 6 s ()]. Interestingly, all these episodes were recorded during the day-time and did not associate with syncope or dizziness. No AV nodal conduction abnormality was recorded during sleeping. Dual chamber pacemaker (PM) was successfully implanted after patient informed consent. 24-h ambulatory ECG monitoring showed ventricular pacing during day-time (). The patient was under the follow-up during 6 months. According to PM follow-up cumulative percent of ventricular pacing was 6%. She started to eat normally just after implantation, and 5 kg weight gain was recorded after month. She was completely active, did well in math school, no any kind of physical or laboratory disorder were revealed, no eating disorder recorded during 6 months. She has been under the control in paediatric and cardiac clinics, no any structural changes reported at 6th month, weight 42 kg, height 148 cm, BMI =19.2 kg/cm2, which was categorized as normal weight. Parents’ consent form was presented.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [42.0, 'kg'], 'height': [148.0, 'cm']}",1.31403,1.24833,1.37973,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 148.0 cm. 
The patient's weight is 42.0 kg. 
Therefore, the patient's bsa is sqrt((42.0 (in kgs) * 148.0 (in cm))/3600) = 1.31403 m^2."
7242,60,Body Surface Area Calculator,physical,decimal,pmc-5809710-1,Extracted,"A 35-year-old man (66 kg, 182 cm) was selected for forearm VCA. He had a medical history of left forearm amputation due to trauma 18 months prior to the consultation (). At the time of the forearm transplantation, he had no coexisting medical conditions or psychological issues. A 49-year-old brain-dead male donor was selected on the basis of blood typing and human leukocyte antigen typing.
Before the surgery, the patient had fasted for eight hours; no premedication was administered. Noninvasive blood pressure, electrocardiogram, and oxygen saturation (SpO2) monitoring were initiated. Anesthesia was induced with propofol (2 mg/kg) and a continuous infusion of remifentanil (1 µg/kg/h). Orotracheal intubation was performed after administration of rocuronium (0.75 mg/kg). Anesthesia was maintained with sevoflurane with 50% oxygen to maintain the bispectral index range between 40 and 60. Remifentanil and rocuronium were continuously administered to provide adequate analgesia and muscular relaxation, respectively. A 20-G vascular catheter was inserted into the right radial artery for invasive monitoring of arterial pressure, arterial blood gas analysis (ABGA), and laboratory testing during surgery. A triple-lumen vascular catheter was introduced into the right subclavian vein to monitor central venous pressure (CVP) and administer fluids and medication. A 16-G vascular catheter was also placed in a superficial vein in the left leg. A warm blanket with a heated circuit, fluid warmer, and forced-air warmer were used to maintain normothermia during surgery.
Intravenous ceftriaxone (2 g), acyclovir (250 mg), and fluconazole (500 mg) were administered preoperatively for antimicrobial prophylaxis. Immunosuppression was induced with basiliximab (IL-2 receptor blocker, 20 mg) and maintained with triple-drug therapy using methylprednisolone (125 mg), mycophenolate mofetil (an inhibitor of inosine monophosphate dehydrogenase, 750 mg), and tacrolimus (a calcineurin inhibitor, 5 mg).
Preparation of the donor's forearm and dissection of the recipient's forearm were performed simultaneously. The left forearm of the donor was procured at the proximal humeral level before aortic cross-clamping and immediately perfused with a cold histidine-tryptophan-ketoglutarate solution before transplantation (). The recipient's forearm was dissected under a pneumatic tourniquet inflated to 300 mmHg with intermittent deflation over 125 minutes. The forearm preparation was followed by bony fixation with a plate at the distal radius and ulna, followed by end-to-end anastomoses of the ulnar and anterior interosseous arteries and four venae comitantes (). Intravenous heparin (5000 units) was administered just before the forearm was reperfused.
The patient's esophageal temperature was maintained at 36–37℃. The transplanted hand turned pinkish immediately after arterial anastomosis and reperfusion. The ischemic-time the retrieval of the donor's forearm to reperfusion following transplantation was 210 minutes. Although the patient continued to bleed from the surgical site during the vascular anastomoses, the mean arterial pressure (MAP) and heart rate were maintained at 65–85 mmHg and 80–100 beats/min, respectively, by administration of fluid and packed red blood cells (pRBCs, ). Low-dose dopamine (3–5 µg/kg/min) was infused to maintain MAP above 65 mmHg during the reconstruction of the tendons and the ulnar, median, and radial nerves. Skin grafting for monitoring acute rejection was then performed. On completion of the surgery, the patient underwent ultrasound-guided axillary brachial plexus block (BPB) with ropivacaine (0.375%, 20 ml) to provide postoperative analgesia and adequate blood flow to the allograft. Immediately after surgery, the transplanted hand was slightly edematous but pinkish (). SpO2 values measured on the right and left second fingers were 100% and 98%, respectively.
The duration of surgery and anesthesia was 8 hours 10 minutes and 9 hours 10 minutes, respectively. The estimated blood loss was 1,500 ml, and urine output was 2,230 ml. The patient received 11,100 ml (168 ml/kg) of crystalloid, 1,000 ml (15 ml/kg) of colloid, and 4 units of pRBCs. Because excessive bleeding or coagulopathy was not observed during surgery, hemostatic management guided by a thromboelastogram and coagulation panels including a prothrombin time, partial thromboplastin time, international normalized ratio, and fibrinogen level was not performed. The patient was extubated with sugammadex (3 mg/kg) after the return of consciousness and adequate spontaneous ventilation.
The forearm and hand remained pinkish and slightly edematous in the immediate postoperative period. Adequate blood flow to the transplanted forearm was confirmed by Doppler ultrasound. SpO2 measured at the left second finger was maintained in a range of 98–100%. The visual analog scale was 3 in the immediate postoperative period and maintained between 2 and 3 after receiving intravenous meperidine (12.5 mg) on the first postoperative day.
Two episodes of acute rejection occurred at days 6 and 47 post-transplantation. In both episodes, rejection was suspected due to erythematous changes on the transplanted hand. The graft-skin biopsy confirmed mild acute rejection (Grade I: mild infiltration of lymphocytes in the dermis) []. The patient received steroid pulse therapy and anti-thymocyte globulin, according to the immunosuppression protocol; tacrolimus ointment was applied to the areas of skin showing signs of rejection. The patient was discharged from hospital 22 days postoperatively. Once graft viability was confirmed, an early rehabilitation protocol was initiated. The patient had recovered his pain and tactile sensation and could grasp a baseball with his fingers at first discharge. His second admission due to acute rejection also resolved with tacrolimus ointment, increased in immunosuppressive dosage, and plasma exchange.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [66.0, 'kg'], 'height': [182.0, 'cm']}",1.82665,1.73532,1.91798,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 182.0 cm. 
The patient's weight is 66.0 kg. 
Therefore, the patient's bsa is sqrt((66.0 (in kgs) * 182.0 (in cm))/3600) = 1.82665 m^2."
7243,60,Body Surface Area Calculator,physical,decimal,usmle-1535,Extracted,"A 26-year-old medical student comes to the physician for a chest x-ray to rule out active pulmonary tuberculosis. He needs a medical and radiological report before starting a medical internship in South Africa. He has no history of serious illness and does not complain of any symptoms. He has smoked 1 pack of cigarettes daily for the past 6 years. He does not drink alcohol. He is 190 cm (6 ft 3 in) tall and weighs 75 kg (165 lbs); BMI is 20.8 kg/m2. His temperature is 37°C (98.6°F), pulse is 80/min, respirations are 18/min, and blood pressure is 128/89 mm Hg. The lungs are clear to auscultation. Cardiac examination shows no abnormalities. The x-ray of the chest shows a small pneumothorax (rim of < 2 cm) between the upper left lung margin and the chest wall.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [75.0, 'kg'], 'height': [190.0, 'cm']}",1.98956,1.89008,2.08904,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 190.0 cm. 
The patient's weight is 75.0 kg. 
Therefore, the patient's bsa is sqrt((75.0 (in kgs) * 190.0 (in cm))/3600) = 1.98956 m^2."
7244,60,Body Surface Area Calculator,physical,decimal,pmc-3720184-2,Extracted,"A 36-year-old woman was referred for partial lipodystrophy. She was born from non-consanguineous healthy parents of Sicilian and French origin. Her two siblings, a 34-yr old sister and a 38-yr old brother, were also reported to be healthy. Her medical history was uneventful until age 30, when she underwent surgical removal of a chondrosarcoma of the right distal femur (with total knee prosthetic replacement). At this time a 2 g/l fasting glycemia was observed, in the absence of antibodies directed against glutamic acid decarboxylase 65 and tyrosine phosphatase (anti-GAD and anti-IA2); BMI was 20.3 kg/m2. Hypertriglyceridemia reached 4 g/l, and liver steatosis was diagnosed on ultrasonographic appearance and elevated ALT and GGT in the absence of any other cause. Metabolic alterations were controlled using diet, fibrates and α-glucosidase inhibitors. Regarding gynecological history, puberty was normal, with spontaneous menarche at age 11, and regular menstrual cycles of 28 days. A first-trimester spontaneous miscarriage was reported at age 34. Since then, she did not conceive and consulted for 2 year infertility. At examination, she presented a partial lipodystrophy phenotype, with lipoatrophy and loss of muscle mass of the four limbs, palms and soles, which progressively appeared since age 20. Lipoatrophy spared the face, which contrasted with truncal and abdominal subcutaneous fat accumulation (Figure and Figure A). Height was 144 cm, weight 39 kg (BMI: 18.8 kg/m2), waist and hip perimeters 76 cm. A high-pitched voice was noted. Skin examination revealed livedo reticularis on the limbs, with dry, tight, atrophied skin and hyperkeratosis, predominant in the extremities (Figure ). No acanthosis nigricans or hirsutism were observed. Blood pressure was 110/60 mmHg. Cardiac examination was normal but doppler monitoring revealed diffuse atherosclerosis. Further inquiry revealed that hair graying appeared since age 12, and bilateral cataracts were diagnosed at age 34.
OGTT revealed severe hyperinsulinemia (fasting and T120 min values, 371 and 8884 pmol/L, respectively) with diabetes (glycemia was normal at fast but reached 12.2 mmol/L at T120 min OGTT) (Table and Figure ). Hypertriglyceridemia was associated with slightly low HDL-cholesterol and elevated ALT and GGT. Leptin was normal for BMI. SHBG and adiponectin levels were low. FSH and testosterone levels were normal, but AMH and inhibin B very low (Table ).
Peripheral lipoatrophy was assessed by skinfold thickness measurements (Figure A) and by MRI imaging. As for patient 1, MRI showed asymmetrical distribution of subcutaneous fat in the thighs and increased intra-abdominal fat stores (Figure ). DEXA confirmed that fat was predominant in the trunk and reduced in the lower limbs (Figure B). Bone mineral density was low (−2 and −2.8 SD at the vertebral and the femoral levels, respectively).
WRN sequencing revealed previously undescribed compound heterozygous mutations, with a c.3769C>T transition in exon 32 predicting a p.Q1257X truncation, and a c.3986delT frameshift deletion in exon 34 predicting the synthesis of a 1333 amino acid p.M1329fs WRN truncated protein, both mutated proteins lacking their nuclear localization signal. These mutations were absent in 100 unrelated control subjects.
Metformin was added to the treatment of the patient, and she became pregnant two months later. Insulin therapy was needed from the second month of pregnancy. A prophylactic cervical cerclage was performed at 15 weeks of gestation, but premature rupture of membranes with preterm labor occurred at 21 weeks. Treatment allowed the maintenance of pregnancy until 31 weeks, when a caesarean section was performed for chorioamnionitis. The patient gave birth to a healthy female child of 2310 g (normal for gestational age) with normal clinical examination except for the presence of a receding forehead without radiological signs of craniodysostosis. X-ray analysis of the whole skeleton, and cardiac and abdominal echography were normal. Placental histological examination confirmed the diagnosis of chorioamnionitis but did not reveal other specific alterations.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [39.0, 'kg'], 'height': [144.0, 'cm']}",1.249,1.18655,1.31145,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 144.0 cm. 
The patient's weight is 39.0 kg. 
Therefore, the patient's bsa is sqrt((39.0 (in kgs) * 144.0 (in cm))/3600) = 1.249 m^2."
7245,60,Body Surface Area Calculator,physical,decimal,pmc-4495851-1,Extracted,"A 77-year-old woman underwent an annual medical checkup and was diagnosed with a cystic tumor in the pancreas by computed tomography (CT) of the abdomen. The patient was referred to our hospital for further examination. Her medical history included a radical parotidectomy for a parotid gland tumor and a total knee replacement for the right leg. In addition, she was receiving treatment for hypertension and osteoporosis. On admission, she had no clinical symptoms. Her height was 154 cm and her body weight was 61 kg. There was no superficial lymphadenopathy or palpable mass in the abdomen. Her serum amylase level was 211 U/L (normal range; 30–120 U/L), and other biochemical data, including tumor marker levels, fasting plasma glucose, and hemoglobin A1c, were within normal ranges. An upper gastrointestinal endoscopy showed esophageal hiatal hernia and short-segment Barrett’s esophagus. Colonoscopy showed diverticula in the sigmoid colon. Contrast-enhanced abdominal CT scanning demonstrated a cystic tumor in the head of the pancreas measuring 40 mm in diameter with slightly enhancing mural nodules within the cyst (Fig. ). Magnetic resonance cholangiopancreatography (MRCP) revealed a cystic tumor in the head of the pancreas along with a normal, non-dilated dorsal pancreatic duct throughout the pancreas (Fig. ). The presence of a connection between the cystic lesion and the main pancreatic duct was unclear. Endoscopic retrograde pancreatography (ERP) via the major duodenal papilla showed a cystic tumor and a slightly dilated main pancreatic duct, but the main pancreatic duct was abruptly interrupted at the head of the pancreas (Fig. ). The major duodenal papilla was enlarged and the orifice was filled with abundant mucin (Fig. ). The minor duodenal papilla was normal in size and ERP via the minor papilla was not possible. The diagnosis based on pancreatic juice cytology was “highly suspicious for adenocarcinoma,” suggestive of an intraductal papillary mucinous carcinoma (IPMC) arising in the ventral pancreas of pancreas divisum. The patient underwent a pylorus-preserving pancreaticoduodenectomy (PPPD) with regional lymphadenectomy. The postoperative course was uneventful, except for a Grade A pancreatic fistula (staged according to the International Study Group on Pancreatic Fistula clinical criteria []), and the patient was discharged on postoperative day 29.
A pancreatography via the major and minor duodenal papillae on the surgical specimen revealed no connection between the ventral and dorsal pancreatic duct systems (Fig. ). Macroscopically, a multilocular cystic tumor, 40 × 35 × 25 mm in size, with abundant accumulation of mucin was identified in the ventral pancreas. Microscopically, the tumor was composed of atypical epithelial cells showing nuclear enlargement, clear nucleoli, and disordered polarity (Fig. ). They formed prominent papillary structures. The Mib-1 index was up to 80 %. The tumor cells slightly progressed into the main pancreatic duct. Finally, the tumor was determined to be a mixed type IPMC (well-differentiated adenocarcinoma) with partial microinvasion. The pancreas bearing the tumor was drained by the pancreatic duct, which opened into the major papilla, suggesting that it was the ventral pancreas. The region surrounding the IPMC was mainly composed of fibrous tissue, which was clearly distinguished from the normal pancreas (Fig. ). The normal pancreas was relatively rich in adipose tissue and the islets of Langerhans were typically oval in shape, features consistent with the dorsal pancreas. Furthermore, the pancreatic duct in the region of the normal pancreas was linked to the minor papilla, also suggesting a dorsal pancreas origin.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.0, 'kg'], 'height': [154.0, 'cm']}",1.61538,1.53461,1.69615,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 154.0 cm. 
The patient's weight is 61.0 kg. 
Therefore, the patient's bsa is sqrt((61.0 (in kgs) * 154.0 (in cm))/3600) = 1.61538 m^2."
7246,60,Body Surface Area Calculator,physical,decimal,usmle-3528,Extracted,A 43-year-old man from Chile comes to the physician because of a 1-day history of upper back pain and difficulty swallowing. He has had pain in his shoulder and knee joints over the past 10 years. He is 190 cm (6 ft 3 in) tall and weighs 70.3 kg (155 lb); BMI is 19.4 kg/m2. His blood pressure is 142/86 mm Hg in the right arm and 130/70 mg Hg in the left arm. Physical examination shows a depression in the sternum and a grade 3/6 diastolic murmur at the right upper sternal border. A CT scan of the chest with contrast is shown.,What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.3, 'kg'], 'height': [190.0, 'cm']}",1.92621,1.8299,2.02252,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 190.0 cm. 
The patient's weight is 70.3 kg. 
Therefore, the patient's bsa is sqrt((70.3 (in kgs) * 190.0 (in cm))/3600) = 1.92621 m^2."
7247,60,Body Surface Area Calculator,physical,decimal,pmc-3150201-1,Extracted,"A 52-year-old female with a history of admission to the hospital 5 times in the last 5 years because of frequent hypoglycemic attacks was admitted to our hospital.
At the age of 36, her urine examination showed excessive glucose levels but she did not receive further medical treatment. The following year, she consulted a doctor due to general malaise and bilateral lower leg edema. She was then diagnosed with diabetes mellitus and hypoalbuminemia of unknown cause. Glibenclamide was administered for the treatment of diabetes at age of 40, but poor control persisted. She was referred to our hospital for the first time at the age of 43 because of exacerbation of her lower leg edema. Protein-losing gastroenteropathy (PLGE) due to idiopathic gastrointestinal lymphangiectasia was diagnosed by functional and histopathological examinations. She had been treated with elemental diet and steroid therapy for her PLGE, but those treatments were not effective. At the same time, insulin therapy was started because of the poorly controlled diabetes (HbA1c, approximately 10%). After the age of 47, her average blood glucose levels were keeping consistently high (300 to 400 mg/dL) and even hypoglycemic attacks had been recognized. When she was hospitalized at the age of 48, the cause of the hypoglycemic attacks was unidentified (2004). Around the age of 50, the frequency of hypoglycemic attacks (defined as blood glucose level less than 70 mg/dL) had increased to about 40 times per month. The attacks occurred at postprandial and preprandial times. Her medication history suggested that hypoglycemia was not related to her insulin therapy. Precise examination of hypoglycemia was performed during the current hospitalization at the age of 52.
On admission, her body height was 137 cm and body weight was 44 kg (BMI, 23.4 kg/m2). Blood pressure was 128/78 mmHg and heart rate was 87. Physical examination revealed bilateral lower leg pitting edema, no Achilles tendon reflexes, and reduced sensation of vibration (C128 Hz, 4 s (rt.)/4 s (lt.)). Chest X-ray revealed no pleural effusions and no cardiomegaly. Diabetic complications were confirmed, that is, bilateral proliferative retinopathy, nephropathy (stage 2), and peripheral neuropathy. She was treated with a combination of rapid-acting and NPH insulin injection for her diabetes. The results of laboratory tests were as follows: total protein: 4.0 g/dL; serum albumin: 2.3 g/dL; total cholesterol: 172 mg/dL; triglyceride: 104 mg/dL; HDL-c: 47.4 mg/dL; LDL-c: 116.7 mg/dL; creatinine: 0.49 mg/dL; HbA1c: 15.5%; urinary C-peptide: 125 μg/day; anti-GAD and anti-IA-2 antibodies: negative; urinary microalbumin: 73.8 mg/g·Cre; creatinine clearance: 109.4 mL/min/m2. Blood glucose profiles appeared unstable, with periodic (2 to 3 days) alternation between hyperglycemia (>300 mg/dL) and hypoglycemia (<70 mg/dL). Representative blood glucose profiles are shown in , and the frequency of hypoglycemia is shown in . A glucagon loading/stimulation test revealed that the ability of insulin secretion was retained (ΔCPR = 4.8 ng/mL). No abnormalities were found in other endocrine hormones.
Because the hypoglycemic attacks occurred at a time after cessation of insulin injections sufficiently longer than the effective time of the insulin, we were convinced that hypoglycemia was not related to the injections. Therefore, we suspected that it was induced by an endogenous cause. The result of a fasting test was positive (). After a 17 h fast, hypoglycemia (plasma glucose 45 mg/dL) appeared and serum insulin concentration was 9.92 μU/mL (normal, <6.0), C-peptide level was 0.98 ng/mL (<0.6), and proinsulin level was 15.3 pmol/L (<5.0). Service's and Turner's criteria for diagnosing insulinoma were satisfied (Grunt 4.54 (positive, <2.5), Fajans 0.22 (>0.3), Turner 66.1 (>50), and Service 9.92 (>6)). Serum C-peptide and proinsulin levels at the time of hypoglycemia attack were significantly high, and the values satisfied the criteria for hyperinsulinism defined by Service []. Also, the proinsulin level was above 5 pmol/L, and this parameter and threshold level have been reported as the best criteria for diagnosis of endogenous hyperinsulinism during the fasting test []. Counterregulatory response to hypoglycemia was not impaired; before and at the time of hypoglycemia, testing showed the following respective levels: glucagon 150 pg/mL and 230 pg/mL; cortisol 6.09 μg/dL and 27.45 μg/dL; growth hormone 0.33 ng/mL and 11.70 ng/mL; adrenaline <10 pg/mL and 583 pg/mL. Tests for both anti-insulin antibody and anti-insulin receptor antibody were negative. We excluded the specific hypoglycemic conditions induced by medicines, insulin autoimmunity, factitious hypoglycemia, and other conditions/diseases such as renal failure or liver cirrhosis. We did not measure plasma sulfonylurea concentration as we were aware that the patient had not been taking the medicine. To investigate the possible involvement of glucose-dependent insulinotropic polypeptide (GIP) or glucagon-like peptide 1 (GLP-1) in the hypoglycemia, we measured serum concentrations of total GIP (Human GIP Assay Kit, Immuno-Biological Laboratories, Fujioka, Japan) and total GLP-1 (YK160 GLP-1 EIA Kit, Yanaihara Institute, Fujinomiya, Japan) by enzyme-linked immunosorbent assays in her fasting, postprandial, and hypoglycemic state. Serum concentrations of total GIP were 7.6, 30.2, and 6.0 pg/mL, whereas those of total GLP-1 were 4.7, 4.2, and 4.1 ng/mL in fasting, postprandial, and hypoglycemic state, respectively. Taken together, these results suggested that inappropriate endogenous hyperinsulinemia was responsible for her hypoglycemia, possibly due to insulinoma, nesidioblastosis, or β cell dysfunction.
Thus far, all efforts for obtaining diagnostic imaging of an insulinoma via CT scan, MRI scan, and endoscopic ultrasound were unsuccessful. SACI tests with calcium gluconate (Ca2+ 0.025 mEq/kg) were performed twice in 2004 (age 48) and 2008 (age 52). In keeping with other researchers, an increment in plasma immunoreactive insulin levels greater than 2-fold over prestimulation levels was considered indicative of a tumor or other responsive lesion in the vascular territory of the artery studied []. The results, confirmed twice, were positive only after stimulations of the supramesenteric artery (SMA) (2.53-fold increase in 2004 and 3.36 in 2008 versus before stimulation; Figures and , resp.). No anatomical variant was apparent on review of the angiogram, but there seemed to be backflow slightly in the gastroduodenal artery (GDA) on the examination only in 2008. Exploratory laparotomy was refused by the patient and her family.
Since she had been suffering mostly from frequent hypoglycemic attacks, we focused primarily on the management of hypoglycemia by medication. We considered the use of octreotide (Sandostatin, Novartis, Basel, Switzerland), a long-acting somatostatin analog, because this medicine suppresses insulin secretion [] and has been reported to be effective for PLGE due to idiopathic gastrointestinal lymphangiectasia []. At first, we tried a single dose (50 μg) of octreotide to evaluate its effects on serum insulin and glucose levels (). As we observed no remarkable changes in glucose levels and suppression of insulin levels, we started her on octreotide (50 μg, twice a day) for 2 weeks, monitoring its tolerability. Since almost no side effects except for controllable constipation were determined, we switched to octreotide LAR (Sandostatin LAR, Novartis, 20 mg per month), which is a very long-acting octreotide. After using octreotide LAR for 4 months, although hyperglycemia was uncontrollable even with multiple insulin injections (), the frequency of hypoglycemic attacks was surprisingly reduced (). This effect was sustained for 20 months until her death from acute heart failure (54 years, 2010). On the other hand, serum albumin was slightly increased (2.3 g/dL and 3.0 g/dL; before and after treatment, resp.), but her leg edema was unchanged.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [44.0, 'kg'], 'height': [137.0, 'cm']}",1.294,1.2293,1.3587,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 137.0 cm. 
The patient's weight is 44.0 kg. 
Therefore, the patient's bsa is sqrt((44.0 (in kgs) * 137.0 (in cm))/3600) = 1.294 m^2."
7248,60,Body Surface Area Calculator,physical,decimal,pmc-5647821-1,Extracted,"The patient was a 2-year-old girl, 72.9 cm in height and 6.2 kg in weight. She was born through a normal delivery and weighed 2010 g at birth. Using gene analysis, she was diagnosed with Wolf-Hirschhorn syndrome. She had short stature, congenital heart disease, including ASD and ventricular septal defect (VSD), mental retardation, and bilateral cleft palate, but no micrognathia or seizures. She was scheduled for cleft palate repair under general anesthesia. Her past surgical history included an ASD and VSD closure.
On preoperative anesthesia evaluation, echocardiogram and electrocardiogram (ECG) were normal. In addition, chest radiographic findings were normal and laboratory test results were also within normal limits. The tracheal diameter at the level of the sixth cervical (C6) vertebra on her chest radiograph was 5.4 mm. She could speak only a few words, but we could not communicate with her. She could take a sitting position, but could not stand by herself. The clinical assessment of her airway was difficult.
On admission, her heart rate (HR) was 135 beats/min, and her oxygen saturation (SpO2) was 98% in room air. No premedication was given before she was transferred to the operating room. Anesthesia was induced with inhalation of sevoflurane 1-8% in oxygen after the start of noninvasive monitoring for SpO2 (100%). After loss of consciousness, standard non-invasive monitoring was conducted, including ECG, HR (96 beats/min), blood pressure (BP) (85/40 mmHg), and bispectral index (BIS value: 54; spectral edge frequency [SEF]: 14-20 Hz, signal quality index [SQI]: 95%). Rocuronium (4 mg) was also administered intravenously to facilitate tracheal intubation. We could smoothly intubate by using a laryngoscope with a tracheal tube (inner diameter, 4.0 mm; Mallinckrodt Medical, Athlone, Ireland). The air leak around the tube was 20 cm H2O pressure. The correct position of the tube was confirmed using 5-point auscultation and capnography. Anesthesia was maintained with desflurane 8.5-9.0%, remifentanil 0.1-0.15 µg/kg/min in air, and oxygen (FiO2: 0.4). BP was maintained at 75-95/45-57 mmHg, HR was 122-140 beats/min, end-tidal carbon dioxide was 35-40 mmHg, and BIS value was maintained between 40 and 58 with an SEF of 10-15 Hz and SQI of 95%. In addition, intermittent boluses of fentanyl were administered with reference to the BIS and hemodynamics. In addition, the patient's cardiac status was monitored using Aesculon® with a noninvasive cardiac function monitor. During anesthesia, BP was maintained at 80-110/50-70 mmHg, cardiac output was 3.1-3.9 L/min, cardiac index was 2.6-3.0 L/min/m2, stroke volume was 10-14 ml, and stroke volume variation was 6-11%. The surgical procedure was completed uneventfully. The patient's body temperature was maintained at 36.4-37.5℃ with a warming blanket during surgery. The operation was completed in 236 minutes without any surgical or anesthetic problems. There was minimal blood loss during the operation, and she subsequently received a total of 225 ml of lactated Ringer's solution, and her urine volume was 27 ml. She emerged from general anesthesia in 4 minutes after stopping desflurane inhalation. She was extubated after confirming sufficient spontaneous respiration. After extubation, her respiratory and hemodynamic conditions were stable.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [6.2, 'kg'], 'height': [72.9, 'cm']}",0.35433,0.33661,0.37205,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 72.9 cm. 
The patient's weight is 6.2 kg. 
Therefore, the patient's bsa is sqrt((6.2 (in kgs) * 72.9 (in cm))/3600) = 0.35433 m^2."
7249,60,Body Surface Area Calculator,physical,decimal,pmc-6461826-1,Extracted,"A 68-year-old man with 21-year history of type 2 diabetes presented with an ulcer on the left heel. Height was 162 cm; body weight was 69 kg; body mass index was 26.3. The patient had been diagnosed with lower extremity atherosclerotic obliterans 7 years earlier. The left lower limb has been numb for 6 years, with intermittent claudication and rest pain for 1 year. The patient reported that his sleep was affected, but his degree of pain was decreased with the intermittent use of analgesic agents. For the left lower limb with claudication, walking distance was 90 m.
The patient was hospitalized on 10 July 2017. Twenty days before hospitalization, irritation and pain developed on the lateral skin of the toes of the left foot, with no obvious inducement. Purulent exudate was observed after skin ulceration, and the patient’s body temperature increased to 39.5 °C. During hospitalization, the five toes of the left foot were black, necrotic, and associated with aggravated rest pain. Although the dose of oral analgesics was increased, the patient’s pain was not relieved, and his sleep was severely affected.
The patient’s appearance on initial evaluation is shown in Fig. a and b. The five toes of the left foot were almost entirely black and necrotic. The skin extending from the bottom of the foot to the 5th metatarsophalangeal joint was red and swollen, with obvious tenderness; skin temperature was normal. The muscles of the left foot had clearly atrophied; the skin was thin, bright, and hypertonic. Incision and drainage (approx. 5.0-cm long) was immediately performed between the 4th and 5th toes. Necrotic tissue, minimal purulent exudation, and limited bleeding were observed.
The diagnostic results on obtained on July 13 are shown.Secretion cultures displayed Pseudomonas aeruginosa and Staphylococcus aureus. X-ray film showed in Fig. c and d revealed no obvious destruction in foot bone. The lower limb computed tomographic angiography (CTA) is shown in Fig. e.
The magnetic resonance imaging (MRI) of the foot obtained on July 14th is shown in Fig. f and g. Subcutaneous inflammatory tissue in the lateral 5th humerus bone was confirmed as an infectious submerged cavity (Fig. ). The first incision performed at the bedside resulted in limited purulent exudation, as well as decreased local tension and reduced foot swelling. However, progressive necrosis of the skin margin was noted (Fig. a and b).
On July 17, basal therapy consisted in controlling blood sugar with insulin (58 units/day). The initial antimicrobial application of ceftazidime infusion (2 g, twice daily) was replaced by the sensitive drug Sulperazon (Cefoperazone Sodium and Sulbactam Sodium for Injection, Pfizer), according to the bacterial culture result of the secretion, and the application of antibiotics was stopped after July 22. The patient showed improved circulation and blood pressure. Treatment was maintained with protein and iron supplements.
On July 18th, interventional therapy was performed on the lower limb. The balloon was expanded in the superficial femoral artery, anterior tibia artery, iliac artery, and tendon. A thrombus had formed in the lower segment of the superficial femoral artery. The catheter for thrombolysis was left in place until July 20 (Fig. c, d, e and f). Skin temperature in the left foot increased, and swelling extended to the center of the foot. The amount of purulent exudation increased, as did pain and body temperature. The foot was therefore incised and drained, once more. Multiple subcavities were found (Fig. ).
On July 21st, we performed patella truncation and debridement on toes 4 and 5. The procedure was performed in the operating room, with the patient under sciatic nerve block. Results are presented in Fig. . Submerged cavities were filled with povidone-iodine gauze. The amount of nonviable tissue in the submerged cavity gradually decreased. The submerged space became shallow, and the granulation filled. All subsequent treatments were performed in the outpatient department.
From July 25th to September 30th, the left foot plaster was fixed at a functional position and applied intermittently (Fig. a, b, c, d, e and f). After October 1st, the plaster was removed. The patient was given diabetic shoes, and walking was guided. The first signs of wound healing were observed on November 19 (Fig. g, h and i).",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [69.0, 'kg'], 'height': [162.0, 'cm']}",1.7621,1.67399,1.85021,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 162.0 cm. 
The patient's weight is 69.0 kg. 
Therefore, the patient's bsa is sqrt((69.0 (in kgs) * 162.0 (in cm))/3600) = 1.7621 m^2."
7250,60,Body Surface Area Calculator,physical,decimal,pmc-6849219-1,Extracted,"A 32-year old Egyptian male (bodyweight 80 kg, height 180 cm), infected with HCV, was admitted to Hepatic Viruses Center, Faculty of Medicine, Cairo University, Cairo, Egypt, in April 2018. He was complaining from high levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in the blood (70 and 100 U/L, respectively). A test for serum anti-HCV antibody was positive. At the same time, Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) (using 7500 Fast Real-time PCR system) analysis of RNA from plasma demonstrated that the HCV-RNA level was 2 × 106 IU/ml. The patient didn’t have any history of liver disease, there was no pallor, no jaundice, and no splenomegaly. Also, there were no signs suggesting liver cirrhosis. Laboratory investigations of complete blood picture revealed a hemoglobin value of 14.3 g/dl, a white blood cell count of 5.5x103cells/μl (50% lymphocyte, 5.4% monocyte and 44.6% granules). The platelets count was 2.1 × 105 cells/μl and blood biochemical investigations were normal (Table ). The biochemical investigations were repeated monthly during the treatment periods. Abdominal ultrasonography identified a fatty liver. Based on these tests, the patient was treated with a combination of DAA for 12 weeks (sofosbuvir 400 mg and daclatasvir 60 mg once a day).
Before the treatment, the blood sample was collected on EDTA containing tube. RNA sample library was prepared using the TruSeq RNA Sample Preparation Kit v2 (Illumina, San Diego, CA, USA). RNA fragmentation, cDNA synthesis/indexing, PCR amplification/clean-up, and library normalization/pooling steps were conducted according to the manufacturer’s instructions. Sequencing was performed on a MiSeq sequencer with the MiSeq reagent kit v2 (300 cycles; Illumina), as described previously []. Paired-end reads (2 × 150 nucleotide) were analyzed to identify the virus. An in-house workflow was used, as previously described []. The identification on the HPgV isolate was done as followed: the first step in the pipeline included removal of the adaptor sequence from the reads and trimming low-quality bases using the program Fastx toolkit []. The next step was to map the reads to a database of viral sequences using the specific programs SNAP DB [] and BWA []. The reads mapped to the same taxa were grouped together and assembled with SPAdes program, to yield a set of contigs. The Un-mapped reads (which could represent novel sub-sequences) were collected and assembled with the contigs to close any potential gaps and to improve the assembly. Then final contigs were aligned to the reference genome of each group using pairwise clustalw2. Furthermore, the whole viral genome sequences for the most significant group were collected from the GenBank database and the contig was aligned to each of them in order to check if the target sequence has better similarity to a sequence rather than those in the RefSeq database. The assembly yielded a single contig of 9370 bases for the HPgV sequence and another contig of 9291 bases for the HCV sequence, which was submitted to GenBank database and assigned with accession numbers MK234885 and MK799639, respectively. The contig was identified as HPgV by matching the sequences to the set of whole-genome pegivirus sequences in the GenBank database. The most significant hits were 75 sequences with a minimum average depth 100× and minimum 90% genome coverage (Additional file ). The supplementary file also included the statistics for our sequence alignment and each pegivirus sequence in the hit list. These results indicate a high level of confidence in viral identification and give a strong hint regarding its genotype.
The best alignment in this list was to the sequence JN127373.1 (GB virus C isolate UU1), which had 98.77% coverage, 91.1% identity, and 172× average depth (Fig. ) (Additional file ). The variants were distributed throughout the whole genome (Fig. ). Further data analysis using DNAStar software of 9370 bp for HPgv genotype-2 showed the identification of 808 SNPs that consisted of 806 coding SNPs (cSNPs) and 2 non-coding SNPs (Additional file ). According to the type of SNPs for HPgV genome, transition substitutions were more predominant than transversions (73.2% vs 26.8%). Transitions C↔T and A↔G are over-represented with 46 and 26.3% of the total substitutions respectively. The frequency of transitions between coding region were significantly different (73.2% vs 26.8% respectively; χ2 = 5.86, P < 0.01). This confirms that SNPs occur more frequently as transitions in coding regions than in non-coding regions.
After HCV-treatment, HCV-RNA was no longer detected in the plasma by qRT-PCR, whereas HPgV-RNA was still detected with conventional RT-PCR (Fig. ). Conventional RT-PCR was done as followed: the complementary DNA (cDNA) synthesis was performed with a high-capacity cDNA kit (Applied Biosystems) according to the manufacturer’s instructions. The PCR reaction targeting the 5′ UTR consisted of 1 × PCR buffer, 200 μM dNTPs, 1.5 mM MgCl2, 300 nM UTR-F (5′-GATGCCAGGGTTGGTAGGTC-3′; positions 120–139), 300 nM UTR-R (5′-CTCGGTTTAACGACGAGCCT-3′; positions 293–274), 2.5 U Hot start Taq DNA polymerase (Qiagen, Germany), and 1 μl cDNA. Thermal-cycling parameters were as follows: an initial denaturation for 5 min at 95 °C, followed by 40 cycles of denaturation for 60 s at 95 °C, annealing for 90 s at 55 °C, and extension for 120 s at 72 °C; final extension for 10 min at 72 °C. The PCR product was subjected to electrophoresis on 2.5% agarose gel, stained with ethidium bromide (0.5 μg/ml) and visualized with ultraviolet trans-illuminator.
To confirm the HPgV genotyping of the Egyptian isolate, the genotype information was extracted for most of the sequences from the literature and inferred the others using BLAST analysis (Additional file ). Then multiple sequence alignment was performed using DNADynamo software, followed by phylogenetic inference using our isolate sequence and the list of all whole-genome sequences of pegivirus in the hit list. For phylogenetic tree reconstruction, the analysis was conducted with MEGA X software [] using Maximum Likelihood method with default parameters (including bootstrapping with 1000 replicates) and confirmed that this isolate resembles HPgV genotype-2 (Fig. ). Also, based on the bioinformatics analysis of reads obtained by deep sequencing of a relevant genome sequence the genotype of HCV was 4n. Alignments of the NS5A and NS5B protein structures of HCV and HPgV revealed that there were many differences in the protein sequences between HPgV and HCV (Additional files and ).",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [80.0, 'kg'], 'height': [180.0, 'cm']}",2,1.9,2.1,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 180.0 cm. 
The patient's weight is 80.0 kg. 
Therefore, the patient's bsa is sqrt((80.0 (in kgs) * 180.0 (in cm))/3600) = 2.0 m^2."
7251,60,Body Surface Area Calculator,physical,decimal,pmc-4646992-2,Extracted,"Patient B, brother to Patient A and half brother to Patient C, is a 23-year-old man who was referred to the sleep clinic for the first time when he was 18 years old to rule out OSA and to assess his sleep-related problems. He and his mother were concerned about his sleep given that he reported feeling tired most of the day. During sleep he was observed to snore loudly, experience apneic-like events during which he stopped breathing, talk in his sleep, and occasionally experience jerky body movements.
Patient B is prone to frequent upper-airway infections. The PWS genetic test was performed when he was 14 years old and confirmed the diagnosis as a paternal chromosome deletion.
Patient B was delivered by cesarean section (due to a failure of labor to progress). His birth weight was 5 lbs. His early childhood developmental milestones were delayed and he experienced feeding difficulties. He is on risperidone 1.5 mg daily and testosterone 0.25 mg daily, and he was on human growth hormone injections previously. He had not been prescribed Modafinil as the main treatment goals for him were to improve his nighttime sleep quality in order to reduce his daytime fatigue. He is also adhering to the “red-yellow-green” diet for PWS patients [] and has achieved good body weight control success.
Patient B has cryptorchidism and a history of thyroid hypofunction, which is controlled with medications, and osteopenia due to androgen deficiency.
He also has a history of bipolar disorder, type I, for which he is taking valproic acid, quetiapine, Topiramate, and lorazepam. He had previously been hospitalized for his mood disorder with manic episode exacerbation when he was 21 years old.
He graduated from Grade 12 when he was 18 years old. He was enrolled in a special education plan and his academic performance was good. He currently works as a retail clerical assistant. He has learning difficulty and is exempt from Education Quality and Accountability Office (EQAO) tests, both for mathematics in Grade 9 and for the literacy test in Grade 10.
His first physical examination in our sleep clinic was performed when he was 21 years old and it showed the following pertinent features. He was 159 cm tall and his weight was 73.4 kg. His BMI was 29 kg per m2. He demonstrated decreased muscle tone without hyperflexibility. A neurological exam showed a slowed response and evinced echolalic speech. Cranial nerves II to XII were normal. His deep tendon reflexes were hypoactive 1+/1+, his plantar responses were flexor, his gait was normal, Romberg's test was negative, and his sensory examination was grossly intact.
An initial PSG study was conducted when Patient B was 18 years old to investigate possible OSA and parasomnia. A multiple sleep latency test (MSLT) was carried out on the following day to assess the severity and nature of his excessive daytime sleepiness. The sleep study showed normal sleep onset latency and sleep efficiency, mildly increased AHI in total sleep (12.8/h), and moderately increased AHI in REM sleep (20.4/h). The increase during REM was predominantly due to central respiratory events associated with significant oxygen desaturations (minimum of 74%) and occasional mild to loud snoring. The test also showed that his sleep was fragmented, with an arousal index of 12.2 per hour. There were some polysomnographic (PSG) features suggestive of NREM parasomnia.
The mean sleep latency observed on the MSLT was normal. Given that central apnea episodes are occasionally associated with brain tumors and that the most common cause of OSA in the pediatric population is tonsillar hypertrophy, Patient B was referred for neurological and ENT assessments to rule out the presence of other medical disorders.
A second PSG study was conducted three years later when Patient B was 21 years old. He was then observed to have difficulties initiating sleep, moderate central sleep apnea syndrome with an AHI of 19.4 per hour in total sleep, and a central apnea index of 18.2 per hour. Bilevel positive airway pressure (BiPAP) treatment was initiated. During the BiPAP titration, Patient B was found to require an unexpectedly high pressure (17/12 cm H2O) potentially due to the hypotonia typically associated with PWS. Patient B's subjective daytime alertness and his mood improved after this treatment with BiPAP was initiated.
Computed tomography (CT) of the head was conducted when Patient B was 22 years old. It showed nonspecific frontal subcortical white matter changes. No mass was identified. Following neuroimaging, Patient B was seen by a neurologist and he and his mother were informed that individuals with PWS have been found in the literature to demonstrate patchy white matter changes of unknown pathogenesis. These lesions may be related to underlying metabolic disorders experienced by these individuals, which predispose these individuals to premature cardiovascular disease in the microvasculature. A magnetic resonance imaging scan was not recommended at this time.
A follow-up PSG study was conducted for Patient B when he was 23 years old. At this time his BMI remained at 29 kg per m2. The study demonstrated successful breathing control with BiPAP at 15/10 cm of water pressure. Patient B was found to have normal sleep onset latency and sleep efficiency and decreased SWS. His medications at the time of assessment were lithium 900 mg, levothyroxine 0.05 mg, Topiramate 225 mg, calcium 1200 mg, omega 3, vitamin D, and a multivitamin complex.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [73.4, 'kg'], 'height': [159.0, 'cm']}",1.80051,1.71048,1.89054,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 159.0 cm. 
The patient's weight is 73.4 kg. 
Therefore, the patient's bsa is sqrt((73.4 (in kgs) * 159.0 (in cm))/3600) = 1.80051 m^2."
7252,60,Body Surface Area Calculator,physical,decimal,pmc-4754277-1,Extracted,"A 48-year-old female of 163 cm height and 55 kg weight was scheduled for an open radical hysterectomy and bilateral pelvic lymph node dissection. Her physical and laboratory examinations were unremarkable, with an American Society of Anesthesiologists I preoperative physical status classification. Her Mallampati score was I, and her mouth opening and thyromental distance were normal. She did not report a history of chronic renal failure, diabetes mellitus, corticosteroid use, laryngomalacia, or acromegaly.
Anesthesia was induced by the resident anesthesiologists on duty under the supervision of an experienced anesthesiologist with a continuous target-controlled infusion of 5 µg/ml of propofol and 3 ng/ml of remifentanil. After loss of consciousness that was confirmed by Bispectral Index score (BIS, Covidien, Mansfield, MA, USA), 7 mg of vecuronium was injected for intubation. After 4 min, without using stylet, an ID 7.0 mm plain endotracheal tube was smoothly inserted into the patient's trachea without difficulty under direct laryngoscopic view (Macintosh 3 laryngoscope blade) upon first attempt. The epiglottis was short, but the glottis was Cormack-Lehane Grade I. The patient did not cough or move during the intubation. The tube was fixed at the right lip corner and secured properly with the tube holder. After anesthetic induction, the patient was carefully moved caudally for surgical positioning. Otherwise, she was not moved, because the operation was open laparotomy, which is performed in only supine position without any required movement of the operating bed. Besides, there was no movement of head and neck to place intravenous catheters. An esophageal stethoscope (18 Fr, DeRoyal Industries, Powell, TN, USA) was inserted for temperature monitoring and a nasogastric (NG) tube (18Fr, INSUNG Medical, Co., Daegu, Korea) was inserted at the surgeon's request. A resident anesthesiologist inserted the NG tube and esophageal stethoscope without reporting any difficulty.
During the 4 hour operation, anesthesia was maintained with propofol, remifentanil, and vecuronium. The surgery was uneventful, and after the operation, the endotracheal tube cuff was deflated and the patient was extubated; severe coughing did not occur during the emergence. During the stay in post anesthesia care unit (PACU), she did not complain of any symptoms such as hoarseness or laryngeal pain. On the first postoperative day in the ward, she complained of moderate hoarseness. The physician expected the symptom would resolve spontaneously, but the patient complained of persistent hoarseness on the fourth day after the operation. There were no symptoms other than hoarseness. On the sixth day after the operation, fiber-optic laryngoscopy was performed by the laryngologist.
On laryngoscopy, the left vocal cord was fixed in the paramedian position, however minimal movement of arytenoid during phonation was observed. The left vocal cord did not show any movement even following a deep inspiration. Left arytenoid was placed with anteromedial side. A difference in level between the 2 vocal cords caused by the infra-placement of the left vocal cord was observed (). Arytenoid dislocation was suspected, and surgical reduction under general anesthesia was scheduled.
Reduction was attempted by repeatedly applying force to the left arytenoid cartilage toward the posterolateral side using the peanut surgical instrument (Sipjasung Wize, Co., Seoul, Korea). After reduction and just before the patient woke from the anesthesia, the movement of the both vocal cords was confirmed under direct laryngoscopic view (Macintosh 3 laryngoscope blade). The patient's voice was improved immediately after the surgery; and a month after the surgery, movement of the vocal cords was completely normal. showed an image taken 3 weeks after surgical reduction. Written informed consent was obtained from the patient for publication of this case report and the accompanying images.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.0, 'kg'], 'height': [163.0, 'cm']}",1.57806,1.49916,1.65696,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 163.0 cm. 
The patient's weight is 55.0 kg. 
Therefore, the patient's bsa is sqrt((55.0 (in kgs) * 163.0 (in cm))/3600) = 1.57806 m^2."
7253,60,Body Surface Area Calculator,physical,decimal,pmc-8101148-1,Extracted,"The 42-year-old Caucasian female patient was hospitalized for further evaluation because frequent TLOC in recent weeks had resulted in drastically reduced quality of life and potentially harmful incidents. TLOC had started appearing 11 months earlier (see “Timeline”), right after she had been hospitalized for a herpes zoster oticus infection with involvement of the vestibular nerve. Ten months earlier, she had experienced three symptomatic hypertensive emergencies with headaches and impaired vision. She had been prescribed 2.5 mg bisoprolol daily; however, compliance was poor, as she reported significant fatigue as a side effect. The patient reported recurrent TLOC especially during light exercise such as walking. In some instances, prodromes such as dizziness and sweating preceded TLOC; other times they occurred suddenly, leading to falls including serious injury. Dyspnea or angina pectoris-like symptoms were not present.
During presentation, we initially took a detailed history and were able to establish that she indeed suffered from TLOC during these episodes. She also reported long-lasting psychosocial distress as she and her partner had been suffering from unintended childlessness. This had fortunately been resolved when they adopted a child 13 months ago.
The physical examination did not show any abnormalities. Height was 174 cm, weight 64 kg, body mass index (BMI) 21.1 kg/m2. Heart rate was regular and palpable symmetrically in all extremities (67 beats per minute), and blood pressure was 130/75 mmHg, with no heart murmurs, normal auscultation of the lungs, and no peripheral edema. The abdominal examination revealed no masses and no tenderness.
Recommended basal evaluation of syncopes and TLOC including history, physical examination, electrocardiography (ECG), blood pressure measurements, and orthostatic testing did not yield any pathological findings.
We focused on further evaluating a potential cardiac cause of TLOC. A treadmill cardiac stress test showed normal physical fitness, no arrhythmias, normal blood pressure and heart rate response, and the absence of relevant ST changes. A 24-hour Holter ECG revealed no pathological findings. To account for rare causes of syncopes, Brugada syndrome was ruled out by performing an ajmaline test. Echocardiography showed normal ejection fraction and no valvular dysfunction or other structural disease. No hint of arrhythmogenic right ventricular cardiomyopathy could be detected in cardiac magnetic resonance imaging (MRI). Urinary levels of catecholamines and their metabolites were normal.
Upon repeated history-taking about preceding situations and potential triggers, we could elaborate on an association with the intake of carbohydrate-rich foods. The patient reported that the TLOC followed carbohydrate-rich meals by approximately 1–2 hours. She had already intuitively changed her diet by abstaining from carbohydrate-rich meals. To evaluate the association with meals, we performed an oral glucose tolerance test. One hundred and eighty minutes after ingestion of 75 g of glucose, the serum glucose level dropped to 39 mg/dL (see Fig. ), which induced the same aura symptoms that were familiar to the patient from her previous TLOC with dizziness and rapidly fading consciousness. To prevent complete loss of consciousness, glucose was injected intravenously. Taken together, this provocation test and the detailed medical history proved the hypoglycemic etiology. We therefore established the diagnosis of a pathological glucose tolerance and hyperinsulinism resulting in hypoglycemia and TLOC.
Magnetic resonance imaging (MRI) showed a normal pancreas. A 72-hour-fasting glucose test had been performed and insulinoma had been ruled out. Insulin-like growth factor 1 (IGF-1) levels were normal. Cortisol showed normal levels in serial testing throughout the day. There was no hint of adrenal insufficiency, with normal morning cortisol of 16.2 µg/dL. No insulin antibodies were measurable. Noninsulinoma pancreatogenous hypoglycemia syndrome (NIPHS) is a very rare disease causing postprandial hypoglycemia. Testing includes stimulation of pancreatic β-cells by invasive calcium administration, [] which was not performed in our patient. Given the relief of symptoms after lifestyle and dietary changes, further invasive testing to distinguish prediabetes from NIPHS was not performed. We recommended primarily dietary changes including frequent small meals to reduce the frequency of hypoglycemic episodes and avoidance of carbohydrate-rich meals as treatment. We discontinued the β-blocker therapy to avoid interference with glycogenolysis. If symptoms persisted, an off-label metformin therapy for the treatment of her pathological glucose resistance or a treatment test with acarbose, which delays hydrolysis of ingested complex carbohydrates and reduces postprandial glucose and insulin peaks, was suggested. At a follow-up consultation 3 months later, the patient reported no further TLOC after the suggested dietary changes, which led to a markedly improved quality of life.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [64.0, 'kg'], 'height': [174.0, 'cm']}",1.75879,1.67085,1.84673,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 174.0 cm. 
The patient's weight is 64.0 kg. 
Therefore, the patient's bsa is sqrt((64.0 (in kgs) * 174.0 (in cm))/3600) = 1.75879 m^2."
7254,60,Body Surface Area Calculator,physical,decimal,pmc-5366765-1,Extracted,"A 14-year-old boy was referred by his General Practitioner with history of abdominal pain and rash on his back for 12 months. The rash was treated with multiple topical agents including antifungal, antibiotic, and steroid ointments with no improvement. There was no history of loss of appetite, loose stools, diarrhoea, or bloating. He had no significant past medical history or medical problems within the family. He was weaned to solids without any difficulties and had no known food allergies.
On examination, he had a maculopapular and urticarial rash on his back and knees. The rest of his examination was normal.
Investigations including FBC, LFT, U&E, ESR, CRP, anti-tTG, IgA, IgG, and IgM all were normal, but anti-endomysial antibody was weakly positive.
Upper GI endoscopy showed normal oesophagus, mild antral erythema (negative CLO test), and normal mucosa in the duodenum. Partial villous atrophy with crypt lengthening and increasing intraepithelial lymphocytes was seen on histology. A diagnosis of seronegative CD was made. Quick mucosal lactase test was mildly suggestive of lactose intolerance.
The patient noticed a significant improvement in his rash within 12 days of starting gluten-free diet (GFD). He continued to improve on a GFD and when seen in the follow-up clinic a year later reported complete resolution of symptoms. His weight improved from 66.5 kg to 75 kg and height improved from 179.3 cm to 183.6 cm. Repeat investigations including anti-tTG antibody were normal. As there was improvement in his clinical symptoms, height, and weight, we did repeat endoscopy or do HLA-DQ2 and HLA-DQ8 investigations.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [75.0, 'kg'], 'height': [183.6, 'cm']}",1.95576,1.85797,2.05355,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 183.6 cm. 
The patient's weight is 75.0 kg. 
Therefore, the patient's bsa is sqrt((75.0 (in kgs) * 183.6 (in cm))/3600) = 1.95576 m^2."
7255,60,Body Surface Area Calculator,physical,decimal,pmc-3643850-1,Extracted,"A 50-year-old woman patient without medical history and any cardiovascular risk factors was hospitalized for exertional dyspnea and palpitations from three months and signifiant weight loss. She related worsening of symptoms in the last week before admission.
On admission, she was in the poor condition, cachectic, weighing 45 kg for a height of 1, 65 m and a BMI 17 kg/ m2, blood pressure was 100/60 mm Hg, heart rate was regular 120/min, respiratory rate was 29 breaths/ min and she was afebrile. Oxygen saturation was 98%. Physical examination revealed bilateral lung crepitations. A full blood cell count showed a mild normocytic anemia (hemoglobin = 11.5 g/dl). A chest radiograph showed left atrial enlargement and data of left cardiac failure. The electrocardiogram showed sinusal tachycardia.
Transthoracic echocardiography performed in emergency showed a giant left atrial mobile mass (72× 53 mm) attached to the interatrial septum and confined to the left atrium in systole (Figure ). In diastole (Figure ) the tumor was seen prolapsing across the mitral valve into the left ventricle and partially obstructing it and causing severe functional mitral stenosis with a mean gradient of 21,3 mmHg. A mild mitral regurgitation was also found. Severe pulmonary hypertension was confirmed by Doppler PAPs =137 mmHg. The patient was scheduled for cardiac surgery. During the operation, the tumor was excised through a sternotomy from a transseptal approach with a small portion of the atrial wall and the histopathological analysis found atrial myxoma. The clinical course was uncomplicated and the patient was discharged after three weeks with good outcome.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.0, 'kg'], 'height': [1.65, 'm']}",1.43614,1.36433,1.50795,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 1.65 m, which is 1.65 m * 100 cm/m = 165.0 cm. 
The patient's weight is 45.0 kg. 
Therefore, the patient's bsa is sqrt((45.0 (in kgs) * 165.0 (in cm))/3600) = 1.43614 m^2."
7256,60,Body Surface Area Calculator,physical,decimal,pmc-7232722-1,Extracted,"An 80-year-old woman (46 kg, 154 cm) was transported to our intensive care unit intubated and ventilated with recovery of spontaneous circulation after cardiopulmonary arrest (no-flow 15 minutes, low-flow 10 minutes). She reported dyspnea and syncope in her toilets following a pushing effort. She had no previous history of respiratory or cardiac disease. She is followed for giant cell arteritis and myelodysplasia without other medical history.
Initial evolution was rapidly favorable, and the patient regained consciousness without sequelae. Etiologic assessment carried out initially did not explain this episode of cardiopulmonary arrest. CT-chest performed initially when the patient was intubated found a megaesophagus but no tracheal compression ().
A week later, the patient presented an episode of acute respiratory distress with bradycardia during a meal. Faced by suspicion of inhalation pneumopathy, a bronchoscopy was performed but not finding of foreign bodies. In view of the presence of a pulmonary focus on chest X-ray (), diagnosis of aspiration pneumonia was retained. The patient improved and returned home after few weeks.
Three months later, the patient was rehospitalized in a state of acute respiratory distress, once again after a meal. At this time, new CT-chest without intubation found megaesophagus, this time with tracheal compression (). Bronchoscopy performed at this time revealed a TM with complete expiratory collapse and 80% inspiratory collapse associated with an inflammatory mucosa ().
In view of all these elements, we have retained the diagnosis of acute airway obstruction and cardiopulmonary arrest due to TM caused by megaesophagus compression secondary to achalasia. Achalasia was subsequently confirmed by esophageal manometry. No other cause of TM, in particular, no arguments for systemic infection or collagen vascular disease, was highlighted on various examinations. Please note that the patient's giant cell arteritis was perfectly controlled during these respiratory episodes.
On therapeutic plan, in front of patient advanced age and history of myelodysplasia with severe pancytopenia, surgery was not proposed. We proposed intraesophageal botulinum toxin injections under endoscopy to try to treat achalasia. The best treatment for TM is that of the cause. Following this treatment, the patient has not presented any cardiopulmonary arrest but she continued to have repeated lung infections. Unfortunately, she died two years later from a complicated lung infection.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [46.0, 'kg'], 'height': [154.0, 'cm']}",1.40278,1.33264,1.47292,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 154.0 cm. 
The patient's weight is 46.0 kg. 
Therefore, the patient's bsa is sqrt((46.0 (in kgs) * 154.0 (in cm))/3600) = 1.40278 m^2."
7257,60,Body Surface Area Calculator,physical,decimal,pmc-6759807-1,Extracted,"A 26-month-old boy was admitted to our hospital due to repeated melena and hematemesis. Eight months prior, intermittent hematemesis as well as melena initiated due to CTPV, diagnosed in another hospital. Six months prior, azygoportal disconnection without splenectomy was performed to control the symptoms. However, 5 months prior, melena recurred and haematemesis happened 3 times afterwards till readmission. His previous medical history included esophageal atresia (cured previously in another hospital by surgery) and atrial septal defect (untreated due to good cardiac function). Umbilical cord infection was ruled out.
On admission, the patient was stable. His heart rate was 95 bpm and body temperature was 36.5°C. His height was 90 cm (z-score 0.645) and body weight was 12.4 kg (z-score 0.000). Relevant laboratory results are listed in . Computed tomography (CT) found esophageal varices and splenomegaly without ascites (). Branches of portal vein were not distinguishable and replaced by multiple convolute collateral vessels, which was consistent with features of CTPV (). Esophagogastroduodenoscopy demonstrated grade 3 gastroesophageal varices ().
In view of poor response of surgery and after careful consideration, TIPS under general anesthesia was thought to be the safest option and could relieve portal hypertension.
Before TIPS, his CT scan was evaluated to make sure that Rupus-100 (Cook Incorporated, Bloomington, IN, USA), the TIPS kit for adults, was accessible to his vasculature since pediatric TIPS sets are lacking. After general anesthesia, his right internal jugular vein was punctured. Access to the portal vein from the right hepatic vein was guided by X-ray. Portography revealed that the main portal vein at the hepatic hilus was occluded entirely with formation of multiple convolute collateral vessels. Also, splenic vein flowed hepatofugally, and esophageal varices were evidenced (). The portosystemic pressure gradient was 22 mmHg. Because the portal vein diameter was measured to be 9 mm, a 6 ×60 mm covered Fluency stent (Bard Incorporated, Karlsruhe, Germany) and a 6 ×60 mm bare SMART stent (Cordis, FL, USA) were inserted between the hepatic vein and portal vein after dilatation of the intrahepatic tract. Patency of portal vein and stent was confirmed by portography afterwards (), and the portosystemic pressure gradient was reduced to 6 mmHg. Recovery from anesthesia was uneventful. His condition was stable and he was discharged 3 days after TIPS placement.
Six months post-TIPS, relapse of melena and hematemesis, and occurrence of hepatic encephalopathy were not noticed. Relevant follow-up laboratory results are listed in . The shunt functioned well as determined by ultrasound and CT. The size of the spleen was smaller and the varices were relieved dramatically, determined by CT and the esophagogastroduodenoscopy (). Furthermore, his development was not impaired. His height increased to 95 cm (z-score 0.912), which was 5 cm taller than 6 months before. Body weight increased to 14.5 kg (z-score 0.750), which was 3 kg heavier than 6 months before. The growth level and velocity were both within normal range. Language development was also normal.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [12.4, 'kg'], 'height': [90.0, 'cm']}",0.55678,0.52894,0.58462,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 90.0 cm. 
The patient's weight is 12.4 kg. 
Therefore, the patient's bsa is sqrt((12.4 (in kgs) * 90.0 (in cm))/3600) = 0.55678 m^2."
7258,60,Body Surface Area Calculator,physical,decimal,pmc-8028123-1,Extracted,"A 26-year-old male patient experienced a car accident and was diagnosed with an open fracture (Gustilo-Anderson type IIIB) of the right distal humerus with massive bone defects and severe intra-articular involvement, without neurovascular injuries or other associated injuries. Within 24 h after the injury, he was treated by surgical debridement, negative pressure vacuum sealing drainage, and immobilization by casting in a local hospital. Due to severe contamination and a poor soft tissue condition, the wound was surgically debrided again and closed 15 days later. Two months after the initial operation, the wound had finally healed, and the soft tissue was in good condition, without infection or effusion. The CRP (C-reactive protein) and ESR (erythrocyte sedimentation rate) levels returned to normal, and the patient was transferred to our department for additional treatment.
The patient’s height was 175 cm, and his weight was 130 kg. The preoperative anteroposterior (AP) and lateral X-rays (see Fig. ) and 3D-CT scans (see Fig. ) of the right elbow joint showed massive bone defects at the supracondylar level as well as a comminuted articular surface. According to the Association for Osteosynthesis/Association for the Study of Internal Fixation (AO/ASIF) criteria, the fracture was classified as a type 13-C3 fracture []. The physical examination revealed pseudarthrosis at the fracture site, which made it much more difficult to reconstruct the distal humerus.
After the induction of general anesthesia, the patient was placed in the supine position with elbow flexion and forearm crossing chest [], and a longitudinal incision was made along the midline of the posterior aspect of the elbow and medially curved at the olecranon tip. The ulnar nerve was dissected carefully and protected by a rubber strip, and then, a V-shaped osteotomy was performed in the proximal olecranon. The proximal bone fragment and triceps muscle were flipped upward to expose the distal part of the humerus.
Then, we removed all the fibrous scar tissue as well as the anterior and posterior capsules to release the elbow. The dead bones and redundant calli were debrided until fresh bone was evidently revealed, and then the bone callus was kept for grafting. The original articular cartilage was preserved to the greatest extent possible, but the trochlear groove was too severely comminuted to be reconstructed. Therefore, the fracture fragments and adhesive fibrous tissue were removed to facilitate reconstruction.
The trochlear and capitellar articular surfaces of the distal humerus were aligned with the olecranon and radial head articular surfaces, respectively. Then, we measured the width of the trochlear groove defect, harvested a cylindrical autograft of an appropriate size and shape from the iliac crest, and inserted the graft into the defect to reconstruct the distal humerus. The cortical bone surface of the graft was directed towards the articular cavity but was located 2 mm proximal to the cartilage. We stabilized the distal fragments using K-wires (Kirschner wires) for temporary reduction. Then, the intercondylar fracture was converted to a supracondylar fracture of the distal humerus.
Next, the humeral shaft and both columns were reduced. First, the medullary canal was opened by a 3.5 mm diameter drill to promote fracture healing. The supracondylar bone defects were measured to be approximately 3 cm at the medial column and 5 cm at the lateral column. We performed shortening by 2 cm at the supracondylar level. Then, 2 pieces of autografts harvested from the iliac crest were trimmed according to the size and shape of the bony defects to reconstruct the medial and lateral columns, respectively. The cortical bone was directed outward, and the cancellous side was directed inward. The total bone loss was estimated by measuring the humeral length. Then, K-wires were inserted for temporary fixation.
Finally, to optimize the stability of the bony structure, the distal humerus was stabilized using anatomical locking compression plates via a parallel configuration (Zimmer Biomet, USA). Several K-wires were left for the fixation of the tiny fragments.
After internal fixation, the elbow joint exhibited almost full range of motion during passive flexion and extension (see Fig. ). The remaining iliac crest autografts and bone callus were cut into several strip-shaped bone chips and implanted around the supracondylar level.
Finally, the olecranon osteotomy site was reduced and fixed by tension band wires. We performed subcutaneous transposition of the ulnar nerve using soft tissue sling to prevent direct contact and irritation from the hardware. The muscles and deep fascia were sutured carefully to cover the bone grafts and internal fixation site. The donor site was closed by direct suturing.
After the surgery, standard AP and lateral radiographs of the elbow joint were taken to evaluate the quality of reconstruction (see Fig. ).
The drainage tube was removed 24 h after surgery. Active exercises of the hand and wrist, isometric contractions of the biceps and forearm muscles, and active elbow flexion and extension exercises were initiated on the second day after surgery.
Routine follow-ups were carried out. The fracture healed at 3 months postoperatively, and the radiographs showed the presence of a continuous callus passing through the fracture line. Six months after the index surgery, the patient had a painless elbow joint and almost full recovery (125° elbow flexion and 0° extension, 90° forearm supination and 65° pronation). The Mayo elbow performance score (MEPS) was 100 (excellent).
Three years after the index surgery, the patient came to our department for hardware removal due to psychological factors. He was pain free at the affected elbow joint. The flexion-extension range of motion was 130–0°, and the supination-pronation range of rotation was 90–80°. The MEPS was 100 points. The patients was very satisfied.
Secondary displacement or the loss of reduction, implant loosening or internal fixation breakage, and obvious articular degeneration were not observed. No other postoperative complications, such as infection, nonunion, delayed union, ulnar nerve symptoms, or donor site pain, occurred after the initial internal fixation procedure. After hardware removal, the overall bony structure of the affected elbow joint remained intact with only a partial deformity at the lateral column, which had no significant influence on the overall functional outcome (see Fig. ).",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [130.0, 'kg'], 'height': [175.0, 'cm']}",2.51385,2.38816,2.63954,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 175.0 cm. 
The patient's weight is 130.0 kg. 
Therefore, the patient's bsa is sqrt((130.0 (in kgs) * 175.0 (in cm))/3600) = 2.51385 m^2."
7259,60,Body Surface Area Calculator,physical,decimal,pmc-5757101-1,Extracted,"A 41-year-old white European woman presented to our clinic with a 7-year history of unexplained progressive unilateral left thigh pain during cycling, starting at moderate intensity and increasing upon maximal exertion. She had been a spinning instructor for 13 years, with an average of 5 hours per week, before onset of symptoms. In addition, she worked as a firefighter, where she experienced identical complaints during rapid actions, like climbing the stairs. The patient reported a sensation of unilateral muscle fatigue and pain in the left thigh, starting at the vastus medialis and spreading all over the quadriceps, adductors, and biceps femoris, without symptoms in the gluteal region or calf. Complaints vanished within 3 minutes after cessation of exercise and were highly reproducible. There was no history of trauma, while her medical history included right-sided congenital hip dysplasia, primary Raynaud's phenomenon, and attention deficit hyperactivity disorder (ADHD), for which she used clomipramine for 10 years. She was on no other drug therapy at time of presentation and had no history of smoking, diabetes, hypertension, hypercholesterolemia, peripheral artery disease, or coronary heart disease. Family history was positive for familial hyperhomocysteinemia, but this was never diagnosed in her.
The woman presented with a height of 172 cm and body weight of 65 kg (body mass index of 22 kg/m2). Her resting blood pressure was 120/75 mmHg with a heart rate of 61 beats per minute (bpm). Musculoskeletal investigation showed normal back mobility and a full range of motion of hips and knees with normal muscular strength of both legs. In addition, neurological examination was normal in our patient.
Admission laboratory findings included complete blood count, which was unremarkable (). In addition, haemostatic tests, including activated partial thromboplastin time (aPTT), prothrombin time (PT), INR, fibrinogen, D-dimer, DNA testing for Factor V Leiden and prothrombin G20210A carriership, protein C activity, activated protein C resistance, and free protein S level, were all normal, while no lupus anticoagulants or anti-cardiolipin antibodies were detectable.
Transthoracic echocardiography showed normal anatomy with normal left ventricular ejection fraction (LVEF) and systolic and diastolic volumes but suggested a slight increase in total peripheral vascular resistance ().
Since symptoms appeared during exercise, a maximal treadmill exercise test was obtained with increasing resistance, starting at 100 Watt and elevating 15 Watt every minute, until exhaustion. Complaints started at 130 Watt and the test was ceased at 260 Watt due to unilateral thigh pain and muscular fatigue. The exercise electrocardiogram (ECG) showed no abnormalities and systolic pressures were obtained before and after exercise from the left brachial and bilateral calf for ankle-brachial index (ABI) calculation. The ABI before exercise was 1.1 on both sides, whereas directly after exercise ABI was reduced for both legs (right: 0.75; left: 0.59), where no alterations upon exercise were expected in a healthy young woman [] ().
Prompted by bilateral reduced ABI after exercise and the suggested increased vascular resistance, further vascular examinations were performed. Normal lower limb pulses without audible murmurs and a normal capillary refill (<2 sec) were found in both legs. To investigate whether this patient suffered from endofibrosis, resting arterial duplex ultrasonography was done, which revealed no stenosis and normal diameters of the external iliac artery and common iliac artery, where femoral arteries appeared to be relatively wide, as might be expected in well-trained individuals [] (). In addition, femoral intima-media thickness was within normal range (0.78 mm, reference cut off: <0.9 mm), accompanied by normal peak systolic velocity during hip extension (1.41 m/sec) and flexion (1.54 m/sec) []. At the venous level, no signs of (previous) deep vein thrombosis were observed.
Additionally, obstructive vascular pathologies were investigated by multiphase computer tomography angiography (CTA), showing no signs of intraluminal pathologies or aberrant morphology, thereby corroborating the duplex examinations and excluding endofibrosis, popliteal entrapment syndrome, arterial-venous shunts, and venous malformations.
Next, we evaluated arterial function by ultrasonic examination of carotid and brachial artery and tonometric measurement of carotid-femoral pulse wave velocity (cfPWV). Carotid intima-media thickness (0.68 mm, reference cut off: <0.9 mm []) and cfPWV (6.74 m/s, reference cut off: <10 m/s []) were unremarkable. However, carotid distensibility coefficient was lower than expected (16 × 10−3/kPa, reference value: 20–30 × 10−3/kPa) [].
Brachial flow-mediated dilation (FMD, was 1%, reference value: 3.0–8.4% []) and nitroglycerine-mediated dilation, 8%, (reference value: 9.6–18.0% []) were markedly reduced. Microcirculatory studies showed normal capillary density before (74/mm2, reference value: 40.4–85.6/mm2) and after (109 mm2, reference value: 69.5–117.1/mm2) venous congestion []. Furthermore, heat-induced cutaneous microvascular dilatation was within normal limits (+1356%, reference value: 324–1762%).
Based on the symptoms and test results, we postulated impaired arterial vasodilation and therapy with isosorbide mononitrate 30 mg twice daily was started, without any effects on the symptoms. This appeared to exclude a lack of nitrous oxide as major underlying defect. In another approach, we prescribed a vasodilating agent, the long-acting calcium antagonist diltiazem 200 mg once daily, through which claudication symptoms were well controlled and blood pressure remained within normal range (24 h measurement: average 110/80 mmHg) without any symptoms of orthostasis. During 2-year follow-up, she experienced no side effects and was able to continue her work as a fire fighter and spinning instructor.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [65.0, 'kg'], 'height': [172.0, 'cm']}",1.76226,1.67415,1.85037,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 172.0 cm. 
The patient's weight is 65.0 kg. 
Therefore, the patient's bsa is sqrt((65.0 (in kgs) * 172.0 (in cm))/3600) = 1.76226 m^2."
7260,60,Body Surface Area Calculator,physical,decimal,pmc-4563191-1,Extracted,"A fifteen-year-old girl presented to our clinic with the complaint of primary amenorrhea. In her medical history, thelarche and pubarche were reported to occur at ages of 10 and 11 years, respectively. Family history was unremarkable and the parents were not related. On physical examination, weight was 55.2 kg [0.25 standard deviation (SD) for age and sex]; height was 165.5 cm (0.95 SD) and body mass index was 20.1 kg/m2 (0.10 SD). Her external genitalia were completely female. She had breast development and pubic hair of Tanner stage V (). The rest of the physical examination was normal with no apparent somatic abnormalities and no clitoral enlargement or any other evidence of virilization. Laboratory findings revealed normal biochemistry. Hormone levels were as follows; follicle stimulating hormone, 121 mIU/mL (normal, 0.3-10); luteinizing hormone, 13 mIU/mL (normal, 0.3-31); estradiol, 66 pg/mL (normal, 15-350); total testosterone, <20 ng/dL (normal, 15-181); prolactin, 5.3 ng/mL (normal, 1.9-25); beta human chorionic gonadotropin, <1 mIU/mL (normal, 0-10); adrenocorticotropic hormone, 50.3 pg/mL (normal, 0-46) and cortisol, 14 µg/dL (normal, 5-25). Her bone age was consistent with 13.5 years according to the Greulich & Pyle method. Pelvic ultrasound revealed a right gonad of 1.4 cm3 and a left gonad of 2.4 cm3 in volume, with a uterus of 60x25x23 mm in size and an endometrial thickness of 7 mm. In magnetic resonance imaging, the gonads were observed to be smaller than normal. The uterus was of normal size and there was no evidence of a tumor (). Chromosome analysis revealed a 46,XY karyotype (30 metaphase cells counted). SRY gene expression was confirmed by multiplex polymerase chain reaction. Direct sequencing on genomic DNA did not reveal a mutation in the SRY, SF1 and Wilms’ tumor 1 (WT1) genes. After the diagnosis of Swyer syndrome was made, the patient started to have spontaneous but irregular vaginal bleedings and therefore, she decided to quit her scheduled follow-up visits. After nine months, when she returned for a follow-up visit, the patient underwent a diagnostic laparoscopy. Frozen examination of multiple biopsies from gonad tissues revealed gonadoblastoma. Thus, the resection of the primary lesions and proper surgical staging (peritoneal washings, omental and peritoneal biopsies) were done to determine the presence of any occult metastasis. The uterus and other pelvic organs, except for the small streak gonads, were all normal and no palpable paraaortic or pelvic lymph nodes were detected. Histopathological examination of the dysgenetic gonads revealed bilateral pure gonadoblastoma and absence of follicular structures while the stroma was in a form resembling an ovarian structure. The patient underwent combined hormone replacement therapy with estrogen and progesterone, which provided regular monthly vaginal bleedings.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.2, 'kg'], 'height': [165.5, 'cm']}",1.59301,1.51336,1.67266,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 165.5 cm. 
The patient's weight is 55.2 kg. 
Therefore, the patient's bsa is sqrt((55.2 (in kgs) * 165.5 (in cm))/3600) = 1.59301 m^2."
7261,60,Body Surface Area Calculator,physical,decimal,pmc-5615275-3,Extracted,"A morbidly obese 62-year old Caucasian male patient was transferred from a Nursing Home in June 2017 by ambulance with worsening dyspnea, oxygen desaturation of about 70% and hypotension to our Emergency Department. Past medical history was significant for morbid obesity, likely sleep apnea, chronic hypercapnic respiratory failure from COPD, peripheral vascular disease, venous insufficiency, generalized debility, preserved left ventricular ejection fraction of 72%, and hypertension with early stage II CKD, with baseline serum creatinine of less than 1 mg/dL. Pertinent outpatient medications included potassium chloride 40 mEq twice daily, spironolactone 25 mg daily which was started two days before this admission, Furosemide 20 mg twice daily, Duonebs, baby Aspirin, Gabapentin 600 mg twice daily, Oxycodone 10 mg extended release twice daily, pantoprazole and Atorvastatin. The patient had undergone an aortogram with run off followed by a left lower extremity angioplasty for a high-grade proximal left femoral-popliteal bypass in situ vein stenosis two days prior to the admission—he had required temporary intubation for this procedure that was otherwise successful and without other complications.
Initial blood pressure was 88/63, pulse 71/min and oxygen saturation quickly improved to 99% on BIPAP. He weighed 133.5 kg, height was 190 cm, with a BMI of 36.84 kg/m2. He had 2+ bilateral lower extremity edema, and chest examination revealed reduced breath sounds with bibasilar inspiratory rales heard posteriorly. Serum creatinine was 3.14 mg/dL, a significant increase from a week previously (). Other pertinent laboratory indices were serum potassium 7 mmol/L, serum bicarbonate 27 mmol/L, phosphorus 7.1 mg/dL with a normal anion gap of 13 mmol/L. He was in respiratory acidosis and respiratory failure with arterial blood gas pH of 7.18, pCO2 of 84 mm Hg, and bicarbonate of 30 mmol/L. His Pro B Naturetic Peptide level that was nearly normal in August 2016 at 151 pg/mL was grossly elevated at 1426 pg/mL in mid May 2017, and had further escalated to 5503 pg/mL on the day of admission in June 2017 (Pro B Naturetic Peptide reference range ≤ 125 pg/mL). There was in addition, mild rhabdomyolysis with total CK of 1720 U/L, ALT was normal at 17 U/L but AST was mildly elevated at 54 U/L. Lactic acid was normal. EKG was abnormal but the first degree AV block, possible inferior infarct and prolonged QT interval were not new and T waves were not prominent. Chest radiograph revealed worsening cardiomegaly when compared to October 2016, hypoventilation, pulmonary vascular congestion and basal atelectatic changes without overt infiltrates evident. Echocardiogram was not available. He received two 500 cc boluses of normal saline and his blood pressure stabilized with SBP > 120 mm Hg. Other emergent therapies for the hyperkalemia included Ipratropium-Albuterol nebulizer treatments, two ampoules of intravenous Dextrose 50 (25 gm each) infusions, intravenous regular insulin and oral Kayexalate, 15 gm in 60 mL given once [].
Nephrology service was consulted. Evaluation confirmed gross 2+ to 3+ bilateral lower extremity edema, ascites, anasarca with reduced breath sounds with bibasilar inspiratory rales heard posteriorly. A Foley catheter was inserted due to evidence of urinary retention. The working diagnosis was contrast-induced nephropathy, further complicated by severe dyspnea likely the combination of chronic obstructive pulmonary exacerbation, narcotic/Gabapentin toxicity, with volume overload and diastolic congestive heart failure, given an otherwise normal echocardiogram in August 2016 with left ventricular ejection fraction of 72%. Spironolactone, Oxycodone, Gabapentin and potassium chloride were promptly discontinued. Continuous intravenous Furosemide infusion was started at 20 mg/h together with concurrently administered intravenous Chlorothiazide 500 mg every 8 h, and serum creatinine and electrolytes were monitored every 6 h. In addition, oral Doxycycline for longstanding cough and discolored sputum production, together with oral Prednisone and inhaled steroids were added later during the admission. He also went back on the BiPaP machine, which had been discontinued by the patient some months earlier for unclear reasons.
Overnight, the patient exhibited a very prompt, excellent and sustained diuresis with the combination diuretic regimen as he made nearly 10 L of urine the first admission day (). He felt much better, was off the BiPaP during the day, was less dyspneic and leg swelling was significantly reduced bilaterally. His weight quickly dropped, and the serum potassium was normalized about 15 h into the admission and continued to decrease thereafter ( and ). Simultaneously, serum bicarbonate had risen sharply, a reflection of contraction alkalosis. Moreover, hyperphosphatemia improved concurrently with acutely falling serum creatinine values ( and ).
By day 3, he was feeling so much better that intravenous diuretics were discontinued and he was switched to oral Furosemide 40 mg 2 times a day together with oral Metolazone 2.5 mg daily with continued monitoring of intake/output and daily chemistry. The Foley catheter was also discontinued. He continued to improve, lost more weight with loss of anasarca and edema fluids and was discharged after 5 days on the combination oral Furosemide 40 mg twice daily (double the preadmission dose) and oral Metolazone 2.5 mg daily (a new additional diuretic). At discharge, four days later, serum creatinine had fallen to 1.32 mg/dL, phosphorus was normal and he needed potassium supplements for hypokalemia. Besides, the serum bicarbonate was beginning to trend towards normal levels again (). Discharge medications included Prednisone taper and he was to complete five days of oral Doxycycline. Lisinopril and Spironolactone remained discontinued at the time of the discharge. He was seen the following week at follow up, in the Nephrology office, on 12 June 2017, much improved, and his weight had come down from a peak of 327 lb to 293 lb, serum creatinine was down to 1.05 mg/dL and he was requiring more potassium chloride supplements, on the same dose of Furosemide (40 mg twice daily) and Metolazone (2.5 mg daily), together with Spironolactone that was reintroduced by his Internist sometime after discharge, at a lower dose of 12.5 mg daily.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [133.5, 'kg'], 'height': [190.0, 'cm']}",2.6544,2.52168,2.78712,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 190.0 cm. 
The patient's weight is 133.5 kg. 
Therefore, the patient's bsa is sqrt((133.5 (in kgs) * 190.0 (in cm))/3600) = 2.6544 m^2."
7262,60,Body Surface Area Calculator,physical,decimal,pmc-6967330-1,Extracted,"A 169-cm, 65-kg, 51-year-old, right-handed man with right-side hemiparesis and dysarthria underwent screening magnetic resonance imaging (MRI) 2 years before craniotomy: a diffuse parietal tumor was misdiagnosed as cerebral infarction. Anticonvulsant polytherapy (carbamazepine, 200 mg daily; levetiracetam, 1000 mg daily) was started for symptomatic epilepsy. Right-hand and oro-facial motor paresis worsened beginning 4 months before surgery, and he was diagnosed with malignant glioma. He was referred to our institution 2 months before surgery. MRI demonstrated a T1 hypointense, T2/fluid-attenuated inversion recovery hyperintense area in the left lower parietal lobe with a gadolinium-positive mass in the postcentral gyrus. 11C-methionine positron emission tomography showed a high accumulation of methionine mainly in the postcentral gyrus. The results of a manual muscle test (MMT) showed reduced function (3/5) in his right-upper extremity.
The patient’s hypertension was well-controlled with telmisartan (40 mg, daily) and hydrochlorothiazide (12.5 mg, daily). Diabetes was treated with glimepiride (1 mg, daily) and anagliptin (400 mg, daily). Obstructive sleep apnea syndrome (OSAS) was suspected due to a history of snoring. Electrolyte imbalance was not observed. Although carbamazepine was increased to 400 mg daily beginning 17 days before surgery, epileptic seizure in his right-upper limb occurred every 2–3 days. Levetiracetam was increased to 2000 mg daily upon admission 4 days before surgery.
The lesion, suspected grade III glioma according to the World Health Organization (WHO) guidelines [], was distributed throughout the primary motor and sensory areas of his dominant hemisphere. We chose awake craniotomy using the “Asleep-Awake-Asleep” technique combined with intraoperative MRI for removal of his glioma. Uncontrollable seizure suggested rapid growth of the tumor. The patient was evaluated as American Society of Anesthesiologists (ASA) Physical Status Class 2. While the preoperative blood examination at admission indicated that his plasma sodium level (reference 136–145 mEq/L) had decreased from 140 to 130 mEq/L, he was asymptomatic. Preoperative correction of hyponatremia was ruled out to avoid neurological deterioration due to further growth of the glioma. Additional blood or urine examinations were not performed.
No premedication was given. Besides standard ASA monitoring, invasive arterial pressure and processed electroencephalogram monitoring were adopted. Following the intravenous administration of 100 μg fentanyl, general anesthesia was commenced and maintained with the target-controlled infusion of propofol (4.0 μg/mL) and the continuous infusion of remifentanil (0.5 μg/kg/min). After several attempts, a supraglottic airway (SGA) was inserted without muscle relaxant. Ventilation was adjusted to maintain an EtCO2 level around 35 mmHg. Normal saline and bicarbonate Ringer’s solution were given. Scalp blocks and infiltration analgesia were provided with 60 mL of 0.3% ropivacaine and 20 mL of 1% lidocaine with 0.01% epinephrine, respectively. Arterial blood gas (ABG) analysis (STAT PROFILE® Critical Care Express; Nova Biomedical, Waltham, MA) after induction showed mild hyponatremia (Table , T1).
Hypotension followed by induction was stabilized by three boluses each of ephedrine 4 mg and phenylephrine 0.1 mg until the beginning of surgery. Before dural incision, 200 mL of 20% mannitol was administered over 10 min. ABG analysis 117 min after induction, 25 min into mannitol infusion, revealed hyponatremia with hyperkalemia (Table , T2). Neither pathological electrocardiogram changes nor arrhythmia was observed. Sodium bicarbonate 2.8 g was given. Glucose-insulin (40 mL of 50% glucose containing 8 units of insulin) was infused simultaneously with another ABG analysis, which was performed to exclude mechanical failure (Table , T3). Hyponatremia was not treated promptly because of the risk of central pontine myelinolysis. ABG analysis 191 min from induction indicated persistent hyponatremia without hyperkalemia (Table , T4). In the planned transition to the awake phase, we anticipated insufficient wakefulness, intractable seizure, and deterioration of upper airway patency. Thus, the entire procedure was performed under general anesthesia. The remaining operation was uneventful, although the plasma sodium level remained less than 125 mEq/L (Table , T5–7). Anesthetics were discontinued, and SGA was removed 415 min after induction. The patient’s cardiorespiratory status was stable, but the patient could not follow orders. An intravenous transfusion of 1500 mL bicarbonate Ringer’s solution, 300 mL 1% glucose-containing acetated Ringer’s solution, 650 mL normal saline, and 200 mL mannitol was given. Total urine output was 1300 mL, and estimated blood loss was 36 mL. Surgery and anesthesia lasted 433 and 354 min, respectively.
The patient regained consciousness 1 h after the operation. MMTs of his right upper and lower extremities showed 1/5 and 3/5, respectively. Motor aphasia persisted until eight postoperative days (POD), and he walked unaided on POD 24. His plasma sodium concentration normalized by POD 35, before discharge on POD 39. MMTs at discharge were 2/5 and 4/5, respectively. Since the pathological examination revealed an oligoastrocytoma (WHO grade II), he received adjuvant chemotherapy. Prophylactic anticonvulsant polytherapy was continued, and there was no evidence of tumor recurrence at 36 months follow-up.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [65.0, 'kg'], 'height': [169.0, 'cm']}",1.74682,1.65948,1.83416,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 169.0 cm. 
The patient's weight is 65.0 kg. 
Therefore, the patient's bsa is sqrt((65.0 (in kgs) * 169.0 (in cm))/3600) = 1.74682 m^2."
7263,60,Body Surface Area Calculator,physical,decimal,pmc-2687573-1,Extracted,"A 28-year-old obese man presented at the Emergency Room of our hospital complaining of epigastric pain radiated to the back for one day. He had been admitted to our hospital 3 times previously due to acute pancreatitis with hyperlipidemia. He had type 2 diabetes mellitus and active pulmonary tuberculosis. He was treated with dietary restriction, daily NPH insulin injection, and lipid lowing medication such as fibrate derivatives. His father was noted to have hypertension, old cerebral infarction and type 2 diabetes mellitus. His mother had hyperlipidemia (type IV) and his elder brother had recurrent acute pancreatitis and diabetes mellitus. He didn't have xanthoma or xanthelasma. He had no alcohol drinking history and no biliary calculus disease. His height was 176 cm and weight was 87 kg, showing marked obesity. On physical examination, his abdomen was slightly distended with hypoactive bowel sounds and he had direct tenderness on epigastrium without rebound tenderness. On admission, laboratory data showed white blood cell count of 15,210/mm3. Blood chemistry tests revealed fasting blood sugar level of 228 mg/dL, lactate dehydrogenase level of 379 IU/L, and aspartate aminotransferase level of 20 IU/L. The serum amylase level of 160 mg/dL was slightly higher than the normal range (25~125 mg/dL). Serum lipase level was increased to 1596 U/L (normal range of 13~60 U/L). Serum calcium level and blood urea nitrogen level were within normal limits. The lipid profiles such as total cholesterol, triglyceride, high density cholesterol and low density cholesterol were 272 mg/dL, 605 mg/dL, 28 mg/dL and 98 mg/dL, respectively. A diagnosis of type IIb hyperlipoproteinemia was made based on serum lipoprotein electrophoresis [0% of chylomicron (0-2.0), 62.9% of β-lipoprotein (36.5-59.1), 22.5% of pre-β-lipoprotein (3.8-33.8), and 14.6% of α-lipoprotein (20.4-46.4)]. Hemoglobin A1c level was 10.4% and fasting C-peptide and postprandial C-peptide were 2.7 and 3.7 ng/mL, respectively. Abdominal CT scan revealed diffusely enlarged pancreas, peripancreatic fat infiltration and pelvic ascites, which were compatible with acute pancreatitis grade C (). He was treated with dietary restriction, hydration, NPH insulin injection and lipid lowering agents. For the purpose of distinguishing infective pancreatitis from hyperlipidemic pancreatitis, we prescribed antibiotics (2 g of meropenem® per day) for two days until abdominal CT information was obtained. His abdominal pain was resolved within a few days, and white blood cell count was normalized. He was discharged after 8 days, with complete recovery from acute pancreatitis.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [87.0, 'kg'], 'height': [176.0, 'cm']}",2.06236,1.95924,2.16548,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 176.0 cm. 
The patient's weight is 87.0 kg. 
Therefore, the patient's bsa is sqrt((87.0 (in kgs) * 176.0 (in cm))/3600) = 2.06236 m^2."
7264,60,Body Surface Area Calculator,physical,decimal,pmc-5590420-1,Extracted,"A 12-year-old boy presented with sudden onset weakness of both upper and lower limbs. He had history of polydipsia, increased frequency of urination, fatigue and muscle weakness of week duration. There was no history of recurrent carpopedal spasms. The boy had a previous episode of sudden onset weakness of both upper and lower limbs about 4 months ago. His parents' marriage was nonconsanguineous. There was no history of maternal polyhydramnios or premature delivery. There was no history of failure to thrive, salt craving, vomiting, and constipation. He had normal developmental milestones. However, the scholastic performance of boy was poor. Blood pressure was 90/60 mmHg. Height was 138 cm. Weight was 29 kg. Oral cavity examination revealed yellowish teeth [] presenting rough surfaces and conspicuous and irregular defects. The enamel alterations were generalized, affecting teeth in both arches. The gingivae were without signs of inflammation. The systemic examination was unremarkable. The investigations are given in .",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [29.0, 'kg'], 'height': [138.0, 'cm']}",1.05436,1.00164,1.10708,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 138.0 cm. 
The patient's weight is 29.0 kg. 
Therefore, the patient's bsa is sqrt((29.0 (in kgs) * 138.0 (in cm))/3600) = 1.05436 m^2."
7265,60,Body Surface Area Calculator,physical,decimal,pmc-8422010-1,Extracted,"A 48-year-old male patient (186 cm, 88 kg) was referred to our orthopedic outpatient clinic with a history of atraumatic persisting left shoulder pain lasting for several months. Physiotherapy, oral analgesics, and subacromial infiltrations showed no lasting effect. Magnetic resonance imaging revealed an RCT of M. supraspinatus (Patte Grade I; Goutallier/Fuchs Type I) and M. subscapularis (Lafosse Type I) [, , ].
The patient underwent ARCR using a suture bridge-like construct (SpeedBridge™ [SB], Arthrex, Naples, Florida, USA) for rotator cuff repair as well as an LHB tenodesis through one BioComposite SwiveLock™ (Arthrex, Naples, Florida, USA). The cranial part of the partially torn subscapularis tendon was attached to the LHB anchor.
At 6-week follow-up, the patient showed an adequate range of passive motion and no signs of shoulder stiffness. Nine weeks postoperatively, the patient suffered a low-velocity trauma to his left shoulder. He presented to the emergency room with immobilizing pain rated 9/10 on the numeric analog scale. Radiographic examination (, ) and a computer tomography scan (CT, , ) revealed an isolated fracture of the proximal humeral head (AO/OTA fracture and dislocation classification 11C1.3) []. The fracture line was located right at the lateral site of the suture bridge construct close to the anatomic neck (Neer Type II, []). Due to a displacement of 1 cm, surgical refixation was advised.
Under general anesthesia, the fracture site was exposed using a delta split approach. Total reruptures of previously reconstructed rotator cuff tendons were detected, and anchor material was removed. The fracture was reduced, and definitive fixation was performed with a PHILOS™-Plate system (DePuy Synthes, Warsaw, Indiana, USA). Rotator cuff tendons were reconstructed and additionally attached to the plate through Ethibond® fibers (Ethicon, Somerville, Massachusetts) in Mason-Allen technique.
Post-operative radiographs showed good reduction of the fracture so that post-operative rehabilitation following a standardized protocol was initiated ().
At 3-month follow-up, the fracture healed anatomically with the patient’s passive range of motion already within normal limits. Constant score was 68 and improved to 92 points at 1-year and 2-year follow-up. Radiographic examination at 1-year follow-up revealed adequate fracture consolidation (, ).",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [88.0, 'kg'], 'height': [186.0, 'cm']}",2.13229,2.02568,2.2389,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 186.0 cm. 
The patient's weight is 88.0 kg. 
Therefore, the patient's bsa is sqrt((88.0 (in kgs) * 186.0 (in cm))/3600) = 2.13229 m^2."
7266,60,Body Surface Area Calculator,physical,decimal,pmc-6377774-2,Extracted,"Patient 3 (P3) was a 9-year-old girl whose weight was 21,000 g, length 110 cm, and head circumference was 51 cm. At the age of 6 years, her weight was 15,000 g (−2SD), length 98 cm (−5SD), and head circumference was 48 cm (−2SD). She was evaluated for severe speech delay, light growth retardation, low anterior hairline, hypoplastic maxilla, heavy and arched eyebrows, synophrys, long eyelashes, iris hypoplasia, strabismus, broad nasal bridge, widely spaced incisors, an atypical smile, persistent fingertip pads, polydactyly of toes, hairy back and forehead and laryngeal cartilage dysplasia (Fig. c). Her great toes, broad terminal phalanges and grimacing smile as characteristics of RSTS seemed support the diagnosis of it. Nevertheless, we did not observe a beaked nose in her profile that can be seen in a majority of patients (Fig. c). Her polydactyly is also rare in RSTS but is common in CdLS. And some features like low anterior hairline, hypoplastic maxilla, heavy and arched eyebrows, synophrys, long eyelashes indeed overlapped with CdLS. The chromosome karyotype and CNV-seq result were normal.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [21.0, 'kg'], 'height': [110.0, 'cm']}",0.80104,0.76099,0.84109,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 110.0 cm. 
The patient's weight is 21.0 kg. 
Therefore, the patient's bsa is sqrt((21.0 (in kgs) * 110.0 (in cm))/3600) = 0.80104 m^2."
7267,60,Body Surface Area Calculator,physical,decimal,pmc-8665721-1,Extracted,"We present the case of a 15-year-old Caucasian female patient who was admitted to the hospital with symptoms of vomiting, epigastric pain, weight loss, progressive postprandial abdominal discomfort, and nausea. All symptoms were relieved after vomiting. On inspection, she was ill looking and pale, as well as dehydrated, while, based on her body weight, she was falling on the lower limit of the growth curve (Weight = 46kgr, Height = 150 cm). Her vital signs on admission were the following: Temperature = 36.9°C, Heart Rate = 83, Respiratory Rate = 21, and Blood Pressure = 98/59 mmHg. The patient was taking no medication and had no other underlying medical condition or intellectual disability. Furthermore, she had no history of previous surgical interventions.
The clinical examination revealed halitosis, a mobile palpable mass occupying the region between the umbilicus and the xiphoid process with size 25 × 9 cm, normal bowel sounds, and no muscle contraction of the abdominal wall or any other signs indicative of peritonitis. In addition, there was no blood or palpable mass on digital rectal examination. No abnormal signs were found during physical examination of the cardiopulmonary and urogenital systems.
The blood tests revealed anemia (Hemoglobin concentration = 7.1 g/dl with normal values ranging between 11.9 and 14.7 g/dl and Hematocrit = 25.1% with normal values ranging between 36.8% and 45.6%). All other blood test results were falling within normal range (Table ).
On admission, an abdominal X-ray was performed, but it was not diagnostic, followed by an abdominal ultrasound (U/S) which revealed a well-defined mass with dimensions 26cm × 9cm × 9cm in the epigastric region. To determine its origin and composition, an abdominal computerized tomography (CT) was ordered. The imaging results were in accordance with those of U/S, demonstrating the presence of a large, well-circumscribed, non-homogeneous mass, which lacked blood supply and occupied the whole stomach. The dimensions of that mass were 26,6cm × 9,7cm × 9,8cm. The images were strongly suggestive of a bezoar (Figure ).
An upper GI endoscopy was performed on the second day after admission, confirming the diagnosis of trichobezoar, but failing to extract the mass of hairs. The patient underwent an exploratory laparotomy with an upper midline incision on the same day. Intraoperatively, the diagnosis of trichobezoar was confirmed. An intraluminal mass was seen and felt inside the stomach. A 10 cm incision was made in the anterior wall of the gastric antrum, and a massive trichobezoar in the shape of the stomach with size 27cm × 10cm × 10cm was extracted (Figures and ).
The patient had an uneventful recovery and was discharged on the 4th postoperative day. Intraoperatively she received a single dose of Cefoxitin 1g and Metronidazole 500 mg. Postoperatively, she received the same antibiotic combination for 3 consecutive days. Paracetamol and Tramadol were administered intravenously as analgesics, along with intravenous fluids, for the same number of days. Oral feeding was initiated on the 3rd postoperative day.
Despite the patient and her parents initially denying a history of trichophagia, it was later revealed, upon the first psychiatric consultation, that the patient was exhibiting both trichotillomania and trichophagia. Today, five years after the surgical procedure, she has been attending regular meetings with a psychiatrist.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [46.0, 'kg'], 'height': [150.0, 'cm']}",1.38444,1.31522,1.45366,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 150.0 cm. 
The patient's weight is 46.0 kg. 
Therefore, the patient's bsa is sqrt((46.0 (in kgs) * 150.0 (in cm))/3600) = 1.38444 m^2."
7268,60,Body Surface Area Calculator,physical,decimal,pmc-8120524-1,Extracted,"A 4-year-old male, 14.5 kg and 85.5 cm, with PA diagnosed when he was 3 days old. Patient initially presented with lethargy and decreased oral intake. Laboratory workup at that time resulted in elevated serum ammonia level and increased urinary ketones. Genetic laboratory testing was performed, which revealed him to be homozygous for the PCCB (propionyl-CoA carboxylase subunit B) gene mutation. He had several more episodes of hyperammonemia in his first 2 years of life, but each resolved with carglumic acid treatment at home, which accelerated ammonia elimination. He was fed with low-protein formula and supplemented with L-carnitine. He had global developmental delay, for which he received speech therapy, occupational therapy, and physical therapy. He was followed-up by genetics, gastroenterology, and a nutritionist. Due to decreased oral intake, he was gastric tube feeding dependent. No metabolic crises had occurred within the year prior to the transplant.
The patient was listed for orthotopic liver transplantation (OLT) to treat PA. Preoperative evaluation and workup for liver transplantation included a computer tomography scan of the abdomen, an ultrasound of the liver, and an echocardiogram, which were all normal. On admission, blood was drawn for baseline laboratory levels, which included total and free carnitine, acylcarnitine profile, plasma and urine amino acids, ammonia, urinalysis, and a complete metabolic profile, which were all within normal limits. As per the pediatric gastroenterology and genetics specialists, the patient continued his home dose L-carnitine but intravenous (1.4 g IV) as an inpatient, and was started on IV parenteral nutrition with dextrose 10% at 1.5 times maintenance plus appropriate electrolytes and intravenous intralipids at 2 g/kg/day.
Intraoperatively, patient underwent IV induction with propofol (50 mg), glycopyrrolate (0.2 mg), and cisatracurium (4 mg) via a 22-gauge peripheral IV, followed by uneventful endotracheal intubation with a 4.0 endotracheal tube. Central venous access was obtained under ultrasound guidance to the right internal jugular vein with a 5 Fr, 10 cm catheter and a right radial arterial line for frequent blood sampling and intraoperative real-time blood pressure monitoring. Following intraoperative discussion and recommendation from genetics, IV total parenteral nutrition infusions and intralipids were continued intraoperatively at the same rate, and a bolus dose of IV L-carnitine was given before incision (0.7 g IV bolus over 3 minutes). Additionally, an IV insulin infusion was started at 1 unit/hour after induction, and adjusted based on patient’s serum glucose levels (target glucose levels: 100-200 mg/dL). Urine ketones, blood ammonia, glucose, and an arterial blood gas were checked every hour and corrected accordingly. Urine ketones were normal throughout the case.
After induction, baseline laboratory tests were drawn, which revealed a normal pH, lactate level of 3.6 mmol/L (normal range = 0.5-1 mmol/L), serum ammonia level of less than 9 µmol/L (normal range = 21-50 µmol/L), and negative urinary ketones. During the anhepatic phase, the lactate level increased to 4.6 mmol/L and serum ammonia level increased to 25 µmol/L, and both normalized after liver reperfusion. Urinary ketones remained negative throughout the case. Sodium bicarbonate (0.5 mEq/kg) boluses were administered during the anhepatic and post-reperfusion phase to correct metabolic acidosis. He was hemodynamically stable throughout the case and did not require any vasoactive drugs or experience any significant clinical decompensation. Total amount of fluids administered were 2 L of crystalloids and 250 mL of albumin 5%. The total blood loss was approximately 50 mL, and urine output was 250 mL. Duration of surgery was 292 minutes. He was extubated after the surgery was finalized in the OR and was transported to the pediatric intensive care unit (PICU) without any vasopressors in a stable condition. He spent a total of 5 days in the PICU during his postoperative course.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [14.5, 'kg'], 'height': [85.5, 'cm']}",0.58683,0.55749,0.61617,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 85.5 cm. 
The patient's weight is 14.5 kg. 
Therefore, the patient's bsa is sqrt((14.5 (in kgs) * 85.5 (in cm))/3600) = 0.58683 m^2."
7269,60,Body Surface Area Calculator,physical,decimal,pmc-2841068-1,Extracted,"A 26 year old man with a background of Morquio syndrome, was admitted for an elective left total hip replacement. Osteoarthritis of the hips secondary to avascular necrosis of the head of femur bilaterally had been diagnosed. There was no past medical history of note; however review of systems revealed snoring and daytime somnolence, suggestive of obstructive sleep apnoea. Clinical inspection demonstrated a man of short stature, his weight was 63 Kg and height 150 cm, with a large head and short neck, the head appeared to be sitting directly on his thorax. On inspection the thorax had an increased anterior-posterior diameter and kyphosis. Clinical examination including respiratory, neurological and cardiovascular systems were normal. Pulmonary function testing and baseline laboratory tests were normal.
Preoperative airway examination demonstrated bulky soft tissue in the pharynx, grade 2 macroglossia, an enlarged uvula and tonsils, an exuberant gag reflex and a Mallampatti grade II airway. Preanaesthetic neutral and extension cervical x-rays were performed and demonstrated a hypoplastic odontoid process, and widening of the atlanto axial joint upon flexion, the joint measured 3 mm in diameter, the upper limit of normal (figure ). Magnetic Resonance Imaging (MRI) of the cervical spine revealed an intermedullary syrinx extending from the second cervical vertebra spine down to the thoracic spine (figure ), this findings ruled out regional spinal anaesthesia. Based on these findings and after discussion with the patient, an awake fibreoptic intubation for the procedure was planned.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [63.0, 'kg'], 'height': [150.0, 'cm']}",1.62019,1.53918,1.7012,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 150.0 cm. 
The patient's weight is 63.0 kg. 
Therefore, the patient's bsa is sqrt((63.0 (in kgs) * 150.0 (in cm))/3600) = 1.62019 m^2."
7270,60,Body Surface Area Calculator,physical,decimal,pmc-3600137-1,Extracted,"B.P. was a 36-year-old man at the time of presentation to the plastic surgery service for management of massive scrotal edema of three years' duration. This morbidly obese gentleman described a chronic course of slowly enlarging scrotum, abdomen, and lower extremities. His scrotal size made walking difficult and required specially tailored trousers. During this period, he had been hospitalized three times with diagnoses including cardiomegaly, right ventricular strain, polycythemia, obstructive sleep apnea, possible chronic obstructive pulmonary disease, lower extremity cellulitis, and elephantiasis.
On admission, the patient demonstrated a dusky color, mental dullness, and a tendency to fall asleep, but denied shortness of breath, chest pain, orthopnea, paroxysmal nocturnal dyspnea, or palpitations. In response to questions regarding his sleep, he related that he had been told he snored very loudly, but had no information about nocturnal breath cessation. He alleged that he slept four to twelve hours a night and denied any morning somnolence or headache.
On physical examination his blood pressure was 130/90, his pulse was 95, his respiratory rate was 24, and he was afebrile. His weight was 198 kg, and his height was 178 cm. He demonstrated severe obesity, and intertrigo was evident in the large lower abdominal folds and in the groin. Direct examination of the oropharynx showed a large tongue, tonsils, uvula, and soft palate. Direct examination and nasal endoscopic examination revealed significantly reduced caliber of the oropharynx. There were no external or intrinsic masses, exudates, or ulcers. The neck was extremely thickened. Auscultation of the lungs revealed end-expiratory wheezing throughout the lung fields. There were no crackles. He showed severe edema of his lower legs, and a scrotum of massive proportions (). The skin over the lower abdomen, scrotum, and lower extremities showed a peau d'orange appearance. The penis was not visible, as the enlarged scrotum extended so far forward that there was only a slit through which urine issued during voiding. The scrotum measured approximately 30 cm by 60 cm in dimension. The testes were not palpable. Deep pitting edema was present from the upper thighs downward, and chronic venous stasis changes of the lower extremity were noted.
Laboratory data included a hemoglobin of 19.5 g/dL with a hematocrit of 59.8%. Arterial blood gasses on room air were pH 7.31, pCO2 63.2 mm Hg, pO2 34 mm Hg, and bicarbonate 31.9 mEq/L. The hemoglobin was 53% saturated, and the alveolar-arterial oxygen tension gradient was 50 mm Hg. Pulmonary function testing revealed a mixed pattern of dysfunction with severe restriction and mild obstruction. The forced vital capacity (FVC) was 2.10 L (37% of predicted value), the forced expiratory volume in one second (FEV1) 1.44 L (34% of predicted value), and the FEV1/FVC ratio was 68%.
Pulmonary medicine and cardiology consultations were immediately sought. The patient was placed on continuous monitoring with ECG and pulse oximetry monitors. Chest X-ray revealed diffuse bilateral alveolar infiltrates and an enlarged heart. ECG demonstrated sinus rhythm of 100 beats per minute, right ventricular hypertrophy, and a right bundle branch block. Medical therapy with diuretics and inotropic agents was begun. Supplemental oxygen was initially withheld because even very low flow rates resulted in marked progression of his hypercapnia and respiratory acidemia.
During the first few days of his hospitalization, our patient demonstrated daytime hypersomnolence, confusion, and extreme irritability—mental status changes attributed to his prolonged hypoxia. During sleep at night, he was noted to snore loudly and experience mild chest collapse on inspiration. Apneic episodes of variable duration were noted at the bedside with the patient demonstrating inspiratory effort and a lack of air movement. After several days, nocturnal oxygen was administered by a 24% Venturi oxygen mask. Despite this therapy, fingertip pulse oximetry revealed saturations in the 49–72% range.
Following this dramatic desaturation, preliminary diagnostic polysomnography was conducted during a daytime nap in the sleep laboratory and revealed severe obstructive sleep apnea with an average of 120 abnormal obstructed breathing events (apneas plus hypopneas) per hour of sleep, each lasting greater than 10 seconds. These events were associated with profound oxyhemoglobin desaturations to as low as 50% and frequent arousals and awakenings from sleep. Though this study allows for prompt diagnosis of OSA with high sensitivity, specificity, and accuracy, it does not allow for the observation of sufficient REM sleep to measure disordered breathing episodes during this stage []. However, in this patient's case, enough apneic episodes were observed to make the diagnosis of OSA based on this preliminary testing. Nighttime polysomnography was later conducted and confirmed that the patient was suffering from OSA.
Tracheostomy was performed. Serial arterial blood gases subsequently demonstrated improved oxygenation. The patient was maintained on 24% humidified O2 at night by tracheostomy collar, and he began to make dramatic clinical improvement.
Over the next two weeks in the hospital, this gentleman lost approximately 70 lbs. (31.8 kg). His mental status and mood improved, his exercise tolerance increased, and his lymphedematous scrotum decreased markedly in size (). He was discharged on furosemide 40 mg PO daily, potassium supplementation, and nystatin powder for his intertrigo. The patient was able to walk comfortably and resume wearing trousers without modification.
Followup at two months demonstrated marked improvement in mental status. Arterial blood gases revealed normal pH and pCO2 and only mild hypoxemia (pO2 66 mm Hg). Subsequent outpatient follow-up visits documented additional improvement and continued weight loss.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [198.0, 'kg'], 'height': [178.0, 'cm']}",3.1289,2.97245,3.28534,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 178.0 cm. 
The patient's weight is 198.0 kg. 
Therefore, the patient's bsa is sqrt((198.0 (in kgs) * 178.0 (in cm))/3600) = 3.1289 m^2."
7271,60,Body Surface Area Calculator,physical,decimal,pmc-5090078-1,Extracted,"A 17-year-old female with no medical history complained of general fatigue and bradycardia from three months before. Her height, body weight, and body mass index (BMI) were 161 cm, 45 kg, and 17.4 kg/m2, respectively. A physical examination indicated that the blood pressure and heart rate are 87/46 mmHg and 38 beats/min, respectively. Laboratory data indicated an elevation of hepatic enzymes (aspartate aminotransferase, 21 IU/L; alanine aminotransferase, 28 IU/L), hypoproteinemia (total protein, 6.1 g/dL; albumin, 3.9 g/dL), hypoglycemia (blood glucose, 67 mg/dL), and a decrease in free triiodothironene (FT3) and free thyroxine (FT4) levels (FT3, 0.87 pg/mL; FT4 0.87 ng/dL). Thyroid stimulating hormone (4.610 μIU/L) was normal. The total blood ketone level was high (114 mmol/L), but the levels of thiamin (2.7 μg/dL), cobalamin (548 pg/mL), folic acid (4.8 ng/mL), growth hormone (6.17 ng/mL), and adrenocorticotropic hormone (31.3 pg/mL) were within normal limits. An electrocardiogram showed bradycardia with junctional rhythm and prolonged QT interval (). A cardiac echocardiogram showed reduced left ventricular ejection fraction (LVEF 45%) with apical wall motion decline of both ventricles and both ventricles were dilated (LV diastolic dimension: LVDd 52 mm) (). A coronary angiogram showed no stenosis or obstruction, and cardiac magnetic resonance imaging (MRI) did not show late gadolinium enhancement. An endomyocardial biopsy revealed moderate vacuolar degeneration, hypertrophy, and attenuation of the myocardium as well as moderate interstitial fibrosis. Any inflammatory cell infiltrate, myocardial edema, or necrosis was not observed (). The patient was diagnosed with idiopathic dilated cardiomyopathy with sick sinus syndrome at the time.
An angiotensin-converting-enzyme inhibitor (perindopril) was prescribed without pacemaker implantation since the fatigue was clearly not related to the bradycardia. During the follow-up, cardiac echocardiographic findings after four months did not improve (LVEF 44%, LVDd 49 mm); her body weight reduced to 34.1 kg (BMI 13.6 kg/m2) after losing 16 kg in six months, and she was diagnosed with anorexia nervosa (AN) by a psychiatrist. The patient received nutritional counseling and appropriate psychotherapy to increase her caloric intake. One month later, her body weight increased to 43.5 kg (BMI 16.8 kg/m2), heart rate (HR) increased to 66 beats/min with sinus rhythm, and LVEF increased to 55%. One year later, her body weight increased to 54 kg (BMI 20.8 kg/m2), HR increased to 70 beats/min, and LVEF rose to 60%.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.0, 'kg'], 'height': [161.0, 'cm']}",1.41863,1.3477,1.48956,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 161.0 cm. 
The patient's weight is 45.0 kg. 
Therefore, the patient's bsa is sqrt((45.0 (in kgs) * 161.0 (in cm))/3600) = 1.41863 m^2."
7272,60,Body Surface Area Calculator,physical,decimal,pmc-4371897-1,Extracted,"A 68-year-old female without ocular complaints had been taking HC for 8 years for management of Sjögren’s syndrome. She was 155 cm tall and weighed 68 kg. Her daily dose based on ideal body weight was 7.34 mg/kg/day and her cumulative dose was 1,168 g. She had no concomitant liver or renal disease.
Her visual acuities with correction were OD (right eye) 20/25+1 and OS (left eye) 20/30+3.
HC toxicity was diagnosed based on taking a potentially toxic dose of HC in conjunction with a paracentral depression on visual field testing and SD OCT showing paracentral thinning of the outer retinal layers in both eyes (). Although ophthalmoscopy revealed no apparent pigmentary abnormalities, the near infrared reflectance images showed a bull’s eye pattern of increased paracentral reflectance (). FAF revealed no evidence of hyperautofluorescence in either macula (). Color fundus photography () and fluorescein angiography also failed to show a bull’s eye maculopathy.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [68.0, 'kg'], 'height': [155.0, 'cm']}",1.71108,1.62553,1.79663,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 155.0 cm. 
The patient's weight is 68.0 kg. 
Therefore, the patient's bsa is sqrt((68.0 (in kgs) * 155.0 (in cm))/3600) = 1.71108 m^2."
7273,60,Body Surface Area Calculator,physical,decimal,pmc-3170628-1,Extracted,"An infant girl was born at 36 weeks gestation to a healthy 23-year-old mother and 28-year-old father. Her birth weight was 2690 g (50th centile for gestational age), her birth length was 47 cm (25th centile), her head circumference was 32.5 cm (25th centile) and her Apgar score was 9/9. After the birth there were no major concerns, although patent ductus arteriosus and haemodynamically significant atrial septal defect (ASD) had been diagnosed, and pronounced dysmorphic features had been observed. She had upward and slanted palpebral fissures with ptosis of both. This was more pronounced in the left upper palpable. Hypertelorism was also observed and the nose was small in size and saddle-shaped. She had a prominent frontal part of the skull, giving the false impression of macrocrania. Her ears were low-set, asymmetrical, triangular and slightly protuberant. Both lips were accentuated in shape and sometimes stretched in an asymmetrical manner (Figure ). A high-arched palate was also observed. There was evidence of general muscular hypotonia and her developmental milestones were delayed. She sat up without help at 12 months and started walking at 18 months. Her speech development was also late, and only developed after she was three years old. Her social and psychical development were surprisingly good. A magnetic resonance imaging (MRI) scan of the brain showed hyperintensive changes in the white matter and hypoplastic corpus callosum. The electroencephalogram (EEG) was normal and there were no convulsions.
At 12 months, she suffered from serious acute pyelonephritis, and bilateral vesicoureteral reflux (VUR) was diagnosed thereafter. The ultrasound kidney volumes were normal with no major dilatation of the renal pyelon. The endoscopic treatment of the VUR was performed on two occasions. Lastly, after classical surgical treatment, the VUR was successfully treated. At that time, her neurodevelopment was equivalent to that of a 9-month-old infant.
Assessments of the child are being carried out every six months. With the exception of one case of pneumonia and one case of acute laryngitis, no additional health problems had been reported. There were no recurrent urinary tract infections.
The girl is currently 5 years old. She weighs 15.5 kg (10th centile), has a height of 110 cm (50th centile) and a head circumference of 49 cm (10th centile). The dysmorphic features are still prominent. She has lower basic muscle tone, especially in the shoulder muscles and the pelvic girdle. Her muscle strength is fairly good and her reflexes are normal. There are no major problems with fine motorics and there are no abnormal movements or contractures. Her palms, especially hypothenar, are hypoplastic and her fingers are thin. Her foot arches are prominent. Hips incline to internal rotation with knees adduction and inward feet rotation, which has no major impact on her gait. Both renal function and blood pressure are normal. At present, she is preparing for the correction of a congenital heart defect.
She is managed with a team of experts and receives special logopaedic, psychological, and defectological assistance. The girl is motivated, cooperates and strives for success and progress. She is pleasant, friendly, good-natured and no emotional or behavioural problems have been observed. Despite her relatively normal development, a psychological examination (Goodenough Draw, Gessell Drawing Test, Brunet-Lesine scale, Vineland Social Maturity Scale, Wechsler Intelligence Scale for Children - WISC) reveals some cognition deficits and borderline intellectual functioning, requiring specialised help and causing delays in her formal education. She follows and understands simple instructions, speaks in sentences, but her pronunciation is unclear. Her global intelligence quotient is 76 (WISC test). Her social maturity meets the requirements of a 5-year-old child (Vineland Social Maturity Scale). According to the Brunet-Lezine scale, her mental age is that of a 4.6 year old child.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [15.5, 'kg'], 'height': [110.0, 'cm']}",0.68819,0.65378,0.7226,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 110.0 cm. 
The patient's weight is 15.5 kg. 
Therefore, the patient's bsa is sqrt((15.5 (in kgs) * 110.0 (in cm))/3600) = 0.68819 m^2."
7274,60,Body Surface Area Calculator,physical,decimal,pmc-3505917-1,Extracted,"The patient was a 72-year-old female with bilateral Crowe type IV developmental dysplasia of the hip. Her chief complaint was enlargement and pain in her left buttock. Her history included congenital dislocated hips and elderly depression. She underwent a valve replacement 2 years prior due to mitral insufficiency and had been taking 1 mg of warfarin and 100 mg of aspirin daily. There was no appreciable family history.
She experienced enlargement and severe pain in the left buttock on April 26 without an obvious etiology such as trauma. The severe pain led to self-injury, and she was transported to an emergency hospital in hemorrhagic shock. She was diagnosed with elderly depression and was transferred to a psychiatric hospital on May 7th. Her laboratory tests showed that she had severe anemia (Hgb 5.1 g/dL). Thus, she was transferred to Hospital A on June 8th and underwent systemic examinations for anemia, including colonofiberscopy. However, a bleeding source such as gastrointestinal hemorrhage was not found. She was transferred to Hospital B on June 19th for further examinations and then came to our hospital on July 1st due to a suspected hematoma in her left hip joint as well as suppurative hip arthritis.
At the time of admission, her height was 148 cm, and her weight was 40 kg. Her blood pressure was 93/58 mmHg with a pulse of 62/min. Her body temperature was 35.9 degrees Celsius. She experienced severe motion pain in her left hip joint with flexion contracture. Her left buttock, groin, and proximal thigh were significantly enlarged, and the skin was tense. The blood laboratory tests revealed high levels of WBC at 10700/μL, and the CRP was 10.8 mg/dL. The severe anemia was reported as follows: RBC 171 × 104/dL, Hb 5.5 g/dL, Ht 18%, and platelets 28.5 × 104/dL, PT-INR 1.34. Ultrasonography expressed a cystic lesion in her left buttock, and echo-guided paracentesis showed a blood-like fluid.
Radiograph showed bilateral Crowe type IV developmental dysplasia of the hip (). A plain CT showed a cavity that expanded from the left hip joint to the buttock and the thigh. A contrast-enhanced CT revealed extravasation of the contrast medium into the cavity, indicating arterial bleeding (). Angiography revealed hemorrhaging from a lateral femoral circumflex artery, and regurgitation from the cavity (Figures and ). We diagnosed her with a deep femoral artery pseudoaneurysm.
The embolization was chosen for the treatment. A catheter was inserted through the right femoral artery. After a balloon catheter was placed in the left deep femoral arterial circumflex branch to prevent regurgitation, embolization was performed with 3 IDC coils as percutaneous transcatheter angioplasty (PTA).
Her anemia was improved after transfusion and embolization, and the CRP levels dropped to normal levels (). Angiography after the embolization showed no signs of hemorrhage or regurgitation from the cavity (). A contrast-enhanced CT taken 2 months after the embolization showed no hemorrhage, and the size of the hematoma was reduced (). The enlargement and pain in the buttock became mild, and she could walk with a cane at 2 months after embolization.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [40.0, 'kg'], 'height': [148.0, 'cm']}",1.28236,1.21824,1.34648,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 148.0 cm. 
The patient's weight is 40.0 kg. 
Therefore, the patient's bsa is sqrt((40.0 (in kgs) * 148.0 (in cm))/3600) = 1.28236 m^2."
7275,60,Body Surface Area Calculator,physical,decimal,pmc-5385993-1,Extracted,"A 14-year-old girl was admitted to our emergency department with a four-day history
of generalized myalgia, muscular weakness and dark urine. On the day of admission,
she noted much-reduced diuresis and had difficulty walking. During the previous
days, the patient had been participating in a dance festival in hot conditions.
There was no past history of muscle cramps or hospital admissions due to
rhabdomyolysis. She was the only child of non-consanguineous parents.
At presentation, she was dehydrated. Her blood pressure was 120/60 (90th
percentile). Her muscle strengths in the proximal and distal muscles of the upper
and lower extremities were 4/5. Deep tendon reflexes were normal, and there was no
neurologic deficit. The remainder of her physical examination was normal. Her weight
was 57kg, and her height was 165cm.
The laboratory evaluation revealed ARF with a blood urea nitrogen of 263mg/dL (range
19.3 - 44.9mg/dL), a blood creatinine of 9.59mg/dL (range 0.60 - 1.30mg/dL) and a
glomerular filtration rate calculated according to the original Schwartz formula of
11.6mL/min/1.73m2. The blood gases showed metabolic acidosis (pH
7.30; HCO3 17.7mmol/L; base excess - 7.9; lactate 1.4mmol/L). Blood
biochemistries were as follows: sodium 129mmol/L (range 136 - 145mmol/L), potassium
6.12 (range 3.4 - 5.1mmol/L), ionized calcium 1.03mmol/L (range 1.13 - 1.32mmol/L),
phosphorus 9.3mg/dL (3.1 - 5.5mg/dL), magnesium 1.8mg/dL (range 1.6 - 2.3mg/dL),
myoglobin 28173mg/dL (range 9 - 82mg/dL), creatine kinase > 400,000UI/L (range 28
- 142UI/L), aspartate aminotransferase 3266UI/L (range 0 - 26), alanine
aminotransferase 1310UI/L (range 19 - 44UI/L).
Because of massive rhabdomyolysis, the patient was admitted to our pediatric
intensive care unit and was given intravenous fluid combined with diuretic therapy
to reverse ARF, glucose and insulin therapy to correct hyperkalemia and calcium
gluconate to prevent cardiac arrhythmias secondary to ion changes. During the first
hours of admission, she presented anuria that was unresponsive to medical therapy.
After eight hours of receiving supportive therapy, she was started on continuous
veno-venous hemodiafiltration (Gambro Prismaflex® System, Lisbon;
Portugal).
A hemodialysis catheter (12F; triple lumen) was inserted in the right femoral vein.
Hemodiafltration was performed using the hemofilter ST 60, and heparin was the
anticoagulant chosen. The following initial settings were used: blood-pump
150mL/min, dialysate (Prismasol 4®) 1000mL/hr, pre-filter
replacement solution (Prismasol 4®) 500mL/hr, post-filter
replacement solution (Prismasol 4®) 500mL/hr and fluid removal
50mL/hr. During the first two days of therapy, the main problem with
hemodiafiltration was easy coagulability of the hemofilter due to high levels of
myoglobin in circulation. To overcome this problem, higher pre-dilution flow rates
were used (maximum 1500mL/h). After 48 hours, she had asymptomatic hypophosphatemia
of 2.7mg/dL that was corrected after adding phosphorous to the replacement
solutions. On day 5, intermittent hemodialysis was started, and three sessions on
alternate days were performed. A calcium antagonist was prescribed on day six due to
worsening hypertension.
Signs and symptoms were controlled with medical treatment and renal replacement
therapy. Creatinine kinase and myoglobin returned to normal values in two weeks. Her
diuresis started to recover after the second day of therapy. At discharge, her renal
function was recovering, and she had a glomerular filtration rate of
88.9mL/min/1.73m2.
Regarding the investigation of the underlying insult, an acylcarnitine analysis by
tandem mass spectrometry of the patient's dried blood spot revealed a deficiency of
very long-chain acyl-CoA dehydrogenase (VLCAD). A genetic study revealed the
following mutations in compound heterozygosity of the VLCAD gene: p.P65Tfs*7 (c.
187_192insA) and p.R336H (c.1097G > A).
Frequent meals with carbohydrate-rich intake before exercise and restriction of
long-chain fatty acids intake along with medium-chain fatty acid supplementation
were recommended to prevent further attacks.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [57.0, 'kg'], 'height': [165.0, 'cm']}",1.61632,1.5355,1.69714,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 165.0 cm. 
The patient's weight is 57.0 kg. 
Therefore, the patient's bsa is sqrt((57.0 (in kgs) * 165.0 (in cm))/3600) = 1.61632 m^2."
7276,60,Body Surface Area Calculator,physical,decimal,pmc-3763621-3,Extracted,"A 9-month old female infant, with weight 5.6 kg, length 65.9 cm (weight-for-length z-score −3.04, weight-for-age z-score −3.29, length-for-age z-score −1.89) presented in icddr,b's Dhaka Hospital. She had a history of soft stool and cough for five days, fever for three days, vomiting for one day, and respiratory distress for 10 hours. On admission, physical examination revealed a temperature of 36.6 ºC, heart rate 118/min, respiration rate 60/min, and blood pressure 60/40 mmHg. In addition, the patient was very lethargic, there was lower chest wall-indrawing and some dehydration. On auscultation, coarse crackles were found in the right lung, and the heart sounds were normal. The abdomen was soft, non-tender, and bowel sounds were present. Chest x-ray showed patchy shadowing in the right lung field, and plasma electrolyte tests revealed hypokalaemia (K 2.05 mmol/L) and hypophosphataemia (P 2.5 mg/dL). Based on the physical findings and laboratory results, an initial diagnosis of severe pneumonia complicated by severe malnutrition, sepsis, hypokalaemia, and hypophosphataemia was made. Initial treatment was given with intravenous antibiotics and fluid therapy, with additional management given according to the icddr,b's standardized management protocol for severely-malnourished children. On the second day, plasma electrolyte analysis revealed a rise in potassium (K 2.87 mmol/L) but a drop in phosphate (P 1.1 mg/dL) levels. By the 7th day of admission, the patient became afebrile, clinically much improved, and the plasma electrolytes were almost corrected (Na 138.3 mmol/L, K 2.93 mmol/L, Ca 2.0 mmol/L, and P 2.8 mg/dL). Unfortunately, the family members removed the patient from the hospital against medical advice at this point.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [5.6, 'kg'], 'height': [65.9, 'cm']}",0.32017,0.30416,0.33618,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 65.9 cm. 
The patient's weight is 5.6 kg. 
Therefore, the patient's bsa is sqrt((5.6 (in kgs) * 65.9 (in cm))/3600) = 0.32017 m^2."
7277,60,Body Surface Area Calculator,physical,decimal,pmc-2740281-1,Extracted,"A 57-year-old Caucasian female presented to our emergency department complaining of neck pain one month after having a fall from a height and an injury on her occipital bone. The patient was non-smoking, non-drinking and with a free medical history. She weighed 61 kg and had a height of 162 cm.
The patient had already visited two physicians. The first assessment was made at the day of the injury at a hospital elsewhere. This first clinical examination revealed pain at the cervical spine and deficiency in the range of the cervical spine motion but no neurologic impairment was present. No radiologic examination was ordered and the patient received analgesics and recommendation for physiotherapy sessions. Persistence of pain led to a second assessment by another physician one week later at another hospital. Analgesics were once more prescribed and radiological screening was once more not considered essential.
On examination in our department, the patient showed no neurologic deficit, whereas restriction of range of motion and pain remained. Three-view radiographs (lateral, anteroposterior and odondoid) ordered by the attending emergency physician showed bilateral C5-C6 dislocation causing instability (Figure ). CT and MRI scan showed olisthesis of C5 over C6, anterior angulation and narrowing of the spinal canal without spinal cord pressure from disc material (Figure ). The electrophysiological testing was normal.
The patient was transferred to the operating theatre at the day of the admission. Open reduction of the bilateral dislocation and spinal fusion with posterior instrumentation were performed under continuous intraoperative neurophysiological monitoring (Figure ). Duration of hospitalization was four days. Mobilization began the second postoperative day and the patient was discharged using a Philadelphia collar. After twelve months of follow up, the patient reported free of complaints and with excellent return to her every day activities.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.0, 'kg'], 'height': [162.0, 'cm']}",1.6568,1.57396,1.73964,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 162.0 cm. 
The patient's weight is 61.0 kg. 
Therefore, the patient's bsa is sqrt((61.0 (in kgs) * 162.0 (in cm))/3600) = 1.6568 m^2."
7278,60,Body Surface Area Calculator,physical,decimal,pmc-8076790-1,Extracted,"A 74-year-old female patient who had mitral valve regurgitation (MR) was admitted to our hospital because of progressive dyspnea for 6 years, and her illness worsened during the previous 2 months. Her body weight and height were 56 kg and 152 cm, respectively. She had been diagnosed with MR for 2 years and had received diuretic and inotropic therapy for a couple of months. After a preoperative physical examination, a systolic murmur (grade 4/6) was identified by cardiac auscultation at the heart apex, and the boundary of heart dullness was found to expand to the left. Transthoracic echocardiography (TTE) revealed a posterior mitral valve leaf prolapse with severe MR. In addition, the patient still had mild-to-moderate tricuspid valve regurgitation, and the pressure gradient was estimated to be 67 mmHg according to the Bernoulli equation. The left ventricular diameter was 52 mm at the section of papillary muscles, and the ejection fraction (EF) value was 74.5%. An electrocardiogram (ECG) showed sinus rhythm with a heart rate (HR) of 73 beats per minute (bpm). A chest computed tomography (CT) scan did not reveal any obvious abnormalities except for a sign of heart shadow enlargement. The patient denied any previous disease history and did not take any medication before this illness. Preoperative anesthetic assessments indicated that she was classified as American Society of Anesthesiologists III status (ASA III) and the surgical risk score was 6 (EuroSCORE of 6). The surgeons decided to replace her mitral valve under cardiopulmonary bypass (CPB).
Before anesthesia induction, the invasive blood pressure (IBP) was 138/62 mmHg after left radial artery A-line establishment. The ECG demonstrated sinus rhythm and the HR was 62 bpm. The pulse oxygen saturation (SpO2) value was 94% at room air. After induction of anesthesia with 4 mg midazolam, 50 mg propofol, 0.5 mg fentanyl, and 16 mg vecuronium bromide, the patient underwent tracheal intubation with an ID 7.0 mm tube and was then connected to an anesthetic machine for ventilation. At first, the tidal volume was 450 ml and the respiratory rate was 10 bpm. The inspiratory to expiratory ratio was set at 1:2 without an inspiratory pause. The peak airway pressure was 20 cmH2O with the presence of a positive end-expiratory pressure (PEEP) of 5 cmH2O. End-tidal carbon dioxide (ETCO2) was maintained between 35 and 45 mmHg by subsequently adjusting the ventilation frequency. The patient’s hemodynamics, SpO2, and ETCO2 were stable and were maintained in the normal range during anesthesia induction. After placement of a transesophageal echocardiography (TEE) probe and a Swan-Ganz catheter, the central venous pressure (CVP), pulmonary artery pressure (PAP), and cardiac output were monitored. The baseline PAP was 56/22 mmHg after Swan-Ganz catheter placement. Anesthesia was maintained with sevoflurane, cis-atracurium, intermittent fentanyl, and the bispectral index (BIS) value was maintained at 40–60 during most time of the surgical procedure.
After about 60 min of mitral valve replacement, the heart began to re-beat successfully after releasing the aortic clamp. The heart contractility seemed good with the help of dobutamine administered at a rate of 5 μg/kg/min. The anesthesiologist found that the peak airway pressure increased gradually from 20 to 38 cmH2O after resuming ventilation under the previous ventilator settings. The PAP was not high (10 mmHg) because the patient was still dependent on the CPB machine. The anesthesiologist excluded an inadequate anesthesia depth, airway circuit obstruction, anesthetic machine problems, pleural cavity, or mediastinal abnormalities for a short period of time. Fibrotic bronchoscopy did not reveal bronchus intubation or any obvious secretions. Bronchospasm was initially diagnosed and bronchial dilators together with sevoflurane were administered, but without any obvious effect to relieve the airway pressure. Because bronchospasm usually happens in light anesthetic state and what is more, volatile anesthetics can dilate bronchus directly. Even if it was difficult to listen to breath sound because of aseptic towel, we tried to obtain the breath sound in the two lungs. As pulmonary auscultation did not indicate obvious wet or dry rales and ETCO2 waveform did not indicate small airway obstruction, the anesthesiologist began to consider cardiogenic factors. At that time, the IBP was 75/65 mmHg and HR was 90 bpm.
Transesophageal echocardiography examination did not reveal any obvious myocardial contraction abnormalities and the CPB machine perfusion rate was 3.2 L/min. The blood reservoir showed significantly decreased venous return during this period but the surgeons did not note any obvious bleeding around the surgical field. The Swan-Ganz catheter indicated that the right heart stroke volume was much more than the sum of left ventricular outflow tract (LVOT) blood flow volume and the left atrial suction rate. Through echo measurements and calculation, we can get the left ventricle output according to the formula VTI × π × (1/2DLVOT)2 (VTI, velocity-time integral; DLVOT, diameter of LVOT). DLVOT was 0.97 cm and VTI was 5.38 cm. Therefore the stroke volume of left ventricle was almost 4 ml, but the right heart stroke volume was 12 ml through Swan-Ganz catcher measurement. The surgeons confirmed that the left atrial suction tube was working well and excluded an increase of left atrial pressure or left ventricular distension. Due to pulmonary artery blood supply and pulmonary venous return mismatching (), pulmonary congestion was diagnosed as there was no intracardiac shunt at that time. It seemed that there was no cardiac function problems and there were no effective methods to treat this congestion. In addition, the arterial blood gas (ABG) and body temperature was almost in normal ranges. The medical team decided to wean the patient off CPB gradually. Interestingly, the peak airway pressure began to decrease with progressive weaning, and almost recovered to the baseline level finally. The right heart stroke volume was then closer to the stroke volume which was detected by TEE. After the patient was weaned off CPB, DLVOT was 1.57 cm and VTI was 15.1 cm. Stroke volume of the left ventricle became to be 29.2 ml and the right stroke volume was 30 ml at that moment. The PAP was 45/17 mmHg when the patient was completely weaned off CPB. After that, the airway pressure returned to normal and did not increase again during the rest of operation. Subsequently, the patient recovered very well after the surgery.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [56.0, 'kg'], 'height': [152.0, 'cm']}",1.53768,1.4608,1.61456,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 152.0 cm. 
The patient's weight is 56.0 kg. 
Therefore, the patient's bsa is sqrt((56.0 (in kgs) * 152.0 (in cm))/3600) = 1.53768 m^2."
7279,60,Body Surface Area Calculator,physical,decimal,pmc-6211884-1,Extracted,"A 13-year-old Japanese girl with obesity, but no symptoms of chronic liver disease, was referred to our hospital because of unexplained transaminase elevations. She was born after an uncomplicated pregnancy and delivery to healthy parents having no consanguinity. She had no history of drug or alcohol intake. She had no physical findings suggesting a liver disorder, such as hepatosplenomegaly or jaundice. Vital signs and neurologic findings were normal. Height, body weight, and body mass index, respectively, were 158 cm (+0.4 SD), 67.4 kg (+2.2 SD), and 27 kg/m2 (normal range, 18.5–24.9).
Initial laboratory results included serum aspartate aminotransferase (AST), 160 U/L (normal range, <33); alanine aminotransferase (ALT), 338 U/L (<30); γ-glutamyltransferase (GGT), 99 U/L (<47); total/direct bilirubin, 0.96/0.09 mg/dL (<1.2/<0.6); albumin, 4.6 g/dL (4.0–5.0); total bile acids, 2.7 μmol/L (<10); type IV collagen, 133.0 ng/mL (<140); low-density lipoprotein cholesterol, 132 mg/dL (<139); high-density lipoprotein cholesterol 48 mg/dL (>40); fasting plasma glucose 95 mg/dL (<109); HbA1c 5.5% (4.9–6.0); and prothrombin time–international normalized ratio, 0.89 (0.87–1.25). The complete blood cell count was normal. Various causes of chronic liver disease such as autoimmune hepatitis, viral hepatitis, and other metabolic conditions were excluded by appropriate laboratory tests. Abdominal ultrasonography showed fatty liver (ultrasonographic grade 3), with a marked increase in fine echoes and little or no visualization of intrahepatic vessel outlines, the diaphragm, and the posterior right lobe of the liver (Table ).[ Liver biopsy was not performed because signs of steatohepatitis with fibrosis such as thrombocytopenia, coagulopathy, cholestasis, and elevation of serum type IV collagen all were absent.
We clinically diagnosed the patient with NAFLD and obesity, to be treated with diet and exercise. However, body weight increased. As breast enlargement at 11 years and pubic hair growth at 12 years were neither accompanied nor followed by menstruation, endocrine functions were assessed. Luteinizing hormone was <0.2 mIU/mL (0.05–2.44); follicle-stimulating hormone, 1.9 mIU/mL (0.92–3.29); free thyroxine, 0.98 ng/dL (0.93–1.70); thyroid-stimulating hormone, 0.94 μIU/mL (0.50–5.00); estradiol, <25 pg/mL (<42.8); and prolactin, 485.6 ng/mL (4.1–28.9). Cranial magnetic resonance imaging (MRI) including contrast administration showed a pituitary mass consistent with macroadenoma (Fig. A). We diagnosed the patient with PRLoma and treated her with cabergoline, a dopamine agonist, at a dose of 0.25 to 3.5 mg/wk (Table ). In addition to tumor shrinkage demonstrated by MRI (Fig. B), her weight and serum AST/ALT and GGT decreased, as did the ultrasonographic grade of fatty liver disease (Table ). Menarche occurred 21 months after initiation of cabergoline, when serum prolactin was 32.8 ng/mL.
Currently, 2 years after initiation of cabergoline, the patient is receiving cabergoline at a dose of 3.5 mg/wk.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [67.4, 'kg'], 'height': [158.0, 'cm']}",1.71992,1.63392,1.80592,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 158.0 cm. 
The patient's weight is 67.4 kg. 
Therefore, the patient's bsa is sqrt((67.4 (in kgs) * 158.0 (in cm))/3600) = 1.71992 m^2."
7280,60,Body Surface Area Calculator,physical,decimal,pmc-7674726-1,Extracted,"A 71-year-old man (55 kg, 149 cm) was admitted to the hospital for total laparoscopic distal gastrectomy under general anesthesia. During surgery, insufficient muscle relaxation was reported repeatedly by surgical team.
General anesthesia was induced and maintained with 2% propofol and remifentanil using target-controlled infusion. When the patient became unconscious, TOF stimulation of the right ulnar nerve was initiated using a peripheral nerve stimulator (NMT module of the Carescape monitor B850; GE Healthcare, Madison, WI, United States). The initial TOF ratio was 0.98, and the patient then received a bolus injection of rocuronium 50 mg (0.9 mg/kg). According to routine practice, we waited to perform intubation until a TOF count of 0 was observed. The TOF ratio decreased at an unusually slow rate, and a TOF count of 0 was detected approximately 7 min after the administration of rocuronium (Figure ). After successful endotracheal intubation, however, a TOF count of 1 was detected within 1 min, and a TOF ratio of 12% was detected within 2 min. Rocuronium 5 mg was then injected followed by a continuous infusion at a rate of 9 µg/kg/min for deep neuromuscular blockade (post-tetanic count of 1-2). However, a TOF count of 4 (TOF ratio < 10%) was continuously recorded and visually detected. The surgical team noted insufficient muscle relaxation 20 min after the start of the laparoscopic procedure.
The patient had previously been diagnosed with dementia and mild parkinsonism with tremor and had been taking donepezil 5 mg, quetiapine 25 mg, and pregabalin 75 mg twice a day for 16 mo. He had been taking anti-hypertensive medication for 11 years and had undergone diaphragm surgery in our hospital 7 and 10 years prior. During these two surgeries, he required rocuronium 50 mg during 195 min of balanced anesthesia with sevoflurane-remifentanil and rocuronium 60 mg during 225 min of TIVA with propofol-remifentanil. No specific events or comments regarding insufficient muscle relaxation were identified from a review of his anesthesia records of previous surgeries.
The patient had no history of smoking or alcohol abuse. He had no family history of cancer or any other hereditary diseases.
During general anesthesia, vascular access for intravenous anesthetics and NMBAs was well secured, and the patient’s vital signs and state entropy (Entropy module of the Carescape monitor B850; GE Healthcare, Madison, WI, United States) were within the normal ranges, which indicated adequate depth of anesthesia. Using forced-air warming blankets, the central core temperature and skin temperature over the adductor pollicis muscle were maintained above 35.5 °C and 32 °C, respectively. The preoperative physical examination was unremarkable.
The results of preoperative laboratory tests and electrocardiography were normal.
The preoperative chest X-ray showed elevation of the left diaphragm, which was considered evidence of previous diaphragm surgeries.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.0, 'kg'], 'height': [149.0, 'cm']}",1.50877,1.43333,1.58421,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 149.0 cm. 
The patient's weight is 55.0 kg. 
Therefore, the patient's bsa is sqrt((55.0 (in kgs) * 149.0 (in cm))/3600) = 1.50877 m^2."
7281,60,Body Surface Area Calculator,physical,decimal,pmc-3668108-3,Extracted,"A 64-year-old man, 67 kg, 163 cm, ASA physical classification status II with esophageal cancer, was scheduled for a esophagogastrectomy, through a right thoracotomy approach. The preoperative CT examination revealed a displaced right upper lobe bronchus, approximately 1 cm above the carina (). Left-sided OLV, using a 37 F DLT, instead of a blocker, was planned. After anesthetic induction, a left-sided DLT was placed. A fiberoptic bronchoscope was then passed down the tube and confirmed the presence of a RUL bronchus, located in an aforementioned site (). The right lung isolation was satisfactory and the case proceeded uneventfully.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [67.0, 'kg'], 'height': [163.0, 'cm']}",1.74173,1.65464,1.82882,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 163.0 cm. 
The patient's weight is 67.0 kg. 
Therefore, the patient's bsa is sqrt((67.0 (in kgs) * 163.0 (in cm))/3600) = 1.74173 m^2."
7282,60,Body Surface Area Calculator,physical,decimal,pmc-8409215-1,Extracted,"A previously healthy 12-year-old boy was admitted to the hospital on February 12, 2016 with complaints of blepharoptosis, voice hoarseness, fever, and the inability to walk and talk.
The patient exhibited persistent blepharoptosis, voice hoarseness, and fever for about 2 mo. He then became severely agitated with the main complaints of sleepiness, dysphagia, limb weakness, and respiratory and circulatory failure. The patient unfortunately died soon thereafter.
The patient was diagnosed with subacute ptosis at 12-years-old.
The patient was delivered vaginally at term with a birth weight of 3250 g and without developmental delay. His height was 156 cm and weight was 50 kg upon admission to the hospital. The patient's mother exhibited no abnormal symptoms after the birth. The family history of the patient regarding a similar condition was negative.
Clinical examination showed that the patient presented with pyramidal signs and very easily elicited reflexes and extensor toe signs on both feet.
The routine blood and urine tests, urinary sediment examination, routine fecal tests, and occult blood test were performed, which all showed normal results. The arterial blood gas was tested and the pH value was 7.32. The oxygen pressure was 11.3 kPa, the carbon dioxide pressure was 4.9 kPa, and the oxygen saturation was 99%. The arterial plasma lactate level was slightly elevated to 3 mg/dL. Ammonia and blood sugar levels were normal. Other blood biochemistry indexes were also normal. The cytological and biochemical examination showed the normal presence of cerebrospinal fluid (CSF)-positive antibodies to acetylcholine, presynaptic membrane receptor, and thymoma in the blood, and positive oligoclonal bands in the CSF. The antibody tests to Mycoplasma pneumoniae, herpes simplex virus, and Epstein-Barr virus were negative. Gene sequencing analysis revealed a T-to-C transition at nucleotide 9176 of the mitochondrial ATPase 6 gene (Leu to Pro) in the patient and a heteroplasmic mutation in the patient’s mother (Figure ).
Electroencephalogram analysis revealed slow-waves of background activity. The brain MRI scan showed symmetrical abnormal signals in the basal ganglia, medial thalami, periaqueductal region of the midbrain and pons, and the bilateral white matter around the lateral ventricles (Figure ).",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [50.0, 'kg'], 'height': [156.0, 'cm']}",1.47196,1.39836,1.54556,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 156.0 cm. 
The patient's weight is 50.0 kg. 
Therefore, the patient's bsa is sqrt((50.0 (in kgs) * 156.0 (in cm))/3600) = 1.47196 m^2."
7283,60,Body Surface Area Calculator,physical,decimal,pmc-7463145-2,Extracted,"A girl named G, 7 years old, with LMA, 2nd day of treatment. At the time of assessment, the child had had a fever for two days with a peak of 40°C. The child also complained of nausea and of having vomited twice, one day before admission to hospital. There were petechiae in the child’s right hand. Conjunctiva anemic, Hb value: 6.8 gr/dL, Ht: 18.4%, leukocytes: 330/mm3, platelets: 5000/mm3, ANC 39/mm3, BP: 89/65 mmHg, HR: 140 x/minute, RR: 30 x/minute, body temperature 40.30°C, SpO2: 98%, BW: 23 kg, BH: 120 cm. The child’s nutritional status was good, with mild chest retraction. The child’s hydration status was adequate, with a positive fluid balance and without any signs of overload. The child’s rest and sleep statuses were adequate.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [23.0, 'kg'], 'height': [120.0, 'cm']}",0.8756,0.83182,0.91938,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 120.0 cm. 
The patient's weight is 23.0 kg. 
Therefore, the patient's bsa is sqrt((23.0 (in kgs) * 120.0 (in cm))/3600) = 0.8756 m^2."
7284,60,Body Surface Area Calculator,physical,decimal,pmc-2816343-1,Extracted,"A 54-yr-old man was hospitalized following a suicide attempt. For the last 2 months the patient had suffered from depression, anxiety, insomnia, and delusion. At the time of admission, physical examination of this man showed normal blood pressure, heart rate, and body temperature. His body weight was 66.8 kg and he was 165.5 cm in height. EKG finding was unremarkable. Results of routine laboratory tests were normal.
After initial assessment, he was diagnosed as major depression with psychotic symptoms. NT (50 mg/day), lorazepam (1 mg/day), and risperidone (2 mg/day) were initially prescribed. Supportive psychotherapy was also provided. The patient's dose of NT was then increased gradually to 100 mg/day, administered on a divided-dose schedule. Determination of plasma NT level was performed by high-performance liquid chromatography using Hewlett Packard 1090 system (Hewlett Packard GmbH, Waldbronn, Germany). The plasma concentration of NT after 6 days of treatment with 100 mg of daily dose was 181.4 ng/mL (recommended therapeutic range: 50-150 ng/mL).
However, in an attempt to achieve further clinical improvement, the NT dosage was increased to 150 mg/day over 20 days, which resulted in plasma concentrations of 470.6 ng/mL after 6 days. He reported experiencing dry mouth, constipation, and dizziness. Because of this unexpectedly high drug level and worsening of anticholinergic side effects, the patient's dosage was reduced to 100 mg/day. The following measurements indicate that NT concentrations were reduced (198.7-222.7 ng/mL) but still remained higher than the recommended therapeutic range. The patient was discharged after 1 month of hospitalization with a maintenance dose of 100 mg/day.
This patient underwent CYP2D6 genotyping test after informed consent. CYP2D6 gene was amplified by long PCR, to analyze all 9 exons of CYP2D6 gene (). All PCR products were sequenced using ABI PRISIM BigDye Terminator Cycle Sequencing Kit (Applied Biosystems, Foster City, CA, U.S.A.) and an ABI Prism 3100 Genetic Analyzer (Applied Biosystems). CYP2D6*5 allele was detected using long PCR as described by Hersberger et al. (). A fragment specific for deletion of CYP2D6 gene was obtained with the forward primer specific for exon 9 of CYP2D7 and the reverse primer specific for the 3'flanking region of CYP2D6. The patient was found to have CYP2D6*5/*10B, which results in low CYP2D6 activity (, ).
He has been continuing supportive psychotherapy at the outpatient clinic monthly and remains improved, even though his NT dose has been reduced to 50 mg/day.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [66.8, 'kg'], 'height': [165.5, 'cm']}",1.75241,1.66479,1.84003,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 165.5 cm. 
The patient's weight is 66.8 kg. 
Therefore, the patient's bsa is sqrt((66.8 (in kgs) * 165.5 (in cm))/3600) = 1.75241 m^2."
7285,60,Body Surface Area Calculator,physical,decimal,pmc-7716315-1,Extracted,"A 74-year-old man presented with dyspnea on exertion that started two months earlier.
The patient presented anemia and a hemoglobin level of 6.4 g/dL during an ophthalmology consultation for cataract treatment. The patient presented dyspnea on exertion, a symptom that had aggravated over the past two months. The patient visited the hematological department.
The patient had a past medical history of cataract and ossification of a posterior longitudinal ligament.
The patient had been a smoker for 50 years.
Vital signs were within normal limits at presentation, with a heart rate of 80 bpm, blood pressure of 135/60 mmHg, and a temperature of 36.1 ℃. His height and weight were 171 cm and 75 kg, respectively.
Laboratory tests indicated a WBC count of 2190 cells/µL, a hemoglobin level of 6.2 g/dL, a platelet count of 7.4 × 104/µL, a lactate dehydrogenase level of 283 IU/L, and a ferritin level of 620.41 ng/mL. The WT1 mRNA was 4800/µg RNA of peripheral WBCs, and the serum d-ROM level was 435 Carratelli units. The bone marrow aspiration was dry tap, and the bone marrow biopsy showed MDS with fibrosis.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [75.0, 'kg'], 'height': [171.0, 'cm']}",1.88746,1.79309,1.98183,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 171.0 cm. 
The patient's weight is 75.0 kg. 
Therefore, the patient's bsa is sqrt((75.0 (in kgs) * 171.0 (in cm))/3600) = 1.88746 m^2."
7286,60,Body Surface Area Calculator,physical,decimal,pmc-4430750-1,Extracted,"We present a case report of a 73-year-old male (91.5 kg, height - 184 cm) referred to our hospital with acute on chronic COPD exacerbation and Type 2 respiratory failure not responding to conventional nonivasive ventilation. Later patient developed multiple organ dysfunction syndrome with Type 2 respiratory failure with mixed acidosis.
His presenting blood gases showed profound acidemia. pH - 7.057, base excess - 7.5, PCO2-11.23 kPa, PaO2-13.7 kPa on FiO2-50%. P: F ratio was around 200. His inflammatory markers were high (total leukocyte count [TLC] 26 × 109/L, procalcitonin 11.2 mcg/L, C-reactive protein [CRP] 104 mg/L) and renal functions worsened and he was oliguric.
He was started on appropriate antibiotics and noninvasive ventilation. He was started on noradrenaline infusion to target mean arterial pressure of 70 mm Hg. Continuous veno-venous hemodiafiltration instituted to manage his renal failure with an aim for a negative fluid balance of 1.5 L. Hemodynamic monitoring was done by pulse-induced contour cardiac output.
After 12 h, he continued to be acidotic profoundly because of raised PaCO2-10.86 kPa. Failure to remove CO2 was noted despite being on non-invasive ventilation. His chest was clear B/L on auscultation. His vasopressors requirements increased as he continued to be acidotic due to high PaCO2 levels.
Extracorporeal carbon dioxide removal veno-venous (Hemo Lung Respiratory Assist System: Alung Technologies Inc.) was instituted at that time to normalize his acid-base imbalance, which was due to increased PaCO2.
He was started on pump flow - 0.56 L/min, sweep flow - 10 L/min, sweep FiO2-1.0, CO2 removal at 6-10 L of sweep flow, which removed CO2 about 75-100 ml/min. His activated partial thromboplastin time ratio was targeted around 1.2-1.6. Platelets, fibrinogen, and Hb monitored periodically to recognize any signs of bleed/disseminated intravascular coagulation.
Sweep flows were adjusted according to blood gas CO2 values. Heparin infusions were initially avoided as he was coagulopathic, but added later during weaning phase.
It was noted that after starting him on ECCO2R, pH improved to 7.30 as PaCO2 normalized to around 6.5 kPa.
He was continued on non-invasive ventilation on bi-level positive airway pressure MODE with aim Sats >90%, pH >7.3, R/R <30. His inflammatory markers improved. TLC was 16 × 109/L, CRP 46 mg/L, procalcitonin was 0.9 mcg/L enteral nutrition was continued throughout.
Extracorporeal carbon dioxide removal and adjusting sweep flows and actually to be able to monitor CO2 levels removed per minute helped to adjust his ventilator settings accordingly.
Continuous veno-venous hemodiafiltration was turned off as renal function recovered.
Unfortunately patient had sepsis relapse. He turned acidotic and work of breathing worsened. Sweep flows on veno-venous CO2 removal were again adjusted as per demand. This helped to manage the patient without increasing any support on conventional ventilation and hence no increased sedation/paralyzing agents were required.
Extracorporeal carbon dioxide removal was turned off after 20 days when his infection was treated adequately.
Sweep flows were gradually taken down to minimal levels to provide minimal CO2 removal. A decrease in every liter of gas flow was made only after when a patient had been stable on it for 6-10 h. A sweep flow of 4 L/min accounted for 80 ml/min as opposed to about 45 ml/min when on 1 L/min.
He developed critical illness related weakness and had a prolonged weaning and rehabilitation by extensive physiotherapy, after which he was successfully decannulated and discharged from the intensive care unit.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [91.5, 'kg'], 'height': [184.0, 'cm']}",2.16256,2.05443,2.27069,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 184.0 cm. 
The patient's weight is 91.5 kg. 
Therefore, the patient's bsa is sqrt((91.5 (in kgs) * 184.0 (in cm))/3600) = 2.16256 m^2."
7287,60,Body Surface Area Calculator,physical,decimal,pmc-7315195-1,Extracted,"The case involves a then 43-year-old female presenting at the family physician in September 2014 with two painless lumps of about 5 mm in diameter on both the upper and the lower eyelid of the right eye. Initially, the physician advised her to clean the eyelids thoroughly, avoid application of cosmetic products, and frequently apply hot compresses to the lumps. She also suffered from dry eyes for which he prescribed hypromellose 3% eye drops. After 1 month, the lumps decreased in size to almost half the initial diameter. However, at this stage they became red and painful. The patient received an antibiotic ointment (tetracycline 1%). After about 2 weeks, she still suffered from the inflamed lumps. The physician then referred her to an ophthalmic clinic.
The ophthalmologist diagnosed the lesions as chalazia and planned for surgery. On December 12, 2014, he performed the first incision and curettage while he excised the second one similarly on January 12, 2015. The patient recovered without complications. In April 2015, two other chalazia occurred on the upper lid of the left eye, while a small one presented on a different location of the upper eyelid of the right eye. On July 24, 2015, the ophthalmologist performed the surgical procedure on the chalazia of the left eye. In August 2015, the recent right eye chalazion achieved a size of about 5 mm and became inflamed. Another chalazion had occurred on the upper left eyelid. Since the patient was due to travel abroad shortly after that, it was decided to inject the lumps with triamcinolone (40 mg/mL). Both lesions regressed in size within 2 weeks.
However, after returning to the country at the end of September, they regained their original size. In October and November 2015, they were excised. By February 2016 there were already two lesions again, and by the end of 2016 she had undergone an additional three surgical procedures to remove chalazia. In December 2016 there were still two lesions in the upper lids of both eyes. The patient was very annoyed at this point and refused further invasive procedures. She decided to leave it as is and to continue with hot compresses, however, without much success.
In a last attempt, the physician performed routine laboratory tests including a lipid profile and evaluation of the reproductive hormones (estrogen, progesterone, luteinizing hormone, follicle-stimulating hormone, prolactin, and testosterone) and thyroid-stimulating hormone (TSH). All results were well within the normal range. However, the TSH was 3.9 mIU/L, which was close to the upper limit. Based on this result he did a full evaluation of the thyroid hormones. These results were 4.2 mIU/L (0.4–4.0 mIU/L) for TSH, 70 nmol/L for thyroxine (T4) (70–163 nmol/L), 8 pmol/L for free T4 (fT4; 10–24 pmol/L), and 1.0 nmol/L for tri-iodothyronine (T3) (1.1–2.6 nmol/L).
There were no clinical signs of hypothyroidism. She was not overtly obese (157 cm in height and 59 kg in weight) and the resting heart rate varied from 70 to 90 beats/min. In general, she always felt well, had a good appetite with regular stools, and a menstrual cycle of 28 ± 2 days. Suspecting a borderline subclinical hypothyroidism, the physician started treatment with a low dose of levothyroxine (6.25 μg/day) and gradually increased it to 12.5 μg/day within the span of 3 weeks. The patient did not show any adverse reactions to this treatment. Remarkably, both the original chalazia and a third one that developed in the meantime in the upper left eyelid gradually reduced in size. Concomitantly, the inflammation also disappeared and 4 months later, in August 2017, they had all vanished. No new chalazia had developed and the dry eyes were no longer an issue. TSH reduced to 1.4 mIU/L, T4, fT4, and T3 increased to 86 nmol/L, 14 pmol/L, and 1.3 nmol/L, respectively.
In January 2018, the physician decided to taper off the treatment in the course of 2 months under monitoring of the thyroid hormones. In April 2018, after cessation of the levothyroxine supplementation, a lump started to grow in the lower right eyelid. Laboratory values revealed again borderline values for the hormones T4 (80 nmol/L), fT4 (12 pmol/L), and T3 (1.0 nmol/L). TSH was within the normal range at 2.0 mIU/L. After 2 months, the lesion started to grow quickly and another one was developing in the lower left eyelid. In July 2018, treatment with levothyroxine was restarted at 12.5 μg/day. By October, both lumps had disappeared completely. From January 2019 the dose of levothyroxine was reduced to 6.25 μg/day. No new chalazia occurred up to October 2019 . The patient remains on a low-dose regimen of thyroxine.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [59.0, 'kg'], 'height': [157.0, 'cm']}",1.60407,1.52387,1.68427,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 157.0 cm. 
The patient's weight is 59.0 kg. 
Therefore, the patient's bsa is sqrt((59.0 (in kgs) * 157.0 (in cm))/3600) = 1.60407 m^2."
7288,60,Body Surface Area Calculator,physical,decimal,pmc-3127315-1,Extracted,"An 18-year-old female patient with body weight 145 kg, height 164 cm, and body -mass index (BMI) 53.9 was posted for LSG. Preoperatively, her blood pressure was 118/68 mmHg, pulse 70/min, temperature 36.8°C, and she had a history of occasional attacks of bronchial asthma (seasonal). Her preoperative SaO2 % on room air was 99%, and there was no history suggestive of obstructive sleep apnea. Her pre-operative investigations did not reveal any abnormality except a large fatty liver. She was pre-medicated with omeprazole 40 mg IV and metoclopramide 10 mg IV 2h before surgery and midazolam 2 mg IV was administered in the receiving area of the operation theatre. She had received 3500 IU of tinaparin 2 h earlier. Graduated compression stockings were applied before the surgery. Ceftriaxone1000 mg was administered intravenously an hour prior to the surgery.
On arrival to the operation room, the monitors were attached and she was pre-oxygenated for 2 min. Anaesthesia was induced, with the patient in the 30° anti-trendelenberg position, with IV fentanyl 100 μg, IV lignocaine 60mg, IV propofol 200mg, and cisatracurium 18mg. Her trachea was intubated with a 7 mm ID oro-tracheal cuffed Portex tube. Anaesthesia was maintained with 80% oxygen, sevoflurane (end-tidal 2%), alfentanil infusion, and intermittent doses of cisatracurium, as required. The lungs were ventilated with tidal volume of 500 ml, at the rate of 14-18/min and PEEP of 7 cm of H2O using a low flow technique. ECG, NIBP, SaO2 %, end-tidal CO2, nasopharyngeal temperature, and TOF were monitored. She received 2000 ml of lactated Ringer's solution and 500 ml of 6% hydroxyl-ethyl starch (Haesteril 6%, Fresenius Kabi); during anaesthesia which lasted for 120 min.
Almost 20 min after induction of anaesthesia, when the patient was positioned for surgery, fentanyl 50 μg IV bolus was administered while the surgeon introduced the Veress needle through the upper left quadrant of the abdomen in the supine position. The intra-peritoneal insufflation using CO2 was started with high flows to achieve intra-abdominal pressure of 20 mmHg. Within less than 1 min, the end-tidal CO2 dropped from 35 to 9 mmHg, the patient was cyanosed and SaO2 % dropped to 67%. Her heart rate increased to 130/min from 78/min. However, her arterial blood pressure was maintained at 128/78 mmHg. The airway pressure was between 32 and 35 cm of H2O.
Gas embolism was suspected and the surgeon was informed immediately. FiO2 was increased to 1, fresh gas flow increased to 8L/min, sevoflurane stopped, and manual bag ventilation was carried out. The surgeon stopped the insufflation. Tredelenburg position was given immediately and intravenous 6% hydroxyl-ethyl starch was infused fast to raise the venous pressure to prevent further entrainment of the gas. Within 5 min SaO2 % increased to 100%, and end-tidal CO2 increased to 25 mmHg and later to 42 mmHg. The auscultation of chest revealed bilateral good and equal air entry, which excluded pneumothorax, and no mill-wheel murmur was detected. The pupils were bilaterally equal, small and reacting well to light. When heart rate dropped to 110/min, sevoflurane and alfentanil infusion 500 μg/h were resumed. Arterial blood gas analysis 15 min after the insult showed respiratory acidosis: pH 7.24, PCO2 67mmHg, PO2 220 mmHg, HCO3 28.5 mmol/L. FiO2 was decreased to 0.7 at this stage.
After almost 30 min, after the patient was stabilized, the surgeon directed the Veress needle more caudad and insufflated at lower flows to achieve the pressure of 10 mmHg under vision. A small hole on the anterior surface of the left lobe of the liver could be seen from where the gas was being entrained [Figures and ]. The surgeon covered this bleeding hole with a wet gauze [Figures and ] and applied pressure laparoscopically and later sealed it with surgicel. Since there was no further entrainment of the gas, he carried out the surgery uneventfully.
The arterial blood gas analysis after 1 h from the insult showed complete recovery: pH 7.36, PCO2 42 mmHg, PO2 147 mmHg, HCO3 23.2 mmol/L; though the airway pressure maintained between 32 and 35 cm of H2O and the heart rate was consistently around 110/min throughout the surgery.
At the end of the operation the neuromuscular blockade was reversed with atropine 1mg and neostigmine 2.5mg. The trachea was extubated when the T1:T4 ratio reached 87% and she was completely awake.
The patient stayed in the PACU (post anaesthesia care unit) for 2 h under complete monitoring and observation. She was vitally stable. Blood pressure was 140/80 mmHg, SaO2 % was 100% on O2 6 L/min through Hudson's mask, and 96% on room air. The pulse rate was 90-110/min and the respiratory rate was 16-18/min. Pain was relieved by IV infusion of paracetamol (Perfalgan, Bristol-Myers Squibb Pharmaceuticals Ltd) 1G and small boluses of IV pethidine.
The patient was shifted to the ward in stable condition under observation of vital signs and SaO2 % in the ward. O2 6 L/min through Hudson's facemask was given for 24 h. Incentive spirometry and chest physiotherapy were begun within 4 h after the surgery. The patient was discharged home after 2 days without any complications.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [145.0, 'kg'], 'height': [164.0, 'cm']}",2.57013,2.44162,2.69864,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 164.0 cm. 
The patient's weight is 145.0 kg. 
Therefore, the patient's bsa is sqrt((145.0 (in kgs) * 164.0 (in cm))/3600) = 2.57013 m^2."
7289,60,Body Surface Area Calculator,physical,decimal,pmc-7718640-1,Extracted,"A 37-year-old female patient presented to us with complaints of continuous, dull abdominal pain for six months. She reported an acute exacerbation of the epigastric pain with radiation to the back for five days. She had a history of fever for the past five days with a maximal temperature of 101°F, for which she was treated with acetaminophen tablets (500 mg). Additional complaints included halitosis and early satiety. Ten years ago, she was diagnosed with trichotillomania with anxiety and trichophagia. She reported receiving behavioural therapy and medication (sertraline 50 mg/day) for about one year, following which she had no recurrence of symptoms and was not on any medication. She had no history of pica or any eating disorders.
The height and weight of the patient were 162 cm and 54 kg, respectively, and the body mass index was 20.6. On clinical examination, she had icterus. Abdominal examination revealed a mobile mass in the epigastrium extending to the right hypochondrium with visible gastric peristalsis. Abdominal ultrasound showed a large heteroechoic intragastric mass. Upper gastrointestinal endoscopy revealed that her entire stomach was filled with hair and the scope could not be negotiated into the duodenum. Laboratory investigations revealed increased bilirubin levels (5.2 mg/dL) and elevated total leukocyte count (17,200 cells per μL). The lipase (550 IU/L; normal – 0–160 IU/L) and amylase (450 IU/L; normal – 30–110 IU/L) levels were increased. The AST and ALT levels were 53 U/L (normal – 5–40 U/L) and 58 U/L (7–50 U/L), respectively. The ALP level was 158 U/L (normal 45–115 U/L), and the GGT level was 150 U/L (normal 9–48 U/L). ESR was also elevated at 50 mm/h, and the CRP levels were not evaluated.
The contrast-enhanced computed tomography (CECT) scan revealed an intraluminal mottled mass of mesh-like appearance occupying the entire stomach and extending beyond the second part of the duodenum, delineated by the oral contrast circumferentially, suggestive of a trichobezoar (). The lack of any findings of biliary dilation or the presence of gallstones on the ultrasound further narrowed down the diagnosis.
Hence, due to evidence on the CT scan, a preoperative diagnosis of a trichobezoar was made. The large size and high density of the bezoar made fragmentation and removal by endoscopy, a high-risk procedure with high chances of failure. Failure of endoscopy could cause fragmentation and dislocation of parts of the bezoar. Written informed consent was obtained from the patient to perform the surgery, after a clear presentation of all available treatment options.
Given the large size of the trichobezoar and the presence of cholangitis and pancreatitis, the patient was scheduled for surgery. The abdomen was entered by a midline incision. The anterior gastrotomy was done between stay sutures which revealed a large, entangled mass of hair in the stomach with the tail extending to the second part of the duodenum (). The tail of the trichobezoar was found to be obstructing the Ampulla of Vater, which confirmed the diagnosis of Rapunzel syndrome with complications of acute cholangitis and pancreatitis (). The trichobezoar was removed in-toto without peritoneal contamination (). She had an uneventful postoperative recovery and was discharged after detailed psychiatric counselling. She was also advised regular follow-up, and three years later, the patient reports no complications. At the three years of follow-up (2019), informed consent was obtained from the patient for this study.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [54.0, 'kg'], 'height': [162.0, 'cm']}",1.55885,1.48091,1.63679,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 162.0 cm. 
The patient's weight is 54.0 kg. 
Therefore, the patient's bsa is sqrt((54.0 (in kgs) * 162.0 (in cm))/3600) = 1.55885 m^2."
7290,60,Body Surface Area Calculator,physical,decimal,pmc-4141401-1,Extracted,"The present case report is about a 62-year-old male patient with KD, weighing 70 kg and 173 cm tall, was scheduled for frontal sinusectomy due to sinusitis. He first noticed muscle weakness in the proximal part of the lower limbs at the age of 43. At 2 years later, he was diagnosed with KD. Pre-operative physical examination revealed muscular atrophy, weakness and fasciculation in the lower upper limb muscles and diminished deep tendon reflexes in the lower and upper extremities. He had slurred speech and slight difficulties in swallowing. Other findings included fasciculation and atrophy of the tongue and facial muscles, but he had not experienced laryngospasms []. Pre-operative blood tests were within the normal range except for a plasma creatine kinase concentration of 335 μl (normal range: 24-195 μl). His older brother had died as a result of KD 2 years earlier.
The patient was not premedicated and was monitored with electrocardiography, noninvasive blood pressure and pulse oximetry. Following pre-oxygenation, general anesthesia was induced via propofol 80 mg and remifentanil 0.25 μg/kg/h. After the loss of consciousness, neuromuscular monitoring was applied and calibrated using objective evoked electromyography of the adductor pollicis muscle using an NS-272 neuromuscular transmission nerve stimulator (Fisher and Paykel Health care Ltd., New Zealand). The left or right ulnar nerve was stimulated at the wrist with supramaximal and square-wave stimuli of 0.2 ms duration, 2 Hz every 15 s. The fade was not detected before the administration of rocuronium.
After induced anesthesia, train of four (TOF) ratios was indicated 1.0. We then administered 40 mg rocuronium boluses and deep neuromuscular blockade was achieved (T4/T1 = 0.0) after 120 s. We performed the tracheal intubation without any complications. Anesthesia was maintained uneventfully with 5-8 mg/kg/h propofol and remifentanil 0.2-0.25 μg/kg/min in oxygen and air.
During the operation, 60 min after the administration of rocuronium, the Anesthesiologist could detect a T1 response. Before the end of the operation, fentanyl (200 μg) and flurbiprofen axeti (50 mg) were injected for post-operative analgesia. The propofol and remifentanil infusions were terminated at the end of surgery. After 10 min, the neuromuscular monitoring remained indicated T1, we administered 2.0 mg/kg (150 mg) sugammadex. Within 180 s of the administration of sugammadex, we detected a T4 response (T4/T1 = 1.0) and could no longer detect a fade. The patient could lift his head and arms, open his eyes and protrude his tongue. We therefore extubated the patient 300 s after the administration of sugammadex. The post-operative course was uneventful and no respiratory complications were observed.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [70.0, 'kg'], 'height': [173.0, 'cm']}",1.83409,1.74239,1.92579,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 173.0 cm. 
The patient's weight is 70.0 kg. 
Therefore, the patient's bsa is sqrt((70.0 (in kgs) * 173.0 (in cm))/3600) = 1.83409 m^2."
7291,60,Body Surface Area Calculator,physical,decimal,pmc-3060377-2,Extracted,"A 52-yr-old man with uncompensated cirrhosis due to hepatitis C received an LDLT from his healthy daughter. His BMI was 30 kg m−2 (height, 158 cm; weight, 62 kg). He had previously experienced episodes of massive oesophageal variceal bleeding treated by EIS and endoscopic variceal ligation (EVL). However, preoperative oesophageal endoscopy showed no signs or symptoms of rupture. Laboratory evaluations included: haemoglobin, 10.1 g dl−1; white blood cell count, 6140 μl−1; platelet count, 69 000 μl−1; AST, 44 IU litre−1; ALT, 26 IU litre−1; Alb, 2.4 g dl−1; PT–INR, 1.32; T-Bil, 3.42 mg dl−1; creatinine, 3.48 mg dl−1; and NH3, 133 μg dl−1. His Child–Turcotte–Pugh score was 14, and MELD score was 26. Collateral veins including splenorenal and periumbilical shunts were observed on preoperative abdominal contrast CT. Prophylactic splenic artery modulation for decompression of portal hypertension was not conducted due to his poor condition, particularly renal dysfunction. Anaesthesia was induced with midazolam, remifentanil, and isoflurane, with rocuronium for tracheal intubation. Intraoperative anaesthesia was maintained with isoflurane and remifentanil. The patient was haemodynamically fairly stable during the pre-anhepatic phase but, when the portal vein was clamped, there was immediate bleeding from the mouth and nasogastric tube. Massive transfusion and inotropic support with norepinephrine was needed to maintain arterial pressure. Bleeding from an oesophageal gastric varix rupture was suspected and confirmed by endoscopy. Bleeding could not be controlled endoscopically, so an SB tube was introduced. The position of the tube was confirmed by chest X-ray. Bleeding was controlled gradually as surgery progressed. Collateral veins were ligated directly after implantation. The SB tube was removed immediately after transplantation, and bleeding from the nasal tube did not reoccur. In total, 86 units of packed red cells, 110 units of FFP, and 40 units of platelets were required. The haemodynamic status gradually stabilized without inotropic support. No further transfusion was required and on postoperative days 1, 2, and 3, haemoglobin was 9, 9.2, and 11.2 mg dl−1 and INR was 1.17, 1.12, and 1.13. The trachea was extubated on the intensive care unit on postoperative day 1 after endoscopic examination. The postoperative course was unremarkable regarding general condition, including the lung, liver, and renal function.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [62.0, 'kg'], 'height': [158.0, 'cm']}",1.64958,1.5671,1.73206,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 158.0 cm. 
The patient's weight is 62.0 kg. 
Therefore, the patient's bsa is sqrt((62.0 (in kgs) * 158.0 (in cm))/3600) = 1.64958 m^2."
7292,60,Body Surface Area Calculator,physical,decimal,pmc-6434354-2,Extracted,"A 36-year-old woman was referred to our hospital because of repeated swelling and pain in her left upper extremity during work. She was an office worker with no smoking history or family history of PSS. She also did not have an exercise habit. She was 161 cm tall and weighed 59 kg. As in case 1, no coagulopathy was noted and serum tumor markers and antinuclear antibodies were not elevated in the blood examination. CT and ultrasonography revealed a thrombosis in the left SCV. Venography demonstrated complete obstruction of the left SCV with the development of collateral veins (), suggesting chronic SCV compression. She was diagnosed as having PSS and underwent anticoagulant therapy with systemic heparinization (15,000 U/day) for a day, followed by oral administration of dabigatran (300 mg/day) for 6 months. Although thrombolysis was achieved, her symptoms recurred within 2 months after finishing the anticoagulant therapy. She underwent first rib resection using an infraclavicular approach in the same manner as case 1. The patient did not need SCV reconstruction. Anticoagulant therapy was discontinued after the surgery. Venography revealed successful recanalization of the left SCV without major collaterals (). She was discharged on the fourth postoperative day in good condition. Her postoperative course was uneventful, and she had no recurrence of PSS 1 year postoperatively.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [59.0, 'kg'], 'height': [161.0, 'cm']}",1.62438,1.54316,1.7056,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 161.0 cm. 
The patient's weight is 59.0 kg. 
Therefore, the patient's bsa is sqrt((59.0 (in kgs) * 161.0 (in cm))/3600) = 1.62438 m^2."
7293,60,Body Surface Area Calculator,physical,decimal,usmle-2234,Extracted,"A 61-year-old man with hypertension and hyperlipidemia comes to the physician for a 4-month history of recurrent episodes of retrosternal chest pain, shortness of breath, dizziness, and nausea. The episodes usually start after physical activity and subside within minutes of resting. He has smoked one pack of cigarettes daily for 40 years. He is 176 cm (5 ft 9 in) tall and weighs 95 kg (209 lb); BMI is 30 kg/m2. His blood pressure is 160/100 mm Hg. Coronary angiography shows an atherosclerotic lesion with stenosis of the left anterior descending artery. Compared to normal healthy coronary arteries, increased levels of platelet-derived growth factor (PDGF) are found in this lesion.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [95.0, 'kg'], 'height': [176.0, 'cm']}",2.1551,2.04734,2.26286,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 176.0 cm. 
The patient's weight is 95.0 kg. 
Therefore, the patient's bsa is sqrt((95.0 (in kgs) * 176.0 (in cm))/3600) = 2.1551 m^2."
7294,60,Body Surface Area Calculator,physical,decimal,pmc-8522239-1,Extracted,"A 68-year-old man, who was 175 cm height and 75 kg weight with a body mass index (BMI) of 24.5, suffered from syncope for several times, the ECG showed paroxysmal atrial fibrillation with long RR intervals for up to 9.3 s (Fig. ). The echocardiography showed mild-to-moderate tricuspid regurgitation, normal ventricular wall motion and normal left ventricular ejection fraction. The medical history included end-stage renal disease (ESRD) requiring hemodialysis for 6 years, diabetic gangrene of right foot for 5 months. Indication for pacemaker implantation was established according to the ECG results, in order to prevent transvenous pocket inflammation or systemic inflammation from the gangrenous foot, the Micra leadless pacemaker (Medtronic, Inc. Minneapolis, USA) was recommended and the informed consent was approved by the patient.
The right femoral vein was successfully punctured and inserted with a 6 French sheath, and a bolus of 3000 IU unfractionated heparin (UFH) was intravenous administrated at the beginning of the procedure. The access site was gradually dilated by 8- and 12-French dilators, and a 23-French delivery sheath was introduced into the inferior vena cava, then the pacemaker delivery catheter was connected to the sheath. All delivery devices were flushed and connected with heparinized saline properly. The Micra pacemaker was advanced and conducted into the mid-septum of right ventricle and the fluoroscopic location was acceptable. However, electrical measurement showed a low sensing amplitude of only 2.8 mV, suggesting that the pacemaker needed to be repositioned again.
For recapture, the tether connected to the handle was pulled with constant tension and the pacemaker was closed to the recapture cone, different fluoroscopic angles were viewed to confirm the devices were coaxial. Since then the delivery cup could not be advanced due to great resistance, the pacemaker was not able to be withdrew into the catheter (Fig. , Additional file ). Finally, the whole delivery catheter had to be removed from the delivery sheath (Fig. , Additional file ).
Luckily no valvular or myocardial tissues were found at the tip of the catheter, instead the lumen was fully filled with heavy thrombi (Fig. ). An instant ACT level of 104 s revealed that procedural anticoagulant therapy was insufficient, thus, additional 4000 IU (a total amount of 7000 IU) UFH was administrated immediately and the ACT level turned to 248 s 10 min later. After being removed all the thrombi the structure and mobility of the delivery catheter recovered (Fig. ), which in turn proved that the failure of recapture was caused by the thrombi within the lumen. For preventing thromboembolism, a new pacemaker system was applied and successfully implanted. The final electrical measurement was satisfied: pacing threshold was 0.5 V at 0.24 ms, sensing amplitude was 7.9 mV, and pacing impedance was 560 Ω. The final ACT level was 204 s.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [75.0, 'kg'], 'height': [175.0, 'cm']}",1.90941,1.81394,2.00488,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 175.0 cm. 
The patient's weight is 75.0 kg. 
Therefore, the patient's bsa is sqrt((75.0 (in kgs) * 175.0 (in cm))/3600) = 1.90941 m^2."
7295,60,Body Surface Area Calculator,physical,decimal,pmc-5403097-1,Extracted,"A 59-year-old woman of 146 cm in height and 53 kg in weight was diagnosed with a right rotator cuff tendon tear and was scheduled for an open acromioplasty and rotator cuff repair under general anesthesia. The patient's medical history included hypothyroidism of unknown origin, rheumatoid arthritis involving her hands and no previous surgeries. Her preoperative examination and laboratory data were all within normal limits other than a slight sinus bradycardia, and her heart rate was 57 beats per minute on an electrocardiogram. The American Society of Anesthesiologists classification of her physical status was II. A preoperative airway evaluation revealed adequate mouth opening with a Mallampati score of grade II. The patient had normal dentition; adequate neck motion without limitation and her thyromental distance was more than a 3 finger width. There were no symptoms of shortness of breath, hoarseness, or any history of voice change. The anesthetic plan for this patient was general anesthesia with endotracheal intubation and mechanical ventilation under inhaled anesthetics with continuous ISB for preemptive and postoperative analgesia.
In the operating room, basic monitors consisted of a 3-lead electrocardiogram, and pulse oximetry, noninvasive blood pressure, and capnography were applied. Then, 1 mg of midazolam and 50 μg of fentanyl were intravenously injected for the patient comfort during ISB procedure. Before induction of general anesthesia, a right side ISB was performed with the patient in the left lateral position. Under all aseptic precautions, the brachial plexus was identified between the right anterior and middle scalene muscles using a 6 to 15 MHz linear array transducer (HGL50x; Sonosite, Bothell, WA). Two percent lidocaine was injected to anesthetize skin approximately 2 to 3 cm from the edge of the transducer. An 18-gauge 50-mm Tuohy stimulating needle (StimuLong NanoLine: Pajunk GmbH, Geisingen, Germany) was introduced in-plane under ultrasound guidance with a posterior approach[ through the middle scalene muscle. The successful position of the needle tip was identified immediately posterior to the interscalene brachial plexus nerve roots and was further confirmed by a nerve stimulator (Fig. ). The stimulation current was started at 0.5 mA and, once the desired stimulation response was elicited, 10 mL of 0.2% ropivacaine was injected with intermittent aspiration under real-time ultrasound guidance. Following this injection, a continuous catheter for postoperative pain control was advanced approximately 1 to 2 cm beyond the needle tip and its appropriate position adjacent to the brachial plexus nerve roots was confirmed with a 1- to 2-mL injection of local anesthetics. The catheter was tunneled subcutaneously and then sutured using 4–0 nylon and a transparent aseptic dressing was applied. An ipsilateral skin sensory decrease at the upper shoulder and decrease in motor strength during shoulder abduction confirmed a successful block. Immediate complications were also evaluated after nerve block injection and indwelling catheter placement and the patient showed no signs or symptoms of respiratory failure such as dyspnea and hoarseness.
Following the ISB with continuous catheter placement, general anesthesia was induced with lidocaine (40 mg) and propofol (80 mg) and tracheal intubation was facilitated with rocuronium (40 mg). The vocal cord of the patient was fully exposed under direct laryngoscopy and endotracheal intubation was successfully performed without difficulty or trauma. A 7.0-mm silastic endotracheal tube was inserted and fixed at a depth of 19.5 cm from the incisor teeth after confirmation of equal bilateral lung sounds. Anesthesia was maintained with desflurane (6%–7%) with oxygen and nitrous oxide (50%), with the fresh gas flow set at 1.2 L/min. The shoulder surgery was performed in the beach chair position, and the patient's vital signs remained stable throughout the procedure. The lowest measured blood pressure and heart rate during anesthesia were 90/50 mmHg and 55 beats per minute, respectively.
After the end of surgery, a second 10-mL bolus of 0.2% ropivacaine was injected through the catheter for immediate postoperative pain management and to confirm good catheter function. A nerve-blocking patient-controlled analgesia (PCA) consisting of 0.2% ropivacaine was connected before emergence. The PCA was set at a continuous infusion of 5 mL and bolus infusion of 3 mL with a lockout time of 20 minutes and a total volume of 250 mL. Intravenous glycopyrrolate (0.4 mg) with neostigmine (2.0 mg) was administered to reverse the neuromuscular blockade. The trachea was extubated when the patient was awakened with adequate spontaneous respiration. There was no sign of any respiratory defect or difficulty immediately after extubation. The total operation time was 114 minutes and the total general anesthesia time was 158 minutes from intubation to extubation.
The patient was transferred to the postanesthesia care unit (PACU) after emergence, but subsequently complained of a sore throat and hoarseness. Horner's syndrome was not observed. Because the patient did not present with any respiratory insufficiency or shortness of breath, and the pulse oximeter showed an oxygen saturation of >96% at room air with all other vital signs within normal range, we regarded this as a minor complication of the endotracheal intubation and the patient was reassured that it might be because of a mucosal injury from the intubation. Her pain score of the surgical site was 0 on the numerical rating scale. The patient was evaluated with the modified Aldrete scoring system and was given a score of 9, which indicated a sufficient recovery to be transferred from the PACU to the general ward. Upon transfer to the general ward, the hoarseness and sore throat symptoms remained overnight and the patient also complained of mild breathing discomfort. However, there were no signs of acute respiratory obstruction or desaturation at the general ward.
On the morning of the first postoperative day, the patient still complained of mild dyspnea, dysphonia, odynophagia, and slight aspiration when swallowing water. An otolaryngologist examined her upper airway using endoscopic laryngoscopy and diagnosed paresis of both vocal cords with only a 2-mm gap observed between them (Fig. ). Vocal cord edema was not observed. The continuous ISB catheter was immediately removed and the dyspnea and hoarseness had improved within 2 hours, although mild aspiration when drinking water was still present.
On the fourth postoperative day, the right vocal cord movement had returned to normal but the left vocal cord paresis still remained upon laryngoscopy examination. (Fig. ) Her subjective symptoms had all improved but mild hoarseness and aspiration still persisted. She was discharged without any other complications and with an appointment for the otolaryngology outpatient clinic.
Upon visiting the otolaryngology outpatient clinic one month later, the patient still complained of mild aspiration when drinking water, hoarseness, and a foreign body sense in the throat. A laryngeal nerve electromyography (EMG) test demonstrated persistent left recurrent laryngeal neuropathy.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [53.0, 'kg'], 'height': [146.0, 'cm']}",1.4661,1.3928,1.5394,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 146.0 cm. 
The patient's weight is 53.0 kg. 
Therefore, the patient's bsa is sqrt((53.0 (in kgs) * 146.0 (in cm))/3600) = 1.4661 m^2."
7296,60,Body Surface Area Calculator,physical,decimal,usmle-1718,Extracted,"A 40-year-old man comes to the physician because of a 6-week history of increasing shortness of breath, fatigue, and fever. He has had a cough productive of foul-smelling sputum for 4 weeks. He was hospitalized for alcohol intoxication twice over the past 6 months. He has hypertension and depression. He has smoked one pack of cigarettes daily for 20 years and drinks 6 alcoholic beverages daily. Current medications include ramipril and fluoxetine. He appears malnourished. He is 185 cm (6 ft 1 in) tall and weighs 65.7 kg (145 lb); BMI is 19.1 kg/m2. His temperature is 38.3°C (100.9°F), pulse is 118/min, respirations are 24/min, and blood pressure is 147/96 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 94%. Examination of the chest shows dullness to percussion over the right upper lung field. An x-ray of the chest shows a lung cavity with an air-fluid level and surrounding infiltrate in the right upper lobe of the lung.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [65.7, 'kg'], 'height': [185.0, 'cm']}",1.83746,1.74559,1.92933,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 185.0 cm. 
The patient's weight is 65.7 kg. 
Therefore, the patient's bsa is sqrt((65.7 (in kgs) * 185.0 (in cm))/3600) = 1.83746 m^2."
7297,60,Body Surface Area Calculator,physical,decimal,pmc-3512220-1,Extracted,"The proband is a 30-year-old woman. She was born after an uneventful pregnancy at full term. Her parents were nonconsanguineous. SD was diagnosed at 3 years of age on the basis of clinical symptoms and increased level of free sialic acid in the urine.
The patient's development during the first year of life was relatively normal, but crawling was unstable and muscular hypotonia and nystagmus were noticed. The patient spoke her first words at 1 year of age and her first sentences at 2 years of age. She learned to walk by 1.5 years of age, but her gait and balance were abnormal. At 3 years of age, her cognitive development was assessed as normal, except for mild slowness and clumsiness when performing fine motor skills. The followup evaluations showed mild delays in motor tasks, eye-hand coordination, and concentration. Her verbal development was slightly delayed, and verbal dyspraxia was reported. At 6 years of age, the developmental delay was approximately 2 years.
Inattentiveness, hyperactivity, and problems with sleep were reported during childhood. The patient also had problems with balance and body awareness. Ataxic symptoms were prominent in childhood, but improved during the teenage years.
During her school years, the neurocognitive development fluctuated notably. Verbal performance was consistently better than visual performance or fine motor skills. Intellectual disability was considered to be mild.
At the age of 12 years, the patient's verbal skills, as assessed using the Wechsler Intelligence Scale for Children-R test [], were at the level of a 7 year old, and her performance skills varied between those typical of a child of 5 years 6 months and 6 years 6 months of age. Two years later, her verbal skills had improved. At 14 years of age, no progression was noted in the neurocognitive deficits. The developmental age of the patient varied between 4 and 8 years, and her verbal skills were notably better than her motor and visual abilities.
At the age of 30 years, the proband was living alone with support. She was a social person, keen on the arts and team sports. She was 157 cm in height and weighed 56 kg. She was taking no medications. On examination, auscultation of the heart and lungs was unremarkable, her blood pressure was 114/74 mmHg, and the electrocardiogram was normal. Her facial features were slightly coarse. The proband could walk without aid, but both legs were in a pes planus position. When walking, she had some athetotic movements in her upper extremities. Muscle strength and skin sensation were normal, tendon reflexes were symmetrical and normal, and the plantar responses were in flexion. Both Achilles tendons were slightly shortened and there was mild spasticity in both legs. Neurological examination revealed only mild ataxia. There was mild instability in the Romberg test and the patient was unable to stand with her eyes closed. There was no ataxia or dysmetria shown by coordination tests, but her hand movements were clumsy. She suffered from marked myopia and used six dioptre corrective lenses. Clear outward strabismus was seen in her right eye. However, the eye movements were normal and nystagmus was not detected. The neurological condition of the patient had not deteriorated during the previous 10 years.
There had been no deterioration of the patient's motor skills in adulthood. Her skills had improved with respect to balance, coordination of body movements, and reciprocal motor actions, as well as processing the sequences of movements. The speed of motor actions had become slightly slower during the last few years.
The electroencephalogram (EEG) was normal at 3 years of age, but showed mild generalized background abnormality with occasional spikes and sharp waves at the left temporo-parieto-central region at 5 years of age. Quantitative EEG was normal at 15 years of age. There was no history of epileptic seizures, but symptoms that resembled the startle reflex were noticed in response to sudden noises.
The methods that were used for neuropsychological evaluation of the patient are presented in . Her developmental age, as assessed by Wechsler Intelligence Scale for Children-III [] at the age of 30 years, was 7 years 9 months for the verbal scale and 5 years 4 months for the perceptual scale. Her neurocognitive performance was remarkably better than those of other patients with the conventional type of SD and the SallaFIN mutation []. Other patients with SD (n = 37) have been evaluated using the Bayley Scales of Infant Development-II [], because the tasks that are used in the Wechsler children's tests were too demanding.
There was a slowing in visuomotor speed as well as eye-hand coordination during the followup of our patient after her teenage years. Visual reasoning and spatial orientation were mildly delayed, and the visuoconstructive skills were diminished. However, verbal skills had improved. Repetition of nonsense words and oromotor sequences were difficult for the proband because of verbal and oral dyspraxia, but the proband was able to learn and repeat long, logical stories. She had difficulties with time orientation.
Motor problems were evident but the symptoms had not progressed during the followup. The proband was able to walk on the toes and sides of the feet, but the forward tandem walk was insecure, and motor persistence and motor coordination were clumsy. Static cerebellar tests were performed quite well, with only slight problems with balance. Two of the dynamic cerebellar tests—finger-to-thumb tapping and toe tapping—were performed slowly but correctly. Visuomotor deficits were evident, but the proband managed the test of basic functional mobility quite well.
Brain imaging performed at 15 years of age showed dysmyelination. The corpus callosum was hypoplastic, but the cerebellum, pons, and the proximal part of the cervical cord were normal. There was no enlargement of the ventricles or signs of cortical atrophy. The MRI findings at 30 years of age were mild ().",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [56.0, 'kg'], 'height': [157.0, 'cm']}",1.56276,1.48462,1.6409,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 157.0 cm. 
The patient's weight is 56.0 kg. 
Therefore, the patient's bsa is sqrt((56.0 (in kgs) * 157.0 (in cm))/3600) = 1.56276 m^2."
7298,60,Body Surface Area Calculator,physical,decimal,pmc-3277484-1,Extracted,"Our patient was the third child of non-consanguineous Caucasian parents; her father died from cystic kidney disease when she was three years old. Her birth and neonatal development were uneventful.
At the age of three years, skull asymmetry became visible, which was more and more pronounced in the following years. Fibrous dysplasia was identified by computed tomography, involving in particular the left skull base with the optic canal. Café-au-lait spots were not visible. Beginning at the age of five, the girl underwent five subsequent surgical interventions for plastic reconstruction of her face. However, after each surgery, the girl experienced a marked regrowth of the dysplasia leading to massive facial disfigurement (Figure ).
Finally, at the age of eleven years, our patient presented with gigantism, leading to endocrinological examinations. Her pubertal development now showed Tanner stage PH2-3, B2-3; her body weight was 80.8 kg and length 175.2 cm (both above than the 97th percentile). Besides the asymmetrical skull dysplasia, the girl also presented with an acromegalic appearance. Laboratory evaluations revealed a massive hyperprolactinemia of 5475 mU/L (normal range < 500 mU/L), high growth hormone levels (that is, 43.2 mU/mL at 8 a.m.), and an elevated insulin-like growth factor 1 (IGF-1) of 892 ng/mL (age-related normal range, 111 ng/mL to 693 ng/mL). Her alkaline phosphatase was 690 U/L (normal range, 51 U/L to 332 U/L). A pituitary adenoma was seen on magnetic resonance imaging, located within the massively expanded dysplastic skull base (Figure ). An ophthalmological examination revealed neither diplopia nor any other subjective impairment of her vision. There was a mild paleness of her optic nerve papilla and mild left-sided hemianopia.
The case was discussed in a multidisciplinary conference for the four problems, that is, her facial disfigurement, possible danger to her left visual nerve and the pituitary tumor leading to local pressure and acromegaly. Besides the futility and probable enormous difficulty of cosmetic surgery, our patient and her mother refused any further surgical interventions for this purpose. A surgical intervention at her pituitary gland appeared difficult due to its complete impaction within the dysmorphic, fibrous bone of her skull base. Therefore, we did not obtain a histopathology specimen, and so it was not possible to tell whether the pituitary tumor was a lesion of acidophils, prolactin cells or both. Radiotherapy of her pituitary gland by conventional or gamma-knife irradiation was considered as too toxic, especially since malignant transformation is a well-known possible late effect, particularly in fibrous dysplasia tissues [].
Thus, based on published experiences in McCune-Albright syndrome [,,,], at the age of twelve years, our patient started pharmacological treatment. First, to treat the fibrous dysplasia, we initiated parenteral bisphosphonate therapy with pamidronic acid (Aredia), given every four weeks with a dosage of 30 mg, which equals about 0.4 mg per kilogram body weight. This was done by continuous infusion over four hours with cardiorespiratory monitoring and included regular examination of her kidney and liver function parameters.
In parallel, cabergoline, as the current standard therapy of prolactinomas, was given with a stepwise escalation of the dosage to reach a level of 2 mg twice weekly, which was tolerated well. Regular controls of blood pressure and cardiac function were included.
The clinical course was monitored regularly in monthly to three monthly intervals. The therapy was tolerated well. No acute side effects, such as rash, nausea, electrolyte disturbances, cardiovascular, pulmonary or renal impairment, occurred. Further, the continuous treatment, which has been extended without change for two and a half years, was not associated with osseous necrosis of the jaw or elsewhere, nephrocalcinosis or cardiac valve fibrosis.
Magnetic resonance imaging showed no further progression of the fibrous dysplasia; her osseous status has remained unchanged for two and a half years. Her alkaline phosphatase, initially elevated up to 690 U/L, declined to 587 U/L after one year, and 417 U/L after two years of therapy.
Her visually evoked potentials showed a mild prolongation after the first six months of therapy, which did not go along with any subjective symptoms.
Endocrinological tests showed an immediate and rapid response of prolactin, which fell to the normal range within two months of therapy and have remained completely suppressed since. In parallel, we observed a normalization of her growth hormone levels, and her IGF-1 level fell to normal levels after four months. The growth of our patient slowed down, her final length of 180 cm was, however, much higher than her mid parental expectation. Our patient achieved menarche about one year after the initiation of treatment, that is, several months after normalization of her prolactin levels. Magnetic resonance imaging of her skull base showed a marked shrinkage of the hypophyseal tumor.
In summary, we observed stabilization both of the osseous and the endocrinological symptoms of the disease in our patient, allowing a significant improvement in the quality of life of our patient without further surgical interventions.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [80.8, 'kg'], 'height': [175.2, 'cm']}",1.98299,1.88384,2.08214,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 175.2 cm. 
The patient's weight is 80.8 kg. 
Therefore, the patient's bsa is sqrt((80.8 (in kgs) * 175.2 (in cm))/3600) = 1.98299 m^2."
7299,60,Body Surface Area Calculator,physical,decimal,pmc-7887160-1,Extracted,"A male child aged 5 years was referred to the dental OPD with the chief complaint of decayed upper and lower front and back teeth. On examination, significant medical history was found. The child was born in the first pregnancy to nonconsanguineous phenotypically normal parents. At birth, parental age was 30 for mother and 33 for father. The mother had pregnancy preeclampsia and the pregnancy was completed by the lower segment cesarean section. Examination at birth revealed that the baby had perinatal asphyxia, meconium-stained amniotic fluid (MSAF), and he did not cry immediately after birth. Birth weight was 2.4 kg and height was 106 cm. The patient had persistent thrombocytopenia and was admitted in NICU for 11 days.
After birth, he was prone to upper respiratory tract infections frequently. At 5 years of age when examined, it was noted that patient had microcephaly with alar facies, blue sclera, upslanting eyes, overhanging columella, prominent cup-shaped ears, reduced mouth opening, protruding tongue, triangular-shaped face with small chin, and fifth finger clinodactyly. He was identified with noticeable speech delay and behavioral inhibition, difficulty in adapting to new situations, and speaks loudly at times showing hyperactive behavior.
Several investigations like 2D echo and DNA chromosome analysis, ophthalmology, ENT, and audiology evaluation were carried out. In ENT evaluation, it was found that moderate hearing loss was seen with respect to the right and left ears. Ophthalmology evaluation was found normal. The 2D echo analysis has shown small atrioseptal defects.
On intraoral examination, inflamed gingiva in relation to maxillary anteriors and normal appearing mucosa, freni, and tongue was observed. The patient had a full set of primary dentitions with mesial step molar relation on both right and left sides with anterior proclination and high arched palate. The patient had a habit of mouth breathing. The patient had undergone restorations in relation to 54, 55, 64, 65, 74, 75, 84, and 85. The mother reported the history of bottle feeding from 5 months to 4 years. 51, 52, 61, and 62 had deep dentinal caries suggestive of chronic irreversible pulpitis and secondary caries was noted in relation to 55, 64, 74, 84, and 85.
The glass ionomer cement (GIC) restorations were done in relation to 55, 64, 74, and 84. Pulpectomy followed by composite restoration in relation to 52 was done; Pulpectomy followed by stainless steel crown in relation to 85 was performed. Stainless steel crowns in relation to 54, 55, 64, 65, 74, 75, and 84 were cemented. Extraction of 51, 61, and 62 was carried out.
For the mouth breathing habit, underlying etiology, i.e., frequent upper respiratory tract infection, has to be corrected, which will allow this habit to correct automatically.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [2.4, 'kg'], 'height': [106.0, 'cm']}",0.26583,0.25254,0.27912,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 106.0 cm. 
The patient's weight is 2.4 kg. 
Therefore, the patient's bsa is sqrt((2.4 (in kgs) * 106.0 (in cm))/3600) = 0.26583 m^2."
7300,60,Body Surface Area Calculator,physical,decimal,pmc-4127081-1,Extracted,"A 58-years-old man with a height of 1,78 m and a weight of 185 kg, suffered from a large ventral abdominal hernia. He was admitted for elective Pitanquy operation with hernia repair, which was done together with Lichtenstein hernioplasty. Patient suffered postoperatively from respiratory insufficiency and surgical site infection with necrotizing fasciitis. He plunged into massive sepsis with multiple organ dysfunction syndrome. With necessary necrectomy the patient ended with the defect in the abdominal wall sized 55 cm × 18 cm. Together with systemic intensive organ support we provided the defect with two Parietene 3020 dual sided meshes (Covidien, Dublin, Ireland) (sized 30 × 20 cm) sublay laterally to the lumbar region. We applied negative pressure wound therapy on the mesh (VAC ATS, KCI, Texas). Patient was hospitalized in anesthesiology department, with intensive organ support, artificial ventilation, and circulatory support with noradrenalin. Antibiotic therapy with combination of cephalosporins, quinolones, metronidazole was administered, at the time of initiation of NPWT changed to carbapenems. Meropenem was discontinued on 12th day after initiation of NPWT. 4 weeks after initiation of treatment the patient underwent split skin grafting. During this time patient recovered from sepsis and MODS and was released from the hospital. He had no wound complications in the outpatient setting and no need for further surgery arisen. His quality of life is characterized by good mobility and self-care, appropriate adjustment for everyday work, and occasional use of painkillers.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [185.0, 'kg'], 'height': [1.78, 'm']}",3.02444,2.87322,3.17566,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 1.78 m, which is 1.78 m * 100 cm/m = 178.0 cm. 
The patient's weight is 185.0 kg. 
Therefore, the patient's bsa is sqrt((185.0 (in kgs) * 178.0 (in cm))/3600) = 3.02444 m^2."
7301,60,Body Surface Area Calculator,physical,decimal,pmc-6112871-1,Extracted,"In October 2017, a 71-year-old man visited our hospital due to moving difficulties and visual hallucination after experiencing general fatigue for 3 months. He reported dizziness and increased fatigue, 3 weeks prior to presentation, followed by urinary frequency, urinary incontinence, and a fall, 2 weeks later. To investigate his symptoms, head computed tomography (CT) and blood examination were conducted, which revealed a sodium level of 119 mEq/L, and he was hospitalized. Upon admittance, the patient underwent a physical examination that revealed a height of 138.5 cm, a weight of 49.0 kg, and a body mass index of 25.5 kg/m2. His temperature was 36.2°C and blood pressure 127/67 mm Hg. Pigmentations were detected, which were more visible around the lips, on the tongue, and fingers. Although the penis and scrotum were normal in size, the testicles measured small on an ultrasound scan.
His medical history revealed a growth spurt at approximately 8 years of age and the appearance of pubic hair at 10. His height did not increase past 139 cm from the age of 12. In his thirties, he suspected infertility, which was not investigated. At 49 years old in January 1996, he underwent a left adrenalectomy because of a heterogenous incidentaloma, with a size of approximately 3 to 4 cm. Laboratory investigations at the time revealed adrenocorticotropic hormone (ACTH): 102.2 (7.2–63.3) pg/mL, cortisol: 14.6 (6.24–18.0) μg/dL. 17-Ketosteroids (17-KS) were also reported to be elevated. The detailed results of these tests are summarized in Table . Because malignancy could not be fully excluded, adrenalectomy was performed. The mass was pathologically diagnosed as an adenoma and not malignant. After operation, although he was prescribed prednisolone, he did not keep up with his follow-up visits at the hospital because of no symptoms.
Abdominal CT revealed almost normal right adrenal gland (Fig. ). Laboratory evaluations revealed ACTH level of 1820 (7.2–63.3) pg/mL and cortisol level of 3.11 (6.24–18.0) μg/dL. The results of the other tests are presented in Table . Therefore, a diagnosis of primary adrenal insufficiency was suspected, and the patient immediately received a dose of 100 mg hydrocortisone intravenously. This initial dose was followed by a maintenance regimen of intravenous hydrocortisone diluted in saline as follows: 200 mg for 2 days, 150 mg for 3 days, 100 mg for 3 days, and 50 mg for 3 days. Thereafter, he received 15 mg hydrocortisone orally. During this time, the patient also received approximately a liter of physiologic saline per day. Sodium levels were monitored and reached 126 meq/L on day 2, 131 meq/L on day 3, and 138 meq/L on day 7 after hospitalization. As a result, the patient's symptoms improved after a few days. An ACTH-stimulating test was performed, with the results revealing low response of cortisol 17-hydroxyprogesterone (17-OHP). The basal levels were low in the former and high in the latter. The complete results are summarized in Table . Therefore, a diagnosis of primary adrenal insufficiency was made. No anti-adrenal cortex antibody was detected. The patient was discharged on day 34 with a daily oral dose of 15 mg of hydrocortisone.
We suspected nonclassical 21-OHD, and searched for the most common CYP21A2 mutations by polymerase chain reaction (PCR) as per previous studies,[ using the primers previously reported for these mutations,[ after obtaining the patient's informed consent, looking for the large gene deletion or conversion, and the following 9 micro conversion-derived mutations: P30L in exon 1, 656A/C > G in intron 2, I172N in exon 4, V281L in exon 7, Q318X in exon 8, R356W in exon 8, the cluster I236N, V237E and M239K in exon 6, L307+T in exon 7, and 8 bp-del in exon 3.[ The mutations positive in our patient were micro mutation I172N and heterozygous large gene deletion or conversion leading to the diagnosis of nonclassical 21-OHD.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [49.0, 'kg'], 'height': [138.5, 'cm']}",1.373,1.30435,1.44165,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 138.5 cm. 
The patient's weight is 49.0 kg. 
Therefore, the patient's bsa is sqrt((49.0 (in kgs) * 138.5 (in cm))/3600) = 1.373 m^2."
7302,60,Body Surface Area Calculator,physical,decimal,pmc-7206672-1,Extracted,"A 65-year-old male was admitted to our hospital for “a mediastinal tumor with cough for more than two months” on March 22, 2018. Two months prior, the patient fell during mountain climbing, resulting in a painful left chest. He was conscious when he was injured and started coughing. He went to the local hospital emergency department, and a chest CT showed a “left posterior mediastinum mass”. The patient received conservative treatment for the pain. As the patient kept experiencing symptoms, such as coughing and feeling uncomfortable, he came to our hospital for further treatment. The patient had a 4-year history of hypertension, for which he took 20 mg/day of sustained-release nifedipine. This was enough to keep his blood pressure stable within the normal range. He had no family history and no history of diabetes, surgery, or smoking and drinking. He is 162 cm in height and weighed 49.3 kg. His physical examination revealed heavy breathing sounds, but no other abnormalities were found. His blood pressure was 138/81 mmHg, heart rate 88 beats/min, respiratory rate 21 beats/min, and temperature 36 °C. His laboratory tests, such as CRP, blood routine, liver and kidney function, tumor markers, and blood gas analysis were all within the normal range. His fasting blood glucose was 7 mmol/l. His chest enhanced CT suggested: 1. Left posterior mediastinal mass, and therefore a neurogenic tumor was considered; 2. Chronic bronchitis, emphysema, multiple pulmonary bullae in the apex of both lungs; 3. Little inflammation in the lower right lung (Fig. ). No obvious abnormality was found on his ECG, nor by abdominal and cardiac ultrasound. The pulmonary function examination displayed “Mildly restrictive pulmonary ventilation dysfunction”. Given these characteristics, our initial diagnosis was: “left posterior mediastinum tumor; chronic bronchitis; hypertension”. The patient continued to use nifedipine after admission, and his blood pressure was well-controlled.
On March 28, 2018, the patient underwent thoracoscopic mediastinal tumor resection under general anesthesia. When he arrived in the operation room, the invasive arterial blood pressure (ABP), electrocardiogram (ECG), oxygen saturation (SPO2), heart rate (HR), and respiratory rate (RR) were measured for baseline values and were continued to be monitored throughout the surgery. The baseline ABP was 147/78 mmHg, HR was 85 beats per min (bpm), and the SPO2 was 98%. Intravenous anesthesia was induced and he was intubated successfully. During the operation, intravenous anesthesia, combined with inhalation anesthesia, was used. The patient was placed in the right lateral position for thoracoscopic surgery. The ABP (115–140/64-80 mmHg) and HR (80-89 bpm) were stable but suddenly increased during the exploration of the tumor. His ABP sharply increased to 214/81 mmHg, HR increased to 110 bpm, and the SPO2 was steady at 97%. Deeper anesthesia and urapidil (10 mg) iv were used to attempt to control the hypertension, but this was ineffective. The anesthesiologist suspected that the tumor was secreting catecholamines. Nicardipine was given as a continuous infusion at 2 ~ 10 μg/(kg.min) to control the blood pressure. Esmolol 0.5 mg/kg was repeatedly administered to control the heart rate, and 500 ml colloid solution was given to expand the blood volume. When the patient’s blood pressure returned to 140/63 mmHg, and the heart rate dropped to 95 bpm, Nicardipine and Esmolol were discontinued while the tumor was completely removed. After tumor resection, the patient showed circulatory fluctuations again, with the ABP decreasing between 101 and 110/59–80 mmHg and the HR between 95 and 104 bpm. After reducing the depth of the anesthesia, the patient’s blood pressure still showed a decreasing trend (ABP 74/45 mmHg, HR 97 bpm, SPO2 96%). The liquid infusion rate was increased, and 0.03 ~ 0.15 μg/(kg.min) norepinephrine was given to maintain the blood pressure at 100–110/60–70 mmHg. During the whole operation (3 h), a total of 2600 ml liquid was injected into the patient, of which 500 ml was colloidal liquid. Surgical bleeding was 300 ml, and the urine volume was 300 ml. Considering the intraoperative hemodynamic fluctuations, the patient was transferred to the ICU for intensive care after surgery. The vasoactive agents were continuously decreased under surveillance. Four hours after the operation, the patient’s hemodynamics returned to a stable state, and the endotracheal tube was successfully removed. The patient was transferred back to the ward on the first day after surgery. The drainage tube was removed on the third day after the operation, and he was discharged after ten days.
Postoperative immunohistochemistry results showed that the tumor was positive for CgA, CD56, NSE, and SYN (Fig. ), and negative for CK (AE1/AE3), MelanA, ki-67, and s-100. The mass was diagnosed as PGL by postoperative immunohistochemical tests (neuroendocrine markers (CgA, CD56, SYN) were positive) and by a chest enhanced CT scan (uniform enhancement of the tumor).
The patient was followed up in the outpatient clinic for over a year and did not present with recurrences or metastasis of the tumor, and his blood pressure and heart rate remained stable at 135/77 mmHg and 76 bpm with o.p. sustained-release nifedipine.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [49.3, 'kg'], 'height': [162.0, 'cm']}",1.48946,1.41499,1.56393,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 162.0 cm. 
The patient's weight is 49.3 kg. 
Therefore, the patient's bsa is sqrt((49.3 (in kgs) * 162.0 (in cm))/3600) = 1.48946 m^2."
7303,60,Body Surface Area Calculator,physical,decimal,pmc-7394979-1,Extracted,"A 30-year-old female presented with dysphagia. She was obese, with a height of 157.8 cm and a weight of 86.8 kg. Her body mass index (BMI) was 34.9.
She had been aware of the dysphagia for approximately 6 months before presentation. During a medical check-up for work, a chest X-ray showed a shadow on the mediastinum, so the patient visited a doctor. The chest CT showed a 55-mm circular shadow. Three years ago, an upper GI endoscopy revealed a raised lesion in the left anterior wall of the oesophagus. At that time, the lesion was 1/3 of a circle and approximately 25 mm in size. This lesion was diagnosed as leiomyoma and was monitored. The patient had no medical history and no specific mention of a family medical history.
Blood tests showed a slight increase in white blood cell count and CRP. CEA, CA 19-9, NSE, SCC, and p53 levels were within the reference ranges. The chest X-ray showed shadows in the right mediastinum (Fig. a). Barium fluoroscopy revealed a semicircular raised lesion in the lower oesophagus (Fig. a). Upper gastrointestinal endoscopy revealed a type 1 oesophageal tumour centred on the posterior wall 26–35 cm from the incisors (Fig. b). The surface was ulcerated, and the tumour was exposed (Fig. b). The tumour was hard and white. The affected area showed no iodine uptake. The EUS showed an isoechoic mass. The CT scan showed a mass of 71 × 61 × 55 mm in the beginning of the lower oesophagus with low density mass (Fig. a) and swelling of the right recurrent nerve lymph node to 12 mm (Fig. b). On FDG-PET, the tumour showed an SUVmax of 11.05, and no abnormal accumulation was found in lymph nodes or other organs (Fig. c). The MRI showed a hyperintense mass on the T2WI, which had prolonged contrast enhancement, and no findings of invasion into surrounding tissue were found. The endoscopic biopsy showed cascading spindle cells with different-sized nuclei (Fig. a), and immunostaining showed S-100 (+) (Fig. b), keratin (−), CD34 (−), and desmin (−) staining. The MIB-1 LI was approximately 25% (Fig. c), which led to the diagnosis of malignant schwannoma.
We performed right thoracotomy and open thoracic oesophagectomy. There were no pleural effusions or adhesions in the pleural cavity. The swollen right recurrent nerve lymph node was negative for tumours by rapid pathological diagnosis during the operation. We dissected all of the thoracic oesophagus with tumours to achieve radical resection. We placed a gastric tube through the intrathoracic route for reconstruction. Intrathoracic oesophagogastric anastomosis was performed using the circular stapling technique. The resected tumour was white, hard, and 75 × 45 × 45 mm in size (Fig. ). A large bulging lesion in the neck with degenerative necrosis was observed in the specimen. The raised part of the tumour was covered with normal mucosa (Fig. c).
Histologically, spindle cells with different-sized nuclei were mixed throughout the tissue (Fig. a). Some regions showed nuclear polymorphism or a storiform pattern, and locally, there were approximately 7 mitoses/10 HPFs (Fig. b). The MIB-1 LI was approximately 25% (Fig. c). The margin was relatively clear, but spindle-shaped tumour cells infiltrated the surrounding interstitium and basal myoepithelium, and the patient was diagnosed with MPNST (Fig. a, b). Immunostaining showed S-100 (+) (Fig. d), CD34 (−), and HMB-45 (−) staining. These results led to a diagnosis of MPNST. In this case, the postoperative course was good, and 16 months after the operation, the patient is currently under observation at the outpatient stage without recurrence.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [86.8, 'kg'], 'height': [157.8, 'cm']}",1.95057,1.85304,2.0481,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 157.8 cm. 
The patient's weight is 86.8 kg. 
Therefore, the patient's bsa is sqrt((86.8 (in kgs) * 157.8 (in cm))/3600) = 1.95057 m^2."
7304,60,Body Surface Area Calculator,physical,decimal,pmc-7972857-1,Extracted,"A 64-year-old female (height: 155 cm, weight: 120 kg, BMI: 50 kg/m2, and thigh circumference: 78 cm) with hypertension and type two diabetes mellitus presented in November 2017 with right-leg recurrent varicose veins, swelling of the ankle, pigmentation, and a history of right lower thigh venous ulceration (clinical, etiological, anatomical, and pathological clinical classification C5EpApPTPVr []). Her medications were a calcium blocker, an angiotensin converting enzyme inhibitor, and insulin. Previously, in 2010, she had presented with symptomatic varicose veins in the same leg. Ultrasonography had shown reflux in her right GSV without reflux in other veins. She underwent EVTA for her GSV and stab phlebectomy for the surface varicosities at another hospital. She had worn elastic stockings after first procedure, but she stopped wearing it since 2012. In 2017, she presented with a 1-year history of recurrent varicose veins in her leg. Ultrasonography showed the previously ablated GSV had atrophied. There appeared to be reflux in her axial vein at the knee, but the source of the recurrent varicose veins from the ultrasonography assessment was unclear due to her thick thighs. Therefore, we performed venography to identify the source of REVAS. Venography showed the IPV connected to her axial vein (Figures and ), and thereafter, ultrasonography confirmed the reflux in the IPV. Therefore, we decided to ablate the IPV which caused the REVAS. We crossed a 0.025 wire from axial vein to the FV () and advanced RFA catheter to the FV over the wire (). We withdrew the RFA catheter and adjusted its tip to the border between FV and IPV, while contrasting from the catheter lumen under fluoroscopy guidance (Figures and ). We performed TLA and subsequent ablation from the IPV to the axial vein. The patient was discharged the day after the procedure with no deep vein thrombosis, renal damage, or any other complications. She had worn elastic stockings for a year after the procedure. After 2 years, she continued to have no symptoms, and there had been no recurrence of her varicose veins. Ultrasonography at 1-year and 2-year follow-ups showed that the ablated IPV had atrophied, and there were no deep vein thrombosis and reflux in any veins.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [120.0, 'kg'], 'height': [155.0, 'cm']}",2.27303,2.15938,2.38668,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 155.0 cm. 
The patient's weight is 120.0 kg. 
Therefore, the patient's bsa is sqrt((120.0 (in kgs) * 155.0 (in cm))/3600) = 2.27303 m^2."
7305,60,Body Surface Area Calculator,physical,decimal,pmc-4868890-1,Extracted,"An 18-year-old woman was admitted to our hospital with breathlessness and hypertension. Her medical history included arterial hypertension for one year with no history of traumatic injury or Takayasu's arteritis. On physical examination, height was 150 cm and weight was 40 kg, pulse rate was 89 bpm with blood pressure of 162/95 mmHg in both arms, and all pulses were palpable. However, lower extremity pulses were diminished with a typical radial-to-femoral delay and systolic pressure difference between brachial and ankle was 80 mmHg. Routine blood tests and urine analysis were normal. A grade 3/6 systolic ejection murmur could be heard along the left intercostal area and severe S1 sound was audible. The examination of the respiratory and other systems was normal. Transthoracic echocardiography examination showed increased wall thickness of left ventricle (interventricular septum 1.3 cm and posterior wall 1.3 cm), normal left ventricular ejection fraction (65%), and increased pulmonary artery systolic pressure (45 mmHg). Aortic valve was bicuspid and normal functioning. The maximum peak flow velocity in the left ventricular outflow tract measured 1.6 m/s (corresponding to maximal gradient of 10.3 mmHg), indicating no significant left ventricular outflow tract gradient. An increased peak flow velocity of 3.8 m/s (corresponding to a maximal gradient of 58 mmHg) together with the typical color Doppler pattern indicated severe stenosis of the descending aorta (Figures and ). The parasternal short-axis views revealed a PDA () and pulmonary to systemic flow ratio (Qp/Qs) was calculated as 1.8. Thorax computed tomography (CT) angiography showed that diameter of aorta at the preductal level is 20 mm, 11 mm at coarcted segment, and 23 mm at the postductal level. Also the diagnosis of PDA was confirmed with thorax CT angiography ().
Percutaneous treatment of the CoA and PDA with a generally preferred balloon expandable covered stent was planned. But balloon expandable covered stents dedicated for CoA were not available at those days. For this reason, we decided to use a self-expandable thoracic stent graft. Because of their small size detected on CT angiography, common femoral arteries (3.0 mm, both) and external iliac arteries (4.0 mm, both) were not suitable for thoracic stent graft implantation. So we decided to use left common iliac artery (CIA) via RP approach which was 5.5 mm in diameter (right CIA was 5.3 mm). The procedure was performed under general anesthesia. A 6-F pigtail catheter was placed via right femoral artery to the descending aorta, but the catheter could not pass the coarcted segment (). The coarcted segment could be crossed using 0.035-inch hydrophilic guide wire (Radifocus, Terumo Corporation, Tokyo, Japan) and 5-F multipurpose diagnostic catheter (Cordis Corporation, Miami, Florida, USA). This catheter was changed with a 5-F marker pigtail catheter (Cook Inc., Bloomington, USA). Gradient across coarcted segment was measured as 85 mmHg. For retroperitoneal approach of left CIA, an incision was made in the skin of left lower quadrant of abdomen about 3 cm above from the inguinal ligament. Then, left CIA was reached and a 6-F introducer sheath was placed by Seldinger technique. Coarcted segment was passed with hydrophilic guidewire and 5-F multipurpose catheter via the sheath in left CIA. Hydrophilic guidewire was changed with extra stiff Amplatz guidewire (Amplatz Extra Stiff 0.035 inches, Boston Scientific, MA, USA). The sheath in left CIA was exchanged with a 22 Fr E-asy Plus hemostatic valved introducer sheath (Jotec GmbH, Hechingen, Germany). A 26 mm × 100 mm sized thoracic stent graft (Ankura, Lifetech Scientific Ltd., Shenzhen, China) was placed over the coarcted segment via the 22 Fr sheath (). After confirmation of optimal position, the stent was released and then dilated with a balloon catheter (E-xpand, Jotec GmbH, Hechingen, Germany) with high atmosphere for optimal dilatation of the stenosed segment to exclude residual gradient and complete apposition of the stent (). Control aortography confirmed that the coarcted segment is optimally dilated and the PDA is completely covered by stent graft without any leak. The measured gradient across coarcted segment after stent placement was 5 mmHg. Similar findings were confirmed by echocardiographic assessment. Also intravascular pressure difference between ascending aorta and femoral artery was 5 mmHg. The patient recovered well and was discharged three days after the procedure. Before discharge, control CT angiography showed fully expanded thoracic stent graft with complete exclusion of PDA (). The patient was asymptomatic after two years.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [40.0, 'kg'], 'height': [150.0, 'cm']}",1.29099,1.22644,1.35554,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 150.0 cm. 
The patient's weight is 40.0 kg. 
Therefore, the patient's bsa is sqrt((40.0 (in kgs) * 150.0 (in cm))/3600) = 1.29099 m^2."
7306,60,Body Surface Area Calculator,physical,decimal,pmc-4384410-1,Extracted,"A 35-year-old female (weight, 65 kg; height, 159 cm) was scheduled to undergo a planned repeat CS. She had undergone a CS under spinal anesthesia 2 years previously. Her medical history revealed no seizures or other neurological disorder during her current or previous pregnancies. Preoperative evaluation revealed no remarkable risk factors such as hypertension or glucose intolerance. Thus, the patient was considered to have an American Society of Anesthesiologists physical status of I during the preoperative consultation, and a combined spinalepidural anesthesia technique was planned. The patient was not premedicated. Monitoring involved electrocardiography, noninvasive blood pressure, and pulse oximetry. Body temperature was monitored by a thermistor equipped at the top of a urinary catheter.
With the patient fully awake, the epidural catheter was placed at the T12/L1 space, and a spinal tap was performed at the L2/L3 space with a 25-G Quincke needle in the left lateral decubitus position after skin sterilization with 0.5 w/v% chlorhexidine gluconate/ethanol. After backflow of clear cerebrospinal fluid, 12.5 mg of hyperbaric 0.5% bupivacaine without preservatives (AstraZeneca, Osaka, Japan) with 15 µg of fentanyl (Janssen Pharmaceuticals) were injected into the subarachnoid space. The patient was then placed in the supine position. Discernible sensory block to cold sensation was promptly observed. Finally, before the start of the surgical incision, a sensory block to cold to the T3 level with accompanying motor block was obtained. Vasopressors, including 8.0 mg of ephedrine and 0.6 mg of phenylephrine, were administrated to maintain systolic blood pressure at >100 mmHg during the operation. In total, 900 ml of a crystalloid and 500 ml of a colloid were administrated intravenously.
The surgical procedure proceeded uneventfully, and a live male infant and placenta were delivered 9 and 11 min after skin incision, respectively. All other surgical findings were unremarkable, and routine antibiotics and uterotonic oxytocin were administered. No drugs were administered into the epidural space. Because no hypnotics were used for sedation, the patient was awake during the operation.
The operation was completed 1 h 10 min after the spinal tap. At the time of completion, involuntary movements began ( and ). The movement was observed in both upper extremities, but the movement of the left side was more pronounced (). No remarkable vital sign changes were observed before or during the movement. The patient's systolic blood pressure, diastolic blood pressure, and heart rate were 105 mmHg, 74 mmHg, and 87 beats/min before the beginning of the movement and 110 mmHg, 69 mmHg, and 93 beats/min immediately after the beginning of the movement, respectively. The sensory block to cold subsided to the T8 level, and sensory and motor functions in her upper extremities were intact. The patient was fully conscious, calm, and responsive. She complained that she could not stop the movement. She did not complain that she felt cold. The body temperature at her bladder was 36.8℃, and no coldness of the upper extremities was observed. Because she was alert and in a calm mental state, she was untreated until examination by a neurologist. After the examination, 2 mg of midazolam were administered after 33 min of involuntary movement. Three minutes after administration, the involuntary movement stopped ().
The patient was subsequently transferred to the ward, and the involuntary movement did not recur. Five hours after the surgery, the spinal block had completely subsided. No abnormal sensation or spontaneous pain of the upper or lower extremities was observed. The patient was discharged on foot on postoperative day 3.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [65.0, 'kg'], 'height': [159.0, 'cm']}",1.69435,1.60963,1.77907,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 159.0 cm. 
The patient's weight is 65.0 kg. 
Therefore, the patient's bsa is sqrt((65.0 (in kgs) * 159.0 (in cm))/3600) = 1.69435 m^2."
7307,60,Body Surface Area Calculator,physical,decimal,pmc-5139799-1,Extracted,"A 12 years old female child was admitted with mild pain and deformity at both knee joints which was progressive over 6 months. There was no history of swelling or morning stiffness of joints, no history of repeated fractures or similar illness in family. She was admitted for jaundice 3 years back. She was given mega doses of vitamin D before she referred to our center.
On examination she was normally built and nourished with height 138 cm and weight 27 kg, and vital signs and parameters were normal. On Local examination, knee joint was normal and there was genu valgum with bimalleolar distance of 13 cm; angulations were more in right than left (). Rest of systemic examination was found to be normal.
Investigations revealed Hb10.4 gm/dl, TLC 4.8 x 103/µL, PC 208 x 103/µL, ESR 25 mm/ h, ALT 30 U/L, AST 22 U/L, bilirubin 0.8 mg/dl, Urea 28 mg/dL, Cratinine 1.1 mg/dL, Na 149 mEq/L, K 3.1 mEq/L, Ca 7.5 mg/dL, Phosphate 4.8 mg/dL (2.9 - 5.4), AlkPO4 203 units/L (105 - 420). X-ray local part (knee) was suggestive of mild osteoporotic changes.
Urine examination showed urine pH 7.5, urine anion gap +26, urinary calcium 700mg (100 - 250) and urinary phosphate 300mg (900 - 1300). ABG revealed pH 7.29, PO2 108 mmHg, PCO2 36 mmHg, and HCO3 17 mEq/L with anion gap of 14. Parathormone level was 25.5 pg/ml (12 - 95) and Vitamin D3 level was 27 ng/ml (5.9 - 59).
We suspected Wilson’s disease in this unexplained bone disease. Slit lamp examination of her eyes revealed Keyser-Fleisher ring. Ceruloplasmin level was 2.81 mg/dL (25 - 60). Urinary copper excretion was 1140 µg/day. USG abdomen revealed diffuse fatty infiltration of liver. MRI brain showed copper deposits in caudate nucleus and putamina. So diagnosis of Wilson’s disease with rickets due to renal tubular acidosis was made. She was given zinc acetate, D-penicillamine, sohl solution and oral calcium; and asked to follow up in OPD to observe improvement.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [27.0, 'kg'], 'height': [138.0, 'cm']}",1.01735,0.96648,1.06822,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 138.0 cm. 
The patient's weight is 27.0 kg. 
Therefore, the patient's bsa is sqrt((27.0 (in kgs) * 138.0 (in cm))/3600) = 1.01735 m^2."
7308,60,Body Surface Area Calculator,physical,decimal,pmc-7337418-1,Extracted,"A 58-year-old Chinese female was admitted to our department of neurology with weakness of both arms and legs. Two months prior to admission, she had developed weakness in her bilateral limbs as well as pain in both shoulders. So, she went to a local hospital and reported that she felt the pain ease after receiving traditional Chinese medicine therapy. However, the weakness of her limbs gradually increased. So, she came to our hospital for further diagnosis and treatment. Her past medical history included well-controlled hypertension and diabetes mellitus. Furthermore, she had experienced pyrexia at times in recent years but without the detection of a raised temperature, and she did not seek diagnosis and treatment. She had no history of smoking, alcohol consumption, or recreational drug use. Her family history was unremarkable.
On admission, her height was 158 cm, body weight was 42 kg, body temperature was 38.9°C, pulse was regular at 122 beats/min, respiratory rate was 28 breaths/min, and blood pressure was 170/98 mm Hg. The physical examination revealed that multiple lymphadenopathies were present in the bilateral axillary and the right side of the middle neck triangle, hyperpigmentation in the abdomen, and bilateral pitting pedal edema. The neurological examination showed bilateral upper and lower limb muscle weakness. The upper and lower extremity strength scores, as determined by manual muscle testing, were 3/5 and 4/5, respectively. Tendon reflexes were absent in all extremities, and pathological reflexes were negative. The patient was lucid, and the neurological examination revealed no cranial nerve abnormalities.
Laboratory data on admission (Table ) revealed an elevated platelet count, but the coagulation profile was normal. The erythrocyte sedimentation rate was 41 mm/h (normal range 0 to 20 mm/h). The concentration of C-reactive protein was increased. The testing showed strongly raised creatine kinase (CK) activity (7845 U/L, normal range 40–200 U/L) and elevated liver enzymes in the serum. Blood tests showed a glucose level of 5.88 mmol/L and a glycosylated hemoglobin level of 7.1%. The renal function testing revealed that her creatinine level was normal, but Cystatin C was elevated, and her glomerular filtration rate was decreased. Meanwhile, her urine protein content was 133.35 mg/L (normal range 0 to 10 mg/L). Furthermore, her creatine kinase-MB, MB, and hs-TnT concentrations were significantly increased. Thyroid function tests revealed hypothyroidism. The thyroxin stimulating hormone level was 12.069 uIU/mL (normal range 0.35–4.94 uIU/mL), but the free-T3 and T4 concentrations were normal. The adrenocorticotropic hormone concentration was 3.24 pg/mL (normal range 4.7 to 48.8 pg/mL). The cortisol concentration was 1.1 ug/dL in 4pm (normal range 2.9 to 17.3 ug/dL). Human immunodeficiency virus, serology for hepatitis B and C, and tumor markers (cancer antigen 125, alphafetoprotein, careinoembryonic, carbohydrate antigen 199, cancer antigen 153, cancer antigen 242, prostate specific antigen and neuron specific enolase) were negative. Electrodiagnostic study showed that the motor conduction velocities, sensory nerve action potential, compound muscle action potential, and F wave latency were in the normal range in the bilateral median, ulnar, sural, and tibial nerves. Electromyography analysis showed there were mass abnormal spontaneous activities (fibrillation and positive sharp wave) in the left first dorsal interossei, biceps brachii, tibialis anterior, and the medial head of quadriceps femoris muscle, and myotonic potential in the left iliopsoas and tibialis anterior muscles. The neck triangle lymph node biopsy showed lymphadenosis, but the patient refused an immunohistochemical examination. On the thorax computed tomography (CT) scan, multiple enlarged axillary lymph nodes were observed (Fig. A). The flexor carpi radialis muscle biopsy showed many infiltrated lymphocytes, and the congo red staining test was negative. Combined with the symptoms, physical examination, and laboratory tests, we made a diagnosis of myositis. Hence, we treated the patient with methylprednisolone. However, she did not show a significant improvement, despite receiving standard therapy. Thus, immunoelectrophoresis was performed. Immunoelectrophoresis showed monoclonal IgA lambda serum. A bone marrow biopsy examination revealed that the plasma cell content was slightly elevated (0.84%). Furthermore, the concentrations of serum IgA and lambda free light chains were elevated. Serum IgG, IgM, and IgE levels and complements of C3, C4, and kappa free light chains were within the normal range. Furthermore, the VEGF concentration was slightly elevated. In addition, a X-ray of the skull revealed a small bone defect in the frontal lobe (Fig. B). Ultrasonography showed no cardiomegaly, hepatosplenomegaly, or pleuroperitoneal fluids. Based on the observed skin manifestations, lymphadenopathies, pedal edema, IgA-λ restricted paraproteinemia, plasma cell dyscrasia in bone marrow, elevation of VEGF, and other features, we made a diagnosis of atypical POEMS syndrome without polyneuropathy.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [42.0, 'kg'], 'height': [158.0, 'cm']}",1.35769,1.28981,1.42557,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 158.0 cm. 
The patient's weight is 42.0 kg. 
Therefore, the patient's bsa is sqrt((42.0 (in kgs) * 158.0 (in cm))/3600) = 1.35769 m^2."
7309,60,Body Surface Area Calculator,physical,decimal,pmc-3780926-1,Extracted,"Sacrum of the 28 year old female patient were fractured while moving an object seven months before visiting a hospital so she received conservative treatment. Two months before visiting the hospital, thoracic vertebra radiography was performed since she claimed lower back pain. Compression fractures were diagnosed on 12th thoracic vertebra and then she visited orthopedics in our hospital. A dual energy X-ray absorptiometry (DXA) of lumbar spine and femur revealed relatively low BMD for her age and she was referred to endocrinology department for further investigation. There was no medication history of taking calcium, vitamin D supplement, and oriental medicine etc. Menarche was began when she was 13 years old but menstruation was stopped one year before the hospital visit; but there was no unusual finding in obstetrics examination so she was still being monitored. There was no alcohol drinking and smoking history, family history of osteoporosis and fractures, and other unusual findings.
At the time of her visiting, she complained severe back to pain and had 154.4 cm of height, 45.2 kg of body weight, 19 kg/m2 of body mass index (BMI), 130/100 mmHg of blood pressure, 87 times/minute of pulse, 18 times/minute of breathing, and 36.9℃ of body temperature. Moon face was not clearly shown but mild edema on the face and truncal obesity. The upper and bottom limbs were relatively thin and skin became thin as well. Purple spots were exhibited.
A blood test, leukocyte, hemoglobin, platelets were 7,630 mm3 (neutrophils 84.7%, lymphocyte 8.7%, eosinocyte 0.3%), 13.4 g/dL, 169,000/µL. Fasting glucose, albumin, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and creatinine were 112 mg/dL, 4.1 g/dL, 19 IU/L, 27 IU/L, 409 IU/L, and 0.8 mg/dL, respectively. Total calcium and phosphate were 9.1 mg/dL and 2.7 mg/dL, respectively, and albumin/globulin ratio was not reversed. In addition, serum intact parathyroid hormone, osteocalcin, C-telopeptide, and concentration of plasma 25-hydroxy vitamin D were 36.43 pg/mL (normal range: 13-54), 5 ng/mL (normal range: 4-20), 0.83 ng/mL (normal range: < 0.573), and 33.18 ng/mL, respectively. Thyroid function tests resulted in free T4 1.3 ng/dL, thyroid stimulating hormone (TSH) 0.43 mIU/L, and T3 57.2 ng/dL, indicating a normal range.
A compression fracture were observed at 12th thoracic vertebra in spine x-ray () and Z-score of lumbar vertebrae (L1-4) and femoral neck were -2.9 and -2.1 on DXA, respectively, representing below the expected range for age ().
While being hospitalized, the patient put on brace for conservative treatment with regards to the vertebral compression fracture. As the patient claimed chest pain during the treatment, plain radiography was performed. In the result, fractures were exhibited at right 7th and 10th ribs. Cushing's syndrome was considered due to repetitive pathologic fractures, low BMD regarding age, and the gross findings. Then, free cortisol in urine and 17-hydroxycorticosteroid were tested and then resulted 1,062 µg/day and 17.3 mg/day (normal range: 3-15), respectively, indicating cortisol excess. In order to confirm the diagnosis, a low-dose dexamethasone suppression test was carried out. As a result, we confirmed diagnosis of Cushing's syndrome because basal cortisol was 29.34 µg/dL and cortisol on 3rd day was 28.40 µg/dL indicating that it was not suppressed. Since adrenocorticotrophic hormone was relatively low (10.26 pg/mL), abdomen computed tomography (CT) was performed without a high-dose dexamethasone suppression test considering Cushing's syndrome caused by adrenal adenoma. A 2.7 × 2.4 sized adenoma was observed on left adrenal gland (), so that the patient received laparoscopic left adreanalectomy and was given 30 mg of hydrocortisone a day after the operation. However, after 2 months, the patient visited the hospital again due to severe pain on the lower back again and new compression fractures were taken place at 6th, 8th, 9th, and 11th thoracic vertebrae and 2th and 3rd lumbar vertebrae. Then, 750 mg of calcium citrate and 10 µg of cholecalciferol were given once a day and 20 µg of 1-34 parathyroid hormone (teriparatide) was injected once a day for 6 months total. In DXA performed 11 months after the treatment, BMD of lumbar vertebrae (L1-4) and femoral neck were increased by 4.5%, 1.9%, and 5.5%, respectively. Serum alkaline phosphatase, intact parathyroid hormone, osteocalcin, and concentration of blood 25-hydroxyl vitamin D were 304 IU/L, 28.57 pg/mL (normal range: 13-54), 16.1 ng/mL (normal range: 4-20), and 21.5 ng/mL, respectively. Currently, hydrocortisone was reduced to 10 mg a day; the patient is still being monitored without further fracture occurrences.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.2, 'kg'], 'height': [154.4, 'cm']}",1.39233,1.32271,1.46195,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 154.4 cm. 
The patient's weight is 45.2 kg. 
Therefore, the patient's bsa is sqrt((45.2 (in kgs) * 154.4 (in cm))/3600) = 1.39233 m^2."
7310,60,Body Surface Area Calculator,physical,decimal,pmc-6477550-1,Extracted,"A 16-year-old female adolescent was referred to our hospital with severe hypertension (systolic pressure 178 mmHg), which was first detected 7 months prior to presentation during a routine annual physical examination. She complained of intermittent headache for about 1 year, and her previous blood pressure, measured 1 month prior to her detection of hypertension, had been normal. She showed mild hypokalemia (3.4 mmol/L) in a routine blood test, and an additional workup considering secondary hypertension was planned. Despite taking amlodipine (0.1 mg/kg twice a day), her blood pressure remained uncontrolled.
Upon admission to our hospital, her systolic and diastolic blood pressures were 155 mmHg (>99th percentile) and 111 mmHg (>99th percentile) respectively. She was 162.8 cm tall (50th–75th percentile) and weighed 55 kg (50th–75th percentile). Physical examination including ophthalmological examination revealed no abnormality other than hypertension, and her family history was negative for hypertension or renal diseases. Laboratory examination revealed normal levels of hemoglobin (14.4 g/dL), serum creatinine (0.57 mg/dL), serum total cholesterol (144 mg/dL), and normal urinalysis. Serum sodium, potassium, chloride, and total carbon dioxide levels were 134 mmol/L, 3.4 mmol/L, 102 mmol/L, and 27 mmol/L, respectively. Plasma renin activity was 9.83 ng/mL/hr (normal, 0.5–3.3 ng/mL/hr), and serum aldosterone level was 77.3 ng/dL (normal, 4–48 ng/dL). Urinary levels of vanillylmandelic acid, epinephrine, norepinephrine, dopamine, metanephrine, and normetanephrine were normal, and plasma levels of epinephrine, norepinephrine, and dopamine were also normal. Chest radiography, electrocardiography, and echocardiography showed normal findings. Renal Doppler ultrasonography revealed an avascular bilobed cyst in the lower pole of the right kidney (). Abdominal computed tomography (CT) angiography showed bilaterally normal renal arteries and an eccentric soft tissue component at the peripheral aspect of the cystic lesion (). The mass remained unenhanced during the arterial phase, and its margin was indistinguishable from the surrounding tissue (). During the delayed phase, its eccentric capsule showed enhancement, and an intact mass could be observed (), consistent with CT findings of JGC tumors.
A right partial nephrectomy was performed, and a clear resection margin was identified. The well-encapsulated mass measured 2.5 cm ×2.2 cm×2.0 cm in size with a partially cystic-appearing cut surface. Microscopic examination revealed sheets of polygonal tumor cells with amphophilic cytoplasm. Immunohistochemical examination showed that the tumor cells stained positive for CD34 and focally positive for CD117 (C-Kit) and smooth muscle actin. ()
Postoperatively, her blood pressure returned to normal (105/63 mmHg) without using any antihypertensive medication. On the 3rd postoperative day, the plasma renin activity (0.52 ng/mL/hr), serum aldosterone (3.9 ng/dL), and serum potassium (3.6 mmol/L) levels returned to normal. Her blood pressure and laboratory findings remained within the reference range over the next 3 years postoperatively until her last follow-up.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.0, 'kg'], 'height': [162.8, 'cm']}",1.57709,1.49824,1.65594,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 162.8 cm. 
The patient's weight is 55.0 kg. 
Therefore, the patient's bsa is sqrt((55.0 (in kgs) * 162.8 (in cm))/3600) = 1.57709 m^2."
7311,60,Body Surface Area Calculator,physical,decimal,pmc-6867760-1,Extracted,"A 62-year-old otherwise healthy Caucasian man (80 kg, 173 cm, body mass index [BMI] 26.7) was found to have clinical stage T2c prostate cancer as transrectal ultrasound (TRUS)-guided biopsy revealed Gleason 3 + 4 = 7, and Prostate-specific antigen (PSA) was 13.5 ng/dL). The patient underwent an uncomplicated RALP with bilateral dissection of the obturator and external iliac lymph nodes. Two days after surgery, he was discharged home. One the day after discharge, the patient was referred to the pain therapist as he complained severe pain (numeral rate scale [NRS] 6–7) located in the perianal areas. The clinical evaluation showed perianal pain, which was worsened by sitting. Paresthesia and an anal crushing sensation that impaired the patient's HRQoL were also described. Patient underwent to a multimodal therapy with the calcium channel alpha-2-delta ligand pregabalin (75 mg orally twice a day for 3 days and then 75 mg twice a day for 30 days), the association of the weak opioid tramadol plus paracetamol (film-coated tablets 37.5 mg/325 mg 3 times a day for 7 days), and l-acetyl-carnitine (1000 mg twice daily orally for 30 days). Concerning the painful features of the case, clinical results were quickly satisfactory as pain relief was achieved within 4 days. Furthermore, paresthesia resolved within 15 days. However, the anal crushing sensation lasted for approximately 1 month.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [80.0, 'kg'], 'height': [173.0, 'cm']}",1.96073,1.86269,2.05877,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 173.0 cm. 
The patient's weight is 80.0 kg. 
Therefore, the patient's bsa is sqrt((80.0 (in kgs) * 173.0 (in cm))/3600) = 1.96073 m^2."
7312,60,Body Surface Area Calculator,physical,decimal,pmc-2358884-1,Extracted,"A 66-year-old woman was admitted with the symptoms of acute dyspnoe, orthopnoe and progressive dysphagia. The inspection of the oral cavity revealed an extensive lesion of the tongue (Fig. ) with areas of exophytic growth of the tumor as well as a large ulcus located at the dorsal part of the tongue. This large tumor of the tongue occupied nearly the whole oral cavity and the anterior part of the tongue's margin clearly showed biting traces. These inspectatory findings were accompanied by a respective halitosis. Both the general and nutritional status of the patient were clearly reduced with a body mass index (BMI) of 15.6 kg/m2 (body weight of 40 kg and height of 1.60 m). The medical examination revealed the presence of bilateral large cervical conglomerates of lymph nodes that sonographically measured 6 cm in diameter. An acute obstruction of the upper airway by the tumor mass could be excluded by native computed tomography (CT) imaging of the neck and therefore a tracheotomy was not performed. At admission, the diameter of the tumor was already greater than 10 cm (Fig. ). At the same time, a bioptic tissue probe was analyzed histologically and revealed a low grade differenciated (G3) SCC (Fig. ). Imaging by fluorine 18-fluoro-2-deoxy-glucose-positron emission tomography (18F-FDG-PET; Fig. , ) scans showed cervical hypermetabolic foci along the nerve-vessel-sheaths of both sides that were suspect for malignancy and assessed as metastases with regard to sensitivity and specifity of PET and CT scan. Multiple metastatic lesions were also present in the lung. Furthermore, foci that were suspect for metastases were also found unilaterally in the muscular system of both the left part of the back and left anterior thoracic wall. On the basis of these rather atypical findings, we performed a total body CT in order to exclude the simultaneous presence of a second malignoma.
Altogether, one suspect soft tissue metastasis could be identified near the left upper ventral thoracal wall (Fig. ). A further and smaller soft tissue metastasis was found caudal of the sterno-costal base of the first rib in close vicinity to the internal mammary artery. Another metastasis emerged within the thoracic cavity in the right paraaortal soft tissue sheath. A metastasis measuring approximately 1 cm in diameter was detected in the right iliocostal lumborum muscle near the pelvic rim (Fig. ). In the right vastus medialis/intermedius muscle one soft tissue metastasis of a diameter of several centimeters was found (Fig. ). Also, more caudal, a metastasis of approx. 1 cm in diameter was shown in the right adductor magnus muscle. In the long head of the left biceps femoris muscle another metastasis measuring a few millimeters was identified.
In summary, the tumor staging according to the UICC (Union internationale contre le cancer) revealed a terminal cT4cN3cM1(G3)(C3) tumor. At this advanced stage, surgical therapy with curative intention was not indicated. At the same time, the patient strictly refused a surgical reduction of the tumor, a palliative radiochemotherapy as well as the application of a PEG-device. Therefore, she was transferred to the palliative care unit. The patient finally deceased after 5 weeks of hospitalization by a cardiopulmonary failure as a consequence of the tumor progression. The histologic confirmation of the suspect radiologic diagnoses, which included the spreading of the neoplasia, could be made only for the intraoral findings within the limits of the primary diagnostics, because the patient's relatives did not consent to perform an autopsy despite our request.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [40.0, 'kg'], 'height': [1.6, 'm']}",1.33333,1.26666,1.4,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 1.6 m, which is 1.6 m * 100 cm/m = 160.0 cm. 
The patient's weight is 40.0 kg. 
Therefore, the patient's bsa is sqrt((40.0 (in kgs) * 160.0 (in cm))/3600) = 1.33333 m^2."
7313,60,Body Surface Area Calculator,physical,decimal,pmc-7383216-1,Extracted,"A 71-year-old woman (height, 142 cm; body weight, 49.0 kg; Eastern Cooperative Oncology Group performance status, 1) who presented with vomiting was diagnosed with type III advanced GC of the gastroesophageal junction (Siewert type II []) using an upper gastrointestinal endoscopy (Fig. ). Concurrently, an enhanced computed tomography (eCT) scan revealed thickening of the upper gastric wall and enlarged lymph nodes along the cardiac region and lower mediastinum (Fig. ). Lung and liver metastases were not observed on eCT.
Biopsy results from the gastric tumor indicated a diagnosis of poorly differentiated adenocarcinoma, and the HER2 status was negative, as assessed by immunohistochemistry. The clinical diagnosis was GE-Circ type 3 T3 N3 M0 H0 stage III (according to the 15th edition of the Japanese Classification of Gastric Cancer []). For this patient, we chose S-1 (100 mg/day) and oxaliplatin (100 mg/m2) as chemotherapeutics (SOX) because curative resection was considered to be an excessively invasive procedure with thoracotomy. After 3 cycles of SOX, severe anorexia and diarrhea (grade 3; National Cancer Institute Common Terminology Criteria for Adverse Events version 3.0) were observed despite a dose reduction in S-1 and oxaliplatin. Therefore, we converted the regimen from systemic chemotherapy to ramucirumab (RAM) monotherapy.
Four months after the start of RAM monotherapy, the diameter of the metastatic lymph nodes was slightly decreased, but the tumor was still stable according to RECIST version 1.1 []. An eCT following 7 months of RAM monotherapy revealed progression of both metastasis in the lymph nodes and the primary tumor in the stomach (Fig. ), and we initiated nivolumab monotherapy as third-line chemotherapy. Three months of nivolumab administration (7 cycles) led to a 47% reduction in the metastatic lymph nodes, and no new metastatic lesions were seen on eCT. After 7 months of nivolumab monotherapy (a total of 14 cycles of nivolumab were administered), the diameter of the target lymph nodes showed an 81% reduction from baseline and each had reduced to less than 10 mm in size (Fig. ). Although the primary lesion of the gastroesophageal junction was still present as seen with an upper gastrointestinal endoscopy (Fig. ), there was no evidence of malignancy from pathological assessment with a biopsy of the primary tumor. The patient did not exhibit any adverse events and has survived with nivolumab monotherapy for approximately 2 years from her first visit.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [49.0, 'kg'], 'height': [142.0, 'cm']}",1.39024,1.32073,1.45975,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 142.0 cm. 
The patient's weight is 49.0 kg. 
Therefore, the patient's bsa is sqrt((49.0 (in kgs) * 142.0 (in cm))/3600) = 1.39024 m^2."
7314,60,Body Surface Area Calculator,physical,decimal,pmc-7002563-1,Extracted,"A 69-year-old woman was admitted to the emergency room of our hospital for sudden headache with occipital topography, associated with nape pain and visual loss.
She was under treatment by FLOT regimen (5-fluorouracil 4,200 mg, oxaliplatin 147.58 mg, docetaxel 87.5 mg, and folinic acid 350 mg) for a gastric adenocarcinoma at stage IIB (T3N0M0). The neoplasm infiltrated tunica serosa without lymph node infiltration or metastasis. The FLOT regimen was administered as a neoadjuvant treatment to prepare for the surgical procedure of removal of the lesion. She had received a unique dose of chemotherapy 2 months before admission. Chemotherapy was complicated by infectious pneumonia (Streptococcus pneumoniae) leading to septic shock, treated with intravenous infusion of amoxicillin/clavulanic acid, with acute renal failure requiring dialysis. For this reason, the chemotherapy was interrupted after administration. She had a personal history of arterial hypertension, vena cava and iliac deep vein thrombosis, polymyalgia rheumatica, hypercholesterolemia, chronic obstructive pulmonary disease (COPD), and blindness in the right eye. She was taking amiodarone, acetylsalicylic acid, tinzaparin, hydralazine, and lorazepam, but she was not taking any treatment for COPD.
On admission, blood pressure was 136/76 mmHg, weight 58.9 kg, height 1.63 m, heart rate 92 pulse/minute, body temperature 36.0°C, and capillary blood glucose 136 mg/dl. General physical examination was unremarkable. Neurological examination showed visual loss in the left eye and weakness of the lower limbs. Blood tests showed normal values of sodium and magnesium. Lactic acid dehydrogenase (LDH) levels were within normal limits. C-reactive protein (CRP) level was slightly increased, and albumin level was slightly decreased.
Brain computed tomography (CT) showed two ischemic-like occipital lesions without hemorrhage (). Angiographic sequences revealed breakdown of the blood–brain barrier (BBB) in the corresponding regions. Cerebral magnetic resonance imaging (MRI) demonstrated bilateral parieto-occipital lesions: most parts of the lesions were T1 hypointensity and T2 hyperintensity, which demonstrated vasogenic edema. The rest of the parts of the lesions were T1 hyperintensity, T2 hyperintensity, and diffusion-weighted imaging (DWI) hyperintensity, which might indicate cortical laminar necrosis. After gadolinium injection, a linear enhancement of the cortex was observed. Multiple micro-ischemic lesions were observed in the periventricular regions, indicating a background of chronic ischemic leukoencephalopathy. No lesion was demonstrated in the posterior fossa. Dynamic susceptibility contrast (DSC)-MRI was not performed. MRI angiographic sequences did not show any abnormality in the vertebrobasilar system or in Willis polygon (). In particular, there was no evidence of vasospasm.
Lumbar puncture was not performed in our patient owing to absence of clinical evidence of infectious meningitis. The electroencephalography (EEG) was unremarkable. The diagnosis of PRES was made, and the patient was admitted in our cerebrovascular unit to monitor her blood pressure and cardiorespiratory function. Regarding the blood pressure monitoring, she presented one single peak of hypertension (183/91 mmHg) a few hours after admission (see ).
She was administered with oral nimodipine 360 mg/day because of the neuroprotective effect of this drug (, ). She left the hospital 48 h later with continuation of nimodipine at home and was followed up by ambulatory care as an outpatient.
The clinical evolution was characterized by resolution of headache 1 month after discharge. The radiological follow-up with MRI 1 month later showed ischemic-like parieto-occipital bilateral lesions (). There was no rechallenge with FLOT. The patient is alive 15 months after occurrence of PRES, with permanent visual sequelae and residual paraparesis.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [58.9, 'kg'], 'height': [1.63, 'm']}",1.63305,1.5514,1.7147,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 1.63 m, which is 1.63 m * 100 cm/m = 163.0 cm. 
The patient's weight is 58.9 kg. 
Therefore, the patient's bsa is sqrt((58.9 (in kgs) * 163.0 (in cm))/3600) = 1.63305 m^2."
7315,60,Body Surface Area Calculator,physical,decimal,pmc-5572599-1,Extracted,"A 5-year-old boy (43 inches, 50th percentile, and 42 lbs, 50th percentile) presented to Parkside Medical Group (Upland, CA) for a neurological evaluation. His mother remembered being told that he might have intellectual disability based on blood tests and an amniocentesis; however, these test results were not available. Otherwise, the pregnancy history and delivery were normal. He weighed 6 lbs 10 oz (20th percentile) at birth, walked at 14 months, and said “mama” and “papa” at 8-9 months. During early childhood he did not want to be around other children. He adhered to routines; for example, when his father would change his favorite TV channel he would become very angry. He spoke Spanish and some English. He attended special education at a preschool level and he could count up to 100. However, he could not focus in school. He was diagnosed with ADHD and mild autism based on the DSM V criteria by a child psychologist six months prior to the neurology visit. He was started on amphetamine-dextroamphetamine ER 10 mg daily, which improved his behavior both at home and at school. He started participating more in group activities. On exam, he was found to have a high anterior hairline, a triangular face, a short chin, widely spaced eyes, prominent nasal bridge, and conical teeth (). There were no corneal opacities or preauricular scales. He was able to answer questions about his name, age, and what he liked, but there was a lack of reciprocity and eye contact. There were no tics. However, he was fidgety, could not wait his turn, was wandering about, was talking excessively in Spanish, and was interrupting his parents at times. Therefore, his Adderall XR was increased to 20 mg daily, but he became weepy and emotional; hence the dose was lowered back to 10 mg daily, but 7 months later the dose had to be increased back to 15 mg daily due to his persistent symptoms of ADHD. He was also treated for insomnia with guanfacine 0.5 mg at night. Of note, he had a history of asthma and was being treated with budesonide 0.5 mg/2 mL suspension and montelukast 4 mg daily. Family history was unremarkable. He has an 11-year-old healthy sister. There was no history of consanguinity. His EKG was normal. There was no history of seizures; EEG was not performed due to lack of cooperation. His lab results were all normal (cholesterol, TG, HDL, LDL, FSH, LH, TSH, ACTH, vitamin A, free retinol, and plac Lp PLA2) except for human growth hormone, which was elevated (1.6 ng/ml; normal range 0.01–0.97 ng/ml). He tested negative for fragile X syndrome with 29 CGG repeats. Chromosomal microarray (CMA), performed at the Mayo Clinic (Rochester, MN), demonstrated a 1.7 Mb deletion at Xp22.31 (), which included 6 genes; STS, pseudouridine 5′-phosphatase (PUDP), microRNA 4767 (MIR4767), variable charge, X-linked (VCX), patatin-like phospholipase domain containing 4 (PNPLA4), and microRNA 651 (MIR651), which was consistent with the diagnosis of XLI [, ]. CMA was performed using both copy number and single-nucleotide polymorphism (SNP) probes on a whole genome array (CytoScan HD platform) (Affymetrix). The genome-wide functional resolution of this array is approximately 30 kb for deletions and 60 kb for duplications. The presence of dry, scaly skin on his abdomen and pretibial areas () was confirmed after receiving the results of the array. There were no signs of cryptorchidism. The patient's mother could not be tested due to lack of insurance coverage.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [42.0, 'lbs'], 'height': [43.0, 'in']}",0.76025,0.72224,0.79826,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 43.0 in, which is 43.0 in * 2.54 cm/in = 109.22 cm. 
The patient's weight is 42.0 lbs so this converts to 42.0 lbs * 0.453592 kg/lbs = 19.05086 kg. 
Therefore, the patient's bsa is sqrt((19.05086 (in kgs) * 109.22 (in cm))/3600) = 0.76025 m^2."
7316,60,Body Surface Area Calculator,physical,decimal,pmc-8671579-1,Extracted,"An 88-year-old woman (height, 150 cm; weight, 41 kg) with no history of drug allergy or general anesthesia was scheduled for transfemoral TAVI because of severe aortic stenosis (AS). The surgery was performed under general anesthesia to facilitate the use of transesophageal echocardiography and to manage any intraoperative complications. She was taking 0.625 mg/day bisoprolol, a selective β-1 blocker, for hypertension and chronic atrial fibrillation. Additionally, she was taking amlodipine for hypertension. Preoperative transthoracic echocardiography showed severe AS (aortic valve peak flow velocity: 4.73 m/s; mean aortic valve pressure gradient: 47 mmHg; aortic valve area: 0.41 cm2) and myocardial hypertrophy (left ventricular posterior wall thickness and interventricular septum thickness: 14 mm).
Pre-anesthetic medication for sedation was not administered. She received bisoprolol and amlodipine 3 h before entering the operating room. Figure shows the anesthesia record. General anesthesia was induced using midazolam and remifentanil; additionally, rocuronium was administered to facilitate tracheal intubation. She received total intravenous anesthesia: continuous infusions of propofol and remifentanil. Noradrenaline and dopamine were infused continuously through the central venous catheter to maintain blood pressure. AS disappeared after valve implantation. During the surgery, complete atrioventricular block occurred, and ventricular pacing (VVI mode: 60 ppm) was initiated. No other complications were associated with the surgical procedure. Postoperatively, she received 100 mg sugammadex through the central venous catheter, but 2 min later, her systolic arterial blood pressure (ABP) decreased unexpectedly to less than 40 mmHg. Simultaneously, ventilator monitoring revealed elevated peak and plateau airway pressures (60 and 40 cmH2O, respectively). No skin rash was observed on the body surface. Transthoracic echocardiography showed underfilling of the left ventricle without right ventricular dilatation or pericardial effusion. No abnormalities were observed in left ventricular wall motion.
The patient developed distributive shock, which was clinically diagnosed as anaphylactic shock caused by sugammadex because of the rapid onset of severe hypotension and bronchospasm. First, two boluses of 0.05 mg adrenaline were administered through the central venous catheter, followed by rapid volume resuscitation using crystalloid (1 L infusion within 30 min). The dose of noradrenaline was increased to 0.3 μg/kg/min. Consequently, the airway pressures returned to the original level, but the hypotension persisted. Thereafter, adrenaline was administered via bolus (0.1 mg twice) and continuous infusion (0.1 μg/kg/min); however, the increase in her ABP was minimal. Therefore, 1 mg glucagon was administered intravenously, and her systolic ABP immediately rose to 130 mmHg. An erythematous rash also appeared on her neck with the increase in ABP. Her general condition was stable after the therapeutic interventions. Ventricular pacing was continued because bradycardia with complete atrioventricular block was persistent during the interventions. She was admitted to the intensive care unit under tracheal intubation. Subsequently, the continuous infusion of adrenaline was discontinued, and the continuous infusion of noradrenaline was reduced. We also administered 125 mg methylprednisolone for 3 days. She was extubated 9 h after the onset of anaphylaxis, and circulatory agonists were discontinued the following day. She was discharged without complications on postoperative day 9. Blood tests revealed a total serum tryptase level of 7.3 ng/mL and 1.2 ng/mL at 1 h and 24 h after onset, respectively. We advised the patient to undergo allergy tests, such as skin prick tests or intradermal tests, to identify the cause of anaphylaxis. However, the patient refused these tests because she was elderly and unlikely to undergo surgery under general anesthesia in the future.
Written informed consent was obtained from the patient for the publication of this case report. This report was approved by the Institutional Review Board of Nagasaki University Hospital (Approval number: 21041932).",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [41.0, 'kg'], 'height': [150.0, 'cm']}",1.30703,1.24168,1.37238,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 150.0 cm. 
The patient's weight is 41.0 kg. 
Therefore, the patient's bsa is sqrt((41.0 (in kgs) * 150.0 (in cm))/3600) = 1.30703 m^2."
7317,60,Body Surface Area Calculator,physical,decimal,pmc-7476783-1,Extracted,"A 32-year-old man underwent primary THA for osteonecrosis of the femoral head. The patient was 1.72 m in height and 68 kg in weight (body mass index, 22.91 kg/m2). He had been under steroid therapy for 10 years because of dermatomyositis. This patient was informed that data from the case would be submitted for publication, and he gave his consent.
Staged THAs were performed with an interval of one month. The components used for the right hip were PLASMACUP SC® 56 mm (Aesculap, Tuttlingen, Germany), 3rd generation BIOLOX® forte liner (CeramTec), 3rd generation BIOLOX® forte 28 mm head with short neck, and BiCONTACT® (Aesculap) SD type stem of size 16. The components used for the left hip were PLASMACUP SC® 54 mm, BIOLOX® forte liner, BIOLOX® forte 28 mm head with medium neck, and BiCONTACT® SD type stem of size 17. There were no intra- or postoperative complications. On the right side, the inclination of the cup was 40.3° and the anteversion of the cup by the method of Bachhal et al. was 20.0°. On the left side, the inclination of the cup was 30.1° and the anteversion of the cup was 20.9°. The patient had been under annual routine follow-up with satisfactory clinical results. There was no overt negative symptoms, including squeaking.
At 14 years after surgery, the patient heard a pop in his right hip while pulling heavy luggage and visited the emergency room because of sustained pain and a clicking sound. Plain radiographs revealed a ceramic head fracture (). Revision surgery through trans-trochanteric approach was performed. During the revision surgery, ceramic liner fractures at multiple sites of its outer edge were identified in addition to the ceramic head fracture (). After meticulous removal of the fractured ceramic fragments, the remaining main body of the ceramic liner was extracted. After copious irrigation, a new ceramic liner and a 32 mm head with short neck were inserted. Both were made with the 4th generation alumina, BIOLOX® delta, and the head was coupled with a metal sleeve.
Postoperatively, the patient returned to normal activity after using crutches for eight weeks. At approximately 10 weeks after the operation, the patient experienced remarkable pain in his right hip immediately after falling resulting from a sudden forceful crush by a stranger while sitting in the squat position. The crushing force caused the right hip in the squatting position to be more flexed and abducted. He experienced persistent pain and crepitus in the right hip and visited the outpatient clinic at postoperative 12 weeks. Simple radiographs revealed multiple ceramic fragments presumed to be from the ceramic liner (). Re-revision surgery to exchange the ceramic head and liner with new ones was performed. During the operation, eight fractured segments and multiple smaller flakes of ceramic were identified originating from the edge of the ceramic liner. The fracture site occurred between 8 and 12 o'clock of the liner. When engaging in passive range of motion (ROM) of his right hip joint, impingement between the outer margin of the liner and the shoulder of the stem was observed. A notch on the shoulder-side of the stem was also observed (). All detected fragments were removed and the head and liner were exchanged after copious irrigation. The new head and liner were made of 4th generation BIOLOX® delta and a long neck head was used to prevent impingement between the stem shoulder and the liner. The patient is currently in satisfactory condition three years after re-revision surgery.
We retrospectively reviewed the patient's serial simple radiographs to detect signs of impingement between the ceramic liner and the stem shoulder. The notch on the medial side of the stem shoulder was continuously observed starting at 5 years after the initial operation ().",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [68.0, 'kg'], 'height': [1.72, 'm']}",1.80247,1.71235,1.89259,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 1.72 m, which is 1.72 m * 100 cm/m = 172.0 cm. 
The patient's weight is 68.0 kg. 
Therefore, the patient's bsa is sqrt((68.0 (in kgs) * 172.0 (in cm))/3600) = 1.80247 m^2."
7318,60,Body Surface Area Calculator,physical,decimal,pmc-8293099-1,Extracted,"A 32-year-old primiparous woman sought medical attention for the appearance of a rapidly enlarging and painful pelvic mass 6 months after vaginal delivery, accompanied by irregular uterine bleeding. She had a history of infertility attributed to endometriosis and treated with hormonotherapy (dienogest). She was a nonsmoker and had no history of drug or alcohol abuse. The physical examination showed a woman measuring 160 cm with a weight of 85 kg, approximately. Imaging studies revealed a large abdominopelvic mass of malignant appearance with no lymphadenopathy and no distant metastases. During preparation for elective surgery, she presented for severe abdominal pain to the Emergency Department where the diagnosis of an intraabdominal perforation was entertained. An urgent laparotomy was immediately performed, resulting in the palliative resection and debulking of a perforated mass of pelvic origin with extensive involvement of the abdominal cavity.
The pathology report described a 24 cm tumor with honeycomb appearance and cystic degeneration, made up of benign mullerian-type glands admixed with a malignant stromal/mesenchymal hypermitotic and cytologically atypical component, diagnostic of mullerian adenosarcoma with extensive high-grade sarcomatous stromal overgrowth and without heterologous components. The malignant cells stained with ER, PR, cyclin D1 and WT1, suggestive of a gynecologic origin. It was not possible to determine whether the primary site was uterine or extra-uterine. Immunohistochemistry showed no mismatch repair (MMR) protein loss. An inhouse next-generation sequencing platform of the tumor designed to detect DNA and RNA alterations in 52 genes () only revealed a KRAS mutation (p.Gly12Asp). PD-L1 expression on tumor cells was 0%.
The patient was started on doxorubicin for residual disease and received six cycles, which resulted in disease stabilization, as best response. Radiotherapy also had to be given for a bleeding intra-rectal lesion. At progression, chemotherapy was changed to gemcitabine/docetaxel, with disease stabilization; this treatment had to be stopped for toxicity (fatigue and thrombocytopenia) after 4 months. Stability was maintained for another 5 months with anastrozole. For major disease progression with the appearance of new lesions and partial bowel obstruction, ifosfamide was given but, despite short-term stabilization, did not prevent further progression. On the basis of the success of lenvatinib/pembrolizumab in endometrial cancer, this regimen was prescribed to the patient after informed consent through a compassionate program. A clinically meaningful tumor reduction was observed, although not qualifying for partial response per RECIST criteria, after 9 weeks of treatment. Regrowth of a tumor implant was seen after 18 weeks, which did not respond to tumor embolization. Frank disease progression was evident with new tumor deposits after 8 months of lenvatinib/pembrolizumab. Two cycles of trabectedin were unsuccessful and the patient died after opting for palliative care. Survival was 29 months between surgery and death. The various tumor sizes through treatment stages are listed in .",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [85.0, 'kg'], 'height': [160.0, 'cm']}",1.94365,1.84647,2.04083,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 160.0 cm. 
The patient's weight is 85.0 kg. 
Therefore, the patient's bsa is sqrt((85.0 (in kgs) * 160.0 (in cm))/3600) = 1.94365 m^2."
7319,60,Body Surface Area Calculator,physical,decimal,pmc-4161720-1,Extracted,"A 38-year-old primiparous pregnant Japanese woman was transferred to our hospital because of pregnancy-induced hypertension at 37 + 0 weeks’ gestation. Until that time, her pregnancy had been uneventful. On admission, the patient’s height was 156 cm, her body weight was 66 kg, and her blood pressure was 144/67 mmHg. Proteinuria was negative. The patient’s labor progressed rapidly on the day of admission, with full dilation of the cervix 8 hours after the onset of labor. Because of prolonged deceleration on cardiotocogram, vacuum extraction was performed when the fetal head reached the +2 station. The 2,405 g male neonate had an Apgar score of 8 at 1 min and 9 at 5 min after delivery. A vaginal laceration extending 5 cm from the introitus at the 6 o’clock position was repaired. Two hours after delivery, massive bleeding from the vaginal sutures was found. When all sutures were released, pulsatile bleeding was confirmed, necessitating a second repair.Two hours after the second repair, transvaginal ultrasonography showed a hyperechoic 18 × 20 mm mass at the 5 o’clock position on the vaginal wall, suggestive of a hematoma, within which a 6 × 7 mm anechoic mass with pulsation was described (Figure 
A). Power-Doppler ultrasonography showed blood flow signals in the anechoic mass (Figure 
B), and arterial waveforms were detected in pulsed-Doppler mode. Contrast-enhanced CT revealed an 8 mm diameter pooling of contrast adjacent to an 18 × 32 mm mass in the pelvis (Figure 
C, D).
By the fourth postpartum day, the pseudoaneurysm had grown to 10 mm in diameter (Figure 
A). Because of the risk of rupture, elective embolization was planned. On the sixth postpartum day, the patient experienced abdominal pain and massive vaginal bleeding of 260 ml. Contrast-enhanced CT showed that the pseudoaneurysm had grown to 14 mm (Figure 
B). Emergency selective angiography showed strong staining with extravasation from a peripheral branching vessel of the left vaginal artery, indicating ruptured pseudoaneurysm (Figure 
). Selective embolization was performed using n-butyl-2-cyanoacryate. No blood transfusion was necessary. The patient was discharged without further complications on the 13th postpartum day.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [66.0, 'kg'], 'height': [156.0, 'cm']}",1.69115,1.60659,1.77571,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 156.0 cm. 
The patient's weight is 66.0 kg. 
Therefore, the patient's bsa is sqrt((66.0 (in kgs) * 156.0 (in cm))/3600) = 1.69115 m^2."
7320,60,Body Surface Area Calculator,physical,decimal,pmc-6099042-1,Extracted,"Twin B of a spontaneous dichorionic and diamniotic twin pregnancy of a 30-year-old multigravida was found to have symmetrical intrauterine growth restriction (IUGR) at 25-week gestation (estimated fetal weight (EFW) <3rd percentile, intertwin weight discordance 28%), with abnormal Dopplers indicating increased placental resistance and cranial sparing with cephalization of blood flow. Also noted were mild right lateral cerebral ventriculomegaly, small stomach, and enlarged gallbladder. Aneuploidy screening results were low-risk, with cell-free DNA negative for trisomy 21, 18, and 13. Amniocentesis was declined. Maternal viral serology for cytomegalovirus, toxoplasmosis, and parvovirus was negative for recent infection. From 27 weeks onward, persistently absent end-diastolic flow of the umbilical artery was noted. Ventriculomegaly worsened to moderate range at 28 and 33 weeks, with bitemporal skull narrowing and strawberry-shaped skull appearance noted at 31 weeks (Figure ). Anhydramnios for Twin B was noted at 36-week gestation. As diagnosis of aneuploidy would affect postnatal management, bladder aspiration of Twin B was performed, but cell culture was without growth. At 38 weeks, the EFW for Twin B was 1559 g, with twin discordance of 48%.
The patient was born at 38 weeks and 3 days gestation, via scheduled repeat cesarean delivery. Apgar scores were 5, 7, and 8 at 1, 5, and 10 minutes of life, respectively. He was small for gestational age (SGA) with birthweight 1133 g (Z-score: −5.49), birth length 39.4 cm (Z-score: −4.43), and head circumference 29.5 cm (Z-score: −3.23). Physical examination was significant for small facies with underdeveloped chin, relative macrocephaly, overlapping cranial sutures, mild crumpling of the ears, wide-spaced nipples, second and fifth fingers of the right hand overlapping the third and fourth fingers, and a small sacral hemangioma (Figure ). The patient developed hypoglycemia and hypophosphatemia, likely secondary to his IUGR/SGA status, which responded to modifications in intravenous fluids. He tolerated full enteral feeds by the second week of life, but due to poor oromotor skills, he was fully nasogastric tube-dependent. Patient developed self-resolving leukopenia. Thrombocytopenia, reaching a nadir on day of life (DOL) 2, responded to 1 platelet transfusion. Mild self-resolving anemia was noted with a high reticulocyte count. Second anemia nadir at fourth week of life was treated with epoetin alfa, with normalization of erythrocyte indices. From DOL 5 onward, patient had a prolonged need for respiratory support, attributed to chronic microaspirations, with a waxing-and-waning degree of respiratory distress, which was subsequently attributed to a hiatal hernia. Gastrointestinal contrast study showed approximately half the stomach within the thoracic cavity, along with an incidental finding of inguinal hernia.
During the patient's hospital course, extensive workup was completed as part of evaluation for the chromosome 19p deletion (see Section ). Initial head ultrasound showed a small hyperechogenic focus inferior to the third ventricle. Noncontrast brain MRI performed on DOL 23 showed normal findings. Follow-up head ultrasound performed on DOL 50 showed resolution of the previously described echogenic focus, with a new finding of mild dilation of frontal horns of lateral ventricles. Spinal ultrasound was significant for a low lying conus and a tethered spinal cord. Whole spine MRI confirmed this finding, additionally showing 6 lumbar vertebrae. Abdominal and focused renal ultrasounds were normal. Echocardiogram was significant for suspected interrupted inferior vena cava with hemiazygos continuation to the left superior vena cava draining to the coronary sinus; no right superior vena cava was noted. Suspected cervical aortic arch was present with mild tortuosity of transverse arch without evidence of coarctation. Normal pulmonary venous drainage and a patent foramen ovale with left-to-right shunt were also seen. Ophthalmologic examination performed on DOL 13 showed a thin iris with rugged pupils. Mild stippling of the left retina with irregularly shaped optic disk was also noted.
On DOL 53, laparoscopy was performed to repair the hiatal hernia. Intraoperative diagnoses were: type I paraesophageal hernia with almost the entire stomach located within the chest, and a significant pyloric stenosis. The infant underwent paraesophageal hernia repair, Nissen fundoplication, G-tube placement, and pyloromyotomy. On postoperative day four, the patient developed a firm abdomen and respiratory compromise. Abdominal X-ray revealed intestinal pneumatosis and presence of portal vein gas. Emergent laparotomy found a 3 mm gastric perforation and necrotic small bowel. Unfortunately, the patient passed away intraoperatively. Cause of death was shock secondary to gastric perforation, peritonitis, and bowel necrosis.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [1133.0, 'g'], 'height': [39.4, 'cm']}",0.11136,0.10579,0.11693,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 39.4 cm. 
The patient's weight is 1133.0 g so this converts to 1133.0 lbs * kg/1000 g = 1.133 kg. 
Therefore, the patient's bsa is sqrt((1.133 (in kgs) * 39.4 (in cm))/3600) = 0.11136 m^2."
7321,60,Body Surface Area Calculator,physical,decimal,pmc-3602076-1,Extracted,"Our patient was a 10-year-old Han Chinese girl, observed at our clinic for genetic counseling, who was the product of an unremarkable pregnancy and delivery. She did not exhibit any abnormal symptoms until the age of five months, when she developed skin thickening over the extensor surface of her joints followed by progressive difficulty in extending her fingers. Shortly thereafter, she began to lose her hair. Her younger brother has a physical appearance similar to his sister. The living blood relatives of the parents are negative for the phenotype, and the parents have no blood relationship.
On examination, the girl was found to have an extremely short stature (height 93.5cm; weight 6.5kg) and a head circumference of 47.3cm. She was bald, had no eyebrows or eyelashes, and had prominent scalp veins. She also had prominent eyes, a small face and large head, a convex nasal ridge, micrognathia and crowded teeth, narrow shoulders and a horse-riding stance, and a high-pitched voice. There was a generalized paucity of subcutaneous fat. Her atrophic skin was thin, dry and taut, and was marked with diffusely scattered hyperpigmented foci. There was a fixed flexion deformity in all of her fingers. Her anterior fontanel was open (1.5cm×1.5cm).
Radiography revealed generalized and marked osteoporosis with relative expansion of the metaphyseal areas of her bones, a large cranium and a relatively small viscerocranium. Both her maxillae and mandibles were hypoplastic with crowded teeth, malocclusion and protrusion of her upper teeth. Both of her clavicles were completely absent, the bilateral posterior segments of her first to fourth ribs were partially osteolytic, and the costal head of her right 12th rib was absent. She had severe scoliotic deformities: her cervical segment showed fixed flexion deformities and her fifth lumbar segment had a slightly forward olisthe. There was complete osteolysis and resorption of the superior fragment of both radii, the inferior segment of her right ulnoradial joint had a dislocation, and there was an old, healed fracture of the inside of her right ulna. There were fixed flexion deformities of her phalanges: the middle phalanges of her fingers became more slender, and the distal phalanges of the second to fifth fingers were absent (Figure A-C).
Magnetic resonance imaging revealed normal brain tissue with mastoiditis of both middle ears. Our patient had a small pituitary gland with a concavity of the superior border (height about 1mm. Figure D). Audiologic testing revealed conductive hearing loss in the low-frequency range (250Hz to 500Hz) in both ears. Echocardiography revealed left ventricular hypertrophy with a mild regurgitation of the tricuspid valve and pulmonary valve (Figure D). Carotid ultrasonography detected a narrow carotid artery intima-media thickness.
Laboratory results of hepatic function and her levels of blood calcium, blood phosphonium, blood free tri-iodothyronine, free thyroxin, thyroid-stimulating hormone, serum cholesterol, triglyceride, lipoproteins, fast blood glucose, prothrombin time and hemoglobin were all within the normal ranges. Her renal function showed a low level of creatinine (29.6μmol/L; normal range 53 to 132.6μmol/L). Her platelet count was elevated.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [6.5, 'kg'], 'height': [93.5, 'cm']}",0.41088,0.39034,0.43142,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 93.5 cm. 
The patient's weight is 6.5 kg. 
Therefore, the patient's bsa is sqrt((6.5 (in kgs) * 93.5 (in cm))/3600) = 0.41088 m^2."
7322,60,Body Surface Area Calculator,physical,decimal,pmc-3892610-1,Extracted,"On September 15th, 2009, a 29-year-old woman, 61 kg, 1.69 m stature, Caucasian, with no comorbidities, post-graduated, Brazilian, from Recife-PE was submitted to an elective bilateral reductive mammoplasty on a private hospital of Recife-PE to remove 200 mL of each breast using the L technique for resections of excess of skin and breast tissue. Then an ampoule of adrenaline was infiltrated into her breasts, the bandage was realized using saline and Polivinilpirrolidone-iodine. The surgical procedure was concluded in 3 hours. The patient made her bandages at home using water, soap and an antiseptic solution of chlorhexidine gluconate. Healing occurred normally, with no trauma and no presence of inflammatory signs. One year after surgical procedure, on October 17th, 2010, the patient referred edema, heat and pain on her left breast. Although left breast presented no blush and normal aspect of scar.
It was requested a breast ultrasonography (USG) and it was prescribed a non-hormonal anti-inflammatory, Nimesulide 100 mg, one pill a day for 5 days, with no improvement of the signs and symptoms. USG revealed an image of a fluid collection filled by thin echoes, extending from 9 o’clock to 3 o’clock, with an antero-posterior diameter with approximately 2.3 cm, far around 2 cm of the skin with an increase of the echogenicity of the subcutaneous tissue on the region (). It was then prescribed treatment with cephalexin, 500 mg every six hours and Nimesulide, 100 mg, one pill a day for 5 days.
As there was no improvement of the clinical conditions, an aspiration of the fluid collection was performed in November 23rd, 2010 on patient’s left breast with an entry on the intern superior upper quadrant, obtaining a greenish secretion which was sent for automatized culture and antibiogram, both negative for bacterial growth. After the procedure, it was prescribed ciprofloxacin, 500 mg, 2 pills every twelve hours for 2 days and one pill every twelve hours totaling 10 days, without improvement of the condition. On November 30th, 2010, the patient was submitted to a surgery to drain the breast’s abscess, maintaining ciprofloxacin 500 mg, one pill every twelve hours, Diclofenac sodium, 100 mg one pill a day and Dipyrone one pill every six hours for 7 days.
The sample collected in this procedure was sent for automatized culture with antibiogram and for smear tests on acid fast bacilli (AFB), both showing negative results.
After the end of the treatment with antibiotics, on December 13th, 2010 an USG showed an increase of the echogenicity on the cellular subcutaneous tissue and on the breast’s fat, associated with 2 collections which presented debris in suspension and irregular and inaccurate contours, measuring: 8.8×3.1×1.7 cm (vol =24.2 cm3), located on the superior upper quadrants of the left breast and another with 2.2×1.2×0.8 cm (vol=1.1 cm3); deeper than the previous one, which was located on the transition of the left lower quadrants, presenting 2 reactive lymph nodes on the left axilla, measuring 1.8 cm and the 1.4 cm, respectively.
After confirming the presence of the collections, another aspiration was performed using USG, on the same breast in December 14th, 2010, and it was also requested in a private laboratory of the city. Another culture and cytological exam of the collected sample, showed one inflammatory cyst and growth of AFB on a specific culture medium, but the mycobacterium specie was not identified due to fungus contamination on the sample.
A Chest X-ray was requested, and it didn’t show abnormalities, another USG was performed on January 24th, 2011, which revealed a new fluid collection, homogeneous, measuring: 2.0×0.7×1.5 cm located on the internal superior upper quadrant of the left breast. It was then prescribed vibramycin, 100 mg, one pill every twelve hours and trimethropim sulfamethoxazole, 400/160, one pill every twelve hours for 6 months, and it was also requested a new drainage. The drained material was sent to the Public Health’s Central Laboratory – Dr. Milton Bezerra Sobral (LACEN-PE), being isolated non-tuberculous mycobacteria in the culture medium. Mycobacterium wolinskyi was identified by sequencing specific genes; this technique was performed at Aggeu Magalhães Research Center, FIOCRUZ-PE. As the patient presented an evident improvement of the clinical conditions, the treatment scheme proceeded for more 6 months, independent on the antibiogram’s result () remaining asymptomatic for almost 11 months.
After this period, on January 9th, 2012, the inflammatory signs and symptoms reappeared on the left breast, an USG showed 4 cystic images, the biggest at 12 o’clock measuring: 0.7×0.6 cm; the second had slightly thick walls associated with hyperechogenicity of the cellular subjacent subcutaneous tissue at 1 o’clock, measuring: 0.7×0.6×0.5 cm, far 1 cm of the skin and about 4 cm of the nipple; the third cyst presented an heterogeneous content with two adjacent cysts, located at 10 o’clock and measuring: 1.4×1.3×1 cm and 1.3×1.1×0.8 cm, far 3 cm of the nipple and 2 cm of the skin; and the fourth image was located at 5 o’clock measuring: 2.9×1.9×1 cm, far 1 cm of the skin and 4 cm of the nipple. The patient was then submitted to a new surgical procedure to drain the collection and to withdraw the necrotic tissue. This tissue culture revealed one more time the presence of Mycobacterium wolinsky, identified by sequencing specific genes. The prescribed therapy was an association of antibiotics, initially under hospital regimen, amikacin 1 g injectable per day with ciprofloxacin 500 mg every twelve hours and doxycycline 100 mg. Amikacin was maintained for 10 weeks under domiciliary regimen, 1 g intramuscular 3 times a week. The other 2 classes of antibiotics were also maintained for 6 months. After this period the patient was released from the therapeutic scheme with complete regression of the clinical symptoms.
The bacilloscopy performed with the samples was negative for AFB. The culture on Löwenstein-Jensen medium revealed AFB growth on less than 7 days, suggesting RGM. The colonies did not show any coloring, they were resistant to the para-nitrobenzoic acid (PNB) and to the Hydrazide of the 2-carboxilic acid (TCH); they did not show rope spoilage and the test for the presence of niacin was negative.
A 764-bp fragment was amplified and sequenced with primers MycoF (5_-GCAAGGTCACCCCGAAGGG-3_) and MycoR (5_-AGCGGCTGCTGGGTGATCATC-3_). A total of 5 μL of each DNA solution (50 μg/mL) was added to 45 μL of a PCR mixture containing 50 mM KCl, 20 mM Tris-HCl (pH 8.4), 2.5 mM MgCl2, 200 μM each dNTP, 1 μM primers, and 1.0 U of Taq DNA polymerase (Promega). PCR mixtures were heated at 95°C for 1 min and then subjected to 35 cycles of denaturation at 94°C for 30 s, annealing at 64°C for 30 s, and extension at 72°C for 90 s, with a final step of 72°C for 5 min. Amplicons were purified with GFX PCR DNA and a Gel Band purification kit (G&E) and sequenced in an ABI PRISM 3100 sequencer with a BigDye Terminator cycle sequencing kit (Applied Biosystems). The sequences found were edited and aligned by analyzing the sequencing electropherograms using the program BioEdit v7.0.9. The sequences obtained were compared with those deposited in the GenBank database by using BLAST (http://www.ncbi.nlm.nih.gov/BLAST). The isolate had partial sequence of the rpoB gene with 99% (683/689) similar to GenBank accession number AY262743, which corresponds to Mycobacterium wolinskyi type strain ATCC 700010. The in vitro susceptibility test to antibiotics was performed using the microdilution broth assay (MIC) ().",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.0, 'kg'], 'height': [1.69, 'm']}",1.69222,1.60761,1.77683,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 1.69 m, which is 1.69 m * 100 cm/m = 169.0 cm. 
The patient's weight is 61.0 kg. 
Therefore, the patient's bsa is sqrt((61.0 (in kgs) * 169.0 (in cm))/3600) = 1.69222 m^2."
7323,60,Body Surface Area Calculator,physical,decimal,pmc-5540565-1,Extracted,"A 29-year-old male of Turkish decent presented with progressive gait ataxia, external ophthalmoplegia, ptosis, sensorineural hearing loss (meanwhile supplied with cochlear implants), cachexia (body weight/height/BMI before HMD: 55 kg/1.55 m/22.9 kg/m2; after HMD: 50 kg/1.55 m/20.8 kg/m2), advanced leukencephalopathy (Fig. ) and recurrent, diarrhea since age 18 years. Clinical examination showed short stature (149 cm), dysmorphic auricles, congenital Pes cavus and severe demyelinating sensorimotor polyneuropathy. Serum lactate (2.8–3.1 mmol/l; reference range: 0.5–2.2 mmol/l) and CSF lactate (3.5–4.6 mmol/l; reference range: 0–2.2 mmol/l) were elevated. Whole-exome sequencing (WES) revealed a homozygous TYMP stop mutation (c.112G > T, p.Glu38Stop) confirming the diagnosis of MNGIE (for WES methods and family pedigree, see Additional file ).
Effectiveness of HMD was determined by the following predefined outcome measures: 25-m walking-time and -steps, vibratory sensation, nerve conduction studies and levels of thymidine and deoxyuridine in serum, urine and CSF. HMD was delivered for 12 months with an initial frequency of 3 times weekly, escalated to 4 times weekly after 6 months (for details of clinical and molecular outcome assessments and HMD parameters, see Additional file ).
After 12-month of HMD, all clinical outcome parameters indicated progression of disease, demonstrated by worsening of SARA score (Scale for the assessment of Ataxia; 11 to 13 points), decline in MoCA score (Montréal Cognitive Assessment; 27/30 to 24/30 points) and nerve conduction measures (Fig. ). Corresponding to these these clinical observations of progressive worsening, also the subject himself did not perceive any deceleration of disease progression within the 12 months of HMD compared to the pre-HMD disease progression.
Serial testing of serum and urine levels of thymidine and deoxyuridine showed transient decreases each time after dialysis, demonstrating a reproducible immediate effect of HMD. However, they returned to baseline levels within 24 h and did not decrease after 6 and 12 months (Fig. ). CSF levels changed neither short-term (within 24 h) nor long term (at months 6 and 12) (Fig. ).",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [50.0, 'kg'], 'height': [149.0, 'cm']}",1.43856,1.36663,1.51049,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 149.0 cm. 
The patient's weight is 50.0 kg. 
Therefore, the patient's bsa is sqrt((50.0 (in kgs) * 149.0 (in cm))/3600) = 1.43856 m^2."
7324,60,Body Surface Area Calculator,physical,decimal,pmc-7931020-4,Extracted,"A 77-year-old Caucasian male patient (body mass: 77 kg; height: 178 cm; BMI: 24.3 kg/m2) presented with a grade 2 [] open fracture of the femur (AO 33 C1) and a closed tibial and fibular fracture (AO 43 A3) following a bicycle accident (collision against a truck). He was treated with an ORIF and plate osteosynthesis of the femur (less invasive stabilization system (LISS) plate, DePuy Synthes, USA) as well as ORIF and plate osteosynthesis of the tibia (distal tibia LCP plate, DePuy Synthes, USA) and fibula (1/3 tubular plate, DePuy Synthes, USA). Eighteen months later an atrophic nonunion was diagnosed and revision surgery of both femur (LISS pate) and tibia (distal tibia LCP plate) was performed. This procedure included decortication, re-osteosynthesis, and application of autologous cancellous bone from the iliac crest. Intraoperative samples showed no sign of infection. The fracture of the femur showed normal healing. Once again, the tibial fracture showed no healing tendency and the diagnosis of an atrophic nonunion (a) was made 11 months after the revision surgery operation and 29 months after the initial injury. The patient was referred for further osteological treatment of the tibia. Biomechanical analysis showed a correct anatomical reduction and therefore the decision against further operations was made. Calcium and vitamin D supplementation was initiated and a teriparatide treatment was conducted over a period of 21 months. CTX increased by 83% after the teriparatide therapy. The fracture gap showed gradual callus build-up on the serial x rays (b,c). A radiological and clinical union was achieved 4 years after the initial injury (d).",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [77.0, 'kg'], 'height': [178.0, 'cm']}",1.95121,1.85365,2.04877,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 178.0 cm. 
The patient's weight is 77.0 kg. 
Therefore, the patient's bsa is sqrt((77.0 (in kgs) * 178.0 (in cm))/3600) = 1.95121 m^2."
7325,60,Body Surface Area Calculator,physical,decimal,pmc-8074484-1,Extracted,"A 21-year-old parturient (weight, 55 kg; height, 155 cm), gravida 1, with twin pregnancy at 34+ 5 weeks was scheduled to undergo planned cesarean delivery because of intrahepatic cholestasis of pregnancy (ICP). Her past medical history was unremarkable. She was not taking anticoagulants. Laboratory testing results were as follows: hemoglobin (Hb), 135 g/L; platelet count, 147 × 109/L; prothrombin time (PT), 12.5 s; activated partial thromboplastin time (APTT), 26.9 s; international normalized ratio (INR), 1.18; total bile acid (TBA), 21.3 umol/L; alanine aminotransferase (ALT) 78 U/L; aspartate aminotransferase (AST) 84 U/L. Base line heart rate was 79 beats/min, respiratory rate was 18 breaths/min, and blood pressure (BP) was 120/67 mm Hg.
CSE was attempted at the L3–4 intervertebral space using an 18G Tuohy needle (ZHEJIANG HAISHENG MEDICAL DEVICE CO., LTD). After loss of resistance to air, access to the epidural space was presumed and a 25G Sprotte needle was inserted; however, cerebrospinal fluid (CSF) outflow was not obtained. A second senior anesthesiologist then attempted to repeat puncture at the L3–4 level but failed to obtain CSF outflow. An attempt was made at the L2–3 interspace: breakthrough was felt with the spinal needle but CSF outflow was still not obtained. We considered that a “valve” may have formed because of the needle design, causing poor CSF outflow. Furthermore, puncture was difficult. Therefore, a trial dose of bupivacaine (2.5 mL, 0.5 % plain) was administered via the spinal needle to verify subarachnoid space access. This produced only asymmetric blockade. The left side was blocked up to T10 with almost no blockade on the right. Next, a trial dose of epidural lidocaine (3 mL, 1.5 % with 1/200,000 epinephrine) was administered, which resulted in no evidence of local anesthetic toxicity or total spinal anesthesia. Epidural 2-chlorprocaine (5 mL, 3 %) was then administered, which caused an unexpectedly high blockade above T2 as well as tinnitus, difficulty breathing, and inability to speak. The patient’s SpO2 gradually decreased and mask-assisted ventilation was initiated. However, the SpO2 continued decreasing to 68 % even with 100 % oxygen. Propofol 100 mg and succinylcholine 100 mg were administered intravenously and a 6.5 mm internal diameter endotracheal tube was inserted under video laryngoscopic guidance. Her SpO2 increased to 100 % and the twins were delivered. Intraoperative blood loss was 400 mL and 1000 mL of crystalloid fluid was infused. However, the patient’s BP decreased to 80/40 mm Hg a few minutes before surgery was completed, which responded to repeated administration of phenylephrine. Ten minutes after the operation, the patient was awake with a normal tidal volume and the endotracheal tube was removed. Her level of anesthesia remained above T2 and she was unable to move her hands. SpO2 remained at 97 % with face mask oxygen and she was transferred to the intensive care unit for further observation. Two hours after surgery, sensation and movement in her right leg had recovered; however, her left leg remained numb and paralyzed. Left leg sensation and motor function completely recovered 3 h later. She denied headache, low back pain, or other neurologic deficit. It was unclear why sensorimotor recovery was significantly slower on the left. Magnetic resonance imaging (MRI) suggested a small (no more than 3 mL) subdural hematoma extending from T12 to the cauda equina (Fig. ). Postoperative PT, APTT, and INR were 23.4 s, 27 s, and 1.21, respectively. Sensory examination was normal. A neurosurgical consultant recommended in-hospital observation as hematoma absorption was expected. The patient was discharged 6 days after surgery. One month later, repeat MRI was normal.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.0, 'kg'], 'height': [155.0, 'cm']}",1.53885,1.46191,1.61579,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 155.0 cm. 
The patient's weight is 55.0 kg. 
Therefore, the patient's bsa is sqrt((55.0 (in kgs) * 155.0 (in cm))/3600) = 1.53885 m^2."
7326,60,Body Surface Area Calculator,physical,decimal,pmc-7201552-1,Extracted,"A 67-year-old woman was diagnosed with secondary coxarthrosis due to developmental dysplasia of the hip with high hip center. She presented to our hospital for right coxalgia and gait disability due to leg length discrepancy. The contralateral side of her hip joint showed radiographical osteoarthritic change with acetabular dysplasia; however, the symptoms were mild. She was on an aspirin regimen due to a past history of angina. Her height, body weight, and body mass index were 161 cm, 61 kg, 23.5 kg/m2, respectively. She was limping with a T-cane, and her activities of daily living were considerably limited because of right coxalgia. Flexion and external rotation contractures were notable in the right hip joint (), and the right leg length was 2 cm shorter than the left side by measuring the spinal malleolar distance. A radiograph of the hip joint showed right subluxated osteoarthritis classified as Crowe's group 3 [] (). Scoliosis with the convex to the right topped the L1 vertebrae, and a Cobb angle of 22 degrees was measured via standing lumbar anteroposterior radiograph (). Flexion contracture of the hip joint caused an increase in lumbar lordosis, and the pelvis was anteverted in the lateral lumbar to pelvic radiograph (). The femorotibial angle (FTA) was used to determine the standing bilateral lower limb alignment; the right and left legs measured 178 and 173 degrees, respectively (). The values of dual-energy X-ray absorptiometry (DEXA) are shown in ; the right femoral neck decreased slightly, but the others were in the normal range. Laboratory findings were C-reactive protein (CRP): 0.04 (normal range: 0-0.5 mg/dl); alkaline phosphatase: 196 (40-150 IU/l); calcium: 9.6 (8.4-10.2 mg/dl); phosphorus: 3.6 (2.3-4.7 mg/dl); and albumin (3.9-4.9 g/d). Bone turnover markers were tartrate-resistant acid phosphatase 5b (TRACP-5b), 516 (premenopausal normal range: 120-420 mU/dl) and total procollagen type 1 N-terminal propeptide (total P1NP), 45.5 (26.4~98.2 ng/ml). She had no fracture episodes, including fragility fractures.
Cementless total hip arthroplasty with acetabular reconstruction using a bulk bone graft was performed in this case (Continuum Acetabular System Trabecular Metal Shell, Biolox Delta Modular Ceramic Head, Taperloc Complete Primary Femoral Porous Coated Stem Reduced Distal High Offset type: Zimmer Biomet, TN, USA) (). The center of the femoral head moved inferiorly and medially (21 and 45 mm, respectively) postoperation. The leg length discrepancy was resolved in radiographic measurement. Full weight bearing was allowed immediately after surgery as postoperative therapy. Her postoperative process was successful; she could ambulate without a cane three months after the surgery.
However, she presented with right lateral ankle pain during ambulation and edema of the right foot, without any episode of trauma five months after surgery. A few days later, she visited a different hospital for her symptoms and a radiograph of the right ankle joint was obtained, which did not reveal an obvious fracture (Figures and ). The symptoms persisted and she visited our hospital six months after the surgery. A physical examination revealed localized swelling and tenderness around the right lateral malleolus. A radiograph of the right ankle joint revealed a transverse fracture 5 cm proximal to the lateral malleolus tip (Figures and ). Right and left standing lower limb alignments measured 168 and 176 degrees, respectively, via FTA (). A loosening of the implant was not obvious and the grafted bulk bone appeared to union in the radiograph of the hip joint (). MRI of the ankle joint showed bone marrow edema of the fibula and soft tissue edema. There were no findings of fracture and edema in the tibia ( and ). These image results demonstrated an isolated distal fibular fracture. Regarding the range of motion six months after the surgery, flexion and external rotation contractures improved obviously compared to the preoperative value (). The value of the 25(OH) vitamin D was 9.0 ng/dl, and she was diagnosed with vitamin D deficiency. We considered this fracture a result of the increased stress concentrated on the distal fibular from the lower limb alignment change following the total hip arthroplasty. Factors of fragility fracture, such as vitamin D deficiency and local osteoporosis from disuse, might also contribute to this etiology. We administered eldecalcitol 0.75 μg per day orally for vitamin D deficiency and a U-shape splint for fracture. Weight bearing was allowed with splint and T-cane use. Bone union was confirmed on a follow-up radiograph three months after splinting (). The resultant recovery process was favorable.
Informed consent to be published for publication was obtained from the patient, and this study was approved by our institution's ethics review board.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [61.0, 'kg'], 'height': [161.0, 'cm']}",1.65168,1.5691,1.73426,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 161.0 cm. 
The patient's weight is 61.0 kg. 
Therefore, the patient's bsa is sqrt((61.0 (in kgs) * 161.0 (in cm))/3600) = 1.65168 m^2."
7327,60,Body Surface Area Calculator,physical,decimal,pmc-6379869-1,Extracted,"A 41-year-old woman with refractory hypothyroidism was referred to our hospital. She was diagnosed with Graves' disease with thyrotoxicosis at the age of 36 years (thyroid weight: 51.1 g, TSH: <0.001 μU/mL (reference range; 0.4 to 4.0), FT3: 21.85 pg/mL (reference range; 2.36 to 5.00). FT4: 4.00 ng/dL (reference range; 0.88 to 1.67), TSH receptor antibody (TRAb) 22.7 IU/L (reference range; < 2.0)). Neither methimazole, iodine potassium, nor three times of 131I ablation therapy ameliorated thyrotoxicosis. At the age of 39 years, she underwent total thyroidectomy, and oral LT4 replacement was initiated after surgery. Although the dose of LT4 was increased to 650 μg/day (11.8 μg/kg/day), with 150 μg/day of liothyronine (LT3) also being administered, severe hypothyroidism persisted.
She had general fatigue, mild diarrhea, anasarca, hair loss, peripheral coldness, and dry skin. She was hospitalized for further examination to exclude malabsorption.
She was 161.6 cm in height and 55 kg in weight and had a body temperature of 36.3°C. Physical examinations showed a blood pressure of 101/67 mmHg with a heart rate of 56 beats/min, and laboratory findings revealed anemia, mild renal dysfunction, and hypercholesterolemia. Her serum TSH levels were extremely high as 146.8 μIU/mL and FT3 and FT4 levels were undetectable (). Glucose tolerance (fasting plasma glucose of 71 mg/dL and HbA1c of 5.4%) and adrenal and pituitary hormone levels were within normal ranges. Autoimmune antibodies other than thyroid peroxidase antibody (TPOAb) were all negative (). Ultrasonic cardiography showed pericardial effusion with normal cardiac output, and electrocardiography revealed a very low voltage and mild bradycardia (data not shown). She was not receiving any concomitant medication that may have interfered with the absorption or metabolism of LT4 []. Her serum albumin levels were within normal range, suggesting no evidence of malabsorption (). Moreover, anemia and hypocalcemia prior to admission to our hospital were successfully treated by the administration of iron and calcium, respectively. Helicobacter pylori and other gastrointestinal tract infections were negative. A stool examination was normal. Upper and lower gastrointestinal endoscopies were performed and were also normal. Duodenal biopsy was performed and did not show pathological abnormalities consistent with malabsorptive disorder. After her admission to our hospital, the patient was handed LT4 tablets by nurses every morning; however, her intake was not confirmed.
Since the additional rectal administration of LT4 suppository preparation (100 μg/day) did not ameliorate hypothyroidism, we attempted its intravenous administration to treat refractory hypothyroidism under the permission and approval of the Ethical Committee of Tokyo Medical and Dental University Hospital and written informed consent was obtained from the patient and her father. An intravenous LT4 formula was dispensed in the Department of Pharmacy of the Tokyo Medical and Dental University hospital, following a previously reported prescription []. In brief, LT4 sodium salt pentahydrate (Sigma-Aldrich T2501, #6106-07-6) was dissolved by 0.1 N NaOH solution and diluted to a concentration of 200 μg/2 mL by saline. A total of 300 μg of LT4 was then diluted in 50 mL of saline and administered to the patient by intravenous drip infusion in 15 min. Since the patient had suffered from severe hypothyroidism for a long time, we did not really know whether her adrenal function was potentially normal or not. Therefore, prior to the intravenous administration of LT4, we administered 100 mg/day of hydrocortisone (HDC) in an intravenous drip to avoid relative adrenal insufficiency caused by rapid increases in thyroid hormone levels. Six days after the daily intravenous administration HDC, her thyroid hormone levels markedly improved. Therefore, we tapered oral administration of LT4 to 200 μg/day and intravenously a bolus of LT4 was administered (100 μg/day). Following the intravenous administration of a single bolus of LT4 (100 μg/day), her serum FT4 levels were rapidly and markedly increased in 1 hour (). At the time of discharge, we decided to administer 200 μg/day of LT4 orally without the intravenous administration. Since we had already administered 100 mg/day of HDC in an intravenous drip for 10 days, we tapered oral administration of HDC to 20 mg/day upon the discharge. However, 7 days after her discharge, her thyroid hormone levels markedly decreased under the prescription. Thus, in the outpatient clinic, we administered 300 μg of LT4 by intravenous bolus injection weekly for several weeks. Then, we examined the time course of serum FT4, FT3 and TSH levels for optimization (). Serum FT4 and FT3 levels increased within 3 days of the administration and deceased thereafter (Figures and ). Within seven days following the bolus intravenous administration, serum FT4 and FT3 levels remained mostly within normal range. Serum TSH levels increased again 14 days after the intravenous administration of a bolus of LT4 (300 μg) in accordance with the decreases observed in serum FT4 and FT3 levels (). Based on these results, we selected the weekly intravenous administration of LT4 (300 μg). Since then, her serum FT4 and FT3 levels had been maintained as low-normal with the weekly intravenous administration of LT4 for 14 months, whereas serum TSH levels had vary (). At the time of the intravenous bolus administration of high dose LT4 (300 μg) in the outpatient clinic, since HDC administration was already started, we decided to administer 20 mg/day of PSL orally instead of increasing the dose of HDC to avoid relative adrenal insufficiency. However, no symptom of adrenal insufficiency was found and her plasma ACTH and serum potassium levels decreased, possibly due to the administration of PSL. Therefore, we tapered the dose of PSL to 10 mg/day in a month after the onset of the weekly intravenous administration of LT4 (300 μg). Thereafter, we carefully tapered the daily doses of PSL by 1 mg per month to avoid steroid withdrawal syndrome and subsequently withdrew PSL administration ().
Twelve months after weekly intravenous administration of LT4 (300 μg), her hemoglobin levels increased, while serum creatinine, low-dense lipoprotein cholesterol, creatine kinase, and prolactin levels decreased to the normal range. No liver dysfunction or cardiovascular events were detected (). Under oral administration of 200 μg/day of LT4, we attempted the intravenous administration of LT4 (300 μg) once in two weeks, which resulted in the relapse of severe hypothyroidism, suggesting the pseudomalabsorption of LT4 due to poor compliance (). We then attempted the single oral bolus administration (1400 μg) under direct observation instead of the weekly intravenous administration of LT4 [, ]. The dose of LT4 selected was 7-fold the usual daily dose, which was 200 μg/day [, ]. Following the oral administration of a single bolus of LT4, her serum FT4 levels rapidly elevated within 2 hours (0.52 to 4.56 ng/dL) as shown in . Her serum FT4, FT3, and TSH levels were maintained within normal range for 15 days after the single bolus oral administration, and hypothyroidism relapsed thereafter (). Based on the results, we employed 700 μg of LT4 for a weekly oral administration protocol, which was 100 μg of LT4 daily, because when we administered 1400 μg of LT4, her FT4 levels after 2 hours were extremely high, which were clearly harmful and had remained elevated for more than one week. Under the weekly oral administration of 700 μg of LT4, her serum FT4 and FT3 levels were elevated for 2 hours (FT4: 0.96 to 1.36 ng/dL, FT3: 1.41 to 1.56 pg/mL), and TSH levels decreased (52.8 to 48.6 μIU/mL) without liver dysfunction or electrocardiogram abnormalities (). Her serum FT4 and FT3 levels were maintained within normal ranges for 8 days after the single bolus oral administration, which demonstrates the relevance of the weekly oral administration of 700 μg of LT4 ().
Six months after the weekly oral administration of LT4, her renal and liver dysfunction and lipid profile improved (). We concluded that she developed severe hypothyroidism due to poor compliance to the daily oral LT4 replacement, even though she denied the poor compliance. Shi is currently being followed up at the psychiatric clinic. To date, her euthyroid status is maintained under the weekly oral administration of LT4 (700 μg) for two years.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.0, 'kg'], 'height': [161.6, 'cm']}",1.57127,1.49271,1.64983,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 161.6 cm. 
The patient's weight is 55.0 kg. 
Therefore, the patient's bsa is sqrt((55.0 (in kgs) * 161.6 (in cm))/3600) = 1.57127 m^2."
7328,60,Body Surface Area Calculator,physical,decimal,pmc-6967071-1,Extracted,"A 77-year-old man, 55 kg in weight and 165 cm in height, was scheduled to undergo m-ECT, due to a decreasing efficacy of drug treatment for depression over 9 years.
Seven years earlier, coronary computed tomography (CT) showed two CAAs with diameters of 7 × 8 mm and 6 × 11 mm at the distal first diagonal branch of the left coronary artery and right ventricular fistula formation (Fig. ). The diameter of CAAs had no changes during the follow-up observation for 7 years. In adenosine myocardial load scintigraphy as a preoperative examination, neither myocardial ischemia nor infarction was detected. We surmised that the infarct range of the heart would be limited even if a thrombus was formed because the CAAs were located at the distal side of the left first diagonal branch. For that reason, we decided to prioritize m-ECT for depression rather than treatment for the CAAs.
Upon entering the operation room for the first m-ECT, the patient exhibited noninvasive blood pressure (NIBP) of 124/79 mmHg, and the BP on the ClearSight™ system was 132/74 mmHg (Fig. a). For setting the ClearSight™ system, we measured NIBP five times and confirmed that there was not much difference between NIBP and BP on the ClearSight™ system, and blood pressure was measured by this system throughout the procedure. General anesthesia was induced with propofol 1 mg kg-1, and after he lost consciousness, rocuronium 0.35 mg kg-1 was administered. Nine minutes after rocuronium administration, the psychiatrist performed electrical stimulation. As soon as the seizure started, HR increased from 83 beats min-1 to 102 beats min-1, and BP increased from 101/59 mmHg to 143/85 mmHg. The seizure duration was 51 s on the electroencephalogram. When the seizure stopped, the BP rapidly decreased to 120/75 mmHg without the use of any antihypertensive agent. After completing the seizure, sugammadex sodium 2 mg kg-1 was administered. When the patient regained consciousness, the BP was 112/71 mmHg. Neither asynergy nor pericardial effusion was detected by transthoracic echocardiography.
At the second m-ECT performed 4 days after the first procedure, when entering the operation room, NIBP was 144/111 mmHg, and the BP was 152/89 mmHg (Fig. b). General anesthesia was performed by referring to the first m-ECT. As soon as the seizure began after electrical stimulation, the BP increased from 155/93 mmHg to 186/105 mmHg. Therefore, nicardipine 0.01 mg kg-1 was administered, and BP decreased to 155/89 mmHg immediately. After completing the seizure, the BP was 164/92 mmHg. The seizure duration was 50 s on the electroencephalogram. We confirmed that there was no asynergy or pericardial effusion in the transthoracic echocardiography when he regained consciousness.
Both m-ECTs increased HR and BP. However, no decrease in HR or BP due to parasympathetic nervous stimulation or asystole was recognized. With reference to the first and second m-ECTs, we administered nicardipine hydrochloride prophylactically prior to the start of electrical stimulation every time after the third procedure. We performed a total of 10 m-ECTs, and the maximum NIBP in the all m-ECT procedures was 171/99 mmHg.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.0, 'kg'], 'height': [165.0, 'cm']}",1.58771,1.50832,1.6671,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 165.0 cm. 
The patient's weight is 55.0 kg. 
Therefore, the patient's bsa is sqrt((55.0 (in kgs) * 165.0 (in cm))/3600) = 1.58771 m^2."
7329,60,Body Surface Area Calculator,physical,decimal,pmc-4412829-1,Extracted,"66 year old woman (156 cm, 80 kg, BMI 32) presented for elective mastectomy due to breast cancer. She suffered from severe COPD and also bullous emphysema. FVC 1.59 l; FEV1 0.55 l; FEV1 %FVC 34.6. She was on home oxygen therapy. Chronic right heart failure, hypertension and obesity were the other problems.
The paravertebral block was performed using the multi-shot percutaneous technique at Th3, Th4, Th5 and Th6. We used 22 ml of 0.75 % ropivakaine with 0.2 mg of fentanyl. For confirmation, of proper analgesia range, control of temperature changes, using infrared camera was performed. Then light general anesthesia with laryngeal mask (LMA) and sevoflurane was performed.
Infrared photo were made from around 0.5 m distance with FLIR i7 camera, with preservation of proper standards []. Patient was uncovered while performing the exam. First picture was made before performing of paravertebral blockade procedure. Paravertebral multi-shot procedure took 6 min to perform. First control photo was made 20 min after the blockade and next 10 min after. Temperature average was marked for chosen representative area for every segment needed to be anesthetized to perform planed surgery. For every marked area we observed rise in temperature reading from infrared camera photo, which was indirect confirmation of proper paravertebral blockade. Data shown in Table , Fig. .
Similar method of confirmation was previously used in S.P.S Cheema study of paravertebral analgesia. They have received confirmation of proper range of analgesia corresponding to ipsilateral temperature changes marked in infrared technique in six patients. Thus different level of paravertebral block was used in that study [].
Infrared photo showed rise of temperature count in every marked region after 20 min from injection. Latter infrared temperature reading also showed further increase of marked temperature confirming sympathetic nervous system blockade and indirectly proper range of analgesia. Example infrared pictures are in Figs. and .
The patient received very good intraoperative analgesia with high cardiovascular stability and very good respiratory function preservation.
There were no hemodynamic and pulmonary complications postoperatively.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [80.0, 'kg'], 'height': [156.0, 'cm']}",1.8619,1.7688,1.955,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 156.0 cm. 
The patient's weight is 80.0 kg. 
Therefore, the patient's bsa is sqrt((80.0 (in kgs) * 156.0 (in cm))/3600) = 1.8619 m^2."
7330,60,Body Surface Area Calculator,physical,decimal,pmc-7512091-1,Extracted,"Our patient, a 12-year-old girl (160 cm, 45 kg), presented at the emergency department for febrile abdominal pain with repeated vomiting after a violent physical aggression 12 hours before. An adolescent boy (175 cm, 60 kg) tied up the patient and jumped on her belly and kicked her several times. Heart rate and blood pressure were in the normal range.
The first blood tests showed increased plasma lipase (10 N) and liver cytolysis (10 N) without cholestasis or haemostasis disorders, suggesting acute posttraumatic pancreatitis. Furthermore, biological results showed metabolic acidosis with increased anion gap and normal plasma lactate level and acute renal failure (BUN: 25 mmol/L, serum creatinine: 503 umol/L). There were no electrolyte disturbances, but there were proteinuria (240 mg/mmol creatU) and hypoalbuminaemia (25 g/L), normal phosphate and calcium levels, increased LDH (3826 UI/L) and CPK (924 UI/L), and microscopic hematuria without myoglobinuria. There was no evidence for abdominal compartment syndrome.
She had normocytic anemia (Hb: 10.4 g/dL), without schistocytes, and elevated inflammatory markers (CRP: 311 mg/L and leucocytes: 24 × 109/L including 20 × 109/L neutrophils and fibrinogen at 7.1 g/L).
A CT scan performed 12 hours after initial presentation () revealed a haemoperitoneum without pneumoperitoneum, an increase of pancreatic head size, and a heterogeneous and bilateral diminished enhancement of the kidney, suggestive of bilateral renal necrosis.
A second CT scan was performed on day 7 (), showing a bilateral pleural, pericardial, and peritoneal effusion and persistence of lesions compatible with infarction in multiple zones of the renal parenchyma, with a patchy distribution. No artery dissection and no thrombosis were identified. A unilateral sign of left renal arterial thrombosis was suspected but identified as an artefact because there was no blood flow interruption.
A Doppler sonography on day 15 confirmed the integrity of the blood flow, especially at the renal artery ostium. Doppler sonography was repeated several times during the first three months after initial presentation and blood flow remained normal.
As no causative lesion could be identified on vascular CT scans, we performed a renal biopsy on day 7, which revealed complete ischemic necrosis of the renal parenchyma, affecting the proximal and distal tubules, but also the glomeruli and interstitial oedema.
A complete immunologic and viral work-up was negative. Renal failure with oliguria and hyperkalemia (creatinine max: 700 umol/L on day 5) required three hemodialysis sessions between day 5 and day 13. On day 18, she became polyuric requiring IV hydration. We noted a progressive improvement of her renal function with a stable serum creatinine level at 120 umol/L (eGFR: 65 ml/min/1.73 m2) after three months with normal blood pressure.
Abdominal pain decreased until day 30, and plasma lipase normalized after three months.
A thrombophilia work-up was performed after normalisation of inflammation parameters, and it showed an isolated deficiency in S protein (25%).
Ultrasound of the supra-aortic trunks and cardiac ultrasound were performed in order to rule out an embolic cause for renal ischemic necrosis. Preventive anticoagulation was started after confirmation of the S protein deficiency.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [45.0, 'kg'], 'height': [160.0, 'cm']}",1.41421,1.3435,1.48492,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 160.0 cm. 
The patient's weight is 45.0 kg. 
Therefore, the patient's bsa is sqrt((45.0 (in kgs) * 160.0 (in cm))/3600) = 1.41421 m^2."
7331,60,Body Surface Area Calculator,physical,decimal,pmc-3030032-1,Extracted,"A 50-year-old, 168 cm, 68 kg man without significant past medical history, was admitted to emergency room following a slip-down accident. On admission, the patient was alert and complained of moderate headache and dizziness. Cerebrospinal fluid (CSF) rhinorrhea and the left periorbital swelling were noted. Neurologic examination confirmed a Glasgow coma scale (GCS) of 15, and the pupils were symmetrical and reactive. Emergent skull X-ray series, facial computerized tomography (CT) and forearm X-ray revealed fracture of the frontal sinus, skull base, and right distal radius fracture. Computed tomography (CT) of the brain showed multiple small subdural pneumocephalus (). Emergent lumbar drainage was performed to manage CSF rhinorrhea and empirical prophylactic antibiotic treatment was given. Pneumocephalus subsided spontaneously within 7 days as confirmed by repeat CT scan (). With conservative treatment the patient's post-traumatic symptoms improved gradually in the surgical intensive care unit.
At post-trauma 8 days, following trauma, the patient underwent orthopedic surgery for distal radius fracture under general anesthesia. Preoperative laboratory findings were unremarkable. Intramuscular glycopyrrolate 0.2 mg was administered as premedication. Standard monitoring including BIS (A-2000 BIS XP: Aspect Medical System Inc. Natick, MA, USA) was applied before anesthesia induction. Anesthesia was induced with intravenous thiopental 300 mg and 0.5 µg/kg/min remifentanil infusion. Endotracheal intubation was performed after administering 50 mg rocuronium injection with 100% oxygen mask ventilation for 3 min without any difficulties. Anesthesia was maintained with oxygen (2 L/min)-air (2 L/min)-sevoflurane (1-1.5 vol%), continuous infusion of 0.125-0.5 µg/kg/min remifentanil and 10-15 mg/h of rocuronium. Tidal volume and respiratory rate were adjusted to maintain end-tidal carbon dioxide tension at 30-35 mmHg. The 3-hour operation was uneventful. Following surgery, the patient was extubated in the operation room after gaining consciousness and spontaneous ventilation. He was then transferred to the post-anesthesia care unit where he recovered fully without complications.
Ten hours later, the patient complained of severe, increasing, headache and exhibited abrupt deterioration in mental state. In view of his clinical aggravation, tension pneumocephalus was suspected. Neurologic examination demonstrated a GCS 11 and emergent brain CT showed large quantity of both frontal and right occipital pneumocephalus (). PPMV during anesthesia induction was suspected to be the cause of recurred pneumocephalus. High flow (8 L/min) oxygen via a partial non-rebreathing mask was administered in conjunction with supportive care for 2 days. The condition of the patient improved gradually and his GCS subsequently normalized. The last CT () performed 16 days following the operation revealed complete resolution of pneumocephalus. No infectious neuromeningeal complications occurred during hospitalization, and the patient was discharged at post-trauma day 32.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [68.0, 'kg'], 'height': [168.0, 'cm']}",1.78139,1.69232,1.87046,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 168.0 cm. 
The patient's weight is 68.0 kg. 
Therefore, the patient's bsa is sqrt((68.0 (in kgs) * 168.0 (in cm))/3600) = 1.78139 m^2."
7332,60,Body Surface Area Calculator,physical,decimal,pmc-5311478-1,Extracted,"The patient is a 59-year-old woman who was diagnosed with MCTD at the age of 52. She had been largely affected by systemic scleroderma, which resulted in reduced gastrointestinal motility. At 55 years of age, she experienced the onset of superior mesenteric artery (SMA)-like syndrome. Since then, she had received oral drugs, such as a proton-pump inhibitor and prednisolone, and a small amount of water and was provided sustenance with a total parenteral nutrition solution. She presented at our hospital with queasiness and peri-umbilical abdominal pain, which had persisted for 3 mo. She was 159 cm in height and weighed 41 kg.
Abdominal computed tomography scans showed a highly absorbing round substance, which was 7 cm in size, with layered calcification in the transverse colon, resulting in a diagnosis of fecaloma (Figure ). A colonoscopy revealed that a giant brown fecaloma occupied the lumen of the dilated transverse colon. A shallow 3-cm ulcer covered with a white coat was present near the fecaloma. The white coat was adherent to the fecaloma, suggesting it to be the cause of the ulcer (Figure ).
As the fecaloma was huge and actually occupied the colonic lumen, endoscopic extraction was attempted without laxatives because it was thought that the oral administration of laxatives, such as polyethylene glycol, might cause an intestinal obstruction. The surface of the fecaloma was hard, large and slippery, and fragmentation was not possible despite the use of biopsy forceps (Radial Jaw 4 Biopsy Forceps Standard Capacity, Boston Scientific, United States), an injection needle for endoscopic treatment (Impact Flow, Top, Japan), a needle knife (KD-10Q-1-A, Olympus, Japan), and a snare for endoscopic mucosal resection (EMR) (Snare Master, Olympus, Japan). Consequently, the surface of the fecaloma was shaved using jumbo forceps (Radial Jaw 4 Jumbo Cold Polypectomy Forceps, Boston Scientific, Japan) with about ten passes, which scraped the surface and made it possible to advance the forceps into the fecaloma. The same procedure was then repeated several hundred times, aiming for the center of the fecaloma and resulting in gradual fragmentation (Figure ). A total of 6 h over 2 d were required to break the fecaloma into fragments of a size that could pass through the anus. We used the midazolam as a sedative and the pentazocine as an analgesic. Midazolam was administered intravenously according to the degree of affliction and administered 5 mg per time of the procedure. Pentazocine was administered 15 mg per each procedure. The fecaloma was then eliminated using laxatives (Figure ).",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [41.0, 'kg'], 'height': [159.0, 'cm']}",1.34567,1.27839,1.41295,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 159.0 cm. 
The patient's weight is 41.0 kg. 
Therefore, the patient's bsa is sqrt((41.0 (in kgs) * 159.0 (in cm))/3600) = 1.34567 m^2."
7333,60,Body Surface Area Calculator,physical,decimal,pmc-3978401-1,Extracted,"A 78-year-old Japanese woman presented to our hospital because of colicky left abdominal pain. She had no history of any hip or neuromuscular disease. Her past medical history was only a Cesarean section. Physical examination revealed her height as 155 cm and weight as 35 kg (body mass index 14.5), and she was afebrile and in good general health. Blood examination and urinalysis was normal. She complained of left costovertebral angle tenderness. Computed tomography (CT) revealed dilated left ureter with herniation of the ureter into the sciatic foramen (). Drip infusion pyelography (DIP) identified that the left ureter was dilated and ran an unusual and convoluted course laterally through the pelvis (). We diagnosed her case as left ureteric sciatic hernia on the basis of these findings.
The patient's symptoms spontaneously are resolved before long. We followed up her closely without treatment for four months. However, the patient's symptoms recurred occasionally, and the left hydroureter remained unchanged. We decided to laparoscopically repair the hernia.
Operative Management. The patient was positioned in a head-down right semilateral position after general anesthesia. A balloon trocar was placed superior to the umbilicus. Three accessory ports (5 mm) were placed under direct laparoscopic control, and a three-dimensional (3D) laparoscopy system (Shinko Optical, Tokyo, Japan) was used. The peritoneum overlying the common iliac artery was elevated and transected, and the left ureter was identified on the artery. The ureter was mobilized all the way to the sciatic foramen by blunt dissection. The herniated ureter was reduced with light traction. A small defect was identified and repaired by suturing the edges of the surrounding connective tissue in order to close the hernia sac. The patient had an uneventful recovery. A month after the laparoscopic repair, DIP revealed that the left ureter had returned to its normal anatomical position without ureteral obstruction. Eight months after the surgery, the patient remains asymptomatic.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [35.0, 'kg'], 'height': [155.0, 'cm']}",1.22758,1.1662,1.28896,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 155.0 cm. 
The patient's weight is 35.0 kg. 
Therefore, the patient's bsa is sqrt((35.0 (in kgs) * 155.0 (in cm))/3600) = 1.22758 m^2."
7334,60,Body Surface Area Calculator,physical,decimal,pmc-3161475-1,Extracted,"A 48-years-old man weighing 68 kg, and of height 170 cm, was brought to the emergency unit after sustaining an open fracture right femur in a road traffic accident. He was scheduled for external fixation. On examination, the patient was conscious and well oriented. There was no history of loss of consciousness, vomiting or bleeding from oral and nasal cavities. The patient was a smoker since last 25 years (10 cigarettes/day). He denied any other medical comorbidity or surgical treatment in the past. Non-contrast computed tomography (CT) of head was normal, blunt trauma chest and abdomen was ruled out, no cervical spine injury was observed and hemodynamic parameters were also stable. Airway examination revealed mouth opening of 3 cm, thyromental distance of 8 cm, and full range of neck movements. Airway was classified as Mallampatti class II. Preoperative chest radiograph was normal and electrocardiography (ECG) showed normal sinus rhythm. Hemogram, coagulogram and renal and liver function tests were within normal limits. Functional capacity was more than 4 metabolic equivalents (METS).
After explaining the procedure and risk involved to the patient, written informed consent was taken. In the operating room, ECG, noninvasive blood pressure (NIBP), and pulse oximetry were attached and baseline parameters noted. An 18-G intravenous cannula was secured. Preoperative heart rate (HR) was 90/min, blood pressure (BP) 130/80 mm Hg, respiratory rate 16/min, and SpO2 (on room air) was 97%. Arterial blood gases (ABG) showed pH 7.35, pO2 98, pCO2 26, HCO3 15, BE –5, and SaO2 97%.
An 18-G epidural catheter was inserted via the L3-L4 space with the patient in a sitting position, using midline approach, and fixed at 11 cm. At the same level, 15 mg of 0.5% bupivacaine heavy was administered in the subarachnoid with a 25-G Quincke's spinal needle. Supplemented oxygen was administered by a venturi facemask (FiO2 0.5). A sensory loss up to T10 level was achieved with adequate motor paralysis after 9 min and surgery was then started. ECG, NIBP, and SpO2 were monitored. About 35 minutes after the administration of the subarachnoid block, the patient complained of dyspnea and chest pain. There was a sudden fall in SpO2 to 82% from 100%. The patient became tachypneic, started coughing and his HR rose to 126/ min. However, BP was within normal limits and ECG showed no marked changes. ABG showed pH 7.36, pO2 65.6, pCO2 45, HCO3 17.2, BE –6.1, and SaO2 82%. The patient was given continuous positive airway pressure of 100% oxygen with a facemask. SpO2 increased from 82% to 96%. A sample for D-dimer test was sent with the suspicion of pulmonary embolism. The patient had another bout of cough and SpO2 fell to 79-80%, BP to 81/54 mm Hg, and HR was 125/min. Dopamine infusion was started. On chest auscultation, there was reduced breath sounds on the right side. ABG values were pH 7.32, pO2 55.5, pCO2 54.2, HCO3 17, BE –6.9, and SaO2 80%. Anesthesia was induced with intravenous fentanyl 70 μg and thiopental 300 mg. Intravenous vecuronium 7 mg was administered and trachea secured with 8.5 mm endotracheal tube. The position of the tracheal tube was confirmed by capnography. Anesthesia was maintained with isoflurane in 100% oxygen. A chest radiograph was taken immediately, which showed a right-sided pneumothorax. Cardiothoracic consultation was taken and an underwater seal intercostal drain placed. After 5 minutes, HR improved to 80/min, BP 110/69 mm Hg, and SpO2 97%. The surgery lasted for 130 minutes and was completed without any further complication. Postoperatively, SpO2 was 97%, BP 105/62 mm Hg, and HR 113/min. The patient was shifted to the intensive care unit (ICU) and mechanically ventilated on Synchronized Intermittent Mandatory Ventilation (SIMV) mode with pressure support.
In ICU, the patient was monitored closely with invasive blood pressure, central venous pressure, oxygen saturation, airway pressure, and serial ABG. The D-dimer test report showed elevated values and color Doppler of lower limbs showed deep vein thrombosis of the right lower limb. Low-molecular-weight heparin therapy (enoxaparin 1 mg/kg subcutaneously 12 hourly) was started. Bed-side two-dimensional echocardiography in the ICU showed mild tricuspid regurgitation, mild pulmonary hypertension [RV systolic pressure (RVSP) = right atrial pressure (RAP) + 31 mm Hg], and hypokinesia of the right ventricular wall.
Postoperative analgesia was achieved with epidural injection of 8 ml of 0.125% bupivacaine 6 hourly, and epidural catheter was removed after 48 hours. The patient was weaned off ventilator support after three days and the trachea was extubated. Oxygen supplementation with venturi facemask (FiO2 0.5) was given for another two days. Inotropic support was removed on the fourth day and the patient shifted to the ward on the fifth day. Chest drain was removed after 9 days, and he was discharged to home on the 15th postoperative day.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [68.0, 'kg'], 'height': [170.0, 'cm']}",1.79196,1.70236,1.88156,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 170.0 cm. 
The patient's weight is 68.0 kg. 
Therefore, the patient's bsa is sqrt((68.0 (in kgs) * 170.0 (in cm))/3600) = 1.79196 m^2."
7335,60,Body Surface Area Calculator,physical,decimal,pmc-8637043-1,Extracted,"A 38-years-old, 124 kg, 163 cm, BMI 46.7 kg/ m2, American Society of Anesthesiologists Classification (ASA) III level female. She had a history of 5 years hyperthyroidism (propylthiouracil 300 mg qd.) and Obstructive sleep apnea (OSA) for over 10 years, abdominal hernia for over 2 years, habitual mandibular dislocation, thyroidectomy and two cesarean deliveries without any significant personal or familial past history. Long-term high calorie diet and eating habits led her to gain weight gradually. Preoperative airway assessment included a Mallampati class III, a 7.5 cm thyromental distance, a 5 cm interincisor distance and a 46 cm neck circumference. Physical examination showed nutritional obesity, abdominal distension, two old transverse scars in the lower abdomen, and a transverse scar of about 5 cm in the neck. Admission diagnosis: Morbidly obese, Obstructive sleep apnea, Abdominal hernia, Hyperthyroidism, After thyroidectomy, After cesarean section.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [124.0, 'kg'], 'height': [163.0, 'cm']}",2.36948,2.25101,2.48795,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 163.0 cm. 
The patient's weight is 124.0 kg. 
Therefore, the patient's bsa is sqrt((124.0 (in kgs) * 163.0 (in cm))/3600) = 2.36948 m^2."
7336,60,Body Surface Area Calculator,physical,decimal,pmc-7882454-1,Extracted,"A 44-year-old female patient, 148 cm height and 43 kg weight, was admitted to the First Affiliated Hospital, Zhejiang University School of Medicine for “blood in sputum for 11 months.” Chest computed tomography (CT) of the patient showed dilatation of the bronchi in both lungs and nodular high-density shadows and air crescent sign in some cavities (); hence, diagnosis of aspergilloma was considered. The patient was positive for specific IgG of Aspergillus fumigatus and galactomannan (GM) positive for alveolar lavage fluid in the right upper lobe. Subsequently, A. fumigatus was cultured, and the diagnosis was CPA. Voriconazole (VRCZ) tablets (200 mg every 12 hours) were taken orally from January 22, 2019. The patient had a history of rheumatoid arthritis and regularly administered leflunomide tablets 10 mg QD for a long duration and had a history of sinus tachycardia, as well as metoprolol sustained-release tablets (47.5mg QD) for a long period.
Before administering VRCZ, the liver enzymes and the total cholesterol were normal, while the triglyceride was 2.64-fold of the upper limit of the reference value. After ingesting VRCZ tablets for 14 days, the liver enzyme levels were higher, while the blood lipids were similar to the baseline values. After administering the tablets for 30 days, the symptoms of blood in sputum disappeared. And the liver enzymes were normal while the blood lipids were significantly higher than the baseline values. Simultaneously, the trough concentration of VRCZ was 6.6 μg/mL. Considering the possibility of hyperlipidemia caused by the drug, VRCZ was withdrawn, and itraconazole (200 mg every 12 hours) was administered.
After 28 days of itraconazole treatment, the liver enzymes and blood lipids recovered to baseline levels. While, the patient’s symptoms of blood in sputum occurred.Then, the patient was given VRCZ tablets (200 mg every 12 hours) again.
After 24 days of VRCZ treatment, the liver enzyme levels were normal while triglycerides increased significantly, and the trough concentration of VRCZ was 3.2 μg/mL. The symptom of blood in sputum was improved significantly. The increase in blood lipids may be related to the trough concentration of VRCZ. The patient agreed to continue taking VRCZ tablets after communication. Therefore, the therapeutic regimen of voriconazole was adjusted to 100 mg every 12 hours. After 49 days of this therapeutic regimen, the liver enzymes and blood lipids recovered to the baseline levels again, with the trough concentration of voriconazole of 1.5 μg/mL. After 155 days of continuous use of antifungal agents, considering the full course, the voriconazole was withdrawn. During the administration and after the withdrawal of VRCZ, the liver enzymes and blood lipids were similar to the baseline levels. During the whole treatment process, the diet and living habits of the patients were consistent with those before the treatment, and no significant change was detected in height and weight compared to those before the treatment. During the treatment, the specific values of liver enzymes, total cholesterol, and triglyceride of the patient are shown in , .
According to the treatment process of the patient, Naranjo′s rating scale was used to evaluate the adverse reactions, and the final score was 10 points, establishing a positive correlation between VRCZ and dyslipidemia, which was likely to be related to the trough concentration of VRCZ.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [43.0, 'kg'], 'height': [148.0, 'cm']}",1.32958,1.2631,1.39606,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 148.0 cm. 
The patient's weight is 43.0 kg. 
Therefore, the patient's bsa is sqrt((43.0 (in kgs) * 148.0 (in cm))/3600) = 1.32958 m^2."
7337,60,Body Surface Area Calculator,physical,decimal,pmc-3385260-1,Extracted,"A 38-year-old woman was scheduled for elective surgery for a two liver hydatid cyst located in segment VII and VII diagnosed by computed tomography with a dimension of 5 × 6 × 5.5 cm. At the preoperative visit the patient measuring 176 cm and weighing 78 kg with a body mass index of 25.18 kg/m2. Her blood pressure was 132/67 mmHg, with a pulse rate of 82 beats/min. No personnel or familial history of allergy was documented. Preoperative examinations of the cardiovascular and respiratory systems were normal. Electrocardiography (ECG) and chest X-ray were unremarkable. Laboratory tests including alanine transaminase, aspartate transaminase, international normalized ratio, fibrinogen, urea, creatinine, and blood glucose concentrations were normal.
The day before surgery, a blood test with a request for a 2 pockets was made. After a premedication with hydroxyzine (75 mg), the patient was admitted in operative room where a standard monitoring including heart rate, arterial oxygen saturation (SpO2), and non invasive pression (NIP) has been installed. After a catheterization of a peripheral vein, an IV 2 g of cefazolin was administered without problems notably; the hemodynamic of patient remained stable. The initial parameters with a heart rate (HR) at 78 beats/min, NIP at 124/76 mmHg, and SpO2 at 99% have allowed induction of anesthesia with propofol (3 mg/kg), fentanyl (2.5 μg/ kg), and cisatracurium (0.15 mg/kg). Tracheal intubation with a normal tube was successful realized with a standard laryngoscope. The patient was connected to respirator and anesthesia was maintained with isoflurane (1%–1.5%) in a mixture of nitrous oxide and oxygen (50%:50%). With ventilation by a tidal volume of 480 mL, and rate of 13 breaths/min, SpO2 was 99%, capnography [endtidal CO2 (ETCO2)] was 38 mmHg and peak airway pressure (PAwP) was 21 cmH2O. Surgical incision was made after a bolus of fentanyl (50 μg). Five minutes after the opening of the second cyst (segment VIII), patient had presented hypotension (NIP: 65/34 mmHg), tachycardia (HR: 110 beats/min) without desaturation (SPO2: 98%). Surgical manipulations were stopped. Inhalator agent (isoflurane) was closed and oxygen fraction was increased to 100%. Pulmonary auscultation was normal and symmetric; in particular there was no wheeze. EtCO2 (39 mmHg) and airway pressure (20 cmH2O) had not changed. Monitoring did not notice any changes in ECG and no macroscopic evidence of infection was noted by surgeon. No cutaneous signs were noted on the face or neck. Blood loss was low (approximately ≈150 mL). Provisional diagnosis of anaphylactic shock was made. A second peripheral venous catheter (16 gauge), and arterial catheter were placed. Fluid resuscitation (saline 0.9%) 500 mL per 500 mL (with a total of 1500 mL) and IV boluses of ephedrine (30 mg total) allowed only a slight improvement (NIP: 69/43 mmHg). Epinephrine boluses (100 μg to a total of 300 μg) were administered and relayed by continuous infusion (0.08 μg/ kg/min) via a central venous catheter. This therapeutic has stabilized the hemodynamic status (NIP: 109/56 mmHg and HR: 90 beats/min) and so continue the surgery. A bolus of 200 mg of hydrocortisone was administered. No need for additional bolus of epinephrine or an increase in infusion rate were required for the rest of the surgery. After removing of surgical draping, presence of skin signs all over the body has attracted attention of the team [Figures and ]. Diagnosis of anaphylactic shock was then strongly suspected. Serum tryptase was not measured because of its nonavailability in our hospital. The patient was transferred to ICU. Postoperative course was unremarkable with extubation 1 h later and a withdrawal of drugs 3 h later. The patient was discharged home after 5 days of hospitalization.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [78.0, 'kg'], 'height': [176.0, 'cm']}",1.95278,1.85514,2.05042,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 176.0 cm. 
The patient's weight is 78.0 kg. 
Therefore, the patient's bsa is sqrt((78.0 (in kgs) * 176.0 (in cm))/3600) = 1.95278 m^2."
7338,60,Body Surface Area Calculator,physical,decimal,pmc-6966997-1,Extracted,"A 72-year-old woman (140 cm, 56.9 kg) complained of low back pain and numbness and was admitted to our institution for posterior lumbar interbody fusion (PLIF) at L5-S1 and partial laminectomy at L2-L4. She had a prior history of PLIF at L4-5 at 68 years of age. She had no significant medical history except hypertension but no history of epilepsy. Her preoperative laboratory tests were within normal limits. Anesthesia was induced with propofol 70 mg and remifentanil 0.3 μg/kg/min. The trachea was intubated with an aid of rocuronium 50 mg. Anesthesia was maintained with desflurane 3–4% and remifentanil 0.1–0.2 μg/kg/min. Fentanyl 300 μg and rocuronium 20 mg were added during surgery. Bispectral index (BIS) was not monitored. Cerebrospinal fluid (CSF) leakage was not detected, even when inflation of the lungs by employing sustained positive end-expiratory pressure of 20 cm H2O for 5 s. The intraoperative course was uneventful and her hemodynamics remained stable during the 4 h and 55 min surgery. A 5-mm-diameter subfascial drainage tube was placed on the dorsal side of the lamina and opened about 10 min before the surgery was completed. After she was moved to the supine position, all anesthetics were stopped and the muscular relaxant was reversed with sugammadex 100 mg. Immediately thereafter, she developed symmetric, generalized, tonic seizure beginning in the upper extremities and advancing to the lower extremities. The seizure was immediately suppressed with propofol 80 mg; however, the cause of the seizure remained unclear. In order to rule out intracranial hemorrhage, brain computed tomography (CT) was performed under sedation with midazolam 10 mg. Brain CT showed no hemorrhage (Fig. ). Arterial blood gas analysis showed normal acid-base balance, serum electrolytes, and glucose. Propofol was continued because of subsequent repeated seizure.
Although there was minimal output from the drainage tube, our surgical team suspected cauda equina incarceration or the other unknown cause of seizure in the surgical field, because they knew that any neurologic manifestation could appear by intracranial hypotension after spinal surgeries [, ]. Six hours after the initial surgery, the patient was taken back to the surgical suite to confirm and repair a suspected spinal dural laceration. The re-opened surgical field was wet with diluted blood. We suspected that the blood was diluted with the leaked CSF, because the fluid over there might not have the others of the CSF. However, an evident point of dural laceration was not found. There was no cauda equina incarceration. The dura was covered with fibrin glue.
On the first postoperative day, generalized seizure reappeared when sedation was held. Valproic acid 800 mg and levetiracetam 500 mg were added for anticonvulsive therapy. Brain magnetic resonance imaging (MRI) revealed a subarachnoid hemorrhage (SAH) at the right cerebellopontine angle (Fig. ). At that time, we retrospectively noticed that a CSF cavity on the post-surgical brain CT had not been present (Fig. ), suggesting intracranial hypotension. Ultimately, the cause of the seizure was thought to be SAH due to intracranial hypotension. The seizure resolved on postoperative day 2, and her trachea was extubated. She suffered severe headache with typical signs of a classic post-dual puncture headache. Therefore, she was maintained in the Trendelenburg position until postoperative day 3. She was discharged on postoperative day 27 without any neurologic sequelae, and valproic acid and levetiracetam were continued for an additional 3 weeks.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [56.9, 'kg'], 'height': [140.0, 'cm']}",1.48754,1.41316,1.56192,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 140.0 cm. 
The patient's weight is 56.9 kg. 
Therefore, the patient's bsa is sqrt((56.9 (in kgs) * 140.0 (in cm))/3600) = 1.48754 m^2."
7339,60,Body Surface Area Calculator,physical,decimal,pmc-5903165-1,Extracted,"A 69-year-old man complained of difficulty swallowing his morning medication and of variation in the time required to reach an “on” state. He was previously diagnosed with internuclear ophthalmoplegia at the age of 64 years, which had resolved in 1 day. The family and lifestyle histories were unremarkable.
At 60 years of age, the patient's left leg began dragging when he walked, and at 62 years dysarthria developed. Oral administration of L-DOPA 100 mg/carbidopa 10 mg (LDCD) was initiated based on a diagnosis of PD, and walking and dysarthria improved. At 64 years, the patient regularly began to choke during breakfast, and by 65 years, wearing-off phenomena had begun. At 66 years, it became difficult for the patient to receive oral medication, and he began consuming his medication with jelly. Between 65 and 66 years, his weight decreased from 73 kg to 65 kg. By 68 years, completing breakfast required 3–4 h. In the “on” state, the patient was independent in activities of daily living. At 69 years, LDCD 600 mg and entacapone 600 mg were each received in six portions, selegiline hydrochloride 10 mg in two portions, and zonisamide 25 mg and trihexyphenidyl hydrochloride 2 mg in one portion. To assist swallowing, tablets were wrapped in a water-soluble film, but it remained easier for the patient to swallow the wrapped tablets with jelly. However, he sometimes later expelled the tablets through coughing. Doses were frequently accompanied by “delayed-on” or “no-on” phenomena.
The patient's height was 162 cm and his weight was 55 kg. There were no auscultatory abnormalities of the chest or abdomen. Mild right flexion was observed in the standing position. The Mini-Mental State Examination score was 29/30. No abnormalities in cranial nerves, muscle strength, or deep tendon reflexes were found. No pathological reflexes were present. Muscle rigidity was observed in the neck and all four limbs, and the patient was without tremor. He could walk independently in the “on” state, but experienced retropulsion in the “off” state. The Hoehn and Yahr classification was stage III in the “on” state and stage IV in the “off” state. The “off” state was characterized by strong akinesia and bradykinesia, sialorrhea, reduced vocal intensity, and poor speech intelligibility; all symptoms improved in the “on” state.
There were no abnormalities in the general blood tests or on head magnetic resonance imaging (Fig. ). A videofluorographic examination of swallowing (VFG) was performed in which the patient consumed 10 mL of barium-containing thickened water (Ba) and four tablets wrapped in a water-soluble film. VFG showed that the tongue barely moved, and the time required for the Ba to pass the lower border of the mandible and transfer to the pharynx was 27 s (typically 2 s in normal individuals). A swallowing reflex was induced after the Ba reached the pyriform sinuses. The backward movement of the tongue root was very limited, and the tablets remained in the epiglottic vallecula (Fig. ). Respiratory status was unchanged, and no aspiration was observed. After consumption of the medication, 2 h were needed for the patient to reach the “on” state, at which point, tongue movement improved and nothing remained in the pharynx.
The patient was further examined with a L-DOPA test []. One tablet of LDCD was grounded and administered to the patient with jelly in a fasting state after he awakened in the morning. Blood levels of L-DOPA were measured from before the medicine was administered until 240 min afterward (seven time points), and symptoms of parkinsonism were assessed. The patient choked when swallowing the medicine and required suctioning during the L-DOPA test. There was no improvement in parkinsonian symptoms even 4 h after administration, and the blood L-DOPA level only rose to 0.78 nmol/mL (Fig. ).
The patient was shown a video of his swallowing process and was informed that in the “off” state his lingual movement was insufficient to transfer food from his mouth to his pharynx. Tongue resistance training was then initiated. First, the patient held the plastic probe of the tongue pressure-measuring instrument (25 × 1.8 mm) in his mouth. Then, he was asked to press the probe hard with his tongue tip. The probe was pressed between the tongue tip and the upper incisors for 5 s with maximum power, and the tongue pressure was measured. The patient performed this training five times before each meal. In addition, he was instructed to press his tongue tip to the palatal side of the upper incisors without the probe before swallowing.
The L-DOPA test was repeated 8 days after the training began. The patient swallowed the tablets quickly with jelly and reached the “on” state after 30 min, with improvements in akinesia, bradykinesia, hypokinetic dysarthria, and swallowing. The highest blood level of the drug was 9.99 nmol/mL 30 min after administration (Fig. ). The highest tongue pressure measured in the “on” state improved to 28.8 kPa from 23.7 kPa over 10 days. The frequency of reaching the “on” state 30 min after receiving the medicine increased from 2 times/week before training to 5 times/week after training. Additionally, transdermal rotigotine (RTG) was initiated at a maintenance dose of 9.0 mg. The patient reported improvement in swallowing, and the frequency of “no-on” phenomena decreased. The patient gained 3 kg 3 months after RTG treatment without edema.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [55.0, 'kg'], 'height': [162.0, 'cm']}",1.57321,1.49455,1.65187,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 162.0 cm. 
The patient's weight is 55.0 kg. 
Therefore, the patient's bsa is sqrt((55.0 (in kgs) * 162.0 (in cm))/3600) = 1.57321 m^2."
7340,60,Body Surface Area Calculator,physical,decimal,pmc-5597972-1,Extracted,"Patient 1 was a 19-year-old male, who had attended the endocrinology outpatient clinic since the age of 14 years, complaining from tall stature. His birth weight was 3150 g and he had a left undescended testis, that was rescued by hCG administration for 6 weeks when he was 2 years old. He was also diagnosed for a moderate mental and psychomotor retardation, crossness, uneasiness and he had a marked defective speech capacity. The cardiologic counseling revealed no abnormality.
On physical examination, he had high-arched palate, ptosis and scoliosis. At the age of 8 years, he weighed 56.2 kg (>97th percentile), he was 144.9 cm (>99th percentile) tall and had a cranial circumference (CC) that measured 56 cm (>97th percentile). At the age of 14 years, these measurements were, respectively, 97 kg (>97th percentile), 176 cm (90th percentile) and 57.5 cm (>97th percentile). The testicular volume (TV) was 4 mL bilaterally and both testes had an increased consistency. Basal serum luteotropin hormone (LH), follicle-stimulating hormone (FSH) and testosterone (T) levels were 5.61 IU/mL (normal values (n.v.): 1.5–9.3 IU/mL), 5.37 IU/mL (n.v.: 1.4–18.1 IU/mL) and 1.87 ng/mL (n.v.: 3–9 ng/mL), respectively. When he was 15 years old, the TV measured 8 mL bilaterally, and the T levels were 2.9 ng/mL. When he was 17 years old, he was at Tanner stage 3, he had a triangular distribution of pubic hair and a bilateral TV of 12 mL. Serum LH, FSH and T levels were, in turn, 4.8 IU/mL, 9.1 IU/mL and 3.96 ng/mL, and the IGF1 levels were 411.3 ng/mL (n.v.: 119–395 ng/mL). He was 180 cm (50th–75th percentile; target height: 166.5 cm) tall. At the age of 19 years, the sperm analysis detected a severe oligoasthenoteratozoospermia (total sperm count 0.5 million/ejaculate – n.v. >39 million/ejaculate, forward sperm motility 3% – n.v. >32%, total sperm motility 10% – n.v. >40%, normally shaped spermatozoa 2% – n.v. >4%).
Genetic analysis excluded both Prader–Willi and Kallmann syndrome (KAL1, FGFR1, PROK2, PROK2R were evaluated and no mutations resulted). He had a 46,XY karyotype and a 568 kb pure duplication on the 15q26.3 chromosome, diagnosed by array-CGH. This duplication was not detected in the mother. The father could not be evaluated because he was not alive. The patient sister had a normal psychophysical development, and she did not show overgrowth.",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [97.0, 'kg'], 'height': [180.0, 'cm']}",2.20227,2.09216,2.31238,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 180.0 cm. 
The patient's weight is 97.0 kg. 
Therefore, the patient's bsa is sqrt((97.0 (in kgs) * 180.0 (in cm))/3600) = 2.20227 m^2."
7341,60,Body Surface Area Calculator,physical,decimal,pmc-6506424-2,Extracted,"The second patient was a 20-year-old female (height: 1.52 m, weight: 79.8 kg) with a history of ileocolonic CD who had undergone an ileocecal resection five years prior. The patient was receiving adalimumab once every two weeks. The patient was admitted to the gastroenterology service due to abdominal pain of a few weeks' duration. The morning of the admission, the patient had multiple episodes of non-bloody, non-bilious emesis and non-bloody diarrhea. The patient's most recent colonoscopy from six months prior had demonstrated a tight surgical anastomosis through which the scope could not be passed. During her admission, contrast US demonstrated minimal enhancement of the surgical anastomosis and mild enhancement of the more proximal ileum, greater than seen near the anastomosis. The measured mean elastography value was 1.57 m/s at the surgical anastomosis. Kinetic perfusion parameters are reported in . MRE demonstrated mild hyperenhancement of the small bowel loops without definite wall thickening or mesenteric hyperemia. Additionally, there was no high-grade ileal stricture, abscess, or fistula that was demonstrated at that time ().",What is the patient's body surface area? Please output your answer in terms of m². You should use the patient's medical values and health status when they were first admitted to the hospital prior to any treatment.,"{'weight': [79.8, 'kg'], 'height': [1.52, 'm']}",1.83557,1.74379,1.92735,"For the body surface area computation, the formula is sqrt((weight (in kgs) * height (in cm))/3600, where the units of weight is in kg and the units of height is in cm.
The patient's height is 1.52 m, which is 1.52 m * 100 cm/m = 152.0 cm. 
The patient's weight is 79.8 kg. 
Therefore, the patient's bsa is sqrt((79.8 (in kgs) * 152.0 (in cm))/3600) = 1.83557 m^2."
7342,60,Body Surface Area Calculator,physical,decimal,pmc-5296625-1,Extracted,"A 42-year-old G2P1001 presented for a routine growth ultrasound at 36 wk 5 d. The fetus was found to have a vein of Galen malformation, which had not been identified during the 20-wk anatomy scan (Figure ). A review of her medical history was significant for a prior uncomplicated full-term vaginal delivery. Her living child is alive and well, meeting all appropriate milestones. The patient denied any significant family history for congenital anomalies or social history for toxic environmental or occupational exposures. Prenatal care was otherwise uneventful. Fetal MRI confirmed the diagnosis of VOGM, demonstrating a persistent median prosencephalic vein, which measured up to 22 mm in the transverse dimension and 74 mm in length (Figure and C). There was a network of feeding vessels (greater on the right as compared to the left) in the region of the medial temporal lobe, midbrain, and thalami, which likely represented feeder vessels emanating from the posterior cerebral arteries. Torcula and bilateral transverse sinuses were also enlarged. The lateral ventricles and cortical sulci were appropriate for the patient's gestational age. The infratentorial brain appeared normal, with no mass effect or midline shift.
A fetal echocardiogram showed cardiomegaly with preserved biventricular systolic function. The superior vena cava (SVC) was moderately dilated. The right atrium was severely dilated whereas the left atrium was only mildly dilated and there was an aneurysmal patent foramen ovale (PFO) with right to left shunting. The right ventricle (RV) was moderately dilated with qualitatively good RV systolic function. There was marked reversal of flow in the distal aortic arch, apparently draining predominantly to the brachiocephalic artery.
Over the next 2 d, repeat sonographic evaluation demonstrated new polyhydramnios and abnormal Doppler studies. The fetus developed an abnormal fetal heart rate tracing with areas of minimal variability and non-reactivity. At this point, because of the massive VOGM causing a steal phenomenon, evidence of heart failure, worsening dopp